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+FOS	drug	opioid	32407964	The consequences of exciting or destroying the prelimbic cortex (PrL) or the basolateral amygdala (BLA) remain unclear, including the effects on <b>morphine</b> induced conditioned taste aversion (CTA) in the conditioning and extinction phases, plasma corticosterone (CORT) levels, and c <strong>Fos</strong>/p ERK expressions in the subareas of the medial prefrontal cortex (i.e., PrL, infralimbic cortex [IL], cingulate cortex 1 [Cg1]), basolateral amygdala (BLA), central amygdala (CeA), hippocampus (i.e., CA1, CA2, CA3, and dentate gyrus [DG]), nucleus accumbens (NAc), lateral hypothalamus (LH), and piriform cortex (PC).
+FOS	addiction	aversion	32407964	The consequences of exciting or destroying the prelimbic cortex (PrL) or the basolateral amygdala (BLA) remain unclear, including the effects on morphine induced conditioned taste <b>aversion</b> (<b>CTA</b>) in the conditioning and extinction phases, plasma corticosterone (CORT) levels, and c <strong>Fos</strong>/p ERK expressions in the subareas of the medial prefrontal cortex (i.e., PrL, infralimbic cortex [IL], cingulate cortex 1 [Cg1]), basolateral amygdala (BLA), central amygdala (CeA), hippocampus (i.e., CA1, CA2, CA3, and dentate gyrus [DG]), nucleus accumbens (NAc), lateral hypothalamus (LH), and piriform cortex (PC).
+FOS	drug	opioid	32407964	During conditioning, excitation of the PrL glutamate neurons via NMDA injections disrupted <b>morphine</b> induced CTA and decreased plasma CORT levels; moreover, c <strong>Fos</strong> and p ERK expression was hyperactive in the PrL and IL but hypoactive in the Cg1 and BLA.
+FOS	addiction	aversion	32407964	During conditioning, excitation of the PrL glutamate neurons via NMDA injections disrupted morphine induced <b>CTA</b> and decreased plasma CORT levels; moreover, c <strong>Fos</strong> and p ERK expression was hyperactive in the PrL and IL but hypoactive in the Cg1 and BLA.
+FOS	drug	opioid	32407964	In extinction, excitation of the PrL glutamatergic neurons via NMDA injections facilitated <b>morphine</b> induced CTA extinction and did not affect plasma CORT levels; moreover, the expression of c <strong>Fos</strong> and p ERK was hypoactive in the Cg1, PrL, and IL but hyperactive in the BLA.
+FOS	addiction	aversion	32407964	In extinction, excitation of the PrL glutamatergic neurons via NMDA injections facilitated morphine induced <b>CTA</b> extinction and did not affect plasma CORT levels; moreover, the expression of c <strong>Fos</strong> and p ERK was hypoactive in the Cg1, PrL, and IL but hyperactive in the BLA.
+FOS	drug	cannabinoid	32353393	Locomotor activity and c <strong>Fos</strong> IR changes induced by <b>THC</b> challenge were altered by nicotine pre exposure and modified by age and sex.
+FOS	drug	nicotine	32353393	Locomotor activity and c <strong>Fos</strong> IR changes induced by THC challenge were altered by <b>nicotine</b> pre exposure and modified by age and sex.
+FOS	drug	cannabinoid	32353393	<b>THC</b> increased c <strong>Fos</strong> IR in the caudate, nucleus accumbens, stria terminalis, septum, amygdala, hypothalamus, and thalamus.
+FOS	drug	opioid	32341122	The effect of microbiome depletion on the activation of neuronal ensembles was measured by detecting <strong>Fos</strong> positive (<strong>Fos</strong>+) neuron activation during intoxication and withdrawal using a rat model of <b>oxycodone</b> dependence.
+FOS	addiction	dependence	32341122	The effect of microbiome depletion on the activation of neuronal ensembles was measured by detecting <strong>Fos</strong> positive (<strong>Fos</strong>+) neuron activation during intoxication and withdrawal using a rat model of oxycodone <b>dependence</b>.
+FOS	addiction	intoxication	32341122	The effect of microbiome depletion on the activation of neuronal ensembles was measured by detecting <strong>Fos</strong> positive (<strong>Fos</strong>+) neuron activation during <b>intoxication</b> and withdrawal using a rat model of oxycodone dependence.
+FOS	addiction	withdrawal	32341122	The effect of microbiome depletion on the activation of neuronal ensembles was measured by detecting <strong>Fos</strong> positive (<strong>Fos</strong>+) neuron activation during intoxication and <b>withdrawal</b> using a rat model of oxycodone dependence.
+FOS	drug	opioid	32341122	Daily <b>oxycodone</b> administration (2 mg/kg) increased pain thresholds and increased <strong>Fos</strong>+ neurons in the basolateral amygdala (BLA) during intoxication, with a decrease in pain thresholds and increase in <strong>Fos</strong>+ neurons in the periaqueductal gray (PAG), central nucleus of the amygdala (CeA), locus coeruleus (LC), paraventricular nucleus of the thalamus (PVT), agranular insular cortex (AI), bed nucleus of the stria terminalis (BNST), and lateral habenula medial parvocellular region during withdrawal.
+FOS	addiction	intoxication	32341122	Daily oxycodone administration (2 mg/kg) increased pain thresholds and increased <strong>Fos</strong>+ neurons in the basolateral amygdala (BLA) during <b>intoxication</b>, with a decrease in pain thresholds and increase in <strong>Fos</strong>+ neurons in the periaqueductal gray (PAG), central nucleus of the amygdala (CeA), locus coeruleus (LC), paraventricular nucleus of the thalamus (PVT), agranular insular cortex (AI), bed nucleus of the stria terminalis (BNST), and lateral habenula medial parvocellular region during withdrawal.
+FOS	addiction	withdrawal	32341122	Daily oxycodone administration (2 mg/kg) increased pain thresholds and increased <strong>Fos</strong>+ neurons in the basolateral amygdala (BLA) during intoxication, with a decrease in pain thresholds and increase in <strong>Fos</strong>+ neurons in the periaqueductal gray (PAG), central nucleus of the amygdala (CeA), locus coeruleus (LC), paraventricular nucleus of the thalamus (PVT), agranular insular cortex (AI), bed nucleus of the stria terminalis (BNST), and lateral habenula medial parvocellular region during <b>withdrawal</b>.
+FOS	drug	alcohol	32329567	Finally, we found that in mice pretreated with sazetidine A, <b>alcohol</b> induced <strong>Fos</strong> transcript in Th , but not Gad2 expressing neurons in the VTA as measured by increased <strong>Fos</strong> transcript expression.
+FOS	drug	opioid	32319158	<b>Morphine</b> improved the expression levels of orexin1 receptor (OX1R) and c <strong>FOS</strong>, the p/t ERK/PKC as well.
+FOS	drug	opioid	32319158	The c <strong>FOS</strong> protein level and p/t ERK/PKC were significantly elevated by <b>morphine</b> + OXA.
+FOS	addiction	relapse	32205443	shPKCδ CeL injections decreased <strong>Fos</strong> in CeL PKCδ expressing neurons, increased <strong>Fos</strong> in CeM output neurons, and reversed the inhibitory effect of social choice induced abstinence on incubated drug <b>seeking</b> on day 15.
+FOS	addiction	relapse	32205443	In contrast, shSOM CeL injections decreased <strong>Fos</strong> in CeL SOM expressing neurons, decreased <strong>Fos</strong> in CeM output neurons, and decreased incubated drug <b>seeking</b> after 15 forced abstinence days.
+FOS	drug	cocaine	32124535	c <strong>fos</strong> mRNA levels were investigated by quantitative polymerase chain reaction (qPCR) to measure neural activation after exposure to the <b>cocaine</b> associated context.
+FOS	drug	opioid	32113678	The nNOS PSD 95 coupling and c <strong>Fos</strong> expression in the medial prefrontal cortex (mPFC) was significantly increased after extinction of <b>morphine</b> CPP.
+FOS	addiction	reward	32113678	The nNOS PSD 95 coupling and c <strong>Fos</strong> expression in the medial prefrontal cortex (mPFC) was significantly increased after extinction of morphine <b>CPP</b>.
+FOS	addiction	relapse	32074627	Finally, we evaluated the effects of low dose guanfacine on BNST <strong>cFOS</strong> immunoreactivity and stress induced <b>reinstatement</b>.
+FOS	addiction	relapse	32051327	In both sexes, <b>relapse</b> after food choice induced abstinence was associated with increased expression of the activity marker <strong>Fos</strong> in OFC.
+FOS	addiction	relapse	32051327	We then determined projection specific activation of OFC afferents during the <b>relapse</b> test by using <strong>Fos</strong> plus the retrograde tracer cholera toxin B (injected into OFC).
+FOS	drug	opioid	32051327	Relapse to <b>fentanyl</b> seeking was associated with increased <strong>Fos</strong> expression in piriform cortex (Pir) neurons projecting to OFC, but not in projections from basolateral amygdala and thalamus.
+FOS	addiction	relapse	32051327	<b>Relapse</b> to fentanyl <b>seeking</b> was associated with increased <strong>Fos</strong> expression in piriform cortex (Pir) neurons projecting to OFC, but not in projections from basolateral amygdala and thalamus.
+FOS	drug	opioid	32032645	These compounds were also found to produce neuroadaptive changes as evidenced by the increased expression levels of c <strong>Fos</strong>, glucocorticoid receptor, N methyl d aspartate receptor1 and μ <b>opioid</b> receptor (21 & 28 d).
+FOS	drug	alcohol	31926294	Follow up studies did find however, that pharmacological inhibition of the EWcp increased body temperature and prevented <b>alcohol</b> induced increases in c <strong>Fos</strong> expression in the EWcp.
+FOS	drug	alcohol	31926294	Additionally, the present studies provide further evidence for the involvement of the EWcp in thermoregulation and help elucidate the molecular mechanism by which <b>alcohol</b> increases c <strong>Fos</strong> in the EWcp.
+FOS	addiction	reward	31836960	Excessive "disgust" was accompanied by recruitment of neural <strong>Fos</strong> activation in several subcortical structures, including the posterior medial shell of nucleus accumbens (which also contains another GABAergic "disgust" inducing "<b>hedonic</b> cold spot"), the bed nucleus of stria terminalis, lateral habenula, hypothalamus, and midbrain ventral tegmentum.
+FOS	addiction	reward	31836960	<strong>Fos</strong> suppression was found in cortical limbic regions, including previously identified <b>hedonic</b> hot spots in the anteromedial orbitofrontal cortex and posterior insula.
+FOS	drug	alcohol	31818977	Using RNAScope in situ hybridization to characterize activity of different VP cell types during relapse to <b>alcohol</b> seeking provoked by renewal (context induced reinstatement), we found that VP Gad1 and parvalbumin (PV), but not vGlut2, neurons show relapse associated changes in c <strong>Fos</strong> expression.
+FOS	addiction	relapse	31818977	Using RNAScope in situ hybridization to characterize activity of different VP cell types during <b>relapse</b> to alcohol <b>seeking</b> provoked by renewal (context induced <b>reinstatement</b>), we found that VP Gad1 and parvalbumin (PV), but not vGlut2, neurons show <b>relapse</b> associated changes in c <strong>Fos</strong> expression.
+FOS	drug	alcohol	31778691	By contrast, intra LHb infusion of the selective 5 HT2CR agonist WAY161503 induced AB and increased c <strong>Fos</strong> expression in the LHb in <b>alcohol</b> naive but not Post EtOH rats.
+FOS	drug	alcohol	31698029	Effects of the hallucinogenic beverage ayahuasca on voluntary <b>ethanol</b> intake by rats and on <strong>cFos</strong> expression in brain areas relevant to drug addiction.
+FOS	drug	psychedelics	31698029	Effects of the hallucinogenic beverage <b>ayahuasca</b> on voluntary ethanol intake by rats and on <strong>cFos</strong> expression in brain areas relevant to drug addiction.
+FOS	addiction	addiction	31698029	Effects of the hallucinogenic beverage ayahuasca on voluntary ethanol intake by rats and on <strong>cFos</strong> expression in brain areas relevant to drug <b>addiction</b>.
+FOS	drug	alcohol	31698029	<b>Ethanol</b> intake was estimated throughout the experiment, and <strong>cFos</strong> expression was evaluated in medial orbital cortex (MO), ventral orbital cortex (VO), lateral orbital cortex (LO), nucleus accumbens (NAc), and striatum.
+FOS	drug	alcohol	31698029	<b>Ethanol</b> significantly increased <strong>cFos</strong> expression in the MO region for control (p < 0.0001), NTX (p < 0.05), Aya1 (p < 0.001), and Aya2 (p < 0.0001) groups.
+FOS	drug	psychedelics	31698029	Furthermore, NTX and Aya0.5 treatment decreased <strong>cFos</strong> expression compared to controls in the MO region (p < 0.05 and p < 0.01, respectively), but only the <b>ayahuasca</b> group reached levels not significantly different from the naïve group.
+FOS	drug	psychedelics	31698029	Additionally, the role of <b>ayahuasca</b> in mediating <strong>cFos</strong> expression in other selected brain regions and its relationship with the serotoninergic/dopaminergic systems and drug addiction need further investigation.
+FOS	addiction	addiction	31698029	Additionally, the role of ayahuasca in mediating <strong>cFos</strong> expression in other selected brain regions and its relationship with the serotoninergic/dopaminergic systems and drug <b>addiction</b> need further investigation.
+FOS	addiction	reward	31667531	After the <b>CPP</b> test, <strong>cFos</strong> staining was employed as a marker of neuronal activation in the hippocampus.
+FOS	addiction	reward	31667531	AM251 and JWH133 also prevented neuronal activation (c <strong>Fos</strong> expression) in the hippocampus of <b>CPP</b> exposed animals.
+FOS	drug	cocaine	31614186	Using the TetTag mouse model and <strong>Fos</strong> immunohistochemistry, we measured neurons engaged by novelty and acute <b>cocaine</b> exposure, respectively in the prefrontal cortex (PFC) and nucleus accumbens (NAc).
+FOS	drug	cocaine	31614186	While there was no significant impact of novelty exposure on the size of the EGFP+ ensemble, we found that <b>cocaine</b> engaged significantly more <strong>Fos</strong>+ neurons in the NAc, while stress increased the size of the <strong>Fos</strong>+ ensemble in the PFC.
+FOS	drug	alcohol	31556948	We trained male Long Evans rats to self administer <b>alcohol</b> (12% w/v), extinguished <b>alcohol</b> reinforced responding, and then determined the effects of prazosin (1 mg/kg) on U50,488 (2.5 mg/kg) induced reinstatement and regional <strong>Fos</strong> expression.
+FOS	addiction	relapse	31556948	We trained male Long Evans rats to self administer alcohol (12% w/v), extinguished alcohol reinforced responding, and then determined the effects of prazosin (1 mg/kg) on U50,488 (2.5 mg/kg) induced <b>reinstatement</b> and regional <strong>Fos</strong> expression.
+FOS	addiction	relapse	31556948	Prazosin blocked U50,488 induced <b>reinstatement</b> and decreased U50,488 induced <strong>Fos</strong> expression in the orbitofrontal cortex, nucleus accumbens core, ventral bed nucleus of the stria terminalis, central and basolateral amygdalar nuclei and ventral tegmental area.
+FOS	drug	cocaine	31542987	c <strong>Fos</strong> immunohistochemistry revealed a different pattern of activation based on <b>cocaine</b> paired conditioning or the presence of social stimulus.
+FOS	addiction	withdrawal	31523363	Furthermore, during acute <b>withdrawal</b>, <strong>Fos</strong> positive nuclei were increased in the prefrontal cortex, anterior cingulate cortex (ACC), nucleus accumbens (NAc), amygdala and lateral habenula (LHb) in the females, versus only in the ACC, amygdala, and LHb in the males.
+FOS	drug	amphetamine	31521799	The c <strong>Fos</strong> or p ERK immunohistochemical activity showed that the cingulated cortex area 1 (Cg1), infralimbic cortex (IL), prelimbic cortex (PrL), basolateral amygdala (BLA), nucleus accumbens (NAc), and dentate gyrus (DG) of the hippocampus were overexpressed in aversive CTA induced by <b>methamphetamine</b>.
+FOS	addiction	aversion	31521799	The c <strong>Fos</strong> or p ERK immunohistochemical activity showed that the cingulated cortex area 1 (Cg1), infralimbic cortex (IL), prelimbic cortex (PrL), basolateral amygdala (BLA), nucleus accumbens (NAc), and dentate gyrus (DG) of the hippocampus were overexpressed in <b>aversive</b> <b>CTA</b> induced by methamphetamine.
+FOS	drug	opioid	31521796	In contrast to <b>morphine</b>, chronic intrathecal treatments with DN 9 did not induce analgesic tolerance, c <strong>Fos</strong> expression or microglial activation.
+FOS	addiction	sensitization	31506004	CB1 receptor antagonism disrupted the expression of CORT response habituation and some of the c <strong>fos</strong> mRNA reduction associated with it and facilitated novel stressor <b>sensitization</b> in doses that did not potentiate acute responses to these stressors.
+FOS	addiction	aversion	31433552	Activation of the insula, as measured by c <strong>fos</strong> expression, occurred during <b>aversion</b> resistant drinking and was further enhanced by elimination of PNNs.
+FOS	drug	opioid	31433241	Results: <b>Morphine</b> elevated OX1R (2.92 times), c <strong>fos</strong> (2.06 times), p/t ERK (2.04 times) and p/t PKC (2.4 times), Beclin 1 (3.2 times) and LC3 II/LC3 I (3.96 times) expression in HT22 cells.
+FOS	drug	opioid	31433241	The silence of MEG3 lowered the Beclin 1 (1.85 times), LC3 II/LC3 I (2.12 times), c <strong>fos</strong> (1.39 times) and p/t ERK (1.44 times) expressions in <b>morphine</b> treated HT22 cells.
+FOS	drug	opioid	31433241	Conclusions: Up regulation of MEG3 attended to the <b>morphine</b> caused autophagy of HT22 cells might be through elevating c <strong>fos</strong> expression and promoting ERK pathway activation.
+FOS	drug	amphetamine	31422417	Incubated <b>methamphetamine</b> seeking after voluntary abstinence was associated with a selective increase of <strong>Fos</strong> expression in the NAc core, but not shell, and <strong>Fos</strong> was colabeled with both Drd1  and Drd2 MSNs.
+FOS	addiction	relapse	31422417	Incubated methamphetamine <b>seeking</b> after voluntary abstinence was associated with a selective increase of <strong>Fos</strong> expression in the NAc core, but not shell, and <strong>Fos</strong> was colabeled with both Drd1  and Drd2 MSNs.
+FOS	addiction	reward	31374323	BT at orexigenic doses increases c <strong>Fos</strong> immunoreactivity (IR) in brain areas associated with feeding for energy as well as for <b>reward</b>, including the paraventricular nucleus of the hypothalamus, central nucleus of the amygdala and nucleus of the solitary tract.
+FOS	drug	amphetamine	31364821	Distinct gene alterations between <strong>Fos</strong> expressing striatal and thalamic neurons after withdrawal from <b>methamphetamine</b> self administration.
+FOS	addiction	withdrawal	31364821	Distinct gene alterations between <strong>Fos</strong> expressing striatal and thalamic neurons after <b>withdrawal</b> from methamphetamine self administration.
+FOS	drug	amphetamine	31364821	Here, we examined molecular alterations in DMS and AIT neurons activated (identified by neuronal activity marker <strong>Fos</strong>) during "incubated" <b>Meth</b> seeking relapse test after prolonged withdrawal.
+FOS	addiction	relapse	31364821	Here, we examined molecular alterations in DMS and AIT neurons activated (identified by neuronal activity marker <strong>Fos</strong>) during "incubated" Meth <b>seeking</b> <b>relapse</b> test after prolonged withdrawal.
+FOS	addiction	withdrawal	31364821	Here, we examined molecular alterations in DMS and AIT neurons activated (identified by neuronal activity marker <strong>Fos</strong>) during "incubated" Meth seeking relapse test after prolonged <b>withdrawal</b>.
+FOS	addiction	relapse	31364821	Using fluorescence activated cell sorting, we examined gene expression in <strong>Fos</strong> positive (activated during a 2 hr <b>relapse</b> test) and <strong>Fos</strong> negative (nonactivated) DMS and AIT neurons.
+FOS	addiction	relapse	31364821	These results demonstrated that transcriptional regulations in <strong>Fos</strong> positive neurons activated during the <b>relapse</b> tests are brain region specific but are not uniquely associated with drug exposure during the self administration training.
+FOS	drug	cocaine	31332816	Treatment of the mice with BD1047, a σ 1 receptor antagonist, significantly attenuated both <b>cocaine</b> induced CPP and c <strong>Fos</strong> immunoreactivity (c <strong>Fos</strong> IR) in WT and GPx 1 KO mice, although the effects were more evident in the latter group.
+FOS	addiction	reward	31332816	Treatment of the mice with BD1047, a σ 1 receptor antagonist, significantly attenuated both cocaine induced <b>CPP</b> and c <strong>Fos</strong> immunoreactivity (c <strong>Fos</strong> IR) in WT and GPx 1 KO mice, although the effects were more evident in the latter group.
+FOS	drug	cocaine	31332816	Despite the protective effects of BD1047 on <b>cocaine</b> induced CPP and c <strong>Fos</strong> in non TG mice, there were no additional protective effects in <b>cocaine</b> treated GPx 1 TG mice, indicating that the σ 1 receptor is a critical target for GPx 1 mediated psychoprotective activity.
+FOS	addiction	reward	31332816	Despite the protective effects of BD1047 on cocaine induced <b>CPP</b> and c <strong>Fos</strong> in non TG mice, there were no additional protective effects in cocaine treated GPx 1 TG mice, indicating that the σ 1 receptor is a critical target for GPx 1 mediated psychoprotective activity.
+FOS	drug	cocaine	31331999	Using <b>cocaine</b> self administration (3 h/d for 14 d) and extinction procedures, we demonstrated that vmPFC was similarly activated (indexed by <strong>Fos</strong>) during <b>cocaine</b> seeking tests after 0 (no extinction) or 7 extinction sessions.
+FOS	addiction	relapse	31331999	Using cocaine self administration (3 h/d for 14 d) and extinction procedures, we demonstrated that vmPFC was similarly activated (indexed by <strong>Fos</strong>) during cocaine <b>seeking</b> tests after 0 (no extinction) or 7 extinction sessions.
+FOS	drug	cocaine	31331999	Here, we used the Daun02 chemogenetic inactivation procedure, which allows selective inhibition of neuronal ensembles identified by the activity marker <strong>Fos</strong>, to demonstrate that different ensembles for <b>cocaine</b> self administration and extinction memories coexist in the ventral mPFC and interact with distinct subregions of the nucleus accumbens.
+FOS	drug	alcohol	31288295	Dynamic c <strong>Fos</strong> changes in mouse brain during acute and protracted withdrawal from chronic intermittent <b>ethanol</b> exposure and relapse drinking.
+FOS	addiction	relapse	31288295	Dynamic c <strong>Fos</strong> changes in mouse brain during acute and protracted withdrawal from chronic intermittent ethanol exposure and <b>relapse</b> drinking.
+FOS	addiction	withdrawal	31288295	Dynamic c <strong>Fos</strong> changes in mouse brain during acute and protracted <b>withdrawal</b> from chronic intermittent ethanol exposure and relapse drinking.
+FOS	drug	alcohol	31288295	In the current study, we used this model to evaluate changes in neuronal activity (as indexed by c <strong>Fos</strong> expression) throughout acute and protracted withdrawal from CIE (combined with or without a history of <b>ethanol</b> drinking).
+FOS	addiction	withdrawal	31288295	In the current study, we used this model to evaluate changes in neuronal activity (as indexed by c <strong>Fos</strong> expression) throughout acute and protracted <b>withdrawal</b> from CIE (combined with or without a history of ethanol drinking).
+FOS	addiction	withdrawal	31288295	We analyzed c <strong>Fos</strong> protein expression in 29 brain regions in mice sacrificed 2, 10, 26, and 74 hours or 7 days after <b>withdrawal</b> from 5 cycles of CIE.
+FOS	drug	alcohol	31288295	Results revealed dynamic time  and brain region dependent changes in c <strong>Fos</strong> activity over the time course of withdrawal from CIE exposure, as compared with nondependent air exposed control mice, beginning with markedly low expression levels upon removal from the <b>ethanol</b> vapor chambers (2 hours), reflecting intoxication.
+FOS	addiction	intoxication	31288295	Results revealed dynamic time  and brain region dependent changes in c <strong>Fos</strong> activity over the time course of withdrawal from CIE exposure, as compared with nondependent air exposed control mice, beginning with markedly low expression levels upon removal from the ethanol vapor chambers (2 hours), reflecting <b>intoxication</b>.
+FOS	addiction	withdrawal	31288295	Results revealed dynamic time  and brain region dependent changes in c <strong>Fos</strong> activity over the time course of <b>withdrawal</b> from CIE exposure, as compared with nondependent air exposed control mice, beginning with markedly low expression levels upon removal from the ethanol vapor chambers (2 hours), reflecting intoxication.
+FOS	addiction	withdrawal	31288295	c <strong>Fos</strong> expression was enhanced during acute CIE <b>withdrawal</b> (10 and 26 hours), followed by widespread reductions at the beginning of protracted <b>withdrawal</b> (74 hours) in several brain areas.
+FOS	addiction	withdrawal	31288295	Persistent reductions in c <strong>Fos</strong> expression were observed during prolonged <b>withdrawal</b> (7 days) in prelimbic cortex, nucleus accumbens shell, dorsomedial striatum, paraventricular nucleus of thalamus, and ventral subiculum.
+FOS	drug	alcohol	31288295	A history of <b>ethanol</b> drinking altered acute CIE withdrawal effects and caused widespread reductions in c <strong>Fos</strong> that persisted during extended abstinence even without CIE exposure.
+FOS	addiction	withdrawal	31288295	A history of ethanol drinking altered acute CIE <b>withdrawal</b> effects and caused widespread reductions in c <strong>Fos</strong> that persisted during extended abstinence even without CIE exposure.
+FOS	drug	cocaine	31266052	We also tested the ability of ceftriaxone to attenuate the reinstatement of <b>cocaine</b> seeking and assessed reinstatement induced <strong>Fos</strong> expression in several regions critical for reinstatement.
+FOS	addiction	relapse	31266052	We also tested the ability of ceftriaxone to attenuate the <b>reinstatement</b> of cocaine <b>seeking</b> and assessed <b>reinstatement</b> induced <strong>Fos</strong> expression in several regions critical for <b>reinstatement</b>.
+FOS	drug	alcohol	31266052	A history of cocaine + <b>alcohol</b> also altered patterns of reinstatement induced <strong>Fos</strong> expression.
+FOS	drug	cocaine	31266052	A history of <b>cocaine</b> + alcohol also altered patterns of reinstatement induced <strong>Fos</strong> expression.
+FOS	addiction	relapse	31266052	A history of cocaine + alcohol also altered patterns of <b>reinstatement</b> induced <strong>Fos</strong> expression.
+FOS	drug	alcohol	31242442	Using <strong>Fos</strong> staining, site specific infusion of NK1R antagonist, and viral vector overexpression, we examined the influence of NK1R on the sensitivity to yohimbine induced reinstatement of <b>alcohol</b> seeking.
+FOS	addiction	relapse	31242442	Using <strong>Fos</strong> staining, site specific infusion of NK1R antagonist, and viral vector overexpression, we examined the influence of NK1R on the sensitivity to yohimbine induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+FOS	drug	amphetamine	31202809	Finally, we quantified <strong>cFos</strong> immunofluorescence in the NAcc as a proxy for downstream neuronal activity following a PrL infusion of OXY (0, 1 μg/side) prior to <b>METH</b> primed reinstatement.
+FOS	addiction	relapse	31202809	Finally, we quantified <strong>cFos</strong> immunofluorescence in the NAcc as a proxy for downstream neuronal activity following a PrL infusion of OXY (0, 1 μg/side) prior to METH primed <b>reinstatement</b>.
+FOS	drug	amphetamine	31202809	Additionally, intra PrL OXY reduced <b>METH</b> induced <strong>cFos</strong> expression in the rostral but not caudal pole of the NAcc.
+FOS	drug	alcohol	31066114	Therefore, we counted <strong>Fos</strong> protein positive nuclei across 42 brain regions in <b>alcohol</b> experienced <b>alcohol</b> preferring rats that received either yohimbine in the home cage (1 mg/kg i.p.)
+FOS	addiction	relapse	31066114	Yohimbine induced <b>reinstatement</b> increased the number of <strong>Fos</strong> protein expressing nuclei in multiple other regions including the thalamus, hypothalamus and hippocampus.
+FOS	drug	alcohol	31066114	We then examined inter regional correlations in <strong>Fos</strong> protein expression for all 42 brain regions, which showed <strong>Fos</strong> expression was more strongly positively correlated following yohimbine induced reinstatement of <b>alcohol</b> seeking, compared to home cage yohimbine.
+FOS	addiction	relapse	31066114	We then examined inter regional correlations in <strong>Fos</strong> protein expression for all 42 brain regions, which showed <strong>Fos</strong> expression was more strongly positively correlated following yohimbine induced <b>reinstatement</b> of alcohol <b>seeking</b>, compared to home cage yohimbine.
+FOS	drug	alcohol	31060041	Using a chronic <b>ethanol</b> vapor exposure paradigm that renders rats physically dependent on <b>ethanol</b>, we observed significant withdrawal induced enhancement of <strong>cFos</strong> expression in the RMTg.
+FOS	addiction	withdrawal	31060041	Using a chronic ethanol vapor exposure paradigm that renders rats physically dependent on ethanol, we observed significant <b>withdrawal</b> induced enhancement of <strong>cFos</strong> expression in the RMTg.
+FOS	drug	alcohol	31060041	Both measures followed a similar time course to RMTg <strong>cFos</strong> expression with peak symptom severity occurring 12 h following cessation of <b>ethanol</b> exposure.
+FOS	drug	cocaine	31058522	Neuronal activation in orbitofrontal cortex subregions: <strong>Cfos</strong> expression following cue induced reinstatement of <b>cocaine</b> seeking behavior.
+FOS	addiction	relapse	31058522	Neuronal activation in orbitofrontal cortex subregions: <strong>Cfos</strong> expression following cue induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+FOS	addiction	relapse	31058522	<strong>Cfos</strong> protein expression was utilized to measure potential changes in neural activation between the <b>reinstatement</b> test groups.
+FOS	drug	amphetamine	31042352	Mice expressing <b>Meth</b> CPP had elevated numbers of <strong>FOS</strong>+ cells in the ventral tegmental area (VTA) and basolateral amygdala (BlA) and reduced <strong>FOS</strong>+ cells in the central amygdala (CeA) compared to saline controls.
+FOS	addiction	reward	31042352	Mice expressing Meth <b>CPP</b> had elevated numbers of <strong>FOS</strong>+ cells in the ventral tegmental area (VTA) and basolateral amygdala (BlA) and reduced <strong>FOS</strong>+ cells in the central amygdala (CeA) compared to saline controls.
+FOS	drug	amphetamine	31042352	CP94253 given before the expression test, but not acutely in drug naive mice, enhanced <strong>FOS</strong>+ cells in the VTA, the nucleus accumbens (NAc) shell and core, and the dorsomedial striatum and reversed the <b>Meth</b> conditioned changes in <strong>FOS</strong> in the BlA and CeA.
+FOS	drug	amphetamine	30967896	<strong>FOS</strong> and FOSB, which are implicated in the <b>amphetamine</b> addiction pathway, were up regulated in schizophrenia fibroblast samples.
+FOS	addiction	addiction	30967896	<strong>FOS</strong> and FOSB, which are implicated in the amphetamine <b>addiction</b> pathway, were up regulated in schizophrenia fibroblast samples.
+FOS	drug	amphetamine	30967896	Protein protein interaction (PPI) network analysis revealed that proteins closely interacting with <strong>FOS</strong> encoded protein were also involved in the <b>amphetamine</b> addiction pathway.
+FOS	addiction	addiction	30967896	Protein protein interaction (PPI) network analysis revealed that proteins closely interacting with <strong>FOS</strong> encoded protein were also involved in the amphetamine <b>addiction</b> pathway.
+FOS	drug	amphetamine	30967896	Pearson correlation test indicated that <strong>FOS</strong> showed positive correlation with genes in the <b>amphetamine</b> pathway.
+FOS	drug	opioid	30919988	Effect of pretreatment with intracerebroventricular injection of minocycline on <b>morphine</b> induced memory impairment in passive avoidance test: Role of P CREB and c <strong>Fos</strong> expression in the dorsal hippocampus and basolateral amygdala regions.
+FOS	addiction	withdrawal	30902659	In the present study, male and female mice were injected with MA (5 mg/kg) or saline once daily for 10 days, and during early <b>withdrawal</b> were assessed for alterations in immediate early gene (c <strong>Fos</strong>) responses to a forced swim stressor.
+FOS	drug	cocaine	30845266	A subset of the GFP(+) afferents are c <strong>FOS</strong>(+) following acute administration of <b>cocaine</b>, showing that NAc somatostatin interneurons are innervated by some cells that respond to rewarding stimuli.
+FOS	drug	amphetamine	30831183	The present study used dual immunolabeling and fluorescent in situ hybridization (RNAscope) to examine acute <b>amph</b> induced activation of <strong>cFos</strong> expression in phenotypically identified cNTS neurons in ad lib fed vs. overnight fasted male Sprague Dawley rats.
+FOS	drug	cocaine	30803445	This behavioral alteration in spinophilin knockout mice was accompanied by attenuated c <strong>Fos</strong> and ∆FosB expression following <b>cocaine</b> administration and blunted <b>cocaine</b> induced phosphorylation of ERK1/2 in the striatum, with no change in other relevant signaling molecules.
+FOS	drug	cocaine	30803445	Therefore, we suggest spinophilin fulfills an essential role in <b>cocaine</b> induced behavioral sensitization, likely via ERK1/2 phosphorylation and induction of c <strong>Fos</strong> and ∆FosB in the striatum, a mechanism that may underlie specific processes in <b>cocaine</b> addiction.
+FOS	addiction	addiction	30803445	Therefore, we suggest spinophilin fulfills an essential role in cocaine induced behavioral sensitization, likely via ERK1/2 phosphorylation and induction of c <strong>Fos</strong> and ∆FosB in the striatum, a mechanism that may underlie specific processes in cocaine <b>addiction</b>.
+FOS	addiction	sensitization	30803445	Therefore, we suggest spinophilin fulfills an essential role in cocaine induced behavioral <b>sensitization</b>, likely via ERK1/2 phosphorylation and induction of c <strong>Fos</strong> and ∆FosB in the striatum, a mechanism that may underlie specific processes in cocaine addiction.
+FOS	drug	alcohol	30797833	<strong>Fos</strong> activation patterns related to acute <b>ethanol</b> and conditioned taste aversion in adolescent and adult rats.
+FOS	addiction	aversion	30797833	<strong>Fos</strong> activation patterns related to acute ethanol and conditioned taste <b>aversion</b> in adolescent and adult rats.
+FOS	drug	alcohol	30797833	The current study examined early adolescent (postnatal day [P]28 30) and adult (P72 74) Sprague Dawley male rats for conditioned taste aversion (CTA) after doses of 0, 1.0, or 2.5 g/kg <b>ethanol</b>, and patterns of neuronal activation in response to <b>ethanol</b> using <strong>Fos</strong> like immunohistochemistry (<strong>Fos</strong>+) to uncover regions where age differences in activation are associated with <b>ethanol</b> aversion.
+FOS	addiction	aversion	30797833	The current study examined early adolescent (postnatal day [P]28 30) and adult (P72 74) Sprague Dawley male rats for conditioned taste <b>aversion</b> (<b>CTA</b>) after doses of 0, 1.0, or 2.5 g/kg ethanol, and patterns of neuronal activation in response to ethanol using <strong>Fos</strong> like immunohistochemistry (<strong>Fos</strong>+) to uncover regions where age differences in activation are associated with ethanol <b>aversion</b>.
+FOS	drug	alcohol	30797833	An adolescent specific <b>ethanol</b> induced increase in <strong>Fos</strong>+ staining was seen within the nucleus accumbens shell and core.
+FOS	drug	alcohol	30797833	An age difference was also noted within the Edinger Westphal nucleus (EW) following administration of the lower dose of <b>ethanol</b>, with 1 g/kg <b>ethanol</b> producing CTA in adults but not in adolescents and inducing a greater EW <strong>Fos</strong> response in adults than adolescents.
+FOS	addiction	aversion	30797833	An age difference was also noted within the Edinger Westphal nucleus (EW) following administration of the lower dose of ethanol, with 1 g/kg ethanol producing <b>CTA</b> in adults but not in adolescents and inducing a greater EW <strong>Fos</strong> response in adults than adolescents.
+FOS	addiction	aversion	30797833	Regression analysis revealed that greater numbers of <strong>Fos</strong>+ neurons within the EW and insula (Ins) were related to lower consumption of the conditioned stimulus (CS) on test day (reflecting greater <b>CTA</b>).
+FOS	drug	alcohol	30797833	In the BNST (but not PrL), <b>ethanol</b> induced increases in <strong>Fos</strong> immunoreactivity (IR) were evident at both ages.
+FOS	addiction	relapse	30728447	Cues paired during estrus also increased c <strong>fos</strong> expression to a greater extent in striatal regions, an effect that may underlie the observed increases in <b>seeking</b> induced by these cues, even weeks later.
+FOS	drug	psychedelics	30700692	Effects of Electroacupuncture on Expression of D1 Receptor (D1R), Phosphorylation of Extracellular Regulated Protein Kinase 1/2 (p ERK1/2), and c <strong>Fos</strong> in the Insular Cortex of <b>Ketamine</b> Addicted Rats.
+FOS	drug	psychedelics	30700692	BACKGROUND The aim of this study was to investigate the effects of electroacupuncture (EA) on expression of the D1 receptor (D1R), phosphorylation of extracellular regulated protein kinase 1/2 (p ERK1/2) and c <strong>Fos</strong> in the insular cortex (IC) of <b>ketamine</b> addicted rats.
+FOS	drug	psychedelics	30700692	CONCLUSIONS <b>Ketamine</b> addiction induces c <strong>Fos</strong> overexpression in the IC by increasing the expression of D1R and p ERK1/2.
+FOS	addiction	addiction	30700692	CONCLUSIONS Ketamine <b>addiction</b> induces c <strong>Fos</strong> overexpression in the IC by increasing the expression of D1R and p ERK1/2.
+FOS	drug	cocaine	30685319	<b>Cocaine</b> induced drug dependence was followed by increases in c <strong>Fos</strong> immunoreactivity (c <strong>Fos</strong> IR) in the nucleus accumbens.
+FOS	addiction	dependence	30685319	Cocaine induced drug <b>dependence</b> was followed by increases in c <strong>Fos</strong> immunoreactivity (c <strong>Fos</strong> IR) in the nucleus accumbens.
+FOS	addiction	relapse	30659838	U50,488 increased <strong>Fos</strong> expression in brain areas involved in stress induced <b>relapse</b>, and <strong>Fos</strong> activation in the ventral BNST was greater in vapor exposed rats.
+FOS	drug	alcohol	30612041	Finally, we explored the brain basis of cue elicited <b>alcohol</b> seeking using c <strong>Fos</strong> immunohistochemistry.
+FOS	addiction	relapse	30612041	Finally, we explored the brain basis of cue elicited alcohol <b>seeking</b> using c <strong>Fos</strong> immunohistochemistry.
+FOS	drug	alcohol	30509960	We next examined the putative circuitry of context induced relapse to <b>alcohol</b> seeking following prolonged abstinence using <strong>Fos</strong> as a marker of neuronal activation.
+FOS	addiction	relapse	30509960	We next examined the putative circuitry of context induced <b>relapse</b> to alcohol <b>seeking</b> following prolonged abstinence using <strong>Fos</strong> as a marker of neuronal activation.
+FOS	drug	alcohol	30509960	The anterior insular cortex (AI) was the only brain region examined where <strong>Fos</strong> expression correlated with <b>alcohol</b> seeking behavior in Context B after prolonged abstinence.
+FOS	addiction	relapse	30509960	The anterior insular cortex (AI) was the only brain region examined where <strong>Fos</strong> expression correlated with alcohol <b>seeking</b> behavior in Context B after prolonged abstinence.
+FOS	drug	cocaine	30498893	Here, we show that <b>cocaine</b> SA decreased PrL NA core spine head diameter, nuclear <strong>Fos</strong> IR and pCREB IR, and GluA1 IR and GluA2 IR in putative mushroom type spines 2 h after the end of <b>cocaine</b> SA, whereas the opposite occurred following 1 week of abstinence.
+FOS	drug	cocaine	30484727	Adolescent <b>cocaine</b> exposure enhanced negative affect following drug re exposure in adult rats: Attenuation of c <strong>Fos</strong> activation.
+FOS	drug	cocaine	30484727	In this regard, the results showed that adolescent <b>cocaine</b> exposure did not modulate cell proliferation (Ki 67+ cells) or c <strong>Fos</strong> protein activation in the dentate gyrus region of the hippocampus, but attenuated c <strong>Fos</strong> activation in the dorsal striatum.
+FOS	drug	alcohol	30390064	Using a mouse model of chronic <b>alcohol</b> consumption followed by forced abstinence (CDFA), prolonged <b>alcohol</b> abstinence increased c <strong>fos</strong> expression and spontaneous glutamatergic neurotransmission in the dorsal bed nucleus of the stria terminalis (dBNST), a region heavily implicated in negative affect in both humans and rodents.
+FOS	drug	opioid	30373717	Here, we monitor genetically encoded DA and calcium indicators as well as <strong>cFos</strong> in mice to reveal that <b>heroin</b> activates DA neurons located in the medial part of the VTA, preferentially projecting to the medial shell of the nucleus accumbens (NAc).
+FOS	addiction	relapse	30355627	Both shock induced <b>reinstatement</b> and the prelimbic cortex <strong>Fos</strong> response were prevented by bilateral intra VTA injections of the CRF receptor 1 (CRFR1) antagonist, antalarmin.
+FOS	drug	amphetamine	29770212	The effect of d <b>amphetamine</b> on neural activity was inferred by quantifying <strong>cfos</strong> expression in the nucleus accumbens and dorsal hippocampus following CPP training.
+FOS	addiction	reward	29770212	The effect of d amphetamine on neural activity was inferred by quantifying <strong>cfos</strong> expression in the nucleus accumbens and dorsal hippocampus following <b>CPP</b> training.
+FOS	drug	opioid	30342963	In this paper, using immunohistochemical and single cell microinjection techniques, combining behavioral assay, we found that (1) contextual withdrawal conditioning increases the expression of c <strong>Fos</strong>, but not Arc, in the ACC in <b>morphine</b> withdrawal mice; (2) at the first day after conditioning, conditioned context has no influence on the expression of c <strong>Fos</strong> and Arc in the ACC in <b>morphine</b> withdrawal mice; (3) at the 14th day after conditioning, conditioned context increases the expression of both c <strong>Fos</strong> and Arc in the ACC in <b>morphine</b> withdrawal mice; (4) the inhibition of dendritic spines of the ACC or projection neurons from the CA3 of the hippocampus to the ACC attenuates the conditioned context induced increase of Arc expression in the ACC and abolishes the retrieval of withdrawal memory at the 14th day after conditioning.
+FOS	addiction	withdrawal	30342963	In this paper, using immunohistochemical and single cell microinjection techniques, combining behavioral assay, we found that (1) contextual <b>withdrawal</b> conditioning increases the expression of c <strong>Fos</strong>, but not Arc, in the ACC in morphine <b>withdrawal</b> mice; (2) at the first day after conditioning, conditioned context has no influence on the expression of c <strong>Fos</strong> and Arc in the ACC in morphine <b>withdrawal</b> mice; (3) at the 14th day after conditioning, conditioned context increases the expression of both c <strong>Fos</strong> and Arc in the ACC in morphine <b>withdrawal</b> mice; (4) the inhibition of dendritic spines of the ACC or projection neurons from the CA3 of the hippocampus to the ACC attenuates the conditioned context induced increase of Arc expression in the ACC and abolishes the retrieval of <b>withdrawal</b> memory at the 14th day after conditioning.
+FOS	drug	cocaine	30318755	We have previously shown that methyl supplementation via L Methionine (MET) administration attenuates <b>cocaine</b> seeking behavior and reverses expression and methylation patterns of the immediate early gene c <strong>fos</strong>, suggesting that MET may act by altering the excitability of this circuitry during <b>cocaine</b> reinstatement.
+FOS	addiction	relapse	30318755	We have previously shown that methyl supplementation via L Methionine (MET) administration attenuates cocaine <b>seeking</b> behavior and reverses expression and methylation patterns of the immediate early gene c <strong>fos</strong>, suggesting that MET may act by altering the excitability of this circuitry during cocaine <b>reinstatement</b>.
+FOS	drug	cocaine	30307667	<strong>Fos</strong> expression results indicated that only the prelimbic cortex (PL) was activated by both heroin and <b>cocaine</b> cues; in contrast, no significant cue induced neuronal activation was observed in other brain areas.
+FOS	drug	opioid	30307667	<strong>Fos</strong> expression results indicated that only the prelimbic cortex (PL) was activated by both <b>heroin</b> and cocaine cues; in contrast, no significant cue induced neuronal activation was observed in other brain areas.
+FOS	drug	cocaine	30307667	RNA in situ hybridization indicated that the proportion of glutamatergic and GABAergic markers in PL <strong>Fos</strong> expressing cells was similar for the heroin and <b>cocaine</b> cue activated neurons.
+FOS	drug	opioid	30307667	RNA in situ hybridization indicated that the proportion of glutamatergic and GABAergic markers in PL <strong>Fos</strong> expressing cells was similar for the <b>heroin</b> and cocaine cue activated neurons.
+FOS	drug	cocaine	30296530	Additionally, we demonstrated that adolescent onset social isolation increased <b>cocaine</b> induced neuronal activation, as assessed by c <strong>Fos</strong> expression, within the nucleus accumbens core and shell, ventral pallidum, dorsal bed nucleus of the stria terminalis, lateral septum and basolateral amygdala.
+FOS	drug	opioid	30284123	Sustained <b>morphine</b> treatment did not markedly modify certain LC parameters in CCI 30d animals, such as [Met5] enkephalin induced potassium outward currents or burst activity and c <strong>Fos</strong> rebound after <b>naloxone</b> precipitation, which may limit the development of some typical <b>opioid</b> drug related adaptations.
+FOS	drug	opioid	30170186	Modulatory role of the intra accumbal CB1 receptor in protein level of the c <strong>fos</strong> and pCREB/CREB ratio in the nucleus accumbens and ventral tegmental area in extinction and <b>morphine</b> seeking in the rats.
+FOS	addiction	relapse	30170186	Modulatory role of the intra accumbal CB1 receptor in protein level of the c <strong>fos</strong> and pCREB/CREB ratio in the nucleus accumbens and ventral tegmental area in extinction and morphine <b>seeking</b> in the rats.
+FOS	drug	opioid	30170186	The present study tried to investigate the role of the intra accumbal CB1 receptor in the c <strong>fos</strong> level and pCREB/CREB ratio in the NAc and the VTA during reinstatement phase of <b>morphine</b> induced conditioned place preference (CPP) by western blotting.
+FOS	addiction	relapse	30170186	The present study tried to investigate the role of the intra accumbal CB1 receptor in the c <strong>fos</strong> level and pCREB/CREB ratio in the NAc and the VTA during <b>reinstatement</b> phase of morphine induced conditioned place preference (CPP) by western blotting.
+FOS	addiction	reward	30170186	The present study tried to investigate the role of the intra accumbal CB1 receptor in the c <strong>fos</strong> level and pCREB/CREB ratio in the NAc and the VTA during reinstatement phase of morphine induced conditioned place preference (<b>CPP</b>) by western blotting.
+FOS	drug	opioid	30170186	The present data reveals that intra accumbal administration of CB1 agonist, WIN55,212 2 (0.5, 1 and 2 mM/0.5 μl DMSO) before/during extinction period of <b>morphine</b> induced CPP, significantly decreased the NAc and the VTA c <strong>fos</strong> protein level in the reinstatement phase; whereas the pre reinstatement administration of the CB1 agonist, increased the c <strong>fos</strong> protein level.
+FOS	addiction	relapse	30170186	The present data reveals that intra accumbal administration of CB1 agonist, WIN55,212 2 (0.5, 1 and 2 mM/0.5 μl DMSO) before/during extinction period of morphine induced CPP, significantly decreased the NAc and the VTA c <strong>fos</strong> protein level in the <b>reinstatement</b> phase; whereas the pre <b>reinstatement</b> administration of the CB1 agonist, increased the c <strong>fos</strong> protein level.
+FOS	addiction	reward	30170186	The present data reveals that intra accumbal administration of CB1 agonist, WIN55,212 2 (0.5, 1 and 2 mM/0.5 μl DMSO) before/during extinction period of morphine induced <b>CPP</b>, significantly decreased the NAc and the VTA c <strong>fos</strong> protein level in the reinstatement phase; whereas the pre reinstatement administration of the CB1 agonist, increased the c <strong>fos</strong> protein level.
+FOS	drug	opioid	30170186	Also, the present data show that intra accumbal administration of CB1 antagonist, AM251 (15, 45 and 90 μM/0.5 μl DMSO) during/after extinction period of <b>morphine</b> induced CPP affects the NAc and the VTA c <strong>fos</strong> protein level in the reinstatement phase.
+FOS	addiction	relapse	30170186	Also, the present data show that intra accumbal administration of CB1 antagonist, AM251 (15, 45 and 90 μM/0.5 μl DMSO) during/after extinction period of morphine induced CPP affects the NAc and the VTA c <strong>fos</strong> protein level in the <b>reinstatement</b> phase.
+FOS	addiction	reward	30170186	Also, the present data show that intra accumbal administration of CB1 antagonist, AM251 (15, 45 and 90 μM/0.5 μl DMSO) during/after extinction period of morphine induced <b>CPP</b> affects the NAc and the VTA c <strong>fos</strong> protein level in the reinstatement phase.
+FOS	drug	cannabinoid	30170186	In conclusion, the results presented here provide compelling evidence of the modulation and involvement of the c <strong>fos</strong> and the CREB molecules in the <b>cannabinoid</b> opioid interaction of the brain reward system in the CPP paradigm.
+FOS	drug	opioid	30170186	In conclusion, the results presented here provide compelling evidence of the modulation and involvement of the c <strong>fos</strong> and the CREB molecules in the cannabinoid <b>opioid</b> interaction of the brain reward system in the CPP paradigm.
+FOS	addiction	reward	30170186	In conclusion, the results presented here provide compelling evidence of the modulation and involvement of the c <strong>fos</strong> and the CREB molecules in the cannabinoid opioid interaction of the brain <b>reward</b> system in the <b>CPP</b> paradigm.
+FOS	drug	nicotine	30170085	Our results showed that systemic administration of <b>nicotine</b> during contextual fear extinction increased c <strong>fos</strong> expression in the vHPC and BLA while not affecting dHPC, IL or PL.
+FOS	drug	nicotine	30170085	Finally, using c <strong>fos</strong>/GAD65/67 double immunofluorescence, we showed that <b>nicotine</b> mainly increased c <strong>fos</strong> expression in non GABAergic ventral hippocampal cells, indicating that acute <b>nicotine</b> increases vHPC excitability.
+FOS	drug	amphetamine	30105771	Examination of neuronal activation patterns of the <b>METH</b> primed reinstatement session identified c <strong>Fos</strong> immunoreactivity in the basolateral amygdala (BLA) as correlated with SD score, a measure of defeat latency.
+FOS	addiction	relapse	30105771	Examination of neuronal activation patterns of the METH primed <b>reinstatement</b> session identified c <strong>Fos</strong> immunoreactivity in the basolateral amygdala (BLA) as correlated with SD score, a measure of defeat latency.
+FOS	drug	amphetamine	30105771	Rapidly defeated rats showed potentiated <b>METH</b> primed reinstatement and elevated BLA c <strong>Fos</strong> compared with controls.
+FOS	addiction	relapse	30105771	Rapidly defeated rats showed potentiated METH primed <b>reinstatement</b> and elevated BLA c <strong>Fos</strong> compared with controls.
+FOS	drug	amphetamine	30105771	Conversely, rats that were undefeated during the social stress did not show potentiated <b>METH</b> primed reinstatement or elevated BLA c <strong>Fos</strong>.
+FOS	addiction	relapse	30105771	Conversely, rats that were undefeated during the social stress did not show potentiated METH primed <b>reinstatement</b> or elevated BLA c <strong>Fos</strong>.
+FOS	drug	cannabinoid	30101419	injections of <b>cannabinoid</b> related drugs followed by cocaine, and were then tested for cocaine induced hyperlocomotion, c <strong>Fos</strong> expression in the nucleus accumbens and conditioned place preference.
+FOS	drug	cocaine	30101419	injections of cannabinoid related drugs followed by <b>cocaine</b>, and were then tested for <b>cocaine</b> induced hyperlocomotion, c <strong>Fos</strong> expression in the nucleus accumbens and conditioned place preference.
+FOS	drug	cannabinoid	30101419	The CB2 receptor antagonist, AM630, reversed the inhibitory effects of <b>rimonabant</b> in cocaine induced hyperlocomotion and c <strong>Fos</strong> expression in the nucleus accumbens.
+FOS	drug	cocaine	30101419	The CB2 receptor antagonist, AM630, reversed the inhibitory effects of rimonabant in <b>cocaine</b> induced hyperlocomotion and c <strong>Fos</strong> expression in the nucleus accumbens.
+FOS	drug	nicotine	30009210	Consistent with our previous studies low  and high dose <b>nicotine</b> both induced c <strong>Fos</strong> activation of various intensities at multiple sites in VTA.
+FOS	drug	nicotine	30009210	Double labeling of c <strong>Fos</strong> activated cells with GAD67 GFP positive cells identified a subpopulation of GABAergic neurons in Substantia Nigra Compact part Medial tier (SNCM) that were activated by high  but not by low dose <b>nicotine</b>.
+FOS	drug	nicotine	30009210	Of 217 GABAergic cells counted at this site, 48.9% exhibited <b>nicotine</b> induced c <strong>fos</strong> immunoreactivity.
+FOS	drug	alcohol	29926762	The galanin receptor 3 antagonist, SNAP 37889, inhibits cue induced reinstatement of <b>alcohol</b> seeking and increases c <strong>Fos</strong> expression in the nucleus accumbens shell of <b>alcohol</b> preferring rats.
+FOS	addiction	relapse	29926762	The galanin receptor 3 antagonist, SNAP 37889, inhibits cue induced <b>reinstatement</b> of alcohol <b>seeking</b> and increases c <strong>Fos</strong> expression in the nucleus accumbens shell of alcohol preferring rats.
+FOS	drug	alcohol	29926762	This study aimed to investigate the effects of the galanin 3 receptor antagonist, SNAP 37889, on c <strong>Fos</strong> protein expression after cue induced reinstatement of <b>alcohol</b> seeking in the brains of <b>alcohol</b> preferring rats.
+FOS	addiction	relapse	29926762	This study aimed to investigate the effects of the galanin 3 receptor antagonist, SNAP 37889, on c <strong>Fos</strong> protein expression after cue induced <b>reinstatement</b> of alcohol <b>seeking</b> in the brains of alcohol preferring rats.
+FOS	addiction	relapse	29926762	To examine the effect of SNAP 37889 and cue induced <b>reinstatement</b> on neuronal activation, c <strong>Fos</strong> expression was measured in subregions of the medial prefrontal cortex and nucleus accumbens.
+FOS	drug	nicotine	29888787	c <strong>Fos</strong> marking of identified midbrain neurons coactive after <b>nicotine</b> administration in vivo.
+FOS	drug	nicotine	29888787	We performed double immunohistochemistry for the immediate early gene and surrogate activity sensor, c <strong>Fos</strong>, and markers for either cholinergic, dopaminergic or GABAergic cell types in mice treated with <b>nicotine</b>.
+FOS	drug	nicotine	29888787	Twenty four hours of <b>nicotine</b> withdrawal after chronic <b>nicotine</b> treatment suppressed c <strong>Fos</strong> activation in the MT.
+FOS	addiction	withdrawal	29888787	Twenty four hours of nicotine <b>withdrawal</b> after chronic nicotine treatment suppressed c <strong>Fos</strong> activation in the MT.
+FOS	drug	cocaine	29888304	However, high <strong>Fos</strong> expression was seen after <b>cocaine</b> in both reward  and stress related brain regions of LBN rats, including nucleus accumbens core, central amygdala, and lateral habenula.
+FOS	addiction	reward	29888304	However, high <strong>Fos</strong> expression was seen after cocaine in both <b>reward</b>  and stress related brain regions of LBN rats, including nucleus accumbens core, central amygdala, and lateral habenula.
+FOS	drug	opioid	29878268	In the brain, neuropeptide mRNAs in the hypothalamus and c <strong>Fos</strong> protein and <b>opioid</b> and dopaminergic receptor mRNAs in the nucleus accumbens (NAcc) were measured.
+FOS	drug	opioid	29878268	In contrast, in rats adapted to an HP diet compared with an NP diet, energy intake was lower; and in the NAcc, meal induced c <strong>Fos</strong> protein expression was 20% lower, and mRNA expression was 17% higher for dopamine receptor 2 (Drd2) receptors and 38% lower for κ <b>opioid</b> receptor (Oprk1) receptors.
+FOS	drug	cocaine	29740282	Immediate early gene (IEG) expression (<strong>cFos</strong> and FosB) induced by repeated <b>cocaine</b> injections was significantly increased in the forebrain of M4R D1RCre mice, whereas it remained normal in the M4R ChATCre mice.
+FOS	drug	cocaine	29671014	To investigate a relationship between OXT, sex, and <b>cocaine</b> seeking, we examined <strong>Fos</strong> on ED1 in OXT neurons of paraventricular (PVN) and supraoptic nuclei (SON) compared to homecage (<b>cocaine</b> experienced) or naïve male and female rats.
+FOS	addiction	relapse	29671014	To investigate a relationship between OXT, sex, and cocaine <b>seeking</b>, we examined <strong>Fos</strong> on ED1 in OXT neurons of paraventricular (PVN) and supraoptic nuclei (SON) compared to homecage (cocaine experienced) or naïve male and female rats.
+FOS	addiction	withdrawal	29671014	OXT neurons had decreased activity (as reflected by <strong>Fos</strong> protein) in PVN and SON on <b>withdrawal</b> day 1 (homecage) compared to naïve rats.
+FOS	drug	cocaine	29671014	<strong>Fos</strong> in OXT neurons was further decreased on ED1, compared to homecage controls, in both males and females even though in SON, <b>cocaine</b> exposure increased the number of OXT expressing neurons.
+FOS	drug	alcohol	29567624	Next, we determined the effect of context induced renewal of <b>alcohol</b> seeking behavior on the expression of <strong>Fos</strong> (a neuronal activity marker) in the OFC.
+FOS	addiction	relapse	29567624	Next, we determined the effect of context induced renewal of alcohol <b>seeking</b> behavior on the expression of <strong>Fos</strong> (a neuronal activity marker) in the OFC.
+FOS	drug	alcohol	29567624	Re exposure to Context A, but not Context B, reinstated <b>alcohol</b> seeking behavior and increased expression of the neural activity marker <strong>Fos</strong> in the OFC.
+FOS	addiction	relapse	29567624	Re exposure to Context A, but not Context B, reinstated alcohol <b>seeking</b> behavior and increased expression of the neural activity marker <strong>Fos</strong> in the OFC.
+FOS	drug	amphetamine	29501631	Interestingly, m BDNF regulation paralleled hippocampal c <strong>Fos</strong> protein content, indicating decreased neuronal activity, and thus reinforcing the persisting negative effects induced by <b>methamphetamine</b> in rat hippocampus following prolonged withdrawal.
+FOS	addiction	reward	29501631	Interestingly, m BDNF regulation paralleled hippocampal c <strong>Fos</strong> protein content, indicating decreased neuronal activity, and thus <b>reinforcing</b> the persisting negative effects induced by methamphetamine in rat hippocampus following prolonged withdrawal.
+FOS	addiction	withdrawal	29501631	Interestingly, m BDNF regulation paralleled hippocampal c <strong>Fos</strong> protein content, indicating decreased neuronal activity, and thus reinforcing the persisting negative effects induced by methamphetamine in rat hippocampus following prolonged <b>withdrawal</b>.
+FOS	drug	nicotine	29472642	TAAR1 activation was sufficient to block <b>nicotine</b> induced c <strong>Fos</strong> expression in the NAc, while also reducing <b>nicotine</b> induced dopamine release in the NAc.
+FOS	drug	amphetamine	29441405	In rats that reinstated <b>methamphetamine</b> seeking, these altered electrophysiological properties of GCNs were associated with enhanced expression of <strong>Fos</strong>, GluN2A subunits and PSD95 and reduced expression of GABAA subunits in the DG and enhanced expression of synaptic PSD in the molecular layer.
+FOS	addiction	relapse	29441405	In rats that reinstated methamphetamine <b>seeking</b>, these altered electrophysiological properties of GCNs were associated with enhanced expression of <strong>Fos</strong>, GluN2A subunits and PSD95 and reduced expression of GABAA subunits in the DG and enhanced expression of synaptic PSD in the molecular layer.
+FOS	drug	amphetamine	29383398	In the brain, chronic <b>METH</b> treatment enhanced the number of c <strong>Fos</strong> neurons and the CRF neurons with c <strong>Fos</strong> signal (CRF+/c <strong>Fos</strong>+) in PVN and ovBNST.
+FOS	drug	alcohol	29378212	Furthermore, in the CPP trained Swiss mice, ki16425 prevented the effects of <b>ethanol</b> on basal c <strong>Fos</strong> expression in the medial prefrontal cortex and on adult neurogenesis in the hippocampus.
+FOS	addiction	reward	29378212	Furthermore, in the <b>CPP</b> trained Swiss mice, ki16425 prevented the effects of ethanol on basal c <strong>Fos</strong> expression in the medial prefrontal cortex and on adult neurogenesis in the hippocampus.
+FOS	addiction	relapse	29371321	We first measured projection specific activation on day 30 <b>relapse</b> test by using cholera toxin b (retrograde tracer) + <strong>Fos</strong> (activity marker) double labeling in projection areas.
+FOS	drug	alcohol	29348799	We showed here that an intraperitoneal injection of <b>ethanol</b> (0.25 g/kg), resulting in a blood <b>ethanol</b> concentration of 5.6 mM, significantly increased the number of <strong>cFos</strong> immunoreactive (IR) neurons in the LHb.
+FOS	drug	alcohol	29348799	Most of the <b>ethanol</b> activated <strong>cFos</strong> IR LHb neurons expressed vGluT2 (vesicular glutamate transporters 2, a marker of a glutamatergic phenotype).
+FOS	drug	alcohol	29306704	At transcriptional level, <b>ethanol</b> reduced the upregulation of a subset of IEGs encoding for transcription factors such as Atf3, c <strong>Fos</strong>, FosB, Egr1, Egr3 and Npas4 but did not affect the upregulation of others (e.g.
+FOS	drug	alcohol	29306704	Notably, the majority of genes were sensitive to <b>ethanol</b> only when administered before TBI and not afterwards (the exceptions being c <strong>Fos</strong>, Egr1 and Dusp5).
+FOS	drug	cocaine	29294029	Ovariectomized mice were treated with 17β estradiol or agonists selective for ERα or ERβ and tested for <b>cocaine</b> conditioned place preference and for c <strong>fos</strong> expression in the nucleus accumbens.
+FOS	drug	cocaine	29268097	Mdivi 1, a demonstrated fission inhibitor, blunts <b>cocaine</b> seeking and locomotor sensitization, while blocking c <strong>Fos</strong> induction and excitatory input onto dopamine receptor 1 (D1) containing NAc medium spiny neurons (MSNs).
+FOS	addiction	relapse	29268097	Mdivi 1, a demonstrated fission inhibitor, blunts cocaine <b>seeking</b> and locomotor sensitization, while blocking c <strong>Fos</strong> induction and excitatory input onto dopamine receptor 1 (D1) containing NAc medium spiny neurons (MSNs).
+FOS	addiction	sensitization	29268097	Mdivi 1, a demonstrated fission inhibitor, blunts cocaine seeking and locomotor <b>sensitization</b>, while blocking c <strong>Fos</strong> induction and excitatory input onto dopamine receptor 1 (D1) containing NAc medium spiny neurons (MSNs).
+FOS	drug	cocaine	29204804	This study examined whether manipulation of E2 in the mPOA modulates differing behavioral responses to <b>cocaine</b> and whether this is reflected in differing levels of c <strong>Fos</strong> in the NAc following <b>cocaine</b> administration.
+FOS	drug	cocaine	29204804	Finally, animals that received <b>cocaine</b> had increased NAc core and shell c <strong>Fos</strong> relative to animals that received saline, with animals receiving both E2 microinjections and systemic <b>cocaine</b> expressing the highest activation in the caudal NAc, compared to rats receiving aCSF microinjections and systemic <b>cocaine</b> (p = 0.05, d = 0.70).
+FOS	drug	benzodiazepine	29183829	Chronic administration of both paroxetine and <b>alprazolam</b> decreased these responses with morphological correlates between the panicolytic effect of both drugs administered at the highest dose and decreases in <strong>Fos</strong> protein immunolabeled perikarya found in the amygdaloid complex, hypothalamus and periaqueductal gray matter columns, which are structures that make up the encephalic aversion system.
+FOS	addiction	aversion	29183829	Chronic administration of both paroxetine and alprazolam decreased these responses with morphological correlates between the panicolytic effect of both drugs administered at the highest dose and decreases in <strong>Fos</strong> protein immunolabeled perikarya found in the amygdaloid complex, hypothalamus and periaqueductal gray matter columns, which are structures that make up the encephalic <b>aversion</b> system.
+FOS	drug	cocaine	29165565	We assessed <strong>Fos</strong> expression in prelimbic cortex neurons that project to contralateral nucleus accumbens core following cued reinstatement of <b>cocaine</b> or sucrose seeking.
+FOS	addiction	relapse	29165565	We assessed <strong>Fos</strong> expression in prelimbic cortex neurons that project to contralateral nucleus accumbens core following cued <b>reinstatement</b> of cocaine or sucrose <b>seeking</b>.
+FOS	drug	cocaine	29139213	Therefore, using c <strong>fos</strong> as a marker, we here examined neuronal activity in LHb in rats that self administered <b>cocaine</b> for either 10 or 60 days.
+FOS	drug	cocaine	29139213	After 10 days of <b>cocaine</b> self administration, both the density and intensity of c <strong>fos</strong> positive cells were significantly increased in LHbL, but not LHbM, while after 60 days, an increased density (but not intensity) of labeled neurons in both LHbL and LHbM was observed.
+FOS	drug	alcohol	29111360	Voluntary Binge like <b>Ethanol</b> Consumption Site specifically Increases c <strong>Fos</strong> Immunoexpression in Male C57BL6/J Mice.
+FOS	addiction	intoxication	29111360	Voluntary <b>Binge</b> like Ethanol Consumption Site specifically Increases c <strong>Fos</strong> Immunoexpression in Male C57BL6/J Mice.
+FOS	drug	alcohol	29111360	The assessment of binge <b>ethanol</b> induced neuronal activation, using c <strong>Fos</strong> immunoreactivity (IR) as a marker of neuronal activity, is typically accomplished via forced <b>ethanol</b> exposure, such as intraperitoneal injection or gavage.
+FOS	addiction	intoxication	29111360	The assessment of <b>binge</b> ethanol induced neuronal activation, using c <strong>Fos</strong> immunoreactivity (IR) as a marker of neuronal activity, is typically accomplished via forced ethanol exposure, such as intraperitoneal injection or gavage.
+FOS	drug	alcohol	29111360	Additionally, studies assessing <b>ethanol</b> elicited neuronal activation may or may not involve stereotaxic surgery, which could impact c <strong>Fos</strong> IR.
+FOS	drug	alcohol	29111360	The experiments detailed herein aimed to assess the effects of voluntary binge like <b>ethanol</b> consumption on c <strong>Fos</strong> IR in brain regions implicated in <b>ethanol</b> intake in animals with and without surgery experience.
+FOS	addiction	intoxication	29111360	The experiments detailed herein aimed to assess the effects of voluntary <b>binge</b> like ethanol consumption on c <strong>Fos</strong> IR in brain regions implicated in ethanol intake in animals with and without surgery experience.
+FOS	drug	alcohol	29111360	Relative to water consuming controls, mice with BECs ≥ 80 mg/dl showed significantly elevated c <strong>Fos</strong> IR in several brain regions implicated in neurobiological responses to <b>ethanol</b>.
+FOS	drug	alcohol	29111360	In general, the brain regions exhibiting binge induced c <strong>Fos</strong> IR were the same between studies, though differences were noted, highlighting the need for caution when interpreting <b>ethanol</b> induced c <strong>Fos</strong> IR when subjects have a prior history of surgery.
+FOS	addiction	intoxication	29111360	In general, the brain regions exhibiting <b>binge</b> induced c <strong>Fos</strong> IR were the same between studies, though differences were noted, highlighting the need for caution when interpreting ethanol induced c <strong>Fos</strong> IR when subjects have a prior history of surgery.
+FOS	addiction	reward	29093669	Gene expression analysis after <b>CPP</b> test revealed specific up regulation in the CAF COC group of Drd1a, <strong>cFos</strong>, and FosB in the NAc, and <strong>cFos</strong>, Egr1, and Npas4 in the mPFC.
+FOS	drug	cocaine	29093348	Moreover, after the posttest, the number of <strong>cFos</strong> positive mPFC neurons in rats that were conditioned with <b>cocaine</b> was significantly larger than that with saline.
+FOS	drug	alcohol	29089891	<b>Ethanol</b> associated context induced the reinstatement of <b>ethanol</b> seeking and increased the expression of <strong>Fos</strong> in the prelimbic cortex.
+FOS	addiction	relapse	29089891	Ethanol associated context induced the <b>reinstatement</b> of ethanol <b>seeking</b> and increased the expression of <strong>Fos</strong> in the prelimbic cortex.
+FOS	drug	opioid	29073109	<b>Opioid</b>/orexin stimulations in either cortical hotspot activated <strong>Fos</strong> throughout a distributed "hedonic circuit" involving cortical and subcortical structures.
+FOS	addiction	reward	29073109	Opioid/orexin stimulations in either cortical hotspot activated <strong>Fos</strong> throughout a distributed "<b>hedonic</b> circuit" involving cortical and subcortical structures.
+FOS	drug	opioid	29054430	NMDA receptor dependent changes in c <strong>fos</strong> and p CREB signaling following extinction and reinstatement of <b>morphine</b> place preference.
+FOS	addiction	relapse	29054430	NMDA receptor dependent changes in c <strong>fos</strong> and p CREB signaling following extinction and <b>reinstatement</b> of morphine place preference.
+FOS	drug	opioid	29054430	Therefore, in the present study, we tried to evaluate the effect of antagonism of NMDA glutamate receptors on the p CREB/CREB ratio and c <strong>fos</strong> expression in the NAc, PFC and HIP during these two phases of <b>morphine</b> CPP in male adult albino Wistar rats.
+FOS	addiction	reward	29054430	Therefore, in the present study, we tried to evaluate the effect of antagonism of NMDA glutamate receptors on the p CREB/CREB ratio and c <strong>fos</strong> expression in the NAc, PFC and HIP during these two phases of morphine <b>CPP</b> in male adult albino Wistar rats.
+FOS	drug	opioid	29054430	Therefore, it can be assumed that consolidation and reconsolidation of <b>morphine</b> memory via intra PFC,  NAc and  HIP NMDA glutamate receptors are in accordance with changes in p CREB/CREB ratio and c <strong>fos</strong> levels.
+FOS	drug	nicotine	29038792	Neuroanatomical Relationships between Orexin/Hypocretin Containing Neurons/Nerve Fibers and <b>Nicotine</b> Induced c <strong>Fos</strong> Activated Cells of the Reward Addiction Neurocircuitry.
+FOS	addiction	addiction	29038792	Neuroanatomical Relationships between Orexin/Hypocretin Containing Neurons/Nerve Fibers and Nicotine Induced c <strong>Fos</strong> Activated Cells of the Reward <b>Addiction</b> Neurocircuitry.
+FOS	addiction	reward	29038792	Neuroanatomical Relationships between Orexin/Hypocretin Containing Neurons/Nerve Fibers and Nicotine Induced c <strong>Fos</strong> Activated Cells of the <b>Reward</b> Addiction Neurocircuitry.
+FOS	drug	nicotine	29038792	In the present study in mice, we first used c <strong>Fos</strong> immunohistochemistry to identify CNS cells stimulated by an acute single injection of <b>nicotine</b> (NIC, 2 mg/kg, IP).
+FOS	addiction	addiction	29038792	Sequential double labelling was then performed to identify the location of orexin containing neurons and nerve fibers with respect to NIC induced c <strong>Fos</strong> activated cells and/or tyrosine hydroxylase (TH) immunoreactive (IR) cells of the mesocorticolimbic reward <b>addiction</b> pathways.
+FOS	addiction	reward	29038792	Sequential double labelling was then performed to identify the location of orexin containing neurons and nerve fibers with respect to NIC induced c <strong>Fos</strong> activated cells and/or tyrosine hydroxylase (TH) immunoreactive (IR) cells of the mesocorticolimbic <b>reward</b> addiction pathways.
+FOS	addiction	addiction	29038792	Orexin IR nerve fibers and terminals were detected at multiple sites of the NIC reward <b>addiction</b> circuitry in close apposition to, and intermingled with, NIC induced c <strong>Fos</strong> IR cells of locus coeruleus (LC), ventral tegmental area (VTA), nucleus accumbens (Acb), LH and paraventricular thalamic nucleus (PVT).
+FOS	addiction	reward	29038792	Orexin IR nerve fibers and terminals were detected at multiple sites of the NIC <b>reward</b> addiction circuitry in close apposition to, and intermingled with, NIC induced c <strong>Fos</strong> IR cells of locus coeruleus (LC), ventral tegmental area (VTA), nucleus accumbens (Acb), LH and paraventricular thalamic nucleus (PVT).
+FOS	drug	cocaine	28977525	Oxytocin Reduces <b>Cocaine</b> Cued <strong>Fos</strong> Activation in a Regionally Specific Manner.
+FOS	drug	cocaine	28977525	Here, we studied <strong>Fos</strong> expression following <b>cocaine</b> cued reinstatement in both male and female rats.
+FOS	addiction	relapse	28977525	Here, we studied <strong>Fos</strong> expression following cocaine cued <b>reinstatement</b> in both male and female rats.
+FOS	drug	cocaine	28977525	Oxytocin decreased reinstated <b>cocaine</b> seeking, increased <strong>Fos</strong> activation in the paraventricular nucleus of the hypothalamus and central amygdala, but normalized cue induced <strong>Fos</strong> activation in the medial prefrontal cortex, nucleus accumbens core, and subthalamic nucleus, thereby demonstrating regionally specific activation patterns.
+FOS	addiction	relapse	28977525	Oxytocin decreased reinstated cocaine <b>seeking</b>, increased <strong>Fos</strong> activation in the paraventricular nucleus of the hypothalamus and central amygdala, but normalized cue induced <strong>Fos</strong> activation in the medial prefrontal cortex, nucleus accumbens core, and subthalamic nucleus, thereby demonstrating regionally specific activation patterns.
+FOS	drug	cocaine	28977525	No sex differences were seen for the effects of oxytocin on <b>cocaine</b> seeking and <strong>Fos</strong> activation, indicating that oxytocin acts on similar central neural circuits critical to reinstated <b>cocaine</b> seeking in both males and females.
+FOS	addiction	relapse	28977525	No sex differences were seen for the effects of oxytocin on cocaine <b>seeking</b> and <strong>Fos</strong> activation, indicating that oxytocin acts on similar central neural circuits critical to reinstated cocaine <b>seeking</b> in both males and females.
+FOS	drug	cocaine	28957664	Exposure to <b>cocaine</b> and the test chamber induced rapid and transient NPAS4 expression in a small subpopulation of <strong>FOS</strong> positive neurons in the NAc.
+FOS	addiction	sensitization	28941277	Chronic EtOH also caused a lasting <b>sensitization</b> of stress induced microglial CD11b, but not neuronal c <strong>Fos</strong>.
+FOS	drug	amphetamine	28860974	Moreover, we demonstrated a pathway specific activation pattern of D1 MSNs and D2 MSNs in a manic like mouse model induced by D <b>Amphetamine</b> by utilizing this double transgenic mice and c <strong>fos</strong> immunoreactivity.
+FOS	drug	amphetamine	28857482	In addition, Cdkn1cBACx1 animals were hypersensitive to <b>amphetamine</b> as showed by c <strong>fos</strong> expression in the nucleus accumbens.
+FOS	drug	amphetamine	28840858	<b>AMPH</b> induced significantly more expression of the activity dependent gene <strong>Fos</strong> in both D1 and D2 dopamine receptor expressing medium spiny neurons (MSNs) of the NAc of PV+ interneuron silenced mice, suggesting a function for PV+ interneuron mediated MSN inhibition in the expression of <b>AMPH</b> induced locomotor sensitization and CPP.
+FOS	addiction	reward	28840858	AMPH induced significantly more expression of the activity dependent gene <strong>Fos</strong> in both D1 and D2 dopamine receptor expressing medium spiny neurons (MSNs) of the NAc of PV+ interneuron silenced mice, suggesting a function for PV+ interneuron mediated MSN inhibition in the expression of AMPH induced locomotor sensitization and <b>CPP</b>.
+FOS	addiction	sensitization	28840858	AMPH induced significantly more expression of the activity dependent gene <strong>Fos</strong> in both D1 and D2 dopamine receptor expressing medium spiny neurons (MSNs) of the NAc of PV+ interneuron silenced mice, suggesting a function for PV+ interneuron mediated MSN inhibition in the expression of AMPH induced locomotor <b>sensitization</b> and CPP.
+FOS	drug	alcohol	28802560	Further, mice that sustained a juvenile TBI exhibited a significantly reduced activation of <strong>cFos</strong> in the urocortin positive cells of the Edinger Westphal nucleus in response to <b>ethanol</b> administration.
+FOS	drug	opioid	28762073	We then compared the level of neuronal activation using <strong>cFos</strong> immunohistochemistry in 15 brain areas between rats that underwent <b>morphine</b> withdrawal and saline control rats after a test of reversal learning.
+FOS	addiction	withdrawal	28762073	We then compared the level of neuronal activation using <strong>cFos</strong> immunohistochemistry in 15 brain areas between rats that underwent morphine <b>withdrawal</b> and saline control rats after a test of reversal learning.
+FOS	drug	opioid	28762073	<strong>cFos</strong> expression significantly increased in the dorsomedial striatum and major subregions of the medial prefrontal cortex (mPFC) in the <b>morphine</b> group.
+FOS	drug	opioid	28762073	Rats that underwent prolonged <b>morphine</b> withdrawal exhibited no significant changes in <strong>cFos</strong> expression in the dorsolateral striatum, nucleus accumbens, amygdala, paraventricular thalamic nucleus, or motor cortex.
+FOS	addiction	withdrawal	28762073	Rats that underwent prolonged morphine <b>withdrawal</b> exhibited no significant changes in <strong>cFos</strong> expression in the dorsolateral striatum, nucleus accumbens, amygdala, paraventricular thalamic nucleus, or motor cortex.
+FOS	addiction	withdrawal	28762073	The rats that underwent short term <b>withdrawal</b> did not present any changes in <strong>cFos</strong> expression in any of these brain regions.
+FOS	drug	cocaine	28741623	Finally, suvorexant did not alter <strong>Fos</strong> immunoreactivity within tyrosine hydroxylase immunolabeled neurons of VTA, but did attenuate <b>cocaine</b>  and orexin induced increases in calcium transient amplitude within neurons of VTA.
+FOS	drug	cocaine	28729221	Moreover, <b>cocaine</b> induced c <strong>Fos</strong> activity was assessed in different brain regions involved in processing of rewarding stimuli.
+FOS	drug	alcohol	28726252	Furthermore, yohimbine induced reinstatement of <b>alcohol</b> seeking increased <strong>Fos</strong> activation in CeA corticotrophin releasing factor, dynorphin and GABA neurons compared with naïve and vehicle controls.
+FOS	addiction	relapse	28726252	Furthermore, yohimbine induced <b>reinstatement</b> of alcohol <b>seeking</b> increased <strong>Fos</strong> activation in CeA corticotrophin releasing factor, dynorphin and GABA neurons compared with naïve and vehicle controls.
+FOS	drug	cocaine	28710498	In particular, we identified an <strong>AP 1</strong> regulated transcriptional network in dlPFC neurons associated with <b>cocaine</b> use disorder that contains several differentially expressed hub genes.
+FOS	addiction	relapse	28695893	However, dorsal hippocampus inputs to LS showed enhanced neuronal activation (as measured by <strong>Fos</strong> expression) during context induced, but not cue induced <b>reinstatement</b>.
+FOS	drug	cocaine	28661034	Here, we determined the model's generality to <b>cocaine</b> and have begun to explore brain mechanisms of context induced relapse to <b>cocaine</b> seeking after punishment imposed abstinence, using the activity marker <strong>Fos</strong>.
+FOS	addiction	addiction	28661034	Here, we determined the model's generality to cocaine and have begun to explore brain mechanisms of context induced relapse to cocaine seeking after <b>punishment</b> imposed abstinence, using the activity marker <strong>Fos</strong>.
+FOS	addiction	relapse	28661034	Here, we determined the model's generality to cocaine and have begun to explore brain mechanisms of context induced <b>relapse</b> to cocaine <b>seeking</b> after punishment imposed abstinence, using the activity marker <strong>Fos</strong>.
+FOS	addiction	relapse	28661034	2, we used <strong>Fos</strong> immunoreactivity to determine <b>relapse</b> associated neuronal activation in brain regions of rats exposed to context A, context B or neither context.
+FOS	drug	alcohol	28589966	Here, we used the neuronal activity marker <strong>Fos</strong> and site specific injections of the KOR antagonist nor BNI and U50,488 to study brain mechanisms of U50,488 induced reinstatement of <b>alcohol</b> seeking.
+FOS	addiction	relapse	28589966	Here, we used the neuronal activity marker <strong>Fos</strong> and site specific injections of the KOR antagonist nor BNI and U50,488 to study brain mechanisms of U50,488 induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+FOS	addiction	relapse	28589966	Next, we correlated regional <strong>Fos</strong> expression with <b>reinstatement</b> induced by the most effective U50,488 dose (5 mg/kg).
+FOS	drug	alcohol	28589966	Based on the correlational <strong>Fos</strong> results, we determined the effect of bed nucleus of the stria terminalis (BNST) injections of nor BNI (4 μg/side) on U50,488 induced reinstatement of <b>alcohol</b> seeking, and reinstatement induced by injections of U50,488 (0, 0.3, 1, and 3 μg/side) into the BNST.
+FOS	addiction	relapse	28589966	Based on the correlational <strong>Fos</strong> results, we determined the effect of bed nucleus of the stria terminalis (BNST) injections of nor BNI (4 μg/side) on U50,488 induced <b>reinstatement</b> of alcohol <b>seeking</b>, and <b>reinstatement</b> induced by injections of U50,488 (0, 0.3, 1, and 3 μg/side) into the BNST.
+FOS	drug	alcohol	28589966	U50,488 induced reinstatement of <b>alcohol</b> seeking was associated with increased <strong>Fos</strong> expression in multiple brain areas, including the BNST, where it was significantly correlated with lever pressing.
+FOS	addiction	relapse	28589966	U50,488 induced <b>reinstatement</b> of alcohol <b>seeking</b> was associated with increased <strong>Fos</strong> expression in multiple brain areas, including the BNST, where it was significantly correlated with lever pressing.
+FOS	drug	cocaine	28585320	We used c <strong>Fos</strong>, quantitative RT PCR and RNA sequencing methods for insights into cellular and molecular networks supporting SERT dependent <b>cocaine</b> actions.
+FOS	drug	amphetamine	28580417	Post synaptically, pHFD animals display an increase in NAc D2 receptors and c <strong>Fos</strong> expression after <b>amphetamine</b> injection.
+FOS	drug	cocaine	28547130	Either dose of <b>cocaine</b> increased immunoreactivity for c <strong>Fos</strong> in the NA shell of both strains, with greater elevations observed in HS rats.
+FOS	drug	cocaine	28540927	Regional Differences in Striatal Neuronal Ensemble Excitability Following <b>Cocaine</b> and Extinction Memory Retrieval in <strong>Fos</strong> GFP Mice.
+FOS	drug	cocaine	28540927	Using a <b>cocaine</b> conditioned locomotion (CL) procedure, the present study assessed the excitability of neuronal ensembles in the nucleus accumbens core and shell (NAccore and NAcshell), and dorsal striatum (DS) following <b>cocaine</b> conditioning and EXT in <strong>Fos</strong> GFP mice that express green fluorescent protein (GFP) in activated neurons (GFP+).
+FOS	addiction	sensitization	28431969	Moreover, the enhancement in locomotor <b>sensitization</b> was paralleled by a selective increase in the number of the c <strong>Fos</strong>+ cells, the level of CRFR1 mRNA in the ventromedial caudate putamen (vmCPu).
+FOS	addiction	reward	28419642	NIC induced rewarding effects in the <b>CPP</b> paradigm and increased dopamine levels in Acb and PFC, α4β2nAChRs density in VTA and c <strong>Fos</strong> expression in Acb shell (AcbSh), VTA and PFC.
+FOS	drug	cannabinoid	28366798	Post sensitization treatment with <b>rimonabant</b> blocks the expression of cocaine induced behavioral sensitization and c <strong>Fos</strong> protein in mice.
+FOS	drug	cocaine	28366798	Post sensitization treatment with rimonabant blocks the expression of <b>cocaine</b> induced behavioral sensitization and c <strong>Fos</strong> protein in mice.
+FOS	addiction	sensitization	28366798	Post <b>sensitization</b> treatment with rimonabant blocks the expression of cocaine induced behavioral <b>sensitization</b> and c <strong>Fos</strong> protein in mice.
+FOS	drug	cocaine	28366798	c <strong>Fos</strong> protein expression was evaluated in the nucleus accumbens (NAcc), ventral tegmental area (VTA), basolateral amygdala (BLA), medial prefrontal cortex (mPFC) and caudate putamen (CPu) after the last (<b>cocaine</b>) challenge.
+FOS	addiction	reward	28366798	These behavioral effects were accompanied by significant changes in c <strong>Fos</strong> expression in the brain <b>reward</b> system.
+FOS	drug	cannabinoid	28366798	Chronic cocaine sensitization blunted a subsequent acute cocaine induced increase in c <strong>Fos</strong> protein in the NAcc, effect that was reversed by previous treatment with <b>rimonabant</b>.
+FOS	drug	cocaine	28366798	Chronic <b>cocaine</b> sensitization blunted a subsequent acute <b>cocaine</b> induced increase in c <strong>Fos</strong> protein in the NAcc, effect that was reversed by previous treatment with rimonabant.
+FOS	addiction	sensitization	28366798	Chronic cocaine <b>sensitization</b> blunted a subsequent acute cocaine induced increase in c <strong>Fos</strong> protein in the NAcc, effect that was reversed by previous treatment with rimonabant.
+FOS	drug	cannabinoid	28366798	Treatment with 10mg/kg <b>rimonabant</b> also attenuated the significant increase in c <strong>Fos</strong> expression in the CPu, mPFC and BLA induced by previous chronic sensitization with cocaine.
+FOS	drug	cocaine	28366798	Treatment with 10mg/kg rimonabant also attenuated the significant increase in c <strong>Fos</strong> expression in the CPu, mPFC and BLA induced by previous chronic sensitization with <b>cocaine</b>.
+FOS	addiction	sensitization	28366798	Treatment with 10mg/kg rimonabant also attenuated the significant increase in c <strong>Fos</strong> expression in the CPu, mPFC and BLA induced by previous chronic <b>sensitization</b> with cocaine.
+FOS	drug	alcohol	28294133	Finally, we sought to identify the brain regions through which ADX71441 may act to prevent relapse like behavior by mapping the neuronal activation induced by stress induced reinstatement of <b>alcohol</b> seeking using c <strong>Fos</strong> immunohistochemistry.
+FOS	addiction	relapse	28294133	Finally, we sought to identify the brain regions through which ADX71441 may act to prevent <b>relapse</b> like behavior by mapping the neuronal activation induced by stress induced <b>reinstatement</b> of alcohol <b>seeking</b> using c <strong>Fos</strong> immunohistochemistry.
+FOS	addiction	relapse	28294133	Finally, pretreatment with 3 mg/kg of ADX71441 before stress induced <b>reinstatement</b> significantly decreased c <strong>Fos</strong> expression in a network of brain regions implicated in stress induced <b>relapse</b>, comprising the nucleus accumbens shell, the dorsal raphe nucleus and the medial prefrontal cortex.
+FOS	addiction	reward	28280884	Social defeat blunted <b>reward</b> learning (manifested as reduced response bias toward a more frequently rewarded stimulus) and was associated with increased nociceptin/orphanin FQ (N/OFQ) peptide mRNA levels in the striatum and decreased <strong>Fos</strong> mRNA levels in the VTA.
+FOS	drug	cocaine	28262947	As expected, acute <b>cocaine</b> increased c <strong>Fos</strong> expression, but MDPV pretreatment negatively influenced its expression.
+FOS	drug	opioid	28185645	We characterized the genetic deletion by histology, electrophysiology, and microdialysis; probed neuronal activation by c <strong>Fos</strong> immunohistochemistry and resting state functional magnetic resonance imaging; and investigated main behavioral responses to opiates, including motivation to obtain <b>heroin</b> and palatable food.
+FOS	drug	cocaine	28138095	Relevant hippocampal features [basal c <strong>Fos</strong> activity, GABA+, parvalbumin (PV)+ and neuropeptide Y (NPY)+ interneurons and adult neurogenesis (cell proliferation and immature neurons)] were immunohistochemically assessed 73 days after the chronic <b>cocaine</b> or vehicle protocol.
+FOS	drug	cocaine	28138095	All the <b>cocaine</b> withdrawn groups, independent of whether they were submitted to behavioral assessment or not, showed enhanced basal c <strong>Fos</strong> expression and an increased number of GABA+ cells in the dentate gyrus.
+FOS	drug	amphetamine	28123032	Between tests, the rats underwent voluntary abstinence (using a discrete choice procedure between <b>methamphetamine</b> and food; 20 trials/d) for 19 d. We used in situ hybridization to measure the colabeling of the activity marker <strong>Fos</strong> with Drd1 and Drd2 in DMS and DLS after the tests.
+FOS	drug	amphetamine	28123032	The incubated response was associated with increased <strong>Fos</strong> expression in DMS but not in DLS; <strong>Fos</strong> was colabeled with both Drd1 and Drd2 DMS injections of SCH39166 or raclopride selectively decreased <b>methamphetamine</b> seeking after 21 abstinence days.
+FOS	addiction	relapse	28123032	The incubated response was associated with increased <strong>Fos</strong> expression in DMS but not in DLS; <strong>Fos</strong> was colabeled with both Drd1 and Drd2 DMS injections of SCH39166 or raclopride selectively decreased methamphetamine <b>seeking</b> after 21 abstinence days.
+FOS	drug	amphetamine	28123032	In <strong>Fos</strong> lacZ transgenic rats, selective inactivation of relapse test activated <strong>Fos</strong> neurons in DMS on abstinence day 18 decreased incubated <b>methamphetamine</b> seeking on day 21.
+FOS	addiction	relapse	28123032	In <strong>Fos</strong> lacZ transgenic rats, selective inactivation of <b>relapse</b> test activated <strong>Fos</strong> neurons in DMS on abstinence day 18 decreased incubated methamphetamine <b>seeking</b> on day 21.
+FOS	drug	opioid	28089665	Lastly, formalin induced <strong>cFos</strong> expression and the effects of systemic <b>morphine</b> were examined in the superficial dorsal horn of the spinal cord.
+FOS	drug	opioid	28089665	Intraplantar formalin produced robust expression of <strong>cFos</strong>; however, <b>morphine</b> did not attenuate the <strong>cFos</strong> expression.
+FOS	drug	amphetamine	28057490	Blockade of patch based μ opioid receptors reduced <b>METH</b> induced CPP, and reduced patch enhanced c <strong>Fos</strong> expression in the striatum following <b>METH</b> mediated CPP.
+FOS	drug	opioid	28057490	Blockade of patch based μ <b>opioid</b> receptors reduced METH induced CPP, and reduced patch enhanced c <strong>Fos</strong> expression in the striatum following METH mediated CPP.
+FOS	addiction	reward	28057490	Blockade of patch based μ opioid receptors reduced METH induced <b>CPP</b>, and reduced patch enhanced c <strong>Fos</strong> expression in the striatum following METH mediated <b>CPP</b>.
+FOS	drug	amphetamine	28034961	The encounter increased c <strong>Fos</strong> expression in the prefrontal cortex, dorsal raphe nucleus and ventral tegmental area in <b>methamphetamine</b> sensitized mice, while it did not in control mice.
+FOS	drug	alcohol	27989609	Here, using c <strong>Fos</strong> induction as a high resolution marker of neuronal activation, we report that male Alcdp1/Alcw1 congenic animals demonstrate significantly less <b>alcohol</b> withdrawal associated neural activation compared to appropriate background strain animals in the prelimbic and cingulate cortices of the prefrontal cortex as well as discrete regions of the extended amygdala (i.e., basolateral) and extended basal ganglia (i.e., dorsolateral striatum, and caudal substantia nigra pars reticulata).
+FOS	addiction	withdrawal	27989609	Here, using c <strong>Fos</strong> induction as a high resolution marker of neuronal activation, we report that male Alcdp1/Alcw1 congenic animals demonstrate significantly less alcohol <b>withdrawal</b> associated neural activation compared to appropriate background strain animals in the prelimbic and cingulate cortices of the prefrontal cortex as well as discrete regions of the extended amygdala (i.e., basolateral) and extended basal ganglia (i.e., dorsolateral striatum, and caudal substantia nigra pars reticulata).
+FOS	addiction	intoxication	27801508	Indeed, c <strong>Fos</strong> expression was specifically increased in the dorsal dentate gyrus (DG) of the hippocampus after the <b>binge</b> exposure, but then became significantly lower in adulthood both in the DG and the CA1 part of the hippocampus compared with adult saline pretreated mice.
+FOS	drug	cocaine	27789280	Fourth ventricular <b>cocaine</b> robustly increased <strong>cFos</strong> immunoreactivity in the nucleus of the solitary tract (NTS), suggesting a neural substrate for hindbrain <b>cocaine</b> mediated effects on [DA]max.
+FOS	drug	cocaine	27734601	Similarly, NGB2904 and SCH23390 showed opposite/differential effects on <b>cocaine</b> induced structural plasticity, conditioned place preference and locomotor activity and signaling activation, including the activation of ERK, CREB and NR1 and the expression of c <strong>fos</strong> and Cdk5.
+FOS	drug	opioid	27730727	In addition, treatment with another selective TRPV1 antagonist, AMG9810, not only significantly prevented <b>morphine</b> self administration but also prevented <b>morphine</b> induced c <strong>fos</strong> expression in the nucleus accumbens.
+FOS	drug	amphetamine	27703043	After the second dose of <b>amphetamine</b>, the LR rats exhibited more c <strong>Fos</strong> and GluN2B activation in layers II and III of the M1/M2 motor cortex area and prefrontal cortex (PRE, PRL, IL) and also presented with more GluN2B activation in the basal amygdala.
+FOS	addiction	relapse	27656031	After <b>reinstatement</b> testing, we visualized robust c <strong>fos</strong> expression in the basolateral amygdala (BLA), which was reduced in mice pretreated with norBNI.
+FOS	addiction	relapse	27558790	Orx/Hcrt neuronal activation in the lateral hypothalamus, dorsomedial hypothalamus and perifornical area, determined by dual c <strong>fos</strong>/orx immunocytochemistry, was quantified in rat brains, following <b>reinstatement</b> of reward <b>seeking</b> induced by a discriminative stimulus (S+) conditioned to COC or SCM.
+FOS	addiction	reward	27558790	Orx/Hcrt neuronal activation in the lateral hypothalamus, dorsomedial hypothalamus and perifornical area, determined by dual c <strong>fos</strong>/orx immunocytochemistry, was quantified in rat brains, following reinstatement of <b>reward</b> seeking induced by a discriminative stimulus (S+) conditioned to COC or SCM.
+FOS	drug	alcohol	27543844	As such, rats were administered water or <b>alcohol</b> (1 g/kg, IG) and brain tissue was processed for c <strong>Fos</strong> immunoreactivity (IR), a marker of neuronal activity.
+FOS	drug	alcohol	27543844	<b>Alcohol</b> decreased c <strong>Fos</strong> IR in the mPFC, IC, Rh and AcbC.
+FOS	drug	cocaine	27535915	These regions express <strong>Fos</strong> (a marker of neural activity) during cue induced reinstatement of <b>cocaine</b> seeking, but only subpopulations of neurons within these regions drive drug seeking.
+FOS	addiction	relapse	27535915	These regions express <strong>Fos</strong> (a marker of neural activity) during cue induced <b>reinstatement</b> of cocaine <b>seeking</b>, but only subpopulations of neurons within these regions drive drug <b>seeking</b>.
+FOS	drug	cocaine	27535915	In rats, we examined <strong>Fos</strong> expression during cue induced reinstatement of <b>cocaine</b>  and sucrose seeking in prelimbic cortex (PL), infralimbic cortex (IL), BLA, and vSub neurons that project to NAc core (NAcC) or NAc shell (NAcSh).
+FOS	addiction	relapse	27535915	In rats, we examined <strong>Fos</strong> expression during cue induced <b>reinstatement</b> of cocaine  and sucrose <b>seeking</b> in prelimbic cortex (PL), infralimbic cortex (IL), BLA, and vSub neurons that project to NAc core (NAcC) or NAc shell (NAcSh).
+FOS	drug	cocaine	27535915	Neurons in PL, BLA, and vSub that project to NAcC, but not NAcSh, expressed <strong>Fos</strong> during cue induced <b>cocaine</b> seeking, but not sucrose seeking.
+FOS	addiction	relapse	27535915	Neurons in PL, BLA, and vSub that project to NAcC, but not NAcSh, expressed <strong>Fos</strong> during cue induced cocaine <b>seeking</b>, but not sucrose <b>seeking</b>.
+FOS	drug	cocaine	27535915	Prelimbic cortex (PL) projections to nucleus accumbens core (NAcC) uniquely expressed <strong>Fos</strong> in a manner that positively correlated with <b>cocaine</b> seeking, but not sucrose seeking, behavior.
+FOS	addiction	relapse	27535915	Prelimbic cortex (PL) projections to nucleus accumbens core (NAcC) uniquely expressed <strong>Fos</strong> in a manner that positively correlated with cocaine <b>seeking</b>, but not sucrose <b>seeking</b>, behavior.
+FOS	drug	nicotine	27535909	We also used the neuronal activity marker <strong>Fos</strong> and the Daun02 chemogenetic inactivation procedure to identify cue activated neuronal ensembles that mediate incubation of <b>nicotine</b> craving.
+FOS	addiction	relapse	27535909	We also used the neuronal activity marker <strong>Fos</strong> and the Daun02 chemogenetic inactivation procedure to identify cue activated neuronal ensembles that mediate incubation of nicotine <b>craving</b>.
+FOS	addiction	withdrawal	27535909	Analysis of <strong>Fos</strong> expression in different brain areas of adolescent and adult rats on <b>withdrawal</b> days 1 and 14 showed time dependent increases in the number of <strong>Fos</strong> positive neurons in central and basolateral amygdala, orbitofrontal cortex, ventral and dorsal medial prefrontal cortex, and nucleus accumbens core and shell.
+FOS	drug	nicotine	27535909	In adult <strong>Fos</strong> lacZ transgenic rats, selective inactivation of <b>nicotine</b> cue activated <strong>Fos</strong> neurons in central amygdala, but not orbitofrontal cortex, decreased "incubated" <b>nicotine</b> seeking on withdrawal day 14.
+FOS	addiction	relapse	27535909	In adult <strong>Fos</strong> lacZ transgenic rats, selective inactivation of nicotine cue activated <strong>Fos</strong> neurons in central amygdala, but not orbitofrontal cortex, decreased "incubated" nicotine <b>seeking</b> on withdrawal day 14.
+FOS	addiction	withdrawal	27535909	In adult <strong>Fos</strong> lacZ transgenic rats, selective inactivation of nicotine cue activated <strong>Fos</strong> neurons in central amygdala, but not orbitofrontal cortex, decreased "incubated" nicotine seeking on <b>withdrawal</b> day 14.
+FOS	drug	nicotine	27535909	Here, we used a rat model of incubation of drug craving, the neuronal activity marker <strong>Fos</strong>, and the Daun02 chemogenetic inactivation method to demonstrate that incubation of <b>nicotine</b> craving is also observed after adolescent onset <b>nicotine</b> self administration and that neuronal ensembles in the central nucleus of the amygdala play a critical role in this incubation in adult rats.
+FOS	addiction	relapse	27535909	Here, we used a rat model of incubation of drug <b>craving</b>, the neuronal activity marker <strong>Fos</strong>, and the Daun02 chemogenetic inactivation method to demonstrate that incubation of nicotine <b>craving</b> is also observed after adolescent onset nicotine self administration and that neuronal ensembles in the central nucleus of the amygdala play a critical role in this incubation in adult rats.
+FOS	drug	amphetamine	27507424	Rats showing low and high sensitization of frequency modulated 50 kHz vocalization response to <b>amphetamine</b> differ in <b>amphetamine</b> induced brain <strong>Fos</strong> expression.
+FOS	addiction	sensitization	27507424	Rats showing low and high <b>sensitization</b> of frequency modulated 50 kHz vocalization response to amphetamine differ in amphetamine induced brain <strong>Fos</strong> expression.
+FOS	drug	amphetamine	27507424	We compared <b>amphetamine</b> induced <strong>Fos</strong> expression in 16 brain regions considered important for the development of addiction between rats preselected for low and high sensitization of the response and next given nine daily <b>amphetamine</b> doses followed by a 2 week withdrawal and final <b>amphetamine</b> challenge.
+FOS	addiction	addiction	27507424	We compared amphetamine induced <strong>Fos</strong> expression in 16 brain regions considered important for the development of <b>addiction</b> between rats preselected for low and high sensitization of the response and next given nine daily amphetamine doses followed by a 2 week withdrawal and final amphetamine challenge.
+FOS	addiction	sensitization	27507424	We compared amphetamine induced <strong>Fos</strong> expression in 16 brain regions considered important for the development of addiction between rats preselected for low and high <b>sensitization</b> of the response and next given nine daily amphetamine doses followed by a 2 week withdrawal and final amphetamine challenge.
+FOS	addiction	withdrawal	27507424	We compared amphetamine induced <strong>Fos</strong> expression in 16 brain regions considered important for the development of addiction between rats preselected for low and high sensitization of the response and next given nine daily amphetamine doses followed by a 2 week <b>withdrawal</b> and final amphetamine challenge.
+FOS	drug	amphetamine	27507424	Compared to those in <b>amphetamine</b> untreated controls, <strong>Fos</strong> positive nuclei counts were significantly and markedly (2 6 times) higher in 12 regions in high sensitized rats, whereas in low sensitized rats they were significantly higher in the cingulate cortex and dorsomedial striatum only.
+FOS	drug	nicotine	27491589	Nicotinic receptor blockade decreases <strong>fos</strong> immunoreactivity within orexin/hypocretin expressing neurons of <b>nicotine</b> exposed rats.
+FOS	drug	nicotine	27491589	Results demonstrate that nicotinic receptor blockade leads to reduced orexin cell activity, as indicated by lowered <strong>Fos</strong> immunoreactivity, and suggest that this underlying cellular activity may be associated with symptoms of <b>nicotine</b> withdrawal as effects were most prominently observed in rats given chronic <b>nicotine</b>.
+FOS	addiction	withdrawal	27491589	Results demonstrate that nicotinic receptor blockade leads to reduced orexin cell activity, as indicated by lowered <strong>Fos</strong> immunoreactivity, and suggest that this underlying cellular activity may be associated with symptoms of nicotine <b>withdrawal</b> as effects were most prominently observed in rats given chronic nicotine.
+FOS	drug	opioid	27468916	In rats, we assessed <strong>Fos</strong> response to lithium chloride (LiCl), β carboline, <b>naloxone</b>, lipopolysaccharide (LPS), inflammatory pain, neuropathic pain, foot shock, restraint stress, forced swimming, predator odor, and opiate withdrawal.
+FOS	addiction	withdrawal	27468916	In rats, we assessed <strong>Fos</strong> response to lithium chloride (LiCl), β carboline, naloxone, lipopolysaccharide (LPS), inflammatory pain, neuropathic pain, foot shock, restraint stress, forced swimming, predator odor, and opiate <b>withdrawal</b>.
+FOS	drug	opioid	27468916	<b>Naloxone</b> precipitated opiate withdrawal induced <strong>Fos</strong> in μ <b>opioid</b> receptor positive (15%) and  negative (85%) tVTA cells, suggesting the presence of both direct and indirect mechanisms in tVTA recruitment during withdrawal.
+FOS	addiction	withdrawal	27468916	Naloxone precipitated opiate <b>withdrawal</b> induced <strong>Fos</strong> in μ opioid receptor positive (15%) and  negative (85%) tVTA cells, suggesting the presence of both direct and indirect mechanisms in tVTA recruitment during <b>withdrawal</b>.
+FOS	addiction	relapse	27449798	To study circuit wide activations after DBS of the VS, c <strong>fos</strong> immunohistochemistry was performed in regions involved in the extinction of drug <b>seeking</b> behaviors.
+FOS	addiction	reward	27435419	For Experiment 1, brain tissue was collected 90min following the <b>CPP</b> expression test and processed for <strong>Fos</strong> immunohistochemistry.
+FOS	drug	nicotine	27435419	We found that rats conditioned with <b>nicotine</b> with or without a social partner exhibited CPP; however, we found no group differences in <strong>Fos</strong> expression in any brain region analyzed, with the exception of the nucleus accumbens core that exhibited a social induced attenuation in <strong>Fos</strong> expression.
+FOS	addiction	reward	27435419	We found that rats conditioned with nicotine with or without a social partner exhibited <b>CPP</b>; however, we found no group differences in <strong>Fos</strong> expression in any brain region analyzed, with the exception of the nucleus accumbens core that exhibited a social induced attenuation in <strong>Fos</strong> expression.
+FOS	drug	nicotine	27421892	Acute <b>nicotine</b> enhances spontaneous recovery of contextual fear and changes c <strong>fos</strong> early gene expression in infralimbic cortex, hippocampus, and amygdala.
+FOS	drug	nicotine	27421892	In the present study, we tested the effects of acute <b>nicotine</b> administration on SR of extinguished contextual fear memories and c <strong>fos</strong> immediate early gene immunohistochemistry in mice.
+FOS	drug	nicotine	27421892	C <strong>fos</strong> immunoreactive (IR) cells in the ventral hippocampus and basolateral amygdala were increased in the <b>nicotine</b> treated mice following testing for SR, whereas the number of IR cells in the infralimbic cortex was decreased in the same group.
+FOS	addiction	aversion	27388762	Both EtOH  and LiCl induced <b>CTA</b> significantly enhanced <strong>cFos</strong> expression in the RMTg and LHb but not the hippocampus.
+FOS	addiction	aversion	27388762	Similar to behavioral measures, no significant effect of sex on <b>CTA</b> induced <strong>cFos</strong> expression was observed.
+FOS	addiction	aversion	27388762	<strong>cFos</strong> expression in both the RMTg and LHb was significantly correlated with <b>CTA</b> magnitude with greater <strong>cFos</strong> being associated with more pronounced <b>CTA</b>.
+FOS	drug	alcohol	27388762	Furthermore, increased <strong>cFos</strong> expression in the RMTg following EtOH induced CTA suggests that this region plays a role in signaling <b>alcohol</b>'s aversive properties.
+FOS	addiction	aversion	27388762	Furthermore, increased <strong>cFos</strong> expression in the RMTg following EtOH induced <b>CTA</b> suggests that this region plays a role in signaling alcohol's <b>aversive</b> properties.
+FOS	drug	cocaine	27362504	We predicted that LC NE neurons would exhibit <strong>Fos</strong> activation on ED1, and that blocking CRF1 signaling would decrease drug seeking on ED1 measured by responding on an active lever previously associated with <b>cocaine</b> self  administration.
+FOS	addiction	relapse	27362504	We predicted that LC NE neurons would exhibit <strong>Fos</strong> activation on ED1, and that blocking CRF1 signaling would decrease drug <b>seeking</b> on ED1 measured by responding on an active lever previously associated with cocaine self  administration.
+FOS	drug	nicotine	27347434	In the present study in mice, we first used c <strong>Fos</strong> immunohistochemistry to identify CNS cells stimulated by <b>nicotine</b> (NIC, 40 μg/kg, IP) and by a peripherally acting analog of <b>nicotine</b>, <b>nicotine</b> pyrrolidine methiodide (NIC PM, 30 μg/kg, IP).
+FOS	addiction	addiction	27347434	With the exception of sparse numbers of TH immunoreactive D11 cells, dopamine containing neurons in other areas of the reward <b>addiction</b> circuitry, namely periaqueductal gray, and dorsal raphe, were also devoid of c <strong>Fos</strong> immunoreactivity.
+FOS	addiction	reward	27347434	With the exception of sparse numbers of TH immunoreactive D11 cells, dopamine containing neurons in other areas of the <b>reward</b> addiction circuitry, namely periaqueductal gray, and dorsal raphe, were also devoid of c <strong>Fos</strong> immunoreactivity.
+FOS	drug	alcohol	27234303	c <strong>Fos</strong> protein expression and the frequency of both spontaneous action potential firings and spontaneous excitatory postsynaptic currents were higher in LHb neurons of <b>ethanol</b> withdrawn rats compared to their <b>ethanol</b> naïve counterparts.
+FOS	drug	opioid	27212105	Previous studies indicated that the dopamine D4 receptor (D4 R) activation counteracts <b>morphine</b> induced adaptive changes of the μ <b>opioid</b> receptor (MOR) signaling in the striosomes of the caudate putamen (CPu), as well as the induction of several <strong>Fos</strong> family transcription factors.
+FOS	drug	cocaine	27163750	Here, we investigated the conditioned place preference (CPP) in social (conspecific) vs <b>cocaine</b> conditioning, and the expression of central c <strong>Fos</strong>, hypothalamic oxytocin (OT) and vasopressin (AVP) in ICR mice.
+FOS	addiction	reward	27163750	Here, we investigated the conditioned place preference (<b>CPP</b>) in social (conspecific) vs cocaine conditioning, and the expression of central c <strong>Fos</strong>, hypothalamic oxytocin (OT) and vasopressin (AVP) in ICR mice.
+FOS	drug	cocaine	27163750	We observed differential expression of c <strong>Fos</strong> immunoreactive neurons in the ventral anterior cingulate cortex, posterior cingulate cortex, accumbens (shell and core), medial nucleus of the amygdale and the ventral pallidum when comparing the control (CK), social (SC) or <b>cocaine</b> conditioning (CC) group, and social vs <b>cocaine</b> conditioning (SCC) group.
+FOS	drug	opioid	27155000	Activation of dura sensitive trigeminal neurons and increased c <strong>Fos</strong> protein induced by <b>morphine</b> withdrawal in the rostral ventromedial medulla.
+FOS	addiction	withdrawal	27155000	Activation of dura sensitive trigeminal neurons and increased c <strong>Fos</strong> protein induced by morphine <b>withdrawal</b> in the rostral ventromedial medulla.
+FOS	drug	opioid	27155000	Results In chronic <b>morphine</b> treated animals, <b>naloxone</b> methiodide microinjections produced a significant increase both in ongoing and facial heat evoked activity and an increase in <strong>Fos</strong> positive neurons in the Vc and in the nucleus reticularis dorsalis, a brainstem region involved in diffuse noxious inhibitory controls.
+FOS	drug	alcohol	27126842	We found similar reduced social recognition, increased motor stereotypies and increased anxiety with relevant c <strong>fos</strong> response alterations in morphine, nicotine, THC and <b>alcohol</b> abstinent mice.
+FOS	drug	cannabinoid	27126842	We found similar reduced social recognition, increased motor stereotypies and increased anxiety with relevant c <strong>fos</strong> response alterations in morphine, nicotine, <b>THC</b> and alcohol abstinent mice.
+FOS	drug	nicotine	27126842	We found similar reduced social recognition, increased motor stereotypies and increased anxiety with relevant c <strong>fos</strong> response alterations in morphine, <b>nicotine</b>, THC and alcohol abstinent mice.
+FOS	drug	opioid	27126842	We found similar reduced social recognition, increased motor stereotypies and increased anxiety with relevant c <strong>fos</strong> response alterations in <b>morphine</b>, nicotine, THC and alcohol abstinent mice.
+FOS	addiction	withdrawal	27091613	To identify the anatomical substrates associated with PCP induced social <b>withdrawal</b> and the contrasting effects of URB597 on SI in PCP  versus saline treated rats, we analyzed SI induced c <strong>Fos</strong> expression in 28 brain areas relevant to schizophrenia and/or social behavior following vehicle or URB597 administration.
+FOS	drug	alcohol	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (CREB) and c <strong>fos</strong> have important role in morphine induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and <b>alcohol</b>.
+FOS	drug	cocaine	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (CREB) and c <strong>fos</strong> have important role in morphine induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, <b>cocaine</b>, nicotine, and alcohol.
+FOS	drug	nicotine	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (CREB) and c <strong>fos</strong> have important role in morphine induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, <b>nicotine</b>, and alcohol.
+FOS	drug	opioid	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (CREB) and c <strong>fos</strong> have important role in <b>morphine</b> induced conditioned place preference (CPP) induced by drugs of abuse, such as <b>morphine</b>, cocaine, nicotine, and alcohol.
+FOS	addiction	reward	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (CREB) and c <strong>fos</strong> have important role in morphine induced conditioned place preference (<b>CPP</b>) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.
+FOS	drug	opioid	27053349	Therefore, in the present study, we investigated the changes in phosphorylated CREB (p CREB) and c <strong>fos</strong> induction within the nucleus accumbens (NAc), HIP, and PFC after intracerebroventricular (ICV) administration of different doses of CNQX or vehicle during extinction period or reinstatement of <b>morphine</b> induced CPP.
+FOS	addiction	relapse	27053349	Therefore, in the present study, we investigated the changes in phosphorylated CREB (p CREB) and c <strong>fos</strong> induction within the nucleus accumbens (NAc), HIP, and PFC after intracerebroventricular (ICV) administration of different doses of CNQX or vehicle during extinction period or <b>reinstatement</b> of morphine induced CPP.
+FOS	addiction	reward	27053349	Therefore, in the present study, we investigated the changes in phosphorylated CREB (p CREB) and c <strong>fos</strong> induction within the nucleus accumbens (NAc), HIP, and PFC after intracerebroventricular (ICV) administration of different doses of CNQX or vehicle during extinction period or reinstatement of morphine induced <b>CPP</b>.
+FOS	drug	opioid	27040714	Following the treatment with the <b>opioid</b> receptor antagonist <b>naloxone</b> methiodide (5mg/kg, s.c.), the administration of ketanserin failed to inhibit the repeated inflammation induced increase in NADPH d reactivity and c <strong>Fos</strong> expression in the spinal dorsal horn.
+FOS	addiction	relapse	26985037	First, we measured double labeling of the neuronal activity marker <strong>Fos</strong> with the retrograde tracer cholera toxin subunit B (injected in NAc shell) and demonstrated that context induced <b>relapse</b> is associated with selective activation of the vSub→NAc shell projection.
+FOS	drug	amphetamine	26979294	As expected, compared with Controls, Paired rats administered IP <b>amphetamine</b> subsequently showed a conditioned locomotor response when challenged with saline in the open field, an effect accompanied by an increase in c <strong>Fos</strong>+ neurons in the medial NAcc.
+FOS	drug	amphetamine	26979294	In contrast, Paired rats previously exposed to VTA <b>amphetamine</b> showed neither conditioned locomotion nor conditioned c <strong>Fos</strong>+ expression.
+FOS	drug	amphetamine	26979294	Together, these results suggest a role for c <strong>Fos</strong>+ neurons in the medial NAcc and rapid changes in the morphology of their dendritic spines in the expression of conditioning evoked by <b>amphetamine</b> paired contextual stimuli.
+FOS	drug	amphetamine	26896754	In addition, <b>methamphetamine</b> administration and withdrawal increased striatal MOPr binding, as well as c <strong>Fos</strong>(+)/CRF(+) neuronal expression in the amygdala, whereas an increase in plasma corticosterone levels was observed following <b>METH</b> administration, but not withdrawal.
+FOS	addiction	withdrawal	26896754	In addition, methamphetamine administration and <b>withdrawal</b> increased striatal MOPr binding, as well as c <strong>Fos</strong>(+)/CRF(+) neuronal expression in the amygdala, whereas an increase in plasma corticosterone levels was observed following METH administration, but not <b>withdrawal</b>.
+FOS	drug	cannabinoid	26883973	β caryophyllene, a dietary <b>cannabinoid</b>, complexed with β cyclodextrin produced anti hyperalgesic effect involving the inhibition of <strong>Fos</strong> expression in superficial dorsal horn.
+FOS	drug	cocaine	26861675	The ERK CREB <strong>Fos</strong> pathway and the NMDA receptor NR2B subunits in the NAc were involved in the <b>cocaine</b> induced behavioral sensitization.
+FOS	addiction	sensitization	26861675	The ERK CREB <strong>Fos</strong> pathway and the NMDA receptor NR2B subunits in the NAc were involved in the cocaine induced behavioral <b>sensitization</b>.
+FOS	drug	psychedelics	26807959	Furthermore, <b>ibogaine</b> has been shown to interact with the acetylcholine, serotonin and dopamine systems; it alters the expression of several proteins including substance P, brain derived neurotrophic factor (BDNF), c <strong>fos</strong> and egr 1.
+FOS	drug	cannabinoid	26803309	CB1 <b>Cannabinoid</b> Agonist (WIN55,212 2) Within the Basolateral Amygdala Induced Sensitization to Morphine and Increased the Level of μ Opioid Receptor and c <strong>fos</strong> in the Nucleus Accumbens.
+FOS	drug	opioid	26803309	CB1 Cannabinoid Agonist (WIN55,212 2) Within the Basolateral Amygdala Induced Sensitization to <b>Morphine</b> and Increased the Level of μ <b>Opioid</b> Receptor and c <strong>fos</strong> in the Nucleus Accumbens.
+FOS	addiction	sensitization	26803309	CB1 Cannabinoid Agonist (WIN55,212 2) Within the Basolateral Amygdala Induced <b>Sensitization</b> to Morphine and Increased the Level of μ Opioid Receptor and c <strong>fos</strong> in the Nucleus Accumbens.
+FOS	drug	opioid	26803309	In this study, effects of intra BLA administration of CB1R agonist on sensitization to antinociceptive effect of <b>morphine</b> and changes in the levels of μ <b>opioid</b> receptor (MOR), p CREB, and c <strong>fos</strong> in the NAc were investigated.
+FOS	addiction	sensitization	26803309	In this study, effects of intra BLA administration of CB1R agonist on <b>sensitization</b> to antinociceptive effect of morphine and changes in the levels of μ opioid receptor (MOR), p CREB, and c <strong>fos</strong> in the NAc were investigated.
+FOS	drug	opioid	26803309	The results indicated that intra BLA injection of WIN55,212 2 during sensitization period resulted in the induction of antinociceptive responses by ineffective dose of <b>morphine</b> and caused a significant increase in the MOR and c <strong>fos</strong> levels but not p CREB/CREB ratio in the NAc.
+FOS	addiction	sensitization	26803309	The results indicated that intra BLA injection of WIN55,212 2 during <b>sensitization</b> period resulted in the induction of antinociceptive responses by ineffective dose of morphine and caused a significant increase in the MOR and c <strong>fos</strong> levels but not p CREB/CREB ratio in the NAc.
+FOS	drug	opioid	26803309	It seems that c <strong>fos</strong> is one of the important factors involved in the induction of sensitization to antinociceptive effect of <b>morphine</b>.
+FOS	addiction	sensitization	26803309	It seems that c <strong>fos</strong> is one of the important factors involved in the induction of <b>sensitization</b> to antinociceptive effect of morphine.
+FOS	drug	cannabinoid	26799708	The expression of c <strong>Fos</strong> after <b>THC</b> treatment was analysed in several brain areas in wild type mice and in mice lacking the PPO gene.
+FOS	drug	cannabinoid	26799708	<b>THC</b> induced increase in c <strong>Fos</strong> expression was reduced in the central amygdala, medial preoptic area and lateral septum in these mutant mice.
+FOS	drug	alcohol	26786746	<b>Alcohol</b> consumption increases locomotion in an open field and induces <strong>Fos</strong> immunoreactivity in reward and approach/withdrawal related neurocircuitries.
+FOS	addiction	reward	26786746	Alcohol consumption increases locomotion in an open field and induces <strong>Fos</strong> immunoreactivity in <b>reward</b> and approach/withdrawal related neurocircuitries.
+FOS	addiction	withdrawal	26786746	Alcohol consumption increases locomotion in an open field and induces <strong>Fos</strong> immunoreactivity in reward and approach/<b>withdrawal</b> related neurocircuitries.
+FOS	drug	alcohol	26786746	Additionally, <b>alcohol</b> intake increased <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> ir) in the prefrontal cortex, in the shell region of the nucleus accumbens, in the medial and central amygdala, in the bed nucleus of the stria terminalis, in the septal region, and in the paraventricular and dorsomedial hypothalamus, structures that have been linked to reward and to approach/withdrawal behavior.
+FOS	addiction	reward	26786746	Additionally, alcohol intake increased <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> ir) in the prefrontal cortex, in the shell region of the nucleus accumbens, in the medial and central amygdala, in the bed nucleus of the stria terminalis, in the septal region, and in the paraventricular and dorsomedial hypothalamus, structures that have been linked to <b>reward</b> and to approach/withdrawal behavior.
+FOS	addiction	withdrawal	26786746	Additionally, alcohol intake increased <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> ir) in the prefrontal cortex, in the shell region of the nucleus accumbens, in the medial and central amygdala, in the bed nucleus of the stria terminalis, in the septal region, and in the paraventricular and dorsomedial hypothalamus, structures that have been linked to reward and to approach/<b>withdrawal</b> behavior.
+FOS	drug	alcohol	26775553	Acute <b>ethanol</b> treatment significantly increased <strong>Fos</strong> immunoreactivity in the BNST and the central amygdala.
+FOS	drug	alcohol	26750264	To investigate the role of ORX neurons in <b>ethanol</b> (EtOH) seeking, we measured <strong>Fos</strong> activation of ORX neurons in rats following three different measures of EtOH seeking and preference: (i) context induced reinstatement, or ABA renewal; (ii) cue induced reinstatement of extinguished responding for EtOH; and (iii) a home cage task in which preference for EtOH (vs. water) was measured in the absence of either reinforcer.
+FOS	addiction	relapse	26750264	To investigate the role of ORX neurons in ethanol (EtOH) <b>seeking</b>, we measured <strong>Fos</strong> activation of ORX neurons in rats following three different measures of EtOH <b>seeking</b> and preference: (i) context induced <b>reinstatement</b>, or ABA renewal; (ii) cue induced <b>reinstatement</b> of extinguished responding for EtOH; and (iii) a home cage task in which preference for EtOH (vs. water) was measured in the absence of either reinforcer.
+FOS	addiction	relapse	26750264	In addition, <strong>Fos</strong> activation in ORX neurons in the dorsomedial hypothalamic and perifornical areas was correlated with context and home cage <b>seeking</b>/preference, respectively.
+FOS	drug	alcohol	26727528	<b>Alcohol</b> Induces Parallel Changes in Hippocampal Histone H3 Phosphorylation and c <strong>Fos</strong> Protein Expression in Male Rats.
+FOS	addiction	withdrawal	26727528	Subsequent examination of c <strong>fos</strong>, a gene known to be regulated by H3S10ph, revealed that EtOH and <b>withdrawal</b> associated changes in c <strong>fos</strong> closely paralleled changes in H3S10ph.
+FOS	drug	cocaine	26674058	We aimed to clarify the regulatory role of the NAc in the <b>cocaine</b> memory reconsolidation process, by examining the effect of applying different pharmacological interventions to the NAc on Zif 268 and <strong>Fos</strong> B expression in the entire reward circuit after <b>cocaine</b> memory reactivation.
+FOS	addiction	reward	26674058	We aimed to clarify the regulatory role of the NAc in the cocaine memory reconsolidation process, by examining the effect of applying different pharmacological interventions to the NAc on Zif 268 and <strong>Fos</strong> B expression in the entire <b>reward</b> circuit after cocaine memory reactivation.
+FOS	drug	cocaine	26674058	Through the <b>cocaine</b> induced conditioned place preference (CPP) model, immunohistochemical and immunofluorescence staining for Zif 268 and <strong>Fos</strong> B were used to explore the functional activated brain nuclei after <b>cocaine</b> memory reactivation.
+FOS	addiction	reward	26674058	Through the cocaine induced conditioned place preference (<b>CPP</b>) model, immunohistochemical and immunofluorescence staining for Zif 268 and <strong>Fos</strong> B were used to explore the functional activated brain nuclei after cocaine memory reactivation.
+FOS	addiction	addiction	26674058	Further, bilateral NAc shell infusion of MK 801 and SCH 23390, but not raclopride or propranolol, prior to <b>addictive</b> memory reconsolidation, decreased Zif 268 and <strong>Fos</strong> B expression in the entire reward circuit, except for the amygdala, and effectively disturbed subsequent CPP related behavior.
+FOS	addiction	reward	26674058	Further, bilateral NAc shell infusion of MK 801 and SCH 23390, but not raclopride or propranolol, prior to addictive memory reconsolidation, decreased Zif 268 and <strong>Fos</strong> B expression in the entire <b>reward</b> circuit, except for the amygdala, and effectively disturbed subsequent <b>CPP</b> related behavior.
+FOS	drug	cocaine	26674058	In summary, N methyl d aspartate (NMDA) and dopamine D1 receptors, but not dopamine D2 or β adrenergic receptors, within the NAc shell, may regulate Zif 268 and <strong>Fos</strong> B expression in most brain nuclei of the reward circuit after <b>cocaine</b> memory reactivation.
+FOS	addiction	reward	26674058	In summary, N methyl d aspartate (NMDA) and dopamine D1 receptors, but not dopamine D2 or β adrenergic receptors, within the NAc shell, may regulate Zif 268 and <strong>Fos</strong> B expression in most brain nuclei of the <b>reward</b> circuit after cocaine memory reactivation.
+FOS	drug	opioid	26655477	These results suggest that multiple phenotypic regions are mediated by NMDAR and <strong>Fos</strong>/ΔFosB during <b>morphine</b> withdrawal, such as the motivational (AcbC, AcbSh), limbic (CeC, VTA) and executive (Cg) system pathways, and may be the primary targets of NMDAR and <strong>Fos</strong>/ΔfosB that impact <b>morphine</b> withdrawal behaviors.
+FOS	addiction	withdrawal	26655477	These results suggest that multiple phenotypic regions are mediated by NMDAR and <strong>Fos</strong>/ΔFosB during morphine <b>withdrawal</b>, such as the motivational (AcbC, AcbSh), limbic (CeC, VTA) and executive (Cg) system pathways, and may be the primary targets of NMDAR and <strong>Fos</strong>/ΔfosB that impact morphine <b>withdrawal</b> behaviors.
+FOS	addiction	reward	26602173	In addition, we quantified the expression of tyrosine hydroxylase (TH) in the ventral tegmental area (VTA) and c <strong>Fos</strong> in the anterior cingulate cortex (ACC) as a response to <b>reward</b> learning and pain response.
+FOS	drug	cocaine	26598422	Increased expression after <b>cocaine</b> self administration was found for 6 IEGs in dorsal and ventral striatum (c <strong>fos</strong>, Mkp1, Fosb/ΔFosb, Egr2, Egr4, and Arc) and 10 IEGs in mPFC (same 6 IEGs as in striatum, plus Bdnf, Homer1, Sgk1 and Rgs2).
+FOS	drug	amphetamine	26515740	Reductions in c <strong>Fos</strong> related immunoreactivity were found in dorsomedial striatum (DMS) but not dorsolateral striatum after exposure to the <b>METH</b> context suggesting this effect reflected a loss specifically in goal directed control in the <b>METH</b> context.
+FOS	drug	amphetamine	26515740	This reduction in c <strong>Fos</strong> was localized to non enkephalin expressing neurons in the DMS, likely dopamine D1 expressing direct pathway neurons, suggesting a relative change in control by the D1 direct versus D2 indirect pathways originating in the DMS may have been induced by <b>METH</b> context exposure.
+FOS	drug	amphetamine	26496011	We detected six downregulated genes in the frontal cortex and the hippocampus of chronic <b>METH</b> treated mice, including five IEGs (Arc, Egr2, <strong>Fos</strong>, Klf10, and Nr4a1) and one neuronal receptor gene (Grm1), compared with normal saline treated group, but only four genes (Arc, Egr2, <strong>Fos</strong>, and Nr4a1) were confirmed to be different.
+FOS	drug	amphetamine	26496011	Furthermore, we found several CpG sites of the Arc and the <strong>Fos</strong> that had significant changes in DNA methylation status in the frontal cortex of chronic <b>METH</b> treated mice, while the klf10 and the Nr4a1 that had significant changes in the hippocampus.
+FOS	drug	amphetamine	26433325	We also found that <b>AMPH</b> administration completely blocked the forced swim induced expression of the corticotropin releasing hormone (hnCRH) and it partially reduced c <strong>fos</strong> expression in the paraventricular nucleus of the hypothalamus (PVN).
+FOS	drug	amphetamine	26391065	Here, we examined the influence of intra NAc MK 801 infusions on sex experience induced NAc deltaFosB and <strong>cFos</strong> expression, as well as mating  and <b>Amph</b> induced CPP in adult male rats.
+FOS	addiction	reward	26391065	Here, we examined the influence of intra NAc MK 801 infusions on sex experience induced NAc deltaFosB and <strong>cFos</strong> expression, as well as mating  and Amph induced <b>CPP</b> in adult male rats.
+FOS	drug	amphetamine	26391065	Together, these results provide evidence that NAc NMDA receptor activation during sexual behavior plays a key role in mating induced <strong>cFos</strong> and deltaFosB expression and subsequent experience induced cross sensitization to <b>Amph</b> reward.
+FOS	addiction	reward	26391065	Together, these results provide evidence that NAc NMDA receptor activation during sexual behavior plays a key role in mating induced <strong>cFos</strong> and deltaFosB expression and subsequent experience induced cross sensitization to Amph <b>reward</b>.
+FOS	addiction	sensitization	26391065	Together, these results provide evidence that NAc NMDA receptor activation during sexual behavior plays a key role in mating induced <strong>cFos</strong> and deltaFosB expression and subsequent experience induced cross <b>sensitization</b> to Amph reward.
+FOS	drug	cocaine	26386479	We used <strong>Fos</strong> GFP transgenic mice that contained a transgene with a <strong>Fos</strong> promoter driving expression of green fluorescent protein (GFP) to detect neurons that were strongly activated during associative learning, in this case, context independent and context specific <b>cocaine</b> induced locomotor sensitization.
+FOS	addiction	sensitization	26386479	We used <strong>Fos</strong> GFP transgenic mice that contained a transgene with a <strong>Fos</strong> promoter driving expression of green fluorescent protein (GFP) to detect neurons that were strongly activated during associative learning, in this case, context independent and context specific cocaine induced locomotor <b>sensitization</b>.
+FOS	addiction	relapse	26344108	We combined <strong>Fos</strong> with the retrograde tracer Fluoro Gold (FG) to determine projection specific activation during the context induced <b>reinstatement</b> tests.
+FOS	drug	opioid	26344108	Context induced reinstatement of <b>heroin</b> seeking was associated with increased <strong>Fos</strong> expression in vSub neurons, including those projecting to NAc shell and vmPFC.
+FOS	addiction	relapse	26344108	Context induced <b>reinstatement</b> of heroin <b>seeking</b> was associated with increased <strong>Fos</strong> expression in vSub neurons, including those projecting to NAc shell and vmPFC.
+FOS	drug	alcohol	26302652	3 showed that <b>ethanol</b> cue induced c <strong>Fos</strong> immunoreactivity in the BNST was reduced by hM4Di activation (Experiment 4) and in the absence of hM4Di, CNO did not affect <b>ethanol</b> CPP (Experiment 5).
+FOS	addiction	reward	26302652	3 showed that ethanol cue induced c <strong>Fos</strong> immunoreactivity in the BNST was reduced by hM4Di activation (Experiment 4) and in the absence of hM4Di, CNO did not affect ethanol <b>CPP</b> (Experiment 5).
+FOS	drug	alcohol	26283508	In agreement with these findings, c <strong>Fos</strong> immunoreactivity in LHb regions was enhanced after a single administration of a low dose of <b>ethanol</b> (0.25 g/kg i.p.).
+FOS	drug	alcohol	26224858	Cue induced reinstatement of <b>alcohol</b> seeking activates a subset of mPFC neurons in rats, identified by their common expression of the activity marker <strong>cFos</strong> and comprised of both principal and interneurons.
+FOS	addiction	relapse	26224858	Cue induced <b>reinstatement</b> of alcohol <b>seeking</b> activates a subset of mPFC neurons in rats, identified by their common expression of the activity marker <strong>cFos</strong> and comprised of both principal and interneurons.
+FOS	addiction	sensitization	26217204	These manifestations of central <b>sensitization</b> were associated with augmented c <strong>Fos</strong> expression in spinal cord, thalamus, hypothalamus, amygdala and prefrontal cortex.
+FOS	addiction	aversion	26217204	Intrarectal allyl isothiocyanate (AITC) evoked <b>aversive</b> behavior (freezing, reduction of locomotion and exploration) in association with p42/44 MAPK and c <strong>Fos</strong> activation in spinal cord and brain.
+FOS	drug	opioid	26192542	Finally, BLA c <strong>fos</strong> expression was reduced by clonidine, and blockade of BLA β and α1 receptors prevented <b>heroin</b> reacquisition.
+FOS	drug	alcohol	26188146	Here, we administered an NK1R antagonist or vehicle prior to footshock induced reinstatement of <b>alcohol</b> seeking, and mapped the resulting neuronal activation using <strong>Fos</strong> immunohistochemistry.
+FOS	addiction	relapse	26188146	Here, we administered an NK1R antagonist or vehicle prior to footshock induced <b>reinstatement</b> of alcohol <b>seeking</b>, and mapped the resulting neuronal activation using <strong>Fos</strong> immunohistochemistry.
+FOS	drug	nicotine	26169054	Many studies have demonstrated that repeated injections of <b>nicotine</b> can produce progressive increases in locomotor activity and enhanced expression of c <strong>fos</strong> and tyrosine hydroxylase (TH) in brain dopaminergic areas.
+FOS	drug	nicotine	26169054	This study was carried out to investigate the effects of PJ on repeated <b>nicotine</b> induced behavioral sensitization of locomotor activity and c <strong>Fos</strong> and TH expression in the rat brain using immunohistochemistry.
+FOS	addiction	sensitization	26169054	This study was carried out to investigate the effects of PJ on repeated nicotine induced behavioral <b>sensitization</b> of locomotor activity and c <strong>Fos</strong> and TH expression in the rat brain using immunohistochemistry.
+FOS	drug	nicotine	26169054	Pretreatment with PJ decreased the development of <b>nicotine</b> induced sensitization, c <strong>Fos</strong> expression in the nucleus accumbens and striatum, and TH expression in the ventral tegmental area.
+FOS	addiction	sensitization	26169054	Pretreatment with PJ decreased the development of nicotine induced <b>sensitization</b>, c <strong>Fos</strong> expression in the nucleus accumbens and striatum, and TH expression in the ventral tegmental area.
+FOS	drug	nicotine	26111579	α2 Null mutant mice have altered levels of neuronal activity in restricted midbrain and limbic brain regions during <b>nicotine</b> withdrawal as demonstrated by <strong>cfos</strong> expression.
+FOS	addiction	withdrawal	26111579	α2 Null mutant mice have altered levels of neuronal activity in restricted midbrain and limbic brain regions during nicotine <b>withdrawal</b> as demonstrated by <strong>cfos</strong> expression.
+FOS	drug	nicotine	26111579	Using alpha(α)2 nAChR subunit null mutant mice, the current study evaluates whether the absence of this gene product during mecamylamine precipitated <b>nicotine</b> withdrawal eliminates neuronal activity within selective midbrain and limbic brain regions, as determined by the expression of the immediate early gene, <strong>cfos</strong>.
+FOS	addiction	withdrawal	26111579	Using alpha(α)2 nAChR subunit null mutant mice, the current study evaluates whether the absence of this gene product during mecamylamine precipitated nicotine <b>withdrawal</b> eliminates neuronal activity within selective midbrain and limbic brain regions, as determined by the expression of the immediate early gene, <strong>cfos</strong>.
+FOS	drug	nicotine	26111579	Overall, our findings demonstrate that α2 null mutant mice have altered <strong>cfos</strong> expression in distinct populations of neurons within selective midbrain and limbic brain structures that mediate baseline and <b>nicotine</b> withdrawal induced neuronal activity.
+FOS	addiction	withdrawal	26111579	Overall, our findings demonstrate that α2 null mutant mice have altered <strong>cfos</strong> expression in distinct populations of neurons within selective midbrain and limbic brain structures that mediate baseline and nicotine <b>withdrawal</b> induced neuronal activity.
+FOS	addiction	relapse	26096647	PVT sections were obtained following completion of the <b>reinstatement</b> tests and labeled for <strong>Fos</strong>.
+FOS	addiction	relapse	26096647	Moreover, <strong>Fos</strong> expression was significantly correlated with the number of <b>reinstatement</b> responses that were induced by the COC S+ .
+FOS	drug	cocaine	26072178	Based on the anatomical distribution of GLP 1 receptors in the brain and the well established effects of GLP 1 on food reward, we decided to investigate the effect of the GLP 1 analogue exendin 4 on <b>cocaine</b>  and dopamine D1 receptor agonist induced hyperlocomotion, on acute and chronic <b>cocaine</b> self administration, on <b>cocaine</b> induced striatal dopamine release in mice and on <b>cocaine</b> induced c <strong>fos</strong> activation.
+FOS	addiction	reward	26072178	Based on the anatomical distribution of GLP 1 receptors in the brain and the well established effects of GLP 1 on food <b>reward</b>, we decided to investigate the effect of the GLP 1 analogue exendin 4 on cocaine  and dopamine D1 receptor agonist induced hyperlocomotion, on acute and chronic cocaine self administration, on cocaine induced striatal dopamine release in mice and on cocaine induced c <strong>fos</strong> activation.
+FOS	drug	cocaine	26072178	In addition, we show that peripheral administration of exendin 4 reduces <b>cocaine</b> induced elevation of striatal dopamine levels and striatal c <strong>fos</strong> expression implicating central GLP 1 receptors in these responses.
+FOS	drug	cocaine	26063926	Methyl supplementation attenuates <b>cocaine</b> seeking behaviors and <b>cocaine</b> induced c <strong>Fos</strong> activation in a DNA methylation dependent manner.
+FOS	addiction	relapse	26063926	Methyl supplementation attenuates cocaine <b>seeking</b> behaviors and cocaine induced c <strong>Fos</strong> activation in a DNA methylation dependent manner.
+FOS	drug	cocaine	26063926	When compared with vehicle pretreated rats, the immediate early gene c <strong>Fos</strong> (a marker of neuronal activation) was upregulated in the NAc and mPFC of <b>cocaine</b> pretreated rats after <b>cocaine</b> primed reinstatement, and chronic MET treatment blocked its induction in both regions.
+FOS	addiction	relapse	26063926	When compared with vehicle pretreated rats, the immediate early gene c <strong>Fos</strong> (a marker of neuronal activation) was upregulated in the NAc and mPFC of cocaine pretreated rats after cocaine primed <b>reinstatement</b>, and chronic MET treatment blocked its induction in both regions.
+FOS	drug	cocaine	26063926	<b>Cocaine</b> induced c <strong>Fos</strong> expression in the NAc was associated with reduced methylation at CpG dinucleotides in the c <strong>Fos</strong> gene promoter, effects reversed by MET treatment.
+FOS	addiction	relapse	26063926	Overall, these data suggest that drug <b>seeking</b> behaviors are, in part, attributable to a DNA methylation dependent process, likely occurring at specific gene loci (e.g., c <strong>Fos</strong>) in the reward pathway.
+FOS	addiction	reward	26063926	Overall, these data suggest that drug seeking behaviors are, in part, attributable to a DNA methylation dependent process, likely occurring at specific gene loci (e.g., c <strong>Fos</strong>) in the <b>reward</b> pathway.
+FOS	drug	cocaine	26048642	Less studied is the fact that the shell can be further subdivided into a dorsomedial shell (NAcDMS) and an intermediate zone (NAcINT) based on differential expression of transient c <strong>Fos</strong> and long acting immediate early gene ΔFosB upon <b>cocaine</b> sensitization.
+FOS	addiction	sensitization	26048642	Less studied is the fact that the shell can be further subdivided into a dorsomedial shell (NAcDMS) and an intermediate zone (NAcINT) based on differential expression of transient c <strong>Fos</strong> and long acting immediate early gene ΔFosB upon cocaine <b>sensitization</b>.
+FOS	drug	amphetamine	26019338	Incubation of <b>methamphetamine</b> craving is associated with selective increases in expression of Bdnf and trkb, glutamate receptors, and epigenetic enzymes in cue activated <strong>fos</strong> expressing dorsal striatal neurons.
+FOS	addiction	relapse	26019338	Incubation of methamphetamine <b>craving</b> is associated with selective increases in expression of Bdnf and trkb, glutamate receptors, and epigenetic enzymes in cue activated <strong>fos</strong> expressing dorsal striatal neurons.
+FOS	addiction	relapse	26019338	Next, using fluorescence activated cell sorting, we compared gene expression in <strong>Fos</strong> positive dorsal striatal neurons, which were activated during "incubated" cue induced drug <b>seeking</b> tests after prolonged withdrawal, with nonactivated <strong>Fos</strong> negative neurons.
+FOS	addiction	withdrawal	26019338	Next, using fluorescence activated cell sorting, we compared gene expression in <strong>Fos</strong> positive dorsal striatal neurons, which were activated during "incubated" cue induced drug seeking tests after prolonged <b>withdrawal</b>, with nonactivated <strong>Fos</strong> negative neurons.
+FOS	drug	amphetamine	26019338	Finally, we found that DS injections of SCH23390 (C17H18ClNO), a D1 family receptor antagonist known to block cue induced <strong>Fos</strong> induction, decreased incubated cue induced <b>methamphetamine</b> seeking after prolonged withdrawal.
+FOS	addiction	relapse	26019338	Finally, we found that DS injections of SCH23390 (C17H18ClNO), a D1 family receptor antagonist known to block cue induced <strong>Fos</strong> induction, decreased incubated cue induced methamphetamine <b>seeking</b> after prolonged withdrawal.
+FOS	addiction	withdrawal	26019338	Finally, we found that DS injections of SCH23390 (C17H18ClNO), a D1 family receptor antagonist known to block cue induced <strong>Fos</strong> induction, decreased incubated cue induced methamphetamine seeking after prolonged <b>withdrawal</b>.
+FOS	addiction	reward	26007337	In Experiment 1, animals self administered pellets containing 55% F + 45% G or 30% F + 70% G, and <strong>Fos</strong> immunoreactivity was assessed in hypothalamic regions regulating food intake and <b>reward</b>.
+FOS	drug	cocaine	25982833	Neuronal reactivity was analyzed through the expression of two immediate early genes (Arc and c <strong>Fos</strong>) to decipher cellular responses to STN HFS and <b>cocaine</b>.
+FOS	drug	cocaine	25982833	Interestingly, and despite some differential effects on Arc and c <strong>Fos</strong> expression, STN HFS diminished the c <strong>Fos</strong> response induced by acute <b>cocaine</b> in the striatum.
+FOS	drug	cocaine	25870909	Adult hippocampal neurogenesis was pharmacologically reduced with temozolomide (TMZ), and mice were tested for <b>cocaine</b> induced CPP to study c <strong>Fos</strong> expression in the hippocampus and in extrahippocampal addiction related areas.
+FOS	addiction	addiction	25870909	Adult hippocampal neurogenesis was pharmacologically reduced with temozolomide (TMZ), and mice were tested for cocaine induced CPP to study c <strong>Fos</strong> expression in the hippocampus and in extrahippocampal <b>addiction</b> related areas.
+FOS	addiction	reward	25870909	Adult hippocampal neurogenesis was pharmacologically reduced with temozolomide (TMZ), and mice were tested for cocaine induced <b>CPP</b> to study c <strong>Fos</strong> expression in the hippocampus and in extrahippocampal addiction related areas.
+FOS	drug	amphetamine	25855177	Context induced reinstatement of <b>methamphetamine</b> seeking is associated with unique molecular alterations in <strong>Fos</strong> expressing dorsolateral striatum neurons.
+FOS	addiction	relapse	25855177	Context induced <b>reinstatement</b> of methamphetamine <b>seeking</b> is associated with unique molecular alterations in <strong>Fos</strong> expressing dorsolateral striatum neurons.
+FOS	drug	amphetamine	25855177	In this study, we found that context induced reinstatement of <b>methamphetamine</b> seeking increased expression of the neural activity marker <strong>Fos</strong> in dorsal but not ventral striatum.
+FOS	addiction	relapse	25855177	In this study, we found that context induced <b>reinstatement</b> of methamphetamine <b>seeking</b> increased expression of the neural activity marker <strong>Fos</strong> in dorsal but not ventral striatum.
+FOS	addiction	relapse	25855177	Based on our previous findings that <strong>Fos</strong> expressing neurons play a critical role in conditioned drug effects, we assessed whether context induced <b>reinstatement</b> was associated with molecular alterations selectively induced within context activated <strong>Fos</strong> expressing neurons.
+FOS	addiction	relapse	25855177	We used fluorescence activated cell sorting to isolate <b>reinstatement</b> activated <strong>Fos</strong> positive neurons from <strong>Fos</strong> negative neurons in dorsal striatum and used quantitative PCR to assess gene expression within these two populations of neurons.
+FOS	addiction	relapse	25855177	Context induced <b>reinstatement</b> was associated with increased expression of the immediate early genes <strong>Fos</strong> and FosB and the NMDA receptor subunit gene Grin2a in only <strong>Fos</strong> positive neurons.
+FOS	drug	amphetamine	25855177	Our results demonstrate an important role of dorsolateral striatum in context induced reinstatement of <b>methamphetamine</b> seeking and that this reinstatement is associated with unique gene alterations in <strong>Fos</strong> expressing neurons.
+FOS	addiction	relapse	25855177	Our results demonstrate an important role of dorsolateral striatum in context induced <b>reinstatement</b> of methamphetamine <b>seeking</b> and that this <b>reinstatement</b> is associated with unique gene alterations in <strong>Fos</strong> expressing neurons.
+FOS	drug	amphetamine	25813745	PCA allowed for the examination of the relative contribution of our variables of interest to the variance in the data obtained from multiple behavioural tasks, including the skilled reaching task, the Morris water task, the discriminative fear conditioning to context task, the elevated plus maze task and the conditioned place preference task to a low dose of <b>amphetamine</b>, as well as volumetric estimates of brain volumes and <strong>cfos</strong> activation.
+FOS	drug	cocaine	25733538	Finally, when re exposed to the previously <b>cocaine</b> associated context, female H mice displayed greater <strong>Fos</strong> activation in the cingulate cortex, nucleus accumbens, and basolateral amygdala.
+FOS	drug	alcohol	25727639	Using markers of neuronal activation c <strong>Fos</strong>, EGR1, and phophorylated extracellar signal regulated kinase (pERK1/2), adult responses to a moderate and binge drinking <b>ethanol</b> challenge, e.g., 2 or 4 g/kg, were determined.
+FOS	addiction	intoxication	25727639	Using markers of neuronal activation c <strong>Fos</strong>, EGR1, and phophorylated extracellar signal regulated kinase (pERK1/2), adult responses to a moderate and <b>binge</b> drinking ethanol challenge, e.g., 2 or 4 g/kg, were determined.
+FOS	drug	alcohol	25700946	Here, we show an <b>alcohol</b>  and cocaine induced increase in c <strong>fos</strong> expression in the hippocampal dentate gyrus, which is absent in αCaMKII(T286A) autophosphorylation deficient mice.
+FOS	drug	cocaine	25700946	Here, we show an alcohol  and <b>cocaine</b> induced increase in c <strong>fos</strong> expression in the hippocampal dentate gyrus, which is absent in αCaMKII(T286A) autophosphorylation deficient mice.
+FOS	drug	opioid	25582704	<b>Morphine</b> withdrawal induced an enhancement of NA turnover in PVN in parallel with an increase in TH neurons expressing c <strong>Fos</strong> in VLM in wild type mice.
+FOS	addiction	withdrawal	25582704	Morphine <b>withdrawal</b> induced an enhancement of NA turnover in PVN in parallel with an increase in TH neurons expressing c <strong>Fos</strong> in VLM in wild type mice.
+FOS	drug	opioid	25582704	The main finding of the present study was that NA turnover, TH positive neurons that express c <strong>Fos</strong>, TH phosphorylated at serine 40 and PKA expression observed during <b>morphine</b> withdrawal were significantly inhibited in CRF1R KO mice.
+FOS	addiction	withdrawal	25582704	The main finding of the present study was that NA turnover, TH positive neurons that express c <strong>Fos</strong>, TH phosphorylated at serine 40 and PKA expression observed during morphine <b>withdrawal</b> were significantly inhibited in CRF1R KO mice.
+FOS	drug	cocaine	25566008	The increased <b>cocaine</b> CPP was associated with an increased expression of the immediate early genes (IEGs) c <strong>Fos</strong> and Early Growth Related Protein 1 (EGR1) in the accumbens corridor, i.e., a region stretching from the anterior commissure to the interhemispheric border and comprising the medial nucleus accumbens core and shell, the major island of Calleja and intermediate part of the lateral septum, as well as the vertical limb of the diagonal band and medial septum.
+FOS	addiction	reward	25566008	The increased cocaine <b>CPP</b> was associated with an increased expression of the immediate early genes (IEGs) c <strong>Fos</strong> and Early Growth Related Protein 1 (EGR1) in the accumbens corridor, i.e., a region stretching from the anterior commissure to the interhemispheric border and comprising the medial nucleus accumbens core and shell, the major island of Calleja and intermediate part of the lateral septum, as well as the vertical limb of the diagonal band and medial septum.
+FOS	drug	cocaine	25566008	With respect to the activation by contingent vs. non contingent <b>cocaine</b> EGR1 seemed to be a more sensitive marker than c <strong>Fos</strong>.
+FOS	drug	opioid	25556110	CP 154 526 antagonised the enhancement in c <strong>Fos</strong> expression evoked by <b>morphine</b> induced CPP in the VTA and NAc, and the activation of the orexinergic neurons in the LLH.
+FOS	addiction	reward	25556110	CP 154 526 antagonised the enhancement in c <strong>Fos</strong> expression evoked by morphine induced <b>CPP</b> in the VTA and NAc, and the activation of the orexinergic neurons in the LLH.
+FOS	drug	nicotine	25515333	Target prediction and pathway enrichment analyses showed daf 4, daf 1, <strong>fos</strong> 1, cmk 1, and unc 30 to be potential effectors of <b>nicotine</b> addiction.
+FOS	addiction	addiction	25515333	Target prediction and pathway enrichment analyses showed daf 4, daf 1, <strong>fos</strong> 1, cmk 1, and unc 30 to be potential effectors of nicotine <b>addiction</b>.
+FOS	drug	benzodiazepine	25482326	The aim of this study was to examine the effects of <b>benzodiazepine</b> (<b>midazolam</b>) administration on rat conditioned fear responses and on local brain activity (c <strong>Fos</strong> and CRF expressions) of low  (LR) and high  (HR)anxiety rats after the first and second contextual fear test sessions.
+FOS	drug	benzodiazepine	25482326	The pretreatment of rats with <b>midazolam</b> before the second exposure to the aversive context significantly attenuated the conditioned fear response, lowered the serum corticosterone concentration, decreased c <strong>Fos</strong> and CRF expressions in the MeA and in the BLA, and increased CRF complex density in M1 area only in the LR group.
+FOS	addiction	aversion	25482326	The pretreatment of rats with midazolam before the second exposure to the <b>aversive</b> context significantly attenuated the conditioned fear response, lowered the serum corticosterone concentration, decreased c <strong>Fos</strong> and CRF expressions in the MeA and in the BLA, and increased CRF complex density in M1 area only in the LR group.
+FOS	drug	opioid	25481016	<b>Morphine</b> induced conditioned place preference and the alterations of p ERK, p CREB and c <strong>fos</strong> levels in hypothalamus and hippocampus: the effects of physical stress.
+FOS	drug	opioid	25481016	In the current study, effects of acute and subchronic stress on the alteration of p ERK, p CREB and c <strong>fos</strong> levels in the hypothalamus and hippocampus of saline  or <b>morphine</b> treated animals during <b>morphine</b> induced conditioned place preference (CPP) procedure were investigated.
+FOS	addiction	reward	25481016	In the current study, effects of acute and subchronic stress on the alteration of p ERK, p CREB and c <strong>fos</strong> levels in the hypothalamus and hippocampus of saline  or morphine treated animals during morphine induced conditioned place preference (<b>CPP</b>) procedure were investigated.
+FOS	addiction	reward	25481016	In all of groups, the <b>CPP</b> procedure was done, afterward the alternation of p ERK/ERK ratio, p CREB/CREB ratio and c <strong>fos</strong> level in the hypothalamus and hippocampus were estimated by Western blot analysis.
+FOS	drug	opioid	25481016	The results indicated that in saline  or <b>morphine</b> treated animals, p ERK/ERK ratio, p CREB/CREB ratio and c <strong>fos</strong> level increased after application of acute and subchronic stress (except for p ERK/ERK ratio in <b>morphine</b> control group).
+FOS	drug	opioid	25481016	Our findings revealed that in saline  or <b>morphine</b> treated animals, acute and subcronic stress increased the p ERK/ERK ratio, p CREB/CREB ratio and c <strong>fos</strong> level in the hypothalamus and hippocampus and this enhancement in <b>morphine</b> treated animals, was more considerable than that in saline treated animals.
+FOS	drug	cocaine	25451087	Region specific effects of isoflurane anesthesia on <strong>Fos</strong> immunoreactivity in response to intravenous <b>cocaine</b> challenge in rats with a history of repeated <b>cocaine</b> administration.
+FOS	drug	cocaine	25451087	administration of <b>cocaine</b> increases <strong>Fos</strong> immunoreactivity in rats under isoflurane anesthesia.
+FOS	drug	cocaine	25451087	Given that <strong>Fos</strong> expression is a marker of neural activation, the results suggested that isoflurane is appropriate for imaging <b>cocaine</b> effects under anesthesia.
+FOS	drug	cocaine	25451087	We found that challenge injections of <b>cocaine</b> following a regimen of repeated <b>cocaine</b> exposure resulted in <strong>Fos</strong> expression in the prefrontal cortex and striatum roughly equivalent to that found in rats who had received the <b>cocaine</b> challenge after a history of vehicle injections.
+FOS	drug	cocaine	25451087	Additionally, isoflurane anesthesia resulted in a heterogeneous attenuation of <b>cocaine</b> induced <strong>Fos</strong> expression, with the most robust effect in the orbital cortex but no effect in the nucleus accumbens core (NAcC).
+FOS	drug	cocaine	25451087	These results indicate that <b>cocaine</b> induced <strong>Fos</strong> is preserved in the NAcC under isoflurane, suggesting that isoflurane can be used in imaging studies involving <b>cocaine</b> effects in this region.
+FOS	drug	amphetamine	25446574	At the end of behavioral experiments, in order to evaluate the effect of LV siRNA on D1aR expression, rats were challenged with <b>amphetamine</b> and the brains were processed for immunohistochemical detection of c <strong>Fos</strong> and D1aR.
+FOS	drug	cocaine	25446574	Infusion of LV siRNAs in the medial NAc shell reduced D1aR density and the number of c <strong>Fos</strong> positive nuclei in the NAc shell, while sparing the core, and prevented the acquisition of <b>cocaine</b>, but not heroin SA.
+FOS	drug	opioid	25446574	Infusion of LV siRNAs in the medial NAc shell reduced D1aR density and the number of c <strong>Fos</strong> positive nuclei in the NAc shell, while sparing the core, and prevented the acquisition of cocaine, but not <b>heroin</b> SA.
+FOS	drug	cocaine	25446574	In turn, LV siRNAs infusion in the core reduced D1aR density and the number of c <strong>Fos</strong> positive nuclei in the same area, while sparing the shell, and failed to affect acquisition of <b>cocaine</b>.
+FOS	drug	nicotine	25430056	Both <strong>cFos</strong> and phosphorylated cJun (p cJun) were immediately increased in the nucleus, together with an increase of calmodulin kinase (CaMK) IV but not CaMKII expression after <b>nicotine</b> exposure.
+FOS	drug	nicotine	25430056	A nonselective inhibitor of CaMKs, KN 93, and a calcium chelating regent, BAPTA AM, completely suppressed the expression of <strong>cFos</strong> and p cJun in the nucleus as well as the <b>nicotine</b> induced IP3 R 1 upregulation.
+FOS	drug	nicotine	25430056	These results indicate that nAChR activation by <b>nicotine</b> upregulates IP3 R 1 via increase of activator protein 1, which is a <strong>cFos</strong> and cJun dimmer, in the nucleus, with activation of Ca(2+) signaling transduction processes.
+FOS	drug	opioid	25425322	Lastly, food and <b>opioid</b> cues engaged similar amygdalo striatal thalamic circuitry to a much greater extent in STs than GTs, as indicated by <strong>Fos</strong> expression.
+FOS	drug	opioid	25424867	Retrieval of <b>morphine</b> associated context induces <strong>cFos</strong> in dentate gyrus neurons.
+FOS	addiction	reward	25424867	This associative learning has a cellular correlate, as there are more <strong>cFos</strong>+ neurons in the hippocampal dentate gyrus (DG) after psychostimulant conditioned place preference (<b>CPP</b>) versus saline controls.
+FOS	addiction	reward	25424867	To explore this, we employed an unbiased, counterbalanced, and shortened <b>CPP</b> design that led to place preference and more DG <strong>cFos</strong>+ cells.
+FOS	drug	opioid	25424867	<b>Morphine</b> paired mice sequestered to CS+ had ∼30% more DG <strong>cFos</strong>+ cells than saline paired mice.
+FOS	drug	opioid	25424867	Furthermore, Bregma analysis revealed <b>morphine</b> paired mice had more <strong>cFos</strong>+ cells in CS+ compared to CS  controls.
+FOS	drug	opioid	25424867	Notably, there was no significant difference in DG <strong>cFos</strong>+ cell number after handling alone or after receiving <b>morphine</b> in home cage.
+FOS	drug	alcohol	25336083	The results suggest the following: (i) BF nicotine infusion induced c <strong>Fos</strong> in both core and the shell region of NAc at levels comparable to those observed after systemic <b>alcohol</b> administration; (ii) BF nicotine infusion with systemic <b>alcohol</b> induced a significant additive increase in c <strong>Fos</strong> expression only in the NAc shell region.
+FOS	drug	nicotine	25336083	The results suggest the following: (i) BF <b>nicotine</b> infusion induced c <strong>Fos</strong> in both core and the shell region of NAc at levels comparable to those observed after systemic alcohol administration; (ii) BF <b>nicotine</b> infusion with systemic alcohol induced a significant additive increase in c <strong>Fos</strong> expression only in the NAc shell region.
+FOS	drug	cocaine	25332000	This study was designed to reveal neuronal c <strong>Fos</strong>, Zif268 expression pattern in 10 brain regions following <b>cocaine</b> context associated reward memory retrieval in mice, combining animal behavioral study and immunofluorescence method.
+FOS	addiction	reward	25332000	This study was designed to reveal neuronal c <strong>Fos</strong>, Zif268 expression pattern in 10 brain regions following cocaine context associated <b>reward</b> memory retrieval in mice, combining animal behavioral study and immunofluorescence method.
+FOS	drug	cocaine	25332000	The results showed that: Neuronal c <strong>Fos</strong>, Zif268 protein expression levels in nucleus accumbens (NAc) core both were elevated in <b>Cocaine</b> retrieval group compared with those in Saline retrieval (Control) group during <b>cocaine</b> context associated reward memory retrieval.
+FOS	addiction	reward	25332000	The results showed that: Neuronal c <strong>Fos</strong>, Zif268 protein expression levels in nucleus accumbens (NAc) core both were elevated in Cocaine retrieval group compared with those in Saline retrieval (Control) group during cocaine context associated <b>reward</b> memory retrieval.
+FOS	drug	opioid	25308750	The purpose of this study was to investigate the effects of MR blockade on: brain stress system responses to <b>naloxone</b> induced <b>morphine</b> withdrawal, the somatic signs of abstinence; the effects of <b>morphine</b> withdrawal on noradrenaline (NA) turnover in the paraventricular nucleus (PVN), c <strong>Fos</strong> expression and tyrosine hydroxylase (TH) phosphorylated at Ser31 levels in the nucleus tractus solitarius noradrenergic cell group (NTS A2); and finally, hypothalamus pituitary adrenocortical (HPA) axis activity.
+FOS	addiction	withdrawal	25308750	The purpose of this study was to investigate the effects of MR blockade on: brain stress system responses to naloxone induced morphine <b>withdrawal</b>, the somatic signs of abstinence; the effects of morphine <b>withdrawal</b> on noradrenaline (NA) turnover in the paraventricular nucleus (PVN), c <strong>Fos</strong> expression and tyrosine hydroxylase (TH) phosphorylated at Ser31 levels in the nucleus tractus solitarius noradrenergic cell group (NTS A2); and finally, hypothalamus pituitary adrenocortical (HPA) axis activity.
+FOS	drug	opioid	25308750	On the other hand, pretreatment with spironolactone resulted in no significant modification of the increased NA turnover, TH activation, c <strong>Fos</strong> expression or HPA axis activity that occurred during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	25308750	On the other hand, pretreatment with spironolactone resulted in no significant modification of the increased NA turnover, TH activation, c <strong>Fos</strong> expression or HPA axis activity that occurred during morphine <b>withdrawal</b>.
+FOS	drug	cocaine	25294309	Therefore, these experiments explored the role of newly generated neurons in drug reward context association by examining the activation, as determined by expression of the immediate early gene <strong>cfos</strong>, of young and mature granule cells in the septal and temporal dentate gyrus of adult rats that were re exposed to a drug paired environment following the development of <b>cocaine</b> place preference.
+FOS	addiction	reward	25294309	Therefore, these experiments explored the role of newly generated neurons in drug <b>reward</b> context association by examining the activation, as determined by expression of the immediate early gene <strong>cfos</strong>, of young and mature granule cells in the septal and temporal dentate gyrus of adult rats that were re exposed to a drug paired environment following the development of cocaine place preference.
+FOS	drug	cocaine	25294309	However, the number of activated new neurons (DCX + <strong>cfos</strong>) was greater in the temporal dentate gyrus of <b>cocaine</b> conditioned rats re exposed to the drug paired environment as compared to those re exposed to a neutral environment.
+FOS	drug	cocaine	25290264	Under <b>cocaine</b>, the attenuated DA and 5 HT activation in αCaMKII(T286A) mice was followed by impaired c <strong>Fos</strong> activation in the NAcc.
+FOS	drug	opioid	25290009	Although <b>morphine</b> was previously reported to produce an instant induction of c <strong>fos</strong> in the striatum, our recent studies have demonstrated that the expression of numerous immediate early genes (IEGs) is significantly elevated at delayed time points (several hours) after <b>morphine</b> administration.
+FOS	drug	opioid	25290009	To better dissect the time course of <b>opioid</b> produced IEG induction, we used in situ hybridization to examine the expression of the IEGs c <strong>fos</strong>, zif268 and arc in the mouse forebrain at several time points after acute <b>morphine</b> injection.
+FOS	drug	amphetamine	25273280	Immunohistochemical analysis of brain tissue demonstrated that wheel running during withdrawal did not regulate markers of <b>methamphetamine</b> neurotoxicity (neurogenesis, neuronal nitric oxide synthase, vesicular monoamine transporter 2) and cellular activation (c <strong>Fos</strong>) in brain regions involved in relapse to drug seeking.
+FOS	addiction	relapse	25273280	Immunohistochemical analysis of brain tissue demonstrated that wheel running during withdrawal did not regulate markers of methamphetamine neurotoxicity (neurogenesis, neuronal nitric oxide synthase, vesicular monoamine transporter 2) and cellular activation (c <strong>Fos</strong>) in brain regions involved in <b>relapse</b> to drug <b>seeking</b>.
+FOS	addiction	withdrawal	25273280	Immunohistochemical analysis of brain tissue demonstrated that wheel running during <b>withdrawal</b> did not regulate markers of methamphetamine neurotoxicity (neurogenesis, neuronal nitric oxide synthase, vesicular monoamine transporter 2) and cellular activation (c <strong>Fos</strong>) in brain regions involved in relapse to drug seeking.
+FOS	addiction	withdrawal	25229718	Using immunohistochemistry and whole cell patch clamp electrophysiology, we also found that CIE increased <strong>FOS</strong> IR and enhanced neuronal excitability in the ventral BNST (vBNST) 24 h into <b>withdrawal</b> in a 5HT2c R dependent manner.
+FOS	drug	nicotine	25223294	Mouse brains were examined by immunohistochemistry for c <strong>Fos</strong> protein after intraperitoneal injection of either <b>nicotine</b> hydrogen tartrate salt (NIC; 30 and 40 μg/kg) or <b>nicotine</b> pyrrolidine methiodide (NIC PM; 20 and 30 μg/kg).
+FOS	drug	alcohol	25149913	In the present study, <b>alcohol</b> induced adaptations in (1) anxiety like behavior, (2) patterns of c <strong>Fos</strong> activation and (3) subcellular distribution of corticotropin releasing factor receptor in locus coeruleus (LC) neurons was investigated in male and female Sprague Dawley rats that were chronically exposed to <b>ethanol</b> using a liquid diet.
+FOS	drug	alcohol	25149913	<b>Ethanol</b> induced sex differences were observed with increased c <strong>Fos</strong> expression in LC neurons of female <b>ethanol</b> treated subjects compared to controls or male subjects.
+FOS	drug	amphetamine	25145867	Combining quantitative analyses of <strong>cfos</strong> expression with neuronal subtype specific markers at single cell resolution, we show that acute d <b>amphetamine</b> administration leads to both increased neuronal activation and the recruitment of neurons in the medial (Dm) and the lateral (Dl) domains of the adult zebrafish pallium, which contain homologous structures to the mammalian amygdala and hippocampus, respectively.
+FOS	drug	alcohol	25126745	Herein, we examined whether the decrease in IFN γ is resulted from altered expression of miRNA155 and transcription factors  NFAT, Tbx21, Jun and <strong>Fos</strong>  in T cells following <b>ethanol</b> and burn injury.
+FOS	drug	alcohol	25126745	We observed a significant decrease in miRNA155, NFAT, Tbx21, Jun and <strong>Fos</strong> expression as well as IFN γ release in T cells cultured with anti CD3 following <b>ethanol</b> and burn injury compared with shams.
+FOS	drug	opioid	25086310	To test whether these substances act similarly on the same neuronal populations in specific brain areas mediating these behaviors, we administered the substances short term, using the same methods and within the same experiment, and measured their effects, in areas of the hypothalamus (HYPO), amygdala (AMYG), and nucleus accumbens (NAc), on mRNA levels of the <b>opioid</b> peptide, enkephalin (ENK), using in situ hybridization and on c <strong>Fos</strong> immunoreactivity (ir) to indicate neuronal activity, using immunofluorescence histochemistry.
+FOS	drug	alcohol	25086310	Fat, <b>ethanol</b>, and nicotine, but not sucrose, increased the single  and double labeling of ENK and c <strong>Fos</strong> ir in precisely the same brain areas, the middle parvocellular but not lateral area of the paraventricular nucleus, central but not basolateral nucleus of the AMYG, and core but not shell of the NAc.
+FOS	drug	nicotine	25086310	Fat, ethanol, and <b>nicotine</b>, but not sucrose, increased the single  and double labeling of ENK and c <strong>Fos</strong> ir in precisely the same brain areas, the middle parvocellular but not lateral area of the paraventricular nucleus, central but not basolateral nucleus of the AMYG, and core but not shell of the NAc.
+FOS	drug	cocaine	25050821	<b>Cocaine</b> self administration and extinction alter medullary noradrenergic and limbic forebrain <strong>cFos</strong> responses to acute, noncontingent <b>cocaine</b> injections in adult rats.
+FOS	drug	cocaine	25050821	The present study examined the ability of acute <b>cocaine</b> to induce the immediate early gene product, <strong>cFos</strong>, in NA neurons and stress related neural circuits in rats that were <b>cocaine</b> naïve, or had a history of <b>cocaine</b> self administration with or without extinction.
+FOS	drug	cocaine	25050821	Extinction attenuated <b>cocaine</b> induced <strong>cFos</strong> activation in NA neurons of the caudal ventrolateral medulla (A1/C1 cell groups), and attenuated <strong>cFos</strong> within the paraventricular nucleus of the hypothalamus, the apex of the central neuroendocrine stress axis.
+FOS	drug	cocaine	25050821	<b>Cocaine</b> consistently increased <strong>cFos</strong> in the bed nucleus of the stria terminalis, regardless of history.
+FOS	drug	nicotine	25042794	Baclofen prevented the changes in c <strong>Fos</strong> and brain derived neutrophic factor expressions during mecamylamine precipitated <b>nicotine</b> withdrawal in mice.
+FOS	addiction	withdrawal	25042794	Baclofen prevented the changes in c <strong>Fos</strong> and brain derived neutrophic factor expressions during mecamylamine precipitated nicotine <b>withdrawal</b> in mice.
+FOS	addiction	withdrawal	25042794	To further investigate the mechanisms underlying these effects, we analyzed the c <strong>Fos</strong> and brain derived neutrophic factor (BDNF) expression during NIC <b>withdrawal</b> and its prevention with BAC.
+FOS	addiction	withdrawal	25042794	c <strong>Fos</strong> expression decreased in the dentate gyrus of the hippocampus (DG) and the bed nucleus of the stria terminalis (BST), and increased in the habenular (Hb), accumbens shell (AcbSh) nuclei during NIC <b>withdrawal</b>.
+FOS	addiction	withdrawal	25042794	BAC re established the modified c <strong>Fos</strong> expression only in the DG, BST and AcbSh during NIC <b>withdrawal</b>.
+FOS	addiction	withdrawal	25042794	The results suggest a relationship between BAC's preventive effect of the expression of NIC <b>withdrawal</b> signs, and its ability to restore the changes in c <strong>Fos</strong> and BDNF expression, observed in specific brain areas of NIC withdrawn mice.
+FOS	drug	opioid	25025380	Compared to <b>oxycodone</b> self administering control rats immunized with the carrier alone, rats vaccinated with the OXY KLH immunogen showed increased levels of adenylate cyclase 5 (Adcy5) and decreased levels of early growth response protein 2 (Egr2) and the early immediate gene c <strong>Fos</strong> in the striatum.
+FOS	addiction	reward	24943644	C <strong>Fos</strong> expression analysis revealed differential activation in brain areas related with memory and <b>reward</b> in these knockout mice.
+FOS	drug	alcohol	24905237	Chronic light deprivation inhibits appetitive associative learning induced by <b>ethanol</b> and its respective c <strong>Fos</strong> and pCREB expression.
+FOS	drug	alcohol	24905237	To address the role of mixed anxiety/mood disorder on appetitive associative learning, we verify whether previous chronic light deprivation changes <b>ethanol</b> induced conditioned place preference and its respective expression of c <strong>Fos</strong> and pCREB, markers of neuronal activity and plasticity.
+FOS	drug	alcohol	24905237	<b>Ethanol</b> induced conditioned place preference was accompanied by increases on c <strong>Fos</strong> and pCREB in the hippocampus, prefrontal cortex and striatum.
+FOS	drug	alcohol	24905237	Interestingly, mice previously submitted to light deprivation did not develop either acquisition and/or expression of <b>ethanol</b> induced conditioned place preference or increases in c <strong>Fos</strong> and pCREB.
+FOS	drug	alcohol	24872550	We first determined the effect of context induced renewal of <b>alcohol</b> seeking on <strong>Fos</strong> (a neuronal activity marker) expression in LH.
+FOS	addiction	relapse	24872550	We first determined the effect of context induced renewal of alcohol <b>seeking</b> on <strong>Fos</strong> (a neuronal activity marker) expression in LH.
+FOS	drug	alcohol	24872550	Context induced renewal of <b>alcohol</b> seeking after punishment imposed abstinence was associated with increased <strong>Fos</strong> expression in LH.
+FOS	addiction	addiction	24872550	Context induced renewal of alcohol seeking after <b>punishment</b> imposed abstinence was associated with increased <strong>Fos</strong> expression in LH.
+FOS	addiction	relapse	24872550	Context induced renewal of alcohol <b>seeking</b> after punishment imposed abstinence was associated with increased <strong>Fos</strong> expression in LH.
+FOS	drug	alcohol	24872550	Finally, double labeling analysis of CTb + <strong>Fos</strong> showed that context induced renewal of <b>alcohol</b> seeking after punishment imposed abstinence was associated with selective activation of accumbens shell neurons projecting to LH.
+FOS	addiction	addiction	24872550	Finally, double labeling analysis of CTb + <strong>Fos</strong> showed that context induced renewal of alcohol seeking after <b>punishment</b> imposed abstinence was associated with selective activation of accumbens shell neurons projecting to LH.
+FOS	addiction	relapse	24872550	Finally, double labeling analysis of CTb + <strong>Fos</strong> showed that context induced renewal of alcohol <b>seeking</b> after punishment imposed abstinence was associated with selective activation of accumbens shell neurons projecting to LH.
+FOS	drug	cocaine	24872549	On test day, reexposure to the <b>cocaine</b> associated Context A reinstated <b>cocaine</b> seeking and increased expression of the neural activity marker <strong>Fos</strong> in 3.3% of accumbens shell and 1.6% of accumbens core neurons.
+FOS	addiction	relapse	24872549	On test day, reexposure to the cocaine associated Context A reinstated cocaine <b>seeking</b> and increased expression of the neural activity marker <strong>Fos</strong> in 3.3% of accumbens shell and 1.6% of accumbens core neurons.
+FOS	drug	cocaine	24872549	We trained c <strong>fos</strong> lacZ transgenic rats to self administer <b>cocaine</b> in Context A and extinguished their lever pressing in Context B.
+FOS	drug	cocaine	24872549	On test day, 3 d after induction day, the ability of Context A to reinstate <b>cocaine</b> seeking and increase neuronal activity in accumbens shell was attenuated when Daun02 was previously injected after exposure to Context A. Daun02 injections after exposure to the novel Context C had no effect on context induced reinstatement of <b>cocaine</b> seeking despite much greater numbers of <strong>Fos</strong> expressing neurons induced by Context C. Daun02 injections in accumbens core had no effect.
+FOS	addiction	relapse	24872549	On test day, 3 d after induction day, the ability of Context A to reinstate cocaine <b>seeking</b> and increase neuronal activity in accumbens shell was attenuated when Daun02 was previously injected after exposure to Context A. Daun02 injections after exposure to the novel Context C had no effect on context induced <b>reinstatement</b> of cocaine <b>seeking</b> despite much greater numbers of <strong>Fos</strong> expressing neurons induced by Context C. Daun02 injections in accumbens core had no effect.
+FOS	drug	cocaine	24872521	Here, we used a large scale and high resolution <strong>Fos</strong> mapping approach to identify, beyond the PL PFC, how top down and/or bottom up PFC subcortical circuits are recruited during inhibition of <b>cocaine</b> seeking.
+FOS	addiction	relapse	24872521	Here, we used a large scale and high resolution <strong>Fos</strong> mapping approach to identify, beyond the PL PFC, how top down and/or bottom up PFC subcortical circuits are recruited during inhibition of cocaine <b>seeking</b>.
+FOS	drug	opioid	24825609	Finally, <strong>Fos</strong> expression in the medial prefrontal cortex which was decreased during <b>morphine</b> withdrawal was increased by TFF3 pretreatment.
+FOS	addiction	withdrawal	24825609	Finally, <strong>Fos</strong> expression in the medial prefrontal cortex which was decreased during morphine <b>withdrawal</b> was increased by TFF3 pretreatment.
+FOS	drug	nicotine	24823947	Complementary neuroanalysis revealed that extended <b>nicotine</b> self administration was associated with increased c <strong>Fos</strong> expression in brain regions implicated in habitual control of reward seeking, including activation of the dorsolateral striatum and substantia nigra pars compacta.
+FOS	addiction	relapse	24823947	Complementary neuroanalysis revealed that extended nicotine self administration was associated with increased c <strong>Fos</strong> expression in brain regions implicated in habitual control of reward <b>seeking</b>, including activation of the dorsolateral striatum and substantia nigra pars compacta.
+FOS	addiction	reward	24823947	Complementary neuroanalysis revealed that extended nicotine self administration was associated with increased c <strong>Fos</strong> expression in brain regions implicated in habitual control of <b>reward</b> seeking, including activation of the dorsolateral striatum and substantia nigra pars compacta.
+FOS	drug	cocaine	24813699	Very recently, we have shown that conditioned preference for an odour associated with <b>cocaine</b> was directly correlated with <strong>cFOS</strong> expression in cells at the dorsal region of the granule cell layer of the cerebellar vermis.
+FOS	drug	cocaine	24813699	The main goal of the current investigation was to further extend the description of <strong>cFOS</strong> IR patterns in cerebellar circuitry after training mice in a <b>cocaine</b> odour Pavlovian conditioning procedure, including now the major inputs (the inferior olive and pontine nuclei) and one of the output nuclei (the medial deep nucleus) of the cerebellum.
+FOS	drug	cocaine	24813699	The results showed that the cerebellar hallmark of preference towards an odour cue associated to <b>cocaine</b> is an increase in <strong>cFOS</strong> expression in the dorsal part of the granule cell layer.
+FOS	drug	cocaine	24813699	<strong>cFOS</strong> IR levels expressed in the granule cell layer of mice that did not show <b>cocaine</b> conditioned preference did not differ from the basal levels.
+FOS	drug	cocaine	24813699	Remarkably, mice subjected to a random <b>cocaine</b> odour pairing procedure (the unpaired group) exhibited higher <strong>cFOS</strong> IR in the inferior olive, the pontine nuclei and in the deep medial nucleus.
+FOS	drug	cocaine	24800964	<b>Cocaine</b> withdrawn mice show a genotype independent higher c <strong>fos</strong> expression in the NOR memory relevant perirhinal cortex than drug naïve mice.
+FOS	addiction	intoxication	24763081	MA <b>binge</b> exposure produced recognition memory impairment, reduced social behaviours, and increased DOI induced head twitch response, c <strong>Fos</strong> and Egr 2 expression and field potentials in the medial prefrontal cortex.
+FOS	drug	alcohol	24712379	Compared with those maintained on water and chow only (water group), rats trained to drink pharmacologically relevant levels of <b>ethanol</b> (<b>ethanol</b> group) showed increased neuronal activation in the PVT, specifically the aPVT but not pPVT, as indicated by c <strong>Fos</strong> immunoreactivity.
+FOS	drug	alcohol	24712379	Similarly, <b>ethanol</b> gavage increased double labeling of c <strong>Fos</strong> with OX2R but not OX1R, specifically in the aPVT.
+FOS	drug	benzodiazepine	24681217	Moreover, <b>diazepam</b> increased <strong>Fos</strong> expression in field CA2 and CA3 of the hippocampus, but had no significant effect on <strong>Fos</strong> expression in field CA1 and dentate gyrus (DG) of the hippocampus, indicating that the hippocampus has area specific effects on food hoarding in HFH gerbils.
+FOS	drug	cocaine	24584054	We found that projections to VTA from the rostral ventral pallidum (RVP), but not the caudal ventral pallidum (CVP), were robustly <strong>Fos</strong> activated during cue induced reinstatement of <b>cocaine</b> seeking  a rat model of relapse in addiction.
+FOS	addiction	addiction	24584054	We found that projections to VTA from the rostral ventral pallidum (RVP), but not the caudal ventral pallidum (CVP), were robustly <strong>Fos</strong> activated during cue induced reinstatement of cocaine seeking  a rat model of relapse in <b>addiction</b>.
+FOS	addiction	relapse	24584054	We found that projections to VTA from the rostral ventral pallidum (RVP), but not the caudal ventral pallidum (CVP), were robustly <strong>Fos</strong> activated during cue induced <b>reinstatement</b> of cocaine <b>seeking</b>  a rat model of <b>relapse</b> in addiction.
+FOS	drug	amphetamine	24574986	c <strong>Fos</strong> quantification in the nucleus accumbens further confirmed defective neuronal activation following <b>amphetamine</b> injection.
+FOS	drug	cocaine	24456857	To explore how the <b>cocaine</b> context associated information was processed and integrated, we assessed the activity of NAc MSN targeted brain nuclei and found that the activation of NAc GABAergic neurons during CPP expression resulted in a decrease of c <strong>Fos</strong>+ cells in the ventral palladium.
+FOS	addiction	reward	24456857	To explore how the cocaine context associated information was processed and integrated, we assessed the activity of NAc MSN targeted brain nuclei and found that the activation of NAc GABAergic neurons during <b>CPP</b> expression resulted in a decrease of c <strong>Fos</strong>+ cells in the ventral palladium.
+FOS	drug	cocaine	24452697	MPH + FLX, or <b>cocaine</b> exposure in juvenile mice increased mRNA expression of ERK2 and its downstream targets (CREB, <strong>cFos</strong>, and Zif268), and increased protein phosphorylation of ERK2 and CREB 2 months after drug exposure.
+FOS	addiction	reward	24406724	Extinction of opiate <b>reward</b> reduces dendritic arborization and c <strong>Fos</strong> expression in the nucleus accumbens core.
+FOS	drug	opioid	24406724	In the NAcCore only, <b>morphine</b> CPP/extinguished mice produced less dendritic arborization, and a decrease in neuronal activity marker c <strong>Fos</strong> compared to the <b>morphine</b> CPP/sham extinction group.
+FOS	addiction	reward	24406724	In the NAcCore only, morphine <b>CPP</b>/extinguished mice produced less dendritic arborization, and a decrease in neuronal activity marker c <strong>Fos</strong> compared to the morphine <b>CPP</b>/sham extinction group.
+FOS	drug	alcohol	24379765	We previously demonstrated that repeated treatment with a behaviorally sensitizing dose of <b>ethanol</b> in adult mice induced tolerance or no sensitization in adolescents and that repeated <b>ethanol</b> treated adolescents expressed lower <strong>Fos</strong> and Egr 1 expression than adult mice in the prefrontal cortex (PFC).
+FOS	addiction	sensitization	24379765	We previously demonstrated that repeated treatment with a behaviorally sensitizing dose of ethanol in adult mice induced tolerance or no <b>sensitization</b> in adolescents and that repeated ethanol treated adolescents expressed lower <strong>Fos</strong> and Egr 1 expression than adult mice in the prefrontal cortex (PFC).
+FOS	drug	benzodiazepine	24367698	administration of both <b>triazolam</b> (0.03 mg/kg) and ZP (1.0 mg/kg) decreased BDNF protein levels within the HIP relative to vehicle, without any effect on c <strong>Fos</strong>.
+FOS	drug	cocaine	24342748	Chronic wheel running affects <b>cocaine</b> induced c <strong>Fos</strong> expression in brain reward areas in rats.
+FOS	addiction	reward	24342748	Chronic wheel running affects cocaine induced c <strong>Fos</strong> expression in brain <b>reward</b> areas in rats.
+FOS	drug	cocaine	24342748	The c <strong>Fos</strong> transcription factor is a measure of cellular activity and was used to quantify <b>cocaine</b> induced activation of reward processing areas of the brain: nucleus accumbens (NAc), caudate putamen (CPu), medial prefrontal cortex (mPFC), and orbitofrontal cortex (OFC).
+FOS	addiction	reward	24342748	The c <strong>Fos</strong> transcription factor is a measure of cellular activity and was used to quantify cocaine induced activation of <b>reward</b> processing areas of the brain: nucleus accumbens (NAc), caudate putamen (CPu), medial prefrontal cortex (mPFC), and orbitofrontal cortex (OFC).
+FOS	drug	cocaine	24342748	The mean fold change in <b>cocaine</b> induced c <strong>Fos</strong> cell counts relative to saline induced c <strong>Fos</strong> cell counts was significantly higher in exercising compared to control rats in the NAc core, dorsomedial and dorsolateral CPu, the prelimbic area, and the OFC, indicating differential <b>cocaine</b> specific cellular activation of brain reward circuitry between exercising and control animals.
+FOS	addiction	reward	24342748	The mean fold change in cocaine induced c <strong>Fos</strong> cell counts relative to saline induced c <strong>Fos</strong> cell counts was significantly higher in exercising compared to control rats in the NAc core, dorsomedial and dorsolateral CPu, the prelimbic area, and the OFC, indicating differential cocaine specific cellular activation of brain <b>reward</b> circuitry between exercising and control animals.
+FOS	drug	nicotine	24327734	After exposing adults to <b>nicotine</b>, <strong>fos</strong> expression was activated in subregions of the IPN enriched for specific nicotinic acetylcholine receptor subunits.
+FOS	drug	psychedelics	24308186	[Effect of electroacupuncture intervention at different time points in a day on expression of c <strong>fos</strong> and neuronal nitric oxide synthase in medial prefrontal cortex in <b>ketamine</b> addiction rats].
+FOS	addiction	addiction	24308186	[Effect of electroacupuncture intervention at different time points in a day on expression of c <strong>fos</strong> and neuronal nitric oxide synthase in medial prefrontal cortex in ketamine <b>addiction</b> rats].
+FOS	drug	psychedelics	24308186	To observe the effects of electroacupuncture(EA) stimulation of "Zusanli"(ST 36) and "Sanyinjiao"(SP 6) at different time points of a day on the expression of c <strong>fos</strong> and neuronal nitric oxide synthase (nNOS) in the medial prefrontal cortex (mPFC) in rats with <b>ketamine</b> addiction.
+FOS	addiction	addiction	24308186	To observe the effects of electroacupuncture(EA) stimulation of "Zusanli"(ST 36) and "Sanyinjiao"(SP 6) at different time points of a day on the expression of c <strong>fos</strong> and neuronal nitric oxide synthase (nNOS) in the medial prefrontal cortex (mPFC) in rats with ketamine <b>addiction</b>.
+FOS	drug	psychedelics	24308186	EA of ST 36 and SP 6 at 11 : 00 and 17 : 00 can decrease the expression o fc <strong>fos</strong> and nNOS in the mPFC in <b>ketamine</b> addiction rats, which may contribute to its effects in improving the rats' behavior activity.
+FOS	addiction	addiction	24308186	EA of ST 36 and SP 6 at 11 : 00 and 17 : 00 can decrease the expression o fc <strong>fos</strong> and nNOS in the mPFC in ketamine <b>addiction</b> rats, which may contribute to its effects in improving the rats' behavior activity.
+FOS	drug	opioid	24292370	Changes in the levels of p ERK, p CREB, and c <strong>fos</strong> in rat mesocorticolimbic dopaminergic system after <b>morphine</b> induced conditioned place preference: the role of acute and subchronic stress.
+FOS	drug	opioid	24292370	In this study, we investigated the effects of <b>morphine</b> induced conditioned place preference (CPP) on p ERK/ERK ratio, p CREB/CREB ratio and c <strong>fos</strong> level in the mesocorticolimbic dopaminergic system including the nucleus accumbens (NAc), amygdala (AMY), striatum (Str), and prefrontal cortex (PFC).Our aim was to determine if acute and subchronic stress would affect these alterations.
+FOS	addiction	reward	24292370	In this study, we investigated the effects of morphine induced conditioned place preference (<b>CPP</b>) on p ERK/ERK ratio, p CREB/CREB ratio and c <strong>fos</strong> level in the mesocorticolimbic dopaminergic system including the nucleus accumbens (NAc), amygdala (AMY), striatum (Str), and prefrontal cortex (PFC).Our aim was to determine if acute and subchronic stress would affect these alterations.
+FOS	drug	opioid	24292370	Our findings suggest that in saline  or <b>morphine</b> treated animals, acute and subchronic stress increases p ERK, p CREB, and c <strong>fos</strong> levels in the mesocorticolimbic system.
+FOS	drug	alcohol	24250203	Expression of <strong>cFos</strong> and brain derived neurotrophic factor in cortex and hippocampus of <b>ethanol</b> withdrawn male and female rats.
+FOS	drug	alcohol	24250203	To map areas of brain activation (<strong>cFos</strong>) alongside changes in levels of brain derived neurotrophic factor (BDNF) to provide insights into neuronal mechanisms contributing to previously observed sex differences in behavioral measures of <b>ethanol</b> withdrawal (EW).
+FOS	addiction	withdrawal	24250203	To map areas of brain activation (<strong>cFos</strong>) alongside changes in levels of brain derived neurotrophic factor (BDNF) to provide insights into neuronal mechanisms contributing to previously observed sex differences in behavioral measures of ethanol <b>withdrawal</b> (EW).
+FOS	drug	cannabinoid	24200867	Finally, the cellular underpinnings of the observed sensitized response to acute PCP in adult <b>THC</b> treated rats could be ascribed to the increased <strong>cFos</strong> immunoreactivity and glutamate levels in the PFC and dorsal striatum.
+FOS	drug	amphetamine	24183790	KD of Mll1 reduced H3K4me3, <strong>Fos</strong> and Oxtr levels and disrupted <b>METH</b> associated memory.
+FOS	drug	amphetamine	24140441	Effect of rhynchophylline on the expression of p CREB and sc <strong>Fos</strong> in triatum and hippocampal CA1 area of <b>methamphetamine</b> induced conditioned place preference rats.
+FOS	drug	amphetamine	24140441	To explore the effect of rhynchophylline (Rhy) on the expression of p CREB and c <strong>Fos</strong> in the striatum and hippocampal CA1 area of <b>methamphetamine</b> induced conditioned place preference (CPP) rat, <b>methamphetamine</b> (2 mg/kg) was injected to rats and the conditioned place preference was observed in these rats treated with or without Rhy.
+FOS	addiction	reward	24140441	To explore the effect of rhynchophylline (Rhy) on the expression of p CREB and c <strong>Fos</strong> in the striatum and hippocampal CA1 area of methamphetamine induced conditioned place preference (<b>CPP</b>) rat, methamphetamine (2 mg/kg) was injected to rats and the conditioned place preference was observed in these rats treated with or without Rhy.
+FOS	drug	amphetamine	24140441	<b>Methamphetamine</b> also increased the number of p CREB positive cells in the striatum and hippocampal CA1 zone, as well as p <strong>Fos</strong> positive cells.
+FOS	drug	amphetamine	24140441	These findings show that Rhy can suppress the acquisition of CPP in rats induced by <b>methamphetamine</b> and the action may be related with the reduced expression of p CREB and p <strong>Fos</strong> in the striatum and hippocampus.
+FOS	addiction	reward	24140441	These findings show that Rhy can suppress the acquisition of <b>CPP</b> in rats induced by methamphetamine and the action may be related with the reduced expression of p CREB and p <strong>Fos</strong> in the striatum and hippocampus.
+FOS	drug	amphetamine	24089683	The induction of the immediately early gene c <strong>fos</strong> has been used to define brain activated areas by <b>amphetamine</b>.
+FOS	drug	amphetamine	24089683	The study examined the c <strong>fos</strong> expression in mesocorticolimbic areas induced by <b>amphetamine</b> challenge (0.5 mg/kg i.p) in animals pretreated with candesartan, a selective AT₁ receptor blocker (3 mg/kg p.o × 5 days), and <b>amphetamine</b> (5 mg/kg i.p) 3 weeks before the challenge.
+FOS	drug	amphetamine	24089683	Increased c <strong>fos</strong> immunoreactivity was found in response to the <b>amphetamine</b> challenge in the dorsomedial caudate putamen and nucleus accumbens, and both responses were blunted by the AT₁ receptor blocker pretreatment.
+FOS	drug	amphetamine	24089683	In the infralimbic prefrontal cortex, increased c <strong>fos</strong> immunoreactivity was found in response to <b>amphetamine</b> and saline challenge, and both were prevented by the AT₁ receptor blocker.
+FOS	drug	cocaine	24055298	Effects of either <b>cocaine</b> or dexamethasone alone, or both combined, on <strong>FOS</strong> expression in the LHb were observed via immunohistochemistry.
+FOS	drug	cocaine	24055298	Single administration of either <b>cocaine</b> or dexamethasone increased the number of <strong>FOS</strong> positive neurons in the LHb.
+FOS	drug	cocaine	24055298	Pretreatment with dexamethasone and then <b>cocaine</b> markedly enhanced the number of <strong>FOS</strong> positive neurons in the LHb relative to <b>cocaine</b> treatment alone, suggesting that stress and addictive drugs exert a synergistic effect on the LHb.
+FOS	addiction	addiction	24055298	Pretreatment with dexamethasone and then cocaine markedly enhanced the number of <strong>FOS</strong> positive neurons in the LHb relative to cocaine treatment alone, suggesting that stress and <b>addictive</b> drugs exert a synergistic effect on the LHb.
+FOS	drug	opioid	24048098	At completion of behavioral testing, mu <b>opioid</b> receptor (OPRM1), FosB, <strong>cFos</strong>, and dopamine receptor mRNA expression was measured in the nucleus accumbens as well as OPRM1 and corticotropin releasing hormone mRNA in the paraventricular nucleus.
+FOS	drug	amphetamine	24025783	c <strong>Fos</strong> immunoreactivity of neural cells in intoxication due to high dose <b>methamphetamine</b>.
+FOS	addiction	intoxication	24025783	c <strong>Fos</strong> immunoreactivity of neural cells in <b>intoxication</b> due to high dose methamphetamine.
+FOS	drug	amphetamine	24025783	These results indicate that responsive neurons in the regions containing c <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) may undergo cellular reaction to high dose <b>METH</b> administration.
+FOS	drug	amphetamine	23895375	Detection of molecular alterations in <b>methamphetamine</b> activated <strong>Fos</strong> expressing neurons from a single rat dorsal striatum using fluorescence activated cell sorting (FACS).
+FOS	drug	amphetamine	23895375	<strong>Fos</strong> and NeuN (a neuronal marker) immunohistochemistry indicate that 5 6% of dorsal striatum neurons were activated 90 min after acute <b>methamphetamine</b> injections (5 mg/kg, i.p.)
+FOS	drug	amphetamine	23895375	<b>Methamphetamine</b> induced 3 20 fold increases of immediate early genes arc, homer 2, c <strong>fos</strong>, fosB, and its isoforms (ΔfosB and a novel isoform ΔfosB 2) in <strong>Fos</strong> positive but not <strong>Fos</strong> negative neurons.
+FOS	drug	amphetamine	23895375	We used FACS along with targeted PCR pre amplification to assess acute <b>methamphetamine</b> induced gene expression from as few as 5 <strong>Fos</strong> expressing neurons from a single rat dorsal striatum.
+FOS	drug	amphetamine	23895375	<b>Methamphetamine</b> induced 3 20 fold increases of immediate early genes (IEGs) in <strong>Fos</strong> positive but not <strong>Fos</strong> negative neurons.
+FOS	addiction	sensitization	23880022	Behavioral <b>sensitization</b> was assessed by locomotor activity tests and after the last one, immunoreactivity for orexin and <strong>Fos</strong> (ORX+<strong>Fos</strong> ir) was assessed in the lateral hypothalamic area.
+FOS	drug	alcohol	23880022	Chronic <b>ethanol</b> treatment produced behavioral sensitization and a trend for greater ORX+<strong>Fos</strong> ir.
+FOS	addiction	sensitization	23880022	Chronic ethanol treatment produced behavioral <b>sensitization</b> and a trend for greater ORX+<strong>Fos</strong> ir.
+FOS	addiction	addiction	23878596	The present study was undertaken to investigate the influence of electroacupuncture (EA) on <b>compulsive</b> scratching in mice and c <strong>Fos</strong> expression elicited by subcutaneous (s.c.) administration of a known puritogen, 5' guanidinonaltrindole (GNTI) to the neck.
+FOS	drug	cocaine	23832598	<strong>Fos</strong> expression induced by <b>cocaine</b> conditioned cues in male and female rats.
+FOS	drug	cocaine	23832598	Here, we used a <b>cocaine</b> self administration/reinstatement model to examine neuronal activation, as determined by <strong>Fos</strong> expression, following cue induced reinstatement of <b>cocaine</b> seeking in male and female rats.
+FOS	addiction	relapse	23832598	Here, we used a cocaine self administration/<b>reinstatement</b> model to examine neuronal activation, as determined by <strong>Fos</strong> expression, following cue induced <b>reinstatement</b> of cocaine <b>seeking</b> in male and female rats.
+FOS	drug	cocaine	23832598	These findings indicate that while sexually dimorphic <strong>Fos</strong> activation does occur, the relationship between cue induced <b>cocaine</b> seeking and neuronal activation may be similar for males and females in key brain regions of the relapse circuit.
+FOS	addiction	relapse	23832598	These findings indicate that while sexually dimorphic <strong>Fos</strong> activation does occur, the relationship between cue induced cocaine <b>seeking</b> and neuronal activation may be similar for males and females in key brain regions of the <b>relapse</b> circuit.
+FOS	drug	cocaine	23831243	<b>Cocaine</b> conditioned mice exposed to extinction training showed increased c <strong>Fos</strong> expression in several brain areas in comparison to mice exposed to Sham extinction.
+FOS	drug	opioid	23787292	In this study, we evaluated the role of orexin receptors in the dorsal hippocampus (dHPC) in the development of <b>morphine</b> induced conditioned place preference (CPP) and modification of hippocampal c <strong>Fos</strong> and cyclic AMP response element binding protein (CREB) levels.
+FOS	addiction	reward	23787292	In this study, we evaluated the role of orexin receptors in the dorsal hippocampus (dHPC) in the development of morphine induced conditioned place preference (<b>CPP</b>) and modification of hippocampal c <strong>Fos</strong> and cyclic AMP response element binding protein (CREB) levels.
+FOS	drug	opioid	23787292	Orexin did not enhance the rewarding efficacy of <b>morphine</b> (0.5 mg/kg), but caused a reduction in hippocampal c <strong>Fos</strong>.
+FOS	drug	opioid	23787292	Successful conditioning with <b>morphine</b> (7.5 mg/kg) was associated with increased levels of hippocampal c <strong>Fos</strong> and CREB, but with decreased CREB phosphorylation.
+FOS	drug	opioid	23787292	<b>Morphine</b> reward is related to altered levels of hippocampal c <strong>Fos</strong> and CREB.
+FOS	addiction	reward	23787292	Morphine <b>reward</b> is related to altered levels of hippocampal c <strong>Fos</strong> and CREB.
+FOS	drug	alcohol	23779257	We have previously shown that ablation of β arrestin 2 (Arrb2), a crucial regulator of μ opioid receptor function, attenuates <b>alcohol</b> induced hyperlocomotion and c <strong>fos</strong> activation in the nucleus accumbens.
+FOS	drug	opioid	23779257	We have previously shown that ablation of β arrestin 2 (Arrb2), a crucial regulator of μ <b>opioid</b> receptor function, attenuates alcohol induced hyperlocomotion and c <strong>fos</strong> activation in the nucleus accumbens.
+FOS	drug	alcohol	23773238	In experiment 3, we employed retrograde neural tract tracing together with c <strong>Fos</strong> immunohistochemistry to identify the VP afferents recruited during context induced reinstatement of <b>alcoholic</b> beer seeking.
+FOS	addiction	relapse	23773238	In experiment 3, we employed retrograde neural tract tracing together with c <strong>Fos</strong> immunohistochemistry to identify the VP afferents recruited during context induced <b>reinstatement</b> of alcoholic beer <b>seeking</b>.
+FOS	drug	cocaine	23766142	<strong>Fos</strong> expression in response to dopamine D3 preferring phenylpiperazine drugs given with and without <b>cocaine</b>.
+FOS	drug	cocaine	23766142	Both compounds also increased <strong>Fos</strong> expression relative to saline in the dorsal striatum and nucleus accumbens core and shell, and relative to <b>cocaine</b> alone in the nucleus accumbens shell.
+FOS	drug	nicotine	23765240	We proposed a model where <b>nicotine</b> addiction is mediated by miRNAs' regulation of <strong>fos</strong> 1 and is maintained by epigenetic factors.
+FOS	addiction	addiction	23765240	We proposed a model where nicotine <b>addiction</b> is mediated by miRNAs' regulation of <strong>fos</strong> 1 and is maintained by epigenetic factors.
+FOS	drug	amphetamine	23726845	<b>METH</b> self administration caused increases in mRNA expression of the transcription factors, c <strong>fos</strong> and fosb, the neurotrophic factor, Bdnf, and the synaptic protein, synaptophysin (Syp) in the dorsal striatum.
+FOS	drug	amphetamine	23726845	Importantly, ChIP PCR showed that <b>METH</b> self administration caused enrichment of phosphorylated CREB (pCREB), but not of histone H3 trimethylated at lysine 4 (H3K4me3), on promoters of c <strong>fos</strong>, fosb, Bdnf and Syp at 2h after cessation of drug intake.
+FOS	drug	opioid	23651795	Lastly, the contribution of β4 containing nAChRs receptors in the MHb to <b>morphine</b> withdrawal induced jumping behavior and neuronal activity as indicated by c <strong>fos</strong> expression was assessed.
+FOS	addiction	withdrawal	23651795	Lastly, the contribution of β4 containing nAChRs receptors in the MHb to morphine <b>withdrawal</b> induced jumping behavior and neuronal activity as indicated by c <strong>fos</strong> expression was assessed.
+FOS	drug	opioid	23651795	Knock down of β4 subunit containing nAChRs in the MHb attenuated c <strong>fos</strong> activation, but did not decrease <b>morphine</b> withdrawal induced jumping.
+FOS	addiction	withdrawal	23651795	Knock down of β4 subunit containing nAChRs in the MHb attenuated c <strong>fos</strong> activation, but did not decrease morphine <b>withdrawal</b> induced jumping.
+FOS	drug	cocaine	23616555	c <strong>Fos</strong> experiments further showed that <b>cocaine</b> activated LHb neurons preferentially projected to and activated neurons in the rostromedial tegmental nucleus (RMTg), a recently identified target of LHb axons that is activated by negative motivational stimuli and inhibits dopamine neurons.
+FOS	drug	cocaine	23565937	Here, using a female rat model, we show that the mPOA innervates the VTA in a region specific manner, that lesions of the mPOA augment <b>cocaine</b> induced <strong>Fos</strong> expression in the nucleus accumbens (NAc) and <b>cocaine</b> induced conditioned place preference.
+FOS	drug	opioid	23463152	Mapping results for localization of function, aided by <strong>Fos</strong> plume measures of the local spread of orexin impact, suggested that hedonic enhancement was generated by essentially the same cubic millimeter of posterior VP previously identified as the <b>opioid</b> hotspot.
+FOS	addiction	reward	23463152	Mapping results for localization of function, aided by <strong>Fos</strong> plume measures of the local spread of orexin impact, suggested that <b>hedonic</b> enhancement was generated by essentially the same cubic millimeter of posterior VP previously identified as the opioid hotspot.
+FOS	drug	alcohol	23459588	The attenuated DA response in αCaMKII(T286A) mice was in line with altered c <strong>Fos</strong> activation in the ventral tegmental area after acute and subchronic <b>alcohol</b> administration.
+FOS	drug	cocaine	23447367	c <strong>Fos</strong> expression in NAcc, but not in CPu, was associated with these alterations in <b>cocaine</b> sensitization.
+FOS	addiction	sensitization	23447367	c <strong>Fos</strong> expression in NAcc, but not in CPu, was associated with these alterations in cocaine <b>sensitization</b>.
+FOS	drug	cocaine	23445190	Involving the cerebellum in <b>cocaine</b> induced memory: pattern of <strong>cFos</strong> expression in mice trained to acquire conditioned preference for <b>cocaine</b>.
+FOS	drug	cocaine	23445190	In the present study, we ought to fill this gap by aiming to investigate the pattern of neuronal activation (as revealed by <strong>cFos</strong> expression) in different regions of the prefrontal cortex and cerebellum of mice trained to develop conditioned preference for an olfactory stimulus (CS+) paired with <b>cocaine</b>.
+FOS	drug	cocaine	23445190	At the prefrontal cortex, <strong>cFos</strong> expression seemed to be related to <b>cocaine</b> administration rather than to its ability to establish conditioned preference.
+FOS	addiction	addiction	23287538	As the nucleus accumbens (Nac) is particularly involved in <b>addictive</b> behavior, we analyzed IEI induced long term neuroadaptations in the Nac using c <strong>Fos</strong> immunohistochemistry and an array of neurotransmission related genes.
+FOS	drug	alcohol	23287538	This vulnerability to <b>ethanol</b> abuse was associated with a lower c <strong>Fos</strong> immunoreactivity in the Nac and enduring alterations of the expression of Penk and Slc6a4, 2 neurotransmission related genes that have been shown to play critical roles in the behavioral effects of <b>ethanol</b> and <b>alcoholism</b>.
+FOS	drug	alcohol	23266368	Prenatal <b>ethanol</b> exposure increases <b>ethanol</b> intake and reduces c <strong>Fos</strong> expression in infralimbic cortex of adolescent rats.
+FOS	drug	alcohol	23266368	Subsequent Experiments (2, 3 and 4) tested several variables likely to underlie the effect of gestational <b>ethanol</b> on adolescent <b>ethanol</b> preference, including <b>ethanol</b> induced locomotor activation (LMA), <b>ethanol</b> induced emission of ultrasonic vocalizations (USVs) after exposure to a rough exteroceptive stimulus, and induction of the immediate early gene C <strong>fos</strong> in brain areas associated with processing of reward stimuli and with the retrieval and extinction of associative learning.
+FOS	addiction	reward	23266368	Subsequent Experiments (2, 3 and 4) tested several variables likely to underlie the effect of gestational ethanol on adolescent ethanol preference, including ethanol induced locomotor activation (LMA), ethanol induced emission of ultrasonic vocalizations (USVs) after exposure to a rough exteroceptive stimulus, and induction of the immediate early gene C <strong>fos</strong> in brain areas associated with processing of <b>reward</b> stimuli and with the retrieval and extinction of associative learning.
+FOS	drug	opioid	23244430	The present review further details the potential role of second messengers like calcium (Ca2+) / calmodulin dependent protein kinase (CaMKII), nitric oxide synthase, cytokines, arachidonic acid metabolites, corticotropin releasing factor, <strong>fos</strong> and src kinases in causing <b>opioid</b> withdrawal syndrome.
+FOS	addiction	withdrawal	23244430	The present review further details the potential role of second messengers like calcium (Ca2+) / calmodulin dependent protein kinase (CaMKII), nitric oxide synthase, cytokines, arachidonic acid metabolites, corticotropin releasing factor, <strong>fos</strong> and src kinases in causing opioid <b>withdrawal</b> syndrome.
+FOS	drug	opioid	23238466	Among them, a cluster of 8 genes, including 6 inducible transcription factors (c <strong>fos</strong>, fra 2, junB, zif268 (egr1), egr2, NGFI B) and 2 effector IEG (arc and mkp1) seemed to be regulated in concert in response to <b>morphine</b>.
+FOS	drug	nicotine	23233221	In addition, L theanine treatment inhibited <b>nicotine</b> induced c <strong>Fos</strong> expression in the reward circuit related areas of the mouse brain.
+FOS	addiction	reward	23233221	In addition, L theanine treatment inhibited nicotine induced c <strong>Fos</strong> expression in the <b>reward</b> circuit related areas of the mouse brain.
+FOS	drug	nicotine	23233221	Knockdown of c <strong>Fos</strong> by siRNA inhibited the excitatory status of cells but not the upregulation of TH induced by <b>nicotine</b> in SH SY5Y cells.
+FOS	drug	amphetamine	23222036	Neural substrates of <b>amphetamine</b> induced behavioral sensitization: unconditioned (zero context) and conditioned (switch versus same context) components in c <strong>fos</strong> overexpression.
+FOS	addiction	sensitization	23222036	Neural substrates of amphetamine induced behavioral <b>sensitization</b>: unconditioned (zero context) and conditioned (switch versus same context) components in c <strong>fos</strong> overexpression.
+FOS	drug	amphetamine	23178911	An additional cohort of mice was treated similarly except euthanized at age 58 to measure activation of granule neurons from d <b>amphetamine</b> (by detection of c <strong>Fos</strong>) and cell proliferation (Ki67) at a time when the fate of BrdU cells would have been determined in the first cohort.
+FOS	drug	amphetamine	23178911	Low doses of d <b>amphetamine</b> decreased c <strong>Fos</strong> and ΔFosB in the granule layer.
+FOS	drug	opioid	23153991	Differential regulation of CDK5 and c <strong>Fos</strong> expression by <b>morphine</b> in the brain of Lewis and Fischer 344 rat strains.
+FOS	drug	opioid	23153991	The aim of this study was to comparatively study cyclin dependent kinase 5 (CDK5) and c <strong>Fos</strong> regulation by <b>morphine</b> in the brains of Lewis and Fischer 344 (F344) rats, which are known to differ in their behavioral sensitivities to several drugs of abuse.
+FOS	drug	opioid	23153991	Immunostaining of c <strong>Fos</strong> was very low or absent in the control animals and was consistently up regulated by <b>morphine</b>, especially in the LC and NTS of the F344 rats and the NAC of the Lewis rats.
+FOS	drug	opioid	23153991	We propose that the acute <b>morphine</b> regulation of CDK5 expression in the NAC may predict the rate of drug intake and/or extinction of drug seeking, while the pattern of c <strong>Fos</strong> activation may be more related to the differential acquisition of <b>morphine</b> seeking behaviors.
+FOS	addiction	relapse	23153991	We propose that the acute morphine regulation of CDK5 expression in the NAC may predict the rate of drug intake and/or extinction of drug <b>seeking</b>, while the pattern of c <strong>Fos</strong> activation may be more related to the differential acquisition of morphine <b>seeking</b> behaviors.
+FOS	drug	opioid	23152154	Baclofen did not modify sexually dimorphic c <strong>Fos</strong> expression during <b>morphine</b> withdrawal syndrome.
+FOS	addiction	withdrawal	23152154	Baclofen did not modify sexually dimorphic c <strong>Fos</strong> expression during morphine <b>withdrawal</b> syndrome.
+FOS	drug	opioid	23152154	Considering that early gene expression is induced by drugs of abuse, we evaluated the expression of c <strong>Fos</strong> in several brain areas, in mice of either sex during <b>naloxone</b> (NAL) precipitated withdrawal, and after pretreatment with BAC.
+FOS	addiction	withdrawal	23152154	Considering that early gene expression is induced by drugs of abuse, we evaluated the expression of c <strong>Fos</strong> in several brain areas, in mice of either sex during naloxone (NAL) precipitated <b>withdrawal</b>, and after pretreatment with BAC.
+FOS	drug	opioid	23152154	Our results show a significant decrease in c <strong>Fos</strong> expression in hippocampal dentate gyrus, CA3, and CA1 areas of <b>morphine</b> withdrawn males, vs. their control group.
+FOS	drug	opioid	23152154	BAC pretreatment had no effect on the decreased c <strong>Fos</strong> expression in <b>morphine</b> withdrawn males.
+FOS	drug	opioid	23152154	The preventive action of BAC on the expression of <b>morphine</b> withdrawal would not be related to an effect on c <strong>Fos</strong> expression.
+FOS	addiction	withdrawal	23152154	The preventive action of BAC on the expression of morphine <b>withdrawal</b> would not be related to an effect on c <strong>Fos</strong> expression.
+FOS	drug	nicotine	23131151	c <strong>Fos</strong> activity showed through double labeling, that cell types involved in <b>nicotine</b> action were low threshold (LTS) and fast spiking (FS) inter neurons, which increased in the DA depleted striatum.
+FOS	drug	opioid	23113797	Unique gene alterations are induced in FACS purified <strong>Fos</strong> positive neurons activated during cue induced relapse to <b>heroin</b> seeking.
+FOS	addiction	relapse	23113797	Unique gene alterations are induced in FACS purified <strong>Fos</strong> positive neurons activated during cue induced <b>relapse</b> to heroin <b>seeking</b>.
+FOS	drug	opioid	23113797	Using <strong>Fos</strong> as a marker of neural activity, we describe distinct molecular alterations induced in activated versus non activated neurons during cue induced <b>heroin</b> seeking after prolonged withdrawal.
+FOS	addiction	relapse	23113797	Using <strong>Fos</strong> as a marker of neural activity, we describe distinct molecular alterations induced in activated versus non activated neurons during cue induced heroin <b>seeking</b> after prolonged withdrawal.
+FOS	addiction	withdrawal	23113797	Using <strong>Fos</strong> as a marker of neural activity, we describe distinct molecular alterations induced in activated versus non activated neurons during cue induced heroin seeking after prolonged <b>withdrawal</b>.
+FOS	addiction	relapse	23103203	Behavioral sensitization and CPP <b>reinstatement</b> were evaluated 24h later, as well as the expression of c <strong>Fos</strong> protein, a marker of activated neural sites, in brain regions of interest.
+FOS	addiction	reward	23103203	Behavioral sensitization and <b>CPP</b> reinstatement were evaluated 24h later, as well as the expression of c <strong>Fos</strong> protein, a marker of activated neural sites, in brain regions of interest.
+FOS	addiction	sensitization	23103203	Behavioral <b>sensitization</b> and CPP reinstatement were evaluated 24h later, as well as the expression of c <strong>Fos</strong> protein, a marker of activated neural sites, in brain regions of interest.
+FOS	addiction	relapse	23103203	Compared to the saline treated ones, the ZnE treated animals showed reduced c <strong>Fos</strong> expression in the nucleus accumbens (NAc) associated with behavioral sensitization, and in the NAc, cingulate cortex, dentate gyrus, amygdala, lateral hypothalamus and ventral tegmental area associated with CPP <b>reinstatement</b>.
+FOS	addiction	reward	23103203	Compared to the saline treated ones, the ZnE treated animals showed reduced c <strong>Fos</strong> expression in the nucleus accumbens (NAc) associated with behavioral sensitization, and in the NAc, cingulate cortex, dentate gyrus, amygdala, lateral hypothalamus and ventral tegmental area associated with <b>CPP</b> reinstatement.
+FOS	addiction	sensitization	23103203	Compared to the saline treated ones, the ZnE treated animals showed reduced c <strong>Fos</strong> expression in the nucleus accumbens (NAc) associated with behavioral <b>sensitization</b>, and in the NAc, cingulate cortex, dentate gyrus, amygdala, lateral hypothalamus and ventral tegmental area associated with CPP reinstatement.
+FOS	addiction	addiction	23103203	Together, these results demonstrated that acute olfactory impairment could attenuate already established <b>addiction</b> related behaviors and expression of c <strong>Fos</strong> in drug <b>addiction</b> related brain regions, perhaps by affecting the coordination between reward and motivational systems in the brain.
+FOS	addiction	reward	23103203	Together, these results demonstrated that acute olfactory impairment could attenuate already established addiction related behaviors and expression of c <strong>Fos</strong> in drug addiction related brain regions, perhaps by affecting the coordination between <b>reward</b> and motivational systems in the brain.
+FOS	drug	cocaine	23098798	<b>Cocaine</b> induced c <strong>Fos</strong> protein expression was augmented only in the ipsilateral nucleus accumbens core after mSTN lidocaine pretreatment, consistent with the expectation that inactivation of mSTN would disinhibit nucleus accumbens core, but not shell, activity.
+FOS	drug	opioid	23072838	Similarly, the adolescent onset group failed to show significant neural activation in the prelimbic or infralimbic mPFC during the <b>heroin</b> seeking test, whereas the adult onset <b>heroin</b> self administration group showed two to six times more <strong>Fos</strong> ir(+) neurons than their saline counterparts in both mPFC subregions.
+FOS	addiction	relapse	23072838	Similarly, the adolescent onset group failed to show significant neural activation in the prelimbic or infralimbic mPFC during the heroin <b>seeking</b> test, whereas the adult onset heroin self administration group showed two to six times more <strong>Fos</strong> ir(+) neurons than their saline counterparts in both mPFC subregions.
+FOS	drug	opioid	23071721	In addition, CP 154,526 reduced the number of TH containing neurons expressing c <strong>Fos</strong> in the VTA after <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	23071721	In addition, CP 154,526 reduced the number of TH containing neurons expressing c <strong>Fos</strong> in the VTA after naloxone precipitated morphine <b>withdrawal</b>.
+FOS	drug	alcohol	23071333	To address this issue, we examined FBJ murine osteosarcoma viral oncogene homolog (<strong>Fos</strong>) expression in the mPFC, CeA, hippocampus, and nucleus accumbens and evaluated working memory and anxiety like behavior in rats given continuous (24 h/d for 7 d/wk) or intermittent (3 d/wk) access to <b>alcohol</b> (20% vol/vol) using a two bottle choice paradigm.
+FOS	drug	cocaine	23039920	Using tract tracing combined with <strong>Fos</strong> staining, we examined LH afferents for <strong>Fos</strong> induction during <b>cocaine</b> preference in rats.
+FOS	drug	cocaine	23039920	We found that the ventral bed nucleus of the stria terminalis (vBNST) was a major input to the LH orexin cell field that was significantly <strong>Fos</strong> activated during <b>cocaine</b> conditioned place preference (CPP).
+FOS	addiction	reward	23039920	We found that the ventral bed nucleus of the stria terminalis (vBNST) was a major input to the LH orexin cell field that was significantly <strong>Fos</strong> activated during cocaine conditioned place preference (<b>CPP</b>).
+FOS	addiction	reward	23039920	Surprisingly, such inactivation of the vBNST also increased <strong>Fos</strong> induction in LH orexin neurons; as activity in these cells is normally associated with increased preference, this result indicates that a vBNST orexin connection is unlikely to be responsible for <b>CPP</b> that is dependent on vBNST activity.
+FOS	drug	cocaine	23023294	We recently found that a minority of strongly activated <strong>Fos</strong> expressing accumbens neurons are necessary for <b>cocaine</b> induced psychomotor sensitization, whereas the majority of accumbens neurons are less directly involved.
+FOS	addiction	sensitization	23023294	We recently found that a minority of strongly activated <strong>Fos</strong> expressing accumbens neurons are necessary for cocaine induced psychomotor <b>sensitization</b>, whereas the majority of accumbens neurons are less directly involved.
+FOS	drug	alcohol	22994904	Long term <b>alcohol</b> exposure elevated the foot shock induced c <strong>Fos</strong> expression in the basolateral amygdala in wild type animals, but had the opposite effect in dynorphin deficient mice.
+FOS	drug	cocaine	22993446	<strong>Fos</strong> activation of selective afferents to ventral tegmental area during cue induced reinstatement of <b>cocaine</b> seeking in rats.
+FOS	addiction	relapse	22993446	<strong>Fos</strong> activation of selective afferents to ventral tegmental area during cue induced <b>reinstatement</b> of cocaine <b>seeking</b> in rats.
+FOS	addiction	relapse	22993446	Here we examined 56 VTA afferents from forebrain and midbrain that are <strong>Fos</strong> activated during cue induced <b>reinstatement</b>.
+FOS	drug	cocaine	22993446	On a final test day, animals were exposed to response contingent <b>cocaine</b> associated cues, extinction conditions, a non <b>cocaine</b> predictive CS , or a novel environment, and brains were processed to visualize CTb and <strong>Fos</strong> immunoreactivity to identify VTA afferents activated in relation to behaviors.
+FOS	addiction	relapse	22993446	Surprisingly, though efferents from the lateral hypothalamic orexin field were also <strong>Fos</strong> activated during <b>reinstatement</b>, these were largely non orexinergic.
+FOS	drug	amphetamine	22927669	HAL, but not OLZ, also enhanced <b>AMPH</b> induced psychomotor activation and c <strong>fos</strong> mRNA expression in the caudate putamen.
+FOS	drug	cocaine	22916276	In the medial prefrontal cortex, we evidenced a negative correlation between <strong>Fos</strong> expression in its dorsal part and open arm induced freezing in NaCl treated rats but not in <b>cocaine</b> withdrawn rats.
+FOS	drug	opioid	22915104	Cue induced <b>heroin</b> seeking increased from 1 to 14 d and was accompanied by increased <strong>Fos</strong> expression in ∼12% of OFC neurons.
+FOS	addiction	relapse	22915104	Cue induced heroin <b>seeking</b> increased from 1 to 14 d and was accompanied by increased <strong>Fos</strong> expression in ∼12% of OFC neurons.
+FOS	drug	opioid	22915104	We then used the Daun02 inactivation procedure to assess a causal role of the minority of selectively activated <strong>Fos</strong> expressing OFC neurons (that presumably form cue encoding neuronal ensembles) in cue induced <b>heroin</b> seeking after 14 withdrawal days.
+FOS	addiction	relapse	22915104	We then used the Daun02 inactivation procedure to assess a causal role of the minority of selectively activated <strong>Fos</strong> expressing OFC neurons (that presumably form cue encoding neuronal ensembles) in cue induced heroin <b>seeking</b> after 14 withdrawal days.
+FOS	addiction	withdrawal	22915104	We then used the Daun02 inactivation procedure to assess a causal role of the minority of selectively activated <strong>Fos</strong> expressing OFC neurons (that presumably form cue encoding neuronal ensembles) in cue induced heroin seeking after 14 <b>withdrawal</b> days.
+FOS	drug	opioid	22915104	We trained c <strong>fos</strong> lacZ transgenic rats to self administer <b>heroin</b> and 11 d later reexposed them to <b>heroin</b> associated cues or novel cues for 15 min (induction day), followed by OFC Daun02 or vehicle injections 90 min later; we then tested the rats in extinction tests 3 d later.
+FOS	drug	opioid	22907296	Effects of aquaporin 4 deficiency on the expression of spinal PKCα, PKCγ and c <strong>Fos</strong> in <b>naloxone</b> precipitated <b>morphine</b> withdrawal mice.
+FOS	addiction	withdrawal	22907296	Effects of aquaporin 4 deficiency on the expression of spinal PKCα, PKCγ and c <strong>Fos</strong> in naloxone precipitated morphine <b>withdrawal</b> mice.
+FOS	addiction	dependence	22907296	In the present study, the effects of AQP4 deficiency on the expression of three factors, protein kinase C (PKC) α, PKCγ and c <strong>Fos</strong> in the spinal cord, which are known to be concerned with spinal neuronal sensitization and opiate <b>dependence</b>, were investigated in AQP4 knockout mice using Western blotting analysis.
+FOS	addiction	sensitization	22907296	In the present study, the effects of AQP4 deficiency on the expression of three factors, protein kinase C (PKC) α, PKCγ and c <strong>Fos</strong> in the spinal cord, which are known to be concerned with spinal neuronal <b>sensitization</b> and opiate dependence, were investigated in AQP4 knockout mice using Western blotting analysis.
+FOS	addiction	withdrawal	22907296	Meanwhile, the protein levels of PKCα and c <strong>Fos</strong> in the spinal cord of AQP4 knockout mice were significantly higher than those in the wild type mice; while the expression of PKCγ was decreased remarkably by AQP4 knockout during the <b>withdrawal</b> (P < 0.01).
+FOS	drug	opioid	22907296	These data suggest that AQP4 deficiency attenuated <b>morphine</b> withdrawal responses may be partially attributed to the changes in the spinal expression of PKCα, PKCγ or c <strong>Fos</strong>.
+FOS	addiction	withdrawal	22907296	These data suggest that AQP4 deficiency attenuated morphine <b>withdrawal</b> responses may be partially attributed to the changes in the spinal expression of PKCα, PKCγ or c <strong>Fos</strong>.
+FOS	drug	cocaine	22886755	5 HT(2A) receptor blockade and 5 HT(2C) receptor activation interact to reduce <b>cocaine</b> hyperlocomotion and <strong>Fos</strong> protein expression in the caudate putamen.
+FOS	drug	cocaine	22886755	This study examined whether these drugs interact to reduce <b>cocaine</b> hyperlocomotion and <strong>Fos</strong> expression in the striatum and prefrontal cortex.
+FOS	drug	cocaine	22886755	While neither drug given alone produced any effects, the M100907/MK212 cocktail attenuated <b>cocaine</b> hyperlocomotion as well as <b>cocaine</b> induced <strong>Fos</strong> expression in the dorsolateral caudate putamen (CPu), but had no effect on spontaneous locomotion.
+FOS	drug	cocaine	22886755	The findings suggest that 5 HT(2A) Rs and 5 HT(2C) Rs interact to attenuate <b>cocaine</b> hyperlocomotion and <strong>Fos</strong> expression in the CPu, and that the CPu is a potential locus of the interactive effects between these 5 HT(2) R subtypes on behavior.
+FOS	drug	opioid	22860427	To explore the effects of intrathecal injection of neuronal nitric oxide synthase (nNOS) inhibitors 7 Nitroindazole (7 Ni) and inducible nitric oxide synthase(iNOS) inhibitors aminoguanidine (AG) on the behavioral changes of <b>morphine</b> induced dependent and withdrawal rats; the expression of <strong>Fos</strong>, nNOS and iNOS in spinal cord.
+FOS	addiction	withdrawal	22860427	To explore the effects of intrathecal injection of neuronal nitric oxide synthase (nNOS) inhibitors 7 Nitroindazole (7 Ni) and inducible nitric oxide synthase(iNOS) inhibitors aminoguanidine (AG) on the behavioral changes of morphine induced dependent and <b>withdrawal</b> rats; the expression of <strong>Fos</strong>, nNOS and iNOS in spinal cord.
+FOS	drug	opioid	22860427	One hour after <b>naloxone</b> precipitated withdrawal, <strong>Fos</strong> protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of nNOS and iNOS in the rat spinal cord.
+FOS	addiction	withdrawal	22860427	One hour after naloxone precipitated <b>withdrawal</b>, <strong>Fos</strong> protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of nNOS and iNOS in the rat spinal cord.
+FOS	drug	opioid	22860427	Intrathecal administration of nNOS inhibitor 7 Ni and iNOS inhibitors AG decreased the scores of <b>morphine</b> withdrawal, attenuated <b>morphine</b> withdrawal induced allodynia and also inhibited the increase of <strong>Fos</strong> protein expression in the spinal cord of <b>morphine</b> withdrawal rats.
+FOS	addiction	withdrawal	22860427	Intrathecal administration of nNOS inhibitor 7 Ni and iNOS inhibitors AG decreased the scores of morphine <b>withdrawal</b>, attenuated morphine <b>withdrawal</b> induced allodynia and also inhibited the increase of <strong>Fos</strong> protein expression in the spinal cord of morphine <b>withdrawal</b> rats.
+FOS	drug	alcohol	22851043	<b>Ethanol</b> had little effect on c <strong>Fos</strong> activation.
+FOS	drug	alcohol	22792289	ΔFosB and FosB are members of the <strong>Fos</strong> family of transcription factors implicated in neural plasticity in drug addiction; a connection between electroacupuncture's treatment of <b>alcohol</b> abuse and the <strong>Fos</strong> family has not been established.
+FOS	addiction	addiction	22792289	ΔFosB and FosB are members of the <strong>Fos</strong> family of transcription factors implicated in neural plasticity in drug <b>addiction</b>; a connection between electroacupuncture's treatment of alcohol abuse and the <strong>Fos</strong> family has not been established.
+FOS	drug	psychedelics	22764597	[Effects of electroacupuncture intervention at different time in A day on expression of tyrosine hydroxylase and C <strong>fos</strong> in nucleus accumbens in <b>ketamine</b> addiction rats].
+FOS	addiction	addiction	22764597	[Effects of electroacupuncture intervention at different time in A day on expression of tyrosine hydroxylase and C <strong>fos</strong> in nucleus accumbens in ketamine <b>addiction</b> rats].
+FOS	drug	psychedelics	22764597	To observe the effect of electroacupuncture (EA) intervention at different time in a day on the expression of tyrosine hydroxylase (TH) and c <strong>fos</strong> in the Nucleus Accumbens (NAc) so as to explore its mechanism underlying improvement of <b>ketamine</b> addiction.
+FOS	addiction	addiction	22764597	To observe the effect of electroacupuncture (EA) intervention at different time in a day on the expression of tyrosine hydroxylase (TH) and c <strong>fos</strong> in the Nucleus Accumbens (NAc) so as to explore its mechanism underlying improvement of ketamine <b>addiction</b>.
+FOS	drug	psychedelics	22764597	EA of "Zusanli" (ST 36) and "Sanyinjiao" (SP 6) at 11:00 and 17:00 of the daytime can down regulate <b>ketamine</b> addiction induced increase of expression of TH and c <strong>fos</strong> in the NAc in <b>ketamine</b> addiction rats, which may contribute to its effect in relieving <b>ketamine</b> addiction symptoms in clinic.
+FOS	addiction	addiction	22764597	EA of "Zusanli" (ST 36) and "Sanyinjiao" (SP 6) at 11:00 and 17:00 of the daytime can down regulate ketamine <b>addiction</b> induced increase of expression of TH and c <strong>fos</strong> in the NAc in ketamine <b>addiction</b> rats, which may contribute to its effect in relieving ketamine <b>addiction</b> symptoms in clinic.
+FOS	drug	alcohol	22749946	Chronic self administration of <b>ethanol</b> reduced the expression of the C <strong>fos</strong> gene 4  to 12 fold and increased expression of the COX 2 (up to 4 fold) and Homer1a genes in the rat prefrontal cortex.
+FOS	drug	alcohol	22749946	The <b>ethanol</b> induced reduction in C <strong>fos</strong> gene expression in the prefrontal cortex reveals an abnormal activity of these neurons, which may be relevant in the compulsive consumption of <b>ethanol</b>, the control of reward related areas and the behavioural phenotype of <b>ethanol</b> addiction.
+FOS	addiction	addiction	22749946	The ethanol induced reduction in C <strong>fos</strong> gene expression in the prefrontal cortex reveals an abnormal activity of these neurons, which may be relevant in the <b>compulsive</b> consumption of ethanol, the control of reward related areas and the behavioural phenotype of ethanol <b>addiction</b>.
+FOS	addiction	reward	22749946	The ethanol induced reduction in C <strong>fos</strong> gene expression in the prefrontal cortex reveals an abnormal activity of these neurons, which may be relevant in the compulsive consumption of ethanol, the control of <b>reward</b> related areas and the behavioural phenotype of ethanol addiction.
+FOS	addiction	relapse	22741574	We measured the contents of brain derived neurotrophic factor (BDNF), c <strong>Fos</strong> and Fas associated death domain (FADD) proteins in the medial prefrontal cortex (mPFC) following <b>reinstatement</b>.
+FOS	addiction	relapse	22741574	Reductions in drug <b>seeking</b> during <b>reinstatement</b> were matched by downward shifts in the contents of BDNF, c <strong>Fos</strong> and FADD proteins in the mPFC, which were elevated in relapsing rats.
+FOS	drug	cocaine	22721675	Changes in expression of c <strong>Fos</strong> protein following <b>cocaine</b> cue extinction learning.
+FOS	drug	cocaine	22721675	We used regional analyses of c <strong>Fos</strong> and GluR2 protein expression to delineate neural activity and plasticity that may be associated with <b>cocaine</b> cue extinction learning.
+FOS	drug	cocaine	22721675	Among 11 brain sites examined, extinction training increased c <strong>Fos</strong> expression in basolateral amygdala and prelimbic prefrontal cortex of <b>cocaine</b> cue extinguished rats relative to both control conditions.
+FOS	drug	cocaine	22721675	In dorsal subiculum and infralimbic prefrontal cortex, extinction training increased c <strong>Fos</strong> expression in both <b>cocaine</b> cue and saline cue extinguished rats relative to the no extinction control condition.
+FOS	drug	cocaine	22668854	Thus, we investigated orexin and c <strong>Fos</strong> expression in the LH and PFA using immunohistochemistry in HiS and LoS rats following either control or <b>cocaine</b> (15 mg/kg) injections.
+FOS	drug	opioid	22659588	Using immunohistochemical double staining for tyrosine hydroxylase (TH) and <strong>Fos</strong>, we found that the number of <strong>Fos</strong>(+)TH(+) neurons in the rostral VTA and number of <strong>Fos</strong>(+)TH( ) neurons in the lateral SNr were significantly increased in escalating dose <b>morphine</b> treated rats compared with steady dose <b>morphine</b> treated rats and acute <b>morphine</b> treated rats.
+FOS	drug	opioid	22659588	The number of <strong>Fos</strong>(+)TH(+) neurons was significantly increased by acute <b>morphine</b> in the caudal VTA and SNc, but this number did not increase further with <b>morphine</b> pretreatment.
+FOS	drug	opioid	22626645	In addition, the hypothalamic changes of several signal molecules such as pERK, pCaMK IIα, c <strong>FOS</strong> and pCREB expression were observed during the presence or absence of withdrawal responses induced by <b>morphine</b> or β endorphin administered once or repeatedly.
+FOS	addiction	withdrawal	22626645	In addition, the hypothalamic changes of several signal molecules such as pERK, pCaMK IIα, c <strong>FOS</strong> and pCREB expression were observed during the presence or absence of <b>withdrawal</b> responses induced by morphine or β endorphin administered once or repeatedly.
+FOS	drug	opioid	22626645	Both hypothalamic pCaMK IIα and c <strong>FOS</strong> expressions were increased by <b>naloxone</b> treatment in acutely administered <b>morphine</b> group, whereas only pCaMK IIα expression was elevated by <b>naloxone</b> treatment in repeatedly administered <b>morphine</b> group.
+FOS	drug	opioid	22626645	The pCaMK IIα and the c <strong>FOS</strong> protein expression may play important roles for the regulation of <b>naloxone</b> precipitated withdrawal symptoms such as jumping, diarrhea, weight loss, rearing, penile licking and paw tremor induced by <b>morphine</b> treated group, whereas the phosphorylation of hypothalamic pCaMK IIα appears to be involved only in the regulation of <b>naloxone</b> precipitated withdrawal symptoms such as diarrhea, weight loss and rearing in β endorphin treated group.
+FOS	addiction	withdrawal	22626645	The pCaMK IIα and the c <strong>FOS</strong> protein expression may play important roles for the regulation of naloxone precipitated <b>withdrawal</b> symptoms such as jumping, diarrhea, weight loss, rearing, penile licking and paw tremor induced by morphine treated group, whereas the phosphorylation of hypothalamic pCaMK IIα appears to be involved only in the regulation of naloxone precipitated <b>withdrawal</b> symptoms such as diarrhea, weight loss and rearing in β endorphin treated group.
+FOS	drug	cocaine	22613730	<b>Cocaine</b> induced c <strong>Fos</strong> expression in rats selectively bred for high or low saccharin intake and in rats selected for high or low impulsivity.
+FOS	drug	cocaine	22613730	Subsequently, rats were given an acute injection of <b>cocaine</b> or saline and then c <strong>Fos</strong> expression was observed and analyzed in several brain regions.
+FOS	drug	cocaine	22613730	The low reward seeking phenotypes showed higher <b>cocaine</b> induced c <strong>Fos</strong> expression in several of these regions.
+FOS	addiction	relapse	22613730	The low reward <b>seeking</b> phenotypes showed higher cocaine induced c <strong>Fos</strong> expression in several of these regions.
+FOS	addiction	reward	22613730	The low <b>reward</b> seeking phenotypes showed higher cocaine induced c <strong>Fos</strong> expression in several of these regions.
+FOS	drug	cocaine	22613730	Low saccharin preferring rats showed higher <b>cocaine</b> induced c <strong>Fos</strong> expression in the nucleus accumbens shell, and low impulsive rats showed higher <b>cocaine</b> induced c <strong>Fos</strong> expression in the orbitofrontal cortex and cingulate gyrus 1 area.
+FOS	drug	cocaine	22613730	In addition, both low impulsive and low saccharin rats had higher <b>cocaine</b> induced c <strong>Fos</strong> in the dorsal medial and dorsal lateral caudate putamen.
+FOS	drug	opioid	22590628	Importantly, SB334867 attenuated the somatic symptoms of withdrawal, and reduced <b>morphine</b> withdrawal induced c <strong>Fos</strong> expression in the nucleus accumbens (NAc) shell, bed nucleus of stria terminalis, central amygdala and hypothalamic paraventricular nucleus, but did not modify the HPA axis activity.
+FOS	addiction	withdrawal	22590628	Importantly, SB334867 attenuated the somatic symptoms of <b>withdrawal</b>, and reduced morphine <b>withdrawal</b> induced c <strong>Fos</strong> expression in the nucleus accumbens (NAc) shell, bed nucleus of stria terminalis, central amygdala and hypothalamic paraventricular nucleus, but did not modify the HPA axis activity.
+FOS	drug	nicotine	22578217	Therefore, we investigated the effects of <b>nicotine</b> SA on stress induced neuronal activation in limbic PVN network, using c <strong>Fos</strong> protein immunohistochemistry and retrograde tracing.
+FOS	drug	nicotine	22578217	<b>Nicotine</b> decreased stress induced c <strong>Fos</strong> in prelimbic cortex (PrL), anteroventral BST (avBST), and peri PVN, but increased c <strong>Fos</strong> induction in medial amygdala (MeA), locus coeruleus, and PVN.
+FOS	drug	nicotine	22578217	The stress induced c <strong>Fos</strong> expression in retrograde labeled FG+ neurons was decreased in PrL by <b>nicotine</b>, but increased in MeA, and also reduced in avBST.
+FOS	drug	cocaine	22534624	Novel cues reinstate <b>cocaine</b> seeking behavior and induce <strong>Fos</strong> protein expression as effectively as conditioned cues.
+FOS	addiction	relapse	22534624	Novel cues reinstate cocaine <b>seeking</b> behavior and induce <strong>Fos</strong> protein expression as effectively as conditioned cues.
+FOS	drug	cocaine	22534624	This study examined <strong>Fos</strong> protein expression in response to <b>cocaine</b> cues or to novel cues as a control for activation produced by test novelty.
+FOS	drug	amphetamine	22514626	Repeated <b>methamphetamine</b> administration differentially alters <strong>fos</strong> expression in caudate putamen patch and matrix compartments and nucleus accumbens.
+FOS	drug	amphetamine	22514626	In the present study, we used immunohistochemistry to investigate the effects of pretreatment with <b>methamphetamine</b> on the ability of a subsequent <b>methamphetamine</b> challenge to induce <strong>Fos</strong> protein expression in the patch and matrix compartments of the dorsolateral and dorsomedial caudate putamen and in the ventral striatum (nucleus accumbens).
+FOS	drug	amphetamine	22514626	A <b>methamphetamine</b> challenge increased the number of <strong>Fos</strong> positive cells in all areas of the dorsal and ventral striatum.
+FOS	drug	amphetamine	22514626	However, <b>methamphetamine</b> challenge induced <strong>Fos</strong> expression in more cells in the patch than in the matrix compartment in the dorsolateral and dorsomedial caudate putamen.
+FOS	drug	amphetamine	22514626	Furthermore, past experience with <b>methamphetamine</b> increased the number of <b>methamphetamine</b> induced <strong>Fos</strong> positive cells in the patch compartment of the dorsal caudate putamen, but not in the matrix or in the core or shell of the nucleus accumbens.
+FOS	addiction	relapse	22492053	We also combined the marker of neuronal activity, <strong>Fos</strong>, with the retrograde tracer Fluoro Gold to assess activation in this pathway during context induced <b>reinstatement</b>.
+FOS	addiction	relapse	22492053	Context induced <b>reinstatement</b> was associated with increased <strong>Fos</strong> expression in ventral mPFC neurons, including those projecting to accumbens shell, with higher double labeling in the ipsilateral projection than in the contralateral projection.
+FOS	drug	cocaine	22457508	Here, we examined inputs to the lateral hypothalamus (LH) orexin cell field from the lateral septum (LS) using tract tracing and <strong>Fos</strong> immunohistochemistry after <b>cocaine</b> (10 mg/kg) conditioned place preference (CPP) in Sprague Dawley rats.
+FOS	addiction	reward	22457508	Here, we examined inputs to the lateral hypothalamus (LH) orexin cell field from the lateral septum (LS) using tract tracing and <strong>Fos</strong> immunohistochemistry after cocaine (10 mg/kg) conditioned place preference (<b>CPP</b>) in Sprague Dawley rats.
+FOS	drug	cocaine	22457508	We found that neurons in rostral LS (LSr) that project to LH are <strong>Fos</strong> activated in proportion to <b>cocaine</b> CPP, and that inhibition of LSr neurons with local baclofen and muscimol microinjection (0.3/0.03 nmol) blocks expression of <strong>Fos</strong> in LH orexin cells and <b>cocaine</b> preference.
+FOS	addiction	reward	22457508	We found that neurons in rostral LS (LSr) that project to LH are <strong>Fos</strong> activated in proportion to cocaine <b>CPP</b>, and that inhibition of LSr neurons with local baclofen and muscimol microinjection (0.3/0.03 nmol) blocks expression of <strong>Fos</strong> in LH orexin cells and cocaine preference.
+FOS	drug	cocaine	22454845	Reinforcing properties of pups versus <b>cocaine</b> for fathers and associated central expression of <strong>Fos</strong> and tyrosine hydroxylase in mandarin voles (Microtus mandarinus).
+FOS	addiction	reward	22454845	<b>Reinforcing</b> properties of pups versus cocaine for fathers and associated central expression of <strong>Fos</strong> and tyrosine hydroxylase in mandarin voles (Microtus mandarinus).
+FOS	drug	cocaine	22454845	We also measured neuronal <strong>Fos</strong> and tyrosine hydroxylase (TH) expression underlying the preferences of fathers for pups or <b>cocaine</b>.
+FOS	drug	cocaine	22454845	Fathers preferring <b>cocaine</b> exhibited an increase in <strong>Fos</strong> immunoreactive neurons in the accumbens,medial nucleus of the amygdala, cingulate cortex, medial preoptic area and ventral tegmental area and had more TH IR neurons in the ventral tegmental area compared to fathers preferring PND 5–9 pups.
+FOS	drug	opioid	22454660	Electroacupuncture suppresses discrete cue evoked <b>heroin</b> seeking and <strong>fos</strong> protein expression in the nucleus accumbens core in rats.
+FOS	addiction	relapse	22454660	Electroacupuncture suppresses discrete cue evoked heroin <b>seeking</b> and <strong>fos</strong> protein expression in the nucleus accumbens core in rats.
+FOS	addiction	relapse	22454660	We also applied immunohistochemistry to detect <strong>Fos</strong> positive nuclei in the nucleus accumbens (NACc) core and shell after <b>reinstatement</b> test.
+FOS	drug	cocaine	22453546	This study was conducted to investigate the effects of acupuncture on footshock induced reinstatement of <b>cocaine</b> seeking and the expression of c <strong>Fos</strong> and the transcription factor cAMP response element binding protein (CREB) in the NAc, used as markers of neuronal activation in conditions of stress induced reinstatement to <b>cocaine</b>.
+FOS	addiction	relapse	22453546	This study was conducted to investigate the effects of acupuncture on footshock induced <b>reinstatement</b> of cocaine <b>seeking</b> and the expression of c <strong>Fos</strong> and the transcription factor cAMP response element binding protein (CREB) in the NAc, used as markers of neuronal activation in conditions of stress induced <b>reinstatement</b> to cocaine.
+FOS	drug	cocaine	22453546	Acute footshock stress reinstated <b>cocaine</b> seeking behavior and enhanced c <strong>Fos</strong> expression and phosphorylated CREB (pCREB) activation in the NAc shell in <b>cocaine</b> pre exposed rats.
+FOS	addiction	relapse	22453546	Acute footshock stress reinstated cocaine <b>seeking</b> behavior and enhanced c <strong>Fos</strong> expression and phosphorylated CREB (pCREB) activation in the NAc shell in cocaine pre exposed rats.
+FOS	drug	cocaine	22453546	On the other hand, acupuncture at HT7, but not at control point (LI5), markedly reduced reinstatement of <b>cocaine</b> seeking (86.5 % inhibition vs. control value), c <strong>Fos</strong> expression (81.7% inhibition), and pCREB activation (79.3% inhibition) in the NAc shell.
+FOS	addiction	relapse	22453546	On the other hand, acupuncture at HT7, but not at control point (LI5), markedly reduced <b>reinstatement</b> of cocaine <b>seeking</b> (86.5 % inhibition vs. control value), c <strong>Fos</strong> expression (81.7% inhibition), and pCREB activation (79.3% inhibition) in the NAc shell.
+FOS	drug	opioid	22423101	Male Sprague Dawley rats were used to investigate whether orexin cells that project to VTA exhibit <strong>Fos</strong> activation with <b>morphine</b> conditioned place preference (CPP), and whether these cells exhibit increased <strong>Fos</strong> with <b>morphine</b> CPP during protracted abstinence.
+FOS	addiction	reward	22423101	Male Sprague Dawley rats were used to investigate whether orexin cells that project to VTA exhibit <strong>Fos</strong> activation with morphine conditioned place preference (<b>CPP</b>), and whether these cells exhibit increased <strong>Fos</strong> with morphine <b>CPP</b> during protracted abstinence.
+FOS	addiction	reward	22423101	Triple labeling for WGA Au, <strong>Fos</strong>, and orexin revealed that the percentage of VTA projecting orexin neurons <strong>Fos</strong> activated on the <b>CPP</b> test day significantly increased in post dependent (vs nondependent) rats, and was exclusive to LH orexin neurons (not dorsomedial or perifornical).
+FOS	addiction	reward	22423101	Post dependent animals showed a positive correlation between <b>CPP</b> scores and percentages of <strong>Fos</strong> activated, caudal VTA projecting LH orexin cells.
+FOS	addiction	reward	22423101	Unlike afferents to caudal VTA, percentages of rostral VTA projecting, LH orexin cells that were <strong>Fos</strong> activated showed a positive correlation with <b>CPP</b> only in nondependent animals.
+FOS	addiction	reward	22423101	<strong>Fos</strong> in LC projecting orexin cells was not correlated with <b>CPP</b> in any group.
+FOS	drug	opioid	22410393	Here, immunofluorescence for the activity related immediate early gene, c <strong>Fos</strong>, was examined in transgenic reporter mouse lines by confocal microscopy to study the specific populations of ventral striatal neurons activated by <b>morphine</b> withdrawal and acute <b>morphine</b>.
+FOS	addiction	withdrawal	22410393	Here, immunofluorescence for the activity related immediate early gene, c <strong>Fos</strong>, was examined in transgenic reporter mouse lines by confocal microscopy to study the specific populations of ventral striatal neurons activated by morphine <b>withdrawal</b> and acute morphine.
+FOS	drug	opioid	22410393	After chronic <b>morphine</b>, <b>naloxone</b> precipitated withdrawal strongly increased expression of c <strong>Fos</strong> immunoreactivity, predominantly in D2 receptor (D2R) medium sized spiny neurons (MSNs) of the nucleus accumbens (NAc) core and shell regions.
+FOS	addiction	withdrawal	22410393	After chronic morphine, naloxone precipitated <b>withdrawal</b> strongly increased expression of c <strong>Fos</strong> immunoreactivity, predominantly in D2 receptor (D2R) medium sized spiny neurons (MSNs) of the nucleus accumbens (NAc) core and shell regions.
+FOS	drug	opioid	22410393	By contrast, a single injection of <b>morphine</b> exclusively activated c <strong>Fos</strong> immunoreactivity in D1 receptor expressing (D1R) MSNs of the core and shell of the NAc.
+FOS	drug	cocaine	22367168	We also studied effects of Y5 receptor antagonism on <b>cocaine</b> induced c <strong>fos</strong> expression and extracellular dopamine with microdialysis as well as dopamine transporter mediated uptake of dopamine in vitro.
+FOS	drug	cocaine	22367168	<b>Cocaine</b> failed to increase c <strong>fos</strong> expression in the nucleus accumbens and striatum of L 152,804 treated mice, indicating that the Y5 antagonist could act by influencing neural activity in these regions.
+FOS	drug	opioid	22364199	Mifepristone antagonized the TH phosphorylation at Ser³¹ and the expression of c <strong>Fos</strong> expression induced by <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	22364199	Mifepristone antagonized the TH phosphorylation at Ser³¹ and the expression of c <strong>Fos</strong> expression induced by morphine <b>withdrawal</b>.
+FOS	drug	alcohol	22349397	After treating juvenile and adult rats with intermittent <b>ethanol</b> administration, we found that <b>ethanol</b> treatment upregulates histone acetyl transferase (HAT) activity in adolescent prefrontal cortex and increases histone (H3 or H4) acetylation and H3(K4) dimethylation in the promoter region of <strong>cFos</strong>, Cdk5 and FosB.
+FOS	drug	alcohol	22349397	Inhibition of histone deacetylase by sodium butyrate before <b>ethanol</b> injection enhances both up regulation of HAT activity and histone acetylation of <strong>cFos</strong>, Cdk5 and FosB.
+FOS	drug	alcohol	22285885	Neonatal <b>alcohol</b> exposure and the hippocampus in developing male rats: effects on behaviorally induced CA1 c <strong>Fos</strong> expression, CA1 pyramidal cell number, and contextual fear conditioning.
+FOS	drug	alcohol	22285885	We then examined the relationship between CPFE impairment, hippocampal cell loss, and c <strong>Fos</strong> expression in rats exposed to <b>alcohol</b> over PD 4 9 (Experiment 2).
+FOS	drug	alcohol	22285885	In Experiment 2, SI rats had greater numbers of CA1 c <strong>Fos</strong>+ cells compared with <b>alcohol</b> exposed rats, differing significantly from rats exposed to the high <b>alcohol</b> dose (5.25 g) over PD 4 9.
+FOS	drug	alcohol	22285885	In addition, lower levels of c <strong>Fos</strong>+ cells in <b>alcohol</b> exposed rats following preexposure may be related to general reductions in the number of CA1 pyramidal cells in these rats.
+FOS	drug	amphetamine	22266344	Regional c <strong>Fos</strong> and FosB/ΔFosB expression associated with chronic <b>methamphetamine</b> self administration and <b>methamphetamine</b> seeking behavior in rats.
+FOS	addiction	relapse	22266344	Regional c <strong>Fos</strong> and FosB/ΔFosB expression associated with chronic methamphetamine self administration and methamphetamine <b>seeking</b> behavior in rats.
+FOS	drug	amphetamine	22266344	The regional expression of the transcription factors c <strong>Fos</strong> and FosB/ΔFosB was examined in rats given acute exposure to intravenous <b>methamphetamine</b> (<b>METH</b>) or repeated intravenous <b>METH</b> self administration.
+FOS	drug	amphetamine	22266344	The results showed that acute <b>METH</b> produced a characteristic signature of <strong>Fos</strong> expression with elevations in striatal, cortical, and extended amygdala regions.
+FOS	drug	amphetamine	22266344	Importantly, rats with a 3 week history of <b>METH</b> self administration displayed similar regional <strong>Fos</strong> expression to rats receiving <b>METH</b> for the first time.
+FOS	drug	amphetamine	22266344	Rats seeking, but not receiving, <b>METH</b> on the test day had augmented <strong>Fos</strong> in the lateral hypothalamus, septum, and vertical limb of the diagonal band of Broca, suggesting a primary role for these regions in <b>METH</b> seeking behavior.
+FOS	addiction	relapse	22266344	Rats <b>seeking</b>, but not receiving, METH on the test day had augmented <strong>Fos</strong> in the lateral hypothalamus, septum, and vertical limb of the diagonal band of Broca, suggesting a primary role for these regions in METH <b>seeking</b> behavior.
+FOS	drug	amphetamine	22266344	Overall, these results show persistent upregulated regional brain <strong>Fos</strong> and FosB/ΔFosB expression with chronic <b>METH</b> self administration and indicate a role for the lateral hypothalamus and lateral septum in <b>METH</b> seeking behavior.
+FOS	addiction	relapse	22266344	Overall, these results show persistent upregulated regional brain <strong>Fos</strong> and FosB/ΔFosB expression with chronic METH self administration and indicate a role for the lateral hypothalamus and lateral septum in METH <b>seeking</b> behavior.
+FOS	drug	cocaine	22252051	Finally, <strong>Fos</strong> staining results revealed that a number of BLA neurons were activated by the retrieval of both <b>cocaine</b> induced CPP and PA. We conclude that inactivation of neural activity in BLA immediately following retrieval of a fear or <b>cocaine</b> conditioned memory can impair subsequent expression of both memories.
+FOS	addiction	reward	22252051	Finally, <strong>Fos</strong> staining results revealed that a number of BLA neurons were activated by the retrieval of both cocaine induced <b>CPP</b> and PA. We conclude that inactivation of neural activity in BLA immediately following retrieval of a fear or cocaine conditioned memory can impair subsequent expression of both memories.
+FOS	drug	opioid	22227057	Deleting the NR1 gene in CeA neurons resulted in a reduction of <b>morphine</b> induced <strong>Fos</strong> protein labeling in the ventral BNST.
+FOS	drug	benzodiazepine	22210490	Evidence for a role of inhibition of orexinergic neurons in the anxiolytic and sedative effects of <b>diazepam</b>: A c <strong>Fos</strong> study.
+FOS	addiction	addiction	22210490	We used c <strong>Fos</strong> immunohistochemistry as an indirect way to study neuronal activation or inhibition induced by DZ at anxiolytic and sedative doses (0.5 and 5mg/kg, respectively) in various brain areas involved in anxiety, arousal, sedation and <b>addiction</b> in C57BL/6J mice.
+FOS	drug	amphetamine	22205547	Protracted withdrawal from self administration enhanced the survival of SGZ BrdU cells, and <b>methamphetamine</b> seeking during protracted withdrawal enhanced <strong>Fos</strong> expression in the dentate gyrus and medial prefrontal cortex in LgA rats to a greater extent than in ShA and I ShA rats.
+FOS	addiction	relapse	22205547	Protracted withdrawal from self administration enhanced the survival of SGZ BrdU cells, and methamphetamine <b>seeking</b> during protracted withdrawal enhanced <strong>Fos</strong> expression in the dentate gyrus and medial prefrontal cortex in LgA rats to a greater extent than in ShA and I ShA rats.
+FOS	addiction	withdrawal	22205547	Protracted <b>withdrawal</b> from self administration enhanced the survival of SGZ BrdU cells, and methamphetamine seeking during protracted <b>withdrawal</b> enhanced <strong>Fos</strong> expression in the dentate gyrus and medial prefrontal cortex in LgA rats to a greater extent than in ShA and I ShA rats.
+FOS	drug	alcohol	22198308	Very recent preclinical studies have illustrated a remarkable ability of exogenously delivered oxytocin to inhibit stimulant and <b>alcohol</b> self administration, to alter associated drug induced changes in dopamine, glutamate and <strong>Fos</strong> expression in cortical and basal ganglia sites, and to prevent stress and priming induced relapse to drug seeking.
+FOS	addiction	relapse	22198308	Very recent preclinical studies have illustrated a remarkable ability of exogenously delivered oxytocin to inhibit stimulant and alcohol self administration, to alter associated drug induced changes in dopamine, glutamate and <strong>Fos</strong> expression in cortical and basal ganglia sites, and to prevent stress and priming induced <b>relapse</b> to drug <b>seeking</b>.
+FOS	drug	cocaine	22178542	Alteration of c <strong>Fos</strong> mRNA in the accessory lobe of crayfish is associated with a conditioned <b>cocaine</b> induced reward.
+FOS	addiction	reward	22178542	Alteration of c <strong>Fos</strong> mRNA in the accessory lobe of crayfish is associated with a conditioned cocaine induced <b>reward</b>.
+FOS	drug	cocaine	22178542	We aimed to determine whether novelty in a <b>cocaine</b> paired stimulus is accompanied by changes in c <strong>Fos</strong> mRNA in the accessory lobe of crayfish.
+FOS	drug	cocaine	22178542	Following the expression of reward, we designed a second set of experiments to determine context specificity of the <b>cocaine</b> conditioned novelty effect in altering c <strong>Fos</strong> mRNA expression in the accessory lobe of <b>cocaine</b> treated crayfish.
+FOS	addiction	reward	22178542	Following the expression of <b>reward</b>, we designed a second set of experiments to determine context specificity of the cocaine conditioned novelty effect in altering c <strong>Fos</strong> mRNA expression in the accessory lobe of cocaine treated crayfish.
+FOS	addiction	reward	22178542	This is the first report that characterized context specific alteration of c <strong>Fos</strong> mRNA expression in the accessory lobe of crayfish during drug induced <b>reward</b>.
+FOS	drug	amphetamine	22155611	A <strong>Fos</strong> immunohistochemistry study recently demonstrated that peripheral OXY administration reduced <b>METH</b> induced <strong>Fos</strong> expression within the nucleus accumbens (NAc) core and subthalamic nucleus (STh) in rats.
+FOS	drug	cocaine	22114264	A complete loss of CBP in NAc neurons results in decreased histone acetylation and significantly altered c <strong>fos</strong> expression in response to <b>cocaine</b>.
+FOS	addiction	withdrawal	22097732	Global <b>withdrawal</b> score, Touch evoked agitation scores (TEA score), immunohistochemical and Western blot technique were undertaken to evaluate behavioral changes and expression of <strong>FOS</strong>, nNOS and iNOS in spinal cord respectively.
+FOS	addiction	withdrawal	22097732	<strong>Fos</strong> like positive neurons in dorsal horn of <b>withdrawal</b> group were 380 +/  71, which were higher than those of U0126 group(287 +/  54, P < 0.05).
+FOS	drug	amphetamine	22063717	Brain pattern of histone H3 phosphorylation after acute <b>amphetamine</b> administration: its relationship to brain c <strong>fos</strong> induction is strongly dependent on the particular brain area.
+FOS	addiction	addiction	22063717	c <strong>fos</strong>) to detect brain areas and neurons that are critical for the action of <b>addictive</b> drugs.
+FOS	drug	amphetamine	22063717	Thus, in the present work we studied in adult male rats the effects of a high dose of <b>amphetamine</b> on brain pattern of histone H3 phosphorylation in serine 10 (pH3S(10)) and c <strong>fos</strong> expression.
+FOS	drug	amphetamine	22063717	<b>Amphetamine</b> increased c <strong>fos</strong> expression in medial prefrontal cortex (mPFC), dorsal striatum, nucleus accumbens (Acb), major Island of Calleja (ICjM), central amygdala (CeA), bed nucleus of stria terminalis lateral dorsal (BSTld) and paraventricular nucleus of the hypothalamus (PVN).
+FOS	drug	amphetamine	22063717	The present results give support to the hypothesis that <b>amphetamine</b> induced pH3S(10) IR showed a more restricted pattern than brain c <strong>fos</strong> induction, being this difference strongly dependent on the particular brain area studied.
+FOS	drug	nicotine	22048468	Conditioned response evoked by <b>nicotine</b> conditioned stimulus preferentially induces c <strong>Fos</strong> expression in medial regions of caudate putamen.
+FOS	drug	nicotine	22048468	The purpose of this experiment was to use neurohistochemical analysis of rapidly developing c <strong>Fos</strong> protein to elucidate neurobiological loci involved in the processing of <b>nicotine</b> as an interoceptive conditioned stimulus (CS).
+FOS	drug	nicotine	22048468	On the test day, rats in each condition were challenged with saline or <b>nicotine</b> and later assessed for c <strong>Fos</strong> immunoreactivity.
+FOS	drug	nicotine	22048468	In concordance with previous reports, <b>nicotine</b> induced c <strong>Fos</strong> expression in the majority of areas tested; however, learning dependent expression was specific to dorsomedial and ventromedial regions of caudate putamen (dmCPu, vmCPu).
+FOS	drug	nicotine	22048468	Only rats in the <b>nicotine</b> CS condition, when challenged with <b>nicotine</b>, had higher c <strong>Fos</strong> expression in the dmCPu and vmCPu.
+FOS	drug	alcohol	22020770	To our surprise, the impairment of <strong>AP 1</strong> activation was sufficient to mediate a severe and dose dependent phenotype in human monocytes in vitro at <b>alcohol</b> concentrations as low as 0.16% (or 26 mM).
+FOS	drug	amphetamine	21995495	Patterns of <strong>Fos</strong> expression with mephedrone resembled a combination of those observed with <b>methamphetamine</b> and MDMA, with particularly strong <strong>Fos</strong> expression in the cortex, dorsal and ventral striatum, ventral tegmental area (typical of both MDMA and <b>methamphetamine</b>) and supraoptic nucleus (typical of MDMA).
+FOS	drug	psychedelics	21995495	Patterns of <strong>Fos</strong> expression with mephedrone resembled a combination of those observed with methamphetamine and <b>MDMA</b>, with particularly strong <strong>Fos</strong> expression in the cortex, dorsal and ventral striatum, ventral tegmental area (typical of both <b>MDMA</b> and methamphetamine) and supraoptic nucleus (typical of <b>MDMA</b>).
+FOS	addiction	relapse	21985936	Animals were then tested for <b>reinstatement</b> and sacrificed immediately following the presentation of either the S⁻ or S⁺ discriminative stimuli, and <strong>Fos</strong> protein expression was assessed in thalamic and epithalamic regions.
+FOS	drug	cocaine	21976515	Consequently, TDE altered <b>cocaine</b> induced regulation of genes bearing SRE site(s) in their promoters, including c <strong>fos</strong>, zif268, ΔFosB, and arc/arg3.1 (activity regulated cytoskeleton associated protein).
+FOS	drug	alcohol	21969878	On the other hand, chronic <b>ethanol</b> binge increased mRNA expression of angiotensinogen and c <strong>fos</strong>.
+FOS	addiction	intoxication	21969878	On the other hand, chronic ethanol <b>binge</b> increased mRNA expression of angiotensinogen and c <strong>fos</strong>.
+FOS	drug	opioid	21947312	Using dual immunolabeling for c <strong>Fos</strong>, data show that <b>naloxone</b> induced withdrawal increases the number of TH positive neurons phosphorylated at Ser40 or Ser31 that coexpress c <strong>Fos</strong> in the nucleus of tractus solitarius (NTS) A2 from wild type and CRF( / ) deficient mice.
+FOS	addiction	withdrawal	21947312	Using dual immunolabeling for c <strong>Fos</strong>, data show that naloxone induced <b>withdrawal</b> increases the number of TH positive neurons phosphorylated at Ser40 or Ser31 that coexpress c <strong>Fos</strong> in the nucleus of tractus solitarius (NTS) A2 from wild type and CRF( / ) deficient mice.
+FOS	addiction	intoxication	21946008	Also, epidural application of the same concentration of either antagonist during a <b>binge</b> mAMPH regimen blunted the mAMPH induced striatal DAT depletions with a topography similar to its effects on <strong>Fos</strong> expression.
+FOS	addiction	addiction	21886798	ΔFosB and FosB are members of the <strong>Fos</strong> family of transcription factors that are implicated in neural plasticity in <b>addiction</b>.
+FOS	addiction	sensitization	21886798	Opiate induced <b>sensitization</b> may develop via <strong>Fos</strong>/ΔFosB plasticity in motivational pathways (NAc), motor outputs (CPU), and associative learning (PL, IL, BLA) and stress pathways (CNA).
+FOS	drug	cocaine	21886557	These changes are considered as consequences of <b>cocaine</b> induced molecular adaptation such as CREB and c <strong>Fos</strong>.
+FOS	drug	cocaine	21886557	Recently, methanolic extracts from licorice was reported to decrease <b>cocaine</b> induced dopamine release and c <strong>Fos</strong> expression in the nucleus accumbens.
+FOS	drug	cocaine	21886557	In addition, LQ inhibited CREB phosphorylation and c <strong>Fos</strong> expression in the striatum and the nucleus accumbens induced by acute <b>cocaine</b>.
+FOS	drug	cocaine	21886552	We generated and analyzed genetically engineered mouse models and found that the D1 receptor and c <strong>Fos</strong> expressed in D1 receptor bearing neurons mediate the locomotor sensitization and reinforcing effects of <b>cocaine</b>.
+FOS	addiction	reward	21886552	We generated and analyzed genetically engineered mouse models and found that the D1 receptor and c <strong>Fos</strong> expressed in D1 receptor bearing neurons mediate the locomotor sensitization and <b>reinforcing</b> effects of cocaine.
+FOS	addiction	sensitization	21886552	We generated and analyzed genetically engineered mouse models and found that the D1 receptor and c <strong>Fos</strong> expressed in D1 receptor bearing neurons mediate the locomotor <b>sensitization</b> and reinforcing effects of cocaine.
+FOS	drug	cocaine	21886552	Notably, a lack of <strong>Fos</strong> expression in D1 receptor bearing neurons in mice results in no change in the induction but a significantly delayed extinction of <b>cocaine</b> induced conditioned place preference.
+FOS	drug	cocaine	21886552	These findings suggest that D1 receptor mediated and c <strong>Fos</strong> regulated changes in cell signaling and gene expression may play key roles in the extinction process, and they provide a foundation for further exploring mechanisms underlying extinction of cue elicited <b>cocaine</b> seeking.
+FOS	addiction	relapse	21886552	These findings suggest that D1 receptor mediated and c <strong>Fos</strong> regulated changes in cell signaling and gene expression may play key roles in the extinction process, and they provide a foundation for further exploring mechanisms underlying extinction of cue elicited cocaine <b>seeking</b>.
+FOS	drug	cocaine	21880920	In addition, several lines of evidence suggest that adaptive changes occurred in both the ventral and dorsal striatum in the absence of VGLUT2: DA receptor binding was increased, and basal mRNA levels of the DA induced early genes Nur77 and c <strong>fos</strong> were elevated as after <b>cocaine</b> induction.
+FOS	drug	nicotine	21831361	c <strong>Fos</strong> expression was analyzed in several brain areas related to <b>nicotine</b> dependence by immunofluorescence techniques.
+FOS	addiction	dependence	21831361	c <strong>Fos</strong> expression was analyzed in several brain areas related to nicotine <b>dependence</b> by immunofluorescence techniques.
+FOS	drug	nicotine	21831361	<b>Nicotine</b> withdrawal increased the percentage of hypocretin cells expressing c <strong>Fos</strong> in the perifornical, dorsomedial, and lateral hypothalamus.
+FOS	addiction	withdrawal	21831361	Nicotine <b>withdrawal</b> increased the percentage of hypocretin cells expressing c <strong>Fos</strong> in the perifornical, dorsomedial, and lateral hypothalamus.
+FOS	addiction	withdrawal	21831361	In addition, the increased c <strong>Fos</strong> expression in the PVN during <b>withdrawal</b> was dependent on hypocretin transmission through Hcrtr 1 activation.
+FOS	drug	opioid	21791964	Many studies have suggested that the behavioral and reinforcing effects of <b>morphine</b> are induced by hyperactivation of the mesolimbic dopaminergic system, which results in increases in locomotor activity, c <strong>Fos</strong> expression in the nucleus accumbens (NAc), and tyrosine hydroxylase (TH) in the ventral tegmental area (VTA).
+FOS	addiction	reward	21791964	Many studies have suggested that the behavioral and <b>reinforcing</b> effects of morphine are induced by hyperactivation of the mesolimbic dopaminergic system, which results in increases in locomotor activity, c <strong>Fos</strong> expression in the nucleus accumbens (NAc), and tyrosine hydroxylase (TH) in the ventral tegmental area (VTA).
+FOS	drug	opioid	21791964	In order to investigate the effect of wild ginseng (WG) on treating <b>morphine</b> addiction, we examined the behavioral sensitization of locomotor activity and c <strong>Fos</strong> and TH expression in the rat brain using immunohistochemistry.
+FOS	addiction	addiction	21791964	In order to investigate the effect of wild ginseng (WG) on treating morphine <b>addiction</b>, we examined the behavioral sensitization of locomotor activity and c <strong>Fos</strong> and TH expression in the rat brain using immunohistochemistry.
+FOS	addiction	sensitization	21791964	In order to investigate the effect of wild ginseng (WG) on treating morphine addiction, we examined the behavioral <b>sensitization</b> of locomotor activity and c <strong>Fos</strong> and TH expression in the rat brain using immunohistochemistry.
+FOS	drug	opioid	21791964	Intraperitioneal injection of WG (100 and 200 mg/kg), 30 min before administration of a daily injection of <b>morphine</b> (40 mg/kg, s.c.), significantly inhibited <b>morphine</b> induced increases in c <strong>Fos</strong> expression in NAc and TH expression in VTA as well as in locomotor activity, as compared with Panax ginseng.
+FOS	drug	opioid	21782156	Thus, c <strong>Fos</strong>, FosB/ΔFosB and P CREB immunoreactive profiles were quantified in the rat CPu after either acute or continuous (6 day) administration of <b>morphine</b> and/or PD168,077.
+FOS	drug	opioid	21782156	Interestingly, at some time points, combined treatment with <b>morphine</b> and PD168,077 substantially increased c <strong>Fos</strong>, FosB/ΔFosB and P CREB expression.
+FOS	drug	alcohol	21762292	Moreover, increased <b>ethanol</b> consumption was associated with lowered blood corticosterone levels, indicating a blunted HPA signaling, which was reversed by intra PVN injection of picrotoxin, as indicated by the increased <strong>Fos</strong> immunostaining positive cells in the PVN and the increased blood corticosterone levels.
+FOS	drug	psychedelics	21585054	[Effects of electroacupuncture on expression of tyrosine hydroxylase and c <strong>fos</strong> in hippocampal CA 1 area in <b>ketamine</b> addiction rats].
+FOS	addiction	addiction	21585054	[Effects of electroacupuncture on expression of tyrosine hydroxylase and c <strong>fos</strong> in hippocampal CA 1 area in ketamine <b>addiction</b> rats].
+FOS	drug	psychedelics	21585054	EA of "Zusanli"(ST 36) "Sanyinjiao" (SP 6) can downregulate <b>ketamine</b> addiction induced increase of expression of tyrosine hydroxylase and c <strong>fos</strong> in the hippocampal CA 1 region in <b>ketamine</b> addiction rats, which may contribute to its effect in relieving <b>ketamine</b> addiction symptoms in clinic.
+FOS	addiction	addiction	21585054	EA of "Zusanli"(ST 36) "Sanyinjiao" (SP 6) can downregulate ketamine <b>addiction</b> induced increase of expression of tyrosine hydroxylase and c <strong>fos</strong> in the hippocampal CA 1 region in ketamine <b>addiction</b> rats, which may contribute to its effect in relieving ketamine <b>addiction</b> symptoms in clinic.
+FOS	drug	amphetamine	21570990	Sensitized activation of <strong>Fos</strong> and brain derived neurotrophic factor in the medial prefrontal cortex and ventral tegmental area accompanies behavioral sensitization to <b>amphetamine</b>.
+FOS	addiction	sensitization	21570990	Sensitized activation of <strong>Fos</strong> and brain derived neurotrophic factor in the medial prefrontal cortex and ventral tegmental area accompanies behavioral <b>sensitization</b> to amphetamine.
+FOS	drug	amphetamine	21570990	Here we investigate whether mPFC neurons innervating the VTA exhibit altered <strong>Fos</strong> or BDNF expression during long term sensitization to <b>amphetamine</b>.
+FOS	addiction	sensitization	21570990	Here we investigate whether mPFC neurons innervating the VTA exhibit altered <strong>Fos</strong> or BDNF expression during long term <b>sensitization</b> to amphetamine.
+FOS	drug	amphetamine	21570990	<b>Amphetamine</b> challenge increased <strong>Fos</strong> and BDNF expression in the mPFC regardless of prior drug experience, and further augmented mPFC BDNF expression in sensitized rats.
+FOS	drug	amphetamine	21570990	Similarly, more <strong>Fos</strong> FG and <strong>Fos</strong> BDNF double labeling was observed in the mPFC of sensitized rats compared to drug naïve rats after <b>amphetamine</b> challenge.
+FOS	drug	amphetamine	21570990	Repeated <b>amphetamine</b> treatment also increased VTA BDNF, while both acute and repeated <b>amphetamine</b> treatment increased <strong>Fos</strong> and <strong>Fos</strong> BDNF co labeling, an effect enhanced in sensitized rats.
+FOS	drug	opioid	21524693	<b>Morphine</b> conditioned cue alters c <strong>Fos</strong> protein expression in the brain of crayfish.
+FOS	drug	opioid	21524693	In the third experiment, we found that the c <strong>Fos</strong> profile of <b>morphine</b> treated crayfish in an unconditioned environment did not show a significant increase from the basal level comparable to saline treated crayfish.
+FOS	drug	opioid	21524693	These results indicate that chronic <b>morphine</b> treatment alone is not sufficient to induce changes in the expression of c <strong>Fos</strong>; instead, <b>morphine</b> environment pairing in a specific context contributes to the expression of alterations in c <strong>Fos</strong> regulation.
+FOS	addiction	addiction	21524693	The enhancement of c <strong>Fos</strong> expression in the brain of crayfish seems to reflect the sensory or anticipatory facets of conditioning that suggests that potential and even unanticipated hypotheses in drug <b>addiction</b> can emerge from studies of <b>addiction</b> in crayfish.
+FOS	drug	nicotine	21501256	To determine whether there are different subgroups of 5 HT cells activated during <b>nicotine</b> administration and withdrawal, we mapped the appearance of <strong>Fos</strong>, a marker of neuronal activation, in 5 HT cells of the dorsal raphe nucleus (DR) and median raphe nucleus (MR).
+FOS	addiction	withdrawal	21501256	To determine whether there are different subgroups of 5 HT cells activated during nicotine administration and <b>withdrawal</b>, we mapped the appearance of <strong>Fos</strong>, a marker of neuronal activation, in 5 HT cells of the dorsal raphe nucleus (DR) and median raphe nucleus (MR).
+FOS	addiction	relapse	21492092	The dopaminergic, enkephalinergic, and <strong>fos</strong> gene expressions are important regulatory genetic pathways for food <b>craving</b> behaviors.
+FOS	drug	cocaine	21477638	In the present study, using <strong>Fos</strong> immunohistochemistry, we investigated brain regions involved in the elimination of <b>cocaine</b> conditioned place preference (CPP) produced by a 30 day exposure to EE.
+FOS	addiction	reward	21477638	In the present study, using <strong>Fos</strong> immunohistochemistry, we investigated brain regions involved in the elimination of cocaine conditioned place preference (<b>CPP</b>) produced by a 30 day exposure to EE.
+FOS	addiction	reward	21477638	Expression of <b>CPP</b> was paralleled by significant increases in the expression of <strong>Fos</strong> in the anterior cingulate cortex, the lateral caudate putamen, the shell of the nucleus accumbens, the dentate gyrus of the hippocampus, the basolateral and central nuclei of amygdala, the bed nucleus of the stria terminalis, and the ventral tegmental area.
+FOS	drug	alcohol	21477621	In animals subjected to the acute severe stress of <b>naltrexone</b> induced morphine withdrawal, treatment with the NK(1) antagonist, L733,060, produced reductions in <strong>Fos</strong> LI in the spinal dorsal horn, whereas those treated with the NK(3) antagonist, SSR146,977, 0.3mg/kg, had reduced <strong>Fos</strong> LI in the dorsal horn, adrenal medulla, nucleus accumbens, ventral tegmental area and periaqueductal grey.
+FOS	drug	opioid	21477621	In animals subjected to the acute severe stress of naltrexone induced <b>morphine</b> withdrawal, treatment with the NK(1) antagonist, L733,060, produced reductions in <strong>Fos</strong> LI in the spinal dorsal horn, whereas those treated with the NK(3) antagonist, SSR146,977, 0.3mg/kg, had reduced <strong>Fos</strong> LI in the dorsal horn, adrenal medulla, nucleus accumbens, ventral tegmental area and periaqueductal grey.
+FOS	addiction	withdrawal	21477621	In animals subjected to the acute severe stress of naltrexone induced morphine <b>withdrawal</b>, treatment with the NK(1) antagonist, L733,060, produced reductions in <strong>Fos</strong> LI in the spinal dorsal horn, whereas those treated with the NK(3) antagonist, SSR146,977, 0.3mg/kg, had reduced <strong>Fos</strong> LI in the dorsal horn, adrenal medulla, nucleus accumbens, ventral tegmental area and periaqueductal grey.
+FOS	drug	opioid	21477621	Furthermore, combination of NK(1) and NK(3) antagonists was more effective than either antagonist in reducing the <strong>Fos</strong> LI response to <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	21477621	Furthermore, combination of NK(1) and NK(3) antagonists was more effective than either antagonist in reducing the <strong>Fos</strong> LI response to morphine <b>withdrawal</b>.
+FOS	drug	nicotine	21412223	Neurochemical analyses of c <strong>fos</strong> mRNA expression, and of monoamine transmitter and transporter levels, showed that forebrain limbic systems are continuing to develop during early adolescence, and that this maturation is critically altered by brief <b>nicotine</b> exposure.
+FOS	drug	nicotine	21412223	<b>Nicotine</b> selectively increased c <strong>fos</strong> mRNA expression in the nucleus accumbens shell and basolateral amygdala in adolescent, but not adult animals, and altered serotonin markers in these regions as well as the prefrontal cortex.
+FOS	drug	opioid	21362452	The data suggest that vagus nerve stimulation may inhibit <b>heroin</b>  or <b>heroin</b> cue induced relapse, possibly by regulation of the expression of <strong>Fos</strong> and CREB in nucleus accumbens.
+FOS	addiction	relapse	21362452	The data suggest that vagus nerve stimulation may inhibit heroin  or heroin cue induced <b>relapse</b>, possibly by regulation of the expression of <strong>Fos</strong> and CREB in nucleus accumbens.
+FOS	drug	alcohol	21338584	Prodynorphin promoter SNP associated with <b>alcohol</b> dependence forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+FOS	addiction	dependence	21338584	Prodynorphin promoter SNP associated with alcohol <b>dependence</b> forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+FOS	drug	amphetamine	21326191	This effect was not related to differences in the ability to attribute predictive value to a conditioned stimulus (as measured by conditioned approach behavior), but was potentially linked to the development of behavioral supersensitivity to <b>amphetamine</b> and to augmented <b>amphetamine</b> induced immediate early gene expression (c <strong>fos</strong> and Nur77) in dorsal striatopallidal and striatonigral cells.
+FOS	drug	alcohol	21300146	When another group of adolescent binge drinking rats was administered <b>alcohol</b> in adulthood, the number of colocalized c <strong>fos</strong> ir and PNMT ir cells/brain stem section in the C3 area was significantly decreased, compared to controls.
+FOS	addiction	intoxication	21300146	When another group of adolescent <b>binge</b> drinking rats was administered alcohol in adulthood, the number of colocalized c <strong>fos</strong> ir and PNMT ir cells/brain stem section in the C3 area was significantly decreased, compared to controls.
+FOS	drug	alcohol	21295078	Several lines of evidence have shown that cAMP response element binding protein (CREB), extracellular signal regulated kinase (ERK), and c <strong>fos</strong> have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, nicotine, and <b>alcohol</b>.
+FOS	drug	cocaine	21295078	Several lines of evidence have shown that cAMP response element binding protein (CREB), extracellular signal regulated kinase (ERK), and c <strong>fos</strong> have pivotal role in CPP induced by drugs of abuse, such as morphine, <b>cocaine</b>, nicotine, and alcohol.
+FOS	drug	nicotine	21295078	Several lines of evidence have shown that cAMP response element binding protein (CREB), extracellular signal regulated kinase (ERK), and c <strong>fos</strong> have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, <b>nicotine</b>, and alcohol.
+FOS	drug	opioid	21295078	Several lines of evidence have shown that cAMP response element binding protein (CREB), extracellular signal regulated kinase (ERK), and c <strong>fos</strong> have pivotal role in CPP induced by drugs of abuse, such as <b>morphine</b>, cocaine, nicotine, and alcohol.
+FOS	addiction	reward	21295078	Several lines of evidence have shown that cAMP response element binding protein (CREB), extracellular signal regulated kinase (ERK), and c <strong>fos</strong> have pivotal role in <b>CPP</b> induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.
+FOS	addiction	reward	21295078	Therefore, in the present study, we investigated the changes in phosphorylated CREB (p CREB) and  ERK (p ERK), and c <strong>fos</strong> induction within ventral tegmental area (VTA), hippocampus and prefrontal cortex (PFC) after the acquisition of <b>CPP</b> induced by intra LH administration of carbachol.
+FOS	drug	nicotine	21277949	The results show that acute <b>nicotine</b> injection induces <strong>Fos</strong> expression in 5 HT neurons in a region specific manner.
+FOS	drug	amphetamine	21229349	Acute injection of <b>METH</b> increased c <strong>fos</strong>, fosB, fra2, junB, Egr1 3, Nr4a1 (Nur77), and Nr4a3 (Nor 1) mRNA levels in the striatum of saline pretreated rats.
+FOS	drug	alcohol	21216264	Diverse behavioral, monoaminergic and <strong>Fos</strong> protein responses to opioids in Warsaw high <b>alcohol</b> preferring and Warsaw low <b>alcohol</b> preferring rats.
+FOS	drug	opioid	21216264	Diverse behavioral, monoaminergic and <strong>Fos</strong> protein responses to <b>opioids</b> in Warsaw high alcohol preferring and Warsaw low alcohol preferring rats.
+FOS	drug	alcohol	21216264	We compared the effects of repeated (14 daily doses) morphine (10 mg/kg) or methadone (2 mg/kg) treatment followed by a 2 week withdrawal and a morphine challenge (5 mg/kg) on locomotor activity, brain <strong>Fos</strong> expression and selected brain regional levels of dopamine, serotonin and their metabolites in the 38th generations of selectively bred Warsaw low <b>alcohol</b> preferring (WLP) and Warsaw high <b>alcohol</b> preferring (WHP) rat lines.
+FOS	drug	opioid	21216264	We compared the effects of repeated (14 daily doses) <b>morphine</b> (10 mg/kg) or <b>methadone</b> (2 mg/kg) treatment followed by a 2 week withdrawal and a <b>morphine</b> challenge (5 mg/kg) on locomotor activity, brain <strong>Fos</strong> expression and selected brain regional levels of dopamine, serotonin and their metabolites in the 38th generations of selectively bred Warsaw low alcohol preferring (WLP) and Warsaw high alcohol preferring (WHP) rat lines.
+FOS	addiction	withdrawal	21216264	We compared the effects of repeated (14 daily doses) morphine (10 mg/kg) or methadone (2 mg/kg) treatment followed by a 2 week <b>withdrawal</b> and a morphine challenge (5 mg/kg) on locomotor activity, brain <strong>Fos</strong> expression and selected brain regional levels of dopamine, serotonin and their metabolites in the 38th generations of selectively bred Warsaw low alcohol preferring (WLP) and Warsaw high alcohol preferring (WHP) rat lines.
+FOS	drug	opioid	21216264	<b>Morphine</b> did not significantly enhance, but suppressed <strong>Fos</strong> expression in certain brain regions of drug naïve WLP and WHP rats.
+FOS	drug	opioid	21216264	<strong>Fos</strong> expression revealed considerable differences in the responses of WLP and WHP rats to <b>morphine</b> challenge, particularly after <b>methadone</b> pretreatment.
+FOS	addiction	relapse	21209913	Expression of the protein product of the neuronal activity marker c <strong>fos</strong> was assessed in a number of brain regions of mice that exhibited <b>reinstatement</b> (R mice) versus those which did not (NR mice).
+FOS	addiction	relapse	21209913	<b>Reinstatement</b> generally conferred greater <strong>Fos</strong> expression in cortical and limbic structures previously implicated in drug <b>seeking</b> behaviour, though a number of regions not typically associated with drug <b>seeking</b> were also activated.
+FOS	addiction	sensitization	21184750	The interaction of AF and VCS on <strong>Fos</strong> expression in the MPOA suggests that POEF may enhance vaginal cervical sensory input at parturition to facilitate <b>sensitization</b> of the MPOA, and presumably facilitate maternal behavior onset.
+FOS	drug	nicotine	21125398	Furthermore, <b>nicotine</b> increased c <strong>Fos</strong> expression in the CeA, but not the medial or basolateral amygdaloid nucleus.
+FOS	drug	cocaine	21123561	Neuronal activation, as assessed by <strong>Fos</strong> expression, was greatly reduced in the dorsal and ventral bed nucleus of the stria terminalis (BNST), lateral septum, and nucleus accumbens shell in mice lacking CREB (CREBαΔ mice) after a 6 min swim stress but not after <b>cocaine</b> exposure (20 mg/kg).
+FOS	drug	opioid	21068718	Microinjection of recombinant TNFα into the vlPAG followed by intraperitoneal <b>naloxone</b> resulted in <b>morphine</b> withdrawal like behavioral signs, and upregulation of pERK1/2, expression of <strong>Fos</strong>, and phosphorylation of cAMP response element binding (pCREB) protein.
+FOS	addiction	withdrawal	21068718	Microinjection of recombinant TNFα into the vlPAG followed by intraperitoneal naloxone resulted in morphine <b>withdrawal</b> like behavioral signs, and upregulation of pERK1/2, expression of <strong>Fos</strong>, and phosphorylation of cAMP response element binding (pCREB) protein.
+FOS	drug	opioid	21068718	Microinjection of HSV vector expressing sTNFR into the PAG also significantly reduced the phosphorylation of both ERK1/2 and CREB, and reduced <strong>Fos</strong> immunoreactivity in neurons of the PAG following <b>naloxone</b> precipitated withdrawal.
+FOS	addiction	withdrawal	21068718	Microinjection of HSV vector expressing sTNFR into the PAG also significantly reduced the phosphorylation of both ERK1/2 and CREB, and reduced <strong>Fos</strong> immunoreactivity in neurons of the PAG following naloxone precipitated <b>withdrawal</b>.
+FOS	addiction	relapse	20973776	Immediate <b>reinstatement</b> increased <strong>Fos</strong> expression in the nucleus accumbens (NAc), infra limbic (IL), pre limbic (PrL), orbitofrontal (OFC) and piriform cortices, the lateral and dorsomedial hypothalamus, central amygdala and basolateral amygdala (BLA), and the bed nucleus of the stria terminalis.
+FOS	addiction	relapse	20973776	Following delayed <b>reinstatement</b>, <strong>Fos</strong> expression was further elevated in cortical structures.
+FOS	addiction	relapse	20973776	Concurrent with preventing <b>reinstatement</b>, SB 334867 decreased <strong>Fos</strong> in NAc core, PrL and OFC following immediate <b>reinstatement</b>.
+FOS	addiction	relapse	20973776	Following protracted abstinence, SB 334867 treatment decreased <b>reinstatement</b> induced <strong>Fos</strong> in the PrL, OFC and piriform cortices.
+FOS	addiction	relapse	20973776	The effects of SB 334867 on both behaviour and <strong>Fos</strong> expression suggest that the orexin system is implicated in cue induced <b>reinstatement</b>, although some loci may shift following protracted abstinence.
+FOS	drug	amphetamine	20950675	Effect of bee venom acupuncture on <b>methamphetamine</b> induced hyperactivity, hyperthermia and <strong>Fos</strong> expression in mice.
+FOS	drug	amphetamine	20950675	<b>METH</b> injection significantly increased <strong>Fos</strong> expression in several brain regions including nucleus accumbens (NA), caudate putamen (CPU), ventral tegmental area (VTA), substantia nigra (SN) and locus coeruleus (LC).
+FOS	drug	amphetamine	20950675	Interestingly, BV (1mg/ml) injection into ST36 further increased <b>METH</b> induced <strong>Fos</strong> expression in NA (core and shell), SN and LC.
+FOS	drug	amphetamine	20950675	When we performed sciatic denervation or combination treatment of BV and lidocaine (BV diluted in 5% lidocaine solution), the enhancement of <strong>Fos</strong> elevation by BV was completely blocked in the NA, SN and LC in <b>METH</b> injected mice, indicating that BV induced peripheral nerve stimulation played an important role in the BV effect.
+FOS	drug	amphetamine	20950675	Taken together, these findings suggest that BV acupuncture into ST36 may modulate <b>METH</b> induced hyperactivity, hyperthermia and <strong>Fos</strong> expression through activation of the peripheral nerve and the central α₂ adrenergic activation.
+FOS	addiction	aversion	20937363	The role of the central nucleus of the IC (CIC) on fear and anxiety has been suggested on the basis that rats are able to engage in tasks to decrease the aversiveness of CIC stimulation, increased <strong>Fos</strong> immunolabeling during diverse <b>aversive</b> states and increased CIC auditory evoked potentials (AEP) induced by conditioned fear stimuli.
+FOS	drug	cocaine	20933585	Environmental living conditions introduced during forced abstinence alter <b>cocaine</b> seeking behavior and <strong>Fos</strong> protein expression.
+FOS	addiction	relapse	20933585	Environmental living conditions introduced during forced abstinence alter cocaine <b>seeking</b> behavior and <strong>Fos</strong> protein expression.
+FOS	drug	cocaine	20933585	Subsequently, <b>cocaine</b> seeking behavior (lever presses without <b>cocaine</b> reinforcement) elicited by response contingent cue presentations was assessed for 90 min, after which the rats' brains were immediately harvested for <strong>Fos</strong> protein immunohistochemistry.
+FOS	addiction	relapse	20933585	Subsequently, cocaine <b>seeking</b> behavior (lever presses without cocaine reinforcement) elicited by response contingent cue presentations was assessed for 90 min, after which the rats' brains were immediately harvested for <strong>Fos</strong> protein immunohistochemistry.
+FOS	addiction	reward	20933585	Subsequently, cocaine seeking behavior (lever presses without cocaine <b>reinforcement</b>) elicited by response contingent cue presentations was assessed for 90 min, after which the rats' brains were immediately harvested for <strong>Fos</strong> protein immunohistochemistry.
+FOS	drug	cocaine	20933023	Central injections of noradrenaline induce reinstatement of <b>cocaine</b> seeking and increase c <strong>fos</strong> mRNA expression in the extended amygdala.
+FOS	addiction	relapse	20933023	Central injections of noradrenaline induce <b>reinstatement</b> of cocaine <b>seeking</b> and increase c <strong>fos</strong> mRNA expression in the extended amygdala.
+FOS	addiction	aversion	20832433	After initial exposure to an elevated plus maze (EPM), brainstem neural activation, elicited by exposure to EPM <b>aversive</b> cues, was analyzed using a <strong>Fos</strong> protein immunolabeling technique.
+FOS	drug	alcohol	20807311	Next, we examined c <strong>Fos</strong> expression (marker of neuronal activation) in BF wake promoting neurons during <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	20807311	Next, we examined c <strong>Fos</strong> expression (marker of neuronal activation) in BF wake promoting neurons during ethanol <b>withdrawal</b>.
+FOS	drug	amphetamine	20731630	Strikingly, oxytocin significantly reduced <b>methamphetamine</b> induced <strong>Fos</strong> expression in two regions of the basal ganglia: the subthalamic nucleus and the nucleus accumbens core.
+FOS	addiction	reward	20716371	Administration of the GABAA receptor antagonist picrotoxin into rat supramammillary nucleus induces c <strong>Fos</strong> in <b>reward</b> related brain structures.
+FOS	drug	cocaine	20704593	Our results show that SSRIs potentiate methylphenidate induced expression of the transcription factor genes zif268 and c <strong>fos</strong> in the striatum, rendering these molecular changes more <b>cocaine</b> like.
+FOS	drug	amphetamine	20680358	Repeated administration of <b>methamphetamine</b> blocked cholecystokinin octapeptide injection induced c <strong>fos</strong> mRNA expression without change in capsaicin induced junD mRNA expression in rat cerebellum.
+FOS	drug	amphetamine	20680358	First, injections of CCK 8 were found to induce c <strong>fos</strong> mRNA expression in a vague patchy pattern that is different from single <b>methamphetamine</b> induced Zebrin band like c <strong>fos</strong> mRNA expression, suggesting that the CCK 8 activating mossy fibers induce gene expression differently from the dopamine containing mossy fibers in the ventral tegmental area.
+FOS	drug	amphetamine	20680358	Repeated administration of <b>methamphetamine</b> suppressed the CCK 8 induced c <strong>fos</strong> mRNA expression in the rat cerebellum.
+FOS	drug	amphetamine	20680358	Third, capsaicin injections (physical stress) into a hind limb of the rat increased junD mRNA expression with no effect on c <strong>fos</strong> mRNA expression, and repeated <b>methamphetamine</b> injections had no effect on the capsaicin induced expression of junD mRNA.
+FOS	drug	amphetamine	20680358	Fourth, either single injection of <b>methamphetamine</b> or CCK 8 to mice increased c <strong>fos</strong> mRNA expression in the locus coeruleus, and so noradrenalin, but not dopamine, might interact with CCK 8 activating system.
+FOS	drug	amphetamine	20680358	Thus, we conclude that repeated <b>methamphetamine</b> administration though dopamine selectively inhibits the c <strong>fos</strong> mRNA expression after CCK 8 injection in the cerebellum.
+FOS	drug	cocaine	20633205	Striatal regulation of ΔFosB, FosB, and <strong>cFos</strong> during <b>cocaine</b> self administration and withdrawal.
+FOS	addiction	withdrawal	20633205	Striatal regulation of ΔFosB, FosB, and <strong>cFos</strong> during cocaine self administration and <b>withdrawal</b>.
+FOS	drug	cocaine	20633205	The present study examined regulation of the <strong>Fos</strong> family of transcription factors, specifically cFos, FosB, and ΔFosB, in striatal subregions during and after chronic intravenous <b>cocaine</b> administration in self administering and yoked rats.
+FOS	drug	cocaine	20633205	The present study examined regulation of the <strong>Fos</strong> family of transcription factors, specifically <strong>cFos</strong>, FosB, and ΔFosB, in striatal subregions during and after chronic intravenous <b>cocaine</b> administration in self administering and yoked rats.
+FOS	drug	cocaine	20633205	We found that <strong>cFos</strong>, FosB, and ΔFosB exhibit regionally and temporally distinct expression patterns, with greater accumulation of ΔFosB protein in the nucleus accumbens (NAc) shell and core after chronic <b>cocaine</b> administration, whereas ΔFosB increases in the caudate putamen (CPu) remained similar with either acute or chronic administration.
+FOS	drug	cocaine	20633205	Interestingly, tolerance to <b>cocaine</b> induced <strong>cFos</strong> induction was dependent on volitional control of <b>cocaine</b> intake in ventral but not dorsal striatal regions, whereas regulation of FosB and ΔFosB was similar in <b>cocaine</b> self administering and yoked animals.
+FOS	drug	alcohol	20608999	Using congenic mice that confirm this QTL and c <strong>Fos</strong> expression as a high resolution marker of neuronal activation, we report that congenic mice show significantly less neuronal activity associated with <b>alcohol</b> withdrawal in the rostroventral caudate putamen (rvCP), but not other parts of the striatum, compared with background strain mice.
+FOS	addiction	withdrawal	20608999	Using congenic mice that confirm this QTL and c <strong>Fos</strong> expression as a high resolution marker of neuronal activation, we report that congenic mice show significantly less neuronal activity associated with alcohol <b>withdrawal</b> in the rostroventral caudate putamen (rvCP), but not other parts of the striatum, compared with background strain mice.
+FOS	drug	alcohol	20608999	Using retrograde (fluorogold) and anterograde (Texas Red conjugated dextran amine) tract tracing, we found that ∼25% of c <strong>Fos</strong> immunoreactive rvCP neurons project to caudolateral substantia nigra pars reticulata (clSNr), which we previously found is crucially involved in withdrawal following acute and repeated <b>alcohol</b> exposure.
+FOS	addiction	withdrawal	20608999	Using retrograde (fluorogold) and anterograde (Texas Red conjugated dextran amine) tract tracing, we found that ∼25% of c <strong>Fos</strong> immunoreactive rvCP neurons project to caudolateral substantia nigra pars reticulata (clSNr), which we previously found is crucially involved in <b>withdrawal</b> following acute and repeated alcohol exposure.
+FOS	drug	cocaine	20554270	Within the nucleus accumbens, impaired cellular responses to <b>cocaine</b> are conspicuous; a pronounced deficit in <b>cocaine</b> elicited extracellular dopamine release, expression of the key IEGs c <strong>Fos</strong> and Zif268, and phosphorylation of extracellular signal regulated kinases 1/2 in mutants were observed.
+FOS	drug	opioid	20459597	The first module consisted of activity dependent transcripts (including <strong>Fos</strong> and Npas4), which are induced by psychostimulants and <b>opioids</b>.
+FOS	drug	alcohol	20400272	Increased voluntary <b>ethanol</b> consumption and c <strong>Fos</strong> expression in selected brain areas induced by fear memory retrieval in <b>ethanol</b> withdrawn rats.
+FOS	drug	alcohol	20400272	In <b>ethanol</b> withdrawn rats, context dependent memory retrieval was accompanied by an increased c <strong>Fos</strong> expression in the basolateral amygdala, ventrolateral periaqueductal gray, dentate gyrus and dorsomedial periaqueductal gray.
+FOS	addiction	withdrawal	20367754	Moreover, the <b>withdrawal</b> associated cellular hyperactivity and c <strong>fos</strong> expression was blunted.
+FOS	drug	amphetamine	20357113	We then used immunohistochemical detection of c <strong>Fos</strong> as a marker of neuronal activity, combined with immunohistochemical detection of the orexin and cocaine  and <b>amphetamine</b> related transcript (CART) peptides, to study the profile and phenotype of neural activation during reinstatement produced by AcbSh inactivation.
+FOS	drug	cocaine	20357113	We then used immunohistochemical detection of c <strong>Fos</strong> as a marker of neuronal activity, combined with immunohistochemical detection of the orexin and <b>cocaine</b>  and amphetamine related transcript (CART) peptides, to study the profile and phenotype of neural activation during reinstatement produced by AcbSh inactivation.
+FOS	addiction	relapse	20357113	We then used immunohistochemical detection of c <strong>Fos</strong> as a marker of neuronal activity, combined with immunohistochemical detection of the orexin and cocaine  and amphetamine related transcript (CART) peptides, to study the profile and phenotype of neural activation during <b>reinstatement</b> produced by AcbSh inactivation.
+FOS	drug	cocaine	20338186	For example, <strong>Fos</strong> expression in LH orexin neurons varied in proportion to conditioned place preference (CPP) for food, morphine, or <b>cocaine</b>.
+FOS	drug	opioid	20338186	For example, <strong>Fos</strong> expression in LH orexin neurons varied in proportion to conditioned place preference (CPP) for food, <b>morphine</b>, or cocaine.
+FOS	addiction	reward	20338186	For example, <strong>Fos</strong> expression in LH orexin neurons varied in proportion to conditioned place preference (<b>CPP</b>) for food, morphine, or cocaine.
+FOS	drug	cocaine	20338186	This <strong>Fos</strong> expression was altered accordingly for CPP administered during protracted abstinence from morphine or <b>cocaine</b>, when preference for natural rewards was decreased and drug preference was increased.
+FOS	drug	opioid	20338186	This <strong>Fos</strong> expression was altered accordingly for CPP administered during protracted abstinence from <b>morphine</b> or cocaine, when preference for natural rewards was decreased and drug preference was increased.
+FOS	addiction	reward	20338186	This <strong>Fos</strong> expression was altered accordingly for <b>CPP</b> administered during protracted abstinence from morphine or cocaine, when preference for natural rewards was decreased and drug preference was increased.
+FOS	drug	opioid	20336629	Modulation of basal and <b>morphine</b> induced neuronal activity by a NPFF(2) selective agonist measured by c <strong>Fos</strong> mapping of the mouse brain.
+FOS	drug	opioid	20336629	The expression of the immediate early gene c <strong>Fos</strong> was analyzed to map the distribution of neurons whose activity is regulated by central administration of the NPFF(2) selective agonist dNPA in naive mice and in animals who had received a systemic injection of <b>morphine</b>.
+FOS	drug	opioid	20336629	In contrast, intraperitoneal injection of <b>morphine</b> 5 mg.kg( 1) induced a statistically significant increase in c <strong>Fos</strong> expression in the prelimbic cortex, the nucleus accumbens core and shell, the ventral pallidum, the lateral hypothalamus, and the nucleus of the tractus solitarius.
+FOS	drug	opioid	20159948	The effects of <b>naloxone</b> precipitated <b>morphine</b> withdrawal on noradrenaline (NA) turnover in the paraventricular nucleus (PVN), HPA axis activity, signs of withdrawal, and c <strong>Fos</strong> expression were measured in rats pretreated with vehicle, CP 154526 [N butyl N ethyl 2,5 dimethyl 7 (2,4,6 trimethylphenyl)pyrrolo[3,2 e]pyrimidin 4 amine], or antalarmin (selective CRF1R antagonists).
+FOS	addiction	withdrawal	20159948	The effects of naloxone precipitated morphine <b>withdrawal</b> on noradrenaline (NA) turnover in the paraventricular nucleus (PVN), HPA axis activity, signs of <b>withdrawal</b>, and c <strong>Fos</strong> expression were measured in rats pretreated with vehicle, CP 154526 [N butyl N ethyl 2,5 dimethyl 7 (2,4,6 trimethylphenyl)pyrrolo[3,2 e]pyrimidin 4 amine], or antalarmin (selective CRF1R antagonists).
+FOS	drug	opioid	20159948	Pretreatment with CRF1R antagonists resulted in no significant modification of the increased NA turnover at PVN, plasma corticosterone levels, or c <strong>Fos</strong> expression that was seen during <b>naloxone</b> induced <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	20159948	Pretreatment with CRF1R antagonists resulted in no significant modification of the increased NA turnover at PVN, plasma corticosterone levels, or c <strong>Fos</strong> expression that was seen during naloxone induced morphine <b>withdrawal</b>.
+FOS	drug	nicotine	20147556	Acute <b>nicotine</b> (0.8 mg/kg, s.c.) induced anxiogenic like effects in the elevated plus maze and activated the paraventricular nucleus of the hypothalamus (PVN) as revealed by c <strong>Fos</strong> expression.
+FOS	drug	nicotine	20147556	In addition, an increase of the percentage of c <strong>Fos</strong> positive hypocretin cells in the perifornical and dorsomedial hypothalamic (PFA/DMH) areas was found after <b>nicotine</b> (0.8 mg/kg, s.c.) administration.
+FOS	drug	opioid	20034457	<b>Morphine</b> induced locomotor response and <strong>Fos</strong> expression in rats are inhibited by acupuncture.
+FOS	drug	opioid	20034457	The acupuncture treatment was performed for 1 minute once a day for 3 days of withdrawal period and its effect on <b>morphine</b> induced changes of locomotor activity and <strong>Fos</strong> expression was examined.
+FOS	addiction	withdrawal	20034457	The acupuncture treatment was performed for 1 minute once a day for 3 days of <b>withdrawal</b> period and its effect on morphine induced changes of locomotor activity and <strong>Fos</strong> expression was examined.
+FOS	drug	opioid	20034457	The acupuncture stimulation to HT7 significantly suppressed the <b>morphine</b> induced increases in the locomotor activity and <strong>Fos</strong> expression in the nucleus accumbens and striatum, as compared to the controls of non acupoint or the acupoint on other meridian.
+FOS	drug	alcohol	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after ethanol <b>withdrawal</b>.
+FOS	drug	nicotine	20028457	<b>Nicotine</b> self administration also decreased footshock induced c <strong>Fos</strong> expression in the nucleus of the solitary tract A2/C2 catecholaminergic neurons that project to the PVN.
+FOS	drug	opioid	20026253	Immunohistochemical double labeling technique with <strong>Fos</strong> was used to examine if an intraplantar formalin injection, an acute noxious input, changed the effect of <b>morphine</b> on dopaminergic neurons of the ventral tegmental area (VTA), and serotonergic neurons of the dorsal raphe nucleus (DR).
+FOS	drug	opioid	20026253	Following <b>morphine</b> injection, there was an increase in the number of dopaminergic neurons in the VTA with <strong>Fos</strong> immunolabeling.
+FOS	drug	opioid	20026253	However, noxious stimulation did not detectably change <b>morphine</b>'s effect on <strong>Fos</strong> expression in VTA dopamine neurons.
+FOS	drug	opioid	20026253	In contrast, the number of serotonergic neurons containing <strong>Fos</strong> was increased in the <b>morphine</b>/formalin group compared to all other groups and this effect was topographically selective for the dorsal area of the DR at mid rostro caudal levels.
+FOS	addiction	aversion	20026143	A similar pattern of neuronal <strong>Fos</strong> activation in 10 brain regions following exposure to reward  or <b>aversion</b> associated contextual cues in mice.
+FOS	addiction	reward	20026143	A similar pattern of neuronal <strong>Fos</strong> activation in 10 brain regions following exposure to <b>reward</b>  or aversion associated contextual cues in mice.
+FOS	addiction	aversion	20026143	After measuring each animal for conditioned place preference or <b>aversion</b>, mice were re exposed to the context (CS+ or CS ) in absence of the reinforcer to analyze patterns of <strong>Fos</strong> expression in 10 brain regions chosen from previous literature.
+FOS	drug	cocaine	20026143	Levels of <strong>Fos</strong> in the cingulate cortex, paraventricular thalamic nucleus, paraventricular hypothalamic nucleus, and dentate gyrus differed in CS+ versus CS  groups, but the direction of the differences was the same for both lithium chloride (LiCl) and <b>cocaine</b> reinforcers.
+FOS	drug	cocaine	20026143	In the cingulate cortex, <strong>Fos</strong> was positively correlated with degree of place preference for <b>cocaine</b> or aversion to LiCl whereas in the periaqueductal gray the relationship was positive for LiCl and negative for <b>cocaine</b>.
+FOS	addiction	aversion	20026143	In the cingulate cortex, <strong>Fos</strong> was positively correlated with degree of place preference for cocaine or <b>aversion</b> to LiCl whereas in the periaqueductal gray the relationship was positive for LiCl and negative for cocaine.
+FOS	addiction	aversion	20026143	Results confirm <strong>Fos</strong> responses to reward  or <b>aversion</b> paired cues are similar but specificity is detectable.
+FOS	addiction	reward	20026143	Results confirm <strong>Fos</strong> responses to <b>reward</b>  or aversion paired cues are similar but specificity is detectable.
+FOS	addiction	reward	19940038	ICI 118,551 also attenuated the <strong>FOS</strong> response in the BLA induced by the <b>CPP</b> test.
+FOS	drug	opioid	19917879	We hypothesized that activation of extracellular signal regulated kinases 1 and 2 (ERK1/2) and the expression of c <strong>Fos</strong>, prodynorphin (mRNA), and dynorphin in the spinal cord could participate in the molecular mechanisms underlying postoperative <b>opioid</b> induced sensitization.
+FOS	addiction	sensitization	19917879	We hypothesized that activation of extracellular signal regulated kinases 1 and 2 (ERK1/2) and the expression of c <strong>Fos</strong>, prodynorphin (mRNA), and dynorphin in the spinal cord could participate in the molecular mechanisms underlying postoperative opioid induced <b>sensitization</b>.
+FOS	drug	opioid	19915516	Effect of complete maternal and littermate deprivation on <b>morphine</b> induced <strong>Fos</strong> immunoreactivity in the adult male rat brain.
+FOS	drug	opioid	19915516	Specifically, relative to MR rats, AR rats showed significantly greater <b>morphine</b> induced <strong>Fos</strong> immunoreactivity in brain regions associated with the mesocorticolimbic "reward" pathway.
+FOS	addiction	reward	19915516	Specifically, relative to MR rats, AR rats showed significantly greater morphine induced <strong>Fos</strong> immunoreactivity in brain regions associated with the mesocorticolimbic "<b>reward</b>" pathway.
+FOS	drug	cocaine	19880093	We examined separate and combined effects of neonatal ventral hippocampal lesions (NVHLs) a neurodevelopmental model of schizophrenia (vs. SHAM operated control animals)  and a behaviorally sensitizing <b>cocaine</b> history (15 mg/kg/day x 5 days vs. saline injections) on acute <b>cocaine</b> induced neural activation signaled by c <strong>Fos</strong> expression.
+FOS	drug	cocaine	19815001	<strong>Fos</strong> expression in LH orexin neurons varied in proportion to conditioned place preference (CPP) for morphine, <b>cocaine</b>, or food.
+FOS	drug	opioid	19815001	<strong>Fos</strong> expression in LH orexin neurons varied in proportion to conditioned place preference (CPP) for <b>morphine</b>, cocaine, or food.
+FOS	addiction	reward	19815001	<strong>Fos</strong> expression in LH orexin neurons varied in proportion to conditioned place preference (<b>CPP</b>) for morphine, cocaine, or food.
+FOS	drug	cocaine	19815001	Inputs to the LH orexin cell field from lateral septum and bed nucleus of the stria terminalis were <strong>Fos</strong> activated during <b>cocaine</b> CPP in proportion to the preference expressed in each animal.
+FOS	addiction	reward	19815001	Inputs to the LH orexin cell field from lateral septum and bed nucleus of the stria terminalis were <strong>Fos</strong> activated during cocaine <b>CPP</b> in proportion to the preference expressed in each animal.
+FOS	drug	opioid	19815001	Related studies showed that LH orexin neurons that project to ventral tegmental area (VTA) had greater <strong>Fos</strong> induction in association with elevated <b>morphine</b> preference during protracted withdrawal than non VTA projecting orexin neurons, indicating that the VTA is an important site of action for orexin's role in reward processing.
+FOS	addiction	reward	19815001	Related studies showed that LH orexin neurons that project to ventral tegmental area (VTA) had greater <strong>Fos</strong> induction in association with elevated morphine preference during protracted withdrawal than non VTA projecting orexin neurons, indicating that the VTA is an important site of action for orexin's role in <b>reward</b> processing.
+FOS	addiction	withdrawal	19815001	Related studies showed that LH orexin neurons that project to ventral tegmental area (VTA) had greater <strong>Fos</strong> induction in association with elevated morphine preference during protracted <b>withdrawal</b> than non VTA projecting orexin neurons, indicating that the VTA is an important site of action for orexin's role in reward processing.
+FOS	drug	alcohol	19801271	The brains were processed to assess neural activation associated with <b>ethanol</b> withdrawal indexed by c <strong>Fos</strong> immunostaining.
+FOS	addiction	withdrawal	19801271	The brains were processed to assess neural activation associated with ethanol <b>withdrawal</b> indexed by c <strong>Fos</strong> immunostaining.
+FOS	drug	alcohol	19801271	To our knowledge, these are the first studies to use c <strong>Fos</strong> to identify the brain regions and neurocircuitry that distinguish between chronic and acute <b>ethanol</b> withdrawal severity using informative animal models.
+FOS	addiction	withdrawal	19801271	To our knowledge, these are the first studies to use c <strong>Fos</strong> to identify the brain regions and neurocircuitry that distinguish between chronic and acute ethanol <b>withdrawal</b> severity using informative animal models.
+FOS	drug	cocaine	19794406	<strong>Fos</strong> after single and repeated self administration of <b>cocaine</b> and saline in the rat: emphasis on the Basal forebrain and recalibration of expression.
+FOS	drug	cocaine	19794406	We evaluated a large sample of brain structures, particularly ones comprising basal forebrain macrosystems, and determined in which the immediate early gene product, <strong>Fos</strong>, is expressed following a single and repeated self administrations of <b>cocaine</b>.
+FOS	drug	cocaine	19794406	The caudate putamen and accumbens, comprising the basal ganglia input structures, and the hypothalamic supraoptic and paraventricular nuclei, lateral and medial habenula, mesopontine rostromedial tegmental nucleus and anterior cingulate cortex exhibited <strong>Fos</strong> expression enhanced by acute self administration of <b>cocaine</b> (SAC), but desensitized after repeated administrations.
+FOS	drug	cocaine	19794406	<strong>Fos</strong> expression was mainly enhanced by acutely self administered <b>cocaine</b> in basal ganglia output and intrinsic structures and the intermediate nucleus of lateral septum, medial division of the central amygdaloid nucleus and zona incerta, but, in contrast, was sensitized in these structures after repeated administrations.
+FOS	drug	cocaine	19794406	Acute and repeated SAC left <strong>Fos</strong> expression unaffected or marginally enhanced in most extended amygdala structures, of which nearly all, however, exhibited robustly increased <strong>Fos</strong> expression after repeated saline self administration, occasionally to levels exceeding those elicited by <b>cocaine</b>.
+FOS	drug	cocaine	19794406	Thus, self administered <b>cocaine</b> mainly elicits <strong>Fos</strong> expression, which persists or increases with repeated administrations in some structures, but declines in others.
+FOS	drug	cocaine	19794406	Similar spatiotemporal patterns of <b>cocaine</b>  or saline elicited <strong>Fos</strong> expression characterize functionally related clusters of structures, such as, eg, basal ganglia input structures, basal ganglia output structures, extended amygdala and structures in the brainstem to which forebrain macrosystems project.
+FOS	drug	cannabinoid	19786358	We investigated the effects of bilateral intra BLA administration of the CB1 receptor antagonist/inverse agonist, <b>rimonabant</b>, on formalin evoked nociceptive behaviour, fear conditioned behaviour including analgesia, and associated brain regional alterations in <strong>Fos</strong> expression in rats.
+FOS	drug	cannabinoid	19786358	Formalin evoked nociceptive behaviour was associated with increased <strong>Fos</strong> immunoreactivity (FI) in the CA2/3 region of the hippocampus and rostral ventromedial medulla, effects attenuated by intra BLA <b>rimonabant</b>.
+FOS	drug	amphetamine	19783867	To examine whether deficiency in histamine H(3) receptors influences psychostimulant induced behavioral sensitization and reward, we examined locomotor activity, conditioned place preference (CPP), and c <strong>Fos</strong> expression in histamine H(3) receptor gene knockout mice (H3KO) and their wild type (WT) counterparts before and after treatment with <b>methamphetamine</b> (<b>METH</b>) and 3,4 methylenedioxymethamphetamine (MDMA).
+FOS	drug	psychedelics	19783867	To examine whether deficiency in histamine H(3) receptors influences psychostimulant induced behavioral sensitization and reward, we examined locomotor activity, conditioned place preference (CPP), and c <strong>Fos</strong> expression in histamine H(3) receptor gene knockout mice (H3KO) and their wild type (WT) counterparts before and after treatment with methamphetamine (METH) and 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>).
+FOS	addiction	reward	19783867	To examine whether deficiency in histamine H(3) receptors influences psychostimulant induced behavioral sensitization and <b>reward</b>, we examined locomotor activity, conditioned place preference (<b>CPP</b>), and c <strong>Fos</strong> expression in histamine H(3) receptor gene knockout mice (H3KO) and their wild type (WT) counterparts before and after treatment with methamphetamine (METH) and 3,4 methylenedioxymethamphetamine (MDMA).
+FOS	addiction	sensitization	19783867	To examine whether deficiency in histamine H(3) receptors influences psychostimulant induced behavioral <b>sensitization</b> and reward, we examined locomotor activity, conditioned place preference (CPP), and c <strong>Fos</strong> expression in histamine H(3) receptor gene knockout mice (H3KO) and their wild type (WT) counterparts before and after treatment with methamphetamine (METH) and 3,4 methylenedioxymethamphetamine (MDMA).
+FOS	drug	amphetamine	19783867	Following treatment with <b>METH</b>, the number of c <strong>Fos</strong> positive neurons in the the caudate putamen of histamine H3KO mice was lower than that in the caudate putamen of WT mice.
+FOS	drug	nicotine	19711055	<b>Nicotine</b> conditioned place preference induced CREB phosphorylation and <strong>Fos</strong> expression in the adult rat brain.
+FOS	addiction	aversion	19711055	To identify brain regions activated in CPP, we have measured the levels of phosphorylated cyclic AMP response element binding protein (pCREB) and <strong>Fos</strong> protein using a behavioral CPP and conditioned place <b>aversion</b> (CPA) paradigms.
+FOS	addiction	reward	19711055	To identify brain regions activated in <b>CPP</b>, we have measured the levels of phosphorylated cyclic AMP response element binding protein (pCREB) and <strong>Fos</strong> protein using a behavioral <b>CPP</b> and conditioned place aversion (CPA) paradigms.
+FOS	drug	nicotine	19711055	During <b>nicotine</b> preference and reinstatement behaviors, a significant increase of both pCREB and <strong>Fos</strong> protein expression occurs in the nucleus accumbens (NAc) and ventral tegmental area (VTA) and also in the prefrontal cortex (PFC), dorsal striatum (DStr), amygdala, and hippocampus.
+FOS	addiction	relapse	19711055	During nicotine preference and <b>reinstatement</b> behaviors, a significant increase of both pCREB and <strong>Fos</strong> protein expression occurs in the nucleus accumbens (NAc) and ventral tegmental area (VTA) and also in the prefrontal cortex (PFC), dorsal striatum (DStr), amygdala, and hippocampus.
+FOS	drug	nicotine	19711055	The results indicate that the phosphorylation of CREB and expression of <strong>Fos</strong> protein, as indicators of neural activity, accompany the acquisition and maintenance of <b>nicotine</b> induced CPP but not CPA in mesolimbic areas (NAc, VTA, PFC, and DStr) as well as in memory consolidation structures (hippocampus and amygdala) and nicotinic receptor are involved in this process.
+FOS	addiction	reward	19711055	The results indicate that the phosphorylation of CREB and expression of <strong>Fos</strong> protein, as indicators of neural activity, accompany the acquisition and maintenance of nicotine induced <b>CPP</b> but not CPA in mesolimbic areas (NAc, VTA, PFC, and DStr) as well as in memory consolidation structures (hippocampus and amygdala) and nicotinic receptor are involved in this process.
+FOS	drug	opioid	19708041	Regional <strong>Fos</strong> expression induced by <b>morphine</b> withdrawal in the 7 day old rat.
+FOS	addiction	withdrawal	19708041	Regional <strong>Fos</strong> expression induced by morphine <b>withdrawal</b> in the 7 day old rat.
+FOS	drug	opioid	19705550	Induction of <strong>Fos</strong> proteins in regions of the nucleus accumbens and ventrolateral striatum correlates with catalepsy and stereotypic behaviours induced by <b>morphine</b>.
+FOS	drug	opioid	19705550	We examined the effect of intermittent <b>morphine</b> exposure on the distribution of <strong>Fos</strong> proteins in the basal ganglia following a subsequent <b>morphine</b> challenge administered after a period of drug abstinence.
+FOS	drug	opioid	19705550	We found that such exposures increased c <strong>Fos</strong> induced by a <b>morphine</b> challenge in accumbens core regions that were immunoreactive for the micro <b>opioid</b> receptor, and this correlated with the frequency of stereotypic behaviours displayed by the rats.
+FOS	drug	opioid	19705550	We also found that a history of <b>morphine</b> exposures increased c <strong>Fos</strong> in the ventrolateral striatum in response to a <b>morphine</b> challenge following 14 d but not 24 h of drug abstinence.
+FOS	drug	opioid	19693978	[<b>Tramadol</b> inhibits c <strong>fos</strong> expression in spinal cord dorsal horn and serum IL 6 levels induced by plantar incision in rats].
+FOS	drug	opioid	19693978	To investigate effect of <b>tramadol</b> on c <strong>fos</strong> expression in spinal cord dorsal horn and serum IL 6 levels induced by plantar incision in rats.
+FOS	drug	opioid	19693978	The greatest density of <strong>Fos</strong> positive neurons was located in lamine I II in Group I. Serum IL 6 levels were significantly elevated in Group I. Pretreatment with <b>tramadol</b> showed a dose depended inhibitory effect on c <strong>fos</strong> expression and serum IL 6 production,but not in Group T1.
+FOS	drug	opioid	19693978	Administration of <b>tramadol</b> postoperatively also suppressed the c <strong>fos</strong> expression and serum IL 6 production as showed in PT10 but were weaker than those in Group T10.
+FOS	drug	opioid	19693978	Pretreatment with <b>tramadol</b> can produce dose dependent inhibitory effect on c <strong>fos</strong> expression in spinal cord dorsal horn and then suppress the inflammatory response to the trauma.
+FOS	drug	amphetamine	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and <strong>Fos</strong> (cFos), represent candidates whose expression levels may predict <b>methamphetamine</b> consumption and susceptibility to <b>methamphetamine</b> reward and aversion.
+FOS	addiction	aversion	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and <strong>Fos</strong> (cFos), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine reward and <b>aversion</b>.
+FOS	addiction	reward	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and <strong>Fos</strong> (cFos), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine <b>reward</b> and aversion.
+FOS	drug	amphetamine	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and <strong>Fos</strong> (<strong>cFos</strong>), represent candidates whose expression levels may predict <b>methamphetamine</b> consumption and susceptibility to <b>methamphetamine</b> reward and aversion.
+FOS	addiction	aversion	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and <strong>Fos</strong> (<strong>cFos</strong>), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine reward and <b>aversion</b>.
+FOS	addiction	reward	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and <strong>Fos</strong> (<strong>cFos</strong>), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine <b>reward</b> and aversion.
+FOS	drug	opioid	19683523	Moreover, c <strong>Fos</strong> expression was induced in the PVN after <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	19683523	Moreover, c <strong>Fos</strong> expression was induced in the PVN after naloxone precipitated morphine <b>withdrawal</b>.
+FOS	drug	opioid	19679639	However, <b>morphine</b> tolerance and dependence are believed to be mediated by multiple mechanisms, including well documented biochemical changes in cAMP activity, N methyl D aspartate receptors (NMDARs), glucocorticoid receptors (GRs), and c <strong>fos</strong>.
+FOS	addiction	dependence	19679639	However, morphine tolerance and <b>dependence</b> are believed to be mediated by multiple mechanisms, including well documented biochemical changes in cAMP activity, N methyl D aspartate receptors (NMDARs), glucocorticoid receptors (GRs), and c <strong>fos</strong>.
+FOS	drug	opioid	19679639	Chronic <b>morphine</b> treatment of wild type (WT) mice promoted superactivation of adenylyl cyclase, alterations in NMDARs, and up regulation of GR and c <strong>fos</strong> in distinct brain regions.
+FOS	addiction	reward	19606084	Here, we examined in mice the effects of 3 alpha [bis(4' fluorophenyl)metoxy] tropane (AHN 1055) on motor activity, conditioned place preference (<b>CPP</b>) and c <strong>Fos</strong> expression in the striatum.
+FOS	drug	cocaine	19606084	These observations provide evidence that AHN 1055 does not behave as a classical psychomotor stimulant and that some of its properties, including attenuation of <b>cocaine</b> induced striatal c <strong>Fos</strong> expression, locomotor stimulation, and CPP, support its candidacy, and that of structurally related molecules, as possible pharmacotherapies in <b>cocaine</b> addiction.
+FOS	addiction	addiction	19606084	These observations provide evidence that AHN 1055 does not behave as a classical psychomotor stimulant and that some of its properties, including attenuation of cocaine induced striatal c <strong>Fos</strong> expression, locomotor stimulation, and CPP, support its candidacy, and that of structurally related molecules, as possible pharmacotherapies in cocaine <b>addiction</b>.
+FOS	addiction	reward	19606084	These observations provide evidence that AHN 1055 does not behave as a classical psychomotor stimulant and that some of its properties, including attenuation of cocaine induced striatal c <strong>Fos</strong> expression, locomotor stimulation, and <b>CPP</b>, support its candidacy, and that of structurally related molecules, as possible pharmacotherapies in cocaine addiction.
+FOS	drug	opioid	19605941	The utility of <b>methadone</b> and <b>morphine</b> for analgesia and of <b>methadone</b> for substitution therapy for <b>heroin</b> addiction is a consequence of these drugs acting as <b>opioid</b> receptor agonists.We compared the cataleptogenic and antinociceptive effects of single subcutaneous doses of <b>methadone</b> hydrochloride (1 4 mg/kg) and <b>morphine</b> sulfate (2.5 10 mg/kg) using catalepsy and hot plate tests, and examined the effects of the highest doses of the drugs on <strong>Fos</strong> protein expression in selected brain regions in male Sprague Dawley rats.
+FOS	addiction	addiction	19605941	The utility of methadone and morphine for analgesia and of methadone for substitution therapy for heroin <b>addiction</b> is a consequence of these drugs acting as opioid receptor agonists.We compared the cataleptogenic and antinociceptive effects of single subcutaneous doses of methadone hydrochloride (1 4 mg/kg) and morphine sulfate (2.5 10 mg/kg) using catalepsy and hot plate tests, and examined the effects of the highest doses of the drugs on <strong>Fos</strong> protein expression in selected brain regions in male Sprague Dawley rats.
+FOS	drug	opioid	19605941	There were three response patterns identified: 1) drug exposure, but not stress, significantly elevated <strong>Fos</strong> positive cell counts in the caudate putamen; 2) stress alone and stress combined with drug exposure similarly elevated <strong>Fos</strong> positive cell counts in the nucleus accumbens and cingulate cortex; and 3) <b>methadone</b> and <b>morphine</b> (to a lesser extent) counteracted the stimulatory effect of nonpharmacological stressors on <strong>Fos</strong> protein expression in the somatosensory cortex barrel field, and <strong>Fos</strong> positive cell counts in this region correlated negatively with both the duration of catalepsy and the latency time in the hot plate test.
+FOS	drug	amphetamine	19598248	<b>METH</b> induced behavioral responses paralleled striatal c <strong>Fos</strong> like immunoreactivity.
+FOS	addiction	sensitization	19559544	Pdyn gene deficiency potentiates nalbuphine induced behavioral <b>sensitization</b> of locomotor activity and accumbal c <strong>Fos</strong> expression.
+FOS	drug	cocaine	19533625	c <strong>Fos</strong> expression associated with reinstatement of <b>cocaine</b> seeking behavior by response contingent conditioned cues.
+FOS	addiction	relapse	19533625	c <strong>Fos</strong> expression associated with <b>reinstatement</b> of cocaine <b>seeking</b> behavior by response contingent conditioned cues.
+FOS	drug	cocaine	19533625	We investigated neural activity associated with incentive motivational effects of <b>cocaine</b> cues using c <strong>fos</strong> mRNA and <strong>Fos</strong> protein expression as markers.
+FOS	addiction	reward	19533625	We investigated neural activity associated with <b>incentive</b> motivational effects of cocaine cues using c <strong>fos</strong> mRNA and <strong>Fos</strong> protein expression as markers.
+FOS	drug	cocaine	19533625	We also observed a correlation between <b>cocaine</b> seeking behavior and <strong>Fos</strong> in the agranular insula (AgI) and basolateral amygdala (BLA).
+FOS	addiction	relapse	19533625	We also observed a correlation between cocaine <b>seeking</b> behavior and <strong>Fos</strong> in the agranular insula (AgI) and basolateral amygdala (BLA).
+FOS	drug	opioid	19524022	The aims of the present study were to establish if nalfurafine, a kappa <b>opioid</b> agonist, inhibits compulsive scratching in mice elicited by the s.c. administration (behind the neck) of 5' guanidinonaltrindole (GNTI), a kappa <b>opioid</b> antagonist; to assess if nalfurafine prevents c <strong>fos</strong> expression provoked by GNTI or compound 48/80, two chemically diverse pruritogens; and to distinguish on the basis of neuroanatomy, those neurons in the brainstem activated by either GNTI induced itch or formalin induced pain (both compounds given s.c. to the right cheek).
+FOS	addiction	addiction	19524022	The aims of the present study were to establish if nalfurafine, a kappa opioid agonist, inhibits <b>compulsive</b> scratching in mice elicited by the s.c. administration (behind the neck) of 5' guanidinonaltrindole (GNTI), a kappa opioid antagonist; to assess if nalfurafine prevents c <strong>fos</strong> expression provoked by GNTI or compound 48/80, two chemically diverse pruritogens; and to distinguish on the basis of neuroanatomy, those neurons in the brainstem activated by either GNTI induced itch or formalin induced pain (both compounds given s.c. to the right cheek).
+FOS	drug	opioid	19481580	<b>Methadone</b> is substantially less effective than <b>morphine</b> in modifying locomotor and brain <strong>Fos</strong> responses to subsequent <b>methadone</b> challenge in rats.
+FOS	drug	opioid	19481580	Sensitization of <strong>Fos</strong> response was found in a few regions of the <b>morphine</b> treated rats.
+FOS	addiction	sensitization	19481580	<b>Sensitization</b> of <strong>Fos</strong> response was found in a few regions of the morphine treated rats.
+FOS	drug	opioid	19481580	The rats given the lower <b>methadone</b> dose treatment showed a weak while widespread tendency for an opposite change, which reached significance in cingulate cortex layer II/III and resulted in significant differences in <strong>Fos</strong> response between these rats and the <b>morphine</b> treated rats in most regions studied.
+FOS	addiction	reward	19422887	Immunohistochemistry studies demonstrated that <b>ICSS</b> caused a rapid induction of c <strong>Fos</strong> expression in hippocampal cornu ammonis (CA) 3 and dentatus gyrus areas.
+FOS	drug	amphetamine	19422887	Importantly, 10 of the regulated genes have been previously related with learning and memory or neural plasticity, including the cocaine and <b>amphetamine</b> regulated transcript (Cart), adenylate cyclase activating polypeptide 1 (Adcyap1), serum/glucocorticoid regulated kinase (Sgk), Ret proto oncogene (Ret), and <strong>Fos</strong>.
+FOS	drug	cocaine	19422887	Importantly, 10 of the regulated genes have been previously related with learning and memory or neural plasticity, including the <b>cocaine</b> and amphetamine regulated transcript (Cart), adenylate cyclase activating polypeptide 1 (Adcyap1), serum/glucocorticoid regulated kinase (Sgk), Ret proto oncogene (Ret), and <strong>Fos</strong>.
+FOS	drug	opioid	19422884	Activating mu <b>opioid</b> receptors in the lateral parabrachial nucleus increases c <strong>Fos</strong> expression in forebrain areas associated with caloric regulation, reward and cognition.
+FOS	addiction	reward	19422884	Activating mu opioid receptors in the lateral parabrachial nucleus increases c <strong>Fos</strong> expression in forebrain areas associated with caloric regulation, <b>reward</b> and cognition.
+FOS	drug	cocaine	19245875	The purpose of the present study was to correlate <b>cocaine</b> induced locomotor activity with neuronal activation in subregions of the striatum and cortex by acute <b>cocaine</b> in young adolescent (postnatal (PN) 28) and adult (PN 65) male rats by measuring the induction of the plasticity associated immediate early genes (IEGs) c <strong>fos</strong> and zif268 using in situ hybridization.
+FOS	drug	cocaine	19245875	Low dose <b>cocaine</b> induced more locomotor activity and striatal c <strong>fos</strong> expression in adolescents than adults whereas high dose <b>cocaine</b> induced more locomotor activity, striatal c <strong>fos</strong>, and striatal zif268 expression in adults.
+FOS	addiction	aversion	19235216	Prior studies revealed that <b>aversive</b> stimuli and psychostimulant drugs elicit <strong>Fos</strong> expression in neurons clustered above and behind the interpeduncular nucleus that project strongly to the ventral tegmental area (VTA) and substantia nigra (SN) compacta (C).
+FOS	addiction	relapse	19193880	We then used the retrograde neuronal tracer cholera toxin b subunit (CTb) combined with detection of the c <strong>Fos</strong> protein to identify activated afferents to LH during context induced <b>reinstatement</b> of beer <b>seeking</b>.
+FOS	addiction	relapse	19193880	Double labeling for c <strong>Fos</strong> and CTb revealed a significant recruitment of LH projecting neurons in nucleus accumbens shell (AcbSh) during <b>reinstatement</b>.
+FOS	drug	cocaine	19183268	In response to <b>cocaine</b>, MSK1 controls an early phase of histone H3 phosphorylation at the c <strong>fos</strong> promoter in striatal neurons.
+FOS	drug	cocaine	19183268	H3 phosphorylation by MSK1 is critically involved in c <strong>fos</strong> transcription, and <b>cocaine</b> induced locomotor sensitization.
+FOS	addiction	sensitization	19183268	H3 phosphorylation by MSK1 is critically involved in c <strong>fos</strong> transcription, and cocaine induced locomotor <b>sensitization</b>.
+FOS	drug	cocaine	19181855	Compared with WT mice, tPA /  mice injected with <b>cocaine</b> displayed attenuated phosphorylation of ERK, cAMP response element binding protein (CREB), and dopamine and cAMP regulated phosphoprotein 32 kDa (DARPP 32) and blunted induction of immediate early genes (IEGs) c <strong>Fos</strong>, Egr 1, and Homer 1a in the amygdala and the nucleus accumbens (NAc).
+FOS	drug	cocaine	19169671	Drug context differently regulates <b>cocaine</b> versus heroin self administration and <b>cocaine</b>  versus heroin induced <strong>Fos</strong> mRNA expression in the rat.
+FOS	drug	opioid	19169671	Drug context differently regulates cocaine versus <b>heroin</b> self administration and cocaine  versus <b>heroin</b> induced <strong>Fos</strong> mRNA expression in the rat.
+FOS	drug	cocaine	19169671	The second aim of the study was to investigate <strong>Fos</strong> mRNA expression in Resident and Non Resident rats treated with non contingent intravenous infusion of "self administration doses" of heroin (25.0 microg/kg) and <b>cocaine</b> (400 microg/kg).
+FOS	drug	opioid	19169671	The second aim of the study was to investigate <strong>Fos</strong> mRNA expression in Resident and Non Resident rats treated with non contingent intravenous infusion of "self administration doses" of <b>heroin</b> (25.0 microg/kg) and cocaine (400 microg/kg).
+FOS	drug	cocaine	19169671	We found that: (1) drug taking context differentially modulates intravenous <b>cocaine</b> versus heroin self administration; (2) very low doses of <b>cocaine</b> and heroin are sufficient to induce <strong>Fos</strong> mRNA expression in the posterior caudate; (3) drug administration context differentially modulates <b>cocaine</b>  versus heroin induced <strong>Fos</strong> mRNA expression.
+FOS	drug	opioid	19169671	We found that: (1) drug taking context differentially modulates intravenous cocaine versus <b>heroin</b> self administration; (2) very low doses of cocaine and <b>heroin</b> are sufficient to induce <strong>Fos</strong> mRNA expression in the posterior caudate; (3) drug administration context differentially modulates cocaine  versus <b>heroin</b> induced <strong>Fos</strong> mRNA expression.
+FOS	drug	amphetamine	19116947	Differential regulation of prodynophin, c <strong>fos</strong>, and serotonin transporter mRNA following withdrawal from a chronic, escalating dose regimen of D <b>amphetamine</b>.
+FOS	addiction	withdrawal	19116947	Differential regulation of prodynophin, c <strong>fos</strong>, and serotonin transporter mRNA following <b>withdrawal</b> from a chronic, escalating dose regimen of D amphetamine.
+FOS	addiction	withdrawal	19116947	Changes in the serotonin transporter (SERT) have also been reported in MDD, and changes in the immediate early gene c <strong>fos</strong> have been observed in the context of psychostimulant <b>withdrawal</b>.
+FOS	drug	amphetamine	19116947	This study examined the effects of chronic, escalating doses of D <b>AMPH</b> followed by 24 h of withdrawal on the expression of prodynorphin (PD) and c <strong>fos</strong> mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and SERT mRNA expression in the dorsal raphe nucleus (DRN).
+FOS	addiction	withdrawal	19116947	This study examined the effects of chronic, escalating doses of D AMPH followed by 24 h of <b>withdrawal</b> on the expression of prodynorphin (PD) and c <strong>fos</strong> mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and SERT mRNA expression in the dorsal raphe nucleus (DRN).
+FOS	addiction	withdrawal	19116947	Following 24 h of <b>withdrawal</b>, there was an increase in PD and c <strong>fos</strong> mRNA expression in the CPu and nucleus accumbens (NAc), and a decrease in PD and c <strong>fos</strong> expression in hippocampus and amygdala.
+FOS	addiction	withdrawal	19116947	These data indicate that region specific changes in PD and c <strong>fos</strong> expression occur after <b>withdrawal</b>, while SERT mRNA expression is suppressed, similar to what has been reported in MDD.
+FOS	addiction	withdrawal	19116947	Alterations in PD, c <strong>fos</strong>, and SERT expression could contribute to the depression like syndrome associated with psychostimulant <b>withdrawal</b>.
+FOS	drug	amphetamine	19084559	Expression of c <strong>fos</strong> mRNA in the basal ganglia associated with contingent tolerance to <b>amphetamine</b> induced hypophagia.
+FOS	drug	amphetamine	19084559	Following an acute injection of <b>amphetamine</b>, both of these groups had higher levels of c <strong>fos</strong> mRNA than saline treated controls throughout the striatum, in the nucleus accumbens core, the ventral pallidum and layers V VI of the motor cortex.
+FOS	drug	amphetamine	19084559	In contrast, tolerant rats, which had learned to suppress stereotypy, had higher levels of c <strong>fos</strong> mRNA than both <b>amphetamine</b>  and saline treated controls in the entopeduncular nucleus, globus pallidus, subthalamic nucleus, pedunculopontine nucleus, nucleus accumbens shell, olfactory tubercle, somatosensory cortex, and layers II IV of motor cortex.
+FOS	drug	cocaine	19020866	Persistence of one trial <b>cocaine</b> induced behavioral sensitization in young rats: regional differences in <strong>Fos</strong> immunoreactivity.
+FOS	addiction	sensitization	19020866	Persistence of one trial cocaine induced behavioral <b>sensitization</b> in young rats: regional differences in <strong>Fos</strong> immunoreactivity.
+FOS	addiction	sensitization	19020866	The purpose of this study was to determine whether: (1) the context dependent and context independent <b>sensitization</b> of young rats can be dissociated based on the persistence of the sensitized response and (2) the expression of behavioral <b>sensitization</b> is associated with region specific increases in <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR).
+FOS	drug	cocaine	19020866	When assessed after three abstinence days (i.e., on PD 22), acute treatment with <b>cocaine</b> increased <strong>Fos</strong> IR in various brain regions, but sensitized responding was associated with elevated <strong>Fos</strong> expression in only the caudate putamen (CP) and prefrontal cortex (PFC).
+FOS	addiction	sensitization	19020866	<strong>Fos</strong> data indicate that the CP and PFC may be involved in the mediation of short term behavioral <b>sensitization</b> on PD 22.
+FOS	addiction	reward	18996447	Surprisingly, <strong>Fos</strong> immunoreactivity was not observed with either GHB or baclofen in <b>reward</b> relevant regions such as the nucleus accumbens, striatum and ventral tegmental area.
+FOS	drug	cocaine	18991842	c <strong>Fos</strong> is an intracellular regulator of <b>cocaine</b> induced long term changes.
+FOS	drug	cocaine	18991842	Using a genetically modified mouse in which <strong>Fos</strong> is primarily mutated in D1 receptor bearing neurons in the brain, we examined a potential role of the immediate early gene <strong>Fos</strong>, which is rapidly induced by <b>cocaine</b> via D1 receptors, in mediating <b>cocaine</b> induced persistent neurobiological changes.
+FOS	drug	cocaine	18991842	We found that the composition of AP 1 transcription complexes and expression levels of AP 1 complexes, and several transcription factors, neurotransmitter receptors as well as intracellular signaling molecules following repeated <b>cocaine</b> administration are altered in <strong>Fos</strong> deficient brains.
+FOS	drug	cocaine	18991842	We found that the composition of <strong>AP 1</strong> transcription complexes and expression levels of <strong>AP 1</strong> complexes, and several transcription factors, neurotransmitter receptors as well as intracellular signaling molecules following repeated <b>cocaine</b> administration are altered in <strong>Fos</strong> deficient brains.
+FOS	drug	cocaine	18991842	These findings suggest that c <strong>Fos</strong> expressed in D1 receptor bearing neurons mediates <b>cocaine</b> induced persistent changes.
+FOS	drug	psychedelics	18973603	Acute and sensitized response to 3,4 <b>methylenedioxymethamphetamine</b> in rats: different behavioral profiles reflected in different patterns of <strong>Fos</strong> expression.
+FOS	drug	psychedelics	18973603	Acute <b>MDMA</b> exposure produced a dose dependent increase in locomotion in the peripheral zone of the open field that was related to an increase in <strong>Fos</strong> expression in the ventromedial shell of the nucleus accumbens, ventral pallidum, several hypothalamic nuclei and rhomboid thalamic nucleus.
+FOS	drug	cocaine	18938216	To understand intracellular mechanisms contributing to <b>cocaine</b> induced neuroadaptations, we previously examined the role of the immediate early gene <strong>Fos</strong> using a mouse in which <strong>Fos</strong> is disrupted primarily in D1 receptor expressing neurons in the brain.
+FOS	drug	amphetamine	18834549	<b>Amphetamine</b> and pseudoephedrine cross tolerance measured by c <strong>Fos</strong> protein expression in brains of chronically treated rats.
+FOS	drug	amphetamine	18834549	(ii) In animals chronically treated with <b>amphetamine</b> or pseudoephedrine the acute c <strong>Fos</strong> response to pseudoephedrine and <b>amphetamine</b> was reduced respectively as compared to naïve animals indicating cross tolerance for the two drugs.
+FOS	drug	opioid	18831893	In the VTA, <b>morphine</b> and footshock had an interactive effect on the increase in <strong>Fos</strong> expression.
+FOS	drug	opioid	18831893	Inhibition of the CeA decreased <strong>Fos</strong> expression in the BNSTv regardless of drug experience, whereas in the VTA this effect only occurred in <b>morphine</b> treated rats.
+FOS	drug	opioid	18823165	A <b>morphine</b> paired environment alters c <strong>Fos</strong> expression in the forebrain of rats displaying conditioned place preference or aversion.
+FOS	addiction	aversion	18823165	A morphine paired environment alters c <strong>Fos</strong> expression in the forebrain of rats displaying conditioned place preference or <b>aversion</b>.
+FOS	addiction	reward	18823165	Compared with the control group, the <b>CPP</b> and CPA groups showed a significant increase of c <strong>Fos</strong> expression in the dorsomedial striatum, central medial nucleus of the thalamus, and the basolateral amygdala.
+FOS	drug	cocaine	18822274	Effects of dopamine and NMDA receptors on <b>cocaine</b> induced <strong>Fos</strong> expression in the striatum of Fischer rats.
+FOS	drug	cocaine	18822274	In this study, we show that a single <b>cocaine</b> administration (30 mg/kg) time dependently increases ERK phosphorylation, c <strong>Fos</strong> and FosB protein expression, and MKP 1 phosphorylation (p MKP 1), in the caudate putamen (CPu) and nucleus accumbens (NAc) of Fischer rats.
+FOS	drug	cocaine	18822274	In the CPu, 1 h after <b>cocaine</b> injection, the increase in c <strong>Fos</strong> and FosB protein expressions is totally abolished by pre administration of DA D1 receptor antagonist, SCH23390.
+FOS	drug	cocaine	18822274	In the NAc, SCH23390 also inhibits <b>cocaine</b> induced c <strong>Fos</strong> protein expression.
+FOS	drug	cocaine	18822274	The pre treatment of NMDA receptor antagonist, MK801, partially reduces <b>cocaine</b> activated c <strong>Fos</strong> protein expression in the CPu.
+FOS	drug	alcohol	18815268	Using c <strong>Fos</strong> expression as a high resolution marker of neuronal activation, congenic mice demonstrated significantly less neuronal activity associated with <b>ethanol</b> withdrawal than background strain mice in the substantia nigra pars reticulata (SNr), subthalamic nucleus (STN), rostromedial lateral globus pallidus, and ventral pallidum.
+FOS	addiction	withdrawal	18815268	Using c <strong>Fos</strong> expression as a high resolution marker of neuronal activation, congenic mice demonstrated significantly less neuronal activity associated with ethanol <b>withdrawal</b> than background strain mice in the substantia nigra pars reticulata (SNr), subthalamic nucleus (STN), rostromedial lateral globus pallidus, and ventral pallidum.
+FOS	addiction	addiction	18789904	Induction of immediate early genes (IEG), such as c <strong>Fos</strong> or Egr 1, is used to identify brain areas that become activated in response to various stimuli, including <b>addictive</b> drugs.
+FOS	drug	opioid	18772347	Spinal administration of an EphB receptor blocking reagent EphB2 Fc prevents and/or suppresses behavioral responses to <b>morphine</b> withdrawal and associated induction of c <strong>Fos</strong> and depletion of calcitonin gene related peptide.
+FOS	addiction	withdrawal	18772347	Spinal administration of an EphB receptor blocking reagent EphB2 Fc prevents and/or suppresses behavioral responses to morphine <b>withdrawal</b> and associated induction of c <strong>Fos</strong> and depletion of calcitonin gene related peptide.
+FOS	drug	amphetamine	18766328	Separate experiments assessed the effects of SL 327 (50 mg/kg, intraperitoneally) on (1) the reward potentiating effect of D <b>amphetamine</b> in an intracranial self stimulation protocol, (2) the locomotor activating effect of the D 1 agonist, SKF 82958, and (3) <strong>Fos</strong> immunostaining induced in the NAc by SKF 82958.
+FOS	addiction	reward	18766328	Separate experiments assessed the effects of SL 327 (50 mg/kg, intraperitoneally) on (1) the <b>reward</b> potentiating effect of D amphetamine in an intracranial self stimulation protocol, (2) the locomotor activating effect of the D 1 agonist, SKF 82958, and (3) <strong>Fos</strong> immunostaining induced in the NAc by SKF 82958.
+FOS	drug	alcohol	18755245	Effects of pharmacological stressors on c <strong>fos</strong> and CRF mRNA in mouse brain: relationship to <b>alcohol</b> seeking.
+FOS	addiction	relapse	18755245	Effects of pharmacological stressors on c <strong>fos</strong> and CRF mRNA in mouse brain: relationship to alcohol <b>seeking</b>.
+FOS	drug	alcohol	18755245	The purpose of the present experiment is to determine if these differential effects of yohimbine and FG 7142 on regional c <strong>fos</strong> and CRF mRNA expression generalize to another animal commonly used in <b>alcohol</b> research, the C57 BL/6J mouse.
+FOS	addiction	relapse	18755245	The selective induction of c <strong>fos</strong> in the NACs, BLA and CeA of mice and rats by yohimbine offers further support for the idea that activation of these structures participates in <b>reinstatement</b> induced by such stressors.
+FOS	addiction	reward	18722478	In the limbic system, <strong>Fos</strong> positive neurons were examined following retrieval of the MA <b>CPP</b> memory.
+FOS	addiction	reward	18722478	Moreover, enhanced <strong>Fos</strong> expressions were found in the medial prefrontal cortex and the core of the nucleus accumbens after reactivation of the MA <b>CPP</b> memory.
+FOS	drug	alcohol	18692030	<b>Ethanol</b> induced alterations of c <strong>Fos</strong> immunoreactivity in specific limbic brain regions following <b>ethanol</b> discrimination training.
+FOS	drug	alcohol	18692030	To accomplish this goal, immunohistochemistry was used to assess the effects of <b>ethanol</b> (2 g/kg) on c <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR).
+FOS	drug	alcohol	18692030	Comparisons in <b>ethanol</b> induced <strong>Fos</strong> IR were made between a group of rats that was trained to discriminate the stimulus properties of <b>ethanol</b> (2 g/kg, IG) from water (IG) and a drug/behavior matched control group that did not receive differential reinforcement for lever selection, which precluded acquisition of discriminative stimulus control by <b>ethanol</b>.
+FOS	addiction	reward	18692030	Comparisons in ethanol induced <strong>Fos</strong> IR were made between a group of rats that was trained to discriminate the stimulus properties of ethanol (2 g/kg, IG) from water (IG) and a drug/behavior matched control group that did not receive differential <b>reinforcement</b> for lever selection, which precluded acquisition of discriminative stimulus control by ethanol.
+FOS	drug	alcohol	18692030	In some brain regions discrimination training had no effect on <b>ethanol</b> induced <strong>Fos</strong> IR changes (caudate putamen, bed nucleus of the stria terminalis, and CA1 region of the hippocampus).
+FOS	drug	alcohol	18692030	In contrast, discrimination training altered the pattern of <b>ethanol</b> induced <strong>Fos</strong> IR in the nucleus accumbens (core), medial septum, and the hippocampus (dentate and CA3).
+FOS	drug	alcohol	18692030	These results indicate that having behavior under the stimulus control of <b>ethanol</b> can change <b>ethanol</b> induced <strong>Fos</strong> IR in some brain regions.
+FOS	drug	cocaine	18655797	We found that <strong>Fos</strong> expression in LH orexin neurons varied in proportion to preference for morphine, <b>cocaine</b> or food.
+FOS	drug	opioid	18655797	We found that <strong>Fos</strong> expression in LH orexin neurons varied in proportion to preference for <b>morphine</b>, cocaine or food.
+FOS	drug	opioid	18655797	Recent studies showed that LH orexin neurons that project to ventral tegmental area (VTA) have greater <strong>Fos</strong> induction in association with elevated <b>morphine</b> preference during protracted withdrawal than non VTA projecting orexin neurons, indicating that the VTA is an important site of action for orexin's role in reward processing.
+FOS	addiction	reward	18655797	Recent studies showed that LH orexin neurons that project to ventral tegmental area (VTA) have greater <strong>Fos</strong> induction in association with elevated morphine preference during protracted withdrawal than non VTA projecting orexin neurons, indicating that the VTA is an important site of action for orexin's role in <b>reward</b> processing.
+FOS	addiction	withdrawal	18655797	Recent studies showed that LH orexin neurons that project to ventral tegmental area (VTA) have greater <strong>Fos</strong> induction in association with elevated morphine preference during protracted <b>withdrawal</b> than non VTA projecting orexin neurons, indicating that the VTA is an important site of action for orexin's role in reward processing.
+FOS	addiction	withdrawal	18655205	injection of the sigma 1 receptor agonists PRE 084 (PRE) or carbetapentane (CAR) significantly decreased tail flick latency (TFL) and increased the frequency of paw <b>withdrawal</b> responses to mechanical stimulation (von Frey filament, 0.6 g) as well as the amount of <strong>Fos</strong> expression in the spinal cord dorsal horn induced by noxious paw pinch stimulation.
+FOS	drug	cocaine	18651175	Finally, increased <strong>Fos</strong> activation in the extended amygdala and NTS is associated with the enhanced preference for drugs and decreased preference for natural rewards observed during protracted abstinence from opiates and <b>cocaine</b>, indicating that these areas are involved in the altered reward processing associated with addiction.
+FOS	addiction	addiction	18651175	Finally, increased <strong>Fos</strong> activation in the extended amygdala and NTS is associated with the enhanced preference for drugs and decreased preference for natural rewards observed during protracted abstinence from opiates and cocaine, indicating that these areas are involved in the altered reward processing associated with <b>addiction</b>.
+FOS	addiction	reward	18651175	Finally, increased <strong>Fos</strong> activation in the extended amygdala and NTS is associated with the enhanced preference for drugs and decreased preference for natural rewards observed during protracted abstinence from opiates and cocaine, indicating that these areas are involved in the altered <b>reward</b> processing associated with addiction.
+FOS	drug	psychedelics	18633827	Analysis of neural activation across 39 brain regions using <strong>Fos</strong> immunohistochemistry showed the following results: (1) VEHICLE SOCIAL and VEHICLE ALONE groups did not differ in <strong>Fos</strong> expression, indicating that a social context per se did not affect <strong>Fos</strong> expression, (2) <b>MDMA</b> treated groups showed significantly increased <strong>Fos</strong> expression relative to VEHICLE treated groups in 30 brain regions, (3) the <b>MDMA</b> SOCIAL group showed augmented <strong>Fos</strong> expression relative to the <b>MDMA</b> ALONE group in six brain regions including the caudate putamen (medial), medial preoptic area, paraventricular thalamic nucleus, central amygdala, ventromedial hypothalamic nucleus, and the medial amygdala (posterodorsal), and (4) the <b>MDMA</b> SOCIAL group (but not the <b>MDMA</b> ALONE group) showed augmented <strong>Fos</strong> expression relative to the VEHICLE groups in the nucleus accumbens, ventral tegmental area and periaqueductal grey.
+FOS	drug	amphetamine	18632938	Delta FosB mediates epigenetic desensitization of the c <strong>fos</strong> gene after chronic <b>amphetamine</b> exposure.
+FOS	drug	amphetamine	18632938	We show that accumulation of DeltaFosB in striatum after chronic <b>amphetamine</b> treatment desensitizes c <strong>fos</strong> mRNA induction to a subsequent drug dose.
+FOS	drug	amphetamine	18632938	Accordingly, local knock out of HDAC1 in striatum abolishes <b>amphetamine</b> induced desensitization of the c <strong>fos</strong> gene.
+FOS	drug	amphetamine	18632938	In concert, chronic <b>amphetamine</b> increases histone H3 methylation on the c <strong>fos</strong> promoter, a chromatin modification also known to repress gene activity, as well as expression levels of the H3 histone methyltransferase, KMT1A (lysine methyltransferase 1A, formerly SUV39H1).
+FOS	drug	cocaine	18591217	Alterations in <strong>fos</strong> related antigen 2 and sigma1 receptor gene and protein expression are associated with the development of <b>cocaine</b> induced behavioral sensitization: time course and regional distribution studies.
+FOS	addiction	sensitization	18591217	Alterations in <strong>fos</strong> related antigen 2 and sigma1 receptor gene and protein expression are associated with the development of cocaine induced behavioral <b>sensitization</b>: time course and regional distribution studies.
+FOS	drug	cocaine	18591217	Earlier studies demonstrated that acute administration of <b>cocaine</b> up regulates the immediate early gene <strong>fos</strong> related antigen 2 (fra 2) followed by a later up regulation of sigma(1) receptor gene and protein levels in brain regions involved in addiction and reward.
+FOS	addiction	addiction	18591217	Earlier studies demonstrated that acute administration of cocaine up regulates the immediate early gene <strong>fos</strong> related antigen 2 (fra 2) followed by a later up regulation of sigma(1) receptor gene and protein levels in brain regions involved in <b>addiction</b> and reward.
+FOS	addiction	reward	18591217	Earlier studies demonstrated that acute administration of cocaine up regulates the immediate early gene <strong>fos</strong> related antigen 2 (fra 2) followed by a later up regulation of sigma(1) receptor gene and protein levels in brain regions involved in addiction and <b>reward</b>.
+FOS	drug	cocaine	18588535	<b>Cocaine</b> induced stereotypy and c <strong>fos</strong> mRNA expression in cortex and striatum were also examined.
+FOS	drug	cocaine	18588535	Nicotine exposed adolescents did not self administer the low dose of <b>cocaine</b>, but, at the higher dose, exhibited significantly greater <b>cocaine</b> intake and c <strong>fos</strong> mRNA expression in nucleus accumbens than did controls.
+FOS	drug	nicotine	18588535	<b>Nicotine</b> exposed adolescents did not self administer the low dose of cocaine, but, at the higher dose, exhibited significantly greater cocaine intake and c <strong>fos</strong> mRNA expression in nucleus accumbens than did controls.
+FOS	drug	amphetamine	18562160	Sweetened milk ingestion was associated with increased numbers of c <strong>Fos</strong> positive neurons in the caudal core and shell of the nucleus accumbens (NAc), the paraventricular thalamus (PVT), central nucleus of the amygdala (CEA), the basal lateral amygdala (BLA), in orexin A containing neurons of the lateral hypothalamus (LH), and in cocaine and <b>amphetamine</b> regulated transcript (CART) neurons of the arcuate hypothalamus.
+FOS	drug	cocaine	18562160	Sweetened milk ingestion was associated with increased numbers of c <strong>Fos</strong> positive neurons in the caudal core and shell of the nucleus accumbens (NAc), the paraventricular thalamus (PVT), central nucleus of the amygdala (CEA), the basal lateral amygdala (BLA), in orexin A containing neurons of the lateral hypothalamus (LH), and in <b>cocaine</b> and amphetamine regulated transcript (CART) neurons of the arcuate hypothalamus.
+FOS	drug	cocaine	18550291	In addition, the number of <strong>cFos</strong> positive cells was increased in the motor cortex, medial and ventromedial aspects of the nucleus accumbens shell, basolateral amygdala and caudal VTA during the expression of <b>cocaine</b> place preference, and this increase was attenuated in the animals that received intra accumbens core CTAP during daily <b>cocaine</b> conditioning.
+FOS	drug	opioid	18548233	We show that <b>naloxone</b> induced <b>morphine</b> withdrawal activates extracellular signal regulated kinases(1/2) and increases c <strong>Fos</strong> expression in rat paraventricular nucleus and nucleus tractus solitarius A(2) neurons.
+FOS	addiction	withdrawal	18548233	We show that naloxone induced morphine <b>withdrawal</b> activates extracellular signal regulated kinases(1/2) and increases c <strong>Fos</strong> expression in rat paraventricular nucleus and nucleus tractus solitarius A(2) neurons.
+FOS	drug	cocaine	18539009	Region specific involvement of AMPA/Kainate receptors in <strong>Fos</strong> protein expression induced by <b>cocaine</b> conditioned cues.
+FOS	drug	cocaine	18539009	This study investigated the effects of the AMPA/Kainate receptor antagonist, NBQX, on cue elicited <b>cocaine</b> seeking behavior and concomitant changes in <strong>Fos</strong> protein expression.
+FOS	addiction	relapse	18539009	This study investigated the effects of the AMPA/Kainate receptor antagonist, NBQX, on cue elicited cocaine <b>seeking</b> behavior and concomitant changes in <strong>Fos</strong> protein expression.
+FOS	drug	cocaine	18539009	NBQX markedly attenuated cue elicited <b>cocaine</b> seeking behavior relative to vehicle pretreatment in the No Extinction group and also decreased cue elicited <strong>Fos</strong> protein expression in a region specific manner in the anterior cingulate and orbitofrontal cortices, basolateral amygdala, nucleus accumbens core, and dorsal caudate putamen, suggesting involvement of AMPA glutamate systems in specific subregions of the neuronal circuitry activated by <b>cocaine</b> cues.
+FOS	addiction	relapse	18539009	NBQX markedly attenuated cue elicited cocaine <b>seeking</b> behavior relative to vehicle pretreatment in the No Extinction group and also decreased cue elicited <strong>Fos</strong> protein expression in a region specific manner in the anterior cingulate and orbitofrontal cortices, basolateral amygdala, nucleus accumbens core, and dorsal caudate putamen, suggesting involvement of AMPA glutamate systems in specific subregions of the neuronal circuitry activated by cocaine cues.
+FOS	drug	cocaine	18495107	Inhibition of dopamine release by isoliquiritigenin resulted in attenuation of the expression of c <strong>Fos</strong>, an immediately early gene induced by <b>cocaine</b>.
+FOS	drug	cannabinoid	18493584	In addition, peripheral and central <b>cannabinoid</b> administration similarly induced c <strong>Fos</strong> activation in brain sites suggesting mediation via motivational dopaminergic circuitry.
+FOS	drug	cocaine	18488248	Using an animal model of relapse to <b>cocaine</b> seeking, the present study investigated the expression patterns of three different activity related genes (c <strong>fos</strong>, zif/268, and arc) in cortical and striatal brain regions implicated in compulsive drug seeking in order to determine the neuroadaptations that occur during context induced relapse following brief or prolonged abstinence from <b>cocaine</b> self administration.
+FOS	addiction	addiction	18488248	Using an animal model of relapse to cocaine seeking, the present study investigated the expression patterns of three different activity related genes (c <strong>fos</strong>, zif/268, and arc) in cortical and striatal brain regions implicated in <b>compulsive</b> drug seeking in order to determine the neuroadaptations that occur during context induced relapse following brief or prolonged abstinence from cocaine self administration.
+FOS	addiction	relapse	18488248	Using an animal model of <b>relapse</b> to cocaine <b>seeking</b>, the present study investigated the expression patterns of three different activity related genes (c <strong>fos</strong>, zif/268, and arc) in cortical and striatal brain regions implicated in compulsive drug <b>seeking</b> in order to determine the neuroadaptations that occur during context induced <b>relapse</b> following brief or prolonged abstinence from cocaine self administration.
+FOS	drug	cocaine	18488248	Re exposure to the environment previously associated with <b>cocaine</b> self administration following 22 h or 15 days of abstinence produced a significant increase in zif/268 and arc, but not c <strong>fos</strong> mRNA, in the caudate putamen and nucleus accumbens.
+FOS	drug	opioid	18485622	<b>Morphine</b> and <b>methadone</b> pre exposures differently modify brain regional <strong>Fos</strong> protein expression and locomotor activity responses to <b>morphine</b> challenge in the rat.
+FOS	drug	opioid	18485622	We compared the effects of repeated daily and every other day pre exposure of rats to s.c. <b>morphine</b> and <b>methadone</b> on locomotor activity and CNS neuronal activation (as assessed by <strong>Fos</strong> immunohistochemistry) responses to s.c. <b>morphine</b> challenge given 2 weeks after the completion of the pretreatment.
+FOS	drug	opioid	18485622	Dorsomedial striatum and basolateral amygdaloid nucleus showed robust <b>morphine</b> induced <strong>Fos</strong> protein induction that was unaffected by the pretreatments tested.
+FOS	drug	opioid	18485622	Centrolateral striatum, shell and core of the nucleus accumbens, paraventricular thalamic nucleus and some layers of motor and somatosensory cortices showed but negligible <strong>Fos</strong> protein induction in drug naive rats; this response was markedly enhanced by <b>morphine</b> pretreatment only, which effect might be related to the emergence of opiate addiction.
+FOS	addiction	addiction	18485622	Centrolateral striatum, shell and core of the nucleus accumbens, paraventricular thalamic nucleus and some layers of motor and somatosensory cortices showed but negligible <strong>Fos</strong> protein induction in drug naive rats; this response was markedly enhanced by morphine pretreatment only, which effect might be related to the emergence of opiate <b>addiction</b>.
+FOS	drug	opioid	18485622	Minor <strong>Fos</strong> responses to <b>morphine</b> were also found in layers IV and VI of the somatosensory cortex and layer VI of the insular cortex of the drug naïve rats; these responses were significantly enhanced both by <b>morphine</b> and <b>methadone</b> pretreatment.
+FOS	drug	opioid	18485423	The effects of <b>morphine</b> withdrawal on anxiety induced <strong>Fos</strong> immunolabelling were evaluated in four animals that passed by the light dark transition test randomly chosen for <strong>Fos</strong> protein analysis.
+FOS	addiction	withdrawal	18485423	The effects of morphine <b>withdrawal</b> on anxiety induced <strong>Fos</strong> immunolabelling were evaluated in four animals that passed by the light dark transition test randomly chosen for <strong>Fos</strong> protein analysis.
+FOS	addiction	withdrawal	18485423	Increased <strong>Fos</strong> labelling was also observed in the ventral and dorsal aspects of the PAG, a region involved in anxiety related processes suggesting that this region could be a common neural substrate enlisted during anxiety evoked by dangerous stimuli as well as those elicited by opiate <b>withdrawal</b>.
+FOS	drug	opioid	18474394	The proteins of <strong>Fos</strong> family are a potential candidate to link molecular mechanisms of <b>morphine</b> action with behavioural effects such as <b>morphine</b> induced reward, dependence and tolerance.
+FOS	addiction	dependence	18474394	The proteins of <strong>Fos</strong> family are a potential candidate to link molecular mechanisms of morphine action with behavioural effects such as morphine induced reward, <b>dependence</b> and tolerance.
+FOS	addiction	reward	18474394	The proteins of <strong>Fos</strong> family are a potential candidate to link molecular mechanisms of morphine action with behavioural effects such as morphine induced <b>reward</b>, dependence and tolerance.
+FOS	drug	opioid	18466961	<strong>Fos</strong> expression was also increased after 1 and 14 days of abstinence, but at 14 days this increase was response independent (i.e., it occurred in both the rats with a history of <b>heroin</b> self administration and in the yoked controls).
+FOS	drug	cocaine	18463628	Finally, basal levels of Delta <strong>Fos</strong> B, a transcription factor known to be increased by sustained activation of striatal neurons, are higher in the striatum of EE compared to SE mice and repeated administration of <b>cocaine</b> increases Delta <strong>Fos</strong> B levels in SE mice but decreases them in EE mice.
+FOS	addiction	withdrawal	18423425	<b>Withdrawal</b> was accompanied by an increase in c <strong>Fos</strong> expression in the Acb shell (AcbSh), which was reduced by SB 334867 but had no effect on the VTA or the LC.
+FOS	drug	opioid	18423425	<b>Morphine</b> withdrawal increased c <strong>Fos</strong> expression in the dorsomedial (DMH) and perifornical (PFA) regions but not in the lateral region of the LH (LLH).
+FOS	addiction	withdrawal	18423425	Morphine <b>withdrawal</b> increased c <strong>Fos</strong> expression in the dorsomedial (DMH) and perifornical (PFA) regions but not in the lateral region of the LH (LLH).
+FOS	drug	alcohol	18412612	induced expression of the marker genes c <strong>fos</strong> and egr 1 in brain regions associated with both rewarding and stressful <b>ethanol</b> actions.
+FOS	drug	alcohol	18412612	Under non dependent conditions, <b>ethanol</b> induced c <strong>fos</strong> expression was generally not affected by MEK inhibition, with the exception of the medial amygdala (MeA).
+FOS	drug	alcohol	18412612	In contrast, following a history of dependence, a markedly suppressed c <strong>fos</strong> response to acute <b>ethanol</b> was found in the medial pre frontal/orbitofrontal cortex (OFC), nucleus accumbens shell (AcbSh) and paraventricular nucleus (PVN).
+FOS	addiction	dependence	18412612	In contrast, following a history of <b>dependence</b>, a markedly suppressed c <strong>fos</strong> response to acute ethanol was found in the medial pre frontal/orbitofrontal cortex (OFC), nucleus accumbens shell (AcbSh) and paraventricular nucleus (PVN).
+FOS	drug	cocaine	18396266	The rate of intravenous <b>cocaine</b> administration alters c <strong>fos</strong> mRNA expression and the temporal dynamics of dopamine, but not glutamate, overflow in the striatum.
+FOS	drug	cocaine	18396266	In contrast, although peak levels of dopamine were unaffected by infusion rate, dopamine levels increased more rapidly when <b>cocaine</b> was administered over 5 versus 100 s. Moreover, c <strong>fos</strong> mRNA expression in the region of the striatum sampled was greater when <b>cocaine</b> was administered rapidly than when given slowly.
+FOS	drug	cocaine	18355967	Following a single injection of <b>cocaine</b>, locomotion increased similarly in both the A <strong>FOS</strong> expressing and littermate controls.
+FOS	drug	cocaine	18355967	However, following repeated injections of <b>cocaine</b>, the A <strong>FOS</strong> expressing mice showed increased locomotion relative to littermate controls, an increase that persisted following a week of withdrawal and subsequent <b>cocaine</b> administration.
+FOS	addiction	withdrawal	18355967	However, following repeated injections of cocaine, the A <strong>FOS</strong> expressing mice showed increased locomotion relative to littermate controls, an increase that persisted following a week of <b>withdrawal</b> and subsequent cocaine administration.
+FOS	drug	cocaine	18355967	These results indicate that <strong>AP 1</strong> suppresses this behavioral response to <b>cocaine</b>.
+FOS	drug	cocaine	18355967	We analyzed mRNA from the striatum before and 4 and 24 h after a single <b>cocaine</b> injection in both A <strong>FOS</strong> and control striata using Affymetrix microarrays (430 2.0 Array) to identify genes mis regulated by A <strong>FOS</strong> that may mediate the increased locomotor sensitization to <b>cocaine</b>.
+FOS	addiction	sensitization	18355967	We analyzed mRNA from the striatum before and 4 and 24 h after a single cocaine injection in both A <strong>FOS</strong> and control striata using Affymetrix microarrays (430 2.0 Array) to identify genes mis regulated by A <strong>FOS</strong> that may mediate the increased locomotor <b>sensitization</b> to cocaine.
+FOS	drug	cocaine	18355967	A <strong>FOS</strong> expression did not change gene expression in the basal state or 4 h following <b>cocaine</b> treatment relative to controls.
+FOS	drug	cocaine	18355967	However, 24 h after an acute <b>cocaine</b> treatment, 84 genes were identified that were differentially expressed between the A <strong>FOS</strong> and control mice.
+FOS	drug	opioid	18349210	Suppression of noxious induced c <strong>fos</strong> expression in the rat lumbar spinal cord by isoflurane alone or combined with <b>fentanyl</b>.
+FOS	drug	opioid	18349210	Since the anesthetic mechanisms differ between inhaled anesthetics and <b>opioids</b>, we evaluated the differential effects of isoflurane and <b>fentanyl</b> on c <strong>fos</strong> expression at the lumbar level as a measure of nociceptive information transfer during general anesthesia.
+FOS	drug	opioid	18349210	The main suppressive effects on lumbar c <strong>fos</strong> expression of isoflurane were observed in the superficial lamina II (P = 0.02), whereas <b>fentanyl</b> showed the strongest effects in lamina V (P = 0.05).
+FOS	drug	opioid	18349210	This study demonstrates that the NIWR model combined with spinal <strong>Fos</strong> immunoreactivity is a suitable and useful model for evaluating the differential effects of inhaled anesthetics and <b>opioids</b> on nociceptive information transfer during general anesthesia.
+FOS	addiction	sensitization	18347780	c <strong>fos</strong> positive nuclei were quantified in the nucleus accumbens and prefrontal cortex after expression of <b>sensitization</b> with 1 mg/kg i.p.
+FOS	drug	amphetamine	18347780	The c <strong>fos</strong> response to <b>amphetamine</b> in the accumbens core was augmented in <b>amphetamine</b> pretreated animals with a shift in the distribution of optical density, while no effect of sensitization was seen in the nucleus accumbens shell or prefrontal cortex.
+FOS	addiction	sensitization	18347780	The c <strong>fos</strong> response to amphetamine in the accumbens core was augmented in amphetamine pretreated animals with a shift in the distribution of optical density, while no effect of <b>sensitization</b> was seen in the nucleus accumbens shell or prefrontal cortex.
+FOS	addiction	sensitization	18347780	The increase in c <strong>fos</strong> positive nuclei and shift in the distribution of optical density observed in the nucleus accumbens core suggests recruitment of a new population of neurons during expression of <b>sensitization</b>.
+FOS	drug	nicotine	18337407	Significantly, although chronic <b>nicotine</b> SA did not affect total c <strong>Fos</strong> expression induced by mFSS in pcPVN CRF(+) neurons, the majority of the new CRF(+)/AVP(+) population was activated by this heterotypic stressor.
+FOS	drug	cocaine	18311559	Rats self administered <b>cocaine</b> or received yoked saline for 2 h/day for 10 days followed by 22 h or 2 weeks of abstinence when they were re exposed to the self administration chamber with or without levers available to press for 1 h. Brains were harvested and sections through the prefrontal cortex were processed for in situ hybridization using radioactive oligonucleotide probes encoding c <strong>fos</strong>, zif/268, arc, and bdnf.
+FOS	drug	opioid	18311059	In the present study, we examined the influence of c <strong>Fos</strong> expression in the amygdala in acquisition of conditioned place aversion (CPA) induced by <b>naloxone</b> precipitated withdrawal from a single <b>morphine</b> exposure 24 h earlier.
+FOS	addiction	aversion	18311059	In the present study, we examined the influence of c <strong>Fos</strong> expression in the amygdala in acquisition of conditioned place <b>aversion</b> (CPA) induced by naloxone precipitated withdrawal from a single morphine exposure 24 h earlier.
+FOS	addiction	withdrawal	18311059	In the present study, we examined the influence of c <strong>Fos</strong> expression in the amygdala in acquisition of conditioned place aversion (CPA) induced by naloxone precipitated <b>withdrawal</b> from a single morphine exposure 24 h earlier.
+FOS	drug	cocaine	18310906	It has been shown that repeated injections of <b>cocaine</b> produce an increase in locomotor activity, the expression of the immediate early gene, c <strong>fos</strong>, and the release of dopamine (DA) in the nucleus accumbens (NAc), which is one of the main dopaminergic terminal areas.
+FOS	drug	cocaine	18310906	In order to investigate the effects of GTS on the repeated <b>cocaine</b> induced behavioral and neurochemical alterations, we examined the influence of GTS on the <b>cocaine</b> induced behavioral sensitization and on c <strong>Fos</strong> expression in the brain using immunohistochemistry in rats repeatedly treated with <b>cocaine</b>.
+FOS	addiction	sensitization	18310906	In order to investigate the effects of GTS on the repeated cocaine induced behavioral and neurochemical alterations, we examined the influence of GTS on the cocaine induced behavioral <b>sensitization</b> and on c <strong>Fos</strong> expression in the brain using immunohistochemistry in rats repeatedly treated with cocaine.
+FOS	drug	cocaine	18310906	significantly inhibited the repeated <b>cocaine</b> induced increase in locomotor activity as well as the c <strong>Fos</strong> expression in the core and shell in a dose dependent manner.
+FOS	drug	cocaine	18185499	We examined if KOR activation alters sensitivity to stimulant drugs by assessing the effects of the selective KOR agonist, salvinorin A (SalvA), on <b>cocaine</b> induced locomotor activity and c <strong>Fos</strong> expression.
+FOS	drug	cocaine	18185499	The effects of SalvA on locomotor activity paralleled its effects on <b>cocaine</b> induced c <strong>Fos</strong> expression in the dorsal striatum: acute SalvA attenuated <b>cocaine</b> induced c <strong>Fos</strong>, whereas repeated SalvA potentiated it when administered in the activity chambers but not the home cage.
+FOS	drug	amphetamine	18185498	Consistent with the behavioral findings, cocaine induces less c <strong>Fos</strong> expression in the striatum of these mice, while <b>amphetamine</b> induced c <strong>Fos</strong> expression is intact.
+FOS	drug	cocaine	18185498	Consistent with the behavioral findings, <b>cocaine</b> induces less c <strong>Fos</strong> expression in the striatum of these mice, while amphetamine induced c <strong>Fos</strong> expression is intact.
+FOS	drug	opioid	18184800	In contrast to PENK, no association was detected between PDYN genotype (68 bp repeat element containing one to four copies of <strong>AP 1</strong> binding sites in the promoter region) and <b>heroin</b> abuse, although there was a clear functional association with striatal PDYN mRNA expression: an increased number of inducible repeats (three and four) correlated with higher PDYN levels than adult or fetal subjects with noninducible (one and two) alleles.
+FOS	drug	amphetamine	18184321	To test whether the behavioral phenotype is also accompanied by similar neuroplastic adaptations, the present study evaluated changes in <strong>Fos</strong> and FosB/DeltaFosB transcription factors induced in the brain of C57BL/6J mice behaviorally sensitized by repeated <b>amphetamine</b> or repeated restraint stress.
+FOS	drug	amphetamine	18184321	Both stress  and <b>amphetamine</b> pre treated groups showed changes in <b>amphetamine</b> induced <strong>Fos</strong> expression; however, none of these changes was shared by the two sensitizing treatments.
+FOS	drug	cocaine	18164822	Group ABA showed renewal of extinguished <b>cocaine</b> seeking associated with c <strong>Fos</strong> induction in basolateral amygdala, lateral hypothalamus, and infralimbic prefrontal cortex.
+FOS	addiction	relapse	18164822	Group ABA showed renewal of extinguished cocaine <b>seeking</b> associated with c <strong>Fos</strong> induction in basolateral amygdala, lateral hypothalamus, and infralimbic prefrontal cortex.
+FOS	addiction	reward	18155256	Conditioned place preference tests were conducted first to establish relative potency of each <b>reward</b> and facilitate analysis of correlations between <strong>Fos</strong> and motivation.
+FOS	drug	cocaine	18155256	Food  but not <b>cocaine</b> paired cues increased <strong>Fos</strong> in the paraventricular hypothalamic nucleus whereas the opposite occurred for prefrontal, cingulate and piriform cortices.
+FOS	drug	cocaine	18155256	Individual differences in <b>cocaine</b> place preference were negatively correlated with <strong>Fos</strong> in the prefrontal cortex.
+FOS	drug	cocaine	18093170	Although only 2% of striatal neurons were FosB labeled, 87% of these FosB labeled neurons were co labeled with c <strong>fos</strong> when <b>cocaine</b> was injected in the <b>cocaine</b> paired environment.
+FOS	drug	cocaine	18093170	Furthermore, the total number of c <strong>fos</strong> labeled neurons was greater with either <b>cocaine</b> or saline challenge injections in the <b>cocaine</b> paired environment than in the saline paired environment.
+FOS	drug	amphetamine	18080115	Repeated <b>amphetamine</b> administration induces <strong>Fos</strong> in prefrontal cortical neurons that project to the lateral hypothalamus but not the nucleus accumbens or basolateral amygdala.
+FOS	drug	amphetamine	18080115	Using retrograde labeling techniques, <strong>Fos</strong> activation was evaluated in the predominant projection pathways of the mPFC of sensitized rats after a challenge injection of <b>AMPH</b>.
+FOS	drug	amphetamine	18080115	There was a significant increase in <strong>Fos</strong> immunoreactive cells in the mPFC, nucleus accumbens (NAc), basolateral amygdala (BLA), and lateral hypothalamus (LH) of rats treated repeatedly with <b>AMPH</b> when compared to vehicle treated controls.
+FOS	drug	amphetamine	18080115	The mPFC pyramidal neurons that project to the LH but not the NAc or BLA show a significant induction of <strong>Fos</strong> after repeated <b>AMPH</b> treatment.
+FOS	drug	nicotine	18053328	Repeated injections of <b>nicotine</b> can produce an increase in locomotor activity and the expression of immediate early gene, c <strong>fos</strong>, in the central dopaminergic areas.
+FOS	drug	nicotine	18053328	We examined the influence of CR or BER on repeated <b>nicotine</b> induced locomotor activity in rats and the change of c <strong>Fos</strong> expression in the brain by using immunohistochemistry.
+FOS	drug	nicotine	18053328	significantly inhibited the <b>nicotine</b> induced locomotor activity and expression of c <strong>Fos</strong> in the striatum and the nucleus accumbens.
+FOS	drug	alcohol	18001278	Effects of opioid receptor blockade on the renewal of <b>alcohol</b> seeking induced by context: relationship to c <strong>fos</strong> mRNA expression.
+FOS	drug	opioid	18001278	Effects of <b>opioid</b> receptor blockade on the renewal of alcohol seeking induced by context: relationship to c <strong>fos</strong> mRNA expression.
+FOS	addiction	relapse	18001278	Effects of opioid receptor blockade on the renewal of alcohol <b>seeking</b> induced by context: relationship to c <strong>fos</strong> mRNA expression.
+FOS	drug	alcohol	18001278	Re exposure to the <b>alcohol</b> associated context (ABA) significantly increased operant behaviour on the previously active lever relative to the AAA groups and this increased responding was associated with increased c <strong>fos</strong> mRNA expression in the basal and lateral amygdala and the CA3 subregion of the hippocampus.
+FOS	addiction	reward	18001278	Re exposure to the alcohol associated context (ABA) significantly increased <b>operant</b> behaviour on the previously active lever relative to the AAA groups and this increased responding was associated with increased c <strong>fos</strong> mRNA expression in the basal and lateral amygdala and the CA3 subregion of the hippocampus.
+FOS	drug	alcohol	18001278	<b>Naltrexone</b> pre treatment attenuated context induced <b>alcohol</b> seeking and inhibited c <strong>fos</strong> mRNA expression in the lateral amygdala and CA3.
+FOS	addiction	relapse	18001278	Naltrexone pre treatment attenuated context induced alcohol <b>seeking</b> and inhibited c <strong>fos</strong> mRNA expression in the lateral amygdala and CA3.
+FOS	addiction	sensitization	18000809	Therefore, we investigated whether MCH(1) receptor knockout (KO) mice are more susceptible than wild type (WT) mice to psychostimulant induced locomotor stimulation and <b>sensitization</b>, dopamine receptor mediated phosphorylation events and c <strong>fos</strong> expression within the frontal cortex and ventral striatum.
+FOS	drug	amphetamine	18000809	d <b>Amphetamine</b> (3 mg/kg) increased c <strong>fos</strong> expression within the frontal cortex in MCH(1) receptor KO mice, but not WT mice.
+FOS	drug	amphetamine	18000809	There were no d <b>amphetamine</b> induced changes in c <strong>fos</strong> expression within the ventromedial striatum in KO or WT mice.
+FOS	drug	amphetamine	17970739	We tested the hypothesis that <b>amphetamine</b> (<b>AMPH</b>) induced conditioned motor sensitization is accompanied by cellular activation (measured by <strong>Fos</strong> immunoreactivity) and synaptophysin immunoreactivity in reward related brain areas.
+FOS	addiction	reward	17970739	We tested the hypothesis that amphetamine (AMPH) induced conditioned motor sensitization is accompanied by cellular activation (measured by <strong>Fos</strong> immunoreactivity) and synaptophysin immunoreactivity in <b>reward</b> related brain areas.
+FOS	addiction	sensitization	17970739	We tested the hypothesis that amphetamine (AMPH) induced conditioned motor <b>sensitization</b> is accompanied by cellular activation (measured by <strong>Fos</strong> immunoreactivity) and synaptophysin immunoreactivity in reward related brain areas.
+FOS	drug	amphetamine	17970739	<b>AMPH</b> administered in the <b>AMPH</b> paired context increased the density of both <strong>Fos</strong> and synaptophysin immunoreactivity in the dentate gyrus, cornu ammonis (CA)1, CA3, basolateral amygdala and dorsolateral striatum.
+FOS	drug	amphetamine	17970739	Saline administered in the <b>AMPH</b> paired context increased the density of <strong>Fos</strong> immunoreactivity in the basolateral amygdala and nucleus accumbens core.
+FOS	addiction	relapse	17962567	Drug <b>seeking</b> and malaise both induced <strong>Fos</strong> expression, a marker of neuronal activation, in the insula.
+FOS	drug	amphetamine	17931790	The objective of this study was to characterize the effects of different <b>amphetamine</b> paradigms on the <strong>Fos</strong> activation of GABAergic interneurons that contain parvalbumin in the medial prefrontal cortex.
+FOS	drug	amphetamine	17931790	Although a sensitizing, repeated regimen of <b>amphetamine</b> induced <strong>Fos</strong> in all cortical layers, only layer V parvalbumin immunolabeled cells were activated in the infralimbic and prelimbic cortices.
+FOS	drug	amphetamine	17931790	An acute <b>amphetamine</b> injection to naive rats was associated with an increase in <strong>Fos</strong>, but in parvalbumin positive neurons of the prelimbic cortex, where it was preferentially induced in layer III.
+FOS	drug	opioid	17895918	Brain regional <strong>Fos</strong> expression elicited by the activation of mu  but not delta <b>opioid</b> receptors of the ventral tegmental area: evidence for an implication of the ventral thalamus in opiate reward.
+FOS	addiction	reward	17895918	Brain regional <strong>Fos</strong> expression elicited by the activation of mu  but not delta opioid receptors of the ventral tegmental area: evidence for an implication of the ventral thalamus in opiate <b>reward</b>.
+FOS	drug	opioid	17895918	In brains of mice tested for intra VTA <b>morphine</b> self administration, we analyzed regional <strong>Fos</strong> protein expression to investigate the neural circuitry underlying this behavior.
+FOS	drug	opioid	17895918	<b>Morphine</b> ICSA was associated with an increase in <strong>Fos</strong> within the nucleus accumbens, striatum, limbic cortices, amygdala, hippocampus, the lateral mammillary nucleus (LM), and the ventral posteromedial thalamus (VPM).
+FOS	drug	opioid	17895918	Abolition of <b>morphine</b> reward in MOR /  mice was associated with a decrease in <strong>Fos</strong> positive neurons in the mesocorticolimbic dopamine system, amygdala, hippocampus (CA1), LM, and a complete absence within the VPM.
+FOS	addiction	reward	17895918	Abolition of morphine <b>reward</b> in MOR /  mice was associated with a decrease in <strong>Fos</strong> positive neurons in the mesocorticolimbic dopamine system, amygdala, hippocampus (CA1), LM, and a complete absence within the VPM.
+FOS	addiction	reward	17878407	Because efferent orexinergic projections synapse on many targets through the mammalian brain, including mesotelencephalic regions and limbic systems involved in drug <b>reward</b> and <b>reinforcement</b>, we examined for coexpression of pCREB or c <strong>Fos</strong> double labeling within orexin A immunopositive neurons following sensitization.
+FOS	addiction	sensitization	17878407	Because efferent orexinergic projections synapse on many targets through the mammalian brain, including mesotelencephalic regions and limbic systems involved in drug reward and reinforcement, we examined for coexpression of pCREB or c <strong>Fos</strong> double labeling within orexin A immunopositive neurons following <b>sensitization</b>.
+FOS	drug	alcohol	17851539	<b>Alcohol</b> relapse induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+FOS	addiction	relapse	17851539	Alcohol <b>relapse</b> induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+FOS	drug	alcohol	17851539	In the second experiment, c <strong>Fos</strong> activation after reinstatement of <b>ethanol</b> seeking induced by discrete cues was compared with the activation pattern of its putative partner (c Jun) and regulators (extracellular signal regulated kinases and c Jun N terminal kinases).
+FOS	addiction	relapse	17851539	In the second experiment, c <strong>Fos</strong> activation after <b>reinstatement</b> of ethanol <b>seeking</b> induced by discrete cues was compared with the activation pattern of its putative partner (c Jun) and regulators (extracellular signal regulated kinases and c Jun N terminal kinases).
+FOS	drug	alcohol	17851539	Reexposure to <b>ethanol</b> associated context cues (an extinction session) potentiated c <strong>Fos</strong> expression within the basolateral and central amygdala.
+FOS	drug	alcohol	17851539	Repeated presentation of <b>ethanol</b> associated discrete cues in an extinction/reinstatement session led to even stronger c <strong>Fos</strong> activation in the latter nuclei.
+FOS	addiction	relapse	17851539	Repeated presentation of ethanol associated discrete cues in an extinction/<b>reinstatement</b> session led to even stronger c <strong>Fos</strong> activation in the latter nuclei.
+FOS	drug	alcohol	17723286	Effect of postnatal treadmill exercise on c <strong>Fos</strong> expression in the hippocampus of rat pups born from the <b>alcohol</b> intoxicated mothers.
+FOS	drug	alcohol	17723286	In the present study, we investigated the influence of postnatal treadmill running on the c <strong>Fos</strong> expression in the hippocampus of rat pups born from the <b>alcohol</b> intoxicated mothers.
+FOS	drug	alcohol	17723286	The results obtained show that maternal <b>alcohol</b> intoxication suppressed c <strong>Fos</strong> expression in the hippocampus of rat pups and that postnatal treadmill exercise enhanced c <strong>Fos</strong> expression in the hippocampus of these rat pups.
+FOS	addiction	intoxication	17723286	The results obtained show that maternal alcohol <b>intoxication</b> suppressed c <strong>Fos</strong> expression in the hippocampus of rat pups and that postnatal treadmill exercise enhanced c <strong>Fos</strong> expression in the hippocampus of these rat pups.
+FOS	drug	amphetamine	17720257	Repeated <b>amphetamine</b> administration outside the home cage enhances drug induced <strong>Fos</strong> expression in rat nucleus accumbens.
+FOS	drug	amphetamine	17720257	Induction of the immediate early gene protein product <strong>Fos</strong> has been used extensively to assess neural activation in the striatum after repeated <b>amphetamine</b> administration to rats in their home cages.
+FOS	drug	amphetamine	17720257	We determined the dose response relationship for <b>amphetamine</b> induced psychomotor activity and <strong>Fos</strong> expression in nucleus accumbens and caudate putamen 1 week after repeated administration of <b>amphetamine</b> or saline in locomotor activity chambers.
+FOS	drug	amphetamine	17720257	Repeated administration of <b>amphetamine</b> enhanced <b>amphetamine</b> induced locomotor activity and stereotypy and <strong>Fos</strong> expression in nucleus accumbens, but not in caudate putamen.
+FOS	drug	amphetamine	17720257	In comparison, levels of <strong>Fos</strong> expression induced by 1mg/kg <b>amphetamine</b> were not altered in nucleus accumbens or caudate putamen by repeated <b>amphetamine</b> administration in the home cage.
+FOS	drug	amphetamine	17720257	Furthermore, repeated <b>amphetamine</b> administration increased drug induced <strong>Fos</strong> expression in enkephalin positive, but not enkephalin negative, neurons in nucleus accumbens.
+FOS	drug	amphetamine	17714194	The distribution of VTA projecting neurons activated by <b>amphetamine</b> was examined by combining retrograde transport of the cholera toxin beta subunit (CTb), injected into the VTA, with immunodetection of <strong>Fos</strong>.
+FOS	drug	amphetamine	17714194	The quantitative analysis of CTb <strong>Fos</strong> double labelling demonstrates that <b>amphetamine</b> induced a rapid activation of <strong>Fos</strong> in a large number of brain areas projecting to the VTA.
+FOS	drug	benzodiazepine	17669374	Brainstem areas activated by <b>diazepam</b> withdrawal as measured by <strong>Fos</strong> protein immunoreactivity in rats.
+FOS	addiction	withdrawal	17669374	Brainstem areas activated by diazepam <b>withdrawal</b> as measured by <strong>Fos</strong> protein immunoreactivity in rats.
+FOS	drug	benzodiazepine	17669374	In this study, we examined the <strong>Fos</strong> immunoreactivity in brain structures known to be implicated in the neural substrates of aversion in rats under spontaneous <b>diazepam</b> withdrawal.
+FOS	addiction	aversion	17669374	In this study, we examined the <strong>Fos</strong> immunoreactivity in brain structures known to be implicated in the neural substrates of <b>aversion</b> in rats under spontaneous diazepam withdrawal.
+FOS	addiction	withdrawal	17669374	In this study, we examined the <strong>Fos</strong> immunoreactivity in brain structures known to be implicated in the neural substrates of aversion in rats under spontaneous diazepam <b>withdrawal</b>.
+FOS	drug	opioid	17642469	Some of them are: DREAM which constitututively suppresses transcription of mRNA for <b>opioid</b> peptides, oncostatin M, COX 2 inhibitors, <strong>cFOS</strong> protein, tachykinins, gamma butyric acid agonist, L type Ca++ channels.
+FOS	drug	opioid	17601555	Moreover, <b>morphine</b> withdrawal induces <strong>Fos</strong> expression, increase in cyclic AMP and cyclic GMP levels.
+FOS	addiction	withdrawal	17601555	Moreover, morphine <b>withdrawal</b> induces <strong>Fos</strong> expression, increase in cyclic AMP and cyclic GMP levels.
+FOS	drug	benzodiazepine	17601555	Co administration of rolipram or <b>diazepam</b> with morphine during the pre treatment period significantly reduces the signs of withdrawal symptoms, the enhancement of NA turnover, the increase in cyclic AMP and the <strong>Fos</strong> expression.
+FOS	drug	opioid	17601555	Co administration of rolipram or diazepam with <b>morphine</b> during the pre treatment period significantly reduces the signs of withdrawal symptoms, the enhancement of NA turnover, the increase in cyclic AMP and the <strong>Fos</strong> expression.
+FOS	addiction	withdrawal	17601555	Co administration of rolipram or diazepam with morphine during the pre treatment period significantly reduces the signs of <b>withdrawal</b> symptoms, the enhancement of NA turnover, the increase in cyclic AMP and the <strong>Fos</strong> expression.
+FOS	drug	alcohol	17570346	Animals were exposed to environmental stimuli previously associated with <b>ethanol</b> availability (EtOH S+), and sections from the hypothalamus and paraventricular thalamus (PVT), a recipient of CART and orexin innervation, were dual labeled for <strong>Fos</strong> protein and either CART or orexin.
+FOS	drug	opioid	17549049	We have previously demonstrated that <b>morphine</b> withdrawal induced hyperactivity of the heart by activation of noradrenergic pathways innervating the left and right ventricle, as evaluated by noradrenaline turnover and c <strong>Fos</strong> expression.
+FOS	addiction	withdrawal	17549049	We have previously demonstrated that morphine <b>withdrawal</b> induced hyperactivity of the heart by activation of noradrenergic pathways innervating the left and right ventricle, as evaluated by noradrenaline turnover and c <strong>Fos</strong> expression.
+FOS	drug	opioid	17549049	<b>Naloxone</b> induced <b>morphine</b> withdrawal activated ERK1/2 and increased c <strong>Fos</strong> expression in cardiac tissues.
+FOS	addiction	withdrawal	17549049	Naloxone induced morphine <b>withdrawal</b> activated ERK1/2 and increased c <strong>Fos</strong> expression in cardiac tissues.
+FOS	drug	alcohol	17531293	<strong>FOS</strong> expression induced by an <b>ethanol</b> paired conditioned stimulus.
+FOS	drug	alcohol	17531293	To identify brain areas involved in <b>ethanol</b> induced Pavlovian conditioning, brains of male DBA/2J mice were immunohistochemically analyzed for <strong>FOS</strong> expression after exposure to a conditioned stimulus (CS) previously paired with <b>ethanol</b> (2 g/kg) in two experiments.
+FOS	drug	opioid	17467070	<b>Morphine</b> self administration into the lateral septum depends on dopaminergic mechanisms: Evidence from pharmacology and <strong>Fos</strong> neuroimaging.
+FOS	drug	opioid	17467070	Mice acquired self administration behaviour for intra LS <b>morphine</b> that was associated with increased <strong>Fos</strong> expression in the ventral tegmental area (VTA), dorsal and ventral striatum and prefrontal cortex.
+FOS	drug	nicotine	17420096	Acute <b>nicotine</b> enhances c <strong>fos</strong> mRNA expression differentially in reward related substrates of adolescent and adult rat brain.
+FOS	addiction	reward	17420096	Acute nicotine enhances c <strong>fos</strong> mRNA expression differentially in <b>reward</b> related substrates of adolescent and adult rat brain.
+FOS	drug	nicotine	17420096	To help determine the potential brain circuitry involved, we investigated the effect of acute <b>nicotine</b> administration (0.4 or 0.8mg/kg, s.c.) on the expression of c <strong>fos</strong> mRNA in the brains of adolescent (P35) and adult (P67 70) male Wistar rats using in situ hybridization.
+FOS	drug	nicotine	17420096	<b>Nicotine</b> administration increased c <strong>fos</strong> mRNA expression in several brain regions, including the central amygdala, locus coeruleus, nucleus accumbens core, paraventricular nucleus of the hypothalamus and lateral septum of adolescent and adult rats.
+FOS	drug	nicotine	17420096	<b>Nicotine</b> increased c <strong>fos</strong> mRNA expression more robustly in the bed nucleus of the stria terminalis, nucleus accumbens shell and ventral tegmental area in adolescent rats.
+FOS	drug	opioid	17392735	Modulatory effect of environmental context and drug history on <b>heroin</b> induced psychomotor activity and <strong>fos</strong> protein expression in the rat brain.
+FOS	drug	opioid	17392735	The goal of the present study was to investigate the role of environmental context and drug history in modulating the effects of <b>heroin</b> on locomotor activity and <strong>Fos</strong> protein expression in the neocortex and striatal complex of the rat.
+FOS	drug	opioid	17392735	induced psychomotor sensitization only when the treatment was administered in a relatively 'novel' environment (ie, a unique test environment distinct from the home cage) but not when the same treatment was administered in the home cage; (2) environmental novelty facilitated <b>heroin</b> induced <strong>Fos</strong> expression in the caudate, particularly in its most caudal regions; (3) environmental context also modulated <b>heroin</b> induced <strong>Fos</strong> expression in the nucleus accumbens and in the neocortex; (4) repeated exposures to <b>heroin</b> dramatically altered its effects on <strong>Fos</strong> expression in the caudate and in the neocortex; and (5) <strong>Fos</strong> protein levels in the postero dorsal caudate, in the shell of the nucleus accumbens, and in the barrel field cortex predicted most of the variance in <b>heroin</b> induced activity scores, as shown by multiple regression analysis.
+FOS	addiction	sensitization	17392735	induced psychomotor <b>sensitization</b> only when the treatment was administered in a relatively 'novel' environment (ie, a unique test environment distinct from the home cage) but not when the same treatment was administered in the home cage; (2) environmental novelty facilitated heroin induced <strong>Fos</strong> expression in the caudate, particularly in its most caudal regions; (3) environmental context also modulated heroin induced <strong>Fos</strong> expression in the nucleus accumbens and in the neocortex; (4) repeated exposures to heroin dramatically altered its effects on <strong>Fos</strong> expression in the caudate and in the neocortex; and (5) <strong>Fos</strong> protein levels in the postero dorsal caudate, in the shell of the nucleus accumbens, and in the barrel field cortex predicted most of the variance in heroin induced activity scores, as shown by multiple regression analysis.
+FOS	drug	psychedelics	17383105	<b>MDMA</b> (5 mg/kg) activated oxytocin containing neurons in the supraoptic and paraventricular nuclei of the hypothalamus, as shown by <strong>Fos</strong> immunohistochemistry.
+FOS	drug	alcohol	17360123	ABA renewal of <b>alcohol</b> seeking was associated with selective increases in c <strong>Fos</strong> protein induction in basolateral amygdala, ventral accumbens shell, and lateral hypothalamus (renewal associated <strong>Fos</strong>).
+FOS	addiction	relapse	17360123	ABA renewal of alcohol <b>seeking</b> was associated with selective increases in c <strong>Fos</strong> protein induction in basolateral amygdala, ventral accumbens shell, and lateral hypothalamus (renewal associated <strong>Fos</strong>).
+FOS	drug	alcohol	17360123	However, c <strong>Fos</strong> induction in either lateral hypothalamic orexin negative or orexin positive neurons was positively and significantly correlated with <b>alcohol</b> seeking.
+FOS	addiction	relapse	17360123	However, c <strong>Fos</strong> induction in either lateral hypothalamic orexin negative or orexin positive neurons was positively and significantly correlated with alcohol <b>seeking</b>.
+FOS	addiction	reward	17301168	We found that NAc and VP hotspots reciprocally modulated <strong>Fos</strong> expression in each other and that the two hotspots were needed together to enhance sucrose "liking" reactions, essentially cooperating within a single <b>hedonic</b> NAc VP circuit.
+FOS	drug	psychedelics	17289273	High ambient temperature increases 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>, "<b>ecstasy</b>") induced <strong>Fos</strong> expression in a region specific manner.
+FOS	drug	psychedelics	17289273	The present study investigated whether ambient temperature influences <b>MDMA</b> induced expression of <strong>Fos</strong>, a marker of neural activation.
+FOS	drug	psychedelics	17289273	or saline, and were placed in test chambers for 2 h at either 19 or 30 degrees C. <b>MDMA</b> caused significant hyperthermia at 30 degrees C and a modest hypothermia at 19 degrees C. The 30 degrees C ambient temperature had little effect on <strong>Fos</strong> expression in vehicle treated rats.
+FOS	drug	psychedelics	17289273	However <b>MDMA</b> induced <strong>Fos</strong> expression was augmented in 15 of 30 brain regions at the high temperature.
+FOS	drug	psychedelics	17289273	<b>MDMA</b> induced <strong>Fos</strong> expression was unaffected by ambient temperature at many other sites, and was diminished at high temperature at one site (the islands of Calleja), suggesting that the effect of temperature on <b>MDMA</b> induced <strong>Fos</strong> expression was not a general pharmacokinetic effect.
+FOS	drug	nicotine	17287824	<b>Nicotine</b> induced c <strong>fos</strong> expression in the bed nucleus of the stria terminalis, the central nucleus of the amygdala (CeA), nucleus accumbens, and the superior colliculus (SC) at both ages, whereas it activated the hypothalamic paraventricular nucleus (PVN) and consequent corticosterone secretion only in adults.
+FOS	drug	nicotine	17287824	Acetaldehyde potentiated <b>nicotine</b> induced c <strong>fos</strong> in CeA and SC, and activation of PVN c <strong>fos</strong> expression/plasma corticosterone release; however, this drug interaction was only observed in behaviorally tested animals, not those that were minimally stressed.
+FOS	drug	opioid	17286593	To reveal secretory, activational and transcriptional changes in the hypothalamus of <b>morphine</b> dependent rats during <b>naloxone</b> precipitated <b>opioid</b> withdrawal, we measured corticosterone secretion, c <strong>Fos</strong> induction and heteronuclear (hn)RNA levels of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP) in naïve and <b>morphine</b> dependent animals injected with saline or 5 mg/kg <b>naloxone</b>.
+FOS	addiction	withdrawal	17286593	To reveal secretory, activational and transcriptional changes in the hypothalamus of morphine dependent rats during naloxone precipitated opioid <b>withdrawal</b>, we measured corticosterone secretion, c <strong>Fos</strong> induction and heteronuclear (hn)RNA levels of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP) in naïve and morphine dependent animals injected with saline or 5 mg/kg naloxone.
+FOS	drug	amphetamine	17276509	Both HRs and LRs expressed <b>amphetamine</b> induced sensitized locomotor activation and increased expression of <strong>Fos</strong> protein.
+FOS	addiction	sensitization	17276509	Treatment with SR48692 prevented behavioral <b>sensitization</b> and <strong>Fos</strong> protein expression enhancement in LRs but not in HRs mice.
+FOS	drug	cocaine	17276011	<strong>Fos</strong> and glutamate AMPA receptor subunit coexpression associated with cue elicited <b>cocaine</b> seeking behavior in abstinent rats.
+FOS	addiction	relapse	17276011	<strong>Fos</strong> and glutamate AMPA receptor subunit coexpression associated with cue elicited cocaine <b>seeking</b> behavior in abstinent rats.
+FOS	drug	cocaine	17276011	We have reported an increase in neuronal activation in rats, measured by <strong>Fos</strong> protein expression, in various limbic and cortical regions following exposure to <b>cocaine</b> associated cues.
+FOS	drug	cocaine	17276011	responses without <b>cocaine</b> reinforcement) and <strong>Fos</strong> and AMPA glutamate receptor subunits were measured postmortem using immunocytochemistry.
+FOS	addiction	reward	17276011	responses without cocaine <b>reinforcement</b>) and <strong>Fos</strong> and AMPA glutamate receptor subunits were measured postmortem using immunocytochemistry.
+FOS	drug	cocaine	17276011	The No Extinction group exhibited increases in <b>cocaine</b> seeking behavior and <strong>Fos</strong> expression in limbic and cortical regions relative to the Extinction group.
+FOS	addiction	relapse	17276011	The No Extinction group exhibited increases in cocaine <b>seeking</b> behavior and <strong>Fos</strong> expression in limbic and cortical regions relative to the Extinction group.
+FOS	drug	cocaine	17276011	Importantly, there was an increase in the percentage of cells colabeled with <strong>Fos</strong> and GluR1 in the anterior cingulate and nucleus accumbens shell and cells colabeled with <strong>Fos</strong> and GluR4 in the infralimbic cortex, suggesting that within these regions, a greater, and perhaps even different, population of AMPA receptor subunit expressing neurons is activated in rats engaged in <b>cocaine</b> seeking behavior.
+FOS	addiction	relapse	17276011	Importantly, there was an increase in the percentage of cells colabeled with <strong>Fos</strong> and GluR1 in the anterior cingulate and nucleus accumbens shell and cells colabeled with <strong>Fos</strong> and GluR4 in the infralimbic cortex, suggesting that within these regions, a greater, and perhaps even different, population of AMPA receptor subunit expressing neurons is activated in rats engaged in cocaine <b>seeking</b> behavior.
+FOS	drug	opioid	17216288	Differential involvement of 3', 5' cyclic adenosine monophosphate dependent protein kinase in regulation of <strong>Fos</strong> and tyrosine hydroxylase expression in the heart after <b>naloxone</b> induced <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	17216288	Differential involvement of 3', 5' cyclic adenosine monophosphate dependent protein kinase in regulation of <strong>Fos</strong> and tyrosine hydroxylase expression in the heart after naloxone induced morphine <b>withdrawal</b>.
+FOS	drug	opioid	17216288	We previously demonstrated that <b>morphine</b> withdrawal induced hyperactivity of the heart by the activation of noradrenergic pathways innervating the left and right ventricle, as evaluated by noradrenaline (NA) turnover and <strong>Fos</strong> expression.
+FOS	addiction	withdrawal	17216288	We previously demonstrated that morphine <b>withdrawal</b> induced hyperactivity of the heart by the activation of noradrenergic pathways innervating the left and right ventricle, as evaluated by noradrenaline (NA) turnover and <strong>Fos</strong> expression.
+FOS	drug	opioid	17216288	Moreover, <b>morphine</b> withdrawal induces <strong>Fos</strong> expression, an enhancement of NA turnover and an increase in the total TH levels.
+FOS	addiction	withdrawal	17216288	Moreover, morphine <b>withdrawal</b> induces <strong>Fos</strong> expression, an enhancement of NA turnover and an increase in the total TH levels.
+FOS	drug	opioid	17216288	However, this inhibitor neither modifies the <b>morphine</b> withdrawal induced <strong>Fos</strong> expression nor the increase of nonphosphorylated TH levels.
+FOS	addiction	withdrawal	17216288	However, this inhibitor neither modifies the morphine <b>withdrawal</b> induced <strong>Fos</strong> expression nor the increase of nonphosphorylated TH levels.
+FOS	drug	opioid	17216288	The present findings indicate that an up regulated PKA dependent transduction pathway might contribute to the activation of the cardiac catecholaminergic neurons in response to <b>morphine</b> withdrawal and suggest that <strong>Fos</strong> is not a target of PKA at heart levels.
+FOS	addiction	withdrawal	17216288	The present findings indicate that an up regulated PKA dependent transduction pathway might contribute to the activation of the cardiac catecholaminergic neurons in response to morphine <b>withdrawal</b> and suggest that <strong>Fos</strong> is not a target of PKA at heart levels.
+FOS	drug	alcohol	17190973	Long lasting reductions of <b>ethanol</b> drinking, enhanced <b>ethanol</b> induced sedation, and decreased c <strong>fos</strong> expression in the Edinger Westphal nucleus in Wistar rats exposed to the organophosphate chlorpyrifos.
+FOS	drug	alcohol	17190973	An immunocytochemical assay revealed reduced c <strong>fos</strong> expression in the Edinger Westphal nucleus following CPF treatment, a critical brain area that has been implicated in <b>ethanol</b> intake and sedation.
+FOS	drug	cocaine	17182779	c <strong>Fos</strong> facilitates the acquisition and extinction of <b>cocaine</b> induced persistent changes.
+FOS	drug	cocaine	17182779	We examined a potential role of the immediate early gene <strong>Fos</strong>, which is robustly and rapidly induced by <b>cocaine</b> via D1 receptors, in mediating <b>cocaine</b> induced persistent neurobiological changes by creating and analyzing a mouse in which <strong>Fos</strong> is primarily disrupted in D1 receptor expressing neurons in the brain.
+FOS	drug	cocaine	17182779	We show that the expression levels of several transcription factors, neurotransmitter receptors, and intracellular signaling molecules induced by repeated <b>cocaine</b> administration are altered in <strong>Fos</strong> deficient brains.
+FOS	drug	cocaine	17182779	Our findings indicate that c <strong>Fos</strong> produced in D1 receptor expressing neurons integrates mechanisms to facilitate both the acquisition and extinction of <b>cocaine</b> induced persistent changes.
+FOS	drug	opioid	17173187	Furthermore, following the treatment with BAM22 (10 nmol) on day 8 in <b>morphine</b> tolerance rats, <b>morphine</b> administered on day 9 decreased the expressions of the heat evoked c <strong>Fos</strong> like immunoreactivity (FLI) protein by approximately 80% in laminae I II, III IV and V VI in the spinal cord at L4 L5 compared with that in saline or <b>morphine</b> group.
+FOS	drug	cocaine	17161392	We previously reported that brief (1 h), but not extended (6 h), daily access to <b>cocaine</b> results in a sensitized locomotor response to <b>cocaine</b> and in elevated c <strong>Fos</strong> immunoreactivity and DAT binding in the nucleus accumbens (N.Acc) core.
+FOS	drug	alcohol	17127267	Recent findings indicate that low concentrations of <b>ethanol</b> (10 mM) promote inflammatory processes in brain and in glial cells by up regulating cytokines and inflammatory mediators (iNOS, NO, COX 2), and by activating signaling pathways (IKK, MAPKs) and transcriptional factors (NF kappaB, <strong>AP 1</strong>) implicated in inflammatory injury.
+FOS	drug	opioid	17123639	To determine the brain regions involved in this altered reward behavior, we examined neural activation (as indexed by <strong>Fos</strong> like proteins) induced by a preference test for a food associated environment in 5 week <b>morphine</b> abstinent versus non dependent animals.
+FOS	addiction	reward	17123639	To determine the brain regions involved in this altered <b>reward</b> behavior, we examined neural activation (as indexed by <strong>Fos</strong> like proteins) induced by a preference test for a food associated environment in 5 week morphine abstinent versus non dependent animals.
+FOS	drug	opioid	17123639	In contrast, <strong>Fos</strong> expression in stress associated brain areas, including the ventral lateral bed nucleus of the stria terminalis (VL BNST), central nucleus of the amygdala (CE), and noradrenergic (A2) neurons in the nucleus tractus solitarius (NTS) was significantly elevated only in <b>morphine</b> abstinent animals.
+FOS	addiction	relapse	17098214	Rats were tested in a conditioned <b>reinstatement</b> model of <b>relapse</b> with subsequent examination of brain c <strong>fos</strong> expression patterns elicited by an EtOH S(+) versus a cue associated with nonreward (S( )).
+FOS	drug	alcohol	17098214	<b>Naltrexone</b> suppressed the S(+) induced reinstatement and attenuated hippocampal CA3 c <strong>fos</strong> expression, while increasing neural activity in the extended amygdala and PVN.
+FOS	addiction	relapse	17098214	Naltrexone suppressed the S(+) induced <b>reinstatement</b> and attenuated hippocampal CA3 c <strong>fos</strong> expression, while increasing neural activity in the extended amygdala and PVN.
+FOS	drug	opioid	17079516	Modern neuroscience tools such as <strong>Fos</strong> plume mapping have further identified hedonic hot spots within the accumbens and pallidum, where <b>opioids</b> are especially tuned to magnify 'liking' of food rewards.
+FOS	addiction	reward	17079516	Modern neuroscience tools such as <strong>Fos</strong> plume mapping have further identified <b>hedonic</b> hot spots within the accumbens and pallidum, where opioids are especially tuned to magnify 'liking' of food rewards.
+FOS	drug	amphetamine	17067306	To better understand the brain changes that accompany this process, we used immunohistochemistry for c <strong>Fos</strong> (a neuronal activity marker), synaptophysin (a marker for synaptogenesis) and tyrosine kinase B receptor (a neurotrophic factor receptor that mediates synaptic plasticity) to investigate the neural substrates of <b>amphetamine</b> induced conditioned place preference in rats.
+FOS	drug	amphetamine	17067306	Furthermore, <b>amphetamine</b> conditioning increased the density of c <strong>Fos</strong> immunoreactive cells and these cells were fully colocalized with the tyrosine kinase B receptor in the dentate gyrus, CA1 field and basolateral amygdala.
+FOS	drug	psychedelics	17023106	We selected doses of <b>MDMA</b> (2, 6, 10 mg/kg) previously reported to induce CPP in mice and we measured expression of c <strong>Fos</strong> evoked by the treatments in non confronted mice.
+FOS	addiction	reward	17023106	We selected doses of MDMA (2, 6, 10 mg/kg) previously reported to induce <b>CPP</b> in mice and we measured expression of c <strong>Fos</strong> evoked by the treatments in non confronted mice.
+FOS	drug	psychedelics	17023106	<b>MDMA</b> induced c <strong>Fos</strong> protein in several corticolimbic regions involved in drug induced reward.
+FOS	addiction	reward	17023106	MDMA induced c <strong>Fos</strong> protein in several corticolimbic regions involved in drug induced <b>reward</b>.
+FOS	drug	opioid	17015856	<b>Opioid</b> modulation of <strong>Fos</strong> protein expression and olfactory circuitry plays a pivotal role in what neonates remember.
+FOS	drug	opioid	17015856	Experiment 1 assessed post training <b>opioid</b> modulation of <strong>Fos</strong> protein expression within olfactory circuitry (olfactory bulb, piriform cortex, amygdala).
+FOS	drug	opioid	17015856	Post training <b>opioid</b> receptor antagonism (odor aversion) prevented the learning induced changes in the anterior piriform cortex and also induced significant changes in <strong>Fos</strong> protein expression in the central nucleus of the amygdala.
+FOS	addiction	aversion	17015856	Post training opioid receptor antagonism (odor <b>aversion</b>) prevented the learning induced changes in the anterior piriform cortex and also induced significant changes in <strong>Fos</strong> protein expression in the central nucleus of the amygdala.
+FOS	drug	opioid	17015856	Overall, results demonstrate that <b>opioids</b> modulate memory consolidation in the neonate via modulating <strong>Fos</strong> protein expression in olfactory circuitry.
+FOS	drug	alcohol	17005860	Activation of group II metabotropic glutamate receptors attenuates both stress and cue induced <b>ethanol</b> seeking and modulates c <strong>fos</strong> expression in the hippocampus and amygdala.
+FOS	addiction	relapse	17005860	Activation of group II metabotropic glutamate receptors attenuates both stress and cue induced ethanol <b>seeking</b> and modulates c <strong>fos</strong> expression in the hippocampus and amygdala.
+FOS	drug	opioid	16962578	In addition, agmatine (1 microM) co pretreated with <b>morphine</b> attenuated the <b>naloxone</b> precipitated increases of cAMP responsive element binding protein and extracellular signal regulated kinase 1/2 phosphorylations and c <strong>Fos</strong> expression in CHO mu/IRAS.
+FOS	drug	cannabinoid	16954596	In the latter areas, ERK activation after chronic <b>THC</b> increased the transcription factors cyclic adenosine monophosphate response element binding protein and <strong>Fos</strong> B as well as a downstream protein known as brainderived neurotrophic factor.
+FOS	drug	opioid	16935424	<b>Naloxone</b> challenge to <b>morphine</b> treated animals precipitated an intense withdrawal syndrome that depleted CGRP immunoreactivity and increased <strong>Fos</strong> expression in the dorsal horn.
+FOS	addiction	withdrawal	16935424	Naloxone challenge to morphine treated animals precipitated an intense <b>withdrawal</b> syndrome that depleted CGRP immunoreactivity and increased <strong>Fos</strong> expression in the dorsal horn.
+FOS	addiction	withdrawal	16935424	The <strong>Fos</strong> response primarily occurred in neurons that expressed CGRP receptor component protein (RCP) suggesting CGRP activity contributes to neuronal activation during precipitated <b>withdrawal</b>.
+FOS	drug	cocaine	16930414	<b>Cocaine</b> induced locomotor activity and <strong>Fos</strong> expression in nucleus accumbens are sensitized for 6 months after repeated <b>cocaine</b> administration outside the home cage.
+FOS	drug	cocaine	16930414	Induction of the immediate early gene protein product <strong>Fos</strong> has been used extensively to assess neural activation in the striatum after repeated <b>cocaine</b> administration to rats in their home cages but rarely after repeated administration outside the home cage, which produces more robust locomotor sensitization.
+FOS	addiction	sensitization	16930414	Induction of the immediate early gene protein product <strong>Fos</strong> has been used extensively to assess neural activation in the striatum after repeated cocaine administration to rats in their home cages but rarely after repeated administration outside the home cage, which produces more robust locomotor <b>sensitization</b>.
+FOS	drug	cocaine	16930414	In the present study, we found <b>cocaine</b> induced <strong>Fos</strong> expression in nucleus accumbens, but not caudate putamen, was enhanced 1 and 6 months after repeated drug administration in locomotor activity chambers.
+FOS	drug	cocaine	16930414	In contrast, <b>cocaine</b> induced <strong>Fos</strong> expression was absent altogether in nucleus accumbens and unaltered in caudate putamen 1 month after repeated <b>cocaine</b> administration in the home cage.
+FOS	drug	cocaine	16930414	Bilateral infusions of the GABA agonists baclofen and muscimol (1 microg/side) into nucleus accumbens of sensitized rats blocked <b>cocaine</b> induced <strong>Fos</strong> expression and locomotor activity.
+FOS	drug	amphetamine	16855532	Forty three genes exhibited significant differences in expression in HR vs LR 24 h after <b>METH</b> treatment including a group of immediate early genes (IEGs) (eg, c <strong>fos</strong>, junB, NGFI B, serum regulated glucocorticoid kinase).
+FOS	drug	opioid	16806705	There are two principal findings: (1) intrathecal pretreatment with wortmannin or LY294002, two structurally unrelated PI3K inhibitors, produced a dose dependent increase of <b>naloxone</b> precipitated withdrawal jumping, which was accompanied by an increased expression of spinal <strong>Fos</strong> protein in acute and chronic <b>morphine</b> dependent mice; and (2) the expression of spinal p110gamma, the catalytic subunit PI3K, in the membrane fraction was significantly down regulated by <b>naloxone</b> precipitated withdrawal in acute and chronic <b>morphine</b> dependent mice.
+FOS	addiction	withdrawal	16806705	There are two principal findings: (1) intrathecal pretreatment with wortmannin or LY294002, two structurally unrelated PI3K inhibitors, produced a dose dependent increase of naloxone precipitated <b>withdrawal</b> jumping, which was accompanied by an increased expression of spinal <strong>Fos</strong> protein in acute and chronic morphine dependent mice; and (2) the expression of spinal p110gamma, the catalytic subunit PI3K, in the membrane fraction was significantly down regulated by naloxone precipitated <b>withdrawal</b> in acute and chronic morphine dependent mice.
+FOS	drug	opioid	16787418	Re exposure to the cue after 3 weeks of withdrawal reinstated <b>heroin</b> seeking behaviour, which resulted in IEG expression of ania 3, MKP 1, c <strong>fos</strong> and Nr4a3 in the medial prefrontal cortex (mPFC), and of ania 3 in the orbital frontal cortex (OFC) and nucleus accumbens core (NAC).
+FOS	addiction	relapse	16787418	Re exposure to the cue after 3 weeks of withdrawal reinstated heroin <b>seeking</b> behaviour, which resulted in IEG expression of ania 3, MKP 1, c <strong>fos</strong> and Nr4a3 in the medial prefrontal cortex (mPFC), and of ania 3 in the orbital frontal cortex (OFC) and nucleus accumbens core (NAC).
+FOS	addiction	withdrawal	16787418	Re exposure to the cue after 3 weeks of <b>withdrawal</b> reinstated heroin seeking behaviour, which resulted in IEG expression of ania 3, MKP 1, c <strong>fos</strong> and Nr4a3 in the medial prefrontal cortex (mPFC), and of ania 3 in the orbital frontal cortex (OFC) and nucleus accumbens core (NAC).
+FOS	drug	alcohol	16750178	Lack of evidence of a role for the neurosteroid allopregnanolone in <b>ethanol</b> induced reward and c <strong>fos</strong> expression in DBA/2 mice.
+FOS	addiction	reward	16750178	Lack of evidence of a role for the neurosteroid allopregnanolone in ethanol induced <b>reward</b> and c <strong>fos</strong> expression in DBA/2 mice.
+FOS	drug	alcohol	16750178	induced conditioned place preference and c <strong>fos</strong> expression in DBA/2 mice; a strain known to be particularly sensitive to <b>ethanol</b>.
+FOS	drug	alcohol	16750178	<b>Ethanol</b> administration induced a clear conditioned place preference and widespread c <strong>fos</strong> expression, with elements of the extended amygdala, Edinger Westphal nucleus and paraventricular nucleus being especially sensitive.
+FOS	drug	alcohol	16750178	However, despite an approximately 99% decrease in whole brain allopregnanolone content, finasteride pretreatment had remarkably little effect on either <b>ethanol</b> induced conditioned place preference or <b>ethanol</b> induced c <strong>fos</strong> expression.
+FOS	drug	alcohol	16750178	Thus, aside from a general stimulatory effect on c <strong>fos</strong> expression in the ventral tegmental area, and generally mild depression of locomotor activity, no other effects of finasteride or interaction with <b>ethanol</b> effects were identifiable.
+FOS	drug	amphetamine	16713106	Habituation to the test cage influences <b>amphetamine</b> induced locomotion and <strong>Fos</strong> expression and increases FosB/DeltaFosB like immunoreactivity in mice.
+FOS	drug	amphetamine	16713106	The present experiments tested the effects of repeated exposure to a test cage (1 h daily for four consecutive days) on <b>amphetamine</b> induced locomotion and <strong>Fos</strong> expression as well as on FosB/DeltaFosB like immunoreactivity in mice of the C57BL/6J and DBA/2J inbred strains that differ for the response to <b>amphetamine</b>, stress and novelty.
+FOS	drug	amphetamine	16713106	Moreover, previous habituation to the test cage reduced the locomotor response to a low dose of <b>amphetamine</b> only in DBA mice while it reduced <b>amphetamine</b> induced <strong>Fos</strong> expression in medial prefrontal cortex, dorsal caudate and the accumbens shell of mice of the C57 strain.
+FOS	drug	amphetamine	16713106	Moreover, they suggest that the procedure of daily familiarization influences the pattern of brain <strong>Fos</strong> expression induced by <b>amphetamine</b>.
+FOS	drug	opioid	16712881	U0126 in the spinal cord were accompanied by decreased scores of <b>morphine</b> withdrawal and the inhibited spinal <strong>Fos</strong> protein (a maker for neuronal excitation or activation) expression induced by <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	16712881	U0126 in the spinal cord were accompanied by decreased scores of morphine <b>withdrawal</b> and the inhibited spinal <strong>Fos</strong> protein (a maker for neuronal excitation or activation) expression induced by morphine <b>withdrawal</b>.
+FOS	drug	cocaine	16712814	Brief daily access produced stable consumption of the drug and, after withdrawal, a sensitized locomotor response and an enhanced c <strong>Fos</strong> labeling to a single <b>cocaine</b> challenge.
+FOS	addiction	withdrawal	16712814	Brief daily access produced stable consumption of the drug and, after <b>withdrawal</b>, a sensitized locomotor response and an enhanced c <strong>Fos</strong> labeling to a single cocaine challenge.
+FOS	drug	cocaine	16710312	Furthermore, both compounds also efficiently blocked <b>cocaine</b> induced <strong>Fos</strong> induction in the striatal complex.
+FOS	drug	amphetamine	16687500	c <strong>Fos</strong> positive neurons were increased in the prefrontal cortex in <b>amphetamine</b> treated Adcyap1( / ) mice, suggesting increased inhibitory control by prefrontal neurons.
+FOS	drug	opioid	16650614	The possibility that descending facilitation from the rostral ventromedial medulla is required for the maintenance of central sensitization was examined by determining whether ablation of mu <b>opioid</b> receptor expressing cells within the rostral ventromedial medulla prevented the enhanced expression of repetitive touch evoked <strong>FOS</strong> within the spinal cord of animals with spinal nerve ligation injury as well as nerve injury induced behavioral hypersensitivity.
+FOS	addiction	sensitization	16650614	The possibility that descending facilitation from the rostral ventromedial medulla is required for the maintenance of central <b>sensitization</b> was examined by determining whether ablation of mu opioid receptor expressing cells within the rostral ventromedial medulla prevented the enhanced expression of repetitive touch evoked <strong>FOS</strong> within the spinal cord of animals with spinal nerve ligation injury as well as nerve injury induced behavioral hypersensitivity.
+FOS	drug	nicotine	16631212	Effects of chronic <b>nicotine</b> administration and its withdrawal on striatal FosB/DeltaFosB and c <strong>Fos</strong> expression in rats and mice.
+FOS	addiction	withdrawal	16631212	Effects of chronic nicotine administration and its <b>withdrawal</b> on striatal FosB/DeltaFosB and c <strong>Fos</strong> expression in rats and mice.
+FOS	drug	nicotine	16631212	In mice neither 2  nor 7 week oral <b>nicotine</b> treatment induced expression of long lived DeltaFosB isoforms although during the treatment in the NAcc FosB/DeltaFosB expression was increased as was c <strong>Fos</strong> in the CPu.
+FOS	drug	nicotine	16631212	In rats given <b>nicotine</b> subcutaneously once daily for 5days FosB/DeltaFosB expression was elevated in the NAcc still after 24 h withdrawal suggesting accumulation of DeltaFosB but in the CPu neither FosB/DeltaFosB nor c <strong>Fos</strong> expression was altered.
+FOS	addiction	withdrawal	16631212	In rats given nicotine subcutaneously once daily for 5days FosB/DeltaFosB expression was elevated in the NAcc still after 24 h <b>withdrawal</b> suggesting accumulation of DeltaFosB but in the CPu neither FosB/DeltaFosB nor c <strong>Fos</strong> expression was altered.
+FOS	drug	nicotine	16631212	However, in mice given <b>nicotine</b> via drinking fluid although striatal fosB and c <strong>fos</strong> were activated by <b>nicotine</b> even after 7 week treatment no evidence of accumulation of long lived DeltaFosB was found suggesting perhaps a species difference or more likely a role for the manner of administration.
+FOS	drug	cocaine	16580740	Several reports show <b>cocaine</b> induced c <strong>fos</strong> expression particularly in the intermediate zone after 14, but not 2, drug free days following repeated <b>cocaine</b> administration, suggesting that this region may be involved in sensitization and particularly in the later phase of expression, versus the earlier phase of sensitization.
+FOS	addiction	sensitization	16580740	Several reports show cocaine induced c <strong>fos</strong> expression particularly in the intermediate zone after 14, but not 2, drug free days following repeated cocaine administration, suggesting that this region may be involved in <b>sensitization</b> and particularly in the later phase of expression, versus the earlier phase of <b>sensitization</b>.
+FOS	drug	opioid	16474935	Role of PKC in regulation of <strong>Fos</strong> and TH expression after <b>naloxone</b> induced <b>morphine</b> withdrawal in the heart.
+FOS	addiction	withdrawal	16474935	Role of PKC in regulation of <strong>Fos</strong> and TH expression after naloxone induced morphine <b>withdrawal</b> in the heart.
+FOS	drug	opioid	16474935	We previously demonstrated that <b>morphine</b> withdrawal induced hyperactivity of the heart by activation of noradrenergic pathways innervating the left and right ventricle, as evaluated by noradrenaline (NA) turnover and <strong>Fos</strong> expression.
+FOS	addiction	withdrawal	16474935	We previously demonstrated that morphine <b>withdrawal</b> induced hyperactivity of the heart by activation of noradrenergic pathways innervating the left and right ventricle, as evaluated by noradrenaline (NA) turnover and <strong>Fos</strong> expression.
+FOS	drug	opioid	16474935	The present study was designed to investigate the role of protein kinase C (PKC) in this process, by estimating whether pharmacological inhibition of PKC would attenuate <b>morphine</b> withdrawal induced <strong>Fos</strong> expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels and NA turnover in the left and right ventricle.
+FOS	addiction	withdrawal	16474935	The present study was designed to investigate the role of protein kinase C (PKC) in this process, by estimating whether pharmacological inhibition of PKC would attenuate morphine <b>withdrawal</b> induced <strong>Fos</strong> expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels and NA turnover in the left and right ventricle.
+FOS	drug	opioid	16474935	<b>Morphine</b> withdrawal induced <strong>Fos</strong> expression and increased TH levels and NA turnover in the right and left ventricle.
+FOS	addiction	withdrawal	16474935	Morphine <b>withdrawal</b> induced <strong>Fos</strong> expression and increased TH levels and NA turnover in the right and left ventricle.
+FOS	drug	opioid	16474935	However, this inhibitor produced a reduction in the <b>morphine</b> withdrawal induced <strong>Fos</strong> expression.
+FOS	addiction	withdrawal	16474935	However, this inhibitor produced a reduction in the morphine <b>withdrawal</b> induced <strong>Fos</strong> expression.
+FOS	drug	opioid	16474935	The results of the present study provide new information on the mechanisms that underlie <b>morphine</b> withdrawal induced up regulation of <strong>Fos</strong> expression in the heart and suggest that TH is not a target of PKC during <b>morphine</b> withdrawal at heart levels.
+FOS	addiction	withdrawal	16474935	The results of the present study provide new information on the mechanisms that underlie morphine <b>withdrawal</b> induced up regulation of <strong>Fos</strong> expression in the heart and suggest that TH is not a target of PKC during morphine <b>withdrawal</b> at heart levels.
+FOS	drug	alcohol	16470400	Previous experience of <b>ethanol</b> withdrawal increases withdrawal induced c <strong>fos</strong> expression in limbic areas, but not withdrawal induced anxiety and prevents withdrawal induced elevations in plasma corticosterone.
+FOS	addiction	withdrawal	16470400	Previous experience of ethanol <b>withdrawal</b> increases <b>withdrawal</b> induced c <strong>fos</strong> expression in limbic areas, but not <b>withdrawal</b> induced anxiety and prevents <b>withdrawal</b> induced elevations in plasma corticosterone.
+FOS	drug	alcohol	16470400	Eight hours after <b>ethanol</b> withdrawal, anxiety like behaviour was tested in the elevated plus maze, blood corticosterone levels were measured, and expression level of markers of neuronal activity and plasticity, c <strong>fos</strong> and zif268, was assessed.
+FOS	addiction	withdrawal	16470400	Eight hours after ethanol <b>withdrawal</b>, anxiety like behaviour was tested in the elevated plus maze, blood corticosterone levels were measured, and expression level of markers of neuronal activity and plasticity, c <strong>fos</strong> and zif268, was assessed.
+FOS	drug	cocaine	16395306	Rats trained on a running wheel under the influence of <b>cocaine</b> for 4 days subsequently displayed greater c <strong>fos</strong> induction by <b>cocaine</b> than untrained controls.
+FOS	drug	cocaine	16395306	Wheel training was performed after injection of <b>cocaine</b> (25 mg/kg) or vehicle, and c <strong>fos</strong> induction by a <b>cocaine</b> challenge was measured 24 h later.
+FOS	drug	cocaine	16395306	Rats that trained under <b>cocaine</b> (but not vehicle) showed a greater c <strong>fos</strong> response in the striatum compared to locked wheel controls.
+FOS	addiction	withdrawal	16385558	Attenuated expression of <b>withdrawal</b> behaviors correlated with decreased c <strong>Fos</strong> expression and intracellular signal transduction elements [protein kinase A regulatory subunit II (PKA) and phosphorylated cAMP response element binding protein (pCREB)] in brainstem noradrenergic nuclei.
+FOS	drug	alcohol	16385558	In conclusion, our previously reported decreases in c <strong>Fos</strong> and PKA expression in the NTS following pretreatment with low doses of <b>naltrexone</b> may be partially explained by a greater inhibition of NTS neurons resulting from increased muOR expression in this region.
+FOS	drug	opioid	16360647	We investigated the effects of riluzole on the conditioned place aversion (CPA) induced by <b>naloxone</b> precipitated withdrawal from a single <b>morphine</b> exposure 24 h before, and on c <strong>Fos</strong> expression within the amygdala during the withdrawal period in rats.
+FOS	addiction	aversion	16360647	We investigated the effects of riluzole on the conditioned place <b>aversion</b> (CPA) induced by naloxone precipitated withdrawal from a single morphine exposure 24 h before, and on c <strong>Fos</strong> expression within the amygdala during the withdrawal period in rats.
+FOS	addiction	withdrawal	16360647	We investigated the effects of riluzole on the conditioned place aversion (CPA) induced by naloxone precipitated <b>withdrawal</b> from a single morphine exposure 24 h before, and on c <strong>Fos</strong> expression within the amygdala during the <b>withdrawal</b> period in rats.
+FOS	drug	opioid	16360647	In addition, riluzole appeared to produce nonspecific effects on c <strong>Fos</strong> expression by itself, without specifically modifying c <strong>Fos</strong> expression following <b>naloxone</b> precipitated withdrawal in any region of the amygdala examined, suggesting that the amygdala may not serve as a specific site of action for riluzole.
+FOS	addiction	withdrawal	16360647	In addition, riluzole appeared to produce nonspecific effects on c <strong>Fos</strong> expression by itself, without specifically modifying c <strong>Fos</strong> expression following naloxone precipitated <b>withdrawal</b> in any region of the amygdala examined, suggesting that the amygdala may not serve as a specific site of action for riluzole.
+FOS	drug	opioid	16359817	Enhanced <strong>Fos</strong> expression in glutamic acid decarboxylase immunoreactive neurons of the mouse periaqueductal grey during <b>opioid</b> withdrawal.
+FOS	addiction	withdrawal	16359817	Enhanced <strong>Fos</strong> expression in glutamic acid decarboxylase immunoreactive neurons of the mouse periaqueductal grey during opioid <b>withdrawal</b>.
+FOS	drug	opioid	16359817	Previous studies using c <strong>Fos</strong> immunohistochemistry suggest that a sub population of neurons in the midbrain periaqueductal gray region is activated during <b>opioid</b> withdrawal.
+FOS	addiction	withdrawal	16359817	Previous studies using c <strong>Fos</strong> immunohistochemistry suggest that a sub population of neurons in the midbrain periaqueductal gray region is activated during opioid <b>withdrawal</b>.
+FOS	drug	opioid	16359817	The present study investigated whether GABAergic neurons are activated in the mouse periaqueductal gray during <b>opioid</b> withdrawal using dual antibody immunohistochemistry for <strong>Fos</strong> and glutamic acid decarboxylase.
+FOS	addiction	withdrawal	16359817	The present study investigated whether GABAergic neurons are activated in the mouse periaqueductal gray during opioid <b>withdrawal</b> using dual antibody immunohistochemistry for <strong>Fos</strong> and glutamic acid decarboxylase.
+FOS	drug	opioid	16359817	Both chronic <b>opioid</b> treatment and <b>naloxone</b> precipitated <b>opioid</b> withdrawal increased <strong>Fos</strong> expression in the periaqueductal gray, with the greatest increase being four fold in the caudal ventrolateral subdivision following withdrawal.
+FOS	addiction	withdrawal	16359817	Both chronic opioid treatment and naloxone precipitated opioid <b>withdrawal</b> increased <strong>Fos</strong> expression in the periaqueductal gray, with the greatest increase being four fold in the caudal ventrolateral subdivision following <b>withdrawal</b>.
+FOS	addiction	withdrawal	16359817	Neurons stained for both <strong>Fos</strong> and glutamic acid decarboxylase were greatly enhanced in all subdivisions of the periaqueductal gray following <b>withdrawal</b>, particularly in the lateral and ventrolateral divisions where the increase was up to 70 fold.
+FOS	drug	alcohol	16359808	Effects of environmental and pharmacological stressors on c <strong>fos</strong> and corticotropin releasing factor mRNA in rat brain: Relationship to the reinstatement of <b>alcohol</b> seeking.
+FOS	addiction	relapse	16359808	Effects of environmental and pharmacological stressors on c <strong>fos</strong> and corticotropin releasing factor mRNA in rat brain: Relationship to the <b>reinstatement</b> of alcohol <b>seeking</b>.
+FOS	drug	alcohol	16359808	To this end, we assessed whether stressors effective in inducing reinstatement of <b>alcohol</b> seeking activate a different set of neuronal pathways than do those that are ineffective, using the technique of in situ hybridization of the mRNAs for c <strong>fos</strong>, a marker of neuronal activation, and corticotropin releasing factor (CRF), a stress related peptide we have shown to be critical to footshock induced reinstatement of <b>alcohol</b> seeking.
+FOS	addiction	relapse	16359808	To this end, we assessed whether stressors effective in inducing <b>reinstatement</b> of alcohol <b>seeking</b> activate a different set of neuronal pathways than do those that are ineffective, using the technique of in situ hybridization of the mRNAs for c <strong>fos</strong>, a marker of neuronal activation, and corticotropin releasing factor (CRF), a stress related peptide we have shown to be critical to footshock induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+FOS	drug	alcohol	16359808	We found regionally specific effects of the stressors on c <strong>fos</strong> and CRF mRNA in brain regions associated with the rewarding effects of <b>alcohol</b> and other abused drugs.
+FOS	drug	alcohol	16359808	The two stressors we have previously shown to be effective in inducing reinstatement of <b>alcohol</b> seeking, footshock and yohimbine, induced c <strong>fos</strong> mRNA in the shell of the nucleus accumbens, and the basolateral and central amygdalar nuclei.
+FOS	addiction	relapse	16359808	The two stressors we have previously shown to be effective in inducing <b>reinstatement</b> of alcohol <b>seeking</b>, footshock and yohimbine, induced c <strong>fos</strong> mRNA in the shell of the nucleus accumbens, and the basolateral and central amygdalar nuclei.
+FOS	drug	alcohol	16355445	Acupuncture reduces <b>alcohol</b> withdrawal syndrome and c <strong>Fos</strong> expression in rat brain.
+FOS	addiction	withdrawal	16355445	Acupuncture reduces alcohol <b>withdrawal</b> syndrome and c <strong>Fos</strong> expression in rat brain.
+FOS	drug	alcohol	16355445	In the present study, the effects of acupuncture on <b>alcohol</b> withdrawal syndrome (AWS) and <strong>Fos</strong> like immunoreactivity (FLI) in the striatum and the nucleus accumbens (NAC) of rats were investigated.
+FOS	addiction	withdrawal	16355445	In the present study, the effects of acupuncture on alcohol <b>withdrawal</b> syndrome (AWS) and <strong>Fos</strong> like immunoreactivity (FLI) in the striatum and the nucleus accumbens (NAC) of rats were investigated.
+FOS	drug	opioid	16354936	Here, we used a functional mapping procedure based on microinjection <strong>Fos</strong> plumes to localize <b>opioid</b> substrates in the medial shell of the nucleus accumbens that cause enhanced "liking" reactions to sweet pleasure and that stimulate food intake.
+FOS	drug	alcohol	16340450	Acute <b>alcohol</b> withdrawal is associated with c <strong>Fos</strong> expression in the basal ganglia and associated circuitry: C57BL/6J and DBA/2J inbred mouse strain analyses.
+FOS	addiction	withdrawal	16340450	Acute alcohol <b>withdrawal</b> is associated with c <strong>Fos</strong> expression in the basal ganglia and associated circuitry: C57BL/6J and DBA/2J inbred mouse strain analyses.
+FOS	drug	alcohol	16340450	The question addressed was whether or not <b>ethanol</b> withdrawn D2 and B6 mice differed in c <strong>Fos</strong> induction (neural activation) within circuitry that could explain the severe <b>ethanol</b> withdrawal of the D2 strain and the mild <b>ethanol</b> withdrawal in B6 strain mice.
+FOS	addiction	withdrawal	16340450	The question addressed was whether or not ethanol withdrawn D2 and B6 mice differed in c <strong>Fos</strong> induction (neural activation) within circuitry that could explain the severe ethanol <b>withdrawal</b> of the D2 strain and the mild ethanol <b>withdrawal</b> in B6 strain mice.
+FOS	drug	cocaine	16339038	In MSK1 knock out (KO) mice CREB and H3 phosphorylation in response to <b>cocaine</b> (10 mg/kg) were blocked, and induction of c <strong>Fos</strong> and dynorphin was prevented, whereas the induction of Egr 1 (early growth response 1)/zif268/Krox24 was unaltered.
+FOS	addiction	sensitization	16339038	Our results show that MSK1 is a major striatal kinase, downstream from ERK, responsible for the phosphorylation of CREB and H3 and is required specifically for the induction of c <strong>Fos</strong> and dynorphin as well as for locomotor <b>sensitization</b>.
+FOS	drug	cocaine	16337088	c <strong>Fos</strong> and deltaFosB expression are differentially altered in distinct subregions of the nucleus accumbens shell in <b>cocaine</b> sensitized rats.
+FOS	drug	cocaine	16337088	The present study quantified c <strong>Fos</strong>  and deltaFosB immunoreactive nuclei in subterritories of the nucleus accumbens in animals behaviorally sensitized to <b>cocaine</b>.
+FOS	drug	cocaine	16337088	As previously reported, c <strong>Fos</strong> immunoreactivity was increased in the intermediate zone in <b>cocaine</b> sensitized rats.
+FOS	drug	opioid	16289800	The spinal ERK inhibition or knockdown also reduced <b>morphine</b> withdrawal induced phosphorylation of cAMP response element binding protein (CREB), which is one of the important downstream substrates of ERK pathway, and <strong>Fos</strong> expression.
+FOS	addiction	withdrawal	16289800	The spinal ERK inhibition or knockdown also reduced morphine <b>withdrawal</b> induced phosphorylation of cAMP response element binding protein (CREB), which is one of the important downstream substrates of ERK pathway, and <strong>Fos</strong> expression.
+FOS	drug	cocaine	16271798	<b>Cocaine</b> is an addictive psychostimulant that induces <strong>fos</strong> and opioid gene expression by activating the dopamine receptors and the PKA pathways in dopamine D1 and a glutamate NMDA dependent mechanisms in the striatum.
+FOS	drug	opioid	16271798	Cocaine is an addictive psychostimulant that induces <strong>fos</strong> and <b>opioid</b> gene expression by activating the dopamine receptors and the PKA pathways in dopamine D1 and a glutamate NMDA dependent mechanisms in the striatum.
+FOS	addiction	addiction	16271798	Cocaine is an <b>addictive</b> psychostimulant that induces <strong>fos</strong> and opioid gene expression by activating the dopamine receptors and the PKA pathways in dopamine D1 and a glutamate NMDA dependent mechanisms in the striatum.
+FOS	drug	cocaine	16263220	It has also been shown that extracellular signal regulated kinase activation can regulate <b>cocaine</b> induced expression of c <strong>Fos</strong> and FosB, two possible components of activator protein 1.
+FOS	drug	cocaine	16263220	SL327 pre treatment, however, reduces the DNA binding activity of the activator protein 1 complex induced six hours after an acute <b>cocaine</b> treatment as well as one hour after the last of the chronic <b>cocaine</b> injections, a phenomenon that results from the concomitant reduction of all <b>cocaine</b> induced proteins (c <strong>Fos</strong>, FosB, deltaFosB, JunB).
+FOS	drug	nicotine	16251992	Also, we examined the effects of GTS on <b>nicotine</b> induced locomotor hyperactivity and on <b>nicotine</b> induced <strong>Fos</strong> protein expression in the nucleus accumbens and striatum.
+FOS	drug	nicotine	16251992	GTS decreased <b>nicotine</b> induced <strong>Fos</strong> protein expression in the nucleus accumbens and striatum, reflecting the inhibition by GTS of <b>nicotine</b> induced enhancement of dopaminergic transmission.
+FOS	drug	cocaine	16242920	In situ hybridisation studies indicated significant increases in b ZIP transcription factors (CREM, ICER, CBP, and c <strong>fos</strong>) elicited by MK 801 and decreases in c <strong>fos</strong> elicited by <b>cocaine</b>.
+FOS	drug	opioid	16190878	Role of PKC alpha,gamma isoforms in regulation of c <strong>Fos</strong> and TH expression after <b>naloxone</b> induced <b>morphine</b> withdrawal in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups.
+FOS	addiction	withdrawal	16190878	Role of PKC alpha,gamma isoforms in regulation of c <strong>Fos</strong> and TH expression after naloxone induced morphine <b>withdrawal</b> in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups.
+FOS	drug	opioid	16190878	We previously demonstrated that <b>morphine</b> withdrawal induced hyperactivity of the hypothalamus pituitary adrenocortical axis by activation of noradrenergic pathways innervating the hypothalamic paraventricular nucleus (PVN), as evaluated by <strong>Fos</strong> expression and corticosterone release.
+FOS	addiction	withdrawal	16190878	We previously demonstrated that morphine <b>withdrawal</b> induced hyperactivity of the hypothalamus pituitary adrenocortical axis by activation of noradrenergic pathways innervating the hypothalamic paraventricular nucleus (PVN), as evaluated by <strong>Fos</strong> expression and corticosterone release.
+FOS	drug	opioid	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate <b>morphine</b> withdrawal induced c <strong>Fos</strong> expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+FOS	addiction	withdrawal	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate morphine <b>withdrawal</b> induced c <strong>Fos</strong> expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+FOS	drug	opioid	16190878	<b>Morphine</b> withdrawal induced c <strong>Fos</strong> expression in the PVN and NTS/VLM, indicating an activation of neurons in those nuclei.
+FOS	addiction	withdrawal	16190878	Morphine <b>withdrawal</b> induced c <strong>Fos</strong> expression in the PVN and NTS/VLM, indicating an activation of neurons in those nuclei.
+FOS	drug	opioid	16190878	Infusion of calphostin C, a selective protein kinase C inhibitor, produced a reduction in the <b>morphine</b> withdrawal induced c <strong>Fos</strong> expression.
+FOS	addiction	withdrawal	16190878	Infusion of calphostin C, a selective protein kinase C inhibitor, produced a reduction in the morphine <b>withdrawal</b> induced c <strong>Fos</strong> expression.
+FOS	drug	cocaine	16179556	In the present study, we evaluated the effect of increasing doses of <b>cocaine</b> on the expression of immediate early genes (IEGs), c <strong>fos</strong> and c jun, and closely related transcription factors, SP 1 and NF kbeta, at 24 h after the exposure to <b>cocaine</b> (50, 100, 200, 500, 1000, 2500 microM) in NGF differentiated PC12 cells.
+FOS	drug	cocaine	16179556	<b>Cocaine</b> (50 500 microM) resulted in significant induction of the expression of c <strong>fos</strong>, c jun, SP 1, and NF kbeta.
+FOS	addiction	reward	16157281	We show that COC conditioned place preference (<b>CPP</b>) activates ERK, CREB, Elk 1, and <strong>Fos</strong> in the nucleus accumbens core (AcbC) but not shell.
+FOS	addiction	reward	16157281	Intra AcbC infusions of U0126, an inhibitor of the ERK kinase MEK, prevent both the activation of ERK, CREB, Elk 1, and <strong>Fos</strong> and retrieval of COC <b>CPP</b>.
+FOS	drug	alcohol	16131849	Ataxia and c <strong>Fos</strong> expression in mice drinking <b>ethanol</b> in a limited access session.
+FOS	drug	alcohol	16131849	Thus, the goal of this study was to demonstrate ataxia and to examine changes in c <strong>Fos</strong> expression in mice after self administration of intoxicating doses of <b>ethanol</b>.
+FOS	drug	alcohol	16131849	In a separate experiment, various brain structures from mice drinking water or <b>ethanol</b> were examined for changes in c <strong>Fos</strong> expression two hr after the limited access session.
+FOS	drug	alcohol	16131849	Among mice drinking <b>ethanol</b>, an increase in c <strong>Fos</strong> expression was seen in the Edinger Westphal nucleus, and a decrease in c <strong>Fos</strong> expression was seen in the cingulate cortex, ventral tegmental area, lateral and medial septum, CA1 region of the hippocampus, and basolateral amygdala.
+FOS	drug	alcohol	16131849	Brain regions showing changes in c <strong>Fos</strong> expression after voluntary intoxication were similar to those previously reported, suggesting that these brain regions are involved in regulating behavioral effects of <b>alcohol</b> intoxication.
+FOS	addiction	intoxication	16131849	Brain regions showing changes in c <strong>Fos</strong> expression after voluntary <b>intoxication</b> were similar to those previously reported, suggesting that these brain regions are involved in regulating behavioral effects of alcohol <b>intoxication</b>.
+FOS	drug	cocaine	16123776	Consistent with these behavioral findings, we found that <b>cocaine</b> regulation of gene expression in striatum, including the acute induction of the immediate early genes c <strong>fos</strong> and arc (activity regulated cytoskeletal associated gene), was abolished in DARPP 32 Thr 34 mutants, but not in Thr 75 mutants.
+FOS	drug	cocaine	16115217	The patterns of <b>cocaine</b> induced c <strong>Fos</strong>, JunB and Zif268 protein expression were investigated, using an immunohistochemical approach, within distinct nuclei of the amygdala, either in the presence or absence of a selective inhibitor of the ERK pathway, SL327.
+FOS	drug	cocaine	16115217	In particular, whereas c <strong>Fos</strong> and JunB expressions were augmented following chronic <b>cocaine</b> treatment, as compared with acute treatment, Zif268 expression was decreased by this chronic treatment.
+FOS	drug	cocaine	16115217	Additionally, chronic blocking of ERK activation affected <b>cocaine</b> induced c <strong>Fos</strong> and JunB but not Zif268 expression.
+FOS	drug	amphetamine	16112474	Preference for cocaine  versus pup associated cues differentially activates neurons expressing either <strong>Fos</strong> or cocaine  and <b>amphetamine</b> regulated transcript in lactating, maternal rodents.
+FOS	drug	cocaine	16112474	Preference for <b>cocaine</b>  versus pup associated cues differentially activates neurons expressing either <strong>Fos</strong> or <b>cocaine</b>  and amphetamine regulated transcript in lactating, maternal rodents.
+FOS	drug	amphetamine	16112474	Using c <strong>Fos</strong> or cocaine  and <b>amphetamine</b> regulated transcript (CART) immunocytochemistry, we identified the neuronal groups that are activated when the dams expressed a preference for either cues associated with pups or cues associated with cocaine.
+FOS	drug	cocaine	16112474	Using c <strong>Fos</strong> or <b>cocaine</b>  and amphetamine regulated transcript (CART) immunocytochemistry, we identified the neuronal groups that are activated when the dams expressed a preference for either cues associated with pups or cues associated with <b>cocaine</b>.
+FOS	drug	cocaine	16112474	Dams that preferred the <b>cocaine</b> associated cues had more c <strong>Fos</strong> positive neurons in medial prefrontal cortex, nucleus accumbens, and basolateral nucleus of amygdala than pup associated cue preferring dams or control.
+FOS	drug	nicotine	16084664	To investigate this question, we examined the expression of a number of early response genes (arc, c <strong>fos</strong> and NGFI B) that have been implicated in synaptic plasticity and addiction, following acute <b>nicotine</b> in adolescent and adult rats.
+FOS	addiction	addiction	16084664	To investigate this question, we examined the expression of a number of early response genes (arc, c <strong>fos</strong> and NGFI B) that have been implicated in synaptic plasticity and <b>addiction</b>, following acute nicotine in adolescent and adult rats.
+FOS	drug	nicotine	16084664	c <strong>fos</strong> and NGFI B were also upregulated by <b>nicotine</b>, but not in an age related manner.
+FOS	drug	nicotine	16084664	In contrast, <b>nicotine</b> induced less arc, c <strong>fos</strong>, and NGFI B expression in the somatosensory cortex of adolescents compared with adults.
+FOS	drug	opioid	16056125	Enhanced c <strong>Fos</strong> in periaqueductal grey GABAergic neurons during <b>opioid</b> withdrawal.
+FOS	addiction	withdrawal	16056125	Enhanced c <strong>Fos</strong> in periaqueductal grey GABAergic neurons during opioid <b>withdrawal</b>.
+FOS	drug	psychedelics	16054778	Subsequent analysis of c <strong>Fos</strong> and 5 HT(2A)R immunoreactivity in brain sections demonstrated that DOI treatment decreased the number of (+) <b>MDMA</b> induced c <strong>Fos</strong> immunopositive nuclei and 5 HT(2A)R immunostaining in select cortical and striatal areas.
+FOS	drug	opioid	16044914	[Intrathecal injection of muscarinic receptors or GDNF antisense oligonucleotides inhibits the increase of c <strong>Fos</strong> expression in locus coeruleus of <b>morphine</b> withdrawal rats].
+FOS	addiction	withdrawal	16044914	[Intrathecal injection of muscarinic receptors or GDNF antisense oligonucleotides inhibits the increase of c <strong>Fos</strong> expression in locus coeruleus of morphine <b>withdrawal</b> rats].
+FOS	drug	opioid	16044914	The antisense approach and immunohistochemistry were used to study the effects of different muscarinic receptor (M) subtypes and glial cell derived neurotrophic factor (GDNF) on the scores of <b>morphine</b> withdrawal syndrome and the expression of c <strong>Fos</strong> in locus coeruleus (LC).
+FOS	addiction	withdrawal	16044914	The antisense approach and immunohistochemistry were used to study the effects of different muscarinic receptor (M) subtypes and glial cell derived neurotrophic factor (GDNF) on the scores of morphine <b>withdrawal</b> syndrome and the expression of c <strong>Fos</strong> in locus coeruleus (LC).
+FOS	drug	opioid	16044914	The expression of c <strong>Fos</strong> positive neurons in the LC increased in <b>morphine</b> dependent rats and increased to a greater extent after the injection of <b>naloxone</b> (4mg/kg, ip) in <b>morphine</b> dependent rats.
+FOS	drug	opioid	16044914	Intrathecal injection of M2AS oligo or GDNFAS oligo inhibited the increase of c <strong>Fos</strong> expression in LC during <b>morphine</b> withdrawal, but there was no effect in case of M1AS oligo.
+FOS	addiction	withdrawal	16044914	Intrathecal injection of M2AS oligo or GDNFAS oligo inhibited the increase of c <strong>Fos</strong> expression in LC during morphine <b>withdrawal</b>, but there was no effect in case of M1AS oligo.
+FOS	drug	opioid	16002220	Increased c <strong>Fos</strong> expression in the medial part of the lateral habenula during cue evoked <b>heroin</b> seeking in rats.
+FOS	addiction	relapse	16002220	Increased c <strong>Fos</strong> expression in the medial part of the lateral habenula during cue evoked heroin <b>seeking</b> in rats.
+FOS	addiction	relapse	16002220	c <strong>Fos</strong>, the protein product of the protooncogene c <strong>Fos</strong>, is expressed in neurons when there are drug associated cue induced drug <b>seeking</b> behaviour.
+FOS	drug	opioid	16002220	Findings showed that <b>heroin</b> associated conditioned stimuli could induce robust <b>heroin</b> seeking behavior that was associated with increased c <strong>Fos</strong> immunoreactivity in the medial part of the LHb.
+FOS	addiction	relapse	16002220	Findings showed that heroin associated conditioned stimuli could induce robust heroin <b>seeking</b> behavior that was associated with increased c <strong>Fos</strong> immunoreactivity in the medial part of the LHb.
+FOS	drug	amphetamine	15998197	The authors used c <strong>Fos</strong> immunohistochemistry to demonstrate a conditioned physiological response to <b>methamphetamine</b> (<b>meth</b>) in mice.
+FOS	drug	amphetamine	15998197	The <b>meth</b> paired mice displayed increased c <strong>Fos</strong> in several brain regions, including the nucleus accumbens, prefrontal cortex, orbitofrontal cortex, basolateral amygdala, and bed nucleus of the stria terminalis.
+FOS	drug	amphetamine	15998197	Results implicate specific brain regions in classical conditioning to <b>meth</b> and demonstrate the importance of considering locomotor activity and batch in a c <strong>Fos</strong> study.
+FOS	drug	opioid	15977398	[The effect of ribozyme specially cleaving per1 mRNA on c <strong>fos</strong> mRNA and its expression in hippocampus of <b>morphine</b> addicted mice].
+FOS	drug	opioid	15977398	To study the change of c <strong>fos</strong> mRNA and protein in hippocampus of <b>morphine</b> addicted mice after injected with ribozyme specially cleaving per1 mRNA.
+FOS	drug	opioid	15977398	The ribozyme specially cleaving per1 mRNA has potential function in inhibiting the transcription and expression of c <strong>fos</strong> and blocking the <b>morphine</b> addiction.
+FOS	addiction	addiction	15977398	The ribozyme specially cleaving per1 mRNA has potential function in inhibiting the transcription and expression of c <strong>fos</strong> and blocking the morphine <b>addiction</b>.
+FOS	drug	opioid	15939543	In an immunohistochemical study for c <strong>Fos</strong> protein, <b>naloxone</b> precipitated <b>morphine</b> withdrawal dramatically induced c <strong>Fos</strong> immunoreactive neurons in the capsular part of the Ce, and the lateral and medial divisions of the BST.
+FOS	addiction	withdrawal	15939543	In an immunohistochemical study for c <strong>Fos</strong> protein, naloxone precipitated morphine <b>withdrawal</b> dramatically induced c <strong>Fos</strong> immunoreactive neurons in the capsular part of the Ce, and the lateral and medial divisions of the BST.
+FOS	drug	opioid	15939543	Bilateral excitotoxic lesion of the Ce reduced the number of <b>morphine</b> withdrawal induced c <strong>Fos</strong> immunoreactive neurons in the lateral and medial BST, with significant decreases in the posterior, ventral and juxtacapsular parts of lateral division, and anterior part of the medial division, but not in the ventral part of the medial division of the BST.
+FOS	addiction	withdrawal	15939543	Bilateral excitotoxic lesion of the Ce reduced the number of morphine <b>withdrawal</b> induced c <strong>Fos</strong> immunoreactive neurons in the lateral and medial BST, with significant decreases in the posterior, ventral and juxtacapsular parts of lateral division, and anterior part of the medial division, but not in the ventral part of the medial division of the BST.
+FOS	drug	cannabinoid	15920503	Perinatal exposure to delta(9) <b>tetrahydrocannabinol</b> alters heroin induced place conditioning and <strong>fos</strong> immunoreactivity.
+FOS	drug	opioid	15920503	Perinatal exposure to delta(9) tetrahydrocannabinol alters <b>heroin</b> induced place conditioning and <strong>fos</strong> immunoreactivity.
+FOS	drug	cannabinoid	15920503	In the present study, the effects of perinatal exposure to Delta(9) <b>tetrahydrocannabinol</b> (<b>THC</b>) on heroin induced place conditioning and <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) were examined.
+FOS	drug	opioid	15920503	In the present study, the effects of perinatal exposure to Delta(9) tetrahydrocannabinol (THC) on <b>heroin</b> induced place conditioning and <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) were examined.
+FOS	addiction	reward	15920503	<strong>Fos</strong> IR was examined in several brain regions directly or indirectly involved in <b>reward</b>.
+FOS	drug	opioid	15920503	Acute administration of <b>heroin</b> in vehicle pretreated rats increased <strong>Fos</strong> IR in the central, medial, and dorsomedial caudate putamen (CPu), nucleus accumbens (NAC, core and shell regions), lateral septum, islands of Calleja major (ICjM), bed nucleus of the stria terminalis (BNST), central nucleus of the amygdala (CEA), dorsolateral and dorsomedial periaqueductal gray (PAG), ventral tegmental area (VTA), Edinger Westphal nucleus (EW).
+FOS	drug	cannabinoid	15920503	Perinatal <b>THC</b> exposure significantly increased heroin induced <strong>Fos</strong> IR in the dorsomedial CPu.
+FOS	drug	opioid	15920503	Perinatal THC exposure significantly increased <b>heroin</b> induced <strong>Fos</strong> IR in the dorsomedial CPu.
+FOS	drug	cannabinoid	15920503	Conversely, perinatal <b>THC</b> exposure reduced heroin induced <strong>Fos</strong> IR in the NAC (shell), BNST, CEA, dorsolateral and lateral PAG, VTA, and EW.
+FOS	drug	opioid	15920503	Conversely, perinatal THC exposure reduced <b>heroin</b> induced <strong>Fos</strong> IR in the NAC (shell), BNST, CEA, dorsolateral and lateral PAG, VTA, and EW.
+FOS	drug	opioid	15904717	Expression of c <strong>Fos</strong> in the rat central amygdala accompanies the acquisition but not expression of conditioned place aversion induced by withdrawal from acute <b>morphine</b> dependence.
+FOS	addiction	aversion	15904717	Expression of c <strong>Fos</strong> in the rat central amygdala accompanies the acquisition but not expression of conditioned place <b>aversion</b> induced by withdrawal from acute morphine dependence.
+FOS	addiction	dependence	15904717	Expression of c <strong>Fos</strong> in the rat central amygdala accompanies the acquisition but not expression of conditioned place aversion induced by withdrawal from acute morphine <b>dependence</b>.
+FOS	addiction	withdrawal	15904717	Expression of c <strong>Fos</strong> in the rat central amygdala accompanies the acquisition but not expression of conditioned place aversion induced by <b>withdrawal</b> from acute morphine dependence.
+FOS	drug	opioid	15904717	Expression of c <strong>Fos</strong> in the amygdala (the central nucleus, CeA; the medial nucleus, MeA; the basolateral nucleus, BLA) following <b>naloxone</b> precipitated withdrawal and the CPA test was examined using a range of <b>naloxone</b> doses (0.02, 0.05, 0.1, 0.2, 0.5 and 1.0 mg/kg).
+FOS	addiction	withdrawal	15904717	Expression of c <strong>Fos</strong> in the amygdala (the central nucleus, CeA; the medial nucleus, MeA; the basolateral nucleus, BLA) following naloxone precipitated <b>withdrawal</b> and the CPA test was examined using a range of naloxone doses (0.02, 0.05, 0.1, 0.2, 0.5 and 1.0 mg/kg).
+FOS	drug	opioid	15904717	In CeA, but not MeA with high level constitutive neuronal activity, the <b>naloxone</b> induced modification in c <strong>Fos</strong> immunoreactivity following <b>morphine</b> pretreatment exhibited a dose dependent pattern similar to that seen in the behavioral study.
+FOS	addiction	withdrawal	15904717	On the other hand, none of the three amygdaloid nuclei examined including CeA, MeA and BLA showed notable sensitivity of c <strong>Fos</strong> to the conditioned <b>withdrawal</b> stimulus.
+FOS	drug	cocaine	15901784	The ability of <b>cocaine</b> to increase DA was enhanced in knock outs, whereas c <strong>fos</strong> induction was decreased.
+FOS	drug	opioid	15885214	Electroacupuncture attenuates <b>morphine</b> withdrawal signs and c <strong>Fos</strong> expression in the central nucleus of the amygdala in freely moving rats.
+FOS	addiction	withdrawal	15885214	Electroacupuncture attenuates morphine <b>withdrawal</b> signs and c <strong>Fos</strong> expression in the central nucleus of the amygdala in freely moving rats.
+FOS	drug	opioid	15885214	The present study was performed to evaluate the effect of EA at the acupuncture point Shen Shu (BL.23) on <b>morphine</b> withdrawal signs and c <strong>Fos</strong> expression of the amygdala in freely moving rats or restrained rats.
+FOS	addiction	withdrawal	15885214	The present study was performed to evaluate the effect of EA at the acupuncture point Shen Shu (BL.23) on morphine <b>withdrawal</b> signs and c <strong>Fos</strong> expression of the amygdala in freely moving rats or restrained rats.
+FOS	drug	cocaine	15879001	In the present study, the effects of <b>cocaine</b> and BD1063 on the expression of six <strong>fos</strong> and jun genes were evaluated in mouse brains using cDNA microarrays.
+FOS	drug	amphetamine	15866553	Sensitized attentional performance and <strong>Fos</strong> immunoreactive cholinergic neurons in the basal forebrain of <b>amphetamine</b> pretreated rats.
+FOS	drug	amphetamine	15866553	<strong>Fos</strong> like immunoreactivity (<strong>Fos</strong> IR) in selected regions of these rats' brains was examined to test the hypothesis that <b>AMPH</b> sensitized attentional impairments are associated with increased recruitment of basal forebrain cholinergic neurons.
+FOS	drug	amphetamine	15866553	In <b>AMPH</b> pretreated and  challenged animals, an increased number of <strong>Fos</strong> IR neurons was observed in the basal forebrain.
+FOS	drug	cocaine	15858832	We have found that repeated stimulation of the rat prelimbic cortex with picrotoxin (0.25 microg/0.25 microl, five injections on alternate days followed by 7 day withdrawal) contributed to increase c <strong>Fos</strong> protein expression in the striosomes of the dorsolateral striatum, while producing the opposite effect in the matrix compartment, after a single exposure to <b>cocaine</b> (25 mg/kg).
+FOS	addiction	withdrawal	15858832	We have found that repeated stimulation of the rat prelimbic cortex with picrotoxin (0.25 microg/0.25 microl, five injections on alternate days followed by 7 day <b>withdrawal</b>) contributed to increase c <strong>Fos</strong> protein expression in the striosomes of the dorsolateral striatum, while producing the opposite effect in the matrix compartment, after a single exposure to cocaine (25 mg/kg).
+FOS	drug	amphetamine	15836801	Since we found <b>amphetamine</b> induced <strong>fos</strong> activated cells closely associated with dopamine beta hydroxylase immunoreactive varicosities in the bed nucleus of the stria terminalis (BNST), we investigated the effect of a bilateral micro injection of timolol into this nucleus.
+FOS	drug	opioid	15830100	One hour after <b>naloxone</b> precipitated withdrawal, <strong>Fos</strong> protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of cytosol and membrane fraction of PKC alpha and gamma in the rat spinal cord.
+FOS	addiction	withdrawal	15830100	One hour after naloxone precipitated <b>withdrawal</b>, <strong>Fos</strong> protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of cytosol and membrane fraction of PKC alpha and gamma in the rat spinal cord.
+FOS	drug	opioid	15830100	The results showed that intrathecal administration of CHE decreased the scores of <b>morphine</b> withdrawal, attenuated <b>morphine</b> withdrawal induced allodynia and also inhibited the increase of <strong>Fos</strong> protein expression in the spinal cord of <b>morphine</b> withdrawal rats.
+FOS	addiction	withdrawal	15830100	The results showed that intrathecal administration of CHE decreased the scores of morphine <b>withdrawal</b>, attenuated morphine <b>withdrawal</b> induced allodynia and also inhibited the increase of <strong>Fos</strong> protein expression in the spinal cord of morphine <b>withdrawal</b> rats.
+FOS	drug	amphetamine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of <b>amphetamine</b> or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+FOS	drug	cocaine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or <b>cocaine</b> (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+FOS	addiction	addiction	15814102	In order to approach the astroglial implication of <b>addictive</b> and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+FOS	addiction	dependence	15814102	Because astrocytes interact extensively with the neurons in the brain, our data led us to conclude that oxidation regulated <strong>AP 1</strong> target genes may represent one of the molecular mechanisms underlying neuronal adaptation associated with psychostimulant <b>dependence</b>.
+FOS	addiction	relapse	15813948	Altered <strong>Fos</strong> expression in neural pathways underlying cue elicited drug <b>seeking</b> in the rat.
+FOS	drug	cannabinoid	15812570	Concurrent in situ hybridization analysis of regional c <strong>fos</strong> and ngfi b expression highlighted areas of the prefrontal cortex and striatum that were recruited in response to both <b>THC</b> administration and task performance.
+FOS	drug	cannabinoid	15787710	<b>SR141716</b> (2 mg/kg) itself had no effect on <strong>Fos</strong> but pretreatment with <b>SR141716</b> significantly potentiated restraint induced <strong>Fos</strong> expression in cingulate, LS and Acb.
+FOS	drug	cannabinoid	15787710	Administration of <b>SR141716</b> prior to the fifth restraint episode resulted in greater potentiation of restraint induced <strong>Fos</strong> induction than the first; significant increases occurred within all regions of PFC examined, LS and Acb.
+FOS	drug	cannabinoid	15787710	Because repeated homotypic stress increased both limbic 2 AG and resulted in a greater effect of <b>SR141716</b> on limbic <strong>Fos</strong> expression, we hypothesize that increased CB(1) receptor activity contributes to the expression of habituation to homotypic stress.
+FOS	drug	nicotine	15785859	We previously reported that <b>nicotine</b> withdrawal up regulates transcription of some immediately early genes (IEGs), c <strong>fos</strong> (Ichino et al., 1999) and egr1, nur77 (Ichino et al., 2002) in cultures of pheochromocytoma PC12 cells, which are of neuronal lineage.
+FOS	addiction	withdrawal	15785859	We previously reported that nicotine <b>withdrawal</b> up regulates transcription of some immediately early genes (IEGs), c <strong>fos</strong> (Ichino et al., 1999) and egr1, nur77 (Ichino et al., 2002) in cultures of pheochromocytoma PC12 cells, which are of neuronal lineage.
+FOS	drug	cocaine	15770241	These results suggest that genes encoding certain extracellular factors, membrane receptors and modulators, and intracellular signaling molecules, among others, are regulated by <b>cocaine</b> via the D1 receptor, and these <strong>AP 1</strong> transcription complex regulated genes might contribute to persistent <b>cocaine</b> induced behavioral changes.
+FOS	drug	alcohol	15763170	Influence of maternal <b>alcohol</b> administration on c <strong>Fos</strong> expression in the hippocampus of infant rats.
+FOS	drug	alcohol	15763170	In the present study, the dose dependence of the effect of maternal <b>alcohol</b> on hippocampal c <strong>Fos</strong> expression, which is a marker of hippocampal neuronal activity and which is induced by a variety of stimuli, was examined in infant rats.
+FOS	addiction	dependence	15763170	In the present study, the dose <b>dependence</b> of the effect of maternal alcohol on hippocampal c <strong>Fos</strong> expression, which is a marker of hippocampal neuronal activity and which is induced by a variety of stimuli, was examined in infant rats.
+FOS	drug	alcohol	15763170	In the present study, it was shown that expression of c <strong>Fos</strong> in the hippocampus is decreased following treatment with <b>alcohol</b> in a dose dependent fashion.
+FOS	drug	alcohol	15763170	Based on the results of the present study and the findings of other studies, it can be suggested that suppression of c <strong>Fos</strong> expression in the hippocampus of infant rats with maternal <b>alcohol</b> administration mediates the associated developmental retardation and/or anomalies.
+FOS	drug	benzodiazepine	15740792	Immunocytochemistry, histochemistry and western blot were performed to determine the effect of <b>midazolam</b> on formalin induced expression of <strong>Fos</strong> protein, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH d) and nitric oxide synthase (NOS) in chronic morphine tolerant rats, respectively.
+FOS	drug	opioid	15740792	Immunocytochemistry, histochemistry and western blot were performed to determine the effect of midazolam on formalin induced expression of <strong>Fos</strong> protein, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH d) and nitric oxide synthase (NOS) in chronic <b>morphine</b> tolerant rats, respectively.
+FOS	drug	benzodiazepine	15740792	In chronic morphine tolerant rats, pretreatment with <b>midazolam</b> significantly decreased the formalin induced expression of <strong>Fos</strong> and <strong>Fos</strong>/NADPH d double labeled neurons in the contralateral spinal cord and NADPH d positive neurons in the bilateral spinal cord.
+FOS	drug	opioid	15740792	In chronic <b>morphine</b> tolerant rats, pretreatment with midazolam significantly decreased the formalin induced expression of <strong>Fos</strong> and <strong>Fos</strong>/NADPH d double labeled neurons in the contralateral spinal cord and NADPH d positive neurons in the bilateral spinal cord.
+FOS	drug	nicotine	15705350	We found that increasing the rate of intravenous <b>nicotine</b> infusion potentiated its ability to produce locomotor sensitization, and to induce c <strong>fos</strong> and arc mRNA expression in mesocorticolimbic structures.
+FOS	addiction	sensitization	15705350	We found that increasing the rate of intravenous nicotine infusion potentiated its ability to produce locomotor <b>sensitization</b>, and to induce c <strong>fos</strong> and arc mRNA expression in mesocorticolimbic structures.
+FOS	drug	amphetamine	15680202	Ginsenosides attenuate <b>methamphetamine</b> induced behavioral side effects in mice via activation of adenosine A2A receptors: possible involvements of the striatal reduction in <strong>AP 1</strong> DNA binding activity and proenkephalin gene expression.
+FOS	drug	cocaine	15665076	These effects contributed to attenuation of <b>cocaine</b> induced phosphorylation of cAMP response element binding protein as well as a lesser induction of c <strong>fos</strong> in the striatum.
+FOS	drug	opioid	15663473	Involvement of 3',5' cyclic adenosine monophosphate dependent protein kinase in regulation of <strong>Fos</strong> expression and tyrosine hydroxylase levels during <b>morphine</b> withdrawal in the hypothalamic paraventricular nucleus and medulla oblongata catecholaminergic cell groups.
+FOS	addiction	withdrawal	15663473	Involvement of 3',5' cyclic adenosine monophosphate dependent protein kinase in regulation of <strong>Fos</strong> expression and tyrosine hydroxylase levels during morphine <b>withdrawal</b> in the hypothalamic paraventricular nucleus and medulla oblongata catecholaminergic cell groups.
+FOS	drug	opioid	15663473	We investigated whether cAMP dependent protein kinase (PKA) plays a role in this process by estimating changes in PKA immunoreactivity and the influence of inhibition of PKA on <strong>Fos</strong> protein expression and tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and NTS/VLM during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	15663473	We investigated whether cAMP dependent protein kinase (PKA) plays a role in this process by estimating changes in PKA immunoreactivity and the influence of inhibition of PKA on <strong>Fos</strong> protein expression and tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and NTS/VLM during morphine <b>withdrawal</b>.
+FOS	drug	opioid	15663473	<b>Morphine</b> withdrawal induced expression of <strong>Fos</strong> in the PVN and NTS/VLM, indicating an activation of neurones in those nuclei.
+FOS	addiction	withdrawal	15663473	Morphine <b>withdrawal</b> induced expression of <strong>Fos</strong> in the PVN and NTS/VLM, indicating an activation of neurones in those nuclei.
+FOS	drug	opioid	15663473	When the selective PKA inhibitor HA 1004 was infused it greatly diminished the <strong>Fos</strong> expression observed in <b>morphine</b> withdrawn rats.
+FOS	drug	amphetamine	15659295	<b>Methamphetamine</b> sensitization in nociceptin receptor knockout mice: locomotor and c <strong>fos</strong> expression.
+FOS	addiction	sensitization	15659295	Methamphetamine <b>sensitization</b> in nociceptin receptor knockout mice: locomotor and c <strong>fos</strong> expression.
+FOS	drug	amphetamine	15659295	However, analysis of c <strong>fos</strong> expression revealed significant interactions between chronic <b>methamphetamine</b> treatment and genotype in the nucleus accumbens and lateral septum.
+FOS	drug	amphetamine	15659295	This was due to increased c <strong>fos</strong> expression in chronically <b>methamphetamine</b> treated nociceptin receptor knockout mice contrasted with reduced c <strong>fos</strong> expression in chronically vehicle treated nociceptin receptor knockout mice.
+FOS	drug	amphetamine	15659295	Two further regions (nucleus accumbens core and ventromedial caudate putamen) showed significant interactions between genotype, chronic, and acute <b>methamphetamine</b> treatment due to accentuated c <strong>fos</strong> expression in nociceptin receptor knockout mice sensitized and challenged with <b>methamphetamine</b>.
+FOS	drug	psychedelics	15654138	Pre versus post formalin effects of intrathecal <b>ketamine</b> on spinal <strong>Fos</strong> like immunoreactivity in rats.
+FOS	drug	psychedelics	15654138	We undertook this study to compare a preemptive suppression of noxious stimulation induced spinal <strong>Fos</strong> like immunoreactivity (FLI) after receiving intrathecal <b>ketamine</b> before or after formalin pain.
+FOS	drug	opioid	15588731	<b>Morphine</b> withdrawal also induced an increase in the <strong>Fos</strong> expression, which indicates an activation of cardiac cellular activity.
+FOS	addiction	withdrawal	15588731	Morphine <b>withdrawal</b> also induced an increase in the <strong>Fos</strong> expression, which indicates an activation of cardiac cellular activity.
+FOS	drug	cannabinoid	15548217	We also evaluated the consequences of Delta9 <b>THC</b> administration on c <strong>Fos</strong> expression in several brain structures after chronic nicotine administration and withdrawal.
+FOS	drug	nicotine	15548217	We also evaluated the consequences of Delta9 THC administration on c <strong>Fos</strong> expression in several brain structures after chronic <b>nicotine</b> administration and withdrawal.
+FOS	addiction	withdrawal	15548217	We also evaluated the consequences of Delta9 THC administration on c <strong>Fos</strong> expression in several brain structures after chronic nicotine administration and <b>withdrawal</b>.
+FOS	drug	nicotine	15548217	c <strong>Fos</strong> was decreased in the caudate putamen and the dentate gyrus after mecamylamine precipitated <b>nicotine</b> withdrawal.
+FOS	addiction	withdrawal	15548217	c <strong>Fos</strong> was decreased in the caudate putamen and the dentate gyrus after mecamylamine precipitated nicotine <b>withdrawal</b>.
+FOS	drug	cannabinoid	15548217	However, acute Delta9 <b>THC</b> administration did not modify c <strong>Fos</strong> expression under these experimental conditions.
+FOS	drug	amphetamine	15542722	<strong>Fos</strong> expression associated with the discriminative stimulus effects of <b>methamphetamine</b> in rats.
+FOS	drug	amphetamine	15542722	To identify anatomical substrates for the discriminative stimulus effects of <b>methamphetamine</b> in rats, we examined the drug discrimination associated c <strong>Fos</strong> expression in the brains of rats that were trained to discriminate <b>methamphetamine</b> from saline under a two lever fixed ratio (FR 20) schedule of food reinforcement.
+FOS	addiction	reward	15542722	To identify anatomical substrates for the discriminative stimulus effects of methamphetamine in rats, we examined the drug discrimination associated c <strong>Fos</strong> expression in the brains of rats that were trained to discriminate methamphetamine from saline under a two lever fixed ratio (FR 20) schedule of food <b>reinforcement</b>.
+FOS	drug	amphetamine	15542722	c <strong>Fos</strong> expression in the brains of rats trained to discriminate <b>methamphetamine</b> from saline was significantly increased in the nucleus accumbens (NAc) and the ventral tegmental area (VTA) as compared with the expression in the control rats that were maintained under the FR 20 schedule, but no alternation was observed in other areas including the cerebral cortex, caudate putamen, substantia nigra, hippocampus, amygdala, and habenulla.
+FOS	drug	amphetamine	15542722	<b>Methamphetamine</b> treatment in the trained rats caused a significant increase in c <strong>Fos</strong> expression in the VTA, and a decrease in the NAc core, as compared to saline treatment.
+FOS	drug	amphetamine	15542722	However, c <strong>Fos</strong> expression in the NAc and VTA of rats that received chronic intermittent <b>methamphetamine</b> administration without discrimination training, did not differ from the expression in saline treatment animals.
+FOS	drug	cocaine	15541892	<b>Cocaine</b> pre exposure produces a sensitized and context specific c <strong>fos</strong> mRNA response to footshock stress in the central nucleus of the AMYGDALA.
+FOS	drug	cocaine	15541892	In CeA, footshock produced enhanced expression of c <strong>fos</strong> mRNA in <b>cocaine</b>, but not saline, pre exposed animals.
+FOS	drug	cocaine	15541892	Furthermore, this effect was gated by the environmental context in which <b>cocaine</b> was given; footshock only enhanced c <strong>fos</strong> mRNA expression when it was given in a context that had previously been paired with <b>cocaine</b>.
+FOS	drug	cocaine	15464827	In this study, we examined the effects of PTE on the <b>cocaine</b> induced changes in locomotor activity, conditioned place preference (CPP), <strong>fos</strong> related antigen immunoreactivity (FRA IR), and activator protein (AP) 1 DNA binding activity.
+FOS	addiction	reward	15464827	In this study, we examined the effects of PTE on the cocaine induced changes in locomotor activity, conditioned place preference (<b>CPP</b>), <strong>fos</strong> related antigen immunoreactivity (FRA IR), and activator protein (AP) 1 DNA binding activity.
+FOS	drug	cocaine	15464827	<b>Cocaine</b> induced behavioral effects (hyperlocomotion and CPP) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+FOS	addiction	reward	15464827	Cocaine induced behavioral effects (hyperlocomotion and <b>CPP</b>) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+FOS	drug	amphetamine	15464745	Distinct patterns of <strong>Fos</strong> expression induced by systemic <b>amphetamine</b> in the striatal complex of C57BL/6JICo and DBA/2JICo inbred strains of mice.
+FOS	drug	amphetamine	15464745	We used <strong>Fos</strong> expression as a tool to reveal strain differences in the postsynaptic effects of <b>amphetamine</b> (<b>AMPH</b>; 2.5 mg/kg) within the nucleus accumbens (NAc) (core and shell) and the dorsal caudate (dorsomedial and dorsolateral).
+FOS	drug	amphetamine	15464745	<b>AMPH</b> stimulated <strong>Fos</strong> expression in all striatal regions of mice from both strains.
+FOS	drug	opioid	15464026	The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (NR2A) protein, phosphorylated Ca(2+)/calmodulin kinase II (p CaMKII) protein, c <strong>fos</strong> mRNA, c <strong>Fos</strong> protein, are observed in the specific brain areas of mice and/or rats showing signs of <b>naloxone</b> precipitated withdrawal.
+FOS	addiction	withdrawal	15464026	The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (NR2A) protein, phosphorylated Ca(2+)/calmodulin kinase II (p CaMKII) protein, c <strong>fos</strong> mRNA, c <strong>Fos</strong> protein, are observed in the specific brain areas of mice and/or rats showing signs of naloxone precipitated <b>withdrawal</b>.
+FOS	drug	opioid	15464026	The activation of CaMKII and increased expression of c <strong>Fos</strong> protein in the brain of animals with <b>naloxone</b> precipitated withdrawal syndrome are prevented by NMDA receptor antagonists, whereas the increased levels of extracellular glutamate are not prevented by them.
+FOS	addiction	withdrawal	15464026	The activation of CaMKII and increased expression of c <strong>Fos</strong> protein in the brain of animals with naloxone precipitated <b>withdrawal</b> syndrome are prevented by NMDA receptor antagonists, whereas the increased levels of extracellular glutamate are not prevented by them.
+FOS	drug	amphetamine	15447667	We report that transection of corticostriatal afferents selectively blocks, whereas enhancement of cortical activity with an ampakine selectively augments, the number of <b>amphetamine</b> evoked c <strong>fos</strong> positive striatopallidal (but not striatonigral) neurons.
+FOS	drug	amphetamine	15447667	In addition, blockade of the extracellular signal regulated kinase (ERK)/mitogen activated protein kinase (MAPK) signaling cascade preferentially inhibits the number of <b>amphetamine</b> evoked c <strong>fos</strong> positive striatopallidal neurons.
+FOS	drug	amphetamine	15447664	In the present study, to identify potential anatomical substrates for the discriminative stimulus effects of <b>methamphetamine</b>, we investigated the drug discrimination associated <strong>Fos</strong> expression in Sprague Dawley rats trained to discriminate <b>methamphetamine</b> from saline under a two lever fixed ratio 20 (FR 20) schedule of food reinforcement.
+FOS	addiction	reward	15447664	In the present study, to identify potential anatomical substrates for the discriminative stimulus effects of methamphetamine, we investigated the drug discrimination associated <strong>Fos</strong> expression in Sprague Dawley rats trained to discriminate methamphetamine from saline under a two lever fixed ratio 20 (FR 20) schedule of food <b>reinforcement</b>.
+FOS	drug	amphetamine	15447664	<strong>Fos</strong> expression in the brains of rats that discriminate <b>methamphetamine</b> from saline was significantly increased in the nucleus accumbens (NAc) and the ventral tegmental area (VTA), but not in other areas including the cerebral cortex, caudate putamen, substantia nigra, hippocampus, amygdala and habenulla, as compared with the expression in control rats that were maintained under the FR 20 schedule.
+FOS	addiction	reward	15371743	BP 897 reduced brain regional activation, measured by c <strong>fos</strong> imaging after the <b>CPP</b> test session, in the somatosensory cortex of drd3+/+, but not drd3 /  mice.
+FOS	addiction	withdrawal	15312814	Next, sections through the locus coeruleus (LC) and nucleus of the solitary tract (NTS), brainstem areas exhibiting cellular activation following opiate <b>withdrawal</b>, were processed for c <strong>Fos</strong> to detect early gene expression.
+FOS	drug	alcohol	15312814	Withdrawal was attenuated and c <strong>Fos</strong>, PKA, and pCREB expression was decreased in the NTS and LC of rats receiving chronic very low doses of <b>naltrexone</b>.
+FOS	addiction	withdrawal	15312814	<b>Withdrawal</b> was attenuated and c <strong>Fos</strong>, PKA, and pCREB expression was decreased in the NTS and LC of rats receiving chronic very low doses of naltrexone.
+FOS	addiction	relapse	15295023	To investigate the function of this circuit during drug <b>seeking</b>, we characterized <strong>Fos</strong> immunoreactivity of particular neuron classes in each region.
+FOS	addiction	reward	15295023	Within the BLC and NAcc of drug paired and drug unpaired animals tested for <b>CPP</b>, we observed no significant differences in the percentage of <strong>Fos</strong> immunoreactive (IR) cells that were also GAD67 IR.
+FOS	drug	opioid	15287893	Activation of <strong>AP 1</strong> and CRE dependent gene expression via mu <b>opioid</b> receptor.
+FOS	drug	opioid	15287893	Transcription factors Ca2+/cAMP responsive element binding protein (CREB) and activator protein 1 (<strong>AP 1</strong>) may constitute a direct link between the <b>opioid</b> regulated signal transduction pathways and modulation of gene expression.
+FOS	drug	opioid	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during withdrawal from the <b>opioid</b>.
+FOS	addiction	withdrawal	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during <b>withdrawal</b> from the opioid.
+FOS	drug	cannabinoid	15280883	Using <strong>Fos</strong> as a marker, we tested the hypothesis that environmental stress and CB1 <b>cannabinoid</b> receptor activity interact in the regulation of amygdalar activation in male mice.
+FOS	drug	cannabinoid	15280883	In the basolateral (BLA) and medial amygdala, restraint stress produced a low level of <strong>Fos</strong> induction, which was unaffected by <b>cannabinoid</b> treatment.
+FOS	drug	cannabinoid	15280883	Interestingly, the CB1 receptor antagonist <b>SR141716</b> dose dependently increased <strong>Fos</strong> expression in the BLA and CeA.
+FOS	drug	amphetamine	15261093	Short term effects of the nociceptin receptor antagonist Compound B on the development of <b>methamphetamine</b> sensitization in mice: a behavioral and c <strong>fos</strong> expression mapping study.
+FOS	addiction	sensitization	15261093	Short term effects of the nociceptin receptor antagonist Compound B on the development of methamphetamine <b>sensitization</b> in mice: a behavioral and c <strong>fos</strong> expression mapping study.
+FOS	drug	amphetamine	15261093	Six days later, <b>methamphetamine</b> (1 mg/kg s.c.) was administered and locomotor activity monitored again before determining neural activity by analysis of c <strong>fos</strong> expression.
+FOS	drug	cocaine	15254092	Rapid infusions potentiated the ability of <b>cocaine</b> to block DA reuptake, to induce c <strong>fos</strong> and arc mRNA expression, especially in mesocorticolimbic regions, and to produce psychomotor sensitization.
+FOS	addiction	sensitization	15254092	Rapid infusions potentiated the ability of cocaine to block DA reuptake, to induce c <strong>fos</strong> and arc mRNA expression, especially in mesocorticolimbic regions, and to produce psychomotor <b>sensitization</b>.
+FOS	drug	nicotine	15251884	Using in situ hybridization to quantify mRNA levels of the immediate early gene, <strong>cfos</strong>, the neuronal activating effects of <b>nicotine</b> in limbic and sensory cortices at different developmental stages are evaluated.
+FOS	drug	opioid	15249992	Changes in c <strong>fos</strong> expression in the rat heart during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	15249992	Changes in c <strong>fos</strong> expression in the rat heart during morphine <b>withdrawal</b>.
+FOS	drug	opioid	15249992	We previously demonstrated an increase in <strong>Fos</strong> expression in the heart during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	15249992	We previously demonstrated an increase in <strong>Fos</strong> expression in the heart during morphine <b>withdrawal</b>.
+FOS	drug	opioid	15249992	In the present study we examined the role of beta  and alpha adrenoceptors in <b>naloxone</b> precipitated increases in <strong>Fos</strong> expression in the heart.
+FOS	drug	opioid	15249992	Using immunohistochemical staining of <strong>Fos</strong>, the present results indicate that <b>morphine</b> withdrawal induced marked <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) within the cardiomyocyte nuclei.
+FOS	addiction	withdrawal	15249992	Using immunohistochemical staining of <strong>Fos</strong>, the present results indicate that morphine <b>withdrawal</b> induced marked <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) within the cardiomyocyte nuclei.
+FOS	drug	opioid	15249992	Moreover, Western blot analysis revealed a peak expression of c <strong>fos</strong> in the right and left ventricles after <b>naloxone</b> precipitated withdrawal in parallel with an increase in noradrenaline (NA) turnover.
+FOS	addiction	withdrawal	15249992	Moreover, Western blot analysis revealed a peak expression of c <strong>fos</strong> in the right and left ventricles after naloxone precipitated <b>withdrawal</b> in parallel with an increase in noradrenaline (NA) turnover.
+FOS	addiction	withdrawal	15249992	In the second study, the effects of the administration of adrenoceptor antagonists on <b>withdrawal</b> induced <strong>Fos</strong> expression in the heart were studied.
+FOS	addiction	withdrawal	15249992	Pretreatment with the beta antagonist, propranolol (3 mg/kg intraperitoneally) or alpha1 adrenoceptor antagonist, prazosin (1 mg/kg intraperitoneally) did not block the marked <strong>Fos</strong> IR or the hyperactivity of catecholaminergic neurons observed in the heart during <b>withdrawal</b>.
+FOS	drug	opioid	15249992	However, pre treatment with alpha2 adrenoceptor antagonist, yohimbine (1 mg/kg intraperitoneally), 20 min before <b>naloxone</b> administration to <b>morphine</b> dependent rats antagonized <strong>Fos</strong> expression and the enhancement of NA turnover in the heart.
+FOS	drug	opioid	15249992	Collectively, these results suggest that noradrenergic neurons in the heart are active during <b>morphine</b> withdrawal, and that activation of transcriptional responses mediated by <strong>Fos</strong> are dependent upon cardiac alpha2 adrenoceptor.
+FOS	addiction	withdrawal	15249992	Collectively, these results suggest that noradrenergic neurons in the heart are active during morphine <b>withdrawal</b>, and that activation of transcriptional responses mediated by <strong>Fos</strong> are dependent upon cardiac alpha2 adrenoceptor.
+FOS	drug	opioid	15196794	The present study revealed a significant increase in c <strong>Fos</strong> protein expression in the cortex and thalamus of mice showing <b>naloxone</b> precipitated withdrawal syndrome.
+FOS	addiction	withdrawal	15196794	The present study revealed a significant increase in c <strong>Fos</strong> protein expression in the cortex and thalamus of mice showing naloxone precipitated <b>withdrawal</b> syndrome.
+FOS	drug	opioid	15196794	The combination of dizocilpine and <b>morphine</b> prevented the increase of c <strong>Fos</strong> protein expression in the cortex and thalamus.
+FOS	drug	opioid	15196794	Acute dizocilpine treatment prior to the <b>naloxone</b> challenge and repeated treatment with dizocilpine alone had no effect on analgesia, withdrawal manifestations, p CaMK II levels or c <strong>Fos</strong> protein levels.
+FOS	addiction	withdrawal	15196794	Acute dizocilpine treatment prior to the naloxone challenge and repeated treatment with dizocilpine alone had no effect on analgesia, <b>withdrawal</b> manifestations, p CaMK II levels or c <strong>Fos</strong> protein levels.
+FOS	drug	opioid	15196794	These results showed that co administration of dizocilpine and <b>morphine</b> prevented the development of <b>morphine</b> tolerance and dependence and suggested that the preventive effect of dizocilpine results from the regulation of c <strong>Fos</strong> protein expression, which is possibly involved in the activation of the Ca2+/calmodulin dependent signal cascade in the cortex.
+FOS	addiction	dependence	15196794	These results showed that co administration of dizocilpine and morphine prevented the development of morphine tolerance and <b>dependence</b> and suggested that the preventive effect of dizocilpine results from the regulation of c <strong>Fos</strong> protein expression, which is possibly involved in the activation of the Ca2+/calmodulin dependent signal cascade in the cortex.
+FOS	drug	opioid	15196791	A neuroactive steroid, dehydroepiandrosterone sulfate, prevents the development of <b>morphine</b> dependence and tolerance via c <strong>fos</strong> expression linked to the extracellular signal regulated protein kinase.
+FOS	addiction	dependence	15196791	A neuroactive steroid, dehydroepiandrosterone sulfate, prevents the development of morphine <b>dependence</b> and tolerance via c <strong>fos</strong> expression linked to the extracellular signal regulated protein kinase.
+FOS	drug	opioid	15196791	The expression of c <strong>fos</strong> mRNA was observed in the frontal cortex and thalamus of mice showing signs of <b>naloxone</b> precipitated withdrawal, while the expression of c <strong>fos</strong> mRNA was significantly diminished by co administration of DHEAS with <b>morphine</b>.
+FOS	addiction	withdrawal	15196791	The expression of c <strong>fos</strong> mRNA was observed in the frontal cortex and thalamus of mice showing signs of naloxone precipitated <b>withdrawal</b>, while the expression of c <strong>fos</strong> mRNA was significantly diminished by co administration of DHEAS with morphine.
+FOS	drug	opioid	15196791	These results showed that DHEAS prevented the development of <b>morphine</b> tolerance and dependence and suggested that the attenuating effects of DHEAS might result from the regulation of c <strong>fos</strong> mRNA expression, which is possibly involved the signaling activation of ERK, but not of cAMP pathway.
+FOS	addiction	dependence	15196791	These results showed that DHEAS prevented the development of morphine tolerance and <b>dependence</b> and suggested that the attenuating effects of DHEAS might result from the regulation of c <strong>fos</strong> mRNA expression, which is possibly involved the signaling activation of ERK, but not of cAMP pathway.
+FOS	drug	opioid	15183518	In the NAc shell, <b>morphine</b> administration resulted in upregulation of caspace 9, NF kappaB, NF H, tau, GABA A delta subunit, FGFR1, Ggamma2, synuclein 1, syntaxin 5 and 13, GRK5, and c <strong>fos</strong> mRNAs.
+FOS	addiction	withdrawal	15176483	Whereas earlier studies have primarily demonstrated an early and transient transcriptional activation of members of the <strong>Fos</strong>, Jun, and Krox families, recent microarray studies investigating the delayed response could additionally identify several transcriptional repressors such as cAMP response element modulator (CREM), IkappaB, silencer factor B, helix loop helix proteins, or glucocorticoid induced leucine zipper, indicating the attempt of the brain to re establish homeostasis after <b>withdrawal</b> induced excitation.
+FOS	drug	opioid	15175841	Withdrawal induced c <strong>Fos</strong> expression in the rat centromedial amygdala 24 h following a single <b>morphine</b> exposure.
+FOS	addiction	withdrawal	15175841	<b>Withdrawal</b> induced c <strong>Fos</strong> expression in the rat centromedial amygdala 24 h following a single morphine exposure.
+FOS	drug	opioid	15175841	Subsequently, the expression of the protein product of c <strong>fos</strong> gene (c <strong>Fos</strong>) following <b>naloxone</b> administration was measured within the extended amygdala.
+FOS	drug	opioid	15175841	A significant increase in c <strong>Fos</strong> immunoreactivity was seen in the centromedial amygdala (CMA), but not in the bed nucleus of the stria terminalis (BST) and the shell (AcbSh) of the nucleus accumbens (Acb) in rats treated with both <b>morphine</b> and <b>naloxone</b>.
+FOS	drug	opioid	15147776	Effect of <b>naloxone</b> precipitated <b>morphine</b> withdrawal on c <strong>fos</strong> expression in rat corticotropin releasing hormone neurons in the paraventricular hypothalamus and extended amygdala.
+FOS	addiction	withdrawal	15147776	Effect of naloxone precipitated morphine <b>withdrawal</b> on c <strong>fos</strong> expression in rat corticotropin releasing hormone neurons in the paraventricular hypothalamus and extended amygdala.
+FOS	drug	opioid	15147776	Here, by means of dual immunohistochemical methodology, we examined the co expression of the c <strong>Fos</strong> protein and CRH following <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	15147776	Here, by means of dual immunohistochemical methodology, we examined the co expression of the c <strong>Fos</strong> protein and CRH following naloxone precipitated morphine <b>withdrawal</b>.
+FOS	drug	opioid	15147776	We found that <b>naloxone</b> precipitated withdrawal of <b>morphine</b> dependent rats increased c <strong>Fos</strong> immunoreactivity (IR) in CRH positive neurons in the paraventricular hypothalamus.
+FOS	addiction	withdrawal	15147776	We found that naloxone precipitated <b>withdrawal</b> of morphine dependent rats increased c <strong>Fos</strong> immunoreactivity (IR) in CRH positive neurons in the paraventricular hypothalamus.
+FOS	drug	opioid	15147776	Withdrawal of <b>morphine</b> dependent rats also increased c <strong>Fos</strong> IR in the central amygdala and bed nucleus of the stria terminalis, however these were in CRH negative neurons.
+FOS	addiction	withdrawal	15147776	<b>Withdrawal</b> of morphine dependent rats also increased c <strong>Fos</strong> IR in the central amygdala and bed nucleus of the stria terminalis, however these were in CRH negative neurons.
+FOS	drug	opioid	15138436	<b>Morphine</b> induced c <strong>fos</strong> mRNA expression in striatofugal circuits: modulation by dose, environmental context, and drug history.
+FOS	drug	opioid	15138436	We report that, when given in the home cage, <b>morphine</b> produced a small, but significant increase in the number of c <strong>fos</strong>+ striatonigral cells and c <strong>fos</strong>+ cells in cingulate cortex, but had no effect on the number of c <strong>fos</strong>+ striatopallidal cells.
+FOS	drug	opioid	15138436	When given in a novel test environment, however, <b>morphine</b> dramatically increased the number of c <strong>fos</strong>+ striatonigral cells in a dose dependent fashion, and this effect was maintained following repeated treatment.
+FOS	drug	opioid	15138436	Unexpectedly, <b>morphine</b> treatment in a novel environment produced a dose dependent reduction in the number of c <strong>fos</strong>+ striatopallidal cells and c <strong>fos</strong>+ cells in cingulate cortex, relative to exposure to novelty alone effects that were reversed by repeated <b>morphine</b> treatment.
+FOS	drug	opioid	15138436	We suggest that alterations in c <strong>fos</strong> expression patterns in striatofugal circuits following <b>morphine</b> administration may be involved in drug experience dependent plasticity.
+FOS	drug	cocaine	15128409	), did not alter <b>cocaine</b> induced c <strong>Fos</strong> expression in the caudate putamen or nucleus accumbens core.
+FOS	drug	cocaine	15128409	However, rolipram, but not <b>cocaine</b>, induced c <strong>Fos</strong> in the nucleus accumbens shell.
+FOS	drug	cocaine	15128409	These results indicate that elevation of cAMP in neurons that express PDE4s may attenuate the rewarding properties of <b>cocaine</b> and morphine, but does not alter the <b>cocaine</b> signalling cascade that induces c <strong>Fos</strong> expression.
+FOS	drug	opioid	15128409	These results indicate that elevation of cAMP in neurons that express PDE4s may attenuate the rewarding properties of cocaine and <b>morphine</b>, but does not alter the cocaine signalling cascade that induces c <strong>Fos</strong> expression.
+FOS	drug	alcohol	15100610	<b>Ethanol</b> induced <strong>Fos</strong> immunoreactivity in the extended amygdala and hypothalamus of the rat brain: focus on cholinergic interneurons of the nucleus accumbens.
+FOS	drug	alcohol	15100610	The primary goal of this study was to investigate the effects of varying doses of <b>ethanol</b> on cellular activation, as measured by <strong>Fos</strong> immunoreactivity, in brain areas that have been implicated in the reinforcing and anxiolytic effects of substance abuse and dependence, namely, the extended amygdala and hypothalamus.
+FOS	addiction	dependence	15100610	The primary goal of this study was to investigate the effects of varying doses of ethanol on cellular activation, as measured by <strong>Fos</strong> immunoreactivity, in brain areas that have been implicated in the reinforcing and anxiolytic effects of substance abuse and <b>dependence</b>, namely, the extended amygdala and hypothalamus.
+FOS	addiction	reward	15100610	The primary goal of this study was to investigate the effects of varying doses of ethanol on cellular activation, as measured by <strong>Fos</strong> immunoreactivity, in brain areas that have been implicated in the <b>reinforcing</b> and anxiolytic effects of substance abuse and dependence, namely, the extended amygdala and hypothalamus.
+FOS	drug	alcohol	15100610	A dose of 2 g/kg of <b>ethanol</b> significantly increased the number of <strong>Fos</strong> immunoreactive neurons in the central nucleus of the amygdala by 149%, in the shell nucleus accumbens by 80%, and in the paraventricular nucleus of the hypothalamus by 321%.
+FOS	drug	alcohol	15100610	Additionally, 1 g/kg of <b>ethanol</b> significantly increased the percentage of <strong>Fos</strong> immunoreactive cholinergic neurons in the nucleus accumbens by 59%.
+FOS	drug	opioid	15033383	<b>Morphine</b> withdrawal induced c <strong>fos</strong> expression in the heart: a peripheral mechanism.
+FOS	addiction	withdrawal	15033383	Morphine <b>withdrawal</b> induced c <strong>fos</strong> expression in the heart: a peripheral mechanism.
+FOS	drug	opioid	15033383	In the present study, <b>naloxone</b> methiodide (quaternary derivative of <b>naloxone</b> that does not cross the blood brain barrier) and <b>naloxone</b> were administered to <b>morphine</b> dependent rats and <strong>Fos</strong> immunostaining was used as a reflection of neuronal activity.
+FOS	drug	opioid	15033383	Using immunohistochemical staining of <strong>Fos</strong>, present results indicate that the administration of <b>naloxone</b> methiodide or <b>naloxone</b> to <b>morphine</b> dependent rats induced marked <strong>Fos</strong> immunoreactivity within the cardiomyocyte nuclei.
+FOS	drug	opioid	15033383	Moreover, Western blot analysis revealed a peak expression of c <strong>fos</strong> in the right and left ventricles after <b>naloxone</b> methiodide  or <b>naloxone</b> precipitated withdrawal.
+FOS	addiction	withdrawal	15033383	Moreover, Western blot analysis revealed a peak expression of c <strong>fos</strong> in the right and left ventricles after naloxone methiodide  or naloxone precipitated <b>withdrawal</b>.
+FOS	drug	opioid	15033383	In addition, in the hypothalamic paraventricular nucleus (PVN), <strong>Fos</strong> expression was increased after <b>naloxone</b> but not after <b>naloxone</b> methiodide administration to <b>morphine</b> dependent rats.
+FOS	drug	opioid	15033383	These results suggest that the activation of c <strong>fos</strong> expression observed during <b>morphine</b> withdrawal in the heart is due to intrinsic mechanisms outside the central nervous system (CNS).
+FOS	addiction	withdrawal	15033383	These results suggest that the activation of c <strong>fos</strong> expression observed during morphine <b>withdrawal</b> in the heart is due to intrinsic mechanisms outside the central nervous system (CNS).
+FOS	drug	nicotine	15026155	Acupuncture attenuates repeated <b>nicotine</b> induced behavioral sensitization and c <strong>Fos</strong> expression in the nucleus accumbens and striatum of the rat.
+FOS	addiction	sensitization	15026155	Acupuncture attenuates repeated nicotine induced behavioral <b>sensitization</b> and c <strong>Fos</strong> expression in the nucleus accumbens and striatum of the rat.
+FOS	drug	nicotine	15026155	We examined the effect of acupuncture on <b>nicotine</b> induced behavioral locomotor activity and c <strong>fos</strong> expression in the nucleus accumbens and striatum utilizing the immunocytochemical detection of the <strong>Fos</strong> protein.
+FOS	drug	nicotine	15026155	Acupuncture at zusanli (ST36), but not control, significantly attenuated expected increase in <b>nicotine</b> induced locomotor activity and <strong>Fos</strong> like immunoreactivity in the nucleus accumebns and striatum to subsequent <b>nicotine</b> challenge.
+FOS	drug	cocaine	15019428	One week after a single social defeat stress, cross sensitization to <b>cocaine</b> is evident in terms of enhanced motor activity as well as in terms of increased <strong>Fos</strong> labeling in the periaqueductal grey area, the locus coeruleus, and the dorsal raphe nuclei.
+FOS	addiction	sensitization	15019428	One week after a single social defeat stress, cross <b>sensitization</b> to cocaine is evident in terms of enhanced motor activity as well as in terms of increased <strong>Fos</strong> labeling in the periaqueductal grey area, the locus coeruleus, and the dorsal raphe nuclei.
+FOS	drug	amphetamine	15010207	reduced <b>AMPH</b> stimulated c <strong>fos</strong> mRNA levels in the dorsal (caudoputamen) and ventral (nucleus accumbens) striatum as revealed by quantitative in situ hybridization.
+FOS	drug	amphetamine	15010207	In contrast to c <strong>fos</strong> mRNAs, <b>AMPH</b> stimulated mRNA expression of another IEG, zif/268, was not significantly altered by the blockade of mGluR5 with MPEP in the entire striatum and the three areas of cortex.
+FOS	drug	amphetamine	15010207	These results indicate that an mGluR5 dependent mechanism selectively contributes to c <strong>fos</strong> expression in the striatum and cortex in response to acute exposure to <b>AMPH</b>.
+FOS	drug	benzodiazepine	15009662	In wild type animals, <b>diazepam</b> reduced the expression levels of the alpha subunit of the calcium/calmodulin dependent protein kinase II, as well as brain derived neurotrophic factor, MAP kinase phosphatase, transcription factor GIF, c <strong>fos</strong> and nerve growth factor induced gene A.
+FOS	drug	amphetamine	14751279	Long term behavioral and neuronal cross sensitization to <b>amphetamine</b> induced by repeated brief social defeat stress: <strong>Fos</strong> in the ventral tegmental area and amygdala.
+FOS	addiction	sensitization	14751279	Long term behavioral and neuronal cross <b>sensitization</b> to amphetamine induced by repeated brief social defeat stress: <strong>Fos</strong> in the ventral tegmental area and amygdala.
+FOS	drug	amphetamine	14751279	<b>Amphetamine</b> augmented stress induced <strong>Fos</strong> LI labeling 17 days after the first stress episode in the dorsal striatum, NAc core, and medial amygdala, reflecting a cross sensitization of <strong>Fos</strong> response.
+FOS	addiction	sensitization	14751279	Amphetamine augmented stress induced <strong>Fos</strong> LI labeling 17 days after the first stress episode in the dorsal striatum, NAc core, and medial amygdala, reflecting a cross <b>sensitization</b> of <strong>Fos</strong> response.
+FOS	drug	amphetamine	14751279	<b>Amphetamine</b> challenge 70 days after social stress exposures revealed sensitized <strong>Fos</strong> LI labeling in the VTA and the amygdala.
+FOS	drug	alcohol	14741756	c <strong>fos</strong> and cleaved caspase 3 expression after perinatal exposure to <b>ethanol</b>, cocaine, or the combination of both drugs.
+FOS	drug	cocaine	14741756	c <strong>fos</strong> and cleaved caspase 3 expression after perinatal exposure to ethanol, <b>cocaine</b>, or the combination of both drugs.
+FOS	drug	cocaine	14741756	At birth, the brains of fetuses exposed to <b>cocaine</b> exhibited an increase in <strong>Fos</strong> immunoreactivity in many brain regions.
+FOS	drug	alcohol	14741756	Prenatal exposure to <b>ethanol</b> did not increase <strong>Fos</strong> expression above that observed in control rats at early points after birth.
+FOS	drug	alcohol	14741756	However, <strong>Fos</strong> expression at 24 h after birth was higher after <b>ethanol</b> diet treatment in several brain regions, such as the amygdala, ventromedial hypothalamus, and medial thalamus.
+FOS	drug	alcohol	14741756	Only in the striatum did the combination of <b>ethanol</b> and cocaine cause greater <strong>Fos</strong> expression than either prenatal cocaine or <b>ethanol</b> alone.
+FOS	drug	cocaine	14741756	Only in the striatum did the combination of ethanol and <b>cocaine</b> cause greater <strong>Fos</strong> expression than either prenatal <b>cocaine</b> or ethanol alone.
+FOS	drug	alcohol	14741756	These results indicate that both prenatal cocaine and prenatal <b>ethanol</b> exposure increase <strong>Fos</strong> and cleaved caspase 3 expression in the developing brain in a time  and region dependent manner, but that the combination of low dose, chronic <b>ethanol</b>, and binge cocaine does not cause greater apoptosis.
+FOS	drug	cocaine	14741756	These results indicate that both prenatal <b>cocaine</b> and prenatal ethanol exposure increase <strong>Fos</strong> and cleaved caspase 3 expression in the developing brain in a time  and region dependent manner, but that the combination of low dose, chronic ethanol, and binge <b>cocaine</b> does not cause greater apoptosis.
+FOS	addiction	intoxication	14741756	These results indicate that both prenatal cocaine and prenatal ethanol exposure increase <strong>Fos</strong> and cleaved caspase 3 expression in the developing brain in a time  and region dependent manner, but that the combination of low dose, chronic ethanol, and <b>binge</b> cocaine does not cause greater apoptosis.
+FOS	drug	cocaine	14725964	Morphine  and <b>cocaine</b> induced c <strong>Fos</strong> levels in Lewis and Fischer rat strains.
+FOS	drug	opioid	14725964	<b>Morphine</b>  and cocaine induced c <strong>Fos</strong> levels in Lewis and Fischer rat strains.
+FOS	addiction	aversion	14725964	All animals were subsequently tested for c <strong>Fos</strong> expression in areas of the brain associated with <b>aversion</b> learning (the lateral and medial parabrachial nucleus, intermediate and caudal nucleus tractus solitarius and area postrema), reward (the shell of the nucleus accumbens) and locomotion (the core of the nucleus accumbens and the caudate putamen).
+FOS	addiction	reward	14725964	All animals were subsequently tested for c <strong>Fos</strong> expression in areas of the brain associated with aversion learning (the lateral and medial parabrachial nucleus, intermediate and caudal nucleus tractus solitarius and area postrema), <b>reward</b> (the shell of the nucleus accumbens) and locomotion (the core of the nucleus accumbens and the caudate putamen).
+FOS	drug	cocaine	14725964	The present results indicated that patterns of morphine  and <b>cocaine</b> induced c <strong>Fos</strong> within CTA associated, but not reward  or locomotor associated, brain regions paralleled the differential behavioral sensitivities of LEW and F344 rats to these drugs within CTA learning.
+FOS	drug	opioid	14725964	The present results indicated that patterns of <b>morphine</b>  and cocaine induced c <strong>Fos</strong> within CTA associated, but not reward  or locomotor associated, brain regions paralleled the differential behavioral sensitivities of LEW and F344 rats to these drugs within CTA learning.
+FOS	addiction	aversion	14725964	The present results indicated that patterns of morphine  and cocaine induced c <strong>Fos</strong> within <b>CTA</b> associated, but not reward  or locomotor associated, brain regions paralleled the differential behavioral sensitivities of LEW and F344 rats to these drugs within <b>CTA</b> learning.
+FOS	addiction	reward	14725964	The present results indicated that patterns of morphine  and cocaine induced c <strong>Fos</strong> within CTA associated, but not <b>reward</b>  or locomotor associated, brain regions paralleled the differential behavioral sensitivities of LEW and F344 rats to these drugs within CTA learning.
+FOS	drug	cannabinoid	14694354	A possible link between <b>cannabinoid</b> processes and D3  and/or D2 mediated dopaminergic transmission was further investigated by studying <strong>Fos</strong> protein expression in cortico limbic structures in D3 (D3 / ) and D2 (D2 / ) knockout mice.
+FOS	drug	cannabinoid	14694354	<b>Rimonabant</b> (10 mg/kg) increased <strong>Fos</strong> immunoreactivity in the prefrontal cortex (pFCortex) and in the shell but not the core of the nucleus accumbens (NAcc).
+FOS	drug	cannabinoid	14694354	<strong>Fos</strong> induction by this dose of <b>rimonabant</b> was not seen in mice lacking CB1 receptors, providing clear evidence for the involvement of CB1 receptors.
+FOS	drug	cannabinoid	14694354	In contrast, <strong>Fos</strong> expression by <b>rimonabant</b> in the pFCortex was impervious to D2 or D3 receptor deletion.
+FOS	drug	cocaine	14657156	Indeed, EE mice showed decreased locomotor activity in response to <b>cocaine</b> (10 and 20 mg/kg) as well as a different pattern of c <strong>fos</strong> expression in the striatum compared with SE mice.
+FOS	drug	cocaine	14644470	Coc1h animals showed enhanced c <strong>Fos</strong> reactivity in dopaminergic mesocorticolimbic brain regions and a sensitized locomotor response to IV <b>cocaine</b>.
+FOS	drug	opioid	14610238	We hypothesize that GABA(B) receptor agonist treatment in the VTA blocks <b>morphine</b> induced motor stimulation, motor sensitization, and accumbal <strong>Fos</strong> immunoreactivity by inhibiting the activation of dopaminergic neurons.
+FOS	addiction	sensitization	14610238	We hypothesize that GABA(B) receptor agonist treatment in the VTA blocks morphine induced motor stimulation, motor <b>sensitization</b>, and accumbal <strong>Fos</strong> immunoreactivity by inhibiting the activation of dopaminergic neurons.
+FOS	drug	opioid	14610238	Next, <b>morphine</b> was administered on days 1, 3, 5, and 9 and mice demonstrated sensitization to its motor stimulant effects and concomitant induction of <strong>Fos</strong> immunoreactivity in the NAc shell (NAcS) but not NAc core.
+FOS	addiction	sensitization	14610238	Next, morphine was administered on days 1, 3, 5, and 9 and mice demonstrated <b>sensitization</b> to its motor stimulant effects and concomitant induction of <strong>Fos</strong> immunoreactivity in the NAc shell (NAcS) but not NAc core.
+FOS	drug	opioid	14610238	Intra VTA baclofen administered during <b>morphine</b> pretreatment blocked the acquisition of <b>morphine</b> induced motor sensitization and <strong>Fos</strong> activation in the NAcS.
+FOS	addiction	sensitization	14610238	Intra VTA baclofen administered during morphine pretreatment blocked the acquisition of morphine induced motor <b>sensitization</b> and <strong>Fos</strong> activation in the NAcS.
+FOS	drug	opioid	14610238	Intra VTA baclofen administered only on day 9 blocked the expression of <b>morphine</b> induced motor sensitization and <strong>Fos</strong> activation in the NAcS.
+FOS	addiction	sensitization	14610238	Intra VTA baclofen administered only on day 9 blocked the expression of morphine induced motor <b>sensitization</b> and <strong>Fos</strong> activation in the NAcS.
+FOS	drug	opioid	14610238	A linear relationship was found between <b>morphine</b> induced motor activity and accumbal <strong>Fos</strong> in single  and repeated dose treatment groups.
+FOS	drug	opioid	14601197	<b>Fentanyl</b> increased the threshold level to noxious thermal stimulation, and reduced the formalin induced licking/biting behaviors and the number of <strong>Fos</strong> LI labelled neurons which are predominantly found in the neck of the dorsal horn.
+FOS	drug	opioid	14601197	Unlike <b>fentanyl</b>, nitrous oxide and halothane failed to suppress c <strong>fos</strong> expression.
+FOS	drug	alcohol	14576487	The injurious effects of <b>ethanol</b> on the pancreas may be mediated through (1) sensitization of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) sensitization of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+FOS	addiction	sensitization	14576487	The injurious effects of ethanol on the pancreas may be mediated through (1) <b>sensitization</b> of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) <b>sensitization</b> of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+FOS	drug	alcohol	14574439	Different pattern of brain c <strong>Fos</strong> expression following re exposure to <b>ethanol</b> or sucrose self administration environment.
+FOS	drug	alcohol	14574439	c <strong>Fos</strong> protein expression was used as a marker of neuronal activation.Re exposure to <b>ethanol</b> self administration environment after 30 day but not after 24 h abstinence increased the number of <strong>Fos</strong> positive nuclei in the thalamic paraventricular nucleus, granular insular cortex and medial prefrontal cortex.
+FOS	drug	alcohol	14574439	In general, no differences were found in c <strong>Fos</strong> protein expression between the rats allowed to self administer <b>alcohol</b> and the subjects exposed only to <b>alcohol</b> related stimuli.
+FOS	drug	alcohol	14574230	Recently, we found that nuclear RACK1 mediates acute <b>ethanol</b> induction of immediate early gene c <strong>fos</strong> expression.
+FOS	drug	alcohol	14574230	Therefore, we sought to determine the effects of chronic exposure of cells to <b>ethanol</b> on the cellular compartmentalization of RACK1 and on c <strong>fos</strong> messenger RNA (mRNA) and protein expression.
+FOS	drug	alcohol	14574230	Chronic exposure to <b>ethanol</b> did not result in an increase in mRNA or protein levels of c <strong>fos</strong>.
+FOS	drug	alcohol	14574230	Furthermore, acute <b>ethanol</b> exposure did not increase c <strong>fos</strong> protein levels in cells that were first treated chronically with <b>ethanol</b>.
+FOS	drug	alcohol	14574230	However, transduction of exogenous RACK1 expressed as a Tat fusion protein was able to rescue c <strong>fos</strong> mRNA expression after chronic <b>ethanol</b> exposure.
+FOS	drug	alcohol	14574230	Our data suggest that RACK1 nuclear compartmentalization and <b>ethanol</b> induced c <strong>fos</strong> expression are transient and are desensitized to <b>ethanol</b> during prolonged exposure to high concentrations.
+FOS	drug	alcohol	14574230	Our data further suggest that the altered compartmentalization of RACK1 leads to differences in c <strong>fos</strong> expression upon acute or chronic exposure to <b>ethanol</b>.
+FOS	drug	alcohol	14574230	In summary, RACK1 is an important molecular mediator of the acute and chronic actions of <b>ethanol</b> on the expression of c <strong>fos</strong>.
+FOS	drug	cocaine	14559159	MK 801 attenuates <b>cocaine</b> induction of c <strong>fos</strong> and preprodynorphin mRNA levels in Fischer rats.
+FOS	drug	cocaine	14559159	This study shows that single (15 mg/kg) or binge (3x15 mg/kg) <b>cocaine</b> administration increases c <strong>fos</strong> mRNA levels, but only binge <b>cocaine</b> administration increases preprodynorphin mRNA levels in the caudate/putamen of Fischer rats.
+FOS	addiction	intoxication	14559159	This study shows that single (15 mg/kg) or <b>binge</b> (3x15 mg/kg) cocaine administration increases c <strong>fos</strong> mRNA levels, but only <b>binge</b> cocaine administration increases preprodynorphin mRNA levels in the caudate/putamen of Fischer rats.
+FOS	drug	cocaine	14559159	This increase in both c <strong>fos</strong> and preprodynorphin mRNA levels is attenuated by the noncompetitive NMDA antagonist MK 801 (0.25 mg/kg), suggesting a preferential role for NMDA receptor co activation in cellular events leading to <b>cocaine</b> induced behaviors.
+FOS	drug	opioid	14529807	Selective induction of c <strong>Fos</strong> immunoreactivity in the prelimbic cortex during reinstatement of <b>heroin</b> seeking induced by acute food deprivation in rats.
+FOS	addiction	relapse	14529807	Selective induction of c <strong>Fos</strong> immunoreactivity in the prelimbic cortex during <b>reinstatement</b> of heroin <b>seeking</b> induced by acute food deprivation in rats.
+FOS	addiction	relapse	14529807	For this purpose, we measured, by immunohistochemistry, the expression of c <strong>Fos</strong> following a test for food deprivation induced <b>reinstatement</b>.
+FOS	drug	opioid	14529807	Food deprivation selectively increased c <strong>Fos</strong> immunoreactivity (IR) in the prelimbic cortex of <b>heroin</b> trained, but not saline trained, rats (n=4 per condition).
+FOS	drug	opioid	14529807	Food deprivation also increased c <strong>Fos</strong> IR in both <b>heroin</b>  and saline trained rats in the basolateral amygdala and the ventrolateral bed nucleus of stria terminalis (BNST), but had no effect on c <strong>Fos</strong> expression in the dorsolateral BNST, cingulate cortex, nucleus accumbens, and central amygdala.
+FOS	drug	psychedelics	14517176	injection, <b>MDMA</b> induced a strong c <strong>fos</strong> transcription in brain structures, such as caudate putamen, nucleus accumbens and hippocampus, whereas egr 1 and egr 3 transcripts were only increased in the caudate putamen.
+FOS	drug	psychedelics	14517176	In agreement with these results, <b>MDMA</b> induced c <strong>fos</strong> protein expression was blocked by SL327 in the caudate putamen.
+FOS	drug	opioid	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of <b>opioid</b> physical dependence using behavioural assessment of withdrawal and immunostaining for CGRP and <strong>Fos</strong> protein expression in the spinal cord.
+FOS	addiction	dependence	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of opioid physical <b>dependence</b> using behavioural assessment of withdrawal and immunostaining for CGRP and <strong>Fos</strong> protein expression in the spinal cord.
+FOS	addiction	withdrawal	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of opioid physical dependence using behavioural assessment of <b>withdrawal</b> and immunostaining for CGRP and <strong>Fos</strong> protein expression in the spinal cord.
+FOS	addiction	withdrawal	12970109	challenge precipitated a robust <b>withdrawal</b> syndrome that depleted CGRP like immunoreactivity and increased the number of <strong>Fos</strong> like immunoreactive neurons in the dorsal horn.
+FOS	drug	opioid	12970109	Intrathecal administration of NDGA (10, 20 microg), a nonselective LOX inhibitor, AA 861 (1.5, 3 microg), a 5 LOX selective inhibitor, or baicalein (1.4, 2.8 microg), a 12 LOX selective inhibitor, concurrently with systemic <b>morphine</b> for 5 days or as a single injection immediately preceding <b>naloxone</b> challenge, blocked the depletion of CGRP like immunoreactivity, prevented increase in the number of <strong>Fos</strong> like immunoreactive neurons in the dorsal horn, and significantly attenuated the <b>morphine</b> withdrawal syndrome.
+FOS	addiction	withdrawal	12970109	Intrathecal administration of NDGA (10, 20 microg), a nonselective LOX inhibitor, AA 861 (1.5, 3 microg), a 5 LOX selective inhibitor, or baicalein (1.4, 2.8 microg), a 12 LOX selective inhibitor, concurrently with systemic morphine for 5 days or as a single injection immediately preceding naloxone challenge, blocked the depletion of CGRP like immunoreactivity, prevented increase in the number of <strong>Fos</strong> like immunoreactive neurons in the dorsal horn, and significantly attenuated the morphine <b>withdrawal</b> syndrome.
+FOS	addiction	withdrawal	12969258	Precipitated <b>withdrawal</b> also led to up regulation of c <strong>fos</strong> mRNA in response to SKF 82958.
+FOS	drug	opioid	12956728	c <strong>Fos</strong> and peptide immunoreactivities in the central extended amygdala of <b>morphine</b> dependent rats after <b>naloxone</b> precipitated withdrawal.
+FOS	addiction	withdrawal	12956728	c <strong>Fos</strong> and peptide immunoreactivities in the central extended amygdala of morphine dependent rats after naloxone precipitated <b>withdrawal</b>.
+FOS	drug	opioid	12956728	To test its involvement during opiate withdrawal, we studied the distribution of c <strong>Fos</strong> immunoreactive neurons, in relation to their neuropeptide content, in brain sections from <b>morphine</b> dependent or naive rats, killed 90 min after <b>naloxone</b> or saline intraperitoneal injection.
+FOS	addiction	withdrawal	12956728	To test its involvement during opiate <b>withdrawal</b>, we studied the distribution of c <strong>Fos</strong> immunoreactive neurons, in relation to their neuropeptide content, in brain sections from morphine dependent or naive rats, killed 90 min after naloxone or saline intraperitoneal injection.
+FOS	drug	opioid	12956728	<b>Naloxone</b> treatment in naive rats induced a slight increase in c <strong>Fos</strong> immunoreactivity in the central amygdaloid nucleus, the lateral bed nucleus of the stria terminalis and the interstitial nucleus of the posterior limb of the anterior commissure.
+FOS	drug	opioid	12956728	In <b>morphine</b> dependent rats, <b>naloxone</b> injection significantly increased the number of c <strong>Fos</strong> positive neurons in these structures as well as in the majority of the other central extended amygdala components.
+FOS	drug	opioid	12956728	Corticotropin releasing factor  and methionine enkephakin immunoreactive neurons displayed c <strong>Fos</strong> immunoreactivity in naive rats after <b>naloxone</b> injection, whereas only enkephalinergic neurons were found to be c <strong>Fos</strong> positive in <b>morphine</b> dependent rats after <b>naloxone</b> injection.
+FOS	drug	opioid	12934646	Furthermore, we examined c <strong>fos</strong> expression in the parietal cortex, piriform cortex, striatum, nucleus accumbens, and hippocampus of the <b>morphine</b> induced CPP mouse brain.
+FOS	addiction	reward	12934646	Furthermore, we examined c <strong>fos</strong> expression in the parietal cortex, piriform cortex, striatum, nucleus accumbens, and hippocampus of the morphine induced <b>CPP</b> mouse brain.
+FOS	drug	opioid	12934646	Expression of c <strong>fos</strong> was increased in the cortex, striatum, nucleus accumbens, and hippocampus of the <b>morphine</b> induced CPP mouse brain.
+FOS	addiction	reward	12934646	Expression of c <strong>fos</strong> was increased in the cortex, striatum, nucleus accumbens, and hippocampus of the morphine induced <b>CPP</b> mouse brain.
+FOS	drug	opioid	12934646	Taken together, these results suggest that MCJ inhibits <b>morphine</b> induced CPP through the regulation of c <strong>fos</strong> expression in the mouse brain.
+FOS	addiction	reward	12934646	Taken together, these results suggest that MCJ inhibits morphine induced <b>CPP</b> through the regulation of c <strong>fos</strong> expression in the mouse brain.
+FOS	drug	cocaine	12927219	The main finding of this study is that cholinergic interneurons located in the shell compartment of the nucleus accumbens and the ventromedial striatum were activated, as measured by <strong>Fos</strong> labeling, following a 1 h session of the self administration of <b>cocaine</b> in rats.
+FOS	drug	amphetamine	12890524	Environmental context and drug history modulate <b>amphetamine</b> induced c <strong>fos</strong> mRNA expression in the basal ganglia, central extended amygdala, and associated limbic forebrain.
+FOS	drug	amphetamine	12890524	When given in a novel test environment <b>amphetamine</b> produces greater levels of c <strong>fos</strong> and arc mRNA expression in many brain regions relative to when it is given in the home cage.
+FOS	drug	amphetamine	12890524	The purpose of the current study was to determine if environment and drug history interact to influence <b>amphetamine</b> induced c <strong>fos</strong> mRNA expression.
+FOS	drug	amphetamine	12890524	In most brain regions <b>amphetamine</b> given in the Novel environment produced greater c <strong>fos</strong> mRNA expression than when given it was given at Home, and drug history had no effect on <b>amphetamine</b> induced c <strong>fos</strong> mRNA expression.
+FOS	drug	amphetamine	12890524	However, within the subthalamic nucleus, substantia nigra reticulata, and central nucleus of the amygdala prior experience with <b>amphetamine</b> in the Novel but not Home environment enhanced the effect of an <b>amphetamine</b> challenge injection on c <strong>fos</strong> mRNA expression.
+FOS	drug	amphetamine	12890524	In contrast, there was a decrease in c <strong>fos</strong> mRNA expression in <b>amphetamine</b> pretreated animals, regardless of environmental context, in the ventral portion of the far caudal striatum.
+FOS	drug	amphetamine	12890524	Reexposure to an environment previously paired with <b>amphetamine</b> produced a conditioned increase in c <strong>fos</strong> mRNA expression in portions of the caudate putamen, the subthalamic nucleus, the nucleus accumbens shell and a conditioned decrease in c <strong>fos</strong> mRNA expression in the central nucleus of the amygdala.
+FOS	drug	opioid	12853567	Both c <strong>fos</strong> immunoreactivity, a marker of neuronal activity, and phosphorylation of tyrosine hydroxylase at Ser 40, a marker of cAMP levels, are decreased in the locus coeruleus by galnon treatment after <b>morphine</b> withdrawal, suggesting a possible molecular mechanism for the behavioral effects of galanin.
+FOS	addiction	withdrawal	12853567	Both c <strong>fos</strong> immunoreactivity, a marker of neuronal activity, and phosphorylation of tyrosine hydroxylase at Ser 40, a marker of cAMP levels, are decreased in the locus coeruleus by galnon treatment after morphine <b>withdrawal</b>, suggesting a possible molecular mechanism for the behavioral effects of galanin.
+FOS	drug	cocaine	12821377	Blockade of D1 dopaminergic transmission alleviates c <strong>fos</strong> induction and cleaved caspase 3 expression in the brains of rat pups exposed to prenatal <b>cocaine</b> or perinatal asphyxia.
+FOS	drug	cocaine	12821377	Both <b>cocaine</b> binge (3 x 15 mg/kg) and perinatal asphyxia on embryonic day 22 (E22) induced c <strong>fos</strong> in the striatum as well as in several other brain regions within 3 h after treatment.
+FOS	addiction	intoxication	12821377	Both cocaine <b>binge</b> (3 x 15 mg/kg) and perinatal asphyxia on embryonic day 22 (E22) induced c <strong>fos</strong> in the striatum as well as in several other brain regions within 3 h after treatment.
+FOS	drug	cocaine	12821377	Maternal administration of a D1 dopamine antagonist, SCH 23390, before either <b>cocaine</b> or asphyxia exposure dramatically reduced the numbers of <strong>Fos</strong> immunoreactive cells in the striatum as well as in many other brain regions.
+FOS	drug	amphetamine	12821175	<strong>Fos</strong> but not Cart (cocaine and <b>amphetamine</b> regulated transcript) is overexpressed by several drugs of abuse: a comparative study using real time quantitative polymerase chain reaction in rat brain.
+FOS	drug	cocaine	12821175	<strong>Fos</strong> but not Cart (<b>cocaine</b> and amphetamine regulated transcript) is overexpressed by several drugs of abuse: a comparative study using real time quantitative polymerase chain reaction in rat brain.
+FOS	addiction	addiction	12821175	To establish whether or not Cart can be consider as a valuable marker of <b>addiction</b> we performed a comparative study of the expression of Cart and <strong>Fos</strong> genes by several drugs of abuse.
+FOS	drug	cannabinoid	12821175	As expected, a significant induction of the immediate early gene <strong>Fos</strong> was observed after acute administration of morphine, cocaine, 3, 4 methylenedioxymethamphetamine and Delta(9) <b>Tetrahydrocannabinol</b>.
+FOS	drug	cocaine	12821175	As expected, a significant induction of the immediate early gene <strong>Fos</strong> was observed after acute administration of morphine, <b>cocaine</b>, 3, 4 methylenedioxymethamphetamine and Delta(9) Tetrahydrocannabinol.
+FOS	drug	opioid	12821175	As expected, a significant induction of the immediate early gene <strong>Fos</strong> was observed after acute administration of <b>morphine</b>, cocaine, 3, 4 methylenedioxymethamphetamine and Delta(9) Tetrahydrocannabinol.
+FOS	drug	psychedelics	12821175	As expected, a significant induction of the immediate early gene <strong>Fos</strong> was observed after acute administration of morphine, cocaine, 3, 4 <b>methylenedioxymethamphetamine</b> and Delta(9) Tetrahydrocannabinol.
+FOS	drug	alcohol	12818716	Effects of intracerebroventricular <b>ethanol</b> on ingestive behavior and induction of c <strong>Fos</strong> immunoreactivity in selected brain regions.
+FOS	addiction	aversion	12818716	In the present study, we tested whether ETOH[ICV] could induce a conditioned taste preference (CTP) or <b>aversion</b> (<b>CTA</b>) and alter c <strong>Fos</strong> immunoreactivity (c <strong>Fos</strong> IR) in brain regions associated with feeding, <b>aversion</b>, and/or reward.
+FOS	addiction	reward	12818716	In the present study, we tested whether ETOH[ICV] could induce a conditioned taste preference (CTP) or aversion (CTA) and alter c <strong>Fos</strong> immunoreactivity (c <strong>Fos</strong> IR) in brain regions associated with feeding, aversion, and/or <b>reward</b>.
+FOS	addiction	reward	12818716	ETOH[ICV] significantly increased c <strong>Fos</strong> IR in a number of brain sites associated with feeding and <b>reward</b> including the bed nucleus of the stria terminalis, lateral dorsal area (BSTLD); nucleus accumbens, shell area (AcbSh); hypothalamic paraventricular nucleus (PVN); and lateral septum, ventral area (LSV).
+FOS	addiction	aversion	12818716	Thus, ETOH induced a CTP, not <b>CTA</b>, via central mechanisms; it increased c <strong>Fos</strong> IR in specific sites associated with feeding and reward.
+FOS	addiction	reward	12818716	Thus, ETOH induced a CTP, not CTA, via central mechanisms; it increased c <strong>Fos</strong> IR in specific sites associated with feeding and <b>reward</b>.
+FOS	drug	opioid	12814374	<b>Morphine</b> withdrawal precipitated by specific mu, delta or kappa <b>opioid</b> receptor antagonists: a c <strong>Fos</strong> protein study in the rat central nervous system.
+FOS	addiction	withdrawal	12814374	Morphine <b>withdrawal</b> precipitated by specific mu, delta or kappa opioid receptor antagonists: a c <strong>Fos</strong> protein study in the rat central nervous system.
+FOS	drug	opioid	12814374	We have recently shown concurrent changes in behavioural responses and c <strong>Fos</strong> protein expression in the central nervous system in both naive and <b>morphine</b> dependent rats after systemic administration of the <b>opioid</b> antagonist <b>naloxone</b>.
+FOS	drug	opioid	12814374	However, because <b>naloxone</b> acts on the three major types of <b>opioid</b> receptors, the present study aimed at determining, in the same animals, both changes in behaviour and c <strong>Fos</strong> like immunoreactivity after intravenous injection of selective <b>opioid</b> antagonists, such as mu (beta funaltrexamine, 10 mg/kg), delta (naltrindole, 4 mg/kg) or kappa (nor binaltorphimine, 5 mg/kg) <b>opioid</b> receptor antagonists, in naive or <b>morphine</b> dependent rats.
+FOS	drug	opioid	12814374	A second experimental series in <b>morphine</b> dependent rats showed that beta funaltrexamine had the highest potency in the induction of classical signs of <b>morphine</b> withdrawal syndrome, as well as the increase in c <strong>Fos</strong> expression in the 22 central nervous system structures studied, suggesting a major role of mu <b>opioid</b> receptors in <b>opioid</b> dependence.
+FOS	addiction	dependence	12814374	A second experimental series in morphine dependent rats showed that beta funaltrexamine had the highest potency in the induction of classical signs of morphine withdrawal syndrome, as well as the increase in c <strong>Fos</strong> expression in the 22 central nervous system structures studied, suggesting a major role of mu opioid receptors in opioid <b>dependence</b>.
+FOS	addiction	withdrawal	12814374	A second experimental series in morphine dependent rats showed that beta funaltrexamine had the highest potency in the induction of classical signs of morphine <b>withdrawal</b> syndrome, as well as the increase in c <strong>Fos</strong> expression in the 22 central nervous system structures studied, suggesting a major role of mu opioid receptors in opioid dependence.
+FOS	drug	opioid	12814374	However, our results also demonstrated that naltrindole and, to a lesser extent, nor binaltorphimine were able to induce moderate signs of <b>morphine</b> withdrawal and relatively weak c <strong>Fos</strong> protein expression in restricted central nervous system structures.
+FOS	addiction	withdrawal	12814374	However, our results also demonstrated that naltrindole and, to a lesser extent, nor binaltorphimine were able to induce moderate signs of morphine <b>withdrawal</b> and relatively weak c <strong>Fos</strong> protein expression in restricted central nervous system structures.
+FOS	drug	cannabinoid	12809695	Selective activation of <b>cannabinoid</b> CB(2) receptors suppresses spinal <strong>fos</strong> protein expression and pain behavior in a rat model of inflammation.
+FOS	drug	cannabinoid	12809695	The suppression of carrageenan evoked <strong>Fos</strong> protein expression induced by AM1241 was blocked by coadministration of <b>SR144528</b> in all spinal laminae.
+FOS	drug	cocaine	12786985	<b>Cocaine</b> induced psychomotor activity is associated with its ability to induce c <strong>fos</strong> mRNA expression in the subthalamic nucleus: effects of dose and repeated treatment.
+FOS	drug	amphetamine	12786985	Factors that modulate the psychomotor activating effects of <b>amphetamine</b> and cocaine, such as environmental novelty and dose, also regulate the ability of these drugs to induce c <strong>fos</strong> mRNA expression in the subthalamic nucleus (STN).
+FOS	drug	cocaine	12786985	Factors that modulate the psychomotor activating effects of amphetamine and <b>cocaine</b>, such as environmental novelty and dose, also regulate the ability of these drugs to induce c <strong>fos</strong> mRNA expression in the subthalamic nucleus (STN).
+FOS	addiction	sensitization	12786985	produces behavioural <b>sensitization</b>), also enhances its ability to induce c <strong>fos</strong> expression in the STN.
+FOS	drug	cocaine	12786985	In addition, given that STN activity is thought to be influenced by preproenkephalin mRNA containing (ENK+) neurons in the caudate putamen, we also examined whether repeated <b>cocaine</b> treatment alters c <strong>fos</strong> expression in ENK+ cells.
+FOS	drug	cocaine	12786985	We report that: (i) <b>cocaine</b> pretreatment enhances the ability of a <b>cocaine</b> challenge to induce c <strong>fos</strong> mRNA expression in the STN, and this effect is most robust at challenge doses where behavioural sensitization is observed; (ii) the ability of <b>cocaine</b> to induce c <strong>fos</strong> in the STN is independent of the ability of <b>cocaine</b> to engage ENK+ cells.
+FOS	addiction	sensitization	12786985	We report that: (i) cocaine pretreatment enhances the ability of a cocaine challenge to induce c <strong>fos</strong> mRNA expression in the STN, and this effect is most robust at challenge doses where behavioural <b>sensitization</b> is observed; (ii) the ability of cocaine to induce c <strong>fos</strong> in the STN is independent of the ability of cocaine to engage ENK+ cells.
+FOS	drug	amphetamine	12736179	In contrast, <strong>Fos</strong> expression was not induced in melanin concentrating hormone and cocaine <b>amphetamine</b> related transcript (CART) neurons.
+FOS	drug	cocaine	12736179	In contrast, <strong>Fos</strong> expression was not induced in melanin concentrating hormone and <b>cocaine</b> amphetamine related transcript (CART) neurons.
+FOS	addiction	withdrawal	12721110	Effects of U 50488H and U 50488H <b>withdrawal</b> on c <strong>fos</strong> expression in the rat paraventricular nucleus.
+FOS	drug	opioid	12721110	In the present work, we have studied the expression of <strong>Fos</strong> during acute and chronic administration of the kappa <b>opioid</b> receptor agonist U 50488H and after U 5088H withdrawal in the rat hypothalamic paraventricular nucleus (PVN).
+FOS	addiction	withdrawal	12721110	In the present work, we have studied the expression of <strong>Fos</strong> during acute and chronic administration of the kappa opioid receptor agonist U 50488H and after U 5088H <b>withdrawal</b> in the rat hypothalamic paraventricular nucleus (PVN).
+FOS	drug	opioid	12721110	Interestingly in contrast to <b>morphine</b> withdrawal, present results demonstrate that rats withdrawn from U 50488H did show no changes in <strong>Fos</strong> immunoreactivity in the PVN, NTS or VLM, indicating the absence of dependence on the kappa agonist under the present experimental conditions.
+FOS	addiction	dependence	12721110	Interestingly in contrast to morphine withdrawal, present results demonstrate that rats withdrawn from U 50488H did show no changes in <strong>Fos</strong> immunoreactivity in the PVN, NTS or VLM, indicating the absence of <b>dependence</b> on the kappa agonist under the present experimental conditions.
+FOS	addiction	withdrawal	12721110	Interestingly in contrast to morphine <b>withdrawal</b>, present results demonstrate that rats withdrawn from U 50488H did show no changes in <strong>Fos</strong> immunoreactivity in the PVN, NTS or VLM, indicating the absence of dependence on the kappa agonist under the present experimental conditions.
+FOS	drug	opioid	12716916	Additionally, c <strong>Fos</strong> and the orexin gene itself are induced in orexin cells in the LH during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	12716916	Additionally, c <strong>Fos</strong> and the orexin gene itself are induced in orexin cells in the LH during morphine <b>withdrawal</b>.
+FOS	drug	opioid	12711372	We investigated the ability of dextromethorphan, a clinically available NMDA receptor antagonist, to attenuate the behaviors and the expression of c <strong>fos</strong> mRNA associated with acute <b>morphine</b> withdrawal in the 7 day old rat.
+FOS	addiction	withdrawal	12711372	We investigated the ability of dextromethorphan, a clinically available NMDA receptor antagonist, to attenuate the behaviors and the expression of c <strong>fos</strong> mRNA associated with acute morphine <b>withdrawal</b> in the 7 day old rat.
+FOS	drug	opioid	12711372	The intensity of the acute <b>morphine</b> withdrawal behaviors and the elevation in c <strong>fos</strong> mRNA expression in the brain induced by acute <b>morphine</b> withdrawal were reduced by dextromethorphan.
+FOS	addiction	withdrawal	12711372	The intensity of the acute morphine <b>withdrawal</b> behaviors and the elevation in c <strong>fos</strong> mRNA expression in the brain induced by acute morphine <b>withdrawal</b> were reduced by dextromethorphan.
+FOS	drug	cocaine	12706249	Administration of <b>cocaine</b> induces the <strong>Fos</strong> family of transcription factors in the striatum, including the nucleus accumbens (NAc), a brain region important for the rewarding effects of addictive drugs.
+FOS	addiction	addiction	12706249	Administration of cocaine induces the <strong>Fos</strong> family of transcription factors in the striatum, including the nucleus accumbens (NAc), a brain region important for the rewarding effects of <b>addictive</b> drugs.
+FOS	drug	cocaine	12706249	Several <strong>Fos</strong> proteins are induced acutely by <b>cocaine</b>, with stable isoforms of DeltaFosB predominating after chronic drug administration.
+FOS	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for <strong>AP 1</strong> in the NAc: the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+FOS	drug	cocaine	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying <b>cocaine</b> addiction.
+FOS	addiction	addiction	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying cocaine <b>addiction</b>.
+FOS	drug	amphetamine	12699766	WT and DAT knockout (KO) animals were given vehicle or methylphenidate, <b>amphetamine</b>, or cocaine and brain sections were immunostained for <strong>Fos</strong>.
+FOS	drug	cocaine	12699766	WT and DAT knockout (KO) animals were given vehicle or methylphenidate, amphetamine, or <b>cocaine</b> and brain sections were immunostained for <strong>Fos</strong>.
+FOS	drug	amphetamine	12699766	<b>Amphetamine</b> and cocaine produced similar changes to that for methylphenidate, except these psychostimulants also induced <strong>Fos</strong> LI in the nucleus accumbens of the KO animals.
+FOS	drug	cocaine	12699766	Amphetamine and <b>cocaine</b> produced similar changes to that for methylphenidate, except these psychostimulants also induced <strong>Fos</strong> LI in the nucleus accumbens of the KO animals.
+FOS	drug	cannabinoid	12657697	In vivo <b>THC</b> induced the expression of immediate early genes products (c <strong>Fos</strong> protein, Zif268, and BDNF mRNAs), and this induction was prevented by an inhibitor of MEK.
+FOS	drug	cocaine	12653981	Acute induction of c <strong>fos</strong> (by 25 mg/kg of <b>cocaine</b>), and the c <strong>fos</strong> response and dynorphin expression after repeated <b>cocaine</b> treatment (25 mg/kg, 4 days) were assessed as examples for short term and longer term molecular changes, respectively.
+FOS	drug	cocaine	12653981	However, running wheel training under the influence of <b>cocaine</b> enhanced the c <strong>fos</strong> response to a subsequent <b>cocaine</b> challenge selectively in parts of the caudal sensorimotor striatum.
+FOS	drug	amphetamine	12641732	<b>Amphetamine</b> induced c <strong>fos</strong> mRNA expression in the caudate putamen and subthalamic nucleus: interactions between dose, environment, and neuronal phenotype.
+FOS	drug	amphetamine	12641732	When administered in a novel environment relatively low doses of <b>amphetamine</b> induce c <strong>fos</strong> mRNA in the subthalamic nucleus (STN) and in preproenkephalin mRNA containing (ENK+) neurons in the caudate putamen (CPu).
+FOS	drug	amphetamine	12641732	The purpose of the present experiment therefore was to determine if the effect of context on <b>amphetamine</b> induced c <strong>fos</strong> expression is also dose dependent.
+FOS	drug	amphetamine	12641732	It was found that: (i) No dose of <b>amphetamine</b> tested (1 10 mg/kg) induced c <strong>fos</strong> in many ENK+ cells when given at home.
+FOS	drug	amphetamine	12641732	(ii) When given in a novel environment low to moderate doses of <b>amphetamine</b> (1 5 mg/kg) induced c <strong>fos</strong> in substantial numbers of ENK+ cells, but the highest dose examined (10 mg/kg) did not.
+FOS	drug	amphetamine	12641732	(iii) Environmental novelty enhanced the ability of low to moderate doses of <b>amphetamine</b> to induce c <strong>fos</strong> in the STN, but the highest dose of <b>amphetamine</b> induced robust c <strong>fos</strong> mRNA expression in the STN regardless of context.
+FOS	addiction	sensitization	12641732	The results do not support the idea that engaging ENK+ cells, at least as indicated by c <strong>fos</strong> mRNA expression, is critical to produce robust behavioral <b>sensitization</b>, but do suggest a possible role for the STN.
+FOS	drug	cocaine	12629527	Effects of <b>cocaine</b> on c <strong>fos</strong> and NGFI B mRNA expression in transgenic mice underexpressing glucocorticoid receptors.
+FOS	drug	cocaine	12629527	Transgenic (TG) mice expressing an antisense mRNA against the glucocorticoid receptor (GR), which partially blocks GR expression, were used to assess the role of GR dysfunction on <b>cocaine</b> (COC) induced c <strong>fos</strong> and Nerve Growth Factor Inducible B (NGFI B, or Nur77) gene expression.
+FOS	drug	cannabinoid	12623225	Regional differences in naloxone modulation of Delta(9) <b>THC</b> induced <strong>Fos</strong> expression in rat brain.
+FOS	drug	opioid	12623225	Regional differences in <b>naloxone</b> modulation of Delta(9) THC induced <strong>Fos</strong> expression in rat brain.
+FOS	drug	cannabinoid	12623225	We compared <strong>Fos</strong> immunoreactivity in groups of male albino Wistar rats treated with vehicle, Delta(9) <b>tetrahydrocannabinol</b> (<b>THC</b>, 10 mg/kg, i.p.
+FOS	drug	cannabinoid	12623225	Results showed that naloxone inhibited <b>THC</b> induced <strong>Fos</strong> immunoreactivity in several key brain regions including the ventral tegmental area, ventromedial and dorsomedial hypothalamus, central caudate putamen and ventrolateral periaqueductal grey.
+FOS	drug	opioid	12623225	Results showed that <b>naloxone</b> inhibited THC induced <strong>Fos</strong> immunoreactivity in several key brain regions including the ventral tegmental area, ventromedial and dorsomedial hypothalamus, central caudate putamen and ventrolateral periaqueductal grey.
+FOS	drug	cannabinoid	12623225	Conversely, naloxone and <b>THC</b> had an additive effect on <strong>Fos</strong> immunoreactivity in the central nucleus of the amygdala, the bed nucleus of the stria terminalis (lateral division), the insular cortex, and the paraventricular nucleus of the thalamus.
+FOS	drug	opioid	12623225	Conversely, <b>naloxone</b> and THC had an additive effect on <strong>Fos</strong> immunoreactivity in the central nucleus of the amygdala, the bed nucleus of the stria terminalis (lateral division), the insular cortex, and the paraventricular nucleus of the thalamus.
+FOS	drug	cannabinoid	12623225	The inhibitory effects of naloxone on <b>THC</b> induced ventral tegmentum, hypothalamic and periaqueductal grey <strong>Fos</strong> expression point to these structures as key sites involved in <b>cannabinoid</b> opioid interactions.
+FOS	drug	opioid	12623225	The inhibitory effects of <b>naloxone</b> on THC induced ventral tegmentum, hypothalamic and periaqueductal grey <strong>Fos</strong> expression point to these structures as key sites involved in cannabinoid <b>opioid</b> interactions.
+FOS	drug	opioid	12598416	Activation of c <strong>fos</strong> expression in the heart after <b>morphine</b> but not U 50,488H withdrawal.
+FOS	addiction	withdrawal	12598416	Activation of c <strong>fos</strong> expression in the heart after morphine but not U 50,488H <b>withdrawal</b>.
+FOS	drug	opioid	12598416	In the present work we have studied in the heart the expression of <strong>Fos</strong>, the protein product of the c <strong>fos</strong> proto oncogene and the adaptive changes in noradrenergic neurons after <b>naloxone</b> or nor binaltorphimine (nor BNI) administration to <b>morphine</b> or U 50,488H pretreated rats.
+FOS	drug	opioid	12598416	Using immunohistochemical staining of <strong>Fos</strong>, present results indicate that <b>morphine</b> withdrawal induced marked <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) within the cardiomyocyte nuclei.
+FOS	addiction	withdrawal	12598416	Using immunohistochemical staining of <strong>Fos</strong>, present results indicate that morphine <b>withdrawal</b> induced marked <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) within the cardiomyocyte nuclei.
+FOS	drug	opioid	12598416	Moreover, Western blots analysis revealed a peak expression of c <strong>fos</strong> in right and left ventricle after <b>naloxone</b> induced withdrawal in parallel with an increase in noradrenaline (NA) turnover.
+FOS	addiction	withdrawal	12598416	Moreover, Western blots analysis revealed a peak expression of c <strong>fos</strong> in right and left ventricle after naloxone induced <b>withdrawal</b> in parallel with an increase in noradrenaline (NA) turnover.
+FOS	drug	opioid	12598416	In addition, the administration of nor BNI to rats chronically treated with U 50,488H or <b>morphine</b> did not induce modifications in the <strong>Fos</strong> IR, in the heart.
+FOS	drug	opioid	12598416	These results demonstrated that <b>morphine</b> withdrawal induces the expression of <strong>Fos</strong> protein, as well as an enhancement of noradrenergic activity in the heart.
+FOS	addiction	withdrawal	12598416	These results demonstrated that morphine <b>withdrawal</b> induces the expression of <strong>Fos</strong> protein, as well as an enhancement of noradrenergic activity in the heart.
+FOS	drug	opioid	12598416	In contrast to <b>morphine</b> U 50,488 withdrawal produces no changes in <strong>Fos</strong> IR in parallel with a decrease in NA turnover, indicating that the kappa <b>opioid</b> receptors are not involved in the molecular adaptive mechanisms responsible for the development of <b>opioid</b> dependence in the heart.
+FOS	addiction	dependence	12598416	In contrast to morphine U 50,488 withdrawal produces no changes in <strong>Fos</strong> IR in parallel with a decrease in NA turnover, indicating that the kappa opioid receptors are not involved in the molecular adaptive mechanisms responsible for the development of opioid <b>dependence</b> in the heart.
+FOS	addiction	withdrawal	12598416	In contrast to morphine U 50,488 <b>withdrawal</b> produces no changes in <strong>Fos</strong> IR in parallel with a decrease in NA turnover, indicating that the kappa opioid receptors are not involved in the molecular adaptive mechanisms responsible for the development of opioid dependence in the heart.
+FOS	drug	opioid	12589382	Enhanced <b>morphine</b> preference following prolonged abstinence: association with increased <strong>Fos</strong> expression in the extended amygdala.
+FOS	drug	opioid	12589382	To determine brain regions involved in this behavior, we examined neural activation (as indexed by <strong>Fos</strong> like proteins) induced by a <b>morphine</b> conditioned place preference test.
+FOS	drug	opioid	12589382	Placebo pretreated (P) <b>morphine</b> conditioned rats showed significantly elevated <strong>Fos</strong> in the anterior cingulate cortex (Cg), nucleus accumbens core (Ac C) and shell (Ac S), ventral lateral and dorsal lateral bed nucleus of the stria terminialis (BNST VL and  DL), and central and basolateral amygdala nuclei (ACE, ABL) when compared to nonconditioned P rats.
+FOS	drug	opioid	12589382	Chronically <b>morphine</b> pretreated (M) rats that exhibited enhanced <b>morphine</b> preference 5 weeks after <b>morphine</b> withdrawal showed significantly greater <strong>Fos</strong> in all the same areas except the BNST DL relative to conditioned P or nonconditioned M rats.
+FOS	addiction	withdrawal	12589382	Chronically morphine pretreated (M) rats that exhibited enhanced morphine preference 5 weeks after morphine <b>withdrawal</b> showed significantly greater <strong>Fos</strong> in all the same areas except the BNST DL relative to conditioned P or nonconditioned M rats.
+FOS	drug	cocaine	12581847	<b>Cocaine</b> induced alterations in expression of c <strong>fos</strong> and preprodynorphin mRNAs measured by TaqMan were confirmed by ribonuclease protection assay.
+FOS	drug	opioid	12577398	After single administration of <b>morphine</b> and the motion activity was measured by ambulometer, conditioned place preference paradigm was used to study the reinforcing effect of <b>morphine</b>, climbing behavior was used to evaluate the relation with Dopaminergic system and immediate early expression of c <strong>fos</strong> gene was in brain was showed by immunohistochemical method.
+FOS	addiction	reward	12577398	After single administration of morphine and the motion activity was measured by ambulometer, conditioned place preference paradigm was used to study the <b>reinforcing</b> effect of morphine, climbing behavior was used to evaluate the relation with Dopaminergic system and immediate early expression of c <strong>fos</strong> gene was in brain was showed by immunohistochemical method.
+FOS	drug	opioid	12577398	Tetrandrine could inhibit the c <strong>fos</strong> gene expression in nucleus accumbens, ventral tegmental and prefrontal cortex in place preference model formed by <b>morphine</b>.
+FOS	drug	opioid	12577398	Tetrandrine could inhibit the hyperactivity and conditioned place preference response induced by <b>morphine</b>, it might relate to reducing the c <strong>fos</strong> gene expression in special area of brain in mice.
+FOS	drug	opioid	12567447	[Effects of long term <b>morphine</b> exposure on the cAMP system and c <strong>Fos</strong> phosphorylation in differentiated SH SY5Y cells].
+FOS	drug	opioid	12567447	To further understand the effects of long term <b>morphine</b> exposure on the cAMP system and c <strong>Fos</strong> phosphorylation in differentiated SH SY5Y human neuroblastoma cells.
+FOS	drug	opioid	12567447	But no changes were observed in membrane PKA activity; (3) In <b>morphine</b> dependent like cells decreased c <strong>Fos</strong> phosphorylation level was observed.
+FOS	drug	opioid	12567447	PKA inhibitor could significantly inhibit this change; (4) Concomitant administration of <b>naloxone</b> could block the changes in PKA activity and c <strong>Fos</strong> phosphorylation described above.
+FOS	drug	opioid	12567447	The up regulation of cAMP system in differentiated SH SY5Y cells may be involved in the development of <b>morphine</b> dependent and in <b>morphine</b> dependent like SH SY5Y cells and PKA was suggested to regulate c <strong>Fos</strong> dephosphorylation through activating phosphatase and then activate some genes transcription, which might be one of the important mechanism regardingas cellular adaptive responses underlying dependence to <b>opioid</b> drugs.
+FOS	addiction	dependence	12567447	The up regulation of cAMP system in differentiated SH SY5Y cells may be involved in the development of morphine dependent and in morphine dependent like SH SY5Y cells and PKA was suggested to regulate c <strong>Fos</strong> dephosphorylation through activating phosphatase and then activate some genes transcription, which might be one of the important mechanism regardingas cellular adaptive responses underlying <b>dependence</b> to opioid drugs.
+FOS	drug	cannabinoid	12560108	<b>Cannabinoid</b> induced <strong>Fos</strong> expression within A10 dopaminergic neurons.
+FOS	drug	cannabinoid	12560108	We have examined the role of noradrenergic neurotransmission in the mediation of <b>cannabinoid</b> induced activation of A10 dopaminergic neurons using <strong>Fos</strong> as a marker of neuronal activation in mice.
+FOS	drug	cannabinoid	12560108	Similar results were obtained using the CB(1) receptor agonist Win 55212 2; and pretreatment with the CB(1) receptor antagonist <b>SR141716</b> significantly inhibited CP55940 induced <strong>Fos</strong> expression.
+FOS	drug	cannabinoid	12560108	Our data demonstrate that <b>cannabinoids</b> induce <strong>Fos</strong> expression within A10 dopaminergic neurons in a heterogeneous anatomical pattern, and suggest that enhanced noradrenergic neurotransmission contributes to <b>cannabinoid</b> induced activation of A10 dopaminergic neurons in vivo.
+FOS	drug	opioid	12534973	Regulation of tyrosine hydroxylase levels and activity and <strong>Fos</strong> expression during <b>opioid</b> withdrawal in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups innervating the PVN.
+FOS	addiction	withdrawal	12534973	Regulation of tyrosine hydroxylase levels and activity and <strong>Fos</strong> expression during opioid <b>withdrawal</b> in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups innervating the PVN.
+FOS	drug	opioid	12534973	TH and <strong>Fos</strong> immunoreactivity was determined by quantitative Western blot analysis, combined with immunostaining for TH and <strong>Fos</strong> for immunohistochemical identification of active neurons during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	12534973	TH and <strong>Fos</strong> immunoreactivity was determined by quantitative Western blot analysis, combined with immunostaining for TH and <strong>Fos</strong> for immunohistochemical identification of active neurons during morphine <b>withdrawal</b>.
+FOS	drug	opioid	12534973	<b>Morphine</b> withdrawal induced the expression of <strong>Fos</strong> in the PVN and NTS/VLM, which indicates an activation of neurons in these nuclei.
+FOS	addiction	withdrawal	12534973	Morphine <b>withdrawal</b> induced the expression of <strong>Fos</strong> in the PVN and NTS/VLM, which indicates an activation of neurons in these nuclei.
+FOS	addiction	withdrawal	12534973	Following <b>withdrawal</b>, <strong>Fos</strong> immunoreactivity was present in most of the TH positive neurons of the A2 and A1 neurons.
+FOS	drug	amphetamine	12504868	In addition, DNA binding activities of NF kappaB, <strong>AP 1</strong>, and CREB in the frontal cortex and hippocampus were more pronounced in mice injected with Tat plus <b>METH</b> compared to the effects of Tat or <b>METH</b> alone.
+FOS	drug	opioid	12499582	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal elicits increases in c <strong>fos</strong> mRNA expression in restricted regions of the infant rat brain.
+FOS	addiction	withdrawal	12499582	Naloxone precipitated morphine <b>withdrawal</b> elicits increases in c <strong>fos</strong> mRNA expression in restricted regions of the infant rat brain.
+FOS	drug	opioid	12499582	We examined the effects of <b>naloxone</b> (2 mg/kg) on c <strong>fos</strong> mRNA levels in brains of infant and adult rats following repeated treatment with <b>morphine</b> (20 mg/kg, once daily for 5 days).
+FOS	drug	opioid	12499582	One hour after a single administration of <b>naloxone</b> (<b>naloxone</b> challenge), an increase in c <strong>fos</strong> mRNA was observed in the olfactory bulb, hypothalamus and medulla oblongata of infant rats, and in the olfactory bulb and hypothalamus, but not in the medulla oblongata of adult rats.
+FOS	drug	opioid	12499582	The c <strong>fos</strong> mRNA levels returned to control levels 6 h after the <b>naloxone</b> challenge.
+FOS	drug	opioid	12499582	When MK 801, a non competitive N methyl D aspartate (NMDA) receptor antagonist, was co administered along with <b>morphine</b>, it inhibited the <b>naloxone</b> induced increases in c <strong>fos</strong> mRNA levels in infant rats following repeated <b>morphine</b> administration.
+FOS	drug	opioid	12499582	These results suggest that physical dependence develops in infant rats following repeated <b>morphine</b> administration and that the increment of c <strong>fos</strong> mRNA levels is a useful indicator for <b>naloxone</b> precipitated <b>morphine</b> withdrawal in infant as well as in adult rats.
+FOS	addiction	dependence	12499582	These results suggest that physical <b>dependence</b> develops in infant rats following repeated morphine administration and that the increment of c <strong>fos</strong> mRNA levels is a useful indicator for naloxone precipitated morphine withdrawal in infant as well as in adult rats.
+FOS	addiction	withdrawal	12499582	These results suggest that physical dependence develops in infant rats following repeated morphine administration and that the increment of c <strong>fos</strong> mRNA levels is a useful indicator for naloxone precipitated morphine <b>withdrawal</b> in infant as well as in adult rats.
+FOS	drug	cocaine	12496936	Previous work in rats has shown that cues associated with morphine, <b>cocaine</b>, nicotine or palatable food can elicit enhanced expression of the immediate early gene product <strong>Fos</strong> in discrete brain regions.
+FOS	drug	nicotine	12496936	Previous work in rats has shown that cues associated with morphine, cocaine, <b>nicotine</b> or palatable food can elicit enhanced expression of the immediate early gene product <strong>Fos</strong> in discrete brain regions.
+FOS	drug	opioid	12496936	Previous work in rats has shown that cues associated with <b>morphine</b>, cocaine, nicotine or palatable food can elicit enhanced expression of the immediate early gene product <strong>Fos</strong> in discrete brain regions.
+FOS	drug	amphetamine	12492441	In order to distinguish between these possibilities, we studied <b>amphetamine</b> induced c <strong>fos</strong> immunoreactivity in subregions of rat striatum (patch and matrix compartments of caudate putamen and nucleus accumbens core and shell) in drug naive rats, as well as during long term expression of <b>amphetamine</b> sensitization.
+FOS	addiction	sensitization	12492441	In order to distinguish between these possibilities, we studied amphetamine induced c <strong>fos</strong> immunoreactivity in subregions of rat striatum (patch and matrix compartments of caudate putamen and nucleus accumbens core and shell) in drug naive rats, as well as during long term expression of amphetamine <b>sensitization</b>.
+FOS	drug	amphetamine	12492441	We found that, in sensitized animals, <b>amphetamine</b> (1.0 mg/kg) evoked an increase in the ratio of c <strong>fos</strong> immunopositive cells in striatal patch and matrix compartments, suggesting a preferential involvement of striatal patches in the sensitized response to <b>amphetamine</b>.
+FOS	drug	amphetamine	12492441	In drug naive rats, <b>amphetamine</b> (0.5 5.0 mg/kg) dose dependently increased c <strong>fos</strong> expression in all striatal subregions.
+FOS	drug	amphetamine	12492441	Remarkably, the highest dose of <b>amphetamine</b> also evoked an increase in patch : matrix ratio of c <strong>fos</strong> immunoreactivity.
+FOS	drug	amphetamine	12492441	In nucleus accumbens core and shell of <b>amphetamine</b>  and saline pretreated animals, <b>amphetamine</b> (1.0 mg/kg) evoked comparable increases in c <strong>fos</strong> expression.
+FOS	drug	amphetamine	12492441	In addition, they suggest that the shift in <b>amphetamine</b> induced c <strong>fos</strong> expression from striatal matrix to patches in sensitized animals is the consequence of a change in the sensitivity to <b>amphetamine</b>, rather than a long term circuitry reorganization that is exclusive to the sensitized state.
+FOS	drug	alcohol	12482856	Up regulation of CD14 in liver caused by acute <b>ethanol</b> involves oxidant dependent <strong>AP 1</strong> pathway.
+FOS	drug	alcohol	12482856	Additionally, overexpression of SOD also blunted <b>ethanol</b> induced activation of redox sensitive transcription factors NFkappaB and <strong>AP 1</strong> and production of cytokines.
+FOS	drug	alcohol	12482856	However, only inhibition of <strong>AP 1</strong> with dominant negative TAK1 but not NFkappaB by dominant negative IkappaBalpha significantly blunted <b>ethanol</b> induced increases in CD14, suggesting that <strong>AP 1</strong> is important for CD14 transcriptional regulation.
+FOS	drug	cocaine	12429408	Locomotor sensitization to <b>cocaine</b> is associated with increased <strong>Fos</strong> expression in the accumbens, but not in the caudate.
+FOS	addiction	sensitization	12429408	Locomotor <b>sensitization</b> to cocaine is associated with increased <strong>Fos</strong> expression in the accumbens, but not in the caudate.
+FOS	drug	cocaine	12429408	Although <strong>Fos</strong> immunohistochemistry and c <strong>fos</strong> in situ hybridization have frequently been used to assess changes in <b>cocaine</b> induced neural activity following prior <b>cocaine</b> exposure, these techniques have rarely been used to examine neural activity in the accumbens of behaviorally sensitized animals.
+FOS	drug	cocaine	12429408	In the present experiment, we compared the ability of increasing doses of <b>cocaine</b> to induce <strong>Fos</strong> in the accumbens and caudate of rats following a treatment procedure (7 once daily injections of 15 mg/kg of <b>cocaine</b> or the saline vehicle) shown to produce robust and persistent (1 week) locomotor sensitization.
+FOS	addiction	sensitization	12429408	In the present experiment, we compared the ability of increasing doses of cocaine to induce <strong>Fos</strong> in the accumbens and caudate of rats following a treatment procedure (7 once daily injections of 15 mg/kg of cocaine or the saline vehicle) shown to produce robust and persistent (1 week) locomotor <b>sensitization</b>.
+FOS	drug	cocaine	12429408	In sensitized animals, there was a leftward shift in the dose response curve for <b>cocaine</b> induction of <strong>Fos</strong> in the accumbens, but not in the caudate.
+FOS	drug	cocaine	12429408	These results provide the first parametric evidence for sensitization of <b>cocaine</b> induced <strong>Fos</strong> expression in the accumbens.
+FOS	addiction	sensitization	12429408	These results provide the first parametric evidence for <b>sensitization</b> of cocaine induced <strong>Fos</strong> expression in the accumbens.
+FOS	addiction	withdrawal	12419523	Two hours following initiation of <b>withdrawal</b>, rat brains were obtained and processed for detection of c <strong>fos</strong> and in situ hybridization labeling of preproenkephalin (PPE) mRNA.
+FOS	drug	alcohol	12419523	<b>Naltrexone</b> injections into morphine dependent rats caused a dramatic increase in c <strong>fos</strong> as compared to control rats.
+FOS	drug	opioid	12419523	Naltrexone injections into <b>morphine</b> dependent rats caused a dramatic increase in c <strong>fos</strong> as compared to control rats.
+FOS	drug	opioid	12405997	Using in situ hybridization, we have analysed in the brain of <b>morphine</b> dependent rats the effects of acute withdrawal syndrome precipitated by increasing <b>naloxone</b> doses on c <strong>fos</strong> mRNA expression.
+FOS	addiction	withdrawal	12405997	Using in situ hybridization, we have analysed in the brain of morphine dependent rats the effects of acute <b>withdrawal</b> syndrome precipitated by increasing naloxone doses on c <strong>fos</strong> mRNA expression.
+FOS	drug	opioid	12405997	Our mapping study revealed a dissociation between a set of brain structures (extended amygdala, lateral septal nucleus, basolateral amygdala and field CA1 of the hippocampus) which exhibited c <strong>fos</strong> mRNA dose dependent variations from the lowest <b>naloxone</b> doses, and many other structures (dopaminergic and noradrenergic nuclei, motor striatal areas, hypothalamic nuclei and periaqueductal grey) which were less sensitive and recruited only by the higher doses.
+FOS	drug	opioid	12405997	In addition, we found opposite dose dependent variations of c <strong>fos</strong> gene expression within the central (increase) and the basolateral (decrease) amygdala after acute <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	12405997	In addition, we found opposite dose dependent variations of c <strong>fos</strong> gene expression within the central (increase) and the basolateral (decrease) amygdala after acute morphine <b>withdrawal</b>.
+FOS	drug	cocaine	12379259	Withdrawal duration differentially affects c <strong>fos</strong> expression in the medial prefrontal cortex and discrete subregions of the nucleus accumbens in <b>cocaine</b> sensitized rats.
+FOS	addiction	withdrawal	12379259	<b>Withdrawal</b> duration differentially affects c <strong>fos</strong> expression in the medial prefrontal cortex and discrete subregions of the nucleus accumbens in cocaine sensitized rats.
+FOS	drug	cocaine	12379259	The present study was designed to assess the activation of key neuronal populations in subdivisions of the accumbens and subdivisions of the medial prefrontal cortex in <b>cocaine</b> sensitized rats, using the expression of the immediate early gene, c <strong>fos</strong>, as a marker of neuronal activation.
+FOS	drug	cocaine	12379259	Repeated <b>cocaine</b> administration resulted in robust sensitization that correlated with a significant decrease in the density of c <strong>fos</strong> nuclei in all three subdivisions of the medial prefrontal cortex, and two subdivisions of the nucleus accumbens only in animals challenged after a 2 day withdrawal period.
+FOS	addiction	sensitization	12379259	Repeated cocaine administration resulted in robust <b>sensitization</b> that correlated with a significant decrease in the density of c <strong>fos</strong> nuclei in all three subdivisions of the medial prefrontal cortex, and two subdivisions of the nucleus accumbens only in animals challenged after a 2 day withdrawal period.
+FOS	addiction	withdrawal	12379259	Repeated cocaine administration resulted in robust sensitization that correlated with a significant decrease in the density of c <strong>fos</strong> nuclei in all three subdivisions of the medial prefrontal cortex, and two subdivisions of the nucleus accumbens only in animals challenged after a 2 day <b>withdrawal</b> period.
+FOS	addiction	withdrawal	12379259	After a 2 week <b>withdrawal</b> period, sensitized animals no longer showed any differences in the density of c <strong>fos</strong> nuclei in any of the areas examined, with the exception of a significant increase in the intermediate zone of the shell.
+FOS	drug	opioid	12358736	<b>Morphine</b> withdrawal induced c <strong>fos</strong> expression in the hypothalamic paraventricular nucleus is dependent on the activation of catecholaminergic neurones.
+FOS	addiction	withdrawal	12358736	Morphine <b>withdrawal</b> induced c <strong>fos</strong> expression in the hypothalamic paraventricular nucleus is dependent on the activation of catecholaminergic neurones.
+FOS	drug	opioid	12358736	In the present study, <strong>Fos</strong> immunostaining was used as a reflection of neuronal activity and combined with immunostaining for tyrosine hydroxylase (TH) for immunohistochemical identification of active neurones during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	12358736	In the present study, <strong>Fos</strong> immunostaining was used as a reflection of neuronal activity and combined with immunostaining for tyrosine hydroxylase (TH) for immunohistochemical identification of active neurones during morphine <b>withdrawal</b>.
+FOS	drug	opioid	12358736	<strong>Fos</strong> immunoreactivity in the PVN and also in the nucleus tractus solitarius (NTS) A2 and ventrolateral medulla (VLM) A1 cell groups, which project to the PVN, increased during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	12358736	<strong>Fos</strong> immunoreactivity in the PVN and also in the nucleus tractus solitarius (NTS) A2 and ventrolateral medulla (VLM) A1 cell groups, which project to the PVN, increased during morphine <b>withdrawal</b>.
+FOS	addiction	withdrawal	12358736	Following <b>withdrawal</b>, <strong>Fos</strong> immunoreactivity was present in most of the TH positive neurones of the A2 and A1 neurones.
+FOS	addiction	withdrawal	12358736	In a second study, the effects of administration of adrenoceptor antagonists on <b>withdrawal</b> induced <strong>Fos</strong> expression in the PVN were studied.
+FOS	drug	opioid	12358736	Pre treatment with alpha1  or alpha2 adrenoceptor antagonists, prazosin (1 mg/kg intraperitoneally) and yohimbine (1 mg/kg intraperitoneally), respectively, 20 min before <b>naloxone</b> administration to <b>morphine</b> dependent rats markedly reduced <strong>Fos</strong> expression in the PVN.
+FOS	addiction	withdrawal	12358736	Similarly, pre treatment with the beta antagonist, propranolol (3 mg/kg intraperitoneally), significantly prevented <b>withdrawal</b> induced <strong>Fos</strong> expression.
+FOS	drug	opioid	12358736	Collectively, these results suggest the hypothesis that noradrenergic neurones in the brainstem innervating the PVN are active during <b>morphine</b> withdrawal, and that activation of transcriptional responses mediated by <strong>Fos</strong> in the HPA axis following withdrawal are dependent upon hypothalamic alpha  and beta adrenoceptors.
+FOS	addiction	withdrawal	12358736	Collectively, these results suggest the hypothesis that noradrenergic neurones in the brainstem innervating the PVN are active during morphine <b>withdrawal</b>, and that activation of transcriptional responses mediated by <strong>Fos</strong> in the HPA axis following <b>withdrawal</b> are dependent upon hypothalamic alpha  and beta adrenoceptors.
+FOS	drug	cocaine	12244091	Prior treatment with chronic intermittent <b>cocaine</b> induced motor sensitization and significantly potentiated the striatal expression of <strong>Fos</strong> family early genes in response to stimulation of the motor cortex.
+FOS	addiction	sensitization	12244091	Prior treatment with chronic intermittent cocaine induced motor <b>sensitization</b> and significantly potentiated the striatal expression of <strong>Fos</strong> family early genes in response to stimulation of the motor cortex.
+FOS	drug	amphetamine	12231241	Sensitized <strong>Fos</strong> expression in subterritories of the rat medial prefrontal cortex and nucleus accumbens following <b>amphetamine</b> sensitization as revealed by stereology.
+FOS	addiction	sensitization	12231241	Sensitized <strong>Fos</strong> expression in subterritories of the rat medial prefrontal cortex and nucleus accumbens following amphetamine <b>sensitization</b> as revealed by stereology.
+FOS	drug	amphetamine	12231241	In the present study, we investigated the effects of <b>amphetamine</b> sensitization on <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) in subterritories of the nucleus accumbens (core and shell) and medial prefrontal cortex (mPFC; dorsal and ventral) using stereology.
+FOS	addiction	sensitization	12231241	In the present study, we investigated the effects of amphetamine <b>sensitization</b> on <strong>Fos</strong> immunoreactivity (<strong>Fos</strong> IR) in subterritories of the nucleus accumbens (core and shell) and medial prefrontal cortex (mPFC; dorsal and ventral) using stereology.
+FOS	drug	amphetamine	12231241	Densities of <strong>Fos</strong> positive nuclei were enhanced more in the dorsal than the ventral mPFC subterritory, whereas in the nucleus accumbens, densities of <strong>Fos</strong> positive nuclei were increased more in the core than the shell of <b>amphetamine</b> sensitized rats compared to controls.
+FOS	drug	amphetamine	12231241	These results represent, to our knowledge, the first published report using stereological methods to quantify <strong>Fos</strong> IR in the brain and suggest functional specialization of cortical and limbic regions in the expression of behavioral sensitization to <b>amphetamine</b>.
+FOS	addiction	sensitization	12231241	These results represent, to our knowledge, the first published report using stereological methods to quantify <strong>Fos</strong> IR in the brain and suggest functional specialization of cortical and limbic regions in the expression of behavioral <b>sensitization</b> to amphetamine.
+FOS	drug	opioid	12225868	In search for the underlying neuronal mechanisms we investigated the influence of stress on <b>morphine</b> induced c <strong>fos</strong> expression in the brain, and, vice versa, the influence of <b>morphine</b> application on the brain's c <strong>fos</strong> response to stress.
+FOS	drug	opioid	12225868	The stress induced c <strong>fos</strong> induction was markedly decreased by a moderate (10 mg/kg) dose of <b>morphine</b>.
+FOS	drug	opioid	12225868	On the other hand, <b>morphine</b> alone (50 mg/kg) caused only a weak c <strong>fos</strong> expression in nai;ve animals despite of the rather high dose.
+FOS	drug	opioid	12225868	If, however, this <b>morphine</b> dose was applied in the presence of a stressful stimulus, a pronounced c <strong>fos</strong> expression in the dorsal striatum resulted.
+FOS	drug	opioid	12225868	This c <strong>fos</strong> signal was comparable with the signal seen in <b>morphine</b> sensitized animals.
+FOS	drug	amphetamine	12185403	Effects of the D(3) dopamine receptor antagonist, U99194A, on brain stimulation and d <b>amphetamine</b> reward, motor activity, and c <strong>fos</strong> expression in ad libitum fed and food restricted rats.
+FOS	addiction	reward	12185403	Effects of the D(3) dopamine receptor antagonist, U99194A, on brain stimulation and d amphetamine <b>reward</b>, motor activity, and c <strong>fos</strong> expression in ad libitum fed and food restricted rats.
+FOS	drug	amphetamine	12185403	In experiment 3, effects of a behaviorally active dose of U99194A (5.0 mg/kg) on brain c <strong>fos</strong> expression were measured and compared to those produced by d <b>amphetamine</b> (0.5 mg/kg, IP).
+FOS	drug	amphetamine	12185403	The pattern and intensity of <strong>fos</strong> like immunoreactivity (FLI) induced by U99194A was similar to that produced by d <b>amphetamine</b> and was blocked, in caudate putamen and nucleus accumbens, by SCH 23390.
+FOS	drug	benzodiazepine	12147189	<b>Midazolam</b> pretreatment inhibited the increase of <strong>Fos</strong> protein expression, not cyclic AMP content, in rat spinal cord during morphine withdrawal.
+FOS	drug	opioid	12147189	Midazolam pretreatment inhibited the increase of <strong>Fos</strong> protein expression, not cyclic AMP content, in rat spinal cord during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	12147189	Midazolam pretreatment inhibited the increase of <strong>Fos</strong> protein expression, not cyclic AMP content, in rat spinal cord during morphine <b>withdrawal</b>.
+FOS	drug	alcohol	12130710	<b>Alcohol</b> induced c <strong>Fos</strong> expression in the Edinger Westphal nucleus: pharmacological and signal transduction mechanisms.
+FOS	drug	alcohol	12130710	Herein, we characterize the pharmacological and signal transduction mechanisms related to <b>alcohol</b> induced c <strong>Fos</strong> expression in Edinger Westphal neurons.
+FOS	drug	alcohol	12130710	Using immunohistochemistry, we show that pretreatment with gamma aminobutyric acid (GABA) ergic antagonists (4 mg/kg bicuculline and 45 mg/kg pentylenetetrazole) attenuates induction of c <strong>Fos</strong> expression by <b>alcohol</b> (2.4 g/kg, intraperitoneal).
+FOS	drug	alcohol	12130710	In addition, 10 mg/kg 2 (2,3 dihydro 2 methoxy 1,4 benzodioxin 2 yl)4,5 dihydro 1H imidazole (RX 821002), an alpha(2A/D) adrenoceptor antagonist, and 20 mg/kg haloperidol, a dopamine antagonist, also block <b>alcohol</b> induced c <strong>Fos</strong> expression in Edinger Westphal neurons.
+FOS	drug	alcohol	12130710	No effects were seen in <b>alcohol</b> induced c <strong>Fos</strong> after the pretreatment of 20 mg/kg propranolol (beta adrenoceptor antagonist), 10 mg/kg 2 (2 (4 (2 methoxyphenyl)piperazin 1 yl) ethy) 4,4 dimethyl 1,3 (2H,4H) isoquinolindione dihydrochloride (ARC 239) (alpha(2B/C) adrenoceptor antagonist), or 30 mg/kg <b>naltrexone</b> (opioid antagonist).
+FOS	drug	opioid	12130710	No effects were seen in alcohol induced c <strong>Fos</strong> after the pretreatment of 20 mg/kg propranolol (beta adrenoceptor antagonist), 10 mg/kg 2 (2 (4 (2 methoxyphenyl)piperazin 1 yl) ethy) 4,4 dimethyl 1,3 (2H,4H) isoquinolindione dihydrochloride (ARC 239) (alpha(2B/C) adrenoceptor antagonist), or 30 mg/kg naltrexone (<b>opioid</b> antagonist).
+FOS	drug	benzodiazepine	12130710	Although positive modulators for the GABA(A) receptor (20 mg/kg 3alpha hydroxy 5alpha pregnan 20 one and 10 30 mg/kg <b>chlordiazepoxide</b>) and opioid receptor (10 mg/kg morphine) produced significant elevations, agonists for alpha(2) adrenoceptors (clonidine) and dopamine receptors (apomorphine) had no effect on Edinger Westphal c <strong>Fos</strong> expression.
+FOS	drug	opioid	12130710	Although positive modulators for the GABA(A) receptor (20 mg/kg 3alpha hydroxy 5alpha pregnan 20 one and 10 30 mg/kg chlordiazepoxide) and <b>opioid</b> receptor (10 mg/kg <b>morphine</b>) produced significant elevations, agonists for alpha(2) adrenoceptors (clonidine) and dopamine receptors (apomorphine) had no effect on Edinger Westphal c <strong>Fos</strong> expression.
+FOS	drug	alcohol	12130710	These findings suggest that <b>alcohol</b> induced c <strong>Fos</strong> expression in Edinger Westphal results from direct interactions with GABA(A) receptors, which are modified by alpha(2A/D) adrenoceptors and dopamine receptors.
+FOS	drug	alcohol	12130710	Also using immunohistochemistry to identify potential intracellular mechanisms associated with <b>alcohol</b> induced c <strong>Fos</strong> expression in Edinger Westphal, we show time dependent increases in serine 727 phospho signal transducer and activator of transcription 3 (Stat3) but no changes in phospho cAMP response element binding protein and phospho Elk1.
+FOS	drug	alcohol	12130710	Finally, blockade of ERK 1/2 phosphorylation with the mitogen activated protein kinase (MEK) 1/2 inhibitor SL327 blocked <b>alcohol</b> induced c <strong>Fos</strong> expression, suggesting that <b>alcohol</b> induces c <strong>Fos</strong> in Edinger Westphal neurons through activation of the MEK1/2 ERK1/2 Stat3 pathway.
+FOS	drug	alcohol	12130678	We found that nuclear RACK1 is mediating the induction of the immediate early gene c <strong>fos</strong> expression induced by <b>ethanol</b>.
+FOS	drug	alcohol	12130678	First, transduction of full length RACK1 (Tat RACK1) resulted in the induction of c <strong>fos</strong> expression and enhancement of <b>ethanol</b> activities.
+FOS	drug	alcohol	12130678	Third, we identified a dominant negative fragment of RACK1 that inhibited the nuclear compartmentalization of endogenous RACK1 and inhibited <b>ethanol</b> induction of c <strong>fos</strong> mRNA and protein expression.
+FOS	drug	alcohol	12127099	In the present study we have immunohistochemically compared expression of urocortin and c <strong>Fos</strong> in naive and <b>ethanol</b> treated C57BL/6J and DBA/2J mouse inbred strains.
+FOS	drug	alcohol	12127099	Double label immunohistochemistry showed that <b>ethanol</b> induced c <strong>Fos</strong> expression is present in different sets of Edinger Westphal cells between the strains.
+FOS	drug	amphetamine	12125044	To determine if D(2) dopamine receptor mediated nuclear signaling is altered during the development of <b>amphetamine</b> sensitization, we examined the expression of immediate early gene (IEG) products, <strong>Fos</strong>, Jun, and <strong>Fos</strong> related antigen (FRA), in both controls and <b>amphetamine</b> sensitized rats after a challenge with the D(2) antagonist haloperidol.
+FOS	addiction	sensitization	12125044	To determine if D(2) dopamine receptor mediated nuclear signaling is altered during the development of amphetamine <b>sensitization</b>, we examined the expression of immediate early gene (IEG) products, <strong>Fos</strong>, Jun, and <strong>Fos</strong> related antigen (FRA), in both controls and amphetamine sensitized rats after a challenge with the D(2) antagonist haloperidol.
+FOS	drug	amphetamine	12117572	The food restriction regimen that augments drug reward also increases the induction of c <strong>fos</strong>, by intracerebroventricular <b>amphetamine</b>, in limbic forebrain dopamine (DA) terminal areas.
+FOS	addiction	reward	12117572	The food restriction regimen that augments drug <b>reward</b> also increases the induction of c <strong>fos</strong>, by intracerebroventricular amphetamine, in limbic forebrain dopamine (DA) terminal areas.
+FOS	drug	amphetamine	12112395	Similarly, in the second experiment it was found that the D1R dependent induction by <b>AMPH</b> of <strong>Fos</strong>, FosB, and JunB, but not NGFI A, in the NAc was enhanced in rats exposed 1 week earlier to repeated VTA <b>AMPH</b>.
+FOS	drug	amphetamine	12105094	The expression of c <strong>fos</strong> protein in striatal neurons was much more increased after a single injection of D <b>AMPH</b> (5 mg/kg) than after an equimolar concentration of SYD (23.8 mg/kg) in both the anterior and the posterior part of the striatum.
+FOS	drug	cocaine	12099907	<b>Cocaine</b> cue conditioned c <strong>fos</strong> expression was found in cortical areas, notably in the somatosensory cortex, where it was inhibited by BP 897, and in several regions belonging or linked to the limbic system.
+FOS	drug	alcohol	12045006	Chronic <b>alcohol</b> intoxication was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+FOS	addiction	intoxication	12045006	Chronic alcohol <b>intoxication</b> was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+FOS	drug	alcohol	12045006	Chronic <b>ethanol</b> feeding significantly enhanced MNP 1 binding, but not those of NF kappaB and <strong>AP 1</strong> in endothelial cells.
+FOS	drug	opioid	11976269	Here we have studied the expression of <strong>Fos</strong> after administration of <b>morphine</b> and during <b>morphine</b> withdrawal in the rat hypothalamic PVN and SON.
+FOS	addiction	withdrawal	11976269	Here we have studied the expression of <strong>Fos</strong> after administration of morphine and during morphine <b>withdrawal</b> in the rat hypothalamic PVN and SON.
+FOS	drug	opioid	11976269	<strong>Fos</strong> production was also studied in brainstem regions that innervate hypothalamic nuclei: the nucleus of solitary tract (NTS   A2) and the ventrolateral medulla (VLM   A1) and combined with immunostaining for tyrosine hydroxylase (TH) for immunohistochemical identification of active neurons during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	11976269	<strong>Fos</strong> production was also studied in brainstem regions that innervate hypothalamic nuclei: the nucleus of solitary tract (NTS   A2) and the ventrolateral medulla (VLM   A1) and combined with immunostaining for tyrosine hydroxylase (TH) for immunohistochemical identification of active neurons during morphine <b>withdrawal</b>.
+FOS	drug	opioid	11976269	Acute <b>morphine</b> administration produced an increase in <strong>Fos</strong> expression at hypothalamic nuclei and in the brainstem regions, and tolerance developed towards this effect.
+FOS	drug	opioid	11976269	Precipitated <b>morphine</b> withdrawal induced marked <strong>Fos</strong> immunoreactivity within the PVN and SON.
+FOS	addiction	withdrawal	11976269	Precipitated morphine <b>withdrawal</b> induced marked <strong>Fos</strong> immunoreactivity within the PVN and SON.
+FOS	drug	opioid	11976269	Moreover, catecholaminergic positive neurons in the brainstem showed a significant increase in <strong>Fos</strong> expression in response to <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	11976269	Moreover, catecholaminergic positive neurons in the brainstem showed a significant increase in <strong>Fos</strong> expression in response to morphine <b>withdrawal</b>.
+FOS	drug	opioid	11931859	<b>Heroin</b> sensitization as mapped by c <strong>Fos</strong> immunoreactivity in the rat striatum.
+FOS	addiction	sensitization	11931859	Heroin <b>sensitization</b> as mapped by c <strong>Fos</strong> immunoreactivity in the rat striatum.
+FOS	drug	opioid	11931859	Immunohistochemistry was used to map the induction of c <strong>Fos</strong> protein in the forebrain of rats treated with <b>heroin</b>.
+FOS	drug	opioid	11931859	Acute injection of <b>heroin</b> to drug naive rats caused significant induction of c <strong>Fos</strong> protein in the nucleus accumbens shell, whereas the same dose of <b>heroin</b> given to drug sensitized rats significantly increased c <strong>Fos</strong> immunoreactivity in the dorsomedial caudate putamen.
+FOS	drug	opioid	11931859	These results show that the <b>heroin</b> induced pattern of c <strong>Fos</strong> protein in the rat striatum differs according to the rat's drug history.
+FOS	drug	alcohol	11882344	Immediate early gene expression in concurrent prenatal <b>ethanol</b>  and/or cocaine exposed rat pups: intrauterine differences in cocaine levels and <strong>Fos</strong> expression.
+FOS	drug	cocaine	11882344	Immediate early gene expression in concurrent prenatal ethanol  and/or <b>cocaine</b> exposed rat pups: intrauterine differences in <b>cocaine</b> levels and <strong>Fos</strong> expression.
+FOS	drug	alcohol	11882344	There were increased numbers of <strong>Fos</strong> immunoreactive cells in fetuses exposed to both <b>ethanol</b> and cocaine compared to cocaine binge only.
+FOS	drug	cocaine	11882344	There were increased numbers of <strong>Fos</strong> immunoreactive cells in fetuses exposed to both ethanol and <b>cocaine</b> compared to <b>cocaine</b> binge only.
+FOS	addiction	intoxication	11882344	There were increased numbers of <strong>Fos</strong> immunoreactive cells in fetuses exposed to both ethanol and cocaine compared to cocaine <b>binge</b> only.
+FOS	drug	cocaine	11882344	Additionally, the gradient of c <strong>fos</strong> induction observed as a function of intrauterine position in <b>cocaine</b> treated rats was in the opposite direction: most distal fetuses generally had the most <strong>Fos</strong> immunoreactive cells.
+FOS	drug	amphetamine	11879792	The ability of <b>amphetamine</b> or cocaine to induce the expression of c <strong>fos</strong> mRNA in a number of brain regions is greatly enhanced when these drugs are administered in a distinct and relatively novel environment, relative to when they are given in the home cage.
+FOS	drug	cocaine	11879792	The ability of amphetamine or <b>cocaine</b> to induce the expression of c <strong>fos</strong> mRNA in a number of brain regions is greatly enhanced when these drugs are administered in a distinct and relatively novel environment, relative to when they are given in the home cage.
+FOS	drug	opioid	11850145	The present study examined the ability of LY235959, a competitive N methyl D aspartate (NMDA) receptor antagonist, to attenuate behaviors and c <strong>fos</strong> mRNA expression associated with acute <b>morphine</b> withdrawal in the infant rat.
+FOS	addiction	withdrawal	11850145	The present study examined the ability of LY235959, a competitive N methyl D aspartate (NMDA) receptor antagonist, to attenuate behaviors and c <strong>fos</strong> mRNA expression associated with acute morphine <b>withdrawal</b> in the infant rat.
+FOS	drug	opioid	11850145	Acute <b>morphine</b> withdrawal increased c <strong>fos</strong> mRNA expression in the brain and the spinal cord, which was attenuated by pre treatment of LY235959.
+FOS	addiction	withdrawal	11850145	Acute morphine <b>withdrawal</b> increased c <strong>fos</strong> mRNA expression in the brain and the spinal cord, which was attenuated by pre treatment of LY235959.
+FOS	drug	alcohol	11830185	Immunocytochemical and in situ hybridization studies indicate that acute high dose <b>ethanol</b> administration increases c <strong>fos</strong> expression in GABAergic neurons within the CeA of the rat, suggesting activation of these neurons by <b>ethanol</b>.
+FOS	drug	alcohol	11830185	A similar high dose (4 g/kg <b>ethanol</b>) effect on c <strong>fos</strong> expression in the CeA of C57 mice was also observed, whereas the DBA mice showed increased c <strong>fos</strong> expression in the CeA in the dose range of 1.25 4.0 g/kg.
+FOS	drug	cannabinoid	11815392	<b>THC</b> and nicotine administration induced c <strong>Fos</strong> expression in several brain structures.
+FOS	drug	nicotine	11815392	THC and <b>nicotine</b> administration induced c <strong>Fos</strong> expression in several brain structures.
+FOS	drug	opioid	11796656	We tested the overall hypothesis that circulating gonadal steroids determine the gender differences in <b>morphine</b>  and MK 801 induced behavior and c <strong>Fos</strong> expression.
+FOS	drug	opioid	11796656	<b>Morphine</b> caused a greater expression of c <strong>Fos</strong> in the striatum of intact males than of that females, which was independent of sex steroids.
+FOS	drug	opioid	11796656	MK 801 completely inhibited <b>morphine</b> induced c <strong>Fos</strong> in intact females but only caused partial inhibition in intact males; castrated males showed complete inhibition, which was reversed by testosterone, but gonadal steroids had no effect on this response in females.
+FOS	drug	opioid	11747755	NO mediated increase of <strong>Fos</strong> protein and NMDA1A R mRNA expression in rat spinal cord during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	11747755	NO mediated increase of <strong>Fos</strong> protein and NMDA1A R mRNA expression in rat spinal cord during morphine <b>withdrawal</b>.
+FOS	drug	opioid	11747755	Acute administration of <b>naloxone</b> and chronic administration of <b>morphine</b> did not change the expression of <strong>Fos</strong> protein and NADPH d positive neurons, and there was no expression of <strong>Fos</strong>/NADPH d double labeled neurons in the spinal cord of rats.
+FOS	drug	opioid	11747755	<b>Morphine</b> withdrawal increased the expression of <strong>Fos</strong> protein, NADPH d positive, and <strong>Fos</strong>/NADPH d double labeled neurons, and they were observed in all the laminae of the rat spinal cord.
+FOS	addiction	withdrawal	11747755	Morphine <b>withdrawal</b> increased the expression of <strong>Fos</strong> protein, NADPH d positive, and <strong>Fos</strong>/NADPH d double labeled neurons, and they were observed in all the laminae of the rat spinal cord.
+FOS	drug	opioid	11747755	Intrathecal injection of nNOS antisense oligonucleotides (nNOS AS) inhibited the increase of <strong>Fos</strong> protein and NMDA(1A)R mRNA expression in the rat spinal cord during <b>morphine</b> withdrawal and decreased the scores of <b>morphine</b> withdrawal symptoms.
+FOS	addiction	withdrawal	11747755	Intrathecal injection of nNOS antisense oligonucleotides (nNOS AS) inhibited the increase of <strong>Fos</strong> protein and NMDA(1A)R mRNA expression in the rat spinal cord during morphine <b>withdrawal</b> and decreased the scores of morphine <b>withdrawal</b> symptoms.
+FOS	drug	opioid	11747755	NO mediated the increase of <strong>Fos</strong> protein and NMDA1A R mRNA expression in the rat spinal cord during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	11747755	NO mediated the increase of <strong>Fos</strong> protein and NMDA1A R mRNA expression in the rat spinal cord during morphine <b>withdrawal</b>.
+FOS	drug	opioid	11731061	Although <b>morphine</b> tolerance increased formalin evoked persistent pain behavior and <strong>Fos</strong> LI in wild type mice, there was no difference between placebo  and <b>morphine</b> treated mutant mice, suggesting that PKC gamma also contributes to chronic <b>morphine</b> induced changes in nociceptive processing.
+FOS	drug	cannabinoid	11720732	The distribution of <b>cannabinoid</b> induced <strong>Fos</strong> expression in rat brain: differences between the Lewis and Wistar strain.
+FOS	drug	cannabinoid	11720732	In the present study we compared <strong>Fos</strong> expression, body temperature effects and behavioral effects elicited by the <b>cannabinoid</b> CB(1) receptor agonist CP 55,940 in Lewis and Wistar rats.
+FOS	drug	cocaine	11720732	In a further experiment, Wistar rats and Lewis rats did not differ in the amount of <strong>Fos</strong> immunoreactivity produced by <b>cocaine</b> (15 mg/kg).
+FOS	drug	amphetamine	11716816	Environmental context modulates the ability of cocaine and <b>amphetamine</b> to induce c <strong>fos</strong> mRNA expression in the neocortex, caudate nucleus, and nucleus accumbens.
+FOS	drug	cocaine	11716816	Environmental context modulates the ability of <b>cocaine</b> and amphetamine to induce c <strong>fos</strong> mRNA expression in the neocortex, caudate nucleus, and nucleus accumbens.
+FOS	drug	amphetamine	11716816	We reported previously that environmental novelty enhances the acute psychomotor activating effects of <b>amphetamine</b>, its ability to induce behavioral sensitization, and its ability to induce c <strong>fos</strong> mRNA in the striatum and other structures, relative to when <b>amphetamine</b> is given in the home cage.
+FOS	addiction	sensitization	11716816	We reported previously that environmental novelty enhances the acute psychomotor activating effects of amphetamine, its ability to induce behavioral <b>sensitization</b>, and its ability to induce c <strong>fos</strong> mRNA in the striatum and other structures, relative to when amphetamine is given in the home cage.
+FOS	drug	cocaine	11716816	The purpose of the present experiment was 2 fold: to determine (1) whether environmental novelty has a similar effect on the ability of <b>cocaine</b> to induce c <strong>fos</strong> mRNA, and (2) whether this effect is seen in neurologically intact rats (in previous experiments we studied the intact hemisphere of rats with a unilateral 6 OHDA lesion).
+FOS	drug	amphetamine	11716816	In the dorsal portion of the caudate putamen, core and shell of the nucleus accumbens, and in several cortical regions, both <b>amphetamine</b> (1.5 mg/kg) and cocaine (15 mg/kg) induced higher levels of c <strong>fos</strong> mRNA expression when administered in a novel environment, relative to when they were administered in the home cage.
+FOS	drug	cocaine	11716816	In the dorsal portion of the caudate putamen, core and shell of the nucleus accumbens, and in several cortical regions, both amphetamine (1.5 mg/kg) and <b>cocaine</b> (15 mg/kg) induced higher levels of c <strong>fos</strong> mRNA expression when administered in a novel environment, relative to when they were administered in the home cage.
+FOS	drug	nicotine	11702093	However, anatomical studies of <strong>Fos</strong> expression suggest that <b>nicotine</b> targets primarily non cholinergic neurons in the PPTg, especially GABAergic and glutamatergic neurons.
+FOS	drug	opioid	11698063	Characterization of the signal transduction pathways mediating <b>morphine</b> withdrawal stimulated c <strong>fos</strong> expression in hypothalamic nuclei.
+FOS	addiction	withdrawal	11698063	Characterization of the signal transduction pathways mediating morphine <b>withdrawal</b> stimulated c <strong>fos</strong> expression in hypothalamic nuclei.
+FOS	drug	opioid	11698063	We have shown previously that acute administration of <b>morphine</b> induces the expression of <strong>Fos</strong> in hypothalamic nuclei associated with control of the hypothalamus pituitary adrenocortex axis, such as the paraventricular nucleus and the supraoptic nucleus.
+FOS	drug	opioid	11698063	In the current study, we examined the role of protein kinase A, protein kinase C and Ca2+ entry through L type Ca2+ channels in <b>naloxone</b> precipitated <strong>Fos</strong> expression in the paraventricular and supraoptic nuclei.
+FOS	drug	opioid	11698063	After 7 days of <b>morphine</b> treatment, we did not observe any modification in <strong>Fos</strong> production.
+FOS	drug	opioid	11698063	However, when <b>opioid</b> withdrawal was precipitated with <b>naloxone</b> a dramatic increase in <strong>Fos</strong> immunoreactivity was observed in the parvocellular division of the paraventricular nucleus and in the supraoptic nucleus.
+FOS	addiction	withdrawal	11698063	However, when opioid <b>withdrawal</b> was precipitated with naloxone a dramatic increase in <strong>Fos</strong> immunoreactivity was observed in the parvocellular division of the paraventricular nucleus and in the supraoptic nucleus.
+FOS	drug	opioid	11698063	Chronic co administration of chelerythrine (a selective protein kinase C inhibitor acting at its catalytic domain) with <b>morphine</b> did not affect the increase in <strong>Fos</strong> expression observed in nuclei from <b>morphine</b> withdrawn rats.
+FOS	drug	opioid	11698063	In addition, infusion of calphostin C (another protein kinase C inhibitor, which interacts with its regulatory domain) did not modify the <b>morphine</b> withdrawal induced expression of <strong>Fos</strong>.
+FOS	addiction	withdrawal	11698063	In addition, infusion of calphostin C (another protein kinase C inhibitor, which interacts with its regulatory domain) did not modify the morphine <b>withdrawal</b> induced expression of <strong>Fos</strong>.
+FOS	drug	opioid	11698063	In contrast, when the selective protein kinase A inhibitor, N (2'guanidinoethyl) 5 isoquinolinesulfonamide (HA 1004), was infused it greatly diminished the increased <strong>Fos</strong> production observed in <b>morphine</b> withdrawn rats.
+FOS	drug	opioid	11698063	Furthermore, chronic infusion of the selective L type Ca2+ channel antagonist, nimodipine, significantly inhibited the enhancement of <strong>Fos</strong> induction in the paraventricular and supraoptic nuclei from <b>morphine</b> withdrawn animals.
+FOS	drug	opioid	11698063	Taken together, these data might indicate that protein kinase A activity is necessary for the expression of <strong>Fos</strong> during <b>morphine</b> withdrawal and that an up regulated Ca2+ system might contribute to the activation of <strong>Fos</strong>.
+FOS	addiction	withdrawal	11698063	Taken together, these data might indicate that protein kinase A activity is necessary for the expression of <strong>Fos</strong> during morphine <b>withdrawal</b> and that an up regulated Ca2+ system might contribute to the activation of <strong>Fos</strong>.
+FOS	drug	opioid	11605942	Activation of mu <b>opioid</b> receptor induces expression of c <strong>fos</strong> and junB via mitogen activated protein kinase cascade.
+FOS	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induced c <strong>fos</strong> and junB messenger RNAs, which were inhibited by pretreatment of the cells with pertussis toxin and PD98059, an inhibitor of extracellular signal regulated kinase cascade.
+FOS	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induces c <strong>fos</strong> and junB expression and elevates AP 1 mediated transcriptional activities via the mitogen activated protein kinase cascade.
+FOS	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induces c <strong>fos</strong> and junB expression and elevates <strong>AP 1</strong> mediated transcriptional activities via the mitogen activated protein kinase cascade.
+FOS	drug	opioid	11587712	Withdrawal precipitated with a peripherally acting quaternary <b>opioid</b> antagonist (<b>naloxone</b> methiodide) increased <strong>Fos</strong> expression but caused a more restricted pattern of neuronal activation than systemic withdrawal (precipitated with <b>naloxone</b> which enters the brain).
+FOS	addiction	withdrawal	11587712	<b>Withdrawal</b> precipitated with a peripherally acting quaternary opioid antagonist (naloxone methiodide) increased <strong>Fos</strong> expression but caused a more restricted pattern of neuronal activation than systemic <b>withdrawal</b> (precipitated with naloxone which enters the brain).
+FOS	drug	nicotine	11516821	Using the detection of the immediate early gene product, <strong>Fos</strong>, we examined which regions of the brain are activated by environmental cues associated with <b>nicotine</b> administration, and compared this profile to the pattern induced by cues associated with a natural reward, chocolate.
+FOS	addiction	reward	11516821	Using the detection of the immediate early gene product, <strong>Fos</strong>, we examined which regions of the brain are activated by environmental cues associated with nicotine administration, and compared this profile to the pattern induced by cues associated with a natural <b>reward</b>, chocolate.
+FOS	drug	nicotine	11516821	<b>Nicotine</b> associated sensory cues elicited marked and specific activation of <strong>Fos</strong> expression in prefrontal cortical and limbic regions.
+FOS	drug	amphetamine	11494405	The behavioral effects of <b>amphetamine</b> are diminished during periadolescence (35 days) relative to younger (21 days) and older (>60 days) rats, prompting us to examine <b>amphetamine</b> effects on neuronal activation with the immediate early gene, c <strong>fos</strong>.
+FOS	drug	amphetamine	11494405	When expressed as a percentage of vehicle for each age, <b>amphetamine</b> induced effects on c <strong>fos</strong> immunoreactivity were higher at 21 days of age compared with the effects at 35 and 60 days of age in the nucleus accumbens core and shell, striatum, and prefrontal cortex.
+FOS	drug	alcohol	11371719	Expression of c <strong>Fos</strong> in Alko <b>alcohol</b> rats responding for <b>ethanol</b> in an operant paradigm.
+FOS	addiction	reward	11371719	Expression of c <strong>Fos</strong> in Alko alcohol rats responding for ethanol in an <b>operant</b> paradigm.
+FOS	drug	alcohol	11371719	As an extension of studies mapping changes in neural activity after voluntary <b>ethanol</b> drinking, this study analyzed expression of the inducible transcription factor c <strong>Fos</strong> after <b>ethanol</b> consumption in an operant procedure.
+FOS	addiction	reward	11371719	As an extension of studies mapping changes in neural activity after voluntary ethanol drinking, this study analyzed expression of the inducible transcription factor c <strong>Fos</strong> after ethanol consumption in an <b>operant</b> procedure.
+FOS	drug	alcohol	11371719	In this paradigm, <b>ethanol</b> dose dependently increased c <strong>Fos</strong> expression in the Edinger Westphal nucleus (EW) and decreased expression in the dorsal tenia tecta compared with no <b>ethanol</b> controls.
+FOS	drug	alcohol	11371719	The finding that <b>ethanol</b> attenuated c <strong>Fos</strong> expression in the tenia tecta is novel.
+FOS	drug	opioid	11354804	Acute administration of <b>naloxone</b> and chronic administration of <b>morphine</b> changed neither the expression of <strong>Fos</strong> LI and NADPH d positive neurons nor the expression of <strong>Fos</strong>/NADPH d double labeled neurons in the spinal cord of rats.
+FOS	drug	opioid	11354804	<strong>Fos</strong> LI, NADPH d positive and <strong>Fos</strong>/NADPH d double labeled neurons were increased significantly in number in <b>morphine</b> withdrawal rats and they were observed in all the laminae of the spinal cord.
+FOS	addiction	withdrawal	11354804	<strong>Fos</strong> LI, NADPH d positive and <strong>Fos</strong>/NADPH d double labeled neurons were increased significantly in number in morphine <b>withdrawal</b> rats and they were observed in all the laminae of the spinal cord.
+FOS	drug	opioid	11354804	Intrathecal injection of L NA, nNOS antisense oligonucleotides significantly inhibited the expression of <strong>Fos</strong> LI in the spinal cord and decreased the scores for <b>morphine</b> withdrawal symptoms in <b>morphine</b> withdrawal rats, but not in nNOS S group.
+FOS	addiction	withdrawal	11354804	Intrathecal injection of L NA, nNOS antisense oligonucleotides significantly inhibited the expression of <strong>Fos</strong> LI in the spinal cord and decreased the scores for morphine <b>withdrawal</b> symptoms in morphine <b>withdrawal</b> rats, but not in nNOS S group.
+FOS	drug	opioid	11340648	Inhibitory effect of neuropeptide Y on <b>morphine</b> withdrawal is accompanied by reduced c <strong>fos</strong> expression in specific brain regions.
+FOS	addiction	withdrawal	11340648	Inhibitory effect of neuropeptide Y on morphine <b>withdrawal</b> is accompanied by reduced c <strong>fos</strong> expression in specific brain regions.
+FOS	drug	opioid	11340648	Brain areas involved in the attenuation of <b>morphine</b> withdrawal were delineated by radioactive in situ hybridization for the immediate early gene c <strong>fos</strong>, which is a marker for neuronal activity.
+FOS	addiction	withdrawal	11340648	Brain areas involved in the attenuation of morphine <b>withdrawal</b> were delineated by radioactive in situ hybridization for the immediate early gene c <strong>fos</strong>, which is a marker for neuronal activity.
+FOS	drug	opioid	11340648	Inhibition of behavioral signs of <b>naloxone</b> precipitated <b>morphine</b> withdrawal was accompanied by significantly reduced c <strong>fos</strong> expression in the locus coeruleus, lateral septal nucleus, ventral part of the periaqueductal grey, cingulate and frontal cortices, and septohippocampal nucleus.
+FOS	addiction	withdrawal	11340648	Inhibition of behavioral signs of naloxone precipitated morphine <b>withdrawal</b> was accompanied by significantly reduced c <strong>fos</strong> expression in the locus coeruleus, lateral septal nucleus, ventral part of the periaqueductal grey, cingulate and frontal cortices, and septohippocampal nucleus.
+FOS	drug	alcohol	11311798	Reduced <b>ethanol</b> withdrawal severity and altered withdrawal induced c <strong>fos</strong> expression in various brain regions of mice lacking protein kinase C epsilon.
+FOS	addiction	withdrawal	11311798	Reduced ethanol <b>withdrawal</b> severity and altered <b>withdrawal</b> induced c <strong>fos</strong> expression in various brain regions of mice lacking protein kinase C epsilon.
+FOS	addiction	withdrawal	11311798	In addition, we used c <strong>fos</strong> immunohistochemistry immediately following seizure assessment to identify potential brain regions involved in any observed differences in <b>withdrawal</b> severity.
+FOS	drug	alcohol	11311798	<b>Ethanol</b> fed protein kinase C epsilon null mutant mice also exhibited a decrease in the number of <strong>Fos</strong> positive cells in the lateral septum, and an increase in the number of <strong>Fos</strong> positive cells in the dentate gyrus, mediodorsal thalamus, paraventricular nuclei of the thalamus and hypothalamus, and substantia nigra compared to <b>ethanol</b> fed wild type mice.
+FOS	drug	cocaine	11299316	<strong>fos</strong> and jun proteins, and cyclic AMP response element binding protein) previously shown to be relevant to <b>cocaine</b>'s behavioral actions.
+FOS	drug	opioid	11283964	Sensitivity to <b>naloxone</b> of the behavioral signs of <b>morphine</b> withdrawal and c <strong>Fos</strong> expression in the rat CNS: a quantitative dose response analysis.
+FOS	addiction	withdrawal	11283964	Sensitivity to naloxone of the behavioral signs of morphine <b>withdrawal</b> and c <strong>Fos</strong> expression in the rat CNS: a quantitative dose response analysis.
+FOS	drug	opioid	11283964	Several studies have used c <strong>Fos</strong> expression to delineate the neural substrate underlying <b>naloxone</b> precipitated <b>morphine</b> withdrawal (MW).
+FOS	addiction	withdrawal	11283964	Several studies have used c <strong>Fos</strong> expression to delineate the neural substrate underlying naloxone precipitated morphine <b>withdrawal</b> (MW).
+FOS	drug	opioid	11283964	However, because behavioral manifestations of MW depend on both the degree of dependence and the doses of <b>naloxone</b> (NAL), a comprehensive study would require examining c <strong>Fos</strong> expression in relation with the degree of MW.
+FOS	addiction	dependence	11283964	However, because behavioral manifestations of MW depend on both the degree of <b>dependence</b> and the doses of naloxone (NAL), a comprehensive study would require examining c <strong>Fos</strong> expression in relation with the degree of MW.
+FOS	addiction	reward	11283964	Low c <strong>Fos</strong> expression was detected in some regions involved in motor control or in <b>reward</b>, suggesting either their minor role in MW or a limitation of the technique.
+FOS	drug	cocaine	11282258	Induction of chronic <strong>fos</strong> related antigens by <b>cocaine</b> was also reduced in mutant mice as compared to their wild type siblings, implying that downstream actions of <b>cocaine</b> were also affected by inactivation of the high affinity nAChR.
+FOS	drug	nicotine	11275291	<b>Nicotine</b> induced behavioral sensitization is associated with extracellular dopamine release and expression of c <strong>Fos</strong> in the striatum and nucleus accumbens of the rat.
+FOS	addiction	sensitization	11275291	Nicotine induced behavioral <b>sensitization</b> is associated with extracellular dopamine release and expression of c <strong>Fos</strong> in the striatum and nucleus accumbens of the rat.
+FOS	drug	nicotine	11275291	This study was carried out to investigate the neural mechanisms underlying <b>nicotine</b> induced behavioral sensitization using in vivo microdialysis and <strong>Fos</strong> like immunohistochemistry (FLI).
+FOS	addiction	sensitization	11275291	This study was carried out to investigate the neural mechanisms underlying nicotine induced behavioral <b>sensitization</b> using in vivo microdialysis and <strong>Fos</strong> like immunohistochemistry (FLI).
+FOS	drug	nicotine	11275291	Furthermore, in parallel with the behavioral and biochemical data, systemic challenge with <b>nicotine</b> produced marked <strong>Fos</strong> like immunohistochemistry in the nucleus accumbens and the striatum in the <b>nicotine</b> pretreated rats.
+FOS	drug	nicotine	11275291	Taken together, this study demonstrates that behavioral sensitization is clearly associated with an increase in DA release and activation of <strong>Fos</strong> like immunoreactive cells in the striatum and the nucleus accumbens produced by repeated <b>nicotine</b> treatment.
+FOS	addiction	sensitization	11275291	Taken together, this study demonstrates that behavioral <b>sensitization</b> is clearly associated with an increase in DA release and activation of <strong>Fos</strong> like immunoreactive cells in the striatum and the nucleus accumbens produced by repeated nicotine treatment.
+FOS	drug	amphetamine	11259635	<b>Methamphetamine</b> (MAP) causes the sensitization phenomena not only in MAP induced locomotor activity, dopamine release, and <strong>Fos</strong> expression, but also in MAP induced circadian rhythm.
+FOS	addiction	sensitization	11259635	Methamphetamine (MAP) causes the <b>sensitization</b> phenomena not only in MAP induced locomotor activity, dopamine release, and <strong>Fos</strong> expression, but also in MAP induced circadian rhythm.
+FOS	drug	cocaine	11172061	The effects of reexposure to the S(D) on the recovery of responding at the previously <b>cocaine</b> paired lever and on <strong>Fos</strong> protein expression then were determined in two groups.
+FOS	drug	cocaine	11172061	In both groups, the <b>cocaine</b> S(D), but not the non reward S(D), elicited strong recovery of responding and increased <strong>Fos</strong> immunoreactivity in the basolateral amygdala and medial prefrontal cortex (areas Cg1/Cg3).
+FOS	addiction	reward	11172061	In both groups, the cocaine S(D), but not the non <b>reward</b> S(D), elicited strong recovery of responding and increased <strong>Fos</strong> immunoreactivity in the basolateral amygdala and medial prefrontal cortex (areas Cg1/Cg3).
+FOS	drug	cocaine	11172061	The response reinstatement and <strong>Fos</strong> expression induced by the <b>cocaine</b> S(D) were both reversed by selective dopamine D(1) receptor antagonists.
+FOS	addiction	relapse	11172061	The response <b>reinstatement</b> and <strong>Fos</strong> expression induced by the cocaine S(D) were both reversed by selective dopamine D(1) receptor antagonists.
+FOS	drug	alcohol	11164784	Expression of inducible transcription factors (ITFs) c <strong>Fos</strong> and FosB was investigated during acquisition of <b>alcohol</b> drinking in C57BL/6J mice.
+FOS	drug	alcohol	11164784	A slight but statistically significant increase in c <strong>Fos</strong> expression was found in the Edinger Westphal nucleus (EW) of animals consuming 2% <b>ethanol</b>/10% sucrose for the first time.
+FOS	drug	alcohol	11164784	Stronger expression of c <strong>Fos</strong> in EW was found in animals repeatedly consuming <b>ethanol</b> containing solutions.
+FOS	drug	cocaine	11164086	GR127935 attenuated the ability of <b>cocaine</b> to stimulate locomotion and induce c <strong>fos</strong> expression in the striatum.
+FOS	drug	opioid	11163637	A selective phosphodiesterase IV inhibitor, rolipram blocks both withdrawal behavioral manifestations, and c <strong>Fos</strong> protein expression in <b>morphine</b> dependent mice.
+FOS	addiction	withdrawal	11163637	A selective phosphodiesterase IV inhibitor, rolipram blocks both <b>withdrawal</b> behavioral manifestations, and c <strong>Fos</strong> protein expression in morphine dependent mice.
+FOS	drug	opioid	11163637	Immunohistochemical study of c <strong>Fos</strong> protein revealed a significant increase in the protein expression, 1 h after <b>naloxone</b> induced withdrawal manifestations.
+FOS	addiction	withdrawal	11163637	Immunohistochemical study of c <strong>Fos</strong> protein revealed a significant increase in the protein expression, 1 h after naloxone induced <b>withdrawal</b> manifestations.
+FOS	drug	opioid	11163637	A combination of rolipram and <b>morphine</b> treatment for 5 days prevented the increase of c <strong>Fos</strong> protein expression.
+FOS	drug	opioid	11163637	These results suggest that chronic rolipram treatment in combination with <b>morphine</b> in mice will abolish the development of <b>morphine</b> dependence and the expression of c <strong>Fos</strong> protein induced by <b>naloxone</b> challenge.
+FOS	addiction	dependence	11163637	These results suggest that chronic rolipram treatment in combination with morphine in mice will abolish the development of morphine <b>dependence</b> and the expression of c <strong>Fos</strong> protein induced by naloxone challenge.
+FOS	drug	amphetamine	11160452	Environmental novelty differentially affects c <strong>fos</strong> mRNA expression induced by <b>amphetamine</b> or cocaine in subregions of the bed nucleus of the stria terminalis and amygdala.
+FOS	drug	cocaine	11160452	Environmental novelty differentially affects c <strong>fos</strong> mRNA expression induced by amphetamine or <b>cocaine</b> in subregions of the bed nucleus of the stria terminalis and amygdala.
+FOS	drug	amphetamine	11160452	Here we report that environmental context differentially affects patterns of <b>amphetamine</b>  and cocaine induced c <strong>fos</strong> mRNA expression in the bed nucleus of the stria terminalis (BST) and amygdala of male rats.
+FOS	drug	cocaine	11160452	Here we report that environmental context differentially affects patterns of amphetamine  and <b>cocaine</b> induced c <strong>fos</strong> mRNA expression in the bed nucleus of the stria terminalis (BST) and amygdala of male rats.
+FOS	drug	amphetamine	11160452	<b>Amphetamine</b> given at home did not induce c <strong>fos</strong> mRNA, and when given in the novel environment, did not increase levels beyond that observed for novelty alone.
+FOS	drug	amphetamine	11160452	In the basolateral and lateral amygdala, <b>amphetamine</b> or cocaine at home or exposure to novelty induced c <strong>fos</strong> mRNA.
+FOS	drug	cocaine	11160452	In the basolateral and lateral amygdala, amphetamine or <b>cocaine</b> at home or exposure to novelty induced c <strong>fos</strong> mRNA.
+FOS	drug	amphetamine	11160452	When <b>amphetamine</b> or cocaine was given in a novel environment the c <strong>fos</strong> mRNA response was significantly enhanced.
+FOS	drug	cocaine	11160452	When amphetamine or <b>cocaine</b> was given in a novel environment the c <strong>fos</strong> mRNA response was significantly enhanced.
+FOS	drug	amphetamine	11160452	In the central nucleus of the amygdala (CEA) and oval subnucleus of the BST (BSTov), <b>amphetamine</b> administration at home produced a robust increase in c <strong>fos</strong> mRNA expression, whereas exposure to novelty had little effect.
+FOS	drug	amphetamine	11160452	In contrast to other brain regions examined, the c <strong>fos</strong> mRNA response to <b>amphetamine</b> in a novel versus home environment was significantly smaller.
+FOS	drug	amphetamine	11160452	In both "home" and "novel" <b>amphetamine</b> groups, c <strong>fos</strong> mRNA in the BSTov and CEA was predominantly expressed in enkephalin containing cells; coexpression with corticotropin releasing hormone was rare.
+FOS	drug	opioid	11122358	Mapping of c <strong>fos</strong> gene expression in the brain during <b>morphine</b> dependence and precipitated withdrawal, and phenotypic identification of the striatal neurons involved.
+FOS	addiction	dependence	11122358	Mapping of c <strong>fos</strong> gene expression in the brain during morphine <b>dependence</b> and precipitated withdrawal, and phenotypic identification of the striatal neurons involved.
+FOS	addiction	withdrawal	11122358	Mapping of c <strong>fos</strong> gene expression in the brain during morphine dependence and precipitated <b>withdrawal</b>, and phenotypic identification of the striatal neurons involved.
+FOS	drug	opioid	11122358	Using in situ hybridization, we examined the effects of chronic <b>morphine</b> treatment and withdrawal on c <strong>fos</strong> mRNA in the rat brain, and particularly within identified striatal neurons.
+FOS	addiction	withdrawal	11122358	Using in situ hybridization, we examined the effects of chronic morphine treatment and <b>withdrawal</b> on c <strong>fos</strong> mRNA in the rat brain, and particularly within identified striatal neurons.
+FOS	drug	opioid	11122358	Placebo animals and <b>morphine</b> dependent rats showed a very weak c <strong>fos</strong> mRNA expression in all the structures studied.
+FOS	drug	alcohol	11122358	Our study emphasized the spatial variations in c <strong>fos</strong> mRNA expression, and also revealed a peak expression of c <strong>fos</strong> mRNA at 1 h after <b>naltrexone</b> precipitated withdrawal in the projection areas of dopaminergic neurons, noradrenergic neurons and in several regions expressing opiate receptors.
+FOS	addiction	withdrawal	11122358	Our study emphasized the spatial variations in c <strong>fos</strong> mRNA expression, and also revealed a peak expression of c <strong>fos</strong> mRNA at 1 h after naltrexone precipitated <b>withdrawal</b> in the projection areas of dopaminergic neurons, noradrenergic neurons and in several regions expressing opiate receptors.
+FOS	drug	opioid	11122358	Interestingly, <b>morphine</b> withdrawal induces c <strong>fos</strong> mRNA expression in the two efferent populations of the striatum (i.e.
+FOS	addiction	withdrawal	11122358	Interestingly, morphine <b>withdrawal</b> induces c <strong>fos</strong> mRNA expression in the two efferent populations of the striatum (i.e.
+FOS	addiction	withdrawal	11122358	The activation of striatopallidal neurons suggests a predominant dopaminergic regulation on c <strong>fos</strong> gene expression in the striatum during <b>withdrawal</b>.
+FOS	drug	opioid	11122358	On the contrary, c <strong>fos</strong> induction in striatonigral neurons during withdrawal seems to involve a more complex regulation like <b>opioid</b> dopamine interactions via the mu <b>opioid</b> receptor and the D1 dopamine receptor coexpressed on this neuronal population or the implication of other neurotransmitter systems.
+FOS	addiction	withdrawal	11122358	On the contrary, c <strong>fos</strong> induction in striatonigral neurons during <b>withdrawal</b> seems to involve a more complex regulation like opioid dopamine interactions via the mu opioid receptor and the D1 dopamine receptor coexpressed on this neuronal population or the implication of other neurotransmitter systems.
+FOS	addiction	aversion	11120397	Opiate withdrawal induced <strong>fos</strong> immunoreactivity in the rat extended amygdala parallels the development of conditioned place <b>aversion</b>.
+FOS	addiction	withdrawal	11120397	Opiate <b>withdrawal</b> induced <strong>fos</strong> immunoreactivity in the rat extended amygdala parallels the development of conditioned place aversion.
+FOS	addiction	withdrawal	11120397	Expression of the transcription factor <strong>Fos</strong> is known to increase during opiate <b>withdrawal</b>, but its presence during low dose antagonist precipitated <b>withdrawal</b> has not previously been established.
+FOS	drug	opioid	11120397	In order to determine if there is a relationship between withdrawal induced neuronal activity and conditioned place aversion, immunocytochemical localization of <strong>Fos</strong> was examined in the basal forebrain of opiate dependent animals receiving one of several doses of <b>naloxone</b> (0, 3.25, 7.5, 15, 30, or 1000 microg/kg).
+FOS	addiction	aversion	11120397	In order to determine if there is a relationship between withdrawal induced neuronal activity and conditioned place <b>aversion</b>, immunocytochemical localization of <strong>Fos</strong> was examined in the basal forebrain of opiate dependent animals receiving one of several doses of naloxone (0, 3.25, 7.5, 15, 30, or 1000 microg/kg).
+FOS	addiction	withdrawal	11120397	In order to determine if there is a relationship between <b>withdrawal</b> induced neuronal activity and conditioned place aversion, immunocytochemical localization of <strong>Fos</strong> was examined in the basal forebrain of opiate dependent animals receiving one of several doses of naloxone (0, 3.25, 7.5, 15, 30, or 1000 microg/kg).
+FOS	addiction	aversion	11120397	Significant increases in both immunocytochemical detection of <strong>Fos</strong> and conditioned place <b>aversion</b> were seen at doses >/= 7.5 microg/kg.
+FOS	drug	opioid	11058452	Endogenous <b>opioids</b> inhibit oxytocin neurones in late pregnancy and the <b>opioid</b> antagonist, <b>naloxone</b>, increases <strong>Fos</strong> expression in supraoptic nuclei by preventing inhibition.
+FOS	drug	opioid	11058452	However, progesterone attenuated <b>naloxone</b> induced <strong>Fos</strong> expression in the supraoptic nucleus in late pregnancy and <b>naloxone</b> administered during parturition did not accelerate the duration of births delayed by progesterone administration, indicating that progesterone does not act by hyperactivation of endogenous <b>opioid</b> tone.
+FOS	drug	alcohol	11057525	Enhanced ultrasonic vocalization and <strong>Fos</strong> protein expression following <b>ethanol</b> withdrawal: effects of flumazenil.
+FOS	addiction	withdrawal	11057525	Enhanced ultrasonic vocalization and <strong>Fos</strong> protein expression following ethanol <b>withdrawal</b>: effects of flumazenil.
+FOS	addiction	withdrawal	11057525	The present studies further tested this hypothesis by assessing the effect of flumazenil on <b>withdrawal</b> induced changes in a behavioral task and on the expression of the neuronal protein, <strong>Fos</strong>.
+FOS	drug	alcohol	11057525	Male Sprague Dawley rats were withdrawn from a chronic <b>ethanol</b> regimen and tested, with or without flumazenil pretreatment, for either ultrasonic vocalization in response to air puff or for the induction of <strong>Fos</strong> protein like immunoreactivity (<strong>Fos</strong> LI) in brain.
+FOS	drug	alcohol	11057525	In contrast, flumazenil (5.0 mg/kg), given either 14 h before withdrawal from chronic <b>ethanol</b>, or during hours 3 and 5 following withdrawal, did not attenuate the effects of withdrawal on <strong>Fos</strong> LI.
+FOS	addiction	withdrawal	11057525	In contrast, flumazenil (5.0 mg/kg), given either 14 h before <b>withdrawal</b> from chronic ethanol, or during hours 3 and 5 following <b>withdrawal</b>, did not attenuate the effects of <b>withdrawal</b> on <strong>Fos</strong> LI.
+FOS	drug	alcohol	11057525	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce <strong>Fos</strong> LI in most of the same brain regions as observed following <b>ethanol</b> withdrawal, and that this change in <strong>Fos</strong> protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).
+FOS	drug	benzodiazepine	11057525	Subsequent testing with DMCM confirmed that a <b>benzodiazepine</b> inverse agonist can induce <strong>Fos</strong> LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in <strong>Fos</strong> protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).
+FOS	addiction	withdrawal	11057525	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce <strong>Fos</strong> LI in most of the same brain regions as observed following ethanol <b>withdrawal</b>, and that this change in <strong>Fos</strong> protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).
+FOS	drug	alcohol	11057525	Overall, these results demonstrate that specific behavioral indices of anxiety, but not measures of <strong>Fos</strong> LI, support the contribution of an endogenous BZD inverse agonist in the <b>ethanol</b> withdrawal syndrome.
+FOS	addiction	withdrawal	11057525	Overall, these results demonstrate that specific behavioral indices of anxiety, but not measures of <strong>Fos</strong> LI, support the contribution of an endogenous BZD inverse agonist in the ethanol <b>withdrawal</b> syndrome.
+FOS	drug	amphetamine	11057524	Recent studies point to central adaptive changes insofar as rewarding, locomotor and c <strong>fos</strong> inducing effects of <b>amphetamine</b> and MK 801, injected directly into the lateral ventricle, are greater in food restricted than ad libitum fed rats.
+FOS	addiction	reward	11057524	The increased expression of c <strong>fos</strong> in nucleus accumbens (NAC) shell, in particular, suggests that food restriction may augment drug <b>reward</b> by modulating dopamine (DA) synaptic function in this area.
+FOS	drug	opioid	10998122	Suppression of c <strong>fos</strong> induction in the nucleus accumbens prevents acquisition but not expression of <b>morphine</b> conditioned place preference.
+FOS	drug	opioid	10998122	The c <strong>fos</strong> immediate early gene is induced by <b>morphine</b> and other drugs of abuse in the nucleus accumbens (NAc), a mesolimbic region implicated in drug abuse and reward.
+FOS	addiction	reward	10998122	The c <strong>fos</strong> immediate early gene is induced by morphine and other drugs of abuse in the nucleus accumbens (NAc), a mesolimbic region implicated in drug abuse and <b>reward</b>.
+FOS	addiction	reward	10998122	This study examined the role of c <strong>fos</strong> in the acquisition and expression of the conditioned place paradigm (<b>CPP</b>) in the rat by suppressing <strong>Fos</strong> protein expression with c <strong>fos</strong> antisense oligodeoxynucleotides (ODNs).
+FOS	drug	opioid	10998122	CPP was completely prevented by c <strong>fos</strong> antisense ODN infused bilaterally into the NAc prior to each systemic <b>morphine</b> injection, whereas sense and missense NAc injections had no effect on CPP.
+FOS	addiction	reward	10998122	<b>CPP</b> was completely prevented by c <strong>fos</strong> antisense ODN infused bilaterally into the NAc prior to each systemic morphine injection, whereas sense and missense NAc injections had no effect on <b>CPP</b>.
+FOS	drug	opioid	10998122	NAc administration of c <strong>fos</strong> antisense ODN after the last systemic <b>morphine</b> conditioning session did not affect the expression of <b>morphine</b> CPP.
+FOS	addiction	reward	10998122	NAc administration of c <strong>fos</strong> antisense ODN after the last systemic morphine conditioning session did not affect the expression of morphine <b>CPP</b>.
+FOS	drug	opioid	10998122	These results suggest that c <strong>fos</strong> expression in NAc is necessary for the acquisition but not expression of <b>morphine</b> CPP, and they have important implications for understanding conditioned behaviours and drug craving and addiction.
+FOS	addiction	addiction	10998122	These results suggest that c <strong>fos</strong> expression in NAc is necessary for the acquisition but not expression of morphine CPP, and they have important implications for understanding conditioned behaviours and drug craving and <b>addiction</b>.
+FOS	addiction	relapse	10998122	These results suggest that c <strong>fos</strong> expression in NAc is necessary for the acquisition but not expression of morphine CPP, and they have important implications for understanding conditioned behaviours and drug <b>craving</b> and addiction.
+FOS	addiction	reward	10998122	These results suggest that c <strong>fos</strong> expression in NAc is necessary for the acquisition but not expression of morphine <b>CPP</b>, and they have important implications for understanding conditioned behaviours and drug craving and addiction.
+FOS	drug	cocaine	10986339	The suppressive effects of pentobarbital were not specific to c <strong>Fos</strong>, such that pentobarbital also suppressed expression of ITFs FosB and Egr1 in the striatum of <b>cocaine</b> treated rats.
+FOS	drug	alcohol	10986339	On the other hand, pentobarbital by itself strongly induced c <strong>Fos</strong> expression in the lateral habenula of saline , cocaine , and <b>ethanol</b> injected rats.
+FOS	drug	cocaine	10986339	On the other hand, pentobarbital by itself strongly induced c <strong>Fos</strong> expression in the lateral habenula of saline , <b>cocaine</b> , and ethanol injected rats.
+FOS	drug	cocaine	10971643	A low dose of <b>cocaine</b>, by itself essentially ineffective, produced an increase in c <strong>fos</strong> and NGFI A mRNA in the cerebral cortex in mice that had been drinking caffeine.
+FOS	drug	cocaine	10958117	Leftward shift in the acquisition of <b>cocaine</b> self administration in isolation reared rats: relationship to extracellular levels of dopamine, serotonin and glutamate in the nucleus accumbens and amygdala striatal <strong>FOS</strong> expression.
+FOS	drug	cocaine	10958117	To identify specific changes in monoamine and glutamate function in the nucleus accumbens and c <strong>fos</strong> induction in the amygdala and striatum which may be correlated with altered <b>cocaine</b> self administration in isolates.
+FOS	drug	cocaine	10958117	0.25 or 1.5 mg/kg per IV infusion; FR1), intracerebral microdialysis was used to measure <b>cocaine</b> induced changes in extracellular levels of dopamine, serotonin and glutamate in the nucleus accumbens and the expression of the immediate early gene c <strong>fos</strong> was quantified using quantitative immunocytochemistry of its protein product <strong>Fos</strong> in several amygdala and striatal brain regions following <b>cocaine</b> administration.
+FOS	drug	cocaine	10958117	<b>Cocaine</b> increased <strong>FOS</strong> expression in most amygdala and striatal brain regions examined that were relatively greater in isolation reared rats in core and shell regions of the nucleus accumbens, medial and lateral regions of the dorsal striatum as well as the central nucleus of the amygdala.
+FOS	addiction	withdrawal	10942854	Expression of <strong>fos</strong> related antigens in the nucleus accumbens during opiate <b>withdrawal</b> and their attenuation by a D2 dopamine receptor agonist.
+FOS	addiction	withdrawal	10942854	The present study measured the expression of <strong>Fos</strong> related antigens (FRAs) within the NAc during opiate <b>withdrawal</b> to determine whether decreases in somatic <b>withdrawal</b> signs produced by a D2 receptor agonist are accompanied by related changes in accumbens neuronal activity.
+FOS	drug	nicotine	10942036	Based on the data reviewed in the present study, it is suggested that <b>nicotine</b> by stimulating presynaptic alpha7 nicotinic receptors within the VTA, that are probably localized on glutamatergic afferents from the medial prefrontal cortex, produces sequentially an increase in glutamate concentrations, stimulation of NMDA receptors found on dopamine (DA) containing neurons in the VTA, enhanced firing activity of VTA DA neurons, augmented DA release in the nerve terminal regions, and enhanced c <strong>fos</strong> expression in the dopaminergic projection areas through activation of D1 DA receptors.
+FOS	drug	amphetamine	20575854	Although not widely appreciated, protein phosphorylation cascades and <strong>fos</strong> related antigens also may play a role in the neurotoxic actions of substituted amphetamines such as <b>methamphetamine</b>.
+FOS	drug	amphetamine	20575854	Here we document the involvement of the dopaminoceptive phosphoprotein, DARPP 32, the <strong>fos</strong> related antigen, FRA 2, and the growth associated protein kinase, MAP kinase, in the neurotoxic action of known dopaminergic neurotoxicants, including <b>methamphetamine</b>.
+FOS	drug	cocaine	10869819	In order to understand the underlying mechanisms responsible for the behavior induced by DM, we examined the effects of DM on <b>cocaine</b> induced conditioned place preference (CPP) and locomotor pattern in mice, and <strong>Fos</strong> related antigen immunoreactivity (FRA IR) in the striatal complex (nucleus accumbens and striatum) of the mouse brain.
+FOS	addiction	reward	10869819	In order to understand the underlying mechanisms responsible for the behavior induced by DM, we examined the effects of DM on cocaine induced conditioned place preference (<b>CPP</b>) and locomotor pattern in mice, and <strong>Fos</strong> related antigen immunoreactivity (FRA IR) in the striatal complex (nucleus accumbens and striatum) of the mouse brain.
+FOS	drug	nicotine	10837847	Effect of acute <b>nicotine</b> on <strong>Fos</strong> protein expression in rat brain during chronic <b>nicotine</b> and its withdrawal.
+FOS	addiction	withdrawal	10837847	Effect of acute nicotine on <strong>Fos</strong> protein expression in rat brain during chronic nicotine and its <b>withdrawal</b>.
+FOS	drug	nicotine	10837847	To study the cholinergic regulation of hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei and interpeduncular nucleus (IPN) we investigated the effects of acute <b>nicotine</b> (0.5 mg/kg, SC, 60 min) on <strong>Fos</strong> like immunostaining (IS) during chronic <b>nicotine</b> and its withdrawal in rats.
+FOS	addiction	withdrawal	10837847	To study the cholinergic regulation of hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei and interpeduncular nucleus (IPN) we investigated the effects of acute nicotine (0.5 mg/kg, SC, 60 min) on <strong>Fos</strong> like immunostaining (IS) during chronic nicotine and its <b>withdrawal</b> in rats.
+FOS	drug	nicotine	10837847	In control rats, acute <b>nicotine</b> increased <strong>Fos</strong> IS significantly in all three brain areas studied.
+FOS	drug	nicotine	10837847	After 72 h withdrawal <b>nicotine</b> induced elevation of <strong>Fos</strong> IS was similar to that of control rats in all three areas.
+FOS	addiction	withdrawal	10837847	After 72 h <b>withdrawal</b> nicotine induced elevation of <strong>Fos</strong> IS was similar to that of control rats in all three areas.
+FOS	drug	nicotine	10837795	In addition, expression of p53 showed region  and gender selective alterations consistent with cell damage; c <strong>fos</strong>, which is constitutively overexpressed after gestational <b>nicotine</b> exposure, was unaffected with the adolescent treatment paradigm.
+FOS	drug	cocaine	10814832	Prior experience of morphine application alters the c <strong>fos</strong> response to MDMA ('ecstasy') and <b>cocaine</b> in the rat striatum.
+FOS	drug	opioid	10814832	Prior experience of <b>morphine</b> application alters the c <strong>fos</strong> response to MDMA ('ecstasy') and cocaine in the rat striatum.
+FOS	drug	psychedelics	10814832	Prior experience of morphine application alters the c <strong>fos</strong> response to <b>MDMA</b> ('<b>ecstasy</b>') and cocaine in the rat striatum.
+FOS	drug	psychedelics	10814832	<b>MDMA</b> (3, 4 <b>methylenedioxymethamphetamine</b>, 6 mg/kg) as a single test dose yielded a c <strong>fos</strong> response in a wide range of brain areas.
+FOS	drug	opioid	10814832	In the caudate putamen, the expression pattern of c <strong>fos</strong> was clearly altered if the rats had received repeated <b>morphine</b> application previously.
+FOS	drug	psychedelics	10814832	In this case, the <b>MDMA</b> induced c <strong>fos</strong> expression was markedly confined to the centromedial, mesolimbic aspect of the striatum whereas it had a diffuse appearance in rats not exposed to the opiate earlier.
+FOS	drug	cocaine	10814832	<b>Cocaine</b> application (50 mg/kg) elicited an intense c <strong>fos</strong> expression in the medial striatum if the animals were morphine pretreated; it was virtually absent in drug naive rats after the same <b>cocaine</b> dose.
+FOS	drug	opioid	10814832	Cocaine application (50 mg/kg) elicited an intense c <strong>fos</strong> expression in the medial striatum if the animals were <b>morphine</b> pretreated; it was virtually absent in drug naive rats after the same cocaine dose.
+FOS	drug	cannabinoid	10814832	No difference in the c <strong>fos</strong> expression pattern between morphine and saline pretreated animals was observed in the case of a <b>THC</b> (Delta(9) <b>tetrahydrocannabinol</b>, 25 mg/kg) or an LSD (lysergic acid diethylamide, 1 mg/kg) test application.
+FOS	drug	opioid	10814832	No difference in the c <strong>fos</strong> expression pattern between <b>morphine</b> and saline pretreated animals was observed in the case of a THC (Delta(9) tetrahydrocannabinol, 25 mg/kg) or an LSD (lysergic acid diethylamide, 1 mg/kg) test application.
+FOS	drug	psychedelics	10814832	No difference in the c <strong>fos</strong> expression pattern between morphine and saline pretreated animals was observed in the case of a THC (Delta(9) tetrahydrocannabinol, 25 mg/kg) or an <b>LSD</b> (lysergic acid diethylamide, 1 mg/kg) test application.
+FOS	drug	opioid	10808081	Here, inactivation of G(i/o) proteins by pre treatment of <b>morphine</b> dependent rats with pertussis toxin injected into the left supraoptic nucleus reduced withdrawal induced <strong>Fos</strong> protein expression within the injected nucleus by 41+/ 10% compared to the contralateral nucleus, indicating that functional G(i/o) proteins are essential for the development and/or expression of <b>morphine</b> dependence by oxytocin cells in the supraoptic nucleus.
+FOS	addiction	dependence	10808081	Here, inactivation of G(i/o) proteins by pre treatment of morphine dependent rats with pertussis toxin injected into the left supraoptic nucleus reduced withdrawal induced <strong>Fos</strong> protein expression within the injected nucleus by 41+/ 10% compared to the contralateral nucleus, indicating that functional G(i/o) proteins are essential for the development and/or expression of morphine <b>dependence</b> by oxytocin cells in the supraoptic nucleus.
+FOS	addiction	withdrawal	10808081	Here, inactivation of G(i/o) proteins by pre treatment of morphine dependent rats with pertussis toxin injected into the left supraoptic nucleus reduced <b>withdrawal</b> induced <strong>Fos</strong> protein expression within the injected nucleus by 41+/ 10% compared to the contralateral nucleus, indicating that functional G(i/o) proteins are essential for the development and/or expression of morphine dependence by oxytocin cells in the supraoptic nucleus.
+FOS	drug	opioid	10808081	Finally, pertussis toxin reduced acute <b>morphine</b> inhibition of systemic hypertonic saline induced <strong>Fos</strong> protein expression in the supraoptic nucleus, confirming that pertussis toxin effectively inactivates G(i/o) proteins in the supraoptic nucleus.
+FOS	drug	opioid	10792459	<b>Morphine</b> also induced a higher rate of c <strong>fos</strong> transcription in the shell of the nucleus accumbens in mutant mice.
+FOS	drug	opioid	10792459	These particular behavioural responses to <b>morphine</b> may be associated with the action of the drug on DA release and c <strong>fos</strong> expression in the shell of the nucleus accumbens of DAT /  mice.
+FOS	addiction	reward	10780500	The long term adaptive molecular changes in the target neurons of the terminal fields of the mesocorticolimbic DA system, including transcriptional regulation mediated by c <strong>fos</strong> family gene products on other genes, suggest that the mesolimbic DA projection to the nucleus accumbens is mainly involved in the stimulus <b>reward</b> learning process.
+FOS	drug	alcohol	10776677	Changes in dopamine transporter and c <strong>Fos</strong> expression in the nucleus accumbens of <b>alcohol</b> tolerant rats.
+FOS	drug	alcohol	10776677	In the present study, the effects of chronic <b>alcohol</b> consumption on the functions of the dopamine transporter (DAT) and the expression of c <strong>Fos</strong> proteins were investigated using in vivo brain microdialysis and immunocytochemistry.
+FOS	drug	alcohol	10776677	Increased expression of the c <strong>Fos</strong> like protein was found in the ACC of <b>alcohol</b> treated rats.
+FOS	drug	alcohol	10776677	These results show that (1) chronic <b>alcohol</b> consumption desensitizes or decreases the DAT of DA terminals in the ACC and that (2) EtOH causes cellular hyperexcitability of ACC dopaminergic neurons with increased <strong>Fos</strong> expression during <b>alcohol</b> tolerance.
+FOS	drug	opioid	10773195	<b>Opioid</b> site in nucleus accumbens shell mediates eating and hedonic 'liking' for food: map based on microinjection <strong>Fos</strong> plumes.
+FOS	addiction	reward	10773195	Opioid site in nucleus accumbens shell mediates eating and <b>hedonic</b> 'liking' for food: map based on microinjection <strong>Fos</strong> plumes.
+FOS	drug	opioid	10773195	The accumbens site mediating <b>morphine</b> induced increases in food 'wanting' and 'liking' was identified using a novel method based on local expression of <strong>Fos</strong> induced directly by drug microinjections.
+FOS	drug	opioid	10773195	The plume shaped region of drug induced increase in <strong>Fos</strong> immunoreactivity immediately surrounding a <b>morphine</b> microinjection site (<strong>Fos</strong> plume) was objectively mapped.
+FOS	drug	opioid	10773195	A point sampling procedure was used to measure the shape and size of 'positive' plumes of <strong>Fos</strong> expression triggered by microinjections of <b>morphine</b> at locations that caused increases in eating behavior.
+FOS	drug	benzodiazepine	10762378	Previous experience of withdrawal from chronic <b>diazepam</b> ameliorates the aversiveness of precipitated withdrawal and reduces withdrawal induced c <strong>fos</strong> expression in nucleus accumbens.
+FOS	addiction	withdrawal	10762378	Previous experience of <b>withdrawal</b> from chronic diazepam ameliorates the aversiveness of precipitated <b>withdrawal</b> and reduces <b>withdrawal</b> induced c <strong>fos</strong> expression in nucleus accumbens.
+FOS	addiction	aversion	10762378	The weakening of the <b>aversive</b> properties of precipitated withdrawal may reflect habituation to the withdrawal stimulus, and was accompanied by a loss of the ability of withdrawal to induce c <strong>fos</strong> expression in the shell of the nucleus accumbens, an area sensitive to both novel, and stressful, as well as rewarding stimuli.
+FOS	addiction	withdrawal	10762378	The weakening of the aversive properties of precipitated <b>withdrawal</b> may reflect habituation to the <b>withdrawal</b> stimulus, and was accompanied by a loss of the ability of <b>withdrawal</b> to induce c <strong>fos</strong> expression in the shell of the nucleus accumbens, an area sensitive to both novel, and stressful, as well as rewarding stimuli.
+FOS	drug	cocaine	10762327	The decrease in dopamine observed in the shell had a postsynaptic impact, as shown by less induction of <strong>Fos</strong> like proteins selectively in the shell in response to <b>cocaine</b>.
+FOS	drug	cocaine	10762327	remained unchanged after adrenalectomy, suggesting that the changes in <strong>Fos</strong> expression after <b>cocaine</b> injection were likely to depend on changes in extracellular dopamine levels rather than on changes in postsynaptic sensitivity to dopamine.
+FOS	drug	amphetamine	10751568	Chronic food restriction increases <strong>fos</strong> like immunoreactivity (FLI) induced in rat forebrain by intraventricular <b>amphetamine</b>.
+FOS	drug	amphetamine	10751568	In the absence of <b>amphetamine</b> challenge, there was generally no difference in brain <strong>Fos</strong> like immunoreactivity (FLI) between ad libitum fed and food restricted rats.
+FOS	drug	opioid	10718931	Under basal conditions, <b>naloxone</b> (5 mg/kg) increased oxytocin secretion in all groups, but had no greater effect in sex steroid treated rats, and did not induce <strong>Fos</strong> expression in the supraoptic nucleus.
+FOS	drug	opioid	10712293	Sucrose consumption increases <b>naloxone</b> induced c <strong>Fos</strong> immunoreactivity in limbic forebrain.
+FOS	drug	opioid	10712293	In the central nucleus of the amygdala, <b>naloxone</b> administration to those rats drinking water significantly increased c <strong>Fos</strong> IR, an effect that was significantly enhanced by sucrose consumption, suggesting an upregulation of endogenous <b>opioid</b> tone in this area.
+FOS	drug	opioid	10708732	administration of M&B28,767 (1 pg/rat) attenuated the elevation of c <strong>fos</strong> mRNA during <b>naloxone</b> precipitated withdrawal in many brain regions, including the cerebral cortex, thalamus, hypothalamus and locus coeruleus.
+FOS	addiction	withdrawal	10708732	administration of M&B28,767 (1 pg/rat) attenuated the elevation of c <strong>fos</strong> mRNA during naloxone precipitated <b>withdrawal</b> in many brain regions, including the cerebral cortex, thalamus, hypothalamus and locus coeruleus.
+FOS	drug	opioid	10648731	Local <b>morphine</b> withdrawal increases c <strong>fos</strong> gene, <strong>Fos</strong> protein, and oxytocin gene expression in hypothalamic magnocellular neurosecretory cells.
+FOS	addiction	withdrawal	10648731	Local morphine <b>withdrawal</b> increases c <strong>fos</strong> gene, <strong>Fos</strong> protein, and oxytocin gene expression in hypothalamic magnocellular neurosecretory cells.
+FOS	drug	opioid	10648731	We measured stimulation of c <strong>fos</strong> and oxytocin gene expression during excitation of oxytocin cells induced by systemic or local <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	10648731	We measured stimulation of c <strong>fos</strong> and oxytocin gene expression during excitation of oxytocin cells induced by systemic or local morphine <b>withdrawal</b>.
+FOS	drug	opioid	10648731	Female rats were made <b>morphine</b> dependent by intracerebroventricular <b>morphine</b> infusion over 5 d. <b>Morphine</b> withdrawal, induced by systemic injection of the <b>opioid</b> antagonist <b>naloxone</b> (5 mg/kg) in conscious or anesthetized rats, increased the density of c <strong>fos</strong> messenger RNA and of oxytocin heterogeneous nuclear RNA in supraoptic nucleus cells compared with those of nonwithdrawn rats; c <strong>fos</strong> messenger RNA was also increased in the magnocellular and parvocellular paraventricular nuclei of withdrawn rats.
+FOS	addiction	withdrawal	10648731	Female rats were made morphine dependent by intracerebroventricular morphine infusion over 5 d. Morphine <b>withdrawal</b>, induced by systemic injection of the opioid antagonist naloxone (5 mg/kg) in conscious or anesthetized rats, increased the density of c <strong>fos</strong> messenger RNA and of oxytocin heterogeneous nuclear RNA in supraoptic nucleus cells compared with those of nonwithdrawn rats; c <strong>fos</strong> messenger RNA was also increased in the magnocellular and parvocellular paraventricular nuclei of withdrawn rats.
+FOS	drug	opioid	10648731	<b>Morphine</b> withdrawal increased the number of <strong>Fos</strong> immunoreactive cells in the supraoptic and magnocellular paraventricular nuclei of conscious or pentobarbitone anesthetized rats.
+FOS	addiction	withdrawal	10648731	Morphine <b>withdrawal</b> increased the number of <strong>Fos</strong> immunoreactive cells in the supraoptic and magnocellular paraventricular nuclei of conscious or pentobarbitone anesthetized rats.
+FOS	drug	opioid	10648731	<b>Morphine</b> withdrawal also increased <strong>Fos</strong> immunoreactive cell numbers in the parvocellular paraventricular nucleus of conscious but not anesthetized rats.
+FOS	addiction	withdrawal	10648731	Morphine <b>withdrawal</b> also increased <strong>Fos</strong> immunoreactive cell numbers in the parvocellular paraventricular nucleus of conscious but not anesthetized rats.
+FOS	drug	opioid	10648731	Central administration of the alpha(1) adrenoreceptor antagonist benoxathian (5 microg/min) did not prevent <b>morphine</b> withdrawal induced increases in the numbers of <strong>Fos</strong> immunoreactive neurons in the supraoptic or magnocellular paraventricular nucleus.
+FOS	addiction	withdrawal	10648731	Central administration of the alpha(1) adrenoreceptor antagonist benoxathian (5 microg/min) did not prevent morphine <b>withdrawal</b> induced increases in the numbers of <strong>Fos</strong> immunoreactive neurons in the supraoptic or magnocellular paraventricular nucleus.
+FOS	drug	opioid	10648731	Unilateral microdialysis administration of <b>naloxone</b> (10( 5) M) into the supraoptic nucleus of anesthetized <b>morphine</b> dependent rats increased <strong>Fos</strong> immunoreactive cell numbers compared with the contralateral nucleus.
+FOS	drug	opioid	10648731	Finally, we investigated whether dependence could be induced by chronic unilateral infusion of <b>morphine</b> into a supraoptic nucleus; systemic <b>naloxone</b> (5 mg/kg) increased <strong>Fos</strong> immunoreactive cell numbers in the <b>morphine</b> infused nucleus compared with the contralateral nucleus.
+FOS	addiction	dependence	10648731	Finally, we investigated whether <b>dependence</b> could be induced by chronic unilateral infusion of morphine into a supraoptic nucleus; systemic naloxone (5 mg/kg) increased <strong>Fos</strong> immunoreactive cell numbers in the morphine infused nucleus compared with the contralateral nucleus.
+FOS	drug	opioid	10648731	Thus, <b>morphine</b> withdrawal excitation increases c <strong>fos</strong> and oxytocin gene expression in supraoptic nucleus neurons.
+FOS	addiction	withdrawal	10648731	Thus, morphine <b>withdrawal</b> excitation increases c <strong>fos</strong> and oxytocin gene expression in supraoptic nucleus neurons.
+FOS	drug	cocaine	10632609	<strong>Fos</strong> protein expression and <b>cocaine</b> seeking behavior in rats after exposure to a <b>cocaine</b> self administration environment.
+FOS	addiction	relapse	10632609	<strong>Fos</strong> protein expression and cocaine <b>seeking</b> behavior in rats after exposure to a cocaine self administration environment.
+FOS	drug	cocaine	10632609	To examine neuronal activation associated with incentive motivation for <b>cocaine</b>, <b>cocaine</b> seeking behavior (operant responding without <b>cocaine</b> reinforcement) and <strong>Fos</strong> expression were examined in rats exposed to saline and <b>cocaine</b> priming injections and/or a self administration environment.
+FOS	addiction	relapse	10632609	To examine neuronal activation associated with incentive motivation for cocaine, cocaine <b>seeking</b> behavior (operant responding without cocaine reinforcement) and <strong>Fos</strong> expression were examined in rats exposed to saline and cocaine priming injections and/or a self administration environment.
+FOS	addiction	reward	10632609	To examine neuronal activation associated with <b>incentive</b> motivation for cocaine, cocaine seeking behavior (<b>operant</b> responding without cocaine <b>reinforcement</b>) and <strong>Fos</strong> expression were examined in rats exposed to saline and cocaine priming injections and/or a self administration environment.
+FOS	drug	cocaine	10632609	The priming injections also enhanced <strong>Fos</strong> expression in the anterior cingulate, but only in <b>cocaine</b> experienced groups, suggesting that this enhancement reflects an experience dependent motivational effect of the priming injections.
+FOS	drug	cocaine	11102476	Because SL327 antagonized <b>cocaine</b> induced c <strong>fos</strong> expression and Elk 1 hyperphosphorylation, we suggest that the ERK intracellular signaling cascade is also involved in the prime burst of gene expression underlying long term behavioral changes induced by <b>cocaine</b>.
+FOS	drug	opioid	10627313	Androgenic anabolic steroids blunt <b>morphine</b> induced c <strong>fos</strong> expression in the rat striatum: possible role of beta endorphin.
+FOS	drug	opioid	10627313	In the present study, chronic administration of AAS blunted the striatal c <strong>fos</strong> response to <b>morphine</b>, indicating that AAS can alter the molecular responses to at least one drug of abuse.
+FOS	addiction	reward	10583497	AMPA receptor involvement in c <strong>fos</strong> expression in the medial prefrontal cortex and amygdala dissociates neural substrates of conditioned activity and conditioned <b>reward</b>.
+FOS	drug	amphetamine	10583497	), induced locomotor activity and c <strong>fos</strong> expression (a marker for neuronal activation) in the mouse medial prefrontal cortex (mPFC) and amygdala; acute or repeated <b>amphetamine</b> (1 mg/kg, i.p.)
+FOS	drug	amphetamine	10583497	An alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate (AMPA) receptor antagonist, 2, 3 dihydroxy 6 nitro 7 sulphamoyl benzo(f)quinoxaline (NBQX), blocked expression of conditioned activity, and prevented the increase in c <strong>fos</strong> expression in mPFC, implicating mPFC AMPAergic transmission in the conditioned component of behavioural sensitization to <b>amphetamine</b>.
+FOS	addiction	sensitization	10583497	An alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate (AMPA) receptor antagonist, 2, 3 dihydroxy 6 nitro 7 sulphamoyl benzo(f)quinoxaline (NBQX), blocked expression of conditioned activity, and prevented the increase in c <strong>fos</strong> expression in mPFC, implicating mPFC AMPAergic transmission in the conditioned component of behavioural <b>sensitization</b> to amphetamine.
+FOS	drug	amphetamine	10583497	NBQX failed to block the expression of <b>amphetamine</b> conditioned place preference, a measure of conditioned reward, or conditioned c <strong>fos</strong> expression in the amygdala, an area implicated in the expression of conditioned place preference.
+FOS	addiction	reward	10583497	NBQX failed to block the expression of amphetamine conditioned place preference, a measure of conditioned <b>reward</b>, or conditioned c <strong>fos</strong> expression in the amygdala, an area implicated in the expression of conditioned place preference.
+FOS	drug	nicotine	10579804	Selective c <strong>fos</strong> induction and decreased dopamine release in the central nucleus of amygdala in rats displaying a mecamylamine precipitated <b>nicotine</b> withdrawal syndrome.
+FOS	addiction	withdrawal	10579804	Selective c <strong>fos</strong> induction and decreased dopamine release in the central nucleus of amygdala in rats displaying a mecamylamine precipitated nicotine <b>withdrawal</b> syndrome.
+FOS	drug	nicotine	10579804	In the present study the neuronal expression of <strong>Fos</strong>, the protein product of c <strong>fos</strong>, was used to study changes in neuronal activity in nerve terminal regions of the ascending dopaminergic system during <b>nicotine</b> withdrawal.
+FOS	addiction	withdrawal	10579804	In the present study the neuronal expression of <strong>Fos</strong>, the protein product of c <strong>fos</strong>, was used to study changes in neuronal activity in nerve terminal regions of the ascending dopaminergic system during nicotine <b>withdrawal</b>.
+FOS	addiction	withdrawal	10579804	The number of <strong>Fos</strong> positive nuclei was substantially increased in the central nucleus of amygdala (CNA) in animals undergoing mecamylamine precipitated <b>withdrawal</b>, whereas no significant changes in c <strong>fos</strong> expression were observed in the basolateral amygdaloid nucleus, the core and the shell of the nucleus accumbens, the dorsolateral striatum, or the medial prefrontal cortex.
+FOS	drug	nicotine	10579804	These results indicate that the mecamylamine precipitated <b>nicotine</b> withdrawal reaction is accompanied by a selective induction of c <strong>fos</strong> and a concurrent decrease in DA release in the CNA, which may have a bearing on symptoms such as anxiety and distress, which frequently are associated with the <b>nicotine</b> abstinence reaction in humans.
+FOS	addiction	withdrawal	10579804	These results indicate that the mecamylamine precipitated nicotine <b>withdrawal</b> reaction is accompanied by a selective induction of c <strong>fos</strong> and a concurrent decrease in DA release in the CNA, which may have a bearing on symptoms such as anxiety and distress, which frequently are associated with the nicotine abstinence reaction in humans.
+FOS	drug	alcohol	10575084	Expression of c <strong>Fos</strong> was significantly lower in the dentate gyrus of <b>alcohol</b> consuming animals vs. sucrose consuming animals.
+FOS	drug	alcohol	10575084	Induction of c <strong>Fos</strong> in AcbC, CeMPV and EW was significantly related to blood <b>alcohol</b> concentrations (BAC).
+FOS	drug	cocaine	10564376	Expression of c <strong>fos</strong>, NGFI A and secretogranin II mRNA in brain regions during initiation of <b>cocaine</b> self administration in mice.
+FOS	drug	cocaine	10564376	Intravenous <b>cocaine</b> self administration in mice was studied to find correlates of the acquisition of <b>cocaine</b> oriented operant behaviour in the expression of nerve growth factor induced clone A (NGFI A), c <strong>fos</strong> and secretogranin II mRNAs.
+FOS	addiction	reward	10564376	Intravenous cocaine self administration in mice was studied to find correlates of the acquisition of cocaine oriented <b>operant</b> behaviour in the expression of nerve growth factor induced clone A (NGFI A), c <strong>fos</strong> and secretogranin II mRNAs.
+FOS	drug	cocaine	10564376	Compared with saline, an increase in c <strong>fos</strong> mRNA in lateral and basolateral amygdala was found in active <b>cocaine</b> receiving animals, and a decrease in yoked controls receiving <b>cocaine</b>.
+FOS	drug	cocaine	10564376	In caudate putamen, both contingent and non contingent <b>cocaine</b> increased c <strong>fos</strong> mRNA.
+FOS	drug	cocaine	10564376	As differences in c <strong>fos</strong> and secretogranin II mRNA between active mice and yoked controls were robust, measuring these mRNAs may identify neurons selectively involved in acquisition of <b>cocaine</b> taking behaviour.
+FOS	drug	nicotine	10555165	<b>Nicotine</b> withdrawal up regulates c <strong>Fos</strong> transcription in pheochromocytoma cells.
+FOS	addiction	withdrawal	10555165	Nicotine <b>withdrawal</b> up regulates c <strong>Fos</strong> transcription in pheochromocytoma cells.
+FOS	drug	nicotine	10555165	The influence of <b>nicotine</b> on the expression of <strong>Fos</strong> family proteins, which specifically formed complexes with the AP 1 sequence, was assessed.
+FOS	drug	nicotine	10555165	The influence of <b>nicotine</b> on the expression of <strong>Fos</strong> family proteins, which specifically formed complexes with the <strong>AP 1</strong> sequence, was assessed.
+FOS	drug	nicotine	10555165	mRNA for c <strong>Fos</strong>, c jun and jun B were up regulated at 0.5 h after <b>nicotine</b> treatment, elevated c <strong>Fos</strong> also being apparent after withdrawal.
+FOS	addiction	withdrawal	10555165	mRNA for c <strong>Fos</strong>, c jun and jun B were up regulated at 0.5 h after nicotine treatment, elevated c <strong>Fos</strong> also being apparent after <b>withdrawal</b>.
+FOS	drug	nicotine	10555165	These results indicate that <b>nicotine</b> treatment may affect the transcriptional activity of many genes through c <strong>Fos</strong> and c Jun protein expression in neural cells, and that Fra 1 protein may make a contribution.
+FOS	drug	opioid	10521594	Long lasting sensitization towards <b>morphine</b> in motoric and limbic areas as determined by c <strong>fos</strong> expression in rat brain.
+FOS	addiction	sensitization	10521594	Long lasting <b>sensitization</b> towards morphine in motoric and limbic areas as determined by c <strong>fos</strong> expression in rat brain.
+FOS	drug	opioid	10521594	To identify brain areas involved in these long lasting processes, we studied the expression of the transcription factor c <strong>fos</strong> by in situ hybridization in rat brain as a marker for changes in gene expression after single or repeated <b>morphine</b> applications in the animals.
+FOS	drug	opioid	10521594	The only c <strong>fos</strong> signal that exceeded background after a single dose of <b>morphine</b> (50 mg/kg) was a diffuse expression in the lateral septum.
+FOS	drug	opioid	10521594	In contrast, repeated dosage twice daily for 10 days and ascending from 10 to 50 mg/kg resulted in a sharply delineated <b>morphine</b> induced c <strong>fos</strong> synthesis in the dorsomedial and lateral striatum, lateral septum, medial mammillary nuclei, anterior thalamus and, in part masked by a high background due to injection stress, in the cingulate cortex.
+FOS	drug	opioid	10521594	The c <strong>fos</strong> response was inducible by <b>morphine</b> in pretreated animals for up to 8 weeks after finishing the repeated application scheme.
+FOS	drug	opioid	10521594	Therefore, the sensitization of <b>morphine</b> induced c <strong>fos</strong> expression in parts of the striatum seems to correlate with the locomotor effects of repeated <b>morphine</b> application, whereas the observed sensitization in several limbic brain areas might reflect emotional phenomena like increased self administration in rats or drug craving in humans.
+FOS	addiction	relapse	10521594	Therefore, the sensitization of morphine induced c <strong>fos</strong> expression in parts of the striatum seems to correlate with the locomotor effects of repeated morphine application, whereas the observed sensitization in several limbic brain areas might reflect emotional phenomena like increased self administration in rats or drug <b>craving</b> in humans.
+FOS	addiction	sensitization	10521594	Therefore, the <b>sensitization</b> of morphine induced c <strong>fos</strong> expression in parts of the striatum seems to correlate with the locomotor effects of repeated morphine application, whereas the observed <b>sensitization</b> in several limbic brain areas might reflect emotional phenomena like increased self administration in rats or drug craving in humans.
+FOS	drug	cannabinoid	10521585	Acute injection of drugs with low addictive potential (delta(9) <b>tetrahydrocannabinol</b>, 3,4 methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c <strong>fos</strong> expression in limbic brain areas than highly addicting drugs (cocaine and morphine).
+FOS	drug	cocaine	10521585	Acute injection of drugs with low addictive potential (delta(9) tetrahydrocannabinol, 3,4 methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c <strong>fos</strong> expression in limbic brain areas than highly addicting drugs (<b>cocaine</b> and morphine).
+FOS	drug	opioid	10521585	Acute injection of drugs with low addictive potential (delta(9) tetrahydrocannabinol, 3,4 methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c <strong>fos</strong> expression in limbic brain areas than highly addicting drugs (cocaine and <b>morphine</b>).
+FOS	drug	psychedelics	10521585	Acute injection of drugs with low addictive potential (delta(9) tetrahydrocannabinol, 3,4 <b>methylenedioxymethamphetamine</b>, lysergic acid diamide) causes a much higher c <strong>fos</strong> expression in limbic brain areas than highly addicting drugs (cocaine and morphine).
+FOS	addiction	addiction	10521585	Acute injection of drugs with low <b>addictive</b> potential (delta(9) tetrahydrocannabinol, 3,4 methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c <strong>fos</strong> expression in limbic brain areas than highly addicting drugs (cocaine and morphine).
+FOS	addiction	addiction	10521585	To investigate the connection between <b>addictive</b> potential and stimulation of critical brain areas in more detail, we studied c <strong>fos</strong> accumulation in response to various addicting drugs in direct comparison.
+FOS	drug	cocaine	10521585	<b>Cocaine</b> in a high dose of 50 mg/kg yielded only a discrete c <strong>fos</strong> expression in the medial and central striatum.
+FOS	drug	opioid	10521585	<b>Morphine</b> (50 mg/kg) caused a weak c <strong>fos</strong> synthesis in the lateral septum.
+FOS	drug	cannabinoid	10521585	<b>THC</b> (delta(9) <b>tetrahydrocannabinol</b>), 25 mg/kg, induced c <strong>fos</strong> mRNA again in the lateral septum and furthermore in large parts of the striatum including the nucleus accumbens.
+FOS	drug	cannabinoid	10521585	LSD (lysergic acid diamide), 1 mg/kg, elicited a similar c <strong>fos</strong> expression pattern as <b>THC</b>, but there was additionally a very strong hybridization signal in the cerebral cortex, especially in the upper layers, and in the ventral part of the periaqueductal gray.
+FOS	drug	psychedelics	10521585	<b>LSD</b> (lysergic acid diamide), 1 mg/kg, elicited a similar c <strong>fos</strong> expression pattern as THC, but there was additionally a very strong hybridization signal in the cerebral cortex, especially in the upper layers, and in the ventral part of the periaqueductal gray.
+FOS	drug	psychedelics	10521585	In addition to the regions that responded to <b>LSD</b>, there was a very pronounced c <strong>fos</strong> signal in the nucleus accumbens core and shell and in the mammillary nuclei.
+FOS	drug	cannabinoid	10521585	Taken together, our study revealed that the drugs with the highest addictive potential, cocaine and morphine, yielded a very low c <strong>fos</strong> synthesis throughout the brain whereas the brain regions closely linked to pleasure (especially the nucleus accumbens) responded strongly to drugs with an apparently lower addictive potential (<b>THC</b>, LSD, MDMA).
+FOS	drug	cocaine	10521585	Taken together, our study revealed that the drugs with the highest addictive potential, <b>cocaine</b> and morphine, yielded a very low c <strong>fos</strong> synthesis throughout the brain whereas the brain regions closely linked to pleasure (especially the nucleus accumbens) responded strongly to drugs with an apparently lower addictive potential (THC, LSD, MDMA).
+FOS	drug	opioid	10521585	Taken together, our study revealed that the drugs with the highest addictive potential, cocaine and <b>morphine</b>, yielded a very low c <strong>fos</strong> synthesis throughout the brain whereas the brain regions closely linked to pleasure (especially the nucleus accumbens) responded strongly to drugs with an apparently lower addictive potential (THC, LSD, MDMA).
+FOS	drug	psychedelics	10521585	Taken together, our study revealed that the drugs with the highest addictive potential, cocaine and morphine, yielded a very low c <strong>fos</strong> synthesis throughout the brain whereas the brain regions closely linked to pleasure (especially the nucleus accumbens) responded strongly to drugs with an apparently lower addictive potential (THC, <b>LSD</b>, <b>MDMA</b>).
+FOS	addiction	addiction	10521585	Taken together, our study revealed that the drugs with the highest <b>addictive</b> potential, cocaine and morphine, yielded a very low c <strong>fos</strong> synthesis throughout the brain whereas the brain regions closely linked to pleasure (especially the nucleus accumbens) responded strongly to drugs with an apparently lower <b>addictive</b> potential (THC, LSD, MDMA).
+FOS	drug	opioid	10501478	Sexual dimorphism in the response to N methyl D aspartate receptor antagonists and <b>morphine</b> on behavior and c <strong>Fos</strong> induction in the rat brain.
+FOS	drug	opioid	10501478	Previous studies have shown that, upon administration of <b>morphine</b>, the immediate early gene c <strong>Fos</strong> is induced in the striatum, nucleus accumbens and cortex of the rat brain.
+FOS	drug	opioid	10501478	In male rats treated with <b>morphine</b> (10 mg/kg, s.c.) and killed 2 h later, there was an induction of c <strong>Fos</strong> in the dorsomedial caudate putamen, the nucleus accumbens and in the intralaminar nuclei of the thalamus.
+FOS	drug	opioid	10501478	In females, <b>morphine</b> induced c <strong>Fos</strong> in the caudate putamen, but with more inter animal variability than in males.
+FOS	drug	opioid	10501478	Whereas dizocilpine maleate partially blocked the <b>morphine</b> induced c <strong>Fos</strong> expression in the caudate putamen of males, it completely blocked this response in females.
+FOS	drug	opioid	10501478	In the caudate putamen, <b>morphine</b> induced c <strong>Fos</strong> expression was significantly reduced by NPC 17742 (30 min before <b>morphine</b>) in males and completely blocked in females.
+FOS	drug	cocaine	10499584	Acute exposure to <b>cocaine</b> transiently induces several <strong>Fos</strong> family transcription factors in the nucleus accumbens, a region of the brain that is important for addiction.
+FOS	addiction	addiction	10499584	Acute exposure to cocaine transiently induces several <strong>Fos</strong> family transcription factors in the nucleus accumbens, a region of the brain that is important for <b>addiction</b>.
+FOS	drug	nicotine	10479714	The effects of acute <b>nicotine</b> on the metabolism of dopamine and the expression of <strong>Fos</strong> protein in striatal and limbic brain areas of rats during chronic <b>nicotine</b> infusion and its withdrawal.
+FOS	addiction	withdrawal	10479714	The effects of acute nicotine on the metabolism of dopamine and the expression of <strong>Fos</strong> protein in striatal and limbic brain areas of rats during chronic nicotine infusion and its <b>withdrawal</b>.
+FOS	drug	nicotine	10479714	The effects of acute <b>nicotine</b> (0.5 mg/kg, s.c.) on dopamine (DA) metabolism and <strong>Fos</strong> protein expression in striatal and limbic areas of rats on the seventh day of chronic <b>nicotine</b> infusion (4 mg. kg( 1).
+FOS	drug	nicotine	10479714	Acute <b>nicotine</b> increased <strong>Fos</strong> immunostaining (IS) in the caudate putamen (CPU), the core of nucleus accumbens (NAcc), the cingulate cortex (Cg), and the central nucleus of amygdala (ACe) significantly.
+FOS	drug	nicotine	10479714	During <b>nicotine</b> infusion the <b>nicotine</b> induced responses were attenuated in CPU and NAcc, whereas in ACe and Cg <strong>Fos</strong> immunostaining was increased as in saline infused rats.
+FOS	drug	nicotine	10479714	After 24 hr withdrawal, acute <b>nicotine</b> did not increase <strong>Fos</strong> immunostaining in CPU, NAcc, and Cg, but increased it clearly in ACe.
+FOS	addiction	withdrawal	10479714	After 24 hr <b>withdrawal</b>, acute nicotine did not increase <strong>Fos</strong> immunostaining in CPU, NAcc, and Cg, but increased it clearly in ACe.
+FOS	drug	alcohol	10443996	In this study, immunohistochemical expression analysis of immediate early genes c <strong>fos</strong>, fosB, and zif268 was performed in brain of C57BL/6J mice after voluntary <b>alcohol</b> consumption.
+FOS	drug	alcohol	10443996	Specifically, animals consuming <b>ethanol</b>/sucrose with subsequent exposure to restraint stress had lower c <strong>Fos</strong> expression in the CA3 region of hippocampus, and higher c <strong>Fos</strong> expression in nucleus accumbens than mice exposed to restraint stress after drinking the sucrose solution.
+FOS	drug	cocaine	10415707	<b>Cocaine</b> seeking behavior and <strong>Fos</strong> expression in the amygdala produced by <b>cocaine</b> or a <b>cocaine</b> self administration environment.
+FOS	addiction	relapse	10415707	Cocaine <b>seeking</b> behavior and <strong>Fos</strong> expression in the amygdala produced by cocaine or a cocaine self administration environment.
+FOS	drug	opioid	10415375	Previous studies from this laboratory have demonstrated that acute, systemic administration of <b>morphine</b> results in an induction of the immediate early gene (IEG) proteins, c <strong>Fos</strong> and Jun B, in the dorsomedial portion of the rat caudate putamen (CPu).
+FOS	drug	opioid	10415375	These studies have also shown that <b>morphine</b> can induce c <strong>Fos</strong> in the central medial nucleus of the thalamus (CM).
+FOS	drug	opioid	10415375	As compared to an acute dose of <b>morphine</b> in a naive animal, the induction of c <strong>Fos</strong> was increased in the dorsolateral CPu following challenge injection at 7 days, but not at 14 days.
+FOS	addiction	withdrawal	10415375	Induction of c <strong>Fos</strong> in the CM following the challenge injection was blunted following 7 day, but not at 14 days, of <b>withdrawal</b>.
+FOS	drug	nicotine	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during <b>nicotine</b> dependence.
+FOS	addiction	dependence	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during nicotine <b>dependence</b>.
+FOS	drug	nicotine	10320004	The effects of acute and chronic <b>nicotine</b> treatment on activator protein 1 (<strong>AP 1</strong>) gene transcription factor binding activity in the rat cortex were investigated.
+FOS	drug	nicotine	10320004	It was observed that 1 h after acute <b>nicotine</b> treatment (single injection) <strong>AP 1</strong> DNA binding activity was significantly increased in the rat cortex.
+FOS	drug	nicotine	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of <b>nicotine</b> withdrawal after repeated <b>nicotine</b> treatment (10 days).
+FOS	addiction	withdrawal	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of nicotine <b>withdrawal</b> after repeated nicotine treatment (10 days).
+FOS	drug	nicotine	10320004	However, at 18 and 24 h of <b>nicotine</b> withdrawal after 10 days of <b>nicotine</b> treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+FOS	addiction	withdrawal	10320004	However, at 18 and 24 h of nicotine <b>withdrawal</b> after 10 days of nicotine treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+FOS	drug	nicotine	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to <b>nicotine</b> dependence.
+FOS	addiction	dependence	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to nicotine <b>dependence</b>.
+FOS	drug	amphetamine	10234448	Quantitative analysis of the effects of lithium on the reverse tolerance and the c <strong>Fos</strong> expression induced by <b>methamphetamine</b> in mice.
+FOS	drug	amphetamine	10234448	Nestler, Induction of a long lasting AP 1 complex composed of altered <strong>Fos</strong> like proteins in brain by chronic cocaine and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on <b>methamphetamine</b> induced stereotypy in mice, Jpn.
+FOS	drug	cocaine	10234448	Nestler, Induction of a long lasting AP 1 complex composed of altered <strong>Fos</strong> like proteins in brain by chronic <b>cocaine</b> and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on methamphetamine induced stereotypy in mice, Jpn.
+FOS	drug	amphetamine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered <strong>Fos</strong> like proteins in brain by chronic cocaine and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on <b>methamphetamine</b> induced stereotypy in mice, Jpn.
+FOS	drug	cocaine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered <strong>Fos</strong> like proteins in brain by chronic <b>cocaine</b> and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on methamphetamine induced stereotypy in mice, Jpn.
+FOS	drug	amphetamine	10234448	How the Li sensitive c <strong>Fos</strong> expression in the dorsolateral geniculate nucleus and striatum is related to <b>methamphetamine</b> induced behavioral excitation is unclear.
+FOS	addiction	withdrawal	10188944	Noxious mechanical and chemical stimuli were applied to the toes of the left hind limb of decerebrated, spinalized rabbits and their effects on a hind limb spinal <b>withdrawal</b> reflex and expression of <strong>Fos</strong> like immunoreactivity in the spinal cord were measured.
+FOS	drug	opioid	10103112	(ii) After challenges that increase DA by depolarizing DAergic neurons (injection stress or 2 mg/kg <b>morphine</b>), the shell presented the largest increase in DA levels and <strong>Fos</strong> LI.
+FOS	drug	cocaine	10103106	Repeated <b>cocaine</b> administration increased levels of DeltaFosB, a <strong>Fos</strong> family transcription factor, in the striatum of wild type mice, and this increase was abolished in DARPP 32 mutant mice.
+FOS	drug	opioid	10082881	Differential effects of mu and kappa <b>opioid</b> antagonists on <strong>Fos</strong> like immunoreactivity in extended amygdala.
+FOS	drug	alcohol	10082881	It was previously reported that systemic administration of the nonselective opioid antagonist, <b>naltrexone</b>, induces <strong>Fos</strong> like immunoreactivity (FLI) within the central nucleus of the amygdala (CeA), bed nucleus of the stria terminalis (lateral dorsal division; BSTLD), nucleus accumbens shell (NACshell) and ventral tegmental area (VTA) of free feeding rats.
+FOS	drug	opioid	10082881	It was previously reported that systemic administration of the nonselective <b>opioid</b> antagonist, naltrexone, induces <strong>Fos</strong> like immunoreactivity (FLI) within the central nucleus of the amygdala (CeA), bed nucleus of the stria terminalis (lateral dorsal division; BSTLD), nucleus accumbens shell (NACshell) and ventral tegmental area (VTA) of free feeding rats.
+FOS	drug	alcohol	10082881	Considering the involvement of mesoaccumbens dopamine neurons and components of the 'extended amygdala' in motivated behavior and reward, it was hypothesized that the induction of c <strong>Fos</strong> by <b>naltrexone</b> accounts for the motivational affective consequences of opioid antagonism.
+FOS	drug	opioid	10082881	Considering the involvement of mesoaccumbens dopamine neurons and components of the 'extended amygdala' in motivated behavior and reward, it was hypothesized that the induction of c <strong>Fos</strong> by naltrexone accounts for the motivational affective consequences of <b>opioid</b> antagonism.
+FOS	addiction	reward	10082881	Considering the involvement of mesoaccumbens dopamine neurons and components of the 'extended amygdala' in motivated behavior and <b>reward</b>, it was hypothesized that the induction of c <strong>Fos</strong> by naltrexone accounts for the motivational affective consequences of opioid antagonism.
+FOS	drug	alcohol	10082881	reproduced the effect of <b>naltrexone</b> in BSTLD and CeA, suggesting that the induction of c <strong>Fos</strong> in these two structures is a consequence of kappa receptor blockade.
+FOS	drug	alcohol	10082881	), reproduced the effect of <b>naltrexone</b> in NACshell, suggesting that the induction of c <strong>Fos</strong> in this structure is a consequence of mu receptor blockade.
+FOS	drug	psychedelics	10082844	Pretreatment with the NMDA antagonists (+)MK 801 or CPP attenuated reserpine mediated striatal <strong>Fos</strong> induction whereas pretreatment with <b>ketamine</b> or the inactive isomer ( )MK 801 did not.
+FOS	addiction	reward	10082844	Pretreatment with the NMDA antagonists (+)MK 801 or <b>CPP</b> attenuated reserpine mediated striatal <strong>Fos</strong> induction whereas pretreatment with ketamine or the inactive isomer ( )MK 801 did not.
+FOS	drug	cocaine	10027503	Behavioral sensitization to <b>cocaine</b> after a brief social defeat stress: c <strong>fos</strong> expression in the PAG.
+FOS	addiction	sensitization	10027503	Behavioral <b>sensitization</b> to cocaine after a brief social defeat stress: c <strong>fos</strong> expression in the PAG.
+FOS	drug	cocaine	10027503	The experiments explored the nature and time course of changes in behavior and <strong>Fos</strong> expression in the periaqueductal grey area (PAG) in response to an injection of <b>cocaine</b> that was given following a single episode of social defeat stress.
+FOS	drug	cocaine	10027503	Further experiments used immunohistochemical assays of sections through the caudal ventrolateral PAG and showed a significant increase in <strong>Fos</strong> like immunoreactivity (<strong>Fos</strong> LI) 1 h after the social stress experience or after <b>cocaine</b>.
+FOS	drug	cocaine	10027503	Importantly, concurrent administration of <b>cocaine</b> with social defeat stress produced inhibition of <strong>Fos</strong> expression throughout the PAG.
+FOS	drug	cocaine	10027503	A partial to complete recovery of <b>cocaine</b> induced <strong>Fos</strong> expression was observed 5 7 days after social defeat stress.
+FOS	drug	cocaine	10027503	The initial inhibition of <strong>Fos</strong> expression by concurrent social stress and <b>cocaine</b> may point to a relevant initiating event in the process of sensitization to stimulants.
+FOS	addiction	sensitization	10027503	The initial inhibition of <strong>Fos</strong> expression by concurrent social stress and cocaine may point to a relevant initiating event in the process of <b>sensitization</b> to stimulants.
+FOS	drug	alcohol	9918601	This investigation examined the effects of acute and chronic <b>ethanol</b> exposure and its withdrawal on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+FOS	addiction	withdrawal	9918601	This investigation examined the effects of acute and chronic ethanol exposure and its <b>withdrawal</b> on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+FOS	drug	alcohol	9918601	It was observed that acute <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+FOS	addiction	withdrawal	9918601	It was observed that acute ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+FOS	drug	alcohol	9918601	It was also found that chronic <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+FOS	addiction	withdrawal	9918601	It was also found that chronic ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+FOS	drug	amphetamine	9889345	Differential decreases in c <strong>fos</strong> and aldolase C mRNA expression in the rat cerebellum after repeated administration of <b>methamphetamine</b>.
+FOS	drug	amphetamine	9889345	The effects of repeated <b>methamphetamine</b> administration on c <strong>fos</strong> mRNA and aldolase C (Zebrin) mRNA expression in the rat cerebellum were investigated.
+FOS	drug	amphetamine	9889345	A single dose of <b>methamphetamine</b> induced c <strong>fos</strong> mRNA expression in granule and Purkinje cells of both anterior and posterior lobes.
+FOS	drug	amphetamine	9889345	Repeated <b>methamphetamine</b> injections reduced <b>methamphetamine</b> induced c <strong>fos</strong> mRNA signals in the anterior hemisphere and in part of the posterior vermis (lobule VII) and posterior hemisphere.
+FOS	drug	amphetamine	9889345	Aldolase C mRNA signals in Purkinje cells decreased only in lobules where <b>methamphetamine</b> induced c <strong>fos</strong> signals were not reduced (lobules VI and IX).
+FOS	drug	amphetamine	9889345	Therefore, differential decreases in c <strong>fos</strong> mRNA and aldolase C mRNA expression after repeated <b>methamphetamine</b> administration depend upon the localization of Purkinje cells in the cerebellum.
+FOS	drug	amphetamine	9889345	Since c <strong>fos</strong> mRNA and aldolase C mRNA expressions are markers of excitability and the metabolic state of Purkinje cells, respectively, hypofunction of inhibitory Purkinje cells could be induced if <b>methamphetamine</b> is repeatedly injected.
+FOS	drug	amphetamine	9852603	We examined the effects of acute <b>amphetamine</b> and cocaine administration on expression of <strong>Fos</strong> protein in the thalamic paraventricular nucleus (PVT), which provides glutamatergic inputs to the nucleus accumbens and also receives dopaminergic afferents.
+FOS	drug	cocaine	9852603	We examined the effects of acute amphetamine and <b>cocaine</b> administration on expression of <strong>Fos</strong> protein in the thalamic paraventricular nucleus (PVT), which provides glutamatergic inputs to the nucleus accumbens and also receives dopaminergic afferents.
+FOS	drug	amphetamine	9852603	PVT neurons retrogradely labeled from the nucleus accumbens were among the PVT cells that showed a <strong>Fos</strong> response to <b>amphetamine</b>.
+FOS	drug	amphetamine	9852603	Conversely, the effects of cocaine and <b>amphetamine</b> on PVT <strong>Fos</strong> expression were blocked by pretreatment with the dopamine D2/3 antagonist raclopride.
+FOS	drug	cocaine	9852603	Conversely, the effects of <b>cocaine</b> and amphetamine on PVT <strong>Fos</strong> expression were blocked by pretreatment with the dopamine D2/3 antagonist raclopride.
+FOS	addiction	withdrawal	9845244	However, following opiate <b>withdrawal</b>, virtually no <strong>Fos</strong> expression was observed in NPFF neurons.
+FOS	drug	alcohol	9835277	Repeated <b>alcohol</b> administration differentially affects c <strong>Fos</strong> and FosB protein immunoreactivity in DBA/2J mice.
+FOS	drug	alcohol	9835277	To identify <b>alcohol</b> responsive brain areas, we have immunohistochemically analyzed expression of c <strong>Fos</strong>, FosB, and other <strong>Fos</strong> related antigens in the brain of inbred DBA/2J mice after a single or repeated injection of <b>alcohol</b> (4 g/kg).
+FOS	drug	alcohol	9835277	We observed increased expression of c <strong>Fos</strong> after <b>alcohol</b> administration in the central nucleus of amygdala, paraventricular nuclei of hypothalamus and thalamus, and several other brain areas.
+FOS	drug	alcohol	9835277	Repeated administration of <b>alcohol</b> had the tendency to reduce <b>alcohol</b> induced c <strong>Fos</strong> expression in these areas.
+FOS	drug	alcohol	9835277	In contrast to c <strong>Fos</strong>, FosB expression was found to be elevated significantly higher after repeated than after acute treatment with <b>alcohol</b> in several brain areas, including the shell of nucleus accumbens.
+FOS	drug	alcohol	9835277	In contrast to previous c <strong>Fos</strong> studies, our studies confirm that <b>alcohol</b> administration indeed activates the reward circuits, including the basal ganglia, and suggest that FosB could serve as a more sensitive marker for this activation.
+FOS	addiction	reward	9835277	In contrast to previous c <strong>Fos</strong> studies, our studies confirm that alcohol administration indeed activates the <b>reward</b> circuits, including the basal ganglia, and suggest that FosB could serve as a more sensitive marker for this activation.
+FOS	drug	cocaine	9813326	Behavioral sensitization to <b>cocaine</b> after a brief social stress is accompanied by changes in <strong>fos</strong> expression in the murine brainstem.
+FOS	addiction	sensitization	9813326	Behavioral <b>sensitization</b> to cocaine after a brief social stress is accompanied by changes in <strong>fos</strong> expression in the murine brainstem.
+FOS	drug	cocaine	9813326	The objective of the present study was to determine how c <strong>fos</strong> gene expression in brainstem structures after a brief episode of social defeat stress is related to behavioral sensitization to <b>cocaine</b> challenge.
+FOS	addiction	sensitization	9813326	The objective of the present study was to determine how c <strong>fos</strong> gene expression in brainstem structures after a brief episode of social defeat stress is related to behavioral <b>sensitization</b> to cocaine challenge.
+FOS	drug	cocaine	9813326	Similarly, <b>cocaine</b> administration resulted in a significantly increased number of <strong>Fos</strong> LI nuclei in the same areas.
+FOS	drug	cocaine	9813326	Administration of <b>cocaine</b> immediately following social defeat significantly reduced the number of <strong>Fos</strong> LI nuclei in the DR, PAG and LC.
+FOS	drug	cocaine	9813326	<b>Cocaine</b> induced <strong>Fos</strong> expression returned in the PAG and DR, but not in the LC, 1 week after social stress.
+FOS	drug	cocaine	9813326	In conclusion, the present results suggest that the presence of brainstem <strong>Fos</strong> be related to the ability to express stress induced behavioral sensitization to <b>cocaine</b>.
+FOS	addiction	sensitization	9813326	In conclusion, the present results suggest that the presence of brainstem <strong>Fos</strong> be related to the ability to express stress induced behavioral <b>sensitization</b> to cocaine.
+FOS	drug	cocaine	9813294	In contrast to what has been described for c <strong>fos</strong> and egr 1 immediate early genes, we found that hVH 5 mRNA expression in the NAc and hippocampus was as significant after repeated <b>cocaine</b> injections for 10 days as after a single injection.
+FOS	drug	opioid	9795131	The induction of c <strong>fos</strong> mRNA in rat brain due to <b>morphine</b> treatment was analyzed by in situ hybridization.
+FOS	drug	opioid	9795131	However, rats that were repeatedly pretreated with <b>morphine</b> displayed a marked c <strong>fos</strong> induction in a few brain areas in response to <b>morphine</b> application.
+FOS	addiction	withdrawal	9795131	The c <strong>fos</strong> signal was transient and not due to a residual <b>withdrawal</b>.
+FOS	drug	opioid	9795131	<b>Naloxone</b> precipitated withdrawal led to a more intense c <strong>fos</strong> expression which also encompassed a greater range of brain areas.
+FOS	addiction	withdrawal	9795131	Naloxone precipitated <b>withdrawal</b> led to a more intense c <strong>fos</strong> expression which also encompassed a greater range of brain areas.
+FOS	drug	opioid	9795131	A low <b>morphine</b> dose suppressed the c <strong>fos</strong> expression nearly completely and was not sufficient to elicit the <b>morphine</b> like expression pattern of c <strong>fos</strong>.
+FOS	drug	opioid	9795131	These areas responded to <b>morphine</b> with an elevated c <strong>fos</strong> expression only when <b>morphine</b> was repeatedly given previously.
+FOS	addiction	sensitization	9795122	In addition to the behavioral <b>sensitization</b>, Amp pretreated rats showed a reduction in the ability of the acute Amp challenge to induce c <strong>fos</strong> mRNA in the medial prefrontal cortex and neurotensin/neuromedin N (NT/N) mRNA in the nucleus accumbens shell.
+FOS	addiction	sensitization	9795122	At doses that blocked the initiation of behavioral <b>sensitization</b> to Amp, clozapine fully and haloperidol partially restored the capacity of acute Amp to induce c <strong>fos</strong> and NT/N gene expression.
+FOS	addiction	relapse	9789813	Post mortem brain maps of c <strong>fos</strong> related antigens expression showed specific activation in prefrontal cortex, anterior cingulate and nucleus accumbens for both drugs, but of the anterior cingulate cortex only during <b>relapse</b>, suggesting that a subset of the neural network involved in drug self administration is activated during <b>relapse</b>.
+FOS	drug	alcohol	9768540	In contrast, studies on <b>alcohol</b> mediated changes in expression of this gene confirm selective hippocampal suppression of basal and experience induced expression of c <strong>fos</strong> after acute and repeated administration of <b>alcohol</b>.
+FOS	drug	alcohol	9768540	This hippocampal suppression is in marked contrast with <b>alcohol</b> mediated induction of c <strong>fos</strong> expression in other brain areas.
+FOS	addiction	relapse	9756331	The expression of c <strong>fos</strong> in the brain of '<b>craving</b>' rats was compared with that in rats given free access on the test day ('beer' condition), and to rats which had been repeatedly placed in the drinking environment without ever having access to beer ('control' condition).
+FOS	drug	alcohol	9756331	Rats in the 'craving' condition showed significantly higher c <strong>fos</strong> counts than either the 'beer' or 'control' rats in a variety of corticolimbic and brainstem structures, indicating that activation of these regions occurs when a desirable <b>alcoholic</b> beverage is expected but not received.
+FOS	addiction	relapse	9756331	Rats in the '<b>craving</b>' condition showed significantly higher c <strong>fos</strong> counts than either the 'beer' or 'control' rats in a variety of corticolimbic and brainstem structures, indicating that activation of these regions occurs when a desirable alcoholic beverage is expected but not received.
+FOS	drug	opioid	26735118	<strong>Fos</strong> like immunoreactivity in tyrosine hydroxylase and substance P like immunoreactive neurones in guinea pig brain following intracerebroventricular injection of <b>morphine</b> and U50,488H.
+FOS	drug	opioid	26735118	In the present study twocolour immunohistochemistry was used to investigate whether <strong>Fos</strong> protein was induced in dopaminergic (tyrosine hydroxylase) and substance P containing neurones of guinea pig brain following intracerebroventricular administration of the predominantly mu receptor agonist, <b>morphine</b>, and the kappa receptor agonist, U50,488H, which have been reported to produce rewarding and aversive effects, respectively.
+FOS	addiction	aversion	26735118	In the present study twocolour immunohistochemistry was used to investigate whether <strong>Fos</strong> protein was induced in dopaminergic (tyrosine hydroxylase) and substance P containing neurones of guinea pig brain following intracerebroventricular administration of the predominantly mu receptor agonist, morphine, and the kappa receptor agonist, U50,488H, which have been reported to produce rewarding and <b>aversive</b> effects, respectively.
+FOS	drug	opioid	26735118	The present study has shown that of the large number of neurones showing <strong>Fos</strong> like immunoreactivity following a single injection of <b>morphine</b> or U50,488H, few were tyrosine hydroxylase positive (dopaminergic) but a larger number were substance Plike immunoreactive.
+FOS	drug	cannabinoid	9748483	A comparison of delta 9 <b>THC</b> and anandamide induced c <strong>fos</strong> expression in the rat forebrain.
+FOS	drug	cannabinoid	9748483	delta 9 <b>THC</b> and anandamide caused equally high levels of c <strong>fos</strong> expression in the paraventricular nucleus of the hypothalamus and the lateral septum.
+FOS	drug	cannabinoid	9748483	Both drugs also increased c <strong>fos</strong> expression in the central nucleus of the amygdala although the effect was greater with delta 9 <b>THC</b>.
+FOS	drug	cannabinoid	9748483	Only delta 9 <b>THC</b> caused significant increases in c <strong>fos</strong> expression in the nucleus accumbens and caudate putamen.
+FOS	drug	alcohol	9733960	Neuroanatomical patterns of <strong>fos</strong> like immunoreactivity induced by a palatable meal and meal paired environment in saline  and <b>naltrexone</b> treated rats.
+FOS	drug	opioid	9683006	Kappa <b>opioid</b> mediated behavioral sensitization in the preweanling rat: relationship to <strong>Fos</strong> immunoreactivity.
+FOS	addiction	sensitization	9683006	Kappa opioid mediated behavioral <b>sensitization</b> in the preweanling rat: relationship to <strong>Fos</strong> immunoreactivity.
+FOS	drug	opioid	9683006	When given acutely, drugs that stimulate kappa <b>opioid</b> receptors (e.g., U 50,488) enhance the locomotor activity of preweanling rats and induce regional increases in <strong>Fos</strong> immunoreactivity (IR).
+FOS	drug	opioid	9683006	The purpose of the present study was two fold: first, to determine whether repeated treatment with a kappa <b>opioid</b> agonist would sensitize the locomotor activity of preweanling rats and, second, to determine whether changes in <strong>Fos</strong> IR correspond with the occurrence of locomotor sensitization.
+FOS	addiction	sensitization	9683006	The purpose of the present study was two fold: first, to determine whether repeated treatment with a kappa opioid agonist would sensitize the locomotor activity of preweanling rats and, second, to determine whether changes in <strong>Fos</strong> IR correspond with the occurrence of locomotor <b>sensitization</b>.
+FOS	addiction	sensitization	9683006	Chronic treatment with U 50,488 depressed <strong>Fos</strong> expression in a number of brain regions (relative to acutely treated rats); however, these changes in <strong>Fos</strong> IR did not necessarily coincide with the occurrence of behavioral <b>sensitization</b>.
+FOS	addiction	sensitization	9683006	Repeated treatment with U 50,488 did not produce locomotor <b>sensitization</b> in adult rats, so <strong>Fos</strong> IR was not assessed in this age group.
+FOS	drug	cocaine	9668659	<b>Cocaine</b> and the <strong>AP 1</strong> transcription factor complex.
+FOS	drug	cocaine	9668659	Interestingly, repeated <b>cocaine</b> administration induces novel delta FosB related proteins (called chronic <strong>Fos</strong> related antigens (Fras)) in the NAc and Str that replace the downregulated isoforms of <strong>Fos</strong>.
+FOS	drug	cocaine	9668659	Unlike the acutely induced, short lasting isoforms of <strong>Fos</strong> and FosB, the chronic Fras persist long after the last <b>cocaine</b> administration.
+FOS	drug	cocaine	9668659	We presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain
+FOS	drug	alcohol	9666163	Acute <b>ethanol</b> induces c <strong>fos</strong> immunoreactivity in GABAergic neurons of the central nucleus of the amygdala.
+FOS	drug	alcohol	9666163	Previous studies have shown that acute <b>ethanol</b> administration induces the expression of c <strong>fos</strong> in the CNA of rat brains.
+FOS	drug	nicotine	9661252	Inducibility of c <strong>Fos</strong> protein in visuo motor system and limbic structures after acute and repeated administration of <b>nicotine</b> in the rat.
+FOS	drug	nicotine	9661252	To identify neuroanatomical substrates affected by <b>nicotine</b>, we have studied its effects after acute and repeated administration through the c <strong>Fos</strong> protein inducibility in various brain structures.
+FOS	drug	nicotine	9661252	Ninety minutes after acute <b>nicotine</b> (0.35 mg/kg, s.c.) the number of c <strong>Fos</strong> like immunoreactive nuclei was consistently increased in visuo motor structures such as the superior colliculus, the medial terminal nucleus of accessory optic tract, and the nucleus of the optic tract.
+FOS	drug	nicotine	9661252	In chronically treated rats (0.35 mg/kg s.c., 3 x day for 14 days), the last <b>nicotine</b> injection given on the 15th day was still able to induce 90 minutes later c <strong>Fos</strong> protein in visuo motor, retino limbic, subcortical, and cortical limbic structures.
+FOS	drug	nicotine	9661252	c <strong>Fos</strong> induction after <b>nicotine</b> differs from that reported after other addictive drugs in terms of pattern and chronic inducibility, indicating that different mechanisms are involved for maintaining this transcription factor.
+FOS	addiction	addiction	9661252	c <strong>Fos</strong> induction after nicotine differs from that reported after other <b>addictive</b> drugs in terms of pattern and chronic inducibility, indicating that different mechanisms are involved for maintaining this transcription factor.
+FOS	addiction	sensitization	9655895	Accompanying behavioral <b>sensitization</b> were two postsynaptic neuroadaptive responses: reduction in the ability of Amp to induce c <strong>fos</strong> gene expression in the infralimbic/ventral prelimbic cortex and NT/N mRNA in the accumbal shell.
+FOS	drug	opioid	9592116	We previously reported that withdrawal from <b>morphine</b> induces the expression of <strong>Fos</strong>, a marker of neuronal activity, in spinal cord neurons, particularly in laminae I and II of the superficial dorsal horn, and that the magnitude of <strong>Fos</strong> expression is increased in rats with a midthoracic spinal transection.
+FOS	addiction	withdrawal	9592116	We previously reported that <b>withdrawal</b> from morphine induces the expression of <strong>Fos</strong>, a marker of neuronal activity, in spinal cord neurons, particularly in laminae I and II of the superficial dorsal horn, and that the magnitude of <strong>Fos</strong> expression is increased in rats with a midthoracic spinal transection.
+FOS	addiction	withdrawal	9592116	We suggested that loss of <b>withdrawal</b> associated increases in descending inhibitory controls that arise in the brainstem underlie the increased <strong>Fos</strong> expression after spinal transection.
+FOS	drug	amphetamine	9570795	In addition, <b>amphetamine</b> induction of <strong>fos</strong> is absent, and the basal expression of dynorphin mRNA is reduced in the striatum.
+FOS	drug	alcohol	9581657	Induction of <strong>Fos</strong> like proteins and ultrasonic vocalizations during <b>ethanol</b> withdrawal: further evidence for withdrawal induced anxiety.
+FOS	addiction	withdrawal	9581657	Induction of <strong>Fos</strong> like proteins and ultrasonic vocalizations during ethanol <b>withdrawal</b>: further evidence for <b>withdrawal</b> induced anxiety.
+FOS	drug	alcohol	9581657	Because the extent that specific regions of brain are critical to the generation of this emotional state is unknown, <strong>Fos</strong> like immunoreactivity (<strong>Fos</strong> LI) was used to associate specific regions of the rat brain with the anxiety component of the <b>ethanol</b> withdrawal syndrome exacerbated by an air puff challenge in rats.
+FOS	addiction	withdrawal	9581657	Because the extent that specific regions of brain are critical to the generation of this emotional state is unknown, <strong>Fos</strong> like immunoreactivity (<strong>Fos</strong> LI) was used to associate specific regions of the rat brain with the anxiety component of the ethanol <b>withdrawal</b> syndrome exacerbated by an air puff challenge in rats.
+FOS	addiction	withdrawal	9581657	During <b>withdrawal</b> from either treatment protocol, <strong>Fos</strong> LI was induced most prominently in forebrain areas, although the midbrain and hindbrain were also represented.
+FOS	addiction	withdrawal	9581657	<strong>Fos</strong> LI expression differed mostly in intensity between the two treatment and <b>withdrawal</b> protocols, with the gastric protocol producing the greatest <strong>Fos</strong> LI induction in most brain regions.
+FOS	addiction	withdrawal	9581657	Furthermore, a comparison of the effects of the air puff challenge versus <b>withdrawal</b> on <strong>Fos</strong> LI indicated that the behavioral state induced in these two situations share functional neuroanatomical features.
+FOS	addiction	withdrawal	9581657	Some regions  such as the accumbens core, medial septum, subregions of the amygdala, hippocampus, substantia nigra, and cerebellum  exhibited little <strong>Fos</strong> LI during <b>withdrawal</b> and also did not exhibit strong increases after the addition of the air puff challenge.
+FOS	drug	alcohol	9581657	However, other regions such as the cerebral cortex (medial prefrontal, frontal, cingulate and ventrolateral orbital, claustrum, and tenia tecta), hypothalamus, and locus ceoruleus  exhibited <strong>Fos</strong> LI at levels higher than that seen after either the <b>ethanol</b> withdrawal or puff challenge alone.
+FOS	addiction	withdrawal	9581657	However, other regions such as the cerebral cortex (medial prefrontal, frontal, cingulate and ventrolateral orbital, claustrum, and tenia tecta), hypothalamus, and locus ceoruleus  exhibited <strong>Fos</strong> LI at levels higher than that seen after either the ethanol <b>withdrawal</b> or puff challenge alone.
+FOS	drug	alcohol	9581657	These overlapping patterns of <strong>Fos</strong> LI in specific regions of the brain, activated by both <b>ethanol</b> withdrawal and an anxiety provoking behavioral challenge, suggest that specific neuroanatomical sites in brain are associated with the symptom of anxiety observed during the "<b>ethanol</b> withdrawal syndrome."
+FOS	addiction	withdrawal	9581657	These overlapping patterns of <strong>Fos</strong> LI in specific regions of the brain, activated by both ethanol <b>withdrawal</b> and an anxiety provoking behavioral challenge, suggest that specific neuroanatomical sites in brain are associated with the symptom of anxiety observed during the "ethanol <b>withdrawal</b> syndrome."
+FOS	drug	cocaine	29090793	<b>Cocaine</b> and the <strong>AP 1</strong> Transcription Factor Complex.
+FOS	drug	cocaine	29090793	Interestingly, repeated <b>cocaine</b> administration induces novel delta FosB related proteins (called chronic <strong>Fos</strong> related antigens (Fras)) in the NAc and Str that replace the downregulated isoforms of <strong>Fos</strong>.
+FOS	drug	cocaine	29090793	Unlike the acutely induced, short lasting isoforms of <strong>Fos</strong> and FosB, the chronic Fras persist long after the last <b>cocaine</b> administration.
+FOS	drug	cocaine	29090793	We are presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain.
+FOS	drug	amphetamine	9519282	Behavioral sensitization to <b>amphetamine</b> is not accompanied by a decrease in the number of c <strong>Fos</strong> containing cells in the striatum.
+FOS	addiction	sensitization	9519282	Behavioral <b>sensitization</b> to amphetamine is not accompanied by a decrease in the number of c <strong>Fos</strong> containing cells in the striatum.
+FOS	drug	amphetamine	9519282	The expression of c <strong>Fos</strong> like immunoreactivity (FLI) and chronic <strong>Fos</strong> related antigen like immunoreactivity (FRALI) accompanying behavioral sensitization to <b>amphetamine</b> was assessed in male rat striatum.
+FOS	addiction	sensitization	9519282	The expression of c <strong>Fos</strong> like immunoreactivity (FLI) and chronic <strong>Fos</strong> related antigen like immunoreactivity (FRALI) accompanying behavioral <b>sensitization</b> to amphetamine was assessed in male rat striatum.
+FOS	drug	amphetamine	9519282	These results suggest that the absence of a decrease in the number of striatal FLI positive cells accompanying chronic <b>amphetamine</b> treatment is not due to antibody cross reactivity with chronic FRAs, and that behavioral sensitization to <b>amphetamine</b> is not accompanied by a change in the number of striatal cells expressing c <strong>Fos</strong>.
+FOS	addiction	sensitization	9519282	These results suggest that the absence of a decrease in the number of striatal FLI positive cells accompanying chronic amphetamine treatment is not due to antibody cross reactivity with chronic FRAs, and that behavioral <b>sensitization</b> to amphetamine is not accompanied by a change in the number of striatal cells expressing c <strong>Fos</strong>.
+FOS	drug	amphetamine	9466435	Medial prefrontal cortical injections of c <strong>fos</strong> antisense oligonucleotides transiently lower c <strong>Fos</strong> protein and mimic <b>amphetamine</b> withdrawal behaviours.
+FOS	addiction	withdrawal	9466435	Medial prefrontal cortical injections of c <strong>fos</strong> antisense oligonucleotides transiently lower c <strong>Fos</strong> protein and mimic amphetamine <b>withdrawal</b> behaviours.
+FOS	drug	amphetamine	9466435	Prefrontal cerebral cortical areas display decreased expression of several transcription factor/immediate early genes, including c <strong>fos</strong>, during <b>amphetamine</b> withdrawal.
+FOS	addiction	withdrawal	9466435	Prefrontal cerebral cortical areas display decreased expression of several transcription factor/immediate early genes, including c <strong>fos</strong>, during amphetamine <b>withdrawal</b>.
+FOS	drug	amphetamine	9466435	Antisense strategies can help to test possible roles for this prefrontal c <strong>fos</strong> down regulation in the behavioural correlates of <b>amphetamine</b> withdrawal.
+FOS	addiction	withdrawal	9466435	Antisense strategies can help to test possible roles for this prefrontal c <strong>fos</strong> down regulation in the behavioural correlates of amphetamine <b>withdrawal</b>.
+FOS	drug	amphetamine	9466435	Behavioural changes produced by prefrontal cortical injections of c <strong>fos</strong> antisense oligonucleotides closely mimic alterations recorded during <b>amphetamine</b> withdrawal.
+FOS	addiction	withdrawal	9466435	Behavioural changes produced by prefrontal cortical injections of c <strong>fos</strong> antisense oligonucleotides closely mimic alterations recorded during amphetamine <b>withdrawal</b>.
+FOS	addiction	withdrawal	9466435	Prefrontal c <strong>fos</strong> could thus conceivably play roles in the neurobiological underpinnings of psychostimulant <b>withdrawal</b> and of responses to stressors such as exposure to novel environments.
+FOS	drug	opioid	9460759	Swim stress but not <b>opioid</b> withdrawal increases expression of c <strong>fos</strong> immunoreactivity in rat periaqueductal gray neurons which project to the rostral ventromedial medulla.
+FOS	addiction	withdrawal	9460759	Swim stress but not opioid <b>withdrawal</b> increases expression of c <strong>fos</strong> immunoreactivity in rat periaqueductal gray neurons which project to the rostral ventromedial medulla.
+FOS	drug	opioid	9460759	Expression of c <strong>fos</strong> like immunoreactivity has been used as a marker for neuronal activation and is elevated in the periaqueductal gray following stressful and noxious stimuli, and <b>opioid</b> withdrawal.
+FOS	addiction	withdrawal	9460759	Expression of c <strong>fos</strong> like immunoreactivity has been used as a marker for neuronal activation and is elevated in the periaqueductal gray following stressful and noxious stimuli, and opioid <b>withdrawal</b>.
+FOS	drug	opioid	9460759	The present study examined the staining of c <strong>fos</strong> like immunoreactivity following opiate withdrawal or swim stress (2.5 3 min at 21 degrees C) in periaqueductal gray neurons of the rat which had projections to and through the rostral ventromedial medulla identified by microinjection of the retrograde tracer, Fast Blue, into the nucleus raphe magnus prior to development of <b>morphine</b> dependence.
+FOS	addiction	dependence	9460759	The present study examined the staining of c <strong>fos</strong> like immunoreactivity following opiate withdrawal or swim stress (2.5 3 min at 21 degrees C) in periaqueductal gray neurons of the rat which had projections to and through the rostral ventromedial medulla identified by microinjection of the retrograde tracer, Fast Blue, into the nucleus raphe magnus prior to development of morphine <b>dependence</b>.
+FOS	addiction	withdrawal	9460759	The present study examined the staining of c <strong>fos</strong> like immunoreactivity following opiate <b>withdrawal</b> or swim stress (2.5 3 min at 21 degrees C) in periaqueductal gray neurons of the rat which had projections to and through the rostral ventromedial medulla identified by microinjection of the retrograde tracer, Fast Blue, into the nucleus raphe magnus prior to development of morphine dependence.
+FOS	drug	opioid	9460759	Both <b>naloxone</b> precipitated withdrawal and swim stress increased numbers of neurons expressing c <strong>fos</strong> like immunoreactivity in periaqueductal gray.
+FOS	addiction	withdrawal	9460759	Both naloxone precipitated <b>withdrawal</b> and swim stress increased numbers of neurons expressing c <strong>fos</strong> like immunoreactivity in periaqueductal gray.
+FOS	drug	alcohol	9426840	Expression of c <strong>Fos</strong> protein immunoreactivity in rat brain during <b>ethanol</b> withdrawal is prevented by nifedipine.
+FOS	addiction	withdrawal	9426840	Expression of c <strong>Fos</strong> protein immunoreactivity in rat brain during ethanol <b>withdrawal</b> is prevented by nifedipine.
+FOS	drug	alcohol	9426840	Male rats were made physically dependent on <b>ethanol</b> by inhalation of the vapour for 10 days, and c <strong>Fos</strong> protein like immunoreactivity was visualised in the brain of these animals after various periods of <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	9426840	Male rats were made physically dependent on ethanol by inhalation of the vapour for 10 days, and c <strong>Fos</strong> protein like immunoreactivity was visualised in the brain of these animals after various periods of ethanol <b>withdrawal</b>.
+FOS	drug	alcohol	9426840	Immunostaining for c <strong>Fos</strong> appeared 2 h after <b>ethanol</b> withdrawal, the number of cells increased significantly at 8 h, but c <strong>Fos</strong> had returned to basal level after 24 h. Immunoreactive cells were distributed throughout the brain but were concentrated in cerebral cortex, striatum, and hippocampus.
+FOS	addiction	withdrawal	9426840	Immunostaining for c <strong>Fos</strong> appeared 2 h after ethanol <b>withdrawal</b>, the number of cells increased significantly at 8 h, but c <strong>Fos</strong> had returned to basal level after 24 h. Immunoreactive cells were distributed throughout the brain but were concentrated in cerebral cortex, striatum, and hippocampus.
+FOS	drug	alcohol	9426840	Intraperitoneal injection of the calcium channel antagonist nifedipine (3 x 100 mg/kg) prior to, and during <b>ethanol</b> withdrawal totally prevented c <strong>Fos</strong> protein like expression.
+FOS	addiction	withdrawal	9426840	Intraperitoneal injection of the calcium channel antagonist nifedipine (3 x 100 mg/kg) prior to, and during ethanol <b>withdrawal</b> totally prevented c <strong>Fos</strong> protein like expression.
+FOS	drug	alcohol	9426840	These results suggest that the superinduction of c <strong>Fos</strong> protein in the brain of rats undergoing <b>ethanol</b> withdrawal is induced by calcium influx into neuronal cells, and may be related to previously reported increases in L type voltage operated calcium channels in the brain associated with <b>ethanol</b> dependence.
+FOS	addiction	dependence	9426840	These results suggest that the superinduction of c <strong>Fos</strong> protein in the brain of rats undergoing ethanol withdrawal is induced by calcium influx into neuronal cells, and may be related to previously reported increases in L type voltage operated calcium channels in the brain associated with ethanol <b>dependence</b>.
+FOS	addiction	withdrawal	9426840	These results suggest that the superinduction of c <strong>Fos</strong> protein in the brain of rats undergoing ethanol <b>withdrawal</b> is induced by calcium influx into neuronal cells, and may be related to previously reported increases in L type voltage operated calcium channels in the brain associated with ethanol dependence.
+FOS	drug	cocaine	9387892	Direct comparison of the MDD amplification profiles of duplicate, total RNA samples from the caudate putamen (CPu) of either vehicle or <b>cocaine</b> treated Sprague Dawley rats indicated that the relative induction of a 240 bp (8G247) product, likely to represent c <strong>fos</strong> mRNA, closely paralleled changes in c <strong>fos</strong> mRNA as measured by Northern blot analysis.
+FOS	drug	opioid	9369365	The aim of the study was to measure the changes in cerebral energy metabolism and c <strong>fos</strong> mRNA expression following challenge with <b>heroin</b> in drug naive rats and in animals previously sensitized to the drug.
+FOS	drug	opioid	9334431	Systemic <b>morphine</b> induced <strong>Fos</strong> protein in the rat striatum and nucleus accumbens is regulated by mu <b>opioid</b> receptors in the substantia nigra and ventral tegmental area.
+FOS	drug	opioid	9334431	To characterize how systemic <b>morphine</b> induces <strong>Fos</strong> protein in dorsomedial striatum and nucleus accumbens (NAc), we examined the role of receptors in striatum, substantia nigra (SN), and ventral tegmental area (VTA).
+FOS	drug	opioid	9334431	<b>Morphine</b> injected into medial SN or into VTA of awake rats induced <strong>Fos</strong> in neurons in ipsilateral dorsomedial striatum and NAc.
+FOS	drug	opioid	9334431	<b>Morphine</b> injected into lateral SN induced <strong>Fos</strong> in dorsolateral striatum and globus pallidus.
+FOS	drug	opioid	9334431	Intranigral injections of [D Ala2, N Me Phe4, Gly ol5] enkephalin (DAMGO), a mu <b>opioid</b> receptor agonist, and of bicuculline, a GABAA receptor antagonist, induced <strong>Fos</strong> in ipsilateral striatum.
+FOS	drug	opioid	9334431	<strong>Fos</strong> induction in dorsomedial striatum produced by systemic administration of <b>morphine</b> was blocked by (1) SN and VTA injections of the mu1 <b>opioid</b> antagonist naloxonazine and (2) striatal injections of either MK 801, an NMDA glutamate receptor antagonist, or SCH 23390, a D1 dopamine receptor antagonist.
+FOS	drug	opioid	9334431	<strong>Fos</strong> induction in dorsomedial striatum and NAc after systemic administration of <b>morphine</b> seems to be mediated by dopamine neurons in medial SN and VTA that project to medial striatum and NAc, respectively.
+FOS	addiction	addiction	9334431	The modulation of target gene expression by <strong>Fos</strong> could influence <b>addictive</b> behavioral responses to opiates.
+FOS	drug	cocaine	9294222	FosB mutant mice: loss of chronic <b>cocaine</b> induction of <strong>Fos</strong> related proteins and heightened sensitivity to <b>cocaine</b>'s psychomotor and rewarding effects.
+FOS	drug	cocaine	9294222	We previously have shown that long lasting <strong>Fos</strong> related proteins of 35 37 kDa are induced in the striatum by chronic <b>cocaine</b> administration.
+FOS	drug	cocaine	9294222	The striatum of these mice completely lacked basal levels of the 35  to 37 kDa <strong>Fos</strong> related proteins as well as their induction by chronic <b>cocaine</b> administration.
+FOS	drug	cocaine	9294222	These results establish the long lasting <strong>Fos</strong> related proteins as products of the fosB gene (specifically DeltaFosB isoforms) and suggest that transcriptional regulation by fosB gene products plays a critical role in <b>cocaine</b> induced behavioral responses.
+FOS	drug	cocaine	9294222	This finding demonstrates that a <strong>Fos</strong> family member protein plays a functional role in behavioral responses to drugs of abuse and implicates fosB gene products as important determinants of <b>cocaine</b> abuse.
+FOS	drug	opioid	9284361	The contribution of supraspinal, peripheral and intrinsic spinal circuits to the pattern and magnitude of <strong>Fos</strong> like immunoreactivity in the lumbar spinal cord of the rat withdrawing from <b>morphine</b>.
+FOS	drug	opioid	9284361	Withdrawal from <b>morphine</b> evokes increases in <strong>Fos</strong> like immunoreactivity in the spinal cord, particularly in the superficial dorsal horn, laminae I/II.
+FOS	addiction	withdrawal	9284361	<b>Withdrawal</b> from morphine evokes increases in <strong>Fos</strong> like immunoreactivity in the spinal cord, particularly in the superficial dorsal horn, laminae I/II.
+FOS	drug	opioid	9284361	To determine the origin of the increased <strong>Fos</strong> like immunoreactivity, we selectively targeted central or peripheral <b>opioid</b> receptors with <b>naloxone</b> methiodide, an antagonist that does not cross the blood brain barrier, or induced withdrawal after eliminating possible sources of input to the superficial dorsal horn.
+FOS	addiction	withdrawal	9284361	To determine the origin of the increased <strong>Fos</strong> like immunoreactivity, we selectively targeted central or peripheral opioid receptors with naloxone methiodide, an antagonist that does not cross the blood brain barrier, or induced <b>withdrawal</b> after eliminating possible sources of input to the superficial dorsal horn.
+FOS	addiction	withdrawal	9284361	On day 4, <b>withdrawal</b> was precipitated and after 1 h, the rats were killed, their spinal cords removed and 50 microm transverse sections of the spinal cord immunoreacted with a rabbit polyclonal antiserum directed against the <strong>Fos</strong> protein.
+FOS	drug	opioid	9284361	spinal transection, unilateral dorsal rhizotomy (L4 S2), neonatal capsaicin treatment or direct intrathecal <b>opioid</b> antagonist injection, induced expression of the <strong>Fos</strong> protein.
+FOS	drug	opioid	9284361	Selective withdrawal of <b>morphine</b> from peripheral <b>opioid</b> receptors by <b>naloxone</b> methiodide did not induce <strong>Fos</strong> like immunoreactivity in the lumbar spinal cord greater than that recorded in nonwithdrawing rats.
+FOS	addiction	withdrawal	9284361	Selective <b>withdrawal</b> of morphine from peripheral opioid receptors by naloxone methiodide did not induce <strong>Fos</strong> like immunoreactivity in the lumbar spinal cord greater than that recorded in nonwithdrawing rats.
+FOS	drug	opioid	9284361	However, intrathecal injection of <b>naloxone</b> methiodide increased <strong>Fos</strong> like immunoreactivity in laminae I/II and the ventral horn to a greater extent than did subcutaneous injection of <b>naloxone</b>.
+FOS	addiction	withdrawal	9284361	We hypothesize that the increased <strong>Fos</strong> expression after systemic <b>withdrawal</b> in spinally transected rats results from a loss of descending inhibitory control that is activated during <b>withdrawal</b>.
+FOS	addiction	withdrawal	9284361	The increase in <b>withdrawal</b> induced <strong>Fos</strong> like immunoreactivity after rhizotomy may be secondary to loss of inhibitory controls exerted by large diameter primary afferents or to deafferentation induced reorganization in the dorsal horn.
+FOS	drug	opioid	9284361	Since capsaicin did not alter the magnitude of <strong>Fos</strong> like immunoreactivity in withdrawing rats, we conclude that hyperactivity of <b>opioid</b> receptor laden C fibres is not a necessary contributor to the withdrawal induced increase in <strong>Fos</strong> like immunoreactivity in laminae I and II.
+FOS	addiction	withdrawal	9284361	Since capsaicin did not alter the magnitude of <strong>Fos</strong> like immunoreactivity in withdrawing rats, we conclude that hyperactivity of opioid receptor laden C fibres is not a necessary contributor to the <b>withdrawal</b> induced increase in <strong>Fos</strong> like immunoreactivity in laminae I and II.
+FOS	drug	opioid	9284361	Taken together with the results recorded after intrathecal injection of <b>naloxone</b> methiodide in tolerant rats, we conclude that the pattern of lumbar spinal cord <strong>Fos</strong> expression following systemic withdrawal is primarily a consequence of increased activity in <b>opioid</b> receptor containing circuits intrinsic to the dorsal horn and that the magnitude of <strong>Fos</strong> expression is normally dampened by supraspinal and primary afferent derived inhibitory inputs.
+FOS	addiction	withdrawal	9284361	Taken together with the results recorded after intrathecal injection of naloxone methiodide in tolerant rats, we conclude that the pattern of lumbar spinal cord <strong>Fos</strong> expression following systemic <b>withdrawal</b> is primarily a consequence of increased activity in opioid receptor containing circuits intrinsic to the dorsal horn and that the magnitude of <strong>Fos</strong> expression is normally dampened by supraspinal and primary afferent derived inhibitory inputs.
+FOS	drug	opioid	9284358	<strong>Fos</strong> immunoreactivity in the supraoptic nucleus, and also in the median preoptic nucleus, organum vasculosum of the lamina terminalis and subfornical organ, which project to the supraoptic nucleus, increased following <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	9284358	<strong>Fos</strong> immunoreactivity in the supraoptic nucleus, and also in the median preoptic nucleus, organum vasculosum of the lamina terminalis and subfornical organ, which project to the supraoptic nucleus, increased following morphine <b>withdrawal</b>.
+FOS	drug	opioid	9284358	However, retrograde tracing from the supraoptic nucleus showed that, of the neurons in these regions which project to the supraoptic nucleus, only 0.4 7.1% expressed <strong>Fos</strong> in response to <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	9284358	However, retrograde tracing from the supraoptic nucleus showed that, of the neurons in these regions which project to the supraoptic nucleus, only 0.4 7.1% expressed <strong>Fos</strong> in response to morphine <b>withdrawal</b>.
+FOS	drug	opioid	9284358	Following <b>morphine</b> withdrawal, <strong>Fos</strong> immunoreactivity was present in 39.2% and 19.8% of the tyrosine hydroxylase immunoreactive neurons of the A1/C1 and A2/C2 cell groups.
+FOS	addiction	withdrawal	9284358	Following morphine <b>withdrawal</b>, <strong>Fos</strong> immunoreactivity was present in 39.2% and 19.8% of the tyrosine hydroxylase immunoreactive neurons of the A1/C1 and A2/C2 cell groups.
+FOS	drug	opioid	9284358	Of the cells in these regions identified as projecting to the supraoptic nucleus, 11.3% in the region of the A2 cell group and 12.7% in the region of the A1 cell group expressed <strong>Fos</strong> after <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	9284358	Of the cells in these regions identified as projecting to the supraoptic nucleus, 11.3% in the region of the A2 cell group and 12.7% in the region of the A1 cell group expressed <strong>Fos</strong> after morphine <b>withdrawal</b>.
+FOS	drug	amphetamine	9365026	<b>Amphetamine</b> sensitization augments <b>amphetamine</b> induced <strong>Fos</strong> expression in the lateral habenula.
+FOS	addiction	sensitization	9365026	Amphetamine <b>sensitization</b> augments amphetamine induced <strong>Fos</strong> expression in the lateral habenula.
+FOS	drug	amphetamine	9365026	To investigate the neuroanatomical basis of this phenomenon, we examined the effects of <b>AMPH</b> sensitization on <b>AMPH</b> induced <strong>Fos</strong> expression in 24 regions of the rat brain.
+FOS	addiction	sensitization	9365026	To investigate the neuroanatomical basis of this phenomenon, we examined the effects of AMPH <b>sensitization</b> on AMPH induced <strong>Fos</strong> expression in 24 regions of the rat brain.
+FOS	drug	amphetamine	9365026	As measured by <strong>Fos</strong> immunohistochemistry, the <b>AMPH</b> sensitization procedure enhanced subsequent <b>AMPH</b> induced <strong>Fos</strong> expression in only one structure, the medial part of the lateral habenula.
+FOS	addiction	sensitization	9365026	As measured by <strong>Fos</strong> immunohistochemistry, the AMPH <b>sensitization</b> procedure enhanced subsequent AMPH induced <strong>Fos</strong> expression in only one structure, the medial part of the lateral habenula.
+FOS	drug	amphetamine	9365026	These results indicate that <b>AMPH</b> induced behavioral sensitization is not accompanied by widespread increases in the ability of <b>AMPH</b> to increase regional <strong>Fos</strong> expression in the forebrain.
+FOS	addiction	sensitization	9365026	These results indicate that AMPH induced behavioral <b>sensitization</b> is not accompanied by widespread increases in the ability of AMPH to increase regional <strong>Fos</strong> expression in the forebrain.
+FOS	drug	opioid	9359591	Formalin evoked <strong>Fos</strong> expression in spinal cord is enhanced in <b>morphine</b> tolerant rats.
+FOS	drug	opioid	9359591	To determine if administration of a noxious stimulus can unmask a sensitization of dorsal horn neurons in <b>morphine</b> pelleted rats, we injected <b>morphine</b> tolerant and control rats with formalin into the plantar surface of the hindpaw, counted the number of flinches for 2 h and then processed the lumbar cord for <strong>Fos</strong> immunocytochemistry.
+FOS	addiction	sensitization	9359591	To determine if administration of a noxious stimulus can unmask a <b>sensitization</b> of dorsal horn neurons in morphine pelleted rats, we injected morphine tolerant and control rats with formalin into the plantar surface of the hindpaw, counted the number of flinches for 2 h and then processed the lumbar cord for <strong>Fos</strong> immunocytochemistry.
+FOS	drug	opioid	9359591	Although there was no significant difference in flinching behavior between the <b>morphine</b> tolerant and control groups, we recorded significantly increased total <strong>Fos</strong> like immunoreactivity at the L4/5 and L2 segments both ipsilateral and contralateral to the site of formalin injection in the <b>morphine</b> tolerant rats compared to the control rats.
+FOS	addiction	sensitization	9359591	These results suggest that lumbar spinal cord neurons are sensitized during the development of tolerance, that the <b>sensitization</b> can be unmasked by the administration of a noxious stimulus and that it is manifested as increased expression of the <strong>Fos</strong> protein in the lumbar cord.
+FOS	addiction	withdrawal	9295196	Atipamezole precipitated clonidine <b>withdrawal</b> induces c <strong>Fos</strong> expression in rat central nervous system.
+FOS	addiction	withdrawal	9295196	In conclusion, administration of the selective alpha2 antagonist atipamezole to rats chronically treated with the alpha2 adrenergic agonist clonidine triggers a powerful <b>withdrawal</b> syndrome associated with massive CNS expression of c <strong>Fos</strong> protein.
+FOS	drug	alcohol	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during ethanol <b>withdrawal</b>.
+FOS	drug	alcohol	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during ethanol <b>withdrawal</b>.
+FOS	addiction	withdrawal	9202324	The <strong>AP 1</strong> DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of FosB, c Jun, JunB, and JunD.
+FOS	addiction	withdrawal	9202324	<b>Withdrawal</b> severity did not affect the composition of the <strong>AP 1</strong> DNA binding activities.
+FOS	drug	cannabinoid	9197270	Withdrawal, induced by the <b>cannabinoid</b> antagonist SR 141716A, was accompanied by a marked elevation in extracellular CRF concentration and a distinct pattern of <strong>Fos</strong> activation in the central nucleus of the amygdala.
+FOS	addiction	withdrawal	9197270	<b>Withdrawal</b>, induced by the cannabinoid antagonist SR 141716A, was accompanied by a marked elevation in extracellular CRF concentration and a distinct pattern of <strong>Fos</strong> activation in the central nucleus of the amygdala.
+FOS	drug	amphetamine	9070635	Enhanced CREB phosphorylation and changes in c <strong>Fos</strong> and FRA expression in striatum accompany <b>amphetamine</b> sensitization.
+FOS	addiction	sensitization	9070635	Enhanced CREB phosphorylation and changes in c <strong>Fos</strong> and FRA expression in striatum accompany amphetamine <b>sensitization</b>.
+FOS	drug	amphetamine	9070635	Expression in striatum of c <strong>Fos</strong>, a 35 kDa <strong>Fos</strong> related antigen (FRA) and the phosphorylated form of cyclic AMP response element binding protein (phosphoCREB) was assessed using Western blots in rats that developed behavioral sensitization following repeated <b>amphetamine</b> administration.
+FOS	addiction	sensitization	9070635	Expression in striatum of c <strong>Fos</strong>, a 35 kDa <strong>Fos</strong> related antigen (FRA) and the phosphorylated form of cyclic AMP response element binding protein (phosphoCREB) was assessed using Western blots in rats that developed behavioral <b>sensitization</b> following repeated amphetamine administration.
+FOS	drug	amphetamine	9070635	Similar to previous observations using chronic cocaine administration, <b>amphetamine</b> sensitized animals had decreased c <strong>Fos</strong> and increased FRA proteins in striatum.
+FOS	drug	cocaine	9070635	Similar to previous observations using chronic <b>cocaine</b> administration, amphetamine sensitized animals had decreased c <strong>Fos</strong> and increased FRA proteins in striatum.
+FOS	drug	amphetamine	9070635	Thus, <b>amphetamine</b> sensitization is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+FOS	addiction	sensitization	9070635	Thus, amphetamine <b>sensitization</b> is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+FOS	addiction	sensitization	9070635	These results suggest that alterations in <strong>Fos</strong>, FRA and CREB transcription factors are common neuronal responses to chronic psychostimulant administration and may contribute to regulation of genes important to the neuroplastic changes underlying psychostimulant <b>sensitization</b>.
+FOS	drug	amphetamine	9027869	<b>Amphetamine</b> sensitization enhances regional c <strong>fos</strong> expression produced by conditioned fear.
+FOS	addiction	sensitization	9027869	Amphetamine <b>sensitization</b> enhances regional c <strong>fos</strong> expression produced by conditioned fear.
+FOS	drug	amphetamine	9027869	In an attempt to investigate the neurobiological correlates of this phenomenon, the present study examined the effects of prior D <b>amphetamine</b> sensitization on regional c <strong>fos</strong> expression induced by a psychological stressor.
+FOS	addiction	sensitization	9027869	In an attempt to investigate the neurobiological correlates of this phenomenon, the present study examined the effects of prior D amphetamine <b>sensitization</b> on regional c <strong>fos</strong> expression induced by a psychological stressor.
+FOS	drug	amphetamine	9027869	The <b>amphetamine</b> sensitization procedure significantly enhanced the effects of conditioned fear on c <strong>fos</strong> expression in several brain regions.
+FOS	addiction	sensitization	9027869	The amphetamine <b>sensitization</b> procedure significantly enhanced the effects of conditioned fear on c <strong>fos</strong> expression in several brain regions.
+FOS	drug	opioid	9037396	In this study, we monitored <strong>Fos</strong> like immunoreactivity in the sacral spinal cord to identify neurons that are likely to contribute to the autonomic manifestations of <b>opioid</b> antagonist precipitated withdrawal in <b>morphine</b> tolerant rats.
+FOS	addiction	withdrawal	9037396	In this study, we monitored <strong>Fos</strong> like immunoreactivity in the sacral spinal cord to identify neurons that are likely to contribute to the autonomic manifestations of opioid antagonist precipitated <b>withdrawal</b> in morphine tolerant rats.
+FOS	addiction	withdrawal	9037396	Compared to rats that withdrew systemically, peripherally <b>withdrawal</b> evoked significantly less <strong>Fos</strong> like immunoreactivity in laminae V/VI, X and the SPN.
+FOS	drug	cocaine	8974398	Regional brain activation was assessed by mapping of <strong>Fos</strong> related protein expression in rats trained to self administration of intravenous nicotine and <b>cocaine</b>.
+FOS	drug	nicotine	8974398	Regional brain activation was assessed by mapping of <strong>Fos</strong> related protein expression in rats trained to self administration of intravenous <b>nicotine</b> and cocaine.
+FOS	addiction	sensitization	9403355	During the "central <b>sensitization</b>" phenomenon, noxious stimuli lead to expression of IEGs (c <strong>fos</strong>, c jun, krox 24); their proteic products have been postulated to convert short term stimulations into long lasting responses in dorsal horn neurons.
+FOS	drug	opioid	9403355	The aim of this study was to verify if analgesic drugs, such as <b>morphine</b> and ketorolac, may affect the c <strong>fos</strong> protooncogene expression by using a method highly sensitive and specific, based on transformation of activated c <strong>fos</strong> specific mRNA in cDNA (reverse transcription), its amplification (PCR) and final visualization by electrophoresis on agarose gel.
+FOS	drug	opioid	9403355	When the animals were pretreated with <b>morphine</b> or ketorolac and subsequently exposed to the monolateral sciatic nerve ligature, or treated with ketorolac immediately after the same painful stimulus, we found that only pretreatment with <b>morphine</b> completely blocked c <strong>fos</strong> depression.
+FOS	drug	opioid	9227847	The level of c <strong>fos</strong> mRNA was increased only the dorsal striatum following <b>morphine</b> injections.
+FOS	drug	alcohol	9154216	Differential sensitivity of c <strong>Fos</strong> expression in hippocampus and other brain regions to moderate and low doses of <b>alcohol</b>.
+FOS	drug	alcohol	9154216	To identify these targets we have mapped <b>alcohol</b> induced changes in the expression of the c <strong>Fos</strong> protein in the rat brain.
+FOS	drug	alcohol	9154216	Administration of a moderate dose of <b>alcohol</b> (1.5 g kg 1) led to a suppression of basal and novel environment induced c <strong>Fos</strong> expression in the hippocampus and simultaneous induction of this protein in regions important for the reinforcing as well as aversive properties of drugs.
+FOS	addiction	aversion	9154216	Administration of a moderate dose of alcohol (1.5 g kg 1) led to a suppression of basal and novel environment induced c <strong>Fos</strong> expression in the hippocampus and simultaneous induction of this protein in regions important for the reinforcing as well as <b>aversive</b> properties of drugs.
+FOS	addiction	reward	9154216	Administration of a moderate dose of alcohol (1.5 g kg 1) led to a suppression of basal and novel environment induced c <strong>Fos</strong> expression in the hippocampus and simultaneous induction of this protein in regions important for the <b>reinforcing</b> as well as aversive properties of drugs.
+FOS	drug	alcohol	9154216	Repeated administration of the same dose of <b>alcohol</b> did not decrease <b>alcohol</b> mediated suppression of c <strong>Fos</strong> in the hippocampus, but decreased <b>alcohol</b> induced expression of c <strong>Fos</strong> in other areas.
+FOS	drug	alcohol	9154216	A lower dose of acute <b>alcohol</b> (0.5 g kg 1) reduced basal c <strong>Fos</strong> expression in several areas of the neocortex, hippocampus and hypothalamus.
+FOS	drug	alcohol	9154216	However, while this low dose of <b>alcohol</b> was unable to counteract the environmental novelty induced c <strong>Fos</strong> expression in these areas, it increased c <strong>Fos</strong> expression in the central nucleus of amygdala (an effect similar to the one observed previously for diazepam).
+FOS	drug	benzodiazepine	9154216	However, while this low dose of alcohol was unable to counteract the environmental novelty induced c <strong>Fos</strong> expression in these areas, it increased c <strong>Fos</strong> expression in the central nucleus of amygdala (an effect similar to the one observed previously for <b>diazepam</b>).
+FOS	drug	cocaine	9051741	D1 class dopamine receptors influence <b>cocaine</b> induced persistent expression of <strong>Fos</strong> related proteins in striatum.
+FOS	drug	alcohol	8982717	The anti craving drug <b>acamprosate</b> reduces c <strong>fos</strong> expression in rats undergoing <b>ethanol</b> withdrawal.
+FOS	addiction	relapse	8982717	The anti <b>craving</b> drug acamprosate reduces c <strong>fos</strong> expression in rats undergoing ethanol withdrawal.
+FOS	addiction	withdrawal	8982717	The anti craving drug acamprosate reduces c <strong>fos</strong> expression in rats undergoing ethanol <b>withdrawal</b>.
+FOS	drug	alcohol	8982717	In the present study the expression of the immediate early gene c <strong>fos</strong> in rat hippocampal and cerebellar neurons was used to monitor the modulatory effect of <b>acamprosate</b> on neuronal excitability during <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	8982717	In the present study the expression of the immediate early gene c <strong>fos</strong> in rat hippocampal and cerebellar neurons was used to monitor the modulatory effect of acamprosate on neuronal excitability during ethanol <b>withdrawal</b>.
+FOS	drug	alcohol	8982717	Several hybridization techniques were employed to investigate the effect of <b>acamprosate</b> on c <strong>fos</strong> expression.
+FOS	drug	alcohol	8982717	<b>Acamprosate</b> (200 mg/kg; intraperitoneally) reduced the elevated c <strong>fos</strong> mRNA levels in the hippocampus and the cerebellum following 24 h of <b>ethanol</b> withdrawal, or the application of the convulsant pentylenetetrazole.
+FOS	addiction	withdrawal	8982717	Acamprosate (200 mg/kg; intraperitoneally) reduced the elevated c <strong>fos</strong> mRNA levels in the hippocampus and the cerebellum following 24 h of ethanol <b>withdrawal</b>, or the application of the convulsant pentylenetetrazole.
+FOS	drug	alcohol	8982717	The effect of <b>ethanol</b> withdrawal on c <strong>fos</strong> expression was more pronounced in the cerebellum than in the hippocampus.
+FOS	addiction	withdrawal	8982717	The effect of ethanol <b>withdrawal</b> on c <strong>fos</strong> expression was more pronounced in the cerebellum than in the hippocampus.
+FOS	drug	alcohol	8982717	In the hippocampus (CA1) and the cerebellum <b>acamprosate</b> alone induced a significant increase in c <strong>fos</strong> expression in drug naive animals.
+FOS	drug	alcohol	8982717	Only in the hippocampus did co administration of pentylenetetrazole during <b>ethanol</b> withdrawal induce a further increase in c <strong>fos</strong> expression.
+FOS	addiction	withdrawal	8982717	Only in the hippocampus did co administration of pentylenetetrazole during ethanol <b>withdrawal</b> induce a further increase in c <strong>fos</strong> expression.
+FOS	drug	amphetamine	8962158	We show here that deletion of the D1 dopamine receptor produces a neural phenotype in which <b>amphetamine</b> and cocaine, two addictive psychomotor stimulants, can no longer stimulate neurons in the striatum to express <strong>cFos</strong> or JunB or to regulate dynorphin.
+FOS	drug	cocaine	8962158	We show here that deletion of the D1 dopamine receptor produces a neural phenotype in which amphetamine and <b>cocaine</b>, two addictive psychomotor stimulants, can no longer stimulate neurons in the striatum to express <strong>cFos</strong> or JunB or to regulate dynorphin.
+FOS	addiction	addiction	8962158	We show here that deletion of the D1 dopamine receptor produces a neural phenotype in which amphetamine and cocaine, two <b>addictive</b> psychomotor stimulants, can no longer stimulate neurons in the striatum to express <strong>cFos</strong> or JunB or to regulate dynorphin.
+FOS	addiction	withdrawal	9116193	In animals that underwent behavioural changes consistent with <b>withdrawal</b>, <strong>Fos</strong> and nicotinamide dinucleotide phosphate diaphorase (NADPH D) positive neurones were identified within the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei as well as the brain stem nucleus tractus solitarius (NTS).
+FOS	drug	nicotine	8950089	The reinforcing properties of <b>nicotine</b> are associated with a specific patterning of c <strong>fos</strong> expression in the rat brain.
+FOS	addiction	reward	8950089	The <b>reinforcing</b> properties of nicotine are associated with a specific patterning of c <strong>fos</strong> expression in the rat brain.
+FOS	drug	nicotine	8950089	The effect of <b>nicotine</b> self administration on regional brain activity was studied by mapping changes of c <strong>fos</strong> expression.
+FOS	drug	nicotine	8950089	Specific <b>nicotine</b> effects were determine by comparing the patterning of <strong>Fos</strong> like immunoreactivity (<strong>Fos</strong> Ll) in <b>nicotine</b> self administering rats with that in three different control groups.
+FOS	drug	nicotine	8950089	<b>Nicotine</b> self administration, exposure to saline and food restriction increased <strong>Fos</strong> Ll in 43, 33 and three brain regions, respectively, when compared with the control group fed ad libitum.
+FOS	drug	amphetamine	8947933	<b>Amphetamine</b> , cocaine , and morphine induced c <strong>fos</strong> expression patterns were examined following an injection protocol that has previously been shown to produce behavioral sensitization and enhanced dopamine release in the striatal complex.
+FOS	drug	cocaine	8947933	Amphetamine , <b>cocaine</b> , and morphine induced c <strong>fos</strong> expression patterns were examined following an injection protocol that has previously been shown to produce behavioral sensitization and enhanced dopamine release in the striatal complex.
+FOS	drug	opioid	8947933	Amphetamine , cocaine , and <b>morphine</b> induced c <strong>fos</strong> expression patterns were examined following an injection protocol that has previously been shown to produce behavioral sensitization and enhanced dopamine release in the striatal complex.
+FOS	addiction	sensitization	8947933	Amphetamine , cocaine , and morphine induced c <strong>fos</strong> expression patterns were examined following an injection protocol that has previously been shown to produce behavioral <b>sensitization</b> and enhanced dopamine release in the striatal complex.
+FOS	addiction	sensitization	8947933	Drug specific c <strong>fos</strong> patterns were observed in both acute and <b>sensitization</b> injection paradigms.
+FOS	addiction	sensitization	8947933	A <b>sensitization</b> pretreatment schedule did, however, alter the c <strong>fos</strong> expression patterns induced by all the drugs in the caudate putamen, nucleus accumbens, and the cerebral cortex.
+FOS	drug	alcohol	8944413	Combined effects of <b>ethanol</b> and cocaine on <strong>FOS</strong> like protein and cocaethylene biosynthesis in the rat.
+FOS	drug	cocaine	8944413	Combined effects of ethanol and <b>cocaine</b> on <strong>FOS</strong> like protein and cocaethylene biosynthesis in the rat.
+FOS	drug	alcohol	8944413	To study the simultaneous effects of <b>ethanol</b> and cocaine on striatal <strong>FOS</strong> like protein, rats were exposed to an (8.7%) <b>ethanol</b> solution for 15 days followed by single or daily cocaine injections (20 mg/kg; IP).
+FOS	drug	cocaine	8944413	To study the simultaneous effects of ethanol and <b>cocaine</b> on striatal <strong>FOS</strong> like protein, rats were exposed to an (8.7%) ethanol solution for 15 days followed by single or daily <b>cocaine</b> injections (20 mg/kg; IP).
+FOS	drug	cocaine	8944413	In addition, systemic administration of cocaethylene to rats (60 mumol/kg; molar equivalent of 20 mg/kg <b>cocaine</b>) induced widespread <strong>FOS</strong> like protein in the caudate putamen.
+FOS	drug	cocaine	8959019	However, the induction of the chronic <strong>AP 1</strong> complex and the chronic Fras provides a mechanism capable of underlying long lasting alterations in gene expression following chronic <b>cocaine</b> treatment.
+FOS	drug	alcohol	8892522	c <strong>Fos</strong> induction in rat brainstem in response to <b>ethanol</b>  and lithium chloride induced conditioned taste aversions.
+FOS	drug	alcohol	8892522	Relative to saline controls, animals injected with either LiCl (76 mg/kg) or <b>ethanol</b> (3.5 g/kg) displayed greater c <strong>Fos</strong> expression in area postrema, nucleus of the solitary tract (NTS), and lateral parabrachial nucleus.
+FOS	drug	opioid	8883853	Induction of <strong>Fos</strong> like immunoreactivity by <b>opioids</b> in guinea pig brain.
+FOS	drug	opioid	8883853	administration of 100 nmol of <b>morphine</b>, the selective mu receptor agonist DAMGO, the delta receptor agonist DPDPE and the kappa receptor agonist U50,488H, on the induction of <strong>Fos</strong> like immunoreactivity (<strong>Fos</strong> LI) in the guinea pig brain were investigated using immunohistochemical techniques.
+FOS	drug	opioid	8883853	injection of <b>opioids</b> showed marked increases in the number of <strong>Fos</strong> LI nuclei within a large number of brain regions, several of which, including hypothalamic nuclei, paraventricular thalamic nucleus, the amygdala, periaqueductal gray, superior and inferior colliculi, the piriform and entorhinal cortices, have been shown to be activated under stressful or aversive conditions.
+FOS	addiction	aversion	8883853	injection of opioids showed marked increases in the number of <strong>Fos</strong> LI nuclei within a large number of brain regions, several of which, including hypothalamic nuclei, paraventricular thalamic nucleus, the amygdala, periaqueductal gray, superior and inferior colliculi, the piriform and entorhinal cortices, have been shown to be activated under stressful or <b>aversive</b> conditions.
+FOS	drug	alcohol	8883853	Pretreatment with the opioid antagonist, <b>naltrexone</b>, before administration of morphine or U50,488H, inhibited <strong>Fos</strong> LI induction indicating that the effects of the opioids were mediated by opioid receptors.
+FOS	drug	opioid	8883853	Pretreatment with the <b>opioid</b> antagonist, naltrexone, before administration of <b>morphine</b> or U50,488H, inhibited <strong>Fos</strong> LI induction indicating that the effects of the <b>opioids</b> were mediated by <b>opioid</b> receptors.
+FOS	drug	opioid	8883853	U50,488H administration resulted in higher numbers of <strong>Fos</strong> LI stained neurons compared to <b>morphine</b> in most regions other than the nucleus accumbens and interpeduncular nucleus.
+FOS	drug	opioid	8883853	<b>Morphine</b> and DAMGO produced significantly higher numbers of <strong>Fos</strong> LI neurons in the nucleus accumbens shell region than U50,488H, which may reflect the more powerful reinforcing/rewarding effects of mu receptor agonists.
+FOS	addiction	reward	8883853	Morphine and DAMGO produced significantly higher numbers of <strong>Fos</strong> LI neurons in the nucleus accumbens shell region than U50,488H, which may reflect the more powerful <b>reinforcing</b>/rewarding effects of mu receptor agonists.
+FOS	drug	nicotine	8883897	<b>Nicotine</b> injections into the ventral tegmental area increase locomotion and <strong>Fos</strong> like immunoreactivity in the nucleus accumbens of the rat.
+FOS	drug	nicotine	8883897	The effects of intra tegmental injections of <b>nicotine</b> were further investigated on cells in several target areas for the VTA DA neurons through determination of c <strong>fos</strong> expression by means of <strong>Fos</strong> immunohistochemistry.
+FOS	drug	nicotine	8883897	Intra tegmental injections of <b>nicotine</b> (8.0 micrograms/side) increased <strong>Fos</strong> like immunoreactivity in the NAc, but did not affect the number of <strong>Fos</strong> positive nuclei in the medial prefrontal cortex or in the dorsolateral striatum.
+FOS	drug	opioid	8843097	A mu receptor <b>opioid</b> agonist induces <strong>AP 1</strong> and NF kappa B transcription factor activity in primary cultures of rat cortical neurons.
+FOS	drug	opioid	8843097	The specific mu receptor <b>opioid</b> agonist, Tyr, D Ala2, Gly, N Me Phe4, Gly ol5 (DAMGO), was found to increase <strong>AP 1</strong> and NF kappa B activity in primary cultures of neurons from rat cerebral cortex.
+FOS	drug	opioid	8843097	Acute (2 h, 4 h) and long term (72 h) treatment with DAMGO time dependently increased the DNA binding activity of both <strong>AP 1</strong> and NF kappa B and the stimulation could be abolished or inhibited by concurrent incubation with <b>naloxone</b>.
+FOS	drug	opioid	8843097	However, acute <b>naloxone</b> precipitated withdrawal did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+FOS	addiction	withdrawal	8843097	However, acute naloxone precipitated <b>withdrawal</b> did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+FOS	drug	opioid	8843097	These results indicate a mu <b>opioid</b> receptor related co induction of <strong>AP 1</strong> and NF kappa B transcription factors in cultured cortical neurons.
+FOS	drug	cocaine	8755486	Network level changes in expression of inducible <strong>Fos</strong> Jun proteins in the striatum during chronic <b>cocaine</b> treatment and withdrawal.
+FOS	addiction	withdrawal	8755486	Network level changes in expression of inducible <strong>Fos</strong> Jun proteins in the striatum during chronic cocaine treatment and <b>withdrawal</b>.
+FOS	drug	amphetamine	8753884	We find that in vivo, the NMDA receptor antagonist MK 801 inhibits <b>amphetamine</b> induction of c <strong>fos</strong> acutely and also prevents downregulation of IEG expression with chronic <b>amphetamine</b> administration.
+FOS	drug	opioid	8730720	Spinal cord mechanisms of <b>opioid</b> tolerance and dependence: <strong>Fos</strong> like immunoreactivity increases in subpopulations of spinal cord neurons during withdrawal [corrected].
+FOS	addiction	dependence	8730720	Spinal cord mechanisms of opioid tolerance and <b>dependence</b>: <strong>Fos</strong> like immunoreactivity increases in subpopulations of spinal cord neurons during withdrawal [corrected].
+FOS	addiction	withdrawal	8730720	Spinal cord mechanisms of opioid tolerance and dependence: <strong>Fos</strong> like immunoreactivity increases in subpopulations of spinal cord neurons during <b>withdrawal</b> [corrected].
+FOS	drug	alcohol	8730720	To identify the population of spinal cord neurons that underlies this state, we monitored expression of <strong>Fos</strong> like immunoreactivity, after <b>naltrexone</b> precipitated abstinence in normal and morphine tolerant rats.
+FOS	drug	opioid	8730720	To identify the population of spinal cord neurons that underlies this state, we monitored expression of <strong>Fos</strong> like immunoreactivity, after naltrexone precipitated abstinence in normal and <b>morphine</b> tolerant rats.
+FOS	drug	alcohol	8730720	After daily (five days) implantation of morphine or placebo pellets, the rats received an injection of saline or <b>naltrexone</b> and behavior was monitored for 1 h. The rats were then killed, their spinal cords removed and 50 microns transverse sections of the lumbar cord were immunostained with a rabbit polyclonal antiserum directed against <strong>Fos</strong>.
+FOS	drug	opioid	8730720	After daily (five days) implantation of <b>morphine</b> or placebo pellets, the rats received an injection of saline or naltrexone and behavior was monitored for 1 h. The rats were then killed, their spinal cords removed and 50 microns transverse sections of the lumbar cord were immunostained with a rabbit polyclonal antiserum directed against <strong>Fos</strong>.
+FOS	drug	alcohol	8730720	<b>Naltrexone</b> injection in the placebo group did not increase spinal cord <strong>Fos</strong> expression.
+FOS	drug	alcohol	8730720	<b>Naltrexone</b> precipitated abstinence resulted in an increase in <strong>Fos</strong> expression at all levels of the spinal cord; the greatest increase and densest staining was in laminae I through VI.
+FOS	addiction	withdrawal	8730720	Importantly, when <b>withdrawal</b> was precipitated in anesthetized rats, we recorded a significant reduction in <strong>Fos</strong> expression, particularly in laminae III through VI, but there was persistent expression in the superficial dorsal horn, particularly in lamina I.
+FOS	drug	alcohol	8730720	This sensitization is unmasked by the administration of <b>naltrexone</b> and is manifested by <strong>fos</strong> induction in laminae I/II in awake or anesthetized withdrawing animals.
+FOS	addiction	sensitization	8730720	This <b>sensitization</b> is unmasked by the administration of naltrexone and is manifested by <strong>fos</strong> induction in laminae I/II in awake or anesthetized withdrawing animals.
+FOS	drug	opioid	8738262	Distribution of c <strong>Fos</strong> in guinea pig brain following <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	8738262	Distribution of c <strong>Fos</strong> in guinea pig brain following morphine <b>withdrawal</b>.
+FOS	drug	alcohol	8738262	The distribution of the immediate early gene and transcription factor protein, c <strong>Fos</strong>, was examined in the brains of guinea pigs following treatment with morphine, naloxone or <b>naltrexone</b>, or the induction of morphine withdrawal by these opioid antagonists.
+FOS	drug	opioid	8738262	The distribution of the immediate early gene and transcription factor protein, c <strong>Fos</strong>, was examined in the brains of guinea pigs following treatment with <b>morphine</b>, <b>naloxone</b> or naltrexone, or the induction of <b>morphine</b> withdrawal by these <b>opioid</b> antagonists.
+FOS	addiction	withdrawal	8738262	The distribution of the immediate early gene and transcription factor protein, c <strong>Fos</strong>, was examined in the brains of guinea pigs following treatment with morphine, naloxone or naltrexone, or the induction of morphine <b>withdrawal</b> by these opioid antagonists.
+FOS	drug	alcohol	8738262	In the animals that were treated with morphine and withdrawn with either naloxone or <b>naltrexone</b>, c <strong>Fos</strong> was expressed in neurons in many brain areas, including the frontal and cingulate cortices, olfactory tubercles, ventral pallidum, nucleus accumbens, habenular, paraventricular thalamic nucleus, septal and arcuate nuclei, lateral and posterior hypothalamic areas, ventral tegmental area, central grey, dorsal raphe nucleus, locus coeruleus, raphe magnus, lateral paragigantocellular nucleus and solitary tract nucleus.
+FOS	drug	opioid	8738262	In the animals that were treated with <b>morphine</b> and withdrawn with either <b>naloxone</b> or naltrexone, c <strong>Fos</strong> was expressed in neurons in many brain areas, including the frontal and cingulate cortices, olfactory tubercles, ventral pallidum, nucleus accumbens, habenular, paraventricular thalamic nucleus, septal and arcuate nuclei, lateral and posterior hypothalamic areas, ventral tegmental area, central grey, dorsal raphe nucleus, locus coeruleus, raphe magnus, lateral paragigantocellular nucleus and solitary tract nucleus.
+FOS	drug	alcohol	8738262	In contrast, only low levels of c <strong>Fos</strong> were found in brains of animals that had been treated for three days with morphine followed by saline, or with saline followed by <b>naltrexone</b> or naloxone.
+FOS	drug	opioid	8738262	In contrast, only low levels of c <strong>Fos</strong> were found in brains of animals that had been treated for three days with <b>morphine</b> followed by saline, or with saline followed by naltrexone or <b>naloxone</b>.
+FOS	drug	opioid	8738262	The widespread distribution of c <strong>Fos</strong> induced by <b>morphine</b> withdrawal reflects the complexity of the accompanying behavioural and autonomic responses.
+FOS	addiction	withdrawal	8738262	The widespread distribution of c <strong>Fos</strong> induced by morphine <b>withdrawal</b> reflects the complexity of the accompanying behavioural and autonomic responses.
+FOS	drug	opioid	8609891	Induction of chronic <strong>Fos</strong> related antigens in rat brain by chronic <b>morphine</b> administration.
+FOS	drug	cocaine	8609891	Previous studies have shown that repeated exposure to <b>cocaine</b> or to several other stimuli induces novel 35 37 kDa <strong>Fos</strong> related antigens (chronic Fras) in specific brain regions.
+FOS	drug	opioid	8609891	After 5 days of <b>morphine</b> treatment, we observed increased levels of the chronic Fras and of <strong>AP 1</strong> binding activity in rat striatum and nucleus accumbens, effects that were not seen in most other brain regions that we studied.
+FOS	drug	alcohol	8609891	Withdrawal studies demonstrated robust induction of several known acute Fras, including c <strong>Fos</strong>, FosB, Fra 1, Fra 2, and delta FosB, at 6 hr after <b>naltrexone</b> precipitation of withdrawal in the striatum, nucleus accumbens, and several other brain regions.
+FOS	addiction	withdrawal	8609891	<b>Withdrawal</b> studies demonstrated robust induction of several known acute Fras, including c <strong>Fos</strong>, FosB, Fra 1, Fra 2, and delta FosB, at 6 hr after naltrexone precipitation of <b>withdrawal</b> in the striatum, nucleus accumbens, and several other brain regions.
+FOS	drug	nicotine	8593811	<b>Nicotine</b> induced <strong>cFos</strong> expression in the hypothalamic paraventricular nucleus is dependent on brainstem effects: correlations with <strong>cFos</strong> in catecholaminergic and noncatecholaminergic neurons in the nucleus tractus solitarius.
+FOS	drug	nicotine	8593811	The present study in rats examined 1) the relationship between dose dependent expression of <strong>cFos</strong> in the PVN and that in the nucleus of the solitary tract (NTS) A2, NTS C2 and locus coeruleus (LC), after iv <b>nicotine</b> (0.045 0.18 mg/kg, administered at 0.09 mg/kg per min); 2) the dependence of PVN <strong>cFos</strong> expression on the effects of <b>nicotine</b> in brainstem, using the nicotinic cholinergic antagonist, mecamylamine, administered into the fourth ventricle; and 3) the extent of catecholaminergic involvement in the effect of <b>nicotine</b> on the PVN, measured by immunocytochemical double labeling for <strong>cFos</strong> and tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis.
+FOS	addiction	dependence	8593811	The present study in rats examined 1) the relationship between dose dependent expression of <strong>cFos</strong> in the PVN and that in the nucleus of the solitary tract (NTS) A2, NTS C2 and locus coeruleus (LC), after iv nicotine (0.045 0.18 mg/kg, administered at 0.09 mg/kg per min); 2) the <b>dependence</b> of PVN <strong>cFos</strong> expression on the effects of nicotine in brainstem, using the nicotinic cholinergic antagonist, mecamylamine, administered into the fourth ventricle; and 3) the extent of catecholaminergic involvement in the effect of nicotine on the PVN, measured by immunocytochemical double labeling for <strong>cFos</strong> and tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis.
+FOS	drug	nicotine	8593811	The results showed that the magnitude of <strong>cFos</strong> expression was dependent on the dose of <b>nicotine</b> in all regions studied (P < 0.0006); however, at the two lowest doses, only the NTS and CRH containing region of the PVN expressed <strong>cFos</strong>, whereas the LC and the rest of the PVN were activated only by higher doses.
+FOS	drug	nicotine	8593811	<b>Nicotine</b> also elicited a dose dependent increase in <strong>cFos</strong> expression in the TH+ neurons of the NTS, with C2 more sensitive than A2.
+FOS	drug	nicotine	8593811	Fourth ventricular mecamylamine completely blocked <b>nicotine</b> induced <strong>cFos</strong> expression throughout the NTS, as well as the PVN.
+FOS	drug	amphetamine	21359726	Examples of pharmacological stimuli that lead to long term changes are the highly addictive psychostimulant drugs, <b>amphetamine</b> and cocaine These drugs produce a robust activation of IEGs (e.g., c <strong>fos</strong>, jun B, egr 1) in areas of the brain that are believed to be part of the neural substrates of addiction (4 8) In animal models of epileptogenesis or memory, such as kindling and long term potentiation (LTP), respectively, electrical stimuli produce activation of IEGs within the brain structures thought to underlie the long lasting changes associated with these experimental procedures (9 16).
+FOS	drug	cocaine	21359726	Examples of pharmacological stimuli that lead to long term changes are the highly addictive psychostimulant drugs, amphetamine and <b>cocaine</b> These drugs produce a robust activation of IEGs (e.g., c <strong>fos</strong>, jun B, egr 1) in areas of the brain that are believed to be part of the neural substrates of addiction (4 8) In animal models of epileptogenesis or memory, such as kindling and long term potentiation (LTP), respectively, electrical stimuli produce activation of IEGs within the brain structures thought to underlie the long lasting changes associated with these experimental procedures (9 16).
+FOS	addiction	addiction	21359726	Examples of pharmacological stimuli that lead to long term changes are the highly <b>addictive</b> psychostimulant drugs, amphetamine and cocaine These drugs produce a robust activation of IEGs (e.g., c <strong>fos</strong>, jun B, egr 1) in areas of the brain that are believed to be part of the neural substrates of <b>addiction</b> (4 8) In animal models of epileptogenesis or memory, such as kindling and long term potentiation (LTP), respectively, electrical stimuli produce activation of IEGs within the brain structures thought to underlie the long lasting changes associated with these experimental procedures (9 16).
+FOS	addiction	sensitization	8672390	In rats injected s.c. with formalin, behavioural correlates of the amount and pattern of <strong>Fos</strong> like immunoreactivity (<strong>Fos</strong> Ll) (molecular responses to pain) were studied to test if early phase treatment with 75% nitrous oxide or 2% halothane, or both, suppressed subsequent spinal <b>sensitization</b>.
+FOS	drug	opioid	8672390	The numbers of <strong>Fos</strong> Ll labelled neurones for groups given nitrous oxide, or halothane, or both, were identical to the control, whereas numbers for <b>fentanyl</b> were 47.2% less (P < 0.01).
+FOS	drug	alcohol	8749800	The present study examined fetal <b>alcohol</b> effects (FAE) on the induction of the immediate early genes (IEGs) c <strong>fos</strong>, jun B, c jun, and zif268 mRNAs in the prefrontal cortex, hippocampus, and other brain regions after testing in an alternation task.
+FOS	drug	opioid	8747753	Experiments examining c <strong>fos</strong> expression during <b>morphine</b> withdrawal indicate that NMDA antagonists may exert some of their influence on <b>morphine</b> withdrawal symptoms through actions in the forebrain.
+FOS	addiction	withdrawal	8747753	Experiments examining c <strong>fos</strong> expression during morphine <b>withdrawal</b> indicate that NMDA antagonists may exert some of their influence on morphine <b>withdrawal</b> symptoms through actions in the forebrain.
+FOS	drug	opioid	8747753	Pretreatment with the noncompetitive NMDA antagonist MK801 blocks <b>morphine</b> withdrawal induced increased c <strong>fos</strong> expression in the amygdala, but not in the nucleus accumbens, frontal cortex, or hippocampus.
+FOS	addiction	withdrawal	8747753	Pretreatment with the noncompetitive NMDA antagonist MK801 blocks morphine <b>withdrawal</b> induced increased c <strong>fos</strong> expression in the amygdala, but not in the nucleus accumbens, frontal cortex, or hippocampus.
+FOS	drug	opioid	8747753	Pretreatment with the competitive NMDA antagonist LY274614 (or the alpha2 adrenergic agonist clonidine) blocks <b>morphine</b> withdrawal induced increased c <strong>fos</strong> expression in the amygdala and nucleus accumbens, but not in the frontal cortex or hippocampus.
+FOS	addiction	withdrawal	8747753	Pretreatment with the competitive NMDA antagonist LY274614 (or the alpha2 adrenergic agonist clonidine) blocks morphine <b>withdrawal</b> induced increased c <strong>fos</strong> expression in the amygdala and nucleus accumbens, but not in the frontal cortex or hippocampus.
+FOS	drug	amphetamine	8552240	Repeated <b>amphetamine</b> administration induces a prolonged augmentation of phosphorylated cyclase response element binding protein and <strong>Fos</strong> related antigen immunoreactivity in rat striatum.
+FOS	drug	amphetamine	8552240	Semi quantitative immunocytochemistry was used to investigate the levels of cyclase response element binding protein, phosphorylated cyclase response element binding protein, <strong>Fos</strong> and <strong>Fos</strong> related antigen immunoreactivity in the striatum of rats after acute or repeated <b>amphetamine</b> administration.
+FOS	drug	amphetamine	8552240	<strong>Fos</strong> immunoreactivity was significantly induced in the dorsal striatum following acute and repeated <b>amphetamine</b>.
+FOS	drug	amphetamine	8552240	<strong>Fos</strong> immunoreactivity in the core of the nucleus accumbens was significantly increased following repeated <b>amphetamine</b> only.
+FOS	drug	amphetamine	8552240	Acute <b>amphetamine</b> induced, and repeated <b>amphetamine</b> further augmented, <strong>Fos</strong> related antigen immunoreactivity in the dorsal striatum, while not affecting <strong>Fos</strong> related antigen immunoreactivity in the nucleus accumbens.
+FOS	drug	amphetamine	8552240	These data demonstrate that repeated <b>amphetamine</b> administration results in a prolonged induction of phosphorylated cyclase response element binding protein and <strong>Fos</strong> related antigen immunoreactivity in the dorsal striatum, indicating that alterations in striatal gene expression associated with the development of behavioral sensitization may be mediated, in part, by these transcription factors.
+FOS	addiction	sensitization	8552240	These data demonstrate that repeated amphetamine administration results in a prolonged induction of phosphorylated cyclase response element binding protein and <strong>Fos</strong> related antigen immunoreactivity in the dorsal striatum, indicating that alterations in striatal gene expression associated with the development of behavioral <b>sensitization</b> may be mediated, in part, by these transcription factors.
+FOS	drug	amphetamine	8974658	<b>Amphetamine</b> induction of c <strong>fos</strong> in the nucleus accumbens is not inhibited by glutamate antagonists.
+FOS	drug	amphetamine	8974658	Systemic administration of relatively high doses of <b>amphetamine</b> or cocaine induces expression of c <strong>fos</strong> in the rat striatum and nucleus accumbens.
+FOS	drug	cocaine	8974658	Systemic administration of relatively high doses of amphetamine or <b>cocaine</b> induces expression of c <strong>fos</strong> in the rat striatum and nucleus accumbens.
+FOS	drug	amphetamine	8974658	Therefore, it was determined if low doses of <b>amphetamine</b> capable of eliciting reward and sensitization increase levels of c <strong>Fos</strong> protein in the nucleus accumbens.
+FOS	addiction	reward	8974658	Therefore, it was determined if low doses of amphetamine capable of eliciting <b>reward</b> and sensitization increase levels of c <strong>Fos</strong> protein in the nucleus accumbens.
+FOS	addiction	sensitization	8974658	Therefore, it was determined if low doses of amphetamine capable of eliciting reward and <b>sensitization</b> increase levels of c <strong>Fos</strong> protein in the nucleus accumbens.
+FOS	drug	amphetamine	8974658	<b>Amphetamine</b>, 1 mg/kg, stimulated locomotor activity and increased the number of nucleus accumbens cells immunohistochemically positive for c <strong>Fos</strong> protein to approximately 800 cells per section from a control of approximately 100 cells per section.
+FOS	drug	amphetamine	8974658	Since glutamate antagonists modify various responses to <b>amphetamine</b>, it was then determined whether activation of glutamate receptors is involved in the induction of c <strong>Fos</strong> protein by low doses of <b>amphetamine</b>.
+FOS	drug	amphetamine	8974658	When given before <b>amphetamine</b>, both locomotor activity and extent of c <strong>fos</strong> induction were greater than from <b>amphetamine</b> alone.
+FOS	drug	amphetamine	8974658	When given before <b>amphetamine</b>, locomotor activity was completely attenuated, and the extent of c <strong>fos</strong> induction was greater than from <b>amphetamine</b> alone.
+FOS	drug	amphetamine	8974658	We conclude that low doses of <b>amphetamine</b> do increase abundance of c <strong>Fos</strong> protein in the nucleus accumbens.
+FOS	addiction	withdrawal	7476883	Phosphorylation of cyclic AMP response element binding protein and induction of c <strong>fos</strong> gene expression on <b>withdrawal</b> from chronic treatment with carbachol in NG108 15 cells.
+FOS	addiction	withdrawal	7476883	To determine whether this <b>withdrawal</b> induced increase in cAMP modifies gene expression, we studied phosphorylation of the cAMP response element binding protein (CREB) and expression of the c <strong>fos</strong> gene, known to contain a cAMP response element, in NG108 15 cells after abrupt <b>withdrawal</b> from chronic treatment with carbachol.
+FOS	addiction	withdrawal	7476883	In cells treated with carbachol for 48 hr, induction of <b>withdrawal</b> with the muscarinic antagonist atropine led to a small increase in intracellular cAMP concentration but an 11.6 fold increase in the phosphorylation of CREB and a 3.4 fold increase in accumulation of c <strong>fos</strong> mRNA.
+FOS	addiction	withdrawal	7476883	The adenylyl cyclase inhibitor 2',5' dideoxyadenosine, which attenuated the chronic carbachol induced increase in cAMP concentration, prevented the increased phosphorylation of CREB and the enhanced accumulation of c <strong>fos</strong> mRNA during atropine induced <b>withdrawal</b>.
+FOS	addiction	withdrawal	7476883	These results indicate that expression of the c <strong>fos</strong> gene is induced by the small increments in cAMP concentration that can occur in cells on <b>withdrawal</b> from chronic treatment with drugs such as muscarinic agonists.
+FOS	drug	opioid	8532189	The expression of immediate early genes (IEG)s c <strong>fos</strong>, c jun and zif/268 was studied during <b>naloxone</b> precipitated <b>morphine</b> withdrawal in various organs of the rat.
+FOS	addiction	withdrawal	8532189	The expression of immediate early genes (IEG)s c <strong>fos</strong>, c jun and zif/268 was studied during naloxone precipitated morphine <b>withdrawal</b> in various organs of the rat.
+FOS	drug	opioid	8532189	Increased levels of c <strong>fos</strong> and c jun mRNA were observed in the spinal cord at 40 min of <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	8532189	Increased levels of c <strong>fos</strong> and c jun mRNA were observed in the spinal cord at 40 min of morphine <b>withdrawal</b>.
+FOS	drug	cocaine	8539319	The effects of the kappa agonist U 50,488 on <b>cocaine</b> induced conditioned and unconditioned behaviors and <strong>Fos</strong> immunoreactivity.
+FOS	drug	opioid	8539319	The ability of kappa <b>opioid</b> agonists to modulate dopamine mediated behavior and <strong>Fos</strong> immunoreactivity was assessed in adult rats.
+FOS	addiction	reward	8539319	One hour after <b>CPP</b> testing, rats were killed and <strong>Fos</strong> immunoreactivity was assessed.
+FOS	drug	cocaine	8539319	Rats conditioned with <b>cocaine</b>, but not U 50,488, showed increased <strong>Fos</strong> activity in the anterior cingulate cortex, piriform cortex, lateral septal area, and olfactory tubercles.
+FOS	drug	cocaine	8539319	When considered together, these results suggest that U 50,488 was effective at blocking the unconditioned and conditioned effects of <b>cocaine</b>, as well as <b>cocaine</b> induced neuronal activity (as measured by <strong>Fos</strong> induction).
+FOS	drug	alcohol	7579706	The fall in DG production caused by <b>ethanol</b> and propranolol was accompanied by inhibition of GnRH induced c <strong>fos</strong> expression, whereas agonist induced luteinizing hormone release was not affected.
+FOS	drug	alcohol	7579706	In contrast to their inhibitory actions on GnRH induced early gene expression, neither <b>ethanol</b> nor propranolol affected ET 1 induced c <strong>fos</strong> expression, or GnRH  and ET 1 induced inositol trisphosphate/Ca2+ signaling.
+FOS	addiction	sensitization	7637573	The c <strong>fos</strong> response to D1 receptor activation in adults requires a previous <b>sensitization</b> of dopaminergic receptors by chronic treatment with reserpine or by lesion of the nigro striatal pathway.
+FOS	drug	opioid	7637573	The distribution of this transient c <strong>fos</strong> response corresponded to the early striosomal compartment since it matched with the regions of intense mu <b>opioid</b> and dopamine D1 receptor binding, as assessed by autoradiography performed on adjacent sections.
+FOS	drug	alcohol	7648269	Activation and desensitization of <strong>Fos</strong> immunoreactivity in the rat brain following <b>ethanol</b> administration.
+FOS	drug	alcohol	7648269	Following intraperitoneal injection of <b>ethanol</b> (16% w/v), <strong>Fos</strong> immunoreactivity was induced in several rat brain areas including the bed nucleus of the stria terminalis, paraventricular hypothalamic nucleus, the central nucleus of amygdala, Edinger Westphal nucleus, locus coeruleus nucleus and parabrachial nucleus.
+FOS	drug	alcohol	7648269	<strong>Fos</strong> immunoreactivity in the supraoptic nucleus appeared only when a higher concentration of <b>ethanol</b> was injected.
+FOS	drug	alcohol	7648269	Repeated administration of <b>ethanol</b> twice daily for 17 or 24 days resulted in a desensitization of <strong>Fos</strong> immunoreactivity in these nuclei.
+FOS	drug	alcohol	7648269	These data suggest that induction of <strong>Fos</strong> immunoreactivity can be used to determine the sites at which <b>ethanol</b> acts on the brain, and may provide important information about the mechanisms underlying the tolerance and physical dependence of <b>alcohol</b> usage.
+FOS	addiction	dependence	7648269	These data suggest that induction of <strong>Fos</strong> immunoreactivity can be used to determine the sites at which ethanol acts on the brain, and may provide important information about the mechanisms underlying the tolerance and physical <b>dependence</b> of alcohol usage.
+FOS	drug	opioid	7624831	NMDA antagonists and clonidine block c <strong>fos</strong> expression during <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	7624831	NMDA antagonists and clonidine block c <strong>fos</strong> expression during morphine <b>withdrawal</b>.
+FOS	drug	alcohol	7624831	Induction of c <strong>fos</strong> in certain CNS regions occurs following <b>naltrexone</b> precipitated withdrawal in morphine dependent rats.
+FOS	drug	opioid	7624831	Induction of c <strong>fos</strong> in certain CNS regions occurs following naltrexone precipitated withdrawal in <b>morphine</b> dependent rats.
+FOS	addiction	withdrawal	7624831	Induction of c <strong>fos</strong> in certain CNS regions occurs following naltrexone precipitated <b>withdrawal</b> in morphine dependent rats.
+FOS	drug	opioid	7624831	We determined the levels of c <strong>fos</strong> mRNA by solution hybridization in several brain regions in control and <b>morphine</b> dependent rats following pretreatment with saline, MK801 (1 mg/kg, s.c.), LY274614 (100 mg/kg, i.p.
+FOS	drug	opioid	7624831	<b>Morphine</b> treatment increased c <strong>fos</strong> mRNA levels in striatum (STR) and amygdala (AMY).
+FOS	drug	alcohol	7624831	<b>Naltrexone</b> did not alter c <strong>fos</strong> mRNA levels in placebo treated rats.
+FOS	drug	alcohol	7624831	However, <b>naltrexone</b> increased c <strong>fos</strong> mRNA levels in morphine dependent rats in the nucleus accumbens (NA), frontal cortex (FC), AMY, and hippocampus (HIP) but not in STR or spinal cord.
+FOS	drug	opioid	7624831	However, naltrexone increased c <strong>fos</strong> mRNA levels in <b>morphine</b> dependent rats in the nucleus accumbens (NA), frontal cortex (FC), AMY, and hippocampus (HIP) but not in STR or spinal cord.
+FOS	drug	amphetamine	7477877	Administration of the indirect dopamine agonist <b>amphetamine</b> increased <strong>Fos</strong> expression in the intact striatum, but not in the ipsilateral (lesioned) striatum or globus pallidus, and did not sensitize (prime) animals to behavioural effects of SKF 38393.
+FOS	drug	alcohol	7542145	C <strong>Fos</strong> expression induced by <b>naltrexone</b> precipitated withdrawal was examined in the brainstem of freely moving morphine dependent rats pretreated with clonidine or saline before injection of the opioid antagonist.
+FOS	drug	opioid	7542145	C <strong>Fos</strong> expression induced by naltrexone precipitated withdrawal was examined in the brainstem of freely moving <b>morphine</b> dependent rats pretreated with clonidine or saline before injection of the <b>opioid</b> antagonist.
+FOS	addiction	withdrawal	7542145	C <strong>Fos</strong> expression induced by naltrexone precipitated <b>withdrawal</b> was examined in the brainstem of freely moving morphine dependent rats pretreated with clonidine or saline before injection of the opioid antagonist.
+FOS	drug	opioid	7542145	<b>Morphine</b> withdrawal without clonidine treatment significantly increased the number of <strong>Fos</strong> like immunoreactive (<strong>Fos</strong> LIR) cells in the RVLM and LC.
+FOS	addiction	withdrawal	7542145	Morphine <b>withdrawal</b> without clonidine treatment significantly increased the number of <strong>Fos</strong> like immunoreactive (<strong>Fos</strong> LIR) cells in the RVLM and LC.
+FOS	addiction	withdrawal	7542145	reduced the number of <b>withdrawal</b> activated <strong>Fos</strong> LIR cells in LC by 81%.
+FOS	drug	opioid	7542145	Further, a very large proportion of RVLM neurons that expressed c <strong>Fos</strong> during <b>morphine</b> withdrawal (83%) were immunoreactive for alpha 2A adrenergic receptors.
+FOS	addiction	withdrawal	7542145	Further, a very large proportion of RVLM neurons that expressed c <strong>Fos</strong> during morphine <b>withdrawal</b> (83%) were immunoreactive for alpha 2A adrenergic receptors.
+FOS	drug	amphetamine	7718243	Surprisingly, following chronic administration of <b>amphetamine</b>, levels of phosphorylated CREB are increased above basal in rat striatum in vivo, whereas c <strong>fos</strong> mRNA is suppressed below basal levels.
+FOS	addiction	aversion	7619322	Two experiments used c <strong>fos</strong> expression as a marker of spinal nociceptive processing to study the neural correlates of hypoalgesic responses to conditioned stimuli (CSs) paired with an <b>aversive</b> event.
+FOS	addiction	aversion	7619322	Compared with control rats either not conditioned or conditioned in one environment but tested elsewhere, there were significantly fewer <strong>Fos</strong> ir neurons in the spinal cords of rats displaying hypoalgesic responses when tested in the presence of <b>aversive</b> CSs.
+FOS	drug	opioid	7619322	<b>Naloxone</b> abolished hypoalgesic responses and reinstated spinal <strong>Fos</strong> expression, indicating that aversive CSs activated <b>opioid</b> based antinociceptive mechanisms.
+FOS	addiction	aversion	7619322	Naloxone abolished hypoalgesic responses and reinstated spinal <strong>Fos</strong> expression, indicating that <b>aversive</b> CSs activated opioid based antinociceptive mechanisms.
+FOS	drug	amphetamine	7617160	Acute and chronic <b>amphetamine</b> treatments differently regulate neuropeptide messenger RNA levels and <strong>Fos</strong> immunoreactivity in rat striatal neurons.
+FOS	drug	amphetamine	7617160	In this paper, we investigated the effects of acute (1.5 or 5 mg/kg) and chronic (5 mg/kg/day for 14 days) <b>amphetamine</b> treatment on locomotor activity, stereotypy, <strong>Fos</strong> immunoreactivity and messenger RNA levels of molecules implicated in dopamine transmission in the rat striatum and substantia nigra.
+FOS	drug	amphetamine	7617160	A double labeling procedure with <strong>Fos</strong> immunohistochemistry coupled with in situ hybridization demonstrated that acute <b>amphetamine</b> treatment induces <strong>Fos</strong> immunoreactivity predominantly in striatal neurons expressing substance P messenger RNA (77.07 +/  1.42%).
+FOS	drug	amphetamine	7617160	In chronic <b>amphetamine</b> treated rats, 56.21 +/  1.32% of the <strong>Fos</strong> immunoreactive neurons expressed substance P messenger RNA while 52.12 +/  1.84% expressed preproenkephalin A messenger RNA.
+FOS	drug	amphetamine	7617160	<b>Amphetamine</b> treatments induced <strong>Fos</strong> immunoreactivity in the substantia nigra in non dopamine neurons.
+FOS	drug	amphetamine	7617160	preproenkephalin A and substance P neurons) and the number of <strong>Fos</strong> immunoreactive neurons is reduced as compared with acute; (3) neuropeptide messenger RNA levels, but not dopamine receptor messenger RNAs, are affected in the response to acute or chronic treatment with <b>amphetamine</b>.
+FOS	drug	cocaine	7609608	Several studies have demonstrated that <b>cocaine</b> increases preprodynorphin, c <strong>fos</strong>, and zif/268 mRNAs in rat dorsal striatum.
+FOS	addiction	intoxication	7609608	Therefore, we used a '<b>binge</b>' paradigm to evaluate changes in mRNA for preprodynorphin, preproenkephalin, c <strong>fos</strong> and zif/268.
+FOS	drug	cocaine	7609608	These data indicate that (1) c <strong>fos</strong>, zif/268 and preprodynorphin mRNAs are differentially regulated in dorsal striatum, (2) behavioral tolerance results from chronic binges with 10 and 20 mg/kg <b>cocaine</b> and (3) the preprodynorphin genomic response exhibits tolerance to chronic high dose, but not low dose, <b>cocaine</b> binges.
+FOS	drug	amphetamine	7606439	c <strong>Fos</strong> induction in response to taste stimuli previously paired with <b>amphetamine</b> or LiCl during taste aversion learning.
+FOS	addiction	aversion	7606439	c <strong>Fos</strong> induction in response to taste stimuli previously paired with amphetamine or LiCl during taste <b>aversion</b> learning.
+FOS	drug	amphetamine	7606439	c <strong>Fos</strong> immunohistochemistry was used to define brain regions activated during drug administration and during expression of a CTA using either <b>amphetamine</b> or LiCl as the US drug.
+FOS	addiction	aversion	7606439	c <strong>Fos</strong> immunohistochemistry was used to define brain regions activated during drug administration and during expression of a <b>CTA</b> using either amphetamine or LiCl as the US drug.
+FOS	drug	amphetamine	7606439	Administration of LiCl induced dense c <strong>Fos</strong> like immunoreactivity (c FLI) in the nucleus of the solitary tract (NTS) while <b>amphetamine</b> induced only light staining in this area.
+FOS	addiction	aversion	7606439	This suggests that the pattern of c <strong>Fos</strong> expression to a taste CS after conditioning is characteristic of <b>aversion</b> conditioning, in general, and appears not to represent a matching of the conditioned response to specific unconditioned effects of the drug.
+FOS	drug	amphetamine	7784961	This study illustrates how a 2 week, twice daily 7.5 mg/kg d <b>amphetamine</b> or saline regimen alters rat brain regional expression of transcription factor genes, including c <strong>fos</strong>, <strong>fos</strong> B, jun B, c jun, and zif 268, and seeks potential correlations between those changes and alterations in neurotransmitter levels and behavioral novelty responses.
+FOS	drug	opioid	7540319	In contrast, mRNA levels for c <strong>fos</strong> were dramatically elevated in the LC following <b>naloxone</b> precipitated withdrawal.
+FOS	addiction	withdrawal	7540319	In contrast, mRNA levels for c <strong>fos</strong> were dramatically elevated in the LC following naloxone precipitated <b>withdrawal</b>.
+FOS	drug	opioid	7755894	NMDA and D1 receptors mediate induction of c <strong>fos</strong> and junB genes in striatum following <b>morphine</b> administration: implications for studies of memory.
+FOS	drug	opioid	7755894	The c <strong>fos</strong> and junB immediate early genes (IEGs) were induced in neurons of the medial and ventral striatum following administration of <b>morphine</b>.
+FOS	drug	opioid	7755894	The striatal induction of c <strong>fos</strong> and junB mRNA and <strong>Fos</strong> protein was blocked by <b>naloxone</b>, the D1 dopamine (DA) receptor antagonists, SCH23390 and SCH39166, and the N methyl D aspartate (NMDA) glutamate receptor antagonist, MK801.
+FOS	drug	opioid	7755894	SCH23390 and MK801 did not block <b>morphine</b> induction of c <strong>fos</strong> and junB in septum.
+FOS	drug	amphetamine	7755894	Since the pattern of the morphine induction of c <strong>fos</strong> and junB in striatum and nucleus accumbens was similar to that observed with cocaine and <b>amphetamine</b> [2,18,45,51], these data support current concepts that limbic striatum and nucleus accumbens are among the brain regions that mediate drug abuse [9,10,23,27,49].
+FOS	drug	cocaine	7755894	Since the pattern of the morphine induction of c <strong>fos</strong> and junB in striatum and nucleus accumbens was similar to that observed with <b>cocaine</b> and amphetamine [2,18,45,51], these data support current concepts that limbic striatum and nucleus accumbens are among the brain regions that mediate drug abuse [9,10,23,27,49].
+FOS	drug	opioid	7755894	Since the pattern of the <b>morphine</b> induction of c <strong>fos</strong> and junB in striatum and nucleus accumbens was similar to that observed with cocaine and amphetamine [2,18,45,51], these data support current concepts that limbic striatum and nucleus accumbens are among the brain regions that mediate drug abuse [9,10,23,27,49].
+FOS	addiction	addiction	7755894	The <strong>Fos</strong> induced by this simultaneous activation of NMDA and D1 receptors should lead to long term changes of gene expression that might also be involved in changes of brain circuits that could form the basis for 'memories' relating to prior exposure to <b>addictive</b> drugs.
+FOS	addiction	withdrawal	7746492	Increased <strong>fos</strong> like immunoreactivity in the periaqueductal gray of anaesthetised rats during opiate <b>withdrawal</b>.
+FOS	drug	opioid	7746492	Staining of c <strong>fos</strong> like immunoreactivity (CFIR) in neurones was used to study neuronal activation within subdivisions of periaqueductal gray (PAG), and in locus coeruleus and ventral tegmental area during opiate withdrawal in awake and anaesthetised, <b>morphine</b> dependent rats.
+FOS	addiction	withdrawal	7746492	Staining of c <strong>fos</strong> like immunoreactivity (CFIR) in neurones was used to study neuronal activation within subdivisions of periaqueductal gray (PAG), and in locus coeruleus and ventral tegmental area during opiate <b>withdrawal</b> in awake and anaesthetised, morphine dependent rats.
+FOS	addiction	withdrawal	7746492	Induction of c <strong>fos</strong> in lateral and ventrolateral PAG during <b>withdrawal</b> is consistent with known functions of these regions, involving the integration of autonomic and somatic components of defensive and escape behaviours which are characteristic signs of opiate <b>withdrawal</b>.
+FOS	drug	amphetamine	8535862	Roles of dopamine D1 receptors in striatal <strong>fos</strong> protein induction associated with <b>methamphetamine</b> behavioral sensitization in rats.
+FOS	addiction	sensitization	8535862	Roles of dopamine D1 receptors in striatal <strong>fos</strong> protein induction associated with methamphetamine behavioral <b>sensitization</b> in rats.
+FOS	drug	amphetamine	8535862	To elucidate the roles of dopamine D1 and D2 receptors in mediating strial <strong>Fos</strong> protein induction and behavioral sensitization after <b>methamphetamine</b> administration, we examined the effects of the D1 receptor antagonist SCH 23390 and D2 receptor antagonist sulpiride on these phenomena in rats.
+FOS	addiction	sensitization	8535862	To elucidate the roles of dopamine D1 and D2 receptors in mediating strial <strong>Fos</strong> protein induction and behavioral <b>sensitization</b> after methamphetamine administration, we examined the effects of the D1 receptor antagonist SCH 23390 and D2 receptor antagonist sulpiride on these phenomena in rats.
+FOS	drug	amphetamine	8535862	Intraperitoneal administration of 5.0 mg/kg <b>methamphetamine</b> produced a significant increase in <strong>Fos</strong> immunoreactive cells in the medial striatum.
+FOS	drug	amphetamine	8535862	Pretreatment with SCH 23390 (0.32 mg/kg IP) suppressed significantly the expression of striatal <strong>Fos</strong> protein and the development of acute behavioral sensitization following a single injection of 5.0 mg/kg <b>methamphetamine</b>.
+FOS	addiction	sensitization	8535862	Pretreatment with SCH 23390 (0.32 mg/kg IP) suppressed significantly the expression of striatal <strong>Fos</strong> protein and the development of acute behavioral <b>sensitization</b> following a single injection of 5.0 mg/kg methamphetamine.
+FOS	drug	amphetamine	8535862	Sulpiride (50 mg/kg IP) was also effective in suppressing <b>methamphetamine</b> behavioral sensitization, but did not affect the striatal <strong>Fos</strong> induction.
+FOS	addiction	sensitization	8535862	Sulpiride (50 mg/kg IP) was also effective in suppressing methamphetamine behavioral <b>sensitization</b>, but did not affect the striatal <strong>Fos</strong> induction.
+FOS	drug	amphetamine	8535862	These results suggest that dopamine D1 receptor mediated mechanisms are involved in the striatal <strong>Fos</strong> protein induction associated with behavioral sensitization following exposure to <b>methamphetamine</b>.
+FOS	addiction	sensitization	8535862	These results suggest that dopamine D1 receptor mediated mechanisms are involved in the striatal <strong>Fos</strong> protein induction associated with behavioral <b>sensitization</b> following exposure to methamphetamine.
+FOS	drug	opioid	7838131	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal, a model of <b>opioid</b> dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+FOS	addiction	dependence	7838131	Naloxone precipitated morphine withdrawal, a model of opioid <b>dependence</b>, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+FOS	addiction	withdrawal	7838131	Naloxone precipitated morphine <b>withdrawal</b>, a model of opioid dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+FOS	addiction	dependence	7838131	Rapid increases in c <strong>fos</strong>, <strong>fos</strong> B, jun B, and c jun mRNA levels accompany withdrawal, with the relative level of induction correlating with the severity of physical <b>dependence</b>.
+FOS	addiction	withdrawal	7838131	Rapid increases in c <strong>fos</strong>, <strong>fos</strong> B, jun B, and c jun mRNA levels accompany <b>withdrawal</b>, with the relative level of induction correlating with the severity of physical dependence.
+FOS	addiction	withdrawal	7838131	<strong>AP 1</strong> DNA binding activity and dimer composition also exhibited regulation after <b>withdrawal</b>, presumably as a result of both transcriptional and post translational events.
+FOS	drug	opioid	7838131	Thus, <b>morphine</b> dependence results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+FOS	addiction	dependence	7838131	Thus, morphine <b>dependence</b> results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+FOS	drug	cocaine	7633900	Quantitative in situ hybridization revealed that <b>cocaine</b> self administration increased levels of preprodynorphin, but not preproenkephalin, c <strong>fos</strong>, or zif/268 mRNAs in a patchy pattern in the dorsal striatum.
+FOS	drug	cocaine	7633900	These data demonstrate that the regulation of preprodynorphin gene expression is dissociable from that of c <strong>fos</strong> and zif/268 in dorsal striatum following short term <b>cocaine</b> self administration.
+FOS	drug	amphetamine	7886627	The role of N methyl D aspartate (NMDA) excitatory amino acid receptors in D <b>amphetamine</b> (<b>AMPH</b>) induced behavioral changes and increased expression of the nuclear transcription factors, c <strong>fos</strong> and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.
+FOS	drug	amphetamine	7882006	NMDA receptor mediated expression of <strong>Fos</strong> protein in the rat striatum following <b>methamphetamine</b> administration: relation to behavioral sensitization.
+FOS	addiction	sensitization	7882006	NMDA receptor mediated expression of <strong>Fos</strong> protein in the rat striatum following methamphetamine administration: relation to behavioral <b>sensitization</b>.
+FOS	drug	amphetamine	7882006	In order to clarify the possible involvement of N methyl D aspartate (NMDA) receptors in mediating striatal <strong>Fos</strong> protein induction and behavioral sensitization after <b>methamphetamine</b> administration, we examined the effects of non competitive NMDA receptor antagonist MK 801 on these phenomena in rats.
+FOS	addiction	sensitization	7882006	In order to clarify the possible involvement of N methyl D aspartate (NMDA) receptors in mediating striatal <strong>Fos</strong> protein induction and behavioral <b>sensitization</b> after methamphetamine administration, we examined the effects of non competitive NMDA receptor antagonist MK 801 on these phenomena in rats.
+FOS	drug	amphetamine	7882006	A single administration of 1.0 and 5.0 mg/kg <b>methamphetamine</b> resulted in a dose dependent increase in <strong>Fos</strong> immunoreactive cells in the medial striatum.
+FOS	drug	amphetamine	7882006	Pretreatment with 1.0 mg/kg MK 801 completely prevented both the expression of striatal <strong>Fos</strong> protein and the development of acute behavioral sensitization following a single injection of 5.0 mg/kg <b>methamphetamine</b>.
+FOS	addiction	sensitization	7882006	Pretreatment with 1.0 mg/kg MK 801 completely prevented both the expression of striatal <strong>Fos</strong> protein and the development of acute behavioral <b>sensitization</b> following a single injection of 5.0 mg/kg methamphetamine.
+FOS	drug	amphetamine	7882006	These results suggest that NMDA receptor mediated mechanisms contribute to the expression of striatal <strong>Fos</strong> protein associated with behavioral sensitization that follows exposure to <b>methamphetamine</b>.
+FOS	addiction	sensitization	7882006	These results suggest that NMDA receptor mediated mechanisms contribute to the expression of striatal <strong>Fos</strong> protein associated with behavioral <b>sensitization</b> that follows exposure to methamphetamine.
+FOS	drug	cocaine	7969045	One early cellular response to <b>cocaine</b> administration is a brain region specific alteration in the transcriptional pattern of immediate early genes belonging to the <strong>Fos</strong>/Jun family of nucleotide sequence specific [activator protein 1 (AP 1)] DNA binding proteins.
+FOS	drug	cocaine	7969045	One early cellular response to <b>cocaine</b> administration is a brain region specific alteration in the transcriptional pattern of immediate early genes belonging to the <strong>Fos</strong>/Jun family of nucleotide sequence specific [activator protein 1 (<strong>AP 1</strong>)] DNA binding proteins.
+FOS	drug	cocaine	7969045	The work described here compares <b>cocaine</b> induced transcriptional regulation of immediate early gene mRNA levels, as well as <strong>AP 1</strong> DNA binding activity, within the striatum and cerebellum.
+FOS	drug	cocaine	7969045	In the striatum, acute <b>cocaine</b> administration increases cellular levels of c <strong>fos</strong> and jun B mRNA, whereas transcriptional effects in the cerebellum are limited to c <strong>fos</strong> mRNA.
+FOS	drug	cocaine	7969045	After chronic <b>cocaine</b> treatment a desensitization of c <strong>fos</strong> mRNA induction is observed in the striatum, with sensitization of the same transcriptional effect occurring in the cerebellum.
+FOS	addiction	sensitization	7969045	After chronic cocaine treatment a desensitization of c <strong>fos</strong> mRNA induction is observed in the striatum, with <b>sensitization</b> of the same transcriptional effect occurring in the cerebellum.
+FOS	drug	cocaine	7969045	Gel retention analysis using antibodies to the various <strong>Fos</strong> and Jun proteins was used to characterize <b>cocaine</b> dependent alterations in the composition of striatal and cerebellar AP 1 DNA binding complexes.
+FOS	drug	cocaine	7969045	Gel retention analysis using antibodies to the various <strong>Fos</strong> and Jun proteins was used to characterize <b>cocaine</b> dependent alterations in the composition of striatal and cerebellar <strong>AP 1</strong> DNA binding complexes.
+FOS	drug	cocaine	7969045	In striatum, <b>cocaine</b> increases the relative levels of c <strong>Fos</strong>, <strong>Fos</strong> B, Jun B, and Jun D proteins that bind the AP 1 DNA sequence element, whereas in the cerebellum only c <strong>Fos</strong> and Jun D binding activities are increased.
+FOS	drug	cocaine	7969045	In striatum, <b>cocaine</b> increases the relative levels of c <strong>Fos</strong>, <strong>Fos</strong> B, Jun B, and Jun D proteins that bind the <strong>AP 1</strong> DNA sequence element, whereas in the cerebellum only c <strong>Fos</strong> and Jun D binding activities are increased.
+FOS	drug	cocaine	7854036	Previous studies have demonstrated that the IEGs NGFI A (zif268) and c <strong>fos</strong> are each rapidly induced in the caudate putamen (CP) by treatment with the indirect dopamine agonist <b>cocaine</b>.
+FOS	drug	cocaine	7854036	Levels of NGFI A and c <strong>fos</strong> were measured in the CP of rats by Northern blot analysis, which confirmed that <b>cocaine</b> induced increases of NGFI A and c <strong>fos</strong> mRNA lasts for several hours after drug administration.
+FOS	drug	cocaine	7854036	Immediately following this induction, however, there is a prolonged period during which a marked reduction in the relative amount of mRNA for both NGFI A and c <strong>fos</strong> is observed in <b>cocaine</b> treated animals when compared to matched, vehicle treated controls.
+FOS	drug	alcohol	7839314	Acute administration of <b>alcohol</b> blocks cocaine induced striatal c <strong>fos</strong> immunoreactivity protein in the rat.
+FOS	drug	cocaine	7839314	Acute administration of alcohol blocks <b>cocaine</b> induced striatal c <strong>fos</strong> immunoreactivity protein in the rat.
+FOS	drug	cocaine	7839314	Immediate early genes, such as c <strong>fos</strong>, are induced in the brain by <b>cocaine</b> and other psychotropic drugs.
+FOS	drug	alcohol	7839314	Because <b>alcohol</b> selectively blocks NMDA receptor function, we determined the ability of <b>alcohol</b> to block the expression of c <strong>fos</strong> normally induced by systemic cocaine exposure in perikarya of the rat striatum.
+FOS	drug	cocaine	7839314	Because alcohol selectively blocks NMDA receptor function, we determined the ability of alcohol to block the expression of c <strong>fos</strong> normally induced by systemic <b>cocaine</b> exposure in perikarya of the rat striatum.
+FOS	drug	alcohol	7839314	Separate administration of three doses of <b>alcohol</b> alone (1, 2, or 3 g/kg) was ineffectual in inducing <strong>FOS</strong> like protein in this or other regions of the rat brain.
+FOS	drug	alcohol	7839314	Furthermore, the blockade of cocaine induced <strong>FOS</strong> like protein by <b>alcohol</b> occurred at a dose which produced a blood <b>alcohol</b> concentration of approximately 180 mg/dl (40 mM), comparable to that detected in intoxicating humans.
+FOS	drug	cocaine	7839314	Furthermore, the blockade of <b>cocaine</b> induced <strong>FOS</strong> like protein by alcohol occurred at a dose which produced a blood alcohol concentration of approximately 180 mg/dl (40 mM), comparable to that detected in intoxicating humans.
+FOS	drug	amphetamine	8083758	It has recently been demonstrated that <b>amphetamine</b> regulates the expression of several genes, including c <strong>fos</strong>, via dopamine D1 receptors in rat striatum.
+FOS	drug	amphetamine	8083758	In addition, we show by antisense injection that CREB is necessary for c <strong>fos</strong> induction by <b>amphetamine</b> in vivo.
+FOS	drug	opioid	8078918	<b>Morphine</b> induces c <strong>fos</strong> and junB in striatum and nucleus accumbens via D1 and N methyl D aspartate receptors.
+FOS	drug	opioid	8078918	<b>Morphine</b> induced the c <strong>fos</strong> and junB immediate early genes in neurons of the medial and ventral striatum and nucleus accumbens.
+FOS	drug	opioid	8078918	Induction of c <strong>fos</strong> and junB mRNA and <strong>Fos</strong> protein was blocked by <b>naloxone</b>, the D1 dopamine (DA) receptor antagonists SCH23390 and SCH39166, and the N methyl D aspartate (NMDA) glutamate receptor antagonist MK801.
+FOS	drug	opioid	8078918	SCH23390 attenuated <b>morphine</b> induction of AP 1 binding in striatum, suggesting that c <strong>fos</strong> and junB contribute to AP 1 binding.
+FOS	drug	opioid	8078918	SCH23390 attenuated <b>morphine</b> induction of <strong>AP 1</strong> binding in striatum, suggesting that c <strong>fos</strong> and junB contribute to <strong>AP 1</strong> binding.
+FOS	drug	opioid	8078918	SCH23390 and MK801 did not block <b>morphine</b> induction of c <strong>fos</strong> and junB in septum.
+FOS	drug	amphetamine	8078918	Since the morphine induction of c <strong>fos</strong> and junB in striatum and nucleus accumbens (NA) was similar to that observed with cocaine and <b>amphetamine</b>, these data support current concepts that limbic striatum and NA are among the brain regions that mediate drug abuse.
+FOS	drug	cocaine	8078918	Since the morphine induction of c <strong>fos</strong> and junB in striatum and nucleus accumbens (NA) was similar to that observed with <b>cocaine</b> and amphetamine, these data support current concepts that limbic striatum and NA are among the brain regions that mediate drug abuse.
+FOS	drug	opioid	8078918	Since the <b>morphine</b> induction of c <strong>fos</strong> and junB in striatum and nucleus accumbens (NA) was similar to that observed with cocaine and amphetamine, these data support current concepts that limbic striatum and NA are among the brain regions that mediate drug abuse.
+FOS	addiction	reward	8078918	Furthermore, since DA and NMDA receptors may mediate opiate <b>reward</b> and opiate induction of c <strong>fos</strong> and junB, the DA/NMDA regulation of c <strong>fos</strong> and junB and their target genes may produce long term changes in the striatal and NA circuits that contribute to opiate drug abuse.
+FOS	drug	amphetamine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with <b>methamphetamine</b>, cocaine and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of <b>methamphetamine</b> and cocaine, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+FOS	drug	cocaine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, <b>cocaine</b> and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and <b>cocaine</b>, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+FOS	drug	opioid	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, cocaine and <b>morphine</b>: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and cocaine, 2) CRE binding activity was decreased by chronic <b>morphine</b> treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic <b>morphine</b> treatment in the mouse cerebellum.
+FOS	drug	alcohol	7969881	The baseline expression of the gene c <strong>fos</strong> in the offspring of male <b>alcoholic</b> rats did not differ from the norm; however, a powerful increase in the expression of the gene c <strong>fos</strong> did appear in response to the administration of 2 g/kg of <b>ethanol</b>, in the absence of this effect in the control.
+FOS	drug	nicotine	7913201	<b>Nicotine</b> induced c <strong>fos</strong> expression in the striatum is mediated mostly by dopamine D1 receptor and is dependent on NMDA stimulation.
+FOS	drug	nicotine	7913201	To extend our understanding of <b>nicotine</b> and dopamine interactions, we mapped the pattern of c <strong>fos</strong> expression in the striatum as an important marker of some of the earliest changes that occur at gene transcription level.
+FOS	drug	nicotine	7913201	Acute <b>nicotine</b> injections in rats led to <strong>Fos</strong> expression more prominently in the caudatoputamen than in the nucleus accumbens in a dose dependent fashion.
+FOS	drug	nicotine	7913201	Injections of mecamylamine completely blocked <b>nicotine</b> induced <strong>Fos</strong> expression.
+FOS	drug	nicotine	7913201	Injections of the selective dopamine D1 antagonist SCH 23390, but not D2 antagonist YM 09151 2 or Clozapine, a drug with high affinity to D4 receptors, before <b>nicotine</b> injections, completely blocked <strong>Fos</strong> expression in the striatum.
+FOS	drug	nicotine	7913201	<b>Nicotine</b> induced <strong>Fos</strong> expression was also blocked completely by the NMDA receptor antagonists MK 801 and CPP.
+FOS	addiction	reward	7913201	Nicotine induced <strong>Fos</strong> expression was also blocked completely by the NMDA receptor antagonists MK 801 and <b>CPP</b>.
+FOS	drug	nicotine	7913201	These results suggest that <b>nicotine</b> induced <strong>Fos</strong> expression in the striatum is mediated mostly by dopamine D1 receptors and that the <strong>Fos</strong> expression is also dependent on N methyl D aspartate (NMDA) stimulation.
+FOS	drug	alcohol	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during ethanol <b>withdrawal</b>.
+FOS	drug	alcohol	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing ethanol <b>withdrawal</b>.
+FOS	drug	alcohol	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after ethanol <b>withdrawal</b>.
+FOS	drug	alcohol	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of ethanol <b>withdrawal</b>.
+FOS	drug	alcohol	8974322	The expression of the proteins (C <strong>FOS</strong> and C JUN) encoded by the immediate early genes c <strong>fos</strong> and c jun was investigated in the brains of rats undergoing <b>ethanol</b> withdrawal.
+FOS	addiction	withdrawal	8974322	The expression of the proteins (C <strong>FOS</strong> and C JUN) encoded by the immediate early genes c <strong>fos</strong> and c jun was investigated in the brains of rats undergoing ethanol <b>withdrawal</b>.
+FOS	addiction	withdrawal	8974322	Maximal C <strong>FOS</strong> expression occurred 15 hr after <b>withdrawal</b> while C JUN was maximal at 24 hr.
+FOS	addiction	withdrawal	8974322	Gel shift assays indicated the formation of <strong>AP 1</strong> binding factors in nuclear extracts of the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>withdrawal</b>.
+FOS	addiction	withdrawal	19912955	A large, transient increase in the expression of whole brain c <strong>fos</strong>, c jun, and zif/268 mRNA was observed 12 h after <b>withdrawal</b>, and expression of their protein products was detected 15 to 24 h after <b>withdrawal</b>.
+FOS	addiction	withdrawal	7902768	Autonomic areas of rat brain exhibit increased <strong>Fos</strong> like immunoreactivity during opiate <b>withdrawal</b> in rats.
+FOS	drug	opioid	7902768	We sought to identify the brain areas that might contribute to the increased autonomic activity seen during <b>morphine</b> withdrawal by mapping neuronal expression of c <strong>fos</strong> protein (<strong>Fos</strong>) and <strong>Fos</strong> related antigens.
+FOS	addiction	withdrawal	7902768	We sought to identify the brain areas that might contribute to the increased autonomic activity seen during morphine <b>withdrawal</b> by mapping neuronal expression of c <strong>fos</strong> protein (<strong>Fos</strong>) and <strong>Fos</strong> related antigens.
+FOS	drug	alcohol	7902768	Although some <strong>Fos</strong> LIR was seen in these areas in control rats (either morphine implanted, saline injected, or placebo implanted, saline or <b>naltrexone</b> injected), a significantly higher number of <strong>Fos</strong> LIR positive cells in NTS, CVL and RVL were seen after morphine withdrawal.
+FOS	drug	opioid	7902768	Although some <strong>Fos</strong> LIR was seen in these areas in control rats (either <b>morphine</b> implanted, saline injected, or placebo implanted, saline or naltrexone injected), a significantly higher number of <strong>Fos</strong> LIR positive cells in NTS, CVL and RVL were seen after <b>morphine</b> withdrawal.
+FOS	addiction	withdrawal	7902768	Although some <strong>Fos</strong> LIR was seen in these areas in control rats (either morphine implanted, saline injected, or placebo implanted, saline or naltrexone injected), a significantly higher number of <strong>Fos</strong> LIR positive cells in NTS, CVL and RVL were seen after morphine <b>withdrawal</b>.
+FOS	drug	opioid	7902768	Increased <strong>Fos</strong> LIR was also detected in the paraventricular nucleus of the hypothalamus and the amygdala of <b>morphine</b> withdrawn rats.
+FOS	drug	nicotine	8255178	Acute <b>nicotine</b> injections induce c <strong>fos</strong> mostly in non dopaminergic neurons of the midbrain of the rat.
+FOS	drug	nicotine	8255178	Acute <b>nicotine</b> injections resulted in prominent <strong>Fos</strong> like immunoreactivity ( LI) in the medial terminal nucleus of the accessory optic system, the interpeduncular nucleus, and in the caudal linear subnucleus of VTA.
+FOS	drug	nicotine	8255178	These results suggest that acute <b>nicotine</b> injections induce c <strong>fos</strong> expression mostly in non dopaminergic neurons of the ventral tegmental area of the rat and that <b>nicotine</b> induces c <strong>fos</strong> most intensely in the interpeduncular nucleus, the superior colliculus, and several other subnuclei of the accessory optic system.
+FOS	drug	psychedelics	19912927	In the experiments reported here, we examined the effects of the noncompetitive NMDA receptor antagonists <b>ketamine</b> (2 mg/kg; as an anesthetic mixture) and dizocilpine (MK 801; 1 mg/kg), as well as the competitive NMDA receptor antagonist, 3 (2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (CPP; 5 mg/kg), on the expression of <strong>fos</strong> like protein induced by dl fenfluramine (20 mg/kg), in the rat caudate putamen.
+FOS	addiction	reward	19912927	In the experiments reported here, we examined the effects of the noncompetitive NMDA receptor antagonists ketamine (2 mg/kg; as an anesthetic mixture) and dizocilpine (MK 801; 1 mg/kg), as well as the competitive NMDA receptor antagonist, 3 (2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (<b>CPP</b>; 5 mg/kg), on the expression of <strong>fos</strong> like protein induced by dl fenfluramine (20 mg/kg), in the rat caudate putamen.
+FOS	drug	cocaine	8099817	<b>Cocaine</b> self administration increases preprodynorphin, but not c <strong>fos</strong>, mRNA in rat striatum.
+FOS	drug	cocaine	8099817	The impact of <b>cocaine</b> self administration on the expression of striatal preprodynorphin and c <strong>fos</strong> mRNA was examined with in situ hybridization histochemistry.
+FOS	drug	cocaine	8099817	Expression of c <strong>fos</strong> mRNA in <b>cocaine</b> administering rats did not differ from that in controls in all structures examined.
+FOS	drug	cocaine	8099817	These results indicate that the expression of preprodynorphin, but not c <strong>fos</strong>, is upregulated in rat striatum as a consequence of <b>cocaine</b> self administration.
+FOS	drug	cocaine	8099817	Furthermore, these data indicate that the regulation of preprodynorphin is dissociable from the expression of c <strong>fos</strong> in rats exposed to repeated doses of <b>cocaine</b>.
+FOS	drug	amphetamine	8453468	Sensitization of c <strong>fos</strong> expression in rat striatum following multiple challenges with D <b>amphetamine</b>.
+FOS	addiction	sensitization	8453468	<b>Sensitization</b> of c <strong>fos</strong> expression in rat striatum following multiple challenges with D amphetamine.
+FOS	drug	amphetamine	8453468	D <b>Amphetamine</b> transiently stimulates the expression of the immediate early response gene, c <strong>fos</strong>, in rat striatal cell nuclei.
+FOS	drug	amphetamine	8453468	induced a significantly greater expression of <strong>Fos</strong> like immunoreactivity in striatum of rats treated three days previously with D <b>amphetamine</b> compared to rats treated three days previously with saline.
+FOS	drug	amphetamine	8453468	This sensitization of c <strong>fos</strong> expression following a repeated administration of D <b>amphetamine</b> indicates an increased activation of post synaptic elements in rat striatum.
+FOS	addiction	sensitization	8453468	This <b>sensitization</b> of c <strong>fos</strong> expression following a repeated administration of D amphetamine indicates an increased activation of post synaptic elements in rat striatum.
+FOS	drug	cocaine	8420627	<b>Cocaine</b> induced expression of striatal c <strong>fos</strong> in the rat is inhibited by NMDA receptor antagonists.
+FOS	drug	cocaine	8420627	To assess the possible involvement of NMDA receptors in mediating the expression of striatal c <strong>fos</strong> by <b>cocaine</b> injection, we investigated the effects of the noncompetitive NMDA receptor antagonists, ketamine and (+) 5 methyl 10,11 dihydro 5H dibenzo[a,d]cyclohepten 5,10 imine hydrogen maleate (MK 801), as well as the competitive NMDA receptor antagonist, 3 (2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (CPP), in the perikarya of <b>cocaine</b> treated rat brains.
+FOS	drug	psychedelics	8420627	To assess the possible involvement of NMDA receptors in mediating the expression of striatal c <strong>fos</strong> by cocaine injection, we investigated the effects of the noncompetitive NMDA receptor antagonists, <b>ketamine</b> and (+) 5 methyl 10,11 dihydro 5H dibenzo[a,d]cyclohepten 5,10 imine hydrogen maleate (MK 801), as well as the competitive NMDA receptor antagonist, 3 (2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (CPP), in the perikarya of cocaine treated rat brains.
+FOS	addiction	reward	8420627	To assess the possible involvement of NMDA receptors in mediating the expression of striatal c <strong>fos</strong> by cocaine injection, we investigated the effects of the noncompetitive NMDA receptor antagonists, ketamine and (+) 5 methyl 10,11 dihydro 5H dibenzo[a,d]cyclohepten 5,10 imine hydrogen maleate (MK 801), as well as the competitive NMDA receptor antagonist, 3 (2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (<b>CPP</b>), in the perikarya of cocaine treated rat brains.
+FOS	drug	cocaine	8420627	Pretreatment with MK 801 (1 mg/kg) or CPP (5 mg/kg) also interfered, albeit to a lesser extent, with the expression of c <strong>fos</strong> by <b>cocaine</b> in awake animals.
+FOS	addiction	reward	8420627	Pretreatment with MK 801 (1 mg/kg) or <b>CPP</b> (5 mg/kg) also interfered, albeit to a lesser extent, with the expression of c <strong>fos</strong> by cocaine in awake animals.
+FOS	drug	cocaine	8420627	These results indicate that <b>cocaine</b> induction of cellular c <strong>fos</strong> in the caudate putamen is mediated at least in part by NMDA sensitive receptors.
+FOS	drug	cocaine	8385579	The investigations have focused on the <strong>Fos</strong> Jun family of immediate early gene transcription factors, and the CREB family of transcription factors, as possible mediators of the effects of chronic opiate and <b>cocaine</b> exposure on regulation of neuronal gene expression.
+FOS	drug	alcohol	7748323	Chronic exposure to <b>ethanol</b> vapour did not increase c <strong>fos</strong> expression.
+FOS	drug	alcohol	7748323	However, <b>ethanol</b> withdrawn rats showed a marked increase in c <strong>fos</strong> expression.
+FOS	addiction	withdrawal	7748323	The <b>withdrawal</b> induced expression of c <strong>fos</strong> mRNA could be inhibited by prior administration of MK801.
+FOS	drug	alcohol	1306754	In descendants of white rats with chronic <b>alcoholic</b> intoxication, the contents of DA in the brain and blood plasma, characteristics of GABA and opiate brain receptors, the contents of cAMP and other substances were studied as well as the c <strong>fos</strong> gene expression.
+FOS	addiction	intoxication	1306754	In descendants of white rats with chronic alcoholic <b>intoxication</b>, the contents of DA in the brain and blood plasma, characteristics of GABA and opiate brain receptors, the contents of cAMP and other substances were studied as well as the c <strong>fos</strong> gene expression.
+FOS	drug	nicotine	1422856	Induction of c <strong>fos</strong> immunostaining in the rat brain after the systemic administration of <b>nicotine</b>.
+FOS	drug	nicotine	1422856	To search for evidence of altered neuronal gene expression in response to exposure to the highly addictive drug <b>nicotine</b>, rat brains were examined by immunocytochemistry for the <strong>fos</strong> protein after the systemic administration of <b>nicotine</b>.
+FOS	addiction	addiction	1422856	To search for evidence of altered neuronal gene expression in response to exposure to the highly <b>addictive</b> drug nicotine, rat brains were examined by immunocytochemistry for the <strong>fos</strong> protein after the systemic administration of nicotine.
+FOS	drug	nicotine	1422856	The drug was administered as an IV infusion over 1 h At a dose of 2 mg/kg, the most dramatic <b>nicotine</b> induced <strong>fos</strong> nuclear immunostaining was seen in central visual pathways, including the superficial superior colliculus and the medial terminal nu.
+FOS	drug	nicotine	1422856	Notably, many regions with high levels of <b>nicotine</b> binding sites, including the medial habenula, thalamus, substantia nigra, and ventral tegmental area, failed to express the c <strong>fos</strong> gene with this schedule of <b>nicotine</b> administration.
+FOS	drug	nicotine	1422856	A minimal increase in <strong>fos</strong> immunostaining was seen after a <b>nicotine</b> dose of 0.5 mg/kg, with a much greater response after 1 or 2 mg/kg.
+FOS	drug	nicotine	1422856	c <strong>fos</strong> expression was substantially attenuated in the superficial gray layer of superior colliculus, medial terminal nucleus of the accessory optic tract, and the interpeduncular nucleus by pretreatment with the centrally acting <b>nicotine</b> antagonist mecamylamine, 5 mg/kg IP, but not with the peripherally acting antagonist hexamethonium, 4 mg/kg IP.
+FOS	drug	nicotine	1422856	These observations identify a subset of central nervous system neurons that respond to <b>nicotine</b> with altered expression of the immediate early gene c <strong>fos</strong>.
+FOS	drug	cocaine	1403102	To understand better the neurobiology of <b>cocaine</b> induced environment specific conditioning, <strong>Fos</strong> expression was examined in the forebrain of rats exposed to an environment in which they had previously received <b>cocaine</b>.
+FOS	drug	cocaine	1403102	Consistent with its stimulant actions, <b>cocaine</b> produced an increase in locomotion that was accompanied by an increase in <strong>Fos</strong> expression within specific limbic regions (cingulate cortex, claustrum, piriform cortex, lateral septal nucleus, paraventricular nucleus of the thalamus, lateral habenula, and amygdala) as well as the basal ganglia (dorsomedial striatum and nucleus accumbens).
+FOS	drug	cocaine	1403102	Although the nucleus accumbens is necessary for the reinforcing and locomotor effects of <b>cocaine</b>, it does not exhibit a conditional <strong>Fos</strong> response, suggesting that different neural circuits are involved in the unconditioned and conditioned effects of <b>cocaine</b>.
+FOS	addiction	reward	1403102	Although the nucleus accumbens is necessary for the <b>reinforcing</b> and locomotor effects of cocaine, it does not exhibit a conditional <strong>Fos</strong> response, suggesting that different neural circuits are involved in the unconditioned and conditioned effects of cocaine.
+FOS	drug	cocaine	1631058	Regulation of immediate early gene expression and <strong>AP 1</strong> binding in the rat nucleus accumbens by chronic <b>cocaine</b>.
+FOS	drug	cocaine	1631058	We therefore examined changes in the mRNA levels for the IEGs c <strong>fos</strong>, c jun, fosB, junB, and zif268 in the NAc of rats treated acutely and chronically with <b>cocaine</b>.
+FOS	drug	cocaine	1631058	Similarly, levels of <strong>Fos</strong> like immunoreactivity, which are increased in the NAc by acute <b>cocaine</b>, were reduced to control levels in chronic <b>cocaine</b> treated rats.
+FOS	drug	cocaine	1631058	As would be expected from the RNA data and immunohistochemistry, acute <b>cocaine</b> administration increased <strong>AP 1</strong> binding activity in the NAc, an effect that reverted completely to control levels within 8 12 hr.
+FOS	drug	cocaine	1631058	In contrast, AP 1 binding activity in the NAc of animals treated chronically with <b>cocaine</b> remained elevated at acute levels 18 hr after the last chronic injection, a time at which c <strong>fos</strong> and c jun mRNA levels and <strong>Fos</strong> like immunoreactivity had returned to control values.
+FOS	drug	cocaine	1631058	In contrast, <strong>AP 1</strong> binding activity in the NAc of animals treated chronically with <b>cocaine</b> remained elevated at acute levels 18 hr after the last chronic injection, a time at which c <strong>fos</strong> and c jun mRNA levels and <strong>Fos</strong> like immunoreactivity had returned to control values.
+FOS	drug	cocaine	1631058	An additional acute <b>cocaine</b> challenge did not further increase <strong>AP 1</strong> binding.
+FOS	drug	cocaine	1631058	The data suggest that chronic <b>cocaine</b> treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of <b>cocaine</b> addiction.
+FOS	addiction	addiction	1631058	The data suggest that chronic cocaine treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of cocaine <b>addiction</b>.
+FOS	drug	psychedelics	1319800	To assess the specificity of these effects, we compared the effects on photic induction of <strong>Fos</strong> lir of several treatments: central injection of a competitive NMDA antagonist, CPP; central injection of a non NMDA antagonist, DNQX; and systemic injection of the non competitive NMDA antagonist, <b>ketamine</b>.
+FOS	addiction	reward	1319800	To assess the specificity of these effects, we compared the effects on photic induction of <strong>Fos</strong> lir of several treatments: central injection of a competitive NMDA antagonist, <b>CPP</b>; central injection of a non NMDA antagonist, DNQX; and systemic injection of the non competitive NMDA antagonist, ketamine.
+FOS	drug	psychedelics	1319800	Pretreatment with CPP (greater than 2 nmoles) or <b>ketamine</b> (greater than 100 mg/kg) caused a dose related inhibition of photic induction of <strong>Fos</strong> lir in portions of the SCN.
+FOS	addiction	reward	1319800	Pretreatment with <b>CPP</b> (greater than 2 nmoles) or ketamine (greater than 100 mg/kg) caused a dose related inhibition of photic induction of <strong>Fos</strong> lir in portions of the SCN.
+FOS	drug	alcohol	1355445	Brain structures activated during <b>ethanol</b> withdrawal have been mapped by visualizing c <strong>fos</strong> mRNA expression.
+FOS	addiction	withdrawal	1355445	Brain structures activated during ethanol <b>withdrawal</b> have been mapped by visualizing c <strong>fos</strong> mRNA expression.
+FOS	drug	alcohol	1355445	The regional distribution of c <strong>fos</strong> mRNA in brain during <b>ethanol</b> withdrawal can be mimicked by acute injection of N methyl D aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK 801.
+FOS	addiction	withdrawal	1355445	The regional distribution of c <strong>fos</strong> mRNA in brain during ethanol <b>withdrawal</b> can be mimicked by acute injection of N methyl D aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK 801.
+FOS	addiction	sensitization	1831151	Striatal c <strong>fos</strong> induction by drugs and stress in neonatally dopamine depleted rats given nigral transplants: importance of NMDA activation and relevance to <b>sensitization</b> phenomena.
+FOS	drug	amphetamine	1831151	As revealed by <strong>fos</strong> immunocytochemistry, <b>amphetamine</b> (<b>AMPH</b>) produced c <strong>fos</strong> induction in many cells of the medial two thirds of the striatum of normal rats, with patchy labeling in the lateral third.
+FOS	drug	amphetamine	1831151	In animals DA depleted at birth, few <strong>fos</strong> immunoreactive neurons were present in response to <b>AMPH</b>.
+FOS	drug	amphetamine	1831151	The N methyl D aspartate antagonist MK 801 also blocked c <strong>fos</strong> induction by <b>AMPH</b> within the medial striatum, but intensified c <strong>fos</strong> induction laterally in those animals with DA innervation.
+FOS	drug	amphetamine	1831151	A second set of experiments examined the functional importance of c <strong>fos</strong> induction in the <b>AMPH</b> sensitization of turning behavior that occurs in these animals.
+FOS	addiction	sensitization	1831151	A second set of experiments examined the functional importance of c <strong>fos</strong> induction in the AMPH <b>sensitization</b> of turning behavior that occurs in these animals.
+FOS	drug	amphetamine	1831151	Both <b>AMPH</b> and stress produced turning, but only <b>AMPH</b> produced widespread c <strong>fos</strong> induction, and stress induced turning only occurred after exposure to <b>AMPH</b>.
+FOS	addiction	sensitization	1831151	Thus the <b>sensitization</b> of transplant related behaviors is NMDA dependent and associated with c <strong>fos</strong> induction in host striatal neurons.
+FOS	drug	amphetamine	1682022	Directly acting dopamine agonists of the D1 type (SKF 38393, CY 208 243) and indirectly acting dopamine agonists (<b>amphetamine</b>, cocaine) all produce a rapid and transient increase in <strong>Fos</strong> protein levels in varying patterns in striatum and cerebral cortex.
+FOS	drug	cocaine	1682022	Directly acting dopamine agonists of the D1 type (SKF 38393, CY 208 243) and indirectly acting dopamine agonists (amphetamine, <b>cocaine</b>) all produce a rapid and transient increase in <strong>Fos</strong> protein levels in varying patterns in striatum and cerebral cortex.
+FOS	drug	amphetamine	1682022	Directly acting dopamine agonists only produce c <strong>fos</strong> activation in denervated (supersensitive) striatum whereas cocaine and <b>amphetamine</b> activate c <strong>fos</strong> in striatum in naive animals.
+FOS	drug	cocaine	1682022	Directly acting dopamine agonists only produce c <strong>fos</strong> activation in denervated (supersensitive) striatum whereas <b>cocaine</b> and amphetamine activate c <strong>fos</strong> in striatum in naive animals.
+FOS	addiction	addiction	1682022	Activation of c <strong>fos</strong> and other immediate early genes may play a part in the development of such long term dopamine related effects as dyskinetic movements and <b>addiction</b>.
+FOS	drug	opioid	18415163	Various processes such as expression of C <strong>fos</strong> like protein, modification of the spinal composition of endogenous <b>opioids</b>, and release of neuropeptides may be involved in this newly detected phenomenon.
+FOS	drug	amphetamine	2118661	<b>Amphetamine</b> and cocaine induce drug specific activation of the c <strong>fos</strong> gene in striosome matrix compartments and limbic subdivisions of the striatum.
+FOS	drug	cocaine	2118661	Amphetamine and <b>cocaine</b> induce drug specific activation of the c <strong>fos</strong> gene in striosome matrix compartments and limbic subdivisions of the striatum.
+FOS	addiction	addiction	2118661	Here we report that single doses of these drugs induce rapid expression of the nuclear proto oncogene c <strong>fos</strong> in the forebrain and particularly in the striatum, an extrapyramidal structure implicated in <b>addiction</b> and in long term drug induced changes in motor function.
+FOS	addiction	withdrawal	1701330	Induction of the c <strong>fos</strong> proto oncogene during opiate <b>withdrawal</b> in the locus coeruleus and other regions of rat brain.
+FOS	addiction	withdrawal	1701330	Precipitation of opiate <b>withdrawal</b> in rats, which is known to increase LC firing rates 4 fold, led to a two  to three fold increase in levels of mRNA and protein for c <strong>fos</strong> in the LC 1 2 h after initiation of <b>withdrawal</b>.
+FOS	drug	opioid	1701330	In contrast, levels of c <strong>fos</strong> expression were decreased in LC from rats treated acutely or chronically with <b>morphine</b> but not experiencing withdrawal, conditions under which LC firing rates are depressed.
+FOS	addiction	withdrawal	1701330	In contrast, levels of c <strong>fos</strong> expression were decreased in LC from rats treated acutely or chronically with morphine but not experiencing <b>withdrawal</b>, conditions under which LC firing rates are depressed.
+FOS	addiction	withdrawal	1701330	Similar regulation of c <strong>fos</strong> expression during opiate <b>withdrawal</b> was found in the amygdala, ventral tegmentum, nucleus accumbens, neostriatum, and cerebral cortex, but not in a number of other brain regions studied, which included the hippocampus, dorsal raphe, periaqueductal gray, and paragigantocellularis.
+FOS	addiction	withdrawal	1701330	In the LC and some other brain regions, induction of c <strong>fos</strong> during opiate <b>withdrawal</b> was associated with a parallel induction of c jun, another nuclear proto oncogene, which, like c <strong>fos</strong>, is expressed rapidly in brain in response to certain extracellular stimuli.
+FOS	addiction	withdrawal	1701330	The results demonstrate a novel use of c <strong>fos</strong> in neuropharmacology, namely to map neuronal pathways and neuronal cell types activated in response to acute and chronic opiate administration and during opiate <b>withdrawal</b>, as well as in response to other psychotropic drug treatments.
+FOS	drug	alcohol	2107390	<b>Ethanol</b> withdrawal seizures produce increased c <strong>fos</strong> mRNA in mouse brain.
+FOS	addiction	withdrawal	2107390	Ethanol <b>withdrawal</b> seizures produce increased c <strong>fos</strong> mRNA in mouse brain.
+FOS	drug	alcohol	2107390	mRNA levels for the protooncogene c <strong>fos</strong>, measured by Northern blot analysis, were greatly increased in brains of mice undergoing <b>ethanol</b> withdrawal seizures.
+FOS	addiction	withdrawal	2107390	mRNA levels for the protooncogene c <strong>fos</strong>, measured by Northern blot analysis, were greatly increased in brains of mice undergoing ethanol <b>withdrawal</b> seizures.
+FOS	drug	alcohol	2107390	In mice that were fed <b>ethanol</b> chronically and withdrawn but that did not undergo overt withdrawal seizures, c <strong>fos</strong> mRNA levels were not significantly increased.
+FOS	addiction	withdrawal	2107390	In mice that were fed ethanol chronically and withdrawn but that did not undergo overt <b>withdrawal</b> seizures, c <strong>fos</strong> mRNA levels were not significantly increased.
+FOS	drug	alcohol	2107390	The findings with <b>ethanol</b> withdrawal seizures are similar in many respects to results of earlier studies with chemically induced seizures or kindling, which had led to the suggestion that c <strong>fos</strong> expression may play a role in neuronal adaptation.
+FOS	addiction	withdrawal	2107390	The findings with ethanol <b>withdrawal</b> seizures are similar in many respects to results of earlier studies with chemically induced seizures or kindling, which had led to the suggestion that c <strong>fos</strong> expression may play a role in neuronal adaptation.
+FOS	drug	alcohol	2107390	The present data support the hypothesis that this phenomenon may involve <b>ethanol</b> withdrawal seizure induced increases in c <strong>fos</strong> expression in various brain areas.
+FOS	addiction	withdrawal	2107390	The present data support the hypothesis that this phenomenon may involve ethanol <b>withdrawal</b> seizure induced increases in c <strong>fos</strong> expression in various brain areas.
+FOS	drug	opioid	3144275	<b>Morphine</b> activation of c <strong>fos</strong> expression in rat brain.
+FOS	drug	opioid	3144275	The post receptor mechanism of opiate action has been studied by examining the activation by <b>morphine</b> of the proto oncogene c <strong>fos</strong> and its encoded nucleoprotein pp55c <strong>fos</strong> (<strong>FOS</strong>) in rat caudate putamen, which is rich in the mu type opiate receptor.
+FOS	drug	opioid	3144275	Following an acute <b>morphine</b> treatment, c <strong>fos</strong> mRNA levels in rat caudate putamen were increased to maximum (420% of control level) at 45 minutes and returned to control levels at 90 minutes.
+FOS	drug	opioid	3144275	<strong>Fos</strong> protein, detected by immunocytochemistry, was also increased 3 hours after <b>morphine</b> injection, in the caudate putamen, but not in the olfactory tubercle, which does not have the mu type opiate receptor.
+FOS	drug	opioid	3144275	Upon activation of opiate receptors by <b>morphine</b>, the c <strong>fos</strong> gene is activated and <strong>Fos</strong> protein may act as a signal transducer uniquely involved in the mechanism of opiate addiction at the level of gene regulation.
+FOS	addiction	addiction	3144275	Upon activation of opiate receptors by morphine, the c <strong>fos</strong> gene is activated and <strong>Fos</strong> protein may act as a signal transducer uniquely involved in the mechanism of opiate <b>addiction</b> at the level of gene regulation.
+TH	drug	opioid	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (<strong>TH</strong>), DOPA decarboxylase (DDC), solute carrier family 6 member 3 (SLC6A3) and DA beta hydroxylase (DBH), with six important phenotypes of <b>heroin</b> dependence.
+TH	addiction	dependence	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (<strong>TH</strong>), DOPA decarboxylase (DDC), solute carrier family 6 member 3 (SLC6A3) and DA beta hydroxylase (DBH), with six important phenotypes of heroin <b>dependence</b>.
+TH	drug	opioid	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), DOPA decarboxylase (DDC), solute carrier family 6 member 3 (SLC6A3) and DA beta hydroxylase (DBH), with six important phenotypes of <b>heroin</b> dependence.
+TH	addiction	dependence	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), DOPA decarboxylase (DDC), solute carrier family 6 member 3 (SLC6A3) and DA beta hydroxylase (DBH), with six important phenotypes of heroin <b>dependence</b>.
+TH	drug	alcohol	32669355	First, we used chemogenetic approaches to show a causal role for ventral tegmental area (VTA) tyrosine hydroxylase (<strong>TH</strong>) neurons in two forms of relapse to <b>alcohol</b> seeking: renewal (context induced reinstatement) and reacquisition.
+TH	addiction	relapse	32669355	First, we used chemogenetic approaches to show a causal role for ventral tegmental area (VTA) tyrosine hydroxylase (<strong>TH</strong>) neurons in two forms of <b>relapse</b> to alcohol <b>seeking</b>: renewal (context induced <b>reinstatement</b>) and reacquisition.
+TH	drug	alcohol	32669355	First, we used chemogenetic approaches to show a causal role for ventral tegmental area (VTA) <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) neurons in two forms of relapse to <b>alcohol</b> seeking: renewal (context induced reinstatement) and reacquisition.
+TH	addiction	relapse	32669355	First, we used chemogenetic approaches to show a causal role for ventral tegmental area (VTA) <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) neurons in two forms of <b>relapse</b> to alcohol <b>seeking</b>: renewal (context induced <b>reinstatement</b>) and reacquisition.
+TH	addiction	relapse	32669355	Next we used optogenetic inhibition of VTA <strong>TH</strong> neurons to show distinct causal roles for VTA subregions in distinct forms of <b>relapse</b>.
+TH	drug	opioid	32404265	Furthermore, the Orx1 blockade could decrease the percentage of tyrosine hydroxylase (<strong>TH</strong>)+/CREB+ and <strong>TH</strong>+/PLCβ3+ neurons in LC of <b>morphine</b> treated rats.
+TH	drug	opioid	32404265	Furthermore, the Orx1 blockade could decrease the percentage of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>)+/CREB+ and <strong>TH</strong>+/PLCβ3+ neurons in LC of <b>morphine</b> treated rats.
+TH	drug	alcohol	32329567	Finally, we found that in mice pretreated with sazetidine A, <b>alcohol</b> induced Fos transcript in <strong>Th</strong> , but not Gad2 expressing neurons in the VTA as measured by increased Fos transcript expression.
+TH	drug	amphetamine	32080803	First, we demonstrated that mice pretreated with EGCG 30 min prior to the <b>METH</b> injection (30 mg/kg, ip) showed protection against the striatal <b>METH</b> induced reduction of <strong>tyrosine hydroxylase</strong> without mitigating hyperthermia.
+TH	addiction	intoxication	31887307	MPTP <b>intoxication</b> of mice results in glial activation, tyrosine hydroxylase (<strong>TH</strong>) depletion, and significant behavioral deficits.
+TH	addiction	intoxication	31887307	MPTP <b>intoxication</b> of mice results in glial activation, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) depletion, and significant behavioral deficits.
+TH	drug	alcohol	31842273	Drinking two or more times <b>alcohol</b> per week was associated with greater aBMD of the <strong>TH</strong> (p = 0.04 0.002) and FN (p = 0.043) compared to a lower frequency of <b>alcohol</b> consumption and 2 4 times per month, respectively.
+TH	drug	alcohol	31842273	Young college aged women with greater bone loading physical activity showed greater aBMD at the <strong>TH</strong>, FN, FT, and lumbar spine, while a moderate <b>alcohol</b> intake was associated with greater aBMD of the <strong>TH</strong> and FN.
+TH	drug	amphetamine	31822818	<b>Meth</b> differentially altered dopamine signaling markers (e.g., Dat, Comt, and <strong>Th</strong>) between hBDNFVal/Val and hBDNFMet/Met mice, implicating involvement of BDNF in <b>Meth</b> induced reprogramming of the mesolimbic proteome.
+TH	drug	amphetamine	31622973	We then quantified DA release in the nucleus accumbens (NAc) shell after treatment with d <b>Amphetamine</b> using in vivo microdialysis, quantified levels of tyrosine hydroxylase (<strong>TH</strong>) and dopamine transporter (DAT) mRNA using quantitative polymerase chain reaction (qPCR), and lastly, quantified baseline extracellular DA and function of DAT in vivo using quantitative "no net flux" microdialysis.
+TH	drug	amphetamine	31622973	We then quantified DA release in the nucleus accumbens (NAc) shell after treatment with d <b>Amphetamine</b> using in vivo microdialysis, quantified levels of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine transporter (DAT) mRNA using quantitative polymerase chain reaction (qPCR), and lastly, quantified baseline extracellular DA and function of DAT in vivo using quantitative "no net flux" microdialysis.
+TH	drug	cocaine	31478293	We used male tyrosine hydroxylase (<strong>TH</strong>) IRES Cre+ rats along with optogenetic tools to inhibit directly and briefly VTA DA neurons during conditioned stimulus (CS) induced <b>cocaine</b> seeking under extinction conditions.
+TH	addiction	relapse	31478293	We used male tyrosine hydroxylase (<strong>TH</strong>) IRES Cre+ rats along with optogenetic tools to inhibit directly and briefly VTA DA neurons during conditioned stimulus (CS) induced cocaine <b>seeking</b> under extinction conditions.
+TH	drug	cocaine	31478293	We used male <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) IRES Cre+ rats along with optogenetic tools to inhibit directly and briefly VTA DA neurons during conditioned stimulus (CS) induced <b>cocaine</b> seeking under extinction conditions.
+TH	addiction	relapse	31478293	We used male <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) IRES Cre+ rats along with optogenetic tools to inhibit directly and briefly VTA DA neurons during conditioned stimulus (CS) induced cocaine <b>seeking</b> under extinction conditions.
+TH	drug	cocaine	31478293	We found that brief and nondysphoric/nonsedative pulses of VTA photo inhibition (1 s every 9 s, ie, for 10% of time) attenuated CS induced <b>cocaine</b> seeking under extinction conditions in rats expressing archaerhodopsin selectively on the <strong>TH</strong>+ neurons.
+TH	addiction	relapse	31478293	We found that brief and nondysphoric/nonsedative pulses of VTA photo inhibition (1 s every 9 s, ie, for 10% of time) attenuated CS induced cocaine <b>seeking</b> under extinction conditions in rats expressing archaerhodopsin selectively on the <strong>TH</strong>+ neurons.
+TH	drug	psychedelics	31279579	Furthermore, 25 N <b>NBOMe</b> significantly reduced the expression of <strong>tyrosine hydroxylase</strong> in the NAc but not in the DSt.
+TH	drug	alcohol	31260795	Additionally, we observed that inhibition of serum ADH activity caused a decrease in peak dopamine levels during acute <b>alcohol</b> intake in chronically <b>ethanol</b> fed rats during <b>ethanol</b> withdrawal that was associated with reduced <strong>tyrosine hydroxylase</strong> activity in the striatum.
+TH	addiction	withdrawal	31260795	Additionally, we observed that inhibition of serum ADH activity caused a decrease in peak dopamine levels during acute alcohol intake in chronically ethanol fed rats during ethanol <b>withdrawal</b> that was associated with reduced <strong>tyrosine hydroxylase</strong> activity in the striatum.
+TH	drug	amphetamine	31228610	These effects preceded the activation of cleaved caspase 3 in dopamine cell bodies, as well as decreases in tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity in the substantia nigra and dopamine transporter (DAT) immunoreactivity in the striatum measured at 7 days after <b>Meth</b>.
+TH	drug	amphetamine	31228610	These effects preceded the activation of cleaved caspase 3 in dopamine cell bodies, as well as decreases in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity in the substantia nigra and dopamine transporter (DAT) immunoreactivity in the striatum measured at 7 days after <b>Meth</b>.
+TH	drug	amphetamine	31228610	Intervention with a selective COX 2 inhibitor during EtOH drinking prevented the changes in microglia, and attenuated the increase in cleaved caspase 3, and decreases in <strong>TH</strong> and DAT after <b>Meth</b> administration.
+TH	drug	nicotine	31220484	Additionally, oral <b>nicotine</b> consumption increased nucleus accumbens <strong>tyrosine hydroxylase</strong> levels.
+TH	drug	cannabinoid	31074060	Finally, we analyzed the relative gene expression of tyrosine hydroxylase (<strong>TH</strong>) and μ opioid receptor (OPRM1) and <b>cannabinoid</b> CB1 receptor (CB1 r) in the ventral tegmental area (VTA) and in the nucleus accumbens (NAc), respectively, by real time quantitative PCR.
+TH	drug	opioid	31074060	Finally, we analyzed the relative gene expression of tyrosine hydroxylase (<strong>TH</strong>) and μ <b>opioid</b> receptor (OPRM1) and cannabinoid CB1 receptor (CB1 r) in the ventral tegmental area (VTA) and in the nucleus accumbens (NAc), respectively, by real time quantitative PCR.
+TH	drug	cannabinoid	31074060	Finally, we analyzed the relative gene expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and μ opioid receptor (OPRM1) and <b>cannabinoid</b> CB1 receptor (CB1 r) in the ventral tegmental area (VTA) and in the nucleus accumbens (NAc), respectively, by real time quantitative PCR.
+TH	drug	opioid	31074060	Finally, we analyzed the relative gene expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and μ <b>opioid</b> receptor (OPRM1) and cannabinoid CB1 receptor (CB1 r) in the ventral tegmental area (VTA) and in the nucleus accumbens (NAc), respectively, by real time quantitative PCR.
+TH	drug	alcohol	31074060	Interestingly, females also showed higher expression of <strong>TH</strong> and OPRM1, without any difference in CB1 r. Only the acute administration of CBD at the highest dose (90 mg/kg) reduced significantly <b>ethanol</b> consumption in both sexes.
+TH	drug	cocaine	31009113	Sexual cues influence <b>cocaine</b> induced locomotion, anxiety and the immunoreactivity of oestrogen receptor alpha and <strong>tyrosine hydroxylase</strong> in both sexes.
+TH	drug	cocaine	31009113	LSC up regulated <b>cocaine</b> induced increases in ventral tegmental area (VTA) <strong>TH</strong> immunoreactivity in females only.
+TH	drug	cocaine	31009113	Our present data suggest that interactions between LSC and <b>cocaine</b> led to changes in ERα and <strong>TH</strong> immunoreactivity in a brain region specific manner, which showed subtle differences in both sexes.
+TH	drug	amphetamine	30951972	While FO prevented <b>AMPH</b> induced oxidative damages in the prefrontal cortex, molecular assays allowed us to observe that it was also able to modulate dopaminergic cascade markers (DAT, <strong>TH</strong>, VMAT 2, D1R and D2R) in the same brain area, thus preventing <b>AMPH</b> induced molecular changes.
+TH	addiction	aversion	30862664	Finally, ablation of KORs from dopamine neurons using AAV <strong>TH</strong> cre in KORloxP mice prevented pain induced <b>aversive</b> states as measured by place <b>aversion</b> assays.
+TH	drug	cocaine	30826460	Levels of nicotinic acetylcholine receptor β2, α6 and α7 subunit, Pitx3, and <strong>tyrosine hydroxylase</strong> 1 (TH1) mRNAs were increased in the brain of nicotine  and <b>cocaine</b> sensitized zebrafish.
+TH	drug	nicotine	30826460	Levels of nicotinic acetylcholine receptor β2, α6 and α7 subunit, Pitx3, and <strong>tyrosine hydroxylase</strong> 1 (TH1) mRNAs were increased in the brain of <b>nicotine</b>  and cocaine sensitized zebrafish.
+TH	drug	alcohol	30708098	The expression of HSP27, pHSP27, Trx 1, total <strong>TH</strong> and pTH in the right ventricle was increased after binge <b>ethanol</b> or MDMA alone.
+TH	drug	psychedelics	30708098	The expression of HSP27, pHSP27, Trx 1, total <strong>TH</strong> and pTH in the right ventricle was increased after binge ethanol or <b>MDMA</b> alone.
+TH	addiction	intoxication	30708098	The expression of HSP27, pHSP27, Trx 1, total <strong>TH</strong> and pTH in the right ventricle was increased after <b>binge</b> ethanol or MDMA alone.
+TH	drug	alcohol	30708098	In addition, the combination of binge <b>ethanol</b> + MDMA enhanced <strong>TH</strong> expression and phosphorylation versus their individual administration.
+TH	drug	psychedelics	30708098	In addition, the combination of binge ethanol + <b>MDMA</b> enhanced <strong>TH</strong> expression and phosphorylation versus their individual administration.
+TH	addiction	intoxication	30708098	In addition, the combination of <b>binge</b> ethanol + MDMA enhanced <strong>TH</strong> expression and phosphorylation versus their individual administration.
+TH	drug	alcohol	30648291	Serving as a versatile substrate, Nth AD+ was reduced by <b>alcohol</b> dehydrogenase (ADH) to Nth ADH and afforded <strong>th</strong> ADP ribose (<strong>th</strong> ADPr) upon hydrolysis by NAD+  nucleosidase (NADase).
+TH	addiction	aversion	30648291	Furthermore, Nth AD+ was engaged in cholera toxin A (<b>CTA</b>) catalyzed mono(<strong>th</strong> ADP ribosyl)ation, but was found incapable in promoting PARP1 mediated poly(<strong>th</strong> ADP ribosyl)ation.
+TH	drug	opioid	30634592	Dysregulation of Dopaminergic Regulatory Factors <strong>TH</strong>, Nurr1, and Pitx3 in the Ventral Tegmental Area Associated with Neuronal Injury Induced by Chronic <b>Morphine</b> Dependence.
+TH	addiction	dependence	30634592	Dysregulation of Dopaminergic Regulatory Factors <strong>TH</strong>, Nurr1, and Pitx3 in the Ventral Tegmental Area Associated with Neuronal Injury Induced by Chronic Morphine <b>Dependence</b>.
+TH	drug	opioid	30634592	Immunohistochemistry showed that the number of <strong>TH</strong>⁺, Nurr1⁺, and Pitx3⁺ cells, and the number of <strong>TH</strong>⁺ cells expressing Nurr1 or Pitx3, significantly decreased in the VTA after a long period of <b>morphine</b> dependence.
+TH	addiction	dependence	30634592	Immunohistochemistry showed that the number of <strong>TH</strong>⁺, Nurr1⁺, and Pitx3⁺ cells, and the number of <strong>TH</strong>⁺ cells expressing Nurr1 or Pitx3, significantly decreased in the VTA after a long period of morphine <b>dependence</b>.
+TH	drug	amphetamine	30629943	We did not find a significant effect of <b>methamphetamine</b> on the dopamine neuron markers tyrosine hydroxylase (<strong>TH</strong>) or dopamine transporter (DAT) 7 days after <b>methamphetamine</b> administrations.
+TH	drug	amphetamine	30629943	We did not find a significant effect of <b>methamphetamine</b> on the dopamine neuron markers <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) or dopamine transporter (DAT) 7 days after <b>methamphetamine</b> administrations.
+TH	drug	opioid	30517913	Expression Levels of the <strong>Tyrosine Hydroxylase</strong> Gene and Histone Modifications Around its Promoter in the Locus Coeruleus and Ventral Tegmental Area of Rats during Forced Abstinence from <b>Morphine</b>.
+TH	drug	opioid	30517913	We studied whether <b>morphine</b> induced changes in mRNA levels of the catecholamine biosynthesis enzyme, tyrosine hydroxylase (<strong>TH</strong>), are associated with histone modifications around the promoter of this gene in the locus coeruleus (LC) and ventral tegmental area (VTA) of rats.
+TH	drug	opioid	30517913	We studied whether <b>morphine</b> induced changes in mRNA levels of the catecholamine biosynthesis enzyme, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), are associated with histone modifications around the promoter of this gene in the locus coeruleus (LC) and ventral tegmental area (VTA) of rats.
+TH	drug	opioid	30517913	Analysis of our real time quantitative reverse transcription PCR results by 1 way ANOVA showed significant upregulation (5.13 ± 0.39 folds) of LC levels of the <strong>TH</strong> transcript 24 h after the last injection of <b>morphine</b> to rats, when compared with 2 h and 7 days time points.
+TH	drug	opioid	30517913	Chronic <b>morphine</b> and <b>morphine</b> abstinence failed to cause any significant changes in the levels of <strong>TH</strong> mRNA in the VTA after cessation of <b>morphine</b>.
+TH	drug	opioid	30517913	Consistently, chromatin immunoprecipitation real time quantitative PCR assays revealed that 24 h after the last injection of <b>morphine</b>, levels of H3 acetylation were significantly increased (4.12 ± 0.38 folds) at the promoter of the <strong>TH</strong> gene in the LC but not in the VTA.
+TH	drug	opioid	30517913	Our data also showed that histone H3 trimethylation failed to change around the <strong>TH</strong> gene promoter either in the VTA or in the LC after <b>morphine</b> abstinence.
+TH	drug	opioid	30517913	Results of the present study, for the first time, demonstrate the involvement of histone H3 acetylation in the regulation of <strong>TH</strong> gene expression in the LC of rats during forced abstinence from <b>morphine</b>.
+TH	drug	alcohol	30446531	l DOPA also reverses the selective loss of dendritic "long thin" spines observed in medium spiny neurons of the nucleus accumbens (NAc) shell of <b>alcohol</b> dependent rats during abstinence, as well as the reduction in <strong>tyrosine hydroxylase</strong> immunostaining and postsynaptic density 95 positive elements.
+TH	drug	nicotine	30354182	Here, we determined <b>nicotine</b>'s actions on NTS CA neurons by use of patch clamp techniques in brain slices from transgenic mice expressing enhanced green fluorescent protein driven by the tyrosine hydroxylase promoter (<strong>TH</strong> EGFP).
+TH	drug	nicotine	30354182	Here, we determined <b>nicotine</b>'s actions on NTS CA neurons by use of patch clamp techniques in brain slices from transgenic mice expressing enhanced green fluorescent protein driven by the <strong>tyrosine hydroxylase</strong> promoter (<strong>TH</strong> EGFP).
+TH	drug	cocaine	30321610	Increased expression of Arc, CDK5 and <strong>TH</strong>, and decrease in DAT protein levels persisted longer after withdrawal, pointing to a neuroplastic lasting effect similar to that involved in <b>cocaine</b> addiction.
+TH	addiction	addiction	30321610	Increased expression of Arc, CDK5 and <strong>TH</strong>, and decrease in DAT protein levels persisted longer after withdrawal, pointing to a neuroplastic lasting effect similar to that involved in cocaine <b>addiction</b>.
+TH	addiction	withdrawal	30321610	Increased expression of Arc, CDK5 and <strong>TH</strong>, and decrease in DAT protein levels persisted longer after <b>withdrawal</b>, pointing to a neuroplastic lasting effect similar to that involved in cocaine addiction.
+TH	drug	amphetamine	30296508	Molecular analysis evidenced that <b>AMPH</b> ISO modulated dopaminergic targets (dopamine transporter, <strong>tyrosine hydroxylase</strong> and D1 R), whose immunoreactivity was increased by <b>AMPH</b>.
+TH	drug	amphetamine	30296469	Effect of a binge like dosing regimen of <b>methamphetamine</b> on dopamine levels and <strong>tyrosine hydroxylase</strong> expressing neurons in the rat brain.
+TH	addiction	intoxication	30296469	Effect of a <b>binge</b> like dosing regimen of methamphetamine on dopamine levels and <strong>tyrosine hydroxylase</strong> expressing neurons in the rat brain.
+TH	addiction	intoxication	30296469	The effect of MA <b>binge</b> like dosing on the volume of <strong>tyrosine hydroxylase</strong> containing cell bodies and the area fraction of <strong>tyrosine hydroxylase</strong> containing fibres was also assessed.
+TH	drug	amphetamine	30296469	These findings collectively highlight the importance of the dopaminergic system in <b>methamphetamine</b> induced effects, identify the frontal cortex, amygdala and striatum as key regions that undergo early changes in response to binge like <b>methamphetamine</b> dosing and provide evidence of time dependent effects on the cell bodies and fibres of <strong>tyrosine hydroxylase</strong> expressing neurons.
+TH	addiction	intoxication	30296469	These findings collectively highlight the importance of the dopaminergic system in methamphetamine induced effects, identify the frontal cortex, amygdala and striatum as key regions that undergo early changes in response to <b>binge</b> like methamphetamine dosing and provide evidence of time dependent effects on the cell bodies and fibres of <strong>tyrosine hydroxylase</strong> expressing neurons.
+TH	drug	opioid	30268817	Quantitative real time polymerase chain reaction (qPCR) studies were carried out to evaluate alterations in targets closely related to DA neurotransmission in the reward system, tyrosine hydroxylase (<strong>Th</strong>) in the ventral tegmental area (VTA), and μ <b>opioid</b> receptor (Oprm1) in the nucleus accumbens (NAc).
+TH	addiction	reward	30268817	Quantitative real time polymerase chain reaction (qPCR) studies were carried out to evaluate alterations in targets closely related to DA neurotransmission in the <b>reward</b> system, tyrosine hydroxylase (<strong>Th</strong>) in the ventral tegmental area (VTA), and μ opioid receptor (Oprm1) in the nucleus accumbens (NAc).
+TH	drug	opioid	30268817	Quantitative real time polymerase chain reaction (qPCR) studies were carried out to evaluate alterations in targets closely related to DA neurotransmission in the reward system, <strong>tyrosine hydroxylase</strong> (<strong>Th</strong>) in the ventral tegmental area (VTA), and μ <b>opioid</b> receptor (Oprm1) in the nucleus accumbens (NAc).
+TH	addiction	reward	30268817	Quantitative real time polymerase chain reaction (qPCR) studies were carried out to evaluate alterations in targets closely related to DA neurotransmission in the <b>reward</b> system, <strong>tyrosine hydroxylase</strong> (<strong>Th</strong>) in the ventral tegmental area (VTA), and μ opioid receptor (Oprm1) in the nucleus accumbens (NAc).
+TH	drug	amphetamine	30136629	The levels of dopamine D1 receptor, <strong>tyrosine hydroxylase</strong>, phosphorylated extracellular regulated kinase, and phosphorylated cyclic adenosine monophosphate response element binding protein were decreased in the ventral tegmental area, nucleus accumbens, and prefrontal cortex of mice in the control and negative groups after <b>methamphetamine</b> conditioned place preference extinction, but were inversely increased in thioredoxin 1 siRNA group.
+TH	drug	amphetamine	30091820	In addition, we measured expression levels of dopamine and dopamine related genes (monoamine oxidase A, DA receptor 1, DA receptor 2, DA active transporter, <strong>tyrosine hydroxylase</strong> and cAMP response element binding protein 1) in the striatum of the mice after repeated <b>METH</b> treatments, using qRT PCR.
+TH	drug	opioid	30063884	By means of real time polymerase chain reaction (PCR), we also analysed relative gene expression of tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area (VTA), and of mu <b>opioid</b> receptor (OPRM1), CNR1 and CNR2 in the nucleus accumbens (NAcc).
+TH	drug	opioid	30063884	By means of real time polymerase chain reaction (PCR), we also analysed relative gene expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area (VTA), and of mu <b>opioid</b> receptor (OPRM1), CNR1 and CNR2 in the nucleus accumbens (NAcc).
+TH	drug	nicotine	30009210	Double labeling of GAD67 GFP positive cells with <strong>TH</strong> IR cells showed that the GABAergic neurons that were activated by high dose <b>nicotine</b> were located in close proximity to the dopaminergic neurons of substantia nigra compact part and VTA.
+TH	drug	cocaine	29911172	In summary, in addition to demonstrating a key role of PICK1 in mediating behavioral effects of <b>cocaine</b>, our data reveal a so far unappreciated role of PICK1 in DA homeostasis that possibly involves negative regulation of striatal <strong>TH</strong> levels.
+TH	drug	opioid	29859012	Gene expression analyses of the <b>opioid</b> μ receptor (Oprm1) in the nucleus accumbens (NAc), tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area (VTA) and the 5 HT1A receptor in the dorsal raphe nucleus (DR) were carried out by real time PCR.
+TH	drug	opioid	29859012	Gene expression analyses of the <b>opioid</b> μ receptor (Oprm1) in the nucleus accumbens (NAc), <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area (VTA) and the 5 HT1A receptor in the dorsal raphe nucleus (DR) were carried out by real time PCR.
+TH	drug	opioid	29770121	The DA level and expressions of tyrosine hydroxylase (<strong>TH</strong>) and D1 were induced by <b>morphine</b> in WT mice, which were not induced in Trx 1 TG mice.
+TH	drug	opioid	29770121	The DA level and expressions of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and D1 were induced by <b>morphine</b> in WT mice, which were not induced in Trx 1 TG mice.
+TH	drug	opioid	29770121	Therefore, Trx 1 may play a role in blocking CPP induced by <b>morphine</b> through regulating the expressions of D1, <strong>TH</strong>, and GABABR in the VTA and NAc.
+TH	addiction	reward	29770121	Therefore, Trx 1 may play a role in blocking <b>CPP</b> induced by morphine through regulating the expressions of D1, <strong>TH</strong>, and GABABR in the VTA and NAc.
+TH	drug	opioid	29731707	Finally, oral application of low dose <b>morphine</b> significantly improved midbrain tyrosine hydroxylase (<strong>TH</strong>) expression, decreased apomorphine evoked rotation and attenuated pain hypersensitivity in a 6 OHDA induced PD rat model, without the risks associated with <b>morphine</b> addiction.
+TH	addiction	addiction	29731707	Finally, oral application of low dose morphine significantly improved midbrain tyrosine hydroxylase (<strong>TH</strong>) expression, decreased apomorphine evoked rotation and attenuated pain hypersensitivity in a 6 OHDA induced PD rat model, without the risks associated with morphine <b>addiction</b>.
+TH	drug	opioid	29731707	Finally, oral application of low dose <b>morphine</b> significantly improved midbrain <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) expression, decreased apomorphine evoked rotation and attenuated pain hypersensitivity in a 6 OHDA induced PD rat model, without the risks associated with <b>morphine</b> addiction.
+TH	addiction	addiction	29731707	Finally, oral application of low dose morphine significantly improved midbrain <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) expression, decreased apomorphine evoked rotation and attenuated pain hypersensitivity in a 6 OHDA induced PD rat model, without the risks associated with morphine <b>addiction</b>.
+TH	drug	cocaine	29728703	NAD+ cellular redox and SIRT1 regulate the diurnal rhythms of <strong>tyrosine hydroxylase</strong> and conditioned <b>cocaine</b> reward.
+TH	addiction	reward	29728703	NAD+ cellular redox and SIRT1 regulate the diurnal rhythms of <strong>tyrosine hydroxylase</strong> and conditioned cocaine <b>reward</b>.
+TH	drug	cocaine	29728703	Additionally, we demonstrate that the transcriptional activity of <strong>TH</strong> is modulated by the cellular redox state, and daily rhythms of redox balance in the ventral tegmental area (VTA), along with <strong>TH</strong> transcription, are highly disrupted following chronic <b>cocaine</b> administration.
+TH	addiction	relapse	29690521	However, the mechanism of signal activation, its function in dopaminergic (<strong>TH</strong>+) neurons within the reward circuitry implicated in drug <b>seeking</b> behavior [viz.
+TH	addiction	reward	29690521	However, the mechanism of signal activation, its function in dopaminergic (<strong>TH</strong>+) neurons within the <b>reward</b> circuitry implicated in drug seeking behavior [viz.
+TH	drug	cannabinoid	29624642	Furthermore, gene expression changes in <strong>TH</strong> in the ventral tegmental area, and in the opioid μ receptor (Oprm1), <b>cannabinoid</b> CB1 receptor (Cnr1) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+TH	drug	opioid	29624642	Furthermore, gene expression changes in <strong>TH</strong> in the ventral tegmental area, and in the <b>opioid</b> μ receptor (Oprm1), cannabinoid CB1 receptor (Cnr1) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+TH	drug	amphetamine	29475448	Pre treatment with JTT significantly attenuated <b>METH</b> induced stereotyped responses, and interdicted <b>METH</b> induced changes in the levels of DAT, D2R and <strong>TH</strong> expression.
+TH	drug	amphetamine	29475448	Treatment with JTT after <b>METH</b> administration restored DAT, D2R and <strong>TH</strong> expression to normal levels.
+TH	addiction	withdrawal	29407532	These results indicate that CRF CRF1R pathway could be a critical factor governing opiate <b>withdrawal</b> memory storage and retrieval and might suggest a role for <strong>TH</strong> NA pathway in the effects of <b>withdrawal</b> on memory.
+TH	drug	amphetamine	29383398	In the heart, <b>METH</b> administration induced an increase in soluble (S) COMT and membrane bound (MB) COMT without changes in phospho (p) <strong>TH</strong>, Hsp27, or pHsp27.
+TH	drug	amphetamine	29383398	In contrast to chronic treatment, <b>METH</b> withdrawal enhanced levels of (p)<strong>TH</strong> and (p)Hsp27 in the heart.
+TH	addiction	withdrawal	29383398	In contrast to chronic treatment, METH <b>withdrawal</b> enhanced levels of (p)<strong>TH</strong> and (p)Hsp27 in the heart.
+TH	addiction	withdrawal	29313212	Compared with the model group, HBO2 therapy significantly attenuated the <b>withdrawal</b> symptom scores, body weight loss and the level of norepinephrine level, whereas it increased the dopamine level and <strong>tyrosine hydroxylase</strong> expression in the nucleus accumbens.
+TH	drug	amphetamine	29223637	Repeated intrastriatal injections of a Gαq/11 inhibitor, [D Trp7,9,10] substance P, significantly reduced behavioral sensitization and striatal dopamine (DA) level in response to <b>METH</b>, with no effect on striatal <strong>tyrosine hydroxylase</strong> expression.
+TH	addiction	sensitization	29223637	Repeated intrastriatal injections of a Gαq/11 inhibitor, [D Trp7,9,10] substance P, significantly reduced behavioral <b>sensitization</b> and striatal dopamine (DA) level in response to METH, with no effect on striatal <strong>tyrosine hydroxylase</strong> expression.
+TH	addiction	addiction	29210332	The most significant results were obtained for DA β hydroxylase variants, rs2073837 and rs1611131, which were associated with protection from <b>addiction</b> (q = 0.0172, 0.0415, respectively) and the functional <strong>TH</strong> variant, rs2070762, was associated with more risk (q = 0.0387).
+TH	drug	opioid	29116553	Evidence suggests that the dopamine receptor rate limiting enzyme, tyrosine hydroxylase (<strong>TH</strong>), and the glutamate receptor, N methyl D aspartate receptor 2B (NR2B), contribute to <b>morphine</b> dependence.
+TH	addiction	dependence	29116553	Evidence suggests that the dopamine receptor rate limiting enzyme, tyrosine hydroxylase (<strong>TH</strong>), and the glutamate receptor, N methyl D aspartate receptor 2B (NR2B), contribute to morphine <b>dependence</b>.
+TH	drug	opioid	29116553	Evidence suggests that the dopamine receptor rate limiting enzyme, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and the glutamate receptor, N methyl D aspartate receptor 2B (NR2B), contribute to <b>morphine</b> dependence.
+TH	addiction	dependence	29116553	Evidence suggests that the dopamine receptor rate limiting enzyme, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and the glutamate receptor, N methyl D aspartate receptor 2B (NR2B), contribute to morphine <b>dependence</b>.
+TH	drug	opioid	29116553	Conditioned place preference (CPP) mouse model was established using <b>morphine</b> (9 mg/kg, s.c.), and their expression levels of <strong>TH</strong> and NR2B were observed by immunohistochemistry.
+TH	addiction	reward	29116553	Conditioned place preference (<b>CPP</b>) mouse model was established using morphine (9 mg/kg, s.c.), and their expression levels of <strong>TH</strong> and NR2B were observed by immunohistochemistry.
+TH	drug	opioid	29116553	Results showed that high sinomenine dose (80 mg/kg) effectively attenuated the behavior of CPP mice and reversed increased expression levels of <strong>TH</strong> and NR2B induced by <b>morphine</b>.
+TH	addiction	reward	29116553	Results showed that high sinomenine dose (80 mg/kg) effectively attenuated the behavior of <b>CPP</b> mice and reversed increased expression levels of <strong>TH</strong> and NR2B induced by morphine.
+TH	drug	opioid	29116553	In summary, these data indicate that sinomenine can inhibit <b>morphine</b> dependence by increasing the expression levels of <strong>TH</strong>, NR2B, and MOR in the mouse brain; however, DOR may not contribute to this effect.
+TH	addiction	dependence	29116553	In summary, these data indicate that sinomenine can inhibit morphine <b>dependence</b> by increasing the expression levels of <strong>TH</strong>, NR2B, and MOR in the mouse brain; however, DOR may not contribute to this effect.
+TH	drug	opioid	29039297	There was no effect of PC:EtOH on mRNA expression of the µ <b>opioid</b> receptor, tyrosine hydroxylase (<strong>Th</strong>), dopamine receptor type 2 (Drd2) or dopamine active transporter (Slc6a3).
+TH	drug	opioid	29039297	There was no effect of PC:EtOH on mRNA expression of the µ <b>opioid</b> receptor, <strong>tyrosine hydroxylase</strong> (<strong>Th</strong>), dopamine receptor type 2 (Drd2) or dopamine active transporter (Slc6a3).
+TH	addiction	addiction	29038792	Sequential double labelling was then performed to identify the location of orexin containing neurons and nerve fibers with respect to NIC induced c Fos activated cells and/or tyrosine hydroxylase (<strong>TH</strong>) immunoreactive (IR) cells of the mesocorticolimbic reward <b>addiction</b> pathways.
+TH	addiction	reward	29038792	Sequential double labelling was then performed to identify the location of orexin containing neurons and nerve fibers with respect to NIC induced c Fos activated cells and/or tyrosine hydroxylase (<strong>TH</strong>) immunoreactive (IR) cells of the mesocorticolimbic <b>reward</b> addiction pathways.
+TH	addiction	addiction	29038792	Sequential double labelling was then performed to identify the location of orexin containing neurons and nerve fibers with respect to NIC induced c Fos activated cells and/or <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactive (IR) cells of the mesocorticolimbic reward <b>addiction</b> pathways.
+TH	addiction	reward	29038792	Sequential double labelling was then performed to identify the location of orexin containing neurons and nerve fibers with respect to NIC induced c Fos activated cells and/or <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactive (IR) cells of the mesocorticolimbic <b>reward</b> addiction pathways.
+TH	addiction	reward	29031851	The enhanced duration of <b>CPP</b> was correlated with increased tyrosine hydroxylase (<strong>TH</strong>) expression and dopamine content in the ventral striatum.
+TH	addiction	reward	29031851	The enhanced duration of <b>CPP</b> was correlated with increased <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) expression and dopamine content in the ventral striatum.
+TH	addiction	relapse	29031851	Together, our results suggest that downstream components of GDNF signaling, in this case Ret, may mediate persistent drug <b>seeking</b> behavior through increased <strong>TH</strong> expression and dopamine levels in the mesolimbic dopamine neurons.
+TH	drug	cocaine	28921596	Furthermore, expression levels of two key enzymes related to dopamine synthesis, <strong>tyrosine hydroxylase</strong> and aromatic l amino acid decarboxylase, within the striatum of scanned mice were not significantly affected by acute <b>cocaine</b> pre treatment (p > 0.05).
+TH	drug	alcohol	28864261	However, (+) <b>Naltrexone</b>, like other TLR4 antagonists exhibited off target side effects, with a significant reduction in overall saccharin intake   an effect likely attributable to a reduction in tyrosine hydroxylase (<strong>Th</strong>) mRNA expression levels.
+TH	drug	alcohol	28864261	However, (+) <b>Naltrexone</b>, like other TLR4 antagonists exhibited off target side effects, with a significant reduction in overall saccharin intake   an effect likely attributable to a reduction in <strong>tyrosine hydroxylase</strong> (<strong>Th</strong>) mRNA expression levels.
+TH	drug	cocaine	28741623	Finally, suvorexant did not alter Fos immunoreactivity within <strong>tyrosine hydroxylase</strong> immunolabeled neurons of VTA, but did attenuate <b>cocaine</b>  and orexin induced increases in calcium transient amplitude within neurons of VTA.
+TH	drug	amphetamine	28661099	The aim of this study was to determine whether self administered <b>METH</b> altered the levels of α synuclein, parkin, tyrosine hydroxylase (<strong>TH</strong>), and dopamine β hydroxylase (DβH) in the myenteric plexus of the distal colon ENS.
+TH	drug	amphetamine	28661099	The aim of this study was to determine whether self administered <b>METH</b> altered the levels of α synuclein, parkin, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and dopamine β hydroxylase (DβH) in the myenteric plexus of the distal colon ENS.
+TH	drug	amphetamine	28661099	Levels of α synuclein were increased, while levels of parkin, <strong>TH</strong>, and DβH were decreased in the myenteric plexus in the <b>METH</b> exposed rats at 1 day following the last operant session and returned to the control levels after 14 or 56 days of forced abstinence.
+TH	addiction	reward	28661099	Levels of α synuclein were increased, while levels of parkin, <strong>TH</strong>, and DβH were decreased in the myenteric plexus in the METH exposed rats at 1 day following the last <b>operant</b> session and returned to the control levels after 14 or 56 days of forced abstinence.
+TH	drug	cocaine	28624112	In <strong>TH</strong>::Cre rats, the dopaminergic pathways from the ventral tegmental area to the rostral and caudal regions of the shell were optogenetically stimulated during intraoral delivery of a taste cue signaling delayed <b>cocaine</b>.
+TH	drug	psychedelics	28603026	<b>MDMA</b> reduced density of tyrosine hydroxylase (<strong>TH</strong>) positive neurons in the ventral tegmental area and in the substantia nigra pars compacta, and immunoreactivity of <strong>TH</strong> and DA transporter in the nucleus accumbens (NAc) shell and core, and caudate putamen.
+TH	drug	psychedelics	28603026	<b>MDMA</b> reduced density of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) positive neurons in the ventral tegmental area and in the substantia nigra pars compacta, and immunoreactivity of <strong>TH</strong> and DA transporter in the nucleus accumbens (NAc) shell and core, and caudate putamen.
+TH	drug	amphetamine	28580417	In pHFD exposed animals, a single <b>amphetamine</b> exposure induces an increase in bursting activity of DA cells in the ventral tegmental area (VTA) as well as higher DA release and greater expression of (tyrosine hydroxylase, <strong>TH</strong>) in the nucleus accumbens (NAc).
+TH	drug	amphetamine	28580417	In pHFD exposed animals, a single <b>amphetamine</b> exposure induces an increase in bursting activity of DA cells in the ventral tegmental area (VTA) as well as higher DA release and greater expression of (<strong>tyrosine hydroxylase</strong>, <strong>TH</strong>) in the nucleus accumbens (NAc).
+TH	drug	opioid	28537967	In CCI rats treated with both nortriptyline and <b>morphine</b>, the expression of α2A adrenergic receptors, norepinephrine transporter, and <strong>tyrosine hydroxylase</strong> was markedly decreased in the locus coeruleus, whereas the norepinephrine concentration in the nucleus accumbens was remarkably increased.
+TH	addiction	withdrawal	28468077	Before and after the 14(<strong>th</strong>) day of <b>withdrawal</b>, levels of immunoglobulin (IgM, IgA, IgG), T cell subsets (CD(3)(+), CD(4)(+), CD(8)(+), CD(4)(+)/CD(8)(+)) and cytokines (IL 2, IFN γ, IL 4, IFN γ/IL 4) were detected.
+TH	addiction	withdrawal	28468077	At the 14(<strong>th</strong>) day of <b>withdrawal</b> in placebo group, levels of IL 4 returned to normal while IFN γ/IL 4 ratio increased by 3.43 times (P<0.05).
+TH	addiction	withdrawal	28468077	Compared with placebo group, fluctuation of IgG and IgM decreased in Jitai group during <b>withdrawal</b> period, together with a normal level of IgM at the 14(<strong>th</strong>) day.
+TH	drug	opioid	28468077	Level of IL 4 abnormally rose up by 0.54 times in Jitai tablet plus <b>buprenorphine</b> group, while IFN γ/IL 4 ratio been switched back at the 14(<strong>th</strong>) day of withdrawal.
+TH	addiction	withdrawal	28468077	Level of IL 4 abnormally rose up by 0.54 times in Jitai tablet plus buprenorphine group, while IFN γ/IL 4 ratio been switched back at the 14(<strong>th</strong>) day of <b>withdrawal</b>.
+TH	drug	cannabinoid	28457972	After the SA procedure, HFB mice exhibited reduced levels of the mu opioid receptor (MOr) and increased <b>cannabinoid</b> 1 receptor (CB1r) gene expression in the nucleus accumbens (N Acc), and decreased of tyrosine hydroxylase (<strong>TH</strong>) gene expression in the ventral tegmental area (VTA).
+TH	drug	opioid	28457972	After the SA procedure, HFB mice exhibited reduced levels of the mu <b>opioid</b> receptor (MOr) and increased cannabinoid 1 receptor (CB1r) gene expression in the nucleus accumbens (N Acc), and decreased of tyrosine hydroxylase (<strong>TH</strong>) gene expression in the ventral tegmental area (VTA).
+TH	drug	cannabinoid	28457972	After the SA procedure, HFB mice exhibited reduced levels of the mu opioid receptor (MOr) and increased <b>cannabinoid</b> 1 receptor (CB1r) gene expression in the nucleus accumbens (N Acc), and decreased of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the ventral tegmental area (VTA).
+TH	drug	opioid	28457972	After the SA procedure, HFB mice exhibited reduced levels of the mu <b>opioid</b> receptor (MOr) and increased cannabinoid 1 receptor (CB1r) gene expression in the nucleus accumbens (N Acc), and decreased of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the ventral tegmental area (VTA).
+TH	drug	amphetamine	28400844	In addition, both dopamine and tyrosine hydroxylase (<strong>TH</strong>) levels decreased but monoamine oxidase A (MAO A) levels increased in the NAc of the <b>METH</b> treated mice receiving EA compared with those not receiving EA.
+TH	drug	amphetamine	28400844	In addition, both dopamine and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) levels decreased but monoamine oxidase A (MAO A) levels increased in the NAc of the <b>METH</b> treated mice receiving EA compared with those not receiving EA.
+TH	drug	amphetamine	28400844	EA may be a useful nonpharmacological approach for treating <b>METH</b> induced behavioral changes, probably because it reduces the <b>METH</b> induced <strong>TH</strong> expression and dopamine levels and raises MAO A expression in the NAc.
+TH	addiction	intoxication	28342134	Notably, DA specific deletion of p53 provided protection of substantia nigra pars reticulata (SNpr) tyrosine hydroxylase (<strong>TH</strong>) positive fibers following <b>binge</b> MA, with DAT p53KO mice having less decline of <strong>TH</strong> protein levels in striatum versus WT mice.
+TH	addiction	intoxication	28342134	Notably, DA specific deletion of p53 provided protection of substantia nigra pars reticulata (SNpr) <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) positive fibers following <b>binge</b> MA, with DAT p53KO mice having less decline of <strong>TH</strong> protein levels in striatum versus WT mice.
+TH	drug	cannabinoid	28194850	Gene expression analyses of <strong>tyrosine hydroxylase</strong> in ventral tegmental area and μ opioid (Oprm1), <b>cannabinoid</b> (CB1 r and CB2 r) and GPR55 receptors in nucleus accumbens (NAcc) were carried out by real time polymerase chain reaction.
+TH	drug	opioid	28194850	Gene expression analyses of <strong>tyrosine hydroxylase</strong> in ventral tegmental area and μ <b>opioid</b> (Oprm1), cannabinoid (CB1 r and CB2 r) and GPR55 receptors in nucleus accumbens (NAcc) were carried out by real time polymerase chain reaction.
+TH	drug	amphetamine	28130052	There was no effect of NTR1 agonist on <b>METH</b> induced dopamine terminal degeneration, as evidenced by <strong>tyrosine hydroxylase</strong> levels determined by Western blot.
+TH	drug	amphetamine	28063836	Inhibiting effects of rhynchophylline on <b>methamphetamine</b> dependent zebrafish are related with the expression of tyrosine hydroxylase (<strong>TH</strong>).
+TH	drug	amphetamine	28063836	Inhibiting effects of rhynchophylline on <b>methamphetamine</b> dependent zebrafish are related with the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>).
+TH	drug	amphetamine	28063836	In this study, to study the effect of rhynchophylline on <strong>TH</strong> in midbrain of <b>methamphetamine</b> induced conditioned place preference (CPP) adult zebrafish, place preference adult zebrafish models were established by <b>methamphetamine</b> (40μg/g) and the expression of <strong>TH</strong> was observed by immunohistochemistry technique and Western blot.
+TH	addiction	reward	28063836	In this study, to study the effect of rhynchophylline on <strong>TH</strong> in midbrain of methamphetamine induced conditioned place preference (<b>CPP</b>) adult zebrafish, place preference adult zebrafish models were established by methamphetamine (40μg/g) and the expression of <strong>TH</strong> was observed by immunohistochemistry technique and Western blot.
+TH	drug	amphetamine	28063836	Ketamine (150μg/g), high dose of rhynchophylline (100μg/g) group can significantly reduce the place preference; immunohistochemistry results showed that the number of <strong>TH</strong> positive neurons in midbrain was increased in the <b>methamphetamine</b> model group, whereas less <strong>TH</strong> positive neurons were found in the ketamine group and high dosage rhynchophylline group.
+TH	drug	psychedelics	28063836	<b>Ketamine</b> (150μg/g), high dose of rhynchophylline (100μg/g) group can significantly reduce the place preference; immunohistochemistry results showed that the number of <strong>TH</strong> positive neurons in midbrain was increased in the methamphetamine model group, whereas less <strong>TH</strong> positive neurons were found in the <b>ketamine</b> group and high dosage rhynchophylline group.
+TH	drug	psychedelics	28063836	Western blot results showed that the expression of <strong>TH</strong> protein was significantly increased in the model group, whereas less expression was found in the <b>ketamine</b> group, high dosage rhynchophylline group.
+TH	drug	amphetamine	28063836	Our data pointed out that <strong>TH</strong> plays an important role in the formation of <b>methamphetamine</b> induced place preference in adult zebrafish.
+TH	drug	amphetamine	28063836	Rhynchophylline reversed the expression of <strong>TH</strong> in the midbrain demonstrates the potential effect of mediates <b>methamphetamine</b> induced rewarding effect.
+TH	addiction	reward	27881347	The protein expressions of <strong>TH</strong>, NR2B and GLUR2 in the brain of zebrafish with <b>CPP</b> were detected with Western blotting.
+TH	drug	amphetamine	27881347	Compared with the control group, zebrafish in <b>methamphetamine</b> group showed significant variations in the staying time and swimming distance in the drug box after conditioning (P<0.05) with obvious alterations of NR2B, <strong>TH</strong> and GLUR2 expressions in the brain (P<0.05).
+TH	drug	amphetamine	27881347	Treatment of <b>methamphetamine</b> dependent zebrafish with high dose rhynchophylline significantly reduced the variations in the staying time and swimming distance in the drug box (P<0.05) and in the expressions of NR2B, <strong>TH</strong> and GLUR2 in the brain (P<0.05).
+TH	drug	amphetamine	27881347	Rhynchophylline can inhibit <b>methamphetamine</b> dependence in zebrafish, the mechanism of which may involve the expressions of <strong>TH</strong>, NR2B and GLUR2 proteins in the brain.
+TH	addiction	dependence	27881347	Rhynchophylline can inhibit methamphetamine <b>dependence</b> in zebrafish, the mechanism of which may involve the expressions of <strong>TH</strong>, NR2B and GLUR2 proteins in the brain.
+TH	addiction	relapse	27832596	A reduced cell size may lead to substantial enhancement of cue triggered bursting, which underlies drug <b>craving</b> and reward anticipation, whereas it could also result in DA depletion, as smaller neurons might express low levels of <strong>tyrosine hydroxylase</strong>.
+TH	addiction	reward	27832596	A reduced cell size may lead to substantial enhancement of cue triggered bursting, which underlies drug craving and <b>reward</b> anticipation, whereas it could also result in DA depletion, as smaller neurons might express low levels of <strong>tyrosine hydroxylase</strong>.
+TH	addiction	reward	27686026	While the <b>ICSS</b> experience seems to activate CART cells in the LH, the pVTA showed significant increment in the CART fiber terminals on the dopamine cells, increase in tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity, and CART and synaptophysin colabeled elements.
+TH	addiction	reward	27686026	While the <b>ICSS</b> experience seems to activate CART cells in the LH, the pVTA showed significant increment in the CART fiber terminals on the dopamine cells, increase in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity, and CART and synaptophysin colabeled elements.
+TH	drug	opioid	27696120	To investigate the hypothalamic mechanisms involved in estrogen actions in PRL secretion at the end of pregnancy, we measured the effect of pretreatment with the estrogen antagonist tamoxifen on the expression of tyrosine hydroxylase (<strong>TH</strong>), hormone receptors (ERα and β, PRs, PRLR(long)), and μ  and κ  <b>opioid</b> receptors (ORs) at mRNA (by semiquantitative RT PCR) and protein (by western blot for <strong>TH</strong>, PRLR(long), ERα, PRs, μ  and ORs) levels in extracts of medial basal hypothalamus (MBH) and serum PRL, E2 and P4 levels (by RIA) in mifepristone  and <b>naloxone</b> treated rats.
+TH	drug	opioid	27696120	To investigate the hypothalamic mechanisms involved in estrogen actions in PRL secretion at the end of pregnancy, we measured the effect of pretreatment with the estrogen antagonist tamoxifen on the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), hormone receptors (ERα and β, PRs, PRLR(long)), and μ  and κ  <b>opioid</b> receptors (ORs) at mRNA (by semiquantitative RT PCR) and protein (by western blot for <strong>TH</strong>, PRLR(long), ERα, PRs, μ  and ORs) levels in extracts of medial basal hypothalamus (MBH) and serum PRL, E2 and P4 levels (by RIA) in mifepristone  and <b>naloxone</b> treated rats.
+TH	addiction	withdrawal	27696120	Acting through ERα, E2 modulates hypothalamic dopaminergic neurons activity, regulating <strong>TH</strong>, μ  and κ ORs and PRLR(long) expression, and is necessary for evidencing the effects of P4 <b>withdrawal</b>.
+TH	drug	amphetamine	27687740	We found that acute <b>amphetamine</b> treatment increased Nurr1, p65 and <strong>TH</strong> protein levels in the VTA.
+TH	drug	amphetamine	27687740	On the other hand, chronic <b>amphetamine</b> treatment decreased Nurr1 and p65 protein levels, but <strong>TH</strong> was unchanged.
+TH	drug	cocaine	27596289	<strong>TH</strong> and DAT gene expression in the VTA was significantly lower both with topiramate alone and in combination with <b>cocaine</b> compared with animals receiving only <b>cocaine</b>.
+TH	drug	cocaine	27596289	• Topiramate increases the rewarding properties of <b>cocaine</b> in CPP • Topiramate alters dopaminergic signaling in the mesolimbic circuit • Topiramate delays the extinction of <b>cocaine</b> induced CPP • <strong>TH</strong> and DAT gene expression in the VTA decreases with topiramate and/or with <b>cocaine</b> • Results show that it should limit the use of topiramate in <b>cocaine</b> dependent subjects.
+TH	addiction	reward	27596289	• Topiramate increases the rewarding properties of cocaine in <b>CPP</b> • Topiramate alters dopaminergic signaling in the mesolimbic circuit • Topiramate delays the extinction of cocaine induced <b>CPP</b> • <strong>TH</strong> and DAT gene expression in the VTA decreases with topiramate and/or with cocaine • Results show that it should limit the use of topiramate in cocaine dependent subjects.
+TH	drug	cocaine	27562335	Previous studies demonstrated that the lysine dimethyltransferase G9a/G9a like protein (Glp) complex plays a critical role in <b>cocaine</b> induced central plasticity, and given <b>cocaine</b>'s role in the nerve system is relied on its function on dopamine system, we herein proposed that the reduced inhibition of dopaminergic transmission was from the downregulation of tyrosine hydroxylase expression by G9a/Glp complex through methylating its gene <strong>Th</strong> After approval by the Animal Care and Use Committee, C57BL/6 mice were used for pain behavior using von Frey after spared nerve injury, and <strong>Th</strong> CpG islands methylation was measured using bisulfite sequencing at different nerve areas.
+TH	drug	cocaine	27562335	Previous studies demonstrated that the lysine dimethyltransferase G9a/G9a like protein (Glp) complex plays a critical role in <b>cocaine</b> induced central plasticity, and given <b>cocaine</b>'s role in the nerve system is relied on its function on dopamine system, we herein proposed that the reduced inhibition of dopaminergic transmission was from the downregulation of <strong>tyrosine hydroxylase</strong> expression by G9a/Glp complex through methylating its gene <strong>Th</strong> After approval by the Animal Care and Use Committee, C57BL/6 mice were used for pain behavior using von Frey after spared nerve injury, and <strong>Th</strong> CpG islands methylation was measured using bisulfite sequencing at different nerve areas.
+TH	addiction	addiction	27547496	In human DA neurons, which provide an appropriate cellular milieu, VPA treatment alters the expression of several genes important for dopaminergic neuron function including DAT, Nurr1, and <strong>TH</strong>; this might partly explain its action in regulating <b>addictive</b> behaviors.
+TH	addiction	relapse	27440951	The pattern of anti <b>craving</b> medication, extent of adherence, and drinking outcome was collected at 1(st), 3(rd), 8(<strong>th</strong>), and 12(<strong>th</strong>) week follow up.
+TH	drug	opioid	27385847	Subjective and objective rating for <b>opioid</b> withdrawal was done by subjective opiate withdrawal scale (SOWS) and objective opiate withdrawal scale (OOWS) prepatch and postpatch 3(rd) and 7(<strong>th</strong>) day.
+TH	addiction	withdrawal	27385847	Subjective and objective rating for opioid <b>withdrawal</b> was done by subjective opiate <b>withdrawal</b> scale (SOWS) and objective opiate <b>withdrawal</b> scale (OOWS) prepatch and postpatch 3(rd) and 7(<strong>th</strong>) day.
+TH	addiction	addiction	27347434	With the exception of sparse numbers of <strong>TH</strong> immunoreactive D11 cells, dopamine containing neurons in other areas of the reward <b>addiction</b> circuitry, namely periaqueductal gray, and dorsal raphe, were also devoid of c Fos immunoreactivity.
+TH	addiction	reward	27347434	With the exception of sparse numbers of <strong>TH</strong> immunoreactive D11 cells, dopamine containing neurons in other areas of the <b>reward</b> addiction circuitry, namely periaqueductal gray, and dorsal raphe, were also devoid of c Fos immunoreactivity.
+TH	drug	cannabinoid	27336068	All of the adult patients (≥18 year old) with synthetic <b>cannabinoid</b> intoxication who presented to the Emergency Department throughout the two years of the study (July 1(st) 2012 June 30(<strong>th</strong>) 2014) were enrolled.
+TH	addiction	intoxication	27336068	All of the adult patients (≥18 year old) with synthetic cannabinoid <b>intoxication</b> who presented to the Emergency Department throughout the two years of the study (July 1(st) 2012 June 30(<strong>th</strong>) 2014) were enrolled.
+TH	drug	alcohol	27187237	The data suggest that TLR4 signaling in VTA dopaminergic neurons controls impulsivity related to the regulation of <strong>TH</strong> expression, likely contributing to the initiation of <b>alcohol</b> drinking and its transition to <b>alcohol</b> dependence.
+TH	addiction	dependence	27187237	The data suggest that TLR4 signaling in VTA dopaminergic neurons controls impulsivity related to the regulation of <strong>TH</strong> expression, likely contributing to the initiation of alcohol drinking and its transition to alcohol <b>dependence</b>.
+TH	drug	alcohol	27168749	Antitussive, expectorant and analgesic effects of the <b>ethanol</b> seed extract of Picralima nitida (Stapf) <strong>Th</strong>.
+TH	addiction	withdrawal	27154870	<b>Withdrawal</b> induced a significant volume and neuron loss that was accompanied by an increase in NPY expression without affecting α MSH and <strong>TH</strong> expression.
+TH	drug	opioid	27038750	This group had higher POMC in the arcuate nucleus (ARC), higher tyrosine hydroxylase (<strong>TH</strong>) in the VTA, higher dopa decarboxylase (DDc), higher D2R and μu <b>opioid</b> receptor in the NAc.
+TH	drug	opioid	27038750	This group had higher POMC in the arcuate nucleus (ARC), higher <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the VTA, higher dopa decarboxylase (DDc), higher D2R and μu <b>opioid</b> receptor in the NAc.
+TH	drug	alcohol	27011401	A performa was filled up prospectively for each consecutive new patient seeking treatment for drug/<b>alcohol</b> use (excluding tobacco) at De addiction centres funded by MOH&FW; NGOs under MoSJE and private psychiatrists between 15(<strong>th</strong>) July to 15(<strong>th</strong>) October, 2011.
+TH	drug	nicotine	27011401	A performa was filled up prospectively for each consecutive new patient seeking treatment for drug/alcohol use (excluding <b>tobacco</b>) at De addiction centres funded by MOH&FW; NGOs under MoSJE and private psychiatrists between 15(<strong>th</strong>) July to 15(<strong>th</strong>) October, 2011.
+TH	addiction	addiction	27011401	A performa was filled up prospectively for each consecutive new patient seeking treatment for drug/alcohol use (excluding tobacco) at De <b>addiction</b> centres funded by MOH&FW; NGOs under MoSJE and private psychiatrists between 15(<strong>th</strong>) July to 15(<strong>th</strong>) October, 2011.
+TH	addiction	relapse	27011401	A performa was filled up prospectively for each consecutive new patient <b>seeking</b> treatment for drug/alcohol use (excluding tobacco) at De addiction centres funded by MOH&FW; NGOs under MoSJE and private psychiatrists between 15(<strong>th</strong>) July to 15(<strong>th</strong>) October, 2011.
+TH	drug	amphetamine	27009763	Inhibiting effects of rhynchophylline on zebrafish <b>methamphetamine</b> dependence are associated with amelioration of neurotransmitters content and down regulation of <strong>TH</strong> and NR2B expression.
+TH	addiction	dependence	27009763	Inhibiting effects of rhynchophylline on zebrafish methamphetamine <b>dependence</b> are associated with amelioration of neurotransmitters content and down regulation of <strong>TH</strong> and NR2B expression.
+TH	drug	amphetamine	27009763	The current study investigated the inhibiting effects of rhynchophylline on <b>methamphetamine</b> induced (<b>METH</b> induced) CPP in adult zebrafish and <b>METH</b> induced locomotor activity in tyrosine hydroxylase green fluorescent protein (<strong>TH</strong> GFP) transgenic zebrafish larvae and attempted to confirm the hypothesis that these effects were mediated via regulation of neurotransmitters and dopaminergic and glutamatergic systems.
+TH	addiction	reward	27009763	The current study investigated the inhibiting effects of rhynchophylline on methamphetamine induced (METH induced) <b>CPP</b> in adult zebrafish and METH induced locomotor activity in tyrosine hydroxylase green fluorescent protein (<strong>TH</strong> GFP) transgenic zebrafish larvae and attempted to confirm the hypothesis that these effects were mediated via regulation of neurotransmitters and dopaminergic and glutamatergic systems.
+TH	drug	amphetamine	27009763	The current study investigated the inhibiting effects of rhynchophylline on <b>methamphetamine</b> induced (<b>METH</b> induced) CPP in adult zebrafish and <b>METH</b> induced locomotor activity in <strong>tyrosine hydroxylase</strong> green fluorescent protein (<strong>TH</strong> GFP) transgenic zebrafish larvae and attempted to confirm the hypothesis that these effects were mediated via regulation of neurotransmitters and dopaminergic and glutamatergic systems.
+TH	addiction	reward	27009763	The current study investigated the inhibiting effects of rhynchophylline on methamphetamine induced (METH induced) <b>CPP</b> in adult zebrafish and METH induced locomotor activity in <strong>tyrosine hydroxylase</strong> green fluorescent protein (<strong>TH</strong> GFP) transgenic zebrafish larvae and attempted to confirm the hypothesis that these effects were mediated via regulation of neurotransmitters and dopaminergic and glutamatergic systems.
+TH	drug	amphetamine	27009763	Results revealed that rhynchophylline (100mg/kg) significantly inhibited the acquisition of <b>METH</b> induced CPP, reduced the content of dopamine and glutamate and down regulated the expression of <strong>TH</strong> and NR2B in the CPP zebrafish brains.
+TH	addiction	reward	27009763	Results revealed that rhynchophylline (100mg/kg) significantly inhibited the acquisition of METH induced <b>CPP</b>, reduced the content of dopamine and glutamate and down regulated the expression of <strong>TH</strong> and NR2B in the <b>CPP</b> zebrafish brains.
+TH	drug	amphetamine	27009763	Furthermore, the influence of rhynchophylline on <b>METH</b> induced locomotor activity was also observed in <strong>TH</strong> GFP transgenic zebrafish larvae.
+TH	drug	amphetamine	27009763	Taken together, these data indicate that the inhibition of the formation of <b>METH</b> dependence by rhynchophylline in zebrafish is associated with amelioration of the neurotransmitters dopamine and glutamate content and down regulation of <strong>TH</strong> and NR2B expression.
+TH	addiction	dependence	27009763	Taken together, these data indicate that the inhibition of the formation of METH <b>dependence</b> by rhynchophylline in zebrafish is associated with amelioration of the neurotransmitters dopamine and glutamate content and down regulation of <strong>TH</strong> and NR2B expression.
+TH	drug	amphetamine	26974957	In addition, aSWNTs attenuated <b>METH</b> induced increases in <strong>tyrosine hydroxylase</strong> or synaptic protein expression.
+TH	drug	amphetamine	26946780	Moreover, phosphorylated <strong>tyrosine hydroxylase</strong> serine40 (pTH Ser40) levels in the ventral tegmental area (VTA) were increased by <b>methamphetamine</b>.
+TH	drug	alcohol	26939765	This was correlated with a significant 22% reduction in the number of dopaminergic like neurons in the VTA of naïve MS rats, similar to genetically <b>alcohol</b> preferring (P) rats which show a 35% reduction in tyrosine hydroxylase (<strong>TH</strong>) positive dopaminergic neurons in the VTA.
+TH	drug	alcohol	26939765	This was correlated with a significant 22% reduction in the number of dopaminergic like neurons in the VTA of naïve MS rats, similar to genetically <b>alcohol</b> preferring (P) rats which show a 35% reduction in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) positive dopaminergic neurons in the VTA.
+TH	addiction	addiction	26810004	The one target/gene identified as essential for drug induced behavioral responses across all drugs of abuse was the cat 2 gene coding for <strong>tyrosine hydroxylase</strong>, which is consistent with the role of dopamine neurotransmission in human <b>addiction</b>.
+TH	drug	opioid	26722146	Afterwards, the animals received <b>morphine</b> for 14 days by either of the following regimens: Once daily 45 mg/kg (positive controls)Increasing the interval (each time 6 hours longer than the previous interval)Irregular interval in every 36, 12 and 24 hours until the 21(<strong>th</strong>) day12, 24, 36 hours decreasing doses (each time 2.5 mg/kg less than the former dosage).
+TH	drug	opioid	29624299	<strong>Th</strong> ey usually include acetaminophen, nonsteroidal anti rheumatic drugs, and <b>opioids</b> (mostly weak <b>opioids</b>).
+TH	addiction	reward	26602173	In addition, we quantified the expression of tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area (VTA) and c Fos in the anterior cingulate cortex (ACC) as a response to <b>reward</b> learning and pain response.
+TH	addiction	reward	26602173	In addition, we quantified the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area (VTA) and c Fos in the anterior cingulate cortex (ACC) as a response to <b>reward</b> learning and pain response.
+TH	drug	opioid	26602173	We found an enhanced preference for the low level pain paired cue and enhanced <strong>TH</strong> expression in the VTA of the Placebo and Placebo + <b>Naloxone</b> groups.
+TH	addiction	withdrawal	26598419	In this report, we further characterize the role of glucocorticoid and mineralocorticoid receptor (GR and MR) signalling in DA turnover at the Nacc, and in opiate <b>withdrawal</b> induced tyrosine hydroxylase (<strong>TH</strong>) expression, ERK and CREB phosphorylation (activation) in the nucleus of tractus solitarius (NTS A2).
+TH	addiction	withdrawal	26598419	In this report, we further characterize the role of glucocorticoid and mineralocorticoid receptor (GR and MR) signalling in DA turnover at the Nacc, and in opiate <b>withdrawal</b> induced <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) expression, ERK and CREB phosphorylation (activation) in the nucleus of tractus solitarius (NTS A2).
+TH	drug	opioid	26598419	Six days later rats were pretreated with mifepristone, spironolactone or vehicle 30 min before <b>naloxone</b>, and DA turnover, <strong>TH</strong> expression, ERK and CREB phosphorylation, were measured using HPLC and immunoblotting.
+TH	drug	opioid	26598419	Glucocorticoid receptor blockade attenuated ERK and CREB phosphorylation and the <strong>TH</strong> expression induced by <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	26598419	Glucocorticoid receptor blockade attenuated ERK and CREB phosphorylation and the <strong>TH</strong> expression induced by morphine <b>withdrawal</b>.
+TH	drug	alcohol	26571816	The high positive correlation was obtained between EEC findings at the 5 <strong>th</strong> min of the first <b>ethanol</b> withdrawal and the same findings at the 5 <strong>th</strong> min of <b>ethanol</b> withdrawal in the second and the third episodes of <b>ethanol</b> withdrawal.
+TH	addiction	withdrawal	26571816	The high positive correlation was obtained between EEC findings at the 5 <strong>th</strong> min of the first ethanol <b>withdrawal</b> and the same findings at the 5 <strong>th</strong> min of ethanol <b>withdrawal</b> in the second and the third episodes of ethanol <b>withdrawal</b>.
+TH	drug	alcohol	26569416	Expressions of glutamate transporters, namely the excitatory amino acid transporter 2 (EAAT2) and EAAT3, in white blood cells were measured with the real time polymerase chain reaction (RT PCR) method in early (first day) and late (28(<strong>th</strong>) day) withdrawal in <b>alcoholic</b> patients and once in the controls.
+TH	addiction	withdrawal	26569416	Expressions of glutamate transporters, namely the excitatory amino acid transporter 2 (EAAT2) and EAAT3, in white blood cells were measured with the real time polymerase chain reaction (RT PCR) method in early (first day) and late (28(<strong>th</strong>) day) <b>withdrawal</b> in alcoholic patients and once in the controls.
+TH	drug	alcohol	26558894	Furthermore, by measuring locomotive activity, learning and memory performance, the number of dopaminergic neurons, <strong>tyrosine hydroxylase</strong> expression, and the change in the photoreceptors in the retina, we found that acute and chronic <b>alcohol</b> exposure induced varying degrees of Parkinson like symptoms in zebrafish.
+TH	drug	alcohol	26549324	<b>Ethanol</b> self administration significantly increased <strong>tyrosine hydroxylase</strong> immunoreactivity in pVTA and LC; the response was blocked by DSP 4 pre treatment.
+TH	addiction	addiction	26523857	In a second study, the anatomical basis of high and low CPP in the mouse brain was investigated by studying the number of neurons (neuronal nuclei positive) in two <b>addiction</b> related limbic regions (the medial prefrontal cortex and the basolateral amygdala) and the number of dopaminergic neurons (<strong>tyrosine hydroxylase</strong> positive) in the ventral tegmental area by immunohistochemistry and stereology.
+TH	addiction	reward	26523857	In a second study, the anatomical basis of high and low <b>CPP</b> in the mouse brain was investigated by studying the number of neurons (neuronal nuclei positive) in two addiction related limbic regions (the medial prefrontal cortex and the basolateral amygdala) and the number of dopaminergic neurons (<strong>tyrosine hydroxylase</strong> positive) in the ventral tegmental area by immunohistochemistry and stereology.
+TH	drug	alcohol	26509576	<b>Ethanol</b> and MDMA co administration increased NA turnover and <strong>TH</strong> expression and phosphorylation versus the consumption of each one of these drugs.
+TH	drug	psychedelics	26509576	Ethanol and <b>MDMA</b> co administration increased NA turnover and <strong>TH</strong> expression and phosphorylation versus the consumption of each one of these drugs.
+TH	drug	amphetamine	26465779	Exposure to binge <b>methamphetamine</b> (<b>METH</b>) can result in a permanent or transient loss of dopaminergic (DAergic) markers such as dopamine (DA), dopamine transporter, and tyrosine hydroxylase (<strong>TH</strong>) in the striatum.
+TH	addiction	intoxication	26465779	Exposure to <b>binge</b> methamphetamine (METH) can result in a permanent or transient loss of dopaminergic (DAergic) markers such as dopamine (DA), dopamine transporter, and tyrosine hydroxylase (<strong>TH</strong>) in the striatum.
+TH	drug	amphetamine	26465779	Exposure to binge <b>methamphetamine</b> (<b>METH</b>) can result in a permanent or transient loss of dopaminergic (DAergic) markers such as dopamine (DA), dopamine transporter, and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the striatum.
+TH	addiction	intoxication	26465779	Exposure to <b>binge</b> methamphetamine (METH) can result in a permanent or transient loss of dopaminergic (DAergic) markers such as dopamine (DA), dopamine transporter, and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the striatum.
+TH	drug	amphetamine	26427884	Multiple day dosing with <b>METH</b> enhanced DNA oxidation and decreased <strong>tyrosine hydroxylase</strong> and dopamine transporter staining in the striatum, indicating dopaminergic nerve terminal toxicity, which was more severe in  /  mice, as were deficits in motor coordination and olfactory discrimination.
+TH	drug	opioid	26386147	Therefore, this study investigated <strong>TH</strong> changes in dopaminergic neurons of the ventral tegmental area (VTA) and substantia nigra (SN), as well as the <b>morphine</b> effects on dopaminergic neurons induced by different durations of <b>morphine</b> dependence.
+TH	addiction	dependence	26386147	Therefore, this study investigated <strong>TH</strong> changes in dopaminergic neurons of the ventral tegmental area (VTA) and substantia nigra (SN), as well as the morphine effects on dopaminergic neurons induced by different durations of morphine <b>dependence</b>.
+TH	drug	opioid	26386147	Models of <b>morphine</b> dependence were established in rats, and paraffin embedded sections, immunohistochemistry and western blotting were used to observe the changes in the expression of <strong>TH</strong> protein.
+TH	addiction	dependence	26386147	Models of morphine <b>dependence</b> were established in rats, and paraffin embedded sections, immunohistochemistry and western blotting were used to observe the changes in the expression of <strong>TH</strong> protein.
+TH	drug	opioid	26386147	Immunohistochemistry and western blotting showed that the number of <strong>TH</strong> positive cells and the protein levels in the VTA and SN were significantly decreased in the rats with a long period of <b>morphine</b> dependency.
+TH	drug	amphetamine	26367473	This study examined changes in striatal dopamine transporter (DAT), tyrosine hydroxylase (<strong>TH</strong>) and dopamine receptor 2 (D2) 72 h after withdrawal from <b>METH</b> intravenous self  administration (IVSA).
+TH	addiction	withdrawal	26367473	This study examined changes in striatal dopamine transporter (DAT), tyrosine hydroxylase (<strong>TH</strong>) and dopamine receptor 2 (D2) 72 h after <b>withdrawal</b> from METH intravenous self  administration (IVSA).
+TH	drug	amphetamine	26367473	This study examined changes in striatal dopamine transporter (DAT), <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine receptor 2 (D2) 72 h after withdrawal from <b>METH</b> intravenous self  administration (IVSA).
+TH	addiction	withdrawal	26367473	This study examined changes in striatal dopamine transporter (DAT), <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine receptor 2 (D2) 72 h after <b>withdrawal</b> from METH intravenous self  administration (IVSA).
+TH	addiction	addiction	26266026	The highest scales in the SCL 90 R profile of our patients were those indicating somatic discomfort, anger, phobic anxiety, paranoid ideation, and also obsessive <b>compulsive</b> disorder symptoms (scores above the 39(<strong>th</strong>) percentile).
+TH	drug	amphetamine	26211645	Tyrosine hydroxylase (<strong>TH</strong>) expression was decreased by IH, but increased by <b>AMPH</b> + IH in mPFC.
+TH	drug	amphetamine	26211645	<strong>Tyrosine hydroxylase</strong> (<strong>TH</strong>) expression was decreased by IH, but increased by <b>AMPH</b> + IH in mPFC.
+TH	drug	opioid	26191179	Expression of the μ, κ, and δ <b>opioid</b> receptors and <strong>tyrosine hydroxylase</strong> in MN9D cells.
+TH	drug	nicotine	26169054	Many studies have demonstrated that repeated injections of <b>nicotine</b> can produce progressive increases in locomotor activity and enhanced expression of c fos and tyrosine hydroxylase (<strong>TH</strong>) in brain dopaminergic areas.
+TH	drug	nicotine	26169054	Many studies have demonstrated that repeated injections of <b>nicotine</b> can produce progressive increases in locomotor activity and enhanced expression of c fos and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in brain dopaminergic areas.
+TH	drug	nicotine	26169054	This study was carried out to investigate the effects of PJ on repeated <b>nicotine</b> induced behavioral sensitization of locomotor activity and c Fos and <strong>TH</strong> expression in the rat brain using immunohistochemistry.
+TH	addiction	sensitization	26169054	This study was carried out to investigate the effects of PJ on repeated nicotine induced behavioral <b>sensitization</b> of locomotor activity and c Fos and <strong>TH</strong> expression in the rat brain using immunohistochemistry.
+TH	drug	nicotine	26169054	Pretreatment with PJ decreased the development of <b>nicotine</b> induced sensitization, c Fos expression in the nucleus accumbens and striatum, and <strong>TH</strong> expression in the ventral tegmental area.
+TH	addiction	sensitization	26169054	Pretreatment with PJ decreased the development of nicotine induced <b>sensitization</b>, c Fos expression in the nucleus accumbens and striatum, and <strong>TH</strong> expression in the ventral tegmental area.
+TH	addiction	reward	26047964	Finally, gene expression levels of dopamine receptors 1 and 2 as well as <strong>tyrosine hydroxylase</strong> were measured in <b>reward</b> related brain regions.
+TH	drug	opioid	25988842	Alterations of the corticotropin releasing factor (CRF), glucocorticoid receptor (NR3C1), tyrosine hydroxylase (<strong>TH</strong>), mu <b>opioid</b> receptor (MOr), brain derived neurotrophic factor (BDNF), neuronal nuclei (NeuN), microtubule associated protein 2 (MAP2) and neurofilament heavy (NF200) immunoreactive fibers were studied in the paraventricular nucleus of the hypothalamus (PVN), ventral tegmental area (VTA), nucleus accumbens (NAc) or hippocampus (HIP).
+TH	drug	opioid	25988842	Alterations of the corticotropin releasing factor (CRF), glucocorticoid receptor (NR3C1), <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), mu <b>opioid</b> receptor (MOr), brain derived neurotrophic factor (BDNF), neuronal nuclei (NeuN), microtubule associated protein 2 (MAP2) and neurofilament heavy (NF200) immunoreactive fibers were studied in the paraventricular nucleus of the hypothalamus (PVN), ventral tegmental area (VTA), nucleus accumbens (NAc) or hippocampus (HIP).
+TH	drug	psychedelics	25894683	Antidepressant Effects of <b>Ketamine</b> Are Not Related to ¹⁸F FDG Metabolism or <strong>Tyrosine Hydroxylase</strong> Immunoreactivity in the Ventral Tegmental Area of Wistar Rats.
+TH	drug	psychedelics	25894683	Thus, our aims were to elucidate if <b>ketamine</b> would be able to revert depression like behaviors induced by a chronic unpredictable stress (CUS) protocol and if it could cause alterations to metabolism and tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity in VTA.
+TH	drug	psychedelics	25894683	Thus, our aims were to elucidate if <b>ketamine</b> would be able to revert depression like behaviors induced by a chronic unpredictable stress (CUS) protocol and if it could cause alterations to metabolism and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity in VTA.
+TH	drug	amphetamine	25746685	While wildtype mice show significant losses in striatal levels of the dopamine transporter (65% loss) and <strong>tyrosine hydroxylase</strong> (46% loss) following a 4 × 10 mg/kg <b>METH</b> dosing regimen, VMAT2 HI mice were protected from this damage.
+TH	drug	opioid	25745356	On the 15(<strong>th</strong>) day, thermal withdrawal was measured after s.c. <b>morphine</b> (20 mg/kg), but not melatonin, and <b>morphine</b> tolerance was measured and expressed by MPAE% (percent of maximal possible anti nociceptive effect) of <b>morphine</b>.
+TH	addiction	withdrawal	25745356	On the 15(<strong>th</strong>) day, thermal <b>withdrawal</b> was measured after s.c. morphine (20 mg/kg), but not melatonin, and morphine tolerance was measured and expressed by MPAE% (percent of maximal possible anti nociceptive effect) of morphine.
+TH	drug	alcohol	25660505	We recorded from identified DA neuronal cell bodies within ventral midbrain slices prepared from a transgenic mouse line (<strong>TH</strong> GFP) using long term stable extracellular recordings in a variety of locations and carefully mapped the responses to applied <b>ethanol</b> (EtOH).
+TH	drug	cocaine	25658879	Most of the genes studied (i.e., <strong>tyrosine hydroxylase</strong>, dopamine transporter, forkhead box A2, histone variant H3 family 3B, nuclear factor kappa B inhibitor alpha, growth arrest and DNA damage inducible beta) were found to be differentially expressed in chronic <b>cocaine</b> abusers irrespective of immediate cause of death or perimortem levels of <b>cocaine</b>, suggesting that these may represent core pathophysiological changes arising with chronic drug abuse.
+TH	drug	amphetamine	25629941	CCK 8 pretreatment attenuated <b>METH</b> (10mg/kg) induced hyperthermia, the decrease of tyrosine hydroxylase (<strong>TH</strong>) and dopamine transporter (DAT) in the striatum, and <strong>TH</strong> in the substantia nigra.
+TH	drug	amphetamine	25629941	CCK 8 pretreatment attenuated <b>METH</b> (10mg/kg) induced hyperthermia, the decrease of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine transporter (DAT) in the striatum, and <strong>TH</strong> in the substantia nigra.
+TH	drug	opioid	25626992	Our study has shown the following: (1) pre  and post treatment with JTT were effective at alleviating the wet dog shakes and episodes of writhing; (2) pre treatment with JTT inhibited the <b>morphine</b> induced decreases in dopamine transporter (DAT), dopamine D2 receptor (D2 R) and tyrosine hydroxylase (<strong>TH</strong>) levels in the striatum (p < 0.01, compared with <b>morphine</b> group) and maintained them at normal levels; and (3) post treatment with JTT restored the densities of DAT, D2 R and <strong>TH</strong> in the striatum to normal levels (p < 0.01, compared with <b>morphine</b> group).
+TH	drug	opioid	25626992	Our study has shown the following: (1) pre  and post treatment with JTT were effective at alleviating the wet dog shakes and episodes of writhing; (2) pre treatment with JTT inhibited the <b>morphine</b> induced decreases in dopamine transporter (DAT), dopamine D2 receptor (D2 R) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) levels in the striatum (p < 0.01, compared with <b>morphine</b> group) and maintained them at normal levels; and (3) post treatment with JTT restored the densities of DAT, D2 R and <strong>TH</strong> in the striatum to normal levels (p < 0.01, compared with <b>morphine</b> group).
+TH	drug	alcohol	25612895	<strong>Tyrosine hydroxylase</strong> (prelimbic cortex only) and choline acetyltransferase immunoreactivity levels were decreased in adolescent intermittent <b>ethanol</b> exposed rats compared with controls.
+TH	drug	alcohol	25612895	The decreases in <strong>tyrosine hydroxylase</strong> and choline acetyltransferase immunoreactivity suggest that adolescent intermittent <b>ethanol</b> exposure has enduring neural effects that may lead to altered adult behaviors, such as increased risky decision making.
+TH	drug	opioid	25582704	<b>Morphine</b> withdrawal induced an enhancement of NA turnover in PVN in parallel with an increase in <strong>TH</strong> neurons expressing c Fos in VLM in wild type mice.
+TH	addiction	withdrawal	25582704	Morphine <b>withdrawal</b> induced an enhancement of NA turnover in PVN in parallel with an increase in <strong>TH</strong> neurons expressing c Fos in VLM in wild type mice.
+TH	drug	opioid	25582704	The main finding of the present study was that NA turnover, <strong>TH</strong> positive neurons that express c Fos, <strong>TH</strong> phosphorylated at serine 40 and PKA expression observed during <b>morphine</b> withdrawal were significantly inhibited in CRF1R KO mice.
+TH	addiction	withdrawal	25582704	The main finding of the present study was that NA turnover, <strong>TH</strong> positive neurons that express c Fos, <strong>TH</strong> phosphorylated at serine 40 and PKA expression observed during morphine <b>withdrawal</b> were significantly inhibited in CRF1R KO mice.
+TH	addiction	withdrawal	25561936	After drug <b>withdrawal</b>, the hot plate test was repeated at the 17(<strong>th</strong>), 19(<strong>th</strong>), and 22(nd) days.
+TH	drug	opioid	25561936	At the 8(<strong>th</strong>) day (d8), <b>morphine</b> and <b>tramadol</b> led to the most powerful analgesic effect comparing to the other experimental days (P<0.001).
+TH	drug	opioid	25557842	In dependency tests, withdrawal symptoms were assessed on the 4(<strong>th</strong>) day for each animal 30 minutes after the administration of <b>naloxone</b> (4 mg/kg, i.p.
+TH	addiction	withdrawal	25557842	In dependency tests, <b>withdrawal</b> symptoms were assessed on the 4(<strong>th</strong>) day for each animal 30 minutes after the administration of naloxone (4 mg/kg, i.p.
+TH	drug	amphetamine	25535855	<b>Methamphetamine</b> significantly elevated core body temperature in males and decreased striatal DAT and <strong>TH</strong> content, and this effect was potentiated by early life stress.
+TH	drug	opioid	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single <b>morphine</b> administration, <b>morphine</b> dependence and withdrawal on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (DRD2), DA 1 receptor subtype as well as tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+TH	addiction	dependence	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single morphine administration, morphine <b>dependence</b> and withdrawal on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (DRD2), DA 1 receptor subtype as well as tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+TH	addiction	withdrawal	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single morphine administration, morphine dependence and <b>withdrawal</b> on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (DRD2), DA 1 receptor subtype as well as tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+TH	drug	opioid	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single <b>morphine</b> administration, <b>morphine</b> dependence and withdrawal on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (DRD2), DA 1 receptor subtype as well as <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+TH	addiction	dependence	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single morphine administration, morphine <b>dependence</b> and withdrawal on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (DRD2), DA 1 receptor subtype as well as <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+TH	addiction	withdrawal	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single morphine administration, morphine dependence and <b>withdrawal</b> on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (DRD2), DA 1 receptor subtype as well as <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+TH	addiction	addiction	25377367	High risk of Internet <b>addiction</b> and its relationship with lifetime substance use, psychological and behavioral problems among 10(<strong>th</strong>) grade adolescents.
+TH	addiction	addiction	25377367	The aim of this study was to investigate the relationship of higher risk of Internet <b>addiction</b> (HRIA) with lifetime substance use, psychological and behavioral factors among Turkish 10(<strong>th</strong>) grade students.
+TH	drug	alcohol	25377367	Male gender, lifetime use of tobacco, <b>alcohol</b> and/or drug, depression, attention deficit and hyperactivity symptoms and lack of assertiveness predicted the HRIA in Turkish 10(<strong>th</strong>) grade students.
+TH	drug	nicotine	25377367	Male gender, lifetime use of <b>tobacco</b>, alcohol and/or drug, depression, attention deficit and hyperactivity symptoms and lack of assertiveness predicted the HRIA in Turkish 10(<strong>th</strong>) grade students.
+TH	drug	alcohol	25324733	Medium Spiny Neurons (MSNs) of the Nucleus Accumbens (Nacc) show a reduced number of dendritic spines and a decrease in <strong>TH</strong> positive terminals upon withdrawal from opiates, cannabinoids and <b>alcohol</b>.
+TH	drug	cannabinoid	25324733	Medium Spiny Neurons (MSNs) of the Nucleus Accumbens (Nacc) show a reduced number of dendritic spines and a decrease in <strong>TH</strong> positive terminals upon withdrawal from opiates, <b>cannabinoids</b> and alcohol.
+TH	addiction	withdrawal	25324733	Medium Spiny Neurons (MSNs) of the Nucleus Accumbens (Nacc) show a reduced number of dendritic spines and a decrease in <strong>TH</strong> positive terminals upon <b>withdrawal</b> from opiates, cannabinoids and alcohol.
+TH	drug	opioid	25308750	The purpose of this study was to investigate the effects of MR blockade on: brain stress system responses to <b>naloxone</b> induced <b>morphine</b> withdrawal, the somatic signs of abstinence; the effects of <b>morphine</b> withdrawal on noradrenaline (NA) turnover in the paraventricular nucleus (PVN), c Fos expression and tyrosine hydroxylase (<strong>TH</strong>) phosphorylated at Ser31 levels in the nucleus tractus solitarius noradrenergic cell group (NTS A2); and finally, hypothalamus pituitary adrenocortical (HPA) axis activity.
+TH	addiction	withdrawal	25308750	The purpose of this study was to investigate the effects of MR blockade on: brain stress system responses to naloxone induced morphine <b>withdrawal</b>, the somatic signs of abstinence; the effects of morphine <b>withdrawal</b> on noradrenaline (NA) turnover in the paraventricular nucleus (PVN), c Fos expression and tyrosine hydroxylase (<strong>TH</strong>) phosphorylated at Ser31 levels in the nucleus tractus solitarius noradrenergic cell group (NTS A2); and finally, hypothalamus pituitary adrenocortical (HPA) axis activity.
+TH	drug	opioid	25308750	The purpose of this study was to investigate the effects of MR blockade on: brain stress system responses to <b>naloxone</b> induced <b>morphine</b> withdrawal, the somatic signs of abstinence; the effects of <b>morphine</b> withdrawal on noradrenaline (NA) turnover in the paraventricular nucleus (PVN), c Fos expression and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) phosphorylated at Ser31 levels in the nucleus tractus solitarius noradrenergic cell group (NTS A2); and finally, hypothalamus pituitary adrenocortical (HPA) axis activity.
+TH	addiction	withdrawal	25308750	The purpose of this study was to investigate the effects of MR blockade on: brain stress system responses to naloxone induced morphine <b>withdrawal</b>, the somatic signs of abstinence; the effects of morphine <b>withdrawal</b> on noradrenaline (NA) turnover in the paraventricular nucleus (PVN), c Fos expression and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) phosphorylated at Ser31 levels in the nucleus tractus solitarius noradrenergic cell group (NTS A2); and finally, hypothalamus pituitary adrenocortical (HPA) axis activity.
+TH	drug	opioid	25308750	On the other hand, pretreatment with spironolactone resulted in no significant modification of the increased NA turnover, <strong>TH</strong> activation, c Fos expression or HPA axis activity that occurred during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	25308750	On the other hand, pretreatment with spironolactone resulted in no significant modification of the increased NA turnover, <strong>TH</strong> activation, c Fos expression or HPA axis activity that occurred during morphine <b>withdrawal</b>.
+TH	drug	amphetamine	25273280	However, reduced <b>methamphetamine</b> seeking was associated with running induced reduction (and normalization) of the number of <strong>tyrosine hydroxylase</strong> immunoreactive neurons in the periaqueductal gray (PAG).
+TH	addiction	relapse	25273280	However, reduced methamphetamine <b>seeking</b> was associated with running induced reduction (and normalization) of the number of <strong>tyrosine hydroxylase</strong> immunoreactive neurons in the periaqueductal gray (PAG).
+TH	drug	amphetamine	25261212	Exposure to hot ambient temperature exacerbated <b>METH</b> toxicity evidenced by striatal reductions in <strong>TH</strong> and DAT and increased GFAP immmunoreactivity.
+TH	drug	opioid	25134609	(3) Pre treatment with AJN effectively interdicted the <b>morphine</b> induced decreases in the levels of DAT, D2R, and <strong>TH</strong> in the striatum (p < 0.01) such that they remained at nearly normal levels.
+TH	drug	opioid	25134609	AJN can effectively alleviate <b>opioid</b> withdrawal symptoms and preserve or restore the DAT, D2R, and <strong>TH</strong> levels in the striatum.
+TH	addiction	withdrawal	25134609	AJN can effectively alleviate opioid <b>withdrawal</b> symptoms and preserve or restore the DAT, D2R, and <strong>TH</strong> levels in the striatum.
+TH	drug	alcohol	25129124	; 8 % w/v) was observed from 7(<strong>th</strong>) day of <b>ethanol</b> diet (6 % v/v) consumption.
+TH	drug	alcohol	25129124	as tolerance was observed from 13(<strong>th</strong>)day since commencement of <b>ethanol</b> diet consumption.
+TH	drug	alcohol	25122682	Here we show that <b>ethanol</b> dependent rats display a loss of dendritic spines in medium spiny neurons of the nucleus accumbens (Nacc) shell, accompanied by a reduction of <strong>tyrosine hydroxylase</strong> immunostaining and postsynaptic density 95 positive elements.
+TH	drug	psychedelics	24980763	On 8(<strong>th</strong>) day after L PAM injection, the rats were weighted and blood and liver tissue were taken under <b>Ketamine</b> general anesthesia for biochemical examination.
+TH	drug	alcohol	24964687	The participants were recruited via interview using the <b>alcohol</b> section of the Thai version of Diagnostic Interview for Genetic Studies (<strong>Th</strong> DIGS), which included 165 psychiatric outpatients with <b>alcohol</b> dependence and 165 psychiatric outpatients without <b>alcohol</b> related disorders.
+TH	addiction	dependence	24964687	The participants were recruited via interview using the alcohol section of the Thai version of Diagnostic Interview for Genetic Studies (<strong>Th</strong> DIGS), which included 165 psychiatric outpatients with alcohol <b>dependence</b> and 165 psychiatric outpatients without alcohol related disorders.
+TH	drug	cocaine	24912888	Well known changes in <strong>tyrosine hydroxylase</strong> and protein kinase A were used for confirming biochemical effects of repeated <b>cocaine</b>.
+TH	drug	cocaine	24912888	Repeated <b>cocaine</b> led to well known short term augmentation of <strong>tyrosine hydroxylase</strong> and protein kinase A expressions in the nucleus accumbens, as well as maintained upregulation of <strong>tyrosine hydroxylase</strong> in the ventral tegmental area.
+TH	addiction	sensitization	24912888	It was confirmed that upregulation of <strong>tyrosine hydroxylase</strong> within the ventral tegmental area may participate on the development of motor <b>sensitization</b>.
+TH	drug	opioid	24904720	Following these injections, the percent of maximum possible effect (%MPE) of <b>morphine</b> was measured on the 1(st), 4(<strong>th</strong>), and 8(<strong>th</strong>) days by hot plate test.
+TH	drug	amphetamine	24890790	In the substantia nigra, there was marked reduction of <strong>TH</strong>+ cells, and Fluorogold (retrograde tracer) transport from the striatum to the nigra, at 28 and 56 days after <b>Meth</b>.
+TH	drug	alcohol	24846914	In this review, the roles of key factors of the monoamine system (dopamine receptor genes, 5 hydroxytryptamine receptor genes, transporter genes, <strong>tyrosine hydroxylase</strong> gene, tryptophanhydroxylase gene and monoamine oxidase gene) in <b>alcohol</b> dependence were discussed, and strategies for further studies of molecular mechanisms were proposed based on gene knockout mice models generated in our laboratory.
+TH	addiction	dependence	24846914	In this review, the roles of key factors of the monoamine system (dopamine receptor genes, 5 hydroxytryptamine receptor genes, transporter genes, <strong>tyrosine hydroxylase</strong> gene, tryptophanhydroxylase gene and monoamine oxidase gene) in alcohol <b>dependence</b> were discussed, and strategies for further studies of molecular mechanisms were proposed based on gene knockout mice models generated in our laboratory.
+TH	addiction	withdrawal	24800964	However neither genotype nor drug <b>withdrawal</b> affect the expression of <strong>tyrosine hydroxylase</strong> in the ventral tegmental area or the locus coeruleus and CRF in the central nucleus of the amygdala or the paraventricular nucleus of the hypothalamus, brain regions implicated in stress and drug responses.
+TH	addiction	withdrawal	24753218	After these <b>withdrawal</b> periods, we measured DA extracellular levels by in vivo microdialysis, DA tissue levels, and tyrosine hydroxylase (<strong>TH</strong>) and vesicular monoamine transporter 2 (VMAT2) expression in the LS.
+TH	addiction	withdrawal	24753218	After these <b>withdrawal</b> periods, we measured DA extracellular levels by in vivo microdialysis, DA tissue levels, and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and vesicular monoamine transporter 2 (VMAT2) expression in the LS.
+TH	drug	amphetamine	24748435	Moreover, <b>methamphetamine</b> increased phosphorylated <strong>tyrosine hydroxylase</strong> (pTH) levels in the ventral tegmental area (VTA).
+TH	drug	opioid	24727340	We measured mRNA expression of key components of the reward pathway (mu <b>opioid</b> receptor, proenkephalin, <strong>tyrosine hydroxylase</strong>, D1 and D2 receptors and the dopamine active transporter (DAT)) in the nucleus accumbens (NAc) and ventral tegmental area (VTA) of the offspring of control and cafeteria fed (JF) dams at weaning and after a 10 day <b>naloxone</b> treatment post weaning and determined food preferences in adulthood in the remaining offspring.
+TH	addiction	reward	24727340	We measured mRNA expression of key components of the <b>reward</b> pathway (mu opioid receptor, proenkephalin, <strong>tyrosine hydroxylase</strong>, D1 and D2 receptors and the dopamine active transporter (DAT)) in the nucleus accumbens (NAc) and ventral tegmental area (VTA) of the offspring of control and cafeteria fed (JF) dams at weaning and after a 10 day naloxone treatment post weaning and determined food preferences in adulthood in the remaining offspring.
+TH	drug	opioid	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single <b>morphine</b> administration, <b>morphine</b> dependence and <b>morphine</b> withdrawal on Nurr1 and Pitx3 expression as well as on the DA marker tyrosine hydroxylase (<strong>TH</strong>) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+TH	addiction	dependence	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single morphine administration, morphine <b>dependence</b> and morphine withdrawal on Nurr1 and Pitx3 expression as well as on the DA marker tyrosine hydroxylase (<strong>TH</strong>) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+TH	addiction	withdrawal	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single morphine administration, morphine dependence and morphine <b>withdrawal</b> on Nurr1 and Pitx3 expression as well as on the DA marker tyrosine hydroxylase (<strong>TH</strong>) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+TH	drug	opioid	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single <b>morphine</b> administration, <b>morphine</b> dependence and <b>morphine</b> withdrawal on Nurr1 and Pitx3 expression as well as on the DA marker <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+TH	addiction	dependence	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single morphine administration, morphine <b>dependence</b> and morphine withdrawal on Nurr1 and Pitx3 expression as well as on the DA marker <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+TH	addiction	withdrawal	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single morphine administration, morphine dependence and morphine <b>withdrawal</b> on Nurr1 and Pitx3 expression as well as on the DA marker <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+TH	drug	opioid	24706046	We showed that the three experimental conditions caused induction of Nurr1 and Pitx3 in the VTA, which correlated with changes in <strong>TH</strong> expression during chronic <b>morphine</b> administration.
+TH	drug	opioid	24706046	Furthermore, during <b>morphine</b> dependence, Nurr1 was detected in the nucleus compartment of VTA <strong>TH</strong> positive neurons, whereas Pitx3 was strongly detected in the nucleus of <strong>TH</strong> positive neurons after single <b>morphine</b> administration and during <b>morphine</b> withdrawal.
+TH	addiction	dependence	24706046	Furthermore, during morphine <b>dependence</b>, Nurr1 was detected in the nucleus compartment of VTA <strong>TH</strong> positive neurons, whereas Pitx3 was strongly detected in the nucleus of <strong>TH</strong> positive neurons after single morphine administration and during morphine withdrawal.
+TH	addiction	withdrawal	24706046	Furthermore, during morphine dependence, Nurr1 was detected in the nucleus compartment of VTA <strong>TH</strong> positive neurons, whereas Pitx3 was strongly detected in the nucleus of <strong>TH</strong> positive neurons after single morphine administration and during morphine <b>withdrawal</b>.
+TH	addiction	addiction	24644510	To understand this issue, a cross sectional study was conducted and sixty treatment and non treatment seekers who met the Diagnostic and Statistical Manual of Mental Disorders, 4(<strong>th</strong>) ed., Text Revision (DSM.IV TR) criteria for drug dependence with mean age of 28.7 (± 8.3) years were recruited from 16 <b>addiction</b> clinics and drop in centers (DICs) in Karaj, Iran.
+TH	addiction	dependence	24644510	To understand this issue, a cross sectional study was conducted and sixty treatment and non treatment seekers who met the Diagnostic and Statistical Manual of Mental Disorders, 4(<strong>th</strong>) ed., Text Revision (DSM.IV TR) criteria for drug <b>dependence</b> with mean age of 28.7 (± 8.3) years were recruited from 16 addiction clinics and drop in centers (DICs) in Karaj, Iran.
+TH	drug	cocaine	24634647	Results indicated that acute <b>cocaine</b> exposure decreased DAGLα expression, suggesting a down regulation of 2 arachidonylglycerol (2 AG) production, as well as gene expression of <strong>TH</strong>, KGA, mGluR3 and all ionotropic receptor subunits analyzed in the cerebellum.
+TH	drug	cocaine	24527678	Topiramate and <b>cocaine</b> co administration caused an up regulation of dopamine (Drd1, <strong>Th</strong>) and opioid (Oprm1) receptor genes.
+TH	drug	opioid	24527678	Topiramate and cocaine co administration caused an up regulation of dopamine (Drd1, <strong>Th</strong>) and <b>opioid</b> (Oprm1) receptor genes.
+TH	drug	opioid	24527041	Also the acupuncture stimulation significantly suppressed the increase in the hypothalamic corticotropin releasing factor (CRF) expression, the decrease in the <strong>tyrosine hydroxylase</strong> expression in the locus coeruleus, and the decrease in the hippocampal brain derived neurotrophic factor mRNA expression, induced by repeated injection of <b>morphine</b>.
+TH	drug	opioid	24409147	<b>Morphine</b> withdrawal activates ERK1/2 and phosphorylated tyrosine hydroxylase (<strong>TH</strong>) at Ser31 in the right and left ventricle.
+TH	addiction	withdrawal	24409147	Morphine <b>withdrawal</b> activates ERK1/2 and phosphorylated tyrosine hydroxylase (<strong>TH</strong>) at Ser31 in the right and left ventricle.
+TH	drug	opioid	24409147	<b>Morphine</b> withdrawal activates ERK1/2 and phosphorylated <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) at Ser31 in the right and left ventricle.
+TH	addiction	withdrawal	24409147	Morphine <b>withdrawal</b> activates ERK1/2 and phosphorylated <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) at Ser31 in the right and left ventricle.
+TH	drug	opioid	24409147	When N (2 guanidinoethyl) 5 isoquinolinesulfonamide (HA 1004), a PKA inhibitor was infused, the ability of <b>morphine</b> withdrawal to activate ERK, which phosphorylates <strong>TH</strong> at Ser31, was reduced.
+TH	addiction	withdrawal	24409147	When N (2 guanidinoethyl) 5 isoquinolinesulfonamide (HA 1004), a PKA inhibitor was infused, the ability of morphine <b>withdrawal</b> to activate ERK, which phosphorylates <strong>TH</strong> at Ser31, was reduced.
+TH	drug	opioid	24409147	The present finding demonstrated that the enhancement of ERK1/2 expression and the phosphorylation state of <strong>TH</strong> at Ser31 during <b>morphine</b> withdrawal are dependent on PKA and suggest cross talk between PKA and ERK1/2 transduction pathway mediating <b>morphine</b> withdrawal induced activation of <strong>TH</strong>.
+TH	addiction	withdrawal	24409147	The present finding demonstrated that the enhancement of ERK1/2 expression and the phosphorylation state of <strong>TH</strong> at Ser31 during morphine <b>withdrawal</b> are dependent on PKA and suggest cross talk between PKA and ERK1/2 transduction pathway mediating morphine <b>withdrawal</b> induced activation of <strong>TH</strong>.
+TH	drug	opioid	24399412	Moreover, pre treatment with the antibody could antagonize the effect of GDNF on inhibiting the neuroadaptations induced by chronic <b>morphine</b> exposure, including the decreases of the number and length of neurites and the size of cell bodies of VTA dopamine neurons, as well as the increase of <strong>tyrosine hydroxylase</strong> in the VTA dopamine neurons.
+TH	drug	opioid	24398105	Pre treatment with CRF1 receptor antagonist significantly reduced <b>morphine</b> withdrawal induced increases in plasma adrenocorticotropic hormone (ACTH) levels, NA turnover and <strong>TH</strong> phosphorylation at Ser31 in the right ventricle.
+TH	addiction	withdrawal	24398105	Pre treatment with CRF1 receptor antagonist significantly reduced morphine <b>withdrawal</b> induced increases in plasma adrenocorticotropic hormone (ACTH) levels, NA turnover and <strong>TH</strong> phosphorylation at Ser31 in the right ventricle.
+TH	drug	opioid	24358001	Additionally, <b>opioid</b> prescribing guidelines and educational programs, including World Health Organization published guidelines for the management of cancer pain in 1986 and the American Pain Society's promotion of pain as the 5(<strong>th</strong>) vital sign, have increased the propensity of pharmacists, physicians, and pain specialists to dispense pain treatments.
+TH	drug	cocaine	24238615	<b>Cocaine</b> withdrawal influences paternal behavior and associated central expression of vasopressin, oxytocin and <strong>tyrosine hydroxylase</strong> in mandarin voles.
+TH	addiction	withdrawal	24238615	Cocaine <b>withdrawal</b> influences paternal behavior and associated central expression of vasopressin, oxytocin and <strong>tyrosine hydroxylase</strong> in mandarin voles.
+TH	drug	cocaine	24238615	Last, fewer AVP and OT immunoreactive neurons in the paraventricular nucleus and more <strong>tyrosine hydroxylase</strong> immunoreactive neurons in the ventral tegmental area were observed in <b>cocaine</b> treated fathers.
+TH	drug	amphetamine	24072398	This depressive like profile induced by <b>METH</b> was accompanied by a marked depletion of frontostriatal dopaminergic and serotonergic neurotransmission, indicated by a reduction in the levels of dopamine, DOPAC and HVA, <strong>tyrosine hydroxylase</strong> and serotonin, observed at both 3 and 49 days post administration.
+TH	drug	cocaine	23970867	The abundance of surrogate markers of dopamine signaling and plasticity in the dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC) were examined: glycosylated and non glycosylated forms of the dopamine transporter (efficiency of dopamine transport), tyrosine hydroxylase (<strong>TH</strong>; marker of dopamine synthesis) and phosphorylated <strong>TH</strong> at Serine 30 and 40 (markers of enzyme activity), extracellular signal regulated kinase 1 and 2 (ERK1 and ERK 2), and phosphorylated ERK1 and ERK2 (phosphorylates <strong>TH</strong> Serine 31; markers of synaptic plasticity), and markers of synaptic integrity, spinophilin and post synaptic density protein 95 (roles in dopamine signaling and response to <b>cocaine</b>).
+TH	drug	cocaine	23970867	The abundance of surrogate markers of dopamine signaling and plasticity in the dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC) were examined: glycosylated and non glycosylated forms of the dopamine transporter (efficiency of dopamine transport), <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>; marker of dopamine synthesis) and phosphorylated <strong>TH</strong> at Serine 30 and 40 (markers of enzyme activity), extracellular signal regulated kinase 1 and 2 (ERK1 and ERK 2), and phosphorylated ERK1 and ERK2 (phosphorylates <strong>TH</strong> Serine 31; markers of synaptic plasticity), and markers of synaptic integrity, spinophilin and post synaptic density protein 95 (roles in dopamine signaling and response to <b>cocaine</b>).
+TH	drug	opioid	23927484	<b>Morphine</b> regulates Argonaute 2 and <strong>TH</strong> expression and activity but not miR 133b in midbrain dopaminergic neurons.
+TH	drug	opioid	23927484	These changes were paralleled with enhanced and decreased NAc tyrosine hydroxylase (<strong>TH</strong>) protein (an early DA marker) in <b>morphine</b> dependent rats and after withdrawal, respectively.
+TH	addiction	withdrawal	23927484	These changes were paralleled with enhanced and decreased NAc tyrosine hydroxylase (<strong>TH</strong>) protein (an early DA marker) in morphine dependent rats and after <b>withdrawal</b>, respectively.
+TH	drug	opioid	23927484	These changes were paralleled with enhanced and decreased NAc <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) protein (an early DA marker) in <b>morphine</b> dependent rats and after withdrawal, respectively.
+TH	addiction	withdrawal	23927484	These changes were paralleled with enhanced and decreased NAc <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) protein (an early DA marker) in morphine dependent rats and after <b>withdrawal</b>, respectively.
+TH	drug	opioid	23927484	We also observed changes in <strong>TH</strong> mRNA expression in the VTA that could be related to Ago2 induced translational repression of <strong>TH</strong> mRNA during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	23927484	We also observed changes in <strong>TH</strong> mRNA expression in the VTA that could be related to Ago2 induced translational repression of <strong>TH</strong> mRNA during morphine <b>withdrawal</b>.
+TH	drug	opioid	23927484	Acute <b>morphine</b> administration produced a marked increase in <strong>TH</strong> activity and DA turnover in the NAc (shell).
+TH	drug	opioid	23927484	In contrast, precipitated <b>morphine</b> withdrawal decreased <strong>TH</strong> activation and did not change DA turnover.
+TH	addiction	withdrawal	23927484	In contrast, precipitated morphine <b>withdrawal</b> decreased <strong>TH</strong> activation and did not change DA turnover.
+TH	addiction	addiction	23885543	According to the Act on Counteracting Drug <b>Addiction</b> (20 <strong>th</strong> of March, 2009, Dz.
+TH	drug	amphetamine	23875705	These results suggest that selective inhibition of VMAT2 produces a time dependent decrease in DA release in NAc shell as a result of alterations in <strong>tyrosine hydroxylase</strong> activity, which may play a role in the ability of GZ 793A to decrease <b>METH</b> reward.
+TH	addiction	reward	23875705	These results suggest that selective inhibition of VMAT2 produces a time dependent decrease in DA release in NAc shell as a result of alterations in <strong>tyrosine hydroxylase</strong> activity, which may play a role in the ability of GZ 793A to decrease METH <b>reward</b>.
+TH	drug	opioid	23855434	Tyrosine hydroxylase (<strong>TH</strong>) and μ <b>opioid</b> receptor gene expressions were also measured in the ventral tegmental area and nucleus accumbens (NAcc), respectively.
+TH	drug	opioid	23855434	<strong>Tyrosine hydroxylase</strong> (<strong>TH</strong>) and μ <b>opioid</b> receptor gene expressions were also measured in the ventral tegmental area and nucleus accumbens (NAcc), respectively.
+TH	drug	alcohol	23855434	Acute <b>ethanol</b> administration (1 2 g/kg) increased <strong>TH</strong> and μ opioid receptor gene expressions in CB2 KO mice, whereas the lower dose of <b>ethanol</b> decreased <strong>TH</strong> gene expression in WT mice.
+TH	drug	opioid	23855434	Acute ethanol administration (1 2 g/kg) increased <strong>TH</strong> and μ <b>opioid</b> receptor gene expressions in CB2 KO mice, whereas the lower dose of ethanol decreased <strong>TH</strong> gene expression in WT mice.
+TH	drug	alcohol	23855434	These results suggest that deletion of the CB2 r gene increased preference for and vulnerability to <b>ethanol</b> consumption, at least in part, by increased <b>ethanol</b> induced sensitivity of the <strong>TH</strong> and μ opioid receptor gene expressions in mesolimbic neurons.
+TH	drug	opioid	23855434	These results suggest that deletion of the CB2 r gene increased preference for and vulnerability to ethanol consumption, at least in part, by increased ethanol induced sensitivity of the <strong>TH</strong> and μ <b>opioid</b> receptor gene expressions in mesolimbic neurons.
+TH	drug	alcohol	23825854	Sleep heart rate variability of 20 male <b>alcohol</b> dependent inpatients was recorded on the 5(<strong>th</strong>) day after detoxification.
+TH	drug	opioid	23773348	All Serious Adverse Drug Reactions (SADR) notified with <b>tramadol</b> to the French PharmacoVigilance Centres (CRPV) and pharmaceutical companies between August 1(st), 2010 and July 31(<strong>th</strong>), 2011 were analyzed.
+TH	drug	amphetamine	23574629	RHA rats also showed a higher expression of the <strong>tyrosine hydroxylase</strong> gene in SN/VTA, higher levels of extracellular DA in striatum and augmentation of the DA releasing effects of <b>amphetamine</b> (<b>Amph</b>), suggesting hyperfunctioning of midbrain DA neurons.
+TH	drug	alcohol	23573810	Effects of <b>naltrexone</b> plus topiramate on <b>ethanol</b> self administration and <strong>tyrosine hydroxylase</strong> gene expression changes.
+TH	drug	alcohol	23573810	Real time PCR analyses revealed that <b>naltrexone</b> significantly normalized the increase of <strong>TH</strong> gene expression in the VTA induced by <b>ethanol</b>, whereas the administration of topiramate did not produce any significant effect.
+TH	drug	alcohol	23573810	In the <b>ethanol</b> self administration procedure, the combination of both drugs further reduced <strong>TH</strong> gene expression, reaching statistical significance compared with the vehicle, <b>naltrexone</b> or topiramate groups.
+TH	drug	cocaine	23499958	Treatment with resveratrol (50μM for 30min) enhanced <b>cocaine</b> induced increases in the phosphorylation of DARPP 32 at Thr34 and GluA1 at Ser845, postsynaptic substrates for dopamine/D1 receptor/PKA signaling, and a <b>cocaine</b> induced decrease in the phosphorylation of <strong>tyrosine hydroxylase</strong> at Ser40, a presynaptic substrate for dopamine/D2 receptor signaling.
+TH	drug	cocaine	23447367	In CTL, C+, and PA15, but not in PA19 rats, the expression of <strong>TH</strong> in NAcc was reduced in groups repeatedly treated with <b>cocaine</b>, independently of the challenge test.
+TH	drug	opioid	27392672	All Serious Adverse Drug Reactions (SADR) notified with <b>tramadol</b> to the French PharmacoVigilance Centres (CRPV) and pharmaceutical companies between August 1(st), 2010 and July 31(<strong>th</strong>), 2011 were analyzed.
+TH	drug	nicotine	23437324	The effects of employment conditions on <b>smoking</b> status and <b>smoking</b> intensity: the analysis of Korean labor & income panel 8(<strong>th</strong>) 10(<strong>th</strong>) wave.
+TH	drug	nicotine	23437324	To examine the association between employment condition and <b>smoking</b> status, we selected male respondents aged 20 59 that participated in all of the 8(<strong>th</strong>) 10(<strong>th</strong>) wave of Korean Labor and Income Panel Study(KLIPS) which is a nationally representative data.
+TH	drug	alcohol	23411164	The following factors increased the probability of becoming a smoker (OR and 95%CI): being a female 0.60 (0.53 0.68), being in the 4(<strong>th</strong>) year 1.27 (1.12 1.43), low academic performance 3.38 (2.74 4.17), self reported regular/poor health status 2.81 (2.21 3.58), smoking parents 1.68 (1.45 1.95), <b>alcohol</b> consumption 5.05 (4.35 5.86), having 3 or more problems of mood state 1.22 (1.05 1.41), living without parents 1.59 (1.07 2.38), agreeing with tobacco industry advertising 1.64 (1.45 1.85) and believing that tobacco acts as a relaxant 3.57 (3.23 4.17).
+TH	drug	nicotine	23411164	The following factors increased the probability of becoming a <b>smoker</b> (OR and 95%CI): being a female 0.60 (0.53 0.68), being in the 4(<strong>th</strong>) year 1.27 (1.12 1.43), low academic performance 3.38 (2.74 4.17), self reported regular/poor health status 2.81 (2.21 3.58), <b>smoking</b> parents 1.68 (1.45 1.95), alcohol consumption 5.05 (4.35 5.86), having 3 or more problems of mood state 1.22 (1.05 1.41), living without parents 1.59 (1.07 2.38), agreeing with <b>tobacco</b> industry advertising 1.64 (1.45 1.85) and believing that <b>tobacco</b> acts as a relaxant 3.57 (3.23 4.17).
+TH	drug	opioid	23402719	The nucleus accumbens (NAc) was isolated and mRNA expression of tyrosine hydroxylase (<strong>TH</strong>), dopamine active transporter (DAT), D1 and D2 dopamine receptors, and μ <b>opioid</b> receptor determined by qRT PCR.
+TH	drug	opioid	23402719	The nucleus accumbens (NAc) was isolated and mRNA expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), dopamine active transporter (DAT), D1 and D2 dopamine receptors, and μ <b>opioid</b> receptor determined by qRT PCR.
+TH	drug	amphetamine	23358239	Behaviorally, adolescents were less sensitive to <b>amphetamine</b> but more sensitive to a <strong>TH</strong> inhibitor.
+TH	drug	amphetamine	23313192	In <b>METH</b> exposed rats, the increase in parkin levels attenuated <b>METH</b> induced decreases in striatal <strong>tyrosine hydroxylase</strong> immunoreactivity in a dose dependent manner, indicating that parkin can protect striatal dopaminergic terminals against <b>METH</b> neurotoxicity.
+TH	drug	cocaine	23285158	Via miR 133b <b>cocaine</b> would modulate the expression of pitx3 and subsequently of dopamine receptors, dat and <strong>th</strong>.
+TH	drug	opioid	23269899	The purpose of this study was to evaluate whether berberine (BER) administration could attenuate depression  and anxiety like behaviors and increase corticotrophin releasing factor (CRF) and tyrosine hydroxylase (<strong>TH</strong>) expression following chronic <b>morphine</b> withdrawal in rats.
+TH	addiction	withdrawal	23269899	The purpose of this study was to evaluate whether berberine (BER) administration could attenuate depression  and anxiety like behaviors and increase corticotrophin releasing factor (CRF) and tyrosine hydroxylase (<strong>TH</strong>) expression following chronic morphine <b>withdrawal</b> in rats.
+TH	drug	opioid	23269899	The purpose of this study was to evaluate whether berberine (BER) administration could attenuate depression  and anxiety like behaviors and increase corticotrophin releasing factor (CRF) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) expression following chronic <b>morphine</b> withdrawal in rats.
+TH	addiction	withdrawal	23269899	The purpose of this study was to evaluate whether berberine (BER) administration could attenuate depression  and anxiety like behaviors and increase corticotrophin releasing factor (CRF) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) expression following chronic morphine <b>withdrawal</b> in rats.
+TH	drug	nicotine	23233221	Further studies using high performance liquid chromatography, western blotting and immunofluorescence staining analyses showed that L theanine significantly inhibited <b>nicotine</b> induced tyrosine hydroxylase (<strong>TH</strong>) expression and dopamine production in the midbrain of mice.
+TH	drug	nicotine	23233221	Further studies using high performance liquid chromatography, western blotting and immunofluorescence staining analyses showed that L theanine significantly inhibited <b>nicotine</b> induced <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) expression and dopamine production in the midbrain of mice.
+TH	drug	nicotine	23233221	Knockdown of c Fos by siRNA inhibited the excitatory status of cells but not the upregulation of <strong>TH</strong> induced by <b>nicotine</b> in SH SY5Y cells.
+TH	drug	opioid	23215787	We have examined the effects of acute and chronic <b>morphine</b> and <b>morphine</b> withdrawal on <strong>TH</strong> expression and activity as well as expression of Nurr1, Pitx3 and Ago2 in the ventral tegmental area (VTA) and nucleus accumbens (NAc) of the rat.
+TH	addiction	withdrawal	23215787	We have examined the effects of acute and chronic morphine and morphine <b>withdrawal</b> on <strong>TH</strong> expression and activity as well as expression of Nurr1, Pitx3 and Ago2 in the ventral tegmental area (VTA) and nucleus accumbens (NAc) of the rat.
+TH	drug	opioid	23215787	Acute <b>morphine</b> produced a marked increase in <strong>TH</strong> activity and DA turnover in the NAc, concomitantly with increased Nurr1 and Pitx3 expression in the VTA.
+TH	drug	opioid	23215787	In contrast, precipitated <b>morphine</b> withdrawal decreased <strong>TH</strong> activation, <strong>TH</strong> expression and did not increase DA turnover in the NAc.
+TH	addiction	withdrawal	23215787	In contrast, precipitated morphine <b>withdrawal</b> decreased <strong>TH</strong> activation, <strong>TH</strong> expression and did not increase DA turnover in the NAc.
+TH	drug	opioid	23215787	The combined decrease in Ago2 and increases in Nurr1 and Pitx3 might represent some of the mechanisms that served to protect against accumbal <strong>TH</strong> regulation observed in <b>morphine</b> withdrawn rats, which may be critical for DA bioavailability to influence behaviour.
+TH	drug	nicotine	23202349	Assessments of the effects of <b>nicotine</b> and ketamine using <strong>tyrosine hydroxylase</strong> green fluorescent protein transgenic zebrafish as biosensors.
+TH	drug	psychedelics	23202349	Assessments of the effects of nicotine and <b>ketamine</b> using <strong>tyrosine hydroxylase</strong> green fluorescent protein transgenic zebrafish as biosensors.
+TH	drug	nicotine	23202349	The <strong>TH</strong> GFP transgenic zebrafish were employed as live biosensors to test the effects of the commonly abused drugs <b>nicotine</b> and ketamine.
+TH	drug	psychedelics	23202349	The <strong>TH</strong> GFP transgenic zebrafish were employed as live biosensors to test the effects of the commonly abused drugs nicotine and <b>ketamine</b>.
+TH	drug	amphetamine	23195702	This study investigated the involvements of dopaminergic and glutamatergic transmission in the development of <b>Meth</b> psychosis and dependence by using tyrosine hydroxylase heterozygous mutant (<strong>TH</strong>+/ ) mice and N methyl d aspartate receptor knockout (NR2A / ) mice.
+TH	addiction	dependence	23195702	This study investigated the involvements of dopaminergic and glutamatergic transmission in the development of Meth psychosis and <b>dependence</b> by using tyrosine hydroxylase heterozygous mutant (<strong>TH</strong>+/ ) mice and N methyl d aspartate receptor knockout (NR2A / ) mice.
+TH	drug	amphetamine	23195702	This study investigated the involvements of dopaminergic and glutamatergic transmission in the development of <b>Meth</b> psychosis and dependence by using <strong>tyrosine hydroxylase</strong> heterozygous mutant (<strong>TH</strong>+/ ) mice and N methyl d aspartate receptor knockout (NR2A / ) mice.
+TH	addiction	dependence	23195702	This study investigated the involvements of dopaminergic and glutamatergic transmission in the development of Meth psychosis and <b>dependence</b> by using <strong>tyrosine hydroxylase</strong> heterozygous mutant (<strong>TH</strong>+/ ) mice and N methyl d aspartate receptor knockout (NR2A / ) mice.
+TH	drug	opioid	23071721	However, blockade of CRF1 receptor significantly reduced <b>morphine</b> withdrawal induced increases in plasma adrenocorticotropin (ACTH) levels, DA turnover and <strong>TH</strong> phosphorylation at Ser40 in the NAc.
+TH	addiction	withdrawal	23071721	However, blockade of CRF1 receptor significantly reduced morphine <b>withdrawal</b> induced increases in plasma adrenocorticotropin (ACTH) levels, DA turnover and <strong>TH</strong> phosphorylation at Ser40 in the NAc.
+TH	drug	opioid	23071721	In addition, CP 154,526 reduced the number of <strong>TH</strong> containing neurons expressing c Fos in the VTA after <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	23071721	In addition, CP 154,526 reduced the number of <strong>TH</strong> containing neurons expressing c Fos in the VTA after naloxone precipitated morphine <b>withdrawal</b>.
+TH	drug	amphetamine	23056363	Modafinil also counteracted the decrease in <strong>tyrosine hydroxylase</strong> and dopamine transporter levels and prevented <b>methamphetamine</b> induced increases in the pro apoptotic BAX and decreases in the anti apoptotic Bcl 2 protein expression.
+TH	drug	nicotine	23020022	Between 2009 2011, non compulsory lectures on the diagnosis and treatment of <b>tobacco</b> dependence were provided for 3(rd) to 6(<strong>th</strong>) year students of medicine at the Medical University in Wroclaw (170 students).
+TH	addiction	dependence	23020022	Between 2009 2011, non compulsory lectures on the diagnosis and treatment of tobacco <b>dependence</b> were provided for 3(rd) to 6(<strong>th</strong>) year students of medicine at the Medical University in Wroclaw (170 students).
+TH	drug	amphetamine	22952603	We identified several putative associations; the strongest was between a positive subjective drug response factor and a SNP (rs3784943) in the 8(<strong>th</strong>) intron of cadherin 13 (CDH13; P = 4.58×10( 8)), a gene previously associated with a number of psychiatric traits including <b>methamphetamine</b> dependence.
+TH	addiction	dependence	22952603	We identified several putative associations; the strongest was between a positive subjective drug response factor and a SNP (rs3784943) in the 8(<strong>th</strong>) intron of cadherin 13 (CDH13; P = 4.58×10( 8)), a gene previously associated with a number of psychiatric traits including methamphetamine <b>dependence</b>.
+TH	drug	cocaine	22910534	Sulpiride, but not SCH23390, modifies <b>cocaine</b> induced conditioned place preference and expression of <strong>tyrosine hydroxylase</strong> and elongation factor 1α in zebrafish.
+TH	drug	cocaine	22910534	Acute <b>cocaine</b> exposure also induced a rise in the expression of tyrosine hydroxylase (<strong>TH</strong>), an important enzyme in dopamine synthesis, and a significant decrease in the expression of elongation factor 1α (EF1α), a housekeeping gene that regulates protein synthesis.
+TH	drug	cocaine	22910534	Acute <b>cocaine</b> exposure also induced a rise in the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), an important enzyme in dopamine synthesis, and a significant decrease in the expression of elongation factor 1α (EF1α), a housekeeping gene that regulates protein synthesis.
+TH	drug	cocaine	22910534	<b>Cocaine</b> selectively increased the ratio of <strong>TH</strong>/EF1α in the telencephalon, but not in other brain regions.
+TH	drug	cocaine	22910534	The <b>cocaine</b> induced change in <strong>TH</strong>/EF1α was blocked by co treatment with sulpiride, but not SCH23390, correlating closely with the action of these drugs on the CPP behavioral response.
+TH	addiction	reward	22910534	The cocaine induced change in <strong>TH</strong>/EF1α was blocked by co treatment with sulpiride, but not SCH23390, correlating closely with the action of these drugs on the <b>CPP</b> behavioral response.
+TH	drug	amphetamine	22884891	This <b>methamphetamine</b> regimen also produced dopaminergic terminal degeneration in the striatum, as evidenced by dopamine and <strong>tyrosine hydroxylase</strong> depletion.
+TH	drug	opioid	22796075	Here we determined whether <b>opioid</b> agonists modulate afferent activation of NTS CA neurons using transgenic mice with EGFP expressed under the control of the tyrosine hydroxylase promoter (<strong>TH</strong> EGFP) to identify catecholamine neurons.
+TH	drug	opioid	22796075	Here we determined whether <b>opioid</b> agonists modulate afferent activation of NTS CA neurons using transgenic mice with EGFP expressed under the control of the <strong>tyrosine hydroxylase</strong> promoter (<strong>TH</strong> EGFP) to identify catecholamine neurons.
+TH	drug	opioid	22796075	The <b>opioid</b> agonist Met enkephalin (Met Enk) significantly attenuated solitary tract evoked excitatory postsynaptic currents (ST EPSCs) in NTS <strong>TH</strong> EGFP neurons by 80%, an effect reversed by wash or the mu <b>opioid</b> receptor specific antagonist D Phe Cys Tyr D Trp Orn Thr Pen Thr NH(2) (CTOP).
+TH	drug	psychedelics	22764597	[Effects of electroacupuncture intervention at different time in A day on expression of <strong>tyrosine hydroxylase</strong> and C fos in nucleus accumbens in <b>ketamine</b> addiction rats].
+TH	addiction	addiction	22764597	[Effects of electroacupuncture intervention at different time in A day on expression of <strong>tyrosine hydroxylase</strong> and C fos in nucleus accumbens in ketamine <b>addiction</b> rats].
+TH	drug	psychedelics	22764597	To observe the effect of electroacupuncture (EA) intervention at different time in a day on the expression of tyrosine hydroxylase (<strong>TH</strong>) and c fos in the Nucleus Accumbens (NAc) so as to explore its mechanism underlying improvement of <b>ketamine</b> addiction.
+TH	addiction	addiction	22764597	To observe the effect of electroacupuncture (EA) intervention at different time in a day on the expression of tyrosine hydroxylase (<strong>TH</strong>) and c fos in the Nucleus Accumbens (NAc) so as to explore its mechanism underlying improvement of ketamine <b>addiction</b>.
+TH	drug	psychedelics	22764597	To observe the effect of electroacupuncture (EA) intervention at different time in a day on the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and c fos in the Nucleus Accumbens (NAc) so as to explore its mechanism underlying improvement of <b>ketamine</b> addiction.
+TH	addiction	addiction	22764597	To observe the effect of electroacupuncture (EA) intervention at different time in a day on the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and c fos in the Nucleus Accumbens (NAc) so as to explore its mechanism underlying improvement of ketamine <b>addiction</b>.
+TH	drug	psychedelics	22764597	EA of "Zusanli" (ST 36) and "Sanyinjiao" (SP 6) at 11:00 and 17:00 of the daytime can down regulate <b>ketamine</b> addiction induced increase of expression of <strong>TH</strong> and c fos in the NAc in <b>ketamine</b> addiction rats, which may contribute to its effect in relieving <b>ketamine</b> addiction symptoms in clinic.
+TH	addiction	addiction	22764597	EA of "Zusanli" (ST 36) and "Sanyinjiao" (SP 6) at 11:00 and 17:00 of the daytime can down regulate ketamine <b>addiction</b> induced increase of expression of <strong>TH</strong> and c fos in the NAc in ketamine <b>addiction</b> rats, which may contribute to its effect in relieving ketamine <b>addiction</b> symptoms in clinic.
+TH	drug	opioid	22713675	The purpose of the present study was to evaluate: (i) the turnover of DA, NA and 5 HT in the nucleus accumbens (NAc), one of the most important substrates for aversive states, (ii) the changes in tyrosine hydroxylase (<strong>TH</strong>) gene expression in the ventral tegmental area, and (iii) total <strong>TH</strong> protein levels and <strong>TH</strong> phosphorylation in the NAc after <b>naloxone</b> induced <b>morphine</b> withdrawal.
+TH	addiction	aversion	22713675	The purpose of the present study was to evaluate: (i) the turnover of DA, NA and 5 HT in the nucleus accumbens (NAc), one of the most important substrates for <b>aversive</b> states, (ii) the changes in tyrosine hydroxylase (<strong>TH</strong>) gene expression in the ventral tegmental area, and (iii) total <strong>TH</strong> protein levels and <strong>TH</strong> phosphorylation in the NAc after naloxone induced morphine withdrawal.
+TH	addiction	withdrawal	22713675	The purpose of the present study was to evaluate: (i) the turnover of DA, NA and 5 HT in the nucleus accumbens (NAc), one of the most important substrates for aversive states, (ii) the changes in tyrosine hydroxylase (<strong>TH</strong>) gene expression in the ventral tegmental area, and (iii) total <strong>TH</strong> protein levels and <strong>TH</strong> phosphorylation in the NAc after naloxone induced morphine <b>withdrawal</b>.
+TH	drug	opioid	22713675	The purpose of the present study was to evaluate: (i) the turnover of DA, NA and 5 HT in the nucleus accumbens (NAc), one of the most important substrates for aversive states, (ii) the changes in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the ventral tegmental area, and (iii) total <strong>TH</strong> protein levels and <strong>TH</strong> phosphorylation in the NAc after <b>naloxone</b> induced <b>morphine</b> withdrawal.
+TH	addiction	aversion	22713675	The purpose of the present study was to evaluate: (i) the turnover of DA, NA and 5 HT in the nucleus accumbens (NAc), one of the most important substrates for <b>aversive</b> states, (ii) the changes in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the ventral tegmental area, and (iii) total <strong>TH</strong> protein levels and <strong>TH</strong> phosphorylation in the NAc after naloxone induced morphine withdrawal.
+TH	addiction	withdrawal	22713675	The purpose of the present study was to evaluate: (i) the turnover of DA, NA and 5 HT in the nucleus accumbens (NAc), one of the most important substrates for aversive states, (ii) the changes in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the ventral tegmental area, and (iii) total <strong>TH</strong> protein levels and <strong>TH</strong> phosphorylation in the NAc after naloxone induced morphine <b>withdrawal</b>.
+TH	drug	opioid	22713675	In addition, present data show that <b>naloxone</b> induced CPA positively correlated with an increase of DA and NA turnover in the NAc, which paralleled an increase in <strong>TH</strong> gene expression in the VTA and <strong>TH</strong> phosphorylation and enhanced <strong>TH</strong> protein levels in the NAc.
+TH	drug	opioid	22713675	Thus, the present study indicates that <b>naloxone</b> induced aversion in <b>morphine</b> dependent mice enhances DA and NA activity in the NAc and suggests that transcriptional and post transcriptional regulation of <strong>TH</strong> could be involved in the hyperactivity of mesolimbic dopaminergic system observed in <b>morphine</b> withdrawn mice.
+TH	addiction	aversion	22713675	Thus, the present study indicates that naloxone induced <b>aversion</b> in morphine dependent mice enhances DA and NA activity in the NAc and suggests that transcriptional and post transcriptional regulation of <strong>TH</strong> could be involved in the hyperactivity of mesolimbic dopaminergic system observed in morphine withdrawn mice.
+TH	drug	amphetamine	22692568	Concomitantly, the observations of a decreased gene expression of <strong>tyrosine hydroxylase</strong> in midbrain together with a blunted psychomotor response to <b>amphetamine</b> concurred to indicate a diminished presynaptic DA function following THC.
+TH	drug	cannabinoid	22692568	Concomitantly, the observations of a decreased gene expression of <strong>tyrosine hydroxylase</strong> in midbrain together with a blunted psychomotor response to amphetamine concurred to indicate a diminished presynaptic DA function following <b>THC</b>.
+TH	drug	opioid	22659588	Using immunohistochemical double staining for tyrosine hydroxylase (<strong>TH</strong>) and Fos, we found that the number of Fos(+)<strong>TH</strong>(+) neurons in the rostral VTA and number of Fos(+)<strong>TH</strong>( ) neurons in the lateral SNr were significantly increased in escalating dose <b>morphine</b> treated rats compared with steady dose <b>morphine</b> treated rats and acute <b>morphine</b> treated rats.
+TH	drug	opioid	22659588	Using immunohistochemical double staining for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and Fos, we found that the number of Fos(+)<strong>TH</strong>(+) neurons in the rostral VTA and number of Fos(+)<strong>TH</strong>( ) neurons in the lateral SNr were significantly increased in escalating dose <b>morphine</b> treated rats compared with steady dose <b>morphine</b> treated rats and acute <b>morphine</b> treated rats.
+TH	drug	opioid	22659588	The number of Fos(+)<strong>TH</strong>(+) neurons was significantly increased by acute <b>morphine</b> in the caudal VTA and SNc, but this number did not increase further with <b>morphine</b> pretreatment.
+TH	drug	alcohol	22467995	Diagnosed with <b>alcohol</b> dependence (n = 285), according to the Diagnostic and Statistical Manual of Mental Disorders, 4(<strong>th</strong>) edition.
+TH	addiction	dependence	22467995	Diagnosed with alcohol <b>dependence</b> (n = 285), according to the Diagnostic and Statistical Manual of Mental Disorders, 4(<strong>th</strong>) edition.
+TH	drug	cocaine	22454845	Reinforcing properties of pups versus <b>cocaine</b> for fathers and associated central expression of Fos and <strong>tyrosine hydroxylase</strong> in mandarin voles (Microtus mandarinus).
+TH	addiction	reward	22454845	<b>Reinforcing</b> properties of pups versus cocaine for fathers and associated central expression of Fos and <strong>tyrosine hydroxylase</strong> in mandarin voles (Microtus mandarinus).
+TH	drug	cocaine	22454845	We also measured neuronal Fos and tyrosine hydroxylase (<strong>TH</strong>) expression underlying the preferences of fathers for pups or <b>cocaine</b>.
+TH	drug	cocaine	22454845	We also measured neuronal Fos and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) expression underlying the preferences of fathers for pups or <b>cocaine</b>.
+TH	drug	cocaine	22454845	Fathers preferring <b>cocaine</b> exhibited an increase in Fos immunoreactive neurons in the accumbens,medial nucleus of the amygdala, cingulate cortex, medial preoptic area and ventral tegmental area and had more <strong>TH</strong> IR neurons in the ventral tegmental area compared to fathers preferring PND 5–9 pups.
+TH	drug	cannabinoid	22414816	Dopamine (DA) extracellular levels in the nucleus accumbens (NAcc), and gene expression of tyrosine hydroxylase (<strong>TH</strong>) and DA transporter (DAT) in the ventral tegmental area (VTA), and μ opioid and <b>cannabinoid</b> CB₁ receptors in the NAcc were also studied in both genotypes.
+TH	drug	opioid	22414816	Dopamine (DA) extracellular levels in the nucleus accumbens (NAcc), and gene expression of tyrosine hydroxylase (<strong>TH</strong>) and DA transporter (DAT) in the ventral tegmental area (VTA), and μ <b>opioid</b> and cannabinoid CB₁ receptors in the NAcc were also studied in both genotypes.
+TH	drug	cannabinoid	22414816	Dopamine (DA) extracellular levels in the nucleus accumbens (NAcc), and gene expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and DA transporter (DAT) in the ventral tegmental area (VTA), and μ opioid and <b>cannabinoid</b> CB₁ receptors in the NAcc were also studied in both genotypes.
+TH	drug	opioid	22414816	Dopamine (DA) extracellular levels in the nucleus accumbens (NAcc), and gene expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and DA transporter (DAT) in the ventral tegmental area (VTA), and μ <b>opioid</b> and cannabinoid CB₁ receptors in the NAcc were also studied in both genotypes.
+TH	drug	opioid	22414816	Under baseline conditions, <strong>TH</strong> and DAT gene expression was higher and μ <b>opioid</b> receptor gene expression was lower in CB₂xP than in WT mice.
+TH	drug	cocaine	22414816	However, both genotypes showed similar changes in <strong>TH</strong> and μ opioid receptor gene expression after <b>cocaine</b> challenge independently of the pretreatment received.
+TH	drug	opioid	22414816	However, both genotypes showed similar changes in <strong>TH</strong> and μ <b>opioid</b> receptor gene expression after cocaine challenge independently of the pretreatment received.
+TH	drug	opioid	22396106	Dynamic changes of <strong>tyrosine hydroxylase</strong> and dopamine concentrations in the ventral tegmental area nucleus accumbens projection during the expression of <b>morphine</b> induced conditioned place preference in rats.
+TH	drug	opioid	22396106	However, still unknown are how DA concentrations dynamically change during the <b>morphine</b> induced CPP test and whether tyrosine hydroxylase (<strong>TH</strong>) activity in the ventral tegmental area (VTA) plays a vital role in this process.
+TH	addiction	reward	22396106	However, still unknown are how DA concentrations dynamically change during the morphine induced <b>CPP</b> test and whether tyrosine hydroxylase (<strong>TH</strong>) activity in the ventral tegmental area (VTA) plays a vital role in this process.
+TH	drug	opioid	22396106	However, still unknown are how DA concentrations dynamically change during the <b>morphine</b> induced CPP test and whether <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) activity in the ventral tegmental area (VTA) plays a vital role in this process.
+TH	addiction	reward	22396106	However, still unknown are how DA concentrations dynamically change during the morphine induced <b>CPP</b> test and whether <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) activity in the ventral tegmental area (VTA) plays a vital role in this process.
+TH	drug	opioid	22396106	In the present study, we measured dynamic changes in <strong>TH</strong> and phosphorylated <strong>TH</strong> serine 40 (pTH Ser(40)) and pTH Ser(31) proteins in the VTA, and DA concentrations in the NAc at 5 min intervals during a 30 min <b>morphine</b> induced CPP test.
+TH	addiction	reward	22396106	In the present study, we measured dynamic changes in <strong>TH</strong> and phosphorylated <strong>TH</strong> serine 40 (pTH Ser(40)) and pTH Ser(31) proteins in the VTA, and DA concentrations in the NAc at 5 min intervals during a 30 min morphine induced <b>CPP</b> test.
+TH	addiction	reward	22396106	<strong>TH</strong> and pTH Ser(40) levels, but not pTH Ser(31) levels, in the VTA were enhanced during the <b>CPP</b> test.
+TH	addiction	reward	22396106	These results indicated that <strong>TH</strong> and the phosphorylation of <strong>TH</strong> Ser(40) in the VTA may be responsible for DA synthesis and release in the NAc during the behavioral expression of conditioned <b>reward</b> elicited by a drug associated context.
+TH	addiction	dependence	22364199	Hence, we performed a series of experiments to further characterize the role of GR signalling in opiate withdrawal induced physical signs of <b>dependence</b>, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and tyrosine hydroxylase (<strong>TH</strong>) phosphorylation (activation) as well as GR expression in the nucleus of the solitary tract noradrenergic cell group (NTS A₂).
+TH	addiction	withdrawal	22364199	Hence, we performed a series of experiments to further characterize the role of GR signalling in opiate <b>withdrawal</b> induced physical signs of dependence, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and tyrosine hydroxylase (<strong>TH</strong>) phosphorylation (activation) as well as GR expression in the nucleus of the solitary tract noradrenergic cell group (NTS A₂).
+TH	addiction	dependence	22364199	Hence, we performed a series of experiments to further characterize the role of GR signalling in opiate withdrawal induced physical signs of <b>dependence</b>, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) phosphorylation (activation) as well as GR expression in the nucleus of the solitary tract noradrenergic cell group (NTS A₂).
+TH	addiction	withdrawal	22364199	Hence, we performed a series of experiments to further characterize the role of GR signalling in opiate <b>withdrawal</b> induced physical signs of dependence, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) phosphorylation (activation) as well as GR expression in the nucleus of the solitary tract noradrenergic cell group (NTS A₂).
+TH	drug	opioid	22364199	Six days later, rats were pretreated with mifepristone or vehicle 30 min before <b>naloxone</b> and physical signs of abstinence, NA turnover, <strong>TH</strong> activation, GR expression and the hypothalamus pituitary adrenocortical axis activity were measured using HPLC, immunoblotting and RIA.
+TH	drug	opioid	22364199	Mifepristone antagonized the <strong>TH</strong> phosphorylation at Ser³¹ and the expression of c Fos expression induced by <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	22364199	Mifepristone antagonized the <strong>TH</strong> phosphorylation at Ser³¹ and the expression of c Fos expression induced by morphine <b>withdrawal</b>.
+TH	addiction	withdrawal	22364199	These results suggest that the physical signs of opiate <b>withdrawal</b>, <strong>TH</strong> activation and stimulation of noradrenergic pathways innervating the PVN are modulated by GR signalling.
+TH	drug	amphetamine	22329540	Differential action of <b>methamphetamine</b> on <strong>tyrosine hydroxylase</strong> and dopamine transport in the nigrostriatal pathway of μ opioid receptor knockout mice.
+TH	drug	opioid	22329540	Differential action of methamphetamine on <strong>tyrosine hydroxylase</strong> and dopamine transport in the nigrostriatal pathway of μ <b>opioid</b> receptor knockout mice.
+TH	drug	amphetamine	22329540	The present study assessed whether <b>METH</b> treated μ OR knockout mice exhibit a differential response of the expression of dopamine transporter and tyrosine hydroxylase (<strong>TH</strong>), the rate limiting enzyme for dopamine synthesis and maintaining dopamine levels.
+TH	drug	amphetamine	22329540	The present study assessed whether <b>METH</b> treated μ OR knockout mice exhibit a differential response of the expression of dopamine transporter and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the rate limiting enzyme for dopamine synthesis and maintaining dopamine levels.
+TH	drug	amphetamine	22329540	The expression of <strong>TH</strong> protein in the striatum and the levels of <strong>TH</strong> mRNA and number of <strong>TH</strong> positive neurons in the substantia nigra were reduced in wild type mice treated with <b>METH</b> (2.5 and 10 mg/kg), but not in the μ OR knockout mice.
+TH	drug	amphetamine	22329540	These results suggest that the μ OR contributes to <b>METH</b> induced loss of dopamine and behavioral sensitization by decreasing the expression of <strong>TH</strong>.
+TH	addiction	sensitization	22329540	These results suggest that the μ OR contributes to METH induced loss of dopamine and behavioral <b>sensitization</b> by decreasing the expression of <strong>TH</strong>.
+TH	drug	nicotine	24592049	At the end of the 6(<strong>th</strong>) week, it was determined that 30 (69%) rats out of 43 in the NG and only 7 rats (20%) out of 35 in the control group preferred the <b>nicotine</b> added drinking water (p<0.05).
+TH	drug	opioid	22133920	and spinal administration of the <b>opioid</b> receptor antagonist <b>naloxone</b> (0.1 μg/μl i.<strong>th</strong>.
+TH	drug	opioid	22133920	on the spinal nociceptive responses was prevented by spinal administration of the <b>opioid</b> receptor antagonist <b>naloxone</b> (0.1 μg/μl i.<strong>th</strong>.).
+TH	drug	amphetamine	22133515	Maternal treatment with TURP at gestational day (GD) 15 enhanced the locomotor response to the DA indirect agonist, <b>amphetamine</b> (<b>AMPH</b>), increased the expression of tyrosine hydroxylase (<strong>TH</strong>), an enzyme involved in DA synthesis, DA levels and the expression of the post synaptic protein spinophilin in the nucleus accumbens (NAcc) in the adult offspring.
+TH	drug	amphetamine	22133515	Maternal treatment with TURP at gestational day (GD) 15 enhanced the locomotor response to the DA indirect agonist, <b>amphetamine</b> (<b>AMPH</b>), increased the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), an enzyme involved in DA synthesis, DA levels and the expression of the post synaptic protein spinophilin in the nucleus accumbens (NAcc) in the adult offspring.
+TH	drug	amphetamine	22133515	Neutralization of maternal leptin prevented the enhanced behavioral sensitization and elevation of DA and spinophilin in the NAcc but spared other changes regulated by IL 6, such as increased NAcc <strong>TH</strong> levels and acute locomotor response to <b>AMPH</b>.
+TH	addiction	sensitization	22133515	Neutralization of maternal leptin prevented the enhanced behavioral <b>sensitization</b> and elevation of DA and spinophilin in the NAcc but spared other changes regulated by IL 6, such as increased NAcc <strong>TH</strong> levels and acute locomotor response to AMPH.
+TH	drug	cannabinoid	22017514	<b>Cannabinoid</b> withdrawal decreased tyrosine hydroxylase (<strong>TH</strong>) gene expression in the ventral tegmental area and µ opioid receptor gene expression in the nucleus accumbens (NAcc) and increased CB1 receptor gene expression in the NAcc.
+TH	drug	opioid	22017514	Cannabinoid withdrawal decreased tyrosine hydroxylase (<strong>TH</strong>) gene expression in the ventral tegmental area and µ <b>opioid</b> receptor gene expression in the nucleus accumbens (NAcc) and increased CB1 receptor gene expression in the NAcc.
+TH	addiction	withdrawal	22017514	Cannabinoid <b>withdrawal</b> decreased tyrosine hydroxylase (<strong>TH</strong>) gene expression in the ventral tegmental area and µ opioid receptor gene expression in the nucleus accumbens (NAcc) and increased CB1 receptor gene expression in the NAcc.
+TH	drug	cannabinoid	22017514	<b>Cannabinoid</b> withdrawal decreased <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the ventral tegmental area and µ opioid receptor gene expression in the nucleus accumbens (NAcc) and increased CB1 receptor gene expression in the NAcc.
+TH	drug	opioid	22017514	Cannabinoid withdrawal decreased <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the ventral tegmental area and µ <b>opioid</b> receptor gene expression in the nucleus accumbens (NAcc) and increased CB1 receptor gene expression in the NAcc.
+TH	addiction	withdrawal	22017514	Cannabinoid <b>withdrawal</b> decreased <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the ventral tegmental area and µ opioid receptor gene expression in the nucleus accumbens (NAcc) and increased CB1 receptor gene expression in the NAcc.
+TH	drug	cannabinoid	22017514	Treatment with topiramate or pregabalin blocked the decrease of <strong>TH</strong> and the increase of CB1 gene expressions induced by <b>cannabinoid</b> withdrawal.
+TH	addiction	withdrawal	22017514	Treatment with topiramate or pregabalin blocked the decrease of <strong>TH</strong> and the increase of CB1 gene expressions induced by cannabinoid <b>withdrawal</b>.
+TH	drug	alcohol	21966993	Handling induced convulsion (HIC) associated to <b>alcohol</b>, <b>alcohol</b> induced loss of righting reflex (LORR), hypothermic effects in response to acute <b>ethanol</b> challenge, blood <b>ethanol</b> levels (BELs), conditioned place preference, voluntary <b>ethanol</b> consumption and preference, tyrosine hydroxylase (<strong>TH</strong>), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and µ , δ  and κ opioid agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild type (WT) mice.
+TH	drug	opioid	21966993	Handling induced convulsion (HIC) associated to alcohol, alcohol induced loss of righting reflex (LORR), hypothermic effects in response to acute ethanol challenge, blood ethanol levels (BELs), conditioned place preference, voluntary ethanol consumption and preference, tyrosine hydroxylase (<strong>TH</strong>), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and µ , δ  and κ <b>opioid</b> agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild type (WT) mice.
+TH	drug	alcohol	21966993	Handling induced convulsion (HIC) associated to <b>alcohol</b>, <b>alcohol</b> induced loss of righting reflex (LORR), hypothermic effects in response to acute <b>ethanol</b> challenge, blood <b>ethanol</b> levels (BELs), conditioned place preference, voluntary <b>ethanol</b> consumption and preference, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and µ , δ  and κ opioid agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild type (WT) mice.
+TH	drug	opioid	21966993	Handling induced convulsion (HIC) associated to alcohol, alcohol induced loss of righting reflex (LORR), hypothermic effects in response to acute ethanol challenge, blood ethanol levels (BELs), conditioned place preference, voluntary ethanol consumption and preference, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and µ , δ  and κ <b>opioid</b> agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild type (WT) mice.
+TH	drug	alcohol	21966993	These results suggest that deletion of the PDYN gene increased vulnerability for <b>ethanol</b> consumption by altering, at least in part, PENK, <strong>TH</strong> and DAT gene expression, and µ , δ  and κ opioid receptor functional activity in brain areas closely related to <b>ethanol</b> reinforcement.
+TH	drug	opioid	21966993	These results suggest that deletion of the PDYN gene increased vulnerability for ethanol consumption by altering, at least in part, PENK, <strong>TH</strong> and DAT gene expression, and µ , δ  and κ <b>opioid</b> receptor functional activity in brain areas closely related to ethanol reinforcement.
+TH	addiction	reward	21966993	These results suggest that deletion of the PDYN gene increased vulnerability for ethanol consumption by altering, at least in part, PENK, <strong>TH</strong> and DAT gene expression, and µ , δ  and κ opioid receptor functional activity in brain areas closely related to ethanol <b>reinforcement</b>.
+TH	addiction	intoxication	21953518	<b>Binge</b> mAMPH treatment significantly reduced striatal DAT and <strong>TH</strong> in a regionally specific pattern; with greatest effects in ventral caudate putamen (CP) and relative sparing of the nucleus accumbens septi (NAc).
+TH	drug	opioid	21947312	Negative state associated with <b>opioid</b> withdrawal was examined by using conditioned place aversion (CPA), <strong>TH</strong> expression and <strong>TH</strong> phosphorylation were measured in different brain regions involved in addictive behaviours using immunohistochemistry.
+TH	addiction	addiction	21947312	Negative state associated with opioid withdrawal was examined by using conditioned place aversion (CPA), <strong>TH</strong> expression and <strong>TH</strong> phosphorylation were measured in different brain regions involved in <b>addictive</b> behaviours using immunohistochemistry.
+TH	addiction	aversion	21947312	Negative state associated with opioid withdrawal was examined by using conditioned place <b>aversion</b> (CPA), <strong>TH</strong> expression and <strong>TH</strong> phosphorylation were measured in different brain regions involved in addictive behaviours using immunohistochemistry.
+TH	addiction	withdrawal	21947312	Negative state associated with opioid <b>withdrawal</b> was examined by using conditioned place aversion (CPA), <strong>TH</strong> expression and <strong>TH</strong> phosphorylation were measured in different brain regions involved in addictive behaviours using immunohistochemistry.
+TH	drug	opioid	21947312	Using dual immunolabeling for c Fos, data show that <b>naloxone</b> induced withdrawal increases the number of <strong>TH</strong> positive neurons phosphorylated at Ser40 or Ser31 that coexpress c Fos in the nucleus of tractus solitarius (NTS) A2 from wild type and CRF( / ) deficient mice.
+TH	addiction	withdrawal	21947312	Using dual immunolabeling for c Fos, data show that naloxone induced <b>withdrawal</b> increases the number of <strong>TH</strong> positive neurons phosphorylated at Ser40 or Ser31 that coexpress c Fos in the nucleus of tractus solitarius (NTS) A2 from wild type and CRF( / ) deficient mice.
+TH	drug	cannabinoid	21931637	The antinociceptive properties induced by <b>cannabinoid</b> agonists were assessed on the 5(<strong>th</strong>) and 30(<strong>th</strong>) days after surgery.
+TH	drug	cannabinoid	21931637	Systemic treatment with <b>cannabinoid</b> agonists reduced mechanical allodynia on both the 5(<strong>th</strong>) and 30(<strong>th</strong>) days after surgery, but the greatest results were observed by using central routes of administration, especially at the 30(<strong>th</strong>) day.
+TH	drug	cocaine	21887497	Striatal dopaminergic markers (<strong>tyrosine hydroxylase</strong>, dopamine D1 receptor, and dopamine transporter DAT), were similar in both genotypes and were equally affected by <b>cocaine</b> exposure.
+TH	drug	opioid	21886595	Rats were administered <b>morphine</b> (10 mg/kg, s.c. /day) for 12 days and the spontaneous withdrawal symptoms were developed by cessation of the drug administration on day 13(<strong>th</strong>) that were prominent on day 14(<strong>th</strong>) and continued up to day 15(<strong>th</strong>) (24 to 72 h periods).
+TH	addiction	withdrawal	21886595	Rats were administered morphine (10 mg/kg, s.c. /day) for 12 days and the spontaneous <b>withdrawal</b> symptoms were developed by cessation of the drug administration on day 13(<strong>th</strong>) that were prominent on day 14(<strong>th</strong>) and continued up to day 15(<strong>th</strong>) (24 to 72 h periods).
+TH	addiction	withdrawal	21886595	Furthermore, cerebrolysin reduced the <b>withdrawal</b> symptoms on day 14(<strong>th</strong>) to 15(<strong>th</strong>).
+TH	drug	cannabinoid	21886590	We found that <strong>TH</strong> positive neurons shrink and Golgi stained medium spiny neurons loose dendritic spines in withdrawal rats after chronic <b>cannabinoids</b> administration.
+TH	addiction	withdrawal	21886590	We found that <strong>TH</strong> positive neurons shrink and Golgi stained medium spiny neurons loose dendritic spines in <b>withdrawal</b> rats after chronic cannabinoids administration.
+TH	drug	amphetamine	21798282	Here we further investigated the impact of genotype and age on tyrosine hydroxylase (<strong>TH</strong>) loss and dopamine (DA) metabolism due to a high binge dose of <b>Meth</b> (4 × 5 mg/kg × 2 h × 2 days).
+TH	addiction	intoxication	21798282	Here we further investigated the impact of genotype and age on tyrosine hydroxylase (<strong>TH</strong>) loss and dopamine (DA) metabolism due to a high <b>binge</b> dose of Meth (4 × 5 mg/kg × 2 h × 2 days).
+TH	drug	amphetamine	21798282	Here we further investigated the impact of genotype and age on <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) loss and dopamine (DA) metabolism due to a high binge dose of <b>Meth</b> (4 × 5 mg/kg × 2 h × 2 days).
+TH	addiction	intoxication	21798282	Here we further investigated the impact of genotype and age on <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) loss and dopamine (DA) metabolism due to a high <b>binge</b> dose of Meth (4 × 5 mg/kg × 2 h × 2 days).
+TH	drug	opioid	21791964	Many studies have suggested that the behavioral and reinforcing effects of <b>morphine</b> are induced by hyperactivation of the mesolimbic dopaminergic system, which results in increases in locomotor activity, c Fos expression in the nucleus accumbens (NAc), and tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area (VTA).
+TH	addiction	reward	21791964	Many studies have suggested that the behavioral and <b>reinforcing</b> effects of morphine are induced by hyperactivation of the mesolimbic dopaminergic system, which results in increases in locomotor activity, c Fos expression in the nucleus accumbens (NAc), and tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area (VTA).
+TH	drug	opioid	21791964	Many studies have suggested that the behavioral and reinforcing effects of <b>morphine</b> are induced by hyperactivation of the mesolimbic dopaminergic system, which results in increases in locomotor activity, c Fos expression in the nucleus accumbens (NAc), and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area (VTA).
+TH	addiction	reward	21791964	Many studies have suggested that the behavioral and <b>reinforcing</b> effects of morphine are induced by hyperactivation of the mesolimbic dopaminergic system, which results in increases in locomotor activity, c Fos expression in the nucleus accumbens (NAc), and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area (VTA).
+TH	drug	opioid	21791964	In order to investigate the effect of wild ginseng (WG) on treating <b>morphine</b> addiction, we examined the behavioral sensitization of locomotor activity and c Fos and <strong>TH</strong> expression in the rat brain using immunohistochemistry.
+TH	addiction	addiction	21791964	In order to investigate the effect of wild ginseng (WG) on treating morphine <b>addiction</b>, we examined the behavioral sensitization of locomotor activity and c Fos and <strong>TH</strong> expression in the rat brain using immunohistochemistry.
+TH	addiction	sensitization	21791964	In order to investigate the effect of wild ginseng (WG) on treating morphine addiction, we examined the behavioral <b>sensitization</b> of locomotor activity and c Fos and <strong>TH</strong> expression in the rat brain using immunohistochemistry.
+TH	drug	opioid	21791964	Intraperitioneal injection of WG (100 and 200 mg/kg), 30 min before administration of a daily injection of <b>morphine</b> (40 mg/kg, s.c.), significantly inhibited <b>morphine</b> induced increases in c Fos expression in NAc and <strong>TH</strong> expression in VTA as well as in locomotor activity, as compared with Panax ginseng.
+TH	drug	opioid	24250391	Mothers were exposed to <b>morphine</b> during the 14(<strong>th</strong>) 16(<strong>th</strong>) days of gestational.
+TH	drug	opioid	21594658	<strong>TH</strong> 030418: a potent long acting <b>opioid</b> analgesic with low dependence liability.
+TH	addiction	dependence	21594658	<strong>TH</strong> 030418: a potent long acting opioid analgesic with low <b>dependence</b> liability.
+TH	drug	opioid	21594658	Here, we evaluated the pharmacological activities of <strong>TH</strong> 030418, in comparison with <b>morphine</b>, the prototype <b>opioid</b> analgesic.
+TH	drug	opioid	21594658	In radioligand binding assays, <strong>TH</strong> 030418 bound potently and nonselectively to μ , δ , κ , and ORL1 (<b>opioid</b> receptor like 1) receptors stably expressed in CHO (Chinese hamster ovary) cells with K (i) values of 0.56, 0.73, 0.60, and 1.55 nM, respectively.
+TH	drug	opioid	21594658	When administered subcutaneously, <strong>TH</strong> 030418 was much more potent than <b>morphine</b> in analgesia, with the ED(50) values of 1.37 μg/kg and 1.70 μg/kg in hot plate and acetic acid writhing tests, respectively.
+TH	drug	opioid	21594658	The <b>opioid</b> antagonist <b>naloxone</b> blocked the antinociceptive effect of <strong>TH</strong> 030418, indicating that the action of <strong>TH</strong> 030418 was mediated by <b>opioid</b> receptors.
+TH	drug	opioid	21594658	The antinociceptive effect of s.c. <strong>TH</strong> 030418 in hot plate test lasted for more than 12 h, which is much longer than those of <b>morphine</b> (2.5 h) and dihydroetorphine (1.5 h).
+TH	drug	opioid	21594658	In addition, <b>naloxone</b> did not precipitate withdrawal syndrome in the mice treated with <strong>TH</strong> 030418 previously.
+TH	addiction	withdrawal	21594658	In addition, naloxone did not precipitate <b>withdrawal</b> syndrome in the mice treated with <strong>TH</strong> 030418 previously.
+TH	drug	opioid	21594658	These results indicate that <strong>TH</strong> 030418 is a potent long acting <b>opioid</b> analgesic with low dependence liability and may be of some value in the development of new analgesics.
+TH	addiction	dependence	21594658	These results indicate that <strong>TH</strong> 030418 is a potent long acting opioid analgesic with low <b>dependence</b> liability and may be of some value in the development of new analgesics.
+TH	drug	amphetamine	21590747	We found that mice treated with a <b>METH</b> binge showed a marked decrease in DA and dopaminergic metabolites as well as lower levels of <strong>TH</strong> immunoreactivity in the dorsal striatum.
+TH	addiction	intoxication	21590747	We found that mice treated with a METH <b>binge</b> showed a marked decrease in DA and dopaminergic metabolites as well as lower levels of <strong>TH</strong> immunoreactivity in the dorsal striatum.
+TH	drug	opioid	21589866	<b>Opioid</b> dependence patients (meeting Diagnostic and Statistical Manual of Mental Disorders, [4(<strong>th</strong>) Edition] criteria) from a MMT community program were recruited.
+TH	addiction	dependence	21589866	Opioid <b>dependence</b> patients (meeting Diagnostic and Statistical Manual of Mental Disorders, [4(<strong>th</strong>) Edition] criteria) from a MMT community program were recruited.
+TH	drug	psychedelics	21585054	[Effects of electroacupuncture on expression of <strong>tyrosine hydroxylase</strong> and c fos in hippocampal CA 1 area in <b>ketamine</b> addiction rats].
+TH	addiction	addiction	21585054	[Effects of electroacupuncture on expression of <strong>tyrosine hydroxylase</strong> and c fos in hippocampal CA 1 area in ketamine <b>addiction</b> rats].
+TH	drug	psychedelics	21585054	EA of "Zusanli"(ST 36) "Sanyinjiao" (SP 6) can downregulate <b>ketamine</b> addiction induced increase of expression of <strong>tyrosine hydroxylase</strong> and c fos in the hippocampal CA 1 region in <b>ketamine</b> addiction rats, which may contribute to its effect in relieving <b>ketamine</b> addiction symptoms in clinic.
+TH	addiction	addiction	21585054	EA of "Zusanli"(ST 36) "Sanyinjiao" (SP 6) can downregulate ketamine <b>addiction</b> induced increase of expression of <strong>tyrosine hydroxylase</strong> and c fos in the hippocampal CA 1 region in ketamine <b>addiction</b> rats, which may contribute to its effect in relieving ketamine <b>addiction</b> symptoms in clinic.
+TH	drug	amphetamine	21547080	Animals that received toxic <b>METH</b> challenges showed decreases in dopamine levels and reductions in <strong>tyrosine hydroxylase</strong> protein concentration in the striatum.
+TH	drug	amphetamine	21547080	<b>METH</b> pretreatment protected against loss of striatal dopamine and <strong>tyrosine hydroxylase</strong>.
+TH	drug	opioid	21530574	Increased pain perception and attenuated <b>opioid</b> antinociception in paradoxical sleep deprived rats are associated with reduced <strong>tyrosine hydroxylase</strong> staining in the periaqueductal gray matter and are reversed by L dopa.
+TH	drug	opioid	21530574	Because dopaminergic neurons in the periaqueductal gray matter (PAG) participate in pain modulation and <b>opioid</b> induced antinociception, we evaluated the effects of PSD on thermal pain sensitivity, <b>morphine</b>  and L DOPA induced antinociception and dopaminergic functionality in the PAG by assessing tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity.
+TH	drug	opioid	21530574	Because dopaminergic neurons in the periaqueductal gray matter (PAG) participate in pain modulation and <b>opioid</b> induced antinociception, we evaluated the effects of PSD on thermal pain sensitivity, <b>morphine</b>  and L DOPA induced antinociception and dopaminergic functionality in the PAG by assessing <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity.
+TH	drug	amphetamine	21523347	<b>Methamphetamine</b> (MA) increases extracellular dopamine (DA) and at chronic high doses induces toxicity as indicated by decreased expression of tyrosine hydroxylase (<strong>TH</strong>) and dopamine transporter (DAT).
+TH	drug	amphetamine	21523347	<b>Methamphetamine</b> (MA) increases extracellular dopamine (DA) and at chronic high doses induces toxicity as indicated by decreased expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine transporter (DAT).
+TH	addiction	addiction	21523347	<b>Escalation</b> of MA intake produces both transient and long lasting effects upon DA, <strong>TH</strong>, and DAT in the mesoaccumbens pathway.
+TH	addiction	intoxication	21453757	This experiment examined the effects of a MA <b>binge</b> dosing regimen (10 mg/kg x 4 at 2 h intervals, s.c.) in Sprague Dawley rats on BDNF, tropomyosin receptor kinase B (TrkB), and tyrosine hydroxylase (<strong>TH</strong>) mRNA expression, and plasma corticosterone.
+TH	addiction	intoxication	21453757	This experiment examined the effects of a MA <b>binge</b> dosing regimen (10 mg/kg x 4 at 2 h intervals, s.c.) in Sprague Dawley rats on BDNF, tropomyosin receptor kinase B (TrkB), and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) mRNA expression, and plasma corticosterone.
+TH	addiction	addiction	21431004	Evaluation of effectiveness of various deaddiction regimen; c. Defaulters and dropouts Fifty one patients in a de <b>addiction</b> center were investigated on 0(<strong>th</strong>) , 30(<strong>th</strong>) and 60(<strong>th</strong>) day along with psychiatric evaluation, ADR surveillance was made.
+TH	addiction	sensitization	21409840	The decreased <strong>tyrosine hydroxylase</strong> activity in the locus coeruleus and the beta adrenoceptor down regulation in the amygdaloid complex might be involved in the inhibiton of the delayed augmentation of f ASR by repeated antidepressant treatment, leading to the possibility that the delayed <b>sensitization</b> of CRH response to stress after CVS might contribute to the biological mechanism underlying the formation of pathological states such as anxiety and depressive disorders.
+TH	drug	cocaine	21215761	At each time point, both <b>cocaine</b>  and saline injected mice showed AMPAR GluR1 immunogold labeling in somatodendritic profiles, many of which contained immunoperoxidase labeling for the DA synthesizing enzyme, tyrosine hydroxylase (<strong>TH</strong>).
+TH	drug	cocaine	21215761	At each time point, both <b>cocaine</b>  and saline injected mice showed AMPAR GluR1 immunogold labeling in somatodendritic profiles, many of which contained immunoperoxidase labeling for the DA synthesizing enzyme, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>).
+TH	drug	cocaine	21215761	At 30 min after the last injection, when <b>cocaine</b> was systemically present, only the non <strong>TH</strong> labeled dendrites showed a significant increase in the synaptic/plasmalemmal density of GluR1 immunogold particles.
+TH	drug	cocaine	21215761	At 72 h, when systemic <b>cocaine</b> was depleted, synaptic GluR1 labeling was greatly enhanced in <strong>TH</strong> containing dendrites throughout the VTA and in non <strong>TH</strong> dendrites of the limbic associated paranigral VTA.
+TH	drug	amphetamine	21208167	Over the course of the 20(<strong>th</strong>) century, it became increasingly clear that <b>amphetamine</b> like psychostimulants carried serious abuse liability that has resulted in sociological use patterns that have been described as epidemics.
+TH	drug	cocaine	21205279	Recent studies have identified changes of several specific miRNA expression profiles and polymorphisms affecting the interactions between miRNAs and their targets in various brain disorders, including addiction: miR 16 causes adaptive changes in production of the serotonin transporter; miR 133b is specifically expressed in midbrain dopaminergic neurons, and regulates the production of <strong>tyrosine hydroxylase</strong> and the dopamine transporter; miR 212 affects production of striatal brain derived neurotrophic factor and synaptic plasticity upon <b>cocaine</b>.
+TH	addiction	addiction	21205279	Recent studies have identified changes of several specific miRNA expression profiles and polymorphisms affecting the interactions between miRNAs and their targets in various brain disorders, including <b>addiction</b>: miR 16 causes adaptive changes in production of the serotonin transporter; miR 133b is specifically expressed in midbrain dopaminergic neurons, and regulates the production of <strong>tyrosine hydroxylase</strong> and the dopamine transporter; miR 212 affects production of striatal brain derived neurotrophic factor and synaptic plasticity upon cocaine.
+TH	drug	amphetamine	21151937	Compared to naïve mice that received <b>METH</b> binge treatment for the first time, mice pretreated with <b>METH</b> in adolescence showed a greater loss of tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity in striatum, loss of THir fibers in the substantia nigra reticulata (SNr) as well as decreased dopamine transporter (DAT) level and compromised DA clearance in striatum.
+TH	addiction	intoxication	21151937	Compared to naïve mice that received METH <b>binge</b> treatment for the first time, mice pretreated with METH in adolescence showed a greater loss of tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity in striatum, loss of THir fibers in the substantia nigra reticulata (SNr) as well as decreased dopamine transporter (DAT) level and compromised DA clearance in striatum.
+TH	drug	amphetamine	21151937	Compared to naïve mice that received <b>METH</b> binge treatment for the first time, mice pretreated with <b>METH</b> in adolescence showed a greater loss of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity in striatum, loss of THir fibers in the substantia nigra reticulata (SNr) as well as decreased dopamine transporter (DAT) level and compromised DA clearance in striatum.
+TH	addiction	intoxication	21151937	Compared to naïve mice that received METH <b>binge</b> treatment for the first time, mice pretreated with METH in adolescence showed a greater loss of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity in striatum, loss of THir fibers in the substantia nigra reticulata (SNr) as well as decreased dopamine transporter (DAT) level and compromised DA clearance in striatum.
+TH	drug	opioid	21070820	In addition, semi quantitative in situ hybridization revealed that 6 weeks of wheel running, compared to sedentary housing, increased tyrosine hydroxylase (<strong>TH</strong>) mRNA levels in the ventral tegmental area (VTA), increased delta <b>opioid</b> receptor (DOR) mRNA levels in the Acb shell, and reduced levels of dopamine receptor (DR) D2 mRNA in the Acb core.
+TH	drug	opioid	21070820	In addition, semi quantitative in situ hybridization revealed that 6 weeks of wheel running, compared to sedentary housing, increased <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) mRNA levels in the ventral tegmental area (VTA), increased delta <b>opioid</b> receptor (DOR) mRNA levels in the Acb shell, and reduced levels of dopamine receptor (DR) D2 mRNA in the Acb core.
+TH	drug	nicotine	21047685	NT69L might modulate dopamine neurotransmission implicated in the reinforcing effects of <b>nicotine</b> by modulating <strong>tyrosine hydroxylase</strong> and dopamine receptor mRNA levels in the PFC and striatum.
+TH	addiction	reward	21047685	NT69L might modulate dopamine neurotransmission implicated in the <b>reinforcing</b> effects of nicotine by modulating <strong>tyrosine hydroxylase</strong> and dopamine receptor mRNA levels in the PFC and striatum.
+TH	drug	nicotine	20978107	Participants were 234 9(<strong>th</strong>) and 10(<strong>th</strong>) graders (54% female) who recorded at least one <b>smoking</b> event during 7 days of EMA data collection.
+TH	addiction	dependence	20973778	In this study, a series of experiments were performed to further characterize the role of CRF type 2 receptor (CRF₂) signalling in opiate withdrawal induced physical signs of <b>dependence</b>, hypothalamus pituitary adrenal (HPA) axis activation, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and tyrosine hydroxylase (<strong>TH</strong>) phosphorylation (activation), as well as CRF₂ expression in the nucleus of the solitary tract A₂ noradrenergic cell group (NTS A₂).
+TH	addiction	withdrawal	20973778	In this study, a series of experiments were performed to further characterize the role of CRF type 2 receptor (CRF₂) signalling in opiate <b>withdrawal</b> induced physical signs of dependence, hypothalamus pituitary adrenal (HPA) axis activation, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and tyrosine hydroxylase (<strong>TH</strong>) phosphorylation (activation), as well as CRF₂ expression in the nucleus of the solitary tract A₂ noradrenergic cell group (NTS A₂).
+TH	addiction	dependence	20973778	In this study, a series of experiments were performed to further characterize the role of CRF type 2 receptor (CRF₂) signalling in opiate withdrawal induced physical signs of <b>dependence</b>, hypothalamus pituitary adrenal (HPA) axis activation, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) phosphorylation (activation), as well as CRF₂ expression in the nucleus of the solitary tract A₂ noradrenergic cell group (NTS A₂).
+TH	addiction	withdrawal	20973778	In this study, a series of experiments were performed to further characterize the role of CRF type 2 receptor (CRF₂) signalling in opiate <b>withdrawal</b> induced physical signs of dependence, hypothalamus pituitary adrenal (HPA) axis activation, enhanced noradrenaline (NA) turnover in the hypothalamic paraventricular nucleus (PVN) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) phosphorylation (activation), as well as CRF₂ expression in the nucleus of the solitary tract A₂ noradrenergic cell group (NTS A₂).
+TH	drug	opioid	20973778	Six days later, rats were pretreated with AS 30 or saline 10 min before <b>naloxone</b> and the physical signs of abstinence, the HPA axis activity, NA turnover, <strong>TH</strong> activation and CRF₂ expression were measured using immunoblotting, RIA, HPLC and immunohistochemistry.
+TH	drug	opioid	20973778	Finally, AS 30 antagonized the <strong>TH</strong> phosphorylation at Serine40 induced by <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	20973778	Finally, AS 30 antagonized the <strong>TH</strong> phosphorylation at Serine40 induced by morphine <b>withdrawal</b>.
+TH	addiction	withdrawal	20973778	These results suggest that physical signs of opiate <b>withdrawal</b>, <strong>TH</strong> activation and stimulation of noradrenergic pathways innervating the PVN are modulated by CRF₂ signalling.
+TH	drug	opioid	20924561	Enhanced <strong>tyrosine hydroxylase</strong> phosphorylation in the nucleus accumbens and nucleus tractus solitarius A2 cell group after <b>morphine</b> conditioned place preference.
+TH	drug	opioid	20924561	The purpose of the present study was to evaluate the turnover of DA and NA in the NAc and the site specific phosphorylation of <strong>TH</strong> in the NAc, VTA, and NTS on the CPP mice conditioned by <b>morphine</b>.
+TH	addiction	reward	20924561	The purpose of the present study was to evaluate the turnover of DA and NA in the NAc and the site specific phosphorylation of <strong>TH</strong> in the NAc, VTA, and NTS on the <b>CPP</b> mice conditioned by morphine.
+TH	drug	opioid	20924561	<b>Morphine</b> induced CPP phosphorylates <strong>TH</strong> at serine (Ser)40 but not Ser31 in NAc, which is associated with an enhanced of DA and NA turnover.
+TH	addiction	reward	20924561	Morphine induced <b>CPP</b> phosphorylates <strong>TH</strong> at serine (Ser)40 but not Ser31 in NAc, which is associated with an enhanced of DA and NA turnover.
+TH	drug	opioid	20924561	We also found that <b>morphine</b> induced CPP increased levels of <strong>TH</strong> phosphorylated at Ser31 and Ser40 in the NTS.
+TH	addiction	reward	20924561	We also found that morphine induced <b>CPP</b> increased levels of <strong>TH</strong> phosphorylated at Ser31 and Ser40 in the NTS.
+TH	drug	opioid	20924561	The present study demonstrates that <b>morphine</b> induced CPP might stimulate <strong>TH</strong> activity and accelerate DA and NA turnover in the NAc via a mechanism involving phosphorylation of <strong>TH</strong>.
+TH	addiction	reward	20924561	The present study demonstrates that morphine induced <b>CPP</b> might stimulate <strong>TH</strong> activity and accelerate DA and NA turnover in the NAc via a mechanism involving phosphorylation of <strong>TH</strong>.
+TH	addiction	withdrawal	20920894	Animals exhibiting decreased <b>withdrawal</b> latency time, indicating <strong>TH</strong>, on or before Day 42, were selected for pharmacological intervention.
+TH	drug	opioid	20718739	Rats were intrathecally (i.<strong>th</strong>) injected with a Raf 1 selective small interfering RNA (siRNA) mixture for 3 days and were subsequently infused with saline or <b>morphine</b>, s.c. for 7 days.
+TH	drug	opioid	20718739	Selective knockdown of spinal Raf 1 protein levels by i.<strong>th</strong> Raf 1 selective siRNA pretreatment significantly attenuated sustained <b>morphine</b> mediated up regulation of CGRP immunoreactivity in the spinal cord of rats and prevented the development of thermal hyperalgesia, mechanical allodynia and antinociceptive tolerance.
+TH	drug	opioid	20716624	Using zebrafish embryos as the model, we demonstrate that <b>morphine</b> decreases miR 133b expression, hence increasing the expression of its target, Pitx3, a transcription factor that activates <strong>tyrosine hydroxylase</strong> and dopamine transporter.
+TH	drug	cocaine	20655181	We evaluated the levels of the dopamine transporter (DAT), and the D1  (D1R) and D2 type (D2R) dopaminergic receptors, as well as tyrosine hydroxylase (<strong>TH</strong>) mRNA in dopaminergic areas of the adult, <b>cocaine</b> self administered, rat brain that had been chronically exposed to CP or vehicle (VH) during periadolescence.
+TH	drug	cocaine	20655181	We evaluated the levels of the dopamine transporter (DAT), and the D1  (D1R) and D2 type (D2R) dopaminergic receptors, as well as <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) mRNA in dopaminergic areas of the adult, <b>cocaine</b> self administered, rat brain that had been chronically exposed to CP or vehicle (VH) during periadolescence.
+TH	drug	cocaine	20553819	To test this hypothesis, we used electron microscopic immunolabeling of AMPA GluR1 subunits and tyrosine hydroxylase (<strong>TH</strong>), the enzyme needed for dopamine synthesis, in the cortical associated parabrachial (PB) and in the limbic associated paranigral (PN) VTA of adult male C57BL/6 mice receiving either a single injection (acute) or repeated escalating doses for 14 days (chronic) of <b>cocaine</b>.
+TH	drug	cocaine	20553819	To test this hypothesis, we used electron microscopic immunolabeling of AMPA GluR1 subunits and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the enzyme needed for dopamine synthesis, in the cortical associated parabrachial (PB) and in the limbic associated paranigral (PN) VTA of adult male C57BL/6 mice receiving either a single injection (acute) or repeated escalating doses for 14 days (chronic) of <b>cocaine</b>.
+TH	drug	cocaine	20553819	Acute <b>cocaine</b> resulted in opposing VTA region specific changes in <strong>TH</strong> containing dopaminergic dendrites.
+TH	drug	cocaine	20553819	Conversely, <strong>TH</strong> labeled dendrites within the PN VTA showed greater surface expression of GluR1 with increases in both synaptic and plasmalemmal GluR1 immunogold density after a single injection of <b>cocaine</b>.
+TH	drug	cocaine	20553819	In contrast, non <strong>TH</strong> containing, presumably GABAergic dendrites showed VTA region specific changes only after repeated <b>cocaine</b> administration such that synaptic GluR1 decreased in the PB, but increased in the PN VTA.
+TH	drug	opioid	20540693	DHC possesses approximately 1/6(<strong>th</strong>) of the <b>morphine</b> analgesic effect when drugs are administered orally.
+TH	drug	amphetamine	20460138	Stress induced reinstatement of <b>amphetamine</b> conditioned place preference and changes in <strong>tyrosine hydroxylase</strong> in the nucleus accumbens in adolescent rats.
+TH	addiction	relapse	20460138	Stress induced <b>reinstatement</b> of amphetamine conditioned place preference and changes in <strong>tyrosine hydroxylase</strong> in the nucleus accumbens in adolescent rats.
+TH	addiction	addiction	20460138	In humans and animals, changes in tyrosine hydroxylase (<strong>TH</strong>) have been related to drug <b>addiction</b>.
+TH	addiction	addiction	20460138	In humans and animals, changes in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) have been related to drug <b>addiction</b>.
+TH	addiction	relapse	20460138	We also investigated <strong>TH</strong> levels following the <b>reinstatement</b> of CPP.
+TH	addiction	reward	20460138	We also investigated <strong>TH</strong> levels following the reinstatement of <b>CPP</b>.
+TH	drug	amphetamine	20460138	Moreover the reinstatement of <b>AMPH</b> induced CPP by stress exposure occurred in the presence of decreased <strong>TH</strong> in the nucleus accumbens.
+TH	addiction	relapse	20460138	Moreover the <b>reinstatement</b> of AMPH induced CPP by stress exposure occurred in the presence of decreased <strong>TH</strong> in the nucleus accumbens.
+TH	addiction	reward	20460138	Moreover the reinstatement of AMPH induced <b>CPP</b> by stress exposure occurred in the presence of decreased <strong>TH</strong> in the nucleus accumbens.
+TH	addiction	relapse	20460138	In conclusion, our data add new evidence that neuroadaptations on <strong>TH</strong> may mediate <b>relapse</b> to drug <b>seeking</b> behavior induced by stress within adolescence.
+TH	drug	opioid	20438612	Using immunohistochemistry and western blot, the expression of FosB/DeltaFosB, tyrosine hydroxylase (<strong>TH</strong>), corticotropin releasing factor (CRF) and pro dynorphin (DYN) was measured in different nuclei from the brain stress system in <b>morphine</b> dependent rats and after <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	20438612	Using immunohistochemistry and western blot, the expression of FosB/DeltaFosB, tyrosine hydroxylase (<strong>TH</strong>), corticotropin releasing factor (CRF) and pro dynorphin (DYN) was measured in different nuclei from the brain stress system in morphine dependent rats and after morphine <b>withdrawal</b>.
+TH	drug	opioid	20438612	Using immunohistochemistry and western blot, the expression of FosB/DeltaFosB, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), corticotropin releasing factor (CRF) and pro dynorphin (DYN) was measured in different nuclei from the brain stress system in <b>morphine</b> dependent rats and after <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	20438612	Using immunohistochemistry and western blot, the expression of FosB/DeltaFosB, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), corticotropin releasing factor (CRF) and pro dynorphin (DYN) was measured in different nuclei from the brain stress system in morphine dependent rats and after morphine <b>withdrawal</b>.
+TH	drug	opioid	20438612	<b>Morphine</b> dependence and withdrawal evoked an increase in FosB/DeltaFosB <strong>TH</strong> and FosB/DeltaFosB CRF double labelling in NTS A(2) and PVN, respectively, besides an increase in <strong>TH</strong> levels in NTS A(2) and CRF expression in PVN.
+TH	addiction	dependence	20438612	Morphine <b>dependence</b> and withdrawal evoked an increase in FosB/DeltaFosB <strong>TH</strong> and FosB/DeltaFosB CRF double labelling in NTS A(2) and PVN, respectively, besides an increase in <strong>TH</strong> levels in NTS A(2) and CRF expression in PVN.
+TH	addiction	withdrawal	20438612	Morphine dependence and <b>withdrawal</b> evoked an increase in FosB/DeltaFosB <strong>TH</strong> and FosB/DeltaFosB CRF double labelling in NTS A(2) and PVN, respectively, besides an increase in <strong>TH</strong> levels in NTS A(2) and CRF expression in PVN.
+TH	addiction	reward	20394806	IUGR offspring have six to eightfold over expression of dopamine (DA) related genes (tyrosine hydroxylase (<strong>TH</strong>) and dopamine transporter) in brain regions related to <b>reward</b> processing (ventral tegmental area (VTA), nucleus accumbens, prefrontal cortex (PFC)) and homeostatic control (hypothalamus), as well as increased number of <strong>TH</strong> ir neurons in the VTA and increased dopamine in the PFC.
+TH	addiction	reward	20394806	IUGR offspring have six to eightfold over expression of dopamine (DA) related genes (<strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine transporter) in brain regions related to <b>reward</b> processing (ventral tegmental area (VTA), nucleus accumbens, prefrontal cortex (PFC)) and homeostatic control (hypothalamus), as well as increased number of <strong>TH</strong> ir neurons in the VTA and increased dopamine in the PFC.
+TH	addiction	withdrawal	20367754	We found that the enhanced expression of <strong>tyrosine hydroxylase</strong> normally observed during <b>withdrawal</b> was attenuated in CREB/CREM mutants.
+TH	drug	opioid	20159948	<strong>Tyrosine hydroxylase</strong> positive neurons expressing CRF1R were seen at the level of the nucleus tractus solitarius A(2) cell group in both control and <b>morphine</b> withdrawn rats.
+TH	drug	amphetamine	20143198	In addition, contrary to what we found with other toxins such as MPTP, EE did not diminish the striatal neurotoxicity induced by <b>METH</b> (4 x 10 mg/kg) as measured by dopamine content, <strong>tyrosine hydroxylase</strong> protein levels and apoptosis.
+TH	addiction	reward	19926806	Diurnal variations in natural and drug <b>reward</b>, mesolimbic <strong>tyrosine hydroxylase</strong>, and clock gene expression in the male rat.
+TH	addiction	reward	19926806	To identify potential mechanisms for rhythmicity in <b>reward</b>, levels of tyrosine hydroxylase (<strong>TH</strong>) and core clock proteins (Period1 and Bmal1) were examined across the day in the ventral tegmental area (VTA) and the nucleus accumbens (NAcc).
+TH	addiction	reward	19926806	To identify potential mechanisms for rhythmicity in <b>reward</b>, levels of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and core clock proteins (Period1 and Bmal1) were examined across the day in the ventral tegmental area (VTA) and the nucleus accumbens (NAcc).
+TH	drug	amphetamine	19926806	By contrast, <strong>TH</strong> protein levels were rhythmic in both the NAcc and VTA, but the peaks differed with that in the NAcc coinciding with the peak of sex reward and that in the VTA associated with the peak in <b>amphetamine</b> reward.
+TH	addiction	reward	19926806	By contrast, <strong>TH</strong> protein levels were rhythmic in both the NAcc and VTA, but the peaks differed with that in the NAcc coinciding with the peak of sex <b>reward</b> and that in the VTA associated with the peak in amphetamine <b>reward</b>.
+TH	drug	amphetamine	19926806	The phase relationships between reward rhythms and mesolimbic <strong>TH</strong> protein levels suggest that an increased capacity for the release of dopamine in the NAcc may underlie the rhythms in sex related reward, while <b>amphetamine</b> related reward occurs at a time when the likelihood of evoked NAcc DA release is relatively low.
+TH	addiction	reward	19926806	The phase relationships between <b>reward</b> rhythms and mesolimbic <strong>TH</strong> protein levels suggest that an increased capacity for the release of dopamine in the NAcc may underlie the rhythms in sex related <b>reward</b>, while amphetamine related <b>reward</b> occurs at a time when the likelihood of evoked NAcc DA release is relatively low.
+TH	drug	alcohol	19876496	The mean ages at the first onset of <b>alcohol</b> use, development of the first criterion and International Statistical Classification of Diseases and Related Health Problems 10(<strong>th</strong>) Revision (ICD 10) dependence was 18.72 years (SD, 6.84), 24.33 years (SD, 9.21) and 27.51 years (SD, 9.28), respectively.
+TH	addiction	dependence	19876496	The mean ages at the first onset of alcohol use, development of the first criterion and International Statistical Classification of Diseases and Related Health Problems 10(<strong>th</strong>) Revision (ICD 10) <b>dependence</b> was 18.72 years (SD, 6.84), 24.33 years (SD, 9.21) and 27.51 years (SD, 9.28), respectively.
+TH	drug	alcohol	19860799	Moreover, <b>ethanol</b> intake increased tyrosine hydroxylase (<strong>TH</strong>) gene expression in the substantia nigra (24%) and ventral tegmental area (23%) and corticotrophin releasing gene expression in the paraventricular hypothalamic nucleus (41.6%).
+TH	drug	alcohol	19860799	Moreover, <b>ethanol</b> intake increased <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene expression in the substantia nigra (24%) and ventral tegmental area (23%) and corticotrophin releasing gene expression in the paraventricular hypothalamic nucleus (41.6%).
+TH	drug	opioid	19819303	Biochemical traits related to <b>morphine</b>'s sensitizing effects were altered by intra VTA anti FGF 1 because <b>morphine</b> induced upregulation of both tyrosine hydroxylase (<strong>TH</strong>) and N methyl d aspartate glutamate receptor 1 (NMDAR1) in the VTA was blocked after anti FGF 1.
+TH	drug	opioid	19819303	Biochemical traits related to <b>morphine</b>'s sensitizing effects were altered by intra VTA anti FGF 1 because <b>morphine</b> induced upregulation of both <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and N methyl d aspartate glutamate receptor 1 (NMDAR1) in the VTA was blocked after anti FGF 1.
+TH	drug	alcohol	19673740	Furthermore, the effects of gender on the relationship between Ucn 1 and tyrosine hydroxylase (<strong>TH</strong>) in pIII and <b>alcohol</b> preference in rats have not been previously assessed.
+TH	drug	alcohol	19673740	Furthermore, the effects of gender on the relationship between Ucn 1 and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in pIII and <b>alcohol</b> preference in rats have not been previously assessed.
+TH	drug	alcohol	19673740	Ucn 1  and <strong>TH</strong> positive cells were detected on coronal midbrain sections from 6  to 8 week old <b>alcohol</b> naïve animals using brightfield and fluorescent immunohistochemistry.
+TH	addiction	withdrawal	19639608	Dox <b>withdrawal</b> after 7 weeks, resulted in <strong>TH</strong> levels comparable to the controls at 14 weeks.
+TH	drug	cocaine	19580849	There also were differential effects of <b>cocaine</b> on <strong>tyrosine hydroxylase</strong> and DAT depending on housing, with both increased by <b>cocaine</b> in II but not SE3 rats.
+TH	drug	opioid	19567779	<b>Naloxone</b> induced <b>morphine</b> withdrawal activates ERK1/2 and phosphorylates <strong>TH</strong> at Ser31 in the right and left ventricle, with an increase in the mean arterial blood pressure and heart rate.
+TH	addiction	withdrawal	19567779	Naloxone induced morphine <b>withdrawal</b> activates ERK1/2 and phosphorylates <strong>TH</strong> at Ser31 in the right and left ventricle, with an increase in the mean arterial blood pressure and heart rate.
+TH	drug	opioid	19567779	The ability of <b>morphine</b> withdrawal to activate ERK that phosphorylates <strong>TH</strong> at Ser31 was reduced by HA 1004.
+TH	addiction	withdrawal	19567779	The ability of morphine <b>withdrawal</b> to activate ERK that phosphorylates <strong>TH</strong> at Ser31 was reduced by HA 1004.
+TH	drug	opioid	19567779	The present findings demonstrate that the enhancement of ERK1/2 expression and the phosphorylation state of <strong>TH</strong> at Ser31 during <b>morphine</b> withdrawal are dependent on PKA and suggest cross talk between PKA and ERK1/2 transduction pathway mediating <b>morphine</b> withdrawal induced activation (phosphorylation) of <strong>TH</strong>.
+TH	addiction	withdrawal	19567779	The present findings demonstrate that the enhancement of ERK1/2 expression and the phosphorylation state of <strong>TH</strong> at Ser31 during morphine <b>withdrawal</b> are dependent on PKA and suggest cross talk between PKA and ERK1/2 transduction pathway mediating morphine <b>withdrawal</b> induced activation (phosphorylation) of <strong>TH</strong>.
+TH	drug	opioid	19545278	We found an increased phosphorylation of CREB (pCREB) selectively within tyrosine hydroxylase (<strong>TH</strong>) immunoreactive neurons in the NTS from <b>morphine</b> withdrawn rats, which parallel elevated corticosterone levels.
+TH	drug	opioid	19545278	We found an increased phosphorylation of CREB (pCREB) selectively within <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactive neurons in the NTS from <b>morphine</b> withdrawn rats, which parallel elevated corticosterone levels.
+TH	drug	opioid	19545278	We also measured expression levels of <strong>TH</strong> and phosphorylated ERK(1/2) (pERK(1/2)), and found that both are up regulated following <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	19545278	We also measured expression levels of <strong>TH</strong> and phosphorylated ERK(1/2) (pERK(1/2)), and found that both are up regulated following morphine <b>withdrawal</b>.
+TH	drug	opioid	19545278	SL327, an inhibitor of ERK activation, at doses which reduced the hyperactive pERK(1/2) levels, did not attenuated the rise in pCREB and <strong>TH</strong> immunoreactivity or plasma corticosterone secretion during <b>morphine</b> withdrawal, indicating that ERK kinase/ERK pathway was not directly needed for either activation of CREB and <strong>TH</strong> expression in the NTS or HPA axis hyperactivity.
+TH	addiction	withdrawal	19545278	SL327, an inhibitor of ERK activation, at doses which reduced the hyperactive pERK(1/2) levels, did not attenuated the rise in pCREB and <strong>TH</strong> immunoreactivity or plasma corticosterone secretion during morphine <b>withdrawal</b>, indicating that ERK kinase/ERK pathway was not directly needed for either activation of CREB and <strong>TH</strong> expression in the NTS or HPA axis hyperactivity.
+TH	addiction	withdrawal	19545278	In contrast, PKC inhibitor calphostin C reduced the <b>withdrawal</b> triggered rise in pCREB, pERK(1/2), <strong>TH</strong> expression and corticosterone secretion.
+TH	drug	opioid	19545278	The results indicate that PKC mediates both CREB activation and HPA response by <b>morphine</b> withdrawal and might suggest that CREB activation in the NTS is related to <strong>TH</strong> expression associated with <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	19545278	The results indicate that PKC mediates both CREB activation and HPA response by morphine <b>withdrawal</b> and might suggest that CREB activation in the NTS is related to <strong>TH</strong> expression associated with morphine <b>withdrawal</b>.
+TH	drug	amphetamine	19457119	Increases in cytoplasmic DA produced by reserpine, L DOPA or clorgyline prior to <b>METH</b> uncover damage in the NAc as evidenced by microglial activation and depletion of DA, tyrosine hydroxylase (<strong>TH</strong>), and the DA transporter.
+TH	drug	amphetamine	19457119	Increases in cytoplasmic DA produced by reserpine, L DOPA or clorgyline prior to <b>METH</b> uncover damage in the NAc as evidenced by microglial activation and depletion of DA, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and the DA transporter.
+TH	drug	amphetamine	19457119	None of the treatments that enhance <b>METH</b> toxicity in the NAc and CPu lead to losses of <strong>TH</strong> protein or DA cell bodies in the substantia nigra or the ventral tegmentum.
+TH	drug	cocaine	19429176	The neuronal nitric oxide synthase (nNOS) gene contributes to the regulation of tyrosine hydroxylase (<strong>TH</strong>) by <b>cocaine</b>.
+TH	drug	cocaine	19429176	The neuronal nitric oxide synthase (nNOS) gene contributes to the regulation of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) by <b>cocaine</b>.
+TH	drug	cocaine	19429176	Given the requirement of dopamine (DA) transmission in <b>cocaine</b> induced behavioral sensitization and the interactions between NO and DA systems, the present study investigated the role of the neuronal nitric oxide synthase (nNOS) gene and the effect of <b>cocaine</b> on the expression of tyrosine hydroxylase (<strong>TH</strong>) immunoreactive ( ir) neurons.
+TH	addiction	sensitization	19429176	Given the requirement of dopamine (DA) transmission in cocaine induced behavioral <b>sensitization</b> and the interactions between NO and DA systems, the present study investigated the role of the neuronal nitric oxide synthase (nNOS) gene and the effect of cocaine on the expression of tyrosine hydroxylase (<strong>TH</strong>) immunoreactive ( ir) neurons.
+TH	drug	cocaine	19429176	Given the requirement of dopamine (DA) transmission in <b>cocaine</b> induced behavioral sensitization and the interactions between NO and DA systems, the present study investigated the role of the neuronal nitric oxide synthase (nNOS) gene and the effect of <b>cocaine</b> on the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactive ( ir) neurons.
+TH	addiction	sensitization	19429176	Given the requirement of dopamine (DA) transmission in cocaine induced behavioral <b>sensitization</b> and the interactions between NO and DA systems, the present study investigated the role of the neuronal nitric oxide synthase (nNOS) gene and the effect of cocaine on the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactive ( ir) neurons.
+TH	drug	cocaine	19429176	We report that (a) nNOS KO mice express lower levels of <strong>TH</strong> ir neurons in the VTA compared to WT counterparts, (b) <b>cocaine</b> administration to WT mice significantly increased striatal <strong>TH</strong> expression, and (c) the same <b>cocaine</b> administration to nNOS KO mice significantly decreased striatal <strong>TH</strong> expression.
+TH	drug	psychedelics	19428783	NAC and <b>ketamine</b> exerted a preventive effect against MPTP induced loss of <strong>tyrosine hydroxylase</strong> positive neurons and suppressed the nuclear translocation of JNK3, suggesting that NAC and <b>ketamine</b> can prevent MPTP induced dopaminergic neuronal death by suppressing JNK3 activation.
+TH	drug	nicotine	19406037	<b>Nicotine</b> tolerance to PC12 cell line: acute and chronic exposures modulate dopamine D2 receptor and <strong>tyrosine hydroxylase</strong> expression.
+TH	drug	nicotine	19406037	In this paper, we have demonstrated the tolerance to acute and chronic <b>nicotine</b> administrations on PC12 cell line on the basis of the expressions of dopamine receptors and <strong>tyrosine hydroxylase</strong>, the rate limiting enzyme of dopamine biosynthesis, by Western blot, immunohistochemistry and in situ hybridization.
+TH	drug	nicotine	19406037	In vitro treatment of <b>nicotine</b> resulted in similar expressional changes of dopamine D(2) receptor and <strong>tyrosine hydroxylase</strong> at protein and mRNA levels in dose  and time dependent manner, whereas dopamine D(1) receptor did not reveal any positive output.
+TH	drug	nicotine	19406037	Therefore, this study implied a new approach towards <b>nicotine</b> tolerance which is likely to be related to the modulation of dopamine D(2) receptor and <strong>tyrosine hydroxylase</strong> expressions by chronic and acute <b>nicotine</b> exposures in PC12 cell line.
+TH	drug	amphetamine	19378464	At 14 days after 6 OHDA when <b>AMPH</b> evoked ipsiversive rotation is mediated by the intact hemisphere, rotation was dose dependently reduced by tyrosine hydroxylase (<strong>TH</strong>) inhibition with alpha methyl p tyrosine (alpha MPT) or dopa decarboxylase (DDC) inhibition with 3 hydroxybenzyl hydrazine (NSD 1015), indicating dependence upon newly synthesized DA.
+TH	addiction	dependence	19378464	At 14 days after 6 OHDA when AMPH evoked ipsiversive rotation is mediated by the intact hemisphere, rotation was dose dependently reduced by tyrosine hydroxylase (<strong>TH</strong>) inhibition with alpha methyl p tyrosine (alpha MPT) or dopa decarboxylase (DDC) inhibition with 3 hydroxybenzyl hydrazine (NSD 1015), indicating <b>dependence</b> upon newly synthesized DA.
+TH	drug	amphetamine	19378464	At 14 days after 6 OHDA when <b>AMPH</b> evoked ipsiversive rotation is mediated by the intact hemisphere, rotation was dose dependently reduced by <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) inhibition with alpha methyl p tyrosine (alpha MPT) or dopa decarboxylase (DDC) inhibition with 3 hydroxybenzyl hydrazine (NSD 1015), indicating dependence upon newly synthesized DA.
+TH	addiction	dependence	19378464	At 14 days after 6 OHDA when AMPH evoked ipsiversive rotation is mediated by the intact hemisphere, rotation was dose dependently reduced by <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) inhibition with alpha methyl p tyrosine (alpha MPT) or dopa decarboxylase (DDC) inhibition with 3 hydroxybenzyl hydrazine (NSD 1015), indicating <b>dependence</b> upon newly synthesized DA.
+TH	drug	amphetamine	19269222	The tyrosine hydroxylase (<strong>TH</strong>), dopamine transporter (DAT), and vesicular monoamine transporter 2 (VMAT2) levels and glial reactions in the striata of <b>METH</b> abusers were examined using immunohistochemical technique.
+TH	drug	amphetamine	19269222	The <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), dopamine transporter (DAT), and vesicular monoamine transporter 2 (VMAT2) levels and glial reactions in the striata of <b>METH</b> abusers were examined using immunohistochemical technique.
+TH	drug	amphetamine	19269222	Decreases in <strong>TH</strong> immunoreactivity and DAT levels were evident in <b>METH</b> users.
+TH	addiction	sensitization	19262504	Pulmonary dendritic cells (DCs) are crucially involved in <b>sensitization</b> toward allergens and play an important role in the development of T helper (<strong>Th</strong>)2 mediated allergic airway inflammation.
+TH	drug	opioid	19179436	Elevated glucocorticoid levels are responsible for induction of <strong>tyrosine hydroxylase</strong> mRNA expression, phosphorylation, and enzyme activity in the nucleus of the solitary tract during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	19179436	Elevated glucocorticoid levels are responsible for induction of <strong>tyrosine hydroxylase</strong> mRNA expression, phosphorylation, and enzyme activity in the nucleus of the solitary tract during morphine <b>withdrawal</b>.
+TH	drug	opioid	19179436	This study addressed the role of <b>morphine</b> withdrawal induced corticosterone (CORT) release in regulation of tyrosine hydroxylase (<strong>TH</strong>), the rate limiting enzyme of catecholamine biosynthesis in adrenalectomized (ADX) rats supplemented with low CORT pellet (ADX plus CORT).
+TH	addiction	withdrawal	19179436	This study addressed the role of morphine <b>withdrawal</b> induced corticosterone (CORT) release in regulation of tyrosine hydroxylase (<strong>TH</strong>), the rate limiting enzyme of catecholamine biosynthesis in adrenalectomized (ADX) rats supplemented with low CORT pellet (ADX plus CORT).
+TH	drug	opioid	19179436	This study addressed the role of <b>morphine</b> withdrawal induced corticosterone (CORT) release in regulation of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the rate limiting enzyme of catecholamine biosynthesis in adrenalectomized (ADX) rats supplemented with low CORT pellet (ADX plus CORT).
+TH	addiction	withdrawal	19179436	This study addressed the role of morphine <b>withdrawal</b> induced corticosterone (CORT) release in regulation of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the rate limiting enzyme of catecholamine biosynthesis in adrenalectomized (ADX) rats supplemented with low CORT pellet (ADX plus CORT).
+TH	drug	opioid	19179436	Present results show that in sham ADX rats, noradrenergic neurons in the NTS A(2) became activated during <b>morphine</b> withdrawal, as indicated by increased <strong>TH</strong> mRNA expression.
+TH	addiction	withdrawal	19179436	Present results show that in sham ADX rats, noradrenergic neurons in the NTS A(2) became activated during morphine <b>withdrawal</b>, as indicated by increased <strong>TH</strong> mRNA expression.
+TH	drug	opioid	19179436	However, this induction of <strong>TH</strong> expression is not detected in ADX plus CORT rats that are unable to mount CORT secretory response to <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	19179436	However, this induction of <strong>TH</strong> expression is not detected in ADX plus CORT rats that are unable to mount CORT secretory response to morphine <b>withdrawal</b>.
+TH	drug	opioid	19179436	Total <strong>TH</strong> protein levels were elevated in the NTS A(2) from sham operated rats during <b>morphine</b> dependence and withdrawal, whereas we did not find any alteration in ADX plus CORT animals.
+TH	addiction	dependence	19179436	Total <strong>TH</strong> protein levels were elevated in the NTS A(2) from sham operated rats during morphine <b>dependence</b> and withdrawal, whereas we did not find any alteration in ADX plus CORT animals.
+TH	addiction	withdrawal	19179436	Total <strong>TH</strong> protein levels were elevated in the NTS A(2) from sham operated rats during morphine dependence and <b>withdrawal</b>, whereas we did not find any alteration in ADX plus CORT animals.
+TH	drug	opioid	19179436	Furthermore, high levels of <strong>TH</strong> phosphorylated (activated) at Ser31 (but not at Ser40) were found in the A(2) area from sham <b>morphine</b> withdrawn rats.
+TH	drug	opioid	19179436	However, induction of <b>morphine</b> withdrawal to ADX plus CORT animals did not alter the phosphorylation (activation) of <strong>TH</strong> in NTS A(2) and decreased <strong>TH</strong> activity in the PVN.
+TH	addiction	withdrawal	19179436	However, induction of morphine <b>withdrawal</b> to ADX plus CORT animals did not alter the phosphorylation (activation) of <strong>TH</strong> in NTS A(2) and decreased <strong>TH</strong> activity in the PVN.
+TH	drug	amphetamine	19110059	Minocycline restores striatal <strong>tyrosine hydroxylase</strong> in GDNF heterozygous mice but not in <b>methamphetamine</b> treated mice.
+TH	drug	amphetamine	19110059	Microglial activation in the substantia nigra and a <strong>tyrosine hydroxylase</strong> deficit in the striatum of 3 month old GDNF heterozygous (GDNF(+/ )) mice were previously reported and both were exacerbated by a toxic <b>methamphetamine</b> binge.
+TH	addiction	intoxication	19110059	Microglial activation in the substantia nigra and a <strong>tyrosine hydroxylase</strong> deficit in the striatum of 3 month old GDNF heterozygous (GDNF(+/ )) mice were previously reported and both were exacerbated by a toxic methamphetamine <b>binge</b>.
+TH	drug	amphetamine	19110059	Although minocycline increased <strong>tyrosine hydroxylase</strong> immunoreactivity in GDNF(+/ ) mice, it did not attenuate the <b>methamphetamine</b> induced reduction of <strong>tyrosine hydroxylase</strong>.
+TH	drug	opioid	19104749	<strong>Tyrosine hydroxylase</strong> phosphorylation after <b>naloxone</b> induced <b>morphine</b> withdrawal in the left ventricle.
+TH	addiction	withdrawal	19104749	<strong>Tyrosine hydroxylase</strong> phosphorylation after naloxone induced morphine <b>withdrawal</b> in the left ventricle.
+TH	drug	opioid	19104749	The purpose of the present study was to evaluate the effects of <b>morphine</b> withdrawal on site specific tyrosine hydroxylase (<strong>TH</strong>) phosphorylation in the rat left ventricle.
+TH	addiction	withdrawal	19104749	The purpose of the present study was to evaluate the effects of morphine <b>withdrawal</b> on site specific tyrosine hydroxylase (<strong>TH</strong>) phosphorylation in the rat left ventricle.
+TH	drug	opioid	19104749	The purpose of the present study was to evaluate the effects of <b>morphine</b> withdrawal on site specific <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) phosphorylation in the rat left ventricle.
+TH	addiction	withdrawal	19104749	The purpose of the present study was to evaluate the effects of morphine <b>withdrawal</b> on site specific <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) phosphorylation in the rat left ventricle.
+TH	drug	opioid	19104749	Ninety min after <b>naloxone</b> administration to <b>morphine</b> dependent rats there was an increase in phospho Ser40 <strong>TH</strong> (139.0 +/  13%, P < 0.05) and Ser31 <strong>TH</strong> (135.5 +/  11%, P < 0.05) in the left ventricle which is associated with both an increase in total <strong>TH</strong> levels (114.4 +/  4.6%, P < 0.05, P < 0.01) and an enhancement of <strong>TH</strong> activity (51.0 +/  11 dm/microg protein, P < 0.001).
+TH	drug	opioid	19104749	When HA 1004 (40 nmol/day), inhibitor of cyclic AMP dependent protein kinase (PKA) was infused, concomitantly with <b>morphine</b>, it diminished the increase in noradrenaline (NA) turnover, total <strong>TH</strong> expression (95.76 +/  4.1 %, P < 0.01) and <strong>TH</strong> phosphorylation at Ser40 (85.5 +/  11%, P < 0.01) in <b>morphine</b> withdrawn rats.
+TH	drug	opioid	19104749	The present findings demonstrate that the enhancement of total <strong>TH</strong> expression and the increase of the phosphorylation state of <strong>TH</strong> during <b>morphine</b> withdrawal are dependent on PKA and ERK and suggest that these transduction pathways might contribute to the activation of the cardiac catecholaminergic neurons in response to <b>morphine</b>  withdrawal.
+TH	addiction	withdrawal	19104749	The present findings demonstrate that the enhancement of total <strong>TH</strong> expression and the increase of the phosphorylation state of <strong>TH</strong> during morphine <b>withdrawal</b> are dependent on PKA and ERK and suggest that these transduction pathways might contribute to the activation of the cardiac catecholaminergic neurons in response to morphine  <b>withdrawal</b>.
+TH	drug	cocaine	18992788	Many studies have suggested that behavioral sensitization by repeated injections of <b>cocaine</b> produce an increase in locomotor activity and an increase in the expression of tyrosine hydroxylase (<strong>TH</strong>), in the central dopaminergic system.
+TH	addiction	sensitization	18992788	Many studies have suggested that behavioral <b>sensitization</b> by repeated injections of cocaine produce an increase in locomotor activity and an increase in the expression of tyrosine hydroxylase (<strong>TH</strong>), in the central dopaminergic system.
+TH	drug	cocaine	18992788	Many studies have suggested that behavioral sensitization by repeated injections of <b>cocaine</b> produce an increase in locomotor activity and an increase in the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), in the central dopaminergic system.
+TH	addiction	sensitization	18992788	Many studies have suggested that behavioral <b>sensitization</b> by repeated injections of cocaine produce an increase in locomotor activity and an increase in the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), in the central dopaminergic system.
+TH	drug	cocaine	18992788	In order to investigate the effects of acupuncture on the repeated <b>cocaine</b> induced neuronal and behavioral sensitization alternations, we examined the influence of acupuncture on the repeated <b>cocaine</b> induced locomotor activity and the expression of <strong>TH</strong> in the brain using immunohistochemistry.
+TH	addiction	sensitization	18992788	In order to investigate the effects of acupuncture on the repeated cocaine induced neuronal and behavioral <b>sensitization</b> alternations, we examined the influence of acupuncture on the repeated cocaine induced locomotor activity and the expression of <strong>TH</strong> in the brain using immunohistochemistry.
+TH	drug	cocaine	18992788	<b>Cocaine</b> challenge produced a large increase in the locomotor activity and the expression of <strong>TH</strong> in the ventral tegmental area (VTA).
+TH	drug	cocaine	18955248	Repeated injections of <b>cocaine</b> produce an increase in locomotor activity and the expression of tyrosine hydroxylase (<strong>TH</strong>) in the main dopaminergic areas.
+TH	drug	cocaine	18955248	Repeated injections of <b>cocaine</b> produce an increase in locomotor activity and the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the main dopaminergic areas.
+TH	drug	cocaine	18955248	In order to investigate the effects of CR or BER on the repeated <b>cocaine</b> induced neuronal and behavioral alterations, we examined the influence of CR or BER on the repeated <b>cocaine</b> induced locomotor activity and the expression of <strong>TH</strong> in the brain by using immunohistochemistry.
+TH	drug	cocaine	18955248	<b>Cocaine</b> challenge (15 mg/kg, i.p) produced a larger increase in locomotor activity and expression of <strong>TH</strong> in the central dopaminergic areas.
+TH	drug	cocaine	18955248	30 min before the daily injections of <b>cocaine</b> significantly inhibited the <b>cocaine</b> induced locomotor activity as well as <strong>TH</strong> expression in the central dopaminergic areas.
+TH	drug	opioid	18815253	Therefore, we examined electron microscopic immunolabeling of GluR1 and tyrosine hydroxylase (<strong>TH</strong>) in two VTA regions of rats perfused 1 h after a single injection of <b>morphine</b>, or chronic <b>morphine</b> in intermittent escalating doses for 14 d, and appropriate saline controls.
+TH	drug	opioid	18815253	Therefore, we examined electron microscopic immunolabeling of GluR1 and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in two VTA regions of rats perfused 1 h after a single injection of <b>morphine</b>, or chronic <b>morphine</b> in intermittent escalating doses for 14 d, and appropriate saline controls.
+TH	drug	opioid	18815253	Acute <b>morphine</b> administration produced a significant increase in GluR1 immunogold particles at the plasma membrane and postsynaptic densities in both <strong>TH</strong>  and non <strong>TH</strong> containing dendrites in the parabrachial VTA, a region that contains mainly prefrontal cortical projecting dopaminergic neurons involved in motivation and drug seeking behavior.
+TH	addiction	relapse	18815253	Acute morphine administration produced a significant increase in GluR1 immunogold particles at the plasma membrane and postsynaptic densities in both <strong>TH</strong>  and non <strong>TH</strong> containing dendrites in the parabrachial VTA, a region that contains mainly prefrontal cortical projecting dopaminergic neurons involved in motivation and drug <b>seeking</b> behavior.
+TH	drug	opioid	18815253	Chronic <b>morphine</b> administration maintained the increased synaptic GluR1 labeling in the parabrachial VTA, but also increased the number of GluR1 labeled synapses and <strong>TH</strong> immunoreactivity in dendrites of the paranigral VTA where substantially more dopaminergic neurons project to limbic structures implicated in locomotor activation and reward.
+TH	addiction	reward	18815253	Chronic morphine administration maintained the increased synaptic GluR1 labeling in the parabrachial VTA, but also increased the number of GluR1 labeled synapses and <strong>TH</strong> immunoreactivity in dendrites of the paranigral VTA where substantially more dopaminergic neurons project to limbic structures implicated in locomotor activation and <b>reward</b>.
+TH	drug	amphetamine	18690106	Characterization of behavioral response to <b>amphetamine</b>, <strong>tyrosine hydroxylase</strong> levels, and dopamine receptor levels in neurokinin 3 receptor knockout mice.
+TH	drug	cocaine	18640148	<b>Cocaine</b> induced behavioral sensitization in adolescent rats endures until adulthood: lack of association with GluR1 and NR1 glutamate receptor subunits and <strong>tyrosine hydroxylase</strong>.
+TH	addiction	sensitization	18640148	Cocaine induced behavioral <b>sensitization</b> in adolescent rats endures until adulthood: lack of association with GluR1 and NR1 glutamate receptor subunits and <strong>tyrosine hydroxylase</strong>.
+TH	addiction	sensitization	18606864	The lack of behavioral <b>sensitization</b> correlates with reduced dopamine levels in the striatum and decreased expression of <strong>tyrosine hydroxylase</strong>.
+TH	drug	opioid	18536752	The PKs PKA and ERK 1/2 are involved in phosphorylation of <strong>TH</strong> at Serine 40 and 31 during <b>morphine</b> withdrawal in rat hearts.
+TH	addiction	withdrawal	18536752	The PKs PKA and ERK 1/2 are involved in phosphorylation of <strong>TH</strong> at Serine 40 and 31 during morphine <b>withdrawal</b> in rat hearts.
+TH	drug	opioid	18536752	The purpose of the present study was to evaluate the effects of <b>morphine</b> withdrawal on site specific phosphorylation of <strong>TH</strong> in the heart.
+TH	addiction	withdrawal	18536752	The purpose of the present study was to evaluate the effects of morphine <b>withdrawal</b> on site specific phosphorylation of <strong>TH</strong> in the heart.
+TH	drug	opioid	18536752	<b>Naloxone</b> induced <b>morphine</b> withdrawal induced phosphorylation of <strong>TH</strong> at serine (Ser)40 and Ser31 in the right ventricle, associated with both an increase in total <strong>TH</strong> levels and an enhancement of <strong>TH</strong> activity.
+TH	addiction	withdrawal	18536752	Naloxone induced morphine <b>withdrawal</b> induced phosphorylation of <strong>TH</strong> at serine (Ser)40 and Ser31 in the right ventricle, associated with both an increase in total <strong>TH</strong> levels and an enhancement of <strong>TH</strong> activity.
+TH	drug	opioid	18536752	When HA 1004 (PK A inhibitor) was infused, concomitantly with <b>morphine</b>, it diminished the increase in noradrenaline turnover, total <strong>TH</strong> levels and <strong>TH</strong> phosphorylation at Ser40 in <b>morphine</b> withdrawn rats.
+TH	drug	opioid	18536752	In contrast, the infusion of calphostin C (PKC inhibitor), did not modify the <b>morphine</b> withdrawal induced increase in noradrenaline turnover and total <strong>TH</strong> levels.
+TH	addiction	withdrawal	18536752	In contrast, the infusion of calphostin C (PKC inhibitor), did not modify the morphine <b>withdrawal</b> induced increase in noradrenaline turnover and total <strong>TH</strong> levels.
+TH	drug	opioid	18536752	The present findings demonstrate that the enhancement of total <strong>TH</strong> levels and the increased phosphorylation state of <strong>TH</strong> during <b>morphine</b> withdrawal were dependent on PKA and ERK activities and suggest that these transduction pathways might contribute to the activation of the cardiac catecholaminergic neurons in response to <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	18536752	The present findings demonstrate that the enhancement of total <strong>TH</strong> levels and the increased phosphorylation state of <strong>TH</strong> during morphine <b>withdrawal</b> were dependent on PKA and ERK activities and suggest that these transduction pathways might contribute to the activation of the cardiac catecholaminergic neurons in response to morphine <b>withdrawal</b>.
+TH	drug	cocaine	18420350	For that purpose, we have measured tyrosine hydroxylase (<strong>TH</strong>) and dopamine transporter (DAT) mRNA and D1  and D2 like receptor binding in C57BL/6 and DBA/2 mice that were i) unoperated, ii) ADX or sham (SHAM) operated, or iii) ADX or SHAM operated and subjected to a <b>cocaine</b> sensitization regimen (15.0 mg/kg <b>cocaine</b> on nine consecutive days, followed by a 7.5 mg/kg challenge after a 5 day withdrawal).
+TH	addiction	sensitization	18420350	For that purpose, we have measured tyrosine hydroxylase (<strong>TH</strong>) and dopamine transporter (DAT) mRNA and D1  and D2 like receptor binding in C57BL/6 and DBA/2 mice that were i) unoperated, ii) ADX or sham (SHAM) operated, or iii) ADX or SHAM operated and subjected to a cocaine <b>sensitization</b> regimen (15.0 mg/kg cocaine on nine consecutive days, followed by a 7.5 mg/kg challenge after a 5 day withdrawal).
+TH	addiction	withdrawal	18420350	For that purpose, we have measured tyrosine hydroxylase (<strong>TH</strong>) and dopamine transporter (DAT) mRNA and D1  and D2 like receptor binding in C57BL/6 and DBA/2 mice that were i) unoperated, ii) ADX or sham (SHAM) operated, or iii) ADX or SHAM operated and subjected to a cocaine sensitization regimen (15.0 mg/kg cocaine on nine consecutive days, followed by a 7.5 mg/kg challenge after a 5 day <b>withdrawal</b>).
+TH	drug	cocaine	18420350	For that purpose, we have measured <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine transporter (DAT) mRNA and D1  and D2 like receptor binding in C57BL/6 and DBA/2 mice that were i) unoperated, ii) ADX or sham (SHAM) operated, or iii) ADX or SHAM operated and subjected to a <b>cocaine</b> sensitization regimen (15.0 mg/kg <b>cocaine</b> on nine consecutive days, followed by a 7.5 mg/kg challenge after a 5 day withdrawal).
+TH	addiction	sensitization	18420350	For that purpose, we have measured <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine transporter (DAT) mRNA and D1  and D2 like receptor binding in C57BL/6 and DBA/2 mice that were i) unoperated, ii) ADX or sham (SHAM) operated, or iii) ADX or SHAM operated and subjected to a cocaine <b>sensitization</b> regimen (15.0 mg/kg cocaine on nine consecutive days, followed by a 7.5 mg/kg challenge after a 5 day withdrawal).
+TH	addiction	withdrawal	18420350	For that purpose, we have measured <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and dopamine transporter (DAT) mRNA and D1  and D2 like receptor binding in C57BL/6 and DBA/2 mice that were i) unoperated, ii) ADX or sham (SHAM) operated, or iii) ADX or SHAM operated and subjected to a cocaine sensitization regimen (15.0 mg/kg cocaine on nine consecutive days, followed by a 7.5 mg/kg challenge after a 5 day <b>withdrawal</b>).
+TH	addiction	sensitization	18420350	Furthermore, ADX prevented the increase in <strong>TH</strong> and DAT mRNA expression in the substantia nigra, and the decrease in D2 binding in the dorsomedial subdivision of the caudal caudate putamen associated with <b>sensitization</b> in SHAM mice.
+TH	drug	cocaine	18420350	During <b>cocaine</b> sensitization, the DBA/2, but not the C57BL/6 strain, was susceptible to ADX in the dopamine system with respect to presynaptic <strong>TH</strong> and DAT and terminal D2 receptor expression.
+TH	addiction	sensitization	18420350	During cocaine <b>sensitization</b>, the DBA/2, but not the C57BL/6 strain, was susceptible to ADX in the dopamine system with respect to presynaptic <strong>TH</strong> and DAT and terminal D2 receptor expression.
+TH	drug	alcohol	18358675	Using a chronic inhalation model of <b>ethanol</b> exposure in mice, we have begun to investigate the effects of <b>alcohol</b> intake on dopaminergic signaling by examining protein levels of <strong>tyrosine hydroxylase</strong> and the dopamine transporter, as well as monoamine metabolites in three different target fields of three different dopaminergic nuclei.
+TH	drug	opioid	18322172	Our previous work demonstrated that <b>morphine</b> withdrawal contributed to <strong>Th</strong> cell differentiation by biasing cells toward the Th2 lineage.
+TH	addiction	withdrawal	18322172	Our previous work demonstrated that morphine <b>withdrawal</b> contributed to <strong>Th</strong> cell differentiation by biasing cells toward the Th2 lineage.
+TH	drug	opioid	18184800	Up regulation of NAc PENK in Met/Met <b>heroin</b> abusers was accompanied by impaired tyrosine hydroxylase (<strong>TH</strong>) mRNA expression in mesolimbic dopamine neurons.
+TH	drug	opioid	18184800	Up regulation of NAc PENK in Met/Met <b>heroin</b> abusers was accompanied by impaired <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) mRNA expression in mesolimbic dopamine neurons.
+TH	drug	opioid	18184800	Altogether, the data suggest that dysfunction of the <b>opioid</b> reward system is significantly linked to opiate abuse vulnerability and that <b>heroin</b> use alters the apparent influence of heritable dopamine tone on mesolimbic PENK and <strong>TH</strong> function.
+TH	addiction	reward	18184800	Altogether, the data suggest that dysfunction of the opioid <b>reward</b> system is significantly linked to opiate abuse vulnerability and that heroin use alters the apparent influence of heritable dopamine tone on mesolimbic PENK and <strong>TH</strong> function.
+TH	drug	opioid	20390081	On the 10(<strong>th</strong>) day after the measurement of tail flick latency, animals were challenged with <b>naloxone</b> (2 mg/kg., i.p.)
+TH	drug	opioid	18057194	We examined mRNA expression levels of DA transporter (DAT), tyrosine hydroxylase (<strong>TH</strong>), dopamine D2 receptor, alpha synuclein, and nuclear receptor related 1 (Nurr1) in discrete mesocorticolimbic and nigrostriatal subpopulations of <b>heroin</b> users and control subjects.
+TH	drug	opioid	18057194	We examined mRNA expression levels of DA transporter (DAT), <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), dopamine D2 receptor, alpha synuclein, and nuclear receptor related 1 (Nurr1) in discrete mesocorticolimbic and nigrostriatal subpopulations of <b>heroin</b> users and control subjects.
+TH	drug	opioid	18057194	<strong>TH</strong> and alpha synuclein mRNA levels were, in contrast, elevated in the VTA PN in <b>heroin</b> users with no change of the D2 receptor.
+TH	drug	alcohol	18036156	Voluntary <b>ethanol</b> intake increased the cerebrocortical concentration of the progesterone metabolite 3alpha hydroxy 5alpha pregnan 20 one (3alpha,5alpha <strong>TH</strong> PROG) that returned to control level 48 h after discontinuation of <b>ethanol</b> intake.
+TH	drug	alcohol	18036156	The 5alpha reductase inhibitor finasteride prevented both the increase in the cerebrocortical concentration of 3alpha,5alpha <strong>TH</strong> PROG apparent after 4 weeks of <b>ethanol</b> intake and the changes in NPY immunoreactivity and transgene expression induced by <b>ethanol</b> discontinuation.
+TH	drug	alcohol	18036156	Data suggest that 3alpha,5alpha <strong>TH</strong> PROG plays an important role in the changes in NPY Y1R signalling in the amygdala during <b>ethanol</b> discontinuation.
+TH	drug	opioid	17823252	Regulation of serine (Ser) 31 and Ser40 <strong>tyrosine hydroxylase</strong> phosphorylation during <b>morphine</b> withdrawal in the hypothalamic paraventricular nucleus and nucleus tractus solitarius A2 cell group: role of ERK1/2.
+TH	addiction	withdrawal	17823252	Regulation of serine (Ser) 31 and Ser40 <strong>tyrosine hydroxylase</strong> phosphorylation during morphine <b>withdrawal</b> in the hypothalamic paraventricular nucleus and nucleus tractus solitarius A2 cell group: role of ERK1/2.
+TH	drug	opioid	17823252	In the present study, the effect of <b>morphine</b> withdrawal on site specific <strong>TH</strong> phosphorylation in the PVN and NTS A(2) was determined by quantitative blot immunolabeling and immunohistochemistry using phosphorylation state specific antibodies.
+TH	addiction	withdrawal	17823252	In the present study, the effect of morphine <b>withdrawal</b> on site specific <strong>TH</strong> phosphorylation in the PVN and NTS A(2) was determined by quantitative blot immunolabeling and immunohistochemistry using phosphorylation state specific antibodies.
+TH	drug	opioid	17823252	We show that <b>naloxone</b> induced <b>morphine</b> withdrawal phosphorylates <strong>TH</strong> at Serine (Ser) 31 but not Ser40 in PVN and NTS A(2), which is associated with both an increase in total <strong>TH</strong> immunoreactivity in NTS A(2) and an enhanced <strong>TH</strong> activity in the PVN.
+TH	addiction	withdrawal	17823252	We show that naloxone induced morphine <b>withdrawal</b> phosphorylates <strong>TH</strong> at Serine (Ser) 31 but not Ser40 in PVN and NTS A(2), which is associated with both an increase in total <strong>TH</strong> immunoreactivity in NTS A(2) and an enhanced <strong>TH</strong> activity in the PVN.
+TH	drug	opioid	17823252	We then tested whether pharmacological inhibition of ERK activation by ERK kinase contributes to <b>morphine</b> withdrawal induced phosphorylation of <strong>TH</strong> at Ser31.
+TH	addiction	withdrawal	17823252	We then tested whether pharmacological inhibition of ERK activation by ERK kinase contributes to morphine <b>withdrawal</b> induced phosphorylation of <strong>TH</strong> at Ser31.
+TH	drug	opioid	17823252	These results suggest that <b>morphine</b> withdrawal increases noradrenaline turnover in the PVN, at least in part, via ERK(1/2) dependent phosphorylation of <strong>TH</strong> at Ser31.
+TH	addiction	withdrawal	17823252	These results suggest that morphine <b>withdrawal</b> increases noradrenaline turnover in the PVN, at least in part, via ERK(1/2) dependent phosphorylation of <strong>TH</strong> at Ser31.
+TH	drug	amphetamine	17699663	Two weeks after a <b>methamphetamine</b> binge (4 x 10 mg/kg, i.p., at 2 h intervals), GDNF(+/ ) mice had a significantly greater reduction of <strong>tyrosine hydroxylase</strong> immunoreactivity in the medial striatum, a proportionally greater depletion of dopamine and 3,4 dihydroxyphenylacetic acid (DOPAC) levels in the striatum, and a greater increase in activated microglia in the substantia nigra than wild type mice.
+TH	addiction	intoxication	17699663	Two weeks after a methamphetamine <b>binge</b> (4 x 10 mg/kg, i.p., at 2 h intervals), GDNF(+/ ) mice had a significantly greater reduction of <strong>tyrosine hydroxylase</strong> immunoreactivity in the medial striatum, a proportionally greater depletion of dopamine and 3,4 dihydroxyphenylacetic acid (DOPAC) levels in the striatum, and a greater increase in activated microglia in the substantia nigra than wild type mice.
+TH	drug	amphetamine	17699663	At 12 months of age, <b>methamphetamine</b> treated GDNF(+/ ) mice exhibited less motor activity and lower levels of <strong>tyrosine hydroxylase</strong> immunoreactivity, dopamine, DOPAC, and serotonin than wild type mice.
+TH	drug	cannabinoid	17655884	These axon terminal types carried presynaptic CB(1) <b>cannabinoid</b> receptors on the opposite side of DGL alpha containing synapses and double immunostaining confirmed that DGL alpha is present on the plasma membrane of both tyrosine hydroxylase (<strong>TH</strong>) positive (dopaminergic) and <strong>TH</strong> negative dendrites.
+TH	drug	cannabinoid	17655884	These axon terminal types carried presynaptic CB(1) <b>cannabinoid</b> receptors on the opposite side of DGL alpha containing synapses and double immunostaining confirmed that DGL alpha is present on the plasma membrane of both <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) positive (dopaminergic) and <strong>TH</strong> negative dendrites.
+TH	drug	amphetamine	17651730	<strong>Tyrosine hydroxylase</strong> immunostaining in the midbrain was unaffected by <b>methamphetamine</b>, suggesting that dopamine neurotoxicity was localized to the caudate.
+TH	drug	opioid	17604969	In addition, repeated <b>morphine</b> also increased the expression of <strong>tyrosine hydroxylase</strong> mRNA in the VTA after 4 days of <b>morphine</b> pretreatment, while decreasing the expression of dynorphin mRNA at 3 days after withdrawal.
+TH	addiction	withdrawal	17604969	In addition, repeated morphine also increased the expression of <strong>tyrosine hydroxylase</strong> mRNA in the VTA after 4 days of morphine pretreatment, while decreasing the expression of dynorphin mRNA at 3 days after <b>withdrawal</b>.
+TH	drug	opioid	17604969	Agmatine inhibited <b>morphine</b> induced changes in dynorphin, but not in <strong>tyrosine hydroxylase</strong> mRNA expression.
+TH	drug	amphetamine	17592122	The powerfully rewarding effects of <b>methamphetamine</b> are attributed to multiple neuropharmacological actions such as its ability to block plasma membrane transporters of all monoamines, reduce dopamine transporter expression, and inhibit monoamine oxidase activity while increasing <strong>tyrosine hydroxylase</strong> activity.
+TH	drug	cocaine	17538232	GDNF inhibits the <b>cocaine</b> induced upregulation of <strong>tyrosine hydroxylase</strong> activity in the ventral tegmental area and blocks behavioral responses to <b>cocaine</b>.
+TH	drug	cocaine	17505818	<b>Cocaine</b> induced sensitization is associated with altered dynamics of transcriptional responses of the dopamine transporter, <strong>tyrosine hydroxylase</strong>, and dopamine D2 receptors in C57Bl/6J mice.
+TH	addiction	sensitization	17505818	Cocaine induced <b>sensitization</b> is associated with altered dynamics of transcriptional responses of the dopamine transporter, <strong>tyrosine hydroxylase</strong>, and dopamine D2 receptors in C57Bl/6J mice.
+TH	drug	cocaine	17505818	As compared to vehicle challenge, <b>cocaine</b> challenge in vehicle pretreated mice induced a rapid increase (+208%) in DAT mRNA (45 min) followed by a delayed decrease ( 70%) (24 h), while <strong>TH</strong> and D2 mRNA were both increased (+45%) 24 h after the challenge.
+TH	addiction	sensitization	17439498	In contrast, <b>sensitization</b> to presynaptic regulation of synapsin(S9) phosphorylation developed in the hippocampal CA3 subregion while cAMP dependent <strong>tyrosine hydroxylase</strong>(S40) phosphorylation decreased in striatal dopamine terminals.
+TH	drug	amphetamine	17239369	In addition to the severe behavioral and societal consequences associated with <b>methamphetamine</b> abuse, <b>methamphetamine</b> can cause persistent damage to monoaminergic nerve terminals in rats, as measured by either monoamine concentrations or activity of the rate limiting synthetic enzymes, <strong>tyrosine hydroxylase</strong> and tryptophan hydroxylase.
+TH	drug	opioid	17216288	Differential involvement of 3', 5' cyclic adenosine monophosphate dependent protein kinase in regulation of Fos and <strong>tyrosine hydroxylase</strong> expression in the heart after <b>naloxone</b> induced <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	17216288	Differential involvement of 3', 5' cyclic adenosine monophosphate dependent protein kinase in regulation of Fos and <strong>tyrosine hydroxylase</strong> expression in the heart after naloxone induced morphine <b>withdrawal</b>.
+TH	drug	opioid	17216288	Moreover, <b>morphine</b> withdrawal induces Fos expression, an enhancement of NA turnover and an increase in the total <strong>TH</strong> levels.
+TH	addiction	withdrawal	17216288	Moreover, morphine <b>withdrawal</b> induces Fos expression, an enhancement of NA turnover and an increase in the total <strong>TH</strong> levels.
+TH	drug	opioid	17216288	When the selective PKA inhibitor HA 1004 was infused, concomitantly with <b>morphine</b> pellets, it diminished the increase in NA turnover and the total <strong>TH</strong> levels observed in <b>morphine</b> withdrawn rats.
+TH	drug	opioid	17216288	However, this inhibitor neither modifies the <b>morphine</b> withdrawal induced Fos expression nor the increase of nonphosphorylated <strong>TH</strong> levels.
+TH	addiction	withdrawal	17216288	However, this inhibitor neither modifies the morphine <b>withdrawal</b> induced Fos expression nor the increase of nonphosphorylated <strong>TH</strong> levels.
+TH	drug	amphetamine	17161385	<b>Methamphetamine</b> administration caused marked decreases in dopamine (DA) levels and <strong>TH</strong> like immunostaining in the mouse OB.
+TH	drug	amphetamine	17161385	Moreover, there was <b>METH</b> induced expression of activated caspase 3 in <strong>TH</strong> positive cells.
+TH	addiction	dependence	17156761	Diurnal differences in dopamine transporter and <strong>tyrosine hydroxylase</strong> levels in rat brain: <b>dependence</b> on the suprachiasmatic nucleus.
+TH	addiction	dependence	17156761	We conclude that DAT and <strong>TH</strong> within these brain regions exhibit diurnal variation and <b>dependence</b> on the SCN.
+TH	drug	alcohol	17109703	Of these, 34 had 4(<strong>th</strong>) edition Diagnostic and Statistical Manual diagnosis of <b>alcohol</b> dependence, 38 had schizophrenia, and 28 had bipolar disorder.
+TH	addiction	dependence	17109703	Of these, 34 had 4(<strong>th</strong>) edition Diagnostic and Statistical Manual diagnosis of alcohol <b>dependence</b>, 38 had schizophrenia, and 28 had bipolar disorder.
+TH	drug	alcohol	17091218	We examined the association between total hip (<strong>TH</strong>) and femoral neck (FN) BMD and <b>alcohol</b> intake of men and pre  and postmenopausal women.
+TH	drug	alcohol	17063152	Voluntary <b>ethanol</b> consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+TH	drug	cannabinoid	17063152	Voluntary ethanol consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, <b>cannabinoid</b> CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+TH	drug	opioid	17063152	Voluntary ethanol consumption altered mu <b>opioid</b> receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (<strong>TH</strong>) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+TH	drug	alcohol	17063152	Voluntary <b>ethanol</b> consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+TH	drug	cannabinoid	17063152	Voluntary ethanol consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, <b>cannabinoid</b> CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+TH	drug	opioid	17063152	Voluntary ethanol consumption altered mu <b>opioid</b> receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+TH	drug	alcohol	17063152	These results point to a role for the mu opioid receptor, <strong>TH</strong>, PENK, CRF, CB1 R, and 5 HTT genes in specific brain regions in the modulation of neuroadaptative mechanisms associated to the decrease of <b>ethanol</b> intake induced by <b>naltrexone</b>.
+TH	drug	opioid	17063152	These results point to a role for the mu <b>opioid</b> receptor, <strong>TH</strong>, PENK, CRF, CB1 R, and 5 HTT genes in specific brain regions in the modulation of neuroadaptative mechanisms associated to the decrease of ethanol intake induced by naltrexone.
+TH	drug	alcohol	16938628	We found that chronic <b>alcohol</b> did not alter the number of <strong>TH</strong> im terminals in the extended amygdala in either the C Alc or RD Alc drinking paradigms.
+TH	drug	benzodiazepine	16824587	By using a transgenic mouse model carrying the murine Y(1)R gene promoter fused to the lacZ reporter gene (Y(1)R/LacZ mice), we showed that prolonged pharmacologically or physiologically induced changes in the cerebrocortical concentrations of the neuroactive steroids 3alpha hydroxy 5alpha pregnan  20 one (3alpha,5alpha <strong>TH</strong> PROG) and tetrahydrodeoxycorticosterone (3alpha,5alpha <strong>TH</strong> DOC) increases Y(1)R/LacZ transgene expression in the central and medial amygdala, an effect similar to that induced by long term treatment with positive modulators of the GABA(A) receptor complex (<b>diazepam</b> or abecarnil).
+TH	drug	alcohol	16824587	We also demonstrated that fluctuations in the cerebrocortical concentrations of 3alpha,5alpha <strong>TH</strong> PROG and 3alpha,5alpha <strong>TH</strong> DOC during voluntary <b>ethanol</b> consumption and <b>ethanol</b> withdrawal induces a marked increase in Y(1)R gene expression that becomes apparent 48 h after withdrawal.
+TH	addiction	withdrawal	16824587	We also demonstrated that fluctuations in the cerebrocortical concentrations of 3alpha,5alpha <strong>TH</strong> PROG and 3alpha,5alpha <strong>TH</strong> DOC during voluntary ethanol consumption and ethanol <b>withdrawal</b> induces a marked increase in Y(1)R gene expression that becomes apparent 48 h after <b>withdrawal</b>.
+TH	drug	amphetamine	16760923	Administration of <b>METH</b> (5 mg/kg x 3) to Swiss Webster mice decreased striatal tyrosine hydroxylase (<strong>TH</strong>) immunoreactive neurons and significantly increased glial fibrillary acidic protein (GFAP) expression, confirming the neurotoxic potential of <b>METH</b> in mice.
+TH	drug	amphetamine	16760923	Administration of <b>METH</b> (5 mg/kg x 3) to Swiss Webster mice decreased striatal <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactive neurons and significantly increased glial fibrillary acidic protein (GFAP) expression, confirming the neurotoxic potential of <b>METH</b> in mice.
+TH	drug	amphetamine	16733807	Complex I immunoreactivity was inhibited in both cocaine and <b>METH</b> treated mice, whereas tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity was decreased in <b>METH</b> treated mice and increased in cocaine treated mice.
+TH	drug	cocaine	16733807	Complex I immunoreactivity was inhibited in both <b>cocaine</b> and METH treated mice, whereas tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity was decreased in METH treated mice and increased in <b>cocaine</b> treated mice.
+TH	drug	amphetamine	16733807	Complex I immunoreactivity was inhibited in both cocaine and <b>METH</b> treated mice, whereas <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity was decreased in <b>METH</b> treated mice and increased in cocaine treated mice.
+TH	drug	cocaine	16733807	Complex I immunoreactivity was inhibited in both <b>cocaine</b> and METH treated mice, whereas <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity was decreased in METH treated mice and increased in <b>cocaine</b> treated mice.
+TH	addiction	dependence	16712807	Since incomplete reduction of <strong>TH</strong> levels in normal mice does not produce behavioral effects, <strong>TH</strong> siRNA experiments were carried out in DAT knockout animals that show increased <b>dependence</b> on newly synthesized dopamine.
+TH	drug	amphetamine	16622715	In this study, we examined the suitability of the immunohistochemical detection of tyrosine hydroxylase (<strong>TH</strong>), dopamine transporter (DAT), and vesicular monoamine transporter 2 (VMAT2) levels, and caspase 3 activation in the striatum to diagnose <b>METH</b> abuse.
+TH	drug	amphetamine	16622715	In this study, we examined the suitability of the immunohistochemical detection of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), dopamine transporter (DAT), and vesicular monoamine transporter 2 (VMAT2) levels, and caspase 3 activation in the striatum to diagnose <b>METH</b> abuse.
+TH	drug	amphetamine	16622715	Decreases in <strong>TH</strong> immunoreactivity in the nucleus accumbens and DAT in the nucleus accumbens and putamen were induced in <b>METH</b> users, whereas a significant difference of VMAT2 was not evident between <b>METH</b> and control groups.
+TH	drug	cocaine	16580740	The nucleus accumbens (NAc), a major termination site of dopaminergic neurons, is believed to be involved in behavioral sensitization and studies have demonstrated that the NAc shell can be split into five zones of analysis; the vertex, arch, cone, intermediate and ventrolateral zones [Todtenkopf MS, Stellar JR. Assessment of <strong>tyrosine hydroxylase</strong> immunoreactive innervation in five subregions of the nucleus accumbens shell in rats treated with repeated <b>cocaine</b>.
+TH	addiction	sensitization	16580740	The nucleus accumbens (NAc), a major termination site of dopaminergic neurons, is believed to be involved in behavioral <b>sensitization</b> and studies have demonstrated that the NAc shell can be split into five zones of analysis; the vertex, arch, cone, intermediate and ventrolateral zones [Todtenkopf MS, Stellar JR. Assessment of <strong>tyrosine hydroxylase</strong> immunoreactive innervation in five subregions of the nucleus accumbens shell in rats treated with repeated cocaine.
+TH	drug	amphetamine	16555063	Effect of <b>methamphetamine</b> self administration on <strong>tyrosine hydroxylase</strong> and dopamine transporter levels in mesolimbic and nigrostriatal dopamine pathways of the rat.
+TH	drug	amphetamine	16555063	We studied the effect of <b>methamphetamine</b> self administration on two key regulators of dopamine transmission, tyrosine hydroxylase (<strong>TH</strong>), and dopamine transporter (DAT), in components of the mesolimbic and nigrostriatal dopamine pathways.
+TH	drug	amphetamine	16555063	We studied the effect of <b>methamphetamine</b> self administration on two key regulators of dopamine transmission, <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and dopamine transporter (DAT), in components of the mesolimbic and nigrostriatal dopamine pathways.
+TH	drug	amphetamine	16555063	<strong>TH</strong> mRNA and protein levels were increased in the ventral tegmental area (VTA, the cell body region of the mesolimbic dopamine system) and the substantia nigra pars compacta (SNC, the cell body region of the nigrostriatal dopamine system) after 1 day, but not 30 days, of forced abstinence from <b>methamphetamine</b>.
+TH	drug	amphetamine	16555063	In contrast, <b>methamphetamine</b> self administration had no effect on <strong>TH</strong> protein levels in dopaminergic terminals located in the nucleus accumbens and caudate putamen.
+TH	drug	opioid	16474935	Role of PKC in regulation of Fos and <strong>TH</strong> expression after <b>naloxone</b> induced <b>morphine</b> withdrawal in the heart.
+TH	addiction	withdrawal	16474935	Role of PKC in regulation of Fos and <strong>TH</strong> expression after naloxone induced morphine <b>withdrawal</b> in the heart.
+TH	drug	opioid	16474935	The present study was designed to investigate the role of protein kinase C (PKC) in this process, by estimating whether pharmacological inhibition of PKC would attenuate <b>morphine</b> withdrawal induced Fos expression and changes in tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity levels and NA turnover in the left and right ventricle.
+TH	addiction	withdrawal	16474935	The present study was designed to investigate the role of protein kinase C (PKC) in this process, by estimating whether pharmacological inhibition of PKC would attenuate morphine <b>withdrawal</b> induced Fos expression and changes in tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity levels and NA turnover in the left and right ventricle.
+TH	drug	opioid	16474935	The present study was designed to investigate the role of protein kinase C (PKC) in this process, by estimating whether pharmacological inhibition of PKC would attenuate <b>morphine</b> withdrawal induced Fos expression and changes in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity levels and NA turnover in the left and right ventricle.
+TH	addiction	withdrawal	16474935	The present study was designed to investigate the role of protein kinase C (PKC) in this process, by estimating whether pharmacological inhibition of PKC would attenuate morphine <b>withdrawal</b> induced Fos expression and changes in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity levels and NA turnover in the left and right ventricle.
+TH	drug	opioid	16474935	<b>Morphine</b> withdrawal induced Fos expression and increased <strong>TH</strong> levels and NA turnover in the right and left ventricle.
+TH	addiction	withdrawal	16474935	Morphine <b>withdrawal</b> induced Fos expression and increased <strong>TH</strong> levels and NA turnover in the right and left ventricle.
+TH	drug	opioid	16474935	Infusion of calphostin C, a selective PKC inhibitor, did not modify the <b>morphine</b> withdrawal induced increase in NA turnover and <strong>TH</strong> levels.
+TH	addiction	withdrawal	16474935	Infusion of calphostin C, a selective PKC inhibitor, did not modify the morphine <b>withdrawal</b> induced increase in NA turnover and <strong>TH</strong> levels.
+TH	drug	opioid	16474935	The results of the present study provide new information on the mechanisms that underlie <b>morphine</b> withdrawal induced up regulation of Fos expression in the heart and suggest that <strong>TH</strong> is not a target of PKC during <b>morphine</b> withdrawal at heart levels.
+TH	addiction	withdrawal	16474935	The results of the present study provide new information on the mechanisms that underlie morphine <b>withdrawal</b> induced up regulation of Fos expression in the heart and suggest that <strong>TH</strong> is not a target of PKC during morphine <b>withdrawal</b> at heart levels.
+TH	drug	nicotine	16344718	A study of TH01 and IGF2 INS <strong>TH</strong> haplotypes in relation to <b>smoking</b> initiation in three independent surveys.
+TH	drug	nicotine	16344718	Recent studies suggest an association between a microsatellite locus (TH01) located in intron 1 of the tyrosine hydroxylase gene (<strong>TH</strong>) and <b>nicotine</b> dependence.
+TH	addiction	dependence	16344718	Recent studies suggest an association between a microsatellite locus (TH01) located in intron 1 of the tyrosine hydroxylase gene (<strong>TH</strong>) and nicotine <b>dependence</b>.
+TH	drug	nicotine	16344718	Recent studies suggest an association between a microsatellite locus (TH01) located in intron 1 of the <strong>tyrosine hydroxylase</strong> gene (<strong>TH</strong>) and <b>nicotine</b> dependence.
+TH	addiction	dependence	16344718	Recent studies suggest an association between a microsatellite locus (TH01) located in intron 1 of the <strong>tyrosine hydroxylase</strong> gene (<strong>TH</strong>) and nicotine <b>dependence</b>.
+TH	drug	nicotine	16344718	We aimed here to study whether both TH01 and haplotypes of the wider IGF2 INS <strong>TH</strong> region influence initiation of regular <b>smoking</b> in current <b>smokers</b>.
+TH	drug	nicotine	16344718	However, an IGF2 INS <strong>TH</strong> haplotype (*5) was found to be nominally associated with AFRS at younger ages in adult <b>smokers</b>.
+TH	drug	amphetamine	16338084	Compared with controls, <b>methamphetamine</b>+Tat treated animals showed extensive silver staining and loss of <strong>tyrosine hydroxylase</strong> immunoreactivity and protein levels in the ipsilateral striatum.
+TH	drug	opioid	16292327	Following repeated <b>heroin</b>, large PAG neurons and small RLi/ventral PAG cells (not periaqueductal neurons) were activated, since <strong>tyrosine hydroxylase</strong> was adaptively induced, without changes in protein kinase Aalpha.
+TH	drug	opioid	16190878	Role of PKC alpha,gamma isoforms in regulation of c Fos and <strong>TH</strong> expression after <b>naloxone</b> induced <b>morphine</b> withdrawal in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups.
+TH	addiction	withdrawal	16190878	Role of PKC alpha,gamma isoforms in regulation of c Fos and <strong>TH</strong> expression after naloxone induced morphine <b>withdrawal</b> in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups.
+TH	drug	opioid	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate <b>morphine</b> withdrawal induced c Fos expression and changes in tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+TH	addiction	withdrawal	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate morphine <b>withdrawal</b> induced c Fos expression and changes in tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+TH	drug	opioid	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate <b>morphine</b> withdrawal induced c Fos expression and changes in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+TH	addiction	withdrawal	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate morphine <b>withdrawal</b> induced c Fos expression and changes in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+TH	drug	opioid	16190878	<strong>TH</strong> immunoreactivity was increased in the NTS/VLM after induction of <b>morphine</b> withdrawal, whereas there was a decrease in <strong>TH</strong> levels in the PVN.
+TH	addiction	withdrawal	16190878	<strong>TH</strong> immunoreactivity was increased in the NTS/VLM after induction of morphine <b>withdrawal</b>, whereas there was a decrease in <strong>TH</strong> levels in the PVN.
+TH	drug	opioid	16190878	Additionally, the changes in <strong>TH</strong> levels in the PVN and NTS/VLM were significantly modified by calphostin C. The present results suggest that activated PKC in the PVN and catecholaminergic brainstem cell groups may be critical for the activation of the hypothalamic pituitary adrenocortical axis in response to <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	16190878	Additionally, the changes in <strong>TH</strong> levels in the PVN and NTS/VLM were significantly modified by calphostin C. The present results suggest that activated PKC in the PVN and catecholaminergic brainstem cell groups may be critical for the activation of the hypothalamic pituitary adrenocortical axis in response to morphine <b>withdrawal</b>.
+TH	drug	amphetamine	16126238	Dopamine transporter, but not <strong>tyrosine hydroxylase</strong>, may be implicated in determining individual differences in behavioral sensitization to <b>amphetamine</b>.
+TH	addiction	sensitization	16126238	Dopamine transporter, but not <strong>tyrosine hydroxylase</strong>, may be implicated in determining individual differences in behavioral <b>sensitization</b> to amphetamine.
+TH	drug	amphetamine	16126238	<strong>Tyrosine hydroxylase</strong> mRNA in the VTA and SN was upregulated in both HR and LR rats pretreated with <b>amphetamine</b> when compared to HR and LR rats pretreated with saline.
+TH	drug	amphetamine	16126238	These results demonstrate the existence of individual differences in behavioral sensitization to <b>amphetamine</b> and suggest that dopamine transporter, but not <strong>tyrosine hydroxylase</strong>, may be a critical factor in the development and expression of behavioral sensitization to the locomotor activating effects of <b>amphetamine</b>.
+TH	addiction	sensitization	16126238	These results demonstrate the existence of individual differences in behavioral <b>sensitization</b> to amphetamine and suggest that dopamine transporter, but not <strong>tyrosine hydroxylase</strong>, may be a critical factor in the development and expression of behavioral <b>sensitization</b> to the locomotor activating effects of amphetamine.
+TH	drug	opioid	16081842	<b>Morphine</b> withdrawal contributes to <strong>Th</strong> cell differentiation by biasing cells toward the Th2 lineage.
+TH	addiction	withdrawal	16081842	Morphine <b>withdrawal</b> contributes to <strong>Th</strong> cell differentiation by biasing cells toward the Th2 lineage.
+TH	drug	opioid	16081842	In previous work, we have demonstrated that <b>morphine</b> treatment contributes to immunosuppression by polarizing <strong>Th</strong> cells toward the Th2 lineage.
+TH	drug	amphetamine	15985712	The remaining animals were additionally treated on the 34 <strong>th</strong> day (one day after the last D <b>amphetamine</b> injection) with 6 OHDA HBr (300 microg in 10 microl i.c.v., salt form, half in each lateral ventricle) or its vehicle.
+TH	drug	alcohol	15897221	We assessed mRNA levels of tyrosine hydroxylase (<strong>TH</strong>), a major regulatory enzyme in the dopamine synthesis and levels of dopamine and its metabolites after chronic <b>ethanol</b> administration with and without concomitant <b>naltrexone</b>.
+TH	drug	alcohol	15897221	We assessed mRNA levels of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), a major regulatory enzyme in the dopamine synthesis and levels of dopamine and its metabolites after chronic <b>ethanol</b> administration with and without concomitant <b>naltrexone</b>.
+TH	drug	alcohol	15897221	Chronic <b>ethanol</b> consumption increased <strong>TH</strong> mRNA levels in the VTA, but did not cause any significant change in the SN.
+TH	drug	alcohol	15897221	With <b>naltrexone</b> treatment, <b>ethanol</b> induced increase in the <strong>TH</strong> mRNA level was reduced in the VTA.
+TH	drug	alcohol	15851399	Erythrocyte thiamine (<strong>Th</strong>) esters: a major factor of the <b>alcohol</b> withdrawal syndrome or a candidate marker for <b>alcoholism</b> itself?
+TH	addiction	withdrawal	15851399	Erythrocyte thiamine (<strong>Th</strong>) esters: a major factor of the alcohol <b>withdrawal</b> syndrome or a candidate marker for alcoholism itself?
+TH	drug	alcohol	15851399	Thiamine (<strong>Th</strong>) deficiency is a major problem in <b>alcoholics</b>.
+TH	drug	alcohol	15851399	In this study, the relationship of <b>alcohol</b> withdrawal syndrome (AWS) to <strong>Th</strong> and its esters, as well as the diagnostic power of <strong>Th</strong> and its esters were investigated.
+TH	addiction	withdrawal	15851399	In this study, the relationship of alcohol <b>withdrawal</b> syndrome (AWS) to <strong>Th</strong> and its esters, as well as the diagnostic power of <strong>Th</strong> and its esters were investigated.
+TH	drug	alcohol	15851399	<strong>Th</strong> and its esters were assessed in a series of chronic <b>alcoholics</b> (and in controls) using an improved method.
+TH	drug	nicotine	15823687	We hypothesize that the illnesses associated with <b>smoking</b> may be partly attributable to autonomic dysfunction, sympathetic bias, and T helper (<strong>Th</strong>)2 inflammation induced by a paradoxical compensatory response to intermittent nicotinic exposure.
+TH	drug	amphetamine	15765258	In experiments 1 and 2 (examining the agonistic actions of terguride), preweanling rats were either given an escalating regimen of <b>amphetamine</b> to induce a state of <b>amphetamine</b> withdrawal or pretreated with the <strong>tyrosine hydroxylase</strong> inhibitor AMPT.
+TH	addiction	withdrawal	15765258	In experiments 1 and 2 (examining the agonistic actions of terguride), preweanling rats were either given an escalating regimen of amphetamine to induce a state of amphetamine <b>withdrawal</b> or pretreated with the <strong>tyrosine hydroxylase</strong> inhibitor AMPT.
+TH	drug	alcohol	15722952	<strong>Tyrosine hydroxylase</strong> Val 81 Met polymorphism associated with early onset <b>alcoholism</b>.
+TH	drug	alcohol	15722952	The present study examined the association of the <strong>Tyrosine hydroxylase</strong> Val 81 Met polymorphism with <b>alcohol</b> dependence.
+TH	addiction	dependence	15722952	The present study examined the association of the <strong>Tyrosine hydroxylase</strong> Val 81 Met polymorphism with alcohol <b>dependence</b>.
+TH	drug	alcohol	15722952	Our results suggest a role for <strong>tyrosine hydroxylase</strong> in early onset <b>alcoholism</b>.
+TH	drug	opioid	15663473	Involvement of 3',5' cyclic adenosine monophosphate dependent protein kinase in regulation of Fos expression and <strong>tyrosine hydroxylase</strong> levels during <b>morphine</b> withdrawal in the hypothalamic paraventricular nucleus and medulla oblongata catecholaminergic cell groups.
+TH	addiction	withdrawal	15663473	Involvement of 3',5' cyclic adenosine monophosphate dependent protein kinase in regulation of Fos expression and <strong>tyrosine hydroxylase</strong> levels during morphine <b>withdrawal</b> in the hypothalamic paraventricular nucleus and medulla oblongata catecholaminergic cell groups.
+TH	drug	opioid	15663473	We investigated whether cAMP dependent protein kinase (PKA) plays a role in this process by estimating changes in PKA immunoreactivity and the influence of inhibition of PKA on Fos protein expression and tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity levels in the PVN and NTS/VLM during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	15663473	We investigated whether cAMP dependent protein kinase (PKA) plays a role in this process by estimating changes in PKA immunoreactivity and the influence of inhibition of PKA on Fos protein expression and tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity levels in the PVN and NTS/VLM during morphine <b>withdrawal</b>.
+TH	drug	opioid	15663473	We investigated whether cAMP dependent protein kinase (PKA) plays a role in this process by estimating changes in PKA immunoreactivity and the influence of inhibition of PKA on Fos protein expression and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity levels in the PVN and NTS/VLM during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	15663473	We investigated whether cAMP dependent protein kinase (PKA) plays a role in this process by estimating changes in PKA immunoreactivity and the influence of inhibition of PKA on Fos protein expression and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity levels in the PVN and NTS/VLM during morphine <b>withdrawal</b>.
+TH	drug	opioid	15663473	<strong>TH</strong> immunoreactivity in NTS/VLM was increased 90 min after induction of <b>morphine</b> withdrawal, whereas there was a decrease in <strong>TH</strong> levels in the PVN at the same time point.
+TH	addiction	withdrawal	15663473	<strong>TH</strong> immunoreactivity in NTS/VLM was increased 90 min after induction of morphine <b>withdrawal</b>, whereas there was a decrease in <strong>TH</strong> levels in the PVN at the same time point.
+TH	drug	cocaine	15659224	Neuroadaptations of total levels of adenylate cyclase, protein kinase A, <strong>tyrosine hydroxylase</strong>, cdk5 and neurofilaments in the nucleus accumbens and ventral tegmental area do not correlate with expression of sensitized or tolerant locomotor responses to <b>cocaine</b>.
+TH	drug	nicotine	15631874	From the 9(<strong>th</strong>) to the 14(<strong>th</strong>) month, once a week a patch without <b>nicotine</b> and an oral placebo substituted <b>nicotine</b> and fluoxetine.
+TH	drug	opioid	15588731	Increase of <strong>tyrosine hydroxylase</strong> levels and activity during <b>morphine</b> withdrawal in the heart.
+TH	addiction	withdrawal	15588731	Increase of <strong>tyrosine hydroxylase</strong> levels and activity during morphine <b>withdrawal</b> in the heart.
+TH	drug	opioid	15588731	We studied the alterations in <strong>tyrosine hydroxylase</strong> (the rate limiting enzyme in catecholamines biosynthesis) and <strong>tyrosine hydroxylase</strong> activity in the heart (right and left ventricle) during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	15588731	We studied the alterations in <strong>tyrosine hydroxylase</strong> (the rate limiting enzyme in catecholamines biosynthesis) and <strong>tyrosine hydroxylase</strong> activity in the heart (right and left ventricle) during morphine <b>withdrawal</b>.
+TH	drug	opioid	15588731	The results show a significant increase in <strong>tyrosine hydroxylase</strong> levels and activity in the right and left ventricle 30 or 90 min after <b>naloxone</b> precipitated withdrawal in parallel with an increase in noradrenaline turnover.
+TH	addiction	withdrawal	15588731	The results show a significant increase in <strong>tyrosine hydroxylase</strong> levels and activity in the right and left ventricle 30 or 90 min after naloxone precipitated <b>withdrawal</b> in parallel with an increase in noradrenaline turnover.
+TH	drug	opioid	15588731	Our results suggest that an increase in <strong>tyrosine hydroxylase</strong> protein levels and <strong>tyrosine hydroxylase</strong> enzyme activity might contribute to the enhanced noradrenergic activity in the heart in response to <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	15588731	Our results suggest that an increase in <strong>tyrosine hydroxylase</strong> protein levels and <strong>tyrosine hydroxylase</strong> enzyme activity might contribute to the enhanced noradrenergic activity in the heart in response to morphine <b>withdrawal</b>.
+TH	drug	cannabinoid	15545023	These disturbances are likely originated by the capability of <b>cannabinoids</b> to influence the expression of key genes for both neurotransmitters, in particular, the enzyme <strong>tyrosine hydroxylase</strong> and the opioid precursor proenkephalin.
+TH	drug	opioid	15545023	These disturbances are likely originated by the capability of cannabinoids to influence the expression of key genes for both neurotransmitters, in particular, the enzyme <strong>tyrosine hydroxylase</strong> and the <b>opioid</b> precursor proenkephalin.
+TH	drug	amphetamine	15542715	Exposure to <b>METH</b> induces long term deficits in dopamine transporter (DAT) and tyrosine hydroxylase (<strong>TH</strong>) levels as well as induction of glial fibrillary acidic protein (GFAP) in the caudate putamen (CPu) and the nucleus accumbens (NAc).
+TH	drug	amphetamine	15542715	Exposure to <b>METH</b> induces long term deficits in dopamine transporter (DAT) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) levels as well as induction of glial fibrillary acidic protein (GFAP) in the caudate putamen (CPu) and the nucleus accumbens (NAc).
+TH	drug	amphetamine	15542715	Moreover, pretreatment with WIN 51,708 also prevented the reduction of <strong>TH</strong> levels induced by <b>METH</b> as well as the induction of GFAP in astrocytes.
+TH	drug	opioid	15541421	The induction of <strong>tyrosine hydroxylase</strong> after <b>morphine</b> exposure was also reduced in locus coeruleus when agmatine was administered along with <b>morphine</b>.
+TH	drug	nicotine	15521060	To explore further the relationship between the mesencephalic dopaminergic neurons and PFC GABAergic neurons, we investigated the effects of <b>nicotine</b> and passive exposure to cigarette smoke on the regulation of tyrosine hydroxylase (<strong>TH</strong>) in VTA and substantia nigra (SNC) and dopamine (DA) D1 receptor levels in nucleus accumbens (NAc) and caudate putamen (CPu).
+TH	drug	nicotine	15521060	To explore further the relationship between the mesencephalic dopaminergic neurons and PFC GABAergic neurons, we investigated the effects of <b>nicotine</b> and passive exposure to cigarette smoke on the regulation of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in VTA and substantia nigra (SNC) and dopamine (DA) D1 receptor levels in nucleus accumbens (NAc) and caudate putamen (CPu).
+TH	drug	nicotine	15521060	The results showed that chronic <b>nicotine</b> and <b>smoking</b> treatment differentially changed the levels of <strong>TH</strong> protein in VTA and SNC and DA D1 receptor levels in Nac and CPu.
+TH	drug	cocaine	15466321	Extinction training normalizes <strong>tyrosine hydroxylase</strong> levels in the nucleus accumbens (NAc) shell, an effect that could help ameliorate dysphoria and depression associated with withdrawal from chronic <b>cocaine</b> use.
+TH	addiction	withdrawal	15466321	Extinction training normalizes <strong>tyrosine hydroxylase</strong> levels in the nucleus accumbens (NAc) shell, an effect that could help ameliorate dysphoria and depression associated with <b>withdrawal</b> from chronic cocaine use.
+TH	drug	cocaine	15447670	Finally, phospho Ser31 <strong>TH</strong> levels were increased in dopaminergic neurons of rats trained to chronically self administer <b>cocaine</b>.
+TH	drug	cocaine	15447670	These results demonstrate direct and indirect regulation of the phosphorylation state of a Cdk5/ERK1/2 site on <strong>TH</strong> and suggest a role for these pathways in the neuroadaptive changes associated with chronic <b>cocaine</b> exposure.
+TH	drug	nicotine	15345197	We investigated the association of <b>smoking</b>, atopy and helper T (<strong>Th</strong>) cytokines with sensitization to methyltetrahydrophthalic anhydride (MTHPA) in occupationally exposed subjects.
+TH	addiction	sensitization	15345197	We investigated the association of smoking, atopy and helper T (<strong>Th</strong>) cytokines with <b>sensitization</b> to methyltetrahydrophthalic anhydride (MTHPA) in occupationally exposed subjects.
+TH	drug	alcohol	15240366	<strong>Tyrosine hydroxylase</strong> gene expression was elevated 80% to 90% by <b>alcohol</b> consumption in both experiments (P < 0.001) compared with adlib control rats.
+TH	drug	nicotine	15077008	<b>Nicotine</b> dependence in a prospective population based study of adolescents: the protective role of a functional <strong>tyrosine hydroxylase</strong> polymorphism.
+TH	addiction	dependence	15077008	Nicotine <b>dependence</b> in a prospective population based study of adolescents: the protective role of a functional <strong>tyrosine hydroxylase</strong> polymorphism.
+TH	addiction	reward	15077008	Dopamine is a key neurotransmitter of the mesolimbic <b>reward</b> pathway in the human brain, and tyrosine hydroxylase (<strong>TH</strong>) is the rate limiting enzyme in dopamine biosynthesis.
+TH	addiction	reward	15077008	Dopamine is a key neurotransmitter of the mesolimbic <b>reward</b> pathway in the human brain, and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) is the rate limiting enzyme in dopamine biosynthesis.
+TH	addiction	addiction	15077008	Consequently, the gene encoding <strong>TH</strong> is a strong candidate for involvement in the genetic component of <b>addiction</b>.
+TH	drug	nicotine	15077008	The importance of this gene in <b>nicotine</b> dependence is supported by many studies showing a link between <b>nicotine</b> administration and <strong>TH</strong> expression.
+TH	addiction	dependence	15077008	The importance of this gene in nicotine <b>dependence</b> is supported by many studies showing a link between nicotine administration and <strong>TH</strong> expression.
+TH	drug	nicotine	15077008	A functional tetranucleotide repeat polymorphism within intron 1 of the <strong>TH</strong> gene (HUMTH01 VNTR) has been shown to modify <b>tobacco</b> use in two independent Caucasian samples from the USA and Australia.
+TH	drug	nicotine	14739699	Association between dependent <b>smoking</b> and a polymorphism in the <strong>tyrosine hydroxylase</strong> gene in a prospective population based study of adolescent health.
+TH	drug	nicotine	14739699	This study reports pilot data on an association between <b>tobacco</b> dependence and a five allele tetranucleotide repeat polymorphism in the first intron of the tyrosine hydroxylase (<strong>TH</strong>) gene.
+TH	addiction	dependence	14739699	This study reports pilot data on an association between tobacco <b>dependence</b> and a five allele tetranucleotide repeat polymorphism in the first intron of the tyrosine hydroxylase (<strong>TH</strong>) gene.
+TH	drug	nicotine	14739699	This study reports pilot data on an association between <b>tobacco</b> dependence and a five allele tetranucleotide repeat polymorphism in the first intron of the <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene.
+TH	addiction	dependence	14739699	This study reports pilot data on an association between tobacco <b>dependence</b> and a five allele tetranucleotide repeat polymorphism in the first intron of the <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene.
+TH	drug	nicotine	14739699	These preliminary results replicate a previous association between <b>tobacco</b> use and the K4 allele of the <strong>TH</strong> gene (Lerman et al., 1997).
+TH	drug	nicotine	14739699	The potential significance of including time to first cigarette in definitions of <b>tobacco</b> dependence and the possible role that these <strong>TH</strong> variants might play in <b>tobacco</b> dependence are discussed.
+TH	addiction	dependence	14739699	The potential significance of including time to first cigarette in definitions of tobacco <b>dependence</b> and the possible role that these <strong>TH</strong> variants might play in tobacco <b>dependence</b> are discussed.
+TH	drug	nicotine	12932857	<b>Nicotine</b> and cotinine plasmatic concentration was quantified by the HPLC method, and degeneration of the nigrostriatal system was assessed by tyrosine hydroxylase (<strong>TH</strong>) immunohistochemistry.
+TH	drug	nicotine	12932857	<b>Nicotine</b> and cotinine plasmatic concentration was quantified by the HPLC method, and degeneration of the nigrostriatal system was assessed by <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunohistochemistry.
+TH	drug	opioid	12853567	Both c fos immunoreactivity, a marker of neuronal activity, and phosphorylation of <strong>tyrosine hydroxylase</strong> at Ser 40, a marker of cAMP levels, are decreased in the locus coeruleus by galnon treatment after <b>morphine</b> withdrawal, suggesting a possible molecular mechanism for the behavioral effects of galanin.
+TH	addiction	withdrawal	12853567	Both c fos immunoreactivity, a marker of neuronal activity, and phosphorylation of <strong>tyrosine hydroxylase</strong> at Ser 40, a marker of cAMP levels, are decreased in the locus coeruleus by galnon treatment after morphine <b>withdrawal</b>, suggesting a possible molecular mechanism for the behavioral effects of galanin.
+TH	drug	cannabinoid	12831997	The expression of central <b>cannabinoid</b> (CB1) receptors in tyrosine hydroxylase (<strong>TH</strong>) containing neurones was demonstrated.
+TH	drug	cannabinoid	12831997	The expression of central <b>cannabinoid</b> (CB1) receptors in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) containing neurones was demonstrated.
+TH	drug	cocaine	12787079	In the accumbens of <b>cocaine</b> trained rats, GluR1 and NMDAR1 levels were increased on days 1 and 90, while GluR2 levels were increased on days 1 and 30, but not day 90; PKA activity levels were increased on days 1 and 30, but not day 90, while AC activity, <strong>TH</strong> and cdk5 levels were unaltered.
+TH	drug	cocaine	12787079	In the VTA of <b>cocaine</b> trained rats, NMDAR1 levels were increased for up to 90 days, while GluR2 levels were increased only on day 1; <strong>TH</strong> and Cdk5 levels were increased only on day 1, while PKA and AC activity levels were unaltered.
+TH	drug	cannabinoid	12668119	Because T cells play a key role in the pathophysiology of allergic asthma by expressing T helper cell (<strong>Th</strong>)2 cytokines, the objective of the present studies was to examine the effect of <b>cannabinoids</b> on immunologic and pathologic features associated with the allergic airway response induced by ovalbumin (Ova).
+TH	drug	cannabinoid	12641731	Spontaneous <b>cannabinoid</b> withdrawal produced time related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (<strong>TH</strong>) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (PENK) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus.
+TH	addiction	withdrawal	12641731	Spontaneous cannabinoid <b>withdrawal</b> produced time related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (<strong>TH</strong>) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (PENK) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus.
+TH	drug	cannabinoid	12641731	Spontaneous <b>cannabinoid</b> withdrawal produced time related significant alterations in gene transcription: (i) decreased (20%) <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (PENK) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus.
+TH	addiction	withdrawal	12641731	Spontaneous cannabinoid <b>withdrawal</b> produced time related significant alterations in gene transcription: (i) decreased (20%) <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (PENK) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus.
+TH	drug	nicotine	12614343	<strong>TH</strong> levels increased in both the amygdala and prefrontal cortex, supporting the hypothesis that increased catecholaminergic tone contributes to <b>nicotine</b> reinforcement.
+TH	addiction	reward	12614343	<strong>TH</strong> levels increased in both the amygdala and prefrontal cortex, supporting the hypothesis that increased catecholaminergic tone contributes to nicotine <b>reinforcement</b>.
+TH	drug	opioid	12581178	We investigated the effects of chronic <b>morphine</b> administration and withdrawal on the morphological properties of immuno labelled <strong>tyrosine hydroxylase</strong> positive neurons of the rat ventrotegmental area with a confocal laser scanning microscope.
+TH	addiction	withdrawal	12581178	We investigated the effects of chronic morphine administration and <b>withdrawal</b> on the morphological properties of immuno labelled <strong>tyrosine hydroxylase</strong> positive neurons of the rat ventrotegmental area with a confocal laser scanning microscope.
+TH	drug	opioid	12581178	Morphological evaluation revealed a reduction in the area and perimeter of <strong>tyrosine hydroxylase</strong> positive somata in <b>morphine</b> withdrawn rats.
+TH	drug	opioid	12581178	Collectively, the present results indicate that withdrawal from a chronic <b>morphine</b> treatment, and not chronic <b>morphine</b> per se, modifies cellular morphology of <strong>tyrosine hydroxylase</strong> positive, presumably dopamine containing, neurons of the rat VTA.
+TH	addiction	withdrawal	12581178	Collectively, the present results indicate that <b>withdrawal</b> from a chronic morphine treatment, and not chronic morphine per se, modifies cellular morphology of <strong>tyrosine hydroxylase</strong> positive, presumably dopamine containing, neurons of the rat VTA.
+TH	drug	opioid	12534973	Regulation of <strong>tyrosine hydroxylase</strong> levels and activity and Fos expression during <b>opioid</b> withdrawal in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups innervating the PVN.
+TH	addiction	withdrawal	12534973	Regulation of <strong>tyrosine hydroxylase</strong> levels and activity and Fos expression during opioid <b>withdrawal</b> in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups innervating the PVN.
+TH	drug	opioid	12534973	We studied the alterations in tyrosine hydroxylase (<strong>TH</strong>; the rate limiting enzyme in catecholamines biosynthesis) immunoreactivity levels and <strong>TH</strong> enzyme activity in the rat NTS A2/VLM A1 noradrenergic cell groups and in the PVN during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	12534973	We studied the alterations in tyrosine hydroxylase (<strong>TH</strong>; the rate limiting enzyme in catecholamines biosynthesis) immunoreactivity levels and <strong>TH</strong> enzyme activity in the rat NTS A2/VLM A1 noradrenergic cell groups and in the PVN during morphine <b>withdrawal</b>.
+TH	drug	opioid	12534973	We studied the alterations in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>; the rate limiting enzyme in catecholamines biosynthesis) immunoreactivity levels and <strong>TH</strong> enzyme activity in the rat NTS A2/VLM A1 noradrenergic cell groups and in the PVN during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	12534973	We studied the alterations in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>; the rate limiting enzyme in catecholamines biosynthesis) immunoreactivity levels and <strong>TH</strong> enzyme activity in the rat NTS A2/VLM A1 noradrenergic cell groups and in the PVN during morphine <b>withdrawal</b>.
+TH	drug	opioid	12534973	<strong>TH</strong> and Fos immunoreactivity was determined by quantitative Western blot analysis, combined with immunostaining for <strong>TH</strong> and Fos for immunohistochemical identification of active neurons during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	12534973	<strong>TH</strong> and Fos immunoreactivity was determined by quantitative Western blot analysis, combined with immunostaining for <strong>TH</strong> and Fos for immunohistochemical identification of active neurons during morphine <b>withdrawal</b>.
+TH	drug	opioid	12534973	<strong>TH</strong> immunoreactivity in the NTS/VLM was increased 90 min after <b>morphine</b> withdrawal, whereas there was a decrease in <strong>TH</strong> levels in the PVN at the same time point.
+TH	addiction	withdrawal	12534973	<strong>TH</strong> immunoreactivity in the NTS/VLM was increased 90 min after morphine <b>withdrawal</b>, whereas there was a decrease in <strong>TH</strong> levels in the PVN at the same time point.
+TH	addiction	withdrawal	12534973	Following <b>withdrawal</b>, Fos immunoreactivity was present in most of the <strong>TH</strong> positive neurons of the A2 and A1 neurons.
+TH	drug	opioid	12534973	The present results suggest that an increase in <strong>TH</strong> protein levels and <strong>TH</strong> enzyme activity might contribute to the enhanced noradrenergic activity in the PVN in response to <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	12534973	The present results suggest that an increase in <strong>TH</strong> protein levels and <strong>TH</strong> enzyme activity might contribute to the enhanced noradrenergic activity in the PVN in response to morphine <b>withdrawal</b>.
+TH	drug	amphetamine	12468030	This <b>AMPH</b> paradigm affected fewer cortical regions, and caused smaller reduction in striatal tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity than previous 1 day <b>AMPH</b> regimens generating seizures or severe (above 40 degrees C) hyperthermia.
+TH	drug	amphetamine	12468030	This <b>AMPH</b> paradigm affected fewer cortical regions, and caused smaller reduction in striatal <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity than previous 1 day <b>AMPH</b> regimens generating seizures or severe (above 40 degrees C) hyperthermia.
+TH	drug	opioid	12399106	Orphanin FQ/nociceptin blocks chronic <b>morphine</b> induced <strong>tyrosine hydroxylase</strong> upregulation.
+TH	drug	opioid	12399106	One manifestation of the behavioral changes resulting from chronic use of <b>morphine</b> is the upregulation of tyrosine hydroxylase (<strong>TH</strong>, the rate limiting enzyme in catecholamine biosynthesis), which contributes to the dramatic increases in catecholamine release in the target regions of the locus coeruleus (LC) and the ventral tegmental area (VTA).
+TH	drug	opioid	12399106	One manifestation of the behavioral changes resulting from chronic use of <b>morphine</b> is the upregulation of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>, the rate limiting enzyme in catecholamine biosynthesis), which contributes to the dramatic increases in catecholamine release in the target regions of the locus coeruleus (LC) and the ventral tegmental area (VTA).
+TH	drug	opioid	12399106	The present study sought to determine the molecular mechanism(s) by which OFQ/N modulates the chronic actions of <b>morphine</b> by utilizing human neuroblastoma cell lines [BE(2) C and SH SY5Y] that endogenously express <strong>TH</strong>, and mu and ORL1 receptors.
+TH	drug	opioid	12399106	<b>Morphine</b> induced <strong>TH</strong> upregulation was blocked upon inclusion of a MEK 1 (mitogen activated protein kinase kinase 1) inhibitor (PD98059), confirming the role for ERKs in this adaptive response to <b>morphine</b>.
+TH	drug	opioid	12399106	Inclusion of OFQ/N during chronic <b>morphine</b> exposure also blocked <b>morphine</b> induced <strong>TH</strong> upregulation.
+TH	drug	opioid	12399106	Furthermore, chronic OFQ/N exposure increased levels of the <strong>TH</strong> gene repressor, Oct 2, irrespective of the presence or absence of <b>morphine</b>.
+TH	drug	cocaine	12394414	Effect of <b>cocaine</b> and sucrose withdrawal period on extinction behavior, cue induced reinstatement, and protein levels of the dopamine transporter and <strong>tyrosine hydroxylase</strong> in limbic and cortical areas in rats.
+TH	addiction	relapse	12394414	Effect of cocaine and sucrose withdrawal period on extinction behavior, cue induced <b>reinstatement</b>, and protein levels of the dopamine transporter and <strong>tyrosine hydroxylase</strong> in limbic and cortical areas in rats.
+TH	addiction	withdrawal	12394414	Effect of cocaine and sucrose <b>withdrawal</b> period on extinction behavior, cue induced reinstatement, and protein levels of the dopamine transporter and <strong>tyrosine hydroxylase</strong> in limbic and cortical areas in rats.
+TH	drug	cocaine	12394414	We also examined whether the time dependent changes in <b>cocaine</b> seeking correlate with the levels of the dopamine transporter (DAT) and tyrosine hydroxylase (<strong>TH</strong>) proteins in the amygdala, nucleus accumbens, prefrontal cortex and orbitofrontal cortex.
+TH	addiction	relapse	12394414	We also examined whether the time dependent changes in cocaine <b>seeking</b> correlate with the levels of the dopamine transporter (DAT) and tyrosine hydroxylase (<strong>TH</strong>) proteins in the amygdala, nucleus accumbens, prefrontal cortex and orbitofrontal cortex.
+TH	drug	cocaine	12394414	We also examined whether the time dependent changes in <b>cocaine</b> seeking correlate with the levels of the dopamine transporter (DAT) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) proteins in the amygdala, nucleus accumbens, prefrontal cortex and orbitofrontal cortex.
+TH	addiction	relapse	12394414	We also examined whether the time dependent changes in cocaine <b>seeking</b> correlate with the levels of the dopamine transporter (DAT) and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) proteins in the amygdala, nucleus accumbens, prefrontal cortex and orbitofrontal cortex.
+TH	drug	cocaine	12394414	The levels of DAT, but not <strong>TH</strong>, were greater in the prefrontal cortex of <b>cocaine</b> trained rats than in sucrose trained rats on both days 1 and 15 of withdrawal.
+TH	addiction	withdrawal	12394414	The levels of DAT, but not <strong>TH</strong>, were greater in the prefrontal cortex of cocaine trained rats than in sucrose trained rats on both days 1 and 15 of <b>withdrawal</b>.
+TH	drug	cocaine	12394414	The levels of DAT and <strong>TH</strong> in other brain areas were not altered following withdrawal from <b>cocaine</b> or sucrose self administration.
+TH	addiction	withdrawal	12394414	The levels of DAT and <strong>TH</strong> in other brain areas were not altered following <b>withdrawal</b> from cocaine or sucrose self administration.
+TH	addiction	relapse	12394414	These data suggest that the withdrawal can modulate reward <b>seeking</b> of both drug and non drug reinforcers, and that alterations in DAT and <strong>TH</strong> levels in the brain regions examined do not mediate this effect.
+TH	addiction	reward	12394414	These data suggest that the withdrawal can modulate <b>reward</b> seeking of both drug and non drug reinforcers, and that alterations in DAT and <strong>TH</strong> levels in the brain regions examined do not mediate this effect.
+TH	addiction	withdrawal	12394414	These data suggest that the <b>withdrawal</b> can modulate reward seeking of both drug and non drug reinforcers, and that alterations in DAT and <strong>TH</strong> levels in the brain regions examined do not mediate this effect.
+TH	drug	opioid	12358736	In the present study, Fos immunostaining was used as a reflection of neuronal activity and combined with immunostaining for tyrosine hydroxylase (<strong>TH</strong>) for immunohistochemical identification of active neurones during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	12358736	In the present study, Fos immunostaining was used as a reflection of neuronal activity and combined with immunostaining for tyrosine hydroxylase (<strong>TH</strong>) for immunohistochemical identification of active neurones during morphine <b>withdrawal</b>.
+TH	drug	opioid	12358736	In the present study, Fos immunostaining was used as a reflection of neuronal activity and combined with immunostaining for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) for immunohistochemical identification of active neurones during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	12358736	In the present study, Fos immunostaining was used as a reflection of neuronal activity and combined with immunostaining for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) for immunohistochemical identification of active neurones during morphine <b>withdrawal</b>.
+TH	addiction	withdrawal	12358736	Following <b>withdrawal</b>, Fos immunoreactivity was present in most of the <strong>TH</strong> positive neurones of the A2 and A1 neurones.
+TH	drug	amphetamine	12165394	The effect of crude water extracts (0.1 g/ml) of <strong>TH</strong> and SY on K(+) (20 mM) stimulated dopamine release from rat striatal slices were compared with <b>amphetamine</b> (10( 4) M) using high performance liquid chromatography with electrochemical detection to measure endogenous dopamine.
+TH	drug	amphetamine	12165394	<b>Amphetamine</b> and <strong>TH</strong>, but not SY, significantly increased K(+) stimulated dopamine release (P < 0.001) from rat striatal slices when compared with K(+) stimulated alone.
+TH	drug	amphetamine	12165394	<strong>TH</strong> potentiated the effect of <b>amphetamine</b> on K(+) stimulated dopamine release (P < 0.001) when compared with <b>amphetamine</b> alone.
+TH	drug	amphetamine	12165394	The results indicate that <strong>TH</strong> may stimulate dopamine release in the same manner as <b>amphetamine</b>.
+TH	drug	amphetamine	12105090	A high dose of <b>METH</b> given to mice and rats causes long lasting depletion of <strong>tyrosine hydroxylase</strong> activity, dopamine (DA), and DA transporter (DAT) binding sites in the striatum.
+TH	drug	opioid	12019333	Here we report that noradrenergic locus ceruleus (LC) neurons of mice with a conditional deletion of BDNF in postnatal brain respond to chronic <b>morphine</b> treatment with a paradoxical downregulation of cAMP mediated excitation and lack of dynamic regulation of <strong>TH</strong> expression.
+TH	drug	opioid	11979726	The heterozygous mice for the tyrosine hydroxylase (<strong>TH</strong>) gene and for the cyclic AMP (cAMP) response element binding protein (CREB) binding protein (CBP) gene showed the impairment of latent learning in the water finding task, and these mice did not develop <b>morphine</b> dependence.
+TH	addiction	dependence	11979726	The heterozygous mice for the tyrosine hydroxylase (<strong>TH</strong>) gene and for the cyclic AMP (cAMP) response element binding protein (CREB) binding protein (CBP) gene showed the impairment of latent learning in the water finding task, and these mice did not develop morphine <b>dependence</b>.
+TH	drug	opioid	11979726	The heterozygous mice for the <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene and for the cyclic AMP (cAMP) response element binding protein (CREB) binding protein (CBP) gene showed the impairment of latent learning in the water finding task, and these mice did not develop <b>morphine</b> dependence.
+TH	addiction	dependence	11979726	The heterozygous mice for the <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene and for the cyclic AMP (cAMP) response element binding protein (CREB) binding protein (CBP) gene showed the impairment of latent learning in the water finding task, and these mice did not develop morphine <b>dependence</b>.
+TH	drug	opioid	11976269	Fos production was also studied in brainstem regions that innervate hypothalamic nuclei: the nucleus of solitary tract (NTS   A2) and the ventrolateral medulla (VLM   A1) and combined with immunostaining for tyrosine hydroxylase (<strong>TH</strong>) for immunohistochemical identification of active neurons during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	11976269	Fos production was also studied in brainstem regions that innervate hypothalamic nuclei: the nucleus of solitary tract (NTS   A2) and the ventrolateral medulla (VLM   A1) and combined with immunostaining for tyrosine hydroxylase (<strong>TH</strong>) for immunohistochemical identification of active neurons during morphine <b>withdrawal</b>.
+TH	drug	opioid	11976269	Fos production was also studied in brainstem regions that innervate hypothalamic nuclei: the nucleus of solitary tract (NTS   A2) and the ventrolateral medulla (VLM   A1) and combined with immunostaining for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) for immunohistochemical identification of active neurons during <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	11976269	Fos production was also studied in brainstem regions that innervate hypothalamic nuclei: the nucleus of solitary tract (NTS   A2) and the ventrolateral medulla (VLM   A1) and combined with immunostaining for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) for immunohistochemical identification of active neurons during morphine <b>withdrawal</b>.
+TH	drug	alcohol	11750910	Reduced <strong>TH</strong> immunoreactive fibers in the limbic system of Sardinian <b>alcohol</b> preferring rats.
+TH	drug	alcohol	11744078	We discuss how GABAergic neurosteroids, including 3alpha,5alpha <strong>TH</strong> PROG and 3alpha,5alpha <strong>TH</strong> DOC, produced in response to systemic <b>ethanol</b> administration contribute to several of the effects of <b>ethanol</b> associated with modulation of GABA(A) receptors in rodents.
+TH	drug	alcohol	11744078	There is an essential correlation between the time course of <b>ethanol</b> induced 3alpha,5alpha <strong>TH</strong> PROG production in the brain and specific behavioral and neural effects of <b>ethanol</b>.
+TH	drug	alcohol	11744078	Furthermore, <b>ethanol</b> induction of 3alpha,5alpha <strong>TH</strong> PROG is diminished in tolerant and dependent animals.
+TH	drug	alcohol	11744078	Together, we suggest that 3alpha,5alpha <strong>TH</strong> PROG and 3alpha,5alpha <strong>TH</strong> DOC contribute to <b>ethanol</b> action and this interaction may represent a new mechanism of <b>ethanol</b> action.
+TH	drug	cocaine	11284443	Sensitization to the behavioural effects of <b>cocaine</b>: alterations in <strong>tyrosine hydroxylase</strong> or endogenous opioid mRNAs are not necessarily involved.
+TH	drug	opioid	11284443	Sensitization to the behavioural effects of cocaine: alterations in <strong>tyrosine hydroxylase</strong> or endogenous <b>opioid</b> mRNAs are not necessarily involved.
+TH	addiction	sensitization	11284443	<b>Sensitization</b> to the behavioural effects of cocaine: alterations in <strong>tyrosine hydroxylase</strong> or endogenous opioid mRNAs are not necessarily involved.
+TH	drug	cocaine	11284443	The mRNA for tyrosine hydroxylase (<strong>TH</strong>) in substantia nigra + ventral tegmental area was significantly elevated to about 140% of saline controls both in the "repeated <b>cocaine</b>" and the "acute <b>cocaine</b>" group as compared with the "saline group".
+TH	drug	cocaine	11284443	The mRNA for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in substantia nigra + ventral tegmental area was significantly elevated to about 140% of saline controls both in the "repeated <b>cocaine</b>" and the "acute <b>cocaine</b>" group as compared with the "saline group".
+TH	drug	cocaine	11264329	Extinction training regulates <strong>tyrosine hydroxylase</strong> during withdrawal from <b>cocaine</b> self administration.
+TH	addiction	withdrawal	11264329	Extinction training regulates <strong>tyrosine hydroxylase</strong> during <b>withdrawal</b> from cocaine self administration.
+TH	drug	cocaine	11264329	In this study, 12 d of <b>cocaine</b> self administration in rats (4 hr/d) reduced <strong>TH</strong> immunoreactivity by 29% in the nucleus accumbens (NAc) shell, but not core, after a 1 week withdrawal period.
+TH	addiction	withdrawal	11264329	In this study, 12 d of cocaine self administration in rats (4 hr/d) reduced <strong>TH</strong> immunoreactivity by 29% in the nucleus accumbens (NAc) shell, but not core, after a 1 week <b>withdrawal</b> period.
+TH	addiction	withdrawal	11264329	In contrast, <strong>TH</strong> immunoreactivity in the NAc was completely restored in animals that experienced extinction training (4 hr/d) during the same <b>withdrawal</b> period.
+TH	drug	cocaine	11264329	Extinction training also increased <strong>TH</strong> levels in the ventral tegmental area (VTA) by 45%, whereas <strong>TH</strong> was not altered in the VTA by <b>cocaine</b> withdrawal alone.
+TH	addiction	withdrawal	11264329	Extinction training also increased <strong>TH</strong> levels in the ventral tegmental area (VTA) by 45%, whereas <strong>TH</strong> was not altered in the VTA by cocaine <b>withdrawal</b> alone.
+TH	drug	cocaine	11264329	A similar extinction training regimen failed to alter <strong>TH</strong> levels in the NAc or VTA of rats trained to self administer sucrose pellets, indicating that <strong>TH</strong> regulation in <b>cocaine</b> trained animals is not a generalized effect of extinction learning per se.
+TH	drug	cocaine	11264329	The ability of extinction training to restore NAc <strong>TH</strong> levels is hypothesized to accelerate recovery from dopamine depletion and anhedonia during <b>cocaine</b> withdrawal.
+TH	addiction	withdrawal	11264329	The ability of extinction training to restore NAc <strong>TH</strong> levels is hypothesized to accelerate recovery from dopamine depletion and anhedonia during cocaine <b>withdrawal</b>.
+TH	drug	opioid	11233292	To investigate the involvement of catecholamines and/or the cyclic AMP (cAMP) systems in the development of drug dependence, we examined whether <b>morphine</b> dependence was developed in tyrosine hydroxylase (<strong>TH</strong>) heterozygous (<strong>TH</strong>+/ ) and cAMP response element binding protein (CREB) binding protein (CBP) heterozygous (CBP+/ ) mice.
+TH	addiction	dependence	11233292	To investigate the involvement of catecholamines and/or the cyclic AMP (cAMP) systems in the development of drug <b>dependence</b>, we examined whether morphine <b>dependence</b> was developed in tyrosine hydroxylase (<strong>TH</strong>) heterozygous (<strong>TH</strong>+/ ) and cAMP response element binding protein (CREB) binding protein (CBP) heterozygous (CBP+/ ) mice.
+TH	drug	opioid	11233292	To investigate the involvement of catecholamines and/or the cyclic AMP (cAMP) systems in the development of drug dependence, we examined whether <b>morphine</b> dependence was developed in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) heterozygous (<strong>TH</strong>+/ ) and cAMP response element binding protein (CREB) binding protein (CBP) heterozygous (CBP+/ ) mice.
+TH	addiction	dependence	11233292	To investigate the involvement of catecholamines and/or the cyclic AMP (cAMP) systems in the development of drug <b>dependence</b>, we examined whether morphine <b>dependence</b> was developed in <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) heterozygous (<strong>TH</strong>+/ ) and cAMP response element binding protein (CREB) binding protein (CBP) heterozygous (CBP+/ ) mice.
+TH	drug	opioid	11233292	In the <strong>TH</strong>+/  and CBP+/  mice, however, we could not find any <b>morphine</b> induced place preference.
+TH	drug	alcohol	11207375	Western blotting revealed a mean 20% decrease in <strong>tyrosine hydroxylase</strong> protein levels in the dorsal and ventral striatum of <b>alcohol</b> fed animals while dopamine transporter protein levels from the same animals were significantly increased compared to controls (mean 60% increase for the dorsal and ventral striatum).
+TH	drug	cocaine	11181904	Moreover, DA depletion resulting from administration of the <strong>tyrosine hydroxylase</strong> inhibitor alpha methyl p tyrosine had <b>cocaine</b> like effects.
+TH	drug	cannabinoid	11134671	These include genes encoding the dopamine D(3) and D(5) receptors, serotonin receptors, <strong>tyrosine hydroxylase</strong>, trytophan 2,3 dioxygenase, opioid receptors, and <b>cannabinoid</b> receptors.
+TH	drug	opioid	11134671	These include genes encoding the dopamine D(3) and D(5) receptors, serotonin receptors, <strong>tyrosine hydroxylase</strong>, trytophan 2,3 dioxygenase, <b>opioid</b> receptors, and cannabinoid receptors.
+TH	addiction	sensitization	11123184	The process of <b>sensitization</b> (development of IgE antibodies) is a complex process which involves interaction of antigen presenting cells and lymphocytes of the <strong>Th</strong> 2 cell type.
+TH	drug	amphetamine	11050146	Using the Borna disease rat, an animal model of viral induced encephalopathy wherein sensitivity to the locomotor and stereotypic behavioral effects of d <b>amphetamine</b> and cocaine is enhanced (Solbrig et al., 1994, 1998), we identify a specific neurotrophin expression pattern triggered by striatal viral injury that increases <strong>tyrosine hydroxylase</strong> activity, an early step in DA synthesis, to produce a phenotype of enhanced <b>amphetamine</b> sensitivity.
+TH	drug	cocaine	11050146	Using the Borna disease rat, an animal model of viral induced encephalopathy wherein sensitivity to the locomotor and stereotypic behavioral effects of d amphetamine and <b>cocaine</b> is enhanced (Solbrig et al., 1994, 1998), we identify a specific neurotrophin expression pattern triggered by striatal viral injury that increases <strong>tyrosine hydroxylase</strong> activity, an early step in DA synthesis, to produce a phenotype of enhanced amphetamine sensitivity.
+TH	drug	cocaine	11020229	Assessment of <strong>tyrosine hydroxylase</strong> immunoreactive innervation in five subregions of the nucleus accumbens shell in rats treated with repeated <b>cocaine</b>.
+TH	drug	cocaine	11020229	To explore the effects of behavioral sensitization on the anatomy of the nucleus accumbens shell, we employed a typical <b>cocaine</b> dosing paradigm and assessed <strong>tyrosine hydroxylase</strong> immunoreactive varicosities in five different areas of the shell, as well as the core of the nucleus accumbens.
+TH	addiction	sensitization	11020229	To explore the effects of behavioral <b>sensitization</b> on the anatomy of the nucleus accumbens shell, we employed a typical cocaine dosing paradigm and assessed <strong>tyrosine hydroxylase</strong> immunoreactive varicosities in five different areas of the shell, as well as the core of the nucleus accumbens.
+TH	drug	cocaine	11020229	Compared to saline controls, the <b>cocaine</b> treated animals showed a significant augmentation in <strong>tyrosine hydroxylase</strong> immunoreactivity in two of the five subregions after 2 days of withdrawal in the shell, but not in the core.
+TH	addiction	withdrawal	11020229	Compared to saline controls, the cocaine treated animals showed a significant augmentation in <strong>tyrosine hydroxylase</strong> immunoreactivity in two of the five subregions after 2 days of <b>withdrawal</b> in the shell, but not in the core.
+TH	addiction	sensitization	11020229	These data are the first to suggest that increases in nucleus accumbens presynaptic <strong>tyrosine hydroxylase</strong> may play a role in the development of behavioral <b>sensitization</b>, but not in the long term expression of this phenomenon.
+TH	addiction	sensitization	10931782	The tendency to develop specific IgE antibodies to allergens (<b>sensitization</b>) is associated with and may be preceded by the development of a T helper (<strong>Th</strong>)2 profile of cytokine release.
+TH	drug	cocaine	10922520	Repeated <b>cocaine</b> treatment alters <strong>tyrosine hydroxylase</strong> in the rat nucleus accumbens.
+TH	drug	cocaine	10922520	To determine whether repeated exposure of <b>cocaine</b> affects the dopaminergic innervation of the nucleus accumbens, we employed a typical <b>cocaine</b> dosing regimen in adult male Sprague Dawley rats followed by an immunocytochemical analysis of tyrosine hydroxylase (<strong>TH</strong>).
+TH	drug	cocaine	10922520	To determine whether repeated exposure of <b>cocaine</b> affects the dopaminergic innervation of the nucleus accumbens, we employed a typical <b>cocaine</b> dosing regimen in adult male Sprague Dawley rats followed by an immunocytochemical analysis of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>).
+TH	addiction	withdrawal	10922520	After 2 or 14 days of <b>withdrawal</b>, sections of the nucleus accumbens (NAc) were processed for <strong>tyrosine hydroxylase</strong> and the number of immunoreactive varicosities in the core and shell were quantified.
+TH	drug	opioid	10863042	Before inclusion, all the patients had their pain controlled by daily intrathecal (I <strong>Th</strong>) <b>morphine</b> administration.
+TH	drug	opioid	10863042	The main evaluation criteria of analgesic activity of the chromaffin cell allograft was the complementary requirement of analgesics and in particular the consumption of I <strong>Th</strong> <b>morphine</b> required to maintain effective pain control.
+TH	drug	opioid	10863042	Out of the 12 patients who profited from enhanced analgesia with long term follow up (average 4.5 months), five no longer required the I <strong>Th</strong> <b>morphine</b> (with prolonged interruption of systemic <b>opioids</b> as well), two durably decreased I <strong>Th</strong> <b>morphine</b> intake and five were stabilized until the end of their follow up.
+TH	drug	opioid	10708732	Double in situ hybridization analysis revealed that in the locus coeruleus most of the <strong>tyrosine hydroxylase</strong> mRNA positive neurons expressed mu <b>opioid</b> receptor mRNA and more than half of these neurons were positive for prostanoid EP(3) receptor mRNA.
+TH	drug	opioid	10528105	The peptidic <b>opioid</b> delta(1) agonist [D Pen(2),D Pen(5)]enkephalin (DPDPE) or delta(2) agonist [D Ala(2),Glu(4)]deltorphin (DELT) were given into the rostral ventral medulla (RVM), intrathecally (i.<strong>th</strong>.)
+TH	drug	alcohol	10490712	To determine the role of genes in the chromosomal regions 11p15 and 4p12 in the development of <b>alcohol</b> dependence, a sample of <b>alcoholics</b> (n = 133) and normal controls (n = 89) were screened using polymorphisms in the dopamine D4 receptor (DRD4), tyrosine hydroxylase (<strong>TH</strong>), and GABA receptor beta1 (GABRbeta1) genes.
+TH	addiction	dependence	10490712	To determine the role of genes in the chromosomal regions 11p15 and 4p12 in the development of alcohol <b>dependence</b>, a sample of alcoholics (n = 133) and normal controls (n = 89) were screened using polymorphisms in the dopamine D4 receptor (DRD4), tyrosine hydroxylase (<strong>TH</strong>), and GABA receptor beta1 (GABRbeta1) genes.
+TH	drug	alcohol	10490712	To determine the role of genes in the chromosomal regions 11p15 and 4p12 in the development of <b>alcohol</b> dependence, a sample of <b>alcoholics</b> (n = 133) and normal controls (n = 89) were screened using polymorphisms in the dopamine D4 receptor (DRD4), <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and GABA receptor beta1 (GABRbeta1) genes.
+TH	addiction	dependence	10490712	To determine the role of genes in the chromosomal regions 11p15 and 4p12 in the development of alcohol <b>dependence</b>, a sample of alcoholics (n = 133) and normal controls (n = 89) were screened using polymorphisms in the dopamine D4 receptor (DRD4), <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and GABA receptor beta1 (GABRbeta1) genes.
+TH	drug	alcohol	10490712	The allele distributions of the polymorphisms in the DRD4 and <strong>TH</strong> genes in <b>alcoholics</b> and normal controls were similar and their differences were not significant.
+TH	drug	alcohol	10490712	Results with <strong>TH</strong> and DRD4 genes indicate that these two genes may not play major roles in the development of <b>alcoholism</b>.
+TH	drug	alcohol	10470972	Chronic <b>alcoholism</b> is associated with an imbalanced production of <strong>Th</strong> 1/<strong>Th</strong> 2 cytokines by peripheral blood T cells.
+TH	addiction	withdrawal	10470972	After a <b>withdrawal</b> period of > or =1 yr, ALC patients did not show significant changes in the cytoplasmic expression of <strong>Th</strong> 1 associated cytokines compared with the control group; in contrast, these patients showed a marked increase on the proportion of CD4+ and CD8strong+ T cells expressing IL 4, a <strong>Th</strong> 2 associated cytokine (p<0.01).
+TH	drug	alcohol	10470972	Our results showed that in patients with chronic <b>alcoholism</b>, active EtOH intake is associated with a <strong>Th</strong> 1 pattern of cytokine production by PB T cells.
+TH	drug	opioid	10422661	Piroxicam, NS 398, <b>morphine</b> and vehicle (90% DMSO) were without significant antiallodynic effect when administered alone, but moderate antiallodynic effects were produced by i.<strong>th</strong>.
+TH	drug	opioid	10422661	Finally, <b>morphine</b>, but not ketorolac, given i.<strong>th</strong>.
+TH	addiction	sensitization	10336516	ALE 0540 given i.<strong>th</strong>., at doses of 30 and 60 microgram, also blocked tactile allodynia in the thermal <b>sensitization</b> model.
+TH	addiction	aversion	9819806	and alpha methyl rho tyrosine (AMPT; 100 mg/kg), a <strong>tyrosine hydroxylase</strong> inhibitor, did not affect the <b>aversive</b> effect of PCP.
+TH	drug	alcohol	9754624	Systematic search for variations in the <strong>tyrosine hydroxylase</strong> gene and their associations with schizophrenia, affective disorders, and <b>alcoholism</b>.
+TH	drug	alcohol	9754624	To find variants in the tyrosine hydroxylase (<strong>TH</strong>) gene that are associated with schizophrenia, mood disorders, or <b>alcohol</b> dependence, all of the exons, the exon intron boundaries, and the 5' promoter region of the <strong>TH</strong> gene were systematically screened for variants by single strand conformation polymorphism analysis followed by direct nucleotide sequencing.
+TH	addiction	dependence	9754624	To find variants in the tyrosine hydroxylase (<strong>TH</strong>) gene that are associated with schizophrenia, mood disorders, or alcohol <b>dependence</b>, all of the exons, the exon intron boundaries, and the 5' promoter region of the <strong>TH</strong> gene were systematically screened for variants by single strand conformation polymorphism analysis followed by direct nucleotide sequencing.
+TH	drug	alcohol	9754624	To find variants in the <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene that are associated with schizophrenia, mood disorders, or <b>alcohol</b> dependence, all of the exons, the exon intron boundaries, and the 5' promoter region of the <strong>TH</strong> gene were systematically screened for variants by single strand conformation polymorphism analysis followed by direct nucleotide sequencing.
+TH	addiction	dependence	9754624	To find variants in the <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene that are associated with schizophrenia, mood disorders, or alcohol <b>dependence</b>, all of the exons, the exon intron boundaries, and the 5' promoter region of the <strong>TH</strong> gene were systematically screened for variants by single strand conformation polymorphism analysis followed by direct nucleotide sequencing.
+TH	drug	alcohol	9754624	Our study indicates that the <strong>TH</strong> gene is not likely to play a major role in the genetic predisposition to schizophrenia, mood disorders, or <b>alcohol</b> dependence.
+TH	addiction	dependence	9754624	Our study indicates that the <strong>TH</strong> gene is not likely to play a major role in the genetic predisposition to schizophrenia, mood disorders, or alcohol <b>dependence</b>.
+TH	drug	opioid	26735118	Fos like immunoreactivity in <strong>tyrosine hydroxylase</strong> and substance P like immunoreactive neurones in guinea pig brain following intracerebroventricular injection of <b>morphine</b> and U50,488H.
+TH	drug	opioid	26735118	In the present study twocolour immunohistochemistry was used to investigate whether Fos protein was induced in dopaminergic (<strong>tyrosine hydroxylase</strong>) and substance P containing neurones of guinea pig brain following intracerebroventricular administration of the predominantly mu receptor agonist, <b>morphine</b>, and the kappa receptor agonist, U50,488H, which have been reported to produce rewarding and aversive effects, respectively.
+TH	addiction	aversion	26735118	In the present study twocolour immunohistochemistry was used to investigate whether Fos protein was induced in dopaminergic (<strong>tyrosine hydroxylase</strong>) and substance P containing neurones of guinea pig brain following intracerebroventricular administration of the predominantly mu receptor agonist, morphine, and the kappa receptor agonist, U50,488H, which have been reported to produce rewarding and <b>aversive</b> effects, respectively.
+TH	drug	opioid	26735118	The present study has shown that of the large number of neurones showing Fos like immunoreactivity following a single injection of <b>morphine</b> or U50,488H, few were <strong>tyrosine hydroxylase</strong> positive (dopaminergic) but a larger number were substance Plike immunoreactive.
+TH	drug	nicotine	9695129	Since we have proposed that interactions between mediobasohypothalamic (MBH) dopaminergic and beta endorphinergic mechanisms have a key role in neuroendocrine integration, we investigated the effects of chronic <b>nicotine</b> treatment and withdrawal on: (1) MBH concentrations of proopiomelanocortin (POMC, precursor for beta endorphin biosynthesis) mRNA; (2) MBH concentrations of tyrosine hydroxylase (<strong>TH</strong>, rate limiting enzyme in catecholamine biosynthesis) mRNA; (3) corresponding serum prolacin, corticosterone, luteinizing hormone (LH), and testosterone concentrations.
+TH	addiction	withdrawal	9695129	Since we have proposed that interactions between mediobasohypothalamic (MBH) dopaminergic and beta endorphinergic mechanisms have a key role in neuroendocrine integration, we investigated the effects of chronic nicotine treatment and <b>withdrawal</b> on: (1) MBH concentrations of proopiomelanocortin (POMC, precursor for beta endorphin biosynthesis) mRNA; (2) MBH concentrations of tyrosine hydroxylase (<strong>TH</strong>, rate limiting enzyme in catecholamine biosynthesis) mRNA; (3) corresponding serum prolacin, corticosterone, luteinizing hormone (LH), and testosterone concentrations.
+TH	drug	nicotine	9695129	Since we have proposed that interactions between mediobasohypothalamic (MBH) dopaminergic and beta endorphinergic mechanisms have a key role in neuroendocrine integration, we investigated the effects of chronic <b>nicotine</b> treatment and withdrawal on: (1) MBH concentrations of proopiomelanocortin (POMC, precursor for beta endorphin biosynthesis) mRNA; (2) MBH concentrations of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>, rate limiting enzyme in catecholamine biosynthesis) mRNA; (3) corresponding serum prolacin, corticosterone, luteinizing hormone (LH), and testosterone concentrations.
+TH	addiction	withdrawal	9695129	Since we have proposed that interactions between mediobasohypothalamic (MBH) dopaminergic and beta endorphinergic mechanisms have a key role in neuroendocrine integration, we investigated the effects of chronic nicotine treatment and <b>withdrawal</b> on: (1) MBH concentrations of proopiomelanocortin (POMC, precursor for beta endorphin biosynthesis) mRNA; (2) MBH concentrations of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>, rate limiting enzyme in catecholamine biosynthesis) mRNA; (3) corresponding serum prolacin, corticosterone, luteinizing hormone (LH), and testosterone concentrations.
+TH	drug	nicotine	9695129	Chronic daily <b>nicotine</b> administration induced significant changes in serum corticosterone, serum prolactin, MBH <strong>TH</strong> mRNA, and MBH POMC mRNA concentrations that tended to persist through day 3 of withdrawal; serum prolactin and MBH POMC mRNA concentrations were suppressed whereas serum corticosterone and MBH <strong>TH</strong> mRNA concentrations were stimulated.
+TH	addiction	withdrawal	9695129	Chronic daily nicotine administration induced significant changes in serum corticosterone, serum prolactin, MBH <strong>TH</strong> mRNA, and MBH POMC mRNA concentrations that tended to persist through day 3 of <b>withdrawal</b>; serum prolactin and MBH POMC mRNA concentrations were suppressed whereas serum corticosterone and MBH <strong>TH</strong> mRNA concentrations were stimulated.
+TH	drug	alcohol	9564682	Possible allelic association of a <strong>tyrosine hydroxylase</strong> polymorphism with vulnerability to <b>alcohol</b> withdrawal delirium.
+TH	addiction	withdrawal	9564682	Possible allelic association of a <strong>tyrosine hydroxylase</strong> polymorphism with vulnerability to alcohol <b>withdrawal</b> delirium.
+TH	drug	alcohol	9564682	The genotype of the <strong>TH</strong> tetranucleotide polymorphism was assessed in 204 German controls and 311 German <b>alcohol</b> dependent subjects, including 63 <b>alcoholics</b> with a history of visual hallucinations during withdrawal delirium.
+TH	addiction	withdrawal	9564682	The genotype of the <strong>TH</strong> tetranucleotide polymorphism was assessed in 204 German controls and 311 German alcohol dependent subjects, including 63 alcoholics with a history of visual hallucinations during <b>withdrawal</b> delirium.
+TH	drug	alcohol	9564682	The possible allelic association suggests that allelic variation at the <strong>TH</strong> locus mediates vulnerability to <b>alcohol</b> withdrawal delirium in a small proportion of <b>alcohol</b> dependent subjects.
+TH	addiction	withdrawal	9564682	The possible allelic association suggests that allelic variation at the <strong>TH</strong> locus mediates vulnerability to alcohol <b>withdrawal</b> delirium in a small proportion of alcohol dependent subjects.
+TH	drug	opioid	9608348	In the first study, <b>methadone</b> maintenance patients were randomly assigned to one of two 8 week baseline take home (<strong>TH</strong>) conditions differing in frequency of clinic visits per week.
+TH	drug	cocaine	9608348	In the second study, fluoxetine (0 , 20 , 40 mg) <strong>TH</strong> doses were similarly contingent in treatment of <b>cocaine</b> dependence.
+TH	addiction	dependence	9608348	In the second study, fluoxetine (0 , 20 , 40 mg) <strong>TH</strong> doses were similarly contingent in treatment of cocaine <b>dependence</b>.
+TH	drug	amphetamine	9495865	<b>Methamphetamine</b> (<b>METH</b>) is a powerful psychostimulant that produces dopaminergic neurotoxicity manifested by a decrease in the levels of dopamine, <strong>tyrosine hydroxylase</strong> activity and dopamine transporter (DAT) binding sites in the nigrostriatal system.
+TH	drug	amphetamine	9440865	In contrast, many more <strong>TH</strong>+ cells typically survived transplantation in the recipients of graft tissue derived from the youngest donors and <b>amphetamine</b> induced rotation was significantly reduced in this group alone.
+TH	drug	opioid	9416730	The identification of colocalization of glutamate with <strong>tyrosine hydroxylase</strong> in most locus ceruleus neurons suggests a role for cerulospinal glutamatergic neurotransmission in <b>fentanyl</b> induced muscular rigidity.
+TH	drug	nicotine	9396226	[Effect of <b>nicotine</b> administration on <strong>tyrosine hydroxylase</strong> containing neuron in the rat forebrain; immunohistochemical study with semiquantitative morphometric analysis].
+TH	drug	nicotine	9396226	We studied the effects of <b>nicotine</b> administration (5 mg/kg x 2/day, 7 days) on immunoreactivity for tyrosine hydroxylase (<strong>TH</strong>), the rate limiting enzyme of catecholamine synthesis, in the rat forebrain including the cerebral cortex, hippocampus, striatum and hypothalamus to investigate the influence on catecholaminergic neurons.
+TH	drug	nicotine	9396226	We studied the effects of <b>nicotine</b> administration (5 mg/kg x 2/day, 7 days) on immunoreactivity for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the rate limiting enzyme of catecholamine synthesis, in the rat forebrain including the cerebral cortex, hippocampus, striatum and hypothalamus to investigate the influence on catecholaminergic neurons.
+TH	drug	nicotine	9396226	In the <b>nicotine</b> administration group, both the number and intensity of <strong>TH</strong> immunoreactive fibers and terminals increased in the fronto parietal cortex, anterior cingulate cortex and hippocampus in comparison with those of the control group, and a significant difference was demonstrated by computer assisted morphometric analysis.
+TH	drug	opioid	9315909	The infusions also blocked the <b>morphine</b> induced upregulation of <strong>tyrosine hydroxylase</strong> but not of Gialpha, two other proteins induced in the LC by chronic <b>morphine</b> treatment.
+TH	drug	opioid	9284358	Following <b>morphine</b> withdrawal, Fos immunoreactivity was present in 39.2% and 19.8% of the <strong>tyrosine hydroxylase</strong> immunoreactive neurons of the A1/C1 and A2/C2 cell groups.
+TH	addiction	withdrawal	9284358	Following morphine <b>withdrawal</b>, Fos immunoreactivity was present in 39.2% and 19.8% of the <strong>tyrosine hydroxylase</strong> immunoreactive neurons of the A1/C1 and A2/C2 cell groups.
+TH	drug	cocaine	9232210	This study evaluated the effect of an acute reduction in catecholamine synthesis produced by alpha methyl para tyrosine (AMPT), a <strong>tyrosine hydroxylase</strong> inhibitor, on <b>cocaine</b> induced euphoria.
+TH	drug	alcohol	9303735	[Characteristics of <strong>tyrosine hydroxylase</strong> gene expression in the brain of rats with different <b>ethanol</b> consumption after chronic <b>alcoholic</b> intoxication].
+TH	addiction	intoxication	9303735	[Characteristics of <strong>tyrosine hydroxylase</strong> gene expression in the brain of rats with different ethanol consumption after chronic alcoholic <b>intoxication</b>].
+TH	drug	nicotine	9197282	<b>Nicotine</b> regulates mRNA level of <strong>tyrosine hydroxylase</strong> gene but not that of nicotinic acetylcholine receptor genes in PC12 cells.
+TH	drug	nicotine	9197282	To understand the molecular mechanism of <b>nicotine</b> addiction, we examined the mRNA level of the tyrosine hydroxylase (<strong>TH</strong>) gene and that of the nicotinic acetylcholine receptor (nAChR) genes by long term <b>nicotine</b> treatment.
+TH	addiction	addiction	9197282	To understand the molecular mechanism of nicotine <b>addiction</b>, we examined the mRNA level of the tyrosine hydroxylase (<strong>TH</strong>) gene and that of the nicotinic acetylcholine receptor (nAChR) genes by long term nicotine treatment.
+TH	drug	nicotine	9197282	To understand the molecular mechanism of <b>nicotine</b> addiction, we examined the mRNA level of the <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene and that of the nicotinic acetylcholine receptor (nAChR) genes by long term <b>nicotine</b> treatment.
+TH	addiction	addiction	9197282	To understand the molecular mechanism of nicotine <b>addiction</b>, we examined the mRNA level of the <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) gene and that of the nicotinic acetylcholine receptor (nAChR) genes by long term nicotine treatment.
+TH	drug	nicotine	9197282	However, the mRNA level of <strong>TH</strong> gene did not change by forskolin under long term <b>nicotine</b> treatment.
+TH	drug	nicotine	9197282	The <strong>TH</strong> gene may be regulated by a <b>nicotine</b> related signaling pathway, whereas alpha3, alpha5, alpha7, and beta4 nAChR genes may be further regulated by a protein kinase A (PKA) pathway under long term <b>nicotine</b> treatment.
+TH	drug	amphetamine	8923661	Contrasting effects of repeated treatment vs. withdrawal of <b>methamphetamine</b> on <strong>tyrosine hydroxylase</strong> messenger RNA levels in the ventral tegmental area and substantia nigra zona compacta of the rat brain.
+TH	addiction	withdrawal	8923661	Contrasting effects of repeated treatment vs. <b>withdrawal</b> of methamphetamine on <strong>tyrosine hydroxylase</strong> messenger RNA levels in the ventral tegmental area and substantia nigra zona compacta of the rat brain.
+TH	drug	amphetamine	8923661	We have assessed the effect of repeated treatment with <b>methamphetamine</b> (<b>METH</b>) on the abundance of the messenger ribonucleic acid molecules encoding the enzyme tyrosine hydroxylase (<strong>TH</strong>) and preprocholecystokinin (PPCCK) in the substantia nigra zona compacta (SNc) and the ventral tegmental area (VTA) by in situ hybridization histochemistry.
+TH	drug	amphetamine	8923661	We have assessed the effect of repeated treatment with <b>methamphetamine</b> (<b>METH</b>) on the abundance of the messenger ribonucleic acid molecules encoding the enzyme <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) and preprocholecystokinin (PPCCK) in the substantia nigra zona compacta (SNc) and the ventral tegmental area (VTA) by in situ hybridization histochemistry.
+TH	drug	amphetamine	8923661	<strong>TH</strong> mRNA in the VTA was unaffected by repeated <b>METH</b> treatment but was decreased 25% relative to controls in the SNc.
+TH	drug	amphetamine	8923661	Concurrent administration of <b>METH</b> and MK 801 decreased <strong>TH</strong> mRNA levels in the SNc to 47% relative to controls.
+TH	drug	amphetamine	8923661	In contrast, <strong>TH</strong> mRNA levels were found increased in the VTA (42%) but not SNc 15 days post <b>METH</b> treatment.
+TH	drug	amphetamine	8923661	Coadministration of MK 801 with <b>METH</b> prevented the increase in <strong>TH</strong> mRNA in the VTA.
+TH	drug	amphetamine	8923661	The results demonstrate that exposure to repeated <b>methamphetamine</b> elicits changes of <strong>TH</strong> mRNA levels in the VTA that become manifest 2 weeks after withdrawal from this psychostimulant drug.
+TH	addiction	withdrawal	8923661	The results demonstrate that exposure to repeated methamphetamine elicits changes of <strong>TH</strong> mRNA levels in the VTA that become manifest 2 weeks after <b>withdrawal</b> from this psychostimulant drug.
+TH	drug	amphetamine	8959049	Neurochemical analysis of the <strong>tyrosine hydroxylase</strong> expression in <b>methamphetamine</b> sensitized rats.
+TH	addiction	sensitization	8959049	To elucidate the expression of <strong>TH</strong> mRNA in MAP induced behavioral <b>sensitization</b>, rats were daily injected with MAP (5 mg/kg i.p.)
+TH	drug	amphetamine	8640565	We found reduced levels of three dopamine nerve terminal markers (dopamine, <strong>tyrosine hydroxylase</strong> and the dopamine transporter) in post mortem striatum (nucleus accumbens, caudate, putamen) of chronic <b>methamphetamine</b> users.
+TH	addiction	dependence	8613958	and i.<strong>th</strong>., as expected if modulation of mu* activity played a role in <b>dependence</b>.
+TH	drug	opioid	8613958	or i.<strong>th</strong>., indicating that CTAP competes with <b>naloxone</b> at mu*.
+TH	drug	benzodiazepine	8650291	According to WWO criteria the improvement index was significantly higher on the 3 rd and 7 <strong>th</strong> day in two groups whereas in one group <b>chlordiazepoxide</b> and nifedipine action was equal.
+TH	drug	nicotine	8593811	The present study in rats examined 1) the relationship between dose dependent expression of cFos in the PVN and that in the nucleus of the solitary tract (NTS) A2, NTS C2 and locus coeruleus (LC), after iv <b>nicotine</b> (0.045 0.18 mg/kg, administered at 0.09 mg/kg per min); 2) the dependence of PVN cFos expression on the effects of <b>nicotine</b> in brainstem, using the nicotinic cholinergic antagonist, mecamylamine, administered into the fourth ventricle; and 3) the extent of catecholaminergic involvement in the effect of <b>nicotine</b> on the PVN, measured by immunocytochemical double labeling for cFos and tyrosine hydroxylase (<strong>TH</strong>), the rate limiting enzyme in catecholamine synthesis.
+TH	addiction	dependence	8593811	The present study in rats examined 1) the relationship between dose dependent expression of cFos in the PVN and that in the nucleus of the solitary tract (NTS) A2, NTS C2 and locus coeruleus (LC), after iv nicotine (0.045 0.18 mg/kg, administered at 0.09 mg/kg per min); 2) the <b>dependence</b> of PVN cFos expression on the effects of nicotine in brainstem, using the nicotinic cholinergic antagonist, mecamylamine, administered into the fourth ventricle; and 3) the extent of catecholaminergic involvement in the effect of nicotine on the PVN, measured by immunocytochemical double labeling for cFos and tyrosine hydroxylase (<strong>TH</strong>), the rate limiting enzyme in catecholamine synthesis.
+TH	drug	nicotine	8593811	The present study in rats examined 1) the relationship between dose dependent expression of cFos in the PVN and that in the nucleus of the solitary tract (NTS) A2, NTS C2 and locus coeruleus (LC), after iv <b>nicotine</b> (0.045 0.18 mg/kg, administered at 0.09 mg/kg per min); 2) the dependence of PVN cFos expression on the effects of <b>nicotine</b> in brainstem, using the nicotinic cholinergic antagonist, mecamylamine, administered into the fourth ventricle; and 3) the extent of catecholaminergic involvement in the effect of <b>nicotine</b> on the PVN, measured by immunocytochemical double labeling for cFos and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the rate limiting enzyme in catecholamine synthesis.
+TH	addiction	dependence	8593811	The present study in rats examined 1) the relationship between dose dependent expression of cFos in the PVN and that in the nucleus of the solitary tract (NTS) A2, NTS C2 and locus coeruleus (LC), after iv nicotine (0.045 0.18 mg/kg, administered at 0.09 mg/kg per min); 2) the <b>dependence</b> of PVN cFos expression on the effects of nicotine in brainstem, using the nicotinic cholinergic antagonist, mecamylamine, administered into the fourth ventricle; and 3) the extent of catecholaminergic involvement in the effect of nicotine on the PVN, measured by immunocytochemical double labeling for cFos and <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the rate limiting enzyme in catecholamine synthesis.
+TH	drug	nicotine	8593811	<b>Nicotine</b> also elicited a dose dependent increase in cFos expression in the <strong>TH</strong>+ neurons of the NTS, with C2 more sensitive than A2.
+TH	drug	opioid	8869161	Tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity was increased (31 38%) in the VTA and decreased (11%) in the NAc of <b>heroin</b> exposed rats relative to controls.
+TH	drug	opioid	8869161	<strong>Tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity was increased (31 38%) in the VTA and decreased (11%) in the NAc of <b>heroin</b> exposed rats relative to controls.
+TH	drug	alcohol	8869159	Indeed, as seen for chronic morphine and cocaine treatments, we show here that chronic <b>ethanol</b> treatment increased levels of <strong>tyrosine hydroxylase</strong> and glial fibrillary acidic protein immunoreactivity, and decreases levels of neurofilament protein immunoreactivity, in the VTA.
+TH	drug	cocaine	8869159	Indeed, as seen for chronic morphine and <b>cocaine</b> treatments, we show here that chronic ethanol treatment increased levels of <strong>tyrosine hydroxylase</strong> and glial fibrillary acidic protein immunoreactivity, and decreases levels of neurofilament protein immunoreactivity, in the VTA.
+TH	drug	opioid	8869159	Indeed, as seen for chronic <b>morphine</b> and cocaine treatments, we show here that chronic ethanol treatment increased levels of <strong>tyrosine hydroxylase</strong> and glial fibrillary acidic protein immunoreactivity, and decreases levels of neurofilament protein immunoreactivity, in the VTA.
+TH	drug	cocaine	8545003	Previous research has shown an increase in <strong>tyrosine hydroxylase</strong> in the ventral tegmental area following chronic morphine and chronic <b>cocaine</b> treatments.
+TH	drug	opioid	8545003	Previous research has shown an increase in <strong>tyrosine hydroxylase</strong> in the ventral tegmental area following chronic <b>morphine</b> and chronic cocaine treatments.
+TH	drug	cocaine	8545003	Brain derived neurotrophic factor, which by itself tended to decrease <strong>tyrosine hydroxylase</strong> levels in the ventral tegmental area, prevented the characteristic increase in <strong>tyrosine hydroxylase</strong> following morphine and <b>cocaine</b> exposure and reversed the increase in rats pretreated with morphine.
+TH	drug	opioid	8545003	Brain derived neurotrophic factor, which by itself tended to decrease <strong>tyrosine hydroxylase</strong> levels in the ventral tegmental area, prevented the characteristic increase in <strong>tyrosine hydroxylase</strong> following <b>morphine</b> and cocaine exposure and reversed the increase in rats pretreated with <b>morphine</b>.
+TH	drug	cocaine	8545003	In contrast, ciliary neurotrophic factor infusions alone resulted in an increase in <strong>tyrosine hydroxylase</strong> levels, with no additional increase induced by morphine or <b>cocaine</b> coadministration.
+TH	drug	opioid	8545003	In contrast, ciliary neurotrophic factor infusions alone resulted in an increase in <strong>tyrosine hydroxylase</strong> levels, with no additional increase induced by <b>morphine</b> or cocaine coadministration.
+TH	drug	opioid	8545003	Nerve growth factor alone had no effect on <strong>tyrosine hydroxylase</strong> or glial fibrillary acidic protein levels and did not affect <b>morphine</b>'s ability to induce these proteins.
+TH	drug	cocaine	7675174	Strain selective effects of corticosterone on locomotor sensitization to <b>cocaine</b> and on levels of <strong>tyrosine hydroxylase</strong> and glucocorticoid receptor in the ventral tegmental area.
+TH	addiction	sensitization	7675174	Strain selective effects of corticosterone on locomotor <b>sensitization</b> to cocaine and on levels of <strong>tyrosine hydroxylase</strong> and glucocorticoid receptor in the ventral tegmental area.
+TH	drug	opioid	7540319	Lack of effect of chronic <b>morphine</b> treatment and <b>naloxone</b> precipitated withdrawal on <strong>tyrosine hydroxylase</strong>, galanin, and neuropeptide Y mRNA levels in the rat locus coeruleus.
+TH	addiction	withdrawal	7540319	Lack of effect of chronic morphine treatment and naloxone precipitated <b>withdrawal</b> on <strong>tyrosine hydroxylase</strong>, galanin, and neuropeptide Y mRNA levels in the rat locus coeruleus.
+TH	drug	opioid	7540319	Messenger RNA (mRNA) levels for tyrosine hydroxylase (<strong>TH</strong>), the rate limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and neuropeptide Y (NPY), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic <b>morphine</b> treatment or <b>naloxone</b> precipitated withdrawal.
+TH	addiction	withdrawal	7540319	Messenger RNA (mRNA) levels for tyrosine hydroxylase (<strong>TH</strong>), the rate limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and neuropeptide Y (NPY), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic morphine treatment or naloxone precipitated <b>withdrawal</b>.
+TH	drug	opioid	7540319	Messenger RNA (mRNA) levels for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the rate limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and neuropeptide Y (NPY), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic <b>morphine</b> treatment or <b>naloxone</b> precipitated withdrawal.
+TH	addiction	withdrawal	7540319	Messenger RNA (mRNA) levels for <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the rate limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and neuropeptide Y (NPY), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic morphine treatment or naloxone precipitated <b>withdrawal</b>.
+TH	drug	opioid	7540319	Although long term adaptations of LC neurons have previously been implicated in the development of <b>morphine</b> tolerance, dependence, and withdrawal, alterations in the levels of <strong>TH</strong>, GAL, or NPY mRNA in the LC apparently do not underlie this process.
+TH	addiction	dependence	7540319	Although long term adaptations of LC neurons have previously been implicated in the development of morphine tolerance, <b>dependence</b>, and withdrawal, alterations in the levels of <strong>TH</strong>, GAL, or NPY mRNA in the LC apparently do not underlie this process.
+TH	addiction	withdrawal	7540319	Although long term adaptations of LC neurons have previously been implicated in the development of morphine tolerance, dependence, and <b>withdrawal</b>, alterations in the levels of <strong>TH</strong>, GAL, or NPY mRNA in the LC apparently do not underlie this process.
+TH	addiction	withdrawal	7550547	The change in the level of LENK in the thalamus (<strong>Th</strong>), hippocampus and mesencephalon and in the level of MENK in the hypothalamus and mesencephalon persisted after <b>withdrawal</b> of anesthesia.
+TH	drug	cannabinoid	7805282	Changes in <strong>tyrosine hydroxylase</strong> gene expression in mesencephalic catecholaminergic neurons of immature and adult male rats perinatally exposed to <b>cannabinoids</b>.
+TH	drug	cannabinoid	7805282	We have previously reported that the perinatal exposure of pregnant rats to <b>cannabinoids</b> affected the activity of tyrosine hydroxylase (<strong>TH</strong>) in the striatum of their male offspring at peripubertal ages.
+TH	drug	cannabinoid	7805282	We have previously reported that the perinatal exposure of pregnant rats to <b>cannabinoids</b> affected the activity of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) in the striatum of their male offspring at peripubertal ages.
+TH	drug	cannabinoid	7805282	In summary, perinatal <b>cannabinoid</b> exposure enhances the expression of the <strong>TH</strong> gene in mesencephalic catecholaminergic neurons during early peripubertal ages, coinciding with hashish treatment.
+TH	addiction	withdrawal	7805282	Normality was found after hashish <b>withdrawal</b> and an interesting decrease in the amount of <strong>TH</strong> mRNA appeared in adulthood, although with no reflection on the amount of <strong>TH</strong> protein.
+TH	drug	alcohol	7969718	The superior cervical ganglia (SCG) of the young (4 months) and the 2 year old rats responded to a 12 day or 4 week <b>ethanol</b> exposure with significantly increased catecholamine turnover, while the ganglia of the middle aged rats (12 months) showed only a minor increase in the intensity of catecholamine fluorescence and <strong>tyrosine hydroxylase</strong> immunoreactivity.
+TH	drug	cocaine	7902421	Chronic <b>cocaine</b> administration increases CNS <strong>tyrosine hydroxylase</strong> enzyme activity and mRNA levels and tryptophan hydroxylase enzyme activity levels.
+TH	drug	cocaine	7902421	Tyrosine hydroxylase (<strong>TH</strong>) and tryptophan hydroxylase (TPH) catalyze the rate limiting steps in dopamine and serotonin biosynthesis, respectively, and are the subject of dynamic regulatory mechanisms that could be sensitive to the actions of <b>cocaine</b>.
+TH	drug	cocaine	7902421	<strong>Tyrosine hydroxylase</strong> (<strong>TH</strong>) and tryptophan hydroxylase (TPH) catalyze the rate limiting steps in dopamine and serotonin biosynthesis, respectively, and are the subject of dynamic regulatory mechanisms that could be sensitive to the actions of <b>cocaine</b>.
+TH	drug	cocaine	7902421	This study assessed the effects of chronic <b>cocaine</b> on brain <strong>TH</strong> and TPH activities.
+TH	drug	cocaine	7902421	In summary, the chronic response independent administration of <b>cocaine</b> produces increases in the expression of <strong>TH</strong> mRNA and activity in both the cell bodies of motor (nigrostriatal) and reinforcement (mesolimbic) dopamine pathways.
+TH	addiction	reward	7902421	In summary, the chronic response independent administration of cocaine produces increases in the expression of <strong>TH</strong> mRNA and activity in both the cell bodies of motor (nigrostriatal) and <b>reinforcement</b> (mesolimbic) dopamine pathways.
+TH	drug	cocaine	19912951	We have demonstrated previously that chronic morphine and <b>cocaine</b> treatments increase levels of tyrosine hydroxylase (<strong>TH</strong>), and decrease levels of neurofilament (NF) proteins, in the ventral tegmental area (VTA), a major dopaminergic brain reward region, of outbred Sprague Dawley rats.
+TH	drug	opioid	19912951	We have demonstrated previously that chronic <b>morphine</b> and cocaine treatments increase levels of tyrosine hydroxylase (<strong>TH</strong>), and decrease levels of neurofilament (NF) proteins, in the ventral tegmental area (VTA), a major dopaminergic brain reward region, of outbred Sprague Dawley rats.
+TH	addiction	reward	19912951	We have demonstrated previously that chronic morphine and cocaine treatments increase levels of tyrosine hydroxylase (<strong>TH</strong>), and decrease levels of neurofilament (NF) proteins, in the ventral tegmental area (VTA), a major dopaminergic brain <b>reward</b> region, of outbred Sprague Dawley rats.
+TH	drug	cocaine	19912951	We have demonstrated previously that chronic morphine and <b>cocaine</b> treatments increase levels of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and decrease levels of neurofilament (NF) proteins, in the ventral tegmental area (VTA), a major dopaminergic brain reward region, of outbred Sprague Dawley rats.
+TH	drug	opioid	19912951	We have demonstrated previously that chronic <b>morphine</b> and cocaine treatments increase levels of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and decrease levels of neurofilament (NF) proteins, in the ventral tegmental area (VTA), a major dopaminergic brain reward region, of outbred Sprague Dawley rats.
+TH	addiction	reward	19912951	We have demonstrated previously that chronic morphine and cocaine treatments increase levels of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), and decrease levels of neurofilament (NF) proteins, in the ventral tegmental area (VTA), a major dopaminergic brain <b>reward</b> region, of outbred Sprague Dawley rats.
+TH	drug	cocaine	19912951	We have also found inherent differences in levels of these proteins in the VTA of inbred rat strains that differ in their behavioral responses to opiates, <b>cocaine</b>, and other drugs of abuse, with the Lewis rat showing higher levels of <strong>TH</strong> and lower levels of NFs in the VTA compared to the Fischer 344 rat.
+TH	drug	cocaine	8101222	Time course of <strong>tyrosine hydroxylase</strong> expression after behavioral sensitization to <b>cocaine</b>.
+TH	addiction	sensitization	8101222	Time course of <strong>tyrosine hydroxylase</strong> expression after behavioral <b>sensitization</b> to cocaine.
+TH	drug	cocaine	8101222	Levels of tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity and mRNA in the ventral tegmental area (VTA) and <strong>TH</strong> immunoreactivity in the nucleus accumbens were measured after early (24 hr) and late (3 weeks) withdrawal times from acute and repeated <b>cocaine</b> treatment.
+TH	addiction	withdrawal	8101222	Levels of tyrosine hydroxylase (<strong>TH</strong>) immunoreactivity and mRNA in the ventral tegmental area (VTA) and <strong>TH</strong> immunoreactivity in the nucleus accumbens were measured after early (24 hr) and late (3 weeks) <b>withdrawal</b> times from acute and repeated cocaine treatment.
+TH	drug	cocaine	8101222	Levels of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity and mRNA in the ventral tegmental area (VTA) and <strong>TH</strong> immunoreactivity in the nucleus accumbens were measured after early (24 hr) and late (3 weeks) withdrawal times from acute and repeated <b>cocaine</b> treatment.
+TH	addiction	withdrawal	8101222	Levels of <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>) immunoreactivity and mRNA in the ventral tegmental area (VTA) and <strong>TH</strong> immunoreactivity in the nucleus accumbens were measured after early (24 hr) and late (3 weeks) <b>withdrawal</b> times from acute and repeated cocaine treatment.
+TH	drug	cocaine	8101222	At the early withdrawal time, <strong>TH</strong> immunoreactivity and <strong>TH</strong> mRNA levels were measured 2 or 24 hr after the <b>cocaine</b> or saline challenge, and at the late withdrawal, measurements were made 24 hr after the challenge.
+TH	addiction	withdrawal	8101222	At the early <b>withdrawal</b> time, <strong>TH</strong> immunoreactivity and <strong>TH</strong> mRNA levels were measured 2 or 24 hr after the cocaine or saline challenge, and at the late <b>withdrawal</b>, measurements were made 24 hr after the challenge.
+TH	drug	cocaine	8101222	At early withdrawal, after both doses of repeated <b>cocaine</b> treatment, <strong>TH</strong> immunoreactivity in the VTA increased to 125% of saline controls by 24 hr after the <b>cocaine</b> challenge, with no significant changes in <strong>TH</strong> mRNA levels at either 2 or 24 hr after the <b>cocaine</b> challenge.
+TH	addiction	withdrawal	8101222	At early <b>withdrawal</b>, after both doses of repeated cocaine treatment, <strong>TH</strong> immunoreactivity in the VTA increased to 125% of saline controls by 24 hr after the cocaine challenge, with no significant changes in <strong>TH</strong> mRNA levels at either 2 or 24 hr after the cocaine challenge.
+TH	drug	cocaine	8101222	At the late withdrawal time, levels of <strong>TH</strong> immunoreactivity or mRNA in the VTA were not statistically altered 24 hr after a saline or <b>cocaine</b> challenge.
+TH	addiction	withdrawal	8101222	At the late <b>withdrawal</b> time, levels of <strong>TH</strong> immunoreactivity or mRNA in the VTA were not statistically altered 24 hr after a saline or cocaine challenge.
+TH	drug	cocaine	8101222	The data do not indicate a clear association between the regulation of <strong>TH</strong> expression and enduring behavioral sensitization to daily <b>cocaine</b> pretreatments.
+TH	addiction	sensitization	8101222	The data do not indicate a clear association between the regulation of <strong>TH</strong> expression and enduring behavioral <b>sensitization</b> to daily cocaine pretreatments.
+TH	drug	cocaine	8518951	In previous studies, we demonstrated that <strong>tyrosine hydroxylase</strong> and neurofilament proteins are regulated by chronic morphine and chronic <b>cocaine</b> treatments in the ventral tegmental area in Sprague Dawley rats and that the inbred Lewis and Fischer 344 rat strains, under drug naive conditions, show different levels of these proteins specifically in this brain region.
+TH	drug	opioid	8518951	In previous studies, we demonstrated that <strong>tyrosine hydroxylase</strong> and neurofilament proteins are regulated by chronic <b>morphine</b> and chronic cocaine treatments in the ventral tegmental area in Sprague Dawley rats and that the inbred Lewis and Fischer 344 rat strains, under drug naive conditions, show different levels of these proteins specifically in this brain region.
+TH	drug	amphetamine	8095821	<b>Amphetamine</b> withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (<strong>TH</strong>), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).
+TH	addiction	withdrawal	8095821	Amphetamine <b>withdrawal</b> could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (<strong>TH</strong>), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).
+TH	drug	amphetamine	8095821	<b>Amphetamine</b> withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).
+TH	addiction	withdrawal	8095821	Amphetamine <b>withdrawal</b> could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding <strong>tyrosine hydroxylase</strong> (<strong>TH</strong>), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).
+TH	addiction	withdrawal	8095821	<strong>TH</strong> mRNA levels are modestly enhanced over the same week of <b>withdrawal</b>, during which dopamine levels and behavioral novelty responses are both depressed.
+TH	drug	amphetamine	8095821	Altered <strong>TH</strong> and/or SVAT gene expression might contribute to restoring normal function to neurons "withdrawing" from <b>amphetamine</b> treatments.
+TH	drug	opioid	1362292	A similar strain difference was observed in chronic <b>morphine</b> regulation of <strong>tyrosine hydroxylase</strong>, with <b>morphine</b> increasing enzyme immunoreactivity in the VTA of F344 rats (as has been observed previously in Sprague Dawley rats [Beitner Johnson, D., and Nestler, E.J.:J.
+TH	addiction	addiction	1362292	In view of the observations that LEW and F344 rats show different levels of preference for several types of drugs of abuse, and of the evidence supporting a central role of the mesolimbic dopamine system in drug reward mechanisms, the results of the current study suggest the possibility that levels of NFs and <strong>tyrosine hydroxylase</strong> may mediate some aspects of drug reinforcement and contribute to individual genetic differences in vulnerability to drug <b>addiction</b>.
+TH	addiction	reward	1362292	In view of the observations that LEW and F344 rats show different levels of preference for several types of drugs of abuse, and of the evidence supporting a central role of the mesolimbic dopamine system in drug <b>reward</b> mechanisms, the results of the current study suggest the possibility that levels of NFs and <strong>tyrosine hydroxylase</strong> may mediate some aspects of drug <b>reinforcement</b> and contribute to individual genetic differences in vulnerability to drug addiction.
+TH	drug	nicotine	1525312	To identify the characteristics of the physician, of the demand for care, of the reason for the clinical consultation, of the patient's pathology and of the case's length of time under care, all of these in connection with the assessment by the Primary Care physician or nurse of both arterial tension (AT) and of the <b>tobacco</b> habit (<strong>TH</strong>) in the general population aged between 20 and 65.
+TH	drug	cocaine	1376774	In a previous study, we demonstrated that chronic morphine and <b>cocaine</b> exert common actions on <strong>tyrosine hydroxylase</strong>, the rate limiting enzyme in catecholamine biosynthesis, in this dopaminergic brain reward region (Beitner Johnson and Nestler, 1991).
+TH	drug	opioid	1376774	In a previous study, we demonstrated that chronic <b>morphine</b> and cocaine exert common actions on <strong>tyrosine hydroxylase</strong>, the rate limiting enzyme in catecholamine biosynthesis, in this dopaminergic brain reward region (Beitner Johnson and Nestler, 1991).
+TH	addiction	reward	1376774	In a previous study, we demonstrated that chronic morphine and cocaine exert common actions on <strong>tyrosine hydroxylase</strong>, the rate limiting enzyme in catecholamine biosynthesis, in this dopaminergic brain <b>reward</b> region (Beitner Johnson and Nestler, 1991).
+TH	drug	cocaine	1686743	Dopaminergic brain reward regions of Lewis and Fischer rats display different levels of <strong>tyrosine hydroxylase</strong> and other morphine  and <b>cocaine</b> regulated phosphoproteins.
+TH	drug	opioid	1686743	Dopaminergic brain reward regions of Lewis and Fischer rats display different levels of <strong>tyrosine hydroxylase</strong> and other <b>morphine</b>  and cocaine regulated phosphoproteins.
+TH	addiction	reward	1686743	Dopaminergic brain <b>reward</b> regions of Lewis and Fischer rats display different levels of <strong>tyrosine hydroxylase</strong> and other morphine  and cocaine regulated phosphoproteins.
+TH	drug	cocaine	1675665	Morphine and <b>cocaine</b> exert common chronic actions on <strong>tyrosine hydroxylase</strong> in dopaminergic brain reward regions.
+TH	drug	opioid	1675665	<b>Morphine</b> and cocaine exert common chronic actions on <strong>tyrosine hydroxylase</strong> in dopaminergic brain reward regions.
+TH	addiction	reward	1675665	Morphine and cocaine exert common chronic actions on <strong>tyrosine hydroxylase</strong> in dopaminergic brain <b>reward</b> regions.
+TH	drug	cocaine	1675665	We studied levels of <strong>tyrosine hydroxylase</strong> immunoreactivity and phosphorylation state in the ventral tegmental area (VTA) and nucleus accumbens (NAc) in an effort to understand better the mechanisms by which these brain reward regions are influenced by opiates and <b>cocaine</b>.
+TH	addiction	reward	1675665	We studied levels of <strong>tyrosine hydroxylase</strong> immunoreactivity and phosphorylation state in the ventral tegmental area (VTA) and nucleus accumbens (NAc) in an effort to understand better the mechanisms by which these brain <b>reward</b> regions are influenced by opiates and cocaine.
+TH	drug	cocaine	1675665	In the VTA, chronic, but not acute, administration of either morphine or <b>cocaine</b> increased levels of <strong>tyrosine hydroxylase</strong> immunoreactivity by 30 40%, with no change observed in the relative phosphorylation state of the enzyme.
+TH	drug	opioid	1675665	In the VTA, chronic, but not acute, administration of either <b>morphine</b> or cocaine increased levels of <strong>tyrosine hydroxylase</strong> immunoreactivity by 30 40%, with no change observed in the relative phosphorylation state of the enzyme.
+TH	drug	cocaine	1675665	In the NAc, chronic, but not acute, morphine and <b>cocaine</b> treatments decreased the phosphorylation state of <strong>tyrosine hydroxylase</strong>, without a change in its total amount.
+TH	drug	opioid	1675665	In the NAc, chronic, but not acute, <b>morphine</b> and cocaine treatments decreased the phosphorylation state of <strong>tyrosine hydroxylase</strong>, without a change in its total amount.
+TH	drug	cocaine	1675665	In contrast, morphine and <b>cocaine</b> did not regulate <strong>tyrosine hydroxylase</strong> in the substantia nigra or caudate/putamen, brain regions generally not implicated in drug reward.
+TH	drug	opioid	1675665	In contrast, <b>morphine</b> and cocaine did not regulate <strong>tyrosine hydroxylase</strong> in the substantia nigra or caudate/putamen, brain regions generally not implicated in drug reward.
+TH	addiction	reward	1675665	In contrast, morphine and cocaine did not regulate <strong>tyrosine hydroxylase</strong> in the substantia nigra or caudate/putamen, brain regions generally not implicated in drug <b>reward</b>.
+TH	drug	cocaine	1675665	Morphine and <b>cocaine</b> regulation of <strong>tyrosine hydroxylase</strong> could represent part of a common biochemical basis of morphine and <b>cocaine</b> addiction and craving.
+TH	drug	opioid	1675665	<b>Morphine</b> and cocaine regulation of <strong>tyrosine hydroxylase</strong> could represent part of a common biochemical basis of <b>morphine</b> and cocaine addiction and craving.
+TH	addiction	addiction	1675665	Morphine and cocaine regulation of <strong>tyrosine hydroxylase</strong> could represent part of a common biochemical basis of morphine and cocaine <b>addiction</b> and craving.
+TH	addiction	relapse	1675665	Morphine and cocaine regulation of <strong>tyrosine hydroxylase</strong> could represent part of a common biochemical basis of morphine and cocaine addiction and <b>craving</b>.
+TH	drug	cannabinoid	1922791	In the striatum, <strong>tyrosine hydroxylase</strong> activity was constantly decreased during <b>cannabinoid</b> exposure in males.
+TH	addiction	aversion	1672462	The possible involvement of catecholamines (CA) in the mediation of acetaldehyde's conditioned taste <b>aversion</b> (<b>CTA</b>) was examined by testing the effects of alpha methyl para tyrosine (AMPT, a <strong>tyrosine hydroxylase</strong> inhibitor) on the CTAs produced by acetaldehyde.
+TH	drug	amphetamine	2322845	Bilateral microinjections of a <strong>tyrosine hydroxylase</strong> inhibitor, alpha methyl p tyrosine (alpha MPT), decreased (+) <b>amphetamine</b> locomotor stimulation in a dose dependent fashion.
+TH	drug	cannabinoid	2138936	Most of these effects disappeared after cessation of <b>cannabinoid</b> treatment, but the decrease in striatal <strong>TH</strong> activity in males was maintained during drug withdrawal.
+TH	addiction	withdrawal	2138936	Most of these effects disappeared after cessation of cannabinoid treatment, but the decrease in striatal <strong>TH</strong> activity in males was maintained during drug <b>withdrawal</b>.
+TH	addiction	withdrawal	2895003	Immediately prior to <b>withdrawal</b> assessment, rats were injected with dynorphin A (1 13) either i.<strong>th</strong>.
+TH	addiction	withdrawal	2823970	injection to mice 20 min prior to testing in the warm water (55 degrees C) tail <b>withdrawal</b> test (+10 min for i.<strong>th</strong>.
+TH	drug	opioid	2823970	<b>morphine</b> dose response curve to the right without affecting the i.<strong>th</strong>.
+TH	drug	opioid	3022095	<b>naloxone</b> against DPDPE and DAGO; the i.<strong>th</strong>.
+TH	drug	opioid	3022095	Additionally, while the affinity of <b>naloxone</b> appears different for the receptors activated by i.<strong>th</strong>.
+TH	drug	opioid	4039756	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal in the rat has been shown to deplete adrenal epinephrine and to increase adrenal and locus ceruleus <strong>tyrosine hydroxylase</strong> activities.
+TH	addiction	withdrawal	4039756	Naloxone precipitated morphine <b>withdrawal</b> in the rat has been shown to deplete adrenal epinephrine and to increase adrenal and locus ceruleus <strong>tyrosine hydroxylase</strong> activities.
+TH	addiction	withdrawal	4039756	Clonidine also blocked the increases in <strong>tyrosine hydroxylase</strong> activity seen in the adrenal and locus ceruleus during <b>withdrawal</b>.
+TH	drug	alcohol	2862881	Similarly, no changes in the activities of choline acetyltransferase, <strong>tyrosine hydroxylase</strong> or MAO B were observed in brains of <b>alcoholics</b> as compared to the control population.
+TH	drug	opioid	2860239	<b>Morphine</b> treatment increased adrenal <strong>tyrosine hydroxylase</strong> activity to 160% of control.
+TH	drug	opioid	2860239	Precipitation of withdrawal with <b>naloxone</b> further increased adrenal <strong>tyrosine hydroxylase</strong> activity to 240% of control after 1 day; the enzyme activity returned to control values at day 7.
+TH	addiction	withdrawal	2860239	Precipitation of <b>withdrawal</b> with naloxone further increased adrenal <strong>tyrosine hydroxylase</strong> activity to 240% of control after 1 day; the enzyme activity returned to control values at day 7.
+TH	drug	opioid	4039289	The rats of 4 groups were abruptly withdrawn from <b>morphine</b>, and the rats of another 4 groups were given <b>naloxone</b> (3 mg/kg, s.c.) at 20:00 on the 8 <strong>th</strong> day and 2:00, 8:00 and 14:00 on the 9 <strong>th</strong> day after the <b>morphine</b> administration, respectively.
+TH	drug	opioid	6541792	Both inhibition of <strong>tyrosine hydroxylase</strong> by alpha methyl p tyrosine (alpha MPT) and inhibition of DA receptors by pimozide interfere with the effect of Z Pro D Leu on <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+TH	addiction	withdrawal	6541792	Both inhibition of <strong>tyrosine hydroxylase</strong> by alpha methyl p tyrosine (alpha MPT) and inhibition of DA receptors by pimozide interfere with the effect of Z Pro D Leu on naloxone precipitated morphine <b>withdrawal</b>.
+TH	drug	alcohol	6137968	<strong>Tyrosine hydroxylase</strong> activity in the brain and adrenal gland of rats following chronic administration of <b>ethanol</b>.
+TH	drug	alcohol	6137968	The effects of chronic administration and <b>ethanol</b> withdrawal on the activity of <strong>tyrosine hydroxylase</strong> were examined in the adrenal gland and six brain regions, including the frontal cortex, hippocampus, locus coeruleus, striatum, substantia nigra, and hypothalamus.
+TH	addiction	withdrawal	6137968	The effects of chronic administration and ethanol <b>withdrawal</b> on the activity of <strong>tyrosine hydroxylase</strong> were examined in the adrenal gland and six brain regions, including the frontal cortex, hippocampus, locus coeruleus, striatum, substantia nigra, and hypothalamus.
+TH	drug	alcohol	6137968	Forty hr following the last <b>ethanol</b> intubation, <strong>tyrosine hydroxylase</strong> activity was significantly increased above control values in both the adrenal gland and locus coeruleus.
+TH	drug	alcohol	6137968	<strong>Tyrosine hydroxylase</strong> activity in the remaining five brain areas was unaffected by <b>ethanol</b> treatment.
+TH	drug	alcohol	6137968	Immunotitration studies indicate that the increases in <strong>tyrosine hydroxylase</strong> activity found in the adrenal gland and locus coeruleus 40 hr after <b>ethanol</b> administration were due to an increase in enzyme protein.
+TH	drug	alcohol	6137968	These data indicate that high blood <b>ethanol</b> concentrations maintained over a period of time (48 hr) do not affect adrenal gland or brain <strong>tyrosine hydroxylase</strong> activity.
+TH	drug	alcohol	6137968	However, withdrawal from <b>ethanol</b> following 48 hr of treatment does produce an increase in <strong>tyrosine hydroxylase</strong> activity in the adrenal gland and locus coeruleus, similar to that seen following other stresses.
+TH	addiction	withdrawal	6137968	However, <b>withdrawal</b> from ethanol following 48 hr of treatment does produce an increase in <strong>tyrosine hydroxylase</strong> activity in the adrenal gland and locus coeruleus, similar to that seen following other stresses.
+TH	drug	nicotine	7116761	Approximately 26% of <strong>th</strong> original material was recovered from the pipe after <b>smoking</b>.
+TH	drug	alcohol	7043008	Compared with the placebo, cimetidine produced a small increase in both the peak plasma <b>ethanol</b> level (from 146 +/  5.2 to 163 +/  7.6 mg/dL, mean +/  SEM) and <strong>th</strong> area under the <b>ethanol</b> concentration time curve (from 717 +/  17 to 771 +/  44 mg/dLXhr).
+TH	drug	amphetamine	6115646	Catecholamine levels and <strong>tyrosine hydroxylase</strong> activities in rat brain regions after chronic treatment with, and withdrawal of, <b>methamphetamine</b>.
+TH	addiction	withdrawal	6115646	Catecholamine levels and <strong>tyrosine hydroxylase</strong> activities in rat brain regions after chronic treatment with, and <b>withdrawal</b> of, methamphetamine.
+TH	addiction	dependence	7013801	Theory is developed for <strong>th</strong> pH <b>dependence</b> of isotope effects in a mechanism where a pH dependent step precedes the isotope sensitive bond breaking step, and the rate of the latter varies only slightly with the state of protonation of the acid base catalytic group on the enzyme.
+TH	drug	nicotine	6782600	The voluntary <b>smoking</b> model described in the present paper should be useful for studying the factors involved in initiating and maintaining <b>smoking</b> behavior and for studying the psychopharmacological effects of <b>smoking</b>, while the schedule controlled <b>smoking</b> model should be useful for studying the physiological effects of <b>smoking</b> and for studying <strong>th</strong> relationship of <b>smoking</b> with various disease entities.
+TH	drug	alcohol	6105829	These effects cannot be interpreted as resulting either from DA receptor subsensitivity or supersensitivity, but suggest instead that coupling between DA receptors and <strong>tyrosine hydroxylase</strong> is perturbed by <b>ethanol</b> treatment.
+TH	drug	alcohol	42080	<strong>Tyrosine hydroxylase</strong> activity in adrenal medulla of rats following acute and chronic administration of <b>ethanol</b>.
+TH	drug	opioid	690627	The disappearance rate of brain NA after inhibition of <strong>tyrosine hydroxylase</strong> by alpha methyltyrosine methylester (250 mg/kg), the utilization of NA, was accelerated by <b>morphine</b>, whereas that of DA was not affected.
+TH	drug	alcohol	21065	In mice chronically treated with <b>ethanol</b> (in a liquid diet containing 6% <b>ethanol</b> ad libitum for 2 weeks), brain tryptophan hydroxylase (TPH) activity was increased (by 30 45% in whole brain), while brain <strong>tyrosine hydroxylase</strong> activity remained unchanged.
+TH	drug	alcohol	239396	<strong>Tyrosine hydroxylase</strong> and dopamine (DA) beta hydroxylase acitvities in guinea pig brain and heart were determined at various time after <b>disulfiram</b> (DS) and sodium diethyldithiocarbamate (DDC) injections.
+TH	drug	opioid	4153650	Effect of chronic <b>morphine</b> implantation on <strong>tyrosine hydroxylase</strong> activity in the rat caudate.
+TH	drug	alcohol	5690148	Oral administration of alpha methyl p tyrosine, a <strong>tyrosine hydroxylase</strong> inhibitor that depletes brain catecholamines, slightly reduced selection of <b>alcohol</b>, but preference returned to normal as soon as alpha methyl p tyrosine was terminated.
+BDNF	drug	psychedelics	32745661	Rapid release of brain derived neurotrophic factor (<strong>BDNF</strong>) in the medial prefrontal cortex (mPFC) plays a critical role in the rapid and sustained antidepressant actions of <b>ketamine</b>, an N methyl d aspartate receptor antagonist.
+BDNF	drug	psychedelics	32745661	Rapid release of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the medial prefrontal cortex (mPFC) plays a critical role in the rapid and sustained antidepressant actions of <b>ketamine</b>, an N methyl d aspartate receptor antagonist.
+BDNF	addiction	reward	32745661	Herein, we examined the duration of the antidepressant like effects of intra mPFC infusion of <strong>BDNF</strong> using male C57BL/6 J mice in two different behavioral paradigms namely, despair (forced swim test, FST) and motivation/<b>reward</b> (female urine sniffing test, FUST).
+BDNF	drug	psychedelics	32745661	These results indicate that the antidepressant like effects of a single intra mPFC infusion of <strong>BDNF</strong> last for approximately one week and that this duration is similar to that of the antidepressant actions of <b>ketamine</b>.
+BDNF	drug	cannabinoid	32714224	ii) Nominally significant differences were observed in the levels of IL 1RA (p = 0.0059), YKL40 (p = 0.0069), CatS (p = 0.013), sTNFR1 (p = 0.031), and <strong>BDNF</strong> (p = 0.020), where these factors exhibited higher plasma levels in <b>Cannabis</b> user SCZ patients than in non users.
+BDNF	drug	alcohol	32657509	Finally, we found that aversive counterconditioning preceded by <b>alcohol</b> memory retrieval was characterized by the upregulation of brain derived neurotrophic factor (<strong>Bdnf</strong>) mRNA expression in the medial prefrontal cortex, suggesting that <strong>BDNF</strong> may play a role in the memory updating process.
+BDNF	addiction	aversion	32657509	Finally, we found that <b>aversive</b> counterconditioning preceded by alcohol memory retrieval was characterized by the upregulation of brain derived neurotrophic factor (<strong>Bdnf</strong>) mRNA expression in the medial prefrontal cortex, suggesting that <strong>BDNF</strong> may play a role in the memory updating process.
+BDNF	drug	alcohol	32657509	Finally, we found that aversive counterconditioning preceded by <b>alcohol</b> memory retrieval was characterized by the upregulation of <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) mRNA expression in the medial prefrontal cortex, suggesting that <strong>BDNF</strong> may play a role in the memory updating process.
+BDNF	addiction	aversion	32657509	Finally, we found that <b>aversive</b> counterconditioning preceded by alcohol memory retrieval was characterized by the upregulation of <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) mRNA expression in the medial prefrontal cortex, suggesting that <strong>BDNF</strong> may play a role in the memory updating process.
+BDNF	drug	alcohol	32588398	Among others, <strong>BDNF</strong> (brain derived neurotrophic factor) is believed to control voluntary <b>ethanol</b> intake in rodents.
+BDNF	drug	alcohol	32588398	Among others, <strong>BDNF</strong> (<strong>brain derived neurotrophic factor</strong>) is believed to control voluntary <b>ethanol</b> intake in rodents.
+BDNF	drug	alcohol	32588398	Meanwhile, expression of <strong>BDNF</strong> exons in brain regions and epigenetic mechanisms underlying <b>alcohol</b> intake pattern remain obscure.
+BDNF	drug	alcohol	32588398	The main goal was to study whether voluntary <b>alcohol</b> drinking pattern affects expression of <strong>BDNF</strong> exons in selected rat brain regions during early abstinence.
+BDNF	drug	alcohol	32588398	Finally, the IA2BC rats with growing <b>alcohol</b> intake showed elevation of <strong>BDNF</strong> mRNA containing exon VI in the hippocampus associated with an enhanced H3K9ac occupancy at the respective promoter.
+BDNF	drug	alcohol	32588398	Thus, rats differentially consuming <b>alcohol</b> in the IA2BC paradigm differ in epigenetically determined expression of <strong>BDNF</strong> exon VI in the hippocampus during early abstinence.
+BDNF	drug	alcohol	32569950	Finally, the effect of resveratrol on the <b>alcohol</b> induced alteration of brain derived neurotrophic factors (<strong>BDNF</strong>) in the liver was investigated.
+BDNF	drug	alcohol	32569950	Moreover, resveratrol supplementation can counteract <b>alcohol</b> induced <strong>BDNF</strong> elevation in the liver, which is the main target of organ <b>alcohol</b> induced damage.
+BDNF	drug	alcohol	32569950	The consumption of resveratrol through metabolite formation may play a protective role by decreasing free radical formation and modulating the <strong>BDNF</strong> involved in hepatic disruption induced by chronic <b>alcohol</b> consumption.
+BDNF	drug	opioid	32477481	Comparing the Efficacy of Anodal, Cathodal, and Sham Transcranial Direct Current Stimulation on <strong>Brain Derived Neurotrophic Factor</strong> and Psychological Symptoms in <b>Opioid</b> Addicted Patients.
+BDNF	drug	opioid	32477481	This research aimed at comparing the efficacy of anodal, cathodal, and sham transcranial Direct Current Stimulation (tDCS) on the Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) and psychological symptoms in <b>opioid</b> addicted patients.
+BDNF	drug	opioid	32477481	This research aimed at comparing the efficacy of anodal, cathodal, and sham transcranial Direct Current Stimulation (tDCS) on the <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) and psychological symptoms in <b>opioid</b> addicted patients.
+BDNF	drug	opioid	32477481	Stimulating the Dorsolateral Prefrontal Cortex (DLPFC) led to a significant change in increasing the level of <strong>BDNF</strong> (P=0.031) and reducing the degree of depression (P=0.018), anxiety (P=0.001), stress (P=0.012), and decreased the level of craving (P=0.001) in <b>opioid</b> addicted patients.
+BDNF	addiction	relapse	32477481	Stimulating the Dorsolateral Prefrontal Cortex (DLPFC) led to a significant change in increasing the level of <strong>BDNF</strong> (P=0.031) and reducing the degree of depression (P=0.018), anxiety (P=0.001), stress (P=0.012), and decreased the level of <b>craving</b> (P=0.001) in opioid addicted patients.
+BDNF	addiction	relapse	32477481	The stimulation of the right DLPFC (group B) significantly increased <strong>BDNF</strong> in comparison with the sham group (sham tDCS) and decreased anxiety and <b>craving</b>.
+BDNF	addiction	relapse	32477481	The stimulation of the left DLPFC (group A) significantly reduced depression, anxiety, stress, and <b>craving</b> compared with the sham group, while there was no change in <strong>BDNF</strong>.
+BDNF	drug	alcohol	32477119	In addition, <strong>Bdnf</strong> expression was upregulated after either chronic <b>alcohol</b> or cocaine intake.
+BDNF	drug	cocaine	32477119	In addition, <strong>Bdnf</strong> expression was upregulated after either chronic alcohol or <b>cocaine</b> intake.
+BDNF	drug	amphetamine	32466633	MeBib Suppressed <b>Methamphetamine</b> Self Administration Response via Inhibition of <strong>BDNF</strong>/ERK/CREB Signal Pathway in the Hippocampus.
+BDNF	addiction	intoxication	32458406	Our findings show that <b>binge</b> KET impaired memory, increased pro <strong>BDNF</strong> and TrkB levels in the hippocampus, and increased lipid peroxidation (LP) in the kidney and hippocampus, while SbChro KET impaired memory, increased pro <strong>BDNF</strong>, and decreased both <strong>BDNF</strong> and TrkB levels in the hippocampus, and increased LP in the kidney, liver, and hippocampus.
+BDNF	drug	opioid	32428531	Impairment of cost benefit decision making in <b>morphine</b> dependent rats is partly mediated via the alteration of <strong>BDNF</strong> and p CREB levels in the nucleus accumbens.
+BDNF	drug	opioid	32428531	In the current study, we assessed the effects of <b>morphine</b> dependence and its withdrawal on cost benefit decision making and furthermore the involvement of <strong>BDNF</strong> and p CREB in the nucleus accumbens, a key brain area involved in decision making was measured.
+BDNF	addiction	dependence	32428531	In the current study, we assessed the effects of morphine <b>dependence</b> and its withdrawal on cost benefit decision making and furthermore the involvement of <strong>BDNF</strong> and p CREB in the nucleus accumbens, a key brain area involved in decision making was measured.
+BDNF	addiction	withdrawal	32428531	In the current study, we assessed the effects of morphine dependence and its <b>withdrawal</b> on cost benefit decision making and furthermore the involvement of <strong>BDNF</strong> and p CREB in the nucleus accumbens, a key brain area involved in decision making was measured.
+BDNF	drug	opioid	32428531	During effort based decision making in <b>morphine</b> dependent rats, <strong>BDNF</strong> decreased but there was no significant change in p CREB.
+BDNF	drug	opioid	32428531	Besides, during delay based decision making in the <b>morphine</b> dependent group, both <strong>BDNF</strong> and p CREB did not show any significant change.
+BDNF	drug	opioid	32428531	In addition, impairment of effort based decision making in <b>morphine</b> dependent rats is related to the decrease of <strong>BDNF</strong> level but not p CREB/CREB ratio in the NAc.
+BDNF	drug	opioid	32428531	However, delay based decision making defects in <b>morphine</b> dependent rats did not associate with the change in <strong>BDNF</strong> and p CREB levels in the NAc.
+BDNF	drug	nicotine	32417176	Expression analysis of hippocampal and amygdala CREB <strong>BDNF</strong> signaling pathway in <b>nicotine</b> induced reward under stress in rats.
+BDNF	addiction	reward	32417176	Expression analysis of hippocampal and amygdala CREB <strong>BDNF</strong> signaling pathway in nicotine induced <b>reward</b> under stress in rats.
+BDNF	drug	nicotine	32417176	The present study includes an expression analysis to identify the possible role of hippocampal and amygdala CREB (cAMP response element binding protein) and <strong>BDNF</strong> (Brain derived neurotrophic factor) activation in <b>nicotine</b> induced conditioned place preference (CPP) under exposure to acute or sub chronic stress.
+BDNF	addiction	reward	32417176	The present study includes an expression analysis to identify the possible role of hippocampal and amygdala CREB (cAMP response element binding protein) and <strong>BDNF</strong> (Brain derived neurotrophic factor) activation in nicotine induced conditioned place preference (<b>CPP</b>) under exposure to acute or sub chronic stress.
+BDNF	drug	nicotine	32417176	The present study includes an expression analysis to identify the possible role of hippocampal and amygdala CREB (cAMP response element binding protein) and <strong>BDNF</strong> (<strong>Brain derived neurotrophic factor</strong>) activation in <b>nicotine</b> induced conditioned place preference (CPP) under exposure to acute or sub chronic stress.
+BDNF	addiction	reward	32417176	The present study includes an expression analysis to identify the possible role of hippocampal and amygdala CREB (cAMP response element binding protein) and <strong>BDNF</strong> (<strong>Brain derived neurotrophic factor</strong>) activation in nicotine induced conditioned place preference (<b>CPP</b>) under exposure to acute or sub chronic stress.
+BDNF	drug	nicotine	32417176	The hippocampal level of <strong>BDNF</strong> was increased following <b>nicotine</b> administration and in the <b>nicotine</b> treated animals exposed to acute stress.
+BDNF	drug	nicotine	32417176	Acute stress induced increase of <b>nicotine</b> reward increased <strong>BDNF</strong> levels in the hippocampus.
+BDNF	addiction	reward	32417176	Acute stress induced increase of nicotine <b>reward</b> increased <strong>BDNF</strong> levels in the hippocampus.
+BDNF	addiction	reward	32417176	Moreover, the animals' exposure to the <b>CPP</b> apparatus without any drug administration increased the ratios of pCREB/tCREB and <strong>BDNF</strong>/β actin in the targeted sites.
+BDNF	drug	nicotine	32417176	In summary, the present study indicate that the alterations of the ratio of pCREB/CREB and also the level of <strong>BDNF</strong> in the hippocampus may be critical for enhancing <b>nicotine</b> reward under stress condition.
+BDNF	addiction	reward	32417176	In summary, the present study indicate that the alterations of the ratio of pCREB/CREB and also the level of <strong>BDNF</strong> in the hippocampus may be critical for enhancing nicotine <b>reward</b> under stress condition.
+BDNF	drug	alcohol	32399021	Among Adolescents, <strong>BDNF</strong> and Pro <strong>BDNF</strong> Lasting Changes with <b>Alcohol</b> Use Are Stage Specific.
+BDNF	drug	alcohol	32399021	Given the importance of brain derived neurotrophic factor (mature <strong>BDNF</strong>) in this development stage, the current study investigated its relationship with <b>alcohol</b> use.
+BDNF	drug	alcohol	32399021	Given the importance of <strong>brain derived neurotrophic factor</strong> (mature <strong>BDNF</strong>) in this development stage, the current study investigated its relationship with <b>alcohol</b> use.
+BDNF	drug	alcohol	32399021	Then, the onset and frequency of <b>alcohol</b> use from ages 11 to 18 were collected to determine how the relationship between <b>alcohol</b>, pro <strong>BDNF</strong>, and m <strong>BDNF</strong> unfolds over time.
+BDNF	drug	alcohol	32399021	On the other hand, levels of mature <strong>BDNF</strong> steadily increased (974.896 ± 275 pg/ml) in those starting <b>alcohol</b> use after the age of 15.
+BDNF	drug	amphetamine	32388619	Binge <b>METH</b> (40 mg/kg, i.p., over 1 day) dramatically altered striatal and hippocampal dopamine, DOPAC, 5 HT, 5 HIAA, <strong>BDNF</strong>, and TrkB 75 days after drug exposure.
+BDNF	addiction	intoxication	32388619	<b>Binge</b> METH (40 mg/kg, i.p., over 1 day) dramatically altered striatal and hippocampal dopamine, DOPAC, 5 HT, 5 HIAA, <strong>BDNF</strong>, and TrkB 75 days after drug exposure.
+BDNF	drug	amphetamine	32388619	In contrast, 6 h LgA <b>METH</b> self administration (cumulative 24.8 48.9 mg <b>METH</b>, i.v., over 16 days) altered hippocampal <strong>BDNF</strong> in both contingent and yoked animals but reduced striatal 5 HIAA in only contingent animals.
+BDNF	drug	alcohol	32372985	Exploring <strong>Brain Derived Neurotrophic Factor</strong> and Cell Adhesion Molecules as Biomarkers for the Transdiagnostic Symptom Anhedonia in <b>Alcohol</b> Use Disorder and Comorbid Depression.
+BDNF	drug	alcohol	32369970	Reduced brain derived neurotrophic factor (<strong>BDNF</strong>) expression has been associated with AUD and <b>alcohol</b> addiction, however the effects of activation of <strong>BDNF</strong> signalling in the brain on voluntary <b>alcohol</b> intake reinstatement and relapse are unknown.
+BDNF	addiction	addiction	32369970	Reduced brain derived neurotrophic factor (<strong>BDNF</strong>) expression has been associated with AUD and alcohol <b>addiction</b>, however the effects of activation of <strong>BDNF</strong> signalling in the brain on voluntary alcohol intake reinstatement and relapse are unknown.
+BDNF	addiction	relapse	32369970	Reduced brain derived neurotrophic factor (<strong>BDNF</strong>) expression has been associated with AUD and alcohol addiction, however the effects of activation of <strong>BDNF</strong> signalling in the brain on voluntary alcohol intake <b>reinstatement</b> and <b>relapse</b> are unknown.
+BDNF	drug	alcohol	32369970	Reduced <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression has been associated with AUD and <b>alcohol</b> addiction, however the effects of activation of <strong>BDNF</strong> signalling in the brain on voluntary <b>alcohol</b> intake reinstatement and relapse are unknown.
+BDNF	addiction	addiction	32369970	Reduced <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression has been associated with AUD and alcohol <b>addiction</b>, however the effects of activation of <strong>BDNF</strong> signalling in the brain on voluntary alcohol intake reinstatement and relapse are unknown.
+BDNF	addiction	relapse	32369970	Reduced <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression has been associated with AUD and alcohol addiction, however the effects of activation of <strong>BDNF</strong> signalling in the brain on voluntary alcohol intake <b>reinstatement</b> and <b>relapse</b> are unknown.
+BDNF	drug	cocaine	32361384	The <strong>BDNF</strong> Val66Met Polymorphism Moderates the Relationship Between Posttraumatic Stress Disorder and Trauma Script evoked Attentional Bias to <b>Cocaine</b> Cues Among Patients with <b>Cocaine</b> Dependence.
+BDNF	addiction	dependence	32361384	The <strong>BDNF</strong> Val66Met Polymorphism Moderates the Relationship Between Posttraumatic Stress Disorder and Trauma Script evoked Attentional Bias to Cocaine Cues Among Patients with Cocaine <b>Dependence</b>.
+BDNF	drug	cocaine	32361384	A common polymorphism in brain derived neurotrophic factor (<strong>BDNF</strong>), Val66met, is associated with risk for stimulant addiction, and thus, was examined as a moderator of the association between PTSD and <b>cocaine</b> related AB following trauma script exposure in this study.
+BDNF	addiction	addiction	32361384	A common polymorphism in brain derived neurotrophic factor (<strong>BDNF</strong>), Val66met, is associated with risk for stimulant <b>addiction</b>, and thus, was examined as a moderator of the association between PTSD and cocaine related AB following trauma script exposure in this study.
+BDNF	drug	cocaine	32361384	A common polymorphism in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), Val66met, is associated with risk for stimulant addiction, and thus, was examined as a moderator of the association between PTSD and <b>cocaine</b> related AB following trauma script exposure in this study.
+BDNF	addiction	addiction	32361384	A common polymorphism in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), Val66met, is associated with risk for stimulant <b>addiction</b>, and thus, was examined as a moderator of the association between PTSD and cocaine related AB following trauma script exposure in this study.
+BDNF	drug	cocaine	32361384	PTSD CD patients homozygous for the <strong>BDNF</strong> Val/Val genotype exhibited greater bias for attending to <b>cocaine</b> related stimuli following trauma script exposure than those carrying the Met allele.
+BDNF	drug	cocaine	32361384	The PTSD by <strong>BDNF</strong> interaction did not predict response time variability on trials for which only neutral stimuli were presented, thus increasing confidence that the observed effect is specific to <b>cocaine</b> related stimuli.
+BDNF	drug	cocaine	32361384	PTSD CD patients homozygous for the <strong>BDNF</strong> Val/Val genotype may be at particularly high risk for negative clinical outcomes (e.g., relapse, treatment dropout) as a function of prolonged attentional engagement with <b>cocaine</b> cues when exposed to trauma reminders.
+BDNF	addiction	relapse	32361384	PTSD CD patients homozygous for the <strong>BDNF</strong> Val/Val genotype may be at particularly high risk for negative clinical outcomes (e.g., <b>relapse</b>, treatment dropout) as a function of prolonged attentional engagement with cocaine cues when exposed to trauma reminders.
+BDNF	drug	alcohol	32329706	A polymorphism in the gene for <strong>BDNF</strong> has been linked to the risk of developing deficiences in colour vision sometimes observed in <b>alcoholics</b>.
+BDNF	drug	psychedelics	32125485	<b>Ketamine</b> relieves depression like behaviors induced by chronic postsurgical pain in rats through anti inflammatory, anti oxidant effects and regulating <strong>BDNF</strong> expression.
+BDNF	drug	psychedelics	32125485	Additionally, <b>ketamine</b> reduced proinflammatory cytokines, inhibited oxidative stress, and elevated <strong>BDNF</strong> levels in rat hippocampus.
+BDNF	drug	psychedelics	32125485	<b>Ketamine</b> can rapidly relieve CPSP induced depression in rats, which may be related to the reduction of proinflammatory cytokines, regulating oxidative stress and increasing <strong>BDNF</strong> in the hippocampus.
+BDNF	drug	psychedelics	32103409	Toxicity of <b>ayahuasca</b> after 28 days daily exposure and effects on monoamines and brain derived neurotrophic factor (<strong>BDNF</strong>) in brain of Wistar rats.
+BDNF	drug	psychedelics	32103409	Toxicity of <b>ayahuasca</b> after 28 days daily exposure and effects on monoamines and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in brain of Wistar rats.
+BDNF	drug	psychedelics	32103409	The objectives of this study were to evaluate the potential toxic effects of <b>ayahuasca</b> on rats after chronic exposure, and the levels of monoamines, their metabolites and the brain derived neurotrophic factor (<strong>BDNF</strong>) in the brain.
+BDNF	drug	psychedelics	32103409	The objectives of this study were to evaluate the potential toxic effects of <b>ayahuasca</b> on rats after chronic exposure, and the levels of monoamines, their metabolites and the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the brain.
+BDNF	drug	psychedelics	32103409	The mechanisms involved in the increase in serotonin, dopamine turnover and <strong>BDNF</strong> levels observed in <b>ayahuasca</b> treated animals should be further investigated in specific brain areas.
+BDNF	drug	alcohol	32081048	Evolution of <strong>BDNF</strong> serum levels during the first six months after <b>alcohol</b> withdrawal.
+BDNF	addiction	withdrawal	32081048	Evolution of <strong>BDNF</strong> serum levels during the first six months after alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	32081048	Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) has been associated to <b>alcohol</b> dependence and appear to vary after withdrawal, although the link with the withdrawal outcome on the long term is unknown.We aimed to assess the evolution of <strong>BDNF</strong> levels during the six months following withdrawal, and determine the association with the status of <b>alcohol</b> consumption.
+BDNF	addiction	dependence	32081048	Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) has been associated to alcohol <b>dependence</b> and appear to vary after withdrawal, although the link with the withdrawal outcome on the long term is unknown.We aimed to assess the evolution of <strong>BDNF</strong> levels during the six months following withdrawal, and determine the association with the status of alcohol consumption.
+BDNF	addiction	withdrawal	32081048	Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) has been associated to alcohol dependence and appear to vary after <b>withdrawal</b>, although the link with the <b>withdrawal</b> outcome on the long term is unknown.We aimed to assess the evolution of <strong>BDNF</strong> levels during the six months following <b>withdrawal</b>, and determine the association with the status of alcohol consumption.
+BDNF	drug	alcohol	32081048	<strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) has been associated to <b>alcohol</b> dependence and appear to vary after withdrawal, although the link with the withdrawal outcome on the long term is unknown.We aimed to assess the evolution of <strong>BDNF</strong> levels during the six months following withdrawal, and determine the association with the status of <b>alcohol</b> consumption.
+BDNF	addiction	dependence	32081048	<strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) has been associated to alcohol <b>dependence</b> and appear to vary after withdrawal, although the link with the withdrawal outcome on the long term is unknown.We aimed to assess the evolution of <strong>BDNF</strong> levels during the six months following withdrawal, and determine the association with the status of alcohol consumption.
+BDNF	addiction	withdrawal	32081048	<strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) has been associated to alcohol dependence and appear to vary after <b>withdrawal</b>, although the link with the <b>withdrawal</b> outcome on the long term is unknown.We aimed to assess the evolution of <strong>BDNF</strong> levels during the six months following <b>withdrawal</b>, and determine the association with the status of alcohol consumption.
+BDNF	drug	alcohol	32081048	Serum <strong>BDNF</strong> levels of <b>alcohol</b> dependent patients (n = 248) and biological and clinical parameters were determined at the time of <b>alcohol</b> cessation (D0), 14 days (D14), 28 days (D28), and 2, 4, and 6 months after (M2, M4, M6).
+BDNF	drug	alcohol	32081048	<strong>BDNF</strong> levels increased by 14 days after withdrawal and remained elevated throughout the six month period, independently of <b>alcohol</b> consumption.
+BDNF	addiction	withdrawal	32081048	<strong>BDNF</strong> levels increased by 14 days after <b>withdrawal</b> and remained elevated throughout the six month period, independently of alcohol consumption.
+BDNF	addiction	withdrawal	32081048	The prescription of baclofen at the time of <b>withdrawal</b> was associated with higher serum <strong>BDNF</strong> levels throughout the follow up and that of anti inflammatory drugs with lower <strong>BDNF</strong> levels.
+BDNF	drug	alcohol	32081048	A link between <strong>BDNF</strong> levels, liver function, and the inflammatory state in the context of <b>alcohol</b> abuse and not only with <b>alcohol</b> dependence itself is proposed.
+BDNF	addiction	dependence	32081048	A link between <strong>BDNF</strong> levels, liver function, and the inflammatory state in the context of alcohol abuse and not only with alcohol <b>dependence</b> itself is proposed.
+BDNF	drug	alcohol	32063838	Activation of Melanocortin 4 Receptor Inhibits Both Neuroinflammation Induced by Early Exposure to <b>Ethanol</b> and Subsequent Voluntary <b>Alcohol</b> Intake in Adulthood in Animal Models: Is <strong>BDNF</strong> the Key Mediator?
+BDNF	drug	alcohol	32063838	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been implicated in <b>alcohol</b> drinking motivation, dependence and withdrawal, and its levels are reduced in <b>alcoholics</b>.
+BDNF	addiction	dependence	32063838	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been implicated in alcohol drinking motivation, <b>dependence</b> and withdrawal, and its levels are reduced in alcoholics.
+BDNF	addiction	withdrawal	32063838	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been implicated in alcohol drinking motivation, dependence and <b>withdrawal</b>, and its levels are reduced in alcoholics.
+BDNF	drug	alcohol	32063838	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been implicated in <b>alcohol</b> drinking motivation, dependence and withdrawal, and its levels are reduced in <b>alcoholics</b>.
+BDNF	addiction	dependence	32063838	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been implicated in alcohol drinking motivation, <b>dependence</b> and withdrawal, and its levels are reduced in alcoholics.
+BDNF	addiction	withdrawal	32063838	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been implicated in alcohol drinking motivation, dependence and <b>withdrawal</b>, and its levels are reduced in alcoholics.
+BDNF	drug	alcohol	32063838	Deficiencies in <strong>BDNF</strong> levels increased <b>ethanol</b> self administration in rats.
+BDNF	drug	alcohol	32063838	Further, <strong>BDNF</strong> triggers important anti inflammatory effects in the brain, and this could be one of the mechanisms by which <strong>BDNF</strong> reduces chronic <b>alcohol</b> intake.
+BDNF	drug	alcohol	32063838	We hypothesize that <b>ethanol</b> exposure during adolescence decreases the expression of α MSH and hence MC4R signaling in the hippocampus, leading to a lower <strong>BDNF</strong> activity that causes dramatic changes in the brain (e.g., neuroinflammation and decreased neurogenesis) that predispose to maintain <b>alcohol</b> abuse until adulthood.
+BDNF	drug	alcohol	32063838	The activation of MC4R either by α MSH or by synthetic agonist peptides can induce the expression of <strong>BDNF</strong>, which would trigger several processes that lead to lower <b>alcohol</b> consumption.
+BDNF	drug	alcohol	32001926	A review of peripheral <strong>brain derived neurotrophic factor</strong> levels in <b>alcohol</b> dependent patients: Current understanding.
+BDNF	drug	alcohol	32001926	Brain derived neurotrophic factor (<strong>BDNF</strong>) plays a crucial role in neuroplasticity of the brain, and its role in <b>alcohol</b> dependence has been explored in the recent past.
+BDNF	addiction	dependence	32001926	Brain derived neurotrophic factor (<strong>BDNF</strong>) plays a crucial role in neuroplasticity of the brain, and its role in alcohol <b>dependence</b> has been explored in the recent past.
+BDNF	drug	alcohol	32001926	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) plays a crucial role in neuroplasticity of the brain, and its role in <b>alcohol</b> dependence has been explored in the recent past.
+BDNF	addiction	dependence	32001926	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) plays a crucial role in neuroplasticity of the brain, and its role in alcohol <b>dependence</b> has been explored in the recent past.
+BDNF	drug	alcohol	32001926	Animal studies suggest that <strong>BDNF</strong> may function as a protective factor in transition from social drinking to an <b>alcohol</b> use disorder.
+BDNF	drug	alcohol	32001926	In order to obtain a comprehensive understanding, the current review aims to evaluate the existing literature on the role of <strong>BDNF</strong> in <b>alcohol</b> dependence.
+BDNF	addiction	dependence	32001926	In order to obtain a comprehensive understanding, the current review aims to evaluate the existing literature on the role of <strong>BDNF</strong> in alcohol <b>dependence</b>.
+BDNF	drug	alcohol	32001926	A total of 13 studies were found which compared <strong>BDNF</strong> levels in <b>alcohol</b> dependent patients with control population.
+BDNF	drug	alcohol	32001926	The current review supports the notion that <strong>BDNF</strong> plays an important role in the neuroplasticity of <b>alcohol</b> dependence.
+BDNF	addiction	dependence	32001926	The current review supports the notion that <strong>BDNF</strong> plays an important role in the neuroplasticity of alcohol <b>dependence</b>.
+BDNF	drug	alcohol	32001926	Future studies with longer follow ups, larger sample size, comparing early and late periods of <b>alcohol</b> abstinence are required for better understanding of the role <strong>BDNF</strong> in <b>alcohol</b> dependence.
+BDNF	addiction	dependence	32001926	Future studies with longer follow ups, larger sample size, comparing early and late periods of alcohol abstinence are required for better understanding of the role <strong>BDNF</strong> in alcohol <b>dependence</b>.
+BDNF	drug	alcohol	31874240	Remarkably, hippocampal levels of NMDA R2B were reduced only in <b>ethanol</b> exposed male, while total <strong>BDNF</strong> levels were increased in both male and female <b>ethanol</b> exposed mice.
+BDNF	drug	opioid	31838222	<b>Naloxone</b> precipitated withdrawal ameliorates impairment of cost benefit decision making in <b>morphine</b> treated rats: Involvement of <strong>BDNF</strong>, p GSK3 β, and p CREB in the amygdala.
+BDNF	addiction	withdrawal	31838222	Naloxone precipitated <b>withdrawal</b> ameliorates impairment of cost benefit decision making in morphine treated rats: Involvement of <strong>BDNF</strong>, p GSK3 β, and p CREB in the amygdala.
+BDNF	drug	opioid	31838222	Therefore, in the current study, we investigated the effect of subchronic exposure to <b>morphine</b> and its withdrawal on effort  and/or delay based forms of cost benefit decision making and alterations in p CREB/CREB ratio, p GSK3β/GSK3β ratio, and <strong>BDNF</strong> level during decision making in the amygdala.
+BDNF	addiction	withdrawal	31838222	Therefore, in the current study, we investigated the effect of subchronic exposure to morphine and its <b>withdrawal</b> on effort  and/or delay based forms of cost benefit decision making and alterations in p CREB/CREB ratio, p GSK3β/GSK3β ratio, and <strong>BDNF</strong> level during decision making in the amygdala.
+BDNF	drug	opioid	31838222	In <b>morphine</b> treated rats, level of <strong>BDNF</strong> and p CREB/CREB ratio reduced during both forms of decision making while p GSK3β/GSK3β ratio increased during delay based and did not have a significant difference with the control group during effort based decision making.
+BDNF	drug	opioid	31838222	On the withdrawal day, <strong>BDNF</strong> level raised while p GSK3β/GSK3β ratio attenuated compared to <b>morphine</b> treated group in both form of decision making.
+BDNF	addiction	withdrawal	31838222	On the <b>withdrawal</b> day, <strong>BDNF</strong> level raised while p GSK3β/GSK3β ratio attenuated compared to morphine treated group in both form of decision making.
+BDNF	drug	opioid	31838222	In conclusion, our data revealed that subchronic exposure to <b>morphine</b> interferes with the cost benefit decision making may be via changes in level of <strong>BDNF</strong>, p CREB/CREB and p GSK3β/GSK3β ratio in the amygdala.
+BDNF	drug	amphetamine	31830601	Effect of chronic <b>methamphetamine</b> injection on levels of <strong>BDNF</strong> mRNA and its CpG island methylation in prefrontal cortex of rats.
+BDNF	drug	amphetamine	31830601	Brain derived neurotrophic factor (<strong>BDNF</strong>), plays important roles in modulating different aspects of addiction, and is implicated in psychiatric conditions reminiscent of those suffered by <b>METH</b> abusers.
+BDNF	addiction	addiction	31830601	Brain derived neurotrophic factor (<strong>BDNF</strong>), plays important roles in modulating different aspects of <b>addiction</b>, and is implicated in psychiatric conditions reminiscent of those suffered by METH abusers.
+BDNF	drug	amphetamine	31830601	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), plays important roles in modulating different aspects of addiction, and is implicated in psychiatric conditions reminiscent of those suffered by <b>METH</b> abusers.
+BDNF	addiction	addiction	31830601	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), plays important roles in modulating different aspects of <b>addiction</b>, and is implicated in psychiatric conditions reminiscent of those suffered by METH abusers.
+BDNF	drug	amphetamine	31830601	The relative expression of <strong>BDNF</strong> IV in <b>METH</b> treated group was 2.15 fold higher than the control group.
+BDNF	drug	psychedelics	31829932	We will show that although <b>ketamine</b> and serotonergic <b>psychedelics</b> have affinity for very different receptors (NMDA, 5 HT2A), they ultimately initiate similar plastic adaptations in the prefrontal cortex through the involvement of the brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	psychedelics	31829932	We will show that although <b>ketamine</b> and serotonergic <b>psychedelics</b> have affinity for very different receptors (NMDA, 5 HT2A), they ultimately initiate similar plastic adaptations in the prefrontal cortex through the involvement of the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	psychedelics	31829932	We will see that although <b>MDMA</b> uses the same receptors as serotonergic <b>psychedelics</b> to alleviate PTSD symptoms, its effect on <strong>BDNF</strong> levels seem paradoxical and quite different.
+BDNF	drug	cocaine	31826099	Effects of childhood trauma on <strong>BDNF</strong> and TBARS during crack <b>cocaine</b> withdrawal.
+BDNF	addiction	withdrawal	31826099	Effects of childhood trauma on <strong>BDNF</strong> and TBARS during crack cocaine <b>withdrawal</b>.
+BDNF	drug	cocaine	31826099	To evaluate the association between childhood trauma (CT) and serum levels of brain derived neurotrophic factor (<strong>BDNF</strong>) and thiobarbituric acid reactive substances (TBARS) during crack <b>cocaine</b> withdrawal.
+BDNF	addiction	withdrawal	31826099	To evaluate the association between childhood trauma (CT) and serum levels of brain derived neurotrophic factor (<strong>BDNF</strong>) and thiobarbituric acid reactive substances (TBARS) during crack cocaine <b>withdrawal</b>.
+BDNF	drug	cocaine	31826099	To evaluate the association between childhood trauma (CT) and serum levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and thiobarbituric acid reactive substances (TBARS) during crack <b>cocaine</b> withdrawal.
+BDNF	addiction	withdrawal	31826099	To evaluate the association between childhood trauma (CT) and serum levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and thiobarbituric acid reactive substances (TBARS) during crack cocaine <b>withdrawal</b>.
+BDNF	drug	amphetamine	31822818	Chronic <b>methamphetamine</b> interacts with <strong>BDNF</strong> Val66Met to remodel psychosis pathways in the mesocorticolimbic proteome.
+BDNF	drug	amphetamine	31822818	Brain derived neurotrophic factor (<strong>BDNF</strong>) is implicated in both <b>Meth</b> effects and schizophrenia.
+BDNF	drug	amphetamine	31822818	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is implicated in both <b>Meth</b> effects and schizophrenia.
+BDNF	drug	amphetamine	31822818	<b>Meth</b> differentially altered dopamine signaling markers (e.g., Dat, Comt, and Th) between hBDNFVal/Val and hBDNFMet/Met mice, implicating involvement of <strong>BDNF</strong> in <b>Meth</b> induced reprogramming of the mesolimbic proteome.
+BDNF	drug	amphetamine	31822818	In addition, these data reveal that long term <b>Meth</b> induced brain changes are strongly dependent upon <strong>BDNF</strong> genetic variation, illustrating how drug induced psychosis may be modulated at the molecular level by a single genetic locus.
+BDNF	drug	cannabinoid	31779002	<strong>Brain Derived Neurotrophic Factor</strong> and Oxidative Stress in <b>Cannabis</b> Dependence.
+BDNF	addiction	dependence	31779002	<strong>Brain Derived Neurotrophic Factor</strong> and Oxidative Stress in Cannabis <b>Dependence</b>.
+BDNF	drug	cannabinoid	31779002	We found significantly increased <strong>BDNF</strong>, ceruloplasmin, and lipid hydroperoxide, and decreased free thiol levels in patients with <b>cannabis</b> dependence.
+BDNF	addiction	dependence	31779002	We found significantly increased <strong>BDNF</strong>, ceruloplasmin, and lipid hydroperoxide, and decreased free thiol levels in patients with cannabis <b>dependence</b>.
+BDNF	addiction	addiction	31779002	Increased <strong>BDNF</strong> might be a sign of impaired neuronal plasticity that is crucial for memory formation and adaptive response to drug <b>addiction</b>.
+BDNF	drug	cannabinoid	31779002	In conclusion, <b>cannabis</b> dependency alters <strong>BDNF</strong> levels and increases oxidative stress.
+BDNF	drug	opioid	31773433	Impact of different intensities of forced exercise on deficits of spatial and aversive memory, anxiety like behavior, and hippocampal <strong>BDNF</strong> during <b>morphine</b> abstinence period in male rats.
+BDNF	addiction	aversion	31773433	Impact of different intensities of forced exercise on deficits of spatial and <b>aversive</b> memory, anxiety like behavior, and hippocampal <strong>BDNF</strong> during morphine abstinence period in male rats.
+BDNF	drug	opioid	31773433	Forced exercise at a moderate intensity alleviated anxiety, cognitive and <strong>BDNF</strong> defects in <b>morphine</b> abstinent animals.
+BDNF	drug	nicotine	31752015	Cognitive rigidity and <strong>BDNF</strong> mediated frontostriatal glutamate neuroadaptations during spontaneous <b>nicotine</b> withdrawal.
+BDNF	addiction	withdrawal	31752015	Cognitive rigidity and <strong>BDNF</strong> mediated frontostriatal glutamate neuroadaptations during spontaneous nicotine <b>withdrawal</b>.
+BDNF	drug	nicotine	31752015	Because frontostriatal circuits are critical for cognitive flexibility and brain derived neurotrophic factor (<strong>BDNF</strong>) modulates glutamate plasticity in these circuits, we also explored the effects of <b>nicotine</b> withdrawal on these neurochemical substrates.
+BDNF	addiction	withdrawal	31752015	Because frontostriatal circuits are critical for cognitive flexibility and brain derived neurotrophic factor (<strong>BDNF</strong>) modulates glutamate plasticity in these circuits, we also explored the effects of nicotine <b>withdrawal</b> on these neurochemical substrates.
+BDNF	drug	nicotine	31752015	Because frontostriatal circuits are critical for cognitive flexibility and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) modulates glutamate plasticity in these circuits, we also explored the effects of <b>nicotine</b> withdrawal on these neurochemical substrates.
+BDNF	addiction	withdrawal	31752015	Because frontostriatal circuits are critical for cognitive flexibility and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) modulates glutamate plasticity in these circuits, we also explored the effects of nicotine <b>withdrawal</b> on these neurochemical substrates.
+BDNF	drug	nicotine	31752015	<strong>BDNF</strong> mRNA expression increased in the medial prefrontal cortex (mPFC) following <b>nicotine</b> withdrawal.
+BDNF	addiction	withdrawal	31752015	<strong>BDNF</strong> mRNA expression increased in the medial prefrontal cortex (mPFC) following nicotine <b>withdrawal</b>.
+BDNF	addiction	withdrawal	31752015	DS <strong>BDNF</strong> protein positively correlated with perseverative and maintenance errors, suggesting mPFC DS overflow of <strong>BDNF</strong> during <b>withdrawal</b>.
+BDNF	drug	nicotine	31752015	Taken together, these data suggest that spontaneous <b>nicotine</b> withdrawal impairs distinct components of cognitive set shifting and these deficits may be linked to <strong>BDNF</strong> mediated alterations in glutamate signaling dynamics in discrete frontostriatal circuits.
+BDNF	addiction	withdrawal	31752015	Taken together, these data suggest that spontaneous nicotine <b>withdrawal</b> impairs distinct components of cognitive set shifting and these deficits may be linked to <strong>BDNF</strong> mediated alterations in glutamate signaling dynamics in discrete frontostriatal circuits.
+BDNF	drug	alcohol	31740576	Infusion of miR 137 antagomir directly into the central nucleus of the amygdala (CeA) rescues AIE induced <b>alcohol</b> drinking and anxiety like behaviors via normalization of decreased Lsd1 expression, decreased LSD1 occupancy, and decreased <strong>Bdnf</strong> IV expression due to increased H3K9 dimethylation in AIE adult rats.
+BDNF	drug	alcohol	31722379	Preclinical studies suggest that decreased levels of <strong>brain derived neurotrophic factor</strong> in the amygdala play a role in anxiety and <b>alcohol</b> use disorder.
+BDNF	drug	alcohol	31722379	The association between <strong>brain derived neurotrophic factor</strong> levels and amygdala function in humans with <b>alcohol</b> use disorder is still unclear, although neuroimaging studies have also implicated the amygdala in <b>alcohol</b> use disorder and suggest that <b>alcohol</b> use disorder is associated with disrupted functional connectivity between the amygdala and prefrontal cortex during aversive states.
+BDNF	addiction	aversion	31722379	The association between <strong>brain derived neurotrophic factor</strong> levels and amygdala function in humans with alcohol use disorder is still unclear, although neuroimaging studies have also implicated the amygdala in alcohol use disorder and suggest that alcohol use disorder is associated with disrupted functional connectivity between the amygdala and prefrontal cortex during <b>aversive</b> states.
+BDNF	drug	alcohol	31722379	The current study investigated whether plasma <strong>brain derived neurotrophic factor</strong> levels in individuals with and without <b>alcohol</b> use disorder (n = 57) were associated with individual differences in amygdala reactivity and amygdala prefrontal cortex functional connectivity during 2 forms of aversive responding captured via functional magnetic resonance imaging: anxiety elicited by unpredictable threat of shock and fear elicited by predictable threat of shock.
+BDNF	addiction	aversion	31722379	The current study investigated whether plasma <strong>brain derived neurotrophic factor</strong> levels in individuals with and without alcohol use disorder (n = 57) were associated with individual differences in amygdala reactivity and amygdala prefrontal cortex functional connectivity during 2 forms of <b>aversive</b> responding captured via functional magnetic resonance imaging: anxiety elicited by unpredictable threat of shock and fear elicited by predictable threat of shock.
+BDNF	drug	alcohol	31722379	We also examined whether <strong>brain derived neurotrophic factor</strong> and brain function were associated with binge drinking episodes and <b>alcohol</b> use disorder age of onset.
+BDNF	addiction	intoxication	31722379	We also examined whether <strong>brain derived neurotrophic factor</strong> and brain function were associated with <b>binge</b> drinking episodes and alcohol use disorder age of onset.
+BDNF	drug	alcohol	31722379	In addition, within individuals with <b>alcohol</b> use disorder (only), lower levels of <strong>brain derived neurotrophic factor</strong> and amygdala medial prefrontal cortex functional connectivity during anxiety were associated with more binge episodes within the past 60 days and a lower age of <b>alcohol</b> use disorder onset.
+BDNF	addiction	intoxication	31722379	In addition, within individuals with alcohol use disorder (only), lower levels of <strong>brain derived neurotrophic factor</strong> and amygdala medial prefrontal cortex functional connectivity during anxiety were associated with more <b>binge</b> episodes within the past 60 days and a lower age of alcohol use disorder onset.
+BDNF	drug	alcohol	31721205	Co administration of <b>ethanol</b> and nicotine heightens sensitivity to <b>ethanol</b> reward within the nucleus accumbens (NAc) shell and increasing NAc shell <strong>BDNF</strong> is sufficient to enhance <b>ethanol</b> reward in naïve Wistar rats.
+BDNF	drug	nicotine	31721205	Co administration of ethanol and <b>nicotine</b> heightens sensitivity to ethanol reward within the nucleus accumbens (NAc) shell and increasing NAc shell <strong>BDNF</strong> is sufficient to enhance ethanol reward in naïve Wistar rats.
+BDNF	addiction	reward	31721205	Co administration of ethanol and nicotine heightens sensitivity to ethanol <b>reward</b> within the nucleus accumbens (NAc) shell and increasing NAc shell <strong>BDNF</strong> is sufficient to enhance ethanol <b>reward</b> in naïve Wistar rats.
+BDNF	addiction	reward	31721205	The concluding experiment evaluated the effect of NAc shell pretreatment with <strong>BDNF</strong> on EtOH <b>reward</b> utilizing ICSA within that region.
+BDNF	addiction	reward	31721205	<strong>BDNF</strong> pretreatment in the NAc shell was also sufficient to enhance the <b>reinforcing</b> properties of EtOH in the NAc shell.
+BDNF	drug	nicotine	31694445	<strong>BDNF</strong> closely followed the behavioral results: CGS 21680 alleviated the enhancement in NAcc <strong>BDNF</strong> in NQ treated animals, and eliminated the increase in NAcc <strong>BDNF</strong> produced by <b>nicotine</b> in controls.
+BDNF	addiction	reward	31694445	Both <strong>BDNF</strong> and GDNF correlated with <b>CPP</b> performance.
+BDNF	drug	amphetamine	31693929	Time and region dependent manner of increased <strong>brain derived neurotrophic factor</strong> and TrkB in rat brain after binge like <b>methamphetamine</b> exposure.
+BDNF	addiction	intoxication	31693929	Time and region dependent manner of increased <strong>brain derived neurotrophic factor</strong> and TrkB in rat brain after <b>binge</b> like methamphetamine exposure.
+BDNF	addiction	intoxication	31693929	This study investigated the effect of <b>binge</b> like MA dosing (4 x 4 mg/kg, s.c., 2 h (h) apart) at a range of different time points (from 2 h to 7 days after treatment) on brain derived neurotrophic factor (<strong>BDNF</strong>) levels and its receptors, TrkB and p75NTR.
+BDNF	addiction	intoxication	31693929	This study investigated the effect of <b>binge</b> like MA dosing (4 x 4 mg/kg, s.c., 2 h (h) apart) at a range of different time points (from 2 h to 7 days after treatment) on <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels and its receptors, TrkB and p75NTR.
+BDNF	addiction	intoxication	31693929	In the striatum, <strong>BDNF</strong> expression was increased at 12 and 24 h after <b>binge</b> like MA treatment and had returned to normal at 36 h. Increased expression of the TrkB receptor was observed in the frontal cortex at 2, 24 and 48 h after MA treatment and in the striatum at 24 and 48 h after the MA regimen.
+BDNF	addiction	intoxication	31693929	These findings show that the <b>binge</b> like regimen of MA affects expression of <strong>BDNF</strong> and its receptors, particularly the TrkB receptor, in a time and region dependent manner, and highlights the importance of the frontal cortex and the striatum in the response following MA <b>binge</b> like dosing.
+BDNF	drug	opioid	31666179	corticotropin releasing hormone (CRH), <b>opioids</b>, brain derived neurotrophic factor (<strong>BDNF</strong>), and the adrenal glucocorticoids.
+BDNF	drug	opioid	31666179	corticotropin releasing hormone (CRH), <b>opioids</b>, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), and the adrenal glucocorticoids.
+BDNF	drug	psychedelics	31634774	In order to substantiate the '<b>psilocybin</b> telomere hypothesis' potential neuropsychopharmacological, endocrinological, and genetic mechanisms of action are discussed (e.g., HPA axis reactivity, hippocampal neurogenesis, neurotropic growth factors such as <strong>BDNF</strong>, 5 HT2A receptor agonism, neuroplasticity/synaptoplasticity, brain wide alterations in neuronal functional connectivity density, involvement of the SLC6A4 serotonin transporter gene, inter alia).
+BDNF	drug	alcohol	31625062	Selank, Peptide Analogue of Tuftsin, Protects Against <b>Ethanol</b> Induced Memory Impairment by Regulating of <strong>BDNF</strong> Content in the Hippocampus and Prefrontal Cortex in Rats.
+BDNF	drug	alcohol	31625062	The effects of a peptide anxiolytic Selank synthesized on the basis of the endogenous peptide tuftsin on memory impairment and content of brain derived neurotrophic factor (<strong>BDNF</strong>) in brain structures were analyzed in outbred rats receiving 10% <b>ethanol</b> as the only source of fluid for 30 weeks.
+BDNF	drug	alcohol	31625062	The effects of a peptide anxiolytic Selank synthesized on the basis of the endogenous peptide tuftsin on memory impairment and content of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in brain structures were analyzed in outbred rats receiving 10% <b>ethanol</b> as the only source of fluid for 30 weeks.
+BDNF	drug	alcohol	31625062	In ex vivo experiments, Selank prevented <b>ethanol</b> induced increase in <strong>BDNF</strong> content in the hippocampus and frontal cortex (p<0.05).
+BDNF	drug	alcohol	31625062	These results indicate positive effects of the tuftsin analogue on age related memory disturbances associated with chronic <b>alcohol</b> intoxication and confirm the involvement of the neurotrophin mechanism related to <strong>BDNF</strong> production into the effect of Selank.
+BDNF	addiction	intoxication	31625062	These results indicate positive effects of the tuftsin analogue on age related memory disturbances associated with chronic alcohol <b>intoxication</b> and confirm the involvement of the neurotrophin mechanism related to <strong>BDNF</strong> production into the effect of Selank.
+BDNF	drug	opioid	31609135	Moreover, we conclude that altered <strong>BDNF</strong> levels and HPA axis activity may be the mechanisms involved in the effects of FR on <b>morphine</b> induced behavior.
+BDNF	drug	cocaine	31606593	Deletion of the serotonin transporter perturbs <strong>BDNF</strong> signaling in the central amygdala following long access <b>cocaine</b> self administration.
+BDNF	drug	cocaine	31606593	One key plasticity factor that modulates effects of <b>cocaine</b> on the brain is Brain Derived Neurotrophic Factor (<strong>BDNF</strong>).
+BDNF	drug	cocaine	31606593	One key plasticity factor that modulates effects of <b>cocaine</b> on the brain is <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	cocaine	31606593	A wealth of evidence shows that <b>cocaine</b> exposure alters <strong>BDNF</strong> signaling in corticolimbic structures, but, surprisingly, such evidence is very limited for the amygdala.
+BDNF	drug	cocaine	31606593	Additionally, while <strong>BDNF</strong> is strongly regulated by serotonin levels and inherited serotonin transporter down regulation is associated with increased vulnerability to <b>cocaine</b> addiction, the effects of serotonin transporter genotype on <strong>BDNF</strong> signaling in the amygdala under naïve and <b>cocaine</b> exposure conditions are unknown.
+BDNF	addiction	addiction	31606593	Additionally, while <strong>BDNF</strong> is strongly regulated by serotonin levels and inherited serotonin transporter down regulation is associated with increased vulnerability to cocaine <b>addiction</b>, the effects of serotonin transporter genotype on <strong>BDNF</strong> signaling in the amygdala under naïve and cocaine exposure conditions are unknown.
+BDNF	drug	cocaine	31606593	We measured <strong>BDNF</strong> signaling in the central amygdala of wild type and serotonin transporter knockout rats 24 h into withdrawal from long access <b>cocaine</b> self administration.
+BDNF	addiction	withdrawal	31606593	We measured <strong>BDNF</strong> signaling in the central amygdala of wild type and serotonin transporter knockout rats 24 h into <b>withdrawal</b> from long access cocaine self administration.
+BDNF	drug	cocaine	31606593	Interestingly, <b>cocaine</b> exposed serotonin transporter knockout rats showed increased <strong>BDNF</strong> levels, with no signs of phospho TrkB receptor coupling to phospho Akt and phospho ERK1.
+BDNF	drug	cocaine	31606593	Long access <b>cocaine</b> self administration dysregulates <strong>BDNF</strong> signaling in the central amygdala.
+BDNF	drug	alcohol	31518024	Compared to mice transplanted with fecal microbiota from healthy male adults, the mice accepting fecal microbiota from patients with <b>alcoholism</b> showed (a) anxiety like and depression like behaviors, (b) decreased social interaction behaviors, (c) spontaneous <b>alcohol</b> preference, and (d) decreased brain derived neurotrophic factor (<strong>BDNF</strong>), alpha 1 subunit of GABA type A receptor (α1GABAA R) in mPFC and decreased metabotropic glutamate receptors 1 (mGluR1), protein kinase C (PKC) ε in NAc.
+BDNF	drug	alcohol	31518024	Compared to mice transplanted with fecal microbiota from healthy male adults, the mice accepting fecal microbiota from patients with <b>alcoholism</b> showed (a) anxiety like and depression like behaviors, (b) decreased social interaction behaviors, (c) spontaneous <b>alcohol</b> preference, and (d) decreased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), alpha 1 subunit of GABA type A receptor (α1GABAA R) in mPFC and decreased metabotropic glutamate receptors 1 (mGluR1), protein kinase C (PKC) ε in NAc.
+BDNF	drug	psychedelics	31473552	Vinpocetine is a nootropic phosphodiesterase 1 (PDE 1) inhibitor that can reverse <b>ketamine</b> induced schizophrenia like deficits by increasing <strong>BDNF</strong> expression.
+BDNF	drug	psychedelics	31473552	<b>Ketamine</b> induced drastic schizophrenia like behaviors, lower protein levels of <strong>BDNF</strong> and PSD 95, and a change in the synaptic ultrastructure in the PCC.
+BDNF	drug	psychedelics	31473552	Vinpocetine can reverse the synaptic ultrastructure by regulating <strong>BDNF</strong> related PSD 95 to alleviate schizophrenia like deficits induced by <b>ketamine</b> in rats.
+BDNF	drug	opioid	31454827	Studies in primary cortical cultures show that d <b>methadone</b> also increases <strong>BDNF</strong> release, as well as phospho p70S6 kinase.
+BDNF	drug	cocaine	31417375	Infralimbic Estradiol Enhances Neuronal Excitability and Facilitates Extinction of <b>Cocaine</b> Seeking in Female Rats via a <strong>BDNF</strong>/TrkB Mechanism.
+BDNF	addiction	relapse	31417375	Infralimbic Estradiol Enhances Neuronal Excitability and Facilitates Extinction of Cocaine <b>Seeking</b> in Female Rats via a <strong>BDNF</strong>/TrkB Mechanism.
+BDNF	drug	cocaine	31417375	Our findings suggest that pharmacological enhancement of E2 or <strong>BDNF</strong>/TrkB signaling during extinction based therapies would improve therapeutic outcome in <b>cocaine</b> addicted women.
+BDNF	drug	opioid	31376054	NGF, <strong>BDNF</strong> and Arc mRNA Expression in the Hippocampus of Rats After Administration of <b>Morphine</b>.
+BDNF	drug	opioid	31376054	<b>Morphine</b> can influence immediate early genes (IEG) of activity regulated cytoskeletal associated protein (Arc) and brain derived neurotrophic factor (<strong>BDNF</strong>) which are activated in response to physiological stimuli during learning, as well as the nerve growth factor (NGF) gene which increases the expression of several IEGs for memory formation.
+BDNF	drug	opioid	31376054	<b>Morphine</b> can influence immediate early genes (IEG) of activity regulated cytoskeletal associated protein (Arc) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) which are activated in response to physiological stimuli during learning, as well as the nerve growth factor (NGF) gene which increases the expression of several IEGs for memory formation.
+BDNF	drug	opioid	31376054	The purpose of the current study was first to evaluate the effect of acute (1 day) and subchronic (15 days) <b>morphine</b> administration on memory retrieval of rats and second to determine the hippocampal expression of NGF, <strong>BDNF</strong> and Arc genes as potential contributors in the observed effects in each setting.
+BDNF	drug	opioid	31376054	We did not detect a significant change in the hippocampal expression of Arc, <strong>BDNF</strong> or NGF genes after a single episode of <b>morphine</b> treatment.
+BDNF	drug	opioid	31376054	However, subchronic <b>morphine</b> administration (15 and 20 mg/kg) increased the expression of Arc and <strong>BDNF</strong> genes in a dose dependent manner.
+BDNF	drug	alcohol	31374324	In the present study, we aimed to investigate whether URB597, an inhibitor of the metabolic enzyme of the endocannabinoid anandamide (AEA), altered the effects of acute and chronic <b>alcohol</b> administration beginning during rat adolescence on recognition memory, neuroinflammation and brain derived neurotrophic factor (<strong>BDNF</strong>) levels.
+BDNF	drug	cannabinoid	31374324	In the present study, we aimed to investigate whether URB597, an inhibitor of the metabolic enzyme of the <b>endocannabinoid</b> anandamide (AEA), altered the effects of acute and chronic alcohol administration beginning during rat adolescence on recognition memory, neuroinflammation and brain derived neurotrophic factor (<strong>BDNF</strong>) levels.
+BDNF	drug	alcohol	31374324	In the present study, we aimed to investigate whether URB597, an inhibitor of the metabolic enzyme of the endocannabinoid anandamide (AEA), altered the effects of acute and chronic <b>alcohol</b> administration beginning during rat adolescence on recognition memory, neuroinflammation and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels.
+BDNF	drug	cannabinoid	31374324	In the present study, we aimed to investigate whether URB597, an inhibitor of the metabolic enzyme of the <b>endocannabinoid</b> anandamide (AEA), altered the effects of acute and chronic alcohol administration beginning during rat adolescence on recognition memory, neuroinflammation and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels.
+BDNF	drug	alcohol	31374324	The chronic binge <b>alcohol</b> administration increased the interferon (IFN) γ and tumor necrosis factor (TNF) α levels in the PFC and hippocampus and the interleukin (IL) 10 and <strong>BDNF</strong> levels in the PFC, and these effects were prevented by URB597.
+BDNF	addiction	intoxication	31374324	The chronic <b>binge</b> alcohol administration increased the interferon (IFN) γ and tumor necrosis factor (TNF) α levels in the PFC and hippocampus and the interleukin (IL) 10 and <strong>BDNF</strong> levels in the PFC, and these effects were prevented by URB597.
+BDNF	drug	cocaine	31364211	<b>Cocaine</b> significantly increased the binding of phosphorylated BRD4 (pBRD4) at the promoter of Gria2 and <strong>Bdnf</strong> genes in the NAc.
+BDNF	drug	cocaine	31364211	(+)JQ1, a selective BRD4 inhibitor, markedly reduced the reinforcement and reinstatement of <b>cocaine</b> seeking behaviors, which was accompanied by the decreased expressions of GRIA2 and <strong>BDNF</strong>.
+BDNF	addiction	relapse	31364211	(+)JQ1, a selective BRD4 inhibitor, markedly reduced the reinforcement and <b>reinstatement</b> of cocaine <b>seeking</b> behaviors, which was accompanied by the decreased expressions of GRIA2 and <strong>BDNF</strong>.
+BDNF	addiction	reward	31364211	(+)JQ1, a selective BRD4 inhibitor, markedly reduced the <b>reinforcement</b> and reinstatement of cocaine seeking behaviors, which was accompanied by the decreased expressions of GRIA2 and <strong>BDNF</strong>.
+BDNF	drug	cocaine	31364211	Furthermore, chromatin immunoprecipitation assay showed that (+)JQ1 clearly attenuated <b>cocaine</b> enhanced binding of pBRD4 at the promotor of Gria2 and <strong>Bdnf</strong> genes.
+BDNF	drug	nicotine	31316930	Expressions of <strong>brain derived neurotrophic factor</strong> and tyrosine kinase B (TrkB) were decreased in the <b>nicotine</b> withdrawal rats, in contrast, treadmill running increased <strong>brain derived neurotrophic factor</strong> and TrkB expressions.
+BDNF	addiction	withdrawal	31316930	Expressions of <strong>brain derived neurotrophic factor</strong> and tyrosine kinase B (TrkB) were decreased in the nicotine <b>withdrawal</b> rats, in contrast, treadmill running increased <strong>brain derived neurotrophic factor</strong> and TrkB expressions.
+BDNF	drug	nicotine	31315660	Additionally, brain derived neurotrophic factor (<strong>BDNF</strong>) levels can be altered significantly after repeated <b>nicotine</b> exposure, suggesting a potential mechanism contributing to <b>nicotine</b> induced behavioral phenotypes.
+BDNF	drug	nicotine	31315660	Additionally, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels can be altered significantly after repeated <b>nicotine</b> exposure, suggesting a potential mechanism contributing to <b>nicotine</b> induced behavioral phenotypes.
+BDNF	drug	nicotine	31315660	The present study investigated the role of sex on <b>nicotine</b> induced changes to stimulus response behavior and associated <strong>BDNF</strong> protein levels.
+BDNF	drug	nicotine	31315660	In contrast to prior studies, neither repeated exposure to <b>nicotine</b> nor sex significantly affected <strong>BDNF</strong> expression.
+BDNF	drug	nicotine	31315660	Further, non significant changes to <strong>BDNF</strong> expression in brain regions highly associated with PCA indicate that <strong>BDNF</strong> is unlikely to drive <b>nicotine</b> enhanced conditioned behavior.
+BDNF	drug	alcohol	31294671	Early <b>alcohol</b> exposure produces a decrease in <strong>BDNF</strong> levels in the hippocampus (HPC) and prefrontal cortex, a reduction of neurogenesis in the DG and increased activity levels of the HDAC4 in the HPC.
+BDNF	drug	opioid	31282111	Conditioned aversive memory associated with <b>morphine</b> withdrawal increases <strong>brain derived neurotrophic factor</strong> in dentate gyrus and basolateral amygdala.
+BDNF	addiction	aversion	31282111	Conditioned <b>aversive</b> memory associated with morphine withdrawal increases <strong>brain derived neurotrophic factor</strong> in dentate gyrus and basolateral amygdala.
+BDNF	addiction	withdrawal	31282111	Conditioned aversive memory associated with morphine <b>withdrawal</b> increases <strong>brain derived neurotrophic factor</strong> in dentate gyrus and basolateral amygdala.
+BDNF	drug	opioid	31282111	<b>Morphine</b> has been shown to increase the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in the brain.
+BDNF	drug	opioid	31282111	<b>Morphine</b> has been shown to increase the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the brain.
+BDNF	drug	opioid	31282111	However, little is known about the effect of conditioned <b>naloxone</b> precipitated <b>morphine</b> withdrawal on <strong>BDNF</strong> and its precursor protein, proBDNF.
+BDNF	addiction	withdrawal	31282111	However, little is known about the effect of conditioned naloxone precipitated morphine <b>withdrawal</b> on <strong>BDNF</strong> and its precursor protein, proBDNF.
+BDNF	addiction	aversion	31282111	We used the conditioned place <b>aversion</b> (CPA) paradigm to evaluate the role of corticotropin releasing factor (CRF)/CRF1 receptor signaling on the <strong>BDNF</strong> expression and corticosterone plasma levels after CPA expression and extinction.
+BDNF	drug	opioid	31282111	Mice subjected to conditioned <b>naloxone</b> induced <b>morphine</b> withdrawal showed an increased expression of <strong>BDNF</strong> (in DG and BLA) in parallel with an enhancement of corticosterone plasma levels.
+BDNF	addiction	withdrawal	31282111	Mice subjected to conditioned naloxone induced morphine <b>withdrawal</b> showed an increased expression of <strong>BDNF</strong> (in DG and BLA) in parallel with an enhancement of corticosterone plasma levels.
+BDNF	addiction	aversion	31282111	These results demonstrated that <strong>BDNF</strong> expression together with the increased activity of hypothalamic pituitary adrenocortical (HPA) axis are critical to the acquisition of <b>aversive</b> memory.
+BDNF	addiction	aversion	31282111	However, we have observed a decrease in corticosterone plasma levels and <strong>BDNF</strong> expression after CPA extinction reaffirming the importance of <strong>BDNF</strong> in the maintenance of <b>aversive</b> memory.
+BDNF	drug	opioid	31282111	In addition, the pre treatment with the CRF1 receptor antagonist CP 154 526 before <b>naloxone</b> conditioning session impaired <b>morphine</b> withdrawal induced aversive memory acquisition, the increased corticosterone plasma levels, and the expression of <strong>BDNF</strong> observed after CPA expression in the DG and BLA.
+BDNF	addiction	aversion	31282111	In addition, the pre treatment with the CRF1 receptor antagonist CP 154 526 before naloxone conditioning session impaired morphine withdrawal induced <b>aversive</b> memory acquisition, the increased corticosterone plasma levels, and the expression of <strong>BDNF</strong> observed after CPA expression in the DG and BLA.
+BDNF	addiction	withdrawal	31282111	In addition, the pre treatment with the CRF1 receptor antagonist CP 154 526 before naloxone conditioning session impaired morphine <b>withdrawal</b> induced aversive memory acquisition, the increased corticosterone plasma levels, and the expression of <strong>BDNF</strong> observed after CPA expression in the DG and BLA.
+BDNF	addiction	aversion	31282111	Altogether, present results are suggesting a clear connection between HPA axis and <strong>BDNF</strong> in the formation and extinction of <b>aversive</b> memory.
+BDNF	drug	alcohol	31229451	Treatment with the DNMT inhibitor 5 azacytidine (5 azaC) at adulthood normalizes the AIE induced DNA hypermethylation of Npy and <strong>Bdnf</strong> exon IV with concomitant reversal of AIE induced anxiety like and <b>alcohol</b> drinking behaviors.
+BDNF	drug	psychedelics	31218603	We believe that <b>MDMA</b> acts by stimulating neurotrophin/trkB systems in the orbitofrontal cortex (OFC), a region involved in prospectively evaluating the consequences of one's action, because 1) <b>MDMA</b> also increased brain derived neurotrophic factor (<strong>BDNF</strong>) in the OFC, 2) <b>MDMA</b> corrected habit biases due to <strong>Bdnf</strong> loss in the OFC, and 3) overexpression of a truncated isoform of trkB occluded the memory enhancing effects of <b>MDMA</b>.
+BDNF	drug	psychedelics	31218603	We believe that <b>MDMA</b> acts by stimulating neurotrophin/trkB systems in the orbitofrontal cortex (OFC), a region involved in prospectively evaluating the consequences of one's action, because 1) <b>MDMA</b> also increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the OFC, 2) <b>MDMA</b> corrected habit biases due to <strong>Bdnf</strong> loss in the OFC, and 3) overexpression of a truncated isoform of trkB occluded the memory enhancing effects of <b>MDMA</b>.
+BDNF	drug	cocaine	31218603	Thus, selecting actions based on their consequences requires <strong>BDNF</strong> trkB in the OFC, the stimulation of which may improve goal attainment in both drug naïve and <b>cocaine</b> exposed individuals.
+BDNF	drug	nicotine	31208140	Interactions of Glutamatergic Neurotransmission and <strong>Brain Derived Neurotrophic Factor</strong> in the Regulation of Behaviors after <b>Nicotine</b> Administration.
+BDNF	drug	nicotine	31208140	In parallel with glutamate increases, <b>nicotine</b> exposure elevates brain derived neurotrophic factor (<strong>BDNF</strong>) release through anterograde and retrograde targeting of the synapses of glutamatergic terminals and GABAergic neurons.
+BDNF	drug	nicotine	31208140	In parallel with glutamate increases, <b>nicotine</b> exposure elevates <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) release through anterograde and retrograde targeting of the synapses of glutamatergic terminals and GABAergic neurons.
+BDNF	drug	nicotine	31208140	This article reviews <b>nicotine</b> exposure induced elevations of glutamatergic neurotransmission, the bidirectional targeting of <strong>BDNF</strong> in the striatum, and the potential regulatory role played by <strong>BDNF</strong> in behavioral responses to <b>nicotine</b> exposure.
+BDNF	drug	cocaine	31206907	Hippocampal <strong>BDNF</strong> regulates a shift from flexible, goal directed to habit memory system function following <b>cocaine</b> abstinence.
+BDNF	drug	cocaine	31206907	Using viral mediated gene transfer, we overexpressed <strong>BDNF</strong> in the dHPC during <b>cocaine</b> abstinence and new maze learning.
+BDNF	drug	nicotine	31193084	In our study, we explored the role of <strong>BDNF</strong>, Wnt/β catenin and Shh signalling in depression and the involvement of these signalling pathways in providing an antidepressant effect by <b>nicotine</b>.
+BDNF	addiction	relapse	31161451	We propose that exercise, by upregulating dorsal medial prefrontal cortex (dmPFC) nucleus accumbens (NAc) transmission, offsets deficits in pathways targeting glutamate, <strong>BDNF</strong>, and dopamine during early abstinence, and in doing so, normalizes neuroadaptations that underlie <b>relapse</b>.
+BDNF	drug	cocaine	31161451	Exercise initiated during early, but not late abstinence, reduced <b>cocaine</b> seeking; this effect was strongly associated with dmPFC Grm5 expression (gene encoding mGlu5), and modestly associated with dmPFC Grin1 and <strong>Bdnf</strong> IV expression.
+BDNF	addiction	relapse	31161451	Exercise initiated during early, but not late abstinence, reduced cocaine <b>seeking</b>; this effect was strongly associated with dmPFC Grm5 expression (gene encoding mGlu5), and modestly associated with dmPFC Grin1 and <strong>Bdnf</strong> IV expression.
+BDNF	drug	alcohol	31156431	Reduced <b>Alcohol</b> Seeking and Withdrawal Symptoms in Mice Lacking the <strong>BDNF</strong> Receptor SorCS2.
+BDNF	addiction	relapse	31156431	Reduced Alcohol <b>Seeking</b> and Withdrawal Symptoms in Mice Lacking the <strong>BDNF</strong> Receptor SorCS2.
+BDNF	addiction	withdrawal	31156431	Reduced Alcohol Seeking and <b>Withdrawal</b> Symptoms in Mice Lacking the <strong>BDNF</strong> Receptor SorCS2.
+BDNF	drug	alcohol	31156431	The <strong>BDNF</strong> signaling mechanism is complex and depends on two receptor systems, TrkB and p75NTR, which appear to have opposite effects on <b>alcohol</b> seeking behavior in animal models.
+BDNF	addiction	relapse	31156431	The <strong>BDNF</strong> signaling mechanism is complex and depends on two receptor systems, TrkB and p75NTR, which appear to have opposite effects on alcohol <b>seeking</b> behavior in animal models.
+BDNF	drug	nicotine	31129809	Likewise, <b>nicotine</b> induced CPP was associated with elevation of pro  brain derived neurotropic factor (<strong>BDNF</strong>) and <strong>BDNF</strong> protein levels in WT mice, but not in D2RKO mice.
+BDNF	addiction	reward	31129809	Likewise, nicotine induced <b>CPP</b> was associated with elevation of pro  brain derived neurotropic factor (<strong>BDNF</strong>) and <strong>BDNF</strong> protein levels in WT mice, but not in D2RKO mice.
+BDNF	drug	opioid	31071414	<b>Oxycodone</b> CPP males have: a) increases in <strong>Bdnf</strong> (brain derived neurotrophic factor) expression, which is known to be produced in granule cells, relative to females; b) elevated Mapk1 expression and pMAPK ir in the dentate hilus which harbors newly generated granule cells; and c) increases in CRHR1 ir in CA3 pyramidal cell soma.
+BDNF	addiction	reward	31071414	Oxycodone <b>CPP</b> males have: a) increases in <strong>Bdnf</strong> (brain derived neurotrophic factor) expression, which is known to be produced in granule cells, relative to females; b) elevated Mapk1 expression and pMAPK ir in the dentate hilus which harbors newly generated granule cells; and c) increases in CRHR1 ir in CA3 pyramidal cell soma.
+BDNF	drug	opioid	31071414	<b>Oxycodone</b> CPP males have: a) increases in <strong>Bdnf</strong> (<strong>brain derived neurotrophic factor</strong>) expression, which is known to be produced in granule cells, relative to females; b) elevated Mapk1 expression and pMAPK ir in the dentate hilus which harbors newly generated granule cells; and c) increases in CRHR1 ir in CA3 pyramidal cell soma.
+BDNF	addiction	reward	31071414	Oxycodone <b>CPP</b> males have: a) increases in <strong>Bdnf</strong> (<strong>brain derived neurotrophic factor</strong>) expression, which is known to be produced in granule cells, relative to females; b) elevated Mapk1 expression and pMAPK ir in the dentate hilus which harbors newly generated granule cells; and c) increases in CRHR1 ir in CA3 pyramidal cell soma.
+BDNF	drug	alcohol	31071339	In conclusion, Binge <b>ethanol</b> drinking causes spatial memory deficiency by reduction of <strong>BDNF</strong>, and the combination of curcumin and swimming training improves impaired spatial memory after binge <b>ethanol</b> drinking.
+BDNF	addiction	intoxication	31071339	In conclusion, <b>Binge</b> ethanol drinking causes spatial memory deficiency by reduction of <strong>BDNF</strong>, and the combination of curcumin and swimming training improves impaired spatial memory after <b>binge</b> ethanol drinking.
+BDNF	drug	alcohol	31068789	Oleoylethanolamide Modulates <strong>BDNF</strong> ERK Signaling and Neurogenesis in the Hippocampi of Rats Exposed to Δ9 THC and <b>Ethanol</b> Binge Drinking During Adolescence.
+BDNF	drug	cannabinoid	31068789	<b>Oleoylethanolamide</b> Modulates <strong>BDNF</strong> ERK Signaling and Neurogenesis in the Hippocampi of Rats Exposed to Δ9 <b>THC</b> and Ethanol Binge Drinking During Adolescence.
+BDNF	addiction	intoxication	31068789	Oleoylethanolamide Modulates <strong>BDNF</strong> ERK Signaling and Neurogenesis in the Hippocampi of Rats Exposed to Δ9 THC and Ethanol <b>Binge</b> Drinking During Adolescence.
+BDNF	drug	alcohol	31068789	In the present study we further analyze the role of OEA in hippocampal neurogenesis, <strong>BDNF</strong> ERK signaling, and spatial memory that are affected by <b>alcohol</b>.
+BDNF	drug	alcohol	31068789	OEA restored <b>ethanol</b>/THC related decreases in both short term spatial memory (spontaneous alternation by Y maze) and circulating levels of <strong>BDNF</strong>, reduced cell proliferation (Mki67 and IdU+ cells) and maturation (Dcx, Calb1), and improved cell survival (Casp3 and BrdU+ cells) in the dorsal hippocampus.
+BDNF	drug	cannabinoid	31068789	OEA restored ethanol/<b>THC</b> related decreases in both short term spatial memory (spontaneous alternation by Y maze) and circulating levels of <strong>BDNF</strong>, reduced cell proliferation (Mki67 and IdU+ cells) and maturation (Dcx, Calb1), and improved cell survival (Casp3 and BrdU+ cells) in the dorsal hippocampus.
+BDNF	drug	alcohol	31068789	Interestingly, OEA alone or combined with THC also decreased the mRNA levels of neurotrophic factors (<strong>Bdnf</strong>, Ntf3) and the NT3 receptor TrkC, but increased the <strong>BDNF</strong> receptor TrkB in the hippocampus of <b>ethanol</b> exposed rats.
+BDNF	drug	cannabinoid	31068789	Interestingly, OEA alone or combined with <b>THC</b> also decreased the mRNA levels of neurotrophic factors (<strong>Bdnf</strong>, Ntf3) and the NT3 receptor TrkC, but increased the <strong>BDNF</strong> receptor TrkB in the hippocampus of ethanol exposed rats.
+BDNF	drug	alcohol	31068789	These results suggest a regulatory role of OEA in short term spatial memory and hippocampal neurogenesis through <strong>BDNF</strong>/AKT/ERK1 signaling in response to acute THC in an <b>alcoholic</b> context during adolescence.
+BDNF	drug	cannabinoid	31068789	These results suggest a regulatory role of OEA in short term spatial memory and hippocampal neurogenesis through <strong>BDNF</strong>/AKT/ERK1 signaling in response to acute <b>THC</b> in an alcoholic context during adolescence.
+BDNF	addiction	relapse	31062481	Notably, DRL but not CMS rats, displayed higher rates of <b>relapse</b> than controls, and expressed higher levels of <strong>BDNF</strong> in the prelimbic cortex (PLC).
+BDNF	drug	cocaine	31062481	The increase in PLC <strong>BDNF</strong> levels is consistent with previous rat models of depression, and concomitantly, with its suggested role in promoting <b>cocaine</b> seeking.
+BDNF	addiction	relapse	31062481	The increase in PLC <strong>BDNF</strong> levels is consistent with previous rat models of depression, and concomitantly, with its suggested role in promoting cocaine <b>seeking</b>.
+BDNF	drug	alcohol	31032138	Parallel to these behavioral observations, both ketamine and NBQX normalized the reduction in hippocampal <strong>BDNF</strong> caused by <b>alcohol</b> withdrawal.
+BDNF	drug	psychedelics	31032138	Parallel to these behavioral observations, both <b>ketamine</b> and NBQX normalized the reduction in hippocampal <strong>BDNF</strong> caused by alcohol withdrawal.
+BDNF	addiction	withdrawal	31032138	Parallel to these behavioral observations, both ketamine and NBQX normalized the reduction in hippocampal <strong>BDNF</strong> caused by alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	31032138	These results suggest that either NMDA or AMPA/kainate receptor antagonists, acting at least partially through hippocampal <strong>BDNF</strong>, may be of therapeutic potential in <b>alcohol</b> use disorder.
+BDNF	drug	opioid	31010055	We evaluated the mechanical paw withdrawal threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) <b>opioid</b> receptor, brain derived neurotrophic factor (<strong>BDNF</strong>), Substance P, and calcitonin gene related peptide (CGRP) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real time quantitative polymerase chain reaction (RT PCR).
+BDNF	addiction	withdrawal	31010055	We evaluated the mechanical paw <b>withdrawal</b> threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) opioid receptor, brain derived neurotrophic factor (<strong>BDNF</strong>), Substance P, and calcitonin gene related peptide (CGRP) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real time quantitative polymerase chain reaction (RT PCR).
+BDNF	drug	opioid	31010055	We evaluated the mechanical paw withdrawal threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) <b>opioid</b> receptor, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), Substance P, and calcitonin gene related peptide (CGRP) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real time quantitative polymerase chain reaction (RT PCR).
+BDNF	addiction	withdrawal	31010055	We evaluated the mechanical paw <b>withdrawal</b> threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) opioid receptor, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), Substance P, and calcitonin gene related peptide (CGRP) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real time quantitative polymerase chain reaction (RT PCR).
+BDNF	drug	amphetamine	30993081	Possible Role of Cyclic AMP Response Element Binding/<strong>Brain Derived Neurotrophic Factor</strong> Signaling Pathway in Mediating the Pharmacological Effects of Duloxetine against <b>Methamphetamine</b> Use Induced Cognitive Impairment and Withdrawal Induced Anxiety and Depression in Rats.
+BDNF	addiction	withdrawal	30993081	Possible Role of Cyclic AMP Response Element Binding/<strong>Brain Derived Neurotrophic Factor</strong> Signaling Pathway in Mediating the Pharmacological Effects of Duloxetine against Methamphetamine Use Induced Cognitive Impairment and <b>Withdrawal</b> Induced Anxiety and Depression in Rats.
+BDNF	drug	amphetamine	30993081	In both experiments, duloxetine activated cAMP, CREB, and <strong>BDNF</strong> proteins' expression in <b>methamphetamine</b> treated rats.
+BDNF	drug	amphetamine	30993081	Duloxetine can protect the brain against <b>methamphetamine</b> withdrawal induced mood and motor disturbances and can also inhibit <b>methamphetamine</b> induced cognitive impairment, possibly via cAMP/CREB/<strong>BDNF</strong> signaling pathway.
+BDNF	addiction	withdrawal	30993081	Duloxetine can protect the brain against methamphetamine <b>withdrawal</b> induced mood and motor disturbances and can also inhibit methamphetamine induced cognitive impairment, possibly via cAMP/CREB/<strong>BDNF</strong> signaling pathway.
+BDNF	drug	amphetamine	30904722	Alteration level of hippocampus <strong>BDNF</strong> expression and long term potentiation upon microinjection of BRL15572 hydrochloride in a rat model of <b>methamphetamine</b> relapse.
+BDNF	addiction	relapse	30904722	Alteration level of hippocampus <strong>BDNF</strong> expression and long term potentiation upon microinjection of BRL15572 hydrochloride in a rat model of methamphetamine <b>relapse</b>.
+BDNF	drug	amphetamine	30904722	<b>Methamphetamine</b> (<b>METH</b>) relapse affects the function of the serotonergic system, which this system important for synaptic plasticity and brain derived neurotrophic factor (<strong>BDNF</strong>) level.
+BDNF	addiction	relapse	30904722	Methamphetamine (METH) <b>relapse</b> affects the function of the serotonergic system, which this system important for synaptic plasticity and brain derived neurotrophic factor (<strong>BDNF</strong>) level.
+BDNF	drug	amphetamine	30904722	<b>Methamphetamine</b> (<b>METH</b>) relapse affects the function of the serotonergic system, which this system important for synaptic plasticity and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) level.
+BDNF	addiction	relapse	30904722	Methamphetamine (METH) <b>relapse</b> affects the function of the serotonergic system, which this system important for synaptic plasticity and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) level.
+BDNF	drug	amphetamine	30904722	This article assessed effects of BRL15572 hydrochloride (5 HT1D receptor antagonist) on behavior, long term potentiation (LTP), and <strong>BDNF</strong> level in reinstated <b>METH</b> rats.
+BDNF	drug	amphetamine	30904722	Furthermore, <strong>BDNF</strong> expression significantly increased in the <b>METH</b> group although it decreased markedly upon treatment with BRL.
+BDNF	drug	psychedelics	30890941	<b>Ibogaine</b> Administration Modifies GDNF and <strong>BDNF</strong> Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits.
+BDNF	drug	psychedelics	30890941	Although previous reports have shown <b>ibogaine</b>'s ability to induce GDNF expression in rat midbrain, there are no studies addressing its effect on the expression of GDNF and other neurotrophic factors (NFs) such as Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) or Nerve Growth Factor (NGF) in distinct brain regions containing dopaminergic neurons.
+BDNF	drug	psychedelics	30890941	Although previous reports have shown <b>ibogaine</b>'s ability to induce GDNF expression in rat midbrain, there are no studies addressing its effect on the expression of GDNF and other neurotrophic factors (NFs) such as <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) or Nerve Growth Factor (NGF) in distinct brain regions containing dopaminergic neurons.
+BDNF	drug	amphetamine	30877026	MMP 9 <strong>BDNF</strong> pathway is implicated in cognitive impairment of male individuals with <b>methamphetamine</b> addiction during early withdrawal.
+BDNF	addiction	addiction	30877026	MMP 9 <strong>BDNF</strong> pathway is implicated in cognitive impairment of male individuals with methamphetamine <b>addiction</b> during early withdrawal.
+BDNF	addiction	withdrawal	30877026	MMP 9 <strong>BDNF</strong> pathway is implicated in cognitive impairment of male individuals with methamphetamine addiction during early <b>withdrawal</b>.
+BDNF	drug	amphetamine	30877026	As evidence indicates that brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with <b>METH</b> addiction, the present study aimed to investigate whether <strong>BDNF</strong> and the proteins regulating the <strong>BDNF</strong> signaling pathway might be implicated in the cognitive impairment of the <b>METH</b> abusers during early withdrawal.
+BDNF	addiction	addiction	30877026	As evidence indicates that brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with METH <b>addiction</b>, the present study aimed to investigate whether <strong>BDNF</strong> and the proteins regulating the <strong>BDNF</strong> signaling pathway might be implicated in the cognitive impairment of the METH abusers during early withdrawal.
+BDNF	addiction	withdrawal	30877026	As evidence indicates that brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with METH addiction, the present study aimed to investigate whether <strong>BDNF</strong> and the proteins regulating the <strong>BDNF</strong> signaling pathway might be implicated in the cognitive impairment of the METH abusers during early <b>withdrawal</b>.
+BDNF	drug	amphetamine	30877026	As evidence indicates that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with <b>METH</b> addiction, the present study aimed to investigate whether <strong>BDNF</strong> and the proteins regulating the <strong>BDNF</strong> signaling pathway might be implicated in the cognitive impairment of the <b>METH</b> abusers during early withdrawal.
+BDNF	addiction	addiction	30877026	As evidence indicates that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with METH <b>addiction</b>, the present study aimed to investigate whether <strong>BDNF</strong> and the proteins regulating the <strong>BDNF</strong> signaling pathway might be implicated in the cognitive impairment of the METH abusers during early withdrawal.
+BDNF	addiction	withdrawal	30877026	As evidence indicates that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with METH addiction, the present study aimed to investigate whether <strong>BDNF</strong> and the proteins regulating the <strong>BDNF</strong> signaling pathway might be implicated in the cognitive impairment of the METH abusers during early <b>withdrawal</b>.
+BDNF	drug	amphetamine	30877026	The results provide the prospective evidence that the MMP 9 <strong>BDNF</strong> pathway may underlie the pathogenesis of cognitive impairment in <b>METH</b> abusers during early withdrawal.
+BDNF	addiction	withdrawal	30877026	The results provide the prospective evidence that the MMP 9 <strong>BDNF</strong> pathway may underlie the pathogenesis of cognitive impairment in METH abusers during early <b>withdrawal</b>.
+BDNF	drug	cocaine	30818133	Short term withdrawal from repeated exposure to <b>cocaine</b> during adolescence modulates dynorphin mRNA levels and <strong>BDNF</strong> signaling in the rat nucleus accumbens.
+BDNF	addiction	withdrawal	30818133	Short term <b>withdrawal</b> from repeated exposure to cocaine during adolescence modulates dynorphin mRNA levels and <strong>BDNF</strong> signaling in the rat nucleus accumbens.
+BDNF	drug	opioid	30818133	Moreover, since brain derived neurotrophic factor (<strong>BDNF</strong>) may undergo simultaneous alterations with the <b>opioid</b> peptide dynorphin, we also evaluated its signaling pathway as well.
+BDNF	drug	opioid	30818133	Moreover, since <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) may undergo simultaneous alterations with the <b>opioid</b> peptide dynorphin, we also evaluated its signaling pathway as well.
+BDNF	drug	opioid	30818133	After short  (PND45) or long term (PND90) abstinence, prodynorphin κ <b>opioid</b> receptor (pDYN KOP) and pronociceptin nociceptin receptor (pN/OFQ NOP) gene expression were evaluated in the nucleus accumbens (NAc) and hippocampus (Hip) together with the analysis of <strong>BDNF</strong> signaling pathways.
+BDNF	drug	cocaine	30818133	Our results indicate that the short term withdrawal from adolescent <b>cocaine</b> exposure is characterized by a parallel pDYN mRNA and <strong>BDNF</strong> signaling increase in the NAc.
+BDNF	addiction	withdrawal	30818133	Our results indicate that the short term <b>withdrawal</b> from adolescent cocaine exposure is characterized by a parallel pDYN mRNA and <strong>BDNF</strong> signaling increase in the NAc.
+BDNF	drug	nicotine	30815604	Effect of genetic polymorphism of <strong>brain derived neurotrophic factor</strong> and serotonin transporter on <b>smoking</b> phenotypes: A pilot study of Japanese participants.
+BDNF	drug	nicotine	30815604	This study investigated whether a gene polymorphism causing a Val66Met substitution (rs6265) in brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with <b>smoking</b> initiation, <b>smoking</b> cessation, <b>nicotine</b> dependence and age of <b>smoking</b> initiation, in Japanese participants.
+BDNF	addiction	dependence	30815604	This study investigated whether a gene polymorphism causing a Val66Met substitution (rs6265) in brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with smoking initiation, smoking cessation, nicotine <b>dependence</b> and age of smoking initiation, in Japanese participants.
+BDNF	drug	nicotine	30815604	This study investigated whether a gene polymorphism causing a Val66Met substitution (rs6265) in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with <b>smoking</b> initiation, <b>smoking</b> cessation, <b>nicotine</b> dependence and age of <b>smoking</b> initiation, in Japanese participants.
+BDNF	addiction	dependence	30815604	This study investigated whether a gene polymorphism causing a Val66Met substitution (rs6265) in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with smoking initiation, smoking cessation, nicotine <b>dependence</b> and age of smoking initiation, in Japanese participants.
+BDNF	drug	nicotine	30815604	Additionally, this study examined whether the S allele of the serotonin transporter gene linked polymorphic region (5 HTTLPR) is associated with the <strong>BDNF</strong> Val66Met polymorphism on <b>smoking</b> phenotypes.
+BDNF	drug	nicotine	30815604	The genotypic proportion of the polymorphism responsible for <strong>BDNF</strong> Val66Met was determined in 148 participants including 88 current <b>smokers</b>, 21 former <b>smokers</b>, and 39 never <b>smokers</b>, and Fisher's exact test was used to investigate the relationship between this polymorphism and <b>smoking</b> cessation and initiation as well as the association between the genotypes of current <b>smokers</b> with a heavy <b>smoking</b> index (HSI) and the age of <b>smoking</b> initiation.
+BDNF	drug	nicotine	30815604	Moreover, the 5 HTTLPR polymorphism was associated with the age of <b>smoking</b> initiation in current <b>smokers</b> carrying the <strong>BDNF</strong> Met allele, in both the whole study sample (P = 0.041) and the male subgroup (P = 0.041).
+BDNF	drug	nicotine	30815604	On the other hand, no association was observed between the <strong>BDNF</strong> Val66Met polymorphism, either alone or in combination with the 5 HTTLPR polymorphism, and the age of <b>smoking</b> cessation.
+BDNF	drug	nicotine	30815604	Finally, no independent effects of the <strong>BDNF</strong> Val66Met genotype on the age of <b>smoking</b> initiation were detected.
+BDNF	drug	nicotine	30815604	This pilot study provides preliminary findings regarding the influence of <strong>BDNF</strong> Val66Met on <b>smoking</b> phenotypes and the interacting effect of 5 HTTLPR on the association between <strong>BDNF</strong> Val66Met and <b>smoking</b> phenotypes in Japanese participants.
+BDNF	drug	cocaine	30738029	7,8 Dihydroxyflavone blocks the development of behavioral sensitization to MDPV, but not to <b>cocaine</b>: Differential role of the <strong>BDNF</strong> TrkB pathway.
+BDNF	addiction	sensitization	30738029	7,8 Dihydroxyflavone blocks the development of behavioral <b>sensitization</b> to MDPV, but not to cocaine: Differential role of the <strong>BDNF</strong> TrkB pathway.
+BDNF	drug	cocaine	30738029	In this study we aimed to investigate the bidirectional cross sensitization between MDPV and <b>cocaine</b>, as well as to evaluate the role of the <strong>BDNF</strong> TrkB signaling pathway in the development of locomotor sensitization to both drugs.
+BDNF	addiction	sensitization	30738029	In this study we aimed to investigate the bidirectional cross <b>sensitization</b> between MDPV and cocaine, as well as to evaluate the role of the <strong>BDNF</strong> TrkB signaling pathway in the development of locomotor <b>sensitization</b> to both drugs.
+BDNF	drug	cocaine	30738029	For biochemical determinations, MDPV (1.5 mg/kg) or <b>cocaine</b> (15 mg/kg) were administered acutely or repeatedly, and <strong>BDNF</strong>, D3R and G9a transcription levels as well as pro  and mature <strong>BDNF</strong> protein levels were determined.
+BDNF	drug	cocaine	30738029	Interestingly, such decline was involved in the development of locomotor sensitization, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a TrkB agonist, blocked the development of sensitization to MDPV but not to <b>cocaine</b>, for which no changes in the <strong>BDNF</strong> TrkB signaling pathway were observed at early withdrawal.
+BDNF	addiction	sensitization	30738029	Interestingly, such decline was involved in the development of locomotor <b>sensitization</b>, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a TrkB agonist, blocked the development of <b>sensitization</b> to MDPV but not to cocaine, for which no changes in the <strong>BDNF</strong> TrkB signaling pathway were observed at early withdrawal.
+BDNF	addiction	withdrawal	30738029	Interestingly, such decline was involved in the development of locomotor sensitization, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a TrkB agonist, blocked the development of sensitization to MDPV but not to cocaine, for which no changes in the <strong>BDNF</strong> TrkB signaling pathway were observed at early <b>withdrawal</b>.
+BDNF	addiction	sensitization	30738029	Our findings suggest that decreased <strong>BDNF</strong> TrkB signaling has an important role in the behavioral <b>sensitization</b> to MDPV, pointing TrkB modulation as a target to prevent MDPV <b>sensitization</b>.
+BDNF	drug	amphetamine	30699853	<strong>BDNF</strong>, NGF, and GDNF levels were decreased, while NT 3 and NT 4 levels were increased in brains after d <b>AMPH</b> sensitization.
+BDNF	addiction	sensitization	30699853	<strong>BDNF</strong>, NGF, and GDNF levels were decreased, while NT 3 and NT 4 levels were increased in brains after d AMPH <b>sensitization</b>.
+BDNF	drug	amphetamine	30680641	Different doses of <b>methamphetamine</b> alter long term potentiation, level of <strong>BDNF</strong> and neuronal apoptosis in the hippocampus of reinstated rats.
+BDNF	drug	amphetamine	30680641	Therefore, we investigated the effects of different doses of <b>METH</b> on long term potentiation (LTP), <strong>BDNF</strong> expression and neuronal apoptosis in the hippocampus of reinstated rats.
+BDNF	addiction	relapse	30680641	Following implementation of the <b>reinstatement</b> model, electrophysiology, western blotting and TUNEL assay were performed to assess behavior, LTP components, <strong>BDNF</strong> expression, and neuronal apoptosis, respectively.
+BDNF	drug	amphetamine	30680641	The results demonstrated that the preference scores, population spike amplitude and <strong>BDNF</strong> expression markedly decreased in the <b>METH</b> (10 mg/kg) group compared with the other groups.
+BDNF	drug	amphetamine	30680641	These results suggest that alterations in synaptic plasticity, expression of <strong>BDNF</strong> and neuronal apoptosis in the hippocampus has a vital role in the context induced reinstatement of <b>METH</b> seeking.
+BDNF	addiction	relapse	30680641	These results suggest that alterations in synaptic plasticity, expression of <strong>BDNF</strong> and neuronal apoptosis in the hippocampus has a vital role in the context induced <b>reinstatement</b> of METH <b>seeking</b>.
+BDNF	drug	nicotine	30659208	Effects of <b>smoking</b> on cognition and <strong>BDNF</strong> levels in a male Chinese population: relationship with <strong>BDNF</strong> Val66Met polymorphism.
+BDNF	drug	nicotine	30659208	Recent studies demonstrate that brain derived neurotrophic factor (<strong>BDNF</strong>) might be associated with <b>nicotine</b> addiction, and circulating <strong>BDNF</strong> is a biomarker of memory and general cognitive function.
+BDNF	addiction	addiction	30659208	Recent studies demonstrate that brain derived neurotrophic factor (<strong>BDNF</strong>) might be associated with nicotine <b>addiction</b>, and circulating <strong>BDNF</strong> is a biomarker of memory and general cognitive function.
+BDNF	drug	nicotine	30659208	Recent studies demonstrate that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) might be associated with <b>nicotine</b> addiction, and circulating <strong>BDNF</strong> is a biomarker of memory and general cognitive function.
+BDNF	addiction	addiction	30659208	Recent studies demonstrate that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) might be associated with nicotine <b>addiction</b>, and circulating <strong>BDNF</strong> is a biomarker of memory and general cognitive function.
+BDNF	drug	nicotine	30659208	We aimed to explore the relationships between <b>smoking</b>, cognitive performance and <strong>BDNF</strong> in a normal Chinese Han population.
+BDNF	drug	nicotine	30659208	We recruited 628 male healthy subjects, inducing 322 <b>smokers</b> and 306 nonsmokers, and genotyped them the <strong>BDNF</strong> Val66Met polymorphism.
+BDNF	drug	nicotine	30659208	Of these, we assessed 114 <b>smokers</b> and 98 nonsmokers on the repeatable battery for the assessment of neuropsychological status (RBANS), and 103 <b>smokers</b> and 89 nonsmokers on serum <strong>BDNF</strong> levels.
+BDNF	drug	nicotine	30659208	<strong>BDNF</strong> levels among the <b>smokers</b> who were Val allele carriers were correlated with the degree of cognitive impairments, especially attention, as well as with the carbon monoxide concentrations.
+BDNF	drug	nicotine	30659208	The association between higher <strong>BDNF</strong> levels and cognitive impairment, mainly attention in <b>smokers</b> appears to be dependent on the <strong>BDNF</strong> Val66Met polymorphism.
+BDNF	drug	nicotine	30616127	Current <b>smokers</b> had significantly higher mean <strong>BDNF</strong> concentrations than never <b>smokers</b>.
+BDNF	drug	nicotine	30616127	In this study, higher BMI and <b>smoking</b> were associated with higher concentrations of serum <strong>BDNF</strong>, while nutrients that have been linked to depression were not associated with <strong>BDNF</strong> concentrations among Japanese workers.
+BDNF	drug	opioid	30550948	Distinct regulation pattern of Egr 1, <strong>BDNF</strong> and Arc during <b>morphine</b> withdrawal conditioned place aversion paradigm: Role of glucocorticoids.
+BDNF	addiction	aversion	30550948	Distinct regulation pattern of Egr 1, <strong>BDNF</strong> and Arc during morphine withdrawal conditioned place <b>aversion</b> paradigm: Role of glucocorticoids.
+BDNF	addiction	withdrawal	30550948	Distinct regulation pattern of Egr 1, <strong>BDNF</strong> and Arc during morphine <b>withdrawal</b> conditioned place aversion paradigm: Role of glucocorticoids.
+BDNF	addiction	aversion	30550948	qPCR was employed to detect the expression of brain derived neurotrophic factor (<strong>Bdnf</strong>) and the immediate early genes (IEG) early growth response 1 (Egr 1) and activity regulated cytoskeletal associated protein (Arc) mRNAs in the VTA and mPFC at different time points of the conditioned place <b>aversion</b> (CPA) paradigm: after the conditioning phase and after the test phase.
+BDNF	addiction	aversion	30550948	qPCR was employed to detect the expression of <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) and the immediate early genes (IEG) early growth response 1 (Egr 1) and activity regulated cytoskeletal associated protein (Arc) mRNAs in the VTA and mPFC at different time points of the conditioned place <b>aversion</b> (CPA) paradigm: after the conditioning phase and after the test phase.
+BDNF	drug	opioid	30550948	<strong>Bdnf</strong> induction seemed to be glucocorticoid dependent, given that was correlated with HPA axis function and was not observed in <b>morphine</b> dependent ADX animals.
+BDNF	addiction	aversion	30550948	In addition, <strong>BDNF</strong> regulation and function was opposite in the VTA and mPFC during <b>aversive</b> withdrawal memory retrieval.
+BDNF	addiction	withdrawal	30550948	In addition, <strong>BDNF</strong> regulation and function was opposite in the VTA and mPFC during aversive <b>withdrawal</b> memory retrieval.
+BDNF	addiction	withdrawal	30550948	Our results suggest that IEGs and <strong>BDNF</strong> in these brain regions may play key roles in mediating the negative motivational component of opiate <b>withdrawal</b>.
+BDNF	drug	amphetamine	30544074	Additional experiments showed that expression of brain derived neurotrophic factor (<strong>BDNF</strong>), phosphorylated tropomyosin receptor kinase B (p TrkB), phosphorylated extracellular signal related kinase 1/2 (p ERK1/2) and phosphorylated cAMP response element binding protein (p CREB) were decreased in the hippocampus and prefrontal cortex of mice in <b>METH</b> group and the level of mitogen activated protein kinase phosphatase 1 (MKP 1) was increased.
+BDNF	drug	amphetamine	30544074	Additional experiments showed that expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), phosphorylated tropomyosin receptor kinase B (p TrkB), phosphorylated extracellular signal related kinase 1/2 (p ERK1/2) and phosphorylated cAMP response element binding protein (p CREB) were decreased in the hippocampus and prefrontal cortex of mice in <b>METH</b> group and the level of mitogen activated protein kinase phosphatase 1 (MKP 1) was increased.
+BDNF	drug	amphetamine	30544074	Combined, our data show that withdrawal from chronic <b>METH</b> exposure induces anxiety and depression like behavior associated with aberrant changes of proteins in <strong>BDNF</strong> ERK CREB pathway, providing new evidence for the involvement of <strong>BDNF</strong> pathway in the negative emotional states induced by withdrawal from <b>METH</b>.
+BDNF	addiction	withdrawal	30544074	Combined, our data show that <b>withdrawal</b> from chronic METH exposure induces anxiety and depression like behavior associated with aberrant changes of proteins in <strong>BDNF</strong> ERK CREB pathway, providing new evidence for the involvement of <strong>BDNF</strong> pathway in the negative emotional states induced by <b>withdrawal</b> from METH.
+BDNF	drug	alcohol	30457048	In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and <b>alcohol</b> dependence, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand receptor systems, voltage gated calcium channels (VGCCs) and brain derived neurotrophic factor (<strong>BDNF</strong>) tyrosine kinase B (TrkB).
+BDNF	addiction	dependence	30457048	In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and alcohol <b>dependence</b>, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand receptor systems, voltage gated calcium channels (VGCCs) and brain derived neurotrophic factor (<strong>BDNF</strong>) tyrosine kinase B (TrkB).
+BDNF	drug	alcohol	30457048	In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and <b>alcohol</b> dependence, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand receptor systems, voltage gated calcium channels (VGCCs) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) tyrosine kinase B (TrkB).
+BDNF	addiction	dependence	30457048	In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and alcohol <b>dependence</b>, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand receptor systems, voltage gated calcium channels (VGCCs) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) tyrosine kinase B (TrkB).
+BDNF	drug	cocaine	30421552	ARC and <strong>BDNF</strong> expression after <b>cocaine</b> self administration or cue induced reinstatement of <b>cocaine</b> seeking in adolescent and adult male rats.
+BDNF	addiction	relapse	30421552	ARC and <strong>BDNF</strong> expression after cocaine self administration or cue induced <b>reinstatement</b> of cocaine <b>seeking</b> in adolescent and adult male rats.
+BDNF	drug	cocaine	30421552	Two neuroplasticity related genes, activity regulated cytoskeletal associated gene (Arc) and brain derived neurotrophic factor (<strong>Bdnf</strong>), influence <b>cocaine</b> self administration and cue induced reinstatement.
+BDNF	addiction	relapse	30421552	Two neuroplasticity related genes, activity regulated cytoskeletal associated gene (Arc) and brain derived neurotrophic factor (<strong>Bdnf</strong>), influence cocaine self administration and cue induced <b>reinstatement</b>.
+BDNF	drug	cocaine	30421552	Two neuroplasticity related genes, activity regulated cytoskeletal associated gene (Arc) and <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>), influence <b>cocaine</b> self administration and cue induced reinstatement.
+BDNF	addiction	relapse	30421552	Two neuroplasticity related genes, activity regulated cytoskeletal associated gene (Arc) and <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>), influence cocaine self administration and cue induced <b>reinstatement</b>.
+BDNF	addiction	relapse	30421552	These data partially support the hypothesis that higher levels of Arc and/or <strong>Bdnf</strong> gene expression in reinforcement related brain regions of younger animals contribute to lower rates of extinction responding and/or <b>reinstatement</b>.
+BDNF	addiction	reward	30421552	These data partially support the hypothesis that higher levels of Arc and/or <strong>Bdnf</strong> gene expression in <b>reinforcement</b> related brain regions of younger animals contribute to lower rates of extinction responding and/or reinstatement.
+BDNF	drug	cocaine	30421552	Future studies should include mechanistic analysis of Arc, <strong>Bdnf</strong>, and their signaling pathways in age dependent effects of <b>cocaine</b>.
+BDNF	drug	opioid	30418215	Postfracture expression levels of several genes previously associated with <b>opioid</b> induced hyperalgesia, including <strong>brain derived neurotrophic factor</strong> and prodynorphin, were unchanged, but neuroinflammation involving Toll like receptor 4 receptor expressing microglia was observed (6.8 ± 1.5 [mean ± SD] cells per high power field for fracture + vehicle vs. 12 ± 2.8 fracture + <b>morphine</b>, P < 0.001, n = 8 per /group).
+BDNF	drug	alcohol	30417952	Chronic <b>alcohol</b> exposure induced gut microbiota dysbiosis and its correlations with neuropsychic behaviors and brain <strong>BDNF</strong>/Gabra1 changes in mice.
+BDNF	drug	alcohol	30417952	was positively correlated with <b>alcohol</b> preference and negatively correlated with anxiety like behavior and <strong>BDNF</strong>/Gabra1 changes in PFC.
+BDNF	drug	alcohol	30417952	and <b>alcohol</b> preference and <strong>BDNF</strong> changes.
+BDNF	drug	alcohol	30417952	Taken together, our study showed that gut microbiota dysbiosis during chronic <b>alcohol</b> exposure was closely correlated with <b>alcohol</b> induced neuropsychic behaviors and <strong>BDNF</strong>/Gabra1 expression, which provides a new perspective for understanding underlying mechanisms in <b>alcohol</b> addiction.
+BDNF	addiction	addiction	30417952	Taken together, our study showed that gut microbiota dysbiosis during chronic alcohol exposure was closely correlated with alcohol induced neuropsychic behaviors and <strong>BDNF</strong>/Gabra1 expression, which provides a new perspective for understanding underlying mechanisms in alcohol <b>addiction</b>.
+BDNF	addiction	sensitization	30414958	We tested the hypothesis that activation of CB2 receptor by MDA7 modulates microglial dysregulation, suppresses the overexpression of brain derived neurotrophic factor (<strong>BDNF</strong>) in microglia in the dorsal horn, and attenuates the central <b>sensitization</b> and pain behavior induced by paclitaxel.
+BDNF	addiction	sensitization	30414958	We tested the hypothesis that activation of CB2 receptor by MDA7 modulates microglial dysregulation, suppresses the overexpression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in microglia in the dorsal horn, and attenuates the central <b>sensitization</b> and pain behavior induced by paclitaxel.
+BDNF	addiction	sensitization	30414958	Perspective: This study provides evidence that paclitaxel induced microglia dysregulation and epigenetically upregulated the microglial expression of <strong>BDNF</strong>, which led to <b>sensitization</b> of dorsal horn neurons and mechanical allodynia in rats.
+BDNF	drug	cocaine	30405186	Intermittent intake of rapid <b>cocaine</b> injections promotes the risk of relapse and increases mesocorticolimbic <strong>BDNF</strong> levels during abstinence.
+BDNF	addiction	relapse	30405186	Intermittent intake of rapid cocaine injections promotes the risk of <b>relapse</b> and increases mesocorticolimbic <strong>BDNF</strong> levels during abstinence.
+BDNF	addiction	relapse	30405186	Brain derived neurotrophic factor (<strong>BDNF</strong>) activity in the brain regulates <b>reinstatement</b> behaviour.
+BDNF	addiction	relapse	30405186	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) activity in the brain regulates <b>reinstatement</b> behaviour.
+BDNF	addiction	relapse	30405186	Thus, 24 h after <b>reinstatement</b> tests, we measured <strong>BDNF</strong> protein concentrations in mesocorticolimbic regions.
+BDNF	drug	cocaine	30405186	Only 5s rats showed time dependent increases in <strong>BDNF</strong> concentrations in the prelimbic cortex, nucleus accumbens core and ventral tegmental area after withdrawal from <b>cocaine</b> (day 45 > day 1).
+BDNF	addiction	withdrawal	30405186	Only 5s rats showed time dependent increases in <strong>BDNF</strong> concentrations in the prelimbic cortex, nucleus accumbens core and ventral tegmental area after <b>withdrawal</b> from cocaine (day 45 > day 1).
+BDNF	drug	alcohol	30347311	Subgroup analysis revealed lower levels of serum <strong>BDNF</strong> in <b>alcohol</b> users (SMD =  0.70, 95%CI  1.15 to  0.25, I2 = 89.81) and crack/cocaine users (SMD =  1.78, 95%CI  2.92 to  0.65, I2 = 97.59) than controls.
+BDNF	drug	cocaine	30347311	Subgroup analysis revealed lower levels of serum <strong>BDNF</strong> in alcohol users (SMD =  0.70, 95%CI  1.15 to  0.25, I2 = 89.81) and crack/<b>cocaine</b> users (SMD =  1.78, 95%CI  2.92 to  0.65, I2 = 97.59) than controls.
+BDNF	addiction	addiction	30347311	Altogether, these findings suggest that <strong>BDNF</strong> levels may be related to acute use and <b>addiction</b> severity and also point to <strong>BDNF</strong>'s potential utility as a biomarker in this population.
+BDNF	drug	alcohol	30277635	<b>Alcohol</b> induced cognitive deficits are associated with decreased circulating levels of the neurotrophin <strong>BDNF</strong> in humans and rats.
+BDNF	drug	alcohol	30277635	For further investigation, a cross sectional study was performed to evaluate the association of cognitive impairment, by using frontal assessment battery, and memory loss, using memory failures everyday, with the circulating levels of the neurotrophin brain derived neurotrophic factor (<strong>BDNF</strong>) and neurotrophin 3 (NT 3) in abstinent subjects with <b>alcohol</b> use disorders (AUDs, N = 58, average of 17.9 years of problematic use and 4.3 months of abstinence) compared with healthy control subjects (N = 22).
+BDNF	drug	alcohol	30277635	For further investigation, a cross sectional study was performed to evaluate the association of cognitive impairment, by using frontal assessment battery, and memory loss, using memory failures everyday, with the circulating levels of the neurotrophin <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and neurotrophin 3 (NT 3) in abstinent subjects with <b>alcohol</b> use disorders (AUDs, N = 58, average of 17.9 years of problematic use and 4.3 months of abstinence) compared with healthy control subjects (N = 22).
+BDNF	drug	alcohol	30277635	In the <b>ethanol</b> exposed rats, the plasma levels of <strong>BDNF</strong> and NT 3 were also decreased, and a negative correlation between hippocampal <strong>Bdnf</strong> mRNA levels and recognition memory was found.
+BDNF	drug	alcohol	30277635	The <b>ethanol</b> exposed rat hippocampus showed a decrease in the mRNA levels of neurotrophic (<strong>Bdnf</strong> and Ntf 3) and neurogenic (Mki67, Sox2, Dcx, Ncam1 and Calb1) factors, associated to a deactivation of the neurogenic regulator mitogen activated protein kinase extracellular signal regulated kinase.
+BDNF	drug	alcohol	30277635	Results suggest a relevant role of <strong>BDNF</strong>/extracellular signal regulated kinase 2 signaling in <b>alcohol</b> induced cognitive impairment and suggest that early <b>alcohol</b> exposure derived effects on cognition are associated with neurotrophin signaling deficits.
+BDNF	drug	cannabinoid	30273593	In parallel, CBD increased expression of type 1 <b>cannabinoid</b> receptor, MAPK CREB phosphorylation, <strong>BDNF</strong> expression, and neural cell proliferation in the hippocampus, and reduced the GluA1/2 AMPA subunit receptor ratio in the striatum.
+BDNF	drug	nicotine	30227235	Our data suggest that response similar to <b>nicotine</b> withdrawal or/and hypoxia induced by childhood chronic asthma enhances the <strong>BDNF</strong> Cdc42/RhoA signaling pathway and activates cofilin1, leading to the remodeling of actin, causing the loss of dendritic spines and atrophy of dendrites, eventually resulting in behavioral alterations.
+BDNF	addiction	withdrawal	30227235	Our data suggest that response similar to nicotine <b>withdrawal</b> or/and hypoxia induced by childhood chronic asthma enhances the <strong>BDNF</strong> Cdc42/RhoA signaling pathway and activates cofilin1, leading to the remodeling of actin, causing the loss of dendritic spines and atrophy of dendrites, eventually resulting in behavioral alterations.
+BDNF	drug	alcohol	30188517	Protein or mRNA expression studies following Gsk3b over expression identified synaptojanin 2, <strong>brain derived neurotrophic factor</strong> and the neuropeptide Y Y5 receptor as potential downstream factors altering <b>ethanol</b> behaviors.
+BDNF	drug	cocaine	30185459	Divergent Prelimbic Cortical Pathways Interact with <strong>BDNF</strong> to Regulate <b>Cocaine</b> seeking.
+BDNF	addiction	relapse	30185459	Divergent Prelimbic Cortical Pathways Interact with <strong>BDNF</strong> to Regulate Cocaine <b>seeking</b>.
+BDNF	drug	cocaine	30185459	A single <strong>BDNF</strong> microinfusion into prelimbic (PrL) cortex immediately after the last <b>cocaine</b> self administration session decreases relapse to <b>cocaine</b> seeking.
+BDNF	addiction	relapse	30185459	A single <strong>BDNF</strong> microinfusion into prelimbic (PrL) cortex immediately after the last cocaine self administration session decreases <b>relapse</b> to cocaine <b>seeking</b>.
+BDNF	addiction	relapse	30185459	To determine whether synaptic activity in putative excitatory projection neurons in PrL cortex is sufficient for <strong>BDNF</strong>'s effect on <b>relapse</b>, the PrL cortex of male rats was infused with an inhibitory Designer Receptor Exclusively Activated by Designer Drugs (DREADD) viral vector driven by an αCaMKII promoter.
+BDNF	drug	cocaine	30185459	Immediately after the last <b>cocaine</b> self administration session, rats were injected with clozapine N oxide 30 min before an intra PrL <strong>BDNF</strong> microinfusion.
+BDNF	drug	cocaine	30185459	DREADD mediated inhibition of the PrL cortex blocked the <strong>BDNF</strong> induced decrease in <b>cocaine</b> seeking after abstinence and cue induced reinstatement after extinction.
+BDNF	addiction	relapse	30185459	DREADD mediated inhibition of the PrL cortex blocked the <strong>BDNF</strong> induced decrease in cocaine <b>seeking</b> after abstinence and cue induced <b>reinstatement</b> after extinction.
+BDNF	drug	cocaine	30185459	Next, using a cre dependent retroviral approach, we tested the ability of DREADD inhibition of PrL projections to the NAc core or the paraventricular thalamic nucleus (PVT) to alter <b>cocaine</b> seeking in <strong>BDNF</strong>  and PBS infused rats.
+BDNF	addiction	relapse	30185459	Next, using a cre dependent retroviral approach, we tested the ability of DREADD inhibition of PrL projections to the NAc core or the paraventricular thalamic nucleus (PVT) to alter cocaine <b>seeking</b> in <strong>BDNF</strong>  and PBS infused rats.
+BDNF	drug	cocaine	30185459	Selective inhibition of the PrL NAc pathway at the end of <b>cocaine</b> self administration blocked the <strong>BDNF</strong> induced decrease in <b>cocaine</b> seeking but had no effect in PBS infused rats.
+BDNF	addiction	relapse	30185459	Selective inhibition of the PrL NAc pathway at the end of cocaine self administration blocked the <strong>BDNF</strong> induced decrease in cocaine <b>seeking</b> but had no effect in PBS infused rats.
+BDNF	drug	cocaine	30185459	In contrast, selective inhibition of the PrL PVT pathway in PBS infused rats decreased <b>cocaine</b> seeking, and this effect was prevented in <strong>BDNF</strong> infused rats.
+BDNF	addiction	relapse	30185459	In contrast, selective inhibition of the PrL PVT pathway in PBS infused rats decreased cocaine <b>seeking</b>, and this effect was prevented in <strong>BDNF</strong> infused rats.
+BDNF	drug	cocaine	30185459	Thus, activity in the PrL NAc pathway is responsible for the therapeutic effect of <strong>BDNF</strong> on <b>cocaine</b> seeking whereas inhibition of activity in the PrL pPVT pathway elicits a similar therapeutic effect in the absence of <strong>BDNF</strong>.SIGNIFICANCE STATEMENT The major issue in <b>cocaine</b> addiction is the high rate of relapse.
+BDNF	addiction	addiction	30185459	Thus, activity in the PrL NAc pathway is responsible for the therapeutic effect of <strong>BDNF</strong> on cocaine seeking whereas inhibition of activity in the PrL pPVT pathway elicits a similar therapeutic effect in the absence of <strong>BDNF</strong>.SIGNIFICANCE STATEMENT The major issue in cocaine <b>addiction</b> is the high rate of relapse.
+BDNF	addiction	relapse	30185459	Thus, activity in the PrL NAc pathway is responsible for the therapeutic effect of <strong>BDNF</strong> on cocaine <b>seeking</b> whereas inhibition of activity in the PrL pPVT pathway elicits a similar therapeutic effect in the absence of <strong>BDNF</strong>.SIGNIFICANCE STATEMENT The major issue in cocaine addiction is the high rate of <b>relapse</b>.
+BDNF	addiction	relapse	30185459	Using a pathway specific chemogenetic approach, we found that <strong>BDNF</strong> differentially regulates two key prelimbic pathways to guide long term <b>relapse</b>.
+BDNF	drug	cocaine	30185459	Infusion of <strong>BDNF</strong> in the prelimbic cortex during early withdrawal from <b>cocaine</b> self administration decreases relapse that is prevented when neurons projecting from the prelimbic cortex to the nucleus accumbens core are inhibited.
+BDNF	addiction	relapse	30185459	Infusion of <strong>BDNF</strong> in the prelimbic cortex during early withdrawal from cocaine self administration decreases <b>relapse</b> that is prevented when neurons projecting from the prelimbic cortex to the nucleus accumbens core are inhibited.
+BDNF	addiction	withdrawal	30185459	Infusion of <strong>BDNF</strong> in the prelimbic cortex during early <b>withdrawal</b> from cocaine self administration decreases relapse that is prevented when neurons projecting from the prelimbic cortex to the nucleus accumbens core are inhibited.
+BDNF	addiction	relapse	30185459	In contrast, <strong>BDNF</strong> restores <b>relapse</b> when neurons projecting from the prelimbic cortex to the posterior paraventricular thalamic nucleus are inhibited.
+BDNF	drug	cocaine	30185459	This study demonstrates that two divergent cortical outputs mediate relapse that is regulated in opposite directions by infusing <strong>BDNF</strong> in the prelimbic cortex during early withdrawal from <b>cocaine</b>.
+BDNF	addiction	relapse	30185459	This study demonstrates that two divergent cortical outputs mediate <b>relapse</b> that is regulated in opposite directions by infusing <strong>BDNF</strong> in the prelimbic cortex during early withdrawal from cocaine.
+BDNF	addiction	withdrawal	30185459	This study demonstrates that two divergent cortical outputs mediate relapse that is regulated in opposite directions by infusing <strong>BDNF</strong> in the prelimbic cortex during early <b>withdrawal</b> from cocaine.
+BDNF	drug	alcohol	30154658	We found that administration of ketamine with <b>ethanol</b> led to a significant increase of DA in the VTA associated with differential regulation of mRNA levels of the four DA metabolism genes and protein levels of <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	psychedelics	30154658	We found that administration of <b>ketamine</b> with ethanol led to a significant increase of DA in the VTA associated with differential regulation of mRNA levels of the four DA metabolism genes and protein levels of <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	opioid	30118972	The most studied candidate genes have included the mu <b>opioid</b> receptor (OPRM1), the delta <b>opioid</b> receptor (OPRD1), the dopamine D2 receptor (DRD2), and brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	opioid	30118972	The most studied candidate genes have included the mu <b>opioid</b> receptor (OPRM1), the delta <b>opioid</b> receptor (OPRD1), the dopamine D2 receptor (DRD2), and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	alcohol	30072053	Surprisingly, moderate <b>alcohol</b> consumption may trigger, on the long term, changes of <strong>BDNF</strong> expression and of its epigenetic elements that are somehow similar to those produced by antidepressant drugs.
+BDNF	drug	alcohol	30056122	Increasing Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) in medial prefrontal cortex selectively reduces excessive drinking in <b>ethanol</b> dependent mice.
+BDNF	drug	alcohol	30056122	Increasing <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) in medial prefrontal cortex selectively reduces excessive drinking in <b>ethanol</b> dependent mice.
+BDNF	drug	alcohol	30056122	The neurotrophin Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) has been implicated in a number of neuropsychiatric disorders, including <b>alcohol</b> use disorder.
+BDNF	drug	alcohol	30056122	The neurotrophin <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) has been implicated in a number of neuropsychiatric disorders, including <b>alcohol</b> use disorder.
+BDNF	drug	alcohol	30056122	Studies have shown that <strong>BDNF</strong> activity in cortical regions, such as the medial prefrontal cortex (mPFC) mediates various <b>ethanol</b> related behaviors.
+BDNF	drug	alcohol	30056122	We previously reported a significant down regulation in <strong>Bdnf</strong> mRNA in mPFC following chronic <b>ethanol</b> exposure compared to control mice.
+BDNF	drug	alcohol	30056122	The present study was conducted to extend these findings by examining whether chronic <b>ethanol</b> treatment reduces <strong>BDNF</strong> protein expression in mPFC and whether reversing this deficit via direct injection of <strong>BDNF</strong> or viral mediated overexpression of <strong>BDNF</strong> in mPFC alters voluntary <b>ethanol</b> consumption in dependent and nondependent mice.
+BDNF	drug	alcohol	30056122	Results indicated that CIE treatment significantly increased <b>ethanol</b> intake and this was accompanied by a significant decrease in <strong>BDNF</strong> protein in mPFC that lasted at least 72 h after CIE exposure.
+BDNF	drug	alcohol	30056122	In a separate study, once dependence related increased drinking was established, bilateral infusion of <strong>BDNF</strong> (0, 0.25, 0.50 μg) into mPFC significantly decreased <b>ethanol</b> intake in a dose related manner in dependent mice but did not affect moderate drinking in nondependent mice.
+BDNF	addiction	dependence	30056122	In a separate study, once <b>dependence</b> related increased drinking was established, bilateral infusion of <strong>BDNF</strong> (0, 0.25, 0.50 μg) into mPFC significantly decreased ethanol intake in a dose related manner in dependent mice but did not affect moderate drinking in nondependent mice.
+BDNF	addiction	addiction	30056122	In a third study, viral mediated overexpression of <strong>BDNF</strong> in mPFC prevented <b>escalation</b> of drinking in dependent mice but did not alter intake in nondependent mice.
+BDNF	drug	alcohol	30056122	Collectively, these results provide evidence that adaptations in cortical (mPFC) <strong>BDNF</strong> activity resulting from chronic <b>ethanol</b> exposure play a role in mediating excessive <b>ethanol</b> drinking associated with dependence.
+BDNF	addiction	dependence	30056122	Collectively, these results provide evidence that adaptations in cortical (mPFC) <strong>BDNF</strong> activity resulting from chronic ethanol exposure play a role in mediating excessive ethanol drinking associated with <b>dependence</b>.
+BDNF	drug	opioid	29946108	The conceptual framework of this review is to focus on hormonal, chromosomal, and epigenetic organizational and contingent, sex dependent mechanisms of four neural systems that are known primarily in males to be key players in addiction: dopamine, mu <b>opioid</b> receptors (MOR), kappa <b>opioid</b> receptors (KOR), and brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	addiction	addiction	29946108	The conceptual framework of this review is to focus on hormonal, chromosomal, and epigenetic organizational and contingent, sex dependent mechanisms of four neural systems that are known primarily in males to be key players in <b>addiction</b>: dopamine, mu opioid receptors (MOR), kappa opioid receptors (KOR), and brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	opioid	29946108	The conceptual framework of this review is to focus on hormonal, chromosomal, and epigenetic organizational and contingent, sex dependent mechanisms of four neural systems that are known primarily in males to be key players in addiction: dopamine, mu <b>opioid</b> receptors (MOR), kappa <b>opioid</b> receptors (KOR), and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	addiction	addiction	29946108	The conceptual framework of this review is to focus on hormonal, chromosomal, and epigenetic organizational and contingent, sex dependent mechanisms of four neural systems that are known primarily in males to be key players in <b>addiction</b>: dopamine, mu opioid receptors (MOR), kappa opioid receptors (KOR), and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	opioid	29936268	Effects of treadmill exercise on <b>methadone</b> withdrawal induced locomotor sensitization and the ventral pallidum and ventral tegmental area <strong>BDNF</strong> levels in <b>morphine</b> withdrawn rats receiving <b>methadone</b> maintenance treatment.
+BDNF	addiction	sensitization	29936268	Effects of treadmill exercise on methadone withdrawal induced locomotor <b>sensitization</b> and the ventral pallidum and ventral tegmental area <strong>BDNF</strong> levels in morphine withdrawn rats receiving methadone maintenance treatment.
+BDNF	addiction	withdrawal	29936268	Effects of treadmill exercise on methadone <b>withdrawal</b> induced locomotor sensitization and the ventral pallidum and ventral tegmental area <strong>BDNF</strong> levels in morphine withdrawn rats receiving methadone maintenance treatment.
+BDNF	drug	opioid	29936268	This study examined the effects of treadmill exercise on the <b>methadone</b> withdrawal  induced locomotor sensitization, the ventral tegmental area (VTA) and ventral pallidum (VP) <strong>BDNF</strong> levels in <b>morphine</b> withdrawn rats receiving <b>methadone</b> maintenance treatment (MMT).
+BDNF	addiction	sensitization	29936268	This study examined the effects of treadmill exercise on the methadone withdrawal  induced locomotor <b>sensitization</b>, the ventral tegmental area (VTA) and ventral pallidum (VP) <strong>BDNF</strong> levels in morphine withdrawn rats receiving methadone maintenance treatment (MMT).
+BDNF	addiction	withdrawal	29936268	This study examined the effects of treadmill exercise on the methadone <b>withdrawal</b>  induced locomotor sensitization, the ventral tegmental area (VTA) and ventral pallidum (VP) <strong>BDNF</strong> levels in morphine withdrawn rats receiving methadone maintenance treatment (MMT).
+BDNF	drug	amphetamine	29936268	The VP <strong>BDNF</strong> level and the locomotors response were higher and lower, respectively in the D/<b>Meth</b>/Sed and D/Sal/Exc than the D/Sal/Sed rats.
+BDNF	drug	opioid	29936268	Exercise had no effect on the locomotors response and the VP <strong>BDNF</strong> levels in <b>morphine</b> dependent rats receiving MMT.
+BDNF	drug	opioid	29936268	Our results showed that the sedentary <b>morphine</b> dependent rats challenged to <b>morphine</b> enhanced the <b>morphine</b> induced hyperlocomotion, whereas decreased the VP <strong>BDNF</strong> levels.
+BDNF	drug	amphetamine	29936268	Exercise had no effect on the locomotors response and the VTA VP <strong>BDNF</strong> levels in the D/<b>Meth</b>/Exc.
+BDNF	drug	alcohol	29896126	Synaptic Ultrastructure Might Be Involved in HCN1 Related <strong>BDNF</strong> mRNA in Withdrawal Anxiety After <b>Ethanol</b> Dependence.
+BDNF	addiction	dependence	29896126	Synaptic Ultrastructure Might Be Involved in HCN1 Related <strong>BDNF</strong> mRNA in Withdrawal Anxiety After Ethanol <b>Dependence</b>.
+BDNF	addiction	withdrawal	29896126	Synaptic Ultrastructure Might Be Involved in HCN1 Related <strong>BDNF</strong> mRNA in <b>Withdrawal</b> Anxiety After Ethanol Dependence.
+BDNF	drug	cocaine	29890020	Accumbens brain derived neurotrophic factor (<strong>BDNF</strong>) transmission inhibits <b>cocaine</b> seeking.
+BDNF	addiction	relapse	29890020	Accumbens brain derived neurotrophic factor (<strong>BDNF</strong>) transmission inhibits cocaine <b>seeking</b>.
+BDNF	drug	cocaine	29890020	Accumbens <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) transmission inhibits <b>cocaine</b> seeking.
+BDNF	addiction	relapse	29890020	Accumbens <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) transmission inhibits cocaine <b>seeking</b>.
+BDNF	addiction	addiction	29890020	Brain derived neurotrophic factor (<strong>BDNF</strong>) regulates a variety of physiological processes, and several studies have explored the role of <strong>BDNF</strong> in <b>addiction</b> related brain regions like the nucleus accumbens core (NAcore).
+BDNF	addiction	addiction	29890020	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) regulates a variety of physiological processes, and several studies have explored the role of <strong>BDNF</strong> in <b>addiction</b> related brain regions like the nucleus accumbens core (NAcore).
+BDNF	drug	cocaine	29890020	We sought to understand the rapid effects of endogenous <strong>BDNF</strong> on <b>cocaine</b> seeking.
+BDNF	addiction	relapse	29890020	We sought to understand the rapid effects of endogenous <strong>BDNF</strong> on cocaine <b>seeking</b>.
+BDNF	addiction	relapse	29890020	Blocking TrkB or inactivating <strong>BDNF</strong> in NAcore potentiated active lever pressing, showing that endogenous <strong>BDNF</strong> tone was present and supplying inhibitory tone on cue induced <b>reinstatement</b>.
+BDNF	addiction	relapse	29890020	To determine if exogenous <strong>BDNF</strong> also negatively regulated <b>reinstatement</b>, <strong>BDNF</strong> was microinjected into NAcore 15 minutes before cue induced <b>reinstatement</b>.
+BDNF	drug	cocaine	29890020	<strong>BDNF</strong> decreased <b>cocaine</b> seeking through TrkB receptor binding, but had no effect on inactive lever pressing, spontaneous or <b>cocaine</b> induced locomotion, or on reinstated sucrose seeking.
+BDNF	addiction	relapse	29890020	<strong>BDNF</strong> decreased cocaine <b>seeking</b> through TrkB receptor binding, but had no effect on inactive lever pressing, spontaneous or cocaine induced locomotion, or on reinstated sucrose <b>seeking</b>.
+BDNF	addiction	relapse	29890020	<strong>BDNF</strong> infusion potentiated within trial extinction when microinjected in the NAcore during cue  and context + cue induced <b>reinstatement</b>, and the inhibition of lever pressing lasted at least 3 days post injection.
+BDNF	addiction	relapse	29890020	Although decreased <b>reinstatement</b> endured for 3 days when <strong>BDNF</strong> was administered prior to a <b>reinstatement</b> session, when microinjected before an extinction session or in the home cage, <strong>BDNF</strong> did not alter subsequent cued <b>reinstatement</b>.
+BDNF	drug	cocaine	29890020	Together, these data show that endogenous <strong>BDNF</strong> acts on TrKB to provide inhibitory tone on reinstated <b>cocaine</b> seeking, and this effect was recapitulated by exogenous <strong>BDNF</strong>.
+BDNF	addiction	relapse	29890020	Together, these data show that endogenous <strong>BDNF</strong> acts on TrKB to provide inhibitory tone on reinstated cocaine <b>seeking</b>, and this effect was recapitulated by exogenous <strong>BDNF</strong>.
+BDNF	drug	opioid	29859931	Serum <strong>BDNF</strong> levels in patients with <b>opioid</b> dependence during the early withdrawal period: A case control study.
+BDNF	addiction	dependence	29859931	Serum <strong>BDNF</strong> levels in patients with opioid <b>dependence</b> during the early withdrawal period: A case control study.
+BDNF	addiction	withdrawal	29859931	Serum <strong>BDNF</strong> levels in patients with opioid dependence during the early <b>withdrawal</b> period: A case control study.
+BDNF	drug	opioid	29859931	Brain Derived Neurotrophic Factor (<strong>BDNF</strong>), a neuropeptide important for neural growth and differentiation has been explored in patients with <b>opioid</b> dependence.
+BDNF	addiction	dependence	29859931	Brain Derived Neurotrophic Factor (<strong>BDNF</strong>), a neuropeptide important for neural growth and differentiation has been explored in patients with opioid <b>dependence</b>.
+BDNF	drug	opioid	29859931	<strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>), a neuropeptide important for neural growth and differentiation has been explored in patients with <b>opioid</b> dependence.
+BDNF	addiction	dependence	29859931	<strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>), a neuropeptide important for neural growth and differentiation has been explored in patients with opioid <b>dependence</b>.
+BDNF	drug	opioid	29859931	We aimed to compare the serum <strong>BDNF</strong> levels in patients with <b>opioid</b> dependence with age and gender matched controls, and to assess change in <strong>BDNF</strong> levels during initial withdrawal period.
+BDNF	addiction	dependence	29859931	We aimed to compare the serum <strong>BDNF</strong> levels in patients with opioid <b>dependence</b> with age and gender matched controls, and to assess change in <strong>BDNF</strong> levels during initial withdrawal period.
+BDNF	addiction	withdrawal	29859931	We aimed to compare the serum <strong>BDNF</strong> levels in patients with opioid dependence with age and gender matched controls, and to assess change in <strong>BDNF</strong> levels during initial <b>withdrawal</b> period.
+BDNF	drug	opioid	29859931	Additionally, <strong>BDNF</strong> levels were measured in patients with <b>opioid</b> dependence after 10 days of inpatient detoxification.
+BDNF	addiction	dependence	29859931	Additionally, <strong>BDNF</strong> levels were measured in patients with opioid <b>dependence</b> after 10 days of inpatient detoxification.
+BDNF	drug	nicotine	29859931	<strong>BDNF</strong> levels did not correlate with severity of <b>nicotine</b> dependence, age of the cases or duration of opioid dependence.
+BDNF	drug	opioid	29859931	<strong>BDNF</strong> levels did not correlate with severity of nicotine dependence, age of the cases or duration of <b>opioid</b> dependence.
+BDNF	addiction	dependence	29859931	<strong>BDNF</strong> levels did not correlate with severity of nicotine <b>dependence</b>, age of the cases or duration of opioid <b>dependence</b>.
+BDNF	drug	opioid	29859931	The results from the study provide further insights into the relationship of <strong>BDNF</strong> levels and <b>opioid</b> dependence.
+BDNF	addiction	dependence	29859931	The results from the study provide further insights into the relationship of <strong>BDNF</strong> levels and opioid <b>dependence</b>.
+BDNF	drug	cocaine	29859319	<b>Cocaine</b> mediated activation of microglia and microglial MeCP2 and <strong>BDNF</strong> production.
+BDNF	drug	cocaine	29859319	Methyl CpG binding protein 2 (MeCP2) binds to the promoter region of <strong>BDNF</strong> to negatively regulate its expression and <b>cocaine</b> can recruit MeCP2 to alter the expression of genes such as <strong>BDNF</strong> that are involved in synaptic plasticity.
+BDNF	drug	cocaine	29859319	For several decades, <strong>BDNF</strong> has been implicated in mediating synaptic plasticity associated with <b>cocaine</b> abuse, and most studies report that neurons are the primary source for <strong>BDNF</strong> production in the brain.
+BDNF	drug	cocaine	29859319	The current study assessed the effects of intravenous <b>cocaine</b> self administration on microglial activation, and MeCP2 and <strong>BDNF</strong> expression in reward regions of the brain in vivo, as well as determined specific effects of <b>cocaine</b> exposure on MeCP2 and <strong>BDNF</strong> expression in human primary neurons and microglia.
+BDNF	addiction	reward	29859319	The current study assessed the effects of intravenous cocaine self administration on microglial activation, and MeCP2 and <strong>BDNF</strong> expression in <b>reward</b> regions of the brain in vivo, as well as determined specific effects of cocaine exposure on MeCP2 and <strong>BDNF</strong> expression in human primary neurons and microglia.
+BDNF	drug	cocaine	29859319	The results from this study highlight a distinct molecular pathway in microglia through which <b>cocaine</b> increases <strong>BDNF</strong>, including the phosphorylation of MeCP2 its subsequent translocation from the nucleus to the cytosol, which frees the <strong>BDNF</strong> promoter and permits its transcriptional activation.
+BDNF	drug	cocaine	29859319	Results from these studies show for the first time that <b>cocaine</b> self administration increases microglial activation, and that microglial MeCP2 is a sensitive target of <b>cocaine</b> resulting in increased release of <strong>BDNF</strong> from microglia, and possibly contributing to <b>cocaine</b> induced synaptic plasticity.
+BDNF	addiction	withdrawal	29752970	The reduced <strong>BDNF</strong> level observed shortly after BEI recovered upon <b>withdrawal</b>, whereas increased GFAP immunoreactivity was persistent up to 14 days post administration in adulthood.
+BDNF	drug	alcohol	29752970	These findings show that repeated binge like <b>ethanol</b> episodes from adolescence to adulthood in female rats cause consistent and long term alterations of anxiety and hippocampal astrogliosis, whereas they trigger a recognition memory deficit paralleled by lower hippocampal <strong>BDNF</strong> levels, both recovering upon <b>ethanol</b> withdrawal.
+BDNF	addiction	intoxication	29752970	These findings show that repeated <b>binge</b> like ethanol episodes from adolescence to adulthood in female rats cause consistent and long term alterations of anxiety and hippocampal astrogliosis, whereas they trigger a recognition memory deficit paralleled by lower hippocampal <strong>BDNF</strong> levels, both recovering upon ethanol withdrawal.
+BDNF	addiction	withdrawal	29752970	These findings show that repeated binge like ethanol episodes from adolescence to adulthood in female rats cause consistent and long term alterations of anxiety and hippocampal astrogliosis, whereas they trigger a recognition memory deficit paralleled by lower hippocampal <strong>BDNF</strong> levels, both recovering upon ethanol <b>withdrawal</b>.
+BDNF	drug	alcohol	29656414	We investigated whether add on memantine to regular valproic acid treatment ameliorated clinical symptoms, reduced <b>alcohol</b> use, and cytokine levels, and increased plasma brain derived neurotrophic factor (<strong>BDNF</strong>) in BD II patients with comorbid <b>alcohol</b> dependence.
+BDNF	addiction	dependence	29656414	We investigated whether add on memantine to regular valproic acid treatment ameliorated clinical symptoms, reduced alcohol use, and cytokine levels, and increased plasma brain derived neurotrophic factor (<strong>BDNF</strong>) in BD II patients with comorbid alcohol <b>dependence</b>.
+BDNF	drug	alcohol	29656414	We investigated whether add on memantine to regular valproic acid treatment ameliorated clinical symptoms, reduced <b>alcohol</b> use, and cytokine levels, and increased plasma <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in BD II patients with comorbid <b>alcohol</b> dependence.
+BDNF	addiction	dependence	29656414	We investigated whether add on memantine to regular valproic acid treatment ameliorated clinical symptoms, reduced alcohol use, and cytokine levels, and increased plasma <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in BD II patients with comorbid alcohol <b>dependence</b>.
+BDNF	drug	alcohol	29656414	Symptom severity, <b>alcohol</b> use, cytokine (plasma tumor necrosis factor α and C reactive protein [CRP], transforming growth factor β1 [TGF β1], interleukin 8 [IL 8], IL 10), and plasma <strong>BDNF</strong> levels were regularly assessed.
+BDNF	drug	alcohol	29656414	Mean within group decreases in Hamilton Depression Rating Scale (HDRS) and Young Mania Rating Scale (YMRS) scores, <b>alcohol</b> use, CRP, <strong>BDNF</strong>, and IL 8 levels were significantly different from baseline after 12 weeks of treatment.
+BDNF	drug	alcohol	29656414	BD II comorbid with <b>alcohol</b> dependence might benefit from add on memantine treatment, which significantly reduced clinical severity, <b>alcohol</b> use, and plasma cytokine levels, and increased <strong>BDNF</strong> levels.
+BDNF	addiction	dependence	29656414	BD II comorbid with alcohol <b>dependence</b> might benefit from add on memantine treatment, which significantly reduced clinical severity, alcohol use, and plasma cytokine levels, and increased <strong>BDNF</strong> levels.
+BDNF	drug	psychedelics	29576706	Rhynchophylline Downregulates Phosphorylated cAMP Response Element Binding Protein, Nuclear Receptor related 1, and <strong>Brain derived Neurotrophic Factor</strong> Expression in the Hippocampus of <b>Ketamine</b> induced Conditioned Place Preference Rats.
+BDNF	addiction	addiction	29576706	Increasing evidence supports the contributions of cAMP response element binding protein (CREB), nuclear receptor related 1 (Nurr1), and brain derived neurotrophic factor (<strong>BDNF</strong>) in modulating neural and behavioral plasticity which was induced by <b>addictive</b> drugs.
+BDNF	addiction	addiction	29576706	Increasing evidence supports the contributions of cAMP response element binding protein (CREB), nuclear receptor related 1 (Nurr1), and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in modulating neural and behavioral plasticity which was induced by <b>addictive</b> drugs.
+BDNF	drug	psychedelics	29576706	To investigate the effects of Rhy on the behavior and the levels of phosphorylated CREB (p CREB), Nurr1, and <strong>BDNF</strong> in the hippocampus of <b>ketamine</b> induced conditioned place preference (CPP) rats.
+BDNF	addiction	reward	29576706	To investigate the effects of Rhy on the behavior and the levels of phosphorylated CREB (p CREB), Nurr1, and <strong>BDNF</strong> in the hippocampus of ketamine induced conditioned place preference (<b>CPP</b>) rats.
+BDNF	drug	psychedelics	29576706	At the same time, expression of p CREB, Nurr1, and <strong>BDNF</strong>, which was significantly increased by <b>ketamine</b>, was restored in the Rhy  treated group.
+BDNF	drug	psychedelics	29576706	This study indicates that Rhy can reverse the reward effect induced by <b>ketamine</b> in rats and the mechanism can probably be related to regulate the hippocampal protein expression of p CREB, Nurr1, and <strong>BDNF</strong>.
+BDNF	addiction	reward	29576706	This study indicates that Rhy can reverse the <b>reward</b> effect induced by ketamine in rats and the mechanism can probably be related to regulate the hippocampal protein expression of p CREB, Nurr1, and <strong>BDNF</strong>.
+BDNF	drug	psychedelics	29576706	P CREB, Nurr1 and <strong>BDNF</strong> play an important role in the formation of <b>ketamine</b> induced place preference in ratsRhynchophylline reversed the expression of p CREB, Nurr1 and <strong>BDNF</strong> which was activated by <b>ketamine</b> in the hippocampusRhynchophylline demonstrates the potential effect of mediates <b>ketamine</b> induced rewarding effect.
+BDNF	drug	amphetamine	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; <strong>BDNF</strong>: Brain derived neurotrophic factor; CPP: Conditioned place preference; NMDA: N methyl D aspartic acid; <b>METH</b>: <b>Methamphetamine</b>; CNS: Central nervous system; PFA: Paraformaldehyde; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+BDNF	addiction	reward	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; <strong>BDNF</strong>: Brain derived neurotrophic factor; <b>CPP</b>: Conditioned place preference; NMDA: N methyl D aspartic acid; METH: Methamphetamine; CNS: Central nervous system; PFA: Paraformaldehyde; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+BDNF	drug	amphetamine	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; <strong>BDNF</strong>: <strong>Brain derived neurotrophic factor</strong>; CPP: Conditioned place preference; NMDA: N methyl D aspartic acid; <b>METH</b>: <b>Methamphetamine</b>; CNS: Central nervous system; PFA: Paraformaldehyde; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+BDNF	addiction	reward	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; <strong>BDNF</strong>: <strong>Brain derived neurotrophic factor</strong>; <b>CPP</b>: Conditioned place preference; NMDA: N methyl D aspartic acid; METH: Methamphetamine; CNS: Central nervous system; PFA: Paraformaldehyde; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+BDNF	drug	alcohol	29520063	A number of studies have suggested that <strong>BDNF</strong> (mature <strong>BDNF</strong>) and its precursor (proBDNF) play important roles in the <b>alcohol</b> dependence.
+BDNF	addiction	dependence	29520063	A number of studies have suggested that <strong>BDNF</strong> (mature <strong>BDNF</strong>) and its precursor (proBDNF) play important roles in the alcohol <b>dependence</b>.
+BDNF	drug	amphetamine	29501631	The main results showed that a history of <b>methamphetamine</b> administration (PND 54 57) induced enduring hippocampal cell damage (i.e., observed on PND 91) by decreasing cell survival (BrdU + cells) and mature <strong>BDNF</strong> (m <strong>BDNF</strong>) protein content, associated with neuronal survival, growth and differentiation.
+BDNF	drug	amphetamine	29501631	Interestingly, m <strong>BDNF</strong> regulation paralleled hippocampal c Fos protein content, indicating decreased neuronal activity, and thus reinforcing the persisting negative effects induced by <b>methamphetamine</b> in rat hippocampus following prolonged withdrawal.
+BDNF	addiction	reward	29501631	Interestingly, m <strong>BDNF</strong> regulation paralleled hippocampal c Fos protein content, indicating decreased neuronal activity, and thus <b>reinforcing</b> the persisting negative effects induced by methamphetamine in rat hippocampus following prolonged withdrawal.
+BDNF	addiction	withdrawal	29501631	Interestingly, m <strong>BDNF</strong> regulation paralleled hippocampal c Fos protein content, indicating decreased neuronal activity, and thus reinforcing the persisting negative effects induced by methamphetamine in rat hippocampus following prolonged <b>withdrawal</b>.
+BDNF	drug	psychedelics	29476799	In summary, miR 331 5p is a key regulatory factor of Nurr1, and rhynchophylline can participate in the process of resistance to <b>ketamine</b> addiction through the miR 331 5p/Nurr1/<strong>BDNF</strong> pathway or inhibition of CREB phosphorylation.
+BDNF	addiction	addiction	29476799	In summary, miR 331 5p is a key regulatory factor of Nurr1, and rhynchophylline can participate in the process of resistance to ketamine <b>addiction</b> through the miR 331 5p/Nurr1/<strong>BDNF</strong> pathway or inhibition of CREB phosphorylation.
+BDNF	drug	opioid	29445295	The activation of glial cells (microglia and astrocytes), expression of brain derived neurotrophic factor (<strong>BDNF</strong>) and μ <b>opioid</b> receptor in the spinal dorsal horn and endogenous <b>opioid</b> in the midbrain were examined using immunohistochemistry.
+BDNF	drug	opioid	29445295	The activation of glial cells (microglia and astrocytes), expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and μ <b>opioid</b> receptor in the spinal dorsal horn and endogenous <b>opioid</b> in the midbrain were examined using immunohistochemistry.
+BDNF	drug	opioid	29445295	The development of neuropathic pain was related to the activation of glial cells, increased <strong>BDNF</strong> expression, and downregulation of the μ <b>opioid</b> receptor in the ipsilateral spinal dorsal horn.
+BDNF	drug	opioid	29445295	In both exercise groups, the alleviation of neuropathic pain was accelerated through the regulation of glial activation, <strong>BDNF</strong> expression, and the endogenous <b>opioid</b> system.
+BDNF	drug	opioid	29445295	The expression of <strong>BDNF</strong> and endogenous <b>opioid</b> in relation to exercise induced alleviation of neuropathic pain differed in the HFE and LFE groups.
+BDNF	drug	opioid	29445295	Our findings indicated that aerobic exercise induced alleviated neuropathic pain through the regulation of glial cell activation, expression of <strong>BDNF</strong> in the ipsilateral spinal dorsal horn, and the endogenous <b>opioid</b> system.
+BDNF	drug	alcohol	29391279	Using quantitative real time polymerase chain reaction, we further confirmed that the expression of genes implicated in <b>alcohol</b> addiction, <strong>BDNF</strong>, CRHR1 and OPRM1, was also altered by transplantation of gut microbes from <b>alcohol</b> exposed donors.
+BDNF	addiction	addiction	29391279	Using quantitative real time polymerase chain reaction, we further confirmed that the expression of genes implicated in alcohol <b>addiction</b>, <strong>BDNF</strong>, CRHR1 and OPRM1, was also altered by transplantation of gut microbes from alcohol exposed donors.
+BDNF	drug	cocaine	29380665	Repeated <b>cocaine</b> exposure dysregulates <strong>BDNF</strong> expression and signaling in the mesocorticolimbic pathway of the adolescent rat.
+BDNF	drug	cocaine	29380665	Objectives: Long term abstinence following <b>cocaine</b> exposure up regulates brain derived neurotrophic factor (<strong>BDNF</strong>) expression in the mesocorticolimbic pathway.
+BDNF	drug	cocaine	29380665	Objectives: Long term abstinence following <b>cocaine</b> exposure up regulates <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression in the mesocorticolimbic pathway.
+BDNF	drug	cocaine	29380665	Given the increased vulnerability to drug abuse typical of adolescence, we hypothesized that changes in <strong>BDNF</strong> expression may become manifest early after the end of <b>cocaine</b> treatment in the adolescent brain.Methods: Rats received <b>cocaine</b> injections from postnatal day 28 (PND28) to PND42 and the mesocorticolimbic expression of <strong>BDNF</strong> was measured by real time PCR and Western blotting at PND43.Results: In the ventral tegmental area, <strong>BDNF</strong> tropomyosin receptor kinase B (TrΚB) expression and phosphorylation are enhanced while the intracellular signaling is unaltered.
+BDNF	drug	cocaine	29380665	To evaluate the role of glutamate on <strong>BDNF</strong> independent changes, we investigated the expression of the transporter GLT 1 and the activation of the NMDA receptor subunit GluN2B, which were both increased in the PL cortex while reduced in the IL cortex.Conclusions: Our results show that adolescent <b>cocaine</b> exposure modulates <strong>BDNF</strong> system early after treatment in the mesocorticolimbic pathway, identifying a complex but specific set of changes that could provide clues for treatment.
+BDNF	addiction	withdrawal	29374540	Alteration of biological markers of oxidative stress and brain derived neurotrophic factor (<strong>BDNF</strong>) could be related to the severity of crack <b>withdrawal</b> symptoms in patients undergoing rehabilitation.
+BDNF	addiction	withdrawal	29374540	Alteration of biological markers of oxidative stress and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) could be related to the severity of crack <b>withdrawal</b> symptoms in patients undergoing rehabilitation.
+BDNF	drug	alcohol	29357295	Association study of <strong>BDNF</strong> and DRD3 genes with <b>alcohol</b> use disorder in Schizophrenia.
+BDNF	drug	alcohol	29357295	The brain derived neurotrophic factor (<strong>BDNF</strong>) and dopamine D3 receptor (DRD3) have been implicated in <b>alcohol</b> drinking behaviour.
+BDNF	drug	alcohol	29357295	The <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and dopamine D3 receptor (DRD3) have been implicated in <b>alcohol</b> drinking behaviour.
+BDNF	drug	alcohol	29357295	Previous genetic studies of the <strong>BDNF</strong> and DRD3 genes produced mixed findings; however, only one study investigated two <strong>BDNF</strong> genetic markers with <b>alcohol</b> dependence in schizophrenia patients.
+BDNF	addiction	dependence	29357295	Previous genetic studies of the <strong>BDNF</strong> and DRD3 genes produced mixed findings; however, only one study investigated two <strong>BDNF</strong> genetic markers with alcohol <b>dependence</b> in schizophrenia patients.
+BDNF	drug	alcohol	29357295	We investigated 15 single nucleotide polymorphisms (SNPs) in DRD3 and four SNPs in <strong>BDNF</strong> for possible association with <b>alcohol</b> abuse or dependence in schizophrenia patients of European ancestry (N = 195).
+BDNF	addiction	dependence	29357295	We investigated 15 single nucleotide polymorphisms (SNPs) in DRD3 and four SNPs in <strong>BDNF</strong> for possible association with alcohol abuse or <b>dependence</b> in schizophrenia patients of European ancestry (N = 195).
+BDNF	drug	alcohol	29357295	We found the <strong>BDNF</strong> Val66Met to be associated with <b>alcohol</b> dependence (p = 0.004).
+BDNF	addiction	dependence	29357295	We found the <strong>BDNF</strong> Val66Met to be associated with alcohol <b>dependence</b> (p = 0.004).
+BDNF	drug	alcohol	29357295	We also found haplotypes across <strong>BDNF</strong> to be nominally associated with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	29357295	We also found haplotypes across <strong>BDNF</strong> to be nominally associated with alcohol <b>dependence</b>.
+BDNF	drug	alcohol	29357295	Our findings support a role of the <strong>BDNF</strong> gene in <b>alcohol</b> dependence in schizophrenia patients.
+BDNF	addiction	dependence	29357295	Our findings support a role of the <strong>BDNF</strong> gene in alcohol <b>dependence</b> in schizophrenia patients.
+BDNF	addiction	addiction	29348190	DAT KO rats also demonstrate cognitive deficits in working memory and sensorimotor gating tests, less propensity to develop <b>compulsive</b> behaviors, and strong dysregulation in frontostriatal <strong>BDNF</strong> function.
+BDNF	drug	amphetamine	29338492	These preliminary findings indicate that genetic variability in GRIA3 may interact with a functional <strong>BDNF</strong> polymorphism to provide a strong risk factor for the development of <b>METH</b> dependence in the Thai population.
+BDNF	addiction	dependence	29338492	These preliminary findings indicate that genetic variability in GRIA3 may interact with a functional <strong>BDNF</strong> polymorphism to provide a strong risk factor for the development of METH <b>dependence</b> in the Thai population.
+BDNF	drug	alcohol	29306704	While a subset of IEGs encoding for effector proteins (such as <strong>Bdnf</strong>, InhbA and Dusp5) were downregulated by <b>ethanol</b>, others (such as Il 6) were unaffected.
+BDNF	drug	opioid	29294331	Effects of <strong>BDNF</strong> receptor antagonist on the severity of physical and psychological dependence, <b>morphine</b> induced locomotor sensitization and the ventral tegmental area nucleus accumbens <strong>BDNF</strong> levels in <b>morphine</b>  dependent and withdrawn rats.
+BDNF	addiction	dependence	29294331	Effects of <strong>BDNF</strong> receptor antagonist on the severity of physical and psychological <b>dependence</b>, morphine induced locomotor sensitization and the ventral tegmental area nucleus accumbens <strong>BDNF</strong> levels in morphine  dependent and withdrawn rats.
+BDNF	addiction	sensitization	29294331	Effects of <strong>BDNF</strong> receptor antagonist on the severity of physical and psychological dependence, morphine induced locomotor <b>sensitization</b> and the ventral tegmental area nucleus accumbens <strong>BDNF</strong> levels in morphine  dependent and withdrawn rats.
+BDNF	drug	opioid	29294331	This study examined the effects of systemic administration of the TrkB receptor antagonist (ANA 12) on the severity of physical and psychological dependence and <b>morphine</b> induced locomotor sensitization, the ventral tegmental area (VTA) nucleus accumbens (NAc) <strong>BDNF</strong> levels in <b>morphine</b> dependent and withdrawn rats.
+BDNF	addiction	dependence	29294331	This study examined the effects of systemic administration of the TrkB receptor antagonist (ANA 12) on the severity of physical and psychological <b>dependence</b> and morphine induced locomotor sensitization, the ventral tegmental area (VTA) nucleus accumbens (NAc) <strong>BDNF</strong> levels in morphine dependent and withdrawn rats.
+BDNF	addiction	sensitization	29294331	This study examined the effects of systemic administration of the TrkB receptor antagonist (ANA 12) on the severity of physical and psychological dependence and morphine induced locomotor <b>sensitization</b>, the ventral tegmental area (VTA) nucleus accumbens (NAc) <strong>BDNF</strong> levels in morphine dependent and withdrawn rats.
+BDNF	drug	opioid	29294331	The VTA NAc <strong>BDNF</strong> levels were assessed in <b>morphine</b> dependent and withdrawn rats.
+BDNF	drug	opioid	29294331	There was no significant difference in the locomotor activity and the VTA NAc <strong>BDNF</strong> levels between D/Sal/<b>morphine</b> and D/ANA 12/<b>morphine</b> groups after <b>morphine</b> withdrawal.
+BDNF	addiction	withdrawal	29294331	There was no significant difference in the locomotor activity and the VTA NAc <strong>BDNF</strong> levels between D/Sal/morphine and D/ANA 12/morphine groups after morphine <b>withdrawal</b>.
+BDNF	drug	opioid	29294331	However, ANA 12 did not affect <b>morphine</b> induced locomotor sensitization and the VTA NAc <strong>BDNF</strong> levels in <b>morphine</b> dependent and withdrawn rats.
+BDNF	addiction	sensitization	29294331	However, ANA 12 did not affect morphine induced locomotor <b>sensitization</b> and the VTA NAc <strong>BDNF</strong> levels in morphine dependent and withdrawn rats.
+BDNF	drug	nicotine	29266170	We investigated, in a mouse model, the effect of exercise intensity during chronic <b>nicotine</b> exposure on <b>nicotine</b> withdrawal severity, binding of α4β2*, α7 nicotinic acetylcholine (nAChR), μ opioid (μ receptors) and D2 dopamine receptors and on brain derived neurotrophic factor (<strong>BDNF</strong>) and plasma corticosterone levels.
+BDNF	drug	opioid	29266170	We investigated, in a mouse model, the effect of exercise intensity during chronic nicotine exposure on nicotine withdrawal severity, binding of α4β2*, α7 nicotinic acetylcholine (nAChR), μ <b>opioid</b> (μ receptors) and D2 dopamine receptors and on brain derived neurotrophic factor (<strong>BDNF</strong>) and plasma corticosterone levels.
+BDNF	addiction	withdrawal	29266170	We investigated, in a mouse model, the effect of exercise intensity during chronic nicotine exposure on nicotine <b>withdrawal</b> severity, binding of α4β2*, α7 nicotinic acetylcholine (nAChR), μ opioid (μ receptors) and D2 dopamine receptors and on brain derived neurotrophic factor (<strong>BDNF</strong>) and plasma corticosterone levels.
+BDNF	drug	nicotine	29266170	We investigated, in a mouse model, the effect of exercise intensity during chronic <b>nicotine</b> exposure on <b>nicotine</b> withdrawal severity, binding of α4β2*, α7 nicotinic acetylcholine (nAChR), μ opioid (μ receptors) and D2 dopamine receptors and on <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and plasma corticosterone levels.
+BDNF	drug	opioid	29266170	We investigated, in a mouse model, the effect of exercise intensity during chronic nicotine exposure on nicotine withdrawal severity, binding of α4β2*, α7 nicotinic acetylcholine (nAChR), μ <b>opioid</b> (μ receptors) and D2 dopamine receptors and on <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and plasma corticosterone levels.
+BDNF	addiction	withdrawal	29266170	We investigated, in a mouse model, the effect of exercise intensity during chronic nicotine exposure on nicotine <b>withdrawal</b> severity, binding of α4β2*, α7 nicotinic acetylcholine (nAChR), μ opioid (μ receptors) and D2 dopamine receptors and on <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and plasma corticosterone levels.
+BDNF	drug	nicotine	29266170	Neither exercise nor <b>nicotine</b> treatment affected μ or D2 receptor binding or <strong>BDNF</strong> levels.
+BDNF	drug	cannabinoid	29231147	Inclusion criteria were: 1) full text available in English; 2) published in a peerreviewed journal and using the following keywords: neurotransmitters (AgRP, <strong>BDNF</strong>, αMSH, NP Y, <b>endocannabinoids</b>, adiponectin, CCK, ghrelin, GLP 1, insulin, leptin, PP, PYY), hormones (FSH, LH, estrogen, progesterone, testosterone) and bulimia nervosa, eating disorders.
+BDNF	drug	opioid	29217257	The present findings indicate that the <strong>BDNF</strong> and IL 1ß induction within the dorsal horn may be linked to the development of hyperalgesia, and that <b>opioid</b> analgesics and probably inhibitors of glial cell activation can prevent sensitization in the pain pathway at spinal level.
+BDNF	addiction	sensitization	29217257	The present findings indicate that the <strong>BDNF</strong> and IL 1ß induction within the dorsal horn may be linked to the development of hyperalgesia, and that opioid analgesics and probably inhibitors of glial cell activation can prevent <b>sensitization</b> in the pain pathway at spinal level.
+BDNF	drug	alcohol	29158111	Brain derived neurotrophic factor (<strong>BDNF</strong>) determines a sex difference in cue conditioned <b>alcohol</b> seeking in rats.
+BDNF	addiction	relapse	29158111	Brain derived neurotrophic factor (<strong>BDNF</strong>) determines a sex difference in cue conditioned alcohol <b>seeking</b> in rats.
+BDNF	drug	alcohol	29158111	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) determines a sex difference in cue conditioned <b>alcohol</b> seeking in rats.
+BDNF	addiction	relapse	29158111	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) determines a sex difference in cue conditioned alcohol <b>seeking</b> in rats.
+BDNF	drug	alcohol	29158111	Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) is implicated in substance abuse disorders including <b>alcoholism</b>.
+BDNF	drug	alcohol	29158111	<strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) is implicated in substance abuse disorders including <b>alcoholism</b>.
+BDNF	drug	alcohol	29158111	As the vast majority of previous animal model studies have concentrated on males only, the aim of this study was to determine whether endogenous <strong>BDNF</strong> mediates <b>alcohol</b> seeking in a sex specific manner.
+BDNF	addiction	relapse	29158111	As the vast majority of previous animal model studies have concentrated on males only, the aim of this study was to determine whether endogenous <strong>BDNF</strong> mediates alcohol <b>seeking</b> in a sex specific manner.
+BDNF	drug	alcohol	29158111	We used an operant self administration paradigm where the animals were trained in operant chambers to self administer a 10% <b>ethanol</b> solution, and compared male and female <strong>BDNF</strong> heterozygous (HET) and wildtype (WT) rats.
+BDNF	addiction	reward	29158111	We used an <b>operant</b> self administration paradigm where the animals were trained in <b>operant</b> chambers to self administer a 10% ethanol solution, and compared male and female <strong>BDNF</strong> heterozygous (HET) and wildtype (WT) rats.
+BDNF	drug	alcohol	29158111	However, a significant difference between male and female WT rats following <b>alcohol</b> primed reinstatement was completely absent in <strong>BDNF</strong> HET rats suggesting a role of <strong>BDNF</strong> in sex differences in <b>alcohol</b> seeking after abstinence.
+BDNF	addiction	relapse	29158111	However, a significant difference between male and female WT rats following alcohol primed <b>reinstatement</b> was completely absent in <strong>BDNF</strong> HET rats suggesting a role of <strong>BDNF</strong> in sex differences in alcohol <b>seeking</b> after abstinence.
+BDNF	drug	alcohol	29158111	Female <strong>BDNF</strong> HET rats showed significantly higher number of <b>alcohol</b> paired lever presses during reinstatement than female WT controls.
+BDNF	addiction	relapse	29158111	Female <strong>BDNF</strong> HET rats showed significantly higher number of alcohol paired lever presses during <b>reinstatement</b> than female WT controls.
+BDNF	drug	alcohol	29158111	These findings suggest that <strong>BDNF</strong> regulatory pathways are involved in sex differences in reinstatement of <b>alcohol</b> intake and emphasize the need to include both male and female animals to explore sex specific interactions in addiction neurocircuitry.
+BDNF	addiction	addiction	29158111	These findings suggest that <strong>BDNF</strong> regulatory pathways are involved in sex differences in reinstatement of alcohol intake and emphasize the need to include both male and female animals to explore sex specific interactions in <b>addiction</b> neurocircuitry.
+BDNF	addiction	relapse	29158111	These findings suggest that <strong>BDNF</strong> regulatory pathways are involved in sex differences in <b>reinstatement</b> of alcohol intake and emphasize the need to include both male and female animals to explore sex specific interactions in addiction neurocircuitry.
+BDNF	addiction	withdrawal	29139560	This increase persisted during EtOH <b>withdrawal</b>, along with an increase in NR2B Y1472 phosphorylation, mature <strong>brain derived neurotrophic factor</strong>, and phosphorylated TrkB.
+BDNF	drug	opioid	29111854	We observed differential methylation of <strong>Bdnf</strong> and Il6 in the pons, Nr3c1 in the cerebellum, and Il1b in the hippocampus in response to acute <b>morphine</b> exposure (all P value < 0.05).
+BDNF	drug	alcohol	29108028	Decreased plasma concentrations of <strong>BDNF</strong> and IGF 1 in abstinent patients with <b>alcohol</b> use disorders.
+BDNF	drug	alcohol	29108028	In order to further clarify the impact of chronic <b>alcohol</b> consumption on circulating growth factors, a cross sectional study was performed in abstinent AUD patients (<b>alcohol</b> group, N = 91) and healthy control subjects (control group, N = 55) to examine plasma concentrations of brain derived neurotrophic factor (<strong>BDNF</strong>), insulin like growth factor 1 (IGF 1) and IGF 1 binding protein 3 (IGFBP 3).
+BDNF	drug	alcohol	29108028	In order to further clarify the impact of chronic <b>alcohol</b> consumption on circulating growth factors, a cross sectional study was performed in abstinent AUD patients (<b>alcohol</b> group, N = 91) and healthy control subjects (control group, N = 55) to examine plasma concentrations of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), insulin like growth factor 1 (IGF 1) and IGF 1 binding protein 3 (IGFBP 3).
+BDNF	drug	alcohol	29108028	Plasma <strong>BDNF</strong> and IGF 1 concentrations were significantly lower in the <b>alcohol</b> group than in the control group (p<0.001).
+BDNF	drug	alcohol	29108028	These results suggest that further research is necessary to elucidate the role of <strong>BDNF</strong> in <b>alcohol</b> induced toxicity and the biological significance of the lack of correlation between age and plasma IGF 1 levels in abstinent AUD patients.
+BDNF	addiction	reward	29076919	<strong>Brain derived neurotrophic factor</strong> mediated projection specific regulation of depressive like and nociceptive behaviors in the mesolimbic <b>reward</b> circuitry.
+BDNF	drug	opioid	29076919	Furthermore, the relief of depressive like behaviors induced by intra VTA injection of <b>morphine</b> in CMS mice could be prevented by blocking brain derived neurotrophic factor (<strong>BDNF</strong>) signaling and mimicked by the administration of exogenous <strong>BDNF</strong> in mPFC rather than in NAc shell.
+BDNF	drug	opioid	29076919	Furthermore, the relief of depressive like behaviors induced by intra VTA injection of <b>morphine</b> in CMS mice could be prevented by blocking <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling and mimicked by the administration of exogenous <strong>BDNF</strong> in mPFC rather than in NAc shell.
+BDNF	drug	opioid	29076919	Nociceptive responses induced by the activation of VTA DA neurons with <b>morphine</b> in CMS mice could be prevented by blocking <strong>BDNF</strong> signaling or mimicked by administration of exogenous <strong>BDNF</strong> in NAc shell, but not in mPFC.
+BDNF	drug	nicotine	29075117	We investigated the following biological markers for any alterations during <b>smoking</b> cessation in the absence of pharmacotherapy: the dopamine metabolite homovanillic acid (HVA), the noradrenaline metabolite 3 methoxy 4 hydroxyphenylglycol (MHPG) and brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	nicotine	29075117	We investigated the following biological markers for any alterations during <b>smoking</b> cessation in the absence of pharmacotherapy: the dopamine metabolite homovanillic acid (HVA), the noradrenaline metabolite 3 methoxy 4 hydroxyphenylglycol (MHPG) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	nicotine	29075117	The hardcore <b>smoker</b> group had higher MHPG and <strong>BDNF</strong> levels than the non <b>smoker</b> group (p=0.002 and p<0.001, respectively).
+BDNF	drug	amphetamine	29065400	Collectively, this data highlights the importance of the frontal cortex in <b>methamphetamine</b> induced effects, and also the similar dose response effect of <b>methamphetamine</b> on dopamine and <strong>BDNF</strong> expression.
+BDNF	drug	nicotine	29042206	In addition, the effect of α asarone or bupropion on the hippocampal pCREB, CREB and <strong>BDNF</strong> levels during <b>nicotine</b> withdrawal were measured.
+BDNF	addiction	withdrawal	29042206	In addition, the effect of α asarone or bupropion on the hippocampal pCREB, CREB and <strong>BDNF</strong> levels during nicotine <b>withdrawal</b> were measured.
+BDNF	drug	opioid	29031903	In conclusion, we found that agmatine abolished chronic <b>morphine</b> induced decrease in proliferation of hippocampal progenitors in vivo and in vitro, which may be due to the increase in cAMP CREB <strong>BDNF</strong> signaling.
+BDNF	drug	alcohol	28889008	The interplay between ventro striatal <strong>BDNF</strong> levels and the effects of valproic acid on the acquisition of <b>ethanol</b> induced conditioned place preference in mice.
+BDNF	drug	alcohol	28889008	In addition, neuroadaptive changes mediated by the brain derived neurotrophic factor (<strong>BDNF</strong>) seems to be an interesting pharmacological target for <b>alcoholism</b> treatment.
+BDNF	drug	alcohol	28889008	In addition, neuroadaptive changes mediated by the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) seems to be an interesting pharmacological target for <b>alcoholism</b> treatment.
+BDNF	drug	alcohol	28889008	VPA pretreatment increased <strong>BDNF</strong> levels when compared to <b>ethanol</b> induced CPP.
+BDNF	addiction	reward	28889008	VPA pretreatment increased <strong>BDNF</strong> levels when compared to ethanol induced <b>CPP</b>.
+BDNF	drug	alcohol	28882570	Taurine restores the exploratory behavior following <b>alcohol</b> withdrawal and decreases <strong>BDNF</strong> mRNA expression in the frontal cortex of chronic <b>alcohol</b> treated rats.
+BDNF	addiction	withdrawal	28882570	Taurine restores the exploratory behavior following alcohol <b>withdrawal</b> and decreases <strong>BDNF</strong> mRNA expression in the frontal cortex of chronic alcohol treated rats.
+BDNF	drug	alcohol	28882570	Therefore, we investigated the effects of taurine on behavior in the open field test (OFT), the GABAAR α2 subunit and <strong>BDNF</strong> mRNA expression in the frontal cortex of rats after chronic <b>alcohol</b> treatment or upon withdrawal.
+BDNF	addiction	withdrawal	28882570	Therefore, we investigated the effects of taurine on behavior in the open field test (OFT), the GABAAR α2 subunit and <strong>BDNF</strong> mRNA expression in the frontal cortex of rats after chronic alcohol treatment or upon <b>withdrawal</b>.
+BDNF	drug	alcohol	28882570	Chronic <b>alcohol</b> treatment or withdrawal did not change the GABAAR α2 subunit or <strong>BDNF</strong> mRNA expression in the frontal cortex, but taurine decreased the α2 subunit level in control rats and to the <strong>BDNF</strong> levels in the <b>alcohol</b> rat group.
+BDNF	addiction	withdrawal	28882570	Chronic alcohol treatment or <b>withdrawal</b> did not change the GABAAR α2 subunit or <strong>BDNF</strong> mRNA expression in the frontal cortex, but taurine decreased the α2 subunit level in control rats and to the <strong>BDNF</strong> levels in the alcohol rat group.
+BDNF	drug	alcohol	28882570	We conclude that taurine restored exploratory behavior after <b>alcohol</b> withdrawal but that this effect was not related to the GABAAR α2 subunit or <strong>BDNF</strong> mRNA expression in the frontal cortex of the rats.
+BDNF	addiction	withdrawal	28882570	We conclude that taurine restored exploratory behavior after alcohol <b>withdrawal</b> but that this effect was not related to the GABAAR α2 subunit or <strong>BDNF</strong> mRNA expression in the frontal cortex of the rats.
+BDNF	drug	nicotine	28857504	Persistent histone modifications at the <strong>BDNF</strong> and Cdk 5 promoters following extinction of <b>nicotine</b> seeking in rats.
+BDNF	addiction	relapse	28857504	Persistent histone modifications at the <strong>BDNF</strong> and Cdk 5 promoters following extinction of nicotine <b>seeking</b> in rats.
+BDNF	drug	nicotine	28857504	A history of <b>nicotine</b> exposure significantly decreased H3K14 acetylation at the brain derived neurotrophic factor (<strong>BDNF</strong>) exon IV promoter, and this effect was abolished with NaB treatment.
+BDNF	drug	nicotine	28857504	A history of <b>nicotine</b> exposure significantly decreased H3K14 acetylation at the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) exon IV promoter, and this effect was abolished with NaB treatment.
+BDNF	drug	nicotine	28857504	In contrast, <b>nicotine</b> self administration alone, resulted in a significant decrease in histone methylation at the H3K27me3 and H3K9me2 marks in the promoter regions of <strong>BDNF</strong> exon IV and cyclin dependent kinase 5 (Cdk 5).
+BDNF	drug	nicotine	28857504	Quantitative PCR identified changes in several genes associated with NaB treatment that were independent of <b>nicotine</b> exposure; however, an interaction of <b>nicotine</b> history and NaB treatment was detected only in the expression of <strong>BDNF</strong> IV and <strong>BDNF</strong> IX.
+BDNF	drug	nicotine	28857504	Together these results suggest that <b>nicotine</b> self administration leads to a number of epigenetic changes at both the <strong>BDNF</strong> and Cdk 5 promoters, and that these changes may contribute to the enhanced extinction of <b>nicotine</b> seeking by NaB.
+BDNF	addiction	relapse	28857504	Together these results suggest that nicotine self administration leads to a number of epigenetic changes at both the <strong>BDNF</strong> and Cdk 5 promoters, and that these changes may contribute to the enhanced extinction of nicotine <b>seeking</b> by NaB.
+BDNF	drug	cocaine	28857460	Working memory and salivary <strong>brain derived neurotrophic factor</strong> as developmental predictors of <b>cocaine</b> seeking in male and female rats.
+BDNF	addiction	relapse	28857460	Working memory and salivary <strong>brain derived neurotrophic factor</strong> as developmental predictors of cocaine <b>seeking</b> in male and female rats.
+BDNF	drug	cocaine	28857460	We sought to determine in rats whether juvenile traits, specifically poor working memory and low salivary brain derived neurotrophic factor (<strong>BDNF</strong>), are related to elevated <b>cocaine</b> taking and relapse in adolescence and adulthood.
+BDNF	addiction	relapse	28857460	We sought to determine in rats whether juvenile traits, specifically poor working memory and low salivary brain derived neurotrophic factor (<strong>BDNF</strong>), are related to elevated cocaine taking and <b>relapse</b> in adolescence and adulthood.
+BDNF	drug	cocaine	28857460	We sought to determine in rats whether juvenile traits, specifically poor working memory and low salivary <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), are related to elevated <b>cocaine</b> taking and relapse in adolescence and adulthood.
+BDNF	addiction	relapse	28857460	We sought to determine in rats whether juvenile traits, specifically poor working memory and low salivary <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), are related to elevated cocaine taking and <b>relapse</b> in adolescence and adulthood.
+BDNF	drug	cocaine	28857460	Saliva was assayed at P20 for <strong>BDNF</strong> before <b>cocaine</b> self administration on P28 [0.75 or 0.25 mg/kg/infusion for 30 days under a fixed ratio (FR) 1 to FR5 schedule] and on P94 before relapse after 30 day abstinence in adulthood.
+BDNF	addiction	relapse	28857460	Saliva was assayed at P20 for <strong>BDNF</strong> before cocaine self administration on P28 [0.75 or 0.25 mg/kg/infusion for 30 days under a fixed ratio (FR) 1 to FR5 schedule] and on P94 before <b>relapse</b> after 30 day abstinence in adulthood.
+BDNF	addiction	relapse	28857460	These elevated <b>relapse</b> rates in male rats were significantly associated with P20 object discrimination and salivary <strong>BDNF</strong>.
+BDNF	drug	cocaine	28857460	In conclusion, poor working memory and low salivary <strong>BDNF</strong> in juvenile male rats may represent biomarkers for later <b>cocaine</b> use.
+BDNF	drug	alcohol	28851339	This study examined how <b>alcohol</b> use disorder (AUD) patients with post traumatic stress disorder (PTSD) differed from those without PTSD in terms of demography, drinking patterns and C reactive protein, inflammatory cytokines, tryptophan metabolism parameters, and brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	alcohol	28851339	This study examined how <b>alcohol</b> use disorder (AUD) patients with post traumatic stress disorder (PTSD) differed from those without PTSD in terms of demography, drinking patterns and C reactive protein, inflammatory cytokines, tryptophan metabolism parameters, and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	addiction	relapse	28848444	Moreover, prazosin treated mice that had extinguished CS preference showed increased mRNA expression of brain derived neurotrophic factor (<strong>BDNF</strong>) and post synaptic density 95 (PSD 95) in the nucleus accumbens shell or core, respectively, thus suggesting that prelimbic α1 adrenergic receptor blockade triggers neural adaptations in subcortical areas that could contribute to the extinction of cue induced drug <b>seeking</b> behavior.
+BDNF	addiction	relapse	28848444	Moreover, prazosin treated mice that had extinguished CS preference showed increased mRNA expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and post synaptic density 95 (PSD 95) in the nucleus accumbens shell or core, respectively, thus suggesting that prelimbic α1 adrenergic receptor blockade triggers neural adaptations in subcortical areas that could contribute to the extinction of cue induced drug <b>seeking</b> behavior.
+BDNF	drug	alcohol	28847297	NGF and <strong>BDNF</strong> Alterations by Prenatal <b>Alcohol</b> Exposure.
+BDNF	drug	alcohol	28847297	Neurotrophins, in particular nerve growth factor (NGF) and brain derived neurotrophic factor (<strong>BDNF</strong>), are molecules playing a pivotal role in the survival, development and function of the peripheral and central nervous systems but also in the pathogenesis of developmental defects caused by <b>alcohol</b> exposure.
+BDNF	drug	alcohol	28847297	Neurotrophins, in particular nerve growth factor (NGF) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), are molecules playing a pivotal role in the survival, development and function of the peripheral and central nervous systems but also in the pathogenesis of developmental defects caused by <b>alcohol</b> exposure.
+BDNF	drug	alcohol	28847297	NGF and <strong>BDNF</strong> changes play a subtle role in short  and long lasting effects of <b>alcohol</b> in <b>ethanol</b> target tissues, including neuronal cell death and severe cognitive and physiological deficits in the newborns.
+BDNF	drug	opioid	28847022	This study was aimed to investigate the attenuation effect of Cerebrolysin, a mixture of potent growth factors (<strong>BDNF</strong>, GDNF, NGF, CNTF etc,), on the development of <b>Morphine</b> induced dependence and tolerance.
+BDNF	addiction	dependence	28847022	This study was aimed to investigate the attenuation effect of Cerebrolysin, a mixture of potent growth factors (<strong>BDNF</strong>, GDNF, NGF, CNTF etc,), on the development of Morphine induced <b>dependence</b> and tolerance.
+BDNF	drug	cannabinoid	28822116	Almost consistently, these studies revealed that polymorphisms in COMT, <strong>BDNF</strong>, and FKBP5 genes might interact with early life stress and <b>cannabis</b> abuse or dependence, influencing various outcomes of schizophrenia spectrum disorders and BD.
+BDNF	addiction	dependence	28822116	Almost consistently, these studies revealed that polymorphisms in COMT, <strong>BDNF</strong>, and FKBP5 genes might interact with early life stress and cannabis abuse or <b>dependence</b>, influencing various outcomes of schizophrenia spectrum disorders and BD.
+BDNF	drug	alcohol	28819238	Effects of environmental enrichment upon <b>ethanol</b> induced conditioned place preference and pre frontal <strong>BDNF</strong> levels in adolescent and adult mice.
+BDNF	drug	alcohol	28819238	Among SC, but not among EE, adolescents, <strong>BDNF</strong> levels were significantly lower in those treated with <b>ethanol</b> than in those given vehicle.
+BDNF	drug	alcohol	28819238	<b>Ethanol</b> significantly reduced <strong>BDNF</strong> levels in adolescents reared under standard housing conditions, but not in adult mice nor in adolescents given EE housing conditions.
+BDNF	drug	opioid	28811779	Effect of exercise and <b>morphine</b> on psychological and physical dependencies, <strong>BDNF</strong> and TrkB gene expression in rat's hippocampus.
+BDNF	drug	opioid	28811779	Correlation between exercise level, <b>morphine</b> injection, concurrent <b>morphine</b> administration and exercise with <b>morphine</b> CPP, <strong>BDNF</strong> and TrkB genes was determined.
+BDNF	addiction	reward	28811779	Correlation between exercise level, morphine injection, concurrent morphine administration and exercise with morphine <b>CPP</b>, <strong>BDNF</strong> and TrkB genes was determined.
+BDNF	addiction	reward	28811779	Voluntary exercise in different levels potentiates the brain rewarding system, <b>CPP</b> scale, and hippocampal <strong>BDNF</strong> and TrKB expressions.
+BDNF	drug	cocaine	28808012	<strong>BDNF</strong> TrkB controls <b>cocaine</b> induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors.
+BDNF	addiction	addiction	28808012	<strong>BDNF</strong> TrkB controls cocaine induced dendritic spines in rodent nucleus accumbens dissociated from increases in <b>addictive</b> behaviors.
+BDNF	drug	cocaine	28808012	Here we show that brain derived neurotrophic factor (<strong>BDNF</strong>) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is necessary for <b>cocaine</b> induced dendritic spine formation by using either localized TrkB knockout or viral mediated expression of a dominant negative, kinase dead TrkB mutant.
+BDNF	drug	cocaine	28808012	Here we show that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is necessary for <b>cocaine</b> induced dendritic spine formation by using either localized TrkB knockout or viral mediated expression of a dominant negative, kinase dead TrkB mutant.
+BDNF	drug	cocaine	28808012	Together, these findings indicate that <strong>BDNF</strong> TrkB signaling both mediates and reverses <b>cocaine</b> induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in addictive behavior.
+BDNF	addiction	addiction	28808012	Together, these findings indicate that <strong>BDNF</strong> TrkB signaling both mediates and reverses cocaine induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in <b>addictive</b> behavior.
+BDNF	drug	alcohol	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, ADH1C, OPRM1, DRD2, <strong>BDNF</strong>, and ALDH2 genes on <b>alcohol</b> dependence in a Caucasian population.
+BDNF	addiction	dependence	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, ADH1C, OPRM1, DRD2, <strong>BDNF</strong>, and ALDH2 genes on alcohol <b>dependence</b> in a Caucasian population.
+BDNF	drug	opioid	28777966	Long term <b>heroin</b> use was associated with the downregulation of systemic platelets, <strong>BDNF</strong>, and TGF β1, and it contributed to the disruption of executive function in Taiwanese Han Chinese.
+BDNF	drug	opioid	28777966	Long term <b>heroin</b> addicts have low plasma brain derived neurotrophic factor (<strong>BDNF</strong>) levels.
+BDNF	drug	opioid	28777966	Long term <b>heroin</b> addicts have low plasma <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels.
+BDNF	drug	opioid	28777966	However, the mechanisms and effects of systemic disturbances of <strong>BDNF</strong> caused by <b>heroin</b> remain unclear.
+BDNF	drug	opioid	28777966	Thus, we investigated the effects of <b>heroin</b> on platelets, <strong>BDNF</strong> and TGF β1, the association between blood platelets, <strong>BDNF</strong>, TGF β1, and executive function in long term <b>heroin</b> addicts.
+BDNF	drug	opioid	28777966	Plasma <strong>BDNF</strong> and TGF β1 levels were significantly downregulated in long term <b>heroin</b> addicts.
+BDNF	drug	opioid	28777966	<strong>BDNF</strong>, TGF β1, and platelet levels were lower in patients who had used <b>heroin</b> for more than 6 years than in those who had used it for less than 6 years.
+BDNF	drug	opioid	28777966	In long term <b>heroin</b> addicts, lower platelet counts contributed to lower plasma <strong>BDNF</strong> and TGF β1 levels, which, in turn, contributed to the disruption of executive function after long term <b>heroin</b> use.
+BDNF	drug	alcohol	28776866	RNA Seq analysis confirmed a prenatal AR mediated control of adult expression of <b>alcohol</b> drinking related genes like <strong>Bdnf</strong> and Per2.
+BDNF	drug	opioid	28776309	<b>Morphine</b> Withdrawal Increases <strong>Brain Derived Neurotrophic Factor</strong> Precursor.
+BDNF	addiction	withdrawal	28776309	Morphine <b>Withdrawal</b> Increases <strong>Brain Derived Neurotrophic Factor</strong> Precursor.
+BDNF	drug	opioid	28776309	<b>Morphine</b> has been shown to increase the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in the brain.
+BDNF	drug	opioid	28776309	<b>Morphine</b> has been shown to increase the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the brain.
+BDNF	drug	opioid	28776309	However, little is known about the effect of <b>morphine</b> withdrawal on <strong>BDNF</strong> and its precursor protein, or proBDNF, which induces neuronal apoptosis.
+BDNF	addiction	withdrawal	28776309	However, little is known about the effect of morphine <b>withdrawal</b> on <strong>BDNF</strong> and its precursor protein, or proBDNF, which induces neuronal apoptosis.
+BDNF	drug	opioid	28776309	In this work, we examined whether <strong>BDNF</strong> and proBDNF levels change in rats chronically injected with escalating doses of <b>morphine</b> and those who undergo spontaneous withdrawal for 60 h. We observed, in the frontal cortex and striatum, that the ratio of <strong>BDNF</strong> to proBDNF changed depending upon the experimental paradigm.
+BDNF	addiction	withdrawal	28776309	In this work, we examined whether <strong>BDNF</strong> and proBDNF levels change in rats chronically injected with escalating doses of morphine and those who undergo spontaneous <b>withdrawal</b> for 60 h. We observed, in the frontal cortex and striatum, that the ratio of <strong>BDNF</strong> to proBDNF changed depending upon the experimental paradigm.
+BDNF	drug	opioid	28776309	<b>Morphine</b> treatment and <b>morphine</b> withdrawal increased both <strong>BDNF</strong> and proBDNF levels.
+BDNF	addiction	withdrawal	28776309	Morphine treatment and morphine <b>withdrawal</b> increased both <strong>BDNF</strong> and proBDNF levels.
+BDNF	drug	opioid	28776309	To examine the mechanisms whereby chronic <b>morphine</b> treatment and <b>morphine</b> withdrawal differentially affects <strong>BDNF</strong>/proBDNF, the levels MMP 3 and MMP 7, furin, and tPA were analyzed.
+BDNF	addiction	withdrawal	28776309	To examine the mechanisms whereby chronic morphine treatment and morphine <b>withdrawal</b> differentially affects <strong>BDNF</strong>/proBDNF, the levels MMP 3 and MMP 7, furin, and tPA were analyzed.
+BDNF	drug	opioid	28776309	To confirm the involvement of tPA in the <b>morphine</b> mediated effect on <strong>BDNF</strong>/proBDNF, we exposed cortical neurons to <b>morphine</b> in the presence of the tPA inhibitor plasminogen activator inhibitor 1 (PAI 1).
+BDNF	drug	opioid	28776309	This inhibitor reversed the <b>morphine</b> mediated decrease in proBDNF, supporting the hypothesis that <b>morphine</b> increases the availability of <strong>BDNF</strong> by promoting the extracellular processing of proBDNF by tPA.
+BDNF	drug	opioid	28692418	Contribution of Genetic Polymorphisms and Haplotypes in DRD2, <strong>BDNF</strong>, and <b>Opioid</b> Receptors to <b>Heroin</b> Dependence and Endophenotypes Among the Han Chinese.
+BDNF	addiction	dependence	28692418	Contribution of Genetic Polymorphisms and Haplotypes in DRD2, <strong>BDNF</strong>, and Opioid Receptors to Heroin <b>Dependence</b> and Endophenotypes Among the Han Chinese.
+BDNF	drug	opioid	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (<strong>BDNF</strong>), as well as the <b>opioid</b> receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to <b>heroin</b> dependence in populations worldwide.
+BDNF	addiction	dependence	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (<strong>BDNF</strong>), as well as the opioid receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug <b>dependence</b>, but relatively little is known on their contributions to heroin <b>dependence</b> in populations worldwide.
+BDNF	addiction	reward	28692418	<b>Reward</b>  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (<strong>BDNF</strong>), as well as the opioid receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to heroin dependence in populations worldwide.
+BDNF	drug	opioid	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), as well as the <b>opioid</b> receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to <b>heroin</b> dependence in populations worldwide.
+BDNF	addiction	dependence	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), as well as the opioid receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug <b>dependence</b>, but relatively little is known on their contributions to heroin <b>dependence</b> in populations worldwide.
+BDNF	addiction	reward	28692418	<b>Reward</b>  and memory related candidate genes dopamine D2 receptor (DRD2) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), as well as the opioid receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to heroin dependence in populations worldwide.
+BDNF	drug	opioid	28692418	Homozygotes AA at rs6265 (<strong>BDNF</strong>), TT at rs16917234 (<strong>BDNF</strong>), and CC at rs508448 (OPRD1) also appeared as risk factors for the endophenotype earlier age of onset for <b>heroin</b> use.
+BDNF	addiction	sensitization	28670835	Intrathecal/intracisternal <strong>BDNF</strong> in rodents produces long lasting hyperalgesia/allodynia, which implies <strong>BDNF</strong> plays a role in the establishment and maintenance of central <b>sensitization</b>.
+BDNF	drug	psychedelics	28670835	Chronic <b>ketamine</b> prevented the mechanical hyperalgesia induced by <strong>BDNF</strong>, without affecting locomotion and food and water consumption.
+BDNF	addiction	sensitization	28670835	Intrathecal <strong>BDNF</strong> induces long lasting central <b>sensitization</b> via a glial likely <strong>BDNF</strong> self regenerating mechanism, whose behavioural expression depends on downstream activation of NMDA receptors.
+BDNF	drug	alcohol	28663110	Sucrose and <b>naltrexone</b> prevent increased pain sensitivity and impaired long term memory induced by repetitive neonatal noxious stimulation: Role of <strong>BDNF</strong> and β endorphin.
+BDNF	drug	alcohol	28663110	<b>Naltrexone</b> and/or sucrose prevented neonatal pain induced impairment of long term memory, while neonatal pain decreased levels of <strong>BDNF</strong> in the hippocampus; this decrease was averted by sucrose and <b>naltrexone</b>.
+BDNF	drug	alcohol	28663110	In conclusion, <b>naltrexone</b> and sucrose can reverse increased pain sensitivity and impaired long term memory induced by acute repetitive neonatal pain probably by normalizing <strong>BDNF</strong> expression and increasing β endorphin levels.
+BDNF	drug	amphetamine	28647666	<strong>Brain derived neurotrophic factor</strong> levels and depression during <b>methamphetamine</b> withdrawal.
+BDNF	addiction	withdrawal	28647666	<strong>Brain derived neurotrophic factor</strong> levels and depression during methamphetamine <b>withdrawal</b>.
+BDNF	drug	amphetamine	28647666	Except for the role in the pathophysiology of depression symptoms, brain derived neurotrophic factor (<strong>BDNF</strong>) is also involved in the <b>METH</b> dependence.
+BDNF	addiction	dependence	28647666	Except for the role in the pathophysiology of depression symptoms, brain derived neurotrophic factor (<strong>BDNF</strong>) is also involved in the METH <b>dependence</b>.
+BDNF	drug	amphetamine	28647666	Except for the role in the pathophysiology of depression symptoms, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is also involved in the <b>METH</b> dependence.
+BDNF	addiction	dependence	28647666	Except for the role in the pathophysiology of depression symptoms, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is also involved in the METH <b>dependence</b>.
+BDNF	drug	amphetamine	28647666	The present study aims to explore whether <strong>BDNF</strong> plays a role in the development of depression symptoms during <b>METH</b> withdrawal.
+BDNF	addiction	withdrawal	28647666	The present study aims to explore whether <strong>BDNF</strong> plays a role in the development of depression symptoms during METH <b>withdrawal</b>.
+BDNF	drug	amphetamine	28647666	Serum <strong>BDNF</strong> levels (≤ 1251.0pg/ml) were independently associated with the development of depression symptoms during <b>METH</b> withdrawal (OR = 3.50, 95% CI, 1.14 10.73, p = 0.028).
+BDNF	addiction	withdrawal	28647666	Serum <strong>BDNF</strong> levels (≤ 1251.0pg/ml) were independently associated with the development of depression symptoms during METH <b>withdrawal</b> (OR = 3.50, 95% CI, 1.14 10.73, p = 0.028).
+BDNF	drug	amphetamine	28647666	Our study demonstrated that patients with serum <strong>BDNF</strong> levels ≤ 1251.0pg/ml had higher risk of depression symptoms during <b>METH</b> withdrawal.
+BDNF	addiction	withdrawal	28647666	Our study demonstrated that patients with serum <strong>BDNF</strong> levels ≤ 1251.0pg/ml had higher risk of depression symptoms during METH <b>withdrawal</b>.
+BDNF	drug	amphetamine	28645061	<b>METH</b> self administration reduced striatal DAT in both sexes, but only males that self administered <b>METH</b> had elevated hippocampal <strong>BDNF</strong> levels.
+BDNF	drug	nicotine	28641491	<b>Nicotine</b> and cigarette smoke modulate Nrf2 <strong>BDNF</strong> dopaminergic signal and neurobehavioral disorders in adult rat cerebral cortex.
+BDNF	drug	nicotine	28641491	Overall, our data strongly suggest that the intervention of DA and <strong>BDNF</strong>, and depletion of antioxidants are important factors during <b>nicotine</b>/CS induced cerebral cortex pathological changes leading to neurobehavioral impairments, which could underpin the novel therapeutic approaches targeted at <b>tobacco</b> <b>smoking</b>/<b>nicotine</b>'s neuropsychological disorders including cognition and drug addiction.
+BDNF	addiction	addiction	28641491	Overall, our data strongly suggest that the intervention of DA and <strong>BDNF</strong>, and depletion of antioxidants are important factors during nicotine/CS induced cerebral cortex pathological changes leading to neurobehavioral impairments, which could underpin the novel therapeutic approaches targeted at tobacco smoking/nicotine's neuropsychological disorders including cognition and drug <b>addiction</b>.
+BDNF	drug	opioid	28630256	Here, we report that extinction of conditioned place aversion (CPA) to <b>naloxone</b> precipitated opiate withdrawal in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a <strong>BDNF</strong> dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+BDNF	addiction	aversion	28630256	Here, we report that extinction of conditioned place <b>aversion</b> (CPA) to naloxone precipitated opiate withdrawal in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a <strong>BDNF</strong> dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+BDNF	addiction	withdrawal	28630256	Here, we report that extinction of conditioned place aversion (CPA) to naloxone precipitated opiate <b>withdrawal</b> in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a <strong>BDNF</strong> dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+BDNF	drug	cocaine	28618284	To measure the variation in Brain Derived Neurotrophic Factor (<strong>BDNF</strong>), Thiobarbituric Acid Reactive Substances (TBARS) and interleukin (IL) levels in crack <b>cocaine</b> dependent adolescents after 21days of abstinence, comparing to levels found in a group of healthy controls.
+BDNF	drug	cocaine	28618284	To measure the variation in <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>), Thiobarbituric Acid Reactive Substances (TBARS) and interleukin (IL) levels in crack <b>cocaine</b> dependent adolescents after 21days of abstinence, comparing to levels found in a group of healthy controls.
+BDNF	drug	amphetamine	28612521	<b>AMPH</b> also increased pro brain derived neurotrophic factor (<strong>BDNF</strong>), tyrosine kinase receptor B, dopamine transporter, D1R and decreased <strong>BDNF</strong> and D2R immunoreactivity.
+BDNF	drug	amphetamine	28612521	<b>AMPH</b> also increased pro <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), tyrosine kinase receptor B, dopamine transporter, D1R and decreased <strong>BDNF</strong> and D2R immunoreactivity.
+BDNF	drug	opioid	28598964	Changes in Expression of Dopamine, Its Receptor, and Transporter in Nucleus Accumbens of <b>Heroin</b> Addicted Rats with Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) Overexpression.
+BDNF	drug	opioid	28598964	Changes in Expression of Dopamine, Its Receptor, and Transporter in Nucleus Accumbens of <b>Heroin</b> Addicted Rats with <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) Overexpression.
+BDNF	drug	opioid	28598964	BACKGROUND The aim of this study was to explore how changes in the expression of <strong>BDNF</strong> in MLDS change the effect of <strong>BDNF</strong> on dopamine (DA) neurons, which may have therapeutic implications for <b>heroin</b> addiction.
+BDNF	addiction	addiction	28598964	BACKGROUND The aim of this study was to explore how changes in the expression of <strong>BDNF</strong> in MLDS change the effect of <strong>BDNF</strong> on dopamine (DA) neurons, which may have therapeutic implications for heroin <b>addiction</b>.
+BDNF	drug	opioid	28598964	MATERIAL AND METHODS We established a rat model of <b>heroin</b> addiction and observed changes in the expression of <strong>BDNF</strong>, DA, dopamine receptor (DRD), dopamine transporter (DAT), and other relevant pathways in NAc.
+BDNF	addiction	addiction	28598964	MATERIAL AND METHODS We established a rat model of heroin <b>addiction</b> and observed changes in the expression of <strong>BDNF</strong>, DA, dopamine receptor (DRD), dopamine transporter (DAT), and other relevant pathways in NAc.
+BDNF	drug	opioid	28598964	We also assessed the effect of <strong>BDNF</strong> overexpression in the NAc, behavioral changes of <b>heroin</b> conditioned place preference (CPP), and <b>naloxone</b> withdrawal in rats with high levels of <strong>BDNF</strong>.
+BDNF	addiction	reward	28598964	We also assessed the effect of <strong>BDNF</strong> overexpression in the NAc, behavioral changes of heroin conditioned place preference (<b>CPP</b>), and naloxone withdrawal in rats with high levels of <strong>BDNF</strong>.
+BDNF	addiction	withdrawal	28598964	We also assessed the effect of <strong>BDNF</strong> overexpression in the NAc, behavioral changes of heroin conditioned place preference (CPP), and naloxone <b>withdrawal</b> in rats with high levels of <strong>BDNF</strong>.
+BDNF	drug	opioid	28598964	CONCLUSIONS <strong>BDNF</strong> and DA in the NAc are involved in <b>heroin</b> addiction.
+BDNF	addiction	addiction	28598964	CONCLUSIONS <strong>BDNF</strong> and DA in the NAc are involved in heroin <b>addiction</b>.
+BDNF	drug	opioid	28598964	<strong>BDNF</strong> overexpression in NAc reduces withdrawal symptoms and craving behavior for medicine induced by environmental cues for <b>heroin</b> addicted rats.
+BDNF	addiction	relapse	28598964	<strong>BDNF</strong> overexpression in NAc reduces withdrawal symptoms and <b>craving</b> behavior for medicine induced by environmental cues for heroin addicted rats.
+BDNF	addiction	withdrawal	28598964	<strong>BDNF</strong> overexpression in NAc reduces <b>withdrawal</b> symptoms and craving behavior for medicine induced by environmental cues for heroin addicted rats.
+BDNF	drug	cocaine	28585567	Role of Src Family Kinases in <strong>BDNF</strong> Mediated Suppression of <b>Cocaine</b> Seeking and Prevention of <b>Cocaine</b> Induced ERK, GluN2A, and GluN2B Dephosphorylation in the Prelimbic Cortex.
+BDNF	addiction	relapse	28585567	Role of Src Family Kinases in <strong>BDNF</strong> Mediated Suppression of Cocaine <b>Seeking</b> and Prevention of Cocaine Induced ERK, GluN2A, and GluN2B Dephosphorylation in the Prelimbic Cortex.
+BDNF	drug	cocaine	28585567	A single <strong>BDNF</strong> infusion into the PrL cortex following a final <b>cocaine</b> SA session results in attenuation of reinstatement of <b>cocaine</b> seeking.
+BDNF	addiction	relapse	28585567	A single <strong>BDNF</strong> infusion into the PrL cortex following a final cocaine SA session results in attenuation of <b>reinstatement</b> of cocaine <b>seeking</b>.
+BDNF	addiction	relapse	28585567	Inhibiting <strong>BDNF</strong>'s receptor, TrkB, ERK/MAP kinase activation, or NMDA receptors blocks this attenuating effect, indicating that the interaction between glutamate mediated synaptic activity and TrkB signaling is imperative to <strong>BDNF</strong>'s suppressive effect on drug <b>seeking</b>.
+BDNF	drug	cocaine	28585567	We hypothesized that infusion of the SFK inhibitor, PP2, into the PrL cortex prior to a <strong>BDNF</strong> infusion, immediately after the end of the last <b>cocaine</b> SA session, would block <strong>BDNF</strong>'s ability to suppress reinstatement of <b>cocaine</b> seeking in rats with a <b>cocaine</b> SA history.
+BDNF	addiction	relapse	28585567	We hypothesized that infusion of the SFK inhibitor, PP2, into the PrL cortex prior to a <strong>BDNF</strong> infusion, immediately after the end of the last cocaine SA session, would block <strong>BDNF</strong>'s ability to suppress <b>reinstatement</b> of cocaine <b>seeking</b> in rats with a cocaine SA history.
+BDNF	addiction	relapse	28585567	PP2, but not the negative control, PP3, blocked <strong>BDNF</strong>'s suppressive effect on context induced <b>relapse</b> after 1 week of abstinence and cue induced <b>reinstatement</b> after extinction.
+BDNF	drug	cocaine	28585567	As previously reported, infusion of <strong>BDNF</strong> into the PrL cortex blocked <b>cocaine</b> SA induced dephosphorylation of ERK, GluN2A, and GluN2B containing receptors.
+BDNF	drug	cocaine	28585567	These data indicate that SFK activity is necessary for <strong>BDNF</strong> mediated suppression of <b>cocaine</b> seeking and reversal of <b>cocaine</b> induced dephosphorylation of key phosphoproteins in the prefrontal cortex related to synaptic plasticity.
+BDNF	addiction	relapse	28585567	These data indicate that SFK activity is necessary for <strong>BDNF</strong> mediated suppression of cocaine <b>seeking</b> and reversal of cocaine induced dephosphorylation of key phosphoproteins in the prefrontal cortex related to synaptic plasticity.
+BDNF	drug	alcohol	28568647	Besides, <b>alcohol</b> treatment increased <strong>brain derived neurotrophic factor</strong> and interleukin 10 levels in prefrontal cortex, which was not reverted by P. incarnata.
+BDNF	drug	alcohol	28554528	Abstinence from chronic <b>ethanol</b> exposure also decreased brain derived neurotrophic factor (<strong>BDNF</strong>) in the dentate gyrus and CA3 region of the hippocampus.
+BDNF	drug	alcohol	28554528	Abstinence from chronic <b>ethanol</b> exposure also decreased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the dentate gyrus and CA3 region of the hippocampus.
+BDNF	drug	opioid	28538519	Neurotrophins, brain derived neurotrophic factors (<strong>BDNF</strong>), neurotrophin 3 (NT 3), and neurotrophin 4 (NT 4), have been implicated in the modulation of <b>heroin</b> dependency.
+BDNF	drug	opioid	28538519	This study was designed to explore the expression alterations of <strong>BDNF</strong>, NT 3, and NT 4 in the context of <b>heroin</b> dependence and withdrawal in the rat nucleus accumbens (NAc).
+BDNF	addiction	dependence	28538519	This study was designed to explore the expression alterations of <strong>BDNF</strong>, NT 3, and NT 4 in the context of heroin <b>dependence</b> and withdrawal in the rat nucleus accumbens (NAc).
+BDNF	addiction	withdrawal	28538519	This study was designed to explore the expression alterations of <strong>BDNF</strong>, NT 3, and NT 4 in the context of heroin dependence and <b>withdrawal</b> in the rat nucleus accumbens (NAc).
+BDNF	drug	opioid	28538519	The results showed that the expression levels of <strong>BDNF</strong> and NT 4 were significantly decreased in the NAc of rats with <b>heroin</b> addiction in comparison with the control group, whereas there was a significant increase in <strong>BDNF</strong> and NT 4 expressions in the groups of rats with both <b>naloxone</b> induced and spontaneous withdrawal.
+BDNF	addiction	addiction	28538519	The results showed that the expression levels of <strong>BDNF</strong> and NT 4 were significantly decreased in the NAc of rats with heroin <b>addiction</b> in comparison with the control group, whereas there was a significant increase in <strong>BDNF</strong> and NT 4 expressions in the groups of rats with both naloxone induced and spontaneous withdrawal.
+BDNF	addiction	withdrawal	28538519	The results showed that the expression levels of <strong>BDNF</strong> and NT 4 were significantly decreased in the NAc of rats with heroin addiction in comparison with the control group, whereas there was a significant increase in <strong>BDNF</strong> and NT 4 expressions in the groups of rats with both naloxone induced and spontaneous <b>withdrawal</b>.
+BDNF	drug	opioid	28538519	These results indicated that chronic administration of <b>heroin</b> results in the alterations of <strong>BDNF</strong>, NT 3, and NT 4 expressions in the rat NAc.
+BDNF	drug	opioid	28538519	<strong>BDNF</strong>, NT 3, and NT 4 may play a critical role in the development of <b>heroin</b> dependency and withdrawal.
+BDNF	addiction	withdrawal	28538519	<strong>BDNF</strong>, NT 3, and NT 4 may play a critical role in the development of heroin dependency and <b>withdrawal</b>.
+BDNF	drug	alcohol	28525828	Significant sex×<b>alcohol</b> dependence history interactions were observed for plasma levels of tissue inhibitor of metalloproteinase 1 (TIMP 1) and brain derived neurotrophic factor (<strong>BDNF</strong>), with women in the <b>alcohol</b> dependent group exhibiting increased levels of both analytes (p<0.05) relative to controls.
+BDNF	addiction	dependence	28525828	Significant sex×alcohol <b>dependence</b> history interactions were observed for plasma levels of tissue inhibitor of metalloproteinase 1 (TIMP 1) and brain derived neurotrophic factor (<strong>BDNF</strong>), with women in the alcohol dependent group exhibiting increased levels of both analytes (p<0.05) relative to controls.
+BDNF	drug	alcohol	28525828	Significant sex×<b>alcohol</b> dependence history interactions were observed for plasma levels of tissue inhibitor of metalloproteinase 1 (TIMP 1) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), with women in the <b>alcohol</b> dependent group exhibiting increased levels of both analytes (p<0.05) relative to controls.
+BDNF	addiction	dependence	28525828	Significant sex×alcohol <b>dependence</b> history interactions were observed for plasma levels of tissue inhibitor of metalloproteinase 1 (TIMP 1) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), with women in the alcohol dependent group exhibiting increased levels of both analytes (p<0.05) relative to controls.
+BDNF	drug	alcohol	28485899	Determinants of Blood <strong>Brain Derived Neurotrophic Factor</strong> Blood Levels in Patients with <b>Alcohol</b> Use Disorder.
+BDNF	addiction	addiction	28485899	Blood brain derived neurotrophic factor (<strong>BDNF</strong>) levels are influenced by both <b>addiction</b> and mood disorders, as well as somatic conditions, gender, and genetic polymorphisms, leading to widely varying results.
+BDNF	addiction	addiction	28485899	Blood <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels are influenced by both <b>addiction</b> and mood disorders, as well as somatic conditions, gender, and genetic polymorphisms, leading to widely varying results.
+BDNF	drug	alcohol	28485899	Depressive symptoms and episodes are frequently observed in patients with <b>alcohol</b> use disorder, and vary widely over time, making it a challenge to determine which aspects are specifically involved in variations of serum <strong>BDNF</strong> levels in this population.
+BDNF	drug	alcohol	28485899	The presence of the Met allele, 2 markers of the history of <b>alcohol</b> dependence (gamma glutamyl transferase and the number of past treatments in detoxification programs), and the presence of a depressive episode (but not depressive score) were significantly associated with the 2 blood levels of <strong>BDNF</strong> at baseline and after 6 months.
+BDNF	addiction	dependence	28485899	The presence of the Met allele, 2 markers of the history of alcohol <b>dependence</b> (gamma glutamyl transferase and the number of past treatments in detoxification programs), and the presence of a depressive episode (but not depressive score) were significantly associated with the 2 blood levels of <strong>BDNF</strong> at baseline and after 6 months.
+BDNF	drug	alcohol	28485899	Low serum <strong>BDNF</strong> levels are associated with characteristics related to <b>alcohol</b> consumption and mood disorders, and variants of the <strong>BDNF</strong> gene in <b>alcohol</b> use disorder patients.
+BDNF	drug	alcohol	28485899	The factors that most strongly influenced changes in serum <strong>BDNF</strong> levels following treatment in an <b>alcohol</b> detoxification program were variants of the <strong>BDNF</strong> gene and ongoing depression.
+BDNF	drug	psychedelics	28479397	Additionally, males administered 5 mg/kg <b>ketamine</b> displayed increased protein expression of ΔfosB, calcium calmodulin kinase II alpha (CaMKIIα), and brain derived neurotrophic factor (<strong>BDNF</strong>), an effect not observed in females administered either dose of <b>ketamine</b>.
+BDNF	drug	psychedelics	28479397	Additionally, males administered 5 mg/kg <b>ketamine</b> displayed increased protein expression of ΔfosB, calcium calmodulin kinase II alpha (CaMKIIα), and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), an effect not observed in females administered either dose of <b>ketamine</b>.
+BDNF	drug	alcohol	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during <b>alcohol</b> dependence and stress disorders, and among these, brain derived neurotrophic factor (<strong>BDNF</strong>), corticotropin releasing factor (CRF), neuropeptide Y (NPY) and opioid peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and <b>alcohol</b>.
+BDNF	drug	opioid	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol dependence and stress disorders, and among these, brain derived neurotrophic factor (<strong>BDNF</strong>), corticotropin releasing factor (CRF), neuropeptide Y (NPY) and <b>opioid</b> peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and alcohol.
+BDNF	addiction	dependence	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol <b>dependence</b> and stress disorders, and among these, brain derived neurotrophic factor (<strong>BDNF</strong>), corticotropin releasing factor (CRF), neuropeptide Y (NPY) and opioid peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and alcohol.
+BDNF	drug	alcohol	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during <b>alcohol</b> dependence and stress disorders, and among these, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), corticotropin releasing factor (CRF), neuropeptide Y (NPY) and opioid peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and <b>alcohol</b>.
+BDNF	drug	opioid	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol dependence and stress disorders, and among these, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), corticotropin releasing factor (CRF), neuropeptide Y (NPY) and <b>opioid</b> peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and alcohol.
+BDNF	addiction	dependence	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol <b>dependence</b> and stress disorders, and among these, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), corticotropin releasing factor (CRF), neuropeptide Y (NPY) and opioid peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and alcohol.
+BDNF	drug	psychedelics	28473755	The Combination of Long term <b>Ketamine</b> and Extinction Training Contributes to Fear Erasure by <strong>Bdnf</strong> Methylation.
+BDNF	drug	psychedelics	28473755	Here we investigated the role of DNA methylation of the brain derived neurotrophic factor (<strong>Bdnf</strong>) gene in the therapeutic effects of <b>ketamine</b> in combination with extinction training in a mouse model of post traumatic stress disorder (PTSD) induced by inescapable electric foot shocks (IFS).
+BDNF	drug	psychedelics	28473755	Here we investigated the role of DNA methylation of the <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) gene in the therapeutic effects of <b>ketamine</b> in combination with extinction training in a mouse model of post traumatic stress disorder (PTSD) induced by inescapable electric foot shocks (IFS).
+BDNF	addiction	relapse	28473755	Mice, subjected to IFS, exhibited anxiety like behavior and fear <b>relapse</b>, accompanied by the increased levels of DNA methyltransferases, hyper methylation of <strong>Bdnf</strong> gene, and decreased <strong>BDNF</strong> mRNA expression in the medial prefrontal cortex (mPFC) and hippocampus (HIP).
+BDNF	drug	psychedelics	28473755	These results suggest that long term <b>ketamine</b> treatment in combination with extinction training may ameliorate fear relapse in the murine model of PTSD, at least in part, by normalizing DNA methylation of <strong>Bdnf</strong> gene.
+BDNF	addiction	relapse	28473755	These results suggest that long term ketamine treatment in combination with extinction training may ameliorate fear <b>relapse</b> in the murine model of PTSD, at least in part, by normalizing DNA methylation of <strong>Bdnf</strong> gene.
+BDNF	drug	psychedelics	28472632	The involvement of <strong>brain derived neurotrophic factor</strong> in 3,4 <b>methylenedioxymethamphetamine</b> induced place preference and behavioral sensitization.
+BDNF	addiction	sensitization	28472632	The involvement of <strong>brain derived neurotrophic factor</strong> in 3,4 methylenedioxymethamphetamine induced place preference and behavioral <b>sensitization</b>.
+BDNF	drug	psychedelics	28472632	This study aimed to investigate the role of <strong>BDNF</strong> in <b>MDMA</b> induced dependence and psychosis.
+BDNF	addiction	dependence	28472632	This study aimed to investigate the role of <strong>BDNF</strong> in MDMA induced <b>dependence</b> and psychosis.
+BDNF	drug	psychedelics	28472632	A single dose of <b>MDMA</b> (10mg/kg) induced <strong>BDNF</strong> mRNA expression in the prefrontal cortex, nucleus accumbens, and amygdala, but not in the striatum or the hippocampus.
+BDNF	drug	psychedelics	28472632	However, repeated <b>MDMA</b> administration for 7 days induced <strong>BDNF</strong> mRNA expression in the striatum and hippocampus.
+BDNF	drug	psychedelics	28472632	Dopamine receptor antagonists attenuated the effect of repeated <b>MDMA</b> administration on <strong>BDNF</strong> mRNA expression in the nucleus accumbens.
+BDNF	drug	psychedelics	28472632	To examine the role of endogenous <strong>BDNF</strong> in the behavioral and neurochemical effects of <b>MDMA</b>, we used mice with heterozygous deletions of the <strong>BDNF</strong> gene.
+BDNF	drug	psychedelics	28472632	<b>MDMA</b> induced place preference, behavioral sensitization, and an increase in the levels of extracellular serotonin and dopamine within the nucleus accumbens, were attenuated in <strong>BDNF</strong> heterozygous knockout mice.
+BDNF	addiction	sensitization	28472632	MDMA induced place preference, behavioral <b>sensitization</b>, and an increase in the levels of extracellular serotonin and dopamine within the nucleus accumbens, were attenuated in <strong>BDNF</strong> heterozygous knockout mice.
+BDNF	drug	psychedelics	28472632	These results suggest that <strong>BDNF</strong> is implicated in <b>MDMA</b> induced dependence and psychosis by activating the midbrain serotonergic and dopaminergic neurons.
+BDNF	addiction	dependence	28472632	These results suggest that <strong>BDNF</strong> is implicated in MDMA induced <b>dependence</b> and psychosis by activating the midbrain serotonergic and dopaminergic neurons.
+BDNF	drug	cocaine	28466092	The aim of the present study was to compare the long term effects of RSD on the conditioned rewarding effects of <b>cocaine</b> and levels of the transcription factors Pitx3 and Nurr1 in the ventral tegmental area (VTA), the dopamine transporter (DAT), the D2 dopamine receptor (D2DR) and precursor of <strong>brain derived neurotrophic factor</strong> (proBDNF) signaling pathways, and the tropomyosin related kinase B (TrkB) receptor in the nucleus accumbens (NAc) in adult and adolescent mice.
+BDNF	drug	alcohol	28454718	Moreover, treatment involving low  or high dose ketamine with or without <b>ethanol</b> caused a differential regulatory response in the mRNA levels of the four DA metabolism genes and the cellular protein abundance of <strong>BDNF</strong> via the cortex striatum circuitry.
+BDNF	drug	psychedelics	28454718	Moreover, treatment involving low  or high dose <b>ketamine</b> with or without ethanol caused a differential regulatory response in the mRNA levels of the four DA metabolism genes and the cellular protein abundance of <strong>BDNF</strong> via the cortex striatum circuitry.
+BDNF	drug	alcohol	28430931	In this study we investigated a possible association between alterations in the methylation of the <strong>BDNF</strong> IV/NGF I gene promoter and the cytokines tumor necrosis factor α (TNF α) and interleukin 6 (IL 6) in 55 male <b>alcohol</b> dependent patients.
+BDNF	addiction	withdrawal	28430931	Mean methylation of the promoter of the <strong>BDNF</strong> gene was significantly associated with the TNF α serum levels and the CIWA score during <b>withdrawal</b> (P < 0.001).
+BDNF	drug	alcohol	28430931	Our results suggest an association between the epigenetic regulation of both neurotrophins, <strong>BDNF</strong> and NGF, cytokine release and the symptomatology of <b>alcohol</b> dependence.
+BDNF	addiction	dependence	28430931	Our results suggest an association between the epigenetic regulation of both neurotrophins, <strong>BDNF</strong> and NGF, cytokine release and the symptomatology of alcohol <b>dependence</b>.
+BDNF	drug	opioid	28403087	Increased <strong>BDNF</strong> may not be associated with cognitive impairment in <b>heroin</b> dependent patients.
+BDNF	drug	opioid	28403087	<b>Heroin</b> addiction has a series of cognitive impairments that may be associated with <strong>BDNF</strong>.
+BDNF	addiction	addiction	28403087	Heroin <b>addiction</b> has a series of cognitive impairments that may be associated with <strong>BDNF</strong>.
+BDNF	drug	opioid	28403087	In this study, we explored the association of <strong>BDNF</strong> with cognitive function in <b>heroin</b> dependent patients.We enrolled 86 <b>heroin</b> dependent patients and 238 normal control subjects and examined their cognition by the repeatable battery for the assessment of neuropsychological status (RBANS) and serum <strong>BDNF</strong> levels in 2 groups.<strong>BDNF</strong> levels were significantly higher in patients than controls (P < .001).
+BDNF	drug	opioid	28403087	Unfortunately, we found no positive association between <strong>BDNF</strong> and cognitive function in patients, except that <strong>BDNF</strong> was positively associated with visuospatial/constructional index in control groups.Our findings suggest that <strong>BDNF</strong> may not be involved in the pathophysiology of <b>heroin</b> dependence, but more studies about cognitive impairment in <b>heroin</b> addiction are needed.
+BDNF	addiction	addiction	28403087	Unfortunately, we found no positive association between <strong>BDNF</strong> and cognitive function in patients, except that <strong>BDNF</strong> was positively associated with visuospatial/constructional index in control groups.Our findings suggest that <strong>BDNF</strong> may not be involved in the pathophysiology of heroin dependence, but more studies about cognitive impairment in heroin <b>addiction</b> are needed.
+BDNF	addiction	dependence	28403087	Unfortunately, we found no positive association between <strong>BDNF</strong> and cognitive function in patients, except that <strong>BDNF</strong> was positively associated with visuospatial/constructional index in control groups.Our findings suggest that <strong>BDNF</strong> may not be involved in the pathophysiology of heroin <b>dependence</b>, but more studies about cognitive impairment in heroin addiction are needed.
+BDNF	drug	nicotine	28306606	Spinal microglial P2X4 receptor <strong>brain derived neurotrophic factor</strong> signaling regulates <b>nicotine</b> withdrawal induced hyperalgesia.
+BDNF	addiction	withdrawal	28306606	Spinal microglial P2X4 receptor <strong>brain derived neurotrophic factor</strong> signaling regulates nicotine <b>withdrawal</b> induced hyperalgesia.
+BDNF	addiction	addiction	28306543	Brain derived neurotrophic factor (<strong>BDNF</strong>) is a central neurotrophin involved in many neuronal processes, and it has been related to several psychiatric diseases and <b>addictive</b> disorders.
+BDNF	addiction	addiction	28306543	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is a central neurotrophin involved in many neuronal processes, and it has been related to several psychiatric diseases and <b>addictive</b> disorders.
+BDNF	addiction	withdrawal	28306543	Also, opiates may modify epigenetic processes that may be associated with peripheral concentrations of <strong>BDNF</strong>, and in this line, <b>withdrawal</b> could reflect recovering processes in the CNS.
+BDNF	drug	alcohol	28303373	Using Pearson's correlation, results showed a strong negative relationship between MyT1 mRNA and anxiety parameters and <b>ethanol</b> consumption and a positive correlation between MyT1 and <strong>BDNF</strong> mRNAs.
+BDNF	drug	alcohol	28257889	Chronic intermittent <b>ethanol</b> exposure leads to alterations in <strong>brain derived neurotrophic factor</strong> within the frontal cortex and impaired behavioral flexibility in both adolescent and adult rats.
+BDNF	addiction	intoxication	28257889	Experiment 2 examined changes in brain derived neurotrophic factor (<strong>BDNF</strong>) levels within the frontal cortex (FC) and hippocampus (HPC) at four time points: during <b>intoxication</b>, 24 h after the final EtOH exposure (acute abstinence), 3 weeks following abstinence (recovery) and after behavioral testing.
+BDNF	addiction	intoxication	28257889	Experiment 2 examined changes in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels within the frontal cortex (FC) and hippocampus (HPC) at four time points: during <b>intoxication</b>, 24 h after the final EtOH exposure (acute abstinence), 3 weeks following abstinence (recovery) and after behavioral testing.
+BDNF	addiction	intoxication	28257889	During <b>intoxication</b>, <strong>BDNF</strong> was suppressed in the FC, regardless of the age of exposure.
+BDNF	addiction	intoxication	28257889	Our results indicate that intermittent <b>binge</b> like EtOH exposure leads to acute disruptions in FC <strong>BDNF</strong> levels and long lasting behavioral deficits.
+BDNF	drug	psychedelics	28251011	Given MXE's structural similarities to <b>ketamine</b> and recent work showing that <b>ketamine</b> reduces PTSD symptoms, we hypothesize that MXE alleviated this veteran's PTSD symptoms through action at the NMDA receptor and via influences on brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	psychedelics	28251011	Given MXE's structural similarities to <b>ketamine</b> and recent work showing that <b>ketamine</b> reduces PTSD symptoms, we hypothesize that MXE alleviated this veteran's PTSD symptoms through action at the NMDA receptor and via influences on <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	amphetamine	28249787	Effects of prolonged abstinence from <b>METH</b> on the hippocampal <strong>BDNF</strong> levels, neuronal numbers and apoptosis in <b>methamphetamine</b> sensitized rats.
+BDNF	drug	amphetamine	28249787	This study evaluated serum and hippocampal <strong>BDNF</strong> levels, neuronal numbers and apoptosis in <b>METH</b> sensitized and abstinent rats.
+BDNF	drug	amphetamine	28249787	All rats were evaluated for neuron counting, the TUNEL test and serum and hippocampal <strong>BDNF</strong> levels after 30 days of forced abstinence from <b>METH</b>.
+BDNF	drug	amphetamine	28249787	The results showed that increased <strong>BDNF</strong> levels in the hippocampus and serum of <b>METH</b> sensitized rats returned to control level after 30 days of abstinence.
+BDNF	drug	cocaine	28237884	Effects of crack <b>cocaine</b> addiction and stress related genes on peripheral <strong>BDNF</strong> levels.
+BDNF	addiction	addiction	28237884	Effects of crack cocaine <b>addiction</b> and stress related genes on peripheral <strong>BDNF</strong> levels.
+BDNF	drug	cocaine	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), corticotropin releasing hormone receptor 1 (CRHR1), and brain derived neurotrophic factor (<strong>BDNF</strong>) genes on susceptibility to crack <b>cocaine</b> addiction and <strong>BDNF</strong> levels.
+BDNF	addiction	addiction	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), corticotropin releasing hormone receptor 1 (CRHR1), and brain derived neurotrophic factor (<strong>BDNF</strong>) genes on susceptibility to crack cocaine <b>addiction</b> and <strong>BDNF</strong> levels.
+BDNF	drug	cocaine	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), corticotropin releasing hormone receptor 1 (CRHR1), and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) genes on susceptibility to crack <b>cocaine</b> addiction and <strong>BDNF</strong> levels.
+BDNF	addiction	addiction	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), corticotropin releasing hormone receptor 1 (CRHR1), and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) genes on susceptibility to crack cocaine <b>addiction</b> and <strong>BDNF</strong> levels.
+BDNF	drug	cocaine	28237884	Crack <b>cocaine</b> addicted patients showed significantly lower serum <strong>BDNF</strong> levels.
+BDNF	drug	cocaine	28237884	This study suggests that SNPs in the NR3C1 and CRHR1 genes may influence <strong>BDNF</strong> levels, but this effect is blunted in the context of crack <b>cocaine</b> addiction.
+BDNF	addiction	addiction	28237884	This study suggests that SNPs in the NR3C1 and CRHR1 genes may influence <strong>BDNF</strong> levels, but this effect is blunted in the context of crack cocaine <b>addiction</b>.
+BDNF	drug	cocaine	28237884	Therefore, our data may be interpreted in light of several studies showing pronounced effects of crack <b>cocaine</b> on <strong>BDNF</strong> levels.
+BDNF	addiction	addiction	28237884	Since peripheral <strong>BDNF</strong> is a biomarker for several psychiatric phenotypes, our results may be useful in interpreting previous associations between stress related SNPs, drug <b>addiction</b>, and depression.
+BDNF	drug	nicotine	28235586	In Experiment 1, we analyzed the role of α7 and α4β2 nicotinic receptors (nAChRs) in <b>nicotine</b> behavioral sensitization and on the brain derived neurotrophic factor (<strong>BDNF</strong>) response to <b>nicotine</b> in NQ  and neonatally saline (NS) treated rats.
+BDNF	addiction	sensitization	28235586	In Experiment 1, we analyzed the role of α7 and α4β2 nicotinic receptors (nAChRs) in nicotine behavioral <b>sensitization</b> and on the brain derived neurotrophic factor (<strong>BDNF</strong>) response to nicotine in NQ  and neonatally saline (NS) treated rats.
+BDNF	drug	nicotine	28235586	In Experiment 1, we analyzed the role of α7 and α4β2 nicotinic receptors (nAChRs) in <b>nicotine</b> behavioral sensitization and on the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) response to <b>nicotine</b> in NQ  and neonatally saline (NS) treated rats.
+BDNF	addiction	sensitization	28235586	In Experiment 1, we analyzed the role of α7 and α4β2 nicotinic receptors (nAChRs) in nicotine behavioral <b>sensitization</b> and on the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) response to nicotine in NQ  and neonatally saline (NS) treated rats.
+BDNF	drug	nicotine	28235586	NQ enhanced the NAcc <strong>BDNF</strong> response to <b>nicotine</b> which was blocked by both antagonists.
+BDNF	drug	nicotine	28235586	These results suggest a relationship between accumbal <strong>BDNF</strong> and α4β2 nAChRs and their role in the behavioral response to <b>nicotine</b> in the NQ model which has relevance to schizophrenia, a behavioral disorder with high rates of <b>tobacco</b> <b>smoking</b>.
+BDNF	drug	alcohol	28095363	Curcumin confers neuroprotection against <b>alcohol</b> induced hippocampal neurodegeneration via CREB <strong>BDNF</strong> pathway in rats.
+BDNF	drug	alcohol	28095363	Furthermore, <b>alcohol</b> induced significant reduction were observed in reduced form of glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and CREB, <strong>BDNF</strong> and Bcl 2 levels.
+BDNF	drug	alcohol	28095363	Curcumin can act as a neuroprotective agent against neurodegenerative effects of <b>alcohol</b> abuse, probably via activation of CREB <strong>BDNF</strong> signaling pathway.
+BDNF	drug	cocaine	28086206	VTA <strong>BDNF</strong> enhances social stress induced compulsive <b>cocaine</b> bingeing.
+BDNF	addiction	addiction	28086206	VTA <strong>BDNF</strong> enhances social stress induced <b>compulsive</b> cocaine bingeing.
+BDNF	drug	opioid	28063398	Brain derived neurotrophic factor (<strong>BDNF</strong>) and oxidative stress in <b>heroin</b> dependent male patients undergoing <b>methadone</b> maintenance treatment.
+BDNF	drug	opioid	28063398	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and oxidative stress in <b>heroin</b> dependent male patients undergoing <b>methadone</b> maintenance treatment.
+BDNF	drug	opioid	28063398	Brain derived neurotrophic factor (<strong>BDNF</strong>) and oxidative stress may play a role in patients with <b>heroin</b> dependence.
+BDNF	addiction	dependence	28063398	Brain derived neurotrophic factor (<strong>BDNF</strong>) and oxidative stress may play a role in patients with heroin <b>dependence</b>.
+BDNF	drug	opioid	28063398	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and oxidative stress may play a role in patients with <b>heroin</b> dependence.
+BDNF	addiction	dependence	28063398	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and oxidative stress may play a role in patients with heroin <b>dependence</b>.
+BDNF	drug	opioid	28063398	The aim of this study was to investigate the serum levels and activities of <strong>BDNF</strong> and oxidative stress markers, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC), and 8 hydroxy 2' deoxyguanosine (8 OHdG), in <b>heroin</b> dependent patients undergoing <b>methadone</b> maintenance treatment (MMT).
+BDNF	drug	opioid	28063398	In conclusion, our results suggest that MMT increases <strong>BDNF</strong> levels in <b>heroin</b> dependent patients, and that patients undergoing MMT might be in a balanced state of reduced oxidation.
+BDNF	drug	alcohol	28032807	Research has shown that the brain derived neurotrophic factor (<strong>BDNF</strong>) plays an important role in <b>alcohol</b> addiction.
+BDNF	addiction	addiction	28032807	Research has shown that the brain derived neurotrophic factor (<strong>BDNF</strong>) plays an important role in alcohol <b>addiction</b>.
+BDNF	drug	alcohol	28032807	Research has shown that the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) plays an important role in <b>alcohol</b> addiction.
+BDNF	addiction	addiction	28032807	Research has shown that the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) plays an important role in alcohol <b>addiction</b>.
+BDNF	drug	alcohol	28032807	However, the effects of proBDNF and <strong>BDNF</strong> in <b>alcohol</b> addiction are not fully known.
+BDNF	addiction	addiction	28032807	However, the effects of proBDNF and <strong>BDNF</strong> in alcohol <b>addiction</b> are not fully known.
+BDNF	drug	alcohol	28032807	The objective was to identify the expression patterns and effects of proBDNF and <strong>BDNF</strong> after chronic <b>alcohol</b> exposure.
+BDNF	drug	alcohol	28032807	A mouse psychomotor sensitization (PS) model was established to explore the effects of <strong>BDNF</strong> and proBDNF treatment following chronic <b>alcohol</b> exposure.
+BDNF	addiction	sensitization	28032807	A mouse psychomotor <b>sensitization</b> (PS) model was established to explore the effects of <strong>BDNF</strong> and proBDNF treatment following chronic alcohol exposure.
+BDNF	drug	alcohol	28032807	Reverse transcription PCR (RT PCR) was performed to measure mRNA levels for <strong>BDNF</strong>, TrkB, P75NTR, and sortilin in the prefrontal cortex, hippocampus, and dorsal striatum of Kunming mice after chronic <b>alcohol</b> exposure.
+BDNF	drug	alcohol	28032807	In Kunming mice, chronic <b>alcohol</b> exposure up regulated <strong>BDNF</strong> and TrkB mRNA levels in the prefrontal cortex, but decreased sortilin and P75 mRNA levels in the dorsal striatum.
+BDNF	drug	alcohol	28032807	Chronic <b>alcohol</b> exposure induced the region specific expression of <strong>BDNF</strong> and proBDNF and their respective receptors in the brain.
+BDNF	drug	alcohol	28032807	These results suggest that <strong>BDNF</strong> and proBDNF signaling pathways may play major roles in <b>alcohol</b> preference and addiction.
+BDNF	addiction	addiction	28032807	These results suggest that <strong>BDNF</strong> and proBDNF signaling pathways may play major roles in alcohol preference and <b>addiction</b>.
+BDNF	drug	nicotine	27940499	The effects of adolescent methylphenidate exposure on the behavioral and <strong>brain derived neurotrophic factor</strong> response to <b>nicotine</b>.
+BDNF	drug	nicotine	27940499	This study analyzed the interaction of adolescent methylphenidate on the behavioral response to <b>nicotine</b> and the effects of these drug treatments on <strong>brain derived neurotrophic factor</strong> in the nucleus accumbens and hippocampus in male and female Sprague Dawley rats.
+BDNF	drug	nicotine	27940499	In addition, methylphenidate and <b>nicotine</b> increased nucleus accumbens <strong>brain derived neurotrophic factor</strong> in females and methylphenidate enhanced hippocampus <strong>brain derived neurotrophic factor</strong> in males and females.
+BDNF	drug	nicotine	27940499	Methylphenidate adolescent exposure using a clinically relevant dose and regimen results in changes in the behavioral and <strong>brain derived neurotrophic factor</strong> responses to <b>nicotine</b> in adolescence that are sex dependent.
+BDNF	drug	opioid	27927738	Altered Acoustic Startle Reflex, Prepulse Inhibition, and Peripheral <strong>Brain Derived Neurotrophic Factor</strong> in <b>Morphine</b> Self Administered Rats.
+BDNF	addiction	withdrawal	27927738	Previous studies suggested that opiate <b>withdrawal</b> may increase anxiety and disrupt <strong>brain derived neurotrophic factor</strong> function, but the effects of i.v.
+BDNF	drug	opioid	27927738	The blood <strong>brain derived neurotrophic factor</strong> levels were decreased in the <b>morphine</b> self administration group at self administration days 3 and 5, while the corticosterone levels remained unchanged throughout the study.
+BDNF	drug	opioid	27927738	<b>morphine</b> self administration may have transient effects on acoustic startle, sensorimotor gating, and peripheral <strong>brain derived neurotrophic factor</strong> levels, and these changes may contribute to the adverse effects of opiate withdrawal.
+BDNF	addiction	withdrawal	27927738	morphine self administration may have transient effects on acoustic startle, sensorimotor gating, and peripheral <strong>brain derived neurotrophic factor</strong> levels, and these changes may contribute to the adverse effects of opiate <b>withdrawal</b>.
+BDNF	drug	alcohol	27898499	COMT and <strong>BDNF</strong> Gene Variants Help to Predict <b>Alcohol</b> Consumption in <b>Alcohol</b> dependent Patients.
+BDNF	drug	alcohol	27898499	The relationship between <b>alcohol</b> consumption and single nucleotide polymorphisms, Val66Met in the brain derived neurotrophic factor (<strong>BDNF</strong>), and Val158Met in the catechol O methyltransferase (COMT), was analyzed among 281 <b>alcohol</b> dependent individuals.
+BDNF	drug	alcohol	27898499	The relationship between <b>alcohol</b> consumption and single nucleotide polymorphisms, Val66Met in the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), and Val158Met in the catechol O methyltransferase (COMT), was analyzed among 281 <b>alcohol</b> dependent individuals.
+BDNF	drug	alcohol	27898499	Patients carrying both the <strong>BDNF</strong> Val66Val and COMT Met158Met variants had higher <b>alcohol</b> consumption.
+BDNF	drug	alcohol	27898499	These effects may be influenced by the effects of <strong>BDNF</strong> and COMT on dopamine responses to <b>alcohol</b>.
+BDNF	drug	opioid	27647760	The relationship between polymorphisms of BDNFOS and <strong>BDNF</strong> genes and <b>heroin</b> addiction in the Han Chinese population.
+BDNF	addiction	addiction	27647760	The relationship between polymorphisms of BDNFOS and <strong>BDNF</strong> genes and heroin <b>addiction</b> in the Han Chinese population.
+BDNF	addiction	addiction	27647760	We aimed to investigate the associations between single nucleotide polymorphisms (SNPs) in LIN7C, BDNFOS and <strong>BDNF</strong> genes and drug <b>addiction</b> in the Han Chinese population.
+BDNF	drug	opioid	27647760	Additionally, we found that rs6265, rs11030104 and rs10767664 in <strong>BDNF</strong> were associated with a decreased risk of <b>heroin</b> addiction (p < 0.05).
+BDNF	addiction	addiction	27647760	Additionally, we found that rs6265, rs11030104 and rs10767664 in <strong>BDNF</strong> were associated with a decreased risk of heroin <b>addiction</b> (p < 0.05).
+BDNF	drug	cocaine	27765467	Glutamatergic neurotransmission in the prefrontal cortex mediates the suppressive effect of intra prelimbic cortical infusion of <strong>BDNF</strong> on <b>cocaine</b> seeking.
+BDNF	addiction	relapse	27765467	Glutamatergic neurotransmission in the prefrontal cortex mediates the suppressive effect of intra prelimbic cortical infusion of <strong>BDNF</strong> on cocaine <b>seeking</b>.
+BDNF	drug	cocaine	27765467	<b>Cocaine</b> self administration disturbs glutamatergic transmission in the nucleus accumbens that is prevented by infusion of brain derived neurotrophic factor (<strong>BDNF</strong>) into the prelimbic area of the prefrontal cortex.
+BDNF	drug	cocaine	27765467	<b>Cocaine</b> self administration disturbs glutamatergic transmission in the nucleus accumbens that is prevented by infusion of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) into the prelimbic area of the prefrontal cortex.
+BDNF	drug	cocaine	27765467	Intra prelimbic infusion of <strong>BDNF</strong> decreases <b>cocaine</b> seeking in a TrkB ERK MAP kinase dependent manner.
+BDNF	addiction	relapse	27765467	Intra prelimbic infusion of <strong>BDNF</strong> decreases cocaine <b>seeking</b> in a TrkB ERK MAP kinase dependent manner.
+BDNF	drug	cocaine	27765467	In the present study, infusion of the GluN2A containing NMDA receptor antagonist, TCN 201, or the GluN2B containing NMDA receptor antagonist, Ro 25 6981, into the prelimbic cortex of rats blocked the suppressive effect of <strong>BDNF</strong> on <b>cocaine</b> seeking.
+BDNF	addiction	relapse	27765467	In the present study, infusion of the GluN2A containing NMDA receptor antagonist, TCN 201, or the GluN2B containing NMDA receptor antagonist, Ro 25 6981, into the prelimbic cortex of rats blocked the suppressive effect of <strong>BDNF</strong> on cocaine <b>seeking</b>.
+BDNF	drug	cocaine	27765467	During early withdrawal from <b>cocaine</b> self administration, tyrosine phosphorylation of ERK, GluN2A, and GluN2B in the prelimbic cortex was reduced and this reduction of phospho proteins was prevented by intra prelimbic <strong>BDNF</strong> infusion.
+BDNF	addiction	withdrawal	27765467	During early <b>withdrawal</b> from cocaine self administration, tyrosine phosphorylation of ERK, GluN2A, and GluN2B in the prelimbic cortex was reduced and this reduction of phospho proteins was prevented by intra prelimbic <strong>BDNF</strong> infusion.
+BDNF	drug	cocaine	27765467	These data demonstrate that <strong>BDNF</strong> mediated activation of GluN2A  and GluN2B containing NMDA receptors underlies ERK activation in the prelimbic cortex during early withdrawal, preventing subsequent relapse to <b>cocaine</b> seeking.
+BDNF	addiction	relapse	27765467	These data demonstrate that <strong>BDNF</strong> mediated activation of GluN2A  and GluN2B containing NMDA receptors underlies ERK activation in the prelimbic cortex during early withdrawal, preventing subsequent <b>relapse</b> to cocaine <b>seeking</b>.
+BDNF	addiction	withdrawal	27765467	These data demonstrate that <strong>BDNF</strong> mediated activation of GluN2A  and GluN2B containing NMDA receptors underlies ERK activation in the prelimbic cortex during early <b>withdrawal</b>, preventing subsequent relapse to cocaine seeking.
+BDNF	drug	alcohol	27683907	Brain derived neurotrophic factor (<strong>BDNF</strong>) signaling in the dorsolateral striatum (DLS) keeps <b>alcohol</b> intake in moderation.
+BDNF	drug	alcohol	27683907	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling in the dorsolateral striatum (DLS) keeps <b>alcohol</b> intake in moderation.
+BDNF	drug	alcohol	27683907	For example, activation of the <strong>BDNF</strong> receptor tropomyosin receptor kinase B (TrkB) in the DLS reduces intake in rats that consume moderate amounts of <b>alcohol</b>.
+BDNF	drug	alcohol	27683907	Here, we tested whether long term excessive consumption of <b>alcohol</b> produces neuroadaptations in <strong>BDNF</strong> signaling in the rat DLS.
+BDNF	drug	alcohol	27683907	We found that <strong>BDNF</strong> was no longer able to gate <b>alcohol</b> self administration after a history of repeated cycles of binge <b>alcohol</b> drinking and withdrawal.
+BDNF	addiction	intoxication	27683907	We found that <strong>BDNF</strong> was no longer able to gate alcohol self administration after a history of repeated cycles of <b>binge</b> alcohol drinking and withdrawal.
+BDNF	addiction	withdrawal	27683907	We found that <strong>BDNF</strong> was no longer able to gate alcohol self administration after a history of repeated cycles of binge alcohol drinking and <b>withdrawal</b>.
+BDNF	drug	alcohol	27683907	We then elucidated the possible neuroadaptations that could block the ability of <strong>BDNF</strong> to keep consumption of <b>alcohol</b> in moderation.
+BDNF	drug	alcohol	27683907	Together, our results suggest that excessive <b>alcohol</b> consumption produces a change in <strong>BDNF</strong> signaling in the DLS, which is mediated by the recruitment of p75NTR.
+BDNF	drug	alcohol	27683907	We previously showed that <strong>brain derived neurotrophic factor</strong> and its receptor, TrkB, in the dorsolateral striatum (DLS), are part of an endogenous system that keeps <b>alcohol</b> drinking in moderation.
+BDNF	drug	alcohol	27683907	Here, we show that a history of excessive <b>alcohol</b> intake produces neuroadaptations in the DLS that preclude <strong>BDNF</strong>'s ability to gate <b>alcohol</b> self administration in rats by the recruitment of the low affinity neurotrophin receptor, p75NTR, whose activities opposes those of the Trk receptors.
+BDNF	drug	psychedelics	27660449	This has resulted in novel treatments being adopted, including subanesthetic doses of <b>ketamine</b>, which affects aberrant neuroplastic circuits, glutamatergic signaling, and the production of <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	psychedelics	27660449	It was found that a single 15 mg/kg dose of <b>ketamine</b> did indeed induce rapid antidepressant like effects in the forced swim test but did not affect brain levels of the <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	opioid	27599867	Downregulation of miR 219 enhances <strong>brain derived neurotrophic factor</strong> production in mouse dorsal root ganglia to mediate <b>morphine</b> analgesic tolerance by upregulating CaMKIIγ.
+BDNF	drug	opioid	27599867	The protein and mRNA expression of <strong>brain derived neurotrophic factor</strong> were also induced in dorsal root ganglia by prolonged <b>morphine</b> exposure in a time dependent manner, which were transcriptionally regulated by miR 219 and CaMKIIγ.
+BDNF	drug	opioid	27599867	Scavenging <strong>brain derived neurotrophic factor</strong> via tyrosine receptor kinase B Fc partially attenuated <b>morphine</b> tolerance.
+BDNF	drug	opioid	27599867	These results demonstrate that miR 219 contributes to the development of chronic tolerance to <b>morphine</b> analgesia in mouse dorsal root ganglia by targeting CaMKIIγ and enhancing CaMKIIγ dependent <strong>brain derived neurotrophic factor</strong> expression.
+BDNF	drug	alcohol	27597545	Impact of exercise and a complex environment on hippocampal dendritic morphology, <strong>Bdnf</strong> gene expression, and DNA methylation in male rat pups neonatally exposed to <b>alcohol</b>.
+BDNF	drug	alcohol	27597545	The current study investigated whether third trimester equivalent binge like <b>alcohol</b> exposure (AE) [postnatal days (PD) 4 9] affects dendritic morphology of immature dentate gyrus granule cells, and brain derived neurotrophic factor (<strong>Bdnf</strong>) gene expression and DNA methylation in hippocampal tissue in adult male rats.
+BDNF	addiction	intoxication	27597545	The current study investigated whether third trimester equivalent <b>binge</b> like alcohol exposure (AE) [postnatal days (PD) 4 9] affects dendritic morphology of immature dentate gyrus granule cells, and brain derived neurotrophic factor (<strong>Bdnf</strong>) gene expression and DNA methylation in hippocampal tissue in adult male rats.
+BDNF	drug	alcohol	27597545	The current study investigated whether third trimester equivalent binge like <b>alcohol</b> exposure (AE) [postnatal days (PD) 4 9] affects dendritic morphology of immature dentate gyrus granule cells, and <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) gene expression and DNA methylation in hippocampal tissue in adult male rats.
+BDNF	addiction	intoxication	27597545	The current study investigated whether third trimester equivalent <b>binge</b> like alcohol exposure (AE) [postnatal days (PD) 4 9] affects dendritic morphology of immature dentate gyrus granule cells, and <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) gene expression and DNA methylation in hippocampal tissue in adult male rats.
+BDNF	drug	opioid	30695408	[Effect of a Single Injection of <strong>Brain Derived Neurotrophic Factor</strong> into Midline Ventral Tegmental Area on <b>Morphine</b> Reinforcing Properties].
+BDNF	addiction	reward	30695408	[Effect of a Single Injection of <strong>Brain Derived Neurotrophic Factor</strong> into Midline Ventral Tegmental Area on Morphine <b>Reinforcing</b> Properties].
+BDNF	drug	opioid	30695408	According to the literature, <strong>BDNF</strong> (brain derived neurotrophic factor) in the lateral ventral tegmental area (VTA) could modulate <b>morphine</b> reinforcement, but the role of <strong>BDNF</strong> in the midline VTA has not been studied yet.
+BDNF	addiction	reward	30695408	According to the literature, <strong>BDNF</strong> (brain derived neurotrophic factor) in the lateral ventral tegmental area (VTA) could modulate morphine <b>reinforcement</b>, but the role of <strong>BDNF</strong> in the midline VTA has not been studied yet.
+BDNF	drug	opioid	30695408	According to the literature, <strong>BDNF</strong> (<strong>brain derived neurotrophic factor</strong>) in the lateral ventral tegmental area (VTA) could modulate <b>morphine</b> reinforcement, but the role of <strong>BDNF</strong> in the midline VTA has not been studied yet.
+BDNF	addiction	reward	30695408	According to the literature, <strong>BDNF</strong> (<strong>brain derived neurotrophic factor</strong>) in the lateral ventral tegmental area (VTA) could modulate morphine <b>reinforcement</b>, but the role of <strong>BDNF</strong> in the midline VTA has not been studied yet.
+BDNF	drug	opioid	30695408	CPP procedure was composed of eight conditioning sessions (one session per day): <b>morphine</b> (i.p., 10 mg/kg) and saline injections were paired to the compartments and counterbalanced.Recombinant human <strong>BDNF</strong> (0.75 ug) or phosphate buffered saline (PBS) as a vehicle were injected once into the midline VTA one day before or after conditioning.
+BDNF	addiction	reward	30695408	<b>CPP</b> procedure was composed of eight conditioning sessions (one session per day): morphine (i.p., 10 mg/kg) and saline injections were paired to the compartments and counterbalanced.Recombinant human <strong>BDNF</strong> (0.75 ug) or phosphate buffered saline (PBS) as a vehicle were injected once into the midline VTA one day before or after conditioning.
+BDNF	drug	opioid	30695408	After a single <strong>BDNF</strong> injection into the midline VTA be  fore conditioning, but not after conditioning, differences in time spent in <b>morphine</b> and saline paired compartments did not reach significance (p > 0.05).
+BDNF	drug	opioid	30695408	Thus, taking into account limitations of the results, we sug  gest that <strong>BDNF</strong> in the midline VTA may block <b>morphine</b> reinforcement.
+BDNF	addiction	reward	30695408	Thus, taking into account limitations of the results, we sug  gest that <strong>BDNF</strong> in the midline VTA may block morphine <b>reinforcement</b>.
+BDNF	drug	opioid	27550421	Synergistic Effects of Social Isolation and <b>Morphine</b> Addiction on Reduced Neurogenesis and <strong>BDNF</strong> Levels and the Resultant Deficits in Cognition and Emotional State in Male Rats.
+BDNF	addiction	addiction	27550421	Synergistic Effects of Social Isolation and Morphine <b>Addiction</b> on Reduced Neurogenesis and <strong>BDNF</strong> Levels and the Resultant Deficits in Cognition and Emotional State in Male Rats.
+BDNF	drug	opioid	27550421	Neurogenesis and <strong>BDNF</strong> levels were reduced in isolated and <b>morphine</b> treated isolated rats as compared to group housed rats and <b>morphine</b> treated group housed rats, respectively.
+BDNF	drug	alcohol	27514572	Association of testosterone and <strong>BDNF</strong> serum levels with craving during <b>alcohol</b> withdrawal.
+BDNF	addiction	relapse	27514572	Association of testosterone and <strong>BDNF</strong> serum levels with <b>craving</b> during alcohol withdrawal.
+BDNF	addiction	withdrawal	27514572	Association of testosterone and <strong>BDNF</strong> serum levels with craving during alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	27514572	<strong>BDNF</strong> and testosterone have been independently reported to influence <b>alcohol</b> consumption.
+BDNF	drug	alcohol	27514572	Therefore, we aimed to investigate a possible interplay of testosterone and <strong>BDNF</strong> contributing to <b>alcohol</b> dependence.
+BDNF	addiction	dependence	27514572	Therefore, we aimed to investigate a possible interplay of testosterone and <strong>BDNF</strong> contributing to alcohol <b>dependence</b>.
+BDNF	drug	alcohol	27514572	We investigated testosterone and <strong>BDNF</strong> serum levels in a sample of 99 male <b>alcohol</b> dependent patients during <b>alcohol</b> withdrawal (day 1, 7, and 14) and compared them to a healthy male control group (n = 17).
+BDNF	addiction	withdrawal	27514572	We investigated testosterone and <strong>BDNF</strong> serum levels in a sample of 99 male alcohol dependent patients during alcohol <b>withdrawal</b> (day 1, 7, and 14) and compared them to a healthy male control group (n = 17).
+BDNF	drug	alcohol	27514572	The decrease of testosterone serum levels during <b>alcohol</b> withdrawal (days 1 7) was significantly associated with the <strong>BDNF</strong> serum levels (day 1: p = 0.008).
+BDNF	addiction	withdrawal	27514572	The decrease of testosterone serum levels during alcohol <b>withdrawal</b> (days 1 7) was significantly associated with the <strong>BDNF</strong> serum levels (day 1: p = 0.008).
+BDNF	drug	alcohol	27514572	In a subgroup of patients showing high cortisol serum levels (putatively mirroring high HPA activity), we found a significant association of <strong>BDNF</strong> and testosterone as well as with <b>alcohol</b> craving measured by the Obsessive and Compulsive Drinking Scale (OCDS).
+BDNF	addiction	addiction	27514572	In a subgroup of patients showing high cortisol serum levels (putatively mirroring high HPA activity), we found a significant association of <strong>BDNF</strong> and testosterone as well as with alcohol craving measured by the Obsessive and <b>Compulsive</b> Drinking Scale (OCDS).
+BDNF	addiction	relapse	27514572	In a subgroup of patients showing high cortisol serum levels (putatively mirroring high HPA activity), we found a significant association of <strong>BDNF</strong> and testosterone as well as with alcohol <b>craving</b> measured by the Obsessive and Compulsive Drinking Scale (OCDS).
+BDNF	drug	alcohol	27514572	Our data suggest a possible association of <strong>BDNF</strong> and testosterone serum levels, which may be relevant for the symptomatology of <b>alcohol</b> dependence.
+BDNF	addiction	dependence	27514572	Our data suggest a possible association of <strong>BDNF</strong> and testosterone serum levels, which may be relevant for the symptomatology of alcohol <b>dependence</b>.
+BDNF	drug	cocaine	27488635	<b>Cocaine</b> exposure alters brain derived neurotrophic factor (<strong>BDNF</strong>) expression in the brain.
+BDNF	drug	cocaine	27488635	<b>Cocaine</b> exposure alters <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression in the brain.
+BDNF	drug	cocaine	27488635	<strong>BDNF</strong> signaling through TrkB receptors differentially modulates <b>cocaine</b> self administration, depending on the brain regions involved.
+BDNF	drug	cocaine	27488635	Brain derived neurotrophic factor (<strong>BDNF</strong>) signaling through TrkB receptors plays a well established role in <b>cocaine</b> reinforcement.
+BDNF	addiction	reward	27488635	Brain derived neurotrophic factor (<strong>BDNF</strong>) signaling through TrkB receptors plays a well established role in cocaine <b>reinforcement</b>.
+BDNF	drug	cocaine	27488635	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling through TrkB receptors plays a well established role in <b>cocaine</b> reinforcement.
+BDNF	addiction	reward	27488635	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling through TrkB receptors plays a well established role in cocaine <b>reinforcement</b>.
+BDNF	drug	cocaine	27488635	However, local manipulation of <strong>BDNF</strong> signaling yields divergent effects, depending on the brain region, thereby questioning the viability of systemic TrkB targeting for the treatment of <b>cocaine</b> use disorders.
+BDNF	drug	cocaine	27473943	High levels of <strong>brain derived neurotrophic factor</strong> are associated with treatment adherence among crack <b>cocaine</b> users.
+BDNF	drug	cocaine	27473943	Therefore, we aim to evaluate the association of Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) and Thiobarbituric Acid Reactive Substances (TBARS) levels in crack  <b>cocaine</b> users with treatment adherence and with drug addiction severity.
+BDNF	addiction	addiction	27473943	Therefore, we aim to evaluate the association of Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) and Thiobarbituric Acid Reactive Substances (TBARS) levels in crack  cocaine users with treatment adherence and with drug <b>addiction</b> severity.
+BDNF	drug	cocaine	27473943	Therefore, we aim to evaluate the association of <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) and Thiobarbituric Acid Reactive Substances (TBARS) levels in crack  <b>cocaine</b> users with treatment adherence and with drug addiction severity.
+BDNF	addiction	addiction	27473943	Therefore, we aim to evaluate the association of <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) and Thiobarbituric Acid Reactive Substances (TBARS) levels in crack  cocaine users with treatment adherence and with drug <b>addiction</b> severity.
+BDNF	drug	cocaine	27473943	A sample of 47 male inpatient crack  <b>cocaine</b> users were recruited in a treatment unit, and blood samples were collected at admission and discharge in order to measure <strong>BDNF</strong> and TBARS serum levels.
+BDNF	drug	cocaine	27473943	These findings suggest an association between higher levels of <strong>BDNF</strong> and better clinical outcomes in crack  <b>cocaine</b> users after detoxification.
+BDNF	drug	cocaine	27473943	We believe that the variation in <strong>BDNF</strong> and TBARS found here add evidence to literature data that propose that such biomarkers could be used to better understand the physiopathology of crack  <b>cocaine</b> addiction.
+BDNF	addiction	addiction	27473943	We believe that the variation in <strong>BDNF</strong> and TBARS found here add evidence to literature data that propose that such biomarkers could be used to better understand the physiopathology of crack  cocaine <b>addiction</b>.
+BDNF	drug	cannabinoid	27461790	Blockade of <b>Cannabinoid</b> CB1 receptor attenuates the acquisition of morphine induced conditioned place preference along with a downregulation of ERK, CREB phosphorylation, and <strong>BDNF</strong> expression in the nucleus accumbens and hippocampus.
+BDNF	drug	opioid	27461790	Blockade of Cannabinoid CB1 receptor attenuates the acquisition of <b>morphine</b> induced conditioned place preference along with a downregulation of ERK, CREB phosphorylation, and <strong>BDNF</strong> expression in the nucleus accumbens and hippocampus.
+BDNF	drug	opioid	27461790	In the present study, we investigated the relationship between CB1R and the extracellular signal regulated kinase (ERK), cAMP response element binding protein (CREB), brain derived neurotrophic factor (<strong>BDNF</strong>) signaling in the nucleus accumbens (NAc) and hippocampus in <b>morphine</b> induced conditioned place preference (CPP), which is used to assess the <b>morphine</b> induced reward memory.
+BDNF	addiction	reward	27461790	In the present study, we investigated the relationship between CB1R and the extracellular signal regulated kinase (ERK), cAMP response element binding protein (CREB), brain derived neurotrophic factor (<strong>BDNF</strong>) signaling in the nucleus accumbens (NAc) and hippocampus in morphine induced conditioned place preference (<b>CPP</b>), which is used to assess the morphine induced <b>reward</b> memory.
+BDNF	drug	opioid	27461790	In the present study, we investigated the relationship between CB1R and the extracellular signal regulated kinase (ERK), cAMP response element binding protein (CREB), <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling in the nucleus accumbens (NAc) and hippocampus in <b>morphine</b> induced conditioned place preference (CPP), which is used to assess the <b>morphine</b> induced reward memory.
+BDNF	addiction	reward	27461790	In the present study, we investigated the relationship between CB1R and the extracellular signal regulated kinase (ERK), cAMP response element binding protein (CREB), <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling in the nucleus accumbens (NAc) and hippocampus in morphine induced conditioned place preference (<b>CPP</b>), which is used to assess the morphine induced <b>reward</b> memory.
+BDNF	drug	opioid	27461790	Both <b>morphine</b> CPP and NO CPP induced an upregulation of ERK, CREB phosphorylation and <strong>BDNF</strong> expression.
+BDNF	addiction	reward	27461790	Both morphine <b>CPP</b> and NO <b>CPP</b> induced an upregulation of ERK, CREB phosphorylation and <strong>BDNF</strong> expression.
+BDNF	drug	opioid	27461790	Furthermore, pretreatment with AM251 before <b>morphine</b> attenuated the CPP acquisition and CB1R expression as well as the activation of ERK CREB <strong>BDNF</strong> cascade.
+BDNF	addiction	reward	27461790	Furthermore, pretreatment with AM251 before morphine attenuated the <b>CPP</b> acquisition and CB1R expression as well as the activation of ERK CREB <strong>BDNF</strong> cascade.
+BDNF	drug	opioid	27461790	(2) CB1R antagonist mediated blockade of ERK CREB <strong>BDNF</strong> signaling activation in the NAc and hippocampus may be an important mechanism underlying the attenuation of <b>morphine</b> CPP.
+BDNF	addiction	reward	27461790	(2) CB1R antagonist mediated blockade of ERK CREB <strong>BDNF</strong> signaling activation in the NAc and hippocampus may be an important mechanism underlying the attenuation of morphine <b>CPP</b>.
+BDNF	drug	alcohol	27396498	The present study examined the association between self reported concussion history and genetics (apolipoprotein E [APOE], brain derived neurotrophic factor [<strong>BDNF</strong>], and D2 dopamine receptor genes [DRD2]), trait personality measures (impulsive sensation seeking and trait aggression hostility), and current <b>alcohol</b> use.
+BDNF	addiction	relapse	27396498	The present study examined the association between self reported concussion history and genetics (apolipoprotein E [APOE], brain derived neurotrophic factor [<strong>BDNF</strong>], and D2 dopamine receptor genes [DRD2]), trait personality measures (impulsive sensation <b>seeking</b> and trait aggression hostility), and current alcohol use.
+BDNF	drug	alcohol	27396498	The present study examined the association between self reported concussion history and genetics (apolipoprotein E [APOE], <strong>brain derived neurotrophic factor</strong> [<strong>BDNF</strong>], and D2 dopamine receptor genes [DRD2]), trait personality measures (impulsive sensation seeking and trait aggression hostility), and current <b>alcohol</b> use.
+BDNF	addiction	relapse	27396498	The present study examined the association between self reported concussion history and genetics (apolipoprotein E [APOE], <strong>brain derived neurotrophic factor</strong> [<strong>BDNF</strong>], and D2 dopamine receptor genes [DRD2]), trait personality measures (impulsive sensation <b>seeking</b> and trait aggression hostility), and current alcohol use.
+BDNF	drug	cocaine	27392631	Increased <b>cocaine</b> induced conditioned place preference during periadolescence in maternally separated male BALB/c mice: the role of cortical <strong>BDNF</strong>, microRNA 212, and MeCP2.
+BDNF	drug	cocaine	27392631	MicroRNA 212 (miR 212) and methyl CpG binding protein 2 (MeCP2) have recently emerged as key regulators of brain derived neurotrophic factor (<strong>BDNF</strong>) signaling during the acquisition and maintenance of <b>cocaine</b> seeking behaviors.
+BDNF	addiction	relapse	27392631	MicroRNA 212 (miR 212) and methyl CpG binding protein 2 (MeCP2) have recently emerged as key regulators of brain derived neurotrophic factor (<strong>BDNF</strong>) signaling during the acquisition and maintenance of cocaine <b>seeking</b> behaviors.
+BDNF	drug	cocaine	27392631	MicroRNA 212 (miR 212) and methyl CpG binding protein 2 (MeCP2) have recently emerged as key regulators of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling during the acquisition and maintenance of <b>cocaine</b> seeking behaviors.
+BDNF	addiction	relapse	27392631	MicroRNA 212 (miR 212) and methyl CpG binding protein 2 (MeCP2) have recently emerged as key regulators of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) signaling during the acquisition and maintenance of cocaine <b>seeking</b> behaviors.
+BDNF	drug	cocaine	27392631	We therefore investigated the effect of maternal separation (MS) on <b>cocaine</b> induced conditioned place preference (CPP) during periadolescence and how this influences miR 212, Mecp2, and <strong>Bdnf</strong> expressions in the prefrontal cortex.
+BDNF	addiction	reward	27392631	We therefore investigated the effect of maternal separation (MS) on cocaine induced conditioned place preference (<b>CPP</b>) during periadolescence and how this influences miR 212, Mecp2, and <strong>Bdnf</strong> expressions in the prefrontal cortex.
+BDNF	drug	cocaine	27392631	MS increased <b>cocaine</b> induced CPP and decreased <strong>Bdnf</strong> exon IV expression, which correlated with higher CPP scores in such animals.
+BDNF	addiction	reward	27392631	MS increased cocaine induced <b>CPP</b> and decreased <strong>Bdnf</strong> exon IV expression, which correlated with higher <b>CPP</b> scores in such animals.
+BDNF	drug	cocaine	27392631	Together, our results suggest that early life stress can enhance the motivational salience for <b>cocaine</b> paired cues during periadolescence, and that altered expression of miR 212, Mecp2, and <strong>Bdnf</strong> in the prefrontal cortex is involved in this process.
+BDNF	drug	alcohol	27370019	Contingent and non contingent recreational like exposure to <b>ethanol</b> alters <strong>BDNF</strong> expression and signaling in the cortico accumbal network differently.
+BDNF	drug	alcohol	27370019	Although brain derived neurotrophic factor (<strong>BDNF</strong>) is part of a homeostatic pathway involved in the development of <b>alcohol</b> dependence, it is not clear whether this is also true after recreational <b>ethanol</b> consumption.
+BDNF	addiction	dependence	27370019	Although brain derived neurotrophic factor (<strong>BDNF</strong>) is part of a homeostatic pathway involved in the development of alcohol <b>dependence</b>, it is not clear whether this is also true after recreational ethanol consumption.
+BDNF	drug	alcohol	27370019	Although <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is part of a homeostatic pathway involved in the development of <b>alcohol</b> dependence, it is not clear whether this is also true after recreational <b>ethanol</b> consumption.
+BDNF	addiction	dependence	27370019	Although <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is part of a homeostatic pathway involved in the development of alcohol <b>dependence</b>, it is not clear whether this is also true after recreational ethanol consumption.
+BDNF	drug	alcohol	27370019	A single <b>ethanol</b> exposure transiently reduced <strong>BDNF</strong> mRNA levels in the medial prefrontal cortex (mPFC) of Y Et.
+BDNF	drug	alcohol	27370019	A rapid intervention targeting the <strong>BDNF</strong> system might be useful to prevent escalation to <b>alcohol</b> abuse.
+BDNF	addiction	addiction	27370019	A rapid intervention targeting the <strong>BDNF</strong> system might be useful to prevent <b>escalation</b> to alcohol abuse.
+BDNF	drug	psychedelics	27343386	In a second part, we found an effective disruption of contextual fear reconsolidation by the N methyl d aspartate receptor antagonist <b>ketamine</b>, associated with a down regulation of early growth response 1 (Egr1) in the hippocampal CA1 area, and up regulation of brain derived neurotrophic factor (<strong>Bdnf</strong>) mRNA levels in the prelimbic and infralimbic cortices.
+BDNF	drug	psychedelics	27343386	In a second part, we found an effective disruption of contextual fear reconsolidation by the N methyl d aspartate receptor antagonist <b>ketamine</b>, associated with a down regulation of early growth response 1 (Egr1) in the hippocampal CA1 area, and up regulation of <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) mRNA levels in the prelimbic and infralimbic cortices.
+BDNF	drug	opioid	27312092	Furthermore, the protein expression levels of extracellular signal regulated kinase (ERK) and phosphorylated ERK (p ERK), histone H3 lysine 9 acetylation (aceH3K9) and brain derived neurotrophic factor (<strong>BDNF</strong>) in the VLO in <b>morphine</b> induced behavioral sensitization were examined.
+BDNF	addiction	sensitization	27312092	Furthermore, the protein expression levels of extracellular signal regulated kinase (ERK) and phosphorylated ERK (p ERK), histone H3 lysine 9 acetylation (aceH3K9) and brain derived neurotrophic factor (<strong>BDNF</strong>) in the VLO in morphine induced behavioral <b>sensitization</b> were examined.
+BDNF	drug	opioid	27312092	Furthermore, the protein expression levels of extracellular signal regulated kinase (ERK) and phosphorylated ERK (p ERK), histone H3 lysine 9 acetylation (aceH3K9) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the VLO in <b>morphine</b> induced behavioral sensitization were examined.
+BDNF	addiction	sensitization	27312092	Furthermore, the protein expression levels of extracellular signal regulated kinase (ERK) and phosphorylated ERK (p ERK), histone H3 lysine 9 acetylation (aceH3K9) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the VLO in morphine induced behavioral <b>sensitization</b> were examined.
+BDNF	drug	opioid	27312092	Moreover, the protein levels of p ERK, aceH3K9 and <strong>BDNF</strong> except ERK in the VLO were significantly upregulated in <b>morphine</b> treated rats in the expression phase.
+BDNF	drug	opioid	27312092	The upregulated expression of p ERK, aceH3K9 and <strong>BDNF</strong> in the VLO might be the underlying mechanism of histone acetylation enhancing the <b>morphine</b> induced behavioral sensitization.
+BDNF	addiction	sensitization	27312092	The upregulated expression of p ERK, aceH3K9 and <strong>BDNF</strong> in the VLO might be the underlying mechanism of histone acetylation enhancing the morphine induced behavioral <b>sensitization</b>.
+BDNF	drug	amphetamine	27287203	Intravenous Prenatal Nicotine Exposure Alters <b>METH</b> Induced Hyperactivity, Conditioned Hyperactivity, and <strong>BDNF</strong> in Adult Rat Offspring.
+BDNF	drug	nicotine	27287203	Intravenous Prenatal <b>Nicotine</b> Exposure Alters METH Induced Hyperactivity, Conditioned Hyperactivity, and <strong>BDNF</strong> in Adult Rat Offspring.
+BDNF	drug	amphetamine	27287203	We also determined whether PN and/or <b>METH</b> exposure altered protein levels of <strong>BDNF</strong> (brain derived neurotrophic factor) in the nucleus accumbens, the dorsal striatum, and the prefrontal cortex of adult offspring.
+BDNF	drug	amphetamine	27287203	We also determined whether PN and/or <b>METH</b> exposure altered protein levels of <strong>BDNF</strong> (<strong>brain derived neurotrophic factor</strong>) in the nucleus accumbens, the dorsal striatum, and the prefrontal cortex of adult offspring.
+BDNF	addiction	sensitization	27287203	<strong>BDNF</strong> was of interest because of its role in the development and maintenance of the mesocorticolimbic pathway and its ability to modulate neural processes that contribute to drug abuse, such as <b>sensitization</b> of the dopamine system.
+BDNF	drug	amphetamine	27287203	PN and <b>METH</b> exposure produced changes in <strong>BDNF</strong> protein levels in all three regions, and complex interactions were observed between these two factors.
+BDNF	drug	nicotine	27287203	The PN induced alterations in mesocorticolimbic <strong>BDNF</strong> protein lend further support for the hypothesis that maternal <b>smoking</b> during pregnancy produces alterations in neuronal plasticity that contribute to drug abuse vulnerability.
+BDNF	drug	cocaine	27154426	Overexpression of <strong>BDNF</strong> in the ventral tegmental area enhances binge <b>cocaine</b> self administration in rats exposed to repeated social defeat.
+BDNF	addiction	intoxication	27154426	Overexpression of <strong>BDNF</strong> in the ventral tegmental area enhances <b>binge</b> cocaine self administration in rats exposed to repeated social defeat.
+BDNF	addiction	sensitization	27154426	Intra VTA <strong>BDNF</strong> overexpression enhances social defeat stress induced cross <b>sensitization</b> to psychostimulants and induces nucleus accumbens (NAc) ΔFosB expression.
+BDNF	drug	cocaine	27154426	While stress alone increased intake during the 12 h binge session, socially defeated rats that received VTA <strong>BDNF</strong> overexpression exhibited even greater <b>cocaine</b> intake compared to the GFP stressed group.
+BDNF	addiction	intoxication	27154426	While stress alone increased intake during the 12 h <b>binge</b> session, socially defeated rats that received VTA <strong>BDNF</strong> overexpression exhibited even greater cocaine intake compared to the GFP stressed group.
+BDNF	addiction	intoxication	27154426	However, VTA <strong>BDNF</strong> overexpression alone did not alter <b>binge</b> intake.
+BDNF	drug	cocaine	27154426	<strong>BDNF</strong> expression in the VTA was also positively correlated with total <b>cocaine</b> intake during binge session.
+BDNF	addiction	intoxication	27154426	<strong>BDNF</strong> expression in the VTA was also positively correlated with total cocaine intake during <b>binge</b> session.
+BDNF	drug	cocaine	27154426	Here we demonstrate that VTA <strong>BDNF</strong> overexpression increases long access <b>cocaine</b> intake, but only under stressful conditions.
+BDNF	addiction	addiction	27154426	Therefore, enhanced VTA <strong>BDNF</strong> expression may be a facilitator for stress induced increases in drug abuse related behavior specifically under conditions that capture <b>compulsive</b> like drug intake.
+BDNF	drug	cocaine	27137405	The effects of resistance exercise on <b>cocaine</b> self administration, muscle hypertrophy, and <strong>BDNF</strong> expression in the nucleus accumbens.
+BDNF	drug	cocaine	27137405	This study examined the effects of resistance exercise (strength training) on <b>cocaine</b> self administration and <strong>BDNF</strong> expression, a marker of neuronal activation regulated by aerobic exercise.
+BDNF	drug	cocaine	27137405	These data indicate that resistance exercise decreases <b>cocaine</b> self administration and reduces <strong>BDNF</strong> expression in the nucleus accumbens after a history of <b>cocaine</b> exposure.
+BDNF	drug	alcohol	27107672	Serum levels of <strong>brain derived neurotrophic factor</strong> in <b>alcohol</b> dependent patients receiving high dose baclofen.
+BDNF	addiction	addiction	27107672	The neurotrophin brain derived neurotrophic factor (<strong>BDNF</strong>) has been suggested to be involved in the development and maintenance of <b>addictive</b> and other psychiatric disorders.
+BDNF	addiction	addiction	27107672	The neurotrophin <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been suggested to be involved in the development and maintenance of <b>addictive</b> and other psychiatric disorders.
+BDNF	drug	alcohol	27107672	The objective of this study was to investigate serum levels of <strong>BDNF</strong> over time in <b>alcohol</b> dependent patients receiving individually titrated high dose treatment (30 270mg/d) with the GABA B receptor agonist baclofen or placebo for up to 20 weeks.
+BDNF	drug	alcohol	27107672	Based on these findings, it seems unlikely that baclofen exerts a direct effect on serum levels of <strong>BDNF</strong> in <b>alcohol</b> dependent patients.
+BDNF	drug	alcohol	27107672	Future studies are needed to further explore the mechanism of action of baclofen and its possible relationship to <strong>BDNF</strong> in <b>alcohol</b> use disorders.
+BDNF	drug	opioid	27094549	The expression of <strong>Bdnf</strong> and Pdyn (qPCR) was increased after <b>morphine</b> treatment and incision.
+BDNF	drug	opioid	27094549	Chromatin immunoprecipitation assays demonstrated that the Pdyn and <strong>Bdnf</strong> promoters were more strongly associated with acetylated H3K9 after <b>morphine</b> plus incision than in the <b>morphine</b> or incision alone groups.
+BDNF	drug	opioid	27094549	Spinal epigenetic changes involving <strong>Bdnf</strong> and Pdyn may contribute to the enhanced postoperative nociceptive sensitization and analgesic tolerance observed after continuous <b>opioid</b> exposure.
+BDNF	addiction	sensitization	27094549	Spinal epigenetic changes involving <strong>Bdnf</strong> and Pdyn may contribute to the enhanced postoperative nociceptive <b>sensitization</b> and analgesic tolerance observed after continuous opioid exposure.
+BDNF	addiction	reward	27063080	Furthermore, it may also play a role in the regulation of behavior given it readily enters the central nervous system, where it induces <strong>BDNF</strong> expression in several brain areas linked to <b>reward</b> processing, e.g.
+BDNF	drug	alcohol	27038596	Ingenuity Pathway Analysis of putative miRNA targets illustrated that miRNAs identified in this study are involved in biological pathways that mediate the effects of <b>alcohol</b>, such as <strong>brain derived neurotrophic factor</strong>, ERK1/2, and PI3K/AKT signaling.
+BDNF	addiction	addiction	26976342	A significant association between <strong>BDNF</strong> promoter methylation and the risk of drug <b>addiction</b>.
+BDNF	addiction	addiction	26976342	The aim of our work was to evaluate the role of <strong>BDNF</strong> promoter methylation in drug <b>addiction</b>.
+BDNF	addiction	addiction	26976342	Our results suggest that <strong>BDNF</strong> promoter methylation is associated with drug <b>addiction</b>, although further studies are needed to understand the mechanisms by which <strong>BDNF</strong> promoter methylation contributes to the pathophysiology of drug <b>addiction</b>.
+BDNF	drug	amphetamine	26965573	Altered social cognition in male <strong>BDNF</strong> heterozygous mice and following chronic <b>methamphetamine</b> exposure.
+BDNF	drug	amphetamine	26965573	We recently found that brain derived neurotrophic factor (<strong>BDNF</strong>) heterozygous mice show disrupted sensitization to <b>methamphetamine</b>, supporting other work suggesting an important role of this neurotrophin in the pathophysiology of psychosis and the neuronal response to stimulant drugs.
+BDNF	addiction	sensitization	26965573	We recently found that brain derived neurotrophic factor (<strong>BDNF</strong>) heterozygous mice show disrupted <b>sensitization</b> to methamphetamine, supporting other work suggesting an important role of this neurotrophin in the pathophysiology of psychosis and the neuronal response to stimulant drugs.
+BDNF	drug	amphetamine	26965573	We recently found that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) heterozygous mice show disrupted sensitization to <b>methamphetamine</b>, supporting other work suggesting an important role of this neurotrophin in the pathophysiology of psychosis and the neuronal response to stimulant drugs.
+BDNF	addiction	sensitization	26965573	We recently found that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) heterozygous mice show disrupted <b>sensitization</b> to methamphetamine, supporting other work suggesting an important role of this neurotrophin in the pathophysiology of psychosis and the neuronal response to stimulant drugs.
+BDNF	drug	amphetamine	26965573	In the current study, we assessed social and cognitive behaviours in <b>methamphetamine</b> treated <strong>BDNF</strong> heterozygous mice and wildtype littermate controls.
+BDNF	drug	amphetamine	26965573	Vehicle treated male <strong>BDNF</strong> heterozygous mice showed a similar impairment in social novelty preference, with a trend for no further disruption by <b>methamphetamine</b> exposure.
+BDNF	drug	amphetamine	26965573	Together these findings suggest that dynamic regulation of <strong>BDNF</strong> signalling is necessary to mediate the effects of <b>methamphetamine</b> on behaviours relevant to schizophrenia.
+BDNF	addiction	reward	26960698	However, treatment with a <strong>BDNF</strong> tropomyosin receptor kinase B (TrkB) receptor antagonist, K252a (5 μg/kg), did not affect rottlerin's suppressing effect on COC induced <b>CPP</b> and treatment with 7,8 dihydroxyflavone (10 mg/kg x 6, 7,8 DHF), a selective TrkB agonist, prior to each conditioning trial did not affect COC induced <b>CPP</b>.
+BDNF	drug	alcohol	26941165	A role for histone acetylation mechanisms in adolescent <b>alcohol</b> exposure induced deficits in hippocampal <strong>brain derived neurotrophic factor</strong> expression and neurogenesis markers in adulthood.
+BDNF	drug	alcohol	26941165	We investigated the effects of adolescent intermittent <b>ethanol</b> (AIE) exposure, as opposed to normal saline (AIS) exposure, on histone acetylation mediated regulation of brain derived neurotrophic factor (<strong>BDNF</strong>) expression and developmental stages of neurogenesis (proliferating and immature neurons) in the hippocampus in adulthood.
+BDNF	drug	alcohol	26941165	We investigated the effects of adolescent intermittent <b>ethanol</b> (AIE) exposure, as opposed to normal saline (AIS) exposure, on histone acetylation mediated regulation of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression and developmental stages of neurogenesis (proliferating and immature neurons) in the hippocampus in adulthood.
+BDNF	drug	cocaine	26923993	Prefrontal cortical <strong>BDNF</strong>: A regulatory key in <b>cocaine</b>  and food reinforced behaviors.
+BDNF	drug	cocaine	26923993	Recent evidence also points to important, yet complex, roles for <strong>BDNF</strong> in rodent models of <b>cocaine</b> abuse and addiction.
+BDNF	addiction	addiction	26923993	Recent evidence also points to important, yet complex, roles for <strong>BDNF</strong> in rodent models of cocaine abuse and <b>addiction</b>.
+BDNF	drug	cocaine	26923993	Here we examine the role of prefrontal cortical (PFC) <strong>BDNF</strong> in reward related decision making and behavioral sensitivity to, and responding for, <b>cocaine</b>.
+BDNF	addiction	reward	26923993	Here we examine the role of prefrontal cortical (PFC) <strong>BDNF</strong> in <b>reward</b> related decision making and behavioral sensitivity to, and responding for, cocaine.
+BDNF	drug	cocaine	26923993	We focus on <strong>BDNF</strong> within the medial and orbital PFC, its regulation by <b>cocaine</b> during early postnatal development and in adulthood, and how <strong>BDNF</strong> in turn influences responding for drug reinforcement, including in reinstatement models.
+BDNF	addiction	relapse	26923993	We focus on <strong>BDNF</strong> within the medial and orbital PFC, its regulation by cocaine during early postnatal development and in adulthood, and how <strong>BDNF</strong> in turn influences responding for drug reinforcement, including in <b>reinstatement</b> models.
+BDNF	addiction	reward	26923993	We focus on <strong>BDNF</strong> within the medial and orbital PFC, its regulation by cocaine during early postnatal development and in adulthood, and how <strong>BDNF</strong> in turn influences responding for drug <b>reinforcement</b>, including in reinstatement models.
+BDNF	drug	cocaine	26912258	Demethylation of c MYB binding site mediates upregulation of <strong>Bdnf</strong> IV in <b>cocaine</b> conditioned place preference.
+BDNF	addiction	addiction	26912258	However, the mechanisms regulating expression of <strong>Bdnf</strong> in drug <b>addiction</b> remain elusive.
+BDNF	drug	cocaine	26912258	In the present study, using the conditioned place preference (CPP) model, we showed that expression of <strong>Bdnf</strong> IV is upregulated in the nucleus accumbens (NAc) of conditioned animals while <strong>Bdnf</strong> I is upregulated in <b>cocaine</b> treated mice irrespective of conditioning.
+BDNF	addiction	reward	26912258	In the present study, using the conditioned place preference (<b>CPP</b>) model, we showed that expression of <strong>Bdnf</strong> IV is upregulated in the nucleus accumbens (NAc) of conditioned animals while <strong>Bdnf</strong> I is upregulated in cocaine treated mice irrespective of conditioning.
+BDNF	drug	cocaine	26912258	The methylation level of a putative c MYB binding site in the promoter region of <strong>Bdnf</strong> IV was significantly decreased in the NAc under <b>cocaine</b> CPP conditioning but remained unchanged without conditioning, concurrently with increased binding of c MYB to this site.
+BDNF	addiction	reward	26912258	The methylation level of a putative c MYB binding site in the promoter region of <strong>Bdnf</strong> IV was significantly decreased in the NAc under cocaine <b>CPP</b> conditioning but remained unchanged without conditioning, concurrently with increased binding of c MYB to this site.
+BDNF	drug	cocaine	26912258	Administration of methionine, a precursor of SAM, inhibited <b>cocaine</b> CPP, reversed demethylation of c MYB binding site and induction of <strong>Bdnf</strong> IV expression by <b>cocaine</b> CPP.
+BDNF	addiction	reward	26912258	Administration of methionine, a precursor of SAM, inhibited cocaine <b>CPP</b>, reversed demethylation of c MYB binding site and induction of <strong>Bdnf</strong> IV expression by cocaine <b>CPP</b>.
+BDNF	drug	cocaine	26912258	Our results imply that <strong>Bdnf</strong> IV demethylation at c MYB binding site is involved in <b>cocaine</b> triggered seeking behavior, whereas <strong>Bdnf</strong> I responds to the immediate pharmacological effects of <b>cocaine</b>.
+BDNF	addiction	relapse	26912258	Our results imply that <strong>Bdnf</strong> IV demethylation at c MYB binding site is involved in cocaine triggered <b>seeking</b> behavior, whereas <strong>Bdnf</strong> I responds to the immediate pharmacological effects of cocaine.
+BDNF	drug	amphetamine	26844469	Time Dependent Serum <strong>Brain Derived Neurotrophic Factor</strong> Decline During <b>Methamphetamine</b> Withdrawal.
+BDNF	addiction	withdrawal	26844469	Time Dependent Serum <strong>Brain Derived Neurotrophic Factor</strong> Decline During Methamphetamine <b>Withdrawal</b>.
+BDNF	drug	amphetamine	26844469	Studies on the role of brain derived neurotrophic factor (<strong>BDNF</strong>) in human <b>METH</b> addicts are limited and inconsistent.
+BDNF	drug	amphetamine	26844469	Studies on the role of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in human <b>METH</b> addicts are limited and inconsistent.
+BDNF	drug	amphetamine	26844469	The purposes of this study are to compare the serum <strong>BDNF</strong> levels between <b>METH</b> addicts and healthy controls during early withdrawal, and explore the changes of serum <strong>BDNF</strong> levels during the first month after <b>METH</b> withdrawal.179 <b>METH</b> addicts and 90 age  and gender matched healthy controls were recruited in this study.
+BDNF	addiction	withdrawal	26844469	The purposes of this study are to compare the serum <strong>BDNF</strong> levels between METH addicts and healthy controls during early <b>withdrawal</b>, and explore the changes of serum <strong>BDNF</strong> levels during the first month after METH <b>withdrawal</b>.179 METH addicts and 90 age  and gender matched healthy controls were recruited in this study.
+BDNF	drug	amphetamine	26844469	We measured serum <strong>BDNF</strong> levels at baseline (both <b>METH</b> addicts and healthy controls) and at 1 month after abstinence of <b>METH</b> (<b>METH</b> addicts only).Serum <strong>BDNF</strong> levels of <b>METH</b> addicts at baseline were significantly higher than controls (1460.28 ± 490.69 vs 1241.27 ± 335.52 pg/mL; F = 14.51, P < 0.001).
+BDNF	drug	amphetamine	26844469	The serum <strong>BDNF</strong> levels of 40 <b>METH</b> addicts were re examined after 1 month of <b>METH</b> abstinence, which were significantly lower than that at baseline (1363.70 ± 580.59 vs 1621.41 ± 591.07 pg/mL; t = 2.26, P = .03), but showed no differences to the controls (1363.70 ± 580.59 vs 1241.27 ± 335.52 pg/mL; F = 2.29, P = 0.13).Our study demonstrated that serum <strong>BDNF</strong> levels were higher in <b>METH</b> addicts than controls during early withdrawal, and were time dependent decreased during the first month of abstinence.
+BDNF	addiction	withdrawal	26844469	The serum <strong>BDNF</strong> levels of 40 METH addicts were re examined after 1 month of METH abstinence, which were significantly lower than that at baseline (1363.70 ± 580.59 vs 1621.41 ± 591.07 pg/mL; t = 2.26, P = .03), but showed no differences to the controls (1363.70 ± 580.59 vs 1241.27 ± 335.52 pg/mL; F = 2.29, P = 0.13).Our study demonstrated that serum <strong>BDNF</strong> levels were higher in METH addicts than controls during early <b>withdrawal</b>, and were time dependent decreased during the first month of abstinence.
+BDNF	drug	amphetamine	26844469	These findings may provide further evidence that increased serum <strong>BDNF</strong> levels may be associated with the pathophysiology of <b>METH</b> addiction and withdrawal and may be a protective response against the subsequent <b>METH</b> induced neurotoxicity.
+BDNF	addiction	addiction	26844469	These findings may provide further evidence that increased serum <strong>BDNF</strong> levels may be associated with the pathophysiology of METH <b>addiction</b> and withdrawal and may be a protective response against the subsequent METH induced neurotoxicity.
+BDNF	addiction	withdrawal	26844469	These findings may provide further evidence that increased serum <strong>BDNF</strong> levels may be associated with the pathophysiology of METH addiction and <b>withdrawal</b> and may be a protective response against the subsequent METH induced neurotoxicity.
+BDNF	drug	psychedelics	26807959	Furthermore, <b>ibogaine</b> has been shown to interact with the acetylcholine, serotonin and dopamine systems; it alters the expression of several proteins including substance P, brain derived neurotrophic factor (<strong>BDNF</strong>), c fos and egr 1.
+BDNF	drug	psychedelics	26807959	Furthermore, <b>ibogaine</b> has been shown to interact with the acetylcholine, serotonin and dopamine systems; it alters the expression of several proteins including substance P, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), c fos and egr 1.
+BDNF	drug	alcohol	26805422	Binge <b>ethanol</b> treated rats demonstrated a significant increase in KLF11, both MAO isoforms, protein oxidation and caspase 3, as well as a reduction in <strong>BDNF</strong> expression in the frontal cortex compared to control rats.
+BDNF	addiction	intoxication	26805422	<b>Binge</b> ethanol treated rats demonstrated a significant increase in KLF11, both MAO isoforms, protein oxidation and caspase 3, as well as a reduction in <strong>BDNF</strong> expression in the frontal cortex compared to control rats.
+BDNF	drug	opioid	26801497	Brain derived neurotrophic factor (<strong>BDNF</strong>) appears to play a crucial role in the reward response to drugs such as <b>heroin</b>.
+BDNF	addiction	reward	26801497	Brain derived neurotrophic factor (<strong>BDNF</strong>) appears to play a crucial role in the <b>reward</b> response to drugs such as heroin.
+BDNF	drug	opioid	26801497	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) appears to play a crucial role in the reward response to drugs such as <b>heroin</b>.
+BDNF	addiction	reward	26801497	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) appears to play a crucial role in the <b>reward</b> response to drugs such as heroin.
+BDNF	drug	opioid	26801497	According to these findings, methylation of the <strong>BDNF</strong> IV promoter showed the highest level in patients receiving levomethadone without heroine co use (linear mixed model: control vs. levomethadone group without heroine co use: p = 0.008, with <b>heroin</b> co use: p = 0.050, diamorphine vs. levomethadone group with heroine co use: p = 0.077 and without heroine co use: p = 0.015.).
+BDNF	addiction	addiction	26792050	In addition, <strong>BDNF</strong> alterations contribute to neurological, mental, and <b>addictive</b> disorders.
+BDNF	drug	cocaine	26792050	We described two cases of patients with <b>cocaine</b> dependence who presented with CIP and had changes in their <strong>BDNF</strong> levels during the psychotic episode.
+BDNF	addiction	dependence	26792050	We described two cases of patients with cocaine <b>dependence</b> who presented with CIP and had changes in their <strong>BDNF</strong> levels during the psychotic episode.
+BDNF	drug	alcohol	26792039	This study aims to reveal the relationship of depression with growth factors such as brain derived neurotrophic factor (<strong>BDNF</strong>), nerve growth factor (NGF), and insulin like growth factor 1 (IGF 1) in inpatients diagnosed with <b>alcohol</b> dependence, and to identify candidate growth factors as biological markers to indicate the comorbid of <b>alcohol</b> dependence and depression.
+BDNF	addiction	dependence	26792039	This study aims to reveal the relationship of depression with growth factors such as brain derived neurotrophic factor (<strong>BDNF</strong>), nerve growth factor (NGF), and insulin like growth factor 1 (IGF 1) in inpatients diagnosed with alcohol <b>dependence</b>, and to identify candidate growth factors as biological markers to indicate the comorbid of alcohol <b>dependence</b> and depression.
+BDNF	drug	alcohol	26792039	This study aims to reveal the relationship of depression with growth factors such as <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), nerve growth factor (NGF), and insulin like growth factor 1 (IGF 1) in inpatients diagnosed with <b>alcohol</b> dependence, and to identify candidate growth factors as biological markers to indicate the comorbid of <b>alcohol</b> dependence and depression.
+BDNF	addiction	dependence	26792039	This study aims to reveal the relationship of depression with growth factors such as <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), nerve growth factor (NGF), and insulin like growth factor 1 (IGF 1) in inpatients diagnosed with alcohol <b>dependence</b>, and to identify candidate growth factors as biological markers to indicate the comorbid of alcohol <b>dependence</b> and depression.
+BDNF	drug	alcohol	26792039	<strong>BDNF</strong> and NGF showed no significant difference between <b>alcohol</b> dependent patients with and without depression, but IGF 1 was significantly higher in those with than in those without depression.
+BDNF	drug	opioid	26789010	Baclofen prevents the elevated plus maze behavior and <strong>BDNF</strong> expression during <b>naloxone</b> precipitated <b>morphine</b> withdrawal in male and female mice.
+BDNF	addiction	withdrawal	26789010	Baclofen prevents the elevated plus maze behavior and <strong>BDNF</strong> expression during naloxone precipitated morphine <b>withdrawal</b> in male and female mice.
+BDNF	drug	opioid	26789010	There are no previous reports regarding sex differences in the elevated plus maze (EPM) and the expression of <strong>BDNF</strong> in <b>morphine</b> withdrawn mice.
+BDNF	drug	opioid	26789010	<strong>BDNF</strong> expression decreased in the AcbC, BNST, CeC, and CA3 of the hippocampus while increased in the BLA of <b>morphine</b> withdrawn male.
+BDNF	drug	opioid	26789010	Baclofen pretreatment prevented the <strong>BDNF</strong> expression observed in <b>morphine</b> withdrawn male mice in all the brain areas studied except in the CeC.
+BDNF	drug	opioid	26789010	Baclofen prevention of the EPM behavior associated to <b>morphine</b> withdrawal could be partially related to changes in <strong>BDNF</strong> expression.
+BDNF	addiction	withdrawal	26789010	Baclofen prevention of the EPM behavior associated to morphine <b>withdrawal</b> could be partially related to changes in <strong>BDNF</strong> expression.
+BDNF	addiction	withdrawal	26775017	Cognitive control deficits during mecamylamine precipitated <b>withdrawal</b> in mice: Possible links to frontostriatal <strong>BDNF</strong> imbalance.
+BDNF	drug	nicotine	26775017	Thus, we examined the effects of mecamylamine precipitated <b>nicotine</b> withdrawal on prefrontal and striatal <strong>BDNF</strong> protein expression.
+BDNF	addiction	withdrawal	26775017	Thus, we examined the effects of mecamylamine precipitated nicotine <b>withdrawal</b> on prefrontal and striatal <strong>BDNF</strong> protein expression.
+BDNF	drug	nicotine	26775017	The striatal/prefrontal <strong>BDNF</strong> ratios robustly increased following precipitated <b>nicotine</b> withdrawal.
+BDNF	addiction	withdrawal	26775017	The striatal/prefrontal <strong>BDNF</strong> ratios robustly increased following precipitated nicotine <b>withdrawal</b>.
+BDNF	drug	nicotine	26775017	Collectively, our findings illustrate that mecamylamine induced <b>nicotine</b> withdrawal disrupts cognitive control processes and that these changes are possibly linked to perturbations in frontostriatal <strong>BDNF</strong> signaling.
+BDNF	addiction	withdrawal	26775017	Collectively, our findings illustrate that mecamylamine induced nicotine <b>withdrawal</b> disrupts cognitive control processes and that these changes are possibly linked to perturbations in frontostriatal <strong>BDNF</strong> signaling.
+BDNF	drug	opioid	26774004	<strong>Brain derived neurotrophic factor</strong> serum levels in <b>heroin</b> dependent patients after 26weeks of withdrawal.
+BDNF	addiction	withdrawal	26774004	<strong>Brain derived neurotrophic factor</strong> serum levels in heroin dependent patients after 26weeks of <b>withdrawal</b>.
+BDNF	drug	opioid	26774004	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been implicated in the pathophysiology of <b>heroin</b> dependence.
+BDNF	addiction	dependence	26774004	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been implicated in the pathophysiology of heroin <b>dependence</b>.
+BDNF	drug	opioid	26774004	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been implicated in the pathophysiology of <b>heroin</b> dependence.
+BDNF	addiction	dependence	26774004	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been implicated in the pathophysiology of heroin <b>dependence</b>.
+BDNF	addiction	withdrawal	26774004	<strong>BDNF</strong> expression is dramatically changed during drug <b>withdrawal</b>, and is associated with drug <b>withdrawal</b> syndrome.
+BDNF	drug	opioid	26774004	This study aimed to explore (1) alterations of <strong>BDNF</strong> serum levels in <b>heroin</b> dependent patients after long term abstinence; and (2) the association between <strong>BDNF</strong> serum levels and protracted withdrawal syndrome.
+BDNF	addiction	withdrawal	26774004	This study aimed to explore (1) alterations of <strong>BDNF</strong> serum levels in heroin dependent patients after long term abstinence; and (2) the association between <strong>BDNF</strong> serum levels and protracted <b>withdrawal</b> syndrome.
+BDNF	drug	opioid	26774004	We measured <strong>BDNF</strong> serum levels at baseline and 26 weeks after <b>heroin</b> abstinence.
+BDNF	drug	opioid	26774004	We found that baseline <strong>BDNF</strong> serum levels were significantly lower in <b>heroin</b> dependent patients compared to controls (p<0.01).
+BDNF	drug	opioid	26774004	There was also a significantly difference in <strong>BDNF</strong> serum levels among <b>heroin</b> dependent patients at baseline and 26 week follow up (p<0.01).
+BDNF	drug	opioid	26774004	The results show that the <strong>BDNF</strong> serum levels in <b>heroin</b> dependent patients are lower than those of healthy controls at baseline and increased after 26 weeks of abstinence, although the <strong>BDNF</strong> serum levels are still lower than those of the healthy controls.
+BDNF	addiction	withdrawal	26774004	A negative correlation between the change in <strong>BDNF</strong> serum levels and protracted <b>withdrawal</b> symptoms was found but needs to be confirmed in further study.
+BDNF	addiction	dependence	26774004	The results revealed that <strong>BDNF</strong> serum level is worth paying attention to in order to further investigate the possibility of it being a biomarker of treatment outcome for opiate <b>dependence</b>.
+BDNF	drug	alcohol	26730594	In PFC a module containing <strong>Bdnf</strong> was identified as highly CIE responsive in a biphasic manner, with peak changes at 0 hours and 5 days following CIE, suggesting a possible role in mechanisms underlying long term molecular and behavioral response to CIE. Bioinformatics analysis of this network and several other modules identified Let 7 family microRNAs as potential regulators of gene expression changes induced by CIE. Our results suggest a complex temporal and regional pattern of widespread gene network responses involving neuroinflammatory and neuroplasticity related genes as contributing to physiological and behavioral responses to chronic <b>ethanol</b>.
+BDNF	drug	opioid	28635745	No Genom Wide Association studies of ВЕD has been performed and the analysis of the results of candidate genes studies gives reason to believe that pathogenetically substantiated panel of genes, including serotonin system, <strong>BDNF</strong> and, especially dopamine and endogenous <b>opioid</b> system, would be most useful, taking into account the mechanism of action of drugs for the ВЕD treatment.
+BDNF	drug	alcohol	26711851	We previously reported that acute and repeated exposure to <b>ethanol</b> during the third trimester equivalent inhibits long term potentiation of GABAA receptor dependent synaptic currents in CA3 pyramidal neurons through a mechanism that depends on retrograde release of <strong>brain derived neurotrophic factor</strong> driven by activation of voltage gated Ca(2+) channels (Zucca and Valenzuela, 2010).
+BDNF	drug	psychedelics	26706783	The modulation of <strong>BDNF</strong> expression and signalling dissects the antidepressant from the reinforcing properties of <b>ketamine</b>: Effects of single infusion vs. chronic self administration in rats.
+BDNF	addiction	reward	26706783	The modulation of <strong>BDNF</strong> expression and signalling dissects the antidepressant from the <b>reinforcing</b> properties of ketamine: Effects of single infusion vs. chronic self administration in rats.
+BDNF	addiction	reward	26706783	To this end, we focused our attention on <strong>BDNF</strong>, a neurotrophin that has been shown to play a role in both antidepressant and <b>reinforcing</b> properties of several drugs.
+BDNF	drug	psychedelics	26706783	Taken together, we here point to <strong>BDNF</strong> and its downstream signalling pathway as a finely tuned mechanism whose modulation might subserve the different features of <b>ketamine</b>.
+BDNF	drug	alcohol	26686767	Using wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with <b>ethanol</b> (3g/kg) for 2 weeks, we showed that binge like <b>ethanol</b> treatment in adolescent mice promotes short  and long term alterations in synaptic plasticity and epigenetic changes in the promoter region of <strong>bdnf</strong> and fosb, which increased their expression in the mPFC of young adult animals.
+BDNF	addiction	intoxication	26686767	Using wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with ethanol (3g/kg) for 2 weeks, we showed that <b>binge</b> like ethanol treatment in adolescent mice promotes short  and long term alterations in synaptic plasticity and epigenetic changes in the promoter region of <strong>bdnf</strong> and fosb, which increased their expression in the mPFC of young adult animals.
+BDNF	drug	alcohol	26659122	<b>Alcohol</b> dependence induced regulation of the proliferation and survival of adult brain progenitors is associated with altered <strong>BDNF</strong> TrkB signaling.
+BDNF	addiction	dependence	26659122	Alcohol <b>dependence</b> induced regulation of the proliferation and survival of adult brain progenitors is associated with altered <strong>BDNF</strong> TrkB signaling.
+BDNF	addiction	withdrawal	26659122	<b>Withdrawal</b> from CIE increased <strong>BDNF</strong> levels in the hippocampus and mPFC, and subsequently increased proliferation in the hippocampus and mPFC compared to nondependent rats and controls.
+BDNF	drug	alcohol	26659122	These results suggest a novel relationship between <strong>BDNF</strong> and progenitors in the hippocampus and mPFC, in which increased <b>ethanol</b> drinking may alter hippocampal and cortical function in <b>alcohol</b> dependent subjects by altering the cellular composition of newly born progenitors in the hippocampus and mPFC.
+BDNF	drug	cocaine	26598422	Increased expression after <b>cocaine</b> self administration was found for 6 IEGs in dorsal and ventral striatum (c fos, Mkp1, Fosb/ΔFosb, Egr2, Egr4, and Arc) and 10 IEGs in mPFC (same 6 IEGs as in striatum, plus <strong>Bdnf</strong>, Homer1, Sgk1 and Rgs2).
+BDNF	drug	opioid	26567727	Formation of aversive memories associated with conditioned drug withdrawal requires <strong>BDNF</strong> expression in the amygdala in acute <b>morphine</b> dependent rats.
+BDNF	addiction	aversion	26567727	Formation of <b>aversive</b> memories associated with conditioned drug withdrawal requires <strong>BDNF</strong> expression in the amygdala in acute morphine dependent rats.
+BDNF	addiction	withdrawal	26567727	Formation of aversive memories associated with conditioned drug <b>withdrawal</b> requires <strong>BDNF</strong> expression in the amygdala in acute morphine dependent rats.
+BDNF	drug	opioid	26567727	In the present study, we investigated the roles of <strong>BDNF</strong> in aversive memories associated with conditioned drug withdrawal in acute <b>morphine</b> dependent rats.
+BDNF	addiction	aversion	26567727	In the present study, we investigated the roles of <strong>BDNF</strong> in <b>aversive</b> memories associated with conditioned drug withdrawal in acute morphine dependent rats.
+BDNF	addiction	withdrawal	26567727	In the present study, we investigated the roles of <strong>BDNF</strong> in aversive memories associated with conditioned drug <b>withdrawal</b> in acute morphine dependent rats.
+BDNF	drug	opioid	26567727	In some rats, <strong>BDNF</strong> receptor antagonist K252a (8.5 ng per side) or <strong>BDNF</strong> scavenger TrkB FC (0.65 μg per side) was bilaterally microinjected into amygdala before <b>naloxone</b> injection.
+BDNF	drug	opioid	26567727	CPA behavior was induced in rats by the <b>naloxone</b> precipitated <b>morphine</b> withdrawal, which was accompanied by significantly increased levels of <strong>BDNF</strong> mRNA and protein in the amygdala.
+BDNF	addiction	withdrawal	26567727	CPA behavior was induced in rats by the naloxone precipitated morphine <b>withdrawal</b>, which was accompanied by significantly increased levels of <strong>BDNF</strong> mRNA and protein in the amygdala.
+BDNF	drug	opioid	26567727	Formation of aversive memories associated with conditioned drug withdrawal in acute <b>morphine</b> dependent rats requires <strong>BDNF</strong> expression in the amygdala.
+BDNF	addiction	aversion	26567727	Formation of <b>aversive</b> memories associated with conditioned drug withdrawal in acute morphine dependent rats requires <strong>BDNF</strong> expression in the amygdala.
+BDNF	addiction	withdrawal	26567727	Formation of aversive memories associated with conditioned drug <b>withdrawal</b> in acute morphine dependent rats requires <strong>BDNF</strong> expression in the amygdala.
+BDNF	drug	cocaine	26558777	Investigating the underlying mechanisms, we found that repeated <b>cocaine</b> injections enhanced the binding of BRD4, but not BRD3, to the promoter region of <strong>Bdnf</strong> in the NAc, whereas systemic injection of JQ1 attenuated <b>cocaine</b> induced expression of <strong>Bdnf</strong> in the NAc.
+BDNF	drug	cocaine	26538265	The Results showed that <b>cocaine</b> sensitization was associated with increased <strong>BDNF</strong>, ILK activity, phospho Akt Ser(473), p75(NTR), and TrkB protein levels in the mPFC and NAc core.
+BDNF	addiction	sensitization	26538265	The Results showed that cocaine <b>sensitization</b> was associated with increased <strong>BDNF</strong>, ILK activity, phospho Akt Ser(473), p75(NTR), and TrkB protein levels in the mPFC and NAc core.
+BDNF	drug	cocaine	26538265	Results suggested that the <strong>BDNF</strong> TrkA/p75(NTR) ILK Akt signaling pathway may be active in <b>cocaine</b> sensitization and associated neural plasticity in the mPFC and NAc core.
+BDNF	addiction	sensitization	26538265	Results suggested that the <strong>BDNF</strong> TrkA/p75(NTR) ILK Akt signaling pathway may be active in cocaine <b>sensitization</b> and associated neural plasticity in the mPFC and NAc core.
+BDNF	drug	alcohol	26518023	Effects of cigarette smoking and <b>alcohol</b> use on neurocognition and <strong>BDNF</strong> levels in a Chinese population.
+BDNF	drug	nicotine	26518023	Effects of cigarette <b>smoking</b> and alcohol use on neurocognition and <strong>BDNF</strong> levels in a Chinese population.
+BDNF	drug	alcohol	26518023	This is the first study to examine the neurocognitive consequences of cigarette smoking combined with chronic <b>alcohol</b> consumption and their relationship to serum <strong>BDNF</strong> levels in a Chinese Han population.
+BDNF	drug	nicotine	26518023	This is the first study to examine the neurocognitive consequences of cigarette <b>smoking</b> combined with chronic alcohol consumption and their relationship to serum <strong>BDNF</strong> levels in a Chinese Han population.
+BDNF	drug	nicotine	26518023	We did not find an association between <strong>BDNF</strong> and <b>smoking</b> or drinking status or between <strong>BDNF</strong> and cognitive performance.
+BDNF	drug	nicotine	26518023	In the <b>smoking</b> group, there was a significant correlation between <strong>BDNF</strong> and carbon monoxide concentration, and between <strong>BDNF</strong> and the Fagerstrom Test for <b>Nicotine</b> Dependence (FTND) total score.
+BDNF	addiction	dependence	26518023	In the smoking group, there was a significant correlation between <strong>BDNF</strong> and carbon monoxide concentration, and between <strong>BDNF</strong> and the Fagerstrom Test for Nicotine <b>Dependence</b> (FTND) total score.
+BDNF	drug	nicotine	26518023	Our results suggest that <b>smoking</b> is associated with cognitive decline, but not with <strong>BDNF</strong> levels in a normal population.
+BDNF	drug	nicotine	26518023	However, <b>smoking</b> severity is positively associated with <strong>BDNF</strong> levels.
+BDNF	drug	amphetamine	26506052	<strong>BDNF</strong> TrkB signaling in the nucleus accumbens shell of mice has key role in <b>methamphetamine</b> withdrawal symptoms.
+BDNF	addiction	withdrawal	26506052	<strong>BDNF</strong> TrkB signaling in the nucleus accumbens shell of mice has key role in methamphetamine <b>withdrawal</b> symptoms.
+BDNF	drug	amphetamine	26506052	In this study, we examined the role of <strong>BDNF</strong> TrkB signaling in different brain regions of male mice with <b>METH</b> withdrawal symptoms.
+BDNF	addiction	withdrawal	26506052	In this study, we examined the role of <strong>BDNF</strong> TrkB signaling in different brain regions of male mice with METH <b>withdrawal</b> symptoms.
+BDNF	drug	amphetamine	26506052	Western blot analysis showed that <strong>BDNF</strong> levels in the nucleus accumbens (NAc) of <b>METH</b> treated mice were significantly higher than those of control mice whereas <strong>BDNF</strong> levels in other regions, including the prefrontal cortex and hippocampus, were not altered.
+BDNF	drug	amphetamine	26506052	These findings suggest that increased <strong>BDNF</strong> TrkB signaling in the NAc shell has an important role in the behavioral abnormalities after withdrawal from repeated <b>METH</b> administration, and that TrkB antagonists are potential therapeutic drugs for withdrawal symptoms in <b>METH</b> abusers.
+BDNF	addiction	withdrawal	26506052	These findings suggest that increased <strong>BDNF</strong> TrkB signaling in the NAc shell has an important role in the behavioral abnormalities after <b>withdrawal</b> from repeated METH administration, and that TrkB antagonists are potential therapeutic drugs for <b>withdrawal</b> symptoms in METH abusers.
+BDNF	drug	cocaine	26482898	Cerebellar proBDNF and mature <strong>BDNF</strong> levels were both enhanced by <b>cocaine</b>.
+BDNF	drug	amphetamine	26453694	<strong>BDNF</strong> Deficient Mice Show Reduced Psychosis Related Behaviors Following Chronic <b>Methamphetamine</b>.
+BDNF	drug	amphetamine	26453694	<strong>Brain derived neurotrophic factor</strong> has been implicated in both psychosis and neuronal responses to <b>methamphetamine</b>.
+BDNF	drug	amphetamine	26453694	We therefore examined persistent psychosis like behavioral effects of <b>methamphetamine</b> in <strong>brain derived neurotrophic factor</strong> heterozygous mice.
+BDNF	drug	amphetamine	26453694	<b>Methamphetamine</b> treated wild type mice, but not <strong>brain derived neurotrophic factor</strong> heterozygous mice, showed locomotor sensitization to acute 3mg/kg D <b>amphetamine</b>.
+BDNF	addiction	sensitization	26453694	Methamphetamine treated wild type mice, but not <strong>brain derived neurotrophic factor</strong> heterozygous mice, showed locomotor <b>sensitization</b> to acute 3mg/kg D amphetamine.
+BDNF	drug	amphetamine	26453694	Qualitative analysis of exploration revealed tolerance to D <b>amphetamine</b> effects on entropy in <b>methamphetamine</b> treated <strong>brain derived neurotrophic factor</strong> heterozygous mice, but not wild type mice.
+BDNF	drug	amphetamine	26453694	Chronic <b>methamphetamine</b> exposure induces contrasting profiles of behavioral changes in wild type and <strong>brain derived neurotrophic factor</strong> heterozygous mice, with attenuation of behaviors relevant to psychosis in <b>methamphetamine</b> treated <strong>brain derived neurotrophic factor</strong> heterozygous mice.
+BDNF	drug	amphetamine	26453694	This suggests that <strong>brain derived neurotrophic factor</strong> signalling changes may contribute to development of psychosis in <b>methamphetamine</b> users.
+BDNF	drug	nicotine	28123805	<strong>BDNF</strong>/TRK/KCC2 pathway in <b>nicotine</b> withdrawal induced hyperalgesia.
+BDNF	addiction	withdrawal	28123805	<strong>BDNF</strong>/TRK/KCC2 pathway in nicotine <b>withdrawal</b> induced hyperalgesia.
+BDNF	drug	nicotine	28123805	To investigate the effect of brain derived neurotrophic factor (<strong>BDNF</strong>)/tropomyosin receptor kinase (Trk) on potassium chloride cotransporter 2 (KCC2) in rats following <b>nicotine</b> withdrawal and the roles played by <strong>BDNF</strong>/Trk/KCC2 pathway in <b>nicotine</b> withdrawal induced hyperalgesia.
+BDNF	addiction	withdrawal	28123805	To investigate the effect of brain derived neurotrophic factor (<strong>BDNF</strong>)/tropomyosin receptor kinase (Trk) on potassium chloride cotransporter 2 (KCC2) in rats following nicotine <b>withdrawal</b> and the roles played by <strong>BDNF</strong>/Trk/KCC2 pathway in nicotine <b>withdrawal</b> induced hyperalgesia.
+BDNF	drug	nicotine	28123805	To investigate the effect of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>)/tropomyosin receptor kinase (Trk) on potassium chloride cotransporter 2 (KCC2) in rats following <b>nicotine</b> withdrawal and the roles played by <strong>BDNF</strong>/Trk/KCC2 pathway in <b>nicotine</b> withdrawal induced hyperalgesia.
+BDNF	addiction	withdrawal	28123805	To investigate the effect of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>)/tropomyosin receptor kinase (Trk) on potassium chloride cotransporter 2 (KCC2) in rats following nicotine <b>withdrawal</b> and the roles played by <strong>BDNF</strong>/Trk/KCC2 pathway in nicotine <b>withdrawal</b> induced hyperalgesia.
+BDNF	drug	nicotine	28123805	<strong>BDNF</strong>/Trk signaling may contribute to <b>nicotine</b> withdrawal induced hyperalgesia via downregulation of KCC2.
+BDNF	addiction	withdrawal	28123805	<strong>BDNF</strong>/Trk signaling may contribute to nicotine <b>withdrawal</b> induced hyperalgesia via downregulation of KCC2.
+BDNF	drug	opioid	26437921	Contribution of <strong>BDNF</strong> and DRD2 genetic polymorphisms to continued <b>opioid</b> use in patients receiving <b>methadone</b> treatment for <b>opioid</b> use disorder: an observational study.
+BDNF	drug	opioid	26437921	The aim of this study was to investigate the effect of brain derived neurotrophic factor (<strong>BDNF</strong>) and dopamine receptor D2 (DRD2) polymorphisms on continued <b>opioid</b> use among patients on <b>methadone</b> treatment for <b>opioid</b> use disorder.
+BDNF	drug	opioid	26437921	The aim of this study was to investigate the effect of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and dopamine receptor D2 (DRD2) polymorphisms on continued <b>opioid</b> use among patients on <b>methadone</b> treatment for <b>opioid</b> use disorder.
+BDNF	drug	opioid	26437921	<strong>BDNF</strong> 196G>A (rs6265) and DRD2 241A>G (rs1799978) genetic variants were examined in patients with <b>opioid</b> use disorder who were recruited from <b>methadone</b> treatment clinics across Southern Ontario, Canada.
+BDNF	drug	opioid	26437921	Despite an association of <strong>BDNF</strong> rs6265 and DRD2 rs1799978 with addictive behaviors, these variants were not associated with continued illicit <b>opioid</b> use in patients treated with <b>methadone</b>.
+BDNF	addiction	addiction	26437921	Despite an association of <strong>BDNF</strong> rs6265 and DRD2 rs1799978 with <b>addictive</b> behaviors, these variants were not associated with continued illicit opioid use in patients treated with methadone.
+BDNF	drug	alcohol	26405456	The relationship between <strong>brain derived neurotrophic factor</strong> and cognitive functions in <b>alcohol</b> dependent patients: a preliminary study.
+BDNF	drug	alcohol	26405456	The purpose of this study was to investigate the relationship between cognitive functions and <strong>BDNF</strong> in <b>alcohol</b> dependent patients.
+BDNF	drug	alcohol	26405456	<strong>BDNF</strong> might play an important role in the detection of neurocognitive function among individuals with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	26405456	<strong>BDNF</strong> might play an important role in the detection of neurocognitive function among individuals with alcohol <b>dependence</b>.
+BDNF	drug	alcohol	26404404	Do changes in the <strong>BDNF</strong> promoter methylation indicate the risk of <b>alcohol</b> relapse?
+BDNF	addiction	relapse	26404404	Do changes in the <strong>BDNF</strong> promoter methylation indicate the risk of alcohol <b>relapse</b>?
+BDNF	drug	alcohol	26404404	The neurotrophic growth factor brain derived neurotrophic factor (<strong>BDNF</strong>) was linked to the risk of <b>alcohol</b> relapse in clinical studies.
+BDNF	addiction	relapse	26404404	The neurotrophic growth factor brain derived neurotrophic factor (<strong>BDNF</strong>) was linked to the risk of alcohol <b>relapse</b> in clinical studies.
+BDNF	drug	alcohol	26404404	The neurotrophic growth factor <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) was linked to the risk of <b>alcohol</b> relapse in clinical studies.
+BDNF	addiction	relapse	26404404	The neurotrophic growth factor <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) was linked to the risk of alcohol <b>relapse</b> in clinical studies.
+BDNF	drug	alcohol	26404404	In this study we investigated alterations in the methylation of the <strong>BDNF</strong> gene during <b>alcohol</b> withdrawal (day 1, 7 and 14) in 99 male <b>alcohol</b> dependent patients compared to age matched healthy males (n=33).
+BDNF	addiction	withdrawal	26404404	In this study we investigated alterations in the methylation of the <strong>BDNF</strong> gene during alcohol <b>withdrawal</b> (day 1, 7 and 14) in 99 male alcohol dependent patients compared to age matched healthy males (n=33).
+BDNF	drug	alcohol	26404404	In particular, we aimed to investigate a possible association between the <strong>BDNF</strong> promoter methylation and the self reported duration of <b>alcohol</b> abstinence before relapse.
+BDNF	addiction	relapse	26404404	In particular, we aimed to investigate a possible association between the <strong>BDNF</strong> promoter methylation and the self reported duration of alcohol abstinence before <b>relapse</b>.
+BDNF	drug	alcohol	26404404	Mean methylation of the <strong>BDNF</strong> promoter was significantly increased in <b>alcohol</b> dependent patients compared to the healthy controls (F=10.014, p<0.001) and decreased significantly during <b>alcohol</b> withdrawal (F=10.014, p<0.001).
+BDNF	addiction	withdrawal	26404404	Mean methylation of the <strong>BDNF</strong> promoter was significantly increased in alcohol dependent patients compared to the healthy controls (F=10.014, p<0.001) and decreased significantly during alcohol <b>withdrawal</b> (F=10.014, p<0.001).
+BDNF	drug	alcohol	26404404	Our results suggest an association between <strong>BDNF</strong> expression and the symptomatology of <b>alcohol</b> withdrawal and imply that changes in the methylation of the <strong>BDNF</strong> IV gene may contribute to <b>alcohol</b> consumption.
+BDNF	addiction	withdrawal	26404404	Our results suggest an association between <strong>BDNF</strong> expression and the symptomatology of alcohol <b>withdrawal</b> and imply that changes in the methylation of the <strong>BDNF</strong> IV gene may contribute to alcohol consumption.
+BDNF	drug	amphetamine	26401760	<strong>BDNF</strong> (Val66Met) genetic polymorphism is associated with vulnerability for <b>methamphetamine</b> dependence.
+BDNF	addiction	dependence	26401760	<strong>BDNF</strong> (Val66Met) genetic polymorphism is associated with vulnerability for methamphetamine <b>dependence</b>.
+BDNF	drug	amphetamine	26401760	Association of the brain derived neurotrophic factor (<strong>BDNF</strong>) genetic polymorphism rs6265 (Val66Met) with <b>methamphetamine</b> (<b>METH</b>) dependence and <b>METH</b> induced psychosis was investigated in the Thai population.
+BDNF	addiction	dependence	26401760	Association of the brain derived neurotrophic factor (<strong>BDNF</strong>) genetic polymorphism rs6265 (Val66Met) with methamphetamine (METH) <b>dependence</b> and METH induced psychosis was investigated in the Thai population.
+BDNF	drug	amphetamine	26401760	Association of the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) genetic polymorphism rs6265 (Val66Met) with <b>methamphetamine</b> (<b>METH</b>) dependence and <b>METH</b> induced psychosis was investigated in the Thai population.
+BDNF	addiction	dependence	26401760	Association of the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) genetic polymorphism rs6265 (Val66Met) with methamphetamine (METH) <b>dependence</b> and METH induced psychosis was investigated in the Thai population.
+BDNF	drug	alcohol	26361715	Effects of acute <b>ethanol</b> exposure on class I HDACs family enzymes in wild type and <strong>BDNF</strong>(+/ ) mice.
+BDNF	drug	alcohol	26361715	Alterations of brain derived neurotrophic factor (<strong>BDNF</strong>) have been associated with the development of addiction to different drugs of abuse, including <b>ethanol</b> (EtOH).
+BDNF	addiction	addiction	26361715	Alterations of brain derived neurotrophic factor (<strong>BDNF</strong>) have been associated with the development of <b>addiction</b> to different drugs of abuse, including ethanol (EtOH).
+BDNF	drug	alcohol	26361715	Alterations of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) have been associated with the development of addiction to different drugs of abuse, including <b>ethanol</b> (EtOH).
+BDNF	addiction	addiction	26361715	Alterations of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) have been associated with the development of <b>addiction</b> to different drugs of abuse, including ethanol (EtOH).
+BDNF	addiction	addiction	26361715	We investigated the effects induced by acute EtOH exposure on the protein levels of class I HDAC 1 3 isoforms of wild type (WT) and <strong>BDNF</strong> heterozygous mice (<strong>BDNF</strong>(+/ )), in nuclear and cytoplasmic extracts of specific brain regions associated with EtOH <b>addiction</b>.
+BDNF	drug	opioid	26346883	Expression of <strong>BDNF</strong> and TrkB Phosphorylation in the Rat Frontal Cortex During <b>Morphine</b> Withdrawal are NO Dependent.
+BDNF	addiction	withdrawal	26346883	Expression of <strong>BDNF</strong> and TrkB Phosphorylation in the Rat Frontal Cortex During Morphine <b>Withdrawal</b> are NO Dependent.
+BDNF	drug	opioid	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of <b>morphine</b> dependence on the expression of brain derived neurotrophic factor (<strong>BDNF</strong>), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous <b>morphine</b> withdrawal in dependent animals.
+BDNF	addiction	dependence	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine <b>dependence</b> on the expression of brain derived neurotrophic factor (<strong>BDNF</strong>), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine withdrawal in dependent animals.
+BDNF	addiction	withdrawal	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine dependence on the expression of brain derived neurotrophic factor (<strong>BDNF</strong>), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine <b>withdrawal</b> in dependent animals.
+BDNF	drug	opioid	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of <b>morphine</b> dependence on the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous <b>morphine</b> withdrawal in dependent animals.
+BDNF	addiction	dependence	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine <b>dependence</b> on the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine withdrawal in dependent animals.
+BDNF	addiction	withdrawal	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine dependence on the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine <b>withdrawal</b> in dependent animals.
+BDNF	drug	opioid	26346883	The expression of the <strong>BDNF</strong>, GDNF, NGF, IGF1, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after <b>morphine</b> withdrawal.
+BDNF	addiction	withdrawal	26346883	The expression of the <strong>BDNF</strong>, GDNF, NGF, IGF1, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after morphine <b>withdrawal</b>.
+BDNF	drug	opioid	26346883	<b>Morphine</b> withdrawal was accompanied by upregulation of <strong>BDNF</strong>, IGF1, and their receptors TrkB and IGF1R, respectively, on the mRNA level in the frontal cortex, and only <strong>BDNF</strong> in hippocampus and midbrain.
+BDNF	addiction	withdrawal	26346883	Morphine <b>withdrawal</b> was accompanied by upregulation of <strong>BDNF</strong>, IGF1, and their receptors TrkB and IGF1R, respectively, on the mRNA level in the frontal cortex, and only <strong>BDNF</strong> in hippocampus and midbrain.
+BDNF	addiction	dependence	26346883	Thus, NO signaling during induction of <b>dependence</b> may be involved in the mechanisms of <strong>BDNF</strong> expression and processing at abstinence, thereby affecting signaling through TrkB in the frontal cortex.
+BDNF	drug	opioid	26343470	Serum <strong>brain derived neurotrophic factor</strong> levels and psychotic symptoms in <b>heroin</b> dependence.
+BDNF	addiction	dependence	26343470	Serum <strong>brain derived neurotrophic factor</strong> levels and psychotic symptoms in heroin <b>dependence</b>.
+BDNF	drug	opioid	26343470	Low serum brain derived neurotrophic factor (<strong>BDNF</strong>) levels have been reported in schizophrenia and psychosis; however, studies assessing the relationship between serum <strong>BDNF</strong> levels and psychotic symptoms in <b>heroin</b> dependence are lacking.
+BDNF	addiction	dependence	26343470	Low serum brain derived neurotrophic factor (<strong>BDNF</strong>) levels have been reported in schizophrenia and psychosis; however, studies assessing the relationship between serum <strong>BDNF</strong> levels and psychotic symptoms in heroin <b>dependence</b> are lacking.
+BDNF	drug	opioid	26343470	Low serum <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels have been reported in schizophrenia and psychosis; however, studies assessing the relationship between serum <strong>BDNF</strong> levels and psychotic symptoms in <b>heroin</b> dependence are lacking.
+BDNF	addiction	dependence	26343470	Low serum <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels have been reported in schizophrenia and psychosis; however, studies assessing the relationship between serum <strong>BDNF</strong> levels and psychotic symptoms in heroin <b>dependence</b> are lacking.
+BDNF	drug	opioid	26343470	<strong>BDNF</strong> levels were not found to be correlated with sex, age, age of onset, duration of <b>heroin</b> use, average daily dose of <b>heroin</b> use, frequency of <b>heroin</b> use, SDS scores, BAI scores and BDI scores in the psychotic subsamples (all P>0.05).
+BDNF	drug	amphetamine	26334786	<b>Methamphetamine</b> blocks exercise effects on <strong>Bdnf</strong> and Drd2 gene expression in frontal cortex and striatum.
+BDNF	addiction	relapse	26334786	Additionally, <strong>Bdnf</strong> in the striatum has been shown to play a role in flexible reward <b>seeking</b> behavior.
+BDNF	addiction	reward	26334786	Additionally, <strong>Bdnf</strong> in the striatum has been shown to play a role in flexible <b>reward</b> seeking behavior.
+BDNF	drug	amphetamine	26334786	Given that voluntary aerobic exercise can affect the expression of these proteins in healthy subjects, and that exercise has shown promise as an anti addictive therapy, we set out to quantify changes in D2 and <strong>Bdnf</strong> expression in <b>methamphetamine</b> exposed rats given access to running wheels.
+BDNF	addiction	addiction	26334786	Given that voluntary aerobic exercise can affect the expression of these proteins in healthy subjects, and that exercise has shown promise as an anti <b>addictive</b> therapy, we set out to quantify changes in D2 and <strong>Bdnf</strong> expression in methamphetamine exposed rats given access to running wheels.
+BDNF	drug	amphetamine	26334786	Drd2 and <strong>Bdnf</strong> mRNA levels were impacted independently by exercise and <b>methamphetamine</b>, but exposure to <b>methamphetamine</b> prior to the initiation of exercise blocked the exercise induced changes seen in rats treated with saline.
+BDNF	drug	amphetamine	26280836	The Effects of <strong>BDNF</strong> Val66Met Gene Polymorphism on Serum <strong>BDNF</strong> and Cognitive Function in <b>Methamphetamine</b> Dependent Patients and Normal Controls: A Case Control Study.
+BDNF	drug	amphetamine	26280836	Studies suggest that a functional polymorphism of the brain derived neurotrophic factor gene (<strong>BDNF</strong> Val66Met) may contribute to <b>methamphetamine</b> dependence.
+BDNF	addiction	dependence	26280836	Studies suggest that a functional polymorphism of the brain derived neurotrophic factor gene (<strong>BDNF</strong> Val66Met) may contribute to methamphetamine <b>dependence</b>.
+BDNF	drug	amphetamine	26280836	Studies suggest that a functional polymorphism of the <strong>brain derived neurotrophic factor</strong> gene (<strong>BDNF</strong> Val66Met) may contribute to <b>methamphetamine</b> dependence.
+BDNF	addiction	dependence	26280836	Studies suggest that a functional polymorphism of the <strong>brain derived neurotrophic factor</strong> gene (<strong>BDNF</strong> Val66Met) may contribute to methamphetamine <b>dependence</b>.
+BDNF	drug	amphetamine	26280836	We hypothesized that this polymorphism had a role in cognitive deficits in <b>methamphetamine</b> dependent patients and in the relationship of serum <strong>BDNF</strong> with cognitive impairments.
+BDNF	drug	amphetamine	26280836	We conducted a case control study by assessing 194 <b>methamphetamine</b> dependent patients and 378 healthy volunteers without history of drug use on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) and the presence of the <strong>BDNF</strong> Val66Met polymorphism and serum <strong>BDNF</strong> levels.
+BDNF	drug	amphetamine	26280836	The serum <strong>BDNF</strong> levels in <b>methamphetamine</b> dependent patients were significantly higher than those of the healthy controls.
+BDNF	drug	amphetamine	26280836	We demonstrated significant impairment on some aspects of cognitive function and increased <strong>BDNF</strong> levels in <b>methamphetamine</b> dependent patients as well as genotypic differences in the relationships between <strong>BDNF</strong> levels and RBANS scores on the <strong>BDNF</strong> Val66Met polymorphism only in these patients.
+BDNF	drug	alcohol	26228024	<b>Alcohol</b> enhances the psychostimulant and conditioning effects of mephedrone in adolescent mice; postulation of unique roles of D3 receptors and <strong>BDNF</strong> in place preference acquisition.
+BDNF	addiction	reward	26228024	The D3 receptor antagonist SB 277011A and the <strong>BDNF</strong> receptor antagonist ANA 12 completely prevented <b>CPP</b> as well as the increases in Drd3 in all groups.
+BDNF	addiction	reward	26228024	D3 receptors and <strong>BDNF</strong> play a key role in the establishment of <b>CPP</b> by mephedrone, although an accompanying increase in other synaptic plasticity related genes may also be necessary.
+BDNF	drug	alcohol	26204799	The <strong>BDNF</strong> Valine 68 to Methionine Polymorphism Increases Compulsive <b>Alcohol</b> Drinking in Mice That Is Reversed by Tropomyosin Receptor Kinase B Activation.
+BDNF	addiction	addiction	26204799	The <strong>BDNF</strong> Valine 68 to Methionine Polymorphism Increases <b>Compulsive</b> Alcohol Drinking in Mice That Is Reversed by Tropomyosin Receptor Kinase B Activation.
+BDNF	drug	alcohol	26204799	Our findings suggest that carrying this <strong>BDNF</strong> allele increases the risk of developing uncontrolled and excessive <b>alcohol</b> drinking that can be reversed by directly activating the <strong>BDNF</strong> receptor, tropomyosin receptor kinase B.
+BDNF	drug	alcohol	26204172	Association study between reward dependence and a functional <strong>BDNF</strong> polymorphism in adult women offspring of <b>alcohol</b> dependent probands.
+BDNF	addiction	dependence	26204172	Association study between reward <b>dependence</b> and a functional <strong>BDNF</strong> polymorphism in adult women offspring of alcohol dependent probands.
+BDNF	addiction	reward	26204172	Association study between <b>reward</b> dependence and a functional <strong>BDNF</strong> polymorphism in adult women offspring of alcohol dependent probands.
+BDNF	drug	alcohol	26204172	Thirty five healthy adult women offspring of <b>alcohol</b> dependent probands (AWOA) were compared with 63 healthy controls to test whether personality dimensions on the Temperament and Character Inventory questionnaire were associated with the <strong>brain derived neurotrophic factor</strong> Val66Met polymorphism in offspring.
+BDNF	addiction	dependence	26204172	The <strong>brain derived neurotrophic factor</strong> Val66Met polymorphism may be involved in this difference as the lower reward <b>dependence</b> score was found only in AWOA carrying the Val allele.
+BDNF	addiction	reward	26204172	The <strong>brain derived neurotrophic factor</strong> Val66Met polymorphism may be involved in this difference as the lower <b>reward</b> dependence score was found only in AWOA carrying the Val allele.
+BDNF	drug	opioid	26202104	<b>Opioid</b> induced microglial activation resulted in an increase in brain derived neurotrophic factor (<strong>BDNF</strong>) expression and a reduction in the expression and function of the K(+)Cl( ) co transporter KCC2 within VTA GABAergic neurons.
+BDNF	drug	opioid	26202104	<b>Opioid</b> induced microglial activation resulted in an increase in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression and a reduction in the expression and function of the K(+)Cl( ) co transporter KCC2 within VTA GABAergic neurons.
+BDNF	drug	cocaine	26202104	Inhibition of microglial activation or interfering with <strong>BDNF</strong> signaling prevented the loss of Cl( ) extrusion capacity and restored the rewarding effects of <b>cocaine</b> in opioid dependent animals.
+BDNF	drug	opioid	26202104	Inhibition of microglial activation or interfering with <strong>BDNF</strong> signaling prevented the loss of Cl( ) extrusion capacity and restored the rewarding effects of cocaine in <b>opioid</b> dependent animals.
+BDNF	drug	cocaine	26202104	Consistent with a microglial derived <strong>BDNF</strong> induced disruption of reward, intra VTA injection of <strong>BDNF</strong> or a KCC2 inhibitor resulted in a loss of <b>cocaine</b> induced place preference in opioid naïve animals.
+BDNF	drug	opioid	26202104	Consistent with a microglial derived <strong>BDNF</strong> induced disruption of reward, intra VTA injection of <strong>BDNF</strong> or a KCC2 inhibitor resulted in a loss of cocaine induced place preference in <b>opioid</b> naïve animals.
+BDNF	addiction	reward	26202104	Consistent with a microglial derived <strong>BDNF</strong> induced disruption of <b>reward</b>, intra VTA injection of <strong>BDNF</strong> or a KCC2 inhibitor resulted in a loss of cocaine induced place preference in opioid naïve animals.
+BDNF	drug	opioid	26202104	This study directly implicates microglial derived <strong>BDNF</strong> as a negative regulator of reward in <b>opioid</b> dependent states, identifying new therapeutic targets for opiate addictive behaviors.
+BDNF	addiction	addiction	26202104	This study directly implicates microglial derived <strong>BDNF</strong> as a negative regulator of reward in opioid dependent states, identifying new therapeutic targets for opiate <b>addictive</b> behaviors.
+BDNF	addiction	reward	26202104	This study directly implicates microglial derived <strong>BDNF</strong> as a negative regulator of <b>reward</b> in opioid dependent states, identifying new therapeutic targets for opiate addictive behaviors.
+BDNF	drug	amphetamine	26188494	Cross Generational trans Fat Consumption Favors Self Administration of <b>Amphetamine</b> and Changes Molecular Expressions of <strong>BDNF</strong>, DAT, and D1/D2 Receptors in the Cortex and Hippocampus of Rats.
+BDNF	addiction	reward	26041913	Treatment with minocycline or interfering with <strong>BDNF</strong> signaling restored chloride transport within these neurons and recovered DA dependent <b>reward</b> behavior.
+BDNF	drug	cocaine	26022436	<strong>Brain Derived Neurotrophic Factor</strong> and Delayed Verbal Recall in Crack/<b>Cocaine</b> Dependents.
+BDNF	drug	cocaine	26022436	Considering the role of brain derived neurotrophic factor (<strong>BDNF</strong>) in memory processes and its peripheral response during the detoxification of <b>cocaine</b>, the aim of this study was to investigate whether plasma <strong>BDNF</strong> levels could be related to memory performance in women with crack/<b>cocaine</b> dependence.
+BDNF	addiction	dependence	26022436	Considering the role of brain derived neurotrophic factor (<strong>BDNF</strong>) in memory processes and its peripheral response during the detoxification of cocaine, the aim of this study was to investigate whether plasma <strong>BDNF</strong> levels could be related to memory performance in women with crack/cocaine <b>dependence</b>.
+BDNF	drug	cocaine	26022436	Considering the role of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in memory processes and its peripheral response during the detoxification of <b>cocaine</b>, the aim of this study was to investigate whether plasma <strong>BDNF</strong> levels could be related to memory performance in women with crack/<b>cocaine</b> dependence.
+BDNF	addiction	dependence	26022436	Considering the role of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in memory processes and its peripheral response during the detoxification of cocaine, the aim of this study was to investigate whether plasma <strong>BDNF</strong> levels could be related to memory performance in women with crack/cocaine <b>dependence</b>.
+BDNF	drug	amphetamine	26019338	Incubation of <b>methamphetamine</b> craving is associated with selective increases in expression of <strong>Bdnf</strong> and trkb, glutamate receptors, and epigenetic enzymes in cue activated fos expressing dorsal striatal neurons.
+BDNF	addiction	relapse	26019338	Incubation of methamphetamine <b>craving</b> is associated with selective increases in expression of <strong>Bdnf</strong> and trkb, glutamate receptors, and epigenetic enzymes in cue activated fos expressing dorsal striatal neurons.
+BDNF	drug	alcohol	26013579	Protracted <b>alcohol</b> abstinence induces analgesia in rats: Possible relationships with <strong>BDNF</strong> and interleukin 10.
+BDNF	drug	alcohol	26013579	Exposure to <b>ethanol</b> alters the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in central regions such as, the hippocampus, cortex and striatum.
+BDNF	drug	alcohol	26013579	Exposure to <b>ethanol</b> alters the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in central regions such as, the hippocampus, cortex and striatum.
+BDNF	drug	alcohol	26013579	In addition, we evaluated <strong>BDNF</strong> and interleukin 10 (IL 10) in the cerebral prefrontal cortex, brainstem and hippocampus of rats after protracted <b>alcohol</b> abstinence.
+BDNF	drug	alcohol	26013579	There was a significant increase in the prefrontal cortex <strong>BDNF</strong> levels in the <b>alcohol</b> group in relation to the water group, after 11days of <b>alcohol</b> abstinence.
+BDNF	drug	opioid	25988842	Alterations of the corticotropin releasing factor (CRF), glucocorticoid receptor (NR3C1), tyrosine hydroxylase (TH), mu <b>opioid</b> receptor (MOr), brain derived neurotrophic factor (<strong>BDNF</strong>), neuronal nuclei (NeuN), microtubule associated protein 2 (MAP2) and neurofilament heavy (NF200) immunoreactive fibers were studied in the paraventricular nucleus of the hypothalamus (PVN), ventral tegmental area (VTA), nucleus accumbens (NAc) or hippocampus (HIP).
+BDNF	drug	opioid	25988842	Alterations of the corticotropin releasing factor (CRF), glucocorticoid receptor (NR3C1), tyrosine hydroxylase (TH), mu <b>opioid</b> receptor (MOr), <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), neuronal nuclei (NeuN), microtubule associated protein 2 (MAP2) and neurofilament heavy (NF200) immunoreactive fibers were studied in the paraventricular nucleus of the hypothalamus (PVN), ventral tegmental area (VTA), nucleus accumbens (NAc) or hippocampus (HIP).
+BDNF	drug	amphetamine	25986696	D <b>Amphetamine</b> withdrawal induced decreases in <strong>brain derived neurotrophic factor</strong> in sprague dawley rats are reversed by treatment with ketamine.
+BDNF	drug	psychedelics	25986696	D Amphetamine withdrawal induced decreases in <strong>brain derived neurotrophic factor</strong> in sprague dawley rats are reversed by treatment with <b>ketamine</b>.
+BDNF	addiction	withdrawal	25986696	D Amphetamine <b>withdrawal</b> induced decreases in <strong>brain derived neurotrophic factor</strong> in sprague dawley rats are reversed by treatment with ketamine.
+BDNF	drug	psychedelics	25986696	Diminished levels of brain derived neurotrophic factor (<strong>BDNF</strong>), particularly in the hippocampus has been observed after exposure to stress, and recent data indicate that treatment with the N methyl D aspartate (NMDA) receptor antagonist, <b>ketamine</b> may reverse these changes.
+BDNF	drug	psychedelics	25986696	Diminished levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), particularly in the hippocampus has been observed after exposure to stress, and recent data indicate that treatment with the N methyl D aspartate (NMDA) receptor antagonist, <b>ketamine</b> may reverse these changes.
+BDNF	drug	amphetamine	25986696	However, it is unclear whether <strong>BDNF</strong> levels in the hippocampus or other regions of the limbic system are altered following the stress of D <b>AMPH</b> withdrawal and it is not currently known if treatment with ketamine has any effect on these changes.
+BDNF	drug	psychedelics	25986696	However, it is unclear whether <strong>BDNF</strong> levels in the hippocampus or other regions of the limbic system are altered following the stress of D AMPH withdrawal and it is not currently known if treatment with <b>ketamine</b> has any effect on these changes.
+BDNF	addiction	withdrawal	25986696	However, it is unclear whether <strong>BDNF</strong> levels in the hippocampus or other regions of the limbic system are altered following the stress of D AMPH <b>withdrawal</b> and it is not currently known if treatment with ketamine has any effect on these changes.
+BDNF	drug	amphetamine	25986696	The goals of this study were to examine <strong>BDNF</strong> levels throughout the limbic system following D <b>AMPH</b> withdrawal and determine whether ketamine treatment would alter D <b>AMPH</b> induced changes in <strong>BDNF</strong>.
+BDNF	drug	psychedelics	25986696	The goals of this study were to examine <strong>BDNF</strong> levels throughout the limbic system following D AMPH withdrawal and determine whether <b>ketamine</b> treatment would alter D AMPH induced changes in <strong>BDNF</strong>.
+BDNF	addiction	withdrawal	25986696	The goals of this study were to examine <strong>BDNF</strong> levels throughout the limbic system following D AMPH <b>withdrawal</b> and determine whether ketamine treatment would alter D AMPH induced changes in <strong>BDNF</strong>.
+BDNF	drug	amphetamine	25986696	Sprague Dawley rats were treated with D <b>AMPH</b> and <strong>BDNF</strong> protein examined in the prefrontal cortex, nucleus accumbens, amygdala and hippocampus at 24 h and 4 days of withdrawal.
+BDNF	addiction	withdrawal	25986696	Sprague Dawley rats were treated with D AMPH and <strong>BDNF</strong> protein examined in the prefrontal cortex, nucleus accumbens, amygdala and hippocampus at 24 h and 4 days of <b>withdrawal</b>.
+BDNF	drug	amphetamine	25986696	Our data show that at 24 h post D <b>AMPH</b>, <strong>BDNF</strong> levels were increased in the nucleus accumbens and decreased in the hippocampus.
+BDNF	drug	amphetamine	25986696	At 4 d post D <b>AMPH</b>, <strong>BDNF</strong> protein levels were decreased in all areas examined, and these decreases were reversed by treatment with ketamine.
+BDNF	drug	psychedelics	25986696	At 4 d post D AMPH, <strong>BDNF</strong> protein levels were decreased in all areas examined, and these decreases were reversed by treatment with <b>ketamine</b>.
+BDNF	drug	amphetamine	25986696	These data suggest that diminished <strong>BDNF</strong> may contribute to the negative affect seen following D <b>AMPH</b> withdrawal, and that ketamine treatment could offer relief from these symptoms.
+BDNF	drug	psychedelics	25986696	These data suggest that diminished <strong>BDNF</strong> may contribute to the negative affect seen following D AMPH withdrawal, and that <b>ketamine</b> treatment could offer relief from these symptoms.
+BDNF	addiction	withdrawal	25986696	These data suggest that diminished <strong>BDNF</strong> may contribute to the negative affect seen following D AMPH <b>withdrawal</b>, and that ketamine treatment could offer relief from these symptoms.
+BDNF	drug	alcohol	25940002	Paternal <b>alcohol</b> exposure in mice alters brain NGF and <strong>BDNF</strong> and increases <b>ethanol</b> elicited preference in male offspring.
+BDNF	drug	alcohol	25940002	DAT was affected in the olfactory lobes in PAE animals treated with 0.5 g/kg of <b>ethanol</b> while no differences were found on D1/D2 receptors and for pro NGF or pro <strong>BDNF</strong>.
+BDNF	drug	alcohol	25940002	In conclusion, this study shows that: PAE affects NGF and <strong>BDNF</strong> expression in the mouse brain; PAE may induce <b>ethanol</b> intake preference in the male offspring.
+BDNF	drug	alcohol	25939814	CREB <strong>BDNF</strong> pathway influences <b>alcohol</b> cue elicited activation in drinkers.
+BDNF	drug	alcohol	25939814	The genetic component derived from the cAMP response element binding protein and  brain derived neurotrophic factor (CREB <strong>BDNF</strong>) pathway reference was significantly associated (r =  0.38, P = 3.98 × 10( 12)) with an imaging component reflecting hyperactivation in precuneus, superior parietal lobule, and posterior cingulate for drinkers with more severe <b>alcohol</b> dependence symptoms.
+BDNF	addiction	dependence	25939814	The genetic component derived from the cAMP response element binding protein and  brain derived neurotrophic factor (CREB <strong>BDNF</strong>) pathway reference was significantly associated (r =  0.38, P = 3.98 × 10( 12)) with an imaging component reflecting hyperactivation in precuneus, superior parietal lobule, and posterior cingulate for drinkers with more severe alcohol <b>dependence</b> symptoms.
+BDNF	drug	alcohol	25939814	The genetic component derived from the cAMP response element binding protein and  <strong>brain derived neurotrophic factor</strong> (CREB <strong>BDNF</strong>) pathway reference was significantly associated (r =  0.38, P = 3.98 × 10( 12)) with an imaging component reflecting hyperactivation in precuneus, superior parietal lobule, and posterior cingulate for drinkers with more severe <b>alcohol</b> dependence symptoms.
+BDNF	addiction	dependence	25939814	The genetic component derived from the cAMP response element binding protein and  <strong>brain derived neurotrophic factor</strong> (CREB <strong>BDNF</strong>) pathway reference was significantly associated (r =  0.38, P = 3.98 × 10( 12)) with an imaging component reflecting hyperactivation in precuneus, superior parietal lobule, and posterior cingulate for drinkers with more severe alcohol <b>dependence</b> symptoms.
+BDNF	drug	alcohol	25881894	In the <b>ethanol</b> treated cerebellar granule neurons we find an increased expression of genes related to apoptosis (Mapk8 and Bax), but also of genes previously described as neuroprotective (Dhcr24 and <strong>Bdnf</strong>), which might suggest an actively maintained viability.
+BDNF	drug	opioid	25881704	Expression levels of H3K14 acetylation and brain derived neurotrophic factor (<strong>BDNF</strong>) in BLA were evaluated by Western blotting.The results showed that CPP could be established by intraperitoneal injection of <b>morphine</b>.
+BDNF	addiction	reward	25881704	Expression levels of H3K14 acetylation and brain derived neurotrophic factor (<strong>BDNF</strong>) in BLA were evaluated by Western blotting.The results showed that <b>CPP</b> could be established by intraperitoneal injection of morphine.
+BDNF	drug	opioid	25881704	Expression levels of H3K14 acetylation and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in BLA were evaluated by Western blotting.The results showed that CPP could be established by intraperitoneal injection of <b>morphine</b>.
+BDNF	addiction	reward	25881704	Expression levels of H3K14 acetylation and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in BLA were evaluated by Western blotting.The results showed that <b>CPP</b> could be established by intraperitoneal injection of morphine.
+BDNF	drug	opioid	25881704	Compared with control groups, a stronger place preference was established and expression of H3K14 acetylation and <strong>BDNF</strong> was significantly increased in the group treated with TSA and <b>morphine</b>.
+BDNF	drug	opioid	25881704	Inhibition of the activity of histone deacetylases in BLA can promote the formation of cue associated memory induced by <b>morphine</b> and the involvement of <strong>BDNF</strong> in BLA maybe was regulated by histone acetylation.
+BDNF	drug	alcohol	25873205	Serum <strong>brain derived neurotrophic factor</strong> levels in relation to comorbid depression and cytokine levels in Nepalese men with <b>alcohol</b> use disorders.
+BDNF	addiction	intoxication	25873205	Although serum <strong>BDNF</strong> levels were unrelated to MD history, patients with recent depressive symptoms (n=42) had lower (mean±SD) <strong>BDNF</strong> serum levels compared to those without (n=110) (21.6±8.1 ng/mL vs. 26.0±9.6 ng/mL; p=0.010), and patients with higher AUD severity and <b>binge</b> drinking patterns had higher mean serum <strong>BDNF</strong> levels compared to lower AUD severity and non binging (25.9±9.7 ng/mL vs. 22.1±8.7 ng/mL; p=0.022 and 25.7±9.3 vs. 21.8±9.7 ng/mL; p=0.029, respectively).
+BDNF	drug	alcohol	25873205	These findings show that in <b>alcohol</b> using populations, peripheral <strong>BDNF</strong> levels are related to severity of AUD as well as presence of depressive symptoms.
+BDNF	drug	alcohol	25814047	AIE also induced anxiety like behaviors and enhanced <b>ethanol</b> intake in adulthood, which was attenuated by TSA treatment via normalization of deficits in histone H3 acetylation of <strong>BDNF</strong> and Arc genes.
+BDNF	drug	alcohol	25801118	Corticostriatal <strong>BDNF</strong> and <b>alcohol</b> addiction.
+BDNF	addiction	addiction	25801118	Corticostriatal <strong>BDNF</strong> and alcohol <b>addiction</b>.
+BDNF	drug	alcohol	25801118	This review details the intricate interaction between the Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) and <b>alcohol</b>, and provides evidence to suggest that corticostriatal <strong>BDNF</strong> signaling acts to keep <b>alcohol</b> drinking in moderation.
+BDNF	drug	alcohol	25801118	This review details the intricate interaction between the <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) and <b>alcohol</b>, and provides evidence to suggest that corticostriatal <strong>BDNF</strong> signaling acts to keep <b>alcohol</b> drinking in moderation.
+BDNF	drug	alcohol	25801118	Specifically, we describe studies in rodent models suggesting that moderate consumption of <b>alcohol</b> increases <strong>BDNF</strong> levels in the dorsal striatum, which in turn act to suppress <b>alcohol</b> intake by activating a Mitogen Activated Protein Kinase (MAPK) dependent genomic mechanism.
+BDNF	drug	alcohol	25801118	We further provide data to suggest that <b>alcohol</b> intake levels escalate when the endogenous corticostriatal <strong>BDNF</strong> pathway becomes dysregulated.
+BDNF	drug	cannabinoid	25770649	Rs6265 in <strong>BDNF</strong> was associated with smoking initiation, as in the original meta analysis and also with lifetime <b>cannabis</b> use.
+BDNF	drug	nicotine	25770649	Rs6265 in <strong>BDNF</strong> was associated with <b>smoking</b> initiation, as in the original meta analysis and also with lifetime cannabis use.
+BDNF	drug	amphetamine	25764907	The analysis of <strong>BDNF</strong> gene polymorphism haplotypes and impulsivity in <b>methamphetamine</b> abusers.
+BDNF	addiction	dependence	25764907	Data from genetic scans in humans suggest that brain derived neurotrophic factor (<strong>BDNF</strong>), a member of the neurotrophic factor family, may be associated with substance abuse or <b>dependence</b>.
+BDNF	addiction	dependence	25764907	Data from genetic scans in humans suggest that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), a member of the neurotrophic factor family, may be associated with substance abuse or <b>dependence</b>.
+BDNF	drug	amphetamine	25764907	To test the hypothesis that the <strong>BDNF</strong> gene polymorphism is involved in <b>methamphetamine</b> abuse, we compared three single nucleotide polymorphisms (SNPs, rs16917204, rs16917234, and rs2030324) of the <strong>BDNF</strong> gene in 200 <b>methamphetamine</b> abusers and 219 healthy individuals.
+BDNF	drug	amphetamine	25764907	Our findings suggest that the <strong>BDNF</strong> gene polymorphism may contribute to the impulsivity in <b>methamphetamine</b> abusers.
+BDNF	drug	cannabinoid	25762688	<strong>BDNF</strong> interacts with <b>endocannabinoids</b> to regulate cocaine induced synaptic plasticity in mouse midbrain dopamine neurons.
+BDNF	drug	cocaine	25762688	<strong>BDNF</strong> interacts with endocannabinoids to regulate <b>cocaine</b> induced synaptic plasticity in mouse midbrain dopamine neurons.
+BDNF	drug	cannabinoid	25762688	Brain derived neurotrophic factor (<strong>BDNF</strong>) and <b>endocannabinoids</b> (eCBs) have been individually implicated in behavioral effects of cocaine.
+BDNF	drug	cocaine	25762688	Brain derived neurotrophic factor (<strong>BDNF</strong>) and endocannabinoids (eCBs) have been individually implicated in behavioral effects of <b>cocaine</b>.
+BDNF	drug	cannabinoid	25762688	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and <b>endocannabinoids</b> (eCBs) have been individually implicated in behavioral effects of cocaine.
+BDNF	drug	cocaine	25762688	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and endocannabinoids (eCBs) have been individually implicated in behavioral effects of <b>cocaine</b>.
+BDNF	drug	cocaine	25762688	The present study examined how <strong>BDNF</strong> eCB interaction regulates <b>cocaine</b> induced synaptic plasticity in the ventral tegmental area and behavioral effects.
+BDNF	drug	cocaine	25762688	Using Cre loxP technology to specifically delete <strong>BDNF</strong> in dopamine neurons, we showed that eCB mediated I LTD, <b>cocaine</b> induced reduction of GABAergic inhibition, and potentiation of glutamatergic excitation remained intact in wild type control mice, but were impaired in <strong>BDNF</strong> conditional knock out mice.
+BDNF	drug	cocaine	25762688	We also showed that <b>cocaine</b> induced conditioned place preference was attenuated in <strong>BDNF</strong> conditional knock out mice, in vivo pretreatments with DHF before place conditioning restored <b>cocaine</b> conditioned place preference in these mice, and the behavioral effect of DHF was blocked by a CB₁ receptor antagonist.
+BDNF	drug	cocaine	25762688	Together, these results suggest that <strong>BDNF</strong> in dopamine neurons regulates eCB responses, <b>cocaine</b> induced synaptic plasticity, and associative learning.
+BDNF	drug	alcohol	25743187	In the medial prefrontal cortex, 2.5g/kg <b>ethanol</b> decreased mRNA expression of <strong>brain derived neurotrophic factor</strong>, NMDA NR2A subunit, mGluR8 receptor, Homer1, the glutamate transporters SLC1a1 and SLC1a6 and Srr.
+BDNF	drug	nicotine	25744957	Effects of the <strong>BDNF</strong> Val66Met Polymorphism on Anxiety Like Behavior Following <b>Nicotine</b> Withdrawal in Mice.
+BDNF	addiction	withdrawal	25744957	Effects of the <strong>BDNF</strong> Val66Met Polymorphism on Anxiety Like Behavior Following Nicotine <b>Withdrawal</b> in Mice.
+BDNF	drug	nicotine	25744957	In the current study we used a mouse model of a non synonymous single nucleotide polymorphism in the translated region of the brain derived neurotrophic factor (<strong>BDNF</strong>) gene that substitutes a valine (Val) for a methionine (Met) amino acid (Val66Met) to examine the relationship between the Val66Met single nucleotide polymorphism and <b>nicotine</b> dependence.
+BDNF	addiction	dependence	25744957	In the current study we used a mouse model of a non synonymous single nucleotide polymorphism in the translated region of the brain derived neurotrophic factor (<strong>BDNF</strong>) gene that substitutes a valine (Val) for a methionine (Met) amino acid (Val66Met) to examine the relationship between the Val66Met single nucleotide polymorphism and nicotine <b>dependence</b>.
+BDNF	drug	nicotine	25744957	In the current study we used a mouse model of a non synonymous single nucleotide polymorphism in the translated region of the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene that substitutes a valine (Val) for a methionine (Met) amino acid (Val66Met) to examine the relationship between the Val66Met single nucleotide polymorphism and <b>nicotine</b> dependence.
+BDNF	addiction	dependence	25744957	In the current study we used a mouse model of a non synonymous single nucleotide polymorphism in the translated region of the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene that substitutes a valine (Val) for a methionine (Met) amino acid (Val66Met) to examine the relationship between the Val66Met single nucleotide polymorphism and nicotine <b>dependence</b>.
+BDNF	drug	nicotine	25744957	This study measured proBDNF and the <strong>BDNF</strong> prodomain levels following <b>nicotine</b> and <b>nicotine</b> withdrawal and examined a mouse model of a common polymorphism in this protein (<strong>BDNF</strong>(Met/Met)) in three behavioral paradigms: novelty induced hypophagia, marble burying, and the open field test.
+BDNF	addiction	withdrawal	25744957	This study measured proBDNF and the <strong>BDNF</strong> prodomain levels following nicotine and nicotine <b>withdrawal</b> and examined a mouse model of a common polymorphism in this protein (<strong>BDNF</strong>(Met/Met)) in three behavioral paradigms: novelty induced hypophagia, marble burying, and the open field test.
+BDNF	drug	nicotine	25744957	Using the <strong>BDNF</strong> knock in mouse containing the <strong>BDNF</strong> Val66Met polymorphism we found: (1) blunted anxiety like behavior in <strong>BDNF</strong>(Met/Met) mice following withdrawal in three behavioral paradigms: novelty induced hypophagia, marble burying, and the open field test; (2) the anxiolytic effects of chronic <b>nicotine</b> are absent in <strong>BDNF</strong>(Met/Met) mice; and (3) an increase in <strong>BDNF</strong> prodomain in <strong>BDNF</strong>(Met/Met) mice following <b>nicotine</b> withdrawal.
+BDNF	addiction	withdrawal	25744957	Using the <strong>BDNF</strong> knock in mouse containing the <strong>BDNF</strong> Val66Met polymorphism we found: (1) blunted anxiety like behavior in <strong>BDNF</strong>(Met/Met) mice following <b>withdrawal</b> in three behavioral paradigms: novelty induced hypophagia, marble burying, and the open field test; (2) the anxiolytic effects of chronic nicotine are absent in <strong>BDNF</strong>(Met/Met) mice; and (3) an increase in <strong>BDNF</strong> prodomain in <strong>BDNF</strong>(Met/Met) mice following nicotine <b>withdrawal</b>.
+BDNF	drug	nicotine	25744957	Our study is the first to examine the effect of the <strong>BDNF</strong> Val66Met polymorphism on the affective symptoms of withdrawal from <b>nicotine</b> in mice.
+BDNF	addiction	withdrawal	25744957	Our study is the first to examine the effect of the <strong>BDNF</strong> Val66Met polymorphism on the affective symptoms of <b>withdrawal</b> from nicotine in mice.
+BDNF	addiction	withdrawal	25744957	In these mice, a single nucleotide polymorphism in the translated region of the <strong>BDNF</strong> gene can result in a blunted <b>withdrawal</b>, as measured by decreased anxiety like behavior.
+BDNF	drug	nicotine	25744957	The significant increase in the <strong>BDNF</strong> prodomain in <strong>BDNF</strong>(Met/Met) mice following <b>nicotine</b> cessation suggests a possible role of this ligand in the circuitry remodeling after withdrawal.
+BDNF	addiction	withdrawal	25744957	The significant increase in the <strong>BDNF</strong> prodomain in <strong>BDNF</strong>(Met/Met) mice following nicotine cessation suggests a possible role of this ligand in the circuitry remodeling after <b>withdrawal</b>.
+BDNF	drug	cocaine	25734326	Plasma concentrations of <strong>BDNF</strong> and IGF 1 in abstinent <b>cocaine</b> users with high prevalence of substance use disorders: relationship to psychiatric comorbidity.
+BDNF	drug	cocaine	25734326	Because the neurotrophic factors are involved in neural plasticity, neurogenesis and neuronal survival, we have determined plasma concentrations of brain derived neurotrophic factor (<strong>BDNF</strong>), insulin like growth factor 1 (IGF 1) and IGF 1 binding protein 3 (IGFBP 3) in a cross sectional study with abstinent <b>cocaine</b> users who sought outpatient treatment for <b>cocaine</b> (n = 100) and age/body mass matched controls (n = 85).
+BDNF	drug	cocaine	25734326	Because the neurotrophic factors are involved in neural plasticity, neurogenesis and neuronal survival, we have determined plasma concentrations of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), insulin like growth factor 1 (IGF 1) and IGF 1 binding protein 3 (IGFBP 3) in a cross sectional study with abstinent <b>cocaine</b> users who sought outpatient treatment for <b>cocaine</b> (n = 100) and age/body mass matched controls (n = 85).
+BDNF	drug	cocaine	25734326	Correlation analyses were performed between these peptides and other molecules sensitive to addiction: <strong>BDNF</strong> concentrations were not associated with inflammatory mediators, lipid derivatives or IGF 1 in <b>cocaine</b> users, but correlated with chemokines (fractalkine/CX3CL1 and SDF 1/CXCL12) and N acyl ethanolamines (N palmitoyl , N oleoyl , N arachidonoyl , N linoleoyl  and N dihomo γ linolenoyl ethanolamine) in controls; IGF 1 concentrations only showed association with IGFBP 3 concentrations in controls; and IGFBP 3 was only correlated with N stearoyl ethanolamine concentrations in <b>cocaine</b> users.
+BDNF	addiction	addiction	25734326	Correlation analyses were performed between these peptides and other molecules sensitive to <b>addiction</b>: <strong>BDNF</strong> concentrations were not associated with inflammatory mediators, lipid derivatives or IGF 1 in cocaine users, but correlated with chemokines (fractalkine/CX3CL1 and SDF 1/CXCL12) and N acyl ethanolamines (N palmitoyl , N oleoyl , N arachidonoyl , N linoleoyl  and N dihomo γ linolenoyl ethanolamine) in controls; IGF 1 concentrations only showed association with IGFBP 3 concentrations in controls; and IGFBP 3 was only correlated with N stearoyl ethanolamine concentrations in cocaine users.
+BDNF	drug	cocaine	25734326	Interestingly, plasma <strong>BDNF</strong> concentrations were exclusively found to be decreased in users diagnosed with both primary and <b>cocaine</b> induced disorders for mood and anxiety disorders.
+BDNF	drug	cocaine	25734326	In summary, <strong>BDNF</strong>, IGF 1 and IGFBP 3 were not affected by a history of pathological use of <b>cocaine</b> supported by the absence of associations with other molecules sensitive to <b>cocaine</b> addiction.
+BDNF	addiction	addiction	25734326	In summary, <strong>BDNF</strong>, IGF 1 and IGFBP 3 were not affected by a history of pathological use of cocaine supported by the absence of associations with other molecules sensitive to cocaine <b>addiction</b>.
+BDNF	drug	cocaine	25734326	Further research is necessary to elucidate the role of <strong>BDNF</strong> and IGF 1 in the transition to <b>cocaine</b> addiction and associated psychiatric comorbidity.
+BDNF	addiction	addiction	25734326	Further research is necessary to elucidate the role of <strong>BDNF</strong> and IGF 1 in the transition to cocaine <b>addiction</b> and associated psychiatric comorbidity.
+BDNF	drug	cocaine	25733538	Moreover, female H mice acquired <b>cocaine</b> associated context learning much faster than I and NH mice, a facilitating effect that was associated to a rapid increase in striatal and accumbal brain derived neurotrophic factor levels (<strong>BDNF</strong>; up to 35% 24 h after <b>cocaine</b> conditioning).
+BDNF	drug	cocaine	25733538	Moreover, female H mice acquired <b>cocaine</b> associated context learning much faster than I and NH mice, a facilitating effect that was associated to a rapid increase in striatal and accumbal <strong>brain derived neurotrophic factor</strong> levels (<strong>BDNF</strong>; up to 35% 24 h after <b>cocaine</b> conditioning).
+BDNF	drug	cocaine	25733538	Our data indicate that neurobiological mechanisms such as alterations in associative learning, striato accumbal <strong>BDNF</strong> expression, and limbic cortico striatal circuit reactivity could mediate enhanced <b>cocaine</b> vulnerability in female depressive like mice.
+BDNF	drug	opioid	25729949	In this study, we used dopamine receptor mutant mice to explore the roles of the D1 and D3 receptors in locomotion and <b>morphine</b> induced place preference; furthermore, we investigated the effects of <b>morphine</b> on <strong>BDNF</strong> expression in the NAc and PFC of the mouse brain.
+BDNF	drug	opioid	25729949	Furthermore, D1 receptor mutant mice did not acquire <b>morphine</b> conditioned place preference (D1:  18.3 ± 59.9, D3: 217.7 ± 64.1) and showed decreased <strong>BDNF</strong> expression in the NAc (D1: 0.33 ± 0.07 fold, D3: 2.21 ± 0.18 fold) and PFC (D1: 0.74 ± 0.15 fold, D3: 1.68 ± 0.22 fold) compared with wild type and D3 receptor mutant mice.
+BDNF	drug	opioid	25729949	The dopamine receptor D1 but not the D3 is also critical for <b>morphine</b> induced <strong>BDNF</strong> expression in the NAc and PFC.
+BDNF	drug	opioid	25716777	However, changes in plasma cytokine levels, <strong>BDNF</strong> levels, and the <b>methadone</b> dose required in the three groups were not significantly different.
+BDNF	drug	alcohol	25660313	Meta analysis of six genes (<strong>BDNF</strong>, DRD1, DRD3, DRD4, GRIN2B and MAOA) involved in neuroplasticity and the risk for <b>alcohol</b> dependence.
+BDNF	addiction	dependence	25660313	Meta analysis of six genes (<strong>BDNF</strong>, DRD1, DRD3, DRD4, GRIN2B and MAOA) involved in neuroplasticity and the risk for alcohol <b>dependence</b>.
+BDNF	drug	alcohol	25650137	<strong>BDNF</strong> Val66Met and reward related brain function in adolescents: role for early <b>alcohol</b> consumption.
+BDNF	addiction	reward	25650137	<strong>BDNF</strong> Val66Met and <b>reward</b> related brain function in adolescents: role for early alcohol consumption.
+BDNF	addiction	reward	25650137	The nonsynonymous single nucleotide polymorphism in the brain derived neurotrophic factor (<strong>BDNF</strong>) gene (rs6265/Val66Met) modulates the central nervous system activity of neurotransmitters involved in <b>reward</b> processing such as serotonin, dopamine, and glutamate.
+BDNF	addiction	reward	25650137	The nonsynonymous single nucleotide polymorphism in the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene (rs6265/Val66Met) modulates the central nervous system activity of neurotransmitters involved in <b>reward</b> processing such as serotonin, dopamine, and glutamate.
+BDNF	drug	alcohol	25650137	However, studies in humans on the association of <strong>BDNF</strong> Val66Met and reward related brain functions and its role for <b>alcohol</b> consumption, a significant predictor of later <b>alcohol</b> addiction, are missing.
+BDNF	addiction	addiction	25650137	However, studies in humans on the association of <strong>BDNF</strong> Val66Met and reward related brain functions and its role for alcohol consumption, a significant predictor of later alcohol <b>addiction</b>, are missing.
+BDNF	addiction	reward	25650137	However, studies in humans on the association of <strong>BDNF</strong> Val66Met and <b>reward</b> related brain functions and its role for alcohol consumption, a significant predictor of later alcohol addiction, are missing.
+BDNF	drug	alcohol	25650137	This study indicates a possible effect of <strong>BDNF</strong> Val66Met on <b>alcohol</b> addiction related phenotypes in adolescence.
+BDNF	addiction	addiction	25650137	This study indicates a possible effect of <strong>BDNF</strong> Val66Met on alcohol <b>addiction</b> related phenotypes in adolescence.
+BDNF	drug	alcohol	25638740	A comparison of dexmedetomidine and placebo on the plasma concentrations of NGF, <strong>BDNF</strong>, GDNF, and epinephrine during severe <b>alcohol</b> withdrawal.
+BDNF	addiction	withdrawal	25638740	A comparison of dexmedetomidine and placebo on the plasma concentrations of NGF, <strong>BDNF</strong>, GDNF, and epinephrine during severe alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	25638740	<b>Alcohol</b> withdrawal and therapies may affect nerve growth factor (NGF), brain derived neurotrophic growth factor (<strong>BDNF</strong>), glial derived neurotrophic growth factor (GDNF), and epinephrine (EPI).
+BDNF	addiction	withdrawal	25638740	Alcohol <b>withdrawal</b> and therapies may affect nerve growth factor (NGF), brain derived neurotrophic growth factor (<strong>BDNF</strong>), glial derived neurotrophic growth factor (GDNF), and epinephrine (EPI).
+BDNF	drug	alcohol	25638740	This study evaluated dexmedetomidine (DEX) on NGF, <strong>BDNF</strong>, GDNF, and EPI in severe <b>alcohol</b> withdrawal and related their plasma concentrations to DEX concentrations.
+BDNF	addiction	withdrawal	25638740	This study evaluated dexmedetomidine (DEX) on NGF, <strong>BDNF</strong>, GDNF, and EPI in severe alcohol <b>withdrawal</b> and related their plasma concentrations to DEX concentrations.
+BDNF	drug	alcohol	25638740	In summary, the plasma concentrations of NGF, <strong>BDNF</strong>, GDNF, and EPI during <b>alcohol</b> withdrawal are variable and the effects of DEX were marginal.
+BDNF	addiction	withdrawal	25638740	In summary, the plasma concentrations of NGF, <strong>BDNF</strong>, GDNF, and EPI during alcohol <b>withdrawal</b> are variable and the effects of DEX were marginal.
+BDNF	drug	alcohol	25623403	The aim of this study was to investigate the alterations in serum neurotrophin levels (brain derived neurotrophic factor [<strong>BDNF</strong>], glial derived neurotrophic factor [GDNF], and nerve growth factor [NGF]) in <b>alcohol</b> use disorder in a young population, and thus possibly representing the early stages of the illness.
+BDNF	drug	alcohol	25623403	The aim of this study was to investigate the alterations in serum neurotrophin levels (<strong>brain derived neurotrophic factor</strong> [<strong>BDNF</strong>], glial derived neurotrophic factor [GDNF], and nerve growth factor [NGF]) in <b>alcohol</b> use disorder in a young population, and thus possibly representing the early stages of the illness.
+BDNF	drug	cocaine	25619460	In the present study, we investigated the effects of a chronic <b>cocaine</b> treatment on molecular and structural plasticity in the cerebellum, including <strong>BDNF</strong>, D3 dopamine receptors, ΔFosB, the Glu2 AMPA receptor subunit, structural modifications in Purkinje neurons and, finally, the evaluation of perineuronal nets (PNNs) in the projection neurons of the medial nucleus, the output of the cerebellar vermis.
+BDNF	drug	cocaine	25619460	In the current experimental conditions in which repeated <b>cocaine</b> treatment was followed by a 1 week withdrawal period and a new <b>cocaine</b> challenge, our results showed that <b>cocaine</b> induced a large increase in cerebellar proBDNF levels and its expression in Purkinje neurons, with the mature <strong>BDNF</strong> expression remaining unchanged.
+BDNF	addiction	withdrawal	25619460	In the current experimental conditions in which repeated cocaine treatment was followed by a 1 week <b>withdrawal</b> period and a new cocaine challenge, our results showed that cocaine induced a large increase in cerebellar proBDNF levels and its expression in Purkinje neurons, with the mature <strong>BDNF</strong> expression remaining unchanged.
+BDNF	drug	nicotine	25618300	Effect of variation in <strong>BDNF</strong> Val(66)Met polymorphism, <b>smoking</b>, and <b>nicotine</b> dependence on symptom severity of depressive and anxiety disorders.
+BDNF	addiction	dependence	25618300	Effect of variation in <strong>BDNF</strong> Val(66)Met polymorphism, smoking, and nicotine <b>dependence</b> on symptom severity of depressive and anxiety disorders.
+BDNF	drug	nicotine	25618300	We investigated the effect of brain derived neurotrophic factor (<strong>BDNF</strong>) Val(66)Met polymorphism on the severity of depressive and anxiety symptoms in never <b>smokers</b>, former <b>smokers</b>, non dependent, and <b>nicotine</b> dependent <b>smokers</b> with a current diagnosis of depression and/or anxiety.
+BDNF	drug	nicotine	25618300	We investigated the effect of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) Val(66)Met polymorphism on the severity of depressive and anxiety symptoms in never <b>smokers</b>, former <b>smokers</b>, non dependent, and <b>nicotine</b> dependent <b>smokers</b> with a current diagnosis of depression and/or anxiety.
+BDNF	drug	nicotine	25618300	Independent variables were <b>smoking</b> status and <strong>BDNF</strong> genotype.
+BDNF	drug	nicotine	25618300	In patients with a current diagnosis of depression or anxiety, the relationship between <b>nicotine</b> dependence and symptom severity may be moderated by <strong>BDNF</strong> Val(66)Met.
+BDNF	addiction	dependence	25618300	In patients with a current diagnosis of depression or anxiety, the relationship between nicotine <b>dependence</b> and symptom severity may be moderated by <strong>BDNF</strong> Val(66)Met.
+BDNF	drug	alcohol	25611260	Corticosterone protects against memory impairments and reduced hippocampal <strong>BDNF</strong> levels induced by a chronic low dose of <b>ethanol</b> in C57BL/6J mice.
+BDNF	drug	alcohol	25611260	<strong>BDNF</strong> contributes to memory function and toxic effects of <b>ethanol</b>, therefore its levels were quantified in the hippocampus and frontal cortex.
+BDNF	drug	alcohol	25611260	The chronic exposure to a low dose of <b>ethanol</b> caused spatial and non spatial memory deficits after withdrawal associated with a reduction in hippocampal <strong>BDNF</strong> levels, which were prevented by co treatment with corticosterone (~21 mg/kg/day).
+BDNF	addiction	withdrawal	25611260	The chronic exposure to a low dose of ethanol caused spatial and non spatial memory deficits after <b>withdrawal</b> associated with a reduction in hippocampal <strong>BDNF</strong> levels, which were prevented by co treatment with corticosterone (~21 mg/kg/day).
+BDNF	drug	cocaine	25592977	Changes in brain derived neurotrophic factor (<strong>BDNF</strong>) during abstinence could be associated with relapse in <b>cocaine</b> dependent patients.
+BDNF	addiction	relapse	25592977	Changes in brain derived neurotrophic factor (<strong>BDNF</strong>) during abstinence could be associated with <b>relapse</b> in cocaine dependent patients.
+BDNF	drug	cocaine	25592977	Changes in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) during abstinence could be associated with relapse in <b>cocaine</b> dependent patients.
+BDNF	addiction	relapse	25592977	Changes in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) during abstinence could be associated with <b>relapse</b> in cocaine dependent patients.
+BDNF	drug	cocaine	25592977	Brain derived neurotrophic factor (<strong>BDNF</strong>) is involved in <b>cocaine</b> craving in humans and drug seeking in rodents.
+BDNF	addiction	relapse	25592977	Brain derived neurotrophic factor (<strong>BDNF</strong>) is involved in cocaine <b>craving</b> in humans and drug <b>seeking</b> in rodents.
+BDNF	drug	cocaine	25592977	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is involved in <b>cocaine</b> craving in humans and drug seeking in rodents.
+BDNF	addiction	relapse	25592977	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is involved in cocaine <b>craving</b> in humans and drug <b>seeking</b> in rodents.
+BDNF	drug	cocaine	25592977	Based on this, the aim of this study was to explore the possible role of serum <strong>BDNF</strong> in <b>cocaine</b> relapse in abstinent addicts.
+BDNF	addiction	relapse	25592977	Based on this, the aim of this study was to explore the possible role of serum <strong>BDNF</strong> in cocaine <b>relapse</b> in abstinent addicts.
+BDNF	drug	cocaine	25592977	These results suggest that <strong>BDNF</strong> has a role in relapse to <b>cocaine</b> consumption in abstinent addicts, although the underlying neurobiological mechanisms remain to be clarified.
+BDNF	addiction	relapse	25592977	These results suggest that <strong>BDNF</strong> has a role in <b>relapse</b> to cocaine consumption in abstinent addicts, although the underlying neurobiological mechanisms remain to be clarified.
+BDNF	drug	psychedelics	25582786	The rapid synaptic and behavioral actions of <b>ketamine</b> occur via increased <strong>BDNF</strong> regulation of synaptic protein synthesis.
+BDNF	drug	cocaine	25576963	We found a significant association between <b>cocaine</b> and methylphenidate treatments and age progression in the prefrontal protein expression of brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	cocaine	25576963	We found a significant association between <b>cocaine</b> and methylphenidate treatments and age progression in the prefrontal protein expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	cannabinoid	25550231	The purpose of this review is to outline the literature showing how pharmacological interventions targeting neurotransmitter systems including serotonin, dopamine, noradrenaline, histamine, glutamate, GABA, <b>cannabinoids</b>, neuropeptides (oxytocin, neuropeptides Y and S, opioids) and other targets (neurotrophins <strong>BDNF</strong> and FGF2, glucocorticoids, L type calcium channels, epigenetic modifications) as well as their downstream signaling pathways, can augment fear extinction and strengthen extinction memory persistently in preclinical models.
+BDNF	drug	opioid	25550231	The purpose of this review is to outline the literature showing how pharmacological interventions targeting neurotransmitter systems including serotonin, dopamine, noradrenaline, histamine, glutamate, GABA, cannabinoids, neuropeptides (oxytocin, neuropeptides Y and S, <b>opioids</b>) and other targets (neurotrophins <strong>BDNF</strong> and FGF2, glucocorticoids, L type calcium channels, epigenetic modifications) as well as their downstream signaling pathways, can augment fear extinction and strengthen extinction memory persistently in preclinical models.
+BDNF	drug	cocaine	25522421	Temporal regulation of peripheral <strong>BDNF</strong> levels during <b>cocaine</b> and morphine withdrawal: comparison with a natural reward.
+BDNF	drug	opioid	25522421	Temporal regulation of peripheral <strong>BDNF</strong> levels during cocaine and <b>morphine</b> withdrawal: comparison with a natural reward.
+BDNF	addiction	reward	25522421	Temporal regulation of peripheral <strong>BDNF</strong> levels during cocaine and morphine withdrawal: comparison with a natural <b>reward</b>.
+BDNF	addiction	withdrawal	25522421	Temporal regulation of peripheral <strong>BDNF</strong> levels during cocaine and morphine <b>withdrawal</b>: comparison with a natural reward.
+BDNF	addiction	addiction	25522421	Brain derived neurotrophic factor (<strong>BDNF</strong>) is a neurotrophin that has long been studied in the field of <b>addiction</b> and its importance in regulating drug <b>addiction</b> related behavior has been widely demonstrated.
+BDNF	addiction	addiction	25522421	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is a neurotrophin that has long been studied in the field of <b>addiction</b> and its importance in regulating drug <b>addiction</b> related behavior has been widely demonstrated.
+BDNF	addiction	reward	25522421	The aim of our study was to analyze the consequences of a repeated exposure to drugs of abuse or natural <b>reward</b> on plasma <strong>BDNF</strong> levels during withdrawal.
+BDNF	addiction	withdrawal	25522421	The aim of our study was to analyze the consequences of a repeated exposure to drugs of abuse or natural reward on plasma <strong>BDNF</strong> levels during <b>withdrawal</b>.
+BDNF	addiction	reward	25522421	Blood collection was performed on the 1st (withdrawal day 1 or WD1) or on (WD14), either at the same time point rats had been exposed to drugs or natural <b>reward</b> or at a different time point (used to quantify basal <strong>brain derived neurotrophic factor</strong> levels).
+BDNF	addiction	withdrawal	25522421	Blood collection was performed on the 1st (<b>withdrawal</b> day 1 or WD1) or on (WD14), either at the same time point rats had been exposed to drugs or natural reward or at a different time point (used to quantify basal <strong>brain derived neurotrophic factor</strong> levels).
+BDNF	drug	cocaine	25522421	<b>Cocaine</b> treatment led to a rapid (WD1) and persistent (WD14) decrease of basal <strong>BDNF</strong> levels compared with saline treated animals, whereas morphine induced an increase on WD14 without any alteration on WD1.
+BDNF	drug	opioid	25522421	Cocaine treatment led to a rapid (WD1) and persistent (WD14) decrease of basal <strong>BDNF</strong> levels compared with saline treated animals, whereas <b>morphine</b> induced an increase on WD14 without any alteration on WD1.
+BDNF	addiction	reward	25522421	On the contrary, the natural <b>reward</b> induced a significant increase of basal <strong>brain derived neurotrophic factor</strong> levels only on WD1.
+BDNF	addiction	reward	25522421	The analysis of <strong>BDNF</strong> levels at the usual time point at which animals had been exposed showed that both drugs, but not the natural <b>reward</b>, increased <strong>BDNF</strong> levels compared with basal levels.
+BDNF	drug	cocaine	25522393	A single <strong>brain derived neurotrophic factor</strong> infusion into the dorsomedial prefrontal cortex attenuates <b>cocaine</b> self administration induced phosphorylation of synapsin in the nucleus accumbens during early withdrawal.
+BDNF	addiction	withdrawal	25522393	A single <strong>brain derived neurotrophic factor</strong> infusion into the dorsomedial prefrontal cortex attenuates cocaine self administration induced phosphorylation of synapsin in the nucleus accumbens during early <b>withdrawal</b>.
+BDNF	drug	cocaine	25522393	We have previously demonstrated that one intra dorsomedial prefrontal cortex brain derived neurotrophic factor (<strong>BDNF</strong>) infusion immediately following the last <b>cocaine</b> self administration session caused a long lasting inhibition of <b>cocaine</b> seeking and normalized the <b>cocaine</b> induced disturbance of glutamate transmission in the nucleus accumbens after extinction and a <b>cocaine</b> prime.
+BDNF	addiction	relapse	25522393	We have previously demonstrated that one intra dorsomedial prefrontal cortex brain derived neurotrophic factor (<strong>BDNF</strong>) infusion immediately following the last cocaine self administration session caused a long lasting inhibition of cocaine <b>seeking</b> and normalized the cocaine induced disturbance of glutamate transmission in the nucleus accumbens after extinction and a cocaine prime.
+BDNF	drug	cocaine	25522393	We have previously demonstrated that one intra dorsomedial prefrontal cortex <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) infusion immediately following the last <b>cocaine</b> self administration session caused a long lasting inhibition of <b>cocaine</b> seeking and normalized the <b>cocaine</b> induced disturbance of glutamate transmission in the nucleus accumbens after extinction and a <b>cocaine</b> prime.
+BDNF	addiction	relapse	25522393	We have previously demonstrated that one intra dorsomedial prefrontal cortex <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) infusion immediately following the last cocaine self administration session caused a long lasting inhibition of cocaine <b>seeking</b> and normalized the cocaine induced disturbance of glutamate transmission in the nucleus accumbens after extinction and a cocaine prime.
+BDNF	drug	cocaine	25522393	However, the molecular mechanism mediating the <strong>brain derived neurotrophic factor</strong> effect on <b>cocaine</b> induced alterations in extracellular glutamate levels is unknown.
+BDNF	drug	cocaine	25522393	In the present study, we determined the effects of <strong>brain derived neurotrophic factor</strong> on <b>cocaine</b> induced changes in the phosphorylation of synapsin (p synapsin), a family of presynaptic proteins that mediate synaptic vesicle mobilization, in the nucleus accumbens during early withdrawal.
+BDNF	addiction	withdrawal	25522393	In the present study, we determined the effects of <strong>brain derived neurotrophic factor</strong> on cocaine induced changes in the phosphorylation of synapsin (p synapsin), a family of presynaptic proteins that mediate synaptic vesicle mobilization, in the nucleus accumbens during early <b>withdrawal</b>.
+BDNF	drug	cocaine	25522393	Elevations at both time points were attenuated by an intra dorsomedial prefrontal cortex <strong>brain derived neurotrophic factor</strong> infusion immediately after the end of <b>cocaine</b> self administration.
+BDNF	drug	cocaine	25522393	<strong>Brain derived neurotrophic factor</strong> also reduced <b>cocaine</b> self administration withdrawal induced phosphorylation of the protein phosphatase 2A C subunit, suggesting that <strong>brain derived neurotrophic factor</strong> disinhibits protein phosphatase 2A C subunit, consistent with p synapsin Ser9 dephosphorylation.
+BDNF	addiction	withdrawal	25522393	<strong>Brain derived neurotrophic factor</strong> also reduced cocaine self administration <b>withdrawal</b> induced phosphorylation of the protein phosphatase 2A C subunit, suggesting that <strong>brain derived neurotrophic factor</strong> disinhibits protein phosphatase 2A C subunit, consistent with p synapsin Ser9 dephosphorylation.
+BDNF	drug	cocaine	25522393	Further, co immunoprecipitation demonstrated that protein phosphatase 2A C subunit and synapsin are associated in a protein protein complex that was reduced after 2 hours of withdrawal from <b>cocaine</b> self administration and reversed by <strong>brain derived neurotrophic factor</strong>.
+BDNF	addiction	withdrawal	25522393	Further, co immunoprecipitation demonstrated that protein phosphatase 2A C subunit and synapsin are associated in a protein protein complex that was reduced after 2 hours of <b>withdrawal</b> from cocaine self administration and reversed by <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	cocaine	25522393	Taken together, these findings demonstrate that <strong>brain derived neurotrophic factor</strong> normalizes the <b>cocaine</b> self administration induced elevation of p synapsin in nucleus accumbens that may underlie a disturbance in the probability of neurotransmitter release or represent a compensatory neuroadaptation in response to the hypofunction within the prefrontal cortex nucleus accumbens pathway during <b>cocaine</b> withdrawal.
+BDNF	addiction	withdrawal	25522393	Taken together, these findings demonstrate that <strong>brain derived neurotrophic factor</strong> normalizes the cocaine self administration induced elevation of p synapsin in nucleus accumbens that may underlie a disturbance in the probability of neurotransmitter release or represent a compensatory neuroadaptation in response to the hypofunction within the prefrontal cortex nucleus accumbens pathway during cocaine <b>withdrawal</b>.
+BDNF	drug	alcohol	25510982	The <strong>BDNF</strong> p.Val66Met polymorphism, childhood trauma, and brain volumes in adolescents with <b>alcohol</b> abuse.
+BDNF	drug	alcohol	25510982	p.Met66 allele of <strong>BDNF</strong>), and <b>alcohol</b> dependence, on brain structure in adolescents is limited.
+BDNF	addiction	dependence	25510982	p.Met66 allele of <strong>BDNF</strong>), and alcohol <b>dependence</b>, on brain structure in adolescents is limited.
+BDNF	drug	alcohol	25510982	We examined whether the <strong>BDNF</strong> p.Val66Met polymorphism interacts with childhood trauma to predict alterations in brain volume in adolescents with <b>alcohol</b> use disorders (AUDs).
+BDNF	addiction	withdrawal	25479464	We analysed the time course of the global <b>withdrawal</b> score, the anxiety like effects, monoamine concentrations, the brain derived neurotrophic factor (<strong>BDNF</strong>) expression, the corticosterone plasmatic levels and [(3)H]epibatidine binding sites during NIC <b>withdrawal</b> precipitated by mecamylamine, a nicotinic receptor antagonist (MEC).
+BDNF	addiction	withdrawal	25479464	We analysed the time course of the global <b>withdrawal</b> score, the anxiety like effects, monoamine concentrations, the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression, the corticosterone plasmatic levels and [(3)H]epibatidine binding sites during NIC <b>withdrawal</b> precipitated by mecamylamine, a nicotinic receptor antagonist (MEC).
+BDNF	addiction	withdrawal	25479464	In NIC withdrawn wild type mice, we observed a global <b>withdrawal</b> score, an anxiety like effect in the elevated plus maze, a decrease of the striatal dopamine and 3,4 dihydroxyphenylacetic acid concentrations, an increase of corticosterone plasma levels, a reduction of <strong>BDNF</strong> expression in several brain areas and an increase of [(3)H]epibatidine binding sites in specific brain regions.
+BDNF	drug	amphetamine	25463524	<b>Methamphetamine</b> differentially affects <strong>BDNF</strong> and cell death factors in anatomically defined regions of the hippocampus.
+BDNF	drug	amphetamine	25463524	Expression of brain derived neurotrophic factor (<strong>BDNF</strong>; a regulator of LTP and neurogenesis), and its receptor tropomyosin related kinase B (TrkB) were studied in the dorsal and ventral hippocampal tissue lysates in rats that intravenously self administered <b>methamphetamine</b> in a limited access (1h/day) or extended access (6h/day) paradigm for 17days post baseline sessions.
+BDNF	drug	amphetamine	25463524	Expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>; a regulator of LTP and neurogenesis), and its receptor tropomyosin related kinase B (TrkB) were studied in the dorsal and ventral hippocampal tissue lysates in rats that intravenously self administered <b>methamphetamine</b> in a limited access (1h/day) or extended access (6h/day) paradigm for 17days post baseline sessions.
+BDNF	drug	amphetamine	25463524	Extended access <b>methamphetamine</b> enhanced expression of <strong>BDNF</strong> with significant effects observed in the dorsal and ventral hippocampus.
+BDNF	drug	amphetamine	25463524	<b>Methamphetamine</b> induced enhancements in <strong>BDNF</strong> expression were not associated with TrkB receptor activation as indicated by phospho (p) TrkB 706 levels.
+BDNF	drug	nicotine	25455509	<b>Smoking</b> and <strong>BDNF</strong> Val66Met polymorphism in male schizophrenia: a case control study.
+BDNF	drug	nicotine	25455509	Some recent studies show an association between a functional polymorphism of <strong>BDNF</strong> gene (Val66Met) and the susceptibility to <b>nicotine</b> dependence and we hypothesized that this polymorphism was associated with <b>smoking</b> in both schizophrenia patients and healthy controls.
+BDNF	addiction	dependence	25455509	Some recent studies show an association between a functional polymorphism of <strong>BDNF</strong> gene (Val66Met) and the susceptibility to nicotine <b>dependence</b> and we hypothesized that this polymorphism was associated with smoking in both schizophrenia patients and healthy controls.
+BDNF	drug	nicotine	25455509	The <strong>BDNF</strong> Val66Met gene polymorphism was genotyped in 690 chronic male schizophrenia patients (<b>smoker</b>/nonsmoker = 522/169) and 628 male controls (<b>smoker</b>/nonsmoker = 322/306) using a case control design.
+BDNF	drug	nicotine	25455509	The results showed no significant differences in <strong>BDNF</strong> Val66Met genotype and allele distributions between the patients and healthy controls or between <b>smokers</b> and nonsmokers in either patients or healthy controls alone.
+BDNF	drug	nicotine	25455509	These results suggest that the <strong>BDNF</strong> Val66Met polymorphism may affect a <b>smoker</b>'s response to <b>nicotine</b> in both schizophrenia and healthy controls from a Chinese Han population, but with differential effects in different aspects of <b>smoking</b> behaviors.
+BDNF	drug	cocaine	25453740	Since GM1 pretreatment did not modify <b>cocaine</b>'s pharmacokinetic parameters, we suspected that the increased rewarding effect found might be mediated by <strong>BDNF</strong>, a neurotrophic factor closely related to <b>cocaine</b> addiction.
+BDNF	addiction	addiction	25453740	Since GM1 pretreatment did not modify cocaine's pharmacokinetic parameters, we suspected that the increased rewarding effect found might be mediated by <strong>BDNF</strong>, a neurotrophic factor closely related to cocaine <b>addiction</b>.
+BDNF	drug	cocaine	25453740	This study was performed to investigate the possibility that GM1 may induce changes in <strong>BDNF</strong> levels in the nucleus accumbens (NAc), a core structure in the brain's reward circuitry, of rats submitted to three conditioning sessions with <b>cocaine</b> (10 mg/kg, i.p.).
+BDNF	addiction	reward	25453740	This study was performed to investigate the possibility that GM1 may induce changes in <strong>BDNF</strong> levels in the nucleus accumbens (NAc), a core structure in the brain's <b>reward</b> circuitry, of rats submitted to three conditioning sessions with cocaine (10 mg/kg, i.p.).
+BDNF	drug	cocaine	25453740	The results demonstrate that GM1 administration, which showed no rewarding effect by itself in the CPP, induced a significant increase of <strong>BDNF</strong> protein levels in the NAc, which may account for the increased rewarding effect of <b>cocaine</b> shown in the CPP paradigm.
+BDNF	addiction	reward	25453740	The results demonstrate that GM1 administration, which showed no rewarding effect by itself in the <b>CPP</b>, induced a significant increase of <strong>BDNF</strong> protein levels in the NAc, which may account for the increased rewarding effect of cocaine shown in the <b>CPP</b> paradigm.
+BDNF	addiction	addiction	25451116	<strong>Brain derived neurotrophic factor</strong> and <b>addiction</b>: Pathological versus therapeutic effects on drug seeking.
+BDNF	addiction	relapse	25451116	<strong>Brain derived neurotrophic factor</strong> and addiction: Pathological versus therapeutic effects on drug <b>seeking</b>.
+BDNF	addiction	addiction	25451116	Many abused drugs lead to changes in endogenous brain derived neurotrophic factor (<strong>BDNF</strong>) expression in neural circuits responsible for <b>addictive</b> behaviors.
+BDNF	addiction	addiction	25451116	Many abused drugs lead to changes in endogenous <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression in neural circuits responsible for <b>addictive</b> behaviors.
+BDNF	addiction	relapse	25451116	Here we explore the role of <strong>BDNF</strong> in extinction circuits, compared to <b>seeking</b> circuits that "incubate" over prolonged withdrawal periods.
+BDNF	addiction	withdrawal	25451116	Here we explore the role of <strong>BDNF</strong> in extinction circuits, compared to seeking circuits that "incubate" over prolonged <b>withdrawal</b> periods.
+BDNF	drug	cocaine	25451116	We begin by discussing the role of <strong>BDNF</strong> in extinction memory for fear and <b>cocaine</b> seeking behaviors, where extinction circuits overlap in infralimbic prefrontal cortex (PFC).
+BDNF	addiction	relapse	25451116	We begin by discussing the role of <strong>BDNF</strong> in extinction memory for fear and cocaine <b>seeking</b> behaviors, where extinction circuits overlap in infralimbic prefrontal cortex (PFC).
+BDNF	addiction	relapse	25451116	We highlight the ability of estrogen to promote <strong>BDNF</strong> like effects in hippocampal prefrontal circuits and consider the role of sex differences in extinction and incubation of drug <b>seeking</b> behaviors.
+BDNF	drug	alcohol	25451116	Finally, we examine how opiates and <b>alcohol</b> "break the mold" in terms of <strong>BDNF</strong> function in extinction circuits.
+BDNF	drug	cocaine	25449839	Multiple faces of <strong>BDNF</strong> in <b>cocaine</b> addiction.
+BDNF	addiction	addiction	25449839	Multiple faces of <strong>BDNF</strong> in cocaine <b>addiction</b>.
+BDNF	addiction	addiction	25449839	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been found to play roles in many types of plasticity including drug <b>addiction</b>.
+BDNF	addiction	addiction	25449839	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been found to play roles in many types of plasticity including drug <b>addiction</b>.
+BDNF	drug	cocaine	25449839	Here, we focus on rodent studies over the past two decades that have demonstrated diverse roles of <strong>BDNF</strong> in models of <b>cocaine</b> addiction.
+BDNF	addiction	addiction	25449839	Here, we focus on rodent studies over the past two decades that have demonstrated diverse roles of <strong>BDNF</strong> in models of cocaine <b>addiction</b>.
+BDNF	drug	cocaine	25449839	First, we will provide an overview of studies showing that <b>cocaine</b> exposure alters (and generally increases) <strong>BDNF</strong> levels in reward related regions including the ventral tegmental area, nucleus accumbens, prefrontal cortex, and amygdala.
+BDNF	addiction	reward	25449839	First, we will provide an overview of studies showing that cocaine exposure alters (and generally increases) <strong>BDNF</strong> levels in <b>reward</b> related regions including the ventral tegmental area, nucleus accumbens, prefrontal cortex, and amygdala.
+BDNF	drug	cocaine	25449839	Then we will review evidence that <strong>BDNF</strong> contributes to behavioral changes in animal models of <b>cocaine</b> addiction, focusing on conditioned place preference, behavioral sensitization, maintenance and reinstatement of self administration, and incubation of <b>cocaine</b> craving.
+BDNF	addiction	addiction	25449839	Then we will review evidence that <strong>BDNF</strong> contributes to behavioral changes in animal models of cocaine <b>addiction</b>, focusing on conditioned place preference, behavioral sensitization, maintenance and reinstatement of self administration, and incubation of cocaine craving.
+BDNF	addiction	relapse	25449839	Then we will review evidence that <strong>BDNF</strong> contributes to behavioral changes in animal models of cocaine addiction, focusing on conditioned place preference, behavioral sensitization, maintenance and <b>reinstatement</b> of self administration, and incubation of cocaine <b>craving</b>.
+BDNF	addiction	sensitization	25449839	Then we will review evidence that <strong>BDNF</strong> contributes to behavioral changes in animal models of cocaine addiction, focusing on conditioned place preference, behavioral <b>sensitization</b>, maintenance and reinstatement of self administration, and incubation of cocaine craving.
+BDNF	drug	cocaine	25449839	Last, we will review the role of <strong>BDNF</strong> in synaptic plasticity, particularly as it relates to plasticity of AMPA receptor transmission after <b>cocaine</b> exposure.
+BDNF	drug	cocaine	25449839	We conclude that <strong>BDNF</strong> regulates <b>cocaine</b> induced behaviors in a highly complex manner that varies depending on the brain region (and even among different cell types within the same brain region), the nature of <b>cocaine</b> exposure, and the "addiction phase" examined (e.g., acquisition vs maintenance; early vs late withdrawal).
+BDNF	addiction	addiction	25449839	We conclude that <strong>BDNF</strong> regulates cocaine induced behaviors in a highly complex manner that varies depending on the brain region (and even among different cell types within the same brain region), the nature of cocaine exposure, and the "<b>addiction</b> phase" examined (e.g., acquisition vs maintenance; early vs late withdrawal).
+BDNF	addiction	withdrawal	25449839	We conclude that <strong>BDNF</strong> regulates cocaine induced behaviors in a highly complex manner that varies depending on the brain region (and even among different cell types within the same brain region), the nature of cocaine exposure, and the "addiction phase" examined (e.g., acquisition vs maintenance; early vs late <b>withdrawal</b>).
+BDNF	drug	cocaine	25449839	These complexities make <strong>BDNF</strong> a daunting therapeutic target for treating <b>cocaine</b> addiction.
+BDNF	addiction	addiction	25449839	These complexities make <strong>BDNF</strong> a daunting therapeutic target for treating cocaine <b>addiction</b>.
+BDNF	drug	cocaine	25449839	However, recent clinical evidence suggests that the serum <strong>BDNF</strong> level may serve as a biomarker in <b>cocaine</b> addicts to predict future relapse, providing an alternative direction for exploring <strong>BDNF</strong>'s potential relevance to treating <b>cocaine</b> addiction.
+BDNF	addiction	addiction	25449839	However, recent clinical evidence suggests that the serum <strong>BDNF</strong> level may serve as a biomarker in cocaine addicts to predict future relapse, providing an alternative direction for exploring <strong>BDNF</strong>'s potential relevance to treating cocaine <b>addiction</b>.
+BDNF	addiction	relapse	25449839	However, recent clinical evidence suggests that the serum <strong>BDNF</strong> level may serve as a biomarker in cocaine addicts to predict future <b>relapse</b>, providing an alternative direction for exploring <strong>BDNF</strong>'s potential relevance to treating cocaine addiction.
+BDNF	drug	alcohol	25447477	Voluntary exercise decreases <b>ethanol</b> preference and consumption in C57BL/6 adolescent mice: sex differences and hippocampal <strong>BDNF</strong> expression.
+BDNF	addiction	reward	25447477	Given previously known effects of exercise in increasing the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in the hippocampus and its role in regulating the <b>reward</b> system, <strong>BDNF</strong> mRNA and protein levels were measured at the end of the behavioral experiment.
+BDNF	addiction	reward	25447477	Given previously known effects of exercise in increasing the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the hippocampus and its role in regulating the <b>reward</b> system, <strong>BDNF</strong> mRNA and protein levels were measured at the end of the behavioral experiment.
+BDNF	drug	amphetamine	25446676	Knockdown of ventral tegmental area mu opioid receptors in rats prevents effects of social defeat stress: implications for <b>amphetamine</b> cross sensitization, social avoidance, weight regulation and expression of <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	opioid	25446676	Knockdown of ventral tegmental area mu <b>opioid</b> receptors in rats prevents effects of social defeat stress: implications for amphetamine cross sensitization, social avoidance, weight regulation and expression of <strong>brain derived neurotrophic factor</strong>.
+BDNF	addiction	sensitization	25446676	Knockdown of ventral tegmental area mu opioid receptors in rats prevents effects of social defeat stress: implications for amphetamine cross <b>sensitization</b>, social avoidance, weight regulation and expression of <strong>brain derived neurotrophic factor</strong>.
+BDNF	addiction	sensitization	25446676	Social defeat stress causes social avoidance and long lasting cross <b>sensitization</b> to psychostimulants, both of which are associated with increased brain derived neurotrophic factor (<strong>BDNF</strong>) expression in the ventral tegmental area (VTA).
+BDNF	addiction	sensitization	25446676	Social defeat stress causes social avoidance and long lasting cross <b>sensitization</b> to psychostimulants, both of which are associated with increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression in the ventral tegmental area (VTA).
+BDNF	drug	amphetamine	25446676	At the time point corresponding to <b>amphetamine</b> challenge, immunohistochemical analysis was performed to examine the effect of stress on VTA <strong>BDNF</strong> expression.
+BDNF	drug	opioid	25392083	Elevation of <strong>BDNF</strong> exon I specific transcripts in the frontal cortex and midbrain of rat during spontaneous <b>morphine</b> withdrawal is accompanied by enhanced pCreb1 occupancy at the corresponding promoter.
+BDNF	addiction	withdrawal	25392083	Elevation of <strong>BDNF</strong> exon I specific transcripts in the frontal cortex and midbrain of rat during spontaneous morphine <b>withdrawal</b> is accompanied by enhanced pCreb1 occupancy at the corresponding promoter.
+BDNF	addiction	dependence	25392083	Brain derived neurotrophic factor (<strong>BDNF</strong>) is believed to play a crucial role in the mechanisms underlying opiate <b>dependence</b>; however, little is known about specific features and mechanisms regulating its expression in the brain under these conditions.
+BDNF	addiction	dependence	25392083	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is believed to play a crucial role in the mechanisms underlying opiate <b>dependence</b>; however, little is known about specific features and mechanisms regulating its expression in the brain under these conditions.
+BDNF	drug	opioid	25392083	The aim of this study was to investigate the effects of acute <b>morphine</b> intoxication and withdrawal from chronic intoxication on expression of <strong>BDNF</strong> exon I , II , IV , VI  and IX containing transcripts in the rat frontal cortex and midbrain.
+BDNF	addiction	intoxication	25392083	The aim of this study was to investigate the effects of acute morphine <b>intoxication</b> and withdrawal from chronic <b>intoxication</b> on expression of <strong>BDNF</strong> exon I , II , IV , VI  and IX containing transcripts in the rat frontal cortex and midbrain.
+BDNF	addiction	withdrawal	25392083	The aim of this study was to investigate the effects of acute morphine intoxication and <b>withdrawal</b> from chronic intoxication on expression of <strong>BDNF</strong> exon I , II , IV , VI  and IX containing transcripts in the rat frontal cortex and midbrain.
+BDNF	drug	opioid	25392083	Acute <b>morphine</b> intoxication did not affect levels of <strong>BDNF</strong> exons in brain regions, while spontaneous <b>morphine</b> withdrawal in dependent rats was accompanied by an elevation of the <strong>BDNF</strong> exon I containing mRNAs both in the frontal cortex and midbrain.
+BDNF	addiction	intoxication	25392083	Acute morphine <b>intoxication</b> did not affect levels of <strong>BDNF</strong> exons in brain regions, while spontaneous morphine withdrawal in dependent rats was accompanied by an elevation of the <strong>BDNF</strong> exon I containing mRNAs both in the frontal cortex and midbrain.
+BDNF	addiction	withdrawal	25392083	Acute morphine intoxication did not affect levels of <strong>BDNF</strong> exons in brain regions, while spontaneous morphine <b>withdrawal</b> in dependent rats was accompanied by an elevation of the <strong>BDNF</strong> exon I containing mRNAs both in the frontal cortex and midbrain.
+BDNF	drug	opioid	25392083	The association of MeCP2 with <strong>BDNF</strong> promoters during spontaneous <b>morphine</b> withdrawal did not change.
+BDNF	addiction	withdrawal	25392083	The association of MeCP2 with <strong>BDNF</strong> promoters during spontaneous morphine <b>withdrawal</b> did not change.
+BDNF	drug	opioid	25392083	Thus, <strong>BDNF</strong> exon specific transcripts are differentially expressed in brain regions during spontaneous <b>morphine</b> withdrawal in dependent rats and pCreb1 may be at least partially responsible for these alterations.
+BDNF	addiction	withdrawal	25392083	Thus, <strong>BDNF</strong> exon specific transcripts are differentially expressed in brain regions during spontaneous morphine <b>withdrawal</b> in dependent rats and pCreb1 may be at least partially responsible for these alterations.
+BDNF	drug	alcohol	25330738	The <strong>BDNF</strong> signaling pathway is activated by moderate intake of <b>alcohol</b> to prevent escalation to excessive drinking.
+BDNF	addiction	addiction	25330738	The <strong>BDNF</strong> signaling pathway is activated by moderate intake of alcohol to prevent <b>escalation</b> to excessive drinking.
+BDNF	drug	alcohol	25330738	Specifically, a mouse paradigm that mimics binge <b>alcohol</b> drinking in humans produced a robust reduction in <strong>BDNF</strong> mRNA levels in the medial PFC (mPFC), which was associated with increased expression of several miRNAs including miR 30a 5p.
+BDNF	addiction	intoxication	25330738	Specifically, a mouse paradigm that mimics <b>binge</b> alcohol drinking in humans produced a robust reduction in <strong>BDNF</strong> mRNA levels in the medial PFC (mPFC), which was associated with increased expression of several miRNAs including miR 30a 5p.
+BDNF	drug	alcohol	25330738	Conversely, inhibition of miR 30a 5p in the mPFC using a Locked Nucleic Acid sequence that targets miR 30a 5p restored <strong>BDNF</strong> levels and decreased excessive <b>alcohol</b> intake.
+BDNF	drug	cocaine	25268928	<b>Cocaine</b> self administration causes signaling deficits in corticostriatal circuitry that are reversed by <strong>BDNF</strong> in early withdrawal.
+BDNF	addiction	withdrawal	25268928	Cocaine self administration causes signaling deficits in corticostriatal circuitry that are reversed by <strong>BDNF</strong> in early <b>withdrawal</b>.
+BDNF	drug	cocaine	25268928	Infusion of brain derived neurotrophic factor (<strong>BDNF</strong>) into the dmPFC immediately following a final session of <b>cocaine</b> self administration blocks the <b>cocaine</b> induced changes in phosphorylation and attenuates relapse to <b>cocaine</b> seeking for as long as three weeks.
+BDNF	addiction	relapse	25268928	Infusion of brain derived neurotrophic factor (<strong>BDNF</strong>) into the dmPFC immediately following a final session of cocaine self administration blocks the cocaine induced changes in phosphorylation and attenuates <b>relapse</b> to cocaine <b>seeking</b> for as long as three weeks.
+BDNF	drug	cocaine	25268928	Infusion of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) into the dmPFC immediately following a final session of <b>cocaine</b> self administration blocks the <b>cocaine</b> induced changes in phosphorylation and attenuates relapse to <b>cocaine</b> seeking for as long as three weeks.
+BDNF	addiction	relapse	25268928	Infusion of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) into the dmPFC immediately following a final session of cocaine self administration blocks the cocaine induced changes in phosphorylation and attenuates <b>relapse</b> to cocaine <b>seeking</b> for as long as three weeks.
+BDNF	drug	cocaine	25268928	The intra dmPFC <strong>BDNF</strong> infusion also prevents <b>cocaine</b> induced deficits in prefronto accumbens glutamatergic transmission that are implicated in <b>cocaine</b> seeking.
+BDNF	addiction	relapse	25268928	The intra dmPFC <strong>BDNF</strong> infusion also prevents cocaine induced deficits in prefronto accumbens glutamatergic transmission that are implicated in cocaine <b>seeking</b>.
+BDNF	drug	cocaine	25268928	Thus, intervention with <strong>BDNF</strong> in the dmPFC during early withdrawal has local and distal effects in target areas that are critical to mediating <b>cocaine</b> induced neuroadaptations that lead to <b>cocaine</b> seeking.
+BDNF	addiction	relapse	25268928	Thus, intervention with <strong>BDNF</strong> in the dmPFC during early withdrawal has local and distal effects in target areas that are critical to mediating cocaine induced neuroadaptations that lead to cocaine <b>seeking</b>.
+BDNF	addiction	withdrawal	25268928	Thus, intervention with <strong>BDNF</strong> in the dmPFC during early <b>withdrawal</b> has local and distal effects in target areas that are critical to mediating cocaine induced neuroadaptations that lead to cocaine seeking.
+BDNF	drug	nicotine	25262572	We aimed to characterize the effects of select comorbid (i.e., cigarette <b>smoking</b>) and premorbid factors (brain derived neurotrophic factor [<strong>BDNF</strong>] genotype [Val66Met rs6265]) on hippocampal volume in an ALC cohort followed longitudinally into extended abstinence.
+BDNF	drug	nicotine	25262572	We aimed to characterize the effects of select comorbid (i.e., cigarette <b>smoking</b>) and premorbid factors (<strong>brain derived neurotrophic factor</strong> [<strong>BDNF</strong>] genotype [Val66Met rs6265]) on hippocampal volume in an ALC cohort followed longitudinally into extended abstinence.
+BDNF	drug	nicotine	25262572	One hundred twenty one adult ALC in treatment (76 <b>smokers</b>, 45 non <b>smokers</b>) and 35 non <b>smoking</b> light drinking controls underwent quantitative magnetic resonance imaging, <strong>BDNF</strong> genotyping, and neurocognitive assessments.
+BDNF	drug	nicotine	25262572	These findings suggest that <strong>BDNF</strong> genotype, but not <b>smoking</b> status or measures of drinking severity, regulate functionally relevant hippocampal volume recovery in abstinent ALC.
+BDNF	drug	opioid	25252306	[Association study of CNR1, GAD1 and <strong>BDNF</strong> polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan].
+BDNF	addiction	dependence	25252306	[Association study of CNR1, GAD1 and <strong>BDNF</strong> polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan].
+BDNF	drug	cannabinoid	25252306	In order to analyze the association of CNR1(<b>Cannabinoid</b> receptor 1), GAD1(Glutamate decarboxylase 1), and <strong>BDNF</strong>(Brain derived neurotrophic factor) polymorphisms with male heroin dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+BDNF	drug	opioid	25252306	In order to analyze the association of CNR1(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and <strong>BDNF</strong>(Brain derived neurotrophic factor) polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+BDNF	addiction	dependence	25252306	In order to analyze the association of CNR1(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and <strong>BDNF</strong>(Brain derived neurotrophic factor) polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+BDNF	drug	cannabinoid	25252306	In order to analyze the association of CNR1(<b>Cannabinoid</b> receptor 1), GAD1(Glutamate decarboxylase 1), and <strong>BDNF</strong>(<strong>Brain derived neurotrophic factor</strong>) polymorphisms with male heroin dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+BDNF	drug	opioid	25252306	In order to analyze the association of CNR1(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and <strong>BDNF</strong>(<strong>Brain derived neurotrophic factor</strong>) polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+BDNF	addiction	dependence	25252306	In order to analyze the association of CNR1(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and <strong>BDNF</strong>(<strong>Brain derived neurotrophic factor</strong>) polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+BDNF	drug	opioid	25252306	A case control study was performed with 8 SNPs from CNR1, GAD1, and <strong>BDNF</strong> genes in 165 <b>heroin</b> dependent males and 170 healthy males of the Dai population.
+BDNF	drug	opioid	25252306	Furthermore, polymorphisms in CNR1 (rs1049353), GAD1 (rs1978340 and rs11542313), and <strong>BDNF</strong> (rs6265 and rs13306221) were associated with <b>heroin</b> dependence in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be <b>heroin</b> dependent.
+BDNF	addiction	dependence	25252306	Furthermore, polymorphisms in CNR1 (rs1049353), GAD1 (rs1978340 and rs11542313), and <strong>BDNF</strong> (rs6265 and rs13306221) were associated with heroin <b>dependence</b> in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be heroin dependent.
+BDNF	drug	psychedelics	25231918	The effect of <b>ketamine</b> on behavioral changes after exposure to TDS was also investigated, and the levels of brain derived neurotrophic factor (<strong>BDNF</strong>) in the hippocampus were measured.
+BDNF	drug	psychedelics	25231918	The effect of <b>ketamine</b> on behavioral changes after exposure to TDS was also investigated, and the levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the hippocampus were measured.
+BDNF	drug	psychedelics	25231918	Furthermore, <b>ketamine</b> normalized the decreased <strong>BDNF</strong> level in the hippocampus in post TDS rats.
+BDNF	drug	psychedelics	25231918	Taken together, these results suggest that <b>ketamine</b> exerts a therapeutic effect on PTSD that might be at least partially mediated by an influence on <strong>BDNF</strong> signaling in the hippocampus.
+BDNF	drug	cocaine	25217125	Thus, agents modifying <strong>BDNF</strong> 5 HT interactions might have therapeutic potential for <b>cocaine</b> dependence by reversing the altered brain structure that underlies relapse after <b>cocaine</b> withdrawal.
+BDNF	addiction	dependence	25217125	Thus, agents modifying <strong>BDNF</strong> 5 HT interactions might have therapeutic potential for cocaine <b>dependence</b> by reversing the altered brain structure that underlies relapse after cocaine withdrawal.
+BDNF	addiction	relapse	25217125	Thus, agents modifying <strong>BDNF</strong> 5 HT interactions might have therapeutic potential for cocaine dependence by reversing the altered brain structure that underlies <b>relapse</b> after cocaine withdrawal.
+BDNF	addiction	withdrawal	25217125	Thus, agents modifying <strong>BDNF</strong> 5 HT interactions might have therapeutic potential for cocaine dependence by reversing the altered brain structure that underlies relapse after cocaine <b>withdrawal</b>.
+BDNF	drug	cocaine	25217125	On the basis of the available literature, the authors propose an interaction between <strong>BDNF</strong> and the serotonergic system in the response to <b>cocaine</b> and during <b>cocaine</b> intake.
+BDNF	drug	cocaine	25217125	Recent studies are beginning to elucidate the role of 5 HT and <strong>BDNF</strong> in <b>cocaine</b> addiction.
+BDNF	addiction	addiction	25217125	Recent studies are beginning to elucidate the role of 5 HT and <strong>BDNF</strong> in cocaine <b>addiction</b>.
+BDNF	addiction	addiction	25217125	Based on the current evidence, the authors believe that <strong>BDNF</strong>, as a modulator of the serotonergic pathway, or 5 HT, as a modulator of the <strong>BDNF</strong> system, represent a valuable target to treat drug <b>addiction</b>, which may yield novel therapeutics in the future.
+BDNF	drug	opioid	25206816	Results suggested that acupuncture at Baihui and Dazhui protected brain neurons against injury in rats with <b>heroin</b> relapse by promoting <strong>brain derived neurotrophic factor</strong> and glial cell line derived neurotrophic factor expression.
+BDNF	addiction	relapse	25206816	Results suggested that acupuncture at Baihui and Dazhui protected brain neurons against injury in rats with heroin <b>relapse</b> by promoting <strong>brain derived neurotrophic factor</strong> and glial cell line derived neurotrophic factor expression.
+BDNF	drug	nicotine	25183693	Association between <b>smoking</b>, <b>nicotine</b> dependence, and <strong>BDNF</strong> Val66Met polymorphism with <strong>BDNF</strong> concentrations in serum.
+BDNF	addiction	dependence	25183693	Association between smoking, nicotine <b>dependence</b>, and <strong>BDNF</strong> Val66Met polymorphism with <strong>BDNF</strong> concentrations in serum.
+BDNF	drug	nicotine	25183693	<b>Nicotine</b> use is associated with the upregulation of brain derived neurotrophic factor (<strong>BDNF</strong>) in serum.
+BDNF	drug	nicotine	25183693	<b>Nicotine</b> use is associated with the upregulation of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in serum.
+BDNF	drug	nicotine	25183693	An association between <b>smoking</b> and the <strong>BDNF</strong> Val(66)Met polymorphism has also been found.
+BDNF	drug	nicotine	25183693	The aim of this study is to examine the levels of serum <strong>BDNF</strong> in never <b>smokers</b>, former <b>smokers</b>, and current <b>smokers</b> with and without <b>nicotine</b> dependence and to examine the interaction of the polymorphism and <b>smoking</b> status with serum <strong>BDNF</strong>.
+BDNF	addiction	dependence	25183693	The aim of this study is to examine the levels of serum <strong>BDNF</strong> in never smokers, former smokers, and current smokers with and without nicotine <b>dependence</b> and to examine the interaction of the polymorphism and smoking status with serum <strong>BDNF</strong>.
+BDNF	drug	nicotine	25183693	We used baseline serum and gene data of <strong>BDNF</strong> on 2,088 participants from the Netherlands Study of Depression and Anxiety (NESDA) to investigate <b>smoking</b> <strong>BDNF</strong> association while controlling for potential confounding variables.
+BDNF	drug	nicotine	25183693	<b>Smokers</b> with and without <b>nicotine</b> dependence had higher levels of serum <strong>BDNF</strong> than former and never <b>smokers</b>.
+BDNF	addiction	dependence	25183693	Smokers with and without nicotine <b>dependence</b> had higher levels of serum <strong>BDNF</strong> than former and never smokers.
+BDNF	drug	nicotine	25183693	<b>Nicotine</b> dependence and number of cigarettes smoked per day did not add to the prediction of serum <strong>BDNF</strong>; however, total number of <b>smoking</b> years was a significant predictor of serum <strong>BDNF</strong>.
+BDNF	addiction	dependence	25183693	Nicotine <b>dependence</b> and number of cigarettes smoked per day did not add to the prediction of serum <strong>BDNF</strong>; however, total number of smoking years was a significant predictor of serum <strong>BDNF</strong>.
+BDNF	drug	nicotine	25183693	There was no association of <strong>BDNF</strong> Val(66)Met, nor an interaction of this polymorphism and <b>smoking</b> status, with serum <strong>BDNF</strong>.
+BDNF	drug	nicotine	25183693	Current <b>smoking</b> and higher number of <b>smoking</b> years are associated with higher levels of serum <strong>BDNF</strong>, and this is independent of the <strong>BDNF</strong> genotype.
+BDNF	drug	nicotine	25183693	<b>Nicotine</b> dependence itself is not associated with a further increase or decrease of serum <strong>BDNF</strong>.
+BDNF	addiction	dependence	25183693	Nicotine <b>dependence</b> itself is not associated with a further increase or decrease of serum <strong>BDNF</strong>.
+BDNF	drug	nicotine	25183693	Longitudinal investigations that address changes in serum <strong>BDNF</strong> in incident <b>smokers</b> and/or in quitters may be useful to understand the association of <b>smoking</b> with <strong>BDNF</strong>.
+BDNF	drug	amphetamine	25168604	An association between <strong>BDNF</strong> Val66Met polymorphism and impulsivity in <b>methamphetamine</b> abusers.
+BDNF	drug	amphetamine	25168604	Recent studies showed an association between a functional polymorphism of <strong>BDNF</strong> gene (Val66Met) and the susceptibility to <b>methamphetamine</b> addiction.
+BDNF	addiction	addiction	25168604	Recent studies showed an association between a functional polymorphism of <strong>BDNF</strong> gene (Val66Met) and the susceptibility to methamphetamine <b>addiction</b>.
+BDNF	drug	amphetamine	25168604	The association of the Val66Met polymorphism of the <strong>BDNF</strong> gene and impulsivity in 138 <b>methamphetamine</b> abusers were assessed using Barratt Impulsivity Scale 11(BIS 11) Chinese version.
+BDNF	drug	amphetamine	25168604	Our findings suggest that the <strong>BDNF</strong> Val66Met gene polymorphism may influence attentional impulsivity in <b>methamphetamine</b> abusers.
+BDNF	drug	amphetamine	25168604	Moreover, the <strong>BDNF</strong> Val66Met gene polymorphism may contribute to onset age of <b>methamphetamine</b> use.
+BDNF	drug	alcohol	25155311	EtOH and nicotine directly administered into the pVTA resulted in alterations in gene expression in the AcbSh (50.8 fold increase in brain derived neurotrophic factor (<strong>BDNF</strong>), 2.4 fold decrease in glial cell line derived neurotrophic factor (GDNF), 10.3 fold increase in vesicular glutamate transporter 1 (Vglut1)) that were not observed following microinjections of equivalent concentrations/doses of <b>ethanol</b> or nicotine.
+BDNF	drug	nicotine	25155311	EtOH and <b>nicotine</b> directly administered into the pVTA resulted in alterations in gene expression in the AcbSh (50.8 fold increase in brain derived neurotrophic factor (<strong>BDNF</strong>), 2.4 fold decrease in glial cell line derived neurotrophic factor (GDNF), 10.3 fold increase in vesicular glutamate transporter 1 (Vglut1)) that were not observed following microinjections of equivalent concentrations/doses of ethanol or <b>nicotine</b>.
+BDNF	drug	alcohol	25155311	EtOH and nicotine directly administered into the pVTA resulted in alterations in gene expression in the AcbSh (50.8 fold increase in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), 2.4 fold decrease in glial cell line derived neurotrophic factor (GDNF), 10.3 fold increase in vesicular glutamate transporter 1 (Vglut1)) that were not observed following microinjections of equivalent concentrations/doses of <b>ethanol</b> or nicotine.
+BDNF	drug	nicotine	25155311	EtOH and <b>nicotine</b> directly administered into the pVTA resulted in alterations in gene expression in the AcbSh (50.8 fold increase in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), 2.4 fold decrease in glial cell line derived neurotrophic factor (GDNF), 10.3 fold increase in vesicular glutamate transporter 1 (Vglut1)) that were not observed following microinjections of equivalent concentrations/doses of ethanol or <b>nicotine</b>.
+BDNF	drug	alcohol	25089150	We investigated the association between serum proBDNF, a precursor of brain derived neurotrophic factor (<strong>BDNF</strong>), and response to fluvoxamine in patients with major depressive disorder (MDD) using the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM IV TR): physically healthy and free of current <b>alcohol</b> or drug abuse, comorbid anxiety, or personality disorders.
+BDNF	drug	alcohol	25089150	We investigated the association between serum proBDNF, a precursor of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), and response to fluvoxamine in patients with major depressive disorder (MDD) using the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM IV TR): physically healthy and free of current <b>alcohol</b> or drug abuse, comorbid anxiety, or personality disorders.
+BDNF	drug	cocaine	25072653	Previously we have shown that <b>cocaine</b> induced increases in brain derived neurotrophic factor (<strong>BDNF</strong>) expression in the medial prefrontal cortex (PFC) is a neuroadaptive mechanism that blunts the reinforcing efficacy of <b>cocaine</b>.
+BDNF	addiction	reward	25072653	Previously we have shown that cocaine induced increases in brain derived neurotrophic factor (<strong>BDNF</strong>) expression in the medial prefrontal cortex (PFC) is a neuroadaptive mechanism that blunts the <b>reinforcing</b> efficacy of cocaine.
+BDNF	drug	cocaine	25072653	Previously we have shown that <b>cocaine</b> induced increases in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression in the medial prefrontal cortex (PFC) is a neuroadaptive mechanism that blunts the reinforcing efficacy of <b>cocaine</b>.
+BDNF	addiction	reward	25072653	Previously we have shown that cocaine induced increases in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression in the medial prefrontal cortex (PFC) is a neuroadaptive mechanism that blunts the <b>reinforcing</b> efficacy of cocaine.
+BDNF	drug	cocaine	25072653	As <strong>BDNF</strong> is known to affect neuronal survival and synaptic plasticity, we tested the hypothesis that abstinence from <b>cocaine</b> self administration would lead to alterations in neuronal morphology and synaptic density in the PFC.
+BDNF	drug	psychedelics	25064020	Serum <strong>brain derived neurotrophic factor</strong> and nerve growth factor decreased in chronic <b>ketamine</b> abusers.
+BDNF	drug	psychedelics	25064020	This study investigated the serum levels of brain derived neurotrophic factor (<strong>BDNF</strong>) and nerve growth factor (NGF) in a group of chronic <b>ketamine</b> abusers in comparison to healthy controls.
+BDNF	drug	psychedelics	25064020	This study investigated the serum levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and nerve growth factor (NGF) in a group of chronic <b>ketamine</b> abusers in comparison to healthy controls.
+BDNF	drug	psychedelics	25064020	The correlations between the serum <strong>BDNF</strong>, NGF level with the subjects' demographic, pattern of <b>ketamine</b> use were also examined.
+BDNF	drug	psychedelics	25064020	Both serum levels of <strong>BDNF</strong> and NGF were significant lower in the <b>ketamine</b> users compared to the healthy control subjects (9.50±6.68 versus 14.37±6.07 ng/ml, p=0.019 for <strong>BDNF</strong>; 1.93±0.80 versus 2.60±1.07 ng/ml, p=0.011 for NGF).
+BDNF	drug	psychedelics	25064020	<strong>BDNF</strong> level was negatively associated with current frequency of <b>ketamine</b> use (r= 0.209, p=0.045).
+BDNF	drug	psychedelics	25064020	Both <strong>BDNF</strong> and NGF serum concentrations were significantly lower among chronic <b>ketamine</b> users than among health controls.
+BDNF	drug	alcohol	25044407	Innate <strong>BDNF</strong> expression is associated with <b>ethanol</b> intake in <b>alcohol</b> preferring AA and <b>alcohol</b> avoiding ANA rats.
+BDNF	drug	alcohol	25044407	We have shown recently that acute administration of <b>ethanol</b> modulates the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in several rat brain areas known to be involved in the development of addiction to <b>ethanol</b> and other drugs of abuse, suggesting that <strong>BDNF</strong> may be a factor contributing to the neuroadaptive changes set in motion by <b>ethanol</b> exposure.
+BDNF	addiction	addiction	25044407	We have shown recently that acute administration of ethanol modulates the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in several rat brain areas known to be involved in the development of <b>addiction</b> to ethanol and other drugs of abuse, suggesting that <strong>BDNF</strong> may be a factor contributing to the neuroadaptive changes set in motion by ethanol exposure.
+BDNF	drug	alcohol	25044407	We have shown recently that acute administration of <b>ethanol</b> modulates the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in several rat brain areas known to be involved in the development of addiction to <b>ethanol</b> and other drugs of abuse, suggesting that <strong>BDNF</strong> may be a factor contributing to the neuroadaptive changes set in motion by <b>ethanol</b> exposure.
+BDNF	addiction	addiction	25044407	We have shown recently that acute administration of ethanol modulates the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in several rat brain areas known to be involved in the development of <b>addiction</b> to ethanol and other drugs of abuse, suggesting that <strong>BDNF</strong> may be a factor contributing to the neuroadaptive changes set in motion by ethanol exposure.
+BDNF	drug	alcohol	25044407	The purpose of the present study was to further clarify the role of <strong>BDNF</strong> in reinforcement from <b>ethanol</b> and in the development of addiction to <b>ethanol</b> by specifying the effect of acute administration of <b>ethanol</b> (1.5 or 3.0 g/kg i.p.)
+BDNF	addiction	addiction	25044407	The purpose of the present study was to further clarify the role of <strong>BDNF</strong> in reinforcement from ethanol and in the development of <b>addiction</b> to ethanol by specifying the effect of acute administration of ethanol (1.5 or 3.0 g/kg i.p.)
+BDNF	addiction	reward	25044407	The purpose of the present study was to further clarify the role of <strong>BDNF</strong> in <b>reinforcement</b> from ethanol and in the development of addiction to ethanol by specifying the effect of acute administration of ethanol (1.5 or 3.0 g/kg i.p.)
+BDNF	drug	alcohol	25044407	on the expression profile of <strong>BDNF</strong> mRNA in the ventral tegmental area and in the terminal areas of the mesolimbic dopamine pathway in the brain of <b>alcohol</b> preferring AA and <b>alcohol</b> avoiding ANA rats, selected for high and low voluntary <b>ethanol</b> intake, respectively.
+BDNF	drug	alcohol	25044407	Furthermore, there was a difference between the AA and ANA lines in the effect of <b>ethanol</b>, the ANA rats showing an increase in <strong>BDNF</strong> mRNA levels while such a change was not seen in AA rats.
+BDNF	drug	alcohol	25044407	These findings suggest that the innate levels of <strong>BDNF</strong> expression may play a role in the mediation of the reinforcing effects of <b>ethanol</b> and in the control of <b>ethanol</b> intake.
+BDNF	addiction	reward	25044407	These findings suggest that the innate levels of <strong>BDNF</strong> expression may play a role in the mediation of the <b>reinforcing</b> effects of ethanol and in the control of ethanol intake.
+BDNF	addiction	withdrawal	25042794	To further investigate the mechanisms underlying these effects, we analyzed the c Fos and brain derived neutrophic factor (<strong>BDNF</strong>) expression during NIC <b>withdrawal</b> and its prevention with BAC.
+BDNF	addiction	withdrawal	25042794	Conversely, <strong>BDNF</strong> expression decreased in the CA1 and CA3 area of the hippocampus, the Hb, and caudate putamen (CPu) during NIC <b>withdrawal</b>.
+BDNF	addiction	withdrawal	25042794	Finally, BAC restored the decreased <strong>BDNF</strong> expression during NIC <b>withdrawal</b> in the CA1, CA3, Hb, and CPu.
+BDNF	addiction	withdrawal	25042794	The results suggest a relationship between BAC's preventive effect of the expression of NIC <b>withdrawal</b> signs, and its ability to restore the changes in c Fos and <strong>BDNF</strong> expression, observed in specific brain areas of NIC withdrawn mice.
+BDNF	drug	alcohol	24993285	<strong>BDNF</strong> SNPs are implicated in comorbid <b>alcohol</b> dependence in schizophrenia but not in <b>alcohol</b> dependent patients without schizophrenia.
+BDNF	addiction	dependence	24993285	<strong>BDNF</strong> SNPs are implicated in comorbid alcohol <b>dependence</b> in schizophrenia but not in alcohol dependent patients without schizophrenia.
+BDNF	drug	alcohol	24993285	The functional <strong>BDNF</strong> single nucleotide polymorphism (SNP) rs6265 has been associated with many disorders including schizophrenia and <b>alcohol</b> dependence.
+BDNF	addiction	dependence	24993285	The functional <strong>BDNF</strong> single nucleotide polymorphism (SNP) rs6265 has been associated with many disorders including schizophrenia and alcohol <b>dependence</b>.
+BDNF	drug	alcohol	24993285	In the replication study, we were able to detect allelic associations between both <strong>BDNF</strong> SNPs and comorbid <b>alcohol</b> dependence (rs6265, P = 0.006; rs7103411, P = 0.014).
+BDNF	addiction	dependence	24993285	In the replication study, we were able to detect allelic associations between both <strong>BDNF</strong> SNPs and comorbid alcohol <b>dependence</b> (rs6265, P = 0.006; rs7103411, P = 0.014).
+BDNF	drug	alcohol	24993285	We conclude that these <strong>BDNF</strong> SNPs play a role in development of comorbid <b>alcohol</b> dependence in schizophrenia while our data do not indicate that they play a role in <b>alcohol</b> dependent patients who do not have schizophrenia.
+BDNF	addiction	dependence	24993285	We conclude that these <strong>BDNF</strong> SNPs play a role in development of comorbid alcohol <b>dependence</b> in schizophrenia while our data do not indicate that they play a role in alcohol dependent patients who do not have schizophrenia.
+BDNF	drug	cocaine	24968785	In the embryonic brains of prenatally <b>cocaine</b> exposed mice, we observed a delay in the tangential migration of GABA neurons to the cerebral cortex as a result of a significant but transient decrease in the expression of the neurotrophin brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	cocaine	24968785	In the embryonic brains of prenatally <b>cocaine</b> exposed mice, we observed a delay in the tangential migration of GABA neurons to the cerebral cortex as a result of a significant but transient decrease in the expression of the neurotrophin <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	cocaine	24968785	In adult prenatally <b>cocaine</b> exposed mice, we observed a behavioral deficit in the recall of an extinguished cue conditioned fear, which was rescued by administration of exogenous recombinant <strong>BDNF</strong> protein directly into the infralimbic cortex of the mPFC, which may result from altered activity driven transcriptional regulation of <strong>BDNF</strong>.
+BDNF	drug	opioid	24949623	In the presence of glia, selective neurotoxic measures were significantly enhanced and interactions with <b>morphine</b> were also augmented, perhaps related to a decreased level of <strong>BDNF</strong>.
+BDNF	addiction	sensitization	24930805	Targeting metabolic (e.g., ketogenic diets) and neurotrophic factors (e.g., decreasing <strong>brain derived neurotrophic factor</strong>) are promising new avenues for diminishing hyperexcitability of the CNS in central <b>sensitization</b> pain patients.
+BDNF	drug	opioid	24853771	Loss of <strong>BDNF</strong> signaling in D1R expressing NAc neurons enhances <b>morphine</b> reward by reducing GABA inhibition.
+BDNF	addiction	reward	24853771	Loss of <strong>BDNF</strong> signaling in D1R expressing NAc neurons enhances morphine <b>reward</b> by reducing GABA inhibition.
+BDNF	drug	opioid	24853771	In the present study, we show that GABAergic activity is selectively modulated in D1 type MSNs of the NAc by signaling of brain derived neurotrophic factor (<strong>BDNF</strong>) and its receptor, tyrosine receptor kinase B (TrkB), and that such adaptations control rewarding responses to <b>morphine</b>.
+BDNF	drug	opioid	24853771	In the present study, we show that GABAergic activity is selectively modulated in D1 type MSNs of the NAc by signaling of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and its receptor, tyrosine receptor kinase B (TrkB), and that such adaptations control rewarding responses to <b>morphine</b>.
+BDNF	drug	opioid	24853771	Together, these data provide evidence for the enhancement of <b>morphine</b> reward through reduction of inhibitory GABAAR responses, an adaptation mediated by <b>morphine</b> induced reduction of <strong>BDNF</strong> TrkB signaling in D1 type MSNs.
+BDNF	addiction	reward	24853771	Together, these data provide evidence for the enhancement of morphine <b>reward</b> through reduction of inhibitory GABAAR responses, an adaptation mediated by morphine induced reduction of <strong>BDNF</strong> TrkB signaling in D1 type MSNs.
+BDNF	drug	amphetamine	24820626	The D1 D2 receptor heteromer, for instance, has been associated with calcium calmodulin kinase IIα, <strong>brain derived neurotrophic factor</strong> and glycogen synthase kinase 3 (GSK 3) signaling, three proteins highly implicated in the regulation of glutamate transmission and synaptic plasticity and which regulate addiction to <b>amphetamine</b>, opioids and cocaine.
+BDNF	drug	cocaine	24820626	The D1 D2 receptor heteromer, for instance, has been associated with calcium calmodulin kinase IIα, <strong>brain derived neurotrophic factor</strong> and glycogen synthase kinase 3 (GSK 3) signaling, three proteins highly implicated in the regulation of glutamate transmission and synaptic plasticity and which regulate addiction to amphetamine, opioids and <b>cocaine</b>.
+BDNF	drug	opioid	24820626	The D1 D2 receptor heteromer, for instance, has been associated with calcium calmodulin kinase IIα, <strong>brain derived neurotrophic factor</strong> and glycogen synthase kinase 3 (GSK 3) signaling, three proteins highly implicated in the regulation of glutamate transmission and synaptic plasticity and which regulate addiction to amphetamine, <b>opioids</b> and cocaine.
+BDNF	addiction	addiction	24820626	The D1 D2 receptor heteromer, for instance, has been associated with calcium calmodulin kinase IIα, <strong>brain derived neurotrophic factor</strong> and glycogen synthase kinase 3 (GSK 3) signaling, three proteins highly implicated in the regulation of glutamate transmission and synaptic plasticity and which regulate <b>addiction</b> to amphetamine, opioids and cocaine.
+BDNF	addiction	withdrawal	24810885	Increased serum <strong>brain derived neurotrophic factor</strong> levels during opiate <b>withdrawal</b>.
+BDNF	addiction	addiction	24810885	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been implicated in the pathophysiology of opiate <b>addiction</b>.
+BDNF	addiction	addiction	24810885	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been implicated in the pathophysiology of opiate <b>addiction</b>.
+BDNF	drug	opioid	24810885	Both increased and decreased serum <strong>BDNF</strong> levels have been reported in <b>heroin</b> addicts.
+BDNF	drug	opioid	24810885	Moreover, the role of <strong>BDNF</strong> in <b>heroin</b> dependent patients during withdrawal has not been studied.
+BDNF	addiction	withdrawal	24810885	Moreover, the role of <strong>BDNF</strong> in heroin dependent patients during <b>withdrawal</b> has not been studied.
+BDNF	drug	opioid	24810885	This study aimed to explore the differences in serum <strong>BDNF</strong> levels of <b>heroin</b> addicts and healthy controls, and investigate the changes of serum <strong>BDNF</strong> levels in <b>heroin</b> addicts at baseline and at one month after <b>heroin</b> cessation.
+BDNF	drug	opioid	24810885	We measured serum <strong>BDNF</strong> levels at baseline (both <b>heroin</b> addicts and healthy controls) and one month after <b>heroin</b> cessation (<b>heroin</b> addicts only).
+BDNF	drug	opioid	24810885	We found that baseline serum <strong>BDNF</strong> levels were significantly higher in <b>heroin</b> addicts compared to controls (F=36.5, p=0.001).
+BDNF	drug	opioid	24810885	There was no difference in serum <strong>BDNF</strong> levels among <b>heroin</b> addicts at baseline and one month after <b>heroin</b> cessation (F=1.101, p=0.301).
+BDNF	addiction	addiction	24810885	These results indicate that <strong>BDNF</strong> may play a critical role in the course of opiate <b>addiction</b> and withdrawal.
+BDNF	addiction	withdrawal	24810885	These results indicate that <strong>BDNF</strong> may play a critical role in the course of opiate addiction and <b>withdrawal</b>.
+BDNF	drug	cocaine	24798661	To address this issue, we exposed laboratory rats to subchronic regimens of heroin or <b>cocaine</b> and tested long term effects on (i) depressive like behaviors, (ii) brain derived neurotrophic factor (<strong>BDNF</strong>) levels in reward related brain regions, and (iii) depressive like behavior following an additional chronic mild stress procedure.
+BDNF	drug	opioid	24798661	To address this issue, we exposed laboratory rats to subchronic regimens of <b>heroin</b> or cocaine and tested long term effects on (i) depressive like behaviors, (ii) brain derived neurotrophic factor (<strong>BDNF</strong>) levels in reward related brain regions, and (iii) depressive like behavior following an additional chronic mild stress procedure.
+BDNF	addiction	reward	24798661	To address this issue, we exposed laboratory rats to subchronic regimens of heroin or cocaine and tested long term effects on (i) depressive like behaviors, (ii) brain derived neurotrophic factor (<strong>BDNF</strong>) levels in <b>reward</b> related brain regions, and (iii) depressive like behavior following an additional chronic mild stress procedure.
+BDNF	drug	cocaine	24798661	To address this issue, we exposed laboratory rats to subchronic regimens of heroin or <b>cocaine</b> and tested long term effects on (i) depressive like behaviors, (ii) <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels in reward related brain regions, and (iii) depressive like behavior following an additional chronic mild stress procedure.
+BDNF	drug	opioid	24798661	To address this issue, we exposed laboratory rats to subchronic regimens of <b>heroin</b> or cocaine and tested long term effects on (i) depressive like behaviors, (ii) <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels in reward related brain regions, and (iii) depressive like behavior following an additional chronic mild stress procedure.
+BDNF	addiction	reward	24798661	To address this issue, we exposed laboratory rats to subchronic regimens of heroin or cocaine and tested long term effects on (i) depressive like behaviors, (ii) <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels in <b>reward</b> related brain regions, and (iii) depressive like behavior following an additional chronic mild stress procedure.
+BDNF	drug	cocaine	24798661	Both <b>cocaine</b> and heroin exposure induced alterations in <strong>BDNF</strong> levels that are similar to those observed in several animal models of depression.
+BDNF	drug	opioid	24798661	Both cocaine and <b>heroin</b> exposure induced alterations in <strong>BDNF</strong> levels that are similar to those observed in several animal models of depression.
+BDNF	drug	cocaine	24798661	Our results demonstrate that short term, subchronic administration of either <b>cocaine</b> or heroin promotes some depressive like behaviors, while inducing alterations in <strong>BDNF</strong> protein levels similar to alterations observed in several animal models of depression.
+BDNF	drug	opioid	24798661	Our results demonstrate that short term, subchronic administration of either cocaine or <b>heroin</b> promotes some depressive like behaviors, while inducing alterations in <strong>BDNF</strong> protein levels similar to alterations observed in several animal models of depression.
+BDNF	drug	alcohol	26501066	Mood Disorders and <strong>BDNF</strong> Relationship with <b>Alcohol</b> Drinking Trajectories among PLWH Receiving Care.
+BDNF	drug	alcohol	26501066	Therefore, the present study was geared toward determining: 1) the rates of mood disorders and its relationship with HAU, and 2) to assess the impact of Brain Derived Neurotrophic Factor (<strong>BDNF</strong>), a well known regulator of <b>alcohol</b> and mood disorders.
+BDNF	drug	alcohol	26501066	Therefore, the present study was geared toward determining: 1) the rates of mood disorders and its relationship with HAU, and 2) to assess the impact of <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>), a well known regulator of <b>alcohol</b> and mood disorders.
+BDNF	drug	alcohol	26501066	Findings suggest that <strong>BDNF</strong> and social support seems to be a logical target as it seems to be the bridge linking mood disorders and <b>alcohol</b> consumption.
+BDNF	drug	cocaine	24760865	Infralimbic <strong>BDNF</strong>/TrkB enhancement of GluN2B currents facilitates extinction of a <b>cocaine</b> conditioned place preference.
+BDNF	drug	opioid	24755993	SNPs in the genes for brain derived neurotrophic factor (<strong>BDNF</strong>), the muscarinic acetylcholine receptor M2 (CHRM2), the dopamine receptor D4 (DRD4) and the μ1 <b>opioid</b> receptor (OPRM1) significantly moderated the impact of treatment condition over time on PA. Genetic variation in the genes for CHRM2 and OPRM1 specifically had an impact on the level of PA following MBCT.
+BDNF	drug	opioid	24755993	SNPs in the genes for <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), the muscarinic acetylcholine receptor M2 (CHRM2), the dopamine receptor D4 (DRD4) and the μ1 <b>opioid</b> receptor (OPRM1) significantly moderated the impact of treatment condition over time on PA. Genetic variation in the genes for CHRM2 and OPRM1 specifically had an impact on the level of PA following MBCT.
+BDNF	drug	cocaine	24752656	We also investigated the effects of <b>cocaine</b> delivery speed on corticostriatal expression of brain derived neurotrophic factor (<strong>BDNF</strong>) and tropomyosin receptor kinase B (TrkB) mRNA.
+BDNF	drug	cocaine	24752656	We also investigated the effects of <b>cocaine</b> delivery speed on corticostriatal expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and tropomyosin receptor kinase B (TrkB) mRNA.
+BDNF	drug	cocaine	24752656	In parallel, only rats self administering rapid <b>cocaine</b> injections had altered <strong>BDNF</strong> and TrkB mRNA levels in corticostriatal regions.
+BDNF	drug	cocaine	24737916	Early life <b>cocaine</b> interferes with <strong>BDNF</strong> mediated behavioral plasticity.
+BDNF	drug	cocaine	24737916	A history of adolescent <b>cocaine</b> exposure, however, occludes the "beneficial" effects of <strong>Bdnf</strong> knockdown.
+BDNF	drug	cocaine	24712995	Brain derived neurotrophic factor (<strong>BDNF</strong>) plays a critical role in plasticity at glutamate synapses and in the effects of repeated <b>cocaine</b> exposure.
+BDNF	drug	cocaine	24712995	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) plays a critical role in plasticity at glutamate synapses and in the effects of repeated <b>cocaine</b> exposure.
+BDNF	drug	cocaine	24712995	We recently showed that intracranial injection of <strong>BDNF</strong> into the rat nucleus accumbens (NAc), a key region for <b>cocaine</b> addiction, rapidly increases α amino 3 hyroxy 5 methyl 4 isoxazole propionic acid receptor (AMPAR) surface expression.
+BDNF	addiction	addiction	24712995	We recently showed that intracranial injection of <strong>BDNF</strong> into the rat nucleus accumbens (NAc), a key region for cocaine <b>addiction</b>, rapidly increases α amino 3 hyroxy 5 methyl 4 isoxazole propionic acid receptor (AMPAR) surface expression.
+BDNF	addiction	withdrawal	24682499	Further, repeated treatment with lobeline or 3 (pyridine 3́ yl) cytisine decreased immobility time in the FST and reduced <b>withdrawal</b> induced increased <strong>BDNF</strong> and p CREB expression in the hippocampus.
+BDNF	drug	nicotine	24682499	Taken together, our results indicate that lobeline attenuated <b>nicotine</b> withdrawal induced depression like behavior likely by targeting brain nAChRs, noradrenergic neurotransmission, and/or hippocampal <strong>BDNF</strong>.
+BDNF	addiction	withdrawal	24682499	Taken together, our results indicate that lobeline attenuated nicotine <b>withdrawal</b> induced depression like behavior likely by targeting brain nAChRs, noradrenergic neurotransmission, and/or hippocampal <strong>BDNF</strong>.
+BDNF	drug	cocaine	24676990	Oxidative stress and <strong>BDNF</strong> as possible markers for the severity of crack <b>cocaine</b> use in early withdrawal.
+BDNF	addiction	withdrawal	24676990	Oxidative stress and <strong>BDNF</strong> as possible markers for the severity of crack cocaine use in early <b>withdrawal</b>.
+BDNF	drug	cocaine	24676990	This study aims to evaluate alteration of TBARS and <strong>BDNF</strong> levels among crack <b>cocaine</b> users during early drug withdrawal and its relationship to severity of drug use.
+BDNF	addiction	withdrawal	24676990	This study aims to evaluate alteration of TBARS and <strong>BDNF</strong> levels among crack cocaine users during early drug <b>withdrawal</b> and its relationship to severity of drug use.
+BDNF	drug	cocaine	24676990	There is a positive correlation between TBARS levels and severity of crack <b>cocaine</b> use (R = 0.304, p = 0.04) and a negative correlation between <strong>BDNF</strong> and severity of crack <b>cocaine</b> use (R =  0.359, p = 0.01) at discharge.
+BDNF	drug	alcohol	24672003	microRNA 206 in rat medial prefrontal cortex regulates <strong>BDNF</strong> expression and <b>alcohol</b> drinking.
+BDNF	drug	alcohol	24672003	Viral mediated overexpression of miR 206 in the mPFC of nondependent rats reproduced the escalation of <b>alcohol</b> self administration seen following a history of dependence and significantly inhibited <strong>BDNF</strong> expression.
+BDNF	addiction	addiction	24672003	Viral mediated overexpression of miR 206 in the mPFC of nondependent rats reproduced the <b>escalation</b> of alcohol self administration seen following a history of dependence and significantly inhibited <strong>BDNF</strong> expression.
+BDNF	addiction	dependence	24672003	Viral mediated overexpression of miR 206 in the mPFC of nondependent rats reproduced the escalation of alcohol self administration seen following a history of <b>dependence</b> and significantly inhibited <strong>BDNF</strong> expression.
+BDNF	drug	alcohol	24672003	In conclusion, recruitment of miR 206 in the mPFC contributes to escalated <b>alcohol</b> consumption following a history of dependence, with <strong>BDNF</strong> as a possible mediator of its action.
+BDNF	addiction	dependence	24672003	In conclusion, recruitment of miR 206 in the mPFC contributes to escalated alcohol consumption following a history of <b>dependence</b>, with <strong>BDNF</strong> as a possible mediator of its action.
+BDNF	drug	amphetamine	24650575	<b>Methamphetamine</b> self administration attenuates hippocampal serotonergic deficits: role of <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	amphetamine	24650575	The current study investigated changes in hippocampal <strong>BDNF</strong> protein and SERT function in rats exposed to saline or <b>METH</b> self administration prior to a binge exposure to <b>METH</b> or saline.
+BDNF	addiction	intoxication	24650575	The current study investigated changes in hippocampal <strong>BDNF</strong> protein and SERT function in rats exposed to saline or METH self administration prior to a <b>binge</b> exposure to METH or saline.
+BDNF	drug	amphetamine	24650575	Results revealed that <b>METH</b> self administration increased hippocampal mature <strong>BDNF</strong> (mBDNF) immunoreactivity compared to saline treated rats as assessed 24 h after the start of the last session.
+BDNF	drug	alcohol	24584330	<b>Ethanol</b> intake increased the expression of RACK1 and brain derived neurotrophic factor (<strong>BDNF</strong>) in both WT and D3R( / ); in WT there was also a robust overexpression of D3R.
+BDNF	drug	alcohol	24584330	<b>Ethanol</b> intake increased the expression of RACK1 and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in both WT and D3R( / ); in WT there was also a robust overexpression of D3R.
+BDNF	drug	alcohol	24584330	Thus, increased expression of D3R associated with activation of RACK1/<strong>BDNF</strong> seems to operate as a reinforcing mechanism in voluntary <b>ethanol</b> intake.
+BDNF	addiction	reward	24584330	Thus, increased expression of D3R associated with activation of RACK1/<strong>BDNF</strong> seems to operate as a <b>reinforcing</b> mechanism in voluntary ethanol intake.
+BDNF	drug	alcohol	24584330	Indeed, blockade of the <strong>BDNF</strong> pathway by the TrkB selective antagonist ANA 12 reversed chronic stable <b>ethanol</b> intake and strongly decreased the striatal expression of D3R.
+BDNF	drug	opioid	24583192	Fifteen weeks of cafeteria diet suppressed μ <b>opioid</b> and CB1 receptor mRNA in the VTA, but elevated amygdala GR, and 6 weeks of cafeteria diet reduced <strong>BDNF</strong>, compared to chow fed rats.
+BDNF	drug	opioid	24527041	Also the acupuncture stimulation significantly suppressed the increase in the hypothalamic corticotropin releasing factor (CRF) expression, the decrease in the tyrosine hydroxylase expression in the locus coeruleus, and the decrease in the hippocampal <strong>brain derived neurotrophic factor</strong> mRNA expression, induced by repeated injection of <b>morphine</b>.
+BDNF	addiction	aversion	24523535	<strong>BDNF</strong> deletion or TrkB impairment in amygdala inhibits both appetitive and <b>aversive</b> learning.
+BDNF	addiction	aversion	24523535	Although the necessity of amygdala <strong>bdnf</strong> expression and TrkB activation for associative learning within <b>aversive</b> contexts has been explored, it is unclear to what extent this interaction is involved in appetitive learning.
+BDNF	addiction	aversion	24523535	Together, these data suggest that <strong>BDNF</strong> TrkB signaling is critical for amygdala dependent learning of both appetitive and <b>aversive</b> emotional memories.
+BDNF	drug	amphetamine	24440750	Elevated <strong>BDNF</strong> mRNA expression in the medial prefrontal cortex after d <b>amphetamine</b> reinstated conditioned place preference in rats.
+BDNF	addiction	addiction	24440750	Drug <b>addiction</b> behavior that is established and maintained by psychostimulants has been shown to be associated with the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in the mesolimbic dopamine (DA) system.
+BDNF	addiction	addiction	24440750	Drug <b>addiction</b> behavior that is established and maintained by psychostimulants has been shown to be associated with the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the mesolimbic dopamine (DA) system.
+BDNF	addiction	relapse	24440750	To fill this gap, the present study was designed to test whether <strong>BDNF</strong> mRNA expression levels in the DA terminal regions were changed specifically by d AMP induced conditioned place preference (CPP) followed by drug primed <b>reinstatement</b>.
+BDNF	addiction	reward	24440750	To fill this gap, the present study was designed to test whether <strong>BDNF</strong> mRNA expression levels in the DA terminal regions were changed specifically by d AMP induced conditioned place preference (<b>CPP</b>) followed by drug primed reinstatement.
+BDNF	addiction	relapse	24440750	The <strong>BDNF</strong> mRNA levels in the selected brain areas were determined by real time polymerase chain reaction (PCR) after the CPP and <b>reinstatement</b>.
+BDNF	addiction	reward	24440750	The <strong>BDNF</strong> mRNA levels in the selected brain areas were determined by real time polymerase chain reaction (PCR) after the <b>CPP</b> and reinstatement.
+BDNF	addiction	relapse	24440750	The <strong>BDNF</strong> mRNA level in the medial prefrontal cortex (mPFC) was significantly increased after the <b>reinstatement</b>, but not the CPP test.
+BDNF	addiction	reward	24440750	The <strong>BDNF</strong> mRNA level in the medial prefrontal cortex (mPFC) was significantly increased after the reinstatement, but not the <b>CPP</b> test.
+BDNF	addiction	relapse	24440750	And, none of the other four assessed brain areas showed any change in <strong>BDNF</strong> mRNA level after d AMP CPP or <b>reinstatement</b>.
+BDNF	addiction	reward	24440750	And, none of the other four assessed brain areas showed any change in <strong>BDNF</strong> mRNA level after d AMP <b>CPP</b> or reinstatement.
+BDNF	addiction	relapse	24440750	These findings support the notion that <strong>BDNF</strong> is involved in drug <b>seeking</b> behavior and indicate that d AMP <b>reinstatement</b> after extinction may be linked to an increase in <strong>BDNF</strong> mRNA expression in the mPFC.
+BDNF	addiction	intoxication	24416161	In addition, we measured the effects of <b>binge</b> EtOH exposure on hippocampal Drosha and Dicer mRNA levels, as well as the putative miR target genes, <strong>BDNF</strong> and SIRT1.
+BDNF	drug	amphetamine	24407463	The purpose of the present study was to investigate the individual effects of MS and <b>methamphetamine</b> administration during adolescence and the combined effects of both stressors on brain derived neurotrophic factor (<strong>BDNF</strong>) and nerve growth factor (NGF) levels in the dorsal and ventral hippocampus (HC) in adulthood.
+BDNF	drug	amphetamine	24407463	The purpose of the present study was to investigate the individual effects of MS and <b>methamphetamine</b> administration during adolescence and the combined effects of both stressors on <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and nerve growth factor (NGF) levels in the dorsal and ventral hippocampus (HC) in adulthood.
+BDNF	drug	amphetamine	24407463	<b>Methamphetamine</b> administration (1 mg/kg, daily from postnatal day (PND) 33 to 36 and from PND 39 to 42), MS and the combination of the two stressors resulted in decreased <strong>BDNF</strong> levels in both the dorsal and ventral HC.
+BDNF	addiction	addiction	24369067	The striatal <strong>BDNF</strong>/TrkB system is thereby implicated in many physiologic and pathophysiologic processes, the latter including mood disorders, <b>addiction</b>, and Huntington's disease.
+BDNF	drug	benzodiazepine	24367698	Alterations in <strong>brain derived neurotrophic factor</strong> in the mouse hippocampus following acute but not repeated <b>benzodiazepine</b> treatment.
+BDNF	drug	benzodiazepine	24367698	administration of both <b>triazolam</b> (0.03 mg/kg) and ZP (1.0 mg/kg) decreased <strong>BDNF</strong> protein levels within the HIP relative to vehicle, without any effect on c Fos.
+BDNF	drug	amphetamine	24354924	In this study, we examined the necessity for <strong>BDNF</strong> TrkB signaling in the NAc shell during social defeat stress induced cross sensitization to <b>amphetamine</b>.
+BDNF	addiction	sensitization	24354924	In this study, we examined the necessity for <strong>BDNF</strong> TrkB signaling in the NAc shell during social defeat stress induced cross <b>sensitization</b> to amphetamine.
+BDNF	addiction	sensitization	24354924	These findings indicated that <strong>BDNF</strong> TrkB signaling in the NAc shell was required for social defeat stress induced cross <b>sensitization</b>.
+BDNF	addiction	sensitization	24354924	NAc TrkB <strong>BDNF</strong> signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc ΔFosB accumulation that could trigger cross <b>sensitization</b> after social defeat stress.
+BDNF	drug	nicotine	24301752	<strong>BDNF</strong> Val66Met polymorphism and serum concentrations of <strong>BDNF</strong> with <b>smoking</b> in Thai males.
+BDNF	drug	nicotine	24301752	Many studies have suggested that brain derived neurotrophic factor (<strong>BDNF</strong>) is involved in the reward system of addiction, and that <b>nicotine</b> may induce alterations in <strong>BDNF</strong> gene expression and its protein level within the mesocorticolimbic system.
+BDNF	addiction	addiction	24301752	Many studies have suggested that brain derived neurotrophic factor (<strong>BDNF</strong>) is involved in the reward system of <b>addiction</b>, and that nicotine may induce alterations in <strong>BDNF</strong> gene expression and its protein level within the mesocorticolimbic system.
+BDNF	addiction	reward	24301752	Many studies have suggested that brain derived neurotrophic factor (<strong>BDNF</strong>) is involved in the <b>reward</b> system of addiction, and that nicotine may induce alterations in <strong>BDNF</strong> gene expression and its protein level within the mesocorticolimbic system.
+BDNF	drug	nicotine	24301752	Many studies have suggested that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is involved in the reward system of addiction, and that <b>nicotine</b> may induce alterations in <strong>BDNF</strong> gene expression and its protein level within the mesocorticolimbic system.
+BDNF	addiction	addiction	24301752	Many studies have suggested that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is involved in the reward system of <b>addiction</b>, and that nicotine may induce alterations in <strong>BDNF</strong> gene expression and its protein level within the mesocorticolimbic system.
+BDNF	addiction	reward	24301752	Many studies have suggested that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is involved in the <b>reward</b> system of addiction, and that nicotine may induce alterations in <strong>BDNF</strong> gene expression and its protein level within the mesocorticolimbic system.
+BDNF	drug	nicotine	24301752	We investigated the <strong>BDNF</strong> levels and biochemical hematological parameters of <b>smoker</b> and non <b>smoker</b> groups, and examined the association of the Val66Met <strong>BDNF</strong> gene polymorphism with <strong>BDNF</strong> serum levels and cigarette <b>smoking</b>.
+BDNF	drug	nicotine	24301752	The <b>smoker</b> group had significantly higher serum <strong>BDNF</strong> levels than the non <b>smoker</b> group (8.3 vs 6.5 ng/mL, P < 0.05).
+BDNF	drug	nicotine	24301752	The <strong>BDNF</strong> Val66Met polymorphism was not significantly associated with the <b>smoking</b> status of the Thai males in this study.
+BDNF	drug	nicotine	24301752	Cigarette <b>smoking</b> may be one factor that determines the serum <strong>BDNF</strong> level, but the <strong>BDNF</strong> Val66Met polymorphism probably does not influence susceptibility to <b>smoking</b> among Thai males.
+BDNF	addiction	addiction	24279859	<strong>BDNF</strong> rs6265 polymorphism and drug <b>addiction</b>: a systematic review and meta analysis.
+BDNF	addiction	dependence	24279859	A majority of studies have shown a link between the common functional rs6265 polymorphism of the <strong>BDNF</strong> gene and susceptibility to drug <b>dependence</b>.
+BDNF	drug	alcohol	24250203	Expression of cFos and <strong>brain derived neurotrophic factor</strong> in cortex and hippocampus of <b>ethanol</b> withdrawn male and female rats.
+BDNF	drug	alcohol	24250203	To map areas of brain activation (cFos) alongside changes in levels of brain derived neurotrophic factor (<strong>BDNF</strong>) to provide insights into neuronal mechanisms contributing to previously observed sex differences in behavioral measures of <b>ethanol</b> withdrawal (EW).
+BDNF	addiction	withdrawal	24250203	To map areas of brain activation (cFos) alongside changes in levels of brain derived neurotrophic factor (<strong>BDNF</strong>) to provide insights into neuronal mechanisms contributing to previously observed sex differences in behavioral measures of ethanol <b>withdrawal</b> (EW).
+BDNF	drug	alcohol	24250203	To map areas of brain activation (cFos) alongside changes in levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) to provide insights into neuronal mechanisms contributing to previously observed sex differences in behavioral measures of <b>ethanol</b> withdrawal (EW).
+BDNF	addiction	withdrawal	24250203	To map areas of brain activation (cFos) alongside changes in levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) to provide insights into neuronal mechanisms contributing to previously observed sex differences in behavioral measures of ethanol <b>withdrawal</b> (EW).
+BDNF	drug	alcohol	24239693	Hippocampal <strong>Bdnf</strong> mRNA increased in response to exercise and decreased in response to <b>ethanol</b>.
+BDNF	addiction	reward	24239693	These data suggest an important role for this pathway, and especially for <strong>Bdnf</strong> and Slc18a2 in regulating <b>hedonic</b> substitution.
+BDNF	drug	cannabinoid	24219803	Dominant negative DISC1 mutant mice display specific social behaviour deficits and aberration in <strong>BDNF</strong> and <b>cannabinoid</b> receptor expression.
+BDNF	drug	cannabinoid	24219803	Western blot was employed to measure <strong>BDNF</strong> receptor (TrkB) and <b>cannabinoid</b> receptor CB1.
+BDNF	drug	cocaine	24173624	Dose dependent effects of wheel running on <b>cocaine</b> seeking and prefrontal cortex <strong>Bdnf</strong> exon IV expression in rats.
+BDNF	addiction	relapse	24173624	Dose dependent effects of wheel running on cocaine <b>seeking</b> and prefrontal cortex <strong>Bdnf</strong> exon IV expression in rats.
+BDNF	drug	cocaine	24173624	In this study, we examined the dose dependent effects of wheel running, an animal model of exercise, during abstinence on subsequent <b>cocaine</b> seeking and associated changes in prefrontal cortex (PFC) brain derived neurotrophic factor (<strong>Bdnf</strong>) exon IV expression, a marker of epigenetic regulation implicated in <b>cocaine</b> relapse and known to be regulated by exercise.
+BDNF	addiction	relapse	24173624	In this study, we examined the dose dependent effects of wheel running, an animal model of exercise, during abstinence on subsequent cocaine <b>seeking</b> and associated changes in prefrontal cortex (PFC) brain derived neurotrophic factor (<strong>Bdnf</strong>) exon IV expression, a marker of epigenetic regulation implicated in cocaine <b>relapse</b> and known to be regulated by exercise.
+BDNF	drug	cocaine	24173624	In this study, we examined the dose dependent effects of wheel running, an animal model of exercise, during abstinence on subsequent <b>cocaine</b> seeking and associated changes in prefrontal cortex (PFC) <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) exon IV expression, a marker of epigenetic regulation implicated in <b>cocaine</b> relapse and known to be regulated by exercise.
+BDNF	addiction	relapse	24173624	In this study, we examined the dose dependent effects of wheel running, an animal model of exercise, during abstinence on subsequent cocaine <b>seeking</b> and associated changes in prefrontal cortex (PFC) <strong>brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) exon IV expression, a marker of epigenetic regulation implicated in cocaine <b>relapse</b> and known to be regulated by exercise.
+BDNF	drug	cocaine	24173624	<b>Cocaine</b> increased <strong>Bdnf</strong> exon IV expression, and wheel running dose dependently attenuated this increase, with complete blockade in rats given 6 h/day access.
+BDNF	drug	psychedelics	24158501	We have demonstrated that <b>MDMA</b> caused an increase in brain derived neurotrophic factor (<strong>BDNF</strong>) expression.
+BDNF	drug	psychedelics	24158501	We have demonstrated that <b>MDMA</b> caused an increase in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression.
+BDNF	drug	psychedelics	24158501	This study provides support for the conclusion that binge administration of <b>MDMA</b>, known to be associated to neurotoxic damage of hippocampal serotonergic terminals, increases <strong>BDNF</strong> expression and stimulates synaptic plasticity when associated with training.
+BDNF	addiction	intoxication	24158501	This study provides support for the conclusion that <b>binge</b> administration of MDMA, known to be associated to neurotoxic damage of hippocampal serotonergic terminals, increases <strong>BDNF</strong> expression and stimulates synaptic plasticity when associated with training.
+BDNF	addiction	relapse	24109187	<strong>BDNF</strong> also induces drug related behaviors like self administration and <b>relapse</b>.
+BDNF	drug	alcohol	24103311	Reversal of deficits in dendritic spines, <strong>BDNF</strong> and Arc expression in the amygdala during <b>alcohol</b> dependence by HDAC inhibitor treatment.
+BDNF	addiction	dependence	24103311	Reversal of deficits in dendritic spines, <strong>BDNF</strong> and Arc expression in the amygdala during alcohol <b>dependence</b> by HDAC inhibitor treatment.
+BDNF	drug	alcohol	24103311	Development of anxiety like behaviours during <b>ethanol</b> withdrawal has been correlated with increased histone deacetylase (HDAC) activity and decreased brain derived neurotrophic factor (<strong>BDNF</strong>) and activity regulated cytoskeleton associated protein (Arc) gene expression in the amygdala.
+BDNF	addiction	withdrawal	24103311	Development of anxiety like behaviours during ethanol <b>withdrawal</b> has been correlated with increased histone deacetylase (HDAC) activity and decreased brain derived neurotrophic factor (<strong>BDNF</strong>) and activity regulated cytoskeleton associated protein (Arc) gene expression in the amygdala.
+BDNF	drug	alcohol	24103311	Development of anxiety like behaviours during <b>ethanol</b> withdrawal has been correlated with increased histone deacetylase (HDAC) activity and decreased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and activity regulated cytoskeleton associated protein (Arc) gene expression in the amygdala.
+BDNF	addiction	withdrawal	24103311	Development of anxiety like behaviours during ethanol <b>withdrawal</b> has been correlated with increased histone deacetylase (HDAC) activity and decreased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and activity regulated cytoskeleton associated protein (Arc) gene expression in the amygdala.
+BDNF	drug	alcohol	24103311	In this study we used the HDAC inhibitor trichostatin A (TSA) to determine whether HDAC inhibition could prevent <b>ethanol</b> withdrawal induced deficits in dendritic spine density (DSD), <strong>BDNF</strong> or Arc expression in the amygdala of rats.
+BDNF	addiction	withdrawal	24103311	In this study we used the HDAC inhibitor trichostatin A (TSA) to determine whether HDAC inhibition could prevent ethanol <b>withdrawal</b> induced deficits in dendritic spine density (DSD), <strong>BDNF</strong> or Arc expression in the amygdala of rats.
+BDNF	drug	alcohol	24103311	It was found that decreased <strong>BDNF</strong> and Arc expression in the central (CeA) and medial nucleus of amygdala (MeA), observed during withdrawal after chronic <b>ethanol</b> exposure, were normalized following acute TSA treatment.
+BDNF	addiction	withdrawal	24103311	It was found that decreased <strong>BDNF</strong> and Arc expression in the central (CeA) and medial nucleus of amygdala (MeA), observed during <b>withdrawal</b> after chronic ethanol exposure, were normalized following acute TSA treatment.
+BDNF	drug	alcohol	24103311	Taken together, these findings demonstrate that correcting the deficits in histone acetylation through TSA treatment also amends downstream synaptic plasticity related deficits such as <strong>BDNF</strong> and Arc expression, and DSD in the CeA and MeA as well as attenuates anxiety like behaviours in rats during withdrawal after chronic <b>ethanol</b> exposure.
+BDNF	addiction	withdrawal	24103311	Taken together, these findings demonstrate that correcting the deficits in histone acetylation through TSA treatment also amends downstream synaptic plasticity related deficits such as <strong>BDNF</strong> and Arc expression, and DSD in the CeA and MeA as well as attenuates anxiety like behaviours in rats during <b>withdrawal</b> after chronic ethanol exposure.
+BDNF	drug	alcohol	24076087	Chronic binge like <b>alcohol</b> consumption in adolescence causes depression like symptoms possibly mediated by the effects of <strong>BDNF</strong> on neurogenesis.
+BDNF	addiction	intoxication	24076087	Chronic <b>binge</b> like alcohol consumption in adolescence causes depression like symptoms possibly mediated by the effects of <strong>BDNF</strong> on neurogenesis.
+BDNF	drug	alcohol	24076087	Here we investigated whether changes in neurogenesis and brain derived neurotrophic factor (<strong>BDNF</strong>) expression are possible mechanisms involved in the depression like symptom during the withdrawal/abstinence period after chronic binge pattern <b>alcohol</b> consumption given the limited number of studies addressing the link between these factors in the adolescent brain.
+BDNF	addiction	intoxication	24076087	Here we investigated whether changes in neurogenesis and brain derived neurotrophic factor (<strong>BDNF</strong>) expression are possible mechanisms involved in the depression like symptom during the withdrawal/abstinence period after chronic <b>binge</b> pattern alcohol consumption given the limited number of studies addressing the link between these factors in the adolescent brain.
+BDNF	addiction	withdrawal	24076087	Here we investigated whether changes in neurogenesis and brain derived neurotrophic factor (<strong>BDNF</strong>) expression are possible mechanisms involved in the depression like symptom during the <b>withdrawal</b>/abstinence period after chronic binge pattern alcohol consumption given the limited number of studies addressing the link between these factors in the adolescent brain.
+BDNF	drug	alcohol	24076087	Here we investigated whether changes in neurogenesis and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression are possible mechanisms involved in the depression like symptom during the withdrawal/abstinence period after chronic binge pattern <b>alcohol</b> consumption given the limited number of studies addressing the link between these factors in the adolescent brain.
+BDNF	addiction	intoxication	24076087	Here we investigated whether changes in neurogenesis and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression are possible mechanisms involved in the depression like symptom during the withdrawal/abstinence period after chronic <b>binge</b> pattern alcohol consumption given the limited number of studies addressing the link between these factors in the adolescent brain.
+BDNF	addiction	withdrawal	24076087	Here we investigated whether changes in neurogenesis and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression are possible mechanisms involved in the depression like symptom during the <b>withdrawal</b>/abstinence period after chronic binge pattern alcohol consumption given the limited number of studies addressing the link between these factors in the adolescent brain.
+BDNF	drug	alcohol	24076087	Our data showed that: (1) self administration of <b>alcohol</b> in a binge like pattern causes inebriation as defined by the National Institute on <b>Alcohol</b> Abuse and <b>Alcoholism</b> and this pattern of <b>alcohol</b> exposure is associated with the development of a depression like symptom; (2) no significant difference in blood <b>alcohol</b> levels between the two <b>ethanol</b> groups; and (3) chronic binge drinking resulted in the development of a depressive phenotype, decreased survival and neuronal differentiation of neural progenitor cells in the hippocampus, and decreased <strong>BDNF</strong> effect during the withdrawal period.
+BDNF	addiction	intoxication	24076087	Our data showed that: (1) self administration of alcohol in a <b>binge</b> like pattern causes inebriation as defined by the National Institute on Alcohol Abuse and Alcoholism and this pattern of alcohol exposure is associated with the development of a depression like symptom; (2) no significant difference in blood alcohol levels between the two ethanol groups; and (3) chronic <b>binge</b> drinking resulted in the development of a depressive phenotype, decreased survival and neuronal differentiation of neural progenitor cells in the hippocampus, and decreased <strong>BDNF</strong> effect during the withdrawal period.
+BDNF	addiction	withdrawal	24076087	Our data showed that: (1) self administration of alcohol in a binge like pattern causes inebriation as defined by the National Institute on Alcohol Abuse and Alcoholism and this pattern of alcohol exposure is associated with the development of a depression like symptom; (2) no significant difference in blood alcohol levels between the two ethanol groups; and (3) chronic binge drinking resulted in the development of a depressive phenotype, decreased survival and neuronal differentiation of neural progenitor cells in the hippocampus, and decreased <strong>BDNF</strong> effect during the <b>withdrawal</b> period.
+BDNF	drug	alcohol	24076087	But the most important finding in our study is that augmenting <strong>BDNF</strong> actions through the use of tyrosine kinase B (TrkB, a <strong>BDNF</strong> receptor) agonist restored neurogenesis and abolished the <b>alcohol</b> induced anhedonia and despair behaviors seen during the withdrawal/abstinence period.
+BDNF	addiction	withdrawal	24076087	But the most important finding in our study is that augmenting <strong>BDNF</strong> actions through the use of tyrosine kinase B (TrkB, a <strong>BDNF</strong> receptor) agonist restored neurogenesis and abolished the alcohol induced anhedonia and despair behaviors seen during the <b>withdrawal</b>/abstinence period.
+BDNF	drug	alcohol	24076087	Our results suggest that <strong>BDNF</strong> might be a molecule that can be targeted for interventions in <b>alcoholism</b> depression co incidence.
+BDNF	drug	cocaine	24067327	Increase in <strong>brain derived neurotrophic factor</strong> expression in early crack <b>cocaine</b> withdrawal.
+BDNF	addiction	withdrawal	24067327	Increase in <strong>brain derived neurotrophic factor</strong> expression in early crack cocaine <b>withdrawal</b>.
+BDNF	addiction	relapse	24067327	Recent reports suggest that brain derived neurotrophic factor (<strong>BDNF</strong>) could be a biomarker for <b>relapse</b>, drug <b>craving</b> and withdrawal severity.
+BDNF	addiction	withdrawal	24067327	Recent reports suggest that brain derived neurotrophic factor (<strong>BDNF</strong>) could be a biomarker for relapse, drug craving and <b>withdrawal</b> severity.
+BDNF	addiction	relapse	24067327	Recent reports suggest that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) could be a biomarker for <b>relapse</b>, drug <b>craving</b> and withdrawal severity.
+BDNF	addiction	withdrawal	24067327	Recent reports suggest that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) could be a biomarker for relapse, drug craving and <b>withdrawal</b> severity.
+BDNF	drug	cocaine	24067327	In particular, elevated <strong>BDNF</strong> levels among former <b>cocaine</b> users have been associated with higher rates of relapse in 90 d. However, no data are available on <strong>BDNF</strong> levels at baseline and during crack <b>cocaine</b> withdrawal.
+BDNF	addiction	relapse	24067327	In particular, elevated <strong>BDNF</strong> levels among former cocaine users have been associated with higher rates of <b>relapse</b> in 90 d. However, no data are available on <strong>BDNF</strong> levels at baseline and during crack cocaine withdrawal.
+BDNF	addiction	withdrawal	24067327	In particular, elevated <strong>BDNF</strong> levels among former cocaine users have been associated with higher rates of relapse in 90 d. However, no data are available on <strong>BDNF</strong> levels at baseline and during crack cocaine <b>withdrawal</b>.
+BDNF	drug	cocaine	24067327	This study evaluated <strong>BDNF</strong> among crack <b>cocaine</b> users during inpatient treatment, before and after withdrawal, vs. healthy controls.
+BDNF	addiction	withdrawal	24067327	This study evaluated <strong>BDNF</strong> among crack cocaine users during inpatient treatment, before and after <b>withdrawal</b>, vs. healthy controls.
+BDNF	drug	cocaine	24067327	Our findings show that <strong>BDNF</strong> levels increase during early crack <b>cocaine</b> withdrawal, at an inverse correlation with number of crack rocks used in the last 30 d and years of crack use.
+BDNF	addiction	withdrawal	24067327	Our findings show that <strong>BDNF</strong> levels increase during early crack cocaine <b>withdrawal</b>, at an inverse correlation with number of crack rocks used in the last 30 d and years of crack use.
+BDNF	drug	alcohol	24061482	Our primary interest is the examination of how regions that receive BF cholinergic projections are influenced by short term <b>ethanol</b> exposure through alterations in the mRNA levels of neurotrophic factors [nerve growth factor/TrkA, <strong>brain derived neurotrophic factor</strong>/TrkB, and glial derived neurotrophic factor (GDNF)/GDNF family receptor α1].
+BDNF	drug	nicotine	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, CHRNB2, <strong>BDNF</strong>, and NTRK2 associated with <b>nicotine</b> dependence in the Study of Addiction: Genetics and Environment sample, suggesting the biological role of these genes in <b>nicotine</b> dependence development.
+BDNF	addiction	addiction	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, CHRNB2, <strong>BDNF</strong>, and NTRK2 associated with nicotine dependence in the Study of <b>Addiction</b>: Genetics and Environment sample, suggesting the biological role of these genes in nicotine dependence development.
+BDNF	addiction	dependence	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, CHRNB2, <strong>BDNF</strong>, and NTRK2 associated with nicotine <b>dependence</b> in the Study of Addiction: Genetics and Environment sample, suggesting the biological role of these genes in nicotine <b>dependence</b> development.
+BDNF	drug	opioid	24055683	Gene expression for brain derived neurotrophic factor (<strong>BDNF</strong>), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ <b>opioid</b> receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of <b>morphine</b> exposure, withdrawal and post withdrawal stress.
+BDNF	addiction	withdrawal	24055683	Gene expression for brain derived neurotrophic factor (<strong>BDNF</strong>), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ opioid receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of morphine exposure, <b>withdrawal</b> and post <b>withdrawal</b> stress.
+BDNF	drug	opioid	24055683	Gene expression for <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ <b>opioid</b> receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of <b>morphine</b> exposure, withdrawal and post withdrawal stress.
+BDNF	addiction	withdrawal	24055683	Gene expression for <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ opioid receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of morphine exposure, <b>withdrawal</b> and post <b>withdrawal</b> stress.
+BDNF	drug	opioid	24055683	Expression levels of <strong>BDNF</strong>, TrkB and CRF R1 mRNA were decreased during both <b>morphine</b> exposure and following 7days of withdrawal.
+BDNF	addiction	withdrawal	24055683	Expression levels of <strong>BDNF</strong>, TrkB and CRF R1 mRNA were decreased during both morphine exposure and following 7days of <b>withdrawal</b>.
+BDNF	drug	cocaine	24051573	Serum <strong>brain derived neurotrophic factor</strong> levels and <b>cocaine</b> induced transient psychotic symptoms.
+BDNF	drug	cocaine	24051573	Improvements in depression (Beck Depression Inventory, BDI, p = 0.003) and withdrawal symptoms (<b>Cocaine</b> Selective Severity Assessment, CSSA, p = 0.013) show a significant positive correlation with serum <strong>BDNF</strong> levels in the non CIP group, whereas no correlation between the same variables was found in the CIP group.
+BDNF	addiction	withdrawal	24051573	Improvements in depression (Beck Depression Inventory, BDI, p = 0.003) and <b>withdrawal</b> symptoms (Cocaine Selective Severity Assessment, CSSA, p = 0.013) show a significant positive correlation with serum <strong>BDNF</strong> levels in the non CIP group, whereas no correlation between the same variables was found in the CIP group.
+BDNF	drug	cocaine	24051573	This study suggests that <strong>BDNF</strong> plays a role in the transient psychotic symptoms associated with <b>cocaine</b> consumption.
+BDNF	drug	cocaine	24051573	In the non CIP group, the increase in serum <strong>BDNF</strong> appears to be driven by the effects of chronic <b>cocaine</b> consumption and withdrawal.
+BDNF	addiction	withdrawal	24051573	In the non CIP group, the increase in serum <strong>BDNF</strong> appears to be driven by the effects of chronic cocaine consumption and <b>withdrawal</b>.
+BDNF	drug	amphetamine	23934209	Several lines of evidence suggest a role for brain derived neurotrophic factor (<strong>BDNF</strong>) and its specific receptor, tropomyosin related kinase (TrkB), in <b>METH</b> induced behavioral abnormalities.
+BDNF	drug	amphetamine	23934209	Several lines of evidence suggest a role for <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and its specific receptor, tropomyosin related kinase (TrkB), in <b>METH</b> induced behavioral abnormalities.
+BDNF	drug	amphetamine	23872394	We found that peri pubertal treatment with <b>AMPH</b> induces long lasting changes in the expression of <strong>bdnf</strong> and of activity regulated genes in the hippocampus and in the prefrontal/frontal cortex, and leads to alterations of their short term modulation in response to a subsequent acute <b>AMPH</b> challenge.
+BDNF	addiction	sensitization	23847084	These findings demonstrate a cellular mechanism by which the hyperactivity of NRM MOR expressing neurons, presumably responsible for descending pain facilitation, contributes to pain <b>sensitization</b> through the signaling cascade of <strong>BDNF</strong> KCC2 GABA impairment in the development of chronic pain.
+BDNF	drug	alcohol	25309774	Parallel to the behavioral changes, chronic <b>alcohol</b> resulted in a significant decrease in hippocampal <strong>BDNF</strong>, which was normalized by nicotine.
+BDNF	drug	nicotine	25309774	Parallel to the behavioral changes, chronic alcohol resulted in a significant decrease in hippocampal <strong>BDNF</strong>, which was normalized by <b>nicotine</b>.
+BDNF	addiction	withdrawal	23727437	Finally, elevation of brain derived neurotrophic factor (<strong>BDNF</strong>) levels in the NAc may contribute to maintenance of incubation after months of <b>withdrawal</b>, although incubation related increases in <strong>BDNF</strong> accumulation do not account for CP AMPAR accumulation.
+BDNF	addiction	withdrawal	23727437	Finally, elevation of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels in the NAc may contribute to maintenance of incubation after months of <b>withdrawal</b>, although incubation related increases in <strong>BDNF</strong> accumulation do not account for CP AMPAR accumulation.
+BDNF	drug	amphetamine	23726845	<b>METH</b> self administration caused increases in mRNA expression of the transcription factors, c fos and fosb, the neurotrophic factor, <strong>Bdnf</strong>, and the synaptic protein, synaptophysin (Syp) in the dorsal striatum.
+BDNF	drug	amphetamine	23726845	<b>METH</b> also caused changes in ΔFosB, <strong>BDNF</strong> and TrkB protein levels, with increases after 2 and 24h, but decreases after 1month of drug abstinence.
+BDNF	drug	amphetamine	23726845	Importantly, ChIP PCR showed that <b>METH</b> self administration caused enrichment of phosphorylated CREB (pCREB), but not of histone H3 trimethylated at lysine 4 (H3K4me3), on promoters of c fos, fosb, <strong>Bdnf</strong> and Syp at 2h after cessation of drug intake.
+BDNF	drug	cocaine	23717324	Second, miR 212 was also shown to regulate <b>cocaine</b> intake by repressing striatal expression of methyl CpG binding protein 2 (MeCP2), consequently decreasing protein levels of brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	cocaine	23717324	Second, miR 212 was also shown to regulate <b>cocaine</b> intake by repressing striatal expression of methyl CpG binding protein 2 (MeCP2), consequently decreasing protein levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	cocaine	23717324	The concerted actions of miR 212 on striatal CREB and MeCP2/<strong>BDNF</strong> activity greatly attenuate the motivational effects of <b>cocaine</b>.
+BDNF	drug	amphetamine	23689674	<strong>BDNF</strong> overexpression in the ventral tegmental area prolongs social defeat stress induced cross sensitization to <b>amphetamine</b> and increases ΔFosB expression in mesocorticolimbic regions of rats.
+BDNF	addiction	sensitization	23689674	<strong>BDNF</strong> overexpression in the ventral tegmental area prolongs social defeat stress induced cross <b>sensitization</b> to amphetamine and increases ΔFosB expression in mesocorticolimbic regions of rats.
+BDNF	addiction	sensitization	23689674	The present research examined whether ventral tegmental area (VTA) <strong>BDNF</strong> overexpression would prolong the time course of cross <b>sensitization</b> after a single social defeat stress, which normally produces transient cross <b>sensitization</b> lasting <1 week.
+BDNF	addiction	sensitization	23689674	AAV <strong>BDNF</strong> rats exposed to stress showed prolonged cross <b>sensitization</b> and facilitated <b>sensitization</b> to the second drug challenge.
+BDNF	drug	amphetamine	23689674	Immunohistochemistry showed that the combination of virally enhanced VTA <strong>BDNF</strong>, stress, and <b>AMPH</b> resulted in increased ΔFosB in the NAc shell compared with the other groups.
+BDNF	addiction	sensitization	23689674	Thus, elevation of VTA <strong>BDNF</strong> prolongs cross <b>sensitization</b>, facilitates <b>sensitization</b>, and increases ΔFosB in mesocorticolimbic terminal regions.
+BDNF	addiction	addiction	23653680	Use of neuroprotective agent; brain derived neurotropic factor (<strong>BDNF</strong>), which protects neurons against these effects, could be of therapeutic benefit in the treatment of opiate <b>addiction</b>.
+BDNF	drug	opioid	23653680	We found that transmigrated <strong>BDNF</strong> was effective in suppressing the <b>morphine</b> induced apoptosis, inducing CREB expression and restoring the spine density.
+BDNF	drug	cocaine	23651226	oPFC striatal disconnection and oPFC <strong>Bdnf</strong> knockdown blocked sensitivity to outcome predictive relationships in both food reinforced and <b>cocaine</b> associated settings.
+BDNF	drug	opioid	23651024	Out of the 110 variants analyzed, 12 SNPs (in <strong>BDNF</strong>, NTRK2, OPRM1, DRD2 and ANKK1) were associated with <b>methadone</b> dose (nominal p < 0.05).
+BDNF	drug	opioid	23623815	Region specific expression of <strong>brain derived neurotrophic factor</strong> splice variants in <b>morphine</b> conditioned place preference in mice.
+BDNF	addiction	addiction	23623815	It is well established that brain derived neurotrophic factor (<strong>BDNF</strong>) plays a pivotal role in brain plasticity related processes, such as learning, memory and drug <b>addiction</b>.
+BDNF	addiction	addiction	23623815	It is well established that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) plays a pivotal role in brain plasticity related processes, such as learning, memory and drug <b>addiction</b>.
+BDNF	drug	opioid	23623815	However, changes in expression of <strong>BDNF</strong> splice variants after acquisition, extinction and reinstatement of cue elicited <b>morphine</b> seeking behavior have not yet been investigated.
+BDNF	addiction	relapse	23623815	However, changes in expression of <strong>BDNF</strong> splice variants after acquisition, extinction and <b>reinstatement</b> of cue elicited morphine <b>seeking</b> behavior have not yet been investigated.
+BDNF	drug	opioid	23623815	Real time PCR was used to assess <strong>BDNF</strong> splice variants (I, II, IV and VI) in various brain regions during acquisition, extinction and reinstatement of <b>morphine</b> conditioned place preference (CPP) in mice.
+BDNF	addiction	relapse	23623815	Real time PCR was used to assess <strong>BDNF</strong> splice variants (I, II, IV and VI) in various brain regions during acquisition, extinction and <b>reinstatement</b> of morphine conditioned place preference (CPP) in mice.
+BDNF	addiction	reward	23623815	Real time PCR was used to assess <strong>BDNF</strong> splice variants (I, II, IV and VI) in various brain regions during acquisition, extinction and reinstatement of morphine conditioned place preference (<b>CPP</b>) in mice.
+BDNF	drug	opioid	23623815	Levels of <strong>BDNF</strong> splice variants decreased after extinction training and continued to decrease during reinstatement induced by a <b>morphine</b> priming injection (10mg/kg, i.p.).
+BDNF	addiction	relapse	23623815	Levels of <strong>BDNF</strong> splice variants decreased after extinction training and continued to decrease during <b>reinstatement</b> induced by a morphine priming injection (10mg/kg, i.p.).
+BDNF	addiction	relapse	23623815	However, after <b>reinstatement</b> induced by exposure to 6 min of forced swimming (FS), expression of <strong>BDNF</strong> splice variants II, IV and VI was increased in the hippocampus, CPu, NAcc and prefrontal cortex (PFC).
+BDNF	addiction	relapse	23623815	After <b>reinstatement</b> induced by 40 min of restraint, expression of <strong>BDNF</strong> splice variants was increased in PFC.
+BDNF	drug	opioid	23623815	These results show that exposure to either <b>morphine</b> or acute stress can induce reinstatement of drug seeking, but expression of <strong>BDNF</strong> splice variants is differentially affected by chronic <b>morphine</b> and acute stress.
+BDNF	addiction	relapse	23623815	These results show that exposure to either morphine or acute stress can induce <b>reinstatement</b> of drug <b>seeking</b>, but expression of <strong>BDNF</strong> splice variants is differentially affected by chronic morphine and acute stress.
+BDNF	drug	opioid	23623815	Furthermore, <strong>BDNF</strong> splice variants II, IV and VI may play a role in learning and memory for <b>morphine</b> addiction in the hippocampus, CPu and NAcc.
+BDNF	addiction	addiction	23623815	Furthermore, <strong>BDNF</strong> splice variants II, IV and VI may play a role in learning and memory for morphine <b>addiction</b> in the hippocampus, CPu and NAcc.
+BDNF	drug	alcohol	23601049	Striatal modulation of <strong>BDNF</strong> expression using microRNA124a expressing lentiviral vectors impairs <b>ethanol</b> induced conditioned place preference and voluntary <b>alcohol</b> consumption.
+BDNF	drug	alcohol	23601049	In fact, <strong>BDNF</strong> mRNA was upregulated following <b>ethanol</b> drinking.
+BDNF	drug	alcohol	23601049	We used lentiviral vector (LV) gene transfer technology to further address the role of miR124a and its direct target <strong>BDNF</strong> in <b>ethanol</b> induced CPP and <b>alcohol</b> consumption.
+BDNF	addiction	reward	23601049	We used lentiviral vector (LV) gene transfer technology to further address the role of miR124a and its direct target <strong>BDNF</strong> in ethanol induced <b>CPP</b> and alcohol consumption.
+BDNF	drug	alcohol	23601049	Moreover, miR124a silencer (LV siR124a) as well as LV <strong>BDNF</strong> infusion in the DLS attenuates <b>ethanol</b> induced CPP as well as voluntary <b>alcohol</b> consumption.
+BDNF	addiction	reward	23601049	Moreover, miR124a silencer (LV siR124a) as well as LV <strong>BDNF</strong> infusion in the DLS attenuates ethanol induced <b>CPP</b> as well as voluntary alcohol consumption.
+BDNF	drug	alcohol	23601049	Our findings indicate that striatal miR124a and <strong>BDNF</strong> signaling have crucial roles in <b>alcohol</b> consumption and <b>ethanol</b> conditioned reward.
+BDNF	addiction	reward	23601049	Our findings indicate that striatal miR124a and <strong>BDNF</strong> signaling have crucial roles in alcohol consumption and ethanol conditioned <b>reward</b>.
+BDNF	drug	cocaine	23597759	We report here changes in inflammation markers, oxidative damage and <strong>brain derived neurotrophic factor</strong> in a sample of outpatients with crack <b>cocaine</b> use disorders.
+BDNF	drug	cocaine	23597759	Crack <b>cocaine</b> use was associated with higher <strong>BDNF</strong> levels when compared to controls, present only in those who used crack <b>cocaine</b> in the last month.
+BDNF	drug	alcohol	23588198	Binge <b>alcohol</b> induced alterations in <strong>BDNF</strong> and GDNF expression in central extended amygdala and pyriform cortex on infant rats.
+BDNF	addiction	intoxication	23588198	<b>Binge</b> alcohol induced alterations in <strong>BDNF</strong> and GDNF expression in central extended amygdala and pyriform cortex on infant rats.
+BDNF	drug	alcohol	23588198	Our goal was to study whether brain derived neurotrophic factor (<strong>BDNF</strong>) and glial derived neurotrophic factor (GDNF) expression were affected by <b>alcohol</b> in central extended amygdala (CEXA) and pyriform cortex (Pyr), structures strongly involved in emotional/social behaviors.
+BDNF	drug	alcohol	23588198	Our goal was to study whether <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and glial derived neurotrophic factor (GDNF) expression were affected by <b>alcohol</b> in central extended amygdala (CEXA) and pyriform cortex (Pyr), structures strongly involved in emotional/social behaviors.
+BDNF	drug	alcohol	23588198	Results showed: (1) <b>alcohol</b> induced enhancement of <strong>BDNF</strong> positive cells on PND 7 and 20, a decrease on PND 15 in the CEXA, and no changes in the Pyr on PND 7 and 20, but a diminished on PND 15; (2) GDNF positive cells rise after <b>alcohol</b> administration for the three ages in the CEXA and Pyr except on PND 15, where there was a decline; and (3) pharmacokinetics analysis demonstrated age related differences showing equal BALs on PND 7 and 20 but higher BALs on PND 15.
+BDNF	drug	cocaine	23583595	Reduced <b>cocaine</b> seeking behavior in heterozygous <strong>BDNF</strong> knockout rats.
+BDNF	addiction	relapse	23583595	Reduced cocaine <b>seeking</b> behavior in heterozygous <strong>BDNF</strong> knockout rats.
+BDNF	drug	cocaine	23583595	Using conditioned place preference, the current study investigated the hypothesis that a partial knockout of the <strong>BDNF</strong> gene in rats (<strong>BDNF</strong>(+/ )) would attenuate the rewarding effects of <b>cocaine</b>.
+BDNF	drug	cocaine	23583595	In contrast, <strong>BDNF</strong>(+/ ) rats did not show <b>cocaine</b> seeking behavior one day after conditioning, nor did they respond to drug priming.
+BDNF	addiction	relapse	23583595	In contrast, <strong>BDNF</strong>(+/ ) rats did not show cocaine <b>seeking</b> behavior one day after conditioning, nor did they respond to drug priming.
+BDNF	drug	cocaine	23583595	A median split of rats based on <strong>BDNF</strong> levels in sera collected prior to behavioral procedures revealed that wildtype rats with high <strong>BDNF</strong> levels showed stronger conditioned place preference and reinstatement to <b>cocaine</b>.
+BDNF	addiction	relapse	23583595	A median split of rats based on <strong>BDNF</strong> levels in sera collected prior to behavioral procedures revealed that wildtype rats with high <strong>BDNF</strong> levels showed stronger conditioned place preference and <b>reinstatement</b> to cocaine.
+BDNF	drug	cocaine	23583595	Together, the results support the hypothesis that a partial knockout of the <strong>BDNF</strong> gene attenuates the rewarding properties of <b>cocaine</b>.
+BDNF	drug	cocaine	23583595	Additionally, individual differences in <strong>BDNF</strong> levels may predict future <b>cocaine</b> seeking behavior.
+BDNF	addiction	relapse	23583595	Additionally, individual differences in <strong>BDNF</strong> levels may predict future cocaine <b>seeking</b> behavior.
+BDNF	drug	alcohol	23582695	Brain derived neurotrophic factor (<strong>BDNF</strong>) Val66Met polymorphism and its implication in executive functions in adult offspring of <b>alcohol</b> dependent probands.
+BDNF	drug	alcohol	23582695	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) Val66Met polymorphism and its implication in executive functions in adult offspring of <b>alcohol</b> dependent probands.
+BDNF	drug	alcohol	23582695	These results suggest that the <strong>BDNF</strong> Val66Met polymorphism may contribute to <b>alcohol</b> dependence vulnerability via lower EFs performance.
+BDNF	addiction	dependence	23582695	These results suggest that the <strong>BDNF</strong> Val66Met polymorphism may contribute to alcohol <b>dependence</b> vulnerability via lower EFs performance.
+BDNF	drug	alcohol	23485013	Acute <b>ethanol</b> exposure decreased amygdaloid HDAC activity and HDAC2 protein levels, increased global and gene (<strong>Bdnf</strong> and Arc) specific histone acetylation, and attenuated anxiety like behaviors in P rats but had no effects in NP rats.
+BDNF	drug	alcohol	23485013	The HDAC2 knockdown in the CeA attenuated anxiety like behaviors and voluntary <b>alcohol</b> but not sucrose consumption in P rats and increased histone acetylation of <strong>Bdnf</strong> and Arc with a resultant increase in protein levels that correlated with increased dendritic spine density.
+BDNF	drug	opioid	23454521	Photoactivation of optoMOR decreased the Ca(2+) influx and inhibited the forskolin induced cAMP generation, activation of CREB, and <strong>BDNF</strong> levels in optoMOR expressing cells similar to the activation of native μ <b>opioid</b> receptor by DAMGO.
+BDNF	drug	alcohol	23414063	<strong>Brain derived neurotrophic factor</strong> mediates the suppression of <b>alcohol</b> self administration by memantine.
+BDNF	drug	alcohol	23414063	Brain derived neurotrophic factor (<strong>BDNF</strong>) within the striatum is part of a homeostatic pathway regulating <b>alcohol</b> consumption.
+BDNF	drug	alcohol	23414063	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) within the striatum is part of a homeostatic pathway regulating <b>alcohol</b> consumption.
+BDNF	drug	cocaine	23359110	Here we review how alterations in histone modifications, DNA methylation, and microRNAs regulate gene expression and contribute to psychostimulant addiction with a focus on the epigenetic mechanisms that regulate brain derived neurotrophic factor (<strong>BDNF</strong>) expression following chronic <b>cocaine</b> exposure.
+BDNF	addiction	addiction	23359110	Here we review how alterations in histone modifications, DNA methylation, and microRNAs regulate gene expression and contribute to psychostimulant <b>addiction</b> with a focus on the epigenetic mechanisms that regulate brain derived neurotrophic factor (<strong>BDNF</strong>) expression following chronic cocaine exposure.
+BDNF	drug	cocaine	23359110	Here we review how alterations in histone modifications, DNA methylation, and microRNAs regulate gene expression and contribute to psychostimulant addiction with a focus on the epigenetic mechanisms that regulate <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression following chronic <b>cocaine</b> exposure.
+BDNF	addiction	addiction	23359110	Here we review how alterations in histone modifications, DNA methylation, and microRNAs regulate gene expression and contribute to psychostimulant <b>addiction</b> with a focus on the epigenetic mechanisms that regulate <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression following chronic cocaine exposure.
+BDNF	drug	cocaine	23333681	Enhanced nicotine seeking behavior following pre exposure to repeated <b>cocaine</b> is accompanied by changes in <strong>BDNF</strong> in the nucleus accumbens of rats.
+BDNF	drug	nicotine	23333681	Enhanced <b>nicotine</b> seeking behavior following pre exposure to repeated cocaine is accompanied by changes in <strong>BDNF</strong> in the nucleus accumbens of rats.
+BDNF	addiction	relapse	23333681	Enhanced nicotine <b>seeking</b> behavior following pre exposure to repeated cocaine is accompanied by changes in <strong>BDNF</strong> in the nucleus accumbens of rats.
+BDNF	drug	opioid	23333681	The dynorphin (DYN), μ <b>opioid</b> receptor (mu <b>opioid</b>), neuropeptide Y (NPY), brain derived neurotrophic factor (<strong>BDNF</strong>), tropomyosin related tyrosine kinase B receptor (TrkB) and corticotropin releasing factor receptor type 1 (CRF R1) gene expression were measured by the reverse transcription polymerase chain reaction (RT PCR).
+BDNF	drug	opioid	23333681	The dynorphin (DYN), μ <b>opioid</b> receptor (mu <b>opioid</b>), neuropeptide Y (NPY), <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), tropomyosin related tyrosine kinase B receptor (TrkB) and corticotropin releasing factor receptor type 1 (CRF R1) gene expression were measured by the reverse transcription polymerase chain reaction (RT PCR).
+BDNF	drug	cocaine	23327740	Developmentally divergent effects of Rho kinase inhibition on <b>cocaine</b>  and <strong>BDNF</strong> induced behavioral plasticity.
+BDNF	addiction	addiction	23327740	By contrast, when administered in adulthood, HA 1077 had no psychomotor consequences and normalized food reinforced instrumental responding after orbitofrontal selective knockdown of <strong>Brain derived neurotrophic factor</strong>, a potential factor in <b>addiction</b>.
+BDNF	drug	cocaine	23325250	Different roles of <strong>BDNF</strong> in nucleus accumbens core versus shell during the incubation of cue induced <b>cocaine</b> craving and its long term maintenance.
+BDNF	addiction	relapse	23325250	Different roles of <strong>BDNF</strong> in nucleus accumbens core versus shell during the incubation of cue induced cocaine <b>craving</b> and its long term maintenance.
+BDNF	drug	cocaine	23325250	Brain derived neurotrophic factor (<strong>BDNF</strong>) contributes to diverse types of plasticity, including <b>cocaine</b> addiction.
+BDNF	addiction	addiction	23325250	Brain derived neurotrophic factor (<strong>BDNF</strong>) contributes to diverse types of plasticity, including cocaine <b>addiction</b>.
+BDNF	drug	cocaine	23325250	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) contributes to diverse types of plasticity, including <b>cocaine</b> addiction.
+BDNF	addiction	addiction	23325250	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) contributes to diverse types of plasticity, including cocaine <b>addiction</b>.
+BDNF	drug	cocaine	23325250	We investigated the role of <strong>BDNF</strong> in the rat nucleus accumbens (NAc) in the incubation of <b>cocaine</b> craving over 3 months of withdrawal from extended access <b>cocaine</b> self administration.
+BDNF	addiction	relapse	23325250	We investigated the role of <strong>BDNF</strong> in the rat nucleus accumbens (NAc) in the incubation of cocaine <b>craving</b> over 3 months of withdrawal from extended access cocaine self administration.
+BDNF	addiction	withdrawal	23325250	We investigated the role of <strong>BDNF</strong> in the rat nucleus accumbens (NAc) in the incubation of cocaine craving over 3 months of <b>withdrawal</b> from extended access cocaine self administration.
+BDNF	drug	cocaine	23325250	First, we confirmed by immunoblotting that <strong>BDNF</strong> levels are elevated after this <b>cocaine</b> regimen on withdrawal day 45 (WD45) and showed that <strong>BDNF</strong> mRNA levels are not altered.
+BDNF	addiction	withdrawal	23325250	First, we confirmed by immunoblotting that <strong>BDNF</strong> levels are elevated after this cocaine regimen on <b>withdrawal</b> day 45 (WD45) and showed that <strong>BDNF</strong> mRNA levels are not altered.
+BDNF	drug	cocaine	23325250	Attenuating <strong>BDNF</strong> TrkB signaling in shell did not affect <b>cocaine</b> seeking on WD1 or WD45 but significantly decreased <b>cocaine</b> seeking on WD90.
+BDNF	addiction	relapse	23325250	Attenuating <strong>BDNF</strong> TrkB signaling in shell did not affect cocaine <b>seeking</b> on WD1 or WD45 but significantly decreased cocaine <b>seeking</b> on WD90.
+BDNF	drug	cocaine	23325250	These results suggest that basal levels of <strong>BDNF</strong> transmission in the NAc core exert a suppressive effect on <b>cocaine</b> seeking in early withdrawal (WD1), whereas the late elevation of <strong>BDNF</strong> protein in NAc shell contributes to incubation in late withdrawal (WD90).
+BDNF	addiction	relapse	23325250	These results suggest that basal levels of <strong>BDNF</strong> transmission in the NAc core exert a suppressive effect on cocaine <b>seeking</b> in early withdrawal (WD1), whereas the late elevation of <strong>BDNF</strong> protein in NAc shell contributes to incubation in late withdrawal (WD90).
+BDNF	addiction	withdrawal	23325250	These results suggest that basal levels of <strong>BDNF</strong> transmission in the NAc core exert a suppressive effect on cocaine seeking in early <b>withdrawal</b> (WD1), whereas the late elevation of <strong>BDNF</strong> protein in NAc shell contributes to incubation in late <b>withdrawal</b> (WD90).
+BDNF	addiction	withdrawal	23325250	Finally, <strong>BDNF</strong> protein levels in the NAc were significantly increased after ampakine treatment, supporting the novel hypothesis that the gradual increase of <strong>BDNF</strong> levels in NAc accompanying incubation could be caused by increased AMPAR transmission during <b>withdrawal</b>.
+BDNF	drug	cannabinoid	23313276	Dysfunctions of leptin, ghrelin, <strong>BDNF</strong> and <b>endocannabinoids</b> in eating disorders: beyond the homeostatic control of food intake.
+BDNF	drug	cannabinoid	23313276	In the present review, the evidences supporting a role of leptin, ghrelin, <strong>brain derived neurotrophic factor</strong> and <b>endocannabinoids</b> in the homeostatic and non homeostatic dysregulations of patients with AN and BN will be presented.
+BDNF	drug	nicotine	23291224	In addition, neonatal quinpirole increased the accumbal <strong>BDNF</strong> in response to <b>nicotine</b> compared to all other groups, and <b>nicotine</b> alone also produced significant increases in striatal and accumbal <strong>BDNF</strong>.
+BDNF	drug	nicotine	23291224	This study reveals that neonatal quinpirole enhanced adolescent <b>nicotine</b> sensitization, accumbal dopamine overflow, and <strong>BDNF</strong> protein in response to <b>nicotine</b>, which may be related to changes in the brain's reward system.
+BDNF	addiction	reward	23291224	This study reveals that neonatal quinpirole enhanced adolescent nicotine sensitization, accumbal dopamine overflow, and <strong>BDNF</strong> protein in response to nicotine, which may be related to changes in the brain's <b>reward</b> system.
+BDNF	addiction	sensitization	23291224	This study reveals that neonatal quinpirole enhanced adolescent nicotine <b>sensitization</b>, accumbal dopamine overflow, and <strong>BDNF</strong> protein in response to nicotine, which may be related to changes in the brain's reward system.
+BDNF	drug	alcohol	23291223	Susceptibility to <b>ethanol</b> sensitization is differentially associated with changes in pCREB, trkB and <strong>BDNF</strong> mRNA expression in the mouse brain.
+BDNF	addiction	sensitization	23291223	Susceptibility to ethanol <b>sensitization</b> is differentially associated with changes in pCREB, trkB and <strong>BDNF</strong> mRNA expression in the mouse brain.
+BDNF	drug	alcohol	23291223	The goal of the present study was to examine whether variability in the sensitization response to <b>ethanol</b> (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely <strong>BDNF</strong> and its receptor trkB, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after withdrawal from chronic, intermittent EtOH exposure.
+BDNF	addiction	sensitization	23291223	The goal of the present study was to examine whether variability in the <b>sensitization</b> response to ethanol (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely <strong>BDNF</strong> and its receptor trkB, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after withdrawal from chronic, intermittent EtOH exposure.
+BDNF	addiction	withdrawal	23291223	The goal of the present study was to examine whether variability in the sensitization response to ethanol (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely <strong>BDNF</strong> and its receptor trkB, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after <b>withdrawal</b> from chronic, intermittent EtOH exposure.
+BDNF	addiction	sensitization	23291223	The observed decrease in <strong>BDNF</strong> and trkB mRNA in the Non sensitized group suggests the possibility that EtOH may have neurotoxic effects in a subpopulation of mice, which might in turn prevent the development of behavioural <b>sensitization</b>.
+BDNF	addiction	sensitization	23291223	The lack of a difference in <strong>BDNF</strong> and trkB mRNA expression between Sensitized and SAL mice suggests that EtOH <b>sensitization</b> may be mediated by mechanisms different from those mediating <b>sensitization</b> to other psychostimulants.
+BDNF	drug	nicotine	23285275	<strong>BDNF</strong> Val66Met variant and <b>smoking</b> in a Chinese population.
+BDNF	drug	nicotine	23285275	Several recent studies have supported the hypothesis that brain derived neurotrophic factor (<strong>BDNF</strong>), a member of the neurotrophic factor family, might be associated with <b>nicotine</b> addiction.
+BDNF	addiction	addiction	23285275	Several recent studies have supported the hypothesis that brain derived neurotrophic factor (<strong>BDNF</strong>), a member of the neurotrophic factor family, might be associated with nicotine <b>addiction</b>.
+BDNF	drug	nicotine	23285275	Several recent studies have supported the hypothesis that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), a member of the neurotrophic factor family, might be associated with <b>nicotine</b> addiction.
+BDNF	addiction	addiction	23285275	Several recent studies have supported the hypothesis that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), a member of the neurotrophic factor family, might be associated with nicotine <b>addiction</b>.
+BDNF	drug	nicotine	23285275	Association studies have also suggested that the <strong>BDNF</strong> gene might play a role in the susceptibility to <b>nicotine</b> dependence but results appear contradictory.
+BDNF	addiction	dependence	23285275	Association studies have also suggested that the <strong>BDNF</strong> gene might play a role in the susceptibility to nicotine <b>dependence</b> but results appear contradictory.
+BDNF	drug	nicotine	23285275	The present work was therefore undertaken to examine the association of <b>smoking</b> with the <strong>BDNF</strong> Val66Met gene polymorphism in Chinese population.
+BDNF	drug	nicotine	23285275	The <strong>BDNF</strong> Val66Met gene polymorphism was examined in 628 healthy male volunteers including 322 <b>smokers</b> and 306 non <b>smokers</b>.
+BDNF	drug	nicotine	23285275	Also, the <strong>BDNF</strong> serum levels were measured in 136 <b>smokers</b> and 97 nonsmokers.
+BDNF	drug	nicotine	23285275	Our results showed no significant association between the <strong>BDNF</strong> Val66Met polymorphism or serum levels among <b>smokers</b> and non <b>smokers</b>.
+BDNF	drug	nicotine	23285275	Our findings suggest that the <strong>BDNF</strong> Val66Met polymorphism may not be involved in susceptibility to <b>smoking</b> among the Chinese male population, but may influence the age at which <b>smoking</b> is initiated.
+BDNF	addiction	addiction	25408911	The neurotrophins brain derived neurotrophic factor (<strong>BDNF</strong>) and neurotrophic factor 3 (NT3) could play a role in <b>addictive</b> behavior.
+BDNF	addiction	addiction	25408911	The neurotrophins <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and neurotrophic factor 3 (NT3) could play a role in <b>addictive</b> behavior.
+BDNF	drug	alcohol	25408911	Interactions between <strong>BDNF</strong> and dopamine transmission influence the <b>alcohol</b> intake.
+BDNF	drug	alcohol	25408911	It has been hypothesized that extensive <b>alcohol</b> consumption leads to diminished circulating <strong>BDNF</strong> levels and impaired <strong>BDNF</strong> mediated protective mechanisms.
+BDNF	drug	alcohol	25408911	In this study, we tested the hypothesis that <b>alcohol</b> withdrawal increases the serum levels of <strong>BDNF</strong> in <b>alcoholic</b> patients and investigated correlations between serum <strong>BDNF</strong> and NT3 and <b>alcohol</b> in breath as well as with the body mass index (BMI), lipoprotein profiles and lifestyle factors in 110 male in patients diagnosed with <b>alcohol</b> addiction on the first day after admission and at discharge.
+BDNF	addiction	addiction	25408911	In this study, we tested the hypothesis that alcohol withdrawal increases the serum levels of <strong>BDNF</strong> in alcoholic patients and investigated correlations between serum <strong>BDNF</strong> and NT3 and alcohol in breath as well as with the body mass index (BMI), lipoprotein profiles and lifestyle factors in 110 male in patients diagnosed with alcohol <b>addiction</b> on the first day after admission and at discharge.
+BDNF	addiction	withdrawal	25408911	In this study, we tested the hypothesis that alcohol <b>withdrawal</b> increases the serum levels of <strong>BDNF</strong> in alcoholic patients and investigated correlations between serum <strong>BDNF</strong> and NT3 and alcohol in breath as well as with the body mass index (BMI), lipoprotein profiles and lifestyle factors in 110 male in patients diagnosed with alcohol addiction on the first day after admission and at discharge.
+BDNF	drug	alcohol	25408911	The intoxication level (<b>alcohol</b> in breath at admission) was significantly correlated with liver enzymes and <strong>BDNF</strong> concentrations (R = .28; p = .004).
+BDNF	addiction	intoxication	25408911	The <b>intoxication</b> level (alcohol in breath at admission) was significantly correlated with liver enzymes and <strong>BDNF</strong> concentrations (R = .28; p = .004).
+BDNF	drug	alcohol	25408911	Other than expected, the levels of NT3 and to a lesser extent <strong>BDNF</strong> levels, were found to be significantly increased in acute <b>alcohol</b> abuse.
+BDNF	addiction	aversion	23250006	Prelimbic <strong>BDNF</strong> and TrkB signaling regulates consolidation of both appetitive and <b>aversive</b> emotional learning.
+BDNF	drug	cocaine	23250006	The site specific TrkB antagonism and viral mediated <strong>bdnf</strong> deletion within the PL resulted in deficits in both <b>cocaine</b> dependent associative learning and fear expression.
+BDNF	addiction	aversion	23250006	Deficiencies were rescued by the novel TrkB agonist 7,8 dihydroxyflavone, indicating that PL <strong>BDNF</strong> expression and downstream signaling through the TrkB receptor are required for memory formation in both appetitive and <b>aversive</b> domains.
+BDNF	drug	cocaine	23242310	Brain derived neurotrophic factor (<strong>Bdnf</strong>) mRNA and <strong>BDNF</strong> protein were increased in the medial prefrontal cortex (mPFC), and there was an increased association of acetylated histone H3 with <strong>Bdnf</strong> promoters in only the male offspring of <b>cocaine</b> experienced sires.
+BDNF	drug	cocaine	23242310	<strong>Brain derived neurotrophic factor</strong> (<strong>Bdnf</strong>) mRNA and <strong>BDNF</strong> protein were increased in the medial prefrontal cortex (mPFC), and there was an increased association of acetylated histone H3 with <strong>Bdnf</strong> promoters in only the male offspring of <b>cocaine</b> experienced sires.
+BDNF	drug	cocaine	23242310	Administration of a <strong>BDNF</strong> receptor antagonist (the TrkB receptor antagonist ANA 12) reversed the diminished <b>cocaine</b> self administration in male <b>cocaine</b> sired rats.
+BDNF	drug	cocaine	23242310	In addition, the association of acetylated histone H3 with <strong>Bdnf</strong> promoters was increased in the sperm of sires that self administered <b>cocaine</b>.
+BDNF	drug	cocaine	23239946	Regulation of <strong>BDNF</strong> expression by <b>cocaine</b>.
+BDNF	drug	cocaine	23239946	This review will discuss how exposure to <b>cocaine</b>, one of the most addictive drugs known to mankind, can produce alterations in <strong>BDNF</strong> gene expression, especially in the mesolimbic dopaminergic system, which lead to alterations in the reward mediated behaviors involved in addiction.
+BDNF	addiction	addiction	23239946	This review will discuss how exposure to cocaine, one of the most <b>addictive</b> drugs known to mankind, can produce alterations in <strong>BDNF</strong> gene expression, especially in the mesolimbic dopaminergic system, which lead to alterations in the reward mediated behaviors involved in <b>addiction</b>.
+BDNF	addiction	reward	23239946	This review will discuss how exposure to cocaine, one of the most addictive drugs known to mankind, can produce alterations in <strong>BDNF</strong> gene expression, especially in the mesolimbic dopaminergic system, which lead to alterations in the <b>reward</b> mediated behaviors involved in addiction.
+BDNF	drug	opioid	23224818	Neonatal <b>morphine</b> administration leads to changes in hippocampal <strong>BDNF</strong> levels and antioxidant enzyme activity in the adult life of rats.
+BDNF	drug	opioid	23224818	Thus, the aim of this investigation was to assess hippocampal levels of <strong>BDNF</strong>, oxidative stress markers associated with cell viability, and TNF α in the short, medium and long term after repeated <b>morphine</b> treatment in early life.
+BDNF	drug	opioid	23224818	For the first time, we observed that <b>morphine</b> treatment in early life modulates <strong>BDNF</strong> levels in the medium and long term and also modulates superoxide dismutase activity in the long term.
+BDNF	drug	alcohol	23189980	<strong>BDNF</strong> mediated regulation of <b>ethanol</b> consumption requires the activation of the MAP kinase pathway and protein synthesis.
+BDNF	drug	alcohol	23189980	We previously found that the brain derived neurotrophic factor (<strong>BDNF</strong>) in the dorsolateral striatum (DLS) is part of a homeostatic pathway that gates <b>ethanol</b> self administration [Jeanblanc et al.
+BDNF	drug	alcohol	23189980	We previously found that the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the dorsolateral striatum (DLS) is part of a homeostatic pathway that gates <b>ethanol</b> self administration [Jeanblanc et al.
+BDNF	drug	alcohol	23189980	Specifically, we showed that moderate levels (10%) of <b>ethanol</b> consumption increase <strong>BDNF</strong> expression within the DLS, and that direct infusion of <strong>BDNF</strong> into the DLS decreases operant self administration of a 10% <b>ethanol</b> solution.
+BDNF	addiction	reward	23189980	Specifically, we showed that moderate levels (10%) of ethanol consumption increase <strong>BDNF</strong> expression within the DLS, and that direct infusion of <strong>BDNF</strong> into the DLS decreases <b>operant</b> self administration of a 10% ethanol solution.
+BDNF	drug	alcohol	23189980	Thus, here, we set out to identify which of these intracellular pathway(s) plays a role in the regulation of <b>ethanol</b> consumption by <strong>BDNF</strong>.
+BDNF	drug	alcohol	23189980	We found that inhibition of the MAPK, but not PLC γ or PI3K, activity blocks the <strong>BDNF</strong> mediated reduction of <b>ethanol</b> consumption.
+BDNF	drug	alcohol	23189980	As activation of the MAPK pathway leads to the initiation of transcription and/or translation events, we tested whether the <strong>BDNF</strong> mediated reduction of <b>ethanol</b> self administration requires de novo protein synthesis.
+BDNF	drug	alcohol	23189980	We found that the inhibitory effect of <strong>BDNF</strong> on <b>ethanol</b> intake is blocked by the protein synthesis inhibitor cycloheximide.
+BDNF	drug	alcohol	23189980	Together, our results show that <strong>BDNF</strong> attenuates <b>ethanol</b> drinking via activation of the MAPK pathway in a protein synthesis dependent manner within the DLS.
+BDNF	drug	cocaine	23164369	Region specific effects on <strong>BDNF</strong> expression after contingent or non contingent <b>cocaine</b> i.v.
+BDNF	drug	cocaine	23164369	Brain derived neurotrophic factor (<strong>BDNF</strong>) dynamic changes were investigated in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) during use and the early phases of <b>cocaine</b> abstinence after 14 sessions (2 h self administration/d; 0.25 mg/0.1 ml.6 s infusion) by employing a 'yoked control operant paradigm'.
+BDNF	addiction	reward	23164369	Brain derived neurotrophic factor (<strong>BDNF</strong>) dynamic changes were investigated in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) during use and the early phases of cocaine abstinence after 14 sessions (2 h self administration/d; 0.25 mg/0.1 ml.6 s infusion) by employing a 'yoked control <b>operant</b> paradigm'.
+BDNF	drug	cocaine	23164369	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) dynamic changes were investigated in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) during use and the early phases of <b>cocaine</b> abstinence after 14 sessions (2 h self administration/d; 0.25 mg/0.1 ml.6 s infusion) by employing a 'yoked control operant paradigm'.
+BDNF	addiction	reward	23164369	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) dynamic changes were investigated in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) during use and the early phases of cocaine abstinence after 14 sessions (2 h self administration/d; 0.25 mg/0.1 ml.6 s infusion) by employing a 'yoked control <b>operant</b> paradigm'.
+BDNF	addiction	withdrawal	23164369	The effect on <strong>BDNF</strong> was region specific and dependent on the <b>withdrawal</b> time.
+BDNF	drug	cocaine	23164369	In the NAc, <strong>BDNF</strong> protein levels increased immediately after the last self administration session, with a larger increase in passively <b>cocaine</b> exposed rats.
+BDNF	drug	cocaine	23164369	These findings indicate a finely tuned modulation of <strong>BDNF</strong> expression during use and early phases of <b>cocaine</b> abstinence.
+BDNF	drug	alcohol	23128606	Serum <strong>brain derived neurotrophic factor</strong> and nerve growth factor concentrations change after <b>alcohol</b> withdrawal: preliminary data of a case control comparison.
+BDNF	addiction	withdrawal	23128606	Serum <strong>brain derived neurotrophic factor</strong> and nerve growth factor concentrations change after alcohol <b>withdrawal</b>: preliminary data of a case control comparison.
+BDNF	drug	alcohol	23128606	In this study, we addressed the question whether <strong>BDNF</strong> and NGF serum concentrations change during subacute <b>alcohol</b> withdrawal in patients with <b>alcohol</b> dependence compared to healthy controls.
+BDNF	addiction	dependence	23128606	In this study, we addressed the question whether <strong>BDNF</strong> and NGF serum concentrations change during subacute alcohol withdrawal in patients with alcohol <b>dependence</b> compared to healthy controls.
+BDNF	addiction	withdrawal	23128606	In this study, we addressed the question whether <strong>BDNF</strong> and NGF serum concentrations change during subacute alcohol <b>withdrawal</b> in patients with alcohol dependence compared to healthy controls.
+BDNF	drug	alcohol	23128606	Mean <strong>BDNF</strong> levels (7.8 ng/ml, IQR = 4.4 10.7 vs. 16.5 ng/ml, IQR = 13.9 25.6; Z =  3.8, p < 0.0001) and NGF levels (5.8 pg/ml, IQR = 3.8 13.0 vs. 18.4 pg/ml, IQR = 10.9 25.1; Z =  2.5, p = 0.012) were significantly decreased in <b>alcohol</b> dependent subjects when compared to healthy matched controls.
+BDNF	addiction	withdrawal	23128606	Mean <strong>BDNF</strong> concentrations showed a tendency to increase after <b>withdrawal</b> from day 3 to day 14 (Z = 1.7; p = 0.078).
+BDNF	drug	alcohol	23128606	Decreased NGF and <strong>BDNF</strong> concentrations in patients suffering from <b>alcohol</b> dependence, which stabilize after physical withdrawal, are in line with withdrawal symptoms and neurological risk factors.
+BDNF	addiction	dependence	23128606	Decreased NGF and <strong>BDNF</strong> concentrations in patients suffering from alcohol <b>dependence</b>, which stabilize after physical withdrawal, are in line with withdrawal symptoms and neurological risk factors.
+BDNF	addiction	withdrawal	23128606	Decreased NGF and <strong>BDNF</strong> concentrations in patients suffering from alcohol dependence, which stabilize after physical <b>withdrawal</b>, are in line with <b>withdrawal</b> symptoms and neurological risk factors.
+BDNF	addiction	withdrawal	23128606	In turn, increase of <strong>BDNF</strong> after acute <b>withdrawal</b> might be connected to neurobiological and behavioral stabilization.
+BDNF	drug	amphetamine	23111884	Estimation of <strong>BDNF</strong> gene polymorphism and predisposition to dependence development for selected psychoactive compounds: genetic aspects of addiction with the selected drugs, <b>amphetamine</b>, tetrahydrocannabinol and opiates.
+BDNF	drug	cannabinoid	23111884	Estimation of <strong>BDNF</strong> gene polymorphism and predisposition to dependence development for selected psychoactive compounds: genetic aspects of addiction with the selected drugs, amphetamine, <b>tetrahydrocannabinol</b> and opiates.
+BDNF	addiction	addiction	23111884	Estimation of <strong>BDNF</strong> gene polymorphism and predisposition to dependence development for selected psychoactive compounds: genetic aspects of <b>addiction</b> with the selected drugs, amphetamine, tetrahydrocannabinol and opiates.
+BDNF	addiction	dependence	23111884	Estimation of <strong>BDNF</strong> gene polymorphism and predisposition to <b>dependence</b> development for selected psychoactive compounds: genetic aspects of addiction with the selected drugs, amphetamine, tetrahydrocannabinol and opiates.
+BDNF	addiction	dependence	23111884	The purpose of this research was to reveal the relationship between the Val66Met <strong>BDNF</strong> gene polymorphism and <b>dependence</b> of psychoactive agent.
+BDNF	drug	nicotine	23103711	As frontostriatal circuits involving discrete regions of dorsal striatum contribute directly to decision making processes, and <strong>BDNF</strong> modulates synaptic plasticity and learning, we also assessed the effects of <b>nicotine</b> on striatal <strong>BDNF</strong> expression.
+BDNF	drug	nicotine	23103711	Moreover, striatal <strong>BDNF</strong> may play a critical role in <b>nicotine</b> induced alterations in cognitive flexibility.
+BDNF	drug	alcohol	23087644	Associations of Cigarette Smoking and Polymorphisms in <strong>Brain Derived Neurotrophic Factor</strong> and Catechol O Methyltransferase with Neurocognition in <b>Alcohol</b> Dependent Individuals during Early Abstinence.
+BDNF	drug	nicotine	23087644	Associations of Cigarette <b>Smoking</b> and Polymorphisms in <strong>Brain Derived Neurotrophic Factor</strong> and Catechol O Methyltransferase with Neurocognition in Alcohol Dependent Individuals during Early Abstinence.
+BDNF	drug	nicotine	23087644	Chronic cigarette <b>smoking</b> and polymorphisms in brain derived neurotrophic factor (<strong>BDNF</strong>) and catechol O methyltransferase (COMT) are associated with neurocognition in normal controls and those with various neuropsychiatric conditions.
+BDNF	drug	nicotine	23087644	Chronic cigarette <b>smoking</b> and polymorphisms in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and catechol O methyltransferase (COMT) are associated with neurocognition in normal controls and those with various neuropsychiatric conditions.
+BDNF	drug	alcohol	23087644	The influence of <strong>BDNF</strong> and COMT on neurocognition in <b>alcohol</b> dependence is unclear.
+BDNF	addiction	dependence	23087644	The influence of <strong>BDNF</strong> and COMT on neurocognition in alcohol <b>dependence</b> is unclear.
+BDNF	drug	alcohol	23087644	The primary goal of this report was to investigate the associations of single nucleotide polymorphisms (SNPs) in <strong>BDNF</strong> Val66Met (rs6265) and COMT Val158Met (rs4680) with neurocognition in a treatment seeking <b>alcohol</b> dependent cohort and determine if neurocognitive differences between non smokers and smokers previously observed in this cohort persist when controlled for these functional SNPs.
+BDNF	drug	nicotine	23087644	The primary goal of this report was to investigate the associations of single nucleotide polymorphisms (SNPs) in <strong>BDNF</strong> Val66Met (rs6265) and COMT Val158Met (rs4680) with neurocognition in a treatment seeking alcohol dependent cohort and determine if neurocognitive differences between non <b>smokers</b> and <b>smokers</b> previously observed in this cohort persist when controlled for these functional SNPs.
+BDNF	addiction	relapse	23087644	The primary goal of this report was to investigate the associations of single nucleotide polymorphisms (SNPs) in <strong>BDNF</strong> Val66Met (rs6265) and COMT Val158Met (rs4680) with neurocognition in a treatment <b>seeking</b> alcohol dependent cohort and determine if neurocognitive differences between non smokers and smokers previously observed in this cohort persist when controlled for these functional SNPs.
+BDNF	drug	nicotine	23087644	After controlling for COMT and <strong>BDNF</strong> genotypes, <b>smoking</b> ALC performed significantly worse than non <b>smoking</b> ALC on the domains of auditory verbal and visuospatial learning and memory, cognitive efficiency, general intelligence, processing speed, and global neurocognition.
+BDNF	drug	nicotine	23087644	Results also indicated that the poorer performance of <b>smoking</b> compared to non <b>smoking</b> ALC across multiple neurocognitive domains was not mediated by COMT or <strong>BDNF</strong> genotype.
+BDNF	drug	amphetamine	23076832	The present study aims to evaluate the effects of TMX on biochemical targets of Li, such as glycogen synthase kinase 3β (GSK 3β), PKC, PKA, CREB, <strong>BDNF</strong> and NGF, in the brain of rats subjected to an animal model of mania induced by d <b>amphetamine</b> (d <b>AMPH</b>).
+BDNF	drug	amphetamine	23076832	Western blot showed that d <b>AMPH</b> significantly increased GSK 3 and PKC levels, and decreased pGSK 3, PKA, NGF, <strong>BDNF</strong> and CREB levels in the structures analyzed.
+BDNF	drug	opioid	23042896	<strong>BDNF</strong> is a negative modulator of <b>morphine</b> action.
+BDNF	drug	cocaine	23042896	Brain derived neurotrophic factor (<strong>BDNF</strong>) is a key positive regulator of neural plasticity, promoting, for example, the actions of stimulant drugs of abuse such as <b>cocaine</b>.
+BDNF	drug	cocaine	23042896	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is a key positive regulator of neural plasticity, promoting, for example, the actions of stimulant drugs of abuse such as <b>cocaine</b>.
+BDNF	drug	opioid	23042896	We discovered a surprising opposite role for <strong>BDNF</strong> in countering responses to chronic <b>morphine</b> exposure.
+BDNF	drug	opioid	23042896	The suppression of <strong>BDNF</strong> in the ventral tegmental area (VTA) enhanced the ability of <b>morphine</b> to increase dopamine (DA) neuron excitability and promote reward.
+BDNF	addiction	reward	23042896	The suppression of <strong>BDNF</strong> in the ventral tegmental area (VTA) enhanced the ability of morphine to increase dopamine (DA) neuron excitability and promote <b>reward</b>.
+BDNF	drug	opioid	23042896	In contrast, optical stimulation of VTA DA terminals in nucleus accumbens (NAc) completely reversed the suppressive effect of <strong>BDNF</strong> on <b>morphine</b> reward.
+BDNF	addiction	reward	23042896	In contrast, optical stimulation of VTA DA terminals in nucleus accumbens (NAc) completely reversed the suppressive effect of <strong>BDNF</strong> on morphine <b>reward</b>.
+BDNF	drug	opioid	23042896	Furthermore, we identified numerous genes in the NAc, a major target region of VTA DA neurons, whose regulation by <strong>BDNF</strong> in the context of chronic <b>morphine</b> exposure mediated this counteractive function.
+BDNF	drug	opioid	23035088	Extinction of aversive memories associated with <b>morphine</b> withdrawal requires ERK mediated epigenetic regulation of <strong>brain derived neurotrophic factor</strong> transcription in the rat ventromedial prefrontal cortex.
+BDNF	addiction	aversion	23035088	Extinction of <b>aversive</b> memories associated with morphine withdrawal requires ERK mediated epigenetic regulation of <strong>brain derived neurotrophic factor</strong> transcription in the rat ventromedial prefrontal cortex.
+BDNF	addiction	withdrawal	23035088	Extinction of aversive memories associated with morphine <b>withdrawal</b> requires ERK mediated epigenetic regulation of <strong>brain derived neurotrophic factor</strong> transcription in the rat ventromedial prefrontal cortex.
+BDNF	addiction	aversion	23035088	In this study, we used conditioned place <b>aversion</b> (CPA), a highly sensitive model for measuring <b>aversive</b> memory of drug withdrawal, to investigate the role of epigenetic regulation of brain derived neurotrophic factor (<strong>BDNF</strong>) gene expression in extinction of <b>aversive</b> memory.
+BDNF	addiction	withdrawal	23035088	In this study, we used conditioned place aversion (CPA), a highly sensitive model for measuring aversive memory of drug <b>withdrawal</b>, to investigate the role of epigenetic regulation of brain derived neurotrophic factor (<strong>BDNF</strong>) gene expression in extinction of aversive memory.
+BDNF	addiction	aversion	23035088	In this study, we used conditioned place <b>aversion</b> (CPA), a highly sensitive model for measuring <b>aversive</b> memory of drug withdrawal, to investigate the role of epigenetic regulation of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene expression in extinction of <b>aversive</b> memory.
+BDNF	addiction	withdrawal	23035088	In this study, we used conditioned place aversion (CPA), a highly sensitive model for measuring aversive memory of drug <b>withdrawal</b>, to investigate the role of epigenetic regulation of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene expression in extinction of aversive memory.
+BDNF	drug	opioid	23035088	We found that CPA extinction training induced an increase in recruiting cAMP response element binding protein (CREB) to and acetylation of histone H3 at the promoters of <strong>BDNF</strong> exon I transcript and increased <strong>BDNF</strong> mRNA and protein expression in the ventromedial prefrontal cortex (vmPFC) of acute <b>morphine</b> dependent rats and that such epigenetic regulation of <strong>BDNF</strong> gene transcription could be facilitated or diminished by intra vmPFC infusion of HDAC inhibitor trichostatin A or extracellular signal regulated kinase (ERK) inhibitor U0126 (1,4 diamino 2,3 dicyano 1,4 bis(methylthio)butadiene) before extinction training.
+BDNF	drug	opioid	23035088	We conclude that extinction of aversive memory of <b>morphine</b> withdrawal requires epigenetic regulation of <strong>BDNF</strong> gene transcription in the vmPFC through activation of the ERK CREB signaling pathway perhaps in a NMDA receptor dependent manner.
+BDNF	addiction	aversion	23035088	We conclude that extinction of <b>aversive</b> memory of morphine withdrawal requires epigenetic regulation of <strong>BDNF</strong> gene transcription in the vmPFC through activation of the ERK CREB signaling pathway perhaps in a NMDA receptor dependent manner.
+BDNF	addiction	withdrawal	23035088	We conclude that extinction of aversive memory of morphine <b>withdrawal</b> requires epigenetic regulation of <strong>BDNF</strong> gene transcription in the vmPFC through activation of the ERK CREB signaling pathway perhaps in a NMDA receptor dependent manner.
+BDNF	drug	alcohol	23023098	<strong>Brain derived neurotrophic factor</strong> Val66Met polymorphism and <b>alcohol</b> related phenotypes.
+BDNF	addiction	addiction	23023098	Brain derived neurotrophic factor (<strong>BDNF</strong>) regulates mood, response to stress and interacts with neurotransmitters and stress systems involved in reward pathways and <b>addiction</b>.
+BDNF	addiction	reward	23023098	Brain derived neurotrophic factor (<strong>BDNF</strong>) regulates mood, response to stress and interacts with neurotransmitters and stress systems involved in <b>reward</b> pathways and addiction.
+BDNF	addiction	addiction	23023098	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) regulates mood, response to stress and interacts with neurotransmitters and stress systems involved in reward pathways and <b>addiction</b>.
+BDNF	addiction	reward	23023098	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) regulates mood, response to stress and interacts with neurotransmitters and stress systems involved in <b>reward</b> pathways and addiction.
+BDNF	drug	alcohol	23023098	Aim of the study was to evaluate the association between a single nucleotide polymorphism (<strong>BDNF</strong> Val66Met or rs6265) and <b>alcohol</b> related phenotypes in Caucasian patients.
+BDNF	drug	alcohol	23023098	In ethnically homogenous Caucasian subjects of the Croatian origin, the <strong>BDNF</strong> Val66Met genotype distribution was determined in 549 male and 126 female patients with <b>alcohol</b> dependence and in 655 male and 259 female healthy non <b>alcoholic</b> control subjects.
+BDNF	addiction	dependence	23023098	In ethnically homogenous Caucasian subjects of the Croatian origin, the <strong>BDNF</strong> Val66Met genotype distribution was determined in 549 male and 126 female patients with alcohol <b>dependence</b> and in 655 male and 259 female healthy non alcoholic control subjects.
+BDNF	drug	alcohol	23023098	The results showed no significant association between <strong>BDNF</strong> Val66Met variants and <b>alcohol</b> dependence and/or any of the <b>alcohol</b> related phenotypes in either Caucasian women, or men, with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	23023098	The results showed no significant association between <strong>BDNF</strong> Val66Met variants and alcohol <b>dependence</b> and/or any of the alcohol related phenotypes in either Caucasian women, or men, with alcohol <b>dependence</b>.
+BDNF	drug	alcohol	23023098	In conclusion, these data do not support the view that <strong>BDNF</strong> Val66Met polymorphism correlates with the specific <b>alcohol</b> related phenotypes in ethnically homogenous medication free Caucasian subjects with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	23023098	In conclusion, these data do not support the view that <strong>BDNF</strong> Val66Met polymorphism correlates with the specific alcohol related phenotypes in ethnically homogenous medication free Caucasian subjects with alcohol <b>dependence</b>.
+BDNF	drug	cocaine	23021567	<strong>Brain derived neurotrophic factor</strong> serum levels in <b>cocaine</b> dependent patients during early abstinence.
+BDNF	drug	cocaine	23021567	Preclinical studies indicate that brain derived neurotrophic factor (<strong>BDNF</strong>) is involved in neuroplastic changes underlying enduring <b>cocaine</b> seeking following withdrawal.
+BDNF	addiction	relapse	23021567	Preclinical studies indicate that brain derived neurotrophic factor (<strong>BDNF</strong>) is involved in neuroplastic changes underlying enduring cocaine <b>seeking</b> following withdrawal.
+BDNF	addiction	withdrawal	23021567	Preclinical studies indicate that brain derived neurotrophic factor (<strong>BDNF</strong>) is involved in neuroplastic changes underlying enduring cocaine seeking following <b>withdrawal</b>.
+BDNF	drug	cocaine	23021567	Preclinical studies indicate that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is involved in neuroplastic changes underlying enduring <b>cocaine</b> seeking following withdrawal.
+BDNF	addiction	relapse	23021567	Preclinical studies indicate that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is involved in neuroplastic changes underlying enduring cocaine <b>seeking</b> following withdrawal.
+BDNF	addiction	withdrawal	23021567	Preclinical studies indicate that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is involved in neuroplastic changes underlying enduring cocaine seeking following <b>withdrawal</b>.
+BDNF	drug	cocaine	23021567	However, little is known about temporal changes in serum <strong>BDNF</strong> levels or the involvement of <strong>BDNF</strong> in craving and abstinence in early abstinent <b>cocaine</b> dependent patients.
+BDNF	addiction	relapse	23021567	However, little is known about temporal changes in serum <strong>BDNF</strong> levels or the involvement of <strong>BDNF</strong> in <b>craving</b> and abstinence in early abstinent cocaine dependent patients.
+BDNF	drug	cocaine	23021567	Significantly lower serum <strong>BDNF</strong> levels (p<.0001) were observed for <b>cocaine</b> dependent patients at baseline compared to healthy controls.
+BDNF	addiction	relapse	23021567	Baseline <strong>BDNF</strong> levels correlated with <b>craving</b> (p=.034).
+BDNF	addiction	relapse	23021567	Post detoxification <strong>BDNF</strong> levels correlated with <b>craving</b> (p=.018), loss of control (p<.000), abstinence measures (p=0.031), depression (p=0.036), and anxiety (p=0.036).
+BDNF	addiction	relapse	23021567	Post detoxification <strong>BDNF</strong> levels also had predictive value for the loss of control measure of <b>craving</b>.
+BDNF	drug	cocaine	23021567	Chronic <b>cocaine</b> use is associated with decreased serum <strong>BDNF</strong>.
+BDNF	drug	cocaine	23021567	A progressive increase in serum <strong>BDNF</strong> levels during early abstinence correlates with <b>cocaine</b> craving and abstinence symptoms and may reflect increasing <strong>BDNF</strong> levels in different brain regions.
+BDNF	addiction	relapse	23021567	A progressive increase in serum <strong>BDNF</strong> levels during early abstinence correlates with cocaine <b>craving</b> and abstinence symptoms and may reflect increasing <strong>BDNF</strong> levels in different brain regions.
+BDNF	drug	cocaine	23021567	These findings suggest that serum <strong>BDNF</strong> may be a biomarker for <b>cocaine</b> addiction.
+BDNF	addiction	addiction	23021567	These findings suggest that serum <strong>BDNF</strong> may be a biomarker for cocaine <b>addiction</b>.
+BDNF	drug	alcohol	23020045	Chronic cocaine and <b>alcohol</b> treatment activate and repress many genes such as FosB, Cdk5, and <strong>Bdnf</strong>, where their dysregulation, at the chromatin level, contribute to the development and maintenance of addiction.
+BDNF	drug	cocaine	23020045	Chronic <b>cocaine</b> and alcohol treatment activate and repress many genes such as FosB, Cdk5, and <strong>Bdnf</strong>, where their dysregulation, at the chromatin level, contribute to the development and maintenance of addiction.
+BDNF	addiction	addiction	23020045	Chronic cocaine and alcohol treatment activate and repress many genes such as FosB, Cdk5, and <strong>Bdnf</strong>, where their dysregulation, at the chromatin level, contribute to the development and maintenance of <b>addiction</b>.
+BDNF	drug	alcohol	22989210	<strong>Brain derived neurotrophic factor</strong> genotype is associated with brain gray and white matter tissue volumes recovery in abstinent <b>alcohol</b> dependent individuals.
+BDNF	drug	alcohol	22989210	Here we assessed the effects of the <strong>BDNF</strong> Val66Met (rs6265) polymorphism on regional brain tissue volumes and their recovery during short term abstinence in treatment seeking <b>alcohol</b> dependent individuals.
+BDNF	addiction	relapse	22989210	Here we assessed the effects of the <strong>BDNF</strong> Val66Met (rs6265) polymorphism on regional brain tissue volumes and their recovery during short term abstinence in treatment <b>seeking</b> alcohol dependent individuals.
+BDNF	drug	alcohol	22989210	The findings suggest that functionally significant brain tissue volume recovery during abstinence from <b>alcohol</b> is influenced by <strong>BDNF</strong> genotype.
+BDNF	drug	alcohol	22974102	The effects of <b>alcohol</b> abstinence on <strong>BDNF</strong>, ghrelin, and leptin secretions in <b>alcohol</b> dependent patients with glucose intolerance.
+BDNF	drug	alcohol	22974102	<b>Alcohol</b> use affecting the risk of type 2 diabetes mellitus (T2DM) is poorly identified as well as the role of brain derived neurotrophic factor (<strong>BDNF</strong>), ghrelin, and leptin in <b>alcohol</b> dependence with T2DM.
+BDNF	addiction	dependence	22974102	Alcohol use affecting the risk of type 2 diabetes mellitus (T2DM) is poorly identified as well as the role of brain derived neurotrophic factor (<strong>BDNF</strong>), ghrelin, and leptin in alcohol <b>dependence</b> with T2DM.
+BDNF	drug	alcohol	22974102	<b>Alcohol</b> use affecting the risk of type 2 diabetes mellitus (T2DM) is poorly identified as well as the role of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), ghrelin, and leptin in <b>alcohol</b> dependence with T2DM.
+BDNF	addiction	dependence	22974102	Alcohol use affecting the risk of type 2 diabetes mellitus (T2DM) is poorly identified as well as the role of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), ghrelin, and leptin in alcohol <b>dependence</b> with T2DM.
+BDNF	drug	alcohol	22974102	We tested the hypothesis that <b>alcohol</b> abstinence affects diabetes related factors and <strong>BDNF</strong>, ghrelin, and leptin secretions in <b>alcohol</b> dependent patients with glucose intolerance.
+BDNF	drug	alcohol	22974102	All participants got <b>alcohol</b> dependence rehabilitation treatment for 30 days, and then we compared changes in <strong>BDNF</strong>, ghrelin, and leptin between pre  and post <b>alcohol</b> abstinence.
+BDNF	addiction	dependence	22974102	All participants got alcohol <b>dependence</b> rehabilitation treatment for 30 days, and then we compared changes in <strong>BDNF</strong>, ghrelin, and leptin between pre  and post alcohol abstinence.
+BDNF	drug	nicotine	22959963	Moreover, these behavioral effects of <b>nicotine</b> are accompanied by a persistent imbalance between neuropeptide Y and corticotrophin releasing factor systems, and a persistent increase in brain derived neurotrophic factor (<strong>BDNF</strong>) and spinophilin mRNA levels in the amygdala.
+BDNF	drug	nicotine	22959963	Moreover, these behavioral effects of <b>nicotine</b> are accompanied by a persistent imbalance between neuropeptide Y and corticotrophin releasing factor systems, and a persistent increase in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and spinophilin mRNA levels in the amygdala.
+BDNF	drug	cannabinoid	22959963	Furthermore, treatment with the <b>cannabinoid</b> receptor 1 antagonist, AM251 (5 mg/kg) during a short (1 wk) abstinence is ineffective in reversing nicotine induced anxiety, fluctuations in <strong>BDNF</strong> and spinophilin mRNAs, and the neuropeptidergic dysregulations in the amygdala; although this treatment is effective in reversing the expression of locomotor sensitization to challenge nicotine even after a long abstinence.
+BDNF	drug	nicotine	22959963	Furthermore, treatment with the cannabinoid receptor 1 antagonist, AM251 (5 mg/kg) during a short (1 wk) abstinence is ineffective in reversing <b>nicotine</b> induced anxiety, fluctuations in <strong>BDNF</strong> and spinophilin mRNAs, and the neuropeptidergic dysregulations in the amygdala; although this treatment is effective in reversing the expression of locomotor sensitization to challenge <b>nicotine</b> even after a long abstinence.
+BDNF	addiction	sensitization	22959963	Furthermore, treatment with the cannabinoid receptor 1 antagonist, AM251 (5 mg/kg) during a short (1 wk) abstinence is ineffective in reversing nicotine induced anxiety, fluctuations in <strong>BDNF</strong> and spinophilin mRNAs, and the neuropeptidergic dysregulations in the amygdala; although this treatment is effective in reversing the expression of locomotor <b>sensitization</b> to challenge nicotine even after a long abstinence.
+BDNF	drug	nicotine	22959963	Interestingly, the identical AM251 treatment administered during the late phase of a long abstinence further augments anxiety and associated changes in <strong>BDNF</strong> and spinophilin mRNA in the basolateral nucleus of the amygdala in <b>nicotine</b> pre exposed HRs.
+BDNF	drug	opioid	22856871	Influence of <strong>brain derived neurotrophic factor</strong> genetic polymorphisms on the ages of onset for <b>heroin</b> dependence in a Chinese population.
+BDNF	addiction	dependence	22856871	Influence of <strong>brain derived neurotrophic factor</strong> genetic polymorphisms on the ages of onset for heroin <b>dependence</b> in a Chinese population.
+BDNF	drug	opioid	22856871	The study aims at evaluating the association between brain derived neurotrophic factor (<strong>BDNF</strong>) gene polymorphisms and <b>heroin</b> dependent patients in the Chinese population.
+BDNF	drug	opioid	22856871	The study aims at evaluating the association between <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene polymorphisms and <b>heroin</b> dependent patients in the Chinese population.
+BDNF	drug	opioid	22856871	Three polymorphisms of the <strong>BDNF</strong> gene (rs10835210, rs16917234, and rs6265) in 486 <b>heroin</b> dependent patients and in 226 healthy controls were genotyped for analyzing the association of these polymorphisms with age of onset of <b>heroin</b> dependence.
+BDNF	addiction	dependence	22856871	Three polymorphisms of the <strong>BDNF</strong> gene (rs10835210, rs16917234, and rs6265) in 486 heroin dependent patients and in 226 healthy controls were genotyped for analyzing the association of these polymorphisms with age of onset of heroin <b>dependence</b>.
+BDNF	drug	opioid	22856871	We defined the healthy cases as "unknown phenotype" and used the endophenotype (behavior traits) to stratify the <b>heroin</b> dependents group on the basis of self reporting traits for examining the association between <strong>BDNF</strong> polymorphisms (rs10835210, rs16917234, and rs6265) and <b>heroin</b> dependence.
+BDNF	addiction	dependence	22856871	We defined the healthy cases as "unknown phenotype" and used the endophenotype (behavior traits) to stratify the heroin dependents group on the basis of self reporting traits for examining the association between <strong>BDNF</strong> polymorphisms (rs10835210, rs16917234, and rs6265) and heroin <b>dependence</b>.
+BDNF	drug	opioid	22856871	Allelic distributions of <strong>BDNF</strong> gene polymorphisms did not differ significantly between <b>heroin</b> dependent patients and controls.
+BDNF	drug	opioid	22856871	However, we found that the AA carriers of <strong>BDNF</strong> rs6265 had an earlier onset of <b>heroin</b> dependence and a clearer tendency of family history of <b>heroin</b> dependent than GG carriers after controlling behavior characteristics across rs6265 genotypes.
+BDNF	addiction	dependence	22856871	However, we found that the AA carriers of <strong>BDNF</strong> rs6265 had an earlier onset of heroin <b>dependence</b> and a clearer tendency of family history of heroin dependent than GG carriers after controlling behavior characteristics across rs6265 genotypes.
+BDNF	drug	opioid	22856871	Our findings suggested that the <strong>BDNF</strong> genetic polymorphism (rs6265) may have effects on the age of onset of <b>heroin</b> dependence among the Chinese population.
+BDNF	addiction	dependence	22856871	Our findings suggested that the <strong>BDNF</strong> genetic polymorphism (rs6265) may have effects on the age of onset of heroin <b>dependence</b> among the Chinese population.
+BDNF	drug	opioid	22856871	The <strong>BDNF</strong> gene could contribute to vulnerabilities to <b>heroin</b> dependence.
+BDNF	addiction	dependence	22856871	The <strong>BDNF</strong> gene could contribute to vulnerabilities to heroin <b>dependence</b>.
+BDNF	addiction	addiction	22854676	Brain derived neurotrophic factor (<strong>BDNF</strong>) plays important roles in neurotransmitter release and synaptic plasticity and has been hypothesized to be involved in the development and maintenance of <b>addictive</b> disorders.
+BDNF	addiction	addiction	22854676	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) plays important roles in neurotransmitter release and synaptic plasticity and has been hypothesized to be involved in the development and maintenance of <b>addictive</b> disorders.
+BDNF	addiction	addiction	22854676	The objective of this study was to investigate alterations of <strong>BDNF</strong> expression in a non substance related <b>addiction</b>, i.e.
+BDNF	drug	nicotine	22854676	Serum levels of <strong>BDNF</strong> were assessed in male patients with PG (n = 14) and healthy control subjects (n = 13) carefully matched for sex, age, body mass index, <b>smoking</b> status and urbanicity.
+BDNF	addiction	addiction	22854676	Our results show alterations of <strong>BDNF</strong> serum levels in patients suffering from a behavioural <b>addiction</b> and suggest that non substance related addictions like PG might be associated with neuroendocrinological changes similar to the changes observed in substance related addictions.
+BDNF	drug	cocaine	22832183	Companions reverse stressor induced decreases in neurogenesis and <b>cocaine</b> conditioning possibly by restoring <strong>BDNF</strong> and NGF levels in dentate gyrus.
+BDNF	drug	cocaine	22832183	Intra ventricular infusion with K252a, a mixed TrkA and TrkB antagonist, did not affect the protective effects of companions on local NGF, <strong>BDNF</strong> levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and <b>cocaine</b> induced CPP.
+BDNF	addiction	reward	22832183	Intra ventricular infusion with K252a, a mixed TrkA and TrkB antagonist, did not affect the protective effects of companions on local NGF, <strong>BDNF</strong> levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and cocaine induced <b>CPP</b>.
+BDNF	drug	cocaine	22832183	These results, taken together, indicate that stressor decreased NGF and <strong>BDNF</strong> levels in DG could be involved in the stressor decreased DG neurogenesis and <b>cocaine</b> conditioning.
+BDNF	drug	cocaine	22832183	The presence of companions reverses the stressor decreased DG neurogenesis and <b>cocaine</b> conditioning possibly by restoring <strong>BDNF</strong> and NGF levels in DG.
+BDNF	drug	opioid	22790874	Association of time dependent changes in mu <b>opioid</b> receptor mRNA, but not <strong>BDNF</strong>, TrkB, or MeCP2 mRNA and protein expression in the rat nucleus accumbens with incubation of <b>heroin</b> craving.
+BDNF	addiction	relapse	22790874	Association of time dependent changes in mu opioid receptor mRNA, but not <strong>BDNF</strong>, TrkB, or MeCP2 mRNA and protein expression in the rat nucleus accumbens with incubation of heroin <b>craving</b>.
+BDNF	drug	opioid	22790874	We investigated whether this incubation is associated with time dependent changes in brain derived neurotrophic factor (<strong>BDNF</strong>) and methyl CpG binding protein 2 (MeCP2) signaling and mu <b>opioid</b> receptor (MOR) expression in nucleus accumbens (NAc), dorsal striatum (DS), and medial prefrontal cortex (mPFC).
+BDNF	drug	opioid	22790874	We investigated whether this incubation is associated with time dependent changes in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and methyl CpG binding protein 2 (MeCP2) signaling and mu <b>opioid</b> receptor (MOR) expression in nucleus accumbens (NAc), dorsal striatum (DS), and medial prefrontal cortex (mPFC).
+BDNF	drug	opioid	22790874	We trained rats to self administer <b>heroin</b> or saline for 9 10 days and then dissected the NAc, DS, and mPFC at different abstinence days and measured mRNA and protein levels of <strong>BDNF</strong>, TrkB, and MeCP2, as well as MOR mRNA (Oprm1).
+BDNF	drug	cocaine	22790874	As previous studies implicated NAc <strong>BDNF</strong> in incubation of <b>cocaine</b> craving, our data suggest that different mechanisms contribute to incubation of heroin versus <b>cocaine</b> craving.
+BDNF	drug	opioid	22790874	As previous studies implicated NAc <strong>BDNF</strong> in incubation of cocaine craving, our data suggest that different mechanisms contribute to incubation of <b>heroin</b> versus cocaine craving.
+BDNF	addiction	relapse	22790874	As previous studies implicated NAc <strong>BDNF</strong> in incubation of cocaine <b>craving</b>, our data suggest that different mechanisms contribute to incubation of heroin versus cocaine <b>craving</b>.
+BDNF	addiction	relapse	22741574	We measured the contents of brain derived neurotrophic factor (<strong>BDNF</strong>), c Fos and Fas associated death domain (FADD) proteins in the medial prefrontal cortex (mPFC) following <b>reinstatement</b>.
+BDNF	addiction	relapse	22741574	We measured the contents of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), c Fos and Fas associated death domain (FADD) proteins in the medial prefrontal cortex (mPFC) following <b>reinstatement</b>.
+BDNF	addiction	relapse	22741574	Reductions in drug <b>seeking</b> during <b>reinstatement</b> were matched by downward shifts in the contents of <strong>BDNF</strong>, c Fos and FADD proteins in the mPFC, which were elevated in relapsing rats.
+BDNF	addiction	dependence	22682406	These results demonstrate that atorvastatin exerts an antidepressant like effect and point to <b>dependence</b> on the inhibition of NMDA receptors and NO cGMP synthesis, and on the increase of hippocampal <strong>BDNF</strong> levels.
+BDNF	drug	alcohol	22546227	<strong>Brain derived neurotrophic factor</strong> expression after acute administration of <b>ethanol</b>.
+BDNF	addiction	reward	22546227	Earlier findings suggest that, in addition to its well known neurotrophic role, brain derived neurotrophic factor (<strong>BDNF</strong>) is also involved in the rewarding and <b>reinforcing</b> effects of drugs of abuse.
+BDNF	addiction	reward	22546227	Earlier findings suggest that, in addition to its well known neurotrophic role, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is also involved in the rewarding and <b>reinforcing</b> effects of drugs of abuse.
+BDNF	drug	alcohol	22546227	<b>Ethanol</b> decreased <strong>BDNF</strong> mRNA levels dose dependently in the hippocampus, and after the higher <b>ethanol</b> dose in the frontal cortex, nucleus accumbens and amygdala, while increasing them in the ventral tegmental area.
+BDNF	drug	alcohol	22546227	These data suggest that <strong>BDNF</strong> is involved in the acute effects of <b>ethanol</b>, but separate brain areas may be differentially engaged in the mediation of these effects.
+BDNF	addiction	sensitization	22521816	Here, we hypothesized that social defeat stress would increase ΔFosB expression in <strong>BDNF</strong> containing mesocorticolimbic neurons at a time when cross <b>sensitization</b> is evident.
+BDNF	addiction	sensitization	22521816	Increased ΔFosB/<strong>BDNF</strong> co expression and persistent functional activation of corticolimbic neurons after stress may contribute to mechanisms underlying cross <b>sensitization</b> to psychostimulants.
+BDNF	drug	amphetamine	22458544	Serum <strong>brain derived neurotrophic factor</strong> levels were reduced during <b>methamphetamine</b> early withdrawal.
+BDNF	addiction	withdrawal	22458544	Serum <strong>brain derived neurotrophic factor</strong> levels were reduced during methamphetamine early <b>withdrawal</b>.
+BDNF	drug	amphetamine	22458544	Animal studies have shown that brain derived neurotrophic factor (<strong>BDNF</strong>) decreased after repeated <b>amphetamine</b> administration and increased at 30 and 90 days from psychostimulant withdrawal, suggesting that there might be a psychostimulant induced neuroprotective dysfunction followed by a neuroadaptive process in the brain.
+BDNF	addiction	withdrawal	22458544	Animal studies have shown that brain derived neurotrophic factor (<strong>BDNF</strong>) decreased after repeated amphetamine administration and increased at 30 and 90 days from psychostimulant <b>withdrawal</b>, suggesting that there might be a psychostimulant induced neuroprotective dysfunction followed by a neuroadaptive process in the brain.
+BDNF	drug	amphetamine	22458544	Animal studies have shown that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) decreased after repeated <b>amphetamine</b> administration and increased at 30 and 90 days from psychostimulant withdrawal, suggesting that there might be a psychostimulant induced neuroprotective dysfunction followed by a neuroadaptive process in the brain.
+BDNF	addiction	withdrawal	22458544	Animal studies have shown that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) decreased after repeated amphetamine administration and increased at 30 and 90 days from psychostimulant <b>withdrawal</b>, suggesting that there might be a psychostimulant induced neuroprotective dysfunction followed by a neuroadaptive process in the brain.
+BDNF	drug	amphetamine	22458544	However, current research on the role of <strong>BDNF</strong> in human <b>METH</b> addiction is limited, particularly during early withdrawal.
+BDNF	addiction	addiction	22458544	However, current research on the role of <strong>BDNF</strong> in human METH <b>addiction</b> is limited, particularly during early withdrawal.
+BDNF	addiction	withdrawal	22458544	However, current research on the role of <strong>BDNF</strong> in human METH addiction is limited, particularly during early <b>withdrawal</b>.
+BDNF	drug	amphetamine	22458544	The aim of this study was to assess the serum <strong>BDNF</strong> levels in <b>METH</b> abusers during the early withdrawal stage.
+BDNF	addiction	withdrawal	22458544	The aim of this study was to assess the serum <strong>BDNF</strong> levels in METH abusers during the early <b>withdrawal</b> stage.
+BDNF	drug	amphetamine	22458544	We found that serum <strong>BDNF</strong> levels were significantly and constantly lower in the <b>METH</b> abusers during early withdrawal than those of the healthy controls.
+BDNF	addiction	withdrawal	22458544	We found that serum <strong>BDNF</strong> levels were significantly and constantly lower in the METH abusers during early <b>withdrawal</b> than those of the healthy controls.
+BDNF	drug	amphetamine	22458544	This indicates that <b>METH</b> abusers might have severe <strong>BDNF</strong> dysfunction and an impaired neuroprotective function after repetitive <b>METH</b> misuse.
+BDNF	drug	amphetamine	22445683	Gender, <strong>brain derived neurotrophic factor</strong> Val66Met, and frequency of <b>methamphetamine</b> use.
+BDNF	drug	opioid	22410736	Expression levels of the <strong>BDNF</strong> gene and histone modifications around its promoters in the ventral tegmental area and locus ceruleus of rats during forced abstinence from <b>morphine</b>.
+BDNF	addiction	addiction	22410736	Brain derived neurotrophic factor (<strong>BDNF</strong>) plays a role in mediating molecular, cellular, and behavioral adaptations underlying drug <b>addiction</b>.
+BDNF	addiction	addiction	22410736	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) plays a role in mediating molecular, cellular, and behavioral adaptations underlying drug <b>addiction</b>.
+BDNF	drug	opioid	22410736	Here, we examined the influence of withdrawal from repeated <b>morphine</b> treatment on the expression of <strong>BDNF</strong> mRNA in the ventral tegmental area (VTA) and locus coeruleus (LC) of the rat brain.
+BDNF	addiction	withdrawal	22410736	Here, we examined the influence of <b>withdrawal</b> from repeated morphine treatment on the expression of <strong>BDNF</strong> mRNA in the ventral tegmental area (VTA) and locus coeruleus (LC) of the rat brain.
+BDNF	drug	opioid	22410736	Results of qRT PCR showed that levels of <strong>BDNF</strong> mRNA in both VTA and LC were significantly increased 7 days rather than 2 h or 24 h following the last injection of <b>morphine</b>.
+BDNF	drug	opioid	22410736	Consistently, CHIP and qPCR analysis revealed that on day 7 of <b>morphine</b> abstinence, both VTA and LC levels of histone methylation at <strong>BDNF</strong> promoters II and III of <b>morphine</b> treated rats were significantly lower than control animals.
+BDNF	drug	cocaine	22394056	Enhanced extinction of <b>cocaine</b> seeking in <strong>brain derived neurotrophic factor</strong> Val66Met knock in mice.
+BDNF	addiction	relapse	22394056	Enhanced extinction of cocaine <b>seeking</b> in <strong>brain derived neurotrophic factor</strong> Val66Met knock in mice.
+BDNF	drug	cocaine	22394056	Therefore, we examined operant learning and extinction of both food and <b>cocaine</b> self administration behavior in an inbred genetic knock in mouse strain expressing the variant <strong>Bdnf</strong>.
+BDNF	addiction	reward	22394056	Therefore, we examined <b>operant</b> learning and extinction of both food and cocaine self administration behavior in an inbred genetic knock in mouse strain expressing the variant <strong>Bdnf</strong>.
+BDNF	addiction	reward	22394056	<strong>BDNF</strong>(Met/Met) mice exhibited a severe deficit in <b>operant</b> learning as demonstrated by an inability to learn the food self administration task.
+BDNF	drug	cocaine	22394056	Therefore, extinction experiments were performed comparing wildtype (<strong>BDNF</strong>(Val/Val)) animals to mice heterozygous for the Met allele (<strong>BDNF</strong>(Val/Met)), which did not differ in food or <b>cocaine</b> self administration behavior.
+BDNF	drug	cocaine	22394056	In contrast to the deficit in fear extinction previously demonstrated in these mice, we found that <strong>BDNF</strong>(Val/Met) mice exhibited more rapid extinction of <b>cocaine</b> responding compared to wildtype mice.
+BDNF	addiction	aversion	22394056	These results suggest that the molecular mechanisms underlying <b>aversive</b> and appetitive extinction are distinct from one another and <strong>BDNF</strong> may play opposing roles in the two phenomena.
+BDNF	drug	opioid	22339949	<strong>BDNF</strong> Val(66)Met genotype is associated with drug seeking phenotypes in <b>heroin</b> dependent individuals: a pilot study.
+BDNF	addiction	relapse	22339949	<strong>BDNF</strong> Val(66)Met genotype is associated with drug <b>seeking</b> phenotypes in heroin dependent individuals: a pilot study.
+BDNF	addiction	addiction	22339949	To examine its relevance for <b>addiction</b>, we examined <strong>BDNF</strong> genotype differences in drug seeking behavior.
+BDNF	addiction	relapse	22339949	To examine its relevance for addiction, we examined <strong>BDNF</strong> genotype differences in drug <b>seeking</b> behavior.
+BDNF	drug	opioid	22339949	<strong>BDNF</strong> Val(66)Met genotype predicted 18.4% of variance in 'weekly <b>heroin</b> investment' (purchasing time × amount × frequency).
+BDNF	addiction	reward	22339949	These data suggest that the <strong>BDNF</strong> Met allele may confer a 'preferred drug invested' phenotype, resistant to moderating effects of higher drug prices and non drug <b>reinforcement</b>.
+BDNF	drug	amphetamine	22217949	COMT Val158Met, <strong>BDNF</strong> Val66Met, and OPRM1 Asn40Asp and <b>methamphetamine</b> dependence treatment response: preliminary investigation.
+BDNF	addiction	dependence	22217949	COMT Val158Met, <strong>BDNF</strong> Val66Met, and OPRM1 Asn40Asp and methamphetamine <b>dependence</b> treatment response: preliminary investigation.
+BDNF	drug	cocaine	22209827	Because <b>cocaine</b> seeking is associated with increased brain derived neurotrophic factor (<strong>BDNF</strong>) in the brain, we examined whether synthetic mouse TCAP 1 has the potential to regulate <strong>BDNF</strong> expression in immortalized mouse neurons.
+BDNF	addiction	relapse	22209827	Because cocaine <b>seeking</b> is associated with increased brain derived neurotrophic factor (<strong>BDNF</strong>) in the brain, we examined whether synthetic mouse TCAP 1 has the potential to regulate <strong>BDNF</strong> expression in immortalized mouse neurons.
+BDNF	drug	cocaine	22209827	Because <b>cocaine</b> seeking is associated with increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the brain, we examined whether synthetic mouse TCAP 1 has the potential to regulate <strong>BDNF</strong> expression in immortalized mouse neurons.
+BDNF	addiction	relapse	22209827	Because cocaine <b>seeking</b> is associated with increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the brain, we examined whether synthetic mouse TCAP 1 has the potential to regulate <strong>BDNF</strong> expression in immortalized mouse neurons.
+BDNF	drug	opioid	22205542	To clarify the effects of chronic <b>morphine</b> and low dose memantine, serum and brain levels of cytokines and brain derived neurotrophic factor (<strong>BDNF</strong>) were measured.
+BDNF	drug	opioid	22205542	To clarify the effects of chronic <b>morphine</b> and low dose memantine, serum and brain levels of cytokines and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) were measured.
+BDNF	drug	opioid	22205542	After 6 days of <b>morphine</b> treatment, cytokine (IL 1β, IL 6) levels had significantly increased in serum; IL 1β and IL 6 mRNA levels had significantly increased in the nucleus accumbens and medial prefrontal cortex, both addiction related brain areas; and <strong>BDNF</strong> levels had significantly decreased, both in serum and in addiction related brain areas.
+BDNF	addiction	addiction	22205542	After 6 days of morphine treatment, cytokine (IL 1β, IL 6) levels had significantly increased in serum; IL 1β and IL 6 mRNA levels had significantly increased in the nucleus accumbens and medial prefrontal cortex, both <b>addiction</b> related brain areas; and <strong>BDNF</strong> levels had significantly decreased, both in serum and in <b>addiction</b> related brain areas.
+BDNF	drug	opioid	22205542	We hypothesize that neuronal inflammation and <strong>BDNF</strong> downregulation are related to the progression of <b>opioid</b> addiction.
+BDNF	addiction	addiction	22205542	We hypothesize that neuronal inflammation and <strong>BDNF</strong> downregulation are related to the progression of opioid <b>addiction</b>.
+BDNF	drug	alcohol	22129841	The analysis used logistic and Cox regression methods to evaluate the contributions of age; sex; number of intake <b>alcohol</b>, drug use, and depression symptoms; and either GABRA2, CHRM2, ANKK1, <strong>BDNF</strong>, or KIBRA SNP genotypes to outcome.
+BDNF	drug	alcohol	22126132	Environmental enrichment blocks <b>ethanol</b> induced locomotor sensitization and decreases <strong>BDNF</strong> levels in the prefrontal cortex in mice.
+BDNF	addiction	sensitization	22126132	Environmental enrichment blocks ethanol induced locomotor <b>sensitization</b> and decreases <strong>BDNF</strong> levels in the prefrontal cortex in mice.
+BDNF	drug	alcohol	22126132	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been associated with behaviors related to <b>ethanol</b> addiction.
+BDNF	addiction	addiction	22126132	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been associated with behaviors related to ethanol <b>addiction</b>.
+BDNF	drug	alcohol	22126132	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been associated with behaviors related to <b>ethanol</b> addiction.
+BDNF	addiction	addiction	22126132	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been associated with behaviors related to ethanol <b>addiction</b>.
+BDNF	drug	alcohol	22126132	The aim of the present study was to evaluate the effects of EE on <b>ethanol</b> induced behavioral sensitization and <strong>BDNF</strong> expression.
+BDNF	addiction	sensitization	22126132	The aim of the present study was to evaluate the effects of EE on ethanol induced behavioral <b>sensitization</b> and <strong>BDNF</strong> expression.
+BDNF	drug	alcohol	22126132	Both repeated <b>ethanol</b> and EE decreased <strong>BDNF</strong> levels in the prefrontal cortex but not in the hippocampus.
+BDNF	drug	alcohol	22126132	However, <strong>BDNF</strong> levels were lower in <b>ethanol</b> treated mice exposed to EE.
+BDNF	addiction	addiction	22126132	Additionally, EE alters <strong>BDNF</strong> levels, which regulate <b>addiction</b> related behaviors.
+BDNF	drug	cocaine	22072694	CREB also increased the effort exerted by rats to obtain <b>cocaine</b> on more demanding progressive ratio schedules, an effect highly correlated with viral induced modulation of <strong>BDNF</strong> protein in the NAc shell.
+BDNF	drug	alcohol	22047728	Cerebellum volume in high risk offspring from multiplex <b>alcohol</b> dependence families: association with allelic variation in GABRA2 and <strong>BDNF</strong>.
+BDNF	addiction	dependence	22047728	Cerebellum volume in high risk offspring from multiplex alcohol <b>dependence</b> families: association with allelic variation in GABRA2 and <strong>BDNF</strong>.
+BDNF	drug	cocaine	22043863	Increased brain derived neurotrophic factor (<strong>BDNF</strong>) expression in the ventral tegmental area during <b>cocaine</b> abstinence is associated with increased histone acetylation at <strong>BDNF</strong> exon I containing promoters.
+BDNF	drug	cocaine	22043863	Increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression in the ventral tegmental area during <b>cocaine</b> abstinence is associated with increased histone acetylation at <strong>BDNF</strong> exon I containing promoters.
+BDNF	drug	cocaine	22043863	Specifically, incubation of <b>cocaine</b> seeking behavior coincides with increased brain derived neurotrophic factor (<strong>BDNF</strong>) protein expression in the ventral tegmental area (VTA).
+BDNF	addiction	relapse	22043863	Specifically, incubation of cocaine <b>seeking</b> behavior coincides with increased brain derived neurotrophic factor (<strong>BDNF</strong>) protein expression in the ventral tegmental area (VTA).
+BDNF	drug	cocaine	22043863	Specifically, incubation of <b>cocaine</b> seeking behavior coincides with increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) protein expression in the ventral tegmental area (VTA).
+BDNF	addiction	relapse	22043863	Specifically, incubation of cocaine <b>seeking</b> behavior coincides with increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) protein expression in the ventral tegmental area (VTA).
+BDNF	drug	cocaine	22043863	However, the molecular mechanisms that regulate time dependent changes in VTA <strong>BDNF</strong> protein expression during <b>cocaine</b> abstinence are unclear.
+BDNF	drug	cocaine	22043863	The goal of these experiments was to determine whether VTA <strong>BDNF</strong> transcript levels are altered following <b>cocaine</b> abstinence and identify the molecular mechanisms regulating <b>cocaine</b> induced changes in VTA <strong>BDNF</strong> transcription.
+BDNF	drug	cocaine	22043863	<strong>BDNF</strong> protein and exon I containing transcripts were significantly increased in the VTA of <b>cocaine</b> experienced rats following 7 days of forced drug abstinence compared to yoked saline controls.
+BDNF	drug	cocaine	22043863	<b>Cocaine</b> induced changes in <strong>BDNF</strong> mRNA were associated with increased acetylation of histone 3 and binding of CREB binding protein to exon I containing promoters in the VTA.
+BDNF	drug	cocaine	22043863	Taken together, these results suggest that drug abstinence following <b>cocaine</b> self administration remodels chromatin in the VTA resulting in increased expression of <strong>BDNF</strong>, which may contribute to neuroadaptations underlying <b>cocaine</b> craving and relapse.
+BDNF	addiction	relapse	22043863	Taken together, these results suggest that drug abstinence following cocaine self administration remodels chromatin in the VTA resulting in increased expression of <strong>BDNF</strong>, which may contribute to neuroadaptations underlying cocaine <b>craving</b> and <b>relapse</b>.
+BDNF	drug	cannabinoid	22029953	Intense exercise increases circulating <b>endocannabinoid</b> and <strong>BDNF</strong> levels in humans  possible implications for reward and depression.
+BDNF	addiction	reward	22029953	Intense exercise increases circulating endocannabinoid and <strong>BDNF</strong> levels in humans  possible implications for <b>reward</b> and depression.
+BDNF	drug	cannabinoid	22029953	The <b>endocannabinoid</b> system is known to have positive effects on depression partly through its actions on neurotrophins, such as Brain Derived Neurotrophic Factor (<strong>BDNF</strong>).
+BDNF	drug	cannabinoid	22029953	The <b>endocannabinoid</b> system is known to have positive effects on depression partly through its actions on neurotrophins, such as <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	cannabinoid	22029953	As <strong>BDNF</strong> is also considered the major candidate molecule for exercise induced brain plasticity, we hypothesized that the <b>endocannabinoid</b> system represents a crucial signaling system mediating the beneficial antidepressant effects of exercise.
+BDNF	drug	cannabinoid	22029953	Here we investigated, in 11 healthy trained male cyclists, the effects of an intense exercise (60 min at 55% followed by 30 min at 75% W(max)) on plasma levels of <b>endocannabinoids</b> (anandamide, AEA and 2 arachidonoylglycerol, 2 AG) and their possible link with serum <strong>BDNF</strong>.
+BDNF	drug	alcohol	22005582	Ameliorative effect of <strong>BDNF</strong> on prenatal <b>ethanol</b> and stress exposure induced behavioral disorders.
+BDNF	drug	alcohol	22005582	The present experiments investigated whether <strong>BDNF</strong> ameliorates the damaging effect of prenatal <b>ethanol</b> and stress exposure on behavior in offspring.
+BDNF	drug	nicotine	21990022	Gestational IV <b>nicotine</b> produces elevated <strong>brain derived neurotrophic factor</strong> in the mesocorticolimbic dopamine system of adolescent rat offspring.
+BDNF	drug	amphetamine	21990022	In this experiment, a novel intravenous (IV) exposure model was used to determine if gestational nicotine (GN) treatment produced alterations in <b>methamphetamine</b> induced sensitization and the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in the mesocorticolimbic dopamine (DA) system of adolescent offspring.
+BDNF	drug	nicotine	21990022	In this experiment, a novel intravenous (IV) exposure model was used to determine if gestational <b>nicotine</b> (GN) treatment produced alterations in methamphetamine induced sensitization and the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in the mesocorticolimbic dopamine (DA) system of adolescent offspring.
+BDNF	addiction	sensitization	21990022	In this experiment, a novel intravenous (IV) exposure model was used to determine if gestational nicotine (GN) treatment produced alterations in methamphetamine induced <b>sensitization</b> and the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in the mesocorticolimbic dopamine (DA) system of adolescent offspring.
+BDNF	drug	amphetamine	21990022	In this experiment, a novel intravenous (IV) exposure model was used to determine if gestational nicotine (GN) treatment produced alterations in <b>methamphetamine</b> induced sensitization and the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the mesocorticolimbic dopamine (DA) system of adolescent offspring.
+BDNF	drug	nicotine	21990022	In this experiment, a novel intravenous (IV) exposure model was used to determine if gestational <b>nicotine</b> (GN) treatment produced alterations in methamphetamine induced sensitization and the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the mesocorticolimbic dopamine (DA) system of adolescent offspring.
+BDNF	addiction	sensitization	21990022	In this experiment, a novel intravenous (IV) exposure model was used to determine if gestational nicotine (GN) treatment produced alterations in methamphetamine induced <b>sensitization</b> and the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the mesocorticolimbic dopamine (DA) system of adolescent offspring.
+BDNF	drug	amphetamine	21990022	Interestingly, GN, but not adolescent <b>methamphetamine</b> treatment, elevated levels of <strong>BDNF</strong> in the NAcc and Str; however, the GN induced increase in <strong>BDNF</strong> in the FC was attenuated by adolescent <b>methamphetamine</b> treatment.
+BDNF	drug	amphetamine	21990022	Both GN and adolescent <b>methamphetamine</b> treatment increased <strong>BDNF</strong> in the Hipp.
+BDNF	drug	amphetamine	21990022	These findings indicate that GN exposure will result in increased levels of <strong>BDNF</strong> protein throughout the mesocorticolimbic DA system during adolescent development and suggests that <b>methamphetamine</b> abuse will modulate the expression of <strong>BDNF</strong> in motivational circuitries of adolescent offspring exposed to GN.
+BDNF	drug	cocaine	21967984	Is <strong>brain derived neurotrophic factor</strong> a selective biomarker that predicts <b>cocaine</b> relapse outcomes?
+BDNF	addiction	relapse	21967984	Is <strong>brain derived neurotrophic factor</strong> a selective biomarker that predicts cocaine <b>relapse</b> outcomes?
+BDNF	addiction	relapse	21890593	Serum levels of <strong>BDNF</strong> are associated with <b>craving</b> in opiate dependent patients.
+BDNF	addiction	addiction	21890593	Preclinical study results suggest that brain derived neurotrophic factor (<strong>BDNF</strong>) and glial cell line derived neurotrophic factor (GDNF) are involved in the modulation of <b>addictive</b> behaviour.
+BDNF	addiction	addiction	21890593	Preclinical study results suggest that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and glial cell line derived neurotrophic factor (GDNF) are involved in the modulation of <b>addictive</b> behaviour.
+BDNF	drug	opioid	21890593	<strong>BDNF</strong> serum levels were significantly associated with craving for <b>heroin</b> (measured by the <b>Heroin</b> Craving Questionnaire (r = 0.420, p = 0.029) and by the General Craving Scale (r = 0.457, p = 0.016), whereas GDNF serum levels were not associated with psychometric dimensions of <b>heroin</b> craving.
+BDNF	addiction	relapse	21890593	<strong>BDNF</strong> serum levels were significantly associated with <b>craving</b> for heroin (measured by the Heroin <b>Craving</b> Questionnaire (r = 0.420, p = 0.029) and by the General <b>Craving</b> Scale (r = 0.457, p = 0.016), whereas GDNF serum levels were not associated with psychometric dimensions of heroin <b>craving</b>.
+BDNF	addiction	relapse	21890593	In conclusion, our results show a positive association between <strong>BDNF</strong> serum levels and opiate <b>craving</b> in opiate dependent patients.
+BDNF	drug	opioid	21886595	Since activation of pain pathways result in exhaustion of growth factors, we examined the influence of cerebrolysin, a mixture of potent growth factors (<strong>BDNF</strong>, GDNF, NGF, CNTF etc,) on <b>morphine</b> induced HSP expression.
+BDNF	addiction	addiction	21886571	Low <strong>BDNF</strong> levels are seen in many <b>addictive</b> disorders and <strong>BDNF</strong> is elevated in recovering MA addicts, suggesting <strong>BDNF</strong> may be a marker of MA <b>addiction</b>.
+BDNF	drug	opioid	21885037	RACK1 affects <b>morphine</b> reward via <strong>BDNF</strong>.
+BDNF	addiction	reward	21885037	RACK1 affects morphine <b>reward</b> via <strong>BDNF</strong>.
+BDNF	addiction	addiction	21885037	Brain derived neurotrophic factor (<strong>BDNF</strong>) has been implicated in <b>addiction</b> related pathology in animal studies.
+BDNF	addiction	addiction	21885037	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been implicated in <b>addiction</b> related pathology in animal studies.
+BDNF	drug	opioid	21885037	The present study was designed to investigate if shRACK1 (a short hairpin RNA of RACK1) could reverse the mice's behavioral responses to <b>morphine</b> and <strong>BDNF</strong> expression in hippocampus and prefrontal cortex.
+BDNF	drug	opioid	21885037	No significant changes were observed in vehicle infused mice which received no <b>morphine</b> treatment (CONC) and shRACK1 infused mice which received no <b>morphine</b> treatment (CONR), whereas vehicle infused mice preceded the <b>morphine</b> injection (MIC) showed increased <strong>BDNF</strong> expression in hippocampus and prefrontal cortex, as compared to vehicle infused mice which received no <b>morphine</b> treatment (CONC).
+BDNF	drug	opioid	21885037	Intracerebroventricular shRACK1 treatment reversed these, and in fact, ShRACK1 infused mice preceded the <b>morphine</b> injection (MIR) showed reduced <strong>BDNF</strong> expression in hippocampus and prefrontal cortex, as compared to MIC.
+BDNF	drug	opioid	21885037	Combined behavioral and molecular approaches have support the possibility that the RACK1 <strong>BDNF</strong> system plays an important role in the response to <b>morphine</b> induced reward.
+BDNF	addiction	reward	21885037	Combined behavioral and molecular approaches have support the possibility that the RACK1 <strong>BDNF</strong> system plays an important role in the response to morphine induced <b>reward</b>.
+BDNF	drug	alcohol	21880305	The <strong>brain derived neurotrophic factor</strong> is associated with <b>alcohol</b> dependence related depression and antidepressant response.
+BDNF	addiction	dependence	21880305	The <strong>brain derived neurotrophic factor</strong> is associated with alcohol <b>dependence</b> related depression and antidepressant response.
+BDNF	drug	alcohol	21880305	Here, we investigated the possible association between three single nucleotide polymorphisms (SNPs) of the <strong>BDNF</strong> gene (rs13306221, rs6265, rs16917204) and AD D. Of 548 patients with <b>alcohol</b> dependence (AD), 166 had AD D and 312 healthy controls.
+BDNF	addiction	dependence	21880305	Here, we investigated the possible association between three single nucleotide polymorphisms (SNPs) of the <strong>BDNF</strong> gene (rs13306221, rs6265, rs16917204) and AD D. Of 548 patients with alcohol <b>dependence</b> (AD), 166 had AD D and 312 healthy controls.
+BDNF	drug	opioid	21872672	Voluntary exercise ameliorates cognitive deficits in <b>morphine</b> dependent rats: the role of hippocampal <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	opioid	21872672	If an effect of exercise was observed, we aimed to investigate the possible role of hippocampal brain derived neurotrophic factor (<strong>BDNF</strong>) in the exercise induced enhancement of learning and memory in <b>morphine</b> dependent rats.
+BDNF	drug	opioid	21872672	If an effect of exercise was observed, we aimed to investigate the possible role of hippocampal <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the exercise induced enhancement of learning and memory in <b>morphine</b> dependent rats.
+BDNF	drug	cocaine	21867882	This resilience was mediated, in part, through repression of <strong>BDNF</strong> TrkB CREB signaling, which was induced after repeated <b>cocaine</b> or stress.
+BDNF	drug	alcohol	21848960	<strong>Brain derived neurotrophic factor</strong> serum levels in <b>alcohol</b> dependent subjects 6 months after <b>alcohol</b> withdrawal.
+BDNF	addiction	withdrawal	21848960	<strong>Brain derived neurotrophic factor</strong> serum levels in alcohol dependent subjects 6 months after alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	21848960	The neuroadaptive changes associated with <b>alcohol</b> dependence involve markers such as brain derived neurotrophic factor (<strong>BDNF</strong>), which regulate neuronal plasticity.
+BDNF	addiction	dependence	21848960	The neuroadaptive changes associated with alcohol <b>dependence</b> involve markers such as brain derived neurotrophic factor (<strong>BDNF</strong>), which regulate neuronal plasticity.
+BDNF	drug	alcohol	21848960	The neuroadaptive changes associated with <b>alcohol</b> dependence involve markers such as <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), which regulate neuronal plasticity.
+BDNF	addiction	dependence	21848960	The neuroadaptive changes associated with alcohol <b>dependence</b> involve markers such as <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), which regulate neuronal plasticity.
+BDNF	drug	alcohol	21848960	Serum levels of <strong>BDNF</strong> have been reported to decrease during <b>alcohol</b> dependence and may be restored to normal soon after <b>alcohol</b> is withdrawn.
+BDNF	addiction	dependence	21848960	Serum levels of <strong>BDNF</strong> have been reported to decrease during alcohol <b>dependence</b> and may be restored to normal soon after alcohol is withdrawn.
+BDNF	drug	alcohol	21848960	We investigated serum <strong>BDNF</strong> levels in 101 abstinent and relapsing <b>alcohol</b> dependent subjects at the moment of hospitalization for <b>alcohol</b> withdrawal (M0) and 6 months later (M6) and compared them to the serum <strong>BDNF</strong> levels of 41 nondependent subjects.
+BDNF	addiction	withdrawal	21848960	We investigated serum <strong>BDNF</strong> levels in 101 abstinent and relapsing alcohol dependent subjects at the moment of hospitalization for alcohol <b>withdrawal</b> (M0) and 6 months later (M6) and compared them to the serum <strong>BDNF</strong> levels of 41 nondependent subjects.
+BDNF	drug	alcohol	21848960	The <strong>BDNF</strong> levels of the <b>alcohol</b> dependent subjects were compared to their serum gamma glutamyl transferase (GGT) levels, mean corpuscular volume (MCV) values, and their score on the Beck Depression Inventory (BDI) questionnaire.
+BDNF	drug	alcohol	21848960	Serum <strong>BDNF</strong> levels of the abstinent group at M6 were significantly higher than those of the original group of <b>alcohol</b> dependent subjects at M0 (p = 0.034).
+BDNF	drug	alcohol	21848960	Our data confirm that serum <strong>BDNF</strong> levels do not correlate with either chronic <b>alcohol</b> consumption or peripheral toxicity but may be linked to neuronal aspects of <b>alcohol</b> consumption and dependence.
+BDNF	addiction	dependence	21848960	Our data confirm that serum <strong>BDNF</strong> levels do not correlate with either chronic alcohol consumption or peripheral toxicity but may be linked to neuronal aspects of alcohol consumption and <b>dependence</b>.
+BDNF	drug	alcohol	21848960	The increased serum levels of <strong>BDNF</strong> may reflect the concomitant activation of <strong>BDNF</strong> synthesis that accompanies the neuronal remodeling triggered by <b>alcohol</b> withdrawal and suggests that <strong>BDNF</strong> synthesis may have a role in the long term maintenance of abstinence.
+BDNF	addiction	withdrawal	21848960	The increased serum levels of <strong>BDNF</strong> may reflect the concomitant activation of <strong>BDNF</strong> synthesis that accompanies the neuronal remodeling triggered by alcohol <b>withdrawal</b> and suggests that <strong>BDNF</strong> synthesis may have a role in the long term maintenance of abstinence.
+BDNF	drug	alcohol	21848960	Monitoring the serum <strong>BDNF</strong> levels of <b>alcoholics</b> undergoing treatment could help to characterize <b>alcohol</b> dependence profiles and predict relapse.
+BDNF	addiction	dependence	21848960	Monitoring the serum <strong>BDNF</strong> levels of alcoholics undergoing treatment could help to characterize alcohol <b>dependence</b> profiles and predict relapse.
+BDNF	addiction	relapse	21848960	Monitoring the serum <strong>BDNF</strong> levels of alcoholics undergoing treatment could help to characterize alcohol dependence profiles and predict <b>relapse</b>.
+BDNF	drug	alcohol	21796371	Neuropeptide Y (NPY) and brain derived neurotrophic factor (<strong>BDNF</strong>) have been implicated in both the stress response and <b>alcohol</b> addiction.
+BDNF	addiction	addiction	21796371	Neuropeptide Y (NPY) and brain derived neurotrophic factor (<strong>BDNF</strong>) have been implicated in both the stress response and alcohol <b>addiction</b>.
+BDNF	drug	alcohol	21796371	Neuropeptide Y (NPY) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) have been implicated in both the stress response and <b>alcohol</b> addiction.
+BDNF	addiction	addiction	21796371	Neuropeptide Y (NPY) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) have been implicated in both the stress response and alcohol <b>addiction</b>.
+BDNF	drug	alcohol	21796371	However, few studies have assessed the NPY and <strong>BDNF</strong> response to stress in <b>alcohol</b> dependent participants and the concurrent measure of NPY and <strong>BDNF</strong> has not been reported in human participants.
+BDNF	drug	alcohol	21796371	The purpose of this study was to concurrently assess serum NPY and <strong>BDNF</strong>, as well as adrenocorticotropin (ACTH) and cortisol, in control and race  and aged matched abstinent <b>alcohol</b> dependent participants in response to a stress inducing public speaking task.
+BDNF	drug	alcohol	21796371	Basal and post stress serum values of NPY and <strong>BDNF</strong>, as well as ACTH and cortisol, were assessed in 14 abstinent <b>alcohol</b> dependent and ten healthy control male participants.
+BDNF	drug	alcohol	21796371	Differences in basal and stress induced responses of NPY and <strong>BDNF</strong> were not supported between control and abstinent <b>alcohol</b> dependent subjects.
+BDNF	drug	alcohol	21792305	Is serum <strong>brain derived neurotrophic factor</strong> related to craving for or use of <b>alcohol</b>, cocaine, or methamphetamine?
+BDNF	drug	amphetamine	21792305	Is serum <strong>brain derived neurotrophic factor</strong> related to craving for or use of alcohol, cocaine, or <b>methamphetamine</b>?
+BDNF	drug	cocaine	21792305	Is serum <strong>brain derived neurotrophic factor</strong> related to craving for or use of alcohol, <b>cocaine</b>, or methamphetamine?
+BDNF	addiction	relapse	21792305	Is serum <strong>brain derived neurotrophic factor</strong> related to <b>craving</b> for or use of alcohol, cocaine, or methamphetamine?
+BDNF	addiction	addiction	21792305	Data suggests that brain derived neurotropic factor (<strong>BDNF</strong>) plays a neuroadaptive role in <b>addiction</b>.
+BDNF	drug	alcohol	21792305	Whether serum <strong>BDNF</strong> levels are different in <b>alcohol</b> or psychostimulants as a function of craving is unknown.
+BDNF	addiction	relapse	21792305	Whether serum <strong>BDNF</strong> levels are different in alcohol or psychostimulants as a function of <b>craving</b> is unknown.
+BDNF	drug	alcohol	21792305	Here, we examined craving and serum <strong>BDNF</strong> levels in persons with <b>alcohol</b> versus psychostimulant dependence.
+BDNF	addiction	dependence	21792305	Here, we examined craving and serum <strong>BDNF</strong> levels in persons with alcohol versus psychostimulant <b>dependence</b>.
+BDNF	addiction	relapse	21792305	Here, we examined <b>craving</b> and serum <strong>BDNF</strong> levels in persons with alcohol versus psychostimulant dependence.
+BDNF	addiction	relapse	21792305	Our goals were to explore <strong>BDNF</strong> as an objective biomarker for 1) <b>craving</b> 2) abstinence, and 3) years of chronic substance use.
+BDNF	drug	cocaine	21741029	Increased serum <strong>brain derived neurotrophic factor</strong> is predictive of <b>cocaine</b> relapse outcomes: a prospective study.
+BDNF	addiction	relapse	21741029	Increased serum <strong>brain derived neurotrophic factor</strong> is predictive of cocaine <b>relapse</b> outcomes: a prospective study.
+BDNF	drug	cocaine	21741029	Extending preclinical research showing a role for central brain derived neurotrophic factor (<strong>BDNF</strong>) in <b>cocaine</b> seeking, we examined whether serum <strong>BDNF</strong> is altered in abstinent, early recovering, <b>cocaine</b> dependent individuals and whether it is predictive of subsequent relapse risk.
+BDNF	addiction	relapse	21741029	Extending preclinical research showing a role for central brain derived neurotrophic factor (<strong>BDNF</strong>) in cocaine <b>seeking</b>, we examined whether serum <strong>BDNF</strong> is altered in abstinent, early recovering, cocaine dependent individuals and whether it is predictive of subsequent <b>relapse</b> risk.
+BDNF	drug	cocaine	21741029	Extending preclinical research showing a role for central <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in <b>cocaine</b> seeking, we examined whether serum <strong>BDNF</strong> is altered in abstinent, early recovering, <b>cocaine</b> dependent individuals and whether it is predictive of subsequent relapse risk.
+BDNF	addiction	relapse	21741029	Extending preclinical research showing a role for central <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in cocaine <b>seeking</b>, we examined whether serum <strong>BDNF</strong> is altered in abstinent, early recovering, cocaine dependent individuals and whether it is predictive of subsequent <b>relapse</b> risk.
+BDNF	drug	cocaine	21741029	Significantly higher mean serum <strong>BDNF</strong> levels were observed for the <b>cocaine</b> dependent patients compared with healthy control participants (p < .001).
+BDNF	drug	cocaine	21741029	Higher serum <strong>BDNF</strong> levels predicted shorter subsequent time to <b>cocaine</b> relapse (hazard ratio: 1.09, p < .05), greater number of days (p < .05), and higher total amounts of <b>cocaine</b> used (p = .05).
+BDNF	addiction	relapse	21741029	Higher serum <strong>BDNF</strong> levels predicted shorter subsequent time to cocaine <b>relapse</b> (hazard ratio: 1.09, p < .05), greater number of days (p < .05), and higher total amounts of cocaine used (p = .05).
+BDNF	drug	cocaine	21741029	High serum <strong>BDNF</strong> levels in recovering <b>cocaine</b> dependent individuals are predictive of future <b>cocaine</b> relapse outcomes and may represent a clinically relevant marker of relapse risk.
+BDNF	addiction	relapse	21741029	High serum <strong>BDNF</strong> levels in recovering cocaine dependent individuals are predictive of future cocaine <b>relapse</b> outcomes and may represent a clinically relevant marker of <b>relapse</b> risk.
+BDNF	drug	cocaine	21741029	These data suggest that serum <strong>BDNF</strong> levels may provide an indication of relapse risk during early recovery from <b>cocaine</b> dependence.
+BDNF	addiction	dependence	21741029	These data suggest that serum <strong>BDNF</strong> levels may provide an indication of relapse risk during early recovery from cocaine <b>dependence</b>.
+BDNF	addiction	relapse	21741029	These data suggest that serum <strong>BDNF</strong> levels may provide an indication of <b>relapse</b> risk during early recovery from cocaine dependence.
+BDNF	drug	cocaine	21734276	Escalated or suppressed <b>cocaine</b> reward, tegmental <strong>BDNF</strong>, and accumbal dopamine caused by episodic versus continuous social stress in rats.
+BDNF	addiction	reward	21734276	Escalated or suppressed cocaine <b>reward</b>, tegmental <strong>BDNF</strong>, and accumbal dopamine caused by episodic versus continuous social stress in rats.
+BDNF	drug	cocaine	21734276	These stress experiences result in (1) increased intravenous <b>cocaine</b> self administration under a fixed ratio schedule with prolonged binge like access in episodically defeated intruder rats but suppressed <b>cocaine</b> intake by continuously subordinate rats; (2) deteriorated sugar preference and intake and decreased exploratory behavior in subordinate, but not intermittently defeated, rats; and (3) a sensitized dopamine (DA) response in the nucleus accumbens via in vivo microdialysis and increased tegmental brain derived neural growth factor (<strong>BDNF</strong>) in episodically defeated rats, whereas the continuously subordinate rats show suppression of the DA and <strong>BDNF</strong> responses.
+BDNF	addiction	intoxication	21734276	These stress experiences result in (1) increased intravenous cocaine self administration under a fixed ratio schedule with prolonged <b>binge</b> like access in episodically defeated intruder rats but suppressed cocaine intake by continuously subordinate rats; (2) deteriorated sugar preference and intake and decreased exploratory behavior in subordinate, but not intermittently defeated, rats; and (3) a sensitized dopamine (DA) response in the nucleus accumbens via in vivo microdialysis and increased tegmental brain derived neural growth factor (<strong>BDNF</strong>) in episodically defeated rats, whereas the continuously subordinate rats show suppression of the DA and <strong>BDNF</strong> responses.
+BDNF	drug	opioid	21703297	These results suggest that the μ <b>opioid</b> receptor is involved in the behavioral sequelae of psychosocial stress and consequent regulation of <strong>BDNF</strong> expression in the hippocampus, and may play an important role in psychiatric disorders for which stress is an important predisposing or precipitating factor, such as depression, posttraumatic stress disorder, and social anxiety disorder.
+BDNF	drug	alcohol	21640793	Association between Val66Met polymorphism of Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) gene and a deficiency of colour vision in <b>alcohol</b> dependent male patients.
+BDNF	drug	alcohol	21640793	Association between Val66Met polymorphism of <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) gene and a deficiency of colour vision in <b>alcohol</b> dependent male patients.
+BDNF	drug	alcohol	21640793	The <strong>BDNF</strong> polymorphism Val66Met (rs6265) has been studied in the context of etiology of mental diseases including <b>alcoholism</b>.
+BDNF	drug	alcohol	21640793	The A allele containing 66Met promotes <strong>BDNF</strong> expression and this may protect humans against CVD induced by long term excessive <b>alcohol</b> intake.
+BDNF	drug	alcohol	21640793	The present findings indicate that <b>alcohol</b> induced CVD does not depend solely on excessive <b>alcohol</b> consumption but is significantly influenced by genetic predisposition in the form of a specific <strong>BDNF</strong> polymorphism.
+BDNF	drug	cocaine	21640333	Enhanced <b>cocaine</b> conditioned place preference and associated brain regional levels of <strong>BDNF</strong>, p ERK1/2 and p Ser845 GluA1 in food restricted rats.
+BDNF	drug	amphetamine	21570990	Sensitized activation of Fos and <strong>brain derived neurotrophic factor</strong> in the medial prefrontal cortex and ventral tegmental area accompanies behavioral sensitization to <b>amphetamine</b>.
+BDNF	addiction	sensitization	21570990	Sensitized activation of Fos and <strong>brain derived neurotrophic factor</strong> in the medial prefrontal cortex and ventral tegmental area accompanies behavioral <b>sensitization</b> to amphetamine.
+BDNF	addiction	sensitization	21570990	Both the medial prefrontal cortex (mPFC) and ventral tegmental area (VTA) influence behavioral <b>sensitization</b> and display increased immediate early gene and <strong>BDNF</strong> expression after psychostimulant administration.
+BDNF	drug	amphetamine	21570990	Here we investigate whether mPFC neurons innervating the VTA exhibit altered Fos or <strong>BDNF</strong> expression during long term sensitization to <b>amphetamine</b>.
+BDNF	addiction	sensitization	21570990	Here we investigate whether mPFC neurons innervating the VTA exhibit altered Fos or <strong>BDNF</strong> expression during long term <b>sensitization</b> to amphetamine.
+BDNF	drug	amphetamine	21570990	<b>Amphetamine</b> challenge increased Fos and <strong>BDNF</strong> expression in the mPFC regardless of prior drug experience, and further augmented mPFC <strong>BDNF</strong> expression in sensitized rats.
+BDNF	drug	amphetamine	21570990	Similarly, more Fos FG and Fos <strong>BDNF</strong> double labeling was observed in the mPFC of sensitized rats compared to drug naïve rats after <b>amphetamine</b> challenge.
+BDNF	drug	amphetamine	21570990	Repeated <b>amphetamine</b> treatment also increased VTA <strong>BDNF</strong>, while both acute and repeated <b>amphetamine</b> treatment increased Fos and Fos <strong>BDNF</strong> co labeling, an effect enhanced in sensitized rats.
+BDNF	drug	amphetamine	21570990	These findings point to a role of cortico tegmental <strong>BDNF</strong> in long term <b>amphetamine</b> sensitization.
+BDNF	addiction	sensitization	21570990	These findings point to a role of cortico tegmental <strong>BDNF</strong> in long term amphetamine <b>sensitization</b>.
+BDNF	drug	alcohol	21463342	Alterations of <strong>brain derived neurotrophic factor</strong> serum levels in patients with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	21463342	Alterations of <strong>brain derived neurotrophic factor</strong> serum levels in patients with alcohol <b>dependence</b>.
+BDNF	drug	alcohol	21463342	The role of <strong>BDNF</strong> and its signaling in the mechanisms of <b>alcohol</b> dependence has been well documented in studies of animal models, but a few studies have been conducted in human peripheral tissues.
+BDNF	addiction	dependence	21463342	The role of <strong>BDNF</strong> and its signaling in the mechanisms of alcohol <b>dependence</b> has been well documented in studies of animal models, but a few studies have been conducted in human peripheral tissues.
+BDNF	drug	alcohol	21463342	On the basis of this rationale, we compared <strong>BDNF</strong> levels in both serum and plasma in <b>alcohol</b> dependent patients and healthy volunteers.
+BDNF	drug	alcohol	21463342	In conclusion, our data show an alteration of <strong>BDNF</strong> peripheral content in patients with <b>alcohol</b> dependence, suggesting the involvement of this neurotrophin in this psychopathology.
+BDNF	addiction	dependence	21463342	In conclusion, our data show an alteration of <strong>BDNF</strong> peripheral content in patients with alcohol <b>dependence</b>, suggesting the involvement of this neurotrophin in this psychopathology.
+BDNF	drug	opioid	21458533	Polymorphisms of <strong>brain derived neurotrophic factor</strong> associated with <b>heroin</b> dependence.
+BDNF	addiction	dependence	21458533	Polymorphisms of <strong>brain derived neurotrophic factor</strong> associated with heroin <b>dependence</b>.
+BDNF	drug	opioid	21458533	To identify genetic variants associated with <b>heroin</b> dependence, we compared four single nucleotide polymorphisms (SNPs, rs13306221, rs6265, rs56164415, and rs16917204) of the <strong>BDNF</strong> gene in 487 subjects with <b>heroin</b> dependence and 492 healthy individuals.
+BDNF	addiction	dependence	21458533	To identify genetic variants associated with heroin <b>dependence</b>, we compared four single nucleotide polymorphisms (SNPs, rs13306221, rs6265, rs56164415, and rs16917204) of the <strong>BDNF</strong> gene in 487 subjects with heroin <b>dependence</b> and 492 healthy individuals.
+BDNF	drug	opioid	21458533	These findings support a role of <strong>BDNF</strong> rs6265 and rs13306221 polymorphisms in <b>heroin</b> dependence and may guide future studies to identify other genetic risk factors for <b>heroin</b> dependence.
+BDNF	addiction	dependence	21458533	These findings support a role of <strong>BDNF</strong> rs6265 and rs13306221 polymorphisms in heroin <b>dependence</b> and may guide future studies to identify other genetic risk factors for heroin <b>dependence</b>.
+BDNF	drug	amphetamine	21453757	Neurotoxic (+) <b>methamphetamine</b> treatment in rats increases <strong>brain derived neurotrophic factor</strong> and tropomyosin receptor kinase B expression in multiple brain regions.
+BDNF	addiction	intoxication	21453757	This experiment examined the effects of a MA <b>binge</b> dosing regimen (10 mg/kg x 4 at 2 h intervals, s.c.) in Sprague Dawley rats on <strong>BDNF</strong>, tropomyosin receptor kinase B (TrkB), and tyrosine hydroxylase (TH) mRNA expression, and plasma corticosterone.
+BDNF	drug	cocaine	21411660	Furthermore, the levels of brain derived neurotrophic factor (<strong>BDNF</strong>) protein in the NAc shell increased progressively after <b>cocaine</b> withdrawal, and the impairment of DHPG LTD in the NAc shell was not found in slices from <strong>BDNF</strong> knock out mice after <b>cocaine</b> withdrawal.
+BDNF	addiction	withdrawal	21411660	Furthermore, the levels of brain derived neurotrophic factor (<strong>BDNF</strong>) protein in the NAc shell increased progressively after cocaine <b>withdrawal</b>, and the impairment of DHPG LTD in the NAc shell was not found in slices from <strong>BDNF</strong> knock out mice after cocaine <b>withdrawal</b>.
+BDNF	drug	cocaine	21411660	Furthermore, the levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) protein in the NAc shell increased progressively after <b>cocaine</b> withdrawal, and the impairment of DHPG LTD in the NAc shell was not found in slices from <strong>BDNF</strong> knock out mice after <b>cocaine</b> withdrawal.
+BDNF	addiction	withdrawal	21411660	Furthermore, the levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) protein in the NAc shell increased progressively after cocaine <b>withdrawal</b>, and the impairment of DHPG LTD in the NAc shell was not found in slices from <strong>BDNF</strong> knock out mice after cocaine <b>withdrawal</b>.
+BDNF	drug	cocaine	21411660	These results suggest that withdrawal from repeated <b>cocaine</b> exposure may result in increased <strong>BDNF</strong> levels in the NAc shell, which leads to a selective downregulation of mGluR5 and thereby impairs the induction of mGluR dependent LTD.
+BDNF	addiction	withdrawal	21411660	These results suggest that <b>withdrawal</b> from repeated cocaine exposure may result in increased <strong>BDNF</strong> levels in the NAc shell, which leads to a selective downregulation of mGluR5 and thereby impairs the induction of mGluR dependent LTD.
+BDNF	addiction	addiction	21375485	This review discusses targeting growth factors such as glial derived neurotrophic factor (GDNF) and brain derived neurotrophic factor (<strong>BDNF</strong>) to treat Parkinson's disease and/or drug <b>addiction</b> and compiles recent evidences to propose the pleiotrophin/receptor protein tyrosine phosphatase β/ζ signaling pathway as a new therapeutic target to treat Parkinson's disease and to prevent drug of abuse induced neurotoxicity and <b>addictive</b> effects.
+BDNF	addiction	addiction	21375485	This review discusses targeting growth factors such as glial derived neurotrophic factor (GDNF) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) to treat Parkinson's disease and/or drug <b>addiction</b> and compiles recent evidences to propose the pleiotrophin/receptor protein tyrosine phosphatase β/ζ signaling pathway as a new therapeutic target to treat Parkinson's disease and to prevent drug of abuse induced neurotoxicity and <b>addictive</b> effects.
+BDNF	drug	alcohol	21367572	Opposite effects of acute <b>ethanol</b> exposure on GAP 43 and <strong>BDNF</strong> expression in the hippocampus versus the cerebellum of juvenile rats.
+BDNF	drug	alcohol	21367572	The present study addresses the effects of a single acute <b>ethanol</b> exposure on growth associated protein 43 (GAP 43) and brain derived neurotrophic factor (<strong>BDNF</strong>) gene expression in neurons in the cerebellum and hippocampus of adolescent rats.
+BDNF	drug	alcohol	21367572	The present study addresses the effects of a single acute <b>ethanol</b> exposure on growth associated protein 43 (GAP 43) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene expression in neurons in the cerebellum and hippocampus of adolescent rats.
+BDNF	drug	alcohol	21367572	In situ hybridizations revealed that GAP 43 and <strong>BDNF</strong> mRNA levels were primarily increased by <b>alcohol</b> exposure in hippocampal dentate granule cells and CA3 neurons.
+BDNF	addiction	intoxication	21367572	Overall, the reported alterations in the expression of the plasticity associated genes GAP 43 and <strong>BDNF</strong> in juvenile rats are consistent with the known deleterious effects of <b>binge</b> drinking on motor coordination and cognitive function.
+BDNF	addiction	sensitization	21366724	<b>Sensitization</b> by MET decreased <strong>BDNF</strong> mRNAs by 40% in the hippocampus.
+BDNF	drug	opioid	21358750	Brain derived neurotrophic factor (<strong>BDNF</strong>) was shown to affect the response to <b>methadone</b> maintenance treatment.
+BDNF	drug	opioid	21358750	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) was shown to affect the response to <b>methadone</b> maintenance treatment.
+BDNF	drug	alcohol	21322143	<strong>Brain derived neurotrophic factor</strong>, on the contrary, increases the addictive activity of cocaine suppressing the development of the syndrome of psychic dependence on <b>ethanol</b>.
+BDNF	drug	cocaine	21322143	<strong>Brain derived neurotrophic factor</strong>, on the contrary, increases the addictive activity of <b>cocaine</b> suppressing the development of the syndrome of psychic dependence on ethanol.
+BDNF	addiction	addiction	21322143	<strong>Brain derived neurotrophic factor</strong>, on the contrary, increases the <b>addictive</b> activity of cocaine suppressing the development of the syndrome of psychic dependence on ethanol.
+BDNF	addiction	dependence	21322143	<strong>Brain derived neurotrophic factor</strong>, on the contrary, increases the addictive activity of cocaine suppressing the development of the syndrome of psychic <b>dependence</b> on ethanol.
+BDNF	drug	opioid	21277174	Roles of <strong>BDNF</strong>, dopamine D(3) receptors, and their interactions in the expression of <b>morphine</b> induced context specific locomotor sensitization.
+BDNF	addiction	sensitization	21277174	Roles of <strong>BDNF</strong>, dopamine D(3) receptors, and their interactions in the expression of morphine induced context specific locomotor <b>sensitization</b>.
+BDNF	drug	opioid	21277174	The present study used a conditioning procedure to assess the roles of <strong>BDNF</strong>, Drd3, and their interactions in the NAc in the expression of <b>morphine</b> induced context specific locomotor sensitization.
+BDNF	addiction	sensitization	21277174	The present study used a conditioning procedure to assess the roles of <strong>BDNF</strong>, Drd3, and their interactions in the NAc in the expression of morphine induced context specific locomotor <b>sensitization</b>.
+BDNF	drug	opioid	21277174	We showed that the expression of locomotor sensitization in the <b>morphine</b> paired environment was accompanied by significantly increased expression of Drd3 mRNA and <strong>BDNF</strong> mRNA and protein levels.
+BDNF	addiction	sensitization	21277174	We showed that the expression of locomotor <b>sensitization</b> in the morphine paired environment was accompanied by significantly increased expression of Drd3 mRNA and <strong>BDNF</strong> mRNA and protein levels.
+BDNF	addiction	sensitization	21277174	Furthermore, intra NAc infusion of the Drd3 selective antagonist SB 277011A significantly decreased the expression of context specific locomotor <b>sensitization</b> and upregulated <strong>BDNF</strong> mRNA.
+BDNF	drug	opioid	21277174	Altogether, these results suggest that <strong>BDNF</strong>/TrkB signaling and activation of Drd3 in the NAc are required for the expression of <b>morphine</b> induced context specific locomotor sensitization.
+BDNF	addiction	sensitization	21277174	Altogether, these results suggest that <strong>BDNF</strong>/TrkB signaling and activation of Drd3 in the NAc are required for the expression of morphine induced context specific locomotor <b>sensitization</b>.
+BDNF	addiction	addiction	21273656	The molecular basis of <b>addiction</b> remains poorly understood, but diverse lines of evidence suggest that neurotrophins (<strong>BDNF</strong>, NT 3 and NT 4) play a role in the regulation of synaptic plasticity.
+BDNF	drug	cocaine	21248106	The suppressive effect of an intra prefrontal cortical infusion of <strong>BDNF</strong> on <b>cocaine</b> seeking is Trk receptor and extracellular signal regulated protein kinase mitogen activated protein kinase dependent.
+BDNF	addiction	relapse	21248106	The suppressive effect of an intra prefrontal cortical infusion of <strong>BDNF</strong> on cocaine <b>seeking</b> is Trk receptor and extracellular signal regulated protein kinase mitogen activated protein kinase dependent.
+BDNF	drug	cocaine	21248106	We have previously demonstrated that infusion of <strong>BDNF</strong> into the dorsomedial prefrontal cortex (dmPFC) immediately after the last of 10 <b>cocaine</b> SA sessions attenuates contextual, cue  and <b>cocaine</b> prime induced reinstatement of <b>cocaine</b> seeking (Berglind et al., 2007) and normalizes <b>cocaine</b> induced disruption of glutamatergic transmission in the nucleus accumbens (Berglind et al., 2009).
+BDNF	addiction	relapse	21248106	We have previously demonstrated that infusion of <strong>BDNF</strong> into the dorsomedial prefrontal cortex (dmPFC) immediately after the last of 10 cocaine SA sessions attenuates contextual, cue  and cocaine prime induced <b>reinstatement</b> of cocaine <b>seeking</b> (Berglind et al., 2007) and normalizes cocaine induced disruption of glutamatergic transmission in the nucleus accumbens (Berglind et al., 2009).
+BDNF	drug	cocaine	21248106	In the present study, the suppressive effect of intra dmPFC <strong>BDNF</strong> on <b>cocaine</b> seeking is shown to depend on Trk receptor mediated activation of extracellular signal regulated kinase (ERK) signaling in the dmPFC.
+BDNF	addiction	relapse	21248106	In the present study, the suppressive effect of intra dmPFC <strong>BDNF</strong> on cocaine <b>seeking</b> is shown to depend on Trk receptor mediated activation of extracellular signal regulated kinase (ERK) signaling in the dmPFC.
+BDNF	drug	cocaine	21248106	The tyrosine kinase inhibitor, K252a, and the mitogen activated protein/extracellular signal regulated kinase kinase inhibitor, U0126 (1,4 diamino 2,3 dicyano 1,4 bis[2 aminophenylthio]butadiene), prevented <strong>BDNF</strong>'s suppressive effects on <b>cocaine</b> seeking.
+BDNF	addiction	relapse	21248106	The tyrosine kinase inhibitor, K252a, and the mitogen activated protein/extracellular signal regulated kinase kinase inhibitor, U0126 (1,4 diamino 2,3 dicyano 1,4 bis[2 aminophenylthio]butadiene), prevented <strong>BDNF</strong>'s suppressive effects on cocaine <b>seeking</b>.
+BDNF	drug	cocaine	21248106	Vehicle infused rats with a <b>cocaine</b> SA history showed significant decreases in ERK and cyclic AMP response element binding protein (CREB), but not Akt, phosphorylation after the final <b>cocaine</b> SA session that were reversed by intra dmPFC <strong>BDNF</strong>.
+BDNF	drug	cocaine	21248106	Additionally, <strong>BDNF</strong>'s ability to normalize <b>cocaine</b> mediated decreases in ERK and CREB phosphorylation was blocked by U0126, demonstrating that ERK/MAPK activation mediated the behavioral effects.
+BDNF	drug	cocaine	21248106	This study elucidates a mechanism whereby <strong>BDNF</strong>/TrkB (tropomyosin receptor kinase B) activates ERK regulated CREB phosphorylation in the dmPFC to counteract the neuroadaptations induced by <b>cocaine</b> SA and subsequent relapse to <b>cocaine</b> seeking.
+BDNF	addiction	relapse	21248106	This study elucidates a mechanism whereby <strong>BDNF</strong>/TrkB (tropomyosin receptor kinase B) activates ERK regulated CREB phosphorylation in the dmPFC to counteract the neuroadaptations induced by cocaine SA and subsequent <b>relapse</b> to cocaine <b>seeking</b>.
+BDNF	drug	cannabinoid	21243477	In this chapter, the ED literature dealing with ghrelin, <strong>brain derived neurotrophic factor</strong>, opioid peptides, and <b>endocannabinoids</b>, which have prominent effects on eating behavior, body weight, reward, emotional, and cognitive functions, is reviewed in view of the above suggested links.
+BDNF	drug	opioid	21243477	In this chapter, the ED literature dealing with ghrelin, <strong>brain derived neurotrophic factor</strong>, <b>opioid</b> peptides, and endocannabinoids, which have prominent effects on eating behavior, body weight, reward, emotional, and cognitive functions, is reviewed in view of the above suggested links.
+BDNF	addiction	reward	21243477	In this chapter, the ED literature dealing with ghrelin, <strong>brain derived neurotrophic factor</strong>, opioid peptides, and endocannabinoids, which have prominent effects on eating behavior, body weight, <b>reward</b>, emotional, and cognitive functions, is reviewed in view of the above suggested links.
+BDNF	drug	cannabinoid	21243475	serotonergic, opioid, <b>cannabinoid</b> and dopaminergic receptors, and brain derived neurotrophic factor (<strong>BDNF</strong>)], appetite regulatory peptides and their receptors [leptin, ghrelin, agouti related protein (AgRP), melanocortin receptors, neuropeptide Y], energy balance systems (e.g.
+BDNF	drug	opioid	21243475	serotonergic, <b>opioid</b>, cannabinoid and dopaminergic receptors, and brain derived neurotrophic factor (<strong>BDNF</strong>)], appetite regulatory peptides and their receptors [leptin, ghrelin, agouti related protein (AgRP), melanocortin receptors, neuropeptide Y], energy balance systems (e.g.
+BDNF	drug	cannabinoid	21243475	serotonergic, opioid, <b>cannabinoid</b> and dopaminergic receptors, and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>)], appetite regulatory peptides and their receptors [leptin, ghrelin, agouti related protein (AgRP), melanocortin receptors, neuropeptide Y], energy balance systems (e.g.
+BDNF	drug	opioid	21243475	serotonergic, <b>opioid</b>, cannabinoid and dopaminergic receptors, and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>)], appetite regulatory peptides and their receptors [leptin, ghrelin, agouti related protein (AgRP), melanocortin receptors, neuropeptide Y], energy balance systems (e.g.
+BDNF	drug	opioid	21243475	Candidate gene association has implicated <strong>BDNF</strong>, delta 1 <b>opioid</b> receptor (OPDR1) and AgRP.
+BDNF	drug	nicotine	21232579	Alterations in <strong>BDNF</strong> and phospho CREB levels following chronic oral <b>nicotine</b> treatment and its withdrawal in dopaminergic brain areas of mice.
+BDNF	addiction	withdrawal	21232579	Alterations in <strong>BDNF</strong> and phospho CREB levels following chronic oral nicotine treatment and its <b>withdrawal</b> in dopaminergic brain areas of mice.
+BDNF	drug	nicotine	21232579	Here we studied the effects of chronic oral <b>nicotine</b> treatment and <b>nicotine</b> treatment cessation on two well characterised markers of neuronal plasticity, brain derived neurotrophic factor (<strong>BDNF</strong>) and phosphorylated cAMP responsive element binding protein (pCREB), in several dopaminergic brain areas.
+BDNF	drug	nicotine	21232579	Here we studied the effects of chronic oral <b>nicotine</b> treatment and <b>nicotine</b> treatment cessation on two well characterised markers of neuronal plasticity, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and phosphorylated cAMP responsive element binding protein (pCREB), in several dopaminergic brain areas.
+BDNF	drug	nicotine	21232579	<strong>BDNF</strong> levels were not altered by chronic <b>nicotine</b> treatment, but they were significantly increased in the nucleus accumbens (NAc) after 24h and 29 days of <b>nicotine</b> abstinence and in the ventral tegmental area (VTA) and substantia nigra after 29 days of <b>nicotine</b> abstinence.
+BDNF	drug	nicotine	21232579	These findings suggest that <b>nicotine</b> abstinence promotes long lasting neuroadaptations in dopaminergic neurocircuits by inducing <strong>BDNF</strong> production.
+BDNF	drug	nicotine	21232579	In conclusion, the current results suggest the involvement of <strong>BDNF</strong>  and CREB related neuronal processes in <b>nicotine</b> induced neurochemical, behavioural, and neuroplastic changes in dopaminergic neurocircuits.
+BDNF	drug	alcohol	21208596	Chronic, moderate PTSD due to civilian trauma, without psychotic symptoms and without significant rates of comorbid depression, <b>alcohol</b> dependence, or substance dependence, is not associated with abnormalities in CSF CRF, IL 6, <strong>BDNF</strong>, IGF 1, or substance P levels.
+BDNF	addiction	dependence	21208596	Chronic, moderate PTSD due to civilian trauma, without psychotic symptoms and without significant rates of comorbid depression, alcohol <b>dependence</b>, or substance <b>dependence</b>, is not associated with abnormalities in CSF CRF, IL 6, <strong>BDNF</strong>, IGF 1, or substance P levels.
+BDNF	drug	cocaine	21205279	Recent studies have identified changes of several specific miRNA expression profiles and polymorphisms affecting the interactions between miRNAs and their targets in various brain disorders, including addiction: miR 16 causes adaptive changes in production of the serotonin transporter; miR 133b is specifically expressed in midbrain dopaminergic neurons, and regulates the production of tyrosine hydroxylase and the dopamine transporter; miR 212 affects production of striatal <strong>brain derived neurotrophic factor</strong> and synaptic plasticity upon <b>cocaine</b>.
+BDNF	addiction	addiction	21205279	Recent studies have identified changes of several specific miRNA expression profiles and polymorphisms affecting the interactions between miRNAs and their targets in various brain disorders, including <b>addiction</b>: miR 16 causes adaptive changes in production of the serotonin transporter; miR 133b is specifically expressed in midbrain dopaminergic neurons, and regulates the production of tyrosine hydroxylase and the dopamine transporter; miR 212 affects production of striatal <strong>brain derived neurotrophic factor</strong> and synaptic plasticity upon cocaine.
+BDNF	drug	alcohol	21163332	<b>Ethanol</b> induced increases in extracellular dopamine are blunted in <strong>brain derived neurotrophic factor</strong> heterozygous mice.
+BDNF	drug	alcohol	21163332	Brain derived neurotrophic factor (<strong>BDNF</strong>) is suggested to have a protective role in regulating the reinforcing effects of <b>ethanol</b>.
+BDNF	addiction	reward	21163332	Brain derived neurotrophic factor (<strong>BDNF</strong>) is suggested to have a protective role in regulating the <b>reinforcing</b> effects of ethanol.
+BDNF	drug	alcohol	21163332	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is suggested to have a protective role in regulating the reinforcing effects of <b>ethanol</b>.
+BDNF	addiction	reward	21163332	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is suggested to have a protective role in regulating the <b>reinforcing</b> effects of ethanol.
+BDNF	drug	alcohol	21163332	In the present study, we evaluated the effects of an acute, systemic injection of <b>ethanol</b> (2 g/kg) on <strong>BDNF</strong> protein levels and extracellular dopamine concentrations, measured by in vivo microdialysis, in the caudate putamen of wildtype and heterozygous <strong>BDNF</strong> mice.
+BDNF	drug	alcohol	21163332	In both genotypes, the peak increase in extracellular dopamine following <b>ethanol</b> coincided temporally with a decrease in <strong>BDNF</strong> protein levels following a similar <b>ethanol</b> treatment.
+BDNF	drug	alcohol	21163332	Moreover, the effect of <b>ethanol</b> to increase extracellular dopamine was blunted in heterozygous <strong>BDNF</strong> mice compared to wildtype mice.
+BDNF	drug	alcohol	21163332	While the magnitude of decrease in <strong>BDNF</strong> protein induced by <b>ethanol</b> was similar between genotypes (two fold), <b>ethanol</b> treatment induced significantly lower <strong>BDNF</strong> protein levels in heterozygous <strong>BDNF</strong> mice overall.
+BDNF	drug	alcohol	21163332	These findings suggest the effects of <b>ethanol</b> are influenced by an interaction between <strong>BDNF</strong> and dopamine transmission, which may relate to the pathway through which <strong>BDNF</strong> regulates <b>ethanol</b> intake.
+BDNF	drug	alcohol	21098877	Family based study of brain derived neurotrophic factor (<strong>BDNF</strong>) gene polymorphism in <b>alcohol</b> dependence.
+BDNF	addiction	dependence	21098877	Family based study of brain derived neurotrophic factor (<strong>BDNF</strong>) gene polymorphism in alcohol <b>dependence</b>.
+BDNF	drug	alcohol	21098877	Family based study of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene polymorphism in <b>alcohol</b> dependence.
+BDNF	addiction	dependence	21098877	Family based study of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene polymorphism in alcohol <b>dependence</b>.
+BDNF	addiction	addiction	21098877	<strong>BDNF</strong> is thought to be involved in the pathogenesis of bipolar disorder, schizophrenia, eating disorders and <b>addiction</b>.
+BDNF	drug	alcohol	21098877	We hypothesize that a functionally relevant polymorphism of the <strong>BDNF</strong> gene promoter may be associated with the pathogenesis of <b>alcohol</b> dependence.
+BDNF	addiction	dependence	21098877	We hypothesize that a functionally relevant polymorphism of the <strong>BDNF</strong> gene promoter may be associated with the pathogenesis of alcohol <b>dependence</b>.
+BDNF	drug	alcohol	21098877	An association between the <strong>BDNF</strong> Val66Met gene polymorphism and <b>alcoholism</b> was not found.
+BDNF	drug	alcohol	21039634	Differential patterns of serum <strong>brain derived neurotrophic factor</strong> levels in <b>alcoholic</b> patients with and without delirium tremens during acute withdrawal.
+BDNF	addiction	withdrawal	21039634	Differential patterns of serum <strong>brain derived neurotrophic factor</strong> levels in alcoholic patients with and without delirium tremens during acute <b>withdrawal</b>.
+BDNF	drug	alcohol	21039634	Brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with <b>alcohol</b> addiction and withdrawal related neurotoxicity.
+BDNF	addiction	addiction	21039634	Brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with alcohol <b>addiction</b> and withdrawal related neurotoxicity.
+BDNF	addiction	withdrawal	21039634	Brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with alcohol addiction and <b>withdrawal</b> related neurotoxicity.
+BDNF	drug	alcohol	21039634	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with <b>alcohol</b> addiction and withdrawal related neurotoxicity.
+BDNF	addiction	addiction	21039634	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with alcohol <b>addiction</b> and withdrawal related neurotoxicity.
+BDNF	addiction	withdrawal	21039634	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with alcohol addiction and <b>withdrawal</b> related neurotoxicity.
+BDNF	drug	alcohol	21039634	In this study, we explored the differences in serum <strong>BDNF</strong> levels, measured at baseline and 1 week after <b>alcohol</b> withdrawal among <b>alcoholic</b> patients with and without DT.
+BDNF	addiction	withdrawal	21039634	In this study, we explored the differences in serum <strong>BDNF</strong> levels, measured at baseline and 1 week after alcohol <b>withdrawal</b> among alcoholic patients with and without DT.
+BDNF	drug	alcohol	21039634	We collected blood samples of the patient groups on the first and seventh days of <b>alcohol</b> withdrawal and measured serum <strong>BDNF</strong> levels by sandwich enzyme linked immunosorbent assay.
+BDNF	addiction	withdrawal	21039634	We collected blood samples of the patient groups on the first and seventh days of alcohol <b>withdrawal</b> and measured serum <strong>BDNF</strong> levels by sandwich enzyme linked immunosorbent assay.
+BDNF	drug	alcohol	21039634	One week after <b>alcohol</b> withdrawal, the <strong>BDNF</strong> levels increased significantly for both <b>alcoholic</b> groups.
+BDNF	addiction	withdrawal	21039634	One week after alcohol <b>withdrawal</b>, the <strong>BDNF</strong> levels increased significantly for both alcoholic groups.
+BDNF	drug	alcohol	21039634	Additionally, <strong>BDNF</strong> levels elevated after prompt <b>alcohol</b> detoxification treatment.
+BDNF	drug	alcohol	21039634	These findings indicate that <strong>BDNF</strong> could involve modifying the phenotypes of AWS as well as the pertinent neuroadaptive processes of <b>alcohol</b> dependence.
+BDNF	addiction	dependence	21039634	These findings indicate that <strong>BDNF</strong> could involve modifying the phenotypes of AWS as well as the pertinent neuroadaptive processes of alcohol <b>dependence</b>.
+BDNF	drug	alcohol	20978454	<strong>Brain derived neurotrophic factor</strong>, Val66Met single nucleotide polymorphism is not associated with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	20978454	<strong>Brain derived neurotrophic factor</strong>, Val66Met single nucleotide polymorphism is not associated with alcohol <b>dependence</b>.
+BDNF	drug	cocaine	20947769	Cell type specific loss of <strong>BDNF</strong> signaling mimics optogenetic control of <b>cocaine</b> reward.
+BDNF	addiction	reward	20947769	Cell type specific loss of <strong>BDNF</strong> signaling mimics optogenetic control of cocaine <b>reward</b>.
+BDNF	drug	cocaine	20947769	We show that deletion of TrkB, the brain derived neurotrophic factor (<strong>BDNF</strong>) receptor, selectively from D1+ or D2+ neurons oppositely affects <b>cocaine</b> reward.
+BDNF	addiction	reward	20947769	We show that deletion of TrkB, the brain derived neurotrophic factor (<strong>BDNF</strong>) receptor, selectively from D1+ or D2+ neurons oppositely affects cocaine <b>reward</b>.
+BDNF	drug	cocaine	20947769	We show that deletion of TrkB, the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) receptor, selectively from D1+ or D2+ neurons oppositely affects <b>cocaine</b> reward.
+BDNF	addiction	reward	20947769	We show that deletion of TrkB, the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) receptor, selectively from D1+ or D2+ neurons oppositely affects cocaine <b>reward</b>.
+BDNF	drug	cocaine	20890399	Decoding <strong>BDNF</strong> LTP coupling in <b>cocaine</b> addiction.
+BDNF	addiction	addiction	20890399	Decoding <strong>BDNF</strong> LTP coupling in cocaine <b>addiction</b>.
+BDNF	drug	cocaine	20890399	New work by Lu and coworkers in this issue of Neuron now identifies <strong>BDNF</strong> as a gatekeeper of synaptic and behavioral plasticity in <b>cocaine</b> sensitization.
+BDNF	addiction	sensitization	20890399	New work by Lu and coworkers in this issue of Neuron now identifies <strong>BDNF</strong> as a gatekeeper of synaptic and behavioral plasticity in cocaine <b>sensitization</b>.
+BDNF	drug	cocaine	20826313	Elevated <strong>BDNF</strong> after <b>cocaine</b> withdrawal facilitates LTP in medial prefrontal cortex by suppressing GABA inhibition.
+BDNF	addiction	withdrawal	20826313	Elevated <strong>BDNF</strong> after cocaine <b>withdrawal</b> facilitates LTP in medial prefrontal cortex by suppressing GABA inhibition.
+BDNF	drug	cocaine	20826313	Here, we report that after terminating repeated <b>cocaine</b> exposure in rats, a gradual increase in the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) in the mPFC facilitates activity induced long term potentiation (LTP) of excitatory synapses on layer V pyramidal neurons.
+BDNF	drug	cocaine	20826313	Here, we report that after terminating repeated <b>cocaine</b> exposure in rats, a gradual increase in the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the mPFC facilitates activity induced long term potentiation (LTP) of excitatory synapses on layer V pyramidal neurons.
+BDNF	drug	cocaine	20826313	Thus, elevated <strong>BDNF</strong> expression after <b>cocaine</b> withdrawal sensitizes the excitatory synapses in the mPFC to undergo activity induced persistent potentiation that may contribute to cue induced drug craving and drug seeking behavior.
+BDNF	addiction	relapse	20826313	Thus, elevated <strong>BDNF</strong> expression after cocaine withdrawal sensitizes the excitatory synapses in the mPFC to undergo activity induced persistent potentiation that may contribute to cue induced drug <b>craving</b> and drug <b>seeking</b> behavior.
+BDNF	addiction	withdrawal	20826313	Thus, elevated <strong>BDNF</strong> expression after cocaine <b>withdrawal</b> sensitizes the excitatory synapses in the mPFC to undergo activity induced persistent potentiation that may contribute to cue induced drug craving and drug seeking behavior.
+BDNF	drug	cocaine	20810894	<b>Cocaine</b> induced chromatin remodeling increases <strong>brain derived neurotrophic factor</strong> transcription in the rat medial prefrontal cortex, which alters the reinforcing efficacy of <b>cocaine</b>.
+BDNF	addiction	reward	20810894	Cocaine induced chromatin remodeling increases <strong>brain derived neurotrophic factor</strong> transcription in the rat medial prefrontal cortex, which alters the <b>reinforcing</b> efficacy of cocaine.
+BDNF	drug	cocaine	20810894	Compared with yoked saline control rats, <b>cocaine</b> self administration resulted in increased brain derived neurotrophic factor (<strong>BDNF</strong>) protein levels in the rat medial prefrontal cortex (mPFC).
+BDNF	drug	cocaine	20810894	Compared with yoked saline control rats, <b>cocaine</b> self administration resulted in increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) protein levels in the rat medial prefrontal cortex (mPFC).
+BDNF	drug	cocaine	20810894	To examine the functional relevance of this finding, <b>cocaine</b> self administration maintained under a progressive ratio schedule of reinforcement was assessed after short hairpin RNA induced suppression of <strong>BDNF</strong> expression in the mPFC.
+BDNF	addiction	reward	20810894	To examine the functional relevance of this finding, cocaine self administration maintained under a progressive ratio schedule of <b>reinforcement</b> was assessed after short hairpin RNA induced suppression of <strong>BDNF</strong> expression in the mPFC.
+BDNF	drug	cocaine	20810894	Decreased <strong>BDNF</strong> expression in the mPFC increased the <b>cocaine</b> self administration breakpoint.
+BDNF	drug	cocaine	20810894	Next, the effect of <b>cocaine</b> self administration on specific <strong>BDNF</strong> exons was assessed; results revealed selectively increased <strong>BDNF</strong> exon IV containing transcripts in the mPFC.
+BDNF	drug	cocaine	20810894	Moreover, there were significant <b>cocaine</b> induced increases in acetylated histone H3 (AcH3) and phospho cAMP response element binding protein (pCREB) association with <strong>BDNF</strong> promoter IV.
+BDNF	drug	cocaine	20810894	In contrast, there was decreased methyl CpG binding protein 2 (MeCP2) association with <strong>BDNF</strong> promoter IV in the mPFC of rats that previously self administered <b>cocaine</b>.
+BDNF	drug	cocaine	20810894	Together, these results indicate that <b>cocaine</b> induced increases in <strong>BDNF</strong> promoter IV transcript in the mPFC are driven by increased binding of AcH3 and pCREB as well as decreased MeCP2 binding at this <strong>BDNF</strong> promoter.
+BDNF	drug	cocaine	20810894	Collectively, these results indicate that <b>cocaine</b> self administration remodels chromatin in the mPFC, resulting in increased expression of <strong>BDNF</strong>, which appears to represent a compensatory neuroadaptation that reduces the reinforcing efficacy of <b>cocaine</b>.
+BDNF	addiction	reward	20810894	Collectively, these results indicate that cocaine self administration remodels chromatin in the mPFC, resulting in increased expression of <strong>BDNF</strong>, which appears to represent a compensatory neuroadaptation that reduces the <b>reinforcing</b> efficacy of cocaine.
+BDNF	drug	amphetamine	20736000	Association of <strong>brain derived neurotrophic factor</strong> (Val66Met) genetic polymorphism with <b>methamphetamine</b> dependence in a Malaysian population.
+BDNF	addiction	dependence	20736000	Association of <strong>brain derived neurotrophic factor</strong> (Val66Met) genetic polymorphism with methamphetamine <b>dependence</b> in a Malaysian population.
+BDNF	addiction	dependence	20736000	Previous studies suggested that the <strong>BDNF</strong> gene may be involved in the mechanisms underlying substance <b>dependence</b>.
+BDNF	drug	amphetamine	20736000	This study investigated the association of the <strong>BDNF</strong> gene Val66Met polymorphism with <b>methamphetamine</b> dependence and with psychosis in a Malaysian population with different ethnicities.
+BDNF	addiction	dependence	20736000	This study investigated the association of the <strong>BDNF</strong> gene Val66Met polymorphism with methamphetamine <b>dependence</b> and with psychosis in a Malaysian population with different ethnicities.
+BDNF	drug	amphetamine	20736000	The <strong>BDNF</strong> Val66Met polymorphism was genotyped by PCR RFLP in 186 male <b>methamphetamine</b> dependent subjects and in 154 male controls of four different ethnicities, namely, Malay, Chinese, Kadazan Dusun, and Bajau.
+BDNF	drug	amphetamine	20736000	Our results showed that the distribution of the <strong>BDNF</strong> Val66Met genotype in Chinese subjects with <b>methamphetamine</b> dependence (OR=2.6, p=0.015) and <b>methamphetamine</b> psychosis (OR=0.2, p = 0.034) were significant compared with controls.
+BDNF	addiction	dependence	20736000	Our results showed that the distribution of the <strong>BDNF</strong> Val66Met genotype in Chinese subjects with methamphetamine <b>dependence</b> (OR=2.6, p=0.015) and methamphetamine psychosis (OR=0.2, p = 0.034) were significant compared with controls.
+BDNF	drug	amphetamine	20736000	Our findings suggest that the <strong>BDNF</strong> Val66Met polymorphism may contribute to <b>methamphetamine</b> dependence and psychosis in the Chinese population but not in other Malaysian ethnicities.
+BDNF	addiction	dependence	20736000	Our findings suggest that the <strong>BDNF</strong> Val66Met polymorphism may contribute to methamphetamine <b>dependence</b> and psychosis in the Chinese population but not in other Malaysian ethnicities.
+BDNF	drug	cocaine	20711185	MeCP2 controls <strong>BDNF</strong> expression and <b>cocaine</b> intake through homeostatic interactions with microRNA 212.
+BDNF	drug	cocaine	20711185	MeCP2 regulates <b>cocaine</b> intake through homeostatic interactions with microRNA 212 (miR 212) to control the effects of <b>cocaine</b> on striatal brain derived neurotrophic factor (<strong>BDNF</strong>) levels.
+BDNF	drug	cocaine	20711185	MeCP2 regulates <b>cocaine</b> intake through homeostatic interactions with microRNA 212 (miR 212) to control the effects of <b>cocaine</b> on striatal <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels.
+BDNF	addiction	intoxication	20702043	Our final multivariate regression analysis revealed that a non fasting state of blood draw (β= .067; p=.019), later measurement (β= .065; p=.022), longer sample storage (β= .082; p=.004) and being a <b>binge</b> drinker (β= .063; p=.035) all resulted in attenuated <strong>BDNF</strong> levels.
+BDNF	drug	nicotine	20702043	This was in contrast to <b>smoking</b> (β=.098; p=.001) and living in an urban area (β=.109; p<.001), which resulted in increased <strong>BDNF</strong> levels.
+BDNF	drug	alcohol	20702043	Future studies on serum levels of <strong>BDNF</strong> in humans should correct for the time of blood withdrawal, storage, urbanicity, age, sex, smoking status and food and <b>alcohol</b> intake.
+BDNF	drug	nicotine	20702043	Future studies on serum levels of <strong>BDNF</strong> in humans should correct for the time of blood withdrawal, storage, urbanicity, age, sex, <b>smoking</b> status and food and alcohol intake.
+BDNF	addiction	withdrawal	20702043	Future studies on serum levels of <strong>BDNF</strong> in humans should correct for the time of blood <b>withdrawal</b>, storage, urbanicity, age, sex, smoking status and food and alcohol intake.
+BDNF	drug	nicotine	20661552	<b>Nicotine</b> dependence and serum <strong>BDNF</strong> levels in male patients with schizophrenia.
+BDNF	addiction	dependence	20661552	Nicotine <b>dependence</b> and serum <strong>BDNF</strong> levels in male patients with schizophrenia.
+BDNF	drug	nicotine	20661552	The purposes of this study were to compare <strong>BDNF</strong> levels in <b>smokers</b> to nonsmokers with schizophrenia and examine the association between <strong>BDNF</strong> levels and psychopathological symptoms.
+BDNF	drug	nicotine	20661552	Serum <strong>BDNF</strong> levels were measured in 139 male inpatients with DSM IV schizophrenia: 102 <b>smokers</b> and 37 nonsmokers.
+BDNF	drug	nicotine	20661552	<strong>BDNF</strong> levels were significantly higher in <b>smokers</b> than in nonsmokers (p < 0.05).
+BDNF	drug	nicotine	20661552	Higher <strong>BDNF</strong> levels correlated with fewer negative symptoms and with <b>smoking</b> more cigarettes.
+BDNF	drug	nicotine	20661552	The fewer positive symptoms in <b>smokers</b> and fewer negative symptoms in those who smoked more cigarettes may be associated with <b>nicotine</b> induced upregulation of <strong>BDNF</strong>.
+BDNF	drug	opioid	20655300	Influence of <strong>brain derived neurotrophic factor</strong> (val66met) genetic polymorphism on the ages of onset for <b>heroin</b> abuse in males.
+BDNF	addiction	addiction	20655300	Previous studies have shown that one of the genetic variants <strong>BDNF</strong> val66met polymorphism is associated with drug <b>addiction</b>.
+BDNF	drug	opioid	20655300	We conducted an exploratory research to investigate the association of <strong>BDNF</strong> val66met genetic polymorphism with the ages of onset for <b>heroin</b> abuse in males.
+BDNF	drug	opioid	20655300	Venous blood samples from 96 <b>heroin</b> dependent persons were analyzed by Real Time Fluorogenic PCR Assay to determine the genotype of <strong>BDNF</strong> val66met polymorphism.
+BDNF	drug	opioid	20655300	The effect of <strong>BDNF</strong> val66met genetic polymorphism on the age of onset for <b>heroin</b> abuse was analyzed in the patients of different genotypes.
+BDNF	drug	opioid	20655300	Our findings further illustrate the role of <strong>BDNF</strong> genetic variants in drug abuse and dependence and this study will help to identify who are at risk of becoming <b>heroin</b> dependence in the future and decide the more appropriate timing that interventions should be taken in the high risk groups.
+BDNF	addiction	dependence	20655300	Our findings further illustrate the role of <strong>BDNF</strong> genetic variants in drug abuse and <b>dependence</b> and this study will help to identify who are at risk of becoming heroin <b>dependence</b> in the future and decide the more appropriate timing that interventions should be taken in the high risk groups.
+BDNF	drug	cannabinoid	20554863	<strong>Brain derived neurotrophic factor</strong> controls <b>cannabinoid</b> CB1 receptor function in the striatum.
+BDNF	drug	cannabinoid	20554863	The role of brain derived neurotrophic factor (<strong>BDNF</strong>) in emotional processes suggests an interaction with the <b>endocannabinoid</b> system.
+BDNF	drug	cannabinoid	20554863	The role of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in emotional processes suggests an interaction with the <b>endocannabinoid</b> system.
+BDNF	drug	cannabinoid	20554863	Here, we addressed the functional interplay between <strong>BDNF</strong> and <b>cannabinoid</b> CB(1) receptors (CB(1)Rs) in the striatum, a brain area in which both <strong>BDNF</strong> and CB(1)s play a role in the emotional consequences of stress and of rewarding experiences.
+BDNF	drug	cocaine	20554863	The action of <strong>BDNF</strong> on CB(1)R(GABA) function was tyrosine kinase dependent and was complete even after receptor sensitization with <b>cocaine</b> or environmental manipulations activating the dopamine (DA) dependent reward system.
+BDNF	addiction	reward	20554863	The action of <strong>BDNF</strong> on CB(1)R(GABA) function was tyrosine kinase dependent and was complete even after receptor sensitization with cocaine or environmental manipulations activating the dopamine (DA) dependent <b>reward</b> system.
+BDNF	addiction	sensitization	20554863	The action of <strong>BDNF</strong> on CB(1)R(GABA) function was tyrosine kinase dependent and was complete even after receptor <b>sensitization</b> with cocaine or environmental manipulations activating the dopamine (DA) dependent reward system.
+BDNF	drug	cannabinoid	20554863	Haloperidol also enhanced <strong>BDNF</strong> levels in the striatum, suggesting that this neurotrophin may act as a downstream effector of D(2)Rs in the modulation of <b>cannabinoid</b> signaling.
+BDNF	drug	cocaine	20554863	Accordingly, 5 d <b>cocaine</b> exposure both reduced striatal <strong>BDNF</strong> levels and increased CB(1)R(GABA) activity, through a mechanism dependent on D(2)Rs.
+BDNF	drug	alcohol	20553781	<strong>BDNF</strong> and GDNF serum levels in <b>alcohol</b> dependent patients during withdrawal.
+BDNF	addiction	withdrawal	20553781	<strong>BDNF</strong> and GDNF serum levels in alcohol dependent patients during <b>withdrawal</b>.
+BDNF	addiction	addiction	20553781	Preclinical study results suggest that brain derived neurotrophic factor (<strong>BDNF</strong>) and glial cell line derived neurotrophic factor (GDNF) modulate <b>addictive</b> behaviour.
+BDNF	addiction	addiction	20553781	Preclinical study results suggest that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and glial cell line derived neurotrophic factor (GDNF) modulate <b>addictive</b> behaviour.
+BDNF	drug	alcohol	20553781	Therefore we investigated alterations in <strong>BDNF</strong> (81 male patients) and GDNF serum levels (52 male patients) in <b>alcohol</b> dependent patients during <b>alcohol</b> withdrawal (day 1, 7 and 14) in comparison to healthy controls (41 male controls).
+BDNF	addiction	withdrawal	20553781	Therefore we investigated alterations in <strong>BDNF</strong> (81 male patients) and GDNF serum levels (52 male patients) in alcohol dependent patients during alcohol <b>withdrawal</b> (day 1, 7 and 14) in comparison to healthy controls (41 male controls).
+BDNF	drug	alcohol	20553781	<strong>BDNF</strong> serum levels were not significantly altered in <b>alcohol</b> dependent patients compared to healthy controls (p=0.685).
+BDNF	drug	alcohol	20553781	<strong>BDNF</strong> (p=0.265) and GDNF (p=0.255) serum levels did not change significantly during <b>alcohol</b> withdrawal.
+BDNF	addiction	withdrawal	20553781	<strong>BDNF</strong> (p=0.265) and GDNF (p=0.255) serum levels did not change significantly during alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	20553781	<strong>BDNF</strong> serum levels were significantly negatively associated with <b>alcohol</b> withdrawal severity on day 1 (CIWA Ar score, p=0.004).
+BDNF	addiction	withdrawal	20553781	<strong>BDNF</strong> serum levels were significantly negatively associated with alcohol <b>withdrawal</b> severity on day 1 (CIWA Ar score, p=0.004).
+BDNF	addiction	withdrawal	20553781	Moreover <strong>BDNF</strong> serum levels were found to be associated with <b>withdrawal</b> severity.
+BDNF	drug	amphetamine	20478633	A total of 193 non psychotic males (117 <b>methamphetamine</b> dependent and 76 controls) were genotyped for variants located in six genes (AKT1, ARRB2, <strong>BDNF</strong>, COMT, GSTP1, OPRM1).
+BDNF	addiction	addiction	20472139	More importantly, <strong>BDNF</strong> signaling has recently emerged as a key player in the development of drug <b>addiction</b> and is well known to be involved in adaptation to stress and stress related disorders.
+BDNF	drug	nicotine	20456319	Association of polymorphisms in the <strong>BDNF</strong>, DRD1 and DRD3 genes with <b>tobacco</b> <b>smoking</b> in schizophrenia.
+BDNF	drug	nicotine	20456319	Emerging evidence indicates that the DRD1 <strong>BDNF</strong> DRD3 cluster plays an important role in <b>nicotine</b> addiction.
+BDNF	addiction	addiction	20456319	Emerging evidence indicates that the DRD1 <strong>BDNF</strong> DRD3 cluster plays an important role in nicotine <b>addiction</b>.
+BDNF	drug	nicotine	20456319	The ACCG haplotype consisting of four <strong>BDNF</strong> markers (Val66Met (rs6265), rs11030104, rs2049045 and rs7103411) showed an association with the risk of <b>smoking</b> (p = 0.0002).
+BDNF	drug	nicotine	20456319	Our findings are preliminary; however, they support the involvement of the DRD1, <strong>BDNF</strong> and DRD3 genes in <b>smoking</b> behaviour.
+BDNF	addiction	sensitization	20390474	Some mechanisms appear common to all three types of <b>sensitization</b>, such as decreases of brain derived neuroprotective factor (<strong>BDNF</strong>) in hippocampus and blood, as well as increases in <strong>BDNF</strong> in the nucleus accumbens, suggesting the possibility that single treatments could ameliorate several of these factors at once.
+BDNF	drug	alcohol	20382450	The aim of this study was to investigate changes in nerve growth factor (NGF), brain derived neurotrophic factor (<strong>BDNF</strong>), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF) in brain areas, liver, and kidney of 18 mo old male mice exposed perinatally to <b>ethanol</b> at 11% vol or to red wine at the same <b>ethanol</b> concentration.
+BDNF	drug	alcohol	20382450	The aim of this study was to investigate changes in nerve growth factor (NGF), <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF) in brain areas, liver, and kidney of 18 mo old male mice exposed perinatally to <b>ethanol</b> at 11% vol or to red wine at the same <b>ethanol</b> concentration.
+BDNF	drug	alcohol	20382450	The authors found that <b>ethanol</b> per se elevated NGF, <strong>BDNF</strong>, HGF, and VEGF measured by ELISA in brain limbic system areas.
+BDNF	drug	alcohol	20382450	In the liver, early exposure to <b>ethanol</b> solution and red wine depleted <strong>BDNF</strong> and VEGF concentrations.
+BDNF	drug	nicotine	20373480	Varenicline does not increase serum <strong>BDNF</strong> levels in patients with <b>nicotine</b> dependence.
+BDNF	addiction	dependence	20373480	Varenicline does not increase serum <strong>BDNF</strong> levels in patients with nicotine <b>dependence</b>.
+BDNF	drug	nicotine	20373480	In the present study, we compared serum brain derived neurotrophic factor (<strong>BDNF</strong>) levels of <b>nicotine</b> dependence and nonsmokers, and we investigated changes in serum <strong>BDNF</strong> levels after 8 weeks of treatment with varenicline.
+BDNF	addiction	dependence	20373480	In the present study, we compared serum brain derived neurotrophic factor (<strong>BDNF</strong>) levels of nicotine <b>dependence</b> and nonsmokers, and we investigated changes in serum <strong>BDNF</strong> levels after 8 weeks of treatment with varenicline.
+BDNF	drug	nicotine	20373480	In the present study, we compared serum <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels of <b>nicotine</b> dependence and nonsmokers, and we investigated changes in serum <strong>BDNF</strong> levels after 8 weeks of treatment with varenicline.
+BDNF	addiction	dependence	20373480	In the present study, we compared serum <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels of nicotine <b>dependence</b> and nonsmokers, and we investigated changes in serum <strong>BDNF</strong> levels after 8 weeks of treatment with varenicline.
+BDNF	drug	nicotine	20373480	These results suggest that <b>smoking</b> might decrease serum <strong>BDNF</strong> levels and that treatment with varenicline for 8 weeks, combined with 12 weeks of not <b>smoking</b>, does not increase serum <strong>BDNF</strong> levels in <b>smokers</b>.
+BDNF	drug	cocaine	20176040	Exogenous brain derived neurotrophic factor (<strong>BDNF</strong>) can regulate behavioral sensitization and conditioned place preference (CPP) when animals are exposed to repeated <b>cocaine</b> administration.
+BDNF	addiction	reward	20176040	Exogenous brain derived neurotrophic factor (<strong>BDNF</strong>) can regulate behavioral sensitization and conditioned place preference (<b>CPP</b>) when animals are exposed to repeated cocaine administration.
+BDNF	addiction	sensitization	20176040	Exogenous brain derived neurotrophic factor (<strong>BDNF</strong>) can regulate behavioral <b>sensitization</b> and conditioned place preference (CPP) when animals are exposed to repeated cocaine administration.
+BDNF	drug	cocaine	20176040	Exogenous <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) can regulate behavioral sensitization and conditioned place preference (CPP) when animals are exposed to repeated <b>cocaine</b> administration.
+BDNF	addiction	reward	20176040	Exogenous <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) can regulate behavioral sensitization and conditioned place preference (<b>CPP</b>) when animals are exposed to repeated cocaine administration.
+BDNF	addiction	sensitization	20176040	Exogenous <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) can regulate behavioral <b>sensitization</b> and conditioned place preference (CPP) when animals are exposed to repeated cocaine administration.
+BDNF	drug	cocaine	20176040	However, it is unclear whether <strong>BDNF</strong> signaling through the TrkB receptor can mediate these behavioral responses when animals are given a single <b>cocaine</b> exposure.
+BDNF	drug	benzodiazepine	20140603	<strong>BDNF</strong> plasma levels decrease during <b>benzodiazepine</b> withdrawal in patients suffering from comorbidity of depressive disorder and <b>benzodiazepine</b> dependence.
+BDNF	addiction	dependence	20140603	<strong>BDNF</strong> plasma levels decrease during benzodiazepine withdrawal in patients suffering from comorbidity of depressive disorder and benzodiazepine <b>dependence</b>.
+BDNF	addiction	withdrawal	20140603	<strong>BDNF</strong> plasma levels decrease during benzodiazepine <b>withdrawal</b> in patients suffering from comorbidity of depressive disorder and benzodiazepine dependence.
+BDNF	drug	alcohol	19864562	Endogenous <strong>BDNF</strong> in the dorsolateral striatum gates <b>alcohol</b> drinking.
+BDNF	drug	alcohol	19864562	We previously found that brain derived neurotrophic factor (<strong>BDNF</strong>) haplodeficient mice exhibit greater <b>ethanol</b> induced place preference and psychomotor sensitization, and greater <b>ethanol</b> consumption after deprivation, than control mice.
+BDNF	addiction	sensitization	19864562	We previously found that brain derived neurotrophic factor (<strong>BDNF</strong>) haplodeficient mice exhibit greater ethanol induced place preference and psychomotor <b>sensitization</b>, and greater ethanol consumption after deprivation, than control mice.
+BDNF	drug	alcohol	19864562	We previously found that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) haplodeficient mice exhibit greater <b>ethanol</b> induced place preference and psychomotor sensitization, and greater <b>ethanol</b> consumption after deprivation, than control mice.
+BDNF	addiction	sensitization	19864562	We previously found that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) haplodeficient mice exhibit greater ethanol induced place preference and psychomotor <b>sensitization</b>, and greater ethanol consumption after deprivation, than control mice.
+BDNF	drug	alcohol	19864562	We further observed that, in mice, voluntary <b>ethanol</b> intake increases <strong>BDNF</strong> expression in the dorsal striatum (DS).
+BDNF	drug	alcohol	19864562	Here, we determined whether <strong>BDNF</strong> within the DS regulates <b>ethanol</b> self administration in Long Evans rats trained to self administer a 10% <b>ethanol</b> solution.
+BDNF	drug	alcohol	19864562	We observed a greater increase in <strong>BDNF</strong> expression after <b>ethanol</b> self administration in the dorsolateral striatum (DLS) than in the dorsomedial striatum (DMS).
+BDNF	drug	alcohol	19864562	We further found that downregulation of endogenous <strong>BDNF</strong> using viral mediated siRNA in the DLS, but not in the DMS, significantly increased <b>ethanol</b> self administration.
+BDNF	drug	alcohol	19864562	Infusion of exogenous <strong>BDNF</strong> (0.25 microg/microl/side into the DMS; 0.25 and 0.75 microg/microl/side into the DLS) attenuated responding for <b>ethanol</b> when infused 3 h before the beginning of the self administration session.
+BDNF	drug	alcohol	19864562	Although the decrease in <b>ethanol</b> intake was similar in the DLS and DMS, <strong>BDNF</strong> infused in the DLS, but not in the DMS, induced an early termination of the drinking episode.
+BDNF	drug	alcohol	19864562	Furthermore, the action of <strong>BDNF</strong> in the DLS was specific for <b>ethanol</b>, as infusion of the neurotrophic factor in the DMS, but not DLS, resulted in a reduction of sucrose intake.
+BDNF	drug	alcohol	19864562	Together, these findings demonstrate that the <strong>BDNF</strong> pathway within the DLS controls the level of <b>ethanol</b> self administration.
+BDNF	drug	alcohol	19861148	Short term exposure to <b>ethanol</b> causes a differential response between nerve growth factor and <strong>brain derived neurotrophic factor</strong> ligand/receptor systems in the mouse cerebellum.
+BDNF	drug	alcohol	19861148	We found that exposure to <b>ethanol</b> resulted in elevated levels of nerve growth factor (NGF) and TrkA mRNA expression but a decreased level of brain derived neurotrophic factor (<strong>BDNF</strong>) mRNA expression.
+BDNF	drug	alcohol	19861148	We found that exposure to <b>ethanol</b> resulted in elevated levels of nerve growth factor (NGF) and TrkA mRNA expression but a decreased level of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) mRNA expression.
+BDNF	drug	nicotine	19850105	Changes in plasma <strong>brain derived neurotrophic factor</strong> levels in <b>smokers</b> after <b>smoking</b> cessation.
+BDNF	drug	nicotine	19850105	Several studies have reported that brain derived neurotrophic factor (<strong>BDNF</strong>) might be associated with <b>nicotine</b> dependence.
+BDNF	addiction	dependence	19850105	Several studies have reported that brain derived neurotrophic factor (<strong>BDNF</strong>) might be associated with nicotine <b>dependence</b>.
+BDNF	drug	nicotine	19850105	Several studies have reported that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) might be associated with <b>nicotine</b> dependence.
+BDNF	addiction	dependence	19850105	Several studies have reported that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) might be associated with nicotine <b>dependence</b>.
+BDNF	drug	nicotine	19850105	However, there are few studies on <strong>BDNF</strong> levels in humans with <b>nicotine</b> dependence.
+BDNF	addiction	dependence	19850105	However, there are few studies on <strong>BDNF</strong> levels in humans with nicotine <b>dependence</b>.
+BDNF	drug	nicotine	19850105	In the present study, we compared the differences in plasma <strong>BDNF</strong> levels in patients with <b>nicotine</b> dependence and in healthy nonsmokers, and we investigated serial changes in plasma <strong>BDNF</strong> levels in patients with <b>nicotine</b> dependence following <b>smoking</b> cessation.
+BDNF	addiction	dependence	19850105	In the present study, we compared the differences in plasma <strong>BDNF</strong> levels in patients with nicotine <b>dependence</b> and in healthy nonsmokers, and we investigated serial changes in plasma <strong>BDNF</strong> levels in patients with nicotine <b>dependence</b> following smoking cessation.
+BDNF	drug	nicotine	19850105	Plasma <strong>BDNF</strong> levels were measured at baseline using an enzyme linked immunosorbent assay (both <b>smokers</b> and nonsmokers) and at weeks 4 and 12 after <b>smoking</b> cessation (abstinent <b>smokers</b> only).
+BDNF	drug	nicotine	19850105	Baseline plasma <strong>BDNF</strong> levels were significantly lower in <b>smokers</b> compared to nonsmokers (F=4.410, p=0.002).
+BDNF	drug	nicotine	19850105	The plasma <strong>BDNF</strong> levels in the abstinent <b>smokers</b> significantly increased from baseline after 4 weeks of <b>smoking</b> cessation (z= 2.86, p=0.004) but had a tendency of decrease in the period between weeks 4 and 12.
+BDNF	drug	nicotine	19850105	We could not find differences in the plasma <strong>BDNF</strong> levels among the three <b>smoker</b> subgroups at week 12 following cessation.
+BDNF	drug	nicotine	19850105	Changes in plasma <strong>BDNF</strong> levels might be related to the process of abstinence and the pathophysiology of <b>nicotine</b> dependence.
+BDNF	addiction	dependence	19850105	Changes in plasma <strong>BDNF</strong> levels might be related to the process of abstinence and the pathophysiology of nicotine <b>dependence</b>.
+BDNF	drug	cocaine	19843976	<strong>Brain derived neurotrophic factor</strong> signaling modulates <b>cocaine</b> induction of reward associated ultrasonic vocalization in rats.
+BDNF	addiction	reward	19843976	<strong>Brain derived neurotrophic factor</strong> signaling modulates cocaine induction of <b>reward</b> associated ultrasonic vocalization in rats.
+BDNF	addiction	addiction	19843976	As a crucial mediator of neuroplasticity in diverse functional models, brain derived neurotrophic factor (<strong>BDNF</strong>) could contribute to the mechanisms of <b>addiction</b> related neuroplasticity.
+BDNF	addiction	addiction	19843976	As a crucial mediator of neuroplasticity in diverse functional models, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) could contribute to the mechanisms of <b>addiction</b> related neuroplasticity.
+BDNF	drug	cocaine	19843976	Here, we addressed the hypothesis that <b>cocaine</b> increases synaptic dopamine, which induces <strong>BDNF</strong> protein expression to initiate addiction related behavior in the rat.
+BDNF	addiction	addiction	19843976	Here, we addressed the hypothesis that cocaine increases synaptic dopamine, which induces <strong>BDNF</strong> protein expression to initiate <b>addiction</b> related behavior in the rat.
+BDNF	drug	cocaine	19843976	A single injection of <b>cocaine</b> significantly increased <strong>BDNF</strong> protein expression, but this effect was not further augmented by repeated <b>cocaine</b> administration.
+BDNF	drug	cocaine	19843976	R (+) 7 Chloro 8 hydroxy 3 methyl 1 phenyl 2,3,4,5 tetrahydro 1H 3 benzazepine (SCH23390), but not raclopride, significantly attenuated <b>cocaine</b> induced <strong>BDNF</strong> protein expression, whereas either the D(1) like or D(2) like receptor antagonist blocked <b>cocaine</b> induced USV behavior.
+BDNF	drug	amphetamine	19830406	Expression of brain derived neurotrophic factor (<strong>BDNF</strong>) and phosphorylated c AMP response element binding protein (p CREB) genes were measured under basal conditions and after acute or repeated <b>amphetamine</b> treatments.
+BDNF	drug	amphetamine	19830406	Expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and phosphorylated c AMP response element binding protein (p CREB) genes were measured under basal conditions and after acute or repeated <b>amphetamine</b> treatments.
+BDNF	drug	amphetamine	19830406	Basal expression of p CREB (but not <strong>BDNF</strong>) was higher in D (1) ( / ) than D (1) (+/+) mice and was reduced after <b>amphetamine</b> treatment.
+BDNF	drug	alcohol	19756388	Study of the downstream effectors of CREB have identified several important CREB related genes, such as neuropeptide Y, <strong>brain derived neurotrophic factor</strong>, activity regulated cytoskeleton associated protein, and corticotrophin releasing factor, that may play a crucial role in the behavioral effects of <b>ethanol</b> and molecular changes in the specific neurocircuitry that underlie both <b>alcohol</b> addiction and a genetic predisposition to <b>alcoholism</b>.
+BDNF	addiction	addiction	19756388	Study of the downstream effectors of CREB have identified several important CREB related genes, such as neuropeptide Y, <strong>brain derived neurotrophic factor</strong>, activity regulated cytoskeleton associated protein, and corticotrophin releasing factor, that may play a crucial role in the behavioral effects of ethanol and molecular changes in the specific neurocircuitry that underlie both alcohol <b>addiction</b> and a genetic predisposition to alcoholism.
+BDNF	drug	cocaine	19732758	<strong>Brain derived neurotrophic factor</strong> and <b>cocaine</b> addiction.
+BDNF	addiction	addiction	19732758	<strong>Brain derived neurotrophic factor</strong> and cocaine <b>addiction</b>.
+BDNF	drug	cocaine	19732758	The effects of brain derived neurotrophic factor (<strong>BDNF</strong>) on <b>cocaine</b> seeking are brain region specific.
+BDNF	addiction	relapse	19732758	The effects of brain derived neurotrophic factor (<strong>BDNF</strong>) on cocaine <b>seeking</b> are brain region specific.
+BDNF	drug	cocaine	19732758	The effects of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) on <b>cocaine</b> seeking are brain region specific.
+BDNF	addiction	relapse	19732758	The effects of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) on cocaine <b>seeking</b> are brain region specific.
+BDNF	drug	cocaine	19732758	Infusion of <strong>BDNF</strong> into subcortical structures, like the nucleus accumbens and ventral tegmental area, enhances <b>cocaine</b> induced behavioral sensitization and <b>cocaine</b> seeking.
+BDNF	addiction	relapse	19732758	Infusion of <strong>BDNF</strong> into subcortical structures, like the nucleus accumbens and ventral tegmental area, enhances cocaine induced behavioral sensitization and cocaine <b>seeking</b>.
+BDNF	addiction	sensitization	19732758	Infusion of <strong>BDNF</strong> into subcortical structures, like the nucleus accumbens and ventral tegmental area, enhances cocaine induced behavioral <b>sensitization</b> and cocaine seeking.
+BDNF	drug	cocaine	19732758	Conversely, repeated administration of <strong>BDNF</strong> antiserum into the nucleus accumbens during chronic <b>cocaine</b> self administration attenuates <b>cocaine</b> induced reinstatement.
+BDNF	addiction	relapse	19732758	Conversely, repeated administration of <strong>BDNF</strong> antiserum into the nucleus accumbens during chronic cocaine self administration attenuates cocaine induced <b>reinstatement</b>.
+BDNF	drug	cocaine	19732758	In contrast, <strong>BDNF</strong> infusion into the dorsomedial prefrontal cortex immediately following a final session of <b>cocaine</b> self administration attenuates relapse to <b>cocaine</b> seeking after abstinence, as well as cue  and <b>cocaine</b> prime induced reinstatement of <b>cocaine</b> seeking following extinction.
+BDNF	addiction	relapse	19732758	In contrast, <strong>BDNF</strong> infusion into the dorsomedial prefrontal cortex immediately following a final session of cocaine self administration attenuates <b>relapse</b> to cocaine <b>seeking</b> after abstinence, as well as cue  and cocaine prime induced <b>reinstatement</b> of cocaine <b>seeking</b> following extinction.
+BDNF	drug	cocaine	19732758	<strong>BDNF</strong> induced alterations in the ERK MAP kinase cascade and in prefronto accumbens glutamatergic transmission are implicated in <strong>BDNF</strong>'s ability to alter <b>cocaine</b> seeking.
+BDNF	addiction	relapse	19732758	<strong>BDNF</strong> induced alterations in the ERK MAP kinase cascade and in prefronto accumbens glutamatergic transmission are implicated in <strong>BDNF</strong>'s ability to alter cocaine <b>seeking</b>.
+BDNF	drug	cocaine	19732758	Within 22 hours after infusion into the prefrontal cortex, <strong>BDNF</strong> increases <strong>BDNF</strong> protein in prefrontal cortical targets, including nucleus accumbens, and restores <b>cocaine</b> mediated decreases in phospho ERK expression in the nucleus accumbens.
+BDNF	drug	cocaine	19732758	Furthermore, 3 weeks after <strong>BDNF</strong> infusion in animals with a <b>cocaine</b> self administration history, suppressed basal levels of glutamate are normalized and a <b>cocaine</b> prime induced increase in extracellular glutamate levels in the nucleus accumbens is prevented.
+BDNF	drug	cocaine	19732758	Thus, <strong>BDNF</strong> may have local effects at the site of infusion and distal effects in target areas that are critical to mediating or preventing <b>cocaine</b> induced dysfunctional neuroadaptations.
+BDNF	drug	alcohol	19671462	Previously, we demonstrated that acute <b>ethanol</b> increased preprodynorphin expression via brain derived neurotrophic factor (<strong>BDNF</strong>) in striatal neurons, and that blockade of the KOR attenuated decreases in <b>ethanol</b> intake observed following increased expression of <strong>BDNF</strong>.
+BDNF	drug	alcohol	19671462	Previously, we demonstrated that acute <b>ethanol</b> increased preprodynorphin expression via <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in striatal neurons, and that blockade of the KOR attenuated decreases in <b>ethanol</b> intake observed following increased expression of <strong>BDNF</strong>.
+BDNF	drug	amphetamine	19562947	We have demonstrated that systemic administration of dipeptide Leu Ile increases <strong>BDNF</strong> and GDNF production in the brain, and has a protective role in <b>methamphetamine</b> and morphine dependence.
+BDNF	drug	opioid	19562947	We have demonstrated that systemic administration of dipeptide Leu Ile increases <strong>BDNF</strong> and GDNF production in the brain, and has a protective role in methamphetamine and <b>morphine</b> dependence.
+BDNF	addiction	dependence	19562947	We have demonstrated that systemic administration of dipeptide Leu Ile increases <strong>BDNF</strong> and GDNF production in the brain, and has a protective role in methamphetamine and morphine <b>dependence</b>.
+BDNF	drug	alcohol	19560628	Relation between plasma <strong>brain derived neurotrophic factor</strong> and nerve growth factor in the male patients with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19560628	Relation between plasma <strong>brain derived neurotrophic factor</strong> and nerve growth factor in the male patients with alcohol <b>dependence</b>.
+BDNF	drug	alcohol	19560628	Our aim was to verify the changes in human plasma <strong>BDNF</strong> and NGF concentrations induced by chronic <b>alcohol</b> use.
+BDNF	drug	alcohol	19560628	Mean plasma <strong>BDNF</strong> level was significantly higher in the patients with <b>alcohol</b> dependence (3502.21+/ 1726.9 pg/mL) compared with the healthy subjects (861.75+/ 478.9 pg/mL) (P=.000).
+BDNF	addiction	dependence	19560628	Mean plasma <strong>BDNF</strong> level was significantly higher in the patients with alcohol <b>dependence</b> (3502.21+/ 1726.9 pg/mL) compared with the healthy subjects (861.75+/ 478.9 pg/mL) (P=.000).
+BDNF	drug	alcohol	19560628	Plasma <strong>BDNF</strong> and NGF levels showed significant negative correlation in <b>alcohol</b> dependence group (r= 0.388, P=.012).
+BDNF	addiction	dependence	19560628	Plasma <strong>BDNF</strong> and NGF levels showed significant negative correlation in alcohol <b>dependence</b> group (r= 0.388, P=.012).
+BDNF	drug	alcohol	19560628	Increased plasma <strong>BDNF</strong> and NGF with negative correlation in <b>alcohol</b> dependent patients may have some role in the regeneration of damage done by chronic <b>alcohol</b> use.
+BDNF	drug	alcohol	19548207	Serum levels of <strong>brain derived neurotrophic factor</strong> in comorbidity of depression and <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19548207	Serum levels of <strong>brain derived neurotrophic factor</strong> in comorbidity of depression and alcohol <b>dependence</b>.
+BDNF	drug	alcohol	19548207	The purpose of the present study was to compare serum brain derived neurotrophic factor (<strong>BDNF</strong>) levels between depressive patients with and without <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19548207	The purpose of the present study was to compare serum brain derived neurotrophic factor (<strong>BDNF</strong>) levels between depressive patients with and without alcohol <b>dependence</b>.
+BDNF	drug	alcohol	19548207	The purpose of the present study was to compare serum <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels between depressive patients with and without <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19548207	The purpose of the present study was to compare serum <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels between depressive patients with and without alcohol <b>dependence</b>.
+BDNF	drug	alcohol	19548207	Serum <strong>BDNF</strong> levels in the depressive patients with (9.0 +/  4.3 ng/ml) and without (9.8 +/  5.2 ng/ml) <b>alcohol</b> dependence were significantly lower than those in the healthy subjects (21.1 +/  7.0 ng/ml); however, no significant difference was found in the serum <strong>BDNF</strong> levels of depressive patients with and without <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19548207	Serum <strong>BDNF</strong> levels in the depressive patients with (9.0 +/  4.3 ng/ml) and without (9.8 +/  5.2 ng/ml) alcohol <b>dependence</b> were significantly lower than those in the healthy subjects (21.1 +/  7.0 ng/ml); however, no significant difference was found in the serum <strong>BDNF</strong> levels of depressive patients with and without alcohol <b>dependence</b>.
+BDNF	drug	alcohol	19548207	Eight of the 16 (50%) depressive patients suffering from both depression and <b>alcohol</b> dependence responded to 8 weeks of treatment with antidepressant drugs which significantly increased their serum <strong>BDNF</strong> levels.
+BDNF	addiction	dependence	19548207	Eight of the 16 (50%) depressive patients suffering from both depression and alcohol <b>dependence</b> responded to 8 weeks of treatment with antidepressant drugs which significantly increased their serum <strong>BDNF</strong> levels.
+BDNF	drug	alcohol	19548207	These results suggest that the serum <strong>BDNF</strong> level is a useful biological marker for depression in patients with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19548207	These results suggest that the serum <strong>BDNF</strong> level is a useful biological marker for depression in patients with alcohol <b>dependence</b>.
+BDNF	drug	amphetamine	19462300	COMT, D4 receptor, and <strong>BDNF</strong> polymorphisms are linked to <b>methamphetamine</b> abuse and psychosis.
+BDNF	drug	alcohol	19453942	Escalating <b>ethanol</b> intake is associated with altered corticostriatal <strong>BDNF</strong> expression.
+BDNF	drug	alcohol	19453942	Previously, we identified brain derived neurotrophic factor (<strong>BDNF</strong>) in the dorsal striatum as the central mediator of a homeostatic mechanism which is activated by acute <b>alcohol</b> (<b>ethanol</b>) exposure and functions to decrease the sensitivity of rodents to <b>ethanol</b> related behaviors.
+BDNF	drug	alcohol	19453942	Previously, we identified <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the dorsal striatum as the central mediator of a homeostatic mechanism which is activated by acute <b>alcohol</b> (<b>ethanol</b>) exposure and functions to decrease the sensitivity of rodents to <b>ethanol</b> related behaviors.
+BDNF	drug	alcohol	19453942	We hypothesized that extensive exposure to <b>ethanol</b> would result in dysregulation of this <strong>BDNF</strong> mediated protective mechanism, accompanied by heightened <b>ethanol</b> intake.
+BDNF	drug	alcohol	19453942	In this study, we demonstrate that while a single bout of <b>ethanol</b> intake increases <strong>BDNF</strong> mRNA expression in the dorsal striatum, this effect is no longer observed after 6 weeks of daily <b>ethanol</b> access.
+BDNF	drug	alcohol	19453942	Additionally, 6 weeks of <b>ethanol</b> consumption decreases <strong>BDNF</strong> in the cortex, a main source of <strong>BDNF</strong> for the striatum.
+BDNF	drug	alcohol	19453942	Importantly, these <b>ethanol</b> induced changes in <strong>BDNF</strong> levels are not ameliorated by 2 weeks' abstinence.
+BDNF	drug	alcohol	19453942	Together, these data suggest that the <strong>BDNF</strong> pathway, which is activated following a single bout of <b>ethanol</b> drinking, breaks down by the end of 6 weeks of access and does not recover its protective function after a 2 week deprivation period.
+BDNF	addiction	addiction	19453942	These results suggest that the persistence of altered <strong>BDNF</strong> signaling may contribute to the inflexibility of <b>addictive</b> behaviors.
+BDNF	drug	cocaine	19345340	Ventral tegmental area (VTA) brain derived neurotrophic factor (<strong>BDNF</strong>) contributes to time dependent increases in cue induced <b>cocaine</b> seeking after withdrawal (incubation of <b>cocaine</b> craving).
+BDNF	addiction	relapse	19345340	Ventral tegmental area (VTA) brain derived neurotrophic factor (<strong>BDNF</strong>) contributes to time dependent increases in cue induced cocaine <b>seeking</b> after withdrawal (incubation of cocaine <b>craving</b>).
+BDNF	addiction	withdrawal	19345340	Ventral tegmental area (VTA) brain derived neurotrophic factor (<strong>BDNF</strong>) contributes to time dependent increases in cue induced cocaine seeking after <b>withdrawal</b> (incubation of cocaine craving).
+BDNF	drug	cocaine	19345340	Ventral tegmental area (VTA) <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) contributes to time dependent increases in cue induced <b>cocaine</b> seeking after withdrawal (incubation of <b>cocaine</b> craving).
+BDNF	addiction	relapse	19345340	Ventral tegmental area (VTA) <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) contributes to time dependent increases in cue induced cocaine <b>seeking</b> after withdrawal (incubation of cocaine <b>craving</b>).
+BDNF	addiction	withdrawal	19345340	Ventral tegmental area (VTA) <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) contributes to time dependent increases in cue induced cocaine seeking after <b>withdrawal</b> (incubation of cocaine craving).
+BDNF	drug	cocaine	19345340	Here, we studied the role of glial cell line derived neurotrophic factor (GDNF) in incubation of <b>cocaine</b> craving because, like <strong>BDNF</strong>, GDNF provides trophic support to midbrain dopamine neurons.
+BDNF	addiction	relapse	19345340	Here, we studied the role of glial cell line derived neurotrophic factor (GDNF) in incubation of cocaine <b>craving</b> because, like <strong>BDNF</strong>, GDNF provides trophic support to midbrain dopamine neurons.
+BDNF	drug	cocaine	19321768	A single intra PFC infusion of <strong>BDNF</strong> prevents <b>cocaine</b> induced alterations in extracellular glutamate within the nucleus accumbens.
+BDNF	drug	cocaine	19321768	<strong>BDNF</strong> infusion into the dmPFC attenuates reinstatement to <b>cocaine</b> seeking behavior, as well as some <b>cocaine</b> induced molecular adaptations within the NAc.
+BDNF	addiction	relapse	19321768	<strong>BDNF</strong> infusion into the dmPFC attenuates <b>reinstatement</b> to cocaine <b>seeking</b> behavior, as well as some cocaine induced molecular adaptations within the NAc.
+BDNF	drug	cocaine	19321768	In the present study, it is demonstrated that a single intra dmPFC infusion of <strong>BDNF</strong> prevents <b>cocaine</b> self administration induced reduction in basal extracellular glutamate, as well as <b>cocaine</b> prime induced increases in extracellular glutamate levels within the NAc.
+BDNF	drug	cocaine	19321768	These data suggest that intra PFC <strong>BDNF</strong> attenuates reinstatement to <b>cocaine</b> seeking behavior by normalizing <b>cocaine</b> induced neuroadaptations that alter glutamate neurotransmission within the NAc.
+BDNF	addiction	relapse	19321768	These data suggest that intra PFC <strong>BDNF</strong> attenuates <b>reinstatement</b> to cocaine <b>seeking</b> behavior by normalizing cocaine induced neuroadaptations that alter glutamate neurotransmission within the NAc.
+BDNF	drug	nicotine	19224602	<b>Nicotine</b> sensitization and analysis of <strong>brain derived neurotrophic factor</strong> in adolescent beta arrestin 2 knockout mice.
+BDNF	addiction	sensitization	19224602	Nicotine <b>sensitization</b> and analysis of <strong>brain derived neurotrophic factor</strong> in adolescent beta arrestin 2 knockout mice.
+BDNF	drug	nicotine	19224602	<b>Nicotine</b> sensitization and levels of brain derived neurotrophic factor (<strong>BDNF</strong>) were analyzed in adolescent beta arrestin 2 knockout (betaA 2 KO) and wild type (WT) mice.
+BDNF	addiction	sensitization	19224602	Nicotine <b>sensitization</b> and levels of brain derived neurotrophic factor (<strong>BDNF</strong>) were analyzed in adolescent beta arrestin 2 knockout (betaA 2 KO) and wild type (WT) mice.
+BDNF	drug	nicotine	19224602	<b>Nicotine</b> sensitization and levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) were analyzed in adolescent beta arrestin 2 knockout (betaA 2 KO) and wild type (WT) mice.
+BDNF	addiction	sensitization	19224602	Nicotine <b>sensitization</b> and levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) were analyzed in adolescent beta arrestin 2 knockout (betaA 2 KO) and wild type (WT) mice.
+BDNF	drug	nicotine	19224602	On the <b>nicotine</b> challenge, WT mice administered <b>nicotine</b> demonstrated significantly higher activity levels compared to all groups, and this same group demonstrated significantly higher levels of accumbal <strong>BDNF</strong> compared to all groups.
+BDNF	drug	nicotine	19224602	On the <b>nicotine</b> challenge, WT mice that received <b>nicotine</b> demonstrated a significant increase in activity compared to all groups, and showed increased accumbal <strong>BDNF</strong> compared to all groups.
+BDNF	drug	nicotine	19224602	These results show that the beta arrestin 2 protein is important in induction and expression of <b>nicotine</b> sensitization as well as <b>nicotine</b>'s effects on accumbal <strong>BDNF</strong>.
+BDNF	addiction	sensitization	19224602	These results show that the beta arrestin 2 protein is important in induction and expression of nicotine <b>sensitization</b> as well as nicotine's effects on accumbal <strong>BDNF</strong>.
+BDNF	drug	amphetamine	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, <strong>BDNF</strong>, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with <b>METH</b> psychosis.
+BDNF	addiction	dependence	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, <strong>BDNF</strong>, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.
+BDNF	drug	alcohol	19170664	Association between Val66Met brain derived neurotrophic factor (<strong>BDNF</strong>) gene polymorphism and post treatment relapse in <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19170664	Association between Val66Met brain derived neurotrophic factor (<strong>BDNF</strong>) gene polymorphism and post treatment relapse in alcohol <b>dependence</b>.
+BDNF	addiction	relapse	19170664	Association between Val66Met brain derived neurotrophic factor (<strong>BDNF</strong>) gene polymorphism and post treatment <b>relapse</b> in alcohol dependence.
+BDNF	drug	alcohol	19170664	Association between Val66Met <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene polymorphism and post treatment relapse in <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19170664	Association between Val66Met <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene polymorphism and post treatment relapse in alcohol <b>dependence</b>.
+BDNF	addiction	relapse	19170664	Association between Val66Met <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene polymorphism and post treatment <b>relapse</b> in alcohol dependence.
+BDNF	addiction	relapse	19170664	Genetic polymorphisms in several genes (TPH2, SLC6A4, HTR1A, HTR2A, COMT, and <strong>BDNF</strong>) were tested as predictors of <b>relapse</b> (defined as any drinking during follow up) while controlling for baseline measures.
+BDNF	addiction	relapse	19170664	Patients with the Val allele in the Val66Met <strong>BDNF</strong> polymorphism and the Met allele in the Val158Met COMT polymorphism were more likely to <b>relapse</b>.
+BDNF	addiction	relapse	19170664	Only the <strong>BDNF</strong> Val/Val genotype predicted post treatment <b>relapse</b> [odds ratio (OR) = 2.62; p = 0.019], and time to <b>relapse</b> (OR = 2.57; p = 0.002), after adjusting for baseline measures and other significant genetic markers.
+BDNF	drug	alcohol	19170664	When the analysis was restricted to patients with a family history of <b>alcohol</b> dependence (n = 73), the associations between the <strong>BDNF</strong> Val/Val genotype and relapse (OR = 5.76, p = 0.0045) and time to relapse (hazard ratio = 4.93, p = 0.001) were even stronger.
+BDNF	addiction	dependence	19170664	When the analysis was restricted to patients with a family history of alcohol <b>dependence</b> (n = 73), the associations between the <strong>BDNF</strong> Val/Val genotype and relapse (OR = 5.76, p = 0.0045) and time to relapse (hazard ratio = 4.93, p = 0.001) were even stronger.
+BDNF	addiction	relapse	19170664	When the analysis was restricted to patients with a family history of alcohol dependence (n = 73), the associations between the <strong>BDNF</strong> Val/Val genotype and <b>relapse</b> (OR = 5.76, p = 0.0045) and time to <b>relapse</b> (hazard ratio = 4.93, p = 0.001) were even stronger.
+BDNF	drug	alcohol	19170664	The Val66Met <strong>BDNF</strong> gene polymorphism was associated with a higher risk and earlier occurrence of relapse among patients treated for <b>alcohol</b> dependence.
+BDNF	addiction	dependence	19170664	The Val66Met <strong>BDNF</strong> gene polymorphism was associated with a higher risk and earlier occurrence of relapse among patients treated for alcohol <b>dependence</b>.
+BDNF	addiction	relapse	19170664	The Val66Met <strong>BDNF</strong> gene polymorphism was associated with a higher risk and earlier occurrence of <b>relapse</b> among patients treated for alcohol dependence.
+BDNF	drug	cocaine	18990365	Previous studies found that brain derived neurotrophic factor (<strong>BDNF</strong>) derived from nucleus accumbens (NAc) neurons can mediate persistent behavioral changes that contribute to <b>cocaine</b> addiction.
+BDNF	addiction	addiction	18990365	Previous studies found that brain derived neurotrophic factor (<strong>BDNF</strong>) derived from nucleus accumbens (NAc) neurons can mediate persistent behavioral changes that contribute to cocaine <b>addiction</b>.
+BDNF	drug	cocaine	18990365	Previous studies found that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) derived from nucleus accumbens (NAc) neurons can mediate persistent behavioral changes that contribute to <b>cocaine</b> addiction.
+BDNF	addiction	addiction	18990365	Previous studies found that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) derived from nucleus accumbens (NAc) neurons can mediate persistent behavioral changes that contribute to cocaine <b>addiction</b>.
+BDNF	drug	cocaine	18990365	To further investigate <strong>BDNF</strong> signaling in the mesolimbic dopamine system, we analyzed tropomyosin related kinase B (TrkB) messenger RNA (mRNA) and protein changes in the NAc and ventral tegmental area (VTA) in rats following 3 weeks of <b>cocaine</b> self administration.
+BDNF	drug	cocaine	18990365	To study the role of <strong>BDNF</strong> TrkB activity in the VTA and NAc in <b>cocaine</b> reward, we used localized viral mediated Cre recombinase expression in floxed <strong>BDNF</strong> and floxed TrkB mice to knockdown <strong>BDNF</strong> or TrkB in the VTA and NAc in <b>cocaine</b> place conditioning tests and TrkB in the NAc in <b>cocaine</b> self administration tests.
+BDNF	addiction	reward	18990365	To study the role of <strong>BDNF</strong> TrkB activity in the VTA and NAc in cocaine <b>reward</b>, we used localized viral mediated Cre recombinase expression in floxed <strong>BDNF</strong> and floxed TrkB mice to knockdown <strong>BDNF</strong> or TrkB in the VTA and NAc in cocaine place conditioning tests and TrkB in the NAc in cocaine self administration tests.
+BDNF	drug	cocaine	18990365	Localized <strong>BDNF</strong> knockdown in either region reduced <b>cocaine</b> reward in place conditioning, whereas only TrkB knockdown in the NAc reduced <b>cocaine</b> reward.
+BDNF	addiction	reward	18990365	Localized <strong>BDNF</strong> knockdown in either region reduced cocaine <b>reward</b> in place conditioning, whereas only TrkB knockdown in the NAc reduced cocaine <b>reward</b>.
+BDNF	drug	cocaine	18990365	Together, these data suggest that <strong>BDNF</strong> synthesized in either VTA or NAc neurons is important for maintaining sensitivity to <b>cocaine</b> reward but only <strong>BDNF</strong> activation of TrkB receptors in the NAc mediates this effect.
+BDNF	addiction	reward	18990365	Together, these data suggest that <strong>BDNF</strong> synthesized in either VTA or NAc neurons is important for maintaining sensitivity to cocaine <b>reward</b> but only <strong>BDNF</strong> activation of TrkB receptors in the NAc mediates this effect.
+BDNF	drug	cannabinoid	18807247	Preliminary evidence of <b>cannabinoid</b> effects on brain derived neurotrophic factor (<strong>BDNF</strong>) levels in humans.
+BDNF	drug	cannabinoid	18807247	Preliminary evidence of <b>cannabinoid</b> effects on <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) levels in humans.
+BDNF	drug	cannabinoid	18807247	Preclinical studies suggest that <b>cannabinoids</b> modulate brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	cannabinoid	18807247	Preclinical studies suggest that <b>cannabinoids</b> modulate <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	cannabinoid	18807247	Accordingly, we hypothesized that Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>), the principal active component of <b>cannabis</b>, would alter <strong>BDNF</strong> levels in humans.
+BDNF	drug	cannabinoid	18807247	Serum sampled at baseline, after placebo administration, and after Delta(9) <b>THC</b> administration was assayed for <strong>BDNF</strong> using ELISA.
+BDNF	drug	cannabinoid	18807247	Delta(9) <b>THC</b> increased serum <strong>BDNF</strong> levels in healthy controls but not light users of <b>cannabis</b>.
+BDNF	drug	cannabinoid	18807247	Further, light users of <b>cannabis</b> had lower basal <strong>BDNF</strong> levels.
+BDNF	drug	cannabinoid	18807247	The effects of socially relevant doses of <b>cannabinoids</b> on <strong>BDNF</strong> suggest a possible mechanism underlying the consequences of exposure to <b>cannabis</b>.
+BDNF	drug	cannabinoid	18807247	Larger studies to investigate the effects of <b>cannabinoids</b> on <strong>BDNF</strong> and other neurotrophins are warranted.
+BDNF	drug	cocaine	18677617	Stress exposure increased <strong>BDNF</strong> mRNA levels in the ventral tegmental area (VTA) and nucleus accumbens (NAc) only in <b>cocaine</b> experienced mice following a prolonged, but not acute, drug free period.
+BDNF	drug	amphetamine	18654637	First, we discuss the roles of several neurotransmitters and neuropeptides in the functioning of the NAc, including dopamine, glutamate, gamma aminobutyric acid (GABA), acetylcholine, serotonin, dynorphin, enkephaline, brain derived neurotrophic factor (<strong>BDNF</strong>), cAMP response element binding protein (CREB), melanin concentrating hormone (MCH) and cocaine  and <b>amphetamine</b> regulated transcript (CART).
+BDNF	drug	cocaine	18654637	First, we discuss the roles of several neurotransmitters and neuropeptides in the functioning of the NAc, including dopamine, glutamate, gamma aminobutyric acid (GABA), acetylcholine, serotonin, dynorphin, enkephaline, brain derived neurotrophic factor (<strong>BDNF</strong>), cAMP response element binding protein (CREB), melanin concentrating hormone (MCH) and <b>cocaine</b>  and amphetamine regulated transcript (CART).
+BDNF	drug	amphetamine	18654637	First, we discuss the roles of several neurotransmitters and neuropeptides in the functioning of the NAc, including dopamine, glutamate, gamma aminobutyric acid (GABA), acetylcholine, serotonin, dynorphin, enkephaline, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), cAMP response element binding protein (CREB), melanin concentrating hormone (MCH) and cocaine  and <b>amphetamine</b> regulated transcript (CART).
+BDNF	drug	cocaine	18654637	First, we discuss the roles of several neurotransmitters and neuropeptides in the functioning of the NAc, including dopamine, glutamate, gamma aminobutyric acid (GABA), acetylcholine, serotonin, dynorphin, enkephaline, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), cAMP response element binding protein (CREB), melanin concentrating hormone (MCH) and <b>cocaine</b>  and amphetamine regulated transcript (CART).
+BDNF	drug	opioid	18630696	[The expression of <strong>BDNF</strong> and PSD 95 in hippocampal CA1 region of <b>morphine</b> withdrawn rat with different dependent times].
+BDNF	drug	opioid	18630696	To observe the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) and postsynaptic density 95 (PSD 95) in hippocampal CA1 region of rat with <b>morphine</b> dependence for different times and withdrawn for 1 week, and investigate the influence of that <b>morphine</b> dependence is withdrawn on rat hippocampal CA1 area.
+BDNF	addiction	dependence	18630696	To observe the expression of brain derived neurotrophic factor (<strong>BDNF</strong>) and postsynaptic density 95 (PSD 95) in hippocampal CA1 region of rat with morphine <b>dependence</b> for different times and withdrawn for 1 week, and investigate the influence of that morphine <b>dependence</b> is withdrawn on rat hippocampal CA1 area.
+BDNF	drug	opioid	18630696	To observe the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and postsynaptic density 95 (PSD 95) in hippocampal CA1 region of rat with <b>morphine</b> dependence for different times and withdrawn for 1 week, and investigate the influence of that <b>morphine</b> dependence is withdrawn on rat hippocampal CA1 area.
+BDNF	addiction	dependence	18630696	To observe the expression of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and postsynaptic density 95 (PSD 95) in hippocampal CA1 region of rat with morphine <b>dependence</b> for different times and withdrawn for 1 week, and investigate the influence of that morphine <b>dependence</b> is withdrawn on rat hippocampal CA1 area.
+BDNF	drug	opioid	18630696	The expression of <strong>BDNF</strong> and PSD 95 in hippocampal CA1 decreased in the withdrawn group with <b>morphine</b> dependence for 1 week as compared with that in normal saline (NS) group (P < 0.01), and it increased in the withdrawn group with <b>morphine</b> dependence for 2 weeks as compared with that in <b>morphine</b> dependent group for 1 week (P < 0.05) but still decreased as compared with that in NS group (P < 0.01), and it decreased in the withdrawn group with <b>morphine</b> dependence for 4 weeks as compared with the other three groups (P < 0.01).
+BDNF	addiction	dependence	18630696	The expression of <strong>BDNF</strong> and PSD 95 in hippocampal CA1 decreased in the withdrawn group with morphine <b>dependence</b> for 1 week as compared with that in normal saline (NS) group (P < 0.01), and it increased in the withdrawn group with morphine <b>dependence</b> for 2 weeks as compared with that in morphine dependent group for 1 week (P < 0.05) but still decreased as compared with that in NS group (P < 0.01), and it decreased in the withdrawn group with morphine <b>dependence</b> for 4 weeks as compared with the other three groups (P < 0.01).
+BDNF	drug	opioid	18630696	The expression of <strong>BDNF</strong> and PSD 95 in hippocampal CA1 decreases in <b>morphine</b> depended rats withdrawn for 1 week.
+BDNF	drug	cocaine	18551281	Role of accumbens <strong>BDNF</strong> and TrkB in <b>cocaine</b> induced psychomotor sensitization, conditioned place preference, and reinstatement in rats.
+BDNF	addiction	relapse	18551281	Role of accumbens <strong>BDNF</strong> and TrkB in cocaine induced psychomotor sensitization, conditioned place preference, and <b>reinstatement</b> in rats.
+BDNF	addiction	sensitization	18551281	Role of accumbens <strong>BDNF</strong> and TrkB in cocaine induced psychomotor <b>sensitization</b>, conditioned place preference, and reinstatement in rats.
+BDNF	drug	cocaine	18551281	<strong>BDNF</strong> was previously shown to be involved in <b>cocaine</b> reward and relapse, as assessed in rat models.
+BDNF	addiction	relapse	18551281	<strong>BDNF</strong> was previously shown to be involved in cocaine reward and <b>relapse</b>, as assessed in rat models.
+BDNF	addiction	reward	18551281	<strong>BDNF</strong> was previously shown to be involved in cocaine <b>reward</b> and relapse, as assessed in rat models.
+BDNF	drug	cocaine	18551281	The goal of this study is to explore the role of <strong>BDNF</strong> and TrkB in the rat nucleus accumbens (NAc) in <b>cocaine</b> induced psychomotor sensitization and in conditioned place preference acquisition, expression, and reinstatement.
+BDNF	addiction	relapse	18551281	The goal of this study is to explore the role of <strong>BDNF</strong> and TrkB in the rat nucleus accumbens (NAc) in cocaine induced psychomotor sensitization and in conditioned place preference acquisition, expression, and <b>reinstatement</b>.
+BDNF	addiction	sensitization	18551281	The goal of this study is to explore the role of <strong>BDNF</strong> and TrkB in the rat nucleus accumbens (NAc) in cocaine induced psychomotor <b>sensitization</b> and in conditioned place preference acquisition, expression, and reinstatement.
+BDNF	addiction	sensitization	18551281	<strong>BDNF</strong> and/or its receptor TrkB in the NAc enhance drug induced locomotor activity and induce <b>sensitization</b> in rats.
+BDNF	drug	cocaine	18551281	Furthermore, LV <strong>BDNF</strong>  and LV TrkB treated rats display enhanced <b>cocaine</b> induced CPP, delayed CPP extinction upon repeated measurements, and increased CPP reinstatement.
+BDNF	addiction	relapse	18551281	Furthermore, LV <strong>BDNF</strong>  and LV TrkB treated rats display enhanced cocaine induced CPP, delayed CPP extinction upon repeated measurements, and increased CPP <b>reinstatement</b>.
+BDNF	addiction	reward	18551281	Furthermore, LV <strong>BDNF</strong>  and LV TrkB treated rats display enhanced cocaine induced <b>CPP</b>, delayed <b>CPP</b> extinction upon repeated measurements, and increased <b>CPP</b> reinstatement.
+BDNF	addiction	reward	18551281	We show that <strong>BDNF</strong> and TrkB induced <b>CPP</b> takes place during the learning period (conditioning), whereas extinction leads to the loss of <b>CPP</b>.
+BDNF	drug	cocaine	18551281	Extinction is delayed when rats are injected LV <strong>BDNF</strong> or LV TrkB, and in turn, priming injections of 2 mg/kg of <b>cocaine</b> reinstates it.
+BDNF	drug	cocaine	18551281	These results demonstrate the crucial function of <strong>BDNF</strong> through its receptor TrkB in the enhancement of locomotor activity, sensitization, conditioned place preference, CPP reinstatement, and rewarding effects of <b>cocaine</b> in the mesolimbic dopaminergic pathway.
+BDNF	addiction	relapse	18551281	These results demonstrate the crucial function of <strong>BDNF</strong> through its receptor TrkB in the enhancement of locomotor activity, sensitization, conditioned place preference, CPP <b>reinstatement</b>, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+BDNF	addiction	reward	18551281	These results demonstrate the crucial function of <strong>BDNF</strong> through its receptor TrkB in the enhancement of locomotor activity, sensitization, conditioned place preference, <b>CPP</b> reinstatement, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+BDNF	addiction	sensitization	18551281	These results demonstrate the crucial function of <strong>BDNF</strong> through its receptor TrkB in the enhancement of locomotor activity, <b>sensitization</b>, conditioned place preference, CPP reinstatement, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+BDNF	drug	nicotine	18534558	Gene gene interactions among CHRNA4, CHRNB2, <strong>BDNF</strong>, and NTRK2 in <b>nicotine</b> dependence.
+BDNF	addiction	dependence	18534558	Gene gene interactions among CHRNA4, CHRNB2, <strong>BDNF</strong>, and NTRK2 in nicotine <b>dependence</b>.
+BDNF	drug	nicotine	18534558	To determine if gene gene interactions exist among the four genes, we genotyped six single nucleotide polymorphisms (SNPs) for CHRNA4 and <strong>BDNF</strong>, nine SNPs for NTRK2, and four SNPs for CHRNB2 in a case control sample containing 275 unrelated <b>smokers</b> with a Fagerström Test for <b>Nicotine</b> Dependence score of 4.0 or more and 348 unrelated nonsmokers.
+BDNF	addiction	dependence	18534558	To determine if gene gene interactions exist among the four genes, we genotyped six single nucleotide polymorphisms (SNPs) for CHRNA4 and <strong>BDNF</strong>, nine SNPs for NTRK2, and four SNPs for CHRNB2 in a case control sample containing 275 unrelated smokers with a Fagerström Test for Nicotine <b>Dependence</b> score of 4.0 or more and 348 unrelated nonsmokers.
+BDNF	drug	alcohol	18394710	<b>Ethanol</b> <strong>BDNF</strong> interactions: still more questions than answers.
+BDNF	addiction	addiction	18394710	Brain derived neurotrophic factor (<strong>BDNF</strong>) has emerged as a regulator of development, plasticity and, recently, <b>addiction</b>.
+BDNF	addiction	addiction	18394710	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has emerged as a regulator of development, plasticity and, recently, <b>addiction</b>.
+BDNF	drug	alcohol	18394710	This can occur through decreased expression of <strong>BDNF</strong> or through inability of the receptor to transduce signals in the presence of <b>ethanol</b>.
+BDNF	drug	alcohol	18394710	In contrast, recent studies implicate region specific up regulation of <strong>BDNF</strong> and associated signaling pathways in anxiety, addiction and homeostasis after <b>ethanol</b> exposure.
+BDNF	addiction	addiction	18394710	In contrast, recent studies implicate region specific up regulation of <strong>BDNF</strong> and associated signaling pathways in anxiety, <b>addiction</b> and homeostasis after ethanol exposure.
+BDNF	drug	alcohol	18394710	Polymorphisms in the genes coding for <strong>BDNF</strong> and its receptor TrkB are linked to affective, substance abuse and appetitive disorders and therefore may play a role in the development of <b>alcoholism</b>.
+BDNF	drug	alcohol	18394710	This review summarizes historical and pre clinical data on <strong>BDNF</strong> and TrkB as it relates to <b>ethanol</b> toxicity and addiction.
+BDNF	addiction	addiction	18394710	This review summarizes historical and pre clinical data on <strong>BDNF</strong> and TrkB as it relates to ethanol toxicity and <b>addiction</b>.
+BDNF	addiction	addiction	18394710	Many unresolved questions about region specific changes in <strong>BDNF</strong> expression and the precise role of <strong>BDNF</strong> in neuropsychiatric disorders and <b>addiction</b> remain to be elucidated.
+BDNF	addiction	addiction	18355967	Fifty six genes are down regulated while 28 genes are up regulated including previously identified candidates for <b>addiction</b> including <strong>brain derived neurotrophic factor</strong> and period homolog 1.
+BDNF	drug	alcohol	18326550	Alterations of serum <strong>brain derived neurotrophic factor</strong> levels in early <b>alcohol</b> withdrawal.
+BDNF	addiction	withdrawal	18326550	Alterations of serum <strong>brain derived neurotrophic factor</strong> levels in early alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	18326550	In this study, we explored the changes of serum <strong>BDNF</strong> levels in <b>alcoholic</b> patients at baseline and after one week <b>alcohol</b> withdrawal.
+BDNF	addiction	withdrawal	18326550	In this study, we explored the changes of serum <strong>BDNF</strong> levels in alcoholic patients at baseline and after one week alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	18326550	We collected blood samples of the patient group on the first and seventh day of <b>alcohol</b> withdrawal, and measured serum <strong>BDNF</strong> level with sandwich enzyme linked immunosorbent assay.
+BDNF	addiction	withdrawal	18326550	We collected blood samples of the patient group on the first and seventh day of alcohol <b>withdrawal</b>, and measured serum <strong>BDNF</strong> level with sandwich enzyme linked immunosorbent assay.
+BDNF	drug	alcohol	18326550	Serum <strong>BDNF</strong> levels did not differ significantly between <b>alcoholic</b> patients and control subjects.
+BDNF	drug	alcohol	18326550	But <strong>BDNF</strong> levels were found to be significantly increased one week after <b>alcohol</b> withdrawal (from 13.9 +/  3.8 ng/ml to 15.4 +/  3.8 ng/ml, P = 0.03).
+BDNF	addiction	withdrawal	18326550	But <strong>BDNF</strong> levels were found to be significantly increased one week after alcohol <b>withdrawal</b> (from 13.9 +/  3.8 ng/ml to 15.4 +/  3.8 ng/ml, P = 0.03).
+BDNF	addiction	withdrawal	18326550	A significant positive correlation was found between baseline <strong>BDNF</strong> level and baseline <b>withdrawal</b> severity (r = 0.45, P = 0.03).
+BDNF	drug	alcohol	18326550	The present study suggests that elevated serum <strong>BDNF</strong> levels were found in early <b>alcohol</b> withdrawal, implying that <strong>BDNF</strong> may involve in neuroadaptation during the period.
+BDNF	addiction	withdrawal	18326550	The present study suggests that elevated serum <strong>BDNF</strong> levels were found in early alcohol <b>withdrawal</b>, implying that <strong>BDNF</strong> may involve in neuroadaptation during the period.
+BDNF	drug	alcohol	18322102	Here, we report that the anxiolytic effects of acute <b>ethanol</b> were associated with increased brain derived neurotrophic factor (<strong>BDNF</strong>) and tyrosine kinase B (trkB) expression, increased phosphorylation of extracellular signal regulated kinases 1/2 (Erk1/2), Elk 1, and cAMP responsive element binding protein (CREB), increased Arc expression, and increased dendritic spine density (DSD) in both the central amygdala (CeA) and medial amygdala (MeA) but not in the basolateral amygdala (BLA) of rats.
+BDNF	drug	alcohol	18322102	Here, we report that the anxiolytic effects of acute <b>ethanol</b> were associated with increased <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and tyrosine kinase B (trkB) expression, increased phosphorylation of extracellular signal regulated kinases 1/2 (Erk1/2), Elk 1, and cAMP responsive element binding protein (CREB), increased Arc expression, and increased dendritic spine density (DSD) in both the central amygdala (CeA) and medial amygdala (MeA) but not in the basolateral amygdala (BLA) of rats.
+BDNF	drug	alcohol	18322102	Conversely, the anxiogenic effects of withdrawal after long term <b>ethanol</b> exposure were associated with decreased <strong>BDNF</strong> and trkB expression, decreased phosphorylation of Erk1/2, Elk 1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+BDNF	addiction	withdrawal	18322102	Conversely, the anxiogenic effects of <b>withdrawal</b> after long term ethanol exposure were associated with decreased <strong>BDNF</strong> and trkB expression, decreased phosphorylation of Erk1/2, Elk 1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+BDNF	drug	alcohol	18322102	We also showed that <strong>BDNF</strong> infusion into the CeA normalized phosphorylation of Erk1/2, Elk 1, and CREB, and normalized Arc expression, thereby protecting against the onset of <b>ethanol</b> withdrawal related anxiety.
+BDNF	addiction	withdrawal	18322102	We also showed that <strong>BDNF</strong> infusion into the CeA normalized phosphorylation of Erk1/2, Elk 1, and CREB, and normalized Arc expression, thereby protecting against the onset of ethanol <b>withdrawal</b> related anxiety.
+BDNF	drug	alcohol	18322102	These results revealed that <strong>BDNF</strong> Arc signaling and the associated DSD in the CeA, and possibly in the MeA, may be involved in the molecular processes of <b>alcohol</b> dependence and comorbidity of anxiety and <b>alcohol</b> drinking behaviors.
+BDNF	addiction	dependence	18322102	These results revealed that <strong>BDNF</strong> Arc signaling and the associated DSD in the CeA, and possibly in the MeA, may be involved in the molecular processes of alcohol <b>dependence</b> and comorbidity of anxiety and alcohol drinking behaviors.
+BDNF	drug	cocaine	18311559	Rats self administered <b>cocaine</b> or received yoked saline for 2 h/day for 10 days followed by 22 h or 2 weeks of abstinence when they were re exposed to the self administration chamber with or without levers available to press for 1 h. Brains were harvested and sections through the prefrontal cortex were processed for in situ hybridization using radioactive oligonucleotide probes encoding c fos, zif/268, arc, and <strong>bdnf</strong>.
+BDNF	drug	cocaine	18311559	Re exposure to the chamber in which rats previously self administered <b>cocaine</b> but not saline, regardless of lever availability, increased the expression of all genes in the medial prefrontal and orbitofrontal cortices at both time points with one exception: <strong>bdnf</strong> mRNA was significantly increased in the medial prefrontal cortex at 22 h only if levers previously associated with <b>cocaine</b> delivery were available to press.
+BDNF	drug	cocaine	18234897	Because components of the neurotrophin system including <strong>brain derived neurotrophic factor</strong> and TrkB are developmentally regulated, their role in the age specific effects of <b>cocaine</b> was determined using the Trk receptor antagonist K252a.
+BDNF	drug	alcohol	18077569	Also, recent human genetic studies have supported a role of <strong>BDNF</strong> signaling in addictive behaviors by allele , genotype , and haplotype based association of the TrkB gene, which encodes the cognate receptor for <strong>BDNF</strong>, with <b>alcohol</b> dependence.
+BDNF	addiction	addiction	18077569	Also, recent human genetic studies have supported a role of <strong>BDNF</strong> signaling in <b>addictive</b> behaviors by allele , genotype , and haplotype based association of the TrkB gene, which encodes the cognate receptor for <strong>BDNF</strong>, with alcohol dependence.
+BDNF	addiction	dependence	18077569	Also, recent human genetic studies have supported a role of <strong>BDNF</strong> signaling in addictive behaviors by allele , genotype , and haplotype based association of the TrkB gene, which encodes the cognate receptor for <strong>BDNF</strong>, with alcohol <b>dependence</b>.
+BDNF	drug	alcohol	17543031	After adjusting for confounders, results indicated that bipolar patients with a history of TE have <b>alcohol</b> abuse/dependence (p < 0.001), anxiety comorbidity, and lower levels of serum <strong>BDNF</strong> (p < 0.01) compared to those without a history of TE.
+BDNF	addiction	dependence	17543031	After adjusting for confounders, results indicated that bipolar patients with a history of TE have alcohol abuse/<b>dependence</b> (p < 0.001), anxiety comorbidity, and lower levels of serum <strong>BDNF</strong> (p < 0.01) compared to those without a history of TE.
+BDNF	drug	alcohol	17543031	Our findings suggest that TE are associated with significantly increased prevalence of <b>alcohol</b> and anxiety comorbidity as well as lower <strong>BDNF</strong> levels in bipolar patients.
+BDNF	drug	opioid	17945205	Peripheral electrical stimulation reversed the cell size reduction and increased <strong>BDNF</strong> level in the ventral tegmental area in chronic <b>morphine</b> treated rats.
+BDNF	drug	opioid	17945205	Immunohistochemical observations showed that the cell size of dopaminergic neurons in the VTA reduced significantly in the chronic <b>morphine</b> treated rats with a concomitant decrease in the number of <strong>BDNF</strong> positive cells compared to the saline treated rats.
+BDNF	drug	opioid	17945205	A much milder morphological change, accompanying with an increased number of <strong>BDNF</strong> positive cells, was observed in dopaminergic neurons in the rats that received repeated 100 Hz PES after <b>morphine</b> withdrawal.
+BDNF	addiction	withdrawal	17945205	A much milder morphological change, accompanying with an increased number of <strong>BDNF</strong> positive cells, was observed in dopaminergic neurons in the rats that received repeated 100 Hz PES after morphine <b>withdrawal</b>.
+BDNF	drug	opioid	17945205	In another experiment, enzyme linked immunosorbent assay (ELISA) reconfirmed a significant up regulation of <strong>BDNF</strong> protein level in the VTA in the rats received 100 Hz PES after <b>morphine</b> abstinence.
+BDNF	drug	opioid	17945205	These results indicate that PES could facilitate the morphological recovery of the VTA dopaminergic cells damaged by chronic <b>morphine</b> treatment and up regulate the <strong>BDNF</strong> protein level in the VTA.
+BDNF	drug	opioid	17945205	Activation of endogenous <strong>BDNF</strong> by PES may play a role in the recovery of the injured dopaminergic neurons in the <b>morphine</b> addictive rats.
+BDNF	addiction	addiction	17945205	Activation of endogenous <strong>BDNF</strong> by PES may play a role in the recovery of the injured dopaminergic neurons in the morphine <b>addictive</b> rats.
+BDNF	drug	alcohol	17850220	Decreased plasma <strong>brain derived neurotrophic factor</strong> levels in patients with <b>alcohol</b> dependence.
+BDNF	addiction	dependence	17850220	Decreased plasma <strong>brain derived neurotrophic factor</strong> levels in patients with alcohol <b>dependence</b>.
+BDNF	drug	alcohol	17850220	Many reports have suggested possible relationships between brain derived neurotrophic factor (<strong>BDNF</strong>) and <b>alcohol</b> dependence.
+BDNF	addiction	dependence	17850220	Many reports have suggested possible relationships between brain derived neurotrophic factor (<strong>BDNF</strong>) and alcohol <b>dependence</b>.
+BDNF	drug	alcohol	17850220	Many reports have suggested possible relationships between <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and <b>alcohol</b> dependence.
+BDNF	addiction	dependence	17850220	Many reports have suggested possible relationships between <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and alcohol <b>dependence</b>.
+BDNF	drug	alcohol	17850220	A protective effect of <strong>BDNF</strong> against <b>ethanol</b> induced cell damage has been suggested, and this effect may contribute to the development or maintenance of <b>alcohol</b> dependence.
+BDNF	addiction	dependence	17850220	A protective effect of <strong>BDNF</strong> against ethanol induced cell damage has been suggested, and this effect may contribute to the development or maintenance of alcohol <b>dependence</b>.
+BDNF	drug	alcohol	17850220	This study was carried out in order to verify the significance of <strong>BDNF</strong> in <b>alcohol</b> dependence.
+BDNF	addiction	dependence	17850220	This study was carried out in order to verify the significance of <strong>BDNF</strong> in alcohol <b>dependence</b>.
+BDNF	drug	alcohol	17850220	Peripheral <strong>BDNF</strong> levels were measured in <b>alcohol</b> dependent patients and control subjects using an enzyme linked immunosorbent assay.
+BDNF	drug	alcohol	17850220	The mean <strong>BDNF</strong> level was lower in the <b>alcohol</b> dependence group (389.5 +/  501.7 pg/ml) than in the normal controls (822.5 +/  420.7 pg/ml) by analysis of covariance (ANCOVA) (F = 25.79, p < 0.01).
+BDNF	addiction	dependence	17850220	The mean <strong>BDNF</strong> level was lower in the alcohol <b>dependence</b> group (389.5 +/  501.7 pg/ml) than in the normal controls (822.5 +/  420.7 pg/ml) by analysis of covariance (ANCOVA) (F = 25.79, p < 0.01).
+BDNF	drug	alcohol	17850220	The mean <strong>BDNF</strong> level was lower in the <b>alcohol</b> dependent patients with a positive family history of <b>alcohol</b> dependence (247.6 +/  289.2 pg/ml) than in those with a negative family history of <b>alcohol</b> dependence (583.9 +/  652.8 pg/ml) by ANCOVA (F = 6.51, p = 0.01).
+BDNF	addiction	dependence	17850220	The mean <strong>BDNF</strong> level was lower in the alcohol dependent patients with a positive family history of alcohol <b>dependence</b> (247.6 +/  289.2 pg/ml) than in those with a negative family history of alcohol <b>dependence</b> (583.9 +/  652.8 pg/ml) by ANCOVA (F = 6.51, p = 0.01).
+BDNF	drug	alcohol	17850220	Changes in the levels of <strong>BDNF</strong> might play a role in the pathophysiology and inheritance of <b>alcohol</b> dependence.
+BDNF	addiction	dependence	17850220	Changes in the levels of <strong>BDNF</strong> might play a role in the pathophysiology and inheritance of alcohol <b>dependence</b>.
+BDNF	drug	cocaine	17715210	Chronic heroin and <b>cocaine</b> abuse is associated with decreased serum concentrations of the nerve growth factor and <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	opioid	17715210	Chronic <b>heroin</b> and cocaine abuse is associated with decreased serum concentrations of the nerve growth factor and <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	cocaine	17715210	In the present study, we measured by enzyme linked immunosorbent assay (ELISA) the NGF and <strong>BDNF</strong> levels in serum of three groups of subjects: heroin dependent patients, <b>cocaine</b> dependent patients and healthy volunteers.
+BDNF	drug	opioid	17715210	In the present study, we measured by enzyme linked immunosorbent assay (ELISA) the NGF and <strong>BDNF</strong> levels in serum of three groups of subjects: <b>heroin</b> dependent patients, cocaine dependent patients and healthy volunteers.
+BDNF	drug	cocaine	17715210	<strong>BDNF</strong> was decreased in heroin users whereas NGF was decreased in both heroin and <b>cocaine</b> users.
+BDNF	drug	opioid	17715210	<strong>BDNF</strong> was decreased in <b>heroin</b> users whereas NGF was decreased in both <b>heroin</b> and cocaine users.
+BDNF	addiction	addiction	17715210	These findings indicate that NGF and <strong>BDNF</strong> may play a role in the neurotoxicity and <b>addiction</b> induced by these drugs.
+BDNF	drug	opioid	17688944	Alterations of <strong>BDNF</strong> and NT 3 genes expression in the nucleus paragigantocellularis during <b>morphine</b> dependency and withdrawal.
+BDNF	addiction	withdrawal	17688944	Alterations of <strong>BDNF</strong> and NT 3 genes expression in the nucleus paragigantocellularis during morphine dependency and <b>withdrawal</b>.
+BDNF	addiction	dependence	17688944	The present study was designed to evaluate the expression of <strong>BDNF</strong> and NT 3 in the context of opiate <b>dependence</b> and withdrawal in PGi.
+BDNF	addiction	withdrawal	17688944	The present study was designed to evaluate the expression of <strong>BDNF</strong> and NT 3 in the context of opiate dependence and <b>withdrawal</b> in PGi.
+BDNF	drug	opioid	17688944	Results showed that chronic administration of <b>morphine</b> significantly increased <strong>BDNF</strong> and NT 3 gene expression in PGi.
+BDNF	addiction	withdrawal	17688944	In spontaneous <b>withdrawal</b>, <strong>BDNF</strong>/NT 3 genes expression were high in comparison to control group.
+BDNF	drug	nicotine	17662528	Increased plasma <strong>brain derived neurotrophic factor</strong> levels in chronic <b>smokers</b> following unaided <b>smoking</b> cessation.
+BDNF	drug	nicotine	17662528	Recent animal studies have suggested an association between <b>nicotine</b> and alterations in brain derived neurotrophic factor (<strong>BDNF</strong>) expression levels.
+BDNF	drug	nicotine	17662528	Recent animal studies have suggested an association between <b>nicotine</b> and alterations in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression levels.
+BDNF	drug	nicotine	17662528	However, the role of <strong>BDNF</strong> in humans with <b>nicotine</b> dependence has not yet been investigated.
+BDNF	addiction	dependence	17662528	However, the role of <strong>BDNF</strong> in humans with nicotine <b>dependence</b> has not yet been investigated.
+BDNF	drug	nicotine	17662528	In this study, we explored the differences in the plasma <strong>BDNF</strong> levels of chronic <b>smokers</b> and healthy nonsmokers, and we investigated the changes in plasma <strong>BDNF</strong> levels in chronic <b>smokers</b> following unaided <b>smoking</b> cessation.
+BDNF	drug	nicotine	17662528	We measured the plasma <strong>BDNF</strong> levels at baseline (both groups) and at the end of the two month study period (<b>smoker</b> group only) using an enzyme linked immunosorbent assay.
+BDNF	drug	nicotine	17662528	ANCOVA with age and body mass index as covariates showed that the baseline plasma <strong>BDNF</strong> levels in <b>smokers</b> were significantly lower than those in nonsmokers (F=4.626, p=0.038).
+BDNF	drug	nicotine	17662528	The plasma <strong>BDNF</strong> levels in the <b>smokers</b> significantly increased from baseline after the two month <b>smoking</b> cessation period (Z= 3.059, p=0.002).
+BDNF	drug	nicotine	17662528	These findings suggest that <strong>BDNF</strong> may play a role in the pathophysiology of <b>smoking</b> behavior.
+BDNF	drug	cocaine	17657232	A role for <strong>BDNF</strong> in <b>cocaine</b> reward and relapse.
+BDNF	addiction	relapse	17657232	A role for <strong>BDNF</strong> in cocaine reward and <b>relapse</b>.
+BDNF	addiction	reward	17657232	A role for <strong>BDNF</strong> in cocaine <b>reward</b> and relapse.
+BDNF	drug	cocaine	17651427	A <strong>BDNF</strong> infusion into the medial prefrontal cortex suppresses <b>cocaine</b> seeking in rats.
+BDNF	addiction	relapse	17651427	A <strong>BDNF</strong> infusion into the medial prefrontal cortex suppresses cocaine <b>seeking</b> in rats.
+BDNF	drug	cocaine	17651427	The medial prefrontal cortex (mPFC) is critical for reinstatement of <b>cocaine</b> seeking and is the main source of brain derived neurotrophic factor (<strong>BDNF</strong>) to striatal regions of the brain relapse circuitry.
+BDNF	addiction	relapse	17651427	The medial prefrontal cortex (mPFC) is critical for <b>reinstatement</b> of cocaine <b>seeking</b> and is the main source of brain derived neurotrophic factor (<strong>BDNF</strong>) to striatal regions of the brain <b>relapse</b> circuitry.
+BDNF	drug	cocaine	17651427	The medial prefrontal cortex (mPFC) is critical for reinstatement of <b>cocaine</b> seeking and is the main source of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) to striatal regions of the brain relapse circuitry.
+BDNF	addiction	relapse	17651427	The medial prefrontal cortex (mPFC) is critical for <b>reinstatement</b> of cocaine <b>seeking</b> and is the main source of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) to striatal regions of the brain <b>relapse</b> circuitry.
+BDNF	drug	cocaine	17651427	To test the hypothesis that <strong>BDNF</strong> in the mPFC regulates <b>cocaine</b> seeking behavior, rats were trained to press a lever for <b>cocaine</b> infusions (0.2 mg/inf, 2 h/day) paired with light+tone conditioned stimulus (CS) presentations on 10 consecutive days.
+BDNF	addiction	relapse	17651427	To test the hypothesis that <strong>BDNF</strong> in the mPFC regulates cocaine <b>seeking</b> behavior, rats were trained to press a lever for cocaine infusions (0.2 mg/inf, 2 h/day) paired with light+tone conditioned stimulus (CS) presentations on 10 consecutive days.
+BDNF	drug	cocaine	17651427	After the last self administration session, rats received a single infusion of <strong>BDNF</strong> (0.75 microg/0.5 microL/side) into the mPFC; this manipulation produced protracted effects on <b>cocaine</b> seeking behavior (non reinforced lever pressing).
+BDNF	addiction	relapse	17651427	After the last self administration session, rats received a single infusion of <strong>BDNF</strong> (0.75 microg/0.5 microL/side) into the mPFC; this manipulation produced protracted effects on cocaine <b>seeking</b> behavior (non reinforced lever pressing).
+BDNF	drug	cocaine	17651427	<strong>BDNF</strong> pretreatment administered after the last session attenuated <b>cocaine</b> seeking 22 h later and, remarkably, it also blocked <b>cocaine</b> induced suppression of phospho extracellular regulated kinase and elevated <strong>BDNF</strong> immunoreactivity in the nucleus accumbens.
+BDNF	addiction	relapse	17651427	<strong>BDNF</strong> pretreatment administered after the last session attenuated cocaine <b>seeking</b> 22 h later and, remarkably, it also blocked cocaine induced suppression of phospho extracellular regulated kinase and elevated <strong>BDNF</strong> immunoreactivity in the nucleus accumbens.
+BDNF	addiction	relapse	17651427	However, <strong>BDNF</strong> infused into the mPFC had no effect on food <b>seeking</b> behavior.
+BDNF	drug	cocaine	17651427	The suppressive effects of <strong>BDNF</strong> infused into the mPFC on <b>cocaine</b> seeking indicate that <strong>BDNF</strong> regulates cortical pathways implicated in relapse to drug seeking and that corticostriatal <strong>BDNF</strong> adaptations during early abstinence diminish compulsive drug seeking.
+BDNF	addiction	addiction	17651427	The suppressive effects of <strong>BDNF</strong> infused into the mPFC on cocaine seeking indicate that <strong>BDNF</strong> regulates cortical pathways implicated in relapse to drug seeking and that corticostriatal <strong>BDNF</strong> adaptations during early abstinence diminish <b>compulsive</b> drug seeking.
+BDNF	addiction	relapse	17651427	The suppressive effects of <strong>BDNF</strong> infused into the mPFC on cocaine <b>seeking</b> indicate that <strong>BDNF</strong> regulates cortical pathways implicated in <b>relapse</b> to drug <b>seeking</b> and that corticostriatal <strong>BDNF</strong> adaptations during early abstinence diminish compulsive drug <b>seeking</b>.
+BDNF	drug	cocaine	17618281	Dynamic <strong>BDNF</strong> activity in nucleus accumbens with <b>cocaine</b> use increases self administration and relapse.
+BDNF	addiction	relapse	17618281	Dynamic <strong>BDNF</strong> activity in nucleus accumbens with cocaine use increases self administration and <b>relapse</b>.
+BDNF	drug	cocaine	17618281	We found that 4 h of intravenous <b>cocaine</b> self administration in rats induced a transient increase in brain derived neurotrophic factor (<strong>BDNF</strong>) and activation of TrkB mediated signaling in the nucleus accumbens (NAc).
+BDNF	drug	cocaine	17618281	We found that 4 h of intravenous <b>cocaine</b> self administration in rats induced a transient increase in <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and activation of TrkB mediated signaling in the nucleus accumbens (NAc).
+BDNF	drug	cocaine	17618281	Augmenting this dynamic regulation with five daily NAc <strong>BDNF</strong> infusions caused enduring increases in <b>cocaine</b> self administration, and facilitated relapse to <b>cocaine</b> seeking in withdrawal.
+BDNF	addiction	relapse	17618281	Augmenting this dynamic regulation with five daily NAc <strong>BDNF</strong> infusions caused enduring increases in cocaine self administration, and facilitated <b>relapse</b> to cocaine <b>seeking</b> in withdrawal.
+BDNF	addiction	withdrawal	17618281	Augmenting this dynamic regulation with five daily NAc <strong>BDNF</strong> infusions caused enduring increases in cocaine self administration, and facilitated relapse to cocaine seeking in <b>withdrawal</b>.
+BDNF	drug	cocaine	17618281	In contrast, neutralizing endogenous <strong>BDNF</strong> regulation with intra NAc infusions of antibody to <strong>BDNF</strong> subsequently reduced <b>cocaine</b> self administration and attenuated relapse.
+BDNF	addiction	relapse	17618281	In contrast, neutralizing endogenous <strong>BDNF</strong> regulation with intra NAc infusions of antibody to <strong>BDNF</strong> subsequently reduced cocaine self administration and attenuated <b>relapse</b>.
+BDNF	drug	cocaine	17618281	Using localized inducible <strong>BDNF</strong> knockout in mice, we found that <strong>BDNF</strong> originating from NAc neurons was necessary for maintaining increased <b>cocaine</b> self administration.
+BDNF	drug	cocaine	17618281	These findings suggest that dynamic induction and release of <strong>BDNF</strong> from NAc neurons during <b>cocaine</b> use promotes the development and persistence of addictive behavior.
+BDNF	addiction	addiction	17618281	These findings suggest that dynamic induction and release of <strong>BDNF</strong> from NAc neurons during cocaine use promotes the development and persistence of <b>addictive</b> behavior.
+BDNF	drug	cocaine	17556847	<strong>Brain derived neurotrophic factor</strong> and its intracellular signaling pathways in <b>cocaine</b> addiction.
+BDNF	addiction	addiction	17556847	<strong>Brain derived neurotrophic factor</strong> and its intracellular signaling pathways in cocaine <b>addiction</b>.
+BDNF	drug	cocaine	17556847	Within the context of the behavioral and neurochemical actions of <b>cocaine</b>, this paper considers the contribution of brain derived neurotrophic factor (<strong>BDNF</strong>) and its main intracellular signaling mechanisms, including mitogen activated protein kinase/extracellular signal regulated protein kinase (MAPK/ERK) and phosphatidylinositol 3 kinase (PI3K), in psychostimulant addiction.
+BDNF	addiction	addiction	17556847	Within the context of the behavioral and neurochemical actions of cocaine, this paper considers the contribution of brain derived neurotrophic factor (<strong>BDNF</strong>) and its main intracellular signaling mechanisms, including mitogen activated protein kinase/extracellular signal regulated protein kinase (MAPK/ERK) and phosphatidylinositol 3 kinase (PI3K), in psychostimulant <b>addiction</b>.
+BDNF	drug	cocaine	17556847	Within the context of the behavioral and neurochemical actions of <b>cocaine</b>, this paper considers the contribution of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and its main intracellular signaling mechanisms, including mitogen activated protein kinase/extracellular signal regulated protein kinase (MAPK/ERK) and phosphatidylinositol 3 kinase (PI3K), in psychostimulant addiction.
+BDNF	addiction	addiction	17556847	Within the context of the behavioral and neurochemical actions of cocaine, this paper considers the contribution of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and its main intracellular signaling mechanisms, including mitogen activated protein kinase/extracellular signal regulated protein kinase (MAPK/ERK) and phosphatidylinositol 3 kinase (PI3K), in psychostimulant <b>addiction</b>.
+BDNF	drug	cocaine	17556847	Repeated <b>cocaine</b> administration leads to an increase in <strong>BDNF</strong> levels and enhanced activity in the intracellular pathways (PI3K and MAPK/ERK) in the reward related brain areas, which applies especially several days following withdrawal.
+BDNF	addiction	reward	17556847	Repeated cocaine administration leads to an increase in <strong>BDNF</strong> levels and enhanced activity in the intracellular pathways (PI3K and MAPK/ERK) in the <b>reward</b> related brain areas, which applies especially several days following withdrawal.
+BDNF	addiction	withdrawal	17556847	Repeated cocaine administration leads to an increase in <strong>BDNF</strong> levels and enhanced activity in the intracellular pathways (PI3K and MAPK/ERK) in the reward related brain areas, which applies especially several days following <b>withdrawal</b>.
+BDNF	addiction	addiction	17556847	Nevertheless, increased <strong>BDNF</strong> levels could also have a role as a protection factor in <b>addiction</b>.
+BDNF	drug	amphetamine	17434716	Chronic <b>amphetamine</b> treatment reduces NGF and <strong>BDNF</strong> in the rat brain.
+BDNF	drug	amphetamine	17434716	In this study in order to investigate the mechanism of <b>amphetamine</b> induced neurotoxicity and further elucidate the role of neurotrophins in the pathogenesis of schizophrenia we administered intraperitoneally d <b>amphetamine</b> for 8 days to rats and measured the levels of neurotrophins NGF and <strong>BDNF</strong> in selected brain regions by ELISA.
+BDNF	drug	amphetamine	17434716	<b>Amphetamine</b> reduced NGF levels in the hippocampus, occipital cortex and hypothalamus and of <strong>BDNF</strong> in the occipital cortex and hypothalamus.
+BDNF	drug	amphetamine	17434716	Thus the present data indicate that chronic <b>amphetamine</b> can reduce the levels of NGF and <strong>BDNF</strong> in selected brain regions.
+BDNF	drug	nicotine	17186223	Association of the met66 allele of brain derived neurotrophic factor (<strong>BDNF</strong>) with <b>smoking</b>.
+BDNF	drug	nicotine	17186223	Association of the met66 allele of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) with <b>smoking</b>.
+BDNF	addiction	addiction	17186223	It has been suggested that a susceptibility locus near the gene encoding the brain derived neurotrophic factor (<strong>BDNF</strong>) contributes to individual differences in human <b>addiction</b> vulnerability.
+BDNF	addiction	addiction	17186223	It has been suggested that a susceptibility locus near the gene encoding the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) contributes to individual differences in human <b>addiction</b> vulnerability.
+BDNF	drug	amphetamine	17186223	<strong>BDNF</strong> modulates several behaviors that are associated with addictive drugs, and upregulation of <strong>BDNF</strong> was found to be associated with several drugs of abuse such as <b>amphetamine</b>, cocaine, and nicotine.
+BDNF	drug	cocaine	17186223	<strong>BDNF</strong> modulates several behaviors that are associated with addictive drugs, and upregulation of <strong>BDNF</strong> was found to be associated with several drugs of abuse such as amphetamine, <b>cocaine</b>, and nicotine.
+BDNF	drug	nicotine	17186223	<strong>BDNF</strong> modulates several behaviors that are associated with addictive drugs, and upregulation of <strong>BDNF</strong> was found to be associated with several drugs of abuse such as amphetamine, cocaine, and <b>nicotine</b>.
+BDNF	addiction	addiction	17186223	<strong>BDNF</strong> modulates several behaviors that are associated with <b>addictive</b> drugs, and upregulation of <strong>BDNF</strong> was found to be associated with several drugs of abuse such as amphetamine, cocaine, and nicotine.
+BDNF	drug	nicotine	17186223	In this study, we addressed the question if a common <strong>BDNF</strong> missense variation (Val66Met) influences the risk for <b>smoking</b> behavior in otherwise healthy human volunteers.
+BDNF	drug	nicotine	17186223	Our results suggest that humans who carry the Met allele of the <strong>BDNF</strong> missense polymorphism might be more vulnerable to initiate and also maintain <b>smoking</b>.
+BDNF	addiction	addiction	16824691	Evidence from animal and clinical studies suggests that increased central <strong>BDNF</strong> activity may be implicated in the pathogenesis of drug <b>addiction</b>.
+BDNF	drug	cocaine	16824691	For example, <strong>BDNF</strong> infusion into rat midbrain enhances the rewarding effects of <b>cocaine</b> as measured by the condition place preference paradigm.
+BDNF	drug	cocaine	16824691	In contrast, <b>cocaine</b> conditioned place preference was reduced in heterozygous <strong>BDNF</strong> knockout mice.
+BDNF	addiction	addiction	16824691	We found higher <strong>BDNF</strong> 66Val homozygote frequency in people with drug <b>addiction</b> compared with normal controls.
+BDNF	drug	amphetamine	16824691	Furthermore, plasma <strong>BDNF</strong> concentrations of <b>methamphetamine</b> users were significantly higher than controls.
+BDNF	addiction	addiction	16824691	The increased central <strong>BDNF</strong> activity hypothesis of drug <b>addiction</b> may provide new insights for improved therapeutic strategies for the prevention and treatment of drug <b>addiction</b>.
+BDNF	addiction	addiction	16824691	Several strategies to decrease central <strong>BDNF</strong> activity that have potential use in the treatment of drug <b>addiction</b> are proposed.
+BDNF	drug	amphetamine	16823800	An association study of the <strong>brain derived neurotrophic factor</strong> Val66Met polymorphism and <b>amphetamine</b> response.
+BDNF	addiction	addiction	16823800	Brain derived neurotrophic factor (<strong>BDNF</strong>), which has been implicated in the behavioral response to psychomotor stimulants and potentiates neurotransmitters that are strongly linked to <b>addiction</b>, is a logical candidate gene to study.
+BDNF	addiction	addiction	16823800	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), which has been implicated in the behavioral response to psychomotor stimulants and potentiates neurotransmitters that are strongly linked to <b>addiction</b>, is a logical candidate gene to study.
+BDNF	drug	amphetamine	16823800	Using a drug challenge approach, we tested for association between <strong>BDNF</strong> G196A (val66met) genotype and subjective responses to <b>amphetamine</b> (<b>AMPH</b>).
+BDNF	drug	amphetamine	16823800	These results suggest that <strong>BDNF</strong> is related to the subjective and physical response to low doses of <b>AMPH</b>.
+BDNF	addiction	dependence	16649215	Brain derived neurotrophic factor (<strong>BDNF</strong>) gene variants and Alzheimer's disease, affective disorders, posttraumatic stress disorder, schizophrenia, and substance <b>dependence</b>.
+BDNF	addiction	dependence	16649215	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) gene variants and Alzheimer's disease, affective disorders, posttraumatic stress disorder, schizophrenia, and substance <b>dependence</b>.
+BDNF	addiction	dependence	16649215	Genetic variation at the locus encoding the brain derived neurotrophic factor (<strong>BDNF</strong>) has been implicated in some neuropsychiatric disorders such as Alzheimer's disease (AD), affective disorders (AFDs), schizophrenia, and substance <b>dependence</b>.
+BDNF	addiction	dependence	16649215	Genetic variation at the locus encoding the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) has been implicated in some neuropsychiatric disorders such as Alzheimer's disease (AD), affective disorders (AFDs), schizophrenia, and substance <b>dependence</b>.
+BDNF	drug	alcohol	16649215	This variant and two previously reported <strong>BDNF</strong> SNPs (C270T and Val66Met) were genotyped in 295 patients with AD, 108 with AFDs, 96 with posttraumatic stress disorder (PTSD), 84 with schizophrenia, 327 with <b>alcohol</b> and/or drug dependence, and 250 normal control subjects.
+BDNF	addiction	dependence	16649215	This variant and two previously reported <strong>BDNF</strong> SNPs (C270T and Val66Met) were genotyped in 295 patients with AD, 108 with AFDs, 96 with posttraumatic stress disorder (PTSD), 84 with schizophrenia, 327 with alcohol and/or drug <b>dependence</b>, and 250 normal control subjects.
+BDNF	drug	cocaine	16633344	<strong>BDNF</strong> dependent synaptic sensitization in midbrain dopamine neurons after <b>cocaine</b> withdrawal.
+BDNF	addiction	sensitization	16633344	<strong>BDNF</strong> dependent synaptic <b>sensitization</b> in midbrain dopamine neurons after cocaine withdrawal.
+BDNF	addiction	withdrawal	16633344	<strong>BDNF</strong> dependent synaptic sensitization in midbrain dopamine neurons after cocaine <b>withdrawal</b>.
+BDNF	drug	cocaine	16633344	We found that after withdrawal from repeated <b>cocaine</b> exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous brain derived neurotrophic factor tyrosine kinase B (<strong>BDNF</strong> TrkB) signaling.
+BDNF	addiction	withdrawal	16633344	We found that after <b>withdrawal</b> from repeated cocaine exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous brain derived neurotrophic factor tyrosine kinase B (<strong>BDNF</strong> TrkB) signaling.
+BDNF	drug	cocaine	16633344	We found that after withdrawal from repeated <b>cocaine</b> exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous <strong>brain derived neurotrophic factor</strong> tyrosine kinase B (<strong>BDNF</strong> TrkB) signaling.
+BDNF	addiction	withdrawal	16633344	We found that after <b>withdrawal</b> from repeated cocaine exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous <strong>brain derived neurotrophic factor</strong> tyrosine kinase B (<strong>BDNF</strong> TrkB) signaling.
+BDNF	drug	cocaine	16633344	The elevated <strong>BDNF</strong> expression in the VTA after <b>cocaine</b> withdrawal may prime these synapses for potentiation by cue associated activity, triggering drug craving and relapse.
+BDNF	addiction	relapse	16633344	The elevated <strong>BDNF</strong> expression in the VTA after cocaine withdrawal may prime these synapses for potentiation by cue associated activity, triggering drug <b>craving</b> and <b>relapse</b>.
+BDNF	addiction	withdrawal	16633344	The elevated <strong>BDNF</strong> expression in the VTA after cocaine <b>withdrawal</b> may prime these synapses for potentiation by cue associated activity, triggering drug craving and relapse.
+BDNF	drug	alcohol	16441270	BIG news in <b>alcohol</b> addiction: new findings on growth factor pathways <strong>BDNF</strong>, insulin, and GDNF.
+BDNF	addiction	addiction	16441270	BIG news in alcohol <b>addiction</b>: new findings on growth factor pathways <strong>BDNF</strong>, insulin, and GDNF.
+BDNF	drug	alcohol	16441270	The 4 speakers showed that the behavioral effects of <b>alcohol</b> in the adult are regulated by 3 growth factors, insulin, glial cell line derived neurotrophic factor (GDNF), and brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	alcohol	16441270	The 4 speakers showed that the behavioral effects of <b>alcohol</b> in the adult are regulated by 3 growth factors, insulin, glial cell line derived neurotrophic factor (GDNF), and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	alcohol	16441270	Marian Logrip from the Ron and Janak laboratories presented evidence obtained in rodents that low concentrations of <b>alcohol</b> increase the expression of <strong>BDNF</strong> in the brain to regulate <b>alcohol</b> consumption.
+BDNF	drug	alcohol	16441270	Dr. Pandey showed that amygdalar <strong>BDNF</strong> regulates <b>alcohol</b>'s anxiolytic effects and preference.
+BDNF	drug	cocaine	16423334	Alterations in <strong>BDNF</strong> and trkB mRNAs following acute or sensitizing <b>cocaine</b> treatments and withdrawal.
+BDNF	addiction	withdrawal	16423334	Alterations in <strong>BDNF</strong> and trkB mRNAs following acute or sensitizing cocaine treatments and <b>withdrawal</b>.
+BDNF	drug	cocaine	16423334	In the present study, we used in situ hybridization to examine the influence of acute or repeated <b>cocaine</b> administrations and withdrawal from repeated <b>cocaine</b> treatment on the level of brain derived neurotrophic factor (<strong>BDNF</strong>) and its receptor trkB mRNAs in rat brain.
+BDNF	addiction	withdrawal	16423334	In the present study, we used in situ hybridization to examine the influence of acute or repeated cocaine administrations and <b>withdrawal</b> from repeated cocaine treatment on the level of brain derived neurotrophic factor (<strong>BDNF</strong>) and its receptor trkB mRNAs in rat brain.
+BDNF	drug	cocaine	16423334	In the present study, we used in situ hybridization to examine the influence of acute or repeated <b>cocaine</b> administrations and withdrawal from repeated <b>cocaine</b> treatment on the level of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and its receptor trkB mRNAs in rat brain.
+BDNF	addiction	withdrawal	16423334	In the present study, we used in situ hybridization to examine the influence of acute or repeated cocaine administrations and <b>withdrawal</b> from repeated cocaine treatment on the level of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and its receptor trkB mRNAs in rat brain.
+BDNF	drug	cocaine	16423334	On the other hand, <strong>BDNF</strong> mRNA in the rat hippocampus was increased only in the group of rats subjected to <b>cocaine</b> withdrawal.
+BDNF	addiction	withdrawal	16423334	On the other hand, <strong>BDNF</strong> mRNA in the rat hippocampus was increased only in the group of rats subjected to cocaine <b>withdrawal</b>.
+BDNF	drug	cocaine	16423334	Therefore, the increases in the levels of <strong>BDNF</strong> mRNA in the rat hippocampus seem to be correlated with "depressive like" behavioral effects during withdrawal from repeated <b>cocaine</b> treatment.
+BDNF	addiction	withdrawal	16423334	Therefore, the increases in the levels of <strong>BDNF</strong> mRNA in the rat hippocampus seem to be correlated with "depressive like" behavioral effects during <b>withdrawal</b> from repeated cocaine treatment.
+BDNF	drug	cocaine	16423334	In the shell (but not in the core) of the nucleus accumbens, the levels of <strong>BDNF</strong> mRNA were significantly increased following acute and repeated <b>cocaine</b> treatment as well as during <b>cocaine</b> withdrawal, which indicates that the alterations in the neurotrophin level in the brain region important for the expression of <b>cocaine</b> induced sensitization involve other mechanisms.
+BDNF	addiction	sensitization	16423334	In the shell (but not in the core) of the nucleus accumbens, the levels of <strong>BDNF</strong> mRNA were significantly increased following acute and repeated cocaine treatment as well as during cocaine withdrawal, which indicates that the alterations in the neurotrophin level in the brain region important for the expression of cocaine induced <b>sensitization</b> involve other mechanisms.
+BDNF	addiction	withdrawal	16423334	In the shell (but not in the core) of the nucleus accumbens, the levels of <strong>BDNF</strong> mRNA were significantly increased following acute and repeated cocaine treatment as well as during cocaine <b>withdrawal</b>, which indicates that the alterations in the neurotrophin level in the brain region important for the expression of cocaine induced sensitization involve other mechanisms.
+BDNF	drug	cocaine	16376315	Rodent <strong>BDNF</strong> genes, novel promoters, novel splice variants, and regulation by <b>cocaine</b>.
+BDNF	drug	cocaine	16376315	Interestingly, however, neither experimenter  nor self administered chronic <b>cocaine</b> administration enhanced striatal <strong>BDNF</strong> expression.
+BDNF	drug	amphetamine	16218999	Withdrawal of the obesogenic diets decreased gene expression for cocaine and <b>amphetamine</b> regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (<strong>BDNF</strong>) in the VMH, whereas neuropeptide Y (NPY) gene expression in the ARC was increased.
+BDNF	drug	cocaine	16218999	Withdrawal of the obesogenic diets decreased gene expression for <b>cocaine</b> and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (<strong>BDNF</strong>) in the VMH, whereas neuropeptide Y (NPY) gene expression in the ARC was increased.
+BDNF	addiction	withdrawal	16218999	<b>Withdrawal</b> of the obesogenic diets decreased gene expression for cocaine and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (<strong>BDNF</strong>) in the VMH, whereas neuropeptide Y (NPY) gene expression in the ARC was increased.
+BDNF	drug	amphetamine	16218999	Withdrawal of the obesogenic diets decreased gene expression for cocaine and <b>amphetamine</b> regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the VMH, whereas neuropeptide Y (NPY) gene expression in the ARC was increased.
+BDNF	drug	cocaine	16218999	Withdrawal of the obesogenic diets decreased gene expression for <b>cocaine</b> and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the VMH, whereas neuropeptide Y (NPY) gene expression in the ARC was increased.
+BDNF	addiction	withdrawal	16218999	<b>Withdrawal</b> of the obesogenic diets decreased gene expression for cocaine and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the VMH, whereas neuropeptide Y (NPY) gene expression in the ARC was increased.
+BDNF	addiction	withdrawal	16218999	<b>Withdrawal</b> of obesogenic diets induces changes in the gene expression consistent with NPY, CART and <strong>BDNF</strong> attempting to oppose weight gain on either HE or HE + EN.
+BDNF	drug	nicotine	16152573	Significant association of <strong>BDNF</strong> haplotypes in European American male <b>smokers</b> but not in European American female or African American <b>smokers</b>.
+BDNF	addiction	addiction	16152573	Brain derived neurotrophic factor (<strong>BDNF</strong>) influences dopamine and serotonin neurotransmission in the brain, both of which are involved in the reward system of <b>addiction</b>.
+BDNF	addiction	reward	16152573	Brain derived neurotrophic factor (<strong>BDNF</strong>) influences dopamine and serotonin neurotransmission in the brain, both of which are involved in the <b>reward</b> system of addiction.
+BDNF	addiction	addiction	16152573	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) influences dopamine and serotonin neurotransmission in the brain, both of which are involved in the reward system of <b>addiction</b>.
+BDNF	addiction	reward	16152573	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) influences dopamine and serotonin neurotransmission in the brain, both of which are involved in the <b>reward</b> system of addiction.
+BDNF	drug	nicotine	16152573	The <strong>BDNF</strong> gene is located in a genomic region on chromosome 11p where we and others have found 'significant' linkage to <b>nicotine</b> dependence (ND).
+BDNF	addiction	dependence	16152573	The <strong>BDNF</strong> gene is located in a genomic region on chromosome 11p where we and others have found 'significant' linkage to nicotine <b>dependence</b> (ND).
+BDNF	drug	nicotine	16152573	We tested the potential role of variants within <strong>BDNF</strong> in vulnerability to ND, which was assessed by <b>Smoking</b> Quantity (SQ), the Heaviness of <b>Smoking</b> Index (HSI), and the Fagerström Test for ND (FTND).
+BDNF	drug	nicotine	16152573	Six single nucleotide polymorphisms (SNPs) in <strong>BDNF</strong> were analyzed in an extensively phenotyped cohort of 602 nuclear families with <b>smokers</b> and non <b>smokers</b> of African American (AA) or European American (EA) ancestry.
+BDNF	drug	amphetamine	16039058	High concentrations of plasma <strong>brain derived neurotrophic factor</strong> in <b>methamphetamine</b> users.
+BDNF	addiction	addiction	16039058	A growing body of evidence suggests that brain derived neurotrophic factor (<strong>BDNF</strong>) is associated with <b>addictive</b> behavior.
+BDNF	addiction	addiction	16039058	A growing body of evidence suggests that <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) is associated with <b>addictive</b> behavior.
+BDNF	drug	amphetamine	16039058	The present study investigated the changes in plasma <strong>BDNF</strong> concentration that were induced by chronic <b>methamphetamine</b> use.
+BDNF	drug	amphetamine	16039058	Using an enzyme linked immunosorbent assay (ELISA), we measured peripheral <strong>BDNF</strong> levels in <b>methamphetamine</b> users and in a control group.
+BDNF	drug	amphetamine	16039058	The plasma <strong>BDNF</strong> concentrations of <b>methamphetamine</b> users were significantly higher compared with those of controls (2536.3 pg/ml versus 1352.6 pg/ml).
+BDNF	drug	amphetamine	16039058	This finding suggests that <strong>BDNF</strong> plays some role in the neurotoxicity of <b>methamphetamine</b>.
+BDNF	drug	alcohol	15896496	A study of the association of (Val66Met) polymorphism in the <strong>brain derived neurotrophic factor</strong> gene with <b>alcohol</b> dependence and extreme violence in Chinese males.
+BDNF	addiction	dependence	15896496	A study of the association of (Val66Met) polymorphism in the <strong>brain derived neurotrophic factor</strong> gene with alcohol <b>dependence</b> and extreme violence in Chinese males.
+BDNF	drug	alcohol	15896496	From studies of genetic knockout animals, brain derived neurotrophic factor (<strong>BDNF</strong>), a member of the neurotrophin growth factor family, has been implicated in both <b>alcohol</b> preference and aggressive behaviour.
+BDNF	drug	alcohol	15896496	From studies of genetic knockout animals, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), a member of the neurotrophin growth factor family, has been implicated in both <b>alcohol</b> preference and aggressive behaviour.
+BDNF	drug	alcohol	15896496	To test whether a <strong>BDNF</strong> genetic variant may be associated with <b>alcohol</b> dependent and violent behaviours, we studied Val66Met polymorphism of the <strong>BDNF</strong> gene in 110 cases of <b>alcohol</b> dependence, in 134 extremely violent convicts, and in 149 individuals without psychosis or mood disorders.
+BDNF	addiction	dependence	15896496	To test whether a <strong>BDNF</strong> genetic variant may be associated with alcohol dependent and violent behaviours, we studied Val66Met polymorphism of the <strong>BDNF</strong> gene in 110 cases of alcohol <b>dependence</b>, in 134 extremely violent convicts, and in 149 individuals without psychosis or mood disorders.
+BDNF	drug	alcohol	15896496	Based on these findings, it seems reasonable to suggest that this <strong>BDNF</strong> gene Val66Met polymorphism is unlikely to play a major role in the genetic susceptibility to the traits of <b>alcohol</b> dependence or violence proneness.
+BDNF	addiction	dependence	15896496	Based on these findings, it seems reasonable to suggest that this <strong>BDNF</strong> gene Val66Met polymorphism is unlikely to play a major role in the genetic susceptibility to the traits of alcohol <b>dependence</b> or violence proneness.
+BDNF	drug	cannabinoid	15857384	In vivo up regulation of <strong>brain derived neurotrophic factor</strong> in specific brain areas by chronic exposure to Delta <b>tetrahydrocannabinol</b>.
+BDNF	drug	cannabinoid	15857384	Here we show that chronic administration of Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>), the active psychotropic agent in <b>marijuana</b> and hashish, at 1.5 mg per kg per day intraperitoneally for 7 days, increases the expression, at both mRNA and protein levels, of brain derived neurotrophic factor (<strong>BDNF</strong>), in specific rat brain areas, notably in those involved in reward and addiction.
+BDNF	addiction	addiction	15857384	Here we show that chronic administration of Delta(9) tetrahydrocannabinol (Delta(9) THC), the active psychotropic agent in marijuana and hashish, at 1.5 mg per kg per day intraperitoneally for 7 days, increases the expression, at both mRNA and protein levels, of brain derived neurotrophic factor (<strong>BDNF</strong>), in specific rat brain areas, notably in those involved in reward and <b>addiction</b>.
+BDNF	addiction	reward	15857384	Here we show that chronic administration of Delta(9) tetrahydrocannabinol (Delta(9) THC), the active psychotropic agent in marijuana and hashish, at 1.5 mg per kg per day intraperitoneally for 7 days, increases the expression, at both mRNA and protein levels, of brain derived neurotrophic factor (<strong>BDNF</strong>), in specific rat brain areas, notably in those involved in <b>reward</b> and addiction.
+BDNF	drug	cannabinoid	15857384	Here we show that chronic administration of Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>), the active psychotropic agent in <b>marijuana</b> and hashish, at 1.5 mg per kg per day intraperitoneally for 7 days, increases the expression, at both mRNA and protein levels, of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), in specific rat brain areas, notably in those involved in reward and addiction.
+BDNF	addiction	addiction	15857384	Here we show that chronic administration of Delta(9) tetrahydrocannabinol (Delta(9) THC), the active psychotropic agent in marijuana and hashish, at 1.5 mg per kg per day intraperitoneally for 7 days, increases the expression, at both mRNA and protein levels, of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), in specific rat brain areas, notably in those involved in reward and <b>addiction</b>.
+BDNF	addiction	reward	15857384	Here we show that chronic administration of Delta(9) tetrahydrocannabinol (Delta(9) THC), the active psychotropic agent in marijuana and hashish, at 1.5 mg per kg per day intraperitoneally for 7 days, increases the expression, at both mRNA and protein levels, of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), in specific rat brain areas, notably in those involved in <b>reward</b> and addiction.
+BDNF	drug	cannabinoid	15857384	Real time PCR revealed a 10 fold up regulation of <strong>BDNF</strong> mRNA in the nucleus accumbens (NAc) upon chronic Delta(9) <b>THC</b> treatment, but there was no change at 3 or 24 h after a single injection.
+BDNF	drug	cannabinoid	15857384	Altogether, our study indicates that chronic exposure to Delta(9) <b>THC</b> up regulates <strong>BDNF</strong> in specific brain areas involved with reward, and provides evidence for different <strong>BDNF</strong> expression in the anterior and posterior VTA.
+BDNF	addiction	reward	15857384	Altogether, our study indicates that chronic exposure to Delta(9) THC up regulates <strong>BDNF</strong> in specific brain areas involved with <b>reward</b>, and provides evidence for different <strong>BDNF</strong> expression in the anterior and posterior VTA.
+BDNF	drug	cannabinoid	15857384	We suggest that Delta(9) <b>THC</b> up regulation of <strong>BDNF</strong> expression has an important role in inducing the neuroadaptive processes taking place upon exposure to <b>cannabinoids</b>.
+BDNF	drug	alcohol	15745951	<b>Ethanol</b> regulated genes were generally related to neuroplasticity, but regulation of discrete functional groups and pathways was brain region specific: glucocorticoid signaling, neurogenesis, and myelination in the prefrontal cortex; neuropeptide signaling and developmental genes, including factor <strong>Bdnf</strong>, in the nucleus accumbens; and retinoic acid signaling in the ventral tegmental area.
+BDNF	drug	cocaine	15671872	A single <b>cocaine</b> exposure increases <strong>BDNF</strong> and D3 receptor expression: implications for drug conditioning.
+BDNF	drug	cocaine	15671872	Acute <b>cocaine</b> produced a transient increase in <strong>BDNF</strong> mRNA in the prefrontal cortex, associated with a long lasting increase in drd3 mRNA, and a delayed and long lasting increase in Drd3 protein in the nucleus accumbens.
+BDNF	drug	amphetamine	15671872	<b>Methamphetamine</b> and morphine, two drugs known to easily induce drug conditioning, also markedly elevated <strong>BDNF</strong> mRNA.
+BDNF	drug	opioid	15671872	Methamphetamine and <b>morphine</b>, two drugs known to easily induce drug conditioning, also markedly elevated <strong>BDNF</strong> mRNA.
+BDNF	drug	alcohol	15548669	RACK1 and <strong>brain derived neurotrophic factor</strong>: a homeostatic pathway that regulates <b>alcohol</b> addiction.
+BDNF	addiction	addiction	15548669	RACK1 and <strong>brain derived neurotrophic factor</strong>: a homeostatic pathway that regulates alcohol <b>addiction</b>.
+BDNF	drug	alcohol	15548669	Here we demonstrate that <strong>BDNF</strong> plays a role in reducing the behavioral effects of <b>ethanol</b>, including consumption, in rodents.
+BDNF	drug	alcohol	15548669	We found that decreasing the levels of <strong>BDNF</strong> leads to increased behavioral responses to <b>ethanol</b>, whereas increases in the levels of <strong>BDNF</strong>, mediated by the scaffolding protein RACK1, attenuate these behaviors.
+BDNF	drug	alcohol	15548669	Interestingly, we found that acute exposure of neurons to <b>ethanol</b> leads to increased levels of <strong>BDNF</strong> mRNA via RACK1.
+BDNF	drug	alcohol	15548669	Importantly, acute systemic administration of <b>ethanol</b> and voluntary <b>ethanol</b> consumption lead to increased levels of <strong>BDNF</strong> expression in the dorsal striatum.
+BDNF	drug	alcohol	15548669	Taken together, these findings suggest that RACK1 and <strong>BDNF</strong> are part of a regulatory pathway that opposes adaptations that lead to the development of <b>alcohol</b> addiction.
+BDNF	addiction	addiction	15548669	Taken together, these findings suggest that RACK1 and <strong>BDNF</strong> are part of a regulatory pathway that opposes adaptations that lead to the development of alcohol <b>addiction</b>.
+BDNF	drug	alcohol	15547445	Association study of <strong>brain derived neurotrophic factor</strong> gene polymorphism and <b>alcoholism</b>.
+BDNF	addiction	addiction	15547445	Brain derived neurotrophic factor (<strong>BDNF</strong>) influences dopamine and serotonin neurotransmitters that are heavily linked to <b>addiction</b>.
+BDNF	addiction	addiction	15547445	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) influences dopamine and serotonin neurotransmitters that are heavily linked to <b>addiction</b>.
+BDNF	drug	alcohol	15547445	A quantitative trait loci study indicated that genes localized to 11p13, where the <strong>BDNF</strong> gene is mapped (11p13 15), increase the risk for severe <b>alcohol</b> withdrawal.
+BDNF	addiction	withdrawal	15547445	A quantitative trait loci study indicated that genes localized to 11p13, where the <strong>BDNF</strong> gene is mapped (11p13 15), increase the risk for severe alcohol <b>withdrawal</b>.
+BDNF	drug	alcohol	15547445	These lines of evidence suggested that <strong>BDNF</strong> might play some role in the development of or vulnerability to <b>alcoholism</b> and/or clinical characteristics of <b>alcoholic</b> individuals.
+BDNF	drug	alcohol	15547445	Genotype and allele distributions of the <strong>BDNF</strong> gene polymorphism did not differ significantly between <b>alcoholic</b> and control subjects.
+BDNF	drug	alcohol	15547445	These results indicate that <strong>BDNF</strong> gene polymorphism might modify phenotypes of <b>alcoholism</b>.
+BDNF	drug	cannabinoid	15465283	Here, we show that selective isolation of perisomatic inhibitory cells containing either parvalbumin or cholecystokinin reveals major differences in the temporal dynamics of their functional differentiation, and their dependence on target derived signals like <strong>brain derived neurotrophic factor</strong> and <b>endocannabinoids</b>.
+BDNF	addiction	dependence	15465283	Here, we show that selective isolation of perisomatic inhibitory cells containing either parvalbumin or cholecystokinin reveals major differences in the temporal dynamics of their functional differentiation, and their <b>dependence</b> on target derived signals like <strong>brain derived neurotrophic factor</strong> and endocannabinoids.
+BDNF	drug	cocaine	15464139	Incubation of <b>cocaine</b> craving after withdrawal is associated with increases in the levels of brain derived neurotrophic factor (<strong>BDNF</strong>) in mesolimbic dopamine areas.
+BDNF	addiction	relapse	15464139	Incubation of cocaine <b>craving</b> after withdrawal is associated with increases in the levels of brain derived neurotrophic factor (<strong>BDNF</strong>) in mesolimbic dopamine areas.
+BDNF	addiction	withdrawal	15464139	Incubation of cocaine craving after <b>withdrawal</b> is associated with increases in the levels of brain derived neurotrophic factor (<strong>BDNF</strong>) in mesolimbic dopamine areas.
+BDNF	drug	cocaine	15464139	Incubation of <b>cocaine</b> craving after withdrawal is associated with increases in the levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in mesolimbic dopamine areas.
+BDNF	addiction	relapse	15464139	Incubation of cocaine <b>craving</b> after withdrawal is associated with increases in the levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in mesolimbic dopamine areas.
+BDNF	addiction	withdrawal	15464139	Incubation of cocaine craving after <b>withdrawal</b> is associated with increases in the levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in mesolimbic dopamine areas.
+BDNF	drug	amphetamine	15459944	Association study between <strong>brain derived neurotrophic factor</strong> gene polymorphisms and <b>methamphetamine</b> abusers in Japan.
+BDNF	drug	amphetamine	15459944	In this study, we analyzed association of two <strong>BDNF</strong> gene single nucleotide polymorphisms (SNPs), 132C > T (C270T named formerly) in the noncoding region of exon V and 196G > A (val66met) in the coding region of exon XIIIA, with <b>methamphetamine</b> (MAP) abuse in Japan.
+BDNF	addiction	relapse	15459944	Furthermore, there was no difference between clinical parameters (e.g., prognosis psychosis, spontaneous <b>relapse</b>, or poly substance abuse) and the two SNPs of <strong>BDNF</strong> gene.
+BDNF	drug	alcohol	15296847	The parietal cortex was susceptible to <b>ethanol</b> exposure, NGF and <strong>BDNF</strong> content increased, and NT 3 content fell, whereas no changes were detectable in the entorhinal cortex.
+BDNF	drug	alcohol	15296847	Neurotrophin content in the two segments of the basal forebrain was affected; NGF and NT 3 content in the basal forebrain was reduced and NGF and <strong>BDNF</strong> content in the septal nuclei was increased by <b>ethanol</b> exposure.
+BDNF	drug	alcohol	15246696	Alterations of cerebellar mRNA specific for <strong>BDNF</strong>, p75NTR, and TrkB receptor isoforms occur within hours of <b>ethanol</b> administration to 4 day old rat pups.
+BDNF	drug	alcohol	15246696	<b>Ethanol</b> exposure during this vulnerable window induces rapid apoptotic Purkinje cell death that is hypothesized to result from <b>ethanol</b> inhibition in brain derived nerve growth factor (<strong>BDNF</strong>) TrkB neurotrophic signaling that results in loss of apoptotic suppression.
+BDNF	drug	alcohol	15246696	In this study, the effect that different concentrations of <b>ethanol</b> (1.5, 3.0, 4.5 and 6.0 g/kg) have on steady state mRNA expression of <strong>BDNF</strong> and different TrkB receptor isoforms in the cerebellum on PN4 was determined at 1, 4, 6, and 8 h after treatment.
+BDNF	drug	alcohol	15246696	Significant decreases in mRNA specific for <strong>BDNF</strong> and TrkB isoforms were detected within 1 h after <b>ethanol</b> administration.
+BDNF	drug	alcohol	15246696	These results support the hypothesis that <b>ethanol</b> induces a disruption of <strong>BDNF</strong> TrkB signaling that results in loss of apoptotic suppression in vulnerable Purkinje cells by growth factor withdrawal.
+BDNF	addiction	withdrawal	15246696	These results support the hypothesis that ethanol induces a disruption of <strong>BDNF</strong> TrkB signaling that results in loss of apoptotic suppression in vulnerable Purkinje cells by growth factor <b>withdrawal</b>.
+BDNF	drug	alcohol	15163695	Furthermore, <b>alcohol</b> drinking and anxiety like behaviors in CREB haplodeficient mice may possibly be related to decreased expression of NPY and <strong>BDNF</strong> in the brains of these mice.
+BDNF	drug	benzodiazepine	15009662	In wild type animals, <b>diazepam</b> reduced the expression levels of the alpha subunit of the calcium/calmodulin dependent protein kinase II, as well as <strong>brain derived neurotrophic factor</strong>, MAP kinase phosphatase, transcription factor GIF, c fos and nerve growth factor induced gene A.
+BDNF	drug	amphetamine	14985924	The offspring was tested for a) locomotor and exploratory activity with or without a d <b>amphetamine</b> challenge (0, 1, or 2 mg/kg) on postnatal day (pnd) 15; b) social interactions and novelty seeking during adolescence; c) levels of the brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	addiction	relapse	14985924	The offspring was tested for a) locomotor and exploratory activity with or without a d amphetamine challenge (0, 1, or 2 mg/kg) on postnatal day (pnd) 15; b) social interactions and novelty <b>seeking</b> during adolescence; c) levels of the brain derived neurotrophic factor (<strong>BDNF</strong>).
+BDNF	drug	amphetamine	14985924	The offspring was tested for a) locomotor and exploratory activity with or without a d <b>amphetamine</b> challenge (0, 1, or 2 mg/kg) on postnatal day (pnd) 15; b) social interactions and novelty seeking during adolescence; c) levels of the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	addiction	relapse	14985924	The offspring was tested for a) locomotor and exploratory activity with or without a d amphetamine challenge (0, 1, or 2 mg/kg) on postnatal day (pnd) 15; b) social interactions and novelty <b>seeking</b> during adolescence; c) levels of the <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>).
+BDNF	drug	cocaine	14973246	A single infusion of <strong>brain derived neurotrophic factor</strong> into the ventral tegmental area induces long lasting potentiation of <b>cocaine</b> seeking after withdrawal.
+BDNF	addiction	relapse	14973246	A single infusion of <strong>brain derived neurotrophic factor</strong> into the ventral tegmental area induces long lasting potentiation of cocaine <b>seeking</b> after withdrawal.
+BDNF	addiction	withdrawal	14973246	A single infusion of <strong>brain derived neurotrophic factor</strong> into the ventral tegmental area induces long lasting potentiation of cocaine seeking after <b>withdrawal</b>.
+BDNF	drug	cocaine	14973246	Based on these findings, we studied whether <strong>BDNF</strong> infusions into the ventral tegmental area (VTA), the cell body region of mesolimbic dopamine neurons, would potentiate <b>cocaine</b> seeking after withdrawal.
+BDNF	addiction	relapse	14973246	Based on these findings, we studied whether <strong>BDNF</strong> infusions into the ventral tegmental area (VTA), the cell body region of mesolimbic dopamine neurons, would potentiate cocaine <b>seeking</b> after withdrawal.
+BDNF	addiction	withdrawal	14973246	Based on these findings, we studied whether <strong>BDNF</strong> infusions into the ventral tegmental area (VTA), the cell body region of mesolimbic dopamine neurons, would potentiate cocaine seeking after <b>withdrawal</b>.
+BDNF	drug	cocaine	14973246	A single intra VTA infusion of <strong>BDNF</strong>, but not NGF, induced long lasting enhancement of <b>cocaine</b> seeking for up to 30 d, an effect reversed by U0126.
+BDNF	addiction	relapse	14973246	A single intra VTA infusion of <strong>BDNF</strong>, but not NGF, induced long lasting enhancement of cocaine <b>seeking</b> for up to 30 d, an effect reversed by U0126.
+BDNF	addiction	withdrawal	14973246	In contrast, neither <strong>BDNF</strong> infusions into the substantia nigra, nor acute intra VTA <strong>BDNF</strong> infusions 2 hr before testing on day 3 of <b>withdrawal</b>, were effective.
+BDNF	drug	cocaine	14973246	These data suggest that <strong>BDNF</strong> mediated neuroadaptations in mesolimbic areas are involved in the persistent <b>cocaine</b> seeking induced by exposure to drug cues after withdrawal.
+BDNF	addiction	relapse	14973246	These data suggest that <strong>BDNF</strong> mediated neuroadaptations in mesolimbic areas are involved in the persistent cocaine <b>seeking</b> induced by exposure to drug cues after withdrawal.
+BDNF	addiction	withdrawal	14973246	These data suggest that <strong>BDNF</strong> mediated neuroadaptations in mesolimbic areas are involved in the persistent cocaine seeking induced by exposure to drug cues after <b>withdrawal</b>.
+BDNF	drug	alcohol	12967770	I also suggest that, via CREB, NPY might interact with other CREB target genes, such as the gene encoding <strong>brain derived neurotrophic factor</strong>, and that this CREB mediated interaction might be important in the regulation of anxiety and <b>alcohol</b> drinking behaviors.
+BDNF	drug	cocaine	12784114	Reduced behavioral effects of <b>cocaine</b> in heterozygous brain derived neurotrophic factor (<strong>BDNF</strong>) knockout mice.
+BDNF	drug	cocaine	12784114	Reduced behavioral effects of <b>cocaine</b> in heterozygous <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) knockout mice.
+BDNF	drug	cocaine	12784114	Brain derived neurotrophic factor (<strong>BDNF</strong>) affects the development of brain neurotransmitter systems, including dopamine and serotonin systems that are important for <b>cocaine</b>'s rewarding and locomotor stimulatory properties.
+BDNF	drug	cocaine	12784114	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) affects the development of brain neurotransmitter systems, including dopamine and serotonin systems that are important for <b>cocaine</b>'s rewarding and locomotor stimulatory properties.
+BDNF	drug	cocaine	12784114	To assess the effects of lifelong alterations in the levels of <strong>BDNF</strong> expression on a measure of psychostimulant reward, we have compared locomotor stimulant and rewarding effects of <b>cocaine</b> in heterozygous <strong>BDNF</strong> knockout mice with effects in their wild type littermates.
+BDNF	addiction	reward	12784114	To assess the effects of lifelong alterations in the levels of <strong>BDNF</strong> expression on a measure of psychostimulant <b>reward</b>, we have compared locomotor stimulant and rewarding effects of cocaine in heterozygous <strong>BDNF</strong> knockout mice with effects in their wild type littermates.
+BDNF	drug	cocaine	12784114	Heterozygous <strong>BDNF</strong> knockout mice displayed less locomotion during habituation and less locomotion after <b>cocaine</b> injections.
+BDNF	drug	cocaine	12784114	<b>Cocaine</b> conditioned place preferences were reduced in the <strong>BDNF</strong> heterozygotes.
+BDNF	addiction	addiction	12784114	Furthermore, these data support suggestions that differences in human <strong>BDNF</strong> expression may underlie associations between markers near the human <strong>BDNF</strong> gene locus and drug <b>addiction</b>.
+BDNF	drug	cannabinoid	12657697	In vivo <b>THC</b> induced the expression of immediate early genes products (c Fos protein, Zif268, and <strong>BDNF</strong> mRNAs), and this induction was prevented by an inhibitor of MEK.
+BDNF	addiction	sensitization	12642909	As to subcellular neurochemical mechanisms of <b>sensitization</b>, the activation of three main cascades is indispensable, 1) D1 dopamine (DA) receptors/PKA/phospho 34Thr DARPP 32/PP 1 cascade activated by psychostimulant induced enhancement of DA release in the accumbens, 2) NMDA receptors and CaM KII activated by enhanced release of glutamate, 3) activation of MAP kinase cascade by <strong>BDNF</strong> and beta 1 subunit of G protein.
+BDNF	drug	cocaine	12574402	Time dependent increases in <strong>brain derived neurotrophic factor</strong> protein levels within the mesolimbic dopamine system after withdrawal from <b>cocaine</b>: implications for incubation of <b>cocaine</b> craving.
+BDNF	addiction	relapse	12574402	Time dependent increases in <strong>brain derived neurotrophic factor</strong> protein levels within the mesolimbic dopamine system after withdrawal from cocaine: implications for incubation of cocaine <b>craving</b>.
+BDNF	addiction	withdrawal	12574402	Time dependent increases in <strong>brain derived neurotrophic factor</strong> protein levels within the mesolimbic dopamine system after <b>withdrawal</b> from cocaine: implications for incubation of cocaine craving.
+BDNF	addiction	reward	12574402	Other rats were killed without testing on days 1, 30, and 90 of <b>reward</b> withdrawal, and <strong>BDNF</strong> and nerve growth factor (NGF) protein levels were measured in the ventral tegmental area (VTA), accumbens, and amygdala.
+BDNF	addiction	withdrawal	12574402	Other rats were killed without testing on days 1, 30, and 90 of reward <b>withdrawal</b>, and <strong>BDNF</strong> and nerve growth factor (NGF) protein levels were measured in the ventral tegmental area (VTA), accumbens, and amygdala.
+BDNF	drug	cocaine	12574402	<strong>BDNF</strong>, but not NGF, levels in the VTA, accumbens, and amygdala progressively increased after <b>cocaine</b>, but not sucrose, withdrawal.
+BDNF	addiction	withdrawal	12574402	<strong>BDNF</strong>, but not NGF, levels in the VTA, accumbens, and amygdala progressively increased after cocaine, but not sucrose, <b>withdrawal</b>.
+BDNF	drug	cocaine	12574402	Time dependent increases in <strong>BDNF</strong> levels may lead to synaptic modifications that underlie enhanced responsiveness to <b>cocaine</b> cues after prolonged withdrawal periods.
+BDNF	addiction	withdrawal	12574402	Time dependent increases in <strong>BDNF</strong> levels may lead to synaptic modifications that underlie enhanced responsiveness to cocaine cues after prolonged <b>withdrawal</b> periods.
+BDNF	drug	amphetamine	12213320	<strong>Brain derived neurotrophic factor</strong> expression is increased in the rat amygdala, piriform cortex and hypothalamus following repeated <b>amphetamine</b> administration.
+BDNF	addiction	reward	12213320	The amygdala also expresses high levels of brain derived neurotrophic factor (<strong>BDNF</strong>), an activity dependent neurotrophin that can influence the <b>reinforcing</b> and locomotor activating properties of psychostimulants.
+BDNF	addiction	reward	12213320	The amygdala also expresses high levels of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), an activity dependent neurotrophin that can influence the <b>reinforcing</b> and locomotor activating properties of psychostimulants.
+BDNF	drug	amphetamine	12213320	of D <b>amphetamine</b> developed hyperactivity followed by stereotypical behavior but showed no change in the basal expression of <strong>BDNF</strong> mRNA or its immunocytochemical profile in any region except the piriform cortex.
+BDNF	drug	amphetamine	12213320	Repeated injections (5 days) of 5 mg/kg <b>amphetamine</b> were accompanied by an enhanced onset of stereotypical behavior and elevated <strong>BDNF</strong> mRNA in the basolateral amygdala, rostral piriform cortex and paraventricular nucleus of the hypothalamus.
+BDNF	drug	cocaine	12211082	These experiments were designed to assess the influence of neurotrophin 3 (NT 3) and brain derived neurotrophic factor (<strong>BDNF</strong>) in the mesoaccumbens dopamine system on the initiation of behavioral sensitization to <b>cocaine</b>.
+BDNF	addiction	sensitization	12211082	These experiments were designed to assess the influence of neurotrophin 3 (NT 3) and brain derived neurotrophic factor (<strong>BDNF</strong>) in the mesoaccumbens dopamine system on the initiation of behavioral <b>sensitization</b> to cocaine.
+BDNF	drug	cocaine	12211082	These experiments were designed to assess the influence of neurotrophin 3 (NT 3) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the mesoaccumbens dopamine system on the initiation of behavioral sensitization to <b>cocaine</b>.
+BDNF	addiction	sensitization	12211082	These experiments were designed to assess the influence of neurotrophin 3 (NT 3) and <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) in the mesoaccumbens dopamine system on the initiation of behavioral <b>sensitization</b> to cocaine.
+BDNF	drug	cocaine	12211082	A neutralizing antibody for NT 3, <strong>BDNF</strong> or their vehicle was administered into the ventral tegmental area (VTA) or nucleus accumbens prior to each of four daily injections of 15 mg/kg <b>cocaine</b>.
+BDNF	drug	cocaine	12211082	In contrast, pretreatment with anti <strong>BDNF</strong> into the VTA or nucleus accumbens had no influence on the initiation of behavioral sensitization to <b>cocaine</b>.
+BDNF	addiction	sensitization	12211082	In contrast, pretreatment with anti <strong>BDNF</strong> into the VTA or nucleus accumbens had no influence on the initiation of behavioral <b>sensitization</b> to cocaine.
+BDNF	drug	cocaine	12099907	<b>Cocaine</b> conditioned mice had increased levels of D3R mRNA and binding in the nucleus accumbens (NAc), and transcripts of brain derived neurotrophic factor (<strong>BDNF</strong>), a factor controlling D3R expression, in the ventral tegmental area (VTA).
+BDNF	drug	cocaine	12099907	<b>Cocaine</b> conditioned mice had increased levels of D3R mRNA and binding in the nucleus accumbens (NAc), and transcripts of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), a factor controlling D3R expression, in the ventral tegmental area (VTA).
+BDNF	drug	cocaine	12099907	<b>Cocaine</b> had no effects on D3R or <strong>BDNF</strong> genes when administered in home cages.
+BDNF	drug	cocaine	12099907	These results demonstrate a modulation of reactivity to <b>cocaine</b> cues by the D3R, the expression of which is elevated in the NAc by the repeated association of drug effects with a particular context, through a <strong>BDNF</strong> dependent mechanism.
+BDNF	drug	opioid	12019333	Here we report that noradrenergic locus ceruleus (LC) neurons of mice with a conditional deletion of <strong>BDNF</strong> in postnatal brain respond to chronic <b>morphine</b> treatment with a paradoxical downregulation of cAMP mediated excitation and lack of dynamic regulation of TH expression.
+BDNF	addiction	withdrawal	12019333	This was accompanied by a threefold reduction in opiate <b>withdrawal</b> symptoms despite normal antinociceptive tolerance in the <strong>BDNF</strong> deficient mice.
+BDNF	drug	alcohol	11743997	In addition, Purkinje cells are reported to experience a critical switch between <strong>BDNF</strong> dependence and NT3 dependence during the period of highest <b>ethanol</b> sensitivity between postnatal days (PN) 4 6.
+BDNF	addiction	dependence	11743997	In addition, Purkinje cells are reported to experience a critical switch between <strong>BDNF</strong> <b>dependence</b> and NT3 <b>dependence</b> during the period of highest ethanol sensitivity between postnatal days (PN) 4 6.
+BDNF	drug	alcohol	11704927	Positive markers identify the <b>alcohol</b> dehydrogenase (ADH) locus, flank the brain derived neurotropic factor (<strong>BDNF</strong>) locus, and mark seven other regions previously linked to vulnerability to nicotine or <b>alcohol</b> abuse.
+BDNF	drug	nicotine	11704927	Positive markers identify the alcohol dehydrogenase (ADH) locus, flank the brain derived neurotropic factor (<strong>BDNF</strong>) locus, and mark seven other regions previously linked to vulnerability to <b>nicotine</b> or alcohol abuse.
+BDNF	drug	alcohol	11532337	Early postnatal <b>ethanol</b> exposure selectively decreases <strong>BDNF</strong> and truncated TrkB T2 receptor mRNA expression in the rat cerebellum.
+BDNF	drug	alcohol	11532337	We believe that the specific <b>ethanol</b> vulnerability, and the timing of this vulnerability result from alterations in the <strong>BDNF</strong> NT3 interplay.
+BDNF	drug	alcohol	11532337	No significant alterations to the expression of TrkC mRNA were found indicating that <b>ethanol</b> exposure appears to act selectively on the <strong>BDNF</strong> communication system.
+BDNF	drug	alcohol	11169630	Effects of <b>alcohol</b> on <strong>brain derived neurotrophic factor</strong> mRNA expression in discrete regions of the rat hippocampus and hypothalamus.
+BDNF	drug	alcohol	11169630	We showed that chronic <b>alcohol</b> intoxication decreases <strong>brain derived neurotrophic factor</strong> mRNA expression in discrete regions of the rat hippocampus (CA1 region and dentate gyrus) and in the supraoptic nucleus of the hypothalamus.
+BDNF	addiction	intoxication	11169630	We showed that chronic alcohol <b>intoxication</b> decreases <strong>brain derived neurotrophic factor</strong> mRNA expression in discrete regions of the rat hippocampus (CA1 region and dentate gyrus) and in the supraoptic nucleus of the hypothalamus.
+BDNF	drug	alcohol	11169630	Following 12 hr of <b>alcohol</b> withdrawal, a significant increase in <strong>BDNF</strong> mRNA expression was observed in the dentate gyrus and CA3 region of hippocampus and in the hypothalamic supraoptic nucleus.
+BDNF	addiction	withdrawal	11169630	Following 12 hr of alcohol <b>withdrawal</b>, a significant increase in <strong>BDNF</strong> mRNA expression was observed in the dentate gyrus and CA3 region of hippocampus and in the hypothalamic supraoptic nucleus.
+BDNF	drug	nicotine	11146126	Acute <b>nicotine</b> decreases, and chronic <b>nicotine</b> increases the expression of <strong>brain derived neurotrophic factor</strong> mRNA in rat hippocampus.
+BDNF	drug	nicotine	11146126	However, with 7 days <b>nicotine</b> treatment, tolerance developed to the inhibitory effect of <b>nicotine</b> on <strong>BDNF</strong> mRNA expression and there was a significant increase in <strong>BDNF</strong> expression 2 h after the final injection in the CA1 region.
+BDNF	drug	nicotine	11146126	These data suggests that changes in expression of hippocampal <strong>BDNF</strong> may be involved in the behavioural effects of <b>nicotine</b> observed after acute and chronic treatment.
+BDNF	drug	alcohol	10591601	<b>Ethanol</b> pretreatment enhances NMDA excitotoxicity in biogenic amine neurons: protection by <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	alcohol	10591601	Treatment with Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) prevented <b>ethanol</b> sensitization to NMDA excitotoxicity.
+BDNF	addiction	sensitization	10591601	Treatment with Brain Derived Neurotrophic Factor (<strong>BDNF</strong>) prevented ethanol <b>sensitization</b> to NMDA excitotoxicity.
+BDNF	drug	alcohol	10591601	Treatment with <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) prevented <b>ethanol</b> sensitization to NMDA excitotoxicity.
+BDNF	addiction	sensitization	10591601	Treatment with <strong>Brain Derived Neurotrophic Factor</strong> (<strong>BDNF</strong>) prevented ethanol <b>sensitization</b> to NMDA excitotoxicity.
+BDNF	drug	cocaine	10493769	The first experiments evaluated the effect of three daily intra ventral tegmental area (VTA) microinjections of neurotrophin 3 (NT 3) or brain derived neurotrophic factor (<strong>BDNF</strong>) on the behavioral activating effects of a subsequent challenge injection of <b>cocaine</b> in rats.
+BDNF	drug	cocaine	10493769	The first experiments evaluated the effect of three daily intra ventral tegmental area (VTA) microinjections of neurotrophin 3 (NT 3) or <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) on the behavioral activating effects of a subsequent challenge injection of <b>cocaine</b> in rats.
+BDNF	drug	cocaine	10493769	In contrast, <strong>BDNF</strong> microinjections resulted in a progressive increase in behavioral activity but did not influence the subsequent behavioral response to <b>cocaine</b>.
+BDNF	drug	cocaine	10493769	Finally, the effects of acute and repeated <b>cocaine</b> injections on NT 3 and <strong>BDNF</strong> mRNA levels in the VTA, substantia nigra, and hippocampus were assessed.
+BDNF	drug	cocaine	10234039	Enhancement of locomotor activity and conditioned reward to <b>cocaine</b> by <strong>brain derived neurotrophic factor</strong>.
+BDNF	addiction	reward	10234039	Enhancement of locomotor activity and conditioned <b>reward</b> to cocaine by <strong>brain derived neurotrophic factor</strong>.
+BDNF	addiction	sensitization	10234039	Here, we investigated the effect of brain derived neurotrophic factor (<strong>BDNF</strong>), which enhances the survival and function of dopaminergic neurons, on stimulant induced locomotor <b>sensitization</b> and responding for CR.
+BDNF	addiction	sensitization	10234039	Here, we investigated the effect of <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), which enhances the survival and function of dopaminergic neurons, on stimulant induced locomotor <b>sensitization</b> and responding for CR.
+BDNF	drug	cocaine	10234039	In experiment 1, <strong>BDNF</strong> was infused into the nucleus accumbens (NAc) or ventral tegmental area over 2 weeks via chronically implanted minipumps (1 2.5 microgram/d), and the psychomotor stimulant effects of <b>cocaine</b> (5 15 mg/kg, i.p.)
+BDNF	drug	cocaine	10234039	We found that <strong>BDNF</strong> enhanced the initial stimulant effects of <b>cocaine</b> and seemed to facilitate the development of sensitization to repeated <b>cocaine</b> doses.
+BDNF	addiction	sensitization	10234039	We found that <strong>BDNF</strong> enhanced the initial stimulant effects of cocaine and seemed to facilitate the development of <b>sensitization</b> to repeated cocaine doses.
+BDNF	drug	cocaine	10234039	<strong>BDNF</strong> enhanced responding on the CR lever more than four times that seen in control animals after a <b>cocaine</b> injection (10 mg/kg, i.p.).
+BDNF	drug	cocaine	10234039	The enhanced response to <b>cocaine</b> in <strong>BDNF</strong> treated animals persisted for more than a month after the <strong>BDNF</strong> infusions had stopped, indicating long lasting changes in the mesolimbic DA system caused by <strong>BDNF</strong> administration.
+BDNF	drug	cocaine	10234039	In experiment 3, we examined locomotor sensitization to <b>cocaine</b> in heterozygous <strong>BDNF</strong> knock out mice and found that the development of sensitization was delayed compared with wild type littermates.
+BDNF	addiction	sensitization	10234039	In experiment 3, we examined locomotor <b>sensitization</b> to cocaine in heterozygous <strong>BDNF</strong> knock out mice and found that the development of <b>sensitization</b> was delayed compared with wild type littermates.
+BDNF	drug	cocaine	10234039	These results demonstrate the profound effects of <strong>BDNF</strong> on the enhancement of both <b>cocaine</b> induced locomotion and facilitation of CR and suggest a possible role for <strong>BDNF</strong> in long term adaptations of the brain to <b>cocaine</b>.
+BDNF	drug	alcohol	10212287	<strong>Brain derived neurotrophic factor</strong> mediates the anti apoptotic effect of NMDA in cerebellar granule neurons: signal transduction cascades and site of <b>ethanol</b> action.
+BDNF	addiction	dependence	10212287	NMDA treatment reduced caspase 3 like activity in cerebellar granule neurons, and the time course and concentration <b>dependence</b> of the protective effect of NMDA mirrored the ability of NMDA to induce brain derived neurotrophic factor (<strong>BDNF</strong>) expression.
+BDNF	addiction	dependence	10212287	NMDA treatment reduced caspase 3 like activity in cerebellar granule neurons, and the time course and concentration <b>dependence</b> of the protective effect of NMDA mirrored the ability of NMDA to induce <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) expression.
+BDNF	drug	alcohol	10212287	Furthermore, <b>ethanol</b>, which interferes with NMDA receptor function, inhibited the NMDA induced increase in <strong>BDNF</strong> levels but did not block the protective effect of <strong>BDNF</strong>.
+BDNF	drug	alcohol	10212287	These findings further support the role of <strong>BDNF</strong> in the anti apoptotic effect of NMDA in cerebellar granule neurons and suggest that the NMDA <strong>BDNF</strong> interaction may play a key role in in vivo cerebellar granule neuron development, as well as in the deleterious effects of <b>ethanol</b> on the developing cerebellum.
+BDNF	drug	alcohol	9918601	The changes in the immunolabeling of the CREB related target, that is, brain derived neurotrophic factor (<strong>BDNF</strong>), in the rat cortex during chronic <b>ethanol</b> treatment and its withdrawal (24 h) were examined using western blotting.
+BDNF	addiction	withdrawal	9918601	The changes in the immunolabeling of the CREB related target, that is, brain derived neurotrophic factor (<strong>BDNF</strong>), in the rat cortex during chronic ethanol treatment and its <b>withdrawal</b> (24 h) were examined using western blotting.
+BDNF	drug	alcohol	9918601	The changes in the immunolabeling of the CREB related target, that is, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), in the rat cortex during chronic <b>ethanol</b> treatment and its withdrawal (24 h) were examined using western blotting.
+BDNF	addiction	withdrawal	9918601	The changes in the immunolabeling of the CREB related target, that is, <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>), in the rat cortex during chronic ethanol treatment and its <b>withdrawal</b> (24 h) were examined using western blotting.
+BDNF	drug	alcohol	9918601	It was found that 24 h but not 0 h of <b>ethanol</b> withdrawal after 15 days of <b>ethanol</b> treatment caused a significant decrease in the immunolabeling of <strong>BDNF</strong> in the rat cortex.
+BDNF	addiction	withdrawal	9918601	It was found that 24 h but not 0 h of ethanol <b>withdrawal</b> after 15 days of ethanol treatment caused a significant decrease in the immunolabeling of <strong>BDNF</strong> in the rat cortex.
+BDNF	drug	alcohol	9918601	However, when fluoxetine was administered concurrently with <b>ethanol</b> treatment for 15 days, it caused a reversal of the anxiogenic effects of <b>ethanol</b> withdrawal and antagonized the down regulation of CRE DNA binding activity and of the decrease in immunolabeling of <strong>BDNF</strong> in the cortices of <b>ethanol</b> withdrawn rats.
+BDNF	addiction	withdrawal	9918601	However, when fluoxetine was administered concurrently with ethanol treatment for 15 days, it caused a reversal of the anxiogenic effects of ethanol <b>withdrawal</b> and antagonized the down regulation of CRE DNA binding activity and of the decrease in immunolabeling of <strong>BDNF</strong> in the cortices of ethanol withdrawn rats.
+BDNF	addiction	addiction	9852605	The neurotrophins brain derived neurotrophic factor (<strong>BDNF</strong>) and neurotrophin 3 (NT 3) and their receptors trkB and trkC, respectively, are expressed in the locus coeruleus (LC) and ventral tegmental area (VTA), brain regions known to be involved in opiate <b>addiction</b>.
+BDNF	addiction	addiction	9852605	The neurotrophins <strong>brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and neurotrophin 3 (NT 3) and their receptors trkB and trkC, respectively, are expressed in the locus coeruleus (LC) and ventral tegmental area (VTA), brain regions known to be involved in opiate <b>addiction</b>.
+BDNF	drug	opioid	9852605	In this study, <strong>BDNF</strong>, NT 3, trkB, and trkC mRNAs were analyzed in these regions after chronic <b>morphine</b> treatment and during antagonist precipitated withdrawal.
+BDNF	addiction	withdrawal	9852605	In this study, <strong>BDNF</strong>, NT 3, trkB, and trkC mRNAs were analyzed in these regions after chronic morphine treatment and during antagonist precipitated <b>withdrawal</b>.
+BDNF	drug	opioid	9852605	Although chronic <b>morphine</b> exposure resulted in only modest increases in <strong>BDNF</strong> and NT 3 mRNA expression in LC, precipitated withdrawal led to a marked, rapid, and prolonged increase in <strong>BDNF</strong> mRNA and a delayed decrease in NT 3 mRNA.
+BDNF	addiction	withdrawal	9852605	Although chronic morphine exposure resulted in only modest increases in <strong>BDNF</strong> and NT 3 mRNA expression in LC, precipitated <b>withdrawal</b> led to a marked, rapid, and prolonged increase in <strong>BDNF</strong> mRNA and a delayed decrease in NT 3 mRNA.
+BDNF	drug	alcohol	9541742	Brain derived neurotrophic factor (<strong>BDNF</strong>) and nerve growth factor (NGF) have previously been shown to ameliorate <b>ethanol</b> , hypoglycemia  and hypoxia induced neurotoxicity.
+BDNF	drug	alcohol	9541742	<strong>Brain derived neurotrophic factor</strong> (<strong>BDNF</strong>) and nerve growth factor (NGF) have previously been shown to ameliorate <b>ethanol</b> , hypoglycemia  and hypoxia induced neurotoxicity.
+BDNF	drug	alcohol	9541742	<strong>BDNF</strong> afforded similar protection, but not against <b>ethanol</b> + gwHG.
+BDNF	drug	alcohol	9541742	CNTF + <strong>BDNF</strong>, previously shown to act synergistically, protected against <b>ethanol</b> + aHP up to 800 mg/dl <b>ethanol</b>, but not, paradoxically, against <b>ethanol</b> alone, gwHG, or <b>ethanol</b> + gwHG, all conditions <strong>BDNF</strong> alone protected against.
+BDNF	drug	alcohol	8855333	This reduction in cell size was prevented by concomitant treatment of rats with <b>naltrexone</b>, an opioid receptor antagonist, as well as by intra VTA infusion of <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	opioid	8855333	This reduction in cell size was prevented by concomitant treatment of rats with naltrexone, an <b>opioid</b> receptor antagonist, as well as by intra VTA infusion of <strong>brain derived neurotrophic factor</strong>.
+BDNF	drug	alcohol	8666023	<strong>Brain derived neurotrophic factor</strong>, neurotrophin 3 and neurotrophin 4/5 maintain functional tolerance to <b>ethanol</b>.
+BDNF	drug	cocaine	8545003	<strong>Brain derived neurotrophic factor</strong>, which by itself tended to decrease tyrosine hydroxylase levels in the ventral tegmental area, prevented the characteristic increase in tyrosine hydroxylase following morphine and <b>cocaine</b> exposure and reversed the increase in rats pretreated with morphine.
+BDNF	drug	opioid	8545003	<strong>Brain derived neurotrophic factor</strong>, which by itself tended to decrease tyrosine hydroxylase levels in the ventral tegmental area, prevented the characteristic increase in tyrosine hydroxylase following <b>morphine</b> and cocaine exposure and reversed the increase in rats pretreated with <b>morphine</b>.
+BDNF	drug	opioid	8545003	Intra ventral tegmental area infusion of <strong>brain derived neurotrophic factor</strong> (or neurotrophin 4) alone tended to decrease cAMP dependent protein kinase and adenylyl cyclase activity in the nucleus accumbens and prevented the <b>morphine</b> induced increases in these enzymes.
+TNF	drug	opioid	32733481	<b>Opioids</b> bind to TLR4, in a manner parallel to LPS, activating TLR4 signaling, which leads to nuclear factor kappa light chain enhancer of activated B cells (NF κB) expression and the production of the pro inflammatory cytokines tumor necrosis factor (<strong>TNF</strong>) α, interleukin (IL) 1β, and IL 6.
+TNF	drug	opioid	32733481	<b>Opioids</b> bind to TLR4, in a manner parallel to LPS, activating TLR4 signaling, which leads to nuclear factor kappa light chain enhancer of activated B cells (NF κB) expression and the production of the pro inflammatory cytokines <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α, interleukin (IL) 1β, and IL 6.
+TNF	drug	opioid	32733481	The intracellular TLR4/<b>opioid</b> receptor signaling pathway crosstalk induces the formation of the β arrestin 2/<strong>TNF</strong> receptor associated factor 6 (TRAF6) complex, which contributes to <b>morphine</b> induced inhibition of LPS induced <strong>TNF</strong> α secretion in mast cells.
+TNF	drug	opioid	32524520	The <b>morphine</b> induced increases of apoptosis, neuron death, OS, lipid peroxidation, caspase 3 and caspase 9, neuroinflammatory cytokines (IL 1β, <strong>TNF</strong> α, IL 6), and Ca2+ levels in the hippocampal neuron of TRPM2 WT mouse were decreased by the L NAME, ACA, and 2 APB treatments, although cell viability, neuron count, and reduced glutathione and glutathione peroxidase levels were increased by the treatments.
+TNF	drug	opioid	32470337	This review focuses on the contributions of neuropeptide (CRF, melanocortin, <b>opioid</b> peptide) and cytokine (IL 1β, <strong>TNF</strong> α, chemokine) systems in the development and maintenance of substance induced hyperalgesia.
+TNF	drug	alcohol	32139808	Hippocampal <strong>TNF</strong> death receptors, caspase cell death cascades, and IL 8 in <b>alcohol</b> use disorder.
+TNF	addiction	intoxication	32139808	We report here that <strong>tumor necrosis factor</strong> receptor superfamily death receptor 3 (TNFRSF25, DR3) and Fas receptors (Fas) that initiate caspase cell death cascades are increased in AUD hippocampus and following a rat adolescent <b>binge</b> drinking model.
+TNF	drug	alcohol	32116558	Expression levels of inflammatory factors (<strong>TNF</strong> α, IL 1β, and IL 6) were increased in mice after 4 weeks of <b>alcohol</b> exposure.
+TNF	drug	amphetamine	32044305	Increased <strong>tumor necrosis factor</strong> α protein in the retina and elevated norepinephrine levels in plasma were found in <b>METH</b> treated mice.
+TNF	drug	amphetamine	31862507	<b>Methamphetamine</b> induced alterations in intestinal mucosal barrier function occur via the microRNA 181c/ <strong>TNF</strong> α/tight junction axis.
+TNF	drug	alcohol	31821337	Pulmonary and splenic cytokine expression (<strong>TNF</strong> α, GM CSF) remained suppressed, while IL 12/p40 increased in mice administered <b>alcohol</b> 6 or 24 h prior to infection.
+TNF	drug	alcohol	31759072	Acute <b>alcohol</b> consumption alters the peripheral cytokines IL 8 and <strong>TNF</strong> α.
+TNF	drug	alcohol	31759072	In contrast, the pro inflammatory cytokine <strong>TNF</strong> α significantly decreased 6 h after <b>alcohol</b> [F(1,34) =  3.07, p = 0.004, d' = 0.3].
+TNF	drug	alcohol	31759072	In our exploratory data, acute <b>alcohol</b> challenge (120 mg/dL) elicits dynamic changes in the pro inflammatory molecules IL 8 and <strong>TNF</strong> α.
+TNF	drug	alcohol	31747353	When <b>alcohol</b> was consumed for 8 weeks with LGG treatment during the last 2 weeks, we demonstrated that the dose dependence of LGG granules can improve <b>alcohol</b> induced liver injury through decreasing the levels of lipopolysaccharide and <strong>tumor necrosis factor</strong> α in serum and prevent liver steatosis by suppressing triglyceride, free fatty acid, and malondialdehyde production in liver.
+TNF	addiction	dependence	31747353	When alcohol was consumed for 8 weeks with LGG treatment during the last 2 weeks, we demonstrated that the dose <b>dependence</b> of LGG granules can improve alcohol induced liver injury through decreasing the levels of lipopolysaccharide and <strong>tumor necrosis factor</strong> α in serum and prevent liver steatosis by suppressing triglyceride, free fatty acid, and malondialdehyde production in liver.
+TNF	drug	alcohol	31736187	<b>Alcohol</b> craving and serum measures of <strong>tumor necrosis factor</strong> alpha (TNFα), <strong>tumor necrosis factor</strong> receptor 1 (TNFR1), interleukin 6 (IL 6), and interleukin 1 receptor antagonist (IL 1ra) were collected prior to and following imagery exposure.
+TNF	addiction	relapse	31736187	Alcohol <b>craving</b> and serum measures of <strong>tumor necrosis factor</strong> alpha (TNFα), <strong>tumor necrosis factor</strong> receptor 1 (TNFR1), interleukin 6 (IL 6), and interleukin 1 receptor antagonist (IL 1ra) were collected prior to and following imagery exposure.
+TNF	drug	alcohol	31736187	Stress induced suppression of pro inflammatory <strong>TNF</strong> markers may indicate a risk factor for <b>alcohol</b> dependent individuals with co occurring depressive symptoms.
+TNF	drug	alcohol	31666409	The effects of acute (single) and chronic <b>ethanol</b> administration on the level of pro inflammatory cytokines (IL 1β and <strong>TNF</strong> α), as well as on the level of mRNA NF κB, TLR4 and its endogenous agonist, HMGB1 protein, were investigated in rats.
+TNF	drug	opioid	31630319	Co administration of venlafaxine (40 mg/kg) with <b>morphine</b> not only inhibited the <b>naloxone</b> precipitated withdrawal signs including jumping and weight loss, but also reduced the up regulation of <strong>TNF</strong> α, IL 1β, IL 6, NO and MDA contents in mice brain tissue.
+TNF	addiction	withdrawal	31630319	Co administration of venlafaxine (40 mg/kg) with morphine not only inhibited the naloxone precipitated <b>withdrawal</b> signs including jumping and weight loss, but also reduced the up regulation of <strong>TNF</strong> α, IL 1β, IL 6, NO and MDA contents in mice brain tissue.
+TNF	drug	amphetamine	31396089	Ad libitum HRW consumption also had an inhibitory effect on the <b>METH</b> induced increase in the expression of Bax/Bcl 2, cleaved caspase 3, glucose related protein 78 (GRP 78), CCAAT/enhancer binding protein homologous protein (CHOP), and p NF kB p65 expression and elevation of interleukin (IL) 6 and tumor necrosis factor (<strong>TNF</strong>) α levels in the hippocampus.
+TNF	drug	amphetamine	31396089	Ad libitum HRW consumption also had an inhibitory effect on the <b>METH</b> induced increase in the expression of Bax/Bcl 2, cleaved caspase 3, glucose related protein 78 (GRP 78), CCAAT/enhancer binding protein homologous protein (CHOP), and p NF kB p65 expression and elevation of interleukin (IL) 6 and <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α levels in the hippocampus.
+TNF	drug	alcohol	31374324	The chronic binge <b>alcohol</b> administration increased the interferon (IFN) γ and tumor necrosis factor (<strong>TNF</strong>) α levels in the PFC and hippocampus and the interleukin (IL) 10 and BDNF levels in the PFC, and these effects were prevented by URB597.
+TNF	addiction	intoxication	31374324	The chronic <b>binge</b> alcohol administration increased the interferon (IFN) γ and tumor necrosis factor (<strong>TNF</strong>) α levels in the PFC and hippocampus and the interleukin (IL) 10 and BDNF levels in the PFC, and these effects were prevented by URB597.
+TNF	drug	alcohol	31374324	The chronic binge <b>alcohol</b> administration increased the interferon (IFN) γ and <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α levels in the PFC and hippocampus and the interleukin (IL) 10 and BDNF levels in the PFC, and these effects were prevented by URB597.
+TNF	addiction	intoxication	31374324	The chronic <b>binge</b> alcohol administration increased the interferon (IFN) γ and <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α levels in the PFC and hippocampus and the interleukin (IL) 10 and BDNF levels in the PFC, and these effects were prevented by URB597.
+TNF	drug	alcohol	31334440	In active drinkers, quantitative real time polymerase chain reaction revealed <b>alcohol</b> induced activation of <strong>tumor necrosis factor</strong> alpha, interleukin (IL) 1β, and nuclear factor kappa B in liver tissue already at early disease stages.
+TNF	addiction	withdrawal	31333398	We found that neuroinflammatory genes, notably <strong>Tnf</strong>, were upregulated in the <b>withdrawal</b> condition and that astrocytes, in particular, were highly active.
+TNF	drug	nicotine	31330570	Extinction and cue induced reinstatement of <b>nicotine</b> seeking was also associated with increased <strong>tumor necrosis factor</strong> alpha (TNFα) and decreased glial fibrillary acidic protein (GFAP) expression in the NAcore.
+TNF	addiction	relapse	31330570	Extinction and cue induced <b>reinstatement</b> of nicotine <b>seeking</b> was also associated with increased <strong>tumor necrosis factor</strong> alpha (TNFα) and decreased glial fibrillary acidic protein (GFAP) expression in the NAcore.
+TNF	drug	opioid	31209376	<b>Morphine</b> withdrawal driven synaptic plasticity and reduced sociability require tumor necrosis factor α (<strong>TNF</strong> α) release and neuronal <strong>TNF</strong> receptor 1 activation.
+TNF	addiction	withdrawal	31209376	Morphine <b>withdrawal</b> driven synaptic plasticity and reduced sociability require tumor necrosis factor α (<strong>TNF</strong> α) release and neuronal <strong>TNF</strong> receptor 1 activation.
+TNF	drug	opioid	31209376	<b>Morphine</b> withdrawal driven synaptic plasticity and reduced sociability require <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) release and neuronal <strong>TNF</strong> receptor 1 activation.
+TNF	addiction	withdrawal	31209376	Morphine <b>withdrawal</b> driven synaptic plasticity and reduced sociability require <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) release and neuronal <strong>TNF</strong> receptor 1 activation.
+TNF	drug	nicotine	31079306	In stratified models, gender, age, <b>smoking</b> status, and hypertension only led to small modifications in effect estimates, though a few of the estimates for IL 6 and <strong>TNF</strong> α became non significant.
+TNF	drug	amphetamine	31078920	We found that <b>METH</b> exposure increased LPS induced IL 6 and <strong>TNF</strong> α production in the Hip, CPU and NAc regions.
+TNF	drug	alcohol	30908665	Plasma alanine aminotransferase (ALT) and expression of liver <strong>TNF</strong> α were both significantly increased in the <b>alcohol</b> fed mice, which were normalized by ENP1.
+TNF	drug	nicotine	30815825	Table 1 Baseline characteristics of CD patients with primary nonresponse to subcutaneous (SC) tumor necrosis antagonists (<strong>TNF</strong>), subsequently treated with intravenous (IV) <strong>TNF</strong> therapy Characteristics N 17 Mean age, years (range) 37.5 (18 67) Mean BMI, kg/m2 (range) 26.6 (17.8 40.6) Mean albumin prior to infliximab, g/dL (range) RR: 3.5 5.2 g/dL 3.57 (2.5 4.2) Female sex [n (%)] 7 (41.2) <b>Tobacco</b> use [n (%)] Never 15 (88.2) Former 1 (5.88) Current 1 (5.88) Age at diagnosis [n (%)] Less than 17 2 (11.8) 17 40 11 (64.7) Over 40 4 (23.5) Mean disease duration, yrs (range) 7.76 (1 24) Disease extent [n (%)] Ileal 2 (11.8) Colonic 5 (29.4) Ileocolonic 10 (64.7) Disease behavior [n (%)] Nonstenosing, nonpenetrating 10 (58.8) Stenosing 3 (17.6) Penetrating 2 (11.8) Stenosing and penetrating 2 (11.8) History of gastrointestinal surgery [n (%)] 4 (23.5) Ileocecal resection (n) 2 Hemicolectomy (n) 2 Prior therapy [n (%)] IV corticosteroids 3 (17.6) Oral corticosteroids 14 (82.4) 5 ASA 12 (70.6) Thiopurine 14 (82.4) Methotrexate 10 (58.8) Prior biologic therapy Adalimumab only 12 (70.6) Certolizumab pegol only 2 (11.8) Adalimumab and certolizumab pegol 2 (11.8) Adalimumab, certolizumab pegol and golimumab 1 (5.88) Dose escalation of prior SC <strong>TNF</strong> [n (%)] Adalimumab 9 (52.9) Certolizumab pegol 0 (0.0) Golimumab 0 (0.0) During infliximab, concomitant therapy [n (%)] Immunomodulator 13 (76.5) Corticosteroid 5 (29.4) CONCLUSIONS: Patients with moderate severe CD with prior primary nonresponse to SC, fixed dose TNFs, subsequently treated with IV, weight based <strong>TNF</strong> have high rates of clinical and endoscopic response and remission.
+TNF	addiction	addiction	30815825	Table 1 Baseline characteristics of CD patients with primary nonresponse to subcutaneous (SC) tumor necrosis antagonists (<strong>TNF</strong>), subsequently treated with intravenous (IV) <strong>TNF</strong> therapy Characteristics N 17 Mean age, years (range) 37.5 (18 67) Mean BMI, kg/m2 (range) 26.6 (17.8 40.6) Mean albumin prior to infliximab, g/dL (range) RR: 3.5 5.2 g/dL 3.57 (2.5 4.2) Female sex [n (%)] 7 (41.2) Tobacco use [n (%)] Never 15 (88.2) Former 1 (5.88) Current 1 (5.88) Age at diagnosis [n (%)] Less than 17 2 (11.8) 17 40 11 (64.7) Over 40 4 (23.5) Mean disease duration, yrs (range) 7.76 (1 24) Disease extent [n (%)] Ileal 2 (11.8) Colonic 5 (29.4) Ileocolonic 10 (64.7) Disease behavior [n (%)] Nonstenosing, nonpenetrating 10 (58.8) Stenosing 3 (17.6) Penetrating 2 (11.8) Stenosing and penetrating 2 (11.8) History of gastrointestinal surgery [n (%)] 4 (23.5) Ileocecal resection (n) 2 Hemicolectomy (n) 2 Prior therapy [n (%)] IV corticosteroids 3 (17.6) Oral corticosteroids 14 (82.4) 5 ASA 12 (70.6) Thiopurine 14 (82.4) Methotrexate 10 (58.8) Prior biologic therapy Adalimumab only 12 (70.6) Certolizumab pegol only 2 (11.8) Adalimumab and certolizumab pegol 2 (11.8) Adalimumab, certolizumab pegol and golimumab 1 (5.88) Dose <b>escalation</b> of prior SC <strong>TNF</strong> [n (%)] Adalimumab 9 (52.9) Certolizumab pegol 0 (0.0) Golimumab 0 (0.0) During infliximab, concomitant therapy [n (%)] Immunomodulator 13 (76.5) Corticosteroid 5 (29.4) CONCLUSIONS: Patients with moderate severe CD with prior primary nonresponse to SC, fixed dose TNFs, subsequently treated with IV, weight based <strong>TNF</strong> have high rates of clinical and endoscopic response and remission.
+TNF	drug	amphetamine	30793820	The aim of this study was to assess whether CBD prevents reinstatement of <b>METH</b> through change of gene expression of cytokines such as interleukin 1β, interleukin 6, interleukin 10, and tumor necrosis factor α (<strong>TNF</strong> α) in extinguished rats.
+TNF	addiction	relapse	30793820	The aim of this study was to assess whether CBD prevents <b>reinstatement</b> of METH through change of gene expression of cytokines such as interleukin 1β, interleukin 6, interleukin 10, and tumor necrosis factor α (<strong>TNF</strong> α) in extinguished rats.
+TNF	drug	amphetamine	30793820	The aim of this study was to assess whether CBD prevents reinstatement of <b>METH</b> through change of gene expression of cytokines such as interleukin 1β, interleukin 6, interleukin 10, and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) in extinguished rats.
+TNF	addiction	relapse	30793820	The aim of this study was to assess whether CBD prevents <b>reinstatement</b> of METH through change of gene expression of cytokines such as interleukin 1β, interleukin 6, interleukin 10, and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) in extinguished rats.
+TNF	addiction	dependence	30787972	Results showed that EAE/CA/DHQ/KA prevented increases in liver index, ALT, AST, α SMA, collagen I, TβR1, Smad2/3, <strong>TNF</strong> α and p NF κB caused by CCL4 in dose <b>dependence</b>, they also improved the liver morphology, decreased inflammatory cell infiltration and collagenous fiber in dose <b>dependence</b>, CA' efficacy was best in mice; in LX 2, CA also decreased the expression of α SMA, collagen I, TGF β, Smad2/3.
+TNF	drug	opioid	30782159	Changes in brain gene expression levels of induced nitric oxide synthase (iNOS), enzyme responsible for nitric oxide generation, as well as pro inflammatory mediator, tumor necrosis alpha (<strong>TNF</strong> α) were measured in <b>morphine</b> tolerated animals, as well as after withdrawal by real time polymerase chain reaction (RT PCR).
+TNF	addiction	withdrawal	30782159	Changes in brain gene expression levels of induced nitric oxide synthase (iNOS), enzyme responsible for nitric oxide generation, as well as pro inflammatory mediator, tumor necrosis alpha (<strong>TNF</strong> α) were measured in morphine tolerated animals, as well as after <b>withdrawal</b> by real time polymerase chain reaction (RT PCR).
+TNF	drug	opioid	30782159	Increased mRNA expression of iNOS as well as <strong>TNF</strong> α mRNA expression and protein, after both <b>morphine</b> tolerance and withdrawal, were considerably reduced by glucosamine (1000 mg/kg) in the <b>morphine</b> withdrawal animals.
+TNF	addiction	withdrawal	30782159	Increased mRNA expression of iNOS as well as <strong>TNF</strong> α mRNA expression and protein, after both morphine tolerance and <b>withdrawal</b>, were considerably reduced by glucosamine (1000 mg/kg) in the morphine <b>withdrawal</b> animals.
+TNF	addiction	addiction	30701908	Dose <b>escalation</b> in our study required patients with high initial CDAI and previous inefficiencies of the other two inhibitors of <strong>TNF</strong> α.
+TNF	drug	cocaine	30654007	Effects of early life stress on <b>cocaine</b> conditioning and AMPA receptor composition are sex specific and driven by <strong>TNF</strong>.
+TNF	drug	cocaine	30654007	Since MS can elevate adolescent <strong>TNF</strong> levels, the stressor may therefore alter AMPAR subunit composition via neuroimmune signaling, thereby affecting <b>cocaine</b> induced CPP.
+TNF	addiction	reward	30654007	Since MS can elevate adolescent <strong>TNF</strong> levels, the stressor may therefore alter AMPAR subunit composition via neuroimmune signaling, thereby affecting cocaine induced <b>CPP</b>.
+TNF	drug	cocaine	30654007	We tested the specific role of soluble <strong>TNF</strong> in MS induced GluA2 loss and <b>cocaine</b> induced CPP with biologic disruption of <strong>TNF</strong> signaling.
+TNF	addiction	reward	30654007	We tested the specific role of soluble <strong>TNF</strong> in MS induced GluA2 loss and cocaine induced <b>CPP</b> with biologic disruption of <strong>TNF</strong> signaling.
+TNF	addiction	reward	30654007	Moreover, manipulation of the <strong>TNF</strong> signaling pathway represents a novel approach for influencing response to <b>reinforcing</b> effects of drug use.
+TNF	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 <strong>TNF</strong> α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+TNF	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 <strong>TNF</strong> α <strong>tumor necrosis factor</strong> α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+TNF	addiction	intoxication	30485380	Pulmonary cytokine expression (<strong>TNF</strong> α, GM CSF) decreased, while splenic cytokine (IL 10) increased in <b>binge</b> drunk mice.
+TNF	drug	amphetamine	30456731	H2S treatment could significantly increase both superoxide dismutase and glutathione (P < 0.01), and a reduction was observed in malondialdehyde (P < 0.05) and <strong>TNF</strong> α (P < 0.01) versus the <b>METH</b> group.
+TNF	drug	alcohol	30403751	The goal of this project was to establish the effect of <b>alcohol</b> consumption on the circulating levels of the adipose tissue derived protein C1q <strong>TNF</strong> Related Protein 3 (CTRP3).
+TNF	addiction	intoxication	30359672	Our previous study showed that both Kupffer cell eliminator (GdCl3) and tumor necrosis factor α (<strong>TNF</strong> α) receptor antagonist (etanercept) could partially attenuate <b>binge</b> drinking induced liver steatosis.
+TNF	addiction	intoxication	30359672	Our previous study showed that both Kupffer cell eliminator (GdCl3) and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) receptor antagonist (etanercept) could partially attenuate <b>binge</b> drinking induced liver steatosis.
+TNF	drug	alcohol	30359672	These results support the hypothesis that <strong>TNF</strong> α might make a small contribution to <b>ethanol</b> induced fatty liver by stimulating extrahepatic lipolysis.
+TNF	drug	amphetamine	30259275	Crocin treatment could significantly increase superoxide dismutase (P < 0.05) and glutathione (P < 0.01) levels and reduce malondialdehyde and <strong>TNF</strong> α in comparison with the <b>METH</b> group (P < 0.05).
+TNF	addiction	intoxication	30257399	Administration of PD prior to APAP <b>intoxication</b> significantly ameliorated the increase in serum transferases, interleukin 1β (IL 1β), IL 6, tumor necrosis factor alpha (<strong>TNF</strong> α), and hepatic malondialdehyde (MDA) and the depletion of glutathione (GSH) in mice.
+TNF	addiction	intoxication	30257399	Administration of PD prior to APAP <b>intoxication</b> significantly ameliorated the increase in serum transferases, interleukin 1β (IL 1β), IL 6, <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> α), and hepatic malondialdehyde (MDA) and the depletion of glutathione (GSH) in mice.
+TNF	drug	nicotine	30217256	Our data revealed that <b>nicotine</b> induced renal dysfunction manifested by significant abnormal levels of kidney function markers (creatinine and urea) accompanied by increased levels of oxidative stress biomarker (malondialdehyde) and inflammatory markers (nitric oxide, Interleukin 6 and <strong>tumor necrosis factor</strong> α) while antioxidant status as glutathione level and glutathione S transferase activity were found to be decreased significantly as compared with controls.
+TNF	drug	alcohol	30066901	In the present study, the anti‑AD effects of a 70% <b>ethanol</b> extract of TAEE were investigated in 2,4‑dinitrochlorobenzene (DNCB)‑treated mice with AD‑like skin lesions and in tumor necrosis factor (<strong>TNF</strong>)‑α‑ and interferon (IFN)‑γ‑stimulated human keratinocytes (HaCaT cells).
+TNF	drug	alcohol	30066901	In the present study, the anti‑AD effects of a 70% <b>ethanol</b> extract of TAEE were investigated in 2,4‑dinitrochlorobenzene (DNCB)‑treated mice with AD‑like skin lesions and in <strong>tumor necrosis factor</strong> (<strong>TNF</strong>)‑α‑ and interferon (IFN)‑γ‑stimulated human keratinocytes (HaCaT cells).
+TNF	addiction	withdrawal	30060508	However, it is often reversible after anti <strong>TNF</strong> α <b>withdrawal</b>.
+TNF	drug	alcohol	30060508	Anti <strong>TNF</strong> α agents have been tested in advanced stages of severe <b>alcoholic</b> hepatitis and non <b>alcoholic</b> fatty liver disease.
+TNF	drug	cannabinoid	30046349	Δ9 <b>THC</b>/sesame oil therapy showed similar effects to MTX in neutralizing the inflammatory process of AIA, through attenuating erythrocyte sedimentation rate (ESR) scores and proinflammatory cytokines, including tumor necrosis factor alpha (<strong>TNF</strong> α), interleukin 1 beta (IL 1β), and interleukin 6 (IL 6) levels, to normal values.
+TNF	drug	cannabinoid	30046349	Δ9 <b>THC</b>/sesame oil therapy showed similar effects to MTX in neutralizing the inflammatory process of AIA, through attenuating erythrocyte sedimentation rate (ESR) scores and proinflammatory cytokines, including <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> α), interleukin 1 beta (IL 1β), and interleukin 6 (IL 6) levels, to normal values.
+TNF	drug	nicotine	29906478	Increased oxidative stress by tramadol and/or <b>nicotine</b> sequentially augmented nuclear factor kappa B and the proinflammatory cytokine <strong>tumor necrosis factor</strong> α with the induction of apoptosis evident by the increased caspase 3 immunoreactivity.
+TNF	drug	opioid	29906478	Increased oxidative stress by <b>tramadol</b> and/or nicotine sequentially augmented nuclear factor kappa B and the proinflammatory cytokine <strong>tumor necrosis factor</strong> α with the induction of apoptosis evident by the increased caspase 3 immunoreactivity.
+TNF	drug	opioid	29892317	<b>Methadone</b> therapy was associated with lower MMP 9 and <strong>TNF</strong> α level, and higher SOD and catalase activities two weeks after therapy; showing an improvement in oxidative profile.
+TNF	drug	opioid	29729431	Coadministration of AM1241 (3 mg/kg) reduced the production of interleukin 1β, <strong>tumor necrosis factor</strong> α, and interleukin 6 induced by long term and acute <b>morphine</b> treatment.
+TNF	drug	opioid	29657246	The aim of the current study was to investigate the effects of those two modalities on pain behavior and the expression of pro inflammatory cytokines such as interleukin (IL) 1β and IL 6 and tumor necrosis factor α (<strong>TNF</strong> α) in the spinal cord and dorsal root ganglion (DRG) in a rat model of perioperative <b>fentanyl</b> induced hyperalgesia.
+TNF	drug	opioid	29657246	The aim of the current study was to investigate the effects of those two modalities on pain behavior and the expression of pro inflammatory cytokines such as interleukin (IL) 1β and IL 6 and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) in the spinal cord and dorsal root ganglion (DRG) in a rat model of perioperative <b>fentanyl</b> induced hyperalgesia.
+TNF	drug	alcohol	29656414	Symptom severity, <b>alcohol</b> use, cytokine (plasma <strong>tumor necrosis factor</strong> α and C reactive protein [CRP], transforming growth factor β1 [TGF β1], interleukin 8 [IL 8], IL 10), and plasma BDNF levels were regularly assessed.
+TNF	drug	cannabinoid	29607409	The <b>THC</b>+CBD strain was also associated with less desire to smoke, lower levels of subjective drug effects, and lower levels of circulating cytokines (<strong>TNF</strong> α, IL 6, and IL 1β) immediately after use.
+TNF	drug	alcohol	29445009	In vivo and in vitro binge <b>alcohol</b> exposure significantly inhibited the TLR4 MyD88 cytokines <strong>TNF</strong> α and IL 6, as well as the TLR4 TRIF cytokines/chemokines IFN β, IP 10, and RANTES, in human monocytes, but not TLR3 TRIF induced cytokines/chemokines, as detected by quantitative PCR and ELISA.
+TNF	addiction	intoxication	29445009	In vivo and in vitro <b>binge</b> alcohol exposure significantly inhibited the TLR4 MyD88 cytokines <strong>TNF</strong> α and IL 6, as well as the TLR4 TRIF cytokines/chemokines IFN β, IP 10, and RANTES, in human monocytes, but not TLR3 TRIF induced cytokines/chemokines, as detected by quantitative PCR and ELISA.
+TNF	addiction	relapse	29367619	Independent risk factors for S3 US steatosis in IBD patients at the multivariate logistic regression analysis were: more than 1 IBD <b>relapse</b> per year during disease history (OR 17.3, 95% CI 3.6 84), surgery for IBD (OR 15.1, 95% CI 3.1 73.7) and more extensive intestinal involvement (OR 19.4, 95% CI 3.4 110.9); the ongoing anti <strong>Tumor Necrosis Factor</strong> alpha (antiTNFα) therapy was the only independent factor which protect toward the presence of altered liver enzymes (OR 0.15, 95% CI 0 0.8, p = 0.02).
+TNF	drug	opioid	29135586	In this study, we tried to investigate behavioral hyperalgesia, the expression of proinflammatory cytokines, such as interleukin 1β (IL 1β), interleukin 6 (IL 6), and tumor necrosis factor α (<strong>TNF</strong> α), and the activation of microglia in the spinal cord and dorsal root ganglion (DRG) in a rat model of surgical plantar incision with or without perioperative <b>fentanyl</b>.
+TNF	drug	opioid	29135586	In this study, we tried to investigate behavioral hyperalgesia, the expression of proinflammatory cytokines, such as interleukin 1β (IL 1β), interleukin 6 (IL 6), and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α), and the activation of microglia in the spinal cord and dorsal root ganglion (DRG) in a rat model of surgical plantar incision with or without perioperative <b>fentanyl</b>.
+TNF	drug	opioid	29135586	The <b>fentanyl</b> or surgical incision upregulated the expression of IL 1β, IL 6, and <strong>TNF</strong> α in the spinal cord and bilateral DRG for more than 7 days and increase of ionized calcium binding adapter molecule 1 in the spinal cord.
+TNF	drug	opioid	29135586	The combination of <b>fentanyl</b> and incision resulted in higher increase of IL 1β, IL 6, and <strong>TNF</strong> α in the spinal cord and bilateral DRG.
+TNF	drug	opioid	29135586	The surgical plantar incision with or without perioperative <b>fentanyl</b> induced significant mechanical and thermal hyperalgesia, an increased expression of IL 1β, IL 6, <strong>TNF</strong> α in the spinal cord and DRG, and activation of microglia in the spinal cord.
+TNF	drug	alcohol	29113896	Neuroinflammation produced by heavy <b>alcohol</b> intake is due to loops of interactions between Toll like 4 and <strong>TNF</strong> receptors, peroxisome proliferator activated receptors and the central melanocortin system: A novel hypothesis and new therapeutic avenues.
+TNF	drug	alcohol	28965650	Concomitant with a delayed increase of plasma <strong>TNF</strong> α in <b>ethanol</b> treated mice, plasma PTX3 was also suppressed in the early phase of sepsis.
+TNF	drug	alcohol	28965650	Although <strong>TNF</strong> α level in <b>ethanol</b> treated mice exceeded that in saline treated mice 16 h after CLP, PTX3 levels were still suppressed in the former group.
+TNF	drug	alcohol	28965650	Furthermore, JNK phosphorylation in <b>ethanol</b> treated human umbilical vein endothelial cells was suppressed even in the presence of exogenous <strong>TNF</strong> α, resulting in inhibition of PTX3 mRNA and protein expression.
+TNF	drug	alcohol	28965650	Our results suggest that <b>ethanol</b> suppresses de novo PTX3 synthesis via two mechanisms   i.e., suppression of <strong>TNF</strong> α production and inhibition of JNK phosphorylation.
+TNF	drug	alcohol	28951767	Baicalin attenuated <b>ethanol</b> induced proinflammatory molecules such as <strong>TNF</strong> α, IL 1β, MIP 2, and MCP 1 and reversed redox sensitive transcription factor NF κB activation.
+TNF	addiction	intoxication	28882574	This study was designed to investigate the roles of KCs inhibitor (GdCl3) and <strong>TNF</strong> α antagonist (etanercept) on <b>binge</b> drinking induced liver steatosis and to explore the underlying mechanisms.
+TNF	addiction	intoxication	28882574	Taken together, KCs inhibitor and <strong>TNF</strong> α antagonist could partially attenuate <b>binge</b> drinking induced liver steatosis, which might be attributed to the suppression of mobilization of white adipose tissues.
+TNF	addiction	intoxication	28882574	These results suggest that KCs activation may promote <b>binge</b> drinking induced fatty liver by <strong>TNF</strong> α mediated activation of lipolysis in white adipose tissues.
+TNF	drug	cocaine	28813640	<b>Cocaine</b> self administration increased the expression of mRNA for the proinflammatory cytokine interleukin 1ß, but not <strong>tumor necrosis factor</strong> alpha, in the VTA.
+TNF	addiction	intoxication	28776218	Molecular pathology of cerebral <strong>TNF</strong> α, IL 1β, iNOS and Nrf2 in forensic autopsy cases with special regard to deaths due to environmental hazards and <b>intoxication</b>.
+TNF	drug	amphetamine	28776218	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of IL 1β, <strong>TNF</strong> α and iNOS, and lower expression of Nrf2 in <b>methamphetamine</b> intoxication and hyperthermia cases, higher expression of iNOS in phenobarbital intoxication cases, and higher expression of Nrf2 in phenobarbital intoxication and hypothermia cases.
+TNF	addiction	intoxication	28776218	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of IL 1β, <strong>TNF</strong> α and iNOS, and lower expression of Nrf2 in methamphetamine <b>intoxication</b> and hyperthermia cases, higher expression of iNOS in phenobarbital <b>intoxication</b> cases, and higher expression of Nrf2 in phenobarbital <b>intoxication</b> and hypothermia cases.
+TNF	drug	opioid	28750172	Transgenerational modification of hippocampus <strong>TNF</strong> α and S100B levels in the offspring of rats chronically exposed to <b>morphine</b> during adolescence.
+TNF	drug	opioid	28750172	We examined the consequences of chronic <b>morphine</b> consumption by parents before mating on hippocampus <strong>TNF</strong> α and S100B levels in the parents and their offspring.
+TNF	drug	opioid	28750172	Hippocampus <strong>TNF</strong> α levels were significantly increased due to chronic <b>morphine</b> use in both male and female parents compared to those of control parents (P < 0.01).
+TNF	drug	opioid	28750172	Moreover, both male and female offspring of <b>morphine</b> exposed parents showed a significant increase in hippocampus <strong>TNF</strong> α levels compared to those of control offspring (P < 0.01).
+TNF	drug	nicotine	28691127	It is worthy to note that <b>nicotine</b> toxicity induced significant increments in serum inflammatory markers: <strong>tumor necrosis factor</strong> α and vascular cell adhesion protein 1.
+TNF	drug	alcohol	28669319	Our aim is to describe changes in serum concentration for the pro inflammatory factors <strong>TNF</strong> α, IFN γ, IL 1β, IL 8, IL 6, IL 10, IL 12 and MCP 1, for the satiety factor leptin and for factors associated with neuronal changes, neuron specific enolase (NSE) and glial activation S100 beta protein (S100 β), and explore their association with abstinence in <b>alcohol</b> dependent subjects after withdrawal.
+TNF	addiction	withdrawal	28669319	Our aim is to describe changes in serum concentration for the pro inflammatory factors <strong>TNF</strong> α, IFN γ, IL 1β, IL 8, IL 6, IL 10, IL 12 and MCP 1, for the satiety factor leptin and for factors associated with neuronal changes, neuron specific enolase (NSE) and glial activation S100 beta protein (S100 β), and explore their association with abstinence in alcohol dependent subjects after <b>withdrawal</b>.
+TNF	drug	alcohol	28669319	The levels of <strong>TNF</strong> α, IL 1β, IL 8, IL 6, IL 12, MCP 1, and leptin decreased after withdrawal and remained low until M6, regardless of <b>alcohol</b> consumption.
+TNF	addiction	withdrawal	28669319	The levels of <strong>TNF</strong> α, IL 1β, IL 8, IL 6, IL 12, MCP 1, and leptin decreased after <b>withdrawal</b> and remained low until M6, regardless of alcohol consumption.
+TNF	addiction	withdrawal	28654797	Changes in brain gene expression levels of induced nitric oxide synthase (iNOS), astroglia marker, glial fibrillary acidic protein (GFAP), ionized calcium binding protein (Iba1) a microglia activation marker, a pro inflammatory mediator and tumor necrosis alpha (<strong>TNF</strong> α) were measured after <b>withdrawal</b> by real time polymerase chain reaction (RT PCR).
+TNF	drug	opioid	28654797	Administration of <b>naloxone</b> was associated with the increased expression of <strong>TNF</strong> α, GFAP, Iba1 and iNOS in the brain samples of <b>morphine</b> dependent mice, while the nine days treatment with both 5 and 10mg/kg simvastatin reduced such changes.
+TNF	drug	amphetamine	28621212	RAW264.7 macrophages tended to switch to the M1 phenotype, releasing more nitric oxide and proinflammatory cytokines, including <strong>tumor necrosis factor</strong> α (TNFα), interleukin (IL) 12, and IL 1β, while decreasing the release of anti inflammatory cytokine IL 10 after treatment with <b>Meth</b>.
+TNF	drug	amphetamine	28621212	<b>Meth</b> could also upregulate the protein expression of IL 1β and <strong>TNF</strong> α and downregulate the expression of Arg 1 and KLF4.
+TNF	drug	amphetamine	28552341	<b>Meth</b>/gp120 activated caspase 3 and increased caspase 3/7 activity in microglia and inhibition of caspase 3 by its specific inhibitor significantly decreased microglial production of <strong>TNF</strong> α and iNOS and attenuated microglia associated neurotoxic activity.
+TNF	drug	alcohol	28430931	In this study we investigated a possible association between alterations in the methylation of the BDNF IV/NGF I gene promoter and the cytokines tumor necrosis factor α (<strong>TNF</strong> α) and interleukin 6 (IL 6) in 55 male <b>alcohol</b> dependent patients.
+TNF	drug	alcohol	28430931	In this study we investigated a possible association between alterations in the methylation of the BDNF IV/NGF I gene promoter and the cytokines <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) and interleukin 6 (IL 6) in 55 male <b>alcohol</b> dependent patients.
+TNF	addiction	withdrawal	28430931	Mean methylation of the promoter of the BDNF gene was significantly associated with the <strong>TNF</strong> α serum levels and the CIWA score during <b>withdrawal</b> (P < 0.001).
+TNF	drug	alcohol	28408342	These data were supported by functional evidence since chronic <b>alcohol</b> consumption produced no changes in the expression of <strong>TNF</strong> α or COX 2.
+TNF	drug	alcohol	28386694	Although the exercise bout increased LPS stimulated production of <strong>TNF</strong> α (%change from PRE: 5 h POST 109%; 24 h POST 49%; 48 h POST 40%) and decreased LPS stimulated production of IL 8 (5 h POST  40%; 24 h POST  50%; 48 h POST:  43%) and IL 10 (5 h POST:  37%; 24 h POST  32%; 48 h POST  31%), consuming <b>alcohol</b> after exercise did not affect this response.
+TNF	drug	alcohol	28350851	Expression of liver mRNA <strong>tumor necrosis factor</strong> alpha (Tnfα), C X C motif chemokine ligand 1 (Cxcl1) and circulating protein monocyte chemoattractant protein 1 (MCP 1) were also reduced in antibiotic treated <b>alcohol</b> fed mice.
+TNF	drug	alcohol	28319836	These manifest as increased interleukin (IL) 6 and IκBα, and suppressed IL 1β and <strong>tumor necrosis factor</strong> alpha during acute <b>ethanol</b> intoxication.
+TNF	addiction	intoxication	28319836	These manifest as increased interleukin (IL) 6 and IκBα, and suppressed IL 1β and <strong>tumor necrosis factor</strong> alpha during acute ethanol <b>intoxication</b>.
+TNF	drug	alcohol	28257601	Overexpression of miR181b 3p decreased importin α5 expression and normalized lipopolysaccharide stimulated <strong>tumor necrosis factor</strong> α expression in Kupffer cells from <b>ethanol</b> fed rats.
+TNF	drug	amphetamine	28237710	Rats trained to self administer <b>METH</b> also presented a neuroinflammatory profile characterized by microglial activation, astrogliosis and increased pro inflammatory mediators, namely <strong>tumor necrosis factor</strong> alpha, interleukine 1 beta, and matrix metalloproteinase 9.
+TNF	drug	nicotine	28197102	We found that right cervical vagotomy inhibited the cholinergic anti inflammatory pathway, aggravated myocardial lesions, up regulated the expression of <strong>TNF</strong> α, IL 1β, and IL 6, and worsened the impaired left ventricular function in murine viral myocarditis, and these changes were reversed by co treatment with <b>nicotine</b> by activating the cholinergic anti inflammatory pathway.
+TNF	drug	alcohol	28147432	Measures of <strong>tumor necrosis factor</strong> alpha (TNFα), interleukin 6 (IL 6), interleukin 1 receptor antagonist (IL 1ra), <b>alcohol</b> craving, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+TNF	addiction	relapse	28147432	Measures of <strong>tumor necrosis factor</strong> alpha (TNFα), interleukin 6 (IL 6), interleukin 1 receptor antagonist (IL 1ra), alcohol <b>craving</b>, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+TNF	drug	alcohol	28131626	In the present study, we subjected adult male and female rats to different regimens of <b>alcohol</b> vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for <strong>tumor necrosis factor</strong> alpha (TNFα), interleukin 6 (IL 6), and chemokine (C C motif) ligand 2 (CCL2) in reward related brain regions.
+TNF	addiction	reward	28131626	In the present study, we subjected adult male and female rats to different regimens of alcohol vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for <strong>tumor necrosis factor</strong> alpha (TNFα), interleukin 6 (IL 6), and chemokine (C C motif) ligand 2 (CCL2) in <b>reward</b> related brain regions.
+TNF	drug	alcohol	28095363	Also, <b>alcohol</b> administration augmented lipid peroxidation, mitochondrial oxidized glutathione (GSSG), interleukin 1 beta (IL 1β), tumor necrosis factor alpha (<strong>TNF</strong> α) and Bax levels in isolated hippocampal tissues.
+TNF	drug	alcohol	28095363	Also, <b>alcohol</b> administration augmented lipid peroxidation, mitochondrial oxidized glutathione (GSSG), interleukin 1 beta (IL 1β), <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> α) and Bax levels in isolated hippocampal tissues.
+TNF	drug	alcohol	28087985	Hepatic toll like receptor mRNA expression and <strong>tumor necrosis factor</strong> alpha protein expression was induced by <b>ethanol</b>; however, the response was significantly dampened in mice co treated with tributyrin.
+TNF	addiction	withdrawal	28062186	We attempted to verify <b>withdrawal</b> regulation of induced nitric oxide synthase (iNOS), astroglia marker, glial fibrillary acidic protein (GFAP), ionized calcium binding protein (Iba1), a microglia activation marker, a pro inflammatory mediator, tumor necrosis alpha (<strong>TNF</strong> α) and immune receptor, toll like receptor 4 (TLR 4) genes by real time polymerase chain reaction (RT PCR).
+TNF	drug	opioid	28062186	Brain expression levels of <strong>TNF</strong> α, GFAP, Iba1 and iNOS increased in <b>morphine</b> withdrawn animals which were attenuated by nine days treatment with atorvastatin.
+TNF	drug	alcohol	27834881	SDS significantly inhibited protein secretion and mRNA expression of of interleukin (IL) 1β and tumor necrosis factor (<strong>TNF</strong>) α. Additionally C57BL/6 mice were orally administrated SDS for continuous 5 days, followed by three gavages of <b>ethanol</b> every 30 min.
+TNF	drug	alcohol	27834881	SDS significantly inhibited protein secretion and mRNA expression of of interleukin (IL) 1β and <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α. Additionally C57BL/6 mice were orally administrated SDS for continuous 5 days, followed by three gavages of <b>ethanol</b> every 30 min.
+TNF	drug	alcohol	27256567	<b>Alcohol</b> withdrawal partially restored the distribution of monocyte subsets and the frequency of IL 6 producing monocytes and increased the frequency of <strong>TNF</strong> producing cells in response to LPS and PGN stimulation to levels compared with those in HC.
+TNF	addiction	withdrawal	27256567	Alcohol <b>withdrawal</b> partially restored the distribution of monocyte subsets and the frequency of IL 6 producing monocytes and increased the frequency of <strong>TNF</strong> producing cells in response to LPS and PGN stimulation to levels compared with those in HC.
+TNF	drug	alcohol	27527870	<b>Ethanol</b> caused pancreatic inflammation which was indicated by the induction of <strong>TNF</strong> alpha, IL 1beta, IL 6, MCP 1 and CCR2, and the increase of CD68 positive macrophages in the pancreas.
+TNF	drug	opioid	27461080	Toll like Receptor 4 Mediates <b>Morphine</b> Induced Neuroinflammation and Tolerance via Soluble <strong>Tumor Necrosis Factor</strong> Signaling.
+TNF	drug	opioid	27461080	Tumor necrosis factor (<strong>TNF</strong>), a product of TLR4 signaling, promotes inflammation and facilitates glutamatergic signaling, key components of <b>opioid</b> tolerance.
+TNF	drug	opioid	27461080	<strong>Tumor necrosis factor</strong> (<strong>TNF</strong>), a product of TLR4 signaling, promotes inflammation and facilitates glutamatergic signaling, key components of <b>opioid</b> tolerance.
+TNF	drug	opioid	27461080	Therefore, we hypothesize that TLR4 mediated <b>opioid</b> tolerance requires <strong>TNF</strong> signaling.
+TNF	drug	opioid	27461080	By expression of a dominant negative <strong>TNF</strong> peptide via lentiviral vector injection in rat PAG to sequester soluble <strong>TNF</strong> (solTNF), we demonstrate that solTNF mediates <b>morphine</b> tolerance induced by TLR4 signaling, stimulates neuroinflammation (increased IL 1β and TLR4 mRNA), and disrupts glutamate reuptake (decreased GLT 1 and GLAST mRNA).
+TNF	addiction	intoxication	27455577	It was established in experiments on noninbred albino rats that the acute <b>intoxication</b> with methanol (1.0 LD50) decreased cellular and humoral immune responses, Th2 lymphocyte activity (to a greater extent as compared to the function of Th1 cells), reduced the blood concentration of immunoregulatory (IFN g, IL 2, IL 4) and proinflammatory (<strong>TNF</strong>, IL 1b, IL 6) cytokines on the average by 36.5% (p < 0.05), and did not affect the content of anti inflammatory cytokines (IL 10, IL 13).
+TNF	drug	alcohol	27455577	Methanol antidote 4 methylpyrazole (non competitive inhibitor of <b>alcohol</b> dehydrogenase) administered upon acute intoxication with methanol at a dose of 1.0 DL50 partially reduces the intoxication induced suppression of humoral and cellular immune response, activity of T helper cells, and production of IL 4 and restores blood levels of <strong>TNF</strong>, IL 1b, IFN γ, IL 4, IL 2, IL 6 to the control values.
+TNF	addiction	intoxication	27455577	Methanol antidote 4 methylpyrazole (non competitive inhibitor of alcohol dehydrogenase) administered upon acute <b>intoxication</b> with methanol at a dose of 1.0 DL50 partially reduces the <b>intoxication</b> induced suppression of humoral and cellular immune response, activity of T helper cells, and production of IL 4 and restores blood levels of <strong>TNF</strong>, IL 1b, IFN γ, IL 4, IL 2, IL 6 to the control values.
+TNF	addiction	withdrawal	27430907	Further, Pinellia ternata treatment reversed budesonide <b>withdrawal</b> induced increase of interleukin 1[Formula: see text] (IL 1[Formula: see text] and tumor necrosis factor [Formula: see text] (<strong>TNF</strong> [Formula: see text]) levels in bronchoalveolar lavage fluid (BALF).
+TNF	addiction	withdrawal	27430907	Further, Pinellia ternata treatment reversed budesonide <b>withdrawal</b> induced increase of interleukin 1[Formula: see text] (IL 1[Formula: see text] and <strong>tumor necrosis factor</strong> [Formula: see text] (<strong>TNF</strong> [Formula: see text]) levels in bronchoalveolar lavage fluid (BALF).
+TNF	drug	benzodiazepine	27352341	Continuous <b>midazolam</b> treatment induced a significant increase in plasma levels of gelsolin, heat shock protein 70, nitric oxide, superoxide dismutase, and <strong>tumor necrosis factor</strong> alpha (p < 0.05).
+TNF	drug	nicotine	27349339	UC patients experienced relapse during pregnancy more often than CD patients, independent of maternal age, <b>smoking</b>, periconceptional disease activity, previous IBD surgery, and the use of immunosuppressives or anti tumor necrosis factor (<strong>TNF</strong>) (aOR=3.71, 95% CI:1.86 7.40).
+TNF	addiction	relapse	27349339	UC patients experienced <b>relapse</b> during pregnancy more often than CD patients, independent of maternal age, smoking, periconceptional disease activity, previous IBD surgery, and the use of immunosuppressives or anti tumor necrosis factor (<strong>TNF</strong>) (aOR=3.71, 95% CI:1.86 7.40).
+TNF	drug	nicotine	27349339	UC patients experienced relapse during pregnancy more often than CD patients, independent of maternal age, <b>smoking</b>, periconceptional disease activity, previous IBD surgery, and the use of immunosuppressives or anti <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) (aOR=3.71, 95% CI:1.86 7.40).
+TNF	addiction	relapse	27349339	UC patients experienced <b>relapse</b> during pregnancy more often than CD patients, independent of maternal age, smoking, periconceptional disease activity, previous IBD surgery, and the use of immunosuppressives or anti <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) (aOR=3.71, 95% CI:1.86 7.40).
+TNF	drug	alcohol	27273552	Here, we examined the role of interleukin 1 (IL 1) and tumor necrosis factor α (<strong>TNF</strong> α) in regulation of voluntary <b>alcohol</b> consumption, <b>alcohol</b> reward and stress induced drinking.
+TNF	addiction	reward	27273552	Here, we examined the role of interleukin 1 (IL 1) and tumor necrosis factor α (<strong>TNF</strong> α) in regulation of voluntary alcohol consumption, alcohol <b>reward</b> and stress induced drinking.
+TNF	drug	alcohol	27273552	Here, we examined the role of interleukin 1 (IL 1) and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) in regulation of voluntary <b>alcohol</b> consumption, <b>alcohol</b> reward and stress induced drinking.
+TNF	addiction	reward	27273552	Here, we examined the role of interleukin 1 (IL 1) and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) in regulation of voluntary alcohol consumption, alcohol <b>reward</b> and stress induced drinking.
+TNF	drug	alcohol	27273552	We therefore hypothesized that double deletion of both IL 1RI and <strong>TNF</strong> 1 receptors (<strong>TNF</strong> 1R) may reveal the role of these pathways in regulation of <b>alcohol</b> intake.
+TNF	drug	alcohol	27273552	The combined deletion of <strong>TNF</strong> 1R and IL 1RI did not influence <b>alcohol</b> reward, but did prevent increased <b>alcohol</b> consumption resulting from exposure to repeated bouts of social defeat stress.
+TNF	addiction	reward	27273552	The combined deletion of <strong>TNF</strong> 1R and IL 1RI did not influence alcohol <b>reward</b>, but did prevent increased alcohol consumption resulting from exposure to repeated bouts of social defeat stress.
+TNF	drug	alcohol	27273552	Taken together, these data indicate that IL 1RI and <strong>TNF</strong> 1R contribute to regulation of stress induced, negatively reinforced drinking perhaps through overlapping signaling events downstream of these receptors, while leaving rewarding properties of <b>alcohol</b> largely unaffected.
+TNF	drug	alcohol	27260954	Frontline Science: ATF3 is responsible for the inhibition of <strong>TNF</strong> α release and the impaired migration of acute <b>ethanol</b> exposed monocytes and macrophages.
+TNF	drug	alcohol	27260954	We found that there was an inverse correlation between ATF3 and LPS induced <strong>TNF</strong> α production in acute <b>ethanol</b> pretreated murine monocytes and macrophages.
+TNF	drug	alcohol	27260954	The knockdown of ATF3 attenuated the inhibitory effects of acute <b>ethanol</b> treatment on LPS induced <strong>TNF</strong> α production.
+TNF	addiction	intoxication	27260954	In <b>binge</b> drinking mice challenged with LPS, an up regulation of ATF3 and HDAC1 and a concomitant decrease in <strong>TNF</strong> α were observed.
+TNF	drug	alcohol	27260954	Our results revealed that TSA treatment and HDAC1 knockdown prevented acute <b>ethanol</b> induced ATF3 expression and the inhibition of <strong>TNF</strong> α transcription.
+TNF	drug	alcohol	27240410	Specifically, double binge rats had greater OX 42 immunoreactivity, increased ionized calcium binding adapter molecule 1 (Iba 1+) cells, and upregulated tumor necrosis factor α (<strong>TNF</strong> α) compared with the single binge <b>ethanol</b> group.
+TNF	addiction	intoxication	27240410	Specifically, double <b>binge</b> rats had greater OX 42 immunoreactivity, increased ionized calcium binding adapter molecule 1 (Iba 1+) cells, and upregulated tumor necrosis factor α (<strong>TNF</strong> α) compared with the single <b>binge</b> ethanol group.
+TNF	drug	alcohol	27240410	Specifically, double binge rats had greater OX 42 immunoreactivity, increased ionized calcium binding adapter molecule 1 (Iba 1+) cells, and upregulated <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) compared with the single binge <b>ethanol</b> group.
+TNF	addiction	intoxication	27240410	Specifically, double <b>binge</b> rats had greater OX 42 immunoreactivity, increased ionized calcium binding adapter molecule 1 (Iba 1+) cells, and upregulated <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) compared with the single <b>binge</b> ethanol group.
+TNF	drug	alcohol	27208497	Acute <b>ethanol</b> intoxication is associated with Rapid Alterations in Neuroimmune Gene Expression (RANGE), including increased Interleukin (IL) 6 and Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (IκBα), and suppressed IL 1β and Tumor necrosis factor (<strong>TNF</strong>) α, yet little is known about adaptations in cytokines across the first few <b>ethanol</b> exposures.
+TNF	addiction	intoxication	27208497	Acute ethanol <b>intoxication</b> is associated with Rapid Alterations in Neuroimmune Gene Expression (RANGE), including increased Interleukin (IL) 6 and Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (IκBα), and suppressed IL 1β and Tumor necrosis factor (<strong>TNF</strong>) α, yet little is known about adaptations in cytokines across the first few ethanol exposures.
+TNF	drug	alcohol	27208497	Acute <b>ethanol</b> intoxication is associated with Rapid Alterations in Neuroimmune Gene Expression (RANGE), including increased Interleukin (IL) 6 and Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (IκBα), and suppressed IL 1β and <strong>Tumor necrosis factor</strong> (<strong>TNF</strong>) α, yet little is known about adaptations in cytokines across the first few <b>ethanol</b> exposures.
+TNF	addiction	intoxication	27208497	Acute ethanol <b>intoxication</b> is associated with Rapid Alterations in Neuroimmune Gene Expression (RANGE), including increased Interleukin (IL) 6 and Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (IκBα), and suppressed IL 1β and <strong>Tumor necrosis factor</strong> (<strong>TNF</strong>) α, yet little is known about adaptations in cytokines across the first few ethanol exposures.
+TNF	drug	alcohol	27177528	Functional inhibition of SYK activation using a potent SYK inhibitor, R406, was associated with a significant decrease in <b>alcohol</b> induced hepatic inflammation as demonstrated by decreased phospho nuclear factor kappa beta (NF κB) p65, NF κB nuclear binding, <strong>tumor necrosis factor</strong> alpha, and monocyte chemoattractant protein 1 mRNA in the liver.
+TNF	drug	cocaine	27112496	Microglial <strong>TNF</strong> α Suppresses <b>Cocaine</b> Induced Plasticity and Behavioral Sensitization.
+TNF	addiction	sensitization	27112496	Microglial <strong>TNF</strong> α Suppresses Cocaine Induced Plasticity and Behavioral <b>Sensitization</b>.
+TNF	drug	cocaine	27112496	Here we show that repeated administration of <b>cocaine</b> activates striatal microglia and induces <strong>TNF</strong> α production, which in turn depresses glutamatergic synaptic strength in the NAc core and limits the development of behavioral sensitization.
+TNF	addiction	sensitization	27112496	Here we show that repeated administration of cocaine activates striatal microglia and induces <strong>TNF</strong> α production, which in turn depresses glutamatergic synaptic strength in the NAc core and limits the development of behavioral <b>sensitization</b>.
+TNF	drug	cocaine	27112496	Critically, following a period of abstinence, a weak TLR4 agonist can reactivate microglia, increase <strong>TNF</strong> α production, depress striatal synaptic strength, and suppress <b>cocaine</b> induced sensitization.
+TNF	addiction	sensitization	27112496	Critically, following a period of abstinence, a weak TLR4 agonist can reactivate microglia, increase <strong>TNF</strong> α production, depress striatal synaptic strength, and suppress cocaine induced <b>sensitization</b>.
+TNF	drug	alcohol	27058374	Effect of 15% <b>Alcohol</b> Dependence on Alveolar Bone Loss and <strong>TNF</strong> α Secretion in Wistar Rats.
+TNF	addiction	dependence	27058374	Effect of 15% Alcohol <b>Dependence</b> on Alveolar Bone Loss and <strong>TNF</strong> α Secretion in Wistar Rats.
+TNF	drug	alcohol	27058374	The aim of the present study was to evaluate the effect of 15% <b>alcohol</b> dependence on ligature induced alveolar bone loss and <strong>TNF</strong> α secretion in Wistar rats.
+TNF	addiction	dependence	27058374	The aim of the present study was to evaluate the effect of 15% alcohol <b>dependence</b> on ligature induced alveolar bone loss and <strong>TNF</strong> α secretion in Wistar rats.
+TNF	drug	alcohol	27058374	It may be concluded that 15% <b>alcohol</b> dependency was not capable to alter alveolar bone loss and <strong>TNF</strong> α secretion in Wistar rats.
+TNF	drug	nicotine	27018116	<b>Smoking</b> cessation reduced the risk of flaring, regardless of exposure to anti <strong>tumor necrosis factor</strong> agents.
+TNF	drug	alcohol	26996510	Furthermore, both <b>alcohol</b> exposed and SI animals had increased levels of pro inflammatory cytokines IL 1β, <strong>TNF</strong> α, CD11b, and CCL4; in addition, CCL4 was significantly increased in <b>alcohol</b> exposed animals compared to SI as well.
+TNF	drug	alcohol	26857094	Elevations in plasma tumor necrosis factor alpha (<strong>TNF</strong> α) and IL 1β after <b>ethanol</b> were also inhibited by OEA.
+TNF	drug	alcohol	26857094	Elevations in plasma <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> α) and IL 1β after <b>ethanol</b> were also inhibited by OEA.
+TNF	drug	nicotine	26856753	Our aim was to evaluate the current impact of TS on disease relapse and the clinical benefit of quitting <b>smoking</b> in the present era of widespread use of anti <strong>TNF</strong> drugs and immunosuppressants.
+TNF	addiction	relapse	26856753	Our aim was to evaluate the current impact of TS on disease <b>relapse</b> and the clinical benefit of quitting smoking in the present era of widespread use of anti <strong>TNF</strong> drugs and immunosuppressants.
+TNF	drug	nicotine	26856753	In the time dependent analysis, continuing <b>smokers</b> had earlier relapse, regardless of anti <strong>TNF</strong> or immunosuppressant use.
+TNF	addiction	relapse	26856753	In the time dependent analysis, continuing smokers had earlier <b>relapse</b>, regardless of anti <strong>TNF</strong> or immunosuppressant use.
+TNF	addiction	sensitization	26773297	This <b>sensitization</b> enhances the production of various proinflammatory cytokines such as interleukin 1 (IL 1) and <strong>tumor necrosis factor</strong> alpha, thereby contributing to hepatocyte dysfunction, necrosis, and apoptosis and the generation of extracellular matrix proteins leading to fibrosis/cirrhosis.
+TNF	addiction	dependence	26679346	EUF patients did not differ from B2 group regarding anti <strong>TNF</strong> therapy (p = 0.956) and steroid <b>dependence</b> or resistance (p = 0.141).
+TNF	drug	alcohol	26603732	Effects were measured using Western blotting, luciferase reporter assays, fluorescence microscopy and ELISA KEY RESULTS: (+) <b>Naltrexone</b> and (+) naloxone were equi potent inhibitors of the LPS induced TLR4 downstream signalling and induction of the pro inflammatory factors NO and <strong>TNF</strong> α.
+TNF	drug	opioid	26603732	Effects were measured using Western blotting, luciferase reporter assays, fluorescence microscopy and ELISA KEY RESULTS: (+) Naltrexone and (+) <b>naloxone</b> were equi potent inhibitors of the LPS induced TLR4 downstream signalling and induction of the pro inflammatory factors NO and <strong>TNF</strong> α.
+TNF	drug	psychedelics	26589393	Relationship of serum levels of <strong>TNF</strong> α, IL 6 and IL 18 and schizophrenia like symptoms in chronic <b>ketamine</b> abusers.
+TNF	drug	psychedelics	26589393	This study aims to examine the serum <strong>TNF</strong> α, IL 6 and IL 18 levels in chronic human <b>ketamine</b> users as compared to healthy subjects.
+TNF	drug	psychedelics	26589393	Serum IL 6 and IL 18 levels were significantly higher, while serum <strong>TNF</strong> α level was significantly lower among <b>ketamine</b> users than among healthy controls (p<0.05).
+TNF	drug	psychedelics	26589393	Serum levels of <strong>TNF</strong> α, IL 6 and IL 18 were altered in chronic <b>ketamine</b> abusers which may play a role in schizophrenia like symptoms in chronic <b>ketamine</b> abusers.
+TNF	addiction	addiction	26511478	The primary endpoint was failure of thiopurine therapy, defined as treatment with steroids, therapeutic <b>escalation</b> to <strong>TNF</strong> alpha antagonist therapy, or need for surgery.
+TNF	addiction	addiction	26368325	When endoscopic recurrence is identified during follow up, upscaling to anti <strong>TNF</strong> or dose <b>escalation</b> is advocated.
+TNF	drug	amphetamine	26322025	In addition, the serum pro inflammatory (<strong>TNF</strong>, IL12 p70, IL1β, IL 6, and KC GRO) and Th2 (IL 2, IL 10, and IL 4) cytokine profiles were also altered in the presence of <b>METH</b>.
+TNF	drug	alcohol	26178909	In addition, CAE evidently suppressed inflammation and apoptosis in the livers of mice administered with <b>ethanol</b>, by 85% (<strong>tumor necrosis factor</strong> α) and 44% compared to the control group, respectively.
+TNF	addiction	relapse	26075832	Systematic review: factors associated with <b>relapse</b> of inflammatory bowel disease after discontinuation of anti <strong>TNF</strong> therapy.
+TNF	addiction	relapse	26075832	To evaluate the factors associated with <b>relapse</b> of IBD after discontinuation of anti <strong>TNF</strong> therapy.
+TNF	addiction	relapse	26075832	Mucosal healing seems to decrease the risk of <b>relapse</b> after anti <strong>TNF</strong> discontinuation (overall, this risk is 26% at 1 year with mucosal healing and 42% without), although this observation has not been confirmed by some authors.
+TNF	addiction	relapse	26075832	In patients receiving escalated anti <strong>TNF</strong> doses or receiving anti TNFs for the prevention of post operative CD recurrence, the risk of <b>relapse</b> after discontinuation is high (>75%).
+TNF	addiction	relapse	26075832	A high proportion of patients with IBD <b>relapse</b> after discontinuation of anti <strong>TNF</strong> treatment.
+TNF	drug	alcohol	26062839	The aim of this study is to determine the effect of <b>alcohol</b> consumption on the levels of subgingival periodontal pathogens and proinflammatory cytokines (interleukin [IL] 1β and tumor necrosis factor [<strong>TNF</strong>] α) in the gingival fluid among individuals with and without periodontitis.
+TNF	drug	alcohol	26062839	The aim of this study is to determine the effect of <b>alcohol</b> consumption on the levels of subgingival periodontal pathogens and proinflammatory cytokines (interleukin [IL] 1β and <strong>tumor necrosis factor</strong> [<strong>TNF</strong>] α) in the gingival fluid among individuals with and without periodontitis.
+TNF	addiction	sensitization	25960750	Farnesol supplementation significantly (P < 0.05) restored the cytokine secretion ability of peritoneal macrophages that was suppressed as a result of OVA <b>sensitization</b> and challenge and slightly decreased tumor necrosis factor (<strong>TNF</strong> α)/IL 10 cytokine secretion ratios.
+TNF	addiction	sensitization	25960750	Farnesol supplementation significantly (P < 0.05) restored the cytokine secretion ability of peritoneal macrophages that was suppressed as a result of OVA <b>sensitization</b> and challenge and slightly decreased <strong>tumor necrosis factor</strong> (<strong>TNF</strong> α)/IL 10 cytokine secretion ratios.
+TNF	drug	alcohol	25915743	<b>Alcohol</b>+HFD treatment also increased the inflammation (CD45+, CD68+, F4/80+ cells; tumour necrosis factor alpha (<strong>TNF</strong> α), F4/80 mRNAs) and fibrogenesis (vimentin+ activated stellate cells, collagen 1 (Col1) production, transforming growth factor beta (TGF β) and Col 1 mRNAs) in mice livers.
+TNF	addiction	addiction	25874518	Azathioprine discontinuation earlier than 6 months in Crohn's disease patients started on anti <strong>TNF</strong> therapy is associated with loss of response and the need for anti <strong>TNF</strong> dose <b>escalation</b>.
+TNF	addiction	addiction	25874518	We aimed to prospectively determine the predictors and frequency of anti <strong>TNF</strong> loss of response and therefore the need for dose <b>escalation</b> and de <b>escalation</b> in CD patients treated with infliximab or adalimumab.
+TNF	addiction	addiction	25874518	In patients initially responding to anti <strong>TNF</strong> and subsequently losing clinical response after the first 14 weeks of therapy, dose <b>escalation</b> was scheduled.
+TNF	drug	nicotine	25874518	Factors associated with loss of response and therefore the need for anti <strong>TNF</strong> dose escalation were azathioprine discontinuation earlier than 6 months and <b>smoking</b>.
+TNF	addiction	addiction	25874518	Factors associated with loss of response and therefore the need for anti <strong>TNF</strong> dose <b>escalation</b> were azathioprine discontinuation earlier than 6 months and smoking.
+TNF	drug	nicotine	25874518	Azathioprine discontinuation earlier than 6 months and <b>smoking</b> in CD patients started on anti <strong>TNF</strong> therapy is associated with loss of response and the need for anti <strong>TNF</strong> dose escalation.
+TNF	addiction	addiction	25874518	Azathioprine discontinuation earlier than 6 months and smoking in CD patients started on anti <strong>TNF</strong> therapy is associated with loss of response and the need for anti <strong>TNF</strong> dose <b>escalation</b>.
+TNF	drug	opioid	25846801	Various regimens of <b>morphine</b> reduced TWI, cortisol levels, Bax activity, caspase 3, caspase 9, <strong>TNF</strong> α, and IL 1β and lipid peroxidation.
+TNF	drug	cocaine	25762940	The plasma concentrations of interleukin 1 beta (IL 1β), IL 6, IL 10, and <strong>tumor necrosis factor</strong> alpha (TNFα) were affected by history of <b>cocaine</b> addiction and sex.
+TNF	addiction	addiction	25762940	The plasma concentrations of interleukin 1 beta (IL 1β), IL 6, IL 10, and <strong>tumor necrosis factor</strong> alpha (TNFα) were affected by history of cocaine <b>addiction</b> and sex.
+TNF	drug	alcohol	25703252	The serum Adip and tumor necrosis factor alpha (<strong>TNF</strong> α) as well as liver Adip receptors (AdipoR1 and AdipoR2) SIRT1, AMPK, phosphorylated AMPK (p AMPK), sterol regulatory element binding proteins (SREBPs), acetyl CoA carboxylase (ACC), LIP 1, lipocalin 2 (LCN2), and serum amyloid A1 were assessed in the rat model where 16 weeks of gavaged <b>alcohol</b> were administered.
+TNF	drug	alcohol	25703252	The serum Adip and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> α) as well as liver Adip receptors (AdipoR1 and AdipoR2) SIRT1, AMPK, phosphorylated AMPK (p AMPK), sterol regulatory element binding proteins (SREBPs), acetyl CoA carboxylase (ACC), LIP 1, lipocalin 2 (LCN2), and serum amyloid A1 were assessed in the rat model where 16 weeks of gavaged <b>alcohol</b> were administered.
+TNF	drug	amphetamine	25678251	Rats that self administered <b>methamphetamine</b> had a lower frequency of CD4(+) T cells, but more of these cells produced IFN γ. <b>Methamphetamine</b> did not alter the frequency of <strong>TNF</strong> α producing CD4(+) T cells.
+TNF	drug	amphetamine	25678251	<b>Methamphetamine</b> using rats had a higher frequency of CD8(+) T cells, but fewer of them produced <strong>TNF</strong> α. CD11b/c and CD200 expression were unchanged.
+TNF	drug	amphetamine	25678251	Serum cytokine levels of IFN γ, <strong>TNF</strong> α and IL 6 in <b>methamphetamine</b> rats were unchanged.
+TNF	drug	amphetamine	25678251	<b>Methamphetamine</b> lifetime dose inversely correlated with serum <strong>TNF</strong> α levels.
+TNF	drug	opioid	25660662	We tested the cytokine production of IL 1β, IL 6, IL 8, IL 10 and tumor necrosis factor (<strong>TNF</strong>) α from a group of <b>heroin</b> addicts (n=34) and healthy controls (n=20).
+TNF	drug	opioid	25660662	We tested the cytokine production of IL 1β, IL 6, IL 8, IL 10 and <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α from a group of <b>heroin</b> addicts (n=34) and healthy controls (n=20).
+TNF	drug	opioid	25660662	Plasma <strong>TNF</strong> α and IL 6 levels were significantly correlated with the dairy <b>methadone</b> dosage administered, and the IL 1β level was significantly correlated with the duration of <b>methadone</b> maintenance treatment.
+TNF	drug	opioid	25477192	The impact of anti <strong>TNF</strong>, corticosteroid and analgesic therapy on inflammation and pain was evaluated in a novel mono arthritic multi flare rat Streptococcal Cell Wall (SCW) model using Etanercept, Dexamethasone and <b>Buprenorphine</b>.
+TNF	drug	opioid	25446875	The increase in <strong>TNF</strong> α and IL 1β expression induced by chronic <b>morphine</b> exposure was also partially blocked by PDTC pretreatment.
+TNF	addiction	addiction	25350768	The health states included medical remission (azathioprine or antitumor necrosis factor (anti <strong>TNF</strong>), dose <b>escalation</b> of an anti <strong>TNF</strong>, second anti <strong>TNF</strong>, surgery, and death.
+TNF	drug	alcohol	25262503	<strong>TNF</strong> α and IL 6 serum levels: neurobiological markers of <b>alcohol</b> consumption in <b>alcohol</b> dependent patients?
+TNF	drug	alcohol	25262503	We investigated the serum levels of IL 6 and <strong>TNF</strong> α in 30 male <b>alcohol</b> dependent patients during withdrawal (day 1, 7, and 14) and compared them with the levels obtained from 18 healthy male controls.
+TNF	addiction	withdrawal	25262503	We investigated the serum levels of IL 6 and <strong>TNF</strong> α in 30 male alcohol dependent patients during <b>withdrawal</b> (day 1, 7, and 14) and compared them with the levels obtained from 18 healthy male controls.
+TNF	addiction	withdrawal	25262503	<strong>TNF</strong> α (T = 3,202, p = 0.03) serum levels were significantly elevated in the patients' group during the whole period of <b>withdrawal</b>.
+TNF	addiction	withdrawal	25262503	IL 6 serum levels decreased significantly during <b>withdrawal</b> (F = 16.507, p < 0.001), whereas <strong>TNF</strong> α levels did not change significantly (day 1 14).
+TNF	drug	alcohol	25262503	We found an association with the duration of active drinking following the last period of abstinence and the <strong>TNF</strong> α serum levels (day 1:r = 0.354, p = 0.009; day 7: r = 0.323, p = 0.022; day 14: r = 0.303, p = 0.034) as well as an association with the severity of <b>alcohol</b> dependence measured by the SESA scale (r = 0.454, p = 0.015).
+TNF	addiction	dependence	25262503	We found an association with the duration of active drinking following the last period of abstinence and the <strong>TNF</strong> α serum levels (day 1:r = 0.354, p = 0.009; day 7: r = 0.323, p = 0.022; day 14: r = 0.303, p = 0.034) as well as an association with the severity of alcohol <b>dependence</b> measured by the SESA scale (r = 0.454, p = 0.015).
+TNF	drug	alcohol	25262503	Our results support an association between alterations in <strong>TNF</strong> α and IL 6 serum levels and <b>alcohol</b> consumption.
+TNF	drug	opioid	25249941	Maladaptive plasticity is linked to processes that involve kappa <b>opioids</b>, the metabotropic glutamate (mGlu) receptor, glia, and the cytokine tumor necrosis factor (<strong>TNF</strong>).
+TNF	drug	opioid	25249941	Maladaptive plasticity is linked to processes that involve kappa <b>opioids</b>, the metabotropic glutamate (mGlu) receptor, glia, and the cytokine <strong>tumor necrosis factor</strong> (<strong>TNF</strong>).
+TNF	drug	alcohol	25180626	Serum and hepatic triglyceride levels as well as tumor necrosis factor (<strong>TNF</strong>) α mRNA were markedly increased in all <b>ethanol</b> treated OLETF rats.
+TNF	drug	alcohol	25180626	Serum and hepatic triglyceride levels as well as <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α mRNA were markedly increased in all <b>ethanol</b> treated OLETF rats.
+TNF	drug	alcohol	25162931	CMZ also suppressed <b>ethanol</b> induced decline of serum adiponectin level, but did not significantly affect the serum tumor necrosis factor α (<strong>TNF</strong> α) and <b>ethanol</b> levels.
+TNF	drug	alcohol	25162931	CMZ also suppressed <b>ethanol</b> induced decline of serum adiponectin level, but did not significantly affect the serum <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) and <b>ethanol</b> levels.
+TNF	addiction	intoxication	25156612	Although cytokine  and region dependent central IL 6 expression was generally increased and <strong>tumor necrosis factor</strong> alpha decreased during <b>intoxication</b>, IL 1 expression exhibited increases during withdrawal.
+TNF	addiction	withdrawal	25156612	Although cytokine  and region dependent central IL 6 expression was generally increased and <strong>tumor necrosis factor</strong> alpha decreased during intoxication, IL 1 expression exhibited increases during <b>withdrawal</b>.
+TNF	drug	alcohol	25024384	In vitro pre exposure to moderate <b>alcohol</b> reduced subsequent LPS induced NF κB promoter activity and downstream <strong>TNF</strong> α, IL 6 and IL 1β production in monocytes and macrophages, exhibiting endotoxin tolerance.
+TNF	drug	alcohol	25024384	Mechanistic analysis demonstrates that <b>alcohol</b> induced HSF1 binds to the <strong>TNF</strong> α promoter in macrophages at early time points, exerting transrepression and decreased <strong>TNF</strong> α expression.
+TNF	drug	nicotine	24969287	Options for remission maintenance include <b>smoking</b> cessation, thiopurines, methotrexate, anti <strong>TNF</strong> α drugs and surgery.
+TNF	drug	cocaine	24854157	<strong>Tumor necrosis factor</strong> alpha, chemokine (C C motif) ligand 2/monocyte chemotactic protein 1 and chemokine (C X C motif) ligand 12 (CXCL12)/stromal cell derived factor 1 (SDF 1) were decreased in <b>cocaine</b> users, although all cytokines were identified as predictors of a lifetime pathological use of <b>cocaine</b>.
+TNF	drug	opioid	24845379	Upregulation of <strong>tumor necrosis factor</strong> alpha in nucleus accumbens attenuates <b>morphine</b> induced rewarding in a neuropathic pain model.
+TNF	addiction	reward	24845379	The inhibitory effect of SNI on MOR induced <b>CPP</b> was blocked by either genetic deletion of <strong>TNF</strong> receptor 1 (TNFR1) or microinjection of anti <strong>TNF</strong> α into the NAcc and was mimicked by intra NAcc injection of <strong>TNF</strong> α in sham rats.
+TNF	addiction	relapse	24738574	The evidence for prophylactic anti <strong>TNF</strong> use is limited though promising, with its routine use guided by early assessment of <b>relapse</b>.
+TNF	drug	cocaine	24631195	Early life stress and <strong>tumor necrosis factor</strong> superfamily in crack <b>cocaine</b> withdrawal.
+TNF	addiction	withdrawal	24631195	Early life stress and <strong>tumor necrosis factor</strong> superfamily in crack cocaine <b>withdrawal</b>.
+TNF	drug	cocaine	24631195	Considering the role of the tumor necrosis factor system in inflammatory signaling and its association with ELS, the aim of the study was to compare plasma levels of <strong>TNF</strong> alpha, its soluble receptors and ligands during early abstinence of crack <b>cocaine</b>.
+TNF	drug	cocaine	24631195	Considering the role of the <strong>tumor necrosis factor</strong> system in inflammatory signaling and its association with ELS, the aim of the study was to compare plasma levels of <strong>TNF</strong> alpha, its soluble receptors and ligands during early abstinence of crack <b>cocaine</b>.
+TNF	drug	cocaine	24631195	This is the first study to evaluate the newly secreted <strong>tumor necrosis factor</strong> superfamily ligands, TWEAK and TRAIL, during crack <b>cocaine</b> abstinence, supporting the association between early life stress and peripheral pro inflammatory levels.
+TNF	drug	alcohol	24283421	<b>Ethanol</b> intoxication altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (AMPK), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (<strong>TNF</strong> α) expression.
+TNF	addiction	intoxication	24283421	Ethanol <b>intoxication</b> altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (AMPK), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (<strong>TNF</strong> α) expression.
+TNF	drug	alcohol	24283421	<b>Ethanol</b> intoxication altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (AMPK), and nuclear factor kappa B cells (NFκB) and by an increase in <strong>tumor necrosis factor</strong> (<strong>TNF</strong> α) expression.
+TNF	addiction	intoxication	24283421	Ethanol <b>intoxication</b> altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (AMPK), and nuclear factor kappa B cells (NFκB) and by an increase in <strong>tumor necrosis factor</strong> (<strong>TNF</strong> α) expression.
+TNF	drug	opioid	24257399	Intrathecal ultra low dose <b>naloxone</b> enhances the antihyperalgesic effects of <b>morphine</b> and attenuates <strong>tumor necrosis factor</strong> α and <strong>tumor necrosis factor</strong> α receptor 1 expression in the dorsal horn of rats with partial sciatic nerve transection.
+TNF	drug	opioid	24257399	We designed this investigation to examine whether ultra low dose <b>naloxone</b> administered alone or in combination with <b>morphine</b> could alter the concentration of the excitatory amino acids (EAAs) glutamate and aspartate, as well as the expression of tumor necrosis factor α (<strong>TNF</strong> α) and its receptors (TNFR1 and TNFR2) in the spinal cord dorsal horn of rats with partial sciatic nerve transection (PST).
+TNF	drug	opioid	24257399	We designed this investigation to examine whether ultra low dose <b>naloxone</b> administered alone or in combination with <b>morphine</b> could alter the concentration of the excitatory amino acids (EAAs) glutamate and aspartate, as well as the expression of <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) and its receptors (TNFR1 and TNFR2) in the spinal cord dorsal horn of rats with partial sciatic nerve transection (PST).
+TNF	addiction	withdrawal	24257399	Thermal <b>withdrawal</b> latency and mechanical <b>withdrawal</b> threshold, <strong>TNF</strong> α and TNFR expression in the spinal cord and dorsal root ganglia, and EAAs glutamate and aspartate concentration in cerebrospinal fluid dialysates were measured.
+TNF	drug	opioid	24257399	The antihyperalgesic and antiallodynic effects of <b>morphine</b> (10 μg) were abolished by high dose <b>naloxone</b> (15 μg; P = 0.0031) but enhanced by ultra low dose <b>naloxone</b> (15 ng; P = 0.0015), and this was associated with a reduction of <strong>TNF</strong> α (P < 0.0001) and TNFR1 (P = 0.0009) expression in the spinal cord dorsal horn and EAAs concentration (glutamate: P = 0.0001; aspartate: P = 0.004) in cerebrospinal fluid dialysate.
+TNF	drug	opioid	24257399	Ultra low dose <b>naloxone</b> enhances the antihyperalgesia and antiallodynia effects of <b>morphine</b> in PST rats, possibly by reducing <strong>TNF</strong> α and TNFR1 expression, and EAAs concentrations in the spinal dorsal horn.
+TNF	drug	alcohol	24224954	Chronic <b>alcohol</b> exposure results in liver injury that is driven in part by inflammatory cytokines such as tumor necrosis factor α (<strong>TNF</strong>).
+TNF	drug	alcohol	24224954	Chronic <b>alcohol</b> exposure results in liver injury that is driven in part by inflammatory cytokines such as <strong>tumor necrosis factor</strong> α (<strong>TNF</strong>).
+TNF	drug	alcohol	24224954	Hepatocytes are normally resistant to the cytotoxic effects of <strong>TNF</strong>, but they become sensitized to <strong>TNF</strong> by chronic <b>alcohol</b> exposure.
+TNF	drug	alcohol	24224954	Recently, we reported that the decrease in the ratio of S adenosylmethionine (SAM) to S adenosylhomocysteine (SAH) that occurs with <b>alcoholic</b> liver injury renders hepatocytes sensitive to <strong>TNF</strong> cytotoxicity.
+TNF	drug	alcohol	24163503	Acute <b>ethanol</b> intoxication further increased serum levels of GOT, GPT, BUN, Cre, LDH, CPK, <strong>TNF</strong>  α and IL 6 elevation following HS.
+TNF	addiction	intoxication	24163503	Acute ethanol <b>intoxication</b> further increased serum levels of GOT, GPT, BUN, Cre, LDH, CPK, <strong>TNF</strong>  α and IL 6 elevation following HS.
+TNF	drug	alcohol	24070686	Searching for causes of altered vitamin levels, we also assessed liver function, nutritional status, eating habits, <b>alcohol</b> intake, proinflammatory cytokine (<strong>TNF</strong> α, IL 6, IL 8) levels and malondialdehyde (MDA) levels.
+TNF	drug	opioid	23968971	To further define the interaction between CCL5 and inflammation in response to <b>opioids</b>, we have examined the effect of chronic <b>morphine</b> and <b>morphine</b> withdrawal on the in vivo expression of CCL5 as well as of pro inflammatory cytokines interleukin 1β (IL 1β) and tumor necrosis factor α (<strong>TNF</strong> α).
+TNF	addiction	withdrawal	23968971	To further define the interaction between CCL5 and inflammation in response to opioids, we have examined the effect of chronic morphine and morphine <b>withdrawal</b> on the in vivo expression of CCL5 as well as of pro inflammatory cytokines interleukin 1β (IL 1β) and tumor necrosis factor α (<strong>TNF</strong> α).
+TNF	drug	opioid	23968971	To further define the interaction between CCL5 and inflammation in response to <b>opioids</b>, we have examined the effect of chronic <b>morphine</b> and <b>morphine</b> withdrawal on the in vivo expression of CCL5 as well as of pro inflammatory cytokines interleukin 1β (IL 1β) and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α).
+TNF	addiction	withdrawal	23968971	To further define the interaction between CCL5 and inflammation in response to opioids, we have examined the effect of chronic morphine and morphine <b>withdrawal</b> on the in vivo expression of CCL5 as well as of pro inflammatory cytokines interleukin 1β (IL 1β) and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α).
+TNF	drug	alcohol	23968971	No changes were observed in the levels of IL 1β and <strong>TNF</strong> α. <b>Naltrexone</b> blocked the effect of morphine.
+TNF	drug	opioid	23968971	No changes were observed in the levels of IL 1β and <strong>TNF</strong> α. Naltrexone blocked the effect of <b>morphine</b>.
+TNF	drug	alcohol	23828825	Serum samples were collected to measure blood <b>ethanol</b>, aspartate transferase, alanine transferase, creatine phosphokinase, lactate dehydrogenase, amylase, tumor necrosis factor alpha (<strong>TNF</strong> α) and interleukin 6 (IL 6) levels.
+TNF	drug	alcohol	23828825	Serum samples were collected to measure blood <b>ethanol</b>, aspartate transferase, alanine transferase, creatine phosphokinase, lactate dehydrogenase, amylase, <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> α) and interleukin 6 (IL 6) levels.
+TNF	drug	opioid	23796752	Here, we characterized the receptor proximal signaling events that link μ <b>opioid</b> receptors to activation of Akt and ERKs in lipopolysaccharide (LPS) stimulated murine microglial cells with the aim to define the molecular mechanism contributing to the ability of <b>morphine</b> to increase inflammatory mediators such as nitric oxide (NO), tumor necrosis factor (<strong>TNF</strong>) α, interleukin (IL) 1β and IL 6 in activated microglial cells.
+TNF	drug	opioid	23796752	Here, we characterized the receptor proximal signaling events that link μ <b>opioid</b> receptors to activation of Akt and ERKs in lipopolysaccharide (LPS) stimulated murine microglial cells with the aim to define the molecular mechanism contributing to the ability of <b>morphine</b> to increase inflammatory mediators such as nitric oxide (NO), <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α, interleukin (IL) 1β and IL 6 in activated microglial cells.
+TNF	drug	opioid	23796752	Furthermore, we found that <b>morphine</b> enhanced the release of IL 1β, <strong>TNF</strong> α, IL 6, and of NO via μ <b>opioid</b> receptor PKCɛ signaling pathway in activated microglial cells, mediating a proinflammatory phenotype in mouse microglial cells.
+TNF	drug	benzodiazepine	23707757	Ammonia, <b>diazepam</b> and pro inflammatory cytokines such as tumor necrosis factor α (<strong>TNF</strong> α), interferon γ, interleukin 1β induced within 20min astrocyte swelling by about 25% accompanied by nuclear swelling of similar magnitude.
+TNF	drug	benzodiazepine	23707757	Ammonia, <b>diazepam</b> and pro inflammatory cytokines such as <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α), interferon γ, interleukin 1β induced within 20min astrocyte swelling by about 25% accompanied by nuclear swelling of similar magnitude.
+TNF	drug	benzodiazepine	23707757	Astrocyte swelling in response to NH4Cl, <strong>TNF</strong> α or <b>diazepam</b> was abolished by the antioxidant epigallocatechin gallate pointing to an involvement of RNOS.
+TNF	drug	alcohol	23701841	In this paradigm, <b>ethanol</b> did not affect mRNA levels of the cytokines IL 6 or <strong>TNF</strong> α in any of these brain regions in aged animals.
+TNF	drug	alcohol	23532958	Here, we show that chronic plus binge <b>ethanol</b> feeding synergistically up regulated the hepatic expression of interleukin 1β and <strong>tumor necrosis factor</strong> alpha and induced neutrophil accumulation in the liver, compared with chronic or binge feeding alone.
+TNF	addiction	intoxication	23532958	Here, we show that chronic plus <b>binge</b> ethanol feeding synergistically up regulated the hepatic expression of interleukin 1β and <strong>tumor necrosis factor</strong> alpha and induced neutrophil accumulation in the liver, compared with chronic or <b>binge</b> feeding alone.
+TNF	drug	alcohol	23428594	LPS levels increased in peripheral and portal venous plasma (p < 0.05), but mucosal TLR4, TBK1, nuclear NF κB, IFN γ and <strong>TNF</strong> α were unchanged in the <b>ethanol</b> group.
+TNF	drug	alcohol	23428594	LPS treatment in vitro up regulated the level of TLR4, TBK1 and nuclear NF κB as well as the production of IFN γ and <strong>TNF</strong> α in isolated intestinal epithelia in the control (p < 0.05), but not the <b>ethanol</b> group.
+TNF	drug	alcohol	23421770	<b>Ethanol</b> feeding increased hepatic CYP2E1 level, nuclear accumulation of NF κB p65 and <strong>TNF</strong> α expression in rats.
+TNF	drug	alcohol	23421770	Compared with LPS alone, the <b>ethanol</b> induction group produced significantly more <strong>TNF</strong> α, nuclear NF κB p65 and less cytoplasm IκB α under LPS stimuli.
+TNF	drug	alcohol	23421770	CMZ abolished the effects of <b>ethanol</b> on LPS stimulated NF κB translocation and <strong>TNF</strong> α generation in Kupffer cells.
+TNF	drug	alcohol	23421770	In cultured Kupffer cell, using CMZ as inhibitor, <b>ethanol</b> induced CYP2E1 overexpression was proved to contribute to the sensitization of Kupffer cells to LPS stimuli, with amplification of ROS production and activation of NF κB, resulting in increased <strong>TNF</strong> α production.
+TNF	addiction	sensitization	23421770	In cultured Kupffer cell, using CMZ as inhibitor, ethanol induced CYP2E1 overexpression was proved to contribute to the <b>sensitization</b> of Kupffer cells to LPS stimuli, with amplification of ROS production and activation of NF κB, resulting in increased <strong>TNF</strong> α production.
+TNF	drug	opioid	23352192	LPS induced protein expression of <strong>TNF</strong> α, IL 1β, and IL  6 was examined in the spleen of rats with and without <b>morphine</b> tolerance.
+TNF	drug	opioid	23352192	LPS induced IL 1β and <strong>TNF</strong> α protein expression was significantly lower in the spleen of the <b>morphine</b> tolerant animals than in the placebo control animals.
+TNF	drug	opioid	23352192	In response to LPS, expression of 27 genes, including NLRP3, <strong>TNF</strong> α, IL 1β, and IL 6, was significantly increased, and expression of 3 genes was significantly decreased in both the <b>morphine</b> tolerant and placebo control groups compared to the saline treated animals.
+TNF	drug	opioid	23224818	Thus, the aim of this investigation was to assess hippocampal levels of BDNF, oxidative stress markers associated with cell viability, and <strong>TNF</strong> α in the short, medium and long term after repeated <b>morphine</b> treatment in early life.
+TNF	drug	opioid	23047422	Using blood from preterm (≤ 30 weeks gestational age (GA), n=7) and full term (≥ 37 weeks GA, n=19) infants, we investigated the changes in cytokine profile (IL 1β, IL 6, IL 8, IL 10, IL 12p70 and <strong>TNF</strong> α), cyclic adenosine monophosphate (cAMP) levels and μ , δ  and κ  <b>opioid</b> receptor (OPR) gene and protein expression, following in vitro exposure to <b>morphine</b>, <b>methadone</b>, <b>fentanyl</b> or clonidine at increasing concentrations ranging from 0 to 1 mM.
+TNF	drug	opioid	23022502	Using immunohistochemical staining, we demonstrated the administration of MC4R during the induction of <b>morphine</b> tolerance inhibited the activation of astrocytes; reduced the expression of proinflammatory cytokines interleukin 1β, IL 6, and <strong>tumor necrosis factor</strong> α; upregulated the expression of anti inflammatory cytokines IL 10 at the L5 lumbar spinal cord.
+TNF	drug	opioid	22990619	Plasma <strong>TNF</strong> α and IL 8 levels were significantly higher in long term <b>heroin</b> dependent patients than in healthy controls (p < 0.001).
+TNF	drug	opioid	22990619	Chronic <b>heroin</b> use induced <strong>TNF</strong> α and IL 8 levels were significantly (p < 0.05) attenuated in patients treated for 12 weeks with add on dextromethorphan.
+TNF	drug	opioid	22919361	We summarize those neurochemical mechanisms associated with <b>opioid</b> withdrawal including the recently defined importance of TNFα release from activated glial cells that communicate with <strong>TNF</strong> receptors on PAG neurons.
+TNF	addiction	withdrawal	22919361	We summarize those neurochemical mechanisms associated with opioid <b>withdrawal</b> including the recently defined importance of TNFα release from activated glial cells that communicate with <strong>TNF</strong> receptors on PAG neurons.
+TNF	drug	amphetamine	22903344	The present results showed that <b>METH</b> significantly increased inducible nitric oxide synthase (iNOS) expression in a concentration dependent manner and significantly increased the levels of tumor necrosis factor (<strong>TNF</strong>) α mRNA and phosphorylated NF κB, which is translocated into the nucleus.
+TNF	drug	amphetamine	22903344	The present results showed that <b>METH</b> significantly increased inducible nitric oxide synthase (iNOS) expression in a concentration dependent manner and significantly increased the levels of <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) α mRNA and phosphorylated NF κB, which is translocated into the nucleus.
+TNF	drug	amphetamine	22903344	The results show that melatonin significantly decreases the iNOS protein expression and <strong>TNF</strong> α mRNA levels caused by <b>METH</b>.
+TNF	drug	alcohol	22782967	Acute <b>alcohol</b> binge results in immunosuppression and impaired production of proinflammatory cytokines, including <strong>TNF</strong> α. <strong>TNF</strong> α production is induced by LPS, a TLR4 ligand, and is tightly regulated at various levels of the signaling cascade, including the NF κB transcription factor.
+TNF	addiction	intoxication	22782967	Acute alcohol <b>binge</b> results in immunosuppression and impaired production of proinflammatory cytokines, including <strong>TNF</strong> α. <strong>TNF</strong> α production is induced by LPS, a TLR4 ligand, and is tightly regulated at various levels of the signaling cascade, including the NF κB transcription factor.
+TNF	drug	alcohol	22782967	We found that acute <b>alcohol</b> pretreatment resulted in the same attenuating effect as LPS pretreatment on TLR4 induced <strong>TNF</strong> α production in human monocytes and murine RAW 264.7 macrophages.
+TNF	drug	alcohol	22782967	ChIP assays revealed increased occupancy of Bcl 3 and p50 at the promoter region of <strong>TNF</strong> α in <b>alcohol</b> pretreated cells.
+TNF	drug	alcohol	22782967	To confirm that the Bcl 3 p50 complex regulates transcription/production of <strong>TNF</strong> α during acute <b>alcohol</b> exposure, we inhibited Bcl 3 expression using a targeted siRNA.
+TNF	drug	alcohol	22782967	Bcl 3 knockdown prevented the <b>alcohol</b> induced inhibition of <strong>TNF</strong> α mRNA and protein production.
+TNF	drug	alcohol	22782967	In a mouse model of binge <b>alcohol</b>, an increase in Bcl 3 and a concomitant decrease in <strong>TNF</strong> α but no change in IL 10 production were found in mice that received <b>alcohol</b> followed by LPS challenge.
+TNF	addiction	intoxication	22782967	In a mouse model of <b>binge</b> alcohol, an increase in Bcl 3 and a concomitant decrease in <strong>TNF</strong> α but no change in IL 10 production were found in mice that received alcohol followed by LPS challenge.
+TNF	drug	alcohol	22782967	In summary, our novel data suggest that acute <b>alcohol</b> treatment in vitro and in vivo induces molecular signatures of TLR4/LPS tolerance through the induction of Bcl 3, a negative regulator of <strong>TNF</strong> α transcription via its association with NF κB p50/p50 dimers.
+TNF	drug	alcohol	22626265	For qRT PCR studies, we measured the expression of <strong>TNF</strong> α, NOS 2, Ccl2 (MCP 1), MHC II invariant chain CD74, and the <strong>TNF</strong> receptor Tnfrsf1a in CeA and DVC samples from adult male rats exposed to a liquid <b>alcohol</b> diet for thirty five days and in similarly treated animals at four hours and forty eight hours following <b>alcohol</b> withdrawal.
+TNF	addiction	withdrawal	22626265	For qRT PCR studies, we measured the expression of <strong>TNF</strong> α, NOS 2, Ccl2 (MCP 1), MHC II invariant chain CD74, and the <strong>TNF</strong> receptor Tnfrsf1a in CeA and DVC samples from adult male rats exposed to a liquid alcohol diet for thirty five days and in similarly treated animals at four hours and forty eight hours following alcohol <b>withdrawal</b>.
+TNF	drug	alcohol	22626265	Following a chronic <b>alcohol</b> exposure, withdrawal resulted in a statistically significant increase in the expression of mRNAs specific for innate immune markers Ccl2, <strong>TNF</strong> α, NOS 2, Tnfrsf1a, and CD74.
+TNF	addiction	withdrawal	22626265	Following a chronic alcohol exposure, <b>withdrawal</b> resulted in a statistically significant increase in the expression of mRNAs specific for innate immune markers Ccl2, <strong>TNF</strong> α, NOS 2, Tnfrsf1a, and CD74.
+TNF	addiction	withdrawal	22626265	Confocal IHC of samples taken 48 hours into <b>withdrawal</b> demonstrate the presence of <strong>TNF</strong> α staining surrounding cells expressing the neural marker NeuN and endothelial cells colabeled with ICAM 1 (CD54) and RECA 1, markers associated with an inflammatory response.
+TNF	drug	alcohol	22626265	This study demonstrates the rapid induction of Ccl2, <strong>TNF</strong> α, NOS 2, Tnfrsf1a and CD74 expression during <b>alcohol</b> withdrawal in both the CeA and DVC.
+TNF	addiction	withdrawal	22626265	This study demonstrates the rapid induction of Ccl2, <strong>TNF</strong> α, NOS 2, Tnfrsf1a and CD74 expression during alcohol <b>withdrawal</b> in both the CeA and DVC.
+TNF	addiction	withdrawal	22626265	IHC dual labeling showed an increase in <strong>TNF</strong> α surrounding neurons and ICAM 1 on vascular endothelial cells 48 hours into <b>withdrawal</b>, confirming the inflammatory response at the protein level.
+TNF	drug	alcohol	22563259	Cilostazol Decreases <b>Ethanol</b> Mediated <strong>TNFalpha</strong> Expression in RAW264.7 Murine Macrophage and in Liver from Binge Drinking Mice.
+TNF	addiction	intoxication	22563259	Cilostazol Decreases Ethanol Mediated <strong>TNFalpha</strong> Expression in RAW264.7 Murine Macrophage and in Liver from <b>Binge</b> Drinking Mice.
+TNF	drug	alcohol	22563259	<b>Alcoholic</b> hepatitis is a leading cause of liver failure in which the increased production of <strong>tumor necrosis factor</strong> α (TNFα) plays a critical role in progression of <b>alcoholic</b> liver disease.
+TNF	addiction	sensitization	22518321	Induction of miR 155 contributed to increased <strong>TNF</strong> alpha production and to the <b>sensitization</b> of KCs to produce more <strong>TNF</strong> alpha in response to LPS.
+TNF	drug	cannabinoid	22496569	<strong>Tumor necrosis factor</strong> activation of vagal afferent terminal calcium is blocked by <b>cannabinoids</b>.
+TNF	addiction	sensitization	22496569	Our previous work has shown that <strong>TNF</strong> action to excite vagal afferents occurs as a result of <b>sensitization</b> of ryanodine channels in afferent nerve terminals.
+TNF	drug	cannabinoid	22496569	Laser confocal calcium imaging methods were used to directly examine effects of CB1 <b>cannabinoid</b> agonists and <strong>TNF</strong> on visceral afferent signaling in the rat hindbrain.
+TNF	drug	cannabinoid	22496569	These results help to explain the effectiveness of <b>cannabinoids</b> in blocking the malaise generated by <strong>TNF</strong> releasing disease processes by opposing effects on ryanodine channels.
+TNF	drug	opioid	22428664	We examined the effects of µ <b>opioid</b> and CB(2) receptor stimulation on phosphorylation of MAPKs and Akt and on IL 1β, <strong>TNF</strong> α, IL 6 and NO production in primary mouse microglial cells.
+TNF	drug	opioid	22428664	<b>Morphine</b> enhanced release of the proinflammatory cytokines, IL 1β, <strong>TNF</strong> α, IL 6, and of NO via µ <b>opioid</b> receptor in activated microglial cells.
+TNF	drug	opioid	22366510	Moreover, the administration of LXA4ME during the induction of <b>morphine</b> tolerance inhibited the activation of microglia and astrocytes; reduced the expression of proinflammatory cytokines interleukin 1β (IL 1β), IL 6, and tumor necrosis factor α (<strong>TNF</strong> α); upregulated the expression of anti inflammatory cytokines IL 10 and transforming growth factor β1 (TGF β1); and inhibited nuclear factor kappa B (NF κB) activation at the L5 lumbar spinal cord.
+TNF	drug	opioid	22366510	Moreover, the administration of LXA4ME during the induction of <b>morphine</b> tolerance inhibited the activation of microglia and astrocytes; reduced the expression of proinflammatory cytokines interleukin 1β (IL 1β), IL 6, and <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α); upregulated the expression of anti inflammatory cytokines IL 10 and transforming growth factor β1 (TGF β1); and inhibited nuclear factor kappa B (NF κB) activation at the L5 lumbar spinal cord.
+TNF	drug	alcohol	22289614	The mRNA levels of cytochrome P450 2E1, NF κB, <strong>TNF</strong> α and transforming growth factor β1 were found to be increased in the <b>alcohol</b> treated rats, and their expressions were found to be decreased in the co administered group.
+TNF	drug	alcohol	23700666	Dose dependent effects of monoclonal antibodies to tumor necrosis factor alpha (<strong>TNFa</strong>) in the form of infliximab preparation have been studied in Wistar rats upon with <b>alcohol</b> intoxication for 10 weeks (Lieber  De Carli liquid diet).
+TNF	addiction	intoxication	23700666	Dose dependent effects of monoclonal antibodies to tumor necrosis factor alpha (<strong>TNFa</strong>) in the form of infliximab preparation have been studied in Wistar rats upon with alcohol <b>intoxication</b> for 10 weeks (Lieber  De Carli liquid diet).
+TNF	drug	alcohol	23700666	Dose dependent effects of monoclonal antibodies to <strong>tumor necrosis factor</strong> alpha (<strong>TNFa</strong>) in the form of infliximab preparation have been studied in Wistar rats upon with <b>alcohol</b> intoxication for 10 weeks (Lieber  De Carli liquid diet).
+TNF	addiction	intoxication	23700666	Dose dependent effects of monoclonal antibodies to <strong>tumor necrosis factor</strong> alpha (<strong>TNFa</strong>) in the form of infliximab preparation have been studied in Wistar rats upon with alcohol <b>intoxication</b> for 10 weeks (Lieber  De Carli liquid diet).
+TNF	drug	alcohol	23700666	Infliximab administered on the background of <b>alcohol</b> intoxication increases the pool of free amino acids and activates their metabolism in rat blood lymphocytes, which is probably due to inactivation of <strong>TNFalpha</strong> and adaptive changes in the amino acid transport system.
+TNF	addiction	intoxication	23700666	Infliximab administered on the background of alcohol <b>intoxication</b> increases the pool of free amino acids and activates their metabolism in rat blood lymphocytes, which is probably due to inactivation of <strong>TNFalpha</strong> and adaptive changes in the amino acid transport system.
+TNF	drug	nicotine	22180575	Depressed <b>smokers</b> had significantly higher levels of hs CRP (p = .05), IL 6 (p = .039), and <strong>TNF</strong> α (p = .021) compared with nondepressed <b>smokers</b>.
+TNF	drug	nicotine	22180575	These findings demonstrate that depressed <b>smokers</b> had higher hs CRP, IL 6, and <strong>TNF</strong> α levels than nondepressed <b>smokers</b> and had worse physical health outcomes and greater work related disability.
+TNF	drug	amphetamine	22160137	Dissociable role of <strong>tumor necrosis factor</strong> alpha gene deletion in <b>methamphetamine</b> self administration and cue induced relapsing behavior in mice.
+TNF	addiction	addiction	22160137	Previously, we have reported that tumor necrosis factor alpha (<strong>TNF</strong> α) is a critical molecule among endogenous anti <b>addictive</b> modulators using animal models of drug conditioned place preference and drug discrimination.
+TNF	addiction	addiction	22160137	Previously, we have reported that <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> α) is a critical molecule among endogenous anti <b>addictive</b> modulators using animal models of drug conditioned place preference and drug discrimination.
+TNF	drug	amphetamine	22160137	Does targeted deletion of the <strong>TNF</strong> α gene in mice affect <b>methamphetamine</b> (<b>METH</b>) self administration, motivation to self administer <b>METH</b>, cue induced reinstatement of <b>METH</b> seeking behavior, and food reinforcement or seeking behavior?
+TNF	addiction	relapse	22160137	Does targeted deletion of the <strong>TNF</strong> α gene in mice affect methamphetamine (METH) self administration, motivation to self administer METH, cue induced <b>reinstatement</b> of METH <b>seeking</b> behavior, and food reinforcement or <b>seeking</b> behavior?
+TNF	addiction	reward	22160137	Does targeted deletion of the <strong>TNF</strong> α gene in mice affect methamphetamine (METH) self administration, motivation to self administer METH, cue induced reinstatement of METH seeking behavior, and food <b>reinforcement</b> or seeking behavior?
+TNF	drug	amphetamine	22160137	Both <b>METH</b> self administration and reinstatement of drug seeking behavior and food self delivery and food seeking behavior were measured in <strong>TNF</strong> α ( / ) and wild type mice.
+TNF	addiction	relapse	22160137	Both METH self administration and <b>reinstatement</b> of drug <b>seeking</b> behavior and food self delivery and food <b>seeking</b> behavior were measured in <strong>TNF</strong> α ( / ) and wild type mice.
+TNF	drug	amphetamine	22160137	There were an upward shift of dose responses to <b>METH</b> self administration under a fixed ratio schedule of reinforcement and higher breaking points under a progressive ratio schedule of reinforcement in <strong>TNF</strong> α knockout (<strong>TNF</strong> α ( / )) mice as compared with wild type mice.
+TNF	addiction	reward	22160137	There were an upward shift of dose responses to METH self administration under a fixed ratio schedule of <b>reinforcement</b> and higher breaking points under a progressive ratio schedule of <b>reinforcement</b> in <strong>TNF</strong> α knockout (<strong>TNF</strong> α ( / )) mice as compared with wild type mice.
+TNF	drug	amphetamine	22160137	There was no significant difference in cue induced reinstatement of <b>METH</b> seeking behavior, food maintained operant behavior, motivation to natural food, and cue induced food seeking behavior between <strong>TNF</strong> α ( / ) and wild type mice.
+TNF	addiction	relapse	22160137	There was no significant difference in cue induced <b>reinstatement</b> of METH <b>seeking</b> behavior, food maintained operant behavior, motivation to natural food, and cue induced food <b>seeking</b> behavior between <strong>TNF</strong> α ( / ) and wild type mice.
+TNF	addiction	reward	22160137	There was no significant difference in cue induced reinstatement of METH seeking behavior, food maintained <b>operant</b> behavior, motivation to natural food, and cue induced food seeking behavior between <strong>TNF</strong> α ( / ) and wild type mice.
+TNF	drug	amphetamine	22160137	<strong>TNF</strong> α affects <b>METH</b> self administration and motivation to self administer <b>METH</b> but contributes to neither <b>METH</b> associated cue induced relapsing behavior nor food reward and food seeking behavior.
+TNF	addiction	relapse	22160137	<strong>TNF</strong> α affects METH self administration and motivation to self administer METH but contributes to neither METH associated cue induced relapsing behavior nor food reward and food <b>seeking</b> behavior.
+TNF	addiction	reward	22160137	<strong>TNF</strong> α affects METH self administration and motivation to self administer METH but contributes to neither METH associated cue induced relapsing behavior nor food <b>reward</b> and food seeking behavior.
+TNF	addiction	addiction	22160137	<strong>TNF</strong> α may be explored for use as a diagnostic biomarker for the early stage of drug <b>addiction</b>.
+TNF	drug	alcohol	22020770	The <b>alcohol</b> induced cytokine dysregulation was confirmed in a mouse model of isopropanol intoxication in which the production of <strong>TNF</strong> α in response to LPS challenge was virtually abolished.
+TNF	addiction	intoxication	22020770	The alcohol induced cytokine dysregulation was confirmed in a mouse model of isopropanol <b>intoxication</b> in which the production of <strong>TNF</strong> α in response to LPS challenge was virtually abolished.
+TNF	drug	alcohol	21994849	Pentoxifylline, a <strong>tumor necrosis factor</strong> alpha (TNFα) suppressor, and infliximab, an anti TNFα mouse/human chimeric antibody, has been extensively studied in patients with <b>alcoholic</b> hepatitis.
+TNF	drug	amphetamine	21886572	Recently, we have demonstrated that tumor necrosis factor α (<strong>TNF</strong> α) increases dopamine uptake and inhibits <b>methamphetamine</b> induced dependence.
+TNF	addiction	dependence	21886572	Recently, we have demonstrated that tumor necrosis factor α (<strong>TNF</strong> α) increases dopamine uptake and inhibits methamphetamine induced <b>dependence</b>.
+TNF	drug	amphetamine	21886572	Recently, we have demonstrated that <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) increases dopamine uptake and inhibits <b>methamphetamine</b> induced dependence.
+TNF	addiction	dependence	21886572	Recently, we have demonstrated that <strong>tumor necrosis factor</strong> α (<strong>TNF</strong> α) increases dopamine uptake and inhibits methamphetamine induced <b>dependence</b>.
+TNF	drug	amphetamine	21886572	Interestingly, treatment with shati AS also inhibited expression of <strong>TNF</strong> α. Transfection of the vector containing shati cDNA into PC12 cells, dramatically induced the expression of shati and <strong>TNF</strong> α mRNA, accelerated dopamine uptake, and inhibited the <b>methamphetamine</b> induced decrease in dopamine uptake.
+TNF	drug	amphetamine	21886572	These results suggest that the functional roles of shati in <b>methamphetamine</b> induced behavioral changes are mediated through the induction of <strong>TNF</strong> α expression which inhibits the <b>methamphetamine</b> induced increase of dopamine overflow and decrease in dopamine uptake.
+TNF	drug	alcohol	21790532	Elevated serum IL 6 levels as well as hepatic IL 6 and <strong>TNF</strong> α gene expression 2 h after H/R were reduced by <b>ethanol</b>.
+TNF	addiction	addiction	21539588	Dose <b>escalation</b>, reduction of infusion intervals and switch to other anti <strong>TNF</strong> α agents are effective as rescue strategies.
+TNF	drug	nicotine	21407178	Predictors for loss of response or dose escalation were male gender, current/former <b>smoker</b> status, family history of inflammatory bowel disease, isolated colonic disease, extra intestinal manifestations, 80/40 mg induction therapy, longer disease duration, greater baseline Crohn's Disease Activity Index, concomitant corticosteroid use, no deep remission at week 12, low serum trough concentrations of adalimumab, previous infliximab non response and being previously treated with an anti <strong>tumor necrosis factor</strong> agent.
+TNF	addiction	addiction	21407178	Predictors for loss of response or dose <b>escalation</b> were male gender, current/former smoker status, family history of inflammatory bowel disease, isolated colonic disease, extra intestinal manifestations, 80/40 mg induction therapy, longer disease duration, greater baseline Crohn's Disease Activity Index, concomitant corticosteroid use, no deep remission at week 12, low serum trough concentrations of adalimumab, previous infliximab non response and being previously treated with an anti <strong>tumor necrosis factor</strong> agent.
+TNF	drug	alcohol	21322143	Glial cell line derived BNF and <strong>tumor necrosis factor</strong> alpha reduce the addictive potential of cocaine, methamphetamine, morphine and <b>ethanol</b>.
+TNF	drug	amphetamine	21322143	Glial cell line derived BNF and <strong>tumor necrosis factor</strong> alpha reduce the addictive potential of cocaine, <b>methamphetamine</b>, morphine and ethanol.
+TNF	drug	cocaine	21322143	Glial cell line derived BNF and <strong>tumor necrosis factor</strong> alpha reduce the addictive potential of <b>cocaine</b>, methamphetamine, morphine and ethanol.
+TNF	drug	opioid	21322143	Glial cell line derived BNF and <strong>tumor necrosis factor</strong> alpha reduce the addictive potential of cocaine, methamphetamine, <b>morphine</b> and ethanol.
+TNF	addiction	addiction	21322143	Glial cell line derived BNF and <strong>tumor necrosis factor</strong> alpha reduce the <b>addictive</b> potential of cocaine, methamphetamine, morphine and ethanol.
+TNF	drug	cocaine	21277908	Three consecutive days of <b>cocaine</b> conditioning increased interleukin 6 (IL 6) but decreased tumor necrosis factor (<strong>TNF</strong> α) levels in medial prefrontal cortex (mPFC) and nucleus accumbens (Acb).
+TNF	drug	cocaine	21277908	Three consecutive days of <b>cocaine</b> conditioning increased interleukin 6 (IL 6) but decreased <strong>tumor necrosis factor</strong> (<strong>TNF</strong> α) levels in medial prefrontal cortex (mPFC) and nucleus accumbens (Acb).
+TNF	drug	cocaine	21277908	Interestingly, pretreatment with memantine at the lowest effective dose (0.02 mg/kg/injection) reversed <b>cocaine</b> conditioning enhanced IL 6 and  decreased <strong>TNF</strong> α levels in these brain regions.
+TNF	drug	alcohol	21262339	<b>Ethanol</b> did not alter hippocampal ED 1, MHC II, or <strong>TNF</strong> α expression, suggesting that a single period of binge <b>ethanol</b> exposure does not induce a full microglial driven neuroinflammatory response.
+TNF	addiction	intoxication	21262339	Ethanol did not alter hippocampal ED 1, MHC II, or <strong>TNF</strong> α expression, suggesting that a single period of <b>binge</b> ethanol exposure does not induce a full microglial driven neuroinflammatory response.
+TNF	drug	alcohol	21143255	Human PBMCs were cultured in the presence of 100 mM <b>ethanol</b> and/or 100 ng/ml LPS for various time periods (1, 3, 8, and 24 hours) and analyzed for the kinetics of gene expression by quantitative real time PCR of selected transcription factors (T bet, GATA3, Foxp3, and RORγt) and cytokines (<strong>TNF</strong> α, IL 6, IL 10, and IFN γ).
+TNF	drug	alcohol	21143255	<b>Ethanol</b> suppressed the LPS induced gene expression of Foxp3, RORγt, and T bet after 8 hours, expression of <strong>TNF</strong> α and IFN γ was also suppressed after 3 and 8 hours.
+TNF	drug	alcohol	21143255	Markers of inflammation including <strong>TNF</strong> α and IL 1β in supernatant of PBMCs were significantly decreased, while levels of IL 10 and IL 6 remained unchanged following <b>ethanol</b> exposure.
+TNF	drug	alcohol	21143255	<b>Alcohol</b> interferes with the kinetics of Foxp3, RORγt, and T bet gene expression and the production of <strong>TNF</strong> α and IL 1ß and influences the balance of Treg/Th17 cells following LPS exposure.
+TNF	addiction	sensitization	21091930	This <b>sensitization</b> enhances the production of inflammatory mediators, such as <strong>tumor necrosis factor</strong> α and reactive oxygen species that contribute to hepatocyte dysfunction, necrosis and apoptosis of hepatocytes and the generation of extracellular matrix proteins leading to fibrosis.
+TNF	drug	nicotine	21078494	<b>Nicotine</b> did not cause an excessive expression of <strong>TNF</strong> α, IL 8, and IL 6, nor did it affect protein production from the MUC5AC gene.
+TNF	drug	nicotine	21078494	<b>Nicotine</b> not only failed to stimulate production of <strong>TNF</strong> α, IL 8, and IL 6, but its presence was shown to suppress the activation resulting from exposure to CE and LPS (P < 0.05).
+TNF	drug	opioid	21068718	Here we report that chronic <b>morphine</b> withdrawal induced upregulation of glial fibrillary acidic protein (GFAP), <strong>tumor necrosis factor</strong> alpha (TNFα) and phosphorylation of ERK1/2 (pERK1/2) in the caudal ventrolateral PAG (vlPAG).
+TNF	addiction	withdrawal	21068718	Here we report that chronic morphine <b>withdrawal</b> induced upregulation of glial fibrillary acidic protein (GFAP), <strong>tumor necrosis factor</strong> alpha (TNFα) and phosphorylation of ERK1/2 (pERK1/2) in the caudal ventrolateral PAG (vlPAG).
+TNF	drug	opioid	21068718	We used a herpes simplex virus (HSV) based vector expressing p55 soluble <strong>TNF</strong> receptor (sTNFR) microinjected into the PAG to examine the role of the proinflammatory cytokine TNFα in the PAG in the <b>naloxone</b> precipitated withdrawal response.
+TNF	addiction	withdrawal	21068718	We used a herpes simplex virus (HSV) based vector expressing p55 soluble <strong>TNF</strong> receptor (sTNFR) microinjected into the PAG to examine the role of the proinflammatory cytokine TNFα in the PAG in the naloxone precipitated <b>withdrawal</b> response.
+TNF	drug	alcohol	21062897	Additionally, AMPK reactivation of sirtuin 3 prevented the sensitization to the MPT and the enhancement of cell killing by <strong>TNF</strong> in cells exposed to <b>ethanol</b>.
+TNF	addiction	sensitization	21062897	Additionally, AMPK reactivation of sirtuin 3 prevented the <b>sensitization</b> to the MPT and the enhancement of cell killing by <strong>TNF</strong> in cells exposed to ethanol.
+TNF	drug	alcohol	20699198	Rats fed with <b>alcohol</b> (35%) for 10 weeks showed markedly decreased tail flick latency in tail immersion test (thermal hyperalgesia), vocalization threshold in Randall Sellito test (mechanical hyperalgesia) and paw withdrawal threshold in von Frey hair test (mechanical allodynia) along with enhanced oxidative nitrosative stress and inflammatory mediators (<strong>TNF</strong> α, IL 1β and TGF β1 levels).
+TNF	addiction	withdrawal	20699198	Rats fed with alcohol (35%) for 10 weeks showed markedly decreased tail flick latency in tail immersion test (thermal hyperalgesia), vocalization threshold in Randall Sellito test (mechanical hyperalgesia) and paw <b>withdrawal</b> threshold in von Frey hair test (mechanical allodynia) along with enhanced oxidative nitrosative stress and inflammatory mediators (<strong>TNF</strong> α, IL 1β and TGF β1 levels).
+TNF	drug	alcohol	20586751	In addition, administration of rmMFG E8 after <b>alcohol</b> exposure and subsequent sepsis decreases circulating levels of <strong>TNF</strong> alpha and interleukin 6 and attenuates organ injury.
+TNF	addiction	withdrawal	20454616	Conversely, a single injection of PAF near the DRG of naïve rats caused a decrease in the paw <b>withdrawal</b> threshold to mechanical stimulation in a dose dependent manner and an increase in the expression of mRNAs for <strong>TNFalpha</strong> and IL 1beta, both of which were inhibited by pretreatment with a PAFR antagonist.
+TNF	addiction	sensitization	20238399	This <b>sensitization</b> enhances production of inflammatory mediators, such as <strong>tumor necrosis factor</strong> alpha and reactive oxygen species, that contribute to hepatocyte dysfunction, necrosis, apoptosis, and fibrosis.
+TNF	drug	nicotine	20210814	Interaction between early maternal <b>smoking</b> and variants in <strong>TNF</strong> and GSTP1 in childhood wheezing.
+TNF	drug	nicotine	20210814	We studied whether variations in single nucleotide polymorphisms (SNPs) in the <strong>TNF</strong>, glutathione S transferase P1 (GSTP1) and beta2 adrenoreceptor (ADRB2) genes modify the effect of early maternal <b>smoking</b> on the development of childhood asthma, wheeze and allergic sensitization.
+TNF	addiction	sensitization	20210814	We studied whether variations in single nucleotide polymorphisms (SNPs) in the <strong>TNF</strong>, glutathione S transferase P1 (GSTP1) and beta2 adrenoreceptor (ADRB2) genes modify the effect of early maternal smoking on the development of childhood asthma, wheeze and allergic <b>sensitization</b>.
+TNF	drug	nicotine	20210814	An interaction with early maternal <b>smoking</b> was found for three <strong>TNF</strong> SNPs ( 857C/T, Intron 1, Intron 3) with respect to early wheeze (up to 2 years of age).
+TNF	drug	nicotine	20210814	For example, the odds ratio (OR) for developing early wheeze related to early maternal <b>smoking</b> was 2.4 [95% confidence interval (CI) 1.6 3.7] in children with a wild type CC homozygote genotype of the <strong>TNF</strong> 857 SNP, while no <b>tobacco</b> related risk was seen in children carrying the rare T allele.
+TNF	drug	nicotine	20210814	Our results suggest that the risk of early childhood wheeze associated with early maternal <b>smoking</b> may be modified by <strong>TNF</strong> and GSTP1 polymorphisms.
+TNF	addiction	relapse	20203531	The animals were scored clinically throughout the experiment, and axonal degeneration, demyelination, T cells, microglia/macrophages, <strong>TNF</strong> alpha, IL 12, IFN gamma, IL 10 and the T(H)17 response were estimated at the peak of the first <b>relapse</b>.
+TNF	drug	cannabinoid	20203531	Interestingly, treatment at any dosage did not affect the brain levels of <strong>TNF</strong> alpha, IL 12 and IFN gamma (T(H)1 response), whereas high dose <b>cannabinoid</b> treatment reduced the number of T cells and microglia/macrophages in addition to the T(H)17 response.
+TNF	drug	alcohol	20201932	<b>Ethanol</b> induces proinflammatory cytokines <strong>TNFalpha</strong>, MCP 1, and IL 1beta, proinflammatory proteases TACE, and tissue plasminogen activator (tPA) as well as inducible nitric oxide synthase.
+TNF	drug	alcohol	20201932	Neutralizing antibody to proinflammatory cytokine <strong>TNFalpha</strong> reduces <b>ethanol</b> induction of proinflammatory genes, suggesting cytokine propagation of proinflammatory gene induction.
+TNF	drug	alcohol	20090911	Neither <b>ethanol</b> nor ADH affected the expression of ANP, total pro caspase 9, cytosolic and total pro caspase 8, <strong>TNF</strong> alpha, Fas receptor, Fas L and cytosolic AIF.
+TNF	drug	amphetamine	20074221	We observed that <b>METH</b> caused an inflammatory response characterized by astrocytic and microglia reactivity, and tumor necrosis factor (<strong>TNF</strong>) system alterations.
+TNF	drug	amphetamine	20074221	We observed that <b>METH</b> caused an inflammatory response characterized by astrocytic and microglia reactivity, and <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) system alterations.
+TNF	drug	amphetamine	20074221	prevented <b>METH</b> induced glia activation and both <strong>TNF</strong> system and beta III tubulin alterations.
+TNF	drug	alcohol	20052772	Chronic <b>ethanol</b> feeding increases the sensitivity of Kupffer cells, the resident hepatic macrophage, to lipopolysaccharide (LPS), leading to increased tumor necrosis factor alpha (<strong>TNF</strong> alpha) expression.
+TNF	drug	alcohol	20052772	Chronic <b>ethanol</b> feeding increases the sensitivity of Kupffer cells, the resident hepatic macrophage, to lipopolysaccharide (LPS), leading to increased <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) expression.
+TNF	drug	alcohol	20052772	LPS stimulated <strong>TNF</strong> alpha expression in liver was increased in mice after chronic <b>ethanol</b> exposure.
+TNF	drug	alcohol	19764937	The aim of this study was to investigate whether 4 functionally relevant polymorphisms of the interleukin 1 (IL 1) and <strong>tumor necrosis factor</strong> alpha genes were associated with <b>alcohol</b> dependence and with measures of clinical severity and treatment outcome.
+TNF	addiction	dependence	19764937	The aim of this study was to investigate whether 4 functionally relevant polymorphisms of the interleukin 1 (IL 1) and <strong>tumor necrosis factor</strong> alpha genes were associated with alcohol <b>dependence</b> and with measures of clinical severity and treatment outcome.
+TNF	drug	alcohol	19742166	Epistasis between IL1A, IL1B, <strong>TNF</strong>, HTR2A, 5 HTTLPR and TPH2 variations does not impact <b>alcohol</b> dependence disorder features.
+TNF	addiction	dependence	19742166	Epistasis between IL1A, IL1B, <strong>TNF</strong>, HTR2A, 5 HTTLPR and TPH2 variations does not impact alcohol <b>dependence</b> disorder features.
+TNF	drug	alcohol	19742166	In both groups we genotyped 11 genetic variations (rs1800587; rs3087258; rs1799724; 5 HTTLPR; rs1386493; rs1386494; rs1487275; rs1843809; rs4570625; rs2129575; rs6313) located in genes whose impact on <b>alcohol</b> related behaviors and disorders has been hypothesized (IL1A, IL1B, <strong>TNF</strong>, 5 HTTLPR, TPH2 and HTR2A).
+TNF	drug	alcohol	19561104	We hypothesized that in human monocytes, acute <b>alcohol</b> induces hyporesponsiveness to LPS, resulting in decreased <strong>TNF</strong> alpha, whereas chronic <b>alcohol</b> increases <strong>TNF</strong> alpha by sensitization to LPS.
+TNF	addiction	sensitization	19561104	We hypothesized that in human monocytes, acute alcohol induces hyporesponsiveness to LPS, resulting in decreased <strong>TNF</strong> alpha, whereas chronic alcohol increases <strong>TNF</strong> alpha by <b>sensitization</b> to LPS.
+TNF	drug	alcohol	19561104	Inhibition of IRAK M in acute <b>alcohol</b> exposed monocytes using small interfering RNA restored the LPS induced <strong>TNF</strong> alpha production whereas over expression of IRAK M in chronic <b>alcohol</b> macrophages prevented the increase in <strong>TNF</strong> alpha production.
+TNF	drug	alcohol	19561104	Addition of inhibitors of <b>alcohol</b> metabolism did not alter LPS signaling and <strong>TNF</strong> alpha production during chronic <b>alcohol</b> exposure.
+TNF	drug	alcohol	19561104	We determined that acute <b>alcohol</b> decreased but chronic <b>alcohol</b> increased activation of ERK in monocytes and ERK inhibitor, PD98059, prevented the chronic <b>alcohol</b> induced increase in <strong>TNF</strong> alpha.
+TNF	drug	alcohol	19541419	<strong>TNF</strong> alpha and IL 1beta levels were also significantly increased in both serum and sciatic nerve of <b>ethanol</b> treated rats.
+TNF	drug	alcohol	19233636	Since the cell membrane is closely related to the capacitance (or dielectric constant), we have fabricated a capacitance sensor, which can measure the capacitance of cells, and investigated its time dependence during apoptosis and necrosis for TE2 cells induced by <strong>TNF</strong> related apoptosis inducing ligand (TRAIL) and <b>ethanol</b>.
+TNF	addiction	dependence	19233636	Since the cell membrane is closely related to the capacitance (or dielectric constant), we have fabricated a capacitance sensor, which can measure the capacitance of cells, and investigated its time <b>dependence</b> during apoptosis and necrosis for TE2 cells induced by <strong>TNF</strong> related apoptosis inducing ligand (TRAIL) and ethanol.
+TNF	drug	alcohol	19185287	<strong>Tumor necrosis factor</strong> antagonism normalizes rapid eye movement sleep in <b>alcohol</b> dependence.
+TNF	addiction	dependence	19185287	<strong>Tumor necrosis factor</strong> antagonism normalizes rapid eye movement sleep in alcohol <b>dependence</b>.
+TNF	drug	alcohol	19185287	This study was undertaken to test whether blockade of biologically active tumor necrosis factor alpha (<strong>TNF</strong> alpha) normalizes REM sleep in <b>alcohol</b> dependent adults.
+TNF	drug	alcohol	19185287	This study was undertaken to test whether blockade of biologically active <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) normalizes REM sleep in <b>alcohol</b> dependent adults.
+TNF	drug	alcohol	19185287	Pharmacologic neutralization of <strong>TNF</strong> alpha activity is associated with significant reductions in REM sleep in abstinent <b>alcohol</b> dependent patients.
+TNF	drug	alcohol	19155505	<b>Alcohol</b> also suppressed the plasma <strong>TNF</strong> alpha response to bacteremia and inhibited <strong>TNF</strong> alpha induced phenotypic inversion of lin( )c kit(+)Sca 1(+)Sca 1( ) cells in vitro.
+TNF	drug	opioid	19038328	In order to determine the role of inducible nitric oxide synthase (iNOS) and tumor necrosis factor alpha (<strong>TNF</strong> alpha) in the pathogenesis of opiate addiction in humans, the expression of both was analyzed in the locus coeruleus (LC) of patients who died from <b>heroin</b> overdose.
+TNF	addiction	addiction	19038328	In order to determine the role of inducible nitric oxide synthase (iNOS) and tumor necrosis factor alpha (<strong>TNF</strong> alpha) in the pathogenesis of opiate <b>addiction</b> in humans, the expression of both was analyzed in the locus coeruleus (LC) of patients who died from heroin overdose.
+TNF	drug	opioid	19038328	In order to determine the role of inducible nitric oxide synthase (iNOS) and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) in the pathogenesis of opiate addiction in humans, the expression of both was analyzed in the locus coeruleus (LC) of patients who died from <b>heroin</b> overdose.
+TNF	addiction	addiction	19038328	In order to determine the role of inducible nitric oxide synthase (iNOS) and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) in the pathogenesis of opiate <b>addiction</b> in humans, the expression of both was analyzed in the locus coeruleus (LC) of patients who died from heroin overdose.
+TNF	drug	amphetamine	19014384	Recently, we have demonstrated that tumor necrosis factor alpha (<strong>TNF</strong> alpha) increases DA uptake and inhibits <b>METH</b> dependence.
+TNF	addiction	dependence	19014384	Recently, we have demonstrated that tumor necrosis factor alpha (<strong>TNF</strong> alpha) increases DA uptake and inhibits METH <b>dependence</b>.
+TNF	drug	amphetamine	19014384	Recently, we have demonstrated that <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) increases DA uptake and inhibits <b>METH</b> dependence.
+TNF	addiction	dependence	19014384	Recently, we have demonstrated that <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) increases DA uptake and inhibits METH <b>dependence</b>.
+TNF	drug	amphetamine	19014384	<strong>TNF</strong> alpha increased DA uptake via the mitogen activated protein kinase kinase pathway and inhibited the <b>METH</b> induced decrease in DA uptake in PC12 cells.
+TNF	drug	amphetamine	19014384	Transfection of the vector containing shati cDNA into PC12 cells, induced the expression of shati and <strong>TNF</strong> alpha mRNA, accelerated DA uptake, and inhibited the <b>METH</b> induced decrease in DA uptake.
+TNF	drug	amphetamine	19014384	These results suggest that the functional roles of shati in <b>METH</b> regulated behavioral changes are mediated through inhibition of the <b>METH</b> induced decrease in DA uptake via <strong>TNF</strong> alpha.
+TNF	drug	opioid	18973600	The present study sought to determine whether inactivation of the BLA would alter <b>heroin</b>'s conditioned effects on the expression of inducible nitric oxide synthase (iNOS) and the proinflammatory cytokines <strong>TNF</strong> alpha and IL 1beta in the rat.
+TNF	drug	opioid	18973600	Analyses using real time RT PCR indicated that inactivation of the BLA blocked the suppressive effect of <b>heroin</b> associated environmental stimuli on iNOS induction and on the expression of the proinflammatory cytokines <strong>TNF</strong> alpha and IL 1beta in spleen and liver tissue.
+TNF	drug	cocaine	18719314	<b>Cocaine</b> self administered for 18 days induced a significant increase in spleen weight, plasma corticosterone levels, interleukin (IL) 10, and <strong>tumor necrosis factor</strong> alpha production, while concanavalin A stimulated proliferation responses of peripheral blood T lymphocytes and interferon gamma production by splenic lymphocytes were not altered.
+TNF	drug	benzodiazepine	18506841	Also, hypo osmolarity, tumor necrosis factor alpha (<strong>TNF</strong> alpha), and <b>diazepam</b> increase RNA oxidation in cultured astrocytes, suggesting that the action of different HE precipitating factors converges at the level of RNA oxidation.
+TNF	drug	benzodiazepine	18506841	Also, hypo osmolarity, <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha), and <b>diazepam</b> increase RNA oxidation in cultured astrocytes, suggesting that the action of different HE precipitating factors converges at the level of RNA oxidation.
+TNF	drug	opioid	18502094	injection of 1mg/kg of naltroxone 48 h after implantation of 75 mg <b>morphine</b> pellets) did not alter blood to brain transport of IL 1alpha or <strong>TNF</strong> alpha, both the chronic <b>morphine</b> treatment and withdrawal from <b>morphine</b> groups had increased blood to brain transport of IL 2.
+TNF	addiction	withdrawal	18502094	injection of 1mg/kg of naltroxone 48 h after implantation of 75 mg morphine pellets) did not alter blood to brain transport of IL 1alpha or <strong>TNF</strong> alpha, both the chronic morphine treatment and <b>withdrawal</b> from morphine groups had increased blood to brain transport of IL 2.
+TNF	drug	opioid	18502094	Whereas IL 1alpha, IL 2, and <strong>TNF</strong> alpha are all proinflammatory cytokines, <b>morphine</b> exposure has individualized effects on their blood to brain transport.
+TNF	drug	opioid	18294814	An altered Th1/Th2 balance, characterized by reduced IL 4, IFN gamma and <strong>TNF</strong> alpha but normal IL 2 levels, was present in untreated <b>heroin</b> addicted subjects, while the Th1/Th2 balance was well conserved in the <b>methadone</b> and <b>buprenorphine</b> groups.
+TNF	drug	opioid	18294378	Mice treated chronically treated with <b>morphine</b> prior to incision were found to have enhanced skin levels of IL 1beta, IL 6, G CSF, KC and <strong>TNFalpha</strong> after incision at one or more time points compared to saline pretreated controls.
+TNF	drug	alcohol	18267108	Serum alanine aminotransferase activity, <strong>TNFalpha</strong> level, and hepatic malondialdehyde level were increased significantly by <b>ethanol</b> administration.
+TNF	drug	alcohol	18045675	Moreover, by inducing mitochondrial alterations, oxidative stress promotes hepatocyte necrosis and contributes to <b>alcohol</b> induced sensitization of hepatocyte to the pro apoptotic action of <strong>TNF</strong> alpha.
+TNF	addiction	sensitization	18045675	Moreover, by inducing mitochondrial alterations, oxidative stress promotes hepatocyte necrosis and contributes to alcohol induced <b>sensitization</b> of hepatocyte to the pro apoptotic action of <strong>TNF</strong> alpha.
+TNF	drug	opioid	18040852	The splenocytes from protected mice and <b>morphine</b> low concentration treated infected PM, elaborated significantly (p < 0.05) enhanced levels of interleukin 12, interferon gamma, <strong>tumor necrosis factor</strong> alpha, granulocyte macrophage colony stimulating factor and nitrite in the culture medium; a high dose/concentration suppressed their elaboration.
+TNF	drug	alcohol	17980786	<b>Alcohol</b> induced endothelial damage or protection may be related to the synthesis or action of several markers, such as nitric oxide, cortisol, endothelin 1, adhesion molecules, <strong>tumor necrosis factor</strong> alpha, interleukin 6, C reactive protein, and haemostatic factors.
+TNF	drug	alcohol	17900056	[Factors affecting the concentration of plasma tumour necrosis factor alpha (<strong>TNF</strong> alpha) and liver function tests values in <b>alcohol</b> dependent males after <b>alcohol</b> drinking cessation].
+TNF	drug	alcohol	17900056	In our work, the factors affecting the plasma level of cytokine, tumour necrosis factor (<strong>TNF</strong> alpha) and liver function tests values in <b>alcohol</b> dependent males after <b>alcohol</b> abuse period were analysed.
+TNF	drug	alcohol	17900056	Using the step wise method of multiple regression we found, that <strong>TNF</strong> alfa level at the study commencement was determined by history of delirium tremens, Michigan <b>Alcoholism</b> Screening Test score, length of <b>alcohol</b> dependence, ALT activity, % of total monitoring time with gastric pH >3, intensity of antral H. pylori colonisation and number of standard drinks drunk for 90 days before the study start (ns).
+TNF	addiction	dependence	17900056	Using the step wise method of multiple regression we found, that <strong>TNF</strong> alfa level at the study commencement was determined by history of delirium tremens, Michigan Alcoholism Screening Test score, length of alcohol <b>dependence</b>, ALT activity, % of total monitoring time with gastric pH >3, intensity of antral H. pylori colonisation and number of standard drinks drunk for 90 days before the study start (ns).
+TNF	drug	alcohol	17900056	Values of <strong>TNF</strong> alpha and liver function tests two weeks after <b>alcohol</b> withdrawal were independently determined by gastric pH, H.pylori infection and smoking, which suggests their potential synergism with a hepatotoxic effect of <b>alcohol</b> drinking.
+TNF	drug	nicotine	17900056	Values of <strong>TNF</strong> alpha and liver function tests two weeks after alcohol withdrawal were independently determined by gastric pH, H.pylori infection and <b>smoking</b>, which suggests their potential synergism with a hepatotoxic effect of alcohol drinking.
+TNF	addiction	withdrawal	17900056	Values of <strong>TNF</strong> alpha and liver function tests two weeks after alcohol <b>withdrawal</b> were independently determined by gastric pH, H.pylori infection and smoking, which suggests their potential synergism with a hepatotoxic effect of alcohol drinking.
+TNF	drug	alcohol	17887948	This study showed that <b>alcohol</b> drinking for 70 days (1) caused liver inflammation characterized by elevated <strong>tumor necrosis factor</strong> alpha, interleukin 1beta, and matrix metalloproteinase 9 expression and (2) dysregulated lipopolysaccharide (LPS) induced pleurisy.
+TNF	drug	alcohol	17855333	Serum insulin like growth factor 1 (IGF 1), interleukin (IL) 6, IL 8, IL 10, <strong>TNF</strong> alpha, PTH, estradiol, free testosterone, and corticosterone were measured in 36 <b>alcoholics</b>, ten of them cirrhotics, who also underwent brain CT, which recorded the presence of cortical atrophy or cerebellar atrophy, Evan's, Huckmann's, cella media, bicaudate, cortical atrophy, bifrontal, and ventricular indices, and diameter of the third ventricle; subjective nutritional assessment, midarm anthropometry, and evaluation of liver function.
+TNF	drug	alcohol	17574213	<b>Alcohol</b> induced S adenosylhomocysteine accumulation in the liver sensitizes to <strong>TNF</strong> hepatotoxicity: possible involvement of mitochondrial S adenosylmethionine transport.
+TNF	drug	alcohol	17574213	Hepatocytes are resistant to tumor necrosis factor alpha  (<strong>TNF</strong>) induced killing/apoptosis under normal circumstances, but primary hepatocytes from rats chronically fed <b>alcohol</b> have increased <strong>TNF</strong> cytotoxicity.
+TNF	drug	alcohol	17574213	Hepatocytes are resistant to <strong>tumor necrosis factor</strong> alpha  (<strong>TNF</strong>) induced killing/apoptosis under normal circumstances, but primary hepatocytes from rats chronically fed <b>alcohol</b> have increased <strong>TNF</strong> cytotoxicity.
+TNF	drug	alcohol	17574213	Therefore, there must be mechanism(s) by which <b>alcohol</b> exposure "sensitizes" to <strong>TNF</strong> hepatotoxicity.
+TNF	drug	alcohol	17574213	In the current study, we extended our previous observations by further characterizing the effects of chronic <b>alcohol</b> intake on mitochondrial SAM levels in liver and examining its possible involvement in SAH sensitization to <strong>TNF</strong> hepatotoxicity.
+TNF	addiction	sensitization	17574213	In the current study, we extended our previous observations by further characterizing the effects of chronic alcohol intake on mitochondrial SAM levels in liver and examining its possible involvement in SAH <b>sensitization</b> to <strong>TNF</strong> hepatotoxicity.
+TNF	drug	alcohol	17574213	In conclusion, our results demonstrate that depletion of the mitochondrial SAM pool by SAH, which is elevated during chronic <b>alcohol</b> consumption, plays a critical role in SAH induced sensitization to <strong>TNF</strong> hepatotoxicity.
+TNF	addiction	sensitization	17574213	In conclusion, our results demonstrate that depletion of the mitochondrial SAM pool by SAH, which is elevated during chronic alcohol consumption, plays a critical role in SAH induced <b>sensitization</b> to <strong>TNF</strong> hepatotoxicity.
+TNF	drug	alcohol	17551540	administrations of the cytokines IL 1 beta, CCL2 (MCP 1) or <strong>TNFalpha</strong> (cytokine/withdrawal protocol) before exposure and withdrawal from a 5 day cycle of chronic <b>ethanol</b> diet.
+TNF	addiction	withdrawal	17551540	administrations of the cytokines IL 1 beta, CCL2 (MCP 1) or <strong>TNFalpha</strong> (cytokine/<b>withdrawal</b> protocol) before exposure and <b>withdrawal</b> from a 5 day cycle of chronic ethanol diet.
+TNF	drug	benzodiazepine	17551540	Finally, just as found previously with the stress/withdrawal protocol, administration of the <b>benzodiazepine</b> receptor antagonist flumazenil before the LPS or <strong>TNF</strong> treatments prevented anxiety sensitization.
+TNF	addiction	sensitization	17551540	Finally, just as found previously with the stress/withdrawal protocol, administration of the benzodiazepine receptor antagonist flumazenil before the LPS or <strong>TNF</strong> treatments prevented anxiety <b>sensitization</b>.
+TNF	addiction	withdrawal	17551540	Finally, just as found previously with the stress/<b>withdrawal</b> protocol, administration of the benzodiazepine receptor antagonist flumazenil before the LPS or <strong>TNF</strong> treatments prevented anxiety sensitization.
+TNF	addiction	dependence	17538232	The roles of glial cell line derived neurotrophic factor, <strong>tumor necrosis factor</strong> alpha, and an inducer of these factors in drug <b>dependence</b>.
+TNF	addiction	dependence	17538232	In this article, the roles of glial cell line derived neurotrophic factor (GDNF) and tumor necrosis factor alpha (<strong>TNF</strong> alpha) in drug <b>dependence</b> are discussed.
+TNF	addiction	dependence	17538232	In this article, the roles of glial cell line derived neurotrophic factor (GDNF) and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) in drug <b>dependence</b> are discussed.
+TNF	drug	amphetamine	17538232	<strong>TNF</strong> alpha attenuates rewarding effects and locomotor sensitization induced by <b>methamphetamine</b> (<b>METH</b>) and morphine (MOR).
+TNF	drug	opioid	17538232	<strong>TNF</strong> alpha attenuates rewarding effects and locomotor sensitization induced by methamphetamine (METH) and <b>morphine</b> (MOR).
+TNF	addiction	sensitization	17538232	<strong>TNF</strong> alpha attenuates rewarding effects and locomotor <b>sensitization</b> induced by methamphetamine (METH) and morphine (MOR).
+TNF	addiction	dependence	17538232	Moreover, we mentioned the potential of Leu Ile, which induces the expression of GDNF and <strong>TNF</strong> alpha, as a novel therapeutic agent for drug <b>dependence</b>.
+TNF	drug	amphetamine	17538232	The inhibitory effect of Leu Ile on <b>METH</b>  or MOR induced place preference is not observed in GDNF heterozygous and <strong>TNF</strong> alpha knockout mice.
+TNF	drug	amphetamine	17538232	Leu Ile inhibits <b>METH</b>  or MOR induced place preference and sensitization by attenuating the <b>METH</b>  or MOR induced increase in extracellular dopamine levels in the nucleus accumbens via the induction of GDNF and <strong>TNF</strong> alpha expression.
+TNF	addiction	sensitization	17538232	Leu Ile inhibits METH  or MOR induced place preference and <b>sensitization</b> by attenuating the METH  or MOR induced increase in extracellular dopamine levels in the nucleus accumbens via the induction of GDNF and <strong>TNF</strong> alpha expression.
+TNF	drug	alcohol	17386065	Conversely, patients with ALC and at least 1 year of <b>alcohol</b> withdrawal (ALCAW group) showed a decreased number of total circulating DC, whereas ALC patients with active EtOH intake (ALCET group) had an abnormally low production of IL1beta and <strong>TNFalpha</strong> by PB DC.
+TNF	addiction	withdrawal	17386065	Conversely, patients with ALC and at least 1 year of alcohol <b>withdrawal</b> (ALCAW group) showed a decreased number of total circulating DC, whereas ALC patients with active EtOH intake (ALCET group) had an abnormally low production of IL1beta and <strong>TNFalpha</strong> by PB DC.
+TNF	drug	opioid	17377112	Conversely, a prevention of the increase in <strong>TNF</strong> alpha levels was observed only in rats treated with nimesulide or <b>tramadol</b> and paracetamol in combination.
+TNF	drug	alcohol	17374050	Only the T x Hem induced increase in lung <strong>TNF</strong> alpha was prevented by binge <b>alcohol</b> administration.
+TNF	addiction	intoxication	17374050	Only the T x Hem induced increase in lung <strong>TNF</strong> alpha was prevented by <b>binge</b> alcohol administration.
+TNF	drug	alcohol	17374050	While T x Hem did not prevent LPS induced release of <strong>TNF</strong> alpha, IL 1alpha, IL 6, or IL 10 at 6 or 24 hours, <b>alcohol</b> binge suppressed <strong>TNF</strong> alpha, IL 1 and IL 6 release, without altering IL 10 response in cells isolated from blood and pleural compartment.
+TNF	addiction	intoxication	17374050	While T x Hem did not prevent LPS induced release of <strong>TNF</strong> alpha, IL 1alpha, IL 6, or IL 10 at 6 or 24 hours, alcohol <b>binge</b> suppressed <strong>TNF</strong> alpha, IL 1 and IL 6 release, without altering IL 10 response in cells isolated from blood and pleural compartment.
+TNF	drug	amphetamine	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only tumor necrosis factor alpha (<strong>TNF</strong> alpha) but also glial cell line derived neurotrophic factor (GDNF), inhibits <b>methamphetamine</b> (<b>METH</b>) and morphine (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of <strong>TNF</strong> alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for <b>METH</b> and MOR induced dependence.
+TNF	drug	opioid	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only tumor necrosis factor alpha (<strong>TNF</strong> alpha) but also glial cell line derived neurotrophic factor (GDNF), inhibits methamphetamine (METH) and <b>morphine</b> (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of <strong>TNF</strong> alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced dependence.
+TNF	addiction	dependence	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only tumor necrosis factor alpha (<strong>TNF</strong> alpha) but also glial cell line derived neurotrophic factor (GDNF), inhibits methamphetamine (METH) and morphine (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of <strong>TNF</strong> alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced <b>dependence</b>.
+TNF	addiction	sensitization	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only tumor necrosis factor alpha (<strong>TNF</strong> alpha) but also glial cell line derived neurotrophic factor (GDNF), inhibits methamphetamine (METH) and morphine (MOR) induced <b>sensitization</b> and rewarding effects by regulating extracellular dopamine levels via the induction of <strong>TNF</strong> alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced dependence.
+TNF	drug	amphetamine	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) but also glial cell line derived neurotrophic factor (GDNF), inhibits <b>methamphetamine</b> (<b>METH</b>) and morphine (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of <strong>TNF</strong> alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for <b>METH</b> and MOR induced dependence.
+TNF	drug	opioid	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) but also glial cell line derived neurotrophic factor (GDNF), inhibits methamphetamine (METH) and <b>morphine</b> (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of <strong>TNF</strong> alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced dependence.
+TNF	addiction	dependence	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) but also glial cell line derived neurotrophic factor (GDNF), inhibits methamphetamine (METH) and morphine (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of <strong>TNF</strong> alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced <b>dependence</b>.
+TNF	addiction	sensitization	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) but also glial cell line derived neurotrophic factor (GDNF), inhibits methamphetamine (METH) and morphine (MOR) induced <b>sensitization</b> and rewarding effects by regulating extracellular dopamine levels via the induction of <strong>TNF</strong> alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced dependence.
+TNF	drug	alcohol	17266151	Spontaneous and in vitro stimulated production of interleukin (IL) 1alpha (<strong>TNFalpha</strong>) by PB monocytes was analyzed at the single level by flow cytometry in chronic <b>alcoholics</b> without liver disease and active <b>ethanol</b> (EtOH) intake (AWLD group), as well as in patients with <b>alcohol</b> liver cirrhosis (ALC group), who were either actively drinking (ALCET group) or with <b>alcohol</b> withdrawal (ALCAW group).
+TNF	addiction	withdrawal	17266151	Spontaneous and in vitro stimulated production of interleukin (IL) 1alpha (<strong>TNFalpha</strong>) by PB monocytes was analyzed at the single level by flow cytometry in chronic alcoholics without liver disease and active ethanol (EtOH) intake (AWLD group), as well as in patients with alcohol liver cirrhosis (ALC group), who were either actively drinking (ALCET group) or with alcohol <b>withdrawal</b> (ALCAW group).
+TNF	drug	opioid	17217924	<strong>Tumor necrosis factor</strong> alpha and its inducer inhibit <b>morphine</b> induced rewarding effects and sensitization.
+TNF	addiction	sensitization	17217924	<strong>Tumor necrosis factor</strong> alpha and its inducer inhibit morphine induced rewarding effects and <b>sensitization</b>.
+TNF	drug	amphetamine	17217924	We have demonstrated that <strong>TNF</strong> alpha or Leu Ile, a <strong>TNF</strong> alpha inducer, inhibits <b>methamphetamine</b> induced rewarding effects and sensitization.
+TNF	addiction	sensitization	17217924	We have demonstrated that <strong>TNF</strong> alpha or Leu Ile, a <strong>TNF</strong> alpha inducer, inhibits methamphetamine induced rewarding effects and <b>sensitization</b>.
+TNF	drug	opioid	17217924	In this study, we investigated the effects of <strong>TNF</strong> alpha or Leu Ile on <b>morphine</b> (MOR) induced rewarding effects and sensitization.
+TNF	addiction	sensitization	17217924	In this study, we investigated the effects of <strong>TNF</strong> alpha or Leu Ile on morphine (MOR) induced rewarding effects and <b>sensitization</b>.
+TNF	addiction	sensitization	17217924	Effects of <strong>TNF</strong> alpha or Leu Ile on MOR induced rewarding effects and <b>sensitization</b> were investigated by conditioned place preference and locomotor activity tests.
+TNF	drug	opioid	17217924	Effects of <strong>TNF</strong> alpha or Leu Ile on MOR induced antinociceptive effect and withdrawal symptoms were examined by hot plate test and <b>naloxone</b> precipitated withdrawal.
+TNF	addiction	withdrawal	17217924	Effects of <strong>TNF</strong> alpha or Leu Ile on MOR induced antinociceptive effect and <b>withdrawal</b> symptoms were examined by hot plate test and naloxone precipitated <b>withdrawal</b>.
+TNF	drug	opioid	17217924	<b>Morphine</b> induced <strong>TNF</strong> alpha mRNA expression via dopamine and <b>opioid</b> receptors.
+TNF	addiction	sensitization	17217924	Posttreatment with <strong>TNF</strong> alpha or Leu Ile attenuated the MOR induced place preference and <b>sensitization</b> even after their development, as well as pretreatment with <strong>TNF</strong> alpha or Leu Ile blocked them.
+TNF	addiction	sensitization	17217924	These results suggest that <strong>TNF</strong> alpha inhibits MOR induced rewarding effect and <b>sensitization</b> by regulating extracellular dopamine levels, and Leu Ile inhibits them via the induction of <strong>TNF</strong> alpha.
+TNF	drug	alcohol	17117972	However, muscle <strong>TNF</strong> alpha mRNA expression was markedly increased at 10 months post SIV infection in <b>alcohol</b>/SIV(+) animals.
+TNF	drug	amphetamine	17105909	Association study of the <strong>tumor necrosis factor</strong> alpha gene and its 1A receptor gene with <b>methamphetamine</b> dependence.
+TNF	addiction	dependence	17105909	Association study of the <strong>tumor necrosis factor</strong> alpha gene and its 1A receptor gene with methamphetamine <b>dependence</b>.
+TNF	drug	amphetamine	17105909	Recent preclinical findings that repeated treatment with <b>methamphetamine</b> (<b>METH</b>) induced an increase in tumor necrosis factor alpha (<strong>TNF</strong> alpha) mRNA in some brain regions and that <strong>TNF</strong> alpha blocked <b>METH</b> neurotoxicity and rewarding effects suggest <strong>TNF</strong> alpha, a multifunctional pro inflammatory cytokine, may be involved in <b>METH</b> dependence.
+TNF	addiction	dependence	17105909	Recent preclinical findings that repeated treatment with methamphetamine (METH) induced an increase in tumor necrosis factor alpha (<strong>TNF</strong> alpha) mRNA in some brain regions and that <strong>TNF</strong> alpha blocked METH neurotoxicity and rewarding effects suggest <strong>TNF</strong> alpha, a multifunctional pro inflammatory cytokine, may be involved in METH <b>dependence</b>.
+TNF	drug	amphetamine	17105909	Recent preclinical findings that repeated treatment with <b>methamphetamine</b> (<b>METH</b>) induced an increase in <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) mRNA in some brain regions and that <strong>TNF</strong> alpha blocked <b>METH</b> neurotoxicity and rewarding effects suggest <strong>TNF</strong> alpha, a multifunctional pro inflammatory cytokine, may be involved in <b>METH</b> dependence.
+TNF	addiction	dependence	17105909	Recent preclinical findings that repeated treatment with methamphetamine (METH) induced an increase in <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) mRNA in some brain regions and that <strong>TNF</strong> alpha blocked METH neurotoxicity and rewarding effects suggest <strong>TNF</strong> alpha, a multifunctional pro inflammatory cytokine, may be involved in METH <b>dependence</b>.
+TNF	drug	amphetamine	17105909	We hypothesized that genetic polymorphisms of the <strong>TNF</strong> alpha gene and its receptor genes may be associated with vulnerability to <b>METH</b> dependence.
+TNF	addiction	dependence	17105909	We hypothesized that genetic polymorphisms of the <strong>TNF</strong> alpha gene and its receptor genes may be associated with vulnerability to METH <b>dependence</b>.
+TNF	drug	amphetamine	17105909	Genetic association of  308G>A and  857C>T in the promotor region of the <strong>TNF</strong> alpha gene, and 36A>G in exon 1 of the <strong>TNF</strong> receptor 1A gene (TNFR SF1A), were analyzed in patients with <b>METH</b> dependence (n = 185) and healthy controls (n = 221) in a Japanese population.
+TNF	addiction	dependence	17105909	Genetic association of  308G>A and  857C>T in the promotor region of the <strong>TNF</strong> alpha gene, and 36A>G in exon 1 of the <strong>TNF</strong> receptor 1A gene (TNFR SF1A), were analyzed in patients with METH <b>dependence</b> (n = 185) and healthy controls (n = 221) in a Japanese population.
+TNF	drug	amphetamine	17105909	No significant association of alleles or haplotypes of the <strong>TNF</strong> alpha or TNFR SF1A genes with <b>METH</b> dependence was found.
+TNF	addiction	dependence	17105909	No significant association of alleles or haplotypes of the <strong>TNF</strong> alpha or TNFR SF1A genes with METH <b>dependence</b> was found.
+TNF	drug	amphetamine	17105909	These results suggest that genetic variations in the <strong>TNF</strong> alpha gene and its receptor genes may not be involved in individual vulnerability to <b>METH</b> dependence.
+TNF	addiction	dependence	17105909	These results suggest that genetic variations in the <strong>TNF</strong> alpha gene and its receptor genes may not be involved in individual vulnerability to METH <b>dependence</b>.
+TNF	drug	cocaine	17068203	In <b>cocaine</b> dependent volunteers and control subjects, we analyzed monocyte <strong>TNF</strong> alpha and IL 6 expression at rest and in response to the bacterial ligand, lipopolysaccharide (LPS), over a 24 h period.
+TNF	drug	cocaine	17068203	In addition, the in vivo effects of <b>cocaine</b> (40 mg) versus placebo on monocyte expression of <strong>TNF</strong> alpha and IL 6 were profiled over 48 h. <b>Cocaine</b> dependent volunteers showed a decrease in the capacity of monocytes to express <strong>TNF</strong> alpha and IL 6 compared with control subjects.
+TNF	addiction	withdrawal	17068203	Heart rate variability analyses showed that increases of sympathetic activity along with vagal <b>withdrawal</b> were associated with decreases in monocyte expression of <strong>TNF</strong> alpha.
+TNF	drug	amphetamine	17046726	An inducer for glial cell line derived neurotrophic factor and <strong>tumor necrosis factor</strong> alpha protects against <b>methamphetamine</b> induced rewarding effects and sensitization.
+TNF	addiction	sensitization	17046726	An inducer for glial cell line derived neurotrophic factor and <strong>tumor necrosis factor</strong> alpha protects against methamphetamine induced rewarding effects and <b>sensitization</b>.
+TNF	drug	amphetamine	17046726	We investigated the potential of Leu Ile, which induces the expression of glial cell line derived neurotrophic factor (GDNF) and tumor necrosis factor alpha (<strong>TNF</strong> alpha), as a novel therapeutic agent for <b>methamphetamine</b> (<b>METH</b>) induced dependence.
+TNF	addiction	dependence	17046726	We investigated the potential of Leu Ile, which induces the expression of glial cell line derived neurotrophic factor (GDNF) and tumor necrosis factor alpha (<strong>TNF</strong> alpha), as a novel therapeutic agent for methamphetamine (METH) induced <b>dependence</b>.
+TNF	drug	amphetamine	17046726	We investigated the potential of Leu Ile, which induces the expression of glial cell line derived neurotrophic factor (GDNF) and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha), as a novel therapeutic agent for <b>methamphetamine</b> (<b>METH</b>) induced dependence.
+TNF	addiction	dependence	17046726	We investigated the potential of Leu Ile, which induces the expression of glial cell line derived neurotrophic factor (GDNF) and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha), as a novel therapeutic agent for methamphetamine (METH) induced <b>dependence</b>.
+TNF	drug	amphetamine	17046726	An inhibitory effect of Leu Ile on <b>METH</b> induced place preference was observed in neither GDNF heterozygous nor <strong>TNF</strong> alpha knockout mice.
+TNF	drug	amphetamine	17046726	These results suggest that Leu Ile inhibits <b>METH</b> induced rewarding effects and sensitization by regulating extracellular DA levels via the induction of GDNF and <strong>TNF</strong> alpha expression.
+TNF	addiction	sensitization	17046726	These results suggest that Leu Ile inhibits METH induced rewarding effects and <b>sensitization</b> by regulating extracellular DA levels via the induction of GDNF and <strong>TNF</strong> alpha expression.
+TNF	drug	cannabinoid	17017918	Recently, it has been shown that <b>rimonabant</b> prevents indomethacin induced intestinal injury by decreasing the levels of pro inflammatory cytokine tumour necrosis factor alpha (<strong>TNFalpha</strong>), thus indicating that CB1 receptor antagonists might exhibit potential anti inflammatory activity in acute and chronic diseases.
+TNF	drug	alcohol	16958667	Mitochondrial GSH depletion due to <b>alcohol</b> mediated alteration in mitochondrial membrane dynamics underlies the susceptibility of hepatocytes from <b>alcohol</b> fed models to tumor necrosis factor (<strong>TNF</strong>), and in nutritional and genetic models of hepatic steatosis, mGSH depletion occurs due to the enrichment of mitochondria in free cholesterol, resulting in decreased mitochondrial membrane fluidity.
+TNF	drug	alcohol	16958667	Mitochondrial GSH depletion due to <b>alcohol</b> mediated alteration in mitochondrial membrane dynamics underlies the susceptibility of hepatocytes from <b>alcohol</b> fed models to <strong>tumor necrosis factor</strong> (<strong>TNF</strong>), and in nutritional and genetic models of hepatic steatosis, mGSH depletion occurs due to the enrichment of mitochondria in free cholesterol, resulting in decreased mitochondrial membrane fluidity.
+TNF	drug	alcohol	16923312	The available evidence indicates that, by favouring mitochondrial permeability transition, oxidative stress promotes hepatocyte necrosis and/or apoptosis and is implicated in the <b>alcohol</b> induced sensitization of hepatocytes to the pro apoptotic action of <strong>TNF</strong> alpha.
+TNF	addiction	sensitization	16923312	The available evidence indicates that, by favouring mitochondrial permeability transition, oxidative stress promotes hepatocyte necrosis and/or apoptosis and is implicated in the alcohol induced <b>sensitization</b> of hepatocytes to the pro apoptotic action of <strong>TNF</strong> alpha.
+TNF	drug	alcohol	16916584	Interleukin 1 alpha and beta, <strong>TNF</strong> alpha and HTTLPR gene variants study on <b>alcohol</b> toxicity and detoxification outcome.
+TNF	drug	alcohol	16916584	In the present study we investigated the IL 1A rs1800587, IL 1B rs3087258, <strong>TNF</strong> alpha rs1799724 and the HTTLPR variants in a sample of 64 <b>alcohol</b> dependents and 47 relatives versus a set of clinical parameters and outcome measures.
+TNF	drug	alcohol	16916584	In our sample IL 1A, IL 1B, <strong>TNF</strong> alpha and HTTLPR do not appear as liability factors for <b>alcohol</b> toxicity or detoxification outcome, however the small sample size may influence the observed results.
+TNF	drug	alcohol	16783199	Only the hemorrhage induced rise in lung IL 6 and <strong>tumor necrosis factor</strong> alpha was prevented by <b>alcohol</b> administration.
+TNF	drug	opioid	16697650	In vitro studies showed that HIV proteins, gp120 and Tat, Tat + <b>morphine</b> but not tumor necrosis factor alpha (<strong>TNF</strong> alpha), caused increased neurotoxicity in human neuronal cultures with ApoE4 allele.
+TNF	drug	opioid	16697650	In vitro studies showed that HIV proteins, gp120 and Tat, Tat + <b>morphine</b> but not <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha), caused increased neurotoxicity in human neuronal cultures with ApoE4 allele.
+TNF	drug	alcohol	16410364	Adiponectin normalizes LPS stimulated <strong>TNF</strong> alpha production by rat Kupffer cells after chronic <b>ethanol</b> feeding.
+TNF	drug	alcohol	16410364	Chronic <b>ethanol</b> feeding sensitizes Kupffer cells to activation by lipopolysaccharide (LPS), leading to increased production of tumor necrosis factor alpha (<strong>TNF</strong> alpha).
+TNF	drug	alcohol	16410364	Chronic <b>ethanol</b> feeding sensitizes Kupffer cells to activation by lipopolysaccharide (LPS), leading to increased production of <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha).
+TNF	drug	alcohol	16410364	Adiponectin dose dependently inhibited LPS stimulated accumulation of <strong>TNF</strong> alpha mRNA and peptide in Kupffer cells from both pair  and <b>ethanol</b> fed rats.
+TNF	drug	alcohol	16410364	Suppression of LPS stimulated ERK1/2 signaling by low concentrations of gAcrp was associated with normalization of <strong>TNF</strong> alpha production by Kupffer cells after chronic <b>ethanol</b> exposure.
+TNF	drug	alcohol	16385231	LPS induced <strong>TNF</strong> alpha production by Kupffer cells isolated from mice 1 hr after <b>ethanol</b> was reduced to about 60% of values from control Kupffer cells, while LPS induced <strong>TNF</strong> alpha production by Kupffer cells isolated from mice treated with <b>ethanol</b> 21 hrs earlier increased 1.5 fold over control Kupffer cells.
+TNF	drug	alcohol	16317704	<b>Alcohol</b> increases <strong>tumor necrosis factor</strong> alpha and decreases nuclear factor kappab to activate hepatic apoptosis in genetically obese mice.
+TNF	drug	alcohol	16317704	Some obese mice also received pentoxifylline, an inhibitor of tumor necrosis factor alpha (<strong>TNF</strong> alpha) production, before each <b>ethanol</b> administration.
+TNF	drug	alcohol	16317704	Some obese mice also received pentoxifylline, an inhibitor of <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) production, before each <b>ethanol</b> administration.
+TNF	drug	alcohol	16317704	In lean mice, these moderate <b>ethanol</b> doses did not increase plasma <strong>TNF</strong> alpha and hepatic caspase 3 activity, but triggered some apoptotic hepatocytes.
+TNF	drug	alcohol	16317704	<b>Alcohol</b> administration to ob/ob mice did not increase oxidative stress despite increased CYP2E1, but increased plasma <strong>TNF</strong> alpha, further increased Hsp70, and profoundly decreased p65 nuclear factor kappaB (NF kappaB) protein and DNA binding activity in nuclear extracts.
+TNF	drug	alcohol	16317704	Moderate <b>ethanol</b> intoxication does not increase oxidative stress in obese mice, but increases <strong>TNF</strong> alpha and also decreases nuclear NF kappaB activity, thus unleashing the apoptotic effects of <strong>TNF</strong> alpha.
+TNF	addiction	intoxication	16317704	Moderate ethanol <b>intoxication</b> does not increase oxidative stress in obese mice, but increases <strong>TNF</strong> alpha and also decreases nuclear NF kappaB activity, thus unleashing the apoptotic effects of <strong>TNF</strong> alpha.
+TNF	drug	amphetamine	16134406	They evoke possible involvement of cocaine's influence on the anorexigenic cytokine <strong>Tumor Necrosis Factor</strong>, Cocaine and <b>Amphetamine</b> Regulated Transcript, or suppression of the appetite stimulating Neuropeptide Y, or cocaine induced deficits in nicotinic cholinergic neural transmission, all of which have not only been linked to weight and appetite, but also to idiopathic psychosis.
+TNF	drug	cocaine	16134406	They evoke possible involvement of <b>cocaine</b>'s influence on the anorexigenic cytokine <strong>Tumor Necrosis Factor</strong>, <b>Cocaine</b> and Amphetamine Regulated Transcript, or suppression of the appetite stimulating Neuropeptide Y, or <b>cocaine</b> induced deficits in nicotinic cholinergic neural transmission, all of which have not only been linked to weight and appetite, but also to idiopathic psychosis.
+TNF	drug	alcohol	16007126	However, we found that they pay a price for their resistance in that they are more susceptible to clinically relevant forms of tissue injury  they suffer increased hepatic injury in a model of binge <b>alcohol</b> abuse and in response to <strong>TNF</strong> alpha treatment.
+TNF	addiction	intoxication	16007126	However, we found that they pay a price for their resistance in that they are more susceptible to clinically relevant forms of tissue injury  they suffer increased hepatic injury in a model of <b>binge</b> alcohol abuse and in response to <strong>TNF</strong> alpha treatment.
+TNF	drug	alcohol	15961886	Because cytochrome P4502E1 (CYP2E1) is upregulated in Kupffer cells after <b>ethanol</b>, we hypothesized that this effect primes Kupffer cells, sensitizing them to increase <strong>TNF</strong> alpha production in response to LPS.
+TNF	drug	opioid	15913793	<b>Morphine</b> withdrawal sensitizes mice to lipopolysaccharide: elevated <strong>TNF</strong> alpha and nitric oxide with decreased IL 12.
+TNF	addiction	withdrawal	15913793	Morphine <b>withdrawal</b> sensitizes mice to lipopolysaccharide: elevated <strong>TNF</strong> alpha and nitric oxide with decreased IL 12.
+TNF	drug	opioid	15913793	<b>Morphine</b> withdrawn LPS treated animals had elevated serum <strong>TNF</strong> alpha and nitric oxide levels, and depressed IL 12 levels compared to controls.
+TNF	drug	opioid	15913793	Anti <strong>TNF</strong> alpha antibody given prior to LPS challenge afforded significant protection to <b>morphine</b> withdrawn animals.
+TNF	drug	opioid	15913793	These studies show that <b>morphine</b> withdrawal sensitizes to LPS lethality via increased production of <strong>TNF</strong> alpha.
+TNF	addiction	withdrawal	15913793	These studies show that morphine <b>withdrawal</b> sensitizes to LPS lethality via increased production of <strong>TNF</strong> alpha.
+TNF	drug	alcohol	15845418	Depletion of mitochondrial GSH by <b>alcohol</b> is believed to contribute to the sensitization of the liver to <b>alcohol</b> induced injury through tumor necrosis factor (<strong>TNF</strong>) mediated hepatocellular death.
+TNF	addiction	sensitization	15845418	Depletion of mitochondrial GSH by alcohol is believed to contribute to the <b>sensitization</b> of the liver to alcohol induced injury through tumor necrosis factor (<strong>TNF</strong>) mediated hepatocellular death.
+TNF	drug	alcohol	15845418	Depletion of mitochondrial GSH by <b>alcohol</b> is believed to contribute to the sensitization of the liver to <b>alcohol</b> induced injury through <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) mediated hepatocellular death.
+TNF	addiction	sensitization	15845418	Depletion of mitochondrial GSH by alcohol is believed to contribute to the <b>sensitization</b> of the liver to alcohol induced injury through <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) mediated hepatocellular death.
+TNF	drug	nicotine	15710343	The present study aimed at investigating the effect of <b>nicotine</b> on TGF beta1, IL 10, IL 12, and <strong>TNF</strong> alpha production in Cpn infected human peripheral blood mononuclear cells (PBMCs).
+TNF	drug	nicotine	15710343	<b>Nicotine</b> treatment of the Cpn infected cells up regulated IL 10, but not <strong>TNF</strong> alpha and IL 12, and also resulted in significant down regulation of TGF beta1 production which was marked in the Cpn infected control cells.
+TNF	drug	alcohol	15633127	Huh 7 cells expressing core protein, cytochrome P450 2E1, or both were exposed to 0.1 mmol/L tertiary butyl hydroperoxide, <strong>tumor necrosis factor</strong> alpha, and/or 25 mmol/L <b>ethanol</b>.
+TNF	drug	alcohol	15596084	Topics were (1) T cell activation after chronic <b>ethanol</b> ingestion in mice, (2) effect of <b>ethanol</b> consumption on the severity of acute viral mediated pancreatitis, (3) <b>ethanol</b> and alveolar macrophage dysfunction, (4) impaired intestinal immunity and barrier function: a cause for enhanced bacterial translocation in <b>alcohol</b> intoxication and burn injury, (5) immune consequences of the combined insult of acute <b>ethanol</b> exposure and burn injury, (6) consequences of <b>alcohol</b> induced dysregulation of immediate hemodynamic and inflammatory responses to trauma/hemorrhage, (7) regulation of <strong>tumor necrosis factor</strong> alpha production by Kupffer cells after chronic exposure to <b>ethanol</b>, (8) acute exposure to <b>ethanol</b> and suppression of cytokine responses induced through Toll like receptors, and (9) inhibition of antigen presenting cell functions by <b>alcohol</b>: implications for hepatitis C virus infection.
+TNF	addiction	intoxication	15596084	Topics were (1) T cell activation after chronic ethanol ingestion in mice, (2) effect of ethanol consumption on the severity of acute viral mediated pancreatitis, (3) ethanol and alveolar macrophage dysfunction, (4) impaired intestinal immunity and barrier function: a cause for enhanced bacterial translocation in alcohol <b>intoxication</b> and burn injury, (5) immune consequences of the combined insult of acute ethanol exposure and burn injury, (6) consequences of alcohol induced dysregulation of immediate hemodynamic and inflammatory responses to trauma/hemorrhage, (7) regulation of <strong>tumor necrosis factor</strong> alpha production by Kupffer cells after chronic exposure to ethanol, (8) acute exposure to ethanol and suppression of cytokine responses induced through Toll like receptors, and (9) inhibition of antigen presenting cell functions by alcohol: implications for hepatitis C virus infection.
+TNF	drug	nicotine	15339882	Polymorphisms of MHC class III genes (RCCX modules, <strong>TNFA</strong> promoter polymorphisms) were determined in 101 healthy subjects and 232 coronary artery disease (CAD) patients from Hungary with defined <b>tobacco</b> <b>smoking</b> habits.
+TNF	drug	alcohol	15318102	Sensitivity of Kupffer cells to endotoxin [lipopolysaccharide (LPS)] and overproduction of tumor necrosis factor alpha (<strong>TNF</strong> alpha) are critical for progression of <b>alcoholic</b> liver injury.
+TNF	drug	alcohol	15318102	Sensitivity of Kupffer cells to endotoxin [lipopolysaccharide (LPS)] and overproduction of <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) are critical for progression of <b>alcoholic</b> liver injury.
+TNF	drug	alcohol	15318102	Therefore, suppression of <strong>TNF</strong> alpha should prove useful for treatment of <b>alcoholic</b> liver injury.
+TNF	drug	alcohol	15318101	Pioglitazone prevents acute liver injury induced by <b>ethanol</b> and lipopolysaccharide through the suppression of <strong>tumor necrosis factor</strong> alpha.
+TNF	drug	alcohol	15318101	<b>Ethanol</b> and LPS induction of <strong>TNF</strong> alpha mRNA in the liver was blunted by pioglitazone; however, RXR alpha mRNA was not affected.
+TNF	drug	alcohol	15318101	These results suggest that pioglitazone may prevent liver injury induced by <b>ethanol</b> and LPS through the suppression of <strong>TNF</strong> alpha.
+TNF	drug	alcohol	15289211	In 36 <b>alcoholics</b> without liver disease, at the point of commencing withdrawal from <b>alcohol</b>, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (<strong>TNFalpha</strong>, IL1beta, IL1RA, IL4, IL6, IL8, IL10 and IL12).
+TNF	addiction	withdrawal	15289211	In 36 alcoholics without liver disease, at the point of commencing <b>withdrawal</b> from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (<strong>TNFalpha</strong>, IL1beta, IL1RA, IL4, IL6, IL8, IL10 and IL12).
+TNF	addiction	withdrawal	15289211	While IL1  and <strong>TNFalpha</strong> responses normalized after the <b>withdrawal</b> period, impairment of the IL12 response persisted throughout the observation period of 2 weeks.
+TNF	drug	alcohol	15282117	In the current study, our aim was to evaluate and investigate the influence of heavy <b>alcohol</b> intake on serum interleukin (IL) 6, IL 8, IL 10, IL 12, and tumor necrosis factor alpha (<strong>TNF</strong> alpha) concentrations.
+TNF	drug	alcohol	15282117	In the current study, our aim was to evaluate and investigate the influence of heavy <b>alcohol</b> intake on serum interleukin (IL) 6, IL 8, IL 10, IL 12, and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) concentrations.
+TNF	drug	alcohol	15157952	In this study, we investigated whether nocturnal plasma levels of interleukin 6 (IL 6) and tumor necrosis factor alpha (<strong>TNF</strong>) were associated with disordered sleep in <b>alcohol</b> dependence by testing the temporal relationships between these inflammatory cytokines and sleep, before and after sleep deprivation.
+TNF	addiction	dependence	15157952	In this study, we investigated whether nocturnal plasma levels of interleukin 6 (IL 6) and tumor necrosis factor alpha (<strong>TNF</strong>) were associated with disordered sleep in alcohol <b>dependence</b> by testing the temporal relationships between these inflammatory cytokines and sleep, before and after sleep deprivation.
+TNF	drug	alcohol	15157952	In this study, we investigated whether nocturnal plasma levels of interleukin 6 (IL 6) and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong>) were associated with disordered sleep in <b>alcohol</b> dependence by testing the temporal relationships between these inflammatory cytokines and sleep, before and after sleep deprivation.
+TNF	addiction	dependence	15157952	In this study, we investigated whether nocturnal plasma levels of interleukin 6 (IL 6) and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong>) were associated with disordered sleep in alcohol <b>dependence</b> by testing the temporal relationships between these inflammatory cytokines and sleep, before and after sleep deprivation.
+TNF	drug	alcohol	15157952	Coupled with prolonged sleep latency and increased rapid eye movement sleep, <b>alcoholics</b> showed nocturnal elevations of IL 6 and <strong>TNF</strong> as compared to controls after adjustment for <b>alcohol</b> consumption and body mass index.
+TNF	drug	alcohol	15157952	Following sleep deprivation, <b>alcoholics</b> showed greater nocturnal levels of IL 6 and greater nocturnal increases of <strong>TNF</strong> as compared to controls.
+TNF	drug	alcohol	15131799	Activated natural killer T cells induce liver injury by Fas and <strong>tumor necrosis factor</strong> alpha during <b>alcohol</b> consumption.
+TNF	drug	alcohol	15131799	This report analyzes the role of natural killer T cells, Fas, and <strong>TNF</strong> alpha in a model of chronic <b>alcohol</b> consumption.
+TNF	drug	alcohol	15131799	<strong>TNF</strong> alpha plays an additional role as a defect in <strong>TNF</strong> receptor 1 inhibits <b>alcohol</b> associated liver injury.
+TNF	drug	alcohol	15131799	Stimulation of natural killer T cells during <b>alcohol</b> consumption induces serious liver injury by a mechanism that involves concomitant signals by Fas and <strong>tumor necrosis factor</strong> receptor 1 on <b>alcohol</b> stressed hepatocytes.
+TNF	drug	alcohol	15112943	The presentations were (1) Characterization of Synaptic Loss in Cerebella of Mature and Senescent Rats after Lengthy Chronic <b>Ethanol</b> Consumption, (2) <b>Ethanol</b> Withdrawal Both Causes Neurotoxicity and Inhibits Neuronal Recovery Processes in Rat Organotypic Hippocampal Cultures, (3) Binge Drinking Induced Brain Damage: Genetic and Age Related Effects, (4) Binge <b>Ethanol</b> Induced Brain Damage: Involvement of Edema, Arachidonic Acid and Tissue Necrosis Factor alpha (<strong>TNFalpha</strong>), and (5) Cyclic AMP Cascade, Stem Cells and <b>Ethanol</b>.
+TNF	addiction	intoxication	15112943	The presentations were (1) Characterization of Synaptic Loss in Cerebella of Mature and Senescent Rats after Lengthy Chronic Ethanol Consumption, (2) Ethanol Withdrawal Both Causes Neurotoxicity and Inhibits Neuronal Recovery Processes in Rat Organotypic Hippocampal Cultures, (3) <b>Binge</b> Drinking Induced Brain Damage: Genetic and Age Related Effects, (4) <b>Binge</b> Ethanol Induced Brain Damage: Involvement of Edema, Arachidonic Acid and Tissue Necrosis Factor alpha (<strong>TNFalpha</strong>), and (5) Cyclic AMP Cascade, Stem Cells and Ethanol.
+TNF	addiction	withdrawal	15112943	The presentations were (1) Characterization of Synaptic Loss in Cerebella of Mature and Senescent Rats after Lengthy Chronic Ethanol Consumption, (2) Ethanol <b>Withdrawal</b> Both Causes Neurotoxicity and Inhibits Neuronal Recovery Processes in Rat Organotypic Hippocampal Cultures, (3) Binge Drinking Induced Brain Damage: Genetic and Age Related Effects, (4) Binge Ethanol Induced Brain Damage: Involvement of Edema, Arachidonic Acid and Tissue Necrosis Factor alpha (<strong>TNFalpha</strong>), and (5) Cyclic AMP Cascade, Stem Cells and Ethanol.
+TNF	drug	psychedelics	15056370	Specifically, <b>MDMA</b> suppresses neutrophil phagocytosis, suppresses production of the pro inflammatory cytokines tumour necrosis factor alpha (<strong>TNF</strong> alpha) and interleukin (IL) 1beta, and increases production of the endogenous immunosuppressive cytokine (IL 10), thereby promoting an immunosuppressive cytokine phenotype.
+TNF	drug	amphetamine	14999072	Role of <strong>tumor necrosis factor</strong> alpha in <b>methamphetamine</b> induced drug dependence and neurotoxicity.
+TNF	addiction	dependence	14999072	Role of <strong>tumor necrosis factor</strong> alpha in methamphetamine induced drug <b>dependence</b> and neurotoxicity.
+TNF	drug	amphetamine	14999072	In this study, we investigated a role of <strong>TNF</strong> alpha in <b>METH</b> induced dependence and neurotoxicity.
+TNF	addiction	dependence	14999072	In this study, we investigated a role of <strong>TNF</strong> alpha in METH induced <b>dependence</b> and neurotoxicity.
+TNF	drug	amphetamine	14999072	Repeated treatment with <b>METH</b> (2 mg/kg for 5 d) in rats induced a significant increase in <strong>TNF</strong> alpha mRNA and protein expression in the brain.
+TNF	drug	amphetamine	14999072	Exogenous <strong>TNF</strong> alpha (1 4 microg) blocked locomotor stimulating and rewarding effects of <b>METH</b>, as well as <b>METH</b> (4 mg/kg; four times at 2 hr intervals) induced dopaminergic neurotoxicity in mice.
+TNF	drug	amphetamine	14999072	To examine a role of endogenous <strong>TNF</strong> alpha in behavioral and neurochemical effects of <b>METH</b>, we used mice with targeted deletions of the <strong>TNF</strong> alpha gene.
+TNF	drug	amphetamine	14999072	<strong>TNF</strong> alpha ( / ) mice showed enhanced responses to the locomotor sensitizing, rewarding, and neurotoxic effects of <b>METH</b> compared with wild type mice.
+TNF	drug	amphetamine	14999072	We also examined the role of <strong>TNF</strong> alpha in <b>METH</b> induced dopamine (DA) release and uptake in vitro and in vivo in C57BL/6 mice.
+TNF	drug	amphetamine	14999072	Exogenous <strong>TNF</strong> alpha (4 microg) attenuated the <b>METH</b> induced increase in extracellular striatal DA in vivo and potentiated striatal DA uptake into synaptosomes in vitro and in vivo.
+TNF	drug	amphetamine	14999072	Furthermore, <strong>TNF</strong> alpha activated vesicular DA uptake by itself and diminished the <b>METH</b> induced decrease in vesicular DA uptake.
+TNF	drug	amphetamine	14999072	Our findings suggest that <strong>TNF</strong> alpha plays a neuroprotective role in <b>METH</b> induced drug dependence and neurotoxicity by activating plasmalemmal and vesicular DA transporter as well as inhibiting <b>METH</b> induced increase in extracellular DA levels.
+TNF	addiction	dependence	14999072	Our findings suggest that <strong>TNF</strong> alpha plays a neuroprotective role in METH induced drug <b>dependence</b> and neurotoxicity by activating plasmalemmal and vesicular DA transporter as well as inhibiting METH induced increase in extracellular DA levels.
+TNF	drug	nicotine	14745115	These findings indicate that a single systematic administration of <b>nicotine</b> may attenuate the plasma exudation in the PSAR by suppressing the production of NO in the PMNs primed with <strong>TNF</strong> alpha via <b>nicotine</b> induced endogenous glucocorticoid.
+TNF	addiction	withdrawal	14741440	In vivo experiments carried out on mice 24 h post <b>withdrawal</b> showed increased sensitivity to the lethal effects of LPS and increased production of <strong>TNF</strong> alpha, implying a state of macrophage activation.
+TNF	drug	cocaine	14741438	Using experimental rodent models, description of effects of heroin or <b>cocaine</b>, especially self administration of these drugs, on immune cell deficiency and HPA activation, was reviewed as well as effects on important proinflammatory cytokines like <strong>TNFalpha</strong>.
+TNF	drug	opioid	14741438	Using experimental rodent models, description of effects of <b>heroin</b> or cocaine, especially self administration of these drugs, on immune cell deficiency and HPA activation, was reviewed as well as effects on important proinflammatory cytokines like <strong>TNFalpha</strong>.
+TNF	drug	amphetamine	14727530	Repeated treatment with <b>methamphetamine</b> induced an increase in <strong>TNF</strong> alpha mRNA in the some brain regions.
+TNF	drug	amphetamine	14727530	Exogenous <strong>TNF</strong> alpha blocked the <b>methamphetamine</b> rewarding.
+TNF	drug	amphetamine	14727530	<strong>TNF</strong> alpha plays a neuroprotective role in <b>methamphetamine</b> drug dependence.
+TNF	addiction	dependence	14727530	<strong>TNF</strong> alpha plays a neuroprotective role in methamphetamine drug <b>dependence</b>.
+TNF	addiction	dependence	14727530	These results suggest that a stimulator of <strong>TNF</strong> alpha synthesis may be one of therapeutic tools against drug <b>dependence</b>.
+TNF	drug	alcohol	14647036	Biochemical changes induced by <b>alcohol</b> administration included increased hepatic lipid peroxidation, nuclear factor kappaB activation, and <strong>tumor necrosis factor</strong> alpha messenger RNA expression.
+TNF	drug	alcohol	14639920	Two hours after <b>ethanol</b> administration, the LPS induced increases in intracellular calcium concentration and <strong>TNF</strong> alpha release by Kupffer cells was diminished by 50% of control, and these parameters were reciprocally enhanced two fold at 24 hours.
+TNF	drug	alcohol	14639920	Sterilization of the gut with antibiotics blocked both effects of <b>ethanol</b> on intracellular calcium concentration and <strong>TNF</strong> alpha release.
+TNF	drug	alcohol	14639920	In contrast, in Kupffer cells from mice treated with <b>ethanol</b> 21 hours earlier, LPS induced <strong>TNF</strong> alpha production, expression and activity of IRAK were increased 1.5 fold over controls, while NF kappa B activation was elevated 3 fold.
+TNF	drug	nicotine	14622092	The inflammatory cytokine tumor necrosis factor alpha (<strong>TNFalpha</strong>) is also neuroprotective, however, in the presence of <b>nicotine</b>, neuroprotection against NMDA is abolished.
+TNF	drug	nicotine	14622092	The inflammatory cytokine <strong>tumor necrosis factor</strong> alpha (<strong>TNFalpha</strong>) is also neuroprotective, however, in the presence of <b>nicotine</b>, neuroprotection against NMDA is abolished.
+TNF	drug	nicotine	14622092	The specificity of <b>nicotine</b> <strong>TNFalpha</strong> antagonism was further refined using a mouse transgenic dominant negative of nAChRalpha7 in which <b>nicotine</b> failed to induce neuroprotection against NMDA and antagonism of <strong>TNFalpha</strong> was absent.
+TNF	drug	nicotine	14622092	The mechanism of <strong>TNFalpha</strong> mediated neuroprotection and antagonism by <b>nicotine</b> was independent of caspase 8 activation or nuclear factor kappa B translocation in neurons but C6 ceramide addition to neuronal cultures subsequently exposed to NMDA mimicked the neuroprotective effect of <strong>TNFalpha</strong> and, like <strong>TNFalpha</strong>, it was antagonized by cotreatment with <b>nicotine</b>.
+TNF	addiction	withdrawal	14597094	Spleen cells from mice undergoing <b>withdrawal</b> also had decreased splenic mRNA and/or protein levels of IL 1beta, IL 1Ra, <strong>TNF</strong> alpha, IL 12, and IFN gamma.
+TNF	drug	alcohol	12960499	Sensitization of Kupffer cells (KC) to lipopolysaccharide (LPS) and overproduction of tumor necrosis factor (<strong>TNF</strong>) alpha play important roles in the pathogenesis of <b>alcoholic</b> liver damage and sepsis associated organ injury.
+TNF	addiction	sensitization	12960499	<b>Sensitization</b> of Kupffer cells (KC) to lipopolysaccharide (LPS) and overproduction of tumor necrosis factor (<strong>TNF</strong>) alpha play important roles in the pathogenesis of alcoholic liver damage and sepsis associated organ injury.
+TNF	drug	alcohol	12960499	Sensitization of Kupffer cells (KC) to lipopolysaccharide (LPS) and overproduction of <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha play important roles in the pathogenesis of <b>alcoholic</b> liver damage and sepsis associated organ injury.
+TNF	addiction	sensitization	12960499	<b>Sensitization</b> of Kupffer cells (KC) to lipopolysaccharide (LPS) and overproduction of <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha play important roles in the pathogenesis of alcoholic liver damage and sepsis associated organ injury.
+TNF	drug	alcohol	12937155	A critical involvement of oxidative stress in acute <b>alcohol</b> induced hepatic <strong>TNF</strong> alpha production.
+TNF	drug	alcohol	12937155	Tumor necrosis factor alpha (<strong>TNF</strong> alpha) production is a critical factor in the pathogenesis of <b>alcoholic</b> liver injury.
+TNF	drug	alcohol	12937155	<strong>Tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) production is a critical factor in the pathogenesis of <b>alcoholic</b> liver injury.
+TNF	drug	alcohol	12937155	Both oxidative stress and endotoxin have been implicated in the process of <b>alcohol</b> induced <strong>TNF</strong> alpha production.
+TNF	drug	alcohol	12937155	The present study was undertaken to determine the mediators of acute <b>alcohol</b> induced <strong>TNF</strong> alpha production using a mouse model of acute <b>alcohol</b> hepatotoxicity.
+TNF	drug	alcohol	12937155	<b>Alcohol</b> administration via gavage at a dose of 6 g/kg to 129/Sv mice induced hepatic <strong>TNF</strong> alpha production in Kupffer cells as demonstrated by measuring protein levels, immunohistochemical localization, and mRNA expression.
+TNF	drug	alcohol	12937155	Treatment with an endotoxin neutralizing protein significantly suppressed <b>alcohol</b> induced elevation of plasma endotoxin, hepatic lipid peroxidation, and inhibited <strong>TNF</strong> alpha production.
+TNF	drug	alcohol	12937155	Treatment with antioxidants, N ACETYL L CYSTEINE, or dimethylsulfoxide, failed to attenuate plasma endotoxin elevation, but significantly inhibited <b>alcohol</b> induced hepatic lipid peroxidation, <strong>TNF</strong> alpha production and steatosis.
+TNF	drug	alcohol	12937155	This study thus systemically dissected the relationship among plasma endotoxin elevation, hepatic oxidative stress, and <strong>TNF</strong> alpha production following acute <b>alcohol</b> administration, and the results demonstrate that oxidative stress mediates endotoxin induced hepatic <strong>TNF</strong> alpha production in acute <b>alcohol</b> intoxication.
+TNF	addiction	intoxication	12937155	This study thus systemically dissected the relationship among plasma endotoxin elevation, hepatic oxidative stress, and <strong>TNF</strong> alpha production following acute alcohol administration, and the results demonstrate that oxidative stress mediates endotoxin induced hepatic <strong>TNF</strong> alpha production in acute alcohol <b>intoxication</b>.
+TNF	drug	opioid	12927630	<strong>TNF</strong> evoked a time  and dose dependent muscle hyperalgesia within several hours after injection that was totally reversed by systemic treatment with the non <b>opioid</b> analgesic metamizol.
+TNF	addiction	withdrawal	12927630	Paw <b>withdrawal</b> thresholds or latencies to mechanical and thermal stimuli, respectively, were unchanged after intramuscular injection of <strong>TNF</strong> or formalin.
+TNF	drug	alcohol	12805475	On the other hand, sensitization of Kupffer cells to lipopolysaccharide (LPS) and their production of <strong>TNF</strong> alpha are critical for progression of <b>alcoholic</b> liver injury.
+TNF	addiction	sensitization	12805475	On the other hand, <b>sensitization</b> of Kupffer cells to lipopolysaccharide (LPS) and their production of <strong>TNF</strong> alpha are critical for progression of alcoholic liver injury.
+TNF	drug	alcohol	12805475	LPS induced <strong>TNF</strong> alpha production by Kupffer cells from the 4 week <b>ethanol</b> group was 3 to 4 times higher than control.
+TNF	drug	alcohol	12594868	High <b>alcohol</b> concentrations exert an immunosuppressive effect on production of proinflammatory cytokines such as <strong>tumor necrosis factor</strong> and interleukin 1.
+TNF	drug	amphetamine	12504868	Moreover, synergistic effects of Tat plus <b>METH</b> on the <strong>tumor necrosis factor</strong> alpha and interleukin 1beta mRNA levels were observed in the striatal region.
+TNF	drug	opioid	12427855	Chronic administration of <b>morphine</b> to sham operated rats activated spinal glia and upregulated proinflammatory cytokines [interleukin (IL) 1beta, IL 6, and <strong>tumor necrosis factor</strong> alpha].
+TNF	drug	nicotine	12400870	Cultured HCAECs were treated with <b>nicotine</b> at a concentration that correlates with the tissue level of <b>smokers</b> (1 microg/ml), concurrently with tumor necrosis factor alpha (<strong>TNF</strong> alpha) and dexamethasone to induce apoptosis.
+TNF	drug	nicotine	12400870	Cultured HCAECs were treated with <b>nicotine</b> at a concentration that correlates with the tissue level of <b>smokers</b> (1 microg/ml), concurrently with <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) and dexamethasone to induce apoptosis.
+TNF	drug	alcohol	12394292	<b>Alcohol</b> induced increases in insulin like growth factor binding protein 1 are partially mediated by <strong>TNF</strong>.
+TNF	drug	alcohol	12394292	Separate groups of rats were also pretreated with 4 methylpyrazole (4 MP; <b>alcohol</b> dehydrogenase inhibitor), cyanamide (inhibitor of acetaldehyde metabolism), RU486 (glucocorticoid receptor antagonist) or the tumor necrosis factor (<strong>TNF</strong>) antagonist (<strong>TNF</strong>(BP)) prior to EtOH administration.
+TNF	drug	alcohol	12394292	Separate groups of rats were also pretreated with 4 methylpyrazole (4 MP; <b>alcohol</b> dehydrogenase inhibitor), cyanamide (inhibitor of acetaldehyde metabolism), RU486 (glucocorticoid receptor antagonist) or the <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) antagonist (<strong>TNF</strong>(BP)) prior to EtOH administration.
+TNF	drug	alcohol	12394292	However, the <b>alcohol</b> induced increase in IGFBP 1 was attenuated by <strong>TNF</strong>(BP).
+TNF	drug	alcohol	12394292	These data suggest that the acute <b>alcohol</b> induced increase in IGFBP 1 is mediated, at least in part, by <strong>TNF</strong> and is independent of EtOH metabolism and increases in endogenous glucocorticoids.
+TNF	drug	alcohol	12107045	Since the appetite regulating peptide leptin was recently found to be highly correlated with both craving for <b>alcohol</b> and lifetime <b>ethanol</b> intake, the aim of our study was to test the hypothesis whether tumour necrosis factor alpha (<strong>TNF</strong> alpha) might be the factor that links <b>alcohol</b> intake with elevated leptin levels.
+TNF	addiction	relapse	12107045	Since the appetite regulating peptide leptin was recently found to be highly correlated with both <b>craving</b> for alcohol and lifetime ethanol intake, the aim of our study was to test the hypothesis whether tumour necrosis factor alpha (<strong>TNF</strong> alpha) might be the factor that links alcohol intake with elevated leptin levels.
+TNF	drug	alcohol	12107045	<strong>TNF</strong> alpha, leptin, and <b>alcohol</b> craving were assessed in male <b>alcohol</b> addicts at the onset of <b>alcohol</b> withdrawal and in matched controls.
+TNF	addiction	relapse	12107045	<strong>TNF</strong> alpha, leptin, and alcohol <b>craving</b> were assessed in male alcohol addicts at the onset of alcohol withdrawal and in matched controls.
+TNF	addiction	withdrawal	12107045	<strong>TNF</strong> alpha, leptin, and alcohol craving were assessed in male alcohol addicts at the onset of alcohol <b>withdrawal</b> and in matched controls.
+TNF	drug	alcohol	12107045	Increased leptin plasma levels in <b>alcohol</b> addicts correlated significantly with an enhanced secretion of <strong>TNF</strong> alpha, which was itself related to the duration of <b>alcohol</b> misuse.
+TNF	drug	alcohol	12107045	Since leptin was shown to be associated with <b>alcohol</b> craving, a possible vicious circle is suggested, including the components: <b>alcohol</b> intake, increase of <strong>TNF</strong> alpha, enhanced leptin secretion, enhanced <b>alcohol</b> craving, and consecutively increased <b>alcohol</b> intake.
+TNF	addiction	relapse	12107045	Since leptin was shown to be associated with alcohol <b>craving</b>, a possible vicious circle is suggested, including the components: alcohol intake, increase of <strong>TNF</strong> alpha, enhanced leptin secretion, enhanced alcohol <b>craving</b>, and consecutively increased alcohol intake.
+TNF	drug	alcohol	12105857	Thalidomide prevents <b>alcoholic</b> liver injury in rats through suppression of Kupffer cell sensitization and <strong>TNF</strong> alpha production.
+TNF	addiction	sensitization	12105857	Thalidomide prevents alcoholic liver injury in rats through suppression of Kupffer cell <b>sensitization</b> and <strong>TNF</strong> alpha production.
+TNF	drug	alcohol	12105857	Sensitization of Kupffer cells (KCs) to lipopolysaccharide (LPS) and overproduction of tumor necrosis factor (<strong>TNF</strong>) alpha are critical for progression of <b>alcoholic</b> liver injury.
+TNF	addiction	sensitization	12105857	<b>Sensitization</b> of Kupffer cells (KCs) to lipopolysaccharide (LPS) and overproduction of tumor necrosis factor (<strong>TNF</strong>) alpha are critical for progression of alcoholic liver injury.
+TNF	drug	alcohol	12105857	Sensitization of Kupffer cells (KCs) to lipopolysaccharide (LPS) and overproduction of <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha are critical for progression of <b>alcoholic</b> liver injury.
+TNF	addiction	sensitization	12105857	<b>Sensitization</b> of Kupffer cells (KCs) to lipopolysaccharide (LPS) and overproduction of <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha are critical for progression of alcoholic liver injury.
+TNF	drug	alcohol	12105857	KCs were isolated after 4 weeks of <b>ethanol</b> treatment and intracellular Ca2+ ([Ca2+]i) was measured using fura 2, whereas <strong>TNF</strong> alpha was evaluated by reverse transcription polymerase chain reaction and enzyme linked immunosorbent assay.
+TNF	drug	alcohol	12105857	These results collectively indicate that thalidomide prevents <b>alcoholic</b> liver injury through suppression of <strong>TNF</strong> alpha production and abolishment of KC sensitization.
+TNF	addiction	sensitization	12105857	These results collectively indicate that thalidomide prevents alcoholic liver injury through suppression of <strong>TNF</strong> alpha production and abolishment of KC <b>sensitization</b>.
+TNF	drug	alcohol	11956381	<b>Alcohol</b> blunted the hemorrhage induced rise in plasma <strong>TNF</strong> alpha (142 +/  48 pg/mL) and enhanced the hemorrhage induced increase in IL 10 (678 +/  187 pg/mL).
+TNF	drug	alcohol	11956381	<b>Alcohol</b> exacerbated the hemorrhage induced increase in lung <strong>TNF</strong> alpha, and did not alter the IL 1alpha, IL 6, and IL 10 lung responses.
+TNF	drug	alcohol	11939499	The present study was undertaken to examine the effect of acute <b>ethanol</b> pretreatments (producing blood <b>alcohol</b> concentrations of 100+/ 16 mg/dL, and 220+/ 10 mg/dL, considered low and intoxicating doses, respectively) on interleukin 1beta (IL 1beta) and tumor necrosis factor alpha (<strong>TNF</strong> alpha) levels in discrete brain regions.
+TNF	drug	alcohol	11939499	The present study was undertaken to examine the effect of acute <b>ethanol</b> pretreatments (producing blood <b>alcohol</b> concentrations of 100+/ 16 mg/dL, and 220+/ 10 mg/dL, considered low and intoxicating doses, respectively) on interleukin 1beta (IL 1beta) and <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) levels in discrete brain regions.
+TNF	drug	alcohol	11821657	Plasma <strong>tumor necrosis factor</strong> alpha and IL 1beta levels were not affected by <b>alcohol</b> alone.
+TNF	drug	alcohol	11821656	<b>Alcohol</b> intoxication suppressed the MIP 2, CINC, and <strong>TNFalpha</strong> responses in the bloodstream during endotoxemia.
+TNF	addiction	intoxication	11821656	Alcohol <b>intoxication</b> suppressed the MIP 2, CINC, and <strong>TNFalpha</strong> responses in the bloodstream during endotoxemia.
+TNF	drug	alcohol	11821656	These results show that <b>alcohol</b> suppresses the systemic CXC chemokine response to LPS, which is not primarily mediated by <b>ethanol</b> induced suppression of <strong>TNFalpha</strong>.
+TNF	drug	alcohol	11584157	After 12 weeks of <b>ethanol</b> exposure, LPS induced increases in [Ca2+]i and <strong>tumor necrosis factor</strong> alpha production were only approximately 50% as high as peak levels at 4 weeks.
+TNF	drug	alcohol	11454939	The current work shows <b>ethanol</b> also suppresses cytokine induced iNOS expression and reduces interleukin 1beta and <strong>tumor necrosis factor</strong> alpha potency without affecting interferon gamma potency.
+TNF	drug	alcohol	11410742	In isolated Kupffer cells from rats treated with <b>ethanol</b> for 4 weeks, CD14, LPS induced intracellular Ca2+, and <strong>TNF</strong> alpha all were increased.
+TNF	drug	alcohol	11391068	The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated <strong>TNF</strong> signaling in <b>alcoholic</b> liver disease, by Craig J. McClain, S. Joshi Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in <b>ethanol</b> mediated sensitization of the liver, by Anna Colell, Carmen Garcia Ruiz, Neil Kaplowitz, and Jose C. Fernandez Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute <b>ethanol</b> administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S adenosylmethionine affects tumor necrosis factor alpha gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage TNFalpha gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut derived endotoxin in <b>alcoholic</b> liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.
+TNF	addiction	sensitization	11391068	The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated <strong>TNF</strong> signaling in alcoholic liver disease, by Craig J. McClain, S. Joshi Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in ethanol mediated <b>sensitization</b> of the liver, by Anna Colell, Carmen Garcia Ruiz, Neil Kaplowitz, and Jose C. Fernandez Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute ethanol administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S adenosylmethionine affects tumor necrosis factor alpha gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage TNFalpha gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut derived endotoxin in alcoholic liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.
+TNF	drug	alcohol	11391068	The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated <strong>TNF</strong> signaling in <b>alcoholic</b> liver disease, by Craig J. McClain, S. Joshi Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in <b>ethanol</b> mediated sensitization of the liver, by Anna Colell, Carmen Garcia Ruiz, Neil Kaplowitz, and Jose C. Fernandez Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute <b>ethanol</b> administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S adenosylmethionine affects tumor necrosis factor alpha gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage <strong>TNFalpha</strong> gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut derived endotoxin in <b>alcoholic</b> liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.
+TNF	addiction	sensitization	11391068	The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated <strong>TNF</strong> signaling in alcoholic liver disease, by Craig J. McClain, S. Joshi Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in ethanol mediated <b>sensitization</b> of the liver, by Anna Colell, Carmen Garcia Ruiz, Neil Kaplowitz, and Jose C. Fernandez Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute ethanol administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S adenosylmethionine affects tumor necrosis factor alpha gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage <strong>TNFalpha</strong> gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut derived endotoxin in alcoholic liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.
+TNF	drug	alcohol	11391068	The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated <strong>TNF</strong> signaling in <b>alcoholic</b> liver disease, by Craig J. McClain, S. Joshi Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in <b>ethanol</b> mediated sensitization of the liver, by Anna Colell, Carmen Garcia Ruiz, Neil Kaplowitz, and Jose C. Fernandez Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute <b>ethanol</b> administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S adenosylmethionine affects <strong>tumor necrosis factor</strong> alpha gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage <strong>TNFalpha</strong> gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut derived endotoxin in <b>alcoholic</b> liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.
+TNF	addiction	sensitization	11391068	The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated <strong>TNF</strong> signaling in alcoholic liver disease, by Craig J. McClain, S. Joshi Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in ethanol mediated <b>sensitization</b> of the liver, by Anna Colell, Carmen Garcia Ruiz, Neil Kaplowitz, and Jose C. Fernandez Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute ethanol administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S adenosylmethionine affects <strong>tumor necrosis factor</strong> alpha gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage <strong>TNFalpha</strong> gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut derived endotoxin in alcoholic liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.
+TNF	addiction	withdrawal	11368420	At 6 hr on the following morning, <strong>TNF</strong> alpha values were near zero, but following connection of tubing and <b>withdrawal</b> of the initial blood sample, there was a 100 fold increase 1 hr later, followed by a decline over the next 3 hr.
+TNF	drug	alcohol	11062014	In Kupffer cells from mice treated with <b>ethanol</b> 1 h earlier, LPS induced <strong>TNFalpha</strong> production, and IRAK expression and activity and NFkappaB were decreased 50 60% of control.
+TNF	drug	alcohol	11062014	In contrast, in Kupffer cells from mice treated with <b>ethanol</b> 21 h earlier, LPS induced <strong>TNFalpha</strong> production, expression and activity of IRAK were increased 1.5 fold over controls, while NFkappaB was elevated 3 fold.
+TNF	drug	opioid	10936512	In this study, it was shown that injection of an equianalgesic dose of <b>buprenorphine</b> (related to <b>morphine</b>) into the ventral caudal PAG did not alter splenic NK cell, T cell, and macrophage functions, whereas <b>morphine</b> significantly (p<0.001) suppressed splenic NK cell cytotoxic activity (14 50% reduction), splenic and thymic T cell proliferation to concanavalin A (Con A, 43 76% reduction), antiTCR (T cell receptor) (85% reduction) and IL 2 (36 48% reduction), and macrophage functions including nitric oxide (36 41% reduction) and <strong>TNF</strong> alpha production (26%), and phagocytosis of Candida albicans (39%).
+TNF	drug	opioid	10921509	<b>Morphine</b> stimulates mesangial cell <strong>TNF</strong> alpha and nitrite production.
+TNF	drug	opioid	10921509	The effect of <b>morphine</b> was studied on the generation of <strong>TNF</strong> alpha with or without LPS (lipopolysaccharide) by cultured mouse mesangial cells.
+TNF	drug	alcohol	10921509	To evaluate the role of opiate receptors, we studied the effect of naloxone and <b>naltrexone</b> on mesangial cell <strong>TNF</strong> alpha and nitrite production.
+TNF	drug	opioid	10921509	To evaluate the role of opiate receptors, we studied the effect of <b>naloxone</b> and naltrexone on mesangial cell <strong>TNF</strong> alpha and nitrite production.
+TNF	drug	opioid	10921509	To determine the role of <strong>TNF</strong> alpha on mesangial cell nitrite production, we examined the effect of anti <strong>TNF</strong> alpha antibody on <b>morphine</b> induced nitrite production.
+TNF	drug	opioid	10921509	<b>Morphine</b> alone did not enhance the generation of <strong>TNF</strong> alpha by mesangial cells, however, an enhanced (P < 0.001) <strong>TNF</strong> alpha production was observed when mesangial cells were first treated with <b>morphine</b> for 18 h and then activated further with LPS.
+TNF	drug	opioid	10921509	Maximum release of <strong>TNF</strong> alpha was seen at a concentration of 10( 12) M of <b>morphine</b>.
+TNF	drug	opioid	10921509	Anti <strong>TNF</strong> alpha antibody attenuated <b>morphine</b> induced nitrite generation.
+TNF	drug	opioid	10921509	We conclude that <b>morphine</b> stimulates the generation of <strong>TNF</strong> infinity by LPS activated mesangial cells.
+TNF	addiction	sensitization	26368638	In addition, analysis of mediator expression and release over the <b>sensitization</b> phase has revealed that PM exposure can enhance production of Th2 cytokines such as interleukin 5 (IL 5) and the proinflammatory cytokine tumor necrosis factor alpha (<strong>TNF</strong> α).
+TNF	addiction	sensitization	26368638	In addition, analysis of mediator expression and release over the <b>sensitization</b> phase has revealed that PM exposure can enhance production of Th2 cytokines such as interleukin 5 (IL 5) and the proinflammatory cytokine <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> α).
+TNF	addiction	intoxication	10576587	Pathophysiological mechanisms of <strong>TNF</strong> during <b>intoxication</b> with natural or man made toxins.
+TNF	addiction	intoxication	10576587	<b>Intoxication</b> with different natural toxins or man made toxicants has been associated with the induction of tumor necrosis factor alpha (<strong>TNF</strong>).
+TNF	addiction	intoxication	10576587	<b>Intoxication</b> with different natural toxins or man made toxicants has been associated with the induction of <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong>).
+TNF	addiction	intoxication	10576587	In this paper we compile and discuss the current knowledge on the pathophysiological role of <strong>TNF</strong> during <b>intoxication</b> with all mentioned toxins and toxicants.
+TNF	addiction	intoxication	10576587	The development of pharmaceuticals that selectively interfere with the detrimental pathways induced by <strong>TNF</strong> during <b>intoxication</b> with bacteria, viruses, drugs, or other chemicals requires detailed knowledge of the signaling pathways originating from the two <strong>TNF</strong> receptors (TNFR1 and TNFR2).
+TNF	drug	opioid	10469523	<b>Morphine</b> significantly (p <.01) inhibited <strong>TNF</strong> alpha production by LPS activated macrophages (28 +/  8% inhibition compared with PAG injected saline rats).
+TNF	drug	alcohol	10455517	The generation of cytokine induced neutrophil chemoattractant (CINC) by hepatocytes and Kupffer cells of LPS treated rats, as well as <strong>TNF</strong> alpha secretion by Kupffer cells and alveolar macrophages of acutely <b>ethanol</b> intoxicated rats are also gender dependent.
+TNF	drug	alcohol	10417056	During chronic <b>alcohol</b> intoxication, increased levels of serum endotoxin, <strong>TNF</strong>, IL 1, and transaminase were observed and hepatic superoxide anion release was present.
+TNF	addiction	intoxication	10417056	During chronic alcohol <b>intoxication</b>, increased levels of serum endotoxin, <strong>TNF</strong>, IL 1, and transaminase were observed and hepatic superoxide anion release was present.
+TNF	drug	alcohol	10358198	<b>Alcohol</b> (<b>ethanol</b>) inhibits IL 8 and <strong>TNF</strong>: role of the p38 pathway.
+TNF	drug	alcohol	10358198	We examined the effects of LPS and <b>ethanol</b> on p38 activation and the corresponding IL 8 and <strong>TNF</strong> alpha production in human mononuclear cells.
+TNF	addiction	intoxication	10358198	Inhibition of IL 8 and <strong>TNF</strong> alpha production by acute EtOH <b>intoxication</b> may inhibit inflammatory focused neutrophil migration and activation and may be a mechanism explaining the increased risk of trauma  and burn related infections.
+TNF	drug	alcohol	10347108	Kupffer cells were isolated 0 to 24 hours after one intragastric dose of <b>ethanol</b> daily, and intracellular Ca2+ ([Ca2+]i) was measured using fura 2, while tumor necrosis factor alpha (<strong>TNF</strong> alpha) was measured by enzyme linked immunosorbent assay.
+TNF	drug	alcohol	10347108	Kupffer cells were isolated 0 to 24 hours after one intragastric dose of <b>ethanol</b> daily, and intracellular Ca2+ ([Ca2+]i) was measured using fura 2, while <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) was measured by enzyme linked immunosorbent assay.
+TNF	drug	alcohol	10347108	In addition, <strong>TNF</strong> alpha production by Kupffer cells was increased fourfold in cells isolated from rats treated with <b>ethanol</b> 24 hours earlier.
+TNF	drug	alcohol	10347108	Sterilization of the gut with antibiotics blocked all effects of <b>ethanol</b> on [Ca2+]i and <strong>TNF</strong> alpha release completely.
+TNF	drug	alcohol	10228066	Acute <b>ethanol</b> intoxication inhibited tumor necrosis factor (<strong>TNF</strong>) alpha and macrophage inflammatory protein (MIP) 2 production in the lung and suppressed the recruitment of neutrophils into the lung.
+TNF	addiction	intoxication	10228066	Acute ethanol <b>intoxication</b> inhibited tumor necrosis factor (<strong>TNF</strong>) alpha and macrophage inflammatory protein (MIP) 2 production in the lung and suppressed the recruitment of neutrophils into the lung.
+TNF	drug	alcohol	10228066	Acute <b>ethanol</b> intoxication inhibited <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha and macrophage inflammatory protein (MIP) 2 production in the lung and suppressed the recruitment of neutrophils into the lung.
+TNF	addiction	intoxication	10228066	Acute ethanol <b>intoxication</b> inhibited <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha and macrophage inflammatory protein (MIP) 2 production in the lung and suppressed the recruitment of neutrophils into the lung.
+TNF	drug	alcohol	9895030	This study examines i) the activity of serum prolyl endopeptidase (PEP) and dipeptidlyl peptidase IV (DPP IV) in detoxified <b>alcohol</b> dependent patients without liver disease versus normal controls, and ii) the relationships between serum DPP IV and PEP activity and the production of cytokines or cytokine receptors, such as interleukin 6 (IL 6), tumor necrosis factor alpha (<strong>TNF</strong> alpha), interferon y (IFN y), IL 1 receptor antagonist (IL 1RA), and IL 10, and granulocyte macrophage colony stimulatory factor (GM CSF).
+TNF	drug	alcohol	9895030	This study examines i) the activity of serum prolyl endopeptidase (PEP) and dipeptidlyl peptidase IV (DPP IV) in detoxified <b>alcohol</b> dependent patients without liver disease versus normal controls, and ii) the relationships between serum DPP IV and PEP activity and the production of cytokines or cytokine receptors, such as interleukin 6 (IL 6), <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha), interferon y (IFN y), IL 1 receptor antagonist (IL 1RA), and IL 10, and granulocyte macrophage colony stimulatory factor (GM CSF).
+TNF	drug	alcohol	9875556	Such a selective depletion sensitizes hepatocytes from chronic <b>ethanol</b> fed animals to the oxidative effects of cytokines, e.g., tumor necrosis factor (<strong>TNF</strong>).
+TNF	drug	alcohol	9875556	Such a selective depletion sensitizes hepatocytes from chronic <b>ethanol</b> fed animals to the oxidative effects of cytokines, e.g., <strong>tumor necrosis factor</strong> (<strong>TNF</strong>).
+TNF	drug	alcohol	9835289	In previous studies we found acute <b>alcohol</b> intoxication to suppress the tumor necrosis factor alpha (<strong>TNF</strong> alpha) response to in vivo challenges with bacteria or lipopolysaccharide.
+TNF	addiction	intoxication	9835289	In previous studies we found acute alcohol <b>intoxication</b> to suppress the tumor necrosis factor alpha (<strong>TNF</strong> alpha) response to in vivo challenges with bacteria or lipopolysaccharide.
+TNF	drug	alcohol	9835289	In previous studies we found acute <b>alcohol</b> intoxication to suppress the <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) response to in vivo challenges with bacteria or lipopolysaccharide.
+TNF	addiction	intoxication	9835289	In previous studies we found acute alcohol <b>intoxication</b> to suppress the <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) response to in vivo challenges with bacteria or lipopolysaccharide.
+TNF	drug	alcohol	9835289	These results support the postulate that <b>alcohol</b> induced inhibition of <strong>TNF</strong> alpha directly contributes to the adverse effects of <b>alcohol</b> on PMN function by suppressing the normal autocrine amplification pathway responsible for G CSF production.
+TNF	drug	alcohol	9834283	Selective glutathione depletion of mitochondria by <b>ethanol</b> sensitizes hepatocytes to <strong>tumor necrosis factor</strong>.
+TNF	drug	alcohol	9834283	The purpose of this study was to determine the effect of <b>ethanol</b> on the sensitization of hepatocytes to <strong>TNF</strong> alpha.
+TNF	addiction	sensitization	9834283	The purpose of this study was to determine the effect of ethanol on the <b>sensitization</b> of hepatocytes to <strong>TNF</strong> alpha.
+TNF	drug	alcohol	9834283	Cultured hepatocytes from <b>ethanol</b> fed (<b>ethanol</b> hepatocytes) or pair fed (control hepatocytes) rats were exposed to <strong>TNF</strong> alpha, and the extent of oxidative stress, gene expression, and viability were evaluated.
+TNF	drug	alcohol	9834283	<b>Ethanol</b> hepatocytes, which develop a selective deficiency of mitochondrial glutathione (mGSH), showed marked susceptibility to <strong>TNF</strong> alpha.
+TNF	drug	alcohol	9834283	Nuclear factor kappaB activation by <strong>TNF</strong> alpha was significantly greater in <b>ethanol</b> hepatocytes than in control hepatocytes, an effect paralleled by the expression of cytokine induced neutrophil chemoattractant.
+TNF	addiction	sensitization	9834283	Similar <b>sensitization</b> of normal hepatocytes to <strong>TNF</strong> alpha was obtained by depleting the mitochondrial pool of GSH with 3 hydroxyl 4 pentenoate.
+TNF	drug	alcohol	9834283	Restoration of mGSH by S adenosyl L methionine or by GSH ethyl ester prevented the increased susceptibility of <b>ethanol</b> hepatocytes to <strong>TNF</strong> alpha.
+TNF	drug	alcohol	9834283	Its depletion caused by <b>alcohol</b> consumption amplifies the power of <strong>TNF</strong> alpha to generate reactive oxygen species, compromising mitochondrial and cellular functions that culminate in cell death.
+TNF	drug	alcohol	9756533	The goals of this study were to determine if suppression of neutrophil accumulation and <strong>TNF</strong> alpha production in the peritoneal cavity occurs in mice exposed to a chemical stressor [<b>ethanol</b> (EtOH)], to evaluate the role of EtOH induced increases in endogenous glucocorticoids in any such suppression, and to determine if decreased tumor necrosis factor alpha (<strong>TNF</strong> alpha) production is responsible for decreases in neutrophil accumulation in EtOH treated mice.
+TNF	drug	alcohol	9756533	The goals of this study were to determine if suppression of neutrophil accumulation and <strong>TNF</strong> alpha production in the peritoneal cavity occurs in mice exposed to a chemical stressor [<b>ethanol</b> (EtOH)], to evaluate the role of EtOH induced increases in endogenous glucocorticoids in any such suppression, and to determine if decreased <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha) production is responsible for decreases in neutrophil accumulation in EtOH treated mice.
+TNF	drug	alcohol	9679050	Two hours after <b>ethanol</b> administration, the LPS induced increase in [Ca2+]i and <strong>TNF</strong> alpha release by Kupffer cells was diminished by 50%, and these parameters were reciprocally enhanced twofold at 24 hours.
+TNF	drug	alcohol	9679050	Sterilization of the gut with antibiotics blocked all effects of <b>ethanol</b> on [Ca2+]i and <strong>TNF</strong> alpha release completely.
+TNF	drug	amphetamine	9657097	F4614 is known to lack hypotensive effects of human <strong>TNF</strong> alpha without losing its anti tumor effect in mice transplanted with <b>Meth</b> A sarcoma.
+TNF	drug	alcohol	9497367	Accordingly, pretreatment with MG132 reduced JNK dependent apoptosis caused by heat shock or <b>ethanol</b>, but it was unable to block JNK independent apoptosis induced by <strong>TNFalpha</strong>.
+TNF	drug	alcohol	9514301	One potential mechanism of <b>ethanol</b> induced immunosuppression is through its ability to suppress alveolar macrophage production of tumor necrosis factor (<strong>TNF</strong> alpha).
+TNF	drug	alcohol	9514301	One potential mechanism of <b>ethanol</b> induced immunosuppression is through its ability to suppress alveolar macrophage production of <strong>tumor necrosis factor</strong> (<strong>TNF</strong> alpha).
+TNF	drug	alcohol	9514301	Moreover, in a model of acute <b>ethanol</b> intoxication, this vector significantly enhanced lipopolysaccharide induced <strong>TNF</strong> alpha responses and lung polymorphonuclear leukocyte recruitment.
+TNF	addiction	intoxication	9514301	Moreover, in a model of acute ethanol <b>intoxication</b>, this vector significantly enhanced lipopolysaccharide induced <strong>TNF</strong> alpha responses and lung polymorphonuclear leukocyte recruitment.
+TNF	drug	alcohol	9347083	Alterations in <strong>tumor necrosis factor</strong> alpha, interferon gamma, and interleukin 6 production by natural killer cell enriched peripheral blood mononuclear cells in chronic <b>alcoholism</b>: relationship with liver disease and <b>ethanol</b> intake.
+TNF	drug	alcohol	9347083	Accordingly, an increased concentration of this cytokine was detected in the supernatants of cirrhotic patients and active EtOH intake, particularly after IFN alpha stimulation (p < 0.05); whereas, in patients with at least 1 year of <b>alcohol</b> withdrawal, <strong>TNF</strong> alpha levels remained within normal range.
+TNF	addiction	withdrawal	9347083	Accordingly, an increased concentration of this cytokine was detected in the supernatants of cirrhotic patients and active EtOH intake, particularly after IFN alpha stimulation (p < 0.05); whereas, in patients with at least 1 year of alcohol <b>withdrawal</b>, <strong>TNF</strong> alpha levels remained within normal range.
+TNF	drug	alcohol	9347081	In this study, we assessed the effect of <b>alcohol</b> ingestion on the expression of tumor necrosis factor alpha (<strong>TNF</strong> alpha), and the chemokines macrophage inflammatory protein 2 (MIP 2) and macrophage inflammatory protein 1 alpha (MIP 1 alpha) from murine alveolar macrophages (AMs) cultured ex vivo.
+TNF	drug	alcohol	9347081	In this study, we assessed the effect of <b>alcohol</b> ingestion on the expression of <strong>tumor necrosis factor</strong> alpha (<strong>TNF</strong> alpha), and the chemokines macrophage inflammatory protein 2 (MIP 2) and macrophage inflammatory protein 1 alpha (MIP 1 alpha) from murine alveolar macrophages (AMs) cultured ex vivo.
+TNF	drug	alcohol	9347081	Two week <b>ethanol</b> feeding resulted in substantial impairment in the lipopolysaccharide (LPS) induced expression of <strong>TNF</strong> alpha, MIP 2, and MIP 1 alpha mRNA, and protein from LPS stimulated AMs, compared with cytokine production from AMs obtained from CD 1 mice receiving an isocaloric control diet.
+TNF	drug	alcohol	8947315	This study tests two hypotheses: (1) prior exposure to LPS induces cross tolerance for the hepatic effects of subsequent short term <b>alcohol</b> intoxication; and (2) short term <b>alcohol</b> intoxication renders the liver resistant to the effects of acute endotoxemia, resulting in reduced production of superoxide and <strong>tumor necrosis factor</strong>.
+TNF	addiction	intoxication	8947315	This study tests two hypotheses: (1) prior exposure to LPS induces cross tolerance for the hepatic effects of subsequent short term alcohol <b>intoxication</b>; and (2) short term alcohol <b>intoxication</b> renders the liver resistant to the effects of acute endotoxemia, resulting in reduced production of superoxide and <strong>tumor necrosis factor</strong>.
+TNF	drug	alcohol	8947315	Acute <b>ethanol</b> intoxication for 5 hr significantly reduced LPS induced serum <strong>tumor necrosis factor</strong> activity and free radical release by the perfused liver.
+TNF	addiction	intoxication	8947315	Acute ethanol <b>intoxication</b> for 5 hr significantly reduced LPS induced serum <strong>tumor necrosis factor</strong> activity and free radical release by the perfused liver.
+TNF	drug	alcohol	8730220	Interleukin 6 <strong>tumor necrosis factor</strong> alpha clearance and metabolism in vivo and by the isolated, perfused liver in the rat: effect of acute <b>alcohol</b> administration.
+TNF	drug	alcohol	8730220	Plasma clearance and organ distribution of intravenously injected human recombinant [125I]interleukin (IL) 6 and [125I]tumor necrosis factor (<strong>TNF</strong>) alpha were studied in male rats, 2 hr after intravenous <b>alcohol</b> (<b>ethanol</b>) administration (single dose, 2.2 g.kg 1 body weight).
+TNF	drug	alcohol	8730220	Plasma clearance and organ distribution of intravenously injected human recombinant [125I]interleukin (IL) 6 and [125I]<strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha were studied in male rats, 2 hr after intravenous <b>alcohol</b> (<b>ethanol</b>) administration (single dose, 2.2 g.kg 1 body weight).
+TNF	drug	alcohol	8730220	Acute <b>ethanol</b> administration significantly increased plasma clearance rate for both cytokines (36% and 72%, for IL 6 and <strong>TNF</strong> alpha, respectively), decreased the t1/2 alpha (30% and 11%, for IL 6 and <strong>TNF</strong> alpha, respectively), abolished the slow (beta) phase component for <strong>TNF</strong> alpha, and increased t1/2 beta for IL 6 (31%).
+TNF	drug	alcohol	8730220	Although <b>alcohol</b> did not affect organ distribution of <strong>TNF</strong> alpha, it increased the IL 6 content in the liver, kidney, and blood.
+TNF	drug	alcohol	8730220	<b>Ethanol</b> addition to the perfusate (35 mM, final concentration) significantly increased <strong>TNF</strong> alpha uptake (24%), without affecting IL 6 uptake or the degradation rate of either cytokine.
+TNF	drug	alcohol	8730220	Data presented in this study demonstrate that: (1) acute <b>alcohol</b> consumption can alter the kinetic behavior of IL 6 and <strong>TNF</strong> alpha in the bloodstream, mainly by accelerating their clearance which, in turn, may counteract the outcome of cytokine secretion and delivery to the blood; and (2) short exposure of liver to <b>ethanol</b> levels commonly seen in humans after binge drinking may alter its capacity to take up cytokines.
+TNF	addiction	intoxication	8730220	Data presented in this study demonstrate that: (1) acute alcohol consumption can alter the kinetic behavior of IL 6 and <strong>TNF</strong> alpha in the bloodstream, mainly by accelerating their clearance which, in turn, may counteract the outcome of cytokine secretion and delivery to the blood; and (2) short exposure of liver to ethanol levels commonly seen in humans after <b>binge</b> drinking may alter its capacity to take up cytokines.
+TNF	drug	opioid	8032870	Exposure to <b>morphine</b> apparently had limited effect on macrophage function as assessed by production of <strong>tumor necrosis factor</strong>.
+TNF	drug	alcohol	8451312	In the second experiment, the place conditioning paradigm was used to show that <strong>TNF</strong> administered ICV at 2.0 micrograms/rat did not induce aversive or deleterious effects as compared to <b>naltrexone</b> given IP at the equi anorectic dose 5.0 mg/kg.
+TNF	addiction	aversion	8451312	In the second experiment, the place conditioning paradigm was used to show that <strong>TNF</strong> administered ICV at 2.0 micrograms/rat did not induce <b>aversive</b> or deleterious effects as compared to naltrexone given IP at the equi anorectic dose 5.0 mg/kg.
+TNF	drug	alcohol	1320807	Effect of acute <b>alcohol</b> administration on <strong>TNF</strong> alpha binding to neutrophils and isolated liver plasma membranes.
+TNF	drug	alcohol	1320807	In this study we examined the ability of acute <b>alcohol</b> intoxication to alter lipopolysaccharide (LPS) induced changes in tumor necrosis factor (<strong>TNF</strong>) alpha binding to neutrophils and isolated liver plasma membranes.
+TNF	addiction	intoxication	1320807	In this study we examined the ability of acute alcohol <b>intoxication</b> to alter lipopolysaccharide (LPS) induced changes in tumor necrosis factor (<strong>TNF</strong>) alpha binding to neutrophils and isolated liver plasma membranes.
+TNF	drug	alcohol	1320807	In this study we examined the ability of acute <b>alcohol</b> intoxication to alter lipopolysaccharide (LPS) induced changes in <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha binding to neutrophils and isolated liver plasma membranes.
+TNF	addiction	intoxication	1320807	In this study we examined the ability of acute alcohol <b>intoxication</b> to alter lipopolysaccharide (LPS) induced changes in <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) alpha binding to neutrophils and isolated liver plasma membranes.
+TNF	drug	amphetamine	1955383	Effects of <strong>tumor necrosis factor</strong> and hyperthermia on <b>Meth</b> A tumors.
+TNF	drug	amphetamine	1955383	The combined effects of purified human natural tumor necrosis factor (<strong>TNF</strong>) and hyperthermia were investigated in a transplanted <strong>TNF</strong> sensitive <b>Meth</b> A tumor model.
+TNF	drug	amphetamine	1955383	The combined effects of purified human natural <strong>tumor necrosis factor</strong> (<strong>TNF</strong>) and hyperthermia were investigated in a transplanted <strong>TNF</strong> sensitive <b>Meth</b> A tumor model.
+TNF	drug	alcohol	1662988	<b>Ethanol</b> affects release of <strong>TNF</strong> and GM CSF and membrane expression of <strong>TNF</strong> receptors by human macrophages.
+TNF	drug	alcohol	1662988	More recently, <b>ethanol</b> was shown to impair the capacity of pulmonary macrophages to produce superoxide anion and tumor necrosis factor (<strong>TNF</strong>).
+TNF	drug	alcohol	1662988	More recently, <b>ethanol</b> was shown to impair the capacity of pulmonary macrophages to produce superoxide anion and <strong>tumor necrosis factor</strong> (<strong>TNF</strong>).
+TNF	drug	alcohol	1662988	Furthermore, exposure to <b>ethanol</b> compromises macrophage's ability to respond to stimulation with <strong>TNF</strong> and granulocyte macrophage colony stimulating factor (GM CSF), and kill an intracellular pathogen, Mycobacterium avium.
+TNF	drug	alcohol	1662988	Based on these previous findings, we examined whether exposure to <b>ethanol</b> affects superoxide anion production, synthesis of cytokines, and expression of membrane receptors to <strong>TNF</strong> on human monocyte derived macrophages.
+TNF	drug	alcohol	1662988	When macrophages were then treated with lipopolysaccharide (LPS) in the presence of <b>ethanol</b>, high concentrations of <strong>TNF</strong> and GM CSF were produced, but subsequent stimulation with LPS (second stimulus) was associated with significant impairment on synthesis and release of both <strong>TNF</strong> and GM CSF.
+TNF	drug	alcohol	1662988	In addition, although <b>ethanol</b> had no effect on <strong>TNF</strong> binding to resting macrophages and to macrophages infected with M. avium, <b>ethanol</b> significantly reduced the expression of <strong>TNF</strong> receptors on interferon gamma stimulated macrophages.
+TNF	drug	alcohol	2668425	The effects of acute and chronic <b>alcoholism</b> on <strong>tumor necrosis factor</strong> and the inflammatory response.
+TNF	drug	alcohol	2668425	Because the macrophage secretory protein, tumor necrosis factor (<strong>TNF</strong>), plays a central role in the inflammatory cascade, the effect of acute and chronic <b>alcoholism</b> on lipopolysaccharide (LPS) induced <strong>TNF</strong> activity was studied.
+TNF	drug	alcohol	2668425	Because the macrophage secretory protein, <strong>tumor necrosis factor</strong> (<strong>TNF</strong>), plays a central role in the inflammatory cascade, the effect of acute and chronic <b>alcoholism</b> on lipopolysaccharide (LPS) induced <strong>TNF</strong> activity was studied.
+TNF	drug	alcohol	2668425	Intravenous LPS caused a substantial increase in serum <strong>TNF</strong> at 90 min in both normal and chronic <b>alcoholic</b> rats.
+TNF	drug	alcohol	2668425	In marked contrast, peak serum <strong>TNF</strong> levels were significantly suppressed in normal and chronic <b>alcoholic</b> rats given an acute injection of <b>ethanol</b>.
+TNF	drug	alcohol	2668425	Similar levels of <strong>TNF</strong> were found in chronic <b>alcoholic</b> rats after intratracheal LPS.
+TNF	drug	alcohol	2668425	However, acute <b>ethanol</b> intoxication significantly inhibited LPS induced <strong>TNF</strong> in bronchoalveolar lavage fluid.
+TNF	addiction	intoxication	2668425	However, acute ethanol <b>intoxication</b> significantly inhibited LPS induced <strong>TNF</strong> in bronchoalveolar lavage fluid.
+TNF	drug	alcohol	2668425	<b>Alcohol</b> induced inhibition of <strong>TNF</strong> is a potential mechanism of the antiinflammatory effects of <b>ethanol</b>.
+TNF	addiction	dependence	2783463	Sequence <b>dependence</b> of administration of human recombinant <strong>tumor necrosis factor</strong> and interleukin 2 in murine tumor therapy.
+TNF	drug	alcohol	2648095	<b>Alcohol</b> suppresses lipopolysaccharide induced <strong>tumor necrosis factor</strong> activity in serum and lung.
+TNF	drug	alcohol	2648095	Acute <b>ethanol</b> intoxication markedly suppressed both serum and lung <strong>tumor necrosis factor</strong> elicited in response to lipopolysaccharide.
+TNF	addiction	intoxication	2648095	Acute ethanol <b>intoxication</b> markedly suppressed both serum and lung <strong>tumor necrosis factor</strong> elicited in response to lipopolysaccharide.
+TNF	drug	alcohol	2648095	Thus, the anti inflammatory effects of <b>ethanol</b> may be secondary to suppression of macrophage derived <strong>tumor necrosis factor</strong>.
+HTR1A	drug	amphetamine	32315693	Administration of low doses of the <strong>5 HT1A</strong> receptor agonist 8 OH DPAT attenuates the discriminative signal of <b>amphetamine</b> in the conditioned taste aversion procedure.
+HTR1A	addiction	aversion	32315693	Administration of low doses of the <strong>5 HT1A</strong> receptor agonist 8 OH DPAT attenuates the discriminative signal of amphetamine in the conditioned taste <b>aversion</b> procedure.
+HTR1A	drug	cocaine	32315693	Several studies have reported that low doses of the <strong>5 HT1A</strong> receptor agonist 8 OH DPAT reduce <b>cocaine</b> induced locomotor activity.
+HTR1A	drug	amphetamine	32315693	This study aimed to evaluate the effects of low and high doses of the <strong>5 HT1A</strong> agonist 8 OH DPAT on the discriminative signal of <b>AMPH</b> using conditioned taste aversion as a drug discrimination procedure.
+HTR1A	addiction	aversion	32315693	This study aimed to evaluate the effects of low and high doses of the <strong>5 HT1A</strong> agonist 8 OH DPAT on the discriminative signal of AMPH using conditioned taste <b>aversion</b> as a drug discrimination procedure.
+HTR1A	drug	amphetamine	32315693	These data support the hypothesis that <strong>5 HT1A</strong> receptors modulate the behavioral effects of psychostimulant drugs, such as <b>AMPH</b>, through somatodendritic <strong>5 HT1A</strong> autoreceptors in the raphe nucleus indicating that <strong>5 HT1A</strong> receptors may be an important target for the development of pharmacological treatments for psychostimulant addiction.
+HTR1A	addiction	addiction	32315693	These data support the hypothesis that <strong>5 HT1A</strong> receptors modulate the behavioral effects of psychostimulant drugs, such as AMPH, through somatodendritic <strong>5 HT1A</strong> autoreceptors in the raphe nucleus indicating that <strong>5 HT1A</strong> receptors may be an important target for the development of pharmacological treatments for psychostimulant <b>addiction</b>.
+HTR1A	drug	cannabinoid	32199997	Adenosine A1 receptor agonist induces visceral antinociception via <strong>5 HT1A</strong>, 5 HT2A, dopamine D1 or <b>cannabinoid</b> CB1 receptors, and the opioid system in the central nervous system.
+HTR1A	drug	opioid	32199997	Adenosine A1 receptor agonist induces visceral antinociception via <strong>5 HT1A</strong>, 5 HT2A, dopamine D1 or cannabinoid CB1 receptors, and the <b>opioid</b> system in the central nervous system.
+HTR1A	drug	opioid	32199997	These results suggest that <strong>5 HT1A</strong>, 5 HT2A, dopamine D1, CB1 receptors and the <b>opioid</b> system in the CNS may specifically mediate the CPA induced visceral antinociception.
+HTR1A	drug	alcohol	32088264	The <strong>5 HT1A</strong> and 5 HT1B serotonin receptors are abundantly expressed in the CNS and constitute validated as well as putative drug targets in a variety of psychiatric and cognitive disorders, <b>alcoholism</b>/addiction, pain and migraine.
+HTR1A	addiction	addiction	32088264	The <strong>5 HT1A</strong> and 5 HT1B serotonin receptors are abundantly expressed in the CNS and constitute validated as well as putative drug targets in a variety of psychiatric and cognitive disorders, alcoholism/<b>addiction</b>, pain and migraine.
+HTR1A	drug	amphetamine	32007493	Overall, these data further validate our outbred trait anxiety rats: HAn males show anxiety like behavior, <b>AMPH</b> hypersensitivity, greater impulsivity, and varying levels of limbic and midbrain <strong>5 HT1A</strong> and α2 adrenergic receptor proteins.
+HTR1A	drug	alcohol	31954952	Evidence suggests that aripiprazole, a partial dopamine D2 and serotonin <strong>5 HT1A</strong> receptor agonist and 5 HT2A receptor antagonist, show significant efficacy in reducing <b>alcohol</b> use.
+HTR1A	drug	alcohol	31849624	We have previously shown that modulation of NE and 5 HT activity by pharmacological targeting of β adrenoreceptors (β ARs) and <strong>5 HT1A</strong>/1B receptors with pindolol reduces consumption in long term <b>alcohol</b> consuming mice.
+HTR1A	drug	cannabinoid	31437433	<b>Cannabidiol</b> attenuates the rewarding effects of cocaine in rats by CB2, <strong>5 HT1A</strong> and TRPV1 receptor mechanisms.
+HTR1A	drug	cocaine	31437433	Cannabidiol attenuates the rewarding effects of <b>cocaine</b> in rats by CB2, <strong>5 HT1A</strong> and TRPV1 receptor mechanisms.
+HTR1A	drug	cannabinoid	31437433	Strikingly, this reduction in both cocaine self administration and BSR was blocked by AM630 (a <b>cannabinoid</b> CB2 receptor antagonist), WAY100135 (a <strong>5 HT1A</strong> receptor antagonist), or capsazepine (a TRPV1 channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a GPR55 antagonist), or naloxone (an opioid receptor antagonist), suggesting the involvement of CB2, <strong>5 HT1A</strong>, and TRPV1 receptors in CBD action.
+HTR1A	drug	cocaine	31437433	Strikingly, this reduction in both <b>cocaine</b> self administration and BSR was blocked by AM630 (a cannabinoid CB2 receptor antagonist), WAY100135 (a <strong>5 HT1A</strong> receptor antagonist), or capsazepine (a TRPV1 channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a GPR55 antagonist), or naloxone (an opioid receptor antagonist), suggesting the involvement of CB2, <strong>5 HT1A</strong>, and TRPV1 receptors in CBD action.
+HTR1A	drug	opioid	31437433	Strikingly, this reduction in both cocaine self administration and BSR was blocked by AM630 (a cannabinoid CB2 receptor antagonist), WAY100135 (a <strong>5 HT1A</strong> receptor antagonist), or capsazepine (a TRPV1 channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a GPR55 antagonist), or <b>naloxone</b> (an <b>opioid</b> receptor antagonist), suggesting the involvement of CB2, <strong>5 HT1A</strong>, and TRPV1 receptors in CBD action.
+HTR1A	drug	opioid	31282754	Furthermore, a significant abdominal antinociceptive response was obtained in mice, which was totally abolished in the presence of <strong>5 HT1A</strong> receptor antagonist (WAY100635, 0.1 mg/kg, s.c.) and partially by blocking <b>opioid</b> receptors (NX, 1 mg/kg, i.p.
+HTR1A	drug	benzodiazepine	31196061	A hydroalcoholic, thujone free extract from freshly harvested Salvia officinalis leaves (A.Vogel Menosan®) was investigated in an acetylcholinesterase enzyme assay and several receptor binding assays (adrenergic alpha 2A, GABA (<b>benzodiazepine</b> site), GABAB; muscarinic M3, μ opioid, serotonin <strong>5 HT1A</strong>, serotonin 5 HT2B, serotonin 5 HT2C and serotonin transporter).
+HTR1A	drug	opioid	31196061	A hydroalcoholic, thujone free extract from freshly harvested Salvia officinalis leaves (A.Vogel Menosan®) was investigated in an acetylcholinesterase enzyme assay and several receptor binding assays (adrenergic alpha 2A, GABA (benzodiazepine site), GABAB; muscarinic M3, μ <b>opioid</b>, serotonin <strong>5 HT1A</strong>, serotonin 5 HT2B, serotonin 5 HT2C and serotonin transporter).
+HTR1A	drug	opioid	31196061	Strong binding affinity was observed for the adrenergic α2A receptor, μ <b>opioid</b> receptors, muscarinic M3 receptors, and serotonin <strong>5 HT1A</strong> receptors, with IC50 values of 15 μg/ml, 20 μg/ml, 25 μg/ml and 19 μg/ml, respectively.
+HTR1A	drug	cocaine	31045847	<strong>5 HT1A</strong> autoreceptor in dorsal raphe nucleus mediates sensitization of conditioned place preference to <b>cocaine</b> in mice experienced with chronic pain.
+HTR1A	addiction	sensitization	31045847	<strong>5 HT1A</strong> autoreceptor in dorsal raphe nucleus mediates <b>sensitization</b> of conditioned place preference to cocaine in mice experienced with chronic pain.
+HTR1A	drug	cocaine	31045847	The conditioned place preference to <b>cocaine</b> and was abolished by administration of the <strong>5 HT1A</strong> receptor antagonist into the dorsal raphe nucleus (DRN).
+HTR1A	drug	cocaine	31045847	The results reveal that DRN <strong>5 HT1A</strong> receptor mediate the sensitization to <b>cocaine</b> in mice experienced with chronic pain and may be used as a new molecular target for therapeutic interventions to drug addiction influenced by chronic stress.
+HTR1A	addiction	addiction	31045847	The results reveal that DRN <strong>5 HT1A</strong> receptor mediate the sensitization to cocaine in mice experienced with chronic pain and may be used as a new molecular target for therapeutic interventions to drug <b>addiction</b> influenced by chronic stress.
+HTR1A	addiction	sensitization	31045847	The results reveal that DRN <strong>5 HT1A</strong> receptor mediate the <b>sensitization</b> to cocaine in mice experienced with chronic pain and may be used as a new molecular target for therapeutic interventions to drug addiction influenced by chronic stress.
+HTR1A	drug	benzodiazepine	30858018	Cannabinoid CB1 receptors mediate the anxiolytic effects induced by systemic <b>alprazolam</b> and intra periaqueductal gray <strong>5 HT1A</strong> receptor activation.
+HTR1A	drug	cannabinoid	30858018	<b>Cannabinoid</b> CB1 receptors mediate the anxiolytic effects induced by systemic alprazolam and intra periaqueductal gray <strong>5 HT1A</strong> receptor activation.
+HTR1A	drug	benzodiazepine	30858018	Here, we tested the hypothesis that the anxiolytic and panicolytic responses to systemic <b>alprazolam</b> injection and local <strong>5 HT1A</strong> receptor activation in the dorsolateral periaqueductal gray (dlPAG) depend on CB1 receptor activation.
+HTR1A	drug	psychedelics	30385254	However, pre treatment with p CPA (150 mg/kg/day; a 5 HT synthesis inhibitor), WAY100635 (3 mg/kg; a <strong>5 HT1A</strong> receptor antagonist), or L arginine (500 mg/kg; a nitric oxide precursor) did not counteract S <b>ketamine</b> effect in the MBT.
+HTR1A	drug	alcohol	30022582	We have previously shown that systemic administration of the dual beta adrenergic antagonist and <strong>5 HT1A</strong>/1B partial agonist pindolol selectively reduces long term but not short term binge like consumption of <b>ethanol</b> and alters excitatory postsynaptic currents in basolateral amygdala (BLA) principal neurons.
+HTR1A	addiction	intoxication	30022582	We have previously shown that systemic administration of the dual beta adrenergic antagonist and <strong>5 HT1A</strong>/1B partial agonist pindolol selectively reduces long term but not short term <b>binge</b> like consumption of ethanol and alters excitatory postsynaptic currents in basolateral amygdala (BLA) principal neurons.
+HTR1A	drug	alcohol	30022582	We also microinfused RU24969 (<strong>5 HT1A</strong>/1B receptor partial agonist) and CGP12177 (β1/2 adrenergic antagonist) following long term <b>ethanol</b> intake and determined the densities of <strong>5 HT1A</strong>/1B receptors and β1/2 adrenergic in the BLA following short term (4 weeks) and long term <b>ethanol</b> (12 weeks) consumption.
+HTR1A	drug	alcohol	30022582	Additionally, we identified reduced β1/2 adrenergic receptor expression and no change in <strong>5 HT1A</strong>/1B receptor density in the BLA of long term <b>ethanol</b> consuming mice.
+HTR1A	drug	cocaine	29952618	Two such drugs, lorcaserin (Belviq; a drug with serotonin [5 HT]2C receptor agonist properties) and buspirone (Buspar; a drug with <strong>5 HT1A</strong> receptor partial agonist and dopamine D3/D4 receptor antagonist properties) can produce modest decreases in <b>cocaine</b> self administration in rhesus monkeys.
+HTR1A	drug	opioid	29859012	Gene expression analyses of the <b>opioid</b> μ receptor (Oprm1) in the nucleus accumbens (NAc), tyrosine hydroxylase (TH) in the ventral tegmental area (VTA) and the <strong>5 HT1A</strong> receptor in the dorsal raphe nucleus (DR) were carried out by real time PCR.
+HTR1A	drug	alcohol	29859012	The role of <strong>5 HT1A</strong> receptors in the <b>ethanol</b> reduction induced by the administration of CBD + <b>naltrexone</b> was analysed by using the <strong>5 HT1A</strong> receptor antagonist WAY100635 (0.3 mg·kg 1 , i.p.).
+HTR1A	drug	opioid	29782941	Results suggest that <strong>5 HT1A</strong> receptor dependent modulation of dopamine neurotransmission in the CN and NAc is involved in the modulation of the rewarding effects of <b>morphine</b> in buspirone co treated animals.
+HTR1A	drug	opioid	29782941	The findings documenting an important role of <strong>5 HT1A</strong> receptors in drug addiction suggest that synthetic <b>opioid</b> drugs with agonist activity of <strong>5 HT1A</strong> receptors may prove non addictive analgesics.
+HTR1A	addiction	addiction	29782941	The findings documenting an important role of <strong>5 HT1A</strong> receptors in drug <b>addiction</b> suggest that synthetic opioid drugs with agonist activity of <strong>5 HT1A</strong> receptors may prove non <b>addictive</b> analgesics.
+HTR1A	drug	cannabinoid	29773016	It has wide spectrum of action because it acts through <b>endocannabinoid</b> receptors; CB1 and CB2 and it also acts on other receptors, such as GPR18, GPR55, GPR 119, <strong>5HT1A</strong>, and TRPV2.
+HTR1A	drug	cannabinoid	29773016	It has wide spectrum of action because it acts through <b>endocannabinoid</b> receptors; CB1 and CB2 and it also acts on other receptors, such as GPR18, GPR55, GPR 119, <strong><strong>5HT1A</strong></strong>, and TRPV2.
+HTR1A	drug	alcohol	29689260	Recent findings from this laboratory demonstrate that D2, α2 adrenergic and <strong>5HT1A</strong> receptors all decrease the intrinsic excitability of lateral OFC (lOFC) neurons in naïve male mice and that this effect is lost in mice exposed to repeated cycles of chronic intermittent <b>ethanol</b> (CIE) vapor.
+HTR1A	drug	alcohol	29689260	Recent findings from this laboratory demonstrate that D2, α2 adrenergic and <strong><strong>5HT1A</strong></strong> receptors all decrease the intrinsic excitability of lateral OFC (lOFC) neurons in naïve male mice and that this effect is lost in mice exposed to repeated cycles of chronic intermittent <b>ethanol</b> (CIE) vapor.
+HTR1A	drug	cannabinoid	29450258	The antinociceptive and anti inflammatory effects of Δ8THC are mediated primarily via CB1R, whereas that of the <b>cannabinoids</b> CBD and HU 308, involve activation of <strong>5 HT1A</strong> receptors and CB2Rs, respectively.
+HTR1A	drug	alcohol	29391482	<strong>5 HT1A</strong> receptor dependent modulation of emotional and neurogenic deficits elicited by prolonged consumption of <b>alcohol</b>.
+HTR1A	drug	alcohol	29391482	While the involvement of the serotonin receptor 1 A (<strong>5 HT1A</strong>) in the regulation of anxiety like behavior and neurogenesis is well documented, its contribution to <b>alcohol</b> withdrawal induced anxiety and <b>alcohol</b> induced deficits in neurogenesis is less documented.
+HTR1A	addiction	withdrawal	29391482	While the involvement of the serotonin receptor 1 A (<strong>5 HT1A</strong>) in the regulation of anxiety like behavior and neurogenesis is well documented, its contribution to alcohol <b>withdrawal</b> induced anxiety and alcohol induced deficits in neurogenesis is less documented.
+HTR1A	drug	alcohol	29391482	Using the Drinking In the Dark (DID) paradigm to model chronic long term (12 weeks) binge like voluntary <b>alcohol</b> consumption in mice, we show that the selective partial activation of <strong>5 HT1A</strong> receptors by tandospirone (3 mg/kg) prevents <b>alcohol</b> withdrawal induced anxiety in a battery of behavioral tests (marble burying, elevated plus maze, open field), which is accompanied by a robust decrease in binge like <b>ethanol</b> intake (1 and 3 mg/kg).
+HTR1A	addiction	intoxication	29391482	Using the Drinking In the Dark (DID) paradigm to model chronic long term (12 weeks) <b>binge</b> like voluntary alcohol consumption in mice, we show that the selective partial activation of <strong>5 HT1A</strong> receptors by tandospirone (3 mg/kg) prevents alcohol withdrawal induced anxiety in a battery of behavioral tests (marble burying, elevated plus maze, open field), which is accompanied by a robust decrease in <b>binge</b> like ethanol intake (1 and 3 mg/kg).
+HTR1A	addiction	withdrawal	29391482	Using the Drinking In the Dark (DID) paradigm to model chronic long term (12 weeks) binge like voluntary alcohol consumption in mice, we show that the selective partial activation of <strong>5 HT1A</strong> receptors by tandospirone (3 mg/kg) prevents alcohol <b>withdrawal</b> induced anxiety in a battery of behavioral tests (marble burying, elevated plus maze, open field), which is accompanied by a robust decrease in binge like ethanol intake (1 and 3 mg/kg).
+HTR1A	drug	alcohol	29391482	Together, our results confirm previous observations that <strong>5 HT1A</strong> receptors play a pivotal role in <b>alcohol</b> drinking behavior and the associated emotional and neurogenic impairments, and suggest that <strong>5 HT1A</strong> partial agonists represent a promising treatment strategy for <b>alcohol</b> abuse.
+HTR1A	drug	cannabinoid	29338068	<b>Cannabinoid</b> withdrawal signs were assessed following precipitated withdrawal by acute administration of the CB1 receptor antagonist <b>SR141716</b>, the <strong>5 HT1A</strong> receptor antagonist WAY100635, the TRPV1 receptor antagonist capsazepine or the adenosine A2A receptor antagonist SCH58261.
+HTR1A	addiction	withdrawal	29338068	Cannabinoid <b>withdrawal</b> signs were assessed following precipitated <b>withdrawal</b> by acute administration of the CB1 receptor antagonist SR141716, the <strong>5 HT1A</strong> receptor antagonist WAY100635, the TRPV1 receptor antagonist capsazepine or the adenosine A2A receptor antagonist SCH58261.
+HTR1A	drug	cocaine	29217539	Although this effect is partially inhibited by a 5 HT2C receptor antagonist (SB242084), lorcaserin also has effects at 5 HT2A and <strong>5 HT1A</strong> receptors, and the relative contribution of these receptors to its anti <b>cocaine</b> effects has not been investigated.
+HTR1A	drug	cocaine	29217539	Antagonism of 5 HT2C (but not <strong>5 HT1A</strong> or 5 HT2A) receptors blocked the effects of lorcaserin on <b>cocaine</b> and MDPV self administration.
+HTR1A	drug	psychedelics	28890736	This 25B <b>NBOMe</b> induced rhabdomyolysis was inhibited by the 5 HT2A receptor antagonists ritanserin and aripirazole, but not by the <strong>5 HT1A</strong> + 5 HT1B receptor antagonist propranolol and the 5 HT3 receptor antagonist granisetron, indicating 5 HT2A dependent rhabdomyolysis.
+HTR1A	drug	cannabinoid	28268256	Studies show that <b>cannabidiol</b>, the main non psychotomimetic <b>phytocannabinoid</b> found in <b>Cannabis</b> sativa, reduces anxiety via <strong>5 HT1A</strong> and (indirect) <b>cannabinoid</b> receptor activation in paradigms assessing innate responses to threat.
+HTR1A	addiction	reward	27866999	The <strong>5 HT1A</strong>/1B receptor agonist eltoprazine increases both catecholamine release in the prefrontal cortex and dopamine release in the nucleus accumbens and decreases motivation for <b>reward</b> and "waiting" impulsivity, but increases "stopping" impulsivity.
+HTR1A	addiction	relapse	27515792	We observed decreased drug <b>seeking</b> behavior on ED1 following 10 mg/kg S propranolol (β adrenergic and <strong>5 HT1A</strong>/1B receptor antagonist), R propranolol (<strong>5 HT1A</strong>/1B receptor antagonist), or racemic propranolol in both male and female rats.
+HTR1A	addiction	relapse	27515792	Based on these results, we investigated the effects of blocking 5 HT and β adrenoceptor transmission in DH on drug <b>seeking</b> during ED1 by infusing a cocktail of WAY100635 plus GR127935 (<strong>5 HT1A</strong>/1B receptor antagonists), betaxolol plus ICI 118 551 (β1 and β2 antagonists), or S propranolol alone.
+HTR1A	drug	alcohol	27375424	Third Trimester Equivalent <b>Alcohol</b> Exposure Reduces Modulation of Glutamatergic Synaptic Transmission by <strong>5 HT1A</strong> Receptors in the Rat Hippocampal CA3 Region.
+HTR1A	drug	alcohol	27375424	In slices from naïve animals, application of a <strong>5 HT1A</strong> receptor antagonist blocked the effect of 5 HT on the fEPSPs recorded in presence of picrotoxin, suggesting that third trimester <b>ethanol</b> exposure acts by inhibiting the function of these receptors.
+HTR1A	drug	cannabinoid	27289270	<b>Cannabidiol</b>, a therapeutic with potential serotonin (5 hydroxytryptamine; 5 HT) <strong>5 HT1A</strong> receptor agonist activity, is the second most prevalent <b>cannabinoid</b> in <b>Cannabis</b> after Δ(9) <b>THC</b>.
+HTR1A	drug	cannabinoid	27289270	<b>Cannabidiol</b> and the <strong>5 HT1A</strong> receptor agonist (±) 8 hydroxy 2 (dipropylamino)tetralin hydrobromide (8 OH DPAT) were tested in two separate discrimination assays in rhesus monkeys.
+HTR1A	drug	cannabinoid	27289270	In addition to showing that <b>cannabidiol</b> and a <strong>5 HT1A</strong> receptor agonist have overlapping behavioral effects, the current results suggest that <strong>5 HT1A</strong> agonism enhances the CB1 receptor mediated effects of Δ(9) <b>THC</b>.
+HTR1A	drug	alcohol	27273539	Additionally, this effect was blocked by the <strong>5 HT1A</strong>/1B receptor antagonist methiothepin, suggesting that altered serotonergic activity in the BLA may contribute to the efficacy of pindolol to reduce <b>ethanol</b> intake following long term exposure.
+HTR1A	drug	psychedelics	27264435	Doses of the <strong>5 HT1A</strong> antagonist, WAY 100635 (0.1 1.0mg/kg), 5 HT1B antagonist, GR 127935 (1.0 3.0mg/kg), and the 5 HT2A antagonist, ketanserin (1.0 3.0mg/kg) that have previously been shown to decrease self administration of other psychostimulants and that decreased <b>MDMA</b> produced hyperactivity in the present study did not alter <b>MDMA</b> self administration.
+HTR1A	drug	psychedelics	27264435	The <strong>5 HT1A</strong> agonist, 8 OH DPAT (0.1 1.0mg/kg), but not the 5 HT1B/1A agonist, RU 24969 (0.3 3.0mg/kg), decreased drug seeking produced by the reintroduction of a light stimulus that had been paired with self administered <b>MDMA</b> infusions.
+HTR1A	addiction	relapse	27264435	The <strong>5 HT1A</strong> agonist, 8 OH DPAT (0.1 1.0mg/kg), but not the 5 HT1B/1A agonist, RU 24969 (0.3 3.0mg/kg), decreased drug <b>seeking</b> produced by the reintroduction of a light stimulus that had been paired with self administered MDMA infusions.
+HTR1A	drug	psychedelics	27264435	These findings suggest a limited role of activation of <strong>5 HT1A</strong>, 5 HT1B or 5 HT2 receptor mechanisms in <b>MDMA</b> self administration or in <b>MDMA</b> produced drug seeking following extinction.
+HTR1A	addiction	relapse	27264435	These findings suggest a limited role of activation of <strong>5 HT1A</strong>, 5 HT1B or 5 HT2 receptor mechanisms in MDMA self administration or in MDMA produced drug <b>seeking</b> following extinction.
+HTR1A	drug	psychedelics	27264435	The data suggest, however, that <strong>5 HT1A</strong> agonists inhibit cue induced drug seeking following extinction of <b>MDMA</b> self administration and might, therefore, be useful adjuncts to therapies to limit relapse to <b>MDMA</b> use.
+HTR1A	addiction	relapse	27264435	The data suggest, however, that <strong>5 HT1A</strong> agonists inhibit cue induced drug <b>seeking</b> following extinction of MDMA self administration and might, therefore, be useful adjuncts to therapies to limit <b>relapse</b> to MDMA use.
+HTR1A	drug	benzodiazepine	27235743	Prenatal stress alters <b>diazepam</b> withdrawal syndrome and <strong>5HT1A</strong> receptor expression in the raphe nuclei of adult rats.
+HTR1A	addiction	withdrawal	27235743	Prenatal stress alters diazepam <b>withdrawal</b> syndrome and <strong>5HT1A</strong> receptor expression in the raphe nuclei of adult rats.
+HTR1A	drug	benzodiazepine	27235743	Prenatal stress alters <b>diazepam</b> withdrawal syndrome and <strong><strong>5HT1A</strong></strong> receptor expression in the raphe nuclei of adult rats.
+HTR1A	addiction	withdrawal	27235743	Prenatal stress alters diazepam <b>withdrawal</b> syndrome and <strong><strong>5HT1A</strong></strong> receptor expression in the raphe nuclei of adult rats.
+HTR1A	drug	benzodiazepine	27235743	The present experiments were designed to investigate the effects of prenatal stress on <b>diazepam</b> induced withdrawal syndrome and serotonin 1A (<strong>5HT1A</strong>) receptor expression in the raphe nuclei of adult offspring.
+HTR1A	addiction	withdrawal	27235743	The present experiments were designed to investigate the effects of prenatal stress on diazepam induced <b>withdrawal</b> syndrome and serotonin 1A (<strong>5HT1A</strong>) receptor expression in the raphe nuclei of adult offspring.
+HTR1A	drug	benzodiazepine	27235743	The present experiments were designed to investigate the effects of prenatal stress on <b>diazepam</b> induced withdrawal syndrome and serotonin 1A (<strong><strong>5HT1A</strong></strong>) receptor expression in the raphe nuclei of adult offspring.
+HTR1A	addiction	withdrawal	27235743	The present experiments were designed to investigate the effects of prenatal stress on diazepam induced <b>withdrawal</b> syndrome and serotonin 1A (<strong><strong>5HT1A</strong></strong>) receptor expression in the raphe nuclei of adult offspring.
+HTR1A	drug	benzodiazepine	27235743	To our knowledge, this study is the first to demonstrate that maternal exposure to chronic footshock stress enhances <b>diazepam</b> withdrawal symptoms and alters <strong>5HT1A</strong> receptor gene expression in the raphe nuclei of adult offspring.
+HTR1A	addiction	withdrawal	27235743	To our knowledge, this study is the first to demonstrate that maternal exposure to chronic footshock stress enhances diazepam <b>withdrawal</b> symptoms and alters <strong>5HT1A</strong> receptor gene expression in the raphe nuclei of adult offspring.
+HTR1A	drug	benzodiazepine	27235743	To our knowledge, this study is the first to demonstrate that maternal exposure to chronic footshock stress enhances <b>diazepam</b> withdrawal symptoms and alters <strong><strong>5HT1A</strong></strong> receptor gene expression in the raphe nuclei of adult offspring.
+HTR1A	addiction	withdrawal	27235743	To our knowledge, this study is the first to demonstrate that maternal exposure to chronic footshock stress enhances diazepam <b>withdrawal</b> symptoms and alters <strong><strong>5HT1A</strong></strong> receptor gene expression in the raphe nuclei of adult offspring.
+HTR1A	drug	opioid	27178898	The strength of DNIC was reduced by <b>naloxone</b> (μ <b>opioid</b> receptor antagonist, intraperitoneally and intracerebroventricularly), yohimbine (α2 adrenoceptor antagonist, intrathecally), and WAY 100635 (<strong>5 HT1A</strong> receptor antagonist, intrathecally) in the von Frey test.
+HTR1A	drug	cannabinoid	27157263	electronic database was used as source of the studies selected selected based on the studies found by crossing the following keywords: <b>cannabidiol</b> and panic disorder; canabidiol and anxiety, <b>cannabidiol</b> and <strong>5 HT1A</strong> receptor).
+HTR1A	addiction	reward	26856853	The <strong>5 HT1A</strong> and 5 HT1B receptors are both well localized to regulate dopamine (DA) release, and have been implicated in modulating the <b>reinforcing</b> effects of many drugs of abuse, but a role in acquisition of self administration has not been determined.
+HTR1A	drug	psychedelics	26856853	This study was designed to determine the effect of pharmacological manipulation of <strong>5 HT1A</strong> and 5 HT1B receptor mechanisms on the acquisition of <b>MDMA</b> self administration.
+HTR1A	drug	psychedelics	26856853	These data suggest that the initial reinforcing effects of <b>MDMA</b> are modulated by <strong>5 HT1A</strong> and/or 5 HT1B receptor mechanisms.
+HTR1A	addiction	reward	26856853	These data suggest that the initial <b>reinforcing</b> effects of MDMA are modulated by <strong>5 HT1A</strong> and/or 5 HT1B receptor mechanisms.
+HTR1A	addiction	withdrawal	26732231	By contrast, the Dex induced second, but not the first, phase of the prolonged paw <b>withdrawal</b> heat latency was significantly blocked by the lesion of either DLF or thalamic ventromedial (VM) nuclei, and was attenuated by intracerebral administration of either atipamezole (α2 adrenoceptor antagonist) or WAY 100635 (<strong>5 HT1A</strong> receptor antagonist) into the VM nuclei (P < 0.05).
+HTR1A	drug	cannabinoid	26685701	The purpose of this study was to evaluate the efficacy of vilazodone, a selective serotonin receptor inhibitor and partial <strong>5 HT1A</strong> agonist, for treatment of <b>cannabis</b> dependence.
+HTR1A	addiction	dependence	26685701	The purpose of this study was to evaluate the efficacy of vilazodone, a selective serotonin receptor inhibitor and partial <strong>5 HT1A</strong> agonist, for treatment of cannabis <b>dependence</b>.
+HTR1A	drug	cannabinoid	26386827	The purpose of this study was to evaluate the efficacy of buspirone, a partial <strong>5 HT1A</strong> agonist, for treatment of <b>cannabis</b> dependence.
+HTR1A	addiction	dependence	26386827	The purpose of this study was to evaluate the efficacy of buspirone, a partial <strong>5 HT1A</strong> agonist, for treatment of cannabis <b>dependence</b>.
+HTR1A	drug	cocaine	26324408	<strong>5 HT1A</strong> Autoreceptors in the Dorsal Raphe Nucleus Convey Vulnerability to Compulsive <b>Cocaine</b> Seeking.
+HTR1A	addiction	addiction	26324408	<strong>5 HT1A</strong> Autoreceptors in the Dorsal Raphe Nucleus Convey Vulnerability to <b>Compulsive</b> Cocaine Seeking.
+HTR1A	addiction	relapse	26324408	<strong>5 HT1A</strong> Autoreceptors in the Dorsal Raphe Nucleus Convey Vulnerability to Compulsive Cocaine <b>Seeking</b>.
+HTR1A	drug	cocaine	26324408	This study tests the hypothesis that activation of <strong>5 HT1A</strong> autoreceptors, which would lessen 5 HT neuron firing, contributes to <b>cocaine</b> seeking behaviors.
+HTR1A	addiction	relapse	26324408	This study tests the hypothesis that activation of <strong>5 HT1A</strong> autoreceptors, which would lessen 5 HT neuron firing, contributes to cocaine <b>seeking</b> behaviors.
+HTR1A	drug	cocaine	26324408	Using 5 HT neuron specific reduction of <strong>5 HT1A</strong> autoreceptor gene expression in mice, we demonstrate that <strong>5 HT1A</strong> autoreceptors are necessary for <b>cocaine</b> conditioned place preference.
+HTR1A	drug	cocaine	26324408	Finally, using a rat model of compulsive like <b>cocaine</b> self administration, we found that inhibition of dorsal raphe <strong>5 HT1A</strong> autoreceptors attenuates <b>cocaine</b> self administration in rats with 6 h extended access, but not 1 h access to the drug.
+HTR1A	addiction	addiction	26324408	Finally, using a rat model of <b>compulsive</b> like cocaine self administration, we found that inhibition of dorsal raphe <strong>5 HT1A</strong> autoreceptors attenuates cocaine self administration in rats with 6 h extended access, but not 1 h access to the drug.
+HTR1A	drug	cocaine	26324408	Therefore, our findings suggest an important role for <strong>5 HT1A</strong> autoreceptors, and thus DRNNAc 5 HT neuronal activity, in the etiology and vulnerability to <b>cocaine</b> reward and addiction.
+HTR1A	addiction	addiction	26324408	Therefore, our findings suggest an important role for <strong>5 HT1A</strong> autoreceptors, and thus DRNNAc 5 HT neuronal activity, in the etiology and vulnerability to cocaine reward and <b>addiction</b>.
+HTR1A	addiction	reward	26324408	Therefore, our findings suggest an important role for <strong>5 HT1A</strong> autoreceptors, and thus DRNNAc 5 HT neuronal activity, in the etiology and vulnerability to cocaine <b>reward</b> and addiction.
+HTR1A	drug	cocaine	26324408	Moreover, our findings support a strategy for antagonizing <strong>5 HT1A</strong> autoreceptors for treating <b>cocaine</b> addiction.
+HTR1A	addiction	addiction	26324408	Moreover, our findings support a strategy for antagonizing <strong>5 HT1A</strong> autoreceptors for treating cocaine <b>addiction</b>.
+HTR1A	addiction	reward	25902158	Results indicate that tilianin is one of the bioactive metabolites in the anxiolytic like activity of A. mexicana, <b>reinforcing</b> its central nervous system uses, where GABAA/BZD, but not <strong>5 HT1A</strong>, receptors are partially involved.
+HTR1A	drug	nicotine	25896010	Effect of prenatal stress on memory, <b>nicotine</b> withdrawal and <strong>5HT1A</strong> expression in raphe nuclei of adult rats.
+HTR1A	addiction	withdrawal	25896010	Effect of prenatal stress on memory, nicotine <b>withdrawal</b> and <strong>5HT1A</strong> expression in raphe nuclei of adult rats.
+HTR1A	drug	nicotine	25896010	Effect of prenatal stress on memory, <b>nicotine</b> withdrawal and <strong><strong>5HT1A</strong></strong> expression in raphe nuclei of adult rats.
+HTR1A	addiction	withdrawal	25896010	Effect of prenatal stress on memory, nicotine <b>withdrawal</b> and <strong><strong>5HT1A</strong></strong> expression in raphe nuclei of adult rats.
+HTR1A	drug	opioid	25895641	We have recently demonstrated that allyphenyline, behaving as α2C adrenoceptor/serotonin <strong>5 HT1A</strong> receptor agonist and α2A adrenoceptor antagonist, in mice enhanced <b>morphine</b> analgesia, attenuated <b>morphine</b> withdrawal symptoms, showed significant antidepressant like activity and was devoid of sedative side effects.
+HTR1A	addiction	withdrawal	25895641	We have recently demonstrated that allyphenyline, behaving as α2C adrenoceptor/serotonin <strong>5 HT1A</strong> receptor agonist and α2A adrenoceptor antagonist, in mice enhanced morphine analgesia, attenuated morphine <b>withdrawal</b> symptoms, showed significant antidepressant like activity and was devoid of sedative side effects.
+HTR1A	drug	alcohol	25895641	Therefore, the present investigation suggests that allyphenyline might represent an interesting pharmacological tool to investigate the potential of compounds exhibiting α2C adrenoceptor/serotonin <strong>5 HT1A</strong> receptor agonism and α2A adrenoceptor antagonism in the treatment of hyperanxiety and hyperlocomotion occurring during <b>alcohol</b> withdrawal in dependent subjects.
+HTR1A	addiction	withdrawal	25895641	Therefore, the present investigation suggests that allyphenyline might represent an interesting pharmacological tool to investigate the potential of compounds exhibiting α2C adrenoceptor/serotonin <strong>5 HT1A</strong> receptor agonism and α2A adrenoceptor antagonism in the treatment of hyperanxiety and hyperlocomotion occurring during alcohol <b>withdrawal</b> in dependent subjects.
+HTR1A	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, <strong>Htr1a</strong>, Drd1a, Gria1, and Pdyn.
+HTR1A	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, <strong>Htr1a</strong>, Drd1a, Gria1, and Pdyn.
+HTR1A	drug	opioid	25315826	Interaction between μ <b>opioid</b> and <strong>5 HT1A</strong> receptors in the regulation of panic related defensive responses in the rat dorsal periaqueductal grey.
+HTR1A	drug	opioid	25315826	Results that were previously obtained with the elevated T maze test of anxiety/panic suggest that <strong>5 HT1A</strong> and μ <b>opioid</b> receptors in this midbrain area work together to regulate this response.
+HTR1A	drug	opioid	25315826	Therefore, regardless of the aversive nature of the stimulus, μ <b>opioid</b> and <strong>5 HT1A</strong> receptors cooperatively act to regulate escape behaviour.
+HTR1A	addiction	aversion	25315826	Therefore, regardless of the <b>aversive</b> nature of the stimulus, μ opioid and <strong>5 HT1A</strong> receptors cooperatively act to regulate escape behaviour.
+HTR1A	drug	alcohol	25220896	The goal of this work was to directly observe in vivo effects of chronic <b>ethanol</b> self administration on serotonin <strong>5 HT1A</strong> receptor binding with [(18)F]mefway PET neuroimaging in rhesus monkeys.
+HTR1A	drug	alcohol	25220896	Subjects were first imaged <b>alcohol</b> naïve and again during chronic <b>ethanol</b> self administration to quantify changes in <strong>5 HT1A</strong> receptor binding.
+HTR1A	drug	alcohol	25220896	Changes in <strong>5 HT1A</strong> binding during chronic <b>ethanol</b> self administration were examined.
+HTR1A	drug	alcohol	25220896	Widespread increases in <strong>5 HT1A</strong> binding were observed during chronic <b>ethanol</b> self administration, independent of the amount of <b>ethanol</b> consumed.
+HTR1A	drug	alcohol	25220896	A positive correlation between <strong>5 HT1A</strong> binding in the raphe nuclei and average daily <b>ethanol</b> self administration was also observed, indicating that baseline <strong>5 HT1A</strong> binding in this region predicted drinking levels.
+HTR1A	drug	alcohol	25220896	The increase in <strong>5 HT1A</strong> binding levels during chronic <b>ethanol</b> self administration demonstrates an important modulation of the serotonin system due to chronic <b>alcohol</b> exposure.
+HTR1A	drug	alcohol	25220896	Furthermore, the correlation between <strong>5 HT1A</strong> binding in the raphe nuclei and daily <b>ethanol</b> self administration indicates a relationship between the serotonin system and <b>alcohol</b> self administration.
+HTR1A	addiction	withdrawal	24900763	Exploring multitarget interactions, the present investigation suggests that 3 or its (S) enantiomer and 4, endowed with effective α2C AR agonism/α2A AR antagonism/<strong>5 HT1A</strong> R agonism, or 7 and 9 11 producing efficacious α2C AR agonism/α2A AR antagonism/I2 IBS interaction might represent novel multifunctional tools potentially useful for reducing <b>withdrawal</b> syndrome and associated depression.
+HTR1A	addiction	intoxication	24763081	Furthermore, MA <b>binge</b> exposure increased 5 HT2A and decreased mGlu2 receptor expression in the medial frontal cortex, whereas 5 HT2C and <strong>5 HT1A</strong> receptors were unaffected.
+HTR1A	drug	cocaine	24679922	Buspirone, originally characterized as a <strong>5 HT1A</strong> partial agonist and used as an anxiolytic, also binds to D3R and D4R with high affinity, with lower affinity to D2R, and interferes with <b>cocaine</b> reward.
+HTR1A	addiction	reward	24679922	Buspirone, originally characterized as a <strong>5 HT1A</strong> partial agonist and used as an anxiolytic, also binds to D3R and D4R with high affinity, with lower affinity to D2R, and interferes with cocaine <b>reward</b>.
+HTR1A	drug	alcohol	24467872	The effects of chronic <b>ethanol</b> self administration on hippocampal <strong>5 HT1A</strong> receptors in monkeys.
+HTR1A	drug	alcohol	24467872	Hippocampal <strong>5 HT1A</strong> receptors modulate these mechanisms, but the neuroadaptive response of 5HT1A receptors to chronic <b>alcohol</b> self administration is not well understood.
+HTR1A	drug	alcohol	24467872	Hippocampal <strong>5 HT1A</strong> receptors modulate these mechanisms, but the neuroadaptive response of <strong>5HT1A</strong> receptors to chronic <b>alcohol</b> self administration is not well understood.
+HTR1A	drug	alcohol	24467872	Hippocampal <strong>5 HT1A</strong> receptors modulate these mechanisms, but the neuroadaptive response of <strong><strong>5HT1A</strong></strong> receptors to chronic <b>alcohol</b> self administration is not well understood.
+HTR1A	drug	alcohol	24467872	Chronic <b>ethanol</b> self administration was also associated with an up regulation of total and G protein coupled <strong>5 HT1A</strong> receptors in the posterior DG polymorphic layer.
+HTR1A	drug	alcohol	24467872	Chronic, <b>ethanol</b> self administration up regulates hippocampal <strong>5 HT1A</strong> receptor density in a region specific manner that does not appear to be due to alterations at the level of transcription but instead may be due to increased receptor trafficking.
+HTR1A	drug	alcohol	24467872	Further exploration of the mechanisms mediating chronic <b>ethanol</b> induced <strong>5 HT1A</strong> receptor up regulation and how hippocampal neurotransmission is altered is warranted.
+HTR1A	addiction	withdrawal	24076184	injection of the <strong>5 HT1A</strong> receptor antagonist WAY 100635 increased paw <b>withdrawal</b> latency (PWL) above normal level (hypoalgesia) during the late phase of carrageenan evoked inflammation.
+HTR1A	drug	opioid	24076184	The present study suggests that the activation of <strong>5 HT1A</strong> receptors suppressed <b>naloxone</b> reversible antinociception contributing to the maintenance of inflammatory pain, and that the concomitant blockade of <strong>5 HT1A</strong> and 5 HT2A receptors in the periphery produced synergistic effects on inflammatory hyperalgesia.
+HTR1A	drug	opioid	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ <b>opioid</b> receptor (MOR), <strong>5 HT1A</strong> receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of <b>morphine</b> exposure, withdrawal and post withdrawal stress.
+HTR1A	addiction	withdrawal	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ opioid receptor (MOR), <strong>5 HT1A</strong> receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of morphine exposure, <b>withdrawal</b> and post <b>withdrawal</b> stress.
+HTR1A	drug	opioid	24055683	<strong>5 HT1A</strong> receptor mRNA expression was decreased following 3h of <b>morphine</b> exposure, while TPH2 mRNA expression was decreased after 7days of withdrawal with swim stress.
+HTR1A	addiction	withdrawal	24055683	<strong>5 HT1A</strong> receptor mRNA expression was decreased following 3h of morphine exposure, while TPH2 mRNA expression was decreased after 7days of <b>withdrawal</b> with swim stress.
+HTR1A	drug	amphetamine	23994622	This study sought to assess whether aripiprazole, a partial agonist at D2/<strong>5 HT1A</strong> receptors and an antagonist at 5 HT2A receptors, would attenuate the reinforcing and subject rated effects of oral <b>methamphetamine</b>.
+HTR1A	addiction	reward	23994622	This study sought to assess whether aripiprazole, a partial agonist at D2/<strong>5 HT1A</strong> receptors and an antagonist at 5 HT2A receptors, would attenuate the <b>reinforcing</b> and subject rated effects of oral methamphetamine.
+HTR1A	drug	cannabinoid	23929722	qRT PCR analysis of 1 μM nonivamide treated SH SY5Y cells revealed gene regulation of the receptors dopamine D1 and D2, serotonin <strong>HTR1A</strong>, 1B and 2A, <b>cannabinoid</b> 1, and TRPV1.
+HTR1A	drug	cannabinoid	23926240	The role of <strong>5 HT1A</strong> receptors in the anti aversive effects of <b>cannabidiol</b> on panic attack like behaviors evoked in the presence of the wild snake Epicrates cenchria crassus (Reptilia, Boidae).
+HTR1A	addiction	aversion	23926240	The role of <strong>5 HT1A</strong> receptors in the anti <b>aversive</b> effects of cannabidiol on panic attack like behaviors evoked in the presence of the wild snake Epicrates cenchria crassus (Reptilia, Boidae).
+HTR1A	drug	cannabinoid	23926240	These findings demonstrate that <b>cannabidiol</b> modulates the defensive behaviors evoked by the presence of threatening stimuli, and the effects of <b>cannabidiol</b> are at least partially dependent on the recruitment of <strong>5 HT1A</strong> receptors.
+HTR1A	drug	amphetamine	23906987	Inhibition of <b>amphetamine</b> and apomorphine induced behavioral sensitization by co administration of <strong>5 HT 1A</strong> agonists cannot be explained in terms of direct activation of <strong>5 HT 1A</strong> receptors, because activation of pre  as well as postsynaptic <strong>5 HT 1A</strong> receptors tends to increase dopamine neurotransmission.
+HTR1A	addiction	sensitization	23906987	Inhibition of amphetamine and apomorphine induced behavioral <b>sensitization</b> by co administration of <strong>5 HT 1A</strong> agonists cannot be explained in terms of direct activation of <strong>5 HT 1A</strong> receptors, because activation of pre  as well as postsynaptic <strong>5 HT 1A</strong> receptors tends to increase dopamine neurotransmission.
+HTR1A	drug	amphetamine	23906987	Long term use of <b>amphetamine</b> and apomorphine produces adaptive changes in <strong>5 HT 1A</strong> receptor mediated functions, which are prevented by the co use of <strong>5 HT 1A</strong> agonists.
+HTR1A	drug	amphetamine	23906987	In view of extending medicinal use of psychostimulants, it is important to evaluate the effects of co use of <strong>5 HT 1A</strong> agonists on potential therapeutic profile of <b>amphetamine</b> and apomorphine in preclinical research.
+HTR1A	addiction	addiction	23906987	It is also important to evaluate the functional significance of <strong>5 HT 1A</strong> receptors on psychostimulant induced behaviors in other <b>addiction</b> models such as drug self administration and reinstatement of drug seeking behavior.
+HTR1A	addiction	relapse	23906987	It is also important to evaluate the functional significance of <strong>5 HT 1A</strong> receptors on psychostimulant induced behaviors in other addiction models such as drug self administration and <b>reinstatement</b> of drug <b>seeking</b> behavior.
+HTR1A	drug	opioid	23438874	The present study evaluated the effects of cholinesterase inhibitors and serotonin 1A (<strong>5 HT1A</strong>) receptor agonists on <b>morphine</b> (1.0mg/kg, i.v.)
+HTR1A	drug	opioid	23438874	The present study suggests that activation of cholinergic or serotonergic (<strong>5 HT1A</strong>) mechanisms may be a useful therapeutic approach for <b>morphine</b> induced ventilatory depression without loss of its analgesic action.
+HTR1A	drug	alcohol	23216389	Genome wide significant association signals in IPO11 <strong>HTR1A</strong> region specific for <b>alcohol</b> and nicotine codependence.
+HTR1A	drug	nicotine	23216389	Genome wide significant association signals in IPO11 <strong>HTR1A</strong> region specific for alcohol and <b>nicotine</b> codependence.
+HTR1A	drug	alcohol	23216389	We identified a significant risk region for <b>alcohol</b> and nicotine codependence between IPO11 and <strong>HTR1A</strong> on chromosome 5q that was reported to be suggestively associated with <b>alcohol</b> dependence previously.
+HTR1A	drug	nicotine	23216389	We identified a significant risk region for alcohol and <b>nicotine</b> codependence between IPO11 and <strong>HTR1A</strong> on chromosome 5q that was reported to be suggestively associated with alcohol dependence previously.
+HTR1A	addiction	dependence	23216389	We identified a significant risk region for alcohol and nicotine codependence between IPO11 and <strong>HTR1A</strong> on chromosome 5q that was reported to be suggestively associated with alcohol <b>dependence</b> previously.
+HTR1A	drug	alcohol	23216389	We speculate that this IPO11 <strong>HTR1A</strong> region might harbor a causal variant for <b>alcohol</b> and nicotine codependence.
+HTR1A	drug	nicotine	23216389	We speculate that this IPO11 <strong>HTR1A</strong> region might harbor a causal variant for alcohol and <b>nicotine</b> codependence.
+HTR1A	drug	cannabinoid	23041353	Systemic administration of <b>cannabidiol</b> (CBD) is able to attenuate cardiovascular responses to acute restraint stress through activation of <strong>5 HT1A</strong> receptors.
+HTR1A	drug	cannabinoid	22862835	<b>Cannabidiol</b> inhibits the reward facilitating effect of morphine: involvement of <strong>5 HT1A</strong> receptors in the dorsal raphe nucleus.
+HTR1A	drug	opioid	22862835	Cannabidiol inhibits the reward facilitating effect of <b>morphine</b>: involvement of <strong>5 HT1A</strong> receptors in the dorsal raphe nucleus.
+HTR1A	addiction	reward	22862835	Cannabidiol inhibits the <b>reward</b> facilitating effect of morphine: involvement of <strong>5 HT1A</strong> receptors in the dorsal raphe nucleus.
+HTR1A	drug	opioid	24900506	It also highlighted that such positive effects on <b>morphine</b> dependence can even be improved by additional serotoninergic <strong>5 HT1A</strong> receptor (<strong>5 HT1A</strong> R) activation.
+HTR1A	addiction	dependence	24900506	It also highlighted that such positive effects on morphine <b>dependence</b> can even be improved by additional serotoninergic <strong>5 HT1A</strong> receptor (<strong>5 HT1A</strong> R) activation.
+HTR1A	drug	opioid	24900506	Indeed, 1 or the single (S) (+) 1, 2, or both its enantiomers, all behaving as α2C AR agonists/α2A AR antagonists/<strong>5 HT1A</strong> R agonists, alone and at the same low dose, improved <b>morphine</b> withdrawal syndrome and exerted a potent antidepressant like effect.
+HTR1A	addiction	withdrawal	24900506	Indeed, 1 or the single (S) (+) 1, 2, or both its enantiomers, all behaving as α2C AR agonists/α2A AR antagonists/<strong>5 HT1A</strong> R agonists, alone and at the same low dose, improved morphine <b>withdrawal</b> syndrome and exerted a potent antidepressant like effect.
+HTR1A	drug	benzodiazepine	22413490	This chapter outlines the clinician' s guide for prescription of <b>benzodiazepine</b> anxiolytics and <strong>5 HT1A</strong> receptor agonists.
+HTR1A	drug	alcohol	22176604	Serotonin receptor 1A (<strong>5HT1A</strong>) mRNA in BA 9 was elevated in the <b>alcohol</b> dependence without suicide group compared with controls.
+HTR1A	addiction	dependence	22176604	Serotonin receptor 1A (<strong>5HT1A</strong>) mRNA in BA 9 was elevated in the alcohol <b>dependence</b> without suicide group compared with controls.
+HTR1A	drug	alcohol	22176604	Serotonin receptor 1A (<strong><strong>5HT1A</strong></strong>) mRNA in BA 9 was elevated in the <b>alcohol</b> dependence without suicide group compared with controls.
+HTR1A	addiction	dependence	22176604	Serotonin receptor 1A (<strong><strong>5HT1A</strong></strong>) mRNA in BA 9 was elevated in the alcohol <b>dependence</b> without suicide group compared with controls.
+HTR1A	drug	alcohol	22176604	In the <b>alcohol</b> dependence with suicide group, anxiety symptoms were associated with decreased BA 24 SERT mRNA and depressive symptoms with BA 9 <strong>5HT1A</strong> mRNA expression.
+HTR1A	addiction	dependence	22176604	In the alcohol <b>dependence</b> with suicide group, anxiety symptoms were associated with decreased BA 24 SERT mRNA and depressive symptoms with BA 9 <strong>5HT1A</strong> mRNA expression.
+HTR1A	drug	alcohol	22176604	In the <b>alcohol</b> dependence with suicide group, anxiety symptoms were associated with decreased BA 24 SERT mRNA and depressive symptoms with BA 9 <strong><strong>5HT1A</strong></strong> mRNA expression.
+HTR1A	addiction	dependence	22176604	In the alcohol <b>dependence</b> with suicide group, anxiety symptoms were associated with decreased BA 24 SERT mRNA and depressive symptoms with BA 9 <strong><strong>5HT1A</strong></strong> mRNA expression.
+HTR1A	drug	alcohol	21621273	Association of polymorphisms in HTR2A, <strong>HTR1A</strong> and TPH2 genes with suicide attempts in <b>alcohol</b> dependence: a preliminary report.
+HTR1A	addiction	dependence	21621273	Association of polymorphisms in HTR2A, <strong>HTR1A</strong> and TPH2 genes with suicide attempts in alcohol <b>dependence</b>: a preliminary report.
+HTR1A	drug	alcohol	21621273	We investigated a relationship between selected polymorphisms: rs6313 in HTR2A, rs6295 in <strong>HTR1A</strong> and rs1386494 in TPH2, and suicidal behaviour in 150 <b>alcohol</b> dependent patients.
+HTR1A	drug	nicotine	21501256	Shifting topographic activation and <strong>5 HT1A</strong> receptor mediated inhibition of dorsal raphe serotonin neurons produced by <b>nicotine</b> exposure and withdrawal.
+HTR1A	addiction	withdrawal	21501256	Shifting topographic activation and <strong>5 HT1A</strong> receptor mediated inhibition of dorsal raphe serotonin neurons produced by nicotine exposure and <b>withdrawal</b>.
+HTR1A	drug	nicotine	21501256	Using these approaches, we found evidence that acute <b>nicotine</b> exposure activates 5 HT neurons rostrally and in the lateral wings of the DR, whereas there is <strong>5 HT1A</strong> receptor dependent inhibition of cells located ventrally at both the rostral level and mid level.
+HTR1A	drug	nicotine	21501256	Previous chronic <b>nicotine</b> exposure did not modify the pattern of activation produced by acute <b>nicotine</b> exposure, but increased <strong>5 HT1A</strong> receptor dependent inhibition of 5 HT cells in the caudal DR.
+HTR1A	drug	nicotine	21501256	This pattern was nearly reversed during <b>nicotine</b> withdrawal, when there was evidence for caudal activation and mid level and rostral <strong>5 HT1A</strong> receptor dependent inhibition.
+HTR1A	addiction	withdrawal	21501256	This pattern was nearly reversed during nicotine <b>withdrawal</b>, when there was evidence for caudal activation and mid level and rostral <strong>5 HT1A</strong> receptor dependent inhibition.
+HTR1A	drug	nicotine	21501256	These results suggest that the distinct behavioral states produced by <b>nicotine</b> exposure and withdrawal correlate with reciprocal rostral caudal patterns of activation and <strong>5 HT1A</strong> receptor mediated inhibition of DR 5 HT neurons.
+HTR1A	addiction	withdrawal	21501256	These results suggest that the distinct behavioral states produced by nicotine exposure and <b>withdrawal</b> correlate with reciprocal rostral caudal patterns of activation and <strong>5 HT1A</strong> receptor mediated inhibition of DR 5 HT neurons.
+HTR1A	drug	nicotine	21412223	<b>Nicotine</b> alters limbic function in adolescent rat by a <strong>5 HT1A</strong> receptor mechanism.
+HTR1A	drug	cocaine	21412223	Nicotine enhancement of <b>cocaine</b> self administration and quinpirole induced locomotor activity was blocked by co administration of WAY 100 635 (N {2 [4 (2 methoxyphenyl) 1 piperazinyl] ethyl} N (2 pyridinyl)cyclohexanecarboxamide), a selective serotonin 1A (<strong>5 HT1A</strong>) receptor antagonist.
+HTR1A	drug	nicotine	21412223	<b>Nicotine</b> enhancement of cocaine self administration and quinpirole induced locomotor activity was blocked by co administration of WAY 100 635 (N {2 [4 (2 methoxyphenyl) 1 piperazinyl] ethyl} N (2 pyridinyl)cyclohexanecarboxamide), a selective serotonin 1A (<strong>5 HT1A</strong>) receptor antagonist.
+HTR1A	drug	nicotine	21412223	These findings indicate that early adolescent <b>nicotine</b> exposure uniquely alters limbic function by both <strong>5 HT1A</strong> and non <strong>5 HT1A</strong> receptor mechanisms.
+HTR1A	drug	cannabinoid	21148020	<b>Cannabidiol</b> injected into the bed nucleus of the stria terminalis reduces the expression of contextual fear conditioning via <strong>5 HT1A</strong> receptors.
+HTR1A	drug	cannabinoid	20945065	The anxiolytic like effects of <b>cannabidiol</b> injected into the bed nucleus of the stria terminalis are mediated by <strong>5 HT1A</strong> receptors.
+HTR1A	drug	cannabinoid	20621717	<b>Cannabidiol</b> injected into the bed nucleus of the stria terminalis modulates baroreflex activity through <strong>5 HT1A</strong> receptors.
+HTR1A	drug	cannabinoid	20621717	<b>Cannabidiol</b> (CBD) is a non psychotomimetic constituent of the <b>Cannabis</b> sativa plant that inhibits behavioral and cardiovascular responses to aversive situations, facilitating <strong>5 HT1A</strong> mediated neurotransmission.
+HTR1A	addiction	aversion	20621717	Cannabidiol (CBD) is a non psychotomimetic constituent of the Cannabis sativa plant that inhibits behavioral and cardiovascular responses to <b>aversive</b> situations, facilitating <strong>5 HT1A</strong> mediated neurotransmission.
+HTR1A	drug	amphetamine	20614033	In contrast, pretreatment with D1/D5 dopamine receptor antagonist SCH23390 or <strong>5 HT1A</strong> receptor antagonist NAN 190 abrogated the effect of <b>METH</b> on synaptic transmission.
+HTR1A	drug	benzodiazepine	20081241	Gestational manganese intoxication and anxiolytic like effects of <b>diazepam</b> and the <strong>5 HT1A</strong> receptor agonist 8 OH DPAT in male Wistar rats.
+HTR1A	addiction	intoxication	20081241	Gestational manganese <b>intoxication</b> and anxiolytic like effects of diazepam and the <strong>5 HT1A</strong> receptor agonist 8 OH DPAT in male Wistar rats.
+HTR1A	drug	amphetamine	19747927	Several investigations have reported associations the serotonin 1A (5 HT1A) receptor to schizophrenia and psychotic disorders, making 5 HT1A receptor gene (<strong>HTR1A</strong>) an adequate candidate gene for the pathophysiology of schizophrenia and <b>methamphetamine</b> (<b>METH</b>) induced psychosis.
+HTR1A	drug	amphetamine	19747927	Several investigations have reported associations the serotonin 1A (<strong>5 HT1A</strong>) receptor to schizophrenia and psychotic disorders, making <strong>5 HT1A</strong> receptor gene (<strong>HTR1A</strong>) an adequate candidate gene for the pathophysiology of schizophrenia and <b>methamphetamine</b> (<b>METH</b>) induced psychosis.
+HTR1A	drug	amphetamine	19747927	Furthermore, we conducted an analysis of the association of <strong>HTR1A</strong> with <b>METH</b> induced psychosis.
+HTR1A	drug	amphetamine	19747927	In addition, we detected an association between rs6295 and rs878567 in <strong>HTR1A</strong> and <b>METH</b> induced psychosis patients in the haplotype wise analysis.
+HTR1A	drug	amphetamine	19747927	<strong>HTR1A</strong> may play an important role in the pathophysiology of <b>METH</b> induced psychosis in the Japanese population.
+HTR1A	drug	opioid	19555163	When tested for biological activity, compounds 1d f exhibited strong inhibitory effects on the <b>morphine</b> withdrawal syndrome in mice due to their high binding affinities with serotonergic <strong>5 HT1A</strong> receptors.
+HTR1A	addiction	withdrawal	19555163	When tested for biological activity, compounds 1d f exhibited strong inhibitory effects on the morphine <b>withdrawal</b> syndrome in mice due to their high binding affinities with serotonergic <strong>5 HT1A</strong> receptors.
+HTR1A	drug	opioid	19353810	Aripiprazole is an atypical antipsychotic drug primarily characterized by partial agonist activity at dopamine(DA) D2 receptors and serotonin 1A (5 hydroxytryptamine, <strong>5 HT1A</strong>) receptors and minimal side effects.Based on its pharmacological profile, including stabilization of mesocorticolimbic DA activity (a pathway implicated in drug addiction), we investigated the effects of aripiprazole on relapse to <b>morphine</b> seeking in rats.
+HTR1A	addiction	addiction	19353810	Aripiprazole is an atypical antipsychotic drug primarily characterized by partial agonist activity at dopamine(DA) D2 receptors and serotonin 1A (5 hydroxytryptamine, <strong>5 HT1A</strong>) receptors and minimal side effects.Based on its pharmacological profile, including stabilization of mesocorticolimbic DA activity (a pathway implicated in drug <b>addiction</b>), we investigated the effects of aripiprazole on relapse to morphine seeking in rats.
+HTR1A	addiction	relapse	19353810	Aripiprazole is an atypical antipsychotic drug primarily characterized by partial agonist activity at dopamine(DA) D2 receptors and serotonin 1A (5 hydroxytryptamine, <strong>5 HT1A</strong>) receptors and minimal side effects.Based on its pharmacological profile, including stabilization of mesocorticolimbic DA activity (a pathway implicated in drug addiction), we investigated the effects of aripiprazole on <b>relapse</b> to morphine <b>seeking</b> in rats.
+HTR1A	addiction	relapse	19353810	The D2 and <strong>5 HT1A</strong> partial agonist and 5 HT2A antagonist properties of aripiprazole likely account for the blockade of <b>relapse</b> to drug <b>seeking</b>.
+HTR1A	drug	alcohol	19229522	Yohimbine also acts as an agonist of 5 hydroxytryptamine (5 HT) <strong>5 HT1A</strong> receptors, which have been shown to be involved in <b>alcohol</b> seeking.
+HTR1A	addiction	relapse	19229522	Yohimbine also acts as an agonist of 5 hydroxytryptamine (5 HT) <strong>5 HT1A</strong> receptors, which have been shown to be involved in alcohol <b>seeking</b>.
+HTR1A	drug	alcohol	19229522	Here, we determined the contributions of the alpha 2 and <strong>5 HT1A</strong> properties of yohimbine to its effects on <b>alcohol</b> seeking.
+HTR1A	addiction	relapse	19229522	Here, we determined the contributions of the alpha 2 and <strong>5 HT1A</strong> properties of yohimbine to its effects on alcohol <b>seeking</b>.
+HTR1A	addiction	relapse	19229522	The effects of the alpha 2 receptor agonist clonidine, or the <strong>5 HT1A</strong> antagonist WAY 100,635 were then determined on yohimbine induced self administration and <b>reinstatement</b>.
+HTR1A	addiction	relapse	19229522	Blockade of <strong>5 HT1A</strong> receptors reduced both yohimbine induced self administration and <b>reinstatement</b>.
+HTR1A	drug	alcohol	19229522	On the other hand, yohimbine's actions on <strong>5 HT1A</strong> receptors contribute to its effects on both <b>alcohol</b> self administration and reinstatement.
+HTR1A	addiction	relapse	19229522	On the other hand, yohimbine's actions on <strong>5 HT1A</strong> receptors contribute to its effects on both alcohol self administration and <b>reinstatement</b>.
+HTR1A	drug	nicotine	19176807	Inhibition of monoamine oxidases desensitizes <strong>5 HT1A</strong> autoreceptors and allows <b>nicotine</b> to induce a neurochemical and behavioral sensitization.
+HTR1A	addiction	sensitization	19176807	Inhibition of monoamine oxidases desensitizes <strong>5 HT1A</strong> autoreceptors and allows nicotine to induce a neurochemical and behavioral <b>sensitization</b>.
+HTR1A	addiction	relapse	19170664	Genetic polymorphisms in several genes (TPH2, SLC6A4, <strong>HTR1A</strong>, HTR2A, COMT, and BDNF) were tested as predictors of <b>relapse</b> (defined as any drinking during follow up) while controlling for baseline measures.
+HTR1A	drug	benzodiazepine	20581793	We encountered catatonia in a man with neurosyphilis after increasing aripiprazole and valproate (drugs reported to improve catatonia) and reducing doxycycline and <b>temazepam</b> dosages, consistent with identified dopamine D2, serotonin 5HT2, and <strong>5HT1a</strong> (aripiprazole), GABA B (valproate), glutamatergic NMDA (aripiprazole, valproate, doxycycline), and GABA A (aripiprazole, <b>temazepam</b>) mechanisms of catatonia.
+HTR1A	drug	benzodiazepine	20581793	We encountered catatonia in a man with neurosyphilis after increasing aripiprazole and valproate (drugs reported to improve catatonia) and reducing doxycycline and <b>temazepam</b> dosages, consistent with identified dopamine D2, serotonin 5HT2, and <strong><strong>5HT1a</strong></strong> (aripiprazole), GABA B (valproate), glutamatergic NMDA (aripiprazole, valproate, doxycycline), and GABA A (aripiprazole, <b>temazepam</b>) mechanisms of catatonia.
+HTR1A	drug	alcohol	19060480	The role of polymorphisms in the serotonin receptor 1A (<strong>5 HT1A</strong>), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (5 HTT) promotor region (5 HTTLPR) in the manifestation of individual <b>alcohol</b> withdrawal symptoms was investigated in 97 Korean male inpatients with <b>alcohol</b> dependence and 76 Korean healthy male subjects.
+HTR1A	addiction	dependence	19060480	The role of polymorphisms in the serotonin receptor 1A (<strong>5 HT1A</strong>), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (5 HTT) promotor region (5 HTTLPR) in the manifestation of individual alcohol withdrawal symptoms was investigated in 97 Korean male inpatients with alcohol <b>dependence</b> and 76 Korean healthy male subjects.
+HTR1A	addiction	withdrawal	19060480	The role of polymorphisms in the serotonin receptor 1A (<strong>5 HT1A</strong>), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (5 HTT) promotor region (5 HTTLPR) in the manifestation of individual alcohol <b>withdrawal</b> symptoms was investigated in 97 Korean male inpatients with alcohol dependence and 76 Korean healthy male subjects.
+HTR1A	drug	alcohol	19060480	In the <strong>5 HT1A</strong> receptor, the frequency of G  genotype (CC) was significantly higher in patients with <b>alcohol</b> dependence than in normal controls (chi(2) = 5.03, p = 0.025).
+HTR1A	addiction	dependence	19060480	In the <strong>5 HT1A</strong> receptor, the frequency of G  genotype (CC) was significantly higher in patients with alcohol <b>dependence</b> than in normal controls (chi(2) = 5.03, p = 0.025).
+HTR1A	drug	alcohol	19060480	The results suggest that the genetic polymorphism of the <strong>5 HT1A</strong> receptor may play a role in <b>alcohol</b> dependence and polymorphisms of serotonergic genes may be important in withdrawal symptoms of patients with <b>alcohol</b> dependence.
+HTR1A	addiction	dependence	19060480	The results suggest that the genetic polymorphism of the <strong>5 HT1A</strong> receptor may play a role in alcohol <b>dependence</b> and polymorphisms of serotonergic genes may be important in withdrawal symptoms of patients with alcohol <b>dependence</b>.
+HTR1A	addiction	withdrawal	19060480	The results suggest that the genetic polymorphism of the <strong>5 HT1A</strong> receptor may play a role in alcohol dependence and polymorphisms of serotonergic genes may be important in <b>withdrawal</b> symptoms of patients with alcohol dependence.
+HTR1A	addiction	reward	18778728	In the present investigation, using Sprague Dawley rats trained to discriminate DOM (1.0 mg/kg) from saline vehicle under a VI 15 s schedule of <b>reinforcement</b>, it was shown that the stimulus enhancing actions of 8 OH DPAT are related more to its R(+) isomer than to its S( ) enantiomer, and that the (+/ )  and R(+)8 OH DPAT induced effects are antagonized by the <strong>5 HT1A</strong> receptor antagonist NAN 190.
+HTR1A	addiction	withdrawal	18709357	In WIN dependent rats (chronic and <b>withdrawal</b> states), the effect of a low dose of (+/ ) 8 hydroxy 2 (di n propylamino) tetralin (<strong>5 HT1A</strong> agonist; 0.1 mg/kg) on the accumulation of precursor amino acids was markedly potentiated in cerebellum and striatum, indicating the induction of supersensitivity of <strong>5 HT1A</strong> autoreceptors and <strong>5 HT1A</strong> heteroreceptors that regulate the synthesis of 5 HT, noradrenaline, and dopamine in these brain regions.
+HTR1A	drug	cocaine	18581099	Adaptations in pre  and postsynaptic <strong>5 HT1A</strong> receptor function and <b>cocaine</b> supersensitivity in serotonin transporter knockout rats.
+HTR1A	drug	cocaine	18581099	To study the rewarding and motivational properties of <b>cocaine</b> in the serotonin transporter knockout (SERT / ) rat and the involvement of compensatory changes in <strong>5 HT1A</strong> receptor function are the objectives of the study.
+HTR1A	drug	cocaine	18581099	In addition, the function and expression of <strong>5 HT1A</strong> receptors was assessed using telemetry and autoradiography, respectively, and the effect of <strong>5 HT1A</strong> receptor ligands on <b>cocaine</b>'s psychomotor effects were studied.
+HTR1A	drug	cocaine	18581099	These data indicate that SERT /   associated <strong>5 HT1A</strong> receptor adaptations facilitate low dose <b>cocaine</b> effects and attenuate high dose <b>cocaine</b> effects in <b>cocaine</b> supersensitive animals.
+HTR1A	drug	nicotine	18562131	Therefore, 792 cigarette <b>smokers</b> from the Patch in Practice trial were genotyped for the tryptophan hydroxylase (TPH1 A779C), serotonin transporter (SLC6A45 HTTLPR), and 5 HT1A (<strong>HTR1A</strong> C 1019G) polymorphisms.
+HTR1A	drug	nicotine	18562131	Therefore, 792 cigarette <b>smokers</b> from the Patch in Practice trial were genotyped for the tryptophan hydroxylase (TPH1 A779C), serotonin transporter (SLC6A45 HTTLPR), and <strong>5 HT1A</strong> (<strong>HTR1A</strong> C 1019G) polymorphisms.
+HTR1A	drug	nicotine	18562131	Cox regression analysis did not demonstrate significant effects of any of the three genotypes on relapse to <b>smoking</b>: TPH1 (Reference AA; AC: hazard ratio (HR) 0.99, 95% confidence interval (CI) 0.78, 1.24, p=0.90; CC: HR 0.93, 95% CI 0.73, 1.18, p=0.55); 5 HTTLPR (Reference LL; SL: HR 1.01, 95% CI 0.85, 1.20, p=0.90; SS: HR 1.13, 95% CI 0.91, 1.39, p=0.27); <strong>HTR1A</strong> (Reference CC; CG: HR 1.04, 95% CI 0.86, 1.25, p=0.70; GG: HR 1.01, 95% CI 0.82, 1.24, p=0.93).
+HTR1A	addiction	relapse	18562131	Cox regression analysis did not demonstrate significant effects of any of the three genotypes on <b>relapse</b> to smoking: TPH1 (Reference AA; AC: hazard ratio (HR) 0.99, 95% confidence interval (CI) 0.78, 1.24, p=0.90; CC: HR 0.93, 95% CI 0.73, 1.18, p=0.55); 5 HTTLPR (Reference LL; SL: HR 1.01, 95% CI 0.85, 1.20, p=0.90; SS: HR 1.13, 95% CI 0.91, 1.39, p=0.27); <strong>HTR1A</strong> (Reference CC; CG: HR 1.04, 95% CI 0.86, 1.25, p=0.70; GG: HR 1.01, 95% CI 0.82, 1.24, p=0.93).
+HTR1A	drug	amphetamine	18539407	We also examined the effects of <b>amphetamine</b> (<b>AMPH</b>; 0.3 1.0mg/kg) and the <strong>5 HT1A</strong> agonist 8 OH DPAT (0.3 1.0mg/kg) on delay discounting.
+HTR1A	drug	amphetamine	18516987	These observations suggest that the 5 HT system is a neurochemical basis for the behavioral sensitization, and imply that <strong>5 HT1A</strong> and 5 HT2 receptors may have potential therapeutic values in the remission of <b>methamphetamine</b> abuse or psychosis.
+HTR1A	addiction	sensitization	18516987	These observations suggest that the 5 HT system is a neurochemical basis for the behavioral <b>sensitization</b>, and imply that <strong>5 HT1A</strong> and 5 HT2 receptors may have potential therapeutic values in the remission of methamphetamine abuse or psychosis.
+HTR1A	drug	alcohol	18515460	Substantial evidence suggests that both partial dopamine agents and mixed <strong>5 HT1A</strong>/2A receptor drugs independently show significant efficacy in reducing <b>alcohol</b> use in both animals and humans.
+HTR1A	drug	opioid	18242585	In controls, PVN induced antinociception was reversed by spinal administration of a <strong>5 HT1A</strong> receptor or an alpha2 adrenoceptor antagonist but not by an <b>opioid</b> receptor antagonist.
+HTR1A	drug	opioid	18242585	In arthritic animals, PVN induced antinociception was not reversed by a <strong>5 HT1A</strong> receptor antagonist, while the roles of alpha2 adrenoceptors or <b>opioid</b> receptors could not be assessed due to significant actions of antagonists alone.
+HTR1A	drug	alcohol	17891381	We previously found that the inhibition of median raphe nucleus (MRN) 5 HT transmission by local injections of a <strong>5 HT1A</strong> agonist 8 OH DPAT or corticotrophin releasing factor (CRF) mimic the effect of foot shock stress to reinstate <b>alcohol</b> seeking.
+HTR1A	addiction	relapse	17891381	We previously found that the inhibition of median raphe nucleus (MRN) 5 HT transmission by local injections of a <strong>5 HT1A</strong> agonist 8 OH DPAT or corticotrophin releasing factor (CRF) mimic the effect of foot shock stress to reinstate alcohol <b>seeking</b>.
+HTR1A	drug	nicotine	17689233	Moreover, <strong>5 HT1A</strong> expression has been evaluated 30 days after <b>nicotine</b> withdrawal.
+HTR1A	addiction	withdrawal	17689233	Moreover, <strong>5 HT1A</strong> expression has been evaluated 30 days after nicotine <b>withdrawal</b>.
+HTR1A	drug	psychedelics	17653110	Block of both 5 HT4 and beta1 receptors revealed an inhibitory component of the <b>MDMA</b> action mediated by <strong>5 HT1A</strong> receptor.
+HTR1A	drug	nicotine	17562392	Prenatal <b>nicotine</b> exposure elicited persistent suppression of <strong>5HT1A</strong> receptors and upregulation of 5HT2 receptors, effects that were selective for males and that first emerged in young adulthood.
+HTR1A	drug	nicotine	17562392	Prenatal <b>nicotine</b> exposure elicited persistent suppression of <strong><strong>5HT1A</strong></strong> receptors and upregulation of 5HT2 receptors, effects that were selective for males and that first emerged in young adulthood.
+HTR1A	addiction	addiction	17316955	Serotonin and psychostimulant <b>addiction</b>: focus on <strong>5 HT1A</strong> receptors.
+HTR1A	drug	amphetamine	16863654	Attenuation by the <strong>5 HT1A</strong> receptor agonist osemozotan of the behavioral effects of single and repeated <b>methamphetamine</b> in mice.
+HTR1A	drug	amphetamine	16863654	This study examined the effects of the selective <strong>5 HT1A</strong> receptor agonist osemozotan on repeated <b>methamphetamine</b> (<b>METH</b>) induced behavioral sensitization and single <b>METH</b> induced locomotor stimulant effect in mice, and then the neurochemical mechanisms using in vivo microdialysis.
+HTR1A	addiction	sensitization	16863654	This study examined the effects of the selective <strong>5 HT1A</strong> receptor agonist osemozotan on repeated methamphetamine (METH) induced behavioral <b>sensitization</b> and single METH induced locomotor stimulant effect in mice, and then the neurochemical mechanisms using in vivo microdialysis.
+HTR1A	drug	amphetamine	16863654	These results suggest that prefrontal 5 HT release is involved at least partly in the effects of osemozotan on single and repeated <b>METH</b> induced behavioral effects in mice, and imply that the <strong>5 HT1A</strong> receptors may have a potential therapeutic value in the remission of schizophrenia.
+HTR1A	drug	alcohol	16767411	Reduction in repeated <b>ethanol</b> withdrawal induced anxiety like behavior by site selective injections of <strong>5 HT1A</strong> and 5 HT2C ligands.
+HTR1A	addiction	withdrawal	16767411	Reduction in repeated ethanol <b>withdrawal</b> induced anxiety like behavior by site selective injections of <strong>5 HT1A</strong> and 5 HT2C ligands.
+HTR1A	drug	alcohol	16767411	Anxiety like behavior resulting from repeated withdrawals from chronic <b>ethanol</b> diets is counteracted by systemic administration of a 5 HT2C receptor antagonist or a <strong>5 HT1A</strong> receptor partial agonist.
+HTR1A	drug	alcohol	16767411	These results are consistent with the involvement of 5 HT2C receptors in the amygdala and <strong>5 HT1A</strong> autoreceptors in the dorsal raphe nucleus in repeated <b>ethanol</b> withdrawal induced sensitization of anxiety like behavior.
+HTR1A	addiction	sensitization	16767411	These results are consistent with the involvement of 5 HT2C receptors in the amygdala and <strong>5 HT1A</strong> autoreceptors in the dorsal raphe nucleus in repeated ethanol withdrawal induced <b>sensitization</b> of anxiety like behavior.
+HTR1A	addiction	withdrawal	16767411	These results are consistent with the involvement of 5 HT2C receptors in the amygdala and <strong>5 HT1A</strong> autoreceptors in the dorsal raphe nucleus in repeated ethanol <b>withdrawal</b> induced sensitization of anxiety like behavior.
+HTR1A	drug	benzodiazepine	16620882	10 microM LCM did not bind with high affinity to a plethora of rodent, guinea pig or human receptor sites including: AMPA; Kainate; NMDA (glycine/PCP/MK801); GABA(A) (muscimol/<b>benzodiazepine</b>); GABA(B); adenosine A1,2,3; alpha1, alpha2; beta1, beta2; M1,2,3,4,5; H1,2,3; CB1,2; D1,2,3,4,5; <strong>5HT1A</strong>,1B,2A,2C,3,5A,6,7 and KATP.
+HTR1A	drug	benzodiazepine	16620882	10 microM LCM did not bind with high affinity to a plethora of rodent, guinea pig or human receptor sites including: AMPA; Kainate; NMDA (glycine/PCP/MK801); GABA(A) (muscimol/<b>benzodiazepine</b>); GABA(B); adenosine A1,2,3; alpha1, alpha2; beta1, beta2; M1,2,3,4,5; H1,2,3; CB1,2; D1,2,3,4,5; <strong><strong>5HT1A</strong></strong>,1B,2A,2C,3,5A,6,7 and KATP.
+HTR1A	drug	cannabinoid	16479373	The mu opioid receptor agonist morphine, the anti epileptic gabapentin, the anti depressant duloxetine, the <strong>5HT1A</strong> receptor agonist 8 OH DPAT, the GABA(A) receptor agonist gaboxadol and the mixed <b>cannabinoid</b> receptor agonist WIN55,212 2 were tested after systemic administration in the chronic constriction injury (CCI) model of neuropathic pain.
+HTR1A	drug	opioid	16479373	The mu <b>opioid</b> receptor agonist <b>morphine</b>, the anti epileptic gabapentin, the anti depressant duloxetine, the <strong>5HT1A</strong> receptor agonist 8 OH DPAT, the GABA(A) receptor agonist gaboxadol and the mixed cannabinoid receptor agonist WIN55,212 2 were tested after systemic administration in the chronic constriction injury (CCI) model of neuropathic pain.
+HTR1A	drug	cannabinoid	16479373	The mu opioid receptor agonist morphine, the anti epileptic gabapentin, the anti depressant duloxetine, the <strong><strong>5HT1A</strong></strong> receptor agonist 8 OH DPAT, the GABA(A) receptor agonist gaboxadol and the mixed <b>cannabinoid</b> receptor agonist WIN55,212 2 were tested after systemic administration in the chronic constriction injury (CCI) model of neuropathic pain.
+HTR1A	drug	opioid	16479373	The mu <b>opioid</b> receptor agonist <b>morphine</b>, the anti epileptic gabapentin, the anti depressant duloxetine, the <strong><strong>5HT1A</strong></strong> receptor agonist 8 OH DPAT, the GABA(A) receptor agonist gaboxadol and the mixed cannabinoid receptor agonist WIN55,212 2 were tested after systemic administration in the chronic constriction injury (CCI) model of neuropathic pain.
+HTR1A	drug	cocaine	16216323	In the experiments, autoreceptor preferring low doses of either the <strong>5 HT1A</strong> agonist, 8 OHDPAT (8OH) (0.05 mg/kg) or the D1/D2 agonist apomorphine (APO) (0.05 mg/kg) were administered 20 min prior to <b>cocaine</b> administration and test environment placement (paired treatment).
+HTR1A	drug	alcohol	16212943	These <b>ethanol</b> induced increases of the DA release in the VTA and the NACC were significantly attenuated by intra tegmental infusion of SB 216641 (a 5 HT(1B) receptor antagonist), but not BRL 15572 (a 5 HT(1D/1A) receptor antagonist) or WAY 100635 (a <strong>5 HT1A</strong> receptor antagonist).
+HTR1A	drug	alcohol	16001124	Two benzodiazepines, alprazolam and diazepam, and the <strong>5 HT1A</strong> agonist, buspirone, did not substitute for either training drug nor did <b>ethanol</b> or the NMDA antagonists, PCP and ketamine.
+HTR1A	drug	benzodiazepine	16001124	Two benzodiazepines, <b>alprazolam</b> and <b>diazepam</b>, and the <strong>5 HT1A</strong> agonist, buspirone, did not substitute for either training drug nor did ethanol or the NMDA antagonists, PCP and ketamine.
+HTR1A	drug	psychedelics	16001124	Two benzodiazepines, alprazolam and diazepam, and the <strong>5 HT1A</strong> agonist, buspirone, did not substitute for either training drug nor did ethanol or the NMDA antagonists, PCP and <b>ketamine</b>.
+HTR1A	drug	cocaine	15864074	These results suggest that a <strong>5 HT1A</strong> receptor agonist can increase the reinforcing strength of a low <b>cocaine</b> dose relative to a concurrently available non drug reinforcer.
+HTR1A	addiction	reward	15864074	These results suggest that a <strong>5 HT1A</strong> receptor agonist can increase the <b>reinforcing</b> strength of a low cocaine dose relative to a concurrently available non drug reinforcer.
+HTR1A	drug	alcohol	15817184	Early environmental experience alters baseline and <b>ethanol</b> induced cognitive impulsivity: relationship to forebrain <strong>5 HT1A</strong> receptor binding.
+HTR1A	addiction	reward	15817184	Isolation rearing decreased, and enrichment rearing increased <strong>5 HT1A</strong> binding in the frontal pole of the cortex following experience in the delay to <b>reinforcement</b> task.
+HTR1A	addiction	reward	15817184	Isolation reared rats also showed a significant decrease in <strong>5 HT1A</strong> binding in the dentate gyrus of the ventral hippocampus following experience in the delay to <b>reinforcement</b> relative to the go/no go task.
+HTR1A	drug	alcohol	15789863	The early age of onset of <b>alcohol</b> drinking in the P compared to the NP line is associated with (a) higher densities of serotonin 1A (<strong>5 HT1A</strong>) receptors in cerebral cortical and hippocampal regions; (b) lower densities of dopamine (DA) D2 receptors in the ventral tegmental area (VTA); (c) higher functional activity in several limbic, cortical and hippocampal regions; and (d) sensitivity to the low dose stimulating effect of <b>ethanol</b>.
+HTR1A	drug	alcohol	15726114	Prior multiple <b>ethanol</b> withdrawals enhance stress induced anxiety like behavior: inhibition by CRF1  and benzodiazepine receptor antagonists and a <strong>5 HT1a</strong> receptor agonist.
+HTR1A	drug	benzodiazepine	15726114	Prior multiple ethanol withdrawals enhance stress induced anxiety like behavior: inhibition by CRF1  and <b>benzodiazepine</b> receptor antagonists and a <strong>5 HT1a</strong> receptor agonist.
+HTR1A	drug	benzodiazepine	15726114	Drugs (ie a CRF1 receptor antagonist, a <b>benzodiazepine</b> receptor antagonist, and a <strong>5 HT1A</strong> receptor agonist) previously demonstrated to block the cumulative adaptation, when administered during repeated withdrawals, prevented stress induced anxiety like behavior during abstinence.
+HTR1A	drug	cocaine	15713268	Evidence that the <strong>5 HT1A</strong> autoreceptor is an important pharmacological target for the modulation of <b>cocaine</b> behavioral stimulant effects.
+HTR1A	drug	cocaine	15713268	The psychostimulant effects of <b>cocaine</b> critically depend on the serotonergic (5 HT) system, of which the <strong>5 HT1A</strong> receptor is an essential component.
+HTR1A	drug	cocaine	15713268	We recently showed divergent contributions of various pre  and postsynaptic <strong>5 HT1A</strong> receptor populations to the behavioral effects of <b>cocaine</b>.
+HTR1A	drug	cocaine	15713268	Here, we further investigate the role of <strong>5 HT1A</strong> autoreceptors in the acute and chronic stimulant effects of <b>cocaine</b> using <strong>5 HT1A</strong> receptor ligands in autoreceptor preferring doses.
+HTR1A	drug	cocaine	15713268	In experiment 1, four groups of rats (N = 10) received either saline or the <strong>5 HT1A</strong> agonist, 8 OHDPAT (0.05 mg/kg) 20 min prior to a saline or <b>cocaine</b> (10 mg/kg) injection on 9 consecutive days.
+HTR1A	drug	cocaine	15713268	In experiment 2, six groups (N = 10) were given either saline, the <strong>5 HT1A</strong> antagonist, WAY 100635 (0.05 mg/kg) or 8 OHDPAT (0.05 mg/kg) plus WAY 100635 (0.05 mg/kg) 20 min before a saline or <b>cocaine</b> (10.0 mg/kg) treatment on 9 consecutive days.
+HTR1A	drug	cocaine	15713268	These findings demonstrate that low dose autoreceptor preferring treatments with a <strong>5 HT1A</strong> agonist and antagonist can strongly modify the behavioral stimulant effects of <b>cocaine</b> and suggest that the <strong>5 HT1A</strong> autoreceptor may be an important pharmacological target for the development of treatments for <b>cocaine</b> addiction.
+HTR1A	addiction	addiction	15713268	These findings demonstrate that low dose autoreceptor preferring treatments with a <strong>5 HT1A</strong> agonist and antagonist can strongly modify the behavioral stimulant effects of cocaine and suggest that the <strong>5 HT1A</strong> autoreceptor may be an important pharmacological target for the development of treatments for cocaine <b>addiction</b>.
+HTR1A	drug	benzodiazepine	15669223	Recently it has been suggested that the combination of SSRI and <b>benzodiazepine</b> is rational, because each drug has a different mechanism of action, the <b>benzodiazepine</b> enhancing GABAergic transmission, the SSRIs stimulating the <strong>5 HT1A</strong> receptor that may inhibit the postsynaptic neuronal excitability in the amygdala and the prefrontal cortex that comprise the brain circuit of fear and anxiety.
+HTR1A	addiction	withdrawal	15589524	The novel analgesic and high efficacy <strong>5 HT1A</strong> receptor agonist F 13640 inhibits nociceptive responses, wind up, and after discharges in spinal neurons and <b>withdrawal</b> reflexes.
+HTR1A	drug	opioid	15589524	Using a new electrophysiological method of simultaneous recordings in rats we examined the actions of the novel analgesic and high efficacy <strong>5 HT1A</strong> receptor agonist F 13640 as well as those of the <b>opioid</b> receptor agonist <b>fentanyl</b> on simultaneously evoked responses of spinal dorsal horn (DH) wide dynamic range (WDR) neurons and spinal withdrawal reflexes.
+HTR1A	addiction	withdrawal	15589524	Using a new electrophysiological method of simultaneous recordings in rats we examined the actions of the novel analgesic and high efficacy <strong>5 HT1A</strong> receptor agonist F 13640 as well as those of the opioid receptor agonist fentanyl on simultaneously evoked responses of spinal dorsal horn (DH) wide dynamic range (WDR) neurons and spinal <b>withdrawal</b> reflexes.
+HTR1A	drug	opioid	15589524	The inhibitory effects of F 13640 and <b>fentanyl</b> on responses of DH WDR neurons and SMUs were reversed by the specific antagonists WAY 100635 and <b>naloxone</b>, respectively, further indicating that this <strong>5 HT1A</strong> receptor modulated anti nociception is mu <b>opioid</b> receptor independent.
+HTR1A	drug	alcohol	15581381	Buspirone, a serotonin <strong>5 HT1A</strong> partial agonist, does not appear to be an effective treatment for <b>alcoholics</b> without comorbid disease.
+HTR1A	drug	nicotine	15565434	After characterizing a dose response curve for <b>nicotine</b>, we tested the ability of the 5HT(2A/2C) agonists (+/ ) 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane HCL (DOI; 0.18 1.0 mg/kg) and 1 (4 bromo 2, 5 dimethoxyphenyl) 2 aminopropane (DOB; 0.1 1.0 mg/kg), the 5HT2C agonist 6 chloro 2 (1 piperazinyl)pyrazine hydrochloride (MK 212; 0.1 mg/kg 1.0 mg/kg), and the <strong>5HT1A</strong> agonist (+/ ) 8 hydroxy 2 (di n propylamino)tetralin hydrobromide (8 OH DPAT; 0.01 mg/kg 1.0 mg/kg) to modulate <b>nicotine</b>'s discriminative stimulus effects.
+HTR1A	drug	nicotine	15565434	After characterizing a dose response curve for <b>nicotine</b>, we tested the ability of the 5HT(2A/2C) agonists (+/ ) 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane HCL (DOI; 0.18 1.0 mg/kg) and 1 (4 bromo 2, 5 dimethoxyphenyl) 2 aminopropane (DOB; 0.1 1.0 mg/kg), the 5HT2C agonist 6 chloro 2 (1 piperazinyl)pyrazine hydrochloride (MK 212; 0.1 mg/kg 1.0 mg/kg), and the <strong><strong>5HT1A</strong></strong> agonist (+/ ) 8 hydroxy 2 (di n propylamino)tetralin hydrobromide (8 OH DPAT; 0.01 mg/kg 1.0 mg/kg) to modulate <b>nicotine</b>'s discriminative stimulus effects.
+HTR1A	drug	benzodiazepine	15291242	Recently it has been suggested that the combination of SSRI and <b>benzodiazepine</b> is rational, because each drug has a different mechanism of action, the benzodiazepines enhancing GABAergic transmission, and the SSRIs stimulating the <strong>5 HT1A</strong> receptor that may inhibit the postsynaptic neuronal excitability in the amygdala and the prefrontal cortex that comprise the brain circuit of fear and anxiety.
+HTR1A	drug	opioid	15183519	IS potentiation of <b>morphine</b> induced DA efflux in the NAc was also dependent upon activation of 5 HT neurons in the DRN because it was blocked by intra DRN microinjection of the <strong>5 HT1A</strong> autoreceptor agonist 8 hydroxy 2 di n (propylamino) tetralin (1 microg).
+HTR1A	drug	cocaine	15127081	Dissociable roles for the dorsal and median raphé in the facilitatory effect of <strong>5 HT1A</strong> receptor stimulation upon <b>cocaine</b> induced locomotion and sensitization.
+HTR1A	addiction	sensitization	15127081	Dissociable roles for the dorsal and median raphé in the facilitatory effect of <strong>5 HT1A</strong> receptor stimulation upon cocaine induced locomotion and <b>sensitization</b>.
+HTR1A	drug	cocaine	15127081	These data show a differential role for <strong>5 HT1A</strong> receptors in the DRN and MRN in the acute and sensitized effects of <b>cocaine</b>.
+HTR1A	drug	alcohol	12955093	Stress sensitization of <b>ethanol</b> withdrawal induced reduction in social interaction: inhibition by CRF 1 and benzodiazepine receptor antagonists and a <strong>5 HT1A</strong> receptor agonist.
+HTR1A	drug	benzodiazepine	12955093	Stress sensitization of ethanol withdrawal induced reduction in social interaction: inhibition by CRF 1 and <b>benzodiazepine</b> receptor antagonists and a <strong>5 HT1A</strong> receptor agonist.
+HTR1A	addiction	sensitization	12955093	Stress <b>sensitization</b> of ethanol withdrawal induced reduction in social interaction: inhibition by CRF 1 and benzodiazepine receptor antagonists and a <strong>5 HT1A</strong> receptor agonist.
+HTR1A	addiction	withdrawal	12955093	Stress sensitization of ethanol <b>withdrawal</b> induced reduction in social interaction: inhibition by CRF 1 and benzodiazepine receptor antagonists and a <strong>5 HT1A</strong> receptor agonist.
+HTR1A	drug	alcohol	12899673	Chronic <b>ethanol</b> administration and withdrawal decreases <strong>5 HT1A</strong> mRNA, but not 5 HT4 expression in the rat hippocampus.
+HTR1A	addiction	withdrawal	12899673	Chronic ethanol administration and <b>withdrawal</b> decreases <strong>5 HT1A</strong> mRNA, but not 5 HT4 expression in the rat hippocampus.
+HTR1A	drug	opioid	12764106	In seeking ways to improve respiration after SCI, we tested drugs that stimulate serotonin 1A (<strong>5 HT1A</strong>) receptors, based on our previous findings that these agents can counteract respiratory depression produced by <b>morphine</b> overdose.
+HTR1A	addiction	relapse	12764106	In <b>seeking</b> ways to improve respiration after SCI, we tested drugs that stimulate serotonin 1A (<strong>5 HT1A</strong>) receptors, based on our previous findings that these agents can counteract respiratory depression produced by morphine overdose.
+HTR1A	drug	alcohol	12677355	A <strong>5 HT1A</strong> agonist and a 5 HT2c antagonist reduce social interaction deficit induced by multiple <b>ethanol</b> withdrawals in rats.
+HTR1A	addiction	withdrawal	12667911	Modifications in feeding to DR infusions of the <strong>5 HT 1A</strong> receptor agonist, 8 hydroxy 2 (di n propylamino) tetralin (8 OH DPAT), were used to characterize these potential relationships in the DR 5 HT system during NIC administration vs. <b>withdrawal</b>.
+HTR1A	drug	benzodiazepine	12655311	Modulation of passive avoidance in mice by the <strong>5 HT1A</strong> receptor agonist flesinoxan: comparison with the <b>benzodiazepine</b> receptor agonist <b>diazepam</b>.
+HTR1A	drug	opioid	12589380	an acute serotonin (5 HT) inhibition induced by the specific stimulation of <strong>5 HT1A</strong> autoreceptors (8 OHDPAT 5 100 microg/kg), on <b>naloxone</b> induced conditioned place aversion in <b>morphine</b> dependent rats.
+HTR1A	addiction	aversion	12589380	an acute serotonin (5 HT) inhibition induced by the specific stimulation of <strong>5 HT1A</strong> autoreceptors (8 OHDPAT 5 100 microg/kg), on naloxone induced conditioned place <b>aversion</b> in morphine dependent rats.
+HTR1A	drug	alcohol	12223536	Intra MRN infusions of 8 OH DPAT [8 hydroxy 2 (di n propylamino)tetralin] (a <strong>5 HT1A</strong> agonist that decreases 5 HT cell firing and release) reinstated <b>alcohol</b> seeking.
+HTR1A	addiction	relapse	12223536	Intra MRN infusions of 8 OH DPAT [8 hydroxy 2 (di n propylamino)tetralin] (a <strong>5 HT1A</strong> agonist that decreases 5 HT cell firing and release) reinstated alcohol <b>seeking</b>.
+HTR1A	drug	alcohol	12183221	Neuroendocrine evaluation of <strong>5 HT1A</strong> function in male <b>alcoholic</b> patients.
+HTR1A	drug	alcohol	12183221	We assessed the hormonal (prolactin and cortisol) responses to flesinoxan (a highly potent and selective <strong>5 HT1A</strong> agonist) in 12 male inpatients meeting DSM IV criteria for <b>alcohol</b> dependence, 3 weeks after the last reported use of <b>alcohol</b> and antidepressants.
+HTR1A	addiction	dependence	12183221	We assessed the hormonal (prolactin and cortisol) responses to flesinoxan (a highly potent and selective <strong>5 HT1A</strong> agonist) in 12 male inpatients meeting DSM IV criteria for alcohol <b>dependence</b>, 3 weeks after the last reported use of alcohol and antidepressants.
+HTR1A	drug	alcohol	12183221	These results support the implication of the serotonergic system, and particularly a decreased sensitivity of post synaptic <strong>5 HT1A</strong> receptors, in <b>alcoholism</b>.
+HTR1A	drug	cocaine	12112399	<b>Cocaine</b> increases serotonergic activity in the hippocampus and nucleus accumbens in vivo: <strong>5 HT1a</strong> receptor antagonism blocks behavioral but potentiates serotonergic activation.
+HTR1A	drug	alcohol	12072158	<strong>5 HT1A</strong> receptor blockade and the motivational profile of <b>ethanol</b>.
+HTR1A	drug	alcohol	12072158	The present experiments characterized the rewarding, aversive and stimulant effects of <b>ethanol</b> in combination with a specific <strong>5 HT1A</strong> receptor antagonist (pindobind 5HT1A).
+HTR1A	addiction	aversion	12072158	The present experiments characterized the rewarding, <b>aversive</b> and stimulant effects of ethanol in combination with a specific <strong>5 HT1A</strong> receptor antagonist (pindobind 5HT1A).
+HTR1A	drug	alcohol	12072158	The present experiments characterized the rewarding, aversive and stimulant effects of <b>ethanol</b> in combination with a specific <strong>5 HT1A</strong> receptor antagonist (pindobind <strong>5HT1A</strong>).
+HTR1A	addiction	aversion	12072158	The present experiments characterized the rewarding, <b>aversive</b> and stimulant effects of ethanol in combination with a specific <strong>5 HT1A</strong> receptor antagonist (pindobind <strong>5HT1A</strong>).
+HTR1A	drug	alcohol	12072158	The present experiments characterized the rewarding, aversive and stimulant effects of <b>ethanol</b> in combination with a specific <strong>5 HT1A</strong> receptor antagonist (pindobind <strong><strong>5HT1A</strong></strong>).
+HTR1A	addiction	aversion	12072158	The present experiments characterized the rewarding, <b>aversive</b> and stimulant effects of ethanol in combination with a specific <strong>5 HT1A</strong> receptor antagonist (pindobind <strong><strong>5HT1A</strong></strong>).
+HTR1A	drug	alcohol	12072158	In a place conditioning study, adult male Swiss Webster mice received 6 parings of a distinctive tactile stimulus with either 2 g/kg <b>ethanol</b>, 2.5 mg/kg pindobind <strong>5HT1A</strong>, or both drugs in combination.
+HTR1A	drug	alcohol	12072158	In a place conditioning study, adult male Swiss Webster mice received 6 parings of a distinctive tactile stimulus with either 2 g/kg <b>ethanol</b>, 2.5 mg/kg pindobind <strong><strong>5HT1A</strong></strong>, or both drugs in combination.
+HTR1A	drug	alcohol	12072158	<b>Ethanol</b> conditioned preference for the tactile cue was enhanced in mice also receiving pindobind <strong>5HT1A</strong>, which did not produce cue preference in the absence of <b>ethanol</b>.
+HTR1A	drug	alcohol	12072158	<b>Ethanol</b> conditioned preference for the tactile cue was enhanced in mice also receiving pindobind <strong><strong>5HT1A</strong></strong>, which did not produce cue preference in the absence of <b>ethanol</b>.
+HTR1A	drug	alcohol	12072158	In a taste conditioning study, Swiss Webster mice received 4 trials consisting of access to a distinctive NaCl flavor followed by either 4 g/kg <b>ethanol</b>, 2.5 mg/kg pindobind <strong>5HT1A</strong>, or both drugs.
+HTR1A	drug	alcohol	12072158	In a taste conditioning study, Swiss Webster mice received 4 trials consisting of access to a distinctive NaCl flavor followed by either 4 g/kg <b>ethanol</b>, 2.5 mg/kg pindobind <strong><strong>5HT1A</strong></strong>, or both drugs.
+HTR1A	drug	alcohol	12072158	Pindobind <strong>5HT1A</strong> did not reduce or enhance <b>ethanol</b> conditioned flavor aversion.
+HTR1A	addiction	aversion	12072158	Pindobind <strong>5HT1A</strong> did not reduce or enhance ethanol conditioned flavor <b>aversion</b>.
+HTR1A	drug	alcohol	12072158	Pindobind <strong><strong>5HT1A</strong></strong> did not reduce or enhance <b>ethanol</b> conditioned flavor aversion.
+HTR1A	addiction	aversion	12072158	Pindobind <strong><strong>5HT1A</strong></strong> did not reduce or enhance ethanol conditioned flavor <b>aversion</b>.
+HTR1A	addiction	sensitization	12072158	Locomotor <b>sensitization</b> was not altered by co treatment with pindobind <strong>5HT1A</strong>.
+HTR1A	addiction	sensitization	12072158	Locomotor <b>sensitization</b> was not altered by co treatment with pindobind <strong><strong>5HT1A</strong></strong>.
+HTR1A	drug	alcohol	12072158	Overall, the present results show specific effects of <strong>5 HT1A</strong> blockade on <b>ethanol</b> reward.
+HTR1A	addiction	reward	12072158	Overall, the present results show specific effects of <strong>5 HT1A</strong> blockade on ethanol <b>reward</b>.
+HTR1A	drug	opioid	11882917	Supersensitivity of <strong>5 HT1A</strong> autoreceptors and alpha2 adrenoceptors regulating monoamine synthesis in the brain of <b>morphine</b> dependent rats.
+HTR1A	drug	opioid	11882917	The sensitivity of <strong>5 HT1A</strong> serotonin receptors and alpha2 adrenoceptors (autoreceptors and heteroreceptors) modulating brain monoamine synthesis was investigated in rats during <b>morphine</b> treatment and after <b>naloxone</b> precipitated withdrawal.
+HTR1A	addiction	withdrawal	11882917	The sensitivity of <strong>5 HT1A</strong> serotonin receptors and alpha2 adrenoceptors (autoreceptors and heteroreceptors) modulating brain monoamine synthesis was investigated in rats during morphine treatment and after naloxone precipitated <b>withdrawal</b>.
+HTR1A	drug	opioid	11882917	In <b>morphine</b> dependent rats (tolerant and withdrawn states) the inhibitory effects of the <strong>5 HT1A</strong> agonists 8 OH DPAT and buspirone (0.1 mg/kg, 1 h), and that of the alpha2 adrenoceptor agonist clonidine (0.1 mg/kg, 1 h), on the synthesis of 5 HTP/5 HT were potentiated (25% 50%).
+HTR1A	drug	opioid	11882917	In summary, we conclude that <b>morphine</b> addiction is associated with supersensitivity of <strong>5 HT1A</strong> serotonin receptors and alpha2 adrenoceptors (autoreceptors and heteroreceptors) that modulate the synthesis of monoamines in brain.
+HTR1A	addiction	addiction	11882917	In summary, we conclude that morphine <b>addiction</b> is associated with supersensitivity of <strong>5 HT1A</strong> serotonin receptors and alpha2 adrenoceptors (autoreceptors and heteroreceptors) that modulate the synthesis of monoamines in brain.
+HTR1A	drug	benzodiazepine	11862346	The effects of the GABA(A) <b>benzodiazepine</b> receptor agonist <b>chlordiazepoxide</b> (CDP), the <strong>5 HT1A</strong> receptor agonist flesinoxan and the specific 5 HT reuptake inhibitor fluvoxamine on light enhanced startle were studied.
+HTR1A	drug	nicotine	11812255	Over the last decade it has been suggested that <strong>5 HT1A</strong> receptor antagonists may have therapeutic utility in such diseases as depression, anxiety, drug and <b>nicotine</b> withdrawal as well as schizophrenia.
+HTR1A	addiction	withdrawal	11812255	Over the last decade it has been suggested that <strong>5 HT1A</strong> receptor antagonists may have therapeutic utility in such diseases as depression, anxiety, drug and nicotine <b>withdrawal</b> as well as schizophrenia.
+HTR1A	drug	nicotine	11412838	Effects of <strong>5 HT1A</strong> and 5 HT2 receptor agonists on the behavioral and neurochemical consequences of repeated <b>nicotine</b> treatment.
+HTR1A	drug	nicotine	11412838	This study investigated the effects of repeated daily (15 days) treatment with <b>nicotine</b>, alone or in combination with the <strong>5 HT1A</strong>/7 receptor agonist (+/ ) 8 hydroxy 2 (di n propylamino)tetralin (8 OH DPAT) or the 5 HT2 receptor agonist (+/ ) 2,5 dimethoxy 4 iodoamphetamine (DOI) on locomotor sensitization, mesolimbic dopamine neurochemistry and on behavioral inhibition in the rat.
+HTR1A	addiction	sensitization	11412838	This study investigated the effects of repeated daily (15 days) treatment with nicotine, alone or in combination with the <strong>5 HT1A</strong>/7 receptor agonist (+/ ) 8 hydroxy 2 (di n propylamino)tetralin (8 OH DPAT) or the 5 HT2 receptor agonist (+/ ) 2,5 dimethoxy 4 iodoamphetamine (DOI) on locomotor <b>sensitization</b>, mesolimbic dopamine neurochemistry and on behavioral inhibition in the rat.
+HTR1A	drug	nicotine	11412838	Taken together, these findings suggest that the <strong>5 HT1A</strong> and the 5 HT2 receptor subtypes are differentially involved in the effects of repeated <b>nicotine</b> on locomotor sensitization, behavioral inhibition and mesolimbic dopamine neurochemistry.
+HTR1A	addiction	sensitization	11412838	Taken together, these findings suggest that the <strong>5 HT1A</strong> and the 5 HT2 receptor subtypes are differentially involved in the effects of repeated nicotine on locomotor <b>sensitization</b>, behavioral inhibition and mesolimbic dopamine neurochemistry.
+HTR1A	drug	nicotine	11374339	The social interaction test of anxiety was used to investigate the effects of a range of doses of ( ) <b>nicotine</b> (2.5 4000 ng) following DRN infusion, and whether co administration of the specific <strong>5 HT1A</strong> receptor antagonist WAY 100635 could antagonise the anxiolytic action of <b>nicotine</b>.
+HTR1A	drug	nicotine	11374339	The present findings therefore suggest that the DRN plays an important role in mediating the acute effects of <b>nicotine</b> on anxiety, as measured in the social interaction test, and that the anxiolytic effect is mediated by activation of somatodendritic <strong>5 HT1A</strong> autoreceptors.
+HTR1A	drug	alcohol	11198050	Results showed that the 5 HT releaser d fenfluramine, the selective serotonin reuptake inhibitor fluoxetine, the <strong>5 HT1A</strong> receptor agonist 8 hydroxy 2[di n propylamino]tetralin, the partial <strong>5 HT1A</strong> receptor agonist buspirone, and the 5 HT1B/5 HT2C receptor agonist 1 (3 trifluoromethylphenyl)piperazine, but not the 5 HT2A/5 HT2C receptor agonist 1 (2,5 dimethoxy 4 iodophenylaminopropane) 2, selectively reduced responding on a lever leading to presentation of an <b>ethanol</b> paired conditioned stimulus.
+HTR1A	drug	alcohol	11198050	Results are consistent with involvement of the dopaminergic and 5 HT systems, in particular activation of <strong>5 HT1A</strong> and 5 HT1B receptor subtypes, in mediation of the conditioned or secondary reinforcing properties of <b>ethanol</b>.
+HTR1A	addiction	reward	11198050	Results are consistent with involvement of the dopaminergic and 5 HT systems, in particular activation of <strong>5 HT1A</strong> and 5 HT1B receptor subtypes, in mediation of the conditioned or secondary <b>reinforcing</b> properties of ethanol.
+HTR1A	drug	psychedelics	11022403	(+/ )Pindolol attenuated the suppressant effect of the 5 HT autoreceptor agonist lysergic acid diethylamide (<b>LSD</b>) on the firing activity of 5 HT neurons, suggesting that (+/ )pindolol antagonized somatodendritic <strong>5 HT1A</strong> autoreceptors in the dorsal raphe nucleus.
+HTR1A	drug	psychedelics	11022403	However, following a 2 day washout period, the suppressant effect of <b>LSD</b> was still attenuated, indicating rather a desensitization of <strong>5 HT1A</strong> autoreceptors had occurred.
+HTR1A	addiction	relapse	11022403	Although pindolol is capable of antagonizing the <strong>5 HT1A</strong> autoreceptor upon the initiation of a 5 HT reuptake blocker treatment, it also induces a desensitization of this <strong>5 HT1A</strong> autoreceptor, which could explain why patients do not <b>relapse</b> upon its discontinuation when they continue taking a 5 HT reuptake blocker.
+HTR1A	drug	nicotine	10935531	), indicating a possible involvement of somato dendritic <strong>5 HT1A</strong> receptors in the effect of <b>nicotine</b>.
+HTR1A	drug	alcohol	10924015	By means of in vitro quantitative autoradiography, we used [3H]citalopram, [3H]8 OH DPAT, and [3H]GR65630 to label 5 HTT, <strong>5 HT1A</strong> receptors, and 5 HT3 receptors in the brain of <b>alcohol</b> naïve FH rats, Wistar Kyoto (WKY) rats, and FH rats given free access to 5% <b>ethanol</b> and/or after 24 to 48 hr withdrawal.
+HTR1A	addiction	withdrawal	10924015	By means of in vitro quantitative autoradiography, we used [3H]citalopram, [3H]8 OH DPAT, and [3H]GR65630 to label 5 HTT, <strong>5 HT1A</strong> receptors, and 5 HT3 receptors in the brain of alcohol naïve FH rats, Wistar Kyoto (WKY) rats, and FH rats given free access to 5% ethanol and/or after 24 to 48 hr <b>withdrawal</b>.
+HTR1A	drug	alcohol	10924015	In <b>alcohol</b> naïve rats, FH rats displayed significantly higher (p < 0.05) densities of [3H]citalopram binding in the nucleus accumbens (+30%), lateral septum (+37%), ventral pallidum (+21%), and ventral tegmental area (+24%), as well as an increased binding of [3H]8 OH DPAT to <strong>5 HT1A</strong> receptors in the frontal and parietal cortex (+33%), occipital and temporal cortex (+25%), and hippocampal CA3 region (+31%), compared with WKY rats, whereas both strains exhibited comparable [3H]GR65630 binding to 5 HT3 receptors.
+HTR1A	drug	alcohol	10924015	The elevated 5 HT transporters and <strong>5 HT1A</strong> receptors in the mesocorticolimbic areas in FH rats may reflect a potential innate altered transmission at serotonergic synapses, which possibly may affect the high intake of <b>alcohol</b> in FH rats.
+HTR1A	drug	alcohol	10924015	The region specific alterations of <strong>5 HT1A</strong> receptors in FH rat brain after <b>ethanol</b> challenges suggest that <strong>5 HT1A</strong> receptors are sensitive to <b>ethanol</b> challenges, whereas 5 HTT are apparently insensitive.
+HTR1A	drug	amphetamine	10780831	The suppressant actions of RU 24969 on <b>amphetamine</b> self administration and CR responding involve stimulation of 5 HT1B receptors, since they were reversed by the 5 HT1B/1D antagonist GR 127935 (3 mg/kg), but not by the <strong>5 HT1A</strong> antagonist WAY 100635 (1 mg/kg).
+HTR1A	drug	amphetamine	10724448	8 Hydroxy 2 (di n propylamino)tetralin (8 OH DPAT), a <strong>5 HT1A</strong> agonist, dose dependently reduced the expression of <b>AMPH</b> (2.5 mg/kg) induced sensitization.
+HTR1A	addiction	sensitization	10724448	8 Hydroxy 2 (di n propylamino)tetralin (8 OH DPAT), a <strong>5 HT1A</strong> agonist, dose dependently reduced the expression of AMPH (2.5 mg/kg) induced <b>sensitization</b>.
+HTR1A	drug	amphetamine	10724448	These results indicate that <strong>5 HT1A</strong> receptors are not involved in <b>AMPH</b> induced sensitization per se, whereas their pharmacological activation leads to the inhibition of both the development and the expression of <b>AMPH</b> induced sensitization.
+HTR1A	addiction	sensitization	10724448	These results indicate that <strong>5 HT1A</strong> receptors are not involved in AMPH induced <b>sensitization</b> per se, whereas their pharmacological activation leads to the inhibition of both the development and the expression of AMPH induced <b>sensitization</b>.
+HTR1A	drug	alcohol	10647095	Effects of the <strong>5 HT1A</strong> receptor agonist ipsapirone on operant self administration of <b>ethanol</b> in the rat.
+HTR1A	addiction	reward	10647095	Effects of the <strong>5 HT1A</strong> receptor agonist ipsapirone on <b>operant</b> self administration of ethanol in the rat.
+HTR1A	drug	alcohol	10627067	Tiospirone (TSP) is a 5 HT2 receptor antagonist with affinity for D2, <strong>5 HT1a</strong>, and 5 HT7, and sigma receptors, which can decrease consumption of <b>ethanol</b> while increasing food intake.
+HTR1A	addiction	aversion	10475723	The <strong>5 HT1A</strong> receptor agonist flesinoxan increases <b>aversion</b> in a model of panic like anxiety in rats.
+HTR1A	addiction	aversion	10475723	Data suggest that selective activation of <strong>5 HT1A</strong> receptors (pre  and/or post synaptic in brain and/or periphery) following systemic administration of <strong>5 HT1A</strong> receptor full agonists exacerbates <b>aversion</b> in animals or patients with panic anxiety; activation of these receptor subtypes may probably mediate the panicogenic action reported under certain circumstances with non selective 5 HT mimetics.
+HTR1A	drug	alcohol	10371401	Buspirone, a <strong>5 HT1A</strong> agonist, has been shown to decrease the intake of <b>ethanol</b> when given as a single dose to rats with a psychological dependence induced according to our rat model of <b>alcoholism</b>.
+HTR1A	addiction	dependence	10371401	Buspirone, a <strong>5 HT1A</strong> agonist, has been shown to decrease the intake of ethanol when given as a single dose to rats with a psychological <b>dependence</b> induced according to our rat model of alcoholism.
+HTR1A	drug	alcohol	10348615	Systemic administration of agents that (1) increase synaptic levels of serotonin (5 HT) or dopamine (DA); (2) activate <strong>5 HT1A</strong>, 5 HT2, D2, D3, or GABA(A) receptors; or (3) block opioid and 5 HT3 receptors decrease <b>ethanol</b> intake in most animal models.
+HTR1A	drug	opioid	10348615	Systemic administration of agents that (1) increase synaptic levels of serotonin (5 HT) or dopamine (DA); (2) activate <strong>5 HT1A</strong>, 5 HT2, D2, D3, or GABA(A) receptors; or (3) block <b>opioid</b> and 5 HT3 receptors decrease ethanol intake in most animal models.
+HTR1A	drug	psychedelics	10065919	The effects of these drugs were compared to the effects of the non specific serotonergic agonist, lysergic acid diethylamide (<b>LSD</b>); the phenothiazine, chlorpromazine; the atypical antidepressant, trazodone; and the non selective <strong>5 HT1A</strong> antagonists, propranolol and alprenolol.
+HTR1A	drug	alcohol	10064377	Pharmacological and clinical studies have shown that the 5 HT transporter (5 HTT) and the <strong>5 HT1A</strong> receptor appear to be candidate loci for the aetiology of <b>alcohol</b> dependence.
+HTR1A	addiction	dependence	10064377	Pharmacological and clinical studies have shown that the 5 HT transporter (5 HTT) and the <strong>5 HT1A</strong> receptor appear to be candidate loci for the aetiology of alcohol <b>dependence</b>.
+HTR1A	drug	alcohol	10064377	We have analysed the presence of different 5 HTT and <strong>5 HT1A</strong> variants in 104 <b>alcohol</b> dependent patients and 38 controls for a possible association with <b>alcohol</b> dependence.
+HTR1A	addiction	dependence	10064377	We have analysed the presence of different 5 HTT and <strong>5 HT1A</strong> variants in 104 alcohol dependent patients and 38 controls for a possible association with alcohol <b>dependence</b>.
+HTR1A	addiction	reward	10027505	RU 24969, a <strong>5 HT1A</strong>/1B agonist, elevates brain stimulation <b>reward</b> thresholds: an effect reversed by GR 127935, a 5 HT1B/1D antagonist.
+HTR1A	drug	benzodiazepine	9884116	The anxiolytic agents <b>diazepam</b> (<b>benzodiazepine</b>), buspirone and ipsapirone (<strong>5 HT1A</strong> agonists) as well as ritanserin (5 HT2 antagonist) selectively impaired inhibitory avoidance while leaving one way escape unchanged.
+HTR1A	addiction	withdrawal	9884117	Tolerance to acute anxiolysis but no <b>withdrawal</b> anxiogenesis in mice treated chronically with <strong>5 HT1A</strong> receptor antagonist, WAY 100635.
+HTR1A	drug	benzodiazepine	9884117	As tolerance and dependence liability are among the major clinical disadvantages of <b>benzodiazepine</b> therapy, the present study examined the effects of acute drug challenge on the plus maze profiles of mice following daily treatment for 20 days with saline, <b>chlordiazepoxide</b> (CDP; 10.0 mg/kg) or the selective <strong>5 HT1A</strong> receptor antagonist, WAY 100635 (0.1 1.0 mg/kg).
+HTR1A	addiction	dependence	9884117	As tolerance and <b>dependence</b> liability are among the major clinical disadvantages of benzodiazepine therapy, the present study examined the effects of acute drug challenge on the plus maze profiles of mice following daily treatment for 20 days with saline, chlordiazepoxide (CDP; 10.0 mg/kg) or the selective <strong>5 HT1A</strong> receptor antagonist, WAY 100635 (0.1 1.0 mg/kg).
+HTR1A	drug	cocaine	9787882	These data indicate that withdrawal from chronic <b>cocaine</b> renders specific subpopulations of postsynaptic <strong>5 HT1A</strong> receptors subsensitive and 5 HT2A/2C receptors supersensitive.
+HTR1A	addiction	withdrawal	9787882	These data indicate that <b>withdrawal</b> from chronic cocaine renders specific subpopulations of postsynaptic <strong>5 HT1A</strong> receptors subsensitive and 5 HT2A/2C receptors supersensitive.
+HTR1A	drug	cocaine	9787882	No evidence for <b>cocaine</b> induced changes in <strong>5 HT1A</strong> autoreceptor responsiveness was found.
+HTR1A	drug	alcohol	9744857	These results demonstrate that, under the present experimental conditions, activation of central <strong>5 HT1A</strong>, 5 HT1B, and 5 HT2 receptors reduced <b>ethanol</b> intake and reinforced behaviour in an operant paradigm.
+HTR1A	addiction	reward	9744857	These results demonstrate that, under the present experimental conditions, activation of central <strong>5 HT1A</strong>, 5 HT1B, and 5 HT2 receptors reduced ethanol intake and reinforced behaviour in an <b>operant</b> paradigm.
+HTR1A	drug	cocaine	9723786	Downregulation of <strong>5 HT1A</strong> receptors in rat hypothalamus and dentate gyrus after "binge" pattern <b>cocaine</b> administration.
+HTR1A	addiction	intoxication	9723786	Downregulation of <strong>5 HT1A</strong> receptors in rat hypothalamus and dentate gyrus after "<b>binge</b>" pattern cocaine administration.
+HTR1A	drug	cocaine	9723786	The effect of chronic <b>cocaine</b> exposure on the central serotonergic system in the rat was investigated using a selective <strong>5 HT1A</strong> receptor agonist, [3H]8 hydroxy 2 (di N propylamino) tetralin (8 OH DPAT), and a 5 HT2A receptor antagonist, [3H]ketanserin, as tritiated ligands in a quantitative autoradiography study.
+HTR1A	drug	cocaine	9723786	Our data show that the <strong>5 HT1A</strong> component of the serotonergic system is altered following chronic "binge" pattern <b>cocaine</b> administration in an animal model and may be related to changes in the HPA axis and behavior.
+HTR1A	addiction	intoxication	9723786	Our data show that the <strong>5 HT1A</strong> component of the serotonergic system is altered following chronic "<b>binge</b>" pattern cocaine administration in an animal model and may be related to changes in the HPA axis and behavior.
+HTR1A	drug	amphetamine	9694929	A dose response determination for the tricyclic antidepressants, imipramine and desipramine, the selective serotonin (5 hydroxytryptamine; 5 HT) reuptake inhibitor, fluoxetine, the 5 HT2 receptor antagonist, ketanserin, the <strong>5 HT1A</strong> receptor agonist, (+/ )8 hydroxy di propylamino tetralin (8 OH DPAT) and the dopamine releasing compound, <b>amphetamine</b>, were assessed in both rat stocks.
+HTR1A	drug	alcohol	9694030	<b>Ethanol</b> consumption was significantly and selectively reduced by the 5 hydroxytryptamine 1A (<strong>5 HT1A</strong>) full agonist 8 OH DPAT (0.3 1.0 mg/kg) and the 5 HT3 antagonist granisetron (0.1 1.0 mg/kg).
+HTR1A	drug	alcohol	9694030	These studies thus confirm the potential for decreasing <b>ethanol</b> consumption and <b>ethanol</b> preference of <strong>5 HT1A</strong> agonists and 5 HT3 antagonists, but failed to find any selective effects for agents acting at 5 HT1B or 5 HT2 receptors.
+HTR1A	drug	alcohol	9631953	Both <strong>5 HT1A</strong> and 5 HT2A receptors have been implicated in modulating <b>ethanol</b> self administration.
+HTR1A	drug	alcohol	9631953	A novel serotonergic compound, FG 5974, with combined <strong>5 HT1A</strong> agonist/5 HT2A antagonist activities, has shown effects in decreasing <b>ethanol</b> consumption in two bottle choice paradigms.
+HTR1A	drug	alcohol	9631953	In the present study, the effect of this compound on operant responding for <b>ethanol</b> (as well as water and a saccharin solution) was compared to compounds possessing the separate neuropharmacological effects of this drug (the <strong>5 HT1A</strong> agonist, 8 OH DPAT, and the 5 HT2A antagonist, amperozide).
+HTR1A	addiction	reward	9631953	In the present study, the effect of this compound on <b>operant</b> responding for ethanol (as well as water and a saccharin solution) was compared to compounds possessing the separate neuropharmacological effects of this drug (the <strong>5 HT1A</strong> agonist, 8 OH DPAT, and the 5 HT2A antagonist, amperozide).
+HTR1A	drug	alcohol	9631953	These results suggest that combined <strong>5HT1A</strong> agonist/5 HT2A antagonist activity provides a more selective effect on <b>ethanol</b> reinforcement than either neuropharmacological action alone.
+HTR1A	addiction	reward	9631953	These results suggest that combined <strong>5HT1A</strong> agonist/5 HT2A antagonist activity provides a more selective effect on ethanol <b>reinforcement</b> than either neuropharmacological action alone.
+HTR1A	drug	alcohol	9631953	These results suggest that combined <strong><strong>5HT1A</strong></strong> agonist/5 HT2A antagonist activity provides a more selective effect on <b>ethanol</b> reinforcement than either neuropharmacological action alone.
+HTR1A	addiction	reward	9631953	These results suggest that combined <strong><strong>5HT1A</strong></strong> agonist/5 HT2A antagonist activity provides a more selective effect on ethanol <b>reinforcement</b> than either neuropharmacological action alone.
+HTR1A	addiction	addiction	9593223	Behavioral effects of 5 [3 [((2S) 1,4 benzodioxan 2 ylmethyl)amino]propoxy] 1,3 be nzodioxole HCl (MKC 242), a novel <strong>5 HT1A</strong> receptor agonist, were evaluated using animal models of anxiety and obsessive <b>compulsive</b> disorder and compared against reference compounds.
+HTR1A	drug	nicotine	9372532	<b>Nicotine</b> withdrawal leads to increased sensitivity of serotonergic neurons to the <strong>5 HT1A</strong> agonist 8 OH DPAT.
+HTR1A	addiction	withdrawal	9372532	Nicotine <b>withdrawal</b> leads to increased sensitivity of serotonergic neurons to the <strong>5 HT1A</strong> agonist 8 OH DPAT.
+HTR1A	drug	benzodiazepine	9401775	Ritanserin was shown to enhance the disinhibitory potency of other benzodiazepines, <b>chlordiazepoxide</b> (4 fold), <b>temazepam</b> (10 fold) and <b>lorazepam</b> (10 fold), the <strong>5 HT1A</strong> receptor ligands, 8 OH DPAT (25 fold), buspirone (100 fold) and lesopitron (500 fold), the 5 HT3 receptor antagonists, ondansetron (100 fold) R(+) zacopride (100 fold) and S( ) zacopride (greater than a 1000 fold), the substituted benzamides, sulpiride (10 fold) and tiapride (5 to 10 fold) and the cholecystokinin (CCK)A receptor antagonist, devazepide (100 fold).
+HTR1A	drug	alcohol	9394117	These complex findings suggest that biochemical properties other than 5 HT2A receptor antagonism (e.g., <strong>5 HT1A</strong> receptor agonism) may be involved in the effects of amperozide and FG 5974 on <b>alcohol</b> intake and other consummatory behaviors.
+HTR1A	drug	nicotine	9266775	Pretreatment with the <strong>5 HT 1A</strong> agonists (+)8 OH DPAT (0.001 0.1 mg/kg) and LY274600 (0.3 3.0 mg/kg) either had no affect or exacerbated the <b>nicotine</b> withdrawal enhanced startle response.
+HTR1A	addiction	withdrawal	9266775	Pretreatment with the <strong>5 HT 1A</strong> agonists (+)8 OH DPAT (0.001 0.1 mg/kg) and LY274600 (0.3 3.0 mg/kg) either had no affect or exacerbated the nicotine <b>withdrawal</b> enhanced startle response.
+HTR1A	drug	nicotine	9266775	Pretreatment with the <strong>5 HT 1A</strong> antagonists NAN 190 (1 3 mg/kg), LY206130 (1 10 mg/kg), or WAY 100635 (0.1 1.0 mg/kg) blocked the increase in the startle response caused by <b>nicotine</b> withdrawal at doses that had no effect on baseline startle responses.
+HTR1A	addiction	withdrawal	9266775	Pretreatment with the <strong>5 HT 1A</strong> antagonists NAN 190 (1 3 mg/kg), LY206130 (1 10 mg/kg), or WAY 100635 (0.1 1.0 mg/kg) blocked the increase in the startle response caused by nicotine <b>withdrawal</b> at doses that had no effect on baseline startle responses.
+HTR1A	drug	nicotine	9266775	These data indicate that <strong>5 HT 1A</strong> receptors play a role in the neurophysiology of <b>nicotine</b> withdrawal.
+HTR1A	addiction	withdrawal	9266775	These data indicate that <strong>5 HT 1A</strong> receptors play a role in the neurophysiology of nicotine <b>withdrawal</b>.
+HTR1A	drug	nicotine	9266775	In addition, <strong>5 HT 1A</strong> antagonists may be able to relieve some <b>nicotine</b> withdrawal symptoms in man and may represent a novel pharmacotherapy for <b>smoking</b> cessation.
+HTR1A	addiction	withdrawal	9266775	In addition, <strong>5 HT 1A</strong> antagonists may be able to relieve some nicotine <b>withdrawal</b> symptoms in man and may represent a novel pharmacotherapy for smoking cessation.
+HTR1A	drug	psychedelics	9300612	WAY 100,135 had little effect on drug appropriate responding; however, the discrimination of (+) <b>MDMA</b> at 20 min was partly reduced by this <strong>5 HT1A</strong> antagonist.
+HTR1A	drug	cocaine	9300585	The conditioned place preference (CPP) procedure was employed to examine the effects of the 5 hydroxytryptamine1A (<strong>5 HT1A</strong>) receptor agonist, buspirone, on <b>cocaine</b> reinforcement.
+HTR1A	addiction	reward	9300585	The conditioned place preference (<b>CPP</b>) procedure was employed to examine the effects of the 5 hydroxytryptamine1A (<strong>5 HT1A</strong>) receptor agonist, buspirone, on cocaine <b>reinforcement</b>.
+HTR1A	drug	opioid	9359582	A 30 s exposure elicited a shorter duration and lower amplitude 'non <b>opioid</b>' analgesia that was insensitive to <b>naloxone</b>, partially sensitive to either the serotonin 1A (<strong>5 HT1A</strong>) agonist, 8 OH DPAT, or the GABAA antagonist, bicuculline, and blocked by the competitive N methyl D aspartate (NMDA) antagonist, NPC 12626.
+HTR1A	drug	benzodiazepine	9128832	Effects of chronic <b>diazepam</b> treatment on pre  and postsynaptic <strong>5 HT1A</strong> receptors in the rat brain.
+HTR1A	drug	benzodiazepine	9128832	Biochemical and electrophysiological approaches were used to assess possible changes in <strong>5 HT1A</strong> receptors in the rat brain after long term treatment with an anxiolytic <b>benzodiazepine</b>.
+HTR1A	drug	benzodiazepine	9128832	In vitro binding and quantitative autoradiographic experiments with [3H]8 hydroxy 2 (di n propylamino)tetralin ([3H]8 OH DPAT) showed that the characteristics of <strong>5 HT1A</strong> receptor binding sites in the hippocampus and the dorsal raphe nucleus were not significantly altered by the administration of <b>diazepam</b> under the treatment protocols A, B and C. Furthermore, in vitro electrophysiological recordings of serotoninergic neurons in the dorsal raphe nucleus of brain stem slices revealed no modification in the sensitivity of somatodendritic <strong>5 HT1A</strong> autoreceptors in rats treated with <b>diazepam</b> according to the protocols A and B.
+HTR1A	drug	benzodiazepine	9128832	However, they do not support the idea of a reduced anxiolytic efficacy of <strong>5 HT1A</strong> receptor agonists as a result of prior treatment with a <b>benzodiazepine</b>.
+HTR1A	drug	alcohol	9211564	Effects of fluvoxamine, a relatively selective 5 HT uptake inhibitor, and ipsapirone, a relatively selective <strong>5 HT1A</strong> agonist, were studied on the initiation and/or maintenance of the voluntary intake of <b>alcohol</b>, morphine, cocaine, and/or nicotine in rats using the two bottle free choice method.
+HTR1A	drug	cocaine	9211564	Effects of fluvoxamine, a relatively selective 5 HT uptake inhibitor, and ipsapirone, a relatively selective <strong>5 HT1A</strong> agonist, were studied on the initiation and/or maintenance of the voluntary intake of alcohol, morphine, <b>cocaine</b>, and/or nicotine in rats using the two bottle free choice method.
+HTR1A	drug	nicotine	9211564	Effects of fluvoxamine, a relatively selective 5 HT uptake inhibitor, and ipsapirone, a relatively selective <strong>5 HT1A</strong> agonist, were studied on the initiation and/or maintenance of the voluntary intake of alcohol, morphine, cocaine, and/or <b>nicotine</b> in rats using the two bottle free choice method.
+HTR1A	drug	opioid	9211564	Effects of fluvoxamine, a relatively selective 5 HT uptake inhibitor, and ipsapirone, a relatively selective <strong>5 HT1A</strong> agonist, were studied on the initiation and/or maintenance of the voluntary intake of alcohol, <b>morphine</b>, cocaine, and/or nicotine in rats using the two bottle free choice method.
+HTR1A	drug	alcohol	9211564	These results suggest: (1) selective stimulation of <strong>5 HT1A</strong> receptors reduces <b>alcohol</b> preference, (2) stimulation of all 5 HT receptors has no effect on <b>alcohol</b> intake, indicating the presence of inhibitory receptors, (3) stimulation of the serotonergic system in general stimulates morphine preference, (4) the serotonin system does not affect nicotine or cocaine preference and (5) the serotonergic system is not involved in the voluntary consumption of all, but only of some drugs/chemicals of abuse.
+HTR1A	drug	cocaine	9211564	These results suggest: (1) selective stimulation of <strong>5 HT1A</strong> receptors reduces alcohol preference, (2) stimulation of all 5 HT receptors has no effect on alcohol intake, indicating the presence of inhibitory receptors, (3) stimulation of the serotonergic system in general stimulates morphine preference, (4) the serotonin system does not affect nicotine or <b>cocaine</b> preference and (5) the serotonergic system is not involved in the voluntary consumption of all, but only of some drugs/chemicals of abuse.
+HTR1A	drug	nicotine	9211564	These results suggest: (1) selective stimulation of <strong>5 HT1A</strong> receptors reduces alcohol preference, (2) stimulation of all 5 HT receptors has no effect on alcohol intake, indicating the presence of inhibitory receptors, (3) stimulation of the serotonergic system in general stimulates morphine preference, (4) the serotonin system does not affect <b>nicotine</b> or cocaine preference and (5) the serotonergic system is not involved in the voluntary consumption of all, but only of some drugs/chemicals of abuse.
+HTR1A	drug	opioid	9211564	These results suggest: (1) selective stimulation of <strong>5 HT1A</strong> receptors reduces alcohol preference, (2) stimulation of all 5 HT receptors has no effect on alcohol intake, indicating the presence of inhibitory receptors, (3) stimulation of the serotonergic system in general stimulates <b>morphine</b> preference, (4) the serotonin system does not affect nicotine or cocaine preference and (5) the serotonergic system is not involved in the voluntary consumption of all, but only of some drugs/chemicals of abuse.
+HTR1A	drug	benzodiazepine	9151356	As a further test of our hypothesis, we examined the effects of MRN injection of the <strong>5 HT1A</strong> receptor agonist, 8 OH DPAT, on animals withdrawn from <b>diazepam</b> and tested in the low light familiar condition of the social interaction test.
+HTR1A	drug	opioid	10921076	The spontaneous withdrawal from <b>morphine</b> in <b>morphine</b> dependent rats significantly decreased the duration of active interaction in social interaction test and the number of licks during the shock punished period in Vogel's conflict procedure, which were attenuated by buspirone, a <strong>5 HT1A</strong> agonist, as well as para chlorophenylalanine (PCPA), an inhibitor of tryptophan hydroxylase.
+HTR1A	addiction	withdrawal	10921076	The spontaneous <b>withdrawal</b> from morphine in morphine dependent rats significantly decreased the duration of active interaction in social interaction test and the number of licks during the shock punished period in Vogel's conflict procedure, which were attenuated by buspirone, a <strong>5 HT1A</strong> agonist, as well as para chlorophenylalanine (PCPA), an inhibitor of tryptophan hydroxylase.
+HTR1A	addiction	reward	8956376	Pretreatment with the <strong>5 HT1A</strong>/1B receptor agonist CGS 12066B (1 10 mg/kg, IP) dose dependently reduced the self administration of GBR 12909 (83 micrograms/injection) by increasing the interval between drug injections, consistent with a enhancement of the <b>reinforcing</b> effects of GBR 12909.
+HTR1A	drug	alcohol	8944403	Anxiolytic compounds such as the benzodiazepine receptor agonists diazepam and alprazolam, the full <strong>5 HT1A</strong> receptor agonists 8 OH DPAT and flesinoxan, and <b>alcohol</b> reduced isolation calling by the guinea pig pup.
+HTR1A	drug	benzodiazepine	8944403	Anxiolytic compounds such as the <b>benzodiazepine</b> receptor agonists <b>diazepam</b> and <b>alprazolam</b>, the full <strong>5 HT1A</strong> receptor agonists 8 OH DPAT and flesinoxan, and alcohol reduced isolation calling by the guinea pig pup.
+HTR1A	drug	benzodiazepine	8923664	Evidence that conditioned stress enhances outflow of dopamine in rat prefrontal cortex: a search for the influence of <b>diazepam</b> and <strong>5 HT1A</strong> agonists.
+HTR1A	drug	benzodiazepine	8923664	It is concluded that conditioned stress in vivo enhances dopaminergic neurotransmission in the rat prefrontal cortex, this effect being attenuated by <b>diazepam</b>, a classic anxiolytic drug, and by such novel anxiolytics as ipsapirone and buspirone, which operate via serotonergic <strong>5 HT1A</strong> receptors.
+HTR1A	drug	benzodiazepine	8923664	Differential effects of <b>diazepam</b> and <strong>5 HT1A</strong> agonists on basal and stress induced alterations in dopamine outflow are discussed in terms of their possible effectiveness in various types of general anxiety disorders.
+HTR1A	drug	alcohol	8888935	The <strong>5 HT1A</strong> receptor agonist 8 OH DPAT reduces <b>ethanol</b> intake and maintained behavior in female Sprague Dawley rats.
+HTR1A	drug	alcohol	8888935	These results demonstrate that, under the present experimental conditions, the <strong>5 HT1A</strong> receptor agonist 8 OH DPAT reduced <b>ethanol</b> self administration in the rat, and support a role for <strong>5 HT1A</strong> receptors in the mediation of <b>ethanol</b> reinforcement.
+HTR1A	addiction	reward	8888935	These results demonstrate that, under the present experimental conditions, the <strong>5 HT1A</strong> receptor agonist 8 OH DPAT reduced ethanol self administration in the rat, and support a role for <strong>5 HT1A</strong> receptors in the mediation of ethanol <b>reinforcement</b>.
+HTR1A	drug	alcohol	8883849	5 HT (1 100 microM) caused concentration dependent hyperpolarization of the membrane that was not altered by simultaneous 30 mM <b>ethanol</b> treatment, but blunted by 10 microM buspirone, a weak <strong>5 HT1A</strong> agonist.
+HTR1A	drug	alcohol	8905669	Behavioral effects of acute diazepam administration were compared with those of the <strong>5 HT1A</strong> anxiolytic buspirone and those of <b>ethanol</b> in C57BL/6J mice.
+HTR1A	drug	benzodiazepine	8905669	Behavioral effects of acute <b>diazepam</b> administration were compared with those of the <strong>5 HT1A</strong> anxiolytic buspirone and those of ethanol in C57BL/6J mice.
+HTR1A	addiction	reward	8728552	Whatever the experimental parameters and stage of the learning, an acute administration of drugs able to reduce 5 HT neuronal activity (benzodiazepines; <strong>5 HT1A</strong> receptor partial agonists: buspirone and MDL 73005EF) or enhance 5 HT transmission (5 HT reuptake inhibitors: indalpine and zimelidine; <strong>5 HT1A</strong> receptor full agonist: 8 OH DPAT) failed significantly to alter choice strategy (decreased or increased preference for the large but delayed <b>reward</b>, respectively), as they did in other situations such as a T maze procedure.
+HTR1A	drug	alcohol	8801594	The present series of experiments was conducted to investigate whether the previously reported <b>ethanol</b> intake reducing effects of the <strong>5 HT1A</strong> receptor agonist ipsapirone could be based on possible stimulus similarities between both compounds.
+HTR1A	drug	benzodiazepine	8786542	These data indicate that learning is sensitive to disruption by drugs with <strong>5 HT1A</strong> agonist properties, and that atypical anxiolytics with <strong>5 HT1A</strong> agonist properties are no less disruptive to "cognitive" processes than typical anxiolytics such as the <b>benzodiazepine</b> <b>alprazolam</b>.
+HTR1A	addiction	reward	8587903	Drugs with different intrinsic activity at <strong>5 HT1A</strong> receptors and antagonists at 5 HT2A/2C and 5 HT3 receptors were studied for their ability to increase the rates of punished <b>operant</b> responding in rats.
+HTR1A	drug	benzodiazepine	8587903	Like <b>chlordiazepoxide</b> (5 and 10 mg/kg) and <b>diazepam</b> (1.25 and 2.5 mg/kg), 0.125 mg/kg 8 hydroxy 2 (di n propylamino)tetralin (8 OH DPAT), a <strong>5 HT1A</strong> receptor agonist, and 5 and 10 mg/kg ipsapirone, a partial agonist at these receptors, increased the rates of punished responding, whereas (S) WAY 100135, a <strong>5 HT1A</strong> receptor antagonist, had no effect at doses from 1 to 10 mg/kg.
+HTR1A	addiction	reward	8587903	The results show that agents acting as full or partial agonists at <strong>5 HT1A</strong> receptors and blockers of postsynaptic 5 HT2C receptors have anxiolytic like effects in a model of punished <b>operant</b> responding, whereas antagonists at <strong>5 HT1A</strong> and 5 HT3 receptors have no such effect.
+HTR1A	drug	benzodiazepine	8666006	The effect of ipsapirone, a partial agonist at <strong>5 HT1A</strong> receptors, and of <b>diazepam</b> on punished operant responding was studied in rats injected intracerebroventricularly with 150 microg 5,7 dihydroxytryptamine to deplete brain serotonin or pretreated with (S) WAY 100135 (N tert butyl) 3 4 (2 methoxyphenyl)piperazin 1 yl 2 phenylpropanamide dihydrochloride), an antagonist at <strong>5 HT1A</strong> receptors.
+HTR1A	addiction	reward	8666006	The effect of ipsapirone, a partial agonist at <strong>5 HT1A</strong> receptors, and of diazepam on punished <b>operant</b> responding was studied in rats injected intracerebroventricularly with 150 microg 5,7 dihydroxytryptamine to deplete brain serotonin or pretreated with (S) WAY 100135 (N tert butyl) 3 4 (2 methoxyphenyl)piperazin 1 yl 2 phenylpropanamide dihydrochloride), an antagonist at <strong>5 HT1A</strong> receptors.
+HTR1A	addiction	addiction	8666006	The results suggest that ipsapirone releases behaviour that is suppressed by <b>punishment</b> by stimulating presynaptic <strong>5 HT1A</strong> receptors.
+HTR1A	drug	benzodiazepine	8539344	The <b>benzodiazepine</b> receptor agonists <b>chlordiazepoxide</b>, <b>diazepam</b> and <b>alprazolam</b>, the <strong>5 HT1A</strong> receptor agonists flesinoxan and ipsapirone and the 5 HT uptake inhibitor clomipramine selectively (no effect on crossings) reduced SAP.
+HTR1A	drug	benzodiazepine	8539344	In conclusion, SAP and intention movements were reduced selectively by anxiolytic agents from different classes, including <b>benzodiazepine</b> receptor agonists, <strong>5 HT1A</strong> receptor agonists and a 5 HT uptake inhibitor, whereas an alpha 2 adrenoceptor agonist and a MAO inhibitor reduced SAP non selectively.
+HTR1A	drug	benzodiazepine	8539340	Drugs with anxiolytic effects that act on the <b>benzodiazepine</b> GABAA receptor complex and on <strong>5 HT1A</strong> receptors systematically and potently alter specific vocalizations in rodents and primates in a pharmacologically reversible manner; the specificity of these effects on vocalizations is evident due to the effectiveness of low doses that do not compromise other physiological and behavioral processes.
+HTR1A	addiction	withdrawal	8521905	The expression of central <strong>5 HT1A</strong> and 5 HT1B receptors was studied in several brain areas of rats subjected to a 2 week period of chronic alcoholization, followed by 18 h <b>withdrawal</b>.
+HTR1A	drug	alcohol	8521905	Quantitative autoradiography indicated that the <b>ethanol</b> treatment provoked an increase (approximately +30%) in the labeling by [3H]8 hydroxy 2 (di n propylamino)tetralin ([3H]8 OH DPAT) and [3H]N [2 [4 (2 methoxyphenyl) 1 piperazinyl]ethyl] N (2 pyridinyl) cyclohexane carboxamide ([3H]WAY 100635) of <strong>5 HT1A</strong> autoreceptors in the dorsal raphe nucleus, accompanied by a concomitant decrease in the labeling of postsynaptic <strong>5 HT1A</strong> receptors in the hippocampus (approximately  20%), anterior (approximately  30%) and posterior (approximately  32%) cortices.
+HTR1A	drug	alcohol	8521905	These data suggest that altered sensitivity of chronically alcoholized rats to <strong>5 HT1A</strong> and 5 HT1B receptor ligands may result from <b>alcohol</b> induced changes in the transcription of the genes encoding these receptors.
+HTR1A	drug	alcohol	8521904	Modification of behavioral effects of 8 hydroxy 2 (di n propylamino)tetralin following chronic <b>ethanol</b> consumption in the rat: evidence for the involvement of <strong>5 HT1A</strong> receptors in <b>ethanol</b> dependence.
+HTR1A	addiction	dependence	8521904	Modification of behavioral effects of 8 hydroxy 2 (di n propylamino)tetralin following chronic ethanol consumption in the rat: evidence for the involvement of <strong>5 HT1A</strong> receptors in ethanol <b>dependence</b>.
+HTR1A	drug	alcohol	8521904	Taken together, these results indicate that chronic <b>ethanol</b> exposure differentially alters sensitivity to several pharmacological effects of the <strong>5 HT1A</strong> receptor ligand 8 OH DPAT.
+HTR1A	drug	alcohol	8521904	They further support the involvement of 5 HT (5 hydroxytryptamine, serotonin) systems in <b>alcohol</b> abuse and therapeutic interventions using <strong>5 HT1A</strong> ligands.
+HTR1A	drug	psychedelics	8539318	Simultaneous administration of alpha 2 adrenergic agents with <b>LSD</b> shifted the dose response curve to the left only when the adrenergic agent also possessed at least moderate affinity for the <strong>5 HT1A</strong> receptor.
+HTR1A	drug	psychedelics	8539318	While previous studies have suggested that the nature of the <b>LSD</b> cue may be essentially expressed by 5 HT2 receptor activation, the present data show that this cue can be modulated by effects of <b>LSD</b> at <strong>5 HT1A</strong> and at other monoamine neurotransmitter receptors.
+HTR1A	drug	cocaine	7566671	Repeated <b>cocaine</b> administration reduces <strong>5 HT1A</strong> mediated prolactin secretion in rats.
+HTR1A	drug	cocaine	7566671	The prolactin and behavioral responses elicited by the <strong>5 HT1A</strong> agonist 8 OH DPAT (8 hydroxy 2 [di n propylamino]tetralin) were examined in male rats previously exposed to chronic <b>cocaine</b> (15 mg/kg, i.p., b.i.d., 7 days) or saline.
+HTR1A	drug	cocaine	7566671	Our data agree with the findings of others and suggest that <strong>5 HT1A</strong> receptors mediating neuroendocrine secretion become subsensitive after repeated <b>cocaine</b> administration.
+HTR1A	drug	amphetamine	7796132	A significant increase of [3H]SCH 23390 binding to D1 DA receptors was observed in the substantia nigra pars reticulata 1 day but not 15 days after the cessation of <b>AMPH</b> treatment, whereas [3H]8 OH DPAT binding to <strong>5 HT1A</strong> sites was found to be significantly enhanced in the dorsal raphe nucleus at both time points.
+HTR1A	addiction	aversion	7796851	Pindolol and (  ) propranolol, non selective antagonists of beta adrenoceptors and 5 HT1 receptors, 1 (2 methoxyphenyl) 4 [4 (2 phethalimido) butyl] piperazine hydrobromide (NAN 190), a <strong>5 HT1A</strong> receptor antagonist, 3 tropanyl 3,5 dichlorobenzoate (MDL72222) and metoclopramide, 5 HT3 receptor antagonists, significantly inhibited the calcitonin induced anti <b>aversive</b> effects.
+HTR1A	drug	opioid	7796851	These results suggest that beta adrenoceptor, <strong>5 HT1A</strong>, 5 HT3, GABAA and GABAB receptors, but not alpha adrenoceptor, <b>opioid</b> nor 5 HT2A receptors, are involved in the inhibitory effect of calcitonin on intrathecally injected N methyl D aspartate induced aversive behavior in mice.
+HTR1A	addiction	aversion	7796851	These results suggest that beta adrenoceptor, <strong>5 HT1A</strong>, 5 HT3, GABAA and GABAB receptors, but not alpha adrenoceptor, opioid nor 5 HT2A receptors, are involved in the inhibitory effect of calcitonin on intrathecally injected N methyl D aspartate induced <b>aversive</b> behavior in mice.
+HTR1A	drug	cocaine	8594482	These studies demonstrate that prenatal <b>cocaine</b> produces differential changes in neuroendocrine responses following challenge with a 5 HT releaser versus a <strong>5 HT1A</strong> agonist and suggest differential functional alterations in both pre  and postsynaptic components of 5 HT pathways.
+HTR1A	drug	cocaine	8594482	Gender differences in prenatal <b>cocaine</b> effects on postsynaptic receptor function were more clearly shown in study II, which demonstrated that at the same postnatal age, <strong>5 HT1A</strong> mediated neuroendocrine responses were significantly potentiated in male but not female <b>cocaine</b> exposed progeny.
+HTR1A	drug	benzodiazepine	7753959	VA21B7 was compared with standard 5 HT3 receptor antagonists such as ondansetron, tropisetron and granisetron, with the <strong>5 HT1A</strong> agent buspirone and with <b>diazepam</b>.
+HTR1A	drug	benzodiazepine	7724700	The triazolobenzodiazepine <b>alprazolam</b>, the 5 HT uptake inhibitors fluvoxamine and clomipramine, the mixed 5 HT/NA uptake inhibitor imipramine, the full <strong>5 HT1A</strong> receptor agonists 8 OH DPAT and flesinoxan, the partial <strong>5 HT1A</strong> receptor agonists buspirone, ipsapirone and BMY 7378, the alpha 2 adrenoceptor agonist clonidine and the alpha 2 adrenoceptor antagonist yohimbine reduced conditioned USV.
+HTR1A	drug	alcohol	7945982	On the other hand, treatment of intact rats with the <strong>5 HT1A</strong> receptor agonist ipsapirone (2.5 mg/kg), a drug that also decreases <b>ethanol</b> drinking in two bottle intake tests, did increase the duration of aversive groomings, whereas measures of ingestion remained unaffected.
+HTR1A	addiction	aversion	7945982	On the other hand, treatment of intact rats with the <strong>5 HT1A</strong> receptor agonist ipsapirone (2.5 mg/kg), a drug that also decreases ethanol drinking in two bottle intake tests, did increase the duration of <b>aversive</b> groomings, whereas measures of ingestion remained unaffected.
+HTR1A	drug	cocaine	7956751	These results suggest selective alteration of presynaptic <strong>5 HT1A</strong> or postsynaptic 5 HT2A/2C function in <b>cocaine</b> addicts.
+HTR1A	drug	alcohol	7919948	This SIH can be antagonized by benzodiazepines, <b>alcohol</b> and <strong>5 HT1A</strong> receptor agonists, but not by specific 5 HT reuptake inhibitors (SSRIs) or 5 HT3 receptor antagonists.
+HTR1A	drug	cocaine	7813744	Additionally, repeated <b>cocaine</b> exposure produces subsensitive <strong>5 HT1A</strong> mediated hormone responses, and supersensitive 5 HT2 mediated responses.
+HTR1A	addiction	withdrawal	7913228	Effects of <strong>5 HT1A</strong> receptor ligands on a safety signal <b>withdrawal</b> procedure of conflict in the rat.
+HTR1A	addiction	addiction	7913228	The present study evaluated in the rat the ability of various <strong>5 HT1A</strong> receptor agonists to exert an "anxiolytic like" release of the suppression of lever pressing for food induced by the withdrawal of a conditioned signal for safety without presentation of a conditioned signal for <b>punishment</b>.
+HTR1A	addiction	withdrawal	7913228	The present study evaluated in the rat the ability of various <strong>5 HT1A</strong> receptor agonists to exert an "anxiolytic like" release of the suppression of lever pressing for food induced by the <b>withdrawal</b> of a conditioned signal for safety without presentation of a conditioned signal for punishment.
+HTR1A	addiction	reward	8050464	Using a two lever <b>operant</b> drug discrimination procedure, rats were trained to discriminate the <strong>5 HT1A</strong> receptor agonist, flesinoxan (0.5 mg/kg i.p.
+HTR1A	drug	benzodiazepine	8057528	Effects of SUN 8399, a potent and selective <strong>5 HT1A</strong> agonist, on conflict behavior and ambulatory activity in mice: comparison with those of buspirone, tandospirone and <b>diazepam</b>.
+HTR1A	drug	benzodiazepine	8057528	administration of SUN 8399, a selective <strong>5 HT1A</strong> agonist, on the operant behavior under a MULT VI 1.5 min/FR 5 punishment schedule of food reinforcement and on the ambulatory activity were evaluated in mice, and the characteristics were compared with those of other <strong>5 HT1A</strong> agonists, buspirone and tandospirone, and the <b>benzodiazepine</b> <b>diazepam</b>.
+HTR1A	addiction	addiction	8057528	administration of SUN 8399, a selective <strong>5 HT1A</strong> agonist, on the operant behavior under a MULT VI 1.5 min/FR 5 <b>punishment</b> schedule of food reinforcement and on the ambulatory activity were evaluated in mice, and the characteristics were compared with those of other <strong>5 HT1A</strong> agonists, buspirone and tandospirone, and the benzodiazepine diazepam.
+HTR1A	addiction	reward	8057528	administration of SUN 8399, a selective <strong>5 HT1A</strong> agonist, on the <b>operant</b> behavior under a MULT VI 1.5 min/FR 5 punishment schedule of food <b>reinforcement</b> and on the ambulatory activity were evaluated in mice, and the characteristics were compared with those of other <strong>5 HT1A</strong> agonists, buspirone and tandospirone, and the benzodiazepine diazepam.
+HTR1A	drug	amphetamine	8057528	However, SUN 8399 possesses different behavioral characteristics from those of the other two <strong>5 HT1A</strong> agonists in terms of interactions with <b>methamphetamine</b> and scopolamine.
+HTR1A	drug	alcohol	8204202	<strong>5 HT1A</strong> receptor agonists reduce <b>ethanol</b> induced locomotor activity in mice.
+HTR1A	drug	alcohol	8204202	Previous studies have suggested that <strong>5 HT1A</strong> receptor agonists may reduce <b>ethanol</b> preference in rats.
+HTR1A	drug	alcohol	8204202	In the present study on mice, the <strong>5 HT1A</strong> receptor agonists (8 OH DPAT), ipsapirone, and buspirone all antagonized the locomotor activity (LMA) stimulatory effect of <b>ethanol</b> (2.5 g/kg).
+HTR1A	drug	alcohol	8204202	The present results provide further support for the notion that the LMA increasing effect of <b>ethanol</b> may be homologous to its reinforcing properties and that <strong>5 HT1A</strong> receptor agonists may counteract these properties as well.
+HTR1A	addiction	reward	8204202	The present results provide further support for the notion that the LMA increasing effect of ethanol may be homologous to its <b>reinforcing</b> properties and that <strong>5 HT1A</strong> receptor agonists may counteract these properties as well.
+HTR1A	addiction	reward	7846206	In general, the arylpiperazine, <strong>5 HT1A</strong> compounds increased <b>reinforcement</b> rate, decreased response rate and disrupted the profile of the IRT distribution.
+HTR1A	drug	benzodiazepine	7846206	The effects of the four arylpiperazine <strong>5 HT1A</strong> compounds on the IRT distribution profile were different from the AD profile of 5 HTP and the <b>benzodiazepine</b> anxiolytic profile of <b>diazepam</b>.
+HTR1A	drug	benzodiazepine	7846191	Three experiments evaluated the association between USV and "distress" by comparing the effects of <b>diazepam</b> as a prototypic <b>benzodiazepine</b> agonist and the putative anxiolytic gepirone with affinity for 5 hydroxytryptamine (<strong>5 HT1A</strong>) receptors in naive and <b>diazepam</b> withdrawn subjects.
+HTR1A	addiction	dependence	22298627	Assessment of the <b>dependence</b> potential of the potent high efficacy <strong>5 HT1A</strong> agonist S 14506 in rats.
+HTR1A	drug	alcohol	8032152	For example, buspirone, a <strong>5 HT1A</strong> receptor partial agonist, reduced anxiety and <b>alcohol</b> craving, but not AC; a 5 HT partial agonist, m CPP, increased craving in abstinent <b>alcoholics</b>; modest reductions in AC were observed with a 5 HT3 antagonist, ondansetron (0.5 mg/day, but not 4 mg/day).
+HTR1A	addiction	relapse	8032152	For example, buspirone, a <strong>5 HT1A</strong> receptor partial agonist, reduced anxiety and alcohol <b>craving</b>, but not AC; a 5 HT partial agonist, m CPP, increased <b>craving</b> in abstinent alcoholics; modest reductions in AC were observed with a 5 HT3 antagonist, ondansetron (0.5 mg/day, but not 4 mg/day).
+HTR1A	addiction	reward	8032152	For example, buspirone, a <strong>5 HT1A</strong> receptor partial agonist, reduced anxiety and alcohol craving, but not AC; a 5 HT partial agonist, m <b>CPP</b>, increased craving in abstinent alcoholics; modest reductions in AC were observed with a 5 HT3 antagonist, ondansetron (0.5 mg/day, but not 4 mg/day).
+HTR1A	drug	benzodiazepine	8201242	Using measurements of rodent behaviour in the mouse light and dark test box and rat social interaction, anxiolytic agents such as <b>diazepam</b> and putative anxiolytic agents such as the <strong>5 HT1A</strong> and 5 HT3 receptor ligands 8 OH DPAT and low doses of tropisetron release behaviour suppressed by the aversive situation.
+HTR1A	addiction	aversion	8201242	Using measurements of rodent behaviour in the mouse light and dark test box and rat social interaction, anxiolytic agents such as diazepam and putative anxiolytic agents such as the <strong>5 HT1A</strong> and 5 HT3 receptor ligands 8 OH DPAT and low doses of tropisetron release behaviour suppressed by the <b>aversive</b> situation.
+HTR1A	drug	benzodiazepine	7902543	Co administration of buspirone (<strong>5 HT1A</strong> agonist) or ondansetron (5 HT3 antagonist), but not mianserin (5 HT1C antagonist) or ketanserin (5 HT2 antagonist) with <b>diazepam</b> potentiated the hypersensitivity to FG 7142 following chronic treatment with <b>diazepam</b>.
+HTR1A	drug	benzodiazepine	7902543	These results suggest that co administration of buspirone or ondansetron with <b>diazepam</b> may potentiate the development of physical dependence on <b>diazepam</b>; <strong>5 HT1A</strong> and 5 HT3 receptors may be partially involved in the development of physical dependence on <b>diazepam</b>.
+HTR1A	addiction	dependence	7902543	These results suggest that co administration of buspirone or ondansetron with diazepam may potentiate the development of physical <b>dependence</b> on diazepam; <strong>5 HT1A</strong> and 5 HT3 receptors may be partially involved in the development of physical <b>dependence</b> on diazepam.
+HTR1A	drug	cocaine	8405113	Repeated <b>cocaine</b> administration does not affect 5 HT receptor subtypes (<strong>5 HT1A</strong>, 5 HT2) in several rat brain regions.
+HTR1A	drug	cocaine	8405113	In order to examine whether <b>cocaine</b> induced behavioral sensitization is modulated by changes in serotonin receptor subtypes, we measured the binding of [3H]8 hydroxy 2 (di n propylamino)tetralin ([3H]8 OH DPAT) to <strong>5 HT1A</strong> receptors and of [3H] ketanserin to 5 HT2 receptors in various brain regions of <b>cocaine</b> treated and saline treated (control) rats.
+HTR1A	addiction	sensitization	8405113	In order to examine whether cocaine induced behavioral <b>sensitization</b> is modulated by changes in serotonin receptor subtypes, we measured the binding of [3H]8 hydroxy 2 (di n propylamino)tetralin ([3H]8 OH DPAT) to <strong>5 HT1A</strong> receptors and of [3H] ketanserin to 5 HT2 receptors in various brain regions of cocaine treated and saline treated (control) rats.
+HTR1A	drug	cocaine	8405113	These results suggest that the enhanced functional sensitivity of <strong>5 HT1A</strong> or 5 HT2 receptor subtypes seen with <b>cocaine</b> may be associated with alterations in processes distal to receptors rather than changes in the number or the affinity of the receptors.
+HTR1A	drug	cocaine	8332619	The results of Experiment 1 indicated that rats receiving <b>cocaine</b> via osmotic minipumps exhibited marked <strong>5 HT1A</strong> receptor subsensitivity.
+HTR1A	drug	cocaine	8332619	In contrast, rats receiving daily <b>cocaine</b> injections sometimes demonstrated evidence of <strong>5 HT1A</strong> supersensitivity and sometimes demonstrated evidence of <strong>5 HT1A</strong> normosensitivity.
+HTR1A	drug	cocaine	8332619	Overall, the results indicate that, at least in the present behavioral paradigm, the effects of chronic <b>cocaine</b> administration are mediated by changes in <strong>5 HT1A</strong> receptor sensitivity but not by changes in 5 HT1B receptor sensitivity.
+HTR1A	drug	benzodiazepine	7689737	Modulation of <strong>5HT1A</strong> receptors in the hippocampus and the raphe area of rats treated with <b>clonazepam</b>.
+HTR1A	drug	benzodiazepine	7689737	Modulation of <strong><strong>5HT1A</strong></strong> receptors in the hippocampus and the raphe area of rats treated with <b>clonazepam</b>.
+HTR1A	drug	benzodiazepine	7689737	The modulation of 5HT binding sites and <strong>5HT1A</strong> receptors by the administration of <b>clonazepam</b> for various periods of time were studied in the hippocampus and the raphe area by experiments with radioligands.
+HTR1A	drug	benzodiazepine	7689737	The modulation of 5HT binding sites and <strong><strong>5HT1A</strong></strong> receptors by the administration of <b>clonazepam</b> for various periods of time were studied in the hippocampus and the raphe area by experiments with radioligands.
+HTR1A	drug	alcohol	8507391	Systemic administration of the <strong>5 HT1A</strong> agonist ipsapirone (1.25 5.0 mg/kg) caused a dose dependent decrease in <b>ethanol</b> preference and intake, while the 5 HT2 antagonist ritanserin (1.25 5.0 mg/kg) and the 5 HT3 antagonists ondansetron (0.01 1.0 mg/kg) and granisetron (0.5 1.0 mg/kg) failed to alter <b>ethanol</b> consumption.
+HTR1A	drug	alcohol	8507391	These findings support the hypothesis that the 5 HT system is involved in the regulation of <b>ethanol</b> intake, with special emphasis on the involvement of the <strong>5 HT1A</strong> receptor subtype, and may indicate that central reward mediating mechanisms are influenced.
+HTR1A	addiction	reward	8507391	These findings support the hypothesis that the 5 HT system is involved in the regulation of ethanol intake, with special emphasis on the involvement of the <strong>5 HT1A</strong> receptor subtype, and may indicate that central <b>reward</b> mediating mechanisms are influenced.
+HTR1A	addiction	withdrawal	7685916	Further, our data suggests that a compound's effectiveness for the treatment of social <b>withdrawal</b> is at least in part due to its relative affinity for binding to dopamine D1 and serotonin <strong>5 HT1A</strong> receptors.
+HTR1A	drug	alcohol	8517886	The <strong>5 HT1A</strong> agent buspirone reduced <b>alcohol</b> intake and <b>alcohol</b> preference in the group of medium <b>alcohol</b> preferring rats at doses between 0.0025 and 0.63 mg/kg.
+HTR1A	drug	cocaine	8446658	In contrast, rats receiving continuous <b>cocaine</b> tended to exhibit behavior consistent with <strong>5 HT1A</strong> receptor subsensitivity.
+HTR1A	drug	cocaine	8446658	Changes in <strong>5 HT1A</strong> receptor sensitivity may contribute to some of the anxiety and depressive symptoms exhibited by human <b>cocaine</b> abusers.
+HTR1A	addiction	aversion	7871000	Cross familiarisation conditioned taste <b>aversion</b> procedure as a method to reveal stimulus resemblance between drugs: studies on the <strong>5 HT1A</strong> agonist 8 OHDPAT.
+HTR1A	addiction	aversion	7871000	In the present study a cross familiarisation conditioned taste <b>aversion</b> (<b>CTA</b>) paradigm was utilized to reveal stimulus resemblance between the selective <strong>5 HT1A</strong> agonist 8 OHDPAT and a variety of serotonergic and non serotonergic drugs.
+HTR1A	drug	cocaine	7870907	Rats were trained to self administer <b>cocaine</b> (0.5 mg/kg/infusion) and were then pretreated with the <strong>5 HT1A</strong> agonist 8 OH DPAT (0.125, 0.25 or 0.5 mg/kg, SC).
+HTR1A	drug	cocaine	7870907	This effect may be due to the effects at the <strong>5 HT1A</strong> receptor, since 8 OH DPAT produced a similar effect on <b>cocaine</b> self administration.
+HTR1A	drug	alcohol	7748345	The anxiogenic behaviour observed 12 h after <b>ethanol</b> withdrawal was inhibited by the <strong>5 HT1A</strong> partial agonist, buspirone (200 micrograms/kg s.c.), indicating that the increased 5 HT release might underlie the anxiogenic response.
+HTR1A	addiction	withdrawal	7748345	The anxiogenic behaviour observed 12 h after ethanol <b>withdrawal</b> was inhibited by the <strong>5 HT1A</strong> partial agonist, buspirone (200 micrograms/kg s.c.), indicating that the increased 5 HT release might underlie the anxiogenic response.
+HTR1A	drug	alcohol	7748340	This is indicated by (a) lower contents of DA and 5 HT; (b) fewer 5 HT immunostained fibers; (c) lower densities of 5 HT1B, 5 HT2 and D2 receptors; and (d) higher densities of <strong>5 HT1A</strong> receptors in the CNS of P rats compared to the <b>alcohol</b> nonpreferring NP line of rats.
+HTR1A	drug	alcohol	7748304	For example, buspirone, a <strong>5 HT1A</strong> receptor partial agonist, reduced anxiety and <b>alcohol</b> craving, but not AC; a 5 HT partial agonist, m CPP, increased <b>alcohol</b> craving in abstinent <b>alcoholics</b>; modest reductions in AC were observed with a 5 HT3 antagonist, ondansetron (0.5 mg/day, but not 4 mg/day).
+HTR1A	addiction	relapse	7748304	For example, buspirone, a <strong>5 HT1A</strong> receptor partial agonist, reduced anxiety and alcohol <b>craving</b>, but not AC; a 5 HT partial agonist, m CPP, increased alcohol <b>craving</b> in abstinent alcoholics; modest reductions in AC were observed with a 5 HT3 antagonist, ondansetron (0.5 mg/day, but not 4 mg/day).
+HTR1A	addiction	reward	7748304	For example, buspirone, a <strong>5 HT1A</strong> receptor partial agonist, reduced anxiety and alcohol craving, but not AC; a 5 HT partial agonist, m <b>CPP</b>, increased alcohol craving in abstinent alcoholics; modest reductions in AC were observed with a 5 HT3 antagonist, ondansetron (0.5 mg/day, but not 4 mg/day).
+HTR1A	drug	psychedelics	1361990	Low doses of the 5 hydroxytryptamine1A (<strong>5 HT1A</strong>) antagonist NAN 190, the 5 HT2 antagonist pirenperone, and the dopamine antagonist haloperidol were able to somewhat attenuate the <b>MDMA</b> stimulus; however, none of these agents decreased <b>MDMA</b> appropriate responding to less than 46%.
+HTR1A	drug	alcohol	1335222	The effect of short term (15 days) and long term (60 days) <b>ethanol</b> treatment and withdrawal on agonist stimulated phosphoinositide (Pl) hydrolysis, serotonin receptor subtypes (<strong>5HT1A</strong> and 5HT2), and alpha 1 adrenergic receptors were studied in rat cerebral cortex.
+HTR1A	addiction	withdrawal	1335222	The effect of short term (15 days) and long term (60 days) ethanol treatment and <b>withdrawal</b> on agonist stimulated phosphoinositide (Pl) hydrolysis, serotonin receptor subtypes (<strong>5HT1A</strong> and 5HT2), and alpha 1 adrenergic receptors were studied in rat cerebral cortex.
+HTR1A	drug	alcohol	1335222	The effect of short term (15 days) and long term (60 days) <b>ethanol</b> treatment and withdrawal on agonist stimulated phosphoinositide (Pl) hydrolysis, serotonin receptor subtypes (<strong><strong>5HT1A</strong></strong> and 5HT2), and alpha 1 adrenergic receptors were studied in rat cerebral cortex.
+HTR1A	addiction	withdrawal	1335222	The effect of short term (15 days) and long term (60 days) ethanol treatment and <b>withdrawal</b> on agonist stimulated phosphoinositide (Pl) hydrolysis, serotonin receptor subtypes (<strong><strong>5HT1A</strong></strong> and 5HT2), and alpha 1 adrenergic receptors were studied in rat cerebral cortex.
+HTR1A	drug	alcohol	1335222	We also observed that long term <b>ethanol</b> treatment had no significant effect on Bmax and KD of 5HT2, <strong>5HT1A</strong>, and alpha 1 adrenergic receptors, as well as NE and A23187 stimulated [3H] IP1 formation, but significantly decreased the 5HT stimulated [3H] IP1 formation in rat cerebral cortex.
+HTR1A	drug	alcohol	1335222	We also observed that long term <b>ethanol</b> treatment had no significant effect on Bmax and KD of 5HT2, <strong><strong>5HT1A</strong></strong>, and alpha 1 adrenergic receptors, as well as NE and A23187 stimulated [3H] IP1 formation, but significantly decreased the 5HT stimulated [3H] IP1 formation in rat cerebral cortex.
+HTR1A	drug	opioid	1387962	A 30 min exposure to the odors of a parasitized male induced <b>naloxone</b> (1.0 mg/kg) sensitive <b>opioid</b> mediated analgesia in female mice, whereas a brief 1 min exposure to these odors resulted in a lower amplitude, relatively short, nonopioid analgesia that was insensitive to <b>naloxone</b> and blocked by the serotonin 1A (<strong>5 HT1A</strong>), agonist, 8 OH DPAT.
+HTR1A	drug	benzodiazepine	1356807	It is concluded that the reduction in aversive responding caused by pharmacological manipulation at the <b>benzodiazepine</b>, 5 HT receptor subtypes <strong>5 HT1A</strong>, 5 HT1C/5 HT2 and 5 HT3 (but not at the cholecystokin CCKA or angiotensin receptors or inhibition of angiotensin converting enzyme) can be inhibited by R(+) and S( ) zacopride.
+HTR1A	addiction	aversion	1356807	It is concluded that the reduction in <b>aversive</b> responding caused by pharmacological manipulation at the benzodiazepine, 5 HT receptor subtypes <strong>5 HT1A</strong>, 5 HT1C/5 HT2 and 5 HT3 (but not at the cholecystokin CCKA or angiotensin receptors or inhibition of angiotensin converting enzyme) can be inhibited by R(+) and S( ) zacopride.
+HTR1A	drug	alcohol	1386220	Effects of <strong>5 HT 1A</strong> receptor agonists on <b>ethanol</b> preference in the rat.
+HTR1A	drug	benzodiazepine	1357674	We trained different groups of rats to discriminate the <b>benzodiazepine</b> <b>chlordiazepoxide</b> (CDP, 20 mg/kg) or the 5 hydroxytryptamine1A (<strong>5 HT1A</strong>) agonist 8 hydroxy 2 (di n propylamino)tetralin (8 OH DPAT) (0.4 mg/kg) from saline by means of the CTA procedure.
+HTR1A	addiction	aversion	1357674	We trained different groups of rats to discriminate the benzodiazepine chlordiazepoxide (CDP, 20 mg/kg) or the 5 hydroxytryptamine1A (<strong>5 HT1A</strong>) agonist 8 hydroxy 2 (di n propylamino)tetralin (8 OH DPAT) (0.4 mg/kg) from saline by means of the <b>CTA</b> procedure.
+HTR1A	drug	cocaine	1385662	The inhibitory response of single 5 HT neurons in the dorsal raphe (DR) to ( ) <b>cocaine</b>, the 5 HT uptake inhibitor fluoxetine or the <strong>5 HT1A</strong> agonist 8 hydroxy 2 [di N propylamino]tetralin (8 OHDPAT) was significantly enhanced in <b>cocaine</b> treated rats.
+HTR1A	drug	cocaine	1385662	Furthermore, several brain areas that contain either cell bodies (DR) or terminals for 5 HT (medial and sulcal prefrontal cortex, frontal cortex) showed <b>cocaine</b> induced elevations in [3H]imipramine labeled 5 HT uptake sites, while [3H] 8 OHDPAT labeled <strong>5 HT1A</strong> receptors were decreased only in the central medial amygdala.
+HTR1A	drug	cocaine	1584831	In a recent study, we reported that the (+/ ) 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane HCl (DOI) induced HTR was dose dependently reduced by <b>cocaine</b> via indirect stimulation of serotonergic <strong>5 HT1A</strong> and adrenergic alpha 2 receptors.
+HTR1A	drug	cocaine	1584831	Relative to vehicle exposed controls, withdrawal from <b>cocaine</b> treatment enhanced the inhibitory potency of the <strong>5 HT1A</strong> agonist (+ ) 8 hydroxy 2 (di n propylamino)tetralin HBr (8 OH DPAT) on DOI induced HTR.
+HTR1A	addiction	withdrawal	1584831	Relative to vehicle exposed controls, <b>withdrawal</b> from cocaine treatment enhanced the inhibitory potency of the <strong>5 HT1A</strong> agonist (+ ) 8 hydroxy 2 (di n propylamino)tetralin HBr (8 OH DPAT) on DOI induced HTR.
+HTR1A	drug	alcohol	1353126	Voluntary intake of <b>alcohol</b> is attenuated by ipsapirone in mice and role of <strong>5 HT1A</strong> receptor.
+HTR1A	drug	alcohol	1353126	The aim of this study is to examine the effect of ipsapirone, which is a specific <strong>5 HT1A</strong> agonist with a pyrimidinylpiperazine structure, on <b>alcohol</b> consumption in mice (C57BL/6J) by a voluntary <b>alcohol</b> intake paradigm.
+HTR1A	drug	benzodiazepine	1352058	The aim of this study was to use the elevated X maze to compare acute and chronic treatments of a <strong>5 HT1A</strong> partial agonist, ipsapirone, a 5 HT2 antagonist, ritanserin, and a 5 HT3 antagonist, ondansetron, with those of established anxiolytic (<b>diazepam</b>) and anxiogenic (idazoxan) compounds.
+HTR1A	addiction	reward	1351303	Treatment with the <strong>5 HT1A</strong> agonist flesinoxan (0.1 3.0 mg/kg) also dose dependently decreased response rates while at the same time increasing <b>reinforcement</b> rates.
+HTR1A	drug	opioid	1839965	After 15 min of exposure to the presence of an experienced predatory cat, mice displayed a <b>naloxone</b> (1.0 mg/kg) sensitive <b>opioid</b> mediated analgesic response, while after a brief 30 s exposure to the cat mice displayed a lower amplitude, relatively brief, non <b>opioid</b> analgesia that was insensitive to <b>naloxone</b> and blocked by the serotonin 1A (<strong>5 HT1A</strong>) agonist, 8 hydroxy 2 (di n propylamino)tetralin.
+HTR1A	drug	opioid	1839965	Male mice displayed a significantly greater <b>opioid</b> mediated predator induced analgesia than females, whereas female mice showed a significantly greater non <b>opioid</b>, <strong>5 HT1A</strong> sensitive, analgesia than males.
+HTR1A	drug	alcohol	1781924	The anxiolytic like activity of buspirone observed during <b>ethanol</b> withdrawal may be due to a reduction in serotonergic neurotransmission through activation of presynaptic <strong>5 HT1A</strong> autoreceptors.
+HTR1A	addiction	withdrawal	1781924	The anxiolytic like activity of buspirone observed during ethanol <b>withdrawal</b> may be due to a reduction in serotonergic neurotransmission through activation of presynaptic <strong>5 HT1A</strong> autoreceptors.
+HTR1A	drug	alcohol	1781924	The results obtained in this study suggest that pharmacotherapy with selective <strong>5 HT1A</strong> agonists may be beneficial in alleviation of anxiety during <b>ethanol</b> withdrawal.
+HTR1A	addiction	withdrawal	1781924	The results obtained in this study suggest that pharmacotherapy with selective <strong>5 HT1A</strong> agonists may be beneficial in alleviation of anxiety during ethanol <b>withdrawal</b>.
+HTR1A	drug	benzodiazepine	1661879	Such hyperactivity was significantly blocked after 10 days of repeated administration of <b>diazepam</b> (DZP), tandospirone (SM 3997; SM), a <strong>5 HT1A</strong> anxiolytic, and nitrendipene (Nit), a Ca antagonist.
+HTR1A	drug	opioid	1672380	High efficacy <strong>5 HT1A</strong> agonists attenuate <b>morphine</b> induced antinociception in mice in a competitive like manner.
+HTR1A	drug	opioid	1672380	The selective <strong>5 HT1A</strong> agonist, (+ ) 8 hydroxy diprolaminotetralin HBr (8 OH DPAT), dose dependently antagonized <b>morphine</b> induced antinociception (MIA) without affecting the latency to respond when applied alone.
+HTR1A	drug	opioid	1672380	These data show that, over a certain range of doses, the systemic administration of 8 OH DPAT and other high efficacy <strong>5 HT1A</strong> agonists functionally antagonizes the antinociceptive action of systemically applied <b>morphine</b> in a competitive like manner.
+HTR1A	drug	alcohol	1839497	The maximal density of [3H] 8 hydroxy 2 (di n  propylamino)tetralin [(3H] 8 OH DPAT) binding (Bmax) to <strong>5 HT1a</strong> receptors was decreased by 25 and 17% in the hippocampus during chronic <b>ethanol</b> intoxication and withdrawal, respectively.
+HTR1A	addiction	intoxication	1839497	The maximal density of [3H] 8 hydroxy 2 (di n  propylamino)tetralin [(3H] 8 OH DPAT) binding (Bmax) to <strong>5 HT1a</strong> receptors was decreased by 25 and 17% in the hippocampus during chronic ethanol <b>intoxication</b> and withdrawal, respectively.
+HTR1A	addiction	withdrawal	1839497	The maximal density of [3H] 8 hydroxy 2 (di n  propylamino)tetralin [(3H] 8 OH DPAT) binding (Bmax) to <strong>5 HT1a</strong> receptors was decreased by 25 and 17% in the hippocampus during chronic ethanol intoxication and <b>withdrawal</b>, respectively.
+HTR1A	drug	alcohol	1726986	Neurochemical data indicate that high <b>alcohol</b> seeking behavior (when compared with data from rats with low <b>alcohol</b> seeking characteristics) is associated with (a) lower contents of 5 HT in certain limbic regions, e.g., n. accumbens (Acb), frontal cortex, (b) a lower content of DA in the Acb, and (c) higher densities of <strong>5 HT1A</strong> receptors in certain limbic regions, e.g., cerebral cortex.
+HTR1A	addiction	relapse	1726986	Neurochemical data indicate that high alcohol <b>seeking</b> behavior (when compared with data from rats with low alcohol <b>seeking</b> characteristics) is associated with (a) lower contents of 5 HT in certain limbic regions, e.g., n. accumbens (Acb), frontal cortex, (b) a lower content of DA in the Acb, and (c) higher densities of <strong>5 HT1A</strong> receptors in certain limbic regions, e.g., cerebral cortex.
+HTR1A	addiction	aversion	1982355	The putative <strong>5 HT1A</strong> agonists, buspirone and gepirone, had a general inhibitory action on both positive and <b>aversive</b> palatability reactions.
+HTR1A	drug	opioid	2144490	Down regulation of hypothalamic <strong>5 HT1A</strong> receptors in <b>morphine</b> abstinent rats.
+HTR1A	drug	opioid	2144490	The effects of <b>morphine</b> tolerance dependence and abstinence on <strong>5 HT1A</strong> receptors in brain regions and spinal cord of the rat were determined.
+HTR1A	addiction	dependence	2144490	The effects of morphine tolerance <b>dependence</b> and abstinence on <strong>5 HT1A</strong> receptors in brain regions and spinal cord of the rat were determined.
+HTR1A	drug	opioid	2144490	In <b>morphine</b> and placebo tolerant dependent rats the binding of [3H]DPAT to <strong>5 HT1A</strong> receptors in brain regions and spinal cord did not differ.
+HTR1A	drug	opioid	2144490	Since DPAT is believed to have a major action on the presynaptic 5 HT neurons, it is concluded that in <b>morphine</b> abstinent rats <strong>5 HT1A</strong> receptors are down regulated in hypothalamus, but in <b>morphine</b> tolerant dependent rats they are unaffected.
+HTR1A	drug	alcohol	2184832	Neurochemical data indicate that high <b>alcohol</b> seeking behavior (when compared with data from rats with low <b>alcohol</b> seeking characteristics) is associated with: a) lower (10 20%; p less than 0.05) contents of 5 HT in certain limbic regions (e.g., nucleus accumbens, frontal cortex, hypothalamus and hippocampus); b) a lower (10 15%; p less than 0.05) content of DA in the nucleus accumbens; c) higher (20 35%; p less than 0.05) densities of <strong>5 HT1A</strong> binding sites in some limbic regions (e.g., medial nucleus accumbens, medial prefrontal cortex and ventral hippocampus); and d) a greater (20 50%) density of GABA axon terminals in the nucleus accumbens.
+HTR1A	addiction	relapse	2184832	Neurochemical data indicate that high alcohol <b>seeking</b> behavior (when compared with data from rats with low alcohol <b>seeking</b> characteristics) is associated with: a) lower (10 20%; p less than 0.05) contents of 5 HT in certain limbic regions (e.g., nucleus accumbens, frontal cortex, hypothalamus and hippocampus); b) a lower (10 15%; p less than 0.05) content of DA in the nucleus accumbens; c) higher (20 35%; p less than 0.05) densities of <strong>5 HT1A</strong> binding sites in some limbic regions (e.g., medial nucleus accumbens, medial prefrontal cortex and ventral hippocampus); and d) a greater (20 50%) density of GABA axon terminals in the nucleus accumbens.
+HTR1A	drug	benzodiazepine	1973110	The present study has been designed to investigate the effects of the <strong>5 HT1A</strong> receptor agonist, ipsapirone (TVX Q 7821), a representative of a novel class of anxiolytics, and the classical <b>benzodiazepine</b> anxiolytic, <b>diazepam</b>, on cardiac and behavioural responses in an emotional stress situation.
+HTR1A	drug	benzodiazepine	1975107	The <b>benzodiazepine</b> <b>diazepam</b> (5 mg/kg) also failed to reduce immobility time, suggesting that anxiolytic properties of <strong>5 HT1A</strong> agonists did not mediate this behavioral effect.
+HTR1A	drug	benzodiazepine	2574684	The effects of several <strong>5 HT1A</strong> agonists and excitatory amino acid antagonists were compared to the standard benzodiazepines, <b>diazepam</b> and <b>chlordiazepoxide</b> (CDP) in two assays predictive of anxiolytic activity, the social interaction and elevated plus maze procedures.
+HTR1A	addiction	reward	2746512	It is likely that the hypoactivity and PRL responses of m <b>CPP</b> are mediated by 5 HT1B receptors, and the cardiodepressive effects by <strong>5 HT1A</strong> receptors.
+HTR1A	drug	opioid	2566495	8 Hydroxy 2 (di n propylamino)tetralin (8 OH DPAT) and RU 24969 have been used to investigate whether <strong>5 HT1A</strong> and 5 HT1B receptors are involved in the <b>naloxone</b> induced jumping behaviour of the chronically <b>morphine</b> dependent mouse.
+HTR1A	drug	opioid	2826954	Here we describe the potent antinociceptive action of the indolophenanthridine, CY 208 243, which has high affinities to the dopamine D1 binding and the <b>opioid</b> sites as well as to the <strong>5 HT1A</strong> site.
+HTR1A	addiction	reward	2881789	Male Sprague Dawley rats were trained to discriminate the putative <strong>5 HT1A</strong> receptor agonist, 8 hydroxy 2 (di n propylamino) tetralin (8 OH DPAT) from saline in a 2 lever <b>operant</b> drug discrimination paradigm.
+CREB1	drug	amphetamine	32670551	Cannabidiol attenuates <b>methamphetamine</b> induced conditioned place preference via the Sigma1R/AKT/GSK 3β/<strong>CREB</strong> signaling pathway in rats.
+CREB1	drug	cannabinoid	32670551	<b>Cannabidiol</b> attenuates methamphetamine induced conditioned place preference via the Sigma1R/AKT/GSK 3β/<strong>CREB</strong> signaling pathway in rats.
+CREB1	drug	amphetamine	32670551	The present study examines whether CBD has a protective effect on <b>METH</b> induced conditioned place preference (CPP) in rats by regulating the Sigma1R and AKT GSK3β <strong>CREB</strong> signaling pathway.
+CREB1	addiction	reward	32670551	The present study examines whether CBD has a protective effect on METH induced conditioned place preference (<b>CPP</b>) in rats by regulating the Sigma1R and AKT GSK3β <strong>CREB</strong> signaling pathway.
+CREB1	drug	amphetamine	32670551	The expression levels of Sigma1R, p AKT, p GSK3β, and p <strong>CREB</strong> increased significantly in the <b>METH</b> induced CPP model.
+CREB1	addiction	reward	32670551	The expression levels of Sigma1R, p AKT, p GSK3β, and p <strong>CREB</strong> increased significantly in the METH induced <b>CPP</b> model.
+CREB1	drug	amphetamine	32670551	When a pretreatment of CBD is applied, the CBD can weaken CPP in <b>METH</b> induced rats by regulating the SigmaR1/AKT/GSK 3β/<strong>CREB</strong> signaling pathway.
+CREB1	addiction	reward	32670551	When a pretreatment of CBD is applied, the CBD can weaken <b>CPP</b> in METH induced rats by regulating the SigmaR1/AKT/GSK 3β/<strong>CREB</strong> signaling pathway.
+CREB1	drug	alcohol	32599136	Brain area samples were analysed to quantify AMPAR subunits GluR1/2 and pCREB/<strong>CREB</strong> expression following <b>alcohol</b> self administration.
+CREB1	drug	alcohol	32599136	Our findings demonstrate that developmental <b>alcohol</b> exposure enhances <b>alcohol</b> intake during adolescence, which is associated with a decrease in the pCREB/<strong>CREB</strong> ratio in the hippocampus, prefrontal cortex and striatum, while the GluR1/GluR2 ratio showed a decrease in the hippocampus.
+CREB1	drug	alcohol	32599136	Furthermore, a diminished <strong>CREB</strong> signalling and glutamatergic neuroplasticity are proposed as underpinning neurobiological mechanisms involved in the sensitivity to <b>alcohol</b> reinforcing properties.
+CREB1	addiction	reward	32599136	Furthermore, a diminished <strong>CREB</strong> signalling and glutamatergic neuroplasticity are proposed as underpinning neurobiological mechanisms involved in the sensitivity to alcohol <b>reinforcing</b> properties.
+CREB1	drug	amphetamine	32466633	MeBib Suppressed <b>Methamphetamine</b> Self Administration Response via Inhibition of BDNF/ERK/<strong>CREB</strong> Signal Pathway in the Hippocampus.
+CREB1	drug	opioid	32428531	Impairment of cost benefit decision making in <b>morphine</b> dependent rats is partly mediated via the alteration of BDNF and p <strong>CREB</strong> levels in the nucleus accumbens.
+CREB1	drug	opioid	32428531	In the current study, we assessed the effects of <b>morphine</b> dependence and its withdrawal on cost benefit decision making and furthermore the involvement of BDNF and p <strong>CREB</strong> in the nucleus accumbens, a key brain area involved in decision making was measured.
+CREB1	addiction	dependence	32428531	In the current study, we assessed the effects of morphine <b>dependence</b> and its withdrawal on cost benefit decision making and furthermore the involvement of BDNF and p <strong>CREB</strong> in the nucleus accumbens, a key brain area involved in decision making was measured.
+CREB1	addiction	withdrawal	32428531	In the current study, we assessed the effects of morphine dependence and its <b>withdrawal</b> on cost benefit decision making and furthermore the involvement of BDNF and p <strong>CREB</strong> in the nucleus accumbens, a key brain area involved in decision making was measured.
+CREB1	drug	opioid	32428531	During effort based decision making in <b>morphine</b> dependent rats, BDNF decreased but there was no significant change in p <strong>CREB</strong>.
+CREB1	drug	opioid	32428531	Besides, during delay based decision making in the <b>morphine</b> dependent group, both BDNF and p <strong>CREB</strong> did not show any significant change.
+CREB1	drug	opioid	32428531	In addition, impairment of effort based decision making in <b>morphine</b> dependent rats is related to the decrease of BDNF level but not p <strong>CREB</strong>/<strong>CREB</strong> ratio in the NAc.
+CREB1	drug	opioid	32428531	However, delay based decision making defects in <b>morphine</b> dependent rats did not associate with the change in BDNF and p <strong>CREB</strong> levels in the NAc.
+CREB1	drug	nicotine	32417176	Expression analysis of hippocampal and amygdala <strong>CREB</strong> BDNF signaling pathway in <b>nicotine</b> induced reward under stress in rats.
+CREB1	addiction	reward	32417176	Expression analysis of hippocampal and amygdala <strong>CREB</strong> BDNF signaling pathway in nicotine induced <b>reward</b> under stress in rats.
+CREB1	drug	nicotine	32417176	The present study includes an expression analysis to identify the possible role of hippocampal and amygdala <strong>CREB</strong> (cAMP response element binding protein) and BDNF (Brain derived neurotrophic factor) activation in <b>nicotine</b> induced conditioned place preference (CPP) under exposure to acute or sub chronic stress.
+CREB1	addiction	reward	32417176	The present study includes an expression analysis to identify the possible role of hippocampal and amygdala <strong>CREB</strong> (cAMP response element binding protein) and BDNF (Brain derived neurotrophic factor) activation in nicotine induced conditioned place preference (<b>CPP</b>) under exposure to acute or sub chronic stress.
+CREB1	drug	nicotine	32417176	Using western blot technique, <strong>CREB</strong> phosphorylation was shown to increase in the hippocampus and the amygdala following <b>nicotine</b> induced CPP.
+CREB1	addiction	reward	32417176	Using western blot technique, <strong>CREB</strong> phosphorylation was shown to increase in the hippocampus and the amygdala following nicotine induced <b>CPP</b>.
+CREB1	drug	nicotine	32417176	In animals exposed to acute stress, the amygdala ratios of the pCREB/<strong>CREB</strong> decreased, while pre treatment of the animals with <b>nicotine</b> (0.1 mg/kg) decreased this ratio only in the hippocampus.
+CREB1	drug	nicotine	32417176	Interestingly, sub chronic stress induced increase of <b>nicotine</b> reward only decreased the hippocampal pCREB/<strong>CREB</strong> ratio.
+CREB1	addiction	reward	32417176	Interestingly, sub chronic stress induced increase of nicotine <b>reward</b> only decreased the hippocampal pCREB/<strong>CREB</strong> ratio.
+CREB1	drug	nicotine	32417176	In summary, the present study indicate that the alterations of the ratio of pCREB/<strong>CREB</strong> and also the level of BDNF in the hippocampus may be critical for enhancing <b>nicotine</b> reward under stress condition.
+CREB1	addiction	reward	32417176	In summary, the present study indicate that the alterations of the ratio of pCREB/<strong>CREB</strong> and also the level of BDNF in the hippocampus may be critical for enhancing nicotine <b>reward</b> under stress condition.
+CREB1	drug	opioid	32404265	Results showed that cAMP, <strong>CREB</strong> and PLCβ3 levels were suppressed by the application of SB 334867 (as a selective Orx1 antagonist) in <b>morphine</b> dependent rats.
+CREB1	drug	opioid	32404265	Our results unraveled that Orx1 blockade is involved in the development of <b>morphine</b> dependency through diminution of a variety of intracellular events including the cAMP, <strong>CREB</strong> and PLCβ3 levels in <b>morphine</b> dependent rats.
+CREB1	drug	opioid	32404265	Furthermore, the Orx1 blockade could decrease the percentage of tyrosine hydroxylase (TH)+/<strong>CREB</strong>+ and TH+/PLCβ3+ neurons in LC of <b>morphine</b> treated rats.
+CREB1	drug	cocaine	32329565	We also investigated the subsequent alterations on GluR2, GluR1, cAMP response element binding (<strong>CREB</strong>), and <strong>CREB</strong> phosphorylation (pCREB) in ventral tegmental area (VTA) and nucleus accumbens (NAc) induced by both MSEW and <b>cocaine</b> SA.
+CREB1	drug	opioid	32304763	In C57BL/6 mice, 17 AAG decreased <b>morphine</b> induced acute anti nociception in the hot plate test, with an increase in phosphorylated PKA and phosphorylated JNK and a decrease in phosphorylated <strong>CREB</strong> and phosphorylated ERK in murine brains.
+CREB1	drug	opioid	32113678	Significantly reduced phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) in the mPFC was observed in the mice exposed to <b>morphine</b> after the extinction training.
+CREB1	drug	opioid	32113678	Uncoupling nNOS PSD 95 reversed the <b>morphine</b> induced <strong>CREB</strong> dysfunction.
+CREB1	drug	opioid	32113678	Moreover, effects of ZL006 on the reinstatement of <b>morphine</b> CPP and <strong>CREB</strong> activation depended on nNOS PSD 95 target.
+CREB1	addiction	relapse	32113678	Moreover, effects of ZL006 on the <b>reinstatement</b> of morphine CPP and <strong>CREB</strong> activation depended on nNOS PSD 95 target.
+CREB1	addiction	reward	32113678	Moreover, effects of ZL006 on the reinstatement of morphine <b>CPP</b> and <strong>CREB</strong> activation depended on nNOS PSD 95 target.
+CREB1	drug	opioid	32113678	Together, our findings suggest that nNOS PSD 95 in the mPFC contributes to reinstatement of <b>morphine</b> CPP, possibly through <strong>CREB</strong> dysfunction, offering a potential target to prevent relapse of drug abuse.
+CREB1	addiction	relapse	32113678	Together, our findings suggest that nNOS PSD 95 in the mPFC contributes to <b>reinstatement</b> of morphine CPP, possibly through <strong>CREB</strong> dysfunction, offering a potential target to prevent <b>relapse</b> of drug abuse.
+CREB1	addiction	reward	32113678	Together, our findings suggest that nNOS PSD 95 in the mPFC contributes to reinstatement of morphine <b>CPP</b>, possibly through <strong>CREB</strong> dysfunction, offering a potential target to prevent relapse of drug abuse.
+CREB1	drug	opioid	32014377	Stressed mice also showed significant increase in TLR4, Nuclear Factor Kappa B (NF kB), inducible nitric oxide synthase (iNOS), dopamine receptor D2 (DRD2), cyclic adenosine monophosphate (cAMP) response element binding protein 1 (<strong>CREB</strong> 1) and <b>opioid</b> receptor MU 1 (OPRM 1) genes expression compared with control and LPS RS treated stressed mice.
+CREB1	drug	cocaine	31918976	Moreover, we evaluated the effects of <b>cocaine</b> SA in both sexes during adulthood, and the possible changes in GluA1, GluA2, pCREB and <strong>CREB</strong> expressions.
+CREB1	drug	amphetamine	31900897	The Potential Role of PKA/<strong>CREB</strong> Signaling Pathway Concerned with Gastrodin Administration on <b>Methamphetamine</b> Induced Conditioned Place Preference Rats and SH SY5Y Cell Line.
+CREB1	addiction	reward	31900897	In vitro, SH SY5Y cells were exposed to MA (2.0 mM) for 24 h, followed by treatment with GAS (2.0 or 4.0 mM) for 24 h. The expression levels of PKA, P PKA, <strong>CREB</strong>, and P <strong>CREB</strong> proteins in the prefrontal cortex, nucleus accumbens, and ventral tegmental area of MA induced <b>CPP</b> rats and in SH SY5Y cells were detected by Western blot analysis.
+CREB1	addiction	reward	31900897	Results also showed that MA increased the expression levels of PKA, P PKA, <strong>CREB</strong>, and p <strong>CREB</strong> proteins in the prefrontal cortex, nucleus accumbens, and ventral tegmental area of <b>CPP</b> rats and in SH SY5Y cells (p < 0.05).
+CREB1	addiction	reward	31900897	Our study suggests that GAS can attenuate the effects of MA induced <b>CPP</b> in rats by regulating the PKA/<strong>CREB</strong> signaling pathway.
+CREB1	drug	opioid	31838222	<b>Naloxone</b> precipitated withdrawal ameliorates impairment of cost benefit decision making in <b>morphine</b> treated rats: Involvement of BDNF, p GSK3 β, and p <strong>CREB</strong> in the amygdala.
+CREB1	addiction	withdrawal	31838222	Naloxone precipitated <b>withdrawal</b> ameliorates impairment of cost benefit decision making in morphine treated rats: Involvement of BDNF, p GSK3 β, and p <strong>CREB</strong> in the amygdala.
+CREB1	drug	opioid	31838222	Therefore, in the current study, we investigated the effect of subchronic exposure to <b>morphine</b> and its withdrawal on effort  and/or delay based forms of cost benefit decision making and alterations in p <strong>CREB</strong>/<strong>CREB</strong> ratio, p GSK3β/GSK3β ratio, and BDNF level during decision making in the amygdala.
+CREB1	addiction	withdrawal	31838222	Therefore, in the current study, we investigated the effect of subchronic exposure to morphine and its <b>withdrawal</b> on effort  and/or delay based forms of cost benefit decision making and alterations in p <strong>CREB</strong>/<strong>CREB</strong> ratio, p GSK3β/GSK3β ratio, and BDNF level during decision making in the amygdala.
+CREB1	drug	opioid	31838222	In <b>morphine</b> treated rats, level of BDNF and p <strong>CREB</strong>/<strong>CREB</strong> ratio reduced during both forms of decision making while p GSK3β/GSK3β ratio increased during delay based and did not have a significant difference with the control group during effort based decision making.
+CREB1	addiction	withdrawal	31838222	In addition, p <strong>CREB</strong>/<strong>CREB</strong> ratio increased only during delay based decision making on the <b>withdrawal</b> day.
+CREB1	drug	opioid	31838222	In conclusion, our data revealed that subchronic exposure to <b>morphine</b> interferes with the cost benefit decision making may be via changes in level of BDNF, p <strong>CREB</strong>/<strong>CREB</strong> and p GSK3β/GSK3β ratio in the amygdala.
+CREB1	addiction	reward	31801086	Here, to identify the relevant transcriptional factors, we perform proteomic analysis using affinity beads coated with cyclic AMP response element binding protein (<strong>CREB</strong>) binding protein (CBP), a transcriptional coactivator involved in <b>reward</b> related behavior.
+CREB1	drug	cocaine	31704270	Whereas acute <b>cocaine</b> treated mice showed transient increases in p ERK1/2/ERK1/2 and p p65/p65 NFκB ratios after <b>cocaine</b> injection, repeated <b>cocaine</b> treated mice showed transient increases in p ERK1/2/ERK1/2, p p38/p38 MAPK, p NFκB p65/NF κB p65 and p <strong>CREB</strong>/<strong>CREB</strong> ratios.
+CREB1	drug	cocaine	31704270	Baseline p p38/p38 MAPK and p <strong>CREB</strong>/<strong>CREB</strong> ratios were downregulated in repeated <b>cocaine</b> treated mice.
+CREB1	drug	opioid	31689445	Besides, (m CF3 PhSe)2 downregulated the proBDNF/p 75NTR/JNK pro apoptotic pathway without affecting the mBDNF/TrkB/ERK/<strong>CREB</strong> pro survival signaling in the hippocampus of <b>morphine</b> withdrawn mice.
+CREB1	drug	opioid	31639423	The D1R antagonist reduced the withdrawal response in <b>morphine</b> exposed rats and decreased the expression of Ca2+/calmodulin dependent protein kinase II (CaMKII), phosphorylated extracellular signal regulated kinase (p ERK) and cAMP response element binding protein (<strong>CREB</strong>) in the PAG.
+CREB1	addiction	withdrawal	31639423	The D1R antagonist reduced the <b>withdrawal</b> response in morphine exposed rats and decreased the expression of Ca2+/calmodulin dependent protein kinase II (CaMKII), phosphorylated extracellular signal regulated kinase (p ERK) and cAMP response element binding protein (<strong>CREB</strong>) in the PAG.
+CREB1	drug	opioid	31639423	Taken together, the results suggest that D1R antagonist decreased the withdrawal response in <b>morphine</b> exposed rats by downregulating the downstream factors, CaMKII, p ERK and <strong>CREB</strong>.
+CREB1	addiction	withdrawal	31639423	Taken together, the results suggest that D1R antagonist decreased the <b>withdrawal</b> response in morphine exposed rats by downregulating the downstream factors, CaMKII, p ERK and <strong>CREB</strong>.
+CREB1	drug	nicotine	31637050	However, Rap1 protein was elevated and <strong>CREB</strong> phosphorylation was reduced in female <b>nicotine</b> place conditioning mice.
+CREB1	drug	opioid	31616243	oligodeoxynucleotide (ODN) antisense to cAMP responsive element binding protein (<strong>CREB</strong>) attenuated <b>morphine</b> induced hyperalgesia.
+CREB1	drug	opioid	31616243	Real time polymerase chain reaction (RT PCR) analysis showed that <strong>CREB</strong> downstream genes expressions were significantly up regulated 96 h after <b>morphine</b> injection in spinal cord.
+CREB1	drug	opioid	31616243	Together, our data suggest that central ERK is involved in the analgesic and hyperalgesic effects of <b>morphine</b> while JNK, p38, and <strong>CREB</strong> are involved in the <b>morphine</b> induced delayed hyperalgesia.
+CREB1	drug	cocaine	31446159	After CPP induced by <b>cocaine</b>, defeated Cx3cr1 deficient mice showed a decrease in the p p65/p65 NFκB and pCREB/<strong>CREB</strong> ratio in the HPC, and an increase in the hippocampal levels of CX3CL1 and p p38/p38 MAPK relation.
+CREB1	addiction	reward	31446159	After <b>CPP</b> induced by cocaine, defeated Cx3cr1 deficient mice showed a decrease in the p p65/p65 NFκB and pCREB/<strong>CREB</strong> ratio in the HPC, and an increase in the hippocampal levels of CX3CL1 and p p38/p38 MAPK relation.
+CREB1	addiction	sensitization	31378002	Development of <b>sensitization</b> and its expression after withdrawal were tested, as well as threshold for long term potentiation in hippocampus, NOS 1, and <strong>CREB</strong> protein levels and gene expression.
+CREB1	addiction	withdrawal	31378002	Development of sensitization and its expression after <b>withdrawal</b> were tested, as well as threshold for long term potentiation in hippocampus, NOS 1, and <strong>CREB</strong> protein levels and gene expression.
+CREB1	drug	opioid	31253357	The effects of an MCU inhibitor, antisense oligodeoxynucleotide against cyclic adenosine monophosphate response element (CRE) binding protein (<strong>CREB</strong>) or cytoplasmic polyadenylation element binding protein 1 (CPEB1) in <b>morphine</b> tolerance were examined.
+CREB1	drug	opioid	31253357	Spinal <b>morphine</b> tolerance was associated with an increased expression of neuronal MCU, phospho <strong>CREB</strong> (pCREB), and CPEB1 in the spinal cord dorsal horn.
+CREB1	drug	opioid	31253357	Intrathecal antisense oligodeoxynucleotide against <strong>CREB</strong> or CPEB1 restored the anti nociceptive effects of <b>morphine</b> compared with mismatch oligodeoxynucleotide in von Frey test and hotplate test.
+CREB1	drug	amphetamine	31078920	Moreover, phosphorylation of ERK1/2 and <strong>CREB</strong> was increased after <b>METH</b> and LPS exposure but decreased by SCH 23390.
+CREB1	drug	opioid	31042569	The purpose of the present study was to investigate the influence of sex on the expression and duration of spontaneous somatic <b>morphine</b> withdrawal syndrome, and to characterize the relationship between spontaneous somatic withdrawal symptoms and cellular activation (measured as phosphorylated <strong>CREB</strong>; pCREB), in the GABAergic tVTA in male and female rats.
+CREB1	addiction	withdrawal	31042569	The purpose of the present study was to investigate the influence of sex on the expression and duration of spontaneous somatic morphine <b>withdrawal</b> syndrome, and to characterize the relationship between spontaneous somatic <b>withdrawal</b> symptoms and cellular activation (measured as phosphorylated <strong>CREB</strong>; pCREB), in the GABAergic tVTA in male and female rats.
+CREB1	drug	amphetamine	30993081	In both experiments, duloxetine activated cAMP, <strong>CREB</strong>, and BDNF proteins' expression in <b>methamphetamine</b> treated rats.
+CREB1	drug	amphetamine	30993081	Duloxetine can protect the brain against <b>methamphetamine</b> withdrawal induced mood and motor disturbances and can also inhibit <b>methamphetamine</b> induced cognitive impairment, possibly via cAMP/<strong>CREB</strong>/BDNF signaling pathway.
+CREB1	addiction	withdrawal	30993081	Duloxetine can protect the brain against methamphetamine <b>withdrawal</b> induced mood and motor disturbances and can also inhibit methamphetamine induced cognitive impairment, possibly via cAMP/<strong>CREB</strong>/BDNF signaling pathway.
+CREB1	drug	opioid	30919988	Effect of pretreatment with intracerebroventricular injection of minocycline on <b>morphine</b> induced memory impairment in passive avoidance test: Role of P <strong>CREB</strong> and c Fos expression in the dorsal hippocampus and basolateral amygdala regions.
+CREB1	drug	opioid	30919988	The results of immunohistochemistry analysis demonstrated that <b>morphine</b> decreased expression of P <strong>CREB</strong> positive cells compared to saline control group in the BLA, but not in the dorsal hippocampus.
+CREB1	drug	opioid	30919988	In summary, our results indicated that pretreatment with ICV injection of minocycline prevented <b>morphine</b> induced memory impairment and increased P <strong>CREB</strong> expression in the dorsal hippocampus and BLA, which may explain its memory improvement property.
+CREB1	drug	amphetamine	30867225	The AT1R PLCβ <strong>CREB</strong> signaling pathway was found to be associated with the effect of AT1R on the drug taking and drug seeking behavior involving <b>METH</b> use disorder.
+CREB1	addiction	relapse	30867225	The AT1R PLCβ <strong>CREB</strong> signaling pathway was found to be associated with the effect of AT1R on the drug taking and drug <b>seeking</b> behavior involving METH use disorder.
+CREB1	drug	opioid	30654135	It also examines the effects of compounds that alter <strong>CREB</strong> signaling and epigenetic mechanisms in animal model of <b>heroin</b> relapse.
+CREB1	addiction	relapse	30654135	It also examines the effects of compounds that alter <strong>CREB</strong> signaling and epigenetic mechanisms in animal model of heroin <b>relapse</b>.
+CREB1	drug	opioid	30632799	<b>Tramadol</b> induces changes in Δ FosB, µ <b>opioid</b> receptor, and p <strong>CREB</strong> level in the nucleus accumbens and prefrontal cortex of male Wistar rat.
+CREB1	drug	opioid	30632799	In this study, the effects of acute and chronic <b>tramadol</b> treatments on MOR, ΔFosB, and <strong>CREB</strong> levels were studied.
+CREB1	drug	opioid	30632799	In the NAC, acute <b>tramadol</b> exposure increases the levels of MOR and p <strong>CREB</strong>.
+CREB1	drug	opioid	30632799	Moreover, chronic <b>tramadol</b> administration in this region results in elevated levels of MOR, ΔFosB and p <strong>CREB</strong> compared with saline treated rats.
+CREB1	drug	opioid	30632799	The levels of MOR and p <strong>CREB</strong> in the PFC increased in both acute and chronic <b>tramadol</b> exposure.
+CREB1	drug	opioid	30632799	We concluded that both <strong>CREB</strong> and ΔFosB played a role in <b>tramadol</b> dependence.
+CREB1	addiction	dependence	30632799	We concluded that both <strong>CREB</strong> and ΔFosB played a role in tramadol <b>dependence</b>.
+CREB1	drug	cocaine	30622460	Furthermore, we highlight future directions to elucidate the interaction between the prefrontal cortex (PFC) and key intermediaries including ΔFosB, cAMP response element binding protein (<strong>CREB</strong>) and cyclin dependent kinase 5 (CDK5) to highlight possible mechanisms that underlie stress induced acceleration of the progression to a <b>cocaine</b> use disorder diagnosis.
+CREB1	drug	amphetamine	30544074	Additional experiments showed that expression of brain derived neurotrophic factor (BDNF), phosphorylated tropomyosin receptor kinase B (p TrkB), phosphorylated extracellular signal related kinase 1/2 (p ERK1/2) and phosphorylated cAMP response element binding protein (p <strong>CREB</strong>) were decreased in the hippocampus and prefrontal cortex of mice in <b>METH</b> group and the level of mitogen activated protein kinase phosphatase 1 (MKP 1) was increased.
+CREB1	drug	amphetamine	30544074	Combined, our data show that withdrawal from chronic <b>METH</b> exposure induces anxiety and depression like behavior associated with aberrant changes of proteins in BDNF ERK <strong>CREB</strong> pathway, providing new evidence for the involvement of BDNF pathway in the negative emotional states induced by withdrawal from <b>METH</b>.
+CREB1	addiction	withdrawal	30544074	Combined, our data show that <b>withdrawal</b> from chronic METH exposure induces anxiety and depression like behavior associated with aberrant changes of proteins in BDNF ERK <strong>CREB</strong> pathway, providing new evidence for the involvement of BDNF pathway in the negative emotional states induced by <b>withdrawal</b> from METH.
+CREB1	drug	alcohol	30371539	Green tea polyphenols ameliorate <b>ethanol</b> induced spatial learning and memory impairments by enhancing hippocampus NMDAR1 expression and <strong>CREB</strong> activity in rats.
+CREB1	drug	alcohol	30371539	Moreover, 8 week <b>ethanol</b> gavage decreased the density of pyramidal layer neurons, expression of NMDAR1, and <strong>CREB</strong> phosphorylation in the hippocampus region.
+CREB1	drug	alcohol	30371539	The current findings indicated that GTP intervention can improve <b>ethanol</b> induced spatial learning and memory impairments in rats after <b>ethanol</b> withdrawal, which is related to the upregulated density of pyramidal layer neurons, expression of NMDAR1, and <strong>CREB</strong> phosphorylation in the hippocampus region.
+CREB1	addiction	withdrawal	30371539	The current findings indicated that GTP intervention can improve ethanol induced spatial learning and memory impairments in rats after ethanol <b>withdrawal</b>, which is related to the upregulated density of pyramidal layer neurons, expression of NMDAR1, and <strong>CREB</strong> phosphorylation in the hippocampus region.
+CREB1	drug	alcohol	30336151	Because extended amygdala regions have documented roles in stress, reward, and stress induced changes in reward, we also tested the effect of acute <b>alcohol</b> on <strong>CREB</strong> phosphorylation (pCREB) and striatal enriched protein tyrosine phosphatase (STEP) expression in central amygdala (CeA) and bed nucleus of stria terminalis (BNST).
+CREB1	addiction	reward	30336151	Because extended amygdala regions have documented roles in stress, <b>reward</b>, and stress induced changes in <b>reward</b>, we also tested the effect of acute alcohol on <strong>CREB</strong> phosphorylation (pCREB) and striatal enriched protein tyrosine phosphatase (STEP) expression in central amygdala (CeA) and bed nucleus of stria terminalis (BNST).
+CREB1	drug	opioid	30292787	TRPV1 modulates <b>morphine</b> self administration via activation of the CaMKII <strong>CREB</strong> pathway in the nucleus accumbens.
+CREB1	drug	opioid	30292787	We found that treatment with a selective TRPV1 antagonist, SB366791, significantly decreased the <b>morphine</b> SA induced activation of Ca2+/calmodulin dependent protein kinase II (CaMKII), Akt and the cAMP response element binding protein (<strong>CREB</strong>) in the nucleus accumbens (NAc).
+CREB1	drug	opioid	30292787	Taken together, our findings highlight that TRPV1 plays an important role in <b>morphine</b> addiction, likely via activation of the CaMKII <strong>CREB</strong> pathway in the NAc.
+CREB1	addiction	addiction	30292787	Taken together, our findings highlight that TRPV1 plays an important role in morphine <b>addiction</b>, likely via activation of the CaMKII <strong>CREB</strong> pathway in the NAc.
+CREB1	drug	cannabinoid	30273593	In parallel, CBD increased expression of type 1 <b>cannabinoid</b> receptor, MAPK <strong>CREB</strong> phosphorylation, BDNF expression, and neural cell proliferation in the hippocampus, and reduced the GluA1/2 AMPA subunit receptor ratio in the striatum.
+CREB1	drug	opioid	30240785	The expressions of Trx 1, N methyl d aspartate receptor 2B subunit (NR2B), phosphorylated Ca2+/calmodulin dependent protein kinase II (p CaMKII), phosphorylated extracellular signaling regulated kinases (p ERK), and phosphorylated cAMP response element binding protein (p <strong>CREB</strong>) were induced in nucleus accumbens (NAc) and hippocampus by <b>morphine</b> or GGA, whereas these proteins were not changed by <b>morphine</b> in GGA treated mice.
+CREB1	drug	opioid	30227624	Sinomenine Protects Against <b>Morphine</b> Dependence through the NMDAR1/CAMKII/<strong>CREB</strong> Pathway: A Possible Role of Astrocyte Derived Exosomes.
+CREB1	addiction	dependence	30227624	Sinomenine Protects Against Morphine <b>Dependence</b> through the NMDAR1/CAMKII/<strong>CREB</strong> Pathway: A Possible Role of Astrocyte Derived Exosomes.
+CREB1	drug	opioid	30227624	Moreover, sinomenine inhibited the expressions of p NMDAR1/NMDAR1, p CAMKII/CAMKII, and p <strong>CREB</strong>/<strong>CREB</strong> in the hippocampusof <b>morphine</b> dependent mice and SH SY5Y cells.
+CREB1	drug	opioid	30227624	Results showed that Sino exo reduced the level of cAMP, intracellular Ca2+, and the expression of p CAMKII/CAMKII and p <strong>CREB</strong>/<strong>CREB</strong> in <b>morphine</b> treated SH SY5Y cells.
+CREB1	drug	opioid	30227624	In conclusion, we demonstrated that sinomenine exhibited protective effects against <b>morphine</b> dependencein vivo and in vitro through theNMDAR1/CAMKII/<strong>CREB</strong> pathway.
+CREB1	drug	opioid	30170186	Modulatory role of the intra accumbal CB1 receptor in protein level of the c fos and pCREB/<strong>CREB</strong> ratio in the nucleus accumbens and ventral tegmental area in extinction and <b>morphine</b> seeking in the rats.
+CREB1	addiction	relapse	30170186	Modulatory role of the intra accumbal CB1 receptor in protein level of the c fos and pCREB/<strong>CREB</strong> ratio in the nucleus accumbens and ventral tegmental area in extinction and morphine <b>seeking</b> in the rats.
+CREB1	drug	opioid	30170186	The present study tried to investigate the role of the intra accumbal CB1 receptor in the c fos level and pCREB/<strong>CREB</strong> ratio in the NAc and the VTA during reinstatement phase of <b>morphine</b> induced conditioned place preference (CPP) by western blotting.
+CREB1	addiction	relapse	30170186	The present study tried to investigate the role of the intra accumbal CB1 receptor in the c fos level and pCREB/<strong>CREB</strong> ratio in the NAc and the VTA during <b>reinstatement</b> phase of morphine induced conditioned place preference (CPP) by western blotting.
+CREB1	addiction	reward	30170186	The present study tried to investigate the role of the intra accumbal CB1 receptor in the c fos level and pCREB/<strong>CREB</strong> ratio in the NAc and the VTA during reinstatement phase of morphine induced conditioned place preference (<b>CPP</b>) by western blotting.
+CREB1	drug	opioid	30170186	Intra accumbal administration of the CB1 agonist during the extinction period of <b>morphine</b> induced CPP reduced the pCREB/<strong>CREB</strong> ratio in the NAc.
+CREB1	addiction	reward	30170186	Intra accumbal administration of the CB1 agonist during the extinction period of morphine induced <b>CPP</b> reduced the pCREB/<strong>CREB</strong> ratio in the NAc.
+CREB1	drug	cannabinoid	30170186	In conclusion, the results presented here provide compelling evidence of the modulation and involvement of the c fos and the <strong>CREB</strong> molecules in the <b>cannabinoid</b> opioid interaction of the brain reward system in the CPP paradigm.
+CREB1	drug	opioid	30170186	In conclusion, the results presented here provide compelling evidence of the modulation and involvement of the c fos and the <strong>CREB</strong> molecules in the cannabinoid <b>opioid</b> interaction of the brain reward system in the CPP paradigm.
+CREB1	addiction	reward	30170186	In conclusion, the results presented here provide compelling evidence of the modulation and involvement of the c fos and the <strong>CREB</strong> molecules in the cannabinoid opioid interaction of the brain <b>reward</b> system in the <b>CPP</b> paradigm.
+CREB1	drug	opioid	30147637	Over expression of CCK1R reversed <strong>CREB</strong> and ERK1/2 activation in HEK293 hMOR cells exposed to <b>morphine</b>.
+CREB1	drug	opioid	30147637	Our study identifies over expression of CCK1R significantly blocked <b>morphine</b> dependence, which was related with phosphorylation of <strong>CREB</strong>, and ERK1/2 signaling activation.
+CREB1	addiction	dependence	30147637	Our study identifies over expression of CCK1R significantly blocked morphine <b>dependence</b>, which was related with phosphorylation of <strong>CREB</strong>, and ERK1/2 signaling activation.
+CREB1	drug	opioid	30147637	While over expression of CCK2R promoted <b>morphine</b> dependence, which was related with phosphorylation of <strong>CREB</strong> but not ERK1/2 signaling activation.
+CREB1	addiction	dependence	30147637	While over expression of CCK2R promoted morphine <b>dependence</b>, which was related with phosphorylation of <strong>CREB</strong> but not ERK1/2 signaling activation.
+CREB1	drug	alcohol	29991681	Adolescent <b>alcohol</b> exposure epigenetically regulates <strong>CREB</strong> signaling in the adult amygdala.
+CREB1	drug	alcohol	29991681	The transcription factor cAMP response element binding (<strong>CREB</strong>) protein is involved in the neuronal response to adult <b>ethanol</b> exposure, but its role in the enduring effects of adolescent <b>alcohol</b> exposure in adulthood is unknown.
+CREB1	drug	alcohol	29991681	We exposed male rats to adolescent intermittent <b>ethanol</b> (AIE) or saline (AIS) during post natal days 28 41 and evaluated the epigenetic regulation of <strong>CREB</strong> dynamics in the adult amygdala.
+CREB1	drug	alcohol	29991681	AIE exposure also causes deficits in <strong>Creb1</strong>, Cbp, and p300 mRNA expression in the amygdala of AIE adult rats which are normalized after acute <b>ethanol</b> exposure.
+CREB1	drug	alcohol	29991681	Interestingly, occupancy of acetylated histone H3K9/14 proteins at specific locations in the <strong>Creb1</strong>, Cbp, and p300 gene promoter regions was decreased in the amygdala of AIE adult rats and was normalized by acute <b>ethanol</b> exposure.
+CREB1	drug	alcohol	29991681	These results suggest that AIE exposure epigenetically reduces <strong>CREB</strong> and other related transcriptional activators in the amygdala in adulthood that may be associated with the behavioral effects of adolescent <b>alcohol</b> exposure.
+CREB1	drug	amphetamine	29981334	We also examined the expression of N methyl D asparate (NMDA) receptor 2B subunit (GluN2b), the levels of phosphorylated extracellular signal regulated kinase (p ERK) and phosphorylated cAMP response element binding protein (p <strong>CREB</strong>) in the NAc by western blot analysis, and found that the GluN2b expression, p ERK and p <strong>CREB</strong> levels were increased in the NAc in response to low dose <b>METH</b> in AAV shRNA mTrx 1 mice, but were not changed in control and AAV vehicle mice.
+CREB1	drug	amphetamine	29981334	These data indicate that the increased GluN2b expression, and p ERK and p <strong>CREB</strong> levels in the NAc of AAV shRNA mTrx 1 mice may be responsible for the <b>METH</b> primed reinstatement.
+CREB1	addiction	relapse	29981334	These data indicate that the increased GluN2b expression, and p ERK and p <strong>CREB</strong> levels in the NAc of AAV shRNA mTrx 1 mice may be responsible for the METH primed <b>reinstatement</b>.
+CREB1	addiction	reward	29728647	Combining conditioned place preference (<b>CPP</b>) with molecular analyses, we investigated the DA D1 receptor (D1R) and extracellular signal regulated kinase (ERK) cAMP response element binding protein (<strong>CREB</strong>) signaling, as well as DA D2 receptor (D2R) and protein kinase B (PKB or Akt)/glycogen synthase kinase 3 (GSK3) signaling in the ventral hippocampus (vHip) and medial prefrontal cortex (mPFC) during the formation of opiate related associative memories.
+CREB1	drug	opioid	29728647	<b>Morphine</b> CPP acquisition increased the activity of the D1R ERK <strong>CREB</strong> pathway in both the vHip and mPFC.
+CREB1	addiction	reward	29728647	Morphine <b>CPP</b> acquisition increased the activity of the D1R ERK <strong>CREB</strong> pathway in both the vHip and mPFC.
+CREB1	drug	opioid	29728647	Furthermore, integrated D1R ERK <strong>CREB</strong> and D2R Akt GSK3 pathways in the vHip mPFC circuit are required for the acquisition and retrieval of the <b>morphine</b> contextual memory, respectively.
+CREB1	drug	alcohol	29655081	PI3K AKT GSK3β <strong>CREB</strong> signaling pathway regulates anxiety like behavior in rats following <b>alcohol</b> withdrawal.
+CREB1	addiction	withdrawal	29655081	PI3K AKT GSK3β <strong>CREB</strong> signaling pathway regulates anxiety like behavior in rats following alcohol <b>withdrawal</b>.
+CREB1	drug	alcohol	29655081	Moreover, the PI3K AKT GSK3β signaling pathway was activated after <b>alcohol</b> withdrawal, and phosphorylation of the downstream cAMP response element binding protein (<strong>CREB</strong>) was increased.
+CREB1	addiction	withdrawal	29655081	Moreover, the PI3K AKT GSK3β signaling pathway was activated after alcohol <b>withdrawal</b>, and phosphorylation of the downstream cAMP response element binding protein (<strong>CREB</strong>) was increased.
+CREB1	drug	alcohol	29655081	Our results suggest that activating the PI3K AKT GSK3β <strong>CREB</strong> pathway in the mPFC is an important contributor to the molecular mechanisms underlying <b>alcohol</b> withdrawal.
+CREB1	addiction	withdrawal	29655081	Our results suggest that activating the PI3K AKT GSK3β <strong>CREB</strong> pathway in the mPFC is an important contributor to the molecular mechanisms underlying alcohol <b>withdrawal</b>.
+CREB1	drug	amphetamine	29580892	Cocaine  and <b>amphetamine</b> regulated transcript peptide (CART) induced reward behavior is mediated via Gi/o dependent phosphorylation of PKA/ERK/<strong>CREB</strong> pathway.
+CREB1	drug	cocaine	29580892	<b>Cocaine</b>  and amphetamine regulated transcript peptide (CART) induced reward behavior is mediated via Gi/o dependent phosphorylation of PKA/ERK/<strong>CREB</strong> pathway.
+CREB1	addiction	reward	29580892	Cocaine  and amphetamine regulated transcript peptide (CART) induced <b>reward</b> behavior is mediated via Gi/o dependent phosphorylation of PKA/ERK/<strong>CREB</strong> pathway.
+CREB1	addiction	reward	29580892	Herein, we investigate the involvement of Gi/o dependent protein kinase A (PKA)/extracellular signal regulated kinase (ERK)/cAMP response element binding protein (<strong>CREB</strong>) signaling in CART induced <b>reward</b> behavior.
+CREB1	addiction	reward	29580892	<b>ICSS</b> or CART induced <strong>CREB</strong> mRNA expression in Acb and VTA was attenuated by U0126.
+CREB1	addiction	reward	29580892	We suggest that recruitment of Gi/o dependent PKA/ERK/<strong>CREB</strong> phosphorylation signaling in Acb and VTA might play an important role in CART induced <b>reward</b> behavior.
+CREB1	addiction	addiction	29576706	Increasing evidence supports the contributions of cAMP response element binding protein (<strong>CREB</strong>), nuclear receptor related 1 (Nurr1), and brain derived neurotrophic factor (BDNF) in modulating neural and behavioral plasticity which was induced by <b>addictive</b> drugs.
+CREB1	drug	psychedelics	29576706	To investigate the effects of Rhy on the behavior and the levels of phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>), Nurr1, and BDNF in the hippocampus of <b>ketamine</b> induced conditioned place preference (CPP) rats.
+CREB1	addiction	reward	29576706	To investigate the effects of Rhy on the behavior and the levels of phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>), Nurr1, and BDNF in the hippocampus of ketamine induced conditioned place preference (<b>CPP</b>) rats.
+CREB1	drug	psychedelics	29576706	At the same time, expression of p <strong>CREB</strong>, Nurr1, and BDNF, which was significantly increased by <b>ketamine</b>, was restored in the Rhy  treated group.
+CREB1	drug	psychedelics	29576706	This study indicates that Rhy can reverse the reward effect induced by <b>ketamine</b> in rats and the mechanism can probably be related to regulate the hippocampal protein expression of p <strong>CREB</strong>, Nurr1, and BDNF.
+CREB1	addiction	reward	29576706	This study indicates that Rhy can reverse the <b>reward</b> effect induced by ketamine in rats and the mechanism can probably be related to regulate the hippocampal protein expression of p <strong>CREB</strong>, Nurr1, and BDNF.
+CREB1	drug	psychedelics	29576706	P <strong>CREB</strong>, Nurr1 and BDNF play an important role in the formation of <b>ketamine</b> induced place preference in ratsRhynchophylline reversed the expression of p <strong>CREB</strong>, Nurr1 and BDNF which was activated by <b>ketamine</b> in the hippocampusRhynchophylline demonstrates the potential effect of mediates <b>ketamine</b> induced rewarding effect.
+CREB1	drug	amphetamine	29576706	Abbreviations used: Rhy: Rhynchophylline; <strong>CREB</strong>: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; BDNF: Brain derived neurotrophic factor; CPP: Conditioned place preference; NMDA: N methyl D aspartic acid; <b>METH</b>: <b>Methamphetamine</b>; CNS: Central nervous system; PFA: Paraformaldehyde; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+CREB1	addiction	reward	29576706	Abbreviations used: Rhy: Rhynchophylline; <strong>CREB</strong>: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; BDNF: Brain derived neurotrophic factor; <b>CPP</b>: Conditioned place preference; NMDA: N methyl D aspartic acid; METH: Methamphetamine; CNS: Central nervous system; PFA: Paraformaldehyde; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+CREB1	drug	psychedelics	29476799	However, the transcription of the protein upstream of Nurr1, cyclic adenosine monophosphate response element binding protein (<strong>CREB</strong>), did not show any significant differences between the <b>ketamine</b> group and the <b>ketamine</b> + rhynchophylline group.
+CREB1	drug	psychedelics	29476799	However, after rhynchophylline intervention, p <strong>CREB</strong> showed significant differences between the <b>ketamine</b> and the <b>ketamine</b> + rhynchophylline groups.
+CREB1	drug	psychedelics	29476799	In summary, miR 331 5p is a key regulatory factor of Nurr1, and rhynchophylline can participate in the process of resistance to <b>ketamine</b> addiction through the miR 331 5p/Nurr1/BDNF pathway or inhibition of <strong>CREB</strong> phosphorylation.
+CREB1	addiction	addiction	29476799	In summary, miR 331 5p is a key regulatory factor of Nurr1, and rhynchophylline can participate in the process of resistance to ketamine <b>addiction</b> through the miR 331 5p/Nurr1/BDNF pathway or inhibition of <strong>CREB</strong> phosphorylation.
+CREB1	drug	amphetamine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, neuropeptide Y, pro opiomelanocortin, and cocaine  and <b>amphetamine</b> related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (AMPK), mechanistic target of rapamycin and cAMP response element binding protein (<strong>CREB</strong>).
+CREB1	drug	cocaine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, neuropeptide Y, pro opiomelanocortin, and <b>cocaine</b>  and amphetamine related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (AMPK), mechanistic target of rapamycin and cAMP response element binding protein (<strong>CREB</strong>).
+CREB1	drug	nicotine	29100904	<b>Nicotine</b> induced <strong>CREB</strong> and DeltaFosB activity is modified by caffeine in the brain reward system of the rat.
+CREB1	addiction	reward	29100904	Nicotine induced <strong>CREB</strong> and DeltaFosB activity is modified by caffeine in the brain <b>reward</b> system of the rat.
+CREB1	drug	opioid	29054430	NMDA receptor dependent changes in c fos and p <strong>CREB</strong> signaling following extinction and reinstatement of <b>morphine</b> place preference.
+CREB1	addiction	relapse	29054430	NMDA receptor dependent changes in c fos and p <strong>CREB</strong> signaling following extinction and <b>reinstatement</b> of morphine place preference.
+CREB1	drug	opioid	29054430	Therefore, in the present study, we tried to evaluate the effect of antagonism of NMDA glutamate receptors on the p <strong>CREB</strong>/<strong>CREB</strong> ratio and c fos expression in the NAc, PFC and HIP during these two phases of <b>morphine</b> CPP in male adult albino Wistar rats.
+CREB1	addiction	reward	29054430	Therefore, in the present study, we tried to evaluate the effect of antagonism of NMDA glutamate receptors on the p <strong>CREB</strong>/<strong>CREB</strong> ratio and c fos expression in the NAc, PFC and HIP during these two phases of morphine <b>CPP</b> in male adult albino Wistar rats.
+CREB1	drug	opioid	29054430	Therefore, it can be assumed that consolidation and reconsolidation of <b>morphine</b> memory via intra PFC,  NAc and  HIP NMDA glutamate receptors are in accordance with changes in p <strong>CREB</strong>/<strong>CREB</strong> ratio and c fos levels.
+CREB1	drug	nicotine	29042206	In addition, the effect of α asarone or bupropion on the hippocampal pCREB, <strong>CREB</strong> and BDNF levels during <b>nicotine</b> withdrawal were measured.
+CREB1	addiction	withdrawal	29042206	In addition, the effect of α asarone or bupropion on the hippocampal pCREB, <strong>CREB</strong> and BDNF levels during nicotine <b>withdrawal</b> were measured.
+CREB1	drug	opioid	29031903	In conclusion, we found that agmatine abolished chronic <b>morphine</b> induced decrease in proliferation of hippocampal progenitors in vivo and in vitro, which may be due to the increase in cAMP <strong>CREB</strong> BDNF signaling.
+CREB1	drug	amphetamine	28842817	Chromatin immunoprecipitation (ChIP) assays revealed that <b>METH</b> increased the abundance of phosphorylated <strong>CREB</strong> (pCREB) at the promoter of Cartpt but not at Avp or Crh DNA sequences.
+CREB1	drug	amphetamine	28842817	Together, these results indicate that <b>METH</b> produced changes in neuropeptide transcription by both activation of the cAMP/<strong>CREB</strong> pathway and stimulation of TET dependent DNA hydroxymethylation.
+CREB1	drug	amphetamine	28782589	In this study, we examined the rewarding effect after <b>METH</b> administration by conditioned place preference (CPP) of mice, and detected the levels of dopamine and the activity of cAMP responsive element binding protein (<strong>CREB</strong>), the expressions of ΔFosB and cyclin dependent kinase 5 (CDK5) in the ventral tegmental area (VTA) and nucleus accumbens (NAc) in mice.
+CREB1	addiction	reward	28782589	In this study, we examined the rewarding effect after METH administration by conditioned place preference (<b>CPP</b>) of mice, and detected the levels of dopamine and the activity of cAMP responsive element binding protein (<strong>CREB</strong>), the expressions of ΔFosB and cyclin dependent kinase 5 (CDK5) in the ventral tegmental area (VTA) and nucleus accumbens (NAc) in mice.
+CREB1	drug	amphetamine	28782589	The activity of <strong>CREB</strong> and the expressions of ΔFosB and CDK5 were increased by <b>METH</b> in wile type mice, which were not further increased in TG mice.
+CREB1	drug	amphetamine	28782589	These results suggest that overexpression of Trx 1 may occlude the CPP induced by <b>METH</b> through regulating the activity of <strong>CREB</strong> and the expression of ΔFosB.
+CREB1	addiction	reward	28782589	These results suggest that overexpression of Trx 1 may occlude the <b>CPP</b> induced by METH through regulating the activity of <strong>CREB</strong> and the expression of ΔFosB.
+CREB1	drug	amphetamine	28681200	Canonical pathway analysis revealed that a high number of <b>METH</b> addiction related miRNAs play important roles in the MAPK, <strong>CREB</strong>, G Protein Couple Receptor and GnRH Signaling pathways.
+CREB1	addiction	addiction	28681200	Canonical pathway analysis revealed that a high number of METH <b>addiction</b> related miRNAs play important roles in the MAPK, <strong>CREB</strong>, G Protein Couple Receptor and GnRH Signaling pathways.
+CREB1	drug	opioid	28611691	<b>Morphine</b> Reward Promotes Cue Sensitive Learning: Implication of Dorsal Striatal <strong>CREB</strong> Activity.
+CREB1	addiction	reward	28611691	Morphine <b>Reward</b> Promotes Cue Sensitive Learning: Implication of Dorsal Striatal <strong>CREB</strong> Activity.
+CREB1	drug	amphetamine	28319198	<b>Methamphetamine</b> induces Shati/Nat8L expression in the mouse nucleus accumbens via <strong>CREB</strong>  and dopamine D1 receptor dependent mechanism.
+CREB1	drug	amphetamine	28319198	Next, we investigated the response of <b>METH</b> to Shati/Nat8L expression and <strong>CREB</strong> activity using mouse brain slices of NAc, <b>METH</b> administration to mice, and western blotting for <strong>CREB</strong> activity of specific dopamine receptor signals in vivo and ex vivo.
+CREB1	drug	amphetamine	28319198	We found that <b>METH</b> activates <strong>CREB</strong> binding to the Shati/Nat8L promoter to induce the Shati/Nat8L mRNA expression.
+CREB1	drug	amphetamine	28319198	These results showed that the Shati/Nat8L mRNA was increased by <b>METH</b> induced <strong>CREB</strong> pathway via dopamine D1 receptor signaling in mouse NAc.
+CREB1	drug	alcohol	28174112	Acute <b>alcohol</b> exposure produces an anxiolytic response which is associated with the opening of chromatin due to increased histone acetylation, increased <strong>CREB</strong> binding protein (CBP) levels, and histone deacetylase (HDAC) inhibition.
+CREB1	drug	alcohol	28095363	Curcumin confers neuroprotection against <b>alcohol</b> induced hippocampal neurodegeneration via <strong>CREB</strong> BDNF pathway in rats.
+CREB1	drug	alcohol	28095363	Furthermore, <b>alcohol</b> induced significant reduction were observed in reduced form of glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and <strong>CREB</strong>, BDNF and Bcl 2 levels.
+CREB1	drug	alcohol	28095363	Curcumin can act as a neuroprotective agent against neurodegenerative effects of <b>alcohol</b> abuse, probably via activation of <strong>CREB</strong> BDNF signaling pathway.
+CREB1	drug	alcohol	27901267	Similarly, the combination of <b>alcohol</b> and hypergravity suppressed the levels of STAT3, FOXO1/3, C/EBPβ, and <strong>CREB</strong>, transcription factors necessary for cell survival.
+CREB1	drug	nicotine	27848935	Distinct Roles of <strong>CREB</strong> Within the Ventral and Dorsal Hippocampus in Mediating <b>Nicotine</b> Withdrawal Phenotypes.
+CREB1	addiction	withdrawal	27848935	Distinct Roles of <strong>CREB</strong> Within the Ventral and Dorsal Hippocampus in Mediating Nicotine <b>Withdrawal</b> Phenotypes.
+CREB1	drug	nicotine	27848935	Previous work indicates that hippocampal specific alterations in <strong>CREB</strong> signaling and synaptic plasticity may underlie certain <b>nicotine</b> withdrawal phenotypes.
+CREB1	addiction	withdrawal	27848935	Previous work indicates that hippocampal specific alterations in <strong>CREB</strong> signaling and synaptic plasticity may underlie certain nicotine <b>withdrawal</b> phenotypes.
+CREB1	drug	nicotine	27848935	This study examines the effects of <strong>CREB</strong> deletion specifically in the ventral or dorsal hippocampus of animals chronically treated with saline, <b>nicotine</b>, or undergoing 24 h withdrawal.
+CREB1	addiction	withdrawal	27848935	This study examines the effects of <strong>CREB</strong> deletion specifically in the ventral or dorsal hippocampus of animals chronically treated with saline, nicotine, or undergoing 24 h <b>withdrawal</b>.
+CREB1	drug	nicotine	27848935	Deletion of <strong>CREB</strong> in the ventral, but not dorsal, hippocampus resulted in amelioration of <b>nicotine</b> withdrawal induced anxiety like behavior in the Novelty Induced Hypophagia test.
+CREB1	addiction	withdrawal	27848935	Deletion of <strong>CREB</strong> in the ventral, but not dorsal, hippocampus resulted in amelioration of nicotine <b>withdrawal</b> induced anxiety like behavior in the Novelty Induced Hypophagia test.
+CREB1	drug	nicotine	27848935	Collectively, these data provide persuasive evidence towards the distinct roles of <strong>CREB</strong> within the dorsal and ventral hippocampus separately in mediating select <b>nicotine</b> withdrawal phenotypes.
+CREB1	addiction	withdrawal	27848935	Collectively, these data provide persuasive evidence towards the distinct roles of <strong>CREB</strong> within the dorsal and ventral hippocampus separately in mediating select nicotine <b>withdrawal</b> phenotypes.
+CREB1	drug	psychedelics	27713001	Levo tetrahydropalmatine inhibits the acquisition of <b>ketamine</b> induced conditioned place preference by regulating the expression of ERK and <strong>CREB</strong> phosphorylation in rats.
+CREB1	drug	psychedelics	27713001	Furthermore, <b>Ketamine</b> (10mg/kg) promoted the phosphorylation of extracellular regulated kinase (ERK) and cAMP responsive element binding protein (<strong>CREB</strong>) in the hippocampus (Hip) and caudate putamen (CPu), but not in the prefrontal cortex (PFc).
+CREB1	drug	cocaine	27664298	ERK (extracellular regulated kinase), <strong>CREB</strong> (cAMP responsive element binding protein), FosB and ΔFosB proteins were of particular interest due to their involvement in <b>cocaine</b> reward and in synaptic plasticity underlying learning and memory.
+CREB1	addiction	reward	27664298	ERK (extracellular regulated kinase), <strong>CREB</strong> (cAMP responsive element binding protein), FosB and ΔFosB proteins were of particular interest due to their involvement in cocaine <b>reward</b> and in synaptic plasticity underlying learning and memory.
+CREB1	drug	cocaine	27664298	N methyl D aspartate receptor (NMDAR) antagonism prior to <b>cocaine</b> administration during conditioning blocked the acquisition of <b>cocaine</b> CPP and reduced Nucleus Accumbens (NAc) phosphorylated ERK (pERK) and phosphorylated <strong>CREB</strong> (pCREB) levels following the CPP test (drug free).
+CREB1	addiction	reward	27664298	N methyl D aspartate receptor (NMDAR) antagonism prior to cocaine administration during conditioning blocked the acquisition of cocaine <b>CPP</b> and reduced Nucleus Accumbens (NAc) phosphorylated ERK (pERK) and phosphorylated <strong>CREB</strong> (pCREB) levels following the <b>CPP</b> test (drug free).
+CREB1	drug	cocaine	27734601	Similarly, NGB2904 and SCH23390 showed opposite/differential effects on <b>cocaine</b> induced structural plasticity, conditioned place preference and locomotor activity and signaling activation, including the activation of ERK, <strong>CREB</strong> and NR1 and the expression of c fos and Cdk5.
+CREB1	drug	alcohol	27766083	<b>Alcohol</b> induced neuroadaptations involve the dysregulation of numerous signaling cascades, leading to long term changes in transcriptional profiles of genes, through the actions of transcription factors such as [cAMP response element binding protein (<strong>CREB</strong>)] and chromatin remodeling due to posttranslational modifications of histone proteins.
+CREB1	drug	alcohol	27766083	It then highlights the role of cAMP PKA <strong>CREB</strong> signaling cascade and histone acetylation within the PFC and limbic structures in <b>alcohol</b> induced anxiety and behavioral impairments, and how an understanding of functional alterations of these pathways might lead to better treatments for neuropsychiatric disorders.
+CREB1	addiction	aversion	27728875	Moreover, dysregulation of <strong>CREB</strong> signaling, in part through Arc expression, may enhance reconsolidation, resulting in the maintenance of excessive <b>aversive</b> states.
+CREB1	drug	opioid	27699938	This research established that exposure to drugs of abuse or stress increases the activity of the transcription factor <strong>CREB</strong> (cAMP response element binding protein) in the NAc, which leads to elevated expression of the <b>opioid</b> peptide dynorphin that in turn causes core signs of depressive  and anxiety related disorders.
+CREB1	drug	cannabinoid	27461790	Blockade of <b>Cannabinoid</b> CB1 receptor attenuates the acquisition of morphine induced conditioned place preference along with a downregulation of ERK, <strong>CREB</strong> phosphorylation, and BDNF expression in the nucleus accumbens and hippocampus.
+CREB1	drug	opioid	27461790	Blockade of Cannabinoid CB1 receptor attenuates the acquisition of <b>morphine</b> induced conditioned place preference along with a downregulation of ERK, <strong>CREB</strong> phosphorylation, and BDNF expression in the nucleus accumbens and hippocampus.
+CREB1	drug	opioid	27461790	In the present study, we investigated the relationship between CB1R and the extracellular signal regulated kinase (ERK), cAMP response element binding protein (<strong>CREB</strong>), brain derived neurotrophic factor (BDNF) signaling in the nucleus accumbens (NAc) and hippocampus in <b>morphine</b> induced conditioned place preference (CPP), which is used to assess the <b>morphine</b> induced reward memory.
+CREB1	addiction	reward	27461790	In the present study, we investigated the relationship between CB1R and the extracellular signal regulated kinase (ERK), cAMP response element binding protein (<strong>CREB</strong>), brain derived neurotrophic factor (BDNF) signaling in the nucleus accumbens (NAc) and hippocampus in morphine induced conditioned place preference (<b>CPP</b>), which is used to assess the morphine induced <b>reward</b> memory.
+CREB1	drug	opioid	27461790	Both <b>morphine</b> CPP and NO CPP induced an upregulation of ERK, <strong>CREB</strong> phosphorylation and BDNF expression.
+CREB1	addiction	reward	27461790	Both morphine <b>CPP</b> and NO <b>CPP</b> induced an upregulation of ERK, <strong>CREB</strong> phosphorylation and BDNF expression.
+CREB1	drug	opioid	27461790	Furthermore, pretreatment with AM251 before <b>morphine</b> attenuated the CPP acquisition and CB1R expression as well as the activation of ERK <strong>CREB</strong> BDNF cascade.
+CREB1	addiction	reward	27461790	Furthermore, pretreatment with AM251 before morphine attenuated the <b>CPP</b> acquisition and CB1R expression as well as the activation of ERK <strong>CREB</strong> BDNF cascade.
+CREB1	drug	opioid	27461790	(2) CB1R antagonist mediated blockade of ERK <strong>CREB</strong> BDNF signaling activation in the NAc and hippocampus may be an important mechanism underlying the attenuation of <b>morphine</b> CPP.
+CREB1	addiction	reward	27461790	(2) CB1R antagonist mediated blockade of ERK <strong>CREB</strong> BDNF signaling activation in the NAc and hippocampus may be an important mechanism underlying the attenuation of morphine <b>CPP</b>.
+CREB1	drug	cocaine	27261631	Re exposure to the <b>cocaine</b> context triggered <b>cocaine</b> seeking and increase in phosphorylation of cellular PKC substrates, including phospho ERK and phospho <strong>CREB</strong>.
+CREB1	addiction	relapse	27261631	Re exposure to the cocaine context triggered cocaine <b>seeking</b> and increase in phosphorylation of cellular PKC substrates, including phospho ERK and phospho <strong>CREB</strong>.
+CREB1	drug	opioid	27239019	Moreover, administration of exogenous d serine to rats inhibited the development of locomotor sensitization to <b>morphine</b>, attenuated the <b>morphine</b> induced potentiation on conditioned place preference and suppressed the <b>morphine</b> enhanced expression of p <strong>CREB</strong> and ΔFosB in the NAc.
+CREB1	addiction	sensitization	27239019	Moreover, administration of exogenous d serine to rats inhibited the development of locomotor <b>sensitization</b> to morphine, attenuated the morphine induced potentiation on conditioned place preference and suppressed the morphine enhanced expression of p <strong>CREB</strong> and ΔFosB in the NAc.
+CREB1	drug	nicotine	27235579	Learning in the presence of acute <b>nicotine</b> increases the transcription of mitogen activated protein kinase 8 (MAPK8, also known as JNK1), likely through a <strong>CREB</strong> dependent mechanism.
+CREB1	addiction	sensitization	27147595	Changes in <strong>CREB</strong> and deltaFosB are associated with the behavioural <b>sensitization</b> induced by methylenedioxypyrovalerone.
+CREB1	addiction	sensitization	27147595	The objective of this study was to investigate the locomotor <b>sensitization</b> induced by MDPV in adolescent mice, and associated neuroplastic changes in the nucleus accumbens and striatum through deltaFosB and <strong>CREB</strong> expression.
+CREB1	drug	cocaine	27147595	We hypothesize that, similar to <b>cocaine</b>, both <strong>CREB</strong> and deltaFosB play a role in the induction of this behavioural sensitization.
+CREB1	addiction	sensitization	27147595	We hypothesize that, similar to cocaine, both <strong>CREB</strong> and deltaFosB play a role in the induction of this behavioural <b>sensitization</b>.
+CREB1	drug	alcohol	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (<strong>CREB</strong>) and c fos have important role in morphine induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and <b>alcohol</b>.
+CREB1	drug	cocaine	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (<strong>CREB</strong>) and c fos have important role in morphine induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, <b>cocaine</b>, nicotine, and alcohol.
+CREB1	drug	nicotine	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (<strong>CREB</strong>) and c fos have important role in morphine induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, <b>nicotine</b>, and alcohol.
+CREB1	drug	opioid	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (<strong>CREB</strong>) and c fos have important role in <b>morphine</b> induced conditioned place preference (CPP) induced by drugs of abuse, such as <b>morphine</b>, cocaine, nicotine, and alcohol.
+CREB1	addiction	reward	27053349	In addition, several lines of study have indicated that cAMP response element binding protein (<strong>CREB</strong>) and c fos have important role in morphine induced conditioned place preference (<b>CPP</b>) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.
+CREB1	drug	opioid	27053349	Therefore, in the present study, we investigated the changes in phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) and c fos induction within the nucleus accumbens (NAc), HIP, and PFC after intracerebroventricular (ICV) administration of different doses of CNQX or vehicle during extinction period or reinstatement of <b>morphine</b> induced CPP.
+CREB1	addiction	relapse	27053349	Therefore, in the present study, we investigated the changes in phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) and c fos induction within the nucleus accumbens (NAc), HIP, and PFC after intracerebroventricular (ICV) administration of different doses of CNQX or vehicle during extinction period or <b>reinstatement</b> of morphine induced CPP.
+CREB1	addiction	reward	27053349	Therefore, in the present study, we investigated the changes in phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) and c fos induction within the nucleus accumbens (NAc), HIP, and PFC after intracerebroventricular (ICV) administration of different doses of CNQX or vehicle during extinction period or reinstatement of morphine induced <b>CPP</b>.
+CREB1	drug	opioid	27018165	Pharmacological activities are mainly mediated via <b>opioid</b> receptors as well as neuronal Ca2+ channels, expression of cAMP and <strong>CREB</strong> protein and via descending monoaminergic system.
+CREB1	drug	amphetamine	26873080	<b>Methamphetamine</b> addiction: involvement of <strong>CREB</strong> and neuroinflammatory signaling pathways.
+CREB1	addiction	addiction	26873080	Methamphetamine <b>addiction</b>: involvement of <strong>CREB</strong> and neuroinflammatory signaling pathways.
+CREB1	drug	amphetamine	26873080	In addition, gene expression studies using striatal tissues from <b>METH</b> self administering rats revealed increased expression of genes involved in cAMP response element binding protein (<strong>CREB</strong>) signaling pathway and in the activation of neuroinflammatory response in the brain.
+CREB1	drug	cocaine	26861675	The ERK <strong>CREB</strong> Fos pathway and the NMDA receptor NR2B subunits in the NAc were involved in the <b>cocaine</b> induced behavioral sensitization.
+CREB1	addiction	sensitization	26861675	The ERK <strong>CREB</strong> Fos pathway and the NMDA receptor NR2B subunits in the NAc were involved in the cocaine induced behavioral <b>sensitization</b>.
+CREB1	addiction	withdrawal	26860616	To determine the causal role of corticosterone in the <b>withdrawal</b> associated long lasting WM deficits, we further show that a single intraperitoneal injection injection of metyrapone (an inhibitor of corticosterone synthesis) 30 minutes before testing, prevents <b>withdrawal</b> associated WM deficits and reestablishes PFC activity, as assessed by increased phosphorylated C AMP Response Element binding protein (<strong>CREB</strong>) immunoreactivity in withdrawn mice.
+CREB1	drug	opioid	26830449	RACK1 promotes maintenance of <b>morphine</b> associated memory via activation of an ERK <strong>CREB</strong> dependent pathway in hippocampus.
+CREB1	drug	opioid	26830449	Our present study highlights that RACK1 plays an important role in the maintenance of <b>morphine</b> CPP, likely via activation of ERK <strong>CREB</strong> pathway in hippocampus.
+CREB1	addiction	reward	26830449	Our present study highlights that RACK1 plays an important role in the maintenance of morphine <b>CPP</b>, likely via activation of ERK <strong>CREB</strong> pathway in hippocampus.
+CREB1	drug	opioid	26803309	In this study, effects of intra BLA administration of CB1R agonist on sensitization to antinociceptive effect of <b>morphine</b> and changes in the levels of μ <b>opioid</b> receptor (MOR), p <strong>CREB</strong>, and c fos in the NAc were investigated.
+CREB1	addiction	sensitization	26803309	In this study, effects of intra BLA administration of CB1R agonist on <b>sensitization</b> to antinociceptive effect of morphine and changes in the levels of μ opioid receptor (MOR), p <strong>CREB</strong>, and c fos in the NAc were investigated.
+CREB1	drug	opioid	26803309	The results indicated that intra BLA injection of WIN55,212 2 during sensitization period resulted in the induction of antinociceptive responses by ineffective dose of <b>morphine</b> and caused a significant increase in the MOR and c fos levels but not p <strong>CREB</strong>/<strong>CREB</strong> ratio in the NAc.
+CREB1	addiction	sensitization	26803309	The results indicated that intra BLA injection of WIN55,212 2 during <b>sensitization</b> period resulted in the induction of antinociceptive responses by ineffective dose of morphine and caused a significant increase in the MOR and c fos levels but not p <strong>CREB</strong>/<strong>CREB</strong> ratio in the NAc.
+CREB1	drug	cocaine	26740398	Specifically, opiates in several CNS regions including NAc, and <b>cocaine</b> more selectively in NAc, induce expression of certain adenylyl cyclase isoforms and PKA subunits via the transcription factor, <strong>CREB</strong>, and these transcriptional adaptations serve a homeostatic function to oppose drug action.
+CREB1	drug	amphetamine	26736037	Single nucleotide polymorphism near <strong>CREB1</strong>, rs7591784, is associated with pretreatment <b>methamphetamine</b> use frequency and outcome of outpatient treatment for <b>methamphetamine</b> use disorder.
+CREB1	drug	amphetamine	26736037	The <strong>CREB</strong> signaling pathway is involved in gene expression changes related to chronic use of multiple drugs of abuse including <b>methamphetamine</b> and these results suggest that variability in <strong>CREB</strong> signaling may influence pretreatment frequency of <b>methamphetamine</b> use as well as outcomes of outpatient treatment.
+CREB1	drug	amphetamine	26736037	Medications targeting the <strong>CREB</strong> pathway, including phosphodiesterase inhibitors, warrant investigation as pharmacotherapies for <b>methamphetamine</b> use disorders.
+CREB1	drug	nicotine	26687895	Hippocampal kinases such as cAMP dependent protein kinase (PKA), calcium/calmodulin dependent protein kinases (CAMKs), extracellular signal regulated kinases 1 and 2 (ERK1/2), and c jun N terminal kinase 1 (JNK1), and the transcription factor cAMP response element binding protein (<strong>CREB</strong>) that are activated either directly or indirectly by <b>nicotine</b> may modulate hippocampal plasticity and in parallel hippocampus dependent learning and memory.
+CREB1	drug	opioid	26598419	Glucocorticoid receptor but not mineralocorticoid receptor mediates the activation of ERK pathway and <strong>CREB</strong> during <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	26598419	Glucocorticoid receptor but not mineralocorticoid receptor mediates the activation of ERK pathway and <strong>CREB</strong> during morphine <b>withdrawal</b>.
+CREB1	addiction	withdrawal	26598419	In this report, we further characterize the role of glucocorticoid and mineralocorticoid receptor (GR and MR) signalling in DA turnover at the Nacc, and in opiate <b>withdrawal</b> induced tyrosine hydroxylase (TH) expression, ERK and <strong>CREB</strong> phosphorylation (activation) in the nucleus of tractus solitarius (NTS A2).
+CREB1	drug	opioid	26598419	Six days later rats were pretreated with mifepristone, spironolactone or vehicle 30 min before <b>naloxone</b>, and DA turnover, TH expression, ERK and <strong>CREB</strong> phosphorylation, were measured using HPLC and immunoblotting.
+CREB1	drug	opioid	26598419	Glucocorticoid receptor blockade attenuated ERK and <strong>CREB</strong> phosphorylation and the TH expression induced by <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	26598419	Glucocorticoid receptor blockade attenuated ERK and <strong>CREB</strong> phosphorylation and the TH expression induced by morphine <b>withdrawal</b>.
+CREB1	drug	cocaine	26398380	Working memory deficits and alterations of ERK and <strong>CREB</strong> phosphorylation following withdrawal from <b>cocaine</b> self administration.
+CREB1	addiction	withdrawal	26398380	Working memory deficits and alterations of ERK and <strong>CREB</strong> phosphorylation following <b>withdrawal</b> from cocaine self administration.
+CREB1	drug	cocaine	26398380	Upon T maze training and 8 week withdrawal, <b>cocaine</b> pretreated rats had higher levels of p <strong>CREB</strong>/<strong>CREB</strong> in prefrontal cortex and dorsal striatum and lower in hippocampus compared to saline rats.
+CREB1	addiction	withdrawal	26398380	Upon T maze training and 8 week <b>withdrawal</b>, cocaine pretreated rats had higher levels of p <strong>CREB</strong>/<strong>CREB</strong> in prefrontal cortex and dorsal striatum and lower in hippocampus compared to saline rats.
+CREB1	drug	cocaine	26398380	In <b>cocaine</b> pretreated caged rats no changes in p <strong>CREB</strong>/<strong>CREB</strong> levels were observed, while ERK2 levels either decreased (frontal cortex) or increased (nucleus accumbens).
+CREB1	drug	cocaine	26398380	Our results suggest that <b>cocaine</b> self administration results in cognitive impairments and alterations in ERK/<strong>CREB</strong> signaling pathway long after discontinuation of drug use.
+CREB1	drug	opioid	26313266	CP 154,526 Modifies <strong>CREB</strong> Phosphorylation and Thioredoxin 1 Expression in the Dentate Gyrus following <b>Morphine</b> Induced Conditioned Place Preference.
+CREB1	drug	opioid	26313266	We also investigate the effects of the CRF1R antagonist, CP 154,526, on the <b>morphine</b> CPP induced activation of CRF neurons, <strong>CREB</strong> phosphorylation and Trx expression in paraventricular nucleus (PVN) and dentate gyrus (DG) of the mice brain.
+CREB1	addiction	reward	26313266	We also investigate the effects of the CRF1R antagonist, CP 154,526, on the morphine <b>CPP</b> induced activation of CRF neurons, <strong>CREB</strong> phosphorylation and Trx expression in paraventricular nucleus (PVN) and dentate gyrus (DG) of the mice brain.
+CREB1	drug	nicotine	26150803	Intra ventral tegmental area HIV 1 Tat1 86 attenuates <b>nicotine</b> mediated locomotor sensitization and alters mesocorticolimbic ERK and <strong>CREB</strong> signaling in rats.
+CREB1	addiction	sensitization	26150803	Intra ventral tegmental area HIV 1 Tat1 86 attenuates nicotine mediated locomotor <b>sensitization</b> and alters mesocorticolimbic ERK and <strong>CREB</strong> signaling in rats.
+CREB1	drug	nicotine	26150803	We have demonstrated that HIV 1 transgenic rats exhibit attenuated <b>nicotine</b> mediated locomotor activity, altered cAMP response element binding protein (<strong>CREB</strong>) and extracellular regulated kinase (ERK1/2) signaling in the mesocorticolimbic regions.
+CREB1	drug	nicotine	26150803	Thus, these findings indicate that the direct injection of Tat at the VTA may mediate <strong>CREB</strong> and ERK activity in response to <b>nicotine</b> induced locomotor activity.
+CREB1	drug	nicotine	25981209	Expression of <b>nicotine</b> induced CPP was accompanied by an increase of phospho <strong>CREB</strong> (cyclic AMP responsive element binding protein) and HDAC2 (histone deacetylase 2) expression in the nucleus accumbens.
+CREB1	addiction	reward	25981209	Expression of nicotine induced <b>CPP</b> was accompanied by an increase of phospho <strong>CREB</strong> (cyclic AMP responsive element binding protein) and HDAC2 (histone deacetylase 2) expression in the nucleus accumbens.
+CREB1	drug	alcohol	25939814	<strong>CREB</strong> BDNF pathway influences <b>alcohol</b> cue elicited activation in drinkers.
+CREB1	drug	alcohol	25939814	The genetic component derived from the cAMP response element binding protein and  brain derived neurotrophic factor (<strong>CREB</strong> BDNF) pathway reference was significantly associated (r =  0.38, P = 3.98 × 10( 12)) with an imaging component reflecting hyperactivation in precuneus, superior parietal lobule, and posterior cingulate for drinkers with more severe <b>alcohol</b> dependence symptoms.
+CREB1	addiction	dependence	25939814	The genetic component derived from the cAMP response element binding protein and  brain derived neurotrophic factor (<strong>CREB</strong> BDNF) pathway reference was significantly associated (r =  0.38, P = 3.98 × 10( 12)) with an imaging component reflecting hyperactivation in precuneus, superior parietal lobule, and posterior cingulate for drinkers with more severe alcohol <b>dependence</b> symptoms.
+CREB1	drug	nicotine	25847246	Association of MMP7  181A→G Promoter Polymorphism with Gastric Cancer Risk: INFLUENCE OF <b>NICOTINE</b> IN DIFFERENTIAL ALLELE SPECIFIC TRANSCRIPTION VIA INCREASED PHOSPHORYLATION OF cAMP RESPONSE ELEMENT BINDING PROTEIN (<strong>CREB</strong>).
+CREB1	drug	nicotine	25847246	In support, MMP7 promoter reporter assays showed greater transcriptional activity toward A to G transition under basal/<b>nicotine</b> induced/cAMP response element binding protein (<strong>CREB</strong>) overexpressed conditions in gastric adenocarcinoma cells.
+CREB1	drug	nicotine	25847246	Moreover, <b>nicotine</b> (a major component of <b>tobacco</b>) treatment significantly up regulated MMP7 expression due to enhanced <strong>CREB</strong> phosphorylation followed by its nuclear translocation in gastric adenocarcinoma cells.
+CREB1	drug	nicotine	25847246	Altogether, specific binding of phosphorylated <strong>CREB</strong> to the G allele carrying promoter enhances MMP7 gene expression that is further augmented by <b>nicotine</b> due to increased <strong>CREB</strong> phosphorylation and thereby increases the risk for gastric cancer.
+CREB1	drug	opioid	25746394	NAc Shell Arc/Arg3.1 Protein Mediates Reconsolidation of <b>Morphine</b> CPP by Increased GluR1 Cell Surface Expression: Activation of ERK Coupled <strong>CREB</strong> is Required.
+CREB1	addiction	reward	25746394	NAc Shell Arc/Arg3.1 Protein Mediates Reconsolidation of Morphine <b>CPP</b> by Increased GluR1 Cell Surface Expression: Activation of ERK Coupled <strong>CREB</strong> is Required.
+CREB1	drug	opioid	25746394	Arc/Arg3.1 in the NAc shell mediates the reconsolidation of <b>morphine</b> associated context memory via up regulating the level of membrane of GluR1, for which the local activation of the ERK <strong>CREB</strong> signal pathway, as an upstream mechanism of Arc/Arg3.1, is required.
+CREB1	drug	alcohol	25730876	Here we show that acute <b>ethanol</b> exposure also lowers fasting blood glucose concentrations by inhibiting the <strong>CREB</strong> mediated activation of the gluconeogenic program in response to glucagon.
+CREB1	drug	alcohol	25730876	<b>Ethanol</b> exposure blocked the recruitment of <strong>CREB</strong> and its coactivator CRTC2 to gluconeogenic promoters by up regulating ATF3, a transcriptional repressor that also binds to cAMP responsive elements and thereby down regulates gluconeogenic genes.
+CREB1	drug	cocaine	25716852	However, overexpression of <strong>CREB</strong>, which increases excitability of AcbSh neurons, enhances <b>cocaine</b> seeking behavior while producing depression like behavior in tests of mood.
+CREB1	addiction	relapse	25716852	However, overexpression of <strong>CREB</strong>, which increases excitability of AcbSh neurons, enhances cocaine <b>seeking</b> behavior while producing depression like behavior in tests of mood.
+CREB1	drug	opioid	25711798	Decrease of phosphorylated <strong>CREB</strong> and ERK in nucleus accumbens is associated with the incubation of <b>heroin</b> seeking induced by cues after withdrawal.
+CREB1	addiction	relapse	25711798	Decrease of phosphorylated <strong>CREB</strong> and ERK in nucleus accumbens is associated with the incubation of heroin <b>seeking</b> induced by cues after withdrawal.
+CREB1	addiction	withdrawal	25711798	Decrease of phosphorylated <strong>CREB</strong> and ERK in nucleus accumbens is associated with the incubation of heroin seeking induced by cues after <b>withdrawal</b>.
+CREB1	drug	opioid	25711798	cAMP response element binding protein (<strong>CREB</strong>) signaling is involved in the <b>heroin</b> reward, but whether the <strong>CREB</strong> signaling is involved in the incubation of <b>heroin</b> seeking remains unknown.
+CREB1	addiction	relapse	25711798	cAMP response element binding protein (<strong>CREB</strong>) signaling is involved in the heroin reward, but whether the <strong>CREB</strong> signaling is involved in the incubation of heroin <b>seeking</b> remains unknown.
+CREB1	addiction	reward	25711798	cAMP response element binding protein (<strong>CREB</strong>) signaling is involved in the heroin <b>reward</b>, but whether the <strong>CREB</strong> signaling is involved in the incubation of heroin seeking remains unknown.
+CREB1	drug	opioid	25711798	Here we aim to explore the expression of p <strong>CREB</strong> and the p ERK, an upstream molecular of <strong>CREB</strong>, in the nucleus accumbens (NAc) in the incubation of <b>heroin</b> seeking induced by cue after withdrawal.
+CREB1	addiction	relapse	25711798	Here we aim to explore the expression of p <strong>CREB</strong> and the p ERK, an upstream molecular of <strong>CREB</strong>, in the nucleus accumbens (NAc) in the incubation of heroin <b>seeking</b> induced by cue after withdrawal.
+CREB1	addiction	withdrawal	25711798	Here we aim to explore the expression of p <strong>CREB</strong> and the p ERK, an upstream molecular of <strong>CREB</strong>, in the nucleus accumbens (NAc) in the incubation of heroin seeking induced by cue after <b>withdrawal</b>.
+CREB1	addiction	withdrawal	25711798	In contrast, reduction of the expression of p <strong>CREB</strong> was more obvious with exposure to CS after 14 d <b>withdrawal</b>.
+CREB1	drug	opioid	25711798	Furthermore, microinjection of rolipram into the NAc decreased the <b>heroin</b> seeking behavior induced by CS after 14 d withdrawal, which was correlated to an enhancement in the expression of p <strong>CREB</strong> in the NAc.
+CREB1	addiction	relapse	25711798	Furthermore, microinjection of rolipram into the NAc decreased the heroin <b>seeking</b> behavior induced by CS after 14 d withdrawal, which was correlated to an enhancement in the expression of p <strong>CREB</strong> in the NAc.
+CREB1	addiction	withdrawal	25711798	Furthermore, microinjection of rolipram into the NAc decreased the heroin seeking behavior induced by CS after 14 d <b>withdrawal</b>, which was correlated to an enhancement in the expression of p <strong>CREB</strong> in the NAc.
+CREB1	drug	opioid	25711798	These findings suggest that the inactivation of <strong>CREB</strong> and ERK may be involved in the incubation of <b>heroin</b> seeking induced by cues after prolonged withdrawal.
+CREB1	addiction	relapse	25711798	These findings suggest that the inactivation of <strong>CREB</strong> and ERK may be involved in the incubation of heroin <b>seeking</b> induced by cues after prolonged withdrawal.
+CREB1	addiction	withdrawal	25711798	These findings suggest that the inactivation of <strong>CREB</strong> and ERK may be involved in the incubation of heroin seeking induced by cues after prolonged <b>withdrawal</b>.
+CREB1	drug	opioid	25636946	The activation of ERK/cyclic AMP responsive element binding (<strong>CREB</strong>) signaling in the mesocorticolimbic area, glucocorticoid receptors in the basolateral amygdala, and norepinephrine and galanin system in the nucleus accumbens may decrease the acute stress induced inhibition of <b>morphine</b> CPP.
+CREB1	addiction	reward	25636946	The activation of ERK/cyclic AMP responsive element binding (<strong>CREB</strong>) signaling in the mesocorticolimbic area, glucocorticoid receptors in the basolateral amygdala, and norepinephrine and galanin system in the nucleus accumbens may decrease the acute stress induced inhibition of morphine <b>CPP</b>.
+CREB1	drug	cocaine	25522720	Conversely, the higher <b>cocaine</b> dose, independent of environment, resulted in increased NAc FosB, ΔFosB and phosphorylated <strong>CREB</strong> (pCREB) protein levels compared to those conditioned with 5mg/kg <b>cocaine</b> (non CPP expressing).
+CREB1	addiction	reward	25522720	Conversely, the higher cocaine dose, independent of environment, resulted in increased NAc FosB, ΔFosB and phosphorylated <strong>CREB</strong> (pCREB) protein levels compared to those conditioned with 5mg/kg cocaine (non <b>CPP</b> expressing).
+CREB1	drug	opioid	25481016	<b>Morphine</b> induced conditioned place preference and the alterations of p ERK, p <strong>CREB</strong> and c fos levels in hypothalamus and hippocampus: the effects of physical stress.
+CREB1	addiction	reward	25481016	In addition, ERK/<strong>CREB</strong> pathway plays a critical role in the control of cellular responses to stress and <b>reward</b>.
+CREB1	drug	opioid	25481016	In the current study, effects of acute and subchronic stress on the alteration of p ERK, p <strong>CREB</strong> and c fos levels in the hypothalamus and hippocampus of saline  or <b>morphine</b> treated animals during <b>morphine</b> induced conditioned place preference (CPP) procedure were investigated.
+CREB1	addiction	reward	25481016	In the current study, effects of acute and subchronic stress on the alteration of p ERK, p <strong>CREB</strong> and c fos levels in the hypothalamus and hippocampus of saline  or morphine treated animals during morphine induced conditioned place preference (<b>CPP</b>) procedure were investigated.
+CREB1	addiction	reward	25481016	In all of groups, the <b>CPP</b> procedure was done, afterward the alternation of p ERK/ERK ratio, p <strong>CREB</strong>/<strong>CREB</strong> ratio and c fos level in the hypothalamus and hippocampus were estimated by Western blot analysis.
+CREB1	drug	opioid	25481016	The results indicated that in saline  or <b>morphine</b> treated animals, p ERK/ERK ratio, p <strong>CREB</strong>/<strong>CREB</strong> ratio and c fos level increased after application of acute and subchronic stress (except for p ERK/ERK ratio in <b>morphine</b> control group).
+CREB1	drug	opioid	25481016	Our findings revealed that in saline  or <b>morphine</b> treated animals, acute and subcronic stress increased the p ERK/ERK ratio, p <strong>CREB</strong>/<strong>CREB</strong> ratio and c fos level in the hypothalamus and hippocampus and this enhancement in <b>morphine</b> treated animals, was more considerable than that in saline treated animals.
+CREB1	drug	opioid	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for GluR1 AMPA receptor (AMPAR), phosphorylated ERK2 (pERK2), <strong>CREB</strong> (pCREB), TrKB (pTrkB) were performed in brain areas relevant for sensitization from KO and WT and/or <b>naloxone</b>  and vehicle pre treated animals.
+CREB1	addiction	sensitization	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for GluR1 AMPA receptor (AMPAR), phosphorylated ERK2 (pERK2), <strong>CREB</strong> (pCREB), TrKB (pTrkB) were performed in brain areas relevant for <b>sensitization</b> from KO and WT and/or naloxone  and vehicle pre treated animals.
+CREB1	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, <strong>Creb1</strong>, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+CREB1	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, <strong>Creb1</strong>, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+CREB1	drug	alcohol	25388276	Rescuing prefrontal cAMP <strong>CREB</strong> pathway reverses working memory deficits during withdrawal from prolonged <b>alcohol</b> exposure.
+CREB1	addiction	withdrawal	25388276	Rescuing prefrontal cAMP <strong>CREB</strong> pathway reverses working memory deficits during <b>withdrawal</b> from prolonged alcohol exposure.
+CREB1	drug	alcohol	25388276	A candidate signaling cascade contributing to memory deficits during <b>alcohol</b> withdrawal is the protein kinase A (PKA)/cAMP responsive element binding (<strong>CREB</strong>) cascade, although the role of PKA/<strong>CREB</strong> cascade in behavioral and molecular changes during sustained withdrawal period remains largely unknown.
+CREB1	addiction	withdrawal	25388276	A candidate signaling cascade contributing to memory deficits during alcohol <b>withdrawal</b> is the protein kinase A (PKA)/cAMP responsive element binding (<strong>CREB</strong>) cascade, although the role of PKA/<strong>CREB</strong> cascade in behavioral and molecular changes during sustained <b>withdrawal</b> period remains largely unknown.
+CREB1	addiction	withdrawal	25388276	We demonstrated that 1 week (1W) or 6 weeks (6W) <b>withdrawal</b> after 6 month CAC impairs working memory (WM) in a T maze spontaneous alternation task and reduces phosphorylated <strong>CREB</strong> (pCREB) in the PFC but not the dorsal CA1 region (dCA1) of the hippocampus compared with CAC and water conditions.
+CREB1	drug	alcohol	25388276	Collectively, these results provide strong support that dysregulation of PKA/<strong>CREB</strong> dependent processes in prefrontal neurons is a critical molecular signature underlying cognitive decline during <b>alcohol</b> withdrawal.
+CREB1	addiction	withdrawal	25388276	Collectively, these results provide strong support that dysregulation of PKA/<strong>CREB</strong> dependent processes in prefrontal neurons is a critical molecular signature underlying cognitive decline during alcohol <b>withdrawal</b>.
+CREB1	drug	cocaine	25319707	Neurons with increased levels of the transcription factor <strong>CREB</strong> were preferentially recruited or allocated to the <b>cocaine</b> engram.
+CREB1	drug	cocaine	25319707	Ablating or silencing neurons overexpressing <strong>CREB</strong> (but not a similar number of random LA neurons) before testing disrupted the expression of a previously acquired <b>cocaine</b> memory, suggesting that neurons overexpressing <strong>CREB</strong> become a critical hub in what is likely a larger <b>cocaine</b> memory engram.
+CREB1	drug	cocaine	25319707	Consistent with theories that coordinated postencoding reactivation of neurons within an engram or cell assembly is crucial for memory consolidation (Marr, 1971; Buzsáki, 1989; Wilson and McNaughton, 1994; McClelland et al., 1995; Girardeau et al., 2009; Dupret et al., 2010; Carr et al., 2011), we also found that post training suppression, or nondiscriminate activation, of <strong>CREB</strong> overexpressing neurons impaired consolidation of the <b>cocaine</b> memory.
+CREB1	drug	alcohol	25307591	We will provide evidence that alterations in cyclic AMP responsive element binding protein (<strong>CREB</strong>: neurotrophic) and NF κB (neuroimmune) signaling contribute to the development and persistence of <b>alcoholism</b>.
+CREB1	addiction	aversion	25241061	It has also been observed after viral mediated manipulation of GluR1, phospholipase Cγ (PLCγ) and cAMP response element binding protein (<strong>CREB</strong>) expression, with impact on reward and <b>aversion</b> related responses, on anxiety and depression related behaviors and on pain sensitivity.
+CREB1	addiction	reward	25241061	It has also been observed after viral mediated manipulation of GluR1, phospholipase Cγ (PLCγ) and cAMP response element binding protein (<strong>CREB</strong>) expression, with impact on <b>reward</b> and aversion related responses, on anxiety and depression related behaviors and on pain sensitivity.
+CREB1	drug	cocaine	25100957	Further, <b>cocaine</b> regulates proteins related to ERK, <strong>CREB</strong> and AKT signaling.
+CREB1	drug	alcohol	25099937	<b>Ethanol</b> suppresses PGC 1α expression by interfering with the cAMP <strong>CREB</strong> pathway in neuronal cells.
+CREB1	drug	alcohol	25099937	Further analysis show that <b>ethanol</b> decreases steady state intracellular cAMP levels, and thus depletes phosphorylation of cAMP response element binding protein (p <strong>CREB</strong>), the key transcription factor that regulates transcription of PGC 1α gene.
+CREB1	drug	alcohol	25099937	Accordingly, we found PGC 1α promoter activity and transcription was dramatically repressed in neuronal cells when exposed to <b>ethanol</b>, suggesting that <b>ethanol</b> blunts cAMP→<strong>CREB</strong> signaling pathway to interfere with the transcription of PGC 1α.
+CREB1	drug	cocaine	25071493	Corrigendum: <strong>CREB</strong> activity in dopamine D1 receptor expressing neurons regulates <b>cocaine</b> induced behavioral effects.
+CREB1	drug	alcohol	25041461	The aim of the present study was to assess the state of the CB1 receptor, the enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), and the extracellular signal regulated kinase (ERK) and cyclic AMP response element binding protein (<strong>CREB</strong>) in the post mortem prefrontal cortex of <b>alcoholic</b> subjects.
+CREB1	drug	alcohol	25041461	A significant decrease in the active form of ERK and <strong>CREB</strong> levels was also observed in both <b>alcoholic</b> groups.
+CREB1	drug	opioid	25010326	Early TENS decreased p p38 within microglia (P<0.05), the expression levels of protein kinase C (PKC γ), and phosphorylated anti phospho cyclic AMP response element binding protein (p <strong>CREB</strong>) in the superficial spinal dorsal horn neurons (P<0.05), mitogen activated protein (MAP) kinases, and proinflammatory cytokines, and increased the expression levels of <b>opioid</b> receptors (P<0.05).
+CREB1	drug	opioid	25010326	The results suggested that the application of early TENS relieved hyperalgesia in our mouse model of neuropathic pain by inhibiting glial activation, MAP kinase activation, PKC γ, and p <strong>CREB</strong> expression, and proinflammatory cytokines expression, as well as maintenance of spinal <b>opioid</b> receptors.
+CREB1	drug	cocaine	24966820	<strong>CREB</strong> activity in dopamine D1 receptor expressing neurons regulates <b>cocaine</b> induced behavioral effects.
+CREB1	drug	cocaine	24966820	To test the cell specificity of this hypothesis we examined the effects of a dominant negative <strong>CREB</strong> protein variant expressed in dopamine receptor D1 (D1R) neurons on <b>cocaine</b> induced behaviors.
+CREB1	drug	amphetamine	24953280	Repeated exposure to addictive drugs enhances dopamine receptor (DR) signaling and the ultimate phosphorylation of the cyclic adenosine 5' monophosphate (cAMP) response element binding protein (<strong>CREB</strong>) regulated cocaine  and <b>amphetamine</b> regulated transcript (CART) expression in the nucleus accumbens (NAcc).
+CREB1	drug	cocaine	24953280	Repeated exposure to addictive drugs enhances dopamine receptor (DR) signaling and the ultimate phosphorylation of the cyclic adenosine 5' monophosphate (cAMP) response element binding protein (<strong>CREB</strong>) regulated <b>cocaine</b>  and amphetamine regulated transcript (CART) expression in the nucleus accumbens (NAcc).
+CREB1	addiction	addiction	24953280	Repeated exposure to <b>addictive</b> drugs enhances dopamine receptor (DR) signaling and the ultimate phosphorylation of the cyclic adenosine 5' monophosphate (cAMP) response element binding protein (<strong>CREB</strong>) regulated cocaine  and amphetamine regulated transcript (CART) expression in the nucleus accumbens (NAcc).
+CREB1	drug	cocaine	24953280	These results suggest that the phosphorylation of <strong>CREB</strong> by <b>cocaine</b> in the NAcc was blocked by the CART 55 102 peptide via the inhibition of D1R and D2R stimulation, D3R phosphorylation, cAMP/PKA signaling and ERK phosphorylated kinase signaling.
+CREB1	drug	opioid	24950452	<b>Morphine</b> exposure also increased phosphorylation of cortical c Jun whereas levels of phosphorylated cAMP response element binding protein (<strong>CREB</strong>) remained unmodified.
+CREB1	drug	amphetamine	24939695	<b>Methamphetamine</b> induced transcription was found to be regulated via phosphorylated <strong>CREB</strong> dependent events.
+CREB1	drug	opioid	24832929	Finally, the effects of rolipram on <b>heroin</b> seeking behavior were correlated with the increases in expression of phosphorylated <strong>CREB</strong> in the nucleus accumbens.
+CREB1	addiction	relapse	24832929	Finally, the effects of rolipram on heroin <b>seeking</b> behavior were correlated with the increases in expression of phosphorylated <strong>CREB</strong> in the nucleus accumbens.
+CREB1	drug	opioid	24824948	NaHS also inhibited <b>naloxone</b> induced cAMP rebound and cAMP response element binding protein (<strong>CREB</strong>) phosphorylation in rat spinal cord.
+CREB1	addiction	relapse	24704376	Association of <strong>CREB1</strong> gene polymorphism with drug <b>seeking</b> behaviour in eastern Indian addicts.
+CREB1	drug	alcohol	24704376	A study was undertaken to identify the single nucleotide polymorphisms (SNP) at selective areas of <strong>CREB1</strong> gene in heroin as well as in <b>alcohol</b> addicts in comparison with control population.
+CREB1	drug	opioid	24704376	A study was undertaken to identify the single nucleotide polymorphisms (SNP) at selective areas of <strong>CREB1</strong> gene in <b>heroin</b> as well as in alcohol addicts in comparison with control population.
+CREB1	addiction	addiction	24704376	SNPs from several exonic regions of <strong>CREB1</strong> gene were assessed to investigate possible associations with <b>addiction</b>.
+CREB1	addiction	addiction	24704376	The study is the first report on the identification of a role of <strong>CREB1</strong> gene polymorphism with <b>addiction</b>.
+CREB1	drug	opioid	24704371	These results suggested that <strong>CREB</strong> mediated epigenetic upregulation of PSD 95 critically contributed to the enhanced glutamatergic transmission and rewarding behavior induced by <b>morphine</b> conditioning.
+CREB1	addiction	withdrawal	24682499	Further, repeated treatment with lobeline or 3 (pyridine 3́ yl) cytisine decreased immobility time in the FST and reduced <b>withdrawal</b> induced increased BDNF and p <strong>CREB</strong> expression in the hippocampus.
+CREB1	drug	alcohol	24674772	These results suggest that acupuncture at HT7 rescues the depletion of amygdaloid NPY and reverses the decrease in <strong>CREB</strong> phosphorylation to produce anxiolytic effects during <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	24674772	These results suggest that acupuncture at HT7 rescues the depletion of amygdaloid NPY and reverses the decrease in <strong>CREB</strong> phosphorylation to produce anxiolytic effects during ethanol <b>withdrawal</b>.
+CREB1	drug	opioid	24597568	Dorsal hippocampal NMDA receptor blockade impairs extinction of <b>naloxone</b> precipitated conditioned place aversion in acute <b>morphine</b> treated rats by suppressing ERK and <strong>CREB</strong> phosphorylation in the basolateral amygdala.
+CREB1	addiction	aversion	24597568	Dorsal hippocampal NMDA receptor blockade impairs extinction of naloxone precipitated conditioned place <b>aversion</b> in acute morphine treated rats by suppressing ERK and <strong>CREB</strong> phosphorylation in the basolateral amygdala.
+CREB1	drug	cocaine	24560901	Moreover, CART peptides were also found to block <b>cocaine</b> (1μM) induced Ca(2+) influx, CaMKIIα phosphorylation, CaMKIIα D3R interaction, and <strong>CREB</strong> phosphorylation.
+CREB1	drug	cocaine	24452697	MPH + FLX, or <b>cocaine</b> exposure in juvenile mice increased mRNA expression of ERK2 and its downstream targets (<strong>CREB</strong>, cFos, and Zif268), and increased protein phosphorylation of ERK2 and <strong>CREB</strong> 2 months after drug exposure.
+CREB1	drug	alcohol	24379765	Changes in <strong>CREB</strong> activation in the prefrontal cortex and hippocampus blunt <b>ethanol</b> induced behavioral sensitization in adolescent mice.
+CREB1	addiction	sensitization	24379765	Changes in <strong>CREB</strong> activation in the prefrontal cortex and hippocampus blunt ethanol induced behavioral <b>sensitization</b> in adolescent mice.
+CREB1	drug	alcohol	24379765	In the present work, we investigated the effects of acute and repeated <b>ethanol</b> administration on cyclic adenosine monophosphate (cAMP) response element binding protein (<strong>CREB</strong>) DNA binding activity using the electrophoretic mobility shift assay (EMSA) and the phosphorylated <strong>CREB</strong> (pCREB)/<strong>CREB</strong> ratio using immunoblotting in both the PFC and hippocampus in adolescent and adult mice.
+CREB1	drug	alcohol	24379765	The present results indicate that <b>ethanol</b> exposure induces significant and differential neuroadaptive changes in <strong>CREB</strong> DNA binding activity in the PFC and hippocampus in adolescent mice compared with adult mice.
+CREB1	drug	opioid	24292370	Changes in the levels of p ERK, p <strong>CREB</strong>, and c fos in rat mesocorticolimbic dopaminergic system after <b>morphine</b> induced conditioned place preference: the role of acute and subchronic stress.
+CREB1	drug	opioid	24292370	In this study, we investigated the effects of <b>morphine</b> induced conditioned place preference (CPP) on p ERK/ERK ratio, p <strong>CREB</strong>/<strong>CREB</strong> ratio and c fos level in the mesocorticolimbic dopaminergic system including the nucleus accumbens (NAc), amygdala (AMY), striatum (Str), and prefrontal cortex (PFC).Our aim was to determine if acute and subchronic stress would affect these alterations.
+CREB1	addiction	reward	24292370	In this study, we investigated the effects of morphine induced conditioned place preference (<b>CPP</b>) on p ERK/ERK ratio, p <strong>CREB</strong>/<strong>CREB</strong> ratio and c fos level in the mesocorticolimbic dopaminergic system including the nucleus accumbens (NAc), amygdala (AMY), striatum (Str), and prefrontal cortex (PFC).Our aim was to determine if acute and subchronic stress would affect these alterations.
+CREB1	drug	opioid	24292370	Our findings suggest that in saline  or <b>morphine</b> treated animals, acute and subchronic stress increases p ERK, p <strong>CREB</strong>, and c fos levels in the mesocorticolimbic system.
+CREB1	addiction	relapse	24269543	Western blotting results showed that the levels of GLT1, VGLUT2, NR2B, p ERK1/2 and p <strong>CREB</strong> expressions in the mPFC were increased and CaMKII was decreased markedly after the stress priming MAP induced CPP <b>reinstatement</b> test.
+CREB1	addiction	reward	24269543	Western blotting results showed that the levels of GLT1, VGLUT2, NR2B, p ERK1/2 and p <strong>CREB</strong> expressions in the mPFC were increased and CaMKII was decreased markedly after the stress priming MAP induced <b>CPP</b> reinstatement test.
+CREB1	addiction	relapse	24269543	In DHC, the levels of VGLUT2, p ERK1/2 and <strong>CREB</strong> expressions were reduced during the stress induced <b>reinstatement</b>, which could be reversed by OT and further abolished by Ato.
+CREB1	drug	cocaine	24205196	Enhancement of behavioral sensitization, anxiety like behavior, and hippocampal and frontal cortical <strong>CREB</strong> levels following <b>cocaine</b> abstinence in mice exposed to <b>cocaine</b> during adolescence.
+CREB1	addiction	sensitization	24205196	Enhancement of behavioral <b>sensitization</b>, anxiety like behavior, and hippocampal and frontal cortical <strong>CREB</strong> levels following cocaine abstinence in mice exposed to cocaine during adolescence.
+CREB1	drug	cocaine	24205196	Decreases in cyclic adenosine monophosphate response element binding protein (<strong>CREB</strong>) and phosphorylated <strong>CREB</strong> (pCREB) have been reported after repeated <b>cocaine</b> administration in animal models.
+CREB1	drug	cocaine	24205196	We compared the behavioral effects of <b>cocaine</b> and abstinence in adolescent and adult mice and investigated possible age related differences in <strong>CREB</strong> and pCREB levels.
+CREB1	drug	cocaine	24205196	Significant increases in <strong>CREB</strong> levels in the PFC and hippocampus and pCREB in the hippocampus were observed in <b>cocaine</b> abstinent animals compared with the animals treated with <b>cocaine</b> in adulthood.
+CREB1	drug	cocaine	24205196	Interestingly, significant negative correlations were observed between <b>cocaine</b> sensitization and <strong>CREB</strong> levels in both regions.
+CREB1	addiction	sensitization	24205196	Interestingly, significant negative correlations were observed between cocaine <b>sensitization</b> and <strong>CREB</strong> levels in both regions.
+CREB1	drug	amphetamine	24140441	Effect of rhynchophylline on the expression of p <strong>CREB</strong> and sc Fos in triatum and hippocampal CA1 area of <b>methamphetamine</b> induced conditioned place preference rats.
+CREB1	drug	amphetamine	24140441	To explore the effect of rhynchophylline (Rhy) on the expression of p <strong>CREB</strong> and c Fos in the striatum and hippocampal CA1 area of <b>methamphetamine</b> induced conditioned place preference (CPP) rat, <b>methamphetamine</b> (2 mg/kg) was injected to rats and the conditioned place preference was observed in these rats treated with or without Rhy.
+CREB1	addiction	reward	24140441	To explore the effect of rhynchophylline (Rhy) on the expression of p <strong>CREB</strong> and c Fos in the striatum and hippocampal CA1 area of methamphetamine induced conditioned place preference (<b>CPP</b>) rat, methamphetamine (2 mg/kg) was injected to rats and the conditioned place preference was observed in these rats treated with or without Rhy.
+CREB1	drug	amphetamine	24140441	<b>Methamphetamine</b> also increased the number of p <strong>CREB</strong> positive cells in the striatum and hippocampal CA1 zone, as well as p Fos positive cells.
+CREB1	drug	amphetamine	24140441	These findings show that Rhy can suppress the acquisition of CPP in rats induced by <b>methamphetamine</b> and the action may be related with the reduced expression of p <strong>CREB</strong> and p Fos in the striatum and hippocampus.
+CREB1	addiction	reward	24140441	These findings show that Rhy can suppress the acquisition of <b>CPP</b> in rats induced by methamphetamine and the action may be related with the reduced expression of p <strong>CREB</strong> and p Fos in the striatum and hippocampus.
+CREB1	drug	opioid	24073333	Alterations in phosphorylated <strong>CREB</strong> expression in different brain regions following short  and long term <b>morphine</b> exposure: relationship to food intake.
+CREB1	drug	opioid	24073333	Activation of the cyclic adenosine monophosphate (cAMP)/phosphorylated <strong>CREB</strong> (P <strong>CREB</strong>) system in different brain regions has been implicated in mediating <b>opioid</b> tolerance and dependence, while alteration of this system in the lateral hypothalamus (LH) has been suggested to have a role in food intake and body weight.
+CREB1	addiction	dependence	24073333	Activation of the cyclic adenosine monophosphate (cAMP)/phosphorylated <strong>CREB</strong> (P <strong>CREB</strong>) system in different brain regions has been implicated in mediating opioid tolerance and <b>dependence</b>, while alteration of this system in the lateral hypothalamus (LH) has been suggested to have a role in food intake and body weight.
+CREB1	drug	opioid	24073333	Given that <b>opioids</b> regulate food intake, we measured P <strong>CREB</strong> in different brain regions in mice exposed to <b>morphine</b> treatments designed to induce different degrees of tolerance and dependence.
+CREB1	addiction	dependence	24073333	Given that opioids regulate food intake, we measured P <strong>CREB</strong> in different brain regions in mice exposed to morphine treatments designed to induce different degrees of tolerance and <b>dependence</b>.
+CREB1	drug	opioid	24073333	We found that a single <b>morphine</b> injection or daily <b>morphine</b> injections for 8 days did not influence P <strong>CREB</strong> levels, while the escalating dose of <b>morphine</b> regimen raised P <strong>CREB</strong> levels only in the ventral tegmental area (VTA).
+CREB1	drug	opioid	24073333	Chronic <b>morphine</b> pellet implantation for 7 days raised P <strong>CREB</strong> levels in the LH, VTA, and dorsomedial nucleus of the hypothalamus (DM) but not in the nucleus accumbens and amygdala.
+CREB1	drug	opioid	24073333	Increased P <strong>CREB</strong> levels in LH, VTA, and DM following 7 day treatment with <b>morphine</b> pellets and increased P <strong>CREB</strong> levels in the VTA following escalating doses of <b>morphine</b> were associated with decreased food intake and body weight.
+CREB1	drug	opioid	24073333	The <b>morphine</b> regulation of P <strong>CREB</strong> may explain some of the physiological sequelae of <b>opioid</b> exposure including altered food intake and body weight.
+CREB1	drug	nicotine	23999525	We used functional genomic approaches (chromatin immunoprecipitation (ChIP) and whole genome sequencing) to identify cAMP response element binding protein (<strong>CREB</strong>) targets following chronic <b>nicotine</b> administration and withdrawal (WD) in rodents.
+CREB1	addiction	withdrawal	23999525	We used functional genomic approaches (chromatin immunoprecipitation (ChIP) and whole genome sequencing) to identify cAMP response element binding protein (<strong>CREB</strong>) targets following chronic nicotine administration and <b>withdrawal</b> (WD) in rodents.
+CREB1	drug	nicotine	23999525	We found that chronic <b>nicotine</b> and WD differentially modulate <strong>CREB</strong> binding to the gene for neuregulin 3 (NRG3).
+CREB1	drug	alcohol	23912595	Moreover, decreased A2AR function is associated with decreased <strong>CREB</strong> activity in the DMS, which enhances goal oriented behaviors and contributes to excessive <b>ethanol</b> drinking in mice.
+CREB1	drug	alcohol	23903008	PKA and p <strong>CREB</strong> proteins in the limbic forebrain of EtOH conditioned mice on 4th day of withdrawal from continuous EtOH inhalation for 9 days significantly increased, which were completely abolished by <b>acamprosate</b>.
+CREB1	addiction	withdrawal	23903008	PKA and p <strong>CREB</strong> proteins in the limbic forebrain of EtOH conditioned mice on 4th day of <b>withdrawal</b> from continuous EtOH inhalation for 9 days significantly increased, which were completely abolished by acamprosate.
+CREB1	drug	alcohol	23903008	These findings suggest that the signal transduction pathway via the PKA p <strong>CREB</strong> pathway in the limbic forebrain may be functionally related to the development of sensitization of EtOH induced place preference and provide a possible molecular basis for the pharmacological effect of <b>acamprosate</b> to prevent or reduce the relapse of <b>alcohol</b> dependence.
+CREB1	addiction	dependence	23903008	These findings suggest that the signal transduction pathway via the PKA p <strong>CREB</strong> pathway in the limbic forebrain may be functionally related to the development of sensitization of EtOH induced place preference and provide a possible molecular basis for the pharmacological effect of acamprosate to prevent or reduce the relapse of alcohol <b>dependence</b>.
+CREB1	addiction	relapse	23903008	These findings suggest that the signal transduction pathway via the PKA p <strong>CREB</strong> pathway in the limbic forebrain may be functionally related to the development of sensitization of EtOH induced place preference and provide a possible molecular basis for the pharmacological effect of acamprosate to prevent or reduce the <b>relapse</b> of alcohol dependence.
+CREB1	addiction	sensitization	23903008	These findings suggest that the signal transduction pathway via the PKA p <strong>CREB</strong> pathway in the limbic forebrain may be functionally related to the development of <b>sensitization</b> of EtOH induced place preference and provide a possible molecular basis for the pharmacological effect of acamprosate to prevent or reduce the relapse of alcohol dependence.
+CREB1	drug	nicotine	23894483	Moreover, <strong>CREB</strong> phosphorylation, an indicator of neural activity, accompanied the acquisition of <b>nicotine</b> CPP.
+CREB1	addiction	reward	23894483	Moreover, <strong>CREB</strong> phosphorylation, an indicator of neural activity, accompanied the acquisition of nicotine <b>CPP</b>.
+CREB1	drug	opioid	23787292	In this study, we evaluated the role of orexin receptors in the dorsal hippocampus (dHPC) in the development of <b>morphine</b> induced conditioned place preference (CPP) and modification of hippocampal c Fos and cyclic AMP response element binding protein (<strong>CREB</strong>) levels.
+CREB1	addiction	reward	23787292	In this study, we evaluated the role of orexin receptors in the dorsal hippocampus (dHPC) in the development of morphine induced conditioned place preference (<b>CPP</b>) and modification of hippocampal c Fos and cyclic AMP response element binding protein (<strong>CREB</strong>) levels.
+CREB1	drug	opioid	23787292	Successful conditioning with <b>morphine</b> (7.5 mg/kg) was associated with increased levels of hippocampal c Fos and <strong>CREB</strong>, but with decreased <strong>CREB</strong> phosphorylation.
+CREB1	drug	opioid	23787292	Intrahippocampal administration of SB334867 before conditioning sessions disrupted the rewarding effect of <b>morphine</b> (7.5 mg/kg) and blocked <b>morphine</b> induced increases in hippocampal <strong>CREB</strong> protein levels.
+CREB1	drug	opioid	23787292	<b>Morphine</b> reward is related to altered levels of hippocampal c Fos and <strong>CREB</strong>.
+CREB1	addiction	reward	23787292	Morphine <b>reward</b> is related to altered levels of hippocampal c Fos and <strong>CREB</strong>.
+CREB1	drug	opioid	23787292	Inhibition of <b>morphine</b> induced increases in <strong>CREB</strong> levels might be the underlying mechanism for the disruption of <b>morphine</b> CPP.
+CREB1	addiction	reward	23787292	Inhibition of morphine induced increases in <strong>CREB</strong> levels might be the underlying mechanism for the disruption of morphine <b>CPP</b>.
+CREB1	drug	opioid	23745716	<b>Morphine</b> exposure induced an increase in <strong>CREB</strong> phosphorylated at Ser133 in the PVN and central amygdale (CeA), whereas mice exhibiting <b>morphine</b> CPP had higher levels of pCREB in the PVN, CeA and bed nucleus of the stria terminalis (BNST).
+CREB1	addiction	reward	23745716	Morphine exposure induced an increase in <strong>CREB</strong> phosphorylated at Ser133 in the PVN and central amygdale (CeA), whereas mice exhibiting morphine <b>CPP</b> had higher levels of pCREB in the PVN, CeA and bed nucleus of the stria terminalis (BNST).
+CREB1	drug	amphetamine	23726845	<strong>CREB</strong> phosphorylation regulates striatal transcriptional responses in the self administration model of <b>methamphetamine</b> addiction in the rat.
+CREB1	addiction	addiction	23726845	<strong>CREB</strong> phosphorylation regulates striatal transcriptional responses in the self administration model of methamphetamine <b>addiction</b> in the rat.
+CREB1	drug	amphetamine	23726845	Importantly, ChIP PCR showed that <b>METH</b> self administration caused enrichment of phosphorylated <strong>CREB</strong> (pCREB), but not of histone H3 trimethylated at lysine 4 (H3K4me3), on promoters of c fos, fosb, Bdnf and Syp at 2h after cessation of drug intake.
+CREB1	drug	cocaine	23717324	The concerted actions of miR 212 on striatal <strong>CREB</strong> and MeCP2/BDNF activity greatly attenuate the motivational effects of <b>cocaine</b>.
+CREB1	drug	opioid	23682813	Furthermore, NaHS also attenuated <b>morphine</b>/<b>naloxone</b> elevated mRNA levels of AC isoform 1 and 8, production of cAMP, and phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) in mice striatum.
+CREB1	drug	opioid	23682813	Blockade of extracellular regulated protein kinase 1/2 (ERK1/2) with its specific inhibitor attenuated <b>naloxone</b> induced <strong>CREB</strong> phosphorylation.
+CREB1	drug	cocaine	23665060	We investigated whether ERK/<strong>CREB</strong> intracellular responses in the mesocorticolimbic circuitry underlying <b>cocaine</b> environmental associations are sexually dimorphic.
+CREB1	drug	cocaine	23665060	In the nucleus accumbens (NAc) following CPP expression, <b>cocaine</b> treated animals showed increased phosphorylated ERK (pERK), phosphorylated <strong>CREB</strong> (pCREB) and ΔFosB protein levels.
+CREB1	addiction	reward	23665060	In the nucleus accumbens (NAc) following <b>CPP</b> expression, cocaine treated animals showed increased phosphorylated ERK (pERK), phosphorylated <strong>CREB</strong> (pCREB) and ΔFosB protein levels.
+CREB1	drug	cocaine	23665060	CPP scores were positively correlated to NAc pERK, HIP pERK and CPu FosB protein levels, suggesting that similar to males, the ERK/<strong>CREB</strong> intracellular pathway in mesocorticolimbic regions undergoes <b>cocaine</b> induced neuroplasticity in female rats.
+CREB1	addiction	reward	23665060	<b>CPP</b> scores were positively correlated to NAc pERK, HIP pERK and CPu FosB protein levels, suggesting that similar to males, the ERK/<strong>CREB</strong> intracellular pathway in mesocorticolimbic regions undergoes cocaine induced neuroplasticity in female rats.
+CREB1	drug	opioid	23653680	<b>Morphine</b> exposure is known to induce apoptosis, down regulate cAMP response element binding (<strong>CREB</strong>) expression and decrease in dendritic branching and spine density in cultured cells.
+CREB1	drug	opioid	23653680	We found that transmigrated BDNF was effective in suppressing the <b>morphine</b> induced apoptosis, inducing <strong>CREB</strong> expression and restoring the spine density.
+CREB1	drug	cocaine	23624776	Dephosphorylation of extracellular signal regulated kinase (ERK) and cyclic AMP response element binding protein (<strong>CREB</strong>) in the dorsomedial prefrontal cortex (dmPFC) at the end of short access (ShA) <b>cocaine</b> self administration is implicated in <b>cocaine</b> seeking.
+CREB1	addiction	relapse	23624776	Dephosphorylation of extracellular signal regulated kinase (ERK) and cyclic AMP response element binding protein (<strong>CREB</strong>) in the dorsomedial prefrontal cortex (dmPFC) at the end of short access (ShA) cocaine self administration is implicated in cocaine <b>seeking</b>.
+CREB1	drug	cocaine	23624776	However, what receptors and phosphatases mediate this effect and whether ERK/<strong>CREB</strong> and related phospho proteins in the dmPFC react similarly during early withdrawal from long access (LgA) <b>cocaine</b> self administration are unknown.
+CREB1	addiction	withdrawal	23624776	However, what receptors and phosphatases mediate this effect and whether ERK/<strong>CREB</strong> and related phospho proteins in the dmPFC react similarly during early <b>withdrawal</b> from long access (LgA) cocaine self administration are unknown.
+CREB1	drug	cocaine	23624776	Similar to previous findings after ShA <b>cocaine</b>, phospho ERK and phospho <strong>CREB</strong> in the dmPFC were decreased after LgA <b>cocaine</b>.
+CREB1	drug	cocaine	23624776	Activation of phospho STEP may underlie ERK and <strong>CREB</strong> dephosphorylation in the dmPFC as well as internalization and degradation of GluN complexes during early withdrawal from both ShA and LgA <b>cocaine</b> self administration, whereas differential alteration of AMPA receptor subunits after ShA and LgA <b>cocaine</b> self administration depends on <b>cocaine</b> intake.
+CREB1	addiction	withdrawal	23624776	Activation of phospho STEP may underlie ERK and <strong>CREB</strong> dephosphorylation in the dmPFC as well as internalization and degradation of GluN complexes during early <b>withdrawal</b> from both ShA and LgA cocaine self administration, whereas differential alteration of AMPA receptor subunits after ShA and LgA cocaine self administration depends on cocaine intake.
+CREB1	drug	alcohol	23467349	In the present study, we found that decreased A2AR mediated <strong>CREB</strong> activity in the dorsomedial striatum (DMS) enhanced initial behavioral acquisition of goal directed behaviors and the vulnerability to progress to excessive <b>ethanol</b> drinking during operant conditioning in mice lacking <b>ethanol</b> sensitive adenosine transporter ENT1 (ENT1( / )).
+CREB1	addiction	reward	23467349	In the present study, we found that decreased A2AR mediated <strong>CREB</strong> activity in the dorsomedial striatum (DMS) enhanced initial behavioral acquisition of goal directed behaviors and the vulnerability to progress to excessive ethanol drinking during <b>operant</b> conditioning in mice lacking ethanol sensitive adenosine transporter ENT1 (ENT1( / )).
+CREB1	drug	alcohol	23467349	Using mice expressing β galactosidase (lacZ) under the control of seven repeated CRE sites in both genotypes (CRE lacZ/ENT1(+/+) mice and CRE lacZ/ENT1( / ) mice) and the dominant negative form of <strong>CREB</strong>, we found that reduced <strong>CREB</strong> activity in the DMS was causally associated with decreased A2AR signaling and increased goal directed <b>ethanol</b> drinking.
+CREB1	drug	alcohol	23467349	Our results indicate that A2AR mediated <strong>CREB</strong> signaling in the DMS is a key determinant in enhancing the development of goal directed <b>ethanol</b> drinking in mice.
+CREB1	drug	cocaine	23458740	Not all stress is equal: <strong>CREB</strong> is not necessary for restraint stress reinstatement of <b>cocaine</b> conditioned reward.
+CREB1	addiction	relapse	23458740	Not all stress is equal: <strong>CREB</strong> is not necessary for restraint stress <b>reinstatement</b> of cocaine conditioned reward.
+CREB1	addiction	reward	23458740	Not all stress is equal: <strong>CREB</strong> is not necessary for restraint stress reinstatement of cocaine conditioned <b>reward</b>.
+CREB1	drug	cocaine	23458740	Cyclic AMP response element binding protein (<strong>CREB</strong>) is required for swim stress induced reinstatement of <b>cocaine</b> conditioned place preference.
+CREB1	addiction	relapse	23458740	Cyclic AMP response element binding protein (<strong>CREB</strong>) is required for swim stress induced <b>reinstatement</b> of cocaine conditioned place preference.
+CREB1	addiction	relapse	23458740	However, the role of <strong>CREB</strong> in other stress induced <b>reinstatement</b> models has not been examined.
+CREB1	drug	cocaine	23458740	To determine whether <strong>CREB</strong> is required across different stressors we examined the ability of restraint to elicit reinstatement of <b>cocaine</b> conditioned place preference in wild type and CREBαΔ mutant mice.
+CREB1	addiction	relapse	23458740	To determine whether <strong>CREB</strong> is required across different stressors we examined the ability of restraint to elicit <b>reinstatement</b> of cocaine conditioned place preference in wild type and CREBαΔ mutant mice.
+CREB1	drug	opioid	23454521	Photoactivation of optoMOR decreased the Ca(2+) influx and inhibited the forskolin induced cAMP generation, activation of <strong>CREB</strong>, and BDNF levels in optoMOR expressing cells similar to the activation of native μ <b>opioid</b> receptor by DAMGO.
+CREB1	drug	cocaine	23318871	Phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) is also significantly increased in hypocretin neurons in <b>cocaine</b> treated animals, suggesting that <strong>CREB</strong> mediated pathways may contribute to synaptic potentiation in these cells.
+CREB1	drug	opioid	23293139	Although elevated levels of transcriptionally active <strong>CREB</strong> appear to attenuate DA transmission by increasing expression of the endogenous κ <b>opioid</b> receptor (KOR) ligand dynorphin, increased dynorphin transmission may ultimately have undesirable effects that contribute to drug withdrawal states as well as comorbid psychiatric illnesses such as depression.
+CREB1	addiction	withdrawal	23293139	Although elevated levels of transcriptionally active <strong>CREB</strong> appear to attenuate DA transmission by increasing expression of the endogenous κ opioid receptor (KOR) ligand dynorphin, increased dynorphin transmission may ultimately have undesirable effects that contribute to drug <b>withdrawal</b> states as well as comorbid psychiatric illnesses such as depression.
+CREB1	drug	opioid	23242725	Aim of this study was to identify whether hydrogen sulfide (H2S) protects <b>heroin</b> withdrawal rat is related with adenylate cyclase (AC) cAMP protein kinase A (PKA) cAMP response element binding protein (<strong>CREB</strong>) signaling pathway in <b>heroin</b> dependent rat's nucleus accumbens or not.
+CREB1	addiction	withdrawal	23242725	Aim of this study was to identify whether hydrogen sulfide (H2S) protects heroin <b>withdrawal</b> rat is related with adenylate cyclase (AC) cAMP protein kinase A (PKA) cAMP response element binding protein (<strong>CREB</strong>) signaling pathway in heroin dependent rat's nucleus accumbens or not.
+CREB1	drug	opioid	23242725	Exogenous H2S can decrease the high activities of AC, PKA and the high levels of cAMP, p <strong>CREB</strong> caused by <b>heroin</b>.
+CREB1	drug	opioid	23242725	Exogenous H2S decreases <b>naloxone</b> precipitated withdrawal signs, maybe through decreasing AC/cAMP/PKA/<strong>CREB</strong>/NMDR signaling pathway in <b>heroin</b> dependent rats' nucleus accumbens.
+CREB1	addiction	withdrawal	23242725	Exogenous H2S decreases naloxone precipitated <b>withdrawal</b> signs, maybe through decreasing AC/cAMP/PKA/<strong>CREB</strong>/NMDR signaling pathway in heroin dependent rats' nucleus accumbens.
+CREB1	drug	nicotine	23226481	The calcium activated protein, calcium/calmodulin dependent protein kinase IV (CaMKIV) phosphorylates the downstream transcription factor cyclic AMP response element binding protein (<strong>CREB</strong>), which mediates <b>nicotine</b> responses; however the role of CaMKIV in <b>nicotine</b> dependence is unknown.
+CREB1	addiction	dependence	23226481	The calcium activated protein, calcium/calmodulin dependent protein kinase IV (CaMKIV) phosphorylates the downstream transcription factor cyclic AMP response element binding protein (<strong>CREB</strong>), which mediates nicotine responses; however the role of CaMKIV in nicotine <b>dependence</b> is unknown.
+CREB1	drug	nicotine	23226481	Given the proposed role of CaMKIV in <strong>CREB</strong> activation, we hypothesized that CaMKIV might be a crucial molecular component in the development of <b>nicotine</b> dependence.
+CREB1	addiction	dependence	23226481	Given the proposed role of CaMKIV in <strong>CREB</strong> activation, we hypothesized that CaMKIV might be a crucial molecular component in the development of nicotine <b>dependence</b>.
+CREB1	drug	amphetamine	23076832	The present study aims to evaluate the effects of TMX on biochemical targets of Li, such as glycogen synthase kinase 3β (GSK 3β), PKC, PKA, <strong>CREB</strong>, BDNF and NGF, in the brain of rats subjected to an animal model of mania induced by d <b>amphetamine</b> (d <b>AMPH</b>).
+CREB1	drug	amphetamine	23076832	Western blot showed that d <b>AMPH</b> significantly increased GSK 3 and PKC levels, and decreased pGSK 3, PKA, NGF, BDNF and <strong>CREB</strong> levels in the structures analyzed.
+CREB1	drug	opioid	23035088	We found that CPA extinction training induced an increase in recruiting cAMP response element binding protein (<strong>CREB</strong>) to and acetylation of histone H3 at the promoters of BDNF exon I transcript and increased BDNF mRNA and protein expression in the ventromedial prefrontal cortex (vmPFC) of acute <b>morphine</b> dependent rats and that such epigenetic regulation of BDNF gene transcription could be facilitated or diminished by intra vmPFC infusion of HDAC inhibitor trichostatin A or extracellular signal regulated kinase (ERK) inhibitor U0126 (1,4 diamino 2,3 dicyano 1,4 bis(methylthio)butadiene) before extinction training.
+CREB1	drug	opioid	23035088	We conclude that extinction of aversive memory of <b>morphine</b> withdrawal requires epigenetic regulation of BDNF gene transcription in the vmPFC through activation of the ERK <strong>CREB</strong> signaling pathway perhaps in a NMDA receptor dependent manner.
+CREB1	addiction	aversion	23035088	We conclude that extinction of <b>aversive</b> memory of morphine withdrawal requires epigenetic regulation of BDNF gene transcription in the vmPFC through activation of the ERK <strong>CREB</strong> signaling pathway perhaps in a NMDA receptor dependent manner.
+CREB1	addiction	withdrawal	23035088	We conclude that extinction of aversive memory of morphine <b>withdrawal</b> requires epigenetic regulation of BDNF gene transcription in the vmPFC through activation of the ERK <strong>CREB</strong> signaling pathway perhaps in a NMDA receptor dependent manner.
+CREB1	drug	nicotine	22952905	Environmental enrichment alters <b>nicotine</b> mediated locomotor sensitization and phosphorylation of DARPP 32 and <strong>CREB</strong> in rat prefrontal cortex.
+CREB1	addiction	sensitization	22952905	Environmental enrichment alters nicotine mediated locomotor <b>sensitization</b> and phosphorylation of DARPP 32 and <strong>CREB</strong> in rat prefrontal cortex.
+CREB1	drug	nicotine	22952905	The current study determined activation of DARPP 32 (dopamine  and cAMP regulated phosphoprotein 32) and <strong>CREB</strong> (cAMP response element binding protein), and locomotor activity in rats raised in enriched (EC), impoverished (IC), and standard (SC) conditions following repeated administration of <b>nicotine</b> or saline.
+CREB1	drug	nicotine	22952905	Moreover, EC rats had lower basal phosphorylation levels of <strong>CREB</strong> at serine 133 in PFC and nucleus accumbens compared to IC and SC rats, whereas the <b>nicotine</b> induced increase in phosphorylated <strong>CREB</strong> Ser133 was more pronounced in PFC of EC rats relative to IC and SC rats.
+CREB1	drug	nicotine	22791813	The resulting increase in catecholamine production was associated with significant inductions in the phosphorylation of signaling proteins ERK, <strong>CREB</strong>, Src and AKT, upregulated protein expression of nAChR subunits α3, α4, α5 and α7 and increased responsiveness to <b>nicotine</b> in 3 (4,5 dimethylthiazole 2 yl) 2,5 diphenyl tetrazolium bromide and cell migration assays.
+CREB1	drug	opioid	22715022	<b>Hydrocodone</b> and <b>morphine</b> possess similar rewarding effects and reduce ERK and <strong>CREB</strong> phosphorylation in the nucleus accumbens.
+CREB1	drug	opioid	22715022	Moreover, <b>hydrocodone</b> and <b>morphine</b> equally reduced phosphorylation levels of ERK and <strong>CREB</strong> proteins in the nucleus accumbens, suggesting that both drugs exert their effects through signal transduction pathways known to be involved in drug reward and reinforcement.
+CREB1	addiction	reward	22715022	Moreover, hydrocodone and morphine equally reduced phosphorylation levels of ERK and <strong>CREB</strong> proteins in the nucleus accumbens, suggesting that both drugs exert their effects through signal transduction pathways known to be involved in drug <b>reward</b> and <b>reinforcement</b>.
+CREB1	drug	cocaine	22713909	Together, our results suggest that blockade of <b>cocaine</b> induced inhibitory synaptic plasticity (I LTD) and enhancement of <strong>CREB</strong> activation are two putative cellular mechanisms by which PDE4 inhibition impairs the acquisition of <b>cocaine</b> CPP.
+CREB1	addiction	reward	22713909	Together, our results suggest that blockade of cocaine induced inhibitory synaptic plasticity (I LTD) and enhancement of <strong>CREB</strong> activation are two putative cellular mechanisms by which PDE4 inhibition impairs the acquisition of cocaine <b>CPP</b>.
+CREB1	drug	opioid	22666564	<b>Morphine</b> also activates MAPK signaling and downregulates cAMP response element binding protein (<strong>CREB</strong>).
+CREB1	addiction	reward	22649236	Here, we demonstrate a necessary role for two transcription factors, cAMP response element binding protein (<strong>CREB</strong>) and serum response factor (SRF), in mediating this induction within the mouse nucleus accumbens (NAc), a key brain <b>reward</b> region.
+CREB1	drug	cocaine	22649236	<strong>CREB</strong> and SRF are both activated in NAc by <b>cocaine</b> and bind to the fosB gene promoter.
+CREB1	drug	cocaine	22649236	Furthermore, deletion of both SRF and <strong>CREB</strong> from NAc renders animals less sensitive to the rewarding effects of moderate doses of <b>cocaine</b> when tested in the conditioned place preference (CPP) procedure and also blocks locomotor sensitization to higher doses of <b>cocaine</b>.
+CREB1	addiction	reward	22649236	Furthermore, deletion of both SRF and <strong>CREB</strong> from NAc renders animals less sensitive to the rewarding effects of moderate doses of cocaine when tested in the conditioned place preference (<b>CPP</b>) procedure and also blocks locomotor sensitization to higher doses of cocaine.
+CREB1	addiction	sensitization	22649236	Furthermore, deletion of both SRF and <strong>CREB</strong> from NAc renders animals less sensitive to the rewarding effects of moderate doses of cocaine when tested in the conditioned place preference (CPP) procedure and also blocks locomotor <b>sensitization</b> to higher doses of cocaine.
+CREB1	drug	cocaine	22649236	Deletion of <strong>CREB</strong> alone has the opposite effect and enhances both <b>cocaine</b> CPP and locomotor sensitization.
+CREB1	addiction	reward	22649236	Deletion of <strong>CREB</strong> alone has the opposite effect and enhances both cocaine <b>CPP</b> and locomotor sensitization.
+CREB1	addiction	sensitization	22649236	Deletion of <strong>CREB</strong> alone has the opposite effect and enhances both cocaine CPP and locomotor <b>sensitization</b>.
+CREB1	drug	cocaine	22649236	In contrast to ΔFosB induction by <b>cocaine</b>, ΔFosB induction in NAc by chronic social stress, which we have shown previously requires activation of SRF, is unaffected by the deletion of <strong>CREB</strong> alone.
+CREB1	drug	cocaine	22649236	Our results also establish a complex mode of regulation of ΔFosB induction in response to <b>cocaine</b>, which requires the concerted activities of both SRF and <strong>CREB</strong>.
+CREB1	addiction	dependence	22580231	cAMP response element binding protein(<strong>CREB</strong>) and the cAMP cascade play a pivotal role in the opiate <b>dependence</b>.
+CREB1	drug	opioid	22580231	In cells treated with chronic <b>morphine</b>, the expression of <strong>CREB</strong>, adenylyl cyclase (AC) and protein kinase A (PKA) were increased, while in cells infected with LV CREB3, treated with chronic <b>morphine</b> treatment failed to increase the expressions of <strong>CREB</strong> and AC.
+CREB1	drug	opioid	22580231	Consistently, in the rat model for chronic <b>morphine</b> treatment, <b>morphine</b> increased the expression of <strong>CREB</strong>, AC and PKA in LC neurons.
+CREB1	drug	opioid	22580231	In conclusion, the lentiviral vectors expressing <strong>CREB</strong> shRNA inhibited the increase of <strong>CREB</strong> and AC expression induced by chronic <b>morphine</b> treatment both in vivo and in vitro.
+CREB1	drug	nicotine	22521799	The present study examined the short  and long term effects of <b>nicotine</b> and <b>nicotine</b> withdrawal on fear conditioning in pre adolescent, adolescent, and adult mice, and potential underlying substrates that may mediate the developmental effects of <b>nicotine</b>, such as changes in nicotinic acetylcholine receptor (nAChR) binding, <strong>CREB</strong> expression, and <b>nicotine</b> metabolism.
+CREB1	addiction	withdrawal	22521799	The present study examined the short  and long term effects of nicotine and nicotine <b>withdrawal</b> on fear conditioning in pre adolescent, adolescent, and adult mice, and potential underlying substrates that may mediate the developmental effects of nicotine, such as changes in nicotinic acetylcholine receptor (nAChR) binding, <strong>CREB</strong> expression, and nicotine metabolism.
+CREB1	drug	nicotine	22521799	Developmental differences in <b>nicotine</b> metabolism and <strong>CREB</strong> expression were also observed, but were not related to the effects of <b>nicotine</b> withdrawal on contextual learning 24 h post treatment.
+CREB1	addiction	withdrawal	22521799	Developmental differences in nicotine metabolism and <strong>CREB</strong> expression were also observed, but were not related to the effects of nicotine <b>withdrawal</b> on contextual learning 24 h post treatment.
+CREB1	drug	cocaine	22453546	This study was conducted to investigate the effects of acupuncture on footshock induced reinstatement of <b>cocaine</b> seeking and the expression of c Fos and the transcription factor cAMP response element binding protein (<strong>CREB</strong>) in the NAc, used as markers of neuronal activation in conditions of stress induced reinstatement to <b>cocaine</b>.
+CREB1	addiction	relapse	22453546	This study was conducted to investigate the effects of acupuncture on footshock induced <b>reinstatement</b> of cocaine <b>seeking</b> and the expression of c Fos and the transcription factor cAMP response element binding protein (<strong>CREB</strong>) in the NAc, used as markers of neuronal activation in conditions of stress induced <b>reinstatement</b> to cocaine.
+CREB1	drug	cocaine	22453546	Acute footshock stress reinstated <b>cocaine</b> seeking behavior and enhanced c Fos expression and phosphorylated <strong>CREB</strong> (pCREB) activation in the NAc shell in <b>cocaine</b> pre exposed rats.
+CREB1	addiction	relapse	22453546	Acute footshock stress reinstated cocaine <b>seeking</b> behavior and enhanced c Fos expression and phosphorylated <strong>CREB</strong> (pCREB) activation in the NAc shell in cocaine pre exposed rats.
+CREB1	drug	opioid	22355339	Involvement of noradrenergic transmission in the PVN on <strong>CREB</strong> activation, TORC1 levels, and pituitary adrenal axis activity during <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	22355339	Involvement of noradrenergic transmission in the PVN on <strong>CREB</strong> activation, TORC1 levels, and pituitary adrenal axis activity during morphine <b>withdrawal</b>.
+CREB1	drug	opioid	22355339	The present study tested the hypothesis that changes in <strong>CREB</strong> activation and phosphorylated TORC1 levels in the hypothalamic paraventricular nucleus (PVN) after <b>naloxone</b> precipitated <b>morphine</b> withdrawal as well as the HPA axis activity arises from α(1)  and/or β adrenoceptor activation.
+CREB1	addiction	withdrawal	22355339	The present study tested the hypothesis that changes in <strong>CREB</strong> activation and phosphorylated TORC1 levels in the hypothalamic paraventricular nucleus (PVN) after naloxone precipitated morphine <b>withdrawal</b> as well as the HPA axis activity arises from α(1)  and/or β adrenoceptor activation.
+CREB1	drug	opioid	22355339	The effects of <b>morphine</b> dependence and withdrawal on <strong>CREB</strong> phosphorylation (pCREB), phosphorylated TORC1 (pTORC1), and HPA axis response were measured by Western blot, immunohistochemistry and radioimmunoassay in rats pretreated with prazosin (α(1) adrenoceptor antagonist) or propranolol (β adrenoceptor antagonist).
+CREB1	addiction	dependence	22355339	The effects of morphine <b>dependence</b> and withdrawal on <strong>CREB</strong> phosphorylation (pCREB), phosphorylated TORC1 (pTORC1), and HPA axis response were measured by Western blot, immunohistochemistry and radioimmunoassay in rats pretreated with prazosin (α(1) adrenoceptor antagonist) or propranolol (β adrenoceptor antagonist).
+CREB1	addiction	withdrawal	22355339	The effects of morphine dependence and <b>withdrawal</b> on <strong>CREB</strong> phosphorylation (pCREB), phosphorylated TORC1 (pTORC1), and HPA axis response were measured by Western blot, immunohistochemistry and radioimmunoassay in rats pretreated with prazosin (α(1) adrenoceptor antagonist) or propranolol (β adrenoceptor antagonist).
+CREB1	drug	opioid	22355339	Present results suggest that, during acute <b>morphine</b> withdrawal, NA may control the HPA axis activity through <strong>CREB</strong> activation at the PVN level.
+CREB1	addiction	withdrawal	22355339	Present results suggest that, during acute morphine <b>withdrawal</b>, NA may control the HPA axis activity through <strong>CREB</strong> activation at the PVN level.
+CREB1	drug	opioid	22355339	We concluded that the combined increase in <strong>CREB</strong> phosphorylation and decrease in pTORC1 levels might represent, in part, two of the mechanisms of <strong>CREB</strong> activation at the PVN during <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	22355339	We concluded that the combined increase in <strong>CREB</strong> phosphorylation and decrease in pTORC1 levels might represent, in part, two of the mechanisms of <strong>CREB</strong> activation at the PVN during morphine <b>withdrawal</b>.
+CREB1	drug	nicotine	22330674	Stress induces behavioral sensitization, increases <b>nicotine</b> seeking behavior and leads to a decrease of <strong>CREB</strong> in the nucleus accumbens.
+CREB1	addiction	relapse	22330674	Stress induces behavioral sensitization, increases nicotine <b>seeking</b> behavior and leads to a decrease of <strong>CREB</strong> in the nucleus accumbens.
+CREB1	addiction	sensitization	22330674	Stress induces behavioral <b>sensitization</b>, increases nicotine seeking behavior and leads to a decrease of <strong>CREB</strong> in the nucleus accumbens.
+CREB1	drug	nicotine	22330674	The present experiments examined the effects of exposure to variable stress on <b>nicotine</b> induced locomotor activation, cAMP response element binding protein (<strong>CREB</strong>) and extracellular signal regulated kinase (ERK) activity and <b>nicotine</b> intravenous self administration in rats.
+CREB1	drug	nicotine	22330674	Repeated variable stress caused a sensitized motor response to a single challenge of <b>nicotine</b> and decreased <strong>CREB</strong> in the nucleus accumbens.
+CREB1	drug	nicotine	22301350	We examined the hypothesis that adolescent animals who exhibit higher novel stimulus reactivity, exhibit greater locomotor activity in response to <b>nicotine</b> than adolescents who exhibit lower novel stimulus reactivity, and that this difference is associated with alterations in <strong>CREB</strong> expression and activity in the ventral striatum (vStr) and prefrontal cortex (PFC).
+CREB1	drug	nicotine	22301350	Further, HLA adolescents exhibited lower <strong>CREB</strong> activity in the vStr than LLA adolescents and this difference was attenuated by repeated exposure to high, but not low doses of <b>nicotine</b>.
+CREB1	drug	alcohol	22269225	Dysregulated phosphorylation and nuclear translocation of cyclic AMP response element binding protein (<strong>CREB</strong>) in rat liver after chronic <b>ethanol</b> binge.
+CREB1	addiction	intoxication	22269225	Dysregulated phosphorylation and nuclear translocation of cyclic AMP response element binding protein (<strong>CREB</strong>) in rat liver after chronic ethanol <b>binge</b>.
+CREB1	drug	alcohol	22269225	We examined the effects of <b>ethanol</b> on the phosphorylation of <strong>CREB</strong> in hepatocytes, and in vivo in rat liver after chronic <b>ethanol</b> binge.
+CREB1	addiction	intoxication	22269225	We examined the effects of ethanol on the phosphorylation of <strong>CREB</strong> in hepatocytes, and in vivo in rat liver after chronic ethanol <b>binge</b>.
+CREB1	drug	alcohol	22269225	Treatment of hepatocytes with <b>ethanol</b> caused increased phosphorylation of p38 MAPK (mitogen activated protein kinase), MSK 1 (mitogen and stress activated kinase) and <strong>CREB</strong> in the nuclear compartment without activation of ERK1/2 (extracellular regulated kinase); whereas angiotensin II induced activation of <strong>CREB</strong> was accompanied by activation of ERK1/2.
+CREB1	drug	alcohol	22269225	In chronic <b>ethanol</b> binge studies, analysis of the whole cell extracts showed increased phosphorylation of <strong>CREB</strong>, with no effect on <strong>CREB</strong> protein levels; increased phospho ERK1/2, and decreased phospho p38 MAPK.
+CREB1	addiction	intoxication	22269225	In chronic ethanol <b>binge</b> studies, analysis of the whole cell extracts showed increased phosphorylation of <strong>CREB</strong>, with no effect on <strong>CREB</strong> protein levels; increased phospho ERK1/2, and decreased phospho p38 MAPK.
+CREB1	addiction	intoxication	22269225	Reduction in phospho <strong>CREB</strong> and <strong>CREB</strong> proteins in the nuclear extracts was accompanied by suppression of mRNA levels for CPT 1 (carnitine palmitoyl transferase 1) and increase in hepatic steatosis after <b>binge</b>.
+CREB1	drug	alcohol	22269225	It is concluded that binge <b>ethanol</b> causes defect in the nuclear accumulation of <strong>CREB</strong> protein, phospho <strong>CREB</strong>, and an exaggerated hepatic steatosis.
+CREB1	addiction	intoxication	22269225	It is concluded that <b>binge</b> ethanol causes defect in the nuclear accumulation of <strong>CREB</strong> protein, phospho <strong>CREB</strong>, and an exaggerated hepatic steatosis.
+CREB1	drug	cocaine	22197517	Expression of AMPA receptor subunits (GluR1 and GluR2) and CRE binding protein (<strong>CREB</strong>) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of <b>cocaine</b>, with and without ICSS.
+CREB1	addiction	reward	22197517	Expression of AMPA receptor subunits (GluR1 and GluR2) and CRE binding protein (<strong>CREB</strong>) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of cocaine, with and without <b>ICSS</b>.
+CREB1	drug	cocaine	22197517	Repeated <b>cocaine</b> reduced GluR1, GluR2 and <strong>CREB</strong> expression in the NAc, and reductions of GluR1 and GluR2 but not <strong>CREB</strong> were further enhanced by ICSS.
+CREB1	addiction	reward	22197517	Repeated cocaine reduced GluR1, GluR2 and <strong>CREB</strong> expression in the NAc, and reductions of GluR1 and GluR2 but not <strong>CREB</strong> were further enhanced by <b>ICSS</b>.
+CREB1	drug	nicotine	22086359	<strong>CREB</strong> involvement in the regulation of striatal prodynorphin by <b>nicotine</b>.
+CREB1	drug	nicotine	22086359	<strong>CREB</strong> phosphorylation at Ser133 is enhanced by drugs of abuse, including <b>nicotine</b>.
+CREB1	addiction	addiction	22086359	Dynorphin (Dyn) contributes to the <b>addictive</b> process and its precursor gene prodynorphin (PD) is regulated by <strong>CREB</strong>.
+CREB1	drug	nicotine	22086359	These studies investigated PD transcription in mice acutely treated with <b>nicotine</b>, determined the role of <strong>CREB</strong>, and characterized the receptors involved.
+CREB1	drug	nicotine	22086359	Acute <b>nicotine</b> increased adenylyl cyclase activity, cAMP, and pCREB Ser133 levels in striatum and enhanced <strong>CREB</strong> binding to CRE elements (DynCREs) of the PD promoter, preferentially DynCRE3.
+CREB1	drug	nicotine	22086359	Our findings suggest that <b>nicotine</b> regulates PD expression in striatum at the transcriptional level and <strong>CREB</strong> is involved.
+CREB1	drug	cocaine	22072694	Overexpression of <strong>CREB</strong> in the nucleus accumbens shell increases <b>cocaine</b> reinforcement in self administering rats.
+CREB1	addiction	reward	22072694	Overexpression of <strong>CREB</strong> in the nucleus accumbens shell increases cocaine <b>reinforcement</b> in self administering rats.
+CREB1	drug	cocaine	22072694	Chronic exposure to addictive drugs enhances cAMP response element binding protein (<strong>CREB</strong>) regulated gene expression in nucleus accumbens (NAc), and these effects are thought to reduce the positive hedonic effects of passive <b>cocaine</b> administration.
+CREB1	addiction	addiction	22072694	Chronic exposure to <b>addictive</b> drugs enhances cAMP response element binding protein (<strong>CREB</strong>) regulated gene expression in nucleus accumbens (NAc), and these effects are thought to reduce the positive hedonic effects of passive cocaine administration.
+CREB1	addiction	reward	22072694	Chronic exposure to addictive drugs enhances cAMP response element binding protein (<strong>CREB</strong>) regulated gene expression in nucleus accumbens (NAc), and these effects are thought to reduce the positive <b>hedonic</b> effects of passive cocaine administration.
+CREB1	drug	cocaine	22072694	Here, we used viral mediated gene transfer to produce short  and long term regulation of <strong>CREB</strong> activity in NAc shell of rats engaging in volitional <b>cocaine</b> self administration.
+CREB1	drug	cocaine	22072694	Increasing <strong>CREB</strong> expression in NAc shell markedly enhanced <b>cocaine</b> reinforcement of self administration behavior, as indicated by leftward (long term) and upward (short term) shifts in fixed ratio dose response curves.
+CREB1	addiction	reward	22072694	Increasing <strong>CREB</strong> expression in NAc shell markedly enhanced cocaine <b>reinforcement</b> of self administration behavior, as indicated by leftward (long term) and upward (short term) shifts in fixed ratio dose response curves.
+CREB1	drug	cocaine	22072694	<strong>CREB</strong> also increased the effort exerted by rats to obtain <b>cocaine</b> on more demanding progressive ratio schedules, an effect highly correlated with viral induced modulation of BDNF protein in the NAc shell.
+CREB1	drug	cocaine	22072694	<strong>CREB</strong> enhanced <b>cocaine</b> reinforcement when expressed either throughout acquisition of self administration or when expression was limited to postacquisition tests, indicating a direct effect of <strong>CREB</strong> independent of reinforcement related learning.
+CREB1	addiction	reward	22072694	<strong>CREB</strong> enhanced cocaine <b>reinforcement</b> when expressed either throughout acquisition of self administration or when expression was limited to postacquisition tests, indicating a direct effect of <strong>CREB</strong> independent of <b>reinforcement</b> related learning.
+CREB1	drug	cocaine	22072694	Downregulating endogenous <strong>CREB</strong> in NAc shell by expressing a short hairpin RNA reduced <b>cocaine</b> reinforcement in similar tests, while overexpression of a dominant negative <strong>CREB</strong>(S133A) mutant had no significant effect on <b>cocaine</b> self administration.
+CREB1	addiction	reward	22072694	Downregulating endogenous <strong>CREB</strong> in NAc shell by expressing a short hairpin RNA reduced cocaine <b>reinforcement</b> in similar tests, while overexpression of a dominant negative <strong>CREB</strong>(S133A) mutant had no significant effect on cocaine self administration.
+CREB1	drug	cocaine	22072694	Finally, increasing <strong>CREB</strong> expression after withdrawal from self administration enhanced <b>cocaine</b> primed relapse, while reducing <strong>CREB</strong> levels facilitated extinction of <b>cocaine</b> seeking, but neither altered relapse induced by <b>cocaine</b> cues or footshock stress.
+CREB1	addiction	relapse	22072694	Finally, increasing <strong>CREB</strong> expression after withdrawal from self administration enhanced cocaine primed <b>relapse</b>, while reducing <strong>CREB</strong> levels facilitated extinction of cocaine <b>seeking</b>, but neither altered <b>relapse</b> induced by cocaine cues or footshock stress.
+CREB1	addiction	withdrawal	22072694	Finally, increasing <strong>CREB</strong> expression after <b>withdrawal</b> from self administration enhanced cocaine primed relapse, while reducing <strong>CREB</strong> levels facilitated extinction of cocaine seeking, but neither altered relapse induced by cocaine cues or footshock stress.
+CREB1	drug	cocaine	22072694	Together, these findings indicate that <strong>CREB</strong> activity in NAc shell increases the motivation for <b>cocaine</b> during active self administration or after withdrawal from <b>cocaine</b>.
+CREB1	addiction	withdrawal	22072694	Together, these findings indicate that <strong>CREB</strong> activity in NAc shell increases the motivation for cocaine during active self administration or after <b>withdrawal</b> from cocaine.
+CREB1	drug	cocaine	22043863	<b>Cocaine</b> induced changes in BDNF mRNA were associated with increased acetylation of histone 3 and binding of <strong>CREB</strong> binding protein to exon I containing promoters in the VTA.
+CREB1	drug	cocaine	21886557	These changes are considered as consequences of <b>cocaine</b> induced molecular adaptation such as <strong>CREB</strong> and c Fos.
+CREB1	drug	cocaine	21886557	In addition, LQ inhibited <strong>CREB</strong> phosphorylation and c Fos expression in the striatum and the nucleus accumbens induced by acute <b>cocaine</b>.
+CREB1	drug	cocaine	21867882	This resilience was mediated, in part, through repression of BDNF TrkB <strong>CREB</strong> signaling, which was induced after repeated <b>cocaine</b> or stress.
+CREB1	drug	cocaine	21812869	Chronic <b>cocaine</b> self administration modulates ERK1/2 and <strong>CREB</strong> responses to dopamine receptor agonists in striatal slices.
+CREB1	drug	cocaine	21812869	We hypothesized that chronic <b>cocaine</b> self administration could influence dopamine D1 and D2 receptor activation of extracellular signal regulated protein kinase 1 and 2 (ERK1/2) and cyclic adenosine monophosphate response element binding protein (<strong>CREB</strong>) phosphorylation.
+CREB1	drug	cocaine	21812869	<b>Cocaine</b> self administration also reduced D1R agonist induced <strong>CREB</strong> phosphorylation in striatal slices, suggesting a downregulation of D1R signaling.
+CREB1	drug	cocaine	21812869	In contrast, surprisingly, <b>cocaine</b> self administration strongly potentiated D2R agonist induced <strong>CREB</strong> phosphorylation selectively in the NAc portion of the slices.
+CREB1	drug	cocaine	21812869	Our finding that selected cellular D2R responses to <strong>CREB</strong> were strengthened by <b>cocaine</b> self administration could be relevant to understand how dopaminergic receptors participate in <b>cocaine</b> induced behaviors.
+CREB1	drug	opioid	21782156	Thus, c Fos, FosB/ΔFosB and P <strong>CREB</strong> immunoreactive profiles were quantified in the rat CPu after either acute or continuous (6 day) administration of <b>morphine</b> and/or PD168,077.
+CREB1	drug	opioid	21782156	Interestingly, at some time points, combined treatment with <b>morphine</b> and PD168,077 substantially increased c Fos, FosB/ΔFosB and P <strong>CREB</strong> expression.
+CREB1	addiction	reward	21766169	In response to drug exposure, <strong>CREB1</strong> is phosphorylated in the striatum, a structure that is critically involved in <b>reward</b> related learning.
+CREB1	drug	alcohol	21766169	Here we show that <strong>CREB1</strong> mutant mice have increased sensitivity to psychostimulants, an effect that does not generalise to <b>ethanol</b> induced hypnosis.
+CREB1	addiction	addiction	21752352	A polymorphism of the <strong>CREB</strong> binding protein (CREBBP) gene is a risk factor for <b>addiction</b>.
+CREB1	addiction	addiction	21752352	Unequivocal evidences have implicated c AMP response element binding protein (<strong>CREB</strong>) in drug <b>addiction</b>.
+CREB1	drug	amphetamine	21738744	Furthermore, Western blot analysis and quantitative real time reverse transcription polymerase chain reaction demonstrated that ICER overexpression abolished the <b>METH</b> induced increase in <strong>CREB</strong> expression and repressed cocaine  and <b>amphetamine</b> regulated transcript (CART) and prodynorphin (Pdyn) expression in mice.
+CREB1	drug	cocaine	21738744	Furthermore, Western blot analysis and quantitative real time reverse transcription polymerase chain reaction demonstrated that ICER overexpression abolished the METH induced increase in <strong>CREB</strong> expression and repressed <b>cocaine</b>  and amphetamine regulated transcript (CART) and prodynorphin (Pdyn) expression in mice.
+CREB1	drug	cocaine	21632938	Using a combination of viral vector mediated genetic manipulations, biochemistry, and electrophysiology in a locomotor sensitization paradigm with repeated, daily, noncontingent <b>cocaine</b> (15 mg/kg) injections, we show that dominant negative cAMP element binding protein (<strong>CREB</strong>) prevents <b>cocaine</b> induced generation of silent synapses of young (30 d old) rats, whereas constitutively active <strong>CREB</strong> is sufficient to increase the number of NR2B containing NMDA receptors (NMDARs) at synapses and to generate silent synapses.
+CREB1	addiction	sensitization	21632938	Using a combination of viral vector mediated genetic manipulations, biochemistry, and electrophysiology in a locomotor <b>sensitization</b> paradigm with repeated, daily, noncontingent cocaine (15 mg/kg) injections, we show that dominant negative cAMP element binding protein (<strong>CREB</strong>) prevents cocaine induced generation of silent synapses of young (30 d old) rats, whereas constitutively active <strong>CREB</strong> is sufficient to increase the number of NR2B containing NMDA receptors (NMDARs) at synapses and to generate silent synapses.
+CREB1	drug	cocaine	21632938	Our data are consistent with a cellular cascade whereby <b>cocaine</b> induced activation of <strong>CREB</strong> promotes <strong>CREB</strong> dependent transcription of NR2B and synaptic incorporation of NR2B containing NMDARs, which generates new silent synapses within the NAc.
+CREB1	drug	cocaine	21632938	We propose that <b>cocaine</b> induced activation of <strong>CREB</strong> and generation of new silent synapses may serve as key cellular events mediating <b>cocaine</b> induced locomotor sensitization.
+CREB1	addiction	sensitization	21632938	We propose that cocaine induced activation of <strong>CREB</strong> and generation of new silent synapses may serve as key cellular events mediating cocaine induced locomotor <b>sensitization</b>.
+CREB1	drug	opioid	21615389	Here, we investigated changes in activation of the transcription factor, cAMP response element binding protein (<strong>CREB</strong>), in the hypothalamic paraventricular nucleus (PVN) and the kinases that may mediate the <b>morphine</b> withdrawal triggered activation of <strong>CREB</strong> and the response of the hypothalamic pituitary adrenocortical (HPA) axis after <b>naloxone</b> induced <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	21615389	Here, we investigated changes in activation of the transcription factor, cAMP response element binding protein (<strong>CREB</strong>), in the hypothalamic paraventricular nucleus (PVN) and the kinases that may mediate the morphine <b>withdrawal</b> triggered activation of <strong>CREB</strong> and the response of the hypothalamic pituitary adrenocortical (HPA) axis after naloxone induced morphine <b>withdrawal</b>.
+CREB1	drug	opioid	21615389	The effects of <b>morphine</b> dependence and withdrawal, phosphorylated <strong>CREB</strong> (pCREB), corticotrophin releasing factor (CRF) expression in the PVN and HPA axis activity were measured using immunoblotting, immunohistochemistry and radioimmunoassay in controls and in <b>morphine</b> dependent rats, withdrawn with <b>naloxone</b> and pretreated with vehicle, calphostin C, chelerythrine (inhibitors of protein kinase C (PKC) or SL 327 [inhibitor of extracellular signal regulated kinase (ERK) kinase].
+CREB1	addiction	dependence	21615389	The effects of morphine <b>dependence</b> and withdrawal, phosphorylated <strong>CREB</strong> (pCREB), corticotrophin releasing factor (CRF) expression in the PVN and HPA axis activity were measured using immunoblotting, immunohistochemistry and radioimmunoassay in controls and in morphine dependent rats, withdrawn with naloxone and pretreated with vehicle, calphostin C, chelerythrine (inhibitors of protein kinase C (PKC) or SL 327 [inhibitor of extracellular signal regulated kinase (ERK) kinase].
+CREB1	addiction	withdrawal	21615389	The effects of morphine dependence and <b>withdrawal</b>, phosphorylated <strong>CREB</strong> (pCREB), corticotrophin releasing factor (CRF) expression in the PVN and HPA axis activity were measured using immunoblotting, immunohistochemistry and radioimmunoassay in controls and in morphine dependent rats, withdrawn with naloxone and pretreated with vehicle, calphostin C, chelerythrine (inhibitors of protein kinase C (PKC) or SL 327 [inhibitor of extracellular signal regulated kinase (ERK) kinase].
+CREB1	drug	opioid	21615389	PKC mediated, in part, both <strong>CREB</strong> activation and the HPA response to <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	21615389	PKC mediated, in part, both <strong>CREB</strong> activation and the HPA response to morphine <b>withdrawal</b>.
+CREB1	drug	nicotine	21420997	Genetically expressed HIV 1 viral proteins attenuate <b>nicotine</b> induced behavioral sensitization and alter mesocorticolimbic ERK and <strong>CREB</strong> signaling in rats.
+CREB1	addiction	sensitization	21420997	Genetically expressed HIV 1 viral proteins attenuate nicotine induced behavioral <b>sensitization</b> and alter mesocorticolimbic ERK and <strong>CREB</strong> signaling in rats.
+CREB1	drug	nicotine	21420997	In the <b>nicotine</b> treated groups, the levels of phosphorylated <strong>CREB</strong> and ERK2 in the PFC were increased in HIV 1Tg rats, but decreased in F344 animals.
+CREB1	drug	nicotine	21420997	Moreover, repeated <b>nicotine</b> administration reduced phosphorylated ERK2 in the VTA of HIV 1Tg rats and in the NAc of F344 rats, but had no effect on phosphorylated <strong>CREB</strong>, indicating a region specific change of intracellular signaling.
+CREB1	drug	nicotine	21420997	These results demonstrate that HIV 1 viral proteins produce differences in basal and <b>nicotine</b> induced alterations in <strong>CREB</strong> and ERK signaling that may contribute to the alteration in psychomotor sensitization.
+CREB1	addiction	sensitization	21420997	These results demonstrate that HIV 1 viral proteins produce differences in basal and nicotine induced alterations in <strong>CREB</strong> and ERK signaling that may contribute to the alteration in psychomotor <b>sensitization</b>.
+CREB1	drug	nicotine	21420997	Thus, HIV 1 positive <b>smokers</b> are possibly more vulnerable to alterations in <strong>CREB</strong> and ERK signaling and this has implications for motivated behavior, including <b>tobacco</b> <b>smoking</b>, in HIV 1 positive individuals who self administer <b>nicotine</b>.
+CREB1	addiction	aversion	21414930	Here we show in rats that stress (footshock) activates the transcription factor cAMP response element binding protein (<strong>CREB</strong>) within the nucleus accumbens shell (NAS), a brain area involved in encoding reward and <b>aversion</b>.
+CREB1	addiction	reward	21414930	Here we show in rats that stress (footshock) activates the transcription factor cAMP response element binding protein (<strong>CREB</strong>) within the nucleus accumbens shell (NAS), a brain area involved in encoding <b>reward</b> and aversion.
+CREB1	addiction	reward	21414930	Elevated <strong>CREB</strong> produced increases in intracranial self stimulation thresholds, a depressive like sign reflecting anhedonia (decreased sensitivity to <b>reward</b>), whereas disruption of <strong>CREB</strong> function by expression of a dominant negative <strong>CREB</strong> had the opposite effect.
+CREB1	drug	opioid	21414930	To mimic downstream effects of <strong>CREB</strong> activation on expression of the <b>opioid</b> peptide dynorphin, we microinjected the κ <b>opioid</b> receptor (KOR) agonist U50,488 directly into the NAS.
+CREB1	drug	opioid	21362452	The data suggest that vagus nerve stimulation may inhibit <b>heroin</b>  or <b>heroin</b> cue induced relapse, possibly by regulation of the expression of Fos and <strong>CREB</strong> in nucleus accumbens.
+CREB1	addiction	relapse	21362452	The data suggest that vagus nerve stimulation may inhibit heroin  or heroin cue induced <b>relapse</b>, possibly by regulation of the expression of Fos and <strong>CREB</strong> in nucleus accumbens.
+CREB1	drug	opioid	21356274	Moreover, selective attenuation of spinal p ERK5 expression by BIX02188 could significantly relieve <b>morphine</b> withdrawal symptom, accompanying with the decreased phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) in the spinal cord.
+CREB1	addiction	withdrawal	21356274	Moreover, selective attenuation of spinal p ERK5 expression by BIX02188 could significantly relieve morphine <b>withdrawal</b> symptom, accompanying with the decreased phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) in the spinal cord.
+CREB1	drug	alcohol	21295078	Several lines of evidence have shown that cAMP response element binding protein (<strong>CREB</strong>), extracellular signal regulated kinase (ERK), and c fos have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, nicotine, and <b>alcohol</b>.
+CREB1	drug	cocaine	21295078	Several lines of evidence have shown that cAMP response element binding protein (<strong>CREB</strong>), extracellular signal regulated kinase (ERK), and c fos have pivotal role in CPP induced by drugs of abuse, such as morphine, <b>cocaine</b>, nicotine, and alcohol.
+CREB1	drug	nicotine	21295078	Several lines of evidence have shown that cAMP response element binding protein (<strong>CREB</strong>), extracellular signal regulated kinase (ERK), and c fos have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, <b>nicotine</b>, and alcohol.
+CREB1	drug	opioid	21295078	Several lines of evidence have shown that cAMP response element binding protein (<strong>CREB</strong>), extracellular signal regulated kinase (ERK), and c fos have pivotal role in CPP induced by drugs of abuse, such as <b>morphine</b>, cocaine, nicotine, and alcohol.
+CREB1	addiction	reward	21295078	Several lines of evidence have shown that cAMP response element binding protein (<strong>CREB</strong>), extracellular signal regulated kinase (ERK), and c fos have pivotal role in <b>CPP</b> induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.
+CREB1	addiction	reward	21295078	Therefore, in the present study, we investigated the changes in phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) and  ERK (p ERK), and c fos induction within ventral tegmental area (VTA), hippocampus and prefrontal cortex (PFC) after the acquisition of <b>CPP</b> induced by intra LH administration of carbachol.
+CREB1	addiction	reward	21295078	The results indicated a significant increase in level of phosphorylated <strong>CREB</strong> (P<0.01) in VTA, and PFC (P<0.05), during LH stimulation induced <b>CPP</b>, while its level decreased in hippocampus (P<0.05).
+CREB1	addiction	reward	21295078	Our findings suggest that studying the intracellular signals and their changes, such as phosphorylated <strong>CREB</strong>, can elucidate a functional relationship between LH and other brain structures involved in <b>reward</b> processing in rats.
+CREB1	drug	cocaine	21248106	Vehicle infused rats with a <b>cocaine</b> SA history showed significant decreases in ERK and cyclic AMP response element binding protein (<strong>CREB</strong>), but not Akt, phosphorylation after the final <b>cocaine</b> SA session that were reversed by intra dmPFC BDNF.
+CREB1	drug	cocaine	21248106	Additionally, BDNF's ability to normalize <b>cocaine</b> mediated decreases in ERK and <strong>CREB</strong> phosphorylation was blocked by U0126, demonstrating that ERK/MAPK activation mediated the behavioral effects.
+CREB1	drug	cocaine	21248106	This study elucidates a mechanism whereby BDNF/TrkB (tropomyosin receptor kinase B) activates ERK regulated <strong>CREB</strong> phosphorylation in the dmPFC to counteract the neuroadaptations induced by <b>cocaine</b> SA and subsequent relapse to <b>cocaine</b> seeking.
+CREB1	addiction	relapse	21248106	This study elucidates a mechanism whereby BDNF/TrkB (tropomyosin receptor kinase B) activates ERK regulated <strong>CREB</strong> phosphorylation in the dmPFC to counteract the neuroadaptations induced by cocaine SA and subsequent <b>relapse</b> to cocaine <b>seeking</b>.
+CREB1	drug	nicotine	21232579	Alterations in BDNF and phospho <strong>CREB</strong> levels following chronic oral <b>nicotine</b> treatment and its withdrawal in dopaminergic brain areas of mice.
+CREB1	addiction	withdrawal	21232579	Alterations in BDNF and phospho <strong>CREB</strong> levels following chronic oral nicotine treatment and its <b>withdrawal</b> in dopaminergic brain areas of mice.
+CREB1	drug	nicotine	21232579	In conclusion, the current results suggest the involvement of BDNF  and <strong>CREB</strong> related neuronal processes in <b>nicotine</b> induced neurochemical, behavioural, and neuroplastic changes in dopaminergic neurocircuits.
+CREB1	drug	amphetamine	21229349	There were also chronic <b>METH</b> associated decreases in the expression of cAMP responsive element binding protein (<strong>CREB</strong>) which modulates IEG expression via activation of the cAMP/PKA/<strong>CREB</strong> signal transduction pathway.
+CREB1	drug	opioid	21167242	Multiple 100 Hz electroacupuncture treatments produced cumulative effect on the suppression of <b>morphine</b> withdrawal syndrome: Central preprodynorphin mRNA and p <strong>CREB</strong> implicated.
+CREB1	addiction	withdrawal	21167242	Multiple 100 Hz electroacupuncture treatments produced cumulative effect on the suppression of morphine <b>withdrawal</b> syndrome: Central preprodynorphin mRNA and p <strong>CREB</strong> implicated.
+CREB1	drug	opioid	21167242	The findings suggest that down regulation of p <strong>CREB</strong> and acceleration of dynorphin synthesis in spinal cord, PAG and hypothalamus may be implicated in the cumulative effect of multiple 100Hz EA treatment for <b>opioid</b> detoxification.
+CREB1	drug	amphetamine	21159975	Molecular studies to further elucidate the role of Ca(v)1.2 versus Ca(v)1.3 LTCCs in activating signaling pathways in the nucleus accumbens (NAc) of drug naive versus drug preexposed mice examined 14 d later revealed that an acute <b>amphetamine</b> and cocaine challenge in drug naive mice increases Ser133 cAMP response element binding protein (<strong>CREB</strong>) phosphorylation in the NAc via Ca(v)1.3 channels and via a dopamine D(1) dependent mechanism, independent of the extracellular signal regulated kinase (ERK) pathway, an important mediator of psychostimulant induced plasticity.
+CREB1	drug	cocaine	21159975	Molecular studies to further elucidate the role of Ca(v)1.2 versus Ca(v)1.3 LTCCs in activating signaling pathways in the nucleus accumbens (NAc) of drug naive versus drug preexposed mice examined 14 d later revealed that an acute amphetamine and <b>cocaine</b> challenge in drug naive mice increases Ser133 cAMP response element binding protein (<strong>CREB</strong>) phosphorylation in the NAc via Ca(v)1.3 channels and via a dopamine D(1) dependent mechanism, independent of the extracellular signal regulated kinase (ERK) pathway, an important mediator of psychostimulant induced plasticity.
+CREB1	drug	amphetamine	21159975	In contrast, in <b>amphetamine</b>  and cocaine preexposed mice, an <b>amphetamine</b> or cocaine challenge no longer activates <strong>CREB</strong> unless Ca(v)1.2 LTCCs are blocked.
+CREB1	drug	cocaine	21159975	In contrast, in amphetamine  and <b>cocaine</b> preexposed mice, an amphetamine or <b>cocaine</b> challenge no longer activates <strong>CREB</strong> unless Ca(v)1.2 LTCCs are blocked.
+CREB1	addiction	sensitization	21159975	This Ca(v)1.2 dependent blunting of <strong>CREB</strong> activation that underlies expression of locomotor <b>sensitization</b> occurs only after extended drug free periods and involves recruitment of D(1) receptors and the ERK pathway.
+CREB1	drug	cocaine	21138621	<strong>CREB</strong> mediated alterations in the amygdala transcriptome: coordinated regulation of immune response genes following <b>cocaine</b>.
+CREB1	drug	cocaine	21138621	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) is necessary for stress  but not <b>cocaine</b> induced reinstatement of conditioned reward, suggesting that different molecular mechanisms may underlie these two types of reinstatement.
+CREB1	addiction	relapse	21138621	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) is necessary for stress  but not cocaine induced <b>reinstatement</b> of conditioned reward, suggesting that different molecular mechanisms may underlie these two types of <b>reinstatement</b>.
+CREB1	addiction	reward	21138621	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) is necessary for stress  but not cocaine induced reinstatement of conditioned <b>reward</b>, suggesting that different molecular mechanisms may underlie these two types of reinstatement.
+CREB1	drug	cocaine	21138621	Our findings demonstrate that the amygdala transcriptome was altered by <strong>CREB</strong> deficiency more than by previous <b>cocaine</b> experience, with an over representation of genes involved in the immune response.
+CREB1	drug	cocaine	21138621	However, a subset of genes involved in stress and immune response demonstrated a drug×genotype interaction, indicating that <b>cocaine</b> produces different long term alterations in gene expression depending on the presence or absence of <strong>CREB</strong>.
+CREB1	drug	cocaine	21123561	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) is required for stress  but not drug induced reinstatement of <b>cocaine</b> conditioned place preference.
+CREB1	addiction	relapse	21123561	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) is required for stress  but not drug induced <b>reinstatement</b> of cocaine conditioned place preference.
+CREB1	drug	cocaine	21123561	To reveal the neural circuitry associated with this <strong>CREB</strong> dependence, we injected a retrograde tracer into the ventral tegmental area (VTA) and identified afferents that were activated after stress or <b>cocaine</b> exposure in both naive and <b>cocaine</b> conditioned mice.
+CREB1	addiction	dependence	21123561	To reveal the neural circuitry associated with this <strong>CREB</strong> <b>dependence</b>, we injected a retrograde tracer into the ventral tegmental area (VTA) and identified afferents that were activated after stress or cocaine exposure in both naive and cocaine conditioned mice.
+CREB1	drug	cocaine	21123561	Neuronal activation, as assessed by Fos expression, was greatly reduced in the dorsal and ventral bed nucleus of the stria terminalis (BNST), lateral septum, and nucleus accumbens shell in mice lacking <strong>CREB</strong> (CREBαΔ mice) after a 6 min swim stress but not after <b>cocaine</b> exposure (20 mg/kg).
+CREB1	addiction	relapse	21123561	Together, the present studies demonstrate that <strong>CREB</strong> is required for the activation of a unique circuit that converges on the dopamine reward pathway to elicit <b>reinstatement</b> of drug reward and points to the BNST as a key intersection between stress and reward circuits.
+CREB1	addiction	reward	21123561	Together, the present studies demonstrate that <strong>CREB</strong> is required for the activation of a unique circuit that converges on the dopamine <b>reward</b> pathway to elicit reinstatement of drug <b>reward</b> and points to the BNST as a key intersection between stress and <b>reward</b> circuits.
+CREB1	drug	nicotine	21113126	<b>Nicotine</b> mediated RyR2 upregulation was driven by <strong>CREB</strong>, and caused a long lasting reinforcement of Ca2+ signalling via the process of Ca2+ induced Ca2+ release.
+CREB1	addiction	reward	21113126	Nicotine mediated RyR2 upregulation was driven by <strong>CREB</strong>, and caused a long lasting <b>reinforcement</b> of Ca2+ signalling via the process of Ca2+ induced Ca2+ release.
+CREB1	drug	nicotine	21070506	We recently showed that the expression and phosphorylation of cyclic adenosine monophosphate response element (CRE) binding protein (<strong>CREB</strong>) in human buffy coat were associated with <b>smoking</b> behavior.
+CREB1	drug	nicotine	21070506	Because ERK1/2 is known to effect phosphorylation of <strong>CREB</strong>, the aim of the present study was to further elucidate whether cigarette <b>smoking</b> leads to alterations in terms of ERK1/2 in human buffy coat as well.
+CREB1	drug	opioid	21068718	Microinjection of HSV vector expressing sTNFR into the PAG also significantly reduced the phosphorylation of both ERK1/2 and <strong>CREB</strong>, and reduced Fos immunoreactivity in neurons of the PAG following <b>naloxone</b> precipitated withdrawal.
+CREB1	addiction	withdrawal	21068718	Microinjection of HSV vector expressing sTNFR into the PAG also significantly reduced the phosphorylation of both ERK1/2 and <strong>CREB</strong>, and reduced Fos immunoreactivity in neurons of the PAG following naloxone precipitated <b>withdrawal</b>.
+CREB1	drug	amphetamine	21057772	Extracellular signal regulated kinase (ERK), cAMP response element binding protein (<strong>CREB</strong>), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated <b>amphetamine</b> (<b>AMPH</b>) administration.
+CREB1	drug	amphetamine	21057772	The role of the D1 and D2 class of dopamine receptors in the differential phosphorylation of striatal ERK, <strong>CREB</strong>, Thr308 Akt and Ser473 Akt and the expression of behavioral sensitization induced by <b>AMPH</b> challenge in <b>AMPH</b> pretreated rats were determined.
+CREB1	addiction	sensitization	21057772	The role of the D1 and D2 class of dopamine receptors in the differential phosphorylation of striatal ERK, <strong>CREB</strong>, Thr308 Akt and Ser473 Akt and the expression of behavioral <b>sensitization</b> induced by AMPH challenge in AMPH pretreated rats were determined.
+CREB1	drug	amphetamine	21057772	SCH23390, but not eticlopride, significantly decreased ERK, <strong>CREB</strong>, and Thr308 Akt phosphorylation in the striatum 15 min, and ERK and <strong>CREB</strong> phosphorylation 2 h, after <b>AMPH</b> challenge in <b>AMPH</b> sensitized rats.
+CREB1	drug	opioid	20837544	This increased excitability was mediated by direct activation of <b>opioid</b> receptors and up regulation of the cAMP pathway and accompanied by increased cAMP response element binding protein (<strong>CREB</strong>) activity.
+CREB1	drug	opioid	20837544	Overexpression of a dominant negative <strong>CREB</strong> mutant blocked the increase in LC excitability induced by <b>morphine</b>  or cAMP pathway activation.
+CREB1	drug	opioid	20837544	Furthermore, the ability of <b>morphine</b> or <strong>CREB</strong> overexpression to up regulate LC firing was blocked by knockout of the <strong>CREB</strong> target adenylyl cyclase 8.
+CREB1	drug	opioid	20837544	Together, these findings provide direct evidence that prolonged exposure to <b>morphine</b> induces homeostatic plasticity intrinsic to LC neurons, involving up regulation of the cAMP <strong>CREB</strong> signaling pathway, which then enhances LC neuronal excitability.
+CREB1	drug	opioid	20731628	The levels of phosphorylated DARPP32 (Thr34) and phosphorylated <strong>CREB</strong> (Ser133) were increased in the ACG of rats that had maintained the <b>morphine</b> induced place preference, whereas the increases of these levels induced by <b>morphine</b> were blocked by pre treatment of a selective dopamine D1 receptor antagonist SCH23390.
+CREB1	drug	opioid	20731628	The activation of DARPP32 and <strong>CREB</strong> through dopamine D1 receptors in the ACG could be implicated in the maintenance of μ <b>opioid</b> induced place preference.
+CREB1	drug	cocaine	20613834	Striatal microRNA controls <b>cocaine</b> intake through <strong>CREB</strong> signalling.
+CREB1	drug	cocaine	20613834	Striatal miR 212 decreases responsiveness to the motivational properties of <b>cocaine</b> by markedly amplifying the stimulatory effects of the drug on cAMP response element binding protein (<strong>CREB</strong>) signalling.
+CREB1	addiction	sensitization	20613834	This action occurs through miR 212 enhanced Raf1 activity, resulting in adenylyl cyclase <b>sensitization</b> and increased expression of the essential <strong>CREB</strong> co activator TORC (transducer of regulated <strong>CREB</strong>; also known as CRTC).
+CREB1	drug	amphetamine	20451507	Both over expression of cyclic AMP response element binding protein (<strong>CREB</strong>) in the nucleus accumbens (NAc), and intra accumbal injection of cocaine  and <b>amphetamine</b> regulated transcript (CART) peptides, have been shown to decrease cocaine reward.
+CREB1	drug	cocaine	20451507	Both over expression of cyclic AMP response element binding protein (<strong>CREB</strong>) in the nucleus accumbens (NAc), and intra accumbal injection of <b>cocaine</b>  and amphetamine regulated transcript (CART) peptides, have been shown to decrease <b>cocaine</b> reward.
+CREB1	addiction	reward	20451507	Both over expression of cyclic AMP response element binding protein (<strong>CREB</strong>) in the nucleus accumbens (NAc), and intra accumbal injection of cocaine  and amphetamine regulated transcript (CART) peptides, have been shown to decrease cocaine <b>reward</b>.
+CREB1	drug	cocaine	20451507	These data suggest that the effects of <strong>CREB</strong> over expression on blunting <b>cocaine</b> reward could be, at least in part, attributed to the increased expression of the CART gene by direct interaction of P <strong>CREB</strong> with the CART promoter CRE site, rather than by some indirect action.
+CREB1	addiction	reward	20451507	These data suggest that the effects of <strong>CREB</strong> over expression on blunting cocaine <b>reward</b> could be, at least in part, attributed to the increased expression of the CART gene by direct interaction of P <strong>CREB</strong> with the CART promoter CRE site, rather than by some indirect action.
+CREB1	drug	opioid	20367754	Here, we test whether the cAMP dependent transcription factors cAMP responsive element binding protein (<strong>CREB</strong>) and cAMP responsive element modulator (CREM) in noradrenergic neurons control the cellular markers and the physical signs of <b>morphine</b> withdrawal in mice.
+CREB1	addiction	withdrawal	20367754	Here, we test whether the cAMP dependent transcription factors cAMP responsive element binding protein (<strong>CREB</strong>) and cAMP responsive element modulator (CREM) in noradrenergic neurons control the cellular markers and the physical signs of morphine <b>withdrawal</b> in mice.
+CREB1	addiction	withdrawal	20367754	We found that the enhanced expression of tyrosine hydroxylase normally observed during <b>withdrawal</b> was attenuated in <strong>CREB</strong>/CREM mutants.
+CREB1	drug	opioid	20367754	We conclude by a specific genetic approach that the withdrawal associated hyperexcitability of noradrenergic neurons depends on <strong>CREB</strong>/CREM activity in these neurons, but does not mediate several behavioral signs of <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	20367754	We conclude by a specific genetic approach that the <b>withdrawal</b> associated hyperexcitability of noradrenergic neurons depends on <strong>CREB</strong>/CREM activity in these neurons, but does not mediate several behavioral signs of morphine <b>withdrawal</b>.
+CREB1	drug	nicotine	20047710	<b>Smoking</b> behaviour is associated with expression and phosphorylation of <strong>CREB</strong> in human buffy coat.
+CREB1	drug	nicotine	20047710	Nicotinic acetylcholine receptors (nAChRs) are involved in <b>nicotine</b> induced phosphorylation of <strong>CREB</strong> (cyclic AMP response element binding protein) in PC12h cells.
+CREB1	drug	nicotine	20047710	The aim of our study was to determine whether or not there are differences between <b>smokers</b> and non <b>smoking</b> controls in terms of <strong>CREB</strong> expression and phosphorylation in human buffy coat.
+CREB1	drug	nicotine	20047710	Comparing 32 <b>smokers</b> with 76 non <b>smoking</b> controls we found significantly elevated relative (p=0.043) and absolute (p=0.040) <strong>CREB</strong> phosphorylation in the blood of <b>smokers</b> who had smoked two cigarettes in the past 6 h. In contrast, the score of the State and Trait Anxiety Inventory, total <strong>CREB</strong> and mRNA <strong>CREB</strong> were not significantly different.
+CREB1	drug	nicotine	20047710	Multiple regression analysis revealed a significant relation between the number of cigarettes smoked daily (R2=0.143, p=0.023), the Fagerström Test for <b>Nicotine</b> Dependence score (R2=0.145, p=0.022) and the expression of <strong>CREB</strong>.
+CREB1	addiction	dependence	20047710	Multiple regression analysis revealed a significant relation between the number of cigarettes smoked daily (R2=0.143, p=0.023), the Fagerström Test for Nicotine <b>Dependence</b> score (R2=0.145, p=0.022) and the expression of <strong>CREB</strong>.
+CREB1	drug	opioid	22110916	The upregulation of p <strong>CREB</strong> was inhibited by <b>morphine</b> and gabapentin.
+CREB1	addiction	sensitization	19962768	Clozapine also reversed some of the <b>sensitization</b> induced biochemical changes, including increased phosphorylation of GSK 3beta and <strong>CREB</strong>, in the frontal cortex.
+CREB1	drug	opioid	19956087	Modulation of opiate related signaling molecules in <b>morphine</b> dependent conditioned behavior: conditioned place preference to <b>morphine</b> induces <strong>CREB</strong> phosphorylation.
+CREB1	drug	opioid	19956087	We find that <strong>CREB</strong> phosphorylation is specifically induced upon the expression of a sensitized response to <b>morphine</b> induced conditioned behavior in brain areas related to memory consolidation, such as the hippocampus and cortex.
+CREB1	drug	opioid	19956087	These results indicate a critical role for phospho <strong>CREB</strong>, AMPA, and deltaOR activities in mediating the expression of a sensitized response to <b>morphine</b> dependent conditioned behavior.
+CREB1	drug	cocaine	19912338	Context specific modulation of <b>cocaine</b> induced locomotor sensitization and ERK and <strong>CREB</strong> phosphorylation in the rat nucleus accumbens.
+CREB1	addiction	sensitization	19912338	Context specific modulation of cocaine induced locomotor <b>sensitization</b> and ERK and <strong>CREB</strong> phosphorylation in the rat nucleus accumbens.
+CREB1	drug	cocaine	19912338	In contrast, <strong>CREB</strong> and CaMKIV phosphorylation in nucleus accumbens homogenates were decreased by <b>cocaine</b> test injections.
+CREB1	drug	cocaine	19912338	Context specific phosphorylation of ERK and <strong>CREB</strong> in the present study suggests that this signal transduction pathway is selectively activated in the same set of <b>cocaine</b> activated accumbens neurons that mediate this learned association.
+CREB1	drug	opioid	19897079	In this study, we investigated the effect of the opiate (<b>heroin</b>) on D1 receptor (D1R) and DARPP 32 expression and additionally, evaluated the effects of DARPP 32 siRNA gene silencing on protein phosphatase 1 (PP 1), ERK, and cAMP response element binding (<strong>CREB</strong>) gene expression in primary normal human astrocytes (NHA) cells in vitro.
+CREB1	drug	opioid	19897079	Our results indicate that <b>heroin</b> significantly upregulated both D1R and DARPP 32 gene expression, and that DARPP 32 silencing in the NHA cells resulted in the significant modulation of the activity of downstream effector molecules such as PP 1, ERK, and <strong>CREB</strong> which are known to play an important role in opiate abuse induced changes in long term neural plasticity.
+CREB1	drug	amphetamine	19830406	Expression of brain derived neurotrophic factor (BDNF) and phosphorylated c AMP response element binding protein (p <strong>CREB</strong>) genes were measured under basal conditions and after acute or repeated <b>amphetamine</b> treatments.
+CREB1	drug	amphetamine	19830406	Basal expression of p <strong>CREB</strong> (but not BDNF) was higher in D (1) ( / ) than D (1) (+/+) mice and was reduced after <b>amphetamine</b> treatment.
+CREB1	drug	cocaine	19826621	Here we show, in startling contrast, that inhibition of striatal <strong>CREB</strong> facilitates <b>cocaine</b>  and morphine place conditioning and enhances locomotor sensitization to <b>cocaine</b>.
+CREB1	drug	opioid	19826621	Here we show, in startling contrast, that inhibition of striatal <strong>CREB</strong> facilitates cocaine  and <b>morphine</b> place conditioning and enhances locomotor sensitization to cocaine.
+CREB1	addiction	sensitization	19826621	Here we show, in startling contrast, that inhibition of striatal <strong>CREB</strong> facilitates cocaine  and morphine place conditioning and enhances locomotor <b>sensitization</b> to cocaine.
+CREB1	drug	opioid	19826619	To investigate the role of cAMP responsive element binding protein (<strong>CREB</strong>) dependent gene expression in <b>morphine</b> induced behaviors, we examined bitransgenic mice expressing a dominant and strong inhibitor of the <strong>CREB</strong> family of transcription factors, A <strong>CREB</strong>, in striatal neurons in a regulatable manner.
+CREB1	drug	opioid	19826619	The expression of A <strong>CREB</strong> in the striatum enhanced both <b>morphine</b> induced conditioned place preference and <b>morphine</b> withdrawal induced conditioned place avoidance.
+CREB1	addiction	withdrawal	19826619	The expression of A <strong>CREB</strong> in the striatum enhanced both morphine induced conditioned place preference and morphine <b>withdrawal</b> induced conditioned place avoidance.
+CREB1	drug	alcohol	19756388	Acute and chronic <b>ethanol</b> exposure have been shown to modulate function of the activity dependent gene transcription factor, cAMP responsive element binding (<strong>CREB</strong>) protein in the brain, which may be associated with the development of <b>alcoholism</b>.
+CREB1	drug	alcohol	19756388	Study of the downstream effectors of <strong>CREB</strong> have identified several important <strong>CREB</strong> related genes, such as neuropeptide Y, brain derived neurotrophic factor, activity regulated cytoskeleton associated protein, and corticotrophin releasing factor, that may play a crucial role in the behavioral effects of <b>ethanol</b> and molecular changes in the specific neurocircuitry that underlie both <b>alcohol</b> addiction and a genetic predisposition to <b>alcoholism</b>.
+CREB1	addiction	addiction	19756388	Study of the downstream effectors of <strong>CREB</strong> have identified several important <strong>CREB</strong> related genes, such as neuropeptide Y, brain derived neurotrophic factor, activity regulated cytoskeleton associated protein, and corticotrophin releasing factor, that may play a crucial role in the behavioral effects of ethanol and molecular changes in the specific neurocircuitry that underlie both alcohol <b>addiction</b> and a genetic predisposition to alcoholism.
+CREB1	drug	nicotine	19711055	<b>Nicotine</b> conditioned place preference induced <strong>CREB</strong> phosphorylation and Fos expression in the adult rat brain.
+CREB1	drug	nicotine	19711055	The results indicate that the phosphorylation of <strong>CREB</strong> and expression of Fos protein, as indicators of neural activity, accompany the acquisition and maintenance of <b>nicotine</b> induced CPP but not CPA in mesolimbic areas (NAc, VTA, PFC, and DStr) as well as in memory consolidation structures (hippocampus and amygdala) and nicotinic receptor are involved in this process.
+CREB1	addiction	reward	19711055	The results indicate that the phosphorylation of <strong>CREB</strong> and expression of Fos protein, as indicators of neural activity, accompany the acquisition and maintenance of nicotine induced <b>CPP</b> but not CPA in mesolimbic areas (NAc, VTA, PFC, and DStr) as well as in memory consolidation structures (hippocampus and amygdala) and nicotinic receptor are involved in this process.
+CREB1	addiction	reward	19709647	This behavioral phenotype is consistent with low <strong>CREB</strong> activity in the nucleus accumbens, a key brain <b>reward</b> region.
+CREB1	drug	cocaine	19675537	Stress induced potentiation of <b>cocaine</b> reward: a role for CRF R1 and <strong>CREB</strong>.
+CREB1	addiction	reward	19675537	Stress induced potentiation of cocaine <b>reward</b>: a role for CRF R1 and <strong>CREB</strong>.
+CREB1	drug	cocaine	19675537	Previously, we have shown that a single exposure to forced swim (FS) reinstates extinguished conditioned place preference (CPP) to <b>cocaine</b> and that cAMP response element binding protein (<strong>CREB</strong>) is necessary for this response.
+CREB1	addiction	reward	19675537	Previously, we have shown that a single exposure to forced swim (FS) reinstates extinguished conditioned place preference (<b>CPP</b>) to cocaine and that cAMP response element binding protein (<strong>CREB</strong>) is necessary for this response.
+CREB1	drug	cocaine	19675537	The present experiments investigate whether changes in <b>cocaine</b> reward elicited by previous exposure to stress are mediated by <strong>CREB</strong> and/or CRF(R1).
+CREB1	addiction	reward	19675537	The present experiments investigate whether changes in cocaine <b>reward</b> elicited by previous exposure to stress are mediated by <strong>CREB</strong> and/or CRF(R1).
+CREB1	drug	cocaine	19675537	Chronic exposure to FS in advance of conditioning enhances <b>cocaine</b> CPP in wild type mice, but this is blocked in <strong>CREB</strong> deficient mice.
+CREB1	addiction	reward	19675537	Chronic exposure to FS in advance of conditioning enhances cocaine <b>CPP</b> in wild type mice, but this is blocked in <strong>CREB</strong> deficient mice.
+CREB1	addiction	reward	19675537	Taken together, these studies suggest that both <strong>CREB</strong> and CRF(R1) activation are necessary for stress induced potentiation of drug <b>reward</b>.
+CREB1	drug	cocaine	19666831	Deletion of <strong>CREB1</strong> from the dorsal telencephalon reduces motivational properties of <b>cocaine</b>.
+CREB1	drug	cocaine	19666831	To examine whether <strong>CREB1</strong> in cortical glutamatergic neurons was implicated in <b>cocaine</b> use, we developed conditional <strong>CREB1</strong> mutants that exhibit ablation of functional <strong>CREB1</strong> in the cortex and hippocampus.
+CREB1	drug	cocaine	19666831	Here we report that <strong>CREB1</strong> mutants show normal locomotor responses to acute and chronic <b>cocaine</b> and develop a place preference for <b>cocaine</b>.
+CREB1	drug	cocaine	19666831	However, <strong>CREB1</strong> mutants demonstrate a diminished drive to self administer <b>cocaine</b> under operant conditions.
+CREB1	addiction	reward	19666831	However, <strong>CREB1</strong> mutants demonstrate a diminished drive to self administer cocaine under <b>operant</b> conditions.
+CREB1	drug	cocaine	19666831	We conclude that there is a specific role for <strong>CREB1</strong> in telencephalic glutamatergic neurons regulating the motivational properties of <b>cocaine</b>.
+CREB1	drug	opioid	19545278	<b>Morphine</b> withdrawal regulates phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) through PKC in the nucleus tractus solitarius A2 catecholaminergic neurons.
+CREB1	addiction	withdrawal	19545278	Morphine <b>withdrawal</b> regulates phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) through PKC in the nucleus tractus solitarius A2 catecholaminergic neurons.
+CREB1	drug	opioid	19545278	In the current study we used immunoblotting and immunohistochemistry to investigate changes in <strong>CREB</strong> phosphorylation in the NTS and kinases that may mediate the <b>morphine</b> withdrawal triggered activation of <strong>CREB</strong> and hypothalamo pituitary adrenocortical (HPA) axis (another stress system circuit) response after <b>naloxone</b> induced <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	19545278	In the current study we used immunoblotting and immunohistochemistry to investigate changes in <strong>CREB</strong> phosphorylation in the NTS and kinases that may mediate the morphine <b>withdrawal</b> triggered activation of <strong>CREB</strong> and hypothalamo pituitary adrenocortical (HPA) axis (another stress system circuit) response after naloxone induced morphine <b>withdrawal</b>.
+CREB1	drug	opioid	19545278	We found an increased phosphorylation of <strong>CREB</strong> (pCREB) selectively within tyrosine hydroxylase (TH) immunoreactive neurons in the NTS from <b>morphine</b> withdrawn rats, which parallel elevated corticosterone levels.
+CREB1	drug	opioid	19545278	SL327, an inhibitor of ERK activation, at doses which reduced the hyperactive pERK(1/2) levels, did not attenuated the rise in pCREB and TH immunoreactivity or plasma corticosterone secretion during <b>morphine</b> withdrawal, indicating that ERK kinase/ERK pathway was not directly needed for either activation of <strong>CREB</strong> and TH expression in the NTS or HPA axis hyperactivity.
+CREB1	addiction	withdrawal	19545278	SL327, an inhibitor of ERK activation, at doses which reduced the hyperactive pERK(1/2) levels, did not attenuated the rise in pCREB and TH immunoreactivity or plasma corticosterone secretion during morphine <b>withdrawal</b>, indicating that ERK kinase/ERK pathway was not directly needed for either activation of <strong>CREB</strong> and TH expression in the NTS or HPA axis hyperactivity.
+CREB1	drug	opioid	19545278	The results indicate that PKC mediates both <strong>CREB</strong> activation and HPA response by <b>morphine</b> withdrawal and might suggest that <strong>CREB</strong> activation in the NTS is related to TH expression associated with <b>morphine</b> withdrawal.
+CREB1	addiction	withdrawal	19545278	The results indicate that PKC mediates both <strong>CREB</strong> activation and HPA response by morphine <b>withdrawal</b> and might suggest that <strong>CREB</strong> activation in the NTS is related to TH expression associated with morphine <b>withdrawal</b>.
+CREB1	drug	cocaine	19447090	Our findings reveal several interesting principles of gene regulation by <b>cocaine</b> and of the role of DeltaFosB and <strong>CREB</strong>, two prominent <b>cocaine</b> induced transcription factors, in this brain region.
+CREB1	drug	cannabinoid	19429161	Time dependent induction of <strong>CREB</strong> phosphorylation in the hippocampus by the endogenous <b>cannabinoid</b>.
+CREB1	addiction	addiction	19429161	Recent evidence indicates that the transcription factor <strong>CREB</strong> (cAMP response element binding protein) may be an important biochemical substrate for behavioral plasticity that has been associated with the chronic administration of drugs of abuse and <b>addiction</b>.
+CREB1	drug	cannabinoid	19429161	Increased <strong>CREB</strong> activity was reported as a chronic effect of drugs of abuse in the neurons of the nucleus accumbens, a brain reward region that expresses high density levels in the CB1 <b>cannabinoid</b> receptors.
+CREB1	addiction	reward	19429161	Increased <strong>CREB</strong> activity was reported as a chronic effect of drugs of abuse in the neurons of the nucleus accumbens, a brain <b>reward</b> region that expresses high density levels in the CB1 cannabinoid receptors.
+CREB1	drug	cannabinoid	19429161	The present study revealed that <strong>CREB</strong> activities were present in the hippocampal neurons of cultured slice preparations in response to acute and chronic applications of endogenous <b>cannabinoid</b>, anandamide and R(+) methanandamide (a non hydrolyzing form of anandamide).
+CREB1	addiction	reward	19429161	Present findings demonstrate: (1) the hippocampus is vulnerable to the direct chemical effect of anandamide and R(+) methanandamide in isolation of synaptic influences from the midbrain <b>reward</b> neurons, and (2) the effect of R(+) methanandamide is cumulative as evidenced by the sustained elevation of <strong>CREB</strong> activities in response to a chronic dosage that is too low and thus fails to exert any acute effect.
+CREB1	drug	amphetamine	19404615	We measured <b>amphetamine</b> enhancement of brain stimulation reward, changes in sucrose intake, as well as striatal cAMP response element binding protein (<strong>CREB</strong>) activity, a molecular index previously associated with depressant like behavior.
+CREB1	addiction	reward	19404615	We measured amphetamine enhancement of brain stimulation <b>reward</b>, changes in sucrose intake, as well as striatal cAMP response element binding protein (<strong>CREB</strong>) activity, a molecular index previously associated with depressant like behavior.
+CREB1	drug	amphetamine	19404615	Thus, we observed a blunted response to the rewarding properties of <b>amphetamine</b> (1 mg/kg, 21 days post lesion), a long lasting reduction in sucrose intake and increased striatal <strong>CREB</strong> activity.
+CREB1	addiction	addiction	19341783	cAMP responsive element binding protein (<strong>CREB</strong>), a nuclear transcription factor, is a downstream component of the extracellular signal regulated protein kinase (ERK) pathway, which has been shown to regulate different physiological and psychological responses of drug <b>addiction</b>.
+CREB1	addiction	addiction	19341783	We examined if RACK1 is involved in the mechanism of drug <b>addiction</b> by regulating <strong>CREB</strong> in mouse hippocampus and prefrontal cortex.
+CREB1	drug	opioid	19341783	Chronic administration of <b>morphine</b> made the expression of RACK1 and <strong>CREB</strong> mRNA increase in hippocampus and prefrontal cortex.
+CREB1	drug	opioid	19341783	The expression of RACK1 and <strong>CREB</strong> protein was strongly positive in CA1, CA3 and dentate gyrus (DG) of the hippocampus of <b>morphine</b> treated mice brain, especially the pyramidal neurons in the DG of the hippocampus.
+CREB1	drug	opioid	19341783	Using the small interfering RNA technology, we determined that the expression of <strong>CREB</strong> mRNA was decreased in hippocampus and prefrontal cortex of <b>morphine</b> treated mice.
+CREB1	drug	opioid	19341783	These findings suggest that <b>morphine</b> reward can influence the expression of RACK1 in mouse hippocampus and prefrontal cortex through regulating <strong>CREB</strong> transcription.
+CREB1	addiction	reward	19341783	These findings suggest that morphine <b>reward</b> can influence the expression of RACK1 in mouse hippocampus and prefrontal cortex through regulating <strong>CREB</strong> transcription.
+CREB1	drug	opioid	19289113	Chronic <b>morphine</b> administration induces over expression of aldolase C with reduction of <strong>CREB</strong> phosphorylation in the mouse hippocampus.
+CREB1	drug	opioid	19289113	<b>Naloxone</b> pretreatment before <b>morphine</b> administration suppressed withdrawal jumping, weight loss, and overexpression of aldolase C. <strong>CREB</strong> is a transcription factor regulated through phosphorylation on Ser133, which is known to play a key role in the mechanism of <b>morphine</b> dependence.
+CREB1	addiction	dependence	19289113	Naloxone pretreatment before morphine administration suppressed withdrawal jumping, weight loss, and overexpression of aldolase C. <strong>CREB</strong> is a transcription factor regulated through phosphorylation on Ser133, which is known to play a key role in the mechanism of morphine <b>dependence</b>.
+CREB1	addiction	withdrawal	19289113	Naloxone pretreatment before morphine administration suppressed <b>withdrawal</b> jumping, weight loss, and overexpression of aldolase C. <strong>CREB</strong> is a transcription factor regulated through phosphorylation on Ser133, which is known to play a key role in the mechanism of morphine dependence.
+CREB1	drug	opioid	19289113	When detecting the expression of phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) in the mouse hippocampus using Western blot and immunohistochemistry, we found <strong>CREB</strong> phosphorylation was clearly decreased following chronic <b>morphine</b> treatment.
+CREB1	drug	opioid	19289113	The results suggest potential links between the <b>morphine</b> induced alteration of aldolase C and the regulation of <strong>CREB</strong> phosphorylation, a possible mechanism of <b>morphine</b> dependence.
+CREB1	addiction	dependence	19289113	The results suggest potential links between the morphine induced alteration of aldolase C and the regulation of <strong>CREB</strong> phosphorylation, a possible mechanism of morphine <b>dependence</b>.
+CREB1	drug	cocaine	19244515	Our results demonstrate that the Ca(2+) stimulated adenylyl cyclases regulate long lasting <b>cocaine</b> induced behavioral plasticity via activation of the ERK/MSK1/<strong>CREB</strong> signaling pathway in striatonigral MSNs.
+CREB1	addiction	addiction	19243452	The cyclic AMP response element binding (<strong>CREB</strong>) proteins are transcription factors that have been mechanistically linked to some behavioral changes associated with drug <b>addiction</b>.
+CREB1	drug	alcohol	19243452	Here, we show that benzyl <b>alcohol</b> sedation alters expression of both dCREB A and dCREB2 b genes to increase production of positively acting <strong>CREB</strong> isoforms and to reduce expression of negatively acting <strong>CREB</strong> variants.
+CREB1	drug	alcohol	19243452	Using a <strong>CREB</strong> responsive reporter gene, we show that benzyl <b>alcohol</b> sedation increases <strong>CREB</strong> mediated transcription.
+CREB1	drug	alcohol	19243452	These findings suggest that <strong>CREB</strong> positively regulates the expression of slo encoded BK type Ca(2+) activated K(+) channels and that this gives rise to behavioral tolerance to benzyl <b>alcohol</b> sedation.
+CREB1	drug	nicotine	19212318	Nucleus accumbens <strong>CREB</strong> activity is necessary for <b>nicotine</b> conditioned place preference.
+CREB1	drug	cocaine	19212318	Previous studies have implicated nucleus accumbens (NAc) <strong>CREB</strong> activity in the modulation of <b>cocaine</b> and morphine reward, and have shown that nicotine conditioned place preference (CPP) is associated with NAc <strong>CREB</strong> activation.
+CREB1	drug	nicotine	19212318	Previous studies have implicated nucleus accumbens (NAc) <strong>CREB</strong> activity in the modulation of cocaine and morphine reward, and have shown that <b>nicotine</b> conditioned place preference (CPP) is associated with NAc <strong>CREB</strong> activation.
+CREB1	drug	opioid	19212318	Previous studies have implicated nucleus accumbens (NAc) <strong>CREB</strong> activity in the modulation of cocaine and <b>morphine</b> reward, and have shown that nicotine conditioned place preference (CPP) is associated with NAc <strong>CREB</strong> activation.
+CREB1	addiction	reward	19212318	Previous studies have implicated nucleus accumbens (NAc) <strong>CREB</strong> activity in the modulation of cocaine and morphine <b>reward</b>, and have shown that nicotine conditioned place preference (<b>CPP</b>) is associated with NAc <strong>CREB</strong> activation.
+CREB1	drug	nicotine	19212318	It is not clear whether CPP elicits phosphorylation of <strong>CREB</strong> or if elevations in pCREB support <b>nicotine</b> CPP.
+CREB1	addiction	reward	19212318	It is not clear whether <b>CPP</b> elicits phosphorylation of <strong>CREB</strong> or if elevations in pCREB support nicotine <b>CPP</b>.
+CREB1	drug	nicotine	19212318	In the current study, we investigated levels of <strong>CREB</strong> and pCREB during Pavlovian conditioning with <b>nicotine</b> in a novel context in the absence of chamber choice.
+CREB1	drug	nicotine	19212318	To test if <strong>CREB</strong> activity in the NAc shell contributes to cue induced responses that may precipitate <b>nicotine</b> seeking, we used viral mediated gene transfer of a dominant negative <strong>CREB</strong> construct in the NAc shell of C57BL/6J mice and found that disruption of <strong>CREB</strong> activation before training blocked <b>nicotine</b> place preference across a range of doses.
+CREB1	addiction	relapse	19212318	To test if <strong>CREB</strong> activity in the NAc shell contributes to cue induced responses that may precipitate nicotine <b>seeking</b>, we used viral mediated gene transfer of a dominant negative <strong>CREB</strong> construct in the NAc shell of C57BL/6J mice and found that disruption of <strong>CREB</strong> activation before training blocked nicotine place preference across a range of doses.
+CREB1	drug	nicotine	19212318	Taken together, these studies identify the NAc shell as a brain region where <strong>CREB</strong> activity is essential for <b>nicotine</b> CPP.
+CREB1	addiction	reward	19212318	Taken together, these studies identify the NAc shell as a brain region where <strong>CREB</strong> activity is essential for nicotine <b>CPP</b>.
+CREB1	addiction	reward	19211892	We examined how disruption of <strong>CREB</strong> activity affects brain <b>reward</b> processes using intracranial self stimulation (<b>ICSS</b>) and inducible bitransgenic mice with enriched expression of mCREB in forebrain regions including the NAc.
+CREB1	addiction	reward	19211892	Together with previous findings, these studies raise the possibility that disruption of <strong>CREB</strong> in the NAc influences motivation by simultaneously facilitating <b>reward</b> and reducing depressive like states such as anhedonia and dysphoria.
+CREB1	drug	cocaine	19181855	Compared with WT mice, tPA /  mice injected with <b>cocaine</b> displayed attenuated phosphorylation of ERK, cAMP response element binding protein (<strong>CREB</strong>), and dopamine and cAMP regulated phosphoprotein 32 kDa (DARPP 32) and blunted induction of immediate early genes (IEGs) c Fos, Egr 1, and Homer 1a in the amygdala and the nucleus accumbens (NAc).
+CREB1	drug	opioid	19172190	<b>Naloxone</b>'s pentapeptide binding site on filamin A blocks Mu <b>opioid</b> receptor Gs coupling and <strong>CREB</strong> activation of acute <b>morphine</b>.
+CREB1	drug	opioid	19172190	Since ultra low dose NTX also attenuates the addictive properties of <b>opioids</b>, we assessed striatal cAMP production and <strong>CREB</strong> phosphorylation at S(133).
+CREB1	addiction	addiction	19172190	Since ultra low dose NTX also attenuates the <b>addictive</b> properties of opioids, we assessed striatal cAMP production and <strong>CREB</strong> phosphorylation at S(133).
+CREB1	drug	opioid	19172190	Correlating with the Gs coupling, acute <b>morphine</b> induced elevated cAMP levels and a several fold increase in pS(133)<strong>CREB</strong> that were also completely blocked by NLX, NTX or the FLNA pentapeptide.
+CREB1	drug	opioid	19108758	Effects of <b>morphine</b> dependent and withdrawal on activation of the distal cerebrospinal fluid contacting neurons' phosphorylation <strong>CREB</strong> in rat brain.
+CREB1	addiction	withdrawal	19108758	Effects of morphine dependent and <b>withdrawal</b> on activation of the distal cerebrospinal fluid contacting neurons' phosphorylation <strong>CREB</strong> in rat brain.
+CREB1	drug	opioid	19108758	<b>Morphine</b> dependent and withdrawal can activate the distal cerebrospinal fluid contacting neurons phosphorylation <strong>CREB</strong> in rat brain.
+CREB1	addiction	withdrawal	19108758	Morphine dependent and <b>withdrawal</b> can activate the distal cerebrospinal fluid contacting neurons phosphorylation <strong>CREB</strong> in rat brain.
+CREB1	drug	opioid	19106229	The depressive like behaviors seem to be due, at least in part, to <strong>CREB</strong> mediated increases in dynorphin function, because they are mimicked by kappa <b>opioid</b> receptor (KOR) agonists and attenuated by KOR antagonists.
+CREB1	drug	opioid	19084907	Phosphorylation of GluR1, ERK, and <strong>CREB</strong> during spontaneous withdrawal from chronic <b>heroin</b> self administration.
+CREB1	addiction	withdrawal	19084907	Phosphorylation of GluR1, ERK, and <strong>CREB</strong> during spontaneous <b>withdrawal</b> from chronic heroin self administration.
+CREB1	drug	nicotine	19077117	In contrast to control mice, transgenic mice with low level beta2* nAChR expression in the VTA showed no increase in overall levels of cyclic AMP response element binding protein (<strong>CREB</strong>) but did show an increase in <strong>CREB</strong> phosphorylation in response to exposure to a <b>nicotine</b> paired chamber.
+CREB1	drug	nicotine	19077117	Thus, <strong>CREB</strong> activation in the absence of regulation of total <strong>CREB</strong> levels during place preference testing was not sufficient to support <b>nicotine</b> place preference in beta2 trangenic mice.
+CREB1	drug	opioid	19071107	Furthermore, <b>oxycodone</b> (2.5 mg/kg) induced the increased phosphorylation of <strong>CREB</strong> and ERK in nucleus accumbens and hippocampus, but not in prefrontal cortex.
+CREB1	drug	opioid	19071107	All these results suggest that l THP can inhibit <b>oxycodone</b> induced psychological dependence by affecting phosphorylation of <strong>CREB</strong> and ERK in nucleus accumbens and hippocampus of rats.
+CREB1	addiction	dependence	19071107	All these results suggest that l THP can inhibit oxycodone induced psychological <b>dependence</b> by affecting phosphorylation of <strong>CREB</strong> and ERK in nucleus accumbens and hippocampus of rats.
+CREB1	drug	cocaine	19052730	Sex differences in basal and <b>cocaine</b> induced alterations in PKA and <strong>CREB</strong> proteins in the nucleus accumbens.
+CREB1	drug	cocaine	19052730	To this end, protein levels of PKA and phosphorylated <strong>CREB</strong> (pCREB) in the caudate putamen (CPu) and nucleus accumbens (NAc) of male and female rats were measured basally or after acute (one 30 mg/kg intraperitoneal injection) or chronic (twice daily 15 mg/kg injections for 14 days) <b>cocaine</b> administration.
+CREB1	drug	opioid	19052216	The progressive increase in low dose (3 mg/kg) <b>morphine</b> CPP was associated with increased ERK phosphorylation (a measure of ERK activity) and <strong>CREB</strong> (a downstream target of ERK) phosphorylation in central but not basolateral amygdala.
+CREB1	addiction	reward	19052216	The progressive increase in low dose (3 mg/kg) morphine <b>CPP</b> was associated with increased ERK phosphorylation (a measure of ERK activity) and <strong>CREB</strong> (a downstream target of ERK) phosphorylation in central but not basolateral amygdala.
+CREB1	drug	opioid	19052216	Furthermore, inhibition of central but not basolateral amygdala ERK and <strong>CREB</strong> phosphorylation by U0126 [1,4 diamino 2,3 dicyano 1,4 bis(o aminophenylmercapto)butadiene] decreased the enhanced (incubated) drug CPP after 14 d of withdrawal from <b>morphine</b>.
+CREB1	addiction	reward	19052216	Furthermore, inhibition of central but not basolateral amygdala ERK and <strong>CREB</strong> phosphorylation by U0126 [1,4 diamino 2,3 dicyano 1,4 bis(o aminophenylmercapto)butadiene] decreased the enhanced (incubated) drug <b>CPP</b> after 14 d of withdrawal from morphine.
+CREB1	addiction	withdrawal	19052216	Furthermore, inhibition of central but not basolateral amygdala ERK and <strong>CREB</strong> phosphorylation by U0126 [1,4 diamino 2,3 dicyano 1,4 bis(o aminophenylmercapto)butadiene] decreased the enhanced (incubated) drug CPP after 14 d of <b>withdrawal</b> from morphine.
+CREB1	drug	opioid	19052216	Finally, stimulation of central amygdala ERK and <strong>CREB</strong> phosphorylation by NMDA enhanced drug CPP after 1 d of withdrawal from <b>morphine</b>, an effect reversed by U0126.
+CREB1	addiction	reward	19052216	Finally, stimulation of central amygdala ERK and <strong>CREB</strong> phosphorylation by NMDA enhanced drug <b>CPP</b> after 1 d of withdrawal from morphine, an effect reversed by U0126.
+CREB1	addiction	withdrawal	19052216	Finally, stimulation of central amygdala ERK and <strong>CREB</strong> phosphorylation by NMDA enhanced drug CPP after 1 d of <b>withdrawal</b> from morphine, an effect reversed by U0126.
+CREB1	drug	cocaine	19046951	Since over expression of <strong>CREB</strong> was shown to decrease <b>cocaine</b> mediated reward, we hypothesized that CART could be a target gene for <strong>CREB</strong> in the NAc and that over expression of <strong>CREB</strong> would increase CART peptide levels.
+CREB1	addiction	reward	19046951	Since over expression of <strong>CREB</strong> was shown to decrease cocaine mediated <b>reward</b>, we hypothesized that CART could be a target gene for <strong>CREB</strong> in the NAc and that over expression of <strong>CREB</strong> would increase CART peptide levels.
+CREB1	addiction	reward	19046951	The finding that <strong>CREB</strong> can regulate the levels of CART mRNA and peptides in vivo in the NAc supports a role for CART peptides in psychostimulant induced <b>reward</b> and <b>reinforcement</b>.
+CREB1	drug	cocaine	19001277	However, the loss of <strong>CREB</strong> in the forebrain had no effect on either of these behaviors, even though it robustly blunted acute <b>cocaine</b> induced transcription.
+CREB1	drug	cocaine	19001277	To test the relevance of these observations for addiction in humans, we performed an association study of CAMK4 and <strong>CREB</strong> promoter polymorphisms with <b>cocaine</b> addiction in a large sample of addicts.
+CREB1	addiction	addiction	19001277	To test the relevance of these observations for <b>addiction</b> in humans, we performed an association study of CAMK4 and <strong>CREB</strong> promoter polymorphisms with cocaine <b>addiction</b> in a large sample of addicts.
+CREB1	drug	cocaine	19001277	We found that a single nucleotide polymorphism in the CAMK4 promoter was significantly associated with <b>cocaine</b> addiction, whereas variations in the <strong>CREB</strong> promoter regions did not correlate with drug abuse.
+CREB1	addiction	addiction	19001277	We found that a single nucleotide polymorphism in the CAMK4 promoter was significantly associated with cocaine <b>addiction</b>, whereas variations in the <strong>CREB</strong> promoter regions did not correlate with drug abuse.
+CREB1	drug	cocaine	19001277	These findings reveal a critical role for CaMKIV in the development and persistence of <b>cocaine</b> induced behaviors, through mechanisms dissociated from acute effects on gene expression and <strong>CREB</strong> dependent transcription.
+CREB1	addiction	reward	18945553	To evaluate signaling events that correlate with this behavior, brain tissue of these rats were dissected for immunoblot assays of extracellular signal regulated kinase (ERK) and a transcriptional regulator, cAMP response element binding protein (<strong>CREB</strong>) after the <b>CPP</b> test.
+CREB1	addiction	reward	18945553	MP induced <b>CPP</b> was associated with a decrease in phosphorylated <strong>CREB</strong> (pCREB) in the ventral tegmental area, and decreased phosphorylated ERK and pCREB in the nucleus accumbens and treatment with Mirt did not reverse these changes.
+CREB1	addiction	intoxication	18940959	Drugs that block oxidative stress and NF kappaB transcription or increase <strong>CREB</strong> transcription block <b>binge</b> induced neurodegeneration, inhibition of neurogenesis and proinflammatory enzyme induction.
+CREB1	drug	opioid	18850497	Inhibition of Period1 gene attenuates the <b>morphine</b> induced ERK <strong>CREB</strong> activation in frontal cortex, hippocampus, and striatum in mice.
+CREB1	drug	opioid	18850497	We explored the effects of inhibiting expression in brain of Per1 on <b>morphine</b> conditioned place preference (CPP) and <b>morphine</b> induced phosphorylation of extracellular signal regulated kinase (ERK) and cAMP response element binding protein (<strong>CREB</strong>) in mice.
+CREB1	addiction	reward	18850497	We explored the effects of inhibiting expression in brain of Per1 on morphine conditioned place preference (<b>CPP</b>) and morphine induced phosphorylation of extracellular signal regulated kinase (ERK) and cAMP response element binding protein (<strong>CREB</strong>) in mice.
+CREB1	addiction	reward	18850497	After testing <b>CPP</b>, mice were sacrificed and phosphorylated ERK and <strong>CREB</strong> in the frontal cortex, hippocampus, and striatum were examined by immunohistochemistry.
+CREB1	drug	opioid	18850497	Pretreatment with DRz164 significant attenuated the <b>morphine</b> induced activation of ERK and <strong>CREB</strong> in the frontal cortex, hippocampus, and striatum.
+CREB1	drug	opioid	18850497	Our results indicated that per1 plays an important role in <b>morphine</b> reward, and ERK <strong>CREB</strong> pathway was involved in the effects of per1.
+CREB1	addiction	reward	18850497	Our results indicated that per1 plays an important role in morphine <b>reward</b>, and ERK <strong>CREB</strong> pathway was involved in the effects of per1.
+CREB1	drug	amphetamine	18848971	Conversely, repeated treatment with BA or VPA produced <b>amphetamine</b> like effects: enhanced cAMP responsive element binding protein (<strong>CREB</strong>) phosphorylation at Ser(133) position and increased DeltaFosB protein levels in the striatum.
+CREB1	drug	amphetamine	18848971	Furthermore, co administration of BA or VPA with <b>amphetamine</b> produced additive effects on histone H4 acetylation as well as <strong>CREB</strong> phosphorylation in the striatum.
+CREB1	drug	amphetamine	18848971	Finally, the additive effect of VPA/BA and <b>amphetamine</b> on histone H4 acetylation, phosphorylated <strong>CREB</strong>, and DeltaFosB was associated with potentiated <b>amphetamine</b> induced locomotor activity.
+CREB1	addiction	sensitization	18848971	Thus, HDACi may interact additively with psychostimulants at both histone acetylation and <strong>CREB</strong> phosphorylation through the <strong>CREB</strong>:HDAC protein complex in the striatum to modulate DeltaFosB protein levels and psychomotor behavioral <b>sensitization</b>.
+CREB1	drug	opioid	18771713	Therefore, we studied the effects of short term (24 h) and long term (7 day) <b>morphine</b> treatment on the expression of hypothalamic PC1/3 and PC2 and levels of phosphorylated cyclic AMP response element binding protein (P <strong>CREB</strong>).
+CREB1	drug	opioid	18771713	While short term <b>morphine</b> exposure down regulated, long term <b>morphine</b> exposure up regulated P <strong>CREB</strong>, PC1/3 and PC2 protein levels in the rat hypothalamus as determined by Western blot analysis.
+CREB1	drug	opioid	18771713	The down regulation of PC1/3, PC2 and P <strong>CREB</strong> by short term <b>morphine</b> and up regulation by long term <b>morphine</b> treatment may be a signal mediating the switch from drug use to drug abuse.
+CREB1	drug	amphetamine	18654637	First, we discuss the roles of several neurotransmitters and neuropeptides in the functioning of the NAc, including dopamine, glutamate, gamma aminobutyric acid (GABA), acetylcholine, serotonin, dynorphin, enkephaline, brain derived neurotrophic factor (BDNF), cAMP response element binding protein (<strong>CREB</strong>), melanin concentrating hormone (MCH) and cocaine  and <b>amphetamine</b> regulated transcript (CART).
+CREB1	drug	cocaine	18654637	First, we discuss the roles of several neurotransmitters and neuropeptides in the functioning of the NAc, including dopamine, glutamate, gamma aminobutyric acid (GABA), acetylcholine, serotonin, dynorphin, enkephaline, brain derived neurotrophic factor (BDNF), cAMP response element binding protein (<strong>CREB</strong>), melanin concentrating hormone (MCH) and <b>cocaine</b>  and amphetamine regulated transcript (CART).
+CREB1	drug	opioid	18616461	Regulation of ERK1/2 phosphorylation by acute and chronic <b>morphine</b>   implications for the role of cAMP responsive element binding factor (<strong>CREB</strong>) dependent and Ets like protein 1 (Elk 1) dependent transcription; small interfering RNA based strategy.
+CREB1	drug	opioid	18616461	Silencing of <strong>CREB</strong> or Elk 1 significantly increased ERK activation observed after 5 min of <b>morphine</b> stimulation.
+CREB1	drug	opioid	18616461	These differences suggest that both <strong>CREB</strong> dependent and Elk 1 dependent transcription contribute to the expression of proteins regulating <b>morphine</b> induced ERK activity (particular phosphatases, upstream kinases or their activatory proteins).
+CREB1	drug	alcohol	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and <strong>CREB</strong> were analyzed for association with <b>alcohol</b> dependence using multivariate statistical analysis.
+CREB1	addiction	dependence	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and <strong>CREB</strong> were analyzed for association with alcohol <b>dependence</b> using multivariate statistical analysis.
+CREB1	drug	cocaine	18554320	Enhanced <strong>CREB</strong> and DARPP 32 phosphorylation in the nucleus accumbens and <strong>CREB</strong>, ERK, and GluR1 phosphorylation in the dorsal hippocampus is associated with <b>cocaine</b> conditioned place preference behavior.
+CREB1	drug	cocaine	18554320	To better understand the mechanism of <b>cocaine</b> conditioned place preference we have used western blot analysis to examine changes in phosphorylation of cAMP response element binding protein (<strong>CREB</strong>), dopamine  and cyclic AMP regulated phosphoprotein 32 (DARPP 32), extracellular signal regulated kinase (ERK) and GluR1, key molecular substrates altered by <b>cocaine</b>, in the nucleus accumbens (NAc) and dorsal hippocampus (DHC) of C57BL/6 mice.
+CREB1	drug	cocaine	18554320	Our studies revealed that re exposing mice to an environment in which they were previously given <b>cocaine</b> resulted in increased levels of Ser133 phospho <strong>CREB</strong> and Thr34 phospho DARPP 32 with a corresponding decrease in Thr75 phospho DARPP 32 in the NAc.
+CREB1	addiction	reward	18554320	These data suggest that the formation of contextual drug <b>reward</b> associations involves recruitment of the DHC NAc circuit with activation of the DARPP 32/<strong>CREB</strong> pathway in the NAc and the ERK/<strong>CREB</strong> pathway in the DHC.
+CREB1	drug	alcohol	18385331	We found that the anxiolytic effects produced by acute <b>alcohol</b> were associated with a decrease in histone deacetylase (HDAC) activity and increases in acetylation of histones (H3 and H4), levels of <strong>CREB</strong> (cAMP responsive element binding) binding protein (CBP), and neuropeptide Y (NPY) expression in the amygdaloid brain regions of rats.
+CREB1	drug	alcohol	18322102	Here, we report that the anxiolytic effects of acute <b>ethanol</b> were associated with increased brain derived neurotrophic factor (BDNF) and tyrosine kinase B (trkB) expression, increased phosphorylation of extracellular signal regulated kinases 1/2 (Erk1/2), Elk 1, and cAMP responsive element binding protein (<strong>CREB</strong>), increased Arc expression, and increased dendritic spine density (DSD) in both the central amygdala (CeA) and medial amygdala (MeA) but not in the basolateral amygdala (BLA) of rats.
+CREB1	drug	alcohol	18322102	Conversely, the anxiogenic effects of withdrawal after long term <b>ethanol</b> exposure were associated with decreased BDNF and trkB expression, decreased phosphorylation of Erk1/2, Elk 1, and <strong>CREB</strong>, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+CREB1	addiction	withdrawal	18322102	Conversely, the anxiogenic effects of <b>withdrawal</b> after long term ethanol exposure were associated with decreased BDNF and trkB expression, decreased phosphorylation of Erk1/2, Elk 1, and <strong>CREB</strong>, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+CREB1	drug	alcohol	18322102	We also showed that BDNF infusion into the CeA normalized phosphorylation of Erk1/2, Elk 1, and <strong>CREB</strong>, and normalized Arc expression, thereby protecting against the onset of <b>ethanol</b> withdrawal related anxiety.
+CREB1	addiction	withdrawal	18322102	We also showed that BDNF infusion into the CeA normalized phosphorylation of Erk1/2, Elk 1, and <strong>CREB</strong>, and normalized Arc expression, thereby protecting against the onset of ethanol <b>withdrawal</b> related anxiety.
+CREB1	addiction	addiction	18261852	The development of <b>addiction</b> related phenotypes is known to be modulated by regulation of glutamate receptors, as well as activation of transcription factors including cAMP response element binding protein (<strong>CREB</strong>), in the NAc.
+CREB1	drug	nicotine	18261852	We investigated the effects of <b>nicotine</b> pre exposure on <b>nicotine</b> preference and levels of GluR1/2 and <strong>CREB</strong> in the mesolimbic system in male mice C57BL/6J and BALB/c inbred mice.
+CREB1	drug	nicotine	18261852	In addition, alterations in <strong>CREB</strong> and GluR1 levels are not sufficient to explain preference for <b>nicotine</b> in a 2 bottle choice paradigm.
+CREB1	drug	cocaine	18055458	Furthermore, mimicking the effect of <strong>CREB</strong> by pharmacological enhancement of NMDAR function in the NAc in vivo suppressed novelty  and <b>cocaine</b> elicited locomotor activity.
+CREB1	drug	amphetamine	18000809	No significant genotype difference in the effects of d <b>amphetamine</b> on MAPK phosphorylation events within the ventral striatum, phosphorylation at Ser(897) of the NR1 subunit of the NMDA receptor or Ca(2+) and cyclic AMP response element binding protein (<strong>CREB</strong>) at Ser(133) in the frontal cortex was detected.
+CREB1	drug	opioid	17957220	In addition, <b>morphine</b> induced ERK1/2 phosphorylation was increased in the VTA of both wild type and GKO mice, but only the GKO mice showed increases in ERK1/2 and <strong>CREB</strong> phosphorylation in the amygdala or nucleus accumbens.
+CREB1	drug	cocaine	17897358	NMDA induced activation of the NMDA receptor R1 subunit (NR1), Ca(2+)/calmodulin dependent protein kinase II and the cAMP response element binding protein (<strong>CREB</strong>), and <b>cocaine</b> induced <strong>CREB</strong> activation in the CPu are also oppositely regulated by dopamine D(1) and D(3) receptors.
+CREB1	drug	cocaine	17897358	Finally, the blockade of NMDA receptor reduces <b>cocaine</b> induced ERK activation, and inhibits phosphorylation of NR1, Ca(2+)/calmodulin dependent protein kinase II, and <strong>CREB</strong>, while inhibiting ERK activation attenuates <b>cocaine</b> induced <strong>CREB</strong> phosphorylation in the CPu.
+CREB1	drug	nicotine	17592483	<strong>CREB1</strong> haplotypes and the relative reinforcing value of <b>nicotine</b>.
+CREB1	addiction	reward	17592483	<strong>CREB1</strong> haplotypes and the relative <b>reinforcing</b> value of nicotine.
+CREB1	drug	cocaine	17439498	<b>Cocaine</b> induced ERK and <strong>CREB</strong>(S133) phosphorylation were dissociated in many brain regions and failed to develop either tolerance or sensitization with chronic administration.
+CREB1	addiction	sensitization	17439498	Cocaine induced ERK and <strong>CREB</strong>(S133) phosphorylation were dissociated in many brain regions and failed to develop either tolerance or <b>sensitization</b> with chronic administration.
+CREB1	drug	cocaine	17324065	The present study examined the differential <b>cocaine</b> induced activation of the cyclic adenosine monophosphate (cAMP) response element binding protein (<strong>CREB</strong>) throughout discrete zones of analysis of the nucleus accumbens (NAc) in rats.
+CREB1	drug	cocaine	17324065	<strong>CREB</strong> dependent gene transcription, which may underlie long lasting drug induced changes in behavior and the subjective effects of <b>cocaine</b>, varies depending on the stage of drug exposure or withdrawal and the cell population involved.
+CREB1	addiction	withdrawal	17324065	<strong>CREB</strong> dependent gene transcription, which may underlie long lasting drug induced changes in behavior and the subjective effects of cocaine, varies depending on the stage of drug exposure or <b>withdrawal</b> and the cell population involved.
+CREB1	drug	cocaine	17324065	Using immunohistochemistry, the authors analyzed changes in <strong>CREB</strong> phosphorylation in the NAc after 5 days of <b>cocaine</b>, a short or long drug free period, and a subsequent challenge injection.
+CREB1	drug	cocaine	17324065	Repeated <b>cocaine</b> resulted in <strong>CREB</strong> phosphorylation in all analyzed subregions of the NAc excluding the most ventrolateral region of the shell 2 weeks after cessation of repeated <b>cocaine</b>, but rats challenged after 2 drug free days yielded a more localized activation of <strong>CREB</strong> in the 3 most dorsomedial zones of the shell.
+CREB1	drug	cocaine	17324065	The temporal and anatomical determinants of <b>cocaine</b> induced <strong>CREB</strong> activity may indicate functional differences among NAc shell subregions and suggest the involvement of <strong>CREB</strong> in early and late <b>cocaine</b> effects.
+CREB1	drug	opioid	17306231	Antisense pretreated mice showed decreased neurogranin expression, lack of <b>morphine</b> induced phosphorylation of neurogranin and activation of CaMKII and <strong>CREB</strong>, and absence of <b>naloxone</b> induced withdrawal jumping.
+CREB1	addiction	withdrawal	17306231	Antisense pretreated mice showed decreased neurogranin expression, lack of morphine induced phosphorylation of neurogranin and activation of CaMKII and <strong>CREB</strong>, and absence of naloxone induced <b>withdrawal</b> jumping.
+CREB1	drug	opioid	17306231	Taken together, these data suggest that neurogranin plays an essential role in acute <b>opioid</b> dependence, possibly by affecting the CaMKII and <strong>CREB</strong> signaling pathway.
+CREB1	addiction	dependence	17306231	Taken together, these data suggest that neurogranin plays an essential role in acute opioid <b>dependence</b>, possibly by affecting the CaMKII and <strong>CREB</strong> signaling pathway.
+CREB1	drug	opioid	21171355	[Effects of intrathecal injection of U0126 on the expression of phospho <strong>CREB</strong> in spinal cord of <b>morphine</b> induced withdrawal rats].
+CREB1	addiction	withdrawal	21171355	[Effects of intrathecal injection of U0126 on the expression of phospho <strong>CREB</strong> in spinal cord of morphine induced <b>withdrawal</b> rats].
+CREB1	drug	opioid	21171355	To explore effects of intrathecal injection of U0126 on <b>morphine</b> withdrawal response and the spinal Phospho <strong>CREB</strong> expression in <b>morphine</b> induced withdrawal rats.
+CREB1	addiction	withdrawal	21171355	To explore effects of intrathecal injection of U0126 on morphine <b>withdrawal</b> response and the spinal Phospho <strong>CREB</strong> expression in morphine induced <b>withdrawal</b> rats.
+CREB1	drug	opioid	21171355	<b>Morphine</b> withdrawal score, touch evoked agitation scores(TEA score), immunohistochemical and Western blotting technique were used to evaluate <b>morphine</b> withdrawal response and the expression of Phospho <strong>CREB</strong> in the spinal cord.
+CREB1	addiction	withdrawal	21171355	Morphine <b>withdrawal</b> score, touch evoked agitation scores(TEA score), immunohistochemical and Western blotting technique were used to evaluate morphine <b>withdrawal</b> response and the expression of Phospho <strong>CREB</strong> in the spinal cord.
+CREB1	addiction	withdrawal	21171355	Phospho <strong>CREB</strong> positive neurons in the spinal dorsal horn of <b>withdrawal</b> group were 380 +/  71, which is higher than that of U0126 group (293 +/  47, P < 0.05).
+CREB1	addiction	withdrawal	21171355	Compared with <b>withdrawal</b> group, level of Phospho <strong>CREB</strong> protein detected by Western blot in spinal cord of U0126 group was significantly lower.
+CREB1	drug	opioid	17216288	When <b>opioid</b> withdrawal was precipitated, an increase in PKA immunoreactivity and phospho <strong>CREB</strong> (cyclic AMP response element protein) levels were observed in the heart.
+CREB1	addiction	withdrawal	17216288	When opioid <b>withdrawal</b> was precipitated, an increase in PKA immunoreactivity and phospho <strong>CREB</strong> (cyclic AMP response element protein) levels were observed in the heart.
+CREB1	drug	alcohol	17147806	<b>Ethanol</b> sensitivity: a central role for <strong>CREB</strong> transcription regulation in the cerebellum.
+CREB1	drug	alcohol	17147806	Concomitantly, there is evidence for a mediating role of cAMP/PKA/<strong>CREB</strong> signalling in aspects of <b>alcoholism</b> modelled in animals.
+CREB1	drug	alcohol	17147806	These observations collectively suggest that <b>ethanol</b> sensitivity, as it relates to the cerebellum, may be associated with <strong>CREB</strong> transcription activity.
+CREB1	drug	opioid	17117424	Regulation of <b>morphine</b> reward and feeding by <strong>CREB</strong> in the lateral hypothalamus.
+CREB1	addiction	reward	17117424	Regulation of morphine <b>reward</b> and feeding by <strong>CREB</strong> in the lateral hypothalamus.
+CREB1	addiction	reward	17081571	Of particular interest is an upregulation of NMDA receptor dependent MAP kinase and CaM Kinase II signaling, <strong>CREB</strong> phosphorylation, and immediate early and neuropeptide gene expression in nucleus accumbens (NAc) which may facilitate <b>reward</b> related learning, but also play a role in the genesis of maladaptive goal directed behaviors.
+CREB1	drug	alcohol	16961760	Two main factors appear active in the selection: a recruitment of signal transduction networks, including mitogen activated protein kinases and calcium pathways and involving transcription factors such as <strong>Creb</strong>, Myc and Max, to mediate <b>ethanol</b> reinforcement and plasticity.
+CREB1	addiction	reward	16961760	Two main factors appear active in the selection: a recruitment of signal transduction networks, including mitogen activated protein kinases and calcium pathways and involving transcription factors such as <strong>Creb</strong>, Myc and Max, to mediate ethanol <b>reinforcement</b> and plasticity.
+CREB1	addiction	sensitization	16951039	Using immunoblot procedures, limbic brain regions implicated in behavioral <b>sensitization</b> were assayed for extracellular signal regulated kinase and its phosphorylated form (pERK/ERK, a signal transduction kinase), cAMP response element binding protein and its phosphorylated form (pCREB/<strong>CREB</strong>, a constitutively expressed transcriptional regulator), and DeltaFosB (a long lasting transcription factor).
+CREB1	addiction	withdrawal	16951039	pCREB (activated <strong>CREB</strong>) was elevated in the frontal cortex at 3 days <b>withdrawal</b>, but not at 14 days.
+CREB1	drug	opioid	16914643	Furthermore, the significant increase in phosphorylated cAMP response element binding protein (<strong>CREB</strong>) staining in ventral tegmental area induced by long term <b>morphine</b> treatment was not evident in DKO mice, suggesting that <strong>CREB</strong> activation by <b>morphine</b> requires cAMP generated by AC1 and AC8.
+CREB1	drug	amphetamine	16905344	We further found that intraaccumbal <strong>CREB</strong> antisense oligodeoxynucleotide infusion diminished cocaine induced CPP, whereas did not affect the <b>methamphetamine</b> induced CPP.
+CREB1	drug	cocaine	16905344	We further found that intraaccumbal <strong>CREB</strong> antisense oligodeoxynucleotide infusion diminished <b>cocaine</b> induced CPP, whereas did not affect the methamphetamine induced CPP.
+CREB1	addiction	reward	16905344	We further found that intraaccumbal <strong>CREB</strong> antisense oligodeoxynucleotide infusion diminished cocaine induced <b>CPP</b>, whereas did not affect the methamphetamine induced <b>CPP</b>.
+CREB1	drug	amphetamine	16905344	Taken together, these data suggest that protein synthesis and accumbal <strong>CREB</strong> phosphorylation are essential for the learning and consolidation of the cocaine induced CPP, whereas <b>methamphetamine</b> induced CPP may be unrelated to the synthesis of new proteins.
+CREB1	drug	cocaine	16905344	Taken together, these data suggest that protein synthesis and accumbal <strong>CREB</strong> phosphorylation are essential for the learning and consolidation of the <b>cocaine</b> induced CPP, whereas methamphetamine induced CPP may be unrelated to the synthesis of new proteins.
+CREB1	addiction	reward	16905344	Taken together, these data suggest that protein synthesis and accumbal <strong>CREB</strong> phosphorylation are essential for the learning and consolidation of the cocaine induced <b>CPP</b>, whereas methamphetamine induced <b>CPP</b> may be unrelated to the synthesis of new proteins.
+CREB1	drug	opioid	16775132	However, the roles of D1 receptors, <strong>CREB</strong>, and GluR1 in <b>morphine</b> dependence are not well understood.
+CREB1	addiction	dependence	16775132	However, the roles of D1 receptors, <strong>CREB</strong>, and GluR1 in morphine <b>dependence</b> are not well understood.
+CREB1	drug	opioid	16775132	Here, we show that somatic signs of <b>naloxone</b> precipitated withdrawal were associated with increased P <strong>CREB</strong>, but not P GluR1, in the NAc of <b>morphine</b> dependent rats.
+CREB1	addiction	withdrawal	16775132	Here, we show that somatic signs of naloxone precipitated <b>withdrawal</b> were associated with increased P <strong>CREB</strong>, but not P GluR1, in the NAc of morphine dependent rats.
+CREB1	drug	opioid	16775132	Surprisingly, SKF 82958 increased P GluR1, but not P <strong>CREB</strong>, in the NAc, and <b>naloxone</b> reduced SKF 82958 mediated P GluR1 induction specifically in <b>morphine</b> dependent rats.
+CREB1	addiction	aversion	16775132	Together, these results confirm that <b>aversive</b> treatments can increase <strong>CREB</strong> function in the NAc.
+CREB1	addiction	dependence	16775132	Furthermore, they suggest a <b>dependence</b> associated shift in the molecular mechanisms that regulate the consequences of D1 receptor stimulation, favoring activation of GluR1 rather than <strong>CREB</strong>.
+CREB1	drug	cocaine	16710312	Chronic <b>cocaine</b> induces the accumulation of the transcription factor deltaFosB and upregulates cAMP response element binding protein (<strong>CREB</strong>) and dopamine  and cAMP regulated phosphoprotein of 32 kDa (DARPP 32).
+CREB1	drug	opioid	16641242	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) is implicated in mediating the actions of chronic <b>morphine</b> in the locus ceruleus (LC), but direct evidence to support such a role is limited.
+CREB1	addiction	withdrawal	16641242	Here, we investigated the influence of <strong>CREB</strong> on LC neuronal activity and opiate <b>withdrawal</b> behaviors by selectively manipulating <strong>CREB</strong> activity in the LC using viral vectors encoding genes for CREBGFP (wild type <strong>CREB</strong> tagged with green fluorescent protein), caCREBGFP (a constitutively active <strong>CREB</strong> mutant), dnCREBGFP (a dominant negative <strong>CREB</strong> mutant), or GFP alone as a control.
+CREB1	drug	opioid	16641242	Together, these data provide direct evidence that <strong>CREB</strong> plays an important role in controlling the electrical excitability of LC neurons and that <b>morphine</b> induced increases in <strong>CREB</strong> activity contribute to the behavioral and neural adaptations associated with opiate dependence and withdrawal.
+CREB1	addiction	dependence	16641242	Together, these data provide direct evidence that <strong>CREB</strong> plays an important role in controlling the electrical excitability of LC neurons and that morphine induced increases in <strong>CREB</strong> activity contribute to the behavioral and neural adaptations associated with opiate <b>dependence</b> and withdrawal.
+CREB1	addiction	withdrawal	16641242	Together, these data provide direct evidence that <strong>CREB</strong> plays an important role in controlling the electrical excitability of LC neurons and that morphine induced increases in <strong>CREB</strong> activity contribute to the behavioral and neural adaptations associated with opiate dependence and <b>withdrawal</b>.
+CREB1	addiction	addiction	16630062	cAMP response element binding protein (<strong>CREB</strong>), a transcription factor involved in learning, memory and drug <b>addiction</b>, is phosphorylated by calcium calmodulin dependent protein kinase IV (CaMKIV).
+CREB1	drug	opioid	16630062	The increase in phosphorylated <strong>CREB</strong> expression observed in wild type mice after chronic <b>morphine</b> was absent in CaMKIV KO mice, while there was no difference in the expression or phosphorylation of the micro <b>opioid</b> receptor between groups.
+CREB1	drug	opioid	16598705	In addition, prenatal <b>morphine</b> exposure reduced not only the expression of nNOS and the phosphorylation of cAMP responsive element binding protein at serine 133 (<strong>CREB</strong>(Serine 133)), but also the magnitude of long term depression (LTD) at P14.
+CREB1	drug	opioid	16598705	Collectively, the study demonstrates that maternal exposure to <b>morphine</b> decreases the magnitude of PSD 95, nNOS, the phosphorylation of <strong>CREB</strong>(Serine 133), and LTD expression in hippocampal CA1 subregion of young offspring (e.g., P14).
+CREB1	addiction	dependence	16555300	Results show that Ca(2+) activation of the transcription factor cAMP responsive element binding protein (<strong>CREB</strong>) and Ca(2+) induced alterations in the level of the apoptotic enzyme caspase 3 show both dose and age <b>dependence</b> in the early developing Purkinje neurons.
+CREB1	drug	opioid	16421965	Changes of <strong>CREB</strong> in rat hippocampus, prefrontal cortex and nucleus accumbens during three phases of <b>morphine</b> induced conditioned place preference in rats.
+CREB1	drug	opioid	16421965	To investigate the changes in <strong>CREB</strong> (cAMP response element binding protein) in hippocampus, PFC (prefrontal cortex) and NAc (nucleus accumbens) during three phases of <b>morphine</b> induced CPP (conditioned place preference) in rats, and to elucidate the role of <strong>CREB</strong> during the progress of conditioned place preference.
+CREB1	addiction	reward	16421965	To investigate the changes in <strong>CREB</strong> (cAMP response element binding protein) in hippocampus, PFC (prefrontal cortex) and NAc (nucleus accumbens) during three phases of morphine induced <b>CPP</b> (conditioned place preference) in rats, and to elucidate the role of <strong>CREB</strong> during the progress of conditioned place preference.
+CREB1	drug	opioid	16421965	<b>Morphine</b> induced CPP acquisition, extinction and drug primed reinstatement model was established, and <strong>CREB</strong> expression in each brain area was measured by Western Blot methods.
+CREB1	addiction	relapse	16421965	Morphine induced CPP acquisition, extinction and drug primed <b>reinstatement</b> model was established, and <strong>CREB</strong> expression in each brain area was measured by Western Blot methods.
+CREB1	addiction	reward	16421965	Morphine induced <b>CPP</b> acquisition, extinction and drug primed reinstatement model was established, and <strong>CREB</strong> expression in each brain area was measured by Western Blot methods.
+CREB1	addiction	relapse	16421965	During the phases of CPP acquisition and <b>reinstatement</b>, the level of <strong>CREB</strong> expression was significantly changed in different brain areas.
+CREB1	addiction	reward	16421965	During the phases of <b>CPP</b> acquisition and reinstatement, the level of <strong>CREB</strong> expression was significantly changed in different brain areas.
+CREB1	drug	opioid	16421965	It was proved that CPP model can be used as an effective tool to investigate the mechanisms underlying drug induced reinstatement of drug seeking after extinction, and that <b>morphine</b> induced CPP and drug primed reinstatement may involve activation of the transcription factor <strong>CREB</strong> in several brain areas, suggesting that the <strong>CREB</strong> and its target gene regulation pathway may mediate the basic mechanism underlying <b>opioid</b> dependence and its drug seeking behavior.
+CREB1	addiction	dependence	16421965	It was proved that CPP model can be used as an effective tool to investigate the mechanisms underlying drug induced reinstatement of drug seeking after extinction, and that morphine induced CPP and drug primed reinstatement may involve activation of the transcription factor <strong>CREB</strong> in several brain areas, suggesting that the <strong>CREB</strong> and its target gene regulation pathway may mediate the basic mechanism underlying opioid <b>dependence</b> and its drug seeking behavior.
+CREB1	addiction	relapse	16421965	It was proved that CPP model can be used as an effective tool to investigate the mechanisms underlying drug induced <b>reinstatement</b> of drug <b>seeking</b> after extinction, and that morphine induced CPP and drug primed <b>reinstatement</b> may involve activation of the transcription factor <strong>CREB</strong> in several brain areas, suggesting that the <strong>CREB</strong> and its target gene regulation pathway may mediate the basic mechanism underlying opioid dependence and its drug <b>seeking</b> behavior.
+CREB1	addiction	reward	16421965	It was proved that <b>CPP</b> model can be used as an effective tool to investigate the mechanisms underlying drug induced reinstatement of drug seeking after extinction, and that morphine induced <b>CPP</b> and drug primed reinstatement may involve activation of the transcription factor <strong>CREB</strong> in several brain areas, suggesting that the <strong>CREB</strong> and its target gene regulation pathway may mediate the basic mechanism underlying opioid dependence and its drug seeking behavior.
+CREB1	drug	opioid	16417577	Galanin attenuates cyclic AMP regulatory element binding protein (<strong>CREB</strong>) phosphorylation induced by chronic <b>morphine</b> and <b>naloxone</b> challenge in Cath.a cells and primary striatal cultures.
+CREB1	addiction	withdrawal	16417577	The current study demonstrates that acute galanin treatment blocks the consequences of increased cAMP signaling following chronic opiate administration and <b>withdrawal</b> in Cath.a cells and primary cultures of striatal neurons as measured by phosphorylation of the transcription factor cAMP regulatory element binding protein (<strong>CREB</strong>).
+CREB1	drug	cocaine	16380431	<strong>CREB</strong> binding protein controls response to <b>cocaine</b> by acetylating histones at the fosB promoter in the mouse striatum.
+CREB1	drug	cocaine	16380431	Here, we show that histone acetylation by the cAMP response element binding protein (<strong>CREB</strong>) binding protein (CBP) mediates sensitivity to <b>cocaine</b> by regulating expression of the fosB gene and its splice variant, DeltafosB, a transcription factor previously implicated in addiction.
+CREB1	addiction	addiction	16380431	Here, we show that histone acetylation by the cAMP response element binding protein (<strong>CREB</strong>) binding protein (CBP) mediates sensitivity to cocaine by regulating expression of the fosB gene and its splice variant, DeltafosB, a transcription factor previously implicated in <b>addiction</b>.
+CREB1	drug	cocaine	16380431	Thus, CBP, which forms part of the promoter complex with <strong>CREB</strong>, mediates sensitivity to <b>cocaine</b> by acetylating histones.
+CREB1	drug	cocaine	16359811	Repeated <b>cocaine</b> exposure up regulates cyclic AMP signaling and increases the transcriptional activity of cyclic AMP response element binding protein (<strong>CREB</strong>) in the nucleus accumbens.
+CREB1	drug	cocaine	16359811	To study the possibility that nucleus accumbens <strong>CREB</strong> activity regulates self administration behavior, we tested the effects of a single, bilateral infusion of <strong>CREB</strong> antisense oligonucleotide into nucleus accumbens core and shell sub regions on <b>cocaine</b> self administration in rats.
+CREB1	drug	cocaine	16359811	Similar infusions of <strong>CREB</strong> antisense in either core or shell produced a transient downward shift in <b>cocaine</b> self administration dose response curves on a fixed ratio 5 (five responses/injection) reinforcement schedule, indicating a reduction in <b>cocaine</b> reinforcement that fully recovered 3 days after treatment.
+CREB1	addiction	reward	16359811	Similar infusions of <strong>CREB</strong> antisense in either core or shell produced a transient downward shift in cocaine self administration dose response curves on a fixed ratio 5 (five responses/injection) <b>reinforcement</b> schedule, indicating a reduction in cocaine <b>reinforcement</b> that fully recovered 3 days after treatment.
+CREB1	drug	cocaine	16359811	<strong>CREB</strong> antisense also increased the threshold dose of <b>cocaine</b> required for reinstating <b>cocaine</b> self administration, indicating that nucleus accumbens <strong>CREB</strong> levels regulate the incentive properties of <b>cocaine</b>.
+CREB1	addiction	reward	16359811	<strong>CREB</strong> antisense also increased the threshold dose of cocaine required for reinstating cocaine self administration, indicating that nucleus accumbens <strong>CREB</strong> levels regulate the <b>incentive</b> properties of cocaine.
+CREB1	drug	cocaine	16359811	When access to <b>cocaine</b> was less restricted on a fixed ratio 1 schedule, infusion of <strong>CREB</strong> antisense in the core, but not shell, caused a transient (1 2 days) reduction in stabilized <b>cocaine</b> self administration, but had no effect on responding maintained by sucrose pellets, indicating that basal <strong>CREB</strong> levels in the nucleus accumbens core regulate drug intake.
+CREB1	drug	cocaine	16359811	These results suggest a necessary role for nucleus accumbens <strong>CREB</strong> activity in <b>cocaine</b> reinforcement, and, by converse analogy, up regulation in <strong>CREB</strong> activity after chronic <b>cocaine</b> use could contribute to addiction related increases in <b>cocaine</b> self administration.
+CREB1	addiction	addiction	16359811	These results suggest a necessary role for nucleus accumbens <strong>CREB</strong> activity in cocaine reinforcement, and, by converse analogy, up regulation in <strong>CREB</strong> activity after chronic cocaine use could contribute to <b>addiction</b> related increases in cocaine self administration.
+CREB1	addiction	reward	16359811	These results suggest a necessary role for nucleus accumbens <strong>CREB</strong> activity in cocaine <b>reinforcement</b>, and, by converse analogy, up regulation in <strong>CREB</strong> activity after chronic cocaine use could contribute to addiction related increases in cocaine self administration.
+CREB1	drug	cocaine	16339038	<b>Cocaine</b> induced phosphorylation of MSK1 threonine 581 and cAMP response element binding protein (<strong>CREB</strong>) serine 133 (Ser133) were blocked by SL327, a drug that prevents ERK activation.
+CREB1	drug	cocaine	16339038	In MSK1 knock out (KO) mice <strong>CREB</strong> and H3 phosphorylation in response to <b>cocaine</b> (10 mg/kg) were blocked, and induction of c Fos and dynorphin was prevented, whereas the induction of Egr 1 (early growth response 1)/zif268/Krox24 was unaltered.
+CREB1	addiction	sensitization	16339038	Our results show that MSK1 is a major striatal kinase, downstream from ERK, responsible for the phosphorylation of <strong>CREB</strong> and H3 and is required specifically for the induction of c Fos and dynorphin as well as for locomotor <b>sensitization</b>.
+CREB1	drug	opioid	16289800	The spinal ERK inhibition or knockdown also reduced <b>morphine</b> withdrawal induced phosphorylation of cAMP response element binding protein (<strong>CREB</strong>), which is one of the important downstream substrates of ERK pathway, and Fos expression.
+CREB1	addiction	withdrawal	16289800	The spinal ERK inhibition or knockdown also reduced morphine <b>withdrawal</b> induced phosphorylation of cAMP response element binding protein (<strong>CREB</strong>), which is one of the important downstream substrates of ERK pathway, and Fos expression.
+CREB1	drug	cocaine	16271798	Furthermore, this single <b>cocaine</b> administration does not alter the levels of phospho <strong>CREB</strong> protein or <strong>CREB</strong> DNA bindings in the caudate/putamen protein extracts but does increase phospho Elk 1 protein levels in the same extracts.
+CREB1	drug	cocaine	16197514	Deletion of dopamine D1 and D3 receptors differentially affects spontaneous behaviour and <b>cocaine</b> induced locomotor activity, reward and <strong>CREB</strong> phosphorylation.
+CREB1	addiction	reward	16197514	Deletion of dopamine D1 and D3 receptors differentially affects spontaneous behaviour and cocaine induced locomotor activity, <b>reward</b> and <strong>CREB</strong> phosphorylation.
+CREB1	drug	alcohol	16192983	Furthermore, decreased function of PKA may regulate <b>alcohol</b> drinking behaviors via <strong>CREB</strong> mediated decreased expression of NPY in the NAc shell of rats.
+CREB1	addiction	reward	16157281	We show that COC conditioned place preference (<b>CPP</b>) activates ERK, <strong>CREB</strong>, Elk 1, and Fos in the nucleus accumbens core (AcbC) but not shell.
+CREB1	addiction	reward	16157281	Intra AcbC infusions of U0126, an inhibitor of the ERK kinase MEK, prevent both the activation of ERK, <strong>CREB</strong>, Elk 1, and Fos and retrieval of COC <b>CPP</b>.
+CREB1	drug	cocaine	16146347	Third, <strong>CREB</strong> in the nucleus accumbens has been shown to have an opposing effect on <b>cocaine</b> self administration.
+CREB1	addiction	withdrawal	16123760	<strong>CREB</strong> levels did not change in the VP, but there was a significant decrease in levels of its active, phosphorylated form (pCREB) at both 3  and 14 days <b>withdrawal</b>.
+CREB1	drug	cocaine	16046859	Augmented constitutive <strong>CREB</strong> expression in the nucleus accumbens and striatum may contribute to the altered behavioral response to <b>cocaine</b> of adult mice exposed to <b>cocaine</b> in utero.
+CREB1	drug	cocaine	16046859	Tissue samples of the nucleus accumbens (NAc) and striatum (Str) of all four prenatal treatment groups were examined to determine whether alterations in the transcription factor <strong>CREB</strong> or glutamate receptor subunit, GluR1, induced by prenatal <b>cocaine</b> treatment may have contributed to the altered behavioral responses.
+CREB1	drug	cocaine	16046859	Such alterations in constitutive <strong>CREB</strong> levels may contribute to some of the behavioral differences reported in adult mice exposed to <b>cocaine</b> in utero.
+CREB1	drug	nicotine	15953421	Mu opioid receptor and <strong>CREB</strong> activation are required for <b>nicotine</b> reward.
+CREB1	drug	opioid	15953421	Mu <b>opioid</b> receptor and <strong>CREB</strong> activation are required for nicotine reward.
+CREB1	addiction	reward	15953421	Mu opioid receptor and <strong>CREB</strong> activation are required for nicotine <b>reward</b>.
+CREB1	drug	nicotine	15953421	Exposure to an environment previously associated with rewarding properties of <b>nicotine</b> results in an increase of <strong>CREB</strong> phosphorylation similar to that seen following <b>nicotine</b> administration, and this response is absent in MOR( / ) mice.
+CREB1	drug	nicotine	15953421	Moreover, a single administration of an opioid receptor antagonist, naloxone, blocks both the conditioned molecular response (<strong>CREB</strong> phosphorylation) and the conditioned behavioral response (<b>nicotine</b> reward) in a place preference paradigm.
+CREB1	drug	opioid	15953421	Moreover, a single administration of an <b>opioid</b> receptor antagonist, <b>naloxone</b>, blocks both the conditioned molecular response (<strong>CREB</strong> phosphorylation) and the conditioned behavioral response (nicotine reward) in a place preference paradigm.
+CREB1	addiction	reward	15953421	Moreover, a single administration of an opioid receptor antagonist, naloxone, blocks both the conditioned molecular response (<strong>CREB</strong> phosphorylation) and the conditioned behavioral response (nicotine <b>reward</b>) in a place preference paradigm.
+CREB1	drug	nicotine	15953421	However, this effect, along with rewarding properties of <b>nicotine</b>, is blocked in mice with a targeted disruption in the <strong>CREB</strong> gene.
+CREB1	drug	nicotine	15953421	Together, pharmacologic and genetic manipulations indicate that phosphorylation of <strong>CREB</strong> and upregulation of functional MORs are required for <b>nicotine</b> conditioned reward.
+CREB1	addiction	reward	15953421	Together, pharmacologic and genetic manipulations indicate that phosphorylation of <strong>CREB</strong> and upregulation of functional MORs are required for nicotine conditioned <b>reward</b>.
+CREB1	drug	cannabinoid	15913574	Effect of delta9 <b>tetrahydrocannabinol</b> on phosphorylated <strong>CREB</strong> in rat cerebellum: an immunohistochemical study.
+CREB1	drug	cannabinoid	15913574	This immunohistochemical study examines the effect of delta9 <b>tetrahydrocannabinol</b> (delta9 <b>THC</b>), the principal psychoactive component of <b>marijuana</b>, on the levels of phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) in the rat cerebellum.
+CREB1	drug	cannabinoid	15913574	Acute treatments with delta9 <b>THC</b> at doses of 5 or 10 mg/kg induced a significant increase of p <strong>CREB</strong> in the granule cell layer of the cerebellum, an effect blocked by the CB1 receptor antagonist SR 141716A.
+CREB1	drug	cannabinoid	15913574	Following chronic delta9 <b>THC</b> administration (10 mg/kg/day for 4 weeks), the density of p <strong>CREB</strong> was markedly attenuated compared to controls, and this attenuation persisted 3 weeks after withdrawal from delta9 <b>THC</b>.
+CREB1	addiction	withdrawal	15913574	Following chronic delta9 THC administration (10 mg/kg/day for 4 weeks), the density of p <strong>CREB</strong> was markedly attenuated compared to controls, and this attenuation persisted 3 weeks after <b>withdrawal</b> from delta9 THC.
+CREB1	drug	alcohol	15834234	This study was undertaken to examine the effects of acute <b>ethanol</b> on ERK, PKB, and <strong>CREB</strong> activation in the brain.
+CREB1	drug	alcohol	15834234	In cortical cultures, <b>ethanol</b> (100 mM) significantly reduced activity dependent activation of phospho ERK, phospho PKB, and phospho <strong>CREB</strong> by approximately 50%.
+CREB1	drug	alcohol	15834234	Without exception, <b>ethanol</b> inhibited phospho <strong>CREB</strong> in an identical brain region  and age dependent manner as was observed for phospho ERK.
+CREB1	drug	alcohol	15834234	The results demonstrate that acute <b>ethanol</b> inhibits ERK/PKB/<strong>CREB</strong> signaling in brain.
+CREB1	drug	alcohol	15834234	Furthermore, the lack of effect of MK 801 suggests that inhibition of NMDA receptors is unlikely to play a major role in binge <b>ethanol</b> inhibition of ERK/PKB/<strong>CREB</strong> signaling in vivo.
+CREB1	addiction	intoxication	15834234	Furthermore, the lack of effect of MK 801 suggests that inhibition of NMDA receptors is unlikely to play a major role in <b>binge</b> ethanol inhibition of ERK/PKB/<strong>CREB</strong> signaling in vivo.
+CREB1	drug	alcohol	15714041	<strong>CREB</strong> gene transcription factors: role in molecular mechanisms of <b>alcohol</b> and drug addiction.
+CREB1	addiction	addiction	15714041	<strong>CREB</strong> gene transcription factors: role in molecular mechanisms of alcohol and drug <b>addiction</b>.
+CREB1	drug	alcohol	15714041	The presentations were (1) <b>Ethanol</b> Modulation of <strong>CREB</strong>: Role in Dependence and Withdrawal, by Fulton Crews; (2) Effects of D1 Dopamine Receptor Activation During Withdrawal From Chronic Morphine: Enhanced <strong>CREB</strong> Activation and Decreased Conditioned Place Aversion, by Elena H. Chartoff; (3) <strong>CREB</strong> Haplodeficient Mice: Role in Anxiety and <b>Alcohol</b> Drinking Behaviors, by Subhash C. Pandey; and (4) A Role for <strong>CREB</strong> in Stress and Drug Addiction, by Julie A. Blendy.
+CREB1	drug	opioid	15714041	The presentations were (1) Ethanol Modulation of <strong>CREB</strong>: Role in Dependence and Withdrawal, by Fulton Crews; (2) Effects of D1 Dopamine Receptor Activation During Withdrawal From Chronic <b>Morphine</b>: Enhanced <strong>CREB</strong> Activation and Decreased Conditioned Place Aversion, by Elena H. Chartoff; (3) <strong>CREB</strong> Haplodeficient Mice: Role in Anxiety and Alcohol Drinking Behaviors, by Subhash C. Pandey; and (4) A Role for <strong>CREB</strong> in Stress and Drug Addiction, by Julie A. Blendy.
+CREB1	addiction	addiction	15714041	The presentations were (1) Ethanol Modulation of <strong>CREB</strong>: Role in Dependence and Withdrawal, by Fulton Crews; (2) Effects of D1 Dopamine Receptor Activation During Withdrawal From Chronic Morphine: Enhanced <strong>CREB</strong> Activation and Decreased Conditioned Place Aversion, by Elena H. Chartoff; (3) <strong>CREB</strong> Haplodeficient Mice: Role in Anxiety and Alcohol Drinking Behaviors, by Subhash C. Pandey; and (4) A Role for <strong>CREB</strong> in Stress and Drug <b>Addiction</b>, by Julie A. Blendy.
+CREB1	addiction	aversion	15714041	The presentations were (1) Ethanol Modulation of <strong>CREB</strong>: Role in Dependence and Withdrawal, by Fulton Crews; (2) Effects of D1 Dopamine Receptor Activation During Withdrawal From Chronic Morphine: Enhanced <strong>CREB</strong> Activation and Decreased Conditioned Place <b>Aversion</b>, by Elena H. Chartoff; (3) <strong>CREB</strong> Haplodeficient Mice: Role in Anxiety and Alcohol Drinking Behaviors, by Subhash C. Pandey; and (4) A Role for <strong>CREB</strong> in Stress and Drug Addiction, by Julie A. Blendy.
+CREB1	addiction	dependence	15714041	The presentations were (1) Ethanol Modulation of <strong>CREB</strong>: Role in <b>Dependence</b> and Withdrawal, by Fulton Crews; (2) Effects of D1 Dopamine Receptor Activation During Withdrawal From Chronic Morphine: Enhanced <strong>CREB</strong> Activation and Decreased Conditioned Place Aversion, by Elena H. Chartoff; (3) <strong>CREB</strong> Haplodeficient Mice: Role in Anxiety and Alcohol Drinking Behaviors, by Subhash C. Pandey; and (4) A Role for <strong>CREB</strong> in Stress and Drug Addiction, by Julie A. Blendy.
+CREB1	addiction	withdrawal	15714041	The presentations were (1) Ethanol Modulation of <strong>CREB</strong>: Role in Dependence and <b>Withdrawal</b>, by Fulton Crews; (2) Effects of D1 Dopamine Receptor Activation During <b>Withdrawal</b> From Chronic Morphine: Enhanced <strong>CREB</strong> Activation and Decreased Conditioned Place Aversion, by Elena H. Chartoff; (3) <strong>CREB</strong> Haplodeficient Mice: Role in Anxiety and Alcohol Drinking Behaviors, by Subhash C. Pandey; and (4) A Role for <strong>CREB</strong> in Stress and Drug Addiction, by Julie A. Blendy.
+CREB1	drug	opioid	15680959	Alterations in <b>morphine</b> induced reward, locomotor activity, and thermoregulation in <strong>CREB</strong> deficient mice.
+CREB1	addiction	reward	15680959	Alterations in morphine induced <b>reward</b>, locomotor activity, and thermoregulation in <strong>CREB</strong> deficient mice.
+CREB1	drug	opioid	15680959	Previous studies in our lab have shown a robust decrease in the rewarding properties of <b>morphine</b> in <strong>CREB</strong>(alphaDelta) mutant mice.
+CREB1	drug	opioid	15680959	To determine whether the genetic effects of the global <strong>CREB</strong>(alphaDelta) mutation are specific to reward or generalizable, we examined a variety of <b>morphine</b> induced behaviors regulated by different neural circuitry.
+CREB1	addiction	reward	15680959	To determine whether the genetic effects of the global <strong>CREB</strong>(alphaDelta) mutation are specific to <b>reward</b> or generalizable, we examined a variety of morphine induced behaviors regulated by different neural circuitry.
+CREB1	drug	opioid	15680959	At low doses of <b>morphine</b> (5 and 10 mg/kg), <strong>CREB</strong>(alphaDelta) mutant mice show a reduction in reward yet similar locomotor activity in response to <b>morphine</b> compared to wild type littermates.
+CREB1	addiction	reward	15680959	At low doses of morphine (5 and 10 mg/kg), <strong>CREB</strong>(alphaDelta) mutant mice show a reduction in <b>reward</b> yet similar locomotor activity in response to morphine compared to wild type littermates.
+CREB1	addiction	reward	15680959	However, at a high dose (20 mg/kg), <strong>CREB</strong>(alphaDelta) mutant mice show an increase in <b>reward</b> and locomotor activity.
+CREB1	drug	opioid	15680959	<b>Morphine</b> induced thermoregulation is attenuated in <strong>CREB</strong>(alphaDelta) mutant mice at high doses of <b>morphine</b> compared to wild type animals.
+CREB1	drug	opioid	15680959	The behavioral differences in response to <b>morphine</b> seen in <strong>CREB</strong>(alphaDelta) mutant mice are not due to changes in mu <b>opioid</b> receptor (MOR) mRNA expression, as the <strong>CREB</strong> deletion has no effect on baseline MOR mRNA in three of the brain regions involved in mediating these behaviors: the ventral tegmental area (VTA), nucleus accumbens (NAc), and hypothalamus.
+CREB1	drug	opioid	15680959	These data demonstrate that at low doses, deficits in <b>morphine</b> induced changes in <strong>CREB</strong> deficient mice are limited to reward and thermoregulation.
+CREB1	addiction	reward	15680959	These data demonstrate that at low doses, deficits in morphine induced changes in <strong>CREB</strong> deficient mice are limited to <b>reward</b> and thermoregulation.
+CREB1	drug	opioid	15680959	However, at higher doses, <strong>CREB</strong> mutant mice actually find <b>morphine</b> more rewarding and exhibit increased locomotor activity compared to their wild type littermates.
+CREB1	drug	opioid	15680959	Together, these results indicate that the role of <strong>CREB</strong> in dose dependent changes in behaviors induced by <b>morphine</b> is different depending on the brain regions involved in mediating the behavior.
+CREB1	drug	alcohol	15500908	Recent research in molecular neurosciences using animal models have identified the role of extended amygdaloid (shell structures of nucleus accumbens [NAc] and central and medial amygdaloid nuclei) <strong>CREB</strong> signaling in positive and negative affective states of <b>alcohol</b> drinking behaviors.
+CREB1	drug	alcohol	15500908	This review article highlights the current findings on the role of nucleus accumbal and amygdaloid <strong>CREB</strong> signaling in behavioral consequences of <b>alcohol</b> use and abuse.
+CREB1	drug	opioid	15451364	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) plays an important role in <b>opioids</b> dependence.
+CREB1	addiction	dependence	15451364	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) plays an important role in opioids <b>dependence</b>.
+CREB1	drug	opioid	15451364	To better understand the role of <strong>CREB</strong> in <b>opioids</b> dependence and underlying signal pathways, we compared the effects of three ohmfentanyl stereoisomers (( ) cis (3R,4S,2'R) OMF (F9202), (+) cis (3R,4S,2'S) OMF (F9204), ( ) cis (3S,4S,2'R) OMF (F9203)) and <b>morphine</b> on <strong>CREB</strong> phosphorylation and the expression of Ca2+/calmodulin dependent protein kinase IV (CaMKIV) in hippocampus derived from mice which displayed conditioned place preference (CPP) behavior by Western blot, and immunohistochemistry analyses.
+CREB1	addiction	dependence	15451364	To better understand the role of <strong>CREB</strong> in opioids <b>dependence</b> and underlying signal pathways, we compared the effects of three ohmfentanyl stereoisomers (( ) cis (3R,4S,2'R) OMF (F9202), (+) cis (3R,4S,2'S) OMF (F9204), ( ) cis (3S,4S,2'R) OMF (F9203)) and morphine on <strong>CREB</strong> phosphorylation and the expression of Ca2+/calmodulin dependent protein kinase IV (CaMKIV) in hippocampus derived from mice which displayed conditioned place preference (CPP) behavior by Western blot, and immunohistochemistry analyses.
+CREB1	addiction	reward	15451364	To better understand the role of <strong>CREB</strong> in opioids dependence and underlying signal pathways, we compared the effects of three ohmfentanyl stereoisomers (( ) cis (3R,4S,2'R) OMF (F9202), (+) cis (3R,4S,2'S) OMF (F9204), ( ) cis (3S,4S,2'R) OMF (F9203)) and morphine on <strong>CREB</strong> phosphorylation and the expression of Ca2+/calmodulin dependent protein kinase IV (CaMKIV) in hippocampus derived from mice which displayed conditioned place preference (<b>CPP</b>) behavior by Western blot, and immunohistochemistry analyses.
+CREB1	drug	opioid	15451364	Moreover, we studied the effects of OMF and <b>morphine</b> on <strong>CREB</strong> phosphorylation and colocalization of phosphorylated <strong>CREB</strong> (P <strong>CREB</strong>) with CaMKIV in cultured rat hippocampal neurons by Western blot, and confocal fluorescence microscopy analyses.
+CREB1	drug	opioid	15451364	The results showed that F9202, F9204 or <b>morphine</b>, which could induce CPP, enhanced <strong>CREB</strong> phosphorylation and the expression of CaMKIV in hippocampus from CPP mice without affecting total <strong>CREB</strong> protein level.
+CREB1	addiction	reward	15451364	The results showed that F9202, F9204 or morphine, which could induce <b>CPP</b>, enhanced <strong>CREB</strong> phosphorylation and the expression of CaMKIV in hippocampus from <b>CPP</b> mice without affecting total <strong>CREB</strong> protein level.
+CREB1	drug	opioid	15451364	The <strong>CREB</strong> phosphorylation of cultured hippocampal neurons was also enhanced and reached its peak level at 30 min upon exposure to F9202 (100 nM), F9204 (100 nM) or <b>morphine</b> (1 microM), while the total <strong>CREB</strong> protein level was not altered.
+CREB1	drug	opioid	15451364	KN 62 (10 microM), an inhibitor of CaM kinases, prevented <strong>CREB</strong> phosphorylation induced by <b>morphine</b>, F9202, and F9204 without change of total <strong>CREB</strong> level.
+CREB1	addiction	reward	15451364	F9203, which could not induce <b>CPP</b>, failed to increase the <strong>CREB</strong> phosphorylation and the colocalization of P <strong>CREB</strong> with CaMKIV both in hippocampus from <b>CPP</b> mice and in cultured hippocampal neurons.
+CREB1	drug	opioid	15451364	This is the first evidence to suggest that the increased <strong>CREB</strong> phosphorylation via CaMKIV signal pathway in hippocampus is relevant to <b>opioids</b> psychological dependence.
+CREB1	addiction	dependence	15451364	This is the first evidence to suggest that the increased <strong>CREB</strong> phosphorylation via CaMKIV signal pathway in hippocampus is relevant to opioids psychological <b>dependence</b>.
+CREB1	drug	nicotine	15334606	Modulation of <strong>CREB</strong> expression and phosphorylation in the rat nucleus accumbens during <b>nicotine</b> exposure and withdrawal.
+CREB1	addiction	withdrawal	15334606	Modulation of <strong>CREB</strong> expression and phosphorylation in the rat nucleus accumbens during nicotine exposure and <b>withdrawal</b>.
+CREB1	drug	nicotine	15334606	To understand the molecular mechanisms of <b>nicotine</b> addiction, the present investigation examined the effects of acute and chronic <b>nicotine</b> treatment and its withdrawal on cAMP responsive element binding (<strong>CREB</strong>) protein expression and phosphorylation (serine 133) in nucleus accumbens (NAc) structures of rats.
+CREB1	addiction	addiction	15334606	To understand the molecular mechanisms of nicotine <b>addiction</b>, the present investigation examined the effects of acute and chronic nicotine treatment and its withdrawal on cAMP responsive element binding (<strong>CREB</strong>) protein expression and phosphorylation (serine 133) in nucleus accumbens (NAc) structures of rats.
+CREB1	addiction	withdrawal	15334606	To understand the molecular mechanisms of nicotine addiction, the present investigation examined the effects of acute and chronic nicotine treatment and its <b>withdrawal</b> on cAMP responsive element binding (<strong>CREB</strong>) protein expression and phosphorylation (serine 133) in nucleus accumbens (NAc) structures of rats.
+CREB1	drug	nicotine	15334606	it was found that acute treatment (1 and 18 hr of withdrawal) with <b>nicotine</b> had no effects on total <strong>creb</strong> and phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) protein levels in shell or core structures of rat NAc.
+CREB1	addiction	withdrawal	15334606	it was found that acute treatment (1 and 18 hr of <b>withdrawal</b>) with nicotine had no effects on total <strong>creb</strong> and phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) protein levels in shell or core structures of rat NAc.
+CREB1	drug	nicotine	15334606	On the other hand, 18 hr withdrawal after chronic <b>nicotine</b> exposure produced significant reductions in the total <strong>CREB</strong> and p <strong>CREB</strong> protein levels in the shell but not in core structures of nac.
+CREB1	addiction	withdrawal	15334606	On the other hand, 18 hr <b>withdrawal</b> after chronic nicotine exposure produced significant reductions in the total <strong>CREB</strong> and p <strong>CREB</strong> protein levels in the shell but not in core structures of nac.
+CREB1	drug	nicotine	15334606	interestingly, <b>nicotine</b> withdrawal (1 hr) after chronic exposure maintained normal levels of total <strong>CREB</strong> and p <strong>CREB</strong> protein levels in the shell and core structures of NAc.
+CREB1	addiction	withdrawal	15334606	interestingly, nicotine <b>withdrawal</b> (1 hr) after chronic exposure maintained normal levels of total <strong>CREB</strong> and p <strong>CREB</strong> protein levels in the shell and core structures of NAc.
+CREB1	drug	nicotine	15334606	These results suggest the possibility that decreased <strong>CREB</strong> activity in the shell of NAc may be associated with abnormal reward mechanisms during <b>nicotine</b> withdrawal after chronic exposure.
+CREB1	addiction	reward	15334606	These results suggest the possibility that decreased <strong>CREB</strong> activity in the shell of NAc may be associated with abnormal <b>reward</b> mechanisms during nicotine withdrawal after chronic exposure.
+CREB1	addiction	withdrawal	15334606	These results suggest the possibility that decreased <strong>CREB</strong> activity in the shell of NAc may be associated with abnormal reward mechanisms during nicotine <b>withdrawal</b> after chronic exposure.
+CREB1	drug	opioid	15287893	Transcription factors Ca2+/cAMP responsive element binding protein (<strong>CREB</strong>) and activator protein 1 (AP 1) may constitute a direct link between the <b>opioid</b> regulated signal transduction pathways and modulation of gene expression.
+CREB1	drug	opioid	15287893	Acute treatment of Neuro2a MOR neuroblastoma cells with <b>opioids</b> stimulated <strong>CREB</strong> activity; prolonged treatment normalized it, while withdrawal from the drug again elicited an increase in phosphorylated <strong>CREB</strong> levels.
+CREB1	addiction	withdrawal	15287893	Acute treatment of Neuro2a MOR neuroblastoma cells with opioids stimulated <strong>CREB</strong> activity; prolonged treatment normalized it, while <b>withdrawal</b> from the drug again elicited an increase in phosphorylated <strong>CREB</strong> levels.
+CREB1	drug	opioid	15287893	Protein kinase C was responsible for the activation of transcription following acute <b>opioid</b> administration whereas the cAMP pathway activated similar mechanisms during withdrawal, making <strong>CREB</strong> a kind of 'a trigger' reacting to the presence or withdrawal of the <b>opioid</b> signal.
+CREB1	addiction	withdrawal	15287893	Protein kinase C was responsible for the activation of transcription following acute opioid administration whereas the cAMP pathway activated similar mechanisms during <b>withdrawal</b>, making <strong>CREB</strong> a kind of 'a trigger' reacting to the presence or <b>withdrawal</b> of the opioid signal.
+CREB1	drug	opioid	15287893	Apart from the elevated <strong>CREB</strong> phosphorylation, CRE binding activity and expression of luciferase reporter gene regulated by CRE elements were increased after single administration and during withdrawal from the prolonged <b>opioid</b> treatment.
+CREB1	addiction	withdrawal	15287893	Apart from the elevated <strong>CREB</strong> phosphorylation, CRE binding activity and expression of luciferase reporter gene regulated by CRE elements were increased after single administration and during <b>withdrawal</b> from the prolonged opioid treatment.
+CREB1	drug	opioid	15287893	Along with <strong>CREB</strong>, AP 1 binding activity and AP 1 directed transcription were stimulated after single administration and during withdrawal from the <b>opioid</b>.
+CREB1	addiction	withdrawal	15287893	Along with <strong>CREB</strong>, AP 1 binding activity and AP 1 directed transcription were stimulated after single administration and during <b>withdrawal</b> from the opioid.
+CREB1	drug	opioid	15287893	These results provide evidence that both single <b>opioid</b> administration and <b>opioid</b> withdrawal activate <strong>CREB</strong> and CRE dependent transcriptional mechanisms via distinct intracellular signaling pathways.
+CREB1	addiction	withdrawal	15287893	These results provide evidence that both single opioid administration and opioid <b>withdrawal</b> activate <strong>CREB</strong> and CRE dependent transcriptional mechanisms via distinct intracellular signaling pathways.
+CREB1	drug	cocaine	15282271	Furthermore, to determine whether these alterations of <strong>CREB</strong> are necessary in FS or <b>cocaine</b> induced reinstatement, we examined the effect of these stimuli on reinstatement behavior in mice deficient in alpha and Delta isoforms of <strong>CREB</strong>.
+CREB1	addiction	relapse	15282271	Furthermore, to determine whether these alterations of <strong>CREB</strong> are necessary in FS or cocaine induced <b>reinstatement</b>, we examined the effect of these stimuli on <b>reinstatement</b> behavior in mice deficient in alpha and Delta isoforms of <strong>CREB</strong>.
+CREB1	addiction	relapse	15282271	The <strong>CREB</strong>(alphaDelta) mutant mice show deficits in FS induced <b>reinstatement</b> of conditioned place preference.
+CREB1	addiction	relapse	15282271	This deficit in stress but not drug induced <b>reinstatement</b> indicates a specific requirement for <strong>CREB</strong> in stress induced behavioral responses to drugs of abuse.
+CREB1	drug	nicotine	15266655	Repetitive exposures to <b>nicotine</b> induce a hyper responsiveness via the cAMP/PKA/<strong>CREB</strong> signal pathway in Drosophila.
+CREB1	drug	nicotine	15266655	Here we present genetic and pharmacological evidence in Drosophila suggesting that repetitive exposures to <b>nicotine</b> induce a hyper responsiveness through synthesis of new protein(s) via <strong>CREB</strong> mediated gene transcription.
+CREB1	addiction	reward	15207912	Also, given the evidence for involvement of <strong>CREB</strong> in <b>reward</b> and <b>reinforcement</b>, these results are compatible with a role for CART in these processes as well.
+CREB1	drug	opioid	15183518	Caspace 1, D2 dopamine receptor, GABA A alpha1 subunit, GRIA 1/3/4, Galphai2, PSD 95 and <strong>CREB</strong> were down regulated in the NAc shell with <b>morphine</b> administration.
+CREB1	drug	alcohol	15163695	The cAMP response element binding protein (<strong>CREB</strong>) gene transcription factor has been shown to play a role in the synaptic plasticity associated with drug addictive behaviors; however, the causal role of the <strong>CREB</strong> gene in <b>alcohol</b> drinking behaviors is unknown.
+CREB1	addiction	addiction	15163695	The cAMP response element binding protein (<strong>CREB</strong>) gene transcription factor has been shown to play a role in the synaptic plasticity associated with drug <b>addictive</b> behaviors; however, the causal role of the <strong>CREB</strong> gene in alcohol drinking behaviors is unknown.
+CREB1	drug	alcohol	15163695	The present investigation evaluated <b>alcohol</b> drinking behaviors in mice that are haplodeficient in <strong>CREB</strong> as a result of targeted <strong>CREB</strong> (alpha and Delta) gene disruption.
+CREB1	drug	alcohol	15163695	It was found that <strong>CREB</strong> haplodeficient (+/ ) mice have higher preference for <b>ethanol</b> but not for sucrose solution than wild type (+/+) littermates.
+CREB1	drug	alcohol	15163695	It was also found that <strong>CREB</strong> deficient (+/ ) mice displayed more anxiety like behaviors and that acute <b>ethanol</b> exposure produced anxiolytic effects and significantly increased protein levels of p <strong>CREB</strong> and NPY in the central and medial but not in the basolateral amygdala of wild type mice, but these effects are attenuated in <strong>CREB</strong> deficient mice compared with wild type mice.
+CREB1	drug	alcohol	15163695	These results provide the first direct evidence that a haplodeficiency of the <strong>CREB</strong> gene is associated with increased <b>alcohol</b> drinking behaviors.
+CREB1	drug	alcohol	15163695	Furthermore, <b>alcohol</b> drinking and anxiety like behaviors in <strong>CREB</strong> haplodeficient mice may possibly be related to decreased expression of NPY and BDNF in the brains of these mice.
+CREB1	drug	opioid	15029152	Modulation of anxiety like behavior and <b>morphine</b> dependence in <strong>CREB</strong> deficient mice.
+CREB1	addiction	dependence	15029152	Modulation of anxiety like behavior and morphine <b>dependence</b> in <strong>CREB</strong> deficient mice.
+CREB1	addiction	addiction	15029152	The transcription factor cAMP responsive element binding protein (<strong>CREB</strong>) has been shown to regulate different physiological responses including drug <b>addiction</b> and emotional behavior.
+CREB1	addiction	dependence	15029152	Molecular changes including adaptive modifications of the transcription factor <strong>CREB</strong> are produced during drug <b>dependence</b> in many regions of the brain, including the locus coeruleus (LC), but the molecular mechanisms involving <strong>CREB</strong> within these regions have remained controversial.
+CREB1	drug	opioid	15029152	To further investigate the involvement of <strong>CREB</strong> in emotional behavior, drug reward and <b>opioid</b> physical dependence, we used two independently generated <strong>CREB</strong> deficient mice.
+CREB1	addiction	dependence	15029152	To further investigate the involvement of <strong>CREB</strong> in emotional behavior, drug reward and opioid physical <b>dependence</b>, we used two independently generated <strong>CREB</strong> deficient mice.
+CREB1	addiction	reward	15029152	To further investigate the involvement of <strong>CREB</strong> in emotional behavior, drug <b>reward</b> and opioid physical dependence, we used two independently generated <strong>CREB</strong> deficient mice.
+CREB1	drug	cocaine	15029152	Our results emphasize the selective role played by neuronal <strong>CREB</strong> in emotional like behavior and the somatic expression morphine withdrawal, without participating in the rewarding properties induced by morphine and <b>cocaine</b>.
+CREB1	drug	opioid	15029152	Our results emphasize the selective role played by neuronal <strong>CREB</strong> in emotional like behavior and the somatic expression <b>morphine</b> withdrawal, without participating in the rewarding properties induced by <b>morphine</b> and cocaine.
+CREB1	addiction	withdrawal	15029152	Our results emphasize the selective role played by neuronal <strong>CREB</strong> in emotional like behavior and the somatic expression morphine <b>withdrawal</b>, without participating in the rewarding properties induced by morphine and cocaine.
+CREB1	drug	opioid	14975676	These results suggest that the endogenous <b>opioid</b> tone acting on mu /delta receptors tonically stimulate <strong>CREB</strong> activation in the brain.
+CREB1	drug	opioid	14975676	In contrast, chronic <b>morphine</b> treatment in mu KO mice, but not in delta  or kappa KO, resulted in a paradoxical upregulation of Galphai1/2 (12 19%), PKA (19 21%,) and phosphorylated <strong>CREB</strong> (21 73%), but not total <strong>CREB</strong>, in cortex and/or striatum.
+CREB1	drug	cocaine	14727002	Elevations in cAMP response element binding protein (<strong>CREB</strong>) function within the mesolimbic system of rats reduce <b>cocaine</b> reward in place conditioning studies and increase immobility in the forced swim test.
+CREB1	addiction	reward	14727002	Elevations in cAMP response element binding protein (<strong>CREB</strong>) function within the mesolimbic system of rats reduce cocaine <b>reward</b> in place conditioning studies and increase immobility in the forced swim test.
+CREB1	drug	opioid	14727002	Furthermore, each effect appears due to increases in <strong>CREB</strong> mediated expression of dynorphin, since each is attenuated by intracranial injections of the kappa <b>opioid</b> receptor antagonist norBNI.
+CREB1	drug	alcohol	14706555	We recently reported that neuropeptide Y (NPY) protein levels and cAMP responsive element binding (<strong>CREB</strong>) protein phosphorylation are lower in amygdaloid structures during <b>ethanol</b> withdrawal after chronic exposure.
+CREB1	addiction	withdrawal	14706555	We recently reported that neuropeptide Y (NPY) protein levels and cAMP responsive element binding (<strong>CREB</strong>) protein phosphorylation are lower in amygdaloid structures during ethanol <b>withdrawal</b> after chronic exposure.
+CREB1	drug	alcohol	14706555	Furthermore, we reported that normalization of <strong>CREB</strong> phosphorylation by infusing protein kinase A (PKA) activator into the central amygdala prevents anxiety like effects in rats during <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	14706555	Furthermore, we reported that normalization of <strong>CREB</strong> phosphorylation by infusing protein kinase A (PKA) activator into the central amygdala prevents anxiety like effects in rats during ethanol <b>withdrawal</b>.
+CREB1	drug	alcohol	14706555	Here we investigated whether normalization of <strong>CREB</strong> phosphorylation by infusing PKA activator (Sp cAMP) into the central amygdala also normalizes the expression of NPY during <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	14706555	Here we investigated whether normalization of <strong>CREB</strong> phosphorylation by infusing PKA activator (Sp cAMP) into the central amygdala also normalizes the expression of NPY during ethanol <b>withdrawal</b>.
+CREB1	drug	alcohol	14706555	These results suggest that the decreased cellular expression of NPY in the central amygdala may play an important role in the <strong>CREB</strong> mediated regulation of anxiety like behaviors during <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	14706555	These results suggest that the decreased cellular expression of NPY in the central amygdala may play an important role in the <strong>CREB</strong> mediated regulation of anxiety like behaviors during ethanol <b>withdrawal</b>.
+CREB1	drug	opioid	14653953	The effects of the three OMF stereoisomers and <b>morphine</b> (Mor) on cAMP accumulation and <strong>CREB</strong> phosphorylation were monitored by radioimmunoassay and Western blot analysis, respectively.
+CREB1	drug	opioid	14653953	This effect was reversed by <b>naloxone</b>, but F9203 failed to increase <strong>CREB</strong> phosphorylation.
+CREB1	drug	opioid	14653953	KN 62 and staurosporine significantly blocked the <b>opioids</b>  induced <strong>CREB</strong> phosphorylation, while H 89 and PD 98059 had no effect on the actions.
+CREB1	drug	opioid	14653953	Mor, F9202, and F9204, which could induce psychological dependence affected via the micro <b>opioid</b> receptor, stimulated intracellular signal pathways involving Ca2+/calmodulin dependent protein kinases (CCDPK) and protein kinase C (PKC) pathways, which in turn initiated <strong>CREB</strong> phosphorylation.
+CREB1	addiction	dependence	14653953	Mor, F9202, and F9204, which could induce psychological <b>dependence</b> affected via the micro opioid receptor, stimulated intracellular signal pathways involving Ca2+/calmodulin dependent protein kinases (CCDPK) and protein kinase C (PKC) pathways, which in turn initiated <strong>CREB</strong> phosphorylation.
+CREB1	addiction	dependence	14653953	F9203, which could not induce <b>dependence</b>, had no effect on <strong>CREB</strong> phosphorylation in hippocampal neurons.
+CREB1	drug	opioid	14653953	The increased <strong>CREB</strong> phosphorylation in hippocampal neurons may play a role in <b>opioids</b> dependence.
+CREB1	addiction	dependence	14653953	The increased <strong>CREB</strong> phosphorylation in hippocampal neurons may play a role in opioids <b>dependence</b>.
+CREB1	drug	alcohol	14648603	Differences in basal levels of <strong>CREB</strong> and NPY in nucleus accumbens regions between C57BL/6 and DBA/2 mice differing in inborn <b>alcohol</b> drinking behavior.
+CREB1	drug	alcohol	14648603	Furthermore, alterations in cAMP responsive element binding (<strong>CREB</strong>) protein function in the brain have been implicated in <b>alcohol</b> drinking behaviors.
+CREB1	drug	alcohol	14648603	Because the shell structure of the nucleus accumbens has been implicated in reward mechanisms of <b>alcohol</b>, it is possible that lower <strong>CREB</strong> function in this brain structure may be in part associated with the excessive <b>alcohol</b> drinking behavior of C57 mice.
+CREB1	addiction	reward	14648603	Because the shell structure of the nucleus accumbens has been implicated in <b>reward</b> mechanisms of alcohol, it is possible that lower <strong>CREB</strong> function in this brain structure may be in part associated with the excessive alcohol drinking behavior of C57 mice.
+CREB1	drug	opioid	14645671	Collectively, this study demonstrated that <b>fentanyl</b> triggered MOR gene induction was mediated by the sequential activation of <strong>CREB</strong> and the binding of <strong>CREB</strong> and CBP to MOR promoter, thus provides direct evidence for lower propensity of <b>fentanyl</b> to produce tolerance.
+CREB1	addiction	reward	14622103	Differential distribution of <strong>CREB</strong> in the mesolimbic dopamine <b>reward</b> pathway.
+CREB1	addiction	addiction	14622103	The transcription factor cAMP response element binding protein (<strong>CREB</strong>) has been implicated in the long term neuronal plasticity associated with <b>addiction</b>.
+CREB1	addiction	reward	14622103	Studies in which <strong>CREB</strong> levels have been altered, either constitutively throughout the brain via gene targeting or transiently in specific brain regions, demonstrate variable roles for this protein in mediating <b>reinforcing</b> properties of drugs of abuse.
+CREB1	addiction	addiction	14622103	To investigate the complex nature of <strong>CREB</strong> function in <b>addiction</b>, we examined the distribution of <strong>CREB</strong> protein in the nucleus accumbens (NAc) and ventral tegmental area (VTA), two brain regions that are part of the well defined mesolimbic dopamine pathway involved in reward processing.
+CREB1	addiction	reward	14622103	To investigate the complex nature of <strong>CREB</strong> function in addiction, we examined the distribution of <strong>CREB</strong> protein in the nucleus accumbens (NAc) and ventral tegmental area (VTA), two brain regions that are part of the well defined mesolimbic dopamine pathway involved in <b>reward</b> processing.
+CREB1	drug	cocaine	14622103	Phospho <strong>CREB</strong> levels are increased in the NAc of both wild type and CREBalphaDelta mutant animals after <b>cocaine</b>.
+CREB1	drug	opioid	14622103	However, <b>morphine</b> induced increases of phospho <strong>CREB</strong> levels are seen in the VTA of wild type mice but not CREBalphaDelta mutant mice.
+CREB1	drug	cocaine	14566342	Regulation of gene expression and <b>cocaine</b> reward by <strong>CREB</strong> and DeltaFosB.
+CREB1	addiction	reward	14566342	Regulation of gene expression and cocaine <b>reward</b> by <strong>CREB</strong> and DeltaFosB.
+CREB1	addiction	reward	14566342	DeltaFosB (a truncated form of FosB) and <strong>CREB</strong> (cAMP response element binding protein) are transcription factors induced in the brain's <b>reward</b> pathways after chronic exposure to drugs of abuse.
+CREB1	drug	cocaine	14566342	Gene expression induced by short term DeltaFosB and by <strong>CREB</strong> was strikingly similar, and both reduced the rewarding effects of <b>cocaine</b>, whereas prolonged DeltaFosB expression increased drug reward.
+CREB1	addiction	reward	14566342	Gene expression induced by short term DeltaFosB and by <strong>CREB</strong> was strikingly similar, and both reduced the rewarding effects of cocaine, whereas prolonged DeltaFosB expression increased drug <b>reward</b>.
+CREB1	drug	cocaine	14566342	Gene expression after a short <b>cocaine</b> treatment was more dependent on <strong>CREB</strong>, whereas gene expression after a longer <b>cocaine</b> treatment became increasingly DeltaFosB dependent.
+CREB1	drug	cocaine	14566342	These findings help define the molecular functions of <strong>CREB</strong> and DeltaFosB and identify clusters of genes that contribute to <b>cocaine</b> addiction.
+CREB1	addiction	addiction	14566342	These findings help define the molecular functions of <strong>CREB</strong> and DeltaFosB and identify clusters of genes that contribute to cocaine <b>addiction</b>.
+CREB1	drug	opioid	12969258	Dopamine dependent increases in phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) during precipitated <b>morphine</b> withdrawal in primary cultures of rat striatum.
+CREB1	addiction	withdrawal	12969258	Dopamine dependent increases in phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) during precipitated morphine <b>withdrawal</b> in primary cultures of rat striatum.
+CREB1	drug	opioid	12969258	One potential consequence of up regulated cAMP signaling is increased phosphorylation of cAMP response element binding protein (<strong>CREB</strong>), a transcription factor that may regulate neuroadaptations related to <b>morphine</b> dependence.
+CREB1	addiction	dependence	12969258	One potential consequence of up regulated cAMP signaling is increased phosphorylation of cAMP response element binding protein (<strong>CREB</strong>), a transcription factor that may regulate neuroadaptations related to morphine <b>dependence</b>.
+CREB1	drug	opioid	12969258	To determine if <b>morphine</b> withdrawal leads to increased <strong>CREB</strong> phosphorylation in striatal tissues, we examined the effects of <b>naloxone</b> precipitated <b>morphine</b> withdrawal on <strong>CREB</strong> phosphorylation in primary cultures of rat striatal neurons.
+CREB1	addiction	withdrawal	12969258	To determine if morphine <b>withdrawal</b> leads to increased <strong>CREB</strong> phosphorylation in striatal tissues, we examined the effects of naloxone precipitated morphine <b>withdrawal</b> on <strong>CREB</strong> phosphorylation in primary cultures of rat striatal neurons.
+CREB1	drug	opioid	12969258	Precipitated <b>morphine</b> withdrawal was associated with enhanced dopamine , SKF 82958 (D1 receptor agonist) , and forskolin induced <strong>CREB</strong> phosphorylation.
+CREB1	addiction	withdrawal	12969258	Precipitated morphine <b>withdrawal</b> was associated with enhanced dopamine , SKF 82958 (D1 receptor agonist) , and forskolin induced <strong>CREB</strong> phosphorylation.
+CREB1	addiction	withdrawal	12969258	During precipitated <b>withdrawal</b>, D1 receptor mediated <strong>CREB</strong> phosphorylation was dependent on cAMP dependent protein kinase (PKA).
+CREB1	drug	opioid	12969258	<strong>CREB</strong> protein levels were not altered by acute or chronic <b>morphine</b>.
+CREB1	drug	alcohol	12967770	Anxiety and <b>alcohol</b> abuse disorders: a common role for <strong>CREB</strong> and its target, the neuropeptide Y gene.
+CREB1	drug	alcohol	12967770	Here, I propose that cAMP response element binding protein (<strong>CREB</strong>) has a role in anxiety and <b>alcohol</b> drinking behaviors.
+CREB1	drug	alcohol	12967770	The <strong>CREB</strong> gene transcription factor regulates the expression of the gene encoding neuropeptide Y (NPY), and decreased concentrations of NPY are implicated in anxiety and <b>alcohol</b> drinking behaviors.
+CREB1	drug	alcohol	12967770	Therefore, decreased function of <strong>CREB</strong> in the central nucleus of the amygdala might regulate anxiety and <b>alcohol</b> intake via decreased expression of NPY, and might provide a common link between anxiety and <b>alcohol</b> abuse disorders.
+CREB1	drug	alcohol	12967770	I also suggest that, via <strong>CREB</strong>, NPY might interact with other <strong>CREB</strong> target genes, such as the gene encoding brain derived neurotrophic factor, and that this <strong>CREB</strong> mediated interaction might be important in the regulation of anxiety and <b>alcohol</b> drinking behaviors.
+CREB1	drug	alcohol	12966313	The development of tolerance to the sedative effects of <b>ethanol</b> was accompanied by increased expression of phospho <strong>CREB</strong> in the cerebellum, hippocampus, and frontal cortex.
+CREB1	drug	alcohol	12956944	To study the changes in the expression and phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) in the rat nucleus accumbens after chronic <b>ethanol</b> intake and its withdrawal.
+CREB1	addiction	withdrawal	12956944	To study the changes in the expression and phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) in the rat nucleus accumbens after chronic ethanol intake and its <b>withdrawal</b>.
+CREB1	drug	alcohol	12956944	<b>Ethanol</b> given to rats in drinking water decreased the level of p <strong>CREB</strong> protein in the nucleus accumbens ( 75 %) at the time of exposure to <b>ethanol</b>.
+CREB1	drug	alcohol	12956944	The decrement of p <strong>CREB</strong> protein in the nucleus accumbens remained at 24 h ( 35 %) and 72 h ( 28 %) of <b>ethanol</b> withdrawal, which recovered toward control level after 7 d of <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	12956944	The decrement of p <strong>CREB</strong> protein in the nucleus accumbens remained at 24 h ( 35 %) and 72 h ( 28 %) of ethanol <b>withdrawal</b>, which recovered toward control level after 7 d of ethanol <b>withdrawal</b>.
+CREB1	drug	alcohol	12956944	However, chronic <b>ethanol</b>, as well as <b>ethanol</b> withdrawal failed to produce any significant alteration in the level of <strong>CREB</strong> protein in the nucleus accumbens.
+CREB1	addiction	withdrawal	12956944	However, chronic ethanol, as well as ethanol <b>withdrawal</b> failed to produce any significant alteration in the level of <strong>CREB</strong> protein in the nucleus accumbens.
+CREB1	drug	opioid	12956944	<b>Naloxone</b> (alone) treatment of rats had no effect on the levels of <strong>CREB</strong> and p <strong>CREB</strong> protein in the nucleus accumbens.
+CREB1	drug	alcohol	12956944	However, when naloxone was administered concurrently with <b>ethanol</b> treatment, it antagonized the down regulation of p <strong>CREB</strong> protein in the nucleus accumbens (142 %) of rats exposed to <b>ethanol</b>.
+CREB1	drug	opioid	12956944	However, when <b>naloxone</b> was administered concurrently with ethanol treatment, it antagonized the down regulation of p <strong>CREB</strong> protein in the nucleus accumbens (142 %) of rats exposed to ethanol.
+CREB1	drug	alcohol	12956944	A long term intake of <b>ethanol</b> solution down regulates the phosphorylation of <strong>CREB</strong> in the nucleus accumbens, and those changes can be reversed by naloxone, which may be one kind of the molecular mechanisms associated with <b>ethanol</b> dependence.
+CREB1	drug	opioid	12956944	A long term intake of ethanol solution down regulates the phosphorylation of <strong>CREB</strong> in the nucleus accumbens, and those changes can be reversed by <b>naloxone</b>, which may be one kind of the molecular mechanisms associated with ethanol dependence.
+CREB1	addiction	dependence	12956944	A long term intake of ethanol solution down regulates the phosphorylation of <strong>CREB</strong> in the nucleus accumbens, and those changes can be reversed by naloxone, which may be one kind of the molecular mechanisms associated with ethanol <b>dependence</b>.
+CREB1	drug	cocaine	12716423	Correspondingly, western blot analysis revealed VTA selective up regulation of <strong>CREB</strong> (p < 0.01), NMDAR1 (p < 0.01), GluR2 (p < 0.05), GluR5 (p < 0.01) and KA2 (p < 0.05) protein levels of <b>cocaine</b> overdose victims.
+CREB1	drug	cocaine	12716423	The present results indicate that selective alterations of <strong>CREB</strong> and certain ionotropic glutamate receptor (iGluR) subtypes appear to be associated with chronic <b>cocaine</b> use in humans in a region specific manner.
+CREB1	drug	alcohol	12715102	To define the molecular basis of <b>ethanol</b> dependence, changes in the phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) in the nucleus accumbens of rats after acute and chronic <b>ethanol</b> administration were detected using immunohistochemistry.
+CREB1	addiction	dependence	12715102	To define the molecular basis of ethanol <b>dependence</b>, changes in the phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) in the nucleus accumbens of rats after acute and chronic ethanol administration were detected using immunohistochemistry.
+CREB1	drug	alcohol	12715102	The results demonstrate that the expression of phospho <strong>CREB</strong> (p <strong>CREB</strong>) protein in the rat nucleus accumbens significantly increased after 15 min of acute <b>ethanol</b> exposure, reaching a peak at 30 min after <b>ethanol</b> administration.
+CREB1	drug	alcohol	12715102	In contrast, chronic intake of <b>ethanol</b> solution obviously decreased the expression of p <strong>CREB</strong> protein compared to the control rats.
+CREB1	drug	alcohol	12715102	The results suggest that an acute <b>ethanol</b> administration led to an increase in the phosphorylation of <strong>CREB</strong> in the nucleus accumbens, but chronic <b>ethanol</b> administration produced a decrement, which is possibly one of the molecular mechanisms of <b>alcohol</b> dependence.
+CREB1	addiction	dependence	12715102	The results suggest that an acute ethanol administration led to an increase in the phosphorylation of <strong>CREB</strong> in the nucleus accumbens, but chronic ethanol administration produced a decrement, which is possibly one of the molecular mechanisms of alcohol <b>dependence</b>.
+CREB1	drug	alcohol	12658105	The decreased phosphorylation of cyclic adenosine monophosphate (cAMP) response element binding (<strong>CREB</strong>) protein in the central amygdala acts as a molecular substrate for anxiety related to <b>ethanol</b> withdrawal in rats.
+CREB1	addiction	withdrawal	12658105	The decreased phosphorylation of cyclic adenosine monophosphate (cAMP) response element binding (<strong>CREB</strong>) protein in the central amygdala acts as a molecular substrate for anxiety related to ethanol <b>withdrawal</b> in rats.
+CREB1	drug	alcohol	12658105	<b>Ethanol</b> withdrawal but not treatment significantly decreased the phosphorylation of <strong>CREB</strong> protein and protein levels of Ca2+/calmodulin dependent protein kinase IV without modulating the protein levels of total <strong>CREB</strong> and alpha catalytic subunit of protein kinase A (PKA Calpha) in the central and medial amygdala.
+CREB1	addiction	withdrawal	12658105	Ethanol <b>withdrawal</b> but not treatment significantly decreased the phosphorylation of <strong>CREB</strong> protein and protein levels of Ca2+/calmodulin dependent protein kinase IV without modulating the protein levels of total <strong>CREB</strong> and alpha catalytic subunit of protein kinase A (PKA Calpha) in the central and medial amygdala.
+CREB1	drug	alcohol	12658105	We also investigated the effects of manipulation of the phosphorylation status of <strong>CREB</strong> in the central amygdala by infusion of the PKA activator (Sp cAMPS) or inhibitor (Rp cAMPS) on anxiety levels in rats during <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	12658105	We also investigated the effects of manipulation of the phosphorylation status of <strong>CREB</strong> in the central amygdala by infusion of the PKA activator (Sp cAMPS) or inhibitor (Rp cAMPS) on anxiety levels in rats during ethanol <b>withdrawal</b>.
+CREB1	drug	alcohol	12658105	When Sp cAMPS is specifically infused into the central amygdala, it dose dependently normalizes the decrease in <strong>CREB</strong> phosphorylation and prevents the development of anxiety in rats during <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	12658105	When Sp cAMPS is specifically infused into the central amygdala, it dose dependently normalizes the decrease in <strong>CREB</strong> phosphorylation and prevents the development of anxiety in rats during ethanol <b>withdrawal</b>.
+CREB1	drug	alcohol	12658105	On the other hand, Rp cAMPS infusions into the central or basolateral amygdala decrease <strong>CREB</strong> phosphorylation, but only infusion into the central amygdala provokes anxiety and increases <b>alcohol</b> preference in normal rats.
+CREB1	drug	alcohol	12658105	We also found that <b>alcohol</b> preference provoked by decreased <strong>CREB</strong> phosphorylation is related to decreased expression of the neuropeptide Y gene in the central amygdala.
+CREB1	drug	alcohol	12658105	These novel results suggest the possibility that decreased <strong>CREB</strong> phosphorylation in the central amygdala acts as a common molecular correlate for anxiety and <b>alcohol</b> drinking behaviors and also is correlated with anxiety related to <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	12658105	These novel results suggest the possibility that decreased <strong>CREB</strong> phosphorylation in the central amygdala acts as a common molecular correlate for anxiety and alcohol drinking behaviors and also is correlated with anxiety related to ethanol <b>withdrawal</b>.
+CREB1	drug	opioid	12649385	Because <strong>CREB</strong> regulates expression of dynorphin (which acts at kappa <b>opioid</b> receptors) in NAc neurons, these findings raised the possibility that kappa receptors mediate immobility behaviors in the FST.
+CREB1	addiction	reward	12643347	The present study was designed to determine the changes of phosphorylation of cAMP  response element binding protein (<strong>CREB</strong>) in hippocampus induced by ohmefentanyl stereoisomers (F9202 and F9204) in conditioned place preference (<b>CPP</b>) paradigm.
+CREB1	drug	opioid	12643347	We also examined the effects of ketamine, a noncompetitive N mthyl D aspartate receptor (NR) antagonist, on <b>morphine</b> , F9202  and F9204  induced CPP and phosphorylation of <strong>CREB</strong> in hippocampus.
+CREB1	drug	psychedelics	12643347	We also examined the effects of <b>ketamine</b>, a noncompetitive N mthyl D aspartate receptor (NR) antagonist, on morphine , F9202  and F9204  induced CPP and phosphorylation of <strong>CREB</strong> in hippocampus.
+CREB1	addiction	reward	12643347	We also examined the effects of ketamine, a noncompetitive N mthyl D aspartate receptor (NR) antagonist, on morphine , F9202  and F9204  induced <b>CPP</b> and phosphorylation of <strong>CREB</strong> in hippocampus.
+CREB1	drug	opioid	12643347	Ketamine could suppress not only the place preference but also the phosphorylation of <strong>CREB</strong> produced by <b>morphine</b>, F9202 and F9204.
+CREB1	drug	psychedelics	12643347	<b>Ketamine</b> could suppress not only the place preference but also the phosphorylation of <strong>CREB</strong> produced by morphine, F9202 and F9204.
+CREB1	addiction	dependence	12643347	These findings suggest that alterations in the phosphorylation of <strong>CREB</strong> be relevant to opiates signaling and the development of opiates <b>dependence</b>.
+CREB1	drug	nicotine	12614343	In vivo <b>nicotine</b> treatment regulates mesocorticolimbic <strong>CREB</strong> and ERK signaling in C57Bl/6J mice.
+CREB1	drug	nicotine	12614343	<strong>CREB</strong> phosphorylation was reduced in the nucleus accumbens following chronic <b>nicotine</b>, consistent with previous reports that decreased accumbens <strong>CREB</strong> activity increases drug reinforcement.
+CREB1	addiction	reward	12614343	<strong>CREB</strong> phosphorylation was reduced in the nucleus accumbens following chronic nicotine, consistent with previous reports that decreased accumbens <strong>CREB</strong> activity increases drug <b>reinforcement</b>.
+CREB1	drug	nicotine	12614343	In contrast, <strong>CREB</strong> phosphorylation was increased in the prefrontal cortex following chronic <b>nicotine</b> exposure and in the ventral tegmental area during <b>nicotine</b> withdrawal.
+CREB1	addiction	withdrawal	12614343	In contrast, <strong>CREB</strong> phosphorylation was increased in the prefrontal cortex following chronic nicotine exposure and in the ventral tegmental area during nicotine <b>withdrawal</b>.
+CREB1	drug	nicotine	12614343	Overall, these results support a role for ERK and <strong>CREB</strong> activity in neural plasticity associated with <b>nicotine</b> dependence.
+CREB1	addiction	dependence	12614343	Overall, these results support a role for ERK and <strong>CREB</strong> activity in neural plasticity associated with nicotine <b>dependence</b>.
+CREB1	drug	amphetamine	12504868	In addition, DNA binding activities of NF kappaB, AP 1, and <strong>CREB</strong> in the frontal cortex and hippocampus were more pronounced in mice injected with Tat plus <b>METH</b> compared to the effects of Tat or <b>METH</b> alone.
+CREB1	drug	cocaine	12165570	Drugs of abuse activate <strong>CREB</strong> in the nucleus accumbens, an important part of the brain's reward pathways, and local manipulations of <strong>CREB</strong> activity have been shown to affect <b>cocaine</b> reward, suggesting an active role of <strong>CREB</strong> in adaptive processes that follow exposure to drugs of abuse.
+CREB1	addiction	reward	12165570	Drugs of abuse activate <strong>CREB</strong> in the nucleus accumbens, an important part of the brain's <b>reward</b> pathways, and local manipulations of <strong>CREB</strong> activity have been shown to affect cocaine <b>reward</b>, suggesting an active role of <strong>CREB</strong> in adaptive processes that follow exposure to drugs of abuse.
+CREB1	drug	opioid	12165570	Using viral mediated gene transfer to locally alter the activity of <strong>CREB</strong>, we show that this manipulation affects <b>morphine</b> reward, as well as the preference for sucrose, a more natural reward.
+CREB1	addiction	reward	12165570	Using viral mediated gene transfer to locally alter the activity of <strong>CREB</strong>, we show that this manipulation affects morphine <b>reward</b>, as well as the preference for sucrose, a more natural <b>reward</b>.
+CREB1	addiction	aversion	12165570	We then show that local changes in <strong>CREB</strong> activity induce a more general syndrome, by altering reactions to anxiogenic, <b>aversive</b>, and nociceptive stimuli as well.
+CREB1	drug	amphetamine	12125044	Overall, the current study reveals that there is a distinct temporal and spatial profile of haloperidol induced IEG expression and/or <strong>CREB</strong> phosphorylation in <b>amphetamine</b> treated rats, suggesting that there is a critical transition between the early and late withdrawal periods.
+CREB1	addiction	withdrawal	12125044	Overall, the current study reveals that there is a distinct temporal and spatial profile of haloperidol induced IEG expression and/or <strong>CREB</strong> phosphorylation in amphetamine treated rats, suggesting that there is a critical transition between the early and late <b>withdrawal</b> periods.
+CREB1	drug	opioid	11979726	The heterozygous mice for the tyrosine hydroxylase (TH) gene and for the cyclic AMP (cAMP) response element binding protein (<strong>CREB</strong>) binding protein (CBP) gene showed the impairment of latent learning in the water finding task, and these mice did not develop <b>morphine</b> dependence.
+CREB1	addiction	dependence	11979726	The heterozygous mice for the tyrosine hydroxylase (TH) gene and for the cyclic AMP (cAMP) response element binding protein (<strong>CREB</strong>) binding protein (CBP) gene showed the impairment of latent learning in the water finding task, and these mice did not develop morphine <b>dependence</b>.
+CREB1	drug	opioid	11979726	In conclusion, the results of mutant mice suggest that the alternation of catecholamine biosynthesis and cAMP signal pathways may play a key role in development of latent learning and <b>morphine</b> dependence, and they furthermore show that the expression of genes mediated by phosphorylated <strong>CREB</strong> may be involved in the development of latent learning and <b>morphine</b> dependence.
+CREB1	addiction	dependence	11979726	In conclusion, the results of mutant mice suggest that the alternation of catecholamine biosynthesis and cAMP signal pathways may play a key role in development of latent learning and morphine <b>dependence</b>, and they furthermore show that the expression of genes mediated by phosphorylated <strong>CREB</strong> may be involved in the development of latent learning and morphine <b>dependence</b>.
+CREB1	drug	alcohol	11907158	We have shown in the NG108 15 neuroblastoma x glioma hybrid cell line that <b>ethanol</b> increases cellular cAMP levels via activation of adenosine A(2) receptors, leading to phosphorylation of the cAMP response element binding protein (<strong>CREB</strong>).
+CREB1	drug	alcohol	11907158	Here we investigate whether <b>ethanol</b> increases CRE mediated gene expression via endogenous <strong>CREB</strong> using a CRE regulated luciferase reporter construct, transfected into NG108 15 cells.
+CREB1	drug	alcohol	11907158	Coexpression of a dominant negative <strong>CREB</strong> construct blocked <b>ethanol</b> stimulated CRE luciferase expression, further suggesting that <strong>CREB</strong> is required for this response.
+CREB1	drug	alcohol	11907158	Our data suggest that <b>ethanol</b> induces cAMP dependent gene expression regulated by <strong>CREB</strong> and PKA and that this signaling pathway may mediate some of the addictive behaviors underlying <b>alcoholism</b>.
+CREB1	addiction	addiction	11907158	Our data suggest that ethanol induces cAMP dependent gene expression regulated by <strong>CREB</strong> and PKA and that this signaling pathway may mediate some of the <b>addictive</b> behaviors underlying alcoholism.
+CREB1	drug	opioid	11749769	However, <b>naloxone</b> increased [Ca2+]i in two thirds of smc preincubated with <b>morphine</b> 0.1 or 0.5 mmol/L for 48 h from (97 +/  20) to (167 +/  29) nmol/L (n = 9, P < 0.01) and from (106 +/  19) to (225 +/  48) nmol/L (n = 10, P < 0.01), respectively, and it also increased the ratio of positive immunoreaction to phospho <strong>CREB</strong> from (7.7 +/  3.2) % to (19.6 +/  4.7) % (n = 6, P < 0.01) in smc preincubated with <b>morphine</b> 0.5 mmol/L.
+CREB1	drug	alcohol	11742252	Effects of voluntary <b>ethanol</b> intake on the expression of Ca(2+) /calmodulin dependent protein kinase IV and on <strong>CREB</strong> expression and phosphorylation in the rat nucleus accumbens.
+CREB1	drug	alcohol	11742252	To define the molecular basis of <b>alcohol</b> drinking behaviors, the effects of voluntary <b>ethanol</b> intake on the expression of Ca(2+)/calmodulin dependent protein kinase IV (CaM kinase IV) and on the expression and phosphorylation of cAMP responsive element binding protein (<strong>CREB</strong>) [corrected] in the nucleus accumbens (NAc), central amygdala, and frontal cortex of rats were investigated.
+CREB1	drug	alcohol	11742252	Voluntary <b>ethanol</b> intake significantly decreased the expression of CaM kinase IV and <strong>CREB</strong> phosphorylation but not of <strong>CREB</strong> protein levels [corrected], specifically in the shell of NAc.
+CREB1	drug	alcohol	11742252	Mianserin treatment significantly attenuated <b>ethanol</b> intake and antagonized the voluntary <b>ethanol</b> induced reduction in expression of CaM kinase IV and <strong>CREB</strong> phosphorylation in the shell of NAc.
+CREB1	drug	alcohol	11742252	This is the first evidence to suggest that decreased CaM kinase IV dependent <strong>CREB</strong> phosphorylation in the shell region of NAc may play a role in the reward mechanisms of <b>alcohol</b> drinking.
+CREB1	addiction	reward	11742252	This is the first evidence to suggest that decreased CaM kinase IV dependent <strong>CREB</strong> phosphorylation in the shell region of NAc may play a role in the <b>reward</b> mechanisms of alcohol drinking.
+CREB1	addiction	addiction	11717377	Therefore, studying the reinforcing as well as aversive components of drugs of abuse in a single model system will enable us to understand the role of final common mediators, such as cAMP response element binding protein (<strong>CREB</strong>), in the <b>addiction</b> process.
+CREB1	addiction	aversion	11717377	Therefore, studying the reinforcing as well as <b>aversive</b> components of drugs of abuse in a single model system will enable us to understand the role of final common mediators, such as cAMP response element binding protein (<strong>CREB</strong>), in the addiction process.
+CREB1	addiction	reward	11717377	Therefore, studying the <b>reinforcing</b> as well as aversive components of drugs of abuse in a single model system will enable us to understand the role of final common mediators, such as cAMP response element binding protein (<strong>CREB</strong>), in the addiction process.
+CREB1	addiction	dependence	11717377	Previously we have shown that <strong>CREB</strong>(alphaDelta) mutant mice in a mixed genetic background show attenuated signs of physical <b>dependence</b>, as measured by the classic signs of withdrawal.
+CREB1	addiction	withdrawal	11717377	Previously we have shown that <strong>CREB</strong>(alphaDelta) mutant mice in a mixed genetic background show attenuated signs of physical dependence, as measured by the classic signs of <b>withdrawal</b>.
+CREB1	addiction	addiction	11717377	We are now poised to examine a number of complex behavioral phenotypes related to <b>addiction</b> in a well defined <strong>CREB</strong> deficient mouse model.
+CREB1	drug	opioid	11717377	We demonstrate that the aversive properties of <b>morphine</b> are still present in <strong>CREB</strong> mutant mice despite a reduction of physical withdrawal.
+CREB1	addiction	aversion	11717377	We demonstrate that the <b>aversive</b> properties of morphine are still present in <strong>CREB</strong> mutant mice despite a reduction of physical withdrawal.
+CREB1	addiction	withdrawal	11717377	We demonstrate that the aversive properties of morphine are still present in <strong>CREB</strong> mutant mice despite a reduction of physical <b>withdrawal</b>.
+CREB1	drug	cocaine	11717377	In contrast, <strong>CREB</strong> mutant mice demonstrate an enhanced response to the reinforcing properties of <b>cocaine</b> compared with their wild type controls in both conditioned place preference and sensitization behaviors.
+CREB1	addiction	reward	11717377	In contrast, <strong>CREB</strong> mutant mice demonstrate an enhanced response to the <b>reinforcing</b> properties of cocaine compared with their wild type controls in both conditioned place preference and sensitization behaviors.
+CREB1	addiction	sensitization	11717377	In contrast, <strong>CREB</strong> mutant mice demonstrate an enhanced response to the reinforcing properties of cocaine compared with their wild type controls in both conditioned place preference and <b>sensitization</b> behaviors.
+CREB1	drug	cocaine	11549750	Conversely, rats treated with HSV <strong>CREB</strong> spent less time in <b>cocaine</b> associated environments, indicating increased <b>cocaine</b> aversion.
+CREB1	addiction	aversion	11549750	Conversely, rats treated with HSV <strong>CREB</strong> spent less time in cocaine associated environments, indicating increased cocaine <b>aversion</b>.
+CREB1	drug	cocaine	11549750	Studies in which drug environment pairings were varied to coincide with either the early or late effects of <b>cocaine</b> suggest that <strong>CREB</strong> associated place aversions reflect increased <b>cocaine</b> withdrawal.
+CREB1	addiction	withdrawal	11549750	Studies in which drug environment pairings were varied to coincide with either the early or late effects of cocaine suggest that <strong>CREB</strong> associated place aversions reflect increased cocaine <b>withdrawal</b>.
+CREB1	drug	cocaine	11549750	Because <b>cocaine</b> withdrawal can be accompanied by symptoms of depression, we examined how altered <strong>CREB</strong> function in the NAc affects behavior in the forced swim test (FST).
+CREB1	addiction	withdrawal	11549750	Because cocaine <b>withdrawal</b> can be accompanied by symptoms of depression, we examined how altered <strong>CREB</strong> function in the NAc affects behavior in the forced swim test (FST).
+CREB1	drug	opioid	11549750	Moreover, the kappa <b>opioid</b> receptor antagonist nor Binaltorphimine decreased immobility in HSV <strong>CREB</strong>  and HSV mCREB treated rats, suggesting that <strong>CREB</strong> mediated induction of dynorphin (an endogenous kappa receptor ligand) contributes to immobility behavior in the FST.
+CREB1	drug	alcohol	11391048	The presentations were (1) Action of <b>ethanol</b> on cAMP signaling pathways, by M. Yoshimura; (2) Alterations in the G protein adenylyl cyclase system and their mRNA levels in <b>alcoholics</b>, by H. Sohma; (3) The role of the <strong>CREB</strong> gene transcription factor in <b>ethanol</b> dependence and preference, by Subhash C. Pandey; and (4) The efficacy of adenylyl cyclase signal transduction to the nucleus in primary <b>alcoholics</b>, by M. E. Götz.
+CREB1	addiction	dependence	11391048	The presentations were (1) Action of ethanol on cAMP signaling pathways, by M. Yoshimura; (2) Alterations in the G protein adenylyl cyclase system and their mRNA levels in alcoholics, by H. Sohma; (3) The role of the <strong>CREB</strong> gene transcription factor in ethanol <b>dependence</b> and preference, by Subhash C. Pandey; and (4) The efficacy of adenylyl cyclase signal transduction to the nucleus in primary alcoholics, by M. E. Götz.
+CREB1	drug	nicotine	11331423	Effects of protracted <b>nicotine</b> exposure and withdrawal on the expression and phosphorylation of the <strong>CREB</strong> gene transcription factor in rat brain.
+CREB1	addiction	withdrawal	11331423	Effects of protracted nicotine exposure and <b>withdrawal</b> on the expression and phosphorylation of the <strong>CREB</strong> gene transcription factor in rat brain.
+CREB1	drug	nicotine	11331423	Addiction to <b>nicotine</b> may result in molecular adaptations in the neurocircuitry of specific brain structures via changes in the cyclic AMP responsive element binding protein (<strong>CREB</strong>) dependent gene transcription program.
+CREB1	addiction	addiction	11331423	<b>Addiction</b> to nicotine may result in molecular adaptations in the neurocircuitry of specific brain structures via changes in the cyclic AMP responsive element binding protein (<strong>CREB</strong>) dependent gene transcription program.
+CREB1	drug	nicotine	11331423	We therefore investigated the effects of chronic <b>nicotine</b> exposure and its withdrawal on <strong>CREB</strong> and phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) protein levels in the rat brain.
+CREB1	addiction	withdrawal	11331423	We therefore investigated the effects of chronic nicotine exposure and its <b>withdrawal</b> on <strong>CREB</strong> and phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) protein levels in the rat brain.
+CREB1	drug	nicotine	11331423	We report here that chronic <b>nicotine</b> exposure (1 h withdrawal) had no effect on the expression of <strong>CREB</strong> and p <strong>CREB</strong> in the rat cortex and amygdala.
+CREB1	addiction	withdrawal	11331423	We report here that chronic nicotine exposure (1 h <b>withdrawal</b>) had no effect on the expression of <strong>CREB</strong> and p <strong>CREB</strong> in the rat cortex and amygdala.
+CREB1	drug	nicotine	11331423	On the other hand, decreases in the expression of <strong>CREB</strong> protein and phosphorylation of <strong>CREB</strong> occur in the cingulate gyrus, and in the parietal and the piriform but not in the frontal cortex during <b>nicotine</b> withdrawal (18 h) after <b>nicotine</b> exposure.
+CREB1	addiction	withdrawal	11331423	On the other hand, decreases in the expression of <strong>CREB</strong> protein and phosphorylation of <strong>CREB</strong> occur in the cingulate gyrus, and in the parietal and the piriform but not in the frontal cortex during nicotine <b>withdrawal</b> (18 h) after nicotine exposure.
+CREB1	drug	nicotine	11331423	It was also observed that <strong>CREB</strong> and p <strong>CREB</strong> protein levels were significantly decreased in the medial and basolateral, but not in the central amygdala during <b>nicotine</b> withdrawal (18 h) after chronic <b>nicotine</b> exposure.
+CREB1	addiction	withdrawal	11331423	It was also observed that <strong>CREB</strong> and p <strong>CREB</strong> protein levels were significantly decreased in the medial and basolateral, but not in the central amygdala during nicotine <b>withdrawal</b> (18 h) after chronic nicotine exposure.
+CREB1	drug	nicotine	11331423	These results provide the first evidence that decreased <strong>CREB</strong> activity and/or expression in specific cortical and amygdaloid brain structures may be involved in the underlying molecular mechanisms of <b>nicotine</b> dependence.
+CREB1	addiction	dependence	11331423	These results provide the first evidence that decreased <strong>CREB</strong> activity and/or expression in specific cortical and amygdaloid brain structures may be involved in the underlying molecular mechanisms of nicotine <b>dependence</b>.
+CREB1	drug	alcohol	11259782	We examined the amounts of several adenylyl cyclase (AC) isoforms and of cAMP response element binding protein (<strong>CREB</strong>) in <b>alcoholic</b> and control brains.
+CREB1	drug	opioid	11233292	To investigate the involvement of catecholamines and/or the cyclic AMP (cAMP) systems in the development of drug dependence, we examined whether <b>morphine</b> dependence was developed in tyrosine hydroxylase (TH) heterozygous (TH+/ ) and cAMP response element binding protein (<strong>CREB</strong>) binding protein (CBP) heterozygous (CBP+/ ) mice.
+CREB1	addiction	dependence	11233292	To investigate the involvement of catecholamines and/or the cyclic AMP (cAMP) systems in the development of drug <b>dependence</b>, we examined whether morphine <b>dependence</b> was developed in tyrosine hydroxylase (TH) heterozygous (TH+/ ) and cAMP response element binding protein (<strong>CREB</strong>) binding protein (CBP) heterozygous (CBP+/ ) mice.
+CREB1	drug	opioid	11200184	Ca2+/cAMP response element binding protein (<strong>CREB</strong>) is an important factor linking the <b>opioid</b> regulated secondary messenger systems to alterations in gene expression.
+CREB1	drug	opioid	11200184	<b>Opioids</b> regulate <strong>CREB</strong> level, its phosphorylation and binding to its corresponding response element in the promoters of several genes implicated in drug addiction.
+CREB1	addiction	addiction	11200184	Opioids regulate <strong>CREB</strong> level, its phosphorylation and binding to its corresponding response element in the promoters of several genes implicated in drug <b>addiction</b>.
+CREB1	drug	opioid	11200184	<strong>CREB</strong> mediates the action of <b>opioids</b> on the expression of several genes in brain regions responsible for drug seeking behavior and manifestation of signs of dependence.
+CREB1	addiction	dependence	11200184	<strong>CREB</strong> mediates the action of opioids on the expression of several genes in brain regions responsible for drug seeking behavior and manifestation of signs of <b>dependence</b>.
+CREB1	addiction	relapse	11200184	<strong>CREB</strong> mediates the action of opioids on the expression of several genes in brain regions responsible for drug <b>seeking</b> behavior and manifestation of signs of dependence.
+CREB1	drug	cocaine	11200184	Moreover, alterations in <strong>CREB</strong> level can effect the rewarding properties of morphine and regulate the self administration of <b>cocaine</b>.
+CREB1	drug	opioid	11200184	Moreover, alterations in <strong>CREB</strong> level can effect the rewarding properties of <b>morphine</b> and regulate the self administration of cocaine.
+CREB1	drug	opioid	11200184	Cellular studies also highlight the relevance of other ATF/<strong>CREB</strong> family members which can affect Ca2+/cAMP response element (CRE) controlled transcription as well as other transcription factors which make the <b>opioid</b> induction longer lasting.
+CREB1	drug	alcohol	11181917	Effects of chronic <b>ethanol</b> intake and its withdrawal on the expression and phosphorylation of the <strong>creb</strong> gene transcription factor in rat cortex.
+CREB1	addiction	withdrawal	11181917	Effects of chronic ethanol intake and its <b>withdrawal</b> on the expression and phosphorylation of the <strong>creb</strong> gene transcription factor in rat cortex.
+CREB1	drug	alcohol	11181917	This investigation examined the effects of chronic <b>ethanol</b> treatment (15 days) and its withdrawal (24 h) on the expression and phosphorylation of cyclic AMP response element binding (<strong>CREB</strong>) protein in the rat cortex.
+CREB1	addiction	withdrawal	11181917	This investigation examined the effects of chronic ethanol treatment (15 days) and its <b>withdrawal</b> (24 h) on the expression and phosphorylation of cyclic AMP response element binding (<strong>CREB</strong>) protein in the rat cortex.
+CREB1	drug	alcohol	11181917	It was found that <b>ethanol</b> withdrawal but not <b>ethanol</b> treatment produced a significant decrease in the phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) and CaM kinase IV protein levels in the frontal, parietal, and piriform cortex.
+CREB1	addiction	withdrawal	11181917	It was found that ethanol <b>withdrawal</b> but not ethanol treatment produced a significant decrease in the phosphorylated <strong>CREB</strong> (p <strong>CREB</strong>) and CaM kinase IV protein levels in the frontal, parietal, and piriform cortex.
+CREB1	drug	alcohol	11181917	<b>Ethanol</b> treatment and its withdrawal had no effect on the protein levels of total <strong>CREB</strong> in the frontal, parietal, and piriform cortex.
+CREB1	addiction	withdrawal	11181917	Ethanol treatment and its <b>withdrawal</b> had no effect on the protein levels of total <strong>CREB</strong> in the frontal, parietal, and piriform cortex.
+CREB1	drug	alcohol	11181917	On the other hand, <b>ethanol</b> treatment produced a significant reduction in the protein levels of <strong>CREB</strong>, p <strong>CREB</strong>, and CaM kinase IV in the cingulate gyrus, and these changes reverted to normal levels during <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	11181917	On the other hand, ethanol treatment produced a significant reduction in the protein levels of <strong>CREB</strong>, p <strong>CREB</strong>, and CaM kinase IV in the cingulate gyrus, and these changes reverted to normal levels during ethanol <b>withdrawal</b>.
+CREB1	drug	alcohol	11181917	Total <strong>CREB</strong> protein levels were significantly higher in the cingulate gyrus during <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	11181917	Total <strong>CREB</strong> protein levels were significantly higher in the cingulate gyrus during ethanol <b>withdrawal</b>.
+CREB1	drug	alcohol	11181917	It was also observed that mRNA levels of <strong>CREB</strong> were significantly higher in the rat cortex during <b>ethanol</b> withdrawal but not during <b>ethanol</b> treatment.
+CREB1	addiction	withdrawal	11181917	It was also observed that mRNA levels of <strong>CREB</strong> were significantly higher in the rat cortex during ethanol <b>withdrawal</b> but not during ethanol treatment.
+CREB1	drug	alcohol	11181917	Taken together, these results suggest the possibility that decreased <strong>CREB</strong> dependent events in the neurocircuitry of the frontal, parietal, and piriform cortex may play an important role in the phenomenon of <b>alcohol</b> dependence and also that decreased <strong>CREB</strong> dependent events in the neurocircuitry of the cingulate gyrus may play a role in <b>alcohol</b> tolerance.
+CREB1	addiction	dependence	11181917	Taken together, these results suggest the possibility that decreased <strong>CREB</strong> dependent events in the neurocircuitry of the frontal, parietal, and piriform cortex may play an important role in the phenomenon of alcohol <b>dependence</b> and also that decreased <strong>CREB</strong> dependent events in the neurocircuitry of the cingulate gyrus may play a role in alcohol tolerance.
+CREB1	drug	opioid	10737627	Regulation of adenylyl cyclase, ERK1/2, and <strong>CREB</strong> by Gz following acute and chronic activation of the delta <b>opioid</b> receptor.
+CREB1	drug	alcohol	9918601	This investigation examined the effects of acute and chronic <b>ethanol</b> exposure and its withdrawal on the cAMP responsive element binding protein (<strong>CREB</strong>) and the activator protein 1 (AP 1) gene transcription factors in the rat brain.
+CREB1	addiction	withdrawal	9918601	This investigation examined the effects of acute and chronic ethanol exposure and its <b>withdrawal</b> on the cAMP responsive element binding protein (<strong>CREB</strong>) and the activator protein 1 (AP 1) gene transcription factors in the rat brain.
+CREB1	drug	alcohol	9918601	The changes in the immunolabeling of the <strong>CREB</strong> related target, that is, brain derived neurotrophic factor (BDNF), in the rat cortex during chronic <b>ethanol</b> treatment and its withdrawal (24 h) were examined using western blotting.
+CREB1	addiction	withdrawal	9918601	The changes in the immunolabeling of the <strong>CREB</strong> related target, that is, brain derived neurotrophic factor (BDNF), in the rat cortex during chronic ethanol treatment and its <b>withdrawal</b> (24 h) were examined using western blotting.
+CREB1	drug	alcohol	9887443	Recent studies indicate that various postreceptor events of the cAMP signal transduction cascade (i.e., Gs protein, protein kinase A [PKA], and cAMP responsive element binding protein [<strong>CREB</strong>]) in the rodent brain are also modulated by chronic <b>ethanol</b> exposure.
+CREB1	drug	cocaine	9856954	Regulation of <b>cocaine</b> reward by <strong>CREB</strong>.
+CREB1	addiction	reward	9856954	Regulation of cocaine <b>reward</b> by <strong>CREB</strong>.
+CREB1	drug	cocaine	9856954	<b>Cocaine</b> regulates the transcription factor <strong>CREB</strong> (adenosine 3', 5' monophosphate response element binding protein) in rat nucleus accumbens, a brain region that is important for addiction.
+CREB1	addiction	addiction	9856954	Cocaine regulates the transcription factor <strong>CREB</strong> (adenosine 3', 5' monophosphate response element binding protein) in rat nucleus accumbens, a brain region that is important for <b>addiction</b>.
+CREB1	drug	cocaine	9856954	Overexpression of <strong>CREB</strong> in this region decreases the rewarding effects of <b>cocaine</b> and makes low doses of the drug aversive.
+CREB1	addiction	aversion	9856954	Overexpression of <strong>CREB</strong> in this region decreases the rewarding effects of cocaine and makes low doses of the drug <b>aversive</b>.
+CREB1	drug	cocaine	9856954	Conversely, overexpression of a dominant negative mutant <strong>CREB</strong> increases the rewarding effects of <b>cocaine</b>.
+CREB1	drug	cocaine	9856954	Moreover, blockade of kappa opioid receptors (on which dynorphin acts) antagonizes the negative effect of <strong>CREB</strong> on <b>cocaine</b> reward.
+CREB1	drug	opioid	9856954	Moreover, blockade of kappa <b>opioid</b> receptors (on which dynorphin acts) antagonizes the negative effect of <strong>CREB</strong> on cocaine reward.
+CREB1	addiction	reward	9856954	Moreover, blockade of kappa opioid receptors (on which dynorphin acts) antagonizes the negative effect of <strong>CREB</strong> on cocaine <b>reward</b>.
+CREB1	drug	alcohol	9581644	Chronic <b>ethanol</b> exposure impairs phosphorylation of <strong>CREB</strong> and CRE binding activity in rat striatum.
+CREB1	drug	alcohol	9581644	This study examined influences of <b>ethanol</b> exposure on phosphorylation of cAMP response element binding protein (<strong>CREB</strong>) and CRE binding activity in the striatum of rats.
+CREB1	addiction	intoxication	9581644	The phosphorylated form of <strong>CREB</strong> increased 180% during acute <b>intoxication</b>, compared to sham conditions.
+CREB1	drug	alcohol	9581644	After chronic <b>ethanol</b> exposure, induction of <strong>CREB</strong> phosphorylation by an acute <b>ethanol</b> challenge was markedly attenuated (50%) compared with acute <b>ethanol</b> exposure in the pair fed condition.
+CREB1	drug	alcohol	9581644	However, supershift analyses did not show that chronic <b>ethanol</b> exposure altered the dimerization patterns of <strong>CREB</strong> and CEBPbeta within the complexes.
+CREB1	drug	alcohol	9581644	In summary, acute <b>ethanol</b> exposure activates the phosphorylation of <strong>CREB</strong>.
+CREB1	drug	alcohol	9581644	Neuroadaptation to chronic <b>ethanol</b> exposure includes alterations in <strong>CREB</strong> physiology that may impair genes that are dependent upon <strong>CREB</strong> for transcriptional activation.
+CREB1	drug	amphetamine	9465009	As an index of PKA activity in vivo, NAc infusions of Rp cAMPS reduced basal levels of dopamine regulated phosphoprotein 32 phosphorylation and blocked <b>amphetamine</b> induced increases in cAMP response element binding protein (<strong>CREB</strong>) phosphorylation.
+CREB1	addiction	dependence	9315909	<strong>CREB</strong> (cAMP response element binding protein) in the locus coeruleus: biochemical, physiological, and behavioral evidence for a role in opiate <b>dependence</b>.
+CREB1	drug	opioid	9315909	<strong>CREB</strong> antisense oligonucleotide infusions completely blocked the <b>morphine</b> induced upregulation of type VIII adenylyl cyclase but not of PKA.
+CREB1	addiction	dependence	9315909	Intra LC infusions of <strong>CREB</strong> antisense oligonucleotide also reduced the development of physical <b>dependence</b> to opiates, based on attenuation of opiate withdrawal.
+CREB1	addiction	withdrawal	9315909	Intra LC infusions of <strong>CREB</strong> antisense oligonucleotide also reduced the development of physical dependence to opiates, based on attenuation of opiate <b>withdrawal</b>.
+CREB1	drug	opioid	9315909	Together, these findings provide the first direct evidence that <strong>CREB</strong> mediates the <b>morphine</b> induced upregulation of specific components of the cAMP pathway in the LC that contribute to physical opiate dependence.
+CREB1	addiction	dependence	9315909	Together, these findings provide the first direct evidence that <strong>CREB</strong> mediates the morphine induced upregulation of specific components of the cAMP pathway in the LC that contribute to physical opiate <b>dependence</b>.
+CREB1	drug	amphetamine	9070635	Enhanced <strong>CREB</strong> phosphorylation and changes in c Fos and FRA expression in striatum accompany <b>amphetamine</b> sensitization.
+CREB1	addiction	sensitization	9070635	Enhanced <strong>CREB</strong> phosphorylation and changes in c Fos and FRA expression in striatum accompany amphetamine <b>sensitization</b>.
+CREB1	addiction	sensitization	9070635	These results suggest that alterations in Fos, FRA and <strong>CREB</strong> transcription factors are common neuronal responses to chronic psychostimulant administration and may contribute to regulation of genes important to the neuroplastic changes underlying psychostimulant <b>sensitization</b>.
+CREB1	drug	opioid	8662559	Reduction of <b>morphine</b> abstinence in mice with a mutation in the gene encoding <strong>CREB</strong>.
+CREB1	addiction	withdrawal	8662559	The behavioral and biochemical consequences of opiate <b>withdrawal</b> were investigated in mice with a genetic disruption of the alpha and Delta isoforms of the cAMP responsive element binding protein (<strong>CREB</strong>).
+CREB1	addiction	dependence	8662559	Thus, <strong>CREB</strong> dependent gene transcription is a factor in the onset of behavioral manifestations of opiate <b>dependence</b>.
+CREB1	drug	opioid	8558448	Regulation of <strong>CREB</strong> expression: in vivo evidence for a functional role in <b>morphine</b> action in the nucleus accumbens.
+CREB1	drug	opioid	8558448	Chronic, but not acute, <b>morphine</b> administration was found to decrease levels of <strong>CREB</strong> immunoreactivity in the NAc, an effect not seen in other brain regions studied.
+CREB1	drug	opioid	8558448	It was found that the antisense oligonucleotide induced reduction in <strong>CREB</strong> levels mimicked the effect of <b>morphine</b> on certain, but not all, cAMP pathway proteins in this brain region, whereas a large number of other signal transduction proteins tested were unaffected by this treatment.
+CREB1	drug	opioid	8558448	Our results support a role for <strong>CREB</strong> in autoregulation of the cAMP pathway in the nervous system, as well as in mediating some of the effects of <b>morphine</b> on this signaling pathway in the NAc.
+CREB1	addiction	withdrawal	7476883	To determine whether this <b>withdrawal</b> induced increase in cAMP modifies gene expression, we studied phosphorylation of the cAMP response element binding protein (<strong>CREB</strong>) and expression of the c fos gene, known to contain a cAMP response element, in NG108 15 cells after abrupt <b>withdrawal</b> from chronic treatment with carbachol.
+CREB1	addiction	withdrawal	7476883	In cells treated with carbachol for 48 hr, induction of <b>withdrawal</b> with the muscarinic antagonist atropine led to a small increase in intracellular cAMP concentration but an 11.6 fold increase in the phosphorylation of <strong>CREB</strong> and a 3.4 fold increase in accumulation of c fos mRNA.
+CREB1	addiction	withdrawal	7476883	The adenylyl cyclase inhibitor 2',5' dideoxyadenosine, which attenuated the chronic carbachol induced increase in cAMP concentration, prevented the increased phosphorylation of <strong>CREB</strong> and the enhanced accumulation of c fos mRNA during atropine induced <b>withdrawal</b>.
+CREB1	drug	amphetamine	7718243	Surprisingly, following chronic administration of <b>amphetamine</b>, levels of phosphorylated <strong>CREB</strong> are increased above basal in rat striatum in vivo, whereas c fos mRNA is suppressed below basal levels.
+CREB1	drug	opioid	7971989	In the course of investigating effects of chronic <b>morphine</b> on the cAMP pathway in the locus coeruleus, a brain region important for opiate addiction, we found that levels of <strong>CREB</strong> immunoreactivity and CRE binding were increased by chronic <b>morphine</b> administration.
+CREB1	addiction	addiction	7971989	In the course of investigating effects of chronic morphine on the cAMP pathway in the locus coeruleus, a brain region important for opiate <b>addiction</b>, we found that levels of <strong>CREB</strong> immunoreactivity and CRE binding were increased by chronic morphine administration.
+CREB1	drug	amphetamine	8083758	<b>Amphetamine</b> regulates gene expression in rat striatum via transcription factor <strong>CREB</strong>.
+CREB1	drug	amphetamine	8083758	Here we report that <b>amphetamine</b> induces phosphorylation of transcription factor cAMP response element binding protein (<strong>CREB</strong>) in rat striatum in vivo and that dopamine D1 receptor stimulation induces phosphorylation of <strong>CREB</strong> within specific complexes bound to cAMP regulatory elements.
+CREB1	drug	amphetamine	8083758	In addition, we show by antisense injection that <strong>CREB</strong> is necessary for c fos induction by <b>amphetamine</b> in vivo.
+CREB1	drug	amphetamine	8083758	Since <strong>CREB</strong> has been implicated in the activation of a number of immediate early genes as well as several neuropeptide genes, <strong>CREB</strong> phosphorylation may be an important early nuclear event mediating long term consequences of <b>amphetamine</b> administration.
+CREB1	drug	alcohol	8974340	The DNA binding activity of the transcription factors AP 1, <strong>CREB</strong> and OCT was investigated in nuclear extracts of brains from rats undergoing <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	8974340	The DNA binding activity of the transcription factors AP 1, <strong>CREB</strong> and OCT was investigated in nuclear extracts of brains from rats undergoing ethanol <b>withdrawal</b>.
+CREB1	drug	alcohol	8974340	AP 1 DNA binding activity but not that of <strong>CREB</strong> or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>ethanol</b> withdrawal.
+CREB1	addiction	withdrawal	8974340	AP 1 DNA binding activity but not that of <strong>CREB</strong> or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after ethanol <b>withdrawal</b>.
+CREB1	drug	cocaine	8385579	The investigations have focused on the Fos Jun family of immediate early gene transcription factors, and the <strong>CREB</strong> family of transcription factors, as possible mediators of the effects of chronic opiate and <b>cocaine</b> exposure on regulation of neuronal gene expression.
+CREB1	drug	opioid	1531356	Regulation of cyclic AMP response element binding protein (<strong>CREB</strong>) phosphorylation by acute and chronic <b>morphine</b> in the rat locus coeruleus.
+CREB1	drug	opioid	1531356	To understand better the mechanism by which opiates produce these intracellular adaptations, we studied <b>morphine</b> regulation of the state of phosphorylation of cyclic AMP response element binding protein (<strong>CREB</strong>), a transcription factor that mediates some of the effects of the cyclic AMP system on gene expression.
+CREB1	drug	opioid	1531356	We show here, by use of a back phosphorylation and immunoprecipitation procedure, that acute <b>morphine</b> decreases the state of phosphorylation of <strong>CREB</strong>, an effect that becomes completely attenuated after chronic <b>morphine</b> administration.
+CREB1	addiction	withdrawal	1531356	In contrast, acute precipitation of opiate <b>withdrawal</b>, via administration of an opiate receptor antagonist, increases the phosphorylation state of <strong>CREB</strong>.
+CREB1	addiction	addiction	1531356	Such regulation of <strong>CREB</strong> phosphorylation could be part of the molecular pathway by which opiates produce changes in gene expression that lead to <b>addiction</b>.
+DRD2	drug	cocaine	32622465	Elevated abundance of <strong>DRD2</strong> in NAc ChINs was sufficient and necessary to express high <b>cocaine</b> motivation, putatively through reduction of ChIN activity during <b>cocaine</b> exposure.
+DRD2	drug	cocaine	32622465	<strong>DRD2</strong> overexpression in ChINs mimicked <b>cocaine</b> induced effects on the dendritic spine density and the ratios of excitatory inputs between two distinct medium spiny neuron cell types, while <strong>DRD2</strong> depletion precluded <b>cocaine</b> induced synaptic plasticity.
+DRD2	drug	opioid	32588604	Significant association of <strong>DRD2</strong> and ANKK1 genes with rural <b>heroin</b> dependence and relapse in men.
+DRD2	addiction	dependence	32588604	Significant association of <strong>DRD2</strong> and ANKK1 genes with rural heroin <b>dependence</b> and relapse in men.
+DRD2	addiction	relapse	32588604	Significant association of <strong>DRD2</strong> and ANKK1 genes with rural heroin dependence and <b>relapse</b> in men.
+DRD2	drug	cannabinoid	32588603	In the Anxiety trait subscale, a 2% association with the polymorphism <strong>DRD2</strong> Tag1B rs1079597 was detected in subjects using <b>cannabis</b>.
+DRD2	drug	cannabinoid	32588603	However, for the <strong>DRD2</strong> Tag1D rs1800498, there was no effect on the differences in personality traits between rural <b>cannabis</b> users and the control group.
+DRD2	drug	alcohol	32260442	In antisocial <b>alcoholism</b>, epistasis between ANKK1 TaqIA and <strong>DRD2</strong> C957T SNVs has been described.
+DRD2	drug	alcohol	32070691	KB220Z attenuates <b>ethanol</b> drinking and other RDS behaviors in P rats possibly by acting on the dopaminergic system, but not by effecting an increase in NAc <strong>DRD2</strong> mRNA expression.
+DRD2	drug	alcohol	32032698	Our results revealed four distinct <b>ethanol</b> preference phenotypes (Light, Heavy, Negative Reinforcement, and Inflexible), each showing different transcriptional regulation patterns of the drd1, <strong>drd2</strong>, grin1a, gria2a, and gabbr1b receptors.
+DRD2	addiction	reward	32032698	Our results revealed four distinct ethanol preference phenotypes (Light, Heavy, Negative <b>Reinforcement</b>, and Inflexible), each showing different transcriptional regulation patterns of the drd1, <strong>drd2</strong>, grin1a, gria2a, and gabbr1b receptors.
+DRD2	drug	opioid	32014377	Stressed mice also showed significant increase in TLR4, Nuclear Factor Kappa B (NF kB), inducible nitric oxide synthase (iNOS), dopamine receptor D2 (<strong>DRD2</strong>), cyclic adenosine monophosphate (cAMP) response element binding protein 1 (CREB 1) and <b>opioid</b> receptor MU 1 (OPRM 1) genes expression compared with control and LPS RS treated stressed mice.
+DRD2	drug	opioid	32014377	Stressed mice also showed significant increase in TLR4, Nuclear Factor Kappa B (NF kB), inducible nitric oxide synthase (iNOS), <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>), cyclic adenosine monophosphate (cAMP) response element binding protein 1 (CREB 1) and <b>opioid</b> receptor MU 1 (OPRM 1) genes expression compared with control and LPS RS treated stressed mice.
+DRD2	drug	nicotine	31867628	Genetic and Epigenetic Analysis Revealing Variants in the NCAM1 TTC12 ANKK1 <strong>DRD2</strong> Cluster Associated Significantly With <b>Nicotine</b> Dependence in Chinese Han <b>Smokers</b>.
+DRD2	addiction	dependence	31867628	Genetic and Epigenetic Analysis Revealing Variants in the NCAM1 TTC12 ANKK1 <strong>DRD2</strong> Cluster Associated Significantly With Nicotine <b>Dependence</b> in Chinese Han Smokers.
+DRD2	drug	nicotine	31867628	Further, we identified four significant <b>smoking</b> associated DMRs, three of which are located in the <strong>DRD2</strong>/ANKK1 region (p = .0012 .00005).
+DRD2	drug	nicotine	31867628	We found the majority of <b>smoking</b> related DMRs are located in the ANKK1/<strong>DRD2</strong> region, indicating a likely causative relation between non synonymous SNPs and DMRs.
+DRD2	drug	nicotine	31867628	This study shows that there exist significant association of variants and haplotypes in ANKK1/<strong>DRD2</strong> region with ND in Chinese male <b>smokers</b>.
+DRD2	drug	psychedelics	31749223	Pretreatment with SCH23390 (SCH), Haloperidol (HAL), and ketanserin (KS), antagonists of dopamine D1 (DRD1), dopamine D2 (<strong>DRD2</strong>), and serotonin 2A (5 HT2A receptor) receptors, respectively, was utilized during a CPP test to investigate the involvement of the dopaminergic and serotonergic systems in 25B <b>NBOMe</b> mediated effects.
+DRD2	addiction	reward	31749223	Pretreatment with SCH23390 (SCH), Haloperidol (HAL), and ketanserin (KS), antagonists of dopamine D1 (DRD1), dopamine D2 (<strong>DRD2</strong>), and serotonin 2A (5 HT2A receptor) receptors, respectively, was utilized during a <b>CPP</b> test to investigate the involvement of the dopaminergic and serotonergic systems in 25B NBOMe mediated effects.
+DRD2	drug	psychedelics	31749223	Moreover, 25B <b>NBOMe</b> altered the DRD1 , <strong>DRD2</strong> , and dopamine transporter expression and increased dopamine levels.
+DRD2	addiction	reward	31660252	With these disappointing statistics, we are hereby proposing that because of such a high genetic risk as supported by the work of Barr and Kidd showing that NA carriers the <strong>DRD2</strong> A1 allele at the rate of 86%, compared to a highly screened <b>reward</b> deficiency free control of only 3%.
+DRD2	drug	alcohol	31530416	The present study investigated alterations of DNA methylation in the dopamine D2 receptor (<strong>DRD2</strong>) gene in patients suffering from <b>alcohol</b> dependence.
+DRD2	addiction	dependence	31530416	The present study investigated alterations of DNA methylation in the dopamine D2 receptor (<strong>DRD2</strong>) gene in patients suffering from alcohol <b>dependence</b>.
+DRD2	drug	alcohol	31530416	While <strong>DRD2</strong> gene methylation did not differ significantly between patients and controls, we found a significant increase of <strong>DRD2</strong> gene methylation during <b>alcohol</b> withdrawal/early abstinence.
+DRD2	addiction	withdrawal	31530416	While <strong>DRD2</strong> gene methylation did not differ significantly between patients and controls, we found a significant increase of <strong>DRD2</strong> gene methylation during alcohol <b>withdrawal</b>/early abstinence.
+DRD2	addiction	addiction	31530416	Craving, measured with the Obsessive <b>Compulsive</b> Drinking Scale (OCDS), was significantly associated with <strong>DRD2</strong> gene methylation.
+DRD2	addiction	relapse	31530416	<b>Craving</b>, measured with the Obsessive Compulsive Drinking Scale (OCDS), was significantly associated with <strong>DRD2</strong> gene methylation.
+DRD2	drug	nicotine	31530416	Furthermore, <b>smoking</b> significantly influenced <strong>DRD2</strong> gene methylation in both, patients and controls.
+DRD2	drug	alcohol	31530416	As in other types of addictive disorders, <strong>DRD2</strong> gene methylation is altered during <b>alcohol</b> withdrawal/early abstinence.
+DRD2	addiction	addiction	31530416	As in other types of <b>addictive</b> disorders, <strong>DRD2</strong> gene methylation is altered during alcohol withdrawal/early abstinence.
+DRD2	addiction	withdrawal	31530416	As in other types of addictive disorders, <strong>DRD2</strong> gene methylation is altered during alcohol <b>withdrawal</b>/early abstinence.
+DRD2	drug	alcohol	31530416	The findings regarding an association with <b>alcohol</b> craving and tobacco consumption point towards a crucial role of <strong>DRD2</strong> gene methylation in the neurobiology of addictive behavior.
+DRD2	drug	nicotine	31530416	The findings regarding an association with alcohol craving and <b>tobacco</b> consumption point towards a crucial role of <strong>DRD2</strong> gene methylation in the neurobiology of addictive behavior.
+DRD2	addiction	addiction	31530416	The findings regarding an association with alcohol craving and tobacco consumption point towards a crucial role of <strong>DRD2</strong> gene methylation in the neurobiology of <b>addictive</b> behavior.
+DRD2	addiction	relapse	31530416	The findings regarding an association with alcohol <b>craving</b> and tobacco consumption point towards a crucial role of <strong>DRD2</strong> gene methylation in the neurobiology of addictive behavior.
+DRD2	addiction	reward	31474426	Saliva underwent transcriptomic analysis for 4 select genes involved in homeostatic and <b>hedonic</b> feeding regulation (neuropeptide Y2 receptor [NPY2R], proopiomelanocortin [POMC], leptin receptor [LEPR], dopamine type 2 receptor [<strong>DRD2</strong>]).
+DRD2	addiction	reward	31474426	Expression of <strong>DRD2</strong>, a hedonistic/<b>reward</b> regulator, was significantly higher in male newborns compared with female newborns with NOWS (Δ threshold cycle 10.8 ± 3.8 vs 13.9 ± 3.7, P = .01).
+DRD2	addiction	aversion	31462765	The classical view on the field postulates that NAc dopamine receptor D1 expressing medium spiny neurons (D1 MSNs) convey reward signals, while <strong>dopamine receptor D2</strong> expressing MSNs (D2 MSNs) encode <b>aversion</b>.
+DRD2	addiction	reward	31462765	The classical view on the field postulates that NAc dopamine receptor D1 expressing medium spiny neurons (D1 MSNs) convey <b>reward</b> signals, while <strong>dopamine receptor D2</strong> expressing MSNs (D2 MSNs) encode aversion.
+DRD2	addiction	relapse	31422417	Next, we determined the effect of pharmacological inactivation of NAc core and shell by either GABAA and GABAB agonists (muscimol + baclofen, 50 + 50 ng/side), Drd1 <strong>Drd2</strong> antagonist (flupenthixol, 10 µg/side), or the selective Drd1 or <strong>Drd2</strong> antagonists (SCH39166, 1.0 µg/side or raclopride, 1.0 µg/side) during the <b>relapse</b> tests.
+DRD2	drug	amphetamine	31422417	Incubated <b>methamphetamine</b> seeking after voluntary abstinence was associated with a selective increase of Fos expression in the NAc core, but not shell, and Fos was colabeled with both Drd1  and <strong>Drd2</strong> MSNs.
+DRD2	addiction	relapse	31422417	Incubated methamphetamine <b>seeking</b> after voluntary abstinence was associated with a selective increase of Fos expression in the NAc core, but not shell, and Fos was colabeled with both Drd1  and <strong>Drd2</strong> MSNs.
+DRD2	drug	amphetamine	31422417	Together, our results suggest that dopamine transmission through Drd1 and <strong>Drd2</strong> in NAc core is critical to the incubation of <b>methamphetamine</b> craving after voluntary abstinence.
+DRD2	addiction	relapse	31422417	Together, our results suggest that dopamine transmission through Drd1 and <strong>Drd2</strong> in NAc core is critical to the incubation of methamphetamine <b>craving</b> after voluntary abstinence.
+DRD2	addiction	addiction	31330230	The dopamine D2 receptor (<strong>DRD2</strong>) and dopamine transporter (DAT) play a regulatory role in dopaminergic neurotransmission and thus play an important role in drug <b>addiction</b>.
+DRD2	drug	psychedelics	31330230	In this study, we investigate the involvement of PFC <strong>DRD2</strong> and DAT in <b>ketamine</b> addiction effects after <b>ketamine</b> administration for 10 weeks in nonhuman primates.
+DRD2	addiction	addiction	31330230	In this study, we investigate the involvement of PFC <strong>DRD2</strong> and DAT in ketamine <b>addiction</b> effects after ketamine administration for 10 weeks in nonhuman primates.
+DRD2	drug	psychedelics	31330230	After 10 week <b>ketamine</b> administration, the assessment of the manifestations of toxicity in rhesus monkeys revealed significant changes in body weight and behavior, decreased <strong>DRD2</strong> and DAT mRNA and protein expression in the PFC, and histological abnormalities including neuronal eosinophilia, pyknosis and disorderly arrangement of neurons in the PFC.
+DRD2	drug	psychedelics	31330230	These results suggest that the reduced expression of <strong>DRD2</strong> and DAT in PFC could be involved in the behavioral and the neurological changes induced by <b>ketamine</b> administration, which may play an important role in the molecular mechanisms of <b>ketamine</b> addiction.
+DRD2	addiction	addiction	31330230	These results suggest that the reduced expression of <strong>DRD2</strong> and DAT in PFC could be involved in the behavioral and the neurological changes induced by ketamine administration, which may play an important role in the molecular mechanisms of ketamine <b>addiction</b>.
+DRD2	drug	opioid	31025317	Significant association of <strong>DRD2</strong> enhancer variant rs12364283 with <b>heroin</b> addiction in a Pakistani population.
+DRD2	addiction	addiction	31025317	Significant association of <strong>DRD2</strong> enhancer variant rs12364283 with heroin <b>addiction</b> in a Pakistani population.
+DRD2	drug	opioid	31025317	This study identifies rs12364283 of <strong>DRD2</strong> as a potential risk factor for <b>heroin</b> addiction in the Pakistani study population.
+DRD2	addiction	addiction	31025317	This study identifies rs12364283 of <strong>DRD2</strong> as a potential risk factor for heroin <b>addiction</b> in the Pakistani study population.
+DRD2	drug	opioid	31025317	This enhancer variant had been shown to increase <strong>DRD2</strong> mRNA expression, a possible factor in increased vulnerability to <b>heroin</b> addiction.
+DRD2	addiction	addiction	31025317	This enhancer variant had been shown to increase <strong>DRD2</strong> mRNA expression, a possible factor in increased vulnerability to heroin <b>addiction</b>.
+DRD2	drug	cocaine	30952156	Eight day withdrawal from high <b>cocaine</b> escalation was associated, respectively, with increased and decreased dopamine receptor D2 (<strong>DRD2</strong>) and serotonin receptor 2C (HTR2C) expression in the ventral striatum compared with controls.
+DRD2	addiction	addiction	30952156	Eight day withdrawal from high cocaine <b>escalation</b> was associated, respectively, with increased and decreased dopamine receptor D2 (<strong>DRD2</strong>) and serotonin receptor 2C (HTR2C) expression in the ventral striatum compared with controls.
+DRD2	addiction	withdrawal	30952156	Eight day <b>withdrawal</b> from high cocaine escalation was associated, respectively, with increased and decreased dopamine receptor D2 (<strong>DRD2</strong>) and serotonin receptor 2C (HTR2C) expression in the ventral striatum compared with controls.
+DRD2	drug	cocaine	30952156	Eight day withdrawal from high <b>cocaine</b> escalation was associated, respectively, with increased and decreased <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) and serotonin receptor 2C (HTR2C) expression in the ventral striatum compared with controls.
+DRD2	addiction	addiction	30952156	Eight day withdrawal from high cocaine <b>escalation</b> was associated, respectively, with increased and decreased <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) and serotonin receptor 2C (HTR2C) expression in the ventral striatum compared with controls.
+DRD2	addiction	withdrawal	30952156	Eight day <b>withdrawal</b> from high cocaine escalation was associated, respectively, with increased and decreased <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) and serotonin receptor 2C (HTR2C) expression in the ventral striatum compared with controls.
+DRD2	drug	alcohol	30877890	<strong>DRD2</strong> methylation and regional grey matter volumes in young adult offspring from families at ultra high risk for <b>alcohol</b> dependence.
+DRD2	addiction	dependence	30877890	<strong>DRD2</strong> methylation and regional grey matter volumes in young adult offspring from families at ultra high risk for alcohol <b>dependence</b>.
+DRD2	addiction	addiction	30659563	The aim of the study was to determine relationships between the selected <strong>DRD2</strong> gene polymorphisms and drug <b>addiction</b>.
+DRD2	addiction	dependence	30659563	In the presented study, one of selected polymorphisms of <strong>DRD2</strong> gene, revealed to be correlated with substance use disorder (at the limit of statistical significance), which could suggest its impact on <b>dependence</b> endophenotype.
+DRD2	drug	alcohol	30516420	The result obtained with this model point out that the relation among high fat diet consumption and <b>alcohol</b> intake appears to depend on the presence or absence of the diet when <b>alcohol</b> intake is evaluated, and that an imbalance in the mesocorticolimbic dopaminergic pathway, observed by the transcriptional regulation of the dopamine receptors (Drd1/<strong>Drd2</strong>) and GABAB receptors subunit (Gabbr1/Gabbr2), can be driving the <b>alcohol</b> intake.
+DRD2	drug	cocaine	30367264	Effects of <strong>DRD2</strong> splicing regulatory polymorphism and DRD4 48 bp VNTR on crack <b>cocaine</b> addiction.
+DRD2	addiction	addiction	30367264	Effects of <strong>DRD2</strong> splicing regulatory polymorphism and DRD4 48 bp VNTR on crack cocaine <b>addiction</b>.
+DRD2	drug	cocaine	30367264	The influence of <strong>DRD2</strong> rs2283265 and DRD4 48 bp VNTR in exon 3 variants, as well as their interaction on crack <b>cocaine</b> addiction susceptibility and severity were evaluated in women and men separately.
+DRD2	addiction	addiction	30367264	The influence of <strong>DRD2</strong> rs2283265 and DRD4 48 bp VNTR in exon 3 variants, as well as their interaction on crack cocaine <b>addiction</b> susceptibility and severity were evaluated in women and men separately.
+DRD2	drug	cocaine	30367264	An association between the <strong>DRD2</strong> T allele and crack <b>cocaine</b> addiction was found in women.
+DRD2	addiction	addiction	30367264	An association between the <strong>DRD2</strong> T allele and crack cocaine <b>addiction</b> was found in women.
+DRD2	drug	cocaine	30367264	In this same group, interaction analysis demonstrated that the presence of <strong>DRD2</strong> T allele and concomitant absence of DRD4 7R allele were associated with risk for crack <b>cocaine</b> addiction.
+DRD2	addiction	addiction	30367264	In this same group, interaction analysis demonstrated that the presence of <strong>DRD2</strong> T allele and concomitant absence of DRD4 7R allele were associated with risk for crack cocaine <b>addiction</b>.
+DRD2	addiction	addiction	30367264	No influence of <strong>DRD2</strong> and DRD4 variants was observed in men regarding <b>addiction</b> severity.
+DRD2	drug	opioid	30268777	<strong>DRD2</strong> protein level increased in the VTA, NAC and amygdala of <b>opioid</b> abusers when compared with the control.
+DRD2	drug	alcohol	30192917	The current candidate gene and environment interaction (cGxE) study examined whether the effects of an experimentally manipulated psychosocial stressor on self reported drinking urge and implicit attentional bias for <b>alcohol</b> cues differ as a function of a cumulative genetic score of 5 HTTLPR, MAO A, DRD4, DAT1 and <strong>DRD2</strong> genotypes.
+DRD2	drug	opioid	30118972	The most studied candidate genes have included the mu <b>opioid</b> receptor (OPRM1), the delta <b>opioid</b> receptor (OPRD1), the dopamine D2 receptor (<strong>DRD2</strong>), and brain derived neurotrophic factor (BDNF).
+DRD2	drug	nicotine	30104163	A neurobiological pathway to <b>smoking</b> in adolescence: TTC12 ANKK1 <strong>DRD2</strong> variants and reward response.
+DRD2	addiction	reward	30104163	A neurobiological pathway to smoking in adolescence: TTC12 ANKK1 <strong>DRD2</strong> variants and <b>reward</b> response.
+DRD2	drug	nicotine	30104163	The TTC12 ANKK1 <strong>DRD2</strong> gene cluster has been implicated in adult <b>smoking</b>.
+DRD2	drug	nicotine	30104163	Here, we investigated the contribution of individual genes in the TTC12 ANKK1 <strong>DRD2</strong> cluster in <b>smoking</b> and their association with <b>smoking</b> associated reward processing in adolescence.
+DRD2	addiction	reward	30104163	Here, we investigated the contribution of individual genes in the TTC12 ANKK1 <strong>DRD2</strong> cluster in smoking and their association with smoking associated <b>reward</b> processing in adolescence.
+DRD2	drug	nicotine	30104163	A meta analysis of TTC12 ANKK1 <strong>DRD2</strong> variants and self reported <b>smoking</b> behaviours was performed in four European adolescent cohorts (N = 14,084).
+DRD2	addiction	reward	30104163	This risk allele was linked to an increased ventral striatal blood oxygen level dependent (BOLD) response during <b>reward</b> anticipation (n = 1,263) and with higher <strong>DRD2</strong> gene expression in the striatum (p = 0.013), but not with TTC12 or ANKK gene expression.
+DRD2	drug	nicotine	30104163	These data suggest a role for the TTC12 ANKK1 <strong>DRD2</strong> gene cluster in adolescent <b>smoking</b> behaviours, provide evidence for the involvement of <strong>DRD2</strong> in the early stages of addiction and support the notion that genetically driven inter individual differences in dopaminergic transmission mediate reward sensitivity and risk to <b>smoking</b>.
+DRD2	addiction	addiction	30104163	These data suggest a role for the TTC12 ANKK1 <strong>DRD2</strong> gene cluster in adolescent smoking behaviours, provide evidence for the involvement of <strong>DRD2</strong> in the early stages of <b>addiction</b> and support the notion that genetically driven inter individual differences in dopaminergic transmission mediate reward sensitivity and risk to smoking.
+DRD2	addiction	reward	30104163	These data suggest a role for the TTC12 ANKK1 <strong>DRD2</strong> gene cluster in adolescent smoking behaviours, provide evidence for the involvement of <strong>DRD2</strong> in the early stages of addiction and support the notion that genetically driven inter individual differences in dopaminergic transmission mediate <b>reward</b> sensitivity and risk to smoking.
+DRD2	drug	amphetamine	30056065	Analysis of histone 3/4 enrichment at specific promoters revealed: i) distinct effects of the drugs on histone 3 acetylation, with modafinil increasing H3ac at Drd1 and Adra1b promoters, but <b>METH</b> increasing H3ac at Adra1a; ii) distinct effects on histone 4 acetylation enrichment, with modafinil increasing H4ac at the <strong>Drd2</strong> promoter and decreasing it at Hrh1, but <b>METH</b> increasing H4ac at Drd1; iii) comparable effects of both psychostimulants, increasing H3ac at <strong>Drd2</strong>, Hcrtr1, and Hrh1 promoters, decreasing H3ac at Hrh3, increasing H4ac at Hcrtr1, and decreasing H4ac at Hcrtr2, Hrh3, and Grin1 promoters.
+DRD2	drug	opioid	29878268	In contrast, in rats adapted to an HP diet compared with an NP diet, energy intake was lower; and in the NAcc, meal induced c Fos protein expression was 20% lower, and mRNA expression was 17% higher for dopamine receptor 2 (<strong>Drd2</strong>) receptors and 38% lower for κ <b>opioid</b> receptor (Oprk1) receptors.
+DRD2	drug	amphetamine	29702335	<strong>DRD2</strong>/ANKK1 gene polymorphisms in forensic autopsies of <b>methamphetamine</b> intoxication fatalities.
+DRD2	addiction	intoxication	29702335	<strong>DRD2</strong>/ANKK1 gene polymorphisms in forensic autopsies of methamphetamine <b>intoxication</b> fatalities.
+DRD2	addiction	addiction	29702335	Dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (<strong>DRD2</strong>/ANKK1) gene polymorphisms have been associated with responses to psychotropic drugs and <b>addiction</b>.
+DRD2	drug	amphetamine	29702335	We analyzed two <strong>DRD2</strong>/ANKK1 polymorphisms, Taq1A and  141C Ins/Del, in 37 fatal <b>methamphetamine</b> (MA) intoxication cases and 235 control cases in which MA and psychotropic drugs were not detected.
+DRD2	addiction	intoxication	29702335	We analyzed two <strong>DRD2</strong>/ANKK1 polymorphisms, Taq1A and  141C Ins/Del, in 37 fatal methamphetamine (MA) <b>intoxication</b> cases and 235 control cases in which MA and psychotropic drugs were not detected.
+DRD2	addiction	intoxication	29702335	No significant associations were observed between  141C Ins/Del polymorphisms and MA <b>intoxication</b> cases or between <strong>DRD2</strong>/ANKK1 polymorphisms and CSF dopamine concentrations.
+DRD2	addiction	intoxication	29702335	Our findings suggest that the <strong>DRD2</strong>/ANKK1 Taq1A polymorphism is associated with susceptibility to fatal MA <b>intoxication</b>.
+DRD2	drug	alcohol	29568676	Furthermore, voluntary <b>ethanol</b> consumption attenuated stress response and modified expression of reward system genes: enhancing Drd1 and <strong>Drd2</strong>, and reducing Gabbr2 in the striatum.
+DRD2	addiction	reward	29568676	Furthermore, voluntary ethanol consumption attenuated stress response and modified expression of <b>reward</b> system genes: enhancing Drd1 and <strong>Drd2</strong>, and reducing Gabbr2 in the striatum.
+DRD2	drug	opioid	29550268	A 35.8 kilobases haplotype spanning ANKK1 and <strong>DRD2</strong> is associated with <b>heroin</b> dependence in Han Chinese males.
+DRD2	addiction	dependence	29550268	A 35.8 kilobases haplotype spanning ANKK1 and <strong>DRD2</strong> is associated with heroin <b>dependence</b> in Han Chinese males.
+DRD2	drug	opioid	29550268	Ankyrin repeat and kinase domain containing 1 (ANKK1) and dopamine receptor D2 (<strong>DRD2</strong>) gene polymorphisms have long been considered to contribute to susceptibility to <b>heroin</b> dependence.
+DRD2	addiction	dependence	29550268	Ankyrin repeat and kinase domain containing 1 (ANKK1) and dopamine receptor D2 (<strong>DRD2</strong>) gene polymorphisms have long been considered to contribute to susceptibility to heroin <b>dependence</b>.
+DRD2	drug	opioid	29550268	Ankyrin repeat and kinase domain containing 1 (ANKK1) and <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) gene polymorphisms have long been considered to contribute to susceptibility to <b>heroin</b> dependence.
+DRD2	addiction	dependence	29550268	Ankyrin repeat and kinase domain containing 1 (ANKK1) and <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) gene polymorphisms have long been considered to contribute to susceptibility to heroin <b>dependence</b>.
+DRD2	drug	opioid	29550268	Despite their adjacent locations, few studies have elucidated the role of the potential interaction between ANKK1 and <strong>DRD2</strong> in <b>heroin</b> dependence.
+DRD2	addiction	dependence	29550268	Despite their adjacent locations, few studies have elucidated the role of the potential interaction between ANKK1 and <strong>DRD2</strong> in heroin <b>dependence</b>.
+DRD2	drug	opioid	29550268	Notably, a 35.8 kilobases (kb) haplotype spanning ANKK1 and <strong>DRD2</strong> was found to be a strong protective factor for <b>heroin</b> dependence.
+DRD2	addiction	dependence	29550268	Notably, a 35.8 kilobases (kb) haplotype spanning ANKK1 and <strong>DRD2</strong> was found to be a strong protective factor for heroin <b>dependence</b>.
+DRD2	drug	alcohol	29464814	<strong>DRD2</strong> promoter methylation and measures of <b>alcohol</b> reward: functional activation of reward circuits and clinical severity.
+DRD2	addiction	reward	29464814	<strong>DRD2</strong> promoter methylation and measures of alcohol <b>reward</b>: functional activation of <b>reward</b> circuits and clinical severity.
+DRD2	drug	alcohol	29464814	We hypothesized that epigenetic alterations in the promoter region of the dopamine D2 receptor (<strong>DRD2</strong>) gene would be associated with cue elicited activation of neural reward regions, as well as severity of <b>alcohol</b> use behavior.
+DRD2	addiction	reward	29464814	We hypothesized that epigenetic alterations in the promoter region of the dopamine D2 receptor (<strong>DRD2</strong>) gene would be associated with cue elicited activation of neural <b>reward</b> regions, as well as severity of alcohol use behavior.
+DRD2	drug	alcohol	29464814	The current study leveraged functional neuroimaging (fMRI) during an <b>alcohol</b> reward paradigm (n = 383) to test associations among <strong>DRD2</strong> promoter methylation in peripheral tissue, signal change in the striatum during the presentation of <b>alcohol</b> cues, and severity of <b>alcohol</b> use disorder (AUD).
+DRD2	addiction	reward	29464814	The current study leveraged functional neuroimaging (fMRI) during an alcohol <b>reward</b> paradigm (n = 383) to test associations among <strong>DRD2</strong> promoter methylation in peripheral tissue, signal change in the striatum during the presentation of alcohol cues, and severity of alcohol use disorder (AUD).
+DRD2	drug	alcohol	29464814	Controlling for age, <strong>DRD2</strong> promoter methylation was positively associated with responses to <b>alcohol</b> cues in the right accumbens (partial r = 0.144, P = 0.005), left putamen (partial r = 0.133, P = 0.009), right putamen (partial r = 0.106, P = 0.039), left caudate (partial r = 0.117, P = 0.022), and right caudate (partial r = 0.133, P = 0.009), suggesting that <strong>DRD2</strong> methylation was positively associated with robust activation in the striatum in response to reward cues.
+DRD2	addiction	reward	29464814	Controlling for age, <strong>DRD2</strong> promoter methylation was positively associated with responses to alcohol cues in the right accumbens (partial r = 0.144, P = 0.005), left putamen (partial r = 0.133, P = 0.009), right putamen (partial r = 0.106, P = 0.039), left caudate (partial r = 0.117, P = 0.022), and right caudate (partial r = 0.133, P = 0.009), suggesting that <strong>DRD2</strong> methylation was positively associated with robust activation in the striatum in response to <b>reward</b> cues.
+DRD2	drug	alcohol	29464814	Specifically, controlling for age, <strong>DRD2</strong> methylation was associated with <b>Alcohol</b> Use Disorders Identification Test total (partial r = 0.140, P = 0.002); Impaired Control Scale total (partial r = 0.097, P = 0.044) and <b>Alcohol</b> Dependence Scale total (partial r = 0.152, P = 0.001).
+DRD2	addiction	dependence	29464814	Specifically, controlling for age, <strong>DRD2</strong> methylation was associated with Alcohol Use Disorders Identification Test total (partial r = 0.140, P = 0.002); Impaired Control Scale total (partial r = 0.097, P = 0.044) and Alcohol <b>Dependence</b> Scale total (partial r = 0.152, P = 0.001).
+DRD2	drug	alcohol	29464814	Thus, <strong>DRD2</strong> methylation may be a critical mechanism linking D2 receptors with functional striatal brain changes and clinical severity among <b>alcohol</b> users.
+DRD2	drug	cocaine	29454035	Here, we compared the effect of decreased mRNA level of <strong>Drd2</strong> in each region on <b>cocaine</b> self administration in a dose response function.
+DRD2	drug	cocaine	29454035	Animals were trained to self administer <b>cocaine</b> 20 days after <strong>Drd2</strong> shRNA treatment.
+DRD2	drug	cocaine	29454035	Compared to scrambled shRNA treated rats, <strong>Drd2</strong> knockdown in the VTA increased <b>cocaine</b> self administration at all tested doses (0.02 0.56 mg/kg/infusion) producing an upward shift (both the ascending and descending limb) in the dose response curve of <b>cocaine</b> self administration.
+DRD2	drug	alcohol	29383684	A downregulation of DRD1 but not <strong>DRD2</strong> expression was seen in <b>alcoholics</b>.
+DRD2	drug	alcohol	29275025	Genes of the brain pathway of motivation and reward, including <strong>DRD2</strong> and ANKK1, are associated with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	29275025	Genes of the brain pathway of motivation and reward, including <strong>DRD2</strong> and ANKK1, are associated with alcohol <b>dependence</b>.
+DRD2	addiction	reward	29275025	Genes of the brain pathway of motivation and <b>reward</b>, including <strong>DRD2</strong> and ANKK1, are associated with alcohol dependence.
+DRD2	drug	amphetamine	29247759	<b>METH</b> treated mice also showed i) decreased levels of total H3ac and H4ac, and increased levels of 5 mC, ii) decreased H3ac enrichment at promoters of <strong>Drd2</strong>, Hcrtr1/2, Hrh1 and Grin1, and increased H4ac enrichment at Drd1, Hrh1 and Grin1, iii) increased mRNA of Drd1a, Grin1 and Gria1.
+DRD2	drug	alcohol	29236941	TAQ1A1 Allele of the <strong>DRD2</strong> Gene Region Contribute to Shorter Survival Time in <b>Alcohol</b> Dependent Individuals When Controlling for the Influence of Age and Gender.
+DRD2	drug	alcohol	29236941	To investigate the influence of the A1 allele of the TAQ1A polymorphism in the dopamine D2 receptor (<strong>DRD2</strong>) gene region on mortality in adult individuals with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	29236941	To investigate the influence of the A1 allele of the TAQ1A polymorphism in the dopamine D2 receptor (<strong>DRD2</strong>) gene region on mortality in adult individuals with alcohol <b>dependence</b>.
+DRD2	drug	alcohol	29236941	An important contribution of the present study is that in <b>alcohol</b> dependence the Taq1A1 allele of the <strong>DRD2</strong> gene region is a risk factor for premature death of similar importance as the well known risk factors of age and gender.
+DRD2	addiction	dependence	29236941	An important contribution of the present study is that in alcohol <b>dependence</b> the Taq1A1 allele of the <strong>DRD2</strong> gene region is a risk factor for premature death of similar importance as the well known risk factors of age and gender.
+DRD2	drug	alcohol	29236941	We investigated the influence of A1 allele of the TAQ1A polymorphism in <strong>DRD2</strong> receptor gene region on mortality in <b>alcohol</b> dependent individuals in an 18 year follow up.
+DRD2	drug	alcohol	29205397	Long term voluntary <b>alcohol</b> drinking significantly reduced mRNA levels of the long D2R isoform in the nucleus accumbens (NAc) but did not alter CpG methylation levels in the analyzed sequence of the <strong>Drd2</strong> gene.
+DRD2	drug	opioid	29039297	There was no effect of PC:EtOH on mRNA expression of the µ <b>opioid</b> receptor, tyrosine hydroxylase (Th), dopamine receptor type 2 (<strong>Drd2</strong>) or dopamine active transporter (Slc6a3).
+DRD2	drug	opioid	28854834	<strong>DRD2</strong> and ANKK1 genes associate with late onset <b>heroin</b> dependence in men.
+DRD2	addiction	dependence	28854834	<strong>DRD2</strong> and ANKK1 genes associate with late onset heroin <b>dependence</b> in men.
+DRD2	drug	opioid	28854834	Objectives: Dopamine plays an important role in reward system of <b>heroin</b> dependence (HD), and dopaminergic D2 receptor (<strong>DRD2</strong>) gene is a candidate for the aetiology of HD.
+DRD2	addiction	dependence	28854834	Objectives: Dopamine plays an important role in reward system of heroin <b>dependence</b> (HD), and dopaminergic D2 receptor (<strong>DRD2</strong>) gene is a candidate for the aetiology of HD.
+DRD2	addiction	reward	28854834	Objectives: Dopamine plays an important role in <b>reward</b> system of heroin dependence (HD), and dopaminergic D2 receptor (<strong>DRD2</strong>) gene is a candidate for the aetiology of HD.
+DRD2	drug	alcohol	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, ADH1C, OPRM1, <strong>DRD2</strong>, BDNF, and ALDH2 genes on <b>alcohol</b> dependence in a Caucasian population.
+DRD2	addiction	dependence	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, ADH1C, OPRM1, <strong>DRD2</strong>, BDNF, and ALDH2 genes on alcohol <b>dependence</b> in a Caucasian population.
+DRD2	drug	alcohol	28744152	The objectives of this study were to evaluate the correlation between <strong>DRD2</strong>, SLC6A3 (DAT) and COMT genetic polymorphisms and to investigate their effect on the development of adverse drug reactions in patients with <b>alcohol</b> use disorder who received haloperidol.
+DRD2	drug	opioid	28692418	Contribution of Genetic Polymorphisms and Haplotypes in <strong>DRD2</strong>, BDNF, and <b>Opioid</b> Receptors to <b>Heroin</b> Dependence and Endophenotypes Among the Han Chinese.
+DRD2	addiction	dependence	28692418	Contribution of Genetic Polymorphisms and Haplotypes in <strong>DRD2</strong>, BDNF, and Opioid Receptors to Heroin <b>Dependence</b> and Endophenotypes Among the Han Chinese.
+DRD2	drug	opioid	28692418	Reward  and memory related candidate genes dopamine D2 receptor (<strong>DRD2</strong>) and brain derived neurotrophic factor (BDNF), as well as the <b>opioid</b> receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to <b>heroin</b> dependence in populations worldwide.
+DRD2	addiction	dependence	28692418	Reward  and memory related candidate genes dopamine D2 receptor (<strong>DRD2</strong>) and brain derived neurotrophic factor (BDNF), as well as the opioid receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug <b>dependence</b>, but relatively little is known on their contributions to heroin <b>dependence</b> in populations worldwide.
+DRD2	addiction	reward	28692418	<b>Reward</b>  and memory related candidate genes dopamine D2 receptor (<strong>DRD2</strong>) and brain derived neurotrophic factor (BDNF), as well as the opioid receptor genes (OPRM1, OPRD1, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to heroin dependence in populations worldwide.
+DRD2	drug	opioid	28692418	The G allele of rs4654327 (OPRD1), <strong>DRD2</strong> haplotype block CCGCCGTT (rs6277 rs1076560 rs2283265 rs2734833 rs2075652 rs1079596 rs4436578 rs11214607), and OPRD1 haplotypes TACG (rs6669447 rs2236857 rs508448 rs4654327), CG (rs508448 rs4654327), and TG (rs6669447 rs4654327) were significantly associated with <b>heroin</b> dependence phenotype.
+DRD2	addiction	dependence	28692418	The G allele of rs4654327 (OPRD1), <strong>DRD2</strong> haplotype block CCGCCGTT (rs6277 rs1076560 rs2283265 rs2734833 rs2075652 rs1079596 rs4436578 rs11214607), and OPRD1 haplotypes TACG (rs6669447 rs2236857 rs508448 rs4654327), CG (rs508448 rs4654327), and TG (rs6669447 rs4654327) were significantly associated with heroin <b>dependence</b> phenotype.
+DRD2	drug	nicotine	28548579	Genetic Variation of the Mu Opioid Receptor (OPRM1) and Dopamine D2 Receptor (<strong>DRD2</strong>) is Related to <b>Smoking</b> Differences in Patients with Schizophrenia but not Bipolar Disorder.
+DRD2	drug	opioid	28548579	Genetic Variation of the Mu <b>Opioid</b> Receptor (OPRM1) and Dopamine D2 Receptor (<strong>DRD2</strong>) is Related to Smoking Differences in Patients with Schizophrenia but not Bipolar Disorder.
+DRD2	drug	nicotine	28548579	Inasmuch as endogenous opioid and dopaminergic systems are involved in <b>smoking</b> reinforcement, it is important to study mu opioid receptor (OPRM1) A118G (rs1799971), dopamine D2 receptor (<strong>DRD2</strong>) Taq1A (rs1800497) genotypes, and sex differences among patients with schizophrenia or bipolar disorder.
+DRD2	drug	opioid	28548579	Inasmuch as endogenous <b>opioid</b> and dopaminergic systems are involved in smoking reinforcement, it is important to study mu <b>opioid</b> receptor (OPRM1) A118G (rs1799971), dopamine D2 receptor (<strong>DRD2</strong>) Taq1A (rs1800497) genotypes, and sex differences among patients with schizophrenia or bipolar disorder.
+DRD2	addiction	reward	28548579	Inasmuch as endogenous opioid and dopaminergic systems are involved in smoking <b>reinforcement</b>, it is important to study mu opioid receptor (OPRM1) A118G (rs1799971), dopamine D2 receptor (<strong>DRD2</strong>) Taq1A (rs1800497) genotypes, and sex differences among patients with schizophrenia or bipolar disorder.
+DRD2	drug	nicotine	28548579	However, female <b>smokers</b> with schizophrenia who were GG homozygous of the <strong>DRD2</strong> receptor smoked more than the *A male <b>smokers</b> with schizophrenia (p<0.05).
+DRD2	drug	nicotine	28548579	In bipolar patients, there were no OPRM1 and <strong>DRD2</strong> Taq1A genotype differences in <b>smoking</b> status.
+DRD2	drug	nicotine	28548579	Alteration of <strong>DRD2</strong> receptor function also increased <b>smoking</b> behavior in females with schizophrenia.
+DRD2	drug	cocaine	28535798	Selective knockout of Kalirin in dopamine transporter expressing neurons produced a transient enhancement of <b>cocaine</b> induced locomotion, while knockout of Kalirin in Drd1a  or <strong>Drd2</strong> dopamine receptor expressing neurons was without effect.
+DRD2	drug	cocaine	28535798	The <b>cocaine</b> sensitive neuronal pathways which are most sensitive to altered Kalirin function may be the pathways most dependent on GluN2B and <strong>Drd2</strong>.
+DRD2	drug	alcohol	28507526	Patients with chronic addiction exhibit reduced dopamine D2 receptor (<strong>DRD2</strong>) availability in the striatum, and the <strong>DRD2</strong> TaqIA (rs1800497) and C957T (rs6277) genetic polymorphisms have previously been linked to individual differences in striatal dopamine metabolism and clinical risk for <b>alcohol</b> and nicotine dependence.
+DRD2	drug	nicotine	28507526	Patients with chronic addiction exhibit reduced dopamine D2 receptor (<strong>DRD2</strong>) availability in the striatum, and the <strong>DRD2</strong> TaqIA (rs1800497) and C957T (rs6277) genetic polymorphisms have previously been linked to individual differences in striatal dopamine metabolism and clinical risk for alcohol and <b>nicotine</b> dependence.
+DRD2	addiction	addiction	28507526	Patients with chronic <b>addiction</b> exhibit reduced dopamine D2 receptor (<strong>DRD2</strong>) availability in the striatum, and the <strong>DRD2</strong> TaqIA (rs1800497) and C957T (rs6277) genetic polymorphisms have previously been linked to individual differences in striatal dopamine metabolism and clinical risk for alcohol and nicotine dependence.
+DRD2	addiction	dependence	28507526	Patients with chronic addiction exhibit reduced dopamine D2 receptor (<strong>DRD2</strong>) availability in the striatum, and the <strong>DRD2</strong> TaqIA (rs1800497) and C957T (rs6277) genetic polymorphisms have previously been linked to individual differences in striatal dopamine metabolism and clinical risk for alcohol and nicotine <b>dependence</b>.
+DRD2	addiction	addiction	28507526	We suggest that the relatively better memory for rewarded stimuli in carriers of low expressing <strong>DRD2</strong> variants may reflect an intermediate phenotype of <b>addiction</b> memory.
+DRD2	drug	cocaine	28466092	The aim of the present study was to compare the long term effects of RSD on the conditioned rewarding effects of <b>cocaine</b> and levels of the transcription factors Pitx3 and Nurr1 in the ventral tegmental area (VTA), the dopamine transporter (DAT), the D2 dopamine receptor (<strong>D2DR</strong>) and precursor of brain derived neurotrophic factor (proBDNF) signaling pathways, and the tropomyosin related kinase B (TrkB) receptor in the nucleus accumbens (NAc) in adult and adolescent mice.
+DRD2	addiction	reward	28364268	Dopamine D2 receptors (<strong>DRD2</strong>) have been strongly implicated in <b>reward</b> processing of natural stimuli and drugs.
+DRD2	drug	nicotine	28364268	Here, we examined the contribution of the <strong>DRD2</strong> Taq1B polymorphism to <b>smokers</b>' and non <b>smokers</b>' responsivity toward <b>smoking</b> versus naturally rewarding stimuli in the AAT.
+DRD2	drug	nicotine	28364268	<b>Smokers</b> carrying the minor B1 allele of the <strong>DRD2</strong> Taq1B polymorphism showed reduced approach behavior for food related pictures compared to non <b>smokers</b> with the same allele.
+DRD2	drug	nicotine	28364268	This is the first study demonstrating that behavioral shifts in response to <b>smoking</b> relative to natural rewards in <b>smokers</b> are mediated by the <strong>DRD2</strong> Taq1B polymorphism.
+DRD2	drug	nicotine	28364268	Our results indicate a reduced natural reward brain reactivity in <b>smokers</b> with a genetically determined decrease in dopaminergic activity (i.e., reduction of <strong>DRD2</strong> availability).
+DRD2	addiction	reward	28364268	Our results indicate a reduced natural <b>reward</b> brain reactivity in smokers with a genetically determined decrease in dopaminergic activity (i.e., reduction of <strong>DRD2</strong> availability).
+DRD2	drug	amphetamine	28123032	Between tests, the rats underwent voluntary abstinence (using a discrete choice procedure between <b>methamphetamine</b> and food; 20 trials/d) for 19 d. We used in situ hybridization to measure the colabeling of the activity marker Fos with Drd1 and <strong>Drd2</strong> in DMS and DLS after the tests.
+DRD2	drug	amphetamine	28123032	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both Drd1 and <strong>Drd2</strong> DMS injections of SCH39166 or raclopride selectively decreased <b>methamphetamine</b> seeking after 21 abstinence days.
+DRD2	addiction	relapse	28123032	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both Drd1 and <strong>Drd2</strong> DMS injections of SCH39166 or raclopride selectively decreased methamphetamine <b>seeking</b> after 21 abstinence days.
+DRD2	drug	alcohol	30198022	Knowledge of precise polymorphic associations can help in the attenuation of guilt and denial, corroboration of family gene o grams; assistance in risk severity based decisions about appropriate therapies, including pain medications and risk for addiction; choice of the appropriate level of care placement (i.e., inpatient, outpatient, intensive outpatient, residential); determination of the length of stay in treatment; determination of genetic severity based relapse and recovery liability and vulnerability; determination of pharmacogenetic medical monitoring for better clinical outcomes (e.g., the A1 allele of the <strong>DRD2</strong> gene reduces the binding to opioid delta receptors in the brain, thus, reducing <b>Naltrexone</b>'s clinical effectiveness); and supporting medical necessity for insurance scrutiny.
+DRD2	drug	opioid	30198022	Knowledge of precise polymorphic associations can help in the attenuation of guilt and denial, corroboration of family gene o grams; assistance in risk severity based decisions about appropriate therapies, including pain medications and risk for addiction; choice of the appropriate level of care placement (i.e., inpatient, outpatient, intensive outpatient, residential); determination of the length of stay in treatment; determination of genetic severity based relapse and recovery liability and vulnerability; determination of pharmacogenetic medical monitoring for better clinical outcomes (e.g., the A1 allele of the <strong>DRD2</strong> gene reduces the binding to <b>opioid</b> delta receptors in the brain, thus, reducing Naltrexone's clinical effectiveness); and supporting medical necessity for insurance scrutiny.
+DRD2	addiction	addiction	30198022	Knowledge of precise polymorphic associations can help in the attenuation of guilt and denial, corroboration of family gene o grams; assistance in risk severity based decisions about appropriate therapies, including pain medications and risk for <b>addiction</b>; choice of the appropriate level of care placement (i.e., inpatient, outpatient, intensive outpatient, residential); determination of the length of stay in treatment; determination of genetic severity based relapse and recovery liability and vulnerability; determination of pharmacogenetic medical monitoring for better clinical outcomes (e.g., the A1 allele of the <strong>DRD2</strong> gene reduces the binding to opioid delta receptors in the brain, thus, reducing Naltrexone's clinical effectiveness); and supporting medical necessity for insurance scrutiny.
+DRD2	addiction	relapse	30198022	Knowledge of precise polymorphic associations can help in the attenuation of guilt and denial, corroboration of family gene o grams; assistance in risk severity based decisions about appropriate therapies, including pain medications and risk for addiction; choice of the appropriate level of care placement (i.e., inpatient, outpatient, intensive outpatient, residential); determination of the length of stay in treatment; determination of genetic severity based <b>relapse</b> and recovery liability and vulnerability; determination of pharmacogenetic medical monitoring for better clinical outcomes (e.g., the A1 allele of the <strong>DRD2</strong> gene reduces the binding to opioid delta receptors in the brain, thus, reducing Naltrexone's clinical effectiveness); and supporting medical necessity for insurance scrutiny.
+DRD2	addiction	dependence	27819741	Researchers have reported that the dopamine D2 receptor (<strong>DRD2</strong>) is involved in the development of opiate <b>dependence</b>.
+DRD2	drug	opioid	27819741	To identify markers that contribute to the genetic susceptibility to <b>heroin</b> addiction, we examined the potential association between <b>heroin</b> dependence and six polymorphisms of the <strong>DRD2</strong> gene using the MassARRAY system.
+DRD2	addiction	addiction	27819741	To identify markers that contribute to the genetic susceptibility to heroin <b>addiction</b>, we examined the potential association between heroin dependence and six polymorphisms of the <strong>DRD2</strong> gene using the MassARRAY system.
+DRD2	addiction	dependence	27819741	To identify markers that contribute to the genetic susceptibility to heroin addiction, we examined the potential association between heroin <b>dependence</b> and six polymorphisms of the <strong>DRD2</strong> gene using the MassARRAY system.
+DRD2	drug	opioid	27819741	These findings point to a role for <strong>DRD2</strong> polymorphism in <b>heroin</b> dependence in the Chinese Han population, and may be informative for future genetic or neurobiological studies on <b>heroin</b> dependence.
+DRD2	addiction	dependence	27819741	These findings point to a role for <strong>DRD2</strong> polymorphism in heroin <b>dependence</b> in the Chinese Han population, and may be informative for future genetic or neurobiological studies on heroin <b>dependence</b>.
+DRD2	drug	opioid	27580593	We investigated whether variation in the dopamine D2 receptor gene (<strong>DRD2</strong>) and tri dimensional personality questionnaire (TPQ) scores could be used to aid adjustment of daily <b>methadone</b> requirements of <b>heroin</b> addicts.
+DRD2	drug	opioid	27580593	<strong>DRD2</strong> TaqI B polymorphisms and TPQ scores were determined in 138 male Taiwanese <b>heroin</b> addicts who were receiving <b>methadone</b> treatment.
+DRD2	drug	opioid	27580593	No significant differences in age (p = 0.60), mean <b>methadone</b> dose (p = 0.75) or borderline index group (p = 0.25) were observed between subjects bearing the B1/B1, B1/B2 and B2/B2 <strong>DRD2</strong> TaqI genotypes.
+DRD2	drug	opioid	27580593	Although the <strong>DRD2</strong> TaqI B genotype was not associated with <b>methadone</b> use requirements, borderline index was revealed as a potential predictive marker for the adjustment of <b>methadone</b> dosage requirements in <b>heroin</b> addicts.
+DRD2	drug	opioid	27547496	VPA treatment also significantly increased DA D2 receptor (<strong>Drd2</strong>) expression, especially in the <b>opioid</b> dependent iPSC cell lines.
+DRD2	addiction	relapse	27510492	Future research should be directed at asking the question; Would "dopamine agonist therapy" using KB220 variants reduce methylation and increase acetyl groups to enhance <strong>DRD2</strong> expression especially in <strong>DRD2</strong> A1 allele carriers and lead to increased dopamine function and a reduction of drug and non drug <b>seeking</b> behaviors?
+DRD2	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of catechol O methyltransferase (COMT), dopamine receptor D2 (<strong>DRD2</strong>) gene score and <b>smoking</b> cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (ANKK1), dopamine transporter (SLC6A3), dopamine receptor D4 (DRD4) gene score and <b>smoking</b> cessation.
+DRD2	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of catechol O methyltransferase (COMT), <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) gene score and <b>smoking</b> cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (ANKK1), dopamine transporter (SLC6A3), dopamine receptor D4 (DRD4) gene score and <b>smoking</b> cessation.
+DRD2	drug	alcohol	27447243	Association study of <strong>DRD2</strong> A2/A1, DRD3 Ser9Gly, DβH  1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A polymorphisms with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	27447243	Association study of <strong>DRD2</strong> A2/A1, DRD3 Ser9Gly, DβH  1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A polymorphisms with alcohol <b>dependence</b>.
+DRD2	drug	opioid	27447243	Genes of dopaminergic (<strong>DRD2</strong>, DRD3 and DβH), <b>opioid</b> (OPRM1) and glutaminergic (GRIK1) systems mediate the dependent behavior via different mechanisms; however, they all target the serotonergic and dopaminergic pathways in the ventral tegmental area.
+DRD2	drug	alcohol	27447243	In the present study, <strong>DRD2</strong> A2/A1, DRD3 Ser9Gly, DβH  1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A polymorphisms and their interactions were analyzed in 72 <b>alcohol</b> dependent patients and 74 controls of Greek Cypriot origin, using the PCR RFLP method.
+DRD2	drug	alcohol	27447243	No differences were found in the genotype or allele distribution of <strong>DRD2</strong> A2/A1, DRD3 Ser9Gly, DβH  1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A between <b>alcohol</b> dependent patients and controls.
+DRD2	drug	alcohol	27431292	Altogether, the conditional <strong>Drd2</strong> knockout model studied here revealed the overall fundamental contribution of D2R in motor functions and explains some of the side effects elicited by D2R blockers when used in neurological and psychiatric conditions, including schizophrenia, bipolar disorder, Tourette's syndrome, dementia, <b>alcohol</b> induced delusions and obsessive compulsive disorder.
+DRD2	addiction	addiction	27431292	Altogether, the conditional <strong>Drd2</strong> knockout model studied here revealed the overall fundamental contribution of D2R in motor functions and explains some of the side effects elicited by D2R blockers when used in neurological and psychiatric conditions, including schizophrenia, bipolar disorder, Tourette's syndrome, dementia, alcohol induced delusions and obsessive <b>compulsive</b> disorder.
+DRD2	drug	nicotine	27428758	<b>Nicotine</b> increased <strong>Drd2</strong> mRNA expression only in minimum preferring female rats in STR and PFC.
+DRD2	drug	alcohol	27399274	This study investigated the effect of the dopamine related polymorphism in the <strong>DRD2</strong>/ANKK1 gene (rs1800497) and a serotonin related polymorphism in the HTR2A gene (rs6313) on associations between impulsivity, cognition, and <b>alcohol</b> misuse in 120 emerging adults (18 21years).
+DRD2	drug	alcohol	27396498	The present study examined the association between self reported concussion history and genetics (apolipoprotein E [APOE], brain derived neurotrophic factor [BDNF], and D2 dopamine receptor genes [<strong>DRD2</strong>]), trait personality measures (impulsive sensation seeking and trait aggression hostility), and current <b>alcohol</b> use.
+DRD2	addiction	relapse	27396498	The present study examined the association between self reported concussion history and genetics (apolipoprotein E [APOE], brain derived neurotrophic factor [BDNF], and D2 dopamine receptor genes [<strong>DRD2</strong>]), trait personality measures (impulsive sensation <b>seeking</b> and trait aggression hostility), and current alcohol use.
+DRD2	drug	alcohol	27174576	In 1990, Blum and associates provided the first confirmed genetic link between the <strong>DRD2</strong> polymorphisms and <b>alcoholism</b>.
+DRD2	drug	alcohol	27045283	Corrigendum to "<strong>DRD2</strong>/ANKK1 TaqI A genotype moderates the relationship between alexithymia and the relative value of <b>alcohol</b> among male college binge drinkers" [Pharmacol.
+DRD2	addiction	intoxication	27045283	Corrigendum to "<strong>DRD2</strong>/ANKK1 TaqI A genotype moderates the relationship between alexithymia and the relative value of alcohol among male college <b>binge</b> drinkers" [Pharmacol.
+DRD2	addiction	intoxication	26950642	Epistatic interactions involving <strong>DRD2</strong>, DRD4, and COMT polymorphisms and risk of substance abuse in women with <b>binge</b> purge eating disturbances.
+DRD2	addiction	intoxication	26950642	We examined the implications of variations of selected, dopamine relevant polymorphisms (<strong>DRD2</strong> Taq1A, DRD4 7R, and COMT) for risk of substance abuse in women with <b>binge</b> purge eating syndromes.
+DRD2	drug	cannabinoid	26833047	An Information Theoretical Study of the Epistasis Between the CNR1 1359 G/A Polymorphism and the Taq1A and Taq1B <strong>DRD2</strong> Polymorphisms: Assessing the Susceptibility to <b>Cannabis</b> Addiction in a Turkish Population.
+DRD2	addiction	addiction	26833047	An Information Theoretical Study of the Epistasis Between the CNR1 1359 G/A Polymorphism and the Taq1A and Taq1B <strong>DRD2</strong> Polymorphisms: Assessing the Susceptibility to Cannabis <b>Addiction</b> in a Turkish Population.
+DRD2	drug	cannabinoid	26833047	In this study, we discuss the interaction between the 1359 G/A polymorphism of the CNR1 gene and the <strong>DRD2</strong> gene polymorphisms and the net effect of any possible epistasis on the <b>cannabis</b> addiction phenotype in a Turkish population.
+DRD2	addiction	addiction	26833047	In this study, we discuss the interaction between the 1359 G/A polymorphism of the CNR1 gene and the <strong>DRD2</strong> gene polymorphisms and the net effect of any possible epistasis on the cannabis <b>addiction</b> phenotype in a Turkish population.
+DRD2	drug	cannabinoid	26833047	We hypothesize that overlapping expressions of CB1 and D2R is the cause of CB1 D2R interactions in cases of substance abuse and the different polymorphisms of CNR1 and <strong>DRD2</strong> genes may have decisive roles in the nature of these interactions in terms of promoting or alleviating the <b>cannabis</b> addiction risk factor of the individual.
+DRD2	addiction	addiction	26833047	We hypothesize that overlapping expressions of CB1 and D2R is the cause of CB1 D2R interactions in cases of substance abuse and the different polymorphisms of CNR1 and <strong>DRD2</strong> genes may have decisive roles in the nature of these interactions in terms of promoting or alleviating the cannabis <b>addiction</b> risk factor of the individual.
+DRD2	drug	cannabinoid	26756393	The association between young adult patterns of <b>cannabis</b> use or <b>cannabis</b> abuse/dependence was tested with genetic variation in the <b>cannabinoid</b> gene, CNR1, the ANKK1 <strong>DRD2</strong> gene, and childhood developmental trajectories of P300.
+DRD2	addiction	dependence	26756393	The association between young adult patterns of cannabis use or cannabis abuse/<b>dependence</b> was tested with genetic variation in the cannabinoid gene, CNR1, the ANKK1 <strong>DRD2</strong> gene, and childhood developmental trajectories of P300.
+DRD2	drug	alcohol	28300818	[An effect of cabergoline on <b>alcohol</b> consumption and <strong>DRD2</strong> expression in the brain of rats with chronic <b>alcohol</b> intoxication].
+DRD2	addiction	intoxication	28300818	[An effect of cabergoline on alcohol consumption and <strong>DRD2</strong> expression in the brain of rats with chronic alcohol <b>intoxication</b>].
+DRD2	drug	alcohol	28300818	To examine this possibility, cabergoline effects on <b>alcohol</b> consumption and brain <strong>DRD2</strong> expression in rats with chronic <b>alcohol</b> intoxication were studied.
+DRD2	addiction	intoxication	28300818	To examine this possibility, cabergoline effects on alcohol consumption and brain <strong>DRD2</strong> expression in rats with chronic alcohol <b>intoxication</b> were studied.
+DRD2	drug	alcohol	28300818	At the same time, cabergoline elevates the <strong>DRD2</strong> expression in the midbrain and striatum of high <b>alcohol</b> preferring rats but not in intact (<b>alcohol</b> naïve) animals.
+DRD2	drug	alcohol	28300818	The involvement of cabergoline in the <strong>DRD2</strong> expression may lead to the decrease in <b>alcohol</b> motivation.
+DRD2	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (OPRM1), kappa <b>opioid</b> receptors (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (<strong>DRD2</strong>) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (SLC6A3, DAT1) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+DRD2	addiction	relapse	28300812	Regardless of treatment several polymorphisms were associated with high risk of <b>relapse</b>: allele Т (rs510769) OPRM1 (р=0.053), allele А (rs1799971, A118G) OPRM1 (р=0.056), allele S exon III 48 bp DRD4 VNTR (р=0.001; HR=3.1 (ДИ 95% 1.57 6.18); genotype combinations: DRD4   521 С/Т (ТТ) + <strong>DRD2</strong> Nco I (TT), р=0.026; DRD4  521 С/Т (ТТ) + <strong>DRD2</strong>  141 С (II), р=0.011; DRD4   521 С/Т (ТТ) + OPRM1 A118G (rs1799971) (AA), р=0.011; <strong>DRD2</strong> Nco I(ТТ) + ADRA2A (СС), р=0.012; <strong>DRD2</strong> Nco I(ТТ) + OPRM1 A118G (AA), р=0.02.
+DRD2	drug	cannabinoid	26572896	Acute effects of cocaine and <b>cannabis</b> on reversal learning as a function of COMT and <strong>DRD2</strong> genotype.
+DRD2	drug	cocaine	26572896	Acute effects of <b>cocaine</b> and cannabis on reversal learning as a function of COMT and <strong>DRD2</strong> genotype.
+DRD2	drug	cannabinoid	26572896	In this study, we aimed to establish the acute effects of administration of <b>cannabis</b> and cocaine on valence dependent reversal learning as a function of <strong>DRD2</strong> Taq1A (rs1800497) and COMT Val108/158Met (rs4680) genotype.
+DRD2	drug	cocaine	26572896	In this study, we aimed to establish the acute effects of administration of cannabis and <b>cocaine</b> on valence dependent reversal learning as a function of <strong>DRD2</strong> Taq1A (rs1800497) and COMT Val108/158Met (rs4680) genotype.
+DRD2	drug	cocaine	26572896	Effects of <b>cocaine</b> depended on the <strong>DRD2</strong> genotype, as increases in proportion correct were seen only in the A1 carriers, and not in the A2/A2 homozygotes.
+DRD2	drug	alcohol	26509893	Fetal <b>Alcohol</b> Exposure Reduces <strong>Dopamine Receptor D2</strong> and Increases Pituitary Weight and Prolactin Production via Epigenetic Mechanisms.
+DRD2	drug	nicotine	26449981	Parental smoke exposure and the development of <b>nicotine</b> craving in adolescent novice <b>smokers</b>: the roles of <strong>DRD2</strong>, DRD4, and OPRM1 genotypes.
+DRD2	addiction	relapse	26449981	Parental smoke exposure and the development of nicotine <b>craving</b> in adolescent novice smokers: the roles of <strong>DRD2</strong>, DRD4, and OPRM1 genotypes.
+DRD2	drug	nicotine	26449981	The aim of this study was to identify specific genetic (i.e., <strong>DRD2</strong> Taq1A, DRD4 48 bp VNTR, and OPRM1 A118G polymorphisms) and environmental mechanisms that underlie the emergence of both cue induced and cognitive craving among adolescent novice <b>smokers</b>.
+DRD2	addiction	relapse	26449981	The aim of this study was to identify specific genetic (i.e., <strong>DRD2</strong> Taq1A, DRD4 48 bp VNTR, and OPRM1 A118G polymorphisms) and environmental mechanisms that underlie the emergence of both cue induced and cognitive <b>craving</b> among adolescent novice smokers.
+DRD2	addiction	relapse	26449981	For both cue induced and cognitive <b>craving</b>, significant interaction effects were found for <strong>DRD2</strong> Taq1A with parental smoke exposure.
+DRD2	drug	nicotine	26449981	Previous studies identified <strong>DRD2</strong> Taq1A A1 allele carriers as vulnerable to developing <b>nicotine</b> dependence.
+DRD2	addiction	dependence	26449981	Previous studies identified <strong>DRD2</strong> Taq1A A1 allele carriers as vulnerable to developing nicotine <b>dependence</b>.
+DRD2	drug	nicotine	26449981	However, this study showed that parental <b>smoking</b> increased the chances of developing dependence more rapidly for early adolescents who are considered to be less sensitive to the rewarding effects of <b>nicotine</b> according to their <strong>DRD2</strong> Taq1A genotype.
+DRD2	addiction	dependence	26449981	However, this study showed that parental smoking increased the chances of developing <b>dependence</b> more rapidly for early adolescents who are considered to be less sensitive to the rewarding effects of nicotine according to their <strong>DRD2</strong> Taq1A genotype.
+DRD2	drug	alcohol	26447226	Conversely, some alleles of the 12 SNPs from the <strong>DRD2</strong> locus and the 5 from the MAOA locus showed significant associations with excessive <b>alcohol</b> consumption.
+DRD2	drug	alcohol	26447226	Namely, rs10891556 (<strong>DRD2</strong>) proved to be the only SNP positively correlated with excessive <b>alcohol</b> consumption in both sexes.
+DRD2	drug	alcohol	26447226	<strong>DRD2</strong> rs1800497 and rs877138 were significantly associated in men, whereas <strong>DRD2</strong> rs17601612 and rs4936271 and MAOA rs5906898 were associated with excessive <b>alcohol</b> consumption in women.
+DRD2	drug	opioid	26437921	Contribution of BDNF and <strong>DRD2</strong> genetic polymorphisms to continued <b>opioid</b> use in patients receiving <b>methadone</b> treatment for <b>opioid</b> use disorder: an observational study.
+DRD2	drug	opioid	26437921	The aim of this study was to investigate the effect of brain derived neurotrophic factor (BDNF) and dopamine receptor D2 (<strong>DRD2</strong>) polymorphisms on continued <b>opioid</b> use among patients on <b>methadone</b> treatment for <b>opioid</b> use disorder.
+DRD2	drug	opioid	26437921	The aim of this study was to investigate the effect of brain derived neurotrophic factor (BDNF) and <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) polymorphisms on continued <b>opioid</b> use among patients on <b>methadone</b> treatment for <b>opioid</b> use disorder.
+DRD2	drug	opioid	26437921	BDNF 196G>A (rs6265) and <strong>DRD2</strong> 241A>G (rs1799978) genetic variants were examined in patients with <b>opioid</b> use disorder who were recruited from <b>methadone</b> treatment clinics across Southern Ontario, Canada.
+DRD2	drug	opioid	26437921	Despite an association of BDNF rs6265 and <strong>DRD2</strong> rs1799978 with addictive behaviors, these variants were not associated with continued illicit <b>opioid</b> use in patients treated with <b>methadone</b>.
+DRD2	addiction	addiction	26437921	Despite an association of BDNF rs6265 and <strong>DRD2</strong> rs1799978 with <b>addictive</b> behaviors, these variants were not associated with continued illicit opioid use in patients treated with methadone.
+DRD2	drug	nicotine	26416825	Three hundred sixty four Mexican Mestizo Mexico City residents from 87 families with at least one <b>smoker</b> were assessed for association of 12 gene variants of six candidate genes (CHRNA4, CHRNB2, <strong>DRD2</strong>, ANKK1, SLC6A3, and CYP2A6) with cigarette consumption, age of initiation and <b>smoking</b> duration.
+DRD2	drug	amphetamine	26334786	<b>Methamphetamine</b> blocks exercise effects on Bdnf and <strong>Drd2</strong> gene expression in frontal cortex and striatum.
+DRD2	drug	amphetamine	26334786	<strong>Drd2</strong> and Bdnf mRNA levels were impacted independently by exercise and <b>methamphetamine</b>, but exposure to <b>methamphetamine</b> prior to the initiation of exercise blocked the exercise induced changes seen in rats treated with saline.
+DRD2	drug	opioid	26288297	It was genotyped polymorphisms in the following genes: mu <b>opioid</b> receptor (OPRM1), kappa <b>opioid</b> receptor (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (<strong>DRD2</strong>) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (DAT1).
+DRD2	addiction	relapse	26288297	Regardless of treatment several polymorphisms of these genes were associated with high risk of <b>relapse</b>: an allele L (2R) DRD4 120bp (p=0.05; OR (95% CI)=3.3(1.1 10.1)); an allele С <strong>DRD2</strong> NcoI (р=0,051; OR (95% CI)=2,86 (1,09 7,52)); the genotype 9.9 DAT VNTR 40bp (р=0,04; OR (95% CI)=1,4 (1,3 1,5)); on the contrary, (СС+СТ) (ТТ)) variants of OPRK1 DRD2Ncol increased a chance to complete treatment program (р=0,004; OR (95% CI)=7.4 (1.8 30.4)), Kaplan Meier survival analysis (р=0,016).
+DRD2	addiction	intoxication	26260431	Twenty lean females (mean BMI 22) and 25 non <b>binge</b> eating morbidly obese females (mean BMI 41) underwent two positron emission tomography scans with [(11)C]carfentanil and [(11)C]raclopride to measure the MOR and dopamine D2 receptor (<strong>DRD2</strong>) availability, respectively.
+DRD2	addiction	reward	26260431	Moreover, <strong>DRD2</strong> availability in the ventral striatum was associated with MOR availability in other regions of the <b>reward</b> circuitry, particularly in the ventral tegmental area.
+DRD2	drug	nicotine	26192093	Moreover, we observed an overexpression of the <strong>DRD2</strong> gene in adult offspring stressed in utero and a downregulation in the PS NIC group (PS rats treated with <b>nicotine</b>) compared with their control counterparts (C NIC).
+DRD2	drug	alcohol	26146874	Polymorphisms of the <strong>DRD2</strong>, ANKK1, DAT1, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of <b>alcohol</b>, opioid, and cocaine use disorders.
+DRD2	drug	cocaine	26146874	Polymorphisms of the <strong>DRD2</strong>, ANKK1, DAT1, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of alcohol, opioid, and <b>cocaine</b> use disorders.
+DRD2	drug	opioid	26146874	Polymorphisms of the <strong>DRD2</strong>, ANKK1, DAT1, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of alcohol, <b>opioid</b>, and cocaine use disorders.
+DRD2	drug	opioid	26138154	Association between the traditional Chinese medicine pathological factors of <b>opioid</b> addiction and <strong>DRD2</strong>/ANKK1 TaqIA polymorphisms.
+DRD2	addiction	addiction	26138154	Association between the traditional Chinese medicine pathological factors of opioid <b>addiction</b> and <strong>DRD2</strong>/ANKK1 TaqIA polymorphisms.
+DRD2	drug	opioid	26138154	The ANKK1 TaqIA (A1/A2) [rs1800497(T/C)] of the dopamine D2 receptor (<strong>DRD2</strong>) polymorphisms were genotyped in a case control sample consisting of 347 <b>opioid</b> addicts and 155 healthy controls with RT PCR and the TCM pathological factors were collected by means of Syndrome Elements Differentiation in the case control sample.
+DRD2	drug	opioid	26138154	<strong>DRD2</strong>/ANKK1 TaqIA Polymorphisms has no relation with <b>opioid</b> addiction relapse; but for those who were diagnosed with phlegm syndrome, <strong>DRD2</strong>/ANKK1 TaqIA Polymorphisms affect the replapse of apioid addiction (P < 0.05).
+DRD2	addiction	addiction	26138154	<strong>DRD2</strong>/ANKK1 TaqIA Polymorphisms has no relation with opioid <b>addiction</b> relapse; but for those who were diagnosed with phlegm syndrome, <strong>DRD2</strong>/ANKK1 TaqIA Polymorphisms affect the replapse of apioid <b>addiction</b> (P < 0.05).
+DRD2	addiction	relapse	26138154	<strong>DRD2</strong>/ANKK1 TaqIA Polymorphisms has no relation with opioid addiction <b>relapse</b>; but for those who were diagnosed with phlegm syndrome, <strong>DRD2</strong>/ANKK1 TaqIA Polymorphisms affect the replapse of apioid addiction (P < 0.05).
+DRD2	drug	opioid	26138154	<strong>DRD2</strong>/ANKK1 TaqIA is associated with <b>opioid</b> addict and it is obvious in <b>opioid</b> addicts who suffer from the phlegm syndrome.
+DRD2	addiction	addiction	26044620	Connect function from IPA My Pathway toolbox showed that <strong>DRD2</strong> is the gene common to both the list of genetic variations associated with all three <b>addiction</b> phenotypes and the components of the brain neuronal signaling network involved in substance <b>addiction</b>.
+DRD2	drug	alcohol	26029066	Studies have shown that exposure to chronic mild stress decreases <b>ethanol</b> intake and preference in dopamine D2 receptor wild type mice (<strong>Drd2</strong> (+/+)), while it increases intake in heterozygous (<strong>Drd2</strong> (+/ )) and knockout (<strong>Drd2</strong> ( / )) mice.
+DRD2	drug	alcohol	26029066	Receptor levels were measured in the basal forebrain of <strong>Drd2</strong> (+/+), <strong>Drd2</strong> (+/ ), and <strong>Drd2</strong> ( / ) mice belonging to one of four groups: control (C), <b>ethanol</b> intake (E), chronic mild stress exposure (S), and <b>ethanol</b> intake under chronic mild stress (ES).
+DRD2	drug	alcohol	26029066	<b>Ethanol</b> intake in <strong>Drd2</strong> (+/+) mice was negatively correlated with striatal D2 receptor levels.
+DRD2	drug	alcohol	26029066	In <strong>Drd2</strong>( / ) mice, <b>ethanol</b> intake was positively correlated with DAT levels in all regions studied.
+DRD2	drug	alcohol	26029066	In mice with low <strong>Drd2</strong> expression, where <strong>DRD2</strong> levels are not further modulated, <b>ethanol</b> intake is associated with DAT function which is upregulated under stress leading to <b>ethanol</b> overconsumption.
+DRD2	drug	nicotine	26015071	Although the effect of gene gene interaction on <b>nicotine</b> dopamine metabolism for <b>smoking</b> behavior has been reported, polymorphisms of dopamine D2 receptor (<strong>DRD2</strong>) and monoamine oxidase A (MAOA) have not been simultaneously examined among <b>smokers</b>.
+DRD2	drug	nicotine	26015071	In this study, 481 young Taiwanese men completed a self report questionnaire on <b>smoking</b> status, and data were obtained on polymorphisms of <strong>DRD2</strong> rs1800497, <strong>DRD2</strong> rs1079597, MAOA rs309850, and MAOA rs1137070, urinary <b>nicotine</b>, and urinary cotinine.
+DRD2	drug	nicotine	26015071	Among <b>smokers</b> with <strong>DRD2</strong> rs1079597 GG//MAOA rs309850 3 repeat, the OR of heavier <b>smoking</b> was 2.67 times higher (95% confidence interval [CI]: [1.08, 6.59], p = .031) and the score on the Fagerstrom test for <b>nicotine</b> dependence was higher (4.26 vs. 2.83) than in those with <strong>DRD2</strong> rs1079597 AA//MAOA rs309850 3 repeat.
+DRD2	addiction	dependence	26015071	Among smokers with <strong>DRD2</strong> rs1079597 GG//MAOA rs309850 3 repeat, the OR of heavier smoking was 2.67 times higher (95% confidence interval [CI]: [1.08, 6.59], p = .031) and the score on the Fagerstrom test for nicotine <b>dependence</b> was higher (4.26 vs. 2.83) than in those with <strong>DRD2</strong> rs1079597 AA//MAOA rs309850 3 repeat.
+DRD2	drug	nicotine	26015071	These findings suggest that the interaction of <strong>DRD2</strong> rs1079597 and MAOA rs309850 3 repeat affects <b>smoking</b> intensity in young Taiwanese men.
+DRD2	addiction	addiction	25958762	Finally, <strong>DRD2</strong> and ANKK1 genes, involved in the dopaminergic pathway, and which were initially associated with AD, are now considered to be involved in a broader phenotype (<b>addiction</b> to psychoactive substances) including opiates.
+DRD2	drug	nicotine	25907750	In adolescent and adult male rats, we examined (1) alterations occurring in dopamine receptor related mRNAs (DRD1, <strong>DRD2</strong>, DRD3 and D3nf) at two time points during a sensitizing regimen of <b>nicotine</b> and (2) whether DRD3 antagonism either during the initial treatment (induction) or at a later challenge exposure (expression) is able to block <b>nicotine</b> sensitization.
+DRD2	addiction	sensitization	25907750	In adolescent and adult male rats, we examined (1) alterations occurring in dopamine receptor related mRNAs (DRD1, <strong>DRD2</strong>, DRD3 and D3nf) at two time points during a sensitizing regimen of nicotine and (2) whether DRD3 antagonism either during the initial treatment (induction) or at a later challenge exposure (expression) is able to block nicotine <b>sensitization</b>.
+DRD2	drug	nicotine	25907750	Adolescents and adults showed opposite DRD1 mRNA responses to <b>nicotine</b> treatment, while no age  and <b>nicotine</b> related changes in <strong>DRD2</strong> mRNA were observed.
+DRD2	drug	benzodiazepine	25841786	Our results show elevated <strong>Drd2</strong> expression levels in the nucleus accumbens (NAcc) of prenatally stressed rats compared to control subjects, while repeated <b>diazepam</b> administration in adulthood down regulated <strong>Drd2</strong> expression and prevented the effect of prenatal stress.
+DRD2	drug	cocaine	25735756	Moreover, knockout of the gene encoding the D2R receptor (<strong>Drd2</strong>) in dopamine neurons has been shown to enhance the locomotor response to <b>cocaine</b> in mice.
+DRD2	drug	alcohol	25684044	Association study of the SLC6A3 VNTR (DAT) and <strong>DRD2</strong>/ANKK1 Taq1A polymorphisms with <b>alcohol</b> dependence in a population from northeastern Brazil.
+DRD2	addiction	dependence	25684044	Association study of the SLC6A3 VNTR (DAT) and <strong>DRD2</strong>/ANKK1 Taq1A polymorphisms with alcohol <b>dependence</b> in a population from northeastern Brazil.
+DRD2	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., <strong>DRD2</strong>, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+DRD2	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., <strong>DRD2</strong>, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+DRD2	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., <strong>DRD2</strong>, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+DRD2	drug	alcohol	25603899	SNPs in the <b>alcohol</b> metabolizing genes, in the cholinergic gene cluster CHRNA5 CHRNA3 CHRNB4, and in the <strong>DRD2</strong> and ANNK1 genes, are, to date, the most replicated and significant gene variants associated with <b>alcohol</b>  and nicotine related phenotypes.
+DRD2	drug	nicotine	25603899	SNPs in the alcohol metabolizing genes, in the cholinergic gene cluster CHRNA5 CHRNA3 CHRNB4, and in the <strong>DRD2</strong> and ANNK1 genes, are, to date, the most replicated and significant gene variants associated with alcohol  and <b>nicotine</b> related phenotypes.
+DRD2	drug	cocaine	25596492	In the present study, pharmacological inhibition of PKC in the NAc shell attenuated <b>cocaine</b> seeking induced by intra accumbens shell microinjection of a <strong>D2DR</strong> agonist, but not a D1DR agonist.
+DRD2	addiction	relapse	25596492	In the present study, pharmacological inhibition of PKC in the NAc shell attenuated cocaine <b>seeking</b> induced by intra accumbens shell microinjection of a <strong>D2DR</strong> agonist, but not a D1DR agonist.
+DRD2	drug	cocaine	25596492	Following the extinction of <b>cocaine</b> self administration, bath application of a PKC inhibitor produced similar effects on single evoked excitatory and inhibitory post synaptic currents in D1DR  and <strong>D2DR</strong> positive MSNs in the NAc shell.
+DRD2	drug	cocaine	25596492	Taken together, these findings indicate that the reinstatement of <b>cocaine</b> seeking is at least partially due to <strong>D2DR</strong> dependent increases in PKC signaling in the NAc shell, which reduce excitatory synaptic efficacy in <strong>D2DR</strong> expressing MSNs.
+DRD2	addiction	relapse	25596492	Taken together, these findings indicate that the <b>reinstatement</b> of cocaine <b>seeking</b> is at least partially due to <strong>D2DR</strong> dependent increases in PKC signaling in the NAc shell, which reduce excitatory synaptic efficacy in <strong>D2DR</strong> expressing MSNs.
+DRD2	drug	benzodiazepine	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) methadone), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the <b>midazolam</b> test, R,S methadone trough concentration and clinically significant polymorphisms of the OPRM1, <strong>DRD2</strong>, COMT, ABCB1, CYP2B6, CYP3A5, CYP2C19 and CYP2D6 genes.
+DRD2	drug	opioid	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) <b>methadone</b>), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the midazolam test, R,S <b>methadone</b> trough concentration and clinically significant polymorphisms of the OPRM1, <strong>DRD2</strong>, COMT, ABCB1, CYP2B6, CYP3A5, CYP2C19 and CYP2D6 genes.
+DRD2	drug	alcohol	27617300	Earlier work from our laboratory, showing anti addiction activity of a nutraceutical consisting of amino acid precursors and enkephalinase inhibition properties and our discovery of the first polymorphic gene (Dopamine D2 Receptor Gene [<strong>DRD2</strong>]) to associate with severe <b>alcoholism</b> serves as a blue print for the development of "Personalized Medicine" in addiction.
+DRD2	addiction	addiction	27617300	Earlier work from our laboratory, showing anti <b>addiction</b> activity of a nutraceutical consisting of amino acid precursors and enkephalinase inhibition properties and our discovery of the first polymorphic gene (Dopamine D2 Receptor Gene [<strong>DRD2</strong>]) to associate with severe alcoholism serves as a blue print for the development of "Personalized Medicine" in <b>addiction</b>.
+DRD2	drug	nicotine	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (ANKK1), which is adjacent to the dopamine D2 receptor gene (<strong>DRD2</strong>), and the dopamine transporter (SLC6A3) and cytochrome P450 2A6 (CYP2A6) genes influence <b>smoking</b> cessation and <b>nicotine</b> dependence in a Japanese population.
+DRD2	addiction	dependence	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (ANKK1), which is adjacent to the dopamine D2 receptor gene (<strong>DRD2</strong>), and the dopamine transporter (SLC6A3) and cytochrome P450 2A6 (CYP2A6) genes influence smoking cessation and nicotine <b>dependence</b> in a Japanese population.
+DRD2	drug	nicotine	25526961	In 96 current and former <b>smokers</b>, genotyping frequencies for the ANKK1/<strong>DRD2</strong> TaqIA, SLC6A3 VNTR, and CYP2A6 polymorphisms were subjected to chi square analysis, and regression analyses were used to determine the association of the genotypes of current <b>smokers</b> with a Heavy <b>Smoking</b> Index, in addition to evaluating the effect of the subjects' <b>smoking</b> history on the association.
+DRD2	drug	opioid	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single <b>morphine</b> administration, <b>morphine</b> dependence and withdrawal on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (<strong>DRD2</strong>), DA 1 receptor subtype as well as tyrosine hydroxylase (TH) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+DRD2	addiction	dependence	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single morphine administration, morphine <b>dependence</b> and withdrawal on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (<strong>DRD2</strong>), DA 1 receptor subtype as well as tyrosine hydroxylase (TH) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+DRD2	addiction	withdrawal	25522207	Using quantitative real time polymerase chain reaction, immunofluorescence and Western blotting, we studied the effects of single morphine administration, morphine dependence and <b>withdrawal</b> on the DA markers DA transporters (DAT), vesicular monoamine transporters (VMAT2) and DA 2 receptor subtype (<strong>DRD2</strong>), DA 1 receptor subtype as well as tyrosine hydroxylase (TH) in the ventral tegmental area (VTA) and/or nucleus accumbens (NAc).
+DRD2	drug	opioid	25522207	We found that the increased Nurr1 and/or Pitx3 levels during <b>morphine</b> dependence and in <b>morphine</b> withdrawn rats were associated to an increase of DAT, VMAT2 and <strong>DRD2</strong>.
+DRD2	addiction	dependence	25522207	We found that the increased Nurr1 and/or Pitx3 levels during morphine <b>dependence</b> and in morphine withdrawn rats were associated to an increase of DAT, VMAT2 and <strong>DRD2</strong>.
+DRD2	addiction	dependence	25500252	Association between <strong>DRD2</strong>/ANKK1 TaqIA polymorphism and common illicit drug <b>dependence</b>: evidence from a meta analysis.
+DRD2	drug	cannabinoid	25500252	Growing evidence indicated conflicting results about the dopamine receptor D2 (<strong>DRD2</strong>)/kinase domain containing 1 gene (ANKK1) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug dependence risk including stimulants, opioid and <b>marijuana</b>.
+DRD2	drug	opioid	25500252	Growing evidence indicated conflicting results about the dopamine receptor D2 (<strong>DRD2</strong>)/kinase domain containing 1 gene (ANKK1) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug dependence risk including stimulants, <b>opioid</b> and marijuana.
+DRD2	addiction	dependence	25500252	Growing evidence indicated conflicting results about the dopamine receptor D2 (<strong>DRD2</strong>)/kinase domain containing 1 gene (ANKK1) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug <b>dependence</b> risk including stimulants, opioid and marijuana.
+DRD2	drug	cannabinoid	25500252	Growing evidence indicated conflicting results about the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>)/kinase domain containing 1 gene (ANKK1) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug dependence risk including stimulants, opioid and <b>marijuana</b>.
+DRD2	drug	opioid	25500252	Growing evidence indicated conflicting results about the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>)/kinase domain containing 1 gene (ANKK1) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug dependence risk including stimulants, <b>opioid</b> and marijuana.
+DRD2	addiction	dependence	25500252	Growing evidence indicated conflicting results about the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>)/kinase domain containing 1 gene (ANKK1) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug <b>dependence</b> risk including stimulants, opioid and marijuana.
+DRD2	drug	opioid	25500252	We found the <strong>DRD2</strong>/ANKK1 TaqIA polymorphism was significantly associated with increased risk of <b>opioid</b> dependence under homozygote, dominant, and recessive genetic model, respectively (homozygote: OR=1.546, 95%CI=1.279 1.87; dominant: OR=1.265, 95%CI=1.055 1.516; recessive: OR=1.409, 95%CI=1.182 1.680).
+DRD2	addiction	dependence	25500252	We found the <strong>DRD2</strong>/ANKK1 TaqIA polymorphism was significantly associated with increased risk of opioid <b>dependence</b> under homozygote, dominant, and recessive genetic model, respectively (homozygote: OR=1.546, 95%CI=1.279 1.87; dominant: OR=1.265, 95%CI=1.055 1.516; recessive: OR=1.409, 95%CI=1.182 1.680).
+DRD2	drug	cannabinoid	25500252	The current meta analysis suggested that <strong>DRD2</strong>/ANKK1 TaqIA polymorphism might be associated with opioid dependence risk, but not associated with stimulants or <b>marijuana</b> dependence.
+DRD2	drug	opioid	25500252	The current meta analysis suggested that <strong>DRD2</strong>/ANKK1 TaqIA polymorphism might be associated with <b>opioid</b> dependence risk, but not associated with stimulants or marijuana dependence.
+DRD2	addiction	dependence	25500252	The current meta analysis suggested that <strong>DRD2</strong>/ANKK1 TaqIA polymorphism might be associated with opioid <b>dependence</b> risk, but not associated with stimulants or marijuana <b>dependence</b>.
+DRD2	drug	nicotine	25450229	We also observed a significant excess of rare nonsynonymous variants exclusive to EA <b>smokers</b> in NRXN1, CHRNA9, TAS2R38, GRIN3A, DBH, ANKK1/<strong>DRD2</strong>, NRXN3 and CDH13 with WSS P values between 3.5 × 10( 5) and 1 × 10( 6).
+DRD2	drug	alcohol	25415204	Suicidal behavior and haplotypes of the dopamine receptor gene (<strong>DRD2</strong>) and ANKK1 gene polymorphisms in patients with <b>alcohol</b> dependence  preliminary report.
+DRD2	addiction	dependence	25415204	Suicidal behavior and haplotypes of the dopamine receptor gene (<strong>DRD2</strong>) and ANKK1 gene polymorphisms in patients with alcohol <b>dependence</b>  preliminary report.
+DRD2	drug	alcohol	25415204	In our study,  we have analyzed selected SNPs polymorphisms in the <strong>DRD2</strong> and ANKK1 genes in patients with <b>alcohol</b> dependence syndrome (169 Caucasian subjects) including a subgroup of individuals (n = 61) who have experienced at least one suicide attempt.
+DRD2	addiction	dependence	25415204	In our study,  we have analyzed selected SNPs polymorphisms in the <strong>DRD2</strong> and ANKK1 genes in patients with alcohol <b>dependence</b> syndrome (169 Caucasian subjects) including a subgroup of individuals (n = 61) who have experienced at least one suicide attempt.
+DRD2	drug	alcohol	25380208	Association and family studies of <strong>DRD2</strong> gene polymorphisms in <b>alcohol</b> dependence syndrome.
+DRD2	addiction	dependence	25380208	Association and family studies of <strong>DRD2</strong> gene polymorphisms in alcohol <b>dependence</b> syndrome.
+DRD2	drug	alcohol	25380208	The human dopamine receptor 2 gene <strong>DRD2</strong> plays a central role in susceptibility to <b>Alcohol</b> Dependence Syndrome (ADS).
+DRD2	addiction	dependence	25380208	The human dopamine receptor 2 gene <strong>DRD2</strong> plays a central role in susceptibility to Alcohol <b>Dependence</b> Syndrome (ADS).
+DRD2	drug	alcohol	25380208	The aim of this study was to evaluate 3 single nucleotide polymorphisms: D2 (rs1076560), Tag1D (rs1800498), Tag1B (rs1079597) located in dopamine receptor 2 <strong>DRD2</strong> gene and its role in <b>alcohol</b> dependence.
+DRD2	addiction	dependence	25380208	The aim of this study was to evaluate 3 single nucleotide polymorphisms: D2 (rs1076560), Tag1D (rs1800498), Tag1B (rs1079597) located in dopamine receptor 2 <strong>DRD2</strong> gene and its role in alcohol <b>dependence</b>.
+DRD2	drug	alcohol	25380208	Further research is needed to determine the actual contribution of <strong>DRD2</strong> gene in the pathogenesis of <b>alcoholism</b>.
+DRD2	drug	alcohol	25364629	Caudate Volume in Offspring at Ultra High Risk for <b>Alcohol</b> Dependence: COMT Val158Met, <strong>DRD2</strong>, Externalizing Disorders, and Working Memory.
+DRD2	addiction	dependence	25364629	Caudate Volume in Offspring at Ultra High Risk for Alcohol <b>Dependence</b>: COMT Val158Met, <strong>DRD2</strong>, Externalizing Disorders, and Working Memory.
+DRD2	drug	cocaine	25319571	Confirming our previous results, <b>cocaine</b> withdrawal selectively impaired DHPG LTD in NAc shell Drd1 expressing direct and <strong>Drd2</strong> expressing indirect pathway MSNs.
+DRD2	addiction	withdrawal	25319571	Confirming our previous results, cocaine <b>withdrawal</b> selectively impaired DHPG LTD in NAc shell Drd1 expressing direct and <strong>Drd2</strong> expressing indirect pathway MSNs.
+DRD2	drug	alcohol	25307689	Association between dopamine D2 receptor (<strong>DRD2</strong>) genetic variants and <b>alcohol</b> dependence in Han Chinese in Taiwan.
+DRD2	addiction	dependence	25307689	Association between dopamine D2 receptor (<strong>DRD2</strong>) genetic variants and alcohol <b>dependence</b> in Han Chinese in Taiwan.
+DRD2	drug	nicotine	25273375	NCAM1 TTC12 ANKK1 <strong>DRD2</strong> variants and <b>smoking</b> motives as intermediate phenotypes for <b>nicotine</b> dependence.
+DRD2	addiction	dependence	25273375	NCAM1 TTC12 ANKK1 <strong>DRD2</strong> variants and smoking motives as intermediate phenotypes for nicotine <b>dependence</b>.
+DRD2	drug	nicotine	25273375	Based on prior evidence of the role of genetic variation in the NCAM1 TTC12 ANKK1 <strong>DRD2</strong> region on chromosome 11q23 in <b>smoking</b> behavior, associations among 12 region loci with <b>nicotine</b> dependence and PDM phenotypes were examined using haplotype and individual loci approaches.
+DRD2	addiction	dependence	25273375	Based on prior evidence of the role of genetic variation in the NCAM1 TTC12 ANKK1 <strong>DRD2</strong> region on chromosome 11q23 in smoking behavior, associations among 12 region loci with nicotine <b>dependence</b> and PDM phenotypes were examined using haplotype and individual loci approaches.
+DRD2	drug	nicotine	25273375	NCAM1 TTC12 ANKK1 <strong>DRD2</strong> region loci and haplotypes were significantly associated with the motive of Automaticity and, further, Automaticity significantly mediated associations among NCAM1 TTC12 ANKK1 <strong>DRD2</strong> cluster variants and <b>nicotine</b> dependence.
+DRD2	addiction	dependence	25273375	NCAM1 TTC12 ANKK1 <strong>DRD2</strong> region loci and haplotypes were significantly associated with the motive of Automaticity and, further, Automaticity significantly mediated associations among NCAM1 TTC12 ANKK1 <strong>DRD2</strong> cluster variants and nicotine <b>dependence</b>.
+DRD2	drug	nicotine	25273375	Further, NCAM1 TTC12 ANKK1 <strong>DRD2</strong> variants may increase the likelihood that a person will become dependent via a highly automatic <b>smoking</b> ritual that can be elicited with little awareness.
+DRD2	drug	alcohol	25139281	Considering new evidence supporting the association of <strong>DRD2</strong> and its adjacent gene ankyrin repeat and kinase domain containing 1 (ANKK1) with various addictions, in this paper, we provide an updated view of the involvement of variants in <strong>DRD2</strong> and ANKK1 in the etiology of nicotine dependence (ND) and <b>alcohol</b> dependence (AD) based on linkage, association, and molecular studies.
+DRD2	drug	nicotine	25139281	Considering new evidence supporting the association of <strong>DRD2</strong> and its adjacent gene ankyrin repeat and kinase domain containing 1 (ANKK1) with various addictions, in this paper, we provide an updated view of the involvement of variants in <strong>DRD2</strong> and ANKK1 in the etiology of <b>nicotine</b> dependence (ND) and alcohol dependence (AD) based on linkage, association, and molecular studies.
+DRD2	addiction	dependence	25139281	Considering new evidence supporting the association of <strong>DRD2</strong> and its adjacent gene ankyrin repeat and kinase domain containing 1 (ANKK1) with various addictions, in this paper, we provide an updated view of the involvement of variants in <strong>DRD2</strong> and ANKK1 in the etiology of nicotine <b>dependence</b> (ND) and alcohol <b>dependence</b> (AD) based on linkage, association, and molecular studies.
+DRD2	drug	alcohol	25053368	<b>Alcohol</b> abuse and HIV infection: role of <strong>DRD2</strong>.
+DRD2	drug	alcohol	25053368	Although previous studies have shown an association of D(2) dopamine receptor (<strong>DRD2</strong>) polymorphisms with severity of <b>alcohol</b> dependence, the expression of this allele risk on HIV patients with <b>alcohol</b> dependence has not been systematically explored.
+DRD2	addiction	dependence	25053368	Although previous studies have shown an association of D(2) dopamine receptor (<strong>DRD2</strong>) polymorphisms with severity of alcohol <b>dependence</b>, the expression of this allele risk on HIV patients with alcohol <b>dependence</b> has not been systematically explored.
+DRD2	drug	alcohol	25053368	In the current study, <strong>DRD2</strong> Taq1A and C957T SNP genotyping analyses were performed in 165 HIV infected <b>alcohol</b> abusers and the results were examined with immune status and CD4 counts.
+DRD2	drug	opioid	24956254	Nevertheless many genetic factors have been investigated including those affecting its metabolism (CYP2B6 consistent results), efflux transport (P gp inconsistent results), target μ <b>opioid</b> receptor (μ <b>opioid</b> receptor inconsistent results) and a host of other receptors (<strong>DRD2</strong>) and signaling elements (GIRK2 and ARRB2; not replicated).
+DRD2	drug	cannabinoid	26271761	Association of <strong>dopamine receptor D2</strong> TaqI A polymorphism and <b>cannabis</b> use disorder in Lagos, Nigeria.
+DRD2	drug	amphetamine	24785761	We measured striatal dopamine D2/3 receptor (<strong>DRD2</strong>/3) availability and <b>amphetamine</b> induced striatal dopamine release in 15 obese and 15 age matched, normal weight women using [(123)I]iodobenzamide single photon emission computed tomography (SPECT) imaging.
+DRD2	drug	alcohol	24636783	A recent meta analysis suggests that A1 allele of the <strong>DRD2</strong> gene imposes genetic risk for SUD, especially <b>alcoholism</b> and has been implicated in Reward Deficiency Syndrome (RDS).
+DRD2	addiction	reward	24636783	A recent meta analysis suggests that A1 allele of the <strong>DRD2</strong> gene imposes genetic risk for SUD, especially alcoholism and has been implicated in <b>Reward</b> Deficiency Syndrome (RDS).
+DRD2	drug	alcohol	24636783	We hypothesize that dopamine D2 receptor (<strong>DRD2</strong>) gene Taq1 A2 allele is associated with a subtype of non SUD schizophrenics and as such may act as a putative protective agent against the development of addiction to <b>alcohol</b> or other drugs of abuse.
+DRD2	addiction	addiction	24636783	We hypothesize that dopamine D2 receptor (<strong>DRD2</strong>) gene Taq1 A2 allele is associated with a subtype of non SUD schizophrenics and as such may act as a putative protective agent against the development of <b>addiction</b> to alcohol or other drugs of abuse.
+DRD2	addiction	reward	24636783	Schizophrenics with SUD may be carriers of the <strong>DRD2</strong> Taq1 A1 allele, and/or other RDS <b>reward</b> polymorphisms and have hypodopaminergic <b>reward</b> function.
+DRD2	drug	alcohol	24629326	Impulsivity related cognition in <b>alcohol</b> dependence: Is it moderated by <strong>DRD2</strong>/ANKK1 gene status and executive dysfunction?
+DRD2	addiction	dependence	24629326	Impulsivity related cognition in alcohol <b>dependence</b>: Is it moderated by <strong>DRD2</strong>/ANKK1 gene status and executive dysfunction?
+DRD2	drug	alcohol	24629326	These results suggest that, in <b>alcohol</b> dependence, perceived impaired control is a cognitive mediator of impulsivity related constructs that may be unaffected by <strong>DRD2</strong>/ANKK1 and neurocognitive processes underlying the retrieval of verbal information.
+DRD2	addiction	dependence	24629326	These results suggest that, in alcohol <b>dependence</b>, perceived impaired control is a cognitive mediator of impulsivity related constructs that may be unaffected by <strong>DRD2</strong>/ANKK1 and neurocognitive processes underlying the retrieval of verbal information.
+DRD2	drug	opioid	24561386	Using optogenetics we demonstrate that activation of Channelrhodopsin2 in Rgs9 2 expressing neurons, or in D1 dopamine receptor (Drd1) enriched medium spiny neurons, accelerates the development of <b>morphine</b> tolerance, whereas activation of D2 dopamine receptor (<strong>Drd2</strong>) enriched neurons does not significantly affect the development of tolerance.
+DRD2	drug	cocaine	24528631	This study aimed to evaluate whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) gene and/or the dopamine receptor D2 (<strong>DRD2</strong>) gene modulate the subjective effects (reward or non reward response to a stimulus) produced by <b>cocaine</b> administration.
+DRD2	addiction	reward	24528631	This study aimed to evaluate whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) gene and/or the dopamine receptor D2 (<strong>DRD2</strong>) gene modulate the subjective effects (<b>reward</b> or non <b>reward</b> response to a stimulus) produced by cocaine administration.
+DRD2	drug	cocaine	24528631	This study aimed to evaluate whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) gene and/or the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) gene modulate the subjective effects (reward or non reward response to a stimulus) produced by <b>cocaine</b> administration.
+DRD2	addiction	reward	24528631	This study aimed to evaluate whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) gene and/or the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) gene modulate the subjective effects (<b>reward</b> or non <b>reward</b> response to a stimulus) produced by cocaine administration.
+DRD2	drug	cocaine	24528631	The influence of polymorphisms in the ANKK1 and <strong>DRD2</strong> genes on subjective experience of <b>cocaine</b> in the laboratory was tested.
+DRD2	drug	nicotine	24446757	We investigated the role of exposure to <b>smoking</b> (by parents, siblings, and peers) and reward related candidate gene polymorphisms (OPRM1 A118G, <strong>DRD2</strong> TaqlA and DRD4 bp VNTR) in adolescents' responses to initial <b>smoking</b>.
+DRD2	addiction	reward	24446757	We investigated the role of exposure to smoking (by parents, siblings, and peers) and <b>reward</b> related candidate gene polymorphisms (OPRM1 A118G, <strong>DRD2</strong> TaqlA and DRD4 bp VNTR) in adolescents' responses to initial smoking.
+DRD2	drug	nicotine	24446757	Although preliminary, these findings suggest that exposure to environmental <b>smoking</b> and polymorphisms in the OPRM1 and <strong>DRD2</strong> gene may affect initial sensitivity to <b>nicotine</b>, an early phenotype of the risk of dependence.
+DRD2	addiction	dependence	24446757	Although preliminary, these findings suggest that exposure to environmental smoking and polymorphisms in the OPRM1 and <strong>DRD2</strong> gene may affect initial sensitivity to nicotine, an early phenotype of the risk of <b>dependence</b>.
+DRD2	drug	nicotine	24444411	Genetic variants in <strong>DRD2</strong>, DRD4, ANKK1, DAT1, COMT and DBH genes show some promise in informing personalized prescribing of <b>smoking</b> cessation pharmacotherapies.
+DRD2	drug	alcohol	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), <strong>DRD2</strong> (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with <b>alcohol</b>, tobacco and/or cannabis consumption in young individuals (n = 91).
+DRD2	drug	cannabinoid	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), <strong>DRD2</strong> (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, tobacco and/or <b>cannabis</b> consumption in young individuals (n = 91).
+DRD2	drug	nicotine	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), <strong>DRD2</strong> (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, <b>tobacco</b> and/or cannabis consumption in young individuals (n = 91).
+DRD2	drug	opioid	24359476	The dopamine receptor D2 (<strong>DRD2</strong>) SNP rs1076560 is associated with <b>opioid</b> addiction.
+DRD2	addiction	addiction	24359476	The dopamine receptor D2 (<strong>DRD2</strong>) SNP rs1076560 is associated with opioid <b>addiction</b>.
+DRD2	drug	opioid	24359476	The <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) SNP rs1076560 is associated with <b>opioid</b> addiction.
+DRD2	addiction	addiction	24359476	The <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) SNP rs1076560 is associated with opioid <b>addiction</b>.
+DRD2	drug	alcohol	24307790	Thus, genes related to <b>alcohol</b> addiction, such as <strong>dopamine receptor D2</strong> in the brain, or liver <b>alcohol</b> metabolizing enzymes, such as <b>alcohol</b> dehydrogenase class I polypeptide B, cytochrome P450 2E1 and aldehyde dehydrogenase class 2, may vary from one individual to another.
+DRD2	addiction	addiction	24307790	Thus, genes related to alcohol <b>addiction</b>, such as <strong>dopamine receptor D2</strong> in the brain, or liver alcohol metabolizing enzymes, such as alcohol dehydrogenase class I polypeptide B, cytochrome P450 2E1 and aldehyde dehydrogenase class 2, may vary from one individual to another.
+DRD2	drug	alcohol	24247049	The effect of selected polymorphisms of the dopamine receptor gene <strong>DRD2</strong> and the ANKK 1 on the preference of concentrations of sucrose solutions in men with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	24247049	The effect of selected polymorphisms of the dopamine receptor gene <strong>DRD2</strong> and the ANKK 1 on the preference of concentrations of sucrose solutions in men with alcohol <b>dependence</b>.
+DRD2	drug	alcohol	24247049	The aim of the study was to determine the influence of <strong>DRD2</strong> gene polymorphisms in exon 8 G/A (rs 6276) in the promoter region  141 C Ins/Del (rs1799732) and the influence of ANKK 1 gene Taq 1A polymorphism (rs 1800497) on the preference of increasing sucrose concentrations in men with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	24247049	The aim of the study was to determine the influence of <strong>DRD2</strong> gene polymorphisms in exon 8 G/A (rs 6276) in the promoter region  141 C Ins/Del (rs1799732) and the influence of ANKK 1 gene Taq 1A polymorphism (rs 1800497) on the preference of increasing sucrose concentrations in men with alcohol <b>dependence</b>.
+DRD2	addiction	dependence	24078558	DRD1 and <strong>DRD2</strong> have been linked to substance <b>dependence</b>; whether they predict HIV associated neurocognitive disorder (HAND) is unclear.
+DRD2	drug	cocaine	24078558	We observed that both DRD1 and <strong>DRD2</strong> polymorphisms were associated with opiate and <b>cocaine</b> dependence (P < 0.05) in Caucasian subjects, but not African American individuals.
+DRD2	addiction	dependence	24078558	We observed that both DRD1 and <strong>DRD2</strong> polymorphisms were associated with opiate and cocaine <b>dependence</b> (P < 0.05) in Caucasian subjects, but not African American individuals.
+DRD2	addiction	dependence	24078558	The effects differed for substance <b>dependence</b> groups as the direction of the correlations with <strong>DRD2</strong> were opposite to what was seen in subjects without these dependencies.
+DRD2	drug	nicotine	24065931	We examined genetic polymorphisms within the CHRNA5 A3 B4 gene cluster (CHRNA3 rs578776, CHRNA5 rs16969968, LOC123688 rs8034191, and CHRNA3 rs1051730), the ANKK1 gene (rs1800497), and the D2 dopamine receptor gene (<strong>DRD2</strong> rs1079597, <strong>DRD2</strong> rs1799732) from 104 <b>smokers</b> of European ancestry in a <b>smoking</b> cessation trial.
+DRD2	drug	cocaine	24001687	In an effort to identify <b>cocaine</b> induced alterations in D1 r  versus D2 r expressing cells during the initial stages of addiction, we examined cells that expressed D1 rs in Drd1 eGFP mice, or D2 rs in <strong>Drd2</strong> eGFP mice, after an acute, 1 day binge pattern of <b>cocaine</b> administration.
+DRD2	addiction	addiction	24001687	In an effort to identify cocaine induced alterations in D1 r  versus D2 r expressing cells during the initial stages of <b>addiction</b>, we examined cells that expressed D1 rs in Drd1 eGFP mice, or D2 rs in <strong>Drd2</strong> eGFP mice, after an acute, 1 day binge pattern of cocaine administration.
+DRD2	addiction	intoxication	24001687	In an effort to identify cocaine induced alterations in D1 r  versus D2 r expressing cells during the initial stages of addiction, we examined cells that expressed D1 rs in Drd1 eGFP mice, or D2 rs in <strong>Drd2</strong> eGFP mice, after an acute, 1 day <b>binge</b> pattern of cocaine administration.
+DRD2	drug	cocaine	24001687	<strong>Drd2</strong> eGFP mice that received <b>cocaine</b> had fewer D2 r labeled cells in the DL striatum and NAc core compared to saline controls.
+DRD2	drug	cocaine	24001687	<strong>Drd2</strong> eGFP mice that received <b>cocaine</b> also had fewer numbers of D2 r labeled cells in the NAc core compared to saline controls, but no significant differences in the number of D2 r labeled cells in the NAc shell.
+DRD2	drug	opioid	23840506	To study the potential association between allelic variants of dopamine D2 receptor (<strong>DRD2</strong>), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol O methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and <b>heroin</b> dependence in Hungarian patients.
+DRD2	addiction	dependence	23840506	To study the potential association between allelic variants of dopamine D2 receptor (<strong>DRD2</strong>), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol O methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and heroin <b>dependence</b> in Hungarian patients.
+DRD2	drug	opioid	23840506	303 <b>heroin</b> dependent subjects and 555 healthy controls were genotyped for 7 single nucleotide polymorphisms (SNPs) rs4680 of the COMT gene; rs1079597 and rs1800498 of the <strong>DRD2</strong> gene; rs1800497 of the ANKK1 gene; rs1800955, rs936462 and rs747302 of the DRD4 gene.
+DRD2	drug	alcohol	23818181	Association between <strong>DRD2</strong>/DRD4 interaction and conduct disorder: a potential developmental pathway to <b>alcohol</b> dependence.
+DRD2	addiction	dependence	23818181	Association between <strong>DRD2</strong>/DRD4 interaction and conduct disorder: a potential developmental pathway to alcohol <b>dependence</b>.
+DRD2	drug	opioid	23702354	The effect of perinatal lead exposure on <strong>dopamine receptor D2</strong> expression in <b>morphine</b> dependent rats.
+DRD2	drug	nicotine	23691092	Associations of prenatal <b>nicotine</b> exposure and the dopamine related genes ANKK1 and <strong>DRD2</strong> to verbal language.
+DRD2	drug	nicotine	23691092	Our results show that <b>smoking</b> during pregnancy increases the risk for LI and poor performance on language tasks and that ANKK1/<strong>DRD2</strong> contributes to language performance.
+DRD2	drug	nicotine	23691092	Our association of ANKK1/<strong>DRD2</strong> further implicates the role of <b>nicotine</b> related pathways and dopamine signaling in language processing, particularly in comprehension and phonological memory.
+DRD2	drug	alcohol	23685324	Association between <strong>DRD2</strong>, 5 HTTLPR, and ALDH2 genes and specific personality traits in <b>alcohol</b>  and opiate dependent patients.
+DRD2	drug	alcohol	23685324	We concluded that addicts, both <b>alcohol</b>  and opiate dependent patients, have common genetic variants in <strong>DRD2</strong> and 5 HTTLPR but specific for ALDH2.
+DRD2	drug	alcohol	23670889	Drug addiction polymorphisms such as the TaqI A1 allele of the dopamine D2 receptor (<strong>DRD2</strong>) are associated with cocaine, <b>alcohol</b>, and opioid use, but few studies have linked <strong>DRD2</strong> to food craving.
+DRD2	drug	cocaine	23670889	Drug addiction polymorphisms such as the TaqI A1 allele of the dopamine D2 receptor (<strong>DRD2</strong>) are associated with <b>cocaine</b>, alcohol, and opioid use, but few studies have linked <strong>DRD2</strong> to food craving.
+DRD2	drug	opioid	23670889	Drug addiction polymorphisms such as the TaqI A1 allele of the dopamine D2 receptor (<strong>DRD2</strong>) are associated with cocaine, alcohol, and <b>opioid</b> use, but few studies have linked <strong>DRD2</strong> to food craving.
+DRD2	addiction	addiction	23670889	Drug <b>addiction</b> polymorphisms such as the TaqI A1 allele of the dopamine D2 receptor (<strong>DRD2</strong>) are associated with cocaine, alcohol, and opioid use, but few studies have linked <strong>DRD2</strong> to food craving.
+DRD2	addiction	relapse	23670889	Drug addiction polymorphisms such as the TaqI A1 allele of the dopamine D2 receptor (<strong>DRD2</strong>) are associated with cocaine, alcohol, and opioid use, but few studies have linked <strong>DRD2</strong> to food <b>craving</b>.
+DRD2	drug	opioid	23651024	Out of the 110 variants analyzed, 12 SNPs (in BDNF, NTRK2, OPRM1, <strong>DRD2</strong> and ANKK1) were associated with <b>methadone</b> dose (nominal p < 0.05).
+DRD2	drug	amphetamine	23647975	PTSD risk associated with a functional <strong>DRD2</strong> polymorphism in heroin dependent cases and controls is limited to <b>amphetamine</b> dependent individuals.
+DRD2	drug	opioid	23647975	PTSD risk associated with a functional <strong>DRD2</strong> polymorphism in <b>heroin</b> dependent cases and controls is limited to amphetamine dependent individuals.
+DRD2	drug	alcohol	23635803	ANKK1 and <strong>DRD2</strong> pharmacogenetics of <b>disulfiram</b> treatment for cocaine abuse.
+DRD2	drug	cocaine	23635803	ANKK1 and <strong>DRD2</strong> pharmacogenetics of disulfiram treatment for <b>cocaine</b> abuse.
+DRD2	drug	alcohol	23635803	Since dopamine deficiency has been found with cocaine addiction, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) and/or the dopamine receptor D2 (<strong>DRD2</strong>) genes interact with response to treatment with <b>disulfiram</b>.
+DRD2	drug	cocaine	23635803	Since dopamine deficiency has been found with <b>cocaine</b> addiction, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) and/or the dopamine receptor D2 (<strong>DRD2</strong>) genes interact with response to treatment with disulfiram.
+DRD2	addiction	addiction	23635803	Since dopamine deficiency has been found with cocaine <b>addiction</b>, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) and/or the dopamine receptor D2 (<strong>DRD2</strong>) genes interact with response to treatment with disulfiram.
+DRD2	drug	alcohol	23635803	Since dopamine deficiency has been found with cocaine addiction, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) and/or the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) genes interact with response to treatment with <b>disulfiram</b>.
+DRD2	drug	cocaine	23635803	Since dopamine deficiency has been found with <b>cocaine</b> addiction, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) and/or the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) genes interact with response to treatment with disulfiram.
+DRD2	addiction	addiction	23635803	Since dopamine deficiency has been found with cocaine <b>addiction</b>, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (ANKK1) and/or the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) genes interact with response to treatment with disulfiram.
+DRD2	drug	alcohol	23635803	They were genotyped for ANKK1 (rs1800497) and <strong>DRD2</strong> (rs2283265) polymorphisms, and the data were evaluated for an association between a cocaine free state, as assessed by cocaine free urine samples, and <b>disulfiram</b> treatment.
+DRD2	drug	cocaine	23635803	They were genotyped for ANKK1 (rs1800497) and <strong>DRD2</strong> (rs2283265) polymorphisms, and the data were evaluated for an association between a <b>cocaine</b> free state, as assessed by <b>cocaine</b> free urine samples, and disulfiram treatment.
+DRD2	drug	alcohol	23635803	The GT/TT <strong>DRD2</strong> genotype group showed a significant decrease in the number of cocaine positive urine samples on <b>disulfiram</b> (N=9; 67 48%; P ≤ 0.0001), whereas the GG <strong>DRD2</strong> genotype group showed only a marginal decrease (N=23; 84 63%; P=0.04).
+DRD2	drug	cocaine	23635803	The GT/TT <strong>DRD2</strong> genotype group showed a significant decrease in the number of <b>cocaine</b> positive urine samples on disulfiram (N=9; 67 48%; P ≤ 0.0001), whereas the GG <strong>DRD2</strong> genotype group showed only a marginal decrease (N=23; 84 63%; P=0.04).
+DRD2	drug	alcohol	23635803	A patient's genotype for ANKK1, <strong>DRD2</strong>, or both, may be used to identify individuals for whom <b>disulfiram</b> may be an effective pharmacotherapy for cocaine dependence.
+DRD2	drug	cocaine	23635803	A patient's genotype for ANKK1, <strong>DRD2</strong>, or both, may be used to identify individuals for whom disulfiram may be an effective pharmacotherapy for <b>cocaine</b> dependence.
+DRD2	addiction	dependence	23635803	A patient's genotype for ANKK1, <strong>DRD2</strong>, or both, may be used to identify individuals for whom disulfiram may be an effective pharmacotherapy for cocaine <b>dependence</b>.
+DRD2	drug	alcohol	23558112	The association of <strong>DRD2</strong>  141C and ANKK1 TaqIA polymorphisms with <b>alcohol</b> dependence in Korean population classified by the Lesch typology.
+DRD2	addiction	dependence	23558112	The association of <strong>DRD2</strong>  141C and ANKK1 TaqIA polymorphisms with alcohol <b>dependence</b> in Korean population classified by the Lesch typology.
+DRD2	drug	alcohol	23558112	The polymorphisms of dopamine D2 receptor (<strong>DRD2</strong>) genes have been reported to be involved in susceptibility to <b>alcoholism</b>.
+DRD2	drug	alcohol	23558112	Therefore, we investigated the association of three single nucleotide polymorphisms (SNPs) in <strong>DRD2</strong> and ankyrin repeat and kinase domain containing one (ANKK1) genes with <b>alcohol</b> dependence in Korean subjects, who were classified by the criteria of the Lesch typology.
+DRD2	addiction	dependence	23558112	Therefore, we investigated the association of three single nucleotide polymorphisms (SNPs) in <strong>DRD2</strong> and ankyrin repeat and kinase domain containing one (ANKK1) genes with alcohol <b>dependence</b> in Korean subjects, who were classified by the criteria of the Lesch typology.
+DRD2	drug	alcohol	23558112	The <strong>DRD2</strong>  141C (Insertion (Ins)/Deletion (Del)), exon8 (A/G) and the ANKK1 TaqIA (A1/A2) polymorphisms were genotyped in a case control sample consisting of 245 <b>alcohol</b> dependent (AD) patients and 110 healthy controls.
+DRD2	drug	nicotine	23474369	Relative to placebo, 14mg <b>nicotine</b> patch produced shorter overall reaction times (RTs) and individuals with two dopamine type 2 receptor (<strong>DRD2</strong>) A2 alleles exhibited the greatest RT benefit from <b>nicotine</b> following emotionally negative pictures after the longest cue target delay (800ms), but benefitted least from <b>nicotine</b> following positive pictures after the shortest delay (400ms).
+DRD2	drug	alcohol	23443985	<strong>DRD2</strong> and ANKK1 gene polymorphisms and <b>alcohol</b> dependence: a case control study among a Mendelian population of East Asian ancestry.
+DRD2	addiction	dependence	23443985	<strong>DRD2</strong> and ANKK1 gene polymorphisms and alcohol <b>dependence</b>: a case control study among a Mendelian population of East Asian ancestry.
+DRD2	drug	cocaine	23340505	Dopamine transporter DAT and receptor <strong>DRD2</strong> variants affect risk of lethal <b>cocaine</b> abuse: a gene gene environment interaction.
+DRD2	drug	cocaine	23340505	Splicing polymorphism rs2283265 of <strong>DRD2</strong>, encoding D2 receptors, were shown to confer risk of <b>cocaine</b> overdose/death (odds ratio ∼3) in subjects and controls from the Miami Dade County Brain Bank.
+DRD2	drug	cocaine	23340505	DAT rs3836790 and <strong>DRD2</strong> rs2283265 also interacted by modulating DAT protein activity in the ventral putamen of <b>cocaine</b> abusers.
+DRD2	drug	alcohol	23336089	For example, both drinking (<b>alcohol</b>) and obesity seem to cluster in large social networks and are influenced by friends having the same genotype, in particular the <strong>DRD2</strong> A1 allele.
+DRD2	addiction	reward	23336089	Likewise, voting, voting turnout and attachment to a particular political ideology is differentially related to various <b>reward</b> genes (e.g., 5HTT, MOA, <strong>DRD2</strong>, and DRD4), possibly predicting liberalism or conservatism.
+DRD2	drug	opioid	23303482	To examine association of 1430 candidate gene single nucleotide polymorphisms (SNPs) with <b>heroin</b> dependence, reporting here only the 71 SNPs in the chromosome 11 gene cluster (NCAM1, TTC12, ANKK1, <strong>DRD2</strong>) that include the strongest observed associations.
+DRD2	addiction	dependence	23303482	To examine association of 1430 candidate gene single nucleotide polymorphisms (SNPs) with heroin <b>dependence</b>, reporting here only the 71 SNPs in the chromosome 11 gene cluster (NCAM1, TTC12, ANKK1, <strong>DRD2</strong>) that include the strongest observed associations.
+DRD2	drug	opioid	23266708	The ADH1B and <strong>DRD2</strong> gene polymorphism may modify the protective effect of the ALDH2 gene against <b>heroin</b> dependence.
+DRD2	addiction	dependence	23266708	The ADH1B and <strong>DRD2</strong> gene polymorphism may modify the protective effect of the ALDH2 gene against heroin <b>dependence</b>.
+DRD2	addiction	addiction	23266708	In addition, dopamine D2 receptor (<strong>DRD2</strong>) gene may also interact with the dopamine metabolizing genes and link to <b>addiction</b>.
+DRD2	drug	opioid	23266708	Therefore, we investigated the association between the ALDH2, ADH1B and <strong>DRD2</strong> polymorphisms and <b>heroin</b> dependence.
+DRD2	addiction	dependence	23266708	Therefore, we investigated the association between the ALDH2, ADH1B and <strong>DRD2</strong> polymorphisms and heroin <b>dependence</b>.
+DRD2	drug	opioid	23266708	The frequency of the ALDH2*1/*1 genotype was significantly lower in <b>heroin</b> dependent patients than in controls, but the frequency of ADH1B and <strong>DRD2</strong> genotypes was not significantly different.
+DRD2	drug	opioid	23266708	The ALDH2*1/*1, ADH1B*1/*1, and ADH1B*1/*2 genotypes may interact and protect their carriers against <b>heroin</b> dependence and the protective effect may be varied by the <strong>DRD2</strong> gene polymorphism.
+DRD2	addiction	dependence	23266708	The ALDH2*1/*1, ADH1B*1/*1, and ADH1B*1/*2 genotypes may interact and protect their carriers against heroin <b>dependence</b> and the protective effect may be varied by the <strong>DRD2</strong> gene polymorphism.
+DRD2	drug	opioid	23266708	We conclude that the protective effect of the ALDH2 polymorphism against <b>heroin</b> dependence may be modified by the ADH1B and <strong>DRD2</strong> polymorphism.
+DRD2	addiction	dependence	23266708	We conclude that the protective effect of the ALDH2 polymorphism against heroin <b>dependence</b> may be modified by the ADH1B and <strong>DRD2</strong> polymorphism.
+DRD2	drug	alcohol	23238469	Influence of <strong>DRD2</strong> and ANKK1 polymorphisms on the manifestation of withdrawal syndrome symptoms in <b>alcohol</b> addiction.
+DRD2	addiction	addiction	23238469	Influence of <strong>DRD2</strong> and ANKK1 polymorphisms on the manifestation of withdrawal syndrome symptoms in alcohol <b>addiction</b>.
+DRD2	addiction	withdrawal	23238469	Influence of <strong>DRD2</strong> and ANKK1 polymorphisms on the manifestation of <b>withdrawal</b> syndrome symptoms in alcohol addiction.
+DRD2	addiction	withdrawal	23238469	We investigated the relationship between <b>withdrawal</b> syndrome symptoms and dopamine receptor 2 <strong>DRD2</strong> gene polymorphisms 141 C I/D (rs1799732) exon 8 G/A (rs6276) and ANKK1 (Ankyrin Repeat and Kinase Domain Containing 1) gene polymorphism Taq1A (rs1800497).
+DRD2	drug	alcohol	23238469	Our results show statistically significant associations between SNP in exon 8 A/G in the <strong>DRD2</strong> gene and <b>alcohol</b> withdrawal syndrome with seizures, and between SNP in promoter  141 C I/D in the <strong>DRD2</strong> gene and early onset of <b>alcohol</b> dependence (AD).
+DRD2	addiction	dependence	23238469	Our results show statistically significant associations between SNP in exon 8 A/G in the <strong>DRD2</strong> gene and alcohol withdrawal syndrome with seizures, and between SNP in promoter  141 C I/D in the <strong>DRD2</strong> gene and early onset of alcohol <b>dependence</b> (AD).
+DRD2	addiction	withdrawal	23238469	Our results show statistically significant associations between SNP in exon 8 A/G in the <strong>DRD2</strong> gene and alcohol <b>withdrawal</b> syndrome with seizures, and between SNP in promoter  141 C I/D in the <strong>DRD2</strong> gene and early onset of alcohol dependence (AD).
+DRD2	drug	alcohol	23203481	A large scale meta analysis of the association between the ANKK1/<strong>DRD2</strong> Taq1A polymorphism and <b>alcohol</b> dependence.
+DRD2	addiction	dependence	23203481	A large scale meta analysis of the association between the ANKK1/<strong>DRD2</strong> Taq1A polymorphism and alcohol <b>dependence</b>.
+DRD2	drug	nicotine	23153044	A prospective study of the effects of the <strong>DRD2</strong>/ANKK1 TaqIA polymorphism and impulsivity on <b>smoking</b> initiation.
+DRD2	drug	nicotine	23153044	This study tested whether <strong>DRD2</strong>/ANKK1 TaqIA genotype predicted <b>smoking</b> initiation and subsequent use, and effects were mediated by sensation seeking and negative urgency.
+DRD2	addiction	relapse	23153044	This study tested whether <strong>DRD2</strong>/ANKK1 TaqIA genotype predicted smoking initiation and subsequent use, and effects were mediated by sensation <b>seeking</b> and negative urgency.
+DRD2	drug	alcohol	23111884	A relationship between <b>alcoholic</b> disease and the presence of TaqIA1 and <strong>DRD2</strong> alleles permits to initiate another investigation of gene coding <strong>DRD2</strong> dopamine receptor.
+DRD2	drug	amphetamine	23000618	The levels of IP(3)R 1 protein in the NAcc of <b>METH</b> conditioned mice significantly increased, which was completely abolished by microinjection of SCH23390 and raclopride, selective dopamine D1 like and D2 like receptor (D1 and <strong>D2DR</strong>) antagonists respectively, into the mouse NAcc.
+DRD2	drug	alcohol	22970887	The association between <strong>DRD2</strong>/ANKK1 and genetically informed measures of <b>alcohol</b> use and problems.
+DRD2	drug	alcohol	22970887	In 1990, Blum and colleagues first reported an association between <strong>DRD2</strong> and <b>alcoholism</b>.
+DRD2	drug	alcohol	22970887	While there have been subsequent replications of this genetic association, there have also been numerous studies that failed to detect an association between <strong>DRD2</strong> and <b>alcohol</b> dependence.
+DRD2	addiction	dependence	22970887	While there have been subsequent replications of this genetic association, there have also been numerous studies that failed to detect an association between <strong>DRD2</strong> and alcohol <b>dependence</b>.
+DRD2	drug	alcohol	22970887	After correction for multiple testing across SNPs and phenotypes, of the 31 SNPs genotyped across <strong>DRD2</strong>/ANKK1, one SNP (rs10891549) showed significant association with the general <b>alcohol</b> consumption and problems factor score (P = 0.004), and four SNPs (rs10891549, rs1554929, rs6275, rs6279), representing two independent signals after accounting for linkage disequilibrium, showed significant association with the <b>alcohol</b> problems genetic factor score (P = 0.005, P = 0.005, P = 0.003, P = 0.003).
+DRD2	drug	alcohol	22970887	In this study, we provide additional positive evidence for the association between <strong>DRD2</strong>/ANKK1 and <b>alcohol</b> outcomes, including frequency of drinking and drinking problems.
+DRD2	drug	cannabinoid	22745721	Dopamine receptor D2 (<strong>DRD2</strong>) and proenkephalin (PENK) genes have been implicated in animal studies with <b>cannabis</b> exposure.
+DRD2	drug	cannabinoid	22745721	<strong>Dopamine receptor D2</strong> (<strong>DRD2</strong>) and proenkephalin (PENK) genes have been implicated in animal studies with <b>cannabis</b> exposure.
+DRD2	drug	cannabinoid	22745721	Healthy young adults (18 27 years) with <b>cannabis</b> dependence and without a dependence diagnosis were studied (N = 50/group) in relation to a priori determined single nucleotide polymorphisms (SNPs) of the <strong>DRD2</strong> and PENK genes.
+DRD2	addiction	dependence	22745721	Healthy young adults (18 27 years) with cannabis <b>dependence</b> and without a <b>dependence</b> diagnosis were studied (N = 50/group) in relation to a priori determined single nucleotide polymorphisms (SNPs) of the <strong>DRD2</strong> and PENK genes.
+DRD2	addiction	reward	22745721	The findings replicated the known association between the rs6277 <strong>DRD2</strong> SNP and decisions associated with negative <b>reinforcement</b> outcomes.
+DRD2	drug	nicotine	22740151	Impact of COMT Val 108/158 Met and <strong>DRD2</strong> Taq1B gene polymorphisms on vulnerability to cigarette <b>smoking</b> of Thai males.
+DRD2	drug	nicotine	22740151	The purposes of this study were to examine the association between two polymorphisms in COMT Val (108/158) Met and <strong>DRD2</strong> Taq1B and anthropometric biochemical parameters and to ascertain the association between these polymorphisms and cigarette <b>smoking</b>.
+DRD2	drug	nicotine	22740151	<b>Smoking</b> status was significantly associated with COMT Val (108/158) Met polymorphism, but not associated with <strong>DRD2</strong> Taq1B polymorphism.
+DRD2	drug	nicotine	22740151	The results suggest that COMT Val (108/158) Met genetic polymorphisms, but not <strong>DRD2</strong> Taq1B, may influence susceptibility to cigarette <b>smoking</b> among Thai males.
+DRD2	drug	alcohol	22728571	<strong>DRD2</strong>/ANKK1 TaqI A genotype moderates the relationship between alexithymia and the relative value of <b>alcohol</b> among male college binge drinkers.
+DRD2	addiction	intoxication	22728571	<strong>DRD2</strong>/ANKK1 TaqI A genotype moderates the relationship between alexithymia and the relative value of alcohol among male college <b>binge</b> drinkers.
+DRD2	drug	alcohol	22728571	The present study hypothesized that <strong>DRD2</strong>/ANKK1 TaqI A (rs1800497) genotype would moderate the relationship between alexithymia and an <b>alcohol</b> purchase task (APT) among male college binge drinkers.
+DRD2	addiction	intoxication	22728571	The present study hypothesized that <strong>DRD2</strong>/ANKK1 TaqI A (rs1800497) genotype would moderate the relationship between alexithymia and an alcohol purchase task (APT) among male college <b>binge</b> drinkers.
+DRD2	drug	alcohol	22698582	<strong>DRD2</strong>/ANKK1 TaqIA and SLC6A3 VNTR polymorphisms in <b>alcohol</b> dependence: association and gene gene interaction study in a population of Central Italy.
+DRD2	addiction	dependence	22698582	<strong>DRD2</strong>/ANKK1 TaqIA and SLC6A3 VNTR polymorphisms in alcohol <b>dependence</b>: association and gene gene interaction study in a population of Central Italy.
+DRD2	drug	alcohol	22582185	<strong>DRD2</strong> C957T and TaqIA genotyping reveals gender effects and unique low risk and high risk genotypes in <b>alcohol</b> dependence.
+DRD2	addiction	dependence	22582185	<strong>DRD2</strong> C957T and TaqIA genotyping reveals gender effects and unique low risk and high risk genotypes in alcohol <b>dependence</b>.
+DRD2	drug	alcohol	22582185	As recent conflicting reports describe a genetic association between both the C  and the T alleles of the dopamine D2 receptor (<strong>DRD2</strong>) C957T polymorphism (rs6277) in <b>alcohol</b> dependent subjects, our aim was to examine this polymorphism and TaqIA (rs1800497) in Australian <b>alcohol</b> dependent subjects.
+DRD2	drug	alcohol	22582185	Decreased <strong>DRD2</strong> binding associated with the C allele of the <strong>DRD2</strong> C957T polymorphism is likely to be important in the underlying pathophysiology of at least some forms of <b>alcohol</b> dependence, and this effect appears to be limited to males only.
+DRD2	addiction	dependence	22582185	Decreased <strong>DRD2</strong> binding associated with the C allele of the <strong>DRD2</strong> C957T polymorphism is likely to be important in the underlying pathophysiology of at least some forms of alcohol <b>dependence</b>, and this effect appears to be limited to males only.
+DRD2	drug	alcohol	22565782	<strong>DRD2</strong>/DRD4 heteromerization may influence genetic susceptibility to <b>alcohol</b> dependence.
+DRD2	addiction	dependence	22565782	<strong>DRD2</strong>/DRD4 heteromerization may influence genetic susceptibility to alcohol <b>dependence</b>.
+DRD2	drug	cannabinoid	22536882	Analysis of dopamine D2 receptor (<strong>DRD2</strong>) gene polymorphisms in <b>cannabinoid</b> addicts.
+DRD2	addiction	dependence	22536882	The gene encoding the dopamine D2 receptor (<strong>DRD2</strong>) has been suggested as a candidate gene for substance <b>dependence</b>.
+DRD2	drug	cannabinoid	22536882	In this study, the possible association between Taq1A and Taq1B <strong>DRD2</strong> polymorphisms and <b>cannabinoid</b> dependence was investigated.
+DRD2	addiction	dependence	22536882	In this study, the possible association between Taq1A and Taq1B <strong>DRD2</strong> polymorphisms and cannabinoid <b>dependence</b> was investigated.
+DRD2	drug	alcohol	22509987	The COMT Val158Met and <strong>DRD2</strong>/ANKK1 Taq1A genotypes have been suggested to affect both stress sensitivity and the risk for <b>alcohol</b> dependence.
+DRD2	addiction	dependence	22509987	The COMT Val158Met and <strong>DRD2</strong>/ANKK1 Taq1A genotypes have been suggested to affect both stress sensitivity and the risk for alcohol <b>dependence</b>.
+DRD2	drug	alcohol	22509987	This study tested the hypothesis that genetic variation in COMT Val158Met and <strong>DRD2</strong>/ANKK1 Taq1A interacts with childhood adverse experiences to predict <b>alcohol</b> dependence.
+DRD2	addiction	dependence	22509987	This study tested the hypothesis that genetic variation in COMT Val158Met and <strong>DRD2</strong>/ANKK1 Taq1A interacts with childhood adverse experiences to predict alcohol <b>dependence</b>.
+DRD2	drug	alcohol	22509987	Male abstinent <b>alcohol</b> dependent patients (n = 110) and age matched healthy male controls (n = 99) were genotyped for the COMT Val158Met and the <strong>DRD2</strong>/ANKK1 Taq1A genotypes.
+DRD2	drug	alcohol	22509987	The <strong>DRD2</strong>/ANKK1 Taq1A genotype was not related to <b>alcohol</b> dependence, nor did it interact with childhood adversity in predicting <b>alcohol</b> dependence.
+DRD2	addiction	dependence	22509987	The <strong>DRD2</strong>/ANKK1 Taq1A genotype was not related to alcohol <b>dependence</b>, nor did it interact with childhood adversity in predicting alcohol <b>dependence</b>.
+DRD2	drug	alcohol	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, <strong>DRD2</strong>, DRD3, DRD4) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of craving, as well as alpha synuclein (SNCA), which has been previously found to be associated with craving, were associated with <b>alcohol</b> craving in this sample.
+DRD2	addiction	relapse	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, <strong>DRD2</strong>, DRD3, DRD4) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of <b>craving</b>, as well as alpha synuclein (SNCA), which has been previously found to be associated with <b>craving</b>, were associated with alcohol <b>craving</b> in this sample.
+DRD2	drug	alcohol	22474103	Reduced dopamine receptor sensitivity as an intermediate phenotype in <b>alcohol</b> dependence and the role of the COMT Val158Met and <strong>DRD2</strong> Taq1A genotypes.
+DRD2	addiction	dependence	22474103	Reduced dopamine receptor sensitivity as an intermediate phenotype in alcohol <b>dependence</b> and the role of the COMT Val158Met and <strong>DRD2</strong> Taq1A genotypes.
+DRD2	drug	alcohol	22474103	To test central dopamine receptor sensitivity as an intermediate phenotype for <b>alcohol</b> dependence, specifically evaluating the hypothesis that the dopaminergic genes COMT Val158Met and <strong>DRD2</strong> Taq1A affect dopamine receptor sensitivity.
+DRD2	addiction	dependence	22474103	To test central dopamine receptor sensitivity as an intermediate phenotype for alcohol <b>dependence</b>, specifically evaluating the hypothesis that the dopaminergic genes COMT Val158Met and <strong>DRD2</strong> Taq1A affect dopamine receptor sensitivity.
+DRD2	drug	alcohol	22474103	In a logistic regression analysis, reduced dopamine receptor sensitivity on both measures predicted <b>alcohol</b> dependence, without an additive effect of the COMT Val158Met and <strong>DRD2</strong> Taq1A genotypes.
+DRD2	addiction	dependence	22474103	In a logistic regression analysis, reduced dopamine receptor sensitivity on both measures predicted alcohol <b>dependence</b>, without an additive effect of the COMT Val158Met and <strong>DRD2</strong> Taq1A genotypes.
+DRD2	drug	alcohol	22474103	COMT Val158Met and <strong>DRD2</strong> Taq1A may confer their risk of <b>alcohol</b> dependence through reduced dopamine receptor sensitivity in the prefrontal cortex and hindbrain, respectively.
+DRD2	addiction	dependence	22474103	COMT Val158Met and <strong>DRD2</strong> Taq1A may confer their risk of alcohol <b>dependence</b> through reduced dopamine receptor sensitivity in the prefrontal cortex and hindbrain, respectively.
+DRD2	drug	nicotine	22382052	A <strong>DRD2</strong> and ANKK1 haplotype is associated with <b>nicotine</b> dependence.
+DRD2	addiction	dependence	22382052	A <strong>DRD2</strong> and ANKK1 haplotype is associated with nicotine <b>dependence</b>.
+DRD2	drug	nicotine	22382052	To test the importance of the dopamine D2 receptor (<strong>DRD2</strong>) region in <b>nicotine</b> dependence, 150 <b>smokers</b> and 228 controls were genotyped for the <strong>DRD2</strong> C957T,  141delC and ANKK1 TaqIA polymorphisms (rs6277, rs1799732 and rs1800497, respectively).
+DRD2	addiction	dependence	22382052	To test the importance of the dopamine D2 receptor (<strong>DRD2</strong>) region in nicotine <b>dependence</b>, 150 smokers and 228 controls were genotyped for the <strong>DRD2</strong> C957T,  141delC and ANKK1 TaqIA polymorphisms (rs6277, rs1799732 and rs1800497, respectively).
+DRD2	drug	nicotine	22382052	Our findings suggest that the <strong>DRD2</strong> C957T polymorphism and the ANKK1 TaqIA polymorphism are key contributors to the genetic susceptibility to <b>nicotine</b> dependence.
+DRD2	addiction	dependence	22382052	Our findings suggest that the <strong>DRD2</strong> C957T polymorphism and the ANKK1 TaqIA polymorphism are key contributors to the genetic susceptibility to nicotine <b>dependence</b>.
+DRD2	addiction	reward	22342427	Impulsivity has been linked with variation in <b>reward</b> related activation in the ventral striatum (VS), altered dopamine signaling, and functional polymorphisms of <strong>DRD2</strong> and DAT1 genes.
+DRD2	drug	nicotine	22309839	Our results provided confirmation of the previous findings that <strong>DRD2</strong>, DRD3, DDC, CHRNB3, GABBR2 and CHRNA4 are associated with <b>nicotine</b> dependence.
+DRD2	addiction	dependence	22309839	Our results provided confirmation of the previous findings that <strong>DRD2</strong>, DRD3, DDC, CHRNB3, GABBR2 and CHRNA4 are associated with nicotine <b>dependence</b>.
+DRD2	drug	alcohol	22232963	[Research on associations between selected polymorphisms of genes <strong>DRD2</strong>, 5HTT, GRIK3, ADH4 and <b>alcohol</b> dependence syndrome].
+DRD2	addiction	dependence	22232963	[Research on associations between selected polymorphisms of genes <strong>DRD2</strong>, 5HTT, GRIK3, ADH4 and alcohol <b>dependence</b> syndrome].
+DRD2	addiction	addiction	23483116	Previously our laboratory coined the term Reward Deficiency Syndrome (RDS) for common genetic determinants in predicting <b>addictive</b> disorders and reported that the predictive value for future RDS behaviors in subjects carrying the <strong>DRD2</strong> Taq A1 allele was 74%.
+DRD2	addiction	reward	23483116	Previously our laboratory coined the term <b>Reward</b> Deficiency Syndrome (RDS) for common genetic determinants in predicting addictive disorders and reported that the predictive value for future RDS behaviors in subjects carrying the <strong>DRD2</strong> Taq A1 allele was 74%.
+DRD2	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], <strong>DRD2</strong> ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+DRD2	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], <strong>DRD2</strong> ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+DRD2	drug	nicotine	22046326	Compared with carriers of variant alleles, the odds ratio (OR) for being a non <b>smoker</b> in individuals with the wild type genotype of CYP2A6*12 and <strong>DRD2</strong> ANKK1 2137G>A (Taq1A) polymorphisms was 3.60 (95%CI: 1.75, 7.44) and 2.63 (95%CI: 1.41, 4.89) respectively.
+DRD2	drug	nicotine	22046326	We found a significant genotype effect (all P≤0.017) for the following <b>smoking</b> related phenotypes: (i) cigarettes smoked per day and CYP2A13*3; (ii) pack years smoked and CYP2A6*2, CYP2A6*1×2, CYP2A13*7, CYP2B6*4 and <strong>DRD2</strong> ANKK1 2137G>A (Taq1A); (iii) <b>nicotine</b> dependence (assessed with the Fagestrom test) and CYP2A6*9.
+DRD2	addiction	dependence	22046326	We found a significant genotype effect (all P≤0.017) for the following smoking related phenotypes: (i) cigarettes smoked per day and CYP2A13*3; (ii) pack years smoked and CYP2A6*2, CYP2A6*1×2, CYP2A13*7, CYP2B6*4 and <strong>DRD2</strong> ANKK1 2137G>A (Taq1A); (iii) nicotine <b>dependence</b> (assessed with the Fagestrom test) and CYP2A6*9.
+DRD2	drug	nicotine	22028400	Among susceptible youth (N = 246), older age at baseline, living with a <b>smoker</b>, and three different genes (HTR2A, <strong>DRD2</strong>, SLC6A3) predicted experimentation.
+DRD2	drug	cannabinoid	21997315	ANKK1/<strong>DRD2</strong> locus variants are associated with <b>rimonabant</b> efficacy in aiding smoking cessation: pilot data.
+DRD2	drug	nicotine	21997315	ANKK1/<strong>DRD2</strong> locus variants are associated with rimonabant efficacy in aiding <b>smoking</b> cessation: pilot data.
+DRD2	drug	cannabinoid	21997315	The present study determined which polymorphism of the <strong>DRD2</strong> gene had a salutary outcome in administration of <b>rimonabant</b>, a drug used in smoking cessation and obesity studies.
+DRD2	drug	nicotine	21997315	The present study determined which polymorphism of the <strong>DRD2</strong> gene had a salutary outcome in administration of rimonabant, a drug used in <b>smoking</b> cessation and obesity studies.
+DRD2	addiction	reward	21968930	These animals presented prominent changes in the nucleus accumbens (NAcc), a key component of the mesolimbic <b>reward</b> circuitry; specifically, cell numbers and dopamine (DA) levels were significantly reduced, whereas DA receptor 2 (<strong>Drd2</strong>) mRNA expression levels were markedly upregulated in the NAcc.
+DRD2	drug	opioid	21968930	Interestingly, repeated <b>morphine</b> exposure significantly downregulated <strong>Drd2</strong> expression in iuGC exposed animals, in parallel with increased DNA methylation of the <strong>Drd2</strong> gene.
+DRD2	drug	opioid	21968930	Administration of a therapeutic dose of L dopa reverted the hypodopaminergic state in the NAcc of iuGC animals, normalized <strong>Drd2</strong> expression and prevented <b>morphine</b> induced hypermethylation of the <strong>Drd2</strong> promoter.
+DRD2	addiction	reward	21955259	Additionally, striatal dopamine D2 receptor (<strong>DRD2</strong>) availability has been implicated in <b>reward</b> function.
+DRD2	drug	cannabinoid	21955259	This study shows that chronic treatment of rats with <b>rimonabant</b> (1.0 and 3.0 mg/kg/day) dose dependently increased <strong>DRD2</strong> availability in the dorsal striatum (14 and 23%) compared with vehicle.
+DRD2	drug	cannabinoid	21955259	High dose <b>rimonabant</b> also increased <strong>DRD2</strong> availability in the ventral striatum (12%) and reduced weight gain.
+DRD2	drug	cannabinoid	21955259	Thus, up regulation of striatal <strong>DRD2</strong> by chronic <b>rimonabant</b> administration may be an underlying mechanism of action and confirms the interactions of the <b>endocannabinoid</b> and dopaminergic systems.
+DRD2	drug	alcohol	21936764	Our aim was to investigate whether drinking behaviour in the past 12 months and smoking relapse due to <b>alcohol</b> use in TD subjects was associated with polymorphisms flanking the TTC12/ANKK1/<strong>DRD2</strong> region since associations have been found between these genes and AUD and TD as separate disorders.
+DRD2	drug	nicotine	21936764	Our aim was to investigate whether drinking behaviour in the past 12 months and <b>smoking</b> relapse due to alcohol use in TD subjects was associated with polymorphisms flanking the TTC12/ANKK1/<strong>DRD2</strong> region since associations have been found between these genes and AUD and TD as separate disorders.
+DRD2	addiction	relapse	21936764	Our aim was to investigate whether drinking behaviour in the past 12 months and smoking <b>relapse</b> due to alcohol use in TD subjects was associated with polymorphisms flanking the TTC12/ANKK1/<strong>DRD2</strong> region since associations have been found between these genes and AUD and TD as separate disorders.
+DRD2	drug	alcohol	21906503	Case control genetic analyses were conducted for the association between HTR1B, SLC6A4, <strong>DRD2</strong>, and OPRμ1 genes and subgroups of <b>alcohol</b> dependence using a sample of 530 controls screened for <b>alcohol</b> problems.
+DRD2	addiction	dependence	21906503	Case control genetic analyses were conducted for the association between HTR1B, SLC6A4, <strong>DRD2</strong>, and OPRμ1 genes and subgroups of alcohol <b>dependence</b> using a sample of 530 controls screened for alcohol problems.
+DRD2	drug	cannabinoid	21820648	Prenatal <b>cannabis</b> exposure decreased dopamine receptor D2 (<strong>DRD2</strong>) messenger RNA expression in the human ventral striatum (nucleus accumbens [NAc]), a key brain reward region.
+DRD2	addiction	reward	21820648	Prenatal cannabis exposure decreased dopamine receptor D2 (<strong>DRD2</strong>) messenger RNA expression in the human ventral striatum (nucleus accumbens [NAc]), a key brain <b>reward</b> region.
+DRD2	drug	cannabinoid	21820648	Prenatal <b>cannabis</b> exposure decreased <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) messenger RNA expression in the human ventral striatum (nucleus accumbens [NAc]), a key brain reward region.
+DRD2	addiction	reward	21820648	Prenatal cannabis exposure decreased <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) messenger RNA expression in the human ventral striatum (nucleus accumbens [NAc]), a key brain <b>reward</b> region.
+DRD2	drug	cannabinoid	21820648	To explore the mechanisms underlying the <b>cannabis</b> associated disturbances, we exposed pregnant rats to <b>THC</b> and examined the epigenetic regulation of the NAc <strong>Drd2</strong> gene in their offspring at postnatal day 2, comparable to the human fetal period studied, and in adulthood.
+DRD2	drug	cannabinoid	21820648	Chromatin immunoprecipitation of the adult NAc revealed increased 2meH3K9 repressive mark and decreased 3meH3K4 and RNA polymerase II at the <strong>Drd2</strong> gene locus in the <b>THC</b> exposed offspring.
+DRD2	addiction	reward	21820648	Decreased <strong>Drd2</strong> expression was accompanied by reduced dopamine D2 receptor (D(2)R) binding sites and increased sensitivity to opiate <b>reward</b> in adulthood.
+DRD2	drug	opioid	21807019	<b>Heroin</b> had dose related effects on Drd1a mRNA in the hypothalamus and on <strong>Drd2</strong> mRNA in the caudate putamen.
+DRD2	drug	nicotine	21806388	The purpose of the present work was to examine the association of SNPs in the DOPA decarboxylase (DDC), dopamine receptor D2 (<strong>DRD2</strong>) and dopamine transporter (SLC6A3) genes with <b>smoking</b> cessation in a large retrospective study featuring approximately 900 cessation events.
+DRD2	drug	nicotine	21806388	The purpose of the present work was to examine the association of SNPs in the DOPA decarboxylase (DDC), <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) and dopamine transporter (SLC6A3) genes with <b>smoking</b> cessation in a large retrospective study featuring approximately 900 cessation events.
+DRD2	drug	nicotine	21806388	Restricting the analyses to subjects who reported to have regularly smoked > 20 cigarettes per day at some point in their life, we used survival analysis methods to model the time from initiation of regular <b>smoking</b> to cessation (defined as quitting with abstinence lasting until enrollment) and its relation with eight polymorphisms in the aforementioned genes (five in DDC, two in <strong>DRD2</strong> and one in SLC6A3) in 1446 participants.
+DRD2	addiction	addiction	21723677	Determining the influences of genes involved in metabolizing dopamine and encoding dopamine receptors, such as the aldehyde dehydrogenase 2 (ALDH2) and dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (<strong>DRD2</strong>/ANKK1) genes, is critical for understanding <b>addictive</b> behavior.
+DRD2	drug	opioid	21723677	Therefore, we investigated the association between the ALDH2 and <strong>DRD2</strong>/ANKK1 Taq IA polymorphisms and <b>heroin</b> dependence.
+DRD2	addiction	dependence	21723677	Therefore, we investigated the association between the ALDH2 and <strong>DRD2</strong>/ANKK1 Taq IA polymorphisms and heroin <b>dependence</b>.
+DRD2	drug	opioid	21723677	The frequency of ALDH2*1/*2 and *2/*2 genotypes was significantly higher in <b>heroin</b> dependent patients than in controls, but the frequency of <strong>DRD2</strong> Taq IA genotypes was not significantly different.
+DRD2	drug	opioid	21723677	The ALDH2 polymorphism, but not the <strong>DRD2</strong>, was associated with <b>heroin</b> dependence.
+DRD2	addiction	dependence	21723677	The ALDH2 polymorphism, but not the <strong>DRD2</strong>, was associated with heroin <b>dependence</b>.
+DRD2	drug	opioid	21714067	Association between polymorphisms of <strong>DRD2</strong> and DRD4 and <b>opioid</b> dependence: evidence from the current studies.
+DRD2	addiction	dependence	21714067	Association between polymorphisms of <strong>DRD2</strong> and DRD4 and opioid <b>dependence</b>: evidence from the current studies.
+DRD2	drug	opioid	21714067	Several studies have assessed the association between genetic polymorphisms of <strong>DRD2</strong> and DRD4 genes and <b>opioid</b> dependence risk, while the results were inconsistent.
+DRD2	addiction	dependence	21714067	Several studies have assessed the association between genetic polymorphisms of <strong>DRD2</strong> and DRD4 genes and opioid <b>dependence</b> risk, while the results were inconsistent.
+DRD2	drug	opioid	21714067	We performed a meta analysis, including 6,846 <b>opioid</b> dependence cases and 4,187 controls from 22 individual studies, to evaluate the roles of four variants (<strong>DRD2</strong>  141ins/delC, rs1799732; <strong>DRD2</strong> 311 Ser > Cys, rs1801028; <strong>DRD2</strong> related TaqI A, rs1800497 and DRD4 exon III VNTR) in <b>opioid</b> dependence for the first time.
+DRD2	addiction	dependence	21714067	We performed a meta analysis, including 6,846 opioid <b>dependence</b> cases and 4,187 controls from 22 individual studies, to evaluate the roles of four variants (<strong>DRD2</strong>  141ins/delC, rs1799732; <strong>DRD2</strong> 311 Ser > Cys, rs1801028; <strong>DRD2</strong> related TaqI A, rs1800497 and DRD4 exon III VNTR) in opioid <b>dependence</b> for the first time.
+DRD2	drug	opioid	21714067	However, no association was detected between the <strong>DRD2</strong> 311 Ser > Cys polymorphism and <b>opioid</b> dependence.
+DRD2	addiction	dependence	21714067	However, no association was detected between the <strong>DRD2</strong> 311 Ser > Cys polymorphism and opioid <b>dependence</b>.
+DRD2	drug	opioid	21714067	In conclusion, our results suggested that <strong>DRD2</strong>  141ins/delC, <strong>DRD2</strong> related TaqI A and DRD4 exon III VNTR polymorphisms might play important roles in the development of <b>opioid</b> dependence.
+DRD2	addiction	dependence	21714067	In conclusion, our results suggested that <strong>DRD2</strong>  141ins/delC, <strong>DRD2</strong> related TaqI A and DRD4 exon III VNTR polymorphisms might play important roles in the development of opioid <b>dependence</b>.
+DRD2	drug	opioid	21613340	We, therefore, investigated possible associations between dopamine D2 receptor (<strong>DRD2</strong>) and personality traits among intravenous <b>heroin</b> addicts.
+DRD2	drug	alcohol	21613303	Do <b>alcohol</b> dependent individuals with <strong>DRD2</strong> A1 allele have an increased risk of relapse?
+DRD2	addiction	relapse	21613303	Do alcohol dependent individuals with <strong>DRD2</strong> A1 allele have an increased risk of <b>relapse</b>?
+DRD2	drug	alcohol	21613303	The TaqIA polymorphism of the dopamine D2 receptor (<strong>DRD2</strong>) gene has been extensively studied in relation to <b>alcoholism</b>, and the TaqI A1 allele appears to be over represented in <b>alcohol</b> dependent individuals.
+DRD2	drug	alcohol	21613303	In the present study, we investigated whether the TaqI A1 allele of the <strong>DRD2</strong> gene region was associated with a higher relapse rate in <b>alcohol</b> dependent individuals.
+DRD2	addiction	relapse	21613303	In the present study, we investigated whether the TaqI A1 allele of the <strong>DRD2</strong> gene region was associated with a higher <b>relapse</b> rate in alcohol dependent individuals.
+DRD2	drug	alcohol	21606657	Here, we genotyped 31 single nucleotide polymorphisms (SNPs): 1 SNP in the dopamine D₂ receptor (<strong>DRD2</strong>) gene, 20 SNPs in 5 different nicotinic acetylcholine receptor subunit (CHRN*) genes, and 10 SNPs in the genes encoding pro ghrelin (GHRL) and its receptor (GHSR), in a pilot study of type 1 <b>alcoholics</b> (n = 84) and healthy controls (n = 32).
+DRD2	drug	nicotine	21540761	Association between <strong>DRD2</strong>/ANKK1 Taq1A genotypes, depression and <b>smoking</b> cessation with <b>nicotine</b> replacement therapy.
+DRD2	drug	nicotine	21540761	Variant genotypes of the Taq1A (<strong>DRD2</strong>/ANKK1, 32806T, rs1800497) polymorphism have been associated with failure to stop <b>smoking</b> in some studies, but not others.
+DRD2	drug	alcohol	21403585	Lack of allelic association between markers at the <strong>DRD2</strong> and ANKK1 gene loci with the <b>alcohol</b> dependence syndrome and criminal activity.
+DRD2	addiction	dependence	21403585	Lack of allelic association between markers at the <strong>DRD2</strong> and ANKK1 gene loci with the alcohol <b>dependence</b> syndrome and criminal activity.
+DRD2	drug	nicotine	21244814	Waterpipe <b>Smoking</b> And The <strong>DRD2</strong>/ANKK1 Genotype.
+DRD2	drug	nicotine	21244814	A polymorphism (TaqI) in the 3' untranslated region of the dopamine receptor gene (<strong>DRD2</strong>), later localized to the neighboring ANKK1 gene, has been previously linked to cigarette <b>smoking</b>.
+DRD2	drug	nicotine	21244814	Since all <b>tobacco</b> products share the ability of stimulating the dopaminergic reward system, variation in the <strong>DRD2</strong> genotype might be associated with waterpipe <b>smoking</b> addiction.
+DRD2	addiction	addiction	21244814	Since all tobacco products share the ability of stimulating the dopaminergic reward system, variation in the <strong>DRD2</strong> genotype might be associated with waterpipe smoking <b>addiction</b>.
+DRD2	addiction	reward	21244814	Since all tobacco products share the ability of stimulating the dopaminergic <b>reward</b> system, variation in the <strong>DRD2</strong> genotype might be associated with waterpipe smoking addiction.
+DRD2	drug	nicotine	21244814	This study aims to explore genetic variations in <strong>DRD2</strong> gene and waterpipe <b>smoking</b>, motives and addiction in Egyptian rural males.
+DRD2	addiction	addiction	21244814	This study aims to explore genetic variations in <strong>DRD2</strong> gene and waterpipe smoking, motives and <b>addiction</b> in Egyptian rural males.
+DRD2	addiction	relapse	21244814	This study revealed that the maximum duration before experiencing <b>craving</b> to smoke waterpipe and frequency of visiting cafés to smoke may be influenced by an inherited variations in the <strong>DRD2</strong> genotype.
+DRD2	drug	alcohol	21244440	Risky <b>alcohol</b> use in adolescence: the role of genetics (<strong>DRD2</strong>, SLC6A4) and coping motives.
+DRD2	drug	alcohol	21244440	The aim of this study was to examine relationships between the dopamine D2 receptor gene (<strong>DRD2</strong>) Taq1A polymorphism (rs1800497), a serotonin transporter gene (SLC6A4) polymorphism (5 HTTLPR), coping motives, and adolescents' binge drinking and <b>alcohol</b> related problems.
+DRD2	addiction	intoxication	21244440	The aim of this study was to examine relationships between the dopamine D2 receptor gene (<strong>DRD2</strong>) Taq1A polymorphism (rs1800497), a serotonin transporter gene (SLC6A4) polymorphism (5 HTTLPR), coping motives, and adolescents' <b>binge</b> drinking and alcohol related problems.
+DRD2	drug	alcohol	21244440	Coping motives were positively related to both binge drinking and <b>alcohol</b> related problems, while <strong>DRD2</strong> and SLC6A4 genotypes were not.
+DRD2	addiction	intoxication	21244440	Coping motives were positively related to both <b>binge</b> drinking and alcohol related problems, while <strong>DRD2</strong> and SLC6A4 genotypes were not.
+DRD2	drug	alcohol	21244440	The link between coping motives and <b>alcohol</b> outcomes was stronger among those carrying the <strong>DRD2</strong> risk (A1) allele.
+DRD2	drug	alcohol	21244440	An interaction between a vulnerability gene (<strong>DRD2</strong>) and a cognitive factor (coping drinking) was found to be related to adolescents' binge drinking and <b>alcohol</b> related problems.
+DRD2	addiction	intoxication	21244440	An interaction between a vulnerability gene (<strong>DRD2</strong>) and a cognitive factor (coping drinking) was found to be related to adolescents' <b>binge</b> drinking and alcohol related problems.
+DRD2	drug	alcohol	22593996	The purpose of this study was to determine the relationship between the sweet liking phenotype, a subtype of <b>alcoholism</b> according to Lesch and/or Cloninger and gene polymorphism of the <strong>DRD2</strong> dopaminergic system.
+DRD2	drug	alcohol	22593996	Sucrose preference correlated with the TaqI A1 allele of the <strong>DRD2</strong> gene among <b>alcoholics</b> (p = 0.0016).
+DRD2	drug	alcohol	22593996	Changes in the distribution of alleles and genotypes of the TaqI <strong>DRD2</strong> polymorphism correlated with sucrose preference among <b>alcoholics</b> (p = 0.008).
+DRD2	drug	nicotine	21168125	TTC12 ANKK1 <strong>DRD2</strong> and CHRNA5 CHRNA3 CHRNB4 influence different pathways leading to <b>smoking</b> behavior from adolescence to mid adulthood.
+DRD2	drug	nicotine	21168125	CHRNA5 CHRNA3 CHRNB4 and TTC12 ANKK1 <strong>DRD2</strong> gene clusters influence <b>smoking</b> behavior.
+DRD2	addiction	dependence	21130610	Imaging studies in drug dependent subjects show reduced striatal dopamine D(2/3) receptor (<strong>DRD2</strong>/3) availability, and it is hypothesized that increasing <strong>DRD2</strong>/3 availability is a promising strategy to treat drug <b>dependence</b>.
+DRD2	drug	nicotine	21130610	These observations suggest that increased <strong>DRD2</strong>/3 availability may contribute to varenicline's efficacy for <b>smoking</b> cessation and show promise for varenicline as a treatment of other types of drug dependence.
+DRD2	addiction	dependence	21130610	These observations suggest that increased <strong>DRD2</strong>/3 availability may contribute to varenicline's efficacy for smoking cessation and show promise for varenicline as a treatment of other types of drug <b>dependence</b>.
+DRD2	drug	alcohol	21070510	Interaction between ALDH2*1*1 and <strong>DRD2</strong>/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co morbid with <b>alcoholism</b>.
+DRD2	drug	alcohol	20958329	The anatomical proximity of the cannabinoid type 1 (CNR1/CB1R) and the dopamine D2 receptors (<strong>DRD2</strong>), their ability to form CB1R <strong>DRD2</strong> heteromers, their opposing roles in locomotion, and their involvement in <b>ethanol</b>'s reinforcing and addictive properties prompted us to study the levels and distribution of CB1R after chronic <b>ethanol</b> intake, in the presence and absence of <strong>DRD2</strong>.
+DRD2	drug	cannabinoid	20958329	The anatomical proximity of the <b>cannabinoid</b> type 1 (CNR1/CB1R) and the dopamine D2 receptors (<strong>DRD2</strong>), their ability to form CB1R <strong>DRD2</strong> heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and addictive properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of <strong>DRD2</strong>.
+DRD2	addiction	addiction	20958329	The anatomical proximity of the cannabinoid type 1 (CNR1/CB1R) and the dopamine D2 receptors (<strong>DRD2</strong>), their ability to form CB1R <strong>DRD2</strong> heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and <b>addictive</b> properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of <strong>DRD2</strong>.
+DRD2	addiction	reward	20958329	The anatomical proximity of the cannabinoid type 1 (CNR1/CB1R) and the dopamine D2 receptors (<strong>DRD2</strong>), their ability to form CB1R <strong>DRD2</strong> heteromers, their opposing roles in locomotion, and their involvement in ethanol's <b>reinforcing</b> and addictive properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of <strong>DRD2</strong>.
+DRD2	drug	alcohol	20958329	We monitored the drinking patterns and locomotor activity of <strong>Drd2</strong>+/+ and <strong>Drd2</strong> /  mice consuming either water or a 20% (v/v) <b>ethanol</b> solution (forced <b>ethanol</b> intake) for 6 months and used the selective CB1 receptor antagonist [³H]SR141716A to quantify CB1R levels in different brain regions with in vitro receptor autoradiography.
+DRD2	drug	alcohol	20958329	We found that the lack of <strong>DRD2</strong> leads to a marked upregulation (approximately 2 fold increase) of CB1R in the cerebral cortex, the caudate putamen, and the nucleus accumbens, which was reversed by chronic <b>ethanol</b> intake.
+DRD2	drug	alcohol	20958329	The results suggest that <strong>DRD2</strong> mediated dopaminergic neurotransmission and chronic <b>ethanol</b> intake exert an inhibitory effect on cannabinoid receptor expression in cortical and striatal regions implicated in the reinforcing and addictive properties of <b>ethanol</b>.
+DRD2	drug	cannabinoid	20958329	The results suggest that <strong>DRD2</strong> mediated dopaminergic neurotransmission and chronic ethanol intake exert an inhibitory effect on <b>cannabinoid</b> receptor expression in cortical and striatal regions implicated in the reinforcing and addictive properties of ethanol.
+DRD2	addiction	addiction	20958329	The results suggest that <strong>DRD2</strong> mediated dopaminergic neurotransmission and chronic ethanol intake exert an inhibitory effect on cannabinoid receptor expression in cortical and striatal regions implicated in the reinforcing and <b>addictive</b> properties of ethanol.
+DRD2	addiction	reward	20958329	The results suggest that <strong>DRD2</strong> mediated dopaminergic neurotransmission and chronic ethanol intake exert an inhibitory effect on cannabinoid receptor expression in cortical and striatal regions implicated in the <b>reinforcing</b> and addictive properties of ethanol.
+DRD2	drug	alcohol	20924884	Population based case control study of <strong>DRD2</strong> gene polymorphisms and <b>alcoholism</b>.
+DRD2	drug	alcohol	20924884	D2 dopamine receptor (<strong>DRD2</strong>) gene has been among the stronger candidate genes implicated in <b>alcoholism</b>.
+DRD2	drug	alcohol	20924884	Six <strong>DRD2</strong> SNPs were assessed in 81 individuals with <b>alcoholism</b> and 151 controls to evaluate the association between single nucleotide polymorphisms (SNPs) and <b>alcoholism</b>.
+DRD2	drug	alcohol	20924884	Of the three models (dominant, recessive, and additive) tested for association between <b>alcoholism</b> and <strong>DRD2</strong> SNPs, only the additive model shows association for three loci (rs1116313, TaqID, and rs2734835).
+DRD2	drug	cocaine	20801583	Several studies have looked for a link between <b>cocaine</b> addiction and the genes of the dopaminergic system: the genes <strong>DRD2</strong>, COMT, SLC6A3 (coding for the dopamine transporter DAT) and DBH (coding for the dopamine beta hydroxylase) but unfortunately very few well established results.
+DRD2	addiction	addiction	20801583	Several studies have looked for a link between cocaine <b>addiction</b> and the genes of the dopaminergic system: the genes <strong>DRD2</strong>, COMT, SLC6A3 (coding for the dopamine transporter DAT) and DBH (coding for the dopamine beta hydroxylase) but unfortunately very few well established results.
+DRD2	drug	cocaine	20801583	Several functional alterations caused by different mutations of the genes involved in dopaminergic transmission (principally 1021C>T of the gene DBH, but also Val158Met of the gene COMT, TaqI A of the gene <strong>DRD2</strong> and VNTR 9 repeat of the DAT) could result in a <b>cocaine</b> induced psychosis prone phenotype.
+DRD2	drug	nicotine	20712524	This study evaluates the relationship of six polymorphisms found in the CHRNA3, <strong>DRD2</strong> and COMT genes with <b>nicotine</b> dependence, the ability to quit <b>smoking</b> and the occurrence of withdrawal symptoms after short term use of <b>nicotine</b> patch in hospitalized patients.
+DRD2	addiction	dependence	20712524	This study evaluates the relationship of six polymorphisms found in the CHRNA3, <strong>DRD2</strong> and COMT genes with nicotine <b>dependence</b>, the ability to quit smoking and the occurrence of withdrawal symptoms after short term use of nicotine patch in hospitalized patients.
+DRD2	addiction	withdrawal	20712524	This study evaluates the relationship of six polymorphisms found in the CHRNA3, <strong>DRD2</strong> and COMT genes with nicotine dependence, the ability to quit smoking and the occurrence of <b>withdrawal</b> symptoms after short term use of nicotine patch in hospitalized patients.
+DRD2	drug	nicotine	20712524	After correcting for multiple testing, three polymorphisms in the <strong>DRD2</strong> gene (Taq1A, Taq1B and Pro319Pro) were significantly associated with <b>nicotine</b> dependence (p = 0.018, p = 0.048 and p = 0.006, respectively).
+DRD2	addiction	dependence	20712524	After correcting for multiple testing, three polymorphisms in the <strong>DRD2</strong> gene (Taq1A, Taq1B and Pro319Pro) were significantly associated with nicotine <b>dependence</b> (p = 0.018, p = 0.048 and p = 0.006, respectively).
+DRD2	drug	nicotine	20712524	This study confirms the reported association of the CHRNA3 locus with <b>nicotine</b> dependence and shows the involvement of two independent <strong>DRD2</strong> polymorphisms in <b>nicotine</b> dependence.
+DRD2	addiction	dependence	20712524	This study confirms the reported association of the CHRNA3 locus with nicotine <b>dependence</b> and shows the involvement of two independent <strong>DRD2</strong> polymorphisms in nicotine <b>dependence</b>.
+DRD2	drug	cocaine	20643829	Deficiency of Ago2 in dopamine 2 receptor (<strong>Drd2</strong>) expressing neurons greatly reduces the motivation to self administer <b>cocaine</b> in mice.
+DRD2	drug	cocaine	20643829	Comparison of miRNAs affected by Ago2 deficiency with miRNAs that are enriched and/or up regulated in <strong>Drd2</strong> neurons in response to <b>cocaine</b> identified a set of miRNAs that are likely to play a role in <b>cocaine</b> addiction.
+DRD2	addiction	addiction	20643829	Comparison of miRNAs affected by Ago2 deficiency with miRNAs that are enriched and/or up regulated in <strong>Drd2</strong> neurons in response to cocaine identified a set of miRNAs that are likely to play a role in cocaine <b>addiction</b>.
+DRD2	drug	alcohol	20554694	Earlier findings on the associations of <strong>DRD2</strong> and NPY with <b>alcohol</b> dependence were supported: <strong>DRD2</strong>/ANKK1 Taq1A(1) increased (P = 0.04) and NPY Pro7 decreased (P = 0.01) the risk of <b>alcohol</b> dependence.
+DRD2	addiction	dependence	20554694	Earlier findings on the associations of <strong>DRD2</strong> and NPY with alcohol <b>dependence</b> were supported: <strong>DRD2</strong>/ANKK1 Taq1A(1) increased (P = 0.04) and NPY Pro7 decreased (P = 0.01) the risk of alcohol <b>dependence</b>.
+DRD2	drug	alcohol	20554694	The role of <strong>DRD2</strong> and NPY on <b>alcohol</b> dependence was also supported.
+DRD2	addiction	dependence	20554694	The role of <strong>DRD2</strong> and NPY on alcohol <b>dependence</b> was also supported.
+DRD2	drug	cocaine	20505554	Association study between the DAT1, DBH and <strong>DRD2</strong> genes and <b>cocaine</b> dependence in a Spanish sample.
+DRD2	addiction	dependence	20505554	Association study between the DAT1, DBH and <strong>DRD2</strong> genes and cocaine <b>dependence</b> in a Spanish sample.
+DRD2	drug	cocaine	20505554	We genotyped the Int8 and 3'UTR variable number of tandem repeats of the dopamine transporter gene (DAT1/SLC6A3), the TaqIA (rs1800497) and TaqIB (rs1079597) SNP polymorphisms within the <strong>dopamine receptor D2</strong> gene and the 19 bp insertion/deletion and c.444G>A (rs1108580) polymorphisms of the dopamine β hydroxylase gene (DBH) in a Spanish sample of 169 patients with <b>cocaine</b> addiction and 169 sex matched controls.
+DRD2	addiction	addiction	20505554	We genotyped the Int8 and 3'UTR variable number of tandem repeats of the dopamine transporter gene (DAT1/SLC6A3), the TaqIA (rs1800497) and TaqIB (rs1079597) SNP polymorphisms within the <strong>dopamine receptor D2</strong> gene and the 19 bp insertion/deletion and c.444G>A (rs1108580) polymorphisms of the dopamine β hydroxylase gene (DBH) in a Spanish sample of 169 patients with cocaine <b>addiction</b> and 169 sex matched controls.
+DRD2	drug	nicotine	20350135	We examined genotypes at two dopamine related loci, <strong>DRD2</strong>/ANKK1 (rs1800497) and DBH (rs77905), in 577 heavy <b>smokers</b> participating in a prospective study of <b>smoking</b> cessation in general care in Germany.
+DRD2	drug	nicotine	20350135	<b>Smoking</b> status after 1 year was significantly associated with <strong>DRD2</strong>/ANKK1, odds of abstinence being 4.4 fold (95% CI: 1.5 12.9) increased in TT  versus CC homozygous subjects (p = 0.008).
+DRD2	drug	cocaine	20170711	Association analysis between polymorphisms in the dopamine D2 receptor (<strong>DRD2</strong>) and dopamine transporter (DAT1) genes with <b>cocaine</b> dependence.
+DRD2	addiction	dependence	20170711	Association analysis between polymorphisms in the dopamine D2 receptor (<strong>DRD2</strong>) and dopamine transporter (DAT1) genes with cocaine <b>dependence</b>.
+DRD2	drug	cocaine	20170711	<b>Cocaine</b> dependent individuals (n=347) and unaffected controls (n=257) of African descent were genotyped for the polymorphisms in the <strong>DRD2</strong> and DAT1 genes.
+DRD2	drug	alcohol	20146828	The dopamine D2 receptor (<strong>DRD2</strong>) gene on chromosome 11 (q22 q23) has been found to be associated with increased <b>alcohol</b> consumption through mechanisms involving incentive salience attributions and craving in <b>alcoholic</b> patients.
+DRD2	addiction	relapse	20146828	The dopamine D2 receptor (<strong>DRD2</strong>) gene on chromosome 11 (q22 q23) has been found to be associated with increased alcohol consumption through mechanisms involving incentive salience attributions and <b>craving</b> in alcoholic patients.
+DRD2	addiction	reward	20146828	The dopamine D2 receptor (<strong>DRD2</strong>) gene on chromosome 11 (q22 q23) has been found to be associated with increased alcohol consumption through mechanisms involving <b>incentive</b> salience attributions and craving in alcoholic patients.
+DRD2	drug	alcohol	20146828	Therefore, we investigated the association of three single nucleotide polymorphisms (SNP) in <strong>DRD2</strong> gene with <b>alcohol</b> dependence in the north Indian subjects.
+DRD2	addiction	dependence	20146828	Therefore, we investigated the association of three single nucleotide polymorphisms (SNP) in <strong>DRD2</strong> gene with alcohol <b>dependence</b> in the north Indian subjects.
+DRD2	drug	alcohol	20146828	In a retrospective analysis, genetic association of three polymorphisms from <strong>DRD2</strong> gene with <b>alcohol</b> dependence was investigated using a case control approach.
+DRD2	addiction	dependence	20146828	In a retrospective analysis, genetic association of three polymorphisms from <strong>DRD2</strong> gene with alcohol <b>dependence</b> was investigated using a case control approach.
+DRD2	drug	alcohol	20146828	The study showed a significant association of  141C Ins allele and a trend of association of TaqI A1 allele of <strong>DRD2</strong> with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	20146828	The study showed a significant association of  141C Ins allele and a trend of association of TaqI A1 allele of <strong>DRD2</strong> with alcohol <b>dependence</b>.
+DRD2	drug	alcohol	20146828	Two polymorphisms namely,  141C Ins/Del and TaqI A in <strong>DRD2</strong> gene may have clinical implications among Indian <b>alcoholic</b> subjects.
+DRD2	drug	opioid	20119466	diminished euphoric effects from <b>opioids</b> potentially due to <strong>DRD2</strong> polymorphisms decreasing the functioning of the dopaminergic reward system).
+DRD2	addiction	reward	20119466	diminished euphoric effects from opioids potentially due to <strong>DRD2</strong> polymorphisms decreasing the functioning of the dopaminergic <b>reward</b> system).
+DRD2	drug	alcohol	20002020	Results reveal decreased likelihood of DT in <b>alcoholics</b> that carry the <strong>DRD2</strong> rs6276 G allele and SLC6A4 LL genotype.
+DRD2	drug	amphetamine	19968402	Evaluation of genetic variability in the <strong>dopamine receptor D2</strong> in relation to behavioral inhibition and impulsivity/sensation seeking: an exploratory study with d <b>amphetamine</b> in healthy participants.
+DRD2	addiction	relapse	19968402	Evaluation of genetic variability in the <strong>dopamine receptor D2</strong> in relation to behavioral inhibition and impulsivity/sensation <b>seeking</b>: an exploratory study with d amphetamine in healthy participants.
+DRD2	drug	amphetamine	19968402	We secondarily evaluated the <strong>DRD2</strong> SNPs in relation to response to d <b>amphetamine</b> on stop task performance and mood ratings.
+DRD2	addiction	reward	19940429	Another therapeutic conundrum relates to the paradoxical finding that the dopaminergic agonist bromocriptine induces stronger activation of brain <b>reward</b> circuitry in individuals who carry the <strong>DRD2</strong> A1 allele compared with <strong>DRD2</strong> A2 allele carriers.
+DRD2	addiction	relapse	19940429	This term couples the mechanism for <b>relapse</b>, which is "deprivation amplification," especially in <strong>DRD2</strong> A1 allele carriers with natural D2 agonist therapy utilizing amino acid precursors and COMT and enkepalinase inhibition therapy.
+DRD2	drug	cannabinoid	19931559	(3) Feeding motivation  and reward related systems (opioids, OPRD1, <b>cannabinoids</b> (anandamide (AEA), <b>THC</b>, CBR1), dopamine, <strong>DRD2</strong>, DRD3, DRD4, catecholamine O methyl transferase (COMT).
+DRD2	drug	opioid	19931559	(3) Feeding motivation  and reward related systems (<b>opioids</b>, OPRD1, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, <strong>DRD2</strong>, DRD3, DRD4, catecholamine O methyl transferase (COMT).
+DRD2	addiction	reward	19931559	(3) Feeding motivation  and <b>reward</b> related systems (opioids, OPRD1, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, <strong>DRD2</strong>, DRD3, DRD4, catecholamine O methyl transferase (COMT).
+DRD2	drug	alcohol	19914781	[10] provided the first evidence that the dopamine D2 receptor gene (<strong>DRD2</strong>) Taq 1 A1 allele significantly associated with severe <b>alcoholism</b> whereby the author's suggested that they found the first "reward gene" located in the mesolimbic system.
+DRD2	addiction	reward	19914781	[10] provided the first evidence that the dopamine D2 receptor gene (<strong>DRD2</strong>) Taq 1 A1 allele significantly associated with severe alcoholism whereby the author's suggested that they found the first "<b>reward</b> gene" located in the mesolimbic system.
+DRD2	addiction	reward	19914781	In contrast powerful D2 agonists like bromocryptine show a heightened activation of the <b>reward</b> circuitry only in <strong>DRD2</strong> A1 allele carriers.
+DRD2	addiction	reward	19914781	If music causes a powerful activation in spite of the <strong>DRD2</strong> A1 allele due to a strong DA neuronal release which subsequently impinges on existing D2 receptors, then it is reasonable to assume that music is a strong indirect D2 agonist (by virtue of DA neuronal release in the NAc) and may have important therapeutic applicability in <b>Reward</b> Deficiency Syndrome (RDS) related behaviors including Substance Use Disorder (SUD).
+DRD2	drug	nicotine	19904802	To address this issue, we measured DA D2/D3 receptor (<strong>DRD2</strong>/3) availability in twenty eight healthy men (<b>nicotine</b> dependent <b>smokers</b> and never <b>smokers</b>) using positron emission tomography with [18F]fallypride.
+DRD2	drug	nicotine	19904802	The effects of <strong>DRD2</strong>/3 availability in emotion related brain regions and <b>nicotine</b> dependence on amygdala response to unpleasant stimuli were examined by multiple regression analysis.
+DRD2	addiction	dependence	19904802	The effects of <strong>DRD2</strong>/3 availability in emotion related brain regions and nicotine <b>dependence</b> on amygdala response to unpleasant stimuli were examined by multiple regression analysis.
+DRD2	addiction	aversion	19904802	Thus, individuals with high prefrontal <strong>DRD2</strong>/3 availability may be more responsive toward <b>aversive</b> and stressful information.
+DRD2	addiction	addiction	19900188	Polymorphisms of <strong>DRD2</strong> and ANKK1 have been associated with psychiatric syndromes where there is believed to be an underlying learning process deficit such as <b>addiction</b>, post traumatic stress disorder and psychopathy.
+DRD2	drug	alcohol	19900188	We investigated the effects of the <strong>DRD2</strong> C957T and ANKK1 TaqIA single nucleotide polymorphism (SNP), which have been associated with psychopathic traits in <b>alcoholic</b> patients, on fear conditioning and aversive priming in healthy volunteers.
+DRD2	addiction	aversion	19900188	We investigated the effects of the <strong>DRD2</strong> C957T and ANKK1 TaqIA single nucleotide polymorphism (SNP), which have been associated with psychopathic traits in alcoholic patients, on fear conditioning and <b>aversive</b> priming in healthy volunteers.
+DRD2	addiction	aversion	19900188	We found that the <strong>DRD2</strong> C957T SNP, but not the ANKK1 TaqIA SNP, was associated with both differential conditioning of the skin conductance response and the <b>aversive</b> priming effect.
+DRD2	drug	nicotine	19842028	To investigate further the relationships between the <strong>DRD2</strong> genotypes, cigarette use and <b>nicotine</b> dependence, we examined the prevalence of polymorphisms in the TaqIA (A1 and A2) and the TaqIB (B1 and B2) alleles among a series of 608 non Hispanic White bladder cancer patients and 608 matched controls.
+DRD2	addiction	dependence	19842028	To investigate further the relationships between the <strong>DRD2</strong> genotypes, cigarette use and nicotine <b>dependence</b>, we examined the prevalence of polymorphisms in the TaqIA (A1 and A2) and the TaqIB (B1 and B2) alleles among a series of 608 non Hispanic White bladder cancer patients and 608 matched controls.
+DRD2	drug	nicotine	19842028	The present study suggests that the <strong>DRD2</strong> alleles A1 and B1 confer greater vulnerability to <b>tobacco</b> use.
+DRD2	drug	alcohol	19796663	Influence of <strong>DRD2</strong> and ANKK1 genotypes on apomorphine induced growth hormone (GH) response in <b>alcohol</b> dependent patients.
+DRD2	drug	alcohol	19796663	Apomorphine challenge tests measuring GH responses on 5 time points were performed on day 1 of <b>alcohol</b> detoxification in 43 patients with <b>alcohol</b> dependence; patients were genotyped for 11 polymorphisms including <strong>DRD2</strong>, ANKK1, NCAM1 and TTC12.
+DRD2	addiction	dependence	19796663	Apomorphine challenge tests measuring GH responses on 5 time points were performed on day 1 of alcohol detoxification in 43 patients with alcohol <b>dependence</b>; patients were genotyped for 11 polymorphisms including <strong>DRD2</strong>, ANKK1, NCAM1 and TTC12.
+DRD2	drug	alcohol	19796663	This has been the first study showing significant associations between apomorphine induced GH response and SNPs in <strong>DRD2</strong> and ANKK1 in <b>alcohol</b> dependent patients.
+DRD2	drug	alcohol	19764934	<b>Alcoholism</b> is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in opioid receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (<strong>DRD2</strong>) as well as environmental factors (education and marital status) might affect the risk of <b>alcoholism</b>.
+DRD2	drug	opioid	19764934	Alcoholism is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in <b>opioid</b> receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (<strong>DRD2</strong>) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+DRD2	addiction	reward	19764934	Alcoholism is a polygenic disorder resulting from <b>reward</b> deficiency; polymorphisms in <b>reward</b> genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in opioid receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (<strong>DRD2</strong>) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+DRD2	drug	alcohol	19764934	<b>Alcoholism</b> is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in opioid receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) as well as environmental factors (education and marital status) might affect the risk of <b>alcoholism</b>.
+DRD2	drug	opioid	19764934	Alcoholism is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in <b>opioid</b> receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+DRD2	addiction	reward	19764934	Alcoholism is a polygenic disorder resulting from <b>reward</b> deficiency; polymorphisms in <b>reward</b> genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in opioid receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+DRD2	drug	alcohol	19764934	Genotyping of 5 HTTLPR, OPRM1 A118G, and <strong>DRD2</strong> 141C Ins/Del was performed in 365 <b>alcoholics</b> and 338 nonalcoholic controls of Mexican Americans who were gender  and age matched.
+DRD2	drug	alcohol	19764934	Main effect of education, OPRM1, and <strong>DRD2</strong> was detected in <b>alcoholic</b> stratum of moderate and/or largest MAXDRINKS with education < or =12 years, OPRM1 118 A/A, and <strong>DRD2</strong>  141C Ins/Ins being risk factors.
+DRD2	drug	alcohol	19764934	Our results suggest main effect of education background, OPRM1 A118G, and <strong>DRD2</strong>  141C Ins/Del as well as education*OPRM1 interaction in contribution to moderate and/or severe <b>alcoholism</b> in Mexican Americans.
+DRD2	drug	nicotine	19761593	Influences of polymorphic variants of <strong>DRD2</strong> and SLC6A3 genes, and their combinations on <b>smoking</b> in Polish population.
+DRD2	drug	nicotine	19761593	A1 allele of <strong>DRD2</strong> gene is associated with a reduced dopamine D2 receptor density, and it has been hypothesised that A1 carriers are more vulnerable to <b>smoking</b>.
+DRD2	drug	nicotine	19761593	In the present study we investigated whether polymorphic variants of <strong>DRD2</strong> and SLC6A3 genes and their combinations are associated with the <b>smoking</b> habit in the Polish population.
+DRD2	drug	nicotine	19761593	Genotyping for TaqIA polymorphism of <strong>DRD2</strong> and SLC6A3 VNTR polymorphism was performed in 150 ever <b>smokers</b> and 158 never <b>smokers</b>.
+DRD2	drug	nicotine	19761593	At the used alpha levels no association between <strong>DRD2</strong> and SLC6A3 genotypes and <b>smoking</b> status was found.
+DRD2	drug	nicotine	19761593	Polymorphic variants of <strong>DRD2</strong> and SLC6A3 genes may influence some aspects of the <b>smoking</b> behavior, including age of starting regular <b>smoking</b>, the level of cigarette consumption, and periods of abstinence.
+DRD2	drug	opioid	19664686	Potential association of <strong>DRD2</strong> and DAT1 genetic variation with <b>heroin</b> dependence.
+DRD2	addiction	dependence	19664686	Potential association of <strong>DRD2</strong> and DAT1 genetic variation with heroin <b>dependence</b>.
+DRD2	drug	opioid	19664686	The aim of our study was to investigate the potential association of dopamine receptor D2 gene (<strong>DRD2</strong>) TaqI RFLP A (rs1800497) and dopamine transporter gene (DAT) 3'untranslated region VNTR genetic variations with <b>heroin</b> addiction.
+DRD2	addiction	addiction	19664686	The aim of our study was to investigate the potential association of dopamine receptor D2 gene (<strong>DRD2</strong>) TaqI RFLP A (rs1800497) and dopamine transporter gene (DAT) 3'untranslated region VNTR genetic variations with heroin <b>addiction</b>.
+DRD2	drug	opioid	19664686	The aim of our study was to investigate the potential association of <strong>dopamine receptor D2</strong> gene (<strong>DRD2</strong>) TaqI RFLP A (rs1800497) and dopamine transporter gene (DAT) 3'untranslated region VNTR genetic variations with <b>heroin</b> addiction.
+DRD2	addiction	addiction	19664686	The aim of our study was to investigate the potential association of <strong>dopamine receptor D2</strong> gene (<strong>DRD2</strong>) TaqI RFLP A (rs1800497) and dopamine transporter gene (DAT) 3'untranslated region VNTR genetic variations with heroin <b>addiction</b>.
+DRD2	drug	opioid	19664686	Our results showed that <strong>DRD2</strong> TaqI A1 allele carriers (genotypes A1A1 and A1A2) were prone to <b>heroin</b> abuse in models of dominance or co dominance.
+DRD2	drug	opioid	19615406	Finally, <b>opioid</b> dosage requirements may be increased depending on the risk of drug addiction (e.g., <strong>DRD2</strong> polymorphisms decreasing the functioning of the dopaminergic reward system).
+DRD2	addiction	addiction	19615406	Finally, opioid dosage requirements may be increased depending on the risk of drug <b>addiction</b> (e.g., <strong>DRD2</strong> polymorphisms decreasing the functioning of the dopaminergic reward system).
+DRD2	addiction	reward	19615406	Finally, opioid dosage requirements may be increased depending on the risk of drug addiction (e.g., <strong>DRD2</strong> polymorphisms decreasing the functioning of the dopaminergic <b>reward</b> system).
+DRD2	drug	alcohol	19603545	The dopamine D2 receptor (<strong>DRD2</strong>) plays an important role in the reinforcing and motivating effects of <b>ethanol</b>.
+DRD2	addiction	reward	19603545	The dopamine D2 receptor (<strong>DRD2</strong>) plays an important role in the <b>reinforcing</b> and motivating effects of ethanol.
+DRD2	drug	alcohol	19603545	We confirmed the hypothesis that haplotypes, which are supposed to induce a low <strong>DRD2</strong> expression, are associated with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	19603545	We confirmed the hypothesis that haplotypes, which are supposed to induce a low <strong>DRD2</strong> expression, are associated with alcohol <b>dependence</b>.
+DRD2	drug	nicotine	19494806	The <strong>DRD2</strong> SNP appears to represent a novel association with <b>nicotine</b> dependence.
+DRD2	addiction	dependence	19494806	The <strong>DRD2</strong> SNP appears to represent a novel association with nicotine <b>dependence</b>.
+DRD2	drug	alcohol	19376678	The TaqI A <strong>DRD2</strong> polymorphism in type II <b>alcohol</b> dependence: a marker of age at onset or of a familial disease?
+DRD2	addiction	dependence	19376678	The TaqI A <strong>DRD2</strong> polymorphism in type II alcohol <b>dependence</b>: a marker of age at onset or of a familial disease?
+DRD2	addiction	relapse	19376678	Significant association has been reported between the A1 allele of the D2 dopamine receptor (<strong>DRD2</strong>) gene, substance misuse and personality traits of impulsivity and novelty <b>seeking</b>.
+DRD2	drug	alcohol	19376678	We assessed the association between the TaqI A <strong>DRD2</strong> gene polymorphism with Cloninger's typology and family history of <b>alcohol</b> abuse, which is thought to be more frequent in type II <b>alcoholics</b>.
+DRD2	drug	alcohol	19376678	Furthermore, the A1 allele of the <strong>DRD2</strong> was significantly associated with paternal history of <b>alcoholism</b> (chi(2)(1)=4.66; P=.031) and male, first degree, collateral history of <b>alcoholism</b> (chi(2)(1)=4.40; P=.036).
+DRD2	drug	alcohol	19376678	Age at onset of <b>alcohol</b> related problems as main discriminator between type I and type II <b>alcohol</b> dependence does not seem to be associated by the TaqI A <strong>DRD2</strong> polymorphism.
+DRD2	addiction	dependence	19376678	Age at onset of alcohol related problems as main discriminator between type I and type II alcohol <b>dependence</b> does not seem to be associated by the TaqI A <strong>DRD2</strong> polymorphism.
+DRD2	drug	alcohol	19376678	However, the A1 allele of the <strong>DRD2</strong> may be a marker of male familial <b>alcoholism</b>, which has been associated with type II <b>alcohol</b> dependence.
+DRD2	addiction	dependence	19376678	However, the A1 allele of the <strong>DRD2</strong> may be a marker of male familial alcoholism, which has been associated with type II alcohol <b>dependence</b>.
+DRD2	drug	opioid	19373123	Here, we comprehensively analyzed the <strong>DRD2</strong> gene locus, and in addition, the ANKK1 rs1800497C>T single nucleotide polymorphism (SNP), formerly known as 'dopamine D2 receptor Taq1A C>T polymorphism', for associations with the risk of opiate addiction and the <b>methadone</b> dosage requirements.
+DRD2	addiction	addiction	19373123	Here, we comprehensively analyzed the <strong>DRD2</strong> gene locus, and in addition, the ANKK1 rs1800497C>T single nucleotide polymorphism (SNP), formerly known as 'dopamine D2 receptor Taq1A C>T polymorphism', for associations with the risk of opiate <b>addiction</b> and the methadone dosage requirements.
+DRD2	drug	opioid	19373123	Allelic frequencies of <strong>DRD2</strong>/ANKK1 polymorphisms were compared between 85 <b>methadone</b> substituted Caucasian patients and a random sample of 99 healthy Caucasian controls.
+DRD2	drug	opioid	19373123	Within patients, the average and maximum daily <b>methadone</b> dose during the first year of treatment and the time when that maximum dose was reached were analyzed for an association with <strong>DRD2</strong>/ANKK1 genetics.
+DRD2	drug	opioid	19373123	The average and maximum daily <b>methadone</b> doses were significantly associated with the <strong>DRD2</strong> rs6275C>T SNP (P=0.016 and 0.005 for average and maximum dose, respectively).
+DRD2	drug	opioid	19373123	On the basis of an analysis spanning the whole gene locus, from the <strong>DRD2</strong> promoter to the ANKK1 rs1800497C>T polymorphism, <strong>DRD2</strong> genetic polymorphisms modulate both the risk of opiate addiction, leading to the necessity of <b>methadone</b> substitution therapy, and the course of this therapy in terms of dosage requirements.
+DRD2	addiction	addiction	19373123	On the basis of an analysis spanning the whole gene locus, from the <strong>DRD2</strong> promoter to the ANKK1 rs1800497C>T polymorphism, <strong>DRD2</strong> genetic polymorphisms modulate both the risk of opiate <b>addiction</b>, leading to the necessity of methadone substitution therapy, and the course of this therapy in terms of dosage requirements.
+DRD2	drug	opioid	19282821	We targeted three functional polymorphisms related to the D2 receptor (<strong>DRD2</strong>) gene, as well as the functional A118G polymorphism of the mu <b>opioid</b> receptor (OPRM1) gene.
+DRD2	drug	alcohol	19278736	D2 dopamine receptor (<strong>DRD2</strong>) gene, P300, and personality in children of <b>alcoholics</b>.
+DRD2	drug	alcohol	19278736	The D2 dopamine receptor (<strong>DRD2</strong>) gene has been associated with <b>alcoholism</b> and other drug use disorders.
+DRD2	drug	amphetamine	19275926	To test this hypothesis, 6 putatively functional polymorphisms of D2 like receptors,  141C Ins/Del, Ser311Cys and TaqIA of the <strong>DRD2</strong> gene, Ser9Gly of the DRD3 gene, and  521C>T and a variable number of tandem repeats in exon 3 of the DRD4 gene, were analyzed in 202 patients with <b>methamphetamine</b> dependence and/or psychosis and 243 healthy controls in a Japanese population.
+DRD2	addiction	dependence	19275926	To test this hypothesis, 6 putatively functional polymorphisms of D2 like receptors,  141C Ins/Del, Ser311Cys and TaqIA of the <strong>DRD2</strong> gene, Ser9Gly of the DRD3 gene, and  521C>T and a variable number of tandem repeats in exon 3 of the DRD4 gene, were analyzed in 202 patients with methamphetamine <b>dependence</b> and/or psychosis and 243 healthy controls in a Japanese population.
+DRD2	drug	amphetamine	19275926	No polymorphism examined showed significant association with <b>methamphetamine</b> dependence, but two polymorphisms of <strong>DRD2</strong> were associated with the clinical course and prognosis of <b>methamphetamine</b> psychosis.
+DRD2	addiction	dependence	19275926	No polymorphism examined showed significant association with methamphetamine <b>dependence</b>, but two polymorphisms of <strong>DRD2</strong> were associated with the clinical course and prognosis of methamphetamine psychosis.
+DRD2	drug	amphetamine	19275926	The A1/A1 homozygote of <strong>DRD2</strong> was a negative risk factor for a poorer prognosis of psychosis that continues for more than 1 month after the discontinuance of <b>methamphetamine</b> abuse and the beginning of treatment with neuroleptics (p=0.04, odds ratio (OR)=0.42, 95% CI; 0.27 0.65) and the complication of spontaneous relapse of <b>methamphetamine</b> psychosis after remission (p=0.014, OR=0.34, 95% CI; 0.22 0.54).
+DRD2	addiction	relapse	19275926	The A1/A1 homozygote of <strong>DRD2</strong> was a negative risk factor for a poorer prognosis of psychosis that continues for more than 1 month after the discontinuance of methamphetamine abuse and the beginning of treatment with neuroleptics (p=0.04, odds ratio (OR)=0.42, 95% CI; 0.27 0.65) and the complication of spontaneous <b>relapse</b> of methamphetamine psychosis after remission (p=0.014, OR=0.34, 95% CI; 0.22 0.54).
+DRD2	drug	amphetamine	19275926	These findings revealed that genetic variants of <strong>DRD2</strong>, but not DRD3 or DRD4, confer individual risks for rapid onset, prolonged duration, and spontaneous relapse of <b>methamphetamine</b> psychosis.
+DRD2	addiction	relapse	19275926	These findings revealed that genetic variants of <strong>DRD2</strong>, but not DRD3 or DRD4, confer individual risks for rapid onset, prolonged duration, and spontaneous <b>relapse</b> of methamphetamine psychosis.
+DRD2	addiction	withdrawal	19220487	Carrying the A1 allele at the dopamine receptor D2 (<strong>DRD2</strong>) Taq1A polymorphism site moderated the effects of <b>withdrawal</b> on nogo P3 amplitude, suggesting the A1 allele is a vulnerability marker for <b>withdrawal</b> related attentional deficits.
+DRD2	addiction	withdrawal	19220487	Carrying the A1 allele at the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) Taq1A polymorphism site moderated the effects of <b>withdrawal</b> on nogo P3 amplitude, suggesting the A1 allele is a vulnerability marker for <b>withdrawal</b> related attentional deficits.
+DRD2	drug	nicotine	19220487	These findings suggest that <strong>DRD2</strong> status and SNA moderate the effects of <b>smoking</b> status and withdrawal on neurocognitive variation during attentional processing.
+DRD2	addiction	withdrawal	19220487	These findings suggest that <strong>DRD2</strong> status and SNA moderate the effects of smoking status and <b>withdrawal</b> on neurocognitive variation during attentional processing.
+DRD2	addiction	addiction	19179847	Here, we will review the information collected implicating the receptors of the D1 family (DRD1 and DRD5) and of the D2 family (<strong>DRD2</strong>, DRD3 and DRD4) in drug <b>addiction</b>.
+DRD2	drug	alcohol	19179847	A meta analysis of the studies carried out evaluating <strong>DRD2</strong> and <b>alcohol</b> dependence is also provided, which indicates a significant association.
+DRD2	addiction	dependence	19179847	A meta analysis of the studies carried out evaluating <strong>DRD2</strong> and alcohol <b>dependence</b> is also provided, which indicates a significant association.
+DRD2	drug	cannabinoid	19084357	In nonsmokers, impulsive personality, prior <b>marijuana</b> use, and <strong>DRD2</strong> and DRD4 genotypes may moderate nicotine responses in men but apparently not in women.
+DRD2	drug	nicotine	19084357	In nonsmokers, impulsive personality, prior marijuana use, and <strong>DRD2</strong> and DRD4 genotypes may moderate <b>nicotine</b> responses in men but apparently not in women.
+DRD2	drug	alcohol	19077056	Repeated <b>ethanol</b> administration also down regulates the expression of <strong>DRD2</strong> and NMDAR2B phosphorylation in prefrontal cortex of adolescent animals, but not of adult rats.
+DRD2	drug	alcohol	19065655	Increased risk of adenoma recurrence as conferred by <strong>DRD2</strong> genotypes may be related to difference in <b>alcohol</b> and fat intake across genotypes.
+DRD2	addiction	relapse	19014506	Thus, a reduced number of DA receptors, due to carrying the <strong>DRD2</strong> A1 allelic genotype, results in excessive <b>craving</b> behavior; whereas a normal or sufficient amount of DA receptors results in low <b>craving</b> behavior.
+DRD2	drug	alcohol	19014506	In fact as mentioned earlier, this model has been proven in research showing DNA directed compensatory overexpression (a form of gene therapy) of the <strong>DRD2</strong> receptors, resulting in a significant reduction in <b>alcohol</b> craving behavior in <b>alcohol</b> preferring rodents.
+DRD2	addiction	relapse	19014506	In fact as mentioned earlier, this model has been proven in research showing DNA directed compensatory overexpression (a form of gene therapy) of the <strong>DRD2</strong> receptors, resulting in a significant reduction in alcohol <b>craving</b> behavior in alcohol preferring rodents.
+DRD2	drug	alcohol	18828801	Haplotypic variants in <strong>DRD2</strong>, ANKK1, TTC12, and NCAM1 are associated with comorbid <b>alcohol</b> and drug dependence.
+DRD2	addiction	dependence	18828801	Haplotypic variants in <strong>DRD2</strong>, ANKK1, TTC12, and NCAM1 are associated with comorbid alcohol and drug <b>dependence</b>.
+DRD2	drug	alcohol	18828801	Many association studies of <strong>DRD2</strong> and substance dependence (SD), including <b>alcohol</b> dependence (AD) and drug dependence (DD), have been reported; the results have been inconsistent.
+DRD2	addiction	dependence	18828801	Many association studies of <strong>DRD2</strong> and substance <b>dependence</b> (SD), including alcohol <b>dependence</b> (AD) and drug <b>dependence</b> (DD), have been reported; the results have been inconsistent.
+DRD2	drug	nicotine	18781857	Several candidate genes within the dopamine pathway (e.g., <strong>DRD2</strong> and COMT) have been reported to be associated with the efficacy of bupropion and <b>nicotine</b> replacement therapy, and others (e.g., SLC6A3 and DRD4) have been reported to be associated with <b>smoking</b> cessation independent of pharmacotherapy.
+DRD2	drug	nicotine	18690118	The increase in <b>smoking</b> amount owing to negative mood was associated with: dopamine D2 receptor (<strong>DRD2</strong>) C957T (CC>TT or CT), SLC6A3 (presence of 9 repeat>absence of 9), and among those given a <b>nicotine</b> cigarette, DRD4 (presence of 7 repeat>absence of 7) and <strong>DRD2</strong>/ANKK1 TaqIA (TT or CT>CC).
+DRD2	drug	nicotine	18690118	SLC6A3, and <strong>DRD2</strong>/ANKK1 TaqIA were also associated with <b>smoking</b> reward and <b>smoking</b> latency.
+DRD2	addiction	reward	18690118	SLC6A3, and <strong>DRD2</strong>/ANKK1 TaqIA were also associated with smoking <b>reward</b> and smoking latency.
+DRD2	drug	opioid	18690117	Very few or no significant associations were seen for the <strong>DRD2</strong>/ANKK1 TaqIA polymorphism, the serotonin transporter promoter VNTR or 5HTTLPR (SLC6A4), the dopamine transporter 3' VNTR (SLC6A3), and the mu <b>opioid</b> receptor A118G single nucleotide polymorphism (mu <b>opioid</b> receptor polymorphism 1).
+DRD2	drug	opioid	18687376	The polymorphisms of the micro <b>opioid</b> (118A>G), delta <b>opioid</b> (921T>C), dopamine D1 (DdeI) and D2 (TaqI A) receptor genes were not associated with response to MMT and <b>methadone</b> dosing, whereas an association was found with the dopamine D2 receptor (<strong>DRD2</strong>) 957C>T polymorphism.
+DRD2	addiction	addiction	18555060	In addition, carriers of dopamine receptor type 2 (<strong>DRD2</strong>) TaqI A1 have been hypothesized to be potentially vulnerable to <b>addictive</b> behaviors.
+DRD2	addiction	dependence	18555060	Within patients with MA <b>dependence</b>, the subgroup of <strong>DRD2</strong> TaqI A1 carrier had greater NS scores relative to those without, whereas there was only a trend level of lower frontal executive function in the first subgroup.
+DRD2	drug	alcohol	18552399	The aim of this study was to investigate the potential association between functional polymorphisms of dopaminergic [dopamine receptor D2 (<strong>DRD2</strong>), dopamine receptor D3 (DRD3) and dopamine transporter (SLC6A3)] and serotonergic [serotonin 2A receptor (HTR2A) and serotonin transporter (SLC6A4)] genes and treatment outcome in <b>alcohol</b> dependent patients.
+DRD2	drug	alcohol	18552399	The aim of this study was to investigate the potential association between functional polymorphisms of dopaminergic [<strong>dopamine receptor D2</strong> (<strong>DRD2</strong>), dopamine receptor D3 (DRD3) and dopamine transporter (SLC6A3)] and serotonergic [serotonin 2A receptor (HTR2A) and serotonin transporter (SLC6A4)] genes and treatment outcome in <b>alcohol</b> dependent patients.
+DRD2	drug	alcohol	18514919	The current study used path analysis (via structural equation modelling) to explore the relationship between the A(1) allele of the D2 dopamine receptor <strong>DRD2</strong> gene region, age of problem drinking onset, <b>alcohol</b> expectancy and drinking refusal self efficacy towards <b>alcohol</b> consumption and dependence severity.
+DRD2	addiction	dependence	18514919	The current study used path analysis (via structural equation modelling) to explore the relationship between the A(1) allele of the D2 dopamine receptor <strong>DRD2</strong> gene region, age of problem drinking onset, alcohol expectancy and drinking refusal self efficacy towards alcohol consumption and <b>dependence</b> severity.
+DRD2	drug	nicotine	18499348	Thirteen <b>smokers</b> participating in a prior arterial spin labeled (ASL) perfusion MRI study were scanned on two occasions (after >12h abstinence vs. satiety), and were genotyped for variants in the dopamine D2 receptor (<strong>DRD2</strong> 141 Ins/DelC; <strong>DRD2</strong> C957T); a dopamine metabolizing enzyme (COMT val(158) met), and the mu opioid receptor (OPRM1 A118G).
+DRD2	drug	opioid	18499348	Thirteen smokers participating in a prior arterial spin labeled (ASL) perfusion MRI study were scanned on two occasions (after >12h abstinence vs. satiety), and were genotyped for variants in the dopamine D2 receptor (<strong>DRD2</strong> 141 Ins/DelC; <strong>DRD2</strong> C957T); a dopamine metabolizing enzyme (COMT val(158) met), and the mu <b>opioid</b> receptor (OPRM1 A118G).
+DRD2	drug	nicotine	18499348	<b>Smokers</b> with TT genotypes for the <strong>DRD2</strong> C957T exhibited less change in rCBF in abstinence relative to satiety, compared to those with CC or CT genotypes.
+DRD2	drug	nicotine	18434921	<b>Smoking</b> initiation was related to allelic variation in the dopamine D4 receptor gene (DRD4), whereas <b>smoking</b> continuation and dependence showed association with the dopamine D2 receptor gene (<strong>DRD2</strong>).
+DRD2	addiction	dependence	18434921	Smoking initiation was related to allelic variation in the dopamine D4 receptor gene (DRD4), whereas smoking continuation and <b>dependence</b> showed association with the dopamine D2 receptor gene (<strong>DRD2</strong>).
+DRD2	drug	nicotine	18434921	Once <b>smoking</b> started, carriers of the T allele of a single nucleotide polymorphism of <strong>DRD2</strong> (rs4648317) reported higher rates of current <b>smoking</b> and scored higher on <b>nicotine</b> dependence than their allelic counterparts.
+DRD2	addiction	dependence	18434921	Once smoking started, carriers of the T allele of a single nucleotide polymorphism of <strong>DRD2</strong> (rs4648317) reported higher rates of current smoking and scored higher on nicotine <b>dependence</b> than their allelic counterparts.
+DRD2	drug	nicotine	18354387	We examined 16 single nucleotide polymorphisms (SNPs) at <strong>DRD2</strong> and 7 SNPs at ANKK1 in our Mid South <b>Tobacco</b> Family cohort, which consisted of 2037 participants representing two distinct American populations.
+DRD2	drug	alcohol	18214604	<strong>Drd2</strong> expression in the high <b>alcohol</b> preferring and low <b>alcohol</b> preferring mice.
+DRD2	addiction	reward	18214604	The present study examined <strong>Drd2</strong> mRNA expression differences between the HAP1 and LAP1 mice in brain regions important in the dopaminergic <b>reward</b> pathway, including the nucleus accumbens, hippocampus, amygdala, and septum.
+DRD2	drug	alcohol	18214604	Results show that <b>alcohol</b> naïve HAP1 mice exhibited lower levels of <strong>Drd2</strong> mRNA expression in the nucleus accumbens and the hippocampus compared to LAP1 mice.
+DRD2	drug	alcohol	18214604	These results suggest that the SNP may play a role in the differential expression of <strong>Drd2</strong> between the HAP and LAP mice and that the polymorphism in <strong>Drd2</strong> may contribute to <b>alcohol</b> preference.
+DRD2	drug	nicotine	18058350	<strong>DRD2</strong>/ANKK1 TaqI polymorphism and <b>smoking</b> behavior of Egyptian male cigarette <b>smokers</b>.
+DRD2	drug	nicotine	18058350	Logistic regression analysis including <strong>DRD2</strong> genotype, FTND score, age at <b>smoking</b> initiation, marital status, and education as predictors showed that maximum duration of quit time was associated with FTND score (p = .003), <strong>DRD2</strong> genotype (p = .01), marital status (p = .03), and age at <b>smoking</b> initiation (p = .04).
+DRD2	drug	nicotine	18058350	These findings suggest a modest association between <strong>DRD2</strong> genotype and quitting behavior in male cigarette <b>smokers</b> in Egypt.
+DRD2	addiction	addiction	17948902	Animal and human studies of <b>addiction</b> indicate that the D2 dopamine receptor (<strong>DRD2</strong>) plays a critical role in the mechanism of drug reward.
+DRD2	addiction	reward	17948902	Animal and human studies of addiction indicate that the D2 dopamine receptor (<strong>DRD2</strong>) plays a critical role in the mechanism of drug <b>reward</b>.
+DRD2	drug	alcohol	17948902	Previous studies of <strong>DRD2</strong> in association with <b>alcohol</b> dependence using variation in the TaqI A locus were highly controversial.
+DRD2	addiction	dependence	17948902	Previous studies of <strong>DRD2</strong> in association with alcohol <b>dependence</b> using variation in the TaqI A locus were highly controversial.
+DRD2	drug	alcohol	17948902	These results support a role for <strong>DRD2</strong> as a susceptibility gene for <b>alcohol</b> dependence within multiplex families at high risk for developing <b>alcohol</b> dependence.
+DRD2	addiction	dependence	17948902	These results support a role for <strong>DRD2</strong> as a susceptibility gene for alcohol <b>dependence</b> within multiplex families at high risk for developing alcohol <b>dependence</b>.
+DRD2	drug	alcohol	17948892	The association between <strong>DRD2</strong>/ANKK1, 5 HTTLPR gene, and specific personality trait on antisocial <b>alcoholism</b> among Han Chinese in Taiwan.
+DRD2	drug	alcohol	17948892	In the novelty seeking scores, after stratification of <strong>DRD2</strong> TaqI A genotypes, only a significant difference in 5 HTTLPR polymorphisms between antisocial <b>alcoholics</b> and antisocial non <b>alcoholics</b> was found, indicating an interaction between <strong>DRD2</strong> TaqI A1+ (include A1/A1 or A1/A2) and 5 HTTLPR S/S genotype (t = 2.75, P = 0.01) However, no significant difference was found in the harm avoidance personality trait between these two groups of Han Chinese in Taiwan.
+DRD2	addiction	relapse	17948892	In the novelty <b>seeking</b> scores, after stratification of <strong>DRD2</strong> TaqI A genotypes, only a significant difference in 5 HTTLPR polymorphisms between antisocial alcoholics and antisocial non alcoholics was found, indicating an interaction between <strong>DRD2</strong> TaqI A1+ (include A1/A1 or A1/A2) and 5 HTTLPR S/S genotype (t = 2.75, P = 0.01) However, no significant difference was found in the harm avoidance personality trait between these two groups of Han Chinese in Taiwan.
+DRD2	drug	alcohol	17943029	<b>Alcohol</b> consumption is associated with an interaction between <strong>DRD2</strong> exon 8 A/A genotype and self directedness in males.
+DRD2	drug	alcohol	17943029	We examined for interactions between <strong>DRD2</strong> exon 8(rs6276), a polymorphism which has been associated with various <b>alcohol</b> related phenotypes, SDD and <b>alcohol</b> consumption.
+DRD2	drug	alcohol	17943029	Male probands with A/A genotype reported significantly higher <b>alcohol</b> consumption in a typical week (ANOVA; p = 0.024); those with A/A genotype and low SDD showed particularly high consumption levels (interaction <strong>DRD2</strong> x SDD: p = 0.019).
+DRD2	drug	alcohol	17943029	Our findings support a role for a gene personality interaction of <strong>DRD2</strong> exon 8 x SDD in <b>alcohol</b> consumption in males.
+DRD2	drug	alcohol	17850642	Family based association analyses of <b>alcohol</b> dependence phenotypes across <strong>DRD2</strong> and neighboring gene ANKK1.
+DRD2	addiction	dependence	17850642	Family based association analyses of alcohol <b>dependence</b> phenotypes across <strong>DRD2</strong> and neighboring gene ANKK1.
+DRD2	drug	alcohol	17850642	There is an extensive and inconsistent literature on the association of the dopamine D2 receptor gene (<strong>DRD2</strong>) with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	17850642	There is an extensive and inconsistent literature on the association of the dopamine D2 receptor gene (<strong>DRD2</strong>) with alcohol <b>dependence</b>.
+DRD2	drug	alcohol	17850642	To more carefully characterize evidence for association across this region, we genotyped 26 single nucleotide polymorphisms (SNPs) spanning <strong>DRD2</strong> and ANKK1 in a sample of 219 Caucasian families (n = 1,923) from the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA), making this the most extensive analysis to date of association between this region and <b>alcohol</b> dependence.
+DRD2	addiction	dependence	17850642	To more carefully characterize evidence for association across this region, we genotyped 26 single nucleotide polymorphisms (SNPs) spanning <strong>DRD2</strong> and ANKK1 in a sample of 219 Caucasian families (n = 1,923) from the Collaborative Study on the Genetics of Alcoholism (COGA), making this the most extensive analysis to date of association between this region and alcohol <b>dependence</b>.
+DRD2	drug	alcohol	17850642	We used family based analyses robust to population stratification, and we made use of rich phenotypic data to analyze <b>alcohol</b> dependence and subtypes hypothesized in the literature to be more directly influenced by <strong>DRD2</strong>.
+DRD2	addiction	dependence	17850642	We used family based analyses robust to population stratification, and we made use of rich phenotypic data to analyze alcohol <b>dependence</b> and subtypes hypothesized in the literature to be more directly influenced by <strong>DRD2</strong>.
+DRD2	drug	alcohol	17850642	More extensive genotyping across <strong>DRD2</strong> and ANKK1 suggests that the association with <b>alcohol</b> dependence observed in this region may be due to genetic variants in the ANKK1 gene.
+DRD2	addiction	dependence	17850642	More extensive genotyping across <strong>DRD2</strong> and ANKK1 suggests that the association with alcohol <b>dependence</b> observed in this region may be due to genetic variants in the ANKK1 gene.
+DRD2	drug	alcohol	17761687	Association of haplotypic variants in <strong>DRD2</strong>, ANKK1, TTC12 and NCAM1 to <b>alcohol</b> dependence in independent case control and family samples.
+DRD2	addiction	dependence	17761687	Association of haplotypic variants in <strong>DRD2</strong>, ANKK1, TTC12 and NCAM1 to alcohol <b>dependence</b> in independent case control and family samples.
+DRD2	drug	alcohol	17761687	There have been many conflicting reports concerning the association of the <strong>DRD2</strong> locus with <b>alcohol</b> dependence (AD).
+DRD2	addiction	dependence	17761687	There have been many conflicting reports concerning the association of the <strong>DRD2</strong> locus with alcohol <b>dependence</b> (AD).
+DRD2	addiction	relapse	17707567	We attempted to investigate whether the dopamine D2 receptor (<strong>DRD2</strong>) and the serotonin transporter promoter region (5 HTTLPR) genes were involved in Novelty <b>Seeking</b> (NS) and Harm Avoidance (HA) of ANX/DEP ALC.
+DRD2	drug	cocaine	17671965	Polymorphisms TaqI A of the <strong>DRD2</strong>, BalI of the DRD3, exon III repeat of the DRD4, and 3' UTR VNTR of the DAT: association with childhood ADHD in male African Caribbean <b>cocaine</b> dependents?
+DRD2	drug	cocaine	17671965	The potential association of the variants TaqI A of the <strong>DRD2</strong>, BalI of the DRD3, exon III repeat of the DRD4, and 3' UTR VNTR of the DAT was examined in African Caribbean males, smoked <b>cocaine</b> dependents.
+DRD2	drug	nicotine	17654295	<b>Smokers</b> of European ancestry (N = 291), who were randomized to receive bupropion or placebo (12 weeks) plus counseling, were genotyped for the dopamine D2 receptor (<strong>DRD2</strong> Taq1A), dopamine transporter (SLC6A3 3' VNTR), and cytochrome P450 2B6 (CYP2B6 1459 CT) polymorphisms.
+DRD2	drug	nicotine	17654295	We found a significant <strong>DRD2</strong> x bupropion interaction (B = 1.49, SE = 0.59, p = .012) [corrected] and a three way <strong>DRD2</strong> x bupropion x craving interaction on 6 month <b>smoking</b> cessation outcomes (B =  0.45, SE = 0.22, p = .038), such that <b>smokers</b> with the A2/A2 genotype demonstrated the greatest craving reduction and the highest abstinence rates with bupropion.
+DRD2	addiction	relapse	17654295	We found a significant <strong>DRD2</strong> x bupropion interaction (B = 1.49, SE = 0.59, p = .012) [corrected] and a three way <strong>DRD2</strong> x bupropion x <b>craving</b> interaction on 6 month smoking cessation outcomes (B =  0.45, SE = 0.22, p = .038), such that smokers with the A2/A2 genotype demonstrated the greatest <b>craving</b> reduction and the highest abstinence rates with bupropion.
+DRD2	drug	nicotine	17654295	Although these results require replication, the data suggest preliminarily that the <strong>DRD2</strong> Taq1A polymorphism may influence treatment response to bupropion for <b>smoking</b> cessation and, further, that exploration of gene x gene and gene x craving interactions in future, larger studies may provide mechanistic insights into the complex pharmacodynamics of bupropion.
+DRD2	addiction	relapse	17654295	Although these results require replication, the data suggest preliminarily that the <strong>DRD2</strong> Taq1A polymorphism may influence treatment response to bupropion for smoking cessation and, further, that exploration of gene x gene and gene x <b>craving</b> interactions in future, larger studies may provide mechanistic insights into the complex pharmacodynamics of bupropion.
+DRD2	drug	opioid	17597526	Using data from a study of association between <b>heroin</b> dependence and the <strong>DRD2</strong> gene, we obtained estimated haplotype frequencies and the associated likelihood ratio statistic using two different computer programs, MLOCUS and GENECOUNTING.
+DRD2	addiction	dependence	17597526	Using data from a study of association between heroin <b>dependence</b> and the <strong>DRD2</strong> gene, we obtained estimated haplotype frequencies and the associated likelihood ratio statistic using two different computer programs, MLOCUS and GENECOUNTING.
+DRD2	drug	opioid	17543096	Allelic and genotypic associations of <strong>DRD2</strong> TaqI A polymorphism with <b>heroin</b> dependence in Spanish subjects: a case control study.
+DRD2	addiction	dependence	17543096	Allelic and genotypic associations of <strong>DRD2</strong> TaqI A polymorphism with heroin <b>dependence</b> in Spanish subjects: a case control study.
+DRD2	drug	opioid	17543096	Conflicting associations with <b>heroin</b> dependence have been found involving the A1 allele of dopamine D2 receptor gene (<strong>DRD2</strong>) TaqI A polymorphism.
+DRD2	addiction	dependence	17543096	Conflicting associations with heroin <b>dependence</b> have been found involving the A1 allele of dopamine D2 receptor gene (<strong>DRD2</strong>) TaqI A polymorphism.
+DRD2	drug	opioid	17543096	Our results indicate that, in Spanish individuals, genotypes of the <strong>DRD2</strong> TaqI A polymorphism contribute to variations in the risk of <b>heroin</b> dependence, while single alleles contribute only in males.
+DRD2	addiction	dependence	17543096	Our results indicate that, in Spanish individuals, genotypes of the <strong>DRD2</strong> TaqI A polymorphism contribute to variations in the risk of heroin <b>dependence</b>, while single alleles contribute only in males.
+DRD2	drug	alcohol	17476365	Therefore, the present study investigates whether the association between the dopamine D2 receptor (<strong>DRD2</strong>) gene and <b>alcoholism</b> is affected by different polymorphisms of the MAO type A (MAOA) gene.
+DRD2	drug	alcohol	17467918	<b>alcohol</b>) carrying the <strong>DRD2</strong> A1 allele with associated low D2 receptors should, as theorized, increase craving behavior because of a low or hypodopaminergic state causing the individual to seek out substances that increase the release of dopamine for subsequent activation of unbound D2 sites in the nucleus accumbens.
+DRD2	addiction	relapse	17467918	alcohol) carrying the <strong>DRD2</strong> A1 allele with associated low D2 receptors should, as theorized, increase <b>craving</b> behavior because of a low or hypodopaminergic state causing the individual to seek out substances that increase the release of dopamine for subsequent activation of unbound D2 sites in the nucleus accumbens.
+DRD2	drug	alcohol	17446975	Between  and within family association test of the <strong>dopamine receptor D2</strong> TaqIA polymorphism and <b>alcohol</b> abuse and dependence in a general population sample of adults.
+DRD2	addiction	dependence	17446975	Between  and within family association test of the <strong>dopamine receptor D2</strong> TaqIA polymorphism and alcohol abuse and <b>dependence</b> in a general population sample of adults.
+DRD2	drug	alcohol	17446975	A restriction fragment length polymorphism (RFLP) in the 3' untranslated region (3'UTR) of the <strong>DRD2</strong> gene affects gene expression and has been implicated as a risk factor for <b>alcohol</b> dependence.
+DRD2	addiction	dependence	17446975	A restriction fragment length polymorphism (RFLP) in the 3' untranslated region (3'UTR) of the <strong>DRD2</strong> gene affects gene expression and has been implicated as a risk factor for alcohol <b>dependence</b>.
+DRD2	drug	alcohol	17446975	The mixed results of association between the <strong>DRD2</strong> TaqIA polymorphism and <b>alcohol</b> use disorders may be the result of differences in sample size, phenotype definition, heterogeneity of the samples, and genetic admixture.
+DRD2	drug	alcohol	17446975	We examined whether the <strong>DRD2</strong> TaqIA polymorphism was associated with a symptom count measure of <b>alcohol</b> abuse and dependence derived from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and the Craving Withdrawal Model.
+DRD2	addiction	dependence	17446975	We examined whether the <strong>DRD2</strong> TaqIA polymorphism was associated with a symptom count measure of alcohol abuse and <b>dependence</b> derived from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and the Craving Withdrawal Model.
+DRD2	addiction	relapse	17446975	We examined whether the <strong>DRD2</strong> TaqIA polymorphism was associated with a symptom count measure of alcohol abuse and dependence derived from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and the <b>Craving</b> Withdrawal Model.
+DRD2	addiction	withdrawal	17446975	We examined whether the <strong>DRD2</strong> TaqIA polymorphism was associated with a symptom count measure of alcohol abuse and dependence derived from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and the Craving <b>Withdrawal</b> Model.
+DRD2	drug	alcohol	17446975	This study supports other family based association tests that have reported no association between the <strong>DRD2</strong> TaqIA polymorphism and <b>alcohol</b> abuse and dependence.
+DRD2	addiction	dependence	17446975	This study supports other family based association tests that have reported no association between the <strong>DRD2</strong> TaqIA polymorphism and alcohol abuse and <b>dependence</b>.
+DRD2	drug	nicotine	17407504	Dopamine receptor genes (<strong>DRD2</strong>, DRD3 and DRD4) and gene gene interactions associated with <b>smoking</b> related behaviors.
+DRD2	drug	nicotine	17407504	Cigarette <b>smoking</b>, like many addictive behaviors, has a genetic component, and the dopamine D2 like receptor genes (<strong>DRD2</strong>, DRD3 and DRD4) are candidates for contributing to these behaviors.
+DRD2	addiction	addiction	17407504	Cigarette smoking, like many <b>addictive</b> behaviors, has a genetic component, and the dopamine D2 like receptor genes (<strong>DRD2</strong>, DRD3 and DRD4) are candidates for contributing to these behaviors.
+DRD2	drug	nicotine	17407504	Genotype status at the <strong>DRD2</strong> intron 2 simple tandem repeat was related to cigarettes per day (P = 0.035) and heaviness of <b>smoking</b> index (P = 0.049).
+DRD2	drug	nicotine	17387332	These data are consistent with observations from studies of the <strong>DRD2</strong> gene that genetic variants related to relatively decreased dopaminergic tone in the mesocorticolimbic system are associated with increased risk for relapse to <b>smoking</b> following a cessation attempt.
+DRD2	addiction	relapse	17387332	These data are consistent with observations from studies of the <strong>DRD2</strong> gene that genetic variants related to relatively decreased dopaminergic tone in the mesocorticolimbic system are associated with increased risk for <b>relapse</b> to smoking following a cessation attempt.
+DRD2	drug	nicotine	17189962	The <strong>DRD2</strong> TaqI B polymorphism and its relationship to <b>smoking</b> abstinence and withdrawal symptoms.
+DRD2	addiction	withdrawal	17189962	The <strong>DRD2</strong> TaqI B polymorphism and its relationship to smoking abstinence and <b>withdrawal</b> symptoms.
+DRD2	drug	nicotine	17189962	The dopamine receptor D2 (<strong>DRD2</strong>) gene has polymorphisms that have been linked to regulation of the dopamine system and to an increased prevalence of <b>smoking</b>.
+DRD2	drug	nicotine	17189962	The <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) gene has polymorphisms that have been linked to regulation of the dopamine system and to an increased prevalence of <b>smoking</b>.
+DRD2	drug	nicotine	17189962	The present study examined the relationship of the <strong>DRD2</strong> TaqI A and  B polymorphisms with short term clinical outcome (abstinence and withdrawal symptoms), collected from daily (14 pre quit and 42 post quit) diary data among <b>smokers</b> (n=116) treated with the <b>nicotine</b> patch plus either venlafaxine or placebo.
+DRD2	addiction	withdrawal	17189962	The present study examined the relationship of the <strong>DRD2</strong> TaqI A and  B polymorphisms with short term clinical outcome (abstinence and <b>withdrawal</b> symptoms), collected from daily (14 pre quit and 42 post quit) diary data among smokers (n=116) treated with the nicotine patch plus either venlafaxine or placebo.
+DRD2	drug	nicotine	17189962	Significant <strong>DRD2</strong> TaqI B x time interactions were found for several of the withdrawal scales, indicating that those <b>smokers</b> with the B1/B1 or B1/B2 genotypes tended to report more symptoms over time compared to those with the B2/B2 genotype.
+DRD2	addiction	withdrawal	17189962	Significant <strong>DRD2</strong> TaqI B x time interactions were found for several of the <b>withdrawal</b> scales, indicating that those smokers with the B1/B1 or B1/B2 genotypes tended to report more symptoms over time compared to those with the B2/B2 genotype.
+DRD2	drug	nicotine	17108814	<strong>DRD2</strong> genetic variation in relation to <b>smoking</b> and obesity in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.
+DRD2	drug	nicotine	17108814	We investigated the association between <b>smoking</b> behavior and genetic variations in the D2 dopamine receptor (<strong>DRD2</strong>), which mediates <b>nicotine</b> dependence.
+DRD2	addiction	dependence	17108814	We investigated the association between smoking behavior and genetic variations in the D2 dopamine receptor (<strong>DRD2</strong>), which mediates nicotine <b>dependence</b>.
+DRD2	drug	nicotine	17108814	Four single nucleotide polymorphisms in <strong>DRD2</strong> were genotyped in 2374 participants selected randomly from the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial after stratifying by sex, age, and <b>smoking</b> status.
+DRD2	drug	nicotine	17108814	<strong>DRD2</strong> polymorphisms were associated with the risk of remaining a current <b>smoker</b> and obesity.
+DRD2	drug	nicotine	17108814	The <strong>DRD2</strong> haplotype T C T A [TaqIA(C/T) 957(T/C) IVS6 83(G/T)   50977(A/G)] was more common among current than former <b>smokers</b> (OR=1.3, P=0.006), particularly among heavy <b>smokers</b> (21+ cigarettes per day; OR=1.6, P=0.006), and was more common among obese than normal weight individuals (OR=1.4, P=0.02).
+DRD2	drug	nicotine	17108814	Genetic variation in <strong>DRD2</strong> is a modifier of the reward motivated characteristics, <b>smoking</b> and obesity.
+DRD2	addiction	reward	17108814	Genetic variation in <strong>DRD2</strong> is a modifier of the <b>reward</b> motivated characteristics, smoking and obesity.
+DRD2	drug	nicotine	17108814	As fewer than 15% of <b>smokers</b> who attempt to quit are able to maintain abstinence for greater than 3 months, our results support that <strong>DRD2</strong> is an appropriate molecular target for <b>smoking</b> cessation treatments.
+DRD2	drug	nicotine	17085484	Haplotype spanning TTC12 and ANKK1, flanked by the <strong>DRD2</strong> and NCAM1 loci, is strongly associated to <b>nicotine</b> dependence in two distinct American populations.
+DRD2	addiction	dependence	17085484	Haplotype spanning TTC12 and ANKK1, flanked by the <strong>DRD2</strong> and NCAM1 loci, is strongly associated to nicotine <b>dependence</b> in two distinct American populations.
+DRD2	addiction	dependence	17085484	<strong>DRD2</strong> and NCAM1 are functional candidate genes for substance <b>dependence</b>; the TTC12 and ANKK1 loci are not well characterized.
+DRD2	addiction	dependence	17085484	These results provide additional information useful in evaluating the many earlier discrepant findings regarding association of <strong>DRD2</strong> with substance <b>dependence</b>.
+DRD2	drug	alcohol	17079080	Family based and case control study of <strong>DRD2</strong>, DAT, 5HTT, COMT genes polymorphisms in <b>alcohol</b> dependence.
+DRD2	addiction	dependence	17079080	Family based and case control study of <strong>DRD2</strong>, DAT, 5HTT, COMT genes polymorphisms in alcohol <b>dependence</b>.
+DRD2	drug	alcohol	17079080	The paper focuses on such candidate gene polymorphisms that alter <b>alcoholism</b> related intermediate phenotypes including: dopaminergic system polymorphic variants (<strong>DRD2</strong>  141C Ins/Del in promoter region, exon 8 and <strong>DRD2</strong> TaqI A and DAT 40bp VNTR genes polymorphisms) that cause predisposition to severe <b>alcoholism</b> (haplotype Ins/G/A2); COMT Val158Met gene polymorphism related to differences in executive cognitive function and 5 HTT gene promoter polymorphism, which alters stress response and affects anxiety and dysphoria.
+DRD2	addiction	withdrawal	17079080	In the homogenous subgroups of patients with early onset and with <b>withdrawal</b> complications a statistically significant preferential A2 allele transmission was found in <strong>DRD2</strong> TaqIA gene polymorphism.
+DRD2	drug	alcohol	17079080	The results confirmed the fact that the candidate genes (<strong>DRD2</strong> and DAT) are partially responsible for the development of <b>alcohol</b> dependence.
+DRD2	addiction	dependence	17079080	The results confirmed the fact that the candidate genes (<strong>DRD2</strong> and DAT) are partially responsible for the development of alcohol <b>dependence</b>.
+DRD2	drug	alcohol	17069991	We sought to test for an association between early onset (in childhood or adolescence) <b>alcohol</b> use disorders and the <strong>DRD2</strong> TaqIA polymorphism and to resolve some of the hypothesized explanations for previous negative results, utilizing a larger sample than many previous studies.
+DRD2	drug	amphetamine	16916582	Also, the expression of Drd1 gene in the striatum and <strong>Drd2</strong> gene in the mesolimbic structures of wild type mice were up regulated under the influence of <b>amphetamine</b>.
+DRD2	drug	amphetamine	16916582	The lack of development of up regulation of Drd1 and <strong>Drd2</strong> genes after repeated treatment with <b>amphetamine</b> probably explains the reduced place conditioning in CCK(2) receptor deficient mice.
+DRD2	drug	nicotine	16896957	Studies examining the role of genetic variability in modulating individual response to <b>nicotine</b> in humans have increased, with recent work showing that genetic variation at the dopamine D2 receptor (<strong>DRD2</strong>) predicts response to pharmacotherapy for <b>tobacco</b> dependence.
+DRD2	addiction	dependence	16896957	Studies examining the role of genetic variability in modulating individual response to nicotine in humans have increased, with recent work showing that genetic variation at the dopamine D2 receptor (<strong>DRD2</strong>) predicts response to pharmacotherapy for tobacco <b>dependence</b>.
+DRD2	drug	nicotine	16896957	To determine whether a polymorphism of the <strong>DRD2</strong> gene, C957T, that alters <strong>DRD2</strong> binding availability in humans modifies the effects of <b>nicotine</b> on verbal working memory performance and on processing efficiency of brain regions that support verbal working memory.
+DRD2	drug	nicotine	16896957	These findings are consistent with the notion that genetic variation in <strong>DRD2</strong> contributes to individual variation in a range of behavioral and brain responses to <b>nicotine</b> in humans.
+DRD2	drug	alcohol	16766132	Heavy nicotine and <b>alcohol</b> use in <b>alcohol</b> dependence is associated with D2 dopamine receptor (<strong>DRD2</strong>) polymorphism.
+DRD2	drug	nicotine	16766132	Heavy <b>nicotine</b> and alcohol use in alcohol dependence is associated with D2 dopamine receptor (<strong>DRD2</strong>) polymorphism.
+DRD2	addiction	dependence	16766132	Heavy nicotine and alcohol use in alcohol <b>dependence</b> is associated with D2 dopamine receptor (<strong>DRD2</strong>) polymorphism.
+DRD2	drug	alcohol	16766132	The A1 allele of the D2 dopamine receptor (<strong>DRD2</strong>) gene has been independently associated with <b>alcohol</b> and nicotine dependence.
+DRD2	drug	nicotine	16766132	The A1 allele of the D2 dopamine receptor (<strong>DRD2</strong>) gene has been independently associated with alcohol and <b>nicotine</b> dependence.
+DRD2	addiction	dependence	16766132	The A1 allele of the D2 dopamine receptor (<strong>DRD2</strong>) gene has been independently associated with alcohol and nicotine <b>dependence</b>.
+DRD2	drug	alcohol	16759339	No association of dopamine receptor sensitivity in vivo with genetic predisposition for <b>alcoholism</b> and <strong>DRD2</strong>/DRD3 gene polymorphisms in <b>alcohol</b> dependence.
+DRD2	addiction	dependence	16759339	No association of dopamine receptor sensitivity in vivo with genetic predisposition for alcoholism and <strong>DRD2</strong>/DRD3 gene polymorphisms in alcohol <b>dependence</b>.
+DRD2	drug	alcohol	16759339	This study sought to examine dopamine receptor sensitivity among <b>alcoholics</b> in vivo and to explore whether this sensitivity might be associated with functional variations of dopamine D2 (<strong>DRD2</strong>) and D3 (DRD3) receptor genes along with a genetic predisposition for <b>alcoholism</b> as reflected by an <b>alcohol</b> dependent first degree relative.
+DRD2	drug	alcohol	16759339	We analyzed the  141C Ins/Del polymorphism in the promoter region of the <strong>DRD2</strong> gene and the Ser9Gly (BalI) polymorphism in exon 1 of the DRD3 gene in 74 <b>alcohol</b> dependent Caucasian men with or without genetic predisposition for <b>alcoholism</b>.
+DRD2	drug	alcohol	16759339	Given the explorative and preliminary character of this investigation, we cannot provide evidence that in <b>alcohol</b> dependent Caucasian men a genetic predisposition for <b>alcoholism</b> along with functional variants of the <strong>DRD2</strong> and DRD3 genes are associated with differences in dopamine receptor sensitivity.
+DRD2	drug	alcohol	16751215	The taqI <strong>DRD2</strong> A1 allele is associated with <b>alcohol</b> dependence although its effect size is small.
+DRD2	addiction	dependence	16751215	The taqI <strong>DRD2</strong> A1 allele is associated with alcohol <b>dependence</b> although its effect size is small.
+DRD2	drug	alcohol	16751215	Numerous studies of the relationship between the TaqIA <strong>DRD2</strong> A1 allele and <b>alcohol</b> dependence have been performed and many of these have shown an association whereas others have not (Noble, 2003).
+DRD2	addiction	dependence	16751215	Numerous studies of the relationship between the TaqIA <strong>DRD2</strong> A1 allele and alcohol <b>dependence</b> have been performed and many of these have shown an association whereas others have not (Noble, 2003).
+DRD2	drug	alcohol	16751215	In case control studies it has been estimated that to detect the role of genes with small effect size of approximately 2, which is in the range of the <strong>DRD2</strong> A1 allele <b>alcoholism</b> relationship, case control sets of 300 400 subjects are necessary (Noble, 2003).
+DRD2	drug	alcohol	16751215	In the present study, in which the TaqI A1/A2 <strong>DRD2</strong> polymorphism was in Hardy Weinberg equilibrium in the patient group and the two control groups, we found that the TaqI <strong>DRD2</strong> A1/A2 genotype frequency differed significantly between the <b>alcohol</b> dependent group and both the total and screened control groups.
+DRD2	drug	alcohol	16751215	Furthermore, the TaqI <strong>DRD2</strong> A1 allele frequency was significantly overrepresented in the <b>alcohol</b> dependent subjects as compared with both the total and screened control groups.
+DRD2	drug	alcohol	16751215	Consequently, the findings in this study lend further support to the notion of an association between the <strong>DRD2</strong> A1 allele and <b>alcohol</b> dependence, although the effect size of the <strong>DRD2</strong> A1 allele is small.
+DRD2	addiction	dependence	16751215	Consequently, the findings in this study lend further support to the notion of an association between the <strong>DRD2</strong> A1 allele and alcohol <b>dependence</b>, although the effect size of the <strong>DRD2</strong> A1 allele is small.
+DRD2	drug	alcohol	16679343	There were no significant differences in the genotype frequencies of the <strong>DRD2</strong>, ALDH2, 5 HTTLPR, and COMT polymorphisms between <b>alcoholics</b> with and without ADHD.
+DRD2	drug	opioid	16583408	Association between the <strong>DRD2</strong> A1 allele and response to <b>methadone</b> and <b>buprenorphine</b> maintenance treatments.
+DRD2	drug	opioid	16583408	The TaqI A polymorphism (A(1)) of the dopamine D(2) receptor gene (<strong>DRD2</strong>), although not a specific predictor of <b>opioid</b> dependence, has been strongly associated with high levels of prior <b>heroin</b> use and poor treatment outcomes among <b>methadone</b> maintenance patients.
+DRD2	addiction	dependence	16583408	The TaqI A polymorphism (A(1)) of the dopamine D(2) receptor gene (<strong>DRD2</strong>), although not a specific predictor of opioid <b>dependence</b>, has been strongly associated with high levels of prior heroin use and poor treatment outcomes among methadone maintenance patients.
+DRD2	drug	opioid	16583408	In conclusion, the <strong>DRD2</strong> genotype effects did not affect <b>opioid</b> maintenance treatment outcomes.
+DRD2	drug	opioid	16583408	This suggests the need for a further prospective investigation into the role of the <strong>DRD2</strong> A(1) allele in <b>heroin</b> use and response to maintenance pharmacotherapies for <b>opioid</b> dependence.
+DRD2	addiction	dependence	16583408	This suggests the need for a further prospective investigation into the role of the <strong>DRD2</strong> A(1) allele in heroin use and response to maintenance pharmacotherapies for opioid <b>dependence</b>.
+DRD2	drug	opioid	16526040	Significantly stronger cue elicited <b>heroin</b> craving was found in individuals carrying D2 dopamine receptor gene (<strong>DRD2</strong>) TaqI RFLP A1 allele than the non carriers (P < 0.001).
+DRD2	addiction	relapse	16526040	Significantly stronger cue elicited heroin <b>craving</b> was found in individuals carrying D2 dopamine receptor gene (<strong>DRD2</strong>) TaqI RFLP A1 allele than the non carriers (P < 0.001).
+DRD2	drug	cocaine	16492766	After 28 days of <b>cocaine</b> treatment and 2 days of withdrawal, spine density increased in both Drd1 EGFP  and <strong>Drd2</strong> EGFP positive neurons.
+DRD2	addiction	withdrawal	16492766	After 28 days of cocaine treatment and 2 days of <b>withdrawal</b>, spine density increased in both Drd1 EGFP  and <strong>Drd2</strong> EGFP positive neurons.
+DRD2	addiction	withdrawal	16492766	Notably, increased DeltaFosB expression also was observed in Drd1 EGFP  and <strong>Drd2</strong> EGFP positive neurons after 2 days of drug <b>withdrawal</b> but only in Drd1 EGFP positive neurons after 30 days of drug <b>withdrawal</b>.
+DRD2	drug	nicotine	16402081	Interaction between variation in the D2 dopamine receptor (<strong>DRD2</strong>) and the neuronal calcium sensor 1 (FREQ) genes in predicting response to <b>nicotine</b> replacement therapy for <b>tobacco</b> dependence.
+DRD2	addiction	dependence	16402081	Interaction between variation in the D2 dopamine receptor (<strong>DRD2</strong>) and the neuronal calcium sensor 1 (FREQ) genes in predicting response to nicotine replacement therapy for tobacco <b>dependence</b>.
+DRD2	drug	nicotine	16402081	We have previously demonstrated that a functional dopamine D2 receptor promoter variant (<strong>DRD2</strong>  141 Ins/Del) predicts response to <b>nicotine</b> replacement therapy (NRT).
+DRD2	drug	nicotine	16402081	The results indicate a statistically significant interaction effect of <strong>DRD2</strong> 141 and FREQ genotypes on abstinence at the end of the NRT treatment phase; 62% of the <b>smokers</b> with at least one copy of the <strong>DRD2</strong>  141 Del allele and two copies of the FREQ rs1054879 A allele were abstinent from <b>smoking</b>, compared to 29 38% abstinence rates for other <b>smokers</b> in the trial.
+DRD2	drug	nicotine	16123753	Role of functional genetic variation in the dopamine D2 receptor (<strong>DRD2</strong>) in response to bupropion and <b>nicotine</b> replacement therapy for <b>tobacco</b> dependence: results of two randomized clinical trials.
+DRD2	addiction	dependence	16123753	Role of functional genetic variation in the dopamine D2 receptor (<strong>DRD2</strong>) in response to bupropion and nicotine replacement therapy for tobacco <b>dependence</b>: results of two randomized clinical trials.
+DRD2	drug	nicotine	16123753	We investigated the roles of two functional genetic variants in the dopamine D2 receptor (<strong>DRD2</strong>) gene in response to pharmacotherapy for <b>tobacco</b> dependence among participants in two randomized clinical trials with a 6 month follow up period: a double blind placebo controlled trial of bupropion (n=414) and an open label trial of transdermal <b>nicotine</b> vs <b>nicotine</b> nasal spray (n=368).
+DRD2	addiction	dependence	16123753	We investigated the roles of two functional genetic variants in the dopamine D2 receptor (<strong>DRD2</strong>) gene in response to pharmacotherapy for tobacco <b>dependence</b> among participants in two randomized clinical trials with a 6 month follow up period: a double blind placebo controlled trial of bupropion (n=414) and an open label trial of transdermal nicotine vs nicotine nasal spray (n=368).
+DRD2	drug	nicotine	16123753	At the end of the treatment phase, a statistically significant (p=0.01) interaction between the <strong>DRD2</strong>   141C Ins/Del genotype and treatment indicated a more favorable response to bupropion among <b>smokers</b> homozygous for the Ins C allele compared to those carrying a Del C allele.
+DRD2	drug	nicotine	16123753	These results suggest that bupropion may be the preferred pharmacologic treatment for <b>smokers</b> homozygous for the <strong>DRD2</strong>   141 Ins C allele, while NRT may be more beneficial for those who carry the Del C allele.
+DRD2	drug	nicotine	15955630	The TaqIB polymorphism for the Dopamine D2 Receptor gene (<strong>DRD2</strong>) has been previously associated with <b>smoking</b> status, although with some contradictory results.
+DRD2	drug	nicotine	15955630	We investigated whether genetic variants of MAO B intron 13 and <strong>DRD2</strong> TaqIB polymorphism could be associated with <b>smoking</b> status among control subjects.
+DRD2	drug	nicotine	15955630	Similarly, no association with <b>smoking</b> status was observed for the TaqIB polymorphism of <strong>DRD2</strong> itself.
+DRD2	drug	nicotine	15955630	However, among men, there was an interaction between MAO B intron 13 polymorphism and the <strong>DRD2</strong> TaqIB polymorphisms, in which subjects carrying MAO B allele A and genotype B12 of <strong>DRD2</strong> were 2.50 times (95% CI=1.05 5.95) more likely to be ever <b>smokers</b> than the pool of men carrying all other genotype combinations.
+DRD2	drug	nicotine	15955630	These results demonstrate that particular combinations of genotypes for MAO B and <strong>DRD2</strong> genes are associated with significantly higher risk for <b>smoking</b> behavior in men, but not in women.
+DRD2	drug	alcohol	15545020	The TaqIA1 allele of the dopamine receptor gene D2 (<strong>DRD2</strong>) has been associated with <b>alcoholism</b>, as well as with other addictive behaviours.
+DRD2	addiction	addiction	15545020	The TaqIA1 allele of the dopamine receptor gene D2 (<strong>DRD2</strong>) has been associated with alcoholism, as well as with other <b>addictive</b> behaviours.
+DRD2	drug	alcohol	15545020	In this study we found that the presence in the <strong>DRD2</strong> genotype of the TaqIA1 allele in Spanish <b>alcoholics</b> is associated with higher levels of urine homovanillic acid (HVA) when compared to patients homozygous for the TaqIA2 allele.
+DRD2	drug	alcohol	15542698	PCR based assays showed that <b>alcoholism</b> was associated with polymorphisms of the dopamine D2 receptor (<strong>DRD2</strong>) TaqI B (P = .029) and the GABAA beta2 subunit C1412T (P = .012) genes, but not with the glutamate receptor subunit gene NMDAR2B (366C/G), the serotonin transporter gene (5HTTL PR), the dopamine transporter gene DAT1(SLC6A3), the dopamine D2 receptor gene <strong>DRD2</strong> TaqI A, or the GABAA alpha1(A15G), alpha6(T1519C), and gamma2(G3145A) subunit genes.
+DRD2	drug	nicotine	15492764	Dopamine receptor <strong>DRD2</strong> genotype and <b>smoking</b> cessation outcome following treatment with bupropion SR.
+DRD2	addiction	addiction	15492764	The A1 allele of the dopamine D2 receptor gene (<strong>DRD2</strong>) is associated with a reduced number of dopamine binding sites in the brain and with the increased likelihood of substance abuse and <b>addictive</b> behavior.
+DRD2	drug	nicotine	15492764	In a study of <b>smokers</b> enrolled in an open label, randomized effectiveness trial, we investigated whether variants in the <strong>DRD2</strong> receptor gene are associated with <b>smoking</b> cessation outcomes following treatment with a combination of bupropion SR and behavioral counseling.
+DRD2	addiction	relapse	15457501	The dopamine D2 (<strong>DRD2</strong>) gene, and especially its allele TaqI A1 allele and its receptor, also may be involved in comorbid antisocial personality disorder symptoms, high novelty <b>seeking</b>, and related traits.
+DRD2	drug	alcohol	15389757	Association of the  141C Del variant of the dopamine D2 receptor (<strong>DRD2</strong>) with positive family history and suicidality in German <b>alcoholics</b>.
+DRD2	addiction	withdrawal	15389757	Therefore, the  141C Del variant of the <strong>DRD2</strong> might be a protective factor against the development of <b>withdrawal</b> symptoms.
+DRD2	drug	nicotine	15381926	Effects of dopamine D2 receptor (<strong>DRD2</strong>) and transporter (SLC6A3) polymorphisms on <b>smoking</b> cue induced cigarette craving among African American <b>smokers</b>.
+DRD2	addiction	relapse	15381926	Effects of dopamine D2 receptor (<strong>DRD2</strong>) and transporter (SLC6A3) polymorphisms on smoking cue induced cigarette <b>craving</b> among African American smokers.
+DRD2	drug	nicotine	15381926	<b>Smokers</b> carrying either the <strong>DRD2</strong> (D2 dopamine receptor gene) TaqI A1 RFLP or the SLC6A3 (dopamine transporter gene) 9 repeat VNTR polymorphisms had stronger cue induced cravings than noncarriers (Ps <0.05 and 0.01, respectively).
+DRD2	drug	alcohol	15296817	Molecular genetic research has identified promising markers of <b>alcohol</b> dependence, including alleles of the D2 dopamine receptor (<strong>DRD2</strong>) and the GABAA receptor beta3 subunit (GABRB3) genes.
+DRD2	addiction	dependence	15296817	Molecular genetic research has identified promising markers of alcohol <b>dependence</b>, including alleles of the D2 dopamine receptor (<strong>DRD2</strong>) and the GABAA receptor beta3 subunit (GABRB3) genes.
+DRD2	drug	alcohol	15296817	In the present study, A1+ (A1A1 and A1A2 genotypes) and A1  (A2A2 genotype) alleles of the <strong>DRD2</strong> and G1+ (G1G1 and G1 non G1 genotypes) and G1  (non G1 non G1 genotype) alleles of the GABRB3 gene were determined in a group of 56 medically ill patients diagnosed with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	15296817	In the present study, A1+ (A1A1 and A1A2 genotypes) and A1  (A2A2 genotype) alleles of the <strong>DRD2</strong> and G1+ (G1G1 and G1 non G1 genotypes) and G1  (non G1 non G1 genotype) alleles of the GABRB3 gene were determined in a group of 56 medically ill patients diagnosed with alcohol <b>dependence</b>.
+DRD2	drug	alcohol	15288384	78 (2001) 1094] and associates found increases in the dopamine D2 receptors (<strong>DRD2</strong>) via adenoviral vector delivery of the <strong>DRD2</strong> gene into the nucleus accumbens, significantly reduced both <b>ethanol</b> preference (43%) and <b>alcohol</b> intake (64%) of <b>ethanol</b> preferring rats, which recovered as the <strong>DRD2</strong>, returned to baseline levels.
+DRD2	drug	alcohol	15288384	This <strong>DRD2</strong> overexpression similarly produced significant reductions in <b>ethanol</b> non preferring rats, in both <b>alcohol</b> preference (16%) and <b>alcohol</b> intake (75%).
+DRD2	drug	alcohol	15288384	This work further suggests that high levels of <strong>DRD2</strong> may be protective against <b>alcohol</b> abuse [JAMA 263 (1990) 2055; Arch, Gen. Psychiatr.
+DRD2	drug	opioid	15288384	The <strong>DRD2</strong> A1 allele has also been shown to associate with <b>heroin</b> addicts in a number of studies.
+DRD2	drug	nicotine	15203798	Effects of quitting <b>smoking</b> on EEG activation and attention last for more than 31 days and are more severe with stress, dependence, <strong>DRD2</strong> A1 allele, and depressive traits.
+DRD2	addiction	dependence	15203798	Effects of quitting smoking on EEG activation and attention last for more than 31 days and are more severe with stress, <b>dependence</b>, <strong>DRD2</strong> A1 allele, and depressive traits.
+DRD2	drug	opioid	15184239	These results strongly support a role of <strong>DRD2</strong> as a susceptibility gene with <b>heroin</b> dependence in Chinese patients and was associated with low risk of <b>heroin</b> dependence in Germans.
+DRD2	addiction	dependence	15184239	These results strongly support a role of <strong>DRD2</strong> as a susceptibility gene with heroin <b>dependence</b> in Chinese patients and was associated with low risk of heroin <b>dependence</b> in Germans.
+DRD2	addiction	addiction	15146457	If this is the case, then changes in ANKK1 activity may provide an alternative explanation for previously described associations between the <strong>DRD2</strong> Taq1A RFLP and neuropsychiatric disorders such as <b>addiction</b>.
+DRD2	drug	nicotine	15138759	Seventy one <b>smokers</b> of European ancestry were genotyped for the dopamine D2 receptor (<strong>DRD2</strong>) Taq1 polymorphism and randomized to treatment with bupropion (300 mg) or placebo for <b>smoking</b> cessation.
+DRD2	drug	nicotine	15138759	Carriers of the <strong>DRD2</strong> A1 minor allele exhibited significant increases in the rewarding value of food following abstinence from <b>smoking</b>, and these effects were attenuated by bupropion treatment (P=0.03 for medication by genotype interaction).
+DRD2	drug	alcohol	15084894	The role of the dopamine D2 receptor (<strong>DRD2</strong>) gene in the development of <b>alcohol</b> abuse or dependence is controversial.
+DRD2	addiction	dependence	15084894	The role of the dopamine D2 receptor (<strong>DRD2</strong>) gene in the development of alcohol abuse or <b>dependence</b> is controversial.
+DRD2	drug	alcohol	15084894	We hypothesized that the ADH1B and ALDH2 genes might interact with the <strong>DRD2</strong> gene and that the association between the <strong>DRD2</strong> gene and <b>alcohol</b> dependence might be affected by different ADH1B and ALDH2 genotypes.
+DRD2	addiction	dependence	15084894	We hypothesized that the ADH1B and ALDH2 genes might interact with the <strong>DRD2</strong> gene and that the association between the <strong>DRD2</strong> gene and alcohol <b>dependence</b> might be affected by different ADH1B and ALDH2 genotypes.
+DRD2	drug	alcohol	15084894	This study examined whether the <strong>DRD2</strong> gene is associated with specific subtypes of <b>alcohol</b> dependence and evaluated the relationship between the <strong>DRD2</strong> gene and <b>alcohol</b> metabolizing genes in a specific subtype of <b>alcohol</b> dependence.
+DRD2	addiction	dependence	15084894	This study examined whether the <strong>DRD2</strong> gene is associated with specific subtypes of alcohol <b>dependence</b> and evaluated the relationship between the <strong>DRD2</strong> gene and alcohol metabolizing genes in a specific subtype of alcohol <b>dependence</b>.
+DRD2	drug	alcohol	15084894	The <strong>DRD2</strong> gene was not found to be associated with pure <b>alcohol</b> dependence or ANX/DEP, but was found to be associated with ANX/DEP ALC.
+DRD2	addiction	dependence	15084894	The <strong>DRD2</strong> gene was not found to be associated with pure alcohol <b>dependence</b> or ANX/DEP, but was found to be associated with ANX/DEP ALC.
+DRD2	drug	nicotine	15077009	Polymorphisms in the dopamine D2 receptor (<strong>DRD2</strong> C/T and <strong>DRD2</strong> A/G) and in dopamine beta hydroxylase (DBH A/G) have been implicated in modulation of <b>smoking</b> and other reward seeking behaviours.
+DRD2	addiction	relapse	15077009	Polymorphisms in the dopamine D2 receptor (<strong>DRD2</strong> C/T and <strong>DRD2</strong> A/G) and in dopamine beta hydroxylase (DBH A/G) have been implicated in modulation of smoking and other reward <b>seeking</b> behaviours.
+DRD2	addiction	reward	15077009	Polymorphisms in the dopamine D2 receptor (<strong>DRD2</strong> C/T and <strong>DRD2</strong> A/G) and in dopamine beta hydroxylase (DBH A/G) have been implicated in modulation of smoking and other <b>reward</b> seeking behaviours.
+DRD2	drug	nicotine	15077009	In the 755 cases in which DNA was successfully genotyped, we examined associations between the polymorphisms in <strong>DRD2</strong> and DBH, and <b>smoking</b> cessation.
+DRD2	drug	nicotine	15077009	At 1 week, the patch was more effective for <b>smokers</b> with <strong>DRD2</strong> CT/TT genotype [patch/placebo odds ratio (OR) 2.8, 95% confidence interval (CI) 1.7 4.6] than with CC (OR 1.4, 0.9 2.1; P for difference in ORs 0.04).
+DRD2	drug	nicotine	15077009	<b>Smokers</b> with both <strong>DRD2</strong> CT/TT and DBH GA/AA genotypes had an OR of 3.6 (2.0 6.5) compared to 1.4 (1.0 2.1) for others (P = 0.01).
+DRD2	drug	alcohol	15066703	To study the impact of genetic factors that play an important role in an individual's vulnerability to <b>alcohol</b> abuse and dependence, we examined the genetic variations of the major neurotransmitter genes, including the dopamine D2 receptor (<strong>DRD2</strong>) TaqI A, B, and  141C insertion/deletion (Ins/Del) polymorphisms, the serotonin transporter linked polymorphic region (5 HTTLPR), and the gamma aminobutyric acid A (GABA(A)) receptor beta(3) subunit gene (GABRbeta3), for 130 Mexican American <b>alcoholic</b> men and 251 nonalcoholic control subjects (105 men and 146 women).
+DRD2	addiction	dependence	15066703	To study the impact of genetic factors that play an important role in an individual's vulnerability to alcohol abuse and <b>dependence</b>, we examined the genetic variations of the major neurotransmitter genes, including the dopamine D2 receptor (<strong>DRD2</strong>) TaqI A, B, and  141C insertion/deletion (Ins/Del) polymorphisms, the serotonin transporter linked polymorphic region (5 HTTLPR), and the gamma aminobutyric acid A (GABA(A)) receptor beta(3) subunit gene (GABRbeta3), for 130 Mexican American alcoholic men and 251 nonalcoholic control subjects (105 men and 146 women).
+DRD2	drug	alcohol	15066703	The genotype frequency for the <strong>DRD2</strong>  141C Ins/Del allele was significantly different between <b>alcoholic</b> and control subjects (P=.007).
+DRD2	drug	alcohol	15066703	When smokers were excluded from both control and <b>alcoholic</b> groups, the association between the <strong>DRD2</strong>  141C Ins allele, as well as between the 5 HTTLPR S allele, and <b>alcoholism</b> became significant at both genotypic and allelic levels.
+DRD2	drug	nicotine	15066703	When <b>smokers</b> were excluded from both control and alcoholic groups, the association between the <strong>DRD2</strong>  141C Ins allele, as well as between the 5 HTTLPR S allele, and alcoholism became significant at both genotypic and allelic levels.
+DRD2	drug	alcohol	15066703	No positive association was found between <b>alcoholism</b> and the <strong>DRD2</strong> TaqI A or B, or the GABRbeta3, genotype.
+DRD2	drug	alcohol	15066703	Our findings indicate that the <strong>DRD2</strong>  141C Ins allele and the 5 HTTLPR S allele are genetic risk factors for <b>alcoholism</b> in Mexican Americans, and that smoking modulates the association between genetic risk factors and <b>alcoholism</b>.
+DRD2	drug	nicotine	15066703	Our findings indicate that the <strong>DRD2</strong>  141C Ins allele and the 5 HTTLPR S allele are genetic risk factors for alcoholism in Mexican Americans, and that <b>smoking</b> modulates the association between genetic risk factors and alcoholism.
+DRD2	addiction	relapse	14732864	Stress induced cigarette <b>craving</b>: effects of the <strong>DRD2</strong> TaqI RFLP and SLC6A3 VNTR polymorphisms.
+DRD2	addiction	relapse	14732864	Significantly stronger stress induced cigarette <b>craving</b> was found for individuals carrying either the <strong>DRD2</strong> (D2 dopamine receptor gene) A1, or the SLC6A3 (dopamine transporter gene) nine repeat allelic variants.
+DRD2	drug	nicotine	14668077	Does the <strong>DRD2</strong> Taq1 A polymorphism influence treatment response to bupropion hydrochloride for reduction of the <b>nicotine</b> withdrawal syndrome?
+DRD2	addiction	withdrawal	14668077	Does the <strong>DRD2</strong> Taq1 A polymorphism influence treatment response to bupropion hydrochloride for reduction of the nicotine <b>withdrawal</b> syndrome?
+DRD2	addiction	relapse	14668077	Within the bupropion group, subgroup analyses with stratification by genotype demonstrated that <b>craving</b>, irritability, and anxiety were significantly attenuated only among subjects with <strong>DRD2</strong> Taq1 A2/A2 genotypes.
+DRD2	drug	nicotine	14668077	In the <strong>DRD2</strong> Taq1 A1/A1 and A1/A2 groups, no significant reduction was seen in any individual symptom of the <b>nicotine</b> withdrawal syndrome.
+DRD2	addiction	withdrawal	14668077	In the <strong>DRD2</strong> Taq1 A1/A1 and A1/A2 groups, no significant reduction was seen in any individual symptom of the nicotine <b>withdrawal</b> syndrome.
+DRD2	drug	alcohol	14643564	The A1 allele of the <strong>DRD2</strong> gene (TaqI A polymorphisms) is associated with antisocial personality in a sample of <b>alcohol</b> dependent patients.
+DRD2	drug	alcohol	14643564	Presence of A1 allele of the <strong>DRD2</strong> gene has been associated with a predisposition for <b>alcoholism</b> although there are limited data about its phenotypic expression in <b>alcoholism</b>.
+DRD2	drug	nicotine	14570538	Assessments included the dopamine D2 receptor (<strong>DRD2</strong>) genotype, dopamine transporter (SLC6A3) genotype, demographic factors, and <b>nicotine</b> dependence.
+DRD2	addiction	dependence	14570538	Assessments included the dopamine D2 receptor (<strong>DRD2</strong>) genotype, dopamine transporter (SLC6A3) genotype, demographic factors, and nicotine <b>dependence</b>.
+DRD2	drug	nicotine	14570538	The results provided evidence for a significant <strong>DRD2</strong> * SLC6A3 interaction effect on prolonged <b>smoking</b> abstinence and time to relapse at EOT, independent of treatment condition.
+DRD2	addiction	relapse	14570538	The results provided evidence for a significant <strong>DRD2</strong> * SLC6A3 interaction effect on prolonged smoking abstinence and time to <b>relapse</b> at EOT, independent of treatment condition.
+DRD2	drug	alcohol	13679114	Differential associations of sex and D2 dopamine receptor (<strong>DRD2</strong>) genotype with negative affect and other substance abuse risk markers in children of <b>alcoholics</b>.
+DRD2	drug	alcohol	13679114	Because the D2 dopamine receptor (<strong>DRD2</strong>) A1 allele has been associated with <b>alcoholism</b> and other substance use disorders, negative affect, measured by the Beck Depression Inventory (BDI), was determined in four groups of children: boys and girls with the A1+ allele (A1A1 and A1A2 genotypes) and with the A1  allele (A2A2 genotype).
+DRD2	drug	alcohol	12898574	For this study, homogeneous population consisting of 243 young <b>alcohol</b>  and drug naive Koreans who were blood unrelated with a mean age (+/ SD) of 13.87 (+/ 0.30) years old was analyzed for the DRD4 and the <strong>DRD2</strong> polymorphisms with their personality trait by Temperament and character inventory (TCI).
+DRD2	addiction	dependence	12898574	Female subjects who carried the <strong>DRD2</strong> less frequent alleles (TaqI A1, TaqI B1, and Intron6 1) showed higher RD4 scores (<b>dependence</b> vs. independence) of Reward <b>dependence</b> (RD) than those without these alleles (P < 0.05).
+DRD2	addiction	reward	12898574	Female subjects who carried the <strong>DRD2</strong> less frequent alleles (TaqI A1, TaqI B1, and Intron6 1) showed higher RD4 scores (dependence vs. independence) of <b>Reward</b> dependence (RD) than those without these alleles (P < 0.05).
+DRD2	addiction	reward	12898574	These results, thus, confirmed the previous findings in which the long repeats of the DRD4 exon III polymorphism are related to NS personality trait, and also suggested that the <strong>DRD2</strong> less frequent alleles were also associated with the <b>reward</b> dependent trait.
+DRD2	drug	alcohol	12837020	Effects of a <strong>Drd2</strong> deletion mutation on <b>ethanol</b> induced locomotor stimulation and sensitization suggest a role for epistasis.
+DRD2	addiction	sensitization	12837020	Effects of a <strong>Drd2</strong> deletion mutation on ethanol induced locomotor stimulation and <b>sensitization</b> suggest a role for epistasis.
+DRD2	drug	alcohol	12837020	Dopamine D2 receptor (<strong>Drd2</strong>) knockout mice on a C57BL/6 (B6) background show decreased basal locomotion, <b>ethanol</b> preference and <b>ethanol</b> induced ataxia.
+DRD2	drug	alcohol	12837020	The reduced <b>ethanol</b> consumption observed in <b>ethanol</b> naive B6 <strong>Drd2</strong> knockout mice was absent in <b>ethanol</b> sensitized knockout mice.
+DRD2	drug	alcohol	12837020	The impact of the <strong>Drd2</strong> null mutation on a subset of <b>ethanol</b> related behavioral traits is subject to epistatic influences.
+DRD2	drug	alcohol	12782972	Impulsiveness as the intermediate link between the <strong>dopamine receptor D2</strong> gene and <b>alcohol</b> dependence.
+DRD2	addiction	dependence	12782972	Impulsiveness as the intermediate link between the <strong>dopamine receptor D2</strong> gene and alcohol <b>dependence</b>.
+DRD2	drug	alcohol	12782972	Reinforcement and reward processes have been proposed as being an intermediate link between the risk for <b>alcohol</b> dependence and the gene coding for the dopamine receptor D2 (<strong>DRD2</strong>).
+DRD2	addiction	dependence	12782972	Reinforcement and reward processes have been proposed as being an intermediate link between the risk for alcohol <b>dependence</b> and the gene coding for the dopamine receptor D2 (<strong>DRD2</strong>).
+DRD2	addiction	reward	12782972	<b>Reinforcement</b> and <b>reward</b> processes have been proposed as being an intermediate link between the risk for alcohol dependence and the gene coding for the dopamine receptor D2 (<strong>DRD2</strong>).
+DRD2	drug	alcohol	12782972	Reinforcement and reward processes have been proposed as being an intermediate link between the risk for <b>alcohol</b> dependence and the gene coding for the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>).
+DRD2	addiction	dependence	12782972	Reinforcement and reward processes have been proposed as being an intermediate link between the risk for alcohol <b>dependence</b> and the gene coding for the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>).
+DRD2	addiction	reward	12782972	<b>Reinforcement</b> and <b>reward</b> processes have been proposed as being an intermediate link between the risk for alcohol dependence and the gene coding for the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>).
+DRD2	drug	alcohol	12782972	Considering the pro impulsiveness role of <b>ethanol</b> observed in clinical practice and epidemiological studies, we analysed the Barratt impulsiveness scores in a sample of 92 <b>alcohol</b> dependent French patients (57 men and 35 women), according to the TaqI A polymorphism of the <strong>DRD2</strong> gene.
+DRD2	drug	alcohol	12782972	We propose that reward related impulsiveness may constitute a risk factor for <b>alcohol</b> dependence, and that this core temperament could be partly mediated by the <strong>DRD2</strong> gene.
+DRD2	addiction	dependence	12782972	We propose that reward related impulsiveness may constitute a risk factor for alcohol <b>dependence</b>, and that this core temperament could be partly mediated by the <strong>DRD2</strong> gene.
+DRD2	addiction	reward	12782972	We propose that <b>reward</b> related impulsiveness may constitute a risk factor for alcohol dependence, and that this core temperament could be partly mediated by the <strong>DRD2</strong> gene.
+DRD2	drug	alcohol	12543998	Dopamine D2 receptor binding, <strong>Drd2</strong> expression and the number of dopamine neurons in the BXD recombinant inbred series: genetic relationships to <b>alcohol</b> and other drug associated phenotypes.
+DRD2	drug	alcohol	12543998	The current study addresses this issue by measuring D2 dopamine (DA) receptor binding, the expression of <strong>Drd2</strong>, the number of midbrain DA neurons in the BXD recombinant inbred (RI) series and then compares these strain means with those previously reported for a variety of <b>ethanol</b> and other drug related phenotypes.
+DRD2	drug	alcohol	12543998	No significant correlations were detected between <b>ethanol</b> preference and either receptor binding or <strong>Drd2</strong> expression; however, a significant correlation was found between preference and Ncam expression.
+DRD2	drug	alcohol	12543998	Overall, the data suggest <b>ethanol</b> preference and CPP are associated with the expression of <strong>Drd2</strong> or closely linked genetic loci.
+DRD2	addiction	reward	12543998	Overall, the data suggest ethanol preference and <b>CPP</b> are associated with the expression of <strong>Drd2</strong> or closely linked genetic loci.
+DRD2	drug	alcohol	12497624	After the first association of the TaqI A <strong>DRD2</strong> minor (A1) allele with severe <b>alcoholism</b> in 1990, a large number of international studies have followed.
+DRD2	drug	alcohol	12497624	A meta analysis of these studies of Caucasians showed a significantly higher <strong>DRD2</strong> A1 allelic frequency and prevalence in <b>alcoholics</b> when compared to controls.
+DRD2	drug	cocaine	12497624	Variants of the <strong>DRD2</strong> gene have also been associated with other addictive disorders including <b>cocaine</b>, nicotine and opioid dependence and obesity.
+DRD2	drug	nicotine	12497624	Variants of the <strong>DRD2</strong> gene have also been associated with other addictive disorders including cocaine, <b>nicotine</b> and opioid dependence and obesity.
+DRD2	drug	opioid	12497624	Variants of the <strong>DRD2</strong> gene have also been associated with other addictive disorders including cocaine, nicotine and <b>opioid</b> dependence and obesity.
+DRD2	addiction	addiction	12497624	Variants of the <strong>DRD2</strong> gene have also been associated with other <b>addictive</b> disorders including cocaine, nicotine and opioid dependence and obesity.
+DRD2	addiction	dependence	12497624	Variants of the <strong>DRD2</strong> gene have also been associated with other addictive disorders including cocaine, nicotine and opioid <b>dependence</b> and obesity.
+DRD2	addiction	reward	12497624	It is hypothesized that the <strong>DRD2</strong> is a <b>reinforcement</b> or <b>reward</b> gene.
+DRD2	drug	alcohol	12391346	Autosomal dominant <b>alcohol</b> responsive M D is associated with mutations in the epsilon sarcoglycan gene (SGCE) (six families) and with a missense change in the D2 dopamine receptor (<strong>DRD2</strong>)gene (one family).
+DRD2	drug	alcohol	12376935	Male limited association of the <strong>dopamine receptor D2</strong> gene TaqI a polymorphism and <b>alcohol</b> dependence.
+DRD2	addiction	dependence	12376935	Male limited association of the <strong>dopamine receptor D2</strong> gene TaqI a polymorphism and alcohol <b>dependence</b>.
+DRD2	drug	alcohol	12376935	Association studies of the TaqI A allele of the dopamine receptor D2 (<strong>DRD2</strong>) gene with <b>alcohol</b> dependence have produced conflicting findings.
+DRD2	addiction	dependence	12376935	Association studies of the TaqI A allele of the dopamine receptor D2 (<strong>DRD2</strong>) gene with alcohol <b>dependence</b> have produced conflicting findings.
+DRD2	drug	alcohol	12376935	Association studies of the TaqI A allele of the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) gene with <b>alcohol</b> dependence have produced conflicting findings.
+DRD2	addiction	dependence	12376935	Association studies of the TaqI A allele of the <strong>dopamine receptor D2</strong> (<strong>DRD2</strong>) gene with alcohol <b>dependence</b> have produced conflicting findings.
+DRD2	drug	alcohol	12376935	We compared the TaqI A polymorphisms of the <strong>DRD2</strong> gene in 120 French Caucasian <b>alcohol</b> dependent inpatients (62 males and 58 females) and 107 healthy ethnically matched controls (66 males and 41 females).
+DRD2	drug	alcohol	12376935	We thus replicated the allelic association of the A1 allele of the <strong>DRD2</strong> gene with <b>alcohol</b> dependence, but showed a male limited effect of this "vulnerability allele."
+DRD2	addiction	dependence	12376935	We thus replicated the allelic association of the A1 allele of the <strong>DRD2</strong> gene with alcohol <b>dependence</b>, but showed a male limited effect of this "vulnerability allele."
+DRD2	drug	alcohol	12218663	The many association studies that compared the frequencies of alleles of the dopamine D2 receptor (<strong>DRD2</strong>) gene between <b>alcoholics</b> and control groups have produced results, but some have been equivocal.
+DRD2	drug	alcohol	11918988	D(2) dopamine receptor (<strong>DRD2</strong>) polymorphism is associated with severity of <b>alcohol</b> dependence.
+DRD2	addiction	dependence	11918988	D(2) dopamine receptor (<strong>DRD2</strong>) polymorphism is associated with severity of alcohol <b>dependence</b>.
+DRD2	drug	alcohol	11918988	The A(1) allele of the D(2) dopamine receptor (<strong>DRD2</strong>) gene has been associated with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	11918988	The A(1) allele of the D(2) dopamine receptor (<strong>DRD2</strong>) gene has been associated with alcohol <b>dependence</b>.
+DRD2	drug	alcohol	11918988	The present study examines the association between <strong>DRD2</strong> A(1)(+) (A(1)/A(1) and A(1)/A(2) genotypes) and A(1)  (A(2)/A(2) genotype) allele status and key drinking parameters in <b>alcohol</b> dependent patients.
+DRD2	drug	alcohol	11918988	In sum, <b>alcohol</b> dependent patients with the <strong>DRD2</strong> A(1) allele compared to patients without this allele are characterized by greater severity of their disorder across a range of problem drinking indices.
+DRD2	addiction	reward	11901357	The D2 and D4 dopamine receptors (<strong>DRD2</strong> and DRD4) play major roles in the central effects of psychostimulants and in the <b>reward</b> system.
+DRD2	addiction	dependence	11901357	Previous studies, although not all, have demonstrated associations between the <strong>DRD2</strong> TaqI and the DRD4 exon III variable number tandem repeat (VNTR) polymorphisms and substance <b>dependence</b>.
+DRD2	addiction	dependence	11901357	No significant difference was demonstrated for genotype or allele frequency when comparing MAP dependent and control cases for the <strong>DRD2</strong> TaqI and the DRD4 gene exon III VNTR polymorphisms, suggesting that these two polymorphisms do not play major roles in MAP <b>dependence</b> for our sample of Chinese males.
+DRD2	drug	alcohol	11900611	Polymorphisms at the <strong>DRD2</strong> locus in early onset <b>alcohol</b> dependence in the Indian population.
+DRD2	addiction	dependence	11900611	Polymorphisms at the <strong>DRD2</strong> locus in early onset alcohol <b>dependence</b> in the Indian population.
+DRD2	drug	alcohol	11900611	Severe forms of the <b>alcoholism</b> phenotype have been associated with an increased frequency of the Taq A1 allele at the <strong>DRD2</strong> locus.
+DRD2	drug	alcohol	11807408	The results suggest that both the <strong>DRD2</strong> promoter region and the DAT gene do not play a significant role in conferring vulnerability to <b>alcoholism</b>.
+DRD2	drug	alcohol	11692072	Influence of the dopamine D2 receptor (<strong>DRD2</strong>) exon 8 genotype on efficacy of tiapride and clinical outcome of <b>alcohol</b> withdrawal.
+DRD2	addiction	withdrawal	11692072	Influence of the dopamine D2 receptor (<strong>DRD2</strong>) exon 8 genotype on efficacy of tiapride and clinical outcome of alcohol <b>withdrawal</b>.
+DRD2	drug	alcohol	11692072	The findings suggest a pharmacogenetic influence of <strong>DRD2</strong> E8 genotype on tiapride efficacy in <b>alcohol</b> withdrawal.
+DRD2	addiction	withdrawal	11692072	The findings suggest a pharmacogenetic influence of <strong>DRD2</strong> E8 genotype on tiapride efficacy in alcohol <b>withdrawal</b>.
+DRD2	drug	alcohol	11553683	Here we used an adenoviral vector to deliver the dopamine D2 receptor (<strong>DRD2</strong>) gene into the nucleus accumbens of rats, previously trained to self administer <b>alcohol</b>, and to assess if <strong>DRD2</strong> levels regulated <b>alcohol</b> preference and intake.
+DRD2	drug	alcohol	11553683	We show that increases in <strong>DRD2</strong> (52%) were associated with marked reductions in <b>alcohol</b> preference (43%), and <b>alcohol</b> intake (64%) of <b>ethanol</b> preferring rats, which recovered as the <strong>DRD2</strong>, returned to baseline levels.
+DRD2	drug	alcohol	11553683	In addition, this <strong>DRD2</strong> overexpression similarly produced significant reductions in <b>ethanol</b> non preferring rats, in both <b>alcohol</b> preference (16%) and <b>alcohol</b> intake (75%).
+DRD2	drug	alcohol	11553683	This is the first evidence that overexpression of <strong>DRD2</strong> reduces <b>alcohol</b> intake and suggests that high levels of <strong>DRD2</strong> may be protective against <b>alcohol</b> abuse.
+DRD2	drug	alcohol	11347517	More than 80% of <b>alcoholics</b> smoke cigarettes in the U.S.A. Other genetic methods such as linkage analysis, allele sharing methods, association studies and analysis of inbred, transgenic and gene knockout rodents, have partially agreed in showing that the 5HT 1B serotonin receptor and the DRD1, <strong>DRD2</strong> and DRD4 dopamine receptors, as well as the dopamine transporter DAT, play an important role in behaviors related to <b>alcoholism</b> and substance abuse.
+DRD2	drug	alcohol	11256581	The TaqIA D2 dopamine receptor (<strong>DRD2</strong>) minor (A1) allele was first associated with severe <b>alcoholism</b> a decade ago.
+DRD2	drug	alcohol	11256581	However, a meta analysis of a large number of Caucasian <b>alcoholics</b> (both more severe and less severe) and controls (both assessed and unassessed for substance use disorders) revealed a significantly higher frequency (p < 10( 6)) and prevalence (p < 10( 8)) of the <strong>DRD2</strong> A1 allele in the <b>alcoholics</b>.
+DRD2	drug	alcohol	11256581	Further analysis showed that the more severe <b>alcoholics</b> had a 3 fold higher prevalence of the <strong>DRD2</strong> A1 allele than the assessed controls (p < 10( 10)), whereas no difference was found between the less severe <b>alcoholics</b> and the unassessed controls.
+DRD2	drug	alcohol	11256581	<strong>DRD2</strong> exonic or promoter mutations have not yet been associated with <b>alcoholism</b>, although two intronic variants at the TaqIB and intron 6 sites, which are in linkage disequilibrium with the TaqIA site, were associated with this disorder.
+DRD2	drug	cocaine	11256581	Variants of the <strong>DRD2</strong> gene have also been associated with <b>cocaine</b>, nicotine and opioid dependence, obesity and gambling.
+DRD2	drug	nicotine	11256581	Variants of the <strong>DRD2</strong> gene have also been associated with cocaine, <b>nicotine</b> and opioid dependence, obesity and gambling.
+DRD2	drug	opioid	11256581	Variants of the <strong>DRD2</strong> gene have also been associated with cocaine, nicotine and <b>opioid</b> dependence, obesity and gambling.
+DRD2	addiction	dependence	11256581	Variants of the <strong>DRD2</strong> gene have also been associated with cocaine, nicotine and opioid <b>dependence</b>, obesity and gambling.
+DRD2	addiction	reward	11256581	It is hypothesised that the <strong>DRD2</strong> is a <b>reinforcement</b> or <b>reward</b> gene.
+DRD2	drug	alcohol	11236836	We evaluated the role of three polymorphic genes related to <b>alcohol</b> metabolism (CYP2E1) and, possibly, dependence (<strong>DRD2</strong> and SLC6A4 promoter) in a series of 60 <b>alcoholics</b> admitted to a specialized referral center in Florence, Italy.
+DRD2	addiction	dependence	11236836	We evaluated the role of three polymorphic genes related to alcohol metabolism (CYP2E1) and, possibly, <b>dependence</b> (<strong>DRD2</strong> and SLC6A4 promoter) in a series of 60 alcoholics admitted to a specialized referral center in Florence, Italy.
+DRD2	drug	alcohol	11236830	Dopamine D2 receptor gene (<strong>DRD2</strong>) is associated with <b>alcoholism</b> with conduct disorder.
+DRD2	drug	alcohol	11236830	This study examined whether there is evidence for an association between <b>alcoholism</b> with conduct disorder and alleles of the TaqI A and TaqI B polymorphisms, both individually and as haplotypes, at the dopamine D2 receptor gene (<strong>DRD2</strong>).
+DRD2	drug	alcohol	11236830	Significant associations were observed between TaqI A and TaqI B at the <strong>DRD2</strong> locus, tested individually and as haplotypes, and <b>alcoholism</b> with conduct disorder.
+DRD2	drug	alcohol	11236830	Our results suggested that <strong>DRD2</strong> might be associated with conduct disorder or a predisposition to both conduct disorder and <b>alcoholism</b>.
+DRD2	drug	alcohol	11236830	However, this needs to be further investigated by examining the differences among conduct disorder with <b>alcoholism</b>, conduct disorder only, and controls for the TaqI A and B system at <strong>DRD2</strong>.
+DRD2	drug	alcohol	11105655	Studies in the past decade have shown that in various subject groups the Taq I A1 allele of the <strong>DRD2</strong> gene is associated with <b>alcoholism</b>, drug abuse, smoking, obesity, compulsive gambling, and several personality traits.
+DRD2	drug	nicotine	11105655	Studies in the past decade have shown that in various subject groups the Taq I A1 allele of the <strong>DRD2</strong> gene is associated with alcoholism, drug abuse, <b>smoking</b>, obesity, compulsive gambling, and several personality traits.
+DRD2	addiction	addiction	11105655	Studies in the past decade have shown that in various subject groups the Taq I A1 allele of the <strong>DRD2</strong> gene is associated with alcoholism, drug abuse, smoking, obesity, <b>compulsive</b> gambling, and several personality traits.
+DRD2	drug	alcohol	11054774	Family based study of <strong>DRD2</strong> alleles in <b>alcohol</b> and drug dependence.
+DRD2	addiction	dependence	11054774	Family based study of <strong>DRD2</strong> alleles in alcohol and drug <b>dependence</b>.
+DRD2	drug	alcohol	11054774	Numerous case control studies have addressed the hypothesis that variant alleles of the dopamine D2 receptor gene (<strong>DRD2</strong>) increase the liability for <b>alcohol</b> and/or drug dependence, and both positive and negative results have been reported.
+DRD2	addiction	dependence	11054774	Numerous case control studies have addressed the hypothesis that variant alleles of the dopamine D2 receptor gene (<strong>DRD2</strong>) increase the liability for alcohol and/or drug <b>dependence</b>, and both positive and negative results have been reported.
+DRD2	drug	alcohol	11054774	Using the transmission disequilibrium test, the present study examined linkage disequilibrium of <b>alcohol</b> and drug (opioid and/or cocaine) dependence with three <strong>DRD2</strong> polymorphic systems: (a) TaqI A, (b) TaqI D, and (c) the functional  141CIns/Del promoter systems.
+DRD2	drug	cocaine	11054774	Using the transmission disequilibrium test, the present study examined linkage disequilibrium of alcohol and drug (opioid and/or <b>cocaine</b>) dependence with three <strong>DRD2</strong> polymorphic systems: (a) TaqI A, (b) TaqI D, and (c) the functional  141CIns/Del promoter systems.
+DRD2	drug	opioid	11054774	Using the transmission disequilibrium test, the present study examined linkage disequilibrium of alcohol and drug (<b>opioid</b> and/or cocaine) dependence with three <strong>DRD2</strong> polymorphic systems: (a) TaqI A, (b) TaqI D, and (c) the functional  141CIns/Del promoter systems.
+DRD2	addiction	dependence	11054774	Using the transmission disequilibrium test, the present study examined linkage disequilibrium of alcohol and drug (opioid and/or cocaine) <b>dependence</b> with three <strong>DRD2</strong> polymorphic systems: (a) TaqI A, (b) TaqI D, and (c) the functional  141CIns/Del promoter systems.
+DRD2	drug	alcohol	11054774	Because positive association between <strong>DRD2</strong> alleles and <b>alcohol</b> and/or drug dependence has been reported only in populations of European ancestry, we limited the present study to European Americans (EAs).
+DRD2	addiction	dependence	11054774	Because positive association between <strong>DRD2</strong> alleles and alcohol and/or drug <b>dependence</b> has been reported only in populations of European ancestry, we limited the present study to European Americans (EAs).
+DRD2	addiction	dependence	11054774	Together, these studies suggest that the conflicting findings from case control studies of the association between alleles of <strong>DRD2</strong> and substance <b>dependence</b> may be attributable to population stratification in some samples.
+DRD2	drug	alcohol	11054765	The frequency of the TaqI A(1) allele of the D(2) dopamine receptor (<strong>DRD2</strong>) gene was 19.0% in these patients compared with 4.6% in controls free of past and current <b>alcohol</b> and other drug abuse and free of family history of <b>alcohol</b> and other drug abuse (p = 0.009).
+DRD2	drug	opioid	11054765	The results indicate that <strong>DRD2</strong> variants are predictors of <b>heroin</b> use and subsequent <b>methadone</b> treatment outcome and suggest a pharmacogenetic approach to the treatment of <b>opioid</b> dependence.
+DRD2	addiction	dependence	11054765	The results indicate that <strong>DRD2</strong> variants are predictors of heroin use and subsequent methadone treatment outcome and suggest a pharmacogenetic approach to the treatment of opioid <b>dependence</b>.
+DRD2	drug	alcohol	11022024	<b>Alcoholics</b> with the dopamine receptor <strong>DRD2</strong> A1 allele have lower platelet monoamine oxidase B activity than those with the A2 allele: a preliminary study.
+DRD2	drug	alcohol	11022024	Low platelet monoamine oxidase B (MAO B) activity and the presence of the Taq1 A1 allele of the dopamine D2 receptor (<strong>DRD2</strong>) gene have independently been proposed as 'biological/genetic' markers for <b>alcoholism</b>.
+DRD2	drug	alcohol	11022024	In the present study, the relationship between these two markers was investigated in a group of socially stable Caucasian middle aged men with a mean (+/ SD) daily <b>ethanol</b> consumption of 85 +/  57 g. The platelet MAO B activity was significantly lower in individuals with the <strong>DRD2</strong> A1 allele (n = 8), compared to those without it (n = 29).
+DRD2	drug	alcohol	11022024	The finding suggests that <b>alcoholics</b> who are carriers of the <strong>DRD2</strong> A1 allele may have lower platelet MAO B activity.
+DRD2	drug	nicotine	20575861	The dopamine D2 receptor (<strong>DRD2</strong>) gene a genetic risk factor in heavy <b>smoking</b>?
+DRD2	drug	nicotine	20575861	However, our results indicate an association between the <strong>DRD2</strong> Fokl 1 allele and the onset and intensity of <b>smoking</b>.
+DRD2	drug	alcohol	10898904	Allele and genotype frequencies of the TaqI A polymorphism of dopamine D2 receptor (<strong>DRD2</strong>) gene were compared in 115 <b>alcohol</b> dependent Brazilian males and 114 ethnically matched controls.
+DRD2	drug	alcohol	10898904	Regression analyses were performed to test for an interactive effect between the <strong>DRD2</strong> TaqI A1 allele and measures of stress and harm avoidance on severity of <b>alcoholism</b> and number of antisocial personality symptoms.
+DRD2	drug	alcohol	10898904	A slightly positive association of <strong>DRD2</strong> TaqI A1 genotypes with <b>alcoholism</b> was observed, by standard and molecular heterosis approaches.
+DRD2	addiction	dependence	10898904	The <strong>DRD2</strong> TaqI A1 allele showed significant interaction with stress and harm avoidance in predicting the severity of physiologic <b>dependence</b>, and with harm avoidance for the number of antisocial personality symptoms.
+DRD2	drug	alcohol	10893740	[Genetic association between the reduced amplitude of the P300 and the allele A1 of the gene which codifies the D2 dopamine receptor (<strong>DRD2</strong>) as possible biological markers for <b>alcoholism</b>].
+DRD2	drug	alcohol	10893740	The objective of this study is to review part of the literature and find evidence for and against the characteristics observed in the P300 and the possible part played by the <strong>DRD2</strong> gene in the aetiology of <b>alcoholism</b> and the relationship between them.
+DRD2	drug	alcohol	10881206	The <strong>DRD2</strong> gene and the risk for <b>alcohol</b> dependence in bipolar patients.
+DRD2	addiction	dependence	10881206	The <strong>DRD2</strong> gene and the risk for alcohol <b>dependence</b> in bipolar patients.
+DRD2	drug	alcohol	10881206	The regression analysis based on the three variables (bipolar disorder, <b>alcohol</b> dependence and interaction between these two disorders) does not explain the presence of the A1 allele of the <strong>DRD2</strong> gene.
+DRD2	addiction	dependence	10881206	The regression analysis based on the three variables (bipolar disorder, alcohol <b>dependence</b> and interaction between these two disorders) does not explain the presence of the A1 allele of the <strong>DRD2</strong> gene.
+DRD2	drug	alcohol	10881204	Reappraisal of the association between the <strong>DRD2</strong> gene, <b>alcoholism</b> and addiction.
+DRD2	addiction	addiction	10881204	Reappraisal of the association between the <strong>DRD2</strong> gene, alcoholism and <b>addiction</b>.
+DRD2	drug	alcohol	10881204	We thus tested another (dinucleotide STRP) marker within the <strong>DRD2</strong> gene, selected a new homogenous sample of 113 <b>alcoholic</b> patients and 49 unaffected controls strictly matched for ethnic origins, and systematically assessed both samples with a semi structured interview to detect (in both samples) <b>alcohol</b> dependence, but also such related traits as specificities of complications.
+DRD2	addiction	dependence	10881204	We thus tested another (dinucleotide STRP) marker within the <strong>DRD2</strong> gene, selected a new homogenous sample of 113 alcoholic patients and 49 unaffected controls strictly matched for ethnic origins, and systematically assessed both samples with a semi structured interview to detect (in both samples) alcohol <b>dependence</b>, but also such related traits as specificities of complications.
+DRD2	drug	alcohol	10881203	Since 1990, association studies have amassed strong evidence implicating the D(2) dopamine receptor (<strong>DRD2</strong>) gene in <b>alcoholism</b>.
+DRD2	drug	alcohol	10881203	Specifically, the TaqI A minor (A1) allele of the <strong>DRD2</strong> gene has been associated with <b>alcoholism</b>.
+DRD2	drug	cocaine	10881203	The <strong>DRD2</strong> gene has also been found to be involved in other substance use disorders including <b>cocaine</b>, nicotine and opioid dependence, and obesity.
+DRD2	drug	nicotine	10881203	The <strong>DRD2</strong> gene has also been found to be involved in other substance use disorders including cocaine, <b>nicotine</b> and opioid dependence, and obesity.
+DRD2	drug	opioid	10881203	The <strong>DRD2</strong> gene has also been found to be involved in other substance use disorders including cocaine, nicotine and <b>opioid</b> dependence, and obesity.
+DRD2	addiction	dependence	10881203	The <strong>DRD2</strong> gene has also been found to be involved in other substance use disorders including cocaine, nicotine and opioid <b>dependence</b>, and obesity.
+DRD2	drug	nicotine	10710227	Family based study of the association of the dopamine D2 receptor gene (<strong>DRD2</strong>) with habitual <b>smoking</b>.
+DRD2	drug	nicotine	10710227	A recent study showed an association between the dopamine D2 receptor gene (<strong>DRD2</strong>) and <b>smoking</b>.
+DRD2	drug	nicotine	10710227	The purpose of this study was to determine if the familial transmission of <b>smoking</b> is linked to variation at the <strong>DRD2</strong> locus in a genetically informative sample.
+DRD2	drug	nicotine	10710227	There was no significant difference in the frequency between <strong>DRD2</strong> alleles transmitted and not transmitted to habitual <b>smokers</b>.
+DRD2	drug	alcohol	10710227	There also was no evidence for unequal transmission of <strong>DRD2</strong> alleles for the phenotypes "ever smoker" or comorbid <b>alcohol</b> dependence and habitual smoking.
+DRD2	drug	nicotine	10710227	There also was no evidence for unequal transmission of <strong>DRD2</strong> alleles for the phenotypes "ever <b>smoker</b>" or comorbid alcohol dependence and habitual <b>smoking</b>.
+DRD2	addiction	dependence	10710227	There also was no evidence for unequal transmission of <strong>DRD2</strong> alleles for the phenotypes "ever smoker" or comorbid alcohol <b>dependence</b> and habitual smoking.
+DRD2	drug	nicotine	10710227	This study does not support linkage of the <strong>DRD2</strong> with <b>smoking</b>.
+DRD2	drug	nicotine	10597409	This paper explores the relationship between the <strong>DRD2</strong> gene polymorphism, P300, and <b>smoking</b>.
+DRD2	drug	nicotine	10597409	Both <b>smoking</b> and <strong>DRD2</strong> have significant reducing effects on P300 amplitude.
+DRD2	drug	nicotine	10597409	The effect of <b>smoking</b> is apparent only in the presence of the A1 allele of the <strong>DRD2</strong> locus.
+DRD2	drug	nicotine	10597409	Both concordance for <b>smoking</b> and <strong>DRD2</strong> genotype are significant predictors of sib pair similarity in P300 amplitude.
+DRD2	drug	nicotine	10597409	Neurocognitive variation (P300) may moderate the association between <strong>DRD2</strong> and <b>smoking</b>.
+DRD2	drug	nicotine	10597409	Alternatively, <strong>DRD2</strong> genotype may modulate the long term impact of <b>nicotine</b> on neurocognitive functioning.
+DRD2	drug	cocaine	10523822	The <strong>DRD2</strong> gene had an independent and additive effect on <b>cocaine</b> dependence.
+DRD2	addiction	dependence	10523822	The <strong>DRD2</strong> gene had an independent and additive effect on cocaine <b>dependence</b>.
+DRD2	drug	alcohol	10327432	D2 dopamine receptor gene (<strong>DRD2</strong>) allele and haplotype frequencies in <b>alcohol</b> dependent and control subjects: no association with phenotype or severity of phenotype.
+DRD2	drug	alcohol	10327432	Possible association between polymorphisms at the D2 dopamine receptor gene (<strong>DRD2</strong>) and <b>alcohol</b> dependence has been controversial since first proposed in 1990.
+DRD2	addiction	dependence	10327432	Possible association between polymorphisms at the D2 dopamine receptor gene (<strong>DRD2</strong>) and alcohol <b>dependence</b> has been controversial since first proposed in 1990.
+DRD2	drug	alcohol	10327432	To test the hypothesis of an association rigorously, we studied four <strong>DRD2</strong> polymorphic systems in 160 EA <b>alcohol</b> dependent subjects and 136 screened EA control subjects.
+DRD2	drug	alcohol	10327432	Thus, we replicated previous findings of no association between <strong>DRD2</strong> alleles and <b>alcohol</b> dependence.
+DRD2	addiction	dependence	10327432	Thus, we replicated previous findings of no association between <strong>DRD2</strong> alleles and alcohol <b>dependence</b>.
+DRD2	drug	alcohol	10327432	These results are consistent with no effect of <strong>DRD2</strong> polymorphisms on behavioral phenotypes related to <b>alcohol</b> dependence.
+DRD2	addiction	dependence	10327432	These results are consistent with no effect of <strong>DRD2</strong> polymorphisms on behavioral phenotypes related to alcohol <b>dependence</b>.
+DRD2	drug	alcohol	10235293	No association between <strong>DRD2</strong> locus and <b>alcoholism</b> after controlling the ADH and ALDH genotypes in Chinese Han population.
+DRD2	drug	alcohol	10235293	Recent studies on the genetics of <b>alcoholism</b> have examined the association between <b>alcoholism</b> and the dopamine D2 receptor locus (<strong>DRD2</strong>); our study of Chinese Han gave negative results (Lu et al., 1996).
+DRD2	drug	alcohol	10235293	Therefore, association studies of <b>alcoholism</b> in Chinese Han might be more sensitive if controlled for the genotypes of ADH2,ADH3, and ALDH2, when other loci, such as <strong>DRD2</strong>, are examined.
+DRD2	drug	alcohol	10235293	This study employs such controls to evaluate the evidence for an association between <b>alcoholism</b> and TaqI A and TaqI B genotypes and haplotypes at <strong>DRD2</strong> in the Chinese Han population.
+DRD2	drug	alcohol	10235293	Significant linkage disequilibrium was observed between the TaqI A and TaqI B sites at the <strong>DRD2</strong> locus, as previously seen in smaller samples, but no significant association was observed between these genetic variants at the <strong>DRD2</strong> locus and <b>alcoholism</b> in Chinese Han.
+DRD2	drug	alcohol	10235293	Several different stratifications by ADH and ALDH2 genotypes were examined; no genotypes or haplotypes at <strong>DRD2</strong> differ between <b>alcoholics</b> and nonalcoholics except for a small number of nominally significant p values which do not constitute significant results given the many tests done, some of which are not independent of one another due to linkage disequilibrium.
+DRD2	drug	alcohol	10235293	After stratification by the relevant genotypes of ADH2, ADH3, and ALDH2 no significant association exists between the genetic variants at the <strong>DRD2</strong> locus and <b>alcoholism</b> in the Chinese Han population.
+DRD2	drug	alcohol	10235291	Our study examined recent claims of an association of the TaqI A1 allele and the functional  141C Ins allele of the dopamine D2 receptor (<strong>DRD2</strong>) gene with <b>alcohol</b> dependence.
+DRD2	addiction	dependence	10235291	Our study examined recent claims of an association of the TaqI A1 allele and the functional  141C Ins allele of the dopamine D2 receptor (<strong>DRD2</strong>) gene with alcohol <b>dependence</b>.
+DRD2	drug	alcohol	10235291	Our present association results failed to replicate evidence that either the TaqI A1 allele or the functional Ins allele or the A1/Ins haplotype of the <strong>DRD2</strong> gene confers vulnerability to <b>alcohol</b> dependence in the German population.
+DRD2	addiction	dependence	10235291	Our present association results failed to replicate evidence that either the TaqI A1 allele or the functional Ins allele or the A1/Ins haplotype of the <strong>DRD2</strong> gene confers vulnerability to alcohol <b>dependence</b> in the German population.
+DRD2	addiction	reward	10220438	Neurotransmission mediated by <strong>DRD2</strong> is known to have a key role in the control of movement and also has been implicated in <b>reward</b> and <b>reinforcement</b> mechanisms and psychiatric disorders.
+DRD2	drug	alcohol	20575787	The dopaminergic system has been implicated in <b>alcoholism</b>, but most of the past investigations concentrated on the dopamine D2 receptor (<strong>DRD2</strong>), with conflicting results.
+DRD2	drug	cocaine	10023512	No association between D2 dopamine receptor (<strong>DRD2</strong>) alleles or haplotypes and <b>cocaine</b> dependence or severity of <b>cocaine</b> dependence in European  and African Americans.
+DRD2	addiction	dependence	10023512	No association between D2 dopamine receptor (<strong>DRD2</strong>) alleles or haplotypes and cocaine <b>dependence</b> or severity of cocaine <b>dependence</b> in European  and African Americans.
+DRD2	drug	alcohol	10023512	Reports of allelic associations were originally made with <b>alcoholism</b>, but were then extended to other psychiatric disorders; there has been a series of positive reports suggesting an association between <strong>DRD2</strong> alleles and substance dependence in European American (EA) subjects.
+DRD2	addiction	dependence	10023512	Reports of allelic associations were originally made with alcoholism, but were then extended to other psychiatric disorders; there has been a series of positive reports suggesting an association between <strong>DRD2</strong> alleles and substance <b>dependence</b> in European American (EA) subjects.
+DRD2	drug	cocaine	10023512	In an attempt to replicate the reported association between <strong>DRD2</strong> alleles, substance dependence, and severity of substance dependence, we studied allele frequencies for three polymorphic <strong>DRD2</strong> systems (TaqI "A," "B," and "D") in 96 EA and 77 African American (AA) <b>cocaine</b> dependent subjects, and 87 EA and 45 AA control subjects.
+DRD2	addiction	dependence	10023512	In an attempt to replicate the reported association between <strong>DRD2</strong> alleles, substance <b>dependence</b>, and severity of substance <b>dependence</b>, we studied allele frequencies for three polymorphic <strong>DRD2</strong> systems (TaqI "A," "B," and "D") in 96 EA and 77 African American (AA) cocaine dependent subjects, and 87 EA and 45 AA control subjects.
+DRD2	drug	cocaine	10023512	Our data do not support an association between <strong>DRD2</strong> alleles or haplotypes and <b>cocaine</b> dependence, in EA or AA subjects.
+DRD2	addiction	dependence	10023512	Our data do not support an association between <strong>DRD2</strong> alleles or haplotypes and cocaine <b>dependence</b>, in EA or AA subjects.
+DRD2	drug	cocaine	10023512	Moreover, <strong>DRD2</strong> alleles are not associated with severity of <b>cocaine</b> dependence in this sample.
+DRD2	addiction	dependence	10023512	Moreover, <strong>DRD2</strong> alleles are not associated with severity of cocaine <b>dependence</b> in this sample.
+DRD2	drug	nicotine	10022750	Lack of association between the dopamine D2 receptor gene allele <strong>DRD2</strong>*A1 and cigarette <b>smoking</b> in a United Kingdom population.
+DRD2	drug	alcohol	10022750	It has been previously suggested that the lesser allele, <strong>DRD2</strong>*A1, is more prevalent in individuals who are susceptible to impulsive/addictive/compulsive behaviour, for example, <b>alcoholics</b>, polysubstance abusers and tobacco smokers.
+DRD2	drug	nicotine	10022750	It has been previously suggested that the lesser allele, <strong>DRD2</strong>*A1, is more prevalent in individuals who are susceptible to impulsive/addictive/compulsive behaviour, for example, alcoholics, polysubstance abusers and <b>tobacco</b> <b>smokers</b>.
+DRD2	addiction	addiction	10022750	It has been previously suggested that the lesser allele, <strong>DRD2</strong>*A1, is more prevalent in individuals who are susceptible to impulsive/<b>addictive</b>/<b>compulsive</b> behaviour, for example, alcoholics, polysubstance abusers and tobacco smokers.
+DRD2	drug	nicotine	10022750	Furthermore, neither measure of dependence was affected by possession of the A1 allele; the only difference between <strong>DRD2</strong>*A1 bearing and <strong>DRD2</strong>*A2 homozygous individuals in terms of <b>smoking</b> motives was found in the scores for indulgence; the former having a moderately reduced score (by 17%, p < 0.05).
+DRD2	addiction	dependence	10022750	Furthermore, neither measure of <b>dependence</b> was affected by possession of the A1 allele; the only difference between <strong>DRD2</strong>*A1 bearing and <strong>DRD2</strong>*A2 homozygous individuals in terms of smoking motives was found in the scores for indulgence; the former having a moderately reduced score (by 17%, p < 0.05).
+DRD2	drug	nicotine	10022750	This may be caused by the locus being unrelated to impulsive/addictive/compulsive behaviour, the polymorphism being in linkage disequilibrium with another distinct locus or, alternatively, <b>smoking</b> may represent a behaviour that is not directly comparable to impulsive/addictive/compulsive behaviours previously associated with the <strong>DRD2</strong>*A1 allele.
+DRD2	addiction	addiction	10022750	This may be caused by the locus being unrelated to impulsive/<b>addictive</b>/<b>compulsive</b> behaviour, the polymorphism being in linkage disequilibrium with another distinct locus or, alternatively, smoking may represent a behaviour that is not directly comparable to impulsive/<b>addictive</b>/<b>compulsive</b> behaviours previously associated with the <strong>DRD2</strong>*A1 allele.
+DRD2	drug	nicotine	9925041	As a means of investigating the risk of <b>smoking</b> associated with genetic polymorphisms in the dopamine transporter (SLC6A3) and the D2 dopamine receptor (<strong>DRD2</strong>) genes, a case control study of 289 <b>smokers</b> and 233 nonsmoking controls and a case series analysis of <b>smokers</b> were conducted.
+DRD2	drug	nicotine	9925041	A significant effect for SLC6A3 and a significant gene gene interaction were found in a logistic regression model, indicating that individuals with SLC6A3 9 genotypes were significantly less likely to be <b>smokers</b>, especially if they also had <strong>DRD2</strong> A2 genotypes.
+DRD2	drug	alcohol	20575771	The A₁allele of the D₂ dopamine receptor (<strong>DRD2</strong>) gene is a hypothesized risk factor in the development of severe drug dependence and <b>alcoholism</b>.
+DRD2	addiction	dependence	20575771	The A₁allele of the D₂ dopamine receptor (<strong>DRD2</strong>) gene is a hypothesized risk factor in the development of severe drug <b>dependence</b> and alcoholism.
+DRD2	drug	opioid	20575771	The present study compares the frequency of the A₁ allele of the <strong>DRD2</strong> gene among 37 patients presenting to a hepatitis clinic for treatment of hepatitis C, 23 hepatitis C negative drug abusing patients maintained on <b>methadone</b> and 33 non drug abusing controls.
+DRD2	drug	alcohol	9650637	In 1990 Blum, Noble and coworkers reported a significant association between the 1 allele of the Tarq1A polymorphism of the D2 dopamine receptor gene (<strong>DRD2</strong>) and severe <b>alcoholism</b>.
+DRD2	addiction	addiction	9650637	Those rules, and their application to the role of the <strong>DRD2</strong> gene in <b>addictive</b>, impulsive behaviors, are reviewed.
+DRD2	drug	alcohol	9650635	A functionally deficient <strong>DRD2</strong> variant [Ser311Cys] is not linked to <b>alcoholism</b> and substance abuse.
+DRD2	drug	alcohol	9650635	Association studies with the <strong>DRD2</strong> Taq1A marker have been variable in implicating <strong>DRD2</strong> as a "Reward Deficiency Syndrome Gene" for <b>alcoholism</b> and substance abuse.
+DRD2	addiction	reward	9650635	Association studies with the <strong>DRD2</strong> Taq1A marker have been variable in implicating <strong>DRD2</strong> as a "<b>Reward</b> Deficiency Syndrome Gene" for alcoholism and substance abuse.
+DRD2	drug	alcohol	9650635	Genotyping of Ser311Cys, the <strong>DRD2</strong> intron 2 STR, and the Taq1A marker in 459 subjects, including 373 sib pairs and 15 Cys311/Cys311 homozygous individuals, revealed no association to <b>alcoholism</b>, substance use disorders, or schizophrenia.
+DRD2	drug	alcohol	9650635	The implication is that a <strong>DRD2</strong> variant that dramatically impairs receptor function was not sufficient to significantly alter <b>alcoholism</b> vulnerability in a relatively large and also genetically and environmentally homogeneous sample.
+DRD2	drug	alcohol	9603615	The relationship of various dimensions of temperament, measured by the Tridimensional Personality Questionnaire (TPQ), to polymorphisms of the D2 dopamine receptor (<strong>DRD2</strong>) and D4 dopamine receptor (DRD4) genes was determined in 119 healthy Caucasian boys who had not yet begun to consume <b>alcohol</b> and other drugs of abuse.
+DRD2	addiction	relapse	9603615	Total Novelty <b>Seeking</b> score of the TPQ was significantly higher in boys having, in common, all three minor (A1, B1, and Intron 6 1) alleles of the <strong>DRD2</strong> compared to boys without any of these alleles.
+DRD2	addiction	relapse	9603615	However, the greatest difference in Novelty <b>Seeking</b> score was found when boys having all three minor <strong>DRD2</strong> alleles and the DRD4 7R allele were contrasted to those without any of these alleles.
+DRD2	addiction	dependence	9603615	Whereas subjects having all three minor <strong>DRD2</strong> alleles had a significantly higher Reward <b>Dependence</b> 2 (Persistence) score than subjects without any of these alleles, no significant difference in this personality score was found between subjects with and without the DRD4 7R allele.
+DRD2	addiction	reward	9603615	Whereas subjects having all three minor <strong>DRD2</strong> alleles had a significantly higher <b>Reward</b> Dependence 2 (Persistence) score than subjects without any of these alleles, no significant difference in this personality score was found between subjects with and without the DRD4 7R allele.
+DRD2	addiction	relapse	9603615	In conclusion, <strong>DRD2</strong> and DRD4 polymorphisms individually associate with Novelty <b>Seeking</b> behavior.
+DRD2	drug	alcohol	9581660	A family based analysis of the association of the dopamine D2 receptor (<strong>DRD2</strong>) with <b>alcoholism</b>.
+DRD2	drug	alcohol	9581660	The possible association of the <strong>DRD2</strong> locus, and in particular the Taql A1 allele, with <b>alcoholism</b> remains controversial, in part because of differences in allele frequencies among populations.
+DRD2	drug	alcohol	9581660	To avoid problems associated with differences in allele frequencies in different populations, we tested whether the <strong>DRD2</strong> locus is associated with <b>alcohol</b> dependence in a large family based sample.
+DRD2	addiction	dependence	9581660	To avoid problems associated with differences in allele frequencies in different populations, we tested whether the <strong>DRD2</strong> locus is associated with alcohol <b>dependence</b> in a large family based sample.
+DRD2	drug	alcohol	9581660	Neither the transmission/disequilibrium test nor the Affected Family Based Controls test provide any evidence of linkage or association between the <strong>DRD2</strong> locus and <b>alcohol</b> dependence.
+DRD2	addiction	dependence	9581660	Neither the transmission/disequilibrium test nor the Affected Family Based Controls test provide any evidence of linkage or association between the <strong>DRD2</strong> locus and alcohol <b>dependence</b>.
+DRD2	drug	alcohol	9295055	Influence of the dopamine D2 receptor (<strong>DRD2</strong>) genotype on neuroadaptive effects of <b>alcohol</b> and the clinical outcome of <b>alcoholism</b>.
+DRD2	drug	alcohol	9295055	The present study was performed to test the hypotheses that allelic variants at the human dopamine D2 receptor gene locus (<strong>DRD2</strong>) confer susceptibility to <b>alcoholism</b> or are associated with clinical subtypes of <b>alcoholism</b>.
+DRD2	drug	alcohol	9295055	No significant association of the <strong>DRD2</strong> genotype or allele frequencies with <b>alcoholism</b> was found in an association study including 283 <b>alcoholics</b> and 146 non <b>alcoholic</b> controls.
+DRD2	drug	alcohol	9295055	Regression analysis revealed the <strong>DRD2</strong> E8 genotype as the only significant factor determining withdrawal severity in female <b>alcoholics</b>.
+DRD2	addiction	withdrawal	9295055	Regression analysis revealed the <strong>DRD2</strong> E8 genotype as the only significant factor determining <b>withdrawal</b> severity in female alcoholics.
+DRD2	drug	alcohol	9295055	The findings suggest an influence of the <strong>DRD2</strong> genotype on the neuropharmacological effects of chronic <b>alcohol</b> exposure and the clinical course of <b>alcoholism</b>.
+DRD2	drug	alcohol	9259374	Linkage and association of a functional <strong>DRD2</strong> variant [Ser311Cys] and <strong>DRD2</strong> markers to <b>alcoholism</b>, substance abuse and schizophrenia in Southwestern American Indians.
+DRD2	drug	alcohol	9259374	Furthermore, sib pair analysis incorporating information across all three sib pair categories: concordant affected, discordant and concordant unaffected revealed no effect of <strong>DRD2</strong> genotype or haplotype on <b>alcoholism</b> or substance use disorder.
+DRD2	drug	alcohol	9129720	We examined the allelic association between the dopamine D2 receptor (<strong>DRD2</strong>) gene and <b>alcoholism</b> in 100 biologically unrelated Japanese <b>alcoholics</b> and 93 unrelated controls.
+DRD2	drug	alcohol	9129720	The results indicate that the <strong>DRD2</strong> gene is associated with susceptibility to early onset <b>alcoholism</b>, and that each additional A1 allele shifts onset of <b>alcoholism</b> to an earlier age.
+DRD2	drug	alcohol	9129716	Molecular genetic studies have found an association of the D2 dopamine receptor (<strong>DRD2</strong>) A1 allele with <b>alcoholism</b> and drug abuse.
+DRD2	drug	alcohol	9129710	Previous studies examining the putative association between <strong>DRD2</strong> TaqI A1 and <b>alcoholism</b> have produced conflicting results.
+DRD2	drug	alcohol	9129710	To address these issues, we compared the allelic frequency of two polymorphisms of <strong>DRD2</strong>, TaqI A and NcoI, among severe <b>alcoholics</b> and their ethnically matched nonalcoholic controls within four major aboriginal groups and Han (Chinese) in Taiwan.
+DRD2	drug	alcohol	9129710	Severity in medical complications of <b>alcohol</b> dependence with withdrawal symptoms was not associated with higher prevalence of <strong>DRD2</strong> TaqI A1 or NcoI N1 alleles.
+DRD2	addiction	dependence	9129710	Severity in medical complications of alcohol <b>dependence</b> with withdrawal symptoms was not associated with higher prevalence of <strong>DRD2</strong> TaqI A1 or NcoI N1 alleles.
+DRD2	addiction	withdrawal	9129710	Severity in medical complications of alcohol dependence with <b>withdrawal</b> symptoms was not associated with higher prevalence of <strong>DRD2</strong> TaqI A1 or NcoI N1 alleles.
+DRD2	drug	alcohol	9129710	The absence of an association between <strong>DRD2</strong> and <b>alcoholism</b> among the three aboriginal groups suggests either a higher rate of phenocopies among aboriginal <b>alcoholics</b> or genetic heterogeneity in the susceptibility to <b>alcoholism</b>.
+DRD2	drug	alcohol	9034534	The dopaminergic system has been implicated in <b>alcoholism</b> but studies at the dopamine D2 receptor gene (<strong>DRD2</strong>), one of the five dopamine receptors, have not given a consistent picture of an association with <b>alcoholism</b>.
+DRD2	drug	nicotine	9154217	In the TS group and <b>smokers</b> there was a significant additive effect of the DRD1 and <strong>DRD2</strong> genes.
+DRD2	addiction	addiction	9154217	These results support a role for genetic variants of the DRD1 gene in some <b>addictive</b> behaviors, and an interaction of genetic variants at the DRD1 and <strong>DRD2</strong> genes.
+DRD2	addiction	addiction	8873216	These preliminary data suggest that the presence of the <strong>DRD2</strong> A1 allele confirms increased risk not only for obesity, but also for other related <b>addictive</b> behaviours (previously referred to as the Reward Deficiency Syndrome) and that a BMI over 25 by itself (without characterization of macroselection or comorbid substance use disorders) is not a sufficient criterion for association with the <strong>DRD2</strong> A1 allele.
+DRD2	addiction	reward	8873216	These preliminary data suggest that the presence of the <strong>DRD2</strong> A1 allele confirms increased risk not only for obesity, but also for other related addictive behaviours (previously referred to as the <b>Reward</b> Deficiency Syndrome) and that a BMI over 25 by itself (without characterization of macroselection or comorbid substance use disorders) is not a sufficient criterion for association with the <strong>DRD2</strong> A1 allele.
+DRD2	drug	alcohol	8807661	The Taq A1 variant of the human <strong>DRD2</strong> gene has been associated with drug addiction, some forms of severe <b>alcoholism</b>, and other impulsive, addictive behaviours.
+DRD2	addiction	addiction	8807661	The Taq A1 variant of the human <strong>DRD2</strong> gene has been associated with drug <b>addiction</b>, some forms of severe alcoholism, and other impulsive, <b>addictive</b> behaviours.
+DRD2	addiction	addiction	8807661	These results suggest that genetic variants at the <strong>DRD2</strong> gene play a role in pathological gambling, and support the concept that variants of this gene are a risk factor for impulsive and <b>addictive</b> behaviours.
+DRD2	drug	nicotine	8845863	The dopamine D2 receptor (<strong>DRD2</strong>) gene: a genetic risk factor in <b>smoking</b>.
+DRD2	drug	alcohol	8845863	Of a group of 312 non Hispanic Caucasians who smoked at least one pack per day, had unsuccessfully attempted to stop smoking, and were free of <b>alcohol</b> or other drug dependence, 48.7% carried the A1 allele of the <strong>DRD2</strong> gene.
+DRD2	drug	nicotine	8845863	Of a group of 312 non Hispanic Caucasians who smoked at least one pack per day, had unsuccessfully attempted to stop <b>smoking</b>, and were free of alcohol or other drug dependence, 48.7% carried the A1 allele of the <strong>DRD2</strong> gene.
+DRD2	addiction	dependence	8845863	Of a group of 312 non Hispanic Caucasians who smoked at least one pack per day, had unsuccessfully attempted to stop smoking, and were free of alcohol or other drug <b>dependence</b>, 48.7% carried the A1 allele of the <strong>DRD2</strong> gene.
+DRD2	drug	nicotine	8845863	These results suggest the <strong>DRD2</strong> gene is one of a multifactorial set of risk factors associated with <b>smoking</b>.
+DRD2	drug	alcohol	12893451	In animal genetic models of <b>alcoholism</b>, reduced dopamine levels and D2 dopamine receptor (<strong>DRD2</strong>) numbers have been found in the brains of <b>alcohol</b> preferring animals.
+DRD2	drug	alcohol	12893451	Moreover, quantitative trait loci studies in animals suggest the <strong>DRD2</strong> gene and the region proximate to this locus is a chromosomal "hot spot" for <b>alcohol</b> related behaviors.
+DRD2	drug	alcohol	12893451	Molecular genetic studies in humans have identified an association of the Al allele of the <strong>DRD2</strong> gene with <b>alcoholism</b>.
+DRD2	drug	alcohol	12893451	Further, treatment of <b>alcoholics</b> with a dopamine receptor agonist showed more salutary effects on <b>alcoholics</b> who carry than those who do not carry the <strong>DRD2</strong> A1 allele.
+DRD2	addiction	reward	12893451	The emerging evidence suggests that the <strong>DRD2</strong> is a <b>reinforcement</b> or <b>reward</b> gene.
+DRD2	drug	alcohol	8907305	The human dopamine 2 receptor gene (<strong>DRD2</strong>) is an important candidate gene for drug addiction and <b>alcoholism</b>.
+DRD2	addiction	addiction	8907305	The human dopamine 2 receptor gene (<strong>DRD2</strong>) is an important candidate gene for drug <b>addiction</b> and alcoholism.
+DRD2	addiction	addiction	8907305	So far, no mutations within the coding region of <strong>DRD2</strong> have been found to be associated with <b>addiction</b> disorders.
+DRD2	drug	alcohol	8907305	The allele specific PCR allowed the reliable testing of 95 healthy control individuals and 270 <b>alcoholics</b> for analyzing a possible genetic association of this newly characterized polymorphic <strong>DRD2</strong> marker with <b>alcoholism</b> in an ethnically and clinically homogenous group of patients.
+DRD2	drug	alcohol	8825889	Numerous studies on the involvement of dopamine receptors in the genetics of <b>alcoholism</b> focused on associations between a polymorphism of the D2 dopamine receptor (<strong>DRD2</strong>) gene and <b>alcohol</b> dependence.
+DRD2	addiction	dependence	8825889	Numerous studies on the involvement of dopamine receptors in the genetics of alcoholism focused on associations between a polymorphism of the D2 dopamine receptor (<strong>DRD2</strong>) gene and alcohol <b>dependence</b>.
+DRD2	drug	alcohol	8825889	No difference in the DRD3 gene polymorphism emerged between controls and <b>alcoholic</b> patients, regardless of their origin, inclusion criteria, or presence or absence of the <strong>DRD2</strong> TaqI A1 allele.
+DRD2	drug	alcohol	7485259	To address the controversy surrounding <strong>DRD2</strong> and <b>alcoholism</b>, we performed linkage and association studies utilizing <b>alcoholic</b> men from high density families largely uncontaminated by other psychopathology and female <b>alcoholics</b> for whom secondary drug dependence (averaging 10 years later onset) was a prominent feature.
+DRD2	addiction	dependence	7485259	To address the controversy surrounding <strong>DRD2</strong> and alcoholism, we performed linkage and association studies utilizing alcoholic men from high density families largely uncontaminated by other psychopathology and female alcoholics for whom secondary drug <b>dependence</b> (averaging 10 years later onset) was a prominent feature.
+DRD2	drug	alcohol	7550364	While other neurotransmitters have also been implicated, to date the only molecular genetic defect which has been found to associate with <b>alcoholism</b>, drug dependency, obesity, smoking, pathological gambling, attention deficit hyperactivity disorder (ADHD), Tourette syndrome, as well as other related compulsive behaviours, are the variants of the dopamine D2 receptor gene (<strong>DRD2</strong>).
+DRD2	drug	nicotine	7550364	While other neurotransmitters have also been implicated, to date the only molecular genetic defect which has been found to associate with alcoholism, drug dependency, obesity, <b>smoking</b>, pathological gambling, attention deficit hyperactivity disorder (ADHD), Tourette syndrome, as well as other related compulsive behaviours, are the variants of the dopamine D2 receptor gene (<strong>DRD2</strong>).
+DRD2	addiction	addiction	7550364	While other neurotransmitters have also been implicated, to date the only molecular genetic defect which has been found to associate with alcoholism, drug dependency, obesity, smoking, pathological gambling, attention deficit hyperactivity disorder (ADHD), Tourette syndrome, as well as other related <b>compulsive</b> behaviours, are the variants of the dopamine D2 receptor gene (<strong>DRD2</strong>).
+DRD2	addiction	addiction	7550364	In this review of the available data on the subject, we report a number of independent meta analyses that confirm an association of <strong>DRD2</strong> polymorphisms and impulsive additive <b>compulsive</b> behaviour (IACB), which we have termed "Reward Deficiency Syndrome".
+DRD2	addiction	reward	7550364	In this review of the available data on the subject, we report a number of independent meta analyses that confirm an association of <strong>DRD2</strong> polymorphisms and impulsive additive compulsive behaviour (IACB), which we have termed "<b>Reward</b> Deficiency Syndrome".
+DRD2	drug	alcohol	7550364	While we agree that Meta analyses of all exant studies support an association of variants of <strong>DRD2</strong> and IACB, correct negative findings with <b>alcoholism</b> may be due to differences in assessing controls and inclusion/exclusion criteria for selection of diseased probands.
+DRD2	drug	alcohol	7585063	An important role of the mesolimbic dopamine system has been suggested in the reinforcing effects of <b>alcohol</b> and recent molecular genetic studies are implicating the gene for the D2 dopamine receptor (<strong>DRD2</strong>) in <b>alcoholism</b>.
+DRD2	addiction	reward	7585063	An important role of the mesolimbic dopamine system has been suggested in the <b>reinforcing</b> effects of alcohol and recent molecular genetic studies are implicating the gene for the D2 dopamine receptor (<strong>DRD2</strong>) in alcoholism.
+DRD2	drug	alcohol	7585063	In a double blind study, bromocriptine, a <strong>DRD2</strong> agonist, or placebo was administered to <b>alcoholics</b> with either the A1 (A1/A1 and A1/A2 genotypes) or only the A2 (A2/A2 genotype) allele of the <strong>DRD2</strong> gene.
+DRD2	drug	alcohol	8555738	The suggested association between the TaqI A1 allele of the dopamine D2 receptor (<strong>DRD2</strong>) gene with <b>alcoholism</b> was studied comparing the genotypes of 38 controls and 38 ethnic matched <b>alcoholics</b>, drawn from the Mexican population.
+DRD2	drug	alcohol	7704037	In the present investigation, 155 Caucasian male and female diagnosed neuropsychiatrically ill patients with and without comorbid drug and <b>alcohol</b> abuse/dependence were genotyped for the presence or absence of the A1 allele of the D2 dopamine receptor gene (<strong>DRD2</strong>).
+DRD2	addiction	dependence	7704037	In the present investigation, 155 Caucasian male and female diagnosed neuropsychiatrically ill patients with and without comorbid drug and alcohol abuse/<b>dependence</b> were genotyped for the presence or absence of the A1 allele of the D2 dopamine receptor gene (<strong>DRD2</strong>).
+DRD2	drug	alcohol	7695792	The prevalence of TaqI A alleles of the D2 dopamine receptor (<strong>DRD2</strong>) gene was examined in two subgroups of medically ill nonalcoholics (more prevalent and less prevalent substance users, MPSU and LPSU, respectively) and in two subgroups of medically ill <b>alcoholics</b> (more severe and less severe <b>alcoholics</b>, MSA and LSA, respectively).
+DRD2	drug	alcohol	7695792	In conclusion, the severity of <b>alcohol</b> dependence in <b>alcoholics</b> and of substance use behaviors in controls are important variables in <strong>DRD2</strong> allelic association.
+DRD2	addiction	dependence	7695792	In conclusion, the severity of alcohol <b>dependence</b> in alcoholics and of substance use behaviors in controls are important variables in <strong>DRD2</strong> allelic association.
+DRD2	drug	alcohol	7695792	The present report and converging lines of evidence suggest that the <strong>DRD2</strong> locus could represent a prominent gene risk factor for susceptibility to severe <b>alcoholism</b>.
+DRD2	drug	alcohol	8072432	There is now growing evidence that the less prevalent allele (A1) of the D2 dopamine receptor (<strong>DRD2</strong>) gene is strongly associated with severe <b>alcoholism</b>.
+DRD2	addiction	addiction	8033754	To examine the possible role of genetic variants of the dopamine D2 (<strong>DRD2</strong>) gene in susceptibility to drug abuse we determined the prevalence of the TaqI A1 variant of the <strong>DRD2</strong> gene in 200 white patients hospitalized in the <b>Addiction</b> Treatment Unit of a Veterans Administration Hospital.
+DRD2	drug	alcohol	8974314	The A1 (minor) allele of the D2 dopamine receptor (<strong>DRD2</strong>) gene has been shown to be associated with <b>alcoholism</b>, particularly the severe form of this disorder.
+DRD2	addiction	reward	8974314	Moreover, reduced dopaminergic function has been found in subjects carrying the <strong>DRD2</strong> A1 allele, suggesting that the <strong>DRD2</strong> may be a <b>reinforcement</b> or <b>reward</b> gene.
+DRD2	drug	alcohol	8974314	Analysis of the available data suggests that the <strong>DRD2</strong> variants represent one of the most prominent single gene determinants of susceptibility to severe <b>alcoholism</b> and other substance use disorders.
+DRD2	drug	cocaine	8261891	The objective of the present study was to examine allelic prevalence of the D2 dopamine receptor (<strong>DRD2</strong>) gene in male <b>cocaine</b> dependent (CD) Caucasian (non Hispanic) subjects and to determine the relationship of <strong>DRD2</strong> alleles to family history and selected behavioral measures.
+DRD2	drug	cocaine	8261891	The data showing a strong association of the minor alleles (A1 and B1) of the <strong>DRD2</strong> with <b>cocaine</b> dependence suggest that a gene, located on the q22 q23 region of chromosome 11, confers susceptibility to this drug disorder.
+DRD2	addiction	dependence	8261891	The data showing a strong association of the minor alleles (A1 and B1) of the <strong>DRD2</strong> with cocaine <b>dependence</b> suggest that a gene, located on the q22 q23 region of chromosome 11, confers susceptibility to this drug disorder.
+DRD2	drug	alcohol	8488955	<strong>DRD2</strong> dopamine receptor genotype, linkage disequilibrium, and <b>alcoholism</b> in American Indians and other populations.
+DRD2	drug	alcohol	8488955	We defined interpopulation differences in the frequency of the dopamine D2 receptor <strong>DRD2</strong>/Taq1 A1 allele, which has previously been associated with <b>alcoholism</b>.
+DRD2	drug	alcohol	8488955	Legitimate association of the <strong>DRD2</strong>/Taq1 allele to <b>alcoholism</b> would presumably require it to be in linkage disequilibrium (nonrandom association) with a functional mutation at <strong>DRD2</strong> or elsewhere.
+DRD2	drug	alcohol	1347705	Blum et al (1990) have recently examined a restriction fragment length polymorphism (RFLP) detected by TaqI RFLP to the dopamine D2 receptor gene (<strong>DRD2</strong>) in deceased <b>alcoholics</b> and nonalcoholics, and reported an association between <b>alcoholism</b> and the A1 allele.
+DRD2	drug	alcohol	1347705	We have examined the <strong>DRD2</strong> TaqI RFLP in 47 living Caucasian males with severe <b>alcoholism</b>.
+DRD2	drug	alcohol	1832467	No association between an allele at the D2 dopamine receptor gene (<strong>DRD2</strong>) and <b>alcoholism</b>.
+DRD2	drug	alcohol	1832467	We attempted to replicate a positive allelic association between the A1 allele of <strong>DRD2</strong> (the D2 dopamine receptor locus) and <b>alcoholism</b> that has been reported.
+DRD2	drug	alcohol	1832467	We compared allele frequencies at the previously described Taq I restriction fragment length polymorphism system of <strong>DRD2</strong> in <b>alcoholics</b> and random population controls.
+DRD2	drug	alcohol	1832467	There were no significant differences in allele frequencies at the <strong>DRD2</strong> locus between <b>alcoholics</b> and controls.
+DRD2	drug	alcohol	1832467	We conclude that our data do not support an allelic association between the A1 allele at <strong>DRD2</strong> and <b>alcoholism</b>.
+DRD2	drug	alcohol	1832466	The A1 allele of the Taq I polymorphism of the dopamine D2 receptor (<strong>DRD2</strong>) gene has been earlier reported to occur in 69% of <b>alcoholics</b>, compared with 20% of controls.
+DRD2	drug	alcohol	1832466	Other research has reported no significant difference in the prevalence of the A1 allele in <b>alcoholics</b> vs controls and no evidence that the <strong>DRD2</strong> gene was linked to <b>alcoholism</b>.
+SLC6A4	drug	cocaine	32721055	Previous research showed that inherited serotonin transporter (<strong>SERT</strong>) down regulation increases the motor response to <b>cocaine</b>, as well as moderate (as measured during daily 1 hr self administration sessions) and compulsive (as measured during daily 6 hr self administration sessions) intake of this psychostimulant.
+SLC6A4	addiction	addiction	32721055	Previous research showed that inherited serotonin transporter (<strong>SERT</strong>) down regulation increases the motor response to cocaine, as well as moderate (as measured during daily 1 hr self administration sessions) and <b>compulsive</b> (as measured during daily 6 hr self administration sessions) intake of this psychostimulant.
+SLC6A4	drug	amphetamine	32721055	In serotonin transporter knockout (<strong>SERT</strong> / ) and wild type control (<strong>SERT</strong>+/+) rats we assessed the locomotor response to acute <b>amphetamine</b> (<b>AMPH</b>) and intravenous <b>AMPH</b> self administration under short access (ShA: 1 hr daily sessions) and long access (LgA: 6 hr daily sessions) conditions.
+SLC6A4	drug	amphetamine	32721055	We found that <strong>SERT</strong> /  animals displayed an increased <b>AMPH</b> induced locomotor response and increased <b>AMPH</b> self administration under LgA, but not ShA conditions.
+SLC6A4	drug	amphetamine	32721055	We demonstrate that <strong>SERT</strong> gene deletion increases the psychomotor and reinforcing effects of <b>AMPH</b>, and that the latter is potentially mediated, at least in part, by homeostatic changes in the glutamatergic synapse of the nucleus accumbens shell and/or core.
+SLC6A4	addiction	reward	32721055	We demonstrate that <strong>SERT</strong> gene deletion increases the psychomotor and <b>reinforcing</b> effects of AMPH, and that the latter is potentially mediated, at least in part, by homeostatic changes in the glutamatergic synapse of the nucleus accumbens shell and/or core.
+SLC6A4	drug	alcohol	31970627	Correction to: Psychiatric disorders and <strong>SLC6A4</strong> gene variants: possible effects on <b>alcohol</b> dependence and alzheimer's disease.
+SLC6A4	addiction	dependence	31970627	Correction to: Psychiatric disorders and <strong>SLC6A4</strong> gene variants: possible effects on alcohol <b>dependence</b> and alzheimer's disease.
+SLC6A4	addiction	addiction	31652614	Nicotinic acetylcholine receptors (nAChRs), serotonin transporters (<strong>SERT</strong>) and dopamine transporters (DAT) represent targets for the development of novel nicotinic derivatives acting as multiligands associated with different health conditions, such as depressive, anxiety and <b>addiction</b> disorders.
+SLC6A4	drug	psychedelics	31634774	In order to substantiate the '<b>psilocybin</b> telomere hypothesis' potential neuropsychopharmacological, endocrinological, and genetic mechanisms of action are discussed (e.g., HPA axis reactivity, hippocampal neurogenesis, neurotropic growth factors such as BDNF, 5 HT2A receptor agonism, neuroplasticity/synaptoplasticity, brain wide alterations in neuronal functional connectivity density, involvement of the <strong>SLC6A4</strong> serotonin transporter gene, inter alia).
+SLC6A4	drug	alcohol	31595439	Psychiatric disorders and <strong>SLC6A4</strong> gene variants: possible effects on <b>alcohol</b> dependence and alzheimer's disease.
+SLC6A4	addiction	dependence	31595439	Psychiatric disorders and <strong>SLC6A4</strong> gene variants: possible effects on alcohol <b>dependence</b> and alzheimer's disease.
+SLC6A4	drug	alcohol	31595439	<strong>SLC6A4</strong> variants, namely 5HTTLPR, STin2, rs2066713, rs25531, rs4251417, rs6354 and rs7224199 were investigated in 4 independent cohorts of subjects with specific psychiatric disorders, including <b>Alcohol</b> dependence disorder (ALC), Alzheimer disease (ALZ), Schizophrenia (SCZ) and Bipolar disorder (BPD).
+SLC6A4	addiction	dependence	31595439	<strong>SLC6A4</strong> variants, namely 5HTTLPR, STin2, rs2066713, rs25531, rs4251417, rs6354 and rs7224199 were investigated in 4 independent cohorts of subjects with specific psychiatric disorders, including Alcohol <b>dependence</b> disorder (ALC), Alzheimer disease (ALZ), Schizophrenia (SCZ) and Bipolar disorder (BPD).
+SLC6A4	drug	alcohol	31595439	<strong>SLC6A4</strong> variants, namely <strong>5HTTLPR</strong>, STin2, rs2066713, rs25531, rs4251417, rs6354 and rs7224199 were investigated in 4 independent cohorts of subjects with specific psychiatric disorders, including <b>Alcohol</b> dependence disorder (ALC), Alzheimer disease (ALZ), Schizophrenia (SCZ) and Bipolar disorder (BPD).
+SLC6A4	addiction	dependence	31595439	<strong>SLC6A4</strong> variants, namely <strong>5HTTLPR</strong>, STin2, rs2066713, rs25531, rs4251417, rs6354 and rs7224199 were investigated in 4 independent cohorts of subjects with specific psychiatric disorders, including Alcohol <b>dependence</b> disorder (ALC), Alzheimer disease (ALZ), Schizophrenia (SCZ) and Bipolar disorder (BPD).
+SLC6A4	drug	psychedelics	31019304	To elucidate structure based mechanisms for transport in <strong>SERT</strong> we investigated its complexes with <b>ibogaine</b>, a hallucinogenic natural product with psychoactive and anti addictive properties13,14.
+SLC6A4	addiction	addiction	31019304	To elucidate structure based mechanisms for transport in <strong>SERT</strong> we investigated its complexes with ibogaine, a hallucinogenic natural product with psychoactive and anti <b>addictive</b> properties13,14.
+SLC6A4	drug	psychedelics	31019304	Here we report cryo electron microscopy structures of <strong>SERT</strong> <b>ibogaine</b> complexes captured in outward open, occluded and inward open conformations.
+SLC6A4	drug	alcohol	31008507	Lack of Association Between Serotonin Transporter Gene (<strong>SLC6A4</strong>) Promoter Methylation and Amygdala Response During Negative Emotion Processing in Individuals With <b>Alcohol</b> Dependence.
+SLC6A4	addiction	dependence	31008507	Lack of Association Between Serotonin Transporter Gene (<strong>SLC6A4</strong>) Promoter Methylation and Amygdala Response During Negative Emotion Processing in Individuals With Alcohol <b>Dependence</b>.
+SLC6A4	drug	alcohol	31008507	This study investigated the association between <strong>SLC6A4</strong> promoter methylation and threat related amygdala activation in individuals with <b>alcohol</b> dependence (AD).
+SLC6A4	addiction	dependence	31008507	This study investigated the association between <strong>SLC6A4</strong> promoter methylation and threat related amygdala activation in individuals with alcohol <b>dependence</b> (AD).
+SLC6A4	drug	alcohol	30851308	When globally re expressed in serotonergic neurons, wild type <strong>SERT</strong> but not dSERT R599A restored <b>ethanol</b> preference.
+SLC6A4	drug	alcohol	30851308	In contrast, dSERT R599A restored <b>ethanol</b> preference after targeted expression in contralaterally projecting, serotonin immunoreactive deuterocerebral (CSD) interneurons, while expression of wild type <strong>SERT</strong> caused <b>ethanol</b> aversion.
+SLC6A4	addiction	aversion	30851308	In contrast, dSERT R599A restored ethanol preference after targeted expression in contralaterally projecting, serotonin immunoreactive deuterocerebral (CSD) interneurons, while expression of wild type <strong>SERT</strong> caused ethanol <b>aversion</b>.
+SLC6A4	drug	alcohol	30851308	We conclude that, in CSD neurons, (i) somatodendritic <strong>SERT</strong> supports <b>ethanol</b> attraction, (ii) axonal <strong>SERT</strong> specifies <b>ethanol</b> aversion, (iii) the effect of axonal <strong>SERT</strong> can override that of somatodendritic <strong>SERT</strong>.
+SLC6A4	addiction	aversion	30851308	We conclude that, in CSD neurons, (i) somatodendritic <strong>SERT</strong> supports ethanol attraction, (ii) axonal <strong>SERT</strong> specifies ethanol <b>aversion</b>, (iii) the effect of axonal <strong>SERT</strong> can override that of somatodendritic <strong>SERT</strong>.
+SLC6A4	drug	cocaine	30817127	The <strong>SERT</strong> Met172 Mouse: An Engineered Model To Elucidate the Contributions of Serotonin Signaling to <b>Cocaine</b> Action.
+SLC6A4	drug	cocaine	30817127	In particular, a significant body of work points to altered serotonin (5 HT) signaling as one such component, not surprising given that, relative to DAT, <b>cocaine</b> acts as potently to block the 5 HT transporter (<strong>SERT</strong>) as to block DAT, and thereby elevates extracellular 5 HT levels throughout the brain when reward eliciting DA elevations occur.
+SLC6A4	addiction	reward	30817127	In particular, a significant body of work points to altered serotonin (5 HT) signaling as one such component, not surprising given that, relative to DAT, cocaine acts as potently to block the 5 HT transporter (<strong>SERT</strong>) as to block DAT, and thereby elevates extracellular 5 HT levels throughout the brain when <b>reward</b> eliciting DA elevations occur.
+SLC6A4	drug	cocaine	30817127	To elucidate the contribution of <strong>SERT</strong> antagonism to the actions of <b>cocaine</b>, we engineered a mouse model that significantly reduces <b>cocaine</b> potency at <strong>SERT</strong> without disrupting the expression or function of <strong>SERT</strong> in vivo.
+SLC6A4	drug	cocaine	30817127	In this short Perspective, we review the rationale for development of the <strong>SERT</strong> Met172 model, the studies that document the pharmacological impact of the Ile172Met substitution in vitro and in vivo, and our findings with the model that demonstrate serotonergic contributions to the genetic, physiological, and behavioral actions of <b>cocaine</b>.
+SLC6A4	drug	nicotine	30815604	Additionally, this study examined whether the S allele of the serotonin transporter gene linked polymorphic region (<strong>5 HTTLPR</strong>) is associated with the BDNF Val66Met polymorphism on <b>smoking</b> phenotypes.
+SLC6A4	drug	nicotine	30815604	Moreover, the <strong>5 HTTLPR</strong> polymorphism was associated with the age of <b>smoking</b> initiation in current <b>smokers</b> carrying the BDNF Met allele, in both the whole study sample (P = 0.041) and the male subgroup (P = 0.041).
+SLC6A4	drug	nicotine	30815604	On the other hand, no association was observed between the BDNF Val66Met polymorphism, either alone or in combination with the <strong>5 HTTLPR</strong> polymorphism, and the age of <b>smoking</b> cessation.
+SLC6A4	drug	nicotine	30815604	This pilot study provides preliminary findings regarding the influence of BDNF Val66Met on <b>smoking</b> phenotypes and the interacting effect of <strong>5 HTTLPR</strong> on the association between BDNF Val66Met and <b>smoking</b> phenotypes in Japanese participants.
+SLC6A4	drug	cocaine	30748070	Here, we tested this idea by using ultrahigh resolution structural magnetic resonance imaging (MRI) on postmortem tissue of <strong>5 HTT</strong> /  and wild type (<strong>5 HTT</strong>+/+) rats with a history of long access to <b>cocaine</b> or sucrose (control) self administration.
+SLC6A4	drug	cocaine	30748070	We found that <strong>5 HTT</strong> /  rats, compared with wild type control animals, self administered more <b>cocaine</b>, but not sucrose, under long access conditions.
+SLC6A4	drug	cocaine	30748070	Ultrahigh resolution structural MRI subsequently revealed that, independent of sucrose or <b>cocaine</b> self administration, <strong>5 HTT</strong> /  rats had a smaller amygdala.
+SLC6A4	drug	cocaine	30748070	The data point to an important but differential role of the amygdala and dorsal raphe nucleus in <strong>5 HTT</strong> genotype dependent vulnerability to <b>cocaine</b> addiction.
+SLC6A4	addiction	addiction	30748070	The data point to an important but differential role of the amygdala and dorsal raphe nucleus in <strong>5 HTT</strong> genotype dependent vulnerability to cocaine <b>addiction</b>.
+SLC6A4	drug	alcohol	30708239	Serotonin transporter gene linked polymorphism (<strong>5 HTTLPR</strong>) determines progredience of <b>alcohol</b> dependence in Belarusian young males.
+SLC6A4	addiction	dependence	30708239	Serotonin transporter gene linked polymorphism (<strong>5 HTTLPR</strong>) determines progredience of alcohol <b>dependence</b> in Belarusian young males.
+SLC6A4	drug	amphetamine	30578419	Given that <b>amphetamine</b> and methylphenidate, unlike cocaine, lack high affinity interactions with the serotonin (5 HT) transporter (<strong>SERT</strong>), we hypothesized that the lack of cocaine induced hyperlocomotion in DAT Val559 mice arises from <strong>SERT</strong> blockade and augmented 5 HT signaling relative to cocaine actions on wildtype animals.
+SLC6A4	drug	cocaine	30578419	Given that amphetamine and methylphenidate, unlike <b>cocaine</b>, lack high affinity interactions with the serotonin (5 HT) transporter (<strong>SERT</strong>), we hypothesized that the lack of <b>cocaine</b> induced hyperlocomotion in DAT Val559 mice arises from <strong>SERT</strong> blockade and augmented 5 HT signaling relative to <b>cocaine</b> actions on wildtype animals.
+SLC6A4	drug	cocaine	30578419	Consistent with this idea, the <strong>SERT</strong> blocker fluoxetine abolished methylphenidate induced locomotor activity in DAT Val559 mice, mimicking the effects seen with <b>cocaine</b>.
+SLC6A4	drug	cocaine	30578419	Additionally, a <b>cocaine</b> analog (RTI 113) with greater selectivity for DAT over <strong>SERT</strong> retains locomotor activation in DAT Val559 mice.
+SLC6A4	drug	cocaine	30578419	Furthermore, genetic elimination of high affinity <b>cocaine</b> interactions at <strong>SERT</strong> in DAT Val559 mice, or specific inhibition of 5 HT2C receptors in these animals, restored <b>cocaine</b> induced locomotion, but did not restore <b>cocaine</b> induced elevations of extracellular DA.
+SLC6A4	drug	nicotine	30559666	Genetic Interaction Between Two VNTRs in the <strong>SLC6A4</strong> Gene Regulates <b>Nicotine</b> Dependence in Vietnamese Men.
+SLC6A4	addiction	dependence	30559666	Genetic Interaction Between Two VNTRs in the <strong>SLC6A4</strong> Gene Regulates Nicotine <b>Dependence</b> in Vietnamese Men.
+SLC6A4	drug	nicotine	30559666	Association between the <strong>SLC6A4</strong> polymorphisms and <b>nicotine</b> dependence is controversial.
+SLC6A4	addiction	dependence	30559666	Association between the <strong>SLC6A4</strong> polymorphisms and nicotine <b>dependence</b> is controversial.
+SLC6A4	drug	nicotine	30559666	The Fagerström Test (FTND) was used to evaluate the <b>nicotine</b> dependence and PCR was used to determine the <strong>SLC6A4</strong> HTTLPR and STin2 VNTRs.
+SLC6A4	addiction	dependence	30559666	The Fagerström Test (FTND) was used to evaluate the nicotine <b>dependence</b> and PCR was used to determine the <strong>SLC6A4</strong> HTTLPR and STin2 VNTRs.
+SLC6A4	drug	nicotine	30559666	Stratification analysis was used to find the genetic interaction between these two VNTRs in <b>nicotine</b> dependence as they may synergistically regulate the <strong>SLC6A4</strong> expression.
+SLC6A4	addiction	dependence	30559666	Stratification analysis was used to find the genetic interaction between these two VNTRs in nicotine <b>dependence</b> as they may synergistically regulate the <strong>SLC6A4</strong> expression.
+SLC6A4	drug	cocaine	30448991	The similarity between the discriminative stimulus effects of <b>cocaine</b> and mephedrone in male rats suggests an important overlap and the relative importance of the dopamine (DAT) and serotonin (<strong>SERT</strong>) transporters.
+SLC6A4	drug	amphetamine	30305739	Synthetic cathinones are common constituents of abused "bath salts" preparations and represent a large family of structurally related compounds that function as cocaine like inhibitors or <b>amphetamine</b> like substrates of dopamine (DAT), norepinephrine (NET), and serotonin (<strong>SERT</strong>) transporters.
+SLC6A4	drug	cocaine	30305739	Synthetic cathinones are common constituents of abused "bath salts" preparations and represent a large family of structurally related compounds that function as <b>cocaine</b> like inhibitors or amphetamine like substrates of dopamine (DAT), norepinephrine (NET), and serotonin (<strong>SERT</strong>) transporters.
+SLC6A4	addiction	reward	30305739	To this end, we tested the hypothesis that <b>reinforcing</b> effectiveness of cathinone stimulants is positively correlated with their selectivity for DAT relative to <strong>SERT</strong>.
+SLC6A4	drug	cocaine	30305739	Uptake inhibition assays in rat brain synaptosomes were used to directly compare the potency of MDPV, MDPBP, MDPPP, α PVP, α PPP, and <b>cocaine</b> at DAT, NET, and <strong>SERT</strong>, whereas intravenous self administration in rats was used to quantify relative reinforcing effectiveness of the drugs using progressive ratio (PR) and behavioral economic procedures.
+SLC6A4	addiction	reward	30305739	Uptake inhibition assays in rat brain synaptosomes were used to directly compare the potency of MDPV, MDPBP, MDPPP, α PVP, α PPP, and cocaine at DAT, NET, and <strong>SERT</strong>, whereas intravenous self administration in rats was used to quantify relative <b>reinforcing</b> effectiveness of the drugs using progressive ratio (PR) and behavioral economic procedures.
+SLC6A4	drug	cocaine	30305739	All cathinones were more potent at DAT than NET or <strong>SERT</strong>, with a rank order for selectivity at DAT over <strong>SERT</strong> of α PVP > α PPP > MDPV > MDPBP > MDPPP > <b>cocaine</b>.
+SLC6A4	drug	cocaine	30305739	These synthetic cathinones were more effective reinforcers than <b>cocaine</b>, and the measures of reinforcing effectiveness determined by PR and demand curve analyses were highly correlated with selectivity for DAT over <strong>SERT</strong>.
+SLC6A4	addiction	reward	30305739	These synthetic cathinones were more effective reinforcers than cocaine, and the measures of <b>reinforcing</b> effectiveness determined by PR and demand curve analyses were highly correlated with selectivity for DAT over <strong>SERT</strong>.
+SLC6A4	addiction	reward	30305739	Together, these studies provide strong and convergent evidence that the abuse potential of stimulant drugs is mediated by uptake inhibition at DAT, with activity at <strong>SERT</strong> serving as a negative modulator of <b>reinforcing</b> effectiveness.
+SLC6A4	drug	nicotine	30219683	The aim of the current study was to analyze the effect of <strong>SLC6A4</strong> (5HTT_LPR) (rs25531) and HTR2A 1438G/A (rs6311) genetic polymorphisms on the relation between <b>smoking</b> habits and COPD.
+SLC6A4	drug	nicotine	30219683	The association between <strong>SLC6A4</strong> (5HTT_LPR) (rs25531), HTR2A 1438G/A (rs6311), <b>smoking</b> degree and COPD was analyzed in a total of 77 COPD patients (active <b>smokers</b>) and 90 control subjects (active healthy <b>smokers</b>).
+SLC6A4	drug	nicotine	30219683	The distribution of <strong>SLC6A4</strong> genotypes did not vary between healthy <b>smokers</b> and COPD patients (P=0.758).
+SLC6A4	drug	alcohol	30192917	The current candidate gene and environment interaction (cGxE) study examined whether the effects of an experimentally manipulated psychosocial stressor on self reported drinking urge and implicit attentional bias for <b>alcohol</b> cues differ as a function of a cumulative genetic score of <strong>5 HTTLPR</strong>, MAO A, DRD4, DAT1 and DRD2 genotypes.
+SLC6A4	drug	cocaine	30144237	Using serotonin transporter knockout (<strong>SERT</strong> / ) rats, which show depression like behavior and increased <b>cocaine</b> intake, we investigated the effect of <strong>SERT</strong> reduction on expression of genes involved in glutamate neurotransmission under both baseline conditions as well as after short access or long access <b>cocaine</b> (ShA and LgA, respectively) intake.
+SLC6A4	drug	cocaine	30144237	In <b>cocaine</b> naïve animals, <strong>SERT</strong> removal led to reduced baseline Hb mRNA levels of critical determinants of glutamate transmission, such as SLC1A2, the main glutamate transporter and N methyl D aspartate (Grin1, Grin2A and Grin2B) as well as α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (Gria1 and Gria2) receptor subunits, with no changes in the scaffolding protein Dlg4.
+SLC6A4	drug	cocaine	30144237	In response to ShA and LgA <b>cocaine</b> intake, SLC1A2 and Grin1 mRNA levels decreased in <strong>SERT</strong>+/+ rats to levels equal of those of <strong>SERT</strong> /  rats.
+SLC6A4	drug	alcohol	29928152	Meanwhile, rs6354C>A, in <strong>SLC6A4</strong> gene, variant's genotype distribution showed statistically significant difference between the non drinker and <b>alcohol</b> drinker group (distribution of genotypes in the case group: 9/72/172 (CC/CA/AA) and in the control group: 5/7/29, p = 0.0264).
+SLC6A4	addiction	dependence	29673739	Polymorphisms <strong>5 HTTLPR</strong> and STin2 of serotonin and rs2279020 and rs3219151 of the GABA pathway were analyzed and results correlated with age at first use quantity consumed, duration of use, <b>dependence</b> and age at onset of <b>dependence</b>.
+SLC6A4	drug	alcohol	29673739	<strong>5 HTTLPR</strong> was significantly associated with high AUDIT scores and <b>alcohol</b> intake (p < 0.0001), GABAA rs2279020 and rs3219151 with age at first use (p < 0.0001); rs2279020 with higher AUDIT score (p = 0.002) and rs3219151 with quantity (p = 0.0001).
+SLC6A4	addiction	aversion	29560525	Therefore, to continue investigating the relationship between compromised serotonergic function and different classes of drugs, a series of experiments was conducted investigating locomotor activity (LMA) and conditioned taste <b>aversion</b> (<b>CTA</b>) in the serotonin transporter knockout (<strong>SERT</strong> KO) rat model.
+SLC6A4	drug	psychedelics	29560525	<b>MDMA</b> induced hyperactivity was reduced, while <b>MDMA</b> induced CTA was enhanced, in <strong>SERT</strong> KO rats.
+SLC6A4	addiction	aversion	29560525	MDMA induced hyperactivity was reduced, while MDMA induced <b>CTA</b> was enhanced, in <strong>SERT</strong> KO rats.
+SLC6A4	drug	cocaine	29357981	Reduced expression of the serotonin transporter (<strong>SERT</strong>) promotes anxiety and <b>cocaine</b> intake in both humans and rats.
+SLC6A4	drug	cocaine	29357981	<strong>SERT</strong> knockdown in the MRN increased <b>cocaine</b> intake selectively under ShA conditions and, like ShA <b>cocaine</b> self administration, reduced corticotropin releasing factor (CRF) immunodensity in the paraventricular nucleus of the hypothalamus.
+SLC6A4	drug	cocaine	29357981	In contrast, <strong>SERT</strong> knockdown in the DRN increased <b>cocaine</b> intake selectively under LgA conditions and, like LgA <b>cocaine</b> self administration, reduced CRF immunodensity in the central nucleus of the amygdala.
+SLC6A4	drug	cocaine	29357981	<strong>SERT</strong> knockdown in the MRN or DRN produced anxiety like behavior, as did withdrawal from ShA or LgA <b>cocaine</b> self administration.
+SLC6A4	addiction	withdrawal	29357981	<strong>SERT</strong> knockdown in the MRN or DRN produced anxiety like behavior, as did <b>withdrawal</b> from ShA or LgA cocaine self administration.
+SLC6A4	drug	opioid	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, <strong>SLC6A4</strong>) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+SLC6A4	addiction	dependence	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, <strong>SLC6A4</strong>) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+SLC6A4	drug	opioid	29333880	Genotype for 5 HTTLPR in the <strong>SLC6A4</strong> gene was nominally associated with dropout rate when the <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> groups were combined.
+SLC6A4	drug	opioid	29333880	Genotype for <strong>5 HTTLPR</strong> in the <strong>SLC6A4</strong> gene was nominally associated with dropout rate when the <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> groups were combined.
+SLC6A4	drug	opioid	29333880	When the most significant variants associated with dropout rate were analyzed using pairwise analyses, <strong>SLC6A4</strong> (5 HTTLPR) and COMT (Val158Met; rs4860) had nominally significant associations with dropout rate in <b>methadone</b> patients.
+SLC6A4	drug	opioid	29333880	When the most significant variants associated with dropout rate were analyzed using pairwise analyses, <strong>SLC6A4</strong> (<strong>5 HTTLPR</strong>) and COMT (Val158Met; rs4860) had nominally significant associations with dropout rate in <b>methadone</b> patients.
+SLC6A4	addiction	addiction	29333880	Patients with the S/S genotype at 5 HTTLPR in <strong>SLC6A4</strong> or the Val/Val genotype at Val158Met in COMT may require additional treatment to improve their chances of completing <b>addiction</b> treatment.
+SLC6A4	addiction	addiction	29333880	Patients with the S/S genotype at <strong>5 HTTLPR</strong> in <strong>SLC6A4</strong> or the Val/Val genotype at Val158Met in COMT may require additional treatment to improve their chances of completing <b>addiction</b> treatment.
+SLC6A4	drug	nicotine	29310005	In multiple logistic regression, rs1042173 of <strong>Solute carrier family 6 member 4</strong> was significantly related to <b>smoking</b> cessation in additive and dominant model (p=0.03 and 0.02, respectively).
+SLC6A4	drug	cocaine	29292566	Here, we set out to investigate the influence of serotonin transporter (<strong>5 HTT</strong>) genotype on the effectiveness of counter conditioning after extended access to <b>cocaine</b> self administration.
+SLC6A4	addiction	relapse	29292566	To this end, <strong>5 HTT</strong>+/+ and <strong>5 HTT</strong> /  rats underwent a touch screen based approach to test if reward induced <b>reinstatement</b> of responding to a previously counter conditioned cue is reduced, compared with a non counter conditioned cue, in a within subject manner.
+SLC6A4	addiction	reward	29292566	To this end, <strong>5 HTT</strong>+/+ and <strong>5 HTT</strong> /  rats underwent a touch screen based approach to test if <b>reward</b> induced reinstatement of responding to a previously counter conditioned cue is reduced, compared with a non counter conditioned cue, in a within subject manner.
+SLC6A4	drug	cocaine	29292566	We observed an overall extinction deficit of <b>cocaine</b> seeking behavior in <strong>5 HTT</strong> /  rats and a resistance to punishment during the counter conditioning session.
+SLC6A4	addiction	addiction	29292566	We observed an overall extinction deficit of cocaine seeking behavior in <strong>5 HTT</strong> /  rats and a resistance to <b>punishment</b> during the counter conditioning session.
+SLC6A4	addiction	relapse	29292566	We observed an overall extinction deficit of cocaine <b>seeking</b> behavior in <strong>5 HTT</strong> /  rats and a resistance to punishment during the counter conditioning session.
+SLC6A4	drug	cocaine	29292566	Furthermore, we observed a significant decrease in reinstatement to <b>cocaine</b> and sucrose associated cues after counter conditioning but only in <strong>5 HTT</strong>+/+ rats.
+SLC6A4	addiction	relapse	29292566	Furthermore, we observed a significant decrease in <b>reinstatement</b> to cocaine and sucrose associated cues after counter conditioning but only in <strong>5 HTT</strong>+/+ rats.
+SLC6A4	drug	cocaine	28988906	We found that 2 , 3  and 4 FPM inhibit uptake mediated by DAT and NET in HEK293 cells with potencies comparable to <b>cocaine</b> (IC50 values < 2.5 μM), but display less potent effects at <strong>SERT</strong> (IC50 values >80 μM).
+SLC6A4	drug	cannabinoid	28625856	Our aim was to investigate the effect of an endogenous <b>cannabinoid</b>, anandamide (AEA) on the NTG induced changes on serotonin transporter (<strong>5 HTT</strong>) expression in the upper cervical spinal cord (C1 C2) of the rat, where most of the trigeminal nociceptive afferents convey.
+SLC6A4	addiction	withdrawal	28621702	We examined response frequency to mechanical stimulation of the paw, muscle <b>withdrawal</b> thresholds, and expression of phosphorylation of the NR1 subunit of the N methyl D aspartate receptor (p NR1) and serotonin transporter (<strong>SERT</strong>) in the RVM.
+SLC6A4	drug	opioid	28621702	Physically active, <b>naloxone</b> treated, and MOR mice showed significant increases in <strong>SERT</strong> immunoreactivity when compared with wild type physically active control mice.
+SLC6A4	drug	opioid	28621702	These results suggest that analgesia induced by 5 days of wheel running is mediated by mu <b>opioid</b> receptors through the modulation of <strong>SERT</strong>, but not p NR1, in RVM.
+SLC6A4	drug	cocaine	28590957	Genetic moderation of <b>cocaine</b> subjective effects by variation in the TPH1, TPH2, and <strong>SLC6A4</strong> serotonin genes.
+SLC6A4	drug	cocaine	28590957	This study investigated variants of tryptophan hydroxylase (TPH)1, TPH2, and <strong>SLC6A4</strong> in the moderation of the subjective effects of <b>cocaine</b>.
+SLC6A4	drug	cocaine	28590957	These findings indicate that TPH1, TPH2, and <strong>SLC6A4</strong> variants moderate the subjective effects of <b>cocaine</b> in non treatment seeking <b>cocaine</b> dependent participants.
+SLC6A4	addiction	relapse	28590957	These findings indicate that TPH1, TPH2, and <strong>SLC6A4</strong> variants moderate the subjective effects of cocaine in non treatment <b>seeking</b> cocaine dependent participants.
+SLC6A4	drug	cocaine	28585320	To elucidate 5 HT transporter (<strong>SERT</strong>) specific contributions to <b>cocaine</b> action, we evaluated <b>cocaine</b> effects in the <strong>SERT</strong> Met172 knock in mouse, which expresses a <strong>SERT</strong> coding substitution that eliminates high affinity <b>cocaine</b> recognition.
+SLC6A4	drug	cocaine	28585320	We measured the effects of <strong>SERT</strong> Met172 on <b>cocaine</b> antagonism of 5 HT re uptake using ex vivo synaptosome preparations and in vivo microdialysis.
+SLC6A4	drug	cocaine	28585320	We assessed <strong>SERT</strong> dependence of <b>cocaine</b> actions behaviourally through acute and chronic locomotor activation, sensitization, conditioned place preference (CPP) and oral <b>cocaine</b> consumption.
+SLC6A4	addiction	dependence	28585320	We assessed <strong>SERT</strong> <b>dependence</b> of cocaine actions behaviourally through acute and chronic locomotor activation, sensitization, conditioned place preference (CPP) and oral cocaine consumption.
+SLC6A4	addiction	reward	28585320	We assessed <strong>SERT</strong> dependence of cocaine actions behaviourally through acute and chronic locomotor activation, sensitization, conditioned place preference (<b>CPP</b>) and oral cocaine consumption.
+SLC6A4	addiction	sensitization	28585320	We assessed <strong>SERT</strong> dependence of cocaine actions behaviourally through acute and chronic locomotor activation, <b>sensitization</b>, conditioned place preference (CPP) and oral cocaine consumption.
+SLC6A4	drug	cocaine	28585320	We used c Fos, quantitative RT PCR and RNA sequencing methods for insights into cellular and molecular networks supporting <strong>SERT</strong> dependent <b>cocaine</b> actions.
+SLC6A4	drug	cocaine	28585320	<strong>SERT</strong> Met172 mice demonstrated functional insensitivity for <b>cocaine</b> at <strong>SERT</strong>.
+SLC6A4	drug	cocaine	28585320	Distinct <strong>SERT</strong> dependent gene expression networks triggered by acute and chronic <b>cocaine</b> administration were identified, including PrL Akt and nucleus accumbens ERK1/2 signalling.
+SLC6A4	drug	cocaine	28585320	Our studies reveal distinct <strong>SERT</strong> contributions to <b>cocaine</b> action, reinforcing the possibility of targeting specific aspects of <b>cocaine</b> addiction by modulation of 5 HT signalling.
+SLC6A4	addiction	addiction	28585320	Our studies reveal distinct <strong>SERT</strong> contributions to cocaine action, reinforcing the possibility of targeting specific aspects of cocaine <b>addiction</b> by modulation of 5 HT signalling.
+SLC6A4	addiction	reward	28585320	Our studies reveal distinct <strong>SERT</strong> contributions to cocaine action, <b>reinforcing</b> the possibility of targeting specific aspects of cocaine addiction by modulation of 5 HT signalling.
+SLC6A4	drug	psychedelics	28508340	<b>ketamine</b> and oral haloperidol (4 mg/kg), olanzapine (2 mg/kg), or one of two doses of sertraline (<strong>SERT</strong>) (2.5 or 5 mg/kg), respectively.
+SLC6A4	drug	alcohol	28361821	With respect to the 5 hydroxytryptamine (5HT) transporter long promoter region (<strong>5HTTLPR</strong>), cholinergic receptor muscarinic (CHRM2) and <b>alcohol</b> dehydrogenase 1B (ADH1B) genes, there was no significant difference between the cases and the controls.
+SLC6A4	drug	alcohol	28262188	The serotonin transporter linked polymorphic region (5 HTTLPR) of the serotonin transporter gene (<strong>SLC6A4</strong>) has been previously associated with <b>alcohol</b> related risk.
+SLC6A4	drug	alcohol	28262188	The serotonin transporter linked polymorphic region (<strong>5 HTTLPR</strong>) of the serotonin transporter gene (<strong>SLC6A4</strong>) has been previously associated with <b>alcohol</b> related risk.
+SLC6A4	drug	alcohol	28262188	The current prospective study aimed to clarify how and under what circumstances variations in <strong>5 HTTLPR</strong> transmit risk for various <b>alcohol</b> related outcomes.
+SLC6A4	drug	alcohol	28262188	We tested a moderated mediation model with <strong>5 HTTLPR</strong> as the predictor, Self Rating of the Effects of <b>Alcohol</b> (SRE) score as the mediator, <b>alcohol</b> related outcomes as the dependent variables, parental monitoring as the moderator of the SRE to <b>alcohol</b> outcomes path, and prior drinks, sex, age, and body mass index as covariates.
+SLC6A4	drug	alcohol	28262188	Findings suggest that one mechanism by which <strong>5 HTTLPR</strong> variation transmits <b>alcohol</b> related risk is through level of response to <b>alcohol</b>.
+SLC6A4	drug	opioid	28237351	5899 subjects attending twelve centers for addiction treatment (<strong>SERT</strong>) in north Italy following problems due to <b>heroin</b> abuse between 1975 and 2013 were recruited.
+SLC6A4	addiction	addiction	28237351	5899 subjects attending twelve centers for <b>addiction</b> treatment (<strong>SERT</strong>) in north Italy following problems due to heroin abuse between 1975 and 2013 were recruited.
+SLC6A4	drug	opioid	28237351	In the course of time, among <b>heroin</b> users, mortality and the causes of death have changed; for <strong>SERT</strong> clients special attention should be paid to the prevention and treatment of liver related diseases.
+SLC6A4	addiction	reward	27957784	A significant extinction of <b>CPP</b> was observed in <strong>5 HTT</strong>+/+ rats receiving 1 mg/kg i.v.
+SLC6A4	drug	cocaine	27957784	In conclusion, in this study, we show that the dosing of DCS to facilitate the extinction of <b>cocaine</b> seeking behaviour is, at least partially, determined by <strong>5 HTT</strong> genotype.
+SLC6A4	addiction	relapse	27957784	In conclusion, in this study, we show that the dosing of DCS to facilitate the extinction of cocaine <b>seeking</b> behaviour is, at least partially, determined by <strong>5 HTT</strong> genotype.
+SLC6A4	drug	opioid	27942217	A meta analysis was conducted to examine the association of <b>heroin</b> dependence with two common polymorphisms of serotonin transporter gene, in the promoter (5 hydroxytryptamine transporter linked promotor region [<strong>5 httlpr</strong>]) and intron 2 (a various number tandem repeat in serotonin transporter intron 2 [STin2]).
+SLC6A4	addiction	dependence	27942217	A meta analysis was conducted to examine the association of heroin <b>dependence</b> with two common polymorphisms of serotonin transporter gene, in the promoter (5 hydroxytryptamine transporter linked promotor region [<strong>5 httlpr</strong>]) and intron 2 (a various number tandem repeat in serotonin transporter intron 2 [STin2]).
+SLC6A4	drug	opioid	27942217	In the analysis, <b>heroin</b> dependence was found to be significantly associated with the S allele of <strong>5 httlpr</strong> (odds ratio [OR] =1.22, 95% confidence interval [CI] =1.08 1.41, P=0.002).
+SLC6A4	addiction	dependence	27942217	In the analysis, heroin <b>dependence</b> was found to be significantly associated with the S allele of <strong>5 httlpr</strong> (odds ratio [OR] =1.22, 95% confidence interval [CI] =1.08 1.41, P=0.002).
+SLC6A4	drug	opioid	27942217	The association between the S allele of <strong>5 httlpr</strong> and <b>heroin</b> dependence was significant in Caucasian subjects (OR =1.37, 95% CI =1.12 1.68, P=0.003), but not in non Caucasian subjects.
+SLC6A4	addiction	dependence	27942217	The association between the S allele of <strong>5 httlpr</strong> and heroin <b>dependence</b> was significant in Caucasian subjects (OR =1.37, 95% CI =1.12 1.68, P=0.003), but not in non Caucasian subjects.
+SLC6A4	drug	opioid	27942217	The results suggest an ethnic specific effect of the <strong>5 httlpr</strong> polymorphism on the risk for <b>heroin</b> dependence, but the influence of the genetic variance in the patients with comorbidities or intermediate phenotypes of <b>heroin</b> dependence needs to be further examined.
+SLC6A4	addiction	dependence	27942217	The results suggest an ethnic specific effect of the <strong>5 httlpr</strong> polymorphism on the risk for heroin <b>dependence</b>, but the influence of the genetic variance in the patients with comorbidities or intermediate phenotypes of heroin <b>dependence</b> needs to be further examined.
+SLC6A4	drug	psychedelics	27738380	DM exhibited a <b>ketamine</b> like rapid acting antidepressant effect, thought to be mediated by mTOR activation (related to NMDA PCP site antagonism, sigma 1 and beta adrenergic receptor stimulation) and <strong>5HTT</strong> inhibition, resulting in AMPA receptor trafficking, and dendritogenesis, spinogenesis, synaptogenesis, and increased neuronal survival (related to NMDA antagonism and sigma 1 and mTOR signaling).
+SLC6A4	drug	alcohol	27619010	Conditional indirect effects indicated stronger associations between childhood traumatic stress and lability, behavioral disinhibition, <b>alcohol</b> consumption, AUD symptoms, and associated conduct problems via PTSD symptoms among those with the low expression <strong>5 HTTLPR</strong> alleles.
+SLC6A4	drug	amphetamine	27478387	Extracellular serotonin levels are regulated by the serotonin transporter (<strong>SERT</strong>) and organic cation transporter 3 (OCT3), and vHipp OCT3 expression is enhanced during 24 hours of <b>amphetamine</b> withdrawal, while <strong>SERT</strong> expression is unaltered.
+SLC6A4	addiction	withdrawal	27478387	Extracellular serotonin levels are regulated by the serotonin transporter (<strong>SERT</strong>) and organic cation transporter 3 (OCT3), and vHipp OCT3 expression is enhanced during 24 hours of amphetamine <b>withdrawal</b>, while <strong>SERT</strong> expression is unaltered.
+SLC6A4	addiction	withdrawal	27478387	Here, we tested whether OCT3 and <strong>SERT</strong> expression in the CeA is also affected during acute <b>withdrawal</b> to explain opposing regional alterations in limbic serotonergic neurotransmission and if respective changes continued with two weeks of <b>withdrawal</b>.
+SLC6A4	addiction	withdrawal	27478387	OCT3 and <strong>SERT</strong> expression increased in the CeA at both <b>withdrawal</b> timepoints.
+SLC6A4	drug	amphetamine	27478387	These regionally specific changes in limbic OCT3 and <strong>SERT</strong> expression may partially contribute to the serotonergic imbalance and negative affect during <b>amphetamine</b> withdrawal.
+SLC6A4	addiction	withdrawal	27478387	These regionally specific changes in limbic OCT3 and <strong>SERT</strong> expression may partially contribute to the serotonergic imbalance and negative affect during amphetamine <b>withdrawal</b>.
+SLC6A4	drug	alcohol	27161942	In this critical review, we discuss recent literature describing an association between <b>alcohol</b> dependence, the SERT linked polymorphic region (<strong>5 HTTLPR</strong>), and pharmacological response to SSRIs.
+SLC6A4	addiction	dependence	27161942	In this critical review, we discuss recent literature describing an association between alcohol <b>dependence</b>, the SERT linked polymorphic region (<strong>5 HTTLPR</strong>), and pharmacological response to SSRIs.
+SLC6A4	drug	alcohol	27161942	In this critical review, we discuss recent literature describing an association between <b>alcohol</b> dependence, the <strong>SERT</strong> linked polymorphic region (<strong>5 HTTLPR</strong>), and pharmacological response to SSRIs.
+SLC6A4	addiction	dependence	27161942	In this critical review, we discuss recent literature describing an association between alcohol <b>dependence</b>, the <strong>SERT</strong> linked polymorphic region (<strong>5 HTTLPR</strong>), and pharmacological response to SSRIs.
+SLC6A4	drug	alcohol	27161942	Although our current understanding of the role of 5 HT systems in <b>alcohol</b> dependence is incomplete, there is some evidence to suggest that 5 HT3 receptor antagonists are effective in people with the L/L genotype of the <strong>5 HTTLPR</strong> polymorphism while SSRIs may be more beneficial to people with the S/L or S/S genotype.
+SLC6A4	addiction	dependence	27161942	Although our current understanding of the role of 5 HT systems in alcohol <b>dependence</b> is incomplete, there is some evidence to suggest that 5 HT3 receptor antagonists are effective in people with the L/L genotype of the <strong>5 HTTLPR</strong> polymorphism while SSRIs may be more beneficial to people with the S/L or S/S genotype.
+SLC6A4	addiction	addiction	27064247	Polymorphisms in genes such as DAT1, <strong>5HTTLPR</strong>, D4DR4, and MAO A have been linked to attention deficit hyperactivity disorder (ADHD) and susceptibility for opiate <b>addiction</b>.
+SLC6A4	drug	alcohol	27045756	TPH1 and <strong>5 HTTLPR</strong> Genes Specifically Interact in Opiate Dependence but Not in <b>Alcohol</b> Dependence.
+SLC6A4	addiction	dependence	27045756	TPH1 and <strong>5 HTTLPR</strong> Genes Specifically Interact in Opiate <b>Dependence</b> but Not in Alcohol <b>Dependence</b>.
+SLC6A4	drug	alcohol	27045756	We investigated whether 2 serotonergic polymorphisms, TPH1 A218C (rs1800532) and <strong>5 HTT</strong> linked promoter region (5 HTTLPR) (rs25531), are differently associated with <b>alcohol</b> or opiate dependence.
+SLC6A4	addiction	dependence	27045756	We investigated whether 2 serotonergic polymorphisms, TPH1 A218C (rs1800532) and <strong>5 HTT</strong> linked promoter region (5 HTTLPR) (rs25531), are differently associated with alcohol or opiate <b>dependence</b>.
+SLC6A4	drug	alcohol	27045756	We investigated whether 2 serotonergic polymorphisms, TPH1 A218C (rs1800532) and <strong>5 HTT</strong> linked promoter region (<strong>5 HTTLPR</strong>) (rs25531), are differently associated with <b>alcohol</b> or opiate dependence.
+SLC6A4	addiction	dependence	27045756	We investigated whether 2 serotonergic polymorphisms, TPH1 A218C (rs1800532) and <strong>5 HTT</strong> linked promoter region (<strong>5 HTTLPR</strong>) (rs25531), are differently associated with alcohol or opiate <b>dependence</b>.
+SLC6A4	drug	alcohol	27045756	Moreover, there was a significant interaction between the TPH1 A218C A/C and <strong>5 HTTLPR</strong> S+ gene polymorphisms in opiate dependent (OR 2.72, p = 0.01), but not in <b>alcohol</b> dependent patients.
+SLC6A4	drug	alcohol	26979101	Associations of <strong>5HTTLPR</strong> polymorphism with major depressive disorder and <b>alcohol</b> dependence: A systematic review and meta analysis.
+SLC6A4	addiction	dependence	26979101	Associations of <strong>5HTTLPR</strong> polymorphism with major depressive disorder and alcohol <b>dependence</b>: A systematic review and meta analysis.
+SLC6A4	drug	alcohol	26979101	Carrying a genetic variant in the serotonin transporter gene (<strong>5HTT</strong>) may increase the risk of major depressive disorder and <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	26979101	Carrying a genetic variant in the serotonin transporter gene (<strong>5HTT</strong>) may increase the risk of major depressive disorder and alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	26979101	Previous estimates of the association of the S allele of <strong>5HTTLPR</strong> polymorphism with major depressive disorder and <b>alcohol</b> dependence have been inconsistent.
+SLC6A4	addiction	dependence	26979101	Previous estimates of the association of the S allele of <strong>5HTTLPR</strong> polymorphism with major depressive disorder and alcohol <b>dependence</b> have been inconsistent.
+SLC6A4	drug	alcohol	26979101	For the systematic review, we used PubMed MEDLINE and Discovery of The University of Melbourne to search for all relevant case control studies investigating the associations of <strong>5HTTLPR</strong> polymorphism with major depressive disorder and <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	26979101	For the systematic review, we used PubMed MEDLINE and Discovery of The University of Melbourne to search for all relevant case control studies investigating the associations of <strong>5HTTLPR</strong> polymorphism with major depressive disorder and alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	26979101	The summary OR for homozygote carriers of the S allele of <strong>5HTTLPR</strong> polymorphism compared with heterozygote and non carriers combined (SS vs SL+LL genotype) was 1.33 (95% CI = [1.19, 1.48]) for major depressive disorder and 1.18 (95% CI = [1.01, 1.38]) for <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	26979101	The summary OR for homozygote carriers of the S allele of <strong>5HTTLPR</strong> polymorphism compared with heterozygote and non carriers combined (SS vs SL+LL genotype) was 1.33 (95% CI = [1.19, 1.48]) for major depressive disorder and 1.18 (95% CI = [1.01, 1.38]) for alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	26979101	The summary OR per S allele of <strong>5HTTLPR</strong> polymorphism was 1.16 (95% CI = [1.08, 1.23]) for major depressive disorder and 1.12 (95% CI = [1.01, 1.23]) for <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	26979101	The summary OR per S allele of <strong>5HTTLPR</strong> polymorphism was 1.16 (95% CI = [1.08, 1.23]) for major depressive disorder and 1.12 (95% CI = [1.01, 1.23]) for alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	26979101	Our meta analysis confirms that individuals with the homozygous S allele of <strong>5HTTLPR</strong> polymorphism are at increased risks of major depressive disorder as well as <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	26979101	Our meta analysis confirms that individuals with the homozygous S allele of <strong>5HTTLPR</strong> polymorphism are at increased risks of major depressive disorder as well as alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	26979101	Further studies are required to investigate the association between <strong>5HTTLPR</strong> polymorphism and the comorbidity of major depressive disorder and <b>alcohol</b> dependence as well as gene × environmental interactions.
+SLC6A4	addiction	dependence	26979101	Further studies are required to investigate the association between <strong>5HTTLPR</strong> polymorphism and the comorbidity of major depressive disorder and alcohol <b>dependence</b> as well as gene × environmental interactions.
+SLC6A4	drug	nicotine	26886943	Meta analysis of the association between a serotonin transporter <strong>5 HTTLPR</strong> polymorphism and <b>smoking</b> cessation.
+SLC6A4	addiction	addiction	26886943	<strong>5 HTTLPR</strong> is one of the candidate genes influencing <b>addiction</b>.
+SLC6A4	drug	nicotine	26886943	Recent studies have reported that the <strong>5 HTTLPR</strong> genotype is associated with <b>smoking</b> behaviour, but its influence is still controversial.
+SLC6A4	drug	nicotine	26886943	Thus, we reviewed the <b>smoking</b> cessation outcomes among previously reported studies by comparing the <strong>5 HTTLPR</strong> polymorphism.
+SLC6A4	drug	nicotine	26886943	We found no significant association between <strong>5 HTTLPR</strong> and <b>smoking</b> cessation, but <strong>5 HTTLPR</strong> remains an important <b>smoking</b> related candidate gene.
+SLC6A4	drug	nicotine	26742023	Genetic studies have suggested that the serotonin transporter (<strong>SERT</strong>) could be associated with cigarette <b>smoking</b>.
+SLC6A4	drug	nicotine	26742023	The aim of the present study was to examine the <strong>SERT</strong> availability among cigarette <b>smokers</b> by using single photon emission computed tomography (SPECT).
+SLC6A4	drug	nicotine	26742023	No significant difference in <strong>SERT</strong> availability was found between 2 groups in the midbrain (<b>smokers</b>: 2.12 ± 0.70, nonsmokers: 2.13 ± 0.63; P = 0.86), basal ganglia (<b>smokers</b>: 0.83 ± 0.30, nonsmokers:0.90 ± 0.39; P = 0.95), or thalamus (<b>smokers</b>: 1.14 ± 0.41, nonsmokers: 1.20 ± 0.38; P = 0.88).
+SLC6A4	drug	nicotine	26742023	No significant association was found between the <strong>SERT</strong> availability, and either the breath carbon monoxide level or the score of the Fagerström Test for <b>Nicotine</b> Dependence.
+SLC6A4	addiction	dependence	26742023	No significant association was found between the <strong>SERT</strong> availability, and either the breath carbon monoxide level or the score of the Fagerström Test for Nicotine <b>Dependence</b>.
+SLC6A4	drug	nicotine	26742023	Whether the <strong>SERT</strong> availability in the brain is altered in <b>smokers</b> remains unclear.
+SLC6A4	drug	amphetamine	30957071	Results revealed that male and female rats exposed to <b>METH</b> had similar decreases in dopamine (DA) transporter (DAT) immunoreactivity in the striatum, serotonin (5 HT) content and 5 HT transporter (<strong>SERT</strong>) function in the hippocampus, and 5 HT content in the frontal cortex.
+SLC6A4	drug	alcohol	26352193	The severity of the <b>alcohol</b> problems was higher in currently <b>alcohol</b> dependent subjects with the <strong>5 HTTLPR</strong> LL (p = 0.039) and L′L′ genotypes (p = 0.027).
+SLC6A4	drug	alcohol	26352193	Our findings suggest that bi  and triallelic <strong>SLC6A4</strong> 5 HTTLPR has some effects on the severity of <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	26352193	Our findings suggest that bi  and triallelic <strong>SLC6A4</strong> 5 HTTLPR has some effects on the severity of alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	26352193	Our findings suggest that bi  and triallelic <strong>SLC6A4</strong> <strong>5 HTTLPR</strong> has some effects on the severity of <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	26352193	Our findings suggest that bi  and triallelic <strong>SLC6A4</strong> <strong>5 HTTLPR</strong> has some effects on the severity of alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	26352193	Triallelic <strong>5 HTTLPR</strong> was associated with social anxiety, anxiety, and depressive traits in <b>alcohol</b> dependent subjects.
+SLC6A4	drug	psychedelics	26340513	Effects of <b>LSD</b> on grooming behavior in serotonin transporter heterozygous (<strong>Sert</strong>⁺/⁻) mice.
+SLC6A4	addiction	addiction	26340513	In humans, <strong>SERT</strong> genetic variance is linked to the pathogenesis of various psychiatric disorders, including anxiety, autism spectrum disorders (ASD) and obsessive <b>compulsive</b> disorder (OCD).
+SLC6A4	drug	psychedelics	26340513	Here, we examined heterozygous <strong>Sert</strong>(+/ ) mouse behavior following acute administration of <b>LSD</b> (0.32 mg/kg).
+SLC6A4	drug	psychedelics	26340513	Overall, <strong>Sert</strong>(+/ ) mice displayed a longer duration of self grooming behavior regardless of <b>LSD</b> treatment.
+SLC6A4	drug	psychedelics	26340513	In contrast, <b>LSD</b> increased serotonin sensitive behaviors, such as head twitching, tremors and backwards gait behaviors in both <strong>Sert</strong>(+/+) and <strong>Sert</strong>(+/ ) mice.
+SLC6A4	drug	psychedelics	26340513	There were no significant interactions between <b>LSD</b> treatment and <strong>Sert</strong> gene dosage in any of the behavioral domains measured.
+SLC6A4	drug	psychedelics	26340513	These results suggest that <strong>Sert</strong>(+/ ) mice may respond to the behavioral effects of <b>LSD</b> in a similar manner to wild type mice.
+SLC6A4	drug	alcohol	26311211	<strong>SLC6A4</strong>, the gene encoding the serotonin transporter protein (5 HTT), has been extensively examined as a risk factor for <b>alcohol</b> dependence (AD).
+SLC6A4	addiction	dependence	26311211	<strong>SLC6A4</strong>, the gene encoding the serotonin transporter protein (5 HTT), has been extensively examined as a risk factor for alcohol <b>dependence</b> (AD).
+SLC6A4	drug	alcohol	26311211	<strong>SLC6A4</strong>, the gene encoding the serotonin transporter protein (<strong>5 HTT</strong>), has been extensively examined as a risk factor for <b>alcohol</b> dependence (AD).
+SLC6A4	addiction	dependence	26311211	<strong>SLC6A4</strong>, the gene encoding the serotonin transporter protein (<strong>5 HTT</strong>), has been extensively examined as a risk factor for alcohol <b>dependence</b> (AD).
+SLC6A4	drug	alcohol	26265436	Current evidence suggests that genetic variability of the serotonergic biosynthesis enzyme tryptophan hydroxylase 2 (TPH2) and the serotonin transporter (<strong>SLC6A4</strong>) genes mediates the efficacy of several addiction treatments, such as ondansetron and <b>disulfiram</b>, and the antidepressants bupropion, nortriptyline and sertraline.
+SLC6A4	addiction	addiction	26265436	Current evidence suggests that genetic variability of the serotonergic biosynthesis enzyme tryptophan hydroxylase 2 (TPH2) and the serotonin transporter (<strong>SLC6A4</strong>) genes mediates the efficacy of several <b>addiction</b> treatments, such as ondansetron and disulfiram, and the antidepressants bupropion, nortriptyline and sertraline.
+SLC6A4	drug	alcohol	26041607	In this association study of two independent samples, a number of candidate gene variants (5HT2A T102C, <strong>5 HTTLPR</strong>, DRD Ins 141Del, DAT1 VNTR) were related to violent criminal behavior and <b>alcohol</b> related aggressive traits.
+SLC6A4	drug	alcohol	26041607	<strong>5HTTLPR</strong> variant was related to one characteristic of <b>alcohol</b> related violence.
+SLC6A4	drug	cocaine	26019340	In addition, <strong>SERT</strong> is a major molecular target for psychostimulants such as <b>cocaine</b> and amphetamines.
+SLC6A4	drug	amphetamine	26019340	Inhibition of αCaMKII activity markedly decreased <b>amphetamine</b> triggered <strong>SERT</strong> mediated substrate efflux in both cells coexpressing <strong>SERT</strong> and αCaMKII and brain tissue preparations.
+SLC6A4	drug	amphetamine	26019340	Moreover, we found that genetic deletion of αCaMKII impaired the locomotor response of mice to 3,4 methylenedioxymethamphetamine (also known as "ecstasy") and blunted d fenfluramine induced prolactin release, substantiating the importance of αCaMKII modulation for <b>amphetamine</b> action at <strong>SERT</strong> in vivo as well.
+SLC6A4	drug	psychedelics	26019340	Moreover, we found that genetic deletion of αCaMKII impaired the locomotor response of mice to 3,4 <b>methylenedioxymethamphetamine</b> (also known as "<b>ecstasy</b>") and blunted d fenfluramine induced prolactin release, substantiating the importance of αCaMKII modulation for amphetamine action at <strong>SERT</strong> in vivo as well.
+SLC6A4	drug	cocaine	26013962	Thus, we investigated the effects of genetic variations impacting 5 HT activity and of peripheral 5 HT transporter (<strong>5 HTT</strong>) mRNA expression on WM performance in <b>cocaine</b> users and stimulant naive controls.
+SLC6A4	drug	cocaine	26013962	Two hundred twenty participants (126 <b>cocaine</b> users, 94 controls) were assessed with visuospatial, spatial, and verbal WM tasks, genotyped for the length polymorphism in the promoter region of the <strong>5 HTT</strong> (5 HTTLPR), the variable number of tandem repeats in the second intron of the <strong>5 HTT</strong> (VNTR In2), two single nucleotide polymorphisms (rs4570625 and rs1386497) in the tryptophan hydroxylase 2 (TPH2) gene and quantified for peripheral <strong>5 HTT</strong> mRNA expression in whole blood samples.
+SLC6A4	drug	cocaine	26013962	Two hundred twenty participants (126 <b>cocaine</b> users, 94 controls) were assessed with visuospatial, spatial, and verbal WM tasks, genotyped for the length polymorphism in the promoter region of the <strong>5 HTT</strong> (<strong>5 HTTLPR</strong>), the variable number of tandem repeats in the second intron of the <strong>5 HTT</strong> (VNTR In2), two single nucleotide polymorphisms (rs4570625 and rs1386497) in the tryptophan hydroxylase 2 (TPH2) gene and quantified for peripheral <strong>5 HTT</strong> mRNA expression in whole blood samples.
+SLC6A4	drug	cocaine	26013962	Several significant gene × environment interactions between 5 HT genotypes and <b>cocaine</b> use on WM emerged: in <b>cocaine</b> users, the long/long (<strong>5 HTTLPR</strong>), 9+10/9+10 (VNTR In2) and C/C (TPH2 rs1386497) genotypes were risk alleles for WM impairments, whereas in healthy controls these polymorphisms were associated with improved WM performance.
+SLC6A4	drug	cocaine	26013962	Analogously, high <strong>5 HTT</strong> mRNA levels were associated with worse executive WM performance in <b>cocaine</b> users but with increased performance in controls.
+SLC6A4	drug	alcohol	25770138	<b>Alcohol</b> dependence and serotonin transporter functional polymorphisms <strong>5 HTTLPR</strong> and rs25531 in an Italian population.
+SLC6A4	addiction	dependence	25770138	Alcohol <b>dependence</b> and serotonin transporter functional polymorphisms <strong>5 HTTLPR</strong> and rs25531 in an Italian population.
+SLC6A4	drug	alcohol	25770138	The role of the serotonin transporter gene (<strong>SLC6A4</strong>) in <b>alcohol</b> dependence (AD) is still unclear.
+SLC6A4	addiction	dependence	25770138	The role of the serotonin transporter gene (<strong>SLC6A4</strong>) in alcohol <b>dependence</b> (AD) is still unclear.
+SLC6A4	drug	alcohol	25770138	In this paper, we have evaluated the association of the <strong>SLC6A4</strong> gene polymorphisms 5 HTTLPR and rs25531 in AD and assessed the polymorphic patterns both in <b>alcoholics</b> and in healthy people of an Italian population.
+SLC6A4	drug	alcohol	25770138	In this paper, we have evaluated the association of the <strong>SLC6A4</strong> gene polymorphisms <strong>5 HTTLPR</strong> and rs25531 in AD and assessed the polymorphic patterns both in <b>alcoholics</b> and in healthy people of an Italian population.
+SLC6A4	drug	alcohol	25770138	Genotyping of the 5 HTTLPR (L/S) and rs25531 (A/G) polymorphisms of the <strong>SLC6A4</strong> gene was performed on 403 <b>alcoholics</b> outpatients and 427 blood donors.
+SLC6A4	drug	alcohol	25770138	Genotyping of the <strong>5 HTTLPR</strong> (L/S) and rs25531 (A/G) polymorphisms of the <strong>SLC6A4</strong> gene was performed on 403 <b>alcoholics</b> outpatients and 427 blood donors.
+SLC6A4	drug	alcohol	25710844	A meta analysis of the associations between the <strong>SLC6A4</strong> promoter polymorphism (5HTTLPR) and the risk for <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	25710844	A meta analysis of the associations between the <strong>SLC6A4</strong> promoter polymorphism (5HTTLPR) and the risk for alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	25710844	A meta analysis of the associations between the <strong>SLC6A4</strong> promoter polymorphism (<strong>5HTTLPR</strong>) and the risk for <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	25710844	A meta analysis of the associations between the <strong>SLC6A4</strong> promoter polymorphism (<strong>5HTTLPR</strong>) and the risk for alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	25710844	It is plausible that variations in genetically determined <strong>SLC6A4</strong> activity may modify the risk for <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	25710844	It is plausible that variations in genetically determined <strong>SLC6A4</strong> activity may modify the risk for alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	25710844	Overall, the results did not support an association between <b>alcohol</b> dependence and the <strong>SLC6A4</strong> promoter polymorphism for the dominant, recessive, and additive genetic risk models, respectively [odds ratio (OR)=0.99 (95% confidence interval (CI): 0.83, 1.18), OR=0.86 (95% CI: 0.71, 1.03), and OR=0.88 (95% CI: 0.69, 1.13)].
+SLC6A4	addiction	dependence	25710844	Overall, the results did not support an association between alcohol <b>dependence</b> and the <strong>SLC6A4</strong> promoter polymorphism for the dominant, recessive, and additive genetic risk models, respectively [odds ratio (OR)=0.99 (95% confidence interval (CI): 0.83, 1.18), OR=0.86 (95% CI: 0.71, 1.03), and OR=0.88 (95% CI: 0.69, 1.13)].
+SLC6A4	drug	alcohol	25710844	The findings in this meta analysis suggest that the <strong>SLC6A4</strong> promoter polymorphism is not associated with <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	25710844	The findings in this meta analysis suggest that the <strong>SLC6A4</strong> promoter polymorphism is not associated with alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	25656446	Changes in the methylation status of DAT, <strong>SERT</strong>, and MeCP2 gene promoters in the blood cell in families exposed to <b>alcohol</b> during the periconceptional period.
+SLC6A4	drug	alcohol	25656446	These findings suggest that periconceptional <b>alcohol</b> intake may cause epigenetic changes in specific locus of parental and newborn genomes as follows: <b>Alcohol</b> consumption decreases the methylation level of the DAT promoter region of the parent themselves, maternal <b>alcohol</b> drinking during the periconceptional period decreases the methylation level of the <strong>SERT</strong> promoter region of newborns, and maternal <b>alcohol</b> consumption increases the methylation level of the MeCP2 promoter region of newborns.
+SLC6A4	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and <strong>SLC6A4</strong>), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+SLC6A4	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and <strong>SLC6A4</strong>), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+SLC6A4	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and <strong>SLC6A4</strong>), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+SLC6A4	drug	amphetamine	25485646	The present experiments examined serotonergic roles in <b>METH</b> induced locomotor sensitization by assessing: (a) the effect of serotonin transporter (SERT; <strong>Slc6A4</strong>) knockout (KO) on <b>METH</b> induced locomotor sensitization; (b) extracellular monoamine levels in <b>METH</b> treated animals as determined by in vivo microdialysis; and (c) effects of serotonin (5 HT) receptor antagonists on <b>METH</b> induced behavioral sensitization, with focus on effects of the 5 HT1B receptor antagonist SB 216641 and a comparison with the 5 HT2 receptor antagonist ketanserin.
+SLC6A4	addiction	sensitization	25485646	The present experiments examined serotonergic roles in METH induced locomotor <b>sensitization</b> by assessing: (a) the effect of serotonin transporter (SERT; <strong>Slc6A4</strong>) knockout (KO) on METH induced locomotor <b>sensitization</b>; (b) extracellular monoamine levels in METH treated animals as determined by in vivo microdialysis; and (c) effects of serotonin (5 HT) receptor antagonists on METH induced behavioral <b>sensitization</b>, with focus on effects of the 5 HT1B receptor antagonist SB 216641 and a comparison with the 5 HT2 receptor antagonist ketanserin.
+SLC6A4	drug	amphetamine	25485646	The present experiments examined serotonergic roles in <b>METH</b> induced locomotor sensitization by assessing: (a) the effect of serotonin transporter (<strong>SERT</strong>; <strong>Slc6A4</strong>) knockout (KO) on <b>METH</b> induced locomotor sensitization; (b) extracellular monoamine levels in <b>METH</b> treated animals as determined by in vivo microdialysis; and (c) effects of serotonin (5 HT) receptor antagonists on <b>METH</b> induced behavioral sensitization, with focus on effects of the 5 HT1B receptor antagonist SB 216641 and a comparison with the 5 HT2 receptor antagonist ketanserin.
+SLC6A4	addiction	sensitization	25485646	The present experiments examined serotonergic roles in METH induced locomotor <b>sensitization</b> by assessing: (a) the effect of serotonin transporter (<strong>SERT</strong>; <strong>Slc6A4</strong>) knockout (KO) on METH induced locomotor <b>sensitization</b>; (b) extracellular monoamine levels in METH treated animals as determined by in vivo microdialysis; and (c) effects of serotonin (5 HT) receptor antagonists on METH induced behavioral <b>sensitization</b>, with focus on effects of the 5 HT1B receptor antagonist SB 216641 and a comparison with the 5 HT2 receptor antagonist ketanserin.
+SLC6A4	drug	amphetamine	25485646	Repeated <b>METH</b> administration failed to induce behavioral sensitization in homozygous <strong>SERT</strong> KO (<strong>SERT</strong> / ) mice under conditions that produced substantial sensitization in wild type or heterozygous <strong>SERT</strong> KO (<strong>SERT</strong>+/ ) mice.
+SLC6A4	addiction	sensitization	25485646	Repeated METH administration failed to induce behavioral <b>sensitization</b> in homozygous <strong>SERT</strong> KO (<strong>SERT</strong> / ) mice under conditions that produced substantial <b>sensitization</b> in wild type or heterozygous <strong>SERT</strong> KO (<strong>SERT</strong>+/ ) mice.
+SLC6A4	drug	amphetamine	25485646	The selective 5 HT1B antagonist receptor SB 216641 restored <b>METH</b> induced locomotor sensitization in <strong>SERT</strong> /  mice, whereas ketanserin was ineffective.
+SLC6A4	addiction	sensitization	25485646	The selective 5 HT1B antagonist receptor SB 216641 restored METH induced locomotor <b>sensitization</b> in <strong>SERT</strong> /  mice, whereas ketanserin was ineffective.
+SLC6A4	drug	amphetamine	25485646	<b>METH</b> induced increases in extracellular 5 HT (5 HTex) levels were substantially reduced in <strong>SERT</strong> /  mice, although <strong>SERT</strong> genotype had no effect on <b>METH</b> induced increases in extracellular dopamine.
+SLC6A4	drug	alcohol	25294733	Interaction effects between the 5 hydroxy tryptamine transporter linked polymorphic region (<strong>5 HTTLPR</strong>) genotype and family conflict on adolescent <b>alcohol</b> use and misuse.
+SLC6A4	drug	alcohol	25294733	A significant gene environment interaction on <b>alcohol</b> misuse at time 1 was found in both sample 1 (β = 0.57, P = 0.001) and sample 2 (β = 0.19, P = 0.01), indicating that the <strong>5 HTTLPR</strong> low activity allele carriers exposed to higher levels of family conflict were more likely to engage in <b>alcohol</b> misuse than non carriers.
+SLC6A4	drug	alcohol	25294733	Compared with non carriers, adolescents carrying the <strong>5 HTTLPR</strong> low activity allele are more susceptible to the effects of family conflict on <b>alcohol</b> misuse.
+SLC6A4	drug	alcohol	25285331	Amygdala Volume in Offspring from Multiplex for <b>Alcohol</b> Dependence Families: The Moderating Influence of Childhood Environment and <strong>5 HTTLPR</strong> Variation.
+SLC6A4	addiction	dependence	25285331	Amygdala Volume in Offspring from Multiplex for Alcohol <b>Dependence</b> Families: The Moderating Influence of Childhood Environment and <strong>5 HTTLPR</strong> Variation.
+SLC6A4	drug	alcohol	25212749	Ondansetron and sertraline may interact with <strong>5 HTTLPR</strong> and DRD4 polymorphisms to reduce drinking in non treatment seeking <b>alcohol</b> dependent women: exploratory findings.
+SLC6A4	addiction	relapse	25212749	Ondansetron and sertraline may interact with <strong>5 HTTLPR</strong> and DRD4 polymorphisms to reduce drinking in non treatment <b>seeking</b> alcohol dependent women: exploratory findings.
+SLC6A4	drug	alcohol	25212749	The purpose of this exploratory study was to examine the interaction of <strong>5 HTTLPR</strong> and DRD4 exon III polymorphisms with gender in non treatment seeking <b>alcohol</b> dependent (AD) individuals while alternately taking ondansetron and sertraline.
+SLC6A4	addiction	relapse	25212749	The purpose of this exploratory study was to examine the interaction of <strong>5 HTTLPR</strong> and DRD4 exon III polymorphisms with gender in non treatment <b>seeking</b> alcohol dependent (AD) individuals while alternately taking ondansetron and sertraline.
+SLC6A4	drug	alcohol	25072039	Meta analyses suggest that the serotonin transporter linked polymorphic region (<strong>5 HTTLPR</strong>) short (S) allele, relative to the long (L) allele, is associated with risk for <b>alcohol</b> dependence, particularly among individuals with early onset antisocial <b>alcoholism</b>.
+SLC6A4	addiction	dependence	25072039	Meta analyses suggest that the serotonin transporter linked polymorphic region (<strong>5 HTTLPR</strong>) short (S) allele, relative to the long (L) allele, is associated with risk for alcohol <b>dependence</b>, particularly among individuals with early onset antisocial alcoholism.
+SLC6A4	drug	alcohol	25072039	However, <strong>5 HTTLPR</strong> genotype was associated with externalizing behaviors (S and LG > LALA), and externalizing behaviors predicted <b>alcohol</b> and marijuana problem severity at 6 month follow up.
+SLC6A4	drug	cannabinoid	25072039	However, <strong>5 HTTLPR</strong> genotype was associated with externalizing behaviors (S and LG > LALA), and externalizing behaviors predicted alcohol and <b>marijuana</b> problem severity at 6 month follow up.
+SLC6A4	drug	alcohol	25072039	Results indicated an indirect (p < 0.05) and non specific (i.e., both <b>alcohol</b> and marijuana severity) effect of <strong>5 HTTLPR</strong> genotype on youth substance use treatment outcomes, with externalizing behaviors as an important linking factor.
+SLC6A4	drug	cannabinoid	25072039	Results indicated an indirect (p < 0.05) and non specific (i.e., both alcohol and <b>marijuana</b> severity) effect of <strong>5 HTTLPR</strong> genotype on youth substance use treatment outcomes, with externalizing behaviors as an important linking factor.
+SLC6A4	drug	nicotine	24968820	<strong>SLC6A4</strong> STin2 VNTR genetic polymorphism is associated with <b>tobacco</b> use disorder, but not with successful <b>smoking</b> cessation or <b>smoking</b> characteristics: a case control study.
+SLC6A4	drug	nicotine	24968820	The aim of this study was to determine if variable number of tandem repeats (VNTR) in the second intron (STin2) of the serotonin transporter (<strong>SLC6A4</strong>) gene was associated with <b>tobacco</b> use disorder, successful <b>smoking</b> cessation, or <b>smoking</b> characteristics.
+SLC6A4	drug	amphetamine	24959862	We analyzed long term, off drug changes in learning from positive and negative feedback and associated striatal DA transporter (DAT) and frontocortical 5HT transporter (<strong>SERT</strong>) binding in rats pretreated with <b>methamphetamine</b> (mAMPH).
+SLC6A4	drug	cocaine	24950119	Although our data are consistent with <b>cocaine</b> acting through enhanced 5 HT signaling, the nonselective actions of <b>cocaine</b> as an antagonist of monoamine transporters raises the question of whether inhibition of the 5 HT transporter (<strong>SERT</strong>) is key to its circadian effects.
+SLC6A4	drug	cocaine	24950119	Here we investigate this issue using transgenic mice expressing a <strong>SERT</strong> that exhibits normal 5 HT recognition and transport but significantly reduced <b>cocaine</b> potency (<strong>SERT</strong> Met172).
+SLC6A4	drug	cocaine	24950119	However, (1) <b>cocaine</b> administration does not induce phase advances when administered in vivo or in vitro in <strong>SERT</strong> Met172 mice; (2) <b>cocaine</b> does not block photic or glutamate induced phase shifts in <strong>SERT</strong> Met172 mice; and (3) <b>cocaine</b> does not induce long term changes in free running period in <strong>SERT</strong> Met172 mice.
+SLC6A4	drug	cocaine	24950119	We conclude that <strong>SERT</strong> antagonism is required for the phase shifting of the SCN circadian clock induced by <b>cocaine</b>.
+SLC6A4	drug	alcohol	24946437	[The analysis of the polymorphic variations of the dopamine gen transporter (DAT1) and the serotonin transporter (<strong>5 HTTLPR</strong>) in patients with <b>alcohol</b> dependence syndrome with inclusion of the phenotypic feature of sweet liking preference].
+SLC6A4	addiction	dependence	24946437	[The analysis of the polymorphic variations of the dopamine gen transporter (DAT1) and the serotonin transporter (<strong>5 HTTLPR</strong>) in patients with alcohol <b>dependence</b> syndrome with inclusion of the phenotypic feature of sweet liking preference].
+SLC6A4	drug	cocaine	24871545	<b>Cocaine</b> acts as a blocker at the transporters for dopamine (DAT), serotonin (<strong>SERT</strong>), and norepinephrine (NET), but amphetamines are substrates that do not only block the uptake of monoamines but also induce substrate efflux by promoting reverse transport.
+SLC6A4	drug	cocaine	24837582	Using an imaging genetics approach, the current study tested in 62 <b>cocaine</b> abusers and 57 healthy controls the separate and combined effects of variations in the serotonin transporter (<strong>5 HTTLPR</strong>) and monoamine oxidase A (MAOA) genes on processing of aversive information.
+SLC6A4	addiction	aversion	24837582	Using an imaging genetics approach, the current study tested in 62 cocaine abusers and 57 healthy controls the separate and combined effects of variations in the serotonin transporter (<strong>5 HTTLPR</strong>) and monoamine oxidase A (MAOA) genes on processing of <b>aversive</b> information.
+SLC6A4	drug	alcohol	24794154	The role of <strong>5 HTTLPR</strong> polymorphism in <b>alcohol</b> craving experience.
+SLC6A4	addiction	relapse	24794154	The role of <strong>5 HTTLPR</strong> polymorphism in alcohol <b>craving</b> experience.
+SLC6A4	drug	alcohol	24794154	The authors sought to clarify the extent to which <b>alcohol</b> craving could be predicted by a relevant polymorphism in the promoter region of the gene encoding the 5 HT transporter (<strong>5 HTTLPR</strong>).
+SLC6A4	addiction	relapse	24794154	The authors sought to clarify the extent to which alcohol <b>craving</b> could be predicted by a relevant polymorphism in the promoter region of the gene encoding the 5 HT transporter (<strong>5 HTTLPR</strong>).
+SLC6A4	drug	alcohol	24794154	No <strong>5 HTTLPR</strong> genotype effects were observed on <b>alcohol</b> craving experience in a sample of <b>alcohol</b> dependent outpatients.
+SLC6A4	addiction	relapse	24794154	No <strong>5 HTTLPR</strong> genotype effects were observed on alcohol <b>craving</b> experience in a sample of alcohol dependent outpatients.
+SLC6A4	drug	psychedelics	24752593	Intermittent <b>MDMA</b> pretreatment blocked the reductions in serotonin transporter (<strong>SERT</strong>) binding induced by an <b>MDMA</b> binge in a prior study in adolescent male rats.
+SLC6A4	addiction	intoxication	24752593	Intermittent MDMA pretreatment blocked the reductions in serotonin transporter (<strong>SERT</strong>) binding induced by an MDMA <b>binge</b> in a prior study in adolescent male rats.
+SLC6A4	drug	psychedelics	24752593	Similarly, <b>MDMA</b> pretreated animals were resistant to the binge induced <strong>SERT</strong> reductions, especially in the hippocampus.
+SLC6A4	addiction	intoxication	24752593	Similarly, MDMA pretreated animals were resistant to the <b>binge</b> induced <strong>SERT</strong> reductions, especially in the hippocampus.
+SLC6A4	drug	amphetamine	24650575	Preclinical studies suggest that prior treatment with escalating doses of <b>methamphetamine</b> (<b>METH</b>) attenuates the persistent deficits in hippocampal serotonin (5 hydroxytryptamine; 5HT) transporter (<strong>SERT</strong>) function resulting from a subsequent 'binge' <b>METH</b> exposure.
+SLC6A4	addiction	intoxication	24650575	Preclinical studies suggest that prior treatment with escalating doses of methamphetamine (METH) attenuates the persistent deficits in hippocampal serotonin (5 hydroxytryptamine; 5HT) transporter (<strong>SERT</strong>) function resulting from a subsequent '<b>binge</b>' METH exposure.
+SLC6A4	drug	amphetamine	24650575	The current study investigated changes in hippocampal BDNF protein and <strong>SERT</strong> function in rats exposed to saline or <b>METH</b> self administration prior to a binge exposure to <b>METH</b> or saline.
+SLC6A4	addiction	intoxication	24650575	The current study investigated changes in hippocampal BDNF protein and <strong>SERT</strong> function in rats exposed to saline or METH self administration prior to a <b>binge</b> exposure to METH or saline.
+SLC6A4	drug	amphetamine	24650575	Further, mBDNF immunoreactivity was increased and <strong>SERT</strong> function was not altered in rats that self administered <b>METH</b> prior to the binge <b>METH</b> exposure as assessed 24 h after the binge exposure.
+SLC6A4	addiction	intoxication	24650575	Further, mBDNF immunoreactivity was increased and <strong>SERT</strong> function was not altered in rats that self administered METH prior to the <b>binge</b> METH exposure as assessed 24 h after the <b>binge</b> exposure.
+SLC6A4	drug	amphetamine	24650575	These results suggest that prior exposure to contingent <b>METH</b> increases hippocampal mBDNF, and this may contribute to attenuated deficits in <strong>SERT</strong> function.
+SLC6A4	drug	alcohol	24590108	Previous studies have implicated genes encoding the 5 HT3AB receptors (HTR3A and HTR3B) and the serotonin transporter (<strong>SLC6A4</strong>), both independently and interactively, in <b>alcohol</b> (AD), cocaine (CD), and nicotine dependence (ND).
+SLC6A4	drug	cocaine	24590108	Previous studies have implicated genes encoding the 5 HT3AB receptors (HTR3A and HTR3B) and the serotonin transporter (<strong>SLC6A4</strong>), both independently and interactively, in alcohol (AD), <b>cocaine</b> (CD), and nicotine dependence (ND).
+SLC6A4	drug	nicotine	24590108	Previous studies have implicated genes encoding the 5 HT3AB receptors (HTR3A and HTR3B) and the serotonin transporter (<strong>SLC6A4</strong>), both independently and interactively, in alcohol (AD), cocaine (CD), and <b>nicotine</b> dependence (ND).
+SLC6A4	addiction	dependence	24590108	Previous studies have implicated genes encoding the 5 HT3AB receptors (HTR3A and HTR3B) and the serotonin transporter (<strong>SLC6A4</strong>), both independently and interactively, in alcohol (AD), cocaine (CD), and nicotine <b>dependence</b> (ND).
+SLC6A4	drug	nicotine	24590108	We used 1,136 African American (AA) and 2,428 European American (EA) subjects from the Study of Addiction: Genetics and Environment (SAGE) to determine associations between 88 genotyped or imputed variants within HTR3A, HTR3B, and <strong>SLC6A4</strong> and three types of addictions, which were measured by DSM IV diagnoses of AD, CD, and ND and the Fagerström Test for <b>Nicotine</b> Dependence (FTND), an independent measure of ND commonly used in <b>tobacco</b> research.
+SLC6A4	addiction	addiction	24590108	We used 1,136 African American (AA) and 2,428 European American (EA) subjects from the Study of <b>Addiction</b>: Genetics and Environment (SAGE) to determine associations between 88 genotyped or imputed variants within HTR3A, HTR3B, and <strong>SLC6A4</strong> and three types of addictions, which were measured by DSM IV diagnoses of AD, CD, and ND and the Fagerström Test for Nicotine Dependence (FTND), an independent measure of ND commonly used in tobacco research.
+SLC6A4	addiction	dependence	24590108	We used 1,136 African American (AA) and 2,428 European American (EA) subjects from the Study of Addiction: Genetics and Environment (SAGE) to determine associations between 88 genotyped or imputed variants within HTR3A, HTR3B, and <strong>SLC6A4</strong> and three types of addictions, which were measured by DSM IV diagnoses of AD, CD, and ND and the Fagerström Test for Nicotine <b>Dependence</b> (FTND), an independent measure of ND commonly used in tobacco research.
+SLC6A4	addiction	addiction	24590108	Interestingly, most of the SNPs included in the genetic interaction model(s) for each <b>addictive</b> phenotype are either overlapped or in high linkage disequilibrium for both AA and EA samples, suggesting these detected variants in HTR3A, HTR3B, and <strong>SLC6A4</strong> are interactively contributing to etiology of the three <b>addictive</b> phenotypes examined in this study.
+SLC6A4	drug	cocaine	24525654	This study's aim was to determine if treatment with sertraline (<strong>SERT</strong>) or <strong>SERT</strong> plus gabapentin (GBP) improved treatment retention, depressive symptoms, and/or <b>cocaine</b> use.
+SLC6A4	drug	cocaine	24525654	Sertraline, but not <strong>SERT</strong> plus GBP, showed a significantly lower overall percentage of <b>cocaine</b> positive urine samples compared with that of PLA.
+SLC6A4	addiction	relapse	24525654	A significantly greater percentage of participants experienced <b>relapse</b> in the PLA group (88.9%) compared with that of the <strong>SERT</strong> group (65.2%).
+SLC6A4	drug	cocaine	24525654	Sertraline plus GBP may not be superior to <strong>SERT</strong> alone in delaying relapse among abstinent <b>cocaine</b> dependent individuals undergoing cognitive behavioral therapy.
+SLC6A4	addiction	relapse	24525654	Sertraline plus GBP may not be superior to <strong>SERT</strong> alone in delaying <b>relapse</b> among abstinent cocaine dependent individuals undergoing cognitive behavioral therapy.
+SLC6A4	addiction	reward	24486525	m <b>CPP</b> and TFMPP interacted with the <strong>SERT</strong> and serotonergic receptors.
+SLC6A4	drug	alcohol	24408213	Serotonin transporter gene promoter polymorphism (<strong>5 HTTLPR</strong>) and <b>alcohol</b> use in general population: interaction effect with birth cohort.
+SLC6A4	drug	alcohol	24408213	The common genetic variation <strong>5 HTTLPR</strong> (serotonin transporter gene linked polymorphic region) has been related to several aspects of <b>alcohol</b> use and addiction but with mixed results, probably due to different environmental interaction effects.
+SLC6A4	addiction	addiction	24408213	The common genetic variation <strong>5 HTTLPR</strong> (serotonin transporter gene linked polymorphic region) has been related to several aspects of alcohol use and <b>addiction</b> but with mixed results, probably due to different environmental interaction effects.
+SLC6A4	drug	alcohol	24408213	We aimed at assessing whether the association between <b>alcohol</b> use and <strong>5 HTTLPR</strong> genotype is subject to cohort effects as birth cohorts may be raised in significantly different environments.
+SLC6A4	drug	alcohol	24408213	In males, there was no significant cohort × genotype interaction, but the <strong>5 HTTLPR</strong> genotype was associated with <b>alcohol</b> use, the s/s subjects reporting the highest consumption.
+SLC6A4	drug	alcohol	24408213	The <strong>5 HTTLPR</strong> genotype is associated with <b>alcohol</b> consumption in general population, but the effect depends on gender and birth cohort.
+SLC6A4	drug	opioid	24368617	Genetic polymorphisms in the coding or promoter regions of the Mu <b>Opioid</b> Receptor (OPRM1), Corticotropin Releasing Hormone (CRH), Monoamine Oxidase A (MAOA), Dopamine D4 Receptor (DRD4), and Serotonin Transporter (<strong>SLC6A4</strong>) genes have been shown to be functionally similar in humans and rhesus macaques and have been demonstrated to contribute to individual differences in aggression.
+SLC6A4	addiction	addiction	24307794	All illicit drug users (IDUs) visited a Territorial <b>Addiction</b> Service (<strong>SerT</strong>) in the District of Brescia, and hepatitis C antibody (HCVAb) testing positive were offered as part of a standardised hepatologic visit in our Gastroenterology Unit.
+SLC6A4	drug	alcohol	24220019	Genetic analyses of the level of response to <b>alcohol</b>, particularly of the functional OPRM1 A118G polymorphism and 5' and 3' functional polymorphisms in <strong>SLC6A4</strong>, are beginning to provide insights into the etiology of <b>alcoholism</b> and also genotype stratified subgroup responses to <b>naltrexone</b> and SSRIs/ondansetron respectively.
+SLC6A4	addiction	addiction	24152087	The alleles of the rs2180619 are A > G; the G allele has been associated with <b>addiction</b> and high levels of anxiety (when the G allele interacts with the SS genotype of the <strong>5 HTTLPR</strong> gene).
+SLC6A4	drug	nicotine	24127329	The aim of this study was to evaluate the association between the effectiveness of treatment with <b>nicotine</b> or bupropion in heavy <b>smokers</b> (n=70), and 6 candidate polymorphisms in CYP2A6, <strong>5 HTT</strong> and HTR2A genes.
+SLC6A4	drug	nicotine	24127329	Analysis revealed a significant association between "favourable" genotype combination carriers (CYP2A6 "slow metabolizer" or <strong>5HTT</strong> L allele or HTR2A 1438GG) and <b>nicotine</b> treatment outcome (OR=2.69, 95% CI=1.28 5.64).
+SLC6A4	drug	alcohol	24068519	<strong>5 HTT</strong> SS genotype is associated with the pro nociceptive sensation by <b>alcoholic</b> sting.
+SLC6A4	drug	alcohol	24068519	The results suggest that the human triallelic <strong>5 HTT</strong> genotypes are related to individual differences in sensitivity to <b>alcoholic</b> sting.
+SLC6A4	addiction	sensitization	24068519	Taken together, our study supports the hypothesis that the transcription rate of the <strong>5 HTT</strong> transporter may play an important role in the pain sensitivity and central <b>sensitization</b>.
+SLC6A4	drug	alcohol	23927813	To examine the relationship between <strong>SERT</strong> genotype and motivation for <b>alcohol</b>, we compared <b>ethanol</b> self administration in mice with zero (knockout, KO), one (HET) or two copies (WT) of the <strong>SERT</strong> gene.
+SLC6A4	drug	alcohol	23897038	The authors previously reported that the 5' HTTLPR LL and rs1042173 TT (<strong>SLC6A4</strong> LL/TT) genotypes in the serotonin transporter gene predicted a significant reduction in the severity of <b>alcohol</b> consumption among <b>alcoholics</b> receiving the 5 HT3 antagonist ondansetron.
+SLC6A4	drug	amphetamine	23798435	We tested the effects of the verified scarcity of PIP2 on <b>amphetamine</b> triggered <strong>SERT</strong> functions in human cells.
+SLC6A4	drug	amphetamine	23798435	Mutation of the latter resulted in a loss of <b>amphetamine</b> induced <strong>SERT</strong> mediated efflux and currents, as well as a lack of PIP2 dependent effects.
+SLC6A4	drug	amphetamine	23798435	These results open the way to target <b>amphetamine</b> induced <strong>SERT</strong> dependent actions independently of normal <strong>SERT</strong> function and thus to treat psychostimulant addiction.
+SLC6A4	addiction	addiction	23798435	These results open the way to target amphetamine induced <strong>SERT</strong> dependent actions independently of normal <strong>SERT</strong> function and thus to treat psychostimulant <b>addiction</b>.
+SLC6A4	drug	alcohol	23757001	On the basis of the converging evidence showing regulation of drinking behavior by 5 HT3AB receptors and the serotonin transporter, we hypothesized that the interactive effects of genetic variations in the genes HTR3A, HTR3B, and <strong>SLC6A4</strong> confer greater susceptibility to <b>alcohol</b> dependence (AD) than do their effects individually.
+SLC6A4	addiction	dependence	23757001	On the basis of the converging evidence showing regulation of drinking behavior by 5 HT3AB receptors and the serotonin transporter, we hypothesized that the interactive effects of genetic variations in the genes HTR3A, HTR3B, and <strong>SLC6A4</strong> confer greater susceptibility to alcohol <b>dependence</b> (AD) than do their effects individually.
+SLC6A4	drug	alcohol	23739600	Genetic variation in the µ opioid receptor (OPRM1) and the serotonin transporter (<strong>5 HTTLPR</strong>) appear to be associated with treatment outcomes for <b>naltrexone</b> and ondansetron, respectively.
+SLC6A4	drug	opioid	23739600	Genetic variation in the µ <b>opioid</b> receptor (OPRM1) and the serotonin transporter (<strong>5 HTTLPR</strong>) appear to be associated with treatment outcomes for naltrexone and ondansetron, respectively.
+SLC6A4	drug	alcohol	23685324	Association between DRD2, <strong>5 HTTLPR</strong>, and ALDH2 genes and specific personality traits in <b>alcohol</b>  and opiate dependent patients.
+SLC6A4	drug	alcohol	23685324	We concluded that addicts, both <b>alcohol</b>  and opiate dependent patients, have common genetic variants in DRD2 and <strong>5 HTTLPR</strong> but specific for ALDH2.
+SLC6A4	drug	alcohol	23518607	A number of studies have reported associations between the serotonin transporter gene (<strong>SLC6A4</strong>) and <b>alcohol</b>, heroin, cocaine, or methamphetamine abuse.
+SLC6A4	drug	amphetamine	23518607	A number of studies have reported associations between the serotonin transporter gene (<strong>SLC6A4</strong>) and alcohol, heroin, cocaine, or <b>methamphetamine</b> abuse.
+SLC6A4	drug	cocaine	23518607	A number of studies have reported associations between the serotonin transporter gene (<strong>SLC6A4</strong>) and alcohol, heroin, <b>cocaine</b>, or methamphetamine abuse.
+SLC6A4	drug	opioid	23518607	A number of studies have reported associations between the serotonin transporter gene (<strong>SLC6A4</strong>) and alcohol, <b>heroin</b>, cocaine, or methamphetamine abuse.
+SLC6A4	drug	alcohol	23518607	The meta analyses support the associations of <strong>5 HTTLPR</strong> with <b>alcohol</b>, heroin, cocaine, and methamphetamine dependence and abuse (eg, the smallest P values were 0.0058 with odds ratio (OR)=0.54 (0.35, 0.84); 0.0024 with OR=0.77 (0.66, 0.91); 0.018 with OR=1.38 (1.06, 1.81); and 0.028 with OR=0.46 (0.23, 0.92) for <b>alcohol</b>, heroin, cocaine, and methamphetamine dependence/abuse, respectively).
+SLC6A4	drug	amphetamine	23518607	The meta analyses support the associations of <strong>5 HTTLPR</strong> with alcohol, heroin, cocaine, and <b>methamphetamine</b> dependence and abuse (eg, the smallest P values were 0.0058 with odds ratio (OR)=0.54 (0.35, 0.84); 0.0024 with OR=0.77 (0.66, 0.91); 0.018 with OR=1.38 (1.06, 1.81); and 0.028 with OR=0.46 (0.23, 0.92) for alcohol, heroin, cocaine, and <b>methamphetamine</b> dependence/abuse, respectively).
+SLC6A4	drug	cocaine	23518607	The meta analyses support the associations of <strong>5 HTTLPR</strong> with alcohol, heroin, <b>cocaine</b>, and methamphetamine dependence and abuse (eg, the smallest P values were 0.0058 with odds ratio (OR)=0.54 (0.35, 0.84); 0.0024 with OR=0.77 (0.66, 0.91); 0.018 with OR=1.38 (1.06, 1.81); and 0.028 with OR=0.46 (0.23, 0.92) for alcohol, heroin, <b>cocaine</b>, and methamphetamine dependence/abuse, respectively).
+SLC6A4	drug	opioid	23518607	The meta analyses support the associations of <strong>5 HTTLPR</strong> with alcohol, <b>heroin</b>, cocaine, and methamphetamine dependence and abuse (eg, the smallest P values were 0.0058 with odds ratio (OR)=0.54 (0.35, 0.84); 0.0024 with OR=0.77 (0.66, 0.91); 0.018 with OR=1.38 (1.06, 1.81); and 0.028 with OR=0.46 (0.23, 0.92) for alcohol, <b>heroin</b>, cocaine, and methamphetamine dependence/abuse, respectively).
+SLC6A4	addiction	dependence	23518607	The meta analyses support the associations of <strong>5 HTTLPR</strong> with alcohol, heroin, cocaine, and methamphetamine <b>dependence</b> and abuse (eg, the smallest P values were 0.0058 with odds ratio (OR)=0.54 (0.35, 0.84); 0.0024 with OR=0.77 (0.66, 0.91); 0.018 with OR=1.38 (1.06, 1.81); and 0.028 with OR=0.46 (0.23, 0.92) for alcohol, heroin, cocaine, and methamphetamine <b>dependence</b>/abuse, respectively).
+SLC6A4	addiction	reward	23336089	Likewise, voting, voting turnout and attachment to a particular political ideology is differentially related to various <b>reward</b> genes (e.g., <strong>5HTT</strong>, MOA, DRD2, and DRD4), possibly predicting liberalism or conservatism.
+SLC6A4	drug	psychedelics	23318273	Recent studies have demonstrated that a preconditioning regimen (i.e., repeated low doses) of <b>MDMA</b> provides protection against the reductions in tissue concentrations of 5 HT and 5 HT transporter (<strong>SERT</strong>) density and/or expression produced by a subsequent binge regimen of <b>MDMA</b>.
+SLC6A4	addiction	intoxication	23318273	Recent studies have demonstrated that a preconditioning regimen (i.e., repeated low doses) of MDMA provides protection against the reductions in tissue concentrations of 5 HT and 5 HT transporter (<strong>SERT</strong>) density and/or expression produced by a subsequent <b>binge</b> regimen of MDMA.
+SLC6A4	drug	psychedelics	23318273	In the present study, the effects of preconditioning and binge treatment regimens of <b>MDMA</b> on <strong>SERT</strong> function were assessed by synaptosomal 5 HT uptake.
+SLC6A4	addiction	intoxication	23318273	In the present study, the effects of preconditioning and <b>binge</b> treatment regimens of MDMA on <strong>SERT</strong> function were assessed by synaptosomal 5 HT uptake.
+SLC6A4	drug	psychedelics	23318273	The distribution of <strong>SERT</strong> immunoreactivity (ir) in membrane and endosomal fractions of the hippocampus also was evaluated following the preconditioning regimen of <b>MDMA</b>.
+SLC6A4	drug	psychedelics	23318273	The results demonstrate that <strong>SERT</strong> function is transiently reduced in response to a preconditioning regimen of <b>MDMA</b>, while long term reductions in <strong>SERT</strong> function occur in response to a binge regimen of <b>MDMA</b>.
+SLC6A4	addiction	intoxication	23318273	The results demonstrate that <strong>SERT</strong> function is transiently reduced in response to a preconditioning regimen of MDMA, while long term reductions in <strong>SERT</strong> function occur in response to a <b>binge</b> regimen of MDMA.
+SLC6A4	drug	psychedelics	23318273	Moreover, a preconditioning regimen of <b>MDMA</b> provides protection against the long term reductions in <strong>SERT</strong> function evoked by a subsequent binge regimen of the drug.
+SLC6A4	addiction	intoxication	23318273	Moreover, a preconditioning regimen of MDMA provides protection against the long term reductions in <strong>SERT</strong> function evoked by a subsequent <b>binge</b> regimen of the drug.
+SLC6A4	drug	psychedelics	23318273	It is tempting to speculate that the neuroprotective effect of <b>MDMA</b> preconditioning results from a transient down regulation in <strong>SERT</strong> function.
+SLC6A4	drug	nicotine	23290502	Pharmacologic studies implicate a significant role of genes encoding the serotonin transporter (<strong>SLC6A4</strong>) and the 5 HT3AB subunits HTR3A and HTR3B in <b>nicotine</b> dependence (ND).
+SLC6A4	addiction	dependence	23290502	Pharmacologic studies implicate a significant role of genes encoding the serotonin transporter (<strong>SLC6A4</strong>) and the 5 HT3AB subunits HTR3A and HTR3B in nicotine <b>dependence</b> (ND).
+SLC6A4	drug	alcohol	23287538	This vulnerability to <b>ethanol</b> abuse was associated with a lower c Fos immunoreactivity in the Nac and enduring alterations of the expression of Penk and <strong>Slc6a4</strong>, 2 neurotransmission related genes that have been shown to play critical roles in the behavioral effects of <b>ethanol</b> and <b>alcoholism</b>.
+SLC6A4	drug	psychedelics	24648791	Animal studies have demonstrated that high doses of <b>MDMA</b> can lead to long term decreases in forebrain 5 HT concentrations, tryptophan hydroxylase activity, serotonin transporter (<strong>SERT</strong>) expression, and visualization of axons immunoreactive for 5 HT or <strong>SERT</strong>.
+SLC6A4	drug	psychedelics	24648791	Possible neurotoxicity in heavy <b>ecstasy</b> users has been revealed by neuroimaging studies showing reduced <strong>SERT</strong> binding and increased 5 HT2A receptor binding in several cortical and/or subcortical areas.
+SLC6A4	drug	alcohol	23262301	anxiety, family history and onset of <b>alcoholism</b>, and D4 dopamine receptor (DRD4) and <strong>5 HTTLPR</strong> polymorphisms.
+SLC6A4	drug	alcohol	23262301	Yet, baclofen's effects on <b>alcohol</b> consumption were also moderated by <strong>5 HTTLPR</strong> LL genotype.
+SLC6A4	drug	cocaine	23223282	Activation of the dynorphin/κ opioid receptor (KOR) system by repeated stress exposure or agonist treatment produces place aversion, social avoidance, and reinstatement of extinguished <b>cocaine</b> place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (SERT, <strong>SLC6A4</strong>) to the synaptic terminals of serotonergic neurons.
+SLC6A4	drug	opioid	23223282	Activation of the dynorphin/κ <b>opioid</b> receptor (KOR) system by repeated stress exposure or agonist treatment produces place aversion, social avoidance, and reinstatement of extinguished cocaine place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (SERT, <strong>SLC6A4</strong>) to the synaptic terminals of serotonergic neurons.
+SLC6A4	addiction	aversion	23223282	Activation of the dynorphin/κ opioid receptor (KOR) system by repeated stress exposure or agonist treatment produces place <b>aversion</b>, social avoidance, and reinstatement of extinguished cocaine place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (SERT, <strong>SLC6A4</strong>) to the synaptic terminals of serotonergic neurons.
+SLC6A4	addiction	relapse	23223282	Activation of the dynorphin/κ opioid receptor (KOR) system by repeated stress exposure or agonist treatment produces place aversion, social avoidance, and <b>reinstatement</b> of extinguished cocaine place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (SERT, <strong>SLC6A4</strong>) to the synaptic terminals of serotonergic neurons.
+SLC6A4	drug	cocaine	23223282	Activation of the dynorphin/κ opioid receptor (KOR) system by repeated stress exposure or agonist treatment produces place aversion, social avoidance, and reinstatement of extinguished <b>cocaine</b> place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (<strong>SERT</strong>, <strong>SLC6A4</strong>) to the synaptic terminals of serotonergic neurons.
+SLC6A4	drug	opioid	23223282	Activation of the dynorphin/κ <b>opioid</b> receptor (KOR) system by repeated stress exposure or agonist treatment produces place aversion, social avoidance, and reinstatement of extinguished cocaine place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (<strong>SERT</strong>, <strong>SLC6A4</strong>) to the synaptic terminals of serotonergic neurons.
+SLC6A4	addiction	aversion	23223282	Activation of the dynorphin/κ opioid receptor (KOR) system by repeated stress exposure or agonist treatment produces place <b>aversion</b>, social avoidance, and reinstatement of extinguished cocaine place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (<strong>SERT</strong>, <strong>SLC6A4</strong>) to the synaptic terminals of serotonergic neurons.
+SLC6A4	addiction	relapse	23223282	Activation of the dynorphin/κ opioid receptor (KOR) system by repeated stress exposure or agonist treatment produces place aversion, social avoidance, and <b>reinstatement</b> of extinguished cocaine place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (<strong>SERT</strong>, <strong>SLC6A4</strong>) to the synaptic terminals of serotonergic neurons.
+SLC6A4	addiction	aversion	23223282	In addition, <strong>SERT</strong> knock out mice did not show KOR mediated <b>aversion</b>, and selective reexpression of <strong>SERT</strong> by lentiviral injection into the dorsal raphe restored the prodepressive effects of KOR activation.
+SLC6A4	drug	alcohol	23145795	We previously reported moderating effects of age of onset of <b>alcohol</b> dependence (AD) and a functional polymorphism (<strong>5 HTTLPR</strong>) in the gene encoding the serotonin transporter protein in a sample of 134 individuals participating in a 12 week, placebo controlled trial of sertraline.
+SLC6A4	addiction	dependence	23145795	We previously reported moderating effects of age of onset of alcohol <b>dependence</b> (AD) and a functional polymorphism (<strong>5 HTTLPR</strong>) in the gene encoding the serotonin transporter protein in a sample of 134 individuals participating in a 12 week, placebo controlled trial of sertraline.
+SLC6A4	drug	psychedelics	23019496	Drugs of abuse such as <b>MDMA</b> (streetname "<b>ecstasy</b>") and certain 1 phenyl piperazine (PP) analogs such as 1 (3 chlorophenyl) piperazine (mCPP) elicit their stimulatory effect by elevating the synaptic concentration of serotonin by blocking or reversing the normal transport activity of <strong>hSERT</strong>.
+SLC6A4	drug	psychedelics	23019496	Little is still known about the precise mechanism by which <b>MDMA</b> and PP analogs function at <strong>hSERT</strong>, hDAT, and hNET and even less is known about the specific protein ligand interactions.
+SLC6A4	drug	alcohol	22933845	The 5 HT transporter linked polymorphic region S allele, located in <strong>SLC6A4</strong>, has now been modestly associated with <b>alcohol</b> dependence in two large meta analyses.
+SLC6A4	addiction	dependence	22933845	The 5 HT transporter linked polymorphic region S allele, located in <strong>SLC6A4</strong>, has now been modestly associated with alcohol <b>dependence</b> in two large meta analyses.
+SLC6A4	drug	alcohol	22925276	Modifying the role of serotonergic <strong>5 HTTLPR</strong> and TPH2 variants on <b>disulfiram</b> treatment of cocaine addiction: a preliminary study.
+SLC6A4	drug	cocaine	22925276	Modifying the role of serotonergic <strong>5 HTTLPR</strong> and TPH2 variants on disulfiram treatment of <b>cocaine</b> addiction: a preliminary study.
+SLC6A4	addiction	addiction	22925276	Modifying the role of serotonergic <strong>5 HTTLPR</strong> and TPH2 variants on disulfiram treatment of cocaine <b>addiction</b>: a preliminary study.
+SLC6A4	drug	alcohol	22925276	<b>Disulfiram</b> is a cocaine pharmacotherapy that may act through increasing serotonin, benefiting patients with genetically low serotonin transporter levels (<strong>5 HTTLPR</strong>, S' allele carriers) and low serotonin synthesis (TPH2, A allele carriers).
+SLC6A4	drug	cocaine	22925276	Disulfiram is a <b>cocaine</b> pharmacotherapy that may act through increasing serotonin, benefiting patients with genetically low serotonin transporter levels (<strong>5 HTTLPR</strong>, S' allele carriers) and low serotonin synthesis (TPH2, A allele carriers).
+SLC6A4	drug	alcohol	22925276	We genotyped the <strong>SLC6A4</strong> 5 HTTLPR (rs4795541, rs25531) and TPH2 1125A>T (rs4290270) variants and evaluated their role in moderating <b>disulfiram</b> treatment for cocaine dependence.
+SLC6A4	drug	cocaine	22925276	We genotyped the <strong>SLC6A4</strong> 5 HTTLPR (rs4795541, rs25531) and TPH2 1125A>T (rs4290270) variants and evaluated their role in moderating disulfiram treatment for <b>cocaine</b> dependence.
+SLC6A4	addiction	dependence	22925276	We genotyped the <strong>SLC6A4</strong> 5 HTTLPR (rs4795541, rs25531) and TPH2 1125A>T (rs4290270) variants and evaluated their role in moderating disulfiram treatment for cocaine <b>dependence</b>.
+SLC6A4	drug	alcohol	22925276	We genotyped the <strong>SLC6A4</strong> <strong>5 HTTLPR</strong> (rs4795541, rs25531) and TPH2 1125A>T (rs4290270) variants and evaluated their role in moderating <b>disulfiram</b> treatment for cocaine dependence.
+SLC6A4	drug	cocaine	22925276	We genotyped the <strong>SLC6A4</strong> <strong>5 HTTLPR</strong> (rs4795541, rs25531) and TPH2 1125A>T (rs4290270) variants and evaluated their role in moderating disulfiram treatment for <b>cocaine</b> dependence.
+SLC6A4	addiction	dependence	22925276	We genotyped the <strong>SLC6A4</strong> <strong>5 HTTLPR</strong> (rs4795541, rs25531) and TPH2 1125A>T (rs4290270) variants and evaluated their role in moderating disulfiram treatment for cocaine <b>dependence</b>.
+SLC6A4	drug	alcohol	22925276	Cocaine positive urines dropped from 78% to 54% for the <b>disulfiram</b> group and from 77% to 76% for the placebo group among the <strong>5 HTTLPR</strong> S' allele carriers (F = 16.2; df = 1,301; P < 0.0001).
+SLC6A4	drug	cocaine	22925276	<b>Cocaine</b> positive urines dropped from 78% to 54% for the disulfiram group and from 77% to 76% for the placebo group among the <strong>5 HTTLPR</strong> S' allele carriers (F = 16.2; df = 1,301; P < 0.0001).
+SLC6A4	addiction	reward	22916213	In mice treated with the higher doses of haloperidol and CGS an increase in <strong>SERT</strong> concentration in the striatum was detected during acquisition of the <b>CPP</b>, but no changes in DAT were observed.
+SLC6A4	drug	nicotine	22692335	Increased <b>smoking</b> habit was found for the SS genotype of <strong>5 HTT</strong>.
+SLC6A4	drug	amphetamine	22647900	<b>METH</b> self administration per se had no persistent effect on hippocampal 5HT content or <strong>SERT</strong> function.
+SLC6A4	drug	alcohol	22587755	A polymorphism in the serotonin transporter gene <strong>SLC6A4</strong> promoter region appears related to differential treatment response to sertraline depending on the subject's age of onset of <b>alcoholism</b>.
+SLC6A4	drug	alcohol	22557982	The current study investigated the effects of chronic <b>ethanol</b> self administration on hippocampal <strong>SERT</strong> in a layer and field specific manner using a monkey model of human <b>alcohol</b> consumption.
+SLC6A4	drug	alcohol	22557982	[(3)H]Citalopram was used to measure hippocampal <strong>SERT</strong> density in male cynomolgus macaques that voluntarily self administered <b>ethanol</b> for 18 months.
+SLC6A4	drug	alcohol	22557982	<strong>SERT</strong> density was not correlated with measures of <b>ethanol</b> consumption or blood <b>ethanol</b> concentrations, suggesting the possibility that a threshold level of consumption had been met.
+SLC6A4	drug	alcohol	22557982	The lower hippocampal <strong>SERT</strong> density observed suggests that chronic <b>ethanol</b> consumption is associated with altered serotonergic modulation of hippocampal neurotransmission.
+SLC6A4	drug	psychedelics	22451652	<b>Ibogaine</b>, a hallucinogenic alkaloid proposed as a treatment for opiate withdrawal, has been shown to inhibit serotonin transporter (<strong>SERT</strong>) noncompetitively, in contrast to all other known inhibitors, which are competitive with substrate.
+SLC6A4	addiction	withdrawal	22451652	Ibogaine, a hallucinogenic alkaloid proposed as a treatment for opiate <b>withdrawal</b>, has been shown to inhibit serotonin transporter (<strong>SERT</strong>) noncompetitively, in contrast to all other known inhibitors, which are competitive with substrate.
+SLC6A4	drug	psychedelics	22451652	<b>Ibogaine</b> binding to <strong>SERT</strong> increases accessibility in the permeation pathway connecting the substrate binding site with the cytoplasm.
+SLC6A4	drug	psychedelics	22451652	Because of the structural similarity between <b>ibogaine</b> and serotonin, it had been suggested that <b>ibogaine</b> binds to the substrate site of <strong>SERT</strong>.
+SLC6A4	drug	psychedelics	22451652	<b>Ibogaine</b> noncompetitively inhibited transport by both <strong>SERT</strong> and the homologous dopamine transporter (DAT).
+SLC6A4	drug	psychedelics	22451652	When present on the cell exterior, <b>ibogaine</b> inhibited <strong>SERT</strong> substrate induced currents, but not when it was introduced into the cytoplasm through the patch electrode.
+SLC6A4	drug	psychedelics	22451652	The kinetics of inhibitor binding and dissociation, as determined by their effect on <strong>SERT</strong> currents, indicated that <b>ibogaine</b> does not inhibit by forming a long lived complex with <strong>SERT</strong>, but rather binds directly to the transporter in an inward open conformation.
+SLC6A4	drug	alcohol	22355291	We previously have shown that cue induced <b>alcohol</b> craving and propensity for higher drinking are modulated by allelic differences in <strong>SLC6A4</strong> associated with serotonin transporter (5 HTT) expression level alterations.
+SLC6A4	addiction	relapse	22355291	We previously have shown that cue induced alcohol <b>craving</b> and propensity for higher drinking are modulated by allelic differences in <strong>SLC6A4</strong> associated with serotonin transporter (5 HTT) expression level alterations.
+SLC6A4	drug	alcohol	22355291	We previously have shown that cue induced <b>alcohol</b> craving and propensity for higher drinking are modulated by allelic differences in <strong>SLC6A4</strong> associated with serotonin transporter (<strong>5 HTT</strong>) expression level alterations.
+SLC6A4	addiction	relapse	22355291	We previously have shown that cue induced alcohol <b>craving</b> and propensity for higher drinking are modulated by allelic differences in <strong>SLC6A4</strong> associated with serotonin transporter (<strong>5 HTT</strong>) expression level alterations.
+SLC6A4	drug	opioid	22335891	In this two isotope SPECT small sample (N=9) pilot study, the relationship between the availability of serotonin transporter (<strong>SERT</strong>) and dopamine transporter (DAT) and the relapse of <b>heroin</b> users was investigated.
+SLC6A4	addiction	relapse	22335891	In this two isotope SPECT small sample (N=9) pilot study, the relationship between the availability of serotonin transporter (<strong>SERT</strong>) and dopamine transporter (DAT) and the <b>relapse</b> of heroin users was investigated.
+SLC6A4	addiction	relapse	22335891	A significant negative association between <strong>SERT</strong> availability and time to <b>relapse</b> among those who relapsed (N=7) was found.
+SLC6A4	drug	alcohol	22232964	[The influence of parents personality and DRD4 and <strong>5HTT</strong> genes polymorphisms on predisposition to <b>alcohol</b> dependence in their sons].
+SLC6A4	addiction	dependence	22232964	[The influence of parents personality and DRD4 and <strong>5HTT</strong> genes polymorphisms on predisposition to alcohol <b>dependence</b> in their sons].
+SLC6A4	addiction	addiction	22232964	Also the possibility of recognising their genotypes DRD4 (Gene ID: 1815A) and <strong>5HTT</strong> (Gene ID: 6532) could be helpful in predicting predisposition to <b>addiction</b>.
+SLC6A4	drug	alcohol	22232963	[Research on associations between selected polymorphisms of genes DRD2, <strong>5HTT</strong>, GRIK3, ADH4 and <b>alcohol</b> dependence syndrome].
+SLC6A4	addiction	dependence	22232963	[Research on associations between selected polymorphisms of genes DRD2, <strong>5HTT</strong>, GRIK3, ADH4 and alcohol <b>dependence</b> syndrome].
+SLC6A4	drug	alcohol	22232963	The aim of this study was to assess the relation between the <b>alcohol</b> dependence syndrome (ADS) and the polymorphism of the selected genes (GRIK3, <strong>5HTT</strong>, ANKK1, ADH4).
+SLC6A4	addiction	dependence	22232963	The aim of this study was to assess the relation between the alcohol <b>dependence</b> syndrome (ADS) and the polymorphism of the selected genes (GRIK3, <strong>5HTT</strong>, ANKK1, ADH4).
+SLC6A4	addiction	addiction	24474868	We simulated the path for 69,348 patients treated at the outpatient clinics of the <b>Addiction</b> Services (<strong>SerT</strong>), and 38,911 patients discharged from hospital.
+SLC6A4	drug	alcohol	22176604	Serotonin receptor, <strong>SERT</strong> mRNA and correlations with symptoms in males with <b>alcohol</b> dependence and suicide.
+SLC6A4	addiction	dependence	22176604	Serotonin receptor, <strong>SERT</strong> mRNA and correlations with symptoms in males with alcohol <b>dependence</b> and suicide.
+SLC6A4	drug	alcohol	22176604	In the <b>alcohol</b> dependence with suicide group, anxiety symptoms were associated with decreased BA 24 <strong>SERT</strong> mRNA and depressive symptoms with BA 9 5HT1A mRNA expression.
+SLC6A4	addiction	dependence	22176604	In the alcohol <b>dependence</b> with suicide group, anxiety symptoms were associated with decreased BA 24 <strong>SERT</strong> mRNA and depressive symptoms with BA 9 5HT1A mRNA expression.
+SLC6A4	drug	alcohol	22172222	Childhood adversity, serotonin transporter (<strong>5 HTTLPR</strong>) genotype, and risk for cigarette smoking and nicotine dependence in <b>alcohol</b> dependent adults.
+SLC6A4	drug	nicotine	22172222	Childhood adversity, serotonin transporter (<strong>5 HTTLPR</strong>) genotype, and risk for cigarette <b>smoking</b> and <b>nicotine</b> dependence in alcohol dependent adults.
+SLC6A4	addiction	dependence	22172222	Childhood adversity, serotonin transporter (<strong>5 HTTLPR</strong>) genotype, and risk for cigarette smoking and nicotine <b>dependence</b> in alcohol dependent adults.
+SLC6A4	drug	nicotine	22172222	<strong>5 HTTLPR</strong> genotype, gender, and social support did not significantly moderate the relationships among childhood adversity and ever <b>smoking</b> or <b>nicotine</b> dependence.
+SLC6A4	addiction	dependence	22172222	<strong>5 HTTLPR</strong> genotype, gender, and social support did not significantly moderate the relationships among childhood adversity and ever smoking or nicotine <b>dependence</b>.
+SLC6A4	drug	amphetamine	22115899	While only acute <b>meth</b> binge produced signs of neurotoxicity, both <b>meth</b> regimens decreased <strong>SERT</strong> in the perirhinal cortex and hippocampus.
+SLC6A4	addiction	intoxication	22115899	While only acute meth <b>binge</b> produced signs of neurotoxicity, both meth regimens decreased <strong>SERT</strong> in the perirhinal cortex and hippocampus.
+SLC6A4	drug	amphetamine	22115899	<b>Meth</b> induced changes in <strong>SERT</strong> function in the OIP circuitry may underlie memory deficits independently of overt neurotoxic effects.
+SLC6A4	drug	cocaine	22070124	Here we measured DNA methylation at promoter CpG sites of the dopamine transporter (DAT1) and serotonin transporter (<strong>SERT</strong>) and neurokinin3 receptor (NK3 R) receptor (TACR3) coding genes in marmoset monkeys after repeated <b>cocaine</b> injections in a conditioned place preference paradigm.
+SLC6A4	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], <strong>5HTT</strong> LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+SLC6A4	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], <strong>5HTT</strong> LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+SLC6A4	drug	alcohol	21981418	We examined the main and interaction effects with time of 3 between subject factors (medication group, age of onset of AD [late onset <b>alcoholics</b>, LOAs, vs. early onset <b>alcoholics</b>, EOAs], and the tri allelic <strong>5 HTTLPR</strong> genotype) on drinking days (DDs) and heavy drinking days (HDDs).
+SLC6A4	drug	alcohol	21906503	Case control genetic analyses were conducted for the association between HTR1B, <strong>SLC6A4</strong>, DRD2, and OPRμ1 genes and subgroups of <b>alcohol</b> dependence using a sample of 530 controls screened for <b>alcohol</b> problems.
+SLC6A4	addiction	dependence	21906503	Case control genetic analyses were conducted for the association between HTR1B, <strong>SLC6A4</strong>, DRD2, and OPRμ1 genes and subgroups of alcohol <b>dependence</b> using a sample of 530 controls screened for alcohol problems.
+SLC6A4	drug	psychedelics	21886568	Neuroimaging studies further suggest that at least one of these markers, the plasma membrane serotonin transporter (<strong>SERT</strong>), may also be reduced in heavy <b>Ecstasy</b> users.
+SLC6A4	drug	amphetamine	21886565	Recently, we showed that fluoxetine, a selective serotonin reuptake inhibitor (SSRI), decreased <b>METH</b> conditioned place preference (CPP), suggesting that serotonin transporter (<strong>SERT</strong>) inhibition reduces the rewarding effects of <b>METH</b>.
+SLC6A4	addiction	reward	21886565	Recently, we showed that fluoxetine, a selective serotonin reuptake inhibitor (SSRI), decreased METH conditioned place preference (<b>CPP</b>), suggesting that serotonin transporter (<strong>SERT</strong>) inhibition reduces the rewarding effects of METH.
+SLC6A4	drug	amphetamine	21886565	Further, these data suggest that molecules other than the <strong>SERT</strong> [such as G protein activated inwardly rectifying K+ (GIRK) channels] whose activities are modulated by paroxetine and fluoxetine, but not by fluvoxamine, are involved in reducing <b>METH</b> CPP by paroxetine and fluoxetine.
+SLC6A4	addiction	reward	21886565	Further, these data suggest that molecules other than the <strong>SERT</strong> [such as G protein activated inwardly rectifying K+ (GIRK) channels] whose activities are modulated by paroxetine and fluoxetine, but not by fluvoxamine, are involved in reducing METH <b>CPP</b> by paroxetine and fluoxetine.
+SLC6A4	drug	alcohol	21861331	We examined functional changes in serotonin transporter (<strong>SERT</strong>) and serotonin receptors (5 HT(1A) and 5 HT(2A) receptors) related with depression using <b>alcohol</b> physical dependent mice and found correlated changes between depression and <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	21861331	We examined functional changes in serotonin transporter (<strong>SERT</strong>) and serotonin receptors (5 HT(1A) and 5 HT(2A) receptors) related with depression using alcohol physical dependent mice and found correlated changes between depression and alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	21852989	We assessed the methylation level of the serotonin transporter (<strong>5 HTT</strong>) promoter region in control and <b>alcohol</b> dependent patients.
+SLC6A4	drug	alcohol	21852989	We found no differences in the methylation patterns of the serotonin transporter linked promoter region (<strong>5 HTTLPR</strong>) between <b>alcohol</b> dependent and control subjects.
+SLC6A4	drug	alcohol	21852976	The Serotonin Transporter Polymorphism (<strong>5 HTTLPR</strong>) and <b>Alcohol</b> Problems in Heavy Drinkers: Moderation by Depressive Symptoms.
+SLC6A4	drug	alcohol	21852976	These findings extend the emerging literature supporting <strong>5 HTTLPR</strong> genotype as a risk factor for <b>alcohol</b> related problems in the context of co occurring symptoms of depression.
+SLC6A4	drug	cocaine	21790908	Serotonin transporter knockout (<strong>5 HTT</strong>( / )) mice show improved cognitive flexibility in a visual reversal learning task, whereas <strong>5 HTT</strong>( / ) rats self administer increased amounts of <b>cocaine</b>.
+SLC6A4	drug	cocaine	21790908	Here we assessed: (1) whether <strong>5 HTT</strong>( / ) rats also show improved cognitive flexibility (next to mice); and (2) whether this is affected by <b>cocaine</b> self administration, which is increased in these animals.
+SLC6A4	drug	cocaine	21790908	A separate group of rats was subsequently trained to intravenously self administer <b>cocaine</b> (0.5 mg/kg/infusion), and we observed that the <strong>5 HTT</strong>( / ) rats (n = 10) self administered twice as much <b>cocaine</b> [632.7 mg/kg (±26.3)] compared with <strong>5 HTT</strong>(+/+) rats (n = 6) [352.3 mg/kg (±62.0)] over 50 1 hour sessions.
+SLC6A4	drug	cocaine	21790908	Interestingly, like the naïve <strong>5 HTT</strong>( / ) rats, the <b>cocaine</b> exposed <strong>5 HTT</strong>( / ) rats displayed improved cognitive flexibility.
+SLC6A4	drug	cocaine	21790908	In conclusion, we show that improved reversal learning in <strong>5 HTT</strong>( / ) rats reflects a pre existing trait that is preserved during <b>cocaine</b> withdrawal.
+SLC6A4	addiction	withdrawal	21790908	In conclusion, we show that improved reversal learning in <strong>5 HTT</strong>( / ) rats reflects a pre existing trait that is preserved during cocaine <b>withdrawal</b>.
+SLC6A4	drug	cocaine	21790908	As <strong>5 HTT</strong>( / ) rodents model the low activity s allele of the human serotonin transporter linked polymorphic region, these findings may have heuristic value in the treatment of s allele <b>cocaine</b> addicts.
+SLC6A4	drug	nicotine	21626393	Moreover, evidence supporting the beneficial effect of selective serotonin reuptake for quitting <b>smoking</b> suggesting that the serotonin transporter (<strong>5 HTT</strong>) is a plausible target for the understanding and elucidation of <b>smoking</b> behavior.
+SLC6A4	addiction	intoxication	21584865	In animals, <b>binge</b> mAMPH dosing regimens deplete markers for monoamine nerve terminals, for example, dopamine and serotonin transporters (DAT and <strong>SERT</strong>), in striatum and cerebral cortex.
+SLC6A4	addiction	intoxication	21584865	Striatal DAT and cortical, hippocampal, and amygdalar <strong>SERT</strong> were assessed as markers of mAMPH induced neurotoxicity 1 week following <b>binge</b> mAMPH administration.
+SLC6A4	addiction	intoxication	21584865	Blockade of striatal dopamine D1 or D2 receptors during an otherwise neurotoxic <b>binge</b> mAMPH regimen produced widespread protection against mAMPH induced striatal DAT loss and cortical, hippocampal, and amygdalar <strong>SERT</strong> loss.
+SLC6A4	drug	cocaine	21521647	We previously reported that, compared to drug naïve rhesus monkeys, self administration of <b>cocaine</b> but not MDMA was associated with increased serotonin transporter (<strong>SERT</strong>) availability in two mesolimbic regions, the caudate nucleus and putamen, as measured by positron emission tomography (PET) using the <strong>SERT</strong> specific ligand [(11)C] 3 amino 4(2 dimethylamino methyl phenylsulfanyl) benzonitrile ([(11)C]DASB).
+SLC6A4	drug	psychedelics	21521647	We previously reported that, compared to drug naïve rhesus monkeys, self administration of cocaine but not <b>MDMA</b> was associated with increased serotonin transporter (<strong>SERT</strong>) availability in two mesolimbic regions, the caudate nucleus and putamen, as measured by positron emission tomography (PET) using the <strong>SERT</strong> specific ligand [(11)C] 3 amino 4(2 dimethylamino methyl phenylsulfanyl) benzonitrile ([(11)C]DASB).
+SLC6A4	drug	cocaine	21521647	The goal of the present study was to extend this comparison between <b>cocaine</b> and MDMA self administration to <strong>SERT</strong> availability in cortical regions, which have been shown previously to be affected in human drug abusers and are associated with executive function.
+SLC6A4	drug	psychedelics	21521647	The goal of the present study was to extend this comparison between cocaine and <b>MDMA</b> self administration to <strong>SERT</strong> availability in cortical regions, which have been shown previously to be affected in human drug abusers and are associated with executive function.
+SLC6A4	drug	cocaine	21521647	Cortical <strong>SERT</strong> availability was significantly higher in monkeys with a <b>cocaine</b> self administration history compared to controls whereas MDMA self administration resulted in lower levels of <strong>SERT</strong> availability.
+SLC6A4	drug	psychedelics	21521647	Cortical <strong>SERT</strong> availability was significantly higher in monkeys with a cocaine self administration history compared to controls whereas <b>MDMA</b> self administration resulted in lower levels of <strong>SERT</strong> availability.
+SLC6A4	drug	cocaine	21521647	These data extend our previous findings indicating that <b>cocaine</b> and MDMA self administration differentially alter <strong>SERT</strong> availability in subcortical and cortical regions, which may have implications for development of treatment drugs.
+SLC6A4	drug	psychedelics	21521647	These data extend our previous findings indicating that cocaine and <b>MDMA</b> self administration differentially alter <strong>SERT</strong> availability in subcortical and cortical regions, which may have implications for development of treatment drugs.
+SLC6A4	drug	cannabinoid	21497918	We summarize <b>endocannabinoid</b> signaling in pathways related to anxiety and depression, identify the serotonergic system as the most likely candidate to mediate the side effects of CB₁ receptor antagonists, and propose that poloymorphisms in CNR1, <strong>SLC6A4</strong> and certain CYP 450 enzymes could help to identify individuals who may benefit from treatment with CB₁ receptor antagonist without psychiatric side effects.
+SLC6A4	drug	alcohol	21377958	To explore the association of polymorphism in the serotonin transporter gene and the susceptibility to <b>alcohol</b> dependence in Yunnan Han population, PCR and DNA sequencing techniques were used to detect <strong>5 HTT</strong> linked promoter region (5 HTTLPR).
+SLC6A4	addiction	dependence	21377958	To explore the association of polymorphism in the serotonin transporter gene and the susceptibility to alcohol <b>dependence</b> in Yunnan Han population, PCR and DNA sequencing techniques were used to detect <strong>5 HTT</strong> linked promoter region (5 HTTLPR).
+SLC6A4	drug	alcohol	21377958	To explore the association of polymorphism in the serotonin transporter gene and the susceptibility to <b>alcohol</b> dependence in Yunnan Han population, PCR and DNA sequencing techniques were used to detect <strong>5 HTT</strong> linked promoter region (<strong>5 HTTLPR</strong>).
+SLC6A4	addiction	dependence	21377958	To explore the association of polymorphism in the serotonin transporter gene and the susceptibility to alcohol <b>dependence</b> in Yunnan Han population, PCR and DNA sequencing techniques were used to detect <strong>5 HTT</strong> linked promoter region (<strong>5 HTTLPR</strong>).
+SLC6A4	drug	alcohol	21377958	In conclusion, <strong>5 HTTLPR</strong> polymorphism may be associated with <b>alcohol</b> dependent patients, and the genotype L/L or L/S may be a genetic factor that is responsible for decreasing susceptibility of <b>alcohol</b> dependence in Yunnan Han population.
+SLC6A4	addiction	dependence	21377958	In conclusion, <strong>5 HTTLPR</strong> polymorphism may be associated with alcohol dependent patients, and the genotype L/L or L/S may be a genetic factor that is responsible for decreasing susceptibility of alcohol <b>dependence</b> in Yunnan Han population.
+SLC6A4	drug	alcohol	21244440	Risky <b>alcohol</b> use in adolescence: the role of genetics (DRD2, <strong>SLC6A4</strong>) and coping motives.
+SLC6A4	drug	alcohol	21244440	The aim of this study was to examine relationships between the dopamine D2 receptor gene (DRD2) Taq1A polymorphism (rs1800497), a serotonin transporter gene (<strong>SLC6A4</strong>) polymorphism (5 HTTLPR), coping motives, and adolescents' binge drinking and <b>alcohol</b> related problems.
+SLC6A4	addiction	intoxication	21244440	The aim of this study was to examine relationships between the dopamine D2 receptor gene (DRD2) Taq1A polymorphism (rs1800497), a serotonin transporter gene (<strong>SLC6A4</strong>) polymorphism (5 HTTLPR), coping motives, and adolescents' <b>binge</b> drinking and alcohol related problems.
+SLC6A4	drug	alcohol	21244440	The aim of this study was to examine relationships between the dopamine D2 receptor gene (DRD2) Taq1A polymorphism (rs1800497), a serotonin transporter gene (<strong>SLC6A4</strong>) polymorphism (<strong>5 HTTLPR</strong>), coping motives, and adolescents' binge drinking and <b>alcohol</b> related problems.
+SLC6A4	addiction	intoxication	21244440	The aim of this study was to examine relationships between the dopamine D2 receptor gene (DRD2) Taq1A polymorphism (rs1800497), a serotonin transporter gene (<strong>SLC6A4</strong>) polymorphism (<strong>5 HTTLPR</strong>), coping motives, and adolescents' <b>binge</b> drinking and alcohol related problems.
+SLC6A4	drug	alcohol	21244440	Coping motives were positively related to both binge drinking and <b>alcohol</b> related problems, while DRD2 and <strong>SLC6A4</strong> genotypes were not.
+SLC6A4	addiction	intoxication	21244440	Coping motives were positively related to both <b>binge</b> drinking and alcohol related problems, while DRD2 and <strong>SLC6A4</strong> genotypes were not.
+SLC6A4	drug	cocaine	21185387	<b>Cocaine</b> acts to block the dopamine, norepinephrine, and serotonin transporters (DAT, NET, and <strong>SERT</strong>) that clear their respective neurotransmitters from the synapses, helping to terminate cognate neurotransmission.
+SLC6A4	drug	cocaine	21146984	<b>Cocaine</b>, a potent stimulant of the central nervous system, owes its reinforcing and stimulant properties to its ability to inhibit monoamine uptake systems such as the Dopamine Transporter (DAT), and the Serotonin Transporter (<strong>SERT</strong>) located on presynaptic neurons in the striatum.
+SLC6A4	addiction	reward	21146984	Cocaine, a potent stimulant of the central nervous system, owes its <b>reinforcing</b> and stimulant properties to its ability to inhibit monoamine uptake systems such as the Dopamine Transporter (DAT), and the Serotonin Transporter (<strong>SERT</strong>) located on presynaptic neurons in the striatum.
+SLC6A4	drug	nicotine	20981038	A serotonin transporter gene, <strong>SLC6A4</strong>, is thought to be related to <b>nicotine</b> dependence and depression, one of the comorbidities of chronic obstructive pulmonary disease (COPD).
+SLC6A4	addiction	dependence	20981038	A serotonin transporter gene, <strong>SLC6A4</strong>, is thought to be related to nicotine <b>dependence</b> and depression, one of the comorbidities of chronic obstructive pulmonary disease (COPD).
+SLC6A4	drug	nicotine	20981038	To investigate the association between <strong>SLC6A4</strong> variation and <b>tobacco</b> consumption, susceptibility to COPD, and depression status.
+SLC6A4	drug	nicotine	20981038	We conclude that <strong>SLC6A4</strong> variation affects COPD pathogenesis, and this effect depends partly on <b>tobacco</b> consumption.
+SLC6A4	drug	alcohol	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of <b>alcohol</b>, cocaine and heroin dependence and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	drug	cocaine	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, <b>cocaine</b> and heroin dependence and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	drug	opioid	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and <b>heroin</b> dependence and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	addiction	dependence	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and heroin <b>dependence</b> and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	addiction	relapse	20838391	In this study, 360 treatment <b>seeking</b> African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and heroin dependence and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	drug	alcohol	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of <b>alcohol</b>, cocaine and heroin dependence and 187 African American male controls were genotyped for the triallelic <strong>5 HTTLPR</strong> functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	drug	cocaine	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, <b>cocaine</b> and heroin dependence and 187 African American male controls were genotyped for the triallelic <strong>5 HTTLPR</strong> functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	drug	opioid	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and <b>heroin</b> dependence and 187 African American male controls were genotyped for the triallelic <strong>5 HTTLPR</strong> functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	addiction	dependence	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and heroin <b>dependence</b> and 187 African American male controls were genotyped for the triallelic <strong>5 HTTLPR</strong> functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	addiction	relapse	20838391	In this study, 360 treatment <b>seeking</b> African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and heroin dependence and 187 African American male controls were genotyped for the triallelic <strong>5 HTTLPR</strong> functional polymorphism in the 5 HT transporter gene (<strong>SLC6A4</strong>) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and HTR3A, genes encoding 5 HT3 receptors.
+SLC6A4	drug	alcohol	20838391	The HTR3B rs1176744 gain of function Ser129 allele predicted <b>alcohol</b> dependence (P=0.002) and low <strong>5 HTTLPR</strong> activity predicted cocaine/heroin dependence (P=0.01).
+SLC6A4	drug	cocaine	20838391	The HTR3B rs1176744 gain of function Ser129 allele predicted alcohol dependence (P=0.002) and low <strong>5 HTTLPR</strong> activity predicted <b>cocaine</b>/heroin dependence (P=0.01).
+SLC6A4	drug	opioid	20838391	The HTR3B rs1176744 gain of function Ser129 allele predicted alcohol dependence (P=0.002) and low <strong>5 HTTLPR</strong> activity predicted cocaine/<b>heroin</b> dependence (P=0.01).
+SLC6A4	addiction	dependence	20838391	The HTR3B rs1176744 gain of function Ser129 allele predicted alcohol <b>dependence</b> (P=0.002) and low <strong>5 HTTLPR</strong> activity predicted cocaine/heroin <b>dependence</b> (P=0.01).
+SLC6A4	drug	alcohol	20838391	Both the HTR3B Ser129 allele (P=0.014, odds ratio (OR)=1.7 (1.1 2.6)) and low <strong>5 HTTLPR</strong> activity (P=0.011, OR=2.5 (1.3 4.6)) were more common in men with <b>alcohol</b>+drug dependence compared with controls.
+SLC6A4	addiction	dependence	20838391	Both the HTR3B Ser129 allele (P=0.014, odds ratio (OR)=1.7 (1.1 2.6)) and low <strong>5 HTTLPR</strong> activity (P=0.011, OR=2.5 (1.3 4.6)) were more common in men with alcohol+drug <b>dependence</b> compared with controls.
+SLC6A4	drug	alcohol	20838391	Moreover, the HTR3B Ser129 allele and low <strong>5 HTTLPR</strong> activity had an additive (but not an interactive) effect on <b>alcohol</b>+drug dependence (OR=6.0 (2.1 16.6)) that accounted for 13% of the variance.
+SLC6A4	addiction	dependence	20838391	Moreover, the HTR3B Ser129 allele and low <strong>5 HTTLPR</strong> activity had an additive (but not an interactive) effect on alcohol+drug <b>dependence</b> (OR=6.0 (2.1 16.6)) that accounted for 13% of the variance.
+SLC6A4	drug	alcohol	20838024	In the present study, we investigated whether <b>ethanol</b> physical dependence causes changes of serotonin transporter (<strong>SERT</strong>) expression in the brain.
+SLC6A4	addiction	dependence	20838024	In the present study, we investigated whether ethanol physical <b>dependence</b> causes changes of serotonin transporter (<strong>SERT</strong>) expression in the brain.
+SLC6A4	drug	alcohol	20838024	In addition, chronic <b>ethanol</b> treatment increased <strong>SERT</strong> mRNA in the dorsal raphe nucleus from which serotonergic neurons originate, although no <strong>SERT</strong> mRNA was detected in the regions where <strong>SERT</strong> protein increased.
+SLC6A4	drug	alcohol	20838024	These findings suggest that alteration of <strong>SERT</strong> levels in the brain may be related to emotional changes observed in <b>ethanol</b> physical dependence.
+SLC6A4	addiction	dependence	20838024	These findings suggest that alteration of <strong>SERT</strong> levels in the brain may be related to emotional changes observed in ethanol physical <b>dependence</b>.
+SLC6A4	drug	alcohol	20800901	The aim of this study was to determine whether the serotonin transporter gene polymorphism (<strong>5 HTTLPR</strong>) is associated with the treatment outcomes of escitalopram for patients with comorbid major depression and <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	20800901	The aim of this study was to determine whether the serotonin transporter gene polymorphism (<strong>5 HTTLPR</strong>) is associated with the treatment outcomes of escitalopram for patients with comorbid major depression and alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	20642399	Evidence has suggested that the serotonin transporter (SERT) plays a role in the pathogenesis of <b>alcohol</b> dependence, anxiety and depression and that polymorphisms of the serotonin transporter linked promoter region (<strong>5 HTTLPR</strong>) may influence the SERT.
+SLC6A4	addiction	dependence	20642399	Evidence has suggested that the serotonin transporter (SERT) plays a role in the pathogenesis of alcohol <b>dependence</b>, anxiety and depression and that polymorphisms of the serotonin transporter linked promoter region (<strong>5 HTTLPR</strong>) may influence the SERT.
+SLC6A4	drug	alcohol	20642399	Evidence has suggested that the serotonin transporter (<strong>SERT</strong>) plays a role in the pathogenesis of <b>alcohol</b> dependence, anxiety and depression and that polymorphisms of the serotonin transporter linked promoter region (<strong>5 HTTLPR</strong>) may influence the <strong>SERT</strong>.
+SLC6A4	addiction	dependence	20642399	Evidence has suggested that the serotonin transporter (<strong>SERT</strong>) plays a role in the pathogenesis of alcohol <b>dependence</b>, anxiety and depression and that polymorphisms of the serotonin transporter linked promoter region (<strong>5 HTTLPR</strong>) may influence the <strong>SERT</strong>.
+SLC6A4	drug	alcohol	20642399	This study evaluated the differences in SERT availability between healthy controls and <b>alcoholic</b> patients and the impact of <strong>5 HTTLPR</strong> polymorphisms on SERT availability.
+SLC6A4	drug	alcohol	20642399	This study evaluated the differences in <strong>SERT</strong> availability between healthy controls and <b>alcoholic</b> patients and the impact of <strong>5 HTTLPR</strong> polymorphisms on <strong>SERT</strong> availability.
+SLC6A4	drug	alcohol	20642399	Compared to healthy controls, there was a significantly lower availability of <strong>SERT</strong> in the midbrain among patients with pure <b>alcohol</b> dependence (pure ALC).
+SLC6A4	addiction	dependence	20642399	Compared to healthy controls, there was a significantly lower availability of <strong>SERT</strong> in the midbrain among patients with pure alcohol <b>dependence</b> (pure ALC).
+SLC6A4	drug	alcohol	20642399	Of patients with anxiety, depression and <b>alcohol</b> dependence (ANX/DEPALC), the carriers of one L(A) allele showed a significantly higher availability of <strong>SERT</strong> in the striatum compared to non L(A) carriers.
+SLC6A4	addiction	dependence	20642399	Of patients with anxiety, depression and alcohol <b>dependence</b> (ANX/DEPALC), the carriers of one L(A) allele showed a significantly higher availability of <strong>SERT</strong> in the striatum compared to non L(A) carriers.
+SLC6A4	drug	alcohol	20642399	The results suggest that pure <b>alcoholics</b> may have lower SERT availability in the midbrain; the <strong>5HTTLPR</strong> polymorphism may influence SERT availability in ANX/DEP ALC.
+SLC6A4	drug	alcohol	20642399	The results suggest that pure <b>alcoholics</b> may have lower <strong>SERT</strong> availability in the midbrain; the <strong>5HTTLPR</strong> polymorphism may influence <strong>SERT</strong> availability in ANX/DEP ALC.
+SLC6A4	drug	alcohol	20598843	Because the serotonin transporter (5 HTT) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the 5 HTT gene linked polymorphic region [5 HTTLPR] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive compulsive <b>alcohol</b> craving.
+SLC6A4	addiction	addiction	20598843	Because the serotonin transporter (5 HTT) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the 5 HTT gene linked polymorphic region [5 HTTLPR] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive <b>compulsive</b> alcohol craving.
+SLC6A4	addiction	relapse	20598843	Because the serotonin transporter (5 HTT) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the 5 HTT gene linked polymorphic region [5 HTTLPR] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive compulsive alcohol <b>craving</b>.
+SLC6A4	drug	alcohol	20598843	Because the serotonin transporter (<strong>5 HTT</strong>) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the <strong>5 HTT</strong> gene linked polymorphic region [5 HTTLPR] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive compulsive <b>alcohol</b> craving.
+SLC6A4	addiction	addiction	20598843	Because the serotonin transporter (<strong>5 HTT</strong>) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the <strong>5 HTT</strong> gene linked polymorphic region [5 HTTLPR] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive <b>compulsive</b> alcohol craving.
+SLC6A4	addiction	relapse	20598843	Because the serotonin transporter (<strong>5 HTT</strong>) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the <strong>5 HTT</strong> gene linked polymorphic region [5 HTTLPR] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive compulsive alcohol <b>craving</b>.
+SLC6A4	drug	alcohol	20598843	Because the serotonin transporter (<strong>5 HTT</strong>) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the <strong>5 HTT</strong> gene linked polymorphic region [<strong>5 HTTLPR</strong>] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive compulsive <b>alcohol</b> craving.
+SLC6A4	addiction	addiction	20598843	Because the serotonin transporter (<strong>5 HTT</strong>) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the <strong>5 HTT</strong> gene linked polymorphic region [<strong>5 HTTLPR</strong>] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive <b>compulsive</b> alcohol craving.
+SLC6A4	addiction	relapse	20598843	Because the serotonin transporter (<strong>5 HTT</strong>) functions to remove serotonin from the synapse, it is thought that increased reuptake (indicated by the number of high expressing L(A) alleles present in the <strong>5 HTT</strong> gene linked polymorphic region [<strong>5 HTTLPR</strong>] of the <strong>SLC6A4</strong> gene) is associated with an increase in obsessive compulsive alcohol <b>craving</b>.
+SLC6A4	drug	alcohol	20598843	The current pilot investigation sought to explore this hypothesis by examining the extent to which obsessive compulsive <b>alcohol</b> craving varies by <strong>5 HTTLPR</strong> genotype among participants enrolled in an ongoing pharmacogenetics trial.
+SLC6A4	addiction	addiction	20598843	The current pilot investigation sought to explore this hypothesis by examining the extent to which obsessive <b>compulsive</b> alcohol craving varies by <strong>5 HTTLPR</strong> genotype among participants enrolled in an ongoing pharmacogenetics trial.
+SLC6A4	addiction	relapse	20598843	The current pilot investigation sought to explore this hypothesis by examining the extent to which obsessive compulsive alcohol <b>craving</b> varies by <strong>5 HTTLPR</strong> genotype among participants enrolled in an ongoing pharmacogenetics trial.
+SLC6A4	addiction	addiction	20598843	Preliminary findings suggest that <strong>5 HTTLPR</strong> is not predictive of Obsessive <b>Compulsive</b> Drinking Scale total and factor scores.
+SLC6A4	drug	alcohol	20598843	Although the <strong>5 HTTLPR</strong> polymorphism was not related to obsessive compulsive <b>alcohol</b> craving in this pilot study, additional research is needed to clarify the possible role of serotonergic mechanisms in <b>alcohol</b> craving.
+SLC6A4	addiction	addiction	20598843	Although the <strong>5 HTTLPR</strong> polymorphism was not related to obsessive <b>compulsive</b> alcohol craving in this pilot study, additional research is needed to clarify the possible role of serotonergic mechanisms in alcohol craving.
+SLC6A4	addiction	relapse	20598843	Although the <strong>5 HTTLPR</strong> polymorphism was not related to obsessive compulsive alcohol <b>craving</b> in this pilot study, additional research is needed to clarify the possible role of serotonergic mechanisms in alcohol <b>craving</b>.
+SLC6A4	drug	alcohol	20598814	A serotonin transporter polymorphism (<strong>5 HTTLPR</strong>) predicts the development of adolescent <b>alcohol</b> use.
+SLC6A4	drug	alcohol	20598814	The short, low activity allele of a polymorphism (5 HTTLPR) in the serotonin transporter gene (<strong>SLC6A4</strong>) has been related to <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	20598814	The short, low activity allele of a polymorphism (5 HTTLPR) in the serotonin transporter gene (<strong>SLC6A4</strong>) has been related to alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	20598814	The short, low activity allele of a polymorphism (<strong>5 HTTLPR</strong>) in the serotonin transporter gene (<strong>SLC6A4</strong>) has been related to <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	20598814	The short, low activity allele of a polymorphism (<strong>5 HTTLPR</strong>) in the serotonin transporter gene (<strong>SLC6A4</strong>) has been related to alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	20598814	In the current study we tested whether <strong>5 HTTLPR</strong> genotype was associated with adolescent <b>alcohol</b> use both cross sectionally and longitudinally.
+SLC6A4	drug	alcohol	20598814	The <strong>5 HTTLPR</strong> short allele predicted adolescent's growth (slope) in <b>alcohol</b> use over time.
+SLC6A4	drug	alcohol	20598814	Adolescents with the <strong>5 HTTLPR</strong> short allele showed larger increase in <b>alcohol</b> consumption than those without the <strong>5 HTTLPR</strong> short allele.
+SLC6A4	drug	alcohol	20598814	<strong>5 HTTLPR</strong> genotype was not related to the initial level (intercept) of <b>alcohol</b> consumption.
+SLC6A4	drug	nicotine	20585760	The objective of this cross sectional study was to assess the interrelation of cortisol response, thalamic <strong>5 HTT</strong> levels, and anxiety in healthy subjects and two previously published samples of patients with unipolar major depression (UMD) and obsessive compulsive disorder (OCD), controlling for age, gender, <strong>5 HTT</strong> genotype, <b>smoking</b>, and seasonality.
+SLC6A4	addiction	addiction	20585760	The objective of this cross sectional study was to assess the interrelation of cortisol response, thalamic <strong>5 HTT</strong> levels, and anxiety in healthy subjects and two previously published samples of patients with unipolar major depression (UMD) and obsessive <b>compulsive</b> disorder (OCD), controlling for age, gender, <strong>5 HTT</strong> genotype, smoking, and seasonality.
+SLC6A4	drug	nicotine	20585760	Reduced thalamic <strong>5 HTT</strong> BP(ND) was associated with increased cortisol response (r =  0.35, p < 0.05; in patients: r =  0.53, p < 0.01) and with increased state anxiety (r =  0.46, p < 0.01), surviving correction for age, gender, <strong>5 HTT</strong> genotype, <b>smoking</b>, and seasonality (p < 0.05).
+SLC6A4	addiction	intoxication	20579008	<strong>5 HTTLPR</strong> genotype and associations with <b>intoxication</b> and intention to drive: results from a field study of bar patrons.
+SLC6A4	drug	alcohol	20579008	This study reports associations between <strong>5 HTTLPR</strong>, <b>alcohol</b> intoxication and intention to drive among young adult patrons exiting on premise drinking establishments (i.e.
+SLC6A4	addiction	intoxication	20579008	This study reports associations between <strong>5 HTTLPR</strong>, alcohol <b>intoxication</b> and intention to drive among young adult patrons exiting on premise drinking establishments (i.e.
+SLC6A4	drug	alcohol	20579008	An interaction effect involving <strong>5 HTTLPR</strong> and bar sponsored drink specials also had an independent association with BrAC, suggesting that selection of price discounted <b>alcoholic</b> beverages increased intoxication in patrons with an L allele.
+SLC6A4	addiction	intoxication	20579008	An interaction effect involving <strong>5 HTTLPR</strong> and bar sponsored drink specials also had an independent association with BrAC, suggesting that selection of price discounted alcoholic beverages increased <b>intoxication</b> in patrons with an L allele.
+SLC6A4	drug	alcohol	20505557	Our study was aimed at investigating whether distinct haplotypes, defined by polymorphisms associated with the expressions of DAT and <strong>SERT</strong>, were associated with subgroups of <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	20505557	Our study was aimed at investigating whether distinct haplotypes, defined by polymorphisms associated with the expressions of DAT and <strong>SERT</strong>, were associated with subgroups of alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	20505557	Intron 8 variable number of tandem repeats (VNTR), exon 15 rs27072 and VNTR (DAT), promoter VNTR and rs25531, and intron 2 VNTR (<strong>SERT</strong>) were genotyped in a case control sample comprising 360 <b>alcoholics</b> and 368 controls, and in a family based sample of 65 trios, all of German origin.
+SLC6A4	drug	alcohol	20505557	<strong>SERT</strong>: haplotypes SA 10 (OR: 2.3) and LG 12 (OR: 2.5) were more often present in type 2 <b>alcoholics</b> compared with controls.
+SLC6A4	drug	nicotine	20456288	Serotonin transporter (<strong>5 HTT</strong>) gene variation also moderates <b>nicotine</b> induced improvement in spatial working memory.
+SLC6A4	drug	cannabinoid	20434316	We investigated the 5 HTTLPR of the <strong>5 HTT</strong> gene (G) and the presence of childhood sexual abuse and <b>cannabis</b> comorbidity (E) in 137 bipolar patients with (versus without) lifetime psychotic symptoms.
+SLC6A4	drug	cannabinoid	20434316	We investigated the <strong>5 HTTLPR</strong> of the <strong>5 HTT</strong> gene (G) and the presence of childhood sexual abuse and <b>cannabis</b> comorbidity (E) in 137 bipolar patients with (versus without) lifetime psychotic symptoms.
+SLC6A4	drug	cannabinoid	20434316	The short allele of the 5 HTTLPR polymorphism of the <strong>5 HTT</strong> gene was a risk factor for psychotic symptoms in bipolar disorder in the present sample, directly but also indirectly, through the presence of <b>cannabis</b> abuse or dependence, as an exacerbating factor heightening psychotic symptoms.
+SLC6A4	addiction	dependence	20434316	The short allele of the 5 HTTLPR polymorphism of the <strong>5 HTT</strong> gene was a risk factor for psychotic symptoms in bipolar disorder in the present sample, directly but also indirectly, through the presence of cannabis abuse or <b>dependence</b>, as an exacerbating factor heightening psychotic symptoms.
+SLC6A4	drug	cannabinoid	20434316	The short allele of the <strong>5 HTTLPR</strong> polymorphism of the <strong>5 HTT</strong> gene was a risk factor for psychotic symptoms in bipolar disorder in the present sample, directly but also indirectly, through the presence of <b>cannabis</b> abuse or dependence, as an exacerbating factor heightening psychotic symptoms.
+SLC6A4	addiction	dependence	20434316	The short allele of the <strong>5 HTTLPR</strong> polymorphism of the <strong>5 HTT</strong> gene was a risk factor for psychotic symptoms in bipolar disorder in the present sample, directly but also indirectly, through the presence of cannabis abuse or <b>dependence</b>, as an exacerbating factor heightening psychotic symptoms.
+SLC6A4	drug	alcohol	20192950	The present study examined the association between a measure of sociopathy and <strong>5 HTTLPR</strong> genotype in a sample of individuals from Project MATCH, a multi center <b>alcohol</b> treatment trial.
+SLC6A4	drug	alcohol	20192950	The S allele has been associated with a variety of psychiatric disorders and symptoms including <b>alcohol</b> dependence, but it is unknown whether <strong>5 HTTLPR</strong> increases the risk for co morbid sociopathy among those with <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	20192950	The S allele has been associated with a variety of psychiatric disorders and symptoms including alcohol <b>dependence</b>, but it is unknown whether <strong>5 HTTLPR</strong> increases the risk for co morbid sociopathy among those with alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	20192950	Among individuals with <b>alcohol</b> use disorders, the tri allelic <strong>5 HTTLPR</strong> polymorphism had opposite effects on socialization scores in men than women.
+SLC6A4	drug	psychedelics	20169574	We have recently shown that chronic intermittent exposure of adolescent rats to 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b> or <b>Ecstasy</b>) completely blocks the reduction in serotonin transporter (<strong>SERT</strong>) binding and the hypoactivity seen following a subsequent <b>MDMA</b> binge treatment.
+SLC6A4	addiction	intoxication	20169574	We have recently shown that chronic intermittent exposure of adolescent rats to 3,4 methylenedioxymethamphetamine (MDMA or Ecstasy) completely blocks the reduction in serotonin transporter (<strong>SERT</strong>) binding and the hypoactivity seen following a subsequent MDMA <b>binge</b> treatment.
+SLC6A4	drug	psychedelics	20169574	<b>MDMA</b> preexposure protected animals from the reductions in cortical 5 HT levels and <strong>SERT</strong> binding produced by the high dose binge and blocked the postbinge hypoactivity.
+SLC6A4	addiction	intoxication	20169574	MDMA preexposure protected animals from the reductions in cortical 5 HT levels and <strong>SERT</strong> binding produced by the high dose <b>binge</b> and blocked the postbinge hypoactivity.
+SLC6A4	drug	cocaine	20122955	To address the role of serotonin (5 HT) in <b>cocaine</b> induced aversions, the present experiments used the cross drug preexposure design in which the effects of exposure to fluoxetine, a selective 5 HT reuptake inhibitor (SSRI) with 5 HT transporter (<strong>SERT</strong>) inhibitory properties, were examined on aversions induced by <b>cocaine</b> (a nonselective monoamine transport inhibitor) and the effects of <b>cocaine</b> preexposure were examined on fluoxetine induced aversions.
+SLC6A4	drug	nicotine	20060656	<strong>5 HTTLPR</strong> polymorphism of the 5 HT transporter gene and  759C/T (rs3813929) and  697G/C (rs518147) polymorphisms of the 5 HT(2C) receptor gene were analyzed in 172 <b>smoking</b> initiators and 254 non initiators, using PCR RFLP method.
+SLC6A4	drug	nicotine	20060656	We found no differences in the frequency of the <strong>5 HTTLPR</strong> genotypes between <b>smoking</b> initiators and non initiators.
+SLC6A4	drug	nicotine	20060656	<strong>5 HTTLPR</strong> polymorphism was not associated with <b>smoking</b> initiation in either male or female subjects.
+SLC6A4	drug	alcohol	20060655	Previous studies have implicated a relationship between particular allelic variations of the serotonin transporter gene (<strong>5HTTLPR</strong>) and <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	20060655	Previous studies have implicated a relationship between particular allelic variations of the serotonin transporter gene (<strong>5HTTLPR</strong>) and alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	20060655	To provide a current estimate of the strength of this association, particularly in light of inconsistent results for <strong>5HTTLPR</strong>, we conducted a meta analytic review of the association between <strong>5HTTLPR</strong> and a clinical diagnosis of <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	20060655	To provide a current estimate of the strength of this association, particularly in light of inconsistent results for <strong>5HTTLPR</strong>, we conducted a meta analytic review of the association between <strong>5HTTLPR</strong> and a clinical diagnosis of alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	20060655	Therefore, although our review indicates that there is a significant association between <strong>5HTTLPR</strong> and <b>alcohol</b> dependence diagnosis, this result should be interpreted with caution.
+SLC6A4	addiction	dependence	20060655	Therefore, although our review indicates that there is a significant association between <strong>5HTTLPR</strong> and alcohol <b>dependence</b> diagnosis, this result should be interpreted with caution.
+SLC6A4	drug	amphetamine	21423453	An earlier onset of <b>methamphetamine</b> use leads to greater damage to the terminal ends of serotonin neurons, more reduction in serotonin transporter (<strong>5 HTT</strong>) density, and an increased propensity toward further <b>methamphetamine</b> use.
+SLC6A4	drug	amphetamine	21423453	Because the <strong>5 HTT</strong> linked polymorphic region (5' HTTLPR) within the promoter region of the <strong>5 HTT</strong> gene leads to differential expression of the <strong>5 HTT</strong>, we examined, for the first time, whether there is a differential association between the long (L) and short (S) alleles of the 5' HTTLPR and the age of first <b>methamphetamine</b> use (AMU).
+SLC6A4	drug	psychedelics	20002520	Experiment 1 investigated <b>MDMA</b> induced changes in levels of the serotonin transporter (<strong>SERT</strong>) and the vesicular monoamine transporter 2 (VMAT 2) in the hippocampus, a region with sparse dopaminergic innervation, after lesioning noradrenergic input with N (2 chloroethyl) N ethyl 2 bromobenzylamine (DSP 4).
+SLC6A4	drug	psychedelics	20002520	Two weeks following the binge treatment, the DSP 4/<b>MDMA</b> group unexpectedly showed little change in hippocampal VMAT 2 protein expression compared with DSP 4/Saline controls, despite large reductions in <strong>SERT</strong> levels in all regions examined in the <b>MDMA</b> treated animals.
+SLC6A4	addiction	intoxication	20002520	Two weeks following the <b>binge</b> treatment, the DSP 4/MDMA group unexpectedly showed little change in hippocampal VMAT 2 protein expression compared with DSP 4/Saline controls, despite large reductions in <strong>SERT</strong> levels in all regions examined in the MDMA treated animals.
+SLC6A4	drug	psychedelics	20002520	Furthermore, animals treated with binge <b>MDMA</b> (Experiment 2) showed a striking decrease in <strong>SERT</strong> gene expression (and a lesser effect on VMAT 2) measured by quantitative RT PCR in pooled dorsal and median raphe tissue punches, when compared with saline treated controls.
+SLC6A4	addiction	intoxication	20002520	Furthermore, animals treated with <b>binge</b> MDMA (Experiment 2) showed a striking decrease in <strong>SERT</strong> gene expression (and a lesser effect on VMAT 2) measured by quantitative RT PCR in pooled dorsal and median raphe tissue punches, when compared with saline treated controls.
+SLC6A4	drug	alcohol	20002020	Results reveal decreased likelihood of DT in <b>alcoholics</b> that carry the DRD2 rs6276 G allele and <strong>SLC6A4</strong> LL genotype.
+SLC6A4	drug	cocaine	19969013	Monoamine transporter knockout mice have been useful in the study of many different aspects of <b>cocaine</b> effects relevant to human drug use and addiction, yet an assessment of the effects of deletion of the genes for the dopamine, norepinephrine and serotonin transporters (DAT, NET, and <strong>SERT</strong>, respectively) on <b>cocaine</b>'s aversive properties has yet to be performed (Uhl et al., 2002).
+SLC6A4	addiction	addiction	19969013	Monoamine transporter knockout mice have been useful in the study of many different aspects of cocaine effects relevant to human drug use and <b>addiction</b>, yet an assessment of the effects of deletion of the genes for the dopamine, norepinephrine and serotonin transporters (DAT, NET, and <strong>SERT</strong>, respectively) on cocaine's aversive properties has yet to be performed (Uhl et al., 2002).
+SLC6A4	addiction	aversion	19969013	Monoamine transporter knockout mice have been useful in the study of many different aspects of cocaine effects relevant to human drug use and addiction, yet an assessment of the effects of deletion of the genes for the dopamine, norepinephrine and serotonin transporters (DAT, NET, and <strong>SERT</strong>, respectively) on cocaine's <b>aversive</b> properties has yet to be performed (Uhl et al., 2002).
+SLC6A4	drug	cocaine	19969013	When compared to their respective WT controls, dopamine transporter deletion slightly attenuated <b>cocaine</b> induced aversion while deletion of <strong>SERT</strong> or NET resulted in a more significant delay in the onset and strength of <b>cocaine</b> induced taste aversions.
+SLC6A4	addiction	aversion	19969013	When compared to their respective WT controls, dopamine transporter deletion slightly attenuated cocaine induced <b>aversion</b> while deletion of <strong>SERT</strong> or NET resulted in a more significant delay in the onset and strength of cocaine induced taste aversions.
+SLC6A4	drug	cocaine	19969013	The data lead us to conclude that the action of <b>cocaine</b> to inhibit NET contributes most substantially to its aversive effects, with some involvement of <strong>SERT</strong> and minimal contribution of DAT.
+SLC6A4	addiction	aversion	19969013	The data lead us to conclude that the action of cocaine to inhibit NET contributes most substantially to its <b>aversive</b> effects, with some involvement of <strong>SERT</strong> and minimal contribution of DAT.
+SLC6A4	drug	alcohol	19885717	It is predicted that reduced transynaptic 5 HT neurotransmission in <b>alcoholics</b> with the L/L genotype of <strong>5 HTTLPR</strong> would result in a change in DA function compared to the S/S genotype.
+SLC6A4	drug	alcohol	19885717	Dopaminergic sensitivity, <strong>5 HTTLPR</strong> genotype and smoking status were assessed in 121 <b>alcoholics</b>.
+SLC6A4	drug	nicotine	19885717	Dopaminergic sensitivity, <strong>5 HTTLPR</strong> genotype and <b>smoking</b> status were assessed in 121 alcoholics.
+SLC6A4	drug	psychedelics	19878141	<strong>5 HTTLPR</strong> polymorphism, mood disorders and <b>MDMA</b> use in a 3 year follow up study.
+SLC6A4	drug	psychedelics	19878141	<strong>5 HTTLPR</strong> polymorphism was associated with lifetime of primary mood disorders in <b>ecstasy</b> group (P = 0.018).
+SLC6A4	drug	psychedelics	19878141	In the <b>ecstasy</b> users, <strong>5 HTTLPR</strong> polymorphism may result in a high vulnerability to primary mood disorders.
+SLC6A4	drug	psychedelics	19824774	<b>MDMA</b> pretreatment was hypothesized to enhance the effects of CUS leading to enhanced 5 HT transporter (<strong>SERT</strong>) depletion in the hippocampus and increased anxiety and cognitive impairment.
+SLC6A4	drug	psychedelics	19824774	In contrast, <b>MDMA</b> pretreatment led to CUS induced learning impairment in the Morris water maze but not an enhanced depletion of hippocampal <strong>SERT</strong> protein.
+SLC6A4	drug	psychedelics	19824774	These results show that prior exposure to <b>MDMA</b> leads to stress induced impairments in learning behavior that is not otherwise observed with stress alone and appear unrelated to an enhanced depletion of <strong>SERT</strong>.
+SLC6A4	drug	alcohol	19764934	<b>Alcoholism</b> is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (<strong>5 HTT</strong>) linked polymorphic region (5 HTTLPR), A118G in opioid receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of <b>alcoholism</b>.
+SLC6A4	drug	opioid	19764934	Alcoholism is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (<strong>5 HTT</strong>) linked polymorphic region (5 HTTLPR), A118G in <b>opioid</b> receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+SLC6A4	addiction	reward	19764934	Alcoholism is a polygenic disorder resulting from <b>reward</b> deficiency; polymorphisms in <b>reward</b> genes including serotonin transporter (<strong>5 HTT</strong>) linked polymorphic region (5 HTTLPR), A118G in opioid receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+SLC6A4	drug	alcohol	19764934	<b>Alcoholism</b> is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (<strong>5 HTT</strong>) linked polymorphic region (<strong>5 HTTLPR</strong>), A118G in opioid receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of <b>alcoholism</b>.
+SLC6A4	drug	opioid	19764934	Alcoholism is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (<strong>5 HTT</strong>) linked polymorphic region (<strong>5 HTTLPR</strong>), A118G in <b>opioid</b> receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+SLC6A4	addiction	reward	19764934	Alcoholism is a polygenic disorder resulting from <b>reward</b> deficiency; polymorphisms in <b>reward</b> genes including serotonin transporter (<strong>5 HTT</strong>) linked polymorphic region (<strong>5 HTTLPR</strong>), A118G in opioid receptor mu1 (OPRM1), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+SLC6A4	drug	alcohol	19764934	Genotyping of <strong>5 HTTLPR</strong>, OPRM1 A118G, and DRD2 141C Ins/Del was performed in 365 <b>alcoholics</b> and 338 nonalcoholic controls of Mexican Americans who were gender  and age matched.
+SLC6A4	drug	alcohol	19764934	No definite effect of marital status and <strong>5 HTTLPR</strong> in pathogenesis of <b>alcoholism</b> was observed.
+SLC6A4	drug	alcohol	19759277	We examined (1) the association of <strong>SLC6A4</strong> genotypes and <b>alcohol</b> dependence (AD) in a sample of <b>alcoholics</b>; (2) the validity of lifetime occurrence of blacked out violent impulsive behaviour (BOVIB) during binge drinking bouts as a criterion for subtyping AD patients and (3) a mechanistic hypothesis for BOVIB involving tryptophan 2,3 dioxygenase (TDO) activity.
+SLC6A4	addiction	dependence	19759277	We examined (1) the association of <strong>SLC6A4</strong> genotypes and alcohol <b>dependence</b> (AD) in a sample of alcoholics; (2) the validity of lifetime occurrence of blacked out violent impulsive behaviour (BOVIB) during binge drinking bouts as a criterion for subtyping AD patients and (3) a mechanistic hypothesis for BOVIB involving tryptophan 2,3 dioxygenase (TDO) activity.
+SLC6A4	addiction	intoxication	19759277	We examined (1) the association of <strong>SLC6A4</strong> genotypes and alcohol dependence (AD) in a sample of alcoholics; (2) the validity of lifetime occurrence of blacked out violent impulsive behaviour (BOVIB) during <b>binge</b> drinking bouts as a criterion for subtyping AD patients and (3) a mechanistic hypothesis for BOVIB involving tryptophan 2,3 dioxygenase (TDO) activity.
+SLC6A4	drug	alcohol	19742166	Epistasis between IL1A, IL1B, TNF, HTR2A, <strong>5 HTTLPR</strong> and TPH2 variations does not impact <b>alcohol</b> dependence disorder features.
+SLC6A4	addiction	dependence	19742166	Epistasis between IL1A, IL1B, TNF, HTR2A, <strong>5 HTTLPR</strong> and TPH2 variations does not impact alcohol <b>dependence</b> disorder features.
+SLC6A4	drug	alcohol	19742166	In both groups we genotyped 11 genetic variations (rs1800587; rs3087258; rs1799724; <strong>5 HTTLPR</strong>; rs1386493; rs1386494; rs1487275; rs1843809; rs4570625; rs2129575; rs6313) located in genes whose impact on <b>alcohol</b> related behaviors and disorders has been hypothesized (IL1A, IL1B, TNF, <strong>5 HTTLPR</strong>, TPH2 and HTR2A).
+SLC6A4	addiction	addiction	19742166	We detected the following results: the couple rs6313 + rs2129575 affected the Leyton  Trait at admission (p = 0.01) (obsessive <b>compulsive</b> trait), whilst rs1800587 + <strong>5 HTTLPR</strong> impacted the Pilowski test at admission (p = 0.01) (hypochondriac symptoms).
+SLC6A4	drug	amphetamine	19689456	Genes differentially expressed in the drug naï ve state, including <strong>Slc6a4</strong> (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and Fos (cFos), represent candidates whose expression levels may predict <b>methamphetamine</b> consumption and susceptibility to <b>methamphetamine</b> reward and aversion.
+SLC6A4	addiction	aversion	19689456	Genes differentially expressed in the drug naï ve state, including <strong>Slc6a4</strong> (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and Fos (cFos), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine reward and <b>aversion</b>.
+SLC6A4	addiction	reward	19689456	Genes differentially expressed in the drug naï ve state, including <strong>Slc6a4</strong> (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and Fos (cFos), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine <b>reward</b> and aversion.
+SLC6A4	addiction	dependence	19641126	A Cl( ) binding site recently identified in <strong>SERT</strong>, and shown to be important for Cl( ) dependent transport, was also critical for the Cl( ) <b>dependence</b> of antidepressant affinity.
+SLC6A4	drug	opioid	19570226	Genetic variation in the serotonin transporter gene (<strong>5 HTTLPR</strong>, rs25531) influences the analgesic response to the short acting <b>opioid</b> Remifentanil in humans.
+SLC6A4	drug	opioid	19570226	The aim of this study was to investigate if the triallelic <strong>5 HTTLPR</strong> influences pain sensitivity or the analgesic effect of <b>opioids</b> in humans.
+SLC6A4	drug	opioid	19570226	This is the first report showing an influence of the triallelic <strong>5 HTTLPR</strong> on pain sensitivity or the analgesic effect of <b>opioids</b> in humans.
+SLC6A4	drug	opioid	19570226	Previously the 5 HTTLPR s allele has been associated with higher risk of developing chronic pain conditions but in this study we show that the genotype coding for low <strong>5 HTT</strong> expression is associated with a better analgesic effect of an <b>opioid</b>.
+SLC6A4	drug	opioid	19570226	Previously the <strong>5 HTTLPR</strong> s allele has been associated with higher risk of developing chronic pain conditions but in this study we show that the genotype coding for low <strong>5 HTT</strong> expression is associated with a better analgesic effect of an <b>opioid</b>.
+SLC6A4	drug	nicotine	19567154	Polymerase chain reaction restriction fragment length polymorphism (PCR RFLP) was performed to find <strong>5 HTTLPR</strong> gene polymorphisms in 144 <b>smokers</b> and 135 age matched healthy non <b>smokers</b>.
+SLC6A4	drug	nicotine	19567154	There were no significant differences in the proportion of starting <b>smoking</b> before 20 years old (P = 0.219) and those who succeeded in quitting <b>smoking</b> for more than 1 month (P = 0.456) between individuals with different <strong>5 HTTLPR</strong> genotypes in <b>smokers</b>.
+SLC6A4	drug	nicotine	19567154	<strong>5 HTTLPR</strong> polymorphism may be associated with susceptibility to cigarette <b>smoking</b> in Chinese males.
+SLC6A4	drug	amphetamine	19549517	Several well established substrates for human <strong>SERT</strong> including (+/ )MDMA, S (+)<b>amphetamine</b>, RU 24969, and m CPP are not transported by SmSERTs, underscoring the higher selectivity of the schistosomal isoforms.
+SLC6A4	drug	psychedelics	19549517	Several well established substrates for human <strong>SERT</strong> including (+/ )<b>MDMA</b>, S (+)amphetamine, RU 24969, and m CPP are not transported by SmSERTs, underscoring the higher selectivity of the schistosomal isoforms.
+SLC6A4	addiction	reward	19549517	Several well established substrates for human <strong>SERT</strong> including (+/ )MDMA, S (+)amphetamine, RU 24969, and m <b>CPP</b> are not transported by SmSERTs, underscoring the higher selectivity of the schistosomal isoforms.
+SLC6A4	drug	cocaine	19536276	<b>Cocaine</b>, a potent addictive substance, is an inhibitor of monoamine transporters, including DAT (dopamine transporter), <strong>SERT</strong> (serotonin transporter) and NET (norepinephrine transporter).
+SLC6A4	addiction	addiction	19536276	Cocaine, a potent <b>addictive</b> substance, is an inhibitor of monoamine transporters, including DAT (dopamine transporter), <strong>SERT</strong> (serotonin transporter) and NET (norepinephrine transporter).
+SLC6A4	drug	cocaine	19536276	The C. elegans <strong>SERT</strong> MOD 5 is essential for the effect of <b>cocaine</b>, consistent with the role of <b>cocaine</b> in targeting monoamine transporters.
+SLC6A4	drug	cocaine	19482066	The behavioral effects of <b>cocaine</b> are affected by gene knockout (KO) of the dopamine transporter (DAT), the serotonin transporter (<strong>SERT</strong>) and the norepinephrine transporter (NET).
+SLC6A4	drug	cocaine	19482066	To further explore the role of these genes in the rewarding effects of <b>cocaine</b>, the ability of five daily injections of <b>cocaine</b> to induce conditioned locomotion was assessed in DAT, <strong>SERT</strong> and NET KO mice.
+SLC6A4	drug	cocaine	19482066	<b>Cocaine</b> increased locomotor activity acutely during the initial conditioning session in <strong>SERT</strong> KO and NET KO, but not DAT KO, mice.
+SLC6A4	drug	cocaine	19482066	Surprisingly, locomotor responses in the <b>cocaine</b> paired subjects diminished over the five conditioning sessions in <strong>SERT</strong> KO mice, while locomotor responses increased in DAT KO mice, despite the fact that they did not demonstrate any initial locomotor responses to <b>cocaine</b>.
+SLC6A4	drug	alcohol	19426172	These results not only provide support for the hypothesis that <b>alcoholics</b> who are L carriers have greater <b>alcohol</b> craving and possibly greater propensity for drinking but also propose that there is an important <strong>5 HTT</strong> gene by environment interaction that alters cue craving response for <b>alcohol</b>.
+SLC6A4	addiction	relapse	19426172	These results not only provide support for the hypothesis that alcoholics who are L carriers have greater alcohol <b>craving</b> and possibly greater propensity for drinking but also propose that there is an important <strong>5 HTT</strong> gene by environment interaction that alters cue <b>craving</b> response for alcohol.
+SLC6A4	drug	nicotine	19396697	As one of the candidate genes in relation to <b>smoking</b>, the serotonin transporter gene (<strong>5 HTTLPR</strong>) has been suggested, however with conflicting results.
+SLC6A4	drug	nicotine	19396697	The objective of the present study was to investigate the interaction between a variation in the <strong>5 HTTLPR</strong> and family environment in relation to <b>smoking</b> habits, <b>nicotine</b> dependence, and <b>nicotine</b> and cotinine levels in hair samples.
+SLC6A4	addiction	dependence	19396697	The objective of the present study was to investigate the interaction between a variation in the <strong>5 HTTLPR</strong> and family environment in relation to smoking habits, nicotine <b>dependence</b>, and nicotine and cotinine levels in hair samples.
+SLC6A4	drug	nicotine	19396697	A random Swedish adolescent population sample (n = 785), from which 200 individuals were stratified regarding behaviour, was genotyped for <strong>5 HTTLPR</strong> and assessed with semi structured interviews, a questionnaire, and hair analyses of <b>nicotine</b> and cotinine.
+SLC6A4	drug	nicotine	19396697	The <strong>5 HTTLPR</strong> gene interacted with a poor family environment to predict <b>smoking</b> habits, as well as <b>nicotine</b> and cotinine levels.
+SLC6A4	drug	nicotine	19396697	The risk of being a <b>smoker</b> was increased 13 times for an individual with a combination of the <strong>5 HTTLPR</strong> LS genotype and a poor family environment in comparison with the Homozygous Long Long (LL) genotype and a good family environment.
+SLC6A4	drug	cocaine	19376154	Specifically, Experiment 1 assessed the ability of selective monoamine transporter inhibitors, e.g., DAT (vanoxerine), NET (nisoxetine) and <strong>SERT</strong> (fluoxetine), to induce taste aversions (relative to <b>cocaine</b>).
+SLC6A4	drug	alcohol	19358979	Evidence from animal studies supports a role for serotonin transporter gene promoter polymorphism (<strong>5 HTTLPR</strong>) gene environment interaction (G x E) in the development of excessive <b>alcohol</b> intake.
+SLC6A4	drug	alcohol	19358979	The present study aims to further explore G x E between <strong>5 HTTLPR</strong> and exposure to psychosocial adversity on <b>alcohol</b> consumption in a high risk community sample of young adults.
+SLC6A4	drug	alcohol	19358979	At age 19 years, 309 participants (142 male participants, 167 female participants) were genotyped for the biallelic and triallelic <strong>5 HTTLPR</strong> and were administered a 45 day <b>alcohol</b> timeline follow back interview, providing measures of the total number of drinks and the number of binge drinking days.
+SLC6A4	addiction	intoxication	19358979	At age 19 years, 309 participants (142 male participants, 167 female participants) were genotyped for the biallelic and triallelic <strong>5 HTTLPR</strong> and were administered a 45 day alcohol timeline follow back interview, providing measures of the total number of drinks and the number of <b>binge</b> drinking days.
+SLC6A4	drug	alcohol	19331786	[Association of the functional serotonin transporter promoter polymorphism (<strong>5 HTTLPR</strong>) with externalizing and internalizing aggressivity and <b>alcohol</b> abuse].
+SLC6A4	drug	alcohol	19331786	The pathogenesis of <b>alcoholism</b> and anti social behaviour has been connected to serotonergic system dysfunction, given support to examine the association with 44 basepair insertion/deletion polymorphism of serotonin gene transporter (<strong>5 HTT</strong>).
+SLC6A4	drug	alcohol	19331786	Regarding <strong>5 HTTLPR</strong> polymorphism prevalence in <b>alcoholic</b> population, 30.7% were homozygotic to l allele, 19.8% were homozygotic to s allele and 49.5% were heterozygotic l/s.
+SLC6A4	drug	alcohol	19331786	<b>Alcoholic</b> patients carrying the l allele from <strong>5 HTTLPR</strong> genotype showed significant lower scores of aggressivity during acute <b>alcohol</b> consumption, and <b>alcoholic</b> patients carrying the s allele showed significant higher scores of aggressivity (during acute <b>alcohol</b> consumption and abstinence), however, the results were not significant.
+SLC6A4	drug	alcohol	19331786	The results demonstrate an association between <strong>5 HTTLPR</strong> polymorphism and the auto and heteroaggressive behaviour in <b>alcohol</b> dependent population, particularly when aggressivity appears under acute <b>alcohol</b> consumption.
+SLC6A4	drug	alcohol	19328219	This study aimed to investigate whether three serotonergic polymorphisms (HTR2A A 1438G (rs6311), and SCL6A4 <strong>5 HTTLPR</strong> and STin2 VNTR) were associated with <b>alcohol</b> dependence, and, whether the serotonergic polymorphisms played a similar role in conferring vulnerability in <b>alcohol</b> and heroin dependence.
+SLC6A4	drug	opioid	19328219	This study aimed to investigate whether three serotonergic polymorphisms (HTR2A A 1438G (rs6311), and SCL6A4 <strong>5 HTTLPR</strong> and STin2 VNTR) were associated with alcohol dependence, and, whether the serotonergic polymorphisms played a similar role in conferring vulnerability in alcohol and <b>heroin</b> dependence.
+SLC6A4	addiction	dependence	19328219	This study aimed to investigate whether three serotonergic polymorphisms (HTR2A A 1438G (rs6311), and SCL6A4 <strong>5 HTTLPR</strong> and STin2 VNTR) were associated with alcohol <b>dependence</b>, and, whether the serotonergic polymorphisms played a similar role in conferring vulnerability in alcohol and heroin <b>dependence</b>.
+SLC6A4	drug	alcohol	19328219	There was an excess of  1438G and <strong>5 HTTLPR</strong> L carriers in <b>alcoholic</b> patients in comparison to the heroin dependent group (OR (95% CI)=1.98 (1.13 3.45) and 1.92 (1.07 3.44), respectively).
+SLC6A4	drug	opioid	19328219	There was an excess of  1438G and <strong>5 HTTLPR</strong> L carriers in alcoholic patients in comparison to the <b>heroin</b> dependent group (OR (95% CI)=1.98 (1.13 3.45) and 1.92 (1.07 3.44), respectively).
+SLC6A4	drug	alcohol	19328219	The A 1438G and <strong>5 HTTLPR</strong> polymorphisms also interacted in distinguishing <b>alcohol</b> from heroin dependent patients (Wald (df)=10.21 (4), p=0.037).
+SLC6A4	drug	opioid	19328219	The A 1438G and <strong>5 HTTLPR</strong> polymorphisms also interacted in distinguishing alcohol from <b>heroin</b> dependent patients (Wald (df)=10.21 (4), p=0.037).
+SLC6A4	drug	alcohol	19328219	The association of  1438A/G with <b>alcohol</b> dependence was especially pronounced in the presence of <strong>5 HTTLPR</strong> S/S, less evident with <strong>5 HTTLPR</strong> L/S and not present with <strong>5 HTTLPR</strong> L/L.
+SLC6A4	addiction	dependence	19328219	The association of  1438A/G with alcohol <b>dependence</b> was especially pronounced in the presence of <strong>5 HTTLPR</strong> S/S, less evident with <strong>5 HTTLPR</strong> L/S and not present with <strong>5 HTTLPR</strong> L/L.
+SLC6A4	drug	alcohol	19179283	The human serotonin (5 hydroxytryptamine, 5 HT) transporter (hSERT, <strong>SLC6A4</strong>) figures prominently in the etiology and treatment of many prevalent neurobehavioral disorders including anxiety, <b>alcoholism</b>, depression, autism, and obsessive compulsive disorder (OCD).
+SLC6A4	addiction	addiction	19179283	The human serotonin (5 hydroxytryptamine, 5 HT) transporter (hSERT, <strong>SLC6A4</strong>) figures prominently in the etiology and treatment of many prevalent neurobehavioral disorders including anxiety, alcoholism, depression, autism, and obsessive <b>compulsive</b> disorder (OCD).
+SLC6A4	drug	alcohol	19179283	The human serotonin (5 hydroxytryptamine, 5 HT) transporter (<strong>hSERT</strong>, <strong>SLC6A4</strong>) figures prominently in the etiology and treatment of many prevalent neurobehavioral disorders including anxiety, <b>alcoholism</b>, depression, autism, and obsessive compulsive disorder (OCD).
+SLC6A4	addiction	addiction	19179283	The human serotonin (5 hydroxytryptamine, 5 HT) transporter (<strong>hSERT</strong>, <strong>SLC6A4</strong>) figures prominently in the etiology and treatment of many prevalent neurobehavioral disorders including anxiety, alcoholism, depression, autism, and obsessive <b>compulsive</b> disorder (OCD).
+SLC6A4	drug	cocaine	19176817	We tested the hypotheses that mice lacking the dopamine transporter (DAT( / )), the serotonin transporter (<strong>SERT</strong>( / )), or both (DAT( / )<strong>SERT</strong>( / )) exhibit decreased reinforcing effects of <b>cocaine</b>.
+SLC6A4	addiction	reward	19176817	We tested the hypotheses that mice lacking the dopamine transporter (DAT( / )), the serotonin transporter (<strong>SERT</strong>( / )), or both (DAT( / )<strong>SERT</strong>( / )) exhibit decreased <b>reinforcing</b> effects of cocaine.
+SLC6A4	drug	cocaine	19176817	In contrast to those mice, <b>cocaine</b>'s reinforcing effects were not diminished in <strong>SERT</strong>( / ) mice under any of the conditions tested, except for impaired initial acquisition of both food  and <b>cocaine</b> maintained behavior.
+SLC6A4	addiction	reward	19176817	In contrast to those mice, cocaine's <b>reinforcing</b> effects were not diminished in <strong>SERT</strong>( / ) mice under any of the conditions tested, except for impaired initial acquisition of both food  and cocaine maintained behavior.
+SLC6A4	drug	cocaine	19176817	These findings support the notion that the DAT, but not the <strong>SERT</strong>, is critical in mediating the reinforcing effects of <b>cocaine</b>.
+SLC6A4	addiction	reward	19176817	These findings support the notion that the DAT, but not the <strong>SERT</strong>, is critical in mediating the <b>reinforcing</b> effects of cocaine.
+SLC6A4	addiction	relapse	19170664	Genetic polymorphisms in several genes (TPH2, <strong>SLC6A4</strong>, HTR1A, HTR2A, COMT, and BDNF) were tested as predictors of <b>relapse</b> (defined as any drinking during follow up) while controlling for baseline measures.
+SLC6A4	addiction	withdrawal	19116947	Changes in the serotonin transporter (<strong>SERT</strong>) have also been reported in MDD, and changes in the immediate early gene c fos have been observed in the context of psychostimulant <b>withdrawal</b>.
+SLC6A4	drug	amphetamine	19116947	This study examined the effects of chronic, escalating doses of D <b>AMPH</b> followed by 24 h of withdrawal on the expression of prodynorphin (PD) and c fos mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and <strong>SERT</strong> mRNA expression in the dorsal raphe nucleus (DRN).
+SLC6A4	addiction	withdrawal	19116947	This study examined the effects of chronic, escalating doses of D AMPH followed by 24 h of <b>withdrawal</b> on the expression of prodynorphin (PD) and c fos mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and <strong>SERT</strong> mRNA expression in the dorsal raphe nucleus (DRN).
+SLC6A4	drug	amphetamine	19116947	<strong>SERT</strong> mRNA expression was decreased in the DRN, and PD mRNA expression was increased in the adjacent ventrolateral periaqueductal gray (VLPAG) following D <b>AMPH</b> withdrawal.
+SLC6A4	addiction	withdrawal	19116947	<strong>SERT</strong> mRNA expression was decreased in the DRN, and PD mRNA expression was increased in the adjacent ventrolateral periaqueductal gray (VLPAG) following D AMPH <b>withdrawal</b>.
+SLC6A4	addiction	withdrawal	19116947	These data indicate that region specific changes in PD and c fos expression occur after <b>withdrawal</b>, while <strong>SERT</strong> mRNA expression is suppressed, similar to what has been reported in MDD.
+SLC6A4	addiction	withdrawal	19116947	Alterations in PD, c fos, and <strong>SERT</strong> expression could contribute to the depression like syndrome associated with psychostimulant <b>withdrawal</b>.
+SLC6A4	drug	cocaine	19086766	Selective serotonin transporter (<strong>SERT</strong>) inhibitors were also effective in reducing <b>cocaine</b> use and blocked <b>cocaine</b> induced brain activation and increases in extracellular dopamine.
+SLC6A4	drug	cocaine	19086766	The results indicate that combined inhibition of DAT and <strong>SERT</strong> may be a viable approach to treat <b>cocaine</b> addiction.
+SLC6A4	addiction	addiction	19086766	The results indicate that combined inhibition of DAT and <strong>SERT</strong> may be a viable approach to treat cocaine <b>addiction</b>.
+SLC6A4	drug	alcohol	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (<strong>5 HTT</strong>) promotor region (5 HTTLPR) in the manifestation of individual <b>alcohol</b> withdrawal symptoms was investigated in 97 Korean male inpatients with <b>alcohol</b> dependence and 76 Korean healthy male subjects.
+SLC6A4	addiction	dependence	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (<strong>5 HTT</strong>) promotor region (5 HTTLPR) in the manifestation of individual alcohol withdrawal symptoms was investigated in 97 Korean male inpatients with alcohol <b>dependence</b> and 76 Korean healthy male subjects.
+SLC6A4	addiction	withdrawal	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (<strong>5 HTT</strong>) promotor region (5 HTTLPR) in the manifestation of individual alcohol <b>withdrawal</b> symptoms was investigated in 97 Korean male inpatients with alcohol dependence and 76 Korean healthy male subjects.
+SLC6A4	drug	alcohol	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (<strong>5 HTT</strong>) promotor region (<strong>5 HTTLPR</strong>) in the manifestation of individual <b>alcohol</b> withdrawal symptoms was investigated in 97 Korean male inpatients with <b>alcohol</b> dependence and 76 Korean healthy male subjects.
+SLC6A4	addiction	dependence	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (<strong>5 HTT</strong>) promotor region (<strong>5 HTTLPR</strong>) in the manifestation of individual alcohol withdrawal symptoms was investigated in 97 Korean male inpatients with alcohol <b>dependence</b> and 76 Korean healthy male subjects.
+SLC6A4	addiction	withdrawal	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (5 HT2A), and the serotonin transporter gene (<strong>5 HTT</strong>) promotor region (<strong>5 HTTLPR</strong>) in the manifestation of individual alcohol <b>withdrawal</b> symptoms was investigated in 97 Korean male inpatients with alcohol dependence and 76 Korean healthy male subjects.
+SLC6A4	drug	cocaine	19053748	Previous studies showed that the mixed monoamine transporter inhibitor (6, RTI 112) reduced <b>cocaine</b> self administration at a high level of serotonin transporter (<strong>5 HTT</strong>) occupancy with no detectable dopamine transporter (DAT) occupancy.
+SLC6A4	drug	alcohol	19032576	A within group design of nontreatment seeking <strong>5 HTTLPR</strong> genotyped <b>alcohol</b> dependent subjects receiving ondansetron and sertraline.
+SLC6A4	addiction	relapse	19032576	A within group design of nontreatment <b>seeking</b> <strong>5 HTTLPR</strong> genotyped alcohol dependent subjects receiving ondansetron and sertraline.
+SLC6A4	drug	alcohol	19032574	In this study, we investigated whether other <strong>SLC6A4</strong> single nucleotide polymorphisms (SNPs) are associated with drinking intensity among treatment seeking <b>alcoholics</b> and whether these polymorphic variants result in differential <strong>SLC6A4</strong> expression levels.
+SLC6A4	addiction	relapse	19032574	In this study, we investigated whether other <strong>SLC6A4</strong> single nucleotide polymorphisms (SNPs) are associated with drinking intensity among treatment <b>seeking</b> alcoholics and whether these polymorphic variants result in differential <strong>SLC6A4</strong> expression levels.
+SLC6A4	drug	alcohol	19032574	We analyzed associations of drinking intensity in 275 (78.5% male) treatment seeking <b>alcoholics</b> of Caucasian and Hispanic origin, with 6 <strong>SLC6A4</strong> polymorphisms.
+SLC6A4	addiction	relapse	19032574	We analyzed associations of drinking intensity in 275 (78.5% male) treatment <b>seeking</b> alcoholics of Caucasian and Hispanic origin, with 6 <strong>SLC6A4</strong> polymorphisms.
+SLC6A4	drug	psychedelics	18991859	Adult animals treated with high doses of <b>MDMA</b> ("<b>ecstasy</b>") either on a single day or for several consecutive days show numerous behavioral changes as well as persistent reductions in brain serotonin (5 HT) concentrations and 5 HT transporter (<strong>SERT</strong>) protein expression.
+SLC6A4	drug	psychedelics	18991859	<strong>SERT</strong> immunoreactive fiber density is significantly reduced in the hippocampus but not the neocortex, suggesting that the hippocampus may be particularly vulnerable to moderate <b>MDMA</b> exposure during adolescence.
+SLC6A4	drug	amphetamine	18991848	Short allele of <strong>5 HTTLPR</strong> as a risk factor for the development of psychosis in Japanese <b>methamphetamine</b> abusers.
+SLC6A4	addiction	relapse	18841348	Decreased brain <strong>SERT</strong> could also be related to the clinical finding that treatment with a selective serotonin re uptake inhibitor might increase <b>relapse</b> to MA.
+SLC6A4	drug	alcohol	18827956	Serotonin transporter (<strong>5 HTTLPR</strong>) and monoamine oxidase (MAOA) promoter polymorphisms in women with severe <b>alcoholism</b>.
+SLC6A4	drug	alcohol	18827956	Genotyping of two functional polymorphisms in the promoter region of the serotonin transporter and monoamine oxidase A, respectively, (<strong>5 HTT</strong> LPR and MAOA VNTR), was performed in a group of women with severe <b>alcohol</b> addiction.
+SLC6A4	addiction	addiction	18827956	Genotyping of two functional polymorphisms in the promoter region of the serotonin transporter and monoamine oxidase A, respectively, (<strong>5 HTT</strong> LPR and MAOA VNTR), was performed in a group of women with severe alcohol <b>addiction</b>.
+SLC6A4	drug	alcohol	18827956	The pattern of associations between genotypes of <strong>5 HTT</strong> LPR and MAOA VNTR in women with severe <b>alcoholism</b> differs from most corresponding studies on males.
+SLC6A4	drug	opioid	18812655	Association of different susceptibilities to <b>morphine</b> with the expression of <strong>5 HTT</strong> and 5 HT1AR mRNA in brain regions of SD rats.
+SLC6A4	addiction	addiction	18812655	Using in situ hybridization, we examined the mRNA expression of 5 hydroxytryptamine transporter (<strong>5 HTT</strong>) and 5 hydroxytryptamine 1A receptor (5 HT1AR) in 3 crucial regions in <b>addiction</b>, namely the ventral tegmental area (VTA), the nucleus accumbens (NAc), and the medial prefrontal cortex (mPFC), during the dependence and withdrawal.
+SLC6A4	addiction	dependence	18812655	Using in situ hybridization, we examined the mRNA expression of 5 hydroxytryptamine transporter (<strong>5 HTT</strong>) and 5 hydroxytryptamine 1A receptor (5 HT1AR) in 3 crucial regions in addiction, namely the ventral tegmental area (VTA), the nucleus accumbens (NAc), and the medial prefrontal cortex (mPFC), during the <b>dependence</b> and withdrawal.
+SLC6A4	addiction	withdrawal	18812655	Using in situ hybridization, we examined the mRNA expression of 5 hydroxytryptamine transporter (<strong>5 HTT</strong>) and 5 hydroxytryptamine 1A receptor (5 HT1AR) in 3 crucial regions in addiction, namely the ventral tegmental area (VTA), the nucleus accumbens (NAc), and the medial prefrontal cortex (mPFC), during the dependence and <b>withdrawal</b>.
+SLC6A4	addiction	dependence	18812655	During <b>dependence</b> state, the expression of <strong>5 HTT</strong> mRNA in each of the regions in the high preference group was significantly lower than that of the low preference group, while higher expression of 5 HT1AR mRNA in each of the regions in the high preference group than that of the low preference group was found (P < 0.05).
+SLC6A4	addiction	withdrawal	18812655	During <b>withdrawal</b> state, the expression of <strong>5 HTT</strong> mRNA in each of the regions in high preference group was significantly higher than that of the low preference group, while lower expression of 5 HT1AR mRNA in each of the regions in the high preference group than that of the low preference group was found (P < 0.05).
+SLC6A4	drug	opioid	18812655	<strong>5 HTT</strong> and 5 HT1AR may play a role in differences in susceptibility to <b>morphine</b>.
+SLC6A4	drug	psychedelics	18812013	<b>MDMA</b> treatment increased <strong>SERT</strong> in wild type mice, but did not further increase it in S100B mutant mice.
+SLC6A4	drug	nicotine	18778441	To investigate the neuronal mechanisms of the precipitation of depression during <b>smoking</b> cessation, an animal model of <b>nicotine</b> withdrawal was used, and the expression of serotonin transporter (<strong>5HTT</strong>), abnormality of which is implicated in the pathogenesis of depression, was investigated.
+SLC6A4	addiction	withdrawal	18778441	To investigate the neuronal mechanisms of the precipitation of depression during smoking cessation, an animal model of nicotine <b>withdrawal</b> was used, and the expression of serotonin transporter (<strong>5HTT</strong>), abnormality of which is implicated in the pathogenesis of depression, was investigated.
+SLC6A4	drug	nicotine	18778441	Chronic <b>nicotine</b> infusion resulted in the reduction of <strong>5HTT</strong> mRNA expression, which lasted through withdrawal day 2.
+SLC6A4	addiction	withdrawal	18778441	Chronic nicotine infusion resulted in the reduction of <strong>5HTT</strong> mRNA expression, which lasted through <b>withdrawal</b> day 2.
+SLC6A4	drug	nicotine	18778441	Chronic <b>nicotine</b> infusion reduces the synthesis of <strong>5HTT</strong> protein, which may consequently precipitate depression during <b>nicotine</b> withdrawal, but co administration of bupropion may ameliorate withdrawal symptoms by counteracting <b>nicotine</b>'s effect on <strong>5HTT</strong>.
+SLC6A4	addiction	withdrawal	18778441	Chronic nicotine infusion reduces the synthesis of <strong>5HTT</strong> protein, which may consequently precipitate depression during nicotine <b>withdrawal</b>, but co administration of bupropion may ameliorate <b>withdrawal</b> symptoms by counteracting nicotine's effect on <strong>5HTT</strong>.
+SLC6A4	drug	nicotine	18691405	Lack of association between serotonin transporter gene polymorphism <strong>5 HTTLPR</strong> and <b>smoking</b> among Polish population: a case control study.
+SLC6A4	drug	nicotine	18691405	Insertion/deletion polymorphism in the promoter region of the serotonin transporter gene (<strong>5 HTTLPR</strong>) has been linked to vulnerability to <b>smoking</b> and ability to quit.
+SLC6A4	drug	nicotine	18691405	We aimed to determine whether <strong>5 HTTLPR</strong> genotype is associated with <b>smoking</b> behavior in Caucasians from Northern Poland and to investigate other risk factors for <b>tobacco</b> <b>smoking</b>.
+SLC6A4	drug	nicotine	18691405	<strong>5 HTTLPR</strong> genotypes were determined in 149 ever <b>smokers</b> (66 females; mean age 53.0 years) and 158 gender and ethnicity matched never <b>smoking</b> controls (79 females; mean age 45.0 years) to evaluate the association of this polymorphism with ever <b>smoking</b> status.
+SLC6A4	drug	nicotine	18691405	Analysis of <b>smokers</b> was performed to evaluate the role of <strong>5 HTTLPR</strong> in the age of starting regular <b>smoking</b>, the number of cigarettes smoked daily, pack years, FTND score, duration of <b>smoking</b>, and the mean length of the longest abstinence on quitting.
+SLC6A4	drug	nicotine	18691405	<strong>5 HTTLPR</strong> seems to be not a major factor determining cigarette <b>smoking</b> in Poles.
+SLC6A4	drug	nicotine	18690118	OPRM1 (AA>AG or GG) was associated with <b>smoking</b> reward, but <strong>SLC6A4</strong> variable number tandem repeat was unrelated to any of these measures.
+SLC6A4	addiction	reward	18690118	OPRM1 (AA>AG or GG) was associated with smoking <b>reward</b>, but <strong>SLC6A4</strong> variable number tandem repeat was unrelated to any of these measures.
+SLC6A4	drug	opioid	18690117	Very few or no significant associations were seen for the DRD2/ANKK1 TaqIA polymorphism, the serotonin transporter promoter VNTR or 5HTTLPR (<strong>SLC6A4</strong>), the dopamine transporter 3' VNTR (SLC6A3), and the mu <b>opioid</b> receptor A118G single nucleotide polymorphism (mu <b>opioid</b> receptor polymorphism 1).
+SLC6A4	drug	opioid	18690117	Very few or no significant associations were seen for the DRD2/ANKK1 TaqIA polymorphism, the serotonin transporter promoter VNTR or <strong>5HTTLPR</strong> (<strong>SLC6A4</strong>), the dopamine transporter 3' VNTR (SLC6A3), and the mu <b>opioid</b> receptor A118G single nucleotide polymorphism (mu <b>opioid</b> receptor polymorphism 1).
+SLC6A4	drug	cocaine	18606182	In this study, we found that the selective inhibitor of dopamine transporter (DAT) function, 1 [2 [bis(4 fluorophenyl) methoxy]ethyl] 4 (3 phenylpropyl) piperazine (GBR 12909, vanoxerine), but not the selective inhibitors of serotonin and norepinephrine (<strong>SERT</strong> and NET) transporters, sertraline and nizoxetine, emulated <b>cocaine</b> mediated enhancement of Tat neurotoxicity in rat fetal midbrain primary cell cultures.
+SLC6A4	drug	cocaine	18581099	To study the rewarding and motivational properties of <b>cocaine</b> in the serotonin transporter knockout (<strong>SERT</strong> / ) rat and the involvement of compensatory changes in 5 HT1A receptor function are the objectives of the study.
+SLC6A4	drug	cocaine	18581099	The <strong>SERT</strong> /  rat was tested for <b>cocaine</b> induced locomotor activity, <b>cocaine</b> induced conditioned place preference, and intravenous <b>cocaine</b> self administration.
+SLC6A4	drug	cocaine	18581099	<b>Cocaine</b> induced hyperactivity and conditioned place preference, as well as intravenous <b>cocaine</b> self administration were enhanced in <strong>SERT</strong> /  rats.
+SLC6A4	drug	cocaine	18581099	We further found that both 8 OHDPAT and S 15535 pretreatment increased low dose <b>cocaine</b> induced locomotor activity in <strong>SERT</strong> /  rats, but not <strong>SERT</strong>+/+ rats.
+SLC6A4	drug	cocaine	18581099	At a high <b>cocaine</b> dose, only <strong>SERT</strong>+/+ animals responded to 8 OHDPAT and S 15535.
+SLC6A4	drug	cocaine	18581099	These data indicate that <strong>SERT</strong> /   associated 5 HT1A receptor adaptations facilitate low dose <b>cocaine</b> effects and attenuate high dose <b>cocaine</b> effects in <b>cocaine</b> supersensitive animals.
+SLC6A4	drug	nicotine	18562131	Cox regression analysis did not demonstrate significant effects of any of the three genotypes on relapse to <b>smoking</b>: TPH1 (Reference AA; AC: hazard ratio (HR) 0.99, 95% confidence interval (CI) 0.78, 1.24, p=0.90; CC: HR 0.93, 95% CI 0.73, 1.18, p=0.55); <strong>5 HTTLPR</strong> (Reference LL; SL: HR 1.01, 95% CI 0.85, 1.20, p=0.90; SS: HR 1.13, 95% CI 0.91, 1.39, p=0.27); HTR1A (Reference CC; CG: HR 1.04, 95% CI 0.86, 1.25, p=0.70; GG: HR 1.01, 95% CI 0.82, 1.24, p=0.93).
+SLC6A4	addiction	relapse	18562131	Cox regression analysis did not demonstrate significant effects of any of the three genotypes on <b>relapse</b> to smoking: TPH1 (Reference AA; AC: hazard ratio (HR) 0.99, 95% confidence interval (CI) 0.78, 1.24, p=0.90; CC: HR 0.93, 95% CI 0.73, 1.18, p=0.55); <strong>5 HTTLPR</strong> (Reference LL; SL: HR 1.01, 95% CI 0.85, 1.20, p=0.90; SS: HR 1.13, 95% CI 0.91, 1.39, p=0.27); HTR1A (Reference CC; CG: HR 1.04, 95% CI 0.86, 1.25, p=0.70; GG: HR 1.01, 95% CI 0.82, 1.24, p=0.93).
+SLC6A4	drug	alcohol	18552399	The aim of this study was to investigate the potential association between functional polymorphisms of dopaminergic [dopamine receptor D2 (DRD2), dopamine receptor D3 (DRD3) and dopamine transporter (SLC6A3)] and serotonergic [serotonin 2A receptor (HTR2A) and serotonin transporter (<strong>SLC6A4</strong>)] genes and treatment outcome in <b>alcohol</b> dependent patients.
+SLC6A4	drug	alcohol	18552399	Our findings suggest that functional polymorphism of the <strong>SLC6A4</strong> gene may have an influence on treatment outcome in <b>alcohol</b> dependent patients.
+SLC6A4	drug	alcohol	18405071	A case group of males with type 2 <b>alcoholism</b> (N=59) and a control group of healthy males (N=282), both of Croatian origin, were analyzed for the frequency distribution of polymorphisms in 5HT transporter (<strong>5HTT</strong> VNTR2, <strong>5HTT</strong> LPR), monoamine oxidase A (MAOA uVNTR) and B (MAOB A/G) and tryptophan hydroxylase 1 (TPH1 A218C) and 2 (TPH2 G 703T) genes.
+SLC6A4	drug	alcohol	18405071	An increase in the frequencies of 10 repeat allele (p = 0.010; OR = 1.73; 95% CI = 1.14 2.60) and 10/10 genotype (p = 0.006; OR = 2.57; 95% CI = 1.32 5.00) of the <strong>5HTT</strong> VNTR2 polymorphism was found in <b>alcoholic</b> patients.
+SLC6A4	drug	alcohol	18405071	Present results support earlier studies implicating the role of <strong>5HTT</strong> gene in <b>alcoholism</b>.
+SLC6A4	drug	alcohol	18364363	The short (S) allele of the serotonin transporter gene promoter polymorphism (<strong>5 HTTLPR</strong>) contributes to the risk of <b>alcohol</b> dependence and co occurring clinical features.
+SLC6A4	addiction	dependence	18364363	The short (S) allele of the serotonin transporter gene promoter polymorphism (<strong>5 HTTLPR</strong>) contributes to the risk of alcohol <b>dependence</b> and co occurring clinical features.
+SLC6A4	drug	alcohol	18364363	48 <b>alcohol</b> dependent male patients were recruited and genotyped for the <strong>5 HTTLPR</strong>.
+SLC6A4	drug	alcohol	18364363	The S allele of the <strong>5 HTTLPR</strong> polymorphism may influence the risk of relapse in abstinent <b>alcohol</b> dependent patients, possibly through intermediate phenotypes.
+SLC6A4	addiction	relapse	18364363	The S allele of the <strong>5 HTTLPR</strong> polymorphism may influence the risk of <b>relapse</b> in abstinent alcohol dependent patients, possibly through intermediate phenotypes.
+SLC6A4	drug	cocaine	18321529	Preclinical evidence indicates that exposure to <b>cocaine</b> influences the activity of the serotonin transporter (<strong>5 HTT</strong>) as well as several 5 HT receptor subtypes.
+SLC6A4	drug	cocaine	18321529	However, little is known about the relationship between the <strong>5 HTT</strong> and 5 HT receptors following <b>cocaine</b> exposure in humans.
+SLC6A4	drug	cocaine	18321529	We examined the relationship between platelet <strong>5 HTT</strong>, a presynaptic 5 HT measure, and prolactin (PRL) response to meta chlorophenylpiperazine (m CPP), a postsynaptic 5 HT receptor agonist in <b>cocaine</b> dependent individuals.
+SLC6A4	addiction	reward	18321529	We examined the relationship between platelet <strong>5 HTT</strong>, a presynaptic 5 HT measure, and prolactin (PRL) response to meta chlorophenylpiperazine (m <b>CPP</b>), a postsynaptic 5 HT receptor agonist in cocaine dependent individuals.
+SLC6A4	drug	alcohol	18211952	The work by Storvik and colleagues recently published on <b>Alcohol</b> and <b>Alcoholism</b> shows some interesting differences on the <strong>SERT</strong> brain density between the type I and type II <b>alcoholic</b> subtypes.
+SLC6A4	drug	opioid	18182772	The association between the  1438AA vs. AG/GG genotypes and <b>heroin</b> dependence was enhanced in the presence of 12 repeat <strong>5 HTT</strong> VNTR and short 5 HTTLPR alleles [24.8% in <b>heroin</b> dependent patients vs. 12.6% in controls; corrected p = 0.045, OR = 2.28 (95% CI = 1.36 3.82)].
+SLC6A4	addiction	dependence	18182772	The association between the  1438AA vs. AG/GG genotypes and heroin <b>dependence</b> was enhanced in the presence of 12 repeat <strong>5 HTT</strong> VNTR and short 5 HTTLPR alleles [24.8% in heroin dependent patients vs. 12.6% in controls; corrected p = 0.045, OR = 2.28 (95% CI = 1.36 3.82)].
+SLC6A4	drug	opioid	18182772	The association between the  1438AA vs. AG/GG genotypes and <b>heroin</b> dependence was enhanced in the presence of 12 repeat <strong>5 HTT</strong> VNTR and short <strong>5 HTTLPR</strong> alleles [24.8% in <b>heroin</b> dependent patients vs. 12.6% in controls; corrected p = 0.045, OR = 2.28 (95% CI = 1.36 3.82)].
+SLC6A4	addiction	dependence	18182772	The association between the  1438AA vs. AG/GG genotypes and heroin <b>dependence</b> was enhanced in the presence of 12 repeat <strong>5 HTT</strong> VNTR and short <strong>5 HTTLPR</strong> alleles [24.8% in heroin dependent patients vs. 12.6% in controls; corrected p = 0.045, OR = 2.28 (95% CI = 1.36 3.82)].
+SLC6A4	drug	opioid	18182772	Our findings support a contribution of the 5 HT(2A) gene to susceptibility to <b>heroin</b> dependence, as well as a possible synergistic effect of 5 HT(2A) and <strong>5 HTT</strong> genes on susceptibility to <b>heroin</b> dependence.
+SLC6A4	addiction	dependence	18182772	Our findings support a contribution of the 5 HT(2A) gene to susceptibility to heroin <b>dependence</b>, as well as a possible synergistic effect of 5 HT(2A) and <strong>5 HTT</strong> genes on susceptibility to heroin <b>dependence</b>.
+SLC6A4	drug	psychedelics	18005064	Radioligand binding and autoradiography demonstrated lower densities of serotonin transporter sites (<strong>SERT</strong>) in <b>MDMA</b> self administering rats as compared with controls across brain regions.
+SLC6A4	drug	psychedelics	18005064	The reduction in <strong>SERT</strong> densities was comparable in magnitude to rats treated with experimenter administered doses of <b>MDMA</b>.
+SLC6A4	drug	cocaine	18003826	Fluoxetine, a serotonin transporter (<strong>SERT</strong>) inhibitor, produced CPP in DD, but not control mice, suggesting that serotonin mediates <b>cocaine</b> CPP in DD mice.
+SLC6A4	addiction	reward	18003826	Fluoxetine, a serotonin transporter (<strong>SERT</strong>) inhibitor, produced <b>CPP</b> in DD, but not control mice, suggesting that serotonin mediates cocaine <b>CPP</b> in DD mice.
+SLC6A4	drug	cocaine	18003826	These findings are consistent with the hypothesis that, in the absence of dopamine, <b>cocaine</b> mediated <strong>SERT</strong> blockade activates dopamine neurons, which then release some other neurotransmitter that contributes to <b>cocaine</b> reward in DD mice.
+SLC6A4	addiction	reward	18003826	These findings are consistent with the hypothesis that, in the absence of dopamine, cocaine mediated <strong>SERT</strong> blockade activates dopamine neurons, which then release some other neurotransmitter that contributes to cocaine <b>reward</b> in DD mice.
+SLC6A4	drug	alcohol	17987668	The relationship of 5HTT (<strong>SLC6A4</strong>) methylation and genotype on mRNA expression and liability to major depression and <b>alcohol</b> dependence in subjects from the Iowa Adoption Studies.
+SLC6A4	addiction	dependence	17987668	The relationship of 5HTT (<strong>SLC6A4</strong>) methylation and genotype on mRNA expression and liability to major depression and alcohol <b>dependence</b> in subjects from the Iowa Adoption Studies.
+SLC6A4	drug	alcohol	17987668	The relationship of <strong>5HTT</strong> (<strong>SLC6A4</strong>) methylation and genotype on mRNA expression and liability to major depression and <b>alcohol</b> dependence in subjects from the Iowa Adoption Studies.
+SLC6A4	addiction	dependence	17987668	The relationship of <strong>5HTT</strong> (<strong>SLC6A4</strong>) methylation and genotype on mRNA expression and liability to major depression and alcohol <b>dependence</b> in subjects from the Iowa Adoption Studies.
+SLC6A4	drug	alcohol	17987668	Those subjects with a lifetime history of <b>Alcohol</b> Dependence had higher levels of <strong>SLC6A4</strong> mRNA.
+SLC6A4	addiction	dependence	17987668	Those subjects with a lifetime history of Alcohol <b>Dependence</b> had higher levels of <strong>SLC6A4</strong> mRNA.
+SLC6A4	drug	alcohol	17948892	The association between DRD2/ANKK1, <strong>5 HTTLPR</strong> gene, and specific personality trait on antisocial <b>alcoholism</b> among Han Chinese in Taiwan.
+SLC6A4	drug	alcohol	17948892	In the novelty seeking scores, after stratification of DRD2 TaqI A genotypes, only a significant difference in <strong>5 HTTLPR</strong> polymorphisms between antisocial <b>alcoholics</b> and antisocial non <b>alcoholics</b> was found, indicating an interaction between DRD2 TaqI A1+ (include A1/A1 or A1/A2) and <strong>5 HTTLPR</strong> S/S genotype (t = 2.75, P = 0.01) However, no significant difference was found in the harm avoidance personality trait between these two groups of Han Chinese in Taiwan.
+SLC6A4	addiction	relapse	17948892	In the novelty <b>seeking</b> scores, after stratification of DRD2 TaqI A genotypes, only a significant difference in <strong>5 HTTLPR</strong> polymorphisms between antisocial alcoholics and antisocial non alcoholics was found, indicating an interaction between DRD2 TaqI A1+ (include A1/A1 or A1/A2) and <strong>5 HTTLPR</strong> S/S genotype (t = 2.75, P = 0.01) However, no significant difference was found in the harm avoidance personality trait between these two groups of Han Chinese in Taiwan.
+SLC6A4	addiction	addiction	17713719	Reduced availability of brainstem serotonin transporters (<strong>5 HTT</strong>) has been observed in vivo in obsessive <b>compulsive</b> disorder (OCD).
+SLC6A4	drug	nicotine	17713719	<strong>5 HTT</strong> availability in the thalamus and the midbrain was measured in nine drug free OCD patients and compared with 19 healthy controls, matched for the individual combination of <strong>5 HTT</strong> genotype, gender and <b>smoking</b> status.
+SLC6A4	drug	alcohol	17711874	Association of the long allele of the <strong>5 HTTLPR</strong> polymorphism with compulsive craving in <b>alcohol</b> dependence.
+SLC6A4	addiction	addiction	17711874	Association of the long allele of the <strong>5 HTTLPR</strong> polymorphism with <b>compulsive</b> craving in alcohol dependence.
+SLC6A4	addiction	dependence	17711874	Association of the long allele of the <strong>5 HTTLPR</strong> polymorphism with compulsive craving in alcohol <b>dependence</b>.
+SLC6A4	addiction	relapse	17711874	Association of the long allele of the <strong>5 HTTLPR</strong> polymorphism with compulsive <b>craving</b> in alcohol dependence.
+SLC6A4	drug	alcohol	17711874	Various studies have reported a role of the serotonin transporter linked polymorphic region (<strong>5 HTTLPR</strong>) in <b>alcoholism</b>.
+SLC6A4	addiction	addiction	17711874	We found significantly higher <b>compulsive</b> craving in patients with the long allele of the <strong>5 HTTLPR</strong> polymorphism [at admission: analysis of variance (ANOVA): F = 3.48, P = 0.034, general linear model: F = 3.92, P = 0.023; after 7 days: ANOVA: F = 3.12, P = 0.049].
+SLC6A4	addiction	relapse	17711874	We found significantly higher compulsive <b>craving</b> in patients with the long allele of the <strong>5 HTTLPR</strong> polymorphism [at admission: analysis of variance (ANOVA): F = 3.48, P = 0.034, general linear model: F = 3.92, P = 0.023; after 7 days: ANOVA: F = 3.12, P = 0.049].
+SLC6A4	drug	alcohol	17711874	Our results suggest that the long variant of the <strong>5 HTTLPR</strong> polymorphism is associated with higher compulsive <b>alcohol</b> craving at the beginning of <b>alcohol</b> withdrawal.
+SLC6A4	addiction	addiction	17711874	Our results suggest that the long variant of the <strong>5 HTTLPR</strong> polymorphism is associated with higher <b>compulsive</b> alcohol craving at the beginning of alcohol withdrawal.
+SLC6A4	addiction	relapse	17711874	Our results suggest that the long variant of the <strong>5 HTTLPR</strong> polymorphism is associated with higher compulsive alcohol <b>craving</b> at the beginning of alcohol withdrawal.
+SLC6A4	addiction	withdrawal	17711874	Our results suggest that the long variant of the <strong>5 HTTLPR</strong> polymorphism is associated with higher compulsive alcohol craving at the beginning of alcohol <b>withdrawal</b>.
+SLC6A4	addiction	relapse	17707567	We attempted to investigate whether the dopamine D2 receptor (DRD2) and the serotonin transporter promoter region (<strong>5 HTTLPR</strong>) genes were involved in Novelty <b>Seeking</b> (NS) and Harm Avoidance (HA) of ANX/DEP ALC.
+SLC6A4	drug	psychedelics	17698848	<b>Ibogaine</b>, a hallucinogenic alkaloid with purported anti addiction properties, inhibited serotonin transporter (<strong>SERT</strong>) noncompetitively by decreasing V(max) with little change in the K(m) for serotonin (5 HT).
+SLC6A4	addiction	addiction	17698848	Ibogaine, a hallucinogenic alkaloid with purported anti <b>addiction</b> properties, inhibited serotonin transporter (<strong>SERT</strong>) noncompetitively by decreasing V(max) with little change in the K(m) for serotonin (5 HT).
+SLC6A4	drug	cocaine	17698848	Ibogaine also inhibited binding to <strong>SERT</strong> of the <b>cocaine</b> analog 2beta 2 carbomethoxy 3 (4 [(125)I]iodophenyl)tropane.
+SLC6A4	drug	psychedelics	17698848	<b>Ibogaine</b> also inhibited binding to <strong>SERT</strong> of the cocaine analog 2beta 2 carbomethoxy 3 (4 [(125)I]iodophenyl)tropane.
+SLC6A4	drug	psychedelics	17698848	<b>Ibogaine</b> increased the reactivity of cysteine residues positioned in the proposed cytoplasmic permeation pathway of <strong>SERT</strong> but not at nearby positions out of that pathway.
+SLC6A4	drug	cocaine	17698848	These results are consistent with the proposal that ibogaine binds to and stabilizes the state of <strong>SERT</strong> from which 5 HT dissociates to the cytoplasm, in contrast with <b>cocaine</b>, which stabilizes the state that binds extracellular 5 HT.
+SLC6A4	drug	psychedelics	17698848	These results are consistent with the proposal that <b>ibogaine</b> binds to and stabilizes the state of <strong>SERT</strong> from which 5 HT dissociates to the cytoplasm, in contrast with cocaine, which stabilizes the state that binds extracellular 5 HT.
+SLC6A4	drug	psychedelics	17692920	Repeated intermittent <b>MDMA</b> binges reduce DAT density in mice and <strong>SERT</strong> density in rats in reward regions of the adolescent brain.
+SLC6A4	addiction	reward	17692920	Repeated intermittent MDMA binges reduce DAT density in mice and <strong>SERT</strong> density in rats in <b>reward</b> regions of the adolescent brain.
+SLC6A4	addiction	reward	17692920	Behavioral responses in the open field and autoradiographic ligand binding to dopamine (DAT) and serotonin (<strong>SERT</strong>) transporters in <b>reward</b> regions of the brain were measured.
+SLC6A4	drug	psychedelics	17692920	Taken together, our data provide evidence for differential regulation of DAT and <strong>SERT</strong> densities in reward related brain regions of rats and mice after long term intermittent administration of <b>MDMA</b>.
+SLC6A4	addiction	reward	17692920	Taken together, our data provide evidence for differential regulation of DAT and <strong>SERT</strong> densities in <b>reward</b> related brain regions of rats and mice after long term intermittent administration of MDMA.
+SLC6A4	drug	psychedelics	17653110	Block of serotonin transporter (<strong>SERT</strong>) with citalopram or 5 HT depletion with (+/ ) p chlorophenylalanine pretreatment partially inhibited the ESP <b>MDMA</b>.
+SLC6A4	drug	psychedelics	17653110	Block of both <strong>SERT</strong> and NE transporter prevented ESP <b>MDMA</b>, indicating its dependence on release of both 5 HT and NE.
+SLC6A4	addiction	dependence	17653110	Block of both <strong>SERT</strong> and NE transporter prevented ESP MDMA, indicating its <b>dependence</b> on release of both 5 HT and NE.
+SLC6A4	drug	psychedelics	17443127	<strong>SERT</strong> availability did not differ between monkeys with a history of <b>MDMA</b> SA and control monkeys in any region examined.
+SLC6A4	drug	cocaine	17443127	In contrast, monkeys with a history of <b>cocaine</b> SA showed significantly higher levels of <strong>SERT</strong> availability in the caudate nucleus and putamen compared to control subjects.
+SLC6A4	drug	cocaine	17443127	The higher level of <strong>SERT</strong> availability in <b>cocaine</b> experienced monkeys may lead to a reduced inhibitory tone of 5 HT on the DA system, which may explain, in part, differences in the abuse liability between <b>cocaine</b> and MDMA.
+SLC6A4	drug	psychedelics	17443127	The higher level of <strong>SERT</strong> availability in cocaine experienced monkeys may lead to a reduced inhibitory tone of 5 HT on the DA system, which may explain, in part, differences in the abuse liability between cocaine and <b>MDMA</b>.
+SLC6A4	drug	alcohol	17418697	In this preliminary study, possible alterations of [3H]citalopram binding to serotonin transporter (<strong>SERT</strong>) were evaluated in the NAC of Cloninger type 1 and 2 <b>alcoholics</b> (nine and seven subjects, respectively), and nonalcoholic controls (10 subjects) by human postmortem whole hemisphere autoradiography.
+SLC6A4	drug	alcohol	17418697	In addition, there was a strong tendency toward a positive correlation between the <strong>SERT</strong> and dopamine transporter binding in the type 2 <b>alcoholics</b>, but not in the other groups.
+SLC6A4	drug	nicotine	17372541	Regarding interaction between <b>nicotine</b> use and anxiety and depression, the gene encoding for the serotonin transporter (<strong>5 HTT</strong>) may constitute a candidate gene.
+SLC6A4	drug	psychedelics	17306775	The aim of the present study was to determine the contribution of the serotonin transporter (<strong>SERT</strong>) in <b>MDMA</b> self administration behavior by using knockout (KO) mice deficient in <strong>SERT</strong>.
+SLC6A4	drug	psychedelics	17306775	These findings provide evidence for the specific involvement of <strong>SERT</strong> in <b>MDMA</b> reinforcing properties.
+SLC6A4	addiction	reward	17306775	These findings provide evidence for the specific involvement of <strong>SERT</strong> in MDMA <b>reinforcing</b> properties.
+SLC6A4	drug	alcohol	17167343	The objective of this study was to analyze association of the serotonin transporter gene <strong>5 HTTLPR</strong> polymorphism on lifetime depression and <b>alcohol</b> dependence in the Collaborative Study on the Genetics of <b>Alcoholism</b> sample.
+SLC6A4	addiction	dependence	17167343	The objective of this study was to analyze association of the serotonin transporter gene <strong>5 HTTLPR</strong> polymorphism on lifetime depression and alcohol <b>dependence</b> in the Collaborative Study on the Genetics of Alcoholism sample.
+SLC6A4	drug	alcohol	17123474	Predictors of early <b>alcohol</b> use include the following: maltreatment, family loading for <b>alcohol</b> or substance use disorders, and serotonin transporter genotype (5 HTTLPR; locus <strong>SLC6A4</strong>).
+SLC6A4	drug	alcohol	17123474	Predictors of early <b>alcohol</b> use include the following: maltreatment, family loading for <b>alcohol</b> or substance use disorders, and serotonin transporter genotype (<strong>5 HTTLPR</strong>; locus <strong>SLC6A4</strong>).
+SLC6A4	drug	alcohol	17123474	Early <b>alcohol</b> use was predicted by maltreatment, <strong>5 HTTLPR</strong>, and a gene by environment interaction, with increased risk for early <b>alcohol</b> use associated with the s allele.
+SLC6A4	drug	alcohol	17117959	Increasing evidence supports a role for 5 hydroxytryptamine (5 HT) and the 5 HT transporter (<strong>5 HTT</strong>) in modulating the neural and behavioral actions of <b>ethanol</b> (EtOH) and other drugs of abuse.
+SLC6A4	addiction	reward	17117959	<b>Reward</b> related effects of EtOH were assessed in <strong>5 HTT</strong> KO mice using the conditioned place preference (<b>CPP</b>) paradigm.
+SLC6A4	drug	alcohol	17117959	Data extend the finding that loss of <strong>5 HTT</strong> gene function alters certain neural and behavioral effects of EtOH, with implications for better understanding the pathophysiology and treatment of <b>alcoholism</b>.
+SLC6A4	drug	alcohol	17106419	The serotonin transporter promotor polymorphism <strong>5 HTTLPR</strong> is not associated with <b>alcoholism</b> or severe forms of <b>alcohol</b> withdrawal in a German sample.
+SLC6A4	addiction	withdrawal	17106419	The serotonin transporter promotor polymorphism <strong>5 HTTLPR</strong> is not associated with alcoholism or severe forms of alcohol <b>withdrawal</b> in a German sample.
+SLC6A4	drug	cocaine	17105925	Interestingly, the rewarding effects of <b>cocaine</b> are retained in dopamine transporter (DAT) knockout (KO) mice, while serotonin transporter (<strong>SERT</strong>) and DAT double KO mice do not exhibit conditioned place preference (CPP) to <b>cocaine</b>.
+SLC6A4	addiction	reward	17105925	Interestingly, the rewarding effects of cocaine are retained in dopamine transporter (DAT) knockout (KO) mice, while serotonin transporter (<strong>SERT</strong>) and DAT double KO mice do not exhibit conditioned place preference (<b>CPP</b>) to cocaine.
+SLC6A4	drug	cocaine	17105829	Last, the dose of RTI 336 that reduced <b>cocaine</b> maintained behavior by 50% (ED(50)) was coadministered with the selective serotonin transporter (<strong>SERT</strong>) inhibitors fluoxetine (3.0 mg/kg) and citalopram (3.0 mg/kg) to characterize their combined effects on <b>cocaine</b> self administration.
+SLC6A4	drug	cocaine	17105829	Co administration of the ED(50) dose of RTI 336 in combination with either <strong>SERT</strong> inhibitor completely suppressed <b>cocaine</b> self administration without affecting DAT occupancy.
+SLC6A4	drug	cocaine	17105829	Hence, at comparable levels of DAT occupancy, coadministration of <strong>SERT</strong> inhibitors with RTI 336 produced more robust reductions in <b>cocaine</b> self administration compared with RTI 336 alone.
+SLC6A4	drug	cocaine	17105829	Collectively, the results indicate that combined inhibition of DAT and <strong>SERT</strong> warrants consideration as a viable approach in the development of <b>cocaine</b> medications.
+SLC6A4	drug	alcohol	17079080	Family based and case control study of DRD2, DAT, <strong>5HTT</strong>, COMT genes polymorphisms in <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	17079080	Family based and case control study of DRD2, DAT, <strong>5HTT</strong>, COMT genes polymorphisms in alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	17079080	The paper focuses on such candidate gene polymorphisms that alter <b>alcoholism</b> related intermediate phenotypes including: dopaminergic system polymorphic variants (DRD2  141C Ins/Del in promoter region, exon 8 and DRD2 TaqI A and DAT 40bp VNTR genes polymorphisms) that cause predisposition to severe <b>alcoholism</b> (haplotype Ins/G/A2); COMT Val158Met gene polymorphism related to differences in executive cognitive function and <strong>5 HTT</strong> gene promoter polymorphism, which alters stress response and affects anxiety and dysphoria.
+SLC6A4	drug	alcohol	17063152	Voluntary <b>ethanol</b> consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (<strong>5 HTT</strong>) in the dorsal and median raphe nuclei.
+SLC6A4	drug	cannabinoid	17063152	Voluntary ethanol consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, <b>cannabinoid</b> CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (<strong>5 HTT</strong>) in the dorsal and median raphe nuclei.
+SLC6A4	drug	opioid	17063152	Voluntary ethanol consumption altered mu <b>opioid</b> receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, proenkephalin (PENK) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (<strong>5 HTT</strong>) in the dorsal and median raphe nuclei.
+SLC6A4	drug	alcohol	17063152	These results point to a role for the mu opioid receptor, TH, PENK, CRF, CB1 R, and <strong>5 HTT</strong> genes in specific brain regions in the modulation of neuroadaptative mechanisms associated to the decrease of <b>ethanol</b> intake induced by <b>naltrexone</b>.
+SLC6A4	drug	opioid	17063152	These results point to a role for the mu <b>opioid</b> receptor, TH, PENK, CRF, CB1 R, and <strong>5 HTT</strong> genes in specific brain regions in the modulation of neuroadaptative mechanisms associated to the decrease of ethanol intake induced by naltrexone.
+SLC6A4	addiction	reward	17000009	We investigated the relationship of a polymorphism in the 5' promoter region of the serotonin transporter gene (<strong>5 HTTLPR</strong>) with prolactin (PRL) response to meta chlorophenylpiperazine (m <b>CPP</b>) in a sample of 68 African American individuals, 35 CD subjects and 33 controls.
+SLC6A4	addiction	relapse	17000009	We also examined whether measures of impulsivity, hostility and sensation <b>seeking</b> influenced the relationship between the <strong>5 HTTLPR</strong> polymorphism and PRL response to m CPP in this sample.
+SLC6A4	addiction	reward	17000009	We also examined whether measures of impulsivity, hostility and sensation seeking influenced the relationship between the <strong>5 HTTLPR</strong> polymorphism and PRL response to m <b>CPP</b> in this sample.
+SLC6A4	drug	cocaine	16972224	In the present study, parents care perception, aggressive personality traits, and genotype (serotonin transporter promoter gene  <strong>5 HTTLPR</strong>) have been investigated in <b>cocaine</b> users and healthy control subjects.
+SLC6A4	drug	amphetamine	16966188	The separate and combined analyses of the gene linked polymorphic region (<strong>5 HTTLPR</strong>) and the Intron 2 VNTR suggest that these two HTT polymorphisms may contribute to acute subjective responses to d <b>amphetamine</b> with a small effect.
+SLC6A4	drug	alcohol	16819620	The present study was designed to examine the influence of the DA D4 receptor (DRD4) and the serotonin transporter (<strong>5 HTT</strong>) genotype and their interaction on adolescent <b>alcohol</b> and tobacco experimentation.
+SLC6A4	drug	nicotine	16819620	The present study was designed to examine the influence of the DA D4 receptor (DRD4) and the serotonin transporter (<strong>5 HTT</strong>) genotype and their interaction on adolescent alcohol and <b>tobacco</b> experimentation.
+SLC6A4	drug	nicotine	16819620	Girls without the DRD4 7 repeat allele and who were homozygous for the long allele of <strong>5 HTTLPR</strong> displayed the highest <b>smoking</b> and drinking activity.
+SLC6A4	drug	alcohol	16775130	The 5 HT transporter (<strong>5 HTT</strong>) is the principle means of 5 HT reuptake in the brain and an obvious candidate mechanism for the effect of <b>ethanol</b> to inhibit 5 HT clearance.
+SLC6A4	drug	alcohol	16775130	However, our second major finding was that genetic inactivation of the <strong>5 HTT</strong> in a knock out mouse not only failed to prevent <b>ethanol</b> induced inhibition of 5 HT clearance, but actually potentiated this effect.
+SLC6A4	drug	alcohol	16775130	<b>Ethanol</b> induced inhibition of 5 HT clearance was also potentiated in nonmutant mice by cotreatment with a <strong>5 HTT</strong> antagonist.
+SLC6A4	drug	alcohol	16775130	Providing a link with potential behavioral manifestations of this neural phenotype, <strong>5 HTT</strong> knock out mice also exhibited exaggerated sensitivity to behavioral intoxication, as assayed by the sedative/hypnotic effects of <b>ethanol</b>.
+SLC6A4	addiction	intoxication	16775130	Providing a link with potential behavioral manifestations of this neural phenotype, <strong>5 HTT</strong> knock out mice also exhibited exaggerated sensitivity to behavioral <b>intoxication</b>, as assayed by the sedative/hypnotic effects of ethanol.
+SLC6A4	drug	alcohol	16775130	This clearly demonstrates that the <strong>5 HTT</strong> is not necessary for the neural and behavioral effects of <b>ethanol</b> observed herein and that genetic or pharmacological inactivation of the <strong>5 HTT</strong> unmasks involvement of other principle mechanisms.
+SLC6A4	drug	alcohol	16775130	These data are intriguing given growing evidence implicating the <strong>5 HTT</strong> in the pathophysiology and treatment of <b>alcoholism</b> and neuropsychiatric conditions frequently comorbid with <b>alcoholism</b>, such as depression.
+SLC6A4	drug	cocaine	16754872	There are three known high affinity targets for <b>cocaine</b>: the dopamine transporter (DAT), the serotonin transporter (<strong>SERT</strong>), and the norepinephrine transporter (NET).
+SLC6A4	drug	cocaine	16754872	Contrary to expectations, DAT knockout (DAT KO) mice and <strong>SERT</strong> or NET knockout mice still self administer <b>cocaine</b> and/or display conditioned place preference (CPP) to <b>cocaine</b>, which led to the reevaluation of the DA hypothesis and the proposal of redundant reward pathways.
+SLC6A4	addiction	reward	16754872	Contrary to expectations, DAT knockout (DAT KO) mice and <strong>SERT</strong> or NET knockout mice still self administer cocaine and/or display conditioned place preference (<b>CPP</b>) to cocaine, which led to the reevaluation of the DA hypothesis and the proposal of redundant <b>reward</b> pathways.
+SLC6A4	drug	cocaine	16754872	This mouse model is unique in that it is specifically designed to differentiate the role of DAT from the roles of NET and <strong>SERT</strong> in <b>cocaine</b> induced biochemical and behavioral effects.
+SLC6A4	drug	nicotine	16702982	To investigate the potential role of this polymorphism for <b>smoking</b> behavior, <strong>SLC6A4</strong> genotypes were determined in two different studies, the <b>SMOKING</b> GENES case control study (470 current <b>smokers</b> and 419 subjects who had never smoked) and the cross sectional Ludwigshafen risk and cardiovascular health (LURIC) study (777 current <b>smokers</b> and 1178 subjects who had never smoked).
+SLC6A4	drug	nicotine	16702982	In the <b>SMOKING</b> GENES case control study, <strong>SLC6A4</strong> genotype frequencies were not statistically different between <b>smokers</b> (LL: 30.9%; LS: 46.8%; SS: 16.4%) and non <b>smokers</b> (LL: 36.3%; LS: 41.8%; SS: 14.3%; P=0.13).
+SLC6A4	drug	nicotine	16702982	<strong>SLC6A4</strong> genotypes were furthermore not associated with Fagerstrom Tolerance Questionnaire score, packyears, number of cigarettes smoked per day or previous attempts to quit <b>smoking</b>.
+SLC6A4	drug	nicotine	16702982	We conclude that the <strong>SLC6A4</strong> promoter polymorphism is not a major determinant of <b>smoking</b> behavior in Caucasian.
+SLC6A4	drug	alcohol	16691130	The role of the human serotonin transporter protein (<strong>5 HTT</strong>) gene in psychiatric disorders suggests that its variation may influence the comorbidity pattern and the heterogeneity of <b>alcoholism</b>.
+SLC6A4	drug	alcohol	16691130	The aim of the present study is to verify possible associations between the <strong>5 HTTLPR</strong> control region polymorphism with <b>alcoholism</b> and comorbid disorders.
+SLC6A4	drug	alcohol	16691130	They suggest a role of the <strong>5 HTTLPR</strong> polymorphism in a group of comorbid disorders among <b>alcohol</b> dependent individuals, supporting a genetic influence in <b>alcoholism</b> heterogeneity.
+SLC6A4	drug	alcohol	16679343	There were no significant differences in the genotype frequencies of the DRD2, ALDH2, <strong>5 HTTLPR</strong>, and COMT polymorphisms between <b>alcoholics</b> with and without ADHD.
+SLC6A4	drug	psychedelics	16574713	Because 5 HT transporters play a key element in the regulation of synaptic 5 HT transmission it may be important to control for the potential covariance effect of a polymorphism in the 5 HT transporter promoter gene region (<strong>5 HTTLPR</strong>) when studying the effects of <b>MDMA</b> as well as cognitive functioning.
+SLC6A4	drug	psychedelics	16574713	The aim of the study was to investigate the effects of moderate and heavy <b>MDMA</b> use on cognitive function, as well as the effects of long term abstention from <b>MDMA</b>, in subjects genotyped for <strong>5 HTTLPR</strong>.
+SLC6A4	drug	psychedelics	16574713	No effect of <strong>5 HTTLPR</strong> or gender on memory function or <b>MDMA</b> use was observed.
+SLC6A4	drug	psychedelics	16510479	This longitudinal study investigated whether mood, cognition and central serotonin transporters (<strong>SERT</strong>) would deteriorate with continued <b>MDMA</b> use and whether or not they would recover over increasing periods of <b>MDMA</b> abstinence.
+SLC6A4	drug	psychedelics	16510479	The availability of central <strong>SERT</strong> was assessed with positron emission tomography using the McN5652 ligand for all groups at t1, and only for the <b>ecstasy</b> user groups on follow ups.
+SLC6A4	drug	psychedelics	16510479	Reduced <strong>SERT</strong> availability might be a transient effect of heavy <b>ecstasy</b> use, since it partially recovered as the current users reduced their <b>MDMA</b> use.
+SLC6A4	drug	psychedelics	16434566	Adolescent <b>MDMA</b> exposure partially attenuated the hyperthermic effects of the PD 67 <b>MDMA</b> challenge, completely blocked the locomotor hypoactivity otherwise observed on the day after the challenge, and also prevented <b>MDMA</b> induced serotonin neurotoxicity assessed on PD 74 by measuring regional [(3)H]citalopram binding to the serotonin transporter (<strong>SERT</strong>).
+SLC6A4	drug	opioid	16419555	The study sample includes 57 patients with <b>opioid</b> dependence alone (OD) and 41 with <b>opioid</b> dependence and a psychiatric axis I disorder (DD), recruited in 2001 and 2004 at the Drug Addiction Services (<strong>SerT</strong>) of Bolzano and Pontedera (Italy).
+SLC6A4	addiction	addiction	16419555	The study sample includes 57 patients with opioid dependence alone (OD) and 41 with opioid dependence and a psychiatric axis I disorder (DD), recruited in 2001 and 2004 at the Drug <b>Addiction</b> Services (<strong>SerT</strong>) of Bolzano and Pontedera (Italy).
+SLC6A4	addiction	dependence	16419555	The study sample includes 57 patients with opioid <b>dependence</b> alone (OD) and 41 with opioid <b>dependence</b> and a psychiatric axis I disorder (DD), recruited in 2001 and 2004 at the Drug Addiction Services (<strong>SerT</strong>) of Bolzano and Pontedera (Italy).
+SLC6A4	drug	alcohol	16358330	In this study, possible alterations of [(3)H]citalopram binding to serotonin transporter (<strong>SERT</strong>) were evaluated in the dorsal striatum of Cloninger type 1 and 2 <b>alcoholics</b>, and nonalcoholic control subjects by postmortem whole hemisphere autoradiography in humans.
+SLC6A4	drug	alcohol	16358330	The <strong>SERT</strong> binding was significantly lower ( 26%, effect size 1.74) in the caudate body of <b>alcoholics</b>.
+SLC6A4	drug	alcohol	16358330	The <strong>SERT</strong> binding tended to be lower also in the other parts of the dorsal striatum in <b>alcoholics</b>, but the results did not reach significance.
+SLC6A4	drug	alcohol	16358330	In addition, there was a significant positive correlation, especially in type 1 <b>alcoholics</b>, between the <strong>SERT</strong> binding in the body of the caudate and in the perigenual anterior cingulate cortex, an area in which the <strong>SERT</strong> binding has been shown to be lower among <b>alcoholics</b>.
+SLC6A4	drug	alcohol	16358330	These results give preliminary evidence to suggest that the <strong>SERT</strong> binding in the dorsal striatum may be lower in <b>alcoholics</b>, and that the serotonergic system may be affected in cortical and striatal areas simultaneously.
+SLC6A4	drug	cocaine	16337262	Using the conditioned taste aversion (CTA) preparation, the present study examined the role of monoamine uptake inhibition in <b>cocaine</b>'s aversive effects by comparing <b>cocaine</b> to three reuptake inhibitors with relative specificity for the transporters of dopamine (DAT; GBR 12909), norepinephrine (NET; desipramine) and serotonin (<strong>SERT</strong>; clomipramine).
+SLC6A4	addiction	aversion	16337262	Using the conditioned taste <b>aversion</b> (<b>CTA</b>) preparation, the present study examined the role of monoamine uptake inhibition in cocaine's <b>aversive</b> effects by comparing cocaine to three reuptake inhibitors with relative specificity for the transporters of dopamine (DAT; GBR 12909), norepinephrine (NET; desipramine) and serotonin (<strong>SERT</strong>; clomipramine).
+SLC6A4	drug	cocaine	16337262	These results suggest that <b>cocaine</b>'s adrenergic actions resulting from NET inhibition may play a more significant role in the mediation of its aversive effects than its actions at DAT and <strong>SERT</strong>.
+SLC6A4	addiction	aversion	16337262	These results suggest that cocaine's adrenergic actions resulting from NET inhibition may play a more significant role in the mediation of its <b>aversive</b> effects than its actions at DAT and <strong>SERT</strong>.
+SLC6A4	drug	alcohol	16288736	Although variations in many of the genes that encode receptors, enzymes, and transporters of the 5 HT system have been tested as risk factors for <b>alcohol</b> dependence, genetic analyses of 5 HT signaling in <b>alcohol</b> dependence have mainly been focused on the 5 HT transporter (<strong>5 HTT</strong>) gene.
+SLC6A4	addiction	dependence	16288736	Although variations in many of the genes that encode receptors, enzymes, and transporters of the 5 HT system have been tested as risk factors for alcohol <b>dependence</b>, genetic analyses of 5 HT signaling in alcohol <b>dependence</b> have mainly been focused on the 5 HT transporter (<strong>5 HTT</strong>) gene.
+SLC6A4	drug	alcohol	16288736	Due to its central role in the fine tuning serotonergic neurotransmission, a regulatory variant of the <strong>5 HTT</strong>, which is associated with anxiety related traits, is not only a key player in the neurobiological mechanism of gene x environment interaction in the etiology of depression, but also contributes to the risk to develop <b>alcohol</b> dependence with antisocial behavior and suicidality.
+SLC6A4	addiction	dependence	16288736	Due to its central role in the fine tuning serotonergic neurotransmission, a regulatory variant of the <strong>5 HTT</strong>, which is associated with anxiety related traits, is not only a key player in the neurobiological mechanism of gene x environment interaction in the etiology of depression, but also contributes to the risk to develop alcohol <b>dependence</b> with antisocial behavior and suicidality.
+SLC6A4	addiction	dependence	16167465	Dopamine D4 receptor (DRD4) and serotonin transporter (<strong>SERT</strong>) gene polymorphisms were studied, as possible genetic risk factors for substance <b>dependence</b>.
+SLC6A4	drug	opioid	16167465	Association between the  521 CC vs. CT or TT genotypes and <b>heroin</b> dependence was enhanced in the presence of short (s or 14 repeat) <strong>5 HTTLPR</strong> allele (p 0.01).
+SLC6A4	addiction	dependence	16167465	Association between the  521 CC vs. CT or TT genotypes and heroin <b>dependence</b> was enhanced in the presence of short (s or 14 repeat) <strong>5 HTTLPR</strong> allele (p 0.01).
+SLC6A4	drug	opioid	16167465	The odds ratio of 2.14 observed for the  521 CC genotype increased to 4.82 in double homozygotes of  521 CC and <strong>5 HTTLPR</strong> ss, emphasizing the importance of combined analysis of polymorphisms in the dopaminergic and serotonergic systems in <b>heroin</b> dependence.
+SLC6A4	addiction	dependence	16167465	The odds ratio of 2.14 observed for the  521 CC genotype increased to 4.82 in double homozygotes of  521 CC and <strong>5 HTTLPR</strong> ss, emphasizing the importance of combined analysis of polymorphisms in the dopaminergic and serotonergic systems in heroin <b>dependence</b>.
+SLC6A4	drug	alcohol	16125912	One hundred and eleven male patients with <b>alcohol</b> dependence and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 (ADH2), aldehyde dehydrogenase 2 (ALDH2), serotonin transporter (<strong>5 HTT</strong>) and dopamine transporter (DAT1).
+SLC6A4	addiction	dependence	16125912	One hundred and eleven male patients with alcohol <b>dependence</b> and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of alcohol dehydrogenase 2 (ADH2), aldehyde dehydrogenase 2 (ALDH2), serotonin transporter (<strong>5 HTT</strong>) and dopamine transporter (DAT1).
+SLC6A4	drug	alcohol	16125912	Neither <strong>5 HTTLPR</strong> L/S nor DAT1 G2319A SNP genotypes nor alleles discriminated <b>alcoholic</b> patients from normal controls.
+SLC6A4	addiction	addiction	16112691	Mutation at Ile 425 to valine, found in some patients with obsessive <b>compulsive</b> disorder, altered the response of <strong>SERT</strong> to cGMP (Kilic, F., Murphy, D.L., Rudnick, G., 2003.
+SLC6A4	drug	alcohol	16109588	The aims of the study were to investigate whether <strong>5 HTTLPR</strong> genotypes differed in their response to treatment in cocaine  and <b>alcohol</b> abusing patients.
+SLC6A4	drug	cocaine	16109588	The aims of the study were to investigate whether <strong>5 HTTLPR</strong> genotypes differed in their response to treatment in <b>cocaine</b>  and alcohol abusing patients.
+SLC6A4	drug	alcohol	16109588	While we found no association of the <strong>5 HTTLPR</strong> variants with severity of cocaine abuse or any cocaine related outcome measures, the data suggested that the <strong>5 HTTLPR</strong> polymorphism may distinguish responders from non responders to behavioral treatment in terms of <b>alcohol</b> use.
+SLC6A4	drug	cocaine	16109588	While we found no association of the <strong>5 HTTLPR</strong> variants with severity of <b>cocaine</b> abuse or any <b>cocaine</b> related outcome measures, the data suggested that the <strong>5 HTTLPR</strong> polymorphism may distinguish responders from non responders to behavioral treatment in terms of alcohol use.
+SLC6A4	addiction	dependence	16025417	The loudness <b>dependence</b> (LD) of the auditory evoked N1/P2 component has been related to serotonergic neurotransmission, i. e. the allelic variants in the promoter of the 5 hydroxytryptamine transporter (<strong>5 HTT</strong>) gene (SCL6A4).
+SLC6A4	drug	nicotine	16025417	Moreover, <b>smoking</b> behavior has been associated to the <strong>5 HTT</strong> genotype.
+SLC6A4	drug	nicotine	16025417	It was hypothesized that cigarette <b>smoking</b> modulates the LD and this effect was expected to interact with the <strong>5 HTT</strong> genotype.
+SLC6A4	drug	nicotine	16025417	<strong>5 HTT</strong> genotype and LD were determined in 63 healthy <b>smokers</b> and 114 nonsmokers.
+SLC6A4	drug	nicotine	16025417	LD was significantly affected by <b>smoking</b> status (p = 0.008) and <strong>5 HTT</strong> genotype (p = 0.045) but not by <b>smoking</b>*genotype interaction or daily cigarette consumption.
+SLC6A4	drug	nicotine	16025417	<strong>5 HTT</strong> genotype showed no significant effect on <b>smoking</b> behavior.
+SLC6A4	drug	nicotine	16025417	The results indicate a higher serotonergic activity in <b>smokers</b> as compared to nonsmokers independent of <strong>5 HTT</strong> genotype.
+SLC6A4	drug	cocaine	15957006	In in vitro binding in monkey brain tissue, the <b>cocaine</b> analogs had higher affinity for monoamine transporter sites, but similar affinity ratios of <strong>5 HTT</strong>/DAT, compared to <b>cocaine</b>.
+SLC6A4	drug	nicotine	15863794	In an ongoing molecular genetic study of temperament, participants were genotyped to examine the association of <b>smoking</b> with two polymorphisms of the serotonin transporter gene (SERT): the promoter region, <strong>5 HTTLPR</strong>, and an intronic variable number of tandem repeats region (VNTR).
+SLC6A4	drug	nicotine	15863794	In an ongoing molecular genetic study of temperament, participants were genotyped to examine the association of <b>smoking</b> with two polymorphisms of the serotonin transporter gene (<strong>SERT</strong>): the promoter region, <strong>5 HTTLPR</strong>, and an intronic variable number of tandem repeats region (VNTR).
+SLC6A4	drug	nicotine	15863794	There was a significant excess of the <strong>5 HTTLPR</strong> long allele with the 12 repeat VNTR in current <b>smokers</b>, past <b>smokers</b>, and ever <b>smokers</b>, compared to participants who had never smoked.
+SLC6A4	addiction	relapse	15863794	A weak association was observed between novelty <b>seeking</b> and the VNTR polymorphism and between reward and <strong>5 HTTLPR</strong>.
+SLC6A4	addiction	reward	15863794	A weak association was observed between novelty seeking and the VNTR polymorphism and between <b>reward</b> and <strong>5 HTTLPR</strong>.
+SLC6A4	drug	nicotine	15863794	There was a highly significant association between <strong>SERT</strong> and the categorical definition of <b>smoking</b>, irrespective of dependence level, suggesting that this gene influences the initiation of <b>smoking</b>.
+SLC6A4	addiction	dependence	15863794	There was a highly significant association between <strong>SERT</strong> and the categorical definition of smoking, irrespective of <b>dependence</b> level, suggesting that this gene influences the initiation of smoking.
+SLC6A4	drug	nicotine	15863794	Mediation analysis failed to substantiate the hypothesis that novelty seeking partially mediates the effect of <strong>SERT</strong> on <b>smoking</b>.
+SLC6A4	addiction	relapse	15863794	Mediation analysis failed to substantiate the hypothesis that novelty <b>seeking</b> partially mediates the effect of <strong>SERT</strong> on smoking.
+SLC6A4	drug	nicotine	15863794	<strong>SERT</strong> appears to independently contribute to novelty seeking and <b>smoking</b>.
+SLC6A4	addiction	relapse	15863794	<strong>SERT</strong> appears to independently contribute to novelty <b>seeking</b> and smoking.
+SLC6A4	drug	alcohol	15852063	Association between <strong>5 HTTLPR</strong> genotypes and persisting patterns of anxiety and <b>alcohol</b> use: results from a 10 year longitudinal study of adolescent mental health.
+SLC6A4	drug	alcohol	15852063	The purpose of this study was to determine whether (or not) <strong>5 HTTLPR</strong> genotypes moderate known associations between attachment style and adolescent anxiety and <b>alcohol</b> use outcomes.
+SLC6A4	drug	alcohol	15834221	The purpose of the present study was to investigate possible interactions between a polymorphism in the promoter region of the serotonin transporter (<strong>5 HTT</strong>) gene and family relations on adolescent <b>alcohol</b> consumption.
+SLC6A4	drug	alcohol	15834221	<strong>5 HTT</strong> genotype (p=0.029) and family relations (p=0.022) predicted <b>alcohol</b> consumption independently as well as through an interaction with one another (p=0.05).
+SLC6A4	addiction	intoxication	15834221	In a binary logistic model, we found that adolescents with the LS variant of the <strong>5 HTT</strong> gene and with family relations being "neutral" or "bad" had a 12  to 14 fold increased risk for high <b>intoxication</b> frequency.
+SLC6A4	drug	alcohol	15834221	In sum, our results show that a functional polymorphism of the <strong>5 HTT</strong> genotype, family relations, and interactions between these variables predict adolescent <b>alcohol</b> consumption in a randomized sample of adolescents.
+SLC6A4	drug	psychedelics	15831439	<b>MDMA</b> and eight chemically defined byproducts of <b>MDMA</b> synthesis were investigated for their interaction with the primary sites of action of <b>MDMA</b>, namely the human plasmalemmal monamine transporters for norepinephrine, serotonin, and dopamine [(norepinephrine transporter (NET), serotonin transporter (<strong>SERT</strong>), and dopamine transporter (DAT)].
+SLC6A4	drug	psychedelics	15831439	<b>MDMA</b> induced release mediated by NET, <strong>SERT</strong>, or DAT with EC50 values of 0.64, 1.12, and 3.24 microM, respectively.
+SLC6A4	drug	psychedelics	15831439	12 weakly released from NET  and <strong>SERT</strong> expressing cells with maximum effects less than one tenth of that of <b>MDMA</b> and did not release from DAT cells.
+SLC6A4	drug	opioid	15814088	Previous investigations had shown that inhibitor of serotonin reuptake transporter (<strong>SERT</strong>) could attenuate <b>morphine</b> withdrawal syndrome in adult animals.
+SLC6A4	addiction	withdrawal	15814088	Previous investigations had shown that inhibitor of serotonin reuptake transporter (<strong>SERT</strong>) could attenuate morphine <b>withdrawal</b> syndrome in adult animals.
+SLC6A4	drug	opioid	15814088	This result suggests that inhibitor of <strong>SERT</strong> may be of potential in treating neonatal <b>morphine</b> withdrawal syndrome.
+SLC6A4	addiction	withdrawal	15814088	This result suggests that inhibitor of <strong>SERT</strong> may be of potential in treating neonatal morphine <b>withdrawal</b> syndrome.
+SLC6A4	drug	nicotine	15806583	Serotonin transporter promoter polymorphism (<strong>5 HTTLPR</strong>) genotype was previously found associated with <b>smoking</b> behavior, difficulty in quitting <b>smoking</b>, and <b>nicotine</b> addiction; with non replicated findings and contrasting results.
+SLC6A4	addiction	addiction	15806583	Serotonin transporter promoter polymorphism (<strong>5 HTTLPR</strong>) genotype was previously found associated with smoking behavior, difficulty in quitting smoking, and nicotine <b>addiction</b>; with non replicated findings and contrasting results.
+SLC6A4	drug	nicotine	15806583	Aim of the present study was to evaluate the possible association between <strong>5 HTTLPR</strong> genotype and <b>smoking</b> behavior among adolescents, in relationship with psychological characteristics.
+SLC6A4	drug	nicotine	15806583	Our data suggest that a decreased expression of the gene encoding the <strong>5 HTT</strong> transporter, due to "S" promoter polymorphism, may be associated with <b>smoking</b> behavior among adolescents and increased risk to develop <b>nicotine</b> dependence, possibly in relationship to personality traits, temperamental characteristics, and school under achievements.
+SLC6A4	addiction	dependence	15806583	Our data suggest that a decreased expression of the gene encoding the <strong>5 HTT</strong> transporter, due to "S" promoter polymorphism, may be associated with smoking behavior among adolescents and increased risk to develop nicotine <b>dependence</b>, possibly in relationship to personality traits, temperamental characteristics, and school under achievements.
+SLC6A4	drug	alcohol	15804387	This study investigated the association between the serotonin transporter polymorphism (<strong>5 HTTLPR</strong>) and <b>alcoholism</b> in the Korean population.
+SLC6A4	drug	alcohol	15804387	The frequency of the L allele of <strong>5 HTTLPR</strong> was significantly higher in the <b>alcohol</b> dependent patients than in the normal controls (chi(2)=19.11, df=1, p<0.001).
+SLC6A4	drug	alcohol	15804387	This study suggests a putative role of the <strong>5 HTTLPR</strong> for <b>alcoholism</b> in the Korean population.
+SLC6A4	drug	alcohol	15635638	Since activity of the 5 HT transporter protein (<strong>5 HTT</strong>) regulates 5 HT levels, the gene encoding this protein may contribute to the risk of <b>alcohol</b> dependence (AD).
+SLC6A4	addiction	dependence	15635638	Since activity of the 5 HT transporter protein (<strong>5 HTT</strong>) regulates 5 HT levels, the gene encoding this protein may contribute to the risk of alcohol <b>dependence</b> (AD).
+SLC6A4	drug	alcohol	15635638	We conducted a meta analysis of data from 17 published studies (including 3,489 <b>alcoholics</b> and 2,325 controls) investigating the association between <strong>5 HTTLPR</strong> alleles and AD.
+SLC6A4	addiction	intoxication	15635592	The short allelic variant of the serotonin transporter protein promoter polymorphism (<strong>5HTTLPR</strong>) appears to influence <b>binge</b> drinking in college students.
+SLC6A4	addiction	intoxication	15635592	Young Caucasian women carrying higher expression MAOA VNTR alleles homozygous for the short allelic variant of the <strong>5HTTLPR</strong> demonstrated the highest rate of <b>binge</b> drinking by self report, odds ratio (genotype odds: population odds) and 95% confidence intervals, 3.11 (1.14 18.10).
+SLC6A4	addiction	intoxication	15635592	Individuals carrying higher expression MAOA VNTR alleles carrying at least one long <strong>5HTTLPR</strong> allelic variant had the lowest risk of <b>binge</b> drinking 0.46 (0.28 0.71).
+SLC6A4	drug	alcohol	15589566	Male specific association between the <strong>5 HTTLPR</strong> S allele and suicide attempts in <b>alcohol</b> dependent subjects.
+SLC6A4	drug	alcohol	15589566	Previous studies have demonstrated an association between suicide attempts and the <strong>5 HTTLPR</strong> S allele in <b>alcohol</b> dependent subjects.
+SLC6A4	drug	alcohol	15589566	We investigated the frequency of the S allele of <strong>5 HTTLPR</strong> in a sample of 100 French Caucasian <b>alcohol</b> dependent inpatients (48 men and 52 women) with and without a history of suicide attempts.
+SLC6A4	drug	alcohol	15589566	There seems to be an allelic association between the <strong>5 HTTLPR</strong> S allele and suicidal behavior in <b>alcohol</b> dependent subjects, but this relationship is restricted to male subjects.
+SLC6A4	drug	alcohol	15581469	The genetic analyses of serotonin in <b>alcohol</b> dependence are mainly focused on the serotonin transporter gene (<strong>5 HTT</strong>), as one polymorphism within the promoter has a functional impact.
+SLC6A4	addiction	dependence	15581469	The genetic analyses of serotonin in alcohol <b>dependence</b> are mainly focused on the serotonin transporter gene (<strong>5 HTT</strong>), as one polymorphism within the promoter has a functional impact.
+SLC6A4	drug	alcohol	15570522	We investigated phenotype and <strong>5 HTT</strong>/5 HT2c allelic characteristics in 314 <b>alcoholics</b> of German descent.
+SLC6A4	drug	alcohol	15570522	There was no significant difference in <strong>5 HTT</strong>  or 5 HT2c allele distribution between <b>alcoholics</b> and matched controls or between <b>alcoholics</b> with or without ADHD.
+SLC6A4	drug	alcohol	15570522	In our sample the functional relevant <strong>5 HTT</strong> promoter and the 5 HT2c receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	15570522	In our sample the functional relevant <strong>5 HTT</strong> promoter and the 5 HT2c receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and alcohol <b>dependence</b>.
+SLC6A4	drug	cocaine	15542699	We have also identified evidence that, in the absence of DAT, there is greater participation in <b>cocaine</b> reward by serotonin (<strong>SERT</strong>) and norepinephrine (NET) transporters.
+SLC6A4	addiction	reward	15542699	We have also identified evidence that, in the absence of DAT, there is greater participation in cocaine <b>reward</b> by serotonin (<strong>SERT</strong>) and norepinephrine (NET) transporters.
+SLC6A4	drug	cocaine	15542699	The striking elimination of <b>cocaine</b> CPP in combined DAT/<strong>SERT</strong> KO mice contrasts with effects that we have identified in combined NET/<strong>SERT</strong> knockout mice, which display increases in <b>cocaine</b> reward, and with recent reports that suggest that DAT/NET combined KOs retain substantial <b>cocaine</b> CPP.
+SLC6A4	addiction	reward	15542699	The striking elimination of cocaine <b>CPP</b> in combined DAT/<strong>SERT</strong> KO mice contrasts with effects that we have identified in combined NET/<strong>SERT</strong> knockout mice, which display increases in cocaine <b>reward</b>, and with recent reports that suggest that DAT/NET combined KOs retain substantial cocaine <b>CPP</b>.
+SLC6A4	drug	alcohol	15520362	We wanted to determine whether serotonin transporter gene promoter variation (rh <strong>5HTTLPR</strong>) and rearing condition would interact to influence <b>alcohol</b> preference in female rhesus macaques.
+SLC6A4	drug	alcohol	15345266	DRD2A, DRD2B, GABB2, EAAT2, and <strong>5HTT</strong> genotypes did not divide <b>alcoholic</b> cases and controls on N methyl d aspartate (NMDA) receptor parameters.
+SLC6A4	addiction	relapse	15318029	There is no support for linkage of novelty <b>seeking</b> or HA to the regions around DRD4 and <strong>5HTT</strong>, respectively.
+SLC6A4	drug	cocaine	15226739	<b>Cocaine</b> conditioned place preference (CPP) is intact in dopamine transporter (DAT) knockout (KO) mice and enhanced in serotonin transporter (<strong>SERT</strong>) KO mice.
+SLC6A4	addiction	reward	15226739	Cocaine conditioned place preference (<b>CPP</b>) is intact in dopamine transporter (DAT) knockout (KO) mice and enhanced in serotonin transporter (<strong>SERT</strong>) KO mice.
+SLC6A4	drug	cocaine	15226739	However, <b>cocaine</b> CPP is eliminated in double KO mice with no DAT and either no or one <strong>SERT</strong> gene copy.
+SLC6A4	addiction	reward	15226739	However, cocaine <b>CPP</b> is eliminated in double KO mice with no DAT and either no or one <strong>SERT</strong> gene copy.
+SLC6A4	drug	cocaine	15226739	To help determine mechanisms underlying these effects, we now report examination of baselines and drug induced changes of extracellular dopamine (DAex) and serotonin (5 HT(ex)) levels in microdialysates from nucleus accumbens (NAc), caudate putamen (CPu), and prefrontal cortex (PFc) of wild type, homozygous DAT  or <strong>SERT</strong> KO and heterozygous or homozygous DAT/<strong>SERT</strong> double KO mice, which are differentially rewarded by <b>cocaine</b>.
+SLC6A4	drug	cocaine	15226739	Adding <strong>SERT</strong> to DAT deletion attenuates the <b>cocaine</b> induced DAex increases found in CPu, but not those found in PFc.
+SLC6A4	drug	cocaine	15226739	The selective <strong>SERT</strong> blocker fluoxetine increases DAex in CPu of DAT KO mice, while <b>cocaine</b> and the selective DAT blocker GBR12909 increase 5 HT(ex) in CPu of <strong>SERT</strong> KO mice.
+SLC6A4	drug	cocaine	15226739	These data provide evidence that (a) <b>cocaine</b> increases DAex in PFc independently of DAT and that (b), in the absence of <strong>SERT</strong>, CPu levels of 5 HT(ex) can be increased by blocking DAT.
+SLC6A4	drug	cocaine	15226739	<b>Cocaine</b> induced alterations in CPu DA levels in DAT , <strong>SERT</strong> , and DAT/<strong>SERT</strong> double KO mice appear to provide better correlations with <b>cocaine</b> CPP than <b>cocaine</b> induced DA level alterations in NAc or PFc.
+SLC6A4	addiction	reward	15226739	Cocaine induced alterations in CPu DA levels in DAT , <strong>SERT</strong> , and DAT/<strong>SERT</strong> double KO mice appear to provide better correlations with cocaine <b>CPP</b> than cocaine induced DA level alterations in NAc or PFc.
+SLC6A4	drug	alcohol	15112932	Hutchison's and Corbin's papers describe their research on polymorphisms for the serotonin transporter (<strong>SLC6A4</strong>) as a determinant of the subjective effects of <b>alcohol</b> challenge.
+SLC6A4	drug	alcohol	15112932	Dr. Hutchinson's and Ms. Ray's findings indicate that individuals with the short form of the <strong>SLC6A4</strong> alleles (S) demonstrated a low level of response to <b>alcohol</b>, thus supporting previous research that the S allele may be associated with increased risk for <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	15112932	Dr. Hutchinson's and Ms. Ray's findings indicate that individuals with the short form of the <strong>SLC6A4</strong> alleles (S) demonstrated a low level of response to alcohol, thus supporting previous research that the S allele may be associated with increased risk for alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	15112932	In contrast, Dr. Corbin did not find a reliable association between the <strong>SLC6A4</strong> genotype and subjective response to <b>alcohol</b>.
+SLC6A4	drug	cocaine	15091312	Alterations in the serotonin transporter (<strong>5 HTT</strong>) have been implicated in a variety of psychiatric disorders including <b>cocaine</b> dependence.
+SLC6A4	addiction	dependence	15091312	Alterations in the serotonin transporter (<strong>5 HTT</strong>) have been implicated in a variety of psychiatric disorders including cocaine <b>dependence</b>.
+SLC6A4	drug	cocaine	15091312	We investigated whether 5 HTTLPR variants were related to differences in measures of platelet <strong>5 HTT</strong> sites in <b>cocaine</b> dependent patients and healthy volunteers (controls).
+SLC6A4	drug	cocaine	15091312	We investigated whether <strong>5 HTTLPR</strong> variants were related to differences in measures of platelet <strong>5 HTT</strong> sites in <b>cocaine</b> dependent patients and healthy volunteers (controls).
+SLC6A4	drug	cocaine	15091312	Polymerase chain reaction based genotyping of a 44 base pair insertion/deletion polymorphism in <strong>5 HTTLPR</strong> was performed in 138 <b>cocaine</b> dependent African American subjects and 60 African American controls.
+SLC6A4	drug	cocaine	15091312	Bmax values were significantly lower in <b>cocaine</b> dependent patients (640 +/  233) than controls (906 +/  225) (P < 0.001); however, <strong>5 HTTLPR</strong> genotype distributions or allele frequencies did not differ between the two groups.
+SLC6A4	drug	cocaine	15091312	Although platelet <strong>5 HTT</strong> densities are reduced in patients with <b>cocaine</b> dependence compared with healthy volunteers, these genotypic variations in the serotonin transporter do not seem to influence levels of platelet <strong>5 HTT</strong> in <b>cocaine</b> dependent patients or healthy volunteers.
+SLC6A4	addiction	dependence	15091312	Although platelet <strong>5 HTT</strong> densities are reduced in patients with cocaine <b>dependence</b> compared with healthy volunteers, these genotypic variations in the serotonin transporter do not seem to influence levels of platelet <strong>5 HTT</strong> in cocaine dependent patients or healthy volunteers.
+SLC6A4	drug	alcohol	15066703	To study the impact of genetic factors that play an important role in an individual's vulnerability to <b>alcohol</b> abuse and dependence, we examined the genetic variations of the major neurotransmitter genes, including the dopamine D2 receptor (DRD2) TaqI A, B, and  141C insertion/deletion (Ins/Del) polymorphisms, the serotonin transporter linked polymorphic region (<strong>5 HTTLPR</strong>), and the gamma aminobutyric acid A (GABA(A)) receptor beta(3) subunit gene (GABRbeta3), for 130 Mexican American <b>alcoholic</b> men and 251 nonalcoholic control subjects (105 men and 146 women).
+SLC6A4	addiction	dependence	15066703	To study the impact of genetic factors that play an important role in an individual's vulnerability to alcohol abuse and <b>dependence</b>, we examined the genetic variations of the major neurotransmitter genes, including the dopamine D2 receptor (DRD2) TaqI A, B, and  141C insertion/deletion (Ins/Del) polymorphisms, the serotonin transporter linked polymorphic region (<strong>5 HTTLPR</strong>), and the gamma aminobutyric acid A (GABA(A)) receptor beta(3) subunit gene (GABRbeta3), for 130 Mexican American alcoholic men and 251 nonalcoholic control subjects (105 men and 146 women).
+SLC6A4	drug	alcohol	15066703	The frequency of the <strong>5 HTTLPR</strong> short (S) allele was significantly higher in <b>alcoholic</b> individuals (61.5%) than in nonalcoholic control subjects (52.8%; P=.021).
+SLC6A4	drug	alcohol	15066703	When smokers were excluded from both control and <b>alcoholic</b> groups, the association between the DRD2  141C Ins allele, as well as between the <strong>5 HTTLPR</strong> S allele, and <b>alcoholism</b> became significant at both genotypic and allelic levels.
+SLC6A4	drug	nicotine	15066703	When <b>smokers</b> were excluded from both control and alcoholic groups, the association between the DRD2  141C Ins allele, as well as between the <strong>5 HTTLPR</strong> S allele, and alcoholism became significant at both genotypic and allelic levels.
+SLC6A4	drug	alcohol	15066703	Our findings indicate that the DRD2  141C Ins allele and the <strong>5 HTTLPR</strong> S allele are genetic risk factors for <b>alcoholism</b> in Mexican Americans, and that smoking modulates the association between genetic risk factors and <b>alcoholism</b>.
+SLC6A4	drug	nicotine	15066703	Our findings indicate that the DRD2  141C Ins allele and the <strong>5 HTTLPR</strong> S allele are genetic risk factors for alcoholism in Mexican Americans, and that <b>smoking</b> modulates the association between genetic risk factors and alcoholism.
+SLC6A4	drug	alcohol	15048645	A functional polymorphism in the promoter region of the human serotonin transporter gene (<strong>5 HTTLPR</strong>) was recently identified and the presence of the short (S) allele found to be associated with a lower level of expression of the gene, lower levels of 5 HT uptake, type 2 <b>alcoholism</b>, violence and suicidal behavior.
+SLC6A4	drug	alcohol	15048635	For the study, 124 subjects seeking inpatient treatment for primary <b>alcohol</b> dependence were grouped by their <strong>5 HTT</strong> genotype and assessed with the TCI.
+SLC6A4	addiction	dependence	15048635	For the study, 124 subjects seeking inpatient treatment for primary alcohol <b>dependence</b> were grouped by their <strong>5 HTT</strong> genotype and assessed with the TCI.
+SLC6A4	addiction	relapse	15048635	For the study, 124 subjects <b>seeking</b> inpatient treatment for primary alcohol dependence were grouped by their <strong>5 HTT</strong> genotype and assessed with the TCI.
+SLC6A4	drug	alcohol	14691371	Johnson and colleagues proposed a model that attempts to explain the observed treatment response patterns of those with early and late <b>alcoholism</b> onset by focusing on the influence of a common genetic variant in the serotonin transporter regulatory region (<strong>5 HTTLPR</strong>) on serotonin (5 HT) and dopamine (DA) system function.
+SLC6A4	drug	alcohol	14691371	Genotype at <strong>5 HTTLPR</strong> may influence relative reward of drinking <b>alcohol</b> while a person is under pharmacological treatment for <b>alcoholism</b>.
+SLC6A4	addiction	reward	14691371	Genotype at <strong>5 HTTLPR</strong> may influence relative <b>reward</b> of drinking alcohol while a person is under pharmacological treatment for alcoholism.
+SLC6A4	drug	alcohol	14691371	Alternatively, <strong>5 HTTLPR</strong> genotype may influence pathways of <b>alcohol</b> craving.
+SLC6A4	addiction	relapse	14691371	Alternatively, <strong>5 HTTLPR</strong> genotype may influence pathways of alcohol <b>craving</b>.
+SLC6A4	drug	alcohol	14634717	The <strong>SERT</strong> positive innervation density was found to be significantly lower in the medial prefrontal cortex and in the shell of the nucleus accumbens of the <b>ethanol</b> naive sP rats (sP N) when compared with the sNP and unselected Wistar rats.
+SLC6A4	drug	cocaine	14612142	However, the fact that <b>cocaine</b> similarly binds to the serotonin and norepinephrine transporters (<strong>SERT</strong> and NET, respectively), raises the possibility that modulation of mesocorticolimbic dopaminergic transmission might be achieved through alternate pathways.
+SLC6A4	drug	cocaine	14612142	The successful disruption of the genes coding for the DAT, the <strong>SERT</strong> and the NET offered ideal tools to determine the extent of the participation of these transporters and respective monoaminergic systems in the reinforcing effects of <b>cocaine</b>.
+SLC6A4	addiction	reward	14612142	The successful disruption of the genes coding for the DAT, the <strong>SERT</strong> and the NET offered ideal tools to determine the extent of the participation of these transporters and respective monoaminergic systems in the <b>reinforcing</b> effects of cocaine.
+SLC6A4	drug	cocaine	14612142	The reinforcing potency of <b>cocaine</b> is maintained in the absence of the DAT but decreased in the absence of the NET; its motivational rewarding effect is observed in the absence of the <strong>SERT</strong>, but not when both DAT and <strong>SERT</strong> are lacking.
+SLC6A4	addiction	reward	14612142	The <b>reinforcing</b> potency of cocaine is maintained in the absence of the DAT but decreased in the absence of the NET; its motivational rewarding effect is observed in the absence of the <strong>SERT</strong>, but not when both DAT and <strong>SERT</strong> are lacking.
+SLC6A4	drug	cocaine	14612139	Third, most are also conserved in the serotonin transporter (<strong>SERT</strong>), a transporter that is now strongly implicated in <b>cocaine</b> reward based on data from knockout mice.
+SLC6A4	addiction	reward	14612139	Third, most are also conserved in the serotonin transporter (<strong>SERT</strong>), a transporter that is now strongly implicated in cocaine <b>reward</b> based on data from knockout mice.
+SLC6A4	drug	cocaine	14612139	These studies provide a strong basis for redirected studies aimed at producing dopamine  and serotonin sparing <b>cocaine</b> antagonists that would represent combined DAT/<strong>SERT</strong> disinhibitors.
+SLC6A4	drug	alcohol	14574222	We investigated phenotype and <strong>5 HTT</strong>/5 HT2c genotype characteristics in 314 <b>alcoholics</b> of German descent.
+SLC6A4	drug	alcohol	14574222	There was no significant difference in <strong>5 HTT</strong> genotype or 5 HT2c allele distribution between <b>alcoholics</b> and matched controls.
+SLC6A4	drug	alcohol	14574222	There were no differences in <strong>5 HTT</strong> genotype or 5 HT2c allele distribution between the ADHD+ subgroups and <b>alcoholics</b> without comorbidity and matched controls, respectively.
+SLC6A4	drug	alcohol	14574222	In our sample, the functional relevant <strong>5 HTT</strong> promoter and the 5 HT2c receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	14574222	In our sample, the functional relevant <strong>5 HTT</strong> promoter and the 5 HT2c receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	14506400	Because the convergence of these disorders may provide a refined phenotype, we examined the association of serotonin (5 HT) transporter linked polymorphic region (<strong>5 HTTLPR</strong>) alleles to comorbid <b>alcohol</b> dependence and major depression.
+SLC6A4	addiction	dependence	14506400	Because the convergence of these disorders may provide a refined phenotype, we examined the association of serotonin (5 HT) transporter linked polymorphic region (<strong>5 HTTLPR</strong>) alleles to comorbid alcohol <b>dependence</b> and major depression.
+SLC6A4	drug	alcohol	14506400	With respect to the frequency of the short allele at the <strong>SLC6A4</strong> locus (5 HTTLPR), major depression in <b>alcoholics</b> is similar to major depression in nonalcoholics.
+SLC6A4	drug	alcohol	14506400	With respect to the frequency of the short allele at the <strong>SLC6A4</strong> locus (<strong>5 HTTLPR</strong>), major depression in <b>alcoholics</b> is similar to major depression in nonalcoholics.
+SLC6A4	drug	cocaine	12954808	Interestingly, the <strong>5 HTT</strong> selective <b>cocaine</b> analog HD 60 functioned robustly as a reinforcer at several doses in all monkeys tested.
+SLC6A4	addiction	reward	12954808	These data question the dogma regarding the role of pharmacokinetic factors and the relative influence of DAT and <strong>5 HTT</strong> in stimulant <b>reinforcement</b>.
+SLC6A4	drug	alcohol	12915525	In the present study, differences in <b>alcohol</b> consumption behaviour associated with the presence of the short variant (S) of the serotonin transporter promoter polymorphism (<strong>5 HTTLPR</strong>) was investigated in a Caucasian subset (n = 204) of 268 college students.
+SLC6A4	drug	alcohol	12915525	In this Caucasian sample, the <strong>5 HTTLPR</strong> strongly influences <b>alcohol</b> consumption in late pubescence.
+SLC6A4	drug	alcohol	12766626	Decreased sensitivity to <b>alcohol</b> has been demonstrated to be a predictor of <b>alcoholism</b> in humans, and variation in the gene linked polymorphic region of the serotonin transporter (<strong>5 HTTLPR</strong>) is associated with the response to the motor impairing effects of <b>alcohol</b>.
+SLC6A4	drug	amphetamine	12658362	The dopamine transporter (DAT) and the serotonin transporter (<strong>5 HTT</strong>) play important roles in <b>methamphetamine</b> (<b>METH</b>) dependence because they are the target of <b>METH</b> action.
+SLC6A4	addiction	dependence	12658362	The dopamine transporter (DAT) and the serotonin transporter (<strong>5 HTT</strong>) play important roles in methamphetamine (METH) <b>dependence</b> because they are the target of METH action.
+SLC6A4	drug	amphetamine	12658362	For this study, the association between the DAT and <strong>5 HTT</strong> polymorphisms and <b>METH</b> dependence were investigated for a Chinese male sample population.
+SLC6A4	addiction	dependence	12658362	For this study, the association between the DAT and <strong>5 HTT</strong> polymorphisms and METH <b>dependence</b> were investigated for a Chinese male sample population.
+SLC6A4	drug	amphetamine	12658362	No significant difference was demonstrated for genotype or allele frequency, when comparing <b>METH</b> dependent and control cases for the DAT and the <strong>5 HTT</strong> polymorphisms.
+SLC6A4	drug	nicotine	12589524	Although <b>nicotine</b> and other constituents of <b>tobacco</b> smoke may influence serotonin turnover among animals, few studies have examined whether <b>smoking</b> is associated with alteration in <strong>5HTT</strong> in humans.
+SLC6A4	drug	nicotine	12589524	We investigated whether <b>tobacco</b> <b>smokers</b> and non <b>smokers</b> differed in platelet tritiated paroxetine binding, a measure of <strong>5HTT</strong> sites, and whether severity of <b>nicotine</b> dependence (ND) was related to <strong>5HTT</strong> measures.
+SLC6A4	addiction	dependence	12589524	We investigated whether tobacco smokers and non smokers differed in platelet tritiated paroxetine binding, a measure of <strong>5HTT</strong> sites, and whether severity of nicotine <b>dependence</b> (ND) was related to <strong>5HTT</strong> measures.
+SLC6A4	drug	nicotine	12589524	<b>Smoking</b>, in particular higher <b>nicotine</b> dependence, appears to be correlated with decreased density of platelet <strong>5HTT</strong> sites in African Americans.
+SLC6A4	addiction	dependence	12589524	Smoking, in particular higher nicotine <b>dependence</b>, appears to be correlated with decreased density of platelet <strong>5HTT</strong> sites in African Americans.
+SLC6A4	drug	alcohol	12351926	Association studies of a reportedly functional polymorphism in the promoter region (5' HTTLPR) of the gene encoding the serotonin transporter protein (genetic locus <strong>SLC6A4</strong>) in <b>alcoholics</b> have yielded conflicting results.
+SLC6A4	drug	cocaine	12218660	Since the serotonin transporter (<strong>5HTT</strong>) may be involved in modulating effects of <b>cocaine</b>, we investigated whether allelic variants of the <strong>5HTT</strong> gene may confer susceptibility to <b>cocaine</b> dependence among African American individuals.
+SLC6A4	addiction	dependence	12218660	Since the serotonin transporter (<strong>5HTT</strong>) may be involved in modulating effects of cocaine, we investigated whether allelic variants of the <strong>5HTT</strong> gene may confer susceptibility to cocaine <b>dependence</b> among African American individuals.
+SLC6A4	drug	cocaine	12210554	Nevertheless, investigation of the serotonin (<strong>SERT</strong>) and norepinephrine (NET) transporters, as well as other receptor systems, with which <b>cocaine</b> either directly or indirectly interacts, has suggested that the DAT is not solely responsible for the reinforcing effects of <b>cocaine</b>.
+SLC6A4	addiction	reward	12210554	Nevertheless, investigation of the serotonin (<strong>SERT</strong>) and norepinephrine (NET) transporters, as well as other receptor systems, with which cocaine either directly or indirectly interacts, has suggested that the DAT is not solely responsible for the <b>reinforcing</b> effects of cocaine.
+SLC6A4	drug	cocaine	12057823	Considerable evidence indicates that serotonergic mechanisms, particularly the serotonin transporter (<strong>5HTT</strong>), may mediate central effects of <b>cocaine</b> and may also be involved in impulsive and aggressive behavior.
+SLC6A4	drug	cocaine	12057823	We investigated whether polymorphisms in the <strong>5HTT</strong> gene were related to traits of impulsivity, sensation seeking, and aggression among <b>cocaine</b> abusers.
+SLC6A4	addiction	relapse	12057823	We investigated whether polymorphisms in the <strong>5HTT</strong> gene were related to traits of impulsivity, sensation <b>seeking</b>, and aggression among cocaine abusers.
+SLC6A4	drug	cocaine	12057823	Two polymorphisms of the <strong>5HTT</strong> gene were examined involving the 5' promoter (5HTTLPR) region and a 17 base pair variable number tandem repeat (VNTR) marker among <b>cocaine</b> patients.
+SLC6A4	drug	cocaine	12057823	Two polymorphisms of the <strong>5HTT</strong> gene were examined involving the 5' promoter (<strong>5HTTLPR</strong>) region and a 17 base pair variable number tandem repeat (VNTR) marker among <b>cocaine</b> patients.
+SLC6A4	drug	cocaine	12057823	The findings do not seem to support an association between these polymorphisms in the <strong>5HTT</strong> gene and impulsive aggressive traits among <b>cocaine</b> dependent African American individuals.
+SLC6A4	drug	cocaine	12006604	These data rule out the involvement of accumbal NET or <strong>SERT</strong> in the <b>cocaine</b> induced increase in extracellular DA in DAT KO mice.
+SLC6A4	drug	cocaine	11900612	Serotonin transporter (<strong>5 HTT</strong>) gene polymorphisms and susceptibility to <b>cocaine</b> dependence among African American individuals.
+SLC6A4	addiction	dependence	11900612	Serotonin transporter (<strong>5 HTT</strong>) gene polymorphisms and susceptibility to cocaine <b>dependence</b> among African American individuals.
+SLC6A4	drug	cocaine	11900612	Studies indicate that the serotonin system, particularly the serotonin transporter (<strong>5 HTT</strong>), may modulate the central effects of <b>cocaine</b>.
+SLC6A4	drug	cocaine	11900612	We investigated whether a polymorphism in the 5' promotor region (5 HTTLPR) of the <strong>5 HTT</strong> gene confers susceptibility to <b>cocaine</b> dependence.
+SLC6A4	addiction	dependence	11900612	We investigated whether a polymorphism in the 5' promotor region (5 HTTLPR) of the <strong>5 HTT</strong> gene confers susceptibility to cocaine <b>dependence</b>.
+SLC6A4	drug	cocaine	11900612	We investigated whether a polymorphism in the 5' promotor region (<strong>5 HTTLPR</strong>) of the <strong>5 HTT</strong> gene confers susceptibility to <b>cocaine</b> dependence.
+SLC6A4	addiction	dependence	11900612	We investigated whether a polymorphism in the 5' promotor region (<strong>5 HTTLPR</strong>) of the <strong>5 HTT</strong> gene confers susceptibility to cocaine <b>dependence</b>.
+SLC6A4	drug	cocaine	11900612	In conclusion, although comparisons with a heterogeneous control group indicated a possible association between allelic variants of <strong>5 HTTLPR</strong> and <b>cocaine</b> dependence among African American <b>cocaine</b> subjects, this relationship was not observed when the control group was limited to African American people only.
+SLC6A4	addiction	dependence	11900612	In conclusion, although comparisons with a heterogeneous control group indicated a possible association between allelic variants of <strong>5 HTTLPR</strong> and cocaine <b>dependence</b> among African American cocaine subjects, this relationship was not observed when the control group was limited to African American people only.
+SLC6A4	drug	cocaine	11797070	Although <b>cocaine</b> is an indirect DA agonist that binds to all three monoamine transporters, there is much evidence implicating a greater role for the dopamine (DAT) than norepinephrine (NET) and serotonin (<strong>SERT</strong>) transporters in the behavioral effects of <b>cocaine</b>.
+SLC6A4	drug	cocaine	11797070	Analyses indicated that the potency of the compounds to produce <b>cocaine</b> like discriminative stimulus effects was correlated with their affinity for the DAT and the NET but not <strong>SERT</strong>.
+SLC6A4	drug	alcohol	11690601	Association between suicide attempts and <strong>5 HTTLPR</strong> S allele in <b>alcohol</b> dependent and control subjects: further evidence from a German <b>alcohol</b> dependent inpatient sample.
+SLC6A4	drug	alcohol	11690601	A significant association between suicide attempts and the <strong>5 HTT</strong> promoter polymorphisms (5 HTTLPR) S allele has been reported in a sample of French <b>alcohol</b> dependent subjects, and this paper evaluates this phenomenon in a German sample.
+SLC6A4	drug	alcohol	11690601	A significant association between suicide attempts and the <strong>5 HTT</strong> promoter polymorphisms (<strong>5 HTTLPR</strong>) S allele has been reported in a sample of French <b>alcohol</b> dependent subjects, and this paper evaluates this phenomenon in a German sample.
+SLC6A4	drug	alcohol	11690601	<strong>5 HTTLPR</strong> S alleles were seen more frequently in suicidal compared to nonsuicidal <b>alcohol</b> dependent subjects.
+SLC6A4	drug	alcohol	11690601	The results are consistent with an association between the <strong>5 HTTLPR</strong> S allele and suicide attempts in <b>alcohol</b> dependent subjects.
+SLC6A4	drug	alcohol	11449397	Previous studies have indicated associations between a functional biallelic repetitive element in the 5' regulatory region of the serotonin transporter gene (<strong>5 HTTLPR</strong>) and <b>alcoholic</b> subjects who have either dissocial personality disorder or severe withdrawal symptoms.
+SLC6A4	addiction	withdrawal	11449397	Previous studies have indicated associations between a functional biallelic repetitive element in the 5' regulatory region of the serotonin transporter gene (<strong>5 HTTLPR</strong>) and alcoholic subjects who have either dissocial personality disorder or severe <b>withdrawal</b> symptoms.
+SLC6A4	drug	alcohol	11449397	There were no significant differences in the frequencies of either the <strong>5 HTTLPR</strong> genotype or the short vs. long allele in <b>alcoholic</b> and control subjects.
+SLC6A4	drug	alcohol	11449397	The <b>alcoholics</b>' <strong>5 HTTLPR</strong> genotype and allele frequencies did not differ significantly by the severity of withdrawal symptoms or by the number of positive Feighner's diagnostic criteria.
+SLC6A4	addiction	withdrawal	11449397	The alcoholics' <strong>5 HTTLPR</strong> genotype and allele frequencies did not differ significantly by the severity of <b>withdrawal</b> symptoms or by the number of positive Feighner's diagnostic criteria.
+SLC6A4	drug	alcohol	11449397	Although these results indicate an association between <strong>5 HTTLPR</strong> and a subgroup of <b>alcoholics</b> characterized by binge drinking, the authors found no differences in SSS and TCI subscale scores for <b>alcoholics</b> with different <strong>5 HTTLPR</strong> genotypes.
+SLC6A4	addiction	intoxication	11449397	Although these results indicate an association between <strong>5 HTTLPR</strong> and a subgroup of alcoholics characterized by <b>binge</b> drinking, the authors found no differences in SSS and TCI subscale scores for alcoholics with different <strong>5 HTTLPR</strong> genotypes.
+SLC6A4	drug	cocaine	11334571	However, the analogous bivalent ligand 15 comprised of two ( ) trans piperidine units, which is <strong>SERT</strong> selective, was less effective in antagonizing <b>cocaine</b>'s locomotor stimulant activity.
+SLC6A4	drug	cocaine	11320258	<b>Cocaine</b> blocks uptake by neuronal plasma membrane transporters for dopamine (DAT), serotonin (<strong>SERT</strong>), and norepinephrine (NET).
+SLC6A4	drug	cocaine	11320258	<b>Cocaine</b> reward/reinforcement has been linked to actions at DAT or to blockade of <strong>SERT</strong>.
+SLC6A4	addiction	reward	11320258	Cocaine <b>reward</b>/<b>reinforcement</b> has been linked to actions at DAT or to blockade of <strong>SERT</strong>.
+SLC6A4	drug	cocaine	11320258	However, knockouts of neither DAT, <strong>SERT</strong>, or NET reduce <b>cocaine</b> reward/reinforcement, leaving substantial uncertainty about <b>cocaine</b>'s molecular mechanisms for reward.
+SLC6A4	addiction	reward	11320258	However, knockouts of neither DAT, <strong>SERT</strong>, or NET reduce cocaine <b>reward</b>/<b>reinforcement</b>, leaving substantial uncertainty about cocaine's molecular mechanisms for <b>reward</b>.
+SLC6A4	drug	cocaine	11320258	Conceivably, the molecular bases of <b>cocaine</b> reward might display sufficient redundancy that either DAT or <strong>SERT</strong> might be able to mediate <b>cocaine</b> reward in the other's absence.
+SLC6A4	addiction	reward	11320258	Conceivably, the molecular bases of cocaine <b>reward</b> might display sufficient redundancy that either DAT or <strong>SERT</strong> might be able to mediate cocaine <b>reward</b> in the other's absence.
+SLC6A4	drug	cocaine	11320258	Mice with even a single wild type DAT gene copy and no <strong>SERT</strong> copies retain <b>cocaine</b> reward/reinforcement, as measured by conditioned place preference testing.
+SLC6A4	addiction	reward	11320258	Mice with even a single wild type DAT gene copy and no <strong>SERT</strong> copies retain cocaine <b>reward</b>/<b>reinforcement</b>, as measured by conditioned place preference testing.
+SLC6A4	drug	cocaine	11320258	However, mice with no DAT and either no or one <strong>SERT</strong> gene copy display no preference for places where they have previously received <b>cocaine</b>.
+SLC6A4	drug	cocaine	11320258	The serotonin dependence of <b>cocaine</b> reward in DAT knockout mice is thus confirmed by the elimination of <b>cocaine</b> place preference in DAT/<strong>SERT</strong> double knockout mice.
+SLC6A4	addiction	dependence	11320258	The serotonin <b>dependence</b> of cocaine reward in DAT knockout mice is thus confirmed by the elimination of cocaine place preference in DAT/<strong>SERT</strong> double knockout mice.
+SLC6A4	addiction	reward	11320258	The serotonin dependence of cocaine <b>reward</b> in DAT knockout mice is thus confirmed by the elimination of cocaine place preference in DAT/<strong>SERT</strong> double knockout mice.
+SLC6A4	drug	alcohol	11236836	We evaluated the role of three polymorphic genes related to <b>alcohol</b> metabolism (CYP2E1) and, possibly, dependence (DRD2 and <strong>SLC6A4</strong> promoter) in a series of 60 <b>alcoholics</b> admitted to a specialized referral center in Florence, Italy.
+SLC6A4	addiction	dependence	11236836	We evaluated the role of three polymorphic genes related to alcohol metabolism (CYP2E1) and, possibly, <b>dependence</b> (DRD2 and <strong>SLC6A4</strong> promoter) in a series of 60 alcoholics admitted to a specialized referral center in Florence, Italy.
+SLC6A4	drug	cocaine	11207425	We have examined the status of the 5 HT transporter (<strong>SERT</strong>) using ligand binding and autoradiographic methods in subgroups of <b>cocaine</b> overdose deaths.
+SLC6A4	drug	cocaine	11207425	Quantitative autoradiography of [125I]RTI 55 was used to map and measure the effect of chronic <b>cocaine</b> use on <strong>SERT</strong> densities in the striatum, substantia nigra, amygdala, and adjacent paralimbic cortical areas of <b>cocaine</b> overdose (CO) victims with and without preterminal evidence of excited delirium (ED).
+SLC6A4	drug	cocaine	11207425	Chronic <b>cocaine</b> exposure upregulated <strong>SERT</strong> densities in the substantia nigra of the CO, but not ED victims.
+SLC6A4	drug	cocaine	11207425	Adaptive changes in the <strong>SERT</strong> densities may contribute to depressed mood and drug craving associated with acute <b>cocaine</b> abstinence.
+SLC6A4	addiction	relapse	11207425	Adaptive changes in the <strong>SERT</strong> densities may contribute to depressed mood and drug <b>craving</b> associated with acute cocaine abstinence.
+SLC6A4	drug	alcohol	11113619	The serotonin transporter (<strong>5 HTT</strong>) gene is a candidate gene in <b>alcohol</b> dependence because serotonin reuptake inhibitors (SRIs) can alleviate <b>alcohol</b> withdrawal.
+SLC6A4	addiction	dependence	11113619	The serotonin transporter (<strong>5 HTT</strong>) gene is a candidate gene in alcohol <b>dependence</b> because serotonin reuptake inhibitors (SRIs) can alleviate alcohol withdrawal.
+SLC6A4	addiction	withdrawal	11113619	The serotonin transporter (<strong>5 HTT</strong>) gene is a candidate gene in alcohol dependence because serotonin reuptake inhibitors (SRIs) can alleviate alcohol <b>withdrawal</b>.
+SLC6A4	drug	alcohol	11113619	Studies of the <strong>5 HTT</strong> gene in <b>alcohol</b> dependence have not resulted in a consensus.
+SLC6A4	addiction	dependence	11113619	Studies of the <strong>5 HTT</strong> gene in alcohol <b>dependence</b> have not resulted in a consensus.
+SLC6A4	drug	alcohol	11097976	An association between the <strong>5 HTTLPR</strong> short variant polymorphism in the promoter region of the serotonin transporter gene and risk for <b>alcohol</b> dependence has been reported from case control studies that are, however, prone to chance findings related to artifacts of population structure.
+SLC6A4	addiction	dependence	11097976	An association between the <strong>5 HTTLPR</strong> short variant polymorphism in the promoter region of the serotonin transporter gene and risk for alcohol <b>dependence</b> has been reported from case control studies that are, however, prone to chance findings related to artifacts of population structure.
+SLC6A4	drug	alcohol	10980326	Serotonin transporter gene regulatory region polymorphism (<strong>5 HTTLPR</strong>), [3H]paroxetine binding in healthy control subjects and <b>alcohol</b> dependent patients and their relationships to impulsivity.
+SLC6A4	drug	alcohol	10980326	The aim of this study was to investigate [3H]paroxetine binding and impulsivity in <b>alcohol</b> dependent and age matched control subjects in relation to a 5' promoter region serotonin transporter (<strong>5 HTT</strong>) polymorphism (5 HTTLPR).
+SLC6A4	drug	alcohol	10980326	The aim of this study was to investigate [3H]paroxetine binding and impulsivity in <b>alcohol</b> dependent and age matched control subjects in relation to a 5' promoter region serotonin transporter (<strong>5 HTT</strong>) polymorphism (<strong>5 HTTLPR</strong>).
+SLC6A4	drug	alcohol	10980326	<strong>5 HTTLPR</strong> S genotype carriers in both <b>alcohol</b> dependent and control subjects were expected to show significantly fewer binding sites and a lower dissociation constant.
+SLC6A4	drug	alcohol	10980326	Blood samples were taken from both <b>alcohol</b> dependent and control subjects to determine <strong>5 HTTLPR</strong> genotypes using PCR of lymphocyte DNA, and to perform platelet [3H]paroxetine binding (binding capacity: B(max); and dissociation constant: K(D)).
+SLC6A4	drug	alcohol	10980326	This was the first study to investigate platelet [3H]paroxetine binding in <b>alcohol</b> dependent and age matched control subjects in relation to the <strong>5 HTTLPR</strong> genotype.
+SLC6A4	drug	alcohol	10980326	No differences concerning <strong>5 HTTLPR</strong> alleles were found in these groups Furthermore, no significant interaction between these parameters and impulsivity was shown in <b>alcohol</b> dependent subjects.
+SLC6A4	drug	alcohol	10980326	These results do not support previous results of altered [3H]paroxetine binding sites in <b>alcohol</b> dependent subjects or <strong>5 HTTLPR</strong> S allele carriers.
+SLC6A4	drug	alcohol	10960156	The functional polymorphism of the serotonin transporter gene (<strong>5 HTTLPR</strong>) has been associated with different disorders, including <b>alcoholism</b>.
+SLC6A4	drug	alcohol	10960156	Considering the likelihood of heterogeneity in the "<b>alcohol</b> dependence" phenotype, <strong>5 HTTLPR</strong> may be more specifically implicated in subsamples of patients or in related traits of <b>alcoholism</b>, such as impulsivity.
+SLC6A4	addiction	dependence	10960156	Considering the likelihood of heterogeneity in the "alcohol <b>dependence</b>" phenotype, <strong>5 HTTLPR</strong> may be more specifically implicated in subsamples of patients or in related traits of alcoholism, such as impulsivity.
+SLC6A4	drug	alcohol	10960156	The "short" (S) allele of the <strong>5 HTTLPR</strong> appeared to be unrelated to <b>alcohol</b> dependence and comorbid depression in our sample, but was found associated with an increased risk for suicide attempts.
+SLC6A4	addiction	dependence	10960156	The "short" (S) allele of the <strong>5 HTTLPR</strong> appeared to be unrelated to alcohol <b>dependence</b> and comorbid depression in our sample, but was found associated with an increased risk for suicide attempts.
+SLC6A4	drug	alcohol	10924015	By means of in vitro quantitative autoradiography, we used [3H]citalopram, [3H]8 OH DPAT, and [3H]GR65630 to label <strong>5 HTT</strong>, 5 HT1A receptors, and 5 HT3 receptors in the brain of <b>alcohol</b> naïve FH rats, Wistar Kyoto (WKY) rats, and FH rats given free access to 5% <b>ethanol</b> and/or after 24 to 48 hr withdrawal.
+SLC6A4	addiction	withdrawal	10924015	By means of in vitro quantitative autoradiography, we used [3H]citalopram, [3H]8 OH DPAT, and [3H]GR65630 to label <strong>5 HTT</strong>, 5 HT1A receptors, and 5 HT3 receptors in the brain of alcohol naïve FH rats, Wistar Kyoto (WKY) rats, and FH rats given free access to 5% ethanol and/or after 24 to 48 hr <b>withdrawal</b>.
+SLC6A4	drug	alcohol	10924015	The region specific alterations of 5 HT1A receptors in FH rat brain after <b>ethanol</b> challenges suggest that 5 HT1A receptors are sensitive to <b>ethanol</b> challenges, whereas <strong>5 HTT</strong> are apparently insensitive.
+SLC6A4	drug	alcohol	10871694	Reduction in raphe serotonin transporter (<strong>5 HTT</strong>) availability was observed in abstinent male <b>alcoholics</b> and it may be the result of neurodegeneration rather than reversible neuroadaptation.
+SLC6A4	drug	alcohol	10822348	There is abundant evidence that the serotonin (5 HT) system is modulating mood and several behavioural traits and that disturbances in the regulation of this system can be associated with severe behavioural malfunctions, as aggressive implusive and suicidal behaviour.1 Recently a functional polymorphism in the promoter region of the serotonin transporter gene (<strong>5 HTTLPR</strong>) was identified2 and the presence of one or two short alleles was associated with anxiety related personality traits3 and several psychiatric disturbances, such as affective disorder4 or severe <b>alcohol</b> dependence.5 With respect to the importance of the 5 HT transporter in serotonergic transmission, we have genotyped the DNA of 58 Caucasian suicide victims (with unknown psychiatric diagnoses) and 110 healthy controls for the biallelic functional polymorphism in the <strong>5 HTTLPR</strong>.
+SLC6A4	addiction	dependence	10822348	There is abundant evidence that the serotonin (5 HT) system is modulating mood and several behavioural traits and that disturbances in the regulation of this system can be associated with severe behavioural malfunctions, as aggressive implusive and suicidal behaviour.1 Recently a functional polymorphism in the promoter region of the serotonin transporter gene (<strong>5 HTTLPR</strong>) was identified2 and the presence of one or two short alleles was associated with anxiety related personality traits3 and several psychiatric disturbances, such as affective disorder4 or severe alcohol <b>dependence</b>.5 With respect to the importance of the 5 HT transporter in serotonergic transmission, we have genotyped the DNA of 58 Caucasian suicide victims (with unknown psychiatric diagnoses) and 110 healthy controls for the biallelic functional polymorphism in the <strong>5 HTTLPR</strong>.
+SLC6A4	drug	nicotine	10822347	Individual differences in propensity to <b>nicotine</b> dependence appear to be mediated, in part, by genetic factors.1 The serotonin transporter gene has a functional polymorphism (<strong>5 HTTLPR</strong>) which modulates gene transcription and reuptake.2,3 A possible role in <b>nicotine</b> dependence is suggested by a link between <strong>5 HTTLPR</strong> and neuroticism,4 a personality trait which has been related to <b>smoking</b> practices.5 In a cross sectional study of 185 <b>smokers</b>, we utilized multiple linear regression modeling to examine the interacting effects of the <strong>5 HTTLPR</strong> and neuroticism on <b>smoking</b> practices and <b>nicotine</b> dependence.
+SLC6A4	addiction	dependence	10822347	Individual differences in propensity to nicotine <b>dependence</b> appear to be mediated, in part, by genetic factors.1 The serotonin transporter gene has a functional polymorphism (<strong>5 HTTLPR</strong>) which modulates gene transcription and reuptake.2,3 A possible role in nicotine <b>dependence</b> is suggested by a link between <strong>5 HTTLPR</strong> and neuroticism,4 a personality trait which has been related to smoking practices.5 In a cross sectional study of 185 smokers, we utilized multiple linear regression modeling to examine the interacting effects of the <strong>5 HTTLPR</strong> and neuroticism on smoking practices and nicotine <b>dependence</b>.
+SLC6A4	drug	nicotine	10822347	The <strong>5 HTTLPR</strong> by neuroticism interaction effect was statistically significant in the models of <b>nicotine</b> intake (P = 0.05), <b>nicotine</b> dependence (P = 0.001), and <b>smoking</b> motivations (<b>smoking</b> to reduce negative mood (P = 0.01); <b>smoking</b> for stimulation (P = 0.01)).
+SLC6A4	addiction	dependence	10822347	The <strong>5 HTTLPR</strong> by neuroticism interaction effect was statistically significant in the models of nicotine intake (P = 0.05), nicotine <b>dependence</b> (P = 0.001), and smoking motivations (smoking to reduce negative mood (P = 0.01); smoking for stimulation (P = 0.01)).
+SLC6A4	drug	nicotine	10822347	The results suggested that neuroticism was positively associated with these <b>smoking</b> practices among <b>smokers</b> with <strong>5 HTTLPR</strong> S genotypes (s/s or s/l), but not among <b>smokers</b> with the L genotype (l/l).
+SLC6A4	drug	nicotine	10822347	The <strong>5 HTTLPR</strong> may modify the effects of neuroticism on <b>smoking</b> motivations and <b>nicotine</b> dependence.
+SLC6A4	addiction	dependence	10822347	The <strong>5 HTTLPR</strong> may modify the effects of neuroticism on smoking motivations and nicotine <b>dependence</b>.
+SLC6A4	drug	nicotine	10822347	Assessment of <strong>5 HTTLPR</strong> genotype and neuroticism may help to identify <b>smokers</b> who are more responsive to psychotropic medications, such as selective serotonin reuptake inhibitors (SSRIs), which are being used in <b>smoking</b> cessation treatment.
+SLC6A4	addiction	reward	10684896	In an effort to assess the role of 5 HT in drug mediated <b>reward</b>, this study analyzed the serotonergic innervation of NAc using immunocytochemistry for 5 HT and the 5 HT transporter (<strong>SERT</strong>).
+SLC6A4	drug	amphetamine	10684896	These drug resistant 5 HT axons that lack <strong>SERT</strong> densely innervate the caudal one third of the accumbens shell, the same location where dopamine axons are spared after <b>methamphetamine</b>.
+SLC6A4	drug	opioid	10483044	No association between the serotonin transporter promoter region (<strong>5 HTTLPR</strong>) and the dopamine D3 receptor (BalI D3DR) polymorphisms and <b>heroin</b> addiction.
+SLC6A4	addiction	addiction	10483044	No association between the serotonin transporter promoter region (<strong>5 HTTLPR</strong>) and the dopamine D3 receptor (BalI D3DR) polymorphisms and heroin <b>addiction</b>.
+SLC6A4	drug	alcohol	10088053	The 14 men with the LL genotype of the serotonin transporter (<strong>5 HTT</strong>) polymorphism and the seven with the Pro/Ser genotype of the GABAA alpha 6 polymorphism had demonstrated lower LR scores at about age 20, and had significantly higher proportions of <b>alcoholics</b> than the other genotypes for those loci.
+SLC6A4	drug	alcohol	10064377	Pharmacological and clinical studies have shown that the 5 HT transporter (<strong>5 HTT</strong>) and the 5 HT1A receptor appear to be candidate loci for the aetiology of <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	10064377	Pharmacological and clinical studies have shown that the 5 HT transporter (<strong>5 HTT</strong>) and the 5 HT1A receptor appear to be candidate loci for the aetiology of alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	10064377	We have analysed the presence of different <strong>5 HTT</strong> and 5 HT1A variants in 104 <b>alcohol</b> dependent patients and 38 controls for a possible association with <b>alcohol</b> dependence.
+SLC6A4	addiction	dependence	10064377	We have analysed the presence of different <strong>5 HTT</strong> and 5 HT1A variants in 104 alcohol dependent patients and 38 controls for a possible association with alcohol <b>dependence</b>.
+SLC6A4	drug	alcohol	10064377	In <b>alcohol</b> dependent patients, we found a high frequency of the S allele of <strong>5 HTTLPR</strong> (45.5% vs. 29%, chi2 = 6.33, p = 0.0081).
+SLC6A4	drug	alcohol	9654330	We report the association of the low activity, short variant of the <strong>5 HTTLPR</strong> with high <b>ethanol</b> tolerance among young adults in a case control association study (n = 713).
+SLC6A4	drug	alcohol	9654330	The low activity <strong>5 HTTLPR</strong> showed a significantly increased allele frequency (chi2 = 7.30; df = 2; P = 0.007) and genotype frequency among young adults (< or =26 years) with high <b>ethanol</b> tolerance homozygous for the short allele (chi2 = 7.58; df = 1; P = 0.02).
+SLC6A4	drug	alcohol	9654330	This indicates that the low activity <strong>5 HTTLPR</strong> may be involved in the neuronal mechanisms responsible for <b>ethanol</b> tolerance and dependence.
+SLC6A4	addiction	dependence	9654330	This indicates that the low activity <strong>5 HTTLPR</strong> may be involved in the neuronal mechanisms responsible for ethanol tolerance and <b>dependence</b>.
+SLC6A4	drug	cocaine	9636213	Several lines of evidence have suggested that <b>cocaine</b> blockade of the dopamine transporter (DAT), perhaps with additional contributions from serotonin transporter (<strong>5 HTT</strong>) recognition, was key to its rewarding actions.
+SLC6A4	drug	cocaine	9636213	We now report that knockout mice without DAT and mice without <strong>5 HTT</strong> establish <b>cocaine</b> conditioned place preferences.
+SLC6A4	drug	alcohol	9627746	We tested the hypothesis that a functional biallelic repetitive element in the 5' regulatory region of the human serotonin transporter gene (<strong>SLC6A4</strong>) confers susceptibility to serotonin related personality traits underlying <b>alcohol</b> dependence with dissocial behavior.
+SLC6A4	addiction	dependence	9627746	We tested the hypothesis that a functional biallelic repetitive element in the 5' regulatory region of the human serotonin transporter gene (<strong>SLC6A4</strong>) confers susceptibility to serotonin related personality traits underlying alcohol <b>dependence</b> with dissocial behavior.
+SLC6A4	drug	alcohol	9627746	Our association analyses revealed a trend towards a higher frequency of the short (S) allele of the <strong>SLC6A4</strong> polymorphism in dissocial <b>alcoholics</b> compared to 216 German controls (chi 2 = 2.81, df = 1, p = 0.094).
+SLC6A4	drug	alcohol	9627746	Our tentative association findings in dissocial <b>alcoholics</b> suggest that the S allele of the 5' regulatory <strong>SLC6A4</strong> polymorphism confers susceptibility to a temperamental profile of high novelty seeking and low harm avoidance that has been postulated to underlie dissocial (type 2) <b>alcoholism</b> according to Cloninger's neurogenetic theory of personality.
+SLC6A4	addiction	relapse	9627746	Our tentative association findings in dissocial alcoholics suggest that the S allele of the 5' regulatory <strong>SLC6A4</strong> polymorphism confers susceptibility to a temperamental profile of high novelty <b>seeking</b> and low harm avoidance that has been postulated to underlie dissocial (type 2) alcoholism according to Cloninger's neurogenetic theory of personality.
+SLC6A4	drug	alcohol	9394104	The present study tested the hypothesis that the short, low activity variant of a biallelic polymorphism in the 5' regulatory region of the human serotonin transporter (<strong>5 HTT</strong>) gene confers susceptibility to severe <b>alcohol</b> dependence marked by severe withdrawal symptoms.
+SLC6A4	addiction	dependence	9394104	The present study tested the hypothesis that the short, low activity variant of a biallelic polymorphism in the 5' regulatory region of the human serotonin transporter (<strong>5 HTT</strong>) gene confers susceptibility to severe alcohol <b>dependence</b> marked by severe withdrawal symptoms.
+SLC6A4	addiction	withdrawal	9394104	The present study tested the hypothesis that the short, low activity variant of a biallelic polymorphism in the 5' regulatory region of the human serotonin transporter (<strong>5 HTT</strong>) gene confers susceptibility to severe alcohol dependence marked by severe <b>withdrawal</b> symptoms.
+SLC6A4	drug	alcohol	9394104	Further studies are required to test whether the tentative genotype phenotype relationship occurred by chance or reflects a real genotypic association between a recessively modifying effect of the short variant of the functional <strong>5 HTT</strong> promoter polymorphism and <b>alcohol</b> withdrawal vulnerability.
+SLC6A4	addiction	withdrawal	9394104	Further studies are required to test whether the tentative genotype phenotype relationship occurred by chance or reflects a real genotypic association between a recessively modifying effect of the short variant of the functional <strong>5 HTT</strong> promoter polymorphism and alcohol <b>withdrawal</b> vulnerability.
+SLC6A4	drug	cocaine	9387868	The effects of a 'binge' paradigm of <b>cocaine</b> administration on <strong>SERT</strong>, DAT and NET mRNA abundance were compared in the brains of behaviorally sensitized rats.
+SLC6A4	addiction	intoxication	9387868	The effects of a '<b>binge</b>' paradigm of cocaine administration on <strong>SERT</strong>, DAT and NET mRNA abundance were compared in the brains of behaviorally sensitized rats.
+SLC6A4	drug	cocaine	9387868	<b>Cocaine</b> significantly decreased the abundance of the <strong>SERT</strong> mRNA within the dlDR and DAT mRNA abundance within the SNc and the PBP, and increased the abundance of the NET mRNA within the LC.
+SLC6A4	drug	cocaine	9387868	Finally, correlational analysis indicated that post <b>cocaine</b> levels of DAT, <strong>SERT</strong> and NET mRNAs were not associated with <b>cocaine</b> induced sensitization.
+SLC6A4	addiction	sensitization	9387868	Finally, correlational analysis indicated that post cocaine levels of DAT, <strong>SERT</strong> and NET mRNAs were not associated with cocaine induced <b>sensitization</b>.
+SLC6A4	drug	alcohol	6399209	High blood <b>ethanol</b> levels (BEL) were produced through a combination of an initial intubated dose of <b>ethanol</b> sustained <b>ethanol</b> release tube (<strong>SERT</strong>), and <b>ethanol</b> as 37% of total energy in the liquid diet.
+SLC6A4	drug	alcohol	7194802	The following methods are in this category; inhalation, oral intubation, intragastric or intravenous schedule infusions, and <strong>SERT</strong> (sustained <b>ethanol</b> release tubes) implants.
+SLC6A4	drug	alcohol	7208546	The Sustained <b>Ethanol</b> Release Tube (<strong>SERT</strong>) for rats is similar to an earlier device reported for mice, except that only one refill per day is required.
+SLC6A4	drug	alcohol	7208546	Supplementation of <strong>SERT</strong> released <b>ethanol</b> with a Sustacal chocolate flavored diet with 37% of total energy as <b>ethanol</b> produces high, stable BEL for indefinite periods.
+SLC6A4	drug	alcohol	564551	The Silastic device, dubbed <strong>SERT</strong> (sustained <b>ethanol</b> release tube), holds 0.35 milliliter of 95 percent <b>ethanol</b> (by volume) and is implanted under the skin of the back where it releases <b>ethanol</b> for up to 12 hours, with no observable tissue damage.
+OPRM1	drug	nicotine	32763540	Rewarding effects of <b>nicotine</b> from cigarettes are associated, among others, with mu opioid receptors encoded by the <strong>OPRM1</strong> gene.
+OPRM1	drug	opioid	32763540	Rewarding effects of nicotine from cigarettes are associated, among others, with mu <b>opioid</b> receptors encoded by the <strong>OPRM1</strong> gene.
+OPRM1	drug	alcohol	32763540	The aim of the study was to evaluate the association between two <strong>OPRM1</strong> gene polymorphisms, rs1799971 and rs510769, and tobacco smoking in Caucasian patients with schizophrenia, <b>alcohol</b> dependence, and healthy control subjects.
+OPRM1	drug	nicotine	32763540	The aim of the study was to evaluate the association between two <strong>OPRM1</strong> gene polymorphisms, rs1799971 and rs510769, and <b>tobacco</b> <b>smoking</b> in Caucasian patients with schizophrenia, alcohol dependence, and healthy control subjects.
+OPRM1	addiction	dependence	32763540	The aim of the study was to evaluate the association between two <strong>OPRM1</strong> gene polymorphisms, rs1799971 and rs510769, and tobacco smoking in Caucasian patients with schizophrenia, alcohol <b>dependence</b>, and healthy control subjects.
+OPRM1	drug	alcohol	32763540	A significant association was found between the GC haplotype (<strong>OPRM1</strong> rs1799971 and rs510769) and smoking in healthy controls, but not in patients with schizophrenia and <b>alcohol</b> dependence.
+OPRM1	drug	nicotine	32763540	A significant association was found between the GC haplotype (<strong>OPRM1</strong> rs1799971 and rs510769) and <b>smoking</b> in healthy controls, but not in patients with schizophrenia and alcohol dependence.
+OPRM1	addiction	dependence	32763540	A significant association was found between the GC haplotype (<strong>OPRM1</strong> rs1799971 and rs510769) and smoking in healthy controls, but not in patients with schizophrenia and alcohol <b>dependence</b>.
+OPRM1	drug	nicotine	32763540	This is the first study to reveal that <b>nicotine</b> dependence is associated with the GC haplotype of the <strong>OPRM1</strong> rs1799971 and rs510769 in all subjects or specifically in healthy controls.
+OPRM1	addiction	dependence	32763540	This is the first study to reveal that nicotine <b>dependence</b> is associated with the GC haplotype of the <strong>OPRM1</strong> rs1799971 and rs510769 in all subjects or specifically in healthy controls.
+OPRM1	drug	alcohol	32763540	These results did not confirm the strong connection between <strong>OPRM1</strong> polymorphisms and nicotine dependence in schizophrenia or <b>alcohol</b> dependence.
+OPRM1	drug	nicotine	32763540	These results did not confirm the strong connection between <strong>OPRM1</strong> polymorphisms and <b>nicotine</b> dependence in schizophrenia or alcohol dependence.
+OPRM1	addiction	dependence	32763540	These results did not confirm the strong connection between <strong>OPRM1</strong> polymorphisms and nicotine <b>dependence</b> in schizophrenia or alcohol <b>dependence</b>.
+OPRM1	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (<strong>Oprm</strong>), delta (Oprd), and kappa (Oprk), and their endogenous opioid peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+OPRM1	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (<strong>Oprm</strong>), delta (Oprd), and kappa (Oprk), and their endogenous <b>opioid</b> peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+OPRM1	drug	cocaine	32730947	We found that <b>cocaine</b> self administration significantly increased the mRNA levels of <strong>Oprm</strong> and Oprd in both the CPu and PFC, but had no effect on Oprk mRNA levels in either brain region.
+OPRM1	drug	opioid	32561311	The A118G single nucleotide polymorphism (SNP rs1799971) of the <strong>OPRM1</strong> gene encoding the N40D (D40 minor allele) mu <b>opioid</b> receptor (MOR) variant has been linked with individuals who have an AUD.
+OPRM1	drug	opioid	32506472	Dysregulated expression of the alternatively spliced variant mRNAs of the mu <b>opioid</b> receptor gene, <strong>OPRM1</strong>, in the medial prefrontal cortex of male human <b>heroin</b> abusers and <b>heroin</b> self administering male rats.
+OPRM1	drug	opioid	32506472	The mu <b>opioid</b> receptor gene, <strong>OPRM1</strong>, undergoes extensive alternative splicing, creating an array of splice variants that are conserved from rodent to humans.
+OPRM1	drug	opioid	32506472	Increasing evidence suggests that these <strong>OPRM1</strong> splice variants are pharmacologically important in mediating various actions of mu <b>opioids</b>, including analgesia, tolerance, physical dependence, rewarding behavior, as well as addiction.
+OPRM1	addiction	addiction	32506472	Increasing evidence suggests that these <strong>OPRM1</strong> splice variants are pharmacologically important in mediating various actions of mu opioids, including analgesia, tolerance, physical dependence, rewarding behavior, as well as <b>addiction</b>.
+OPRM1	addiction	dependence	32506472	Increasing evidence suggests that these <strong>OPRM1</strong> splice variants are pharmacologically important in mediating various actions of mu opioids, including analgesia, tolerance, physical <b>dependence</b>, rewarding behavior, as well as addiction.
+OPRM1	drug	opioid	32506472	In the present study, we examine expression of the <strong>OPRM1</strong> splice variant mRNAs in the medial prefrontal cortex (mPFC), one of the major brain regions involved in decision making and drug seeking behaviors, of male human <b>heroin</b> abusers and male rats that developed stable <b>heroin</b> seeking behavior using an intravenous <b>heroin</b> self administration (SA) model.
+OPRM1	addiction	relapse	32506472	In the present study, we examine expression of the <strong>OPRM1</strong> splice variant mRNAs in the medial prefrontal cortex (mPFC), one of the major brain regions involved in decision making and drug <b>seeking</b> behaviors, of male human heroin abusers and male rats that developed stable heroin <b>seeking</b> behavior using an intravenous heroin self administration (SA) model.
+OPRM1	drug	opioid	32506472	Moreover, the expressions of several <strong>OPRM1</strong> splice variant mRNAs were dysregulated in the postmortem mPFCs from <b>heroin</b> abusers compared to the control subjects.
+OPRM1	drug	opioid	32506472	These findings suggest potential roles of the <strong>OPRM1</strong> splice variants in <b>heroin</b> addiction that could be mechanistically explored using the rat <b>heroin</b> SA model.
+OPRM1	addiction	addiction	32506472	These findings suggest potential roles of the <strong>OPRM1</strong> splice variants in heroin <b>addiction</b> that could be mechanistically explored using the rat heroin SA model.
+OPRM1	drug	opioid	32492095	Association of <strong>OPRM1</strong> Functional Coding Variant With <b>Opioid</b> Use Disorder: A Genome Wide Association Study.
+OPRM1	drug	opioid	32492095	In 82 707 European American individuals, a functional coding variant (rs1799971, encoding Asn40Asp) in <strong>OPRM1</strong> (μ <b>opioid</b> receptor gene, the main biological target for <b>opioid</b> drugs; OMIM 600018) reached genome wide significance (G allele: mean [SE], β =  0.066 [0.012]; P = 1.51 × 10 8).
+OPRM1	drug	alcohol	32406553	These effects were significant after controlling for <b>alcohol</b> use severity, <strong>OPRM1</strong> genotype, and medication.
+OPRM1	drug	opioid	32388931	We also demonstrated that cells expressing mu <b>opioid</b> receptors (MOR, gene name <strong>Oprm1</strong>) in the MPOA displayed increased Egr1 expression when adolescent rats were engaged in social play using double immunofluorescence labeling of MOR and Egr1.
+OPRM1	drug	opioid	32381649	Here we report the generation of a knock in <strong>Oprm1</strong> Cre mouse line, which allows targeting and manipulating MOR <b>opioid</b> responsive neurons.
+OPRM1	drug	opioid	32381649	The <strong>Oprm1</strong> Cre line is therefore an excellent tool for both mapping and functional studies of MOR positive neurons, and will be of broad interest for <b>opioid</b>, pain, and addiction research.
+OPRM1	addiction	addiction	32381649	The <strong>Oprm1</strong> Cre line is therefore an excellent tool for both mapping and functional studies of MOR positive neurons, and will be of broad interest for opioid, pain, and <b>addiction</b> research.
+OPRM1	drug	alcohol	32344532	<b>Naltrexone</b> Use in Treating Hypersexuality Induced by Dopamine Replacement Therapy: Impact of <strong>OPRM1</strong> A/G Polymorphism on Its Effectiveness.
+OPRM1	drug	opioid	32344532	Our aim was to update the knowledge on this issue, particularly on the influence of an <b>Opioid</b> Receptor Mu 1 (<strong>OPRM1</strong>) genetic polymorphism.
+OPRM1	drug	opioid	32189578	A single nucleotide polymorphism in <strong>OPRM1</strong>(rs483481) and risk for <b>heroin</b> use disorder.
+OPRM1	drug	opioid	32189578	<b>Opioid</b> receptor mu1 (<strong>OPRM1</strong>) is the target of many <b>opioid</b> drugs, and it is known to have affinity toward both endogenous and exogenous <b>opioids</b>, opiate and <b>opioid</b> analgesic drugs.
+OPRM1	drug	opioid	32189578	The present study was undertaken to explore association of single nucleotide polymorphisms (SNPs) in the <strong>OPRM1</strong> gene with <b>heroin</b> use disorder.
+OPRM1	drug	opioid	32189578	<strong>OPRM1</strong> is found to be associated with <b>heroin</b> use disorder in the studied Manipuri cohort.
+OPRM1	drug	alcohol	32029903	An analysis of the effect of mu opioid receptor gene (<strong>OPRM1</strong>) promoter region DNA methylation on the response of <b>naltrexone</b> treatment of <b>alcohol</b> dependence.
+OPRM1	drug	opioid	32029903	An analysis of the effect of mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) promoter region DNA methylation on the response of naltrexone treatment of alcohol dependence.
+OPRM1	addiction	dependence	32029903	An analysis of the effect of mu opioid receptor gene (<strong>OPRM1</strong>) promoter region DNA methylation on the response of naltrexone treatment of alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	32029903	This study explored the effect of <strong>OPRM1</strong> promoter region DNA methylation on the outcome of treatment with the opioid antagonist <b>naltrexone</b> (NTX) for <b>alcohol</b> dependence (AD).
+OPRM1	drug	opioid	32029903	This study explored the effect of <strong>OPRM1</strong> promoter region DNA methylation on the outcome of treatment with the <b>opioid</b> antagonist naltrexone (NTX) for alcohol dependence (AD).
+OPRM1	addiction	dependence	32029903	This study explored the effect of <strong>OPRM1</strong> promoter region DNA methylation on the outcome of treatment with the opioid antagonist naltrexone (NTX) for alcohol <b>dependence</b> (AD).
+OPRM1	addiction	relapse	32029903	No significant effect of individual <strong>OPRM1</strong> promoter CpG units on AD <b>relapse</b> was observed in either AAs or EAs.
+OPRM1	drug	alcohol	32020635	<strong>OPRM1</strong> Moderates Daily Associations of <b>Naltrexone</b> Adherence With <b>Alcohol</b> Consumption: Preliminary Evidence From a Mobile Health Trial.
+OPRM1	drug	alcohol	32020635	Initial evidence that <strong>OPRM1</strong> genotype moderates the clinical response to <b>naltrexone</b> has not been replicated in prospective clinical trials.
+OPRM1	drug	alcohol	32020635	This study leveraged person centered analyses and daily measures of <b>alcohol</b> use, craving, and medication adherence to investigate <strong>OPRM1</strong> as a moderator of changes in clinical outcomes during <b>naltrexone</b> treatment.
+OPRM1	addiction	relapse	32020635	This study leveraged person centered analyses and daily measures of alcohol use, <b>craving</b>, and medication adherence to investigate <strong>OPRM1</strong> as a moderator of changes in clinical outcomes during naltrexone treatment.
+OPRM1	drug	alcohol	32020635	Multilevel modeling and multilevel structural equation modeling analyses evaluated the hypotheses that <strong>OPRM1</strong> genotype would moderate prospective reductions in daily <b>alcohol</b> use and craving, and would also moderate within person associations of daily adherence with same day craving and consumption.
+OPRM1	addiction	relapse	32020635	Multilevel modeling and multilevel structural equation modeling analyses evaluated the hypotheses that <strong>OPRM1</strong> genotype would moderate prospective reductions in daily alcohol use and <b>craving</b>, and would also moderate within person associations of daily adherence with same day <b>craving</b> and consumption.
+OPRM1	addiction	relapse	32020635	<strong>OPRM1</strong> genotype moderated the association of daily adherence with reduced same day consumption (p = 0.007) and <b>craving</b> (p = 0.06), with these associations being stronger for participants with the 118G variant.
+OPRM1	addiction	relapse	32020635	<strong>OPRM1</strong> genotype did not moderate changes in <b>craving</b> and consumption over time.
+OPRM1	drug	opioid	32014377	Stressed mice also showed significant increase in TLR4, Nuclear Factor Kappa B (NF kB), inducible nitric oxide synthase (iNOS), dopamine receptor D2 (DRD2), cyclic adenosine monophosphate (cAMP) response element binding protein 1 (CREB 1) and <strong><b>opioid</b> receptor MU 1</strong> (OPRM 1) genes expression compared with control and LPS RS treated stressed mice.
+OPRM1	drug	opioid	32014377	Stressed mice also showed significant increase in TLR4, Nuclear Factor Kappa B (NF kB), inducible nitric oxide synthase (iNOS), dopamine receptor D2 (DRD2), cyclic adenosine monophosphate (cAMP) response element binding protein 1 (CREB 1) and <strong><b>opioid</b> receptor MU 1</strong> (<strong>OPRM</strong> 1) genes expression compared with control and LPS RS treated stressed mice.
+OPRM1	drug	alcohol	31961981	Systematic review and meta analysis of the moderating effect of rs1799971 in <strong>OPRM1</strong>, the mu opioid receptor gene, on response to <b>naltrexone</b> treatment of <b>alcohol</b> use disorder.
+OPRM1	drug	opioid	31961981	Systematic review and meta analysis of the moderating effect of rs1799971 in <strong>OPRM1</strong>, the mu <b>opioid</b> receptor gene, on response to naltrexone treatment of alcohol use disorder.
+OPRM1	drug	alcohol	31961981	To identify patients who may be most responsive to <b>naltrexone</b> treatment, studies have examined the moderating effect of rs1799971, a single nucleotide polymorphism (SNP) that encodes a non synonymous substitution (Asn40Asp) in the mu opioid receptor gene, <strong>OPRM1</strong>.
+OPRM1	drug	opioid	31961981	To identify patients who may be most responsive to naltrexone treatment, studies have examined the moderating effect of rs1799971, a single nucleotide polymorphism (SNP) that encodes a non synonymous substitution (Asn40Asp) in the mu <b>opioid</b> receptor gene, <strong>OPRM1</strong>.
+OPRM1	drug	alcohol	31961981	From the evidence to date, it remains unclear whether rs1799971, the <strong>OPRM1</strong> Asn40Asp single nucleotide polymorphism, predicts <b>naltrexone</b> treatment response in individuals with <b>alcohol</b> use disorder or heavy drinking.
+OPRM1	drug	opioid	31940240	<b>Heroin</b> acts primarily as a mu <b>opioid</b> receptor (<strong>OPRM1</strong>) agonist.
+OPRM1	drug	opioid	31925906	We speculated that the μ <b>opioid</b> receptor gene (<strong>Oprm1</strong>) impacts <b>morphine</b> response, and genotyped the mice tested for <b>morphine</b> induced hypothermia.
+OPRM1	drug	opioid	31925906	Data from a family of recombinant inbred mouse strains support the influence of <strong>Oprm1</strong> genotype, but not Taar1 genotype, on thermal response to <b>morphine</b>.
+OPRM1	drug	opioid	31925906	These results nominate <strong>Oprm1</strong> as a genetic risk factor for <b>morphine</b> induced hypothermia, and provide additional evidence for a connection between drug preference and drug thermal response.
+OPRM1	addiction	intoxication	31863787	For each unit increase in <b>intoxication</b> level perceived as safe for driving, the odds of past month DUIC increased 18% to 68% (multinomial logistic regression odds ratio   <strong>MOR1</strong> 9 days: 1.18, 95% CI: 1.13 1.23; MOR10 19 days: 1.40, 95% CI: 1.30 1.50; MOR20 30 days: 1.68, 95% CI: 1.57 1.80).
+OPRM1	drug	opioid	31853823	Haplotype Based Association and In Silico Studies of <strong>OPRM1</strong> Gene Variants with Susceptibility to <b>Opioid</b> Dependence Among Addicted Iranians Undergoing <b>Methadone</b> Treatment.
+OPRM1	addiction	dependence	31853823	Haplotype Based Association and In Silico Studies of <strong>OPRM1</strong> Gene Variants with Susceptibility to Opioid <b>Dependence</b> Among Addicted Iranians Undergoing Methadone Treatment.
+OPRM1	drug	opioid	31853823	The associations of <strong>OPRM1</strong> gene variants with <b>opioid</b> dependence have been demonstrated.
+OPRM1	addiction	dependence	31853823	The associations of <strong>OPRM1</strong> gene variants with opioid <b>dependence</b> have been demonstrated.
+OPRM1	drug	opioid	31853823	This study investigated the association of rs495491, rs1799971 (A118G), rs589046, and rs10457090 variants of <strong>OPRM1</strong> gene with opium dependence and their haplotypes among addicted individuals undergoing <b>methadone</b> treatment.
+OPRM1	addiction	dependence	31853823	This study investigated the association of rs495491, rs1799971 (A118G), rs589046, and rs10457090 variants of <strong>OPRM1</strong> gene with opium <b>dependence</b> and their haplotypes among addicted individuals undergoing methadone treatment.
+OPRM1	drug	opioid	31853823	Consequently, rs495491, A118G, rs589046, and rs10457090 were associated with <b>opioid</b> dependence among Iranians; also, A118G might be the most remarkable marker of <strong>OPRM1</strong> owing to its vital structural roles.
+OPRM1	addiction	dependence	31853823	Consequently, rs495491, A118G, rs589046, and rs10457090 were associated with opioid <b>dependence</b> among Iranians; also, A118G might be the most remarkable marker of <strong>OPRM1</strong> owing to its vital structural roles.
+OPRM1	drug	opioid	31819591	<strong>OPRM1</strong> A118G Polymorphisms and Its Role in <b>Opioid</b> Addiction: Implication on Severity and Treatment Approaches.
+OPRM1	addiction	addiction	31819591	<strong>OPRM1</strong> A118G Polymorphisms and Its Role in Opioid <b>Addiction</b>: Implication on Severity and Treatment Approaches.
+OPRM1	drug	opioid	31819591	<strong>OPRM1</strong> nonsynonymous single nucleotide polymorphism rs1799971 (A118G) is the most prominent candidate due to its significant association with onset and treatment of <b>opioid</b> addiction.
+OPRM1	addiction	addiction	31819591	<strong>OPRM1</strong> nonsynonymous single nucleotide polymorphism rs1799971 (A118G) is the most prominent candidate due to its significant association with onset and treatment of opioid <b>addiction</b>.
+OPRM1	drug	opioid	31819591	A more detailed understanding of molecular, epigenetic and genetic variants especially the implication of <strong>OPRM1</strong> A118G polymorphism in an individual may serve as the way forward to address the <b>opioid</b> epidemic.
+OPRM1	drug	opioid	31778689	Murine model of <strong>OPRM1</strong> A118G alters <b>oxycodone</b> self administration and locomotor activation, but not conditioned place preference.
+OPRM1	drug	opioid	31778689	The human mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) contains a functional single nucleotide polymorphism (SNP), A118G, which has been associated with altered <b>opioid</b> addiction risk, however the mechanisms responsible for this are not well understood.
+OPRM1	addiction	addiction	31778689	The human mu opioid receptor gene (<strong>OPRM1</strong>) contains a functional single nucleotide polymorphism (SNP), A118G, which has been associated with altered opioid <b>addiction</b> risk, however the mechanisms responsible for this are not well understood.
+OPRM1	drug	opioid	31778689	To explore this, we examined <b>oxycodone</b> conditioned place preference (CPP) and self administration behavior (SA) in A112G mice, which possess a functionally analogous SNP in the mouse mu <b>opioid</b> receptor gene (<strong>Oprm1</strong>).
+OPRM1	addiction	reward	31778689	To explore this, we examined oxycodone conditioned place preference (<b>CPP</b>) and self administration behavior (SA) in A112G mice, which possess a functionally analogous SNP in the mouse mu opioid receptor gene (<strong>Oprm1</strong>).
+OPRM1	drug	opioid	31775878	The methylation of genes coding for the Toll like receptor 4 (TLR4) as a major mediator of glial contributions to persistent pain or for the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) was analyzed and its association with the pain phenotype was compared with that conferred by global genome wide DNA methylation assessed via quantification of the methylation in the retrotransposon LINE1.
+OPRM1	drug	opioid	31772303	Variation in the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) and experiences of felt security in response to a romantic partner's quarrelsome behavior.
+OPRM1	drug	opioid	31772303	Accordingly, a functional μ <b>opioid</b> receptor (<strong>OPRM1</strong>) polymorphism (C77G in primates, A118G in humans) affecting opioidergic signaling has been associated with separation distress and attachment behavior in nonhuman primates, and social pain sensitivity in humans.
+OPRM1	drug	opioid	31712748	The mu <b>opioid</b> receptors (MOR, <strong>OPRM1</strong>) mediate the effects of beta endorphin and modulate many biological functions including reward processing and addiction.
+OPRM1	addiction	addiction	31712748	The mu opioid receptors (MOR, <strong>OPRM1</strong>) mediate the effects of beta endorphin and modulate many biological functions including reward processing and <b>addiction</b>.
+OPRM1	addiction	reward	31712748	The mu opioid receptors (MOR, <strong>OPRM1</strong>) mediate the effects of beta endorphin and modulate many biological functions including <b>reward</b> processing and addiction.
+OPRM1	drug	opioid	31481756	The <strong>OPRM1</strong> A118G single nucleotide polymorphism (SNP rs1799971) gene variant encoding the N40D µ <b>opioid</b> receptor (MOR) has been associated with dependence on opiates and other drugs of abuse but its mechanism is unknown.
+OPRM1	addiction	dependence	31481756	The <strong>OPRM1</strong> A118G single nucleotide polymorphism (SNP rs1799971) gene variant encoding the N40D µ opioid receptor (MOR) has been associated with <b>dependence</b> on opiates and other drugs of abuse but its mechanism is unknown.
+OPRM1	drug	opioid	31463067	Synthesis and pharmacological characterization of ethylenediamine synthetic <b>opioids</b> in human μ opiate receptor 1 (<strong>OPRM1</strong>) expressing cells.
+OPRM1	drug	alcohol	31370987	Medication enhanced behavior therapy for <b>alcohol</b> use disorder: <b>Naltrexone</b>, <b>Alcoholics</b> Anonymous Facilitation, and <strong>OPRM1</strong> genetic variation.
+OPRM1	drug	alcohol	31370987	The present study examines the treatment benefit of combined outpatient <b>naltrexone</b> (NTX) treatment with <b>Alcoholics</b> Anonymous Facilitation (AAF) behavior therapy, in the context of <strong>OPRM1</strong> genotype.
+OPRM1	drug	alcohol	31370987	The minor <strong>OPRM1</strong> Asp40 G allele has been associated with greater positive reinforcing effects of <b>alcohol</b> consumption and greater <b>alcohol</b> craving, suggesting that individuals carrying the <strong>OPRM1</strong> G allele may have an improved <b>naltrexone</b> response.
+OPRM1	addiction	relapse	31370987	The minor <strong>OPRM1</strong> Asp40 G allele has been associated with greater positive reinforcing effects of alcohol consumption and greater alcohol <b>craving</b>, suggesting that individuals carrying the <strong>OPRM1</strong> G allele may have an improved naltrexone response.
+OPRM1	addiction	reward	31370987	The minor <strong>OPRM1</strong> Asp40 G allele has been associated with greater positive <b>reinforcing</b> effects of alcohol consumption and greater alcohol craving, suggesting that individuals carrying the <strong>OPRM1</strong> G allele may have an improved naltrexone response.
+OPRM1	drug	alcohol	31339663	Persistent alterations of proopiomelanocortin (Pomc) and mu opioid receptor (<strong>Oprm1</strong>) activity and stress responses after <b>alcohol</b> are critically involved in vulnerability to <b>alcohol</b> dependency.
+OPRM1	drug	opioid	31339663	Persistent alterations of proopiomelanocortin (Pomc) and mu <b>opioid</b> receptor (<strong>Oprm1</strong>) activity and stress responses after alcohol are critically involved in vulnerability to alcohol dependency.
+OPRM1	drug	alcohol	31339663	nPE1 /  had lower basal Pomc and Pdyn (prodynorphin) levels compared to nPE1+/+ , coupled with increased basal <strong>Oprm1</strong> and Oprk1 (kappa opioid receptor) levels, and low <b>alcohol</b> drinking increased Pomc and Pdyn to the basal levels of nPE1+/+ in the water group, without significant effects on <strong>Oprm1</strong> and Oprk1.
+OPRM1	drug	opioid	31339663	nPE1 /  had lower basal Pomc and Pdyn (prodynorphin) levels compared to nPE1+/+ , coupled with increased basal <strong>Oprm1</strong> and Oprk1 (kappa <b>opioid</b> receptor) levels, and low alcohol drinking increased Pomc and Pdyn to the basal levels of nPE1+/+ in the water group, without significant effects on <strong>Oprm1</strong> and Oprk1.
+OPRM1	drug	alcohol	31339663	In nPE1+/+ , excessive <b>alcohol</b> intake increased Pomc and <strong>Oprm1</strong>, with no effect on Pdyn or Oprk1.
+OPRM1	drug	opioid	31309790	To study association of µ <b>Opioid</b> Receptor polymorphism in patients of rheumatoid arthritis and its correlation with severity of disease and prevalent alleles of the <strong>OPRM1</strong> genes.
+OPRM1	drug	amphetamine	31274109	Taar1 gene variants have a causal role in <b>methamphetamine</b> intake and response and interact with <strong>Oprm1</strong>.
+OPRM1	drug	opioid	31274109	We nominated the trace amine associated receptor 1 gene, Taar1, as the strongest candidate and identified regulation of the mu <b>opioid</b> receptor 1 gene, <strong>Oprm1</strong>, as another contributor.
+OPRM1	drug	amphetamine	31274109	Both <b>methamphetamine</b> intake and the thermal response mapped to Taar1 and the independent effect of Taar1 was dependent on genotype at <strong>Oprm1</strong>.
+OPRM1	drug	amphetamine	31274109	Our findings encourage investigation of the contribution of Taar1 and <strong>Oprm1</strong> variants to human <b>methamphetamine</b> addiction.
+OPRM1	addiction	addiction	31274109	Our findings encourage investigation of the contribution of Taar1 and <strong>Oprm1</strong> variants to human methamphetamine <b>addiction</b>.
+OPRM1	drug	opioid	31267641	Neurobehavioral effects of neonatal <b>opioid</b> exposure in mice: Influence of the <strong>OPRM1</strong> SNP.
+OPRM1	drug	opioid	31267641	A potential genetic factor is a single nucleotide polymorphism (SNP) in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong> A118G).
+OPRM1	drug	opioid	31267641	To determine whether this SNP modulates the neurobehavioral effects of neonatal <b>opioid</b> exposure and withdrawal, we used mice possessing the equivalent <strong>Oprm1</strong> SNP (A112G).
+OPRM1	addiction	withdrawal	31267641	To determine whether this SNP modulates the neurobehavioral effects of neonatal opioid exposure and <b>withdrawal</b>, we used mice possessing the equivalent <strong>Oprm1</strong> SNP (A112G).
+OPRM1	drug	opioid	31267641	These data suggest the involvement of the <strong>Oprm1</strong> SNP for certain outcomes of neonatal <b>opioid</b> exposure and highlight the importance of considering sex and genetic variability for the prognosis of NOWS.
+OPRM1	addiction	addiction	31246565	The association between the <strong>OPRM1</strong> A118G polymorphism and <b>addiction</b> in a Turkish population.
+OPRM1	drug	opioid	31246565	One important gene in that respect is <strong>OPRM1</strong>, which codes for the μ <b>opioid</b> receptor and has an important role in mediating the rewarding effects of addiction substances.
+OPRM1	addiction	addiction	31246565	One important gene in that respect is <strong>OPRM1</strong>, which codes for the μ opioid receptor and has an important role in mediating the rewarding effects of <b>addiction</b> substances.
+OPRM1	drug	opioid	31246565	The aim of our study was to assess the prevalence of the <strong>OPRM1</strong> A118G polymorphism (rs1799971) in Turkish population and to investigate its association with <b>opioid</b> and other substance addiction.
+OPRM1	addiction	addiction	31246565	The aim of our study was to assess the prevalence of the <strong>OPRM1</strong> A118G polymorphism (rs1799971) in Turkish population and to investigate its association with opioid and other substance <b>addiction</b>.
+OPRM1	drug	alcohol	31160146	Despite known genetic variation across races, studies examining pharmacogenetics of a single nucleotide polymorphism (SNP) of the mu opioid receptor gene (<strong>OPRM1</strong>) on clinical response to <b>naltrexone</b> have been conducted in predominantly Caucasian samples.
+OPRM1	drug	opioid	31160146	Despite known genetic variation across races, studies examining pharmacogenetics of a single nucleotide polymorphism (SNP) of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) on clinical response to naltrexone have been conducted in predominantly Caucasian samples.
+OPRM1	drug	alcohol	31160146	Evidence is mixed for pharmacogenetic <strong>OPRM1</strong> and <b>naltrexone</b> effects on neural responses to <b>alcohol</b> cues.
+OPRM1	drug	alcohol	31160146	The current study tests the pharmacogenetic effects of <b>naltrexone</b> and <strong>OPRM1</strong> on neural responses to <b>alcohol</b> taste cues in heavy drinkers of East Asian descent.
+OPRM1	drug	alcohol	31160146	Analyses tested effects of <b>naltrexone</b>, <strong>OPRM1</strong>, and their interaction in whole brain and region of interest (ROI) analyses of functional activation and functional connectivity in response to <b>alcohol</b> versus water taste cues.
+OPRM1	addiction	reward	31109961	Synaptic Regulation by <strong>OPRM1</strong> Variants in <b>Reward</b> Neurocircuitry.
+OPRM1	drug	opioid	31109961	Susceptibility to <b>opioid</b> addiction is associated with variants in the gene encoding the MOR, <strong>OPRM1</strong> Varying with ethnicity, ∼25% of humans carry a single nucleotide polymorphism (SNP) in <strong>OPRM1</strong> (A118G).
+OPRM1	addiction	addiction	31109961	Susceptibility to opioid <b>addiction</b> is associated with variants in the gene encoding the MOR, <strong>OPRM1</strong> Varying with ethnicity, ∼25% of humans carry a single nucleotide polymorphism (SNP) in <strong>OPRM1</strong> (A118G).
+OPRM1	drug	opioid	31109961	This study provides a better understanding on the neurobiological mechanisms that may underlie risk of addiction development in carriers of the A118G SNP in <strong>OPRM1</strong> SIGNIFICANCE STATEMENT The pandemic of <b>opioid</b> drug abuse is associated with many socioeconomic burdens.
+OPRM1	addiction	addiction	31109961	This study provides a better understanding on the neurobiological mechanisms that may underlie risk of <b>addiction</b> development in carriers of the A118G SNP in <strong>OPRM1</strong> SIGNIFICANCE STATEMENT The pandemic of opioid drug abuse is associated with many socioeconomic burdens.
+OPRM1	drug	opioid	31109961	The primary brain target of <b>opioid</b> drugs is the μ <b>opioid</b> receptor (MOR), encoded by the <strong>OPRM1</strong> gene, which is highly polymorphic in humans.
+OPRM1	drug	cannabinoid	31074060	Finally, we analyzed the relative gene expression of tyrosine hydroxylase (TH) and μ opioid receptor (<strong>OPRM1</strong>) and <b>cannabinoid</b> CB1 receptor (CB1 r) in the ventral tegmental area (VTA) and in the nucleus accumbens (NAc), respectively, by real time quantitative PCR.
+OPRM1	drug	opioid	31074060	Finally, we analyzed the relative gene expression of tyrosine hydroxylase (TH) and μ <b>opioid</b> receptor (<strong>OPRM1</strong>) and cannabinoid CB1 receptor (CB1 r) in the ventral tegmental area (VTA) and in the nucleus accumbens (NAc), respectively, by real time quantitative PCR.
+OPRM1	drug	alcohol	31074060	Interestingly, females also showed higher expression of TH and <strong>OPRM1</strong>, without any difference in CB1 r. Only the acute administration of CBD at the highest dose (90 mg/kg) reduced significantly <b>ethanol</b> consumption in both sexes.
+OPRM1	drug	alcohol	31011876	The prevalence of ADH1B and <strong>OPRM1</strong> alleles predisposing for <b>alcohol</b> consumption are increased in the Hungarian psoriasis population.
+OPRM1	drug	opioid	31004399	Three μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) variants and two κ <b>opioid</b> receptor gene (OPRK1) variants were examined in 314 male patients with AUD and 324 male controls.
+OPRM1	drug	nicotine	30973902	The opioid system is involved in the mesolimbic reward system, which is of great importance in addictive behaviors, such as <b>smoking</b> and is influenced by genes such as the <strong>OPRM1</strong>.
+OPRM1	drug	opioid	30973902	The <b>opioid</b> system is involved in the mesolimbic reward system, which is of great importance in addictive behaviors, such as smoking and is influenced by genes such as the <strong>OPRM1</strong>.
+OPRM1	addiction	addiction	30973902	The opioid system is involved in the mesolimbic reward system, which is of great importance in <b>addictive</b> behaviors, such as smoking and is influenced by genes such as the <strong>OPRM1</strong>.
+OPRM1	addiction	reward	30973902	The opioid system is involved in the mesolimbic <b>reward</b> system, which is of great importance in addictive behaviors, such as smoking and is influenced by genes such as the <strong>OPRM1</strong>.
+OPRM1	drug	nicotine	30973902	There was no significant association between the two markers in <strong>OPRM1</strong> and <b>smoking</b>.
+OPRM1	drug	nicotine	30973902	When mental illness and dental clinical data (tooth loss, dental caries, and periodontitis) were used as covariates, there were associations between heavy <b>smoking</b> and <strong>OPRM1</strong>, when non <b>smokers</b> were used as comparison.
+OPRM1	drug	opioid	30844877	We have previously shown associations between 4 genetic variants in <b>opioid</b> and stress related genes (<strong>OPRM1</strong>, NPYR1/NPYR5, NR3C1, and CRHBP) and prolonged abstinence from <b>heroin</b> without <b>methadone</b> maintenance treatment (MMT).
+OPRM1	addiction	intoxication	30804861	<b>Binge</b> Like Eating Is Not Influenced by the Murine Model of <strong>OPRM1</strong> A118G Polymorphism.
+OPRM1	drug	opioid	30709700	In addition, epigenetic variation in the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene has been associated with differences in NAS hospitalization outcomes.
+OPRM1	drug	opioid	30599218	Interestingly, <b>naloxone</b>, β funaltrexamine, naloxonazine, and naltrindole, but not nor binaltorphimine, could also antagonize the antinociceptive effect markedly, suggesting that <strong>OPRM</strong> (primary μ1 subtype) and OPRD were involved in the antinociceptive response induced by ghrelin(1 7) NH2.
+OPRM1	drug	opioid	30552906	In a functional imaging study, we investigated the influence of the single nucleotide polymorphism of the mu 1 subtype <b>opioid</b> receptor gene (<strong>OPRM1</strong>), implicated in sociability, on correlates of trait and state aggression to delineate the function of these influences in aggression.
+OPRM1	drug	opioid	30508992	Fundamental Considerations for Genetically Guided Pain Management with <b>Opioids</b> Based on CYP2D6 and <strong>OPRM1</strong> Polymorphisms.
+OPRM1	drug	opioid	30508992	Clinically actionable polymorphisms in CYP2D6 (cytochrome p450 2D6) and <strong>OPRM1</strong> (mu 1 <b>opioid</b> receptor), the most important gene coding, respectively, for a metabolizing enzyme and receptor for <b>opioids</b> are reviewed, and functional effects described.
+OPRM1	drug	opioid	30508992	Patients at high risk with dysfunctional CYP2D6 or <strong>OPRM1</strong> account for ~14% of the population and are best managed with non <b>opioids</b>.
+OPRM1	drug	opioid	30508992	Patients at low risk with functional CYP2D6 and <strong>OPRM1</strong> account for ~38% of the population and should be availed to <b>opioid</b> therapy.
+OPRM1	drug	opioid	30508992	Pain management, <b>opioids</b>, CYP2D6, <strong>OPRM1</strong>, clinical decision support, pharmacokinetics, pharmacodynamics, pharmacogenetics, combinatorial genotypes.
+OPRM1	drug	opioid	30420869	<b>Methadone</b> Dosage and Plasma Levels, SNPs of <strong>OPRM1</strong> Gene and Age of First Drug Use Were Associated With Outcomes of <b>Methadone</b> Maintenance Treatment.
+OPRM1	drug	opioid	30420869	Objective: To explore the association between <b>methadone</b> dosage, plasma drug concentration, SNPs of μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>), ATP binding cassette subfamily B member 1 gene (ABCB1), and <b>methadone</b> maintenance treatment (MMT) response.
+OPRM1	drug	opioid	30420869	Nine single nucleotide polymorphisms (SNPs) of the <strong>OPRM1</strong> gene and three SNPs of the ABCB1 gene were genotyped, plasma <b>methadone</b> concentration was detected, and a <b>morphine</b> urine test was taken from all subjects.
+OPRM1	drug	opioid	30420869	A allele and AA genotype carriers of rs562859 (<strong>OPRM1</strong> gene) had better compliance of MMT, and AA genotype carriers had a higher negative rate of <b>morphine</b> urine test.
+OPRM1	drug	opioid	30420869	GG genotype carriers of rs3192723 (<strong>OPRM1</strong> gene) had a significantly lower negative rate of <b>morphine</b> urine test, and the difference was still significant after adjusting influence factors.
+OPRM1	drug	opioid	30420869	The SNPs rs6912029 (OR = 0.021, p = 0.066) and rs6902403 (OR = 0.910, p = 0.007) of the <strong>OPRM1</strong> gene, age at first use (OR = 1.118, p = 0.005), and average <b>methadone</b> dosage (OR = 1.033, p = 0.045) were associated with MMT effect.
+OPRM1	drug	opioid	30420869	Conclusion: Dosage of <b>methadone</b>, plasma <b>methadone</b> concentration, several SNPs (rs3192723, rs6912029, rs6902403) of the <strong>OPRM1</strong> gene, and age of first drug use were associated with better MMT outcomes.
+OPRM1	drug	alcohol	30384381	Some studies show that AUD patients carrying the G allele of the <strong>OPRM1</strong> variant c.118A>G respond better to <b>naltrexone</b>, resulting in reduced relapse rates compared to carriers of the AA genotype.
+OPRM1	addiction	relapse	30384381	Some studies show that AUD patients carrying the G allele of the <strong>OPRM1</strong> variant c.118A>G respond better to naltrexone, resulting in reduced <b>relapse</b> rates compared to carriers of the AA genotype.
+OPRM1	drug	alcohol	30384381	In conclusion, pharmacogenetic treatment allocation of AUD patients to <b>naltrexone</b>, based on <strong>OPRM1</strong> genotype, can be a cost effective strategy, and could have potential individual and societal benefits.
+OPRM1	addiction	relapse	30384381	However, more evidence on the impact of genotype guided treatment allocation on <b>relapse</b> is needed to substantiate these conclusions, as there is contradictory evidence about the effectiveness of <strong>OPRM1</strong> genotyping.
+OPRM1	drug	opioid	30359988	<strong>OPRM1</strong>, as the main receptor of <b>opioids</b>, plays an important role in the pharmacological process of <b>opioids</b> in rodents and human.
+OPRM1	drug	opioid	30359988	We have previously investigated <strong>OPRM1</strong>, the μ <b>opioid</b> receptor gene, which have dozens of alternatively spliced variants probably correlating with <b>opioid</b> induced effects in brain regions of four inbred mouse strains and demonstrated the strain specific expressions of these splice variants.
+OPRM1	drug	opioid	30359988	The mRNA levels of <b>opioid</b> receptor gene splice variants in male and female mice showed significant differences among the brain regions, implying region specific alternative splicing of the <strong>OPRM1</strong> gene, which was consistent with our previous study.
+OPRM1	drug	opioid	30359988	In brief, we put forward that the distinctions among baseline latency, <b>opioid</b> induced tolerance, analgesia and physical dependence in male and female mice might correlate with sex associated differential expressions of <strong>OPRM1</strong> gene.
+OPRM1	addiction	dependence	30359988	In brief, we put forward that the distinctions among baseline latency, opioid induced tolerance, analgesia and physical <b>dependence</b> in male and female mice might correlate with sex associated differential expressions of <strong>OPRM1</strong> gene.
+OPRM1	drug	alcohol	30322771	<strong>OPRM1</strong> A118G and serum β endorphin interact with sex and digit ratio (2D:4D) to influence risk and course of <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	30322771	<strong>OPRM1</strong> A118G and serum β endorphin interact with sex and digit ratio (2D:4D) to influence risk and course of alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	30322771	However, there is conflicting evidence on the relationship between the mu opioid receptor (<strong>OPRM1</strong>) A118G single nucleotide polymorphism (SNP) and <b>alcohol</b> dependence risk.
+OPRM1	drug	opioid	30322771	However, there is conflicting evidence on the relationship between the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) A118G single nucleotide polymorphism (SNP) and alcohol dependence risk.
+OPRM1	addiction	dependence	30322771	However, there is conflicting evidence on the relationship between the mu opioid receptor (<strong>OPRM1</strong>) A118G single nucleotide polymorphism (SNP) and alcohol <b>dependence</b> risk.
+OPRM1	drug	alcohol	30322771	We genotyped 200 <b>alcohol</b> dependent patients and 240 healthy individuals for the <strong>OPRM1</strong> A118G SNP and measured serum β endorphin level at recruitment and after acute withdrawal.
+OPRM1	addiction	withdrawal	30322771	We genotyped 200 alcohol dependent patients and 240 healthy individuals for the <strong>OPRM1</strong> A118G SNP and measured serum β endorphin level at recruitment and after acute <b>withdrawal</b>.
+OPRM1	drug	alcohol	30322771	The <strong>OPRM1</strong> A118G AA genotype associated with elevated risk of <b>alcohol</b> related hospital readmission, more readmissions, and fewer days until first readmission in male patients only.
+OPRM1	drug	alcohol	30322771	After normalizing patient 2D:4D against control 2D:4D, we found that normalized 2D:4D ratios were lower in male 118G patients than male AA patients, suggesting prenatal androgens interact with <strong>OPRM1</strong> to influence <b>alcohol</b> dependence risk.
+OPRM1	addiction	dependence	30322771	After normalizing patient 2D:4D against control 2D:4D, we found that normalized 2D:4D ratios were lower in male 118G patients than male AA patients, suggesting prenatal androgens interact with <strong>OPRM1</strong> to influence alcohol <b>dependence</b> risk.
+OPRM1	drug	opioid	30268817	Quantitative real time polymerase chain reaction (qPCR) studies were carried out to evaluate alterations in targets closely related to DA neurotransmission in the reward system, tyrosine hydroxylase (Th) in the ventral tegmental area (VTA), and μ <b>opioid</b> receptor (<strong>Oprm1</strong>) in the nucleus accumbens (NAc).
+OPRM1	addiction	reward	30268817	Quantitative real time polymerase chain reaction (qPCR) studies were carried out to evaluate alterations in targets closely related to DA neurotransmission in the <b>reward</b> system, tyrosine hydroxylase (Th) in the ventral tegmental area (VTA), and μ opioid receptor (<strong>Oprm1</strong>) in the nucleus accumbens (NAc).
+OPRM1	addiction	reward	30242222	Here we back translated applied behavior analysis (ABA) based behavioral interventions to mice lacking the MOR (<strong>Oprm1</strong> / ), as a model of autism with blunted <b>reward</b> processing.
+OPRM1	addiction	reward	30242222	By associating a positive <b>reinforcement</b>, palatable food <b>reward</b>, to daily encounter with a wild type congener, we were able to rescue durably social interaction and preference in <strong>Oprm1</strong> /  mice.
+OPRM1	drug	opioid	30171993	<b>Opioid</b> related genes, including <strong>OPRM1</strong>, OPRD1, OPRK1, and POMC, are obvious candidates for HD.
+OPRM1	drug	opioid	30118972	The most studied candidate genes have included the mu <b>opioid</b> receptor (<strong>OPRM1</strong>), the delta <b>opioid</b> receptor (OPRD1), the dopamine D2 receptor (DRD2), and brain derived neurotrophic factor (BDNF).
+OPRM1	drug	alcohol	30115121	An exploratory aim is to examine the moderating effects of rs1799971, a polymorphism in <strong>OPRM1</strong>, on the response to <b>naltrexone</b> by comparing Asn40 homozygotes with Asp40 carriers.
+OPRM1	drug	alcohol	30085428	The role of <strong>OPRM1</strong> polymorphism in the etiology of <b>alcoholism</b>.
+OPRM1	drug	alcohol	30085428	Numerous studies have investigated the association between the <strong>OPRM1</strong> A118G polymorphism (rs1799971) and <b>alcohol</b> dependence, but the results have been inconsistent.
+OPRM1	addiction	dependence	30085428	Numerous studies have investigated the association between the <strong>OPRM1</strong> A118G polymorphism (rs1799971) and alcohol <b>dependence</b>, but the results have been inconsistent.
+OPRM1	drug	alcohol	30085428	The aim of this study was to evaluate the role of the A118G polymorphism of the <strong>OPRM1</strong> gene in the pathogenesis of <b>alcohol</b> dependence syndrome (ADS).
+OPRM1	addiction	dependence	30085428	The aim of this study was to evaluate the role of the A118G polymorphism of the <strong>OPRM1</strong> gene in the pathogenesis of alcohol <b>dependence</b> syndrome (ADS).
+OPRM1	drug	alcohol	30085428	The <strong>OPRM1</strong> (rs1799971) polymorphism was investigated in an association study of a group of ADS patients (n = 177) and in subgroups (delirium tremens and/or seizures, age at onset <26 years, dissocial <b>alcoholics</b>, positive familial history of <b>alcoholism</b>, delirium tremens, and seizures).
+OPRM1	drug	opioid	30063884	By means of real time polymerase chain reaction (PCR), we also analysed relative gene expression of tyrosine hydroxylase (TH) in the ventral tegmental area (VTA), and of mu <b>opioid</b> receptor (<strong>OPRM1</strong>), CNR1 and CNR2 in the nucleus accumbens (NAcc).
+OPRM1	drug	opioid	30055180	<b>Oxycodone</b> self administration during pregnancy disrupts the maternal infant dyad and decreases midbrain <strong>OPRM1</strong> expression during early postnatal development in rats.
+OPRM1	drug	opioid	30055180	Neural expression of the mu <b>opioid</b> receptor gene <strong>OPRM1</strong> was examined in offspring on postnatal day 1 (PND1).
+OPRM1	drug	opioid	30055180	In addition, offspring demonstrated region specific effects of <b>oxycodone</b> exposure on <strong>OPRM1</strong> on PND1.
+OPRM1	drug	opioid	30055180	Further, maternal <b>oxycodone</b> self administration alters the maternal offspring dyad in a manner that is dose dependent and results in sex  and region specific effects on <strong>OPRM1</strong> expression.
+OPRM1	drug	opioid	30033503	Implication of <strong>OPRM1</strong> A118G Polymorphism in <b>Opioids</b> Addicts in Pakistan: In vitro and In silico Analysis.
+OPRM1	drug	opioid	30033503	Single nucleotide polymorphism in <strong>OPRM1</strong> gene is associated with hedonic and reinforcing consequences of <b>opioids</b>.
+OPRM1	addiction	reward	30033503	Single nucleotide polymorphism in <strong>OPRM1</strong> gene is associated with <b>hedonic</b> and <b>reinforcing</b> consequences of opioids.
+OPRM1	drug	opioid	30033503	One hundred healthy controls and 100 <b>opioids</b> (predominantly <b>heroin</b>) addicts from Pakistani origin were genotyped for A118G (N40D) polymorphism in <strong>OPRM1</strong>.
+OPRM1	drug	opioid	30033503	However, Haploreg and RegulomeDB predicted <strong>OPRM1</strong> gene repression by chromatin condensation and increased binding affinity of RXRA transcription factor that may reduce protein translation and hence the number of available receptors to bind with drugs, which may trigger underlying mechanisms for <b>opioids</b> addiction.
+OPRM1	addiction	addiction	30033503	However, Haploreg and RegulomeDB predicted <strong>OPRM1</strong> gene repression by chromatin condensation and increased binding affinity of RXRA transcription factor that may reduce protein translation and hence the number of available receptors to bind with drugs, which may trigger underlying mechanisms for opioids <b>addiction</b>.
+OPRM1	drug	opioid	30027498	<strong>OPRM1</strong> A118G, a functional human mu <b>opioid</b> receptor (MOR) polymorphism, is associated with drug dependence and altered stress responsivity in humans as well as altered MOR signaling.
+OPRM1	addiction	dependence	30027498	<strong>OPRM1</strong> A118G, a functional human mu opioid receptor (MOR) polymorphism, is associated with drug <b>dependence</b> and altered stress responsivity in humans as well as altered MOR signaling.
+OPRM1	addiction	reward	29899398	We examined whether touch serves as an unconditioned <b>reward</b> in affective conditioning of human faces, a basic process in social bonding, and whether this process is mediated by variation in mu OP (<strong>OPRM1</strong>) and OXT (rs53576) receptor genes.
+OPRM1	drug	opioid	29859012	Gene expression analyses of the <b>opioid</b> μ receptor (<strong>Oprm1</strong>) in the nucleus accumbens (NAc), tyrosine hydroxylase (TH) in the ventral tegmental area (VTA) and the 5 HT1A receptor in the dorsal raphe nucleus (DR) were carried out by real time PCR.
+OPRM1	drug	opioid	29852138	Prodynorphin (Pdyn) expression was upregulated in the ipsilateral dorsal domains by each the left and right side SNL, while changes in expression of μ <b>opioid</b> receptor (<strong>Oprm1</strong>) and proenkephalin (Penk) genes were dependent on the SNL side.
+OPRM1	addiction	intoxication	29797127	Polymorphism of <strong>Oprm1</strong> Gene and Its Association with Manifestations of N (1 Phenethyl 4 Piperidyl)Propionanilide <b>Intoxication</b> in Rats.
+OPRM1	addiction	intoxication	29797127	We studied association of <strong>Oprm1</strong> gene polymorphisms with signs of N (1 phenethyl 4 piperidyl)propionanilide <b>intoxication</b> in rats.
+OPRM1	drug	opioid	29797127	A polymorphic variant rs105312806 of <strong>Oprm1</strong> gene can be a possible marker of animal sensitivity to <b>opioid</b> receptor agonists.
+OPRM1	drug	opioid	29781244	<strong>OPRM1</strong> influence on and effectiveness of an individualized treatment plan for prescription <b>opioid</b> use disorder patients.
+OPRM1	drug	opioid	29781244	Our ITP showed effectiveness and security in reducing MEDD in <b>opioid</b> dependent patients, with good conversion to <b>buprenorphine</b> that was more pronounced in 118 AA <strong>OPRM1</strong> patients.
+OPRM1	drug	opioid	29649967	Among ALSPAC children, the rs29132 SNP in the Vesicle associated membrane protein associated protein A (VAPA) gene was associated with five sun exposure variables whilst the rs650662 SNP in the <b>Opioid</b> Receptor Mu 1 (<strong>OPRM1</strong>) gene was associated with three.
+OPRM1	drug	cannabinoid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the opioid μ receptor (<strong>Oprm1</strong>), <b>cannabinoid</b> CB1 receptor (Cnr1) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+OPRM1	drug	opioid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the <b>opioid</b> μ receptor (<strong>Oprm1</strong>), cannabinoid CB1 receptor (Cnr1) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+OPRM1	drug	opioid	29564682	<b>Opioid</b> Exposure is Associated with Aberrant DNA Methylation of <strong>OPRM1</strong> Promoter Region in a Chinese Han Population.
+OPRM1	drug	opioid	29564682	The μ <b>opioid</b> receptor (<strong>OPRM1</strong>) plays an important role in opiate addiction.
+OPRM1	addiction	addiction	29564682	The μ opioid receptor (<strong>OPRM1</strong>) plays an important role in opiate <b>addiction</b>.
+OPRM1	drug	opioid	29564682	The <strong>OPRM1</strong> gene promoter showed hypermethylation in lymphocytes of opiate addicts as well as <b>opioid</b> medications users, while the methylation status displayed ethnic diversity.
+OPRM1	drug	opioid	29564682	Our results supported that <b>opioid</b> exposure was associated with methylation status of <strong>OPRM1</strong> promoter and showed ethnic dependence.
+OPRM1	addiction	dependence	29564682	Our results supported that opioid exposure was associated with methylation status of <strong>OPRM1</strong> promoter and showed ethnic <b>dependence</b>.
+OPRM1	drug	alcohol	29497164	The <strong>OPRM1</strong> A118G polymorphism: converging evidence against associations with <b>alcohol</b> sensitivity and consumption.
+OPRM1	drug	opioid	29497164	A functional polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong> A118G, rs1799971) may alter the risk of developing AUD.
+OPRM1	drug	alcohol	29497164	Given this discrepancy, the present study sought to verify whether <strong>OPRM1</strong> A118G was associated with <b>alcohol</b> self administration, subjective response to <b>alcohol</b>, and craving in a sample of 106 social drinkers of European ancestry who completed an intravenous <b>alcohol</b> self administration session.
+OPRM1	addiction	relapse	29497164	Given this discrepancy, the present study sought to verify whether <strong>OPRM1</strong> A118G was associated with alcohol self administration, subjective response to alcohol, and <b>craving</b> in a sample of 106 social drinkers of European ancestry who completed an intravenous alcohol self administration session.
+OPRM1	drug	alcohol	29497164	We found no relationship between <strong>OPRM1</strong> rs1799971 genotype and subjective response to <b>alcohol</b> or craving.
+OPRM1	addiction	relapse	29497164	We found no relationship between <strong>OPRM1</strong> rs1799971 genotype and subjective response to alcohol or <b>craving</b>.
+OPRM1	drug	alcohol	29497164	<strong>OPRM1</strong> genotype was not associated with total <b>alcohol</b> exposure or likelihood of attaining a binge level exposure (80 mg%) during the intravenous <b>alcohol</b> self administration session.
+OPRM1	addiction	intoxication	29497164	<strong>OPRM1</strong> genotype was not associated with total alcohol exposure or likelihood of attaining a <b>binge</b> level exposure (80 mg%) during the intravenous alcohol self administration session.
+OPRM1	drug	alcohol	29497164	Analysis of 90 day Timeline Followback interview data in a larger sample of 965 participants of European ancestry found no relationship between <strong>OPRM1</strong> genotype and <b>alcohol</b> consumption in either <b>alcohol</b> dependent or non dependent participants.
+OPRM1	drug	alcohol	29497164	These findings suggest that there may not be an association between <strong>OPRM1</strong> rs1799971 genotype and <b>alcohol</b> consumption or sensitivity in individuals of European ancestry.
+OPRM1	drug	alcohol	29431852	In a randomized clinical trial, we previously reported that nicotine use/smoking status might be a stronger predictor of <b>naltrexone</b> efficacy than <strong>OPRM1</strong> A118G single nucleotide polymorphism (SNP) genotype.
+OPRM1	drug	nicotine	29431852	In a randomized clinical trial, we previously reported that <b>nicotine</b> use/<b>smoking</b> status might be a stronger predictor of naltrexone efficacy than <strong>OPRM1</strong> A118G single nucleotide polymorphism (SNP) genotype.
+OPRM1	drug	alcohol	29431852	Individuals (n = 146) meeting DSM IV criteria for <b>alcohol</b> dependence who were genotyped for the <strong>OPRM1</strong> A118G SNP and who did, or did not, use nicotine/cigarettes were randomized, in a balanced fashion, to <b>naltrexone</b> (50 mg/d) or placebo and provided medical management (MM) over a 16 week clinical trial.
+OPRM1	drug	nicotine	29431852	Individuals (n = 146) meeting DSM IV criteria for alcohol dependence who were genotyped for the <strong>OPRM1</strong> A118G SNP and who did, or did not, use <b>nicotine</b>/cigarettes were randomized, in a balanced fashion, to naltrexone (50 mg/d) or placebo and provided medical management (MM) over a 16 week clinical trial.
+OPRM1	addiction	dependence	29431852	Individuals (n = 146) meeting DSM IV criteria for alcohol <b>dependence</b> who were genotyped for the <strong>OPRM1</strong> A118G SNP and who did, or did not, use nicotine/cigarettes were randomized, in a balanced fashion, to naltrexone (50 mg/d) or placebo and provided medical management (MM) over a 16 week clinical trial.
+OPRM1	drug	alcohol	29431852	Compared to previous work on the <strong>OPRM1</strong> A118G SNP, it appears that nicotine use might be a more salient predictor of <b>naltrexone</b> treatment response.
+OPRM1	drug	nicotine	29431852	Compared to previous work on the <strong>OPRM1</strong> A118G SNP, it appears that <b>nicotine</b> use might be a more salient predictor of naltrexone treatment response.
+OPRM1	drug	opioid	29413524	A major result of these studies was the discovery that the mu <b>opioid</b> receptor gene, <strong>Oprm1</strong>, undergoes extensive alternative splicing in mice, rats, and humans.
+OPRM1	drug	alcohol	29391279	Using quantitative real time polymerase chain reaction, we further confirmed that the expression of genes implicated in <b>alcohol</b> addiction, BDNF, CRHR1 and <strong>OPRM1</strong>, was also altered by transplantation of gut microbes from <b>alcohol</b> exposed donors.
+OPRM1	addiction	addiction	29391279	Using quantitative real time polymerase chain reaction, we further confirmed that the expression of genes implicated in alcohol <b>addiction</b>, BDNF, CRHR1 and <strong>OPRM1</strong>, was also altered by transplantation of gut microbes from alcohol exposed donors.
+OPRM1	drug	nicotine	29385578	Together with NRT patches, participants were prescribed doses of oral NRT based on either mu opioid receptor (<strong>OPRM1</strong>) genotype or <b>nicotine</b> dependence questionnaire score (phenotype).
+OPRM1	drug	opioid	29385578	Together with NRT patches, participants were prescribed doses of oral NRT based on either mu <b>opioid</b> receptor (<strong>OPRM1</strong>) genotype or nicotine dependence questionnaire score (phenotype).
+OPRM1	addiction	dependence	29385578	Together with NRT patches, participants were prescribed doses of oral NRT based on either mu opioid receptor (<strong>OPRM1</strong>) genotype or nicotine <b>dependence</b> questionnaire score (phenotype).
+OPRM1	drug	opioid	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, <strong>OPRM1</strong>, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+OPRM1	addiction	dependence	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, <strong>OPRM1</strong>, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+OPRM1	drug	opioid	29302220	Additionally, a variant at the µ <b>opioid</b> receptor gene (<strong>OPRM1</strong>), which regulates <strong>OPRM1</strong> expression appears promising.
+OPRM1	drug	opioid	29302220	In pharmacogenetics of <b>opioid</b> addictions, <b>methadone</b> dose may be regulated by variants in cytochrome P450 2B6 (CYP2B6), a <b>methadone</b> metabolizing enzyme, and by a locus 300 kb 5' to <strong>OPRM1</strong>.
+OPRM1	addiction	addiction	29302220	Dans la pharmacogénétique de l'<b>addiction</b> aux opioïdes, la dose de méthadone peut être régulée par des variants du cytochrome P450 2B6 (CYP2B6), une enzyme métabolisant la méthadone, et par le locus situé à 300 kb en en amont du gène <strong>OPRM1</strong>.
+OPRM1	drug	alcohol	29265379	The majority of <b>naltrexone</b> pharmacogenetic studies have focused on a particular single nucleotide polymorphism (SNP) of the mu opioid receptor gene (<strong>OPRM1</strong>; rs1799971; commonly known as the Asn40Asp SNP) in Caucasian samples with decidedly mixed results.
+OPRM1	drug	opioid	29265379	The majority of naltrexone pharmacogenetic studies have focused on a particular single nucleotide polymorphism (SNP) of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>; rs1799971; commonly known as the Asn40Asp SNP) in Caucasian samples with decidedly mixed results.
+OPRM1	drug	opioid	29259946	This prospective association study investigated seven variations in the <strong>OPRM1</strong>, OPRK1 and COMT gene, which encode Mu and KAPPA <b>opioid</b> receptors, and Catechol O methyltransferase enzyme respectively, in a cohort of 129 Tunisian cancer pain patients under oral <b>morphine</b> treatment.
+OPRM1	drug	alcohol	29209387	FPS scores differed significantly between <b>alcohol</b> dependent patients and normal control subjects who had the G allele in <strong>OPRM1</strong> A118G, but not between the two groups with the AA genotype.
+OPRM1	drug	alcohol	29209387	A strong preference for spicy food can be assumed to be a risk factor for <b>alcohol</b> dependence, particularly in those carrying the G allele in <strong>OPRM1</strong> A118G.
+OPRM1	addiction	dependence	29209387	A strong preference for spicy food can be assumed to be a risk factor for alcohol <b>dependence</b>, particularly in those carrying the G allele in <strong>OPRM1</strong> A118G.
+OPRM1	drug	opioid	29170626	This downregulation was required for SNL induced DRG Dnmt3a increase as rescuing miR 143 downregulation through microinjection of miR 143 mimics into injured DRG blocked the SNL induced increase in Dnmt3a and restored the SNL induced decreases in <strong>Oprm1</strong> mRNA and its encoding mu <b>opioid</b> receptor (MOR) in injured DRG, impaired spinal cord central sensitization and neuropathic pain, and improved <b>morphine</b> analgesic effects following SNL.
+OPRM1	addiction	sensitization	29170626	This downregulation was required for SNL induced DRG Dnmt3a increase as rescuing miR 143 downregulation through microinjection of miR 143 mimics into injured DRG blocked the SNL induced increase in Dnmt3a and restored the SNL induced decreases in <strong>Oprm1</strong> mRNA and its encoding mu opioid receptor (MOR) in injured DRG, impaired spinal cord central <b>sensitization</b> and neuropathic pain, and improved morphine analgesic effects following SNL.
+OPRM1	drug	nicotine	29137427	Association of opioid receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with <b>nicotine</b> dependence.
+OPRM1	drug	opioid	29137427	Association of <b>opioid</b> receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with nicotine dependence.
+OPRM1	addiction	dependence	29137427	Association of opioid receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with nicotine <b>dependence</b>.
+OPRM1	drug	nicotine	29137427	Association of <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with <b>nicotine</b> dependence.
+OPRM1	drug	opioid	29137427	Association of <strong><b>opioid</b> receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with nicotine dependence.
+OPRM1	addiction	dependence	29137427	Association of <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with nicotine <b>dependence</b>.
+OPRM1	drug	nicotine	29137427	Whether opioid receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) is associated with <b>nicotine</b> dependence is controversial.
+OPRM1	drug	opioid	29137427	Whether <b>opioid</b> receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) is associated with nicotine dependence is controversial.
+OPRM1	addiction	dependence	29137427	Whether opioid receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) is associated with nicotine <b>dependence</b> is controversial.
+OPRM1	drug	nicotine	29137427	Whether <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) is associated with <b>nicotine</b> dependence is controversial.
+OPRM1	drug	opioid	29137427	Whether <strong><b>opioid</b> receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) is associated with nicotine dependence is controversial.
+OPRM1	addiction	dependence	29137427	Whether <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) is associated with nicotine <b>dependence</b> is controversial.
+OPRM1	drug	nicotine	29137427	<strong>OPRM1</strong> A118G polymorphism (A>G) is not associated with <b>nicotine</b> dependence.
+OPRM1	addiction	dependence	29137427	<strong>OPRM1</strong> A118G polymorphism (A>G) is not associated with nicotine <b>dependence</b>.
+OPRM1	drug	opioid	29129606	In addition, expression of corticotropin releasing hormone (Crh) and mu <b>opioid</b> receptor (<strong>Oprm1</strong>) in the paraventricular nucleus (PVN) were measured using quantitative PCR.
+OPRM1	drug	alcohol	29123234	Predictors of <b>Naltrexone</b> Response in a Randomized Trial: Reward Related Brain Activation, <strong>OPRM1</strong> Genotype, and Smoking Status.
+OPRM1	drug	nicotine	29123234	Predictors of Naltrexone Response in a Randomized Trial: Reward Related Brain Activation, <strong>OPRM1</strong> Genotype, and <b>Smoking</b> Status.
+OPRM1	addiction	reward	29123234	Predictors of Naltrexone Response in a Randomized Trial: <b>Reward</b> Related Brain Activation, <strong>OPRM1</strong> Genotype, and Smoking Status.
+OPRM1	drug	alcohol	29070014	Lack of associations of the opioid receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with <b>alcohol</b> dependence: review and meta analysis of retrospective controlled studies.
+OPRM1	drug	opioid	29070014	Lack of associations of the <b>opioid</b> receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with alcohol dependence: review and meta analysis of retrospective controlled studies.
+OPRM1	addiction	dependence	29070014	Lack of associations of the opioid receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with alcohol <b>dependence</b>: review and meta analysis of retrospective controlled studies.
+OPRM1	drug	alcohol	29070014	Lack of associations of the <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with <b>alcohol</b> dependence: review and meta analysis of retrospective controlled studies.
+OPRM1	drug	opioid	29070014	Lack of associations of the <strong><b>opioid</b> receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with alcohol dependence: review and meta analysis of retrospective controlled studies.
+OPRM1	addiction	dependence	29070014	Lack of associations of the <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with alcohol <b>dependence</b>: review and meta analysis of retrospective controlled studies.
+OPRM1	drug	alcohol	29070014	Studies have sought associations of the opioid receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with <b>alcohol</b> dependence, but findings are inconsistent.
+OPRM1	drug	opioid	29070014	Studies have sought associations of the <b>opioid</b> receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with alcohol dependence, but findings are inconsistent.
+OPRM1	addiction	dependence	29070014	Studies have sought associations of the opioid receptor mu 1 (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with alcohol <b>dependence</b>, but findings are inconsistent.
+OPRM1	drug	alcohol	29070014	Studies have sought associations of the <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with <b>alcohol</b> dependence, but findings are inconsistent.
+OPRM1	drug	opioid	29070014	Studies have sought associations of the <strong><b>opioid</b> receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with alcohol dependence, but findings are inconsistent.
+OPRM1	addiction	dependence	29070014	Studies have sought associations of the <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) A118G polymorphism (rs1799971) with alcohol <b>dependence</b>, but findings are inconsistent.
+OPRM1	drug	opioid	29055075	The aim of this study was to investigate if genetic variants of mu, kappa, and delta <b>opioid</b> receptor genes (<strong>OPRM1</strong>, OPRK1, and OPRD1) and the catechol O methyltransferase gene (COMT) influenced the pain phenotype in patients with osteoarthritis.
+OPRM1	drug	alcohol	28992386	Limited correlational findings, albeit mixed as a function of age, suggest that carriers of a μ opioid receptor (<strong>OPRM1</strong>) G allele may be more vulnerable than noncarriers to <b>alcohol</b> promoting perceived peer environments.
+OPRM1	drug	opioid	28992386	Limited correlational findings, albeit mixed as a function of age, suggest that carriers of a μ <b>opioid</b> receptor (<strong>OPRM1</strong>) G allele may be more vulnerable than noncarriers to alcohol promoting perceived peer environments.
+OPRM1	drug	alcohol	28992386	This study examined whether <strong>OPRM1</strong> modulates the effects of heavy drinking group size on <b>alcohol</b> consumption and explored potential mediators of such <strong>OPRM1</strong> based differences.
+OPRM1	drug	alcohol	28992386	Results showed no significant moderating effects of <strong>OPRM1</strong> in the relationship between the number (or presence) of heavy drinking peers and voluntary <b>alcohol</b> consumption (partial η2 = 0.01).
+OPRM1	drug	alcohol	28992386	In addition, <strong>OPRM1</strong> did not moderate the peer influence on any proposed mediating variables, including craving for <b>alcohol</b> and subjective responses to <b>alcohol</b>.
+OPRM1	addiction	relapse	28992386	In addition, <strong>OPRM1</strong> did not moderate the peer influence on any proposed mediating variables, including <b>craving</b> for alcohol and subjective responses to alcohol.
+OPRM1	drug	alcohol	28992386	Future research on <strong>OPRM1</strong> related susceptibility to <b>alcohol</b> promoting peer environments through meta analytic synthesis and both experimental and prospective, multiwave designs is needed to resolve these mixed findings.
+OPRM1	drug	opioid	28991118	The μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene undergoes extensive alternative precursor messenger ribonucleic acid splicing, generating multiple splice variants that are conserved from rodents to humans.
+OPRM1	addiction	relapse	28976288	Since the stress axis is regulated in part by β endorphin, this functional <strong>OPRM1</strong> SNP may blunt the endogenous stress response and contribute to reduced vulnerability for <b>relapse</b>.
+OPRM1	drug	opioid	28939474	<b>Heroin</b> induced suppression of saccharin intake in <strong>OPRM1</strong> A118G mice.
+OPRM1	drug	alcohol	28939474	The single nucleotide polymorphism of the μ opioid receptor, <strong>OPRM1</strong> A118G, has been associated with greater drug and <b>alcohol</b> use, increased sensitivity to pain, and reduced sensitivity to the antinociceptive effects of opiates.
+OPRM1	drug	opioid	28939474	The single nucleotide polymorphism of the μ <b>opioid</b> receptor, <strong>OPRM1</strong> A118G, has been associated with greater drug and alcohol use, increased sensitivity to pain, and reduced sensitivity to the antinociceptive effects of opiates.
+OPRM1	drug	alcohol	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, ADH1C, <strong>OPRM1</strong>, DRD2, BDNF, and ALDH2 genes on <b>alcohol</b> dependence in a Caucasian population.
+OPRM1	addiction	dependence	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, ADH1C, <strong>OPRM1</strong>, DRD2, BDNF, and ALDH2 genes on alcohol <b>dependence</b> in a Caucasian population.
+OPRM1	drug	alcohol	28780411	The A118G single nucleotide polymorphism (SNP) of the mu opioid receptor gene (<strong>Oprm1</strong>) has been implicated in mediating the rewarding effects of <b>alcohol</b>.
+OPRM1	drug	opioid	28780411	The A118G single nucleotide polymorphism (SNP) of the mu <b>opioid</b> receptor gene (<strong>Oprm1</strong>) has been implicated in mediating the rewarding effects of alcohol.
+OPRM1	drug	opioid	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the <b>opioid</b> receptor genes (<strong>OPRM1</strong>, OPRD1, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to <b>heroin</b> dependence in populations worldwide.
+OPRM1	addiction	dependence	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the opioid receptor genes (<strong>OPRM1</strong>, OPRD1, and OPRK1), have been implicated in drug <b>dependence</b>, but relatively little is known on their contributions to heroin <b>dependence</b> in populations worldwide.
+OPRM1	addiction	reward	28692418	<b>Reward</b>  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the opioid receptor genes (<strong>OPRM1</strong>, OPRD1, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to heroin dependence in populations worldwide.
+OPRM1	drug	opioid	28650467	By unbiased genome wide RNAi screening, we found that among 10 resistant ALL clones, six hits were for <b>opioid</b> receptor mu 1 (<strong>oprm1</strong>), two hits were for carbonic anhydrase 1 (ca1) and another two hits were for ubiquitin conjugating enzyme E2C (ube2c).
+OPRM1	drug	opioid	28650467	<b>Methadone</b>, an agonist of <strong>OPRM1</strong>, enhances the sensitivity of parental leukemic cells, but not <strong>OPRM1</strong> depleted cells, to L asparaginase treatment, indicating that <strong>OPRM1</strong> is required for the synergistic action of L asparaginase and <b>methadone</b>, and that <strong>OPRM1</strong> loss promotes leukemic cell survival likely through downregulation of the <strong>OPRM1</strong> mediated apoptotic pathway.
+OPRM1	drug	nicotine	28548579	Genetic Variation of the Mu Opioid Receptor (<strong>OPRM1</strong>) and Dopamine D2 Receptor (DRD2) is Related to <b>Smoking</b> Differences in Patients with Schizophrenia but not Bipolar Disorder.
+OPRM1	drug	opioid	28548579	Genetic Variation of the Mu <b>Opioid</b> Receptor (<strong>OPRM1</strong>) and Dopamine D2 Receptor (DRD2) is Related to Smoking Differences in Patients with Schizophrenia but not Bipolar Disorder.
+OPRM1	drug	nicotine	28548579	Inasmuch as endogenous opioid and dopaminergic systems are involved in <b>smoking</b> reinforcement, it is important to study mu opioid receptor (<strong>OPRM1</strong>) A118G (rs1799971), dopamine D2 receptor (DRD2) Taq1A (rs1800497) genotypes, and sex differences among patients with schizophrenia or bipolar disorder.
+OPRM1	drug	opioid	28548579	Inasmuch as endogenous <b>opioid</b> and dopaminergic systems are involved in smoking reinforcement, it is important to study mu <b>opioid</b> receptor (<strong>OPRM1</strong>) A118G (rs1799971), dopamine D2 receptor (DRD2) Taq1A (rs1800497) genotypes, and sex differences among patients with schizophrenia or bipolar disorder.
+OPRM1	addiction	reward	28548579	Inasmuch as endogenous opioid and dopaminergic systems are involved in smoking <b>reinforcement</b>, it is important to study mu opioid receptor (<strong>OPRM1</strong>) A118G (rs1799971), dopamine D2 receptor (DRD2) Taq1A (rs1800497) genotypes, and sex differences among patients with schizophrenia or bipolar disorder.
+OPRM1	drug	nicotine	28548579	In bipolar patients, there were no <strong>OPRM1</strong> and DRD2 Taq1A genotype differences in <b>smoking</b> status.
+OPRM1	drug	opioid	28511993	Rats exposed to early life stress (MS360) had increased <b>opioid</b> receptor gene (<strong>Oprm1</strong>, Oprd1 and Oprk1) expression in the dorsal striatum.
+OPRM1	drug	alcohol	28409564	Predictors of <b>Naltrexone</b> Response in a Randomized Trial: Reward Related Brain Activation, <strong>OPRM1</strong> Genotype, and Smoking Status.
+OPRM1	drug	nicotine	28409564	Predictors of Naltrexone Response in a Randomized Trial: Reward Related Brain Activation, <strong>OPRM1</strong> Genotype, and <b>Smoking</b> Status.
+OPRM1	addiction	reward	28409564	Predictors of Naltrexone Response in a Randomized Trial: <b>Reward</b> Related Brain Activation, <strong>OPRM1</strong> Genotype, and Smoking Status.
+OPRM1	drug	alcohol	28409564	This randomized clinical trial tested the effects of <b>naltrexone</b> on drinking and <b>alcohol</b> cue elicited brain activation, evaluated whether <strong>OPRM1</strong> A118G genotype or smoking moderated these effects, and explored whether the effects of medication on cue elicited activation predicted subsequent drinking.
+OPRM1	drug	nicotine	28409564	This randomized clinical trial tested the effects of naltrexone on drinking and alcohol cue elicited brain activation, evaluated whether <strong>OPRM1</strong> A118G genotype or <b>smoking</b> moderated these effects, and explored whether the effects of medication on cue elicited activation predicted subsequent drinking.
+OPRM1	drug	alcohol	28409564	<strong>OPRM1</strong> genotype did not significantly moderate these effects, but G allele carriers who received <b>naltrexone</b> had an accelerated return to heavy drinking after medication was stopped.
+OPRM1	drug	opioid	28343361	<b>Morphine</b> is the prototypic mu <b>opioid</b>, producing its analgesic actions through traditional 7 transmembrane domain (7TM) G protein coupled receptors generated by the mu <b>opioid</b> receptor gene (<strong>Oprm1</strong>).
+OPRM1	addiction	reward	28343361	Groups of male and mixed gender wild type and exon 11 <strong>Oprm1</strong> knockout mice were examined in a series of behavioral assays measuring analgesia, hyperalgesia, respiration, and <b>reward</b> in conditioned place preference assays.
+OPRM1	drug	opioid	28319053	Extensive 3' alternative splicing of the mu <b>opioid</b> receptor gene <strong>OPRM1</strong> creates multiple C terminal splice variants.
+OPRM1	drug	alcohol	28273335	A cis eQTL in <strong>OPRM1</strong> is Associated with Subjective Response to <b>Alcohol</b> and <b>Alcohol</b> Use.
+OPRM1	drug	alcohol	28273335	A functional polymorphism within the μ opioid receptor (<strong>OPRM1</strong>) gene, rs1799971 (A118G), previously has been associated with measures of <b>alcohol</b> use and sensitivity to its effects, but findings have been inconclusive.
+OPRM1	drug	opioid	28273335	A functional polymorphism within the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene, rs1799971 (A118G), previously has been associated with measures of alcohol use and sensitivity to its effects, but findings have been inconclusive.
+OPRM1	drug	opioid	28273335	A recent study suggested that a second nearby variant within <strong>OPRM1</strong>, rs3778150, is robustly associated with <b>heroin</b> dependence and fully explained a smaller observed association with rs1799971.
+OPRM1	addiction	dependence	28273335	A recent study suggested that a second nearby variant within <strong>OPRM1</strong>, rs3778150, is robustly associated with heroin <b>dependence</b> and fully explained a smaller observed association with rs1799971.
+OPRM1	drug	alcohol	28273335	Given evidence that the rs3778150 C allele is associated with decreased <strong>OPRM1</strong> expression levels in the human brain, the current study sought to test the hypothesis that rs3778150 represents a causal variant within <strong>OPRM1</strong> that increases risk for a variety of <b>alcohol</b> use phenotypes.
+OPRM1	drug	alcohol	28273335	Future studies may investigate potential causal relations among genetic variants in <strong>OPRM1</strong>, subjective response to <b>alcohol</b>, and drinking phenotypes to further delineate the effects of rs3778150.
+OPRM1	drug	cannabinoid	28194850	Gene expression analyses of tyrosine hydroxylase in ventral tegmental area and μ opioid (<strong>Oprm1</strong>), <b>cannabinoid</b> (CB1 r and CB2 r) and GPR55 receptors in nucleus accumbens (NAcc) were carried out by real time polymerase chain reaction.
+OPRM1	drug	opioid	28194850	Gene expression analyses of tyrosine hydroxylase in ventral tegmental area and μ <b>opioid</b> (<strong>Oprm1</strong>), cannabinoid (CB1 r and CB2 r) and GPR55 receptors in nucleus accumbens (NAcc) were carried out by real time polymerase chain reaction.
+OPRM1	drug	opioid	28188737	Genetic variation in the behavioral effects of <b>buprenorphine</b> in female mice derived from a murine model of the <strong>OPRM1</strong> A118G polymorphism.
+OPRM1	drug	opioid	28188737	Pharmacogenetic studies have identified the non synonymous single nucleotide polymorphism (A118G) in the human mu <b>opioid</b> receptor (MOR) gene (<strong>OPRM1</strong>) as a critical genetic variant capable of altering the efficacy of <b>opioid</b> therapeutics.
+OPRM1	drug	opioid	28188737	To date few studies have explored the potential impact of the <strong>OPRM1</strong> A118G polymorphism on the pharmacological effects of <b>buprenorphine</b> (BPN), a potent MOR partial agonist and kappa <b>opioid</b> receptor antagonist, which is approved by the FDA for the treatment of <b>opioid</b> addiction and chronic pain.
+OPRM1	addiction	addiction	28188737	To date few studies have explored the potential impact of the <strong>OPRM1</strong> A118G polymorphism on the pharmacological effects of buprenorphine (BPN), a potent MOR partial agonist and kappa opioid receptor antagonist, which is approved by the FDA for the treatment of opioid <b>addiction</b> and chronic pain.
+OPRM1	drug	opioid	28121474	Elevated levels of DNA methylation at the <strong>OPRM1</strong> promoter region in men with <b>opioid</b> use disorder.
+OPRM1	drug	opioid	28121474	The mu <b>opioid</b> receptor, encoded by mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>), has an important role in the development of addiction to <b>opioids</b>.
+OPRM1	addiction	addiction	28121474	The mu opioid receptor, encoded by mu opioid receptor gene (<strong>OPRM1</strong>), has an important role in the development of <b>addiction</b> to opioids.
+OPRM1	drug	opioid	28115739	Genome wide association study of therapeutic <b>opioid</b> dosing identifies a novel locus upstream of <strong>OPRM1</strong>.
+OPRM1	drug	opioid	28115739	<b>Methadone</b> is used to treat <b>opioid</b> dependence (OD), acting as a selective agonist at the μ <b>opioid</b> receptor encoded by the gene <strong>OPRM1</strong>.
+OPRM1	addiction	dependence	28115739	Methadone is used to treat opioid <b>dependence</b> (OD), acting as a selective agonist at the μ opioid receptor encoded by the gene <strong>OPRM1</strong>.
+OPRM1	drug	opioid	28115739	In African American (AA) OD subjects (n=383), we identified a genome wide significant association between therapeutic <b>methadone</b> dose (mean=68.0 mg, s.d.=30.1 mg) and rs73568641 (P=2.8 × 10 8), the nearest gene (306 kilobases) being <strong>OPRM1</strong>.
+OPRM1	drug	opioid	27958381	A polymorphism in the <strong>OPRM1</strong> 3' untranslated region is associated with <b>methadone</b> efficacy in treating <b>opioid</b> dependence.
+OPRM1	addiction	dependence	27958381	A polymorphism in the <strong>OPRM1</strong> 3' untranslated region is associated with methadone efficacy in treating opioid <b>dependence</b>.
+OPRM1	drug	opioid	27725223	Next generation sequencing (NGS) workflow was based on a custom AmpliSeq™ panel and designed for sequencing of human genes related to the <b>opioid</b> receptor group (<strong>OPRM1</strong>, OPRD1, OPRK1, SIGMA1, OPRL1) on an Ion PGM™ Sequencer.
+OPRM1	drug	opioid	27725223	This identified approximately 100 chromosome loci where nucleotides deviated from the reference sequence GRCh37 hg19, including functional variants such as the <strong>OPRM1</strong> rs1799971 SNP (118 A>G) as the most scientifically regarded variant or rs563649 SNP coding for μ <b>opioid</b> receptor splice variants.
+OPRM1	drug	opioid	27671662	We tested whether the sole targeted deletion of the mu <b>opioid</b> receptor gene (<strong>Oprm1</strong>) alters the brain connectome in living mice.
+OPRM1	drug	alcohol	27594419	Neural response to <b>alcohol</b> taste cues in youth: effects of the <strong>OPRM1</strong> gene.
+OPRM1	drug	alcohol	27594419	Genetic variations in the mu opioid receptor (<strong>OPRM1</strong>) gene have been related to high sensitivity to rewarding effects of <b>alcohol</b>.
+OPRM1	drug	opioid	27594419	Genetic variations in the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene have been related to high sensitivity to rewarding effects of alcohol.
+OPRM1	drug	opioid	27515451	CYP2B6 and <strong>OPRM1</strong> Receptor Polymorphisms at <b>Methadone</b> Clinics And Novel <strong>OPRM1</strong> Haplotypes: A Cross Sectional Study.
+OPRM1	drug	opioid	27515451	<b>Methadone</b> responsiveness, however, is affected by a range of CYP450 enzymes and <strong>OPRM1</strong> polymorphisms.
+OPRM1	drug	opioid	27515451	This study sought to detect CYP2B6 and <strong>OPRM1</strong> variants and their genotypes, as major contributors to inter variability in <b>methadone</b> responsiveness and <b>methadone</b> dose requirements.
+OPRM1	drug	alcohol	27510425	Post mortem brain tissue of <b>alcohol</b> dependent subjects and controls (N=43/group) was quantitatively analyzed for MOR ([3H]DAMGO) binding sites and <strong>OPRM1</strong> mRNA in striatal regions.
+OPRM1	addiction	relapse	27510425	In the PET study, a significant interaction of <strong>OPRM1</strong> genotype, binding potential (BPND) for [11C]carfentanil in the ventral striatum, and <b>relapse</b> risk was found.
+OPRM1	drug	nicotine	27459726	It has been proposed that vulnerability to <b>nicotine</b> addiction is moderated by variation at the μ opioid receptor locus (<strong>OPRM1</strong>), but results from human studies vary and prospective studies based on genotype are lacking.
+OPRM1	drug	opioid	27459726	It has been proposed that vulnerability to nicotine addiction is moderated by variation at the μ <b>opioid</b> receptor locus (<strong>OPRM1</strong>), but results from human studies vary and prospective studies based on genotype are lacking.
+OPRM1	addiction	addiction	27459726	It has been proposed that vulnerability to nicotine <b>addiction</b> is moderated by variation at the μ opioid receptor locus (<strong>OPRM1</strong>), but results from human studies vary and prospective studies based on genotype are lacking.
+OPRM1	drug	nicotine	27459726	Here we use this model system together with a cohort of German youth to examine the role of the <strong>OPRM1</strong> A118G variation on <b>nicotine</b> reward.
+OPRM1	addiction	reward	27459726	Here we use this model system together with a cohort of German youth to examine the role of the <strong>OPRM1</strong> A118G variation on nicotine <b>reward</b>.
+OPRM1	drug	alcohol	27447243	Association study of DRD2 A2/A1, DRD3 Ser9Gly, DβH  1021C>T, <strong>OPRM1</strong> A118G and GRIK1 rs2832407C>A polymorphisms with <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	27447243	Association study of DRD2 A2/A1, DRD3 Ser9Gly, DβH  1021C>T, <strong>OPRM1</strong> A118G and GRIK1 rs2832407C>A polymorphisms with alcohol <b>dependence</b>.
+OPRM1	drug	opioid	27447243	Genes of dopaminergic (DRD2, DRD3 and DβH), <b>opioid</b> (<strong>OPRM1</strong>) and glutaminergic (GRIK1) systems mediate the dependent behavior via different mechanisms; however, they all target the serotonergic and dopaminergic pathways in the ventral tegmental area.
+OPRM1	drug	alcohol	27447243	In the present study, DRD2 A2/A1, DRD3 Ser9Gly, DβH  1021C>T, <strong>OPRM1</strong> A118G and GRIK1 rs2832407C>A polymorphisms and their interactions were analyzed in 72 <b>alcohol</b> dependent patients and 74 controls of Greek Cypriot origin, using the PCR RFLP method.
+OPRM1	drug	alcohol	27447243	No differences were found in the genotype or allele distribution of DRD2 A2/A1, DRD3 Ser9Gly, DβH  1021C>T, <strong>OPRM1</strong> A118G and GRIK1 rs2832407C>A between <b>alcohol</b> dependent patients and controls.
+OPRM1	drug	alcohol	27396374	Twenty four healthy male μ opioid receptor (<strong>OPRM1</strong>)118G allele carriers underwent a standardized intravenous and placebo <b>alcohol</b> administration.
+OPRM1	drug	opioid	27396374	Twenty four healthy male μ <b>opioid</b> receptor (<strong>OPRM1</strong>)118G allele carriers underwent a standardized intravenous and placebo alcohol administration.
+OPRM1	drug	opioid	27380026	Here we prove that the miR 212/132 cluster can be regulated by <b>morphine</b>, through the activation of mu <b>opioid</b> receptor (<strong>Oprm1</strong>).
+OPRM1	drug	opioid	27380026	The molecular pathways triggered after <b>morphine</b> administration also induce changes in the levels of expression of <strong>oprm1</strong>.
+OPRM1	drug	opioid	27380026	Moreover, the regulation of both <strong>oprm1</strong> and of the cluster promoter is mediated by MeCP2, acting as a transcriptional repressor on methylated DNA after prolonged <b>morphine</b> administration.
+OPRM1	drug	alcohol	27370058	[μ Opioid Receptor Gene (<strong>OPRM1</strong>) Polymorphisms A118G and C17T in <b>Alcohol</b> Dependence: A Turkish Sample].
+OPRM1	drug	opioid	27370058	[μ <b>Opioid</b> Receptor Gene (<strong>OPRM1</strong>) Polymorphisms A118G and C17T in Alcohol Dependence: A Turkish Sample].
+OPRM1	addiction	dependence	27370058	[μ Opioid Receptor Gene (<strong>OPRM1</strong>) Polymorphisms A118G and C17T in Alcohol <b>Dependence</b>: A Turkish Sample].
+OPRM1	drug	alcohol	27370058	Previous investigations on opioid system genetics have identified polymorphisms of the <strong>OPRM1</strong> gene expressing μ opioid receptors to be significantly associated with some features of <b>alcohol</b> dependence (AD).
+OPRM1	drug	opioid	27370058	Previous investigations on <b>opioid</b> system genetics have identified polymorphisms of the <strong>OPRM1</strong> gene expressing μ <b>opioid</b> receptors to be significantly associated with some features of alcohol dependence (AD).
+OPRM1	addiction	dependence	27370058	Previous investigations on opioid system genetics have identified polymorphisms of the <strong>OPRM1</strong> gene expressing μ opioid receptors to be significantly associated with some features of alcohol <b>dependence</b> (AD).
+OPRM1	drug	alcohol	27370058	In the present study, we evaluated the relationship between single nucleotide polymorphisms (SNP) in the <strong>OPRM1</strong> gene, A118G (rs1799971, Asn40Asp) and C17T (rs1799972, Arg6Val), and AD diagnosis, level of <b>alcohol</b> consumption, and AD severity in a Turkish sample.
+OPRM1	drug	opioid	27288213	Association of the <strong>OPRM1</strong> and COMT genes' polymorphisms with the efficacy of <b>morphine</b> in Tunisian cancer patients: Impact of the high genetic heterogeneity in Tunisia?
+OPRM1	drug	opioid	27288213	The aim of the present study was to investigate the possible association of <b>opioid</b> treatment outcome with single nucleotide polymorphisms (SNPs) in the mμ <b>opioid</b> receptor (<strong>OPRM1</strong>) and catechol o methyltransferase (COMT) genes, in Tunisian cancer pain patients.
+OPRM1	drug	opioid	27288213	We genotyped one hundred and twenty nine cancer patients treated with different doses of <b>morphine</b> for 3 SNPs in <strong>OPRM1</strong> gene (rs17174629, rs1799972 and rs1799971) and one in the COMT gene (rs4680).
+OPRM1	drug	nicotine	27095017	This study investigates differences in μ opioid receptor mediated neurotransmission in healthy controls and overnight abstinent <b>smokers</b>, and potential effects of the <strong>OPRM1</strong> A118G genotype.
+OPRM1	drug	opioid	27095017	This study investigates differences in μ <b>opioid</b> receptor mediated neurotransmission in healthy controls and overnight abstinent smokers, and potential effects of the <strong>OPRM1</strong> A118G genotype.
+OPRM1	drug	alcohol	27063791	Candidate genes for mediating the behavioral interaction between <b>ethanol</b> consumption and wheel running include multiple potassium channel genes, <strong>Oprm1</strong>, Prkcg, Stxbp1, Crhr1, Gabra3, Slc6a13, Stx1b, Pomc, Rassf5 and Camta2.
+OPRM1	drug	opioid	27061230	To examine whether certain genotypes were associated with this, we examined the frequencies of 29 SNPs located in candidate genes related to <b>opioid</b> pharmacology: ABCB1, <strong>OPRM1</strong>, UGT2B7, CYP3A5, CYP2B6, CYP2C19, CYP2D6, COMT, KCNJ6 and SCN9A in 274 deceased patients with OA (DOA), 309 living patients with OA (LOA) and in 394 healthy volunteers (HV).
+OPRM1	drug	opioid	27061086	<b>Opioid</b> genes (e.g., Oprk1, <strong>Oprm1</strong>) and genes for neuropeptides linked to anxiety and panic behaviors (e.g., Npy1r) had mostly decreased expression.
+OPRM1	drug	alcohol	27046326	This study examined the association of subjective responses with subsequent laboratory self administration, also evaluating laboratory phenotypes in relation to putative genetic risk factors [family history (FH) of <b>alcohol</b> dependence and <strong>OPRM1</strong> genotype] and subsequent heavy drinking.
+OPRM1	addiction	dependence	27046326	This study examined the association of subjective responses with subsequent laboratory self administration, also evaluating laboratory phenotypes in relation to putative genetic risk factors [family history (FH) of alcohol <b>dependence</b> and <strong>OPRM1</strong> genotype] and subsequent heavy drinking.
+OPRM1	drug	alcohol	27046326	Although self administration did not differ by FH group, participants with the <strong>OPRM1</strong> 118G allele evidenced steeper breath <b>alcohol</b> concentration (BrAC) trajectories and greater peak BrAC relative to 118A homozygous participants.
+OPRM1	drug	opioid	26976581	The clinical management of severe pain depends heavily on <b>opioids</b> acting through mu <b>opioid</b> receptors encoded by the <strong>Oprm1</strong> gene, which undergoes extensive alternative splicing.
+OPRM1	drug	opioid	26976581	In addition to generating a series of prototypic seven transmembrane domain (7TM) G protein coupled receptors (GPCRs), <strong>Oprm1</strong> also produces a set of truncated splice variants containing only six transmembrane domains (6TM) through which selected <b>opioids</b> such as IBNtxA (3' iodobenzoyl 6β naltrexamide) mediate a potent analgesia without many undesirable effects.
+OPRM1	drug	opioid	26902643	We tested the association between <b>morphine</b> consumption, postoperative pain, and single nucleotide polymorphisms (SNPs) within <b>opioid</b> receptor μ 1 (<strong>OPRM1</strong>), catechol O methyltransferase (COMT), uridine diphosphate glucose glucuronosyltransferase 2B7, and estrogen receptor (ESR1) gene loci to elucidate genetic prediction of <b>opioid</b> consumption.
+OPRM1	drug	opioid	26902643	A haplotype of 7 SNPs in <strong>OPRM1</strong> showed significant additive effects on <b>opioid</b> consumption (P = .007); a linear regression model including age and 9 SNPs in ESR1, <strong>OPRM1</strong>, and COMT explained the highest proportion of variance of <b>morphine</b> consumption (10.7%; P = .001).
+OPRM1	drug	opioid	26902643	Combinations of genetic variants within <strong>OPRM1</strong>, COMT, and ESR1 better explain variability in <b>morphine</b> consumption than single genetic variants.
+OPRM1	drug	opioid	26792136	The AC/AG Diplotype for the 118A>G and IVS2 + 691G>C Polymorphisms of <strong>OPRM1</strong> Gene is Associated with Sleep Quality Among <b>Opioid</b> Dependent Patients on <b>Methadone</b> Maintenance Therapy.
+OPRM1	drug	opioid	26792136	<b>Methadone</b> is a full agonist of the <b>opioid</b> receptor mu 1 which is encoded by the <strong>OPRM1</strong> gene.
+OPRM1	drug	opioid	26792136	This study investigated the association of <strong>OPRM1</strong> polymorphisms with sleep quality among <b>opioid</b> dependent patients on MMT.
+OPRM1	drug	opioid	26792136	Our study indicates that the AC/AG diplotype for the 118A>G and IVS2 + 691G>C polymorphisms of <strong>OPRM1</strong> gene is associated with better sleep quality among males with <b>opioid</b> dependence on MMT.
+OPRM1	addiction	dependence	26792136	Our study indicates that the AC/AG diplotype for the 118A>G and IVS2 + 691G>C polymorphisms of <strong>OPRM1</strong> gene is associated with better sleep quality among males with opioid <b>dependence</b> on MMT.
+OPRM1	drug	cocaine	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, Penk, Pdyn) and cognate receptors (<strong>Oprm</strong>, Oprk and Oprd) in reward related brain regions, after exposure to either <b>cocaine</b> self administration or yoked saline, in the aforementioned translational paradigm.
+OPRM1	drug	opioid	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous <b>opioid</b> peptides (Pomc, Penk, Pdyn) and cognate receptors (<strong>Oprm</strong>, Oprk and Oprd) in reward related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+OPRM1	addiction	reward	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, Penk, Pdyn) and cognate receptors (<strong>Oprm</strong>, Oprk and Oprd) in <b>reward</b> related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+OPRM1	drug	cocaine	26777278	Also, different strain specific <b>cocaine</b> induced mRNA expression of <strong>Oprm</strong> and Oprk was found in DS.
+OPRM1	drug	cocaine	26777278	Moreover, gene expression level of Pdyn, Penk, Oprk, and <strong>Oprm</strong> in the DS was significantly correlated with <b>cocaine</b> intake only in Fischer rats.
+OPRM1	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (<strong>OPRM1</strong>), kappa <b>opioid</b> receptors (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (SLC6A3, DAT1) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+OPRM1	addiction	relapse	28300812	Regardless of treatment several polymorphisms were associated with high risk of <b>relapse</b>: allele Т (rs510769) <strong>OPRM1</strong> (р=0.053), allele А (rs1799971, A118G) <strong>OPRM1</strong> (р=0.056), allele S exon III 48 bp DRD4 VNTR (р=0.001; HR=3.1 (ДИ 95% 1.57 6.18); genotype combinations: DRD4   521 С/Т (ТТ) + DRD2 Nco I (TT), р=0.026; DRD4  521 С/Т (ТТ) + DRD2  141 С (II), р=0.011; DRD4   521 С/Т (ТТ) + <strong>OPRM1</strong> A118G (rs1799971) (AA), р=0.011; DRD2 Nco I(ТТ) + ADRA2A (СС), р=0.012; DRD2 Nco I(ТТ) + <strong>OPRM1</strong> A118G (AA), р=0.02.
+OPRM1	addiction	relapse	28300812	The effects dependent on the treatment group were as follows: 1) in the N+G group, patients with the DRD4  521 С/Т TT genotype had higher probability of completion of treatment program in comparison with other genotypes (CC and CT) (log rank test: p=0.002); 2) in NP + GP group, patients with the <strong>OPRM1</strong> rs510769 T allele had higher risk of <b>relapse</b> compared to the genotype GG (p=0.008) (FDR p<0.0125).
+OPRM1	addiction	withdrawal	26692286	The total <b>withdrawal</b> severity score (based on the COWS) from this procedure was correlated with genotype information for variants of <strong>OPRM1</strong> (rs1799971; rs6848893), OPRD1 (rs10753331; rs2234918; rs581111; rs678849; rs1042114), and OPRK1 (rs6473797; rs963549).
+OPRM1	addiction	withdrawal	26692286	Three polymorphisms were significantly associated with severity of abstinence induced <b>withdrawal</b> (n = 19) in the bivariate analysis (R): <strong>OPRM1</strong> rs6848893 (.45), OPRD1 rs10753331 (.03), and rs678849 (.08), but only the <strong>OPRM1</strong> rs6848893 was retained in the multivariate model (p < .001).
+OPRM1	drug	opioid	26581429	The Opposing Roles of IVS2+691 CC Genotype and AC/AG Diplotype of 118A>G and IVS2+691G>C of <strong>OPRM1</strong> Polymorphisms in Cold Pain Tolerance Among <b>Opioid</b> Dependent Malay Males on <b>Methadone</b> Therapy.
+OPRM1	drug	opioid	26535894	The expression of proopiomelanocortin Pomc encoding β endorphin and <strong>Oprm1</strong> encoding the mu <b>opioid</b> receptor were upregulated peripherally after incision; moreover, <strong>Oprm1</strong> expression was further increased under DNMT inhibitor treatment.
+OPRM1	drug	nicotine	26449981	Parental smoke exposure and the development of <b>nicotine</b> craving in adolescent novice <b>smokers</b>: the roles of DRD2, DRD4, and <strong>OPRM1</strong> genotypes.
+OPRM1	addiction	relapse	26449981	Parental smoke exposure and the development of nicotine <b>craving</b> in adolescent novice smokers: the roles of DRD2, DRD4, and <strong>OPRM1</strong> genotypes.
+OPRM1	drug	nicotine	26449981	The aim of this study was to identify specific genetic (i.e., DRD2 Taq1A, DRD4 48 bp VNTR, and <strong>OPRM1</strong> A118G polymorphisms) and environmental mechanisms that underlie the emergence of both cue induced and cognitive craving among adolescent novice <b>smokers</b>.
+OPRM1	addiction	relapse	26449981	The aim of this study was to identify specific genetic (i.e., DRD2 Taq1A, DRD4 48 bp VNTR, and <strong>OPRM1</strong> A118G polymorphisms) and environmental mechanisms that underlie the emergence of both cue induced and cognitive <b>craving</b> among adolescent novice smokers.
+OPRM1	drug	opioid	26441502	Gene expression analyses implicate the importance of a network enriched in transcription factor genes, some of which regulate the mu <b>opioid</b> receptor gene, <strong>Oprm1</strong>, in risk for MA use.
+OPRM1	addiction	dependence	26392368	Association of the <strong>OPRM1</strong> Variant rs1799971 (A118G) with Non Specific Liability to Substance <b>Dependence</b> in a Collaborative de novo Meta Analysis of European Ancestry Cohorts.
+OPRM1	drug	opioid	26392368	The mu1 <b>opioid</b> receptor gene, <strong>OPRM1</strong>, has long been a high priority candidate for human genetic studies of addiction.
+OPRM1	addiction	addiction	26392368	The mu1 opioid receptor gene, <strong>OPRM1</strong>, has long been a high priority candidate for human genetic studies of <b>addiction</b>.
+OPRM1	addiction	addiction	26392368	Because of its potential functional significance, the non synonymous variant rs1799971 (A118G, Asn40Asp) in <strong>OPRM1</strong> has been extensively studied, yet its role in <b>addiction</b> has remained unclear, with conflicting association findings.
+OPRM1	drug	opioid	26339899	In an exploratory analysis, emotional well being increased in a subgroup of participants with AA genotype of <b>opioid</b> receptor, mu 1 (<strong>OPRM1</strong>) A118G polymorphism (p = 0.02).
+OPRM1	drug	alcohol	26339899	Replication by larger scale studies is warranted to further evaluate <b>naltrexone</b> administration schedules for the treatment of PG and the role of <strong>OPRM1</strong>.
+OPRM1	drug	opioid	26288297	It was genotyped polymorphisms in the following genes: mu <b>opioid</b> receptor (<strong>OPRM1</strong>), kappa <b>opioid</b> receptor (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (DAT1).
+OPRM1	drug	alcohol	26125586	Twenty individuals with <b>alcohol</b> dependence (six females; 90% Caucasian; mean age = 29.4) who were prospectively genotyped on the <strong>OPRM1</strong> gene underwent two functional magnetic resonance imaging (fMRI) sessions, before and after a priming dose of <b>alcohol</b>, each including a gustatory <b>alcohol</b> cue reactivity paradigm and self reported craving measures.
+OPRM1	addiction	dependence	26125586	Twenty individuals with alcohol <b>dependence</b> (six females; 90% Caucasian; mean age = 29.4) who were prospectively genotyped on the <strong>OPRM1</strong> gene underwent two functional magnetic resonance imaging (fMRI) sessions, before and after a priming dose of alcohol, each including a gustatory alcohol cue reactivity paradigm and self reported craving measures.
+OPRM1	addiction	relapse	26125586	Twenty individuals with alcohol dependence (six females; 90% Caucasian; mean age = 29.4) who were prospectively genotyped on the <strong>OPRM1</strong> gene underwent two functional magnetic resonance imaging (fMRI) sessions, before and after a priming dose of alcohol, each including a gustatory alcohol cue reactivity paradigm and self reported <b>craving</b> measures.
+OPRM1	drug	alcohol	26125586	<strong>OPRM1</strong> genotype was also found to moderate <b>alcohol</b> cue reactivity across scans.
+OPRM1	drug	alcohol	26125586	Further, it provides preliminary evidence for moderating roles of <b>alcoholism</b> severity and <strong>OPRM1</strong> genotype on priming related changes in cue reactivity, adding to our understanding of the function of <b>alcohol</b> priming in <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	26125586	Further, it provides preliminary evidence for moderating roles of alcoholism severity and <strong>OPRM1</strong> genotype on priming related changes in cue reactivity, adding to our understanding of the function of alcohol priming in alcohol <b>dependence</b>.
+OPRM1	drug	opioid	26096047	Mechanistic/mammalian target of rapamycin (mTOR) activation by μ <b>opioid</b> receptor (<strong>OPRM1</strong>) participates in antinociceptive tolerance, hyperalgesia, and physical dependence.
+OPRM1	addiction	dependence	26096047	Mechanistic/mammalian target of rapamycin (mTOR) activation by μ opioid receptor (<strong>OPRM1</strong>) participates in antinociceptive tolerance, hyperalgesia, and physical <b>dependence</b>.
+OPRM1	drug	opioid	26096047	<strong>OPRM1</strong> activation by <b>morphine</b> induced time dependent mTOR activation.
+OPRM1	drug	alcohol	26092968	Influence of the A118G Polymorphism of the <strong>OPRM1</strong> Gene and Exon 3 VNTR Polymorphism of the DRD4 Gene on Cigarette Craving After <b>Alcohol</b> Administration.
+OPRM1	addiction	relapse	26092968	Influence of the A118G Polymorphism of the <strong>OPRM1</strong> Gene and Exon 3 VNTR Polymorphism of the DRD4 Gene on Cigarette <b>Craving</b> After Alcohol Administration.
+OPRM1	drug	alcohol	26092968	The current study examined whether the presence of the G allele of the A118G polymorphism of the <strong>OPRM1</strong> gene (rs1799971) and the long allele of exon 3 VNTR polymorphism of the DRD4 gene moderate the effect of <b>alcohol</b> administration on urge to smoke.
+OPRM1	drug	alcohol	26092968	Presence of G allele of the A118G polymorphism of the <strong>OPRM1</strong> gene may lead to greater increases in urge to smoke after a high dose of <b>alcohol</b>.
+OPRM1	drug	opioid	26052934	Although the mechanism which regulates transcription in the 5' UTR of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) in lymphocytes has been well studied, a question remains as to whether there is post transcriptional regulation of <strong>OPRM1</strong> gene in lymphocytes.
+OPRM1	drug	opioid	26052934	Thus, <b>morphine</b> may up regulate receptor level by both stimulating <strong>OPRM1</strong> gene transcription and stabilizing its mRNA.
+OPRM1	drug	opioid	26052934	This finding will be helpful for full understanding of the regulatory mechanism of <strong>OPRM1</strong> gene in lymphocytes, as well as the synergistic mechanism of HIV infection and <b>morphine</b> addiction in the pathogenesis of AIDS.
+OPRM1	addiction	addiction	26052934	This finding will be helpful for full understanding of the regulatory mechanism of <strong>OPRM1</strong> gene in lymphocytes, as well as the synergistic mechanism of HIV infection and morphine <b>addiction</b> in the pathogenesis of AIDS.
+OPRM1	drug	alcohol	26042510	Association between Opioid Receptor mu 1 (<strong>OPRM1</strong>) Gene Polymorphisms and Tobacco and <b>Alcohol</b> Consumption in a Spanish Population.
+OPRM1	drug	nicotine	26042510	Association between Opioid Receptor mu 1 (<strong>OPRM1</strong>) Gene Polymorphisms and <b>Tobacco</b> and Alcohol Consumption in a Spanish Population.
+OPRM1	drug	opioid	26042510	Association between <b>Opioid</b> Receptor mu 1 (<strong>OPRM1</strong>) Gene Polymorphisms and Tobacco and Alcohol Consumption in a Spanish Population.
+OPRM1	drug	alcohol	26042510	Our aim is to assess the influence of genetic variations in the <strong>opioid receptor mu 1</strong> on <b>alcohol</b> and tobacco consumption in a Spanish population.
+OPRM1	drug	nicotine	26042510	Our aim is to assess the influence of genetic variations in the <strong>opioid receptor mu 1</strong> on alcohol and <b>tobacco</b> consumption in a Spanish population.
+OPRM1	drug	opioid	26042510	Our aim is to assess the influence of genetic variations in the <strong><b>opioid</b> receptor mu 1</strong> on alcohol and tobacco consumption in a Spanish population.
+OPRM1	drug	opioid	26042510	Individuals were genotyped for three polymorphisms in the <b>opioid</b> receptor mu 1 (<strong>OPRM1</strong>) gene, using a TaqMan protocol.
+OPRM1	drug	opioid	26011641	μ <b>Opioids</b> act through GPCRs that are generated from the <strong>Oprm1</strong> gene, which undergoes extensive alternative splicing.
+OPRM1	drug	opioid	26011641	The most abundant set of <strong>Oprm1</strong> variants encode classical full length 7 transmembrane domain (7TM) μ <b>opioid</b> receptors that mediate the actions of the traditional μ <b>opioid</b> drugs <b>morphine</b> and <b>methadone</b>.
+OPRM1	drug	opioid	26011641	Here we demonstrated that a truncated 6TM splice variant, mMOR 1G, can rescue IBNtxA analgesia in a μ <b>opioid</b> receptor deficient mouse that lacks all <strong>Oprm1</strong> splice variants, ablating μ <b>opioid</b> activity in these animals.
+OPRM1	drug	opioid	26011641	Intrathecal administration of lentivirus containing the 6TM variant mMOR 1G restored IBNtxA, but not <b>morphine</b>, analgesia in <strong>Oprm1</strong> deficient animals.
+OPRM1	drug	opioid	25986698	A single nucleotide polymorphism (SNP) in the human μ <b>opioid</b> receptor gene (<strong>OPRM1</strong> A118G) has been widely studied for its association in a variety of drug addiction and pain sensitivity phenotypes; however, the extent of these adaptations and the mechanisms underlying these associations remain elusive.
+OPRM1	addiction	addiction	25986698	A single nucleotide polymorphism (SNP) in the human μ opioid receptor gene (<strong>OPRM1</strong> A118G) has been widely studied for its association in a variety of drug <b>addiction</b> and pain sensitivity phenotypes; however, the extent of these adaptations and the mechanisms underlying these associations remain elusive.
+OPRM1	drug	nicotine	25941919	The μ opioid receptor (<strong>OPRM1</strong>) binds the endogenous opioid peptide β endorphin and mediates the reinforcing effects of <b>nicotine</b>, while the GluR5 kainate receptor subunit (encoded by GRIK1 gene), a binding site for known mediators of glutamate neurotransmission, potentially affects the glutaminergic system that is also indirectly implicated in the reward system.
+OPRM1	drug	opioid	25941919	The μ <b>opioid</b> receptor (<strong>OPRM1</strong>) binds the endogenous <b>opioid</b> peptide β endorphin and mediates the reinforcing effects of nicotine, while the GluR5 kainate receptor subunit (encoded by GRIK1 gene), a binding site for known mediators of glutamate neurotransmission, potentially affects the glutaminergic system that is also indirectly implicated in the reward system.
+OPRM1	addiction	reward	25941919	The μ opioid receptor (<strong>OPRM1</strong>) binds the endogenous opioid peptide β endorphin and mediates the <b>reinforcing</b> effects of nicotine, while the GluR5 kainate receptor subunit (encoded by GRIK1 gene), a binding site for known mediators of glutamate neurotransmission, potentially affects the glutaminergic system that is also indirectly implicated in the <b>reward</b> system.
+OPRM1	drug	nicotine	25941919	In the present study, <strong>OPRM1</strong> A118G and GRIK1 rs2832407C>A polymorphisms and their interactions were analyzed in 132 <b>smoking</b> initiators (SI) and 144 non initiators (NI) of Greek origin, using the PCR RFLP method.
+OPRM1	drug	nicotine	25941919	However, we found a significant interaction of <strong>OPRM1</strong> A118G and GRIK1 rs2832407C>A genotypes associated with <b>smoking</b> initiation in a model adjusted for age, sex, BMI and type 2 diabetes mellitus (odds ratio=1.341, 95% CI 1.024 1.755, p=0.033).
+OPRM1	drug	nicotine	25941919	In the present study, we have shown that gene gene interaction of components of different systems associated with <b>nicotine</b> reinforcing effects, such as <strong>OPRM1</strong> and GRIK1, rather than one gene polymorphism, is associated with <b>smoking</b> behavior.
+OPRM1	addiction	reward	25941919	In the present study, we have shown that gene gene interaction of components of different systems associated with nicotine <b>reinforcing</b> effects, such as <strong>OPRM1</strong> and GRIK1, rather than one gene polymorphism, is associated with smoking behavior.
+OPRM1	drug	alcohol	25937240	Increased mesolimbic cue reactivity in carriers of the mu opioid receptor gene <strong>OPRM1</strong> A118G polymorphism predicts drinking outcome: a functional imaging study in <b>alcohol</b> dependent subjects.
+OPRM1	drug	opioid	25937240	Increased mesolimbic cue reactivity in carriers of the mu <b>opioid</b> receptor gene <strong>OPRM1</strong> A118G polymorphism predicts drinking outcome: a functional imaging study in alcohol dependent subjects.
+OPRM1	drug	alcohol	25937240	In particular, a single nucleotide polymorphism rs1799971 (A118G) in the mu opioid receptor gene (<strong>OPRM1</strong>) is suggested to modulate <b>alcohol</b> related phenotypes and neural response in the mesocorticolimbic dopaminergic system.
+OPRM1	drug	opioid	25937240	In particular, a single nucleotide polymorphism rs1799971 (A118G) in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) is suggested to modulate alcohol related phenotypes and neural response in the mesocorticolimbic dopaminergic system.
+OPRM1	addiction	relapse	25937240	This suggests that genotype effects on cue reactivity might link the <strong>OPRM1</strong> A118G risk allele with an increased <b>relapse</b> risk that was reported in earlier studies.
+OPRM1	drug	opioid	25911999	Functional mu <b>opioid</b> receptor polymorphism (<strong>OPRM1</strong> A(118) G) associated with <b>heroin</b> use outcomes in Caucasian males: A pilot study.
+OPRM1	drug	opioid	25911999	The functional polymorphism A(118)G, located in exon 1 of the <strong>OPRM1</strong> gene, results in anatomically specific reductions in MOR expression, which may alter an individual's response to <b>heroin</b>.
+OPRM1	drug	opioid	25911999	Those findings suggest <strong>OPRM1</strong> genotype may impact characteristics of <b>heroin</b> use.
+OPRM1	drug	opioid	25911999	The present pilot study characterized the impact of <strong>OPRM1</strong> genotype (rs1799971, 118G allele carriers vs. 118AA homozygotes) on <b>heroin</b> use phenotypes associated with <b>heroin</b> dependence severity in a sample of male, Caucasian chronic <b>heroin</b> users (n = 86).
+OPRM1	addiction	dependence	25911999	The present pilot study characterized the impact of <strong>OPRM1</strong> genotype (rs1799971, 118G allele carriers vs. 118AA homozygotes) on heroin use phenotypes associated with heroin <b>dependence</b> severity in a sample of male, Caucasian chronic heroin users (n = 86).
+OPRM1	drug	opioid	25911999	These preliminary findings, consistent with extant data, illustrate a role for <strong>OPRM1</strong> allelic variation on <b>heroin</b> use characteristics, and provide support for considering genotype in <b>heroin</b> treatment and relapse prevention.
+OPRM1	addiction	relapse	25911999	These preliminary findings, consistent with extant data, illustrate a role for <strong>OPRM1</strong> allelic variation on heroin use characteristics, and provide support for considering genotype in heroin treatment and <b>relapse</b> prevention.
+OPRM1	drug	opioid	25881115	Receptor Reserve Moderates Mesolimbic Responses to <b>Opioids</b> in a Humanized Mouse Model of the <strong>OPRM1</strong> A118G Polymorphism.
+OPRM1	drug	opioid	25881115	The <strong>OPRM1</strong> A118G polymorphism is the most widely studied μ <b>opioid</b> receptor (MOR) variant.
+OPRM1	drug	opioid	25881115	Prior work has shown that both electrophysiological and analgesic responses to <b>morphine</b> but not to <b>fentanyl</b> are moderated by <strong>OPRM1</strong> A118G variation, but the mechanism behind this dissociation is not known.
+OPRM1	drug	alcohol	25823631	The genetic variability of μ , δ  and κ opioid receptors genes <strong>OPRM1</strong>, OPRD1, and OPRK1 modulates the efficacy of opioid antagonist treatments such as <b>naltrexone</b> and methadone, as well as the cocaine vaccine.
+OPRM1	drug	cocaine	25823631	The genetic variability of μ , δ  and κ opioid receptors genes <strong>OPRM1</strong>, OPRD1, and OPRK1 modulates the efficacy of opioid antagonist treatments such as naltrexone and methadone, as well as the <b>cocaine</b> vaccine.
+OPRM1	drug	opioid	25823631	The genetic variability of μ , δ  and κ <b>opioid</b> receptors genes <strong>OPRM1</strong>, OPRD1, and OPRK1 modulates the efficacy of <b>opioid</b> antagonist treatments such as naltrexone and <b>methadone</b>, as well as the cocaine vaccine.
+OPRM1	drug	alcohol	25760804	Secondary analysis of clinical trial data suggests that a functional polymorphism (rs1799971, Asn40Asp) of the µ opioid receptor gene (<strong>OPRM1</strong>) is associated with the risk of relapse to heavy drinking following treatment with the opioid antagonist <b>naltrexone</b>.
+OPRM1	drug	opioid	25760804	Secondary analysis of clinical trial data suggests that a functional polymorphism (rs1799971, Asn40Asp) of the µ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) is associated with the risk of relapse to heavy drinking following treatment with the <b>opioid</b> antagonist naltrexone.
+OPRM1	addiction	relapse	25760804	Secondary analysis of clinical trial data suggests that a functional polymorphism (rs1799971, Asn40Asp) of the µ opioid receptor gene (<strong>OPRM1</strong>) is associated with the risk of <b>relapse</b> to heavy drinking following treatment with the opioid antagonist naltrexone.
+OPRM1	drug	opioid	25744370	Cis Expression Quantitative Trait Loci Mapping Reveals Replicable Associations with <b>Heroin</b> Addiction in <strong>OPRM1</strong>.
+OPRM1	addiction	addiction	25744370	Cis Expression Quantitative Trait Loci Mapping Reveals Replicable Associations with Heroin <b>Addiction</b> in <strong>OPRM1</strong>.
+OPRM1	drug	opioid	25744370	No <b>opioid</b> receptor, mu 1 (<strong>OPRM1</strong>) gene polymorphisms, including the functional single nucleotide polymorphism (SNP) rs1799971, have been conclusively associated with <b>heroin</b>/other <b>opioid</b> addiction, despite their biological plausibility.
+OPRM1	addiction	addiction	25744370	No opioid receptor, mu 1 (<strong>OPRM1</strong>) gene polymorphisms, including the functional single nucleotide polymorphism (SNP) rs1799971, have been conclusively associated with heroin/other opioid <b>addiction</b>, despite their biological plausibility.
+OPRM1	drug	opioid	25744370	We used evidence of polymorphisms altering <strong>OPRM1</strong> expression in normal human brain tissue to nominate and then test associations with <b>heroin</b> addiction.
+OPRM1	addiction	addiction	25744370	We used evidence of polymorphisms altering <strong>OPRM1</strong> expression in normal human brain tissue to nominate and then test associations with heroin <b>addiction</b>.
+OPRM1	drug	opioid	25744370	Our findings show that common <strong>OPRM1</strong> intron 1 SNPs have replicable associations with <b>heroin</b> addiction.
+OPRM1	addiction	addiction	25744370	Our findings show that common <strong>OPRM1</strong> intron 1 SNPs have replicable associations with heroin <b>addiction</b>.
+OPRM1	drug	opioid	25716856	A single nucleotide polymorphism (SNP) in the human μ <b>opioid</b> receptor gene (<strong>OPRM1</strong> A118G) has been widely studied for its association in drug addiction, pain sensitivity, and, more recently, social behavior.
+OPRM1	addiction	addiction	25716856	A single nucleotide polymorphism (SNP) in the human μ opioid receptor gene (<strong>OPRM1</strong> A118G) has been widely studied for its association in drug <b>addiction</b>, pain sensitivity, and, more recently, social behavior.
+OPRM1	drug	alcohol	25715171	<strong>OPRM1</strong> genotype and <b>naltrexone</b> response in depressed <b>alcohol</b> dependent patients.
+OPRM1	drug	alcohol	25715171	A functional polymorphism rs1799971 (A118G) in the μ opioid receptor gene (<strong>OPRM1</strong>) produces an amino acid substitution Asn40Asp, which is believed to influence <b>naltrexone</b> response in nondepressed <b>alcohol</b> dependent patients.
+OPRM1	drug	opioid	25715171	A functional polymorphism rs1799971 (A118G) in the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) produces an amino acid substitution Asn40Asp, which is believed to influence naltrexone response in nondepressed alcohol dependent patients.
+OPRM1	drug	alcohol	25715171	General linear mixed models examined the effect of the <strong>OPRM1</strong> A118G genotype on <b>alcohol</b> outcomes during treatment.
+OPRM1	drug	opioid	25670515	In Asian populations, the high <strong>OPRM1</strong> 118A>G frequency associates with higher <b>opioid</b> dosage requirements.
+OPRM1	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., <strong>OPRM1</strong>, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+OPRM1	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., <strong>OPRM1</strong>, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+OPRM1	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., <strong>OPRM1</strong>, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+OPRM1	drug	benzodiazepine	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) methadone), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the <b>midazolam</b> test, R,S methadone trough concentration and clinically significant polymorphisms of the <strong>OPRM1</strong>, DRD2, COMT, ABCB1, CYP2B6, CYP3A5, CYP2C19 and CYP2D6 genes.
+OPRM1	drug	opioid	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) <b>methadone</b>), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the midazolam test, R,S <b>methadone</b> trough concentration and clinically significant polymorphisms of the <strong>OPRM1</strong>, DRD2, COMT, ABCB1, CYP2B6, CYP3A5, CYP2C19 and CYP2D6 genes.
+OPRM1	addiction	relapse	25545355	After permutation and FDR adjustment, none of the associations remained statistically significant, although the p values for the association between rs557748 in <strong>OPRM1</strong> and the ND/<b>craving</b> and self medication phenotypes were both 0.076.
+OPRM1	drug	cocaine	25449401	<b>Cocaine</b> induced suppression of saccharin intake and morphine modulation of Ca²⁺ channel currents in sensory neurons of <strong>OPRM1</strong> A118G mice.
+OPRM1	drug	opioid	25449401	Cocaine induced suppression of saccharin intake and <b>morphine</b> modulation of Ca²⁺ channel currents in sensory neurons of <strong>OPRM1</strong> A118G mice.
+OPRM1	drug	alcohol	25449401	Several studies have shown that human carriers of the single nucleotide polymorphism of the μ opioid receptor, <strong>OPRM1</strong> A118G, exhibit greater drug and <b>alcohol</b> use, increased sensitivity to pain, and reduced sensitivity to the antinociceptive effects of opiates.
+OPRM1	drug	opioid	25449401	Several studies have shown that human carriers of the single nucleotide polymorphism of the μ <b>opioid</b> receptor, <strong>OPRM1</strong> A118G, exhibit greater drug and alcohol use, increased sensitivity to pain, and reduced sensitivity to the antinociceptive effects of opiates.
+OPRM1	drug	alcohol	25442002	It has been proposed that therapeutic responses to <b>naltrexone</b> in <b>alcoholism</b> are moderated by variation at the mu opioid receptor gene locus (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	25442002	It has been proposed that therapeutic responses to naltrexone in alcoholism are moderated by variation at the mu <b>opioid</b> receptor gene locus (<strong>OPRM1</strong>).
+OPRM1	drug	alcohol	25442002	Here, we used this model system to examine the role of <strong>OPRM1</strong> A118G variation for opioid antagonist effects on <b>alcohol</b> responses.
+OPRM1	drug	opioid	25442002	Here, we used this model system to examine the role of <strong>OPRM1</strong> A118G variation for <b>opioid</b> antagonist effects on alcohol responses.
+OPRM1	drug	alcohol	25442002	In a model that allows close experimental control, <strong>OPRM1</strong> A118G variation robustly moderates effects of opioid antagonism on <b>alcohol</b> reward and consumption.
+OPRM1	drug	opioid	25442002	In a model that allows close experimental control, <strong>OPRM1</strong> A118G variation robustly moderates effects of <b>opioid</b> antagonism on alcohol reward and consumption.
+OPRM1	addiction	reward	25442002	In a model that allows close experimental control, <strong>OPRM1</strong> A118G variation robustly moderates effects of opioid antagonism on alcohol <b>reward</b> and consumption.
+OPRM1	drug	alcohol	25442002	These findings strongly support a personalized medicine approach to <b>alcoholism</b> treatment that takes into account <strong>OPRM1</strong> genotype.
+OPRM1	drug	alcohol	25410894	Of 15 included studies, eight (n = 1365 participants) assessed variation in <b>naltrexone</b> response and polymorphisms of <strong>OPRM1</strong>.
+OPRM1	drug	alcohol	25410894	Estimates of effect for return to heavy drinking suggest it is possible that patients with at least one G allele of A118G polymorphism of <strong>OPRM1</strong> might be more likely to respond to <b>naltrexone</b>, but confidence intervals were wide; additional studies are needed to improve confidence in the estimates.
+OPRM1	drug	opioid	25343478	Differential expressions of the alternatively spliced variant mRNAs of the µ <b>opioid</b> receptor gene, <strong>OPRM1</strong>, in brain regions of four inbred mouse strains.
+OPRM1	drug	opioid	25343478	The µ <b>opioid</b> receptor gene, <strong>OPRM1</strong>, undergoes extensive alternative pre mRNA splicing in rodents and humans, with dozens of alternatively spliced variants of the <strong>OPRM1</strong> gene.
+OPRM1	drug	opioid	25343478	Using these qPCR assays, we examined the expression of <strong>OPRM1</strong> splice variant mRNAs in selected brain regions of four inbred mouse strains displaying differences in µ <b>opioid</b> induced tolerance and physical dependence: C56BL/6J, 129P3/J, SJL/J and SWR/J.
+OPRM1	addiction	dependence	25343478	Using these qPCR assays, we examined the expression of <strong>OPRM1</strong> splice variant mRNAs in selected brain regions of four inbred mouse strains displaying differences in µ opioid induced tolerance and physical <b>dependence</b>: C56BL/6J, 129P3/J, SJL/J and SWR/J.
+OPRM1	drug	opioid	25336208	Mouse model of the <strong>OPRM1</strong> (A118G) polymorphism: differential <b>heroin</b> self administration behavior compared with wild type mice.
+OPRM1	drug	opioid	25336208	The <strong>OPRM1</strong> A118G genotype results in substantially increased risk of <b>heroin</b> addiction in humans; however, the neurobiological mechanism for this increased risk is not fully understood.
+OPRM1	addiction	addiction	25336208	The <strong>OPRM1</strong> A118G genotype results in substantially increased risk of heroin <b>addiction</b> in humans; however, the neurobiological mechanism for this increased risk is not fully understood.
+OPRM1	drug	opioid	25336208	This study examined <b>heroin</b> self administration (SA) behavior in A112G (G/G) mice, harboring a functionally equivalent SNP in <strong>Oprm1</strong> with a similar amino acid substitution, in extended (4 h) SA sessions.
+OPRM1	drug	opioid	25293312	The human μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>), due to its genetic and structural variation, has been a target of interest in several pharmacogenetic studies.
+OPRM1	drug	alcohol	25293312	The μ opioid receptor (MOR), encoded by <strong>OPRM1</strong>, contributes to regulate the analgesic response to pain and also controls the rewarding effects of many drugs of abuse, including opioids, nicotine, and <b>alcohol</b>.
+OPRM1	drug	nicotine	25293312	The μ opioid receptor (MOR), encoded by <strong>OPRM1</strong>, contributes to regulate the analgesic response to pain and also controls the rewarding effects of many drugs of abuse, including opioids, <b>nicotine</b>, and alcohol.
+OPRM1	drug	opioid	25293312	The μ <b>opioid</b> receptor (MOR), encoded by <strong>OPRM1</strong>, contributes to regulate the analgesic response to pain and also controls the rewarding effects of many drugs of abuse, including <b>opioids</b>, nicotine, and alcohol.
+OPRM1	drug	opioid	25293312	The non synonymous polymorphism A118G of the <strong>OPRM1</strong> has been repeatedly associated with the efficacy of <b>opioid</b> treatments for pain and various types of dependence.
+OPRM1	addiction	dependence	25293312	The non synonymous polymorphism A118G of the <strong>OPRM1</strong> has been repeatedly associated with the efficacy of opioid treatments for pain and various types of <b>dependence</b>.
+OPRM1	drug	nicotine	25266401	It is a complex behaviour that involves the brain reward system and is regulated by genetic and environmental factors, such as the opioid receptor mu 1 gene (<strong>OPRM1</strong>) and prenatal exposure to maternal cigarette <b>smoking</b> (PEMCS).
+OPRM1	drug	opioid	25266401	It is a complex behaviour that involves the brain reward system and is regulated by genetic and environmental factors, such as the <b>opioid</b> receptor mu 1 gene (<strong>OPRM1</strong>) and prenatal exposure to maternal cigarette smoking (PEMCS).
+OPRM1	addiction	reward	25266401	It is a complex behaviour that involves the brain <b>reward</b> system and is regulated by genetic and environmental factors, such as the opioid receptor mu 1 gene (<strong>OPRM1</strong>) and prenatal exposure to maternal cigarette smoking (PEMCS).
+OPRM1	drug	nicotine	25266401	It is a complex behaviour that involves the brain reward system and is regulated by genetic and environmental factors, such as the <strong>opioid receptor mu 1</strong> gene (<strong>OPRM1</strong>) and prenatal exposure to maternal cigarette <b>smoking</b> (PEMCS).
+OPRM1	drug	opioid	25266401	It is a complex behaviour that involves the brain reward system and is regulated by genetic and environmental factors, such as the <strong><b>opioid</b> receptor mu 1</strong> gene (<strong>OPRM1</strong>) and prenatal exposure to maternal cigarette smoking (PEMCS).
+OPRM1	addiction	reward	25266401	It is a complex behaviour that involves the brain <b>reward</b> system and is regulated by genetic and environmental factors, such as the <strong>opioid receptor mu 1</strong> gene (<strong>OPRM1</strong>) and prenatal exposure to maternal cigarette smoking (PEMCS).
+OPRM1	drug	opioid	25225634	Region specific up regulation of oxytocin receptors in the <b>opioid</b> <strong>oprm1</strong> ( / ) mouse model of autism.
+OPRM1	drug	opioid	25225634	To better understand the <b>opioid</b> OXT interplay in the central nervous system, we first determined the expression of the oxytocin receptor (OXTR) in the brain of WT C57BL6/J mice by quantitative autoradiography; we then evaluated OXTR regional alterations in <strong>Oprm1</strong> ( / ) mice.
+OPRM1	drug	alcohol	25217046	There is optimism about potential pharmacogenetic applications for the treatment of <b>alcohol</b> use disorders, with particular interest in the <strong>OPRM1</strong> A118G polymorphism as a moderator of <b>naltrexone</b> response.
+OPRM1	drug	opioid	25122903	A <b>heroin</b> addiction severity associated intronic single nucleotide polymorphism modulates alternative pre mRNA splicing of the μ <b>opioid</b> receptor gene <strong>OPRM1</strong> via hnRNPH interactions.
+OPRM1	addiction	addiction	25122903	A heroin <b>addiction</b> severity associated intronic single nucleotide polymorphism modulates alternative pre mRNA splicing of the μ opioid receptor gene <strong>OPRM1</strong> via hnRNPH interactions.
+OPRM1	drug	opioid	25122903	Single nucleotide polymorphisms (SNPs) in the <strong>OPRM1</strong> gene have been associated with vulnerability to <b>opioid</b> dependence.
+OPRM1	addiction	dependence	25122903	Single nucleotide polymorphisms (SNPs) in the <strong>OPRM1</strong> gene have been associated with vulnerability to opioid <b>dependence</b>.
+OPRM1	drug	opioid	25122903	Individual SNP analysis and haplotype based analysis with additional SNPs in the <strong>OPRM1</strong> locus showed that mild <b>heroin</b> addiction was associated with the AG genotype, whereas severe <b>heroin</b> addiction was associated with the GG genotype.
+OPRM1	addiction	addiction	25122903	Individual SNP analysis and haplotype based analysis with additional SNPs in the <strong>OPRM1</strong> locus showed that mild heroin <b>addiction</b> was associated with the AG genotype, whereas severe heroin <b>addiction</b> was associated with the GG genotype.
+OPRM1	drug	opioid	25122903	Our studies delineate the role of this SNP as a modifier of <strong>OPRM1</strong> alternative splicing via hnRNPH interactions, and suggest a functional link between an SNP containing splicing modifier and the severity of <b>heroin</b> addiction.
+OPRM1	addiction	addiction	25122903	Our studies delineate the role of this SNP as a modifier of <strong>OPRM1</strong> alternative splicing via hnRNPH interactions, and suggest a functional link between an SNP containing splicing modifier and the severity of heroin <b>addiction</b>.
+OPRM1	drug	opioid	25093831	We further demonstrate the dependence of such analgesia on 6 TM μ <b>opioid</b> receptor variants using isobolographic analysis and the testing of <strong>Oprm1</strong> (the μ <b>opioid</b> receptor gene) exon 11 null mutant mice.
+OPRM1	addiction	dependence	25093831	We further demonstrate the <b>dependence</b> of such analgesia on 6 TM μ opioid receptor variants using isobolographic analysis and the testing of <strong>Oprm1</strong> (the μ opioid receptor gene) exon 11 null mutant mice.
+OPRM1	drug	alcohol	25039301	Associations of <strong>OPRM1</strong> A118G and <b>alcohol</b> sensitivity with intravenous <b>alcohol</b> self administration in young adults.
+OPRM1	drug	alcohol	25039301	Human laboratory and animal models implicate variation in the μ opioid receptor gene (<strong>OPRM1</strong>) as relevant for <b>alcohol</b> related reward.
+OPRM1	drug	opioid	25039301	Human laboratory and animal models implicate variation in the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) as relevant for alcohol related reward.
+OPRM1	addiction	reward	25039301	Human laboratory and animal models implicate variation in the μ opioid receptor gene (<strong>OPRM1</strong>) as relevant for alcohol related <b>reward</b>.
+OPRM1	drug	alcohol	25039301	<strong>OPRM1</strong> is associated with <b>alcohol</b> self administration in non human primate studies, but the relevance of this finding to human models is unclear.
+OPRM1	drug	alcohol	25039301	This study used computer assisted self infusion of <b>ethanol</b> (CASE) to examine associations among <strong>OPRM1</strong> A118G genotype, subjective responses to <b>alcohol</b> and intravenous <b>alcohol</b> self administration in young heavy drinkers (n = 40, mean age = 19.95 years, SD = 0.82).
+OPRM1	drug	alcohol	25039301	Those with the <strong>OPRM1</strong> 118G variant (GA or GG genotypes) achieved significantly higher peak BrAC (M = 94.90 mg%, SD = 16.56) than those with the AA genotype (M = 74.46 mg%, SD = 25.36), reflecting a significantly greater number of <b>alcohol</b> requests among GA/GG participants.
+OPRM1	drug	alcohol	25039301	These results offer further support for the feasibility of the CASE paradigm and provide initial evidence for an association of <strong>OPRM1</strong> with <b>alcohol</b> self administration in a human laboratory context.
+OPRM1	drug	opioid	24950410	This study aimed to determine the frequency of occurrence of Single Nucleotide Polymorphism (SNP) in position A118G <strong>OPRM1</strong> (rs1799971) gene and C.3435 (rs1045642) gene in <b>tramadol</b> users in comparison with normal controls.
+OPRM1	drug	alcohol	24837580	Data was culled from two <b>alcohol</b> challenge studies, totalling 91 participants (oversampled on <strong>OPRM1</strong> Asp40 carriers).
+OPRM1	drug	opioid	24755993	SNPs in the genes for brain derived neurotrophic factor (BDNF), the muscarinic acetylcholine receptor M2 (CHRM2), the dopamine receptor D4 (DRD4) and the μ1 <b>opioid</b> receptor (<strong>OPRM1</strong>) significantly moderated the impact of treatment condition over time on PA. Genetic variation in the genes for CHRM2 and <strong>OPRM1</strong> specifically had an impact on the level of PA following MBCT.
+OPRM1	drug	opioid	26574964	Blood samples were taken for the determination of serum levels of racemic <b>methadone</b> and its R and S enantiomers, and for typing of candidate alleles of POR, CYP2B6, ABCB1, GRIN1, <strong>OPRM1</strong>, SLC6A3, DßH and ARRB2 genes, all associated with the metabolism, tissue distribution and mechanism of action of <b>methadone</b>.
+OPRM1	drug	opioid	24619243	Mice lacking the mu <b>opioid</b> receptor gene (<strong>Oprm1</strong>( / )) were recently proposed as a monogenic mouse model of autism, based on severe deficits in social behavior and communication skills.
+OPRM1	drug	alcohol	24533225	Polymorphisms in the μ , δ  and κ opioid receptor genes (<strong>OPRM1</strong>, OPRD1 and OPRK1) have been reported to be associated with substance (<b>alcohol</b> or drug) dependence.
+OPRM1	drug	opioid	24533225	Polymorphisms in the μ , δ  and κ <b>opioid</b> receptor genes (<strong>OPRM1</strong>, OPRD1 and OPRK1) have been reported to be associated with substance (alcohol or drug) dependence.
+OPRM1	addiction	dependence	24533225	Polymorphisms in the μ , δ  and κ opioid receptor genes (<strong>OPRM1</strong>, OPRD1 and OPRK1) have been reported to be associated with substance (alcohol or drug) <b>dependence</b>.
+OPRM1	drug	alcohol	24533225	Genotype data for 13 <strong>OPRM1</strong> Single Nucleotide Polymorphisms (SNPs), 11 OPRD1 SNPs and seven OPRK1 SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with <b>Alcohol</b> Dependence (AD), 171 with Cocaine Dependence (CD), and 91 with Opioid Dependence (OD)] and 338 EA control subjects.
+OPRM1	drug	cocaine	24533225	Genotype data for 13 <strong>OPRM1</strong> Single Nucleotide Polymorphisms (SNPs), 11 OPRD1 SNPs and seven OPRK1 SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with Alcohol Dependence (AD), 171 with <b>Cocaine</b> Dependence (CD), and 91 with Opioid Dependence (OD)] and 338 EA control subjects.
+OPRM1	drug	opioid	24533225	Genotype data for 13 <strong>OPRM1</strong> Single Nucleotide Polymorphisms (SNPs), 11 OPRD1 SNPs and seven OPRK1 SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with Alcohol Dependence (AD), 171 with Cocaine Dependence (CD), and 91 with <b>Opioid</b> Dependence (OD)] and 338 EA control subjects.
+OPRM1	addiction	dependence	24533225	Genotype data for 13 <strong>OPRM1</strong> Single Nucleotide Polymorphisms (SNPs), 11 OPRD1 SNPs and seven OPRK1 SNPs were obtained from 382 European Americans (EAs) affected with substance <b>dependence</b> [among them, 318 with Alcohol <b>Dependence</b> (AD), 171 with Cocaine <b>Dependence</b> (CD), and 91 with Opioid <b>Dependence</b> (OD)] and 338 EA control subjects.
+OPRM1	drug	opioid	24527749	Cellular signalling of non synonymous single nucleotide polymorphisms of the human μ <b>opioid</b> receptor (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	24527749	A number of non synonymous single nucleotide polymorphisms (SNPs) in the coding regions of the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) have been postulated to contribute to this variability.
+OPRM1	drug	cocaine	24527678	Topiramate and <b>cocaine</b> co administration caused an up regulation of dopamine (Drd1, Th) and opioid (<strong>Oprm1</strong>) receptor genes.
+OPRM1	drug	opioid	24527678	Topiramate and cocaine co administration caused an up regulation of dopamine (Drd1, Th) and <b>opioid</b> (<strong>Oprm1</strong>) receptor genes.
+OPRM1	drug	nicotine	24447405	The purpose of the present study was to examine the associations of single nucleotide polymorphisms (SNPs) in the genes encoding mu opioid receptor (MOR) and the MOR interacting proteins (including <strong>OPRM1</strong>, ARRB2, and HINT1) with <b>smoking</b> behaviors in Chinese men.
+OPRM1	drug	opioid	24447405	The purpose of the present study was to examine the associations of single nucleotide polymorphisms (SNPs) in the genes encoding mu <b>opioid</b> receptor (MOR) and the MOR interacting proteins (including <strong>OPRM1</strong>, ARRB2, and HINT1) with smoking behaviors in Chinese men.
+OPRM1	drug	opioid	24447405	Participant samples were genotyped for six SNPs in the <b>opioid</b> pathway genes: rs1799971 in <strong>OPRM1</strong>, rs1045280, rs2036657 and rs3786047 in ARRB2, rs3852209 and rs2278060 in HINT1.
+OPRM1	drug	nicotine	24446757	We investigated the role of exposure to <b>smoking</b> (by parents, siblings, and peers) and reward related candidate gene polymorphisms (<strong>OPRM1</strong> A118G, DRD2 TaqlA and DRD4 bp VNTR) in adolescents' responses to initial <b>smoking</b>.
+OPRM1	addiction	reward	24446757	We investigated the role of exposure to smoking (by parents, siblings, and peers) and <b>reward</b> related candidate gene polymorphisms (<strong>OPRM1</strong> A118G, DRD2 TaqlA and DRD4 bp VNTR) in adolescents' responses to initial smoking.
+OPRM1	drug	nicotine	24446757	Although preliminary, these findings suggest that exposure to environmental <b>smoking</b> and polymorphisms in the <strong>OPRM1</strong> and DRD2 gene may affect initial sensitivity to <b>nicotine</b>, an early phenotype of the risk of dependence.
+OPRM1	addiction	dependence	24446757	Although preliminary, these findings suggest that exposure to environmental smoking and polymorphisms in the <strong>OPRM1</strong> and DRD2 gene may affect initial sensitivity to nicotine, an early phenotype of the risk of <b>dependence</b>.
+OPRM1	drug	alcohol	24421289	Interactive effects of <strong>OPRM1</strong> and DAT1 genetic variation on subjective responses to <b>alcohol</b>.
+OPRM1	drug	alcohol	24421289	The A118G single nucleotide polymorphism (SNP) of the mu opioid receptor (<strong>OPRM1</strong>) gene has been associated with subjective response to <b>alcohol</b>.
+OPRM1	drug	opioid	24421289	The A118G single nucleotide polymorphism (SNP) of the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene has been associated with subjective response to alcohol.
+OPRM1	drug	alcohol	24421289	Recently, the dopamine transporter (DAT1) variable number of tandem repeat (VNTR; SLC6A3) has been found to interact with the <strong>OPRM1</strong> A118G SNP in predicting neural and behavioral responses to <b>naltrexone</b> and to <b>alcohol</b>.
+OPRM1	drug	alcohol	24421289	This exploratory study examines the <strong>OPRM1</strong> × DAT1 interaction on subjective responses to <b>alcohol</b>.
+OPRM1	drug	alcohol	24421289	Following prospective genotyping for the <strong>OPRM1</strong> gene, 43 <b>alcohol</b> dependent individuals were randomized to two intravenous infusion sessions, one of <b>alcohol</b> (target BrAC = 0.06 g/dl) and one of saline.
+OPRM1	drug	alcohol	24421289	Analyses revealed significant <b>Alcohol</b> × <strong>OPRM1</strong> × DAT1 interactions for <b>alcohol</b> induced stimulation, vigor and positive mood as well as significant <b>Alcohol</b> × <strong>OPRM1</strong> × DAT1 × Time interactions for stimulation and positive mood.
+OPRM1	drug	alcohol	24421289	All <b>Alcohol</b> × <strong>OPRM1</strong> × DAT1 interactions remained significant when analyses were restricted to a subsample of Caucasian participants (n = 34); however, 4 way interactions did not reach statistical significance in this subsample.
+OPRM1	drug	alcohol	24421289	This study suggests that the contribution of <strong>OPRM1</strong> genotype to <b>alcohol</b> induced stimulation, vigor and positive mood is moderated by DAT1 genotype.
+OPRM1	drug	alcohol	24411804	This study tested whether subjective responses during <b>alcohol</b> administration predict neural responses to <b>alcohol</b> cues in the scanner and whether these neural responses differ between <strong>OPRM1</strong> genotypes.
+OPRM1	drug	alcohol	24411804	Laboratory assessments of <b>alcohol</b> high, liking, craving, and positive and negative reinforcement during <b>alcohol</b> administration were entered as predictors of neural response to the presentation of <b>alcohol</b> cues versus water cues in the scanner and further tested for <strong>OPRM1</strong> genotype moderation (whole brain cluster corrected at Z > 1.96, p < .05).
+OPRM1	addiction	relapse	24411804	Laboratory assessments of alcohol high, liking, <b>craving</b>, and positive and negative reinforcement during alcohol administration were entered as predictors of neural response to the presentation of alcohol cues versus water cues in the scanner and further tested for <strong>OPRM1</strong> genotype moderation (whole brain cluster corrected at Z > 1.96, p < .05).
+OPRM1	addiction	reward	24411804	Laboratory assessments of alcohol high, liking, craving, and positive and negative <b>reinforcement</b> during alcohol administration were entered as predictors of neural response to the presentation of alcohol cues versus water cues in the scanner and further tested for <strong>OPRM1</strong> genotype moderation (whole brain cluster corrected at Z > 1.96, p < .05).
+OPRM1	drug	alcohol	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and <strong>OPRM1</strong> (rs1799971) genes to identify that SNPs that were more directly associated with <b>alcohol</b>, tobacco and/or cannabis consumption in young individuals (n = 91).
+OPRM1	drug	cannabinoid	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and <strong>OPRM1</strong> (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, tobacco and/or <b>cannabis</b> consumption in young individuals (n = 91).
+OPRM1	drug	nicotine	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and <strong>OPRM1</strong> (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, <b>tobacco</b> and/or cannabis consumption in young individuals (n = 91).
+OPRM1	drug	opioid	24368617	Genetic polymorphisms in the coding or promoter regions of the Mu <b>Opioid</b> Receptor (<strong>OPRM1</strong>), Corticotropin Releasing Hormone (CRH), Monoamine Oxidase A (MAOA), Dopamine D4 Receptor (DRD4), and Serotonin Transporter (SLC6A4) genes have been shown to be functionally similar in humans and rhesus macaques and have been demonstrated to contribute to individual differences in aggression.
+OPRM1	addiction	reward	24273683	We also genotyped the patient using a <b>reward</b> gene panel including (9 genes 18 alleles): DRD 2,3,4; MOA A; COMT; DAT1; 5HTTLLR; <strong>OPRM1</strong>; and GABRA3.
+OPRM1	drug	alcohol	24220019	Genetic analyses of the level of response to <b>alcohol</b>, particularly of the functional <strong>OPRM1</strong> A118G polymorphism and 5' and 3' functional polymorphisms in SLC6A4, are beginning to provide insights into the etiology of <b>alcoholism</b> and also genotype stratified subgroup responses to <b>naltrexone</b> and SSRIs/ondansetron respectively.
+OPRM1	drug	opioid	24217691	When the mu <b>opioid</b> receptor gene (<strong>Oprm1</strong>), located on chromosome 10 in the QTL region, was added to this top ranked transcription factor network, it became a hub in the network.
+OPRM1	drug	amphetamine	24217691	These data are consistent with previously published findings of opioid response and intake differences between the MADR lines and suggest that <strong>Oprm1</strong>, or a gene that impacts activity of the opioid system, plays a role in genetically determined differences in <b>methamphetamine</b> intake.
+OPRM1	drug	opioid	24217691	These data are consistent with previously published findings of <b>opioid</b> response and intake differences between the MADR lines and suggest that <strong>Oprm1</strong>, or a gene that impacts activity of the <b>opioid</b> system, plays a role in genetically determined differences in methamphetamine intake.
+OPRM1	drug	opioid	24201053	The <strong>OPRM1</strong> gene has been a target of interest in a large number of pharmacogenetic studies due to its genetic and structural variation, as well as the role of <b>opioid</b> receptors in a variety of disorders.
+OPRM1	drug	alcohol	24201053	The mu opioid receptor (MOR), encoded by <strong>OPRM1</strong>, naturally regulates the analgesic response to pain and also controls the rewarding effects of many drugs of abuse, including opioids, nicotine, and <b>alcohol</b>.
+OPRM1	drug	nicotine	24201053	The mu opioid receptor (MOR), encoded by <strong>OPRM1</strong>, naturally regulates the analgesic response to pain and also controls the rewarding effects of many drugs of abuse, including opioids, <b>nicotine</b>, and alcohol.
+OPRM1	drug	opioid	24201053	The mu <b>opioid</b> receptor (MOR), encoded by <strong>OPRM1</strong>, naturally regulates the analgesic response to pain and also controls the rewarding effects of many drugs of abuse, including <b>opioids</b>, nicotine, and alcohol.
+OPRM1	addiction	dependence	24201053	Genetic variants in <strong>OPRM1</strong>, particularly the non synonymous polymorphism A118G, have been repeatedly associated with the efficacy of treatments for pain and various types of <b>dependence</b>.
+OPRM1	addiction	addiction	24201053	This review focuses on the current understanding of the pharmacogenetic impact of <strong>OPRM1</strong>, primarily with regard to the treatment of pain and <b>addiction</b>.
+OPRM1	addiction	dependence	24167729	We performed a review of the efficacy of pharmacogenomic markers and their abilities to predict adverse events, <b>dependence</b>, and associated economic costs, focusing on two genes: <strong>OPRM1</strong> and CYP2D6.
+OPRM1	drug	opioid	24086514	Association of polymorphisms in pharmacogenetic candidate genes (OPRD1, GAL, ABCB1, <strong>OPRM1</strong>) with <b>opioid</b> dependence in European population: a case control study.
+OPRM1	addiction	dependence	24086514	Association of polymorphisms in pharmacogenetic candidate genes (OPRD1, GAL, ABCB1, <strong>OPRM1</strong>) with opioid <b>dependence</b> in European population: a case control study.
+OPRM1	drug	opioid	24086514	Moreover, an association of the ATP binding cassette transporter 1 (ABCB1) variant rs1045642 and the Mu <b>Opioid</b> receptor (<strong>OPRM1</strong>) variant rs9479757 with <b>opioid</b> addiction was observed.
+OPRM1	addiction	addiction	24086514	Moreover, an association of the ATP binding cassette transporter 1 (ABCB1) variant rs1045642 and the Mu Opioid receptor (<strong>OPRM1</strong>) variant rs9479757 with opioid <b>addiction</b> was observed.
+OPRM1	drug	opioid	24048098	At completion of behavioral testing, mu <b>opioid</b> receptor (<strong>OPRM1</strong>), FosB, cFos, and dopamine receptor mRNA expression was measured in the nucleus accumbens as well as <strong>OPRM1</strong> and corticotropin releasing hormone mRNA in the paraventricular nucleus.
+OPRM1	drug	opioid	24048098	Also following the <b>morphine</b> challenge, significantly higher levels of <strong>OPRM1</strong> in the nucleus accumbens were observed in WIN F1 animals.
+OPRM1	drug	alcohol	24035285	In this study, single nucleotide polymorphisms within the genes for mu (<strong>OPRM1</strong>) and kappa (OPRK1) opioid receptors and precursors of their ligands   proopiomelanocortin (POMC), coding for beta endorphin and prodynorphin (PDYN) coding for dynorphins, were analyzed in a case control study that included 354 male <b>alcohol</b> dependent and 357 male control subjects from Croatian population.
+OPRM1	drug	opioid	24035285	In this study, single nucleotide polymorphisms within the genes for mu (<strong>OPRM1</strong>) and kappa (OPRK1) <b>opioid</b> receptors and precursors of their ligands   proopiomelanocortin (POMC), coding for beta endorphin and prodynorphin (PDYN) coding for dynorphins, were analyzed in a case control study that included 354 male alcohol dependent and 357 male control subjects from Croatian population.
+OPRM1	drug	alcohol	24035285	Thus, the data obtained suggest no association of the selected polymorphisms of the genes <strong>OPRM1</strong>/POMC and OPRK1/PDYN with <b>alcoholism</b> in Croatian population.
+OPRM1	drug	alcohol	23934621	The effects of GSK1521498 on hedonic and consummatory responses to <b>alcohol</b> and the attentional processing of <b>alcohol</b> related stimuli, and their modulation by the <strong>OPRM1</strong> A118G polymorphism were also explored.
+OPRM1	addiction	reward	23934621	The effects of GSK1521498 on <b>hedonic</b> and consummatory responses to alcohol and the attentional processing of alcohol related stimuli, and their modulation by the <strong>OPRM1</strong> A118G polymorphism were also explored.
+OPRM1	drug	opioid	23911290	Activation of <strong>OPRM1</strong> leads to internalization of a cold sensor TRPM8, which can be reversed by a follow up treatment with the inverse OPRM agonist <b>naloxone</b>.
+OPRM1	drug	opioid	23911290	Activation of <strong>OPRM1</strong> leads to internalization of a cold sensor TRPM8, which can be reversed by a follow up treatment with the inverse <strong>OPRM</strong> agonist <b>naloxone</b>.
+OPRM1	drug	alcohol	23876228	Initial evidence that <strong>OPRM1</strong> genotype moderates ventral and dorsal striatum functional connectivity during <b>alcohol</b> cues.
+OPRM1	drug	alcohol	23876228	This initial study examines dorsal and ventral striatal functional connectivity during <b>alcohol</b> cue processing as a function of the A118G single nucleotide polymorphism of the mu opioid receptor (<strong>OPRM1</strong>) gene.
+OPRM1	drug	opioid	23876228	This initial study examines dorsal and ventral striatal functional connectivity during alcohol cue processing as a function of the A118G single nucleotide polymorphism of the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene.
+OPRM1	drug	alcohol	23876228	Compared to A allele homozygotes, G allele carriers of the <strong>OPRM1</strong> gene showed (i) greater activation of the insula and orbitofrontal cortex and (ii) stronger negative fronto striatal functional connectivity for both ventral and dorsal striatal seed regions during processing of <b>alcohol</b> versus water cues.
+OPRM1	drug	opioid	23803057	Gene polymorphisms of <strong>OPRM1</strong> A118G and ABCB1 C3435T may influence <b>opioid</b> requirements in Chinese patients with cancer pain.
+OPRM1	drug	opioid	23803057	Polymorphisms of <strong>OPRM1</strong> A118G and ABCB1 C3435T have been suggested to contribute to inter individual variability regarding pain sensitivity, <b>opioid</b> usage, tolerance and dependence and incidence of adverse effects in patients with chronic pain.
+OPRM1	addiction	dependence	23803057	Polymorphisms of <strong>OPRM1</strong> A118G and ABCB1 C3435T have been suggested to contribute to inter individual variability regarding pain sensitivity, opioid usage, tolerance and <b>dependence</b> and incidence of adverse effects in patients with chronic pain.
+OPRM1	drug	alcohol	23739600	Genetic variation in the µ opioid receptor (<strong>OPRM1</strong>) and the serotonin transporter (5 HTTLPR) appear to be associated with treatment outcomes for <b>naltrexone</b> and ondansetron, respectively.
+OPRM1	drug	opioid	23739600	Genetic variation in the µ <b>opioid</b> receptor (<strong>OPRM1</strong>) and the serotonin transporter (5 HTTLPR) appear to be associated with treatment outcomes for naltrexone and ondansetron, respectively.
+OPRM1	drug	alcohol	23739600	Pharmacogenetic matching of <b>naltrexone</b> in <b>alcohol</b> dependent carriers of the <strong>OPRM1</strong> G allele currently seems most promising.
+OPRM1	drug	alcohol	23729673	μ Opioid receptor gene (<strong>OPRM1</strong>) polymorphism A118G: lack of association in Finnish populations with <b>alcohol</b> dependence or <b>alcohol</b> consumption.
+OPRM1	drug	opioid	23729673	μ <b>Opioid</b> receptor gene (<strong>OPRM1</strong>) polymorphism A118G: lack of association in Finnish populations with alcohol dependence or alcohol consumption.
+OPRM1	addiction	dependence	23729673	μ Opioid receptor gene (<strong>OPRM1</strong>) polymorphism A118G: lack of association in Finnish populations with alcohol <b>dependence</b> or alcohol consumption.
+OPRM1	drug	alcohol	23729673	The molecular epidemiological studies on the association of the opioid receptor µ 1 (<strong>OPRM1</strong>) polymorphism A118G (Asn40Asp, rs1799971) and <b>alcohol</b> use disorders have given conflicting results.
+OPRM1	drug	opioid	23729673	The molecular epidemiological studies on the association of the <b>opioid</b> receptor µ 1 (<strong>OPRM1</strong>) polymorphism A118G (Asn40Asp, rs1799971) and alcohol use disorders have given conflicting results.
+OPRM1	drug	alcohol	23729673	The association between the <strong>OPRM1</strong> A118G (Asn40Asp, rs1799971) polymorphism and <b>alcohol</b> use disorders and <b>alcohol</b> consumption was analyzed using three different population based samples: (a) a Finnish cohort study, Health 2000, with 503 participants having a DSM IV diagnosis for <b>alcohol</b> dependence and/or <b>alcohol</b> abuse and 506 age  and sex matched controls; (b) a Finnish cohort study, FINRISK (n = 2360) and (c) the Helsinki Birth Cohort Study (n = 1384).
+OPRM1	addiction	dependence	23729673	The association between the <strong>OPRM1</strong> A118G (Asn40Asp, rs1799971) polymorphism and alcohol use disorders and alcohol consumption was analyzed using three different population based samples: (a) a Finnish cohort study, Health 2000, with 503 participants having a DSM IV diagnosis for alcohol <b>dependence</b> and/or alcohol abuse and 506 age  and sex matched controls; (b) a Finnish cohort study, FINRISK (n = 2360) and (c) the Helsinki Birth Cohort Study (n = 1384).
+OPRM1	drug	opioid	23726045	A common variant in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) has been associated with response to <b>opioid</b> analgesia.
+OPRM1	drug	opioid	23726045	These results extend our previous finding on the association of higher self reported pain and <b>morphine</b> use for acute postoperative pain with <strong>OPRM1</strong> 118G to patients who had total hysterectomy under general anesthesia.
+OPRM1	drug	opioid	23702428	ELK1 transcription factor linked to dysregulated striatal mu <b>opioid</b> receptor signaling network and <strong>OPRM1</strong> polymorphism in human <b>heroin</b> abusers.
+OPRM1	drug	opioid	23702428	Striatal ELK1 in <b>heroin</b> abusers associated with the polymorphism rs2075572 in <strong>OPRM1</strong> in a genotype dose dependent manner and correlated with documented history of <b>heroin</b> use, an effect reproduced in an animal model that emphasizes a direct relationship between repeated <b>heroin</b> exposure and ELK1 dysregulation.
+OPRM1	drug	opioid	23702428	ELK1 is a potential key transcriptional regulatory factor in striatal disturbances associated with <b>heroin</b> abuse and relevant to genetic mutation of <strong>OPRM1</strong>.
+OPRM1	drug	opioid	23670889	Other genes such as the leptin receptor gene (LEPR) and mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) that affect appetite and pleasure centers in the brain may also influence food addiction and obesity.
+OPRM1	addiction	addiction	23670889	Other genes such as the leptin receptor gene (LEPR) and mu opioid receptor gene (<strong>OPRM1</strong>) that affect appetite and pleasure centers in the brain may also influence food <b>addiction</b> and obesity.
+OPRM1	drug	opioid	23658070	Future studies that include different single nucleotide polymorphisms of the <strong>OPRM1</strong> gene as well as larger populations will need to be conducted to further elucidate the pharmacogenetic role of the endogenous <b>opioid</b> system in anxiety disorders.
+OPRM1	drug	opioid	23651028	<strong>OPRM1</strong> rs1799971 polymorphism and <b>opioid</b> dependence: evidence from a meta analysis.
+OPRM1	addiction	dependence	23651028	<strong>OPRM1</strong> rs1799971 polymorphism and opioid <b>dependence</b>: evidence from a meta analysis.
+OPRM1	drug	opioid	23651028	The <strong>OPRM1</strong> gene encodes the µ <b>opioid</b> receptor, which is the primary site of action of most <b>opioids</b>.
+OPRM1	drug	opioid	23651028	Several studies and three meta analyses have examined a possible link between the exonic <strong>OPRM1</strong> A118G (rs1799971) polymorphism and <b>opioid</b> dependence; however, results have been inconclusive.
+OPRM1	addiction	dependence	23651028	Several studies and three meta analyses have examined a possible link between the exonic <strong>OPRM1</strong> A118G (rs1799971) polymorphism and opioid <b>dependence</b>; however, results have been inconclusive.
+OPRM1	drug	opioid	23651028	Thirteen studies (n = 9385), comprising 4601 <b>opioid</b> dependents and 4784 controls, which evaluated association of the <strong>OPRM1</strong> rs1799971 polymorphism with susceptibility to <b>opioids</b>, were included in this study.
+OPRM1	drug	opioid	23651028	The nonsynonymous <strong>OPRM1</strong> rs1799971 might be a risk factor for addiction to <b>opioids</b> or <b>heroin</b> in an Asian population.
+OPRM1	addiction	addiction	23651028	The nonsynonymous <strong>OPRM1</strong> rs1799971 might be a risk factor for <b>addiction</b> to opioids or heroin in an Asian population.
+OPRM1	drug	opioid	23651024	Out of the 110 variants analyzed, 12 SNPs (in BDNF, NTRK2, <strong>OPRM1</strong>, DRD2 and ANKK1) were associated with <b>methadone</b> dose (nominal p < 0.05).
+OPRM1	drug	opioid	23632726	Single nucleotide polymorphisms (SNPs) in the μ <b>opioid</b> receptor (<strong>OPRM1</strong>), multidrug resistance (ABCB1), and catechol o methyltransferase (COMT) genes are associated with risk for <b>opioid</b> addiction in adults.
+OPRM1	addiction	addiction	23632726	Single nucleotide polymorphisms (SNPs) in the μ opioid receptor (<strong>OPRM1</strong>), multidrug resistance (ABCB1), and catechol o methyltransferase (COMT) genes are associated with risk for opioid <b>addiction</b> in adults.
+OPRM1	drug	opioid	23566343	In this study, we aimed to determine whether the catechol O methyl transferase (COMT) and <b>opioid</b> receptor μ 1 (<strong>OPRM1</strong>) common functional polymorphisms rs4680 and rs1799971 were associated with the incidence, intensity, or duration of CPP in patients after lower abdominal surgery.
+OPRM1	addiction	reward	23566343	In this study, we aimed to determine whether the catechol O methyl transferase (COMT) and opioid receptor μ 1 (<strong>OPRM1</strong>) common functional polymorphisms rs4680 and rs1799971 were associated with the incidence, intensity, or duration of <b>CPP</b> in patients after lower abdominal surgery.
+OPRM1	addiction	reward	23566343	For <strong>OPRM1</strong> rs1799971, only <b>CPP</b> patients carrying at least one copy of the G allele had higher pain intensity than A118A carriers (p=0.02).
+OPRM1	addiction	reward	23566343	No combined effect of COMT/<strong>OPRM1</strong> polymorphisms on <b>CPP</b> phenotypes was observed.
+OPRM1	addiction	reward	23566343	<strong>OPRM1</strong> genotype influences <b>CPP</b> following lower abdominal surgery.
+OPRM1	drug	alcohol	23543091	A single nucleotide polymorphism (SNP) within the <strong>OPRM1</strong> gene, A118G, leading to an amino acid change (Asn40Asp) in the extracellular portion of the receptor, has been implicated in <b>alcoholism</b> as well as in drug addiction, pain sensitivity and stress response, and in animal and human studies relates to the <b>alcohol</b> dependent phenotype as well as to the treatment response to the µ opioid antagonist <b>naltrexone</b>.
+OPRM1	drug	opioid	23543091	A single nucleotide polymorphism (SNP) within the <strong>OPRM1</strong> gene, A118G, leading to an amino acid change (Asn40Asp) in the extracellular portion of the receptor, has been implicated in alcoholism as well as in drug addiction, pain sensitivity and stress response, and in animal and human studies relates to the alcohol dependent phenotype as well as to the treatment response to the µ <b>opioid</b> antagonist naltrexone.
+OPRM1	addiction	addiction	23543091	A single nucleotide polymorphism (SNP) within the <strong>OPRM1</strong> gene, A118G, leading to an amino acid change (Asn40Asp) in the extracellular portion of the receptor, has been implicated in alcoholism as well as in drug <b>addiction</b>, pain sensitivity and stress response, and in animal and human studies relates to the alcohol dependent phenotype as well as to the treatment response to the µ opioid antagonist naltrexone.
+OPRM1	drug	cocaine	23454283	Low frequency genetic variants in the μ opioid receptor (<strong>OPRM1</strong>) affect risk for addiction to heroin and <b>cocaine</b>.
+OPRM1	drug	opioid	23454283	Low frequency genetic variants in the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) affect risk for addiction to <b>heroin</b> and cocaine.
+OPRM1	addiction	addiction	23454283	Low frequency genetic variants in the μ opioid receptor (<strong>OPRM1</strong>) affect risk for <b>addiction</b> to heroin and cocaine.
+OPRM1	addiction	addiction	23454283	Numerous genetic studies have sought to identify common genetic variation in the gene encoding MOR (<strong>OPRM1</strong>) that affects risk for drug <b>addiction</b>.
+OPRM1	addiction	addiction	23454283	The purpose of this study was to examine the contribution of rare coding variants in <strong>OPRM1</strong> to the risk for <b>addiction</b>.
+OPRM1	addiction	addiction	23454283	This study suggests a potential role for rare <strong>OPRM1</strong> variants in <b>addiction</b> disorders and highlights an area worthy of future study.
+OPRM1	drug	opioid	23443796	To investigate whether A118G single nucleotide polymorphisms of the µ <b>opioid</b> receptor (<strong>OPRM1</strong>) affects epidural patient controlled analgesia with <b>fentanyl</b> after caesarean section.
+OPRM1	drug	opioid	23405975	The mu <b>opioid</b> receptor (<strong>OPRM1</strong>) A118G polymorphism has been associated with decreased analgesic effects of <b>opioids</b> and predisposition to addiction.
+OPRM1	addiction	addiction	23405975	The mu opioid receptor (<strong>OPRM1</strong>) A118G polymorphism has been associated with decreased analgesic effects of opioids and predisposition to <b>addiction</b>.
+OPRM1	addiction	dependence	23377636	Other candidate genes associated with substance <b>dependence</b> phenotypes in Native Americans include <strong>OPRM1</strong>, CRN1, COMT, GABRA2, MAOA, and HTR3 B.
+OPRM1	drug	opioid	23337944	<strong><b>Opioid</b> receptor mu 1</strong> gene, fat intake and obesity in adolescence.
+OPRM1	drug	opioid	23337944	GWAS identified a locus of fat intake in the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>, rs2281617, P=5.2 × 10( 6)), which encodes a receptor expressed in the brain reward system and shown previously to modulate fat preference in animals.
+OPRM1	addiction	reward	23337944	GWAS identified a locus of fat intake in the μ opioid receptor gene (<strong>OPRM1</strong>, rs2281617, P=5.2 × 10( 6)), which encodes a receptor expressed in the brain <b>reward</b> system and shown previously to modulate fat preference in animals.
+OPRM1	drug	opioid	23318993	Genetic variations in the human mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) mediate individual differences in response to pain and opiate addiction.
+OPRM1	addiction	addiction	23318993	Genetic variations in the human mu opioid receptor gene (<strong>OPRM1</strong>) mediate individual differences in response to pain and opiate <b>addiction</b>.
+OPRM1	drug	alcohol	24729984	Variation in Mu Opioid Receptor Gene (<strong>OPRM1</strong>) as a Moderator of <b>Naltrexone</b> Treatment to Reduce Heavy Drinking in a High Functioning Cohort.
+OPRM1	drug	opioid	24729984	Variation in Mu <b>Opioid</b> Receptor Gene (<strong>OPRM1</strong>) as a Moderator of Naltrexone Treatment to Reduce Heavy Drinking in a High Functioning Cohort.
+OPRM1	drug	alcohol	24729984	Recent studies have examined the utility of a functional A118G single nucleotide polymorphism (SNP) of the mu opioid receptor gene (<strong>OPRM1</strong>) as a predictor of <b>naltrexone</b> treatment response.
+OPRM1	drug	opioid	24729984	Recent studies have examined the utility of a functional A118G single nucleotide polymorphism (SNP) of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) as a predictor of naltrexone treatment response.
+OPRM1	drug	alcohol	24729984	These results are consistent with a modest moderating effect of the <strong>OPRM1</strong> 118G allele on the reduction of heavy drinking by <b>naltrexone</b> treatment.
+OPRM1	drug	alcohol	23254216	The A118G (rs 1799971) polymorphism in the mu opioid receptor gene (<strong>OPRM1</strong>) has been reported to be associated with <b>alcohol</b> addiction.
+OPRM1	drug	opioid	23254216	The A118G (rs 1799971) polymorphism in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) has been reported to be associated with alcohol addiction.
+OPRM1	addiction	addiction	23254216	The A118G (rs 1799971) polymorphism in the mu opioid receptor gene (<strong>OPRM1</strong>) has been reported to be associated with alcohol <b>addiction</b>.
+OPRM1	drug	opioid	23240858	A secondary aim of this study was to test the moderating effect of a functional polymorphism (A118G) of the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene.
+OPRM1	drug	alcohol	23240858	Twenty individuals with <b>alcohol</b> dependence (six females; 90% Caucasian; mean age = 29.4) who were prospectively genotyped on the <strong>OPRM1</strong> gene underwent blood oxygen level dependent functional magnetic resonance imaging while performing a Stop Signal Task.
+OPRM1	addiction	dependence	23240858	Twenty individuals with alcohol <b>dependence</b> (six females; 90% Caucasian; mean age = 29.4) who were prospectively genotyped on the <strong>OPRM1</strong> gene underwent blood oxygen level dependent functional magnetic resonance imaging while performing a Stop Signal Task.
+OPRM1	drug	alcohol	23240711	Subjective response to <b>alcohol</b> among <b>alcohol</b> dependent individuals: effects of the μ opioid receptor (<strong>OPRM1</strong>) gene and <b>alcoholism</b> severity.
+OPRM1	drug	opioid	23240711	Subjective response to alcohol among alcohol dependent individuals: effects of the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene and alcoholism severity.
+OPRM1	drug	alcohol	23240711	The A118G single nucleotide polymorphism (SNP) of the mu opioid receptor (<strong>OPRM1</strong>) gene has been previously associated with subjective response to <b>alcohol</b> in heavy drinkers.
+OPRM1	drug	opioid	23240711	The A118G single nucleotide polymorphism (SNP) of the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene has been previously associated with subjective response to alcohol in heavy drinkers.
+OPRM1	drug	alcohol	23240711	This study seeks to extend the literature by examining the effect of <strong>OPRM1</strong> genotype on responses to <b>alcohol</b> in a sample of <b>alcohol</b> dependent individuals.
+OPRM1	drug	alcohol	23240711	These results support the hypothesis that <strong>OPRM1</strong> genotype moderates the hedonic effects of <b>alcohol</b>, but not the sedative and unpleasant effects of <b>alcohol</b>, in a sample of <b>alcohol</b> dependent patients.
+OPRM1	addiction	reward	23240711	These results support the hypothesis that <strong>OPRM1</strong> genotype moderates the <b>hedonic</b> effects of alcohol, but not the sedative and unpleasant effects of alcohol, in a sample of alcohol dependent patients.
+OPRM1	drug	opioid	23226066	Mu <b>opioid</b> receptor (<strong>OPRM1</strong>) as a predictor of treatment outcome in opiate dependent individuals of Arab descent.
+OPRM1	drug	opioid	23226066	A number of research studies on the genetics of opiate dependence have focused on the μ <b>opioid</b> receptor (<strong>OPRM1</strong>), which is a primary target for opiates.
+OPRM1	addiction	dependence	23226066	A number of research studies on the genetics of opiate <b>dependence</b> have focused on the μ opioid receptor (<strong>OPRM1</strong>), which is a primary target for opiates.
+OPRM1	addiction	dependence	23226066	This study is the first report of an association between the <strong>OPRM1</strong> G 172T and G 1510A polymorphisms and treatment response for opiate <b>dependence</b>.
+OPRM1	drug	nicotine	23177301	In line with genetic and pharmacological studies suggesting that neurotransmitter pathways play a role in <b>nicotine</b> dependence, research was conducted in connection with 4 genetic polymorphisms: <strong>OPRM1</strong>, TPH1, ADRA2A and HTR1B.
+OPRM1	addiction	dependence	23177301	In line with genetic and pharmacological studies suggesting that neurotransmitter pathways play a role in nicotine <b>dependence</b>, research was conducted in connection with 4 genetic polymorphisms: <strong>OPRM1</strong>, TPH1, ADRA2A and HTR1B.
+OPRM1	drug	alcohol	23032071	Interacting effects of <b>naltrexone</b> and <strong>OPRM1</strong> and DAT1 variation on the neural response to <b>alcohol</b> cues.
+OPRM1	drug	alcohol	23032071	Variation at a single nucleotide polymorphism in the μ opioid receptor gene (<strong>OPRM1</strong>), A118G (Asn40Asp), may moderate <b>naltrexone</b> (NTX) effects in <b>alcohol</b> dependence.
+OPRM1	drug	opioid	23032071	Variation at a single nucleotide polymorphism in the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>), A118G (Asn40Asp), may moderate naltrexone (NTX) effects in alcohol dependence.
+OPRM1	addiction	dependence	23032071	Variation at a single nucleotide polymorphism in the μ opioid receptor gene (<strong>OPRM1</strong>), A118G (Asn40Asp), may moderate naltrexone (NTX) effects in alcohol <b>dependence</b>.
+OPRM1	addiction	reward	23032071	Polymorphic variation in <strong>OPRM1</strong> and DAT1 should be considered in future studies of NTX, particularly regarding its effects on <b>reward</b> processing.
+OPRM1	drug	alcohol	22954510	Pharmacogenetic effects have been reported such that allelic variation at the gene encoding the mu opioid receptor (<strong>OPRM1</strong>, rs1799971) predicts <b>naltrexone</b> induced blunting of the positively reinforcing effects of <b>alcohol</b>.
+OPRM1	drug	opioid	22954510	Pharmacogenetic effects have been reported such that allelic variation at the gene encoding the mu <b>opioid</b> receptor (<strong>OPRM1</strong>, rs1799971) predicts naltrexone induced blunting of the positively reinforcing effects of alcohol.
+OPRM1	addiction	reward	22954510	Pharmacogenetic effects have been reported such that allelic variation at the gene encoding the mu opioid receptor (<strong>OPRM1</strong>, rs1799971) predicts naltrexone induced blunting of the positively <b>reinforcing</b> effects of alcohol.
+OPRM1	drug	alcohol	22914673	Hypermethylation of <strong>OPRM1</strong> promoter region in European Americans with <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	22914673	Hypermethylation of <strong>OPRM1</strong> promoter region in European Americans with alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	22914673	We hypothesized that altered DNA methylation in the μ opioid receptor gene (<strong>OPRM1</strong>) might influence the vulnerability to <b>alcohol</b> dependence (AD).
+OPRM1	drug	opioid	22914673	We hypothesized that altered DNA methylation in the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) might influence the vulnerability to alcohol dependence (AD).
+OPRM1	addiction	dependence	22914673	We hypothesized that altered DNA methylation in the μ opioid receptor gene (<strong>OPRM1</strong>) might influence the vulnerability to alcohol <b>dependence</b> (AD).
+OPRM1	addiction	intoxication	22914673	A multivariate analysis of covariance was conducted to analyze AD associated methylation changes in the <strong>OPRM1</strong> promoter region, using days of <b>intoxication</b> in the past 30 days, sex, age, ancestry proportion and childhood adversity (CA) as covariates.
+OPRM1	addiction	dependence	22914673	Our findings suggest that <strong>OPRM1</strong> promoter hypermethylation may increase the risk for AD and other substance <b>dependence</b> disorders.
+OPRM1	drug	cocaine	22882391	Among single nucleotide polymorphism markers in 13 candidate genes examined for association with <b>cocaine</b> cue reactivity, two were statistically significant: GABRA2 (coding for GABA A receptor alpha 2 subunit; rs11503014, nominal p= .001) and <strong>OPRM1</strong> (coding for mu opioid receptor; rs2236256, nominal p= .03).
+OPRM1	drug	opioid	22882391	Among single nucleotide polymorphism markers in 13 candidate genes examined for association with cocaine cue reactivity, two were statistically significant: GABRA2 (coding for GABA A receptor alpha 2 subunit; rs11503014, nominal p= .001) and <strong>OPRM1</strong> (coding for mu <b>opioid</b> receptor; rs2236256, nominal p= .03).
+OPRM1	drug	cocaine	22882391	These pilot results suggest that <b>cocaine</b> craving shows variability among <b>cocaine</b> dependent subjects, and that GABRA2 and <strong>OPRM1</strong> polymorphisms have differential influences on <b>cocaine</b> cue reactivity, warranting studies in future research.
+OPRM1	addiction	relapse	22882391	These pilot results suggest that cocaine <b>craving</b> shows variability among cocaine dependent subjects, and that GABRA2 and <strong>OPRM1</strong> polymorphisms have differential influences on cocaine cue reactivity, warranting studies in future research.
+OPRM1	drug	alcohol	22862850	The A118G single nucleotide polymorphism (SNP) of the human μ opioid receptor (MOPR) gene (<strong>OPRM1</strong>) was associated with heightened dopamine release by <b>alcohol</b> intake, better treatment outcome for nicotine and <b>alcohol</b> addiction, and reduced analgesic responses to morphine.
+OPRM1	drug	nicotine	22862850	The A118G single nucleotide polymorphism (SNP) of the human μ opioid receptor (MOPR) gene (<strong>OPRM1</strong>) was associated with heightened dopamine release by alcohol intake, better treatment outcome for <b>nicotine</b> and alcohol addiction, and reduced analgesic responses to morphine.
+OPRM1	drug	opioid	22862850	The A118G single nucleotide polymorphism (SNP) of the human μ <b>opioid</b> receptor (MOPR) gene (<strong>OPRM1</strong>) was associated with heightened dopamine release by alcohol intake, better treatment outcome for nicotine and alcohol addiction, and reduced analgesic responses to <b>morphine</b>.
+OPRM1	addiction	addiction	22862850	The A118G single nucleotide polymorphism (SNP) of the human μ opioid receptor (MOPR) gene (<strong>OPRM1</strong>) was associated with heightened dopamine release by alcohol intake, better treatment outcome for nicotine and alcohol <b>addiction</b>, and reduced analgesic responses to morphine.
+OPRM1	drug	opioid	22841130	One hundred seven <b>methadone</b> maintenance treatment patients, 36 having an ADHD diagnosis, 176 adult patients with ADHD without SUDs, and 500 healthy controls were genotyped for variants in the DRD4 (exon 3 VNTR), DRD5 (upstream VNTR), HTR1B (rs6296), DBH (rs2519152), COMT (rs4680; Val158Met), and <strong>OPRM1</strong> (rs1799971; 118A>G) genes.
+OPRM1	drug	opioid	22790874	We trained rats to self administer <b>heroin</b> or saline for 9 10 days and then dissected the NAc, DS, and mPFC at different abstinence days and measured mRNA and protein levels of BDNF, TrkB, and MeCP2, as well as MOR mRNA (<strong>Oprm1</strong>).
+OPRM1	drug	opioid	22744787	Genetic variations at the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene locus have been associated with opiate addiction.
+OPRM1	addiction	addiction	22744787	Genetic variations at the μ opioid receptor (<strong>OPRM1</strong>) gene locus have been associated with opiate <b>addiction</b>.
+OPRM1	drug	opioid	22715342	In the current review, we examine a variety of mechanisms through which ncRNAs could regulate μ <b>opioid</b> receptor (<strong>OPRM1</strong>) activities and thereby contribute to the development of <b>opioid</b> addiction.
+OPRM1	addiction	addiction	22715342	In the current review, we examine a variety of mechanisms through which ncRNAs could regulate μ opioid receptor (<strong>OPRM1</strong>) activities and thereby contribute to the development of opioid <b>addiction</b>.
+OPRM1	drug	opioid	22715342	Using miR 23b as an example, we present the possible ways in which ncRNA mediated regulation of <strong>OPRM1</strong> expression could impact <b>opioid</b> addiction.
+OPRM1	addiction	addiction	22715342	Using miR 23b as an example, we present the possible ways in which ncRNA mediated regulation of <strong>OPRM1</strong> expression could impact opioid <b>addiction</b>.
+OPRM1	addiction	withdrawal	22682732	Influence of the <strong>OPRM1</strong> gene polymorphism upon children's degree of <b>withdrawal</b> and brain activation in response to facial expressions.
+OPRM1	drug	opioid	22682732	Genetic variation of the A118G polymorphism of the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) predicts individual sensitivity to social rejection and fMRI activation during simulated social rejection in adults, while data on these relationships during childhood are lacking.
+OPRM1	drug	nicotine	22676196	A systematic review of the A118G (Asn40Asp) variant of <strong>OPRM1</strong> in relation to <b>smoking</b> initiation, <b>nicotine</b> dependence and <b>smoking</b> cessation.
+OPRM1	addiction	dependence	22676196	A systematic review of the A118G (Asn40Asp) variant of <strong>OPRM1</strong> in relation to smoking initiation, nicotine <b>dependence</b> and smoking cessation.
+OPRM1	drug	nicotine	22676196	The A118G variant within the <strong>OPRM1</strong> gene has been most often examined in relation to <b>smoking</b>, yielding inconsistent findings.
+OPRM1	drug	nicotine	22676196	The aim of this review was to merge findings of <strong>OPRM1</strong> gene studies in relation to <b>smoking</b> behaviors and to elaborate on the underlying biological mechanism of the A118G variant.
+OPRM1	drug	alcohol	22640768	A few well validated, specific predictors such as <strong>OPRM1</strong>, ADH1B, ALDH2, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand <b>alcohol</b> related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in nicotine metabolism (CYP26), and, potentially, <b>naltrexone</b> treatment response (<strong>OPRM1</strong>).
+OPRM1	drug	nicotine	22640768	A few well validated, specific predictors such as <strong>OPRM1</strong>, ADH1B, ALDH2, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand alcohol related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in <b>nicotine</b> metabolism (CYP26), and, potentially, naltrexone treatment response (<strong>OPRM1</strong>).
+OPRM1	drug	alcohol	22587755	The best studied functional genetic variant relevant to <b>alcoholism</b> treatment is rs1799971, a single nucleotide polymorphism in exon 1 of the <strong>OPRM1</strong> gene that encodes the μ opioid receptor.
+OPRM1	drug	opioid	22587755	The best studied functional genetic variant relevant to alcoholism treatment is rs1799971, a single nucleotide polymorphism in exon 1 of the <strong>OPRM1</strong> gene that encodes the μ <b>opioid</b> receptor.
+OPRM1	drug	alcohol	22551036	<b>Naltrexone</b> modification of drinking effects in a subacute treatment and bar lab paradigm: influence of <strong>OPRM1</strong> and dopamine transporter (SLC6A3) genes.
+OPRM1	drug	alcohol	22551036	The opioid receptor (<strong>OPRM1</strong>) single nucleotide polymorphism (SNP) asn40asp has been shown to alter <b>alcohol</b> and <b>naltrexone</b> response in animals and humans.
+OPRM1	drug	opioid	22551036	The <b>opioid</b> receptor (<strong>OPRM1</strong>) single nucleotide polymorphism (SNP) asn40asp has been shown to alter alcohol and naltrexone response in animals and humans.
+OPRM1	drug	alcohol	22551036	This study investigated the effects of the <strong>OPRM1</strong> SNP and dopamine transporter (DAT) variable number of tandem repeat (VNTR) genetic differences on drinking, <b>alcohol</b> effects, and <b>naltrexone</b> response under controlled conditions in nontreatment seeking <b>alcoholics</b>.
+OPRM1	addiction	relapse	22551036	This study investigated the effects of the <strong>OPRM1</strong> SNP and dopamine transporter (DAT) variable number of tandem repeat (VNTR) genetic differences on drinking, alcohol effects, and naltrexone response under controlled conditions in nontreatment <b>seeking</b> alcoholics.
+OPRM1	drug	alcohol	22551036	Two hundred and sixty five nontreatment seeking individuals with <b>alcohol</b> dependence were genotyped a priori for the <strong>OPRM1</strong> asn40asp SNP and post hoc for DAT (SLC6A3) 9 and 10 VNTRs.
+OPRM1	addiction	dependence	22551036	Two hundred and sixty five nontreatment seeking individuals with alcohol <b>dependence</b> were genotyped a priori for the <strong>OPRM1</strong> asn40asp SNP and post hoc for DAT (SLC6A3) 9 and 10 VNTRs.
+OPRM1	addiction	relapse	22551036	Two hundred and sixty five nontreatment <b>seeking</b> individuals with alcohol dependence were genotyped a priori for the <strong>OPRM1</strong> asn40asp SNP and post hoc for DAT (SLC6A3) 9 and 10 VNTRs.
+OPRM1	drug	alcohol	22551036	There were no significant main effects of <b>naltrexone</b> or <strong>OPRM1</strong> genotype, or any medication by <strong>OPRM1</strong> interaction, on drinking variables.
+OPRM1	drug	alcohol	22551036	However, in individuals who had at least one DAT 9 VNTR, and who were also <strong>OPRM1</strong> asn40 homozygotes, <b>naltrexone</b> reduced drinks/d consumed under natural conditions (p = 0.006), but not in the bar lab.
+OPRM1	drug	alcohol	22551036	<strong>OPRM1</strong> asn40 homozygotes (p = 0.028) and DAT 9 VNTR carriers (p = 0.032) had more stimulation to <b>alcohol</b> after the priming drink.
+OPRM1	drug	alcohol	22551036	This study does not support a salient role for the <strong>OPRM1</strong> asp40 alone in predicting drinking or <b>naltrexone</b> effects.
+OPRM1	drug	alcohol	22551036	However, although exploratory and in need of replication, it introduces the possibility that epistasis between the <strong>OPRM1</strong> gene and DAT gene might need to be taken into account when examining differential genetic response to <b>alcohol</b> or medication treatment, especially in early stage <b>alcoholics</b>.
+OPRM1	drug	alcohol	22515274	Association of µ opioid receptor (<strong>OPRM1</strong>) gene polymorphism with response to <b>naltrexone</b> in <b>alcohol</b> dependence: a systematic review and meta analysis.
+OPRM1	drug	opioid	22515274	Association of µ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene polymorphism with response to naltrexone in alcohol dependence: a systematic review and meta analysis.
+OPRM1	addiction	dependence	22515274	Association of µ opioid receptor (<strong>OPRM1</strong>) gene polymorphism with response to naltrexone in alcohol <b>dependence</b>: a systematic review and meta analysis.
+OPRM1	drug	alcohol	22515274	In particular, the possession of the G allele of the A118G polymorphism of the µ opioid receptor gene (<strong>OPRM1</strong>) has been associated with a better response to <b>naltrexone</b>, although controversial results have been reported.
+OPRM1	drug	opioid	22515274	In particular, the possession of the G allele of the A118G polymorphism of the µ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) has been associated with a better response to naltrexone, although controversial results have been reported.
+OPRM1	drug	alcohol	22515274	We retrieved studies on the relationship between A118G polymorphism in <strong>OPRM1</strong> gene and response to treatment with <b>naltrexone</b> in patients with <b>alcohol</b> dependence by means of electronic database search.
+OPRM1	addiction	dependence	22515274	We retrieved studies on the relationship between A118G polymorphism in <strong>OPRM1</strong> gene and response to treatment with naltrexone in patients with alcohol <b>dependence</b> by means of electronic database search.
+OPRM1	drug	alcohol	22515274	Our results support the fact that the G allele of A118G polymorphism of <strong>OPRM1</strong> moderates the effect of <b>naltrexone</b> in patients with <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	22515274	Our results support the fact that the G allele of A118G polymorphism of <strong>OPRM1</strong> moderates the effect of naltrexone in patients with alcohol <b>dependence</b>.
+OPRM1	drug	nicotine	22509402	In combination with NRT patch, participants were informed that their doses of oral NRT were based either on their mu opioid receptor (<strong>OPRM1</strong>) genotype, or their <b>nicotine</b> dependence questionnaire score (phenotype).
+OPRM1	drug	opioid	22509402	In combination with NRT patch, participants were informed that their doses of oral NRT were based either on their mu <b>opioid</b> receptor (<strong>OPRM1</strong>) genotype, or their nicotine dependence questionnaire score (phenotype).
+OPRM1	addiction	dependence	22509402	In combination with NRT patch, participants were informed that their doses of oral NRT were based either on their mu opioid receptor (<strong>OPRM1</strong>) genotype, or their nicotine <b>dependence</b> questionnaire score (phenotype).
+OPRM1	drug	opioid	22500942	Genes encoding the <b>opioid</b> receptors (<strong>OPRM1</strong>, OPRD1 and OPRK1) are obvious candidates for involvement in risk for <b>heroin</b> dependence.
+OPRM1	addiction	dependence	22500942	Genes encoding the opioid receptors (<strong>OPRM1</strong>, OPRD1 and OPRK1) are obvious candidates for involvement in risk for heroin <b>dependence</b>.
+OPRM1	drug	opioid	22446386	Polymorphisms of the corticotropin releasing hormone binding protein (CRH BP) gene and of the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene were examined as moderators of this relationship.
+OPRM1	drug	alcohol	22436571	The effect of the <strong>OPRM1</strong> and DRD4 polymorphisms on the relation between attentional bias and <b>alcohol</b> use in adolescence and young adulthood.
+OPRM1	drug	alcohol	22436571	The effect of the <strong>OPRM1</strong> c.118A>G polymorphism, associated with liking and wanting, and the DRD4 VNTR polymorphism, related to wanting, on the relation between attentional bias and <b>alcohol</b> use was investigated.
+OPRM1	drug	alcohol	22436571	In Study 1, attentional bias was positively associated with adolescent <b>alcohol</b> use only for <strong>OPRM1</strong> G allele carriers.
+OPRM1	drug	alcohol	22429255	A significant <b>naltrexone</b> × <strong>OPRM1</strong> genotype interaction was observed for intensity of demand.
+OPRM1	drug	opioid	22406240	<b>Methadone</b>, a synthetic racemic <b>opioid</b> that primarily works as a μ <b>opioid</b> receptor (<strong>OPRM1</strong>) agonist, is commonly used for the treatment of <b>heroin</b> addiction.
+OPRM1	addiction	addiction	22406240	Methadone, a synthetic racemic opioid that primarily works as a μ opioid receptor (<strong>OPRM1</strong>) agonist, is commonly used for the treatment of heroin <b>addiction</b>.
+OPRM1	drug	alcohol	22406240	Genetic association studies have reported that the <strong>OPRM1</strong> gene is involved in the physiology of heroin and <b>alcohol</b> addiction.
+OPRM1	drug	opioid	22406240	Genetic association studies have reported that the <strong>OPRM1</strong> gene is involved in the physiology of <b>heroin</b> and alcohol addiction.
+OPRM1	addiction	addiction	22406240	Genetic association studies have reported that the <strong>OPRM1</strong> gene is involved in the physiology of heroin and alcohol <b>addiction</b>.
+OPRM1	drug	opioid	22406240	Our current study is designed to test the hypothesis that genetic polymorphisms in the <strong>OPRM1</strong> gene region are associated with <b>methadone</b> dosage, plasma concentrations, treatment responses, adverse reactions and withdrawal symptoms in a <b>methadone</b> maintenance treatment (MMT) cohort from Taiwan.
+OPRM1	addiction	withdrawal	22406240	Our current study is designed to test the hypothesis that genetic polymorphisms in the <strong>OPRM1</strong> gene region are associated with methadone dosage, plasma concentrations, treatment responses, adverse reactions and <b>withdrawal</b> symptoms in a methadone maintenance treatment (MMT) cohort from Taiwan.
+OPRM1	drug	alcohol	22397905	The Asn40Asp variant (A118G) of the μ opioid receptor (<strong>OPRM1</strong>) gene is thought to contribute to the development and treatment of <b>alcohol</b> dependence.
+OPRM1	drug	opioid	22397905	The Asn40Asp variant (A118G) of the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene is thought to contribute to the development and treatment of alcohol dependence.
+OPRM1	addiction	dependence	22397905	The Asn40Asp variant (A118G) of the μ opioid receptor (<strong>OPRM1</strong>) gene is thought to contribute to the development and treatment of alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	22397905	Second, we examined whether the allelic variants were associated with differences in <strong>OPRM1</strong> occupancy by <b>naltrexone</b> (50 mg) in AD subjects.
+OPRM1	drug	alcohol	22309038	Possible association between <strong>OPRM1</strong> genetic variance at the 118 locus and <b>alcohol</b> dependence in a large treatment sample: relationship to <b>alcohol</b> dependence symptoms.
+OPRM1	addiction	dependence	22309038	Possible association between <strong>OPRM1</strong> genetic variance at the 118 locus and alcohol <b>dependence</b> in a large treatment sample: relationship to alcohol <b>dependence</b> symptoms.
+OPRM1	drug	alcohol	22309038	Conflicting results were reported on the role of the mu opioid receptor (<strong>OPRM1</strong>) polymorphism A118G (Asn40Asp, rs1799971) in the development of <b>alcoholism</b>.
+OPRM1	drug	opioid	22309038	Conflicting results were reported on the role of the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) polymorphism A118G (Asn40Asp, rs1799971) in the development of alcoholism.
+OPRM1	drug	alcohol	22309038	We investigated a total number of 1,845 <b>alcohol</b> dependent subjects recruited from inpatient facilities in Germany and 1,863 controls for the mu opioid receptor (<strong>OPRM1</strong>) polymorphism using chi square statistics.
+OPRM1	drug	opioid	22309038	We investigated a total number of 1,845 alcohol dependent subjects recruited from inpatient facilities in Germany and 1,863 controls for the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) polymorphism using chi square statistics.
+OPRM1	drug	opioid	22240251	Reduced expression of the μ <b>opioid</b> receptor in some, but not all, brain regions in mice with <strong>OPRM1</strong> A112G.
+OPRM1	drug	opioid	22240251	<strong>OPRM1</strong> A118G is a common single nucleotide polymorphism (SNP) in the coding region of the human mu <b>opioid</b> receptor (MOPR) gene <strong>OPRM1</strong>.
+OPRM1	drug	amphetamine	22217949	COMT Val158Met, BDNF Val66Met, and <strong>OPRM1</strong> Asn40Asp and <b>methamphetamine</b> dependence treatment response: preliminary investigation.
+OPRM1	addiction	dependence	22217949	COMT Val158Met, BDNF Val66Met, and <strong>OPRM1</strong> Asn40Asp and methamphetamine <b>dependence</b> treatment response: preliminary investigation.
+OPRM1	addiction	intoxication	22143634	<strong>OPRM1</strong> and diagnosis related posttraumatic stress disorder in <b>binge</b> drinking patients living with HIV.
+OPRM1	drug	alcohol	22143634	The opioid receptor mu 1 (<strong>OPRM1</strong>) gene may play a role in both PTSD and <b>alcohol</b> use.
+OPRM1	drug	opioid	22143634	The <b>opioid</b> receptor mu 1 (<strong>OPRM1</strong>) gene may play a role in both PTSD and alcohol use.
+OPRM1	addiction	intoxication	22143634	We examined the association between PTSD and drinking motives as well as variation in the <strong>OPRM1</strong> as a predictor of both PTSD and drinking motives in a sample of 201 PLH reporting recent <b>binge</b> drinking.
+OPRM1	drug	opioid	22138325	Exons 3 and 4 of OPRK1 and the SNP, A118G of mu <b>opioid</b> receptor 1 (<strong>OPRM1</strong>) in the DNA samples were genotyped by sequencing and restriction fragment length polymorphism respectively.
+OPRM1	drug	opioid	22102848	Recent discoveries show that genetic variations in the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene locus play an essential role in inter individual responses.
+OPRM1	drug	opioid	22102848	Future clinical and basic studies that seek to identify the functional genetic variants within <strong>OPRM1</strong> locus, and associated molecular mechanisms, will result in a better understanding of individual responses to <b>opioid</b> therapy and ultimately to the development new pharmacotherapeutics and diagnostic tools.
+OPRM1	drug	alcohol	22071118	Ethnic specific meta analyses of association between the <strong>OPRM1</strong> A118G polymorphism and <b>alcohol</b> dependence among Asians and Caucasians.
+OPRM1	addiction	dependence	22071118	Ethnic specific meta analyses of association between the <strong>OPRM1</strong> A118G polymorphism and alcohol <b>dependence</b> among Asians and Caucasians.
+OPRM1	drug	alcohol	22071118	Many studies have investigated the association between the <strong>OPRM1</strong> A118G polymorphism (rs1799971) and <b>alcohol</b> dependence, but the results were inconsistent.
+OPRM1	addiction	dependence	22071118	Many studies have investigated the association between the <strong>OPRM1</strong> A118G polymorphism (rs1799971) and alcohol <b>dependence</b>, but the results were inconsistent.
+OPRM1	drug	alcohol	22071118	The <strong>OPRM1</strong> A118G polymorphism may contribute to the susceptibility of <b>alcohol</b> dependence in Asians but not in Caucasians.
+OPRM1	addiction	dependence	22071118	The <strong>OPRM1</strong> A118G polymorphism may contribute to the susceptibility of alcohol <b>dependence</b> in Asians but not in Caucasians.
+OPRM1	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and <strong>OPRM1</strong> 118A>G [rs1799971].
+OPRM1	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and <strong>OPRM1</strong> 118A>G [rs1799971].
+OPRM1	drug	cannabinoid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (<strong>OPRM1</strong>) or <b>cannabinoid</b> receptors (CNR1).
+OPRM1	drug	nicotine	22046326	Overall, our results suggest that genetic variants potentially involved in <b>nicotine</b> metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with <b>smoking</b> related phenotypes, as opposed to genetic variants influencing the brain effects of <b>nicotine</b>, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (<strong>OPRM1</strong>) or cannabinoid receptors (CNR1).
+OPRM1	drug	opioid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), <b>opioid</b> (<strong>OPRM1</strong>) or cannabinoid receptors (CNR1).
+OPRM1	drug	nicotine	22028400	Among committed never <b>smokers</b> (N = 872), three genes (<strong>OPRM1</strong>, SNAP25, HTR1B) were associated with experimentation as were all psychosocial factors.
+OPRM1	drug	opioid	21957825	Elevated levels of DNA methylation at the <strong>OPRM1</strong> promoter in blood and sperm from male <b>opioid</b> addicts.
+OPRM1	drug	opioid	21957825	The <strong>OPRM1</strong> gene was studied for DNA methylation in <b>opioid</b> dependence and possible paternal contribution to epigenetic inheritance of altered methylation profiles.
+OPRM1	addiction	dependence	21957825	The <strong>OPRM1</strong> gene was studied for DNA methylation in opioid <b>dependence</b> and possible paternal contribution to epigenetic inheritance of altered methylation profiles.
+OPRM1	drug	opioid	21957825	Increased DNA methylation in the <strong>OPRM1</strong> gene is associated with <b>opioid</b> dependence.
+OPRM1	addiction	dependence	21957825	Increased DNA methylation in the <strong>OPRM1</strong> gene is associated with opioid <b>dependence</b>.
+OPRM1	drug	alcohol	21946895	<strong>OPRM1</strong> A118G genotype fails to predict the effectiveness of <b>naltrexone</b> treatment for <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	21946895	<strong>OPRM1</strong> A118G genotype fails to predict the effectiveness of naltrexone treatment for alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	21946895	Given the evidence from retrospective studies indicating that <b>alcohol</b> dependent patients with homozygous or heterozygous A118G variant of the μ opioid receptor, <strong>OPRM1</strong>, gene have significantly better outcomes when treated with <b>naltrexone</b>; this study examined this prospectively in 100 <b>alcohol</b> dependent participants prescribed <b>naltrexone</b> for 12 weeks and offered six sessions of cognitive behavioral therapy or intervention.
+OPRM1	drug	opioid	21946895	Given the evidence from retrospective studies indicating that alcohol dependent patients with homozygous or heterozygous A118G variant of the μ <b>opioid</b> receptor, <strong>OPRM1</strong>, gene have significantly better outcomes when treated with naltrexone; this study examined this prospectively in 100 alcohol dependent participants prescribed naltrexone for 12 weeks and offered six sessions of cognitive behavioral therapy or intervention.
+OPRM1	drug	alcohol	21946895	Therefore, while <b>naltrexone</b> was an effective treatment for <b>alcohol</b> dependence, the <strong>OPRM1</strong> A118G genotype was not a predictor of success.
+OPRM1	addiction	dependence	21946895	Therefore, while naltrexone was an effective treatment for alcohol <b>dependence</b>, the <strong>OPRM1</strong> A118G genotype was not a predictor of success.
+OPRM1	drug	opioid	21919606	Many genetic variations have been identified in the human µ <b>opioid</b> receptor MOP gene (<strong>OPRM1</strong>), and their implications have been reported in the effects of <b>opioid</b> drugs and susceptibility to drug dependence.
+OPRM1	addiction	dependence	21919606	Many genetic variations have been identified in the human µ opioid receptor MOP gene (<strong>OPRM1</strong>), and their implications have been reported in the effects of opioid drugs and susceptibility to drug <b>dependence</b>.
+OPRM1	drug	alcohol	21919606	The IVS1+A21573G, IVS1 T17286C, and TAA+A5359G polymorphisms in the <strong>OPRM1</strong> gene may be associated with <b>alcohol</b>, opioid and tobacco dependence, respectively.
+OPRM1	drug	nicotine	21919606	The IVS1+A21573G, IVS1 T17286C, and TAA+A5359G polymorphisms in the <strong>OPRM1</strong> gene may be associated with alcohol, opioid and <b>tobacco</b> dependence, respectively.
+OPRM1	drug	opioid	21919606	The IVS1+A21573G, IVS1 T17286C, and TAA+A5359G polymorphisms in the <strong>OPRM1</strong> gene may be associated with alcohol, <b>opioid</b> and tobacco dependence, respectively.
+OPRM1	addiction	dependence	21919606	The IVS1+A21573G, IVS1 T17286C, and TAA+A5359G polymorphisms in the <strong>OPRM1</strong> gene may be associated with alcohol, opioid and tobacco <b>dependence</b>, respectively.
+OPRM1	drug	opioid	21912675	Functional polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) influences reinforcement learning in humans.
+OPRM1	addiction	reward	21912675	Functional polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) influences <b>reinforcement</b> learning in humans.
+OPRM1	drug	opioid	21912675	Previous reports on the functional effects (i.e., gain or loss of function), and phenotypic outcomes (e.g., changes in addiction vulnerability and stress response) of a commonly occurring functional single nucleotide polymorphism (SNP) of the mu <b>opioid</b> receptor (<strong>OPRM1</strong> A118G) have been inconsistent.
+OPRM1	addiction	addiction	21912675	Previous reports on the functional effects (i.e., gain or loss of function), and phenotypic outcomes (e.g., changes in <b>addiction</b> vulnerability and stress response) of a commonly occurring functional single nucleotide polymorphism (SNP) of the mu opioid receptor (<strong>OPRM1</strong> A118G) have been inconsistent.
+OPRM1	addiction	reward	21912675	Through comparison with other studies using this task, we suggest a possible mechanism by which the <strong>OPRM1</strong> polymorphism may confer reduced response to natural <b>reward</b> through a dopamine mediated decrease during positive <b>reinforcement</b> learning.
+OPRM1	drug	alcohol	21900886	Recent clinical and laboratory studies have shown that the effects of <b>naltrexone</b> for <b>alcoholism</b> may be moderated by the Asn40Asp single nucleotide polymorphism (SNP) of the μ opioid receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	21900886	Recent clinical and laboratory studies have shown that the effects of naltrexone for alcoholism may be moderated by the Asn40Asp single nucleotide polymorphism (SNP) of the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	21871151	The prevalence of CYP2B6 and μ <b>opioid</b> receptor (<strong>OPRM1</strong>) gene variations were examined between a postmortem population where the deaths were associated with <b>methadone</b> and a live nondrug using control population using Taqman™ SNP Genotyping assays.
+OPRM1	drug	opioid	21871151	The prevalence of the <strong>OPRM1</strong> A118G variation was significantly higher in the control population (P = 0.0046), which might indicate a protective mechanism against <b>opioid</b> toxicity.
+OPRM1	drug	opioid	21807019	Within strains, complex patterns of <b>heroin</b> dose dependent changes in the levels of <strong>Oprm1</strong>, Oprk1 and Oprd1 mRNAs were observed in the SN/VTA.
+OPRM1	drug	opioid	21706389	Genes at which variation moderates these phenotypes include those encoding monoamine oxidase A (MAOA LPR), the serotonin transporter (HTTLPR), corticotropin releasing hormone (CRH 248C/T and  2232 C/G), Neuropeptide Y (NPY 1002 T/G), and the μ <b>opioid</b> receptor (<strong>OPRM1</strong> C77G).
+OPRM1	drug	opioid	21629839	The mu <b>opioid</b> receptor is encoded by the <strong>Oprm1</strong> gene and contributes to mother infant behaviors.
+OPRM1	addiction	addiction	21629839	That both LGC and sex have enduring effects on DNA methylation of the <strong>Oprm1</strong> gene in brain regions associated with <b>addiction</b>, stress regulation, motivation, and cognition may suggest one factor that contributes to gender differences in these behaviors.
+OPRM1	drug	nicotine	21576462	Human Mu Opioid Receptor (<strong>OPRM1</strong> A118G) polymorphism is associated with brain mu opioid receptor binding potential in <b>smokers</b>.
+OPRM1	drug	opioid	21576462	Human Mu <b>Opioid</b> Receptor (<strong>OPRM1</strong> A118G) polymorphism is associated with brain mu <b>opioid</b> receptor binding potential in smokers.
+OPRM1	drug	nicotine	21576462	A single nucleotide polymorphism (SNP) in the human MOR gene (<strong>OPRM1</strong> A118G) has been shown to alter receptor protein level in preclinical models and <b>smoking</b> behavior in humans.
+OPRM1	drug	nicotine	21576462	Independent of session, <b>smokers</b> homozygous for the wild type <strong>OPRM1</strong> A allele exhibited significantly higher levels of MOR BP(ND) than <b>smokers</b> carrying the G allele in bilateral amygdala, left thalamus, and left anterior cingulate cortex.
+OPRM1	drug	alcohol	21507151	The mu opioid receptor encoded by the gene <strong>OPRM1</strong> plays a primary role in opiate, <b>alcohol</b>, cocaine and nicotine addiction.
+OPRM1	drug	cocaine	21507151	The mu opioid receptor encoded by the gene <strong>OPRM1</strong> plays a primary role in opiate, alcohol, <b>cocaine</b> and nicotine addiction.
+OPRM1	drug	nicotine	21507151	The mu opioid receptor encoded by the gene <strong>OPRM1</strong> plays a primary role in opiate, alcohol, cocaine and <b>nicotine</b> addiction.
+OPRM1	drug	opioid	21507151	The mu <b>opioid</b> receptor encoded by the gene <strong>OPRM1</strong> plays a primary role in opiate, alcohol, cocaine and nicotine addiction.
+OPRM1	addiction	addiction	21507151	The mu opioid receptor encoded by the gene <strong>OPRM1</strong> plays a primary role in opiate, alcohol, cocaine and nicotine <b>addiction</b>.
+OPRM1	drug	alcohol	21507127	The polymorphism of <strong>opioid receptor mu 1</strong> gene is of interest because it alters the treatment effects of <b>naltrexone</b>.
+OPRM1	drug	opioid	21507127	The polymorphism of <strong><b>opioid</b> receptor mu 1</strong> gene is of interest because it alters the treatment effects of naltrexone.
+OPRM1	drug	alcohol	21463027	Genetic variation at a single nucleotide polymorphism (SNP) in the mu opioid receptor gene (<strong>OPRM1</strong>) of both humans and rhesus macaques Macaca mulatta has been associated with differential affinity to the endogenous ligand beta endorphin as well as alterations in pain sensitivity, drug and <b>alcohol</b> dependence, and social behaviors.
+OPRM1	drug	opioid	21463027	Genetic variation at a single nucleotide polymorphism (SNP) in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) of both humans and rhesus macaques Macaca mulatta has been associated with differential affinity to the endogenous ligand beta endorphin as well as alterations in pain sensitivity, drug and alcohol dependence, and social behaviors.
+OPRM1	addiction	dependence	21463027	Genetic variation at a single nucleotide polymorphism (SNP) in the mu opioid receptor gene (<strong>OPRM1</strong>) of both humans and rhesus macaques Macaca mulatta has been associated with differential affinity to the endogenous ligand beta endorphin as well as alterations in pain sensitivity, drug and alcohol <b>dependence</b>, and social behaviors.
+OPRM1	drug	opioid	21410481	All subjects but one were genotyped for the A118G polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	alcohol	21410481	<b>Naltrexone</b> decreased the <b>ethanol</b> induced 'euphoria' to a priming dose of <b>alcohol</b> in two subgroups: (i) in women, and (ii) in subjects with the A118G polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	21410481	Naltrexone decreased the ethanol induced 'euphoria' to a priming dose of alcohol in two subgroups: (i) in women, and (ii) in subjects with the A118G polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	alcohol	21362114	Thus far, the most promising results were obtained for polymorphisms in the <strong>OPRM1</strong> and CYP2A6 genes, which have been effective in predicting clinical response to <b>naltrexone</b> in <b>alcoholism</b> and nicotine replacement therapy in smoking, respectively.
+OPRM1	drug	nicotine	21362114	Thus far, the most promising results were obtained for polymorphisms in the <strong>OPRM1</strong> and CYP2A6 genes, which have been effective in predicting clinical response to naltrexone in alcoholism and <b>nicotine</b> replacement therapy in <b>smoking</b>, respectively.
+OPRM1	drug	opioid	21277709	No evidence of association between 118A>G <strong>OPRM1</strong> polymorphism and <b>heroin</b> dependence in a large Bulgarian case control sample.
+OPRM1	addiction	dependence	21277709	No evidence of association between 118A>G <strong>OPRM1</strong> polymorphism and heroin <b>dependence</b> in a large Bulgarian case control sample.
+OPRM1	drug	opioid	21277709	The 118A>G (rs1799971) polymorphism in exon 1 of the μ <b>opioid</b> receptor gene (<strong>OPRM1</strong>) leads to an Asn40Asp amino acid change that affects a putative N glycosylation site.
+OPRM1	drug	opioid	21232580	The antinociceptive and antihyperalgesic effect of tapentadol is partially retained in <strong>OPRM1</strong> (μ <b>opioid</b> receptor) knockout mice.
+OPRM1	drug	opioid	21232580	The effect of tapentadol (0.316 31.6 mg/kg IP) and the MOR agonist <b>morphine</b> (3 10 mg/kg IP) was determined in <strong>OPRM1</strong> KO  and congenic wildtype mice.
+OPRM1	drug	opioid	21209234	The aim of this study was to evaluate the plasma dispositions of <b>oxycodone</b> and its demethylates and dose escalation based on genetic polymorphisms of CYP2D6, CYP3A5, ABCB1, and <strong>OPRM1</strong> in cancer patients receiving <b>oxycodone</b>.
+OPRM1	addiction	addiction	21209234	The aim of this study was to evaluate the plasma dispositions of oxycodone and its demethylates and dose <b>escalation</b> based on genetic polymorphisms of CYP2D6, CYP3A5, ABCB1, and <strong>OPRM1</strong> in cancer patients receiving oxycodone.
+OPRM1	drug	opioid	21160491	Recently, we have detected association of two intronic <strong>OPRM1</strong> variants with <b>heroin</b> addiction in European Americans.
+OPRM1	addiction	addiction	21160491	Recently, we have detected association of two intronic <strong>OPRM1</strong> variants with heroin <b>addiction</b> in European Americans.
+OPRM1	drug	opioid	21143246	Following experimentwise permutation, markers in the corticotropin releasing hormone binding protein (CRHBP) the μ <b>opioid</b> receptor (<strong>OPRM1</strong>) and the β1 subunit of GABA A (GABA(A)) receptors (GABRB1) met or exceeded the significance threshold.
+OPRM1	drug	nicotine	21062464	An open label, parallel groups randomised trial in which 630 adult <b>smokers</b> (<b>smoking</b> 10 or more cigarettes daily) using National Health Service (NHS) stop <b>smoking</b> services in primary care are randomly allocated to one of two groups:i. NRT oral dose tailored by DNA analysis (<strong>OPRM1</strong> gene) (genotype), orii.
+OPRM1	drug	alcohol	21039637	Stress induced and cue induced craving for <b>alcohol</b> in heavy drinkers: Preliminary evidence of genetic moderation by the <strong>OPRM1</strong> and CRH BP genes.
+OPRM1	addiction	relapse	21039637	Stress induced and cue induced <b>craving</b> for alcohol in heavy drinkers: Preliminary evidence of genetic moderation by the <strong>OPRM1</strong> and CRH BP genes.
+OPRM1	drug	opioid	21039637	This study examines genetic determinants of stress induced and cue induced craving in heavy drinkers by testing single nucleotide polymorphisms (SNPs) of the corticotrophin releasing hormone binding protein (CRH BP) gene and the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene.
+OPRM1	addiction	relapse	21039637	This study examines genetic determinants of stress induced and cue induced <b>craving</b> in heavy drinkers by testing single nucleotide polymorphisms (SNPs) of the corticotrophin releasing hormone binding protein (CRH BP) gene and the mu opioid receptor (<strong>OPRM1</strong>) gene.
+OPRM1	drug	alcohol	21039637	The Asp40 allele of the <strong>OPRM1</strong> was associated with greater cue induced <b>alcohol</b> craving following the neutral imagery condition.
+OPRM1	addiction	relapse	21039637	The Asp40 allele of the <strong>OPRM1</strong> was associated with greater cue induced alcohol <b>craving</b> following the neutral imagery condition.
+OPRM1	drug	alcohol	21039637	These initial results extend recent preclinical and clinical findings implicating the CRH BP in stress related <b>alcoholism</b> and confirm the role of the Asp40 allele of the <strong>OPRM1</strong> gene in reward driven <b>alcohol</b> phenotypes.
+OPRM1	addiction	reward	21039637	These initial results extend recent preclinical and clinical findings implicating the CRH BP in stress related alcoholism and confirm the role of the Asp40 allele of the <strong>OPRM1</strong> gene in <b>reward</b> driven alcohol phenotypes.
+OPRM1	drug	amphetamine	21029375	<strong>OPRM1</strong> gene variants modulate <b>amphetamine</b> induced euphoria in humans.
+OPRM1	drug	amphetamine	21029375	Associations between levels of self reported Euphoria, Energy and Stimulation [Addiction Research Center Inventory 49 item questionnaire (ARCI 49)] after d <b>amphetamine</b> ingestion and polymorphisms in <strong>OPRM1</strong> were investigated.
+OPRM1	addiction	addiction	21029375	Associations between levels of self reported Euphoria, Energy and Stimulation [<b>Addiction</b> Research Center Inventory 49 item questionnaire (ARCI 49)] after d amphetamine ingestion and polymorphisms in <strong>OPRM1</strong> were investigated.
+OPRM1	drug	opioid	20668445	<strong>OPRM1</strong> and CYP2B6 gene variants as risk factors in <b>methadone</b> related deaths.
+OPRM1	drug	opioid	20668445	We have examined the association between CYP2B6 and micro <b>opioid</b> receptor (<strong>OPRM1</strong>) gene variations and apparent susceptibility to <b>methadone</b> poisoning.
+OPRM1	drug	opioid	20668445	<strong>OPRM1</strong> A118G was also associated with higher postmortem <b>methadone</b> concentrations in blood but not to a level of statistical significance (P = 0.39).
+OPRM1	drug	benzodiazepine	20668445	In these methadone related deaths, <strong>OPRM1</strong> 118GA was associated with higher postmortem <b>benzodiazepine</b> concentrations (P = 0.04), a finding not associated with morphine related deaths.
+OPRM1	drug	opioid	20668445	In these <b>methadone</b> related deaths, <strong>OPRM1</strong> 118GA was associated with higher postmortem benzodiazepine concentrations (P = 0.04), a finding not associated with <b>morphine</b> related deaths.
+OPRM1	drug	opioid	20560679	This study aimed to investigate the associations between response to <b>methadone</b> maintenance treatment (MMT) and polymorphisms in genes coding for the <strong>OPRM1</strong> <b>opioid</b> receptor, the metabotropic glutamate receptors GRM6 and GRM8, the nuclear receptor NR4A2, the photolyase enzyme cryptochrome 1 (CRY1), and the transcription factor myocardin (MYOCD), which have previously been associated with the risk of <b>opioid</b> dependence disorder.
+OPRM1	addiction	dependence	20560679	This study aimed to investigate the associations between response to methadone maintenance treatment (MMT) and polymorphisms in genes coding for the <strong>OPRM1</strong> opioid receptor, the metabotropic glutamate receptors GRM6 and GRM8, the nuclear receptor NR4A2, the photolyase enzyme cryptochrome 1 (CRY1), and the transcription factor myocardin (MYOCD), which have previously been associated with the risk of opioid <b>dependence</b> disorder.
+OPRM1	drug	alcohol	20528823	<b>Naltrexone</b> selectively elevates GABAergic neuroactive steroid levels in heavy drinkers with the Asp40 allele of the <strong>OPRM1</strong> gene: a pilot investigation.
+OPRM1	drug	alcohol	20528823	<b>Naltrexone</b> is thought to blunt the reinforcing effects of <b>alcohol</b>, and a few studies have found that the effects of <b>naltrexone</b> are moderated by the Asn40Asp polymorphisms of the <strong>OPRM1</strong> gene.
+OPRM1	addiction	reward	20528823	Naltrexone is thought to blunt the <b>reinforcing</b> effects of alcohol, and a few studies have found that the effects of naltrexone are moderated by the Asn40Asp polymorphisms of the <strong>OPRM1</strong> gene.
+OPRM1	drug	alcohol	20528823	The present study seeks to integrate these lines of research by testing (i) the moderating role of the functional Asn40Asp polymorphism of the <strong>OPRM1</strong> gene on <b>naltrexone</b> induced alternations in GABAergic neurosteroid levels, namely (3alpha,5alpha) 3 hydroxypregnan 20 one (allopregnanolone, ALLO); and (ii) the combined effects of <b>naltrexone</b> or genotype with <b>alcohol</b> administration on neurosteroid levels in a sample of at risk drinkers.
+OPRM1	drug	opioid	20525224	The major <strong>MOR1</strong> and the alternative MOR1K isoforms mediate opposite cellular effects in response to <b>morphine</b>, with MOR1K driving excitatory processes.
+OPRM1	drug	opioid	20486014	Social hedonic capacity is associated with the A118G polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) in adult healthy volunteers and psychiatric patients.
+OPRM1	addiction	reward	20486014	Social <b>hedonic</b> capacity is associated with the A118G polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) in adult healthy volunteers and psychiatric patients.
+OPRM1	drug	opioid	20486014	Here we investigate whether a common polymorphism (A118G) in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) is associated with alterations in personality traits linked to affiliative behavior and attachment.
+OPRM1	addiction	reward	20486014	In a mixed sample (N = 214) of adult healthy volunteers and psychiatric patients, we analyzed the association between the A118G polymorphism of the <strong>OPRM1</strong> and two different psychological constructs reflecting individual differences in the capacity to experience social <b>reward</b>.
+OPRM1	drug	opioid	20482509	We consider four neurotransmitter systems: opioidergic, dopaminergic, GABAergic, and glutamatergic and focus on one receptor protein in each: <strong>OPRM1</strong> (the &#micro; <b>opioid</b> receptor gene), DRD4 (the D(4) dopamine receptor gene), GABRA2 (GABA(A) receptor alpha 2 subunit gene), and GRIK1 (the kainite receptor GluR5 subunit gene).
+OPRM1	drug	alcohol	20482509	Of greatest clinical relevance is the finding that the presence of an Asp40 allele in <strong>OPRM1</strong> modestly predicts a better response to <b>naltrexone</b> treatment.
+OPRM1	drug	alcohol	20479755	Here, we report that a functional <strong>OPRM1</strong> A118G polymorphism is a major determinant of striatal dopamine responses to <b>alcohol</b>.
+OPRM1	drug	alcohol	20479755	Social drinkers recruited based on <strong>OPRM1</strong> genotype were challenged in separate sessions with <b>alcohol</b> and placebo under pharmacokinetically controlled conditions, and examined for striatal dopamine release using positron emission tomography and [(11)C] raclopride displacement.
+OPRM1	drug	alcohol	20479755	<strong>OPRM1</strong> A118G variation is a genetic determinant of dopamine responses to <b>alcohol</b>, a mechanism by which it likely modulates <b>alcohol</b> reward.
+OPRM1	addiction	reward	20479755	<strong>OPRM1</strong> A118G variation is a genetic determinant of dopamine responses to alcohol, a mechanism by which it likely modulates alcohol <b>reward</b>.
+OPRM1	drug	amphetamine	20478633	A total of 193 non psychotic males (117 <b>methamphetamine</b> dependent and 76 controls) were genotyped for variants located in six genes (AKT1, ARRB2, BDNF, COMT, GSTP1, <strong>OPRM1</strong>).
+OPRM1	drug	opioid	20230086	The purpose of the present investigation was to determine if variation in the catechol O methyltransferase (COMT) and mu <b>opioid</b> receptor (<strong>OPRM1</strong>) genes is associated with pain related positive affective regulation in fibromyalgia (FM).
+OPRM1	drug	opioid	20201854	In addition, we provide the first evidence of a cis acting polymorphism and a functional haplotype in the PDYN gene, of significantly higher DNA methylation rate of the <strong>OPRM1</strong> gene in the lymphocytes of <b>heroin</b> addicts, and significant differences in genotype frequencies of three single nucleotide polymorphisms of the P glycoprotein gene (ABCB1) between "higher" and "lower" <b>methadone</b> doses in <b>methadone</b> maintained patients.
+OPRM1	drug	cannabinoid	20196742	For example, the <b>cannabinoid</b> brain receptor type 1 (CB1) and mu opioid receptor type 1 (<strong>MOR1</strong>) co localize in the same presynaptic nerve terminals and signal through a common receptor mediated G protein pathway.
+OPRM1	drug	opioid	20196742	For example, the cannabinoid brain receptor type 1 (CB1) and mu <b>opioid</b> receptor type 1 (<strong>MOR1</strong>) co localize in the same presynaptic nerve terminals and signal through a common receptor mediated G protein pathway.
+OPRM1	addiction	addiction	20196742	Finally, we discuss genetic studies that reveal significant associations between polymorphisms in <strong>MOR1</strong> and CB1 receptors and drug <b>addiction</b>.
+OPRM1	drug	opioid	20196742	For example, the SNP A118G, which changes the amino acid aspartate to asparagine in the <strong>MOR1</strong> gene, is highly associated with altered <b>opioid</b> system function.
+OPRM1	drug	alcohol	20141248	Polymorphisms of the mu opioid receptor (<strong>OPRM1</strong>) and dopamine D4 receptor (DRD4) genes are associated with subjective responses to <b>alcohol</b> and urge to drink under laboratory conditions.
+OPRM1	drug	opioid	20141248	Polymorphisms of the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) and dopamine D4 receptor (DRD4) genes are associated with subjective responses to alcohol and urge to drink under laboratory conditions.
+OPRM1	drug	alcohol	20141248	Effects of <strong>OPRM1</strong> and DRD4 variable number of tandem repeats genotypes appear to be <b>alcohol</b> dose dependent.
+OPRM1	drug	opioid	20119466	<strong>OPRM1</strong> or GCH1 variants conferring modest "protection" from pain by increasing the tone of the endogenous <b>opioid</b> system or decreasing nitric oxide formation).
+OPRM1	drug	alcohol	20077761	The genotype frequencies of the ADH2 and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) in Korean men and women with <b>alcohol</b> dependence (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for <b>alcoholism</b>.
+OPRM1	drug	opioid	20077761	The genotype frequencies of the ADH2 and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) in Korean men and women with alcohol dependence (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for alcoholism.
+OPRM1	addiction	dependence	20077761	The genotype frequencies of the ADH2 and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) in Korean men and women with alcohol <b>dependence</b> (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for alcoholism.
+OPRM1	drug	alcohol	20077761	These results suggest that, while the risk of <b>alcoholism</b> in Korean men is predominantly affected by the presence of the ALDH2 1/1 genotype, the risk of <b>alcoholism</b> in Korean women is primarily associated with the ADH2 1/1 genotype and G carrier genotype of the <strong>OPRM1</strong> A118G polymorphism.
+OPRM1	drug	nicotine	19959688	<b>Nicotine</b> withdrawal sensitivity, linkage to chr6q26, and association of <strong>OPRM1</strong> SNPs in the <b>SMOking</b> in FAMilies (SMOFAM) sample.
+OPRM1	addiction	withdrawal	19959688	Nicotine <b>withdrawal</b> sensitivity, linkage to chr6q26, and association of <strong>OPRM1</strong> SNPs in the SMOking in FAMilies (SMOFAM) sample.
+OPRM1	drug	nicotine	19959688	The objectives of these analyses were to (a) assess the influence of <b>nicotine</b> withdrawal sensitivity on relapse, (b) conduct autosome wide NPL analysis of <b>nicotine</b> withdrawal sensitivity among 158 pedigrees with 432 individuals with microsatellite genotypes and <b>nicotine</b> withdrawal scores, and (c) explore family based association of single nucleotide polymorphism (SNP) at the mu opioid receptor candidate gene (<strong>OPRM1</strong>) with <b>nicotine</b> withdrawal sensitivity in 172 nuclear pedigrees with 419 individuals with both SNP genotypes and <b>nicotine</b> withdrawal scores.
+OPRM1	drug	opioid	19959688	The objectives of these analyses were to (a) assess the influence of nicotine withdrawal sensitivity on relapse, (b) conduct autosome wide NPL analysis of nicotine withdrawal sensitivity among 158 pedigrees with 432 individuals with microsatellite genotypes and nicotine withdrawal scores, and (c) explore family based association of single nucleotide polymorphism (SNP) at the mu <b>opioid</b> receptor candidate gene (<strong>OPRM1</strong>) with nicotine withdrawal sensitivity in 172 nuclear pedigrees with 419 individuals with both SNP genotypes and nicotine withdrawal scores.
+OPRM1	addiction	relapse	19959688	The objectives of these analyses were to (a) assess the influence of nicotine withdrawal sensitivity on <b>relapse</b>, (b) conduct autosome wide NPL analysis of nicotine withdrawal sensitivity among 158 pedigrees with 432 individuals with microsatellite genotypes and nicotine withdrawal scores, and (c) explore family based association of single nucleotide polymorphism (SNP) at the mu opioid receptor candidate gene (<strong>OPRM1</strong>) with nicotine withdrawal sensitivity in 172 nuclear pedigrees with 419 individuals with both SNP genotypes and nicotine withdrawal scores.
+OPRM1	addiction	withdrawal	19959688	The objectives of these analyses were to (a) assess the influence of nicotine <b>withdrawal</b> sensitivity on relapse, (b) conduct autosome wide NPL analysis of nicotine <b>withdrawal</b> sensitivity among 158 pedigrees with 432 individuals with microsatellite genotypes and nicotine <b>withdrawal</b> scores, and (c) explore family based association of single nucleotide polymorphism (SNP) at the mu opioid receptor candidate gene (<strong>OPRM1</strong>) with nicotine <b>withdrawal</b> sensitivity in 172 nuclear pedigrees with 419 individuals with both SNP genotypes and nicotine <b>withdrawal</b> scores.
+OPRM1	drug	nicotine	19959688	Evaluation of 18 <strong>OPRM1</strong> SNPs via the family based association test with the <b>nicotine</b> withdrawal sensitivity score identified eight tagging SNPs with global P values <0.05 and false discovery rate Q values <0.06.
+OPRM1	addiction	withdrawal	19959688	Evaluation of 18 <strong>OPRM1</strong> SNPs via the family based association test with the nicotine <b>withdrawal</b> sensitivity score identified eight tagging SNPs with global P values <0.05 and false discovery rate Q values <0.06.
+OPRM1	drug	nicotine	19959688	An increased risk of relapse, suggestive linkage at chr6q26, and nominally significant association with multiple <strong>OPRM1</strong> SNPs were found with Rasch modeled <b>nicotine</b> withdrawal sensitivity scores in a multiplex <b>smoking</b> pedigree sample.
+OPRM1	addiction	relapse	19959688	An increased risk of <b>relapse</b>, suggestive linkage at chr6q26, and nominally significant association with multiple <strong>OPRM1</strong> SNPs were found with Rasch modeled nicotine withdrawal sensitivity scores in a multiplex smoking pedigree sample.
+OPRM1	addiction	withdrawal	19959688	An increased risk of relapse, suggestive linkage at chr6q26, and nominally significant association with multiple <strong>OPRM1</strong> SNPs were found with Rasch modeled nicotine <b>withdrawal</b> sensitivity scores in a multiplex smoking pedigree sample.
+OPRM1	drug	nicotine	19959688	Future studies should attempt to replicate these findings and investigate the relationship between <b>nicotine</b> withdrawal symptoms and variation at <strong>OPRM1</strong>.
+OPRM1	addiction	withdrawal	19959688	Future studies should attempt to replicate these findings and investigate the relationship between nicotine <b>withdrawal</b> symptoms and variation at <strong>OPRM1</strong>.
+OPRM1	drug	opioid	19891732	Single nucleotide polymorphism (A118G) in exon 1 of <strong>OPRM1</strong> gene causes alteration in downstream signaling by mu <b>opioid</b> receptor and may contribute to the genetic risk for addiction.
+OPRM1	addiction	addiction	19891732	Single nucleotide polymorphism (A118G) in exon 1 of <strong>OPRM1</strong> gene causes alteration in downstream signaling by mu opioid receptor and may contribute to the genetic risk for <b>addiction</b>.
+OPRM1	drug	opioid	19891732	The <b>opioid</b> receptor mu1 (<strong>OPRM1</strong>) mediates the action of <b>morphine</b>.
+OPRM1	addiction	addiction	19891732	Although genetic background plays an important role in the susceptibility toward abuse of drugs as evident from familial, adoption and twin studies, association of specific single nucleotide polymorphisms of <strong>OPRM1</strong> gene with narcotic <b>addiction</b> is to be established.
+OPRM1	drug	alcohol	19891732	Here, we demonstrate the involvement of A118G polymorphism of exon1 of human <strong>OPRM1</strong> gene (hOPRM1), with heroin and <b>alcohol</b> addiction, in a population in eastern India.
+OPRM1	drug	opioid	19891732	Here, we demonstrate the involvement of A118G polymorphism of exon1 of human <strong>OPRM1</strong> gene (hOPRM1), with <b>heroin</b> and alcohol addiction, in a population in eastern India.
+OPRM1	addiction	addiction	19891732	Here, we demonstrate the involvement of A118G polymorphism of exon1 of human <strong>OPRM1</strong> gene (hOPRM1), with heroin and alcohol <b>addiction</b>, in a population in eastern India.
+OPRM1	drug	alcohol	19860800	Initial evidence of an association between <strong>OPRM1</strong> and adolescent <b>alcohol</b> misuse.
+OPRM1	drug	alcohol	19860800	The purpose of this study was to examine the association between a polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) and <b>alcohol</b> misuse in a sample of youth and to test whether heightened sensitivity to the reinforcing effects of <b>alcohol</b> mediated this relationship.
+OPRM1	drug	opioid	19860800	The purpose of this study was to examine the association between a polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) and alcohol misuse in a sample of youth and to test whether heightened sensitivity to the reinforcing effects of alcohol mediated this relationship.
+OPRM1	addiction	reward	19860800	The purpose of this study was to examine the association between a polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) and alcohol misuse in a sample of youth and to test whether heightened sensitivity to the <b>reinforcing</b> effects of alcohol mediated this relationship.
+OPRM1	drug	alcohol	19860800	Adolescents (n = 187; mean age = 15.4 years; 47.6% female) were genotyped for A118G (rs1799971), a single nucleotide polymorphism (SNP) of the <strong>OPRM1</strong> gene, and assessed for <b>alcohol</b> use disorder (AUD) diagnoses and other psychopathology.
+OPRM1	drug	alcohol	19860800	Those who carried the G allele endorsed drinking to enhance positive affect more strongly than those who were homozygous for the A allele and drinking to enhance positive affect mediated the association between <strong>OPRM1</strong> and <b>alcohol</b> related problems.
+OPRM1	drug	alcohol	19860800	These data build on findings from adult studies and provide the first evidence that a polymorphism of the <strong>OPRM1</strong> receptor gene is associated with the development of early onset <b>alcohol</b> related problems during adolescence, in part, by heightening sensitivity to the reinforcing effects of <b>alcohol</b>.
+OPRM1	addiction	reward	19860800	These data build on findings from adult studies and provide the first evidence that a polymorphism of the <strong>OPRM1</strong> receptor gene is associated with the development of early onset alcohol related problems during adolescence, in part, by heightening sensitivity to the <b>reinforcing</b> effects of alcohol.
+OPRM1	drug	opioid	19819304	KEPI maps onto mouse chromosome 10 close to the locus that contains the mu <b>opioid</b> receptor (<strong>Oprm1</strong>) and provides a major quantitative trait locus for <b>morphine</b> effects.
+OPRM1	drug	alcohol	19764934	<b>Alcoholism</b> is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in opioid receptor mu1 (<strong>OPRM1</strong>), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of <b>alcoholism</b>.
+OPRM1	drug	opioid	19764934	Alcoholism is a polygenic disorder resulting from reward deficiency; polymorphisms in reward genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in <b>opioid</b> receptor mu1 (<strong>OPRM1</strong>), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+OPRM1	addiction	reward	19764934	Alcoholism is a polygenic disorder resulting from <b>reward</b> deficiency; polymorphisms in <b>reward</b> genes including serotonin transporter (5 HTT) linked polymorphic region (5 HTTLPR), A118G in opioid receptor mu1 (<strong>OPRM1</strong>), and  141C Insertion/Deletion (Ins/Del) in dopamine receptor D2 (DRD2) as well as environmental factors (education and marital status) might affect the risk of alcoholism.
+OPRM1	drug	alcohol	19764934	Genotyping of 5 HTTLPR, <strong>OPRM1</strong> A118G, and DRD2 141C Ins/Del was performed in 365 <b>alcoholics</b> and 338 nonalcoholic controls of Mexican Americans who were gender  and age matched.
+OPRM1	drug	alcohol	19764934	Main effect of education, <strong>OPRM1</strong>, and DRD2 was detected in <b>alcoholic</b> stratum of moderate and/or largest MAXDRINKS with education < or =12 years, <strong>OPRM1</strong> 118 A/A, and DRD2  141C Ins/Ins being risk factors.
+OPRM1	drug	alcohol	19764934	Classification tree analysis, GMDR analysis, and PIA 2 program all supported education*<strong>OPRM1</strong> interaction in <b>alcoholics</b> of largest MAXDRINKS with education < or =12 years coupled with <strong>OPRM1</strong> A/A being a high risk factor; dendrogram showed synergistic interaction between these 2 factors; dosage effect response was also observed for education*<strong>OPRM1</strong> interaction.
+OPRM1	drug	alcohol	19764934	Our results suggest main effect of education background, <strong>OPRM1</strong> A118G, and DRD2  141C Ins/Del as well as education*<strong>OPRM1</strong> interaction in contribution to moderate and/or severe <b>alcoholism</b> in Mexican Americans.
+OPRM1	drug	opioid	19759336	One possible candidate is the micro <b>opioid</b> receptor (<strong>Oprm1</strong>) signaling cascade.
+OPRM1	drug	alcohol	19748082	The role of a nonsynonymous A118G polymorphism of the human micro opioid receptor gene (<strong>OPRM1</strong>) for <b>alcohol</b> reward and therapeutic efficacy of <b>naltrexone</b> remains controversial.
+OPRM1	drug	opioid	19748082	The role of a nonsynonymous A118G polymorphism of the human micro <b>opioid</b> receptor gene (<strong>OPRM1</strong>) for alcohol reward and therapeutic efficacy of naltrexone remains controversial.
+OPRM1	addiction	reward	19748082	The role of a nonsynonymous A118G polymorphism of the human micro opioid receptor gene (<strong>OPRM1</strong>) for alcohol <b>reward</b> and therapeutic efficacy of naltrexone remains controversial.
+OPRM1	drug	alcohol	19748082	Twenty one rhesus macaques (13 female rhesus macaques, 8 male rhesus macaques) were genotyped for <strong>OPRM1</strong> C77G and studied during 1 hour sessions for preference between an aspartame sweetened <b>alcohol</b> solution (8.4% vol/vol) and a nonalcoholic control fluid in a baseline session followed by <b>naltrexone</b> (1 mg/kg) and vehicle treatment in a counterbalanced within subject design.
+OPRM1	drug	alcohol	19748082	These results support a critical pharmacogenetic role of <strong>OPRM1</strong> variation for therapeutic efficacy of <b>naltrexone</b>.
+OPRM1	drug	opioid	19615406	Other variants modulate the perception of pain (e.g., <strong>OPRM1</strong> or GCH1 variants conferring modest pain protection by increasing the tone of the endogenous <b>opioid</b> system or decreasing nitric oxide formation).
+OPRM1	drug	opioid	19545447	As mu <b>opioid</b> receptor (<strong>OPRM1</strong>) is known to modulate pain perception and mediate the analgesic effects of <b>opioid</b> compounds in the central nervous system, we examined the influence of two OPRM polymorphisms on acute post operative pain and <b>morphine</b> usage in women undergoing elective caesarean delivery.
+OPRM1	drug	opioid	19545447	As mu <b>opioid</b> receptor (<strong>OPRM1</strong>) is known to modulate pain perception and mediate the analgesic effects of <b>opioid</b> compounds in the central nervous system, we examined the influence of two <strong>OPRM</strong> polymorphisms on acute post operative pain and <b>morphine</b> usage in women undergoing elective caesarean delivery.
+OPRM1	drug	opioid	19545447	We found statistically significant association of the <strong>OPRM</strong> 118A>G with self administered <b>morphine</b> during the first 24 hour postoperative period both in terms of total <b>morphine</b> (p = 1.7 x 10( 5)) and weight adjusted <b>morphine</b> (p = 6.6 x 10( 5)).
+OPRM1	drug	opioid	19545447	<strong>OPRM</strong> 118G homozygotes used more <b>morphine</b> and reported higher pain scores than 118A carriers.
+OPRM1	drug	opioid	19545447	Our results suggest that ethnicity and <strong>OPRM</strong> 118A>G genotype are independent and significant contributors to variation in pain perception and postoperative <b>morphine</b> use in patients undergoing cesarean delivery.
+OPRM1	drug	opioid	19528658	A single nucleotide polymorphism (SNP) in the human mu <b>opioid</b> receptor gene (<strong>OPRM1</strong> A118G) has been widely studied for its association in a variety of drug addiction and pain sensitivity phenotypes; however, the extent of these adaptations and the mechanisms underlying these associations remain elusive.
+OPRM1	addiction	addiction	19528658	A single nucleotide polymorphism (SNP) in the human mu opioid receptor gene (<strong>OPRM1</strong> A118G) has been widely studied for its association in a variety of drug <b>addiction</b> and pain sensitivity phenotypes; however, the extent of these adaptations and the mechanisms underlying these associations remain elusive.
+OPRM1	addiction	addiction	19528658	To clarify the functional mechanisms linking the <strong>OPRM1</strong> A118G SNP to <b>addiction</b> and analgesia phenotypes, we derived a mouse model possessing the equivalent nucleotide/amino acid substitution in the <strong>Oprm1</strong> gene.
+OPRM1	drug	alcohol	19393386	<b>Naltrexone</b> is a competitive antagonist of opioid receptors <strong>OPRM1</strong>, OPRD1 and OPRK1.
+OPRM1	drug	opioid	19393386	Naltrexone is a competitive antagonist of <b>opioid</b> receptors <strong>OPRM1</strong>, OPRD1 and OPRK1.
+OPRM1	drug	opioid	19282821	We targeted three functional polymorphisms related to the D2 receptor (DRD2) gene, as well as the functional A118G polymorphism of the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene.
+OPRM1	drug	amphetamine	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, <strong>OPRM1</strong>, SNCA, and SOD2) with <b>METH</b> psychosis.
+OPRM1	addiction	dependence	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, <strong>OPRM1</strong>, SNCA, and SOD2) with METH psychosis.
+OPRM1	drug	opioid	19198656	We examine, for the first time, the role of <b>opioid</b> systems in impulsivity by testing whether inactivation of the mu  (<strong>Oprm1</strong>) or delta  (Oprd1) <b>opioid</b> receptor gene alters motor impulsivity in mice.
+OPRM1	drug	opioid	23226031	Lack of association between the A118G polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) and <b>opioid</b> dependence: A meta analysis.
+OPRM1	addiction	dependence	23226031	Lack of association between the A118G polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) and opioid <b>dependence</b>: A meta analysis.
+OPRM1	drug	opioid	23226031	Mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene variants, particularly the common A118G single nucleotide polymorphism (SNP), are among the most frequently studied candidate genes associated with <b>opioid</b> dependence.
+OPRM1	addiction	dependence	23226031	Mu opioid receptor (<strong>OPRM1</strong>) gene variants, particularly the common A118G single nucleotide polymorphism (SNP), are among the most frequently studied candidate genes associated with opioid <b>dependence</b>.
+OPRM1	drug	opioid	23226031	In addition, the possibility that other <strong>OPRM1</strong> SNPs albeit rarer may influence the risk of <b>opioid</b> dependence remains to be investigated at this level.
+OPRM1	addiction	dependence	23226031	In addition, the possibility that other <strong>OPRM1</strong> SNPs albeit rarer may influence the risk of opioid <b>dependence</b> remains to be investigated at this level.
+OPRM1	drug	opioid	19059064	The value of CYP2D6 and <strong>OPRM1</strong> pharmacogenetic testing for <b>opioid</b> therapy.
+OPRM1	drug	opioid	19059064	This article focuses on <b>opioid</b> use for pain management, their risks of toxicity and addiction, adverse reactions, undertreatment for fear of addiction, and integration of novel diagnostics, such as the pharmacogenetic biomarkers CYP2D6 and <strong>OPRM1</strong> as holding promise for assessing a patient's risk of adverse events or likelihood of efficacy.
+OPRM1	addiction	addiction	19059064	This article focuses on opioid use for pain management, their risks of toxicity and <b>addiction</b>, adverse reactions, undertreatment for fear of <b>addiction</b>, and integration of novel diagnostics, such as the pharmacogenetic biomarkers CYP2D6 and <strong>OPRM1</strong> as holding promise for assessing a patient's risk of adverse events or likelihood of efficacy.
+OPRM1	drug	alcohol	19016889	This study investigated whether automatic approach action tendencies for <b>alcohol</b> related stimuli were associated with variation in the mu opioid receptor gene (<strong>OPRM1</strong>), previously related to rewarding effects of <b>alcohol</b> and craving.
+OPRM1	drug	opioid	19016889	This study investigated whether automatic approach action tendencies for alcohol related stimuli were associated with variation in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>), previously related to rewarding effects of alcohol and craving.
+OPRM1	addiction	relapse	19016889	This study investigated whether automatic approach action tendencies for alcohol related stimuli were associated with variation in the mu opioid receptor gene (<strong>OPRM1</strong>), previously related to rewarding effects of alcohol and <b>craving</b>.
+OPRM1	drug	alcohol	18795264	Previous studies have demonstrated an association between genetic polymorphisms of the mu opioid receptor gene (<strong>OPRM1</strong>) and response to <b>naltrexone</b> treatment.
+OPRM1	drug	opioid	18795264	Previous studies have demonstrated an association between genetic polymorphisms of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) and response to naltrexone treatment.
+OPRM1	drug	nicotine	18690118	<strong>OPRM1</strong> (AA>AG or GG) was associated with <b>smoking</b> reward, but SLC6A4 variable number tandem repeat was unrelated to any of these measures.
+OPRM1	addiction	reward	18690118	<strong>OPRM1</strong> (AA>AG or GG) was associated with smoking <b>reward</b>, but SLC6A4 variable number tandem repeat was unrelated to any of these measures.
+OPRM1	drug	opioid	18650805	Increased <strong>OPRM1</strong> DNA methylation in lymphocytes of <b>methadone</b> maintained former <b>heroin</b> addicts.
+OPRM1	drug	opioid	18650805	We examined whether there are differences in cytosine:guanine (CpG) dinucleotide methylation in the <strong>OPRM1</strong> promoter between former <b>heroin</b> addicts and controls.
+OPRM1	drug	opioid	18650805	Methylation of these CpG sites may lead to reduced <strong>OPRM1</strong> expression in the lymphocytes of these former <b>heroin</b> addicts.
+OPRM1	drug	opioid	18616461	In this study, we observed a rapid and severe increase in ERK1/2 activity after a 5 min <b>morphine</b> treatment of HEK MOR cells (transfected with the rat mu <b>opioid</b> receptor <strong>MOR1</strong>) expressing mu <b>opioid</b> receptor.
+OPRM1	drug	opioid	18518925	These variants were in noncoding regions of the genes encoding the mu (<strong>OPRM1</strong>; rs510769 and rs3778151), kappa (OPRK1; rs6473797) and delta (OPRD1; rs2236861, rs2236857 and rs3766951) <b>opioid</b> receptors; the neuropeptide galanin (GAL; rs694066); the serotonin receptor subtype 3B (HTR3B; rs3758987) and the casein kinase 1 isoform epsilon (CSNK1E; rs1534891).
+OPRM1	drug	opioid	18518925	Analysis of a combined effect of <strong>OPRM1</strong> and OPRD1 showed that rs510769 and rs2236861 increase the risk of <b>heroin</b> addiction (P = 0.0005).
+OPRM1	addiction	addiction	18518925	Analysis of a combined effect of <strong>OPRM1</strong> and OPRD1 showed that rs510769 and rs2236861 increase the risk of heroin <b>addiction</b> (P = 0.0005).
+OPRM1	drug	nicotine	18499348	Thirteen <b>smokers</b> participating in a prior arterial spin labeled (ASL) perfusion MRI study were scanned on two occasions (after >12h abstinence vs. satiety), and were genotyped for variants in the dopamine D2 receptor (DRD2 141 Ins/DelC; DRD2 C957T); a dopamine metabolizing enzyme (COMT val(158) met), and the mu opioid receptor (<strong>OPRM1</strong> A118G).
+OPRM1	drug	opioid	18499348	Thirteen smokers participating in a prior arterial spin labeled (ASL) perfusion MRI study were scanned on two occasions (after >12h abstinence vs. satiety), and were genotyped for variants in the dopamine D2 receptor (DRD2 141 Ins/DelC; DRD2 C957T); a dopamine metabolizing enzyme (COMT val(158) met), and the mu <b>opioid</b> receptor (<strong>OPRM1</strong> A118G).
+OPRM1	drug	nicotine	18499348	Finally, <b>smokers</b> with <strong>OPRM1</strong> AA genotypes showed significant increases in CBF in regions associated previously with cigarette cravings.
+OPRM1	drug	alcohol	18482155	An exploratory aim examined whether the Asn40Asp polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) predicted response to <b>naltrexone</b>, as had been reported in Caucasians.
+OPRM1	drug	opioid	18482155	An exploratory aim examined whether the Asn40Asp polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) predicted response to naltrexone, as had been reported in Caucasians.
+OPRM1	drug	alcohol	18482155	<b>Naltrexone</b> treatment response was significant within the group of 75 individuals who were homozygous for <strong>OPRM1</strong> Asn40 allele.
+OPRM1	drug	alcohol	18433502	Association between single nucleotide polymorphisms in the mu opioid receptor gene (<strong>OPRM1</strong>) and self reported responses to <b>alcohol</b> in American Indians.
+OPRM1	drug	opioid	18433502	Association between single nucleotide polymorphisms in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) and self reported responses to alcohol in American Indians.
+OPRM1	drug	alcohol	18433502	The purpose of this study was to investigate associations between 13 single nucleotide polymorphisms in the mu opioid receptor gene (<strong>OPRM1</strong>) with self reported responses to <b>alcohol</b>, an endophenotype associated with the development of <b>alcohol</b> dependence, in American Indians living on eight contiguous reservations.
+OPRM1	drug	opioid	18433502	The purpose of this study was to investigate associations between 13 single nucleotide polymorphisms in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) with self reported responses to alcohol, an endophenotype associated with the development of alcohol dependence, in American Indians living on eight contiguous reservations.
+OPRM1	addiction	dependence	18433502	The purpose of this study was to investigate associations between 13 single nucleotide polymorphisms in the mu opioid receptor gene (<strong>OPRM1</strong>) with self reported responses to alcohol, an endophenotype associated with the development of alcohol <b>dependence</b>, in American Indians living on eight contiguous reservations.
+OPRM1	drug	alcohol	18433502	These studies provide data to suggest that the minor allele, for most of the polymorphisms in the <strong>OPRM1</strong> receptor gene investigated, was found to be associated with a more intense, and/or more adverse, response to <b>alcohol</b>, traits that are significantly correlated with lowered quantity of <b>alcohol</b> consumption and less susceptibility to dependence in this Indian population.
+OPRM1	addiction	dependence	18433502	These studies provide data to suggest that the minor allele, for most of the polymorphisms in the <strong>OPRM1</strong> receptor gene investigated, was found to be associated with a more intense, and/or more adverse, response to alcohol, traits that are significantly correlated with lowered quantity of alcohol consumption and less susceptibility to <b>dependence</b> in this Indian population.
+OPRM1	drug	opioid	18396272	The mu <b>opioid</b> receptor encoded by the <strong>Oprm1</strong> gene plays a crucial role in the mediation of food reward and drug induced positive reinforcement, but its genetic deletion has been shown to provide food intake independent, partial protection from diet induced obesity.
+OPRM1	addiction	reward	18396272	The mu opioid receptor encoded by the <strong>Oprm1</strong> gene plays a crucial role in the mediation of food <b>reward</b> and drug induced positive <b>reinforcement</b>, but its genetic deletion has been shown to provide food intake independent, partial protection from diet induced obesity.
+OPRM1	drug	opioid	18378897	Variation at the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) influences attachment behavior in infant primates.
+OPRM1	drug	opioid	18378897	Functional mu <b>opioid</b> receptor gene polymorphisms are present in humans (<strong>OPRM1</strong> A118G) and rhesus macaques (<strong>OPRM1</strong> C77G).
+OPRM1	addiction	reward	18378897	We hypothesized that rhesus infants carrying a gain of function <strong>OPRM1</strong> 77G allele would experience increased <b>reward</b> during maternal contact and would, therefore, display increased measures of attachment.
+OPRM1	drug	alcohol	18250251	An evaluation of mu opioid receptor (<strong>OPRM1</strong>) as a predictor of <b>naltrexone</b> response in the treatment of <b>alcohol</b> dependence: results from the Combined Pharmacotherapies and Behavioral Interventions for <b>Alcohol</b> Dependence (COMBINE) study.
+OPRM1	drug	opioid	18250251	An evaluation of mu <b>opioid</b> receptor (<strong>OPRM1</strong>) as a predictor of naltrexone response in the treatment of alcohol dependence: results from the Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence (COMBINE) study.
+OPRM1	addiction	dependence	18250251	An evaluation of mu opioid receptor (<strong>OPRM1</strong>) as a predictor of naltrexone response in the treatment of alcohol <b>dependence</b>: results from the Combined Pharmacotherapies and Behavioral Interventions for Alcohol <b>Dependence</b> (COMBINE) study.
+OPRM1	drug	alcohol	18250251	Asn40Asp, a functional polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>), might predict <b>naltrexone</b> response.
+OPRM1	drug	opioid	18250251	Asn40Asp, a functional polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>), might predict naltrexone response.
+OPRM1	drug	alcohol	18250251	To evaluate whether individuals with <b>alcoholism</b> who are heterozygous (Asp40/Asn40) or homozygous (Asp40/Asp40) for the <strong>OPRM1</strong> Asp40 allele respond better to <b>naltrexone</b>.
+OPRM1	drug	alcohol	18250251	These results confirm and extend the observation that the functionally significant <strong>OPRM1</strong> Asp40 allele predicts <b>naltrexone</b> treatment response in <b>alcoholic</b> individuals.
+OPRM1	drug	alcohol	18250251	<strong>OPRM1</strong> genotyping in <b>alcoholic</b> individuals might be useful to assist in selecting treatment options.
+OPRM1	drug	opioid	18195715	This approach has identified several new genes potentially associated with <b>heroin</b> addiction and has confirmed the role of <strong>OPRM1</strong> in this disease.
+OPRM1	addiction	addiction	18195715	This approach has identified several new genes potentially associated with heroin <b>addiction</b> and has confirmed the role of <strong>OPRM1</strong> in this disease.
+OPRM1	drug	opioid	18181266	A118g polymorphism in mu <b>opioid</b> receptor gene (<strong>oprm1</strong>): association with opiate addiction in subjects of Indian origin.
+OPRM1	addiction	addiction	18181266	A118g polymorphism in mu opioid receptor gene (<strong>oprm1</strong>): association with opiate <b>addiction</b> in subjects of Indian origin.
+OPRM1	drug	opioid	18181266	The opioidergic hypothesis suggests an association between genetic variations at the <b>opioid</b> receptor mu 1 (<strong>OPRM1</strong>) gene locus and opiate addiction.
+OPRM1	addiction	addiction	18181266	The opioidergic hypothesis suggests an association between genetic variations at the opioid receptor mu 1 (<strong>OPRM1</strong>) gene locus and opiate <b>addiction</b>.
+OPRM1	drug	opioid	18181266	The opioidergic hypothesis suggests an association between genetic variations at the <strong><b>opioid</b> receptor mu 1</strong> (<strong>OPRM1</strong>) gene locus and opiate addiction.
+OPRM1	addiction	addiction	18181266	The opioidergic hypothesis suggests an association between genetic variations at the <strong>opioid receptor mu 1</strong> (<strong>OPRM1</strong>) gene locus and opiate <b>addiction</b>.
+OPRM1	drug	opioid	18181266	The <strong>OPRM1</strong> gene, which encodes for mu <b>opioid</b> receptor, contains several single nucleotide polymorphisms (SNPs) in exon I.
+OPRM1	drug	alcohol	18028530	Polymorphisms in the D4 dopamine receptor (DRD4) gene and the mu opiate receptor (<strong>OPRM1</strong>) gene, family history of <b>alcohol</b> problems, age of onset of <b>alcoholism</b> and gender were explored as potential moderators of NTX's effects.
+OPRM1	drug	alcohol	17979515	Polymorphisms in the mu opioid receptor gene (<strong>OPRM1</strong>) and the implications for <b>alcohol</b> dependence in humans.
+OPRM1	drug	opioid	17979515	Polymorphisms in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) and the implications for alcohol dependence in humans.
+OPRM1	addiction	dependence	17979515	Polymorphisms in the mu opioid receptor gene (<strong>OPRM1</strong>) and the implications for alcohol <b>dependence</b> in humans.
+OPRM1	drug	alcohol	17979515	In attempts to identify the genetic factors involved, association studies have linked the opioid system to <b>alcohol</b> dependence, with a main focus on the <strong>OPRM1</strong> gene encoding the mu opioid receptor.
+OPRM1	drug	opioid	17979515	In attempts to identify the genetic factors involved, association studies have linked the <b>opioid</b> system to alcohol dependence, with a main focus on the <strong>OPRM1</strong> gene encoding the mu <b>opioid</b> receptor.
+OPRM1	addiction	dependence	17979515	In attempts to identify the genetic factors involved, association studies have linked the opioid system to alcohol <b>dependence</b>, with a main focus on the <strong>OPRM1</strong> gene encoding the mu opioid receptor.
+OPRM1	drug	alcohol	17979515	Our aim was to conduct a systematic review of the literature on the associations between polymorphisms in <strong>OPRM1</strong> and <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	17979515	Our aim was to conduct a systematic review of the literature on the associations between polymorphisms in <strong>OPRM1</strong> and alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	17979515	Our review showed that clinical studies do not unequivocally support an association between polymorphisms in <strong>OPRM1</strong> and <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	17979515	Our review showed that clinical studies do not unequivocally support an association between polymorphisms in <strong>OPRM1</strong> and alcohol <b>dependence</b>.
+OPRM1	drug	opioid	17850768	<b>Buprenorphine</b> maintenance showed a dampened HPA axis response to metyrapone, with <strong>OPRM1</strong> 118G carriers showing a significantly attenuated response compared with 118A carriers.
+OPRM1	drug	alcohol	17768272	Clinical trials have suggested a modest effect of <b>naltrexone</b> as a pharmacotherapy for <b>alcoholism</b>, and a recent study has suggested that the effects may be moderated by variations in the mu opioid receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	17768272	Clinical trials have suggested a modest effect of naltrexone as a pharmacotherapy for alcoholism, and a recent study has suggested that the effects may be moderated by variations in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	alcohol	17768272	However, the mechanism by which <b>naltrexone</b> may be differentially effective as a function of the <strong>OPRM1</strong> genotype is unclear.
+OPRM1	drug	alcohol	17768272	(1) To replicate and expand on the association between the A118G single nucleotide polymorphism(SNP) of the <strong>OPRM1</strong> gene and <b>alcohol</b> sensitivity, (2) to examine the effects of <b>naltrexone</b> on <b>alcohol</b> sensitivity, and (3) to test the A118G SNP of the <strong>OPRM1</strong> gene as a moderator of the effects of <b>naltrexone</b> on <b>alcohol</b> sensitivity.
+OPRM1	drug	alcohol	17503481	We analyzed 18 <strong>OPRM1</strong> SNPs, 18 OPRD1 SNPs, 7 PENK SNPs, and 7 POMC SNPs in a sample of 1923 European Americans from 219 multiplex <b>alcohol</b> dependent families.
+OPRM1	drug	opioid	17503481	Secondary analyses employing the narrower phenotype of <b>opioid</b> dependence (83 affected individuals) demonstrated association with SNPs in PENK and POMC, but not in <strong>OPRM1</strong> or OPRD1.
+OPRM1	addiction	dependence	17503481	Secondary analyses employing the narrower phenotype of opioid <b>dependence</b> (83 affected individuals) demonstrated association with SNPs in PENK and POMC, but not in <strong>OPRM1</strong> or OPRD1.
+OPRM1	drug	alcohol	17503481	Therefore, our data provide no support for the idea that variations in <strong>OPRM1</strong>, OPRD1, PENK and POMC are associated with <b>alcohol</b> dependence or general illicit drug dependence, but variations in PENK and POMC appear to be associated with the narrower phenotype of opioid dependence in these families.
+OPRM1	drug	opioid	17503481	Therefore, our data provide no support for the idea that variations in <strong>OPRM1</strong>, OPRD1, PENK and POMC are associated with alcohol dependence or general illicit drug dependence, but variations in PENK and POMC appear to be associated with the narrower phenotype of <b>opioid</b> dependence in these families.
+OPRM1	addiction	dependence	17503481	Therefore, our data provide no support for the idea that variations in <strong>OPRM1</strong>, OPRD1, PENK and POMC are associated with alcohol <b>dependence</b> or general illicit drug <b>dependence</b>, but variations in PENK and POMC appear to be associated with the narrower phenotype of opioid <b>dependence</b> in these families.
+OPRM1	drug	opioid	17416470	Evaluation of <strong>OPRM1</strong> variants in <b>heroin</b> dependence by family based association testing and meta analysis.
+OPRM1	addiction	dependence	17416470	Evaluation of <strong>OPRM1</strong> variants in heroin <b>dependence</b> by family based association testing and meta analysis.
+OPRM1	drug	opioid	17416470	<strong>OPRM1</strong>, which codes for the mu <b>opioid</b> receptor, is the most frequently studied candidate gene for <b>opioid</b> dependence.
+OPRM1	addiction	dependence	17416470	<strong>OPRM1</strong>, which codes for the mu opioid receptor, is the most frequently studied candidate gene for opioid <b>dependence</b>.
+OPRM1	drug	opioid	17416470	Despite numerous allelic association studies, no definitive conclusion has been reached regarding the role of <strong>OPRM1</strong> polymorphisms in determining risk for <b>opioid</b> dependence.
+OPRM1	addiction	dependence	17416470	Despite numerous allelic association studies, no definitive conclusion has been reached regarding the role of <strong>OPRM1</strong> polymorphisms in determining risk for opioid <b>dependence</b>.
+OPRM1	drug	opioid	17416470	First, we genotyped three single nucleotide polymorphisms (SNPs) of <strong>OPRM1</strong> in 1208 individuals from 473 Han Chinese families ascertained on the basis of having two or more siblings with DSM IV defined <b>opioid</b> dependence.
+OPRM1	addiction	dependence	17416470	First, we genotyped three single nucleotide polymorphisms (SNPs) of <strong>OPRM1</strong> in 1208 individuals from 473 Han Chinese families ascertained on the basis of having two or more siblings with DSM IV defined opioid <b>dependence</b>.
+OPRM1	drug	opioid	17416470	Although a role of <strong>OPRM1</strong> polymorphisms in determining risk for <b>opioid</b> dependence cannot be entirely discounted, a major contribution of the Asn40Asp polymorphism seems unlikely.
+OPRM1	addiction	dependence	17416470	Although a role of <strong>OPRM1</strong> polymorphisms in determining risk for opioid <b>dependence</b> cannot be entirely discounted, a major contribution of the Asn40Asp polymorphism seems unlikely.
+OPRM1	drug	opioid	17416470	In addition, it is critical that other <strong>OPRM1</strong> variants, including all haplotype tagging and amino acid coding SNPs, be tested for an influence on risk for <b>opioid</b> dependence, since the Asn40Asp polymorphism is only one of several hundred known mutations in the gene.
+OPRM1	addiction	dependence	17416470	In addition, it is critical that other <strong>OPRM1</strong> variants, including all haplotype tagging and amino acid coding SNPs, be tested for an influence on risk for opioid <b>dependence</b>, since the Asn40Asp polymorphism is only one of several hundred known mutations in the gene.
+OPRM1	drug	alcohol	17374034	Opioid receptor gene (<strong>OPRM1</strong>, OPRK1, and OPRD1) variants and response to <b>naltrexone</b> treatment for <b>alcohol</b> dependence: results from the VA Cooperative Study.
+OPRM1	drug	opioid	17374034	<b>Opioid</b> receptor gene (<strong>OPRM1</strong>, OPRK1, and OPRD1) variants and response to naltrexone treatment for alcohol dependence: results from the VA Cooperative Study.
+OPRM1	addiction	dependence	17374034	Opioid receptor gene (<strong>OPRM1</strong>, OPRK1, and OPRD1) variants and response to naltrexone treatment for alcohol <b>dependence</b>: results from the VA Cooperative Study.
+OPRM1	drug	alcohol	17374034	We studied polymorphic variants at each of the 3 opioid receptor genes  <strong>OPRM1</strong>, OPRD1, and OPRK1, which encode the mu, delta, and kappa opioid receptors, respectively  including the <strong>OPRM1</strong> Asn40Asp variant  as predictors of response to NTX or placebo in 215 <b>alcohol</b> dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "<b>Naltrexone</b> in the Treatment of <b>Alcohol</b> Dependence."
+OPRM1	drug	opioid	17374034	We studied polymorphic variants at each of the 3 <b>opioid</b> receptor genes  <strong>OPRM1</strong>, OPRD1, and OPRK1, which encode the mu, delta, and kappa <b>opioid</b> receptors, respectively  including the <strong>OPRM1</strong> Asn40Asp variant  as predictors of response to NTX or placebo in 215 alcohol dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "Naltrexone in the Treatment of Alcohol Dependence."
+OPRM1	addiction	dependence	17374034	We studied polymorphic variants at each of the 3 opioid receptor genes  <strong>OPRM1</strong>, OPRD1, and OPRK1, which encode the mu, delta, and kappa opioid receptors, respectively  including the <strong>OPRM1</strong> Asn40Asp variant  as predictors of response to NTX or placebo in 215 alcohol dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "Naltrexone in the Treatment of Alcohol <b>Dependence</b>."
+OPRM1	addiction	dependence	17367590	These polymorphisms might be correlated with <strong>OPRM1</strong> mRNA stability and opiate sensitivity, including opiate analgesia, tolerance, and <b>dependence</b>.
+OPRM1	drug	nicotine	17224915	We investigated the association of the <strong>OPRM1</strong> genotype with long term <b>smoking</b> cessation and change in body mass index (BMI) following a <b>smoking</b> cessation attempt among <b>smokers</b> who attempted to quit using the <b>nicotine</b> replacement therapy (NRT) patch or placebo in a randomized controlled trial, and were followed up over an 8 year period following their initial cessation attempt.
+OPRM1	drug	nicotine	17224915	Our results indicate that <strong>OPRM1</strong> genotype may moderate the effect of transdermal <b>nicotine</b> patch compared to placebo during active treatment, with a benefit of active NRT treatment evident in the <strong>OPRM1</strong> AA genotype group only and those carrying one or more copies of the G allele demonstrating no benefit of active NRT versus placebo patch.
+OPRM1	drug	alcohol	17224915	Future studies should also investigate the role of <strong>OPRM1</strong> genotype and smoking cessation on other appetitive and reward behaviours such as <b>alcohol</b> consumption.
+OPRM1	drug	nicotine	17224915	Future studies should also investigate the role of <strong>OPRM1</strong> genotype and <b>smoking</b> cessation on other appetitive and reward behaviours such as alcohol consumption.
+OPRM1	addiction	reward	17224915	Future studies should also investigate the role of <strong>OPRM1</strong> genotype and smoking cessation on other appetitive and <b>reward</b> behaviours such as alcohol consumption.
+OPRM1	drug	alcohol	17207095	A functional polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) influences cue induced craving for <b>alcohol</b> in male heavy drinkers.
+OPRM1	drug	opioid	17207095	A functional polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) influences cue induced craving for alcohol in male heavy drinkers.
+OPRM1	addiction	relapse	17207095	A functional polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) influences cue induced <b>craving</b> for alcohol in male heavy drinkers.
+OPRM1	drug	opioid	17207095	The mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) codes for the mu <b>opioid</b> receptor, which binds beta endorphin.
+OPRM1	drug	opioid	17157823	To evaluate the association of mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) variants with <b>heroin</b> induced positive responses on first use, we studied 336 Chinese Han <b>heroin</b> addicts recruited in Shanghai and divided <b>heroin</b> addicts into two groups (positive vs. negative) according to the self reporting feeling on first use.
+OPRM1	drug	opioid	17157823	Self reported positive responses on first use of <b>heroin</b> were found to be associated with <strong>OPRM1</strong>.
+OPRM1	drug	nicotine	16960700	Association of <strong>OPRM1</strong> A118G variant with the relative reinforcing value of <b>nicotine</b>.
+OPRM1	addiction	reward	16960700	Association of <strong>OPRM1</strong> A118G variant with the relative <b>reinforcing</b> value of nicotine.
+OPRM1	drug	alcohol	16960700	We examined (1) the association of the functional <strong>OPRM1</strong> A118G variant with the relative reinforcing value of nicotine and (2) the main and interacting effects of the mu opioid receptor antagonist <b>naltrexone</b> on nicotine reinforcement.
+OPRM1	drug	nicotine	16960700	We examined (1) the association of the functional <strong>OPRM1</strong> A118G variant with the relative reinforcing value of <b>nicotine</b> and (2) the main and interacting effects of the mu opioid receptor antagonist naltrexone on <b>nicotine</b> reinforcement.
+OPRM1	drug	opioid	16960700	We examined (1) the association of the functional <strong>OPRM1</strong> A118G variant with the relative reinforcing value of nicotine and (2) the main and interacting effects of the mu <b>opioid</b> receptor antagonist naltrexone on nicotine reinforcement.
+OPRM1	addiction	reward	16960700	We examined (1) the association of the functional <strong>OPRM1</strong> A118G variant with the relative <b>reinforcing</b> value of nicotine and (2) the main and interacting effects of the mu opioid receptor antagonist naltrexone on nicotine <b>reinforcement</b>.
+OPRM1	drug	alcohol	16960700	In a within subject, double blind human laboratory study, 30 smokers of each <strong>OPRM1</strong> genotype (A/A vs. A/G or G/G) participated in two experimental sessions following 4 days of orally administered <b>naltrexone</b> 50 mg or placebo.
+OPRM1	drug	nicotine	16960700	In a within subject, double blind human laboratory study, 30 <b>smokers</b> of each <strong>OPRM1</strong> genotype (A/A vs. A/G or G/G) participated in two experimental sessions following 4 days of orally administered naltrexone 50 mg or placebo.
+OPRM1	drug	nicotine	16960700	The relative reinforcing value of <b>nicotine</b> (number of <b>nicotine</b> cigarette puffs) was predicted by a significant <strong>OPRM1</strong> by gender interaction.
+OPRM1	addiction	reward	16960700	The relative <b>reinforcing</b> value of nicotine (number of nicotine cigarette puffs) was predicted by a significant <strong>OPRM1</strong> by gender interaction.
+OPRM1	drug	nicotine	16960700	This study provides initial evidence for an association of the <strong>OPRM1</strong> A118G variant with <b>nicotine</b> reinforcement in women.
+OPRM1	addiction	reward	16960700	This study provides initial evidence for an association of the <strong>OPRM1</strong> A118G variant with nicotine <b>reinforcement</b> in women.
+OPRM1	addiction	relapse	16899031	Polymorphisms in the D4 dopamine receptor (DRD4) gene and mu opiate receptor gene (<strong>OPRM1</strong>) may moderate NTX's effects on <b>craving</b>.
+OPRM1	drug	alcohol	16899031	The non treatment seeking male and female heavy drinkers (62% <b>alcohol</b> dependent) were genotyped for the variable number of tandem repeats polymorphism in the DRD4 gene [L=7 or more (n=34), S=less than 7 (n=56)] and Asn40Asp single nucleotide polymorphism in the <strong>OPRM1</strong> gene [29 aspartate (Asp) carriers and 59 asparagine (Asn) homozygotes].
+OPRM1	addiction	relapse	16899031	The non treatment <b>seeking</b> male and female heavy drinkers (62% alcohol dependent) were genotyped for the variable number of tandem repeats polymorphism in the DRD4 gene [L=7 or more (n=34), S=less than 7 (n=56)] and Asn40Asp single nucleotide polymorphism in the <strong>OPRM1</strong> gene [29 aspartate (Asp) carriers and 59 asparagine (Asn) homozygotes].
+OPRM1	drug	opioid	16887046	The gene encoding the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) is reported to be associated with a range of substance dependence.
+OPRM1	addiction	dependence	16887046	The gene encoding the mu opioid receptor (<strong>OPRM1</strong>) is reported to be associated with a range of substance <b>dependence</b>.
+OPRM1	drug	nicotine	16887046	Additionally, the <strong>OPRM1</strong> gene is located in a region showing linkage to <b>nicotine</b> dependence.
+OPRM1	addiction	dependence	16887046	Additionally, the <strong>OPRM1</strong> gene is located in a region showing linkage to nicotine <b>dependence</b>.
+OPRM1	drug	nicotine	16887046	The <strong>OPRM1</strong> is thus a plausible candidate gene for <b>smoking</b> behavior.
+OPRM1	drug	nicotine	16887046	To investigate whether <strong>OPRM1</strong> contributes to the susceptibility of <b>smoking</b> initiation and <b>nicotine</b> dependence, we genotyped 11 SNPs in the gene for 688 Caucasian subjects of lifetime <b>smokers</b> and nonsmokers.
+OPRM1	addiction	dependence	16887046	To investigate whether <strong>OPRM1</strong> contributes to the susceptibility of smoking initiation and nicotine <b>dependence</b>, we genotyped 11 SNPs in the gene for 688 Caucasian subjects of lifetime smokers and nonsmokers.
+OPRM1	drug	nicotine	16887046	These results suggest that <strong>OPRM1</strong> may be involved in <b>smoking</b> initiation and <b>nicotine</b> dependence.
+OPRM1	addiction	dependence	16887046	These results suggest that <strong>OPRM1</strong> may be involved in smoking initiation and nicotine <b>dependence</b>.
+OPRM1	drug	opioid	16753266	In the acute treatment, expression levels for the encoded mu <b>opioid</b> receptor <strong>Oprm1</strong>, as detected by reverse transcription polymerase chain reaction, were significantly decreased in the periaqueductal gray.
+OPRM1	drug	opioid	16753266	In chronic treatment, both Oprk1 and <strong>Oprm1</strong> expression levels, that encoded kappa and mu <b>opioid</b> receptor respectively, showed significant decreases in the periaqueductal gray and striatum.
+OPRM1	drug	opioid	16682632	Mu <b>opioid</b> receptors are critical for <b>heroin</b> dependence, and A118G SNP of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) has been linked with <b>heroin</b> abuse.
+OPRM1	addiction	dependence	16682632	Mu opioid receptors are critical for heroin <b>dependence</b>, and A118G SNP of the mu opioid receptor gene (<strong>OPRM1</strong>) has been linked with heroin abuse.
+OPRM1	drug	opioid	16682632	Postmortem brain analyses showed the <strong>OPRM1</strong> genotype associated with transcription, translation, and processing of the human striatal <b>opioid</b> neuropeptide system.
+OPRM1	drug	opioid	16682632	Reduced <b>opioid</b> neuropeptide transcription was accompanied by increased dynorphin and enkephalin peptide concentrations exclusively in 118G <b>heroin</b> subjects, suggesting that the peptide processing is associated with the <strong>OPRM1</strong> genotype.
+OPRM1	drug	opioid	16679777	The polymorphism A118G in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) causes the amino acid change Asn40Asp and has been reported to affect the affinity of the ligand for the receptor.
+OPRM1	drug	alcohol	16679777	In the present study, we compared the frequencies of the polymorphism <strong>OPRM1</strong> A118G between patients with <b>alcohol</b> dependence and healthy control subjects living in a Japanese provincial prefecture.
+OPRM1	addiction	dependence	16679777	In the present study, we compared the frequencies of the polymorphism <strong>OPRM1</strong> A118G between patients with alcohol <b>dependence</b> and healthy control subjects living in a Japanese provincial prefecture.
+OPRM1	drug	alcohol	16679777	Both <strong>OPRM1</strong> 118G and ALDH2 1510G were significantly associated with <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	16679777	Both <strong>OPRM1</strong> 118G and ALDH2 1510G were significantly associated with alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	16679777	These results suggest that <strong>OPRM1</strong> 118G in addition to ALDH2 1510G might be one of the risk factors for <b>alcohol</b> dependence in Japanese people.
+OPRM1	addiction	dependence	16679777	These results suggest that <strong>OPRM1</strong> 118G in addition to ALDH2 1510G might be one of the risk factors for alcohol <b>dependence</b> in Japanese people.
+OPRM1	drug	alcohol	16476706	Association between two mu opioid receptor gene (<strong>OPRM1</strong>) haplotype blocks and drug or <b>alcohol</b> dependence.
+OPRM1	drug	opioid	16476706	Association between two mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) haplotype blocks and drug or alcohol dependence.
+OPRM1	addiction	dependence	16476706	Association between two mu opioid receptor gene (<strong>OPRM1</strong>) haplotype blocks and drug or alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	16476706	We examined 13 single nucleotide polymorphisms (SNPs) spanning the coding region of the mu opioid receptor gene (<strong>OPRM1</strong>), among 382 European Americans (EAs) affected with substance dependence [<b>alcohol</b> dependence (AD) and/or drug dependence (DD)] and 338 EA healthy controls.
+OPRM1	drug	opioid	16476706	We examined 13 single nucleotide polymorphisms (SNPs) spanning the coding region of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>), among 382 European Americans (EAs) affected with substance dependence [alcohol dependence (AD) and/or drug dependence (DD)] and 338 EA healthy controls.
+OPRM1	addiction	dependence	16476706	We examined 13 single nucleotide polymorphisms (SNPs) spanning the coding region of the mu opioid receptor gene (<strong>OPRM1</strong>), among 382 European Americans (EAs) affected with substance <b>dependence</b> [alcohol <b>dependence</b> (AD) and/or drug <b>dependence</b> (DD)] and 338 EA healthy controls.
+OPRM1	addiction	dependence	16476706	Logistic regression analyses confirmed the association between <strong>OPRM1</strong> variants and substance <b>dependence</b>, when sex and age of subjects and alleles, genotypes, haplotypes or diplotypes of five tag SNPs were considered.
+OPRM1	addiction	dependence	16451620	This region harbors <strong>OPRM1</strong>, a candidate gene for substance <b>dependence</b>.
+OPRM1	drug	opioid	16415919	Polymorphisms in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) are primary candidate sources of clinical variability in <b>opioid</b> therapy.
+OPRM1	drug	opioid	16415919	Apart from the 118A>G single nucleotide polymorphism, nothing is known about the role of <strong>OPRM1</strong> mutations in <b>opioid</b> therapy.
+OPRM1	drug	opioid	16415919	The influence of the <strong>OPRM1</strong> mutations on <b>opioid</b> pharmacodynamics was assessed in pooled data from 31 healthy volunteers obtained in previous studies with available plasma concentrations and pupil diameters after intravenous administration of <b>morphine</b> or <b>morphine</b> 6 glucuronide (M6G).
+OPRM1	drug	opioid	16415919	Based on <b>morphine</b> and M6G, the present analysis encourages focusing on the 118A>G SNP when investigating the role of <strong>OPRM1</strong> mutations for the activity of <b>opioid</b> analgesics.
+OPRM1	drug	opioid	16415919	This applies to <b>opioid</b> potency in the context of <b>opioid</b> therapy but not to pain processing or substance addiction, in which <b>opioid</b> receptors are involved but other or additional <strong>OPRM1</strong> mutations may be important.
+OPRM1	addiction	addiction	16415919	This applies to opioid potency in the context of opioid therapy but not to pain processing or substance <b>addiction</b>, in which opioid receptors are involved but other or additional <strong>OPRM1</strong> mutations may be important.
+OPRM1	drug	opioid	16402083	We newly identified several polymorphisms and four substantial linkage disequilibrium (LD) blocks in the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) gene.
+OPRM1	drug	opioid	16387451	Studies examining the association of the mu <b>opioid</b> receptor gene (genetic locus <strong>OPRM1</strong>) with substance dependence (SD) have focused on the Asn40Asp (A118G) single nucleotide polymorphism (SNP).
+OPRM1	addiction	dependence	16387451	Studies examining the association of the mu opioid receptor gene (genetic locus <strong>OPRM1</strong>) with substance <b>dependence</b> (SD) have focused on the Asn40Asp (A118G) single nucleotide polymorphism (SNP).
+OPRM1	drug	alcohol	16223057	<strong>OPRM1</strong> Asn40Asp is a common (minor allele frequency 0.10), functional polymorphism of the mu opioid receptor, which may serve as a gatekeeper molecule in <b>naltrexone</b>'s actions and was recently reported to affect <b>naltrexone</b> response.
+OPRM1	drug	opioid	16223057	<strong>OPRM1</strong> Asn40Asp is a common (minor allele frequency 0.10), functional polymorphism of the mu <b>opioid</b> receptor, which may serve as a gatekeeper molecule in naltrexone's actions and was recently reported to affect naltrexone response.
+OPRM1	drug	opioid	16194531	The present study examined the subcellular distribution of the cloned MOR, <strong>MOR1</strong>, in rat C1 neurons following chronic <b>morphine</b> treatment, using RVLM sections that were dually labeled for PNMT immunoperoxidase and <strong>MOR1</strong> immunogold.
+OPRM1	drug	opioid	16194531	Electron microscopic analysis of the subcellular distribution of <strong>MOR1</strong> revealed a lower abundance of plasma membrane associated <strong>MOR1</strong> in C1 dendrites of rats treated with <b>morphine</b>, compared to placebo treated controls, only in distal dendrites.
+OPRM1	drug	opioid	16194531	These results suggest that chronic <b>morphine</b> treatment leads to a decreased presence of <strong>MOR1</strong> at the cell surface, without a significant reduction in cytoplasmic receptor density.
+OPRM1	drug	opioid	16194531	These observations suggest that chronic <b>morphine</b> produces a selective internalization of <strong>MOR1</strong> in C1 neurons, without apparent changes in receptor synthesis or trafficking.
+OPRM1	drug	opioid	16046395	Allelic expression imbalance of human mu <b>opioid</b> receptor (<strong>OPRM1</strong>) caused by variant A118G.
+OPRM1	drug	opioid	16046395	As a primary target for <b>opioid</b> drugs and peptides, the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) plays a key role in pain perception and addiction.
+OPRM1	addiction	addiction	16046395	As a primary target for opioid drugs and peptides, the mu opioid receptor (<strong>OPRM1</strong>) plays a key role in pain perception and <b>addiction</b>.
+OPRM1	addiction	addiction	16046395	Genetic variants of <strong>OPRM1</strong> have been implicated in predisposition to drug <b>addiction</b>, in particular the single nucleotide polymorphism A118G, leading to an N40D substitution, with an allele frequency of 10 32%, and uncertain functions.
+OPRM1	drug	opioid	15925706	Recent studies using inbred and knockout mice have revealed that the mu <b>opioid</b> peptide (MOP) receptor encoded by the <strong>Oprm1</strong> gene has a mandatory role in the analgesic and addictive properties of opiate drugs.
+OPRM1	addiction	addiction	15925706	Recent studies using inbred and knockout mice have revealed that the mu opioid peptide (MOP) receptor encoded by the <strong>Oprm1</strong> gene has a mandatory role in the analgesic and <b>addictive</b> properties of opiate drugs.
+OPRM1	addiction	dependence	15925706	Increasing evidence suggests that differences in <strong>Oprm1</strong> gene sequences affect the amount of <strong>Oprm1</strong> mRNA and sensitivity to opiates, and >100 polymorphisms have been identified in the human <strong>OPRM1</strong> gene, some of which are related to vulnerability to drug <b>dependence</b> in some populations.
+OPRM1	drug	opioid	15680308	The mu <b>opioid</b> receptor (MOR, <strong>OPRM</strong>)  the principal receptor involved in narcotic addiction  has been shown to display basal (spontaneous, constitutive) signaling activity.
+OPRM1	addiction	addiction	15680308	The mu opioid receptor (MOR, <strong>OPRM</strong>)  the principal receptor involved in narcotic <b>addiction</b>  has been shown to display basal (spontaneous, constitutive) signaling activity.
+OPRM1	drug	alcohol	15608594	A polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) and sensitivity to the effects of <b>alcohol</b> in humans.
+OPRM1	drug	opioid	15608594	A polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) and sensitivity to the effects of alcohol in humans.
+OPRM1	drug	opioid	15608594	The A118G polymorphism of the <strong>OPRM1</strong> gene has been shown to confer functional differences to mu <b>opioid</b> receptors, such that the G variant binds beta endorphin three times more strongly than the A variant.
+OPRM1	drug	alcohol	15584875	Functional alleles that alter <b>alcoholism</b> related intermediate phenotypes include common <b>alcohol</b> dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; catechol O methyltransferase (COMT) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (<strong>OPRM1</strong>) Asn40Asp, which may serve as a gatekeeper molecule in the action of <b>naltrexone</b>, a drug used in <b>alcoholism</b> treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+OPRM1	drug	opioid	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; catechol O methyltransferase (COMT) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and <b>opioid</b> function; <b>opioid</b> receptor micro1 (<strong>OPRM1</strong>) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+OPRM1	addiction	addiction	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; catechol O methyltransferase (COMT) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (<strong>OPRM1</strong>) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of <b>addiction</b>, and relapse.
+OPRM1	addiction	aversion	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the <b>aversive</b> flushing reaction; catechol O methyltransferase (COMT) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (<strong>OPRM1</strong>) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+OPRM1	addiction	relapse	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; catechol O methyltransferase (COMT) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (<strong>OPRM1</strong>) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and <b>relapse</b>.
+OPRM1	drug	opioid	15558714	Novel exonic mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) polymorphisms not associated with <b>opioid</b> dependence.
+OPRM1	addiction	dependence	15558714	Novel exonic mu opioid receptor gene (<strong>OPRM1</strong>) polymorphisms not associated with opioid <b>dependence</b>.
+OPRM1	drug	opioid	15558714	Variability in the MOR gene, <strong>OPRM1</strong>, may influence risk for <b>opioid</b> dependence.
+OPRM1	addiction	dependence	15558714	Variability in the MOR gene, <strong>OPRM1</strong>, may influence risk for opioid <b>dependence</b>.
+OPRM1	drug	opioid	15558714	The results indicate that polymorphisms in the novel splice variant are not associated with <b>opioid</b> dependence, but are in LD with other polymorphisms in <strong>OPRM1</strong>.
+OPRM1	addiction	dependence	15558714	The results indicate that polymorphisms in the novel splice variant are not associated with opioid <b>dependence</b>, but are in LD with other polymorphisms in <strong>OPRM1</strong>.
+OPRM1	drug	amphetamine	15542732	We have investigated associations of the mu opioid receptor gene (<strong>OPRM</strong>) variations with <b>methamphetamine</b> (MAP) dependence/psychosis.
+OPRM1	drug	opioid	15542732	We have investigated associations of the mu <b>opioid</b> receptor gene (<strong>OPRM</strong>) variations with methamphetamine (MAP) dependence/psychosis.
+OPRM1	addiction	dependence	15542732	We have investigated associations of the mu opioid receptor gene (<strong>OPRM</strong>) variations with methamphetamine (MAP) <b>dependence</b>/psychosis.
+OPRM1	addiction	dependence	15542732	Further analysis should be capable of identifying associations between the <strong>OPRM</strong> variations and MAP <b>dependence</b>/psychosis.
+OPRM1	drug	opioid	15525999	We have previously demonstrated that the frequently occurring A118G single nucleotide polymorphism (SNP) in exon 1 of the MORgene (<strong>OPRM1</strong>), which encodes an amino acid substitution, is functional and receptors encoded by the variant 118G allele bind the endogenous <b>opioid</b> peptide beta endorphin with three fold greater affinity than prototype receptors.
+OPRM1	drug	alcohol	15525999	In central Sweden, the functional variant 118G allele in exon 1 of <strong>OPRM1</strong> is associated with an increased attributable risk for <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	15525999	In central Sweden, the functional variant 118G allele in exon 1 of <strong>OPRM1</strong> is associated with an increased attributable risk for alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	15252283	The functional polymorphism (A118G) of the mu opioid receptor gene (<strong>OPRM1</strong>) is thought to have clinical significance in the treatment of <b>alcohol</b> dependence.
+OPRM1	drug	opioid	15252283	The functional polymorphism (A118G) of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) is thought to have clinical significance in the treatment of alcohol dependence.
+OPRM1	addiction	dependence	15252283	The functional polymorphism (A118G) of the mu opioid receptor gene (<strong>OPRM1</strong>) is thought to have clinical significance in the treatment of alcohol <b>dependence</b>.
+OPRM1	drug	opioid	15167694	Association study of personality factors and the Asn40Asp polymorphism at the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	15048644	We found correspondence between linkage and microarray/candidate gene studies for genes involved with the mitogen activated protein kinase (MAPK) signaling system, nuclear factor kappa B (NFKB) complex, neuropeptide Y (NPY) neurotransmission, a nicotinic receptor subunit (CHRNA2), the vesicular monoamine transporter (SLC18A2), genes in pathways implicated in human anxiety (HTR7, TDO2, and the endozepine related protein precursor, DKFZP434A2417), and the micro 1 <b>opioid</b> receptor (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	14969743	The mu <b>opioid</b> receptor (<strong>OPRM1</strong>) is expressed in brain regions implicated in reward and locomotor processes.
+OPRM1	addiction	reward	14969743	The mu opioid receptor (<strong>OPRM1</strong>) is expressed in brain regions implicated in <b>reward</b> and locomotor processes.
+OPRM1	addiction	reward	14969743	Reduced <b>reward</b>, not only from opiates, but also from several other abused substances has been observed in mice with lifelong deletions of the <strong>OPRM1</strong> gene.
+OPRM1	drug	cocaine	14969743	In a sensitization study (modeled after the conditions in the dose response experiment) although not observed in WT mice, <strong>OPRM1</strong> /  mice did exhibit <b>cocaine</b> sensitization.
+OPRM1	addiction	sensitization	14969743	In a <b>sensitization</b> study (modeled after the conditions in the dose response experiment) although not observed in WT mice, <strong>OPRM1</strong> /  mice did exhibit cocaine <b>sensitization</b>.
+OPRM1	drug	cocaine	14969743	By stark contrast, and similar to the effects of other rewarding drugs in <strong>OPRM1</strong> KO mice, <b>cocaine</b> reward, as assessed by conditioned place preference, was reduced in both homozygous and heterozygous <strong>OPRM1</strong> KO mice.
+OPRM1	addiction	reward	14969743	By stark contrast, and similar to the effects of other rewarding drugs in <strong>OPRM1</strong> KO mice, cocaine <b>reward</b>, as assessed by conditioned place preference, was reduced in both homozygous and heterozygous <strong>OPRM1</strong> KO mice.
+OPRM1	drug	alcohol	14745298	Nonselective opioid antagonists reduce <b>alcohol</b> consumption under various experimental situations, and several association studies have examined possible roles of opioid receptor mu (<strong>OPRM</strong>), delta (OPRD), and kappa (OPRK) genes in the development of <b>alcohol</b> dependence.
+OPRM1	drug	opioid	14745298	Nonselective <b>opioid</b> antagonists reduce alcohol consumption under various experimental situations, and several association studies have examined possible roles of <b>opioid</b> receptor mu (<strong>OPRM</strong>), delta (OPRD), and kappa (OPRK) genes in the development of alcohol dependence.
+OPRM1	addiction	dependence	14745298	Nonselective opioid antagonists reduce alcohol consumption under various experimental situations, and several association studies have examined possible roles of opioid receptor mu (<strong>OPRM</strong>), delta (OPRD), and kappa (OPRK) genes in the development of alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	14745298	We examined 20 single nucleotide polymorphisms (SNPs) across the <strong>OPRM</strong>, OPRD, and OPRK genes in 158 <b>alcohol</b> dependent subjects and 149 controls.
+OPRM1	drug	opioid	12960749	Studies using animal models also support a role for genetic factors in <b>opioid</b> dependence, and point to a locus of major effect on mouse chromosome 10 (Berrettini et al., 1994; Alexander et al., 1996), which harbors the mu <b>opioid</b> receptor gene (<strong>Mor1</strong>) (Kozak et al., 1994).
+OPRM1	addiction	dependence	12960749	Studies using animal models also support a role for genetic factors in opioid <b>dependence</b>, and point to a locus of major effect on mouse chromosome 10 (Berrettini et al., 1994; Alexander et al., 1996), which harbors the mu opioid receptor gene (<strong>Mor1</strong>) (Kozak et al., 1994).
+OPRM1	drug	opioid	12960749	The gene encoding the human mu <b>opioid</b> receptor (<strong>OPRM1</strong>) is thus an obvious candidate gene for contributing to <b>opioid</b> dependence.
+OPRM1	addiction	dependence	12960749	The gene encoding the human mu opioid receptor (<strong>OPRM1</strong>) is thus an obvious candidate gene for contributing to opioid <b>dependence</b>.
+OPRM1	addiction	dependence	12960749	A recent report (Hoehe et al., 2000) found a significant association between a specific combination of <strong>OPRM1</strong> single nucleotide polymorphisms (SNPs) and substance <b>dependence</b>.
+OPRM1	drug	opioid	12960749	In the current study, we genotyped 213 subjects with severe <b>opioid</b> dependence (89 African Americans, 124 European Americans) and 196 carefully screened "supercontrol" subjects (96 African Americans, 100 European Americans) at five SNPs residing in the <strong>OPRM1</strong> gene.
+OPRM1	addiction	dependence	12960749	In the current study, we genotyped 213 subjects with severe opioid <b>dependence</b> (89 African Americans, 124 European Americans) and 196 carefully screened "supercontrol" subjects (96 African Americans, 100 European Americans) at five SNPs residing in the <strong>OPRM1</strong> gene.
+OPRM1	drug	opioid	12898579	To explore the role of the micro  <b>opioid</b> receptor gene (<strong>OPRM</strong>) in human pain tolerance and <b>opioid</b> addiction, we examined the relationships among <strong>OPRM</strong> genotype and experimental pain tolerance in <b>opioid</b> addicts in <b>methadone</b> treatment (n = 50) and healthy normal controls (n = 59).
+OPRM1	addiction	addiction	12898579	To explore the role of the micro  opioid receptor gene (<strong>OPRM</strong>) in human pain tolerance and opioid <b>addiction</b>, we examined the relationships among <strong>OPRM</strong> genotype and experimental pain tolerance in opioid addicts in methadone treatment (n = 50) and healthy normal controls (n = 59).
+OPRM1	addiction	dependence	12815747	Haplotypes at the <strong>OPRM1</strong> locus are associated with susceptibility to substance <b>dependence</b> in European Americans.
+OPRM1	drug	opioid	12815747	Our objective was to investigate the relationship between the gene encoding the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) and susceptibility to substance dependence in European American (EA) and African American (AA) subjects.
+OPRM1	addiction	dependence	12815747	Our objective was to investigate the relationship between the gene encoding the mu opioid receptor (<strong>OPRM1</strong>) and susceptibility to substance <b>dependence</b> in European American (EA) and African American (AA) subjects.
+OPRM1	addiction	dependence	12815747	Eight single nucleotide polymorphisms (SNPs) at the <strong>OPRM1</strong> locus, i.e.,  2044C/A,  1793T/A,  1699insT,  1469T/C,  1320A/G,  111C/T, +17C/T (Ala6Val), and +118A/G (Asn40Asp) were genotyped in 676 subjects: 318 EA subjects and 124 AA subjects with substance <b>dependence</b>, and 179 EA normal controls, and 55 AA normal controls.
+OPRM1	addiction	dependence	12815747	These findings suggest that <strong>OPRM1</strong> may play a role in the pathophysiology of substance <b>dependence</b> and this role is population  and diagnosis specific.
+OPRM1	drug	alcohol	12813472	A total of 82 patients (71 of European descent) who were randomized to <b>naltrexone</b> and 59 who were randomized to placebo (all of European descent) in one of three randomized, placebo controlled clinical trials of <b>naltrexone</b> were genotyped at the A(+118)G (Asn40Asp) and C(+17)T (Ala6Val) SNPs in the gene encoding the mu opioid receptor (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	12813472	A total of 82 patients (71 of European descent) who were randomized to naltrexone and 59 who were randomized to placebo (all of European descent) in one of three randomized, placebo controlled clinical trials of naltrexone were genotyped at the A(+118)G (Asn40Asp) and C(+17)T (Ala6Val) SNPs in the gene encoding the mu <b>opioid</b> receptor (<strong>OPRM1</strong>).
+OPRM1	drug	alcohol	12813472	These preliminary results are consistent with prior literature demonstrating that the opioid system is involved in the reinforcing properties of <b>alcohol</b> and that allelic variation at <strong>OPRM1</strong> is associated with differential response to a mu receptor antagonist.
+OPRM1	drug	opioid	12813472	These preliminary results are consistent with prior literature demonstrating that the <b>opioid</b> system is involved in the reinforcing properties of alcohol and that allelic variation at <strong>OPRM1</strong> is associated with differential response to a mu receptor antagonist.
+OPRM1	addiction	reward	12813472	These preliminary results are consistent with prior literature demonstrating that the opioid system is involved in the <b>reinforcing</b> properties of alcohol and that allelic variation at <strong>OPRM1</strong> is associated with differential response to a mu receptor antagonist.
+OPRM1	drug	opioid	12657887	The distribution of three polymorphisms of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) was investigated in four different Asian populations, and in <b>heroin</b> dependent subjects deriving from three of these populations.
+OPRM1	drug	opioid	12648891	In a modified case control association study we tested the assumption that two polymorphisms (A(118)G in exon 1 and IVS2+31 in intron 2) of the human mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) confer susceptibility to <b>opioid</b> dependence.
+OPRM1	addiction	dependence	12648891	In a modified case control association study we tested the assumption that two polymorphisms (A(118)G in exon 1 and IVS2+31 in intron 2) of the human mu opioid receptor gene (<strong>OPRM1</strong>) confer susceptibility to opioid <b>dependence</b>.
+OPRM1	drug	opioid	12648891	For the two allelic variants of <strong>OPRM1</strong> under study we did not find evidence for association with <b>opioid</b> dependence.
+OPRM1	addiction	dependence	12648891	For the two allelic variants of <strong>OPRM1</strong> under study we did not find evidence for association with opioid <b>dependence</b>.
+OPRM1	drug	opioid	11933204	Sequence variations in the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) associated with human addiction to <b>heroin</b>.
+OPRM1	addiction	addiction	11933204	Sequence variations in the mu opioid receptor gene (<strong>OPRM1</strong>) associated with human <b>addiction</b> to heroin.
+OPRM1	drug	opioid	11933204	Human mu <b>opioid</b> receptor (<strong>OPRM1</strong>) is the major site for the analgesic action of most <b>opioid</b> drugs such as <b>morphine</b>, <b>methadone</b> and <b>heroin</b>.
+OPRM1	drug	opioid	11933204	Using denaturing high performance liquid chromatography (DHPLC) the complete coding region of the <strong>OPRM1</strong> gene was screened for SNPs in Han Chinese <b>heroin</b> addicts and normal control.
+OPRM1	addiction	dependence	11840318	Our findings and analyses suggest that the <strong>OPRM1</strong> +118 polymorphism is a general risk gene for substance <b>dependence</b>, but is not specific to a particular substance.
+OPRM1	drug	opioid	11424981	Nonreplication of association between mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) A118G polymorphism and substance dependence.
+OPRM1	addiction	dependence	11424981	Nonreplication of association between mu opioid receptor gene (<strong>OPRM1</strong>) A118G polymorphism and substance <b>dependence</b>.
+OPRM1	drug	alcohol	11424981	In the present investigation we hypothesized the A118G (Asn40Asp) polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) as a particular vulnerability factor for heroin and <b>alcohol</b> dependence.
+OPRM1	drug	opioid	11424981	In the present investigation we hypothesized the A118G (Asn40Asp) polymorphism of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) as a particular vulnerability factor for <b>heroin</b> and alcohol dependence.
+OPRM1	addiction	dependence	11424981	In the present investigation we hypothesized the A118G (Asn40Asp) polymorphism of the mu opioid receptor gene (<strong>OPRM1</strong>) as a particular vulnerability factor for heroin and alcohol <b>dependence</b>.
+OPRM1	drug	opioid	11424981	In both patient samples and by both methods we were unable to corroborate the hypothesis of <strong>OPRM1</strong> A118G polymorphism as a particular risk factor for any kind of substance dependence including <b>opioid</b> addiction.
+OPRM1	addiction	addiction	11424981	In both patient samples and by both methods we were unable to corroborate the hypothesis of <strong>OPRM1</strong> A118G polymorphism as a particular risk factor for any kind of substance dependence including opioid <b>addiction</b>.
+OPRM1	addiction	dependence	11424981	In both patient samples and by both methods we were unable to corroborate the hypothesis of <strong>OPRM1</strong> A118G polymorphism as a particular risk factor for any kind of substance <b>dependence</b> including opioid addiction.
+OPRM1	drug	opioid	11146127	The mu <b>opioid</b> receptor (<strong>MOR1</strong>) mediates the main analgesic effects of <b>morphine</b> and several other <b>opioids</b>.
+OPRM1	drug	opioid	11146127	Since the specific pattern of mu <b>opioid</b> receptor regulation in vivo is thought to depend on the cell  and tissue specific complement of protein kinases, we examined the spatial relation between <strong>MOR1</strong> and CaMKII in rat brain using specific antibodies.
+OPRM1	drug	opioid	11146127	Together, we identify CaMKII as a potential protein kinase, which by virtue of its colocalization with <strong>MOR1</strong> may be in a position to phosphorylate the mu <b>opioid</b> receptor and may thus contribute to the development of tolerance to <b>opioid</b> analgesics.
+OPRM1	drug	cocaine	11092766	Using the human mu opioid receptor gene (<strong>OPRM1</strong>) as a model system, we have combined these approaches to test a potential role of <strong>OPRM1</strong> in substance (heroin/<b>cocaine</b>) dependence.
+OPRM1	drug	opioid	11092766	Using the human mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) as a model system, we have combined these approaches to test a potential role of <strong>OPRM1</strong> in substance (<b>heroin</b>/cocaine) dependence.
+OPRM1	addiction	dependence	11092766	Using the human mu opioid receptor gene (<strong>OPRM1</strong>) as a model system, we have combined these approaches to test a potential role of <strong>OPRM1</strong> in substance (heroin/cocaine) <b>dependence</b>.
+OPRM1	drug	opioid	10982041	The three <b>opioid</b> receptor genes, and in particular the mu and delta loci (<strong>OPRM1</strong> and OPRD1, respectively), are compelling candidates to influence risk for substance dependence.
+OPRM1	addiction	dependence	10982041	The three opioid receptor genes, and in particular the mu and delta loci (<strong>OPRM1</strong> and OPRD1, respectively), are compelling candidates to influence risk for substance <b>dependence</b>.
+OPRM1	drug	opioid	10835636	The mu , delta  and kappa  <b>opioid</b> receptors (encoded by <strong>Oprm</strong>, Oprd1 and Oprk1, respectively) mediate the biological activity of <b>opioids</b>.
+OPRM1	drug	opioid	10835636	Our data show no detectable phenotype in Oprk1 /  mutants, suggesting that kappa receptors do not have a role in this aspect of <b>opioid</b> function; opposing phenotypes in <strong>Oprm</strong> /  and Oprd1 /  mutants which contrasts with the classical notion of similar activities of mu  and delta receptors; and consistent anxiogenic  and depressive like responses in Oprd1 /  mice, indicating that delta receptor activity contributes to improvement of mood states.
+OPRM1	drug	alcohol	10523821	Genetics of two mu opioid receptor gene (<strong>OPRM1</strong>) exon I polymorphisms: population studies, and allele frequencies in <b>alcohol</b>  and drug dependent subjects.
+OPRM1	drug	opioid	10523821	Genetics of two mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>) exon I polymorphisms: population studies, and allele frequencies in alcohol  and drug dependent subjects.
+OPRM1	drug	opioid	10523821	The gene encoding the mu <b>opioid</b> receptor, <strong>OPRM1</strong>, contains at least two polymorphisms affecting protein sequence in exon 1, Ala6Val and Asp40Asn.
+OPRM1	drug	alcohol	10399772	The Asn40Asp substitution polymorphism of the human mu opioid receptor (<strong>OPRM</strong>) influences binding of opioids and signal transduction and may, thereby, contribute to the development of <b>alcoholism</b>.
+OPRM1	drug	opioid	10399772	The Asn40Asp substitution polymorphism of the human mu <b>opioid</b> receptor (<strong>OPRM</strong>) influences binding of <b>opioids</b> and signal transduction and may, thereby, contribute to the development of alcoholism.
+OPRM1	drug	alcohol	10399772	The present study tested whether the Asn40Asp substitution polymorphism of the <strong>OPRM</strong> gene is associated with a variation in central dopaminergic sensitivity during <b>alcohol</b> withdrawal in <b>alcoholics</b>.
+OPRM1	addiction	withdrawal	10399772	The present study tested whether the Asn40Asp substitution polymorphism of the <strong>OPRM</strong> gene is associated with a variation in central dopaminergic sensitivity during alcohol <b>withdrawal</b> in alcoholics.
+OPRM1	drug	alcohol	9884158	The present association study tested the hypothesis that the common Asn40Asp substitution polymorphism in the N terminal domain of the human mu opioid receptor (<strong>OPRM</strong>) confers vulnerability to subtypes of <b>alcohol</b> dependence.
+OPRM1	drug	opioid	9884158	The present association study tested the hypothesis that the common Asn40Asp substitution polymorphism in the N terminal domain of the human mu <b>opioid</b> receptor (<strong>OPRM</strong>) confers vulnerability to subtypes of alcohol dependence.
+OPRM1	addiction	dependence	9884158	The present association study tested the hypothesis that the common Asn40Asp substitution polymorphism in the N terminal domain of the human mu opioid receptor (<strong>OPRM</strong>) confers vulnerability to subtypes of alcohol <b>dependence</b>.
+OPRM1	drug	alcohol	9884158	Our results do not provide evidence that the common Asn40Asp substitution polymorphism of the <strong>OPRM</strong> gene contributes a major effect to the pathogenesis of <b>alcohol</b> dependence.
+OPRM1	addiction	dependence	9884158	Our results do not provide evidence that the common Asn40Asp substitution polymorphism of the <strong>OPRM</strong> gene contributes a major effect to the pathogenesis of alcohol <b>dependence</b>.
+OPRM1	drug	opioid	9790747	Population studies of polymorphisms at loci of neuropsychiatric interest (tryptophan hydroxylase (TPH), dopamine transporter protein (SLC6A3), D3 dopamine receptor (DRD3), apolipoprotein E (APOE), mu <b>opioid</b> receptor (<strong>OPRM1</strong>), and ciliary neurotrophic factor (CNTF)).
+OPRM1	drug	opioid	9790747	We determined allele frequencies for polymorphisms at several loci of interest in neuropsychiatry tryptophan hydroxylase (TPH), dopamine transporter protein (SLC6A3), D3 dopamine receptor (DRD3), apolipoprotein E (APOE), ciliary neurotrophic factor (CNTF), and the mu <b>opioid</b> receptor (<strong>OPRM1</strong>) in samples of individuals from populations in several different parts of the world.
+OPRM1	drug	cocaine	9790747	Associations with psychiatric illness have been proposed for specific polymorphisms at TPH (suicide related behaviors and impulsivity), DRD3 (schizophrenia and bipolar affective disorder), SLC6A3 (susceptibility to <b>cocaine</b> induced paranoia and attention deficit disorder), CNTF (psychosis), and <strong>OPRM1</strong> (substance dependence).
+OPRM1	addiction	dependence	9790747	Associations with psychiatric illness have been proposed for specific polymorphisms at TPH (suicide related behaviors and impulsivity), DRD3 (schizophrenia and bipolar affective disorder), SLC6A3 (susceptibility to cocaine induced paranoia and attention deficit disorder), CNTF (psychosis), and <strong>OPRM1</strong> (substance <b>dependence</b>).
+OPRM1	drug	alcohol	9756053	Association of <b>alcohol</b> or other drug dependence with alleles of the mu opioid receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	opioid	9756053	Association of alcohol or other drug dependence with alleles of the mu <b>opioid</b> receptor gene (<strong>OPRM1</strong>).
+OPRM1	addiction	dependence	9756053	Association of alcohol or other drug <b>dependence</b> with alleles of the mu opioid receptor gene (<strong>OPRM1</strong>).
+OPRM1	drug	alcohol	9756053	Consequently, the present study examined the association of a polymorphic (CA)n repeat at the <strong>OPRM1</strong> locus (the gene coding for the mu opioid receptor) to <b>alcohol</b> or drug dependence in 320 Caucasian and 108 African American substance dependent or control subjects.
+OPRM1	drug	opioid	9756053	Consequently, the present study examined the association of a polymorphic (CA)n repeat at the <strong>OPRM1</strong> locus (the gene coding for the mu <b>opioid</b> receptor) to alcohol or drug dependence in 320 Caucasian and 108 African American substance dependent or control subjects.
+OPRM1	addiction	dependence	9756053	Consequently, the present study examined the association of a polymorphic (CA)n repeat at the <strong>OPRM1</strong> locus (the gene coding for the mu opioid receptor) to alcohol or drug <b>dependence</b> in 320 Caucasian and 108 African American substance dependent or control subjects.
+OPRM1	drug	alcohol	9756053	Among Caucasians, suggestion of a modest association, which could be interpreted as statistically significant (p = 0.03), was observed between <strong>OPRM1</strong> alleles and substance (<b>alcohol</b>, cocaine, or opioid) dependence.
+OPRM1	drug	cocaine	9756053	Among Caucasians, suggestion of a modest association, which could be interpreted as statistically significant (p = 0.03), was observed between <strong>OPRM1</strong> alleles and substance (alcohol, <b>cocaine</b>, or opioid) dependence.
+OPRM1	drug	opioid	9756053	Among Caucasians, suggestion of a modest association, which could be interpreted as statistically significant (p = 0.03), was observed between <strong>OPRM1</strong> alleles and substance (alcohol, cocaine, or <b>opioid</b>) dependence.
+OPRM1	addiction	dependence	9756053	Among Caucasians, suggestion of a modest association, which could be interpreted as statistically significant (p = 0.03), was observed between <strong>OPRM1</strong> alleles and substance (alcohol, cocaine, or opioid) <b>dependence</b>.
+OPRM1	addiction	dependence	9756053	Further studies of the association between alleles of the <strong>OPRM1</strong> gene and substance <b>dependence</b> appear warranted, particularly if they use a family based approach to control for population stratification.
+OPRM1	drug	alcohol	9756053	Phenotypes other than a broad diagnostic categorization, such as opioid antagonist effects on drinking behavior in <b>alcoholics</b>, may provide more consistent evidence of a role for <strong>OPRM1</strong> in behavioral variability.
+OPRM1	drug	opioid	9756053	Phenotypes other than a broad diagnostic categorization, such as <b>opioid</b> antagonist effects on drinking behavior in alcoholics, may provide more consistent evidence of a role for <strong>OPRM1</strong> in behavioral variability.
+OPRM1	drug	opioid	9593704	The rat mu <b>opioid</b> receptor is alternatively spliced into two isoforms (<strong>MOR1</strong> and MOR1B) which differ in length and amino acid composition at the carboxyl terminus.
+OPRM1	addiction	withdrawal	9593704	However, the shorter isoform, MOR1B, desensitized at a slower rate during prolonged DAMGO exposure (4 h) but resensitized at a faster rate than <strong>MOR1</strong> during agonist <b>withdrawal</b> (20 min).
+OPRM1	drug	alcohol	9399694	In addition, the murine mu opioid receptor locus, <strong>Oprm</strong>, is implicated as the major quantitative trait locus (QTL) affecting the different levels of morphine consumption between two inbred mouse strains that also exhibit differences in <b>alcohol</b> and cocaine consumption.
+OPRM1	drug	cocaine	9399694	In addition, the murine mu opioid receptor locus, <strong>Oprm</strong>, is implicated as the major quantitative trait locus (QTL) affecting the different levels of morphine consumption between two inbred mouse strains that also exhibit differences in alcohol and <b>cocaine</b> consumption.
+OPRM1	drug	opioid	9399694	In addition, the murine mu <b>opioid</b> receptor locus, <strong>Oprm</strong>, is implicated as the major quantitative trait locus (QTL) affecting the different levels of <b>morphine</b> consumption between two inbred mouse strains that also exhibit differences in alcohol and cocaine consumption.
+OPRM1	drug	opioid	9399694	Detection of genetic variation affecting <strong>OPRM1</strong> expression or mu <b>opioid</b> receptor function would be an important step towards understanding the origins of inter individual variation in response to mu <b>opioid</b> receptor ligands and in diseases of substance dependence.
+OPRM1	addiction	dependence	9399694	Detection of genetic variation affecting <strong>OPRM1</strong> expression or mu opioid receptor function would be an important step towards understanding the origins of inter individual variation in response to mu opioid receptor ligands and in diseases of substance <b>dependence</b>.
+OPRM1	drug	opioid	9399694	We directly sequenced the human mu <b>opioid</b> receptor locus, <strong>OPRM1</strong>, to detect natural variation that might affect function and/or be associated with psychiatric phenotypes related to <b>opioid</b> function.
+OPRM1	drug	alcohol	9399694	<strong>OPRM1</strong> alleles, genotypes and haplotypes from three psychiatrically characterized population samples (US Caucasian [USC, n=100], Finnish Caucasian [FC, n=324] and Southwestern American Indian [SAI, n=367]), were used to perform association and sib pair linkage analyses with <b>alcohol</b> and drug dependence diagnoses.
+OPRM1	addiction	dependence	9399694	<strong>OPRM1</strong> alleles, genotypes and haplotypes from three psychiatrically characterized population samples (US Caucasian [USC, n=100], Finnish Caucasian [FC, n=324] and Southwestern American Indian [SAI, n=367]), were used to perform association and sib pair linkage analyses with alcohol and drug <b>dependence</b> diagnoses.
+OPRM1	drug	alcohol	9399694	This analysis has 80% power to detect a small to moderate effect of <strong>OPRM1</strong> variation on <b>alcohol</b> dependence and 100% power to detect effects of the magnitude of the ALDH2*2 variant.
+OPRM1	addiction	dependence	9399694	This analysis has 80% power to detect a small to moderate effect of <strong>OPRM1</strong> variation on alcohol <b>dependence</b> and 100% power to detect effects of the magnitude of the ALDH2*2 variant.
+OPRM1	drug	alcohol	9399694	While these data do not support a role of the mu opioid receptor in susceptibility to <b>alcohol</b> dependence, the potential relationship between <strong>OPRM1</strong> genetic variation and response to endogenous opioids and exogenous opiates can now be investigated.
+OPRM1	drug	opioid	9399694	While these data do not support a role of the mu <b>opioid</b> receptor in susceptibility to alcohol dependence, the potential relationship between <strong>OPRM1</strong> genetic variation and response to endogenous <b>opioids</b> and exogenous opiates can now be investigated.
+OPRM1	addiction	dependence	9399694	While these data do not support a role of the mu opioid receptor in susceptibility to alcohol <b>dependence</b>, the potential relationship between <strong>OPRM1</strong> genetic variation and response to endogenous opioids and exogenous opiates can now be investigated.
+OPRM1	drug	opioid	7752808	In this study, we completed the localization on mouse chromosomes of the genes encoding mu (<strong>Oprm</strong>) and kappa (Oprk) receptors, as well as the genes for the <b>opioid</b> propeptides proenkephalin (Penk) and prodynorphin (Pdyn).
+IL6	drug	alcohol	32750174	<b>Alcohol</b> craving questionnaire, <b>alcohol</b> consumption (urinary ethylglucuronide/creatinine, Etg), quality of life (QOL), cognition, serum <strong>IL 6</strong> and lipopolysaccharide binding protein (LBP), plasma/stool short chain fatty acids (SCFA) and stool microbiota were tested at baseline and day 15.
+IL6	addiction	relapse	32750174	Alcohol <b>craving</b> questionnaire, alcohol consumption (urinary ethylglucuronide/creatinine, Etg), quality of life (QOL), cognition, serum <strong>IL 6</strong> and lipopolysaccharide binding protein (LBP), plasma/stool short chain fatty acids (SCFA) and stool microbiota were tested at baseline and day 15.
+IL6	drug	opioid	32733481	<b>Opioids</b> bind to TLR4, in a manner parallel to LPS, activating TLR4 signaling, which leads to nuclear factor kappa light chain enhancer of activated B cells (NF κB) expression and the production of the pro inflammatory cytokines tumor necrosis factor (TNF) α, interleukin (IL) 1β, and <strong>IL 6</strong>.
+IL6	drug	cannabinoid	32714224	These findings warrant further investigation into the potential <strong>IL 6</strong> trans signaling modulatory, anti inflammatory, neuroimmune, and biobehavioral cognitive effects of <b>Cannabis</b> use in SCZ.
+IL6	drug	alcohol	32714160	Results revealed that rats challenged with <b>ethanol</b> at either PD35 or PD90 generally exhibited a characteristic cytokine signature of acute intoxication that we have previously reported: increased <strong>Il 6</strong> and IkBα expression, with decreased Il 1β and Tnfα gene expression.
+IL6	addiction	intoxication	32714160	Results revealed that rats challenged with ethanol at either PD35 or PD90 generally exhibited a characteristic cytokine signature of acute <b>intoxication</b> that we have previously reported: increased <strong>Il 6</strong> and IkBα expression, with decreased Il 1β and Tnfα gene expression.
+IL6	drug	alcohol	32714160	While few significant effects of PAE were observed for <b>ethanol</b> induced alterations in cytokine expression, there was a consistent (but nonsignificant) trend for PAE to potentiate the expression of <strong>Il 6</strong> and IkBα in all groups except adult females.
+IL6	drug	alcohol	32634532	<b>Alcohol</b> and <strong>IL 6</strong> Alter Expression of Synaptic Proteins in Cerebellum of Transgenic Mice with Increased Astrocyte Expression of <strong>IL 6</strong>.
+IL6	drug	alcohol	32634532	Recent studies indicate that neuroimmune factors, including the cytokine interleukin 6 (<strong>IL 6</strong>), play a role in the CNS actions of <b>alcohol</b>.
+IL6	drug	alcohol	32634532	Recent studies indicate that neuroimmune factors, including the cytokine <strong>interleukin 6</strong> (<strong>IL 6</strong>), play a role in the CNS actions of <b>alcohol</b>.
+IL6	drug	alcohol	32634532	<strong>IL 6</strong> also alters synaptic transmission, although it is unknown if <strong>IL 6</strong> targets are also targets of <b>alcohol</b>.
+IL6	drug	alcohol	32634532	This is an important issue because <b>alcohol</b> induces glial production of <strong>IL 6</strong>, which could then covertly influence the actions of <b>alcohol</b>.
+IL6	drug	alcohol	32634532	The persistent cerebellar effects of both <strong>IL 6</strong> and <b>alcohol</b> typically involve chronic exposure and, presumably, altered gene and protein expression.
+IL6	drug	alcohol	32634532	Thus, in the current studies we tested the possibility that proteins involved in inhibitory and excitatory synaptic transmission in the cerebellum are common targets of <b>alcohol</b> and <strong>IL 6</strong>.
+IL6	drug	alcohol	32634532	We used transgenic mice that express elevated levels of astrocyte produced <strong>IL 6</strong> to model persistently elevated expression of <strong>IL 6</strong>, as would occur in <b>alcohol</b> use disorders, and a chronic intermittent <b>alcohol</b> exposure/withdrawal paradigm (CIE/withdrawal) that is known to produce <b>alcohol</b> dependence.
+IL6	addiction	dependence	32634532	We used transgenic mice that express elevated levels of astrocyte produced <strong>IL 6</strong> to model persistently elevated expression of <strong>IL 6</strong>, as would occur in alcohol use disorders, and a chronic intermittent alcohol exposure/withdrawal paradigm (CIE/withdrawal) that is known to produce alcohol <b>dependence</b>.
+IL6	addiction	withdrawal	32634532	We used transgenic mice that express elevated levels of astrocyte produced <strong>IL 6</strong> to model persistently elevated expression of <strong>IL 6</strong>, as would occur in alcohol use disorders, and a chronic intermittent alcohol exposure/<b>withdrawal</b> paradigm (CIE/<b>withdrawal</b>) that is known to produce alcohol dependence.
+IL6	addiction	withdrawal	32634532	Results show that <strong>IL 6</strong> and CIE/<b>withdrawal</b> have both unique and common actions that affect synaptic protein expression.
+IL6	drug	alcohol	32634532	These common targets could provide sites for <strong>IL 6</strong>/<b>alcohol</b> exposure/withdrawal interactions and play an important role in cerebellar symptoms of <b>alcohol</b> use such as ataxia.
+IL6	addiction	withdrawal	32634532	These common targets could provide sites for <strong>IL 6</strong>/alcohol exposure/<b>withdrawal</b> interactions and play an important role in cerebellar symptoms of alcohol use such as ataxia.
+IL6	drug	psychedelics	32542550	Use of the adsorber device was associated with a decline in <b>MDMA</b> concentrations in serum from 540 to 140 ng/ml within the first 24 h, a decrease of <strong>interleukin 6</strong> and myoglobin levels, and subsequent clinical improvement.
+IL6	drug	opioid	32524520	The <b>morphine</b> induced increases of apoptosis, neuron death, OS, lipid peroxidation, caspase 3 and caspase 9, neuroinflammatory cytokines (IL 1β, TNF α, <strong>IL 6</strong>), and Ca2+ levels in the hippocampal neuron of TRPM2 WT mouse were decreased by the L NAME, ACA, and 2 APB treatments, although cell viability, neuron count, and reduced glutathione and glutathione peroxidase levels were increased by the treatments.
+IL6	drug	alcohol	32116558	Expression levels of inflammatory factors (TNF α, IL 1β, and <strong>IL 6</strong>) were increased in mice after 4 weeks of <b>alcohol</b> exposure.
+IL6	drug	alcohol	31736187	<b>Alcohol</b> craving and serum measures of tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1 (TNFR1), interleukin 6 (<strong>IL 6</strong>), and interleukin 1 receptor antagonist (IL 1ra) were collected prior to and following imagery exposure.
+IL6	addiction	relapse	31736187	Alcohol <b>craving</b> and serum measures of tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1 (TNFR1), interleukin 6 (<strong>IL 6</strong>), and interleukin 1 receptor antagonist (IL 1ra) were collected prior to and following imagery exposure.
+IL6	drug	alcohol	31736187	<b>Alcohol</b> craving and serum measures of tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1 (TNFR1), <strong>interleukin 6</strong> (<strong>IL 6</strong>), and interleukin 1 receptor antagonist (IL 1ra) were collected prior to and following imagery exposure.
+IL6	addiction	relapse	31736187	Alcohol <b>craving</b> and serum measures of tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1 (TNFR1), <strong>interleukin 6</strong> (<strong>IL 6</strong>), and interleukin 1 receptor antagonist (IL 1ra) were collected prior to and following imagery exposure.
+IL6	drug	alcohol	31736187	Dampened IL 1ra and <strong>IL 6</strong> in response to stress was observed as a function of <b>alcohol</b> dependence and not moderated by depressive symptoms.
+IL6	addiction	dependence	31736187	Dampened IL 1ra and <strong>IL 6</strong> in response to stress was observed as a function of alcohol <b>dependence</b> and not moderated by depressive symptoms.
+IL6	drug	alcohol	31675629	Prior work has established that that an acute <b>ethanol</b> challenge mimicking high intensity <b>alcohol</b> consumption increased <strong>IL 6</strong> and suppressed IL 1β and TNFα mRNA in intoxication, with the opposite pattern seen in withdrawal.
+IL6	addiction	intoxication	31675629	Prior work has established that that an acute ethanol challenge mimicking high intensity alcohol consumption increased <strong>IL 6</strong> and suppressed IL 1β and TNFα mRNA in <b>intoxication</b>, with the opposite pattern seen in withdrawal.
+IL6	addiction	withdrawal	31675629	Prior work has established that that an acute ethanol challenge mimicking high intensity alcohol consumption increased <strong>IL 6</strong> and suppressed IL 1β and TNFα mRNA in intoxication, with the opposite pattern seen in <b>withdrawal</b>.
+IL6	drug	opioid	31630319	Co administration of venlafaxine (40 mg/kg) with <b>morphine</b> not only inhibited the <b>naloxone</b> precipitated withdrawal signs including jumping and weight loss, but also reduced the up regulation of TNF α, IL 1β, <strong>IL 6</strong>, NO and MDA contents in mice brain tissue.
+IL6	addiction	withdrawal	31630319	Co administration of venlafaxine (40 mg/kg) with morphine not only inhibited the naloxone precipitated <b>withdrawal</b> signs including jumping and weight loss, but also reduced the up regulation of TNF α, IL 1β, <strong>IL 6</strong>, NO and MDA contents in mice brain tissue.
+IL6	addiction	relapse	31525567	In our analysis of the biological determinants of personality factors, we identified significant associations between <strong>IL 6</strong> and novelty <b>seeking</b> assessment, and between PIC and neuroticism assessment.
+IL6	drug	cannabinoid	31525567	These data provide evidence of a biological link between metabolites of the kynurenine pathway, the <b>endocannabinoid</b> system and <strong>IL 6</strong> and suggest that these factors may influence personality traits.
+IL6	drug	alcohol	31443893	Mindfulness practice predicts <strong>interleukin 6</strong> responses to a mindfulness based <b>alcohol</b> relapse prevention intervention.
+IL6	addiction	relapse	31443893	Mindfulness practice predicts <strong>interleukin 6</strong> responses to a mindfulness based alcohol <b>relapse</b> prevention intervention.
+IL6	drug	alcohol	31443893	Given that Mindfulness Based Relapse Prevention (MBRP) has been shown to reduce <b>alcohol</b> misuse, MBRP might also be effective in reducing <strong>IL 6</strong> concentrations.
+IL6	addiction	relapse	31443893	Given that Mindfulness Based <b>Relapse</b> Prevention (MBRP) has been shown to reduce alcohol misuse, MBRP might also be effective in reducing <strong>IL 6</strong> concentrations.
+IL6	drug	alcohol	31443893	Building on prior studies, we examined whether between person variability in engagement with mindfulness training (i.e., formal mindfulness practice time) is associated with between person variability in changes in serum <strong>IL 6</strong>, using data from a randomized controlled trial evaluating MBRP for <b>Alcohol</b> Dependence (MBRP A).
+IL6	addiction	dependence	31443893	Building on prior studies, we examined whether between person variability in engagement with mindfulness training (i.e., formal mindfulness practice time) is associated with between person variability in changes in serum <strong>IL 6</strong>, using data from a randomized controlled trial evaluating MBRP for Alcohol <b>Dependence</b> (MBRP A).
+IL6	addiction	addiction	31443893	The association between practice time and <strong>IL 6</strong> changes remained significant when controlling for intervention timing (i.e., immediate or after the 26 week delay), demographic characteristics, and changes in mindful awareness, obsessive <b>compulsive</b> drinking, and depressive symptoms.
+IL6	drug	alcohol	31437534	Increased <strong>IL 6</strong> expression in astrocytes is associated with emotionality, alterations in central amygdala GABAergic transmission, and excitability during <b>alcohol</b> withdrawal.
+IL6	addiction	withdrawal	31437534	Increased <strong>IL 6</strong> expression in astrocytes is associated with emotionality, alterations in central amygdala GABAergic transmission, and excitability during alcohol <b>withdrawal</b>.
+IL6	drug	alcohol	31437534	Accumulating evidence from preclinical and clinical studies has implicated a role for the cytokine <strong>IL 6</strong> in a variety of CNS diseases including anxiety like and depressive like behaviors, as well as <b>alcohol</b> use disorder.
+IL6	drug	alcohol	31398460	We hypothesized that chronic <b>alcohol</b> consumption impairs memory and increases the inflammatory cytokines TNFα, <strong>IL6</strong>, MCP1, and IL1β in the hippocampus and prefrontal cortex regions in the brain.
+IL6	drug	alcohol	31373129	Subsequent epigenetic (chromatin immunoprecipitation [ChIP] sequencing) analysis showed that <b>alcohol</b> induced changes in H3K27me3 were significantly enriched at genes in the <strong>IL 6</strong> signaling pathway, consistent with the well characterized role of KDM6B in modulation of inflammatory responses.
+IL6	drug	alcohol	31334440	Deficient <strong>IL 6</strong>/Stat3 Signaling, High TLR7, and Type I Interferons in Early Human <b>Alcoholic</b> Liver Disease: A Triad for Liver Damage and Fibrosis.
+IL6	addiction	reward	31333427	Following <b>CPP</b>, biological samples were taken to measure striatal levels of interleukin 6 (<strong>IL 6</strong>) and plasmatic levels of oxytocin (OT).
+IL6	addiction	reward	31333427	Following <b>CPP</b>, biological samples were taken to measure striatal levels of <strong>interleukin 6</strong> (<strong>IL 6</strong>) and plasmatic levels of oxytocin (OT).
+IL6	addiction	reward	31333427	Our results confirmed that ISD animals housed in standard condition displayed an anxious phenotype, developed <b>CPP</b> and had increased levels of <strong>IL 6</strong> in the striatum.
+IL6	drug	amphetamine	31282647	Systemically administered <b>METH</b> (1 mg/kg) was found to specifically up regulate expression of both CD11b (microglial activation marker) and the proinflammatory cytokine interleukin 6 (<strong>IL 6</strong>) mRNAs in the ventral tegmental area (VTA), but not in either the nucleus accumbens shell (NAc) or prefrontal cortex (PFC).
+IL6	drug	amphetamine	31282647	Systemically administered <b>METH</b> (1 mg/kg) was found to specifically up regulate expression of both CD11b (microglial activation marker) and the proinflammatory cytokine <strong>interleukin 6</strong> (<strong>IL 6</strong>) mRNAs in the ventral tegmental area (VTA), but not in either the nucleus accumbens shell (NAc) or prefrontal cortex (PFC).
+IL6	drug	amphetamine	31282647	Systemic administration of a nonopioid, blood brain barrier permeable TLR4 antagonist (+) naloxone inhibited <b>METH</b> induced activation of microglia and <strong>IL 6</strong> mRNA overexpression in VTA.
+IL6	drug	opioid	31282647	Systemic administration of a nonopioid, blood brain barrier permeable TLR4 antagonist (+) <b>naloxone</b> inhibited METH induced activation of microglia and <strong>IL 6</strong> mRNA overexpression in VTA.
+IL6	drug	amphetamine	31282647	Furthermore, intra VTA injection of LPS RS or <strong>IL 6</strong> neutralizing antibody suppressed <b>METH</b> induced elevation of extracellular NAc dopamine.
+IL6	drug	amphetamine	31282647	Taken together, this series of studies demonstrate that <b>METH</b> induced neuroinflammation is, at least in part, mediated by TLR4 <strong>IL6</strong> signaling within the VTA, which has the downstream effect of elevating dopamine in the NAc shell.
+IL6	drug	alcohol	31167126	Our results revealed that <b>ethanol</b> challenge overtly compromised echocardiographic, cardiomyocyte contractile, intracellular Ca2+ and ultrastructural properties along with overt apoptosis, inflammation (elevated MIF, IL 1β and <strong>IL 6</strong>) and mitochondrial O2  production (p < 0.01), the effect of which was reconciled by CD74 ablation (p < 0.01 vs. <b>ethanol</b> group) with the exception of MIF expression.
+IL6	drug	nicotine	31079306	In stratified models, gender, age, <b>smoking</b> status, and hypertension only led to small modifications in effect estimates, though a few of the estimates for <strong>IL 6</strong> and TNF α became non significant.
+IL6	drug	amphetamine	31078920	We found that <b>METH</b> exposure increased LPS induced <strong>IL 6</strong> and TNF α production in the Hip, CPU and NAc regions.
+IL6	addiction	reward	30858110	Male and female mice were fed a HFD for 18 weeks, followed by quantitation of glucose tolerance, inflammatory markers of brain tissue (TNFα, <strong>IL 6</strong>, IL 1β, Iba 1), neural excitability in the prelimbic cortex (PLC), as well as assessment of emotional reactivity and <b>hedonic</b> behavior in a battery of behavioral tests.
+IL6	drug	alcohol	30808184	This demonstrates a particular sensitivity of adolescents to <b>alcohol</b> associated cues and neuroimmune learning, whereas prior work indicated that adults require multiple pairings of <b>ethanol</b> to the CS in order to achieve a conditioned amygdala <strong>IL 6</strong> response.
+IL6	drug	alcohol	30803859	The expression of Lcn2 was increased by <b>ethanol</b> treatment, despite unchanged expression of pro inflammatory cytokines Tnfα, <strong>Il6</strong> and Il 1β.
+IL6	drug	amphetamine	30793820	The aim of this study was to assess whether CBD prevents reinstatement of <b>METH</b> through change of gene expression of cytokines such as interleukin 1β, <strong>interleukin 6</strong>, interleukin 10, and tumor necrosis factor α (TNF α) in extinguished rats.
+IL6	addiction	relapse	30793820	The aim of this study was to assess whether CBD prevents <b>reinstatement</b> of METH through change of gene expression of cytokines such as interleukin 1β, <strong>interleukin 6</strong>, interleukin 10, and tumor necrosis factor α (TNF α) in extinguished rats.
+IL6	addiction	reward	30634502	We found that LDOC1 deficiency led to <b>reinforcing</b> a reciprocal loop of <strong>IL 6</strong>/JAK2/STAT3, through which LDOC1 mediates the cancer progression.
+IL6	drug	nicotine	30634502	Overall, our results elucidated a crucial role of LDOC1 in lung cancer and revealed how LDOC1 acts as a bridge between <b>tobacco</b> exposure and the <strong>IL 6</strong>/JAK2/STAT3 loop in this human malignancy.
+IL6	addiction	intoxication	30625475	<b>Binge</b> like consumption resulted in a 67% decrease in IL 10 immunoreactivity but had no effect on IL 4 or <strong>IL 6</strong> compared with the water drinking control group.
+IL6	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; <strong>IL 6</strong> interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+IL6	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; <strong>IL 6</strong> <strong>interleukin 6</strong> iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+IL6	drug	cocaine	30557308	Intraperitoneal administration of the anti inflammatory drug indomethacin before each episode of stress prevented this enhancement of <strong>IL 6</strong> levels and also reversed the increase in the rewarding effects of <b>cocaine</b> in defeated mice.
+IL6	drug	alcohol	30472309	The influence of central <strong>interleukin 6</strong> on behavioral changes associated with acute <b>alcohol</b> intoxication in adult male rats.
+IL6	addiction	intoxication	30472309	The influence of central <strong>interleukin 6</strong> on behavioral changes associated with acute alcohol <b>intoxication</b> in adult male rats.
+IL6	drug	alcohol	30472309	Recent studies have demonstrated brain cytokine fluctuations associated with acute <b>ethanol</b> intoxication (increased <strong>IL 6</strong>) and withdrawal (increased IL 1β and TNFα).
+IL6	addiction	intoxication	30472309	Recent studies have demonstrated brain cytokine fluctuations associated with acute ethanol <b>intoxication</b> (increased <strong>IL 6</strong>) and withdrawal (increased IL 1β and TNFα).
+IL6	addiction	withdrawal	30472309	Recent studies have demonstrated brain cytokine fluctuations associated with acute ethanol intoxication (increased <strong>IL 6</strong>) and <b>withdrawal</b> (increased IL 1β and TNFα).
+IL6	drug	alcohol	30472309	We utilized two tests of <b>ethanol</b> sensitivity to establish a potential role for <strong>IL 6</strong> after high (3.5 4.0 g/kg, intraperitoneally [i.p.])
+IL6	drug	alcohol	30472309	In the first experiments, rats were infused with 25, 50, 100, or 200 ng of <strong>IL 6</strong>; or 0.3, 3.0, or 9.0 μg of the JAK/STAT inhibitor AG490 30 min prior to a high dose <b>ethanol</b> challenge.
+IL6	addiction	aversion	30472309	Next, we assessed whether <strong>IL 6</strong> was sufficient to produce a <b>CTA</b>.
+IL6	drug	alcohol	30472309	Overall, these studies suggest that <strong>IL 6</strong> had only a minor influence on <b>ethanol</b> induced behavioral changes, yet phenotypic differences in sensitivity to <strong>IL 6</strong> were apparent.
+IL6	drug	alcohol	30472309	These studies are among the first to examine a potential functional role for <strong>IL 6</strong> in <b>ethanol</b> related behaviors, and may have important implications for understanding the relationship between acute <b>ethanol</b> intoxication and its associated behavioral alterations.
+IL6	addiction	intoxication	30472309	These studies are among the first to examine a potential functional role for <strong>IL 6</strong> in ethanol related behaviors, and may have important implications for understanding the relationship between acute ethanol <b>intoxication</b> and its associated behavioral alterations.
+IL6	drug	alcohol	30447270	Effect of <b>alcohol</b> on the <strong>interleukin 6</strong> mediated inflammatory response in a new mouse model of acute on chronic liver injury.
+IL6	drug	alcohol	30368255	Acute on chronic <b>alcohol</b> did not induce serum TNFα, <strong>IL 6</strong>, and IL 1β.
+IL6	addiction	intoxication	30257399	Administration of PD prior to APAP <b>intoxication</b> significantly ameliorated the increase in serum transferases, interleukin 1β (IL 1β), <strong>IL 6</strong>, tumor necrosis factor alpha (TNF α), and hepatic malondialdehyde (MDA) and the depletion of glutathione (GSH) in mice.
+IL6	drug	nicotine	30218019	Hyperalgesia induced by PSD prevailed over the antinociceptive action of <b>nicotine</b>, while the association between PSD and ABST synergistically increased <strong>IL 6</strong> concentrations and decreased pain threshold.
+IL6	drug	nicotine	30217256	Our data revealed that <b>nicotine</b> induced renal dysfunction manifested by significant abnormal levels of kidney function markers (creatinine and urea) accompanied by increased levels of oxidative stress biomarker (malondialdehyde) and inflammatory markers (nitric oxide, <strong>Interleukin 6</strong> and tumor necrosis factor α) while antioxidant status as glutathione level and glutathione S transferase activity were found to be decreased significantly as compared with controls.
+IL6	drug	cannabinoid	30046349	Δ9 <b>THC</b>/sesame oil therapy showed similar effects to MTX in neutralizing the inflammatory process of AIA, through attenuating erythrocyte sedimentation rate (ESR) scores and proinflammatory cytokines, including tumor necrosis factor alpha (TNF α), interleukin 1 beta (IL 1β), and interleukin 6 (<strong>IL 6</strong>) levels, to normal values.
+IL6	drug	cannabinoid	30046349	Δ9 <b>THC</b>/sesame oil therapy showed similar effects to MTX in neutralizing the inflammatory process of AIA, through attenuating erythrocyte sedimentation rate (ESR) scores and proinflammatory cytokines, including tumor necrosis factor alpha (TNF α), interleukin 1 beta (IL 1β), and <strong>interleukin 6</strong> (<strong>IL 6</strong>) levels, to normal values.
+IL6	drug	alcohol	29787738	Altered brain activity during withdrawal from chronic <b>alcohol</b> is associated with changes in <strong>IL 6</strong> signal transduction and GABAergic mechanisms in transgenic mice with increased astrocyte expression of <strong>IL 6</strong>.
+IL6	addiction	withdrawal	29787738	Altered brain activity during <b>withdrawal</b> from chronic alcohol is associated with changes in <strong>IL 6</strong> signal transduction and GABAergic mechanisms in transgenic mice with increased astrocyte expression of <strong>IL 6</strong>.
+IL6	drug	alcohol	29787738	Interleukin 6 (<strong>IL 6</strong>) is an important neuroimmune factor that is increased in the brain by <b>alcohol</b> exposure/withdrawal and is thought to play a role in the actions of <b>alcohol</b> on the brain.
+IL6	addiction	withdrawal	29787738	Interleukin 6 (<strong>IL 6</strong>) is an important neuroimmune factor that is increased in the brain by alcohol exposure/<b>withdrawal</b> and is thought to play a role in the actions of alcohol on the brain.
+IL6	drug	alcohol	29787738	<strong>Interleukin 6</strong> (<strong>IL 6</strong>) is an important neuroimmune factor that is increased in the brain by <b>alcohol</b> exposure/withdrawal and is thought to play a role in the actions of <b>alcohol</b> on the brain.
+IL6	addiction	withdrawal	29787738	<strong>Interleukin 6</strong> (<strong>IL 6</strong>) is an important neuroimmune factor that is increased in the brain by alcohol exposure/<b>withdrawal</b> and is thought to play a role in the actions of alcohol on the brain.
+IL6	drug	alcohol	29787738	To gain insight into <strong>IL 6</strong>/<b>alcohol</b>/withdrawal interactions and how these interactions affect the brain, we are studying the effects of chronic binge <b>alcohol</b> exposure on transgenic mice that express elevated levels of <strong>IL 6</strong> in the brain due to increased astrocyte expression (<strong>IL 6</strong> tg) and their non transgenic (non tg) littermate controls.
+IL6	addiction	intoxication	29787738	To gain insight into <strong>IL 6</strong>/alcohol/withdrawal interactions and how these interactions affect the brain, we are studying the effects of chronic <b>binge</b> alcohol exposure on transgenic mice that express elevated levels of <strong>IL 6</strong> in the brain due to increased astrocyte expression (<strong>IL 6</strong> tg) and their non transgenic (non tg) littermate controls.
+IL6	addiction	withdrawal	29787738	To gain insight into <strong>IL 6</strong>/alcohol/<b>withdrawal</b> interactions and how these interactions affect the brain, we are studying the effects of chronic binge alcohol exposure on transgenic mice that express elevated levels of <strong>IL 6</strong> in the brain due to increased astrocyte expression (<strong>IL 6</strong> tg) and their non transgenic (non tg) littermate controls.
+IL6	drug	alcohol	29787738	<strong>IL 6</strong>/<b>alcohol</b>/withdrawal interactions were identified by genotypic differences in spontaneous brain activity in electroencephalogram (EEG) recordings from the mice, and by Western blot analysis of protein activation or expression in hippocampus obtained from the mice after the final <b>alcohol</b> withdrawal period.
+IL6	addiction	withdrawal	29787738	<strong>IL 6</strong>/alcohol/<b>withdrawal</b> interactions were identified by genotypic differences in spontaneous brain activity in electroencephalogram (EEG) recordings from the mice, and by Western blot analysis of protein activation or expression in hippocampus obtained from the mice after the final alcohol <b>withdrawal</b> period.
+IL6	addiction	withdrawal	29787738	Regression analysis revealed that pSTAT3 played a more prominent role during <b>withdrawal</b> in the <strong>IL 6</strong> tg mice than in the non tg mice, and that the role of GABAAR alpha 5 and GABAAR alpha 1 in brain activity varied across genotype and <b>withdrawal</b>.
+IL6	drug	alcohol	29787738	Taken together, our results suggest that <strong>IL 6</strong> can significantly impact mechanisms involved in <b>alcohol</b> withdrawal.
+IL6	addiction	withdrawal	29787738	Taken together, our results suggest that <strong>IL 6</strong> can significantly impact mechanisms involved in alcohol <b>withdrawal</b>.
+IL6	drug	opioid	29729431	Coadministration of AM1241 (3 mg/kg) reduced the production of interleukin 1β, tumor necrosis factor α, and <strong>interleukin 6</strong> induced by long term and acute <b>morphine</b> treatment.
+IL6	drug	amphetamine	29689344	The relationship between <strong>interleukin 6</strong> and functional connectivity in <b>methamphetamine</b> users.
+IL6	addiction	dependence	29689344	Thirty adults diagnosed with MA <b>dependence</b> and 20 control subjects underwent a resting state functional magnetic resonance imaging (fMRI) scan and gave a blood sample for determination of plasma <strong>IL 6</strong> levels.
+IL6	drug	alcohol	29685140	On the other hand, <b>ethanol</b> intoxication caused the increase of serum TNFα, IL 8, <strong>IL 6</strong> and 1Lβ, markers of tissue inflammation.
+IL6	addiction	intoxication	29685140	On the other hand, ethanol <b>intoxication</b> caused the increase of serum TNFα, IL 8, <strong>IL 6</strong> and 1Lβ, markers of tissue inflammation.
+IL6	drug	opioid	29657246	The aim of the current study was to investigate the effects of those two modalities on pain behavior and the expression of pro inflammatory cytokines such as interleukin (IL) 1β and <strong>IL 6</strong> and tumor necrosis factor α (TNF α) in the spinal cord and dorsal root ganglion (DRG) in a rat model of perioperative <b>fentanyl</b> induced hyperalgesia.
+IL6	drug	cannabinoid	29607409	The <b>THC</b>+CBD strain was also associated with less desire to smoke, lower levels of subjective drug effects, and lower levels of circulating cytokines (TNF α, <strong>IL 6</strong>, and IL 1β) immediately after use.
+IL6	drug	nicotine	29578441	In the blood serum of all age groups of rats, pronounced changes in <strong>IL 6</strong> content were observed on the 45th day of exposure to <b>tobacco</b> smoke.
+IL6	drug	alcohol	29576702	EALT supplementation prevented <b>alcoholic</b> liver injury through attenuation of inflammatory mediators such as toll like receptor 4, cytochrome P4502E1, and cyclooxygenase 2, and inflammatory cytokine <strong>interleukin 6</strong>.
+IL6	drug	alcohol	29500107	Among people with only an <b>alcohol</b> use disorder, <strong>IL 6</strong> was positively associated with depression and psychological distress scores, and IL 10 was negatively associated with anxiety score.
+IL6	drug	alcohol	29458194	In non stressed controls, acute <b>ethanol</b> increased expression of <strong>Il 6</strong> and IκBα in the hippocampus.
+IL6	drug	alcohol	29458194	In contrast, rats exposed to footshock 24 h prior to <b>ethanol</b> demonstrated potentiation of hippocampal <strong>Il 6</strong> and IκBα expression relative to <b>ethanol</b> exposed non stressed controls.
+IL6	drug	alcohol	29458194	As expected, acute <b>ethanol</b> increased <strong>Il 6</strong> expression in all structures examined, yet the <strong>Il 6</strong> response was attenuated exclusively in the hippocampus in chronically stressed rats.
+IL6	drug	alcohol	29458194	Together, these experiments demonstrate an intriguing interaction between recent stress history and <b>ethanol</b> induced increases in hippocampal <strong>Il 6</strong>, and may provide insight into novel pharmacotherapeutic targets for prevention and treatment of <b>alcohol</b> related health outcomes based on stress susceptibility.
+IL6	drug	alcohol	29445009	In vivo and in vitro binge <b>alcohol</b> exposure significantly inhibited the TLR4 MyD88 cytokines TNF α and <strong>IL 6</strong>, as well as the TLR4 TRIF cytokines/chemokines IFN β, IP 10, and RANTES, in human monocytes, but not TLR3 TRIF induced cytokines/chemokines, as detected by quantitative PCR and ELISA.
+IL6	addiction	intoxication	29445009	In vivo and in vitro <b>binge</b> alcohol exposure significantly inhibited the TLR4 MyD88 cytokines TNF α and <strong>IL 6</strong>, as well as the TLR4 TRIF cytokines/chemokines IFN β, IP 10, and RANTES, in human monocytes, but not TLR3 TRIF induced cytokines/chemokines, as detected by quantitative PCR and ELISA.
+IL6	drug	alcohol	29369159	Multiple linear regression models adjusted for age, antiretroviral therapy regimen, CD4 T cell count, <strong>interleukin 6</strong>, and <b>alcohol</b> use severity.
+IL6	drug	alcohol	29306704	While a subset of IEGs encoding for effector proteins (such as Bdnf, InhbA and Dusp5) were downregulated by <b>ethanol</b>, others (such as <strong>Il 6</strong>) were unaffected.
+IL6	drug	alcohol	29178411	We found that during abstinence, <b>alcohol</b> binge drinkers had elevated plasma levels of oleoylethanolamide, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (TLR4), pro inflammatory cytokines/chemokines interleukin 1 beta, <strong>interleukin 6</strong> and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+IL6	drug	cannabinoid	29178411	We found that during abstinence, alcohol binge drinkers had elevated plasma levels of <b>oleoylethanolamide</b>, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (TLR4), pro inflammatory cytokines/chemokines interleukin 1 beta, <strong>interleukin 6</strong> and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+IL6	addiction	intoxication	29178411	We found that during abstinence, alcohol <b>binge</b> drinkers had elevated plasma levels of oleoylethanolamide, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (TLR4), pro inflammatory cytokines/chemokines interleukin 1 beta, <strong>interleukin 6</strong> and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+IL6	drug	opioid	29135586	In this study, we tried to investigate behavioral hyperalgesia, the expression of proinflammatory cytokines, such as interleukin 1β (IL 1β), interleukin 6 (<strong>IL 6</strong>), and tumor necrosis factor α (TNF α), and the activation of microglia in the spinal cord and dorsal root ganglion (DRG) in a rat model of surgical plantar incision with or without perioperative <b>fentanyl</b>.
+IL6	drug	opioid	29135586	In this study, we tried to investigate behavioral hyperalgesia, the expression of proinflammatory cytokines, such as interleukin 1β (IL 1β), <strong>interleukin 6</strong> (<strong>IL 6</strong>), and tumor necrosis factor α (TNF α), and the activation of microglia in the spinal cord and dorsal root ganglion (DRG) in a rat model of surgical plantar incision with or without perioperative <b>fentanyl</b>.
+IL6	drug	opioid	29135586	The <b>fentanyl</b> or surgical incision upregulated the expression of IL 1β, <strong>IL 6</strong>, and TNF α in the spinal cord and bilateral DRG for more than 7 days and increase of ionized calcium binding adapter molecule 1 in the spinal cord.
+IL6	drug	opioid	29135586	The combination of <b>fentanyl</b> and incision resulted in higher increase of IL 1β, <strong>IL 6</strong>, and TNF α in the spinal cord and bilateral DRG.
+IL6	drug	opioid	29135586	The surgical plantar incision with or without perioperative <b>fentanyl</b> induced significant mechanical and thermal hyperalgesia, an increased expression of IL 1β, <strong>IL 6</strong>, TNF α in the spinal cord and DRG, and activation of microglia in the spinal cord.
+IL6	drug	opioid	29111854	We observed differential methylation of Bdnf and <strong>Il6</strong> in the pons, Nr3c1 in the cerebellum, and Il1b in the hippocampus in response to acute <b>morphine</b> exposure (all P value < 0.05).
+IL6	addiction	intoxication	28840951	Finally, higher levels of inflammatory markers, mainly monocyte chemoattractant protein 1, as well as LPS, high mobility group box 1, toll like receptor 4, <strong>IL 6</strong> and ciclooxygenase 2, correlated with worse scores on episodic memory and executive functioning tasks in female <b>binge</b> drinkers but not in male <b>binge</b> drinkers.
+IL6	drug	cannabinoid	28821005	This <b>cannabinoid</b> also prevented PTZ induced EEG activity and <strong>interleukin 6</strong> increase in prefrontal cortex.
+IL6	drug	alcohol	28806641	A significant difference in the cytokine profile was still observed 24h post injury in the <b>ethanol</b> pretreated mice, as shown by the delayed peak in <strong>IL 6</strong> and by the suppression of GM CSF, IFN γ, and IL 3.
+IL6	drug	opioid	28697991	In the <b>morphine</b> abuser, a decrease in pain threshold, an increase in <strong>IL 6</strong> and a decrease in IL 10 levels were evident compared with non abuser subjects.
+IL6	drug	alcohol	28669319	Our aim is to describe changes in serum concentration for the pro inflammatory factors TNF α, IFN γ, IL 1β, IL 8, <strong>IL 6</strong>, IL 10, IL 12 and MCP 1, for the satiety factor leptin and for factors associated with neuronal changes, neuron specific enolase (NSE) and glial activation S100 beta protein (S100 β), and explore their association with abstinence in <b>alcohol</b> dependent subjects after withdrawal.
+IL6	addiction	withdrawal	28669319	Our aim is to describe changes in serum concentration for the pro inflammatory factors TNF α, IFN γ, IL 1β, IL 8, <strong>IL 6</strong>, IL 10, IL 12 and MCP 1, for the satiety factor leptin and for factors associated with neuronal changes, neuron specific enolase (NSE) and glial activation S100 beta protein (S100 β), and explore their association with abstinence in alcohol dependent subjects after <b>withdrawal</b>.
+IL6	drug	alcohol	28669319	The levels of TNF α, IL 1β, IL 8, <strong>IL 6</strong>, IL 12, MCP 1, and leptin decreased after withdrawal and remained low until M6, regardless of <b>alcohol</b> consumption.
+IL6	addiction	withdrawal	28669319	The levels of TNF α, IL 1β, IL 8, <strong>IL 6</strong>, IL 12, MCP 1, and leptin decreased after <b>withdrawal</b> and remained low until M6, regardless of alcohol consumption.
+IL6	drug	amphetamine	28621212	<b>Meth</b> upregulated the gene expression of <strong>IL 6</strong>, IL 1β, and TNFα and downregulated the expression of Arg 1, IL 10, and KLF4.
+IL6	drug	alcohol	28430931	In this study we investigated a possible association between alterations in the methylation of the BDNF IV/NGF I gene promoter and the cytokines tumor necrosis factor α (TNF α) and interleukin 6 (<strong>IL 6</strong>) in 55 male <b>alcohol</b> dependent patients.
+IL6	drug	alcohol	28430931	In this study we investigated a possible association between alterations in the methylation of the BDNF IV/NGF I gene promoter and the cytokines tumor necrosis factor α (TNF α) and <strong>interleukin 6</strong> (<strong>IL 6</strong>) in 55 male <b>alcohol</b> dependent patients.
+IL6	addiction	withdrawal	28430931	Moreover, mean methylation of the NGF I promoter was significantly associated with the <strong>IL 6</strong> serum levels and STAI I score during <b>withdrawal</b> (P < 0.001).
+IL6	drug	alcohol	28319836	The hippocampus revealed age dependent shifts in cytokine expression (<strong>IL 6</strong>, IL 1β, and monocyte chemoattractant protein 1), but no changes were observed in the PVN at baseline or following <b>ethanol</b>.
+IL6	drug	alcohol	28242869	Peripheral monocyte response to lipopolysaccharide stimulation was lower in <b>alcohol</b> dependent subjects compared with controls for the proinflammatory cytokines <strong>interleukin 6</strong> and interleukin 8.
+IL6	drug	alcohol	28201924	Re exposure to the odor CS significantly increased <strong>IL 6</strong> levels in HPC and AMG, an effect only evident in paired rats administered <b>ethanol</b> i.p.
+IL6	drug	alcohol	28201924	Overall, this study suggests that <b>ethanol</b> exposure can regulate the levels of <strong>IL 6</strong> at HPC and AMG via classical conditioning mechanisms.
+IL6	drug	alcohol	28201924	The main new finding of the present study was that, after four pairings of <b>ethanol</b>'s unconditioned effects and a distinctive odor, the latter CS increased <strong>IL 6</strong> levels in HPC and AMG.
+IL6	drug	alcohol	28201924	This suggests that <b>ethanol</b>'s effects upon <strong>IL 6</strong> in HPC and AMG may come under conditioned control, particularly after repeated pairings between distinctive odor cues and <b>ethanol</b>'s effects.
+IL6	drug	nicotine	28197102	We found that right cervical vagotomy inhibited the cholinergic anti inflammatory pathway, aggravated myocardial lesions, up regulated the expression of TNF α, IL 1β, and <strong>IL 6</strong>, and worsened the impaired left ventricular function in murine viral myocarditis, and these changes were reversed by co treatment with <b>nicotine</b> by activating the cholinergic anti inflammatory pathway.
+IL6	drug	opioid	28178176	In response to LPS, there was a significant increase in the expression of the pro inflammatory cytokine/chemokine genes interleukin 1 beta (Il 1β), interleukin 6 (<strong>Il 6</strong>), C C motif chemokine ligand 2 (Ccl2), C C motif chemokine ligand 7 (Ccl7), C X C motif chemokine ligand 1 (Cxcl1), and C X C motif chemokine ligand 3 (Cxcl3) and a significant decrease in the anti inflammatory NLRP12 gene in both <b>morphine</b> tolerant and placebo control rats compared to saline treated rats, although the changes were greater in the placebo control animals.
+IL6	drug	opioid	28178176	In response to LPS, there was a significant increase in the expression of the pro inflammatory cytokine/chemokine genes interleukin 1 beta (Il 1β), <strong>interleukin 6</strong> (<strong>Il 6</strong>), C C motif chemokine ligand 2 (Ccl2), C C motif chemokine ligand 7 (Ccl7), C X C motif chemokine ligand 1 (Cxcl1), and C X C motif chemokine ligand 3 (Cxcl3) and a significant decrease in the anti inflammatory NLRP12 gene in both <b>morphine</b> tolerant and placebo control rats compared to saline treated rats, although the changes were greater in the placebo control animals.
+IL6	drug	alcohol	28147432	Measures of tumor necrosis factor alpha (TNFα), interleukin 6 (<strong>IL 6</strong>), interleukin 1 receptor antagonist (IL 1ra), <b>alcohol</b> craving, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+IL6	addiction	relapse	28147432	Measures of tumor necrosis factor alpha (TNFα), interleukin 6 (<strong>IL 6</strong>), interleukin 1 receptor antagonist (IL 1ra), alcohol <b>craving</b>, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+IL6	drug	alcohol	28147432	Measures of tumor necrosis factor alpha (TNFα), <strong>interleukin 6</strong> (<strong>IL 6</strong>), interleukin 1 receptor antagonist (IL 1ra), <b>alcohol</b> craving, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+IL6	addiction	relapse	28147432	Measures of tumor necrosis factor alpha (TNFα), <strong>interleukin 6</strong> (<strong>IL 6</strong>), interleukin 1 receptor antagonist (IL 1ra), alcohol <b>craving</b>, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+IL6	drug	alcohol	28131626	In the present study, we subjected adult male and female rats to different regimens of <b>alcohol</b> vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for tumor necrosis factor alpha (TNFα), interleukin 6 (<strong>IL 6</strong>), and chemokine (C C motif) ligand 2 (CCL2) in reward related brain regions.
+IL6	addiction	reward	28131626	In the present study, we subjected adult male and female rats to different regimens of alcohol vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for tumor necrosis factor alpha (TNFα), interleukin 6 (<strong>IL 6</strong>), and chemokine (C C motif) ligand 2 (CCL2) in <b>reward</b> related brain regions.
+IL6	drug	alcohol	28131626	In the present study, we subjected adult male and female rats to different regimens of <b>alcohol</b> vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for tumor necrosis factor alpha (TNFα), <strong>interleukin 6</strong> (<strong>IL 6</strong>), and chemokine (C C motif) ligand 2 (CCL2) in reward related brain regions.
+IL6	addiction	reward	28131626	In the present study, we subjected adult male and female rats to different regimens of alcohol vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for tumor necrosis factor alpha (TNFα), <strong>interleukin 6</strong> (<strong>IL 6</strong>), and chemokine (C C motif) ligand 2 (CCL2) in <b>reward</b> related brain regions.
+IL6	drug	alcohol	28131626	Results indicated that acute <b>alcohol</b> exposure increased TNFα mRNA expression in the basolateral amygdala (BLA), nucleus accumbens (NAc), and ventral tegmental area (VTA), whereas <strong>IL 6</strong> expression was increased in the VTA, NAc, and ventromedial prefrontal cortex (vmPFC) only in males.
+IL6	drug	alcohol	28131626	Chronic <b>alcohol</b> exposure (6week daily intermittent exposure, 14 h on: 10 h off) increased TNFα mRNA expression in the NAc and increased <strong>IL 6</strong> mRNA in the vmPFC and NAc.
+IL6	addiction	relapse	28126360	In a longitudinal design we measured plasma levels of the pro inflammatory interleukin 6 (<strong>IL 6</strong>), the soluble alpha (Tac) subunit of the interleukin 2 receptor (sIL 2r), and the circulating soluble form of the intercellular adhesion molecule one (sICAM 1), in 79 help <b>seeking</b> UHR individuals (13 25years of age).
+IL6	addiction	relapse	28126360	In a longitudinal design we measured plasma levels of the pro inflammatory <strong>interleukin 6</strong> (<strong>IL 6</strong>), the soluble alpha (Tac) subunit of the interleukin 2 receptor (sIL 2r), and the circulating soluble form of the intercellular adhesion molecule one (sICAM 1), in 79 help <b>seeking</b> UHR individuals (13 25years of age).
+IL6	drug	nicotine	28126360	<strong>IL 6</strong> was weakly inverse associated with omega 6 PUFA, and highly increased in <b>nicotine</b> users.
+IL6	drug	alcohol	27256567	<b>Alcohol</b> withdrawal partially restored the distribution of monocyte subsets and the frequency of <strong>IL 6</strong> producing monocytes and increased the frequency of TNF producing cells in response to LPS and PGN stimulation to levels compared with those in HC.
+IL6	addiction	withdrawal	27256567	Alcohol <b>withdrawal</b> partially restored the distribution of monocyte subsets and the frequency of <strong>IL 6</strong> producing monocytes and increased the frequency of TNF producing cells in response to LPS and PGN stimulation to levels compared with those in HC.
+IL6	drug	alcohol	27711160	Chronic binge <b>alcohol</b> induces adipose tissue inflammation in vivo in female mice, which is illustrated by increased expression of TNFα, <strong>IL 6</strong>, and CCL2, compared to only <strong>IL 6</strong> induction in male adipose tissue.
+IL6	addiction	intoxication	27711160	Chronic <b>binge</b> alcohol induces adipose tissue inflammation in vivo in female mice, which is illustrated by increased expression of TNFα, <strong>IL 6</strong>, and CCL2, compared to only <strong>IL 6</strong> induction in male adipose tissue.
+IL6	drug	alcohol	27699959	The results showed that <b>alcohol</b> intoxication increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, IL 4, <strong>IL 6</strong>, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+IL6	addiction	intoxication	27699959	The results showed that alcohol <b>intoxication</b> increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, IL 4, <strong>IL 6</strong>, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+IL6	drug	alcohol	27679493	MicroRNA 223 ameliorates <b>alcoholic</b> liver injury by inhibiting the <strong>IL 6</strong> p47phox oxidative stress pathway in neutrophils.
+IL6	drug	alcohol	27679493	Finally, miR 223 expression was downregulated, while <strong>IL 6</strong> and p47phox expression were upregulated in peripheral blood neutrophils from <b>alcoholics</b> compared with healthy controls.
+IL6	drug	alcohol	27527870	<b>Ethanol</b> caused pancreatic inflammation which was indicated by the induction of TNF alpha, IL 1beta, <strong>IL 6</strong>, MCP 1 and CCR2, and the increase of CD68 positive macrophages in the pancreas.
+IL6	drug	psychedelics	27497920	Simultaneously, <b>ketamine</b> reduced the levels of <strong>IL 6</strong>, IL 1β, IDO, and KYN/TRP ratio and increased the 5 HT/TRP ratio in the hippocampus.
+IL6	addiction	intoxication	27455577	It was established in experiments on noninbred albino rats that the acute <b>intoxication</b> with methanol (1.0 LD50) decreased cellular and humoral immune responses, Th2 lymphocyte activity (to a greater extent as compared to the function of Th1 cells), reduced the blood concentration of immunoregulatory (IFN g, IL 2, IL 4) and proinflammatory (TNF, IL 1b, <strong>IL 6</strong>) cytokines on the average by 36.5% (p < 0.05), and did not affect the content of anti inflammatory cytokines (IL 10, IL 13).
+IL6	drug	alcohol	27455577	Methanol antidote 4 methylpyrazole (non competitive inhibitor of <b>alcohol</b> dehydrogenase) administered upon acute intoxication with methanol at a dose of 1.0 DL50 partially reduces the intoxication induced suppression of humoral and cellular immune response, activity of T helper cells, and production of IL 4 and restores blood levels of TNF, IL 1b, IFN γ, IL 4, IL 2, <strong>IL 6</strong> to the control values.
+IL6	addiction	intoxication	27455577	Methanol antidote 4 methylpyrazole (non competitive inhibitor of alcohol dehydrogenase) administered upon acute <b>intoxication</b> with methanol at a dose of 1.0 DL50 partially reduces the <b>intoxication</b> induced suppression of humoral and cellular immune response, activity of T helper cells, and production of IL 4 and restores blood levels of TNF, IL 1b, IFN γ, IL 4, IL 2, <strong>IL 6</strong> to the control values.
+IL6	addiction	intoxication	27322363	<b>Intoxication</b> exacerbates postburn hepatic damage through p38 dependent <strong>interleukin 6</strong> production in Kupffer cells.
+IL6	drug	alcohol	27208497	As expected, <b>ethanol</b> led to robust increases in <strong>IL 6</strong> and IκBα gene expression in hippocampus, amygdala and bed nucleus of the stria terminalis (BNST), whereas IL 1β and TNFα were suppressed, thereby replicating our prior work.
+IL6	drug	alcohol	27208497	<b>Ethanol</b> dependent increases in <strong>IL 6</strong> and IκBα remained significant in all structures   even after 6 days of <b>ethanol</b>.
+IL6	drug	alcohol	27058046	<b>Alcohol</b> Intoxication Reduces Systemic <strong>Interleukin 6</strong> Levels and Leukocyte Counts After Severe TBI Compared With Not Intoxicated TBI Patients.
+IL6	addiction	intoxication	27058046	Alcohol <b>Intoxication</b> Reduces Systemic <strong>Interleukin 6</strong> Levels and Leukocyte Counts After Severe TBI Compared With Not Intoxicated TBI Patients.
+IL6	drug	alcohol	27058046	This study shows that positive BAC in TBI patients is associated with lower systemic <strong>IL 6</strong> levels and leukocyte numbers, indicating that positive BAC may have immunosuppressive effects in this cohort of patients compared with TBI patients who were not <b>alcohol</b> intoxicated.
+IL6	drug	cocaine	26790673	Levels of MDA and TNFα in PFC, and levels of MDA, SOD, GSH, <strong>IL 6</strong>, IL 1β, TNFα, caspase 3 and BAX in HP, but not SIRT1 expression in both regions were significantly changed during <b>cocaine</b> withdrawal period.
+IL6	addiction	withdrawal	26790673	Levels of MDA and TNFα in PFC, and levels of MDA, SOD, GSH, <strong>IL 6</strong>, IL 1β, TNFα, caspase 3 and BAX in HP, but not SIRT1 expression in both regions were significantly changed during cocaine <b>withdrawal</b> period.
+IL6	drug	alcohol	26707655	Transgenic mice with increased astrocyte expression of <strong>IL 6</strong> show altered effects of acute <b>ethanol</b> on synaptic function.
+IL6	drug	alcohol	26707655	Recent studies show that <b>ethanol</b> can activate cells of the neuroimmune system, resulting in the elevated production of neuroimmune factors, including the cytokine interleukin 6 (<strong>IL 6</strong>).
+IL6	drug	alcohol	26707655	Recent studies show that <b>ethanol</b> can activate cells of the neuroimmune system, resulting in the elevated production of neuroimmune factors, including the cytokine <strong>interleukin 6</strong> (<strong>IL 6</strong>).
+IL6	drug	alcohol	26707655	Here we analyzed the consequences of this CNS action of <b>ethanol</b> using transgenic mice that express elevated levels of <strong>IL 6</strong> through increased astrocyte expression (<strong>IL 6</strong> tg) to model the increased <strong>IL 6</strong> expression that occurs with <b>ethanol</b> use.
+IL6	drug	alcohol	26707655	Results show that increased <strong>IL 6</strong> expression induces neuroadaptive changes that alter the effects of <b>ethanol</b>.
+IL6	drug	alcohol	26707655	In contrast, acute <b>ethanol</b> enhanced the fEPSP and PS in hippocampal slices from <strong>IL 6</strong> tg mice.
+IL6	drug	alcohol	26707655	Long term synaptic plasticity of the fEPSP (i.e., LTP) showed the expected dose dependent reduction by acute <b>ethanol</b> in non tg hippocampal slices, whereas LTP in the <strong>IL 6</strong> tg hippocampal slices was resistant to this depressive effect of acute <b>ethanol</b>.
+IL6	drug	alcohol	26707655	Consistent with altered effects of acute <b>ethanol</b> on synaptic function in the <strong>IL 6</strong> tg mice, EEG recordings showed a higher level of CNS activity in the <strong>IL 6</strong> tg mice than in the non tg mice during the period of withdrawal from an acute high dose of <b>ethanol</b>.
+IL6	addiction	withdrawal	26707655	Consistent with altered effects of acute ethanol on synaptic function in the <strong>IL 6</strong> tg mice, EEG recordings showed a higher level of CNS activity in the <strong>IL 6</strong> tg mice than in the non tg mice during the period of <b>withdrawal</b> from an acute high dose of ethanol.
+IL6	drug	alcohol	26707655	These results suggest a potential role for neuroadaptive effects of <b>ethanol</b> induced astrocyte production of <strong>IL 6</strong> as a mediator or modulator of the actions of <b>ethanol</b> on the CNS, including persistent changes in CNS function that contribute to cognitive dysfunction and the development of <b>alcohol</b> dependence.
+IL6	addiction	dependence	26707655	These results suggest a potential role for neuroadaptive effects of ethanol induced astrocyte production of <strong>IL 6</strong> as a mediator or modulator of the actions of ethanol on the CNS, including persistent changes in CNS function that contribute to cognitive dysfunction and the development of alcohol <b>dependence</b>.
+IL6	drug	psychedelics	26589393	Relationship of serum levels of TNF α, <strong>IL 6</strong> and IL 18 and schizophrenia like symptoms in chronic <b>ketamine</b> abusers.
+IL6	drug	psychedelics	26589393	This study aims to examine the serum TNF α, <strong>IL 6</strong> and IL 18 levels in chronic human <b>ketamine</b> users as compared to healthy subjects.
+IL6	drug	psychedelics	26589393	Serum <strong>IL 6</strong> and IL 18 levels were significantly higher, while serum TNF α level was significantly lower among <b>ketamine</b> users than among healthy controls (p<0.05).
+IL6	drug	psychedelics	26589393	Serum levels of TNF α, <strong>IL 6</strong> and IL 18 were altered in chronic <b>ketamine</b> abusers which may play a role in schizophrenia like symptoms in chronic <b>ketamine</b> abusers.
+IL6	addiction	dependence	26354917	However, in contrast to prior studies of priming induced by receptor mediated (i.e., TNFα, NGF, or <strong>IL 6</strong> receptor) or direct activation of protein kinase Cε (PKCε), the pronociceptive effects of PGE2 in DAMGO treated rats demonstrated the following: (1) rapid induction (4 h compared with 3 d); (2) protein kinase A (PKA), rather than PKCε, <b>dependence</b>; (3) prolongation of hyperalgesia induced by an activator of PKA, 8 bromo cAMP; (4) failure to be reversed by a protein translation inhibitor; (5) priming in females as well as in males; and (6) lack of <b>dependence</b> on the isolectin B4 positive nociceptor.
+IL6	drug	amphetamine	26322025	In addition, the serum pro inflammatory (TNF, IL12 p70, IL1β, <strong>IL 6</strong>, and KC GRO) and Th2 (IL 2, IL 10, and IL 4) cytokine profiles were also altered in the presence of <b>METH</b>.
+IL6	drug	cocaine	25762940	The plasma concentrations of interleukin 1 beta (IL 1β), <strong>IL 6</strong>, IL 10, and tumor necrosis factor alpha (TNFα) were affected by history of <b>cocaine</b> addiction and sex.
+IL6	addiction	addiction	25762940	The plasma concentrations of interleukin 1 beta (IL 1β), <strong>IL 6</strong>, IL 10, and tumor necrosis factor alpha (TNFα) were affected by history of cocaine <b>addiction</b> and sex.
+IL6	drug	alcohol	25708278	<b>ethanol</b> challenge, <strong>IL 6</strong> and IκBα expression was significantly increased in both ages in the PVN and amygdala, and adults exhibited even greater increases in IκBα than adolescents.
+IL6	drug	alcohol	25708278	administration of <b>ethanol</b> also increased <strong>IL 6</strong> and IκBα expression in all three brain regions, with hippocampal <strong>IL 6</strong> elevated even more so in adults compared to adolescents.
+IL6	drug	amphetamine	25678251	Serum cytokine levels of IFN γ, TNF α and <strong>IL 6</strong> in <b>methamphetamine</b> rats were unchanged.
+IL6	drug	alcohol	25661730	Importantly, several cytokines and chemokines (e.g., MIP 2, MIP 1, IL 4, <strong>IL 6</strong> and osteopontin) involved in neutrophil infiltration were upregulated in hepatic NKT cells isolated from chronic plus binge <b>ethanol</b> fed mice compared to pair fed mice.
+IL6	addiction	intoxication	25661730	Importantly, several cytokines and chemokines (e.g., MIP 2, MIP 1, IL 4, <strong>IL 6</strong> and osteopontin) involved in neutrophil infiltration were upregulated in hepatic NKT cells isolated from chronic plus <b>binge</b> ethanol fed mice compared to pair fed mice.
+IL6	drug	opioid	25660662	We tested the cytokine production of IL 1β, <strong>IL 6</strong>, IL 8, IL 10 and tumor necrosis factor (TNF) α from a group of <b>heroin</b> addicts (n=34) and healthy controls (n=20).
+IL6	drug	opioid	25660662	The results show that production of IL 1β, <strong>IL 6</strong> and IL 8 was significantly higher in the group of <b>methadone</b> maintained patients than in the healthy control group.
+IL6	drug	opioid	25660662	Plasma TNF α and <strong>IL 6</strong> levels were significantly correlated with the dairy <b>methadone</b> dosage administered, and the IL 1β level was significantly correlated with the duration of <b>methadone</b> maintenance treatment.
+IL6	drug	alcohol	25559494	Levels increased directly post consumption and decreased to normal levels within 4 h. LBP, sCD14, and <strong>IL 6</strong> levels were not significantly higher in the <b>alcohol</b> group.
+IL6	drug	alcohol	25262503	TNF α and <strong>IL 6</strong> serum levels: neurobiological markers of <b>alcohol</b> consumption in <b>alcohol</b> dependent patients?
+IL6	drug	alcohol	25262503	We investigated the serum levels of <strong>IL 6</strong> and TNF α in 30 male <b>alcohol</b> dependent patients during withdrawal (day 1, 7, and 14) and compared them with the levels obtained from 18 healthy male controls.
+IL6	addiction	withdrawal	25262503	We investigated the serum levels of <strong>IL 6</strong> and TNF α in 30 male alcohol dependent patients during <b>withdrawal</b> (day 1, 7, and 14) and compared them with the levels obtained from 18 healthy male controls.
+IL6	drug	alcohol	25262503	<strong>IL 6</strong> (day 1: T = 2,593, p = 0.013; day 7: T = 2,315, p = 0.037; day 14: T = 1,650, p = 0.112) serum levels were significantly increased at the beginning of <b>alcohol</b> withdrawal.
+IL6	addiction	withdrawal	25262503	<strong>IL 6</strong> (day 1: T = 2,593, p = 0.013; day 7: T = 2,315, p = 0.037; day 14: T = 1,650, p = 0.112) serum levels were significantly increased at the beginning of alcohol <b>withdrawal</b>.
+IL6	addiction	withdrawal	25262503	<strong>IL 6</strong> serum levels decreased significantly during <b>withdrawal</b> (F = 16.507, p < 0.001), whereas TNF α levels did not change significantly (day 1 14).
+IL6	drug	alcohol	25262503	<strong>IL 6</strong> serum levels were directly associated with <b>alcohol</b> consumption (r = 0.392, p = 0.047) on day 1.
+IL6	drug	alcohol	25262503	Moreover, the <strong>IL 6</strong> serum levels were associated with <b>alcohol</b> craving (PACS total score day 1: r =  0.417, p = 0.022, the score of the obsessive subscale of the OCDS on day 14 [r =  0.549, p = 0.022]), depression (r =  0.507, p = 0.005), and trait anxiety (r =  0.674, p < 0.001) on day 1.
+IL6	addiction	relapse	25262503	Moreover, the <strong>IL 6</strong> serum levels were associated with alcohol <b>craving</b> (PACS total score day 1: r =  0.417, p = 0.022, the score of the obsessive subscale of the OCDS on day 14 [r =  0.549, p = 0.022]), depression (r =  0.507, p = 0.005), and trait anxiety (r =  0.674, p < 0.001) on day 1.
+IL6	drug	alcohol	25262503	Our results support an association between alterations in TNF α and <strong>IL 6</strong> serum levels and <b>alcohol</b> consumption.
+IL6	drug	opioid	25231848	Enzyme Linked Immunosorbent Assay (ELISA) revealed the significant increase of cytokine (IL 1beta, <strong>IL 6</strong>) levels in the repeated <b>morphine</b> treatment rats' cortex and hippocampus regions, which are both addiction related brain areas.
+IL6	addiction	addiction	25231848	Enzyme Linked Immunosorbent Assay (ELISA) revealed the significant increase of cytokine (IL 1beta, <strong>IL 6</strong>) levels in the repeated morphine treatment rats' cortex and hippocampus regions, which are both <b>addiction</b> related brain areas.
+IL6	addiction	intoxication	25156612	Although cytokine  and region dependent central <strong>IL 6</strong> expression was generally increased and tumor necrosis factor alpha decreased during <b>intoxication</b>, IL 1 expression exhibited increases during withdrawal.
+IL6	addiction	withdrawal	25156612	Although cytokine  and region dependent central <strong>IL 6</strong> expression was generally increased and tumor necrosis factor alpha decreased during intoxication, IL 1 expression exhibited increases during <b>withdrawal</b>.
+IL6	addiction	intoxication	25156612	EtOH (4 g/kg), <b>intoxication</b> related increases in <strong>IL 6</strong> expression were again observed in the paraventricular nucleus of the hypothalamus (PVN), although to a lesser extent.
+IL6	addiction	intoxication	25104501	This study tested the hypothesis that <b>intoxication</b> alters the gut liver axis, leading to increased pulmonary inflammation mediated by burn induced <strong>IL 6</strong> in the liver.
+IL6	drug	alcohol	25024384	In vitro pre exposure to moderate <b>alcohol</b> reduced subsequent LPS induced NF κB promoter activity and downstream TNF α, <strong>IL 6</strong> and IL 1β production in monocytes and macrophages, exhibiting endotoxin tolerance.
+IL6	drug	alcohol	24421048	An increased pulmonary bacterial burden was observed in <b>alcohol</b> intoxicated mice at 16 and 24 h and was associated with decreased levels of interleukin 6 (<strong>IL 6</strong>).
+IL6	drug	alcohol	24421048	An increased pulmonary bacterial burden was observed in <b>alcohol</b> intoxicated mice at 16 and 24 h and was associated with decreased levels of <strong>interleukin 6</strong> (<strong>IL 6</strong>).
+IL6	drug	alcohol	24421048	Therefore, acute <b>alcohol</b> intoxication leads to decreased MRSA clearance in part by inhibiting <strong>IL 6</strong>/STAT3 induction of the antimicrobial protein Reg3γ in the pulmonary epithelium.
+IL6	addiction	intoxication	24421048	Therefore, acute alcohol <b>intoxication</b> leads to decreased MRSA clearance in part by inhibiting <strong>IL 6</strong>/STAT3 induction of the antimicrobial protein Reg3γ in the pulmonary epithelium.
+IL6	drug	alcohol	24379525	We also found a similar hematologic response and levels of circulating interleukin 6 (<strong>IL 6</strong>) when either <b>ethanol</b> paradigm achieved intoxication before burn.
+IL6	addiction	intoxication	24379525	We also found a similar hematologic response and levels of circulating interleukin 6 (<strong>IL 6</strong>) when either ethanol paradigm achieved <b>intoxication</b> before burn.
+IL6	drug	alcohol	24379525	We also found a similar hematologic response and levels of circulating <strong>interleukin 6</strong> (<strong>IL 6</strong>) when either <b>ethanol</b> paradigm achieved intoxication before burn.
+IL6	addiction	intoxication	24379525	We also found a similar hematologic response and levels of circulating <strong>interleukin 6</strong> (<strong>IL 6</strong>) when either ethanol paradigm achieved <b>intoxication</b> before burn.
+IL6	drug	alcohol	24163503	Acute <b>ethanol</b> intoxication further increased serum levels of GOT, GPT, BUN, Cre, LDH, CPK, TNF  α and <strong>IL 6</strong> elevation following HS.
+IL6	addiction	intoxication	24163503	Acute ethanol <b>intoxication</b> further increased serum levels of GOT, GPT, BUN, Cre, LDH, CPK, TNF  α and <strong>IL 6</strong> elevation following HS.
+IL6	drug	cocaine	24090796	While viewing the disgusting images, <b>cocaine</b> dependent individuals exhibited aberrant skin conductivity and increased the secretion of the salivary cytokine <strong>interleukin 6</strong> relative to control participants.
+IL6	drug	alcohol	24070686	Searching for causes of altered vitamin levels, we also assessed liver function, nutritional status, eating habits, <b>alcohol</b> intake, proinflammatory cytokine (TNF α, <strong>IL 6</strong>, IL 8) levels and malondialdehyde (MDA) levels.
+IL6	addiction	sensitization	23940384	DIO mice fed for 4 weeks showed no neuronal <b>sensitization</b>, had no signs of gut wall inflammation and showed a smaller increase in leptin, <strong>interleukin 6</strong> and monocyte chemoattractant protein 1 expression in fat tissue.
+IL6	addiction	intoxication	23909743	However, single <b>binge</b> EtOH followed by burn injury induced significant elevations in mRNA and protein concentrations of pro inflammatory mediators interleukin 6 (<strong>IL 6</strong>), KC, and monocyte chemoattractant protein 1 compared with either insult alone or sham vehicle group.
+IL6	addiction	intoxication	23909743	However, single <b>binge</b> EtOH followed by burn injury induced significant elevations in mRNA and protein concentrations of pro inflammatory mediators <strong>interleukin 6</strong> (<strong>IL 6</strong>), KC, and monocyte chemoattractant protein 1 compared with either insult alone or sham vehicle group.
+IL6	drug	alcohol	23828825	Serum samples were collected to measure blood <b>ethanol</b>, aspartate transferase, alanine transferase, creatine phosphokinase, lactate dehydrogenase, amylase, tumor necrosis factor alpha (TNF α) and interleukin 6 (<strong>IL 6</strong>) levels.
+IL6	drug	alcohol	23828825	Serum samples were collected to measure blood <b>ethanol</b>, aspartate transferase, alanine transferase, creatine phosphokinase, lactate dehydrogenase, amylase, tumor necrosis factor alpha (TNF α) and <strong>interleukin 6</strong> (<strong>IL 6</strong>) levels.
+IL6	drug	opioid	23796752	Here, we characterized the receptor proximal signaling events that link μ <b>opioid</b> receptors to activation of Akt and ERKs in lipopolysaccharide (LPS) stimulated murine microglial cells with the aim to define the molecular mechanism contributing to the ability of <b>morphine</b> to increase inflammatory mediators such as nitric oxide (NO), tumor necrosis factor (TNF) α, interleukin (IL) 1β and <strong>IL 6</strong> in activated microglial cells.
+IL6	drug	opioid	23796752	Furthermore, we found that <b>morphine</b> enhanced the release of IL 1β, TNF α, <strong>IL 6</strong>, and of NO via μ <b>opioid</b> receptor PKCɛ signaling pathway in activated microglial cells, mediating a proinflammatory phenotype in mouse microglial cells.
+IL6	drug	alcohol	23701841	In this paradigm, <b>ethanol</b> did not affect mRNA levels of the cytokines <strong>IL 6</strong> or TNF α in any of these brain regions in aged animals.
+IL6	drug	alcohol	23376955	Anti <strong>IL 6</strong> antibody treatment but not <strong>IL 6</strong> knockout improves intestinal barrier function and reduces inflammation after binge <b>ethanol</b> exposure and burn injury.
+IL6	addiction	intoxication	23376955	Anti <strong>IL 6</strong> antibody treatment but not <strong>IL 6</strong> knockout improves intestinal barrier function and reduces inflammation after <b>binge</b> ethanol exposure and burn injury.
+IL6	drug	alcohol	23376955	Previous work in our laboratory has shown that <strong>IL 6</strong> is increased both systemically and in multiple organ systems including the ileum after <b>ethanol</b> exposure and burn injury.
+IL6	drug	alcohol	23376955	As this combined insult causes elevated intestinal morphological damage, tight junction protein localization alterations, and phosphorylated myosin light chain levels, we sought to determine the role of <strong>IL 6</strong> in these intestinal responses using a model of binge <b>ethanol</b> exposure and burn injury.
+IL6	addiction	intoxication	23376955	As this combined insult causes elevated intestinal morphological damage, tight junction protein localization alterations, and phosphorylated myosin light chain levels, we sought to determine the role of <strong>IL 6</strong> in these intestinal responses using a model of <b>binge</b> ethanol exposure and burn injury.
+IL6	drug	alcohol	23376955	Zonula occludens protein 1 and occludin localization was also reestablished in wild type mice given <strong>IL 6</strong> antibody after <b>ethanol</b> and burn.
+IL6	drug	alcohol	23376955	<strong>Interleukin 6</strong> knockout mice given <b>ethanol</b> and burn injury also had reduced intestinal damage; however, no changes in bacterial translocation or tight junction protein localization were observed as compared with similarly treated wild type mice.
+IL6	drug	alcohol	23376955	These data suggest that <strong>IL 6</strong> may have a role in intestinal tissue damage observed after the combined insult of binge <b>ethanol</b> exposure and burn injury, although complete loss of <strong>IL 6</strong> does not seem to be beneficial in this model.
+IL6	addiction	intoxication	23376955	These data suggest that <strong>IL 6</strong> may have a role in intestinal tissue damage observed after the combined insult of <b>binge</b> ethanol exposure and burn injury, although complete loss of <strong>IL 6</strong> does not seem to be beneficial in this model.
+IL6	drug	alcohol	23376955	Modulation of <strong>IL 6</strong> may present a new option for preventing intestinal damage and associated inflammation after a combined insult of <b>ethanol</b> exposure and burn injury.
+IL6	drug	opioid	23352192	In response to LPS, expression of 27 genes, including NLRP3, TNF α, IL 1β, and <strong>IL 6</strong>, was significantly increased, and expression of 3 genes was significantly decreased in both the <b>morphine</b> tolerant and placebo control groups compared to the saline treated animals.
+IL6	drug	opioid	23047422	Using blood from preterm (≤ 30 weeks gestational age (GA), n=7) and full term (≥ 37 weeks GA, n=19) infants, we investigated the changes in cytokine profile (IL 1β, <strong>IL 6</strong>, IL 8, IL 10, IL 12p70 and TNF α), cyclic adenosine monophosphate (cAMP) levels and μ , δ  and κ  <b>opioid</b> receptor (OPR) gene and protein expression, following in vitro exposure to <b>morphine</b>, <b>methadone</b>, <b>fentanyl</b> or clonidine at increasing concentrations ranging from 0 to 1 mM.
+IL6	drug	opioid	23031399	Incision after saline or escalating <b>morphine</b> treatment upregulated skin IL 1β, <strong>IL 6</strong>, G CSF and MIP 1α levels in ppt A( / ) and wt mice similarly.
+IL6	drug	opioid	23022502	Using immunohistochemical staining, we demonstrated the administration of MC4R during the induction of <b>morphine</b> tolerance inhibited the activation of astrocytes; reduced the expression of proinflammatory cytokines interleukin 1β, <strong>IL 6</strong>, and tumor necrosis factor α; upregulated the expression of anti inflammatory cytokines IL 10 at the L5 lumbar spinal cord.
+IL6	drug	alcohol	22803049	Experiments of outbred albino rats showed that chronic <b>ethanol</b> intoxication (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1 cells, increased blood corticosterone concentration, reduced T lymphocyte acetylcholinesterase activity, blood concentrations of IFN γ, IL 2, IL 4, IL 10, and increased <strong>IL 6</strong> level.
+IL6	addiction	intoxication	22803049	Experiments of outbred albino rats showed that chronic ethanol <b>intoxication</b> (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1 cells, increased blood corticosterone concentration, reduced T lymphocyte acetylcholinesterase activity, blood concentrations of IFN γ, IL 2, IL 4, IL 10, and increased <strong>IL 6</strong> level.
+IL6	drug	alcohol	22790598	Elevated morphological damage, ileal IL 1β and <strong>IL 6</strong> levels, and bacterial translocation were seen in mice exposed to <b>ethanol</b> and burn injury relative to either insult alone.
+IL6	drug	alcohol	22709825	<b>Ethanol</b> pretreatment potentiated poly I:C induced brain TNFα (345%), IL 1β (331%), <strong>IL 6</strong> (255%), and MCP 1(190%).
+IL6	drug	alcohol	22521198	Participants were assessed for gut permeability, systemic inflammation (LPS, TNFα, <strong>IL 6</strong>, IL 10, hsCRP) and for depression, anxiety, <b>alcohol</b> craving and selective attention.
+IL6	addiction	relapse	22521198	Participants were assessed for gut permeability, systemic inflammation (LPS, TNFα, <strong>IL 6</strong>, IL 10, hsCRP) and for depression, anxiety, alcohol <b>craving</b> and selective attention.
+IL6	drug	opioid	22428664	We examined the effects of µ <b>opioid</b> and CB(2) receptor stimulation on phosphorylation of MAPKs and Akt and on IL 1β, TNF α, <strong>IL 6</strong> and NO production in primary mouse microglial cells.
+IL6	drug	opioid	22428664	<b>Morphine</b> enhanced release of the proinflammatory cytokines, IL 1β, TNF α, <strong>IL 6</strong>, and of NO via µ <b>opioid</b> receptor in activated microglial cells.
+IL6	drug	opioid	22366510	Moreover, the administration of LXA4ME during the induction of <b>morphine</b> tolerance inhibited the activation of microglia and astrocytes; reduced the expression of proinflammatory cytokines interleukin 1β (IL 1β), <strong>IL 6</strong>, and tumor necrosis factor α (TNF α); upregulated the expression of anti inflammatory cytokines IL 10 and transforming growth factor β1 (TGF β1); and inhibited nuclear factor kappa B (NF κB) activation at the L5 lumbar spinal cord.
+IL6	drug	opioid	22205542	After 6 days of <b>morphine</b> treatment, cytokine (IL 1β, <strong>IL 6</strong>) levels had significantly increased in serum; IL 1β and <strong>IL 6</strong> mRNA levels had significantly increased in the nucleus accumbens and medial prefrontal cortex, both addiction related brain areas; and BDNF levels had significantly decreased, both in serum and in addiction related brain areas.
+IL6	addiction	addiction	22205542	After 6 days of morphine treatment, cytokine (IL 1β, <strong>IL 6</strong>) levels had significantly increased in serum; IL 1β and <strong>IL 6</strong> mRNA levels had significantly increased in the nucleus accumbens and medial prefrontal cortex, both <b>addiction</b> related brain areas; and BDNF levels had significantly decreased, both in serum and in <b>addiction</b> related brain areas.
+IL6	drug	nicotine	22180575	Depressed <b>smokers</b> had significantly higher levels of hs CRP (p = .05), <strong>IL 6</strong> (p = .039), and TNF α (p = .021) compared with nondepressed <b>smokers</b>.
+IL6	drug	nicotine	22180575	These findings demonstrate that depressed <b>smokers</b> had higher hs CRP, <strong>IL 6</strong>, and TNF α levels than nondepressed <b>smokers</b> and had worse physical health outcomes and greater work related disability.
+IL6	drug	alcohol	22140596	In this study, we used a PCR array containing 46 primer pairs of selected genes to compare mRNA expression in the spleen, an immune system organ, of adolescent rats following binge drinking of <b>alcohol</b> solutions containing either 20% or 52% <b>ethanol</b> (v/v, 4.8 g/kg daily dosage), or water (control) for 3 d. We found that, expression of IL 1β, <strong>IL 6</strong>, CCL2, and GABA(A) receptor α2 subunit in the spleen were decreased, and mGluR5 and 5 HT3A receptor expression were increased after administration of an <b>ethanol</b> solution containing 52% <b>ethanol</b>, but not one with 20% <b>ethanol</b>.
+IL6	addiction	intoxication	22140596	In this study, we used a PCR array containing 46 primer pairs of selected genes to compare mRNA expression in the spleen, an immune system organ, of adolescent rats following <b>binge</b> drinking of alcohol solutions containing either 20% or 52% ethanol (v/v, 4.8 g/kg daily dosage), or water (control) for 3 d. We found that, expression of IL 1β, <strong>IL 6</strong>, CCL2, and GABA(A) receptor α2 subunit in the spleen were decreased, and mGluR5 and 5 HT3A receptor expression were increased after administration of an ethanol solution containing 52% ethanol, but not one with 20% ethanol.
+IL6	drug	amphetamine	22133515	Neutralization of maternal leptin prevented the enhanced behavioral sensitization and elevation of DA and spinophilin in the NAcc but spared other changes regulated by <strong>IL 6</strong>, such as increased NAcc TH levels and acute locomotor response to <b>AMPH</b>.
+IL6	addiction	sensitization	22133515	Neutralization of maternal leptin prevented the enhanced behavioral <b>sensitization</b> and elevation of DA and spinophilin in the NAcc but spared other changes regulated by <strong>IL 6</strong>, such as increased NAcc TH levels and acute locomotor response to AMPH.
+IL6	drug	alcohol	21790532	Elevated serum <strong>IL 6</strong> levels as well as hepatic <strong>IL 6</strong> and TNF α gene expression 2 h after H/R were reduced by <b>ethanol</b>.
+IL6	addiction	intoxication	21593683	Furthermore, a significant increase in <strong>IL 6</strong> and MCP 1 was observed in circulation after EtOH <b>intoxication</b> and burn injury compared with either EtOH <b>intoxication</b> or burn injury alone; no other cytokines were detected in circulation.
+IL6	drug	alcohol	21508281	However, <b>alcohol</b> treated animals were found to have increased pulmonary levels of <strong>IL 6</strong>, IL 1β, IL 2, and macrophage inflammatory protein 1α following bilateral femoral fracture.
+IL6	drug	alcohol	21421450	<b>Alcoholics</b> admitted for programmed withdrawal showed higher <strong>IL 6</strong>, IFN γ, IL 10, Il 4 and ICAM 1 serum levels than healthy controls.
+IL6	addiction	withdrawal	21421450	Alcoholics admitted for programmed <b>withdrawal</b> showed higher <strong>IL 6</strong>, IFN γ, IL 10, Il 4 and ICAM 1 serum levels than healthy controls.
+IL6	drug	alcohol	21315785	In female mice, however, corticosterone does appear to mediate the persistent effects of acute <b>ethanol</b> administration on poly I:C  induced <strong>IL 6</strong> levels.
+IL6	drug	alcohol	21315785	Since many <strong>IL 6</strong> related disorders are gender associated, further research into the bidirectional effects of the HPG and HPA axes on alterations in cytokine production mediated by <b>ethanol</b> is warranted.
+IL6	drug	cocaine	21277908	Memantine abolishes the formation of <b>cocaine</b> induced conditioned place preference possibly via its <strong>IL 6</strong> modulating effect in medial prefrontal cortex.
+IL6	drug	cocaine	21277908	Three consecutive days of <b>cocaine</b> conditioning increased interleukin 6 (<strong>IL 6</strong>) but decreased tumor necrosis factor (TNF α) levels in medial prefrontal cortex (mPFC) and nucleus accumbens (Acb).
+IL6	drug	cocaine	21277908	Three consecutive days of <b>cocaine</b> conditioning increased <strong>interleukin 6</strong> (<strong>IL 6</strong>) but decreased tumor necrosis factor (TNF α) levels in medial prefrontal cortex (mPFC) and nucleus accumbens (Acb).
+IL6	drug	cocaine	21277908	Interestingly, pretreatment with memantine at the lowest effective dose (0.02 mg/kg/injection) reversed <b>cocaine</b> conditioning enhanced <strong>IL 6</strong> and  decreased TNF α levels in these brain regions.
+IL6	drug	cocaine	21277908	Finally, intra mPFC infusion of recombinant <strong>IL 6</strong>, but not thalidomide, reversed memantine (0.02 mg/kg/injection × 6) decreased <b>cocaine</b> induced CPP.
+IL6	addiction	reward	21277908	Finally, intra mPFC infusion of recombinant <strong>IL 6</strong>, but not thalidomide, reversed memantine (0.02 mg/kg/injection × 6) decreased cocaine induced <b>CPP</b>.
+IL6	drug	cocaine	21277908	These results, taken together, suggest that <b>cocaine</b> conditioning enhanced <strong>IL 6</strong> in mPFC may be, in part, involved in the acquisition of <b>cocaine</b> induced CPP.
+IL6	addiction	reward	21277908	These results, taken together, suggest that cocaine conditioning enhanced <strong>IL 6</strong> in mPFC may be, in part, involved in the acquisition of cocaine induced <b>CPP</b>.
+IL6	drug	cocaine	21277908	Moreover, an extremely low dose of memantine may decrease the acquisition of <b>cocaine</b> induced CPP by reversing <b>cocaine</b> conditioning increased <strong>IL 6</strong> levels in mPFC.
+IL6	addiction	reward	21277908	Moreover, an extremely low dose of memantine may decrease the acquisition of cocaine induced <b>CPP</b> by reversing cocaine conditioning increased <strong>IL 6</strong> levels in mPFC.
+IL6	drug	alcohol	21254593	It was established in experiments on noninbred rats that their <b>ethanol</b> intoxication (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, IL 2, IL 4, IL 10, increases the concentration of <strong>IL 6</strong>, suppresses the immune responses, and reduces the interrelation IFNgamma/IL 4 in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes.
+IL6	addiction	intoxication	21254593	It was established in experiments on noninbred rats that their ethanol <b>intoxication</b> (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, IL 2, IL 4, IL 10, increases the concentration of <strong>IL 6</strong>, suppresses the immune responses, and reduces the interrelation IFNgamma/IL 4 in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes.
+IL6	drug	alcohol	21208596	Chronic, moderate PTSD due to civilian trauma, without psychotic symptoms and without significant rates of comorbid depression, <b>alcohol</b> dependence, or substance dependence, is not associated with abnormalities in CSF CRF, <strong>IL 6</strong>, BDNF, IGF 1, or substance P levels.
+IL6	addiction	dependence	21208596	Chronic, moderate PTSD due to civilian trauma, without psychotic symptoms and without significant rates of comorbid depression, alcohol <b>dependence</b>, or substance <b>dependence</b>, is not associated with abnormalities in CSF CRF, <strong>IL 6</strong>, BDNF, IGF 1, or substance P levels.
+IL6	drug	alcohol	21143255	Human PBMCs were cultured in the presence of 100 mM <b>ethanol</b> and/or 100 ng/ml LPS for various time periods (1, 3, 8, and 24 hours) and analyzed for the kinetics of gene expression by quantitative real time PCR of selected transcription factors (T bet, GATA3, Foxp3, and RORγt) and cytokines (TNF α, <strong>IL 6</strong>, IL 10, and IFN γ).
+IL6	drug	alcohol	21143255	Markers of inflammation including TNF α and IL 1β in supernatant of PBMCs were significantly decreased, while levels of IL 10 and <strong>IL 6</strong> remained unchanged following <b>ethanol</b> exposure.
+IL6	drug	nicotine	21078494	<b>Nicotine</b> did not cause an excessive expression of TNF α, IL 8, and <strong>IL 6</strong>, nor did it affect protein production from the MUC5AC gene.
+IL6	drug	nicotine	21078494	<b>Nicotine</b> not only failed to stimulate production of TNF α, IL 8, and <strong>IL 6</strong>, but its presence was shown to suppress the activation resulting from exposure to CE and LPS (P < 0.05).
+IL6	drug	alcohol	20608903	Consistent with these findings, pulmonary levels of KC and <strong>IL 6</strong> were increased in wild type mice following burn and <b>ethanol</b> compared to burn injury alone as well as to their TLR4 knockout counterparts.
+IL6	drug	alcohol	20586751	In addition, administration of rmMFG E8 after <b>alcohol</b> exposure and subsequent sepsis decreases circulating levels of TNF alpha and <strong>interleukin 6</strong> and attenuates organ injury.
+IL6	drug	nicotine	19732285	<b>Nicotine</b> suppresses IL 1beta and <strong>IL 6</strong> expression at least in part by inhibiting NFkappaB activation.
+IL6	drug	opioid	19693978	[<b>Tramadol</b> inhibits c fos expression in spinal cord dorsal horn and serum <strong>IL 6</strong> levels induced by plantar incision in rats].
+IL6	drug	opioid	19693978	To investigate effect of <b>tramadol</b> on c fos expression in spinal cord dorsal horn and serum <strong>IL 6</strong> levels induced by plantar incision in rats.
+IL6	drug	opioid	19693978	The greatest density of Fos positive neurons was located in lamine I II in Group I. Serum <strong>IL 6</strong> levels were significantly elevated in Group I. Pretreatment with <b>tramadol</b> showed a dose depended inhibitory effect on c fos expression and serum <strong>IL 6</strong> production,but not in Group T1.
+IL6	drug	opioid	19693978	Administration of <b>tramadol</b> postoperatively also suppressed the c fos expression and serum <strong>IL 6</strong> production as showed in PT10 but were weaker than those in Group T10.
+IL6	drug	alcohol	19406265	Long chain n 3 PUFA intake was inversely associated with plasma concentrations of <strong>interleukin 6</strong> (p = 0.01) and matrix metalloproteinase 3 (p = 0.03) independent of age, body mass index, physical activity, smoking, <b>alcohol</b> consumption, and dietary variables.
+IL6	drug	nicotine	19406265	Long chain n 3 PUFA intake was inversely associated with plasma concentrations of <strong>interleukin 6</strong> (p = 0.01) and matrix metalloproteinase 3 (p = 0.03) independent of age, body mass index, physical activity, <b>smoking</b>, alcohol consumption, and dietary variables.
+IL6	drug	alcohol	19330277	The expression of important regulators of osteoclast maturation and activity such as NF kappabeta (nuclear factor kappabeta) ligand (RANKL) and <strong>interleukin 6</strong> were significantly increased (P < 0.05) by binge <b>alcohol</b>, and osteoprotegerin levels were significantly decreased (P < 0.05) in vertebral bone.
+IL6	addiction	intoxication	19330277	The expression of important regulators of osteoclast maturation and activity such as NF kappabeta (nuclear factor kappabeta) ligand (RANKL) and <strong>interleukin 6</strong> were significantly increased (P < 0.05) by <b>binge</b> alcohol, and osteoprotegerin levels were significantly decreased (P < 0.05) in vertebral bone.
+IL6	drug	alcohol	19185507	Common polymorphisms in interleukin genes (IL4, <strong>IL6</strong>, IL8 and IL12) are not associated with <b>alcoholic</b> liver disease or <b>alcoholism</b> in Spanish men.
+IL6	drug	alcohol	19177625	Age, hour of blood withdrawal, body mass index, pack years of smoking, NT proBNP, systolic blood pressure, high density lipoprotein cholesterol, persistent cough/phlegm and statin use were significantly and independently associated with <strong>IL 6</strong> after adjustment for city, recurrent MI, baseline <b>alcohol</b> intake, current active smoking, tea consumption and extreme anger or stress.
+IL6	drug	nicotine	19177625	Age, hour of blood withdrawal, body mass index, pack years of <b>smoking</b>, NT proBNP, systolic blood pressure, high density lipoprotein cholesterol, persistent cough/phlegm and statin use were significantly and independently associated with <strong>IL 6</strong> after adjustment for city, recurrent MI, baseline alcohol intake, current active <b>smoking</b>, tea consumption and extreme anger or stress.
+IL6	addiction	withdrawal	19177625	Age, hour of blood <b>withdrawal</b>, body mass index, pack years of smoking, NT proBNP, systolic blood pressure, high density lipoprotein cholesterol, persistent cough/phlegm and statin use were significantly and independently associated with <strong>IL 6</strong> after adjustment for city, recurrent MI, baseline alcohol intake, current active smoking, tea consumption and extreme anger or stress.
+IL6	drug	nicotine	18536030	Serum <strong>IL 6</strong> level was also a significant independent predictor of poor survival (HR = 1.22; 95% CI, 1.02 to 1.46; P = .03), as were older age, <b>smoking</b>, cancer site (oral/sinus), higher cancer stage, and comorbidities.
+IL6	addiction	relapse	18536030	Using <strong>IL 6</strong> as a biomarker for recurrence and survival may allow for earlier identification and treatment of disease <b>relapse</b>.
+IL6	drug	opioid	18294378	Mice treated chronically treated with <b>morphine</b> prior to incision were found to have enhanced skin levels of IL 1beta, <strong>IL 6</strong>, G CSF, KC and TNFalpha after incision at one or more time points compared to saline pretreated controls.
+IL6	drug	alcohol	17980786	<b>Alcohol</b> induced endothelial damage or protection may be related to the synthesis or action of several markers, such as nitric oxide, cortisol, endothelin 1, adhesion molecules, tumor necrosis factor alpha, <strong>interleukin 6</strong>, C reactive protein, and haemostatic factors.
+IL6	addiction	withdrawal	17637925	Pooled results show an increase in <strong>IL 6</strong> when concentrations of PNC were elevated 12 17 hr before blood <b>withdrawal</b> [percent change of geometric mean, 2.7; 95% confidence interval (CI), 1.0 4.6].
+IL6	drug	alcohol	17374050	While T x Hem did not prevent LPS induced release of TNF alpha, IL 1alpha, <strong>IL 6</strong>, or IL 10 at 6 or 24 hours, <b>alcohol</b> binge suppressed TNF alpha, IL 1 and <strong>IL 6</strong> release, without altering IL 10 response in cells isolated from blood and pleural compartment.
+IL6	addiction	intoxication	17374050	While T x Hem did not prevent LPS induced release of TNF alpha, IL 1alpha, <strong>IL 6</strong>, or IL 10 at 6 or 24 hours, alcohol <b>binge</b> suppressed TNF alpha, IL 1 and <strong>IL 6</strong> release, without altering IL 10 response in cells isolated from blood and pleural compartment.
+IL6	drug	opioid	17201885	Leukocyte subpopulation NK, CD4+, CD8+ and some cytokines Th1 (IFNgamma, interleukin [IL]2) and Th2 (<strong>IL 6</strong>, IL 10) were evaluated prior to, during and after <b>methadone</b> treatment.
+IL6	drug	cocaine	17068203	In <b>cocaine</b> dependent volunteers and control subjects, we analyzed monocyte TNF alpha and <strong>IL 6</strong> expression at rest and in response to the bacterial ligand, lipopolysaccharide (LPS), over a 24 h period.
+IL6	drug	cocaine	17068203	In addition, the in vivo effects of <b>cocaine</b> (40 mg) versus placebo on monocyte expression of TNF alpha and <strong>IL 6</strong> were profiled over 48 h. <b>Cocaine</b> dependent volunteers showed a decrease in the capacity of monocytes to express TNF alpha and <strong>IL 6</strong> compared with control subjects.
+IL6	drug	alcohol	16783199	Only the hemorrhage induced rise in lung <strong>IL 6</strong> and tumor necrosis factor alpha was prevented by <b>alcohol</b> administration.
+IL6	drug	nicotine	16332510	In the present study, the combined effects of <b>nicotine</b> and bacterial LPS on the expression of <strong>IL 6</strong>, IL 8, GRO alpha and MCP 1 in cell lines of human coronary artery endothelial cells (HCAEC) and pulmonary monocytes (THP 1) were examined by quantitative real time PCR and ELISA.
+IL6	drug	nicotine	16332510	Results showed that <b>nicotine</b> suppressed the LPS induced production of <strong>IL 6</strong> and IL 8 in both cell lines.
+IL6	drug	alcohol	16295318	For this reason, 153 patients with chronic <b>alcoholism</b> were divided into four test lots, in order to determine: the activity and the serum level of ceruloplasmin, plasma level of MDA (malondialdehyde), lactic and pyruvic acids, serum level of transferrin, alpha1 antitrypsin, CRP (C reactive protein), C3 fraction of the complement, IgA, IgG, IgM, IL 1beta, <strong>IL 6</strong> and IL 8, cytosolic level of the cytochrome c in the circulating leukocytes.
+IL6	drug	alcohol	16295318	On the other hand, the <b>ethanol</b> induced apoptosis of leukocytes (especially of the B cells) is very important, probably due to the absence of <strong>IL 6</strong> protective action on these cells.
+IL6	addiction	intoxication	16046881	EtOH <b>intoxication</b> two hr before LPS acutely suppressed the increased <strong>IL 6</strong> mRNA in all tissues and antagonized the increase in plasma and tissue <strong>IL 6</strong> protein concentration.
+IL6	drug	alcohol	15469574	In early septic shock, chronic <b>alcoholic</b> patients had significantly decreased levels of IL 1beta (P < 0.015), <strong>IL 6</strong> (P < 0.016) and IL 8 (P < 0.010).
+IL6	drug	alcohol	15289211	In 36 <b>alcoholics</b> without liver disease, at the point of commencing withdrawal from <b>alcohol</b>, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, IL1RA, IL4, <strong>IL6</strong>, IL8, IL10 and IL12).
+IL6	addiction	withdrawal	15289211	In 36 alcoholics without liver disease, at the point of commencing <b>withdrawal</b> from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, IL1RA, IL4, <strong>IL6</strong>, IL8, IL10 and IL12).
+IL6	drug	alcohol	15282117	criteria for <b>alcohol</b> dependence and estimated by using the Composite International Diagnostic Interview (CIDI), was characterized by increased serum <strong>IL 6</strong> concentration.
+IL6	addiction	dependence	15282117	criteria for alcohol <b>dependence</b> and estimated by using the Composite International Diagnostic Interview (CIDI), was characterized by increased serum <strong>IL 6</strong> concentration.
+IL6	drug	alcohol	15282117	These results indicate that in <b>alcohol</b> dependent individuals there is a significant increase in the serum <strong>IL 6</strong> concentration (P <.05).
+IL6	drug	alcohol	15157952	In this study, we investigated whether nocturnal plasma levels of interleukin 6 (<strong>IL 6</strong>) and tumor necrosis factor alpha (TNF) were associated with disordered sleep in <b>alcohol</b> dependence by testing the temporal relationships between these inflammatory cytokines and sleep, before and after sleep deprivation.
+IL6	addiction	dependence	15157952	In this study, we investigated whether nocturnal plasma levels of interleukin 6 (<strong>IL 6</strong>) and tumor necrosis factor alpha (TNF) were associated with disordered sleep in alcohol <b>dependence</b> by testing the temporal relationships between these inflammatory cytokines and sleep, before and after sleep deprivation.
+IL6	drug	alcohol	15157952	In this study, we investigated whether nocturnal plasma levels of <strong>interleukin 6</strong> (<strong>IL 6</strong>) and tumor necrosis factor alpha (TNF) were associated with disordered sleep in <b>alcohol</b> dependence by testing the temporal relationships between these inflammatory cytokines and sleep, before and after sleep deprivation.
+IL6	addiction	dependence	15157952	In this study, we investigated whether nocturnal plasma levels of <strong>interleukin 6</strong> (<strong>IL 6</strong>) and tumor necrosis factor alpha (TNF) were associated with disordered sleep in alcohol <b>dependence</b> by testing the temporal relationships between these inflammatory cytokines and sleep, before and after sleep deprivation.
+IL6	drug	alcohol	15157952	Coupled with prolonged sleep latency and increased rapid eye movement sleep, <b>alcoholics</b> showed nocturnal elevations of <strong>IL 6</strong> and TNF as compared to controls after adjustment for <b>alcohol</b> consumption and body mass index.
+IL6	drug	alcohol	15157952	Following sleep deprivation, <b>alcoholics</b> showed greater nocturnal levels of <strong>IL 6</strong> and greater nocturnal increases of TNF as compared to controls.
+IL6	drug	opioid	15055740	A significantly higher production of <strong>IL 6</strong> was found in both unstimulated and stimulated PBL from <b>heroin</b> addicts and patients maintained on <b>methadone</b>, when compared with PBL from healthy controls.
+IL6	drug	alcohol	26983653	Association between  174 G/C polymorphism of <strong>interleukin 6</strong> gene and <b>alcoholism</b>.
+IL6	drug	alcohol	26983653	The aim of the present association study was to examine the effect of the G/C  174 polymorphism of the <strong>IL 6</strong> gene on disposition to <b>alcoholism</b>.
+IL6	drug	alcohol	26983653	We investigated the relationship between the G/C  174 polymorphism of the <strong>IL 6</strong> gene and <b>alcohol</b> dependence in 281 <b>alcoholics</b> and 242 control subjects.
+IL6	addiction	dependence	26983653	We investigated the relationship between the G/C  174 polymorphism of the <strong>IL 6</strong> gene and alcohol <b>dependence</b> in 281 alcoholics and 242 control subjects.
+IL6	drug	alcohol	26983653	To our knowledge, this is the first finding providing evidence for an association between <b>alcoholism</b> and the polymorphism of the <strong>IL 6</strong> gene.
+IL6	drug	alcohol	26983653	The background of the relationship between the <strong>IL 6</strong> gene and <b>alcoholism</b> is discussed.
+IL6	drug	opioid	12427855	Chronic administration of <b>morphine</b> to sham operated rats activated spinal glia and upregulated proinflammatory cytokines [interleukin (IL) 1beta, <strong>IL 6</strong>, and tumor necrosis factor alpha].
+IL6	drug	alcohol	11956381	<b>Alcohol</b> exacerbated the hemorrhage induced increase in lung TNF alpha, and did not alter the IL 1alpha, <strong>IL 6</strong>, and IL 10 lung responses.
+IL6	drug	amphetamine	11311862	Wise, <strong>Interleukin 6</strong> increases sensitivity to the locomotor stimulating effects of <b>amphetamine</b> in rats, Brain Res.
+IL6	addiction	relapse	11293664	The mRNA for cytokines IL 1beta, <strong>IL 6</strong>, IL 10 and the chemokines CINC, MIP 1alpha, MCP 1 were significantly (P < 0.05) elevated and persisted for 2 weeks, decreased in 6 weeks and increased again during <b>relapse</b>.
+IL6	drug	alcohol	11109026	Acute <b>ethanol</b> exposure prior to burn injury increases the immune dysfunction seen with burn alone, which has been partially attributed to increased circulating and splenic macrophage production of interleukin 6 (<strong>IL 6</strong>).
+IL6	drug	alcohol	11109026	Acute <b>ethanol</b> exposure prior to burn injury increases the immune dysfunction seen with burn alone, which has been partially attributed to increased circulating and splenic macrophage production of <strong>interleukin 6</strong> (<strong>IL 6</strong>).
+IL6	drug	alcohol	11109026	Interestingly, the increase in macrophage <strong>IL 6</strong> secretion seen at the moderate dose was not augmented at the high dose; however, the circulating <strong>IL 6</strong> levels did reveal a further increase at the high <b>ethanol</b> dose.
+IL6	drug	alcohol	11109026	These results suggest that the dose dependent effects of <b>ethanol</b> on immunity following burn injury are not the result of splenic macrophage <strong>IL 6</strong> production as shown at the moderate dose and that the immune suppressive effects of <b>ethanol</b> in this model persist after it is cleared from the circulation.
+IL6	drug	alcohol	10976010	Influence of acute <b>alcohol</b> intake and <b>alcohol</b> withdrawal on circulating levels of <strong>IL 6</strong>, IL 8, IL 10 and IL 12.
+IL6	addiction	withdrawal	10976010	Influence of acute alcohol intake and alcohol <b>withdrawal</b> on circulating levels of <strong>IL 6</strong>, IL 8, IL 10 and IL 12.
+IL6	drug	alcohol	10976010	The present study was aimed to evaluate the influence of both acute <b>alcohol</b> abstinence (in <b>alcoholics</b>) and acute <b>alcohol</b> intake (in healthy subjects) on serum <strong>IL 6</strong>, IL 8, IL 10, and IL 12 levels.
+IL6	drug	alcohol	10976010	Increased serum levels of <strong>IL 6</strong>, IL 10 and, to a lesser extent IL 8, declined in the few days after <b>alcohol</b> abstinence in patients with <b>alcohol</b> withdrawal syndrome.
+IL6	addiction	withdrawal	10976010	Increased serum levels of <strong>IL 6</strong>, IL 10 and, to a lesser extent IL 8, declined in the few days after alcohol abstinence in patients with alcohol <b>withdrawal</b> syndrome.
+IL6	drug	alcohol	10798594	Decreased natural killer cell responses and altered <strong>interleukin 6</strong> and interleukin 10 production in <b>alcoholism</b>: an interaction between <b>alcohol</b> dependence and African American ethnicity.
+IL6	addiction	dependence	10798594	Decreased natural killer cell responses and altered <strong>interleukin 6</strong> and interleukin 10 production in alcoholism: an interaction between alcohol <b>dependence</b> and African American ethnicity.
+IL6	drug	alcohol	10798594	This study compared NK activity, interleukin (IL) 2 stimulated NK activity, and concanavalin A stimulated peripheral blood mononuclear cell production of Th1 (IL 12 and IL 2), Th2 (IL 10), and proinflammatory (<strong>IL 6</strong>) cytokines in 31 hospitalized chronic <b>alcoholic</b> patients and 31 age matched controls who were stratified on the basis of ethnicity.
+IL6	drug	alcohol	10798594	Compared with the other three groups, African American <b>alcoholics</b> also showed lower levels of <strong>IL 6</strong> (F = 7.2;p < 0.01) and higher levels of IL 10 (F = 4.9;p < 0.05).
+IL6	drug	alcohol	10798594	Regression analyses showed that <b>alcohol</b> dependence and ethnicity predicted NK activity, whereas the interaction between <b>alcohol</b> dependence and ethnicity predicted levels of <strong>IL 6</strong> and IL 10.
+IL6	addiction	dependence	10798594	Regression analyses showed that alcohol <b>dependence</b> and ethnicity predicted NK activity, whereas the interaction between alcohol <b>dependence</b> and ethnicity predicted levels of <strong>IL 6</strong> and IL 10.
+IL6	drug	amphetamine	10575098	<strong>Interleukin 6</strong> increases sensitivity to the locomotor stimulating effects of <b>amphetamine</b> in rats.
+IL6	drug	amphetamine	10575098	Nonetheless, repeated <strong>IL 6</strong> treatment increased sensitivity to the locomotor stimulating effects of 1.0 and 0.5 mg/kg <b>amphetamine</b>, when tested 5, 7, or 14 days following interruption of the cytokine treatment.
+IL6	drug	amphetamine	10575098	The ability of acute <strong>IL 6</strong> injections to alter locomotor activity and the ability of repeated <strong>IL 6</strong> injections to produce long lasting sensitization to the locomotor stimulating effects of <b>amphetamine</b> suggest an interaction of this cytokine with the mesolimbic dopamine system, a system implicated in aspects of schizophrenia, addiction, and movement disorders.
+IL6	addiction	addiction	10575098	The ability of acute <strong>IL 6</strong> injections to alter locomotor activity and the ability of repeated <strong>IL 6</strong> injections to produce long lasting sensitization to the locomotor stimulating effects of amphetamine suggest an interaction of this cytokine with the mesolimbic dopamine system, a system implicated in aspects of schizophrenia, <b>addiction</b>, and movement disorders.
+IL6	addiction	sensitization	10575098	The ability of acute <strong>IL 6</strong> injections to alter locomotor activity and the ability of repeated <strong>IL 6</strong> injections to produce long lasting <b>sensitization</b> to the locomotor stimulating effects of amphetamine suggest an interaction of this cytokine with the mesolimbic dopamine system, a system implicated in aspects of schizophrenia, addiction, and movement disorders.
+IL6	drug	amphetamine	10575098	The fact that <strong>IL 6</strong> caused a lasting change in responsiveness to <b>amphetamine</b> implies a mechanism by which immunogenic stimuli can alter brain circuitry, changing its sensitivity to seemingly unrelated subsequent stimuli or events.
+IL6	drug	alcohol	9895030	This study examines i) the activity of serum prolyl endopeptidase (PEP) and dipeptidlyl peptidase IV (DPP IV) in detoxified <b>alcohol</b> dependent patients without liver disease versus normal controls, and ii) the relationships between serum DPP IV and PEP activity and the production of cytokines or cytokine receptors, such as interleukin 6 (<strong>IL 6</strong>), tumor necrosis factor alpha (TNF alpha), interferon y (IFN y), IL 1 receptor antagonist (IL 1RA), and IL 10, and granulocyte macrophage colony stimulatory factor (GM CSF).
+IL6	drug	alcohol	9895030	This study examines i) the activity of serum prolyl endopeptidase (PEP) and dipeptidlyl peptidase IV (DPP IV) in detoxified <b>alcohol</b> dependent patients without liver disease versus normal controls, and ii) the relationships between serum DPP IV and PEP activity and the production of cytokines or cytokine receptors, such as <strong>interleukin 6</strong> (<strong>IL 6</strong>), tumor necrosis factor alpha (TNF alpha), interferon y (IFN y), IL 1 receptor antagonist (IL 1RA), and IL 10, and granulocyte macrophage colony stimulatory factor (GM CSF).
+IL6	drug	alcohol	9347083	Alterations in tumor necrosis factor alpha, interferon gamma, and <strong>interleukin 6</strong> production by natural killer cell enriched peripheral blood mononuclear cells in chronic <b>alcoholism</b>: relationship with liver disease and <b>ethanol</b> intake.
+IL6	addiction	withdrawal	9347083	The results on the production of <strong>IL 6</strong> and IFN gamma in AWLD and cirrhotic patients showed that only cirrhotic patients with a prolonged EtOH <b>withdrawal</b> period display abnormal production.
+IL6	drug	alcohol	9166969	Enhanced serum IgA concentrations are common in <b>alcoholic</b> liver cirrhosis, but functional differences between IgA subclasses and their relation with interleukin 6 (<strong>IL 6</strong>) have not been described.
+IL6	drug	alcohol	9166969	Enhanced serum IgA concentrations are common in <b>alcoholic</b> liver cirrhosis, but functional differences between IgA subclasses and their relation with <strong>interleukin 6</strong> (<strong>IL 6</strong>) have not been described.
+IL6	drug	alcohol	9166969	Mean IgA1 and IgA2 concentrations were significantly increased (p < 0.001) in <b>alcoholic</b> liver cirrhosis patients (6.13 +/  4.52 g/l and 1.83 +/  1.93 g/l respectively, with an IgA2/IgA1 ratio of 0.32 +/  0.19) and viral hepatitis patients (3.66 +/  2.59 g/l and 0.69 +/  0.67 g/l respectively, with an IgA2/IgA1 ratio of 0.21 +/  0.14) High serum <strong>IL 6</strong> concentrations (34 +/  33 ng/l) were correlated with elevated IgA1 and IgA2 concentrations only in patients with <b>alcoholic</b> liver cirrhosis.
+IL6	drug	opioid	9346391	Neutralizing antibody to <strong>IL 6</strong> inhibited the effect of <b>morphine</b> on RMIC.
+IL6	drug	alcohol	8730220	<strong>Interleukin 6</strong> tumor necrosis factor alpha clearance and metabolism in vivo and by the isolated, perfused liver in the rat: effect of acute <b>alcohol</b> administration.
+IL6	drug	alcohol	8730220	Acute <b>ethanol</b> administration significantly increased plasma clearance rate for both cytokines (36% and 72%, for <strong>IL 6</strong> and TNF alpha, respectively), decreased the t1/2 alpha (30% and 11%, for <strong>IL 6</strong> and TNF alpha, respectively), abolished the slow (beta) phase component for TNF alpha, and increased t1/2 beta for <strong>IL 6</strong> (31%).
+IL6	drug	alcohol	8730220	Although <b>alcohol</b> did not affect organ distribution of TNF alpha, it increased the <strong>IL 6</strong> content in the liver, kidney, and blood.
+IL6	drug	alcohol	8730220	<b>Ethanol</b> addition to the perfusate (35 mM, final concentration) significantly increased TNF alpha uptake (24%), without affecting <strong>IL 6</strong> uptake or the degradation rate of either cytokine.
+IL6	drug	alcohol	8730220	Data presented in this study demonstrate that: (1) acute <b>alcohol</b> consumption can alter the kinetic behavior of <strong>IL 6</strong> and TNF alpha in the bloodstream, mainly by accelerating their clearance which, in turn, may counteract the outcome of cytokine secretion and delivery to the blood; and (2) short exposure of liver to <b>ethanol</b> levels commonly seen in humans after binge drinking may alter its capacity to take up cytokines.
+IL6	addiction	intoxication	8730220	Data presented in this study demonstrate that: (1) acute alcohol consumption can alter the kinetic behavior of <strong>IL 6</strong> and TNF alpha in the bloodstream, mainly by accelerating their clearance which, in turn, may counteract the outcome of cytokine secretion and delivery to the blood; and (2) short exposure of liver to ethanol levels commonly seen in humans after <b>binge</b> drinking may alter its capacity to take up cytokines.
+IL6	drug	alcohol	8116830	<strong>Interleukin 6</strong> and interleukin 8 production by mononuclear cells of chronic <b>alcoholics</b> during treatment.
+IL6	drug	alcohol	8116830	This study was designed to investigate the relationship between chronic <b>alcohol</b> ingestion and cessation with respect to release of interleukin 6 (<strong>IL 6</strong>) and interleukin 8 (IL 8) using highly specific and sensitive ELISA assays, as well as a functional assay, natural killer cell cytotoxic activity.
+IL6	drug	alcohol	8116830	This study was designed to investigate the relationship between chronic <b>alcohol</b> ingestion and cessation with respect to release of <strong>interleukin 6</strong> (<strong>IL 6</strong>) and interleukin 8 (IL 8) using highly specific and sensitive ELISA assays, as well as a functional assay, natural killer cell cytotoxic activity.
+IL6	drug	alcohol	8116830	The abstaining controls, and the <b>alcoholics</b>, after 30 days of abstinence, tended to produce lower amounts of <strong>IL 6</strong> and IL 8, although these differences were not statistically significant.
+NPY	drug	alcohol	32338122	In utero Δ9 tetrahydrocannabinol exposure confers vulnerability towards cognitive impairments and <b>alcohol</b> drinking in the adolescent offspring: Is there a role for <strong>neuropeptide Y</strong>?
+NPY	drug	cannabinoid	32338122	In utero Δ9 <b>tetrahydrocannabinol</b> exposure confers vulnerability towards cognitive impairments and alcohol drinking in the adolescent offspring: Is there a role for <strong>neuropeptide Y</strong>?
+NPY	drug	cannabinoid	32338122	Indeed, since the <b>endocannabinoid</b> system regulates synaptic plasticity, emotional and cognitive processes from early stages of life interfering with it and other excitability endogenous modulators, such as neuropeptide Y (<strong>NPY</strong>), might contribute to the occurrence of a vulnerable phenotype later in life.
+NPY	drug	cannabinoid	32338122	Indeed, since the <b>endocannabinoid</b> system regulates synaptic plasticity, emotional and cognitive processes from early stages of life interfering with it and other excitability endogenous modulators, such as <strong>neuropeptide Y</strong> (<strong>NPY</strong>), might contribute to the occurrence of a vulnerable phenotype later in life.
+NPY	drug	alcohol	32338122	Following in utero THC exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and aversive limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for <strong>NPY</strong> neurons and the PSD proteins Homer 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, <b>alcohol</b> taking, relapse and conflict behaviour in the operant chamber throughout adolescence until early adulthood (cohort 2).
+NPY	drug	cannabinoid	32338122	Following in utero <b>THC</b> exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and aversive limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for <strong>NPY</strong> neurons and the PSD proteins Homer 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, alcohol taking, relapse and conflict behaviour in the operant chamber throughout adolescence until early adulthood (cohort 2).
+NPY	addiction	aversion	32338122	Following in utero THC exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and <b>aversive</b> limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for <strong>NPY</strong> neurons and the PSD proteins Homer 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, alcohol taking, relapse and conflict behaviour in the operant chamber throughout adolescence until early adulthood (cohort 2).
+NPY	addiction	relapse	32338122	Following in utero THC exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and aversive limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for <strong>NPY</strong> neurons and the PSD proteins Homer 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, alcohol taking, <b>relapse</b> and conflict behaviour in the operant chamber throughout adolescence until early adulthood (cohort 2).
+NPY	addiction	reward	32338122	Following in utero THC exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and aversive limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for <strong>NPY</strong> neurons and the PSD proteins Homer 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, alcohol taking, relapse and conflict behaviour in the <b>operant</b> chamber throughout adolescence until early adulthood (cohort 2).
+NPY	drug	alcohol	32338122	In utero THC exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired aversive limbic memory; (d) decreased <strong>NPY</strong> positive neurons in limbic regions; (e) region specific variations in Homer 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased <b>alcohol</b> drinking, relapse and conflict behaviour in the operant chamber.
+NPY	drug	cannabinoid	32338122	In utero <b>THC</b> exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired aversive limbic memory; (d) decreased <strong>NPY</strong> positive neurons in limbic regions; (e) region specific variations in Homer 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased alcohol drinking, relapse and conflict behaviour in the operant chamber.
+NPY	addiction	aversion	32338122	In utero THC exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired <b>aversive</b> limbic memory; (d) decreased <strong>NPY</strong> positive neurons in limbic regions; (e) region specific variations in Homer 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased alcohol drinking, relapse and conflict behaviour in the operant chamber.
+NPY	addiction	relapse	32338122	In utero THC exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired aversive limbic memory; (d) decreased <strong>NPY</strong> positive neurons in limbic regions; (e) region specific variations in Homer 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased alcohol drinking, <b>relapse</b> and conflict behaviour in the operant chamber.
+NPY	addiction	reward	32338122	In utero THC exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired aversive limbic memory; (d) decreased <strong>NPY</strong> positive neurons in limbic regions; (e) region specific variations in Homer 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased alcohol drinking, relapse and conflict behaviour in the <b>operant</b> chamber.
+NPY	drug	cannabinoid	32297119	We also explore the use of sodium glucose co transporter 2 (SGLT 2) inhibitors, amylin mimetics, leptin analogues, ghrelin antagonists and centrally acting agents to suppress appetite [neuropeptide Y (<strong>NPY</strong>) antagonists, melanocortin 4 receptor (MC4R) agonists and <b>cannabinoid</b> 1 receptor antagonists].
+NPY	drug	cannabinoid	32297119	We also explore the use of sodium glucose co transporter 2 (SGLT 2) inhibitors, amylin mimetics, leptin analogues, ghrelin antagonists and centrally acting agents to suppress appetite [<strong>neuropeptide Y</strong> (<strong>NPY</strong>) antagonists, melanocortin 4 receptor (MC4R) agonists and <b>cannabinoid</b> 1 receptor antagonists].
+NPY	drug	alcohol	31743731	We assessed the ability of the opioid antagonist, <b>naltrexone</b>, to reduce the discriminative stimulus effects of 22 h deprivation and of the 22 h deprivation like discriminative stimulus effects of PVN injected hunger mediator, neuropeptide Y (<strong>NPY</strong>).
+NPY	drug	opioid	31743731	We assessed the ability of the <b>opioid</b> antagonist, naltrexone, to reduce the discriminative stimulus effects of 22 h deprivation and of the 22 h deprivation like discriminative stimulus effects of PVN injected hunger mediator, neuropeptide Y (<strong>NPY</strong>).
+NPY	drug	alcohol	31743731	We assessed the ability of the opioid antagonist, <b>naltrexone</b>, to reduce the discriminative stimulus effects of 22 h deprivation and of the 22 h deprivation like discriminative stimulus effects of PVN injected hunger mediator, <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	opioid	31743731	We assessed the ability of the <b>opioid</b> antagonist, naltrexone, to reduce the discriminative stimulus effects of 22 h deprivation and of the 22 h deprivation like discriminative stimulus effects of PVN injected hunger mediator, <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	opioid	31743731	In contrast to PVN <strong>NPY</strong>, centrally or peripherally injected <b>opioid</b> agonists failed to induce discriminative stimuli similar to those of 22 h deprivation.
+NPY	drug	alcohol	31743731	In line with that, <b>naltrexone</b> did not reduce the hunger discriminative stimuli induced by either 22 h deprivation or <strong>NPY</strong> administration in 2 h food restricted subjects, even though doses used therein were sufficient to decrease deprivation induced feeding in a non operant setting in animals familiar with consequences of 2 h and 22 h deprivation.
+NPY	addiction	reward	31743731	In line with that, naltrexone did not reduce the hunger discriminative stimuli induced by either 22 h deprivation or <strong>NPY</strong> administration in 2 h food restricted subjects, even though doses used therein were sufficient to decrease deprivation induced feeding in a non <b>operant</b> setting in animals familiar with consequences of 2 h and 22 h deprivation.
+NPY	drug	opioid	31347421	Serum <strong>NPY</strong> and SP levels have a potential to be used as a biomarker in <b>opioid</b> users before and in the treatment process to account for interactions between biological vulnerabilities and childhood risk factors in predicting behavioural adjustment and more severe drug related problems.
+NPY	drug	cannabinoid	31298176	Within stress diet, the concepts of comfort food and emotional eating are highlighted, as cortisol affects reward pathways and appetite brain centres with a role for insulin, leptin, neuropeptide Y (<strong>NPY</strong>), <b>endocannabinoids</b>, orexin and gastrointestinal hormones.
+NPY	addiction	reward	31298176	Within stress diet, the concepts of comfort food and emotional eating are highlighted, as cortisol affects <b>reward</b> pathways and appetite brain centres with a role for insulin, leptin, neuropeptide Y (<strong>NPY</strong>), endocannabinoids, orexin and gastrointestinal hormones.
+NPY	drug	cannabinoid	31298176	Within stress diet, the concepts of comfort food and emotional eating are highlighted, as cortisol affects reward pathways and appetite brain centres with a role for insulin, leptin, <strong>neuropeptide Y</strong> (<strong>NPY</strong>), <b>endocannabinoids</b>, orexin and gastrointestinal hormones.
+NPY	addiction	reward	31298176	Within stress diet, the concepts of comfort food and emotional eating are highlighted, as cortisol affects <b>reward</b> pathways and appetite brain centres with a role for insulin, leptin, <strong>neuropeptide Y</strong> (<strong>NPY</strong>), endocannabinoids, orexin and gastrointestinal hormones.
+NPY	drug	alcohol	31229451	Treatment with the DNMT inhibitor 5 azacytidine (5 azaC) at adulthood normalizes the AIE induced DNA hypermethylation of <strong>Npy</strong> and Bdnf exon IV with concomitant reversal of AIE induced anxiety like and <b>alcohol</b> drinking behaviors.
+NPY	drug	opioid	31071414	<b>Oxycodone</b> CPP females have: a) increases in ARC (activity regulated cytoskeletal associated protein) immunoreactivity (ir) in CA3 pyramidal cells; b) decreases in <strong>Npy</strong> (neuropeptide Y) gene expression in the medial hippocampus but higher numbers of <strong>NPY</strong> containing hilar interneurons compared to males; c) increases in Crhr2 (corticotropin releasing factor receptor 2) expression in CA2/3; d) increases in Akt1 (AKT serine/threonine kinase 1) expression in medial hippocampus; and e) decreases in phosphorylated MAPK (mitogen activated protein kinase) ir in CA1 and dentate gyrus.
+NPY	addiction	reward	31071414	Oxycodone <b>CPP</b> females have: a) increases in ARC (activity regulated cytoskeletal associated protein) immunoreactivity (ir) in CA3 pyramidal cells; b) decreases in <strong>Npy</strong> (neuropeptide Y) gene expression in the medial hippocampus but higher numbers of <strong>NPY</strong> containing hilar interneurons compared to males; c) increases in Crhr2 (corticotropin releasing factor receptor 2) expression in CA2/3; d) increases in Akt1 (AKT serine/threonine kinase 1) expression in medial hippocampus; and e) decreases in phosphorylated MAPK (mitogen activated protein kinase) ir in CA1 and dentate gyrus.
+NPY	drug	opioid	31071414	<b>Oxycodone</b> CPP females have: a) increases in ARC (activity regulated cytoskeletal associated protein) immunoreactivity (ir) in CA3 pyramidal cells; b) decreases in <strong>Npy</strong> (<strong>neuropeptide Y</strong>) gene expression in the medial hippocampus but higher numbers of <strong>NPY</strong> containing hilar interneurons compared to males; c) increases in Crhr2 (corticotropin releasing factor receptor 2) expression in CA2/3; d) increases in Akt1 (AKT serine/threonine kinase 1) expression in medial hippocampus; and e) decreases in phosphorylated MAPK (mitogen activated protein kinase) ir in CA1 and dentate gyrus.
+NPY	addiction	reward	31071414	Oxycodone <b>CPP</b> females have: a) increases in ARC (activity regulated cytoskeletal associated protein) immunoreactivity (ir) in CA3 pyramidal cells; b) decreases in <strong>Npy</strong> (<strong>neuropeptide Y</strong>) gene expression in the medial hippocampus but higher numbers of <strong>NPY</strong> containing hilar interneurons compared to males; c) increases in Crhr2 (corticotropin releasing factor receptor 2) expression in CA2/3; d) increases in Akt1 (AKT serine/threonine kinase 1) expression in medial hippocampus; and e) decreases in phosphorylated MAPK (mitogen activated protein kinase) ir in CA1 and dentate gyrus.
+NPY	drug	amphetamine	30929417	Lorcaserin stimulates proopiomelanocortin (POMC)/cocaine  and <b>amphetamine</b> regulated transcript (CART) neurons and inhibits neuropeptide Y (<strong>NPY</strong>)/agouti related peptide (AgRP) neurons, which results in the activation of melanocortin 3/4 receptors.
+NPY	drug	cocaine	30929417	Lorcaserin stimulates proopiomelanocortin (POMC)/<b>cocaine</b>  and amphetamine regulated transcript (CART) neurons and inhibits neuropeptide Y (<strong>NPY</strong>)/agouti related peptide (AgRP) neurons, which results in the activation of melanocortin 3/4 receptors.
+NPY	drug	amphetamine	30929417	Lorcaserin stimulates proopiomelanocortin (POMC)/cocaine  and <b>amphetamine</b> regulated transcript (CART) neurons and inhibits <strong>neuropeptide Y</strong> (<strong>NPY</strong>)/agouti related peptide (AgRP) neurons, which results in the activation of melanocortin 3/4 receptors.
+NPY	drug	cocaine	30929417	Lorcaserin stimulates proopiomelanocortin (POMC)/<b>cocaine</b>  and amphetamine regulated transcript (CART) neurons and inhibits <strong>neuropeptide Y</strong> (<strong>NPY</strong>)/agouti related peptide (AgRP) neurons, which results in the activation of melanocortin 3/4 receptors.
+NPY	addiction	reward	30929417	The hypophagic effect of liraglutide is mediated through the direct activation of POMC/CART neurons and the indirect suppression of <strong>NPY</strong>/AgRP neurons through γ aminobutyric acid dependent signaling, with adjunctive suppression of the mesolimbic dopamine <b>reward</b> system.
+NPY	drug	alcohol	30647448	Medial prefrontal cortex <strong>neuropeptide Y</strong> modulates binge like <b>ethanol</b> consumption in C57BL/6J mice.
+NPY	addiction	intoxication	30647448	Medial prefrontal cortex <strong>neuropeptide Y</strong> modulates <b>binge</b> like ethanol consumption in C57BL/6J mice.
+NPY	drug	alcohol	30647448	Neuropeptide Y (<strong>NPY</strong>) signaling via limbic NPY1 and 2 receptors (NPY1R and NPY2R, respectively) is known to modulate binge like <b>ethanol</b> consumption in rodents.
+NPY	addiction	intoxication	30647448	Neuropeptide Y (<strong>NPY</strong>) signaling via limbic NPY1 and 2 receptors (NPY1R and NPY2R, respectively) is known to modulate <b>binge</b> like ethanol consumption in rodents.
+NPY	drug	alcohol	30647448	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) signaling via limbic NPY1 and 2 receptors (NPY1R and NPY2R, respectively) is known to modulate binge like <b>ethanol</b> consumption in rodents.
+NPY	addiction	intoxication	30647448	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) signaling via limbic NPY1 and 2 receptors (NPY1R and NPY2R, respectively) is known to modulate <b>binge</b> like ethanol consumption in rodents.
+NPY	drug	alcohol	30647448	We provide novel evidence that (1) binge like <b>ethanol</b> intake reduces <strong>NPY</strong> levels in the mPFC; (2) activation of NPY1R or blockade of NPY2R reduces binge like <b>ethanol</b> intake; and (3) chemogenetic inhibition of NPY1R+ neurons in the mPFC and NPY1R+ mPFC neurons projecting to the BLA blunts binge like drinking.
+NPY	addiction	intoxication	30647448	We provide novel evidence that (1) <b>binge</b> like ethanol intake reduces <strong>NPY</strong> levels in the mPFC; (2) activation of NPY1R or blockade of NPY2R reduces <b>binge</b> like ethanol intake; and (3) chemogenetic inhibition of NPY1R+ neurons in the mPFC and NPY1R+ mPFC neurons projecting to the BLA blunts <b>binge</b> like drinking.
+NPY	drug	alcohol	30647448	These observations provide the first direct evidence that <strong>NPY</strong> signaling in the mPFC modulates binge like <b>ethanol</b> consumption.
+NPY	addiction	intoxication	30647448	These observations provide the first direct evidence that <strong>NPY</strong> signaling in the mPFC modulates <b>binge</b> like ethanol consumption.
+NPY	drug	alcohol	30590608	Recent studies implicate histone deacetylase mediated histone H3K9 deacetylation in regulating <strong>neuropeptide Y</strong> expression during rapid <b>ethanol</b> tolerance to the anxiolytic effects of <b>ethanol</b>.
+NPY	drug	alcohol	30590608	Therefore, we investigated the role of G9a mediated H3K9me2 in <strong>neuropeptide Y</strong> expression during rapid <b>ethanol</b> tolerance.
+NPY	drug	alcohol	30590608	Acute <b>ethanol</b> produced anxiolysis and decreased global H3K9me2 and G9a protein levels in the central and medial nucleus of the amygdala as well as decreased occupancy levels of H3K9me2 and G9a near a putative binding site for cAMP response element binding protein on the <strong>Npy</strong> gene.
+NPY	drug	alcohol	30590608	Interestingly, treatment with UNC0642, before the second <b>ethanol</b> dose reversed rapid <b>ethanol</b> tolerance, decreased global H3K9me2 and increased <strong>neuropeptide Y</strong> levels in the central and medial nucleus of the amygdala.
+NPY	drug	alcohol	30590608	These results implicate amygdaloid G9a mediated H3K9me2 mechanisms in regulating rapid tolerance to the anxiolytic effects of <b>ethanol</b> via <strong>neuropeptide Y</strong> expression regulation.
+NPY	drug	amphetamine	30396596	Finally, rats were sacrificed and agouti related peptide (AgRP), neuropeptide Y (<strong>NPY</strong>), pro opiomelanocortin (POMC) and cocaine  and <b>amphetamine</b> regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+NPY	drug	cocaine	30396596	Finally, rats were sacrificed and agouti related peptide (AgRP), neuropeptide Y (<strong>NPY</strong>), pro opiomelanocortin (POMC) and <b>cocaine</b>  and amphetamine regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+NPY	drug	amphetamine	30396596	Finally, rats were sacrificed and agouti related peptide (AgRP), <strong>neuropeptide Y</strong> (<strong>NPY</strong>), pro opiomelanocortin (POMC) and cocaine  and <b>amphetamine</b> regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+NPY	drug	cocaine	30396596	Finally, rats were sacrificed and agouti related peptide (AgRP), <strong>neuropeptide Y</strong> (<strong>NPY</strong>), pro opiomelanocortin (POMC) and <b>cocaine</b>  and amphetamine regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+NPY	drug	alcohol	30188517	Protein or mRNA expression studies following Gsk3b over expression identified synaptojanin 2, brain derived neurotrophic factor and the <strong>neuropeptide Y</strong> Y5 receptor as potential downstream factors altering <b>ethanol</b> behaviors.
+NPY	drug	alcohol	29681474	This principle is conserved in Drosophila, where successful copulation is naturally rewarding to male flies, induces long term appetitive memories [5], increases brain levels of neuropeptide F (NPF, the fly homolog of <strong>neuropeptide Y</strong>), and prevents <b>ethanol</b>, known otherwise as rewarding to flies [6, 7], from being rewarding [5].
+NPY	drug	opioid	29437028	Accordingly, feeding is promoted by serotonin, dopamine, and prostaglandin and inhibited by <strong>neuropeptide Y</strong>, norepinephrine, GABA, and <b>opioid</b> peptides.
+NPY	drug	amphetamine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, <strong>neuropeptide Y</strong>, pro opiomelanocortin, and cocaine  and <b>amphetamine</b> related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (AMPK), mechanistic target of rapamycin and cAMP response element binding protein (CREB).
+NPY	drug	cocaine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, <strong>neuropeptide Y</strong>, pro opiomelanocortin, and <b>cocaine</b>  and amphetamine related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (AMPK), mechanistic target of rapamycin and cAMP response element binding protein (CREB).
+NPY	drug	alcohol	29056151	The Role of Neuropeptide Y (<strong>NPY</strong>) in <b>Alcohol</b> and Drug Abuse Disorders.
+NPY	drug	alcohol	29056151	The Role of <strong>Neuropeptide Y</strong> (<strong>NPY</strong>) in <b>Alcohol</b> and Drug Abuse Disorders.
+NPY	drug	alcohol	29056151	There is a long history of research implicating a role for <strong>NPY</strong> in modulating neurobiological responses to <b>alcohol</b> (<b>ethanol</b>) as well as other drugs of abuse.
+NPY	drug	alcohol	29056151	Both <b>ethanol</b> exposure and withdrawal from chronic <b>ethanol</b> have been shown to produce changes in <strong>NPY</strong> and <strong>NPY</strong> receptor protein levels and mRNA expression in the CNS.
+NPY	addiction	withdrawal	29056151	Both ethanol exposure and <b>withdrawal</b> from chronic ethanol have been shown to produce changes in <strong>NPY</strong> and <strong>NPY</strong> receptor protein levels and mRNA expression in the CNS.
+NPY	drug	alcohol	29056151	Importantly, manipulations of <strong>NPY</strong> Y1 and Y2 receptor signaling have been shown to alter <b>ethanol</b> consumption and self administration in a brain region specific manner, with Y1 receptor activation and Y2 receptor blockade in regions of the extended amygdala promoting robust reductions of <b>ethanol</b> intake.
+NPY	drug	alcohol	29056151	When taken together with observations of potential genetic linkage between the <strong>NPY</strong> system and the human <b>alcohol</b> abuse disorders, <strong>NPY</strong> represents a promising target for treating problematic <b>alcohol</b> and drug use, and in protecting individuals from relapse during abstinence.
+NPY	addiction	relapse	29056151	When taken together with observations of potential genetic linkage between the <strong>NPY</strong> system and the human alcohol abuse disorders, <strong>NPY</strong> represents a promising target for treating problematic alcohol and drug use, and in protecting individuals from <b>relapse</b> during abstinence.
+NPY	drug	amphetamine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [proopiomelanocortin (POMC), cocaine  and <b>amphetamine</b> related transcript (CART), neuropeptide Y (<strong>NPY</strong>), and agouti related peptide (AgRP)].
+NPY	drug	cocaine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [proopiomelanocortin (POMC), <b>cocaine</b>  and amphetamine related transcript (CART), neuropeptide Y (<strong>NPY</strong>), and agouti related peptide (AgRP)].
+NPY	drug	amphetamine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [proopiomelanocortin (POMC), cocaine  and <b>amphetamine</b> related transcript (CART), <strong>neuropeptide Y</strong> (<strong>NPY</strong>), and agouti related peptide (AgRP)].
+NPY	drug	cocaine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [proopiomelanocortin (POMC), <b>cocaine</b>  and amphetamine related transcript (CART), <strong>neuropeptide Y</strong> (<strong>NPY</strong>), and agouti related peptide (AgRP)].
+NPY	drug	alcohol	28824541	<strong>Neuropeptide Y</strong> in <b>Alcohol</b> Addiction and Affective Disorders.
+NPY	addiction	addiction	28824541	<strong>Neuropeptide Y</strong> in Alcohol <b>Addiction</b> and Affective Disorders.
+NPY	drug	alcohol	28824541	<strong>NPY</strong> and its receptors have been shown to be of importance in central regulation of events underlying, for example, affective disorders, drug/<b>alcohol</b> use disorders, and energy homeostasis.
+NPY	drug	alcohol	28824541	The potential roles of <strong>NPY</strong> in the etiology and pathophysiology of mood and anxiety disorders, as well as <b>alcohol</b> use disorders, have been extensively studied.
+NPY	drug	alcohol	28824541	These functions of <strong>NPY</strong>, in addition to the peptide's regulation of disease states, suggest that modulation of the activity of the <strong>NPY</strong> system via receptor agonists/antagonists may be a putative treatment mechanism in affective disorders as well as <b>alcohol</b> use disorders.
+NPY	drug	alcohol	28824541	In conclusion, we suggest that modulation of <strong>NPY</strong> ergic activity within the CNS, via ligands aimed at different receptor subtypes, may be attractive targets for treatment development for affective disorders, as well as for <b>alcohol</b> use disorders.
+NPY	drug	amphetamine	28653356	Gene expression of <strong>neuropeptide Y</strong>, agouti related peptide, cocaine  and <b>amphetamine</b> regulated transcript, pro opiomelanocortin, long form leptin receptor and suppressor of cytokine signalling 3 in the hypothalamic arcuate nucleus (ARC), as well as enkephalin, dynorphin, dopamine 2 receptor and dopamine 3 receptor in the nucleus accumbens (NAcc) in the forebrain, were measured by in situ hybridisation.
+NPY	drug	cocaine	28653356	Gene expression of <strong>neuropeptide Y</strong>, agouti related peptide, <b>cocaine</b>  and amphetamine regulated transcript, pro opiomelanocortin, long form leptin receptor and suppressor of cytokine signalling 3 in the hypothalamic arcuate nucleus (ARC), as well as enkephalin, dynorphin, dopamine 2 receptor and dopamine 3 receptor in the nucleus accumbens (NAcc) in the forebrain, were measured by in situ hybridisation.
+NPY	drug	alcohol	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during <b>alcohol</b> dependence and stress disorders, and among these, brain derived neurotrophic factor (BDNF), corticotropin releasing factor (CRF), neuropeptide Y (<strong>NPY</strong>) and opioid peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and <b>alcohol</b>.
+NPY	drug	opioid	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol dependence and stress disorders, and among these, brain derived neurotrophic factor (BDNF), corticotropin releasing factor (CRF), neuropeptide Y (<strong>NPY</strong>) and <b>opioid</b> peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and alcohol.
+NPY	addiction	dependence	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol <b>dependence</b> and stress disorders, and among these, brain derived neurotrophic factor (BDNF), corticotropin releasing factor (CRF), neuropeptide Y (<strong>NPY</strong>) and opioid peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and alcohol.
+NPY	drug	alcohol	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during <b>alcohol</b> dependence and stress disorders, and among these, brain derived neurotrophic factor (BDNF), corticotropin releasing factor (CRF), <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and opioid peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and <b>alcohol</b>.
+NPY	drug	opioid	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol dependence and stress disorders, and among these, brain derived neurotrophic factor (BDNF), corticotropin releasing factor (CRF), <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and <b>opioid</b> peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and alcohol.
+NPY	addiction	dependence	28477725	Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol <b>dependence</b> and stress disorders, and among these, brain derived neurotrophic factor (BDNF), corticotropin releasing factor (CRF), <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and opioid peptides (i.e., nociceptin and dynorphin) are involved in the interaction of stress and alcohol.
+NPY	drug	alcohol	28431971	Additionally, this review focuses on the effects of chronic <b>alcohol</b> induced changes in several pro stress neuropeptides (corticotropin releasing factor, dynorphin) and anti stress neuropeptide systems (nocicepton, <strong>neuropeptide Y</strong>, oxytocin) in contributing to the stress, negative emotional, and motivational consequences of chronic <b>alcohol</b> exposure.
+NPY	drug	alcohol	28302012	Targeting <strong>NPY</strong>, CRF/UCNs and NPS Neuropeptide Systems to Treat <b>Alcohol</b> Use Disorder (AUD).
+NPY	drug	alcohol	28223925	Regarding neuropeptide signaling, <b>alcohol</b> exposed rats displayed lower mRNA levels of the neuropeptide Y signaling, particularly <strong>NPY</strong> receptor 2, in the amygdala and hippocampus and higher mRNA levels of corticotropin releasing factor in the hippocampus.
+NPY	drug	alcohol	28223925	Regarding neuropeptide signaling, <b>alcohol</b> exposed rats displayed lower mRNA levels of the <strong>neuropeptide Y</strong> signaling, particularly <strong>NPY</strong> receptor 2, in the amygdala and hippocampus and higher mRNA levels of corticotropin releasing factor in the hippocampus.
+NPY	drug	cocaine	28138095	Relevant hippocampal features [basal c Fos activity, GABA+, parvalbumin (PV)+ and neuropeptide Y (<strong>NPY</strong>)+ interneurons and adult neurogenesis (cell proliferation and immature neurons)] were immunohistochemically assessed 73 days after the chronic <b>cocaine</b> or vehicle protocol.
+NPY	drug	cocaine	28138095	Relevant hippocampal features [basal c Fos activity, GABA+, parvalbumin (PV)+ and <strong>neuropeptide Y</strong> (<strong>NPY</strong>)+ interneurons and adult neurogenesis (cell proliferation and immature neurons)] were immunohistochemically assessed 73 days after the chronic <b>cocaine</b> or vehicle protocol.
+NPY	drug	cocaine	28138095	Moreover, the <b>cocaine</b> withdrawn mice previously submitted to behavioral training displayed a blunted experience dependent regulation of PV+ and <strong>NPY</strong>+ neurons in the dentate gyrus, and neurogenesis in the hippocampus.
+NPY	drug	amphetamine	28085909	Modulation of the expression of brain neuropeptides and receptors including <strong>NPY</strong>, POMC, AgRP, cocaine  and <b>amphetamine</b> related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+NPY	drug	cocaine	28085909	Modulation of the expression of brain neuropeptides and receptors including <strong>NPY</strong>, POMC, AgRP, <b>cocaine</b>  and amphetamine related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+NPY	drug	amphetamine	28085909	Modulation of the expression of brain neuropeptides and receptors including <strong>NPY</strong>, POMC, AgRP, cocaine  and <b>amphetamine</b> related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (HCRT), and Y2 and Y5 <strong>neuropeptide Y</strong>, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+NPY	drug	cocaine	28085909	Modulation of the expression of brain neuropeptides and receptors including <strong>NPY</strong>, POMC, AgRP, <b>cocaine</b>  and amphetamine related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (HCRT), and Y2 and Y5 <strong>neuropeptide Y</strong>, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+NPY	addiction	withdrawal	27154870	<b>Withdrawal</b> induced a significant volume and neuron loss that was accompanied by an increase in <strong>NPY</strong> expression without affecting α MSH and TH expression.
+NPY	drug	alcohol	27154870	The data also support the hypothesis that the same pathways that regulate the expression of <strong>NPY</strong> and α MSH in long term <b>ethanol</b> intake may regulate food intake.
+NPY	drug	alcohol	27090822	Effects of chronic <b>alcohol</b> consumption, withdrawal and nerve growth factor on <strong>neuropeptide Y</strong> expression and cholinergic innervation of the rat dentate hilus.
+NPY	addiction	withdrawal	27090822	Effects of chronic alcohol consumption, <b>withdrawal</b> and nerve growth factor on <strong>neuropeptide Y</strong> expression and cholinergic innervation of the rat dentate hilus.
+NPY	drug	alcohol	27090822	Because these two systems seem to closely interact in the HF, we sought to study the effects of chronic <b>alcohol</b> consumption (6months) and subsequent withdrawal (2months) on the expression of <strong>NPY</strong> and on the cholinergic innervation of the rat dentate hilus.
+NPY	addiction	withdrawal	27090822	Because these two systems seem to closely interact in the HF, we sought to study the effects of chronic alcohol consumption (6months) and subsequent <b>withdrawal</b> (2months) on the expression of <strong>NPY</strong> and on the cholinergic innervation of the rat dentate hilus.
+NPY	addiction	withdrawal	27090822	<strong>NPY</strong> expression increased after <b>withdrawal</b> and returned to control values after NGF treatment.
+NPY	drug	alcohol	27090822	These results show that the effects of prolonged <b>alcohol</b> intake and protracted withdrawal on the hilar <strong>NPY</strong> expression differ from those induced by shorter exposures to <b>ethanol</b> and by abrupt withdrawal.
+NPY	addiction	withdrawal	27090822	These results show that the effects of prolonged alcohol intake and protracted <b>withdrawal</b> on the hilar <strong>NPY</strong> expression differ from those induced by shorter exposures to ethanol and by abrupt <b>withdrawal</b>.
+NPY	drug	opioid	27055615	Pharmacologically and genetically, the focus will be on the neurotransmitter and neuropeptide systems that have received the most attention: cholinergic, dopaminergic, GABAergic, glutamatergic, serotonergic, noradrenergic, corticotrophin releasing hormone, <b>opioid</b>, and <strong>neuropeptide Y</strong>. Herein, we sought to place the P rat's behavioral and neurochemical phenotypes, and to some extent its genotype, in the context of the clinical literature.
+NPY	drug	cannabinoid	27012427	Enkephalin levels and the number of <strong>neuropeptide Y</strong> containing interneurons in the hippocampus are decreased in female <b>cannabinoid</b> receptor 1 knock out mice.
+NPY	drug	opioid	27012427	This involves activity dependent synaptic plasticity that is partially regulated by endogenous <b>opioid</b> (enkephalin and dynorphin) and non <b>opioid</b> peptides, specifically cholecystokinin, parvalbumin and <strong>neuropeptide Y</strong>, the neuropeptides present in inhibitory interneurons that co express CB1 or selective <b>opioid</b> receptors.
+NPY	drug	cannabinoid	26858616	We report studies using pharmacological manipulations targeting a number of stress related neurotransmitters and neuromodulators [monoamines, opioids, <b>endocannabinoids</b> (eCBs), <strong>neuropeptide Y</strong>, oxytocin, GCs] and behavioral stress induction.
+NPY	drug	opioid	26858616	We report studies using pharmacological manipulations targeting a number of stress related neurotransmitters and neuromodulators [monoamines, <b>opioids</b>, endocannabinoids (eCBs), <strong>neuropeptide Y</strong>, oxytocin, GCs] and behavioral stress induction.
+NPY	drug	alcohol	26779672	<strong>Neuropeptide Y</strong> response to <b>alcohol</b> is altered in nucleus accumbens of mice selectively bred for drinking to intoxication.
+NPY	addiction	intoxication	26779672	<strong>Neuropeptide Y</strong> response to alcohol is altered in nucleus accumbens of mice selectively bred for drinking to <b>intoxication</b>.
+NPY	drug	alcohol	26779672	Previous studies have identified neuropeptide Y (<strong>NPY</strong>) as a potential target for modulating <b>alcohol</b> intake.
+NPY	drug	alcohol	26779672	Previous studies have identified <strong>neuropeptide Y</strong> (<strong>NPY</strong>) as a potential target for modulating <b>alcohol</b> intake.
+NPY	drug	alcohol	26779672	<strong>NPY</strong> expression differs in some rodent lines that have been selected for high and low <b>alcohol</b> drinking phenotypes, as well as inbred mouse strains that differ in <b>alcohol</b> preference.
+NPY	drug	alcohol	26779672	<b>Alcohol</b> drinking and <b>alcohol</b> withdrawal also produce differential effects on <strong>NPY</strong> expression in the brain.
+NPY	addiction	withdrawal	26779672	Alcohol drinking and alcohol <b>withdrawal</b> also produce differential effects on <strong>NPY</strong> expression in the brain.
+NPY	drug	alcohol	26779672	Here, we assessed brain <strong>NPY</strong> protein levels in HDID mice of two replicates of selection and control heterogeneous stock (HS) mice at baseline (water drinking) and after binge like <b>alcohol</b> drinking to determine whether selection is associated with differences in <strong>NPY</strong> expression and its sensitivity to <b>alcohol</b>.
+NPY	addiction	intoxication	26779672	Here, we assessed brain <strong>NPY</strong> protein levels in HDID mice of two replicates of selection and control heterogeneous stock (HS) mice at baseline (water drinking) and after <b>binge</b> like alcohol drinking to determine whether selection is associated with differences in <strong>NPY</strong> expression and its sensitivity to alcohol.
+NPY	drug	alcohol	26779672	HS mice showed a reduction in <strong>NPY</strong> levels in the nucleus accumbens (NAc)   especially in the shell   in <b>ethanol</b> drinking animals vs. water drinking controls.
+NPY	drug	alcohol	26779672	However, HDID mice showed a blunted <strong>NPY</strong> response to <b>alcohol</b> in the NAc core and shell compared to HS mice.
+NPY	drug	alcohol	26779672	These findings suggest that the <strong>NPY</strong> response to <b>alcohol</b> has been altered by selection for drinking to intoxication in a region specific manner.
+NPY	addiction	intoxication	26779672	These findings suggest that the <strong>NPY</strong> response to alcohol has been altered by selection for drinking to <b>intoxication</b> in a region specific manner.
+NPY	drug	alcohol	26779672	Thus, the <strong>NPY</strong> system may represent a potential target for altering binge like <b>alcohol</b> drinking in these mice.
+NPY	addiction	intoxication	26779672	Thus, the <strong>NPY</strong> system may represent a potential target for altering <b>binge</b> like alcohol drinking in these mice.
+NPY	drug	alcohol	26775553	Previous work demonstrates basal anxiety levels in outbred Long Evans rats correlate with differences in voluntary <b>ethanol</b> consumption and that amygdalar Neuropeptide Y (<strong>NPY</strong>) systems may play a role in this relationship.
+NPY	drug	alcohol	26775553	Previous work demonstrates basal anxiety levels in outbred Long Evans rats correlate with differences in voluntary <b>ethanol</b> consumption and that amygdalar <strong>Neuropeptide Y</strong> (<strong>NPY</strong>) systems may play a role in this relationship.
+NPY	drug	alcohol	26775553	The present work explores the possibility that differences in sensitivity to <b>ethanol</b>'s anxiolytic effects contribute to differential <b>ethanol</b> self administration in these animals and examines the potential role of central and peripheral <strong>NPY</strong> in mediating this relationship.
+NPY	drug	alcohol	26775553	Although <strong>NPY</strong> neurons were not significantly activated following <b>ethanol</b> exposure, in saline treated animals lower levels of anxiety like behavior in the LD box (more time in the light arena and more transitions) were correlated with higher <strong>NPY</strong> positive cell density in the central amygdala.
+NPY	drug	alcohol	26775553	Our results suggest that activation of the CeA and BNST are involved in the behavioral expression of <b>ethanol</b> induced anxiolysis, and that differences in basal anxiety state may be correlated with <strong>NPY</strong> systems in the extended amygdala.
+NPY	drug	alcohol	26285061	In anticipation and reaction to aggressive behavior, neuropeptides such as corticotropin releasing factor, <strong>neuropeptide Y</strong>, opioid peptides, and vasopressin interact with monoamines, GABA, and glutamate to attenuate and amplify aggressive behavior in <b>alcohol</b> consuming individuals.
+NPY	drug	opioid	26285061	In anticipation and reaction to aggressive behavior, neuropeptides such as corticotropin releasing factor, <strong>neuropeptide Y</strong>, <b>opioid</b> peptides, and vasopressin interact with monoamines, GABA, and glutamate to attenuate and amplify aggressive behavior in alcohol consuming individuals.
+NPY	drug	alcohol	25929272	<strong>Neuropeptide Y</strong> system in accumbens shell mediates <b>ethanol</b> self administration in posterior ventral tegmental area.
+NPY	drug	alcohol	25929272	Although modulatory effects of neuropeptide Y (<strong>NPY</strong>) on <b>ethanol</b> consumption are well established, its role in <b>ethanol</b> reward, in the framework of mesolimbic dopaminergic system, has not been studied.
+NPY	addiction	reward	25929272	Although modulatory effects of neuropeptide Y (<strong>NPY</strong>) on ethanol consumption are well established, its role in ethanol <b>reward</b>, in the framework of mesolimbic dopaminergic system, has not been studied.
+NPY	drug	alcohol	25929272	Although modulatory effects of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) on <b>ethanol</b> consumption are well established, its role in <b>ethanol</b> reward, in the framework of mesolimbic dopaminergic system, has not been studied.
+NPY	addiction	reward	25929272	Although modulatory effects of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) on ethanol consumption are well established, its role in ethanol <b>reward</b>, in the framework of mesolimbic dopaminergic system, has not been studied.
+NPY	drug	alcohol	25929272	While intra AcbSh <strong>NPY</strong> (1 or 2 ng/rat) or [Leu(31) , Pro(34) ] <strong>NPY</strong> (0.5 or 1 ng/rat) dose dependently increased <b>ethanol</b> self administration, BIBP3226 (0.4 or 0.8 ng/rat) produced opposite effect.
+NPY	drug	alcohol	25929272	The rats conditioned to self administer <b>ethanol</b> showed significant increase in the population of <strong>NPY</strong> immunoreactive cells and fibres in the AcbSh, central nucleus of amygdala (CeA), hypothalamic arcuate nucleus (ARC) and lateral part of bed nucleus of stria terminalis as compared with that in the naïve rats.
+NPY	drug	alcohol	25929272	As <strong>NPY</strong> and dopamine systems in reward areas are known to interact, we suggest that <strong>NPY</strong> inputs from ARC and CeA may play an important role in modulation of the dopaminergic system in the AcbSh and consequently influence the <b>ethanol</b> induced reward and addiction.
+NPY	addiction	addiction	25929272	As <strong>NPY</strong> and dopamine systems in reward areas are known to interact, we suggest that <strong>NPY</strong> inputs from ARC and CeA may play an important role in modulation of the dopaminergic system in the AcbSh and consequently influence the ethanol induced reward and <b>addiction</b>.
+NPY	addiction	reward	25929272	As <strong>NPY</strong> and dopamine systems in <b>reward</b> areas are known to interact, we suggest that <strong>NPY</strong> inputs from ARC and CeA may play an important role in modulation of the dopaminergic system in the AcbSh and consequently influence the ethanol induced <b>reward</b> and addiction.
+NPY	addiction	addiction	25904345	Neuropeptide Y (<strong>NPY</strong>), which is widely expressed in the central nervous system is involved in several neuropathologies including <b>addiction</b>.
+NPY	addiction	addiction	25904345	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>), which is widely expressed in the central nervous system is involved in several neuropathologies including <b>addiction</b>.
+NPY	drug	alcohol	25904345	We report on the effects of psychostimulants [cocaine, amphetamine, methamphetamine, 3,4 methylenedioxymethamphetamine (MDMA) and nicotine], <b>ethanol</b>, and opioids on <strong>NPY</strong> protein levels and expression of different <strong>NPY</strong> receptors.
+NPY	drug	amphetamine	25904345	We report on the effects of psychostimulants [cocaine, <b>amphetamine</b>, <b>methamphetamine</b>, 3,4 methylenedioxymethamphetamine (MDMA) and nicotine], ethanol, and opioids on <strong>NPY</strong> protein levels and expression of different <strong>NPY</strong> receptors.
+NPY	drug	cocaine	25904345	We report on the effects of psychostimulants [<b>cocaine</b>, amphetamine, methamphetamine, 3,4 methylenedioxymethamphetamine (MDMA) and nicotine], ethanol, and opioids on <strong>NPY</strong> protein levels and expression of different <strong>NPY</strong> receptors.
+NPY	drug	nicotine	25904345	We report on the effects of psychostimulants [cocaine, amphetamine, methamphetamine, 3,4 methylenedioxymethamphetamine (MDMA) and <b>nicotine</b>], ethanol, and opioids on <strong>NPY</strong> protein levels and expression of different <strong>NPY</strong> receptors.
+NPY	drug	opioid	25904345	We report on the effects of psychostimulants [cocaine, amphetamine, methamphetamine, 3,4 methylenedioxymethamphetamine (MDMA) and nicotine], ethanol, and <b>opioids</b> on <strong>NPY</strong> protein levels and expression of different <strong>NPY</strong> receptors.
+NPY	drug	psychedelics	25904345	We report on the effects of psychostimulants [cocaine, amphetamine, methamphetamine, 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>) and nicotine], ethanol, and opioids on <strong>NPY</strong> protein levels and expression of different <strong>NPY</strong> receptors.
+NPY	drug	alcohol	25904345	For example methamphetamine and nicotine lead to a consistent increase in <strong>NPY</strong> mRNA and protein levels in different brain sites whereas <b>ethanol</b> and opioids decrease <strong>NPY</strong> mRNA and protein expression.
+NPY	drug	amphetamine	25904345	For example <b>methamphetamine</b> and nicotine lead to a consistent increase in <strong>NPY</strong> mRNA and protein levels in different brain sites whereas ethanol and opioids decrease <strong>NPY</strong> mRNA and protein expression.
+NPY	drug	nicotine	25904345	For example methamphetamine and <b>nicotine</b> lead to a consistent increase in <strong>NPY</strong> mRNA and protein levels in different brain sites whereas ethanol and opioids decrease <strong>NPY</strong> mRNA and protein expression.
+NPY	drug	opioid	25904345	For example methamphetamine and nicotine lead to a consistent increase in <strong>NPY</strong> mRNA and protein levels in different brain sites whereas ethanol and <b>opioids</b> decrease <strong>NPY</strong> mRNA and protein expression.
+NPY	addiction	addiction	25904345	Manipulation of the <strong>NPY</strong> system can have opposing effects on reinforcing and <b>addictive</b> properties of drugs of abuse.
+NPY	addiction	reward	25904345	Manipulation of the <strong>NPY</strong> system can have opposing effects on <b>reinforcing</b> and addictive properties of drugs of abuse.
+NPY	drug	alcohol	25904345	<strong>NPY</strong> can produce pro addictive effects (nicotine and heroin), but can also exert inhibitory effects on addictive behavior (AMPH, <b>ethanol</b>).
+NPY	drug	amphetamine	25904345	<strong>NPY</strong> can produce pro addictive effects (nicotine and heroin), but can also exert inhibitory effects on addictive behavior (<b>AMPH</b>, ethanol).
+NPY	drug	nicotine	25904345	<strong>NPY</strong> can produce pro addictive effects (<b>nicotine</b> and heroin), but can also exert inhibitory effects on addictive behavior (AMPH, ethanol).
+NPY	drug	opioid	25904345	<strong>NPY</strong> can produce pro addictive effects (nicotine and <b>heroin</b>), but can also exert inhibitory effects on addictive behavior (AMPH, ethanol).
+NPY	addiction	addiction	25904345	<strong>NPY</strong> can produce pro <b>addictive</b> effects (nicotine and heroin), but can also exert inhibitory effects on <b>addictive</b> behavior (AMPH, ethanol).
+NPY	drug	amphetamine	25904345	Furthermore, <strong>NPY</strong> can act as a neuroprotective agent in chronically <b>methamphetamine</b> and MDMA treated rodents.
+NPY	drug	psychedelics	25904345	Furthermore, <strong>NPY</strong> can act as a neuroprotective agent in chronically methamphetamine and <b>MDMA</b> treated rodents.
+NPY	addiction	addiction	25904345	In conclusion, manipulation of the <strong>NPY</strong> system seems to be a potential target to counteract neural alterations, <b>addiction</b> related behaviors and cognitive deficits induced by these drugs.
+NPY	drug	alcohol	25751534	<strong>NPY</strong> signaling inhibits extended amygdala CRF neurons to suppress binge <b>alcohol</b> drinking.
+NPY	addiction	intoxication	25751534	<strong>NPY</strong> signaling inhibits extended amygdala CRF neurons to suppress <b>binge</b> alcohol drinking.
+NPY	addiction	reward	25751534	It is thought to do so by hijacking brain systems that regulate stress and <b>reward</b>, including neuropeptide Y (<strong>NPY</strong>) and corticotropin releasing factor (CRF).
+NPY	addiction	reward	25751534	It is thought to do so by hijacking brain systems that regulate stress and <b>reward</b>, including <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and corticotropin releasing factor (CRF).
+NPY	addiction	relapse	25751534	The central actions of <strong>NPY</strong> and CRF have opposing functions in the regulation of emotional and reward <b>seeking</b> behaviors; thus, dysfunctional interactions between these peptidergic systems could be involved in the development of these pathologies.
+NPY	addiction	reward	25751534	The central actions of <strong>NPY</strong> and CRF have opposing functions in the regulation of emotional and <b>reward</b> seeking behaviors; thus, dysfunctional interactions between these peptidergic systems could be involved in the development of these pathologies.
+NPY	drug	alcohol	25751534	We used converging physiological, pharmacological and chemogenetic approaches to identify a precise neural mechanism in the bed nucleus of the stria terminalis (BNST), a limbic brain region involved in pathological reward and anxiety behaviors, underlying the interactions between <strong>NPY</strong> and CRF in the regulation of binge <b>alcohol</b> drinking in both mice and monkeys.
+NPY	addiction	intoxication	25751534	We used converging physiological, pharmacological and chemogenetic approaches to identify a precise neural mechanism in the bed nucleus of the stria terminalis (BNST), a limbic brain region involved in pathological reward and anxiety behaviors, underlying the interactions between <strong>NPY</strong> and CRF in the regulation of <b>binge</b> alcohol drinking in both mice and monkeys.
+NPY	addiction	reward	25751534	We used converging physiological, pharmacological and chemogenetic approaches to identify a precise neural mechanism in the bed nucleus of the stria terminalis (BNST), a limbic brain region involved in pathological <b>reward</b> and anxiety behaviors, underlying the interactions between <strong>NPY</strong> and CRF in the regulation of binge alcohol drinking in both mice and monkeys.
+NPY	drug	alcohol	25751534	We found that <strong>NPY</strong> Y1 receptor (Y1R) activation in the BNST suppressed binge <b>alcohol</b> drinking by enhancing inhibitory synaptic transmission specifically in CRF neurons via a previously unknown Gi mediated, PKA dependent postsynaptic mechanism.
+NPY	addiction	intoxication	25751534	We found that <strong>NPY</strong> Y1 receptor (Y1R) activation in the BNST suppressed <b>binge</b> alcohol drinking by enhancing inhibitory synaptic transmission specifically in CRF neurons via a previously unknown Gi mediated, PKA dependent postsynaptic mechanism.
+NPY	drug	alcohol	25689818	They contrast with other orexigenic neuropeptides, such as melanin concentrating hormone and <strong>neuropeptide Y</strong>, which promote <b>alcohol</b> intake under limited circumstances, are not consistently stimulated by <b>alcohol</b>, and do not enhance reward.
+NPY	addiction	reward	25689818	They contrast with other orexigenic neuropeptides, such as melanin concentrating hormone and <strong>neuropeptide Y</strong>, which promote alcohol intake under limited circumstances, are not consistently stimulated by alcohol, and do not enhance <b>reward</b>.
+NPY	addiction	addiction	25583178	<strong>Neuropeptide Y</strong>, a powerful anti stress neurotransmitter, has a profile of action on <b>compulsive</b> like responding for drugs similar to a CRF1 receptor antagonist.
+NPY	drug	amphetamine	25529631	Based on the importance of paraventricular thalamic nucleus (PVT) as a relay station of energy balance, arousal, and food reward, we aimed in the present study to determine projection patterns of neuropeptide Y (<strong>NPY</strong>), cocaine  and <b>amphetamine</b> regulated transcript (CART), melanin concentrating hormone (MCH), and orexin (ORX) ergic fibers to the PVT.
+NPY	drug	cocaine	25529631	Based on the importance of paraventricular thalamic nucleus (PVT) as a relay station of energy balance, arousal, and food reward, we aimed in the present study to determine projection patterns of neuropeptide Y (<strong>NPY</strong>), <b>cocaine</b>  and amphetamine regulated transcript (CART), melanin concentrating hormone (MCH), and orexin (ORX) ergic fibers to the PVT.
+NPY	addiction	reward	25529631	Based on the importance of paraventricular thalamic nucleus (PVT) as a relay station of energy balance, arousal, and food <b>reward</b>, we aimed in the present study to determine projection patterns of neuropeptide Y (<strong>NPY</strong>), cocaine  and amphetamine regulated transcript (CART), melanin concentrating hormone (MCH), and orexin (ORX) ergic fibers to the PVT.
+NPY	drug	amphetamine	25529631	Based on the importance of paraventricular thalamic nucleus (PVT) as a relay station of energy balance, arousal, and food reward, we aimed in the present study to determine projection patterns of <strong>neuropeptide Y</strong> (<strong>NPY</strong>), cocaine  and <b>amphetamine</b> regulated transcript (CART), melanin concentrating hormone (MCH), and orexin (ORX) ergic fibers to the PVT.
+NPY	drug	cocaine	25529631	Based on the importance of paraventricular thalamic nucleus (PVT) as a relay station of energy balance, arousal, and food reward, we aimed in the present study to determine projection patterns of <strong>neuropeptide Y</strong> (<strong>NPY</strong>), <b>cocaine</b>  and amphetamine regulated transcript (CART), melanin concentrating hormone (MCH), and orexin (ORX) ergic fibers to the PVT.
+NPY	addiction	reward	25529631	Based on the importance of paraventricular thalamic nucleus (PVT) as a relay station of energy balance, arousal, and food <b>reward</b>, we aimed in the present study to determine projection patterns of <strong>neuropeptide Y</strong> (<strong>NPY</strong>), cocaine  and amphetamine regulated transcript (CART), melanin concentrating hormone (MCH), and orexin (ORX) ergic fibers to the PVT.
+NPY	addiction	intoxication	25324788	Effect of Acetaldehyde <b>Intoxication</b> and Withdrawal on <strong>NPY</strong> Expression: Focus on Endocannabinoidergic System Involvement.
+NPY	addiction	withdrawal	25324788	Effect of Acetaldehyde Intoxication and <b>Withdrawal</b> on <strong>NPY</strong> Expression: Focus on Endocannabinoidergic System Involvement.
+NPY	drug	alcohol	25324788	Indeed, the neuropeptide Y (<strong>NPY</strong>) system is altered during <b>alcohol</b> withdrawal in key regions for cerebrocortical excitability and neuroplasticity.
+NPY	addiction	withdrawal	25324788	Indeed, the neuropeptide Y (<strong>NPY</strong>) system is altered during alcohol <b>withdrawal</b> in key regions for cerebrocortical excitability and neuroplasticity.
+NPY	drug	alcohol	25324788	Indeed, the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) system is altered during <b>alcohol</b> withdrawal in key regions for cerebrocortical excitability and neuroplasticity.
+NPY	addiction	withdrawal	25324788	Indeed, the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) system is altered during alcohol <b>withdrawal</b> in key regions for cerebrocortical excitability and neuroplasticity.
+NPY	drug	alcohol	25324788	The primary goal of this research was to investigate the effects of ACD intoxication and withdrawal by recording rat behavior and by measuring <strong>NPY</strong> immunoreactivity in hippocampus and NAcc, two brain regions mainly involved in processes which encompass neuroplasticity in <b>alcohol</b> dependence.
+NPY	addiction	dependence	25324788	The primary goal of this research was to investigate the effects of ACD intoxication and withdrawal by recording rat behavior and by measuring <strong>NPY</strong> immunoreactivity in hippocampus and NAcc, two brain regions mainly involved in processes which encompass neuroplasticity in alcohol <b>dependence</b>.
+NPY	addiction	intoxication	25324788	The primary goal of this research was to investigate the effects of ACD <b>intoxication</b> and withdrawal by recording rat behavior and by measuring <strong>NPY</strong> immunoreactivity in hippocampus and NAcc, two brain regions mainly involved in processes which encompass neuroplasticity in alcohol dependence.
+NPY	addiction	withdrawal	25324788	The primary goal of this research was to investigate the effects of ACD intoxication and <b>withdrawal</b> by recording rat behavior and by measuring <strong>NPY</strong> immunoreactivity in hippocampus and NAcc, two brain regions mainly involved in processes which encompass neuroplasticity in alcohol dependence.
+NPY	drug	alcohol	25324788	Furthermore, on the basis of the involvement of endocannabinoidergic system in <b>alcohol</b> and ACD reinforcing effects, the role of the selective CB1 receptor antagonist AM281 in modulating <strong>NPY</strong> expression during withdrawal was assessed.
+NPY	addiction	reward	25324788	Furthermore, on the basis of the involvement of endocannabinoidergic system in alcohol and ACD <b>reinforcing</b> effects, the role of the selective CB1 receptor antagonist AM281 in modulating <strong>NPY</strong> expression during withdrawal was assessed.
+NPY	addiction	withdrawal	25324788	Furthermore, on the basis of the involvement of endocannabinoidergic system in alcohol and ACD reinforcing effects, the role of the selective CB1 receptor antagonist AM281 in modulating <strong>NPY</strong> expression during <b>withdrawal</b> was assessed.
+NPY	drug	alcohol	25324788	Our results indicate that (i) ACD intoxication induced a reduction in <strong>NPY</strong> expression in hippocampus and NAcc; (ii) symptoms of physical dependence, similar to <b>alcohol</b>'s, were scored at 12 h from the last administration of ACD; and (iii) <strong>NPY</strong> levels increased in early and prolonged acute withdrawal in both brain regions examined.
+NPY	addiction	dependence	25324788	Our results indicate that (i) ACD intoxication induced a reduction in <strong>NPY</strong> expression in hippocampus and NAcc; (ii) symptoms of physical <b>dependence</b>, similar to alcohol's, were scored at 12 h from the last administration of ACD; and (iii) <strong>NPY</strong> levels increased in early and prolonged acute withdrawal in both brain regions examined.
+NPY	addiction	intoxication	25324788	Our results indicate that (i) ACD <b>intoxication</b> induced a reduction in <strong>NPY</strong> expression in hippocampus and NAcc; (ii) symptoms of physical dependence, similar to alcohol's, were scored at 12 h from the last administration of ACD; and (iii) <strong>NPY</strong> levels increased in early and prolonged acute withdrawal in both brain regions examined.
+NPY	addiction	withdrawal	25324788	Our results indicate that (i) ACD intoxication induced a reduction in <strong>NPY</strong> expression in hippocampus and NAcc; (ii) symptoms of physical dependence, similar to alcohol's, were scored at 12 h from the last administration of ACD; and (iii) <strong>NPY</strong> levels increased in early and prolonged acute <b>withdrawal</b> in both brain regions examined.
+NPY	addiction	dependence	25324788	The administration of AM281 was able to blunt signs of ACD induced physical <b>dependence</b>, to modulate <strong>NPY</strong> levels, and to further increase <strong>NPY</strong> expression during ACD withdrawal both in hippocampus and NAcc.
+NPY	addiction	withdrawal	25324788	The administration of AM281 was able to blunt signs of ACD induced physical dependence, to modulate <strong>NPY</strong> levels, and to further increase <strong>NPY</strong> expression during ACD <b>withdrawal</b> both in hippocampus and NAcc.
+NPY	addiction	intoxication	25324788	In conclusion, the present study shows that complex plastic changes take place in <strong>NPY</strong> system during ACD <b>intoxication</b> and subsequent withdrawal in rat hippocampal formation and NAcc.
+NPY	addiction	withdrawal	25324788	In conclusion, the present study shows that complex plastic changes take place in <strong>NPY</strong> system during ACD intoxication and subsequent <b>withdrawal</b> in rat hippocampal formation and NAcc.
+NPY	addiction	reward	25309368	Cholinergic interneurons or GABAergic interneurons positive for parvalbumin, <strong>neuropeptide Y</strong> or calretinin were not involved in these <b>CPP</b> related EGR1 changes.
+NPY	addiction	withdrawal	25307567	Other components of brain stress systems in the extended amygdala that interact with CRF and may contribute to the negative motivational state of <b>withdrawal</b> include increases in norepinephrine function, increases in dynorphin activity, and decreases in <strong>neuropeptide Y</strong>.
+NPY	drug	nicotine	25158103	Moreover, the hippocampus, specifically hippocampal Y2 receptor (Y2R) mediated <strong>neuropeptide Y</strong> signaling is implicated in these <b>nicotine</b> induced behavioral effects observed in HRs.
+NPY	addiction	reward	24936193	Centrally, the α7nAChR modulates activity of hypothalamic neurons involved in food intake regulation, including proopiomelanocortin and <strong>neuropeptide Y</strong>. α7nAChRs also modulate glutamatergic and dopaminergic systems controlling <b>reward</b> processes that affect food intake.
+NPY	drug	alcohol	24893293	Neuropeptide Y (<strong>NPY</strong>)  and acetylcholine containing interneurons of the nucleus accumbens (NAc) seem to play a major role in the rewarding effects of <b>alcohol</b>.
+NPY	drug	alcohol	24893293	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>)  and acetylcholine containing interneurons of the nucleus accumbens (NAc) seem to play a major role in the rewarding effects of <b>alcohol</b>.
+NPY	drug	alcohol	24893293	This study investigated the relationship between chronic <b>alcohol</b> consumption and subsequent withdrawal and the expression of <strong>NPY</strong> and acetylcholine in the NAc, and the possible involvement of nerve growth factor (NGF) in mediating the effects of <b>ethanol</b>.
+NPY	addiction	withdrawal	24893293	This study investigated the relationship between chronic alcohol consumption and subsequent <b>withdrawal</b> and the expression of <strong>NPY</strong> and acetylcholine in the NAc, and the possible involvement of nerve growth factor (NGF) in mediating the effects of ethanol.
+NPY	drug	alcohol	24893293	Rats ingesting an aqueous <b>ethanol</b> solution over 6months and rats subsequently deprived from <b>ethanol</b> during 2months were used to estimate the total number and the somatic volume of <strong>NPY</strong> and cholinergic interneurons, and the numerical density of cholinergic varicosities in the NAc.
+NPY	drug	alcohol	24893293	The number of <strong>NPY</strong> interneurons increased during <b>alcohol</b> ingestion and returned to control values after withdrawal.
+NPY	addiction	withdrawal	24893293	The number of <strong>NPY</strong> interneurons increased during alcohol ingestion and returned to control values after <b>withdrawal</b>.
+NPY	drug	alcohol	24674772	Involvement of amygdaloid <strong>neuropeptide Y</strong> in the anxiolytic effects of acupuncture during <b>ethanol</b> withdrawal in rats.
+NPY	addiction	withdrawal	24674772	Involvement of amygdaloid <strong>neuropeptide Y</strong> in the anxiolytic effects of acupuncture during ethanol <b>withdrawal</b> in rats.
+NPY	drug	alcohol	24674772	The role of neuropeptide Y (<strong>NPY</strong>) in the central nucleus of amygdala (CeA) in the preventive effects of acupuncture against <b>ethanol</b> withdrawal induced anxiety was investigated.
+NPY	addiction	withdrawal	24674772	The role of neuropeptide Y (<strong>NPY</strong>) in the central nucleus of amygdala (CeA) in the preventive effects of acupuncture against ethanol <b>withdrawal</b> induced anxiety was investigated.
+NPY	drug	alcohol	24674772	The role of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in the central nucleus of amygdala (CeA) in the preventive effects of acupuncture against <b>ethanol</b> withdrawal induced anxiety was investigated.
+NPY	addiction	withdrawal	24674772	The role of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in the central nucleus of amygdala (CeA) in the preventive effects of acupuncture against ethanol <b>withdrawal</b> induced anxiety was investigated.
+NPY	drug	alcohol	24674772	Enzyme linked immunosorbent assays and real time polymerase chain reaction analyses showed there was a significant decrease in <strong>NPY</strong> protein and mRNA expression in the CeA during <b>ethanol</b> withdrawal, which was reversed by acupuncture at HT7 but neither at PC6 nor at a non acupoint.
+NPY	addiction	withdrawal	24674772	Enzyme linked immunosorbent assays and real time polymerase chain reaction analyses showed there was a significant decrease in <strong>NPY</strong> protein and mRNA expression in the CeA during ethanol <b>withdrawal</b>, which was reversed by acupuncture at HT7 but neither at PC6 nor at a non acupoint.
+NPY	drug	alcohol	24674772	These results suggest that acupuncture at HT7 rescues the depletion of amygdaloid <strong>NPY</strong> and reverses the decrease in CREB phosphorylation to produce anxiolytic effects during <b>ethanol</b> withdrawal.
+NPY	addiction	withdrawal	24674772	These results suggest that acupuncture at HT7 rescues the depletion of amygdaloid <strong>NPY</strong> and reverses the decrease in CREB phosphorylation to produce anxiolytic effects during ethanol <b>withdrawal</b>.
+NPY	drug	nicotine	24440829	Agmatine attenuates <b>nicotine</b> induced conditioned place preference in mice through modulation of <strong>neuropeptide Y</strong> system.
+NPY	drug	nicotine	24440829	Concomitant administration of neuropeptide Y (<strong>NPY</strong>) (1 pg/mouse, icv) or [Leu(31), Pro(34)] <strong>NPY</strong> (0.1 pg/mouse, icv), selective <strong>NPY</strong> Y1 receptor agonist potentiated the inhibitory effect of agmatine (10 mg/kg, ip) on <b>nicotine</b> CPP.
+NPY	addiction	reward	24440829	Concomitant administration of neuropeptide Y (<strong>NPY</strong>) (1 pg/mouse, icv) or [Leu(31), Pro(34)] <strong>NPY</strong> (0.1 pg/mouse, icv), selective <strong>NPY</strong> Y1 receptor agonist potentiated the inhibitory effect of agmatine (10 mg/kg, ip) on nicotine <b>CPP</b>.
+NPY	drug	nicotine	24440829	Concomitant administration of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) (1 pg/mouse, icv) or [Leu(31), Pro(34)] <strong>NPY</strong> (0.1 pg/mouse, icv), selective <strong>NPY</strong> Y1 receptor agonist potentiated the inhibitory effect of agmatine (10 mg/kg, ip) on <b>nicotine</b> CPP.
+NPY	addiction	reward	24440829	Concomitant administration of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) (1 pg/mouse, icv) or [Leu(31), Pro(34)] <strong>NPY</strong> (0.1 pg/mouse, icv), selective <strong>NPY</strong> Y1 receptor agonist potentiated the inhibitory effect of agmatine (10 mg/kg, ip) on nicotine <b>CPP</b>.
+NPY	drug	nicotine	24440829	Conversely, pretreatment with <strong>NPY</strong> Y1 receptor antagonist, BIBP3226 (0.01 ng/mouse, icv) blocked the effect of agmatine (20 mg/kg, ip) on <b>nicotine</b> induced CPP.
+NPY	addiction	reward	24440829	Conversely, pretreatment with <strong>NPY</strong> Y1 receptor antagonist, BIBP3226 (0.01 ng/mouse, icv) blocked the effect of agmatine (20 mg/kg, ip) on nicotine induced <b>CPP</b>.
+NPY	drug	nicotine	24440829	In immunohistochemical study, <b>nicotine</b> decreased <strong>NPY</strong> immunoreactivity in nucleus accumbens shell (AcbSh), bed nucleus of stria terminalis, lateral part (BNSTl), arcuate nucleus (ARC) and paraventricular nucleus (PVN).
+NPY	drug	nicotine	24440829	Conversely, administration of agmatine prior to the <b>nicotine</b> significantly reversed the effect of <b>nicotine</b> on <strong>NPY</strong> immunoreactivity in the above brain nuclei.
+NPY	drug	alcohol	24406115	Differential patterns of expression of <strong>neuropeptide Y</strong> throughout abstinence in outbred Swiss mice classified as susceptible or resistant to <b>ethanol</b> induced locomotor sensitization.
+NPY	addiction	sensitization	24406115	Differential patterns of expression of <strong>neuropeptide Y</strong> throughout abstinence in outbred Swiss mice classified as susceptible or resistant to ethanol induced locomotor <b>sensitization</b>.
+NPY	addiction	addiction	24406115	The peptide <strong>NPY</strong> plays an important role given its involvement in drug <b>addiction</b>, anxiety, and mood disorders.
+NPY	drug	alcohol	24406115	Here, we investigated whether mice that were either susceptible or resistant to <b>ethanol</b> sensitization differed in their <strong>NPY</strong> expression during abstinence.
+NPY	addiction	sensitization	24406115	Here, we investigated whether mice that were either susceptible or resistant to ethanol <b>sensitization</b> differed in their <strong>NPY</strong> expression during abstinence.
+NPY	drug	alcohol	24406115	To evaluate <strong>NPY</strong> expression, some of the mice were sacrificed at 18 h or 5 days of abstinence, and others were challenged at the 5th day of abstinence with <b>ethanol</b> (1.4 g/kg) and sacrificed after 1.5 h. At 5 days of abstinence, <strong>NPY</strong> expression increased in the orbital cortex, dorsomedial striatum, and dentate gyrus in the EtOH_High mice.
+NPY	drug	alcohol	24406115	Lastly, a decreased level of <strong>NPY</strong> was found in the prelimbic cortex of the EtOH_Low mice at 5 days of abstinence, and this was reversed by <b>ethanol</b> challenge.
+NPY	drug	alcohol	24406115	Therefore, behavioral variability in <b>ethanol</b> sensitization confers differential neurochemical features during the subsequent abstinence, including distinct patterns of <strong>NPY</strong> expression.
+NPY	addiction	sensitization	24406115	Therefore, behavioral variability in ethanol <b>sensitization</b> confers differential neurochemical features during the subsequent abstinence, including distinct patterns of <strong>NPY</strong> expression.
+NPY	addiction	reward	24399943	A large literature has demonstrated that neuropeptide Y (<strong>NPY</strong>) regulates many emotional and <b>reward</b> related behaviors via its primary receptors, Y1R and Y2R.
+NPY	addiction	reward	24399943	A large literature has demonstrated that <strong>neuropeptide Y</strong> (<strong>NPY</strong>) regulates many emotional and <b>reward</b> related behaviors via its primary receptors, Y1R and Y2R.
+NPY	drug	alcohol	24399943	Classically, <strong>NPY</strong> actions at postsynaptic Y1R decrease anxiety, depression, and <b>alcohol</b> drinking, while its actions at presynaptic Y2R produce the opposite behavioral phenotypes.
+NPY	drug	alcohol	24290310	The functional roles of various systems implicated in stress and reward, including opioids, dopamine, corticotropin releasing factor (CRF), glucocorticoids, neuropeptide Y (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and cannabinoids, have been investigated in the context of <b>alcohol</b> dependence.
+NPY	drug	cannabinoid	24290310	The functional roles of various systems implicated in stress and reward, including opioids, dopamine, corticotropin releasing factor (CRF), glucocorticoids, neuropeptide Y (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and <b>cannabinoids</b>, have been investigated in the context of alcohol dependence.
+NPY	drug	opioid	24290310	The functional roles of various systems implicated in stress and reward, including <b>opioids</b>, dopamine, corticotropin releasing factor (CRF), glucocorticoids, neuropeptide Y (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and cannabinoids, have been investigated in the context of alcohol dependence.
+NPY	addiction	dependence	24290310	The functional roles of various systems implicated in stress and reward, including opioids, dopamine, corticotropin releasing factor (CRF), glucocorticoids, neuropeptide Y (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and cannabinoids, have been investigated in the context of alcohol <b>dependence</b>.
+NPY	addiction	reward	24290310	The functional roles of various systems implicated in stress and <b>reward</b>, including opioids, dopamine, corticotropin releasing factor (CRF), glucocorticoids, neuropeptide Y (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and cannabinoids, have been investigated in the context of alcohol dependence.
+NPY	drug	alcohol	24290310	The functional roles of various systems implicated in stress and reward, including opioids, dopamine, corticotropin releasing factor (CRF), glucocorticoids, <strong>neuropeptide Y</strong> (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and cannabinoids, have been investigated in the context of <b>alcohol</b> dependence.
+NPY	drug	cannabinoid	24290310	The functional roles of various systems implicated in stress and reward, including opioids, dopamine, corticotropin releasing factor (CRF), glucocorticoids, <strong>neuropeptide Y</strong> (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and <b>cannabinoids</b>, have been investigated in the context of alcohol dependence.
+NPY	drug	opioid	24290310	The functional roles of various systems implicated in stress and reward, including <b>opioids</b>, dopamine, corticotropin releasing factor (CRF), glucocorticoids, <strong>neuropeptide Y</strong> (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and cannabinoids, have been investigated in the context of alcohol dependence.
+NPY	addiction	dependence	24290310	The functional roles of various systems implicated in stress and reward, including opioids, dopamine, corticotropin releasing factor (CRF), glucocorticoids, <strong>neuropeptide Y</strong> (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and cannabinoids, have been investigated in the context of alcohol <b>dependence</b>.
+NPY	addiction	reward	24290310	The functional roles of various systems implicated in stress and <b>reward</b>, including opioids, dopamine, corticotropin releasing factor (CRF), glucocorticoids, <strong>neuropeptide Y</strong> (<strong>NPY</strong>), γ aminobutyric acid (GABA), norepinephrine, and cannabinoids, have been investigated in the context of alcohol dependence.
+NPY	drug	opioid	24220688	Monoamine oxidase A (Maoa) and <strong>neuropeptide Y</strong> receptor 5 mRNA levels were lower in adolescent mice than in adult mice without <b>oxycodone</b> exposure.
+NPY	drug	alcohol	23914176	<strong>Neuropeptide Y</strong>, a powerful anti stress neurotransmitter, has a profile of action on compulsive like responding for <b>ethanol</b> similar to a CRF1 antagonist.
+NPY	addiction	addiction	23914176	<strong>Neuropeptide Y</strong>, a powerful anti stress neurotransmitter, has a profile of action on <b>compulsive</b> like responding for ethanol similar to a CRF1 antagonist.
+NPY	drug	amphetamine	23864029	In contrast, parallel gene expression changes were observed in the Sleep Dep and Food Restrict groups in hypothalamic energy sensing systems (arcuate nucleus <strong>NPY</strong> was upregulated, and cocaine  and <b>amphetamine</b> regulated transcript was downregulated), in alignment with leptin suppression in both groups.
+NPY	drug	cocaine	23864029	In contrast, parallel gene expression changes were observed in the Sleep Dep and Food Restrict groups in hypothalamic energy sensing systems (arcuate nucleus <strong>NPY</strong> was upregulated, and <b>cocaine</b>  and amphetamine regulated transcript was downregulated), in alignment with leptin suppression in both groups.
+NPY	addiction	withdrawal	23805290	Neuropeptide Y (<strong>NPY</strong>) and arginine vasopressin (AVP) mRNA levels were transiently increased during opiate <b>withdrawal</b>.
+NPY	addiction	withdrawal	23805290	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) and arginine vasopressin (AVP) mRNA levels were transiently increased during opiate <b>withdrawal</b>.
+NPY	drug	alcohol	23792540	Adolescence is a critical developmental period of high vulnerability in which <b>ethanol</b> exposure alters corticotropin releasing factor, <strong>neuropeptide Y</strong>, substance P and neurokinin neuropeptide activities, all of which have key roles in <b>ethanol</b> consumption.
+NPY	drug	alcohol	23652361	Association between <strong>neuropeptide Y</strong> gene polymorphisms and <b>alcohol</b> dependence: a case control study in two independent populations.
+NPY	addiction	dependence	23652361	Association between <strong>neuropeptide Y</strong> gene polymorphisms and alcohol <b>dependence</b>: a case control study in two independent populations.
+NPY	drug	alcohol	23652361	Previous research reported an inverse association between <b>ethanol</b> drinking and cerebral neuropeptide Y (<strong>NPY</strong>) levels.
+NPY	drug	alcohol	23652361	Previous research reported an inverse association between <b>ethanol</b> drinking and cerebral <strong>neuropeptide Y</strong> (<strong>NPY</strong>) levels.
+NPY	drug	alcohol	23652361	There are conflicting results of studies on <strong>NPY</strong> gene polymorphisms in association with <b>alcohol</b> dependence in humans.
+NPY	addiction	dependence	23652361	There are conflicting results of studies on <strong>NPY</strong> gene polymorphisms in association with alcohol <b>dependence</b> in humans.
+NPY	drug	alcohol	23652361	To assess the role of the <strong>NPY</strong> gene in <b>alcohol</b> dependence, we genotyped three polymorphisms  in a sample of 195 subjects from the Kota population (80 <b>alcohol</b> dependence and 115 controls) and 141 subjects from the Badaga population (80 <b>alcohol</b> dependence and 61 controls).
+NPY	addiction	dependence	23652361	To assess the role of the <strong>NPY</strong> gene in alcohol <b>dependence</b>, we genotyped three polymorphisms  in a sample of 195 subjects from the Kota population (80 alcohol <b>dependence</b> and 115 controls) and 141 subjects from the Badaga population (80 alcohol <b>dependence</b> and 61 controls).
+NPY	drug	alcohol	23652361	Association of the <strong>NPY</strong> gene with <b>alcohol</b> dependence was tested by using logistic regression and haplotype analyses and linkage disequilibrium.
+NPY	addiction	dependence	23652361	Association of the <strong>NPY</strong> gene with alcohol <b>dependence</b> was tested by using logistic regression and haplotype analyses and linkage disequilibrium.
+NPY	drug	alcohol	23652361	Haplotype analysis also did not show significant association between the <strong>NPY</strong> gene and <b>alcohol</b> dependence.
+NPY	addiction	dependence	23652361	Haplotype analysis also did not show significant association between the <strong>NPY</strong> gene and alcohol <b>dependence</b>.
+NPY	drug	alcohol	23652361	These data support the hypothesis that <b>alcohol</b> dependence is influenced by the <strong>NPY</strong> G1258A polymorphism in Indian populations.
+NPY	addiction	dependence	23652361	These data support the hypothesis that alcohol <b>dependence</b> is influenced by the <strong>NPY</strong> G1258A polymorphism in Indian populations.
+NPY	drug	opioid	23511250	<strong>NPY</strong> mediates reward activity of <b>morphine</b>, via <strong>NPY</strong> Y1 receptors, in the nucleus accumbens shell.
+NPY	addiction	reward	23511250	<strong>NPY</strong> mediates <b>reward</b> activity of morphine, via <strong>NPY</strong> Y1 receptors, in the nucleus accumbens shell.
+NPY	addiction	reward	23511250	Although the interaction between endogenous neuropeptide Y (<strong>NPY</strong>) and opioidergic systems in processing of <b>reward</b> has been speculated, experimental evidence is lacking.
+NPY	addiction	reward	23511250	Although the interaction between endogenous <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and opioidergic systems in processing of <b>reward</b> has been speculated, experimental evidence is lacking.
+NPY	drug	opioid	23511250	We investigated the role of <strong>NPY</strong>, and its Y1 receptors, in the nucleus accumbens shell (AcbSh) in <b>morphine</b> induced reward and reinforcement behavior.
+NPY	addiction	reward	23511250	We investigated the role of <strong>NPY</strong>, and its Y1 receptors, in the nucleus accumbens shell (AcbSh) in morphine induced <b>reward</b> and <b>reinforcement</b> behavior.
+NPY	drug	opioid	23511250	About 30 70% increase in self stimulation was observed following bilateral intra AcbSh treatment with <b>morphine</b>, <strong>NPY</strong> or [Leu(31), Pro(34)] <strong>NPY</strong> (<strong>NPY</strong> Y1/Y5 receptors agonist), however, BIBP3226 (selective <strong>NPY</strong> Y1 receptors antagonist) produced opposite effect.
+NPY	drug	opioid	23511250	The reward effect of <b>morphine</b> was significantly potentiated by <strong>NPY</strong> or [Leu(31), Pro(34)] <strong>NPY</strong>, but antagonized by BIBP3226.
+NPY	addiction	reward	23511250	The <b>reward</b> effect of morphine was significantly potentiated by <strong>NPY</strong> or [Leu(31), Pro(34)] <strong>NPY</strong>, but antagonized by BIBP3226.
+NPY	addiction	reward	23511250	<strong>NPY</strong> immunoreactivity in the AcbSh, arcuate nucleus (ARC) and lateral part of bed nucleus of stria terminalis (BNSTl) was significantly more in the <b>operant</b> conditioned rats than in naïve control.
+NPY	drug	opioid	23511250	However, <b>morphine</b> administration to the conditioned rats resulted in significant decrease in the <strong>NPY</strong> immunoreactivity in all these anatomical regions.
+NPY	drug	opioid	23511250	Since the role of <b>morphine</b> in modulation of mesolimbic dopaminergic pathway is well established, we suggest that <strong>NPY</strong> system in AcbSh, ARC and BNSTl, perhaps acting via Y1 receptor system, may be an important component of the mesolimbic AcbSh reward circuitry triggered by endogenous <b>opioids</b>.
+NPY	addiction	reward	23511250	Since the role of morphine in modulation of mesolimbic dopaminergic pathway is well established, we suggest that <strong>NPY</strong> system in AcbSh, ARC and BNSTl, perhaps acting via Y1 receptor system, may be an important component of the mesolimbic AcbSh <b>reward</b> circuitry triggered by endogenous opioids.
+NPY	drug	cocaine	23454535	<strong>Neuropeptide Y</strong> Y5 receptor antagonism causes faster extinction and attenuates reinstatement in <b>cocaine</b> induced place preference.
+NPY	addiction	relapse	23454535	<strong>Neuropeptide Y</strong> Y5 receptor antagonism causes faster extinction and attenuates <b>reinstatement</b> in cocaine induced place preference.
+NPY	drug	cocaine	23454535	Several studies have suggested a role for neuropeptide Y (<strong>NPY</strong>) in addiction to drugs of abuse, including <b>cocaine</b>.
+NPY	addiction	addiction	23454535	Several studies have suggested a role for neuropeptide Y (<strong>NPY</strong>) in <b>addiction</b> to drugs of abuse, including cocaine.
+NPY	drug	cocaine	23454535	Several studies have suggested a role for <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in addiction to drugs of abuse, including <b>cocaine</b>.
+NPY	addiction	addiction	23454535	Several studies have suggested a role for <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in <b>addiction</b> to drugs of abuse, including cocaine.
+NPY	drug	cocaine	23454535	Recently, our group showed a role for the <strong>NPY</strong> Y5 receptor in the modulation of acute reinforcing effects of <b>cocaine</b> using self administration and hyperlocomotion paradigms.
+NPY	addiction	reward	23454535	Recently, our group showed a role for the <strong>NPY</strong> Y5 receptor in the modulation of acute <b>reinforcing</b> effects of cocaine using self administration and hyperlocomotion paradigms.
+NPY	drug	cocaine	23454535	Using this model, it was tested whether blockade or deficiency of the <strong>NPY</strong> Y5 receptor could influence the induction, extinction or reinstatement of a conditioned <b>cocaine</b> response.
+NPY	addiction	relapse	23454535	Using this model, it was tested whether blockade or deficiency of the <strong>NPY</strong> Y5 receptor could influence the induction, extinction or <b>reinstatement</b> of a conditioned cocaine response.
+NPY	drug	opioid	23333681	The dynorphin (DYN), μ <b>opioid</b> receptor (mu <b>opioid</b>), neuropeptide Y (<strong>NPY</strong>), brain derived neurotrophic factor (BDNF), tropomyosin related tyrosine kinase B receptor (TrkB) and corticotropin releasing factor receptor type 1 (CRF R1) gene expression were measured by the reverse transcription polymerase chain reaction (RT PCR).
+NPY	drug	opioid	23333681	The dynorphin (DYN), μ <b>opioid</b> receptor (mu <b>opioid</b>), <strong>neuropeptide Y</strong> (<strong>NPY</strong>), brain derived neurotrophic factor (BDNF), tropomyosin related tyrosine kinase B receptor (TrkB) and corticotropin releasing factor receptor type 1 (CRF R1) gene expression were measured by the reverse transcription polymerase chain reaction (RT PCR).
+NPY	drug	amphetamine	23194408	on any of the palatable diets were heavier, fatter and had higher blood leptin than controls, and had reduced <strong>NPY</strong> and increased cocaine  and <b>amphetamine</b> regulated transcript mRNA in the ARC.
+NPY	drug	cocaine	23194408	on any of the palatable diets were heavier, fatter and had higher blood leptin than controls, and had reduced <strong>NPY</strong> and increased <b>cocaine</b>  and amphetamine regulated transcript mRNA in the ARC.
+NPY	drug	opioid	23123350	Pain related behaviors were tested after incision in rats treated with intrathecal <strong>NPY</strong>, Y(1) receptor antagonist (BIBO3304  Chemical Name: N [(1R) 1 [[[[4 [[(Aminocarbonyl)amino]methyl]phenyl]methyl]amino]carbonyl] 4 [(aminoiminomethyl)amino]butyl] α phenyl benzeneacetamide ditrifluoroacetate), Y(2) receptor antagonist (BIIE0246  Chemical Name: N [(1S) 4 [(Aminoiminomethyl)amino] 1 [[[2 (3,5 dioxo 1,2 diphenyl 1,2,4 triazolidin 4 yl)ethyl]amino]carbonyl]butyl] 1 [2 [4 (6,11 dihydro 6 oxo 5H dibenz[b,e]azepin 11 yl) 1 piperazinyl] 2 oxoethyl] cyclopentaneacetamide), combined <strong>NPY</strong>+antagonists, <b>morphine</b>, or vehicle.
+NPY	drug	opioid	23123350	A single intrathecal injection of <strong>NPY</strong> reduced cumulative guarding pain scores, as did <b>morphine</b>.
+NPY	addiction	withdrawal	23123350	Intrathecal Y(2) receptor antagonists and <strong>NPY</strong> improved mechanical threshold and heat <b>withdrawal</b> latency 2h after incision.
+NPY	drug	alcohol	23085848	Pro  (e.g., corticotropin releasing factor [CRF]) and anti stress (e.g., <strong>NPY</strong>, nociceptin) neuropeptides affect <b>alcohol</b>  and anxiety related behaviors, and also alter the <b>alcohol</b> induced effects on CeA neurotransmission.
+NPY	addiction	addiction	23062312	Thus the dynorphin system, acting via <strong>NPY</strong>, may represent a pathway by which higher processes including stress, reward/<b>addiction</b> and depression influence skeletal metabolism.
+NPY	addiction	reward	23062312	Thus the dynorphin system, acting via <strong>NPY</strong>, may represent a pathway by which higher processes including stress, <b>reward</b>/addiction and depression influence skeletal metabolism.
+NPY	drug	amphetamine	23061411	<b>Methamphetamine</b> induced changes in the mice hippocampal <strong>neuropeptide Y</strong> system: implications for memory impairment.
+NPY	drug	amphetamine	23061411	It has been demonstrated that <b>METH</b> induces significant alteration in mice striatal <strong>NPY</strong>, Y(1) and Y(2) receptor mRNA levels.
+NPY	drug	amphetamine	23061411	Thus, in this study, we investigated the effect of <b>METH</b> intoxication on mouse hippocampal <strong>NPY</strong> levels, <strong>NPY</strong> receptors function, and memory performance.
+NPY	addiction	intoxication	23061411	Thus, in this study, we investigated the effect of METH <b>intoxication</b> on mouse hippocampal <strong>NPY</strong> levels, <strong>NPY</strong> receptors function, and memory performance.
+NPY	drug	amphetamine	23061411	Results show that <b>METH</b> increased <strong>NPY</strong>, Y(2) and Y(5) receptor mRNA levels, as well as total <strong>NPY</strong> binding accounted by opposite up  and down regulation of Y(2) and Y(1) functional binding, respectively.
+NPY	drug	amphetamine	23061411	These findings demonstrate that <b>METH</b> interferes with the hippocampal <strong>NPY</strong> system, which seems to be associated with memory failure.
+NPY	drug	nicotine	22959963	Moreover, these behavioral effects of <b>nicotine</b> are accompanied by a persistent imbalance between <strong>neuropeptide Y</strong> and corticotrophin releasing factor systems, and a persistent increase in brain derived neurotrophic factor (BDNF) and spinophilin mRNA levels in the amygdala.
+NPY	drug	alcohol	22938859	Neuropeptide Y (<strong>NPY</strong>) in the extended amygdala is recruited during the transition to <b>alcohol</b> dependence.
+NPY	addiction	dependence	22938859	Neuropeptide Y (<strong>NPY</strong>) in the extended amygdala is recruited during the transition to alcohol <b>dependence</b>.
+NPY	drug	alcohol	22938859	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) in the extended amygdala is recruited during the transition to <b>alcohol</b> dependence.
+NPY	addiction	dependence	22938859	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) in the extended amygdala is recruited during the transition to alcohol <b>dependence</b>.
+NPY	addiction	reward	22938859	<strong>NPY</strong> has been attributed a central role in anxiety like behavior, fear, nociception, and <b>reward</b> in rodents.
+NPY	drug	alcohol	22938859	Deletion of the <strong>NPY</strong> gene in mice produces a high anxiety high <b>alcohol</b> drinking phenotype.
+NPY	drug	alcohol	22938859	<strong>NPY</strong> infused into the brains of rats selectively bred to consume high quantities of <b>alcohol</b> suppresses <b>alcohol</b> drinking by those animals, an effect that is mediated by central amygdala (CeA).
+NPY	drug	alcohol	22938859	Likewise, <b>alcohol</b> preferring rats exhibit basal <strong>NPY</strong> deficits in CeA.
+NPY	drug	alcohol	22938859	<strong>NPY</strong> infused into the brains of <b>alcohol</b> dependent rats blocks excessive <b>alcohol</b> drinking by those animals, an effect that also has been localized to the CeA.
+NPY	drug	alcohol	22938859	<strong>NPY</strong> in CeA may rescue dependence induced increases in anxiety and <b>alcohol</b> drinking via inhibition of downstream effector regions that receive GABAergic inputs from CeA.
+NPY	addiction	dependence	22938859	<strong>NPY</strong> in CeA may rescue <b>dependence</b> induced increases in anxiety and alcohol drinking via inhibition of downstream effector regions that receive GABAergic inputs from CeA.
+NPY	drug	alcohol	22938859	It is hypothesized here that <strong>NPY</strong> modulates anxiety like behavior via Y2R regulation of <strong>NPY</strong> release, whereas <strong>NPY</strong> modulation of <b>alcohol</b> drinking behavior in <b>alcohol</b> dependent animals occurs via Y2R regulation of GABA release.
+NPY	drug	nicotine	22584873	Genetic variation in the <strong>neuropeptide Y</strong> gene promoter is associated with increased risk of <b>tobacco</b> <b>smoking</b>.
+NPY	drug	nicotine	22584873	Neuropeptide Y (<strong>NPY</strong>) is a strong candidate gene regarding the pathophysiology of <b>tobacco</b> dependence.
+NPY	addiction	dependence	22584873	Neuropeptide Y (<strong>NPY</strong>) is a strong candidate gene regarding the pathophysiology of tobacco <b>dependence</b>.
+NPY	drug	nicotine	22584873	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) is a strong candidate gene regarding the pathophysiology of <b>tobacco</b> dependence.
+NPY	addiction	dependence	22584873	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) is a strong candidate gene regarding the pathophysiology of tobacco <b>dependence</b>.
+NPY	drug	alcohol	22560367	Corticotropin releasing factor (CRF) and neuropeptide Y (<strong>NPY</strong>): effects on inhibitory transmission in central amygdala, and anxiety  & <b>alcohol</b> related behaviors.
+NPY	drug	alcohol	22560367	Corticotropin releasing factor (CRF) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>): effects on inhibitory transmission in central amygdala, and anxiety  & <b>alcohol</b> related behaviors.
+NPY	drug	alcohol	22560367	This review focuses on two of these peptides, corticotropin releasing factor (CRF) and neuropeptide Y (<strong>NPY</strong>), that exhibit a high degree of neuroanatomical overlap (e.g., in CeA) and largely opposite behavioral profiles (e.g., in regulating anxiety  and <b>alcohol</b> related behavior).
+NPY	drug	alcohol	22560367	This review focuses on two of these peptides, corticotropin releasing factor (CRF) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>), that exhibit a high degree of neuroanatomical overlap (e.g., in CeA) and largely opposite behavioral profiles (e.g., in regulating anxiety  and <b>alcohol</b> related behavior).
+NPY	drug	alcohol	22560367	CRF and <strong>NPY</strong> systems in the CeA appear to be recruited and/or up regulated during the transition to <b>alcohol</b> dependence.
+NPY	addiction	dependence	22560367	CRF and <strong>NPY</strong> systems in the CeA appear to be recruited and/or up regulated during the transition to alcohol <b>dependence</b>.
+NPY	drug	cocaine	22544368	Mice lacking <strong>neuropeptide Y</strong> show increased sensitivity to <b>cocaine</b>.
+NPY	addiction	addiction	22544368	There is increasing data implicating neuropeptide Y (<strong>NPY</strong>) in the neurobiology of <b>addiction</b>.
+NPY	addiction	addiction	22544368	There is increasing data implicating <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in the neurobiology of <b>addiction</b>.
+NPY	drug	cocaine	22544368	This study explored the possible role of <strong>NPY</strong> in <b>cocaine</b> induced behavior using <strong>NPY</strong> knockout mice.
+NPY	addiction	aversion	22522467	<strong>Neuropeptide Y</strong> receptor expressing dorsal horn neurons: role in nocifensive reflex and operant responses to <b>aversive</b> cold after CFA inflammation.
+NPY	addiction	reward	22522467	<strong>Neuropeptide Y</strong> receptor expressing dorsal horn neurons: role in nocifensive reflex and <b>operant</b> responses to aversive cold after CFA inflammation.
+NPY	addiction	reward	22522467	In the present study, we sought to determine the role of dorsal horn Y1R expressing neurons in pain by destroying them with <strong>NPY</strong> sap and testing the rats on three <b>operant</b> tasks.
+NPY	drug	opioid	22522467	Lumbar intrathecal <strong>NPY</strong> sap (1) reduced Complete Freund's Adjuvant (CFA) induced hyper reflexia on the 10°C cold plate, (2) reduced cold aversion on the thermal preference and escape tasks, (3) was analgesic to noxious heat on the escape task, (4) reduced the CFA induced allodynia to cold temperatures experienced on the thermal preference, feeding interference, and escape tasks, and (5) did not inhibit or interfere with <b>morphine</b> analgesia.
+NPY	addiction	aversion	22522467	Lumbar intrathecal <strong>NPY</strong> sap (1) reduced Complete Freund's Adjuvant (CFA) induced hyper reflexia on the 10°C cold plate, (2) reduced cold <b>aversion</b> on the thermal preference and escape tasks, (3) was analgesic to noxious heat on the escape task, (4) reduced the CFA induced allodynia to cold temperatures experienced on the thermal preference, feeding interference, and escape tasks, and (5) did not inhibit or interfere with morphine analgesia.
+NPY	drug	nicotine	22405889	These studies indicate that corticotropin releasing factor, <strong>Neuropeptide Y</strong>, the hypocretins, and norepinephrine play a pivotal role in <b>nicotine</b> addiction.
+NPY	addiction	addiction	22405889	These studies indicate that corticotropin releasing factor, <strong>Neuropeptide Y</strong>, the hypocretins, and norepinephrine play a pivotal role in nicotine <b>addiction</b>.
+NPY	drug	cocaine	22367168	<strong>Neuropeptide Y</strong> Y5 receptor antagonism attenuates <b>cocaine</b> induced effects in mice.
+NPY	drug	cocaine	22367168	Several studies suggest a role for neuropeptide Y (<strong>NPY</strong>) in addiction to drugs of abuse, including <b>cocaine</b>.
+NPY	addiction	addiction	22367168	Several studies suggest a role for neuropeptide Y (<strong>NPY</strong>) in <b>addiction</b> to drugs of abuse, including cocaine.
+NPY	drug	cocaine	22367168	Several studies suggest a role for <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in addiction to drugs of abuse, including <b>cocaine</b>.
+NPY	addiction	addiction	22367168	Several studies suggest a role for <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in <b>addiction</b> to drugs of abuse, including cocaine.
+NPY	addiction	addiction	22367168	However, the <strong>NPY</strong> receptors mediating <b>addiction</b> related effects remain to be determined.
+NPY	drug	cocaine	22367168	To explore the potential role of Y5 <strong>NPY</strong> receptors in <b>cocaine</b> induced behavioural effects.
+NPY	drug	alcohol	22245775	Finally, recent evidence shows that corticotropin releasing factor (CRF), agouti related protein (AgRP), neuropeptide Y (<strong>NPY</strong>), and ghrelin are also implicated as impacting this pattern of <b>ethanol</b> consumption.
+NPY	drug	alcohol	22245775	Finally, recent evidence shows that corticotropin releasing factor (CRF), agouti related protein (AgRP), <strong>neuropeptide Y</strong> (<strong>NPY</strong>), and ghrelin are also implicated as impacting this pattern of <b>ethanol</b> consumption.
+NPY	drug	alcohol	22218088	Central <strong>neuropeptide Y</strong> modulates binge like <b>ethanol</b> drinking in C57BL/6J mice via Y1 and Y2 receptors.
+NPY	addiction	intoxication	22218088	Central <strong>neuropeptide Y</strong> modulates <b>binge</b> like ethanol drinking in C57BL/6J mice via Y1 and Y2 receptors.
+NPY	drug	alcohol	22218088	Here we employed a mouse model of binge like <b>ethanol</b> drinking to study the role of neuropeptide Y (<strong>NPY</strong>).
+NPY	addiction	intoxication	22218088	Here we employed a mouse model of <b>binge</b> like ethanol drinking to study the role of neuropeptide Y (<strong>NPY</strong>).
+NPY	drug	alcohol	22218088	Here we employed a mouse model of binge like <b>ethanol</b> drinking to study the role of <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	addiction	intoxication	22218088	Here we employed a mouse model of <b>binge</b> like ethanol drinking to study the role of <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	alcohol	22218088	The results indicated that central infusion of <strong>NPY</strong>, a <strong>NPY</strong> Y1 receptor (Y1R) agonist, and a Y2R antagonist significantly blunted binge like <b>ethanol</b> drinking in C57BL/6J mice (that achieved blood <b>ethanol</b> levels >80 mg/dl in control conditions).
+NPY	addiction	intoxication	22218088	The results indicated that central infusion of <strong>NPY</strong>, a <strong>NPY</strong> Y1 receptor (Y1R) agonist, and a Y2R antagonist significantly blunted <b>binge</b> like ethanol drinking in C57BL/6J mice (that achieved blood ethanol levels >80 mg/dl in control conditions).
+NPY	drug	alcohol	22218088	Binge like <b>ethanol</b> drinking reduced <strong>NPY</strong> and Y1R IR in the central nucleus of the amygdala (CeA), and 24 h of <b>ethanol</b> abstinence after a history of binge like drinking promoted increases of Y1R and Y2R IR.
+NPY	addiction	intoxication	22218088	<b>Binge</b> like ethanol drinking reduced <strong>NPY</strong> and Y1R IR in the central nucleus of the amygdala (CeA), and 24 h of ethanol abstinence after a history of <b>binge</b> like drinking promoted increases of Y1R and Y2R IR.
+NPY	drug	alcohol	22218088	Electrophysiological recordings of slice preparations from the CeA showed that binge like <b>ethanol</b> drinking augmented the ability of <strong>NPY</strong> to inhibit GABAergic transmission.
+NPY	addiction	intoxication	22218088	Electrophysiological recordings of slice preparations from the CeA showed that <b>binge</b> like ethanol drinking augmented the ability of <strong>NPY</strong> to inhibit GABAergic transmission.
+NPY	drug	alcohol	22218088	Thus, binge like <b>ethanol</b> drinking in C57BL/6J mice promoted alterations of <strong>NPY</strong> signaling in the CeA, and administration of exogenous <strong>NPY</strong> compounds protected against binge like drinking.
+NPY	addiction	intoxication	22218088	Thus, <b>binge</b> like ethanol drinking in C57BL/6J mice promoted alterations of <strong>NPY</strong> signaling in the CeA, and administration of exogenous <strong>NPY</strong> compounds protected against <b>binge</b> like drinking.
+NPY	drug	opioid	22210742	Ghrelin interacts with <strong>neuropeptide Y</strong> Y1 and <b>opioid</b> receptors to increase food reward.
+NPY	addiction	reward	22210742	Ghrelin interacts with <strong>neuropeptide Y</strong> Y1 and opioid receptors to increase food <b>reward</b>.
+NPY	drug	opioid	22210742	Here we examined the contribution of neuropeptide Y (<strong>NPY</strong>) and <b>opioids</b> to ghrelin's effects on food motivation and intake.
+NPY	drug	opioid	22210742	Here we examined the contribution of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and <b>opioids</b> to ghrelin's effects on food motivation and intake.
+NPY	drug	alcohol	22210742	In separate experiments, we explored the suppressive effects of a selective <strong>NPY</strong> Y1R antagonist or opioid receptor antagonist <b>naltrexone</b>, injected either intracerebroventricularly or intra VTA, on ghrelin induced food reward behavior.
+NPY	drug	opioid	22210742	In separate experiments, we explored the suppressive effects of a selective <strong>NPY</strong> Y1R antagonist or <b>opioid</b> receptor antagonist naltrexone, injected either intracerebroventricularly or intra VTA, on ghrelin induced food reward behavior.
+NPY	addiction	reward	22210742	In separate experiments, we explored the suppressive effects of a selective <strong>NPY</strong> Y1R antagonist or opioid receptor antagonist naltrexone, injected either intracerebroventricularly or intra VTA, on ghrelin induced food <b>reward</b> behavior.
+NPY	drug	alcohol	22210742	The ventricular ghrelin induced increase in sucrose motivated behavior and chow intake were completely blocked by intracerebroventricular pretreatment with either an <strong>NPY</strong> Y1R antagonist or <b>naltrexone</b>.
+NPY	drug	opioid	22210742	Thus, we identify central <strong>NPY</strong> and <b>opioid</b> signaling as the necessary mediators of food intake and reward effects of ghrelin and localize these interactions to the mesolimbic VTA.
+NPY	addiction	reward	22210742	Thus, we identify central <strong>NPY</strong> and opioid signaling as the necessary mediators of food intake and <b>reward</b> effects of ghrelin and localize these interactions to the mesolimbic VTA.
+NPY	drug	alcohol	22120201	Neuropeptide Y (<strong>NPY</strong>) in the central nucleus of the amygdala (CeA) does not affect <b>ethanol</b> reinforced responding in binge drinking, nondependent rats.
+NPY	addiction	intoxication	22120201	Neuropeptide Y (<strong>NPY</strong>) in the central nucleus of the amygdala (CeA) does not affect ethanol reinforced responding in <b>binge</b> drinking, nondependent rats.
+NPY	drug	alcohol	22120201	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) in the central nucleus of the amygdala (CeA) does not affect <b>ethanol</b> reinforced responding in binge drinking, nondependent rats.
+NPY	addiction	intoxication	22120201	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) in the central nucleus of the amygdala (CeA) does not affect ethanol reinforced responding in <b>binge</b> drinking, nondependent rats.
+NPY	drug	alcohol	22120201	Neuropeptide Y (<strong>NPY</strong>) has been investigated as a potential pharmacotherapeutic due to its ability to attenuate <b>ethanol</b> intake, particularly when administered into the CeA.
+NPY	drug	alcohol	22120201	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) has been investigated as a potential pharmacotherapeutic due to its ability to attenuate <b>ethanol</b> intake, particularly when administered into the CeA.
+NPY	drug	alcohol	22120201	Previous research suggests, though the evidence is somewhat conflicting, that the efficacy of <strong>NPY</strong> is contingent upon genetic background and/or prior history of <b>ethanol</b> dependence in rats.
+NPY	addiction	dependence	22120201	Previous research suggests, though the evidence is somewhat conflicting, that the efficacy of <strong>NPY</strong> is contingent upon genetic background and/or prior history of ethanol <b>dependence</b> in rats.
+NPY	drug	alcohol	22120201	However, studies looking at the effects of <strong>NPY</strong> in nonselected animals lacking a history of <b>ethanol</b> dependence have two factors that could impact the interpretation of the results: <b>ethanol</b> history/selection AND relatively low baseline <b>ethanol</b> intakes as compared to <b>ethanol</b> dependent and/or genetically selected controls.
+NPY	addiction	dependence	22120201	However, studies looking at the effects of <strong>NPY</strong> in nonselected animals lacking a history of ethanol <b>dependence</b> have two factors that could impact the interpretation of the results: ethanol history/selection AND relatively low baseline ethanol intakes as compared to ethanol dependent and/or genetically selected controls.
+NPY	drug	alcohol	22120201	The purpose of the present study was to generate higher baseline <b>ethanol</b> intakes upon which to examine the effects of <strong>NPY</strong> on <b>ethanol</b> and sucrose drinking in nonselected rats using a binge drinking model.
+NPY	addiction	intoxication	22120201	The purpose of the present study was to generate higher baseline ethanol intakes upon which to examine the effects of <strong>NPY</strong> on ethanol and sucrose drinking in nonselected rats using a <b>binge</b> drinking model.
+NPY	drug	alcohol	22120201	The results revealed that <strong>NPY</strong> had no effect on either sucrose or <b>ethanol</b> consumption or on appetitive responding (latency to respond).
+NPY	drug	alcohol	22120201	Overall, the findings indicate that even a history of binge like <b>ethanol</b> consumption is not sufficient to recruit CeA <strong>NPY</strong> activity, and are consistent with previous studies showing that the role of <strong>NPY</strong> in regulating <b>ethanol</b> reinforcement in the CeA may be contingent upon a prior history of <b>ethanol</b> dependence.
+NPY	addiction	dependence	22120201	Overall, the findings indicate that even a history of binge like ethanol consumption is not sufficient to recruit CeA <strong>NPY</strong> activity, and are consistent with previous studies showing that the role of <strong>NPY</strong> in regulating ethanol reinforcement in the CeA may be contingent upon a prior history of ethanol <b>dependence</b>.
+NPY	addiction	intoxication	22120201	Overall, the findings indicate that even a history of <b>binge</b> like ethanol consumption is not sufficient to recruit CeA <strong>NPY</strong> activity, and are consistent with previous studies showing that the role of <strong>NPY</strong> in regulating ethanol reinforcement in the CeA may be contingent upon a prior history of ethanol dependence.
+NPY	addiction	reward	22120201	Overall, the findings indicate that even a history of binge like ethanol consumption is not sufficient to recruit CeA <strong>NPY</strong> activity, and are consistent with previous studies showing that the role of <strong>NPY</strong> in regulating ethanol <b>reinforcement</b> in the CeA may be contingent upon a prior history of ethanol dependence.
+NPY	drug	cannabinoid	22101113	Electrophysiology techniques are used to explore the effects of neuropeptides/neuromodulators (CRF, <strong>NPY</strong>, nociceptin, dynorphin, <b>endocannabinoids</b>, galanin) on inhibitory transmission in CeA.
+NPY	drug	opioid	22031036	The purpose of this study was to evaluate whether wild ginseng (WG) administration could attenuate anxiety  and depression like behaviors and expression of corticotrophin releasing factor (CRF) and neuropeptide Y (<strong>NPY</strong>) following withdrawal from repeated <b>morphine</b> administration in rats.
+NPY	addiction	withdrawal	22031036	The purpose of this study was to evaluate whether wild ginseng (WG) administration could attenuate anxiety  and depression like behaviors and expression of corticotrophin releasing factor (CRF) and neuropeptide Y (<strong>NPY</strong>) following <b>withdrawal</b> from repeated morphine administration in rats.
+NPY	drug	opioid	22031036	The purpose of this study was to evaluate whether wild ginseng (WG) administration could attenuate anxiety  and depression like behaviors and expression of corticotrophin releasing factor (CRF) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) following withdrawal from repeated <b>morphine</b> administration in rats.
+NPY	addiction	withdrawal	22031036	The purpose of this study was to evaluate whether wild ginseng (WG) administration could attenuate anxiety  and depression like behaviors and expression of corticotrophin releasing factor (CRF) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) following <b>withdrawal</b> from repeated morphine administration in rats.
+NPY	drug	opioid	22031036	Our results demonstrated that WG extract might be effective at inhibiting the anxiety and depression responses due to <b>morphine</b> withdrawal by possibly modulating the hypothalamus CRF and <strong>NPY</strong> systems.
+NPY	addiction	withdrawal	22031036	Our results demonstrated that WG extract might be effective at inhibiting the anxiety and depression responses due to morphine <b>withdrawal</b> by possibly modulating the hypothalamus CRF and <strong>NPY</strong> systems.
+NPY	drug	alcohol	21999690	Evidence gathered from expression and injection studies suggests that the consumption of drugs, such as <b>ethanol</b> and nicotine, and also of palatable foods rich in fat is stimulated by different orexigenic peptides, such as enkephalin, galanin, orexin, and melaninconcentrating hormone, acting within the hypothalamus or various limbic structures, while another peptide, <strong>neuropeptide Y</strong>, is closely related to carbohydrate consumption and shows an inverse relationship with <b>ethanol</b> and nicotine consumption.
+NPY	drug	nicotine	21999690	Evidence gathered from expression and injection studies suggests that the consumption of drugs, such as ethanol and <b>nicotine</b>, and also of palatable foods rich in fat is stimulated by different orexigenic peptides, such as enkephalin, galanin, orexin, and melaninconcentrating hormone, acting within the hypothalamus or various limbic structures, while another peptide, <strong>neuropeptide Y</strong>, is closely related to carbohydrate consumption and shows an inverse relationship with ethanol and <b>nicotine</b> consumption.
+NPY	drug	alcohol	21995655	<strong>NPY</strong> also has effects on feeding behavior, <b>ethanol</b> intake, sleep regulation, tissue growth and remodeling.
+NPY	addiction	dependence	21917383	We examined whether the functional <strong>NPY</strong> haplotype modulates stress induced <strong>NPY</strong> and anxiety responses, and if plasma <strong>NPY</strong> stress responses are associated with substance <b>dependence</b> outcomes.
+NPY	drug	alcohol	21917383	Thirty seven treatment engaged, abstinent substance dependent (SD) patients and 28 healthy controls (HCs) characterized on <strong>NPY</strong> diplotypes (HH: high expression; HLLL: intermediate/low expression) were exposed to stress, <b>alcohol</b>/drug cues and neutral relaxing cues, using individualized guided imagery, in a 3 session laboratory experiment.
+NPY	addiction	relapse	21917383	The finding that lower stress related <strong>NPY</strong> is predictive of greater <b>relapse</b> severity provides support for therapeutic development of neuropeptide Y targets in the treatment of substance use disorders.
+NPY	addiction	relapse	21917383	The finding that lower stress related <strong>NPY</strong> is predictive of greater <b>relapse</b> severity provides support for therapeutic development of <strong>neuropeptide Y</strong> targets in the treatment of substance use disorders.
+NPY	drug	alcohol	21796371	Serum <strong>NPY</strong> and BNDF response to a behavioral stressor in <b>alcohol</b> dependent and healthy control participants.
+NPY	drug	alcohol	21796371	Neuropeptide Y (<strong>NPY</strong>) and brain derived neurotrophic factor (BDNF) have been implicated in both the stress response and <b>alcohol</b> addiction.
+NPY	addiction	addiction	21796371	Neuropeptide Y (<strong>NPY</strong>) and brain derived neurotrophic factor (BDNF) have been implicated in both the stress response and alcohol <b>addiction</b>.
+NPY	drug	alcohol	21796371	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) and brain derived neurotrophic factor (BDNF) have been implicated in both the stress response and <b>alcohol</b> addiction.
+NPY	addiction	addiction	21796371	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) and brain derived neurotrophic factor (BDNF) have been implicated in both the stress response and alcohol <b>addiction</b>.
+NPY	drug	alcohol	21796371	However, few studies have assessed the <strong>NPY</strong> and BDNF response to stress in <b>alcohol</b> dependent participants and the concurrent measure of <strong>NPY</strong> and BDNF has not been reported in human participants.
+NPY	drug	alcohol	21796371	The purpose of this study was to concurrently assess serum <strong>NPY</strong> and BDNF, as well as adrenocorticotropin (ACTH) and cortisol, in control and race  and aged matched abstinent <b>alcohol</b> dependent participants in response to a stress inducing public speaking task.
+NPY	drug	alcohol	21796371	Basal and post stress serum values of <strong>NPY</strong> and BDNF, as well as ACTH and cortisol, were assessed in 14 abstinent <b>alcohol</b> dependent and ten healthy control male participants.
+NPY	drug	alcohol	21796371	Differences in basal and stress induced responses of <strong>NPY</strong> and BDNF were not supported between control and abstinent <b>alcohol</b> dependent subjects.
+NPY	drug	alcohol	21762289	<strong>Neuropeptide Y</strong> signaling modulates the expression of <b>ethanol</b> induced behavioral sensitization in mice.
+NPY	addiction	sensitization	21762289	<strong>Neuropeptide Y</strong> signaling modulates the expression of ethanol induced behavioral <b>sensitization</b> in mice.
+NPY	drug	alcohol	21762289	Neuropeptide Y (<strong>NPY</strong>) and protein kinase A (PKA) have been implicated in neurobiological responses to <b>ethanol</b>.
+NPY	drug	alcohol	21762289	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) and protein kinase A (PKA) have been implicated in neurobiological responses to <b>ethanol</b>.
+NPY	drug	alcohol	21762289	These observations suggest that elevated <strong>NPY</strong> signaling in the NAc and/or striatum may contribute to the increased sensitivity to <b>ethanol</b> induced behavioral sensitization that is a characteristic of RIIβ /  mice.
+NPY	addiction	sensitization	21762289	These observations suggest that elevated <strong>NPY</strong> signaling in the NAc and/or striatum may contribute to the increased sensitivity to ethanol induced behavioral <b>sensitization</b> that is a characteristic of RIIβ /  mice.
+NPY	drug	alcohol	21762289	Consistently, <strong>NPY</strong> /  mice failed to display <b>ethanol</b> induced behavioral sensitization that was evident in littermate <strong>NPY</strong>+/+ mice.
+NPY	addiction	sensitization	21762289	Consistently, <strong>NPY</strong> /  mice failed to display ethanol induced behavioral <b>sensitization</b> that was evident in littermate <strong>NPY</strong>+/+ mice.
+NPY	drug	alcohol	21762289	To examine more directly the role of <strong>NPY</strong> in the locomotor stimulant effects of <b>ethanol</b>, we infused a recombinant adeno associated virus (rAAV) into the region of the NAc core of DBA/2J mice.
+NPY	drug	alcohol	21762289	Mice treated with the rAAV FIB <strong>NPY</strong>(13 36) vector exhibited reduced expression of <b>ethanol</b> induced behavioral sensitization compared with mice treated with a control vector.
+NPY	addiction	sensitization	21762289	Mice treated with the rAAV FIB <strong>NPY</strong>(13 36) vector exhibited reduced expression of ethanol induced behavioral <b>sensitization</b> compared with mice treated with a control vector.
+NPY	drug	alcohol	21762289	Taken together, the current data provide the first evidence that <strong>NPY</strong> signaling in the NAc core and the Y(2) receptor modulate <b>ethanol</b> induced behavioral sensitization.
+NPY	addiction	sensitization	21762289	Taken together, the current data provide the first evidence that <strong>NPY</strong> signaling in the NAc core and the Y(2) receptor modulate ethanol induced behavioral <b>sensitization</b>.
+NPY	addiction	withdrawal	21744309	Other components of brain stress systems in the extended amygdala that interact with CRF and that may contribute to the negative motivational state of <b>withdrawal</b> include norepinephrine, dynorphin, and <strong>neuropeptide Y</strong>.
+NPY	drug	opioid	21706389	Genes at which variation moderates these phenotypes include those encoding monoamine oxidase A (MAOA LPR), the serotonin transporter (HTTLPR), corticotropin releasing hormone (CRH 248C/T and  2232 C/G), Neuropeptide Y (<strong>NPY</strong> 1002 T/G), and the μ <b>opioid</b> receptor (OPRM1 C77G).
+NPY	drug	opioid	21706389	Genes at which variation moderates these phenotypes include those encoding monoamine oxidase A (MAOA LPR), the serotonin transporter (HTTLPR), corticotropin releasing hormone (CRH 248C/T and  2232 C/G), <strong>Neuropeptide Y</strong> (<strong>NPY</strong> 1002 T/G), and the μ <b>opioid</b> receptor (OPRM1 C77G).
+NPY	drug	nicotine	21653710	<b>Nicotine</b> excites hypothalamic arcuate anorexigenic proopiomelanocortin neurons and orexigenic <strong>neuropeptide Y</strong> neurons: similarities and differences.
+NPY	drug	nicotine	21653710	However, in control experiments <b>nicotine</b> also excited the orexigenic arcuate nucleus neuropeptide Y (<strong>NPY</strong>) cells.
+NPY	drug	nicotine	21653710	However, in control experiments <b>nicotine</b> also excited the orexigenic arcuate nucleus <strong>neuropeptide Y</strong> (<strong>NPY</strong>) cells.
+NPY	drug	nicotine	21653710	<b>Nicotine</b> exerted similar actions on POMC and <strong>NPY</strong> cells, with a slightly greater depolarizing action on POMC cells.
+NPY	drug	nicotine	21653710	We found no differences in the relative desensitization to <b>nicotine</b> between POMC and <strong>NPY</strong> neurons.
+NPY	drug	nicotine	21653710	<b>Nicotine</b> inhibited excitatory synaptic activity recorded in <strong>NPY</strong>, but not POMC, cells.
+NPY	drug	nicotine	21653710	<b>Nicotine</b> also excited hypocretin/orexin neurons that enhance cognitive arousal, but the responses were smaller than in <strong>NPY</strong> or POMC cells.
+NPY	drug	nicotine	21653710	Together, these results indicate that <b>nicotine</b> has a number of similar actions, but also a few different actions, on POMC and <strong>NPY</strong> neurons that could contribute to the weight loss associated with <b>smoking</b>.
+NPY	drug	cannabinoid	21631400	The present review discusses these therapeutic targets including noradrenaline and 5 HT reuptake inhibitors; sodium, calcium and potassium channels; inhibitory and excitatory neurotransmitters; neuropeptides including bradykinin, tachykinin, cholecystokinin, <strong>neuropeptide Y</strong>, vasoactive intestinal peptide, and CGRP; pro inflammatory cytokines; MAP kinases; PPAR γ; Na(+)/Ca(2+) exchanger; nitric oxide; purinergic receptors; neuronal nicotinic receptors; cation dependent chloride transporters; oxidative stress; matrix metalloproteinase and plasminogen activators; growth factors; transient receptor potential (TRP) channels; <b>endocannabinoids</b>; histamine receptors; dopamine; sigma receptors, beta adrenergic receptors, endothelins, and D amino acid oxidase.
+NPY	drug	opioid	21629996	A role for <strong>neuropeptide Y</strong> Y5 but not the Y1 receptor subtype in food deprivation induced reinstatement of <b>heroin</b> seeking in the rat.
+NPY	addiction	relapse	21629996	A role for <strong>neuropeptide Y</strong> Y5 but not the Y1 receptor subtype in food deprivation induced <b>reinstatement</b> of heroin <b>seeking</b> in the rat.
+NPY	addiction	relapse	21629996	We have previously reported that both acute food deprivation (FD) and <strong>NPY</strong> injections can reinstate extinguished drug <b>seeking</b> behavior, a proposed animal model of <b>relapse</b> to drug abuse.
+NPY	addiction	relapse	21629996	However, it is not clear whether the FD effect on drug <b>seeking</b> is dependent on <strong>NPY</strong> transmission.
+NPY	drug	opioid	21629996	Here, we used the reinstatement model to assess the role of <strong>NPY</strong> Y1 and Y5 receptor mediated transmission in FD induced reinstatement of <b>heroin</b> seeking.
+NPY	addiction	relapse	21629996	Here, we used the <b>reinstatement</b> model to assess the role of <strong>NPY</strong> Y1 and Y5 receptor mediated transmission in FD induced <b>reinstatement</b> of heroin <b>seeking</b>.
+NPY	drug	opioid	21629996	Injections of a novel <strong>NPY</strong> Y5 receptor antagonist, Lu AA33810 (0.0, 1.0, or 30.0 mg/kg/IP), resulted in a significant attenuation of FD induced reinstatement of extinguished <b>heroin</b> seeking.
+NPY	addiction	relapse	21629996	Injections of a novel <strong>NPY</strong> Y5 receptor antagonist, Lu AA33810 (0.0, 1.0, or 30.0 mg/kg/IP), resulted in a significant attenuation of FD induced <b>reinstatement</b> of extinguished heroin <b>seeking</b>.
+NPY	drug	opioid	21629996	These results suggest that while signals mediated through <strong>NPY</strong> Y1 receptors play a modest role in reinstatement, activation of Y5 receptors has a critical function in FD induced reinstatement of <b>heroin</b> seeking behavior.
+NPY	addiction	relapse	21629996	These results suggest that while signals mediated through <strong>NPY</strong> Y1 receptors play a modest role in <b>reinstatement</b>, activation of Y5 receptors has a critical function in FD induced <b>reinstatement</b> of heroin <b>seeking</b> behavior.
+NPY	drug	alcohol	21527271	Prolonged chronic <b>ethanol</b> exposure alters <strong>neuropeptide Y</strong> and corticotropin releasing factor levels in the brain of adult Wistar rats.
+NPY	drug	alcohol	21527271	There is evidence to suggest that alterations in neuropeptide Y (<strong>NPY</strong>) and corticotropin releasing factor (CRF) contribute to the escalated voluntary <b>ethanol</b> intake seen following long term chronic <b>ethanol</b> exposure.
+NPY	drug	alcohol	21527271	There is evidence to suggest that alterations in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and corticotropin releasing factor (CRF) contribute to the escalated voluntary <b>ethanol</b> intake seen following long term chronic <b>ethanol</b> exposure.
+NPY	drug	alcohol	21527271	The present study assessed whether the duration of chronic <b>ethanol</b> exposure and abstinence alters brain levels of <strong>NPY</strong> and CRF in adult Wistar rats.
+NPY	drug	alcohol	21527271	<strong>NPY</strong> like immunoreactivity (<strong>NPY</strong> LI) and CRF LI were determined in the amygdala (AMYG), frontal cortex (FCTX), hippocampus (HPC) and parietal cortex (PCTX) of adult Wistar rats after chronic <b>ethanol</b> exposure, and 24 h and 2 weeks following withdrawal (WD).
+NPY	addiction	withdrawal	21527271	<strong>NPY</strong> like immunoreactivity (<strong>NPY</strong> LI) and CRF LI were determined in the amygdala (AMYG), frontal cortex (FCTX), hippocampus (HPC) and parietal cortex (PCTX) of adult Wistar rats after chronic ethanol exposure, and 24 h and 2 weeks following <b>withdrawal</b> (WD).
+NPY	drug	alcohol	21527271	No change in brain levels of <strong>NPY</strong> LI, CRF LI and the <strong>NPY</strong> LI/CRF LI ratio was observed 2 weeks following <b>ethanol</b> exposure, whereas, 8 weeks of <b>ethanol</b> exposure produced a significant effect on <strong>NPY</strong> LI expression in the AMYG and FCTX.
+NPY	drug	alcohol	21527271	Findings from the present study suggest that a longer duration of <b>ethanol</b> vapor, similar to what is required to enhance voluntary drinking, is required to produce changes in <strong>NPY</strong> LI and CRF LI expression in the adult rat brain.
+NPY	drug	cannabinoid	21524263	<b>cannabinoid</b> receptors, CRF, <strong>NPY</strong>, ghrelin).
+NPY	drug	nicotine	21497168	Effects of a selective Y2R antagonist, JNJ 31020028, on <b>nicotine</b> abstinence related social anxiety like behavior, <strong>neuropeptide Y</strong> and corticotropin releasing factor mRNA levels in the novelty seeking phenotype.
+NPY	addiction	relapse	21497168	Effects of a selective Y2R antagonist, JNJ 31020028, on nicotine abstinence related social anxiety like behavior, <strong>neuropeptide Y</strong> and corticotropin releasing factor mRNA levels in the novelty <b>seeking</b> phenotype.
+NPY	drug	nicotine	21497168	Systemic and daily injections of a Y2R antagonist, JNJ 31020028, during abstinence fully reverse <b>nicotine</b> induced social anxiety like behavior, the expression of locomotor sensitization to <b>nicotine</b> challenge, the deficit in the <strong>NPY</strong> mRNA levels in the amygdala and the hippocampus, as well as result an increase in Y2R mRNA levels in the hippocampus and the CRF mRNA levels in the amygdala in HRs.
+NPY	addiction	sensitization	21497168	Systemic and daily injections of a Y2R antagonist, JNJ 31020028, during abstinence fully reverse nicotine induced social anxiety like behavior, the expression of locomotor <b>sensitization</b> to nicotine challenge, the deficit in the <strong>NPY</strong> mRNA levels in the amygdala and the hippocampus, as well as result an increase in Y2R mRNA levels in the hippocampus and the CRF mRNA levels in the amygdala in HRs.
+NPY	drug	alcohol	21459365	<strong>Neuropeptide Y</strong> opposes <b>alcohol</b> effects on gamma aminobutyric acid release in amygdala and blocks the transition to <b>alcohol</b> dependence.
+NPY	addiction	dependence	21459365	<strong>Neuropeptide Y</strong> opposes alcohol effects on gamma aminobutyric acid release in amygdala and blocks the transition to alcohol <b>dependence</b>.
+NPY	drug	alcohol	21459365	This study investigated the role of neuropeptide Y (<strong>NPY</strong>) in excessive <b>alcohol</b> drinking by making rats dependent on <b>alcohol</b> via <b>alcohol</b> vapor inhalation.
+NPY	drug	alcohol	21459365	This study investigated the role of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in excessive <b>alcohol</b> drinking by making rats dependent on <b>alcohol</b> via <b>alcohol</b> vapor inhalation.
+NPY	drug	alcohol	21459365	This study also utilized intracellular and whole cell recording techniques to determine the effects of <strong>NPY</strong> on GABAergic inhibitory transmission in CeA, synaptic mechanisms involved in these <strong>NPY</strong> effects, and <strong>NPY</strong> interactions with <b>alcohol</b> in the CeA of <b>alcohol</b> naive and <b>alcohol</b> dependent rats.
+NPY	drug	alcohol	21459365	Chronic <strong>NPY</strong> treatment blocked excessive operant <b>alcohol</b> reinforced responding associated with <b>alcohol</b> dependence, as well as gradual increases in <b>alcohol</b> responding by intermittently tested nondependent control animals.
+NPY	addiction	dependence	21459365	Chronic <strong>NPY</strong> treatment blocked excessive operant alcohol reinforced responding associated with alcohol <b>dependence</b>, as well as gradual increases in alcohol responding by intermittently tested nondependent control animals.
+NPY	addiction	reward	21459365	Chronic <strong>NPY</strong> treatment blocked excessive <b>operant</b> alcohol reinforced responding associated with alcohol dependence, as well as gradual increases in alcohol responding by intermittently tested nondependent control animals.
+NPY	drug	alcohol	21459365	<strong>Neuropeptide Y</strong> decreased baseline GABAergic transmission and reversed <b>alcohol</b> induced enhancement of inhibitory transmission in CeA by suppressing GABA release via actions at presynaptic Y(2) receptors.
+NPY	drug	alcohol	21459365	These results highlight <strong>NPY</strong> modulation of GABAergic signaling in central amygdala as a promising pharmacotherapeutic target for the treatment of <b>alcoholism</b>.
+NPY	drug	alcohol	21376087	Hippocampal levels of neuropeptide Y (<strong>NPY</strong>) and mGlu1a metabotropic glutamate receptors were increased at the end of <b>ethanol</b> treatment only in unstressed rats.
+NPY	drug	alcohol	21376087	Hippocampal levels of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and mGlu1a metabotropic glutamate receptors were increased at the end of <b>ethanol</b> treatment only in unstressed rats.
+NPY	drug	alcohol	21376087	After <b>ethanol</b> withdrawal, hippocampal levels of mGlu1 receptors were higher in unstressed rats, but lower in PRS rats, whereas <strong>NPY</strong> and CRH levels were similar in the two groups of rats.
+NPY	addiction	withdrawal	21376087	After ethanol <b>withdrawal</b>, hippocampal levels of mGlu1 receptors were higher in unstressed rats, but lower in PRS rats, whereas <strong>NPY</strong> and CRH levels were similar in the two groups of rats.
+NPY	drug	opioid	21328995	[Effect of HANS electroacupuncture on the expression of <strong>NPY</strong> in PAG of <b>heroin</b> addicted rats].
+NPY	drug	opioid	21328995	To examine the effects of Han's acupoint and nerve stimulator (HANS) electroacupuncture on the expression of <strong>NPY</strong> in periaqueductal grey (PAG) of <b>heroin</b> addicted rats.
+NPY	drug	opioid	21328995	(2) The expression of <strong>NPY</strong> of <b>heroin</b> addiction group was lower than that in normal group in PAG, while those of acupuncture group was higher than that in the <b>heroin</b> addiction group (P < 0.05).
+NPY	addiction	addiction	21328995	(2) The expression of <strong>NPY</strong> of heroin <b>addiction</b> group was lower than that in normal group in PAG, while those of acupuncture group was higher than that in the heroin <b>addiction</b> group (P < 0.05).
+NPY	drug	opioid	21328995	The learning and memory induced by <b>heroin</b> addiction could be reversed and the expression of <strong>NPY</strong> in PAG was increased by HANS in rats.
+NPY	addiction	addiction	21328995	The learning and memory induced by heroin <b>addiction</b> could be reversed and the expression of <strong>NPY</strong> in PAG was increased by HANS in rats.
+NPY	drug	cannabinoid	21243475	serotonergic, opioid, <b>cannabinoid</b> and dopaminergic receptors, and brain derived neurotrophic factor (BDNF)], appetite regulatory peptides and their receptors [leptin, ghrelin, agouti related protein (AgRP), melanocortin receptors, <strong>neuropeptide Y</strong>], energy balance systems (e.g.
+NPY	drug	opioid	21243475	serotonergic, <b>opioid</b>, cannabinoid and dopaminergic receptors, and brain derived neurotrophic factor (BDNF)], appetite regulatory peptides and their receptors [leptin, ghrelin, agouti related protein (AgRP), melanocortin receptors, <strong>neuropeptide Y</strong>], energy balance systems (e.g.
+NPY	drug	nicotine	21195134	Vulnerability to <b>nicotine</b> abstinence related social anxiety like behavior: molecular correlates in <strong>neuropeptide Y</strong>, Y2 receptor and corticotropin releasing factor.
+NPY	drug	nicotine	21195134	These findings implicate dysregulations in the <strong>NPY</strong> CRF systems in the HR hippocampus and amygdala associated with the emergence of social anxiety like behavior, and a novel Y2R mediated pathway in <b>nicotine</b> relapse.
+NPY	addiction	relapse	21195134	These findings implicate dysregulations in the <strong>NPY</strong> CRF systems in the HR hippocampus and amygdala associated with the emergence of social anxiety like behavior, and a novel Y2R mediated pathway in nicotine <b>relapse</b>.
+NPY	drug	alcohol	21145691	The novel, selective, brain penetrant <strong>neuropeptide Y</strong> Y2 receptor antagonist, JNJ 31020028, tested in animal models of <b>alcohol</b> consumption, relapse, and anxiety.
+NPY	addiction	relapse	21145691	The novel, selective, brain penetrant <strong>neuropeptide Y</strong> Y2 receptor antagonist, JNJ 31020028, tested in animal models of alcohol consumption, <b>relapse</b>, and anxiety.
+NPY	drug	alcohol	21145691	Neuropeptide Y (<strong>NPY</strong>) signaling has been shown to modulate stress responses and to be involved in regulation of <b>alcohol</b> intake and dependence.
+NPY	addiction	dependence	21145691	Neuropeptide Y (<strong>NPY</strong>) signaling has been shown to modulate stress responses and to be involved in regulation of alcohol intake and <b>dependence</b>.
+NPY	drug	alcohol	21145691	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) signaling has been shown to modulate stress responses and to be involved in regulation of <b>alcohol</b> intake and dependence.
+NPY	addiction	dependence	21145691	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) signaling has been shown to modulate stress responses and to be involved in regulation of alcohol intake and <b>dependence</b>.
+NPY	drug	alcohol	21145691	The present study explores the possibility that blockade of <strong>NPY</strong> Y2 autoreceptors using a novel, blood brain barrier penetrant <strong>NPY</strong> Y2 receptor antagonist, JNJ 31020028 (N (4 {4 [2 (diethylamino) 2 oxo 1 phenylethyl]piperazin 1 yl} 3 fluorophenyl) 2 pyridin 3 ylbenzamide), may achieve a therapeutically useful activation of the <strong>NPY</strong> system in <b>alcohol</b>  and anxiety related behavioral models.
+NPY	drug	alcohol	21145691	JNJ 31020028 (15 mg/kg, s.c.) did reverse the anxiogenic effects of withdrawal from a single bolus dose of <b>alcohol</b> on the elevated plus maze, confirming the anxiolytic like properties of <strong>NPY</strong> Y2 antagonism.
+NPY	addiction	withdrawal	21145691	JNJ 31020028 (15 mg/kg, s.c.) did reverse the anxiogenic effects of <b>withdrawal</b> from a single bolus dose of alcohol on the elevated plus maze, confirming the anxiolytic like properties of <strong>NPY</strong> Y2 antagonism.
+NPY	drug	alcohol	21145691	Our data do not support Y2 antagonism as a mechanism for reducing <b>alcohol</b> consumption or relapse like behavior, but the observed effects on withdrawal induced anxiety suggest that <strong>NPY</strong> Y2 receptor antagonists may be a putative treatment for the negative affective states following <b>alcohol</b> withdrawal.
+NPY	addiction	relapse	21145691	Our data do not support Y2 antagonism as a mechanism for reducing alcohol consumption or <b>relapse</b> like behavior, but the observed effects on withdrawal induced anxiety suggest that <strong>NPY</strong> Y2 receptor antagonists may be a putative treatment for the negative affective states following alcohol withdrawal.
+NPY	addiction	withdrawal	21145691	Our data do not support Y2 antagonism as a mechanism for reducing alcohol consumption or relapse like behavior, but the observed effects on <b>withdrawal</b> induced anxiety suggest that <strong>NPY</strong> Y2 receptor antagonists may be a putative treatment for the negative affective states following alcohol <b>withdrawal</b>.
+NPY	drug	alcohol	21058960	Role of feeding related pathways in <b>alcohol</b> dependence: A focus on sweet preference, <strong>NPY</strong>, and ghrelin.
+NPY	addiction	dependence	21058960	Role of feeding related pathways in alcohol <b>dependence</b>: A focus on sweet preference, <strong>NPY</strong>, and ghrelin.
+NPY	drug	alcohol	20937300	Neuropeptide Y (<strong>NPY</strong>) induced reductions in <b>alcohol</b> intake during continuous access and following <b>alcohol</b> deprivation are not altered by restraint stress in <b>alcohol</b> preferring (P) rats.
+NPY	drug	alcohol	20937300	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) induced reductions in <b>alcohol</b> intake during continuous access and following <b>alcohol</b> deprivation are not altered by restraint stress in <b>alcohol</b> preferring (P) rats.
+NPY	drug	alcohol	20937300	Administration of neuropeptide Y (<strong>NPY</strong>) reduces anxiety like behavior and <b>alcohol</b> intake in <b>alcohol</b> preferring rats.
+NPY	drug	alcohol	20937300	Administration of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) reduces anxiety like behavior and <b>alcohol</b> intake in <b>alcohol</b> preferring rats.
+NPY	drug	alcohol	20937300	The present experiment examined whether the effects of <strong>NPY</strong> on <b>alcohol</b> drinking are modulated by stress exposure during continuous access or following <b>ethanol</b> deprivation.
+NPY	drug	alcohol	20937300	ICV infusions of 5.0 μg <strong>NPY</strong> or aCSF were administered 48 h following the deprivation/stress procedure, after which <b>ethanol</b> was returned.
+NPY	drug	alcohol	20937300	Food and water intake were increased, while <b>ethanol</b> intake was decreased, in rats infused with <strong>NPY</strong>.
+NPY	drug	alcohol	20937300	Stress did not increase <b>ethanol</b> intake or alter the response to <strong>NPY</strong>.
+NPY	drug	alcohol	20937300	Although no stress effects were found, the present experiment replicates previous findings regarding the effectiveness of <strong>NPY</strong> in reducing <b>ethanol</b> consumption.
+NPY	drug	alcohol	20937300	Future studies aimed at determining the extent to which stress may affect relapse to <b>ethanol</b> drinking and response to <strong>NPY</strong> would benefit from implementing different stress paradigms and varying the pattern of <b>ethanol</b> access.
+NPY	addiction	relapse	20937300	Future studies aimed at determining the extent to which stress may affect <b>relapse</b> to ethanol drinking and response to <strong>NPY</strong> would benefit from implementing different stress paradigms and varying the pattern of ethanol access.
+NPY	drug	nicotine	20811389	Association between <strong>neuropeptide Y</strong> receptor 2 polymorphism and the <b>smoking</b> behavior of elderly Japanese.
+NPY	drug	alcohol	20705420	Effects of prolonged <b>ethanol</b> vapor exposure on forced swim behavior, and <strong>neuropeptide Y</strong> and corticotropin releasing factor levels in rat brains.
+NPY	drug	alcohol	20705420	To contribute to the understanding of the neurobiology of chronic <b>ethanol</b> use, we investigated the effects of chronic intermittent <b>ethanol</b> vapor exposure on behaviors in the forced swim test (FST) and neuropeptide Y (<strong>NPY</strong>) and corticotropin releasing factor (CRF) levels in specific brain regions.
+NPY	drug	alcohol	20705420	To contribute to the understanding of the neurobiology of chronic <b>ethanol</b> use, we investigated the effects of chronic intermittent <b>ethanol</b> vapor exposure on behaviors in the forced swim test (FST) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and corticotropin releasing factor (CRF) levels in specific brain regions.
+NPY	drug	alcohol	20705420	Thus, extended <b>ethanol</b> vapor exposure produced long lasting changes in FST behavior and <strong>NPY</strong> levels in the brain.
+NPY	drug	alcohol	20554694	Earlier findings on the associations of DRD2 and <strong>NPY</strong> with <b>alcohol</b> dependence were supported: DRD2/ANKK1 Taq1A(1) increased (P = 0.04) and <strong>NPY</strong> Pro7 decreased (P = 0.01) the risk of <b>alcohol</b> dependence.
+NPY	addiction	dependence	20554694	Earlier findings on the associations of DRD2 and <strong>NPY</strong> with alcohol <b>dependence</b> were supported: DRD2/ANKK1 Taq1A(1) increased (P = 0.04) and <strong>NPY</strong> Pro7 decreased (P = 0.01) the risk of alcohol <b>dependence</b>.
+NPY	drug	alcohol	20554694	The role of DRD2 and <strong>NPY</strong> on <b>alcohol</b> dependence was also supported.
+NPY	addiction	dependence	20554694	The role of DRD2 and <strong>NPY</strong> on alcohol <b>dependence</b> was also supported.
+NPY	drug	cannabinoid	20482506	A variety of systems have been investigated, such as the <b>endocannabinoid</b> system, modulators of glutamatergic transmission, corticotropin releasing factor (CRF), neuropeptide Y (<strong>NPY</strong>), nociceptin, glial cell line derived neurotrophic factor (GDNF), acetaldehyde (ACD), substance P and Neurokinin 1 (NK1) receptor, nicotinic acetylcholine receptors (nAchRs), alpha adrenergic receptor, and many others.
+NPY	drug	cannabinoid	20482506	A variety of systems have been investigated, such as the <b>endocannabinoid</b> system, modulators of glutamatergic transmission, corticotropin releasing factor (CRF), <strong>neuropeptide Y</strong> (<strong>NPY</strong>), nociceptin, glial cell line derived neurotrophic factor (GDNF), acetaldehyde (ACD), substance P and Neurokinin 1 (NK1) receptor, nicotinic acetylcholine receptors (nAchRs), alpha adrenergic receptor, and many others.
+NPY	drug	alcohol	20454655	This dependence on neuropeptides does not involve the <strong>NPY</strong> like receptor npr 1, previously implicated in C. elegans <b>ethanol</b> withdrawal.
+NPY	addiction	dependence	20454655	This <b>dependence</b> on neuropeptides does not involve the <strong>NPY</strong> like receptor npr 1, previously implicated in C. elegans ethanol withdrawal.
+NPY	addiction	withdrawal	20454655	This dependence on neuropeptides does not involve the <strong>NPY</strong> like receptor npr 1, previously implicated in C. elegans ethanol <b>withdrawal</b>.
+NPY	drug	alcohol	20454655	These data resonate with mammalian studies which report involvement of a number of neuropeptides in chronic responses to <b>alcohol</b> including corticotrophin releasing factor (CRF), opioids, tachykinins as well as <strong>NPY</strong>.
+NPY	drug	opioid	20454655	These data resonate with mammalian studies which report involvement of a number of neuropeptides in chronic responses to alcohol including corticotrophin releasing factor (CRF), <b>opioids</b>, tachykinins as well as <strong>NPY</strong>.
+NPY	drug	alcohol	20368518	Functional <strong>NPY</strong> variation as a factor in stress resilience and <b>alcohol</b> consumption in rhesus macaques.
+NPY	drug	alcohol	20368518	Neuropeptide Y (<strong>NPY</strong>) counters stress and is involved in neuroadaptations that drive escalated <b>alcohol</b> drinking in rodents.
+NPY	drug	alcohol	20368518	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) counters stress and is involved in neuroadaptations that drive escalated <b>alcohol</b> drinking in rodents.
+NPY	drug	alcohol	20368518	Genetic variation that affects the <strong>NPY</strong> system could moderate stress resilience and susceptibility to <b>alcohol</b> dependence.
+NPY	addiction	dependence	20368518	Genetic variation that affects the <strong>NPY</strong> system could moderate stress resilience and susceptibility to alcohol <b>dependence</b>.
+NPY	drug	alcohol	20368518	To determine whether functional <strong>NPY</strong> variation influences behavioral adaptation to stress and <b>alcohol</b> consumption in a nonhuman primate model of early adversity (peer rearing).
+NPY	drug	alcohol	20368518	Our results suggest a role for <strong>NPY</strong> promoter variation in the susceptibility to <b>alcohol</b> use disorders and point to <strong>NPY</strong> as a candidate for examining gene x environment interactions in humans.
+NPY	drug	amphetamine	20144693	Microarray analysis uncovered several genes involved in food intake (<strong>neuropeptide Y</strong>, agouti related protein, and cocaine and <b>amphetamine</b> regulated transcript) whose expression was strongly altered by morphine exposure in either the hypothalamus or pituitary.
+NPY	drug	cocaine	20144693	Microarray analysis uncovered several genes involved in food intake (<strong>neuropeptide Y</strong>, agouti related protein, and <b>cocaine</b> and amphetamine regulated transcript) whose expression was strongly altered by morphine exposure in either the hypothalamus or pituitary.
+NPY	drug	opioid	20144693	Microarray analysis uncovered several genes involved in food intake (<strong>neuropeptide Y</strong>, agouti related protein, and cocaine and amphetamine regulated transcript) whose expression was strongly altered by <b>morphine</b> exposure in either the hypothalamus or pituitary.
+NPY	drug	opioid	20097951	The role of endogenous <b>opioids</b> is relatively well known and there is growing evidence for a role of the appetite regulating peptides leptin, ghrelin, <strong>neuropeptide Y</strong>, galanin, and orexins.
+NPY	drug	alcohol	20028355	Gene expression in the <strong>neuropeptide Y</strong> system during <b>ethanol</b> withdrawal kindling in rats.
+NPY	addiction	withdrawal	20028355	Gene expression in the <strong>neuropeptide Y</strong> system during ethanol <b>withdrawal</b> kindling in rats.
+NPY	drug	alcohol	20028355	Previous studies show that a single episode of chronic <b>ethanol</b> intoxication and withdrawal causes prominent changes in neuropeptide Y (<strong>NPY</strong>) and its receptors that have been implicated in regulating withdrawal hyperexcitability.
+NPY	addiction	intoxication	20028355	Previous studies show that a single episode of chronic ethanol <b>intoxication</b> and withdrawal causes prominent changes in neuropeptide Y (<strong>NPY</strong>) and its receptors that have been implicated in regulating withdrawal hyperexcitability.
+NPY	addiction	withdrawal	20028355	Previous studies show that a single episode of chronic ethanol intoxication and <b>withdrawal</b> causes prominent changes in neuropeptide Y (<strong>NPY</strong>) and its receptors that have been implicated in regulating <b>withdrawal</b> hyperexcitability.
+NPY	drug	alcohol	20028355	Previous studies show that a single episode of chronic <b>ethanol</b> intoxication and withdrawal causes prominent changes in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and its receptors that have been implicated in regulating withdrawal hyperexcitability.
+NPY	addiction	intoxication	20028355	Previous studies show that a single episode of chronic ethanol <b>intoxication</b> and withdrawal causes prominent changes in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and its receptors that have been implicated in regulating withdrawal hyperexcitability.
+NPY	addiction	withdrawal	20028355	Previous studies show that a single episode of chronic ethanol intoxication and <b>withdrawal</b> causes prominent changes in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and its receptors that have been implicated in regulating <b>withdrawal</b> hyperexcitability.
+NPY	drug	alcohol	20028355	This study for the first time examined the <strong>NPY</strong> system during <b>ethanol</b> withdrawal kindling.
+NPY	addiction	withdrawal	20028355	This study for the first time examined the <strong>NPY</strong> system during ethanol <b>withdrawal</b> kindling.
+NPY	addiction	withdrawal	20028355	Multiple <b>withdrawal</b> episodes reversibly decreased <strong>NPY</strong> and <strong>NPY</strong> receptor mRNA levels at peak <b>withdrawal</b>, with smaller decreases in <strong>NPY</strong> mRNA levels and augmented decreases in Y1/Y5 mRNA levels compared with a SW episode.
+NPY	drug	alcohol	20028355	These complex changes in <strong>NPY</strong> system gene expression could play a role in the <b>ethanol</b> withdrawal kindling process.
+NPY	addiction	withdrawal	20028355	These complex changes in <strong>NPY</strong> system gene expression could play a role in the ethanol <b>withdrawal</b> kindling process.
+NPY	drug	alcohol	20012021	Neuropeptide Y (<strong>NPY</strong>) suppresses yohimbine induced reinstatement of <b>alcohol</b> seeking.
+NPY	addiction	relapse	20012021	Neuropeptide Y (<strong>NPY</strong>) suppresses yohimbine induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+NPY	drug	alcohol	20012021	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) suppresses yohimbine induced reinstatement of <b>alcohol</b> seeking.
+NPY	addiction	relapse	20012021	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) suppresses yohimbine induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+NPY	drug	alcohol	20012021	Here, we examined whether neuropeptide Y (<strong>NPY</strong>), an endogenous anti stress mediator, blocks reinstatement of <b>alcohol</b> seeking induced by the pharmacological stressor yohimbine.
+NPY	addiction	relapse	20012021	Here, we examined whether neuropeptide Y (<strong>NPY</strong>), an endogenous anti stress mediator, blocks <b>reinstatement</b> of alcohol <b>seeking</b> induced by the pharmacological stressor yohimbine.
+NPY	drug	alcohol	20012021	Here, we examined whether <strong>neuropeptide Y</strong> (<strong>NPY</strong>), an endogenous anti stress mediator, blocks reinstatement of <b>alcohol</b> seeking induced by the pharmacological stressor yohimbine.
+NPY	addiction	relapse	20012021	Here, we examined whether <strong>neuropeptide Y</strong> (<strong>NPY</strong>), an endogenous anti stress mediator, blocks <b>reinstatement</b> of alcohol <b>seeking</b> induced by the pharmacological stressor yohimbine.
+NPY	drug	alcohol	20012021	<strong>NPY</strong> [5.0 or 10.0 mug/rat, intracerebroventricularly (ICV)] dose dependently blocked the reinstatement of <b>alcohol</b> seeking induced by yohimbine (1.25 mg/kg, i.p.)
+NPY	addiction	relapse	20012021	<strong>NPY</strong> [5.0 or 10.0 mug/rat, intracerebroventricularly (ICV)] dose dependently blocked the <b>reinstatement</b> of alcohol <b>seeking</b> induced by yohimbine (1.25 mg/kg, i.p.)
+NPY	drug	alcohol	20012021	These results suggest that <strong>NPY</strong> selectively suppresses relapse to <b>alcohol</b> seeking induced by stressful events and support the <strong>NPY</strong> system as an attractive target for the treatment of <b>alcohol</b> addiction.
+NPY	addiction	addiction	20012021	These results suggest that <strong>NPY</strong> selectively suppresses relapse to alcohol seeking induced by stressful events and support the <strong>NPY</strong> system as an attractive target for the treatment of alcohol <b>addiction</b>.
+NPY	addiction	relapse	20012021	These results suggest that <strong>NPY</strong> selectively suppresses <b>relapse</b> to alcohol <b>seeking</b> induced by stressful events and support the <strong>NPY</strong> system as an attractive target for the treatment of alcohol addiction.
+NPY	drug	alcohol	19913192	Stress related neuropeptides and <b>alcoholism</b>: CRH, <strong>NPY</strong>, and beyond.
+NPY	drug	alcohol	19913192	Dr. Annika Thorsell showed data supporting the significance of the <strong>neuropeptide Y</strong> receptor system in the modulation of behaviors associated with a history of <b>ethanol</b> intoxication.
+NPY	addiction	intoxication	19913192	Dr. Annika Thorsell showed data supporting the significance of the <strong>neuropeptide Y</strong> receptor system in the modulation of behaviors associated with a history of ethanol <b>intoxication</b>.
+NPY	drug	alcohol	19846044	Tolerance to <b>ethanol</b> sedation and withdrawal hyper excitability is mediated via <strong>neuropeptide Y</strong> Y1 and Y5 receptors.
+NPY	addiction	withdrawal	19846044	Tolerance to ethanol sedation and <b>withdrawal</b> hyper excitability is mediated via <strong>neuropeptide Y</strong> Y1 and Y5 receptors.
+NPY	drug	alcohol	19846044	Neuropeptide Y (<strong>NPY</strong>) is widely distributed throughout the brain and has been implicated in some of the actions of <b>ethanol</b>.
+NPY	drug	alcohol	19846044	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) is widely distributed throughout the brain and has been implicated in some of the actions of <b>ethanol</b>.
+NPY	drug	alcohol	19846044	The aim of the present study was to characterize the subtypes of <strong>NPY</strong> receptors in <b>ethanol</b> induced sedation, tolerance and withdrawal hyper excitability.
+NPY	addiction	withdrawal	19846044	The aim of the present study was to characterize the subtypes of <strong>NPY</strong> receptors in ethanol induced sedation, tolerance and <b>withdrawal</b> hyper excitability.
+NPY	drug	alcohol	19846044	injection of <strong>NPY</strong> (5 20 ng per mouse) or <strong>NPY</strong> Y1 and Y5 receptors agonist [Leu(31), Pro(34)] <strong>NPY</strong> (0.02 0.2 ng per mouse) potentiated <b>ethanol</b> induced sedation.
+NPY	drug	alcohol	19846044	The results underscore a role for <strong>NPY</strong> Y1 and Y5 receptors in the <b>ethanol</b> induced sedation, tolerance and withdrawal hyper excitability.
+NPY	addiction	withdrawal	19846044	The results underscore a role for <strong>NPY</strong> Y1 and Y5 receptors in the ethanol induced sedation, tolerance and <b>withdrawal</b> hyper excitability.
+NPY	drug	alcohol	19846044	We suggest that modulation of <strong>NPY</strong> Y1 and Y5 receptors may be a strategy to address the <b>ethanol</b> withdrawal conditions.
+NPY	addiction	withdrawal	19846044	We suggest that modulation of <strong>NPY</strong> Y1 and Y5 receptors may be a strategy to address the ethanol <b>withdrawal</b> conditions.
+NPY	drug	opioid	19804558	In an initial step, reverse transcription polymerase chain reaction (RT PCR) provided the first evidence that transcripts of three different <b>opioid</b> receptors (MOR, DOR, KOR), as well as the <strong>neuropeptide Y</strong> 5 receptor (NPY5R), leptin receptor (LEPR) and proopiomelanocortin (POMC), are expressed in both the porcine amygdala and hypothalamus.
+NPY	drug	alcohol	19756388	Study of the downstream effectors of CREB have identified several important CREB related genes, such as <strong>neuropeptide Y</strong>, brain derived neurotrophic factor, activity regulated cytoskeleton associated protein, and corticotrophin releasing factor, that may play a crucial role in the behavioral effects of <b>ethanol</b> and molecular changes in the specific neurocircuitry that underlie both <b>alcohol</b> addiction and a genetic predisposition to <b>alcoholism</b>.
+NPY	addiction	addiction	19756388	Study of the downstream effectors of CREB have identified several important CREB related genes, such as <strong>neuropeptide Y</strong>, brain derived neurotrophic factor, activity regulated cytoskeleton associated protein, and corticotrophin releasing factor, that may play a crucial role in the behavioral effects of ethanol and molecular changes in the specific neurocircuitry that underlie both alcohol <b>addiction</b> and a genetic predisposition to alcoholism.
+NPY	drug	opioid	19591065	To investigate alterations in cortisol, adrenocorticotrophic hormone (ACTH), beta endorphin (beta EP), leptin, and neuropeptide Y (<strong>NPY</strong>) during the first month of abstinence in <b>heroin</b> addicts.
+NPY	drug	opioid	19591065	To investigate alterations in cortisol, adrenocorticotrophic hormone (ACTH), beta endorphin (beta EP), leptin, and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) during the first month of abstinence in <b>heroin</b> addicts.
+NPY	drug	opioid	19591065	A positive correlation between cortisol level and <b>heroin</b> craving, anxiety, and depression was observed, while a negative correlation was observed between beta EP level and craving and anxiety and between leptin and depression and <strong>NPY</strong> and anxiety.
+NPY	addiction	relapse	19591065	A positive correlation between cortisol level and heroin <b>craving</b>, anxiety, and depression was observed, while a negative correlation was observed between beta EP level and <b>craving</b> and anxiety and between leptin and depression and <strong>NPY</strong> and anxiety.
+NPY	drug	amphetamine	19566775	Association between <strong>neuropeptide Y</strong> gene and its receptor Y1 gene and <b>methamphetamine</b> dependence.
+NPY	addiction	dependence	19566775	Association between <strong>neuropeptide Y</strong> gene and its receptor Y1 gene and methamphetamine <b>dependence</b>.
+NPY	drug	alcohol	19566775	Several lines of evidence suggest a possible involvement of the <strong>NPY</strong> system in the physiological effects of several classes of abused substances including <b>alcohol</b>, phencyclidine, cocaine, and marijuana and in endogenous psychosis.
+NPY	drug	cannabinoid	19566775	Several lines of evidence suggest a possible involvement of the <strong>NPY</strong> system in the physiological effects of several classes of abused substances including alcohol, phencyclidine, cocaine, and <b>marijuana</b> and in endogenous psychosis.
+NPY	drug	cocaine	19566775	Several lines of evidence suggest a possible involvement of the <strong>NPY</strong> system in the physiological effects of several classes of abused substances including alcohol, phencyclidine, <b>cocaine</b>, and marijuana and in endogenous psychosis.
+NPY	drug	amphetamine	19566775	Accordingly, it was hypothesized that the <strong>NPY</strong> system may also be involved in <b>methamphetamine</b> dependence or psychosis.
+NPY	addiction	dependence	19566775	Accordingly, it was hypothesized that the <strong>NPY</strong> system may also be involved in methamphetamine <b>dependence</b> or psychosis.
+NPY	drug	amphetamine	19566775	The single nucleotide polymorphisms rs16147 of the <strong>NPY</strong> gene ( 485C>T) and rs7687423 of the <strong>NPY</strong> receptor Y1 (NPY1R) gene were analyzed in 222 patients with <b>methamphetamine</b> dependence and psychosis and 288 age  and gender matched controls.
+NPY	addiction	dependence	19566775	The single nucleotide polymorphisms rs16147 of the <strong>NPY</strong> gene ( 485C>T) and rs7687423 of the <strong>NPY</strong> receptor Y1 (NPY1R) gene were analyzed in 222 patients with methamphetamine <b>dependence</b> and psychosis and 288 age  and gender matched controls.
+NPY	drug	amphetamine	19566775	Genotypic distribution of the NPY1R gene showed a significant association with <b>methamphetamine</b> dependence and psychosis (P = 0.04), whereas the <strong>NPY</strong> gene had no significant association with them.
+NPY	addiction	dependence	19566775	Genotypic distribution of the NPY1R gene showed a significant association with methamphetamine <b>dependence</b> and psychosis (P = 0.04), whereas the <strong>NPY</strong> gene had no significant association with them.
+NPY	drug	amphetamine	19566775	It is possible that genetic variants of the NPY1R gene affect the <strong>NPY</strong> <strong>NPY</strong> receptor type Y1 signaling system in the brain, which may result in susceptibility to <b>methamphetamine</b> dependence or the development of <b>methamphetamine</b> psychosis, but the present findings need to be confirmed on replication.
+NPY	addiction	dependence	19566775	It is possible that genetic variants of the NPY1R gene affect the <strong>NPY</strong> <strong>NPY</strong> receptor type Y1 signaling system in the brain, which may result in susceptibility to methamphetamine <b>dependence</b> or the development of methamphetamine psychosis, but the present findings need to be confirmed on replication.
+NPY	drug	opioid	19556004	Involvement of <strong>neuropeptide Y</strong> in the acute, chronic and withdrawal responses of <b>morphine</b> in nociception in neuropathic rats: behavioral and neuroanatomical correlates.
+NPY	addiction	withdrawal	19556004	Involvement of <strong>neuropeptide Y</strong> in the acute, chronic and <b>withdrawal</b> responses of morphine in nociception in neuropathic rats: behavioral and neuroanatomical correlates.
+NPY	drug	opioid	19556004	Furthermore, <b>opioid</b> antagonist <b>naloxone</b> attenuated the antinociceptive effect of neuropeptide Y (<strong>NPY</strong>).
+NPY	drug	opioid	19556004	Furthermore, <b>opioid</b> antagonist <b>naloxone</b> attenuated the antinociceptive effect of <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	opioid	19556004	The present study investigated the role of <strong>NPY</strong> and <strong>NPY</strong> Y1/Y5 receptors in acute and chronic actions of <b>morphine</b> in neuropathic rats using thermal paw withdrawal test and immunocytochemistry.
+NPY	addiction	withdrawal	19556004	The present study investigated the role of <strong>NPY</strong> and <strong>NPY</strong> Y1/Y5 receptors in acute and chronic actions of morphine in neuropathic rats using thermal paw <b>withdrawal</b> test and immunocytochemistry.
+NPY	drug	opioid	19556004	In acute study, intracerebroventricular (icv) administration of <b>morphine</b>, <strong>NPY</strong> or <strong>NPY</strong> Y1/Y5 receptors agonist [Leu(31),Pro(34)] <strong>NPY</strong> produced antinociception, whereas selective <strong>NPY</strong> Y1 receptors antagonist BIBP3226 caused hyperalgesia.
+NPY	drug	opioid	19556004	While <strong>NPY</strong> or [Leu(31),Pro(34)] <strong>NPY</strong> potentiated, BIBP3226 attenuated <b>morphine</b> induced antinociception.
+NPY	addiction	withdrawal	19556004	However, co administration of <strong>NPY</strong> or [Leu(31),Pro(34)] <strong>NPY</strong> prevented the development of tolerance and <b>withdrawal</b> hyperalgesia.
+NPY	drug	opioid	19556004	While chronic <b>morphine</b> treatment significantly reduced <strong>NPY</strong> ir fibers in VLPAG and DRD, <b>morphine</b> withdrawal triggered significant augmentation in <strong>NPY</strong> immunoreactivity in the VLPAG.
+NPY	addiction	withdrawal	19556004	While chronic morphine treatment significantly reduced <strong>NPY</strong> ir fibers in VLPAG and DRD, morphine <b>withdrawal</b> triggered significant augmentation in <strong>NPY</strong> immunoreactivity in the VLPAG.
+NPY	drug	opioid	19556004	<strong>NPY</strong> immunoreactivity profile of LC remained unchanged in all the <b>morphine</b> treatment conditions.
+NPY	drug	opioid	19556004	<strong>NPY</strong>, perhaps acting via Y1/Y5 receptors, might profoundly influence the processing of NP information and interact with the endogenous <b>opioid</b> system primarily within the framework of the VLPAG.
+NPY	drug	nicotine	19285064	Involvement of <strong>neuropeptide Y</strong> Y(1) receptors in the acute, chronic and withdrawal effects of <b>nicotine</b> on feeding and body weight in rats.
+NPY	addiction	withdrawal	19285064	Involvement of <strong>neuropeptide Y</strong> Y(1) receptors in the acute, chronic and <b>withdrawal</b> effects of nicotine on feeding and body weight in rats.
+NPY	drug	nicotine	19285064	We investigated the role of <strong>neuropeptide Y</strong> Y(1) receptors in acute, chronic and withdrawal effects of <b>nicotine</b> with reference to feeding behavior.
+NPY	addiction	withdrawal	19285064	We investigated the role of <strong>neuropeptide Y</strong> Y(1) receptors in acute, chronic and <b>withdrawal</b> effects of nicotine with reference to feeding behavior.
+NPY	drug	nicotine	19285064	Rats were administered with <b>nicotine</b>, <strong>neuropeptide Y</strong>, <strong>neuropeptide Y</strong> Y(1) receptor agonist [Leu(31),Pro(34)]<strong>neuropeptide Y</strong> or antagonist BIBP3226 (N(2) diphenylacetyl) N [(4 hydroxy phenyl) methyl] D arginine amide) via i.c.v.
+NPY	drug	nicotine	19285064	While acute <b>nicotine</b> or BIBP3226 reduced food intake, increase was observed following <strong>neuropeptide Y</strong> or [Leu(31),Pro(34)]<strong>neuropeptide Y</strong>. <b>Nicotine</b> induced anorexia was antagonized by pre treatment with <strong>neuropeptide Y</strong> or [Leu(31),Pro(34)]<strong>neuropeptide Y</strong>, and potentiated by BIBP3226.
+NPY	drug	nicotine	19285064	Additionally, immunocytochemical profile of <strong>neuropeptide Y</strong> in the hypothalamus was studied following differential <b>nicotine</b> treatments.
+NPY	drug	nicotine	19285064	Acute <b>nicotine</b> treatment dramatically reduced <strong>neuropeptide Y</strong> immunoreactivity in the arcuate and paraventricular nuclei.
+NPY	drug	nicotine	19285064	Chronic <b>nicotine</b> administration decreased <strong>neuropeptide Y</strong> immunoreactivity in arcuate, but not in paraventricular nucleus.
+NPY	drug	nicotine	19285064	<b>Nicotine</b> withdrawal resulted in significant increase in the <strong>neuropeptide Y</strong> immunoreactivity in both the nuclei.
+NPY	addiction	withdrawal	19285064	Nicotine <b>withdrawal</b> resulted in significant increase in the <strong>neuropeptide Y</strong> immunoreactivity in both the nuclei.
+NPY	drug	nicotine	19285064	The results suggest that <strong>neuropeptide Y</strong> in the arcuate and paraventricular nuclei of hypothalamus may be involved in acute, chronic and withdrawal effects of <b>nicotine</b> on the feeding behavior, possibly via <strong>neuropeptide Y</strong> Y(1) receptors.
+NPY	addiction	withdrawal	19285064	The results suggest that <strong>neuropeptide Y</strong> in the arcuate and paraventricular nuclei of hypothalamus may be involved in acute, chronic and <b>withdrawal</b> effects of nicotine on the feeding behavior, possibly via <strong>neuropeptide Y</strong> Y(1) receptors.
+NPY	drug	alcohol	19267419	Complex plastic changes in the <strong>neuropeptide Y</strong> system during <b>ethanol</b> intoxication and withdrawal in the rat brain.
+NPY	addiction	intoxication	19267419	Complex plastic changes in the <strong>neuropeptide Y</strong> system during ethanol <b>intoxication</b> and withdrawal in the rat brain.
+NPY	addiction	withdrawal	19267419	Complex plastic changes in the <strong>neuropeptide Y</strong> system during ethanol intoxication and <b>withdrawal</b> in the rat brain.
+NPY	drug	alcohol	19267419	Previous studies show that chronic <b>ethanol</b> treatment induces prominent changes in brain neuropeptide Y (<strong>NPY</strong>).
+NPY	drug	alcohol	19267419	Previous studies show that chronic <b>ethanol</b> treatment induces prominent changes in brain <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	alcohol	19267419	The purpose of the present study was to explore <b>ethanol</b> effects at a deeper <strong>NPY</strong> system level, measuring expression of <strong>NPY</strong> and its receptors (Y1, Y2, Y5) as well as <strong>NPY</strong> receptor binding and <strong>NPY</strong> stimulated [(35)S]GTPgammaS functional binding.
+NPY	drug	alcohol	19267419	Rats received intragastric <b>ethanol</b> repeatedly for 4 days, and the <strong>NPY</strong> system was studied in the hippocampal dentate gyrus (DG), CA3, CA1, and piriform cortex (PirCx) and neocortex (NeoCx) during intoxication, peak withdrawal (16 hr), late withdrawal (3 days), and 1 week after last <b>ethanol</b> administration.
+NPY	addiction	intoxication	19267419	Rats received intragastric ethanol repeatedly for 4 days, and the <strong>NPY</strong> system was studied in the hippocampal dentate gyrus (DG), CA3, CA1, and piriform cortex (PirCx) and neocortex (NeoCx) during <b>intoxication</b>, peak withdrawal (16 hr), late withdrawal (3 days), and 1 week after last ethanol administration.
+NPY	addiction	withdrawal	19267419	Rats received intragastric ethanol repeatedly for 4 days, and the <strong>NPY</strong> system was studied in the hippocampal dentate gyrus (DG), CA3, CA1, and piriform cortex (PirCx) and neocortex (NeoCx) during intoxication, peak <b>withdrawal</b> (16 hr), late <b>withdrawal</b> (3 days), and 1 week after last ethanol administration.
+NPY	addiction	intoxication	19267419	<strong>NPY</strong> mRNA levels decreased during <b>intoxication</b> and at 16 hr in hippocampal regions but increased in the PirCx and NeoCx at 16 hr.
+NPY	addiction	intoxication	19267419	Conversely, increases in <strong>NPY</strong> receptor binding occurred in hippocampal regions during <b>intoxication</b> and in functional binding in the DG and NeoCx during <b>intoxication</b> and at 16 hr and in PirCx during <b>intoxication</b> and at 1 week.
+NPY	drug	alcohol	19267419	Thus this study shows that <b>ethanol</b> intoxication and withdrawal induce complex plastic changes in the <strong>NPY</strong> system, with decreased/increased gene expression or binding occurring in a time  and region specific manner.
+NPY	addiction	intoxication	19267419	Thus this study shows that ethanol <b>intoxication</b> and withdrawal induce complex plastic changes in the <strong>NPY</strong> system, with decreased/increased gene expression or binding occurring in a time  and region specific manner.
+NPY	addiction	withdrawal	19267419	Thus this study shows that ethanol intoxication and <b>withdrawal</b> induce complex plastic changes in the <strong>NPY</strong> system, with decreased/increased gene expression or binding occurring in a time  and region specific manner.
+NPY	drug	opioid	19149764	In this respect, while serotonin, dopamine and prostaglandin promote the ingestion of food, by contrast, <strong>neuropeptide Y</strong>, norepinephrine, GABA and <b>opioid</b> peptides inhibit food ingestion, thus, causing the occurence of ED.
+NPY	drug	benzodiazepine	19101875	Also alterations in the expression of neuropeptides like Corticotropin Releasing Hormone and <strong>Neuropeptide Y</strong> are thought to be involved in the development of <b>benzodiazepine</b> dependence.
+NPY	addiction	dependence	19101875	Also alterations in the expression of neuropeptides like Corticotropin Releasing Hormone and <strong>Neuropeptide Y</strong> are thought to be involved in the development of benzodiazepine <b>dependence</b>.
+NPY	drug	cocaine	19063928	<strong>Neuropeptide Y</strong> augments <b>cocaine</b> self administration and <b>cocaine</b> induced hyperlocomotion in rats.
+NPY	drug	opioid	19063928	We have recently demonstrated that <strong>NPY</strong> injections augmented on going <b>heroin</b> self administration and induced a reinstatement of <b>heroin</b> seeking.
+NPY	addiction	relapse	19063928	We have recently demonstrated that <strong>NPY</strong> injections augmented on going heroin self administration and induced a <b>reinstatement</b> of heroin <b>seeking</b>.
+NPY	drug	cocaine	19063928	The present study sought to support and expand our previous finding on <strong>NPY</strong>'s role in addictive drugs related behaviors by examining the effects of <strong>NPY</strong> on <b>cocaine</b> induced locomotor hyperactivity and <b>cocaine</b> self administration.
+NPY	addiction	addiction	19063928	The present study sought to support and expand our previous finding on <strong>NPY</strong>'s role in <b>addictive</b> drugs related behaviors by examining the effects of <strong>NPY</strong> on cocaine induced locomotor hyperactivity and cocaine self administration.
+NPY	drug	cocaine	19063928	In Experiment 1, rats received <strong>NPY</strong> injections (0.0, 2.5, 5.0microg/rat, ICV), followed by <b>cocaine</b> administration (0.0, 1.0, 5.0, and 10.0mg/kg, IP) and their locomotor activity was monitored over 90min.
+NPY	drug	cocaine	19063928	Results revealed that <strong>NPY</strong> injections augmented <b>cocaine</b> induced hyperactivity and moderately increased <b>cocaine</b> self administration.
+NPY	drug	alcohol	18835592	<strong>Neuropeptide Y</strong> suppresses <b>ethanol</b> drinking in <b>ethanol</b> abstinent, but not non <b>ethanol</b> abstinent, Wistar rats.
+NPY	drug	alcohol	18835592	In outbred rats, increases in brain neuropeptide Y (<strong>NPY</strong>) activity suppress <b>ethanol</b> consumption in a variety of access conditions, but only following a history of <b>ethanol</b> dependence.
+NPY	addiction	dependence	18835592	In outbred rats, increases in brain neuropeptide Y (<strong>NPY</strong>) activity suppress ethanol consumption in a variety of access conditions, but only following a history of ethanol <b>dependence</b>.
+NPY	drug	alcohol	18835592	In outbred rats, increases in brain <strong>neuropeptide Y</strong> (<strong>NPY</strong>) activity suppress <b>ethanol</b> consumption in a variety of access conditions, but only following a history of <b>ethanol</b> dependence.
+NPY	addiction	dependence	18835592	In outbred rats, increases in brain <strong>neuropeptide Y</strong> (<strong>NPY</strong>) activity suppress ethanol consumption in a variety of access conditions, but only following a history of ethanol <b>dependence</b>.
+NPY	drug	alcohol	18835592	<strong>NPY</strong> reliably suppresses <b>ethanol</b> drinking in <b>alcohol</b> preferring rats, and this effect is augmented following a period of <b>ethanol</b> abstinence.
+NPY	drug	alcohol	18835592	The purpose of this experiment was to examine the effects of <strong>NPY</strong> on two bottle choice <b>ethanol</b> drinking and feeding in Wistar rats that had undergone chronic <b>ethanol</b> vapor exposure, cycles of <b>ethanol</b> abstinence, or both.
+NPY	drug	alcohol	18835592	Rats were infused intracerebroventricularly with one of four <strong>NPY</strong> doses (0.0, 2.5, 5.0, or 10.0 microg) following the <b>ethanol</b> exposure patterns described above, and tested for <b>ethanol</b> drinking and feeding in a two bottle choice situation.
+NPY	drug	alcohol	18835592	<strong>NPY</strong> dose dependently increased food intake regardless of <b>ethanol</b> exposure history, but suppressed <b>ethanol</b> drinking only in rats that underwent cycles of <b>ethanol</b> access and <b>ethanol</b> abstinence.
+NPY	drug	alcohol	18835592	These results support the notion that dysregulation of brain <strong>NPY</strong> systems during chronic intermittent <b>ethanol</b> exposure is important in the motivational drive for subsequent relapse to <b>ethanol</b> drinking.
+NPY	addiction	relapse	18835592	These results support the notion that dysregulation of brain <strong>NPY</strong> systems during chronic intermittent ethanol exposure is important in the motivational drive for subsequent <b>relapse</b> to ethanol drinking.
+NPY	drug	alcohol	18828811	<strong>Neuropeptide Y</strong> receptor genes are associated with <b>alcohol</b> dependence, <b>alcohol</b> withdrawal phenotypes, and cocaine dependence.
+NPY	drug	cocaine	18828811	<strong>Neuropeptide Y</strong> receptor genes are associated with alcohol dependence, alcohol withdrawal phenotypes, and <b>cocaine</b> dependence.
+NPY	addiction	dependence	18828811	<strong>Neuropeptide Y</strong> receptor genes are associated with alcohol <b>dependence</b>, alcohol withdrawal phenotypes, and cocaine <b>dependence</b>.
+NPY	addiction	withdrawal	18828811	<strong>Neuropeptide Y</strong> receptor genes are associated with alcohol dependence, alcohol <b>withdrawal</b> phenotypes, and cocaine dependence.
+NPY	drug	alcohol	18828811	Several lines of evidence in both human and animal studies suggest that variation in neuropeptide Y (<strong>NPY</strong>) or its receptor genes (NPY1R, NPY2R and NPY5R) is associated with <b>alcohol</b> dependence as well as <b>alcohol</b> withdrawal symptoms.
+NPY	addiction	dependence	18828811	Several lines of evidence in both human and animal studies suggest that variation in neuropeptide Y (<strong>NPY</strong>) or its receptor genes (NPY1R, NPY2R and NPY5R) is associated with alcohol <b>dependence</b> as well as alcohol withdrawal symptoms.
+NPY	addiction	withdrawal	18828811	Several lines of evidence in both human and animal studies suggest that variation in neuropeptide Y (<strong>NPY</strong>) or its receptor genes (NPY1R, NPY2R and NPY5R) is associated with alcohol dependence as well as alcohol <b>withdrawal</b> symptoms.
+NPY	drug	alcohol	18828811	Several lines of evidence in both human and animal studies suggest that variation in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) or its receptor genes (NPY1R, NPY2R and NPY5R) is associated with <b>alcohol</b> dependence as well as <b>alcohol</b> withdrawal symptoms.
+NPY	addiction	dependence	18828811	Several lines of evidence in both human and animal studies suggest that variation in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) or its receptor genes (NPY1R, NPY2R and NPY5R) is associated with alcohol <b>dependence</b> as well as alcohol withdrawal symptoms.
+NPY	addiction	withdrawal	18828811	Several lines of evidence in both human and animal studies suggest that variation in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) or its receptor genes (NPY1R, NPY2R and NPY5R) is associated with alcohol dependence as well as alcohol <b>withdrawal</b> symptoms.
+NPY	drug	cocaine	18828811	Additional studies suggest that <b>cocaine</b> may affect <strong>NPY</strong> expression.
+NPY	drug	alcohol	18828811	A total of 39 single nucleotide polymorphisms (SNPs) were genotyped across <strong>NPY</strong> and its 3 receptor genes in a sample of 1,923 subjects from 219 multiplex <b>alcoholic</b> families of European American descent recruited as part of the Collaborative Studies on the Genetics of <b>Alcoholism</b> (COGA) study.
+NPY	drug	alcohol	18828811	These results indicate that sequence variations in <strong>NPY</strong> receptor genes are associated with <b>alcohol</b> dependence, particularly a severe subtype of <b>alcohol</b> dependence characterized by withdrawal symptoms, comorbid <b>alcohol</b> and cocaine dependence, and cocaine dependence.
+NPY	drug	cocaine	18828811	These results indicate that sequence variations in <strong>NPY</strong> receptor genes are associated with alcohol dependence, particularly a severe subtype of alcohol dependence characterized by withdrawal symptoms, comorbid alcohol and <b>cocaine</b> dependence, and <b>cocaine</b> dependence.
+NPY	addiction	dependence	18828811	These results indicate that sequence variations in <strong>NPY</strong> receptor genes are associated with alcohol <b>dependence</b>, particularly a severe subtype of alcohol <b>dependence</b> characterized by withdrawal symptoms, comorbid alcohol and cocaine <b>dependence</b>, and cocaine <b>dependence</b>.
+NPY	addiction	withdrawal	18828811	These results indicate that sequence variations in <strong>NPY</strong> receptor genes are associated with alcohol dependence, particularly a severe subtype of alcohol dependence characterized by <b>withdrawal</b> symptoms, comorbid alcohol and cocaine dependence, and cocaine dependence.
+NPY	drug	amphetamine	30290413	The best characterized pathways are the orexigenic <strong>neuropeptide Y</strong>/Agouti related protein and the anorexigenic pro opiomelanocortin/cocaine  and <b>amphetamine</b> related transcript neurons in the arcuate nucleus of the hypothalamus.
+NPY	drug	cocaine	30290413	The best characterized pathways are the orexigenic <strong>neuropeptide Y</strong>/Agouti related protein and the anorexigenic pro opiomelanocortin/<b>cocaine</b>  and amphetamine related transcript neurons in the arcuate nucleus of the hypothalamus.
+NPY	addiction	withdrawal	18725236	Other components of brain stress systems in the extended amygdala that interact with CRF and may contribute to the negative motivational state of <b>withdrawal</b> include norepinephrine, dynorphin, and <strong>neuropeptide Y</strong>.
+NPY	drug	alcohol	18675322	A protein kinase C activity localized to <strong>neuropeptide Y</strong> like neurons mediates <b>ethanol</b> intoxication in Drosophila melanogaster.
+NPY	addiction	intoxication	18675322	A protein kinase C activity localized to <strong>neuropeptide Y</strong> like neurons mediates ethanol <b>intoxication</b> in Drosophila melanogaster.
+NPY	drug	alcohol	18675322	Neuropeptide Y (<strong>NPY</strong>) regulates acute <b>ethanol</b> sensitivity and voluntary <b>alcohol</b> consumption in rodents.
+NPY	drug	alcohol	18675322	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) regulates acute <b>ethanol</b> sensitivity and voluntary <b>alcohol</b> consumption in rodents.
+NPY	drug	alcohol	18675322	In Drosophila melanogaster, <strong>NPY</strong> like neuropeptide F (NPF) and its receptor NPFR1 display a parallel function, suggesting that an evolutionarily conserved mechanism may underlie similar behavioral effects of <b>ethanol</b> in diverse organisms.
+NPY	drug	alcohol	18675322	These findings reveal an uncharacterized role of PKC in <strong>NPY</strong>/NPF mediated acute <b>ethanol</b> sensitivity in flies and possibly mammals.
+NPY	drug	opioid	18639589	Food deprivation like effects of <strong>neuropeptide Y</strong> on <b>heroin</b> self administration and reinstatement of <b>heroin</b> seeking in rats.
+NPY	addiction	relapse	18639589	Food deprivation like effects of <strong>neuropeptide Y</strong> on heroin self administration and <b>reinstatement</b> of heroin <b>seeking</b> in rats.
+NPY	drug	opioid	18639589	Here we examined the effect of acute <strong>NPY</strong> administration on the rate of <b>heroin</b> self administration and the reinstatement of extinguished <b>heroin</b> seeking behavior.
+NPY	addiction	relapse	18639589	Here we examined the effect of acute <strong>NPY</strong> administration on the rate of heroin self administration and the <b>reinstatement</b> of extinguished heroin <b>seeking</b> behavior.
+NPY	drug	opioid	18639589	<b>Heroin</b> intake (0.05mg/kg/infusion) was tested using a self administration procedure (FR 1), 10 min post <strong>NPY</strong> injections (0.0, 4.0, and 10microg/rat, ICV).
+NPY	drug	opioid	18639589	In a different group of rats, <strong>NPY</strong> induced reinstatement (0.0, 4.0, and 10microg/rat, ICV) of extinguished <b>heroin</b> seeking was assessed.
+NPY	addiction	relapse	18639589	In a different group of rats, <strong>NPY</strong> induced <b>reinstatement</b> (0.0, 4.0, and 10microg/rat, ICV) of extinguished heroin <b>seeking</b> was assessed.
+NPY	drug	opioid	18639589	<strong>NPY</strong> injections increased on going <b>heroin</b> self administration, and induced a reinstatement of extinguished <b>heroin</b> seeking behavior.
+NPY	addiction	relapse	18639589	<strong>NPY</strong> injections increased on going heroin self administration, and induced a <b>reinstatement</b> of extinguished heroin <b>seeking</b> behavior.
+NPY	addiction	reward	18639589	These findings suggest that <strong>NPY</strong> can modulate the rewarding and conditioned <b>reinforcing</b> effects of drugs of abuse.
+NPY	drug	alcohol	18501411	<strong>Neuropeptide Y</strong> in the central nucleus of the amygdala suppresses dependence induced increases in <b>alcohol</b> drinking.
+NPY	addiction	dependence	18501411	<strong>Neuropeptide Y</strong> in the central nucleus of the amygdala suppresses <b>dependence</b> induced increases in alcohol drinking.
+NPY	drug	alcohol	18501411	The anxiolytic effects of neuropeptide Y (<strong>NPY</strong>) are mediated in part by the central nucleus of the amygdala (CeA), a brain region involved in the regulation of <b>alcohol</b> drinking behaviors.
+NPY	drug	alcohol	18501411	The anxiolytic effects of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) are mediated in part by the central nucleus of the amygdala (CeA), a brain region involved in the regulation of <b>alcohol</b> drinking behaviors.
+NPY	drug	alcohol	18501411	Centrally administered <strong>NPY</strong> suppresses <b>alcohol</b> drinking in subpopulations of rats vulnerable to the development of high <b>alcohol</b> drinking behavior.
+NPY	drug	alcohol	18501411	The purpose of the current study was to determine the role of <strong>NPY</strong> in the CeA on elevated <b>alcohol</b> drinking produced by <b>alcohol</b> dependence.
+NPY	addiction	dependence	18501411	The purpose of the current study was to determine the role of <strong>NPY</strong> in the CeA on elevated alcohol drinking produced by alcohol <b>dependence</b>.
+NPY	drug	alcohol	18501411	Rats were then infused with 4 <strong>NPY</strong> doses (0.0, 0.25, 0.5, 1.0 microg/0.5 microl aCSF) in a within subjects Latin square design during acute withdrawal and tested for operant <b>alcohol</b> responding 30 min later.
+NPY	addiction	reward	18501411	Rats were then infused with 4 <strong>NPY</strong> doses (0.0, 0.25, 0.5, 1.0 microg/0.5 microl aCSF) in a within subjects Latin square design during acute withdrawal and tested for <b>operant</b> alcohol responding 30 min later.
+NPY	addiction	withdrawal	18501411	Rats were then infused with 4 <strong>NPY</strong> doses (0.0, 0.25, 0.5, 1.0 microg/0.5 microl aCSF) in a within subjects Latin square design during acute <b>withdrawal</b> and tested for operant alcohol responding 30 min later.
+NPY	drug	alcohol	18501411	<b>Alcohol</b> dependent rats exhibited higher operant <b>alcohol</b> responding than non dependent rats when infused with vehicle, but responding was similar in the two groups following infusion of all doses of <strong>NPY</strong>.
+NPY	addiction	reward	18501411	Alcohol dependent rats exhibited higher <b>operant</b> alcohol responding than non dependent rats when infused with vehicle, but responding was similar in the two groups following infusion of all doses of <strong>NPY</strong>.
+NPY	drug	alcohol	18501411	These results indicate that <strong>NPY</strong> abolishes dependence induced elevations in <b>alcohol</b> drinking and implicate the recruitment of limbic <strong>NPY</strong> systems in the motivational drive to consume <b>alcohol</b> following the transition to dependence.
+NPY	addiction	dependence	18501411	These results indicate that <strong>NPY</strong> abolishes <b>dependence</b> induced elevations in alcohol drinking and implicate the recruitment of limbic <strong>NPY</strong> systems in the motivational drive to consume alcohol following the transition to <b>dependence</b>.
+NPY	drug	alcohol	18499241	<strong>Neuropeptide Y</strong> administration into the amygdala suppresses <b>ethanol</b> drinking in <b>alcohol</b> preferring (P) rats following multiple deprivations.
+NPY	drug	alcohol	18499241	The present experiment examines the effects of <strong>NPY</strong> administered into the amygdala on <b>ethanol</b> drinking by <b>alcohol</b> preferring P rats following long term continuous <b>ethanol</b> access, with and without multiple periods of imposed <b>ethanol</b> abstinence.
+NPY	drug	alcohol	18499241	Immediately prior to the second <b>ethanol</b> re exposure, 4 groups of rats received bilateral infusions <strong>NPY</strong> (0.25, 0.5, 1.0 microg) or artificial cerebrospinal fluid (aCSF) into the amygdala.
+NPY	drug	alcohol	18499241	Two additional groups were given uninterrupted <b>ethanol</b> access and were infused with a single <strong>NPY</strong> dose (1.0 microg) or aCSF.
+NPY	drug	alcohol	18499241	The highest <strong>NPY</strong> dose (1.0 microg) suppressed <b>ethanol</b> intake for 24 h in rats with a history of <b>ethanol</b> abstinence (i.e.
+NPY	drug	alcohol	18499241	These results suggest that the amygdala mediates the suppressive effects of centrally administered <strong>NPY</strong> on <b>ethanol</b> drinking, and that <strong>NPY</strong> may block relapse like drinking by opposing the anxiogenic effects of <b>ethanol</b> abstinence.
+NPY	addiction	relapse	18499241	These results suggest that the amygdala mediates the suppressive effects of centrally administered <strong>NPY</strong> on ethanol drinking, and that <strong>NPY</strong> may block <b>relapse</b> like drinking by opposing the anxiogenic effects of ethanol abstinence.
+NPY	drug	nicotine	18468678	Effects of <strong>NPY</strong> and the specific Y1 receptor agonist [D His(26)] <strong>NPY</strong> on the deficit in brain reward function and somatic signs associated with <b>nicotine</b> withdrawal in rats.
+NPY	addiction	reward	18468678	Effects of <strong>NPY</strong> and the specific Y1 receptor agonist [D His(26)] <strong>NPY</strong> on the deficit in brain <b>reward</b> function and somatic signs associated with nicotine withdrawal in rats.
+NPY	addiction	withdrawal	18468678	Effects of <strong>NPY</strong> and the specific Y1 receptor agonist [D His(26)] <strong>NPY</strong> on the deficit in brain reward function and somatic signs associated with nicotine <b>withdrawal</b> in rats.
+NPY	addiction	withdrawal	18468678	Previous research suggests that Neuropeptide Y (<strong>NPY</strong>) and Y1 receptor agonists attenuate negative affective states and somatic <b>withdrawal</b> signs.
+NPY	addiction	withdrawal	18468678	Previous research suggests that <strong>Neuropeptide Y</strong> (<strong>NPY</strong>) and Y1 receptor agonists attenuate negative affective states and somatic <b>withdrawal</b> signs.
+NPY	drug	nicotine	18468678	The aim of the present experiments was to investigate the effects of <strong>NPY</strong> and the specific Y1 receptor agonist [D His(26)] <strong>NPY</strong> on the deficit in brain reward function and somatic signs associated with <b>nicotine</b> withdrawal in rats.
+NPY	addiction	reward	18468678	The aim of the present experiments was to investigate the effects of <strong>NPY</strong> and the specific Y1 receptor agonist [D His(26)] <strong>NPY</strong> on the deficit in brain <b>reward</b> function and somatic signs associated with nicotine withdrawal in rats.
+NPY	addiction	withdrawal	18468678	The aim of the present experiments was to investigate the effects of <strong>NPY</strong> and the specific Y1 receptor agonist [D His(26)] <strong>NPY</strong> on the deficit in brain reward function and somatic signs associated with nicotine <b>withdrawal</b> in rats.
+NPY	drug	nicotine	18468678	In the first experiment, <strong>NPY</strong> did not prevent the elevations in brain reward thresholds associated with precipitated <b>nicotine</b> withdrawal and elevated the brain reward thresholds of the saline treated control rats.
+NPY	addiction	reward	18468678	In the first experiment, <strong>NPY</strong> did not prevent the elevations in brain <b>reward</b> thresholds associated with precipitated nicotine withdrawal and elevated the brain <b>reward</b> thresholds of the saline treated control rats.
+NPY	addiction	withdrawal	18468678	In the first experiment, <strong>NPY</strong> did not prevent the elevations in brain reward thresholds associated with precipitated nicotine <b>withdrawal</b> and elevated the brain reward thresholds of the saline treated control rats.
+NPY	drug	nicotine	18468678	Similar to <strong>NPY</strong>, [D His(26)] <strong>NPY</strong> did not prevent the elevations in brain reward thresholds associated with precipitated <b>nicotine</b> withdrawal and elevated the brain reward thresholds of the saline treated control rats.
+NPY	addiction	reward	18468678	Similar to <strong>NPY</strong>, [D His(26)] <strong>NPY</strong> did not prevent the elevations in brain <b>reward</b> thresholds associated with precipitated nicotine withdrawal and elevated the brain <b>reward</b> thresholds of the saline treated control rats.
+NPY	addiction	withdrawal	18468678	Similar to <strong>NPY</strong>, [D His(26)] <strong>NPY</strong> did not prevent the elevations in brain reward thresholds associated with precipitated nicotine <b>withdrawal</b> and elevated the brain reward thresholds of the saline treated control rats.
+NPY	addiction	reward	18468678	In a separate experiment, it was demonstrated that the specific Y1 receptor antagonist BIBP 3226 prevented the <strong>NPY</strong> induced elevations in brain <b>reward</b> thresholds.
+NPY	drug	nicotine	18468678	<strong>NPY</strong> attenuated the overall somatic signs associated with precipitated <b>nicotine</b> withdrawal.
+NPY	addiction	withdrawal	18468678	<strong>NPY</strong> attenuated the overall somatic signs associated with precipitated nicotine <b>withdrawal</b>.
+NPY	drug	nicotine	18468678	[D His(26)] <strong>NPY</strong> did not affect the overall somatic signs associated with precipitated <b>nicotine</b> withdrawal, but decreased the number of abdominal constrictions.
+NPY	addiction	withdrawal	18468678	[D His(26)] <strong>NPY</strong> did not affect the overall somatic signs associated with precipitated nicotine <b>withdrawal</b>, but decreased the number of abdominal constrictions.
+NPY	drug	nicotine	18468678	Both <strong>NPY</strong> and [D His(26)] <strong>NPY</strong> attenuated the overall somatic signs associated with spontaneous <b>nicotine</b> withdrawal.
+NPY	addiction	withdrawal	18468678	Both <strong>NPY</strong> and [D His(26)] <strong>NPY</strong> attenuated the overall somatic signs associated with spontaneous nicotine <b>withdrawal</b>.
+NPY	drug	nicotine	18468678	These findings indicate that <strong>NPY</strong> and [D His(26)] <strong>NPY</strong> attenuate somatic <b>nicotine</b> withdrawal signs, but do not prevent the deficit in brain reward function associated with precipitated <b>nicotine</b> withdrawal.
+NPY	addiction	reward	18468678	These findings indicate that <strong>NPY</strong> and [D His(26)] <strong>NPY</strong> attenuate somatic nicotine withdrawal signs, but do not prevent the deficit in brain <b>reward</b> function associated with precipitated nicotine withdrawal.
+NPY	addiction	withdrawal	18468678	These findings indicate that <strong>NPY</strong> and [D His(26)] <strong>NPY</strong> attenuate somatic nicotine <b>withdrawal</b> signs, but do not prevent the deficit in brain reward function associated with precipitated nicotine <b>withdrawal</b>.
+NPY	drug	alcohol	18385331	We found that the anxiolytic effects produced by acute <b>alcohol</b> were associated with a decrease in histone deacetylase (HDAC) activity and increases in acetylation of histones (H3 and H4), levels of CREB (cAMP responsive element binding) binding protein (CBP), and neuropeptide Y (<strong>NPY</strong>) expression in the amygdaloid brain regions of rats.
+NPY	drug	alcohol	18385331	We found that the anxiolytic effects produced by acute <b>alcohol</b> were associated with a decrease in histone deacetylase (HDAC) activity and increases in acetylation of histones (H3 and H4), levels of CREB (cAMP responsive element binding) binding protein (CBP), and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) expression in the amygdaloid brain regions of rats.
+NPY	drug	alcohol	18385331	However, the anxiety like behaviors during withdrawal after chronic <b>alcohol</b> exposure were associated with an increase in HDAC activity and decreases in acetylation of H3 and H4, and levels of both CBP and <strong>NPY</strong> in the amygdala.
+NPY	addiction	withdrawal	18385331	However, the anxiety like behaviors during <b>withdrawal</b> after chronic alcohol exposure were associated with an increase in HDAC activity and decreases in acetylation of H3 and H4, and levels of both CBP and <strong>NPY</strong> in the amygdala.
+NPY	drug	alcohol	18385331	Blocking the observed increase in HDAC activity during <b>alcohol</b> withdrawal with the HDAC inhibitor, trichostatin A, rescued the deficits in H3 and H4 acetylation and <strong>NPY</strong> expression (mRNA and protein levels) in the amygdala (central and medial nucleus of amygdala) and prevented the development of <b>alcohol</b> withdrawal related anxiety in rats as measured by the elevated plus maze and light/dark box exploration tests.
+NPY	addiction	withdrawal	18385331	Blocking the observed increase in HDAC activity during alcohol <b>withdrawal</b> with the HDAC inhibitor, trichostatin A, rescued the deficits in H3 and H4 acetylation and <strong>NPY</strong> expression (mRNA and protein levels) in the amygdala (central and medial nucleus of amygdala) and prevented the development of alcohol <b>withdrawal</b> related anxiety in rats as measured by the elevated plus maze and light/dark box exploration tests.
+NPY	drug	alcohol	18371990	However, this antagonist was unable to correct the impairment caused by <b>alcohol</b> abstinence in serotonin and <strong>neuropeptide Y</strong>.
+NPY	drug	alcohol	18241322	Analysis of single nucleotide polymorphisms and haplotypes in the <strong>neuropeptide Y</strong> gene: no evidence for association with <b>alcoholism</b> in a German population sample.
+NPY	drug	alcohol	18241322	Several lines of evidence from animal and electrophysiological studies indicate that the neuropeptide Y (<strong>NPY</strong>) gene is involved in the pathophysiology of <b>alcohol</b> dependence.
+NPY	addiction	dependence	18241322	Several lines of evidence from animal and electrophysiological studies indicate that the neuropeptide Y (<strong>NPY</strong>) gene is involved in the pathophysiology of alcohol <b>dependence</b>.
+NPY	drug	alcohol	18241322	Several lines of evidence from animal and electrophysiological studies indicate that the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene is involved in the pathophysiology of <b>alcohol</b> dependence.
+NPY	addiction	dependence	18241322	Several lines of evidence from animal and electrophysiological studies indicate that the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene is involved in the pathophysiology of alcohol <b>dependence</b>.
+NPY	drug	alcohol	18241322	Recent studies have provided evidence for an association between a Leu7Pro polymorphism, as well as 2 promoter single nucleotide polymorphisms (SNPs) in the <strong>NPY</strong> gene (G 602T, T 399C) and <b>alcohol</b> dependence.
+NPY	addiction	dependence	18241322	Recent studies have provided evidence for an association between a Leu7Pro polymorphism, as well as 2 promoter single nucleotide polymorphisms (SNPs) in the <strong>NPY</strong> gene (G 602T, T 399C) and alcohol <b>dependence</b>.
+NPY	drug	alcohol	18241322	We performed single SNP and haplotype studies in 465 <b>alcohol</b> dependent patients and 448 healthy controls with 3 SNPs in the promoter region ( 883ins/del, G 602T, T 399C) and the Leu7Pro polymorphism in exon 2 of the <strong>NPY</strong> gene.
+NPY	drug	alcohol	18241322	In conclusion, our results suggest that the analyzed SNPs, as well as the corresponding haplotypes of the <strong>NPY</strong> gene are unlikely to play a major role in the pathophysiology of <b>alcohol</b> dependence in the investigated sample from the German population.
+NPY	addiction	dependence	18241322	In conclusion, our results suggest that the analyzed SNPs, as well as the corresponding haplotypes of the <strong>NPY</strong> gene are unlikely to play a major role in the pathophysiology of alcohol <b>dependence</b> in the investigated sample from the German population.
+NPY	drug	benzodiazepine	18088080	<b>Benzodiazepine</b> treatment interferes not only with the release of CRH but also with the release of <strong>NPY</strong> and CCK.
+NPY	drug	benzodiazepine	18088080	Depending on the available results possible implications of <strong>NPY</strong> and CCK on <b>benzodiazepine</b> addiction and withdrawal symptoms are reviewed, thereby providing topics for further research.
+NPY	addiction	addiction	18088080	Depending on the available results possible implications of <strong>NPY</strong> and CCK on benzodiazepine <b>addiction</b> and withdrawal symptoms are reviewed, thereby providing topics for further research.
+NPY	addiction	withdrawal	18088080	Depending on the available results possible implications of <strong>NPY</strong> and CCK on benzodiazepine addiction and <b>withdrawal</b> symptoms are reviewed, thereby providing topics for further research.
+NPY	drug	nicotine	18060697	We investigated the effect of acupuncture on anxiety like behavior and corticotrophin releasing factor (CRF) and neuropeptide Y (<strong>NPY</strong>) mRNA expression in the amygdala during <b>nicotine</b> withdrawal.
+NPY	addiction	withdrawal	18060697	We investigated the effect of acupuncture on anxiety like behavior and corticotrophin releasing factor (CRF) and neuropeptide Y (<strong>NPY</strong>) mRNA expression in the amygdala during nicotine <b>withdrawal</b>.
+NPY	drug	nicotine	18060697	We investigated the effect of acupuncture on anxiety like behavior and corticotrophin releasing factor (CRF) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) mRNA expression in the amygdala during <b>nicotine</b> withdrawal.
+NPY	addiction	withdrawal	18060697	We investigated the effect of acupuncture on anxiety like behavior and corticotrophin releasing factor (CRF) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) mRNA expression in the amygdala during nicotine <b>withdrawal</b>.
+NPY	drug	alcohol	18036156	Modulation of <strong>neuropeptide Y</strong> and Y1 receptor expression in the amygdala by fluctuations in the brain content of neuroactive steroids during <b>ethanol</b> drinking discontinuation in Y1R/LacZ transgenic mice.
+NPY	drug	alcohol	18036156	As <b>ethanol</b> is known to increase GABAergic neuroactive steroids, we investigated the relationship between fluctuations in the brain content of neuroactive steroids induced by chronic voluntary <b>ethanol</b> consumption or <b>ethanol</b> discontinuation and both the level of neuropeptide Y (<strong>NPY</strong>) immunoreactivity and Y1R gene expression in the amygdala of Y1R/LacZ transgenic mice.
+NPY	drug	alcohol	18036156	As <b>ethanol</b> is known to increase GABAergic neuroactive steroids, we investigated the relationship between fluctuations in the brain content of neuroactive steroids induced by chronic voluntary <b>ethanol</b> consumption or <b>ethanol</b> discontinuation and both the level of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) immunoreactivity and Y1R gene expression in the amygdala of Y1R/LacZ transgenic mice.
+NPY	drug	alcohol	18036156	<b>Ethanol</b> discontinuation significantly decreased <strong>NPY</strong> immunoreactivity and concomitantly increased Y1R/LacZ transgene expression in the amygdala, whereas chronic <b>ethanol</b> intake failed to affect these parameters.
+NPY	drug	alcohol	18036156	The 5alpha reductase inhibitor finasteride prevented both the increase in the cerebrocortical concentration of 3alpha,5alpha TH PROG apparent after 4 weeks of <b>ethanol</b> intake and the changes in <strong>NPY</strong> immunoreactivity and transgene expression induced by <b>ethanol</b> discontinuation.
+NPY	drug	alcohol	18036156	Data suggest that 3alpha,5alpha TH PROG plays an important role in the changes in <strong>NPY</strong> Y1R signalling in the amygdala during <b>ethanol</b> discontinuation.
+NPY	drug	amphetamine	17910739	Changes in leptin, ghrelin, growth hormone and <strong>neuropeptide Y</strong> after an acute model of MDMA and <b>methamphetamine</b> exposure in rats.
+NPY	drug	psychedelics	17910739	Changes in leptin, ghrelin, growth hormone and <strong>neuropeptide Y</strong> after an acute model of <b>MDMA</b> and methamphetamine exposure in rats.
+NPY	drug	alcohol	17723274	Decreased gene expression of <strong>neuropeptide Y</strong> and its receptors in hippocampal regions during <b>ethanol</b> withdrawal in rats.
+NPY	addiction	withdrawal	17723274	Decreased gene expression of <strong>neuropeptide Y</strong> and its receptors in hippocampal regions during ethanol <b>withdrawal</b> in rats.
+NPY	drug	alcohol	17723274	Expression of <strong>NPY</strong> and its receptors Y1, Y2, and Y5 was studied in hippocampal areas of rats during <b>ethanol</b> withdrawal after repeated intragastric <b>ethanol</b> administration for 2 or 4 days using in situ hybridization.
+NPY	addiction	withdrawal	17723274	Expression of <strong>NPY</strong> and its receptors Y1, Y2, and Y5 was studied in hippocampal areas of rats during ethanol <b>withdrawal</b> after repeated intragastric ethanol administration for 2 or 4 days using in situ hybridization.
+NPY	drug	alcohol	17723274	Withdrawal was associated with decreased hippocampal expression of <strong>NPY</strong> and each of its receptors, particularly Y2, after 2 and/or 4 days of <b>ethanol</b> compared to control rats.
+NPY	addiction	withdrawal	17723274	<b>Withdrawal</b> was associated with decreased hippocampal expression of <strong>NPY</strong> and each of its receptors, particularly Y2, after 2 and/or 4 days of ethanol compared to control rats.
+NPY	drug	alcohol	17723274	These data suggest that the hippocampal <strong>NPY</strong> system is downregulated during <b>ethanol</b> withdrawal and these neuroadaptational changes could play a role in mediating withdrawal hyperexcitability.
+NPY	addiction	withdrawal	17723274	These data suggest that the hippocampal <strong>NPY</strong> system is downregulated during ethanol <b>withdrawal</b> and these neuroadaptational changes could play a role in mediating <b>withdrawal</b> hyperexcitability.
+NPY	drug	alcohol	17669369	Genetic studies on <b>alcoholism</b> examining the metabolism of <b>alcohol</b> and the dopaminergic, GABAergic, glutamatergic, opioid, cholinergic and serotonergic neurotransmitter systems as well as the <strong>neuropeptide Y</strong> are presented.
+NPY	drug	opioid	17669369	Genetic studies on alcoholism examining the metabolism of alcohol and the dopaminergic, GABAergic, glutamatergic, <b>opioid</b>, cholinergic and serotonergic neurotransmitter systems as well as the <strong>neuropeptide Y</strong> are presented.
+NPY	addiction	reward	17543357	Cortisol may influence the <b>reward</b> value of food via neuroendocrine/peptide mediators such as leptin, insulin and neuropeptide Y (<strong>NPY</strong>).
+NPY	addiction	reward	17543357	Cortisol may influence the <b>reward</b> value of food via neuroendocrine/peptide mediators such as leptin, insulin and <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	alcohol	17482381	Elevated anxiety like behavior following <b>ethanol</b> exposure in mutant mice lacking neuropeptide Y (<strong>NPY</strong>).
+NPY	drug	alcohol	17482381	Elevated anxiety like behavior following <b>ethanol</b> exposure in mutant mice lacking <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	alcohol	17482381	Recent evidence suggests that <strong>NPY</strong> modulates neurobiological responses to <b>ethanol</b>.
+NPY	drug	alcohol	17482381	Because withdrawal from <b>ethanol</b> is associated with elevated anxiety like behavior, and because central <strong>NPY</strong> modulates anxiety, we assessed anxiety like behavior in mutant mice lacking normal production of <strong>NPY</strong> (<strong>NPY</strong> / ) and in normal wild type mice (<strong>NPY</strong>+/+) 6h after removal of a liquid diet containing 4.5% <b>ethanol</b>.
+NPY	addiction	withdrawal	17482381	Because <b>withdrawal</b> from ethanol is associated with elevated anxiety like behavior, and because central <strong>NPY</strong> modulates anxiety, we assessed anxiety like behavior in mutant mice lacking normal production of <strong>NPY</strong> (<strong>NPY</strong> / ) and in normal wild type mice (<strong>NPY</strong>+/+) 6h after removal of a liquid diet containing 4.5% ethanol.
+NPY	drug	alcohol	17482381	<strong>NPY</strong> /  and <strong>NPY</strong>+/+ mice on a pure 129/SvEv genetic background were given 6 days of access to a liquid <b>ethanol</b> diet (ED) or control diet (CD).
+NPY	drug	alcohol	17482381	<b>Ethanol</b> withdrawn <strong>NPY</strong> /  mice showed significantly less open arm time and total proportion of time spent in the open arm of the EPM relative to <b>ethanol</b> withdrawn <strong>NPY</strong>+/+ mice and when compared to <strong>NPY</strong> /  and <strong>NPY</strong>+/+ mice that had access to the CD.
+NPY	drug	alcohol	17482381	On the other hand, <b>ethanol</b> withdrawn <strong>NPY</strong>+/+ mice did not show altered EPM behavior relative to controls.
+NPY	drug	alcohol	17482381	Central <strong>NPY</strong> is protective against anxiety like behavior stemming from exposure to and/or withdrawal from <b>ethanol</b>.
+NPY	addiction	withdrawal	17482381	Central <strong>NPY</strong> is protective against anxiety like behavior stemming from exposure to and/or <b>withdrawal</b> from ethanol.
+NPY	drug	alcohol	17482381	Targets aimed at <strong>NPY</strong> receptors may be useful compounds for treating anxiety associated with <b>ethanol</b> dependence.
+NPY	addiction	dependence	17482381	Targets aimed at <strong>NPY</strong> receptors may be useful compounds for treating anxiety associated with ethanol <b>dependence</b>.
+NPY	drug	alcohol	17405766	Viral vector induced amygdala <strong>NPY</strong> overexpression reverses increased <b>alcohol</b> intake caused by repeated deprivations in Wistar rats.
+NPY	drug	alcohol	17405766	Acute administration of neuropeptide Y (<strong>NPY</strong>) modulates <b>alcohol</b> intake in genetic and chemical models of high intake, while leaving intake unaffected during 'normal' or baseline conditions.
+NPY	drug	alcohol	17405766	Acute administration of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) modulates <b>alcohol</b> intake in genetic and chemical models of high intake, while leaving intake unaffected during 'normal' or baseline conditions.
+NPY	drug	alcohol	17405766	In non selected, normal rat lines, <b>alcohol</b> consumption can be increased by prolonged exposure to <b>alcohol</b>, and it is unclear what effect a constitutive increase in <strong>NPY</strong> function will have on <b>alcohol</b> intake.
+NPY	drug	alcohol	17405766	The purpose of the present study was to examine the effects on <b>alcohol</b> intake of an inducible, constitutive overexpression of <strong>NPY</strong>, one of the most abundant neuropeptides in the central nervous system.
+NPY	drug	alcohol	17405766	We then examined the effect of <strong>NPY</strong> overexpression in the amygdala on excessive <b>alcohol</b> intake produced by prolonged exposure to <b>alcohol</b> and <b>alcohol</b> deprivation.
+NPY	drug	alcohol	17239487	Neuropeptide Y (<strong>NPY</strong>) in <b>alcohol</b> intake and dependence.
+NPY	addiction	dependence	17239487	Neuropeptide Y (<strong>NPY</strong>) in alcohol intake and <b>dependence</b>.
+NPY	drug	alcohol	17239487	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) in <b>alcohol</b> intake and dependence.
+NPY	addiction	dependence	17239487	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) in alcohol intake and <b>dependence</b>.
+NPY	drug	alcohol	17239487	<strong>Neuropeptide Y</strong> has a role in <b>alcohol</b> intake and dependence.
+NPY	addiction	dependence	17239487	<strong>Neuropeptide Y</strong> has a role in alcohol intake and <b>dependence</b>.
+NPY	drug	alcohol	17239487	<strong>NPY</strong>'s effect on <b>alcohol</b> intake appears to be in part dependent on the individual's history of <b>alcohol</b> dependence.
+NPY	addiction	dependence	17239487	<strong>NPY</strong>'s effect on alcohol intake appears to be in part dependent on the individual's history of alcohol <b>dependence</b>.
+NPY	drug	alcohol	17239487	In models of high intake such as <b>alcohol</b> preferring, selectively bred rat lines (e.g., the P line and the HAD line), as well as in <b>ethanol</b> vapor exposed subjects, <strong>NPY</strong> modulates <b>alcohol</b> intake while leaving it unaffected during baseline conditions.
+NPY	drug	alcohol	17239487	The primary receptor subtype mediating <strong>NPY</strong>'s effect on <b>ethanol</b> intake remains in question.
+NPY	drug	alcohol	17239487	We propose the <strong>NPY</strong> system to be one of the most interesting target systems for the development of treatments for <b>alcohol</b> abuse and dependence.
+NPY	addiction	dependence	17239487	We propose the <strong>NPY</strong> system to be one of the most interesting target systems for the development of treatments for alcohol abuse and <b>dependence</b>.
+NPY	drug	amphetamine	17105911	The somatostatin/neuropeptide Y (<strong>NPY</strong>)/nitric oxide synthase (NOS) interneurons are not impacted by <b>METH</b>.
+NPY	drug	amphetamine	17105911	The somatostatin/<strong>neuropeptide Y</strong> (<strong>NPY</strong>)/nitric oxide synthase (NOS) interneurons are not impacted by <b>METH</b>.
+NPY	drug	nicotine	17052838	<b>Nicotine</b> withdrawal increases body weight, <strong>neuropeptide Y</strong> and Agouti related protein expression in the hypothalamus and decreases uncoupling protein 3 expression in the brown adipose tissue in high fat fed mice.
+NPY	addiction	withdrawal	17052838	Nicotine <b>withdrawal</b> increases body weight, <strong>neuropeptide Y</strong> and Agouti related protein expression in the hypothalamus and decreases uncoupling protein 3 expression in the brown adipose tissue in high fat fed mice.
+NPY	drug	nicotine	17052838	<b>Nicotine</b> withdrawal is accompanied by increased expression of the orexigenic peptides <strong>neuropeptide Y</strong> and Agouti related protein in the hypothalamus, and decreased expression of the metabolic protein uncoupling protein 3 in brown adipose tissue.
+NPY	addiction	withdrawal	17052838	Nicotine <b>withdrawal</b> is accompanied by increased expression of the orexigenic peptides <strong>neuropeptide Y</strong> and Agouti related protein in the hypothalamus, and decreased expression of the metabolic protein uncoupling protein 3 in brown adipose tissue.
+NPY	drug	amphetamine	17049170	This effect was specific to these genes as tissue plasminogen activator (t PA), neuropeptide Y (<strong>NPY</strong>) and c jun expression in response to <b>AMPH</b> challenge was unaltered or enhanced by <b>amphetamine</b> pretreatments.
+NPY	drug	amphetamine	17049170	This effect was specific to these genes as tissue plasminogen activator (t PA), <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and c jun expression in response to <b>AMPH</b> challenge was unaltered or enhanced by <b>amphetamine</b> pretreatments.
+NPY	drug	nicotine	17010518	These results do not support the direct mediation of the leptin ghrelin neuropeptide Y (<strong>NPY</strong>) system on weight gain after <b>smoking</b> cessation.
+NPY	drug	nicotine	17010518	These results do not support the direct mediation of the leptin ghrelin <strong>neuropeptide Y</strong> (<strong>NPY</strong>) system on weight gain after <b>smoking</b> cessation.
+NPY	drug	opioid	16931647	Striatal <b>opioid</b> peptide gene expression differentially tracks short term satiety but does not vary with negative energy balance in a manner opposite to hypothalamic <strong>NPY</strong>.
+NPY	drug	amphetamine	16840646	Neuropeptide Y (<strong>NPY</strong>) is a neuropeptide that may be involved with emotional regulation and drug addiction and may act as a neuroprotective agent during toxic insults, such as is associated with multiple, high doses of <b>methamphetamine</b> (<b>METH</b>).
+NPY	addiction	addiction	16840646	Neuropeptide Y (<strong>NPY</strong>) is a neuropeptide that may be involved with emotional regulation and drug <b>addiction</b> and may act as a neuroprotective agent during toxic insults, such as is associated with multiple, high doses of methamphetamine (METH).
+NPY	drug	amphetamine	16840646	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) is a neuropeptide that may be involved with emotional regulation and drug addiction and may act as a neuroprotective agent during toxic insults, such as is associated with multiple, high doses of <b>methamphetamine</b> (<b>METH</b>).
+NPY	addiction	addiction	16840646	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) is a neuropeptide that may be involved with emotional regulation and drug <b>addiction</b> and may act as a neuroprotective agent during toxic insults, such as is associated with multiple, high doses of methamphetamine (METH).
+NPY	drug	amphetamine	16840646	The purpose of the present study was to elucidate the nature of <b>METH</b> induced changes in the <strong>NPY</strong> system by examining the effect of multiple, high doses of <b>METH</b> on preproNPY (ppNPY) mRNA expression in the striatum and the role that dopamine (DA) D1 and D2 receptors might play in these changes.
+NPY	drug	alcohol	16824587	These data provide evidence that neuroactive steroids may play an important role in the functional interaction between the GABA(A) receptor and <strong>NPY</strong> Y(1)R mediated pathways in the amygdala, which might represent an important regulatory mechanism for modulation of several functions, including <b>ethanol</b> withdrawal.
+NPY	addiction	withdrawal	16824587	These data provide evidence that neuroactive steroids may play an important role in the functional interaction between the GABA(A) receptor and <strong>NPY</strong> Y(1)R mediated pathways in the amygdala, which might represent an important regulatory mechanism for modulation of several functions, including ethanol <b>withdrawal</b>.
+NPY	drug	alcohol	16634847	Overexpression of <strong>neuropeptide Y</strong> in the central nucleus of the amygdala decreases <b>ethanol</b> self administration in "anxious" rats.
+NPY	drug	alcohol	16634847	Neuropeptide Y (<strong>NPY</strong>) has been implicated in a variety of behaviors including those associated with anxiety and <b>ethanol</b> administration.
+NPY	drug	alcohol	16634847	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) has been implicated in a variety of behaviors including those associated with anxiety and <b>ethanol</b> administration.
+NPY	drug	alcohol	16634847	The current experiment investigated the predictive role of anxiety like behaviors in <b>ethanol</b> self administration and the relationship of <strong>NPY</strong> in the central nucleus of the amygdala (CeA) with anxiety and <b>ethanol</b> self administration.
+NPY	drug	alcohol	16634847	Following 20 day access to 6% <b>ethanol</b>, rats underwent gene transfer surgery with replication defective recombinant herpes simplex 1 vectors encoding prepro <strong>NPY</strong>, an antisense <strong>NPY</strong> RNA, or LacZ (control) into the CeA.
+NPY	drug	alcohol	16634847	In anxious rats, bilateral injections into the CeA with the <strong>NPY</strong> antisense vector increased 6% <b>ethanol</b> preference, while the vector encoding <strong>NPY</strong> decreased 6% <b>ethanol</b> preference.
+NPY	drug	alcohol	16634847	Herpes simplex viral mediated alterations in CeA <strong>NPY</strong> expression did not alter <b>ethanol</b> preference in nonanxious rats.
+NPY	drug	alcohol	16634847	These results suggest that virally mediated alterations in <strong>NPY</strong> levels in the CeA differentially affect <b>ethanol</b> consumption in rats with low and high basal levels of anxiety.
+NPY	drug	alcohol	16611096	In addition to opioid receptors, other neuropeptide receptors including those for corticotrophin releasing factor (CRF), <strong>neuropeptide Y</strong> and nociceptin may represent valid therapeutic targets to regulate <b>alcohol</b> consumption and the affective consequences of <b>alcohol</b> withdrawal.
+NPY	drug	opioid	16611096	In addition to <b>opioid</b> receptors, other neuropeptide receptors including those for corticotrophin releasing factor (CRF), <strong>neuropeptide Y</strong> and nociceptin may represent valid therapeutic targets to regulate alcohol consumption and the affective consequences of alcohol withdrawal.
+NPY	addiction	withdrawal	16611096	In addition to opioid receptors, other neuropeptide receptors including those for corticotrophin releasing factor (CRF), <strong>neuropeptide Y</strong> and nociceptin may represent valid therapeutic targets to regulate alcohol consumption and the affective consequences of alcohol <b>withdrawal</b>.
+NPY	drug	alcohol	16611091	<strong>Neuropeptide y</strong>: role in emotion and <b>alcohol</b> dependence.
+NPY	addiction	dependence	16611091	<strong>Neuropeptide y</strong>: role in emotion and alcohol <b>dependence</b>.
+NPY	drug	alcohol	16611091	Furthermore, recent evidence suggests that <strong>NPY</strong> has a significant role in the neurobiological response to <b>alcohol</b>, including <b>alcohol</b> consumption, dependence, and withdrawal.
+NPY	addiction	dependence	16611091	Furthermore, recent evidence suggests that <strong>NPY</strong> has a significant role in the neurobiological response to alcohol, including alcohol consumption, <b>dependence</b>, and withdrawal.
+NPY	addiction	withdrawal	16611091	Furthermore, recent evidence suggests that <strong>NPY</strong> has a significant role in the neurobiological response to alcohol, including alcohol consumption, dependence, and <b>withdrawal</b>.
+NPY	drug	alcohol	16611091	In addition, <strong>NPY</strong> is beginning to emerge as an important modulator in the etiology of <b>alcoholism</b> that is independent from the addictive and reinforcing properties of the traditional system commonly associated with dopamine and instead, is strongly associated with innate emotionality.
+NPY	addiction	addiction	16611091	In addition, <strong>NPY</strong> is beginning to emerge as an important modulator in the etiology of alcoholism that is independent from the <b>addictive</b> and reinforcing properties of the traditional system commonly associated with dopamine and instead, is strongly associated with innate emotionality.
+NPY	addiction	reward	16611091	In addition, <strong>NPY</strong> is beginning to emerge as an important modulator in the etiology of alcoholism that is independent from the addictive and <b>reinforcing</b> properties of the traditional system commonly associated with dopamine and instead, is strongly associated with innate emotionality.
+NPY	drug	alcohol	16611091	The recent developments elucidating the role of <strong>NPY</strong> in emotion and <b>alcohol</b> dependence are reviewed and the potential of the <strong>NPY</strong> system as a novel therapeutic strategy in the treatment of anxiety, depression and <b>alcohol</b> related disorders is examined.
+NPY	addiction	dependence	16611091	The recent developments elucidating the role of <strong>NPY</strong> in emotion and alcohol <b>dependence</b> are reviewed and the potential of the <strong>NPY</strong> system as a novel therapeutic strategy in the treatment of anxiety, depression and alcohol related disorders is examined.
+NPY	drug	cannabinoid	16545872	These include the <b>cannabinoid</b> CB1 receptor, receptors modulating glutamatergic transmission (mGluR2, 3 and 5), and receptors for stress related neuropeptides corticotropin releasing factor (CRF), neuropeptide Y (<strong>NPY</strong>) and nociceptin.
+NPY	drug	cannabinoid	16545872	These include the <b>cannabinoid</b> CB1 receptor, receptors modulating glutamatergic transmission (mGluR2, 3 and 5), and receptors for stress related neuropeptides corticotropin releasing factor (CRF), <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and nociceptin.
+NPY	drug	opioid	16529722	Changes in neuropeptide FF and <strong>NPY</strong> immunohistochemical patterns in rat brain under <b>heroin</b> treatment.
+NPY	drug	opioid	16529722	Immunohistochemical distribution patterns of neuropeptide FF (NPFF) and neuropeptide tyrosine (<strong>NPY</strong>) were studied in the brain of rats submitted to two different protocols of <b>heroin</b> treatment.
+NPY	drug	opioid	16529722	In drug naive rats, acutely injected <b>heroin</b> significantly depleted NPFF immunoreactive material within the neurons of the nucleus of solitary tract (NTS), significantly decreased the density of NPFF immunoreactive nerve fibers within the median eminence, pituitary stalk, and neurohypophysis, and markedly increased <strong>NPY</strong> immunoreactive neurons and nerve fibers in the thalamic paraventricular nucleus and bed nucleus of stria terminalis.
+NPY	drug	opioid	16529722	In drug sensitized rats, <b>heroin</b> significantly increased the number and immunostaining intensity of the NPFF immunoreactive neurons within the NTS and induced minor changes in the NPFF immunoreactive nerve fiber network of the median eminence, pituitary stalk, and neurohypophysis and a relatively minor increase in <strong>NPY</strong> neurons in the thalamic paraventricular nucleus and bed nucleus of stria terminalis.
+NPY	drug	alcohol	16377459	The <strong>neuropeptide Y</strong> Y5 receptor antagonist L 152,804 decreases <b>alcohol</b> self administration in inbred <b>alcohol</b> preferring (iP) rats.
+NPY	drug	alcohol	16377459	Recent pharmacological evidence indicates that <strong>NPY</strong> activity at this receptor subtype can modulate <b>ethanol</b> reinforcement.
+NPY	addiction	reward	16377459	Recent pharmacological evidence indicates that <strong>NPY</strong> activity at this receptor subtype can modulate ethanol <b>reinforcement</b>.
+NPY	drug	alcohol	16377459	The purpose of this study was to determine if <strong>NPY</strong> Y5 receptor antagonism reduces <b>ethanol</b> self administration and reinforcement in a rodent genetic animal model of <b>alcoholism</b>.
+NPY	addiction	reward	16377459	The purpose of this study was to determine if <strong>NPY</strong> Y5 receptor antagonism reduces ethanol self administration and <b>reinforcement</b> in a rodent genetic animal model of alcoholism.
+NPY	drug	alcohol	16377459	These results indicate that blockade of <strong>NPY</strong> Y5 receptor activity decreases both voluntary <b>ethanol</b> drinking and <b>ethanol</b> reinforcement in a rodent genetic animal model of <b>alcoholism</b>.
+NPY	addiction	reward	16377459	These results indicate that blockade of <strong>NPY</strong> Y5 receptor activity decreases both voluntary ethanol drinking and ethanol <b>reinforcement</b> in a rodent genetic animal model of alcoholism.
+NPY	drug	alcohol	16377459	For this reason, <strong>NPY</strong> Y5 receptor antagonists may be useful in medical management of <b>alcohol</b> abuse and <b>alcoholism</b> in the human population.
+NPY	drug	benzodiazepine	16225749	Changes of brain <strong>neuropeptide Y</strong> and its receptors in rats with <b>flurazepam</b> tolerance and dependence.
+NPY	addiction	dependence	16225749	Changes of brain <strong>neuropeptide Y</strong> and its receptors in rats with flurazepam tolerance and <b>dependence</b>.
+NPY	drug	benzodiazepine	16225749	In order to explore the mechanism of these two adverse reactions, changes of neuropeptide Y (<strong>NPY</strong>) and its receptors in the hippocampus of rat models, in relation to <b>flurazepam</b> (FZP, a member of BDZ) tolerance and dependence, were investigated.
+NPY	addiction	dependence	16225749	In order to explore the mechanism of these two adverse reactions, changes of neuropeptide Y (<strong>NPY</strong>) and its receptors in the hippocampus of rat models, in relation to flurazepam (FZP, a member of BDZ) tolerance and <b>dependence</b>, were investigated.
+NPY	drug	benzodiazepine	16225749	In order to explore the mechanism of these two adverse reactions, changes of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and its receptors in the hippocampus of rat models, in relation to <b>flurazepam</b> (FZP, a member of BDZ) tolerance and dependence, were investigated.
+NPY	addiction	dependence	16225749	In order to explore the mechanism of these two adverse reactions, changes of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and its receptors in the hippocampus of rat models, in relation to flurazepam (FZP, a member of BDZ) tolerance and <b>dependence</b>, were investigated.
+NPY	addiction	dependence	16225749	A decrease of <strong>NPY</strong> in the hippocampus might be involved in anticonvulsant tolerance and <b>dependence</b> following long term treatment with FZP.
+NPY	drug	amphetamine	16218999	Withdrawal of the obesogenic diets decreased gene expression for cocaine and <b>amphetamine</b> regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas neuropeptide Y (<strong>NPY</strong>) gene expression in the ARC was increased.
+NPY	drug	cocaine	16218999	Withdrawal of the obesogenic diets decreased gene expression for <b>cocaine</b> and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas neuropeptide Y (<strong>NPY</strong>) gene expression in the ARC was increased.
+NPY	addiction	withdrawal	16218999	<b>Withdrawal</b> of the obesogenic diets decreased gene expression for cocaine and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas neuropeptide Y (<strong>NPY</strong>) gene expression in the ARC was increased.
+NPY	drug	amphetamine	16218999	Withdrawal of the obesogenic diets decreased gene expression for cocaine and <b>amphetamine</b> regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene expression in the ARC was increased.
+NPY	drug	cocaine	16218999	Withdrawal of the obesogenic diets decreased gene expression for <b>cocaine</b> and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene expression in the ARC was increased.
+NPY	addiction	withdrawal	16218999	<b>Withdrawal</b> of the obesogenic diets decreased gene expression for cocaine and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (ARC), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene expression in the ARC was increased.
+NPY	addiction	withdrawal	16218999	<b>Withdrawal</b> of obesogenic diets induces changes in the gene expression consistent with <strong>NPY</strong>, CART and BDNF attempting to oppose weight gain on either HE or HE + EN.
+NPY	drug	alcohol	16192983	On the other hand, infusion of PKA activator (Sp cAMP) or <strong>NPY</strong> alone into the NAc shell did not produce any changes in <b>alcohol</b> intake; however, when these agents were coinfused with PKA inhibitor, they significantly attenuated the increases in <b>alcohol</b> preference induced by pharmacological inhibition of PKA.
+NPY	drug	alcohol	16192983	Furthermore, decreased function of PKA may regulate <b>alcohol</b> drinking behaviors via CREB mediated decreased expression of <strong>NPY</strong> in the NAc shell of rats.
+NPY	drug	amphetamine	16134406	They evoke possible involvement of cocaine's influence on the anorexigenic cytokine Tumor Necrosis Factor, Cocaine and <b>Amphetamine</b> Regulated Transcript, or suppression of the appetite stimulating <strong>Neuropeptide Y</strong>, or cocaine induced deficits in nicotinic cholinergic neural transmission, all of which have not only been linked to weight and appetite, but also to idiopathic psychosis.
+NPY	drug	cocaine	16134406	They evoke possible involvement of <b>cocaine</b>'s influence on the anorexigenic cytokine Tumor Necrosis Factor, <b>Cocaine</b> and Amphetamine Regulated Transcript, or suppression of the appetite stimulating <strong>Neuropeptide Y</strong>, or <b>cocaine</b> induced deficits in nicotinic cholinergic neural transmission, all of which have not only been linked to weight and appetite, but also to idiopathic psychosis.
+NPY	drug	opioid	16034445	In this study, we analyzed levels of mRNAs encoding the neuropeptide Y (<strong>NPY</strong>) and the <b>opioid</b> peptides dynorphin and enkephalin in hippocampus and correlated these to cell proliferation in the FSL and in the 'nondepressed' Flinders Resistant Line (FRL) strain, with/without access to running wheels.
+NPY	drug	opioid	16034445	In this study, we analyzed levels of mRNAs encoding the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and the <b>opioid</b> peptides dynorphin and enkephalin in hippocampus and correlated these to cell proliferation in the FSL and in the 'nondepressed' Flinders Resistant Line (FRL) strain, with/without access to running wheels.
+NPY	drug	opioid	16034445	Thus, it would appear that the CNS effects of running are different in 'depressed' and control animals; modification of <strong>NPY</strong>, a peptide associated with depression and anxiety, in depressed animals, vs effects on <b>opioids</b>, associated with the reward systems, in healthy controls.
+NPY	addiction	reward	16034445	Thus, it would appear that the CNS effects of running are different in 'depressed' and control animals; modification of <strong>NPY</strong>, a peptide associated with depression and anxiety, in depressed animals, vs effects on opioids, associated with the <b>reward</b> systems, in healthy controls.
+NPY	drug	alcohol	16023707	Sensitized effects of <strong>neuropeptide Y</strong> on multiple ingestive behaviors in P rats following <b>ethanol</b> abstinence.
+NPY	drug	alcohol	16023707	Neuropeptide Y (<strong>NPY</strong>) suppresses <b>ethanol</b> drinking in <b>alcohol</b> preferring (P) rats, an effect which is augmented following a single <b>ethanol</b> abstinence period.
+NPY	drug	alcohol	16023707	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) suppresses <b>ethanol</b> drinking in <b>alcohol</b> preferring (P) rats, an effect which is augmented following a single <b>ethanol</b> abstinence period.
+NPY	drug	alcohol	16023707	Following intracerebroventricular cannula implantation during the third period of <b>ethanol</b> abstinence, groups (n=12 13/dose) were infused with <strong>NPY</strong> (2.5, 5.0, 10.0 microg) or aCSF prior to <b>ethanol</b> reinstatement.
+NPY	addiction	relapse	16023707	Following intracerebroventricular cannula implantation during the third period of ethanol abstinence, groups (n=12 13/dose) were infused with <strong>NPY</strong> (2.5, 5.0, 10.0 microg) or aCSF prior to ethanol <b>reinstatement</b>.
+NPY	drug	alcohol	16023707	Two additional groups (n=11 12/dose) were treated similarly except that <b>ethanol</b> access was uninterrupted, and they were infused with a single <strong>NPY</strong> dose (10.0 microg) or aCSF.
+NPY	drug	alcohol	16023707	<strong>NPY</strong> increased food intake in all groups, and this effect was greater following <b>ethanol</b> abstinence.
+NPY	drug	alcohol	16023707	<strong>NPY</strong> suppressed <b>ethanol</b> intake, and this suppression lasted longer (24 h post infusion) in rats with a history of <b>ethanol</b> abstinence periods than rats with a history of continuous <b>ethanol</b> access (4 h post infusion).
+NPY	drug	alcohol	16023707	These results confirm past findings and indicate that global dysregulation of brain <strong>NPY</strong> systems during <b>ethanol</b> abstinence may render P rats more sensitive to the behavioral effects of <strong>NPY</strong>.
+NPY	drug	amphetamine	15985714	<b>Amphetamine</b> induced effects on <strong>neuropeptide Y</strong> in the rat brain.
+NPY	drug	amphetamine	15985714	Repeated (+) <b>amphetamine</b> sulfate (<b>AMPH</b>) administration (5 mg/kg sc twice daily for 6 days and once on day 7) markedly and reversibly decreased (until 96 h after the final dose) neuropeptide Y like immunoreactivity (<strong>NPY</strong> LI) in the rat striatum (caudate putamen) and nucleus accumbens, and had no effect on <strong>NPY</strong> LI in the hippocampus.
+NPY	drug	amphetamine	15985714	Repeated (+) <b>amphetamine</b> sulfate (<b>AMPH</b>) administration (5 mg/kg sc twice daily for 6 days and once on day 7) markedly and reversibly decreased (until 96 h after the final dose) <strong>neuropeptide Y</strong> like immunoreactivity (<strong>NPY</strong> LI) in the rat striatum (caudate putamen) and nucleus accumbens, and had no effect on <strong>NPY</strong> LI in the hippocampus.
+NPY	drug	amphetamine	15985714	No significant alterations were detected in the hybridization signal of <strong>NPY</strong> mRNA4 and 24 h after the end of <b>AMPH</b> treatment.
+NPY	drug	amphetamine	15985714	A single dose of <b>AMPH</b> (5 mg/kg sc) administered to rats 4 and 24 h prior to sacrifice had no effect on <strong>NPY</strong> LI in the brain structures studied.
+NPY	drug	amphetamine	15985714	Moreover, <b>AMPH</b> injected 8 days after the last dose of repeated <b>AMPH</b> administration did not change <strong>NPY</strong> LI up to 72 h. The minimal dose of haloperidol, the strong mixed dopaminergic D2/D1 receptor antagonist, (0.75 mg/kg injected ip 30 min before each of the multiple <b>AMPH</b> administrations) that was sufficient to completely block stereotypy and hyperlocomotion elicited by multiple <b>AMPH</b> administrations enhanced the <b>AMPH</b> induced decrease in the striatal and accumbens <strong>NPY</strong> LI.
+NPY	drug	amphetamine	15985714	Our results suggest that <strong>NPY</strong> neurons in the striatum, nucleus accumbens and hippocampus are not directly involved in the acute behavioral response to <b>AMPH</b> (stereotypy and hyperlocomotion) as well as in the initiation and expression of <b>AMPH</b> induced behavioral sensitization.
+NPY	addiction	sensitization	15985714	Our results suggest that <strong>NPY</strong> neurons in the striatum, nucleus accumbens and hippocampus are not directly involved in the acute behavioral response to AMPH (stereotypy and hyperlocomotion) as well as in the initiation and expression of AMPH induced behavioral <b>sensitization</b>.
+NPY	drug	alcohol	15976521	<b>Alcohol</b> naïve rats were evaluated in an elevated plus maze after i3vt MCH (10 microg), <strong>neuropeptide Y</strong>, or saline administration.
+NPY	drug	alcohol	15897715	Comparison of basal <strong>neuropeptide Y</strong> and corticotropin releasing factor levels between the high <b>ethanol</b> drinking C57BL/6J and low <b>ethanol</b> drinking DBA/2J inbred mouse strains.
+NPY	drug	alcohol	15897715	Recent genetic and pharmacological evidence indicates that low neuropeptide Y (<strong>NPY</strong>) levels in brain regions involved with neurobiological responses to <b>ethanol</b> promote increased <b>ethanol</b> consumption.
+NPY	drug	alcohol	15897715	Recent genetic and pharmacological evidence indicates that low <strong>neuropeptide Y</strong> (<strong>NPY</strong>) levels in brain regions involved with neurobiological responses to <b>ethanol</b> promote increased <b>ethanol</b> consumption.
+NPY	drug	alcohol	15897715	These data suggest that low <strong>NPY</strong> levels in the amygdala and/or the shell of the NAc, which are not compensated for by similar changes in CRF levels, may contribute to the high <b>ethanol</b> consumption characteristic of C57BL/6J mice.
+NPY	drug	alcohol	15897713	A novel single nucleotide polymorphism of the neuropeptide Y (<strong>NPY</strong>) gene associated with <b>alcohol</b> dependence.
+NPY	addiction	dependence	15897713	A novel single nucleotide polymorphism of the neuropeptide Y (<strong>NPY</strong>) gene associated with alcohol <b>dependence</b>.
+NPY	drug	alcohol	15897713	A novel single nucleotide polymorphism of the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene associated with <b>alcohol</b> dependence.
+NPY	addiction	dependence	15897713	A novel single nucleotide polymorphism of the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene associated with alcohol <b>dependence</b>.
+NPY	drug	alcohol	15897713	Transgenic work with <strong>NPY</strong> and null mutant mice have implicated <strong>NPY</strong> in the control of <b>alcohol</b> consumption, suggesting that genetic variation of the prepro <strong>NPY</strong> gene may also contribute to the heritability of <b>alcoholism</b>.
+NPY	drug	alcohol	15897713	The aim of this study was to examine whether polymorphic variants of the <strong>NPY</strong> gene are associated with the diagnosis of <b>alcohol</b> dependence.
+NPY	addiction	dependence	15897713	The aim of this study was to examine whether polymorphic variants of the <strong>NPY</strong> gene are associated with the diagnosis of alcohol <b>dependence</b>.
+NPY	drug	alcohol	15897713	We compared allele frequencies of 5 <strong>NPY</strong> polymorphisms ( 883 ins/del,  602,  399,  84, and +1128) in a Nordic population of <b>alcohol</b> dependent individuals (n = 428 males; n = 149 females) and ethnically matched controls (n = 84 males; n = 93 females) for whom <b>alcohol</b> dependence or any diagnosis of substance disorder was excluded.
+NPY	addiction	dependence	15897713	We compared allele frequencies of 5 <strong>NPY</strong> polymorphisms ( 883 ins/del,  602,  399,  84, and +1128) in a Nordic population of alcohol dependent individuals (n = 428 males; n = 149 females) and ethnically matched controls (n = 84 males; n = 93 females) for whom alcohol <b>dependence</b> or any diagnosis of substance disorder was excluded.
+NPY	drug	alcohol	15897713	We report a novel polymorphism at position  602 in the 5' region of the <strong>NPY</strong> gene that is significantly associated with <b>alcohol</b> dependence.
+NPY	addiction	dependence	15897713	We report a novel polymorphism at position  602 in the 5' region of the <strong>NPY</strong> gene that is significantly associated with alcohol <b>dependence</b>.
+NPY	drug	alcohol	15834223	Effects of <strong>neuropeptide Y</strong> on appetitive and consummatory behaviors associated with <b>alcohol</b> drinking in wistar rats with a history of <b>ethanol</b> exposure.
+NPY	drug	alcohol	15834223	Neuropeptide Y (<strong>NPY</strong>) reduces <b>ethanol</b> intake under free access conditions in Wistar rats with a history of prolonged <b>ethanol</b> vapor exposure.
+NPY	drug	alcohol	15834223	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) reduces <b>ethanol</b> intake under free access conditions in Wistar rats with a history of prolonged <b>ethanol</b> vapor exposure.
+NPY	drug	alcohol	15834223	The current study was designed to determine whether <strong>NPY</strong> differentially alters <b>ethanol</b> associated appetitive behavior (i.e., lever pressing) or <b>ethanol</b> consumption in Wistar rats with a history of <b>ethanol</b> vapor exposure.
+NPY	drug	alcohol	15834223	Self administration sessions were then reinstituted, and a fixed time (FT) schedule of 10% <b>ethanol</b> access was used to assess the effects of <b>ethanol</b> exposure and <strong>NPY</strong> on lever pressing and drinking behavior.
+NPY	drug	alcohol	15834223	<strong>NPY</strong> significantly reduced <b>ethanol</b> intake but did not significantly reduce lever pressing under the FT schedule.
+NPY	drug	alcohol	15834223	Furthermore, <strong>NPY</strong> has a greater impact on the consummatory factors mediating <b>ethanol</b> intake than appetitive factors mediating <b>ethanol</b> seeking.
+NPY	addiction	relapse	15834223	Furthermore, <strong>NPY</strong> has a greater impact on the consummatory factors mediating ethanol intake than appetitive factors mediating ethanol <b>seeking</b>.
+NPY	drug	alcohol	15749341	Effect of polymorphism on expression of the <strong>neuropeptide Y</strong> gene in inbred <b>alcohol</b> preferring and  nonpreferring rats.
+NPY	drug	alcohol	15749341	Using animal models of <b>alcoholism</b>, previous studies suggest that neuropeptide Y (<strong>NPY</strong>) may be implicated in <b>alcohol</b> preference and consumption due to its role in the modulation of feeding and anxiety.
+NPY	drug	alcohol	15749341	Using animal models of <b>alcoholism</b>, previous studies suggest that <strong>neuropeptide Y</strong> (<strong>NPY</strong>) may be implicated in <b>alcohol</b> preference and consumption due to its role in the modulation of feeding and anxiety.
+NPY	drug	alcohol	15749341	<strong>NPY</strong> mapped to the peak of this QTL region and was prioritized as a candidate gene for <b>alcohol</b> seeking behavior in the iP and iNP rats.
+NPY	addiction	relapse	15749341	<strong>NPY</strong> mapped to the peak of this QTL region and was prioritized as a candidate gene for alcohol <b>seeking</b> behavior in the iP and iNP rats.
+NPY	drug	alcohol	15677721	We have identified a Drosophila signaling system, comprising neurons expressing neuropeptide F (NPF, a homolog of mammalian <strong>neuropeptide Y</strong>) and its receptor, NPFR1, that acutely mediates sensitivity to <b>ethanol</b> sedation.
+NPY	drug	alcohol	15670655	Suppression of <b>ethanol</b> self administration by the neuropeptide Y (<strong>NPY</strong>) Y2 receptor antagonist BIIE0246: evidence for sensitization in rats with a history of dependence.
+NPY	addiction	dependence	15670655	Suppression of ethanol self administration by the neuropeptide Y (<strong>NPY</strong>) Y2 receptor antagonist BIIE0246: evidence for sensitization in rats with a history of <b>dependence</b>.
+NPY	addiction	sensitization	15670655	Suppression of ethanol self administration by the neuropeptide Y (<strong>NPY</strong>) Y2 receptor antagonist BIIE0246: evidence for <b>sensitization</b> in rats with a history of dependence.
+NPY	drug	alcohol	15670655	Suppression of <b>ethanol</b> self administration by the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) Y2 receptor antagonist BIIE0246: evidence for sensitization in rats with a history of dependence.
+NPY	addiction	dependence	15670655	Suppression of ethanol self administration by the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) Y2 receptor antagonist BIIE0246: evidence for sensitization in rats with a history of <b>dependence</b>.
+NPY	addiction	sensitization	15670655	Suppression of ethanol self administration by the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) Y2 receptor antagonist BIIE0246: evidence for <b>sensitization</b> in rats with a history of dependence.
+NPY	drug	alcohol	15670655	Evidence from genetically modified mice suggests a role for <strong>NPY</strong> in regulation of <b>ethanol</b> intake, but results of pharmacological studies have been more variable.
+NPY	drug	alcohol	15670655	We have previously shown that potentiation of <strong>NPY</strong> signaling through antagonism at <strong>NPY</strong> Y2 receptors decreases operant responding for <b>ethanol</b> in Wistar rats without a history of dependence.
+NPY	addiction	dependence	15670655	We have previously shown that potentiation of <strong>NPY</strong> signaling through antagonism at <strong>NPY</strong> Y2 receptors decreases operant responding for ethanol in Wistar rats without a history of <b>dependence</b>.
+NPY	addiction	reward	15670655	We have previously shown that potentiation of <strong>NPY</strong> signaling through antagonism at <strong>NPY</strong> Y2 receptors decreases <b>operant</b> responding for ethanol in Wistar rats without a history of dependence.
+NPY	drug	alcohol	15670655	These data confirm that antagonism at central <strong>NPY</strong> Y2 receptors selectively suppresses motivation to self administer <b>ethanol</b>, and indicate that the <strong>NPY</strong> system is sensitized in animals with a history of dependence.
+NPY	addiction	dependence	15670655	These data confirm that antagonism at central <strong>NPY</strong> Y2 receptors selectively suppresses motivation to self administer ethanol, and indicate that the <strong>NPY</strong> system is sensitized in animals with a history of <b>dependence</b>.
+NPY	drug	alcohol	15670655	This may render the <strong>NPY</strong> system, and Y2 receptors in particular, an attractive target for treatment of <b>alcohol</b> dependence.
+NPY	addiction	dependence	15670655	This may render the <strong>NPY</strong> system, and Y2 receptors in particular, an attractive target for treatment of alcohol <b>dependence</b>.
+NPY	drug	alcohol	15654286	Neither <strong>NPY</strong> nor catalase was associated with either LR or <b>alcoholic</b> outcomes, although the sample did not have sufficient power for definitive conclusions.
+NPY	drug	alcohol	15582675	Allostasis and dysregulation of corticotropin releasing factor and <strong>neuropeptide Y</strong> systems: implications for the development of <b>alcoholism</b>.
+NPY	drug	alcohol	15582675	With regard to <b>alcohol</b>, two neuropeptides appear to be involved in the regulation of <b>alcohol</b> related stress, corticotropin releasing factor (CRF), which is associated with an increased stress response and negative affect, and neuropeptide Y (<strong>NPY</strong>), a neuropeptide with anxiolytic properties.
+NPY	drug	alcohol	15582675	With regard to <b>alcohol</b>, two neuropeptides appear to be involved in the regulation of <b>alcohol</b> related stress, corticotropin releasing factor (CRF), which is associated with an increased stress response and negative affect, and <strong>neuropeptide Y</strong> (<strong>NPY</strong>), a neuropeptide with anxiolytic properties.
+NPY	drug	alcohol	15582675	The hypothesis to be developed in the present review is that a dysregulation of the CRF and <strong>NPY</strong> systems significantly contributes to the motivational basis of continued <b>alcohol</b> seeking behavior during <b>alcohol</b> dependence.
+NPY	addiction	dependence	15582675	The hypothesis to be developed in the present review is that a dysregulation of the CRF and <strong>NPY</strong> systems significantly contributes to the motivational basis of continued alcohol seeking behavior during alcohol <b>dependence</b>.
+NPY	addiction	relapse	15582675	The hypothesis to be developed in the present review is that a dysregulation of the CRF and <strong>NPY</strong> systems significantly contributes to the motivational basis of continued alcohol <b>seeking</b> behavior during alcohol dependence.
+NPY	drug	alcohol	15582675	It appears that increases in CRF contribute to the negative affective state that is strongly associated with <b>alcohol</b> withdrawal, and <strong>NPY</strong> provides a motivational basis to consume <b>alcohol</b> because the anxiolytic effects of <b>alcohol</b>, which are strongly associated with relapse, appear to be regulated in part by this neuropeptide.
+NPY	addiction	relapse	15582675	It appears that increases in CRF contribute to the negative affective state that is strongly associated with alcohol withdrawal, and <strong>NPY</strong> provides a motivational basis to consume alcohol because the anxiolytic effects of alcohol, which are strongly associated with <b>relapse</b>, appear to be regulated in part by this neuropeptide.
+NPY	addiction	withdrawal	15582675	It appears that increases in CRF contribute to the negative affective state that is strongly associated with alcohol <b>withdrawal</b>, and <strong>NPY</strong> provides a motivational basis to consume alcohol because the anxiolytic effects of alcohol, which are strongly associated with relapse, appear to be regulated in part by this neuropeptide.
+NPY	drug	alcohol	15567472	Innate differences in neuropeptide Y (<strong>NPY</strong>) mRNA expression in discrete brain regions between <b>alcohol</b> preferring (P) and  nonpreferring (NP) rats: a significantly low level of <strong>NPY</strong> mRNA in dentate gyrus of the hippocampus and absence of <strong>NPY</strong> mRNA in the medial habenular nucleus of P rats.
+NPY	drug	alcohol	15567472	Innate differences in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) mRNA expression in discrete brain regions between <b>alcohol</b> preferring (P) and  nonpreferring (NP) rats: a significantly low level of <strong>NPY</strong> mRNA in dentate gyrus of the hippocampus and absence of <strong>NPY</strong> mRNA in the medial habenular nucleus of P rats.
+NPY	drug	alcohol	15567472	The neuropeptide Y (<strong>NPY</strong>) gene in rat chromosome 4 has been shown to play an important role in <b>alcohol</b> seeking behavior.
+NPY	addiction	relapse	15567472	The neuropeptide Y (<strong>NPY</strong>) gene in rat chromosome 4 has been shown to play an important role in alcohol <b>seeking</b> behavior.
+NPY	drug	alcohol	15567472	The <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene in rat chromosome 4 has been shown to play an important role in <b>alcohol</b> seeking behavior.
+NPY	addiction	relapse	15567472	The <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene in rat chromosome 4 has been shown to play an important role in alcohol <b>seeking</b> behavior.
+NPY	drug	alcohol	15567472	<strong>NPY</strong> knockout mice drink more <b>alcohol</b> than wild type mice, implicating a link between <strong>NPY</strong> deficiency and high <b>alcohol</b> intake.
+NPY	drug	alcohol	15567472	This is supported by recent studies showing that intracerebroventricular injections of <strong>NPY</strong> reduce <b>alcohol</b> intake in both <b>alcohol</b> preferring (P) and high <b>alcohol</b> drinking rats.
+NPY	drug	alcohol	15567472	However, it is unknown which anatomical <strong>NPY</strong> systems are involved in <b>alcohol</b> preference.
+NPY	drug	alcohol	15567472	This study was designed to investigate whether there are innate differences in <strong>NPY</strong> mRNA in cerebral cortical areas, dentate gyrus (DG) of the hippocampus and medial habenular nucleus (MHb) between P and <b>alcohol</b> nonpreferring (NP) rats, as these discrete brain regions are rich in <strong>NPY</strong> mRNA.
+NPY	drug	cocaine	15547783	Numerous synthetic compounds bind to sigma(1) receptor, playing the role of activator/agonist or blocker/antagonist, and these include benzomorphans, neuroleptics, antidepressants, <b>cocaine</b>, peptides related to <strong>neuropeptide Y</strong> or calcitonin gene related peptide.
+NPY	drug	alcohol	15520048	Recent studies have suggested that leptin and <strong>NPY</strong> play significant roles in the pathophysiology of <b>alcoholism</b>.
+NPY	drug	alcohol	15337375	A role for <strong>neuropeptide Y</strong> in neurobiological responses to <b>ethanol</b> and drugs of abuse.
+NPY	drug	alcohol	15337375	In recent years, evidence has emerged suggesting that neuropeptide Y (<strong>NPY</strong>) is involved with neurobiological responses to <b>ethanol</b> and other drugs of abuse.
+NPY	drug	alcohol	15337375	In recent years, evidence has emerged suggesting that <strong>neuropeptide Y</strong> (<strong>NPY</strong>) is involved with neurobiological responses to <b>ethanol</b> and other drugs of abuse.
+NPY	drug	alcohol	15337375	Here, we provide an overview of physiological, pharmacological, and genetic research showing that: (A) administration of <b>ethanol</b>, as well as <b>ethanol</b> withdrawal, alter central <strong>NPY</strong> expression, (B) <strong>NPY</strong> modulates <b>ethanol</b> consumption under certain conditions, and (C) <strong>NPY</strong> signaling modulates the sedative effects of several drugs, including <b>ethanol</b>, sodium pentobarbital, and ketamine.
+NPY	drug	psychedelics	15337375	Here, we provide an overview of physiological, pharmacological, and genetic research showing that: (A) administration of ethanol, as well as ethanol withdrawal, alter central <strong>NPY</strong> expression, (B) <strong>NPY</strong> modulates ethanol consumption under certain conditions, and (C) <strong>NPY</strong> signaling modulates the sedative effects of several drugs, including ethanol, sodium pentobarbital, and <b>ketamine</b>.
+NPY	addiction	withdrawal	15337375	Here, we provide an overview of physiological, pharmacological, and genetic research showing that: (A) administration of ethanol, as well as ethanol <b>withdrawal</b>, alter central <strong>NPY</strong> expression, (B) <strong>NPY</strong> modulates ethanol consumption under certain conditions, and (C) <strong>NPY</strong> signaling modulates the sedative effects of several drugs, including ethanol, sodium pentobarbital, and ketamine.
+NPY	drug	alcohol	15337375	Evidence suggesting possible mechanism(s) by which <strong>NPY</strong> signaling modulates <b>ethanol</b> consumption are considered.
+NPY	drug	alcohol	15337375	It is suggested that <strong>NPY</strong> may influence <b>ethanol</b> consumption by regulating basal levels of anxiety, by modulating the sedative effects of <b>ethanol</b>, and/or by modulating <b>ethanol</b>'s rewarding properties.
+NPY	drug	alcohol	15203244	Assessment of <b>ethanol</b> consumption and water drinking by <strong>NPY</strong> Y(2) receptor knockout mice.
+NPY	drug	alcohol	15203244	In recent years, pharmacological and genetic evidence have emerged suggesting that neuropeptide Y (<strong>NPY</strong>) and the <strong>NPY</strong> Y(1) receptor are involved with neurobiological responses to <b>ethanol</b>.
+NPY	drug	alcohol	15203244	In recent years, pharmacological and genetic evidence have emerged suggesting that <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and the <strong>NPY</strong> Y(1) receptor are involved with neurobiological responses to <b>ethanol</b>.
+NPY	drug	alcohol	15203244	Pharmacological data implicate a role for the <strong>NPY</strong> Y(2) receptor in <b>ethanol</b> self administration.
+NPY	drug	alcohol	15203244	Here, we report that mutant mice lacking the <strong>NPY</strong> Y(2) receptor (Y(2)( / )), when maintained on a mixed 50% 129/ SvJ x 50 % Balb/cJ background, drink significantly less of solutions containing 3 or 6% (v/v) <b>ethanol</b> relative to wild type (Y(2)(+/+)) mice.
+NPY	drug	alcohol	15203244	However, Y(2)( / ) mice that are backcrossed to a Balb/cJ background show normal consumption of <b>ethanol</b>, indicating that the contributions of the <strong>NPY</strong> Y(2) receptor to <b>ethanol</b> consumption are genetic background dependent.
+NPY	drug	alcohol	15203244	The present results suggest roles for the <strong>NPY</strong> Y(2) receptor in the modulation of <b>ethanol</b> and water consumption.
+NPY	drug	alcohol	15182714	Here we show that allelic variation that alters the functional level of NPR 1, a neuropeptide Y (<strong>NPY</strong>) receptor like protein, can account for natural variation in the acute response to <b>ethanol</b> in wild strains of Caenorhabditis elegans.
+NPY	drug	alcohol	15182714	Here we show that allelic variation that alters the functional level of NPR 1, a <strong>neuropeptide Y</strong> (<strong>NPY</strong>) receptor like protein, can account for natural variation in the acute response to <b>ethanol</b> in wild strains of Caenorhabditis elegans.
+NPY	drug	alcohol	15182714	This suggests an explanation for the conserved function of <strong>NPY</strong> related pathways in <b>ethanol</b> responses across diverse species.
+NPY	drug	alcohol	15163695	It was also found that CREB deficient (+/ ) mice displayed more anxiety like behaviors and that acute <b>ethanol</b> exposure produced anxiolytic effects and significantly increased protein levels of p CREB and <strong>NPY</strong> in the central and medial but not in the basolateral amygdala of wild type mice, but these effects are attenuated in CREB deficient mice compared with wild type mice.
+NPY	drug	alcohol	15163695	Furthermore, <b>alcohol</b> drinking and anxiety like behaviors in CREB haplodeficient mice may possibly be related to decreased expression of <strong>NPY</strong> and BDNF in the brains of these mice.
+NPY	drug	alcohol	15112936	The presentations were (1) Voluntary <b>alcohol</b> consumption is modulated by central melanocortin receptors, by Todd E. Thiele; (2) Central infusion of <strong>neuropeptide Y</strong> reduces <b>alcohol</b> drinking in <b>alcohol</b> preferring P rats, by Robert B. Stewart and Nancy E. Badia Elder; (3) The gut peptide cholecystokinin controls <b>alcohol</b> intake in Sardinian <b>alcohol</b> preferring rats, by Nori Geary and Maurizio Massi; and (4) Hypothalamic galanin: a possible role in excess <b>alcohol</b> drinking, by Sarah F. Leibowitz and Bartley G. Hoebel.
+NPY	drug	amphetamine	15107726	Then are considered, especially at the hypothalamic level, their interpretation by neurones whose transmitters are either neuropeptides such as: <strong>Neuropeptide Y</strong>, Agouti Related Peptide, Cocaine/<b>Amphetamine</b> Regulated Transcript, Melanin Concentrating Hormone, alpha Melanocyte Stimulating Hormone, orexins/hypocretins, octadecaneuropeptide, nociceptin/orphanin FQ, opioid peptides, Interleukin 1, galanin, urocortin 2, Neurotrophic ciliary factor, or monoamines such as: Glutamate, dopamine, Norepinephrine, serotonine, GABA, histamine, acetylcholine.
+NPY	drug	cocaine	15107726	Then are considered, especially at the hypothalamic level, their interpretation by neurones whose transmitters are either neuropeptides such as: <strong>Neuropeptide Y</strong>, Agouti Related Peptide, <b>Cocaine</b>/Amphetamine Regulated Transcript, Melanin Concentrating Hormone, alpha Melanocyte Stimulating Hormone, orexins/hypocretins, octadecaneuropeptide, nociceptin/orphanin FQ, opioid peptides, Interleukin 1, galanin, urocortin 2, Neurotrophic ciliary factor, or monoamines such as: Glutamate, dopamine, Norepinephrine, serotonine, GABA, histamine, acetylcholine.
+NPY	drug	opioid	15107726	Then are considered, especially at the hypothalamic level, their interpretation by neurones whose transmitters are either neuropeptides such as: <strong>Neuropeptide Y</strong>, Agouti Related Peptide, Cocaine/Amphetamine Regulated Transcript, Melanin Concentrating Hormone, alpha Melanocyte Stimulating Hormone, orexins/hypocretins, octadecaneuropeptide, nociceptin/orphanin FQ, <b>opioid</b> peptides, Interleukin 1, galanin, urocortin 2, Neurotrophic ciliary factor, or monoamines such as: Glutamate, dopamine, Norepinephrine, serotonine, GABA, histamine, acetylcholine.
+NPY	drug	opioid	15048644	We found correspondence between linkage and microarray/candidate gene studies for genes involved with the mitogen activated protein kinase (MAPK) signaling system, nuclear factor kappa B (NFKB) complex, neuropeptide Y (<strong>NPY</strong>) neurotransmission, a nicotinic receptor subunit (CHRNA2), the vesicular monoamine transporter (SLC18A2), genes in pathways implicated in human anxiety (HTR7, TDO2, and the endozepine related protein precursor, DKFZP434A2417), and the micro 1 <b>opioid</b> receptor (OPRM1).
+NPY	drug	opioid	15048644	We found correspondence between linkage and microarray/candidate gene studies for genes involved with the mitogen activated protein kinase (MAPK) signaling system, nuclear factor kappa B (NFKB) complex, <strong>neuropeptide Y</strong> (<strong>NPY</strong>) neurotransmission, a nicotinic receptor subunit (CHRNA2), the vesicular monoamine transporter (SLC18A2), genes in pathways implicated in human anxiety (HTR7, TDO2, and the endozepine related protein precursor, DKFZP434A2417), and the micro 1 <b>opioid</b> receptor (OPRM1).
+NPY	drug	opioid	14985834	Co administration of 0.2 nmol of <strong>NPY</strong>(28 36) and 5.5 nmol of <b>naloxone</b> significantly attenuated the <strong>NPY</strong> induced increase in PWLs.
+NPY	drug	opioid	14985834	The results suggest that Y(1) receptor may mediate <strong>NPY</strong> induced anti nociception, and that the <b>opioid</b> receptors in PAG may also be involved in this process in mononeuropathic rats.
+NPY	drug	alcohol	14706555	Effects of PKA modulation on the expression of <strong>neuropeptide Y</strong> in rat amygdaloid structures during <b>ethanol</b> withdrawal.
+NPY	addiction	withdrawal	14706555	Effects of PKA modulation on the expression of <strong>neuropeptide Y</strong> in rat amygdaloid structures during ethanol <b>withdrawal</b>.
+NPY	drug	alcohol	14706555	We recently reported that neuropeptide Y (<strong>NPY</strong>) protein levels and cAMP responsive element binding (CREB) protein phosphorylation are lower in amygdaloid structures during <b>ethanol</b> withdrawal after chronic exposure.
+NPY	addiction	withdrawal	14706555	We recently reported that neuropeptide Y (<strong>NPY</strong>) protein levels and cAMP responsive element binding (CREB) protein phosphorylation are lower in amygdaloid structures during ethanol <b>withdrawal</b> after chronic exposure.
+NPY	drug	alcohol	14706555	We recently reported that <strong>neuropeptide Y</strong> (<strong>NPY</strong>) protein levels and cAMP responsive element binding (CREB) protein phosphorylation are lower in amygdaloid structures during <b>ethanol</b> withdrawal after chronic exposure.
+NPY	addiction	withdrawal	14706555	We recently reported that <strong>neuropeptide Y</strong> (<strong>NPY</strong>) protein levels and cAMP responsive element binding (CREB) protein phosphorylation are lower in amygdaloid structures during ethanol <b>withdrawal</b> after chronic exposure.
+NPY	drug	alcohol	14706555	Here we investigated whether normalization of CREB phosphorylation by infusing PKA activator (Sp cAMP) into the central amygdala also normalizes the expression of <strong>NPY</strong> during <b>ethanol</b> withdrawal.
+NPY	addiction	withdrawal	14706555	Here we investigated whether normalization of CREB phosphorylation by infusing PKA activator (Sp cAMP) into the central amygdala also normalizes the expression of <strong>NPY</strong> during ethanol <b>withdrawal</b>.
+NPY	drug	alcohol	14706555	It was found that chronic <b>ethanol</b> treatment has no effect on mRNA and protein levels of <strong>NPY</strong> in the central, medial, or basolateral amygdala.
+NPY	drug	alcohol	14706555	On the other hand, <b>ethanol</b> withdrawal produced significant reductions in mRNA and protein levels of <strong>NPY</strong> in the central and medial but not in the basolateral amygdala.
+NPY	addiction	withdrawal	14706555	On the other hand, ethanol <b>withdrawal</b> produced significant reductions in mRNA and protein levels of <strong>NPY</strong> in the central and medial but not in the basolateral amygdala.
+NPY	drug	alcohol	14706555	The reductions in mRNA and protein levels of <strong>NPY</strong> were normalized in the central amygdala by infusion with PKA activator in <b>ethanol</b> withdrawn rats.
+NPY	drug	alcohol	14706555	On the other hand, PKA inhibitor infusion does not have any effect on mRNA and protein levels of <strong>NPY</strong> in the central amygdala of <b>ethanol</b> withdrawn rats, but significantly decreased the expression of <strong>NPY</strong> in the central amygdala of control diet fed rats.
+NPY	drug	alcohol	14706555	These results suggest that the decreased cellular expression of <strong>NPY</strong> in the central amygdala may play an important role in the CREB mediated regulation of anxiety like behaviors during <b>ethanol</b> withdrawal.
+NPY	addiction	withdrawal	14706555	These results suggest that the decreased cellular expression of <strong>NPY</strong> in the central amygdala may play an important role in the CREB mediated regulation of anxiety like behaviors during ethanol <b>withdrawal</b>.
+NPY	drug	alcohol	14698675	The present review highlights research aimed at determining if ingestive peptides also regulate voluntary <b>ethanol</b> intake, with an emphasis on the melanocortins and <strong>neuropeptide Y</strong>.
+NPY	drug	alcohol	14691378	<strong>Neuropeptide Y</strong> Y5 receptors modulate the onset and maintenance of operant <b>ethanol</b> self administration.
+NPY	addiction	reward	14691378	<strong>Neuropeptide Y</strong> Y5 receptors modulate the onset and maintenance of <b>operant</b> ethanol self administration.
+NPY	drug	alcohol	14691378	Recent pharmacological and mutant mouse data indicate that <strong>NPY</strong> activity at its receptors can influence <b>ethanol</b> self administration, although the direction and strength of this influence are not clear.
+NPY	drug	alcohol	14691378	Effects of the novel <strong>NPY</strong> Y5 receptor antagonist L 152,804 on the onset and maintenance of operant self administration were examined in male C57BL/6J mice, which were trained to self administer <b>ethanol</b> (10% v/v) versus water via the sucrose substitution method during 16 hr overnight sessions.
+NPY	addiction	reward	14691378	Effects of the novel <strong>NPY</strong> Y5 receptor antagonist L 152,804 on the onset and maintenance of <b>operant</b> self administration were examined in male C57BL/6J mice, which were trained to self administer ethanol (10% v/v) versus water via the sucrose substitution method during 16 hr overnight sessions.
+NPY	drug	alcohol	14691378	These results indicate that blockade <strong>NPY</strong> Y5 receptor activity modulates the onset and maintenance of <b>ethanol</b> self administration.
+NPY	drug	alcohol	14691378	For this reason, <strong>NPY</strong> Y5 receptor antagonists may be useful in medical management of <b>alcohol</b> abuse and <b>alcoholism</b>.
+NPY	drug	alcohol	14691375	Intra amygdala infusion of the <strong>NPY</strong> Y1 receptor antagonist BIBP 3226 attenuates operant <b>ethanol</b> self administration.
+NPY	addiction	reward	14691375	Intra amygdala infusion of the <strong>NPY</strong> Y1 receptor antagonist BIBP 3226 attenuates <b>operant</b> ethanol self administration.
+NPY	drug	alcohol	14691375	Evidence suggests that <strong>NPY</strong> transmission at Y1 receptors may regulate <b>alcohol</b> self administration in rodent models.
+NPY	drug	alcohol	14691375	The purpose of the present study was to test the involvement of <strong>NPY</strong> Y1 receptors in the amygdala in the reinforcing effects of <b>alcohol</b>.
+NPY	addiction	reward	14691375	The purpose of the present study was to test the involvement of <strong>NPY</strong> Y1 receptors in the amygdala in the <b>reinforcing</b> effects of alcohol.
+NPY	drug	alcohol	14691375	Then, the effects of intra amygdala infusion of the high affinity nonpeptide <strong>NPY</strong> Y1 receptor antagonist BIBP 3226 (1, 10, or 20 microMg) were determined on parameters of operant <b>alcohol</b> self administration.
+NPY	addiction	reward	14691375	Then, the effects of intra amygdala infusion of the high affinity nonpeptide <strong>NPY</strong> Y1 receptor antagonist BIBP 3226 (1, 10, or 20 microMg) were determined on parameters of <b>operant</b> alcohol self administration.
+NPY	drug	alcohol	14691375	Results from this study indicate that <b>alcohol</b> reinforced responding is reduced by acute blockade of <strong>NPY</strong> Y1 receptors in the amygdala of rats with a long term history of <b>alcohol</b> self administration.
+NPY	drug	alcohol	14691375	These data are consistent with the hypothesis that <b>alcohol</b> self administration is maintained by <strong>NPY</strong> neurotransmission at Y1 receptors in the central nucleus of the amygdala.
+NPY	drug	alcohol	14648603	Differences in basal levels of CREB and <strong>NPY</strong> in nucleus accumbens regions between C57BL/6 and DBA/2 mice differing in inborn <b>alcohol</b> drinking behavior.
+NPY	drug	alcohol	12967770	Anxiety and <b>alcohol</b> abuse disorders: a common role for CREB and its target, the <strong>neuropeptide Y</strong> gene.
+NPY	drug	alcohol	12967770	The CREB gene transcription factor regulates the expression of the gene encoding neuropeptide Y (<strong>NPY</strong>), and decreased concentrations of <strong>NPY</strong> are implicated in anxiety and <b>alcohol</b> drinking behaviors.
+NPY	drug	alcohol	12967770	The CREB gene transcription factor regulates the expression of the gene encoding <strong>neuropeptide Y</strong> (<strong>NPY</strong>), and decreased concentrations of <strong>NPY</strong> are implicated in anxiety and <b>alcohol</b> drinking behaviors.
+NPY	drug	alcohol	12967770	Therefore, decreased function of CREB in the central nucleus of the amygdala might regulate anxiety and <b>alcohol</b> intake via decreased expression of <strong>NPY</strong>, and might provide a common link between anxiety and <b>alcohol</b> abuse disorders.
+NPY	drug	alcohol	12967770	I also suggest that, via CREB, <strong>NPY</strong> might interact with other CREB target genes, such as the gene encoding brain derived neurotrophic factor, and that this CREB mediated interaction might be important in the regulation of anxiety and <b>alcohol</b> drinking behaviors.
+NPY	addiction	reward	12930156	Of particular interest are the '<b>reward</b> pathway' (serotonin, dopamine, GABA, glutamate, and beta endorphin) and the behavioral stress response system (corticotrophin releasing factor and <strong>neuropeptide Y</strong>).
+NPY	drug	alcohol	12878925	<b>Alcohol</b> withdrawal increases <strong>neuropeptide Y</strong> immunoreactivity in rat brain.
+NPY	addiction	withdrawal	12878925	Alcohol <b>withdrawal</b> increases <strong>neuropeptide Y</strong> immunoreactivity in rat brain.
+NPY	drug	alcohol	12878925	Neuropeptide Y (<strong>NPY</strong>) is widely expressed in the brain and is known to affect consummatory behaviors including drinking <b>alcohol</b> as well as to play a role in seizures.
+NPY	drug	alcohol	12878925	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) is widely expressed in the brain and is known to affect consummatory behaviors including drinking <b>alcohol</b> as well as to play a role in seizures.
+NPY	drug	alcohol	12878925	We investigated the effects of a 4 day binge <b>ethanol</b> treatment model that is known to induce physical dependence and withdrawal seizures to determine the effects of <b>ethanol</b> dependence and withdrawal on <strong>NPY</strong> expression.
+NPY	addiction	dependence	12878925	We investigated the effects of a 4 day binge ethanol treatment model that is known to induce physical <b>dependence</b> and withdrawal seizures to determine the effects of ethanol <b>dependence</b> and withdrawal on <strong>NPY</strong> expression.
+NPY	addiction	intoxication	12878925	We investigated the effects of a 4 day <b>binge</b> ethanol treatment model that is known to induce physical dependence and withdrawal seizures to determine the effects of ethanol dependence and withdrawal on <strong>NPY</strong> expression.
+NPY	addiction	withdrawal	12878925	We investigated the effects of a 4 day binge ethanol treatment model that is known to induce physical dependence and <b>withdrawal</b> seizures to determine the effects of ethanol dependence and <b>withdrawal</b> on <strong>NPY</strong> expression.
+NPY	drug	alcohol	12878925	<strong>NPY</strong> IR was reduced by <b>ethanol</b> treatment in hippocampus and cortex, although at 72 hr of withdrawal there was a dramatic increase in <strong>NPY</strong> IR in the hilus of the dentate gyrus and in CA3 and CA2 fields of hippocampus.
+NPY	addiction	withdrawal	12878925	<strong>NPY</strong> IR was reduced by ethanol treatment in hippocampus and cortex, although at 72 hr of <b>withdrawal</b> there was a dramatic increase in <strong>NPY</strong> IR in the hilus of the dentate gyrus and in CA3 and CA2 fields of hippocampus.
+NPY	drug	alcohol	12878925	<b>Ethanol</b> withdrawal seizures occurred around 12 to 24 hr of withdrawal, preceding the changes in <strong>NPY</strong> IR at 72 hr.
+NPY	addiction	withdrawal	12878925	Ethanol <b>withdrawal</b> seizures occurred around 12 to 24 hr of <b>withdrawal</b>, preceding the changes in <strong>NPY</strong> IR at 72 hr.
+NPY	addiction	withdrawal	12878925	<strong>NPY</strong> IR returned to control levels by 168 hr of <b>withdrawal</b>.
+NPY	drug	alcohol	12878925	These studies suggest that hippocampal <strong>NPY</strong> is reduced during the development of <b>ethanol</b> dependence.
+NPY	addiction	dependence	12878925	These studies suggest that hippocampal <strong>NPY</strong> is reduced during the development of ethanol <b>dependence</b>.
+NPY	drug	alcohol	12878925	<b>Ethanol</b> withdrawal seizures precede a dramatic increase in hippocampal <strong>NPY</strong> IR.
+NPY	addiction	withdrawal	12878925	Ethanol <b>withdrawal</b> seizures precede a dramatic increase in hippocampal <strong>NPY</strong> IR.
+NPY	drug	alcohol	12878925	Thus, the increase in <strong>NPY</strong> IR at 72 hr of withdrawal after binge <b>ethanol</b> treatment may be protective against prolonged withdrawal seizure activity.
+NPY	addiction	intoxication	12878925	Thus, the increase in <strong>NPY</strong> IR at 72 hr of withdrawal after <b>binge</b> ethanol treatment may be protective against prolonged withdrawal seizure activity.
+NPY	addiction	withdrawal	12878925	Thus, the increase in <strong>NPY</strong> IR at 72 hr of <b>withdrawal</b> after binge ethanol treatment may be protective against prolonged <b>withdrawal</b> seizure activity.
+NPY	drug	opioid	12851316	Despite the absence of endogenous beta endorphin, the mutant mice did not differ from wild type mice in their acute feeding responses to beta endorphin or <strong>neuropeptide Y</strong> administered intracerebroventricularly or <b>naloxone</b> administered intraperitoneally.
+NPY	drug	alcohol	12818715	<b>Ethanol</b>, injected daily (0.8 g/kg 10% v/v) for 7 days in male rats, markedly increased the expression of GAL but not of neuropeptide Y (<strong>NPY</strong>).
+NPY	drug	alcohol	12818715	<b>Ethanol</b>, injected daily (0.8 g/kg 10% v/v) for 7 days in male rats, markedly increased the expression of GAL but not of <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	alcohol	12766623	<strong>Neuropeptide Y</strong> reduces oral <b>ethanol</b> intake in <b>alcohol</b> preferring (P) rats following a period of imposed <b>ethanol</b> abstinence.
+NPY	drug	alcohol	12766623	Intracerebroventricular infusion of <strong>NPY</strong> has been shown to reduce <b>ethanol</b> intake in <b>alcohol</b> preferring (P) rats in a limited access procedure.
+NPY	drug	alcohol	12766623	Following the <b>ethanol</b> abstinence period and immediately before <b>ethanol</b> reinstatement, rats received a single infusion of either artificial cerebrospinal fluid or <strong>NPY</strong> (10 microg).
+NPY	addiction	relapse	12766623	Following the ethanol abstinence period and immediately before ethanol <b>reinstatement</b>, rats received a single infusion of either artificial cerebrospinal fluid or <strong>NPY</strong> (10 microg).
+NPY	drug	alcohol	12766623	Following 2 weeks of imposed <b>ethanol</b> abstinence (experiment 1), <strong>NPY</strong> suppressed <b>ethanol</b> intake through postinfusion day 2.
+NPY	drug	alcohol	12766623	After uninterrupted continuous access to <b>ethanol</b> (experiment 2), <strong>NPY</strong> suppressed <b>ethanol</b> intake to a lesser extent and this effect lasted only 24 hr.
+NPY	drug	alcohol	12766623	Previous findings that central administration of <strong>NPY</strong> suppresses <b>ethanol</b> intake in P rats are extended by this study to a continuous access procedure, and the effect is amplified following a period of imposed <b>ethanol</b> abstinence.
+NPY	addiction	addiction	12766623	This effect of <strong>NPY</strong> compares favorably to results obtained with other treatments tested in similar animal models and provides support for a role of <strong>NPY</strong> in an allostasis model of <b>addiction</b>.
+NPY	drug	alcohol	12658105	We also found that <b>alcohol</b> preference provoked by decreased CREB phosphorylation is related to decreased expression of the <strong>neuropeptide Y</strong> gene in the central amygdala.
+NPY	drug	opioid	12612162	In animal studies, fat intake is increased by both <b>opioids</b> and galanin and reduced by enterostatin, whereas carbohydrate intake is increased by neuropeptide Y (<strong>NPY</strong>).
+NPY	drug	opioid	12612162	In animal studies, fat intake is increased by both <b>opioids</b> and galanin and reduced by enterostatin, whereas carbohydrate intake is increased by <strong>neuropeptide Y</strong> (<strong>NPY</strong>).
+NPY	drug	alcohol	12605072	During the development of <b>alcohol</b> dependence, corticotropin releasing factor may be recruited, and the <strong>neuropeptide Y</strong> brain antistress system may be compromised.
+NPY	addiction	dependence	12605072	During the development of alcohol <b>dependence</b>, corticotropin releasing factor may be recruited, and the <strong>neuropeptide Y</strong> brain antistress system may be compromised.
+NPY	drug	alcohol	12605064	<strong>Neuropeptide y</strong> and <b>alcoholism</b>: genetic, molecular, and pharmacological evidence.
+NPY	drug	alcohol	12605064	The presentations were (1) Altered <b>ethanol</b> induced sedation and <b>ethanol</b> drinking in mutant mice lacking specific <strong>NPY</strong> receptor, by Todd E. Thiele; (2) <strong>NPY</strong> in P and NP rats: polymorphism and mRNA expression, by Lucinda G. Carr; (3) The cAMP dependent PKA in the central amygdala regulates <b>alcohol</b> intake through <strong>NPY</strong> gene, by Subhash C. Pandey; (4) Involvement of <strong>NPY</strong> in <b>alcohol</b> dependence: from animal models to human genetics, by Markus Heilig; and (5) Association of neuropeptide Y polymorphism with the occurrence of type 1 and type 2 <b>alcoholism</b>, by Erkki Ilveskoski.
+NPY	addiction	dependence	12605064	The presentations were (1) Altered ethanol induced sedation and ethanol drinking in mutant mice lacking specific <strong>NPY</strong> receptor, by Todd E. Thiele; (2) <strong>NPY</strong> in P and NP rats: polymorphism and mRNA expression, by Lucinda G. Carr; (3) The cAMP dependent PKA in the central amygdala regulates alcohol intake through <strong>NPY</strong> gene, by Subhash C. Pandey; (4) Involvement of <strong>NPY</strong> in alcohol <b>dependence</b>: from animal models to human genetics, by Markus Heilig; and (5) Association of neuropeptide Y polymorphism with the occurrence of type 1 and type 2 alcoholism, by Erkki Ilveskoski.
+NPY	drug	alcohol	12605064	The presentations were (1) Altered <b>ethanol</b> induced sedation and <b>ethanol</b> drinking in mutant mice lacking specific <strong>NPY</strong> receptor, by Todd E. Thiele; (2) <strong>NPY</strong> in P and NP rats: polymorphism and mRNA expression, by Lucinda G. Carr; (3) The cAMP dependent PKA in the central amygdala regulates <b>alcohol</b> intake through <strong>NPY</strong> gene, by Subhash C. Pandey; (4) Involvement of <strong>NPY</strong> in <b>alcohol</b> dependence: from animal models to human genetics, by Markus Heilig; and (5) Association of <strong>neuropeptide Y</strong> polymorphism with the occurrence of type 1 and type 2 <b>alcoholism</b>, by Erkki Ilveskoski.
+NPY	addiction	dependence	12605064	The presentations were (1) Altered ethanol induced sedation and ethanol drinking in mutant mice lacking specific <strong>NPY</strong> receptor, by Todd E. Thiele; (2) <strong>NPY</strong> in P and NP rats: polymorphism and mRNA expression, by Lucinda G. Carr; (3) The cAMP dependent PKA in the central amygdala regulates alcohol intake through <strong>NPY</strong> gene, by Subhash C. Pandey; (4) Involvement of <strong>NPY</strong> in alcohol <b>dependence</b>: from animal models to human genetics, by Markus Heilig; and (5) Association of <strong>neuropeptide Y</strong> polymorphism with the occurrence of type 1 and type 2 alcoholism, by Erkki Ilveskoski.
+NPY	drug	alcohol	12544000	<strong>NPY</strong> Leu7Pro and <b>alcohol</b> dependence in Finnish and Swedish populations.
+NPY	addiction	dependence	12544000	<strong>NPY</strong> Leu7Pro and alcohol <b>dependence</b> in Finnish and Swedish populations.
+NPY	drug	alcohol	12544000	Neuropeptide Y (<strong>NPY</strong>) is a modulator of <b>alcohol</b> intake in animal models of <b>alcoholism</b>, and is potentially involved in <b>alcohol</b> dependence.
+NPY	addiction	dependence	12544000	Neuropeptide Y (<strong>NPY</strong>) is a modulator of alcohol intake in animal models of alcoholism, and is potentially involved in alcohol <b>dependence</b>.
+NPY	drug	alcohol	12544000	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) is a modulator of <b>alcohol</b> intake in animal models of <b>alcoholism</b>, and is potentially involved in <b>alcohol</b> dependence.
+NPY	addiction	dependence	12544000	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) is a modulator of alcohol intake in animal models of alcoholism, and is potentially involved in alcohol <b>dependence</b>.
+NPY	drug	alcohol	12454738	Severity of <b>alcohol</b> withdrawal symptoms and the T1128C polymorphism of the <strong>neuropeptide Y</strong> gene.
+NPY	addiction	withdrawal	12454738	Severity of alcohol <b>withdrawal</b> symptoms and the T1128C polymorphism of the <strong>neuropeptide Y</strong> gene.
+NPY	drug	alcohol	12454738	Neuropeptide Y (<strong>NPY</strong>) modulates <b>ethanol</b> drinking in rodents.
+NPY	drug	alcohol	12454738	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) modulates <b>ethanol</b> drinking in rodents.
+NPY	drug	alcohol	12454738	The C allele of the T1128C polymorphism of the human <strong>NPY</strong> gene has been previously associated with elevated <b>alcohol</b> consumption in a Finn population study.
+NPY	drug	alcohol	12454738	More studies on different ethnic groups are needed to further elucidate the influence of the <strong>NPY</strong> gene on <b>alcoholism</b>.
+NPY	drug	opioid	12405517	Consistent findings with the selected lines include differences in the mesolimbic dopamine reward system, as well as differences in serotonin, GABA, endogenous <b>opioid</b>, and <strong>neuropeptide Y</strong> systems.
+NPY	addiction	reward	12405517	Consistent findings with the selected lines include differences in the mesolimbic dopamine <b>reward</b> system, as well as differences in serotonin, GABA, endogenous opioid, and <strong>neuropeptide Y</strong> systems.
+NPY	drug	alcohol	12377370	Blockade of central neuropeptide Y (<strong>NPY</strong>) Y2 receptors reduces <b>ethanol</b> self administration in rats.
+NPY	drug	alcohol	12377370	Blockade of central <strong>neuropeptide Y</strong> (<strong>NPY</strong>) Y2 receptors reduces <b>ethanol</b> self administration in rats.
+NPY	drug	alcohol	12377370	In addition, experiments in knock out and transgenic mice have suggested a possible role of <strong>NPY</strong> regulation of voluntary <b>ethanol</b> intake.
+NPY	drug	alcohol	12377370	Here, we examined the effects of a selective <strong>NPY</strong> Y2 receptor antagonist, BIIE0246, on operant responding for <b>ethanol</b> in a sweetened solution, or the sweetened solution without <b>ethanol</b>, during 30 min sessions of free choice between the two.
+NPY	addiction	reward	12377370	Here, we examined the effects of a selective <strong>NPY</strong> Y2 receptor antagonist, BIIE0246, on <b>operant</b> responding for ethanol in a sweetened solution, or the sweetened solution without ethanol, during 30 min sessions of free choice between the two.
+NPY	drug	alcohol	12377370	In summary, antagonism at central <strong>NPY</strong> Y2 receptors seems to selectively suppress operant self administration of <b>ethanol</b>.
+NPY	addiction	reward	12377370	In summary, antagonism at central <strong>NPY</strong> Y2 receptors seems to selectively suppress <b>operant</b> self administration of ethanol.
+NPY	drug	alcohol	12377358	<strong>Neuropeptide Y</strong> administration into the amygdala does not affect <b>ethanol</b> consumption.
+NPY	drug	alcohol	12377358	Because findings seem to indicate that <b>ethanol</b> may be self administered partially for its anxiolytic effects, it was hypothesized that <strong>NPY</strong>, microinjected into the central nucleus of the amygdala, would decrease <b>ethanol</b> intake.
+NPY	drug	alcohol	12377358	In this study, we examined the effects of <strong>NPY</strong>, administered into the central nucleus of the amygdala, on <b>ethanol</b>, sucrose, and food consumption, as well as the concomitant effects of <strong>NPY</strong> on cortical electroencephalographic activity.
+NPY	drug	alcohol	12377358	<strong>Neuropeptide Y</strong> (0 250 pmol/0.5 micro l) was infused into the amygdala before drinking sessions, when 10% <b>ethanol</b> (10 E), 2% sucrose (2S), or food was available.
+NPY	drug	alcohol	12359508	Together, these models indicate that stress related behaviors and regulation of voluntary <b>alcohol</b> intake perhaps are among the most important functions of central <strong>NPY</strong>, and may provide attractive targets for developing novel therapies in depression, anxiety disorders and <b>alcohol</b> dependence.
+NPY	addiction	dependence	12359508	Together, these models indicate that stress related behaviors and regulation of voluntary alcohol intake perhaps are among the most important functions of central <strong>NPY</strong>, and may provide attractive targets for developing novel therapies in depression, anxiety disorders and alcohol <b>dependence</b>.
+NPY	drug	alcohol	12215082	A functional <strong>neuropeptide Y</strong> Leu7Pro polymorphism associated with <b>alcohol</b> dependence in a large population sample from the United States.
+NPY	addiction	dependence	12215082	A functional <strong>neuropeptide Y</strong> Leu7Pro polymorphism associated with alcohol <b>dependence</b> in a large population sample from the United States.
+NPY	drug	alcohol	12215082	Quantitative trait locus studies, and observations in animals manipulated for the neuropeptide Y (<strong>NPY</strong>) gene suggest that variation within this gene may contribute to <b>alcoholism</b>.
+NPY	drug	alcohol	12215082	Quantitative trait locus studies, and observations in animals manipulated for the <strong>neuropeptide Y</strong> (<strong>NPY</strong>) gene suggest that variation within this gene may contribute to <b>alcoholism</b>.
+NPY	drug	alcohol	12215082	A recent population study suggested that the Pro7 allele of a functional <strong>NPY</strong> polymorphism (Leu7Pro) may be associated with increased <b>alcohol</b> consumption.
+NPY	drug	alcohol	12215082	These results suggest that the <strong>NPY</strong> Pro7 allele is a risk factor for <b>alcohol</b> dependence.
+NPY	addiction	dependence	12215082	These results suggest that the <strong>NPY</strong> Pro7 allele is a risk factor for alcohol <b>dependence</b>.
+NPY	drug	amphetamine	12213133	Hypothalamic interactions between <strong>neuropeptide Y</strong>, agouti related protein, cocaine  and <b>amphetamine</b> regulated transcript and alpha melanocyte stimulating hormone in vitro in male rats.
+NPY	drug	cocaine	12213133	Hypothalamic interactions between <strong>neuropeptide Y</strong>, agouti related protein, <b>cocaine</b>  and amphetamine regulated transcript and alpha melanocyte stimulating hormone in vitro in male rats.
+NPY	drug	nicotine	12122484	<b>Nicotine</b> and its withdrawal alter feeding induced by paraventricular hypothalamic injections of <strong>neuropeptide Y</strong> in Sprague Dawley rats.
+NPY	addiction	withdrawal	12122484	Nicotine and its <b>withdrawal</b> alter feeding induced by paraventricular hypothalamic injections of <strong>neuropeptide Y</strong> in Sprague Dawley rats.
+NPY	addiction	withdrawal	12122484	To characterize potential differences in PVN <strong>NPY</strong> induced feeding during NIC treatment versus <b>withdrawal</b>.
+NPY	drug	alcohol	12107031	<b>Ethanol</b> withdrawal in rats is attenuated by intracerebroventricular administration of <strong>neuropeptide Y</strong>.
+NPY	addiction	withdrawal	12107031	Ethanol <b>withdrawal</b> in rats is attenuated by intracerebroventricular administration of <strong>neuropeptide Y</strong>.
+NPY	drug	alcohol	12107031	The effects of intracerebroventricular administration of neuropeptide Y (<strong>NPY</strong>) on <b>ethanol</b> withdrawal were studied in rats.
+NPY	addiction	withdrawal	12107031	The effects of intracerebroventricular administration of neuropeptide Y (<strong>NPY</strong>) on ethanol <b>withdrawal</b> were studied in rats.
+NPY	drug	alcohol	12107031	The effects of intracerebroventricular administration of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) on <b>ethanol</b> withdrawal were studied in rats.
+NPY	addiction	withdrawal	12107031	The effects of intracerebroventricular administration of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) on ethanol <b>withdrawal</b> were studied in rats.
+NPY	addiction	withdrawal	12107031	Subsequently, the rats received an injection of <strong>NPY</strong> (12 or 24 nmol) or vehicle and were rated for signs of <b>withdrawal</b>.
+NPY	drug	alcohol	12107031	At both doses, <strong>NPY</strong> significantly reduced <b>ethanol</b> withdrawal, the effect of the larger dose being more pronounced.
+NPY	addiction	withdrawal	12107031	At both doses, <strong>NPY</strong> significantly reduced ethanol <b>withdrawal</b>, the effect of the larger dose being more pronounced.
+NPY	drug	alcohol	12107031	Our results are consistent with the concept that <strong>NPY</strong> receptors are centrally involved in the regulation of neuronal excitability and might form a novel therapeutic target for treatment of <b>ethanol</b> withdrawal and other states of neuronal hyperexcitability.
+NPY	addiction	withdrawal	12107031	Our results are consistent with the concept that <strong>NPY</strong> receptors are centrally involved in the regulation of neuronal excitability and might form a novel therapeutic target for treatment of ethanol <b>withdrawal</b> and other states of neuronal hyperexcitability.
+NPY	drug	alcohol	12068247	The decreased cellular expression of <strong>neuropeptide Y</strong> protein in rat brain structures during <b>ethanol</b> withdrawal after chronic <b>ethanol</b> exposure.
+NPY	addiction	withdrawal	12068247	The decreased cellular expression of <strong>neuropeptide Y</strong> protein in rat brain structures during ethanol <b>withdrawal</b> after chronic ethanol exposure.
+NPY	drug	alcohol	12068247	Neuropeptide Y (<strong>NPY</strong>) has been implicated in the <b>alcohol</b> drinking behaviors of rodents.
+NPY	drug	alcohol	12068247	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) has been implicated in the <b>alcohol</b> drinking behaviors of rodents.
+NPY	drug	alcohol	12068247	This study investigated the possible involvement of <strong>NPY</strong> in the neuroadaptational mechanisms to chronic <b>ethanol</b> exposure and its withdrawal.
+NPY	addiction	withdrawal	12068247	This study investigated the possible involvement of <strong>NPY</strong> in the neuroadaptational mechanisms to chronic ethanol exposure and its <b>withdrawal</b>.
+NPY	drug	alcohol	12068247	It was found that <b>ethanol</b> withdrawal, but not <b>ethanol</b> treatment, produced significant reductions in <strong>NPY</strong> protein levels in (1) layers IV and V of the frontal and parietal cortex, (2) layer II of the piriform cortex, (3) the central and medial nuclei of the amygdala, and (4) the paraventricular nucleus of the hypothalamus in rat brain.
+NPY	addiction	withdrawal	12068247	It was found that ethanol <b>withdrawal</b>, but not ethanol treatment, produced significant reductions in <strong>NPY</strong> protein levels in (1) layers IV and V of the frontal and parietal cortex, (2) layer II of the piriform cortex, (3) the central and medial nuclei of the amygdala, and (4) the paraventricular nucleus of the hypothalamus in rat brain.
+NPY	drug	alcohol	12068247	Chronic <b>ethanol</b> exposure and its withdrawal had no effect on the <strong>NPY</strong> protein levels in layers II, III, and VI of the frontal and parietal cortex or cingulate gyrus, in hippocampal (CA1, CA2, CA3, and dentate gyrus) and striatal (caudate putamen and globus pallidus) structures, or in the ventro medial hypothalamus and basolateral amygdala.
+NPY	addiction	withdrawal	12068247	Chronic ethanol exposure and its <b>withdrawal</b> had no effect on the <strong>NPY</strong> protein levels in layers II, III, and VI of the frontal and parietal cortex or cingulate gyrus, in hippocampal (CA1, CA2, CA3, and dentate gyrus) and striatal (caudate putamen and globus pallidus) structures, or in the ventro medial hypothalamus and basolateral amygdala.
+NPY	drug	alcohol	12068247	However, chronic <b>ethanol</b> exposure and its withdrawal produced significant reductions in <strong>NPY</strong> protein levels in the arcuate nucleus of the hypothalamus and in layers IV and V of the cingulate gyrus.
+NPY	addiction	withdrawal	12068247	However, chronic ethanol exposure and its <b>withdrawal</b> produced significant reductions in <strong>NPY</strong> protein levels in the arcuate nucleus of the hypothalamus and in layers IV and V of the cingulate gyrus.
+NPY	drug	alcohol	12068247	These results suggest that the decreased protein levels of <strong>NPY</strong> in the central and medial nuclei of the amygdala, as well as in the cortical and hypothalamic structures, during <b>ethanol</b> withdrawal may play an important role in the neuromechanisms of some <b>ethanol</b> withdrawal symptoms.
+NPY	addiction	withdrawal	12068247	These results suggest that the decreased protein levels of <strong>NPY</strong> in the central and medial nuclei of the amygdala, as well as in the cortical and hypothalamic structures, during ethanol <b>withdrawal</b> may play an important role in the neuromechanisms of some ethanol <b>withdrawal</b> symptoms.
+NPY	drug	opioid	12020877	Anti nociceptive effect of <strong>neuropeptide Y</strong> in the nucleus accumbens of rats: an involvement of <b>opioid</b> receptors in the effect.
+NPY	addiction	withdrawal	12020877	Intra nucleus accumbens administration of <strong>neuropeptide Y</strong> induced dose dependent increases in the hindpaw <b>withdrawal</b> latency (HWL) to thermal and mechanical stimulation in rats.
+NPY	drug	opioid	12020877	Furthermore, the anti nociceptive effect of <strong>neuropeptide Y</strong> was attenuated by intra nucleus accumbens administration of the <b>opioid</b> antagonist <b>naloxone</b>, suggesting an involvement of the endogenous <b>opioid</b> system in the <strong>neuropeptide Y</strong> induced anti nociception in the nucleus accumbens of rats.
+NPY	drug	opioid	12020877	Moreover, the <strong>neuropeptide Y</strong> induced anti nociception was attenuated by following intra nucleus accumbens injection of the selective <b>opioid</b> antagonists nor binaltorphimine and beta funaltrexamine, but not by naltrindole, illustrating that mu  and kappa <b>opioid</b> receptors, not the delta <b>opioid</b> receptor, were involved in the <strong>neuropeptide Y</strong> induced anti nociception in the nucleus accumbens of rats.
+NPY	drug	alcohol	12013027	Brain neuropeptide Y (<strong>NPY</strong>) in stress and <b>alcohol</b> dependence.
+NPY	addiction	dependence	12013027	Brain neuropeptide Y (<strong>NPY</strong>) in stress and alcohol <b>dependence</b>.
+NPY	drug	alcohol	12013027	Brain <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in stress and <b>alcohol</b> dependence.
+NPY	addiction	dependence	12013027	Brain <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in stress and alcohol <b>dependence</b>.
+NPY	drug	alcohol	12013027	Recent data additionally point to a role of <strong>NPY</strong> in the regulation of <b>alcohol</b> intake, and <b>alcohol</b> dependence emerges as a novel potential indication for compounds targeting the <strong>NPY</strong> system.
+NPY	addiction	dependence	12013027	Recent data additionally point to a role of <strong>NPY</strong> in the regulation of alcohol intake, and alcohol <b>dependence</b> emerges as a novel potential indication for compounds targeting the <strong>NPY</strong> system.
+NPY	drug	alcohol	11875632	<strong>Neuropeptide Y</strong> administration into the third ventricle does not increase sucrose or <b>ethanol</b> self administration but does affect the cortical EEG and increases food intake.
+NPY	drug	alcohol	11875632	Several studies have provided indirect evidence that neuropeptide Y (<strong>NPY</strong>) may play a role in the regulation of <b>ethanol</b> consumption.
+NPY	drug	alcohol	11875632	Several studies have provided indirect evidence that <strong>neuropeptide Y</strong> (<strong>NPY</strong>) may play a role in the regulation of <b>ethanol</b> consumption.
+NPY	drug	alcohol	11875632	However, the direct effects of central <strong>NPY</strong> administration on <b>ethanol</b> drinking are unclear.
+NPY	drug	alcohol	11875632	This study examined the effects of <strong>NPY</strong> on <b>ethanol</b>, sucrose, and food consumption as well as its concomitant effects on the cortical EEG.
+NPY	drug	alcohol	11875632	<strong>NPY</strong> (0 15 microg/3.0 microl) was infused into the third ventricle prior to drinking sessions, when 10% <b>ethanol</b> (10E), 2% sucrose (2S), 0.5% sucrose (0.5S), or food were available.
+NPY	drug	alcohol	11875632	These data suggest that <strong>NPY</strong> administration into the third ventricle preferentially regulates feeding compared to <b>ethanol</b> or sucrose drinking.
+NPY	drug	alcohol	11875632	In addition, since <strong>NPY</strong> significantly altered the cortical EEG in the absence of effects on <b>ethanol</b> and sucrose consumption, these data may indicate that <strong>NPY</strong>'s cortical EEG effects are more related to its sedative or anxiolytic properties, rather than any effect on consumption.
+NPY	drug	opioid	11730241	Within the hypothalamus, decreased activity of both the dynorphin (kappa <b>opioid</b>) and <strong>neuropeptide Y</strong> systems occurs in aging rodents.
+NPY	drug	alcohol	11707630	Differential expression of <strong>NPY</strong> and its receptors in <b>alcohol</b> preferring AA and <b>alcohol</b> avoiding ANA rats.
+NPY	drug	alcohol	11707630	Recently, it has been suggested that <strong>NPY</strong> also has a role in regulation of <b>alcohol</b> consumption.
+NPY	drug	alcohol	11707630	<strong>NPY</strong> and <strong>NPY</strong> receptor expression in genetically selected <b>alcohol</b> preferring (AA), <b>alcohol</b> nonpreferring (ANA), and Wistar rats were investigated.
+NPY	drug	alcohol	11707630	Effects of central <strong>NPY</strong> administration on <b>ethanol</b> self administration were also examined in AA, ANA, and Wistar rats by using oral operant self administration.
+NPY	addiction	reward	11707630	Effects of central <strong>NPY</strong> administration on ethanol self administration were also examined in AA, ANA, and Wistar rats by using oral <b>operant</b> self administration.
+NPY	drug	alcohol	11707630	<strong>NPY</strong> injected intracerebroventricularly (1.5 3.0 nmol) did not affect operant <b>ethanol</b> self administration in any of the three lines examined.
+NPY	addiction	reward	11707630	<strong>NPY</strong> injected intracerebroventricularly (1.5 3.0 nmol) did not affect <b>operant</b> ethanol self administration in any of the three lines examined.
+NPY	drug	alcohol	11707630	The <strong>NPY</strong> system seems to differ in several respects between rat lines with different levels of <b>alcohol</b> preference.
+NPY	drug	alcohol	11707630	Differences observed within the hippocampus could be related to behavioral traits other than <b>alcohol</b> intake but it is also possible that elevated hippocampal expression of <strong>NPY</strong> in the ANA rats contributes to the low <b>alcohol</b> intake of this line.
+NPY	drug	alcohol	11707630	Aberrant <strong>NPY</strong> expression and/function within the amygdala complex could contribute to <b>alcohol</b> preference and constitute an anatomic substrate of the effects of <strong>NPY</strong> expression on <b>alcohol</b> intake observed previously in genetically modified animals.
+NPY	drug	alcohol	11410744	Polymorphism of the <strong>neuropeptide Y</strong> gene: an association study with <b>alcohol</b> withdrawal.
+NPY	addiction	withdrawal	11410744	Polymorphism of the <strong>neuropeptide Y</strong> gene: an association study with alcohol <b>withdrawal</b>.
+NPY	drug	alcohol	11410744	Recent studies have revealed that <strong>NPY</strong> influences <b>alcohol</b> consumption in mice and that <b>alcohol</b> preferring rats showed lower concentrations of <strong>NPY</strong> like immunoreactivity compared with <b>alcohol</b> nonpreferring rats in several brain regions.
+NPY	drug	alcohol	11410744	In the present study, we analyzed the whole coding region and 5' untranslating region of the <strong>NPY</strong> gene for 163 Japanese male <b>alcoholics</b> with different withdrawal symptoms (93 with delirium tremens, 71 with seizures, 49 with hallucinations) and 98 Japanese male controls.
+NPY	addiction	withdrawal	11410744	In the present study, we analyzed the whole coding region and 5' untranslating region of the <strong>NPY</strong> gene for 163 Japanese male alcoholics with different <b>withdrawal</b> symptoms (93 with delirium tremens, 71 with seizures, 49 with hallucinations) and 98 Japanese male controls.
+NPY	drug	alcohol	11410744	Our data suggested that a C to T substitution at the 5671 locus of the <strong>NPY</strong> gene may be associated with seizure during <b>alcohol</b> withdrawal.
+NPY	addiction	withdrawal	11410744	Our data suggested that a C to T substitution at the 5671 locus of the <strong>NPY</strong> gene may be associated with seizure during alcohol <b>withdrawal</b>.
+NPY	drug	opioid	11340648	Inhibitory effect of <strong>neuropeptide Y</strong> on <b>morphine</b> withdrawal is accompanied by reduced c fos expression in specific brain regions.
+NPY	addiction	withdrawal	11340648	Inhibitory effect of <strong>neuropeptide Y</strong> on morphine <b>withdrawal</b> is accompanied by reduced c fos expression in specific brain regions.
+NPY	drug	opioid	11340648	Neuropeptide Y (<strong>NPY</strong>) was previously shown in our laboratory to attenuate behavioral signs of <b>morphine</b> withdrawal.
+NPY	addiction	withdrawal	11340648	Neuropeptide Y (<strong>NPY</strong>) was previously shown in our laboratory to attenuate behavioral signs of morphine <b>withdrawal</b>.
+NPY	drug	opioid	11340648	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) was previously shown in our laboratory to attenuate behavioral signs of <b>morphine</b> withdrawal.
+NPY	addiction	withdrawal	11340648	<strong>Neuropeptide Y</strong> (<strong>NPY</strong>) was previously shown in our laboratory to attenuate behavioral signs of morphine <b>withdrawal</b>.
+NPY	addiction	withdrawal	11340648	To further characterize the anti <b>withdrawal</b> effect of <strong>NPY</strong>, the present study attempted to identify specific brain regions where <strong>NPY</strong> inhibits neuronal activity during <b>withdrawal</b>.
+NPY	drug	opioid	11340648	Rats were pre treated with an intracerebroventricular (icv) injection of <strong>NPY</strong> (12 nmol) or vehicle 30 min before the <b>naloxone</b> challenge.
+NPY	addiction	withdrawal	11340648	The present study confirmed the inhibitory effect of <strong>NPY</strong> on <b>withdrawal</b> behavior.
+NPY	addiction	withdrawal	11340648	Our data suggest that neo  and allo cortical areas as well as specific brainstem nuclei are involved in the anti <b>withdrawal</b> effects of <strong>NPY</strong>.
+NPY	drug	opioid	11311731	<b>Naloxone</b> blocks 'anxiolytic' effects of neuropeptide Y. Intracerebroventricular injection of neuropeptide Y (<strong>NPY</strong>) produces potent 'anxiolytic' effects in animal models of anxiety.
+NPY	drug	opioid	11311731	<b>Naloxone</b> blocks 'anxiolytic' effects of <strong>neuropeptide Y</strong>. Intracerebroventricular injection of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) produces potent 'anxiolytic' effects in animal models of anxiety.
+NPY	drug	opioid	11311731	Administration of <b>opioid</b> receptor antagonists suppresses <strong>NPY</strong> induced food intake and thermogenesis.
+NPY	drug	opioid	11311731	The present study examined whether the opiate antagonist <b>naloxone</b> would also suppress the 'anxiolytic' effects of <strong>neuropeptide Y</strong>.
+NPY	drug	benzodiazepine	11311731	Following training and stabilization of responding in an operant conflict model of anxiety, rats were injected with either <strong>NPY</strong> or <b>diazepam</b>.
+NPY	addiction	reward	11311731	Following training and stabilization of responding in an <b>operant</b> conflict model of anxiety, rats were injected with either <strong>NPY</strong> or diazepam.
+NPY	drug	opioid	11311731	The administration of <b>naloxone</b> (0.25 2.0 mg/kg, s.c.) antagonized the effects of <strong>NPY</strong>.
+NPY	drug	benzodiazepine	11311731	These results support the hypothesis that <strong>NPY</strong> may play an important role in experimental anxiety independent of the <b>benzodiazepine</b> receptor and further implicate the opioid system in the behavioral expression of anxiety.
+NPY	drug	opioid	11311731	These results support the hypothesis that <strong>NPY</strong> may play an important role in experimental anxiety independent of the benzodiazepine receptor and further implicate the <b>opioid</b> system in the behavioral expression of anxiety.
+NPY	drug	amphetamine	11289036	However, in contrast to leptin, cerulenin did not prevent effects of fasting on plasma corticosterone or hypothalamic levels of <strong>neuropeptide Y</strong>, agouti related peptide, pro opiomelanocortin, or cocaine  and <b>amphetamine</b> related peptide mRNA.
+NPY	drug	cocaine	11289036	However, in contrast to leptin, cerulenin did not prevent effects of fasting on plasma corticosterone or hypothalamic levels of <strong>neuropeptide Y</strong>, agouti related peptide, pro opiomelanocortin, or <b>cocaine</b>  and amphetamine related peptide mRNA.
+NPY	drug	alcohol	11287109	<strong>Neuropeptide Y</strong> in the paraventricular nucleus increases <b>ethanol</b> self administration.
+NPY	drug	alcohol	11287109	The role of <strong>NPY</strong> in the PVN on <b>ethanol</b> self administration is unknown.
+NPY	drug	alcohol	11287109	Microinjections of <strong>NPY</strong> and <strong>NPY</strong> antagonists in the PVN were conducted prior to <b>ethanol</b> self administration sessions.
+NPY	drug	alcohol	11287109	All doses of <strong>NPY</strong> significantly increased <b>ethanol</b> self administration and preference, and decreased water intake.
+NPY	drug	alcohol	11287109	The <strong>NPY</strong> antagonist D <strong>NPY</strong> partially reduced <b>ethanol</b> self administration and completely blocked the effects of an intermediate dose of <strong>NPY</strong> (10 fmol) on <b>ethanol</b> intake, preference, and water intake.
+NPY	drug	alcohol	11287109	The competitive non peptide Y1 receptor antagonist BIBP 3226 did not significantly alter <b>ethanol</b> self administration or water intake when administered alone in the PVN but it completely blocked the effect of <strong>NPY</strong> (10 fmol) on <b>ethanol</b> intake.
+NPY	drug	alcohol	11287109	<strong>NPY</strong> infused in the PVN had no effect on <b>ethanol</b> self administration when tested in rats that did not have a long history of <b>ethanol</b> self administration.
+NPY	drug	alcohol	11287109	The doses of <strong>NPY</strong> tested produced no effect on food intake or body weight measured during the 24 h period after infusion in either <b>ethanol</b> experienced or <b>ethanol</b> inexperienced rats.
+NPY	drug	alcohol	11287109	These results indicate that elevation of <strong>NPY</strong> levels in the PVN potently increases <b>ethanol</b> self administration and that this effect is mediated through <strong>NPY</strong> Y1 receptors.
+NPY	addiction	withdrawal	11062340	The neuropeptide Y induced increases in hindpaw <b>withdrawal</b> latency were reversed by following injection of 0.42 nmol of the Y1 antagonist, <strong>NPY</strong>(28 36).
+NPY	addiction	withdrawal	11062340	The <strong>neuropeptide Y</strong> induced increases in hindpaw <b>withdrawal</b> latency were reversed by following injection of 0.42 nmol of the Y1 antagonist, <strong>NPY</strong>(28 36).
+NPY	drug	opioid	11062340	Furthermore, the neuropeptide Y induced increases in hindpaw withdrawal latency were attenuated by following intra nucleus raphe magnus injection of 6 nmol of the <b>opioid</b> antagonist <b>naloxone</b>, indicating that there is an interaction between <strong>NPY</strong> and <b>opioids</b> in nucleus raphe magnus.
+NPY	addiction	withdrawal	11062340	Furthermore, the neuropeptide Y induced increases in hindpaw <b>withdrawal</b> latency were attenuated by following intra nucleus raphe magnus injection of 6 nmol of the opioid antagonist naloxone, indicating that there is an interaction between <strong>NPY</strong> and opioids in nucleus raphe magnus.
+NPY	drug	opioid	11062340	Furthermore, the <strong>neuropeptide Y</strong> induced increases in hindpaw withdrawal latency were attenuated by following intra nucleus raphe magnus injection of 6 nmol of the <b>opioid</b> antagonist <b>naloxone</b>, indicating that there is an interaction between <strong>NPY</strong> and <b>opioids</b> in nucleus raphe magnus.
+NPY	addiction	withdrawal	11062340	Furthermore, the <strong>neuropeptide Y</strong> induced increases in hindpaw <b>withdrawal</b> latency were attenuated by following intra nucleus raphe magnus injection of 6 nmol of the opioid antagonist naloxone, indicating that there is an interaction between <strong>NPY</strong> and opioids in nucleus raphe magnus.
+NPY	addiction	reward	11035216	To clarify the role of <strong>NPY</strong> in mediating <b>reward</b> processes and the possible interaction between <b>reward</b> and feeding, the present study examined the effects of injecting <strong>NPY</strong> bilaterally into the perifornical hypothalamus (PFH) vs. the nucleus accumbens (NAC) on intake of preferred vs. non preferred food types, as well as on conditioned place preference (<b>CPP</b>) learning.
+NPY	addiction	reward	11035216	A <b>CPP</b> that was negatively correlated with food intake occurred with the low (24 pmol/side) dose of <strong>NPY</strong> in the PFH, while a <b>CPP</b> that was not correlated with food intake was produced with the same dose in the NAC.
+NPY	drug	amphetamine	11035216	The extent of the CPPs produced by <strong>NPY</strong> injection in both brain sites mirrored that produced by peripheral injection of <b>amphetamine</b> (2.5 mg/kg).
+NPY	addiction	reward	11035216	These results indicate that <strong>NPY</strong> elicits <b>reward</b> related behavior, but not feeding, from the NAC, and both behaviors from the PFH.
+NPY	drug	opioid	10818386	Neuropeptides mainly involved in the control of GnRH release are <b>opioids</b>, neuropeptide Y (<strong>NPY</strong>), galanin, and corticotropin releasing factor (CRF), whereas neurotransmitters are noradrenaline, dopamine, serotonin, melatonin and gamma aminobutyric acid (GABA).
+NPY	drug	opioid	10818386	Neuropeptides mainly involved in the control of GnRH release are <b>opioids</b>, <strong>neuropeptide Y</strong> (<strong>NPY</strong>), galanin, and corticotropin releasing factor (CRF), whereas neurotransmitters are noradrenaline, dopamine, serotonin, melatonin and gamma aminobutyric acid (GABA).
+NPY	drug	amphetamine	10760371	Inhibition of <b>amphetamine</b>  and apomorphine induced behavioural effects by <strong>neuropeptide Y</strong> Y(1) receptor antagonist BIBO 3304.
+NPY	drug	amphetamine	10760371	These data demonstrate that behavioural response to indirectly (<b>amphetamine</b>) and directly (apomorphine) acting dopaminergic stimulants is inhibited by <strong>NPY</strong> Y(1) receptor antagonists and suggest that <strong>NPY</strong> Y(1) receptor activation might be important in pathophysiology of disorders associated with hyperactivity of dopaminergic pathways, such as psychosis, schizophrenia and drug abuse.
+NPY	drug	amphetamine	10760371	We propose that the effects of BIBO 3304 on <b>amphetamine</b>/apomorphine induced locomotion and apomorphine induced aggressiveness are due to modulation of postsynaptic dopaminergic responses rather than direct effects of <strong>NPY</strong> Y(1) receptor antagonists on dopamine or <strong>NPY</strong> release.
+NPY	drug	alcohol	10627090	Genetic studies, including association and genome wide survey studies in both humans and rodents, implicate serotonin 1b receptor, dopamine D2 receptor, tryptophan hydroxylase and <strong>neuropeptide Y</strong> as candidate targets of genetic susceptibility in these pharmacodynamic actions of <b>ethanol</b>.
+NPY	drug	opioid	10495011	Effects of <strong>neuropeptide Y</strong> on the discriminative stimulus and antinociceptive properties of <b>morphine</b>.
+NPY	drug	opioid	10495011	Previous research indicates that <b>opioid</b> receptor blockade diminishes the effects of neuropeptide Y (<strong>NPY</strong>) on feeding and memory.
+NPY	drug	opioid	10495011	Previous research indicates that <b>opioid</b> receptor blockade diminishes the effects of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) on feeding and memory.
+NPY	drug	opioid	10495011	Conversely, <strong>NPY</strong> attenuates <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+NPY	addiction	withdrawal	10495011	Conversely, <strong>NPY</strong> attenuates naloxone precipitated morphine <b>withdrawal</b>.
+NPY	drug	opioid	10495011	The present study evaluated the effects of <strong>NPY</strong> on the discriminative stimulus and antinociceptive effects produced by the prototypical mu <b>opioid</b>, <b>morphine</b>.
+NPY	drug	opioid	10495011	Across a range of doses (3.0, 5.0, and 10 microg), intracerebroventricular (ICV) injection of <strong>NPY</strong> failed to substitute for, antagonize, or potentiate the discriminative stimulus effects of <b>morphine</b>.
+NPY	drug	opioid	10495011	A warm water tail withdrawal procedure was used to examine the antinociceptive effects of <b>morphine</b> and <strong>NPY</strong>, alone and in combination.
+NPY	addiction	withdrawal	10495011	A warm water tail <b>withdrawal</b> procedure was used to examine the antinociceptive effects of morphine and <strong>NPY</strong>, alone and in combination.
+NPY	drug	opioid	10495011	<strong>NPY</strong> (3.0 and 10 microg, ICV) failed to alter tail withdrawal latencies from 52 degrees and 56 degrees C water, whereas <b>morphine</b> (1.0 30 mg/kg, IP) produced a dose related increase in latencies at both water temperatures.
+NPY	addiction	withdrawal	10495011	<strong>NPY</strong> (3.0 and 10 microg, ICV) failed to alter tail <b>withdrawal</b> latencies from 52 degrees and 56 degrees C water, whereas morphine (1.0 30 mg/kg, IP) produced a dose related increase in latencies at both water temperatures.
+NPY	drug	opioid	10495011	A 10 microg dose of <strong>NPY</strong> also failed to alter the antinociceptive effects of <b>morphine</b>.
+NPY	drug	alcohol	10414603	Effects of chronic <b>ethanol</b> exposure on neurophysiological responses to corticotropin releasing factor and <strong>neuropeptide Y</strong>.
+NPY	drug	alcohol	10414603	The present study examined if prolonged alterations in neurophysiological responses to corticotropin releasing factor (CRF) and neuropeptide Y (<strong>NPY</strong>), peptides known to influence stress responses, would persist during protracted <b>ethanol</b> abstinence.
+NPY	drug	alcohol	10414603	The present study examined if prolonged alterations in neurophysiological responses to corticotropin releasing factor (CRF) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>), peptides known to influence stress responses, would persist during protracted <b>ethanol</b> abstinence.
+NPY	drug	alcohol	10414603	The effects of intracerebroventricular infusions of CRF and <strong>NPY</strong> on electroencephalogram (EEG) and event related potentials (ERPs) were then assessed 10 15 weeks after withdrawal from <b>ethanol</b>.
+NPY	addiction	withdrawal	10414603	The effects of intracerebroventricular infusions of CRF and <strong>NPY</strong> on electroencephalogram (EEG) and event related potentials (ERPs) were then assessed 10 15 weeks after <b>withdrawal</b> from ethanol.
+NPY	drug	alcohol	10414603	This enhanced sensitivity to CRF and <strong>NPY</strong> following chronic <b>ethanol</b> exposure and abstinence suggests that these peptidergic systems may play a role in the symptomatology of the prolonged abstinence syndrome.
+NPY	drug	alcohol	10397286	Innate differences of neuropeptide Y (<strong>NPY</strong>) in hypothalamic nuclei and central nucleus of the amygdala between selectively bred rats with high and low <b>alcohol</b> preference.
+NPY	drug	alcohol	10397286	Innate differences of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) in hypothalamic nuclei and central nucleus of the amygdala between selectively bred rats with high and low <b>alcohol</b> preference.
+NPY	drug	alcohol	10397286	To examine the hypothesis that <strong>NPY</strong> might play a role in <b>alcohol</b> seeking behavior, this study took advantage of the genetic differences of the <b>alcohol</b> preferring (P) rats and <b>alcohol</b> nonpreferring (NP) rats, as well as the high <b>alcohol</b> drinking (HAD) rats and low <b>alcohol</b> drinking (LAD) rats, in voluntary <b>alcohol</b> consumption to examine if <strong>NPY</strong> neurons in the brains differ between these selected lines.
+NPY	addiction	relapse	10397286	To examine the hypothesis that <strong>NPY</strong> might play a role in alcohol <b>seeking</b> behavior, this study took advantage of the genetic differences of the alcohol preferring (P) rats and alcohol nonpreferring (NP) rats, as well as the high alcohol drinking (HAD) rats and low alcohol drinking (LAD) rats, in voluntary alcohol consumption to examine if <strong>NPY</strong> neurons in the brains differ between these selected lines.
+NPY	drug	alcohol	10397286	Therefore, the data indicate that there are innate differences in the <strong>NPY</strong> I in the brain between selectively bred rats with high and low <b>alcohol</b> preference.
+NPY	drug	alcohol	10397286	Because both P rats and HAD rats have high <b>alcohol</b> preference, the disparate finding between these two lines of rats suggests that the hypothalamic <strong>NPY</strong> neurons are probably not associated with <b>alcohol</b> preference.
+NPY	drug	alcohol	10397286	In contrast, consistent findings in the CeA of both P rats and HAD rats suggest that <strong>NPY</strong> in the CeA of P and HAD rats may contribute to the regulation of <b>alcohol</b> consumption.
+NPY	drug	alcohol	10397286	This is substantiated by a recent report showing that <strong>NPY</strong> knockout mice drink significantly more <b>ethanol</b>, and transgenic mice that overexpress the <strong>NPY</strong> gene drink less <b>alcohol</b>, than wild type mice.
+NPY	drug	alcohol	10397286	Together, the findings support the notion that <strong>NPY</strong> agonists that would enhance <strong>NPY</strong> function in the amygdala might be useful for the treatment of anxiety and <b>alcoholism</b>.
+NPY	drug	alcohol	9835294	<strong>Neuropeptide Y</strong> levels in <b>ethanol</b> naive <b>alcohol</b> preferring and nonpreferring rats and in Wistar rats after <b>ethanol</b> exposure.
+NPY	drug	alcohol	9835294	However, the effects of <b>alcohol</b> consumption/deprivation on <strong>NPY</strong> levels remain unknown.
+NPY	drug	alcohol	9835294	The present study sought to determine if brain <strong>NPY</strong> levels were affected by either <b>alcohol</b> exposure and/or correlated with genetic differences in preference for drinking <b>alcohol</b>.
+NPY	drug	alcohol	9835294	In the first experiment, <strong>NPY</strong> like immunoreactivity (<strong>NPY</strong> LI) was compared in <b>alcohol</b> naive, <b>alcohol</b> preferring (P), and nonpreferring (NP) rats.
+NPY	drug	alcohol	9835294	At 7 weeks of <b>alcohol</b> exposure, no significant changes in <strong>NPY</strong> LI in were found.
+NPY	drug	alcohol	9835294	At 1 month after <b>ethanol</b> withdrawal, however, the <b>ethanol</b> exposed animals had significantly higher <strong>NPY</strong> LI in the hypothalamus (F = 4.78, p < 0.04) when compared with the nonexposed controls.
+NPY	addiction	withdrawal	9835294	At 1 month after ethanol <b>withdrawal</b>, however, the ethanol exposed animals had significantly higher <strong>NPY</strong> LI in the hypothalamus (F = 4.78, p < 0.04) when compared with the nonexposed controls.
+NPY	drug	alcohol	9835294	Taken together, these studies suggest that exposure to chronic <b>ethanol</b> may affect <strong>NPY</strong> LI at the level of the hypothalamus in a fashion similar to food restriction, because 4 weeks after <b>alcohol</b> withdrawal, significantly higher <strong>NPY</strong> levels are found.
+NPY	addiction	withdrawal	9835294	Taken together, these studies suggest that exposure to chronic ethanol may affect <strong>NPY</strong> LI at the level of the hypothalamus in a fashion similar to food restriction, because 4 weeks after alcohol <b>withdrawal</b>, significantly higher <strong>NPY</strong> levels are found.
+NPY	drug	alcohol	9835294	In addition, differences in <strong>NPY</strong> LI in limbic areas and frontal cortex between <b>alcohol</b> naive P and NP rats suggest that <strong>NPY</strong> may also play a role in risk for the development of <b>alcohol</b> preference either by modulating the "tension reduction" properties of <b>alcohol</b> or by influencing consummatory behaviors.
+NPY	drug	opioid	9454808	<strong>Neuropeptide Y</strong> attenuates <b>naloxone</b> precipitated <b>morphine</b> withdrawal via Y5 like receptors.
+NPY	addiction	withdrawal	9454808	<strong>Neuropeptide Y</strong> attenuates naloxone precipitated morphine <b>withdrawal</b> via Y5 like receptors.
+NPY	drug	opioid	9454808	The effects of intracerebroventricular injection of neuropeptide Y (<strong>NPY</strong>) and various <strong>NPY</strong> related peptides were studied on <b>naloxone</b> precipitated withdrawal from <b>morphine</b> in rats.
+NPY	addiction	withdrawal	9454808	The effects of intracerebroventricular injection of neuropeptide Y (<strong>NPY</strong>) and various <strong>NPY</strong> related peptides were studied on naloxone precipitated <b>withdrawal</b> from morphine in rats.
+NPY	drug	opioid	9454808	The effects of intracerebroventricular injection of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and various <strong>NPY</strong> related peptides were studied on <b>naloxone</b> precipitated withdrawal from <b>morphine</b> in rats.
+NPY	addiction	withdrawal	9454808	The effects of intracerebroventricular injection of <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and various <strong>NPY</strong> related peptides were studied on naloxone precipitated <b>withdrawal</b> from morphine in rats.
+NPY	drug	opioid	9454808	Our data are consistent with a potential role for <strong>NPY</strong> and Y5 like receptors in basic mechanisms and as a therapeutic target in <b>opioid</b> dependence and withdrawal.
+NPY	addiction	dependence	9454808	Our data are consistent with a potential role for <strong>NPY</strong> and Y5 like receptors in basic mechanisms and as a therapeutic target in opioid <b>dependence</b> and withdrawal.
+NPY	addiction	withdrawal	9454808	Our data are consistent with a potential role for <strong>NPY</strong> and Y5 like receptors in basic mechanisms and as a therapeutic target in opioid dependence and <b>withdrawal</b>.
+NPY	drug	opioid	9322549	In addition, animal studies suggest a decrease in the <b>opioid</b> (dynorphin) feeding drive and possibly in <strong>neuropeptide Y</strong> and nitric oxide.
+NPY	drug	cannabinoid	9272766	SR 141716, a selective central CB1 <b>cannabinoid</b> receptor antagonist, markedly and selectively reduces sucrose feeding and drinking as well as <strong>neuropeptide Y</strong> induced sucrose drinking in rats.
+NPY	drug	opioid	11224469	Utilization of a novel model of food reinforced behavior involving <strong>neuropeptide Y</strong>, insulin, 2 deoxy d glucose and <b>naloxone</b>.
+NPY	addiction	reward	11224469	<strong>NPY</strong>, insulin and 2 DG caused an elevation of the response function obtained by plotting response rates against <b>reinforcement</b> rates but did not affect the slope of the function.
+NPY	drug	opioid	8853202	Behavioral effects of <b>naloxone</b> on <strong>neuropeptide Y</strong> induced feeding.
+NPY	drug	opioid	8853202	We evaluated the effect of <b>naloxone</b> on neuropeptide Y (<strong>NPY</strong>) induced feeding behavior using two methods; operant chambers and observational analysis.
+NPY	addiction	reward	8853202	We evaluated the effect of naloxone on neuropeptide Y (<strong>NPY</strong>) induced feeding behavior using two methods; <b>operant</b> chambers and observational analysis.
+NPY	drug	opioid	8853202	We evaluated the effect of <b>naloxone</b> on <strong>neuropeptide Y</strong> (<strong>NPY</strong>) induced feeding behavior using two methods; operant chambers and observational analysis.
+NPY	addiction	reward	8853202	We evaluated the effect of naloxone on <strong>neuropeptide Y</strong> (<strong>NPY</strong>) induced feeding behavior using two methods; <b>operant</b> chambers and observational analysis.
+NPY	drug	opioid	8853202	Following training, rats were injected with <strong>NPY</strong> (intraventricular, 5 micrograms) and various doses of <b>naloxone</b> (subcutaneous, 0, 0.1, 0.3, 1, 3, and 10 mg/kg).
+NPY	drug	opioid	8853202	<strong>NPY</strong> significantly increased the number of pellets consumed during the one hour session and <b>naloxone</b> (1, 3, and 10 mg/kg) blocked this effect.
+NPY	drug	opioid	8853202	<b>Naloxone</b> (3 and 10 mg/kg) increased the latency to the first response and blocked <strong>NPY</strong>'s effect on completion of the first ratio.
+NPY	drug	opioid	8853202	<strong>NPY</strong> increased food intake during the 1 h session and <b>naloxone</b> blocked this effect.
+NPY	drug	opioid	8853202	<strong>NPY</strong> decreased the latency to eat, but <b>naloxone</b> failed to significantly antagonize this effect.
+NPY	drug	opioid	8853202	The amount of time spent eating was greater in the <strong>NPY</strong> group compared to the saline group and <b>naloxone</b> antagonized this effect.
+NPY	drug	opioid	8853202	Lag sequential analysis indicated that <strong>NPY</strong> induced a move eat move behavioral sequence that disappeared following <b>naloxone</b> administration.
+NPY	drug	opioid	8853202	These data lend support to the notion that <b>opioids</b> are involved in maintenance of <strong>NPY</strong> induced feeding but affect meal initiation in a minor way.
+NPY	drug	opioid	8853202	Only relatively high doses of <b>naloxone</b> (3 and 10 mg/kg) altered <strong>NPY</strong> induced changes in meal initiation.
+NPY	drug	alcohol	7561860	No significant differences in <strong>neuropeptide Y</strong> concentrations were observed between control subjects and victims of suicide with major depression or victims of suicide with <b>alcohol</b> dependence.
+NPY	addiction	dependence	7561860	No significant differences in <strong>neuropeptide Y</strong> concentrations were observed between control subjects and victims of suicide with major depression or victims of suicide with alcohol <b>dependence</b>.
+NPY	drug	nicotine	8523413	In BCC, <b>nicotine</b> (1 10 mumol/l) evoked a release of NE and <strong>NPY</strong> and a transient rise of [Ca2+]i (determined with fura 2) during normoxia which were both dependent on the presence of extracellular calcium.
+NPY	drug	opioid	7540319	Lack of effect of chronic <b>morphine</b> treatment and <b>naloxone</b> precipitated withdrawal on tyrosine hydroxylase, galanin, and <strong>neuropeptide Y</strong> mRNA levels in the rat locus coeruleus.
+NPY	addiction	withdrawal	7540319	Lack of effect of chronic morphine treatment and naloxone precipitated <b>withdrawal</b> on tyrosine hydroxylase, galanin, and <strong>neuropeptide Y</strong> mRNA levels in the rat locus coeruleus.
+NPY	drug	opioid	7540319	Messenger RNA (mRNA) levels for tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and neuropeptide Y (<strong>NPY</strong>), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic <b>morphine</b> treatment or <b>naloxone</b> precipitated withdrawal.
+NPY	addiction	withdrawal	7540319	Messenger RNA (mRNA) levels for tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and neuropeptide Y (<strong>NPY</strong>), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic morphine treatment or naloxone precipitated <b>withdrawal</b>.
+NPY	drug	opioid	7540319	Messenger RNA (mRNA) levels for tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic <b>morphine</b> treatment or <b>naloxone</b> precipitated withdrawal.
+NPY	addiction	withdrawal	7540319	Messenger RNA (mRNA) levels for tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and <strong>neuropeptide Y</strong> (<strong>NPY</strong>), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic morphine treatment or naloxone precipitated <b>withdrawal</b>.
+NPY	drug	opioid	7540319	Although long term adaptations of LC neurons have previously been implicated in the development of <b>morphine</b> tolerance, dependence, and withdrawal, alterations in the levels of TH, GAL, or <strong>NPY</strong> mRNA in the LC apparently do not underlie this process.
+NPY	addiction	dependence	7540319	Although long term adaptations of LC neurons have previously been implicated in the development of morphine tolerance, <b>dependence</b>, and withdrawal, alterations in the levels of TH, GAL, or <strong>NPY</strong> mRNA in the LC apparently do not underlie this process.
+NPY	addiction	withdrawal	7540319	Although long term adaptations of LC neurons have previously been implicated in the development of morphine tolerance, dependence, and <b>withdrawal</b>, alterations in the levels of TH, GAL, or <strong>NPY</strong> mRNA in the LC apparently do not underlie this process.
+NPY	drug	nicotine	7702541	<b>Nicotine</b> induced noradrenaline release was accompanied by <strong>neuropeptide Y</strong> overflow.
+NPY	drug	nicotine	7702541	When added 10 min after the onset of energy depletion, <b>nicotine</b> (10 mumol/l) caused a brief but marked enhancement of exocytotic noradrenaline release, since this release was calcium dependent and was accompanied by a significant rise of <strong>neuropeptide Y</strong> overflow.
+NPY	drug	nicotine	7702541	In absence of extracellular calcium to avoid exocytosis, concomitant administration of <b>nicotine</b> (3 100 mumol/l) and cyanide caused a concentration dependent acceleration of both the overflow of noradrenaline and DOPEG, whereas overflow of <strong>neuropeptide Y</strong> was not increased, thus indicating a nonexocytotic release mechanism.
+NPY	addiction	reward	8278431	Extensive data implicate NAcc DA in <b>reward</b> related learning, raising the possibility that <strong>NPY</strong> microinjected into the NAcc may induce rewarding effects mediated by DA.
+NPY	addiction	reward	8278431	The third experiment showed that intraaccumbens <strong>NPY</strong> (0.1 micrograms in 0.5 microliter on each side) produced a <b>CPP</b>.
+NPY	drug	opioid	1639229	Brain and adrenal monoamines and <strong>neuropeptide Y</strong> in <b>codeine</b> tolerant rats.
+NPY	drug	opioid	1639229	Monoamine turnover and neuropeptide Y (<strong>NPY</strong>) levels were investigated in the central and peripheral nervous systems in adult male rats chronically treated with <b>codeine</b>.
+NPY	drug	opioid	1639229	Monoamine turnover and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) levels were investigated in the central and peripheral nervous systems in adult male rats chronically treated with <b>codeine</b>.
+NPY	drug	opioid	1726061	Distribution of excitatory and inhibitory amino acid, sigma, monoamine, catecholamine, acetylcholine, <b>opioid</b>, neurotensin, substance P, adenosine and <strong>neuropeptide Y</strong> receptors in human motor and somatosensory cortex.
+NPY	drug	benzodiazepine	1726061	Autoradiography was used to visualise N methyl D aspartate, phencyclidine, strychnine insensitive glycine, alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid, kainic acid, <b>benzodiazepine</b>, gamma aminobutyric acid type A, sigma, serotonergic, dopaminergic, alpha 2 adrenergic, beta adrenergic, muscarinic cholinergic, nicotinic, opioid, neurotensin, substance P, adenosine A1 and <strong>neuropeptide Y</strong> receptors in the human primary motor (Brodmann's area 4) and somatosensory cortex (Brodmann's areas 3, 2 and 1).
+NPY	drug	opioid	1726061	Autoradiography was used to visualise N methyl D aspartate, phencyclidine, strychnine insensitive glycine, alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid, kainic acid, benzodiazepine, gamma aminobutyric acid type A, sigma, serotonergic, dopaminergic, alpha 2 adrenergic, beta adrenergic, muscarinic cholinergic, nicotinic, <b>opioid</b>, neurotensin, substance P, adenosine A1 and <strong>neuropeptide Y</strong> receptors in the human primary motor (Brodmann's area 4) and somatosensory cortex (Brodmann's areas 3, 2 and 1).
+NPY	drug	cocaine	2006146	<b>Cocaine</b> induced reduction of brain <strong>neuropeptide Y</strong> synthesis dependent on medial prefrontal cortex.
+NPY	drug	cocaine	2006146	Repeated administration of <b>cocaine</b> elicits substantial, long lasting, but reversible reductions in neuropeptide Y (<strong>NPY</strong>) and <strong>NPY</strong> mRNA in the rat cerebral cortex and nucleus accumbens.
+NPY	drug	cocaine	2006146	Repeated administration of <b>cocaine</b> elicits substantial, long lasting, but reversible reductions in <strong>neuropeptide Y</strong> (<strong>NPY</strong>) and <strong>NPY</strong> mRNA in the rat cerebral cortex and nucleus accumbens.
+NPY	drug	cocaine	2006146	The medial prefrontal cortex appears necessary for maintenance of <b>cocaine</b>'s action on this neuronal network since excitotoxic lesions of this area prevented (lesion before <b>cocaine</b>) and reversed (lesion after <b>cocaine</b>) the reductions in <strong>NPY</strong> elicited by the <b>cocaine</b>.
+NPY	drug	cocaine	2006146	<strong>NPY</strong> may be a sensitive marker for chronic <b>cocaine</b> use.
+NPY	drug	opioid	1761199	The effects of chronic administration of <b>morphine</b> on the levels of brain and adrenal catecholamines and <strong>neuropeptide Y</strong> in rats.
+NPY	drug	opioid	1761199	Monoamine turnover and neuropeptide Y (<strong>NPY</strong>) levels were investigated in the central and peripheral nervous systems in adult male rats chronically treated with <b>morphine</b>.
+NPY	drug	opioid	1761199	Monoamine turnover and <strong>neuropeptide Y</strong> (<strong>NPY</strong>) levels were investigated in the central and peripheral nervous systems in adult male rats chronically treated with <b>morphine</b>.
+NPY	drug	opioid	1761199	Our results contribute to the evidence that brain and adrenal monoamines and <strong>NPY</strong> could be involved in the mechanism of <b>morphine</b> tolerance and/or dependence.
+NPY	addiction	dependence	1761199	Our results contribute to the evidence that brain and adrenal monoamines and <strong>NPY</strong> could be involved in the mechanism of morphine tolerance and/or <b>dependence</b>.
+NPY	drug	nicotine	3184776	<b>Nicotine</b> induced release of noradrenaline and <strong>neuropeptide Y</strong> in guinea pig heart.
+NPY	drug	nicotine	3184776	The effect of <b>nicotine</b> on the release of noradrenaline and <strong>neuropeptide Y</strong> was investigated in isolated perfused guinea pig hearts (Langendorff technique).
+NPY	drug	nicotine	3184776	Endogenous noradrenaline, dihydroxyphenylglycol (both determined by high pressure liquid chromatography) and <strong>neuropeptide Y</strong> (determined by radioimmunoassay) were measured in the coronary venous effluent following the addition of <b>nicotine</b> to the perfusate.
+NPY	drug	nicotine	3184776	<b>Nicotine</b> (2 microM to 2 mM) dose dependently increased both noradrenaline and <strong>neuropeptide Y</strong> overflow, and the release of both transmitters was closely correlated (r = 0.81).
+NPY	drug	nicotine	3184776	Despite ongoing <b>nicotine</b> administration noradrenaline and <strong>neuropeptide Y</strong> levels returned to basal values within 6 min of continuous <b>nicotine</b> administration indicating rapid tachyphylaxis to the effect of <b>nicotine</b>.
+NPY	drug	nicotine	3184776	The <b>nicotine</b> induced release of noradrenaline and <strong>neuropeptide Y</strong> required the presence of extracellular calcium, and the release of both substances was suppressed by hexamethonium or by low concentrations of the inhibitors of the neuronal noradrenaline uptake (uptake1) desipramine and nisoxetine.
+NPY	drug	nicotine	3184776	The close correlation between noradrenaline and <strong>neuropeptide Y</strong> release, its calcium dependence, and the lack of dihydroxyphenylglycol overflow are in agreement with the concept of a common and exocytotic release of noradrenaline and <strong>neuropeptide Y</strong> induced by <b>nicotine</b>.
+NPY	addiction	dependence	3184776	The close correlation between noradrenaline and <strong>neuropeptide Y</strong> release, its calcium <b>dependence</b>, and the lack of dihydroxyphenylglycol overflow are in agreement with the concept of a common and exocytotic release of noradrenaline and <strong>neuropeptide Y</strong> induced by nicotine.
+GRM5	drug	cocaine	32691344	Correction to: Extinction training following <b>cocaine</b> or MDMA self administration produces discrete changes in D2 like and <strong>mGlu5</strong> receptor density in the rat brain.
+GRM5	drug	psychedelics	32691344	Correction to: Extinction training following cocaine or <b>MDMA</b> self administration produces discrete changes in D2 like and <strong>mGlu5</strong> receptor density in the rat brain.
+GRM5	drug	alcohol	32443872	Because a reduction in <b>ethanol</b> associated cues can reduce relapse, <strong>mGlu5</strong> receptor PAM would be useful for therapy of <b>alcoholism</b>.
+GRM5	addiction	relapse	32443872	Because a reduction in ethanol associated cues can reduce <b>relapse</b>, <strong>mGlu5</strong> receptor PAM would be useful for therapy of alcoholism.
+GRM5	drug	alcohol	32416868	Positive allosteric modulators (PAMs) of mGlu2 and negative allosteric modulators of <strong>mGlu5</strong> show particular promise for reducing <b>alcohol</b> intake and/or preventing relapse.
+GRM5	addiction	relapse	32416868	Positive allosteric modulators (PAMs) of mGlu2 and negative allosteric modulators of <strong>mGlu5</strong> show particular promise for reducing alcohol intake and/or preventing <b>relapse</b>.
+GRM5	drug	cannabinoid	32413893	<strong>mGlu5</strong> receptor availability in youth at risk for addictions: effects of vulnerability traits and <b>cannabis</b> use.
+GRM5	drug	cannabinoid	32413893	Together, the study provides evidence that <strong>mGlu5</strong> receptor availability is low in youth at elevated risk for addictions, particularly those who frequently use <b>cannabis</b>.
+GRM5	addiction	relapse	32312578	No differences in <strong>mGluR5</strong> availability, responses during tests of extinction, or cue induced <b>reinstatement</b> were observed between the groups.
+GRM5	drug	nicotine	32150317	At the same time, in both groups, <strong>mGluR5</strong> BPND were significantly lower in <b>smokers</b> (F[27,1] = 15.500; p = .001), but without significant differences between the groups.
+GRM5	drug	nicotine	32150317	They further supply a new perspective on the complex relationship between <b>tobacco</b> addiction and schizophrenia by identifying glutamatergic neurotransmission in particularly <strong>mGluR5</strong> as a possible connection to a shared vulnerability.
+GRM5	addiction	addiction	32150317	They further supply a new perspective on the complex relationship between tobacco <b>addiction</b> and schizophrenia by identifying glutamatergic neurotransmission in particularly <strong>mGluR5</strong> as a possible connection to a shared vulnerability.
+GRM5	drug	psychedelics	31706797	After a molecular analysis of <b>ketamine</b> modulation of GluN2B, GluA1 and <strong>mGluR5</strong> receptors levels in nucleus accumbens, hippocampus and amygdala, two behavioural models were used to investigate <b>ketamine</b> effects: i) context induced renewal of sucrose seeking, and ii) sucrose memory reconsolidation.
+GRM5	addiction	relapse	31706797	After a molecular analysis of ketamine modulation of GluN2B, GluA1 and <strong>mGluR5</strong> receptors levels in nucleus accumbens, hippocampus and amygdala, two behavioural models were used to investigate ketamine effects: i) context induced renewal of sucrose <b>seeking</b>, and ii) sucrose memory reconsolidation.
+GRM5	drug	psychedelics	31706797	At the molecular level, <b>ketamine</b> i) decreased GluN2B, GluA1 and <strong>mGluR5</strong> receptors in hippocampus, ii) decreased GluA1 and <strong>mGluR5</strong> but increased GluN2B in nucleus accumbens and iii) increased GluN2B and <strong>mGluR5</strong> in amygdala.
+GRM5	drug	alcohol	31481578	Animal models of <b>alcohol</b> dependence and relapse demonstrate an important role of the glutamatergic system, in particular, cerebral metabotropic glutamate receptor 5 (<strong>mGluR5</strong>).
+GRM5	addiction	dependence	31481578	Animal models of alcohol <b>dependence</b> and relapse demonstrate an important role of the glutamatergic system, in particular, cerebral metabotropic glutamate receptor 5 (<strong>mGluR5</strong>).
+GRM5	addiction	relapse	31481578	Animal models of alcohol dependence and <b>relapse</b> demonstrate an important role of the glutamatergic system, in particular, cerebral metabotropic glutamate receptor 5 (<strong>mGluR5</strong>).
+GRM5	drug	alcohol	31481578	18F 3 fluoro 5 [(pyridin 3 yl)ethynyl]benzonitrile (18F FPEB) PET has revealed that chronic <b>alcohol</b> use leads to decreased limbic <strong>mGluR5</strong> availability, which was associated with less craving.
+GRM5	addiction	relapse	31481578	18F 3 fluoro 5 [(pyridin 3 yl)ethynyl]benzonitrile (18F FPEB) PET has revealed that chronic alcohol use leads to decreased limbic <strong>mGluR5</strong> availability, which was associated with less <b>craving</b>.
+GRM5	drug	alcohol	31481578	Here, we tested whether the state of decreased <strong>mGluR5</strong> availability in <b>alcohol</b> dependent patients normalizes during abstinence (at 2 and 6 mo of detoxification) and whether initial <strong>mGluR5</strong> imaging parameters can predict individual relapse.
+GRM5	addiction	relapse	31481578	Here, we tested whether the state of decreased <strong>mGluR5</strong> availability in alcohol dependent patients normalizes during abstinence (at 2 and 6 mo of detoxification) and whether initial <strong>mGluR5</strong> imaging parameters can predict individual <b>relapse</b>.
+GRM5	drug	alcohol	31481578	Results: During abstinence, <b>alcohol</b> dependent patients showed sustained recovered <strong>mGluR5</strong> availability in cortical and subcortical regions compared with the baseline, up to the levels observed in controls, after 6 mo in most areas except for the hippocampus, nucleus accumbens, and thalamus.
+GRM5	addiction	relapse	31481578	Higher striatopallidal <strong>mGluR5</strong> availability was observed at the baseline in patients who had a <b>relapse</b> during the 6 mo follow up period (+25.1%).
+GRM5	addiction	relapse	31481578	Also, normalization of striatal <strong>mGluR5</strong> to control levels was associated with reduced <b>craving</b> ("desire and intention to drink" and "negative reinforcement"; r = 0.72 0.94).
+GRM5	addiction	reward	31481578	Also, normalization of striatal <strong>mGluR5</strong> to control levels was associated with reduced craving ("desire and intention to drink" and "negative <b>reinforcement</b>"; r = 0.72 0.94).
+GRM5	drug	alcohol	31481578	Conclusion: Reduced cerebral <strong>mGluR5</strong> availability in <b>alcohol</b> dependent patients recovers during abstinence and is associated with reduced craving.
+GRM5	addiction	relapse	31481578	Conclusion: Reduced cerebral <strong>mGluR5</strong> availability in alcohol dependent patients recovers during abstinence and is associated with reduced <b>craving</b>.
+GRM5	drug	alcohol	31481578	Higher striatal <strong>mGluR5</strong> availability in <b>alcohol</b> dependent users may be associated with long term relapse.
+GRM5	addiction	relapse	31481578	Higher striatal <strong>mGluR5</strong> availability in alcohol dependent users may be associated with long term <b>relapse</b>.
+GRM5	drug	cocaine	31446451	The cognitive cost of reducing relapse to <b>cocaine</b> seeking with <strong>mGlu5</strong> allosteric modulators.
+GRM5	addiction	relapse	31446451	The cognitive cost of reducing <b>relapse</b> to cocaine <b>seeking</b> with <strong>mGlu5</strong> allosteric modulators.
+GRM5	drug	cocaine	31446451	Antagonism of metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) has been demonstrated to decrease <b>cocaine</b> seeking but may also further compromise cognitive function in long term <b>cocaine</b> users.
+GRM5	addiction	relapse	31446451	Antagonism of metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) has been demonstrated to decrease cocaine <b>seeking</b> but may also further compromise cognitive function in long term cocaine users.
+GRM5	drug	cocaine	31446451	Here we assessed the effect of repeated administration of negative or positive allosteric modulators (NAM or PAM) of <strong>mGlu5</strong> on both cognitive performance and (context+cue) primed <b>cocaine</b> seeking after prolonged abstinence (≥ 45 days).
+GRM5	addiction	relapse	31446451	Here we assessed the effect of repeated administration of negative or positive allosteric modulators (NAM or PAM) of <strong>mGlu5</strong> on both cognitive performance and (context+cue) primed cocaine <b>seeking</b> after prolonged abstinence (≥ 45 days).
+GRM5	drug	cocaine	31409665	Although ZIP has no effect on accumbal LTD in slices from naive or yoked saline mice, it is able to restore both NMDA dependent and <strong>mGluR5</strong> dependent LTD in animals after <b>cocaine</b> self administration and withdrawal.
+GRM5	addiction	withdrawal	31409665	Although ZIP has no effect on accumbal LTD in slices from naive or yoked saline mice, it is able to restore both NMDA dependent and <strong>mGluR5</strong> dependent LTD in animals after cocaine self administration and <b>withdrawal</b>.
+GRM5	drug	cocaine	31408786	Extinction training following <b>cocaine</b> or MDMA self administration produces discrete changes in D2 like and <strong>mGlu5</strong> receptor density in the rat brain.
+GRM5	drug	psychedelics	31408786	Extinction training following cocaine or <b>MDMA</b> self administration produces discrete changes in D2 like and <strong>mGlu5</strong> receptor density in the rat brain.
+GRM5	addiction	relapse	31408786	Several studies strongly support the role of the dopamine D2 like and glutamate <strong>mGlu5</strong> receptors in psychostimulant reward and <b>relapse</b>.
+GRM5	addiction	reward	31408786	Several studies strongly support the role of the dopamine D2 like and glutamate <strong>mGlu5</strong> receptors in psychostimulant <b>reward</b> and relapse.
+GRM5	drug	cocaine	31408786	The present study employed <b>cocaine</b> or MDMA self administration with yoked triad procedure in rats to explore whether extinction training affects the drug seeking behavior and the D2 like and <strong>mGlu5</strong> receptor Bmax and Kd values in several regions of the animal brain.
+GRM5	drug	psychedelics	31408786	The present study employed cocaine or <b>MDMA</b> self administration with yoked triad procedure in rats to explore whether extinction training affects the drug seeking behavior and the D2 like and <strong>mGlu5</strong> receptor Bmax and Kd values in several regions of the animal brain.
+GRM5	addiction	relapse	31408786	The present study employed cocaine or MDMA self administration with yoked triad procedure in rats to explore whether extinction training affects the drug <b>seeking</b> behavior and the D2 like and <strong>mGlu5</strong> receptor Bmax and Kd values in several regions of the animal brain.
+GRM5	drug	cocaine	31408786	Interestingly, in the prefrontal cortex a reduction in the <strong>mGlu5</strong> receptor density in <b>cocaine</b>  or MDMA abstinent rats was demonstrated, with significant effects being observed after previous MDMA exposure.
+GRM5	drug	psychedelics	31408786	Interestingly, in the prefrontal cortex a reduction in the <strong>mGlu5</strong> receptor density in cocaine  or <b>MDMA</b> abstinent rats was demonstrated, with significant effects being observed after previous <b>MDMA</b> exposure.
+GRM5	drug	cocaine	31408786	Moreover, rats self administered <b>cocaine</b> showed a rise in the density of <strong>mGlu5</strong> receptor for the nucleus accumbens.
+GRM5	drug	cocaine	31408786	This study first time shows that abstinence followed extinction training after <b>cocaine</b> or MDMA self  or passive injections changes the D2 like and <strong>mGlu5</strong> density and affinity.
+GRM5	drug	psychedelics	31408786	This study first time shows that abstinence followed extinction training after cocaine or <b>MDMA</b> self  or passive injections changes the D2 like and <strong>mGlu5</strong> density and affinity.
+GRM5	drug	alcohol	31366097	Allosteric modulators of metabotropic glutamate 5 receptors (<strong>mGlu5</strong> receptors) have been identified as a promising treatment to independently alleviate both negative affective states and <b>ethanol</b> seeking and intake.
+GRM5	addiction	relapse	31366097	Allosteric modulators of metabotropic glutamate 5 receptors (<strong>mGlu5</strong> receptors) have been identified as a promising treatment to independently alleviate both negative affective states and ethanol <b>seeking</b> and intake.
+GRM5	drug	alcohol	31366097	The current review synthesizes preclinical studies that have observed the role of <strong>mGlu5</strong> receptor modulation in negative affective states following <b>ethanol</b> exposure.
+GRM5	drug	alcohol	31366097	The work done to date supports <strong>mGlu5</strong> receptor modulation as a promising target for mediating negative affective states to reduce <b>ethanol</b> intake or prevent relapse.
+GRM5	addiction	relapse	31366097	The work done to date supports <strong>mGlu5</strong> receptor modulation as a promising target for mediating negative affective states to reduce ethanol intake or prevent <b>relapse</b>.
+GRM5	addiction	relapse	31202811	The <strong>mGlu5</strong> receptor antagonists MPEP and MTEP produced a significant reduction in <b>reinstatement</b> while failing to alter responding where every response produced food.
+GRM5	drug	cocaine	31161451	Mechanisms underlying the efficacy of exercise as an intervention for <b>cocaine</b> relapse: a focus on <strong>mGlu5</strong> in the dorsal medial prefrontal cortex.
+GRM5	addiction	relapse	31161451	Mechanisms underlying the efficacy of exercise as an intervention for cocaine <b>relapse</b>: a focus on <strong>mGlu5</strong> in the dorsal medial prefrontal cortex.
+GRM5	drug	cocaine	31161451	Exercise initiated during early, but not late abstinence, reduced <b>cocaine</b> seeking; this effect was strongly associated with dmPFC <strong>Grm5</strong> expression (gene encoding mGlu5), and modestly associated with dmPFC Grin1 and Bdnf IV expression.
+GRM5	addiction	relapse	31161451	Exercise initiated during early, but not late abstinence, reduced cocaine <b>seeking</b>; this effect was strongly associated with dmPFC <strong>Grm5</strong> expression (gene encoding mGlu5), and modestly associated with dmPFC Grin1 and Bdnf IV expression.
+GRM5	drug	cocaine	31161451	Exercise initiated during early, but not late abstinence, reduced <b>cocaine</b> seeking; this effect was strongly associated with dmPFC <strong>Grm5</strong> expression (gene encoding <strong>mGlu5</strong>), and modestly associated with dmPFC Grin1 and Bdnf IV expression.
+GRM5	addiction	relapse	31161451	Exercise initiated during early, but not late abstinence, reduced cocaine <b>seeking</b>; this effect was strongly associated with dmPFC <strong>Grm5</strong> expression (gene encoding <strong>mGlu5</strong>), and modestly associated with dmPFC Grin1 and Bdnf IV expression.
+GRM5	drug	cocaine	31161451	Activation of <strong>mGlu5</strong> in the dmPFC during early abstinence mimicked the efficacy of early initiated exercise; however, inhibition of these receptors prior to the exercise sessions did not block its efficacy indicating that there may be redundancy in the mechanisms through which exercise reduces <b>cocaine</b> seeking.
+GRM5	addiction	relapse	31161451	Activation of <strong>mGlu5</strong> in the dmPFC during early abstinence mimicked the efficacy of early initiated exercise; however, inhibition of these receptors prior to the exercise sessions did not block its efficacy indicating that there may be redundancy in the mechanisms through which exercise reduces cocaine <b>seeking</b>.
+GRM5	drug	nicotine	31119680	Using positron emission tomography (PET), a profound alteration of the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) was found in human <b>smoking</b> addiction and abstinence.
+GRM5	addiction	addiction	31119680	Using positron emission tomography (PET), a profound alteration of the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) was found in human smoking <b>addiction</b> and abstinence.
+GRM5	drug	nicotine	31119680	As human PET data either reflect the impact of chronic <b>nicotine</b> exposure or a pre existing vulnerability to <b>nicotine</b> addiction, we designed a preclinical, longitudinal study to investigate the effect of chronic <b>nicotine</b> exposure on <strong>mGluR5</strong> with the novel radiotracer [18F]PSS232 using PET.
+GRM5	addiction	addiction	31119680	As human PET data either reflect the impact of chronic nicotine exposure or a pre existing vulnerability to nicotine <b>addiction</b>, we designed a preclinical, longitudinal study to investigate the effect of chronic nicotine exposure on <strong>mGluR5</strong> with the novel radiotracer [18F]PSS232 using PET.
+GRM5	drug	nicotine	31119680	This preliminary longitudinal PET study demonstrates that chronic <b>nicotine</b> administration alters behaviour and <strong>mGluR5</strong> availability.
+GRM5	drug	opioid	31113910	[Role of <strong>mGluR5</strong> in laterocapcular division of central nucleus of amygdala in <b>fentanyl</b> induced hyperalgesia in rats].
+GRM5	drug	opioid	31113910	To investigate the role of metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) in laterocapcular division of the central nucleus of amygdala (CeLC) in <b>fentanyl</b> induced hyperalgesia in rats.
+GRM5	drug	opioid	31113910	Inhibition of the activity of <strong>mGluR5</strong> in the CeLC may alleviate the symptoms of <b>fentanyl</b> induced hyperalgesia.
+GRM5	drug	opioid	31113910	目的：探讨伤害性杏仁核(laterocapcular division of central nucleus of amygdala，CeLC)中代谢型谷氨酸受体5 (metabotropic glutamate receptor 5，<strong>mGluR5</strong>)在芬太尼即阿片类药物诱发的痛觉过敏(<b>opioid</b> induced hyperalgesia，OIH)中的作用。方法：取SD雄性大鼠12只，随机分为正常1组(n=6)与OIH1组(n=6)，OIH1组通过颈下皮肤注射芬太尼制备OIH模型，正常1组注射等量生理盐水。造模后6.5 h分别测量大鼠机械缩足阈值(paw withdrawal mechanical threshold，PWMT)和热缩足潜伏期(paw withdrawal thermal latency，PWTL)以确定造模成功，随后取右侧CeLC组织行蛋白质印迹法检测mGluR5的表达量。另取SD雄性大鼠40只，随机分为OIH+DMSO组、OIH+MTEP(3.0 μg)组、OIH+MTEP(7.5 μg)组、OIH+MTEP(15.0 μg)组4组，每组10只，其中MTEP为mGluR5的选择性抑制剂。每组CeLC置管并恢复1周后制备OIH模型，随后向各组CeLC分别注射0.5 μL DMSO和3.0，7.5，15.0 μg MTEP。观察给药前后大鼠PWMT和PWTL的变化，并取CeLC组织检测mGluR5蛋白的表达水平。另取SD雄性大鼠8只，随机分为正常2组与OIH2组，前者皮下注射生理盐水，后者注射等量芬太尼制备OIH模型，在脑片上记录两组CeLC神经元MTEP(1 μmol/L)给药前后的微小兴奋性突触后电流(miniature excitatory postsynaptic currents，mEPSCs)。结果：与正常1组相比，OIH1组PWMT明显降低且PWTL明显缩短，mGluR5蛋白的表达水平明显升高(P<0.05)。各组造模后PWMT与PWTL均明显下降(P<0.05)，提示造模成功，CeLC中mGluR5的表达水平明显升高，以上变化可被MTEP呈剂量依赖性逆转(P<0.05)。脑片膜片钳电生理记录显示：与正常2组相比，OIH2组mEPSCs幅度与频率均明显升高(P<0.05)，并可被MTEP逆转。结论： CeLC mGluR5的高表达可能参与了OIH的维持，抑制CeLC mGluR5的活性可以减轻芬太尼诱导的痛觉过敏症状。.
+GRM5	addiction	withdrawal	31113910	目的：探讨伤害性杏仁核(laterocapcular division of central nucleus of amygdala，CeLC)中代谢型谷氨酸受体5 (metabotropic glutamate receptor 5，<strong>mGluR5</strong>)在芬太尼即阿片类药物诱发的痛觉过敏(opioid induced hyperalgesia，OIH)中的作用。方法：取SD雄性大鼠12只，随机分为正常1组(n=6)与OIH1组(n=6)，OIH1组通过颈下皮肤注射芬太尼制备OIH模型，正常1组注射等量生理盐水。造模后6.5 h分别测量大鼠机械缩足阈值(paw <b>withdrawal</b> mechanical threshold，PWMT)和热缩足潜伏期(paw <b>withdrawal</b> thermal latency，PWTL)以确定造模成功，随后取右侧CeLC组织行蛋白质印迹法检测mGluR5的表达量。另取SD雄性大鼠40只，随机分为OIH+DMSO组、OIH+MTEP(3.0 μg)组、OIH+MTEP(7.5 μg)组、OIH+MTEP(15.0 μg)组4组，每组10只，其中MTEP为mGluR5的选择性抑制剂。每组CeLC置管并恢复1周后制备OIH模型，随后向各组CeLC分别注射0.5 μL DMSO和3.0，7.5，15.0 μg MTEP。观察给药前后大鼠PWMT和PWTL的变化，并取CeLC组织检测mGluR5蛋白的表达水平。另取SD雄性大鼠8只，随机分为正常2组与OIH2组，前者皮下注射生理盐水，后者注射等量芬太尼制备OIH模型，在脑片上记录两组CeLC神经元MTEP(1 μmol/L)给药前后的微小兴奋性突触后电流(miniature excitatory postsynaptic currents，mEPSCs)。结果：与正常1组相比，OIH1组PWMT明显降低且PWTL明显缩短，mGluR5蛋白的表达水平明显升高(P<0.05)。各组造模后PWMT与PWTL均明显下降(P<0.05)，提示造模成功，CeLC中mGluR5的表达水平明显升高，以上变化可被MTEP呈剂量依赖性逆转(P<0.05)。脑片膜片钳电生理记录显示：与正常2组相比，OIH2组mEPSCs幅度与频率均明显升高(P<0.05)，并可被MTEP逆转。结论： CeLC mGluR5的高表达可能参与了OIH的维持，抑制CeLC mGluR5的活性可以减轻芬太尼诱导的痛觉过敏症状。.
+GRM5	drug	cocaine	31017999	The negative allosteric modulator of <strong>mGluR5</strong>, MPEP, potentiates the rewarding properties of <b>cocaine</b> in priming induced reinstatement of CPP.
+GRM5	addiction	relapse	31017999	The negative allosteric modulator of <strong>mGluR5</strong>, MPEP, potentiates the rewarding properties of cocaine in priming induced <b>reinstatement</b> of CPP.
+GRM5	addiction	reward	31017999	The negative allosteric modulator of <strong>mGluR5</strong>, MPEP, potentiates the rewarding properties of cocaine in priming induced reinstatement of <b>CPP</b>.
+GRM5	drug	cocaine	31017999	The metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) seems to be involved in the reinstatement induced by <b>cocaine</b> associated cues.
+GRM5	addiction	relapse	31017999	The metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) seems to be involved in the <b>reinstatement</b> induced by cocaine associated cues.
+GRM5	drug	cocaine	31017999	The main objective of the study was to evaluate the efficacy of MPEP, a negative allosteric modulator of <strong>mGluR5</strong>, in attenuating or potentiating the reinstatement induced by priming doses of <b>cocaine</b> in the CPP paradigm, ultimately to further knowledge regarding the role of the <strong>mGluR5</strong> in relapse into <b>cocaine</b> abuse.
+GRM5	addiction	relapse	31017999	The main objective of the study was to evaluate the efficacy of MPEP, a negative allosteric modulator of <strong>mGluR5</strong>, in attenuating or potentiating the <b>reinstatement</b> induced by priming doses of cocaine in the CPP paradigm, ultimately to further knowledge regarding the role of the <strong>mGluR5</strong> in <b>relapse</b> into cocaine abuse.
+GRM5	addiction	reward	31017999	The main objective of the study was to evaluate the efficacy of MPEP, a negative allosteric modulator of <strong>mGluR5</strong>, in attenuating or potentiating the reinstatement induced by priming doses of cocaine in the <b>CPP</b> paradigm, ultimately to further knowledge regarding the role of the <strong>mGluR5</strong> in relapse into cocaine abuse.
+GRM5	drug	cocaine	31017999	These findings may help to understand the role of <strong>mGluR5</strong> in the relapse into <b>cocaine</b> abuse.
+GRM5	addiction	relapse	31017999	These findings may help to understand the role of <strong>mGluR5</strong> in the <b>relapse</b> into cocaine abuse.
+GRM5	drug	alcohol	30991250	The function of group I metabotropic glutamate receptors mGluR1 and <strong>mGluR5</strong> is involved in the hyperglutamatergic state caused by chronic <b>alcohol</b>.
+GRM5	drug	cocaine	30948476	Synaptic Depotentiation and <strong>mGluR5</strong> Activity in the Nucleus Accumbens Drive <b>Cocaine</b> Primed Reinstatement of Place Preference.
+GRM5	addiction	relapse	30948476	Synaptic Depotentiation and <strong>mGluR5</strong> Activity in the Nucleus Accumbens Drive Cocaine Primed <b>Reinstatement</b> of Place Preference.
+GRM5	addiction	relapse	30948476	Furthermore, <b>reinstatement</b> was driven by an <strong>mGluR5</strong> dependent reduction in AMPAR signaling.
+GRM5	drug	cocaine	30948476	Intra NAc shell infusion of the <strong>mGluR5</strong> antagonist MTEP blocked <b>cocaine</b> primed reinstatement and corresponding depotentiation, whereas infusion of the <strong>mGluR5</strong> agonist CHPG itself promoted reinstatement and depotentiated synaptic strength in the NAc shell.
+GRM5	addiction	relapse	30948476	Intra NAc shell infusion of the <strong>mGluR5</strong> antagonist MTEP blocked cocaine primed <b>reinstatement</b> and corresponding depotentiation, whereas infusion of the <strong>mGluR5</strong> agonist CHPG itself promoted <b>reinstatement</b> and depotentiated synaptic strength in the NAc shell.
+GRM5	drug	cocaine	30948476	These data support a model in which <strong>mGluR5</strong> mediated reduction in GluA2 containing AMPARs at NAc shell synapses receiving input from the infralimbic cortex is a critical factor in triggering reinstatement of <b>cocaine</b> primed conditioned approach behavior.SIGNIFICANCE STATEMENT These studies identified a sequence of neural events whereby reexposure to <b>cocaine</b> activates a signaling cascade that alters synaptic strength in the NAc shell and triggers a behavioral response driven by a drug associated memory.
+GRM5	addiction	relapse	30948476	These data support a model in which <strong>mGluR5</strong> mediated reduction in GluA2 containing AMPARs at NAc shell synapses receiving input from the infralimbic cortex is a critical factor in triggering <b>reinstatement</b> of cocaine primed conditioned approach behavior.SIGNIFICANCE STATEMENT These studies identified a sequence of neural events whereby reexposure to cocaine activates a signaling cascade that alters synaptic strength in the NAc shell and triggers a behavioral response driven by a drug associated memory.
+GRM5	drug	cocaine	30946882	Further, we found that dysregulated metabolic activity and <strong>mGlu5</strong> receptor signaling in the PrL of <b>cocaine</b> rats correlated with past working memory performance and/or drug seeking, as indicated by the analysis of cytochrome oxidase reactivity, <strong>mGlu5</strong> and Homer 1b/c protein expression, as well as Arc mRNA expression in <strong>mGlu5</strong> positive cells.
+GRM5	addiction	relapse	30946882	Further, we found that dysregulated metabolic activity and <strong>mGlu5</strong> receptor signaling in the PrL of cocaine rats correlated with past working memory performance and/or drug <b>seeking</b>, as indicated by the analysis of cytochrome oxidase reactivity, <strong>mGlu5</strong> and Homer 1b/c protein expression, as well as Arc mRNA expression in <strong>mGlu5</strong> positive cells.
+GRM5	drug	alcohol	30914307	<strong>MGluR5</strong> activity is required for the induction of <b>ethanol</b> behavioral sensitization and associated changes in ERK MAP kinase phosphorylation in the nucleus accumbens shell and lateral habenula.
+GRM5	addiction	sensitization	30914307	<strong>MGluR5</strong> activity is required for the induction of ethanol behavioral <b>sensitization</b> and associated changes in ERK MAP kinase phosphorylation in the nucleus accumbens shell and lateral habenula.
+GRM5	drug	alcohol	30914307	Metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>) activity regulates a variety of behavioral pathologies associated with <b>alcohol</b> addiction.
+GRM5	addiction	addiction	30914307	Metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>) activity regulates a variety of behavioral pathologies associated with alcohol <b>addiction</b>.
+GRM5	drug	alcohol	30914307	The main goal of this study was to determine if <strong>mGluR5</strong> regulates the induction of <b>ethanol</b> induced locomotor sensitization, which is a model of experience dependent plasticity following initial exposure to drugs of abuse.
+GRM5	addiction	sensitization	30914307	The main goal of this study was to determine if <strong>mGluR5</strong> regulates the induction of ethanol induced locomotor <b>sensitization</b>, which is a model of experience dependent plasticity following initial exposure to drugs of abuse.
+GRM5	drug	alcohol	30914307	The extracellular signal regulated kinase (ERK1/2) pathway is downstream of <strong>mGluR5</strong> and implicated in <b>alcohol</b> addiction; however, its role in sensitization remains unexplored.
+GRM5	addiction	addiction	30914307	The extracellular signal regulated kinase (ERK1/2) pathway is downstream of <strong>mGluR5</strong> and implicated in alcohol <b>addiction</b>; however, its role in sensitization remains unexplored.
+GRM5	addiction	sensitization	30914307	The extracellular signal regulated kinase (ERK1/2) pathway is downstream of <strong>mGluR5</strong> and implicated in alcohol addiction; however, its role in <b>sensitization</b> remains unexplored.
+GRM5	drug	alcohol	30914307	We sought to determine if <strong>mGluR5</strong> mediated changes in <b>ethanol</b> induced sensitization are associated with changes in ERK1/2 phosphorylation (pERK1/2) in specific brain regions.
+GRM5	addiction	sensitization	30914307	We sought to determine if <strong>mGluR5</strong> mediated changes in ethanol induced <b>sensitization</b> are associated with changes in ERK1/2 phosphorylation (pERK1/2) in specific brain regions.
+GRM5	drug	alcohol	30914307	Adult male DBA/2 J mice were tested for acute locomotor response to <b>ethanol</b> (0 or 2 g/kg, IP) followed by a 9 day induction period in which the <strong>mGluR5</strong> antagonist MPEP (0 or 30 mg/kg, IP) was administered prior to <b>ethanol</b> (0 or 2.5 g/kg, IP).
+GRM5	addiction	sensitization	30914307	<b>Sensitization</b> was also associated with <strong>mGluR5</strong> independent increases in pERK1/2 IR in the nucleus accumbens core and decreases in the dentate gyrus and lateral septum.
+GRM5	drug	alcohol	30914307	These data indicate that <strong>mGluR5</strong> activity is required for the induction of <b>ethanol</b> locomotor sensitization and associated changes in ERK1/2 phosphorylation in the AcbSh and LHb, which raises the hypothesis that <strong>mGluR5</strong> mediated cell signaling in these brain regions may mediate the induction of sensitization.
+GRM5	addiction	sensitization	30914307	These data indicate that <strong>mGluR5</strong> activity is required for the induction of ethanol locomotor <b>sensitization</b> and associated changes in ERK1/2 phosphorylation in the AcbSh and LHb, which raises the hypothesis that <strong>mGluR5</strong> mediated cell signaling in these brain regions may mediate the induction of <b>sensitization</b>.
+GRM5	drug	amphetamine	30766916	Estradiol Induced Potentiation of Dopamine Release in Dorsal Striatum Following <b>Amphetamine</b> Administration Requires Estradiol Receptors and <strong>mGlu5</strong>.
+GRM5	addiction	addiction	30766916	There is evidence that estradiol receptors collaborate with <strong>mGlu5</strong> within caveoli in DLS and <strong>mGlu5</strong> is hypothesized to mediate many of the effects of estradiol in the <b>addiction</b> processes in females.
+GRM5	drug	amphetamine	30766916	Together, our findings demonstrate that estradiol potentiates <b>amphetamine</b> stimulated DA release in the DLS and this effect requires both estradiol receptors and <strong>mGlu5</strong>.
+GRM5	drug	alcohol	30737312	Increased <b>Alcohol</b> Drinking Induced by Manipulations of <strong>mGlu5</strong> Phosphorylation within the Bed Nucleus of the Stria Terminalis.
+GRM5	drug	alcohol	30737312	We discovered that <strong>mGlu5</strong> signaling in the BNST is linked to excessive <b>alcohol</b> consumption in a manner distinct from behavioral or neuropharmacological endophenotypes that have been previously implicated as triggers for heavy drinking.
+GRM5	drug	alcohol	30737312	Our studies demonstrate that, in male mice, a history of chronic binge <b>alcohol</b> drinking elevates BNST levels of the <strong>mGlu5</strong> scaffolding protein Homer2 and activated extracellular signal regulated kinase (ERK) in an adaptive response to limit <b>alcohol</b> consumption.
+GRM5	addiction	intoxication	30737312	Our studies demonstrate that, in male mice, a history of chronic <b>binge</b> alcohol drinking elevates BNST levels of the <strong>mGlu5</strong> scaffolding protein Homer2 and activated extracellular signal regulated kinase (ERK) in an adaptive response to limit alcohol consumption.
+GRM5	drug	alcohol	30737312	Male and female transgenic mice expressing a point mutation of <strong>mGlu5</strong> that cannot be phosphorylated by ERK exhibit excessive <b>alcohol</b> drinking, despite greater behavioral signs of <b>alcohol</b> intoxication and reduced anxiety, and are insensitive to local manipulations of signaling in the BNST.
+GRM5	addiction	intoxication	30737312	Male and female transgenic mice expressing a point mutation of <strong>mGlu5</strong> that cannot be phosphorylated by ERK exhibit excessive alcohol drinking, despite greater behavioral signs of alcohol <b>intoxication</b> and reduced anxiety, and are insensitive to local manipulations of signaling in the BNST.
+GRM5	drug	alcohol	30737312	Our findings elucidate a novel <strong>mGluR5</strong> linked signaling state within BNST that plays a central and unanticipated role in excessive <b>alcohol</b> consumption.SIGNIFICANCE STATEMENT The bed nucleus of the stria terminalis (BNST) is part of the limbic hypothalamic system important for behavioral responses to stress and <b>alcohol</b>, and glutamate transmission within BNST is implicated in the neurobiology of <b>alcoholism</b>.
+GRM5	drug	alcohol	30737312	The present study provides evidence that a history of excessive <b>alcohol</b> drinking increases signaling through the metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) receptor within the BNST in an adaptive response to limit <b>alcohol</b> consumption.
+GRM5	drug	alcohol	30737312	In particular, disruption of <strong>mGlu5</strong> phosphorylation by extracellular signal regulated kinase within this brain region induces excessive <b>alcohol</b> drinking, which reflects a selective insensitivity to the aversive properties of <b>alcohol</b> intoxication.
+GRM5	addiction	aversion	30737312	In particular, disruption of <strong>mGlu5</strong> phosphorylation by extracellular signal regulated kinase within this brain region induces excessive alcohol drinking, which reflects a selective insensitivity to the <b>aversive</b> properties of alcohol intoxication.
+GRM5	addiction	intoxication	30737312	In particular, disruption of <strong>mGlu5</strong> phosphorylation by extracellular signal regulated kinase within this brain region induces excessive alcohol drinking, which reflects a selective insensitivity to the aversive properties of alcohol <b>intoxication</b>.
+GRM5	drug	alcohol	30737312	These data indicate that a specific signaling state of <strong>mGlu5</strong> within BNST plays a central and unanticipated role in excessive <b>alcohol</b> consumption.
+GRM5	addiction	withdrawal	30733663	We then analyzed the expression levels of presynaptic (vGlut1, vGlut2, CB1 receptor, synaptophysin) and postsynaptic (PSD95, GluN1, GluN2A, GluN2B, GluA1, GluA2, mGluR1 and <strong>mGluR5</strong>) proteins after 7 days EtOH incubation or after EtOH <b>withdrawal</b>.
+GRM5	addiction	withdrawal	30733663	We found that only GluA1 and <strong>mGluR5</strong> expression levels were significantly increased after EtOH <b>withdrawal</b> and, in neuroprotection experiments, we observed that AMPA and <strong>mGluR5</strong> antagonists attenuated EtOH <b>withdrawal</b> induced toxicity.
+GRM5	drug	amphetamine	30599269	In the mPFC, surface expression of <strong>mGlu5</strong> receptors was elevated in rats after <b>amphetamine</b> conditioning.
+GRM5	drug	amphetamine	30599269	<strong>mGlu5</strong> receptors were also increased at synaptic and extrasynaptic sites in <b>amphetamine</b> conditioned rats.
+GRM5	addiction	reward	30515075	<strong>mGluR5</strong> Mediates Dihydrotestosterone Induced Nucleus Accumbens Structural Plasticity, but Not Conditioned <b>Reward</b>.
+GRM5	drug	cannabinoid	30515075	The effect of DHT was dependent on <strong>mGluR5</strong> activity, and local <strong>mGluR5</strong> activation and subsequent <b>endocannabinoid</b> signaling produce an analogous NAc shell spine decrease.
+GRM5	drug	alcohol	30483137	<strong>mGlu5</strong> Receptor Blockade Within the Nucleus Accumbens Shell Reduces Behavioral Indices of <b>Alcohol</b> Withdrawal Induced Anxiety in Mice.
+GRM5	addiction	withdrawal	30483137	<strong>mGlu5</strong> Receptor Blockade Within the Nucleus Accumbens Shell Reduces Behavioral Indices of Alcohol <b>Withdrawal</b> Induced Anxiety in Mice.
+GRM5	addiction	intoxication	30483137	Withdrawal from <b>binge</b> drinking increases negative affect, coinciding with increased expression of the metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) within the shell of the nucleus accumbens (AcbSh).
+GRM5	addiction	withdrawal	30483137	<b>Withdrawal</b> from binge drinking increases negative affect, coinciding with increased expression of the metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) within the shell of the nucleus accumbens (AcbSh).
+GRM5	addiction	intoxication	30483137	Supporting a causal effect relationship, systemic treatment with the <strong>mGlu5</strong> receptor antagonist MTEP [3 ((2 Methyl 4 thiazolyl)ethynyl)pyridine] is anxiolytic in <b>binge</b> drinking adult and adolescent mice.
+GRM5	drug	alcohol	30483137	Here, we employed neuropharmacological approaches to examine the functional relevance of AcbSh <strong>mGlu5</strong> for behavioral indices of <b>alcohol</b> withdrawal induced hyper anxiety.
+GRM5	addiction	withdrawal	30483137	Here, we employed neuropharmacological approaches to examine the functional relevance of AcbSh <strong>mGlu5</strong> for behavioral indices of alcohol <b>withdrawal</b> induced hyper anxiety.
+GRM5	drug	alcohol	30483137	These results implicate AcbSh <strong>mGlu5</strong> in modulating <b>alcohol</b> withdrawal induced negative affect and suggest age differences in the neurobiological effects of <b>alcohol</b> withdrawal and behavioral responsiveness to <strong>mGlu5</strong> blockade within the AcbSh.
+GRM5	addiction	withdrawal	30483137	These results implicate AcbSh <strong>mGlu5</strong> in modulating alcohol <b>withdrawal</b> induced negative affect and suggest age differences in the neurobiological effects of alcohol <b>withdrawal</b> and behavioral responsiveness to <strong>mGlu5</strong> blockade within the AcbSh.
+GRM5	addiction	relapse	30459590	Rats evaluated after >1 month of withdrawal (when incubation of <b>craving</b> is robust) display alterations in excitatory synapses onto medium spiny neurons (MSNs) of the nucleus accumbens (NAc), including elevated levels of Ca2+ permeable AMPA receptors (CP AMPAR) and a transition from group I metabotropic glutamate receptor (mGluR) <strong>mGlu5</strong>  to mGlu1 mediated synaptic depression.
+GRM5	addiction	withdrawal	30459590	Rats evaluated after >1 month of <b>withdrawal</b> (when incubation of craving is robust) display alterations in excitatory synapses onto medium spiny neurons (MSNs) of the nucleus accumbens (NAc), including elevated levels of Ca2+ permeable AMPA receptors (CP AMPAR) and a transition from group I metabotropic glutamate receptor (mGluR) <strong>mGlu5</strong>  to mGlu1 mediated synaptic depression.
+GRM5	drug	cocaine	30459590	Bath application of the nonselective group I mGluR agonist dihydroxyphenylglycine (DHPG) produced a transient <strong>mGlu5</strong> mediated synaptic depression in saline controls, whereas a persistent mGlu1 mediated synaptic depression emerged in <b>cocaine</b> rats.
+GRM5	drug	cocaine	30291225	A novel rat model of comorbid PTSD and addiction reveals intersections between stress susceptibility and enhanced <b>cocaine</b> seeking with a role for <strong>mGlu5</strong> receptors.
+GRM5	addiction	addiction	30291225	A novel rat model of comorbid PTSD and <b>addiction</b> reveals intersections between stress susceptibility and enhanced cocaine seeking with a role for <strong>mGlu5</strong> receptors.
+GRM5	addiction	relapse	30291225	A novel rat model of comorbid PTSD and addiction reveals intersections between stress susceptibility and enhanced cocaine <b>seeking</b> with a role for <strong>mGlu5</strong> receptors.
+GRM5	drug	cocaine	30291225	TMT exposed resilient rats displayed increased <strong>mGlu5</strong> gene expression in the amygdala and medial prefrontal cortex and did not display the enhanced <b>cocaine</b> seeking observed in susceptible rats.
+GRM5	addiction	relapse	30291225	TMT exposed resilient rats displayed increased <strong>mGlu5</strong> gene expression in the amygdala and medial prefrontal cortex and did not display the enhanced cocaine <b>seeking</b> observed in susceptible rats.
+GRM5	drug	cocaine	30291225	Combined treatment with the <strong>mGlu5</strong> positive allosteric modulator 3 Cyano N (1,3 diphenyl 1 H pyrazol 5 yl)benzamide (CDPPB), fear extinction, and ceftriaxone prevented the reinstatement of <b>cocaine</b> seeking in susceptible rats with fear extinction an important mediating condition.
+GRM5	addiction	relapse	30291225	Combined treatment with the <strong>mGlu5</strong> positive allosteric modulator 3 Cyano N (1,3 diphenyl 1 H pyrazol 5 yl)benzamide (CDPPB), fear extinction, and ceftriaxone prevented the <b>reinstatement</b> of cocaine <b>seeking</b> in susceptible rats with fear extinction an important mediating condition.
+GRM5	drug	cocaine	30291225	This work further identifies glutamate homeostasis and <strong>mGlu5</strong> as a target for treating relapse in comorbid PTSD <b>cocaine</b> addiction.
+GRM5	addiction	addiction	30291225	This work further identifies glutamate homeostasis and <strong>mGlu5</strong> as a target for treating relapse in comorbid PTSD cocaine <b>addiction</b>.
+GRM5	addiction	relapse	30291225	This work further identifies glutamate homeostasis and <strong>mGlu5</strong> as a target for treating <b>relapse</b> in comorbid PTSD cocaine addiction.
+GRM5	drug	amphetamine	30267744	<strong>mGluR5</strong> upregulation and the effects of repeated <b>methamphetamine</b> administration and withdrawal on the rewarding efficacy of ketamine and social interaction.
+GRM5	drug	psychedelics	30267744	<strong>mGluR5</strong> upregulation and the effects of repeated methamphetamine administration and withdrawal on the rewarding efficacy of <b>ketamine</b> and social interaction.
+GRM5	addiction	withdrawal	30267744	<strong>mGluR5</strong> upregulation and the effects of repeated methamphetamine administration and <b>withdrawal</b> on the rewarding efficacy of ketamine and social interaction.
+GRM5	addiction	withdrawal	30267744	Likewise, mice receiving the MA <b>withdrawal</b> regimen had high expression in <strong>mGluR5</strong> protein but unaltered EAAT3, Homer2 expression in hippocampal tissues.
+GRM5	addiction	reward	30267744	Pretreatment with MPEP, an <strong>mGluR5</strong> antagonist, prevented the MA withdrawal regimen induced increment in the KE <b>CPP</b> magnitude and impairments in social interaction behavior.
+GRM5	addiction	withdrawal	30267744	Pretreatment with MPEP, an <strong>mGluR5</strong> antagonist, prevented the MA <b>withdrawal</b> regimen induced increment in the KE CPP magnitude and impairments in social interaction behavior.
+GRM5	drug	cannabinoid	30238023	Based on quality of evidence to date, promising first tier neurochemical receptor targets include: noradrenergic (α1 and β antagonist, α2 agonist), kappa opioid antagonist, nociceptin antagonist, orexin 1 antagonist, and <b>endocannabinoid</b> modulation (e.g., <b>cannabidiol</b>, FAAH inhibition); second tier candidates may include corticotropin releasing factor 1 antagonists, serotonergic agents (e.g., 5 HT reuptake inhibitors, 5 HT3 antagonists), glutamatergic agents (e.g., mGluR2/3 agonist/positive allosteric modulator, <strong>mGluR5</strong> antagonist/negative allosteric modulator), GABA promoters (e.g., pregabalin, tiagabine), vasopressin 1b antagonist, NK 1 antagonist, and PPAR γ agonist (e.g., pioglitazone).
+GRM5	drug	opioid	30238023	Based on quality of evidence to date, promising first tier neurochemical receptor targets include: noradrenergic (α1 and β antagonist, α2 agonist), kappa <b>opioid</b> antagonist, nociceptin antagonist, orexin 1 antagonist, and endocannabinoid modulation (e.g., cannabidiol, FAAH inhibition); second tier candidates may include corticotropin releasing factor 1 antagonists, serotonergic agents (e.g., 5 HT reuptake inhibitors, 5 HT3 antagonists), glutamatergic agents (e.g., mGluR2/3 agonist/positive allosteric modulator, <strong>mGluR5</strong> antagonist/negative allosteric modulator), GABA promoters (e.g., pregabalin, tiagabine), vasopressin 1b antagonist, NK 1 antagonist, and PPAR γ agonist (e.g., pioglitazone).
+GRM5	drug	alcohol	29674969	The present study was aimed to further characterize the pharmacological profile of N [4 (trifluoromethyl) benzyl] 4 methoxybutyramide (GET73), a putative negative allosteric modulator (NAM) of metabotropic glutamate subtype 5 receptor (<strong>mGluR5</strong>) under development as a novel medication for the treatment of <b>alcohol</b> dependence.
+GRM5	addiction	dependence	29674969	The present study was aimed to further characterize the pharmacological profile of N [4 (trifluoromethyl) benzyl] 4 methoxybutyramide (GET73), a putative negative allosteric modulator (NAM) of metabotropic glutamate subtype 5 receptor (<strong>mGluR5</strong>) under development as a novel medication for the treatment of alcohol <b>dependence</b>.
+GRM5	drug	cocaine	29654259	Two weeks after five daily non contingent <b>cocaine</b> exposures (15 mg/kg), LTD was attenuated at MDT D1(+) synapses but was rescued by the <strong>mGlu5</strong> positive allosteric modulator (PAM) VU0409551.
+GRM5	drug	alcohol	29628194	This review focuses on the potential involvement of <strong>mGlu5</strong> receptor disruption in major depressive disorder and substance and/or <b>alcohol</b> use disorders.
+GRM5	drug	nicotine	29628194	We provide an overview of the justification of targeting <strong>mGlu5</strong> receptors in the treatment of these disorders, summarize the preclinical evidence for negatively modulating <strong>mGlu5</strong> receptors as a therapeutic target for major depressive disorders and <b>nicotine</b> dependence, and highlight the outcomes of recent clinical trials.
+GRM5	addiction	dependence	29628194	We provide an overview of the justification of targeting <strong>mGlu5</strong> receptors in the treatment of these disorders, summarize the preclinical evidence for negatively modulating <strong>mGlu5</strong> receptors as a therapeutic target for major depressive disorders and nicotine <b>dependence</b>, and highlight the outcomes of recent clinical trials.
+GRM5	drug	cocaine	29622268	We compared basal overall translation and its regulation by metabotropic glutamate receptor 1 (mGlu1), <strong>mGlu5</strong>, and N methyl D aspartate receptors (NMDARs) in drug naïve, saline control, and <b>cocaine</b> rats, and we compared GluA1 and GluA2 translation by immunoprecipitating puromycin labeled proteins.
+GRM5	drug	cocaine	29496988	Glutamatergic Biomarkers for <b>Cocaine</b> Addiction: A Longitudinal Study Using MR Spectroscopy and <strong>mGluR5</strong> PET in Self Administering Rats.
+GRM5	addiction	addiction	29496988	Glutamatergic Biomarkers for Cocaine <b>Addiction</b>: A Longitudinal Study Using MR Spectroscopy and <strong>mGluR5</strong> PET in Self Administering Rats.
+GRM5	drug	cocaine	29496988	We present findings on a rat model of <b>cocaine</b> self administration that was followed up longitudinally using the metabotropic glutamate receptor type 5 (<strong>mGluR5</strong>) tracer 18F 3 fluoro 5 [(pyridin 3 yl)ethynyl]benzonitrile (18F FPEB) PET, proton MR spectroscopy (1H MRS), and behavioral tests.
+GRM5	drug	cocaine	29496988	This decrease was most pronounced bilaterally in the hippocampus, where <strong>mGluR5</strong> availability correlated with the amount of <b>cocaine</b> used during relapse.
+GRM5	addiction	relapse	29496988	This decrease was most pronounced bilaterally in the hippocampus, where <strong>mGluR5</strong> availability correlated with the amount of cocaine used during <b>relapse</b>.
+GRM5	drug	cocaine	29496988	Finally, both glutamate concentration and <strong>mGluR5</strong> availability decrease during exposure to <b>cocaine</b>.
+GRM5	drug	cocaine	29487381	<strong>mGluR5</strong> antagonism inhibits <b>cocaine</b> reinforcement and relapse by elevation of extracellular glutamate in the nucleus accumbens via a CB1 receptor mechanism.
+GRM5	addiction	relapse	29487381	<strong>mGluR5</strong> antagonism inhibits cocaine reinforcement and <b>relapse</b> by elevation of extracellular glutamate in the nucleus accumbens via a CB1 receptor mechanism.
+GRM5	addiction	reward	29487381	<strong>mGluR5</strong> antagonism inhibits cocaine <b>reinforcement</b> and relapse by elevation of extracellular glutamate in the nucleus accumbens via a CB1 receptor mechanism.
+GRM5	drug	cocaine	29487381	Metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonism inhibits <b>cocaine</b> self administration and reinstatement of drug seeking behavior.
+GRM5	addiction	relapse	29487381	Metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonism inhibits cocaine self administration and <b>reinstatement</b> of drug <b>seeking</b> behavior.
+GRM5	drug	cocaine	29487381	Systemic or intra nucleus accumbens (NAc) administration of the <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) dose dependently reduced <b>cocaine</b> (and sucrose) self administration and <b>cocaine</b> induced reinstatement of drug seeking behavior.
+GRM5	addiction	relapse	29487381	Systemic or intra nucleus accumbens (NAc) administration of the <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) dose dependently reduced cocaine (and sucrose) self administration and cocaine induced <b>reinstatement</b> of drug <b>seeking</b> behavior.
+GRM5	drug	cannabinoid	29487381	Together, these results indicate that the therapeutic anti cocaine effects of <strong>mGluR5</strong> antagonists are mediated by elevation of extracellular glutamate in the NAc via an <b>endocannabinoid</b> CB1 receptor disinhibition mechanism.
+GRM5	drug	cocaine	29487381	Together, these results indicate that the therapeutic anti <b>cocaine</b> effects of <strong>mGluR5</strong> antagonists are mediated by elevation of extracellular glutamate in the NAc via an endocannabinoid CB1 receptor disinhibition mechanism.
+GRM5	drug	alcohol	29348321	Animal studies suggest an important role for the metabotropic glutamate receptor subtype 5 (<strong>mGlu5</strong>) in the pathophysiology of <b>alcohol</b> dependence, but direct human evidence is lacking.
+GRM5	addiction	dependence	29348321	Animal studies suggest an important role for the metabotropic glutamate receptor subtype 5 (<strong>mGlu5</strong>) in the pathophysiology of alcohol <b>dependence</b>, but direct human evidence is lacking.
+GRM5	drug	alcohol	29348321	The goal of this study was to investigate cerebral <strong>mGlu5</strong> availability in <b>alcohol</b> dependent subjects versus controls using 18F 3 fluoro 5 [(pyridin 3 yl)ethynyl]benzonitrile (18F FPEB) PET.
+GRM5	drug	alcohol	29348321	Results: <strong>mGlu5</strong> availability was lower in mainly limbic regions of <b>alcohol</b> dependent subjects than in controls (P < 0.05, familywise error corrected), ranging from 14% in the posterior cingulate cortex to 36% in the caudate nucleus.
+GRM5	addiction	relapse	29348321	Lower <strong>mGlu5</strong> availability was associated with higher hair ethyl glucuronide levels for most regions and was related to a lower level of <b>craving</b> specifically in the middle frontal gyrus, cingulate cortex, and inferolateral temporal lobe.
+GRM5	drug	alcohol	29348321	Conclusion: These findings provide human in vivo evidence that limbic <strong>mGlu5</strong> has a role in the pathophysiology of <b>alcohol</b> dependence, possibly involved in a compensatory mechanism helping to reduce craving during abstinence.
+GRM5	addiction	dependence	29348321	Conclusion: These findings provide human in vivo evidence that limbic <strong>mGlu5</strong> has a role in the pathophysiology of alcohol <b>dependence</b>, possibly involved in a compensatory mechanism helping to reduce craving during abstinence.
+GRM5	addiction	relapse	29348321	Conclusion: These findings provide human in vivo evidence that limbic <strong>mGlu5</strong> has a role in the pathophysiology of alcohol dependence, possibly involved in a compensatory mechanism helping to reduce <b>craving</b> during abstinence.
+GRM5	addiction	intoxication	29324247	<strong>mGlu5</strong> dependent modulation of anxiety during early withdrawal from <b>binge</b> drinking in adult and adolescent male mice.
+GRM5	addiction	withdrawal	29324247	<strong>mGlu5</strong> dependent modulation of anxiety during early <b>withdrawal</b> from binge drinking in adult and adolescent male mice.
+GRM5	addiction	intoxication	29324247	<b>Binge</b> induced anxiety during early (24 h) withdrawal is associated with increased expression of metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) within the nucleus accumbens shell (AcbSh) of adult male mice, but was unchanged in anxiety resilient adolescents.
+GRM5	addiction	withdrawal	29324247	Binge induced anxiety during early (24 h) <b>withdrawal</b> is associated with increased expression of metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) within the nucleus accumbens shell (AcbSh) of adult male mice, but was unchanged in anxiety resilient adolescents.
+GRM5	addiction	withdrawal	29324247	Herein, we determined the role of <strong>mGlu5</strong> signaling in <b>withdrawal</b> induced anxiety via pharmacological manipulation using the <strong>mGlu5</strong> negative allosteric modulator MTEP and the positive allosteric modulator CDPPB.
+GRM5	drug	alcohol	29324247	These results demonstrate a causal role for <strong>mGlu5</strong> in withdrawal induced anxiety in adults and suggest age related differences in the behavioral pharmacology of the negative reinforcing properties of <b>alcohol</b>.
+GRM5	addiction	reward	29324247	These results demonstrate a causal role for <strong>mGlu5</strong> in withdrawal induced anxiety in adults and suggest age related differences in the behavioral pharmacology of the negative <b>reinforcing</b> properties of alcohol.
+GRM5	addiction	withdrawal	29324247	These results demonstrate a causal role for <strong>mGlu5</strong> in <b>withdrawal</b> induced anxiety in adults and suggest age related differences in the behavioral pharmacology of the negative reinforcing properties of alcohol.
+GRM5	drug	alcohol	29317611	Preclinical research strongly suggests an implication of G protein coupled metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>) in nicotine addiction and <b>alcohol</b> use disorder.
+GRM5	drug	nicotine	29317611	Preclinical research strongly suggests an implication of G protein coupled metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>) in <b>nicotine</b> addiction and alcohol use disorder.
+GRM5	addiction	addiction	29317611	Preclinical research strongly suggests an implication of G protein coupled metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>) in nicotine <b>addiction</b> and alcohol use disorder.
+GRM5	drug	nicotine	29317611	In humans, <b>smoking</b> is related to a global reduction in <strong>mGluR5</strong> availability.
+GRM5	drug	alcohol	29317611	In the present study, we investigated <strong>mGluR5</strong> in vivo in patients with <b>alcohol</b> use disorder without the confounding effects of smoking.
+GRM5	drug	nicotine	29317611	In the present study, we investigated <strong>mGluR5</strong> in vivo in patients with alcohol use disorder without the confounding effects of <b>smoking</b>.
+GRM5	drug	alcohol	29317611	We did not find altered <strong>mGluR5</strong> DVR in the basal ganglia of subjects recovering from <b>alcohol</b> use disorder.
+GRM5	drug	alcohol	29317611	In conclusion, our study provides clinical evidence for altered <strong>mGluR5</strong> signaling in the amygdala in <b>alcohol</b> use disorder.
+GRM5	addiction	reward	29317611	In addition, this study suggests abnormal <strong>mGluR5</strong> signaling in a network underlying <b>reward</b> related behavioral flexibility.
+GRM5	drug	alcohol	29317611	These findings strengthen the case for pharmacological agents acting on <strong>mGluR5</strong> as promising candidates for the treatment of <b>alcohol</b> use disorder.
+GRM5	drug	alcohol	29294238	In the current study, we investigated the effects of VU 29, positive allosteric modulator of metabotropic glutamate 5 (<strong>mGlu5</strong>) receptor, on the acute <b>ethanol</b>  and <b>ethanol</b> withdrawal induced impairment of novel object recognition (NOR) task in rats.
+GRM5	addiction	withdrawal	29294238	In the current study, we investigated the effects of VU 29, positive allosteric modulator of metabotropic glutamate 5 (<strong>mGlu5</strong>) receptor, on the acute ethanol  and ethanol <b>withdrawal</b> induced impairment of novel object recognition (NOR) task in rats.
+GRM5	drug	alcohol	29294238	Additionally, the effects of VU 29 on expression of <strong>mGlu5</strong> and mGlu2 receptor proteins in the hippocampus, prefrontal cortex, and striatum were determined 48 h after <b>ethanol</b> withdrawal.
+GRM5	addiction	withdrawal	29294238	Additionally, the effects of VU 29 on expression of <strong>mGlu5</strong> and mGlu2 receptor proteins in the hippocampus, prefrontal cortex, and striatum were determined 48 h after ethanol <b>withdrawal</b>.
+GRM5	drug	alcohol	29294238	Our ELISA results show that VU 29 normalized <b>ethanol</b> withdrawal induced increase in expression of <strong>mGlu5</strong> receptor protein in the hippocampus, prefrontal cortex, and striatum, as well as expression of mGlu2 receptor protein in the hippocampus.
+GRM5	addiction	withdrawal	29294238	Our ELISA results show that VU 29 normalized ethanol <b>withdrawal</b> induced increase in expression of <strong>mGlu5</strong> receptor protein in the hippocampus, prefrontal cortex, and striatum, as well as expression of mGlu2 receptor protein in the hippocampus.
+GRM5	drug	alcohol	29294238	Thus, results from our study indicate that positive modulation of <strong>mGlu5</strong> receptor prevented and reversed <b>ethanol</b> induced memory impairment.
+GRM5	drug	alcohol	29294238	Moreover, <strong>mGlu5</strong> (hippocampus, prefrontal cortex, and striatum) and mGlu2 (hippocampus) receptors play an important role in the <b>ethanol</b> induced recognition memory impairment induced by <b>ethanol</b> withdrawal.
+GRM5	addiction	withdrawal	29294238	Moreover, <strong>mGlu5</strong> (hippocampus, prefrontal cortex, and striatum) and mGlu2 (hippocampus) receptors play an important role in the ethanol induced recognition memory impairment induced by ethanol <b>withdrawal</b>.
+GRM5	drug	alcohol	29225043	We identified that <b>ethanol</b> exposure decreases <strong>mGluR5</strong> (metabotropic glutamate receptor 5) expression in the NAc of Ng /  mice and pharmacological inhibition of <strong>mGluR5</strong> reverses NMDAR desensitization in Ng /  mice.
+GRM5	drug	alcohol	29225043	Together these findings specifically suggest that accumbal Ng plays an essential role in the counterbalance between NMDAR and <strong>mGluR5</strong> signaling; which alters NMDAR resistance, and thereby altering aversive motivation for <b>ethanol</b> and may ultimately contribute to susceptibility for <b>alcohol</b> addiction.
+GRM5	addiction	addiction	29225043	Together these findings specifically suggest that accumbal Ng plays an essential role in the counterbalance between NMDAR and <strong>mGluR5</strong> signaling; which alters NMDAR resistance, and thereby altering aversive motivation for ethanol and may ultimately contribute to susceptibility for alcohol <b>addiction</b>.
+GRM5	addiction	aversion	29225043	Together these findings specifically suggest that accumbal Ng plays an essential role in the counterbalance between NMDAR and <strong>mGluR5</strong> signaling; which alters NMDAR resistance, and thereby altering <b>aversive</b> motivation for ethanol and may ultimately contribute to susceptibility for alcohol addiction.
+GRM5	drug	cannabinoid	29143330	This LTD was presynaptic and depended on postsynaptic metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) and retrograde <b>endocannabinoid</b> signalling.
+GRM5	drug	psychedelics	29100629	Unlike the rapidly acting glutamatergic agent <b>ketamine</b>, <strong>mGluR5</strong> specific modulation has not yet shown antidepressant efficacy in MDD and bipolar disorder.
+GRM5	drug	psychedelics	29100629	Although we recently showed that <b>ketamine</b> may work, in part, through significant <strong>mGluR5</strong> modulation, the specific role of <strong>mGluR5</strong> downregulation in <b>ketamine</b>'s antidepressant response is unclear.
+GRM5	addiction	addiction	29100629	There has been relatively little study of posttraumatic stress disorder or obsessive <b>compulsive</b> disorder to date, although there is evidence for the upregulation of <strong>mGluR5</strong> in these disorders.
+GRM5	drug	alcohol	29030082	ADX 47273, a <strong>mGlu5</strong> receptor positive allosteric modulator, attenuates deficits in cognitive flexibility induced by withdrawal from 'binge like' <b>ethanol</b> exposure in rats.
+GRM5	addiction	intoxication	29030082	ADX 47273, a <strong>mGlu5</strong> receptor positive allosteric modulator, attenuates deficits in cognitive flexibility induced by withdrawal from '<b>binge</b> like' ethanol exposure in rats.
+GRM5	addiction	withdrawal	29030082	ADX 47273, a <strong>mGlu5</strong> receptor positive allosteric modulator, attenuates deficits in cognitive flexibility induced by <b>withdrawal</b> from 'binge like' ethanol exposure in rats.
+GRM5	drug	alcohol	29030082	We examined whether (S) (4 fluorophenyl)(3 (3 (4 fluorophenyl) 1,2,4 oxadiazol 5 yl) piperidin 1 yl (ADX 47273), a positive allosteric modulator (PAM) of <strong>mGlu5</strong> receptor, attenuates deficits in reversal learning induced by withdrawal (11 13days) from 'binge like' <b>ethanol</b> input (5.0g/kg, i.g.
+GRM5	addiction	intoxication	29030082	We examined whether (S) (4 fluorophenyl)(3 (3 (4 fluorophenyl) 1,2,4 oxadiazol 5 yl) piperidin 1 yl (ADX 47273), a positive allosteric modulator (PAM) of <strong>mGlu5</strong> receptor, attenuates deficits in reversal learning induced by withdrawal (11 13days) from '<b>binge</b> like' ethanol input (5.0g/kg, i.g.
+GRM5	addiction	withdrawal	29030082	We examined whether (S) (4 fluorophenyl)(3 (3 (4 fluorophenyl) 1,2,4 oxadiazol 5 yl) piperidin 1 yl (ADX 47273), a positive allosteric modulator (PAM) of <strong>mGlu5</strong> receptor, attenuates deficits in reversal learning induced by <b>withdrawal</b> (11 13days) from 'binge like' ethanol input (5.0g/kg, i.g.
+GRM5	drug	alcohol	29030082	In conclusion, positive allosteric modulation of <strong>mGlu5</strong> receptors recovered spatial reversal learning impairment induced by withdrawal from 'binge like' <b>ethanol</b> exposure.
+GRM5	addiction	intoxication	29030082	In conclusion, positive allosteric modulation of <strong>mGlu5</strong> receptors recovered spatial reversal learning impairment induced by withdrawal from '<b>binge</b> like' ethanol exposure.
+GRM5	addiction	withdrawal	29030082	In conclusion, positive allosteric modulation of <strong>mGlu5</strong> receptors recovered spatial reversal learning impairment induced by <b>withdrawal</b> from 'binge like' ethanol exposure.
+GRM5	drug	alcohol	29030082	Thus, our results emphasize the role of <strong>mGlu5</strong> receptor PAM in the adaptive learning impaired by <b>ethanol</b> exposure.
+GRM5	drug	alcohol	28884874	Converging preclinical evidence links extrastriatal dopamine release and glutamatergic transmission via the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) to the rewarding properties of <b>alcohol</b>.
+GRM5	drug	alcohol	28884874	Mesocorticolimbic dopamine release upon intravenous <b>alcohol</b> administration and <strong>mGluR5</strong> availability were measured in 11 moderate social drinkers by single session [18 F]fallypride and [18 F]FPEB positron emission tomography, respectively.
+GRM5	drug	alcohol	28884874	In contrast, baseline <strong>mGluR5</strong> availability was positively correlated with the 'high' effect of <b>alcohol</b> in dorsolateral, ventrolateral and ventromedial PFCs and in the medial temporal lobe, thalamus and caudate nucleus (P < 0.05).
+GRM5	drug	alcohol	28884874	Specifically, prefrontal dopamine release may encode <b>alcohol</b> 'liking' and 'wanting' effects in specific areas underlying value processing and motivation, whereas <strong>mGluR5</strong> availability in distinct prefrontal temporal subcortical regions is more related to the <b>alcohol</b> 'high' effect.
+GRM5	drug	alcohol	28884167	As the role for <strong>mGlu5</strong> in anxiety is well established, we hypothesized that the reduced immobility exhibited by <b>alcohol</b> withdrawn mice when tested in the FST might reflect anxiety, possibly a hyper reactivity to the acute swim stressor.
+GRM5	addiction	withdrawal	28884167	We also determined the functional relevance of the <b>withdrawal</b> induced increase in <strong>mGlu5</strong> expression for FST behavior by comparing the effects of buspirone to a behaviorally effective dose of the <strong>mGlu5</strong> negative allosteric modulator MTEP (3 mg/kg).
+GRM5	drug	alcohol	28884167	These results provide predictive validity for increased swimming/reduced immobility in the FST as a model of anxiety and provide novel evidence in favor of <strong>mGlu5</strong> inhibition as an effective therapeutic strategy for treating hyperanxiety during <b>alcohol</b> withdrawal.
+GRM5	addiction	withdrawal	28884167	These results provide predictive validity for increased swimming/reduced immobility in the FST as a model of anxiety and provide novel evidence in favor of <strong>mGlu5</strong> inhibition as an effective therapeutic strategy for treating hyperanxiety during alcohol <b>withdrawal</b>.
+GRM5	addiction	relapse	28726801	Reinstated drug <b>seeking</b> in animal models of <b>relapse</b> relies on glutamate spillover from cortical terminals synapsing in the nucleus accumbens core (NAcore) to stimulate metabotropic glutamate receptor5 (<strong>mGluR5</strong>) on neuronal nitric oxide synthase (nNOS) interneurons.
+GRM5	addiction	relapse	28726801	Potentiated sucrose <b>reinstatement</b> by mGluR2/3 blockade was reversed by antagonizing <strong>mGluR5</strong>, but reinstated sucrose <b>seeking</b> in the absence of mGluR2/3 blockade was not affected by blocking <strong>mGluR5</strong>.
+GRM5	drug	cocaine	28726801	In <b>cocaine</b> trained rodents <strong>mGluR5</strong> stimulation reinstates drug seeking by activating nNOS, but activating <strong>mGluR5</strong> did not promote reinstated sucrose seeking, nor was potentiated reinstatement after mGluR2/3 blockade reduced by blocking nNOS.
+GRM5	addiction	relapse	28726801	In cocaine trained rodents <strong>mGluR5</strong> stimulation reinstates drug <b>seeking</b> by activating nNOS, but activating <strong>mGluR5</strong> did not promote reinstated sucrose <b>seeking</b>, nor was potentiated <b>reinstatement</b> after mGluR2/3 blockade reduced by blocking nNOS.
+GRM5	drug	cannabinoid	28520841	DSE was mediated by <b>endocannabinoid</b> signaling and modulated by metabotropic glutamate receptor 5 (<strong>mGluR5</strong>).
+GRM5	drug	alcohol	28494749	In the past decade, many studies have highlighted the role of metabotropic glutamate receptor subtype 5 (<strong>mGlu5</strong>) modulators in attenuating <b>alcohol</b> related biological effects such as <b>alcohol</b> consumption, <b>alcohol</b> seeking and relapse like behaviors.
+GRM5	addiction	relapse	28494749	In the past decade, many studies have highlighted the role of metabotropic glutamate receptor subtype 5 (<strong>mGlu5</strong>) modulators in attenuating alcohol related biological effects such as alcohol consumption, alcohol <b>seeking</b> and <b>relapse</b> like behaviors.
+GRM5	drug	alcohol	28494749	In this article, we shall review the following: the effects of acute and chronic <b>alcohol</b> intake on <strong>mGlu5</strong> signaling; the effects of <strong>mGlu5</strong> ligands on <b>alcohol</b> related neurobehavioral changes that are currently being studied both at pre clinical and clinical stages; and the mechanisms underlying the pharmacological effects of these drugs.
+GRM5	drug	alcohol	28320841	Prefrontal Cortex KCa2 Channels Regulate <strong>mGlu5</strong> Dependent Plasticity and Extinction of <b>Alcohol</b> Seeking Behavior.
+GRM5	addiction	relapse	28320841	Prefrontal Cortex KCa2 Channels Regulate <strong>mGlu5</strong> Dependent Plasticity and Extinction of Alcohol <b>Seeking</b> Behavior.
+GRM5	drug	alcohol	28320841	Activation of <strong>mGlu5</strong> receptors in the infralimbic prefrontal cortex (IL PFC) facilitates learning during extinction of cue conditioned <b>alcohol</b> seeking behavior.
+GRM5	addiction	relapse	28320841	Activation of <strong>mGlu5</strong> receptors in the infralimbic prefrontal cortex (IL PFC) facilitates learning during extinction of cue conditioned alcohol <b>seeking</b> behavior.
+GRM5	drug	alcohol	28320841	Positive modulation of IL PFC KCa2 channels significantly attenuated <strong>mGlu5</strong> dependent facilitation of <b>alcohol</b> cue conditioned extinction learning.
+GRM5	drug	nicotine	28243714	Synaptosomal glutamate <strong>mGluR5</strong> and dopamine D4 receptor expression were reduced during chronic <b>nicotine</b> but increased during withdrawal, potentially contributing to cognitive deficits.
+GRM5	addiction	withdrawal	28243714	Synaptosomal glutamate <strong>mGluR5</strong> and dopamine D4 receptor expression were reduced during chronic nicotine but increased during <b>withdrawal</b>, potentially contributing to cognitive deficits.
+GRM5	addiction	relapse	28213190	An optimal dose for <b>relapse</b> prevention may be one that restores extrasynaptic glutamate to physiological levels and predominantly activates mGluR2 and 3, but not <strong>mGluR5</strong> receptors, which are linked to <b>relapse</b>.
+GRM5	drug	cocaine	28123012	We used a rodent self administration/reinstatement model of relapse to show that cue induced t SP and reinstated <b>cocaine</b> seeking result from glutamate spillover, initiating a metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) dependent increase in nitric oxide (NO) production.
+GRM5	addiction	relapse	28123012	We used a rodent self administration/<b>reinstatement</b> model of <b>relapse</b> to show that cue induced t SP and reinstated cocaine <b>seeking</b> result from glutamate spillover, initiating a metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) dependent increase in nitric oxide (NO) production.
+GRM5	addiction	relapse	28123012	Pharmacological stimulation of <strong>mGluR5</strong> in NAcore recapitulated cue induced <b>reinstatement</b> in the absence of drug associated cues.
+GRM5	addiction	relapse	28123012	Using a transgene strategy to express and stimulate designer receptors that mimicked <strong>mGluR5</strong> signaling through Gq in nNOS interneurons, we recapitulated cue induced <b>reinstatement</b> in the absence of cues.
+GRM5	drug	cocaine	28123012	Manipulating the interaction between <strong>mGluR5</strong>, NO production, or MMP 2 and MMP 9 pharmacologically or genetically is sufficient to recapitulate transient synaptic potentiation and reinstate <b>cocaine</b> seeking.
+GRM5	addiction	relapse	28123012	Manipulating the interaction between <strong>mGluR5</strong>, NO production, or MMP 2 and MMP 9 pharmacologically or genetically is sufficient to recapitulate transient synaptic potentiation and reinstate cocaine <b>seeking</b>.
+GRM5	drug	cocaine	27871824	<b>Cocaine</b> self administration, extinction training and drug induced relapse change metabotropic glutamate <strong>mGlu5</strong> receptors expression: Evidence from radioligand binding and immunohistochemistry assays.
+GRM5	addiction	relapse	27871824	Cocaine self administration, extinction training and drug induced <b>relapse</b> change metabotropic glutamate <strong>mGlu5</strong> receptors expression: Evidence from radioligand binding and immunohistochemistry assays.
+GRM5	drug	cocaine	27871824	Several behavioral findings highlight the importance of glutamatergic transmission and its metabotropic receptor type 5 (<strong>mGlu5</strong>) in the controlling of <b>cocaine</b> reward and seeking behaviors.
+GRM5	addiction	relapse	27871824	Several behavioral findings highlight the importance of glutamatergic transmission and its metabotropic receptor type 5 (<strong>mGlu5</strong>) in the controlling of cocaine reward and <b>seeking</b> behaviors.
+GRM5	addiction	reward	27871824	Several behavioral findings highlight the importance of glutamatergic transmission and its metabotropic receptor type 5 (<strong>mGlu5</strong>) in the controlling of cocaine <b>reward</b> and seeking behaviors.
+GRM5	drug	cocaine	27871824	The molecular or neurochemical nature of such interactions is not well recognized, so in the present paper we determine if <b>cocaine</b> self administration and extinction/reinstatement models with the yoked triad control procedure alter <strong>mGlu5</strong> receptor density in rats.
+GRM5	addiction	relapse	27871824	The molecular or neurochemical nature of such interactions is not well recognized, so in the present paper we determine if cocaine self administration and extinction/<b>reinstatement</b> models with the yoked triad control procedure alter <strong>mGlu5</strong> receptor density in rats.
+GRM5	drug	cocaine	27871824	<b>Cocaine</b> self administration and yoked <b>cocaine</b> delivery evoked a significant elevation in <strong>mGlu5</strong> receptors' density in the dorsal striatum, while receptor protein expression was importantly elevated in the substantia nigra and reduced in the nucleus accumbens shell.
+GRM5	drug	cocaine	27871824	<b>Cocaine</b> administration followed by 10 extinction training sessions resulted in biphasic <strong>mGlu5</strong> receptor density changes in the prefrontal cortex nucleus accumbens pathway.
+GRM5	drug	cocaine	27871824	<strong>mGlu5</strong> receptors' up regulation was noted for <b>cocaine</b> self administration and extinction training in the hippocampus and in yoked <b>cocaine</b> controls following drug abstinence in the dorsal striatum.
+GRM5	drug	cocaine	27871824	A <b>cocaine</b> priming dose (but not a saline priming) resulted in a significant decrease of <strong>mGlu5</strong> receptors' density in the nucleus accumbens of rats previously treated with the drug and in the hippocampus of rats previously self administered <b>cocaine</b>.
+GRM5	drug	cocaine	27871824	The latter decrease in <strong>mGlu5</strong> receptors' density and protein expression in the hippocampus was parallel to an increase in [³H]MPEP affinity and opposite to a rise observed after single <b>cocaine</b> administration (ip) to drug naïve yoked saline controls.
+GRM5	drug	nicotine	27847973	The purpose of this paper is to review the evidence from preclinical and clinical studies that drugs that antagonise the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) in the brain are likely to be efficacious as treatments for <b>tobacco</b> dependence.
+GRM5	addiction	dependence	27847973	The purpose of this paper is to review the evidence from preclinical and clinical studies that drugs that antagonise the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) in the brain are likely to be efficacious as treatments for tobacco <b>dependence</b>.
+GRM5	drug	nicotine	27847973	Preclinical results demonstrate that negative allosteric modulators (NAMs) at <strong>mGluR5</strong> attenuate both <b>nicotine</b> self administration and the reinstatement of responding evoked by exposure to conditioned cues paired with <b>nicotine</b> delivery.
+GRM5	addiction	relapse	27847973	Preclinical results demonstrate that negative allosteric modulators (NAMs) at <strong>mGluR5</strong> attenuate both nicotine self administration and the <b>reinstatement</b> of responding evoked by exposure to conditioned cues paired with nicotine delivery.
+GRM5	drug	nicotine	27847973	Although <strong>mGluR5</strong> NAMs attenuate most of the key facets of <b>nicotine</b> dependence, they potentiate the symptoms of <b>nicotine</b> withdrawal.
+GRM5	addiction	dependence	27847973	Although <strong>mGluR5</strong> NAMs attenuate most of the key facets of nicotine <b>dependence</b>, they potentiate the symptoms of nicotine withdrawal.
+GRM5	addiction	withdrawal	27847973	Although <strong>mGluR5</strong> NAMs attenuate most of the key facets of nicotine dependence, they potentiate the symptoms of nicotine <b>withdrawal</b>.
+GRM5	drug	nicotine	27847228	In both groups, <b>smoking</b> was associated with marked global reductions in <strong>mGluR5</strong> availability (on average 23.8%).
+GRM5	drug	nicotine	27847228	Low <strong>mGluR5</strong> DVR in <b>smokers</b> my represent a risk factor for schizophrenia.
+GRM5	drug	nicotine	27847228	Alternatively, <b>smoking</b> may counteract the potential upregulation of <strong>mGluR5</strong> by antipsychotic drugs.
+GRM5	drug	cocaine	27822496	Estradiol Facilitation of <b>Cocaine</b> Self Administration in Female Rats Requires Activation of <strong>mGluR5</strong>.
+GRM5	drug	cocaine	27822496	Hence, we sought to determine whether <strong>mGluR5</strong> activation was essential for estradiol mediated enhancement of <b>cocaine</b> self administration.
+GRM5	drug	cocaine	27822496	In a separate experiment, potentiation of <strong>mGluR5</strong> function with the positive allosteric modulator 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl)benzamide (in the absence of estradiol treatment) failed to increase <b>cocaine</b> self administration.
+GRM5	drug	cocaine	27822496	These data suggest that <strong>mGluR5</strong> activation is necessary for estradiol mediated enhancement of responses to <b>cocaine</b>, but that direct <strong>mGluR5</strong> activation is insufficient to mimic the female response to estradiol.
+GRM5	addiction	addiction	27822496	Building on previous studies in male animals, these findings further highlight the therapeutic potential of <strong>mGluR5</strong> antagonism in the treatment of <b>addiction</b> and suggest that there may be added therapeutic benefit in females.
+GRM5	drug	alcohol	27725153	Deficits in the extinction of <b>ethanol</b> seeking behavior following chronic intermittent <b>ethanol</b> exposure are attenuated with positive allosteric modulation of <strong>mGlu5</strong>.
+GRM5	addiction	relapse	27725153	Deficits in the extinction of ethanol <b>seeking</b> behavior following chronic intermittent ethanol exposure are attenuated with positive allosteric modulation of <strong>mGlu5</strong>.
+GRM5	drug	alcohol	27725153	However, positive allosteric modulation of <strong>mGlu5</strong> with CDPPB enhances the extinction learning of <b>alcohol</b> seeking behavior.
+GRM5	addiction	relapse	27725153	However, positive allosteric modulation of <strong>mGlu5</strong> with CDPPB enhances the extinction learning of alcohol <b>seeking</b> behavior.
+GRM5	drug	alcohol	27725153	The ability to attenuate deficits through modulation of <strong>mGlu5</strong> provides a potential target for pharmacological manipulation that could ultimately reduce relapse in <b>alcoholics</b>.
+GRM5	addiction	relapse	27725153	The ability to attenuate deficits through modulation of <strong>mGlu5</strong> provides a potential target for pharmacological manipulation that could ultimately reduce <b>relapse</b> in alcoholics.
+GRM5	drug	cocaine	27744406	Long Lasting Impairment of <strong>mGluR5</strong> Activated Intracellular Pathways in the Striatum After Withdrawal of <b>Cocaine</b> Self Administration.
+GRM5	addiction	withdrawal	27744406	Long Lasting Impairment of <strong>mGluR5</strong> Activated Intracellular Pathways in the Striatum After <b>Withdrawal</b> of Cocaine Self Administration.
+GRM5	drug	amphetamine	26946431	<strong>mGluR5</strong> activation in the nucleus accumbens is not essential for sexual behavior or cross sensitization of <b>amphetamine</b> responses by sexual experience.
+GRM5	addiction	sensitization	26946431	<strong>mGluR5</strong> activation in the nucleus accumbens is not essential for sexual behavior or cross <b>sensitization</b> of amphetamine responses by sexual experience.
+GRM5	addiction	reward	26946431	Cross sensitization of locomotion or <b>CPP</b> was not prevented by NAc <strong>mGluR5</strong> antagonism during acquisition of sexual experience.
+GRM5	addiction	sensitization	26946431	Cross <b>sensitization</b> of locomotion or CPP was not prevented by NAc <strong>mGluR5</strong> antagonism during acquisition of sexual experience.
+GRM5	drug	amphetamine	26946431	Instead, sexually naive animals that received NAc <strong>mGluR5</strong> antagonists without mating demonstrated sensitized <b>amph</b> induced locomotor responses and enhanced CPP on par with sexually experienced males.
+GRM5	addiction	reward	26946431	Instead, sexually naive animals that received NAc <strong>mGluR5</strong> antagonists without mating demonstrated sensitized amph induced locomotor responses and enhanced <b>CPP</b> on par with sexually experienced males.
+GRM5	drug	amphetamine	26946431	Together, these findings suggest that <strong>mGluR5</strong> activation in the NAc is not essential for the expression of mating, but that experience induced reduction in <strong>mGluR5</strong> protein may contribute to the cross sensitization of <b>amph</b> responses by sexual experience and abstinence.
+GRM5	addiction	sensitization	26946431	Together, these findings suggest that <strong>mGluR5</strong> activation in the NAc is not essential for the expression of mating, but that experience induced reduction in <strong>mGluR5</strong> protein may contribute to the cross <b>sensitization</b> of amph responses by sexual experience and abstinence.
+GRM5	drug	cocaine	26881139	<strong>mGlu5</strong> Receptors and Relapse to <b>Cocaine</b> Seeking: The Role of Receptor Trafficking in Postrelapse Extinction Learning Deficits.
+GRM5	addiction	relapse	26881139	<strong>mGlu5</strong> Receptors and <b>Relapse</b> to Cocaine <b>Seeking</b>: The Role of Receptor Trafficking in Postrelapse Extinction Learning Deficits.
+GRM5	drug	cocaine	26881139	We have previously demonstrated that MTEP, an allosteric antagonist of <strong>mGlu5</strong>, infused into the nucleus accumbens attenuates relapse after abstinence from <b>cocaine</b> self administration.
+GRM5	addiction	relapse	26881139	We have previously demonstrated that MTEP, an allosteric antagonist of <strong>mGlu5</strong>, infused into the nucleus accumbens attenuates <b>relapse</b> after abstinence from cocaine self administration.
+GRM5	drug	cocaine	26881139	Surface biotinylation analysis of protein expression in the dlSTR revealed that, in <b>cocaine</b> animals, intra dlSTR MTEP administration decreased <strong>mGlu5</strong> surface expression and prevented changes in Arc and GluA1/GluA2 observed in their vehicle counterparts.
+GRM5	addiction	relapse	26881139	Thus, blockade of <strong>mGlu5</strong> receptors may be utilized in future treatment strategies for <b>relapse</b> prevention in humans, although the effects of chronic blockade on extinction learning should be further evaluated.
+GRM5	drug	opioid	26861145	Emotional Impairment and Persistent Upregulation of <strong>mGlu5</strong> Receptor following <b>Morphine</b> Abstinence: Implications of an <strong>mGlu5</strong> MOPr Interaction.
+GRM5	addiction	addiction	26802568	Abundant evidence at the anatomical, electrophysiological, and molecular levels implicates metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>) in <b>addiction</b>.
+GRM5	addiction	addiction	26802568	Consistently, the effects of a wide range of doses of different <strong>mGluR5</strong> negative allosteric modulators (NAMs) have been tested in various animal models of <b>addiction</b>.
+GRM5	drug	alcohol	26802568	The review focused on the effects of systemic (i.p., i.v., s.c.) administration of the <strong>mGluR5</strong> NAMs 3 ((2 Methyl 4 thiazolyl)ethynyl)pyridine (MTEP) and 2 Methyl 6 (phenylethynyl)pyridine (MPEP) on paradigms with cocaine, <b>ethanol</b>, nicotine, and food in rats.
+GRM5	drug	cocaine	26802568	The review focused on the effects of systemic (i.p., i.v., s.c.) administration of the <strong>mGluR5</strong> NAMs 3 ((2 Methyl 4 thiazolyl)ethynyl)pyridine (MTEP) and 2 Methyl 6 (phenylethynyl)pyridine (MPEP) on paradigms with <b>cocaine</b>, ethanol, nicotine, and food in rats.
+GRM5	drug	nicotine	26802568	The review focused on the effects of systemic (i.p., i.v., s.c.) administration of the <strong>mGluR5</strong> NAMs 3 ((2 Methyl 4 thiazolyl)ethynyl)pyridine (MTEP) and 2 Methyl 6 (phenylethynyl)pyridine (MPEP) on paradigms with cocaine, ethanol, <b>nicotine</b>, and food in rats.
+GRM5	addiction	addiction	26802568	Altogether, this review suggests a therapeutic window for <strong>mGluR5</strong> NAMs that can be translated to the treatment of substance related and <b>addictive</b> disorders.
+GRM5	drug	cocaine	26784278	Antagonism of the metabotropic glutamate 5 (<strong>mGlu5</strong>) receptor has emerged as a potential treatment, by reducing the reinforcing properties of <b>cocaine</b>.
+GRM5	addiction	reward	26784278	Antagonism of the metabotropic glutamate 5 (<strong>mGlu5</strong>) receptor has emerged as a potential treatment, by reducing the <b>reinforcing</b> properties of cocaine.
+GRM5	drug	cocaine	26784278	These results suggest that <strong>mGlu5</strong> receptor activity is both necessary and sufficient for efficient extinction of a <b>cocaine</b> associated CS.
+GRM5	drug	alcohol	26773198	Binge <b>alcohol</b> intake decreased <strong>mGlu5</strong> levels in females, whereas it decreased indices of phosphoinositide 3 kinase (PI3K), mammalian target of rapamycin (mTOR), 4E binding protein 1, and p70 ribosomal protein S6 kinase in males.
+GRM5	addiction	intoxication	26773198	<b>Binge</b> alcohol intake decreased <strong>mGlu5</strong> levels in females, whereas it decreased indices of phosphoinositide 3 kinase (PI3K), mammalian target of rapamycin (mTOR), 4E binding protein 1, and p70 ribosomal protein S6 kinase in males.
+GRM5	drug	alcohol	26773198	Expression of genes encoding mGlu1, <strong>mGlu5</strong>, the NR2A subunit of the NMDA receptor, and Homer2 were all decreased by binge <b>alcohol</b> consumption in males, while females were relatively resistant (only phosphoinositide dependent protein kinase 1 was decreased).
+GRM5	addiction	intoxication	26773198	Expression of genes encoding mGlu1, <strong>mGlu5</strong>, the NR2A subunit of the NMDA receptor, and Homer2 were all decreased by <b>binge</b> alcohol consumption in males, while females were relatively resistant (only phosphoinositide dependent protein kinase 1 was decreased).
+GRM5	addiction	relapse	26748780	In addition, we found that extinction with metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) activation had similar results to EE: reduced <b>relapse</b> after extinction, decreased synaptic AMPA receptors AMPARs and the AMPA/NMDA ratio.
+GRM5	drug	amphetamine	26748780	These data indicate that EE training elicited inhibition of <b>METH</b> primed reinstatement is mediated by the <strong>mGluR5</strong>.
+GRM5	addiction	relapse	26748780	These data indicate that EE training elicited inhibition of METH primed <b>reinstatement</b> is mediated by the <strong>mGluR5</strong>.
+GRM5	addiction	relapse	26748780	In addition, we found that extinction with the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) activation had similar results to EE: reduced <b>relapse</b> after extinction, decreased synaptic AMPARs and the AMPA/NMDA ratio.
+GRM5	drug	amphetamine	26748780	These data indicate that EE training elicited inhibition of <b>METH</b> primed reinstatement is mediated by <strong>mGluR5</strong> (PAM: positive allosteric modulator).
+GRM5	addiction	relapse	26748780	These data indicate that EE training elicited inhibition of METH primed <b>reinstatement</b> is mediated by <strong>mGluR5</strong> (PAM: positive allosteric modulator).
+GRM5	drug	alcohol	26626323	Metabotropic glutamate receptor subtype 5 (<strong>mGlu5</strong>) and protein kinase C (PKC) epsilon have been reported to mediate acute and chronic effects of <b>ethanol</b>.
+GRM5	drug	alcohol	26626323	This study explores the changes in <strong>mGlu5</strong> and PKC epsilon in the amygdala following acute administration of <b>ethanol</b> during <b>ethanol</b> withdrawal (EW) induced anxiety.
+GRM5	addiction	withdrawal	26626323	This study explores the changes in <strong>mGlu5</strong> and PKC epsilon in the amygdala following acute administration of ethanol during ethanol <b>withdrawal</b> (EW) induced anxiety.
+GRM5	drug	alcohol	26626323	Acute administration of <b>ethanol</b> significantly attenuated EW induced anxiety as well as an EW induced increase in <strong>GRM5</strong>.
+GRM5	drug	alcohol	26521964	The <strong>mGluR5</strong> antagonist MPEP suppresses the expression and reinstatement, but not the acquisition, of the <b>ethanol</b> conditioned place preference in mice.
+GRM5	addiction	relapse	26521964	The <strong>mGluR5</strong> antagonist MPEP suppresses the expression and <b>reinstatement</b>, but not the acquisition, of the ethanol conditioned place preference in mice.
+GRM5	drug	alcohol	26521964	In the present study, we evaluated the effects of 2 methyl 6 (phenylethynyl) pyridine (MPEP), a selective antagonist of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) on the acquisition, expression and reinstatement of <b>ethanol</b> conditioned place preference (CPP).
+GRM5	addiction	relapse	26521964	In the present study, we evaluated the effects of 2 methyl 6 (phenylethynyl) pyridine (MPEP), a selective antagonist of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) on the acquisition, expression and <b>reinstatement</b> of ethanol conditioned place preference (CPP).
+GRM5	addiction	reward	26521964	In the present study, we evaluated the effects of 2 methyl 6 (phenylethynyl) pyridine (MPEP), a selective antagonist of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) on the acquisition, expression and reinstatement of ethanol conditioned place preference (<b>CPP</b>).
+GRM5	drug	alcohol	26521964	The <strong>mGluR5</strong> antagonist MPEP significantly reduced the expression and the reinstatement in dose dependent manner, but not acquisition of <b>ethanol</b> induced CPP.
+GRM5	addiction	relapse	26521964	The <strong>mGluR5</strong> antagonist MPEP significantly reduced the expression and the <b>reinstatement</b> in dose dependent manner, but not acquisition of ethanol induced CPP.
+GRM5	addiction	reward	26521964	The <strong>mGluR5</strong> antagonist MPEP significantly reduced the expression and the reinstatement in dose dependent manner, but not acquisition of ethanol induced <b>CPP</b>.
+GRM5	drug	alcohol	26521964	These results indicate that <strong>mGluR5</strong> may be involved in the expression and reinstatement of conditioned rewarding effects of <b>ethanol</b>, but not the acquisition of <b>ethanol</b>, which provide an evidence that <strong>mGluR5</strong> blockade might make dissociable contributions during the training (acquisition phase), the performance of behavior (expression phase) and reinstatement.
+GRM5	addiction	relapse	26521964	These results indicate that <strong>mGluR5</strong> may be involved in the expression and <b>reinstatement</b> of conditioned rewarding effects of ethanol, but not the acquisition of ethanol, which provide an evidence that <strong>mGluR5</strong> blockade might make dissociable contributions during the training (acquisition phase), the performance of behavior (expression phase) and <b>reinstatement</b>.
+GRM5	drug	alcohol	26442908	Group 1 mGlu family proteins (i.e., mGlu) consist of mGlu1 and <strong>mGlu5</strong> and their activity may influence voluntary <b>ethanol</b> intake.
+GRM5	addiction	withdrawal	26442908	Rat hippocampal explants were exposed to CIE with or without the addition of mGlu1 antagonist (7 hydroxyimino)cyclopropa[b]chromen 1a carboxylate ethyl ester (CPCCOEt; 0.5, 1, and 3μM) or <strong>mGlu5</strong> antagonist (E) 2 methyl 6 styryl pyridine (SIB 1893; 20, 100, and 200μM) to assess sparing of <b>withdrawal</b> induced cytotoxicity.
+GRM5	drug	amphetamine	26365953	Perirhinal Cortex <strong>mGlu5</strong> Receptor Activation Reduces Relapse to <b>Methamphetamine</b> Seeking by Restoring Novelty Salience.
+GRM5	addiction	relapse	26365953	Perirhinal Cortex <strong>mGlu5</strong> Receptor Activation Reduces <b>Relapse</b> to Methamphetamine <b>Seeking</b> by Restoring Novelty Salience.
+GRM5	drug	amphetamine	26365953	The perirhinal cortex is critical for novelty detection, and perirhinal metabotropic glutamate 5 receptors (<strong>mGlu5</strong>) are downregulated after long access <b>meth</b>.
+GRM5	drug	amphetamine	26365953	Perirhinal <strong>mGlu5</strong> are thus a promising pharmacological target for the restoration of cognitive function in <b>meth</b> addicts.
+GRM5	addiction	addiction	26315507	To understand potential therapeutic vs adverse effects in preclinical behavioral assays, we examined the partial <strong>mGlu5</strong> NAMs, M 5MPEP and Br 5MPEPy, in comparison with the full <strong>mGlu5</strong> NAM MTEP across models of <b>addiction</b> and psychotomimetic like activity.
+GRM5	drug	alcohol	26271115	Based on the proposed GET73 mechanism of action, the effects of <strong>mGlu5</strong> receptor negative allosteric modulator, 2 methyl 6 (phenylethynyl) pyridine (MPEP), on <b>ethanol</b> induced reduction of cell viability were also assessed.
+GRM5	drug	amphetamine	26211759	After reaching stable responding for <b>amphetamine</b> (0.03 or 0.1 mg/kg/infusion), rats were injected with five doses (0, 0.3, 1.0, 3.0, and 5.0 mg/kg) of the <strong>mGluR5</strong> antagonist, 3 ((2 methyl 1,3 thiazol 4 yl)ethynyl) pyridine hydrochloride (MTEP), 30 min before self administration sessions.
+GRM5	drug	alcohol	26101849	Importantly, the association between several genetic variants within the mGluR eEF2 AMPAR pathway and <b>alcohol</b> use behavior (i.e., consumption and <b>alcohol</b> related problems) replicated in the Grady Trauma Project (GTP), an independent sample of adults living in Atlanta, Georgia (n = 1034; 95% African American), including individual variants in GRM1, <strong>GRM5</strong>, EEF2, MTOR, GRIA1, GRIA4 and HOMER2 (P < 0.05).
+GRM5	drug	amphetamine	25975203	A critical role of striatal A2A R <strong>mGlu5</strong> R interactions in modulating the psychomotor and drug seeking effects of <b>methamphetamine</b>.
+GRM5	addiction	relapse	25975203	A critical role of striatal A2A R <strong>mGlu5</strong> R interactions in modulating the psychomotor and drug <b>seeking</b> effects of methamphetamine.
+GRM5	drug	alcohol	25975203	Adenosine A2A receptors (A2A R) co localize with metabotropic glutamate 5 receptors (<strong>mGlu5</strong> R) in the striatum and functionally interact to modulate behaviours induced by addictive substances, such as <b>alcohol</b>.
+GRM5	addiction	addiction	25975203	Adenosine A2A receptors (A2A R) co localize with metabotropic glutamate 5 receptors (<strong>mGlu5</strong> R) in the striatum and functionally interact to modulate behaviours induced by <b>addictive</b> substances, such as alcohol.
+GRM5	drug	amphetamine	25975203	Using genetic and pharmacological antagonism of A2A R in mice, we investigated whether A2A R <strong>mGlu5</strong> R interaction can regulate the locomotor, stereotypic and drug seeking effect of <b>methamphetamine</b> and cocaine, two drugs that exhibit distinct mechanism of action.
+GRM5	drug	cocaine	25975203	Using genetic and pharmacological antagonism of A2A R in mice, we investigated whether A2A R <strong>mGlu5</strong> R interaction can regulate the locomotor, stereotypic and drug seeking effect of methamphetamine and <b>cocaine</b>, two drugs that exhibit distinct mechanism of action.
+GRM5	addiction	relapse	25975203	Using genetic and pharmacological antagonism of A2A R in mice, we investigated whether A2A R <strong>mGlu5</strong> R interaction can regulate the locomotor, stereotypic and drug <b>seeking</b> effect of methamphetamine and cocaine, two drugs that exhibit distinct mechanism of action.
+GRM5	addiction	addiction	25975203	Moreover, <strong>mGlu5</strong> R binding was reduced in the nucleus accumbens core of A2A R knockout (KO) mice supporting an interaction between these receptors in a brain region crucial in mediating <b>addiction</b> processes.
+GRM5	drug	amphetamine	25975203	Chronic <b>methamphetamine</b>, but not cocaine administration, resulted in a significant increase in striatal <strong>mGlu5</strong> R binding in wild type mice, which was absent in the A2A R KO mice.
+GRM5	drug	cocaine	25975203	Chronic methamphetamine, but not <b>cocaine</b> administration, resulted in a significant increase in striatal <strong>mGlu5</strong> R binding in wild type mice, which was absent in the A2A R KO mice.
+GRM5	drug	amphetamine	25975203	These data are in support of a critical role of striatal A2A R <strong>mGlu5</strong> R functional interaction in mediating the ambulatory, stereotypic and reinforcing effects of <b>methamphetamine</b> but not cocaine induced hyperlocomotion or stereotypy.
+GRM5	drug	cocaine	25975203	These data are in support of a critical role of striatal A2A R <strong>mGlu5</strong> R functional interaction in mediating the ambulatory, stereotypic and reinforcing effects of methamphetamine but not <b>cocaine</b> induced hyperlocomotion or stereotypy.
+GRM5	addiction	reward	25975203	These data are in support of a critical role of striatal A2A R <strong>mGlu5</strong> R functional interaction in mediating the ambulatory, stereotypic and <b>reinforcing</b> effects of methamphetamine but not cocaine induced hyperlocomotion or stereotypy.
+GRM5	drug	amphetamine	25975203	The present study highlights a distinct and selective mechanistic role for this receptor interaction in regulating <b>methamphetamine</b> induced behaviours and suggests that combined antagonism of A2A R and <strong>mGlu5</strong> R may represent a novel therapy for <b>methamphetamine</b> addiction.
+GRM5	addiction	addiction	25975203	The present study highlights a distinct and selective mechanistic role for this receptor interaction in regulating methamphetamine induced behaviours and suggests that combined antagonism of A2A R and <strong>mGlu5</strong> R may represent a novel therapy for methamphetamine <b>addiction</b>.
+GRM5	drug	nicotine	25861697	We recently showed marked global reductions in metabotropic glutamate receptor type 5 (<strong>mGluR5</strong>) binding in <b>smokers</b> and recent ex <b>smokers</b> (average abstinence duration of 25 weeks).
+GRM5	drug	nicotine	25861697	The goal of this study was to examine the role of <strong>mGluR5</strong> downregulation in <b>nicotine</b> addiction by investigating a group of long term ex <b>smokers</b> (abstinence >1.5 years), and to explore associations between <strong>mGluR5</strong> binding and relapse in recent ex <b>smokers</b>.
+GRM5	addiction	addiction	25861697	The goal of this study was to examine the role of <strong>mGluR5</strong> downregulation in nicotine <b>addiction</b> by investigating a group of long term ex smokers (abstinence >1.5 years), and to explore associations between <strong>mGluR5</strong> binding and relapse in recent ex smokers.
+GRM5	addiction	relapse	25861697	The goal of this study was to examine the role of <strong>mGluR5</strong> downregulation in nicotine addiction by investigating a group of long term ex smokers (abstinence >1.5 years), and to explore associations between <strong>mGluR5</strong> binding and <b>relapse</b> in recent ex smokers.
+GRM5	drug	nicotine	25861697	Images of <strong>mGluR5</strong> receptor binding were acquired in 14 long term ex <b>smokers</b>, using positron emission tomography with radiolabeled [11C]ABP688, which binds to an allosteric site with high specificity.
+GRM5	drug	nicotine	25861697	Long term ex <b>smokers</b> and individuals who had never smoked showed no differences in <strong>mGluR5</strong> binding in any of the brain regions examined.
+GRM5	drug	nicotine	25861697	Long term ex <b>smokers</b> showed significantly higher <strong>mGluR5</strong> binding than recent ex <b>smokers</b>, most prominently in the frontal cortex (42%) and thalamus (57%).
+GRM5	drug	nicotine	25861697	Our findings suggest that downregulation of <strong>mGluR5</strong> is a pathogenetic mechanism underlying <b>nicotine</b> dependence and the high relapse rate in individuals previously exposed to <b>nicotine</b>.
+GRM5	addiction	dependence	25861697	Our findings suggest that downregulation of <strong>mGluR5</strong> is a pathogenetic mechanism underlying nicotine <b>dependence</b> and the high relapse rate in individuals previously exposed to nicotine.
+GRM5	addiction	relapse	25861697	Our findings suggest that downregulation of <strong>mGluR5</strong> is a pathogenetic mechanism underlying nicotine dependence and the high <b>relapse</b> rate in individuals previously exposed to nicotine.
+GRM5	drug	nicotine	25861697	Therefore, <strong>mGluR5</strong> receptor binding appears to be an effective biomarker in <b>smoking</b> and a promising target for the discovery of novel medication for <b>nicotine</b> dependence and other substance related disorders.
+GRM5	addiction	dependence	25861697	Therefore, <strong>mGluR5</strong> receptor binding appears to be an effective biomarker in smoking and a promising target for the discovery of novel medication for nicotine <b>dependence</b> and other substance related disorders.
+GRM5	drug	cocaine	25829143	<b>Cocaine</b> Decreases Metabotropic Glutamate Receptor mGluR1 Currents in Dopamine Neurons by Activating <strong>mGluR5</strong>.
+GRM5	drug	cocaine	25829143	A single injection of <b>cocaine</b> decreased the current activated by mGluR1 in dopamine neurons, and it had no effect on the size of the <strong>mGluR5</strong> mediated current.
+GRM5	drug	cocaine	25829143	When the injection of <b>cocaine</b> was preceded by treatment of the animals with a blocker of <strong>mGluR5</strong> receptors (MPEP), <b>cocaine</b> no longer decreased the mGluR1 current.
+GRM5	drug	cocaine	25829143	Thus, the activation of <strong>mGluR5</strong> was required for the <b>cocaine</b> mediated suppression of mGluR1 mediated currents in dopamine neurons.
+GRM5	drug	cocaine	25829143	The results support the hypothesis that <strong>mGluR5</strong> coordinates a reduction in mGluR1 functional activity after <b>cocaine</b> treatment.
+GRM5	drug	opioid	25736529	<strong>mGluR5</strong> in the nucleus accumbens shell regulates <b>morphine</b> associated contextual memory through reactive oxygen species signaling.
+GRM5	drug	opioid	25736529	Here, we found that microinfusion of the <strong>mGluR5</strong> antagonist 3 ((2 Methyl 1,3 thiazol 4 yl)ethynyl)pyridine (MTEP) into the nucleus accumbens (NAc) shell, but not into the core, significantly attenuated the expression of <b>morphine</b> conditioned place preference (CPP) in rats.
+GRM5	addiction	reward	25736529	Here, we found that microinfusion of the <strong>mGluR5</strong> antagonist 3 ((2 Methyl 1,3 thiazol 4 yl)ethynyl)pyridine (MTEP) into the nucleus accumbens (NAc) shell, but not into the core, significantly attenuated the expression of morphine conditioned place preference (<b>CPP</b>) in rats.
+GRM5	drug	opioid	25736529	Following the expression of <b>morphine</b> CPP, the protein level of membrane <strong>mGluR5</strong> was selectively increased in the NAc shell.
+GRM5	addiction	reward	25736529	Following the expression of morphine <b>CPP</b>, the protein level of membrane <strong>mGluR5</strong> was selectively increased in the NAc shell.
+GRM5	drug	opioid	25736529	Thus, results of the present study suggest that <strong>mGluR5</strong> in the NAc shell, but not in the core, is essential for the retrieval of <b>morphine</b> contextual memory, which is mediated at least in part, through the ROS/ERK signaling pathway.
+GRM5	addiction	addiction	25565255	Negative allosteric modulators (NAMs) of metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) have potential for the treatment of psychiatric diseases including depression, fragile X syndrome (FXS), anxiety, obsessive <b>compulsive</b> disorders, and levodopa induced dyskinesia in Parkinson's disease.
+GRM5	drug	cocaine	25539508	However, in <b>cocaine</b> sensitized mice primed with <b>cocaine</b>, this inhibition was reversed and a strong increase was detected in the <strong>mGluR5</strong>, NR2 subunits, and both GluR1 and GluR3.
+GRM5	drug	cocaine	25522112	Differential regulation of <strong>mGlu5</strong> R and ΜOPr by priming  and cue induced reinstatement of <b>cocaine</b> seeking behaviour in mice.
+GRM5	addiction	relapse	25522112	Differential regulation of <strong>mGlu5</strong> R and ΜOPr by priming  and cue induced <b>reinstatement</b> of cocaine <b>seeking</b> behaviour in mice.
+GRM5	drug	cocaine	25522112	Given the evidence implicating the metabotropic glutamate receptor 5 (<strong>mGlu5</strong> R), μ opioid receptor (MOPr), κ opioid receptor (ΚOPr) and oxytocin receptor (OTR) systems in <b>cocaine</b> addiction and relapse, our aim was to assess the modulation of these receptors using a mouse model of cue  and priming induced reinstatement of <b>cocaine</b> seeking.
+GRM5	drug	opioid	25522112	Given the evidence implicating the metabotropic glutamate receptor 5 (<strong>mGlu5</strong> R), μ <b>opioid</b> receptor (MOPr), κ <b>opioid</b> receptor (ΚOPr) and oxytocin receptor (OTR) systems in cocaine addiction and relapse, our aim was to assess the modulation of these receptors using a mouse model of cue  and priming induced reinstatement of cocaine seeking.
+GRM5	addiction	addiction	25522112	Given the evidence implicating the metabotropic glutamate receptor 5 (<strong>mGlu5</strong> R), μ opioid receptor (MOPr), κ opioid receptor (ΚOPr) and oxytocin receptor (OTR) systems in cocaine <b>addiction</b> and relapse, our aim was to assess the modulation of these receptors using a mouse model of cue  and priming induced reinstatement of cocaine seeking.
+GRM5	addiction	relapse	25522112	Given the evidence implicating the metabotropic glutamate receptor 5 (<strong>mGlu5</strong> R), μ opioid receptor (MOPr), κ opioid receptor (ΚOPr) and oxytocin receptor (OTR) systems in cocaine addiction and <b>relapse</b>, our aim was to assess the modulation of these receptors using a mouse model of cue  and priming induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM5	drug	cocaine	25522112	Quantitative autoradiography of <strong>mGlu5</strong> R, MOPr, KOPr and OTR showed a persistent <b>cocaine</b> induced upregulation of the <strong>mGlu5</strong> R and OTR in the lateral septum and central amygdala, respectively.
+GRM5	addiction	relapse	25522112	Further, we showed that priming  but not cue induced <b>reinstatement</b> upregulates <strong>mGlu5</strong> R and MOPr binding in the nucleus accumbens core and basolateral amygdala, respectively, while cue  but not priming induced <b>reinstatement</b> downregulates MOPr binding in caudate putamen and nucleus accumbens core.
+GRM5	drug	cocaine	25408547	Withdrawal from <b>cocaine</b> self administration and yoked <b>cocaine</b> delivery dysregulates glutamatergic <strong>mGlu5</strong> and NMDA receptors in the rat brain.
+GRM5	addiction	withdrawal	25408547	<b>Withdrawal</b> from cocaine self administration and yoked cocaine delivery dysregulates glutamatergic <strong>mGlu5</strong> and NMDA receptors in the rat brain.
+GRM5	drug	opioid	25399651	Blockade of <strong>mGluR5</strong> in the nucleus accumbens shell but not core attenuates <b>heroin</b> seeking behavior in rats.
+GRM5	addiction	relapse	25399651	Blockade of <strong>mGluR5</strong> in the nucleus accumbens shell but not core attenuates heroin <b>seeking</b> behavior in rats.
+GRM5	drug	opioid	25399651	The aim of this study was to determine whether <strong>mGluR5</strong> in the NAc core or shell involved in <b>heroin</b> seeking behavior in rats.
+GRM5	addiction	relapse	25399651	The aim of this study was to determine whether <strong>mGluR5</strong> in the NAc core or shell involved in heroin <b>seeking</b> behavior in rats.
+GRM5	drug	opioid	25399651	The selective <strong>mGluR5</strong> antagonist 2 methyl 6 phenylethynyl pyridine (MPEP, 5, 15 and 50 nmol per side) was then microinjected into the NAc core or shell 10 min before a <b>heroin</b> seeking test induced by context, cues or <b>heroin</b> priming.
+GRM5	addiction	relapse	25399651	The selective <strong>mGluR5</strong> antagonist 2 methyl 6 phenylethynyl pyridine (MPEP, 5, 15 and 50 nmol per side) was then microinjected into the NAc core or shell 10 min before a heroin <b>seeking</b> test induced by context, cues or heroin priming.
+GRM5	drug	opioid	25399651	Blockade of <strong>mGluR5</strong> in NAc shell in rats specifically suppresses the relapse to <b>heroin</b> seeking and anxiety like behavior, suggesting that <strong>mGluR5</strong> antagonists may be a potential candidate for the therapy of <b>heroin</b> addiction.
+GRM5	addiction	addiction	25399651	Blockade of <strong>mGluR5</strong> in NAc shell in rats specifically suppresses the relapse to heroin seeking and anxiety like behavior, suggesting that <strong>mGluR5</strong> antagonists may be a potential candidate for the therapy of heroin <b>addiction</b>.
+GRM5	addiction	relapse	25399651	Blockade of <strong>mGluR5</strong> in NAc shell in rats specifically suppresses the <b>relapse</b> to heroin <b>seeking</b> and anxiety like behavior, suggesting that <strong>mGluR5</strong> antagonists may be a potential candidate for the therapy of heroin addiction.
+GRM5	drug	cocaine	25319571	<b>Cocaine</b> Withdrawal Impairs <strong>mGluR5</strong> Dependent Long Term Depression in Nucleus Accumbens Shell Neurons of Both Direct and Indirect Pathways.
+GRM5	addiction	withdrawal	25319571	Cocaine <b>Withdrawal</b> Impairs <strong>mGluR5</strong> Dependent Long Term Depression in Nucleus Accumbens Shell Neurons of Both Direct and Indirect Pathways.
+GRM5	drug	cocaine	25319571	We previously reported that animals withdrawn from repeated <b>cocaine</b> exposure exhibited a selective deficit in the ability to elicit metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) dependent long term depression (LTD) in the nucleus accumbens (NAc) shell.
+GRM5	drug	cocaine	25319571	Furthermore, systemic administration of <strong>mGluR5</strong> negative allosteric modulator fenobam before the daily injection of <b>cocaine</b> preserved <strong>mGluR5</strong> function and significantly reduced the expression of <b>cocaine</b> induced behavioral sensitization.
+GRM5	addiction	sensitization	25319571	Furthermore, systemic administration of <strong>mGluR5</strong> negative allosteric modulator fenobam before the daily injection of cocaine preserved <strong>mGluR5</strong> function and significantly reduced the expression of cocaine induced behavioral <b>sensitization</b>.
+GRM5	drug	cocaine	25319571	These results reveal that withdrawal from repeated <b>cocaine</b> exposure may result in the impairment of NAc <strong>mGluR5</strong> LTD in a subregion  but not cell type specific manner and suggests that pharmacological antagonism of <strong>mGluR5</strong> may represent a potential strategy for reducing <b>cocaine</b> induced addictive behaviors.
+GRM5	addiction	addiction	25319571	These results reveal that withdrawal from repeated cocaine exposure may result in the impairment of NAc <strong>mGluR5</strong> LTD in a subregion  but not cell type specific manner and suggests that pharmacological antagonism of <strong>mGluR5</strong> may represent a potential strategy for reducing cocaine induced <b>addictive</b> behaviors.
+GRM5	addiction	withdrawal	25319571	These results reveal that <b>withdrawal</b> from repeated cocaine exposure may result in the impairment of NAc <strong>mGluR5</strong> LTD in a subregion  but not cell type specific manner and suggests that pharmacological antagonism of <strong>mGluR5</strong> may represent a potential strategy for reducing cocaine induced addictive behaviors.
+GRM5	drug	opioid	25284131	Microinjection of the <strong>mGluR5</strong> antagonist MTEP into the nucleus accumbens attenuates the acquisition but not expression of <b>morphine</b> induced conditioned place preference in rats.
+GRM5	drug	opioid	25284131	Previous studies suggest that metabotropic glutamate receptor type 5 (<strong>mGluR5</strong>) plays an important role in modulation of the rewarding properties of <b>morphine</b>.
+GRM5	addiction	reward	25284131	Little is known about the role of <strong>mGluR5</strong> in the nucleus accumbens (NAc), as one of the important regions of the <b>reward</b> circuitry.
+GRM5	drug	opioid	25284131	In the present study, we investigated the effects of intra accumbal injection of <strong>mGluR5</strong> antagonist, 3 [(2 methyl 4 thiazolyl) ethynyl] pyridine, MTEP, on the acquisition and expression of <b>morphine</b> induced Conditioned Place Preference (CPP) in the rats.
+GRM5	addiction	reward	25284131	In the present study, we investigated the effects of intra accumbal injection of <strong>mGluR5</strong> antagonist, 3 [(2 methyl 4 thiazolyl) ethynyl] pyridine, MTEP, on the acquisition and expression of morphine induced Conditioned Place Preference (<b>CPP</b>) in the rats.
+GRM5	drug	opioid	25284131	Our findings indicated that blockade of <strong>mGluR5</strong> reduces rewarding properties of <b>morphine</b>.
+GRM5	drug	opioid	25061818	Analgesic conditioned place preference (aCPP) was used to examine the effects of fenobam (30 mg/kg) and the prototypical <strong>mGluR5</strong> antagonist, MPEP, and these effects were compared to those of a drug with known analgesic properties, <b>morphine</b> (10 mg/kg).
+GRM5	drug	opioid	24930812	Implication of <strong>mGlu5</strong> receptor in the enhancement of <b>morphine</b> induced hyperlocomotion under chronic treatment with zolpidem.
+GRM5	drug	opioid	24930812	To confirm that <strong>mGlu5</strong> receptor is directly involved in dopamine related behavior in mice following chronic treatment with zolpidem, we measured <b>morphine</b> induced hyperlocomotion after chronic treatment with zolpidem in the presence or absence of an <strong>mGlu5</strong> receptor antagonist.
+GRM5	drug	opioid	24930812	Although chronic treatment with zolpidem significantly enhanced <b>morphine</b> induced hyperlocomotion, this enhancement of <b>morphine</b> induced hyperlocomotion was suppressed by treating it with the <strong>mGlu5</strong> receptor antagonist MPEP.
+GRM5	drug	cocaine	24893316	Estradiol facilitation of <b>cocaine</b> induced locomotor sensitization in female rats requires activation of <strong>mGluR5</strong>.
+GRM5	addiction	sensitization	24893316	Estradiol facilitation of cocaine induced locomotor <b>sensitization</b> in female rats requires activation of <strong>mGluR5</strong>.
+GRM5	drug	cocaine	24893316	Recently, we have found that estrogen receptor alpha (ERα) functionally couples with the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) to mediate the effects of estradiol on both cellular activation as well as dendritic spine plasticity in brain regions involved in <b>cocaine</b> induced behavioral sensitization.
+GRM5	addiction	sensitization	24893316	Recently, we have found that estrogen receptor alpha (ERα) functionally couples with the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) to mediate the effects of estradiol on both cellular activation as well as dendritic spine plasticity in brain regions involved in cocaine induced behavioral <b>sensitization</b>.
+GRM5	drug	cocaine	24893316	Thus, we sought to determine whether <strong>mGluR5</strong> activation is required for the facilitative effects of estradiol on locomotor responses to <b>cocaine</b>.
+GRM5	drug	cocaine	24893316	Considered together, these data indicate that <strong>mGluR5</strong> activation is critical for the actions of estradiol on <b>cocaine</b> induced behavioral sensitization.
+GRM5	addiction	sensitization	24893316	Considered together, these data indicate that <strong>mGluR5</strong> activation is critical for the actions of estradiol on cocaine induced behavioral <b>sensitization</b>.
+GRM5	drug	alcohol	24872560	The present study examined the effects of <strong>mGluR5</strong> activation on extinction of <b>ethanol</b> cue maintained responding, relapse like behavior, and neuronal plasticity.
+GRM5	addiction	relapse	24872560	The present study examined the effects of <strong>mGluR5</strong> activation on extinction of ethanol cue maintained responding, <b>relapse</b> like behavior, and neuronal plasticity.
+GRM5	drug	alcohol	24872560	Rats were trained to self administer <b>ethanol</b> and then exposed to extinction training during which they were administered either vehicle or the <strong>mGluR5</strong> positive allosteric modulator 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl) or CDPPB.
+GRM5	drug	alcohol	24872560	These results confirm changes in the PrL and IfL cortex in glutamatergic neurotransmission during extinction learning and demonstrate that manipulation of <strong>mGluR5</strong> facilitates extinction of <b>ethanol</b> cues in association with neuronal plasticity.
+GRM5	drug	cocaine	24811383	<b>Cocaine</b> reward deficits in FMRP deficient mice stem from elevated mGluR5 (or <strong>GRM5</strong>) function, similar to a subset of fragile X symptoms, and do not extend to natural reward.
+GRM5	addiction	reward	24811383	Cocaine <b>reward</b> deficits in FMRP deficient mice stem from elevated mGluR5 (or <strong>GRM5</strong>) function, similar to a subset of fragile X symptoms, and do not extend to natural <b>reward</b>.
+GRM5	drug	cocaine	24811383	<b>Cocaine</b> reward deficits in FMRP deficient mice stem from elevated <strong>mGluR5</strong> (or <strong>GRM5</strong>) function, similar to a subset of fragile X symptoms, and do not extend to natural reward.
+GRM5	addiction	reward	24811383	Cocaine <b>reward</b> deficits in FMRP deficient mice stem from elevated <strong>mGluR5</strong> (or <strong>GRM5</strong>) function, similar to a subset of fragile X symptoms, and do not extend to natural <b>reward</b>.
+GRM5	drug	cocaine	24795154	Limbic system <strong>mGluR5</strong> availability in <b>cocaine</b> dependent subjects: a high resolution PET [(11)C]ABP688 study.
+GRM5	drug	cocaine	24795154	<b>Cocaine</b> self administration decreases type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) tissue concentrations in laboratory rats during early abstinence.
+GRM5	drug	cocaine	24795154	Here, our goal was to measure brain regional <strong>mGluR5</strong> availability in recently abstinent <b>cocaine</b> dependent humans.
+GRM5	drug	cocaine	24795154	Together, these results provide evidence of time related <strong>mGluR5</strong> alterations in striatal and limbic regions in humans during early <b>cocaine</b> abstinence.
+GRM5	addiction	sensitization	24769228	N methyl D aspartate receptor (NMDAR) and metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) play an important role in nociceptive processing and central <b>sensitization</b>.
+GRM5	drug	cocaine	24712397	We investigated the effects of extinguishing action reward versus context reward associations on drug primed reinstatement, and the potential role of the metabotropic glutamate 5 receptor (<strong>mGlu5</strong>) in these different types of extinction in rats that self administer <b>cocaine</b>.
+GRM5	addiction	relapse	24712397	We investigated the effects of extinguishing action reward versus context reward associations on drug primed <b>reinstatement</b>, and the potential role of the metabotropic glutamate 5 receptor (<strong>mGlu5</strong>) in these different types of extinction in rats that self administer cocaine.
+GRM5	addiction	reward	24712397	We investigated the effects of extinguishing action <b>reward</b> versus context <b>reward</b> associations on drug primed reinstatement, and the potential role of the metabotropic glutamate 5 receptor (<strong>mGlu5</strong>) in these different types of extinction in rats that self administer cocaine.
+GRM5	drug	cocaine	24712397	Additionally, systemic injections of the <strong>mGlu5</strong> negative allosteric modulator MTEP (3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine) following each extinction session significantly impaired the ability of context extinction to reduce <b>cocaine</b> primed reinstatement, without affecting reinstatement after lever extinction or passive abstinence.
+GRM5	addiction	relapse	24712397	Additionally, systemic injections of the <strong>mGlu5</strong> negative allosteric modulator MTEP (3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine) following each extinction session significantly impaired the ability of context extinction to reduce cocaine primed <b>reinstatement</b>, without affecting <b>reinstatement</b> after lever extinction or passive abstinence.
+GRM5	addiction	relapse	24612076	We hypothesized that the increased <b>reinstatement</b> after inhibiting NAC induction of GLT 1 resulted from increased extracellular glutamate, and show that augmented <b>reinstatement</b> is prevented by blocking <strong>mGluR5</strong>.
+GRM5	drug	cocaine	24576814	The <strong>mGlu5</strong> receptor regulates extinction of <b>cocaine</b> driven behaviours.
+GRM5	addiction	addiction	24576814	There is extensive evidence implicating the metabotropic glutamate 5 (<strong>mGlu5</strong>) receptor in aspects of <b>addiction</b> related behaviours.
+GRM5	drug	cocaine	24576814	Here, we used a well characterized line of <strong>mGlu5</strong> deficient mice to further examine the role of this receptor in <b>cocaine</b> driven behaviours.
+GRM5	drug	cocaine	24576814	Despite a spatial learning deficit, <strong>mGlu5</strong> deficient mice developed and maintained a conditioned place preference to <b>cocaine</b>, suggesting <b>cocaine</b> reward and Pavlovian conditioning are intact in these animals.
+GRM5	addiction	reward	24576814	Despite a spatial learning deficit, <strong>mGlu5</strong> deficient mice developed and maintained a conditioned place preference to cocaine, suggesting cocaine <b>reward</b> and Pavlovian conditioning are intact in these animals.
+GRM5	drug	cocaine	24576814	Notably, however, <strong>mGlu5</strong> deficient mice exhibited a marked deficit in the extinction of a <b>cocaine</b> conditioned place preference compared to wild type littermates.
+GRM5	drug	cocaine	24576814	Moreover, in a fixed ratio operant intravenous self administration paradigm, both genotypes showed similar responding for <b>cocaine</b> over two different doses, while <strong>mGlu5</strong> deficient mice displayed enhanced responding on a progressive ratio schedule.
+GRM5	addiction	reward	24576814	Moreover, in a fixed ratio <b>operant</b> intravenous self administration paradigm, both genotypes showed similar responding for cocaine over two different doses, while <strong>mGlu5</strong> deficient mice displayed enhanced responding on a progressive ratio schedule.
+GRM5	addiction	relapse	24576814	In addition, cue induced drug <b>seeking</b> after abstinence was exaggerated in <strong>mGlu5</strong> deficient mice.
+GRM5	drug	cocaine	24576814	Collectively, these findings suggest that while the <strong>mGlu5</strong> receptor may be involved in mediating the rewarding effects of <b>cocaine</b>, it appears necessary for the extinction of <b>cocaine</b> driven behaviours.
+GRM5	drug	alcohol	27695144	The Effect of <strong>mGluR5</strong> Antagonism During Binge Drinkingon Subsequent <b>Ethanol</b> Intake in C57BL/6J Mice: Sex  and Age Induced Differences.
+GRM5	addiction	intoxication	27695144	The Effect of <strong>mGluR5</strong> Antagonism During <b>Binge</b> Drinkingon Subsequent Ethanol Intake in C57BL/6J Mice: Sex  and Age Induced Differences.
+GRM5	drug	alcohol	27695144	Collectively, the present findings add to existing evidence implicating the contribution of long term effects of adolescent binge drinking to enhance <b>alcohol</b> abuse in adulthood, while suggesting that <strong>mGluR5</strong> antagonism may not be the best pharmacotherapy to treat binge <b>alcohol</b> consumption in female and adolescent animals.
+GRM5	addiction	intoxication	27695144	Collectively, the present findings add to existing evidence implicating the contribution of long term effects of adolescent <b>binge</b> drinking to enhance alcohol abuse in adulthood, while suggesting that <strong>mGluR5</strong> antagonism may not be the best pharmacotherapy to treat <b>binge</b> alcohol consumption in female and adolescent animals.
+GRM5	addiction	withdrawal	24553949	Rats evaluated after ∼1 month of <b>withdrawal</b> from such regimens ("incubated rats") exhibit changes in medium spiny neurons (MSNs) of the nucleus accumbens (NAc) that include accumulation of Ca(2+) permeable AMPA receptors (CP AMPARs) and a switch in group I metabotropic glutamate receptor (mGluR) mediated suppression of synaptic transmission from <strong>mGluR5</strong> dependent to mGluR1 dependent.
+GRM5	drug	cocaine	24506432	The present study sought to determine the role of accumbens core mGluR1, <strong>mGluR5</strong> and protein kinase C (PKC) in <b>cocaine</b> priming induced reinstatement of drug seeking.
+GRM5	addiction	relapse	24506432	The present study sought to determine the role of accumbens core mGluR1, <strong>mGluR5</strong> and protein kinase C (PKC) in cocaine priming induced <b>reinstatement</b> of drug <b>seeking</b>.
+GRM5	drug	cocaine	24506432	Consistent with these results, administration of an mGluR1 (50.0 μM YM 298198) or <strong>mGluR5</strong> (9.0 μM MPEP) antagonist directly into the accumbens core prior to a priming injection of <b>cocaine</b> (10 mg/kg) attenuated the reinstatement of drug seeking.
+GRM5	addiction	relapse	24506432	Consistent with these results, administration of an mGluR1 (50.0 μM YM 298198) or <strong>mGluR5</strong> (9.0 μM MPEP) antagonist directly into the accumbens core prior to a priming injection of cocaine (10 mg/kg) attenuated the <b>reinstatement</b> of drug <b>seeking</b>.
+GRM5	addiction	relapse	24506432	There were no effects of pharmacological inhibition of mGluR1, <strong>mGluR5</strong> or PKC in the accumbens core on sucrose <b>seeking</b>.
+GRM5	drug	cocaine	24506432	Together, these findings indicate that mGluR1 and <strong>mGluR5</strong> activation in the accumbens core promotes <b>cocaine</b> seeking and that these effects are reinforcer specific.
+GRM5	addiction	relapse	24506432	Together, these findings indicate that mGluR1 and <strong>mGluR5</strong> activation in the accumbens core promotes cocaine <b>seeking</b> and that these effects are reinforcer specific.
+GRM5	drug	cocaine	24506432	Furthermore, stimulation of mGluR1 and <strong>mGluR5</strong> in the accumbens core may regulate <b>cocaine</b> seeking, in part, through activation of PKCγ.
+GRM5	addiction	relapse	24506432	Furthermore, stimulation of mGluR1 and <strong>mGluR5</strong> in the accumbens core may regulate cocaine <b>seeking</b>, in part, through activation of PKCγ.
+GRM5	addiction	reward	24472725	<strong>mGluR5</strong> antagonist induced psychoactive properties: MTEP drug discrimination, a pharmacologically selective non NMDA effect with apparent lack of <b>reinforcing</b> properties.
+GRM5	addiction	reward	24472725	Rats self administered PCP but not MPEP or MTEP, indicating a lack of <b>reinforcing</b> effects of the <strong>mGluR5</strong> antagonists.
+GRM5	addiction	reward	24472725	These data suggest that the <strong>mGluR5</strong> antagonists appear not to have <b>reinforcing</b> properties, that the discriminative effects of <strong>mGluR5</strong> antagonists and PCP are dissimilar, and that <strong>mGluR5</strong> antagonists may produce psychoactive effects different from NMDA antagonists and other drugs with known psychotomimetic properties.
+GRM5	drug	amphetamine	24358885	Positive or negative allosteric modulation of metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) does not alter expression of behavioral sensitization to <b>methamphetamine</b>.
+GRM5	addiction	sensitization	24358885	Positive or negative allosteric modulation of metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) does not alter expression of behavioral <b>sensitization</b> to methamphetamine.
+GRM5	drug	amphetamine	24358885	We investigated the role of metabotropic glutamate receptor type 5 (<strong>mGluR5</strong>) in <b>methamphetamine</b> induced behavioral sensitization.
+GRM5	addiction	sensitization	24358885	We investigated the role of metabotropic glutamate receptor type 5 (<strong>mGluR5</strong>) in methamphetamine induced behavioral <b>sensitization</b>.
+GRM5	drug	amphetamine	24358885	Doses from previous studies showed reduced drug conditioned behavior; however in this study neither CDPPB nor fenobam pretreatment resulted in an altered expression of behavioral sensitization, indicating a lack of <strong>mGluR5</strong> involvement in sensitized <b>methamphetamine</b> induced locomotion.
+GRM5	addiction	sensitization	24358885	Doses from previous studies showed reduced drug conditioned behavior; however in this study neither CDPPB nor fenobam pretreatment resulted in an altered expression of behavioral <b>sensitization</b>, indicating a lack of <strong>mGluR5</strong> involvement in sensitized methamphetamine induced locomotion.
+GRM5	drug	alcohol	24279870	Effects of the <strong>mGluR5</strong> antagonist MPEP on <b>ethanol</b> withdrawal induced anxiety like syndrome in rats.
+GRM5	addiction	withdrawal	24279870	Effects of the <strong>mGluR5</strong> antagonist MPEP on ethanol <b>withdrawal</b> induced anxiety like syndrome in rats.
+GRM5	addiction	addiction	24279870	Recent studies have demonstrated the importance of metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) in <b>addictive</b> behaviours.
+GRM5	drug	alcohol	24279870	This study investigates the effects of the <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) on <b>ethanol</b> withdrawal induced anxiety using two behavioural paradigms.
+GRM5	addiction	withdrawal	24279870	This study investigates the effects of the <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) on ethanol <b>withdrawal</b> induced anxiety using two behavioural paradigms.
+GRM5	drug	cocaine	24035345	Preclinical studies demonstrate that glutamate homeostasis in the striatum is disrupted following <b>cocaine</b> exposure, including a decrease in metabotropic glutamate receptor type 5 (<strong>mGluR5</strong>) expression and reduced glutamate turnover.
+GRM5	drug	cocaine	24035345	Positron emission tomography imaging with the radiotracer [(11)C]ABP688 was used to measure <strong>mGluR5</strong> binding and magnetic resonance spectroscopy was used to measure glutamate glutamine levels in the striatum of <b>cocaine</b> addicted participants (n = 15) compared with healthy control subjects (n = 15).
+GRM5	drug	cocaine	24035345	Following the scans, the <b>cocaine</b> addicted volunteers performed <b>cocaine</b> self administration sessions to investigate the correlation between <b>cocaine</b> seeking behavior and <strong>mGluR5</strong> receptor binding.
+GRM5	addiction	relapse	24035345	Following the scans, the cocaine addicted volunteers performed cocaine self administration sessions to investigate the correlation between cocaine <b>seeking</b> behavior and <strong>mGluR5</strong> receptor binding.
+GRM5	drug	cocaine	24035345	Overall, these results show that long term <b>cocaine</b> use is associated with a decrease in <strong>mGluR5</strong> availability compared with matched healthy control subjects and suggests that this receptor may serve as a viable target for treatment development for this disorder.
+GRM5	drug	benzodiazepine	24003250	Heterotropic activation of the <b>midazolam</b> hydroxylase activity of CYP3A by a positive allosteric modulator of <strong>mGlu5</strong>: in vitro to in vivo translation and potential impact on clinically relevant drug drug interactions.
+GRM5	drug	cocaine	24001208	A novel <strong>mGluR5</strong> antagonist, MFZ 10 7, inhibits <b>cocaine</b> taking and <b>cocaine</b> seeking behavior in rats.
+GRM5	addiction	relapse	24001208	A novel <strong>mGluR5</strong> antagonist, MFZ 10 7, inhibits cocaine taking and cocaine <b>seeking</b> behavior in rats.
+GRM5	addiction	relapse	24001208	Pre clinical studies suggest that negative allosteric modulators (NAMs) of the metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>), including 2 methyl 6 (phenylethynyl)pyridine (MPEP), 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]pyridine (MTEP) and fenobam are highly effective in attenuating drug taking and drug <b>seeking</b> behaviors.
+GRM5	drug	cocaine	24001208	These findings not only provide additional evidence supporting an important role for <strong>mGluR5</strong> in <b>cocaine</b> reward and addiction, but also introduce a new tool for both in vitro and in vivo investigations with which to further characterize this role.
+GRM5	addiction	addiction	24001208	These findings not only provide additional evidence supporting an important role for <strong>mGluR5</strong> in cocaine reward and <b>addiction</b>, but also introduce a new tool for both in vitro and in vivo investigations with which to further characterize this role.
+GRM5	addiction	reward	24001208	These findings not only provide additional evidence supporting an important role for <strong>mGluR5</strong> in cocaine <b>reward</b> and addiction, but also introduce a new tool for both in vitro and in vivo investigations with which to further characterize this role.
+GRM5	drug	alcohol	23995381	Blocking <strong>mGluR5</strong> potently affects various <b>alcohol</b> related behaviors in rodents, and mGluR2/3 agonism also suppresses <b>alcohol</b> consumption.
+GRM5	drug	cocaine	23986250	Stimulation of <strong>mGluR5</strong> in the accumbens shell promotes <b>cocaine</b> seeking by activating PKC gamma.
+GRM5	addiction	relapse	23986250	Stimulation of <strong>mGluR5</strong> in the accumbens shell promotes cocaine <b>seeking</b> by activating PKC gamma.
+GRM5	drug	cocaine	23986250	Recent studies indicate a critical role for metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) in the reinstatement of <b>cocaine</b> seeking.
+GRM5	addiction	relapse	23986250	Recent studies indicate a critical role for metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) in the <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM5	drug	cocaine	23986250	Here, we show that intra accumbens shell administration of an <strong>mGluR5</strong> (9.0 μm MPEP), but not mGluR1 (50.0 μm YM 298198), antagonist before a priming injection of <b>cocaine</b> (10 mg/kg) attenuated the reinstatement of drug seeking in rats.
+GRM5	addiction	relapse	23986250	Here, we show that intra accumbens shell administration of an <strong>mGluR5</strong> (9.0 μm MPEP), but not mGluR1 (50.0 μm YM 298198), antagonist before a priming injection of cocaine (10 mg/kg) attenuated the <b>reinstatement</b> of drug <b>seeking</b> in rats.
+GRM5	drug	cocaine	23986250	Together, these findings indicate that accumbens shell <strong>mGluR5</strong> activation promotes <b>cocaine</b> seeking, in part, through activation of PLC and PKCγ.
+GRM5	addiction	relapse	23986250	Together, these findings indicate that accumbens shell <strong>mGluR5</strong> activation promotes cocaine <b>seeking</b>, in part, through activation of PLC and PKCγ.
+GRM5	drug	cocaine	23973314	Low  and high <b>cocaine</b> locomotor responding rats differ in reinstatement of <b>cocaine</b> seeking and striatal <strong>mGluR5</strong> protein expression.
+GRM5	addiction	relapse	23973314	Low  and high cocaine locomotor responding rats differ in <b>reinstatement</b> of cocaine <b>seeking</b> and striatal <strong>mGluR5</strong> protein expression.
+GRM5	addiction	relapse	23973314	Western blot analysis revealed that <strong>mGluR5</strong> heteromers were significantly higher in the dorsal striatum of HCRs than LCRs following <b>reinstatement</b> testing.
+GRM5	addiction	intoxication	23966068	An intra CeA infusion of mGluR1, <strong>mGluR5</strong> and PLC inhibitors all dose dependently reduced <b>binge</b> intake, without influencing sucrose drinking.
+GRM5	addiction	intoxication	23966068	The effects of co infusing mGluR1 and PLC inhibitors were additive, whereas those of coinhibiting <strong>mGluR5</strong> and PLC were not, indicating that the efficacy of mGluR1 blockade to lower <b>binge</b> intake involves a pathway independent of PLC activation.
+GRM5	addiction	intoxication	23966068	The efficacy of mGluR1, <strong>mGluR5</strong> and PLC inhibitors to reduce <b>binge</b> intake depended upon intact Homer2 expression as revealed through neuropharmacological studies of Homer2 null mutant mice.
+GRM5	addiction	addiction	23911326	The findings elucidate how a coincidence of signals from the nucleus and the synapse can render <strong>mGluR5</strong> accessible to activation with consequences for drug induced dopamine responses and point to depotentiation at corticostriatal synapses as a possible therapeutic target for treating <b>addiction</b>.
+GRM5	addiction	addiction	23862615	Since <strong>mGlu5</strong> receptors play an important role in regulating several central actions of drugs of abuse, and the hippocampus is a crucial brain area involved in <b>addiction</b>, anxiety, and spatial memory, a possible link between <strong>mGlu5</strong> receptor allosteric modulation and the profiles of action of GET73 is proposed, although to date no studies have yet explored GET73 binding at the <strong>mGlu5</strong> receptor orthosteric and/or allosteric sites.
+GRM5	drug	alcohol	23861896	We sought to assess the involvement of the metabotropic glutamate 5 receptor (<strong>mGlu5</strong>) in behaviours relevant to METH addiction because this receptor has been implicated in the actions of other drugs of abuse, including <b>alcohol</b>, cocaine and opiates.
+GRM5	drug	amphetamine	23861896	We sought to assess the involvement of the metabotropic glutamate 5 receptor (<strong>mGlu5</strong>) in behaviours relevant to <b>METH</b> addiction because this receptor has been implicated in the actions of other drugs of abuse, including alcohol, cocaine and opiates.
+GRM5	drug	cocaine	23861896	We sought to assess the involvement of the metabotropic glutamate 5 receptor (<strong>mGlu5</strong>) in behaviours relevant to METH addiction because this receptor has been implicated in the actions of other drugs of abuse, including alcohol, <b>cocaine</b> and opiates.
+GRM5	addiction	addiction	23861896	We sought to assess the involvement of the metabotropic glutamate 5 receptor (<strong>mGlu5</strong>) in behaviours relevant to METH <b>addiction</b> because this receptor has been implicated in the actions of other drugs of abuse, including alcohol, cocaine and opiates.
+GRM5	addiction	sensitization	23861896	<strong>mGlu5</strong> knockout (KO) mice were tested in intravenous self administration, conditioned place preference and locomotor <b>sensitization</b>.
+GRM5	drug	amphetamine	23861896	Acquisition and maintenance of self administration, as well as the motivation to self administer <b>METH</b> was intact in <strong>mGlu5</strong> KO mice.
+GRM5	drug	amphetamine	23861896	Importantly, <strong>mGlu5</strong> KO mice required more extinction sessions to extinguish the operant response for <b>METH</b>, and exhibited an enhanced propensity to reinstate operant responding following exposure to drug associated cues.
+GRM5	addiction	reward	23861896	Importantly, <strong>mGlu5</strong> KO mice required more extinction sessions to extinguish the <b>operant</b> response for METH, and exhibited an enhanced propensity to reinstate <b>operant</b> responding following exposure to drug associated cues.
+GRM5	drug	amphetamine	23861896	These data demonstrate a role for <strong>mGlu5</strong> in the extinction and reinstatement of <b>METH</b> seeking, and suggests a role for <strong>mGlu5</strong> in regulating contextual salience.
+GRM5	addiction	relapse	23861896	These data demonstrate a role for <strong>mGlu5</strong> in the extinction and <b>reinstatement</b> of METH <b>seeking</b>, and suggests a role for <strong>mGlu5</strong> in regulating contextual salience.
+GRM5	drug	cocaine	23850523	We hypothesized that blockade of <strong>mGluR5</strong> within the NAc shell would impair <b>cocaine</b> conditioning in rats.
+GRM5	drug	cocaine	23850523	In contrast, <strong>mGluR5</strong> blockade at 12 nmol and 25 nmol decreased conditioned locomotion in the <b>cocaine</b> paired groups.
+GRM5	drug	cocaine	23850523	Our results suggest that <strong>mGluR5</strong> within the NAc shell could be modulating the expression of memory related to the association of environmental cues with the effects of <b>cocaine</b>.
+GRM5	drug	cocaine	23850523	We suggest that <strong>mGluR5</strong> could be taking into account to further studies related with <b>cocaine</b> exposure and <b>cocaine</b> addiction treatments.
+GRM5	addiction	addiction	23850523	We suggest that <strong>mGluR5</strong> could be taking into account to further studies related with cocaine exposure and cocaine <b>addiction</b> treatments.
+GRM5	drug	opioid	23761764	Null mutations of Homer1a, Homer1, and Homer2, as well as transgenic disruption of <strong>mGluR5</strong> Homer interactions, either attenuated or completely blocked low dose <b>heroin</b> CPP, and none of the CCI mutant strains exhibited <b>heroin</b> induced CPA.
+GRM5	addiction	reward	23761764	Null mutations of Homer1a, Homer1, and Homer2, as well as transgenic disruption of <strong>mGluR5</strong> Homer interactions, either attenuated or completely blocked low dose heroin <b>CPP</b>, and none of the CCI mutant strains exhibited heroin induced CPA.
+GRM5	drug	amphetamine	23711322	Cellular distribution of AMPA receptor subunits and <strong>mGlu5</strong> following acute and repeated administration of morphine or <b>methamphetamine</b>.
+GRM5	drug	opioid	23711322	Cellular distribution of AMPA receptor subunits and <strong>mGlu5</strong> following acute and repeated administration of <b>morphine</b> or methamphetamine.
+GRM5	drug	amphetamine	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (GluA1, GluA2) and <strong>mGlu5</strong>, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated morphine (8 mg/kg) or <b>methamphetamine</b> (1 mg/kg) (treatments producing behavioral sensitization).
+GRM5	drug	opioid	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (GluA1, GluA2) and <strong>mGlu5</strong>, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated <b>morphine</b> (8 mg/kg) or methamphetamine (1 mg/kg) (treatments producing behavioral sensitization).
+GRM5	addiction	sensitization	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (GluA1, GluA2) and <strong>mGlu5</strong>, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated morphine (8 mg/kg) or methamphetamine (1 mg/kg) (treatments producing behavioral <b>sensitization</b>).
+GRM5	drug	amphetamine	23711322	Fourteen days after repeated morphine or <b>methamphetamine</b>, <strong>mGlu5</strong> surface expression increased in VP.
+GRM5	drug	opioid	23711322	Fourteen days after repeated <b>morphine</b> or methamphetamine, <strong>mGlu5</strong> surface expression increased in VP.
+GRM5	drug	amphetamine	23711322	In mPFC, <strong>mGlu5</strong> were unaltered; however, after <b>methamphetamine</b>, STEP61 levels decreased and GluA2 surface expression increased.
+GRM5	drug	amphetamine	23711322	Pre treatment with a <strong>mGlu5</strong> selective negative allosteric modulator, blocked <b>methamphetamine</b> induced behavioral sensitization and changes in mPFC GluA2 and STEP61 .
+GRM5	addiction	sensitization	23711322	Pre treatment with a <strong>mGlu5</strong> selective negative allosteric modulator, blocked methamphetamine induced behavioral <b>sensitization</b> and changes in mPFC GluA2 and STEP61 .
+GRM5	drug	amphetamine	23711322	These data reveal (i) region specific distinctions in glutamate receptor trafficking between acute and repeated treatments of morphine and <b>methamphetamine</b>, and (ii) that <strong>mGlu5</strong> is necessary for <b>methamphetamine</b> induced alterations in mPFC GluA2 and STEP61 .
+GRM5	drug	opioid	23711322	These data reveal (i) region specific distinctions in glutamate receptor trafficking between acute and repeated treatments of <b>morphine</b> and methamphetamine, and (ii) that <strong>mGlu5</strong> is necessary for methamphetamine induced alterations in mPFC GluA2 and STEP61 .
+GRM5	drug	cocaine	23710649	The role of ventral and dorsal striatum <strong>mGluR5</strong> in relapse to <b>cocaine</b> seeking and extinction learning.
+GRM5	addiction	relapse	23710649	The role of ventral and dorsal striatum <strong>mGluR5</strong> in <b>relapse</b> to cocaine <b>seeking</b> and extinction learning.
+GRM5	drug	cocaine	23710649	Here we investigated the role of <strong>mGluR5</strong> in the ventral and dorsal striatum in regulating <b>cocaine</b> seeking following both abstinence and extinction.
+GRM5	addiction	relapse	23710649	Here we investigated the role of <strong>mGluR5</strong> in the ventral and dorsal striatum in regulating cocaine <b>seeking</b> following both abstinence and extinction.
+GRM5	addiction	relapse	23710649	Both drug <b>seeking</b> tests were conducted in the presence of either <strong>mGluR5</strong> negative allosteric modulator, MTEP or vehicle infused into either the nucleus accumbens (NA) core or dorsolateral striatum (dSTR).
+GRM5	drug	cocaine	23710649	Blocking dSTR <strong>mGluR5</strong> had no effect on context  or cue induced <b>cocaine</b> seeking.
+GRM5	addiction	relapse	23710649	Blocking dSTR <strong>mGluR5</strong> had no effect on context  or cue induced cocaine <b>seeking</b>.
+GRM5	drug	cocaine	23710649	Furthermore, <strong>mGluR5</strong> surface expression was reduced and LTD was absent in dSTR slices of animals undergoing 3 weeks of abstinence from <b>cocaine</b> but not sucrose self administration.
+GRM5	drug	cocaine	23710649	Taken together, this data indicates that dSTR <strong>mGluR5</strong> plays an essential role in extinction learning but not <b>cocaine</b> relapse, while NA core <strong>mGluR5</strong> modulates drug seeking following both extinction and abstinence from <b>cocaine</b> self administration.
+GRM5	addiction	relapse	23710649	Taken together, this data indicates that dSTR <strong>mGluR5</strong> plays an essential role in extinction learning but not cocaine <b>relapse</b>, while NA core <strong>mGluR5</strong> modulates drug <b>seeking</b> following both extinction and abstinence from cocaine self administration.
+GRM5	drug	cocaine	23682684	Substituted 1 Phenyl 3 (pyridin 2 yl)urea negative allosteric modulators of <strong>mGlu5</strong>: discovery of a new tool compound VU0463841 with activity in rat models of <b>cocaine</b> addiction.
+GRM5	addiction	addiction	23682684	Substituted 1 Phenyl 3 (pyridin 2 yl)urea negative allosteric modulators of <strong>mGlu5</strong>: discovery of a new tool compound VU0463841 with activity in rat models of cocaine <b>addiction</b>.
+GRM5	drug	cocaine	23682684	Evidence has continued to accumulate that indicates a critical role for the metabotropic glutamate receptor subtype 5 (<strong>mGlu5</strong>) in the modulation of neural circuitry associated with the addictive properties of <b>cocaine</b>.
+GRM5	addiction	addiction	23682684	Evidence has continued to accumulate that indicates a critical role for the metabotropic glutamate receptor subtype 5 (<strong>mGlu5</strong>) in the modulation of neural circuitry associated with the <b>addictive</b> properties of cocaine.
+GRM5	drug	cocaine	23682684	While the small molecule <strong>mGlu5</strong> negative allosteric modulator (NAM) field is relatively advanced, investigation into the potential of small molecule <strong>mGlu5</strong> NAMs for the treatment of <b>cocaine</b> addiction remains an area of high interest.
+GRM5	addiction	addiction	23682684	While the small molecule <strong>mGlu5</strong> negative allosteric modulator (NAM) field is relatively advanced, investigation into the potential of small molecule <strong>mGlu5</strong> NAMs for the treatment of cocaine <b>addiction</b> remains an area of high interest.
+GRM5	addiction	relapse	23628984	In particular, animal models have linked the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) to drug <b>seeking</b> behavior and extinction learning.
+GRM5	drug	cocaine	23628984	Therefore, we investigated if human <b>cocaine</b> users (CU) exhibit altered <strong>mGluR5</strong> availability compared with drug naïve control subjects.
+GRM5	drug	cocaine	23628984	Seventeen male controls (11 smokers) and 18 male <b>cocaine</b> users (13 smokers) underwent positron emission tomography with (11)C ABP688 to quantify <strong>mGluR5</strong> availability in 12 volumes of interest in addiction related brain areas.
+GRM5	drug	nicotine	23628984	Seventeen male controls (11 <b>smokers</b>) and 18 male cocaine users (13 <b>smokers</b>) underwent positron emission tomography with (11)C ABP688 to quantify <strong>mGluR5</strong> availability in 12 volumes of interest in addiction related brain areas.
+GRM5	addiction	addiction	23628984	Seventeen male controls (11 smokers) and 18 male cocaine users (13 smokers) underwent positron emission tomography with (11)C ABP688 to quantify <strong>mGluR5</strong> availability in 12 volumes of interest in <b>addiction</b> related brain areas.
+GRM5	drug	nicotine	23628984	In contrast, <b>smokers</b> (n=24) showed significantly lower <strong>mGluR5</strong> density throughout the brain (mean 20%) compared with non <b>smokers</b> (n=11).
+GRM5	drug	nicotine	23628984	Duration of <b>smoking</b> abstinence was positively associated with <strong>mGluR5</strong> density in all brain regions of interest, indicating that lower <strong>mGluR5</strong> availability was particularly pronounced in individuals who had smoked very recently.
+GRM5	drug	cocaine	23628984	Specifically tobacco smoking was associated with lower <strong>mGluR5</strong> availability in both CU and controls, while <b>cocaine</b> use was not linked to detectable <strong>mGluR5</strong> alterations.
+GRM5	drug	nicotine	23628984	Specifically <b>tobacco</b> <b>smoking</b> was associated with lower <strong>mGluR5</strong> availability in both CU and controls, while cocaine use was not linked to detectable <strong>mGluR5</strong> alterations.
+GRM5	drug	alcohol	23623810	<b>Acamprosate</b> (NMDA and metabotropic glutamate 5 receptor (<strong>mGluR5</strong>) antagonist) at the dose 200 and 400mg/kg showed anxiolytic like effect, thus increasing the percent of time spent in open arms and a number of open arm entries.
+GRM5	drug	alcohol	23623810	<strong>mGluR5</strong> selective antagonist, MTEP (3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]pyridine hydrochloride) and mGluR2/3 agonist, LY354740 (1S,2S,5R,6S) 2 aminobicyclo[3.1.0]hexane 2,6 dicarboxylic acid), caused effects similar to <b>acamprosate</b> at doses 1.25 5mg/kg and 2.5 5mg/kg, respectively.
+GRM5	addiction	addiction	23615919	The metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>) has been reported to be critically involved in drug reward and <b>addiction</b>.
+GRM5	addiction	reward	23615919	The metabotropic glutamate receptor subtype 5 (<strong>mGluR5</strong>) has been reported to be critically involved in drug <b>reward</b> and addiction.
+GRM5	drug	cocaine	23615919	Because the <strong>mGluR5</strong> negative allosteric modulators (NAMs) 2 methyl 6 (phenylethynyl)pyridine (MPEP) and 3 ((2 methyl 1,3 thiazol 4 yl)ethynyl)pyridine (MTEP) significantly inhibit addictivelike behaviors of <b>cocaine</b> and other drugs of abuse in experimental animals, it has been suggested that <strong>mGluR5</strong> NAMs may have translational potential for treatment of addiction in humans.
+GRM5	addiction	addiction	23615919	Because the <strong>mGluR5</strong> negative allosteric modulators (NAMs) 2 methyl 6 (phenylethynyl)pyridine (MPEP) and 3 ((2 methyl 1,3 thiazol 4 yl)ethynyl)pyridine (MTEP) significantly inhibit addictivelike behaviors of cocaine and other drugs of abuse in experimental animals, it has been suggested that <strong>mGluR5</strong> NAMs may have translational potential for treatment of <b>addiction</b> in humans.
+GRM5	addiction	addiction	23615919	Herein, we evaluate a potential candidate for translational <b>addiction</b> research: a new sulfate salt formulation of fenobam, a selective <strong>mGluR5</strong> NAM that has been investigated in humans.
+GRM5	drug	cocaine	23615919	This study provides additional support for the role of <strong>mGluR5</strong> signaling in <b>cocaine</b> addiction and suggests that fenobam sulfate may have translational potential in medication development for the treatment of <b>cocaine</b> addiction in humans.
+GRM5	addiction	addiction	23615919	This study provides additional support for the role of <strong>mGluR5</strong> signaling in cocaine <b>addiction</b> and suggests that fenobam sulfate may have translational potential in medication development for the treatment of cocaine <b>addiction</b> in humans.
+GRM5	drug	alcohol	23564259	In light of the importance of the hippocampal CA1 subregion in <b>alcohol</b> addiction and anxiety like behaviors this in vivo microdialysis study characterized the effect of GET73 on extracellular GABA levels in the hippocampal CA1 region of the freely moving rat including a possible role for <strong>mGlu5</strong> receptor in mediating this effect.
+GRM5	addiction	addiction	23564259	In light of the importance of the hippocampal CA1 subregion in alcohol <b>addiction</b> and anxiety like behaviors this in vivo microdialysis study characterized the effect of GET73 on extracellular GABA levels in the hippocampal CA1 region of the freely moving rat including a possible role for <strong>mGlu5</strong> receptor in mediating this effect.
+GRM5	drug	alcohol	23564259	Furthermore, the present data lead to hypothesize a possible interaction between GET73 and <strong>mGluR5</strong> mediated regulation of hippocampal CA1 GABA transmission, an effect which may be relevant to the ability of GET73 to reduce <b>alcohol</b> intake in an <b>alcohol</b> preferring rat strain.
+GRM5	drug	cocaine	23348064	Antagonism of group I metabotropic glutamate receptors (mGluR1 and <strong>mGluR5</strong>) reduces behavioral effects of drugs of abuse, including <b>cocaine</b>.
+GRM5	drug	nicotine	23248277	Marked global reduction in <strong>mGluR5</strong> receptor binding in <b>smokers</b> and ex <b>smokers</b> determined by [11C]ABP688 positron emission tomography.
+GRM5	drug	nicotine	23248277	Because antagonism of the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) reduced <b>nicotine</b> self administration in rats and mice, <strong>mGluR5</strong> is suggested to be involved in <b>nicotine</b> addiction.
+GRM5	addiction	addiction	23248277	Because antagonism of the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) reduced nicotine self administration in rats and mice, <strong>mGluR5</strong> is suggested to be involved in nicotine <b>addiction</b>.
+GRM5	drug	nicotine	23248277	We found a marked global reduction (20.6%; P < 0.0001) in the <strong>mGluR5</strong> distribution volume ratio (DVR) in the gray matter of 14 <b>smokers</b>.
+GRM5	drug	nicotine	23248277	Compared with 14 nonsmokers, 14 ex <b>smokers</b> had global reductions in the average gray matter <strong>mGluR5</strong> DVR (11.5%; P < 0.005), and there was a significant difference in average gray matter <strong>mGluR5</strong> DVR between <b>smokers</b> and ex <b>smokers</b> (9.2%; P < 0.01).
+GRM5	drug	nicotine	23248277	Clinical variables reflecting current <b>nicotine</b> consumption, dependence and abstinence were not correlated with <strong>mGluR5</strong> DVR.
+GRM5	addiction	dependence	23248277	Clinical variables reflecting current nicotine consumption, <b>dependence</b> and abstinence were not correlated with <strong>mGluR5</strong> DVR.
+GRM5	drug	nicotine	23248277	This decrease in <strong>mGluR5</strong> receptor binding may be an adaptation to chronic increases in glutamate induced by chronic <b>nicotine</b> administration, and the decreased down regulation seen in the ex <b>smokers</b> could be due to incomplete recovery of the receptors, especially because the ex <b>smokers</b> were abstinent for only 25 wk on average.
+GRM5	drug	amphetamine	23189054	Positive Allosteric Modulation of <strong>mGluR5</strong> Accelerates Extinction Learning but Not Relearning Following <b>Methamphetamine</b> Self Administration.
+GRM5	drug	amphetamine	23189054	Here, we investigated the effects of the <strong>mGluR5</strong> positive allosteric modulator CDPPB, a compound known for its cognitive enhancing effects in rodents, on extinction learning in rats with different histories of <b>methamphetamine</b> (<b>METH</b>) training.
+GRM5	drug	amphetamine	23189054	Positive allosteric modulation of <strong>mGluR5</strong> may therefore have some beneficial effects on efforts to facilitate extinction learning and reduce <b>methamphetamine</b> seeking.
+GRM5	addiction	relapse	23189054	Positive allosteric modulation of <strong>mGluR5</strong> may therefore have some beneficial effects on efforts to facilitate extinction learning and reduce methamphetamine <b>seeking</b>.
+GRM5	drug	alcohol	23149043	Type 5 metabotropic glutamate receptor (<strong>mGlur5</strong>) is abundant in brain regions known to be involved in drug reinforcement, yet very little has been published on mGluR1/5 expression in <b>alcoholics</b>.
+GRM5	addiction	reward	23149043	Type 5 metabotropic glutamate receptor (<strong>mGlur5</strong>) is abundant in brain regions known to be involved in drug <b>reinforcement</b>, yet very little has been published on mGluR1/5 expression in alcoholics.
+GRM5	drug	alcohol	22902169	Here, we show that metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) signaling on dopaminoceptive neurons is necessary for both novelty seeking behavior and the abstinence induced escalation of <b>alcohol</b> drinking.
+GRM5	addiction	addiction	22902169	Here, we show that metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) signaling on dopaminoceptive neurons is necessary for both novelty seeking behavior and the abstinence induced <b>escalation</b> of alcohol drinking.
+GRM5	addiction	relapse	22902169	Here, we show that metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) signaling on dopaminoceptive neurons is necessary for both novelty <b>seeking</b> behavior and the abstinence induced escalation of alcohol drinking.
+GRM5	drug	alcohol	22902169	Mice harboring a transgene expressing microRNA hairpins against <strong>mGluR5</strong> messenger RNA under the control of the D1 dopamine receptor gene promoter (<strong>mGluR5</strong>(KD D1)) were tested in a battery of behavioral tests measuring learning abilities, anxiety levels, reactions to novelty, operant sensation seeking, and <b>alcohol</b> sensitivity.
+GRM5	addiction	relapse	22902169	Mice harboring a transgene expressing microRNA hairpins against <strong>mGluR5</strong> messenger RNA under the control of the D1 dopamine receptor gene promoter (<strong>mGluR5</strong>(KD D1)) were tested in a battery of behavioral tests measuring learning abilities, anxiety levels, reactions to novelty, operant sensation <b>seeking</b>, and alcohol sensitivity.
+GRM5	addiction	reward	22902169	Mice harboring a transgene expressing microRNA hairpins against <strong>mGluR5</strong> messenger RNA under the control of the D1 dopamine receptor gene promoter (<strong>mGluR5</strong>(KD D1)) were tested in a battery of behavioral tests measuring learning abilities, anxiety levels, reactions to novelty, <b>operant</b> sensation seeking, and alcohol sensitivity.
+GRM5	drug	alcohol	22902169	When <strong>mGluR5</strong>(KD D1) mice were provided access to <b>alcohol</b>, they showed similar patterns of consumption as wild type animals.
+GRM5	drug	alcohol	22902169	These data identify <strong>mGluR5</strong> receptors on D1 expressing neurons as a common molecular substrate of novelty seeking behaviors and behaviors associated with <b>alcohol</b> abuse.
+GRM5	addiction	relapse	22902169	These data identify <strong>mGluR5</strong> receptors on D1 expressing neurons as a common molecular substrate of novelty <b>seeking</b> behaviors and behaviors associated with alcohol abuse.
+GRM5	addiction	relapse	22820868	Metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) negative allosteric modulators (NAMs) have shown promise in significantly attenuating drug self administration and drug <b>seeking</b> in <b>reinstatement</b> paradigms.
+GRM5	drug	amphetamine	22820868	The current study sought to assess the effect of the <strong>mGluR5</strong> NAM fenobam on <b>METH</b> seeking behavior.
+GRM5	addiction	relapse	22820868	The current study sought to assess the effect of the <strong>mGluR5</strong> NAM fenobam on METH <b>seeking</b> behavior.
+GRM5	drug	amphetamine	22820868	The <strong>mGluR5</strong> NAM fenobam attenuates the reinstatement of <b>METH</b> seeking behavior, but these effects may be due to nonspecific suppression of general appetitive behaviors.
+GRM5	addiction	relapse	22820868	The <strong>mGluR5</strong> NAM fenobam attenuates the <b>reinstatement</b> of METH <b>seeking</b> behavior, but these effects may be due to nonspecific suppression of general appetitive behaviors.
+GRM5	drug	cocaine	22815535	Within the group I family of metabotropic glutamate receptors (mGluRs), substantial evidence points to a role for <strong>mGluR5</strong> mechanisms in <b>cocaine</b>'s abuse related behavioral effects, but less is understood about the contribution of mGluR1, which also belongs to the group I mGluR family.
+GRM5	drug	amphetamine	22732517	<strong>mGluR5</strong> is necessary for maintenance of <b>methamphetamine</b> induced associative learning.
+GRM5	drug	amphetamine	22732517	We hypothesized that the maintenance of <b>Meth</b> induced CPP would also require activated mGluR, and that the role of mGluR1 vs. <strong>mGluR5</strong> group I subtypes may differ.
+GRM5	addiction	reward	22732517	We hypothesized that the maintenance of Meth induced <b>CPP</b> would also require activated mGluR, and that the role of mGluR1 vs. <strong>mGluR5</strong> group I subtypes may differ.
+GRM5	drug	amphetamine	22732517	or its vehicle on days 13 and 14 after <b>Meth</b> conditioning did not influence the maintenance of <b>Meth</b> induced CPP; however, administration of the <strong>mGluR5</strong> NAMs MTEP (3mg/kg, i.p.)
+GRM5	addiction	reward	22732517	or its vehicle on days 13 and 14 after Meth conditioning did not influence the maintenance of Meth induced <b>CPP</b>; however, administration of the <strong>mGluR5</strong> NAMs MTEP (3mg/kg, i.p.)
+GRM5	drug	amphetamine	22732517	These findings suggest a subtype specific role of <strong>mGluR5</strong> receptors in the maintenance of place preference memory and potential of <strong>mGluR5</strong> NAMs as a useful target for <b>Meth</b> addiction therapy.
+GRM5	addiction	addiction	22732517	These findings suggest a subtype specific role of <strong>mGluR5</strong> receptors in the maintenance of place preference memory and potential of <strong>mGluR5</strong> NAMs as a useful target for Meth <b>addiction</b> therapy.
+GRM5	drug	alcohol	22651960	Involvement of <strong>mGlu5</strong> and NMDA receptors in the antidepressant like effect of <b>acamprosate</b> in the tail suspension test.
+GRM5	drug	alcohol	22651960	In the present study we investigated potential antidepressant like effect of a functional NMDA and <strong>mGlu5</strong> receptor antagonist, <b>acamprosate</b>, which has been used in the therapy of human <b>alcoholics</b> as an anti craving drug for more than 20 years and is considered as a safe substance.
+GRM5	addiction	relapse	22651960	In the present study we investigated potential antidepressant like effect of a functional NMDA and <strong>mGlu5</strong> receptor antagonist, acamprosate, which has been used in the therapy of human alcoholics as an anti <b>craving</b> drug for more than 20 years and is considered as a safe substance.
+GRM5	drug	alcohol	22651960	Furthermore we have shown that the antidepressant like effect of <b>acamprosate</b> used at a dose of 200 mg/kg was dependent on NMDA and <strong>mGlu5</strong> receptor blockade, since NMDA (25 mg/kg) and <strong>mGlu5</strong> receptor positive allosteric modulator, CDPPB (3 mg/kg), antagonized its activity in the TST.
+GRM5	drug	alcohol	22651960	These data suggest that <b>acamprosate</b> may induce antidepressant like effect and that NMDA and <strong>mGlu5</strong> receptors are crucial targets of <b>acamprosate</b> in this action.
+GRM5	drug	alcohol	22432643	Nucleus accumbens <strong>mGluR5</strong> associated signaling regulates binge <b>alcohol</b> drinking under drinking in the dark procedures.
+GRM5	addiction	intoxication	22432643	Nucleus accumbens <strong>mGluR5</strong> associated signaling regulates <b>binge</b> alcohol drinking under drinking in the dark procedures.
+GRM5	drug	alcohol	22432643	Limited access <b>alcohol</b> drinking under DID procedures up regulated NAC shell Homer2 levels, concomitant with increases in <strong>mGluR5</strong> and NR2B.
+GRM5	drug	alcohol	22432643	Intra NAC shell blockade of <strong>mGluR5</strong>, Homer2, or PI3K signaling, as well as transgenic disruption of the Homer binding site on <strong>mGluR5</strong>, decreased <b>alcohol</b> consumption in B6 mice.
+GRM5	drug	amphetamine	22428090	The <strong>mGluR5</strong> Positive Allosteric Modulator CDPPB Does Not Alter Extinction or Contextual Reinstatement of <b>Methamphetamine</b> Seeking Behavior in Rats.
+GRM5	addiction	relapse	22428090	The <strong>mGluR5</strong> Positive Allosteric Modulator CDPPB Does Not Alter Extinction or Contextual <b>Reinstatement</b> of Methamphetamine <b>Seeking</b> Behavior in Rats.
+GRM5	drug	amphetamine	22428090	In this study we investigated the effects of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) positive allosteric modulator (PAM) 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl)benzamide (CDPPB) on the extinction and contextual reinstatement of <b>methamphetamine</b> seeking behavior.
+GRM5	addiction	relapse	22428090	In this study we investigated the effects of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) positive allosteric modulator (PAM) 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl)benzamide (CDPPB) on the extinction and contextual <b>reinstatement</b> of methamphetamine <b>seeking</b> behavior.
+GRM5	drug	amphetamine	22428090	We postulate that numerous factors, including <b>methamphetamine</b> induced changes in <strong>mGluR5</strong> receptor expression or function, may have contributed to the observed lack of effects.
+GRM5	drug	amphetamine	22428090	Although these findings initially suggest that <strong>mGluR5</strong> PAMs may be ineffective in facilitating extinction learning or preventing context induced relapse in <b>methamphetamine</b> addiction, additional studies are warranted examining effects of other <strong>mGluR5</strong> PAMs, particularly those with improved pharmacological properties and devoid of potential side effects at higher doses.
+GRM5	addiction	addiction	22428090	Although these findings initially suggest that <strong>mGluR5</strong> PAMs may be ineffective in facilitating extinction learning or preventing context induced relapse in methamphetamine <b>addiction</b>, additional studies are warranted examining effects of other <strong>mGluR5</strong> PAMs, particularly those with improved pharmacological properties and devoid of potential side effects at higher doses.
+GRM5	addiction	relapse	22428090	Although these findings initially suggest that <strong>mGluR5</strong> PAMs may be ineffective in facilitating extinction learning or preventing context induced <b>relapse</b> in methamphetamine addiction, additional studies are warranted examining effects of other <strong>mGluR5</strong> PAMs, particularly those with improved pharmacological properties and devoid of potential side effects at higher doses.
+GRM5	drug	cocaine	22340009	Role of <strong>mGluR5</strong> neurotransmission in reinstated <b>cocaine</b> seeking.
+GRM5	addiction	relapse	22340009	Role of <strong>mGluR5</strong> neurotransmission in reinstated cocaine <b>seeking</b>.
+GRM5	addiction	addiction	22340009	In animal models of <b>addiction</b>, reducing glutamate stimulation of the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) inhibits drug seeking.
+GRM5	addiction	relapse	22340009	In animal models of addiction, reducing glutamate stimulation of the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) inhibits drug <b>seeking</b>.
+GRM5	drug	cocaine	22340009	The present study used the reinstatement model of <b>cocaine</b> seeking to show that blockade of <strong>mGluR5</strong> directly in the core subcompartment of the nucleus accumbens (NAcore) prevented both conditioned cue  and <b>cocaine</b> reinstated drug seeking.
+GRM5	addiction	relapse	22340009	The present study used the <b>reinstatement</b> model of cocaine <b>seeking</b> to show that blockade of <strong>mGluR5</strong> directly in the core subcompartment of the nucleus accumbens (NAcore) prevented both conditioned cue  and cocaine reinstated drug <b>seeking</b>.
+GRM5	addiction	relapse	22340009	Consistent with this finding, microinjection of the <strong>mGluR5</strong> agonist (RS) 2 chloro 5 hydroxyphenylglycine into the NAcore produced modest <b>reinstatement</b> of lever pressing when given alone and significantly potentiated cue induced <b>reinstatement</b>.
+GRM5	drug	cocaine	22340009	Microinjecting a membrane permeable peptide antagonist of Homer binding to <strong>mGluR5</strong> into the NAcore also inhibited cue  and <b>cocaine</b> reinstated lever pressing.
+GRM5	drug	cocaine	22340009	Taken together, these data show that <strong>mGluR5</strong> inhibition and stimulation in the NAcore can regulate <b>cocaine</b> seeking, and demonstrate that one mechanism for this effect is via interactions with Homer proteins.
+GRM5	addiction	relapse	22340009	Taken together, these data show that <strong>mGluR5</strong> inhibition and stimulation in the NAcore can regulate cocaine <b>seeking</b>, and demonstrate that one mechanism for this effect is via interactions with Homer proteins.
+GRM5	drug	alcohol	22296815	<strong>mGluR5</strong> receptors in the basolateral amygdala and nucleus accumbens regulate cue induced reinstatement of <b>ethanol</b> seeking behavior.
+GRM5	addiction	relapse	22296815	<strong>mGluR5</strong> receptors in the basolateral amygdala and nucleus accumbens regulate cue induced <b>reinstatement</b> of ethanol <b>seeking</b> behavior.
+GRM5	drug	alcohol	22296815	Pharmacological blockade of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) attenuates cue induced reinstatement of <b>ethanol</b> seeking behavior, yet the brain regions involved in these effects are not yet known.
+GRM5	addiction	relapse	22296815	Pharmacological blockade of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) attenuates cue induced <b>reinstatement</b> of ethanol <b>seeking</b> behavior, yet the brain regions involved in these effects are not yet known.
+GRM5	drug	alcohol	22296815	The purpose of the present study was to determine if local blockade of <strong>mGluR5</strong> receptors in the basolateral amygdala (BLA) and/or the nucleus accumbens (NAc), two brain regions known to be involved in stimulus reward associations, attenuate the reinstatement of <b>ethanol</b> seeking behavior induced by <b>ethanol</b> paired cues.
+GRM5	addiction	relapse	22296815	The purpose of the present study was to determine if local blockade of <strong>mGluR5</strong> receptors in the basolateral amygdala (BLA) and/or the nucleus accumbens (NAc), two brain regions known to be involved in stimulus reward associations, attenuate the <b>reinstatement</b> of ethanol <b>seeking</b> behavior induced by ethanol paired cues.
+GRM5	addiction	reward	22296815	The purpose of the present study was to determine if local blockade of <strong>mGluR5</strong> receptors in the basolateral amygdala (BLA) and/or the nucleus accumbens (NAc), two brain regions known to be involved in stimulus <b>reward</b> associations, attenuate the reinstatement of ethanol seeking behavior induced by ethanol paired cues.
+GRM5	addiction	relapse	22296815	As a control for possible non specific effects, the effects of <strong>mGluR5</strong> blockade in these regions on cue induced <b>reinstatement</b> of sucrose <b>seeking</b> were also assessed.
+GRM5	addiction	relapse	22296815	Next, animals received infusions of vehicle or the selective <strong>mGluR5</strong> antagonist MTEP (3 μg/μl) into the BLA or NAc prior to cue induced <b>reinstatement</b> testing sessions.
+GRM5	drug	alcohol	22296815	<strong>mGluR5</strong> blockade eliminated cue induced reinstatement of <b>alcohol</b>   but not sucrose seeking behavior.
+GRM5	addiction	relapse	22296815	<strong>mGluR5</strong> blockade eliminated cue induced <b>reinstatement</b> of alcohol   but not sucrose <b>seeking</b> behavior.
+GRM5	drug	alcohol	22296815	Results from this study indicate that <strong>mGluR5</strong> receptors in the BLA and NAc mediate cue induced reinstatement of <b>ethanol</b> seeking behavior, and provide two potential neuroanatomical sites of action where systemically administered <strong>mGluR5</strong> antagonists attenuate cue induced reinstatement.
+GRM5	addiction	relapse	22296815	Results from this study indicate that <strong>mGluR5</strong> receptors in the BLA and NAc mediate cue induced <b>reinstatement</b> of ethanol <b>seeking</b> behavior, and provide two potential neuroanatomical sites of action where systemically administered <strong>mGluR5</strong> antagonists attenuate cue induced <b>reinstatement</b>.
+GRM5	drug	amphetamine	22193724	RGS4 overexpression in the rat dorsal striatum modulates <strong>mGluR5</strong>  and <b>amphetamine</b> mediated behavior and signaling.
+GRM5	drug	amphetamine	22193724	This study aims to investigate whether RGS4, through inhibiting the function of <strong>mGluR5</strong> receptors in the dorsal striatum (dSTR), regulates cellular and behavioral responses to acute <b>amphetamine</b>.
+GRM5	drug	amphetamine	22193724	The effect of RGS4 overexpression on behavioral activity induced by the intrastriatal <strong>mGluR5</strong> agonist, DHPG, or <b>amphetamine</b> was recorded.
+GRM5	drug	amphetamine	22193724	RGS4 overexpression or the <strong>mGluR5</strong> antagonist, 3 ((2 methyl 4 thiazolyl)ethynyl)pyridine (MTEP), attenuated <b>amphetamine</b> induced phospho ERK (but not phospho Akt) levels.
+GRM5	drug	amphetamine	22193724	The present data demonstrate that RGS4 in the dSTR attenuates <b>amphetamine</b> induced ERK signaling and decreases the behavioral efficacy of acute <b>amphetamine</b> likely by limiting <strong>mGluR5</strong> function.
+GRM5	addiction	reward	22147259	The involvement of metabotropic glutamate 5 (<strong>mGlu5</strong>) receptors has been suggested in the <b>reinforcing</b> effects of psychostimulants.
+GRM5	addiction	withdrawal	22147259	The role of <strong>mGlu5</strong> receptors was assessed in the anhedonic and somatic aspects of psychostimulant <b>withdrawal</b>.
+GRM5	drug	nicotine	22147259	or <b>nicotine</b> (40 mg kg( 1) day( 1), base, 28 days, s.c.) administration via osmotic minipumps in <strong>mGlu5</strong> receptor knockout (mGluR5( / )) and wild type (mGluR5(+/+)) mice.
+GRM5	drug	nicotine	22147259	or <b>nicotine</b> (40 mg kg( 1) day( 1), base, 28 days, s.c.) administration via osmotic minipumps in <strong>mGlu5</strong> receptor knockout (<strong>mGluR5</strong>( / )) and wild type (<strong>mGluR5</strong>(+/+)) mice.
+GRM5	drug	nicotine	22147259	<b>Nicotine</b> treated <strong>mGluR5</strong>(+/+) and <strong>mGluR5</strong>( / ) mice demonstrated similar threshold elevations during mecamylamine precipitated withdrawal compared with their saline treated counterparts.
+GRM5	addiction	withdrawal	22147259	Nicotine treated <strong>mGluR5</strong>(+/+) and <strong>mGluR5</strong>( / ) mice demonstrated similar threshold elevations during mecamylamine precipitated <b>withdrawal</b> compared with their saline treated counterparts.
+GRM5	drug	cocaine	22147259	During spontaneous nicotine and <b>cocaine</b> withdrawal, thresholds in drug withdrawing <strong>mGluR5</strong>(+/+), but not <strong>mGluR5</strong>( / ), mice were elevated up to 72 h of nicotine/<b>cocaine</b> withdrawal and then returned to baseline, indicating attenuation of withdrawal induced anhedonia in <strong>mGluR5</strong>( / ) mice.
+GRM5	drug	nicotine	22147259	During spontaneous <b>nicotine</b> and cocaine withdrawal, thresholds in drug withdrawing <strong>mGluR5</strong>(+/+), but not <strong>mGluR5</strong>( / ), mice were elevated up to 72 h of <b>nicotine</b>/cocaine withdrawal and then returned to baseline, indicating attenuation of withdrawal induced anhedonia in <strong>mGluR5</strong>( / ) mice.
+GRM5	addiction	withdrawal	22147259	During spontaneous nicotine and cocaine <b>withdrawal</b>, thresholds in drug withdrawing <strong>mGluR5</strong>(+/+), but not <strong>mGluR5</strong>( / ), mice were elevated up to 72 h of nicotine/cocaine <b>withdrawal</b> and then returned to baseline, indicating attenuation of <b>withdrawal</b> induced anhedonia in <strong>mGluR5</strong>( / ) mice.
+GRM5	drug	nicotine	22147259	<b>Nicotine</b> withdrawing <strong>mGluR5</strong>(+/+), but not <strong>mGluR5</strong>( / ), mice showed increases in somatic signs compared with saline treated counterparts.
+GRM5	addiction	withdrawal	22147259	<strong>mGlu5</strong> receptor null mutation attenuates the anhedonic and somatic effects of psychostimulant <b>withdrawal</b>.
+GRM5	addiction	withdrawal	22147259	This attenuated <b>withdrawal</b> in mGluR5( / ) mice may result from the lack of drug induced adaptations in <strong>mGlu5</strong> receptor function that may occur in mGluR5(+/+) mice with chronic drug administration.
+GRM5	addiction	withdrawal	22147259	This attenuated <b>withdrawal</b> in <strong>mGluR5</strong>( / ) mice may result from the lack of drug induced adaptations in <strong>mGlu5</strong> receptor function that may occur in <strong>mGluR5</strong>(+/+) mice with chronic drug administration.
+GRM5	addiction	dependence	22147259	Thus, these results suggest the involvement of <strong>mGlu5</strong> receptors in psychostimulant <b>dependence</b> and the mediation of the anhedonic and somatic signs of psychostimulant withdrawal.
+GRM5	addiction	withdrawal	22147259	Thus, these results suggest the involvement of <strong>mGlu5</strong> receptors in psychostimulant dependence and the mediation of the anhedonic and somatic signs of psychostimulant <b>withdrawal</b>.
+GRM5	drug	cocaine	22147256	Evidence suggests that Group I metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) is necessary for <b>cocaine</b> sensitization, and stimulation of this receptor in the mPFC potentially alters cell excitability directly through glutamate release or indirectly through downstream signaling cascades.
+GRM5	addiction	sensitization	22147256	Evidence suggests that Group I metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) is necessary for cocaine <b>sensitization</b>, and stimulation of this receptor in the mPFC potentially alters cell excitability directly through glutamate release or indirectly through downstream signaling cascades.
+GRM5	drug	cocaine	22147256	Experiments in this report examined the role of mPFC <strong>mGluR5</strong> in behavioral sensitization to <b>cocaine</b>.
+GRM5	addiction	sensitization	22147256	Experiments in this report examined the role of mPFC <strong>mGluR5</strong> in behavioral <b>sensitization</b> to cocaine.
+GRM5	drug	cocaine	22147256	Intra mPFC DHPG induced an <strong>mGluR5</strong> mediated cross sensitization to <b>cocaine</b> preventable through the prior administration of an AMPA receptor antagonist in the VTA.
+GRM5	addiction	sensitization	22147256	Intra mPFC DHPG induced an <strong>mGluR5</strong> mediated cross <b>sensitization</b> to cocaine preventable through the prior administration of an AMPA receptor antagonist in the VTA.
+GRM5	addiction	sensitization	22147256	Furthermore, <strong>mGluR5</strong> blockade in the mPFC failed to prevent the initiation of <b>sensitization</b>.
+GRM5	drug	cocaine	22147256	However, intra mPFC injections of the <strong>mGluR5</strong> antagonist MTEP prevented the expression of <b>cocaine</b> sensitization at 21, but not 7, days following daily <b>cocaine</b> injections suggesting a possible role for mPFC <strong>mGluR5</strong> in the persistence of the <b>cocaine</b> sensitized state.
+GRM5	addiction	sensitization	22147256	However, intra mPFC injections of the <strong>mGluR5</strong> antagonist MTEP prevented the expression of cocaine <b>sensitization</b> at 21, but not 7, days following daily cocaine injections suggesting a possible role for mPFC <strong>mGluR5</strong> in the persistence of the cocaine sensitized state.
+GRM5	drug	alcohol	22140596	In this study, we used a PCR array containing 46 primer pairs of selected genes to compare mRNA expression in the spleen, an immune system organ, of adolescent rats following binge drinking of <b>alcohol</b> solutions containing either 20% or 52% <b>ethanol</b> (v/v, 4.8 g/kg daily dosage), or water (control) for 3 d. We found that, expression of IL 1β, IL 6, CCL2, and GABA(A) receptor α2 subunit in the spleen were decreased, and <strong>mGluR5</strong> and 5 HT3A receptor expression were increased after administration of an <b>ethanol</b> solution containing 52% <b>ethanol</b>, but not one with 20% <b>ethanol</b>.
+GRM5	addiction	intoxication	22140596	In this study, we used a PCR array containing 46 primer pairs of selected genes to compare mRNA expression in the spleen, an immune system organ, of adolescent rats following <b>binge</b> drinking of alcohol solutions containing either 20% or 52% ethanol (v/v, 4.8 g/kg daily dosage), or water (control) for 3 d. We found that, expression of IL 1β, IL 6, CCL2, and GABA(A) receptor α2 subunit in the spleen were decreased, and <strong>mGluR5</strong> and 5 HT3A receptor expression were increased after administration of an ethanol solution containing 52% ethanol, but not one with 20% ethanol.
+GRM5	drug	amphetamine	22139452	Impact of <strong>mGluR5</strong> during <b>amphetamine</b> induced hyperactivity and conditioned hyperactivity in differentially reared rats.
+GRM5	addiction	reward	22139452	3 ((2 Methyl 1,3 thiazol 4 yl)ethynyl)pyridine hydrochloride (MTEP) is a metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonist that may alter drug sensitivity in differentially reared rats due to its involvement in the psychostimulant <b>reward</b> pathway and plasticity.
+GRM5	addiction	relapse	22137594	Here, we examine the effects of NAC applied directly to the NAcore on <b>relapse</b> and neurotransmission in PFC NAcore synapses, as well as the involvement of the metabotropic glutamate receptors 2/3 (mGluR2/3) and 5 (<strong>mGluR5</strong>).
+GRM5	drug	cocaine	22137594	Finally, we showed that by blocking <strong>mGluR5</strong> the inhibition of <b>cocaine</b> seeking by NAC was potentiated.
+GRM5	addiction	relapse	22137594	Finally, we showed that by blocking <strong>mGluR5</strong> the inhibition of cocaine <b>seeking</b> by NAC was potentiated.
+GRM5	drug	cocaine	22137594	The effect of NAC on relapse to <b>cocaine</b> seeking depends on the balance between stimulating mGluR2/3 and <strong>mGluR5</strong> in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting <strong>mGluR5</strong>.
+GRM5	addiction	relapse	22137594	The effect of NAC on <b>relapse</b> to cocaine <b>seeking</b> depends on the balance between stimulating mGluR2/3 and <strong>mGluR5</strong> in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting <strong>mGluR5</strong>.
+GRM5	addiction	relapse	22129842	The <strong>mGlu5</strong> receptor antagonist MTEP attenuates opiate self administration and cue induced opiate <b>seeking</b> behaviour in mice.
+GRM5	addiction	relapse	22129842	The <strong>mGlu5</strong> receptor (mGluR5) has been implicated in the rewarding effect of various drugs of abuse and drug <b>seeking</b> behaviour.
+GRM5	addiction	relapse	22129842	The <strong>mGlu5</strong> receptor (<strong>mGluR5</strong>) has been implicated in the rewarding effect of various drugs of abuse and drug <b>seeking</b> behaviour.
+GRM5	drug	opioid	22129842	In the present study we investigated the impact of antagonism of <strong>mGluR5</strong> with the selective negative allosteric, modulator 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]pyridine (MTEP) on operant self administration of <b>morphine</b> as well as cue induced drug seeking in adult CD1 mice.
+GRM5	addiction	relapse	22129842	In the present study we investigated the impact of antagonism of <strong>mGluR5</strong> with the selective negative allosteric, modulator 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]pyridine (MTEP) on operant self administration of morphine as well as cue induced drug <b>seeking</b> in adult CD1 mice.
+GRM5	addiction	reward	22129842	In the present study we investigated the impact of antagonism of <strong>mGluR5</strong> with the selective negative allosteric, modulator 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]pyridine (MTEP) on <b>operant</b> self administration of morphine as well as cue induced drug seeking in adult CD1 mice.
+GRM5	addiction	addiction	22129842	Collectively, these data implicate <strong>mGluR5</strong> in the reinforcing effects of opiates and support the proposition that <strong>mGluR5</strong> is a potential therapeutic target for treatment of drug <b>addiction</b>.
+GRM5	addiction	reward	22129842	Collectively, these data implicate <strong>mGluR5</strong> in the <b>reinforcing</b> effects of opiates and support the proposition that <strong>mGluR5</strong> is a potential therapeutic target for treatment of drug addiction.
+GRM5	drug	cocaine	21994370	Interestingly, the effect of DHPG in the <b>cocaine</b> group was mediated by mGluR1 whereas its effect in the saline group was mediated by <strong>mGluR5</strong>.
+GRM5	drug	opioid	21971021	The present study examined the effects of the mGluR1 antagonist JNJ16259685 (JNJ) and the <strong>mGluR5</strong> antagonist 2 methyl 6 phenylethynylpyridine (MPEP) alone and in combination with <b>morphine</b> in two acute pain models (hotplate, warm water tail withdrawal), and a persistent, inflammatory pain model (capsaicin).
+GRM5	addiction	withdrawal	21971021	The present study examined the effects of the mGluR1 antagonist JNJ16259685 (JNJ) and the <strong>mGluR5</strong> antagonist 2 methyl 6 phenylethynylpyridine (MPEP) alone and in combination with morphine in two acute pain models (hotplate, warm water tail <b>withdrawal</b>), and a persistent, inflammatory pain model (capsaicin).
+GRM5	drug	opioid	21971021	The present findings suggest that the effects produced by mGluR1 and <strong>mGluR5</strong> antagonists alone and in combination with <b>morphine</b> can be differentiated in models of both acute and persistent pain.
+GRM5	drug	alcohol	21946112	The objective of the present study was to evaluate the effects of a selective <strong>mGlu5</strong> receptors antagonist  MTEP, and mGlu1 receptors antagonist  EMQMCM, on two processes relevant to <b>alcohol</b> addiction: the expression of <b>ethanol</b> induced conditioned place preference (CPP) paradigm, and <b>ethanol</b> withdrawal audiogenic seizures in rats.
+GRM5	addiction	addiction	21946112	The objective of the present study was to evaluate the effects of a selective <strong>mGlu5</strong> receptors antagonist  MTEP, and mGlu1 receptors antagonist  EMQMCM, on two processes relevant to alcohol <b>addiction</b>: the expression of ethanol induced conditioned place preference (CPP) paradigm, and ethanol withdrawal audiogenic seizures in rats.
+GRM5	addiction	reward	21946112	The objective of the present study was to evaluate the effects of a selective <strong>mGlu5</strong> receptors antagonist  MTEP, and mGlu1 receptors antagonist  EMQMCM, on two processes relevant to alcohol addiction: the expression of ethanol induced conditioned place preference (<b>CPP</b>) paradigm, and ethanol withdrawal audiogenic seizures in rats.
+GRM5	addiction	withdrawal	21946112	The objective of the present study was to evaluate the effects of a selective <strong>mGlu5</strong> receptors antagonist  MTEP, and mGlu1 receptors antagonist  EMQMCM, on two processes relevant to alcohol addiction: the expression of ethanol induced conditioned place preference (CPP) paradigm, and ethanol <b>withdrawal</b> audiogenic seizures in rats.
+GRM5	drug	alcohol	21946112	Our study shows the importance of <strong>mGlu5</strong> and mGlu1 receptors for the expression of <b>ethanol</b> induced CPP and withdrawal seizures, although <strong>mGlu5</strong> receptors antagonist (MTEP) was more potent than the antagonist of mGlu1 receptors (EMQMCM).
+GRM5	addiction	reward	21946112	Our study shows the importance of <strong>mGlu5</strong> and mGlu1 receptors for the expression of ethanol induced <b>CPP</b> and withdrawal seizures, although <strong>mGlu5</strong> receptors antagonist (MTEP) was more potent than the antagonist of mGlu1 receptors (EMQMCM).
+GRM5	addiction	withdrawal	21946112	Our study shows the importance of <strong>mGlu5</strong> and mGlu1 receptors for the expression of ethanol induced CPP and <b>withdrawal</b> seizures, although <strong>mGlu5</strong> receptors antagonist (MTEP) was more potent than the antagonist of mGlu1 receptors (EMQMCM).
+GRM5	drug	nicotine	21896278	Systemic administration of the <strong>mGlu5</strong> receptor antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) was previously shown to selectively attenuate <b>nicotine</b> self administration without affecting food maintained responding in rats.
+GRM5	drug	nicotine	21896278	This lack of effect of 40 μg/0.5 μl/side MPEP on either <b>nicotine</b> or food self administration when administered into the VTA may be attributable either to actions of MPEP at presynaptic <strong>mGlu5</strong> receptors or at targets other than <strong>mGlu5</strong> receptors.
+GRM5	drug	nicotine	21896278	In conclusion, MPEP microinfusions in the VTA or NAcc shell attenuates the reinforcing effects of <b>nicotine</b> possibly via blockade of <strong>mGlu5</strong> receptors located in these regions.
+GRM5	addiction	reward	21896278	In conclusion, MPEP microinfusions in the VTA or NAcc shell attenuates the <b>reinforcing</b> effects of nicotine possibly via blockade of <strong>mGlu5</strong> receptors located in these regions.
+GRM5	drug	amphetamine	21836462	Discriminative stimulus effects of NMDA, AMPA, and <strong>mGluR5</strong> glutamate receptor ligands in <b>methamphetamine</b> trained rats.
+GRM5	drug	cocaine	21816123	<strong>mGlu5</strong> and adenosine A2A receptor interactions regulate the conditioned effects of <b>cocaine</b>.
+GRM5	addiction	relapse	21816123	Adenosine A2A receptors and metabotropic glutamate type 5 (<strong>mGlu5</strong>) receptors are co localized in the striatum and can functionally interact to regulate drug <b>seeking</b>.
+GRM5	drug	cocaine	21816123	These data provide evidence for a functional interaction between adenosine A2A and <strong>mGlu5</strong> receptors in mediating the conditioned effects of <b>cocaine</b> but not direct <b>cocaine</b> induced hyperactivity.
+GRM5	drug	cocaine	21790902	The present study was designed to examine whether antagonizing <strong>mGluR5</strong> or activating mGluR2/3 prevents stress induced reinstatement of <b>cocaine</b> seeking.
+GRM5	addiction	relapse	21790902	The present study was designed to examine whether antagonizing <strong>mGluR5</strong> or activating mGluR2/3 prevents stress induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM5	drug	cocaine	21790902	Both the selective <strong>mGluR5</strong> antagonist 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]piperidine (MTEP) (0 3 mg/kg, intraperitoneally) and the selective mGluR2/3 agonist ( ) 2 oxa 4 aminobicylco[3.1.0]hexane 4,6 dicarboxylic acid (LY379268) (0 3 mg/kg, subcutaneously) prevented <b>cocaine</b> seeking induced by footshock stress following the same dose response function.
+GRM5	addiction	relapse	21790902	Both the selective <strong>mGluR5</strong> antagonist 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]piperidine (MTEP) (0 3 mg/kg, intraperitoneally) and the selective mGluR2/3 agonist ( ) 2 oxa 4 aminobicylco[3.1.0]hexane 4,6 dicarboxylic acid (LY379268) (0 3 mg/kg, subcutaneously) prevented cocaine <b>seeking</b> induced by footshock stress following the same dose response function.
+GRM5	addiction	relapse	21790902	The data show that although mGluR2/3 and <strong>mGluR5</strong> are differentially located on synaptic compartments, both LY379268 and MTEP produced the same behavioral effects in reducing stress induced <b>reinstatement</b>.
+GRM5	addiction	relapse	21790902	These results are important because they demonstrate that a reduction in glutamate mediated neural excitability (albeit via different mechanisms of action) reverses footshock induced <b>reinstatement</b> and suggest that pharmacological manipulations of mGluR2/3 and <strong>mGluR5</strong> can prevent the effects of stress, a major precipitating factor for <b>relapse</b>.
+GRM5	addiction	relapse	21790902	These findings further confirm that mGluR2/3 or <strong>mGluR5</strong> are promising targets for <b>relapse</b> prevention.
+GRM5	drug	alcohol	21790901	Studies have indicated that the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonist 6 methyl 2 (phenylethynyl) pyridine (MPEP) decreases <b>ethanol</b> self administration, and the same receptor type was also suggested to be involved in the mechanism of action of the anti craving substance <b>acamprosate</b>.
+GRM5	addiction	relapse	21790901	Studies have indicated that the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonist 6 methyl 2 (phenylethynyl) pyridine (MPEP) decreases ethanol self administration, and the same receptor type was also suggested to be involved in the mechanism of action of the anti <b>craving</b> substance acamprosate.
+GRM5	drug	amphetamine	21780181	Brain region selective cellular redistribution of <strong>mGlu5</strong> but not GABA(B) receptors following <b>methamphetamine</b> induced associative learning.
+GRM5	addiction	relapse	21780181	Metabotropic glutamate receptor group I, subtype 5 (<strong>mGluR5</strong>) and GABA(B) receptors (GABA(B) R) are critically involved in the development and expression of stimulant induced behaviors, including conditioned place preference (CPP), an index of drug <b>seeking</b>.
+GRM5	addiction	reward	21780181	Metabotropic glutamate receptor group I, subtype 5 (<strong>mGluR5</strong>) and GABA(B) receptors (GABA(B) R) are critically involved in the development and expression of stimulant induced behaviors, including conditioned place preference (<b>CPP</b>), an index of drug seeking.
+GRM5	drug	amphetamine	21780181	There was a decrease in the surface to intracellular ratio of <strong>mGluR5</strong> in the mPFC in <b>Meth</b> conditioned rats, commensurate with an increase in intracellular levels.
+GRM5	drug	amphetamine	21780181	The results suggest that this <b>Meth</b> treatment paradigm likely induced a compensatory change in <strong>mGluR5</strong> surface to intracellular ratio such that the surface remains unaltered while an increase in intracellular protein occurred.
+GRM5	drug	cocaine	21749491	mGluR1, but not <strong>mGluR5</strong>, agonist induced long term potentiation (mGluR1 LTP) in the BLA CeLc pathway was reduced in rats withdrawal from <b>cocaine</b> for 2 and 14 days, and exhibited an altered concentration response to picrotoxin.
+GRM5	addiction	withdrawal	21749491	mGluR1, but not <strong>mGluR5</strong>, agonist induced long term potentiation (mGluR1 LTP) in the BLA CeLc pathway was reduced in rats <b>withdrawal</b> from cocaine for 2 and 14 days, and exhibited an altered concentration response to picrotoxin.
+GRM5	drug	cocaine	21749491	However, CB(1) and CB(2) protein levels were increased in the amygdala of <b>cocaine</b> withdrawn rats while mGluR1 and <strong>mGluR5</strong> remained unchanged.
+GRM5	drug	cocaine	21411660	These results suggest that withdrawal from repeated <b>cocaine</b> exposure may result in increased BDNF levels in the NAc shell, which leads to a selective downregulation of <strong>mGluR5</strong> and thereby impairs the induction of mGluR dependent LTD.
+GRM5	addiction	withdrawal	21411660	These results suggest that <b>withdrawal</b> from repeated cocaine exposure may result in increased BDNF levels in the NAc shell, which leads to a selective downregulation of <strong>mGluR5</strong> and thereby impairs the induction of mGluR dependent LTD.
+GRM5	drug	cocaine	21319882	<strong>mGluR5</strong> positive allosteric modulation enhances extinction learning following <b>cocaine</b> self administration.
+GRM5	drug	cocaine	21319882	In this study, the authors investigated the effects of the Type 5 metabotropic glutamate receptors (<strong>mGluR5</strong>) positive allosteric modulator 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl)benzamide (CDPPB) on the extinction of <b>cocaine</b> seeking behavior in rats with a history of intravenous <b>cocaine</b> self administration.
+GRM5	addiction	relapse	21319882	In this study, the authors investigated the effects of the Type 5 metabotropic glutamate receptors (<strong>mGluR5</strong>) positive allosteric modulator 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl)benzamide (CDPPB) on the extinction of cocaine <b>seeking</b> behavior in rats with a history of intravenous cocaine self administration.
+GRM5	drug	cocaine	21319882	These data indicate that positive allosteric modulation of <strong>mGluR5</strong> receptors facilitates the acquisition and consolidation of extinction learning following <b>cocaine</b> self administration and may provide a novel pharmacological approach to enhancing extinction learning when combined with cue exposure therapy for the treatment of <b>cocaine</b> addiction.
+GRM5	addiction	addiction	21319882	These data indicate that positive allosteric modulation of <strong>mGluR5</strong> receptors facilitates the acquisition and consolidation of extinction learning following cocaine self administration and may provide a novel pharmacological approach to enhancing extinction learning when combined with cue exposure therapy for the treatment of cocaine <b>addiction</b>.
+GRM5	drug	nicotine	21216262	The effects of the <strong>mGluR5</strong> receptor antagonist 6 methyl 2 (phenylethynyl) pyridine (MPEP) on the stimulation of dopamine release evoked by <b>nicotine</b> in the rat brain.
+GRM5	drug	nicotine	21216262	Previous studies have shown that the prior administration of metabotropic glutamate receptor 5 (<strong>MGluR5</strong>) receptor antagonists inhibit responding for <b>nicotine</b> in an intravenous self administration experiment.
+GRM5	drug	nicotine	21216262	However, recent studies in this laboratory have shown that an <strong>mGluR5</strong> receptor antagonist, MPEP (2 methyl 6 (phenylethynyl) pyridine), also attenuates contextually conditioned responding evoked by cues associated with the delivery or availability of <b>nicotine</b>.
+GRM5	drug	nicotine	21216262	Thus, the results to date do not provide unequivocal evidence that the effects of <strong>mGluR5</strong> receptor antagonists on responding for <b>nicotine</b> reflect a direct functional interaction between the antagonists and <b>nicotine</b> per se.
+GRM5	drug	nicotine	21216262	This study employed in vivo microdialysis to test the hypothesis that the prior administration of the <strong>mGluR5</strong> receptor antagonist, MPEP, inhibits a neural response to <b>nicotine</b>, increased dopamine (DA) overflow in the nucleus accumbens, implicated in directly in <b>nicotine</b> reinforcement.
+GRM5	addiction	reward	21216262	This study employed in vivo microdialysis to test the hypothesis that the prior administration of the <strong>mGluR5</strong> receptor antagonist, MPEP, inhibits a neural response to nicotine, increased dopamine (DA) overflow in the nucleus accumbens, implicated in directly in nicotine <b>reinforcement</b>.
+GRM5	drug	nicotine	21216262	It is concluded that the data support the hypothesis that, in addition to their putative role in contextually conditioned responding for <b>nicotine</b>, <strong>mGluR5</strong> receptors are also implicated the primary reinforcing properties of the drug which depend upon increased DA overflow in the nucleus accumbens.
+GRM5	addiction	reward	21216262	It is concluded that the data support the hypothesis that, in addition to their putative role in contextually conditioned responding for nicotine, <strong>mGluR5</strong> receptors are also implicated the primary <b>reinforcing</b> properties of the drug which depend upon increased DA overflow in the nucleus accumbens.
+GRM5	drug	opioid	21172339	The present study was conducted to evaluate the influence of the glutamatergic receptors α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA) and metabotropic glutamate 5 (<strong>mGlu5</strong>) receptors on sensitization to the rewarding effects of <b>morphine</b>.
+GRM5	addiction	sensitization	21172339	The present study was conducted to evaluate the influence of the glutamatergic receptors α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA) and metabotropic glutamate 5 (<strong>mGlu5</strong>) receptors on <b>sensitization</b> to the rewarding effects of morphine.
+GRM5	addiction	relapse	21152045	Operant sensation <b>seeking</b> requires metabotropic glutamate receptor 5 (<strong>mGluR5</strong>).
+GRM5	addiction	reward	21152045	<b>Operant</b> sensation seeking requires metabotropic glutamate receptor 5 (<strong>mGluR5</strong>).
+GRM5	addiction	reward	21152045	Pharmacological and genetic studies have suggested that the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) is critically involved in mediating the <b>reinforcing</b> effects of drugs of abuse, but not food.
+GRM5	addiction	relapse	21152045	The purpose of this study was to use <strong>mGluR5</strong> knockout (KO), heterozygous (Het), and wildtype (WT) mice to determine if <strong>mGluR5</strong> modulates operant sensation <b>seeking</b> (OSS), an operant task that uses varied sensory stimuli as a reinforcer.
+GRM5	addiction	reward	21152045	The purpose of this study was to use <strong>mGluR5</strong> knockout (KO), heterozygous (Het), and wildtype (WT) mice to determine if <strong>mGluR5</strong> modulates <b>operant</b> sensation seeking (OSS), an <b>operant</b> task that uses varied sensory stimuli as a reinforcer.
+GRM5	drug	cocaine	21152045	Further, we assessed <strong>mGluR5</strong> KO, Het and WT mice across a battery of <b>cocaine</b> locomotor, place preference and anxiety related tests.
+GRM5	addiction	reward	21152045	In total, these data demonstrate a key role for <strong>mGluR5</strong> in OSS, indicating an important role for this receptor in <b>reinforcement</b> based behavior.
+GRM5	drug	amphetamine	21150906	Here, we utilized a long access <b>meth</b> self administration (SA) protocol to assess recognition memory and metabotropic glutamate receptor (mGluR) expression, and the possible reversal of cognitive impairments with the <strong>mGluR5</strong> allosteric modulator, 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl) benzamide (CDPPB).
+GRM5	drug	amphetamine	21150906	On day 8, <b>meth</b> intake during SA negatively correlated with mGluR expression in the perirhinal and prefrontal cortex, and <strong>mGluR5</strong> receptor expression was decreased 14 days after discontinuation of <b>meth</b>.
+GRM5	drug	amphetamine	21150906	These results from a clinically relevant animal model of addiction suggest that <strong>mGluR5</strong> receptor modulation may be a potential treatment of cognitive dysfunction in <b>meth</b> addiction.
+GRM5	addiction	addiction	21150906	These results from a clinically relevant animal model of <b>addiction</b> suggest that <strong>mGluR5</strong> receptor modulation may be a potential treatment of cognitive dysfunction in meth <b>addiction</b>.
+GRM5	drug	cocaine	21120457	Dissociable roles of <strong>mGlu5</strong> and dopamine receptors in the rewarding and sensitizing properties of morphine and <b>cocaine</b>.
+GRM5	drug	opioid	21120457	Dissociable roles of <strong>mGlu5</strong> and dopamine receptors in the rewarding and sensitizing properties of <b>morphine</b> and cocaine.
+GRM5	addiction	reward	21120457	Recent studies have implicated the metabotropic glutamate receptor 5 (<strong>mGlu5</strong> receptor) in drug <b>reward</b>, but its role in sensitization is unclear.
+GRM5	addiction	sensitization	21120457	Recent studies have implicated the metabotropic glutamate receptor 5 (<strong>mGlu5</strong> receptor) in drug reward, but its role in <b>sensitization</b> is unclear.
+GRM5	drug	cocaine	21120457	This study aims to evaluate the role of <strong>mGlu5</strong> and dopamine receptors in the development of <b>cocaine</b>  and morphine induced conditioned place preference (CPP) and psychomotor sensitization.
+GRM5	drug	opioid	21120457	This study aims to evaluate the role of <strong>mGlu5</strong> and dopamine receptors in the development of cocaine  and <b>morphine</b> induced conditioned place preference (CPP) and psychomotor sensitization.
+GRM5	addiction	reward	21120457	This study aims to evaluate the role of <strong>mGlu5</strong> and dopamine receptors in the development of cocaine  and morphine induced conditioned place preference (<b>CPP</b>) and psychomotor sensitization.
+GRM5	addiction	sensitization	21120457	This study aims to evaluate the role of <strong>mGlu5</strong> and dopamine receptors in the development of cocaine  and morphine induced conditioned place preference (CPP) and psychomotor <b>sensitization</b>.
+GRM5	addiction	reward	21120457	In contrast, the role of <strong>mGlu5</strong> receptors in <b>reward</b> and sensitization is drug specific.
+GRM5	addiction	sensitization	21120457	In contrast, the role of <strong>mGlu5</strong> receptors in reward and <b>sensitization</b> is drug specific.
+GRM5	drug	opioid	20878582	This conference report highlights selected presentations on negative allosteric modulators of metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) for the treatment of Parkinson's disease, BACE1 inhibitors and γ secretase inhibitors for the prevention or treatment of Alzheimer's disease, <b>opioid</b> modulators for the treatment of reward disorders, SGLT2 inhibitors for the treatment of diabetes, backup compounds to the DPP 4 inhibitor sitagliptin (Januvia) for type 2 diabetes, and MCH R1 inhibitors for the treatment of obesity.
+GRM5	addiction	reward	20878582	This conference report highlights selected presentations on negative allosteric modulators of metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) for the treatment of Parkinson's disease, BACE1 inhibitors and γ secretase inhibitors for the prevention or treatment of Alzheimer's disease, opioid modulators for the treatment of <b>reward</b> disorders, SGLT2 inhibitors for the treatment of diabetes, backup compounds to the DPP 4 inhibitor sitagliptin (Januvia) for type 2 diabetes, and MCH R1 inhibitors for the treatment of obesity.
+GRM5	drug	cocaine	20826661	Incentive learning underlying <b>cocaine</b> seeking requires <strong>mGluR5</strong> receptors located on dopamine D1 receptor expressing neurons.
+GRM5	addiction	relapse	20826661	Incentive learning underlying cocaine <b>seeking</b> requires <strong>mGluR5</strong> receptors located on dopamine D1 receptor expressing neurons.
+GRM5	addiction	reward	20826661	<b>Incentive</b> learning underlying cocaine seeking requires <strong>mGluR5</strong> receptors located on dopamine D1 receptor expressing neurons.
+GRM5	addiction	relapse	20826661	The metabotropic glutamate receptor, <strong>mGluR5</strong>, is potentially important in this respect; it plays a central role in several forms of striatal synaptic plasticity proposed to underpin associative learning and memory processes that enable drug paired stimuli to acquire incentive motivational properties and trigger <b>relapse</b>.
+GRM5	addiction	reward	20826661	The metabotropic glutamate receptor, <strong>mGluR5</strong>, is potentially important in this respect; it plays a central role in several forms of striatal synaptic plasticity proposed to underpin associative learning and memory processes that enable drug paired stimuli to acquire <b>incentive</b> motivational properties and trigger relapse.
+GRM5	drug	cocaine	20826661	Our findings show that glutamate signaling through <strong>mGluR5</strong> located on dopamine D1 receptor expressing neurons is necessary for incentive learning processes that contribute to cue induced reinstatement of <b>cocaine</b> seeking and which may underpin relapse in drug addiction.
+GRM5	addiction	addiction	20826661	Our findings show that glutamate signaling through <strong>mGluR5</strong> located on dopamine D1 receptor expressing neurons is necessary for incentive learning processes that contribute to cue induced reinstatement of cocaine seeking and which may underpin relapse in drug <b>addiction</b>.
+GRM5	addiction	relapse	20826661	Our findings show that glutamate signaling through <strong>mGluR5</strong> located on dopamine D1 receptor expressing neurons is necessary for incentive learning processes that contribute to cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and which may underpin <b>relapse</b> in drug addiction.
+GRM5	addiction	reward	20826661	Our findings show that glutamate signaling through <strong>mGluR5</strong> located on dopamine D1 receptor expressing neurons is necessary for <b>incentive</b> learning processes that contribute to cue induced reinstatement of cocaine seeking and which may underpin relapse in drug addiction.
+GRM5	drug	cannabinoid	20632967	In addition to dopamine receptors, the induction and expression of plasticity mechanisms is regulated by other GPCRs, most importantly adenosine A₂(A) receptors, metabotropic glutamate <strong>mGluR5</strong> receptors and <b>endocannabinoid</b> CB1 receptors.
+GRM5	addiction	addiction	20579001	The <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) potentiates conditioned place preference induced by various <b>addictive</b> and non <b>addictive</b> drugs in rats.
+GRM5	drug	amphetamine	20498134	Blockade of <strong>mGLUR5</strong> receptors differentially alters <b>amphetamine</b> induced enhancement of locomotor activity and of brain stimulation reward.
+GRM5	addiction	reward	20498134	Blockade of <strong>mGLUR5</strong> receptors differentially alters amphetamine induced enhancement of locomotor activity and of brain stimulation <b>reward</b>.
+GRM5	drug	amphetamine	20498134	This study was aimed at determining the role of <strong>mGLUR5</strong> glutamate receptors on <b>amphetamine</b> induced enhancement of locomotion and of brain stimulation reward (BSR).
+GRM5	addiction	reward	20498134	This study was aimed at determining the role of <strong>mGLUR5</strong> glutamate receptors on amphetamine induced enhancement of locomotion and of brain stimulation <b>reward</b> (BSR).
+GRM5	drug	amphetamine	20498134	These findings show that <strong>mGLUR5</strong> glutamate receptors are unlikely to constitute important elements of the reward relevant pathway, and do not intervene in the enhancement effect of <b>amphetamine</b>.
+GRM5	addiction	reward	20498134	These findings show that <strong>mGLUR5</strong> glutamate receptors are unlikely to constitute important elements of the <b>reward</b> relevant pathway, and do not intervene in the enhancement effect of amphetamine.
+GRM5	drug	nicotine	20422403	The effects of the <strong>mGluR5</strong> receptor antagonist 6 methyl 2 (phenylethynyl) pyridine (MPEP) on behavioural responses to <b>nicotine</b>.
+GRM5	drug	nicotine	20422403	Previous studies have shown that blockade of metabotropic glutamate 5 receptors (<strong>mGluR5</strong>) results in inhibition of <b>nicotine</b> self administration in experimental animals.
+GRM5	drug	nicotine	20422403	However, these studies have not established the behavioural mechanisms which mediate these effects or the extent to which the effects of <strong>mGluR5</strong> antagonism on <b>nicotine</b> self administration reflect a selective attenuation of <b>nicotine</b> reinforcement.
+GRM5	addiction	reward	20422403	However, these studies have not established the behavioural mechanisms which mediate these effects or the extent to which the effects of <strong>mGluR5</strong> antagonism on nicotine self administration reflect a selective attenuation of nicotine <b>reinforcement</b>.
+GRM5	drug	nicotine	20422403	To investigate the effects of antagonising <strong>mGluR5</strong> receptors on psychopharmacological responses to <b>nicotine</b> measured using conditioned and unconditioned behaviours.
+GRM5	drug	nicotine	20422403	The results are consistent with the hypothesis that <strong>mGluR5</strong> receptors play an important role in mediating the effects of contextual cues in conditioned behavioural responses to <b>nicotine</b>.
+GRM5	drug	cocaine	20416862	Rats with 1 hour daily <b>cocaine</b> access (short access [ShA]) versus 6 hour access (long access [LgA]) were tested for differences in the effects of the metabotropic glutamate receptor 2/3 (mGluR2/3) agonist ( ) 2 oxa 4 aminobicylco(3.1.0)hexane 4,6 dicarboxylic acid (LY379268) and the metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonist 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine (MTEP) on <b>cocaine</b> reinforced progressive ratio responding and differences in expression levels and functional activity of mGluR2/3 and <strong>mGluR5</strong>.
+GRM5	drug	cocaine	20416862	Long access <b>cocaine</b> exposure was associated with decreased <strong>mGluR5</strong> expression, accompanied by reduced functional <strong>mGluR5</strong> activity in the nucleus accumbens.
+GRM5	drug	cocaine	20416862	Functional upregulation of mGluR2/3 and downregulation of <strong>mGluR5</strong> are likely factors in the transition to <b>cocaine</b> dependence.
+GRM5	addiction	dependence	20416862	Functional upregulation of mGluR2/3 and downregulation of <strong>mGluR5</strong> are likely factors in the transition to cocaine <b>dependence</b>.
+GRM5	drug	cocaine	20416862	The differential behavioral effects of LY379268 and MTEP in rats with a history of long access to <b>cocaine</b> have implications for the treatment target potential of mGluR2/3 and <strong>mGluR5</strong>.
+GRM5	drug	alcohol	20189165	Effects of the mGlu2/3 agonist LY379268 and the <strong>mGlu5</strong> antagonist MTEP on <b>ethanol</b> seeking and reinforcement are differentially altered in rats with a history of <b>ethanol</b> dependence.
+GRM5	addiction	dependence	20189165	Effects of the mGlu2/3 agonist LY379268 and the <strong>mGlu5</strong> antagonist MTEP on ethanol seeking and reinforcement are differentially altered in rats with a history of ethanol <b>dependence</b>.
+GRM5	addiction	relapse	20189165	Effects of the mGlu2/3 agonist LY379268 and the <strong>mGlu5</strong> antagonist MTEP on ethanol <b>seeking</b> and reinforcement are differentially altered in rats with a history of ethanol dependence.
+GRM5	addiction	reward	20189165	Effects of the mGlu2/3 agonist LY379268 and the <strong>mGlu5</strong> antagonist MTEP on ethanol seeking and <b>reinforcement</b> are differentially altered in rats with a history of ethanol dependence.
+GRM5	drug	alcohol	20189165	To extend the understanding of the role of mGluRs in the addiction relevant effects of <b>ethanol</b> as well as of the treatment target potential of these receptors for <b>alcohol</b> abuse, the effects of a selective mGlu2/3 agonist (LY379268) and a selective <strong>mGlu5</strong> antagonist (MTEP) were tested on two processes central to <b>alcohol</b> addiction: <b>ethanol</b> reinforcement and stress induced reinstatement of <b>ethanol</b> seeking in rats with a history of <b>ethanol</b> dependence.
+GRM5	addiction	addiction	20189165	To extend the understanding of the role of mGluRs in the <b>addiction</b> relevant effects of ethanol as well as of the treatment target potential of these receptors for alcohol abuse, the effects of a selective mGlu2/3 agonist (LY379268) and a selective <strong>mGlu5</strong> antagonist (MTEP) were tested on two processes central to alcohol <b>addiction</b>: ethanol reinforcement and stress induced reinstatement of ethanol seeking in rats with a history of ethanol dependence.
+GRM5	addiction	dependence	20189165	To extend the understanding of the role of mGluRs in the addiction relevant effects of ethanol as well as of the treatment target potential of these receptors for alcohol abuse, the effects of a selective mGlu2/3 agonist (LY379268) and a selective <strong>mGlu5</strong> antagonist (MTEP) were tested on two processes central to alcohol addiction: ethanol reinforcement and stress induced reinstatement of ethanol seeking in rats with a history of ethanol <b>dependence</b>.
+GRM5	addiction	relapse	20189165	To extend the understanding of the role of mGluRs in the addiction relevant effects of ethanol as well as of the treatment target potential of these receptors for alcohol abuse, the effects of a selective mGlu2/3 agonist (LY379268) and a selective <strong>mGlu5</strong> antagonist (MTEP) were tested on two processes central to alcohol addiction: ethanol reinforcement and stress induced <b>reinstatement</b> of ethanol <b>seeking</b> in rats with a history of ethanol dependence.
+GRM5	addiction	reward	20189165	To extend the understanding of the role of mGluRs in the addiction relevant effects of ethanol as well as of the treatment target potential of these receptors for alcohol abuse, the effects of a selective mGlu2/3 agonist (LY379268) and a selective <strong>mGlu5</strong> antagonist (MTEP) were tested on two processes central to alcohol addiction: ethanol <b>reinforcement</b> and stress induced reinstatement of ethanol seeking in rats with a history of ethanol dependence.
+GRM5	drug	cocaine	19936864	The aim of the present study was to test, whether group I metabotropic glutamate receptors (mGluRs) antagonists (mGluR1 and <strong>mGluR5</strong>) differentially regulate toxic versus behavioral effects of <b>cocaine</b>, both phenomena relevant to the psychopathology of <b>cocaine</b> addiction in humans.
+GRM5	addiction	addiction	19936864	The aim of the present study was to test, whether group I metabotropic glutamate receptors (mGluRs) antagonists (mGluR1 and <strong>mGluR5</strong>) differentially regulate toxic versus behavioral effects of cocaine, both phenomena relevant to the psychopathology of cocaine <b>addiction</b> in humans.
+GRM5	drug	cocaine	19936864	In the present study, we assessed the impact of mGluR1 antagonist EMQMCM and <strong>mGluR5</strong> antagonist MTEP on the <b>cocaine</b> induced lethality and the expression of sensitization to hyperlocomotor effect of <b>cocaine</b> in mice.
+GRM5	addiction	sensitization	19936864	In the present study, we assessed the impact of mGluR1 antagonist EMQMCM and <strong>mGluR5</strong> antagonist MTEP on the cocaine induced lethality and the expression of <b>sensitization</b> to hyperlocomotor effect of cocaine in mice.
+GRM5	drug	cocaine	19936864	Our results suggest that stimulation of mGluR1 and <strong>mGluR5</strong> is involved in lethal effect of <b>cocaine</b> overdose and <b>cocaine</b> seeking behavior evaluated in behavioral sensitization test.
+GRM5	addiction	relapse	19936864	Our results suggest that stimulation of mGluR1 and <strong>mGluR5</strong> is involved in lethal effect of cocaine overdose and cocaine <b>seeking</b> behavior evaluated in behavioral sensitization test.
+GRM5	addiction	sensitization	19936864	Our results suggest that stimulation of mGluR1 and <strong>mGluR5</strong> is involved in lethal effect of cocaine overdose and cocaine seeking behavior evaluated in behavioral <b>sensitization</b> test.
+GRM5	drug	alcohol	19897175	This study sought to evaluate the functional role of Group I (<strong>mGluR5</strong>) and Group II (mGluR2/3) in mesocorticolimbic brain regions in <b>ethanol</b> self administration.
+GRM5	drug	alcohol	19897175	Microinjection of the <strong>mGluR5</strong> antagonist MPEP in the nucleus accumbens reduced <b>ethanol</b> self administration at a dose that did not alter locomotor activity.
+GRM5	drug	alcohol	19897175	The <strong>mGluR5</strong> involvement showed anatomical specificity as evidenced by lack of effect of MPEP infusion in the dorsomedial caudate or medial prefrontal cortex on <b>ethanol</b> self administration.
+GRM5	drug	alcohol	19897175	These results suggest that <strong>mGluR5</strong> activity specifically in the nucleus accumbens is required for the maintenance of <b>ethanol</b> self administration in individuals with genetic risk for high <b>alcohol</b> consumption.
+GRM5	drug	nicotine	19833142	<b>Nicotine</b> induced conditioned place preference in rats: sex differences and the role of <strong>mGluR5</strong> receptors.
+GRM5	drug	nicotine	19833142	In a series of experiments, the dose response curve was obtained, pairings between the drug and initially non preferred versus preferred compartments were compared, and the involvement of <strong>mGluR5</strong> receptors in <b>nicotine</b> induced CPP was evaluated.
+GRM5	addiction	reward	19833142	In a series of experiments, the dose response curve was obtained, pairings between the drug and initially non preferred versus preferred compartments were compared, and the involvement of <strong>mGluR5</strong> receptors in nicotine induced <b>CPP</b> was evaluated.
+GRM5	drug	nicotine	19833142	Modulation of <b>nicotine</b> induced CPP with <strong>mGluR5</strong> inhibition was obtained by MPEP (2 methyl 6 (phenylethynyl) pyridine hydrochloride).
+GRM5	addiction	reward	19833142	Modulation of nicotine induced <b>CPP</b> with <strong>mGluR5</strong> inhibition was obtained by MPEP (2 methyl 6 (phenylethynyl) pyridine hydrochloride).
+GRM5	drug	nicotine	19833142	The selective <strong>mGluR5</strong> antagonist MPEP inhibited <b>nicotine</b> induced CPP in male rats.
+GRM5	addiction	reward	19833142	The selective <strong>mGluR5</strong> antagonist MPEP inhibited nicotine induced <b>CPP</b> in male rats.
+GRM5	drug	nicotine	19833142	Furthermore, in line with reported findings, our results suggest that <strong>mGluR5</strong> antagonism may be therapeutically useful in <b>smoking</b> cessation during the maintenance of <b>smoking</b> behavior when conditioning plays an important role, notwithstanding the fact that this effect is observed only in male rats, not in females.
+GRM5	drug	alcohol	19641121	Interoceptive effects of <b>alcohol</b> require <strong>mGlu5</strong> receptor activity in the nucleus accumbens.
+GRM5	drug	alcohol	19641121	We found that systemic antagonism of metabotropic glutamate subtype 5 (<strong>mGlu5</strong>) receptors [10 mg/kg 2 methyl 6 (phenylethynyl)pyridine (MPEP) and 3 mg/kg 3 ((2 methyl 1,3 thiazol 4 yl)ethynyl)pyridine], but not mGlu1 receptors ([0.3 3 mg/kg JNJ16259685) (3,4 dihydro 2H pyrano[2,3]beta quinolin 7 yl)(cis 4 methoxycyclohexyl) methanone)], inhibited the discriminative stimulus effects of <b>alcohol</b>.
+GRM5	drug	alcohol	19641121	Accordingly, targeted inhibition of <strong>mGlu5</strong> receptors (20 microg of MPEP) in the nucleus accumbens core blunted the discriminative stimulus effects of <b>alcohol</b> (1 g/kg).
+GRM5	drug	alcohol	19641121	Functional involvement of intra accumbens <strong>mGlu5</strong> receptors was confirmed as activation of <strong>mGlu5</strong> receptors [10 microg of (RS) 2 amino 2 (2 chloro 5 hydroxyphenyl)acetic acid sodium salt] enhanced the discriminative stimulus effects of a low <b>alcohol</b> dose (0.5 g/kg), and <strong>mGlu5</strong> receptor inhibition (20 microg of MPEP) prevented the agonist induced enhancement.
+GRM5	drug	alcohol	19641121	These results show that <strong>mGlu5</strong> receptor activity in the nucleus accumbens is required for the expression of the interoceptive effects of <b>alcohol</b>.
+GRM5	drug	alcohol	19587272	Binge drinking upregulates accumbens <strong>mGluR5</strong> Homer2 PI3K signaling: functional implications for <b>alcoholism</b>.
+GRM5	addiction	intoxication	19587272	<b>Binge</b> drinking upregulates accumbens <strong>mGluR5</strong> Homer2 PI3K signaling: functional implications for alcoholism.
+GRM5	drug	alcohol	19587272	Virus mediated knockdown of NAC Homer2b expression attenuated <b>alcohol</b> intake, as did an intra NAC infusion of the <strong>mGluR5</strong> antagonist MPEP [2 methyl 6 (phenylethynyl)pyridine hydrochloride] (0.1 1 microg/side) and the PI3K antagonist wortmannin (50 ng/side), supporting necessary roles for <strong>mGluR5</strong>/Homer2/PI3K in binge <b>alcohol</b> drinking.
+GRM5	addiction	intoxication	19587272	Virus mediated knockdown of NAC Homer2b expression attenuated alcohol intake, as did an intra NAC infusion of the <strong>mGluR5</strong> antagonist MPEP [2 methyl 6 (phenylethynyl)pyridine hydrochloride] (0.1 1 microg/side) and the PI3K antagonist wortmannin (50 ng/side), supporting necessary roles for <strong>mGluR5</strong>/Homer2/PI3K in <b>binge</b> alcohol drinking.
+GRM5	drug	alcohol	19587272	Moreover, when compared with wild type littermates, transgenic mice with an F1128R point mutation in <strong>mGluR5</strong> that markedly reduces Homer binding exhibited a 50% reduction in binge <b>alcohol</b> drinking, which was related to reduced NAC basal PI3K activity.
+GRM5	addiction	intoxication	19587272	Moreover, when compared with wild type littermates, transgenic mice with an F1128R point mutation in <strong>mGluR5</strong> that markedly reduces Homer binding exhibited a 50% reduction in <b>binge</b> alcohol drinking, which was related to reduced NAC basal PI3K activity.
+GRM5	drug	alcohol	19587272	Consistent with the hypothesis that <strong>mGluR5</strong> Homer PI3K signaling may be a mechanism governing excessive <b>alcohol</b> intake, the "anti binge" effects of MPEP and wortmannin were not additive, nor were they observed in the <strong>mGluR5</strong>(F1128R) transgenic mice.
+GRM5	addiction	intoxication	19587272	Consistent with the hypothesis that <strong>mGluR5</strong> Homer PI3K signaling may be a mechanism governing excessive alcohol intake, the "anti <b>binge</b>" effects of MPEP and wortmannin were not additive, nor were they observed in the <strong>mGluR5</strong>(F1128R) transgenic mice.
+GRM5	drug	alcohol	19587272	Finally, mice genetically selected for a high versus low SHAC phenotype differed in NAC mGluR, Homer2, and PI3K activity, consistent with the hypothesis that augmented NAC <strong>mGluR5</strong> Homer2 PI3K signaling predisposes a high binge <b>alcohol</b> drinking phenotype.
+GRM5	addiction	intoxication	19587272	Finally, mice genetically selected for a high versus low SHAC phenotype differed in NAC mGluR, Homer2, and PI3K activity, consistent with the hypothesis that augmented NAC <strong>mGluR5</strong> Homer2 PI3K signaling predisposes a high <b>binge</b> alcohol drinking phenotype.
+GRM5	drug	alcohol	19587272	Together, these data point to an important role for NAC <strong>mGluR5</strong> Homer2 PI3K signaling in regulating binge like <b>alcohol</b> consumption that has relevance for our understanding of the neurobiology of <b>alcoholism</b> and its pharmacotherapy.
+GRM5	addiction	intoxication	19587272	Together, these data point to an important role for NAC <strong>mGluR5</strong> Homer2 PI3K signaling in regulating <b>binge</b> like alcohol consumption that has relevance for our understanding of the neurobiology of alcoholism and its pharmacotherapy.
+GRM5	drug	cocaine	19545477	<b>Cocaine</b> mediated synaptic potentiation is absent in VTA neurons from <strong>mGlu5</strong> deficient mice.
+GRM5	drug	cocaine	19545477	Moreover, <b>cocaine</b> induced enhancement of this EPSC ratio is also absent in mutant mice, which suggests that <strong>mGlu5</strong> receptors are required for single dose <b>cocaine</b> induced plasticity onto VTA cells.
+GRM5	drug	cocaine	19545477	While the temporal profile of hyperactivity to acute <b>cocaine</b> is altered in <strong>mGlu5</strong> deficient mice; these mice still develop and express sensitized psychomotor responses to <b>cocaine</b>.
+GRM5	drug	cocaine	19545477	These data suggest that the <strong>mGlu5</strong> receptor is required for <b>cocaine</b> induced plasticity in VTA dopaminergic cells.
+GRM5	addiction	addiction	19545477	In contrast, the <strong>mGlu5</strong> receptor may not be essential for psychostimulant behavioural sensitization; although it probably impacts other aspects drug <b>addiction</b>, such as motivation to self administer.
+GRM5	addiction	sensitization	19545477	In contrast, the <strong>mGlu5</strong> receptor may not be essential for psychostimulant behavioural <b>sensitization</b>; although it probably impacts other aspects drug addiction, such as motivation to self administer.
+GRM5	drug	cocaine	19463707	Metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonists attenuate <b>cocaine</b> priming  and cue induced reinstatement of <b>cocaine</b> seeking.
+GRM5	addiction	relapse	19463707	Metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonists attenuate cocaine priming  and cue induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM5	drug	opioid	19326478	We recently reported that the <strong>mGlu5</strong> receptor antagonist 2 methyl 6 (phenylethynyl)pyridine (MPEP) reduces intravenous self administration of ketamine and, to a lesser extent, <b>heroin</b> in rats.
+GRM5	drug	psychedelics	19326478	We recently reported that the <strong>mGlu5</strong> receptor antagonist 2 methyl 6 (phenylethynyl)pyridine (MPEP) reduces intravenous self administration of <b>ketamine</b> and, to a lesser extent, heroin in rats.
+GRM5	drug	cocaine	19258516	To advance understanding of the potential of metabotropic glutamate receptor (mGluR) 5 as treatment targets for <b>cocaine</b> addiction, the effects of MTEP [3 [(2 methyl 1,3 thiazol 4 yl) ethynyl]piperidine] (a selective <strong>mGluR5</strong> antagonist) on conditioned reinstatement of <b>cocaine</b> seeking were examined.
+GRM5	addiction	addiction	19258516	To advance understanding of the potential of metabotropic glutamate receptor (mGluR) 5 as treatment targets for cocaine <b>addiction</b>, the effects of MTEP [3 [(2 methyl 1,3 thiazol 4 yl) ethynyl]piperidine] (a selective <strong>mGluR5</strong> antagonist) on conditioned reinstatement of cocaine seeking were examined.
+GRM5	addiction	relapse	19258516	To advance understanding of the potential of metabotropic glutamate receptor (mGluR) 5 as treatment targets for cocaine addiction, the effects of MTEP [3 [(2 methyl 1,3 thiazol 4 yl) ethynyl]piperidine] (a selective <strong>mGluR5</strong> antagonist) on conditioned <b>reinstatement</b> of cocaine <b>seeking</b> were examined.
+GRM5	drug	cocaine	19258516	The findings implicate <strong>mGluR5</strong> regulated glutamate transmission in appetitive behavior controlled by reward related stimuli but without selectivity for <b>cocaine</b> seeking.
+GRM5	addiction	relapse	19258516	The findings implicate <strong>mGluR5</strong> regulated glutamate transmission in appetitive behavior controlled by reward related stimuli but without selectivity for cocaine <b>seeking</b>.
+GRM5	addiction	reward	19258516	The findings implicate <strong>mGluR5</strong> regulated glutamate transmission in appetitive behavior controlled by <b>reward</b> related stimuli but without selectivity for cocaine seeking.
+GRM5	drug	cocaine	19258516	However, the data suggest a differential role for <strong>mGluR5</strong> in the acute reinforcing effects of <b>cocaine</b> versus conventional reward.
+GRM5	addiction	reward	19258516	However, the data suggest a differential role for <strong>mGluR5</strong> in the acute <b>reinforcing</b> effects of cocaine versus conventional <b>reward</b>.
+GRM5	drug	cocaine	19258516	These observations identify <strong>mGluR5</strong> as potential treatment targets for <b>cocaine</b> relapse prevention, although the profile of action of <strong>mGluR5</strong> antagonists remains to be more closely examined for potential anhedonic effects.
+GRM5	addiction	relapse	19258516	These observations identify <strong>mGluR5</strong> as potential treatment targets for cocaine <b>relapse</b> prevention, although the profile of action of <strong>mGluR5</strong> antagonists remains to be more closely examined for potential anhedonic effects.
+GRM5	drug	alcohol	19225761	Role of protein kinase C epsilon (PKCvarepsilon) in the reduction of <b>ethanol</b> reinforcement due to <strong>mGluR5</strong> antagonism in the nucleus accumbens shell.
+GRM5	addiction	reward	19225761	Role of protein kinase C epsilon (PKCvarepsilon) in the reduction of ethanol <b>reinforcement</b> due to <strong>mGluR5</strong> antagonism in the nucleus accumbens shell.
+GRM5	drug	alcohol	19225761	The type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) and the epsilon isoform of protein kinase C (PKCepsilon) regulate <b>ethanol</b> intake, and we have previously demonstrated that <strong>mGluR5</strong> receptor antagonism reduces <b>ethanol</b> consumption via a PKCepsilon dependent mechanism.
+GRM5	drug	alcohol	19225761	We explored the potential neuroanatomical substrates of regulation of <b>ethanol</b> reinforcement by this <strong>mGluR5</strong> PKCepsilon signaling pathway by infusing selective inhibitors of these proteins into the shell or core region of the nucleus accumbens (NAc).
+GRM5	addiction	reward	19225761	We explored the potential neuroanatomical substrates of regulation of ethanol <b>reinforcement</b> by this <strong>mGluR5</strong> PKCepsilon signaling pathway by infusing selective inhibitors of these proteins into the shell or core region of the nucleus accumbens (NAc).
+GRM5	drug	alcohol	19225761	Male Wistar rats were trained to self administer <b>ethanol</b> intravenously and received intra NAc infusions of vehicle or the selective <strong>mGluR5</strong> antagonist 3 ((2 methyl 1,3 thiazol 4 yl)ethynyl)pyridine (MTEP) alone and in combination with a PKCepsilon translocation inhibitor (epsilonV1 2) or a scrambled control peptide (svarepsilonV1 2).
+GRM5	drug	alcohol	19225761	Blockade of <strong>mGluR5</strong> receptors in the NAc shell reduces <b>ethanol</b> reinforcement via a PKCepsilon dependent mechanism.
+GRM5	addiction	reward	19225761	Blockade of <strong>mGluR5</strong> receptors in the NAc shell reduces ethanol <b>reinforcement</b> via a PKCepsilon dependent mechanism.
+GRM5	drug	cocaine	19118598	Neuroadaptations in the cellular and postsynaptic group 1 metabotropic glutamate receptor <strong>mGluR5</strong> and Homer proteins following extinction of <b>cocaine</b> self administration.
+GRM5	drug	cocaine	19118598	This study examined the role of group1 metabotropic glutamate receptor <strong>mGluR5</strong> and associated postsynaptic scaffolding protein Homer1b/c in behavioral plasticity after three withdrawal treatments from <b>cocaine</b> self administration.
+GRM5	addiction	withdrawal	19118598	This study examined the role of group1 metabotropic glutamate receptor <strong>mGluR5</strong> and associated postsynaptic scaffolding protein Homer1b/c in behavioral plasticity after three <b>withdrawal</b> treatments from cocaine self administration.
+GRM5	drug	cocaine	19118598	<b>Cocaine</b> self administration followed by home cage exposure reduced the <strong>mGluR5</strong> protein in nucleus accumbens (NA) shell and dorsolateral striatum.
+GRM5	addiction	relapse	19118598	Extinction of drug <b>seeking</b> was associated with a significant decrease in the synaptosomal <strong>mGluR5</strong> protein in NAshell and an increase in dorsolateral striatum, while that of NAcore was not modified.
+GRM5	drug	cocaine	19118598	Therefore, extinction of <b>cocaine</b> seeking is associated with neuroadaptations in <strong>mGluR5</strong> expression and distribution that are region specific and consist of extinction induced reversal of <b>cocaine</b> induced adaptations as well as emergent extinction induced alterations.
+GRM5	addiction	relapse	19118598	Therefore, extinction of cocaine <b>seeking</b> is associated with neuroadaptations in <strong>mGluR5</strong> expression and distribution that are region specific and consist of extinction induced reversal of cocaine induced adaptations as well as emergent extinction induced alterations.
+GRM5	drug	cocaine	19100966	Positive allosteric modulation of <strong>mGluR5</strong> receptors facilitates extinction of a <b>cocaine</b> contextual memory.
+GRM5	drug	cocaine	19100966	This study was intended to determine whether potentiation of type 5 metabotropic glutamate receptors (<strong>mGluR5</strong>), which are biochemically and structurally coupled to N methyl D aspartate (NMDA) receptors, would facilitate the extinction of a <b>cocaine</b> associated contextual memory as assessed by the conditioned place preference (CPP) paradigm in rats.
+GRM5	addiction	reward	19100966	This study was intended to determine whether potentiation of type 5 metabotropic glutamate receptors (<strong>mGluR5</strong>), which are biochemically and structurally coupled to N methyl D aspartate (NMDA) receptors, would facilitate the extinction of a cocaine associated contextual memory as assessed by the conditioned place preference (<b>CPP</b>) paradigm in rats.
+GRM5	drug	cocaine	19100966	Following the establishment of a <b>cocaine</b> CPP, rats were treated with the <strong>mGluR5</strong> positive allosteric modulator 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl)benzamide (CDPPB; 0.3, 3 and 30 mg/kg) before extinction test sessions.
+GRM5	addiction	reward	19100966	Following the establishment of a cocaine <b>CPP</b>, rats were treated with the <strong>mGluR5</strong> positive allosteric modulator 3 cyano N (1,3 diphenyl 1H pyrazol 5 yl)benzamide (CDPPB; 0.3, 3 and 30 mg/kg) before extinction test sessions.
+GRM5	drug	cocaine	19100966	Positive allosteric modulation of <strong>mGluR5</strong> function facilitates the extinction of a <b>cocaine</b> associated contextual memory, which may represent a novel approach toward enhancing extinction learning in the context of drug addiction.
+GRM5	addiction	addiction	19100966	Positive allosteric modulation of <strong>mGluR5</strong> function facilitates the extinction of a cocaine associated contextual memory, which may represent a novel approach toward enhancing extinction learning in the context of drug <b>addiction</b>.
+GRM5	addiction	relapse	18991960	Results from studies on selected <strong>mGluR5</strong> antagonists in animal models that simulate drug reward, reinforcement, and <b>relapse</b> appear promising.
+GRM5	addiction	reward	18991960	Results from studies on selected <strong>mGluR5</strong> antagonists in animal models that simulate drug <b>reward</b>, <b>reinforcement</b>, and relapse appear promising.
+GRM5	drug	amphetamine	18991866	A role for <strong>mGluR5</strong> receptors in intravenous <b>methamphetamine</b> self administration.
+GRM5	drug	alcohol	18991866	Selective antagonists of the <strong>mGluR5</strong> receptor attenuate rewarding and reinforcing effects of various drugs of abuse, including <b>alcohol</b>, nicotine, and cocaine.
+GRM5	drug	cocaine	18991866	Selective antagonists of the <strong>mGluR5</strong> receptor attenuate rewarding and reinforcing effects of various drugs of abuse, including alcohol, nicotine, and <b>cocaine</b>.
+GRM5	drug	nicotine	18991866	Selective antagonists of the <strong>mGluR5</strong> receptor attenuate rewarding and reinforcing effects of various drugs of abuse, including alcohol, <b>nicotine</b>, and cocaine.
+GRM5	addiction	reward	18991866	Selective antagonists of the <strong>mGluR5</strong> receptor attenuate rewarding and <b>reinforcing</b> effects of various drugs of abuse, including alcohol, nicotine, and cocaine.
+GRM5	drug	amphetamine	18991866	However, the ability of <strong>mGluR5</strong> antagonists to alter the reinforcing effects of <b>methamphetamine</b> has not yet been explored.
+GRM5	addiction	reward	18991866	However, the ability of <strong>mGluR5</strong> antagonists to alter the <b>reinforcing</b> effects of methamphetamine has not yet been explored.
+GRM5	drug	amphetamine	18991866	After stabilization of <b>methamphetamine</b> or food self administration, the selective <strong>mGluR5</strong> antagonist 3 [(2 methyl 1,3 thiazol 4 yl) ethynyl]pyridine (MTEP; 0.3, 1.0, or 3.0 mg/kg i.p.)
+GRM5	drug	amphetamine	18991866	These data suggest that <strong>mGluR5</strong> receptors are involved in the reinforcing effects of <b>methamphetamine</b>, and that antagonists of this receptor may serve as novel pharmacologic agents for the treatment of addiction to <b>methamphetamine</b>.
+GRM5	addiction	addiction	18991866	These data suggest that <strong>mGluR5</strong> receptors are involved in the reinforcing effects of methamphetamine, and that antagonists of this receptor may serve as novel pharmacologic agents for the treatment of <b>addiction</b> to methamphetamine.
+GRM5	addiction	reward	18991866	These data suggest that <strong>mGluR5</strong> receptors are involved in the <b>reinforcing</b> effects of methamphetamine, and that antagonists of this receptor may serve as novel pharmacologic agents for the treatment of addiction to methamphetamine.
+GRM5	drug	alcohol	18838071	<b>Acamprosate</b> (NMDA and metabotropic glutamate5 (<strong>mGlu5</strong>) receptor antagonist), at a dose of 400 mg/kg showed anxiolytic like effect, thus increasing the percent of time spent in open arms and open arms entries.
+GRM5	drug	alcohol	18838071	Antagonists of group I mGlu receptors, such as MTEP ([(2 methyl 1,3 thiazol 4 yl) ethynyl] pyridine, <strong>mGlu5</strong> receptor) or EMQMCM (3 ethyl 2 methyl quinolin 6 yl (4 methoxy cyclohexyl) methanone methanesulfonate, mGlu1 receptor), caused similar effects to <b>acamprosate</b>.
+GRM5	drug	alcohol	18838071	Our results imply a crucial role of <strong>mGlu5</strong> receptor in an anxiety like effect of <b>ethanol</b> withdrawal because MTEP (a selective <strong>mGlu5</strong> receptor antagonist) and <b>acamprosate</b> (which also indirectly inhibits <strong>mGlu5</strong> receptor) attenuated <b>ethanol</b> withdrawal anxiety like behavior without influence on <b>ethanol</b> withdrawal hypolocomotion and did not show any effect in the saline treated groups.
+GRM5	addiction	withdrawal	18838071	Our results imply a crucial role of <strong>mGlu5</strong> receptor in an anxiety like effect of ethanol <b>withdrawal</b> because MTEP (a selective <strong>mGlu5</strong> receptor antagonist) and acamprosate (which also indirectly inhibits <strong>mGlu5</strong> receptor) attenuated ethanol <b>withdrawal</b> anxiety like behavior without influence on ethanol <b>withdrawal</b> hypolocomotion and did not show any effect in the saline treated groups.
+GRM5	drug	amphetamine	18800068	<strong>mGluR5</strong> antagonism attenuates <b>methamphetamine</b> reinforcement and prevents reinstatement of <b>methamphetamine</b> seeking behavior in rats.
+GRM5	addiction	relapse	18800068	<strong>mGluR5</strong> antagonism attenuates methamphetamine reinforcement and prevents <b>reinstatement</b> of methamphetamine <b>seeking</b> behavior in rats.
+GRM5	addiction	reward	18800068	<strong>mGluR5</strong> antagonism attenuates methamphetamine <b>reinforcement</b> and prevents reinstatement of methamphetamine seeking behavior in rats.
+GRM5	drug	amphetamine	18800068	In the present study, we examined the effects of the selective type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) antagonist 3 ((2 methyl 1,3 thiazol 4 yl)ethynyl)pyridine (MTEP) on intravenous self administration of <b>methamphetamine</b> and reinstatement of <b>methamphetamine</b> seeking behavior.
+GRM5	addiction	relapse	18800068	In the present study, we examined the effects of the selective type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) antagonist 3 ((2 methyl 1,3 thiazol 4 yl)ethynyl)pyridine (MTEP) on intravenous self administration of methamphetamine and <b>reinstatement</b> of methamphetamine <b>seeking</b> behavior.
+GRM5	drug	amphetamine	18800068	Together, these results indicate that <strong>mGluR5</strong> receptors mediate <b>methamphetamine</b> reinforcement and <b>methamphetamine</b> seeking behavior, and that pharmacological inhibitors of <strong>mGluR5</strong> receptor function may represent a novel class of potential therapeutic agents for the treatment of <b>methamphetamine</b> addiction.
+GRM5	addiction	addiction	18800068	Together, these results indicate that <strong>mGluR5</strong> receptors mediate methamphetamine reinforcement and methamphetamine seeking behavior, and that pharmacological inhibitors of <strong>mGluR5</strong> receptor function may represent a novel class of potential therapeutic agents for the treatment of methamphetamine <b>addiction</b>.
+GRM5	addiction	relapse	18800068	Together, these results indicate that <strong>mGluR5</strong> receptors mediate methamphetamine reinforcement and methamphetamine <b>seeking</b> behavior, and that pharmacological inhibitors of <strong>mGluR5</strong> receptor function may represent a novel class of potential therapeutic agents for the treatment of methamphetamine addiction.
+GRM5	addiction	reward	18800068	Together, these results indicate that <strong>mGluR5</strong> receptors mediate methamphetamine <b>reinforcement</b> and methamphetamine seeking behavior, and that pharmacological inhibitors of <strong>mGluR5</strong> receptor function may represent a novel class of potential therapeutic agents for the treatment of methamphetamine addiction.
+GRM5	drug	alcohol	18782337	We measured the effects of <b>acamprosate</b> or MPEP, metabotropic glutamate 5 receptor (<strong>mGluR5</strong>) antagonist, on intake of 20% <b>ethanol</b>, plain tap water or 10% sugar water using the DID procedure in male C57BL/6J mice.
+GRM5	drug	alcohol	18782337	These results support the hypothesis that <strong>mGluR5</strong> signaling plays a role in excessive <b>ethanol</b> intake in DID and suggest DID may have value for screening novel compounds that reduce overactive glutamate signaling for potential pharmaceutical treatment of excessive <b>ethanol</b> drinking behavior.
+GRM5	drug	alcohol	18619984	Cue induced reinstatement of <b>alcohol</b> seeking behavior is associated with increased ERK1/2 phosphorylation in specific limbic brain regions: blockade by the <strong>mGluR5</strong> antagonist MPEP.
+GRM5	addiction	relapse	18619984	Cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior is associated with increased ERK1/2 phosphorylation in specific limbic brain regions: blockade by the <strong>mGluR5</strong> antagonist MPEP.
+GRM5	drug	alcohol	18619984	Emerging evidence indicates that metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonists attenuate relapse to <b>alcohol</b> seeking behavior but the molecular mechanisms of this potential therapeutic effect remain unexplored.
+GRM5	addiction	relapse	18619984	Emerging evidence indicates that metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonists attenuate <b>relapse</b> to alcohol <b>seeking</b> behavior but the molecular mechanisms of this potential therapeutic effect remain unexplored.
+GRM5	addiction	addiction	18619984	The extracellular signal regulated kinase (ERK1/2) pathway is downstream of <strong>mGluR5</strong> and has been implicated in <b>addiction</b>.
+GRM5	drug	alcohol	18619984	We sought to determine if cue induced reinstatement of <b>alcohol</b> seeking behavior, and its reduction by an <strong>mGluR5</strong> antagonist, is associated with changes in ERK1/2 activation in reward related limbic brain regions.
+GRM5	addiction	relapse	18619984	We sought to determine if cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior, and its reduction by an <strong>mGluR5</strong> antagonist, is associated with changes in ERK1/2 activation in reward related limbic brain regions.
+GRM5	addiction	reward	18619984	We sought to determine if cue induced reinstatement of alcohol seeking behavior, and its reduction by an <strong>mGluR5</strong> antagonist, is associated with changes in ERK1/2 activation in <b>reward</b> related limbic brain regions.
+GRM5	addiction	relapse	18619984	Following 9 days of extinction, rats were given an additional extinction trial or injected with the <strong>mGluR5</strong> antagonist MPEP (0, 1, 3, or 10mg/kg) and tested for cue induced <b>reinstatement</b>.
+GRM5	addiction	relapse	18619984	p ERK1/2 IR in the central amygdala and NAcb core was dissociated with the <b>relapse</b> like behavior and the pharmacological effect of <strong>mGluR5</strong> blockade.
+GRM5	drug	alcohol	18619984	Pharmacological compounds, such as <strong>mGluR5</strong> antagonists, that reduce cue induced ERK1/2 activation may be useful for treatment of relapse in <b>alcoholics</b> that is triggered by exposure to environmental events.
+GRM5	addiction	relapse	18619984	Pharmacological compounds, such as <strong>mGluR5</strong> antagonists, that reduce cue induced ERK1/2 activation may be useful for treatment of <b>relapse</b> in alcoholics that is triggered by exposure to environmental events.
+GRM5	drug	alcohol	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; <strong>MGLUR5</strong>; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with <b>alcohol</b> dependence using multivariate statistical analysis.
+GRM5	addiction	dependence	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; <strong>MGLUR5</strong>; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with alcohol <b>dependence</b> using multivariate statistical analysis.
+GRM5	drug	alcohol	18606955	Analysis of study 1 revealed that NR2A and <strong>MGLUR5</strong> have the greatest relevance for human <b>alcohol</b> dependence among the genes selected with odds ratios of 2.35 and 1.69, respectively.
+GRM5	addiction	dependence	18606955	Analysis of study 1 revealed that NR2A and <strong>MGLUR5</strong> have the greatest relevance for human alcohol <b>dependence</b> among the genes selected with odds ratios of 2.35 and 1.69, respectively.
+GRM5	drug	alcohol	18606955	Replication analysis in study 2 confirmed an association of <b>alcohol</b> dependence with NR2A (odds ratio, 2.01) but showed no association with <strong>MGLUR5</strong>.
+GRM5	addiction	dependence	18606955	Replication analysis in study 2 confirmed an association of alcohol <b>dependence</b> with NR2A (odds ratio, 2.01) but showed no association with <strong>MGLUR5</strong>.
+GRM5	drug	alcohol	18540918	New evidence at the molecular and cellular level suggests that <b>acamprosate</b> attenuates hyper glutamatergic states that occur during early abstinence and involves iono (NMDA)  and metabotrotropic (<strong>mGluR5</strong>) glutamate receptors along with augmented intracellular calcium release and electrophysiological changes.
+GRM5	drug	opioid	18520992	We examined the effects of chronic <b>morphine</b> treatment and withdrawal on the expression of metabotropic glutamate (mGlu)1, <strong>mGlu5</strong>, and mGlu2/3 receptors in the nucleus accumbens and caudate putamen.
+GRM5	addiction	withdrawal	18520992	We examined the effects of chronic morphine treatment and <b>withdrawal</b> on the expression of metabotropic glutamate (mGlu)1, <strong>mGlu5</strong>, and mGlu2/3 receptors in the nucleus accumbens and caudate putamen.
+GRM5	drug	cocaine	18509621	Attenuation of <b>cocaine</b> self administration in squirrel monkeys following repeated administration of the <strong>mGluR5</strong> antagonist MPEP: comparison with dizocilpine.
+GRM5	drug	cocaine	18509621	The <strong>mGluR5</strong> antagonist MPEP has effects that suggest potential as a pharmacotherapy for <b>cocaine</b> addiction.
+GRM5	addiction	addiction	18509621	The <strong>mGluR5</strong> antagonist MPEP has effects that suggest potential as a pharmacotherapy for cocaine <b>addiction</b>.
+GRM5	drug	cocaine	18509621	The similar effects of the two drugs raises the possibility that MPEP attenuated the reinforcing effects of <b>cocaine</b>, at least in part, via <strong>mGluR5</strong> mediated inhibition of NMDA receptor activity.
+GRM5	addiction	reward	18509621	The similar effects of the two drugs raises the possibility that MPEP attenuated the <b>reinforcing</b> effects of cocaine, at least in part, via <strong>mGluR5</strong> mediated inhibition of NMDA receptor activity.
+GRM5	addiction	addiction	18479833	There is significant pharmacological and behavioral evidence that group I metabotropic glutamate receptors (mGluR1a and <strong>mGluR5</strong>) in the nucleus accumbens play an important role in the neurochemical and pathophysiological mechanisms that underlie <b>addiction</b> to psychostimulants.
+GRM5	drug	cocaine	18479833	To further address this issue, we undertook a detailed ultrastructural analysis to characterize changes in the subcellular and subsynaptic localization of mGluR1a and <strong>mGluR5</strong> in the core and shell of nucleus accumbens following acute or chronic <b>cocaine</b> administration in rats.
+GRM5	drug	cocaine	18479833	However, neither acute nor chronic <b>cocaine</b> treatments induced significant change in the localization of <strong>mGluR5</strong> in accumbens core and shell, which is in contrast with the significant reduction of plasma membrane bound mGluR1a and <strong>mGluR5</strong> induced by local intra accumbens administration of the group I mGluR agonist, (RS) 3,5 dihydroxyphenylglycine (DHPG).
+GRM5	drug	alcohol	18420113	Effects of the mGluR2/3 agonist LY379268 and the <strong>mGluR5</strong> antagonist MPEP on handling induced convulsions during <b>ethanol</b> withdrawal in mice.
+GRM5	addiction	withdrawal	18420113	Effects of the mGluR2/3 agonist LY379268 and the <strong>mGluR5</strong> antagonist MPEP on handling induced convulsions during ethanol <b>withdrawal</b> in mice.
+GRM5	drug	alcohol	18420113	Therefore, the present study was designed to determine the effects the mGluR2/3 agonist LY379268 and the <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) on <b>ethanol</b> withdrawal induced seizure activity.
+GRM5	addiction	withdrawal	18420113	Therefore, the present study was designed to determine the effects the mGluR2/3 agonist LY379268 and the <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) on ethanol <b>withdrawal</b> induced seizure activity.
+GRM5	drug	alcohol	18420113	These results suggest that inhibition of glutamate transmission by mGluR2/3 agonists or <strong>mGluR5</strong> antagonists does not alter HIC activity during withdrawal from repeated <b>ethanol</b> exposure, and as such these compounds may have limited usefulness in the treatment of central nervous system hyperexcitability during <b>alcohol</b> withdrawal.
+GRM5	addiction	withdrawal	18420113	These results suggest that inhibition of glutamate transmission by mGluR2/3 agonists or <strong>mGluR5</strong> antagonists does not alter HIC activity during <b>withdrawal</b> from repeated ethanol exposure, and as such these compounds may have limited usefulness in the treatment of central nervous system hyperexcitability during alcohol <b>withdrawal</b>.
+GRM5	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, <strong>mGluR5</strong>) in six different brain regions.
+GRM5	drug	alcohol	18400131	The metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) has been implicated in <b>ethanol</b>  and drug seeking behaviours in rodent studies.
+GRM5	addiction	relapse	18400131	The metabotropic glutamate receptor 5 (<strong>mGlu5</strong>) has been implicated in ethanol  and drug <b>seeking</b> behaviours in rodent studies.
+GRM5	drug	alcohol	18400131	Here we examine a number of <b>ethanol</b> related behavioural assays in mice lacking <strong>mGlu5</strong> and wild type littermates.
+GRM5	drug	alcohol	18400131	In a two bottle free choice paradigm, <strong>mGlu5</strong> deficient mice consumed less <b>ethanol</b> with a reduced preference compared to wild type mice.
+GRM5	drug	alcohol	18400131	Indeed, <strong>mGlu5</strong> deficienct mice were <b>ethanol</b> avoiding at both concentrations of <b>ethanol</b> proffered (5% and 10% v/v).
+GRM5	drug	alcohol	18400131	In a conditioned place preference study, <strong>mGlu5</strong> deficient mice displayed a place preference for <b>ethanol</b> when conditioned with a low dose (1g/kg) of <b>ethanol</b>.
+GRM5	drug	alcohol	18400131	Thus, while <strong>mGlu5</strong> deficient mice consume less <b>ethanol</b> (with a reduced preference) than wild type mice, this is not apparently related to impaired hepatic metabolism or a lack of reward from <b>ethanol</b>.
+GRM5	addiction	reward	18400131	Thus, while <strong>mGlu5</strong> deficient mice consume less ethanol (with a reduced preference) than wild type mice, this is not apparently related to impaired hepatic metabolism or a lack of <b>reward</b> from ethanol.
+GRM5	drug	alcohol	18400131	Rather, we provide evidence that deletion of the <strong>mGlu5</strong> receptor increases sensitivity to centrally mediated effects of <b>ethanol</b>.
+GRM5	drug	alcohol	18377703	Metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) regulation of <b>ethanol</b> sedation, dependence and consumption: relationship to <b>acamprosate</b> actions.
+GRM5	addiction	dependence	18377703	Metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) regulation of ethanol sedation, <b>dependence</b> and consumption: relationship to acamprosate actions.
+GRM5	drug	alcohol	18377703	Recent studies have demonstrated that metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonists decrease <b>alcohol</b> self administration and suggest that the anti craving medication, <b>acamprosate</b>, may also act to decrease <strong>mGluR5</strong> function.
+GRM5	addiction	relapse	18377703	Recent studies have demonstrated that metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) antagonists decrease alcohol self administration and suggest that the anti <b>craving</b> medication, acamprosate, may also act to decrease <strong>mGluR5</strong> function.
+GRM5	drug	alcohol	18377703	To address the role of <strong>mGluR5</strong> in behavioural actions of <b>ethanol</b> and <b>acamprosate</b>, we compared mutant mice with deletion of the <strong>mGluR5</strong> gene and mice treated with a <strong>mGluR5</strong> antagonist (MPEP) or <b>acamprosate</b>.
+GRM5	drug	alcohol	18377703	Lack of <strong>mGluR5</strong> or administration of MPEP reduced the severity of <b>alcohol</b> induced withdrawal (AW), increased the sedative effect of <b>alcohol</b> (duration of loss of righting reflex; LORR), and increased basal motor activity.
+GRM5	addiction	withdrawal	18377703	Lack of <strong>mGluR5</strong> or administration of MPEP reduced the severity of alcohol induced <b>withdrawal</b> (AW), increased the sedative effect of alcohol (duration of loss of righting reflex; LORR), and increased basal motor activity.
+GRM5	drug	alcohol	18377703	The motor stimulation produced by <b>ethanol</b> was blocked by deletion of <strong>mGluR5</strong>, but not by injection of MPEP.
+GRM5	drug	alcohol	18377703	No effects of <b>acamprosate</b> or MPEP on <b>ethanol</b> induced LORR and AW were found in <strong>mGluR5</strong> knockout mice, demonstrating that <strong>mGluR5</strong> is required for these actions.
+GRM5	drug	alcohol	18377703	<strong>mGluR5</strong> null mutant mice showed decreased <b>alcohol</b> consumption in some, but not all, tests.
+GRM5	drug	alcohol	18377703	These data show the importance of <strong>mGluR5</strong> for several actions of <b>alcohol</b> and support the hypothesis that some effects of <b>acamprosate</b> require <strong>mGluR5</strong> signalling.
+GRM5	drug	alcohol	18346726	The development of selective type 5 metabotropic glutamate receptor (<strong>mGlu5</strong>) antagonists, such as 2 methyl 6 (phenylethynyl) pyridine (MPEP) and 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine (MTEP), has revealed an important role for these receptors in various disorders of the nervous system including depression, anxiety, epilepsy, Parkinson's disease, drug addiction, and <b>alcoholism</b>.
+GRM5	addiction	addiction	18346726	The development of selective type 5 metabotropic glutamate receptor (<strong>mGlu5</strong>) antagonists, such as 2 methyl 6 (phenylethynyl) pyridine (MPEP) and 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine (MTEP), has revealed an important role for these receptors in various disorders of the nervous system including depression, anxiety, epilepsy, Parkinson's disease, drug <b>addiction</b>, and alcoholism.
+GRM5	drug	alcohol	18162077	Regulation of motivation to self administer <b>ethanol</b> by <strong>mGluR5</strong> in <b>alcohol</b> preferring (P) rats.
+GRM5	drug	alcohol	18162077	Emerging evidence indicates that Group I metabotropic glutamate receptors (mGluR1 and <strong>mGluR5</strong>) differentially regulates <b>ethanol</b> self administration in several rodent behavioral models.
+GRM5	drug	alcohol	18162077	The mGluR1 antagonist, 3,4 dihydro 2H pyrano[2,3]b quinolin 7 yl (cis 4 methoxycyclohexyl) methanone (JNJ 16259685; 0 to 1 mg/kg) and the <strong>mGluR5</strong> antagonist, 6 methyl 2 (phenylethynyl) pyridine (MPEP; 0 to 10 mg/kg) dose dependently reduced <b>ethanol</b> break point.
+GRM5	drug	alcohol	18162077	Together, these results suggest that glutamate activity at <strong>mGluR5</strong> regulates motivation to self administer <b>ethanol</b>.
+GRM5	drug	nicotine	18046312	Metabotropic glutamate 5 receptor (<strong>mGluR5</strong>) antagonists decrease <b>nicotine</b> seeking, but do not affect the reinforcement enhancing effects of <b>nicotine</b>.
+GRM5	addiction	relapse	18046312	Metabotropic glutamate 5 receptor (<strong>mGluR5</strong>) antagonists decrease nicotine <b>seeking</b>, but do not affect the reinforcement enhancing effects of nicotine.
+GRM5	addiction	reward	18046312	Metabotropic glutamate 5 receptor (<strong>mGluR5</strong>) antagonists decrease nicotine seeking, but do not affect the <b>reinforcement</b> enhancing effects of nicotine.
+GRM5	drug	nicotine	18046312	We evaluated the effects of pretreatment with noncompetitive antagonists of the metabotropic glutamate 5 receptor (<strong>mGluR5</strong>) on each reinforcement related effect of <b>nicotine</b> using a model in which a reinforcing visual stimulus (VS) and <b>nicotine</b> infusions were concurrently available.
+GRM5	addiction	reward	18046312	We evaluated the effects of pretreatment with noncompetitive antagonists of the metabotropic glutamate 5 receptor (<strong>mGluR5</strong>) on each <b>reinforcement</b> related effect of nicotine using a model in which a <b>reinforcing</b> visual stimulus (VS) and nicotine infusions were concurrently available.
+GRM5	drug	nicotine	18046312	These findings are consistent with other studies suggesting that <strong>mGlu5</strong> receptors mediate <b>nicotine</b> seeking, but do not alter the reinforcement enhancing effects of <b>nicotine</b>.
+GRM5	addiction	relapse	18046312	These findings are consistent with other studies suggesting that <strong>mGlu5</strong> receptors mediate nicotine <b>seeking</b>, but do not alter the reinforcement enhancing effects of nicotine.
+GRM5	addiction	reward	18046312	These findings are consistent with other studies suggesting that <strong>mGlu5</strong> receptors mediate nicotine seeking, but do not alter the <b>reinforcement</b> enhancing effects of nicotine.
+GRM5	drug	alcohol	17989509	The <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) may be beneficial for drug abuse treatment, as it has been found to reduce self administration of <b>ethanol</b>, nicotine and cocaine in preclinical models.
+GRM5	drug	cocaine	17989509	The <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) may be beneficial for drug abuse treatment, as it has been found to reduce self administration of ethanol, nicotine and <b>cocaine</b> in preclinical models.
+GRM5	drug	nicotine	17989509	The <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) may be beneficial for drug abuse treatment, as it has been found to reduce self administration of ethanol, <b>nicotine</b> and cocaine in preclinical models.
+GRM5	drug	amphetamine	17693584	However, it is not known whether RGS4 and <strong>mGluR5</strong> interactions occur in rat striatum and whether chronic <b>amphetamine</b> (<b>AMPH</b>) treatment produces changes in RGS4 levels that are correlated with <strong>mGluR5</strong> receptor activity.
+GRM5	drug	amphetamine	17693584	In contrast, total levels of <strong>mGluR5</strong> receptors in the striatum were not altered by any <b>AMPH</b> treatment.
+GRM5	drug	amphetamine	17693584	This study further suggests that <b>AMPH</b> induced changes in <strong>mGluR5</strong> associated protein levels (RGS4, Galpha(q/11), and PLCbeta1) may be related to altered coupling of striatal <strong>mGluR5</strong> receptors in animals sensitized to <b>AMPH</b>.
+GRM5	drug	cocaine	17680995	This study further investigated the correlations between <b>cocaine</b> sensitization and modifications in the DARPP 32 phosphorylation pattern, cAMP dependent protein kinase (PKA) activity, and <strong>mGluR5</strong> tone in the medial prefrontal cortex and nucleus accumbens.
+GRM5	addiction	sensitization	17680995	This study further investigated the correlations between cocaine <b>sensitization</b> and modifications in the DARPP 32 phosphorylation pattern, cAMP dependent protein kinase (PKA) activity, and <strong>mGluR5</strong> tone in the medial prefrontal cortex and nucleus accumbens.
+GRM5	drug	cocaine	17680995	Furthermore, in sensitized rats the acute administration of 6 methyl 2 (phenylethynyl) pyridine, a <strong>mGluR5</strong> antagonist, reinstated the phosphorylation levels of Thr75  and Thr34 DARPP 32, GluR1, and NR1 to control values, and a subsequent <b>cocaine</b> challenge did not elicit a sensitized response.
+GRM5	drug	cocaine	17680995	These data suggest that a tonic increase in <strong>mGluR5</strong> transmission in <b>cocaine</b> sensitized rats sustains both the increase in phospho Thr75 DARPP 32 levels and the expression of behavioral sensitization.
+GRM5	addiction	sensitization	17680995	These data suggest that a tonic increase in <strong>mGluR5</strong> transmission in cocaine sensitized rats sustains both the increase in phospho Thr75 DARPP 32 levels and the expression of behavioral <b>sensitization</b>.
+GRM5	drug	cannabinoid	17646043	Therefore, A2A receptors play an important fine tuning role, boosting the efficiency of glutamatergic information flow in the indirect pathway by exerting control, either pre  and/or post synaptically, over other key modulators of glutamatergic synapses, including D2 receptors, group I metabotropic <strong>mGlu5</strong> glutamate receptors and <b>cannabinoid</b> CB1 receptors, and by triggering the cAMP protein kinase A signaling cascade.
+GRM5	drug	nicotine	17631918	Rats were trained to criterion performance and were then pre dosed with either vehicle, the NMDA receptor antagonist (+)3 (2 carboxypiperazin 4 propyl) 1 propenyl 1 phosphonic acid (CPP, 0.3 2.0 mg/kg) or the <strong>mGlu5</strong> antagonist 2 methyl 6 phenylethynyl pyridine (MPEP, 1.0 9.0 mg/kg) and challenged with <b>nicotine</b> (0.2 mg/kg).
+GRM5	addiction	reward	17631918	Rats were trained to criterion performance and were then pre dosed with either vehicle, the NMDA receptor antagonist (+)3 (2 carboxypiperazin 4 propyl) 1 propenyl 1 phosphonic acid (<b>CPP</b>, 0.3 2.0 mg/kg) or the <strong>mGlu5</strong> antagonist 2 methyl 6 phenylethynyl pyridine (MPEP, 1.0 9.0 mg/kg) and challenged with nicotine (0.2 mg/kg).
+GRM5	drug	alcohol	17517168	Combined antagonism of glutamate <strong>mGlu5</strong> and adenosine A2A receptors interact to regulate <b>alcohol</b> seeking in rats.
+GRM5	addiction	relapse	17517168	Combined antagonism of glutamate <strong>mGlu5</strong> and adenosine A2A receptors interact to regulate alcohol <b>seeking</b> in rats.
+GRM5	drug	alcohol	17517168	Furthermore, the combination of a subthreshold dose of SCH 58261 with a subthreshold dose of the <strong>mGlu5</strong> receptor antagonist MTEP also reduced <b>alcohol</b> self administration and increased the latency to the first reinforced response, suggesting a pre ingestive effect.
+GRM5	drug	alcohol	17517168	Collectively, these data suggest a functional interaction between adenosine A2A and <strong>mGlu5</strong> receptors in relation to <b>alcohol</b> seeking and the integration of the drug related cues.
+GRM5	addiction	relapse	17517168	Collectively, these data suggest a functional interaction between adenosine A2A and <strong>mGlu5</strong> receptors in relation to alcohol <b>seeking</b> and the integration of the drug related cues.
+GRM5	drug	cocaine	17347848	Involvement of AMPA/kainate, NMDA, and <strong>mGlu5</strong> receptors in the nucleus accumbens core in cue induced reinstatement of <b>cocaine</b> seeking in rats.
+GRM5	addiction	relapse	17347848	Involvement of AMPA/kainate, NMDA, and <strong>mGlu5</strong> receptors in the nucleus accumbens core in cue induced <b>reinstatement</b> of cocaine <b>seeking</b> in rats.
+GRM5	drug	cocaine	17347848	This study examined the effects of alpha amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA)/kainate, N methyl D aspartate (NMDA) and <strong>mGlu5</strong> receptor blockade in the nucleus accumbens core on cue induced reinstatement of <b>cocaine</b> seeking.
+GRM5	addiction	relapse	17347848	This study examined the effects of alpha amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA)/kainate, N methyl D aspartate (NMDA) and <strong>mGlu5</strong> receptor blockade in the nucleus accumbens core on cue induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM5	addiction	relapse	17347848	The effects of the intra accumbal AMPA/kainate receptor antagonist 6 cyano 7 nitro quinoxaline 2, 3 dione (CNQX; 0, 0.01, and 0.03 microg/side), the NMDA antagonist D 2 amino 5 phosphonopentanoate (D AP5; 0, 1, and 2 microg/side), and the <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP; 0, 0.5, and 1 microg/side) on <b>reinstatement</b> were examined in a within subjects design.
+GRM5	drug	cocaine	17259307	Although metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) is essential for <b>cocaine</b> self administration and drug seeking behavior, there is limited knowledge of the cellular actions of this receptor in the nucleus accumbens (NAc).
+GRM5	addiction	relapse	17259307	Although metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) is essential for cocaine self administration and drug <b>seeking</b> behavior, there is limited knowledge of the cellular actions of this receptor in the nucleus accumbens (NAc).
+GRM5	drug	opioid	17222405	Comparison of the effects of mGluR1 and <strong>mGluR5</strong> antagonists on the expression of behavioral sensitization to the locomotor effect of <b>morphine</b> and the <b>morphine</b> withdrawal jumping in mice.
+GRM5	addiction	sensitization	17222405	Comparison of the effects of mGluR1 and <strong>mGluR5</strong> antagonists on the expression of behavioral <b>sensitization</b> to the locomotor effect of morphine and the morphine withdrawal jumping in mice.
+GRM5	addiction	withdrawal	17222405	Comparison of the effects of mGluR1 and <strong>mGluR5</strong> antagonists on the expression of behavioral sensitization to the locomotor effect of morphine and the morphine <b>withdrawal</b> jumping in mice.
+GRM5	drug	opioid	17222405	The aim of the present study was to compare the influence of group I metabotropic glutamate receptor (mGluR) antagonists (mGluR1 and <strong>mGluR5</strong>) on the expression of sensitization to the locomotor effect of <b>morphine</b>.
+GRM5	addiction	sensitization	17222405	The aim of the present study was to compare the influence of group I metabotropic glutamate receptor (mGluR) antagonists (mGluR1 and <strong>mGluR5</strong>) on the expression of <b>sensitization</b> to the locomotor effect of morphine.
+GRM5	drug	opioid	17222405	The results suggest that both subtypes of the group I mGluRs (mGluR1 and <strong>mGluR5</strong>) take part in the expression of <b>morphine</b> sensitization processes but mGluR1 is not involved in the expression of <b>morphine</b> withdrawal jumps in mice.
+GRM5	addiction	sensitization	17222405	The results suggest that both subtypes of the group I mGluRs (mGluR1 and <strong>mGluR5</strong>) take part in the expression of morphine <b>sensitization</b> processes but mGluR1 is not involved in the expression of morphine withdrawal jumps in mice.
+GRM5	addiction	withdrawal	17222405	The results suggest that both subtypes of the group I mGluRs (mGluR1 and <strong>mGluR5</strong>) take part in the expression of morphine sensitization processes but mGluR1 is not involved in the expression of morphine <b>withdrawal</b> jumps in mice.
+GRM5	drug	nicotine	17113075	Interactive effects of the <strong>mGlu5</strong> receptor antagonist MPEP and the mGlu2/3 receptor antagonist LY341495 on <b>nicotine</b> self administration and reward deficits associated with <b>nicotine</b> withdrawal in rats.
+GRM5	addiction	reward	17113075	Interactive effects of the <strong>mGlu5</strong> receptor antagonist MPEP and the mGlu2/3 receptor antagonist LY341495 on nicotine self administration and <b>reward</b> deficits associated with nicotine withdrawal in rats.
+GRM5	addiction	withdrawal	17113075	Interactive effects of the <strong>mGlu5</strong> receptor antagonist MPEP and the mGlu2/3 receptor antagonist LY341495 on nicotine self administration and reward deficits associated with nicotine <b>withdrawal</b> in rats.
+GRM5	drug	nicotine	17113075	Because both presynaptic inhibitory mGlu2/3 and postsynaptic excitatory <strong>mGlu5</strong> receptors provide potential targets for treatment of aspects of <b>nicotine</b> dependence, we examined interacting effects of <strong>mGlu5</strong> (2 methyl 6 (phenylethynyl) pyridine, MPEP) and mGlu2/3 (LY341495) receptor antagonists on <b>nicotine</b> self administration and brain reward threshold elevations associated with spontaneous <b>nicotine</b> withdrawal in rats.
+GRM5	addiction	dependence	17113075	Because both presynaptic inhibitory mGlu2/3 and postsynaptic excitatory <strong>mGlu5</strong> receptors provide potential targets for treatment of aspects of nicotine <b>dependence</b>, we examined interacting effects of <strong>mGlu5</strong> (2 methyl 6 (phenylethynyl) pyridine, MPEP) and mGlu2/3 (LY341495) receptor antagonists on nicotine self administration and brain reward threshold elevations associated with spontaneous nicotine withdrawal in rats.
+GRM5	addiction	reward	17113075	Because both presynaptic inhibitory mGlu2/3 and postsynaptic excitatory <strong>mGlu5</strong> receptors provide potential targets for treatment of aspects of nicotine dependence, we examined interacting effects of <strong>mGlu5</strong> (2 methyl 6 (phenylethynyl) pyridine, MPEP) and mGlu2/3 (LY341495) receptor antagonists on nicotine self administration and brain <b>reward</b> threshold elevations associated with spontaneous nicotine withdrawal in rats.
+GRM5	addiction	withdrawal	17113075	Because both presynaptic inhibitory mGlu2/3 and postsynaptic excitatory <strong>mGlu5</strong> receptors provide potential targets for treatment of aspects of nicotine dependence, we examined interacting effects of <strong>mGlu5</strong> (2 methyl 6 (phenylethynyl) pyridine, MPEP) and mGlu2/3 (LY341495) receptor antagonists on nicotine self administration and brain reward threshold elevations associated with spontaneous nicotine <b>withdrawal</b> in rats.
+GRM5	drug	nicotine	17113075	We also hypothesized that blocking postsynaptic actions of glutamate on <strong>mGlu5</strong> receptors would exacerbate <b>nicotine</b> withdrawal induced reward deficits, and that this effect would be attenuated by co administration of the mGlu2/3 receptor antagonist LY341495.
+GRM5	addiction	reward	17113075	We also hypothesized that blocking postsynaptic actions of glutamate on <strong>mGlu5</strong> receptors would exacerbate nicotine withdrawal induced <b>reward</b> deficits, and that this effect would be attenuated by co administration of the mGlu2/3 receptor antagonist LY341495.
+GRM5	addiction	withdrawal	17113075	We also hypothesized that blocking postsynaptic actions of glutamate on <strong>mGlu5</strong> receptors would exacerbate nicotine <b>withdrawal</b> induced reward deficits, and that this effect would be attenuated by co administration of the mGlu2/3 receptor antagonist LY341495.
+GRM5	drug	nicotine	17113075	Thus, while <strong>mGlu5</strong> receptor antagonists may be therapeutically useful in decreasing <b>tobacco</b> <b>smoking</b>, they worsen <b>nicotine</b> withdrawal.
+GRM5	addiction	withdrawal	17113075	Thus, while <strong>mGlu5</strong> receptor antagonists may be therapeutically useful in decreasing tobacco smoking, they worsen nicotine <b>withdrawal</b>.
+GRM5	drug	nicotine	17113075	Thus, increasing glutamate transmission via mGlu2/3 autoreceptor blockade reduces the effects of <strong>mGlu5</strong> receptor blockade on <b>nicotine</b> self administration and MPEP induced exacerbation of brain reward deficits associated with <b>nicotine</b> withdrawal.
+GRM5	addiction	reward	17113075	Thus, increasing glutamate transmission via mGlu2/3 autoreceptor blockade reduces the effects of <strong>mGlu5</strong> receptor blockade on nicotine self administration and MPEP induced exacerbation of brain <b>reward</b> deficits associated with nicotine withdrawal.
+GRM5	addiction	withdrawal	17113075	Thus, increasing glutamate transmission via mGlu2/3 autoreceptor blockade reduces the effects of <strong>mGlu5</strong> receptor blockade on nicotine self administration and MPEP induced exacerbation of brain reward deficits associated with nicotine <b>withdrawal</b>.
+GRM5	drug	alcohol	17096086	Assessing appetitive and consummatory phases of <b>ethanol</b> self administration in C57BL/6J mice under operant conditions: regulation by <strong>mGlu5</strong> receptor antagonism.
+GRM5	addiction	reward	17096086	Assessing appetitive and consummatory phases of ethanol self administration in C57BL/6J mice under <b>operant</b> conditions: regulation by <strong>mGlu5</strong> receptor antagonism.
+GRM5	drug	alcohol	17096086	The model provides a useful paradigm for examining both the appetitive and consummatory phases of <b>ethanol</b> consumption in mice; furthermore, the data indicate <strong>mGlu5</strong> receptors are involved in both phases.
+GRM5	drug	alcohol	17081689	Involvement of <strong>mGluR5</strong> in the <b>ethanol</b> induced neuropathic pain like state in the rat.
+GRM5	drug	alcohol	17081689	Under these conditions, an immunohistochemical study showed an increase in metabotropic glutamate receptor 5 (<strong>mGluR5</strong>) immunoreactivity in the superficial spinal dorsal horn of chronic <b>ethanol</b> fed rats.
+GRM5	drug	alcohol	17081689	Furthermore, immunoblot analysis revealed that the protein level of <strong>mGluR5</strong> was clearly increased following chronic <b>ethanol</b> consumption.
+GRM5	drug	alcohol	17081689	These findings support the idea that the increased levels of <strong>mGluR5</strong> in the spinal cord may be, at least in part, involved in the induction of <b>ethanol</b> dependent neuropathic pain like state.
+GRM5	drug	alcohol	17026991	<strong>mGlu5</strong> receptors are involved in the discriminative stimulus effects of self administered <b>ethanol</b> in rats.
+GRM5	drug	cocaine	16896963	These findings indicate that the expression of behavioral sensitization to <b>cocaine</b> induced stimulation of locomotor activity may be modulated by group I mGluR antagonists (mGluR1 rather than <strong>mGluR5</strong>), but these effects occur at the dose levels that attenuate vertical activity.
+GRM5	addiction	sensitization	16896963	These findings indicate that the expression of behavioral <b>sensitization</b> to cocaine induced stimulation of locomotor activity may be modulated by group I mGluR antagonists (mGluR1 rather than <strong>mGluR5</strong>), but these effects occur at the dose levels that attenuate vertical activity.
+GRM5	drug	opioid	16793067	The aims of the present study were to assess: (i) the role of mGlu1 and <strong>mGlu5</strong> receptors in inflammatory pain using selective antagonist EMQMCM, 1.25 5 mg/kg, as the mGlu1 receptor antagonist, and MPEP or MTEP, 2.5 10 mg/kg, as <strong>mGlu5</strong> receptor antagonist; (ii) the possible interaction between mGlu1 and <strong>mGlu5</strong> receptor antagonists and <b>morphine</b>; and (iii) whether tolerance develops to the analgesic effects of these antagonists after prolonged treatment.
+GRM5	drug	opioid	16793067	In the present study, the suppressive effect on formalin induced pain behaviour was much stronger when mGlu1 and <strong>mGlu5</strong> receptor antagonists were co injected compared to administration of a single antagonist, but this effect was not seen when mGlu receptor antagonist was co administered with <b>morphine</b>.
+GRM5	drug	alcohol	16697125	Blockade of the <strong>mGluR5</strong> subtype of Group 1 metabotropic glutamate receptor (mGluRs) reduces the rewarding effects of <b>ethanol</b> (EtOH), while the effects of mGluR1a blockade remain under investigated.
+GRM5	drug	alcohol	16697125	The present study compared the effects of pretreatment with the <strong>mGluR5</strong> antagonist MPEP and the mGluR1a antagonist CPCCPOEt upon behavioral and neurochemical variables associated with EtOH reward in <b>alcohol</b> preferring C57BL/6J mice.
+GRM5	addiction	reward	16697125	The present study compared the effects of pretreatment with the <strong>mGluR5</strong> antagonist MPEP and the mGluR1a antagonist CPCCPOEt upon behavioral and neurochemical variables associated with EtOH <b>reward</b> in alcohol preferring C57BL/6J mice.
+GRM5	drug	cannabinoid	16554472	First, a combined activation of group I mGluRs (mGluR1 and <strong>mGluR5</strong>) induces a transient depression that is <b>cannabinoid</b> 1 receptor dependent.
+GRM5	drug	cannabinoid	16554472	Second, as with <b>endocannabinoid</b> independent group I mGluR long term depression (LTD) in the adult hippocampus, we find that activation of <strong>mGluR5</strong> induces an extracellular signal regulated kinase (ERK) dependent LTD.
+GRM5	drug	alcohol	16292590	The <strong>mGluR5</strong> antagonist MPEP selectively inhibits the onset and maintenance of <b>ethanol</b> self administration in C57BL/6J mice.
+GRM5	drug	alcohol	16292590	Effects of mGluR1, mGluR2/3, and <strong>mGluR5</strong> antagonists were then tested on parameters of <b>ethanol</b> self administration behavior.
+GRM5	drug	alcohol	16292590	These data indicate that <strong>mGlu5</strong> receptors selectively regulate the onset and maintenance of <b>ethanol</b> self administration in a manner that is consistent with reduction in <b>ethanol</b>'s reinforcement function.
+GRM5	addiction	reward	16292590	These data indicate that <strong>mGlu5</strong> receptors selectively regulate the onset and maintenance of ethanol self administration in a manner that is consistent with reduction in ethanol's <b>reinforcement</b> function.
+GRM5	addiction	relapse	16123768	The AMPA/kainate receptor antagonists CNQX and NBQX, the NMDA/glycine site antagonist L 701,324, and the <strong>mGluR5</strong> antagonist MPEP attenuated significantly cue induced <b>reinstatement</b>.
+GRM5	addiction	reward	16109585	Recent studies have revealed the effectiveness of 2 methyl 6 (phenylethynyl)pyridine (MPEP), a highly selective antagonist of metabotropic glutamate receptors subtype 5 (<strong>mGluR5</strong>), in conditioned drug <b>reward</b>.
+GRM5	drug	nicotine	16023685	Metabotropic glutamate receptor (<strong>mGluR5</strong>) antagonist MPEP attenuated cue  and schedule induced reinstatement of <b>nicotine</b> self administration behavior in rats.
+GRM5	addiction	relapse	16023685	Metabotropic glutamate receptor (<strong>mGluR5</strong>) antagonist MPEP attenuated cue  and schedule induced <b>reinstatement</b> of nicotine self administration behavior in rats.
+GRM5	addiction	reward	16023685	Previous studies suggested that metabotropic glutamate 5 (<strong>mGlu5</strong>) receptors play an important role in the <b>reinforcing</b> effects of abused drugs.
+GRM5	drug	nicotine	16023685	In conclusion, the present findings indicate that the blockade of <strong>mGlu5</strong> receptors attenuates cue induced reinstatement of <b>nicotine</b> self administration behavior (but not food seeking) and may produce a general inhibition of schedule induced behaviors, including schedule induced <b>nicotine</b> seeking.
+GRM5	addiction	relapse	16023685	In conclusion, the present findings indicate that the blockade of <strong>mGlu5</strong> receptors attenuates cue induced <b>reinstatement</b> of nicotine self administration behavior (but not food <b>seeking</b>) and may produce a general inhibition of schedule induced behaviors, including schedule induced nicotine <b>seeking</b>.
+GRM5	addiction	relapse	16014750	The metabotropic glutamate 5 receptor (<strong>mGlu5</strong>) receptor has been implicated as having a role in pain modulation, anxiety, and depression, as well as drug <b>seeking</b> behavior.
+GRM5	drug	alcohol	16014750	In the present study, we examined the effect of the selective <strong>mGlu5</strong> receptor antagonist 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine (MTEP) on operant <b>ethanol</b> self administration by two strains of rats, the Fawn Hooded (FH) rat and the inbred <b>alcohol</b> preferring (iP) rat.
+GRM5	addiction	reward	16014750	In the present study, we examined the effect of the selective <strong>mGlu5</strong> receptor antagonist 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine (MTEP) on <b>operant</b> ethanol self administration by two strains of rats, the Fawn Hooded (FH) rat and the inbred alcohol preferring (iP) rat.
+GRM5	drug	alcohol	15907154	Although the precise mechanism(s) of action of the drug remains to be fully elucidated, it appears that it most likely involves beneficial modulation of the glutamatergic neurotransmitter system, including antagonism of the <strong>mGLu5</strong> metabotropic glutamate receptor, to counteract the imbalance between the glutamatergic and GABAergic systems associated with chronic <b>alcohol</b> exposure and <b>alcohol</b> withdrawal.
+GRM5	addiction	withdrawal	15907154	Although the precise mechanism(s) of action of the drug remains to be fully elucidated, it appears that it most likely involves beneficial modulation of the glutamatergic neurotransmitter system, including antagonism of the <strong>mGLu5</strong> metabotropic glutamate receptor, to counteract the imbalance between the glutamatergic and GABAergic systems associated with chronic alcohol exposure and alcohol <b>withdrawal</b>.
+GRM5	drug	alcohol	15717208	The <strong>mGluR5</strong> antagonist MPEP decreases operant <b>ethanol</b> self administration during maintenance and after repeated <b>alcohol</b> deprivations in <b>alcohol</b> preferring (P) rats.
+GRM5	addiction	reward	15717208	The <strong>mGluR5</strong> antagonist MPEP decreases <b>operant</b> ethanol self administration during maintenance and after repeated alcohol deprivations in alcohol preferring (P) rats.
+GRM5	drug	alcohol	15717208	Recent research indicates that blockade of <strong>mGluR5</strong> modifies the reinforcing properties of <b>ethanol</b>.
+GRM5	addiction	reward	15717208	Recent research indicates that blockade of <strong>mGluR5</strong> modifies the <b>reinforcing</b> properties of ethanol.
+GRM5	drug	alcohol	15717208	The present studies examined the effects of <strong>mGluR5</strong> receptor blockade in a genetic model of high <b>ethanol</b> intake, the <b>alcohol</b> preferring (P) rat, on the maintenance of operant <b>ethanol</b> self administration.
+GRM5	addiction	reward	15717208	The present studies examined the effects of <strong>mGluR5</strong> receptor blockade in a genetic model of high ethanol intake, the alcohol preferring (P) rat, on the maintenance of <b>operant</b> ethanol self administration.
+GRM5	drug	alcohol	15717208	After the establishment of operant <b>ethanol</b> self administration, subjects were treated with various metabotropic glutamate receptor (mGluR) subtype antagonists immediately prior to experimental sessions: the <strong>mGluR5</strong> antagonist MPEP (1, 3, and 10 mg/kg); the mGluR2  3 antagonist LY 341495 (1, 3, and 10 mg/kg); and the mGluR1 antagonist CPCCOEt (1, 3, and 10 mg/kg).
+GRM5	addiction	reward	15717208	After the establishment of <b>operant</b> ethanol self administration, subjects were treated with various metabotropic glutamate receptor (mGluR) subtype antagonists immediately prior to experimental sessions: the <strong>mGluR5</strong> antagonist MPEP (1, 3, and 10 mg/kg); the mGluR2  3 antagonist LY 341495 (1, 3, and 10 mg/kg); and the mGluR1 antagonist CPCCOEt (1, 3, and 10 mg/kg).
+GRM5	drug	alcohol	15717208	After determining the role of <strong>mGluR5</strong> in the maintenance of operant <b>ethanol</b> self administration, we examined the role of this receptor in relapse following repeated periods of <b>alcohol</b> deprivation by depriving subjects of <b>ethanol</b> exposure for three 2 week deprivation periods.
+GRM5	addiction	relapse	15717208	After determining the role of <strong>mGluR5</strong> in the maintenance of operant ethanol self administration, we examined the role of this receptor in <b>relapse</b> following repeated periods of alcohol deprivation by depriving subjects of ethanol exposure for three 2 week deprivation periods.
+GRM5	addiction	reward	15717208	After determining the role of <strong>mGluR5</strong> in the maintenance of <b>operant</b> ethanol self administration, we examined the role of this receptor in relapse following repeated periods of alcohol deprivation by depriving subjects of ethanol exposure for three 2 week deprivation periods.
+GRM5	drug	alcohol	15717208	The <strong>mGluR5</strong> antagonist MPEP dose dependently decreased operant <b>ethanol</b> self administration.
+GRM5	addiction	reward	15717208	The <strong>mGluR5</strong> antagonist MPEP dose dependently decreased <b>operant</b> ethanol self administration.
+GRM5	drug	alcohol	15717208	These findings suggest that <strong>mGluR5</strong> receptors may modulate both the maintenance of operant <b>ethanol</b> self administration and abstinence induced increases in <b>ethanol</b> intake.
+GRM5	addiction	reward	15717208	These findings suggest that <strong>mGluR5</strong> receptors may modulate both the maintenance of <b>operant</b> ethanol self administration and abstinence induced increases in ethanol intake.
+GRM5	drug	opioid	15695156	The <strong>mGlu5</strong> receptor antagonists MPEP and MTEP attenuate behavioral signs of <b>morphine</b> withdrawal and <b>morphine</b> withdrawal induced activation of locus coeruleus neurons in rats.
+GRM5	addiction	withdrawal	15695156	The <strong>mGlu5</strong> receptor antagonists MPEP and MTEP attenuate behavioral signs of morphine <b>withdrawal</b> and morphine <b>withdrawal</b> induced activation of locus coeruleus neurons in rats.
+GRM5	drug	opioid	15695156	Since the metabotropic glutamate (mGlu) 5 receptor has been shown to affect glutamate release and modulate NMDA receptor function, we examined the effects of two selective <strong>mGlu5</strong> receptor antagonists, 2 methyl 6 (phenyl ethynyl) pyridine (MPEP) and 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]pyridine (MTEP), on <b>morphine</b> withdrawal.
+GRM5	addiction	withdrawal	15695156	Since the metabotropic glutamate (mGlu) 5 receptor has been shown to affect glutamate release and modulate NMDA receptor function, we examined the effects of two selective <strong>mGlu5</strong> receptor antagonists, 2 methyl 6 (phenyl ethynyl) pyridine (MPEP) and 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]pyridine (MTEP), on morphine <b>withdrawal</b>.
+GRM5	drug	opioid	15695156	These results indicate a role for <strong>mGlu5</strong> receptors in <b>morphine</b> withdrawal and suggest the potential for <strong>mGlu5</strong> antagonists in the treatment of withdrawal from opiates and other drugs of abuse.
+GRM5	addiction	withdrawal	15695156	These results indicate a role for <strong>mGlu5</strong> receptors in morphine <b>withdrawal</b> and suggest the potential for <strong>mGlu5</strong> antagonists in the treatment of <b>withdrawal</b> from opiates and other drugs of abuse.
+GRM5	drug	opioid	15662102	Selective <strong>mGlu5</strong> receptor antagonist MTEP attenuates <b>naloxone</b> induced <b>morphine</b> withdrawal symptoms.
+GRM5	addiction	withdrawal	15662102	Selective <strong>mGlu5</strong> receptor antagonist MTEP attenuates naloxone induced morphine <b>withdrawal</b> symptoms.
+GRM5	drug	opioid	15662102	Given the recent discovery of selective and brain penetrable <strong>mGlu5</strong> receptor antagonists, the effects of 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine (MTEP) were evaluated in the <b>naloxone</b> precipitated <b>morphine</b> withdrawal model.
+GRM5	addiction	withdrawal	15662102	Given the recent discovery of selective and brain penetrable <strong>mGlu5</strong> receptor antagonists, the effects of 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine (MTEP) were evaluated in the naloxone precipitated morphine <b>withdrawal</b> model.
+GRM5	drug	opioid	15662102	Two hours and 15 min after the last dose of <b>morphine</b>, mice were injected with a <strong>mGlu5</strong> receptor antagonist.
+GRM5	addiction	dependence	15662102	The data suggest that selective <strong>mGlu5</strong> receptor antagonists may play a role in the therapy of drug <b>dependence</b> states.
+GRM5	drug	cocaine	15619120	The <strong>mGlu5</strong> receptor is implicated in mediating the reinforcing and incentive motivational properties of nicotine, <b>cocaine</b> and food.
+GRM5	drug	nicotine	15619120	The <strong>mGlu5</strong> receptor is implicated in mediating the reinforcing and incentive motivational properties of <b>nicotine</b>, cocaine and food.
+GRM5	addiction	reward	15619120	The <strong>mGlu5</strong> receptor is implicated in mediating the <b>reinforcing</b> and <b>incentive</b> motivational properties of nicotine, cocaine and food.
+GRM5	addiction	reward	15602687	Evidence is accumulating that metabotropic glutamate 5 (<strong>mGlu5</strong>) receptors play an important role in regulating the <b>reinforcing</b> actions of drugs of abuse.
+GRM5	drug	cocaine	15602687	We examined the effects of the <strong>mGlu5</strong> receptor antagonist MPEP on <b>cocaine</b> consumption and <b>cocaine</b> enhanced brain reward function in rats.
+GRM5	addiction	reward	15602687	We examined the effects of the <strong>mGlu5</strong> receptor antagonist MPEP on cocaine consumption and cocaine enhanced brain <b>reward</b> function in rats.
+GRM5	drug	cocaine	15602687	These data suggest that <strong>mGlu5</strong> receptors regulate the reinforcing properties of <b>cocaine</b>, and that this action of <strong>mGlu5</strong> receptors is independent of the escalation in consumption associated with extended access to <b>cocaine</b> self administration.
+GRM5	addiction	addiction	15602687	These data suggest that <strong>mGlu5</strong> receptors regulate the reinforcing properties of cocaine, and that this action of <strong>mGlu5</strong> receptors is independent of the <b>escalation</b> in consumption associated with extended access to cocaine self administration.
+GRM5	addiction	reward	15602687	These data suggest that <strong>mGlu5</strong> receptors regulate the <b>reinforcing</b> properties of cocaine, and that this action of <strong>mGlu5</strong> receptors is independent of the escalation in consumption associated with extended access to cocaine self administration.
+GRM5	drug	cocaine	15602687	Overall, <strong>mGlu5</strong> receptors appear to play an important role in regulating <b>cocaine</b> consumption, and also in regulating brain reward function.
+GRM5	addiction	reward	15602687	Overall, <strong>mGlu5</strong> receptors appear to play an important role in regulating cocaine consumption, and also in regulating brain <b>reward</b> function.
+GRM5	drug	cocaine	15602687	Further, it is likely that blockade of <strong>mGlu5</strong> receptors may attenuate <b>cocaine</b> consumption, at least in part, by decreasing the baseline activity of brain reward circuitries.
+GRM5	addiction	reward	15602687	Further, it is likely that blockade of <strong>mGlu5</strong> receptors may attenuate cocaine consumption, at least in part, by decreasing the baseline activity of brain <b>reward</b> circuitries.
+GRM5	addiction	relapse	15555632	Recent findings showed an involvement of glutamate in cue induced <b>relapse</b> and suggest that subtype 5 of metabotropic glutamate receptors (<strong>mGluR5</strong>) is involved in conditioned drug reward.
+GRM5	addiction	reward	15555632	Recent findings showed an involvement of glutamate in cue induced relapse and suggest that subtype 5 of metabotropic glutamate receptors (<strong>mGluR5</strong>) is involved in conditioned drug <b>reward</b>.
+GRM5	drug	cocaine	15555632	The present study applied the conditioned place preference (CPP) paradigm to examine the involvement of <strong>mGluR5</strong> in <b>cocaine</b>  and morphine induced behaviours.
+GRM5	drug	opioid	15555632	The present study applied the conditioned place preference (CPP) paradigm to examine the involvement of <strong>mGluR5</strong> in cocaine  and <b>morphine</b> induced behaviours.
+GRM5	addiction	reward	15555632	The present study applied the conditioned place preference (<b>CPP</b>) paradigm to examine the involvement of <strong>mGluR5</strong> in cocaine  and morphine induced behaviours.
+GRM5	drug	cocaine	15555632	In conclusion, <strong>mGluR5</strong> are involved in modulation of spontaneous and <b>cocaine</b> induced locomotion, in state dependent learning and in expression of morphine CPP.
+GRM5	drug	opioid	15555632	In conclusion, <strong>mGluR5</strong> are involved in modulation of spontaneous and cocaine induced locomotion, in state dependent learning and in expression of <b>morphine</b> CPP.
+GRM5	addiction	reward	15555632	In conclusion, <strong>mGluR5</strong> are involved in modulation of spontaneous and cocaine induced locomotion, in state dependent learning and in expression of morphine <b>CPP</b>.
+GRM5	addiction	addiction	15550570	The <strong>mGluR5</strong> subtype, in particular, has come under scrutiny due to its distribution in brain regions associated with drug <b>addiction</b>.
+GRM5	drug	cocaine	15550570	This study investigated interactions between the selective <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) and <b>cocaine</b> in squirrel monkeys whose lever pressing behavior was 1) maintained under a second order schedule of <b>cocaine</b> self administration, 2) extinguished and then reinstated by <b>cocaine</b> priming, and 3) controlled by the discriminative stimulus (DS) effects of <b>cocaine</b>.
+GRM5	drug	cocaine	15550570	The findings point to a significant contribution of <strong>mGluR5</strong> mechanisms in the behavioral effects of <b>cocaine</b> related to its abuse and suggest that MPEP has properties of a functional <b>cocaine</b> antagonist, which are not secondary to antagonism at NMDA receptors.
+GRM5	drug	alcohol	15548766	The <strong>mGluR5</strong> antagonist 6 methyl 2 (phenylethynyl)pyridine decreases <b>ethanol</b> consumption via a protein kinase C epsilon dependent mechanism.
+GRM5	drug	alcohol	15548766	Glutamatergic neurotransmission plays a critical role in addictive behaviors, and recent evidence indicates that genetic or pharmacological inactivation of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) reduces the self administration of cocaine, nicotine, and <b>alcohol</b>.
+GRM5	drug	cocaine	15548766	Glutamatergic neurotransmission plays a critical role in addictive behaviors, and recent evidence indicates that genetic or pharmacological inactivation of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) reduces the self administration of <b>cocaine</b>, nicotine, and alcohol.
+GRM5	drug	nicotine	15548766	Glutamatergic neurotransmission plays a critical role in addictive behaviors, and recent evidence indicates that genetic or pharmacological inactivation of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) reduces the self administration of cocaine, <b>nicotine</b>, and alcohol.
+GRM5	addiction	addiction	15548766	Glutamatergic neurotransmission plays a critical role in <b>addictive</b> behaviors, and recent evidence indicates that genetic or pharmacological inactivation of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>) reduces the self administration of cocaine, nicotine, and alcohol.
+GRM5	drug	alcohol	15548766	Because <strong>mGluR5</strong> is coupled to activation of protein kinase C (PKC), and targeted deletion of the epsilon isoform (PKCepsilon) in mice reduces <b>ethanol</b> self administration, we investigated whether there is a functional link between <strong>mGluR5</strong> and PKCepsilon.
+GRM5	drug	alcohol	15548766	We also show that MPEP dose dependently reduced <b>ethanol</b> consumption in wild type but not in PKCepsilon null mice, suggesting that PKCepsilon is an important signaling target for modulation of <b>ethanol</b> consumption by <strong>mGluR5</strong> antagonists.
+GRM5	drug	alcohol	15548766	Our data indicate that <strong>mGluR5</strong> is coupled to PKCepsilon via a PI3K dependent pathway and that PKCepsilon is required for the ability of the <strong>mGluR5</strong> antagonist MPEP to reduce <b>ethanol</b> consumption.
+GRM5	drug	nicotine	15542754	These results demonstrate that activation of GABAB receptors or blockade of <strong>mGluR5</strong> decreased <b>nicotine</b> self administration.
+GRM5	drug	nicotine	15542754	Thus, compounds that increase GABAergic neurotransmission and antagonists at <strong>mGluR5</strong> have potential as anti <b>smoking</b> medications for humans.
+GRM5	addiction	sensitization	15517195	Behavioral <b>sensitization</b> due to social defeat stress in mice: antagonism at <strong>mGluR5</strong> and NMDA receptors.
+GRM5	drug	amphetamine	15517195	We evaluated the role of <strong>mGluR5</strong> and NMDA glutamate receptors in the development of <b>amphetamine</b> induced and social defeat stress induced sensitization, using the non competitive <strong>mGluR5</strong> antagonist, MPEP, and the non competitive NMDA antagonist, dizocilpine (MK 801).
+GRM5	addiction	sensitization	15517195	We evaluated the role of <strong>mGluR5</strong> and NMDA glutamate receptors in the development of amphetamine induced and social defeat stress induced <b>sensitization</b>, using the non competitive <strong>mGluR5</strong> antagonist, MPEP, and the non competitive NMDA antagonist, dizocilpine (MK 801).
+GRM5	drug	amphetamine	15517195	These data indicate that behavioral sensitization to social defeat stress is dependent on <strong>mGluR5</strong> receptors, whereas low dose <b>amphetamine</b> sensitization may not be.
+GRM5	addiction	sensitization	15517195	These data indicate that behavioral <b>sensitization</b> to social defeat stress is dependent on <strong>mGluR5</strong> receptors, whereas low dose amphetamine <b>sensitization</b> may not be.
+GRM5	drug	alcohol	15365315	In the dentate gyrus, mGlu3 and <strong>mGlu5</strong> receptor mRNA levels were significantly lower in the <b>ethanol</b> treated rats than in the control rats.
+GRM5	drug	alcohol	15365315	In the CA3 region, the mRNA expression of mGlu1, <strong>mGlu5</strong>, and mGlu7 receptors showed substantial decreases after <b>ethanol</b> exposure.
+GRM5	drug	cocaine	15363959	Previous studies in metabotropic glutamate 5 receptor (<strong>mGlu5</strong> receptor) deficient mice have indicated the importance of this receptor in the self administration of <b>cocaine</b> and locomotor sensitisation to this stimulant.
+GRM5	drug	cocaine	15363959	In the present series of experiments we further investigated the role of <strong>mGlu5</strong> receptors on nicotine, <b>cocaine</b>  and food taking behaviour.
+GRM5	drug	nicotine	15363959	In the present series of experiments we further investigated the role of <strong>mGlu5</strong> receptors on <b>nicotine</b>, cocaine  and food taking behaviour.
+GRM5	drug	nicotine	15363959	We also investigated the effects of the <strong>mGlu5</strong> receptor antagonist MPEP (2 methyl 6 (phenylethynyl)pyridine) on the acute locomotor activating effects of <b>nicotine</b>, the expression of sensitisation to its repeated, intermittent administration, and <b>nicotine</b> triggered relapse to <b>nicotine</b> seeking behaviour.
+GRM5	addiction	relapse	15363959	We also investigated the effects of the <strong>mGlu5</strong> receptor antagonist MPEP (2 methyl 6 (phenylethynyl)pyridine) on the acute locomotor activating effects of nicotine, the expression of sensitisation to its repeated, intermittent administration, and nicotine triggered <b>relapse</b> to nicotine <b>seeking</b> behaviour.
+GRM5	addiction	addiction	15363959	Altogether, the present findings strengthen the hypothesis that selective antagonism at <strong>mGlu5</strong> receptors may be a new potential pharmacotherapeutic approach for the treatment of drug dependence and <b>addiction</b>.
+GRM5	addiction	dependence	15363959	Altogether, the present findings strengthen the hypothesis that selective antagonism at <strong>mGlu5</strong> receptors may be a new potential pharmacotherapeutic approach for the treatment of drug <b>dependence</b> and addiction.
+GRM5	drug	opioid	15355330	The aim of the present study was to clarify the role of the metabotropic glutamate 5 (<strong>mGlu5</strong>) receptor subtype in the development of rewarding effect induced by a prototypical mu <b>opioid</b> receptor agonist <b>morphine</b> in the mouse.
+GRM5	drug	opioid	15355330	administration of a selective <strong>mGlu5</strong> receptor antagonist, 2 methyl 6 (phenylethynyl) pyridine (MPEP), attenuated the <b>morphine</b> induced rewarding effects.
+GRM5	drug	opioid	15355330	Furthermore, it should be mentioned that the protein level of <strong>mGlu5</strong> was significantly increased in membrane preparations of the limbic forebrain obtained from <b>morphine</b> conditioned mice compared to those from saline conditioned mice.
+GRM5	drug	opioid	15355330	As well as the result from the immunoblot analysis, we demonstrated using the receptor binding assay that the number of <strong>mGlu5</strong> receptors in the mouse limbic forebrain was significantly increased by <b>morphine</b> conditioning.
+GRM5	drug	opioid	15355330	The present data provide direct evidence that the activation of <strong>mGlu5</strong> receptor linked to the increased PKCgamma isoform in the mouse limbic forebrain is implicated in the development of rewarding effect of <b>morphine</b>.
+GRM5	drug	cocaine	15295029	Both CB1R and <strong>mGluR5</strong> are involved in <b>cocaine</b> related behaviors; however, the impact of in vivo <b>cocaine</b> exposure on eCB mediated retrograde synaptic plasticity remains unknown.
+GRM5	drug	cocaine	15295029	We found that the <b>cocaine</b> induced blockade of retrograde signaling was correlated with enhanced expression levels of Homer scaffolding proteins containing the coiled coil domain and accompanied by a strong reduction of <strong>mGluR5</strong> surface expression.
+GRM5	drug	cocaine	15295029	The results suggest that <b>cocaine</b> induced loss of eCB retrograde signaling is caused by a reduction in the ability of <strong>mGluR5</strong> to translate anterograde glutamate transmission into retrograde eCB signaling.
+GRM5	drug	opioid	15178357	Effects of mGlu1 and <strong>mGlu5</strong> metabotropic glutamate antagonists to reverse <b>morphine</b> tolerance in mice.
+GRM5	drug	cannabinoid	15016425	In the current study, a possible interaction between spinal cord dorsal horn <b>cannabinoid</b> and <strong>mGlu5</strong> receptors was evaluated in rats with a peripheral nerve injury.
+GRM5	drug	amphetamine	15010207	<strong>mGluR5</strong> dependent increases in immediate early gene expression in the rat striatum following acute administration of <b>amphetamine</b>.
+GRM5	drug	amphetamine	15010207	This study investigated the role of <strong>mGluR5</strong> in the mediation of IEG expression in the rat striatum induced by a single dose of <b>AMPH</b> (4 mg/kg, i.p.)
+GRM5	drug	amphetamine	15010207	In contrast to c fos mRNAs, <b>AMPH</b> stimulated mRNA expression of another IEG, zif/268, was not significantly altered by the blockade of <strong>mGluR5</strong> with MPEP in the entire striatum and the three areas of cortex.
+GRM5	drug	amphetamine	15010207	These results indicate that an <strong>mGluR5</strong> dependent mechanism selectively contributes to c fos expression in the striatum and cortex in response to acute exposure to <b>AMPH</b>.
+GRM5	drug	alcohol	14735132	<strong>mGluR5</strong> antagonist MPEP reduces <b>ethanol</b> seeking and relapse behavior.
+GRM5	addiction	relapse	14735132	<strong>mGluR5</strong> antagonist MPEP reduces ethanol <b>seeking</b> and <b>relapse</b> behavior.
+GRM5	drug	alcohol	14735132	Metabotropic glutamate receptors subtype 5 (<strong>mGluR5</strong>) are modulators of glutamatergic neurotransmission and are abundant in brain regions known to be involved in <b>ethanol</b> self administration.
+GRM5	drug	alcohol	14735132	Here, we studied the effects of 2 methyl 6 (phenylethynyl) pyridine (MPEP), a highly potent, noncompetitive <strong>mGlu5</strong> receptor antagonist, on voluntary <b>ethanol</b> consumption and relapse behavior.
+GRM5	addiction	relapse	14735132	Here, we studied the effects of 2 methyl 6 (phenylethynyl) pyridine (MPEP), a highly potent, noncompetitive <strong>mGlu5</strong> receptor antagonist, on voluntary ethanol consumption and <b>relapse</b> behavior.
+GRM5	drug	alcohol	14735132	These results show in two commonly used models of relapse to <b>ethanol</b> that pharmacological targeting of <strong>mGlu5</strong> receptors may be a promising approach for the treatment of <b>alcoholism</b>.
+GRM5	addiction	relapse	14735132	These results show in two commonly used models of <b>relapse</b> to ethanol that pharmacological targeting of <strong>mGlu5</strong> receptors may be a promising approach for the treatment of alcoholism.
+GRM5	drug	cannabinoid	14690633	These strategies focus on altering reward processes in the brain by modulating various neurotransmitter systems: the most promising include dopamine D(3) receptor antagonists, noradrenaline reuptake inhibitors, GABA(B) receptor agonists, metabotropic glutamate 5 (<strong>mGluR5</strong>) receptor antagonists, <b>cannabinoid</b> CB1 receptor antagonists, and corticotropin releasing factor (CRF) 1 receptor antagonists.
+GRM5	addiction	reward	14690633	These strategies focus on altering <b>reward</b> processes in the brain by modulating various neurotransmitter systems: the most promising include dopamine D(3) receptor antagonists, noradrenaline reuptake inhibitors, GABA(B) receptor agonists, metabotropic glutamate 5 (<strong>mGluR5</strong>) receptor antagonists, cannabinoid CB1 receptor antagonists, and corticotropin releasing factor (CRF) 1 receptor antagonists.
+GRM5	drug	nicotine	12682710	The <strong>mGluR5</strong> antagonist MPEP decreased <b>nicotine</b> self administration in rats and mice.
+GRM5	drug	nicotine	12682710	The present study investigated the effects of the <strong>mGluR5</strong> antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) on intravenous <b>nicotine</b> self administration in Wistar rats and DBA/2J mice.
+GRM5	drug	cocaine	12682710	These results indicate that blockade of <strong>mGluR5</strong> decreased nicotine self administration in both rats and mice, and are consistent with findings showing a role of <strong>mGluR5</strong> in <b>cocaine</b> self administration.
+GRM5	drug	nicotine	12682710	These results indicate that blockade of <strong>mGluR5</strong> decreased <b>nicotine</b> self administration in both rats and mice, and are consistent with findings showing a role of <strong>mGluR5</strong> in cocaine self administration.
+GRM5	drug	nicotine	12682710	It is postulated that <strong>mGluR5</strong> plays an essential role in mediating the reinforcing effects of <b>nicotine</b>, possibly but not exclusively, via modulation of mesolimbic dopaminergic neurotransmission.
+GRM5	addiction	reward	12682710	It is postulated that <strong>mGluR5</strong> plays an essential role in mediating the <b>reinforcing</b> effects of nicotine, possibly but not exclusively, via modulation of mesolimbic dopaminergic neurotransmission.
+GRM5	drug	opioid	12527470	<b>Morphine</b> conditioned reward is inhibited by MPEP, the <strong>mGluR5</strong> antagonist.
+GRM5	addiction	reward	12527470	Morphine conditioned <b>reward</b> is inhibited by MPEP, the <strong>mGluR5</strong> antagonist.
+GRM5	drug	opioid	12527470	In the present study we examined the effect of MPEP [2 methyl 6 (phenylethynyl) pyridine] a potent, selective and systemically active metabotropic glutamate receptor (mGluR) type I (subtype <strong>mGluR5</strong>) antagonist on conditioned <b>morphine</b> reward in mice.
+GRM5	addiction	reward	12527470	In the present study we examined the effect of MPEP [2 methyl 6 (phenylethynyl) pyridine] a potent, selective and systemically active metabotropic glutamate receptor (mGluR) type I (subtype <strong>mGluR5</strong>) antagonist on conditioned morphine <b>reward</b> in mice.
+GRM5	drug	opioid	12527470	These data suggest that <strong>mGluR5</strong> may be involved in conditioned <b>morphine</b> reward.
+GRM5	addiction	reward	12527470	These data suggest that <strong>mGluR5</strong> may be involved in conditioned morphine <b>reward</b>.
+GRM5	drug	cocaine	12494407	The <strong>mGluR5</strong> antagonist MPEP reduces the conditioned rewarding effects of <b>cocaine</b> but not other drugs of abuse.
+GRM5	addiction	reward	12494407	We examined the ability of 2 methyl 6 (phenylethynyl) pyridine (MPEP), a selective antagonist of the type 5 metabotropic glutamate receptor (<strong>mGluR5</strong>), to reduce the rewarding effects of various drugs of abuse in the conditioned place preference (<b>CPP</b>) paradigm.
+GRM5	drug	cocaine	12494407	These data provide further support for a role of the <strong>mGluR5</strong> receptor in the rewarding effects of <b>cocaine</b>.
+GRM5	drug	cocaine	11528416	Reinforcing and locomotor stimulant effects of <b>cocaine</b> are absent in <strong>mGluR5</strong> null mutant mice.
+GRM5	addiction	reward	11528416	<b>Reinforcing</b> and locomotor stimulant effects of cocaine are absent in <strong>mGluR5</strong> null mutant mice.
+GRM5	drug	cocaine	11528416	Here we show that mice lacking the <strong>mGluR5</strong> gene do not self administer <b>cocaine</b>, and show no increased locomotor activity following <b>cocaine</b> treatment, despite showing <b>cocaine</b> induced increases in nucleus accumbens (NAcc) dopamine (DA) levels similar to wild type (WT) mice.
+GRM5	drug	cocaine	11528416	These results demonstrate a significant contribution of <strong>mGlu5</strong> receptors to the behavioral effects of <b>cocaine</b>, and suggest that they may be involved in <b>cocaine</b> addiction.
+GRM5	addiction	addiction	11528416	These results demonstrate a significant contribution of <strong>mGlu5</strong> receptors to the behavioral effects of cocaine, and suggest that they may be involved in cocaine <b>addiction</b>.
+GRM5	drug	amphetamine	11418936	Differentially altered mGluR1 and <strong>mGluR5</strong> mRNA expression in rat caudate nucleus and nucleus accumbens in the development and expression of behavioral sensitization to repeated <b>amphetamine</b> administration.
+GRM5	addiction	sensitization	11418936	Differentially altered mGluR1 and <strong>mGluR5</strong> mRNA expression in rat caudate nucleus and nucleus accumbens in the development and expression of behavioral <b>sensitization</b> to repeated amphetamine administration.
+GRM5	drug	amphetamine	11418936	Three hours after acute administration of <b>AMPH</b> to naive rats, mGluR1 and <strong>mGluR5</strong> mRNA expression in the dorsal (caudatoputamen) and ventral (nucleus accumbens) striatum showed no change as compared to acute saline injection.
+GRM5	drug	amphetamine	11418936	Conversely, <strong>mGluR5</strong> levels were markedly reduced 3 h after the final of five daily <b>AMPH</b> treatments in the entire striatum of sensitized rats (34% and 77% of controls in the dorsal and ventral striatum, respectively).
+HTR2A	drug	cocaine	32587535	Methylation Patterns of the <strong>HTR2A</strong> Associate With Relapse Related Behaviors in <b>Cocaine</b> Dependent Participants.
+HTR2A	addiction	relapse	32587535	Methylation Patterns of the <strong>HTR2A</strong> Associate With <b>Relapse</b> Related Behaviors in Cocaine Dependent Participants.
+HTR2A	addiction	relapse	32587535	Preclinical evidence implicates serotonin (5 HT) neurotransmission through the <strong>5 HT2A</strong> receptor (5 HT2AR) as a driver of individual differences in these <b>relapse</b> related behaviors.
+HTR2A	drug	cocaine	32587535	In the present study, we tested the hypothesis that methylation of the <strong>HTR2A</strong> may associate with relapse related behavioral vulnerability in <b>cocaine</b> dependent participants versus healthy controls.
+HTR2A	addiction	relapse	32587535	In the present study, we tested the hypothesis that methylation of the <strong>HTR2A</strong> may associate with <b>relapse</b> related behavioral vulnerability in cocaine dependent participants versus healthy controls.
+HTR2A	drug	cocaine	32587535	DNA methylation at these cytosine residues of the <strong>HTR2A</strong> promoter may be differentially associated with impulsivity or <b>cocaine</b> associated environmental cues.
+HTR2A	addiction	relapse	32587535	Taken together, these data suggest that methylation of the <strong>HTR2A</strong> may contribute to individual differences in <b>relapse</b> related behaviors in CUD.
+HTR2A	drug	opioid	32458577	Effects of <strong>5 HT2A</strong> receptor stimulation on economic demand for <b>fentanyl</b> after intermittent and continuous access self administration in male rats.
+HTR2A	drug	opioid	32458577	Here, we determined how different intake patterns of <b>fentanyl</b>, a μ <b>opioid</b> agonist, alter economic demand for <b>fentanyl</b> and how <strong>5 HT2A</strong> receptor stimulation affects economic demand for <b>fentanyl</b>.
+HTR2A	drug	opioid	32458577	We subsequently tested the acute effects of <strong>5 HT2A</strong> receptor stimulation with psychedelic 2,5 dimethoxy 4 iodoamphetamine (DOI) on economic demand for <b>fentanyl</b>.
+HTR2A	drug	psychedelics	32458577	We subsequently tested the acute effects of <strong>5 HT2A</strong> receptor stimulation with <b>psychedelic</b> 2,5 dimethoxy 4 iodoamphetamine (DOI) on economic demand for fentanyl.
+HTR2A	drug	opioid	32458577	), blocked the effects of DOI, indicating that DOI is acting through <strong>5 HT2A</strong> receptors to alter economic demand for <b>fentanyl</b>.
+HTR2A	drug	opioid	32458577	These results demonstrate that both intermittent and continuous <b>fentanyl</b> experience raise the economic demand for <b>fentanyl</b>, and acute <strong>5 HT2A</strong> receptor activation reduces economic demand for <b>fentanyl</b> and food.
+HTR2A	drug	psychedelics	32371500	The mind altering qualities of <b>psychedelics</b> have been attributed, through serotonin 2A (<strong>5 HT2A</strong>) receptor agonism, to 'reset' areas of functional connectivity (FC) in the brain that play prominent roles in many central neuropathic states.
+HTR2A	drug	psychedelics	32371500	While the mechanisms by which the classic <b>psychedelics</b> may provide analgesia are not clear, several possibilities exist given the similarity between <strong>5 HT2A</strong> activation pathways of <b>psychedelics</b> and the nociceptive modulation pathways in humans.
+HTR2A	drug	psychedelics	32249347	Serotonergic 5 hydroxytryptamine 2A (<strong>5 HT2A</strong>) receptors mediate alterations of perception and cognition that are induced by serotonergic <b>psychedelics</b>.
+HTR2A	drug	cannabinoid	32199997	Adenosine A1 receptor agonist induces visceral antinociception via 5 HT1A, <strong>5 HT2A</strong>, dopamine D1 or <b>cannabinoid</b> CB1 receptors, and the opioid system in the central nervous system.
+HTR2A	drug	opioid	32199997	Adenosine A1 receptor agonist induces visceral antinociception via 5 HT1A, <strong>5 HT2A</strong>, dopamine D1 or cannabinoid CB1 receptors, and the <b>opioid</b> system in the central nervous system.
+HTR2A	drug	opioid	32199997	These results suggest that 5 HT1A, <strong>5 HT2A</strong>, dopamine D1, CB1 receptors and the <b>opioid</b> system in the CNS may specifically mediate the CPA induced visceral antinociception.
+HTR2A	drug	psychedelics	32128596	The behavioural experiments are mainly related with the hallucinogenic effect of 25I <b>NBOMe</b> while the in vitro studies concerning mainly the affinity for <strong>5 HT2A</strong> receptors.
+HTR2A	drug	cannabinoid	32125460	<strong>5 HT2A</strong> receptors but not <b>cannabinoid</b> receptors in the central nervous system mediate levodopa induced visceral antinociception in conscious rats.
+HTR2A	drug	alcohol	31954952	Evidence suggests that aripiprazole, a partial dopamine D2 and serotonin 5 HT1A receptor agonist and <strong>5 HT2A</strong> receptor antagonist, show significant efficacy in reducing <b>alcohol</b> use.
+HTR2A	drug	psychedelics	31915427	25I <b>NBOMe</b> acts as full agonist on serotonergic <strong>5 HT2A</strong> receptors.
+HTR2A	drug	psychedelics	31829932	We will show that although <b>ketamine</b> and serotonergic <b>psychedelics</b> have affinity for very different receptors (NMDA, <strong>5 HT2A</strong>), they ultimately initiate similar plastic adaptations in the prefrontal cortex through the involvement of the brain derived neurotrophic factor (BDNF).
+HTR2A	drug	psychedelics	31749223	Pretreatment with SCH23390 (SCH), Haloperidol (HAL), and ketanserin (KS), antagonists of dopamine D1 (DRD1), dopamine D2 (DRD2), and serotonin 2A (<strong>5 HT2A</strong> receptor) receptors, respectively, was utilized during a CPP test to investigate the involvement of the dopaminergic and serotonergic systems in 25B <b>NBOMe</b> mediated effects.
+HTR2A	addiction	reward	31749223	Pretreatment with SCH23390 (SCH), Haloperidol (HAL), and ketanserin (KS), antagonists of dopamine D1 (DRD1), dopamine D2 (DRD2), and serotonin 2A (<strong>5 HT2A</strong> receptor) receptors, respectively, was utilized during a <b>CPP</b> test to investigate the involvement of the dopaminergic and serotonergic systems in 25B NBOMe mediated effects.
+HTR2A	drug	psychedelics	31749223	In addition, we explored the involvement of <strong>5 HT2A</strong> receptors in the 25B <b>NBOMe</b> induced head twitch response (HTR).
+HTR2A	drug	psychedelics	31749223	25B <b>NBOMe</b> induced HTR and increased <strong>5 HT2A</strong> receptor mRNA levels, effects inhibited by KS.
+HTR2A	drug	psychedelics	31634774	In order to substantiate the '<b>psilocybin</b> telomere hypothesis' potential neuropsychopharmacological, endocrinological, and genetic mechanisms of action are discussed (e.g., HPA axis reactivity, hippocampal neurogenesis, neurotropic growth factors such as BDNF, <strong>5 HT2A</strong> receptor agonism, neuroplasticity/synaptoplasticity, brain wide alterations in neuronal functional connectivity density, involvement of the SLC6A4 serotonin transporter gene, inter alia).
+HTR2A	drug	nicotine	31585211	Inverse agonists of the <strong>5 HT2A</strong> receptor reduce <b>nicotine</b> withdrawal signs in rats.
+HTR2A	addiction	withdrawal	31585211	Inverse agonists of the <strong>5 HT2A</strong> receptor reduce nicotine <b>withdrawal</b> signs in rats.
+HTR2A	drug	nicotine	31585211	Previous work has shown that chronic <b>nicotine</b> administration causes adaptive changes in <strong>5 HT2A</strong> receptor expression.
+HTR2A	drug	nicotine	31585211	Based on this relationship, it was hypothesized that inactivating <strong>5 HT2A</strong> receptors with the inverse agonists pimavanserin and volinanserin (MDL100907), would reduce the symptoms of <b>nicotine</b> withdrawal syndrome.
+HTR2A	addiction	withdrawal	31585211	Based on this relationship, it was hypothesized that inactivating <strong>5 HT2A</strong> receptors with the inverse agonists pimavanserin and volinanserin (MDL100907), would reduce the symptoms of nicotine <b>withdrawal</b> syndrome.
+HTR2A	drug	nicotine	31585211	The results suggest that the <strong>5 HT2A</strong> receptor contributes to mediating <b>nicotine</b> withdrawal syndrome, and thus represents a potential target for interventions to aid <b>smoking</b> cessation.
+HTR2A	addiction	withdrawal	31585211	The results suggest that the <strong>5 HT2A</strong> receptor contributes to mediating nicotine <b>withdrawal</b> syndrome, and thus represents a potential target for interventions to aid smoking cessation.
+HTR2A	drug	psychedelics	31452444	Like other <b>psychedelics</b>, D lysergic acid diethylamide (<b>LSD</b>) affects numerous serotonin receptors, and according to the current dogma, the <strong>5 HT2A</strong> receptors are considered the main target for its hallucinogenic effects.
+HTR2A	drug	psychedelics	31452444	Using male Sprague Dawley rats, we examined the effects of <strong>5 HT2A</strong> and 5 HT5A receptor antagonists on <b>LSD</b> induced stimulus control in the two lever drug discrimination test using a FR10 schedule of reinforcement.
+HTR2A	addiction	reward	31452444	Using male Sprague Dawley rats, we examined the effects of <strong>5 HT2A</strong> and 5 HT5A receptor antagonists on LSD induced stimulus control in the two lever drug discrimination test using a FR10 schedule of <b>reinforcement</b>.
+HTR2A	drug	alcohol	31309240	The effects of DOI were examined using <b>ethanol</b> induced place conditioning (1.8 g/kg <b>ethanol</b>) and 2 bottle choice <b>ethanol</b> drinking (20% v/v), using a dose of DOI (3 mg/kg) that produced the maximal response in the serotonin 2A (<strong>5 HT2A</strong>) receptor dependent head twitch assay.
+HTR2A	drug	alcohol	31309240	DOI induced suppression of <b>alcohol</b> drinking depended upon <strong>5 HT2A</strong> receptors, was selective for <b>alcohol</b> over water, and was selective for high <b>alcohol</b> preferring subjects.
+HTR2A	drug	amphetamine	31104538	Mirtazapine, an antagonist of the α2 adrenoceptor and the <strong>5 HT2A</strong>/C and the 5 HT3 receptors has proven effective in reducing the cocaine, nicotine and <b>methamphetamine</b> behavioural effects in humans and animals.
+HTR2A	drug	cocaine	31104538	Mirtazapine, an antagonist of the α2 adrenoceptor and the <strong>5 HT2A</strong>/C and the 5 HT3 receptors has proven effective in reducing the <b>cocaine</b>, nicotine and methamphetamine behavioural effects in humans and animals.
+HTR2A	drug	nicotine	31104538	Mirtazapine, an antagonist of the α2 adrenoceptor and the <strong>5 HT2A</strong>/C and the 5 HT3 receptors has proven effective in reducing the cocaine, <b>nicotine</b> and methamphetamine behavioural effects in humans and animals.
+HTR2A	drug	nicotine	31061854	This article contains data on the allele and genotype frequency for single nucleotide polymorphisms (SNPs) in candidate genes CHRNA5 (rs16969968, rs17408276, rs680244) CHRNA3 (rs6495307, rs12914385) NRXN1 (rs10865246, rs1882296, rs985919) and <strong>HTR2A</strong> (rs6311, rs6313) previously evaluated as genetic risk variants for cigarette <b>smoking</b> at an early age and relapse to <b>smoking</b> cessation treatment Pérez Rubio et al., 2018.
+HTR2A	addiction	relapse	31061854	This article contains data on the allele and genotype frequency for single nucleotide polymorphisms (SNPs) in candidate genes CHRNA5 (rs16969968, rs17408276, rs680244) CHRNA3 (rs6495307, rs12914385) NRXN1 (rs10865246, rs1882296, rs985919) and <strong>HTR2A</strong> (rs6311, rs6313) previously evaluated as genetic risk variants for cigarette smoking at an early age and <b>relapse</b> to smoking cessation treatment Pérez Rubio et al., 2018.
+HTR2A	drug	alcohol	30998954	In vivo experiments demonstrated that carvedilol increases the <b>ethanol</b> induced loss of the righting reflex and suppresses operant responding in mice, and that these effects are attenuated by pretreatment with the selective <strong>5 HT2A</strong> receptor antagonist M100907.
+HTR2A	addiction	reward	30998954	In vivo experiments demonstrated that carvedilol increases the ethanol induced loss of the righting reflex and suppresses <b>operant</b> responding in mice, and that these effects are attenuated by pretreatment with the selective <strong>5 HT2A</strong> receptor antagonist M100907.
+HTR2A	addiction	relapse	30738094	When the risk of <b>relapse</b> was analyzed one month after the end of treatment, regardless of the age of onset, the T allele (rs6313) of <strong>HTR2A</strong> appeared to be a risk factor for <b>relapse</b> (OR = 2.92, 95% CI = 1.06 8.11); the T allele was found more frequently in those who relapsed (50.0%) compared with people who maintained abstinence (25.4%) (p = 0.0332).
+HTR2A	drug	nicotine	30738094	Our findings suggest that in Mexican mestizos who smoke cigarettes, the presence of the T allele in rs6313 of the <strong>HTR2A</strong> gene increases the risk for the early onset of cigarette <b>smoking</b> as well as the risk for relapsing one month after completing <b>smoking</b> cessation treatment.
+HTR2A	drug	psychedelics	30629611	In the binding (radioligand displacement) studies some of these compounds exhibited only modest selectivity for either <strong>5 HT2A</strong> or 5 HT2C receptors suggesting that a few of them, with affinities in the 10 100 nanomolar range for <strong>5 HT2A</strong> receptors, might presumably be <b>psychedelic</b>.
+HTR2A	drug	psychedelics	30628811	The prototype <strong>5 HT2A</strong> receptor agonist hallucinogens <b>LSD</b>, <b>mescaline</b>, and <b>psilocybin</b> are classified as Schedule 1 drugs of abuse by the U.S. Drug Enforcement Administration.
+HTR2A	drug	psychedelics	30628811	These results extend those of previous preclinical studies to suggest weak expression of abuse related effects by <strong>5 HT2A</strong> agonist hallucinogens and provide supportive evidence for therapeutic effects of repeated <b>LSD</b> dosing to attenuate KOR mediated depressant effects but not abuse potential of psychostimulants.
+HTR2A	addiction	reward	30469095	However, the role of <strong>5 HT2A</strong> receptors on the <b>reinforcing</b> effects of psychostimulant drugs has not been fully elucidated.
+HTR2A	drug	amphetamine	30469095	In the present study, we investigated the effects of the selective <strong>5HT2A</strong> receptor antagonist M100907 alone or in combination with the selective 5HT2C agonist WAY 163909 on intravenous <b>methamphetamine</b> self administration in rhesus macaques (N = 3).
+HTR2A	drug	amphetamine	30469095	Our study indicates that acute selective <strong>5 HT2A</strong> receptor blockade decreases peak <b>methamphetamine</b> intake in nonhuman primates.
+HTR2A	drug	amphetamine	30469095	Combination approaches with sub threshold doses of <strong>5 HT2A</strong> receptor antagonists and 5 HT2C receptor agonists, on the other hand, do not seem to be effective in decreasing <b>methamphetamine</b> reinforcement.
+HTR2A	addiction	reward	30469095	Combination approaches with sub threshold doses of <strong>5 HT2A</strong> receptor antagonists and 5 HT2C receptor agonists, on the other hand, do not seem to be effective in decreasing methamphetamine <b>reinforcement</b>.
+HTR2A	drug	cocaine	30373886	The <strong>5 HT2A</strong> Receptor (5 HT2AR) Regulates Impulsive Action and <b>Cocaine</b> Cue Reactivity in Male Sprague Dawley Rats.
+HTR2A	drug	cocaine	30373886	The investigational serotonin (5 HT) <strong>5 HT2A</strong> receptor (5 HT2AR) antagonist/inverse agonist M100907 suppresses impulsive action, or the inability to withhold premature responses, and <b>cocaine</b> seeking behaviors.
+HTR2A	addiction	relapse	30373886	The investigational serotonin (5 HT) <strong>5 HT2A</strong> receptor (5 HT2AR) antagonist/inverse agonist M100907 suppresses impulsive action, or the inability to withhold premature responses, and cocaine <b>seeking</b> behaviors.
+HTR2A	drug	psychedelics	30318013	Its pharmacodynamic mechanisms of action are primarily attributed to the interaction with the serotonergic <strong>5 HT2A</strong> C receptors, and therefore clinical effects are similar to those elicited by other psychoactive substances, such as lysergic acid diethylamide (<b>LSD</b>) and <b>psilocybin</b>, which include euphoria, hallucinations, depersonalization and psychoses.
+HTR2A	drug	psychedelics	30261175	25D <b>NBOMe</b>, 25E <b>NBOMe</b>, 25H <b>NBOMe</b>, 25I NBOH and 25N <b>NBOMe</b> had very high affinity for, and full efficacy at, <strong>5 HT2A</strong> and 5 HT2C receptors.
+HTR2A	drug	psychedelics	30261175	In the <strong>5 HT2A</strong> receptor functional assay, 25D <b>NBOMe</b>, 25E <b>NBOMe</b>, 25I NBOH and 25N <b>NBOMe</b> had subnanomolar to low nanomolar potencies similar to (+)lysergic acid diethylamide (<b>LSD</b>) while 25H <b>NBOMe</b> had lower potency, similar to serotonin.
+HTR2A	drug	amphetamine	30240581	Chronic <b>methamphetamine</b> self administration dysregulates <strong>5 HT2A</strong> and mGlu2 receptor expression in the rat prefrontal and perirhinal cortex: Comparison to chronic phencyclidine and MK 801.
+HTR2A	drug	amphetamine	30240581	Therefore, in the present study we examined the effects of chronic exposure to three different drugs known to produce persistent deficits in sensorimotor gating and cognition [<b>meth</b>, phencyclidine (PCP) and MK 801] on the expression of <strong>5 HT2A</strong> and mGlu2 within the rat medial prefrontal cortex (mPFC), dorsal hippocampus (dHPC) and perirhinal cortex (PRh).
+HTR2A	drug	amphetamine	30240581	We found that despite different pharmacological mechanism of action, chronic <b>meth</b>, PCP, and MK 801 similarly dysregulated <strong>5 HT2A</strong> and mGlu2, as indicated by an increase in the <strong>5 HT2A</strong>/mGlu2 expression ratio in the mPFC (all three tested drugs), PRh (<b>meth</b> and PCP), and dHPC (MK 801 only).
+HTR2A	drug	amphetamine	30240581	In summary, these data suggest that a shift towards increased availability (and G protein coupling) of cortical <strong>5 HT2A</strong> vs. mGlu2 receptors may represent a common neurobiological mechanism underlying the emergence of psychosis and cognitive deficits observed in subjects with <b>meth</b> use disorder and schizophrenia.
+HTR2A	drug	nicotine	30219683	Association of <strong>HTR2A</strong> 1438G/A Genetic Polymorphism With <b>Smoking</b> and Chronic Obstructive Pulmonary Disease.
+HTR2A	drug	nicotine	30219683	The aim of the current study was to analyze the effect of SLC6A4 (5HTT_LPR) (rs25531) and <strong>HTR2A</strong> 1438G/A (rs6311) genetic polymorphisms on the relation between <b>smoking</b> habits and COPD.
+HTR2A	drug	nicotine	30219683	The association between SLC6A4 (5HTT_LPR) (rs25531), <strong>HTR2A</strong> 1438G/A (rs6311), <b>smoking</b> degree and COPD was analyzed in a total of 77 COPD patients (active <b>smokers</b>) and 90 control subjects (active healthy <b>smokers</b>).
+HTR2A	drug	nicotine	30219683	Our results point a possible role of the A allele of <strong>HTR2A</strong> (rs6311) in COPD pathogenesis, suggesting that this effect depends partly on <b>tobacco</b> consumption due to a gene by environment interaction.
+HTR2A	addiction	relapse	29990431	To investigate large library docking's ability to find molecules with joint activity against on targets and selectivity versus antitargets, the dopamine D2 and serotonin <strong>5 HT2A</strong> receptors were targeted, <b>seeking</b> selectivity against the histamine H1 receptor.
+HTR2A	drug	psychedelics	29753748	<b>Psilocybin</b>, like other <strong>5 HT2A</strong> agonist classic <b>psychedelics</b>, has limited reinforcing effects, supporting marginal, transient non human self administration.
+HTR2A	addiction	reward	29753748	Psilocybin, like other <strong>5 HT2A</strong> agonist classic psychedelics, has limited <b>reinforcing</b> effects, supporting marginal, transient non human self administration.
+HTR2A	drug	opioid	29427652	Psychedelics comprise drugs come from various pharmacological classes including <strong>5 HT2A</strong> agonists, indirect 5 HT agonists, e.g., MDMA, NMDA antagonists and κ <b>opioid</b> receptor agonists.
+HTR2A	drug	psychedelics	29427652	<b>Psychedelics</b> comprise drugs come from various pharmacological classes including <strong>5 HT2A</strong> agonists, indirect 5 HT agonists, e.g., <b>MDMA</b>, NMDA antagonists and κ opioid receptor agonists.
+HTR2A	drug	opioid	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (<strong>HTR2A</strong>, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+HTR2A	addiction	dependence	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (<strong>HTR2A</strong>, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+HTR2A	drug	psychedelics	29302713	We studied ERPs in a serotonergic model of psychosis, induced by <b>psilocybin</b>, a <b>psychedelic</b> with <strong>5 HT2A</strong>/C agonistic properties, in healthy volunteers.
+HTR2A	drug	cocaine	29217539	Although this effect is partially inhibited by a 5 HT2C receptor antagonist (SB242084), lorcaserin also has effects at <strong>5 HT2A</strong> and 5 HT1A receptors, and the relative contribution of these receptors to its anti <b>cocaine</b> effects has not been investigated.
+HTR2A	drug	cocaine	29217539	Antagonism of 5 HT2C (but not 5 HT1A or <strong>5 HT2A</strong>) receptors blocked the effects of lorcaserin on <b>cocaine</b> and MDPV self administration.
+HTR2A	drug	nicotine	28900078	The relationship of HTR4 (rs3995090), <strong>HTR2A</strong> (rs6313), GRIK5 (rs8099939), GRIN2B (rs2268132), and CHRNB4 (rs1948) gene polymorphisms and COPD, as well as the contribution of these polymorphisms to the variations in quantitative characteristics that describe respiratory function, <b>smoking</b> behavior, and <b>nicotine</b> dependence was assessed in an ethnically homogeneous Tatar population.
+HTR2A	addiction	dependence	28900078	The relationship of HTR4 (rs3995090), <strong>HTR2A</strong> (rs6313), GRIK5 (rs8099939), GRIN2B (rs2268132), and CHRNB4 (rs1948) gene polymorphisms and COPD, as well as the contribution of these polymorphisms to the variations in quantitative characteristics that describe respiratory function, smoking behavior, and nicotine <b>dependence</b> was assessed in an ethnically homogeneous Tatar population.
+HTR2A	drug	nicotine	28900078	Importantly, the <strong>HTR2A</strong> (rs6313), GRIN2B (rs2268132), and GRIK5 (rs8099939) polymorphisms were only associated with COPD in <b>smokers</b>.
+HTR2A	drug	nicotine	28900078	The TT genotype of <strong>HTR2A</strong> (rs6313) was associated with a reduced risk of the disease in the group with moderate <b>nicotine</b> dependence (P = 0.02, OR = 0.22).
+HTR2A	addiction	dependence	28900078	The TT genotype of <strong>HTR2A</strong> (rs6313) was associated with a reduced risk of the disease in the group with moderate nicotine <b>dependence</b> (P = 0.02, OR = 0.22).
+HTR2A	drug	nicotine	28900078	The CC genotype of <strong>HTR2A</strong> (rs6313) and the TT genotype of GRIN2B (rs2268132) were associated with higher levels of <b>nicotine</b> dependence according to the Fagerstrõm test (P = 0.0011 and P = 0.037).
+HTR2A	addiction	dependence	28900078	The CC genotype of <strong>HTR2A</strong> (rs6313) and the TT genotype of GRIN2B (rs2268132) were associated with higher levels of nicotine <b>dependence</b> according to the Fagerstrõm test (P = 0.0011 and P = 0.037).
+HTR2A	drug	psychedelics	28890736	The designer drug, 2 (4 bromo 2, 5 dimethoxyphenyl) N (2 methoxybenzyl) ethanamine (25B <b>NBOMe</b>) is considered to be one of the most potent agonists of the serotonin 2A (<strong>5 HT2A</strong>) receptor.
+HTR2A	drug	psychedelics	28890736	This 25B <b>NBOMe</b> induced rhabdomyolysis was inhibited by the <strong>5 HT2A</strong> receptor antagonists ritanserin and aripirazole, but not by the 5 HT1A + 5 HT1B receptor antagonist propranolol and the 5 HT3 receptor antagonist granisetron, indicating <strong>5 HT2A</strong> dependent rhabdomyolysis.
+HTR2A	drug	amphetamine	28855876	3,4 Methylenedioxymethamphetamine (MDMA) and its derivatives, 2,5 dimethoxy 4 bromo <b>amphetamine</b> hydrobromide (DOB) and para methoxyamphetamine (PMA), are recreational drugs whose pharmacological effects have recently been attributed to serotonin <strong>5HT2A</strong>/C receptors.
+HTR2A	drug	psychedelics	28855876	3,4 <b>Methylenedioxymethamphetamine</b> (<b>MDMA</b>) and its derivatives, 2,5 dimethoxy 4 bromo amphetamine hydrobromide (DOB) and para methoxyamphetamine (PMA), are recreational drugs whose pharmacological effects have recently been attributed to serotonin <strong>5HT2A</strong>/C receptors.
+HTR2A	drug	opioid	28831734	A range of agonists or positive allosteric modulators (PAMs) for mostly Gi/o coupled receptors, including metabotropic glutamate2 (mGlu2), adenosine A1, or μ <b>opioid</b> receptors, suppress these effects of <strong>5 HT2A</strong> receptor stimulation.
+HTR2A	addiction	reward	28831734	These effects on <strong>5 HT2A</strong> receptors and related GPCRs appear to play a major role in the behavioral effects of serotonergic hallucinogens, such as head twitches in rodents and higher order behaviors such as rodent lever pressing on the differential <b>reinforcement</b> of low rate 72 s (DRL 72 s) schedule.
+HTR2A	drug	nicotine	28668504	Some studies show that the <strong>5 HT2A</strong>, 5 HT2C, and 5 HT3 receptors have a central role in the induction and expression of <b>nicotine</b> induced locomotor sensitization.
+HTR2A	addiction	sensitization	28668504	Some studies show that the <strong>5 HT2A</strong>, 5 HT2C, and 5 HT3 receptors have a central role in the induction and expression of nicotine induced locomotor <b>sensitization</b>.
+HTR2A	drug	cocaine	28668504	Mirtazapine, an antagonist of the α2 adrenergic receptors, the <strong>5 HT2A</strong>/C, and the 5 HT3 receptors, has proven effective in reducing behavioral effects induced by drugs like <b>cocaine</b> and methamphetamines in human and animal.
+HTR2A	drug	psychedelics	28512684	This chapter reviews what is known about the therapeutic uses of the serotonergic or classic hallucinogens, i.e., psychoactive drugs such as <b>LSD</b> and <b>psilocybin</b> that exert their effects primarily through agonist activity at serotonin 2A (<strong>5HT2A</strong>) receptors.
+HTR2A	drug	cannabinoid	28272498	<b>THC</b> exposure did not influence D2 and <strong>5 HT2A</strong> receptor binding, the major targets of antipsychotic action, but it lowered the brain concentrations of risperidone and its active metabolite, 9 hydroxy risperidone.
+HTR2A	drug	nicotine	28103253	Polymorphisms in <strong>HTR2A</strong> and DRD4 Predispose to <b>Smoking</b> and <b>Smoking</b> Quantity.
+HTR2A	drug	nicotine	28103253	To identify genetic variants in the promoter regions and exons of the DRD4 and <strong>HTR2A</strong> genes associated with <b>tobacco</b> <b>smoking</b> and the degree of <b>nicotine</b> addiction in Mexican mestizos.
+HTR2A	addiction	addiction	28103253	To identify genetic variants in the promoter regions and exons of the DRD4 and <strong>HTR2A</strong> genes associated with tobacco smoking and the degree of nicotine <b>addiction</b> in Mexican mestizos.
+HTR2A	drug	nicotine	28103253	The T allele of rs6313 in <strong>HTR2A</strong> was significantly associated with cigarette <b>smoking</b> and a greater degree of <b>nicotine</b> addiction (p = 4.77E 03, OR = 1.55); the association was maintained in the homozygous genotype (TT) (p = 4.90E 03, OR = 1.96).
+HTR2A	addiction	addiction	28103253	The T allele of rs6313 in <strong>HTR2A</strong> was significantly associated with cigarette smoking and a greater degree of nicotine <b>addiction</b> (p = 4.77E 03, OR = 1.55); the association was maintained in the homozygous genotype (TT) (p = 4.90E 03, OR = 1.96).
+HTR2A	drug	nicotine	28103253	Among Mexican mestizos, the C allele of rs1800955 in the DRD4 gene and the A allele of rs6311 in the <strong>HTR2A</strong> gene are associated with cigarette <b>smoking</b>, whereas the T allele of rs6313 in <strong>HTR2A</strong> is associated with cigarette <b>smoking</b> and the degree of <b>nicotine</b> addiction.
+HTR2A	addiction	addiction	28103253	Among Mexican mestizos, the C allele of rs1800955 in the DRD4 gene and the A allele of rs6311 in the <strong>HTR2A</strong> gene are associated with cigarette smoking, whereas the T allele of rs6313 in <strong>HTR2A</strong> is associated with cigarette smoking and the degree of nicotine <b>addiction</b>.
+HTR2A	drug	opioid	28082900	Blockade of Serotonin <strong>5 HT2A</strong> Receptors Suppresses Behavioral Sensitization and <b>Naloxone</b> Precipitated Withdrawal Symptoms in <b>Morphine</b> Treated Mice.
+HTR2A	addiction	sensitization	28082900	Blockade of Serotonin <strong>5 HT2A</strong> Receptors Suppresses Behavioral <b>Sensitization</b> and Naloxone Precipitated Withdrawal Symptoms in Morphine Treated Mice.
+HTR2A	addiction	withdrawal	28082900	Blockade of Serotonin <strong>5 HT2A</strong> Receptors Suppresses Behavioral Sensitization and Naloxone Precipitated <b>Withdrawal</b> Symptoms in Morphine Treated Mice.
+HTR2A	drug	opioid	28082900	In this study, we examined the effect of blockade of <strong>5 HT2A</strong> receptors (5 HT2ARs) on <b>morphine</b> induced behavioral sensitization and withdrawal in male mice.
+HTR2A	addiction	sensitization	28082900	In this study, we examined the effect of blockade of <strong>5 HT2A</strong> receptors (5 HT2ARs) on morphine induced behavioral <b>sensitization</b> and withdrawal in male mice.
+HTR2A	addiction	withdrawal	28082900	In this study, we examined the effect of blockade of <strong>5 HT2A</strong> receptors (5 HT2ARs) on morphine induced behavioral sensitization and <b>withdrawal</b> in male mice.
+HTR2A	drug	opioid	28082900	(i)Blockade of <strong>5 HT2A</strong> receptors suppresses the expression of <b>morphine</b> induced behavioral sensitization.
+HTR2A	addiction	sensitization	28082900	(i)Blockade of <strong>5 HT2A</strong> receptors suppresses the expression of morphine induced behavioral <b>sensitization</b>.
+HTR2A	drug	opioid	28082900	(ii)Blockade of <strong>5 HT2A</strong> receptors suppresses <b>naloxone</b> precipitated withdrawal in <b>morphine</b> treated mice.
+HTR2A	addiction	withdrawal	28082900	(ii)Blockade of <strong>5 HT2A</strong> receptors suppresses naloxone precipitated <b>withdrawal</b> in morphine treated mice.
+HTR2A	drug	opioid	28082900	(iii)Chronic <b>morphine</b> exposure induces an increase in <strong>5 HT2A</strong> receptor protein level and a decrease in ERK protein phosphorylation in prefrontal cortex.
+HTR2A	drug	opioid	28072812	Active alkaloids isolated from <b>kratom</b> such as mitragynine and 7 hydroxymitragynine are thought to act on mu  and delta <b>opioid</b> receptors as well as alpha 2 adrenergic and <strong>5 HT2A</strong> receptors.
+HTR2A	drug	benzodiazepine	28034961	Pharmacological analysis showed that the encounter induced hyperactivity is mediated by dopamine D1 receptors and <strong>5 HT2A</strong> receptors and attenuated by anxiolytics and antidepressants such as <b>diazepam</b>, osemozotan and selective 5 HT reuptake inhibitors.
+HTR2A	drug	psychedelics	28019026	Scientific interest in serotonergic <b>psychedelics</b> (e.g., <b>psilocybin</b> and <b>LSD</b>; <strong>5 HT2A</strong> receptor agonists) has dramatically increased within the last decade.
+HTR2A	drug	amphetamine	27986974	Thus, we examined the effects of a 5 HT2C receptor agonist, WAY163909, and a <strong>5 HT2A</strong> receptor antagonist, M100907, given alone and in combination, on actigraphy based sleep parameters disrupted by <b>methamphetamine</b> self administration in non human primates.
+HTR2A	drug	psychedelics	27915193	25B <b>NBOMe</b> and 25C <b>NBOMe</b> are potent <strong>5 HT2A</strong> receptor agonists that have been associated with inducing hallucinogenic effects in drug users and severe intoxications.
+HTR2A	drug	cocaine	27857126	Repeated 7 Day Treatment with the 5 HT2C Agonist Lorcaserin or the <strong>5 HT2A</strong> Antagonist Pimavanserin Alone or in Combination Fails to Reduce <b>Cocaine</b> vs Food Choice in Male Rhesus Monkeys.
+HTR2A	drug	cocaine	27857126	Therefore, the present study aim was to determine whether repeated 7 day treatment with the 5 HT2C agonist lorcaserin (0.1 1.0 mg/kg per day, intramuscular; 0.032 0.1 mg/kg/h, intravenous) or the <strong>5 HT2A</strong> inverse agonist/antagonist pimavanserin (0.32 10 mg/kg per day, intramuscular) attenuated <b>cocaine</b> reinforcement under a concurrent 'choice' schedule of <b>cocaine</b> and food availability in rhesus monkeys.
+HTR2A	addiction	reward	27857126	Therefore, the present study aim was to determine whether repeated 7 day treatment with the 5 HT2C agonist lorcaserin (0.1 1.0 mg/kg per day, intramuscular; 0.032 0.1 mg/kg/h, intravenous) or the <strong>5 HT2A</strong> inverse agonist/antagonist pimavanserin (0.32 10 mg/kg per day, intramuscular) attenuated cocaine <b>reinforcement</b> under a concurrent 'choice' schedule of cocaine and food availability in rhesus monkeys.
+HTR2A	drug	cocaine	27857126	These results suggest that neither 5 HT2C receptor activation nor <strong>5 HT2A</strong> receptor blockade are sufficient to produce a therapeutic like decrease in <b>cocaine</b> choice and a complementary increase in food choice.
+HTR2A	drug	cocaine	27857126	Overall, these results do not support the clinical utility of 5 HT2C agonists and <strong>5 HT2A</strong> inverse agonists/antagonists alone or in combination as candidate anti <b>cocaine</b> use disorder pharmacotherapies.
+HTR2A	drug	psychedelics	27649637	Here, we provide evidence that a small subset of <strong>5 HT2A</strong> expressing excitatory neurons is directly activated by <b>psychedelics</b> and subsequently recruits other select cell types including subpopulations of inhibitory somatostatin and parvalbumin GABAergic interneurons, as well as astrocytes, to produce distinct and regional responses.
+HTR2A	drug	opioid	27563418	<strong>5 HT2A</strong> Serotonin Receptor Density in Adult Male Rats' Hippocampus after <b>Morphine</b> based Conditioned Place Preference.
+HTR2A	drug	opioid	27563418	Therefore, the aim of the present study was to assess the influence of <b>morphine</b> and Conditioned Place Preference (CPP) on the density of <strong>5 HT2A</strong> receptor in neurons of rat hippocampal formation.
+HTR2A	addiction	reward	27563418	Therefore, the aim of the present study was to assess the influence of morphine and Conditioned Place Preference (<b>CPP</b>) on the density of <strong>5 HT2A</strong> receptor in neurons of rat hippocampal formation.
+HTR2A	drug	opioid	27563418	The density of <strong>5 HT2A</strong> receptor in different areas of the hippocampus increased significantly at sham <b>morphine</b> and CPP groups (P<0.05).
+HTR2A	addiction	reward	27563418	The density of <strong>5 HT2A</strong> receptor in different areas of the hippocampus increased significantly at sham morphine and <b>CPP</b> groups (P<0.05).
+HTR2A	drug	opioid	27563418	On the other hand, the CPP groups had more <strong>5 HT2A</strong> receptors than sham <b>morphine</b> groups and also the sham <b>morphine</b> groups had more <strong>5 HT2A</strong> receptors than the control groups.
+HTR2A	addiction	reward	27563418	On the other hand, the <b>CPP</b> groups had more <strong>5 HT2A</strong> receptors than sham morphine groups and also the sham morphine groups had more <strong>5 HT2A</strong> receptors than the control groups.
+HTR2A	drug	opioid	27563418	We concluded that the phenomenon of conditioned place preference induced by <b>morphine</b> can cause a significant increase in the number of serotonin <strong>5 HT2A</strong> receptors in neurons of all areas of hippocampus.
+HTR2A	drug	psychedelics	27400739	The dimethoxyphenyl N ((2 methoxyphenyl)methyl)ethanamine (<b>NBOMe</b>) compounds are potent serotonin <strong>5 HT2A</strong> receptor agonists and have recently been subject to recreational use due to their hallucinogenic effects.
+HTR2A	drug	alcohol	27399274	This study investigated the effect of the dopamine related polymorphism in the DRD2/ANKK1 gene (rs1800497) and a serotonin related polymorphism in the <strong>HTR2A</strong> gene (rs6313) on associations between impulsivity, cognition, and <b>alcohol</b> misuse in 120 emerging adults (18 21years).
+HTR2A	drug	alcohol	27399274	<strong>HTR2A</strong> predicted lower positive <b>alcohol</b> expectancy, higher refusal self efficacy, and lower <b>alcohol</b> misuse.
+HTR2A	drug	alcohol	27399274	This is the first report of an association between <strong>HTR2A</strong> and <b>alcohol</b> related cognition.
+HTR2A	drug	psychedelics	27264435	Doses of the 5 HT1A antagonist, WAY 100635 (0.1 1.0mg/kg), 5 HT1B antagonist, GR 127935 (1.0 3.0mg/kg), and the <strong>5 HT2A</strong> antagonist, ketanserin (1.0 3.0mg/kg) that have previously been shown to decrease self administration of other psychostimulants and that decreased <b>MDMA</b> produced hyperactivity in the present study did not alter <b>MDMA</b> self administration.
+HTR2A	drug	amphetamine	27242287	Effects of 7 day repeated treatment with the <strong>5 HT2A</strong> inverse agonist/antagonist pimavanserin on <b>methamphetamine</b> vs. food choice in male rhesus monkeys.
+HTR2A	drug	amphetamine	27242287	Emerging data suggest that serotonin (5 HT)2A receptors modulate mesolimbic dopamine function, such that <strong>5 HT2A</strong> antagonists blunt the abuse related neurochemical effects of monoamine transporter substrates, such as <b>amphetamine</b> or <b>methamphetamine</b>.
+HTR2A	drug	amphetamine	27242287	Whether subchronic <strong>5 HT2A</strong> antagonist treatment attenuates <b>methamphetamine</b> reinforcement in any preclinical drug self administration procedure is unknown.
+HTR2A	addiction	reward	27242287	Whether subchronic <strong>5 HT2A</strong> antagonist treatment attenuates methamphetamine <b>reinforcement</b> in any preclinical drug self administration procedure is unknown.
+HTR2A	drug	amphetamine	27242287	The study aim was therefore to determine 7 day treatment effects with the <strong>5 HT2A</strong> inverse agonist/antagonist pimavanserin on <b>methamphetamine</b> vs. food choice in monkeys.
+HTR2A	drug	amphetamine	27242287	Repeated <strong>5 HT2A</strong> receptor inverse agonist/antagonist treatment did not attenuate <b>methamphetamine</b> reinforcement under a concurrent schedule of intravenous <b>methamphetamine</b> and food presentation in nonhuman primates.
+HTR2A	addiction	reward	27242287	Repeated <strong>5 HT2A</strong> receptor inverse agonist/antagonist treatment did not attenuate methamphetamine <b>reinforcement</b> under a concurrent schedule of intravenous methamphetamine and food presentation in nonhuman primates.
+HTR2A	drug	amphetamine	27242287	Overall, these results do not support the therapeutic potential of <strong>5 HT2A</strong> inverse agonists/antagonists as candidate medications for <b>methamphetamine</b> addiction.
+HTR2A	addiction	addiction	27242287	Overall, these results do not support the therapeutic potential of <strong>5 HT2A</strong> inverse agonists/antagonists as candidate medications for methamphetamine <b>addiction</b>.
+HTR2A	drug	psychedelics	27230395	The mechanisms responsible for the anti addictive properties of <b>ayahuasca</b> and its alkaloids are not clarified, apparently involving both peripheral MAO A inhibition by the β carbolines and central agonism of DMT at <strong>5 HT2A</strong> receptors expressed in brain regions related to the regulation of mood and emotions.
+HTR2A	addiction	addiction	27230395	The mechanisms responsible for the anti <b>addictive</b> properties of ayahuasca and its alkaloids are not clarified, apparently involving both peripheral MAO A inhibition by the β carbolines and central agonism of DMT at <strong>5 HT2A</strong> receptors expressed in brain regions related to the regulation of mood and emotions.
+HTR2A	addiction	sensitization	27040714	These results suggest that <strong>5 HT2A</strong> receptor bioactivity in the inflammatory site plays an important role in repeated inflammation induced central <b>sensitization</b>.
+HTR2A	drug	alcohol	26968030	The Combination of Marketed Antagonists of α1b Adrenergic and <strong>5 HT2A</strong> Receptors Inhibits Behavioral Sensitization and Preference to <b>Alcohol</b> in Mice: A Promising Approach for the Treatment of <b>Alcohol</b> Dependence.
+HTR2A	addiction	dependence	26968030	The Combination of Marketed Antagonists of α1b Adrenergic and <strong>5 HT2A</strong> Receptors Inhibits Behavioral Sensitization and Preference to Alcohol in Mice: A Promising Approach for the Treatment of Alcohol <b>Dependence</b>.
+HTR2A	addiction	sensitization	26968030	The Combination of Marketed Antagonists of α1b Adrenergic and <strong>5 HT2A</strong> Receptors Inhibits Behavioral <b>Sensitization</b> and Preference to Alcohol in Mice: A Promising Approach for the Treatment of Alcohol Dependence.
+HTR2A	addiction	relapse	26968030	Previous studies have indicated that the blockade of two monoaminergic receptors, α1b adrenergic and <strong>5 HT2A</strong>, could inhibit the development of behavioral sensitization to drugs of abuse, a hallmark of drug <b>seeking</b> and drug taking behaviors in rodents.
+HTR2A	addiction	sensitization	26968030	Previous studies have indicated that the blockade of two monoaminergic receptors, α1b adrenergic and <strong>5 HT2A</strong>, could inhibit the development of behavioral <b>sensitization</b> to drugs of abuse, a hallmark of drug seeking and drug taking behaviors in rodents.
+HTR2A	drug	nicotine	26968030	Finally, because α1b adrenergic and <strong>5 HT2A</strong> receptors blockade also inhibits behavioral sensitization to psychostimulants, opioids and <b>tobacco</b>, it cannot be excluded that this combination will exhibit some efficacy in the treatment of addiction to other abused drugs.
+HTR2A	drug	opioid	26968030	Finally, because α1b adrenergic and <strong>5 HT2A</strong> receptors blockade also inhibits behavioral sensitization to psychostimulants, <b>opioids</b> and tobacco, it cannot be excluded that this combination will exhibit some efficacy in the treatment of addiction to other abused drugs.
+HTR2A	addiction	addiction	26968030	Finally, because α1b adrenergic and <strong>5 HT2A</strong> receptors blockade also inhibits behavioral sensitization to psychostimulants, opioids and tobacco, it cannot be excluded that this combination will exhibit some efficacy in the treatment of <b>addiction</b> to other abused drugs.
+HTR2A	addiction	sensitization	26968030	Finally, because α1b adrenergic and <strong>5 HT2A</strong> receptors blockade also inhibits behavioral <b>sensitization</b> to psychostimulants, opioids and tobacco, it cannot be excluded that this combination will exhibit some efficacy in the treatment of addiction to other abused drugs.
+HTR2A	drug	cocaine	26922897	Treatment based on both <strong>5 HT2A</strong>/C and 5 HT3 receptor antagonists attenuate not only the effects of <b>cocaine</b> abuse but also the incentive/motivational effect related to <b>cocaine</b> paired cues.
+HTR2A	addiction	reward	26922897	Treatment based on both <strong>5 HT2A</strong>/C and 5 HT3 receptor antagonists attenuate not only the effects of cocaine abuse but also the <b>incentive</b>/motivational effect related to cocaine paired cues.
+HTR2A	drug	psychedelics	26612618	The tea contains the <b>psychedelic</b> <strong>5 HT2A</strong> receptor agonist N,N dimethyltryptamine (DMT), plus β carboline alkaloids with monoamine oxidase inhibiting properties.
+HTR2A	drug	amphetamine	26508706	We then assessed the effects of a 5 HT2 receptor antagonist (ritanserin; 0.01 and 0.1mg/kg) and of a <strong>5 HT2A</strong> receptor antagonist (MDL100,907; 0.025 0.1mg/kg) on <b>amphetamine</b> induced psychomotor activity.
+HTR2A	drug	cocaine	26484945	The inhibitory effects of 100 μM 5 HT were enhanced in <b>cocaine</b> binge treated <strong>5 HT2A</strong>  /  mice.
+HTR2A	addiction	intoxication	26484945	The inhibitory effects of 100 μM 5 HT were enhanced in cocaine <b>binge</b> treated <strong>5 HT2A</strong>  /  mice.
+HTR2A	drug	psychedelics	26400534	Relevant scientific articles were identified from Medline, Cochrane Central, Scopus, Web of Science, Science Direct, EMBASE and Google Scholar, through June 2015 using the following keywords: "<b>NBOMe</b>", "Nbomb", "Smiles", "intoxication", "toxicity" "fatalities", "death", "pharmacology", "<strong>5 HT2A</strong> receptor", "analysis" and "analytical methods".
+HTR2A	addiction	intoxication	26400534	Relevant scientific articles were identified from Medline, Cochrane Central, Scopus, Web of Science, Science Direct, EMBASE and Google Scholar, through June 2015 using the following keywords: "NBOMe", "Nbomb", "Smiles", "<b>intoxication</b>", "toxicity" "fatalities", "death", "pharmacology", "<strong>5 HT2A</strong> receptor", "analysis" and "analytical methods".
+HTR2A	drug	psychedelics	26400534	The high potency of <b>NBOMes</b> (potent agonists of <strong>5 HT2A</strong> receptor) has led to several severe intoxications, overdose and traumatic fatalities; thus, their increase raises significant public health concerns.
+HTR2A	drug	psychedelics	26108532	25I <b>NBOMe</b>, a new psychoactive substance, is a potent <strong>5 HT2A</strong> receptor agonist with strong hallucinogenic potential.
+HTR2A	drug	psychedelics	26068050	The results showed that chronic <b>MDMA</b> caused hippocampal protein deficits in adolescent and young adult rats at different levels: (1) impaired serotonergic (<strong>5 HT2A</strong> and 5 HT2C post synaptic receptors) and GABAergic (GAD2 enzyme) signaling, and (2) decreased structural cytoskeletal neurofilament proteins (NF H, NF M and NF L).
+HTR2A	drug	alcohol	26041607	In this association study of two independent samples, a number of candidate gene variants (<strong>5HT2A</strong> T102C, 5 HTTLPR, DRD Ins 141Del, DAT1 VNTR) were related to violent criminal behavior and <b>alcohol</b> related aggressive traits.
+HTR2A	drug	nicotine	26031442	Brain <strong>5 HT2A</strong>/2C receptors were analyzed on day 3 of <b>nicotine</b> withdrawal.
+HTR2A	addiction	withdrawal	26031442	Brain <strong>5 HT2A</strong>/2C receptors were analyzed on day 3 of nicotine <b>withdrawal</b>.
+HTR2A	drug	nicotine	26031442	<b>Nicotine</b> withdrawal increased [(3)H]ketanserin binding to <strong>5 HT2A</strong> receptors in the ventral tegmental area and ventral dentate gyrus, yet decreased binding in the nucleus accumbens shell.
+HTR2A	addiction	withdrawal	26031442	Nicotine <b>withdrawal</b> increased [(3)H]ketanserin binding to <strong>5 HT2A</strong> receptors in the ventral tegmental area and ventral dentate gyrus, yet decreased binding in the nucleus accumbens shell.
+HTR2A	drug	nicotine	26031442	These results show that the reduction in the <strong>5 HT2A</strong> receptor transcript level may be an auto regulatory response to the increased receptor density in the hippocampus and ventral tegmental area during <b>nicotine</b> withdrawal, while decreased 5 HT2C receptor mRNA editing may explain the reduction in receptor labeling in the hippocampus.
+HTR2A	addiction	withdrawal	26031442	These results show that the reduction in the <strong>5 HT2A</strong> receptor transcript level may be an auto regulatory response to the increased receptor density in the hippocampus and ventral tegmental area during nicotine <b>withdrawal</b>, while decreased 5 HT2C receptor mRNA editing may explain the reduction in receptor labeling in the hippocampus.
+HTR2A	drug	nicotine	26031442	Here, we show that the reduction in <strong>5 HT2A</strong> receptor transcript level may be an auto regulatory response to the increased receptor number in the hippocampus and ventral tegmental area during <b>nicotine</b> withdrawal, while attenuated 5 HT2C receptor mRNA editing in the hippocampus might explain reduced inverse agonist binding to 5 HT2C receptor and suggest a shift toward a population of more active receptors.
+HTR2A	addiction	withdrawal	26031442	Here, we show that the reduction in <strong>5 HT2A</strong> receptor transcript level may be an auto regulatory response to the increased receptor number in the hippocampus and ventral tegmental area during nicotine <b>withdrawal</b>, while attenuated 5 HT2C receptor mRNA editing in the hippocampus might explain reduced inverse agonist binding to 5 HT2C receptor and suggest a shift toward a population of more active receptors.
+HTR2A	drug	nicotine	25933953	In the present study we used male rats to verify the hypothesis that the binding pattern of <strong>5 HT2A</strong> and 5 HT2C receptors in the brain is altered by chronic <b>nicotine</b> treatment in different environments.
+HTR2A	drug	nicotine	25933953	Repeated treatment with <b>nicotine</b> in home cages evoked significant increases in [(3)H]ketanserin binding to <strong>5 HT2A</strong> receptors in the prefrontal cortex, striatal subregions and ventral tegmental area as well as reductions in [(3)H]mesulergine binding to 5 HT2C receptors in subregions of the prefrontal cortex.
+HTR2A	drug	nicotine	25933953	In contrast, <b>nicotine</b> paired with environmental context produced robust increases in <strong>5 HT2A</strong> receptor labeling in the infralimbic cortex and decreased [(3)H]ketanserin binding in striatal subregions and ventral tegmental area; 5 HT2C receptor labeling in the prefrontal cortex fell.
+HTR2A	drug	nicotine	25933953	The present data indicate that chronic <b>nicotine</b> administration in home cages induces bi directional neuroplastic changes within <strong>5 HT2A</strong> and 5 HT2C receptors in the prefrontal cortex.
+HTR2A	drug	nicotine	25933953	Pairing the <b>nicotine</b> with environmental context potentiates the neuroplastic response in the latter region and evokes opposite changes in <strong>5 HT2A</strong> receptor binding in striatal and tegmental regions compared with <b>nicotine</b> administered in the absence of the context, indicating a modulatory role of environmental context in the expression of <b>nicotine</b> induced sensitization.
+HTR2A	addiction	sensitization	25933953	Pairing the nicotine with environmental context potentiates the neuroplastic response in the latter region and evokes opposite changes in <strong>5 HT2A</strong> receptor binding in striatal and tegmental regions compared with nicotine administered in the absence of the context, indicating a modulatory role of environmental context in the expression of nicotine induced <b>sensitization</b>.
+HTR2A	drug	amphetamine	25588018	Typically, stimulants inhibit the transport of dopamine and noradrenaline (pipradrols, pyrovalerone cathinones) or induce the release of these monoamines (amphetamines and <b>methamphetamine</b> like cathinones), entactogens predominantly enhance serotonin release (phenylpiperazines, aminoindanes, para substituted amphetamines, and MDMA like cathinones) similar to MDMA (ecstasy), and hallucinogens (tryptamines, hallucinogenic phenethylamines) are direct agonists at serotonergic <strong>5 HT2A</strong> receptors.
+HTR2A	drug	psychedelics	25588018	Typically, stimulants inhibit the transport of dopamine and noradrenaline (pipradrols, pyrovalerone cathinones) or induce the release of these monoamines (amphetamines and methamphetamine like cathinones), entactogens predominantly enhance serotonin release (phenylpiperazines, aminoindanes, para substituted amphetamines, and <b>MDMA</b> like cathinones) similar to <b>MDMA</b> (<b>ecstasy</b>), and hallucinogens (tryptamines, hallucinogenic phenethylamines) are direct agonists at serotonergic <strong>5 HT2A</strong> receptors.
+HTR2A	drug	alcohol	25586396	Several lines of evidence suggest that classic (<strong>5HT2A</strong> agonist) hallucinogens have clinically relevant effects in <b>alcohol</b> and drug addiction.
+HTR2A	addiction	addiction	25586396	Several lines of evidence suggest that classic (<strong>5HT2A</strong> agonist) hallucinogens have clinically relevant effects in alcohol and drug <b>addiction</b>.
+HTR2A	drug	cocaine	25505168	However, the <strong>5 HT2A</strong> and 5 HT2C receptors in particular have been implicated as likely candidates for mediating the influence of 5 HT in <b>cocaine</b> abuse as well as to traits (e.g., impulsivity) that contribute to the development of <b>cocaine</b> use disorder and relapse in humans.
+HTR2A	addiction	relapse	25505168	However, the <strong>5 HT2A</strong> and 5 HT2C receptors in particular have been implicated as likely candidates for mediating the influence of 5 HT in cocaine abuse as well as to traits (e.g., impulsivity) that contribute to the development of cocaine use disorder and <b>relapse</b> in humans.
+HTR2A	drug	alcohol	25382408	For example, recently, a novel 4 phenyl 2 N,N dimethylaminotetralin (PAT) drug candidate, that demonstrates 5 HT2C receptor agonist activity together with <strong>5 HT2A</strong>/2B receptor inverse agonist activity, was shown to reduce operant responding for <b>ethanol</b> after peripheral administration to rats.
+HTR2A	addiction	reward	25382408	For example, recently, a novel 4 phenyl 2 N,N dimethylaminotetralin (PAT) drug candidate, that demonstrates 5 HT2C receptor agonist activity together with <strong>5 HT2A</strong>/2B receptor inverse agonist activity, was shown to reduce <b>operant</b> responding for ethanol after peripheral administration to rats.
+HTR2A	drug	nicotine	25366721	Study of polymorphic variants of the serotonin 2A receptor gene (<strong>5 HT2A</strong>) and its possible effects on <b>smoking</b> habits of a population from northeastern Brazil.
+HTR2A	drug	cocaine	25213649	<b>Cocaine</b> potentiates multiple <strong>5 HT2A</strong> receptor signaling pathways and is associated with decreased phosphorylation of <strong>5 HT2A</strong> receptors in vivo.
+HTR2A	drug	cocaine	25213649	Here, we used Sprague Dawley rats injected with either saline (1 ml/kg) or <b>cocaine</b> (15 mg/kg) for 7 days (b.i.d, i.p) to study the effect of <b>cocaine</b> on several components of <strong>5 HT2A</strong> receptor signaling in prefrontal cortex (PFCx).
+HTR2A	drug	cocaine	25213649	We detected enhanced activation of <strong>5 HT2A</strong> receptor mediated phospholipase C beta (PLCβ) and extracellular regulated kinase 1/2 activity in PFCx of <b>cocaine</b> treated rats.
+HTR2A	drug	cocaine	25213649	Our results suggest that decreased phosphorylation of <strong>5 HT2A</strong> receptors could mediate, at least in part, the <b>cocaine</b> induced potentiation of multiple <strong>5 HT2A</strong> receptor signaling pathways in rat PFCx.
+HTR2A	drug	cocaine	25213649	As discussed in this manuscript, we hypothesize that preventing these neuroadaptations in <strong>5 HT2A</strong> receptor signaling may alleviate some of the aversive withdrawal associated symptoms that contribute to relapse to <b>cocaine</b> abuse.
+HTR2A	addiction	aversion	25213649	As discussed in this manuscript, we hypothesize that preventing these neuroadaptations in <strong>5 HT2A</strong> receptor signaling may alleviate some of the <b>aversive</b> withdrawal associated symptoms that contribute to relapse to cocaine abuse.
+HTR2A	addiction	relapse	25213649	As discussed in this manuscript, we hypothesize that preventing these neuroadaptations in <strong>5 HT2A</strong> receptor signaling may alleviate some of the aversive withdrawal associated symptoms that contribute to <b>relapse</b> to cocaine abuse.
+HTR2A	addiction	withdrawal	25213649	As discussed in this manuscript, we hypothesize that preventing these neuroadaptations in <strong>5 HT2A</strong> receptor signaling may alleviate some of the aversive <b>withdrawal</b> associated symptoms that contribute to relapse to cocaine abuse.
+HTR2A	drug	nicotine	25158104	In this study, we assessed roles for dopamine (DA) D1 or D2 receptors, and two serotonin (5 HT) receptor subtypes known to modulate DA activity, the 5 HT2C or <strong>5 HT2A</strong> subtypes, on <b>nicotine</b> enhanced responding for a conditioned reinforcer.
+HTR2A	drug	nicotine	25158104	To examine potential roles for dopamine (DA) and serotonin (5 HT) receptors in this effect, separate groups of animals were used to assess the impact of administering the D1 receptor antagonist SCH 23390, D2 receptor antagonist eticlopride, 5 HT2C receptor agonist Ro 60 0175, or <strong>5 HT2A</strong> receptor antagonist M100907 on <b>nicotine</b> enhanced responding for conditioned reinforcement.
+HTR2A	addiction	reward	25158104	To examine potential roles for dopamine (DA) and serotonin (5 HT) receptors in this effect, separate groups of animals were used to assess the impact of administering the D1 receptor antagonist SCH 23390, D2 receptor antagonist eticlopride, 5 HT2C receptor agonist Ro 60 0175, or <strong>5 HT2A</strong> receptor antagonist M100907 on nicotine enhanced responding for conditioned <b>reinforcement</b>.
+HTR2A	drug	nicotine	25158104	Together, these studies indicate that DA D1 and D2 receptors, but not <strong>5 HT2A</strong> receptors, contribute to the effect of <b>nicotine</b> to enhance responding for a conditioned reinforcer.
+HTR2A	drug	psychedelics	25069786	N,N dimethyltryptamine (DMT) is a widely distributed plant alkaloid that displays partial agonist activity at the <strong>5 HT2A</strong> receptor and induces intense <b>psychedelic</b> effects in humans when administered parenterally.
+HTR2A	drug	psychedelics	24991548	There are at least three different pharmacological ways to induce hallucinations: (1) activation of dopamine D2 receptors (D2Rs) with psychostimulants, (2) activation of serotonin <strong>5HT2A</strong> receptors (HT2ARs) with <b>psychedelics</b>, and (3) blockage of glutamate NMDA receptors (NMDARs) with dissociative anesthetics.
+HTR2A	drug	nicotine	24953434	In contrast, the <strong>5HT2A</strong> and C antagonist ketanserin did not show an effect of reducing <b>nicotine</b> self administration in the same dose range we had found in a previous study to significantly reduce operant lever press <b>nicotine</b> self administration.
+HTR2A	addiction	reward	24953434	In contrast, the <strong>5HT2A</strong> and C antagonist ketanserin did not show an effect of reducing nicotine self administration in the same dose range we had found in a previous study to significantly reduce <b>operant</b> lever press nicotine self administration.
+HTR2A	drug	psychedelics	24779864	The <b>NBOMe</b> compounds are highly potent <strong>5HT2A</strong> receptor agonists and are also agonists at alpha adrenergic receptors, which likely account for their serotonergic and sympathomimetic symptoms.
+HTR2A	drug	amphetamine	24763081	Long lasting alterations in <strong>5 HT2A</strong> receptor after a binge regimen of <b>methamphetamine</b> in mice.
+HTR2A	addiction	intoxication	24763081	Long lasting alterations in <strong>5 HT2A</strong> receptor after a <b>binge</b> regimen of methamphetamine in mice.
+HTR2A	addiction	intoxication	24763081	The present study aimed to examine the effects of MA <b>binge</b> exposure on <strong>5 HT2A</strong> receptors, the subtype of serotonin receptors putatively involved in psychosis.
+HTR2A	addiction	intoxication	24763081	Furthermore, MA <b>binge</b> exposure increased <strong>5 HT2A</strong> and decreased mGlu2 receptor expression in the medial frontal cortex, whereas 5 HT2C and 5 HT1A receptors were unaffected.
+HTR2A	addiction	intoxication	24763081	These data reveal that the increased behavioural, molecular and electrophysiological responses to DOI might be associated with an up regulation of <strong>5 HT2A</strong> receptors in the medial prefrontal cortex after MA <b>binge</b> exposure.
+HTR2A	addiction	relapse	24523680	Together, our findings show that the activation of BLA <strong>5 HT2A</strong>/C receptors inhibits behaviors related to reward <b>seeking</b> by suppressing BLA principal neuron activity.
+HTR2A	addiction	reward	24523680	Together, our findings show that the activation of BLA <strong>5 HT2A</strong>/C receptors inhibits behaviors related to <b>reward</b> seeking by suppressing BLA principal neuron activity.
+HTR2A	drug	psychedelics	24411530	While the hypo activity of serotonin signaling is involved in the pathogenesis of depression, anxiety and obsessive compulsive disorder; <b>LSD</b>, an agonist of serotonin type 2 receptor (5 <strong>HTR2A</strong>) induces psychosis.
+HTR2A	addiction	addiction	24411530	While the hypo activity of serotonin signaling is involved in the pathogenesis of depression, anxiety and obsessive <b>compulsive</b> disorder; LSD, an agonist of serotonin type 2 receptor (5 <strong>HTR2A</strong>) induces psychosis.
+HTR2A	drug	opioid	24355137	The association of 5 <strong>HTR2A</strong> 1438A/G, COMTVal158Met, MAOA LPR, DATVNTR and 5 HTTVNTR gene polymorphisms and borderline personality disorder in female <b>heroin</b> dependent Chinese subjects.
+HTR2A	drug	opioid	24355137	To explore the association between the 5 <strong>HTR2A</strong> 1438A/G, COMTVal158Met, MAOA LPR, DATVNTR and 5 HTTVNTR polymorphisms with co morbid borderline personality disorder (BPD) in female <b>heroin</b> dependent patients.
+HTR2A	drug	opioid	24355137	In a case control study, we compared the polymorphic distributions of 5 <strong>HTR2A</strong> 1438A/G, COMTVal158Met, MAOA LPR, DATVNTR and 5 HTTVNTR in 296 female <b>heroin</b> dependent patients (including 61 patients with BPD and 235 without BPD) and 101 normal females by genotypes, alleles, and interaction between genes.
+HTR2A	drug	amphetamine	24287377	Stress and withdrawal from d <b>amphetamine</b> alter <strong>5 HT2A</strong> receptor mRNA expression in the prefrontal cortex.
+HTR2A	addiction	withdrawal	24287377	Stress and <b>withdrawal</b> from d amphetamine alter <strong>5 HT2A</strong> receptor mRNA expression in the prefrontal cortex.
+HTR2A	drug	amphetamine	24287377	<strong>5 HT2A</strong> receptor (5 HT2AR) mRNA expression in the prefrontal cortex (PFC) is diminished following withdrawal from d <b>amphetamine</b> (<b>AMPH</b>) and may underlie the emotional and cognitive impairments observed in psychostimulant withdrawal, but whether stress affects 5 HT2AR mRNA expression during psychostimulant withdrawal is unknown.
+HTR2A	addiction	withdrawal	24287377	<strong>5 HT2A</strong> receptor (5 HT2AR) mRNA expression in the prefrontal cortex (PFC) is diminished following <b>withdrawal</b> from d amphetamine (AMPH) and may underlie the emotional and cognitive impairments observed in psychostimulant <b>withdrawal</b>, but whether stress affects 5 HT2AR mRNA expression during psychostimulant <b>withdrawal</b> is unknown.
+HTR2A	drug	alcohol	24178752	Association of the <strong>HTR2A</strong> gene with <b>alcohol</b> and heroin abuse.
+HTR2A	drug	opioid	24178752	Association of the <strong>HTR2A</strong> gene with alcohol and <b>heroin</b> abuse.
+HTR2A	drug	alcohol	24178752	Positive genetic associations of rs6313 (102T/C at exon 1) and rs6311 ( 1438A/G) on the 5 hydroxytryptamine (serotonin) 2A receptor gene (<strong>HTR2A</strong> or 5 HT2A) were reported for <b>alcohol</b> and drug abuse; however, other association studies failed to produce consistent results supporting the susceptibility of the two single nucleotide polymorphisms (SNPs).
+HTR2A	drug	alcohol	24178752	Positive genetic associations of rs6313 (102T/C at exon 1) and rs6311 ( 1438A/G) on the 5 hydroxytryptamine (serotonin) 2A receptor gene (<strong>HTR2A</strong> or <strong>5 HT2A</strong>) were reported for <b>alcohol</b> and drug abuse; however, other association studies failed to produce consistent results supporting the susceptibility of the two single nucleotide polymorphisms (SNPs).
+HTR2A	drug	alcohol	24178752	To clarify the associations of the <strong>HTR2A</strong> gene with substance use disorders, we performed a meta analysis based on the genotypes from the available candidate gene association studies of the two SNPs with <b>alcohol</b> and drug abuse from multiple populations.
+HTR2A	drug	alcohol	24178752	Evidence of association was found for <strong>HTR2A</strong> rs6313 in all the combined studies (e.g., allelic P = 0.0048 and OR 0.86, 95 % CI 0.77 0.95) and also in the combined studies of <b>alcohol</b> dependence (abuse) (e.g., allelic P = 0.0001 and OR 0.71, 95 % CI 0.59 0.85).
+HTR2A	addiction	dependence	24178752	Evidence of association was found for <strong>HTR2A</strong> rs6313 in all the combined studies (e.g., allelic P = 0.0048 and OR 0.86, 95 % CI 0.77 0.95) and also in the combined studies of alcohol <b>dependence</b> (abuse) (e.g., allelic P = 0.0001 and OR 0.71, 95 % CI 0.59 0.85).
+HTR2A	drug	alcohol	24178752	The meta analysis supports a contribution of the <strong>HTR2A</strong> gene to the susceptibility to substance use disorders, particularly <b>alcohol</b> dependence.
+HTR2A	addiction	dependence	24178752	The meta analysis supports a contribution of the <strong>HTR2A</strong> gene to the susceptibility to substance use disorders, particularly alcohol <b>dependence</b>.
+HTR2A	drug	nicotine	24127329	The aim of this study was to evaluate the association between the effectiveness of treatment with <b>nicotine</b> or bupropion in heavy <b>smokers</b> (n=70), and 6 candidate polymorphisms in CYP2A6, 5 HTT and <strong>HTR2A</strong> genes.
+HTR2A	drug	nicotine	24127329	Analysis revealed a significant association between "favourable" genotype combination carriers (CYP2A6 "slow metabolizer" or 5HTT L allele or <strong>HTR2A</strong> 1438GG) and <b>nicotine</b> treatment outcome (OR=2.69, 95% CI=1.28 5.64).
+HTR2A	drug	opioid	24076184	The present study suggests that the activation of 5 HT1A receptors suppressed <b>naloxone</b> reversible antinociception contributing to the maintenance of inflammatory pain, and that the concomitant blockade of 5 HT1A and <strong>5 HT2A</strong> receptors in the periphery produced synergistic effects on inflammatory hyperalgesia.
+HTR2A	drug	alcohol	24041931	Ro60 0175, a 5 HT2 family receptor agonist, decreased both <b>ethanol</b> and vehicle responding while ( ) trans PAT, a 5 HT2C receptor agonist with <strong>5 HT2A</strong> 2B receptor inverse agonist activity, selectively reduced only <b>ethanol</b> responding.
+HTR2A	drug	amphetamine	23994622	This study sought to assess whether aripiprazole, a partial agonist at D2/5 HT1A receptors and an antagonist at <strong>5 HT2A</strong> receptors, would attenuate the reinforcing and subject rated effects of oral <b>methamphetamine</b>.
+HTR2A	addiction	reward	23994622	This study sought to assess whether aripiprazole, a partial agonist at D2/5 HT1A receptors and an antagonist at <strong>5 HT2A</strong> receptors, would attenuate the <b>reinforcing</b> and subject rated effects of oral methamphetamine.
+HTR2A	drug	cocaine	23946394	Previous studies indicate that <strong>5 HT2A</strong> receptor antagonists attenuate the reinstatement of <b>cocaine</b> maintained behavior but not <b>cocaine</b> self administration in rodents.
+HTR2A	addiction	relapse	23946394	Previous studies indicate that <strong>5 HT2A</strong> receptor antagonists attenuate the <b>reinstatement</b> of cocaine maintained behavior but not cocaine self administration in rodents.
+HTR2A	drug	cocaine	23946394	To elucidate the neuropharmacological and neuroanatomical mechanisms underlying this phenomenon, we evaluated the effects of the selective <strong>5 HT2A</strong> receptor antagonist M100907 on intravenous <b>cocaine</b> self administration and drug  and cue primed reinstatement in rhesus macaques (Macaca mulatta).
+HTR2A	addiction	relapse	23946394	To elucidate the neuropharmacological and neuroanatomical mechanisms underlying this phenomenon, we evaluated the effects of the selective <strong>5 HT2A</strong> receptor antagonist M100907 on intravenous cocaine self administration and drug  and cue primed <b>reinstatement</b> in rhesus macaques (Macaca mulatta).
+HTR2A	drug	cocaine	23946394	In separate subjects, we evaluated the role of <strong>5 HT2A</strong> receptors in <b>cocaine</b> induced dopamine overflow in the nucleus accumbens (n = 4) and the caudate nucleus (n = 5) using in vivo microdialysis.
+HTR2A	drug	psychedelics	23906865	A Pubmed literature search investigated several lines of evidence: innervation of sensory cortex by serotonin and norepinephrine; antidepressant drugs and depression itself affecting processing of facial expressions of emotion; electroencephalography (EEG) studies of depressed persons and antidepressant drugs; involvement of the serotonergic <strong>5HT2A</strong> receptor in both depression and hallucinogenic drug action; psychotic depression involving sensory distortions; dopamine possibly playing a role in depression; and the antidepressant effect of blocking the NMDA receptor with <b>ketamine</b>.
+HTR2A	drug	psychedelics	23892054	In the present study we have evaluated the capacity of the mixed serotonin (<strong>5 HT2A</strong>)/dopamine (DA D2) antagonist risperidone to block acquisition and reinstatement of <b>MDMA</b> induced CPP.
+HTR2A	addiction	relapse	23892054	In the present study we have evaluated the capacity of the mixed serotonin (<strong>5 HT2A</strong>)/dopamine (DA D2) antagonist risperidone to block acquisition and <b>reinstatement</b> of MDMA induced CPP.
+HTR2A	addiction	reward	23892054	In the present study we have evaluated the capacity of the mixed serotonin (<strong>5 HT2A</strong>)/dopamine (DA D2) antagonist risperidone to block acquisition and reinstatement of MDMA induced <b>CPP</b>.
+HTR2A	drug	psychedelics	23627786	<b>MDMA</b> is a potent monoamine releaser with sympathomimetic effects that may indirectly activate <strong>5 HT2A</strong> receptors.
+HTR2A	drug	psychedelics	23473462	A case of 25I <b>NBOMe</b> (25 I) intoxication: a new potent <strong>5 HT2A</strong> agonist designer drug.
+HTR2A	addiction	intoxication	23473462	A case of 25I NBOMe (25 I) <b>intoxication</b>: a new potent <strong>5 HT2A</strong> agonist designer drug.
+HTR2A	drug	cocaine	23336050	Synergism between a serotonin <strong>5 HT2A</strong> receptor (5 HT2AR) antagonist and 5 HT2CR agonist suggests new pharmacotherapeutics for <b>cocaine</b> addiction.
+HTR2A	addiction	addiction	23336050	Synergism between a serotonin <strong>5 HT2A</strong> receptor (5 HT2AR) antagonist and 5 HT2CR agonist suggests new pharmacotherapeutics for cocaine <b>addiction</b>.
+HTR2A	drug	alcohol	23321485	The CC genotype in the T102C <strong>HTR2A</strong> polymorphism predicts relapse in individuals after <b>alcohol</b> treatment.
+HTR2A	addiction	relapse	23321485	The CC genotype in the T102C <strong>HTR2A</strong> polymorphism predicts <b>relapse</b> in individuals after alcohol treatment.
+HTR2A	drug	alcohol	23321485	However, the potential association between the T102C polymorphism (rs6313) in the type 2A serotonin receptor (<strong>HTR2A</strong>) gene and treatment outcomes in <b>alcohol</b> dependence has not been investigated.
+HTR2A	addiction	dependence	23321485	However, the potential association between the T102C polymorphism (rs6313) in the type 2A serotonin receptor (<strong>HTR2A</strong>) gene and treatment outcomes in alcohol <b>dependence</b> has not been investigated.
+HTR2A	addiction	relapse	23321485	The significant influence on <b>relapse</b> of the CC genotype, which is associated with fewer <strong>5 HT2A</strong> receptors in the central nervous system, suggests the possibility that this genetic polymorphism could influence response to serotonergic medications.
+HTR2A	drug	psychedelics	24648791	Possible neurotoxicity in heavy <b>ecstasy</b> users has been revealed by neuroimaging studies showing reduced SERT binding and increased <strong>5 HT2A</strong> receptor binding in several cortical and/or subcortical areas.
+HTR2A	drug	cocaine	23241418	Single marker analyses provided evidence for association of the serotonin receptor <strong>HTR2A</strong> with <b>cocaine</b> dependence [rs6561333; nominal P value adjusted for age = 1.9e 04, odds ratio = 1.72 (1.29 2.30)].
+HTR2A	addiction	dependence	23241418	Single marker analyses provided evidence for association of the serotonin receptor <strong>HTR2A</strong> with cocaine <b>dependence</b> [rs6561333; nominal P value adjusted for age = 1.9e 04, odds ratio = 1.72 (1.29 2.30)].
+HTR2A	drug	cocaine	23241418	When patients were subdivided according to the presence or absence of psychotic symptoms, we confirmed the association between <b>cocaine</b> dependence and <strong>HTR2A</strong> in both subgroups of patients.
+HTR2A	addiction	dependence	23241418	When patients were subdivided according to the presence or absence of psychotic symptoms, we confirmed the association between cocaine <b>dependence</b> and <strong>HTR2A</strong> in both subgroups of patients.
+HTR2A	drug	alcohol	22661198	Serotonin 2A receptor gene (<strong>HTR2A</strong>) polymorphism in <b>alcohol</b> dependent patients.
+HTR2A	drug	alcohol	22661198	In the present study, a potential relationship between T102C polymorphism in the 5 HT receptor subtype 2Agene (<strong>HTR2A</strong>) and <b>alcohol</b> dependence was examined.
+HTR2A	addiction	dependence	22661198	In the present study, a potential relationship between T102C polymorphism in the 5 HT receptor subtype 2Agene (<strong>HTR2A</strong>) and alcohol <b>dependence</b> was examined.
+HTR2A	drug	alcohol	22661198	The results suggest a potential role of the T102C <strong>HTR2A</strong> polymorphism in development of <b>alcohol</b> dependence.
+HTR2A	addiction	dependence	22661198	The results suggest a potential role of the T102C <strong>HTR2A</strong> polymorphism in development of alcohol <b>dependence</b>.
+HTR2A	drug	cocaine	22434223	Furthermore, chronic fluoxetine treatment causes alterations in <strong>5HT2A</strong> receptors in the frontal cortex that may selectively disrupt <b>cocaine</b> primed reinstatement.
+HTR2A	addiction	relapse	22434223	Furthermore, chronic fluoxetine treatment causes alterations in <strong>5HT2A</strong> receptors in the frontal cortex that may selectively disrupt cocaine primed <b>reinstatement</b>.
+HTR2A	drug	nicotine	22342986	Effects of the 5 HT2C receptor agonist Ro60 0175 and the <strong>5 HT2A</strong> receptor antagonist M100907 on <b>nicotine</b> self administration and reinstatement.
+HTR2A	addiction	relapse	22342986	Effects of the 5 HT2C receptor agonist Ro60 0175 and the <strong>5 HT2A</strong> receptor antagonist M100907 on nicotine self administration and <b>reinstatement</b>.
+HTR2A	drug	opioid	22138326	The association of 5 <strong>HTR2A</strong> 1438A/G, COMTVal158Met, MAOA LPR, DATVNTR and 5 HTTVNTR gene polymorphisms and antisocial personality disorder in male <b>heroin</b> dependent Chinese subjects.
+HTR2A	drug	opioid	22138326	To explore the association between the 5 <strong>HTR2A</strong> 1438A/G, COMTVal158Met, MAOA LPR, DATVNTR and 5 HTTVNTR polymorphisms with comorbidity of antisocial personality disorder in male <b>heroin</b> dependent patients.
+HTR2A	drug	opioid	22138326	In case control study, we compared the polymorphic distributions of 5 <strong>HTR2A</strong> 1438A/G, COMTVal158Met, MAOA LPR, DATVNTR and 5 HTTVNTR in 588 male <b>heroin</b> dependent patients (including 311 patients with antisocial personality disorder and 277 patients without antisocial personality disorder) and 194 normal males by genotypes, alleles, and interaction between genes.
+HTR2A	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, <strong>HTR2A</strong>  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+HTR2A	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, <strong>HTR2A</strong>  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+HTR2A	drug	cannabinoid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (<strong>HTR2A</strong>), opioid (OPRM1) or <b>cannabinoid</b> receptors (CNR1).
+HTR2A	drug	nicotine	22046326	Overall, our results suggest that genetic variants potentially involved in <b>nicotine</b> metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with <b>smoking</b> related phenotypes, as opposed to genetic variants influencing the brain effects of <b>nicotine</b>, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (<strong>HTR2A</strong>), opioid (OPRM1) or cannabinoid receptors (CNR1).
+HTR2A	drug	opioid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (<strong>HTR2A</strong>), <b>opioid</b> (OPRM1) or cannabinoid receptors (CNR1).
+HTR2A	drug	nicotine	22028400	Among susceptible youth (N = 246), older age at baseline, living with a <b>smoker</b>, and three different genes (<strong>HTR2A</strong>, DRD2, SLC6A3) predicted experimentation.
+HTR2A	drug	alcohol	21930285	The CC genotype in <strong>HTR2A</strong> T102C polymorphism is associated with behavioral impulsivity in <b>alcohol</b> dependent patients.
+HTR2A	drug	alcohol	21621273	Association of polymorphisms in <strong>HTR2A</strong>, HTR1A and TPH2 genes with suicide attempts in <b>alcohol</b> dependence: a preliminary report.
+HTR2A	addiction	dependence	21621273	Association of polymorphisms in <strong>HTR2A</strong>, HTR1A and TPH2 genes with suicide attempts in alcohol <b>dependence</b>: a preliminary report.
+HTR2A	drug	alcohol	21621273	We investigated a relationship between selected polymorphisms: rs6313 in <strong>HTR2A</strong>, rs6295 in HTR1A and rs1386494 in TPH2, and suicidal behaviour in 150 <b>alcohol</b> dependent patients.
+HTR2A	drug	alcohol	21621273	There was a significant association between more frequent C102C genotype in <strong>HTR2A</strong> and suicide attempts in <b>alcoholic</b> females.
+HTR2A	drug	amphetamine	21420940	Differential regulation of <strong>5 HT2A</strong> receptor mRNA expression following withdrawal from a chronic escalating dose regimen of D <b>amphetamine</b>.
+HTR2A	addiction	withdrawal	21420940	Differential regulation of <strong>5 HT2A</strong> receptor mRNA expression following <b>withdrawal</b> from a chronic escalating dose regimen of D amphetamine.
+HTR2A	drug	cocaine	21079923	Blockade of <strong>5 HT2A</strong> receptors in the medial prefrontal cortex attenuates reinstatement of cue elicited <b>cocaine</b> seeking behavior in rats.
+HTR2A	addiction	relapse	21079923	Blockade of <strong>5 HT2A</strong> receptors in the medial prefrontal cortex attenuates <b>reinstatement</b> of cue elicited cocaine <b>seeking</b> behavior in rats.
+HTR2A	drug	nicotine	21035274	Cigarette <b>smoking</b> in young adults: the influence of the <strong>HTR2A</strong> T102C polymorphism and punishment sensitivity.
+HTR2A	addiction	addiction	21035274	Cigarette smoking in young adults: the influence of the <strong>HTR2A</strong> T102C polymorphism and <b>punishment</b> sensitivity.
+HTR2A	drug	nicotine	21035274	The C allele of a common polymorphism of the serotonin 2A receptor (<strong>HTR2A</strong>) gene, T102C, results in reduced synthesis of 5 HT2A receptors and has been associated with current <b>smoking</b> status in adults.
+HTR2A	drug	nicotine	21035274	The C allele of a common polymorphism of the serotonin 2A receptor (<strong>HTR2A</strong>) gene, T102C, results in reduced synthesis of <strong>5 HT2A</strong> receptors and has been associated with current <b>smoking</b> status in adults.
+HTR2A	drug	nicotine	21035274	We investigated the contributions of the <strong>HTR2A</strong> gene, chronic psychological stress, and impulsivity to the prediction of cigarette <b>smoking</b> status and dependence in young adults.
+HTR2A	addiction	dependence	21035274	We investigated the contributions of the <strong>HTR2A</strong> gene, chronic psychological stress, and impulsivity to the prediction of cigarette smoking status and <b>dependence</b> in young adults.
+HTR2A	drug	psychedelics	20942998	Involvement of <strong>5 HT2A</strong> receptors in <b>MDMA</b> reinforcement and cue induced reinstatement of <b>MDMA</b> seeking behaviour.
+HTR2A	addiction	relapse	20942998	Involvement of <strong>5 HT2A</strong> receptors in MDMA reinforcement and cue induced <b>reinstatement</b> of MDMA <b>seeking</b> behaviour.
+HTR2A	addiction	reward	20942998	Involvement of <strong>5 HT2A</strong> receptors in MDMA <b>reinforcement</b> and cue induced reinstatement of MDMA seeking behaviour.
+HTR2A	addiction	addiction	20942998	Current evidence indicates that serotonin <strong>5 HT2A</strong> receptors (5 HT2ARs) modulate mesolimbic dopamine (DA) activity and several behavioural responses related to the <b>addictive</b> properties of psychostimulants.
+HTR2A	drug	cocaine	20814782	Blockade of nucleus accumbens <strong>5 HT2A</strong> and 5 HT2C receptors prevents the expression of <b>cocaine</b> induced behavioral and neurochemical sensitization in rats.
+HTR2A	addiction	sensitization	20814782	Blockade of nucleus accumbens <strong>5 HT2A</strong> and 5 HT2C receptors prevents the expression of cocaine induced behavioral and neurochemical <b>sensitization</b> in rats.
+HTR2A	drug	cocaine	20577718	Role of serotonin <strong>5 HT2A</strong> and 5 HT2C receptors on brain stimulation reward and the reward facilitating effect of <b>cocaine</b>.
+HTR2A	addiction	reward	20577718	Role of serotonin <strong>5 HT2A</strong> and 5 HT2C receptors on brain stimulation <b>reward</b> and the <b>reward</b> facilitating effect of cocaine.
+HTR2A	drug	alcohol	20501057	Decreased cerebral cortex and liver <strong>5 HT2A</strong> receptor gene expression and enhanced ALDH activity in <b>ethanol</b> treated rats and hepatocyte cultures.
+HTR2A	drug	alcohol	19742166	Epistasis between IL1A, IL1B, TNF, <strong>HTR2A</strong>, 5 HTTLPR and TPH2 variations does not impact <b>alcohol</b> dependence disorder features.
+HTR2A	addiction	dependence	19742166	Epistasis between IL1A, IL1B, TNF, <strong>HTR2A</strong>, 5 HTTLPR and TPH2 variations does not impact alcohol <b>dependence</b> disorder features.
+HTR2A	drug	alcohol	19742166	In both groups we genotyped 11 genetic variations (rs1800587; rs3087258; rs1799724; 5 HTTLPR; rs1386493; rs1386494; rs1487275; rs1843809; rs4570625; rs2129575; rs6313) located in genes whose impact on <b>alcohol</b> related behaviors and disorders has been hypothesized (IL1A, IL1B, TNF, 5 HTTLPR, TPH2 and <strong>HTR2A</strong>).
+HTR2A	drug	benzodiazepine	19523493	Brain structures implicated in the four plate test in naïve and experienced Swiss mice using injection of <b>diazepam</b> and the <strong>5 HT2A</strong> agonist DOI.
+HTR2A	addiction	relapse	19353810	The D2 and 5 HT1A partial agonist and <strong>5 HT2A</strong> antagonist properties of aripiprazole likely account for the blockade of <b>relapse</b> to drug <b>seeking</b>.
+HTR2A	drug	cocaine	19331461	Blockade of the serotonin <strong>5 HT2A</strong> receptor suppresses cue evoked reinstatement of <b>cocaine</b> seeking behavior in a rat self administration model.
+HTR2A	addiction	relapse	19331461	Blockade of the serotonin <strong>5 HT2A</strong> receptor suppresses cue evoked <b>reinstatement</b> of cocaine <b>seeking</b> behavior in a rat self administration model.
+HTR2A	addiction	relapse	19331461	The serotonin <strong>5 HT2A</strong> receptor (5 HT sub(2A)R) may play a role in <b>reinstatement</b> of drug <b>seeking</b>.
+HTR2A	drug	alcohol	19328219	This study aimed to investigate whether three serotonergic polymorphisms (<strong>HTR2A</strong> A 1438G (rs6311), and SCL6A4 5 HTTLPR and STin2 VNTR) were associated with <b>alcohol</b> dependence, and, whether the serotonergic polymorphisms played a similar role in conferring vulnerability in <b>alcohol</b> and heroin dependence.
+HTR2A	drug	opioid	19328219	This study aimed to investigate whether three serotonergic polymorphisms (<strong>HTR2A</strong> A 1438G (rs6311), and SCL6A4 5 HTTLPR and STin2 VNTR) were associated with alcohol dependence, and, whether the serotonergic polymorphisms played a similar role in conferring vulnerability in alcohol and <b>heroin</b> dependence.
+HTR2A	addiction	dependence	19328219	This study aimed to investigate whether three serotonergic polymorphisms (<strong>HTR2A</strong> A 1438G (rs6311), and SCL6A4 5 HTTLPR and STin2 VNTR) were associated with alcohol <b>dependence</b>, and, whether the serotonergic polymorphisms played a similar role in conferring vulnerability in alcohol and heroin <b>dependence</b>.
+HTR2A	addiction	relapse	19170664	Genetic polymorphisms in several genes (TPH2, SLC6A4, HTR1A, <strong>HTR2A</strong>, COMT, and BDNF) were tested as predictors of <b>relapse</b> (defined as any drinking during follow up) while controlling for baseline measures.
+HTR2A	drug	cocaine	19125118	In contrast, coadministration of the <strong>5 HT2A</strong>/2C agonist (+/ ) 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane (DOI; 0.3 mg/kg) led to partial substitution of DOI for <b>cocaine</b> and enhancement of the stimulus properties of 1.25 mg/kg <b>cocaine</b> in LCRs only.
+HTR2A	drug	alcohol	19111403	The serotonin receptor gene <strong>HTR2A</strong> has been a candidate gene with some evidence for association with <b>alcohol</b> and nicotine dependencies.
+HTR2A	drug	nicotine	19111403	The serotonin receptor gene <strong>HTR2A</strong> has been a candidate gene with some evidence for association with alcohol and <b>nicotine</b> dependencies.
+HTR2A	drug	alcohol	19111403	The aim of the present study was to test for possible associations between the A 1438G polymorphism in the serotonin receptor gene (<strong>HTR2A</strong>) with tobacco smoking combined or not with <b>alcohol</b> dependence.
+HTR2A	drug	nicotine	19111403	The aim of the present study was to test for possible associations between the A 1438G polymorphism in the serotonin receptor gene (<strong>HTR2A</strong>) with <b>tobacco</b> <b>smoking</b> combined or not with alcohol dependence.
+HTR2A	addiction	dependence	19111403	The aim of the present study was to test for possible associations between the A 1438G polymorphism in the serotonin receptor gene (<strong>HTR2A</strong>) with tobacco smoking combined or not with alcohol <b>dependence</b>.
+HTR2A	drug	alcohol	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (<strong>5 HT2A</strong>), and the serotonin transporter gene (5 HTT) promotor region (5 HTTLPR) in the manifestation of individual <b>alcohol</b> withdrawal symptoms was investigated in 97 Korean male inpatients with <b>alcohol</b> dependence and 76 Korean healthy male subjects.
+HTR2A	addiction	dependence	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (<strong>5 HT2A</strong>), and the serotonin transporter gene (5 HTT) promotor region (5 HTTLPR) in the manifestation of individual alcohol withdrawal symptoms was investigated in 97 Korean male inpatients with alcohol <b>dependence</b> and 76 Korean healthy male subjects.
+HTR2A	addiction	withdrawal	19060480	The role of polymorphisms in the serotonin receptor 1A (5 HT1A), serotonin receptor 2A (<strong>5 HT2A</strong>), and the serotonin transporter gene (5 HTT) promotor region (5 HTTLPR) in the manifestation of individual alcohol <b>withdrawal</b> symptoms was investigated in 97 Korean male inpatients with alcohol dependence and 76 Korean healthy male subjects.
+HTR2A	drug	nicotine	18950618	Ketanserin, a <strong>5 HT2a</strong> and 5 HT2c receptor antagonist, significantly attenuates <b>nicotine</b> effects on attention and memory.
+HTR2A	drug	opioid	18801381	Among the 812 differentially expressed candidates, several genes (Adcy5, <strong>Htr2a</strong>) and pathways (Map kinases, G proteins, integrins) have already been described as modulated in the brain of <b>morphine</b> treated rats.
+HTR2A	drug	cocaine	27879921	The rationale for selecting this medication is: ketanserin (a) is an antihypertensive and <b>cocaine</b> and caffeine produce hypertension and (b) acts at <strong>5 HT2A</strong>/2C receptors, prevalent in NAc and implicated in hypertension and <b>cocaine</b> addiction.
+HTR2A	addiction	addiction	27879921	The rationale for selecting this medication is: ketanserin (a) is an antihypertensive and cocaine and caffeine produce hypertension and (b) acts at <strong>5 HT2A</strong>/2C receptors, prevalent in NAc and implicated in hypertension and cocaine <b>addiction</b>.
+HTR2A	drug	alcohol	18552399	The aim of this study was to investigate the potential association between functional polymorphisms of dopaminergic [dopamine receptor D2 (DRD2), dopamine receptor D3 (DRD3) and dopamine transporter (SLC6A3)] and serotonergic [serotonin 2A receptor (<strong>HTR2A</strong>) and serotonin transporter (SLC6A4)] genes and treatment outcome in <b>alcohol</b> dependent patients.
+HTR2A	drug	opioid	18417104	ketanserin (a <strong>5 HT2A</strong> receptor antagonist) on <b>tramadol</b> analgesia was observed.
+HTR2A	drug	opioid	18417104	The expression of the <strong>5 HT2A</strong> receptor mRNA in the nucleus of raphe magnus (NRM), ventrolateral periaqueductal gray (vlPAG) and spinal dorsal horn of mono arthritic rats after a ten day treatment with <b>tramadol</b> was measured with in situ hybridization.
+HTR2A	drug	opioid	18417104	Expression of the <strong>5 HT2A</strong> receptor mRNA in NRM, ipsilateral vlPAG, and the ipsilateral spinal dorsal horn of arthritic rats was significantly increased after <b>tramadol</b> treatment.
+HTR2A	drug	opioid	18417104	These results suggest that <strong>5 HT2A</strong> receptors are involved in the analgesic effect of <b>tramadol</b>.
+HTR2A	drug	opioid	18417104	This study provides evidence for involvement of <strong>5 HT2A</strong> receptors in the <b>tramadol</b> analgesia of inflammatory pain.
+HTR2A	drug	psychedelics	18266547	No particular differences between the capacities of racemic <b>MDMA</b> and its enantiomers to maintain behavior were noted, but antagonism of the <strong>5 HT2A</strong> receptor produces a parallel rightward shift in the dose effect function for the S(+) enantiomer, but insurmountably reduces the reinforcing effects of R( ) <b>MDMA</b>.
+HTR2A	addiction	reward	18266547	No particular differences between the capacities of racemic MDMA and its enantiomers to maintain behavior were noted, but antagonism of the <strong>5 HT2A</strong> receptor produces a parallel rightward shift in the dose effect function for the S(+) enantiomer, but insurmountably reduces the <b>reinforcing</b> effects of R( ) MDMA.
+HTR2A	drug	alcohol	18241316	Family history of <b>alcoholism</b> is associated with lower <strong>5 HT2A</strong> receptor binding in the prefrontal cortex.
+HTR2A	drug	opioid	18182772	Association between <b>heroin</b> dependence and <strong>5 HT2A</strong> receptor gene polymorphisms.
+HTR2A	addiction	dependence	18182772	Association between heroin <b>dependence</b> and <strong>5 HT2A</strong> receptor gene polymorphisms.
+HTR2A	drug	amphetamine	17957734	<b>Methamphetamine</b> induced sensitization includes a functional upregulation of ventral pallidal <strong>5 HT2A</strong>/2C receptors.
+HTR2A	addiction	sensitization	17957734	Methamphetamine induced <b>sensitization</b> includes a functional upregulation of ventral pallidal <strong>5 HT2A</strong>/2C receptors.
+HTR2A	drug	amphetamine	17957734	The current study was designed to ascertain if ventral pallidal neurons are functionally upregulated 3 days after a behaviorally sensitizing treatment regimen of <b>METH</b>, and whether these effects could be revealed by activating the <strong>5 HT2A</strong>/2C receptors.
+HTR2A	drug	amphetamine	17957734	The efficacy of the <strong>5 HT2A</strong>/2C agonist, 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane (DOI) to augment ventral pallidal cell firing also was enhanced in <b>METH</b> sensitized rats.
+HTR2A	addiction	sensitization	17805311	In all cases, this <b>sensitization</b> is prevented by alpha 1b adrenergic and <strong>5 HT2A</strong> receptors blockade, indicating the critical role of these receptors on long term effects of drugs of abuse.
+HTR2A	drug	alcohol	17713649	T102C polymorphism of the serotonin receptor 2A gene (<strong>5 HT2A</strong>) has been shown to be associated with certain diseases such as non fatal acute myocardial infarction, essential hypertension, and <b>alcoholism</b>.
+HTR2A	drug	amphetamine	17510759	Paradoxical constitutive behavioral sensitization to <b>amphetamine</b> in mice lacking <strong>5 HT2A</strong> receptors.
+HTR2A	addiction	sensitization	17510759	Paradoxical constitutive behavioral <b>sensitization</b> to amphetamine in mice lacking <strong>5 HT2A</strong> receptors.
+HTR2A	drug	amphetamine	17510759	Although locomotor response to d <b>amphetamine</b> is considered as mediated by an increased release of dopamine in the ventral striatum, blockade of either alpha1b adrenergic or <strong>5 HT2A</strong> receptors almost completely inhibits d <b>amphetamine</b> induced locomotor response in mice.
+HTR2A	drug	amphetamine	17510759	However, we show here that, paradoxically, mice lacking <strong>5 HT2A</strong> receptors (<strong>5 HT2A</strong> R KO) exhibit a twofold higher locomotor response to d <b>amphetamine</b> than wild type (WT) littermates.
+HTR2A	drug	amphetamine	17510759	Locomotor response and behavioral sensitization to d <b>amphetamine</b> were measured in presence of prazosin and/or SR46349B, alpha1b adrenergic, and <strong>5 HT2A</strong> receptor antagonists, respectively.
+HTR2A	addiction	sensitization	17510759	Locomotor response and behavioral <b>sensitization</b> to d amphetamine were measured in presence of prazosin and/or SR46349B, alpha1b adrenergic, and <strong>5 HT2A</strong> receptor antagonists, respectively.
+HTR2A	drug	amphetamine	17510759	Repeating <b>amphetamine</b> injections still increases <strong>5 HT2A</strong> R KO mice locomotor response to d <b>amphetamine</b> at a level similar to that of sensitized WT mice.
+HTR2A	drug	amphetamine	17510759	One milligrams per kilogram of prazosin completely blocks d <b>amphetamine</b> induced locomotor response in <strong>5 HT2A</strong> R KO naïve animals but 3 mg/kg is necessary in sensitized <strong>5 HT2A</strong> R KO mice.
+HTR2A	drug	amphetamine	17510759	Because naïve <strong>5 HT2A</strong> R KO mice exhibit an increased cortical noradrenergic response to d <b>amphetamine</b>, our data suggest that repeated d <b>amphetamine</b> modifies noradrenergic transmission in <strong>5 HT2A</strong> R KO mice.
+HTR2A	drug	amphetamine	17510759	Dramatic decrease in SR46349B efficiency in sensitized WT mice indicates that a disruption of the regulating role of <strong>5 HT2A</strong> receptors on noradrenergic transmission occurs during sensitization and thus represents the physiological basis of behavioral sensitization to d <b>amphetamine</b>.
+HTR2A	addiction	sensitization	17510759	Dramatic decrease in SR46349B efficiency in sensitized WT mice indicates that a disruption of the regulating role of <strong>5 HT2A</strong> receptors on noradrenergic transmission occurs during <b>sensitization</b> and thus represents the physiological basis of behavioral <b>sensitization</b> to d amphetamine.
+HTR2A	drug	cocaine	17259860	Withdrawal from a single exposure to <b>cocaine</b> increases <strong>5 HT2A</strong> receptor and G protein function.
+HTR2A	addiction	withdrawal	17259860	<b>Withdrawal</b> from a single exposure to cocaine increases <strong>5 HT2A</strong> receptor and G protein function.
+HTR2A	addiction	addiction	17102981	The selective serotonin (5 HT) reuptake inhibitors (SSRIs) represent the first line pharmacotherapy for obsessive <b>compulsive</b> disorder (OCD), and atypical antipsychotic drugs, which block <strong>5 HT2A</strong> receptors, are used in augmentation strategies.
+HTR2A	addiction	addiction	17102981	The <strong>5 HT2A</strong> related behavior (i.e., head twitch) has been related with tics, stereotypes, and <b>compulsive</b> symptoms observed in Tourette syndrome and OCD.
+HTR2A	drug	opioid	17102981	Combined 5 HT and <b>opioid</b> properties result in a greater efficacy in antagonizing <strong>5 HT2A</strong> related behavior.
+HTR2A	drug	cocaine	17055657	<b>Cocaine</b> mediated supersensitivity of <strong>5 HT2A</strong> receptors in hypothalamic paraventricular nucleus is a withdrawal induced phenomenon.
+HTR2A	addiction	withdrawal	17055657	Cocaine mediated supersensitivity of <strong>5 HT2A</strong> receptors in hypothalamic paraventricular nucleus is a <b>withdrawal</b> induced phenomenon.
+HTR2A	drug	cocaine	17055657	We previously reported that treatment and withdrawal from <b>cocaine</b> increases: (1) <strong>5 HT2A</strong> receptor mediated neuroendocrine responses, and (2) Galphaq and Galpha11 G protein levels in the hypothalamic paraventricular nucleus (PVN) at 48 h post treatment.
+HTR2A	addiction	withdrawal	17055657	We previously reported that treatment and <b>withdrawal</b> from cocaine increases: (1) <strong>5 HT2A</strong> receptor mediated neuroendocrine responses, and (2) Galphaq and Galpha11 G protein levels in the hypothalamic paraventricular nucleus (PVN) at 48 h post treatment.
+HTR2A	drug	cocaine	17055657	This study investigates changes in the initial 24 h of withdrawal to discern whether <strong>5 HT2A</strong> receptor supersensitivity is due to <b>cocaine</b> treatment or is induced during the withdrawal period.
+HTR2A	addiction	withdrawal	17055657	This study investigates changes in the initial 24 h of <b>withdrawal</b> to discern whether <strong>5 HT2A</strong> receptor supersensitivity is due to cocaine treatment or is induced during the <b>withdrawal</b> period.
+HTR2A	addiction	withdrawal	17055657	We report here increases in <strong>5 HT2A</strong> receptor mediated neuroendocrine responses only 12 or 24 h post treatment, but not during the initial 4 h <b>withdrawal</b> period.
+HTR2A	drug	cocaine	17055657	However, the density of 125I ( ) 1 (2,5 dimethoxy 4 iodophenyl) 2 amino propane HCl (DOI) labeled high affinity <strong>5 HT2A</strong> receptors in PVN increased 35% in rats withdrawn from <b>cocaine</b> for 24 h. These findings demonstrate that <b>cocaine</b> induced increases in <strong>5 HT2A</strong> receptor function in PVN represents a withdrawal induced phenomena that: (1) is likely attributed to increased G protein coupled/high affinity conformational state of the <strong>5 HT2A</strong> receptor, and (2) occurs in the absence of changes in the levels of associated G proteins during the first 24 h.
+HTR2A	addiction	withdrawal	17055657	However, the density of 125I ( ) 1 (2,5 dimethoxy 4 iodophenyl) 2 amino propane HCl (DOI) labeled high affinity <strong>5 HT2A</strong> receptors in PVN increased 35% in rats withdrawn from cocaine for 24 h. These findings demonstrate that cocaine induced increases in <strong>5 HT2A</strong> receptor function in PVN represents a <b>withdrawal</b> induced phenomena that: (1) is likely attributed to increased G protein coupled/high affinity conformational state of the <strong>5 HT2A</strong> receptor, and (2) occurs in the absence of changes in the levels of associated G proteins during the first 24 h.
+HTR2A	drug	amphetamine	17051415	Effects of d <b>amphetamine</b> and DOI (2,5 dimethoxy 4 iodoamphetamine) on timing behavior: interaction between D1 and <strong>5 HT2A</strong> receptors.
+HTR2A	addiction	dependence	17017968	Serotonin <strong>5 HT2A</strong> and 5 HT2C receptors as potential targets for modulation of psychostimulant use and <b>dependence</b>.
+HTR2A	drug	cocaine	17017968	Two key modulators of DA output are the serotonin (5 HT)2A receptor (<strong>5 HT2A</strong> R) and the 5 HT2C R. These receptors are known to control the neurochemical and behavioral effects of psychostimulants, and in particular, the in vivo effects of <b>cocaine</b>.
+HTR2A	drug	cocaine	17017968	Preclinical studies indicate that <strong>5 HT2A</strong> R antagonists and/or 5 HT2C R agonists may effectively reduce craving and/or relapse, and likewise, enhance abstinence, while 5 HT2C R agonists may also effectively reduce <b>cocaine</b> intake in active <b>cocaine</b> users.
+HTR2A	addiction	relapse	17017968	Preclinical studies indicate that <strong>5 HT2A</strong> R antagonists and/or 5 HT2C R agonists may effectively reduce <b>craving</b> and/or <b>relapse</b>, and likewise, enhance abstinence, while 5 HT2C R agonists may also effectively reduce cocaine intake in active cocaine users.
+HTR2A	drug	cocaine	17017968	At present, the progression of studies to probe the effectiveness of <strong>5 HT2A</strong> R and 5 HT2C R ligands in the clinical setting is hindered by a lack of available selective <strong>5 HT2A</strong> R antagonists or 5 HT2C R agonists for use in human <b>cocaine</b> abusers.
+HTR2A	drug	amphetamine	16326032	Systemic treatment with the 5 HT(2A/2C) receptor agonist 2,5, dimethoxy 4 iodo <b>amphetamine</b> (DOI) (0.25 mg/kg, s.c.) reduced T50; the <strong>5 HT2A</strong> receptor antagonist MDL 100907 (0.5 mg/kg, i.p.)
+HTR2A	drug	nicotine	16272956	CYP2A6, MAOA, DBH, DRD4, and <strong>5HT2A</strong> genotypes, <b>smoking</b> behaviour and cotinine levels in 1518 UK adolescents.
+HTR2A	drug	nicotine	16272956	No significant associations were identified for DBH, MAOA, DRD4 and <strong>5HT2A</strong> markers, with <b>smoking</b> status or cotinine level at either age.
+HTR2A	drug	psychedelics	16005500	When <b>LSD</b> [0.17 mg/kg] was administered in combination with the selective <strong>5 HT2A</strong> antagonist, M100907, <b>LSD</b> appropriate responding was significantly but incompletely reduced to approximately 50%; concurrently, response rates declined significantly.
+HTR2A	drug	benzodiazepine	15918077	The drugs studied were two BZDs, <b>diazepam</b> (1 mg/kg) and <b>alprazolam</b> (0.25 mg/kg); flumazenil, a GABA(A) receptor antagonist (8 mg/kg); atropine sulphate, a muscarinic cholinergic receptor antagonist (4 mg/kg) known for its amnesic properties; paroxetine, a selective serotonin reuptake inhibitor (4 and 8 mg/kg); venlafaxine, a serotonin and noradrenalin reuptake inhibitor (4 and 16 mg/kg); and DOI, a <strong>5 HT2A</strong> agonist (1 mg/kg).
+HTR2A	drug	opioid	15821952	Effect of the blockade of mu1 <b>opioid</b> and <strong>5HT2A</strong> serotonergic/alpha1 noradrenergic receptors on sweet substance induced analgesia.
+HTR2A	drug	opioid	15821952	These data give further evidence for: (a) the involvement of endogenous <b>opioids</b> and a mu1 <b>opioid</b> receptor in the sweet substance induced antinociception; (b) the involvement of monoamines and <strong>5HT2A</strong> serotonergic/alpha1 noradrenergic receptors in the central regulation of the sweet substance produced analgesia.
+HTR2A	drug	psychedelics	15723230	<b>LSD</b> (186 or 372 nmol/kg, 0.08 or 0.16 mg/kg) given 30 min prior to training produced a cue that was completely antagonized by <strong>5 HT2A</strong> antagonists and lasted no longer than 1 h. <b>LSD</b> (372 nmol/kg, 0.16 mg/kg) injected 90 min before training produced a cue that was not fully blocked by <strong>5 HT2A</strong> antagonists, but instead was significantly inhibited by haloperidol.
+HTR2A	drug	nicotine	15682310	The current study served to determine the impact of a relatively selective <strong>5 HT2A</strong> receptor antagonist, ketanserin, on attentional function in rats and the interactions of ketanserin with <b>nicotine</b> administration.
+HTR2A	drug	nicotine	15682310	These data suggest a functional interaction between <b>nicotine</b> and <strong>5 HT2A</strong> receptor antagonist ketanserin.
+HTR2A	addiction	sensitization	15579162	<strong>5 HT2A</strong> and alpha1b adrenergic receptors entirely mediate dopamine release, locomotor response and behavioural <b>sensitization</b> to opiates and psychostimulants.
+HTR2A	drug	opioid	15579162	This acute <b>morphine</b> evoked DA release was completely blocked in alpha1b AR KO mice by SR46349B (1 mg/kg), a <strong>5 HT2A</strong> antagonist.
+HTR2A	drug	amphetamine	15579162	Accordingly, the concomitant blockade of <strong>5 HT2A</strong> and alpha1b adrenergic receptors in WT mice entirely blocked acute locomotor responses but also the development of behavioural sensitization to morphine, D <b>amphetamine</b> or cocaine (10 mg/kg).
+HTR2A	drug	cocaine	15579162	Accordingly, the concomitant blockade of <strong>5 HT2A</strong> and alpha1b adrenergic receptors in WT mice entirely blocked acute locomotor responses but also the development of behavioural sensitization to morphine, D amphetamine or <b>cocaine</b> (10 mg/kg).
+HTR2A	drug	opioid	15579162	Accordingly, the concomitant blockade of <strong>5 HT2A</strong> and alpha1b adrenergic receptors in WT mice entirely blocked acute locomotor responses but also the development of behavioural sensitization to <b>morphine</b>, D amphetamine or cocaine (10 mg/kg).
+HTR2A	addiction	sensitization	15579162	Accordingly, the concomitant blockade of <strong>5 HT2A</strong> and alpha1b adrenergic receptors in WT mice entirely blocked acute locomotor responses but also the development of behavioural <b>sensitization</b> to morphine, D amphetamine or cocaine (10 mg/kg).
+HTR2A	addiction	sensitization	15579162	Because of these latter data and the possible compensation by <strong>5 HT2A</strong> receptors for the genetic deletion of alpha1b adrenergic receptors, we postulate the existence of a functional link between these receptors, which vanishes during the development of behavioural <b>sensitization</b>.
+HTR2A	drug	nicotine	15565434	Attenuation of <b>nicotine</b>'s discriminative stimulus effects in rats and its locomotor activity effects in mice by serotonergic <strong>5 HT2A</strong>/2C receptor agonists.
+HTR2A	drug	nicotine	15565434	Reports have indicated that administration of <b>nicotine</b> inhibits, while withdrawal of chronically administered <b>nicotine</b> augments effects of serotonergic <strong>5HT2A</strong>/2C agonists.
+HTR2A	addiction	withdrawal	15565434	Reports have indicated that administration of nicotine inhibits, while <b>withdrawal</b> of chronically administered nicotine augments effects of serotonergic <strong>5HT2A</strong>/2C agonists.
+HTR2A	drug	nicotine	15565434	It was our objective to determine whether <strong>5HT2A</strong>/2C agonists can modulate the discriminative stimulus effects of <b>nicotine</b> in rats or its locomotor activity effects in mice.
+HTR2A	drug	nicotine	15565434	These results indicate that activation of serotonin <strong>5HT2A</strong>/2C receptors can blunt the discriminative stimulus and locomotor activity effects of <b>nicotine</b> and presents the possibility that activation of these receptors might also be able to attenuate other effects of <b>nicotine</b>.
+HTR2A	drug	nicotine	15564892	Epidemiological and genetic studies on <b>smoking</b> behavior have been performed, and in this study the human serotonin 2A receptor (<strong>HTR2A</strong>) polymorphism was examined in 82 <b>smoking</b> behaviorists and 125 healthy controls.
+HTR2A	drug	nicotine	15564892	The polymorphism in <strong>HTR2A</strong> (102T/C,  1438A/G) was identified by means of the polymerase chain reaction followed by restriction fragment length polymorphism, and the Fagerstrom Test for <b>Nicotine</b> Dependence was used to determine the extent of <b>smoking</b> behavior.
+HTR2A	addiction	dependence	15564892	The polymorphism in <strong>HTR2A</strong> (102T/C,  1438A/G) was identified by means of the polymerase chain reaction followed by restriction fragment length polymorphism, and the Fagerstrom Test for Nicotine <b>Dependence</b> was used to determine the extent of smoking behavior.
+HTR2A	drug	nicotine	15564892	The results suggest that the <strong>HTR2A</strong> (102T/C,  1438G/A) polymorphism might not be associated with susceptibility to a risk factor for developing <b>smoking</b> behavior.
+HTR2A	drug	nicotine	15211639	Polymorphism of <strong>5HT2A</strong> serotonin receptor gene is implicated in <b>smoking</b> addiction.
+HTR2A	addiction	addiction	15211639	Polymorphism of <strong>5HT2A</strong> serotonin receptor gene is implicated in smoking <b>addiction</b>.
+HTR2A	addiction	reward	15103450	Effects of fenfluramine on free <b>operant</b> timing behaviour: evidence for involvement of <strong>5 HT2A</strong> receptors.
+HTR2A	drug	cocaine	15093963	<b>Cocaine</b> acts on accumbens monoamines and locomotor behavior via a <strong>5 HT2A</strong>/2C receptor mechanism as shown by ketanserin: 24 h follow up studies.
+HTR2A	drug	alcohol	15080502	Autoradiographic analysis of 5 hydroxytryptamine <strong>5 HT2A</strong> binding sites in the rat brain after chronic intragastric <b>ethanol</b> treatments.
+HTR2A	drug	alcohol	15080502	Several evidences indicate altered regulation of brain serotonergic mechanisms in <b>alcohol</b> abuse; changes in <strong>5 HT2A</strong> receptor density and functioning have been observed in several lines of <b>alcohol</b> preferring rats.
+HTR2A	drug	alcohol	15080502	Using quantitative autoradiography, the present study investigated the influence of chronic intragastric <b>ethanol</b> treatment on forebrain <strong>5 HT2A</strong> binding sites in rats.
+HTR2A	drug	alcohol	15080502	Administration for 7 days of high doses of <b>ethanol</b>, which induced physical dependence, lowered the levels of <strong>5 HT2A</strong> binding sites in the cingulate cortex, the frontal cortex and in the agranular insular cortex.
+HTR2A	addiction	dependence	15080502	Administration for 7 days of high doses of ethanol, which induced physical <b>dependence</b>, lowered the levels of <strong>5 HT2A</strong> binding sites in the cingulate cortex, the frontal cortex and in the agranular insular cortex.
+HTR2A	drug	alcohol	15080502	Chronic treatment with 6 g/kg of <b>ethanol</b>, which did not induce dependence, did not modify <strong>5 HT2A</strong> binding sites.
+HTR2A	addiction	dependence	15080502	Chronic treatment with 6 g/kg of ethanol, which did not induce <b>dependence</b>, did not modify <strong>5 HT2A</strong> binding sites.
+HTR2A	drug	alcohol	15080502	These long lasting changes in brain <strong>5 HT2A</strong> binding sites observed in the present study might contribute to specific aspects of <b>ethanol</b> dependence, such as development of depression and <b>alcohol</b> craving.
+HTR2A	addiction	dependence	15080502	These long lasting changes in brain <strong>5 HT2A</strong> binding sites observed in the present study might contribute to specific aspects of ethanol <b>dependence</b>, such as development of depression and alcohol craving.
+HTR2A	addiction	relapse	15080502	These long lasting changes in brain <strong>5 HT2A</strong> binding sites observed in the present study might contribute to specific aspects of ethanol dependence, such as development of depression and alcohol <b>craving</b>.
+HTR2A	drug	cocaine	14534355	Serotonin 2A (<strong>5 HT2A</strong>) receptor mediated increases in plasma hormone levels become supersensitive after 42 h of withdrawal from <b>cocaine</b> treatment.
+HTR2A	addiction	withdrawal	14534355	Serotonin 2A (<strong>5 HT2A</strong>) receptor mediated increases in plasma hormone levels become supersensitive after 42 h of <b>withdrawal</b> from cocaine treatment.
+HTR2A	drug	cocaine	14534355	Rats were sacrificed 2 or 7 days after the last <b>cocaine</b> injection, and the levels of membrane and cytosol associated <strong>5 HT2A</strong> receptors, Galphaq, Galpha11, regulators of G protein signaling (RGS)4, and RGS7 proteins were assayed in the hypothalamic paraventricular nucleus, amygdala, and frontal cortex using Western blot analysis.
+HTR2A	drug	cocaine	14534355	The protein levels of the <strong>5 HT2A</strong> receptor, Galphaz protein, and RGS4 or RGS7 proteins were not altered by <b>cocaine</b> withdrawal in any of the above mentioned brain regions.
+HTR2A	addiction	withdrawal	14534355	The protein levels of the <strong>5 HT2A</strong> receptor, Galphaz protein, and RGS4 or RGS7 proteins were not altered by cocaine <b>withdrawal</b> in any of the above mentioned brain regions.
+HTR2A	drug	cocaine	14534355	These findings suggest that the supersensitivity of the <strong>5 HT2A</strong> receptors, during withdrawal from chronic <b>cocaine</b>, is associated with an increase in membrane associated Galphaq and Galpha11 proteins and not with changes in the expression of <strong>5 HT2A</strong> receptors.
+HTR2A	addiction	withdrawal	14534355	These findings suggest that the supersensitivity of the <strong>5 HT2A</strong> receptors, during <b>withdrawal</b> from chronic cocaine, is associated with an increase in membrane associated Galphaq and Galpha11 proteins and not with changes in the expression of <strong>5 HT2A</strong> receptors.
+HTR2A	drug	alcohol	26983355	In the past, there have been many epidemiological and genetic studies of mood disorders, schizophrenia, and <b>alcohol</b> dependence, and in this study, the human serotonin 2A receptor (5 <strong>HTR2A</strong>) polymorphism was examined in 80 patients with mood disorders, 50 patients with schizophrenia and 41 patients with <b>alcohol</b> dependence.
+HTR2A	addiction	dependence	26983355	In the past, there have been many epidemiological and genetic studies of mood disorders, schizophrenia, and alcohol <b>dependence</b>, and in this study, the human serotonin 2A receptor (5 <strong>HTR2A</strong>) polymorphism was examined in 80 patients with mood disorders, 50 patients with schizophrenia and 41 patients with alcohol <b>dependence</b>.
+HTR2A	drug	alcohol	26983355	The results suggest that 5 <strong>HTR2A</strong> (102T/C,  1438G/A) polymorphism might not be associated with susceptibility to schizophrenia or mood disorders, and it might not be a risk factor contributing to <b>alcohol</b> dependency.
+HTR2A	drug	cocaine	12757964	Medications such as olanzapine, which block dopamine D2 receptors, as well as serotonin receptors <strong>5HT2A</strong> and 5HT2C may be able to reduce <b>cocaine</b> use in <b>cocaine</b> dependent patients by reducing the euphoric effects of <b>cocaine</b> and attenuating <b>cocaine</b> craving.
+HTR2A	addiction	relapse	12757964	Medications such as olanzapine, which block dopamine D2 receptors, as well as serotonin receptors <strong>5HT2A</strong> and 5HT2C may be able to reduce cocaine use in cocaine dependent patients by reducing the euphoric effects of cocaine and attenuating cocaine <b>craving</b>.
+HTR2A	addiction	addiction	12054060	This review summarizes information about the association between the <strong>5 HT2A</strong> receptor gene and its relevance to schizophrenia, tardive dyskinesia, major depression, suicidality, anorexia nervosa and obsessive <b>compulsive</b> disorder.
+HTR2A	drug	alcohol	12054060	Evidence is presented that implies that selective <strong>5 HT2A</strong> antagonists may be considered useful in investigating the role of <strong>5 HT2A</strong> receptor function and in the treatment of psychosis, and possibly <b>alcohol</b> and cocaine dependence.
+HTR2A	drug	cocaine	12054060	Evidence is presented that implies that selective <strong>5 HT2A</strong> antagonists may be considered useful in investigating the role of <strong>5 HT2A</strong> receptor function and in the treatment of psychosis, and possibly alcohol and <b>cocaine</b> dependence.
+HTR2A	addiction	dependence	12054060	Evidence is presented that implies that selective <strong>5 HT2A</strong> antagonists may be considered useful in investigating the role of <strong>5 HT2A</strong> receptor function and in the treatment of psychosis, and possibly alcohol and cocaine <b>dependence</b>.
+HTR2A	addiction	dependence	12054060	In conclusion, the ability of selective <strong>5 HT2A</strong> receptor antagonists to interfere with the heightened state of dopamine activity without altering basal tone, suggests that these drugs possess antipsychotic activity and may provide the basis for new therapies for psychosis and drug <b>dependence</b>, in addition to contributing towards a more complete understanding of <strong>5 HT2A</strong> receptor function.
+HTR2A	drug	psychedelics	11705117	It appears that <strong>5 HT2A</strong>, 5 HT2C, and sigma 2 receptors are involved in mediating the stimulus effects of <b>ibogaine</b>.
+HTR2A	drug	psychedelics	11705117	<b>Ibogaine</b>'s hallucinogenic effects may be explained by its interactions with <strong>5 HT2A</strong> and 5 HT2C receptors, while its putative antiaddictive properties may result from its interactions with sigma 2 and opiate receptors.
+HTR2A	drug	cocaine	11596864	In the present study we investigated the role of <strong>5 HT2A</strong>/2C receptors in the development or expression of sensitization to <b>cocaine</b> in rats, using ketanserin, an antagonist at these receptors.
+HTR2A	addiction	sensitization	11596864	In the present study we investigated the role of <strong>5 HT2A</strong>/2C receptors in the development or expression of <b>sensitization</b> to cocaine in rats, using ketanserin, an antagonist at these receptors.
+HTR2A	drug	cocaine	11596864	The above findings indicate a role of <strong>5 HT2A</strong>/2C receptors (but not alpha1 adrenoceptors) in the acute locomotor hyperactivity, as well as in the expression (but not development) of <b>cocaine</b> sensitization.
+HTR2A	addiction	sensitization	11596864	The above findings indicate a role of <strong>5 HT2A</strong>/2C receptors (but not alpha1 adrenoceptors) in the acute locomotor hyperactivity, as well as in the expression (but not development) of cocaine <b>sensitization</b>.
+HTR2A	drug	cocaine	11596864	Since chronic use of <b>cocaine</b> by humans may lead to psychoses or craving for this drug of abuse, our findings also seem to indicate possible importance of <strong>5 HT2A</strong>/2C receptor antagonists in the therapy of <b>cocaine</b> addiction.
+HTR2A	addiction	addiction	11596864	Since chronic use of cocaine by humans may lead to psychoses or craving for this drug of abuse, our findings also seem to indicate possible importance of <strong>5 HT2A</strong>/2C receptor antagonists in the therapy of cocaine <b>addiction</b>.
+HTR2A	addiction	relapse	11596864	Since chronic use of cocaine by humans may lead to psychoses or <b>craving</b> for this drug of abuse, our findings also seem to indicate possible importance of <strong>5 HT2A</strong>/2C receptor antagonists in the therapy of cocaine addiction.
+HTR2A	drug	alcohol	11444684	The authors tested for association of the <strong>5 HT2A</strong> receptor polymorphism (T102C) and the intron 7 tryptophan hydroxylase (TPH) polymorphism (A218C) among 176 <b>alcohol</b> dependent patients, 35 patients with panic disorder, 50 patients with generalized anxiety disorder, 55 patients with narcolepsy and 87 healthy controls.
+HTR2A	drug	alcohol	11444684	Allele and genotype frequencies of the <strong>5 HT2A</strong> receptor polymorphism (T102C), the intron 7 TPH polymorphism (A218C) were almost similar between the patients suffering from <b>alcohol</b> dependence, panic disorder, generalized anxiety disorder and narcolepsy.
+HTR2A	addiction	dependence	11444684	Allele and genotype frequencies of the <strong>5 HT2A</strong> receptor polymorphism (T102C), the intron 7 TPH polymorphism (A218C) were almost similar between the patients suffering from alcohol <b>dependence</b>, panic disorder, generalized anxiety disorder and narcolepsy.
+HTR2A	drug	alcohol	11444684	There was no association between the <strong>5 HT2A</strong> receptor polymorphism (T102C), the intron 7 TPH (A218C) polymorphisms and <b>alcohol</b> dependence, panic disorder, generalized anxiety disorder and narcolepsy in our subsets of German patients.
+HTR2A	addiction	dependence	11444684	There was no association between the <strong>5 HT2A</strong> receptor polymorphism (T102C), the intron 7 TPH (A218C) polymorphisms and alcohol <b>dependence</b>, panic disorder, generalized anxiety disorder and narcolepsy in our subsets of German patients.
+HTR2A	drug	alcohol	11287798	Impulsive traits and <strong>5 HT2A</strong> receptor promoter polymorphism in <b>alcohol</b> dependents: possible association but no influence of personality disorders.
+HTR2A	drug	alcohol	11287798	The aim of this study is to investigate the association between impulsive aggression in <b>alcohol</b> dependents with regard to the G 1438A polymorphism in the promoter region of the <strong>5 HT2A</strong> receptor gene.
+HTR2A	drug	alcohol	11287798	Furthermore, we investigated the statistical interaction between <strong>5 HT2A</strong> alleles, antisocial personality disorder (APD) and impulsive aggression in <b>alcohol</b> dependents.
+HTR2A	drug	alcohol	11287798	Blood samples were taken from <b>alcohol</b> dependents to determine <strong>5 HT2A</strong> promoter polymorphisms using PCR (polymerase chain reaction) of lymphocyte DNA.
+HTR2A	drug	alcohol	11287798	<b>Alcohol</b> dependents with high impulsive traits showed a significant association with <strong>5 HT2A</strong> 1438 A alleles.
+HTR2A	drug	alcohol	11287798	Inpatient <b>alcohol</b> dependents showed a significant association between <strong>5 HT2A</strong> A alleles and impulsive traits, independent of the presence of APD or BPD.
+HTR2A	drug	alcohol	11287798	This is the first report about an association of <strong>5 HT2A</strong> promoter polymorphism and impulsive behavior in <b>alcohol</b> dependents.
+HTR2A	drug	cocaine	11259563	Serotonin (5 hydroxytryptamine; 5 HT) 5 HT(2A) receptors have been shown to modulate dopamine (DA) function and a more thorough appreciation of this modulatory interaction between <strong>5 HT2A</strong> receptors and DA systems may yield insight into novel approaches to treatment of <b>cocaine</b> dependence.
+HTR2A	addiction	dependence	11259563	Serotonin (5 hydroxytryptamine; 5 HT) 5 HT(2A) receptors have been shown to modulate dopamine (DA) function and a more thorough appreciation of this modulatory interaction between <strong>5 HT2A</strong> receptors and DA systems may yield insight into novel approaches to treatment of cocaine <b>dependence</b>.
+HTR2A	drug	cocaine	11259563	The present study examined the effects of two ligands with varying selectivity for <strong>5 HT2A</strong> receptors on the locomotor stimulant and discriminative stimulus effects of <b>cocaine</b> in male rats.
+HTR2A	drug	cocaine	11259563	Locomotor activity was measured following intraperitoneal injection of vehicle (1 ml/kg), the selective <strong>5 HT2A</strong> receptor antagonist M100907 [R (+) (2,3 dimethoxyphenyl) 1 [2 (4 fluorophenylethyl)] 4 piperidine methanol] (0.02 2.0 mg/kg), or the 5 HT(2) receptor antagonist ketanserin (0.04 4 mg/kg) 45 min before administration of saline (1 ml/kg) or <b>cocaine</b> (10 mg/kg); monitoring of activity in photobeam chambers began at once and proceeded for 1 h. Neither M100907 nor ketanserin significantly altered basal locomotor activity, but both drugs attenuated <b>cocaine</b> induced hyperactivity (p < 0.05).
+HTR2A	drug	cocaine	11259563	These results suggest that <strong>5 HT2A</strong> receptors play an important role in the behavioral effects of <b>cocaine</b> and that <strong>5 HT2A</strong> receptors should be considered a viable target for analysis in the search for pharmacotherapies useful in the treatment of <b>cocaine</b> dependence.
+HTR2A	addiction	dependence	11259563	These results suggest that <strong>5 HT2A</strong> receptors play an important role in the behavioral effects of cocaine and that <strong>5 HT2A</strong> receptors should be considered a viable target for analysis in the search for pharmacotherapies useful in the treatment of cocaine <b>dependence</b>.
+HTR2A	drug	alcohol	11198050	Results showed that the 5 HT releaser d fenfluramine, the selective serotonin reuptake inhibitor fluoxetine, the 5 HT1A receptor agonist 8 hydroxy 2[di n propylamino]tetralin, the partial 5 HT1A receptor agonist buspirone, and the 5 HT1B/5 HT2C receptor agonist 1 (3 trifluoromethylphenyl)piperazine, but not the <strong>5 HT2A</strong>/5 HT2C receptor agonist 1 (2,5 dimethoxy 4 iodophenylaminopropane) 2, selectively reduced responding on a lever leading to presentation of an <b>ethanol</b> paired conditioned stimulus.
+HTR2A	drug	alcohol	11121184	Association of <strong>5HT2A</strong> receptor gene polymorphism and <b>alcohol</b> abuse with behavior problems.
+HTR2A	drug	alcohol	11121184	In conclusion, this study demonstrates that <b>alcoholism</b> is heterogeneous and male <b>alcohol</b> abuse with behavioral problems was associated with T/C 102 polymorphism of the <strong>5HT2A</strong> receptor gene.
+HTR2A	drug	alcohol	10754425	The human serotonin receptor gene (<strong>HTR2</strong>) MspI polymorphism in Japanese schizophrenic and <b>alcoholic</b> patients.
+HTR2A	drug	alcohol	10754425	Epidemiological and genetic studies of <b>alcoholism</b> and schizophrenia have been performed, and in this study, the human serotonin receptor (<strong>HTR2</strong>) polymorphism was examined in 75 <b>alcoholics</b> and 31 schizophrenic patients.
+HTR2A	drug	alcohol	10754425	The results suggest that the human <strong>HTR2</strong> MspI polymorphism might not be associated with a risk factor for developing <b>alcohol</b> dependence or susceptibility to schizophrenia.
+HTR2A	addiction	dependence	10754425	The results suggest that the human <strong>HTR2</strong> MspI polymorphism might not be associated with a risk factor for developing alcohol <b>dependence</b> or susceptibility to schizophrenia.
+HTR2A	drug	alcohol	10565156	[Relationship between <b>alcoholism</b> and <strong>HTR2</strong> MspI polymorphism].
+HTR2A	drug	alcohol	10565156	We investigated the human serotonin receptor, <strong>HTR2</strong> genotype among 73 <b>alcoholics</b>.
+HTR2A	drug	alcohol	10565156	We found that there might not be a significant difference between <b>alcoholics</b> and controls in the frequency of <strong>HTR2</strong> C1/C2 gene (MspI polymorphism).
+HTR2A	drug	alcohol	10565156	This result suggested that the <strong>HTR2</strong> C1/C2 gene might not be associated with the risk factor for developing <b>alcohol</b> dependence.
+HTR2A	addiction	dependence	10565156	This result suggested that the <strong>HTR2</strong> C1/C2 gene might not be associated with the risk factor for developing alcohol <b>dependence</b>.
+HTR2A	drug	alcohol	10528815	The serotonin (5 hydroxytryptamine, 5 HT) uptake sites assessed with both [3H]imipramine and [3H]paroxetine, and the <strong>5 HT2A</strong> receptors were simultaneously measured in platelets from 24 male subjects meeting the American Psychiatric Association's DSM IV criteria for <b>alcohol</b> dependence and admitted for inpatient detoxification.
+HTR2A	addiction	dependence	10528815	The serotonin (5 hydroxytryptamine, 5 HT) uptake sites assessed with both [3H]imipramine and [3H]paroxetine, and the <strong>5 HT2A</strong> receptors were simultaneously measured in platelets from 24 male subjects meeting the American Psychiatric Association's DSM IV criteria for alcohol <b>dependence</b> and admitted for inpatient detoxification.
+HTR2A	drug	alcohol	10528815	Abstinence from <b>alcohol</b> for 2 weeks (day 14) resulted in a decrease in the number of 5 HT uptake sites labelled with [3H]paroxetine compared to normal values, together with a significant decrease in the number of <strong>5 HT2A</strong> binding sites.
+HTR2A	drug	alcohol	10334495	The present study evaluated the effects of the selective serotonin (5 hydroxyhyptamine; 5 HT) reuptake inhibitor, fluoxetine, the 5 HT1B receptor agonist, tetrahydro 4 pyridyl[3,2 b]pyridine, CP 94,253 the preferential <strong>5 HT2A</strong> receptor agonist, 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane, DOI and the mixed 5 HT2C/1B receptor agonist, 1 (3 chlorophenyl)piperazine, mCPP, on oral <b>ethanol</b> (10% v/v) self administration in a two lever, fixed ratio:1, water vs. <b>ethanol</b> choice procedure in the rat.
+HTR2A	drug	alcohol	10334495	These findings suggest that operant <b>ethanol</b> self administration can be suppressed in a specific manner by activation of <strong>5 HT2A</strong> and, possibly, 5 HT2C receptors, and in a nonselective manner by activation of 5 HT1B receptors.
+HTR2A	addiction	reward	10334495	These findings suggest that <b>operant</b> ethanol self administration can be suppressed in a specific manner by activation of <strong>5 HT2A</strong> and, possibly, 5 HT2C receptors, and in a nonselective manner by activation of 5 HT1B receptors.
+HTR2A	drug	cannabinoid	10208323	Rats were then tested for the effects of the <strong>5HT2A</strong>/2C receptor antagonist ritanserin (0.625, 2.5 or 10 mg/kg), the opioid receptor antagonist naloxone (0.625, 2.5 or 10 mg/kg) or the <b>cannabinoid</b> CB1 receptor antagonist SR 141716 (0.3, 1 or 3 mg/kg).
+HTR2A	drug	opioid	10208323	Rats were then tested for the effects of the <strong>5HT2A</strong>/2C receptor antagonist ritanserin (0.625, 2.5 or 10 mg/kg), the <b>opioid</b> receptor antagonist <b>naloxone</b> (0.625, 2.5 or 10 mg/kg) or the cannabinoid CB1 receptor antagonist SR 141716 (0.3, 1 or 3 mg/kg).
+HTR2A	drug	alcohol	10089015	Association of a polymorphism of the <strong>5HT2A</strong> receptor gene promoter region with <b>alcohol</b> dependence.
+HTR2A	addiction	dependence	10089015	Association of a polymorphism of the <strong>5HT2A</strong> receptor gene promoter region with alcohol <b>dependence</b>.
+HTR2A	drug	alcohol	10089015	Examination of the  1438 A/G polymorphism of the serotonin 2A (<strong>5HT2A</strong>) receptor gene in 225 Japanese <b>alcoholics</b> with inactive ALDH2 revealed the presence of significantly more of the G allele than was found in 361 control subjects.
+HTR2A	drug	alcohol	10089015	These data suggest that although the effect is relatively small, genetic variability in the <strong>5HT2A</strong> receptor is involved in the development of <b>alcohol</b> dependence.
+HTR2A	addiction	dependence	10089015	These data suggest that although the effect is relatively small, genetic variability in the <strong>5HT2A</strong> receptor is involved in the development of alcohol <b>dependence</b>.
+HTR2A	drug	alcohol	10088053	Selective genotyping for the role of <strong>5 HT2A</strong>, 5 HT2C, and GABA alpha 6 receptors and the serotonin transporter in the level of response to <b>alcohol</b>: a pilot study.
+HTR2A	drug	alcohol	10088053	There was no evidence that two polymorphisms of the <strong>5 HT2A</strong> receptor gene and one of the 5 HT2C receptor gene were related to LR or <b>alcoholism</b> in this sample.
+HTR2A	drug	cocaine	10068147	Amperozide is a <strong>5 HT2A</strong> receptor antagonist that significantly reduces the acquisition and expression, by rats, of a <b>cocaine</b> conditioned place preference.
+HTR2A	drug	psychedelics	9924841	Most <b>psychedelic</b> drugs are potent agonists at <strong>5 HT2A</strong> and 5 HT2C receptors and their binding potency to these receptors is strongly correlated with their human potency as hallucinogens.
+HTR2A	drug	alcohol	9887443	It appears from the literature that PKC plays an important role in the modulation of the function of various neurotransmitter receptors (e.g., gamma aminobutyrate type A [GABAA], N methyl D aspartate [NMDA], serotonin2A [<strong>5 HT2A</strong>], and 5 HT2C, and muscarinic [m1] receptors) resulting from <b>ethanol</b> exposure.
+HTR2A	drug	psychedelics	9829023	Some patients with OCD may experience remission of OCD symptoms during intoxication with <b>psychedelic</b> drugs that have potent <strong>5 HT2A</strong>/2C agonist activity.
+HTR2A	addiction	intoxication	9829023	Some patients with OCD may experience remission of OCD symptoms during <b>intoxication</b> with psychedelic drugs that have potent <strong>5 HT2A</strong>/2C agonist activity.
+HTR2A	drug	cocaine	9787882	These data indicate that withdrawal from chronic <b>cocaine</b> renders specific subpopulations of postsynaptic 5 HT1A receptors subsensitive and <strong>5 HT2A</strong>/2C receptors supersensitive.
+HTR2A	addiction	withdrawal	9787882	These data indicate that <b>withdrawal</b> from chronic cocaine renders specific subpopulations of postsynaptic 5 HT1A receptors subsensitive and <strong>5 HT2A</strong>/2C receptors supersensitive.
+HTR2A	drug	cocaine	9723786	The effect of chronic <b>cocaine</b> exposure on the central serotonergic system in the rat was investigated using a selective 5 HT1A receptor agonist, [3H]8 hydroxy 2 (di N propylamino) tetralin (8 OH DPAT), and a <strong>5 HT2A</strong> receptor antagonist, [3H]ketanserin, as tritiated ligands in a quantitative autoradiography study.
+HTR2A	drug	alcohol	9631953	Both 5 HT1A and <strong>5 HT2A</strong> receptors have been implicated in modulating <b>ethanol</b> self administration.
+HTR2A	drug	alcohol	9631953	A novel serotonergic compound, FG 5974, with combined 5 HT1A agonist/<strong>5 HT2A</strong> antagonist activities, has shown effects in decreasing <b>ethanol</b> consumption in two bottle choice paradigms.
+HTR2A	drug	alcohol	9631953	In the present study, the effect of this compound on operant responding for <b>ethanol</b> (as well as water and a saccharin solution) was compared to compounds possessing the separate neuropharmacological effects of this drug (the 5 HT1A agonist, 8 OH DPAT, and the <strong>5 HT2A</strong> antagonist, amperozide).
+HTR2A	addiction	reward	9631953	In the present study, the effect of this compound on <b>operant</b> responding for ethanol (as well as water and a saccharin solution) was compared to compounds possessing the separate neuropharmacological effects of this drug (the 5 HT1A agonist, 8 OH DPAT, and the <strong>5 HT2A</strong> antagonist, amperozide).
+HTR2A	drug	alcohol	9631953	These results suggest that combined 5HT1A agonist/<strong>5 HT2A</strong> antagonist activity provides a more selective effect on <b>ethanol</b> reinforcement than either neuropharmacological action alone.
+HTR2A	addiction	reward	9631953	These results suggest that combined 5HT1A agonist/<strong>5 HT2A</strong> antagonist activity provides a more selective effect on ethanol <b>reinforcement</b> than either neuropharmacological action alone.
+HTR2A	drug	psychedelics	9566028	In substitution tests, D lysergic acid diethylamide (<b>LSD</b>, 0.02 and 0.04 mg/kg) and quipazine (0.5, 1.5 and 3 mg/kg), <strong>5 HT2A</strong>/2C agonists, evoked dose related responses to the (+/ )DOI appropriate lever, while the non selective 5 HT agonist 1 (3 chlorophenyl)piperazine (m CPP, 0.1, 0.5 and 1 mg/kg), which has the highest binding affinity for 5 HT2C receptors, failed to show substitution.
+HTR2A	addiction	reward	9566028	In substitution tests, D lysergic acid diethylamide (LSD, 0.02 and 0.04 mg/kg) and quipazine (0.5, 1.5 and 3 mg/kg), <strong>5 HT2A</strong>/2C agonists, evoked dose related responses to the (+/ )DOI appropriate lever, while the non selective 5 HT agonist 1 (3 chlorophenyl)piperazine (m <b>CPP</b>, 0.1, 0.5 and 1 mg/kg), which has the highest binding affinity for 5 HT2C receptors, failed to show substitution.
+HTR2A	drug	cocaine	9476970	Mixed D2/<strong>5 HT2A</strong> antagonism of <b>cocaine</b> induced facilitation of brain stimulation reward.
+HTR2A	addiction	reward	9476970	Mixed D2/<strong>5 HT2A</strong> antagonism of cocaine induced facilitation of brain stimulation <b>reward</b>.
+HTR2A	drug	amphetamine	9476970	Previous behavioral, neurochemical and neurophysiological experiments have shown that selective <strong>5 HT2A</strong> and mixed D2/<strong>5 HT2A</strong> antagonists can attenuate some, but not all, responses to <b>amphetamine</b>.
+HTR2A	drug	cocaine	9476970	The generality of these findings were determined in the present experiment by assessing the effect of mixed D2/<strong>5 HT2A</strong> antagonists on <b>cocaine</b> induced facilitation of ventral tegmental area self stimulation in rats.
+HTR2A	drug	amphetamine	9476970	Although <b>amphetamine</b> and cocaine influence activity in monoaminergic neurons through different mechanisms, our previous research has shown that selective D2 and <strong>5 HT2A</strong> antagonists have similar effects on behavioral responses to these psychostimulants.
+HTR2A	drug	cocaine	9476970	Although amphetamine and <b>cocaine</b> influence activity in monoaminergic neurons through different mechanisms, our previous research has shown that selective D2 and <strong>5 HT2A</strong> antagonists have similar effects on behavioral responses to these psychostimulants.
+HTR2A	drug	cocaine	9476970	Haloperidol and the mixed D2/<strong>5 HT2A</strong> antagonists risperidone and MDL 28, 133A antagonized <b>cocaine</b> induced facilitation of self stimulation, but only at doses that increased baseline self stimulation threshold.
+HTR2A	drug	amphetamine	9476970	<strong>5 HT2A</strong> receptors appear not to be involved in mediation of both brain stimulation reward and <b>amphetamine</b>  and cocaine induced facilitation of brain stimulation reward.
+HTR2A	drug	cocaine	9476970	<strong>5 HT2A</strong> receptors appear not to be involved in mediation of both brain stimulation reward and amphetamine  and <b>cocaine</b> induced facilitation of brain stimulation reward.
+HTR2A	addiction	reward	9476970	<strong>5 HT2A</strong> receptors appear not to be involved in mediation of both brain stimulation <b>reward</b> and amphetamine  and cocaine induced facilitation of brain stimulation <b>reward</b>.
+HTR2A	drug	alcohol	9443541	Action of the <strong>5 HT2A</strong> antagonist amperozide on <b>alcohol</b> induced poikilothermia in rats.
+HTR2A	drug	alcohol	9443541	Amperozide, a novel <strong>5 HT2A</strong> receptor antagonist that releases dopamine from mesolimbic neurons suppresses <b>alcohol</b> drinking in rats.
+HTR2A	drug	alcohol	9443541	Further, the 10.0 mg/kg dose of amperozide given prior to the control saline gavage evoked a hyperthermic response in the rats that persisted for 5 h. These results suggest that the antagonism of <strong>5 HT2A</strong> receptors on central serotonergic synapses involved in thermoregulation acts to counteract the potent thermolytic effects of <b>alcohol</b> at an ambient temperature that is below thermoneutrality.
+HTR2A	drug	benzodiazepine	9401775	The <strong>5 HT2A</strong>/2B/2C receptor antagonists ritanserin, MDL11939 and RP62203 and also methysergide, which failed to modify mouse behaviour when administered alone, caused dose related enhancements (4 to 8 fold) in the potency of <b>diazepam</b> to disinhibit behavioural responding to the aversive situation of the test box.
+HTR2A	addiction	aversion	9401775	The <strong>5 HT2A</strong>/2B/2C receptor antagonists ritanserin, MDL11939 and RP62203 and also methysergide, which failed to modify mouse behaviour when administered alone, caused dose related enhancements (4 to 8 fold) in the potency of diazepam to disinhibit behavioural responding to the <b>aversive</b> situation of the test box.
+HTR2A	drug	alcohol	9394117	Selective inhibition of <b>alcohol</b> intake in diverse <b>alcohol</b> preferring rat strains by the <strong>5 HT2A</strong> antagonists amperozide and FG 5974.
+HTR2A	drug	alcohol	9394117	The present studies sought to elucidate the role of <strong>5 HT2A</strong> receptor antagonists in suppressing <b>alcohol</b> intake by comparing the effects of amperozide and FG 5974 on <b>alcohol</b>, food, and water intake in strains of <b>alcohol</b> preferring rats: P, Alko <b>Alcohol</b> (AA), and Fawn Hooded (FH).
+HTR2A	drug	alcohol	9394117	These complex findings suggest that biochemical properties other than <strong>5 HT2A</strong> receptor antagonism (e.g., 5 HT1A receptor agonism) may be involved in the effects of amperozide and FG 5974 on <b>alcohol</b> intake and other consummatory behaviors.
+HTR2A	drug	cocaine	9315505	Withdrawal from chronic <b>cocaine</b> exposure potentiates the ability of direct <strong>5 HT2A</strong> agonists to induce the head twitch response (HTR) in rodents.
+HTR2A	addiction	withdrawal	9315505	<b>Withdrawal</b> from chronic cocaine exposure potentiates the ability of direct <strong>5 HT2A</strong> agonists to induce the head twitch response (HTR) in rodents.
+HTR2A	drug	alcohol	8822536	The purpose of the present experiments was to compare the efficacy of two drugs on the volitional drinking of the HAD rats: the <strong>5 HT2A</strong> receptor antagonist, amperozide, and a nonselective antagonist of opiate receptors, <b>naltrexone</b>.
+HTR2A	drug	alcohol	8822536	A marked dissociation between the temporal patterns of drinking after <b>naltrexone</b> and amperozide treatment suggests that the opiate receptors mediate the immediate reinforcing effects of <b>alcohol</b>, whereas the more vegetative phenomena underlying addictive properties of <b>alcohol</b> are regulated by <strong>5 HT2A</strong> receptors postsynaptic to serotonergic neurons.
+HTR2A	addiction	addiction	8822536	A marked dissociation between the temporal patterns of drinking after naltrexone and amperozide treatment suggests that the opiate receptors mediate the immediate reinforcing effects of alcohol, whereas the more vegetative phenomena underlying <b>addictive</b> properties of alcohol are regulated by <strong>5 HT2A</strong> receptors postsynaptic to serotonergic neurons.
+HTR2A	addiction	reward	8822536	A marked dissociation between the temporal patterns of drinking after naltrexone and amperozide treatment suggests that the opiate receptors mediate the immediate <b>reinforcing</b> effects of alcohol, whereas the more vegetative phenomena underlying addictive properties of alcohol are regulated by <strong>5 HT2A</strong> receptors postsynaptic to serotonergic neurons.
+HTR2A	drug	alcohol	8837935	Opiate and <strong>5 HT2A</strong> receptors in <b>alcohol</b> drinking: preference in HAD rats is inhibited by combination treatment with <b>naltrexone</b> and amperozide.
+HTR2A	drug	alcohol	8837935	Amperozide, a <strong>5 HT2A</strong> receptor antagonist, and <b>naltrexone</b>, an opiate receptor antagonist, have been shown to suppress volitional drinking of <b>alcohol</b> in experimental animals.
+HTR2A	drug	alcohol	8837935	Nevertheless, the results corroborate our previous findings on the suppression of <b>alcohol</b> drinking by antagonists of opiate and <strong>5 HT2A</strong> receptors.
+HTR2A	drug	alcohol	8788509	Studies related to <strong>5 HT2A</strong>/2C receptors and these receptor linked phosphoinositide (PI) system in the rat brain during chronic <b>ethanol</b> treatment and withdrawal are discussed.
+HTR2A	addiction	withdrawal	8788509	Studies related to <strong>5 HT2A</strong>/2C receptors and these receptor linked phosphoinositide (PI) system in the rat brain during chronic ethanol treatment and <b>withdrawal</b> are discussed.
+HTR2A	drug	alcohol	8788509	Chronic <b>ethanol</b> treatment (60 days) has no effect on <strong>5 HT2A</strong>/2C receptors in the cortex and the hippocampus but significantly decreased 5 HT stimulated PI hydrolysis in the rat cortex.
+HTR2A	drug	alcohol	8788509	<b>Ethanol</b> withdrawal (24 h) after chronic <b>ethanol</b> consumption (15 days) results in the down regulation of <strong>5 HT2A</strong> receptors and in a decrease in 5 HT stimulated PI hydrolysis in the rat cortex.
+HTR2A	addiction	withdrawal	8788509	Ethanol <b>withdrawal</b> (24 h) after chronic ethanol consumption (15 days) results in the down regulation of <strong>5 HT2A</strong> receptors and in a decrease in 5 HT stimulated PI hydrolysis in the rat cortex.
+HTR2A	drug	alcohol	8788509	Taken together, these results, along with other reports in the literature, suggest that <strong>5 HT2A</strong>/2C receptors or their function are altered during chronic <b>ethanol</b> consumption and withdrawal.
+HTR2A	addiction	withdrawal	8788509	Taken together, these results, along with other reports in the literature, suggest that <strong>5 HT2A</strong>/2C receptors or their function are altered during chronic ethanol consumption and <b>withdrawal</b>.
+HTR2A	drug	alcohol	8788509	Further studies are needed to explore the role of <strong>5 HT2A</strong>/2C receptors and the PI signal transduction system in the development of <b>ethanol</b> withdrawal symptoms after chronic <b>ethanol</b> consumption.
+HTR2A	addiction	withdrawal	8788509	Further studies are needed to explore the role of <strong>5 HT2A</strong>/2C receptors and the PI signal transduction system in the development of ethanol <b>withdrawal</b> symptoms after chronic ethanol consumption.
+HTR2A	drug	amphetamine	8587922	Mixed D2/<strong>5 HT2A</strong> antagonism of <b>amphetamine</b> induced facilitation of brain stimulation reward.
+HTR2A	addiction	reward	8587922	Mixed D2/<strong>5 HT2A</strong> antagonism of amphetamine induced facilitation of brain stimulation <b>reward</b>.
+HTR2A	addiction	reward	8587922	These findings led to an interest in using <strong>5 HT2A</strong> antagonists to block the effects of psychostimulants on brain <b>reward</b> mechanisms.
+HTR2A	drug	amphetamine	8587922	The present experiments assessed the ability of mixed D2/<strong>5 HT2A</strong> antagonists to reverse <b>amphetamine</b> induced facilitation of self stimulation.
+HTR2A	drug	amphetamine	8587922	The D2/<strong>5 HT2A</strong> antagonists MDL 28,133A and risperidone attenuated the effects of cocaine and <b>amphetamine</b>, but only at antagonist doses that elevated baseline self stimulation thresholds.
+HTR2A	drug	cocaine	8587922	The D2/<strong>5 HT2A</strong> antagonists MDL 28,133A and risperidone attenuated the effects of <b>cocaine</b> and amphetamine, but only at antagonist doses that elevated baseline self stimulation thresholds.
+HTR2A	drug	amphetamine	8587922	<strong>5 HT2A</strong> antagonism makes a negligible contribution to the anti <b>amphetamine</b> effects.
+HTR2A	addiction	reward	8587903	Drugs with different intrinsic activity at 5 HT1A receptors and antagonists at <strong>5 HT2A</strong>/2C and 5 HT3 receptors were studied for their ability to increase the rates of punished <b>operant</b> responding in rats.
+HTR2A	addiction	reward	8570027	These results indicate that the typical antipsychotics, with the exception of lozapine, fail to produce effective in vivo antagonism of <strong>5 HT2A</strong> receptors at doses compatible with the preservation of <b>operant</b> behavior.
+HTR2A	drug	opioid	7796851	Neither <b>naloxone</b>, an <b>opioid</b> receptor antagonist, phentolamine and benextramine, alpha adrenoceptor antagonists, nor ritanserin, a <strong>5 HT2A</strong> receptor antagonist, inhibited the calcitonin induced anti aversive effects.
+HTR2A	addiction	aversion	7796851	Neither naloxone, an opioid receptor antagonist, phentolamine and benextramine, alpha adrenoceptor antagonists, nor ritanserin, a <strong>5 HT2A</strong> receptor antagonist, inhibited the calcitonin induced anti <b>aversive</b> effects.
+HTR2A	drug	opioid	7796851	These results suggest that beta adrenoceptor, 5 HT1A, 5 HT3, GABAA and GABAB receptors, but not alpha adrenoceptor, <b>opioid</b> nor <strong>5 HT2A</strong> receptors, are involved in the inhibitory effect of calcitonin on intrathecally injected N methyl D aspartate induced aversive behavior in mice.
+HTR2A	addiction	aversion	7796851	These results suggest that beta adrenoceptor, 5 HT1A, 5 HT3, GABAA and GABAB receptors, but not alpha adrenoceptor, opioid nor <strong>5 HT2A</strong> receptors, are involved in the inhibitory effect of calcitonin on intrathecally injected N methyl D aspartate induced <b>aversive</b> behavior in mice.
+HTR2A	drug	cocaine	7956751	These results suggest selective alteration of presynaptic 5 HT1A or postsynaptic <strong>5 HT2A</strong>/2C function in <b>cocaine</b> addicts.
+HTR2A	addiction	reward	7846211	Four non selective 5 HT2C/<strong>5 HT2A</strong> receptor antagonists, mianserin (2 8 mg/kg), 1 naphthyl piperazine (1 NP) (0.5 1 mg/kg), ICI 169,369 (20 mg/kg) and LY 53857 (5 mg/kg), increased punished responding for a food <b>reward</b> in the rat Geller Seifter test 30 min after subcutaneous (SC) administration.
+GRIA1	drug	opioid	32717192	Corydaline and l tetrahydropalmatine attenuate <b>morphine</b> induced conditioned place preference and the changes in dopamine D2 and <strong>GluA1</strong> AMPA receptor expression in rats.
+GRIA1	drug	opioid	32717192	Conditioned place preference (CPP) was used to evaluate the rewarding effects of <b>morphine</b> and Western blot immunoreactive assays were used to evaluate <b>morphine</b> induced changes in dopamine D2 receptor and <strong>GluA1</strong> AMPA receptor and GluA2 AMPA receptor expression in the brain of rats.
+GRIA1	addiction	reward	32717192	Conditioned place preference (<b>CPP</b>) was used to evaluate the rewarding effects of morphine and Western blot immunoreactive assays were used to evaluate morphine induced changes in dopamine D2 receptor and <strong>GluA1</strong> AMPA receptor and GluA2 AMPA receptor expression in the brain of rats.
+GRIA1	drug	opioid	32717192	We then examined the expression of dopamine D2 receptor and <strong>GluA1</strong> AMPA receptor and GluA2 AMPA receptor subunit expression in rats after acquisition of <b>morphine</b> induced CPP.
+GRIA1	addiction	reward	32717192	We then examined the expression of dopamine D2 receptor and <strong>GluA1</strong> AMPA receptor and GluA2 AMPA receptor subunit expression in rats after acquisition of morphine induced <b>CPP</b>.
+GRIA1	drug	opioid	32717192	We found that repeated administration of <b>morphine</b> produced a significant reduction in dopamine D2 receptor expression in the prefrontal cortex, hippocamps, and striatum, while an increase in the striatal <strong>GluA1</strong> AMPA receptor expression.
+GRIA1	drug	opioid	32717192	Pretreatment with corydaline or l THP blocked <b>morphine</b> induced dopamine D2 receptor down regulation and <strong>GluA1</strong> AMPA receptor up regulation in these brain regions.
+GRIA1	drug	alcohol	32599136	Brain area samples were analysed to quantify AMPAR subunits <strong>GluR1</strong>/2 and pCREB/CREB expression following <b>alcohol</b> self administration.
+GRIA1	drug	alcohol	32599136	Our findings demonstrate that developmental <b>alcohol</b> exposure enhances <b>alcohol</b> intake during adolescence, which is associated with a decrease in the pCREB/CREB ratio in the hippocampus, prefrontal cortex and striatum, while the <strong>GluR1</strong>/GluR2 ratio showed a decrease in the hippocampus.
+GRIA1	drug	cocaine	32522229	Here, we assess the role of homeostatic mechanisms in the neurobiology of <b>cocaine</b> addiction by providing a brief overview of the parallels between <b>cocaine</b> induced synaptic potentiation and long term synaptic adaptations, focusing on the regulation of <strong>GluA1</strong>  and GluN1  containing receptors.
+GRIA1	addiction	addiction	32522229	Here, we assess the role of homeostatic mechanisms in the neurobiology of cocaine <b>addiction</b> by providing a brief overview of the parallels between cocaine induced synaptic potentiation and long term synaptic adaptations, focusing on the regulation of <strong>GluA1</strong>  and GluN1  containing receptors.
+GRIA1	addiction	withdrawal	32450347	At hippocampal level, the <b>withdrawal</b> induced changes in the levels of AMPA receptor <strong>GluA1</strong> and GluA2/3 subunits, PSD 95 protein, corticotropin releasing factor (Crf) and Crf receptor 1 (CrfR1) mRNA were biphasic: AMPA receptor subunit and PSD95 protein levels initially remained unchanged and decreased after 60 90 days, whereas Crf/CrfR1 mRNA levels initially increased and then markedly decreased after 60 days.
+GRIA1	drug	cocaine	32329565	We also investigated the subsequent alterations on GluR2, <strong>GluR1</strong>, cAMP response element binding (CREB), and CREB phosphorylation (pCREB) in ventral tegmental area (VTA) and nucleus accumbens (NAc) induced by both MSEW and <b>cocaine</b> SA.
+GRIA1	drug	alcohol	32062779	We aimed to investigate whether <b>ethanol</b> (EtOH) and acetaldehyde (AcH) can affect glutamate and its receptors GluN1 and <strong>GluA1</strong> in the hippocampus of Aldh2 knockout (Aldh2 KO) and C57BL/6N (wild type (WT)) mice.
+GRIA1	addiction	intoxication	32062779	Together, these in vivo and ex vivo data suggest that EtOH and AcH decrease extracellular glutamate in the hippocampus of mice with a concomitant decrease in GluN1 and <strong>GluA1</strong> subunits, but these effects require relatively high concentrations and may, therefore, explain the consequences of EtOH <b>intoxication</b>.
+GRIA1	drug	cocaine	31918976	Moreover, we evaluated the effects of <b>cocaine</b> SA in both sexes during adulthood, and the possible changes in <strong>GluA1</strong>, GluA2, pCREB and CREB expressions.
+GRIA1	drug	cocaine	31905369	These findings outline an essential role for the interaction between D1R, Cav1.2, and <strong>GluA1</strong> signaling in the dDG for extinction of <b>cocaine</b> associated contextual memories.
+GRIA1	drug	opioid	31863796	<strong>GluA1</strong> in Central Amygdala Promotes <b>Opioid</b> Use and Reverses Inhibitory Effect of Pain.
+GRIA1	drug	opioid	31863796	Microinjection of NASPM, a selective inhibitor of homomeric <strong>GluA1</strong> AMPARs, into CeA inhibited <b>morphine</b> intake.
+GRIA1	drug	opioid	31863796	Furthermore, viral overexpression of <strong>GluA1</strong> protein in CeA maintained <b>morphine</b> intake at a higher level than controls and reversed the pain induced reduction in <b>morphine</b> intake.
+GRIA1	drug	opioid	31863796	These findings suggest that CeA <strong>GluA1</strong> promotes <b>opioid</b> use and its upregulation is sufficient to increase <b>opioid</b> consumption, which counteracts the acute inhibitory effect of pain on <b>opioid</b> intake.
+GRIA1	drug	opioid	31863796	These results demonstrate that the CeA <strong>GluA1</strong> is a shared target of <b>opioid</b> and pain in regulation of <b>opioid</b> use, which may aid in future development of therapeutic applications in <b>opioid</b> abuse.
+GRIA1	drug	psychedelics	31706797	After a molecular analysis of <b>ketamine</b> modulation of GluN2B, <strong>GluA1</strong> and mGluR5 receptors levels in nucleus accumbens, hippocampus and amygdala, two behavioural models were used to investigate <b>ketamine</b> effects: i) context induced renewal of sucrose seeking, and ii) sucrose memory reconsolidation.
+GRIA1	addiction	relapse	31706797	After a molecular analysis of ketamine modulation of GluN2B, <strong>GluA1</strong> and mGluR5 receptors levels in nucleus accumbens, hippocampus and amygdala, two behavioural models were used to investigate ketamine effects: i) context induced renewal of sucrose <b>seeking</b>, and ii) sucrose memory reconsolidation.
+GRIA1	drug	psychedelics	31706797	At the molecular level, <b>ketamine</b> i) decreased GluN2B, <strong>GluA1</strong> and mGluR5 receptors in hippocampus, ii) decreased <strong>GluA1</strong> and mGluR5 but increased GluN2B in nucleus accumbens and iii) increased GluN2B and mGluR5 in amygdala.
+GRIA1	drug	alcohol	31705540	Furthermore, alterations in glutamatergic excitability (<strong>GluA1</strong>/GluA2 ratio) and ΔFosB expression were found in the prefrontal cortex and the striatum of <b>alcohol</b> exposed mice after cocaine primed reinstatement.
+GRIA1	drug	cocaine	31705540	Furthermore, alterations in glutamatergic excitability (<strong>GluA1</strong>/GluA2 ratio) and ΔFosB expression were found in the prefrontal cortex and the striatum of alcohol exposed mice after <b>cocaine</b> primed reinstatement.
+GRIA1	addiction	relapse	31705540	Furthermore, alterations in glutamatergic excitability (<strong>GluA1</strong>/GluA2 ratio) and ΔFosB expression were found in the prefrontal cortex and the striatum of alcohol exposed mice after cocaine primed <b>reinstatement</b>.
+GRIA1	drug	opioid	31454827	D <b>methadone</b> administration also increased levels of the synaptic proteins, PSD95, <strong>GluA1</strong>, and Synapsin 1 and enhanced synaptic function in the mPFC.
+GRIA1	drug	opioid	31209728	Results showed that membrane expression of <strong>GluA1</strong> and GluA2 in the vmPFC was decreased following the recent retrieval, while the membrane expression of <strong>GluA1</strong> and GluA2 in the vmPFC was increased following the remote retrieval of <b>morphine</b> associated memory.
+GRIA1	drug	cocaine	31146278	Previous biochemical studies revealed that the CP AMPARs accumulating after <b>cocaine</b> incubation are mainly homomeric <strong>GluA1</strong> receptors and that their accumulation is reflected by increased cell surface <strong>GluA1</strong>.
+GRIA1	drug	amphetamine	31146278	Here, for <b>methamphetamine</b>, we observed no significant change in surface or total <strong>GluA1</strong> (GluA2 and GluA3 were also unchanged).
+GRIA1	drug	amphetamine	31146278	Nonetheless, <strong>GluA1</strong> translation was elevated after incubation of <b>methamphetamine</b> craving, as recently found for cocaine.
+GRIA1	drug	cocaine	31146278	Nonetheless, <strong>GluA1</strong> translation was elevated after incubation of methamphetamine craving, as recently found for <b>cocaine</b>.
+GRIA1	addiction	relapse	31146278	Nonetheless, <strong>GluA1</strong> translation was elevated after incubation of methamphetamine <b>craving</b>, as recently found for cocaine.
+GRIA1	drug	amphetamine	31146278	These findings suggest a common role for increased <strong>GluA1</strong> translation, but not decreased mGlu1 function, in the incubation of <b>methamphetamine</b> and cocaine craving.
+GRIA1	drug	cocaine	31146278	These findings suggest a common role for increased <strong>GluA1</strong> translation, but not decreased mGlu1 function, in the incubation of methamphetamine and <b>cocaine</b> craving.
+GRIA1	addiction	relapse	31146278	These findings suggest a common role for increased <strong>GluA1</strong> translation, but not decreased mGlu1 function, in the incubation of methamphetamine and cocaine <b>craving</b>.
+GRIA1	drug	psychedelics	31128500	However, no changes in the p70S6K, PSD 95, <strong>GluA1</strong>, and synapsin immunocontents were found in the hippocampus of <b>ketamine</b> plus guanosine treated mice.
+GRIA1	drug	opioid	30902386	Furthermore, KO mice showed more elevation in the phosphorylation of AMPA receptor <strong>GluR1</strong> S845 than WT mice, while the total expression of <strong>GluR1</strong> remained unchanged after <b>morphine</b> dependence.
+GRIA1	addiction	dependence	30902386	Furthermore, KO mice showed more elevation in the phosphorylation of AMPA receptor <strong>GluR1</strong> S845 than WT mice, while the total expression of <strong>GluR1</strong> remained unchanged after morphine <b>dependence</b>.
+GRIA1	drug	opioid	30902386	Altogether, these data suggest that IRAS may play an important role in the development of <b>morphine</b> tolerance and physical dependence in vivo through modulating MOR expression, as well as AMPA <strong>GluR1</strong> S845 phosphorylation, which might be one of the mechanisms underlying the development of opiate addiction.
+GRIA1	addiction	addiction	30902386	Altogether, these data suggest that IRAS may play an important role in the development of morphine tolerance and physical dependence in vivo through modulating MOR expression, as well as AMPA <strong>GluR1</strong> S845 phosphorylation, which might be one of the mechanisms underlying the development of opiate <b>addiction</b>.
+GRIA1	addiction	dependence	30902386	Altogether, these data suggest that IRAS may play an important role in the development of morphine tolerance and physical <b>dependence</b> in vivo through modulating MOR expression, as well as AMPA <strong>GluR1</strong> S845 phosphorylation, which might be one of the mechanisms underlying the development of opiate addiction.
+GRIA1	addiction	withdrawal	30773388	At the end of e CIG or CIG exposure and during <b>withdrawal</b>, the mice also had a higher AMPA receptors <strong>GluA1</strong>/GluA2 3 ratio in the NAc.
+GRIA1	addiction	withdrawal	30733663	We then analyzed the expression levels of presynaptic (vGlut1, vGlut2, CB1 receptor, synaptophysin) and postsynaptic (PSD95, GluN1, GluN2A, GluN2B, <strong>GluA1</strong>, GluA2, mGluR1 and mGluR5) proteins after 7 days EtOH incubation or after EtOH <b>withdrawal</b>.
+GRIA1	addiction	withdrawal	30733663	We found that only <strong>GluA1</strong> and mGluR5 expression levels were significantly increased after EtOH <b>withdrawal</b> and, in neuroprotection experiments, we observed that AMPA and mGluR5 antagonists attenuated EtOH <b>withdrawal</b> induced toxicity.
+GRIA1	drug	cocaine	30498893	Here, we show that <b>cocaine</b> SA decreased PrL NA core spine head diameter, nuclear Fos IR and pCREB IR, and <strong>GluA1</strong> IR and GluA2 IR in putative mushroom type spines 2 h after the end of <b>cocaine</b> SA, whereas the opposite occurred following 1 week of abstinence.
+GRIA1	drug	opioid	30376459	Normal extinction and reinstatement of <b>morphine</b> induced conditioned place preference in the <strong>GluA1</strong> KO mouse line.
+GRIA1	addiction	relapse	30376459	Normal extinction and <b>reinstatement</b> of morphine induced conditioned place preference in the <strong>GluA1</strong> KO mouse line.
+GRIA1	drug	opioid	30376459	Extinction and reinstatement of <b>morphine</b> induced conditioned place preference were studied in glutamate α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid receptor <strong>GluA1</strong> subunit deficient mice (global <strong>GluA1</strong> KO mice).
+GRIA1	addiction	relapse	30376459	Extinction and <b>reinstatement</b> of morphine induced conditioned place preference were studied in glutamate α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid receptor <strong>GluA1</strong> subunit deficient mice (global <strong>GluA1</strong> KO mice).
+GRIA1	drug	opioid	30376459	In line with previous findings, both acquisition and expression of conditioned place preference to <b>morphine</b> (20 mg/kg, subcutaneously) were fully functional in <strong>GluA1</strong> KO mice compared with wild type littermate controls (<strong>GluA1</strong> WT), thus enabling the study of extinction.
+GRIA1	addiction	relapse	30376459	The results suggest that the <strong>GluA1</strong> subunit may be dispensable or prone to compensation at the neural circuitries delineating extinction and <b>reinstatement</b>.
+GRIA1	drug	cannabinoid	30273593	In parallel, CBD increased expression of type 1 <b>cannabinoid</b> receptor, MAPK CREB phosphorylation, BDNF expression, and neural cell proliferation in the hippocampus, and reduced the <strong>GluA1</strong>/2 AMPA subunit receptor ratio in the striatum.
+GRIA1	drug	cocaine	30144237	In <b>cocaine</b> naïve animals, SERT removal led to reduced baseline Hb mRNA levels of critical determinants of glutamate transmission, such as SLC1A2, the main glutamate transporter and N methyl D aspartate (Grin1, Grin2A and Grin2B) as well as α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (<strong>Gria1</strong> and Gria2) receptor subunits, with no changes in the scaffolding protein Dlg4.
+GRIA1	drug	opioid	29754475	The results of this study show that the NAc specific knockdown of RGS4 significantly increased the behaviors associated with <b>morphine</b> and did so by phosphorylation of the <strong>GluR1</strong> (Ser831) and NR2A (Tyr1325) glutamate receptors in the NAc.
+GRIA1	drug	opioid	29754475	Furthermore, the knock down of RGS4 enhanced the phosphorylation of the <strong>GluR1</strong> and NR2A glutamate receptors in the primary NAc/striatal neurons during spontaneous <b>morphine</b> withdrawal.
+GRIA1	addiction	withdrawal	29754475	Furthermore, the knock down of RGS4 enhanced the phosphorylation of the <strong>GluR1</strong> and NR2A glutamate receptors in the primary NAc/striatal neurons during spontaneous morphine <b>withdrawal</b>.
+GRIA1	drug	cocaine	29622268	We compared basal overall translation and its regulation by metabotropic glutamate receptor 1 (mGlu1), mGlu5, and N methyl D aspartate receptors (NMDARs) in drug naïve, saline control, and <b>cocaine</b> rats, and we compared <strong>GluA1</strong> and GluA2 translation by immunoprecipitating puromycin labeled proteins.
+GRIA1	drug	cocaine	29622268	<b>Cocaine</b>/late withdrawal rats exhibited greater translation of <strong>GluA1</strong> (but not GluA2), which was not further affected by NMDAR blockade.
+GRIA1	addiction	withdrawal	29622268	Cocaine/late <b>withdrawal</b> rats exhibited greater translation of <strong>GluA1</strong> (but not GluA2), which was not further affected by NMDAR blockade.
+GRIA1	drug	amphetamine	29338492	Genotyping of <strong>GRIA1</strong> rs1428920, GRIA2 rs3813296, GRIA3 rs3761554, rs502434 and rs989638 was performed in 102 male Thai controls and 100 <b>METH</b> dependent subjects (53 with <b>METH</b> dependent psychosis).
+GRIA1	drug	amphetamine	29338492	We observed no evidence of association with <b>METH</b> dependence and <b>METH</b> dependent psychosis in the <strong>GRIA1</strong> and GRIA2 polymorphisms, nor with single polymorphisms rs3761554 and rs989638 in GRIA3.
+GRIA1	addiction	dependence	29338492	We observed no evidence of association with METH <b>dependence</b> and METH dependent psychosis in the <strong>GRIA1</strong> and GRIA2 polymorphisms, nor with single polymorphisms rs3761554 and rs989638 in GRIA3.
+GRIA1	drug	cocaine	29317777	Previous work indicated that activation of D1 like dopamine receptors (D1DRs) in the nucleus accumbens shell promoted <b>cocaine</b> seeking through a process involving the activation of PKA and <strong>GluA1</strong> containing AMPA receptors (AMPARs).
+GRIA1	addiction	relapse	29317777	Previous work indicated that activation of D1 like dopamine receptors (D1DRs) in the nucleus accumbens shell promoted cocaine <b>seeking</b> through a process involving the activation of PKA and <strong>GluA1</strong> containing AMPA receptors (AMPARs).
+GRIA1	drug	cocaine	29317777	This viral mediated attenuation of <b>cocaine</b> reinstatement was accompanied by decreased phosphorylation of <strong>GluA1</strong> containing AMPARs and attenuated AMPAR eEPSCs.
+GRIA1	addiction	relapse	29317777	This viral mediated attenuation of cocaine <b>reinstatement</b> was accompanied by decreased phosphorylation of <strong>GluA1</strong> containing AMPARs and attenuated AMPAR eEPSCs.
+GRIA1	drug	amphetamine	29247759	<b>METH</b> treated mice also showed i) decreased levels of total H3ac and H4ac, and increased levels of 5 mC, ii) decreased H3ac enrichment at promoters of Drd2, Hcrtr1/2, Hrh1 and Grin1, and increased H4ac enrichment at Drd1, Hrh1 and Grin1, iii) increased mRNA of Drd1a, Grin1 and <strong>Gria1</strong>.
+GRIA1	addiction	relapse	29197981	A significant increase in AMPA receptor subunit <strong>GluA1</strong> surface expression was also observed during estrus, potentially influencing <b>reinstatement</b>.
+GRIA1	addiction	relapse	29197981	The effects of estrus on <strong>GluA1</strong> expression and <b>reinstatement</b> observed here indicate that females may need additional interventions during some phases of the menstrual cycle.
+GRIA1	drug	cocaine	29196318	Inactivation of NMDA Receptors in the Ventral Tegmental Area during <b>Cocaine</b> Self Administration Prevents <strong>GluA1</strong> Upregulation but with Paradoxical Increases in <b>Cocaine</b> Seeking Behavior.
+GRIA1	addiction	relapse	29196318	Inactivation of NMDA Receptors in the Ventral Tegmental Area during Cocaine Self Administration Prevents <strong>GluA1</strong> Upregulation but with Paradoxical Increases in Cocaine <b>Seeking</b> Behavior.
+GRIA1	drug	cocaine	29196318	<b>Cocaine</b> self administration increases expression of <strong>GluA1</strong> subunits in ventral tegmental area (VTA) dopamine neurons, which subsequently enhance the motivation for <b>cocaine</b>.
+GRIA1	drug	cocaine	29196318	This increase in <strong>GluA1</strong> may be dependent on concomitant NMDA receptor (NMDAR) activation during self administration, similar to <b>cocaine</b> induced long term potentiation in the VTA.
+GRIA1	drug	cocaine	29196318	In this study, we used viral mediated expression of a dominant negative GluN1 subunit (HSV dnGluN1) in VTA neurons to study the effect of transient NMDAR inactivation on the <strong>GluA1</strong> increases induced by chronic <b>cocaine</b> self administration in male rats.
+GRIA1	drug	cocaine	29196318	We found that dnGluN1 expression in the VTA limited to the 3 weeks of <b>cocaine</b> self administration prevents the subsequent increase in tissue <strong>GluA1</strong> levels when compared with control infusions of HSV LacZ.
+GRIA1	drug	cocaine	29196318	Despite blocking tissue <strong>GluA1</strong> increases in <b>cocaine</b> self administering animals, the HSV dnGluN1 treatment resulted in increased membrane levels of <strong>GluA1</strong> and GluN2B, along with markedly higher locomotor responses to intra VTA infusions of AMPA, suggesting a paradoxical increase in VTA AMPA receptor responsiveness.
+GRIA1	drug	cocaine	29196318	Together, these data suggest that NMDARs mediate <b>cocaine</b> induced increases in VTA <strong>GluA1</strong> expression, but such transient NMDAR inactivation also leads to compensatory scaling of synaptic AMPA receptors that enhance the motivational for <b>cocaine</b>.SIGNIFICANCE STATEMENT Dopamine neurons in the ventral tegmental area (VTA) are critical substrates of drug rewards.
+GRIA1	drug	psychedelics	29158578	However, <b>ketamine</b> blunted the increase in the phosphorylation of the <strong>GluA1</strong> subunit of AMPARs at a calcium/calmodulin dependent protein kinase II/protein kinase C site induced by an LTP induction protocol.
+GRIA1	drug	psychedelics	29158578	Moreover, <b>ketamine</b> caused a persistent increased phosphorylation of <strong>GluA1</strong> at a protein kinase A site.
+GRIA1	drug	cocaine	29089442	Finally, conditional knock out of Cav1.2 in dopamine D1 receptor (D1R) expressing cells resulted in attenuation of <b>cocaine</b> CPP extinction and lack of extinction dependent changes in hippocampal PSD CaMKII expression and S831 <strong>GluA1</strong> phosphorylation.
+GRIA1	addiction	reward	29089442	Finally, conditional knock out of Cav1.2 in dopamine D1 receptor (D1R) expressing cells resulted in attenuation of cocaine <b>CPP</b> extinction and lack of extinction dependent changes in hippocampal PSD CaMKII expression and S831 <strong>GluA1</strong> phosphorylation.
+GRIA1	drug	cocaine	29089442	In summary, we demonstrate an essential role for the hippocampal Cav1.2/CaMKII/S831 <strong>GluA1</strong> pathway in <b>cocaine</b> CPP extinction, with data supporting contribution of hippocampal D1R expressing cells in this process.
+GRIA1	addiction	reward	29089442	In summary, we demonstrate an essential role for the hippocampal Cav1.2/CaMKII/S831 <strong>GluA1</strong> pathway in cocaine <b>CPP</b> extinction, with data supporting contribution of hippocampal D1R expressing cells in this process.
+GRIA1	drug	psychedelics	28948570	Since GluN2B, via inhibition of ERK, regulates the membrane expression of <strong>GluA1</strong>, we measured ERK2 phosphorylation in the crude synaptosomal fraction of these brain regions, which was significantly reduced suggesting that <b>ketamine</b> induced phosphorylation of αCaMKII promotes GluN2B (S1303) phosphorylation that, in turn, inhibits ERK 2 signaling, an effect that results in reduced membrane expression and phosphorylation of <strong>GluA1</strong>.
+GRIA1	drug	psychedelics	28948570	Taken together, our findings point to αCaMKII autophosphorylation as a critical signature of <b>ketamine</b> self administration providing an intracellular mechanism to explain the different effects caused by αCaMKII autophosphorylation on the post synaptic GluN2B  and <strong>GluA1</strong> mediated functions.
+GRIA1	drug	alcohol	28865912	Western blotting revealed a higher level of phosphorylated AMPAR <strong>GluA1</strong> subunit at a CaMKII locus (<strong>GluA1</strong> Ser831) in the LHb of <b>ethanol</b> withdrawn rats than that of age matched naïve counterparts.
+GRIA1	addiction	relapse	28495973	Intra NAc xCT knockdown prevented ceftriaxone from attenuating <b>reinstatement</b> and from upregulating GLT 1 and resulted in increased surface expression of AMPA receptor subunits <strong>GluA1</strong> and GluA2.
+GRIA1	addiction	relapse	28495973	Intra NAc GLT 1 knockdown also prevented ceftriaxone from attenuating <b>reinstatement</b> and from upregulating xCT expression, without affecting <strong>GluA1</strong> and GluA2 expression.
+GRIA1	drug	cocaine	28495973	In the absence of <b>cocaine</b> or ceftriaxone treatment, xCT knockdown in the NAc increased the expression of both <strong>GluA1</strong> and GluA2 without affecting GLT 1 expression while GLT 1 knockdown had no effect.
+GRIA1	drug	psychedelics	28479397	However, males and females administered 5 mg/kg <b>ketamine</b> displayed increased protein expression of AMPA receptors (<strong>GluA1</strong>).
+GRIA1	drug	alcohol	28270566	Profiling of the OFC synaptome identified <b>alcohol</b> sensitive proteins that control glutamate release (e.g., SV2A, synaptogyrin 1) and postsynaptic signaling (e.g., <strong>GluA1</strong>, PRRT2) with no changes in synaptic GABAergic proteins.
+GRIA1	drug	amphetamine	28223211	Using protein cross linking, biochemical, subcellular fractionation, and slice electrophysiological approaches in the NAcc, we found that, unlike cocaine, previous exposure to <b>amphetamine</b> did not increase cell surface levels of either <strong>GluA1</strong> or GluA2 AMPA receptor subunits, redistribution of these subunits to the synaptic or perisynaptic cellular membrane domains, protein protein associations required to support the accumulation and retention of AMPA receptors in the PSD, or the peak amplitude of AMPA receptor mediated mEPSCs recorded in NAcc slices.
+GRIA1	drug	cocaine	28223211	Using protein cross linking, biochemical, subcellular fractionation, and slice electrophysiological approaches in the NAcc, we found that, unlike <b>cocaine</b>, previous exposure to amphetamine did not increase cell surface levels of either <strong>GluA1</strong> or GluA2 AMPA receptor subunits, redistribution of these subunits to the synaptic or perisynaptic cellular membrane domains, protein protein associations required to support the accumulation and retention of AMPA receptors in the PSD, or the peak amplitude of AMPA receptor mediated mEPSCs recorded in NAcc slices.
+GRIA1	drug	amphetamine	28223211	On the other hand, exposure to <b>amphetamine</b> significantly slowed mEPSC decay times and increased levels in the PSD of PKA and CaMKII as well as phosphorylation by these kinases of the <strong>GluA1</strong> S845 and S831 residues selectively in this cellular compartment.
+GRIA1	drug	cocaine	28223211	Rather than increase the number of surface and synaptic AMPA receptors as with <b>cocaine</b>, this mechanism could increase NAcc medium spiny neuron reactivity to glutamate afferents by increasing the phosphorylation state of critical regulatory sites in the AMPA receptor <strong>GluA1</strong> subunit in the PSD.
+GRIA1	drug	cocaine	28194001	In the present study, we directly manipulated Cav1.3 channels in Cav1.2 dihydropyridine insensitive mutant mice and found that ventral tegmental area (VTA) Cav1.3 channels mediate <b>cocaine</b> related and depressive like behavior through a common nucleus accumbens (NAc) shell calcium permeable α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid receptor (CP AMPAR) mechanism that requires <strong>GluA1</strong> phosphorylation at S831.
+GRIA1	drug	cocaine	28194001	In contrast to the <b>cocaine</b>  and depression related phenotypes, <strong>GluA1</strong>/A2 AMPARs in the NAc core mediated social deficits, independent of S831 <strong>GluA1</strong> phosphorylation.
+GRIA1	drug	alcohol	28045462	Here we use <b>ethanol</b> (EtOH) to show that interoceptive cues are encoded through the hippocampus by mechanisms that involve increased phosphorylation of <strong>GluR1</strong> on serine 845, and biophysical alterations in neuronal membranes that facilitate stabilization of surface located calcium permeable n 2 amino 3 (5 methyl 3 oxo 1,2 oxazol 4 yl) propanoic acid (AMPA) receptor (AMPAR) into membrane microdomains.
+GRIA1	drug	psychedelics	27934938	Western blot results showed levels of <strong>GluA1</strong>, p S845 and p S831 proteins demonstrated significant decline with <b>ketamine</b> 60 mg/kg until six months administration paradigm.
+GRIA1	drug	psychedelics	27934938	Our results indicate that reduced expression levels and decreased phosphorylation levels of hippocampal post synaptic membrane <strong>GluA1</strong>  containing AMPA receptors maybe involved in cognition impairment after long term <b>ketamine</b> administration.
+GRIA1	addiction	relapse	27863698	Targeted investigation of <strong>GRIA1</strong>, a glutamatergic gene implicated in drug <b>seeking</b> behavior, verified the increased enrichment of lysine 27 acetylated histone H3 at discrete loci, accompanied by enhanced chromatin accessibility at hyperacetylated regions in the gene body.
+GRIA1	drug	alcohol	27796078	Withdrawal from Chronic Nicotine Exposure Produces Region Specific Tolerance to <b>Alcohol</b> Stimulated <strong>GluA1</strong> Phosphorylation.
+GRIA1	drug	nicotine	27796078	Withdrawal from Chronic <b>Nicotine</b> Exposure Produces Region Specific Tolerance to Alcohol Stimulated <strong>GluA1</strong> Phosphorylation.
+GRIA1	addiction	withdrawal	27796078	<b>Withdrawal</b> from Chronic Nicotine Exposure Produces Region Specific Tolerance to Alcohol Stimulated <strong>GluA1</strong> Phosphorylation.
+GRIA1	drug	alcohol	27796078	We examined regional neuroadaptations in nicotine experienced versus nonexperienced animals, focusing on changes in phosphorylation of the AMPA glutamate channel subunit <strong>GluA1</strong> in reward related brain regions as excitatory neuroadaptations are heavily implicated in both <b>alcohol</b> and nicotine addiction.
+GRIA1	drug	nicotine	27796078	We examined regional neuroadaptations in <b>nicotine</b> experienced versus nonexperienced animals, focusing on changes in phosphorylation of the AMPA glutamate channel subunit <strong>GluA1</strong> in reward related brain regions as excitatory neuroadaptations are heavily implicated in both alcohol and <b>nicotine</b> addiction.
+GRIA1	addiction	addiction	27796078	We examined regional neuroadaptations in nicotine experienced versus nonexperienced animals, focusing on changes in phosphorylation of the AMPA glutamate channel subunit <strong>GluA1</strong> in reward related brain regions as excitatory neuroadaptations are heavily implicated in both alcohol and nicotine <b>addiction</b>.
+GRIA1	addiction	reward	27796078	We examined regional neuroadaptations in nicotine experienced versus nonexperienced animals, focusing on changes in phosphorylation of the AMPA glutamate channel subunit <strong>GluA1</strong> in <b>reward</b> related brain regions as excitatory neuroadaptations are heavily implicated in both alcohol and nicotine addiction.
+GRIA1	drug	alcohol	27796078	During withdrawal, nicotine exposure and <b>alcohol</b> challenge (1 g/kg) interactively produced neuroadaptations in <strong>GluA1</strong> phosphorylation in a brain region dependent manner.
+GRIA1	drug	nicotine	27796078	During withdrawal, <b>nicotine</b> exposure and alcohol challenge (1 g/kg) interactively produced neuroadaptations in <strong>GluA1</strong> phosphorylation in a brain region dependent manner.
+GRIA1	addiction	withdrawal	27796078	During <b>withdrawal</b>, nicotine exposure and alcohol challenge (1 g/kg) interactively produced neuroadaptations in <strong>GluA1</strong> phosphorylation in a brain region dependent manner.
+GRIA1	drug	alcohol	27796078	<b>Alcohol</b> robustly increased protein kinase A mediated phosphorylation of <strong>GluA1</strong> at serine 845 in multiple regions.
+GRIA1	drug	alcohol	27796078	This interactive effect suggests a molecular tolerance to <b>alcohol</b> stimulated phosphorylation of <strong>GluA1</strong> in the context of nicotine dependence.
+GRIA1	drug	nicotine	27796078	This interactive effect suggests a molecular tolerance to alcohol stimulated phosphorylation of <strong>GluA1</strong> in the context of <b>nicotine</b> dependence.
+GRIA1	addiction	dependence	27796078	This interactive effect suggests a molecular tolerance to alcohol stimulated phosphorylation of <strong>GluA1</strong> in the context of nicotine <b>dependence</b>.
+GRIA1	drug	cocaine	27376947	When ad libitum fed rats undergo <b>cocaine</b> place preference conditioning (CPP) but are switched to food restriction for testing, CPP becomes resistant to extinction and correlates with phosphorylation of α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA) receptor <strong>GluA1</strong> at Ser845 in nucleus accumbens (NAc) core.
+GRIA1	addiction	reward	27376947	When ad libitum fed rats undergo cocaine place preference conditioning (<b>CPP</b>) but are switched to food restriction for testing, <b>CPP</b> becomes resistant to extinction and correlates with phosphorylation of α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA) receptor <strong>GluA1</strong> at Ser845 in nucleus accumbens (NAc) core.
+GRIA1	drug	opioid	27376947	Food restriction increased persistence of <b>morphine</b> CPP and preference scores correlated with pSer845 <strong>GluA1</strong> in NAc core and shell.
+GRIA1	addiction	reward	27376947	Food restriction increased persistence of morphine <b>CPP</b> and preference scores correlated with pSer845 <strong>GluA1</strong> in NAc core and shell.
+GRIA1	drug	opioid	27376947	Food restriction increased persistence of <b>naloxone</b> CPA and elevated pSer845 <strong>GluA1</strong> in NAc core and shell, and aversion scores were negatively correlated with pERK1 and pERK2 in NAc core.
+GRIA1	addiction	aversion	27376947	Food restriction increased persistence of naloxone CPA and elevated pSer845 <strong>GluA1</strong> in NAc core and shell, and <b>aversion</b> scores were negatively correlated with pERK1 and pERK2 in NAc core.
+GRIA1	drug	opioid	27376947	A mechanistic scheme, attributing these effects to upregulation of pSer845 <strong>GluA1</strong>, but subject to override by CPA specific, pERK2 mediated extinction learning, is explored to accommodate opposite effects of food restriction on LiCl and <b>naloxone</b> CPA.
+GRIA1	drug	opioid	27225765	Using a protein cross linking approach, we found that the surface/intracellular ratio of NAc <strong>GluA1</strong>, but not GluA2, increased with <b>morphine</b> treatment, suggesting postsynaptic insertion of GluA2 lacking AMPARs.
+GRIA1	drug	opioid	27225765	<b>Naloxone</b> decreased the surface/intracellular ratio and synaptosomal membrane levels of NAc <strong>GluA1</strong> in <b>morphine</b> dependent rats, suggesting a compensatory removal of AMPARs from synaptic zones.
+GRIA1	drug	opioid	27225765	Together, these findings indicate that chronic <b>morphine</b> increases synaptic availability of <strong>GluA1</strong> containing AMPARs in the NAc, which is necessary for triggering negative affective states in response to <b>naloxone</b>.
+GRIA1	drug	opioid	27225765	We use a rat model of <b>morphine</b> dependence to show that <strong>GluA1</strong> subunits of AMPA glutamate receptors in the nucleus accumbens (NAc), a brain region critical for modulating affective states, are necessary for aversive effects of <b>morphine</b> withdrawal.
+GRIA1	addiction	aversion	27225765	We use a rat model of morphine dependence to show that <strong>GluA1</strong> subunits of AMPA glutamate receptors in the nucleus accumbens (NAc), a brain region critical for modulating affective states, are necessary for <b>aversive</b> effects of morphine withdrawal.
+GRIA1	addiction	dependence	27225765	We use a rat model of morphine <b>dependence</b> to show that <strong>GluA1</strong> subunits of AMPA glutamate receptors in the nucleus accumbens (NAc), a brain region critical for modulating affective states, are necessary for aversive effects of morphine withdrawal.
+GRIA1	addiction	withdrawal	27225765	We use a rat model of morphine dependence to show that <strong>GluA1</strong> subunits of AMPA glutamate receptors in the nucleus accumbens (NAc), a brain region critical for modulating affective states, are necessary for aversive effects of morphine <b>withdrawal</b>.
+GRIA1	drug	opioid	27225765	Using biochemical methods in NAc tissue, we show that <b>morphine</b> dependence increases cell surface expression of <strong>GluA1</strong>, suggesting that neurons in this area are primed for increased AMPA receptor activation upon withdrawal.
+GRIA1	addiction	dependence	27225765	Using biochemical methods in NAc tissue, we show that morphine <b>dependence</b> increases cell surface expression of <strong>GluA1</strong>, suggesting that neurons in this area are primed for increased AMPA receptor activation upon withdrawal.
+GRIA1	addiction	withdrawal	27225765	Using biochemical methods in NAc tissue, we show that morphine dependence increases cell surface expression of <strong>GluA1</strong>, suggesting that neurons in this area are primed for increased AMPA receptor activation upon <b>withdrawal</b>.
+GRIA1	drug	cocaine	27181066	Rapamycin reduces motivated responding for <b>cocaine</b> and alters <strong>GluA1</strong> expression in the ventral but not dorsal striatum.
+GRIA1	addiction	withdrawal	27038592	Incubation with chronic EtOH for 7 days and its removal from the medium induced a significant decrease in <strong>GluA1</strong> and GluA2 expression levels; a significant reduction in the expression of synaptophysin and GluN2A was observed only after EtOH <b>withdrawal</b>.
+GRIA1	drug	cocaine	26881139	Surface biotinylation analysis of protein expression in the dlSTR revealed that, in <b>cocaine</b> animals, intra dlSTR MTEP administration decreased mGlu5 surface expression and prevented changes in Arc and <strong>GluA1</strong>/GluA2 observed in their vehicle counterparts.
+GRIA1	drug	cocaine	26811312	Results showed that acute <b>cocaine</b> administration induced an overall down regulation of glutamate related gene expression and, specifically, a low phosphorylation level of <strong>GluA1</strong>.
+GRIA1	drug	alcohol	26791202	mTORC1 is critically involved in RNA to protein translation, and we found that the first <b>alcohol</b> session rapidly activated mTORC1 in NAc shell D1+ neurons and increased synaptic expression of the AMPAR subunit <strong>GluA1</strong> and the scaffolding protein Homer.
+GRIA1	drug	alcohol	26742808	Here, we show that low dose <b>alcohol</b> (0.6 g/kg/30 minutes) self administration increases phosphorylation (activation) of AMPAR subtype <strong>GluA1</strong> S831 (pGluA1 S831) in the central amygdala (CeA), basolateral amygdala and nucleus accumbens core (AcbC) of selectively bred <b>alcohol</b> preferring P rats as compared with behavior matched (non drug) sucrose controls.
+GRIA1	drug	alcohol	26742808	Because <strong>GluA1</strong> S831 is a Ca2+/calmodulin dependent protein kinase II (CaMKII) substrate, we sought to determine if AMPAR regulation of enhanced <b>alcohol</b> self administration is dependent on CaMKII activity.
+GRIA1	addiction	relapse	26706696	Here we investigated the effects of ceftriaxone (100 and 200 mg/kg) on context primed <b>relapse</b> following abstinence without extinction training and examined the effects of ceftriaxone on <strong>GluA1</strong>, GluA2 and GLT 1 expression.
+GRIA1	drug	cocaine	26706696	<strong>GluA1</strong> was reduced in the NAc by both doses of ceftriaxone while GluA2 expression was unchanged, indicating that ceftriaxone altered AMPA subunit composition following <b>cocaine</b>.
+GRIA1	addiction	relapse	26639425	Moreover, the expression of <strong>GluR1</strong> in the IL and NAc remarkably increased after treatment with PEPA during the <b>reinstatement</b>.
+GRIA1	drug	alcohol	26609150	Here we evaluated the contribution of mesolimbic NMDARs and AMPARs in mediating <b>alcohol</b> seeking responses induced by environmental stimuli and relapse behavior using four inducible mutant mouse lines lacking the glutamate receptor genes Grin1 or <strong>Gria1</strong> in either DA transporter (DAT) or D1R expressing neurons.
+GRIA1	addiction	relapse	26609150	Here we evaluated the contribution of mesolimbic NMDARs and AMPARs in mediating alcohol <b>seeking</b> responses induced by environmental stimuli and <b>relapse</b> behavior using four inducible mutant mouse lines lacking the glutamate receptor genes Grin1 or <strong>Gria1</strong> in either DA transporter (DAT) or D1R expressing neurons.
+GRIA1	drug	alcohol	26609150	We then show that GluN1 and <strong>GluA1</strong> receptor subunits within these neuronal subpopulations mediate the <b>alcohol</b> deprivation effect, while having no impact on context  plus cue induced reinstatement of <b>alcohol</b> seeking behavior.
+GRIA1	addiction	relapse	26609150	We then show that GluN1 and <strong>GluA1</strong> receptor subunits within these neuronal subpopulations mediate the alcohol deprivation effect, while having no impact on context  plus cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior.
+GRIA1	drug	opioid	26596557	The membrane level of <strong>GluR1</strong> in the CA1 was increased after <b>morphine</b> CPP expression, and this effect was prevented by pre injection of a PKG inhibitor into the CA1.
+GRIA1	addiction	reward	26596557	The membrane level of <strong>GluR1</strong> in the CA1 was increased after morphine <b>CPP</b> expression, and this effect was prevented by pre injection of a PKG inhibitor into the CA1.
+GRIA1	drug	cocaine	26384129	Environmental enrichment facilitates <b>cocaine</b> cue extinction, deters reacquisition of <b>cocaine</b> self administration and alters AMPAR <strong>GluA1</strong> expression and phosphorylation.
+GRIA1	drug	cocaine	26384129	One week later, reacquisition of <b>cocaine</b> self administration was evaluated for 15 sessions, and then <strong>GluA1</strong> expression, a cellular substrate for learning and memory, was measured in selected brain regions.
+GRIA1	drug	cocaine	26384129	<b>Cocaine</b> self administration alone decreased total <strong>GluA1</strong> and/or pSer845GluA1 expression in basolateral amygdala and nucleus accumbens.
+GRIA1	drug	alcohol	26247621	CaMKIIα <strong>GluA1</strong> Activity Underlies Vulnerability to Adolescent Binge <b>Alcohol</b> Drinking.
+GRIA1	addiction	intoxication	26247621	CaMKIIα <strong>GluA1</strong> Activity Underlies Vulnerability to Adolescent <b>Binge</b> Alcohol Drinking.
+GRIA1	addiction	addiction	26247621	In this study, we sought to determine whether binge drinking alters expression or phosphorylation of 2 molecular mechanisms of neuroplasticity, calcium/calmodulin dependent kinase II alpha (CaMKIIα) and the <strong>GluA1</strong> subunit of AMPA receptors (AMPARs) in <b>addiction</b> associated brain regions.
+GRIA1	addiction	intoxication	26247621	In this study, we sought to determine whether <b>binge</b> drinking alters expression or phosphorylation of 2 molecular mechanisms of neuroplasticity, calcium/calmodulin dependent kinase II alpha (CaMKIIα) and the <strong>GluA1</strong> subunit of AMPA receptors (AMPARs) in addiction associated brain regions.
+GRIA1	drug	cocaine	26149358	A Critical Role for the <strong>GluA1</strong> Accessory Protein, SAP97, in <b>Cocaine</b> Seeking.
+GRIA1	addiction	relapse	26149358	A Critical Role for the <strong>GluA1</strong> Accessory Protein, SAP97, in Cocaine <b>Seeking</b>.
+GRIA1	drug	cocaine	26149358	A growing body of evidence indicates that the transport of <strong>GluA1</strong> subunit containing calcium permeable AMPA receptors (CP AMPARs) to synapses in subregions of the nucleus accumbens promotes <b>cocaine</b> seeking.
+GRIA1	addiction	relapse	26149358	A growing body of evidence indicates that the transport of <strong>GluA1</strong> subunit containing calcium permeable AMPA receptors (CP AMPARs) to synapses in subregions of the nucleus accumbens promotes cocaine <b>seeking</b>.
+GRIA1	drug	cocaine	26149358	Moreover, viral mediated overexpression of 'pore dead' <strong>GluA1</strong> subunits (via herpes simplex virus (HSV) <strong>GluA1</strong> Q582E) in the lateral core or medial shell attenuated the reinstatement of <b>cocaine</b> seeking.
+GRIA1	addiction	relapse	26149358	Moreover, viral mediated overexpression of 'pore dead' <strong>GluA1</strong> subunits (via herpes simplex virus (HSV) <strong>GluA1</strong> Q582E) in the lateral core or medial shell attenuated the <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRIA1	drug	cocaine	26149358	The overexpression of wild type <strong>GluA1</strong> subunits (via HSV <strong>GluA1</strong> WT) in the medial shell, but not the lateral core, enhanced the reinstatement of <b>cocaine</b> seeking.
+GRIA1	addiction	relapse	26149358	The overexpression of wild type <strong>GluA1</strong> subunits (via HSV <strong>GluA1</strong> WT) in the medial shell, but not the lateral core, enhanced the <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRIA1	drug	cocaine	26149358	These results indicate that activation of <strong>GluA1</strong> containing AMPARs in subregions of the nucleus accumbens reinstates <b>cocaine</b> seeking.
+GRIA1	addiction	relapse	26149358	These results indicate that activation of <strong>GluA1</strong> containing AMPARs in subregions of the nucleus accumbens reinstates cocaine <b>seeking</b>.
+GRIA1	drug	cocaine	26149358	In contrast, a virus that overexpressed a dominant negative form of a 4.1N C terminal domain (HSV 4.1N CTD), which prevents endogenous 4.1N binding to <strong>GluA1</strong> subunits, had no effect on <b>cocaine</b> seeking.
+GRIA1	addiction	relapse	26149358	In contrast, a virus that overexpressed a dominant negative form of a 4.1N C terminal domain (HSV 4.1N CTD), which prevents endogenous 4.1N binding to <strong>GluA1</strong> subunits, had no effect on cocaine <b>seeking</b>.
+GRIA1	drug	cocaine	26149358	These results indicate that the <strong>GluA1</strong> subunit accessory protein SAP97 may represent a novel target for pharmacotherapeutic intervention in the treatment of <b>cocaine</b> craving.
+GRIA1	addiction	relapse	26149358	These results indicate that the <strong>GluA1</strong> subunit accessory protein SAP97 may represent a novel target for pharmacotherapeutic intervention in the treatment of cocaine <b>craving</b>.
+GRIA1	drug	alcohol	26101849	Importantly, the association between several genetic variants within the mGluR eEF2 AMPAR pathway and <b>alcohol</b> use behavior (i.e., consumption and <b>alcohol</b> related problems) replicated in the Grady Trauma Project (GTP), an independent sample of adults living in Atlanta, Georgia (n = 1034; 95% African American), including individual variants in GRM1, GRM5, EEF2, MTOR, <strong>GRIA1</strong>, GRIA4 and HOMER2 (P < 0.05).
+GRIA1	drug	amphetamine	25871318	We also provide evidence of altered mRNA expression of (1) voltage gated calcium channels P/Q type Cacna1a (Cav 2.1), N type Cacna1b (Cav 2.2), T type Cav 3.1 Cacna1g, Cav 3.2 Cacna1h, Cav 3.3 Cacna1i and the auxiliary subunit Cacna2d1 (α2δ1); (2) hyperpolarization activated cyclic nucleotide gated channels Hcn1 and Hcn2; and (3) glutamate receptors subunits AMPA type <strong>Gria1</strong>, NMDA type Grin1 and metabotropic Grm1 in the mouse mPFC after repeated <b>METH</b> treatment.
+GRIA1	drug	opioid	25746394	NAc Shell Arc/Arg3.1 Protein Mediates Reconsolidation of <b>Morphine</b> CPP by Increased <strong>GluR1</strong> Cell Surface Expression: Activation of ERK Coupled CREB is Required.
+GRIA1	addiction	reward	25746394	NAc Shell Arc/Arg3.1 Protein Mediates Reconsolidation of Morphine <b>CPP</b> by Increased <strong>GluR1</strong> Cell Surface Expression: Activation of ERK Coupled CREB is Required.
+GRIA1	drug	opioid	25746394	The retrieval of <b>morphine</b> CPP in rats specifically increased the Arc/Arg3.1 protein level in the NAc shell, accompanied simultaneously by increases in the phosphorylation of extracellular signal regulated kinase1/2 (pERK1/2), the phosphorylation of Cyclic Adenosine monophosphate (cAMP) response element binding (pCREB), and the up regulation of the membrane α amino 3 hydroxy 5 methyl 4 isoxazole propionate (AMPA) receptors <strong>GluR1</strong> subunit level.
+GRIA1	addiction	reward	25746394	The retrieval of morphine <b>CPP</b> in rats specifically increased the Arc/Arg3.1 protein level in the NAc shell, accompanied simultaneously by increases in the phosphorylation of extracellular signal regulated kinase1/2 (pERK1/2), the phosphorylation of Cyclic Adenosine monophosphate (cAMP) response element binding (pCREB), and the up regulation of the membrane α amino 3 hydroxy 5 methyl 4 isoxazole propionate (AMPA) receptors <strong>GluR1</strong> subunit level.
+GRIA1	drug	opioid	25746394	Intra NAc shell infusion U0126, an inhibitor of the Mitogen activated protein kinase kinase (MEK), prevented the retrieval induced up regulation of pERK1/2, pCREB, Arc/Arg3.1, and membrane <strong>GluR1</strong> immediately after retrieval of <b>morphine</b> CPP.
+GRIA1	addiction	reward	25746394	Intra NAc shell infusion U0126, an inhibitor of the Mitogen activated protein kinase kinase (MEK), prevented the retrieval induced up regulation of pERK1/2, pCREB, Arc/Arg3.1, and membrane <strong>GluR1</strong> immediately after retrieval of morphine <b>CPP</b>.
+GRIA1	drug	opioid	25746394	Furthermore, the specific knockdown of Arc/Arg3.1 in the NAc shell decreased the membrane <strong>GluR1</strong> level, and impaired both the reconsolidation and the reinstatement of <b>morphine</b> CPP.
+GRIA1	addiction	relapse	25746394	Furthermore, the specific knockdown of Arc/Arg3.1 in the NAc shell decreased the membrane <strong>GluR1</strong> level, and impaired both the reconsolidation and the <b>reinstatement</b> of morphine CPP.
+GRIA1	addiction	reward	25746394	Furthermore, the specific knockdown of Arc/Arg3.1 in the NAc shell decreased the membrane <strong>GluR1</strong> level, and impaired both the reconsolidation and the reinstatement of morphine <b>CPP</b>.
+GRIA1	drug	opioid	25746394	Arc/Arg3.1 in the NAc shell mediates the reconsolidation of <b>morphine</b> associated context memory via up regulating the level of membrane of <strong>GluR1</strong>, for which the local activation of the ERK CREB signal pathway, as an upstream mechanism of Arc/Arg3.1, is required.
+GRIA1	drug	opioid	25716866	Persistent pain maintains <b>morphine</b> seeking behavior after <b>morphine</b> withdrawal through reduced MeCP2 repression of <strong>GluA1</strong> in rat central amygdala.
+GRIA1	addiction	relapse	25716866	Persistent pain maintains morphine <b>seeking</b> behavior after morphine withdrawal through reduced MeCP2 repression of <strong>GluA1</strong> in rat central amygdala.
+GRIA1	addiction	withdrawal	25716866	Persistent pain maintains morphine seeking behavior after morphine <b>withdrawal</b> through reduced MeCP2 repression of <strong>GluA1</strong> in rat central amygdala.
+GRIA1	drug	opioid	25716866	In the central nucleus of amygdala (CeA), a limbic structure critically involved in the affective dimension of pain, proteins of <strong>GluA1</strong> subunits of glutamate AMPA receptors were upregulated during <b>morphine</b> withdrawal, and viral knockdown of CeA <strong>GluA1</strong> eliminated the <b>morphine</b> seeking behavior in withdrawn rats of the pain group.
+GRIA1	addiction	relapse	25716866	In the central nucleus of amygdala (CeA), a limbic structure critically involved in the affective dimension of pain, proteins of <strong>GluA1</strong> subunits of glutamate AMPA receptors were upregulated during morphine withdrawal, and viral knockdown of CeA <strong>GluA1</strong> eliminated the morphine <b>seeking</b> behavior in withdrawn rats of the pain group.
+GRIA1	addiction	withdrawal	25716866	In the central nucleus of amygdala (CeA), a limbic structure critically involved in the affective dimension of pain, proteins of <strong>GluA1</strong> subunits of glutamate AMPA receptors were upregulated during morphine <b>withdrawal</b>, and viral knockdown of CeA <strong>GluA1</strong> eliminated the morphine seeking behavior in withdrawn rats of the pain group.
+GRIA1	drug	opioid	25716866	Furthermore, viral overexpression of CeA MeCP2 repressed the <strong>GluA1</strong> level and eliminated the maintenance of <b>morphine</b> seeking behavior after <b>morphine</b> withdrawal.
+GRIA1	addiction	relapse	25716866	Furthermore, viral overexpression of CeA MeCP2 repressed the <strong>GluA1</strong> level and eliminated the maintenance of morphine <b>seeking</b> behavior after morphine withdrawal.
+GRIA1	addiction	withdrawal	25716866	Furthermore, viral overexpression of CeA MeCP2 repressed the <strong>GluA1</strong> level and eliminated the maintenance of morphine seeking behavior after morphine <b>withdrawal</b>.
+GRIA1	drug	opioid	25716866	These results suggest direct MeCp2 repression of <strong>GluA1</strong> function as a likely mechanism for <b>morphine</b> seeking behavior maintained by long lasting affective pain after <b>morphine</b> withdrawal.
+GRIA1	addiction	relapse	25716866	These results suggest direct MeCp2 repression of <strong>GluA1</strong> function as a likely mechanism for morphine <b>seeking</b> behavior maintained by long lasting affective pain after morphine withdrawal.
+GRIA1	addiction	withdrawal	25716866	These results suggest direct MeCp2 repression of <strong>GluA1</strong> function as a likely mechanism for morphine seeking behavior maintained by long lasting affective pain after morphine <b>withdrawal</b>.
+GRIA1	drug	amphetamine	25691515	Among various <b>METH</b> CPP stages, we found that the amount of phospho <strong>GluR1</strong>/Ser845 increased in the VTA at behavioral extinction, but not the acquisition or withdrawal stage.
+GRIA1	addiction	reward	25691515	Among various METH <b>CPP</b> stages, we found that the amount of phospho <strong>GluR1</strong>/Ser845 increased in the VTA at behavioral extinction, but not the acquisition or withdrawal stage.
+GRIA1	addiction	withdrawal	25691515	Among various METH CPP stages, we found that the amount of phospho <strong>GluR1</strong>/Ser845 increased in the VTA at behavioral extinction, but not the acquisition or <b>withdrawal</b> stage.
+GRIA1	drug	amphetamine	25691515	Via surface biotinylation, we found that levels of membrane <strong>GluR1</strong> were significantly increased during <b>METH</b> CPP extinction, while no change was observed at the acquisition stage.
+GRIA1	addiction	reward	25691515	Via surface biotinylation, we found that levels of membrane <strong>GluR1</strong> were significantly increased during METH <b>CPP</b> extinction, while no change was observed at the acquisition stage.
+GRIA1	drug	amphetamine	25691515	Ibotenic acid lesioning of the mPFC did not affect <b>METH</b> CPP acquisition, however, it abolished the extinction stage and reversed the enhanced phospho <strong>GluR1</strong>/Ser845 levels as well as increases in VTA dendritic spines during <b>METH</b> CPP extinction.
+GRIA1	addiction	reward	25691515	Ibotenic acid lesioning of the mPFC did not affect METH <b>CPP</b> acquisition, however, it abolished the extinction stage and reversed the enhanced phospho <strong>GluR1</strong>/Ser845 levels as well as increases in VTA dendritic spines during METH <b>CPP</b> extinction.
+GRIA1	drug	cocaine	25643299	<strong>GluA1</strong> trafficking in LHb was instrumental for these <b>cocaine</b> evoked modifications and drug driven aversive behaviors.
+GRIA1	addiction	aversion	25643299	<strong>GluA1</strong> trafficking in LHb was instrumental for these cocaine evoked modifications and drug driven <b>aversive</b> behaviors.
+GRIA1	drug	cocaine	25589145	When ad libitum fed (AL) rats undergo <b>cocaine</b> place preference conditioning (CPP) but are switched to food restriction (FR) for testing, CPP is enhanced and preference scores correlate with phosphorylation of α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA) receptor <strong>GluA1</strong> at Ser845 in nucleus accumbens (NAc) core.
+GRIA1	addiction	reward	25589145	When ad libitum fed (AL) rats undergo cocaine place preference conditioning (<b>CPP</b>) but are switched to food restriction (FR) for testing, <b>CPP</b> is enhanced and preference scores correlate with phosphorylation of α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA) receptor <strong>GluA1</strong> at Ser845 in nucleus accumbens (NAc) core.
+GRIA1	addiction	reward	25589145	In experiment 1, <b>CPP</b> expression in AL rats was associated with elevated pSer845 <strong>GluA1</strong>, <strong>GluA1</strong>, and GluA2 in NAc.
+GRIA1	addiction	reward	25589145	In experiment 2, the correlation between pSer845 <strong>GluA1</strong> and <b>CPP</b> was localized to NAc core.
+GRIA1	addiction	reward	25589145	In experiment 3, pSer845 <strong>GluA1</strong> following a <b>CPP</b> test was higher in NAc synaptic membranes of FR relative to AL rats.
+GRIA1	drug	cocaine	25589145	Results support a scheme in which pSer845 <strong>GluA1</strong> in NAc core underlies expression of <b>cocaine</b> CPP and does so by stabilizing or trafficking Ca(2+) permeable AMPARs to the synaptic membrane.
+GRIA1	addiction	reward	25589145	Results support a scheme in which pSer845 <strong>GluA1</strong> in NAc core underlies expression of cocaine <b>CPP</b> and does so by stabilizing or trafficking Ca(2+) permeable AMPARs to the synaptic membrane.
+GRIA1	addiction	reward	25589145	The more robust <b>CPP</b> of FR rats may result from upregulation of stimulus induced pSer845 <strong>GluA1</strong>.
+GRIA1	drug	alcohol	25579851	Accordingly, <b>alcohol</b> drinking increased α amino 3 hydroxy 5 methyl 4 isooxazole receptor (AMPAR) in central amygdala (CeA) and phosphorylation of AMPAR <strong>GluA1</strong> subunit at a CaMKII locus (<strong>GluA1</strong> Ser831) in CeA and lateral amygdala.
+GRIA1	drug	alcohol	25579851	Further, CaMKIIα Thr286 and <strong>GluA1</strong> Ser831 phosphorylation was increased in CeA and lateral amygdala of mice that lever pressed for <b>alcohol</b> versus the nondrug reinforcer sucrose.
+GRIA1	drug	cocaine	25539508	However, in <b>cocaine</b> sensitized mice primed with <b>cocaine</b>, this inhibition was reversed and a strong increase was detected in the mGluR5, NR2 subunits, and both <strong>GluR1</strong> and GluR3.
+GRIA1	drug	cocaine	25539504	Immunoprecipitation of oxytocin receptor and <strong>GluA1</strong> subunit receptors further demonstrated a physical interaction between these 2 receptors, although the interaction was not influenced by chronic <b>cocaine</b> or oxytocin treatment.
+GRIA1	addiction	relapse	25539504	Oxytocin also attenuated sucrose <b>seeking</b> in a <strong>GluA1</strong>  or extracellular signal regulated kinase independent manner.
+GRIA1	drug	opioid	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for <strong>GluR1</strong> AMPA receptor (AMPAR), phosphorylated ERK2 (pERK2), CREB (pCREB), TrKB (pTrkB) were performed in brain areas relevant for sensitization from KO and WT and/or <b>naloxone</b>  and vehicle pre treated animals.
+GRIA1	addiction	sensitization	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for <strong>GluR1</strong> AMPA receptor (AMPAR), phosphorylated ERK2 (pERK2), CREB (pCREB), TrKB (pTrkB) were performed in brain areas relevant for <b>sensitization</b> from KO and WT and/or naloxone  and vehicle pre treated animals.
+GRIA1	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, <strong>Gria1</strong>, and Pdyn.
+GRIA1	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, <strong>Gria1</strong>, and Pdyn.
+GRIA1	drug	alcohol	25278838	Our data revealed that out of the 16 ionotropic glutamate receptor subunits, mRNAs encoding two AMPA [2 amino 3 (3 hydroxy 5 methyl isoxazol 4 yl)propanoic acid] receptor subunits <strong>GluA1</strong> and GluA4; one kainate receptor subunit GluK2; one NMDA (N methyl D aspartate) receptor subunit GluN2D and one delta receptor subunit GluD2 were significantly decreased in the CeA of <b>alcoholics</b>.
+GRIA1	drug	cocaine	25268136	After repeated <b>cocaine</b> exposure, the density of <strong>GluR1</strong> was increased, but there was no change in total AMPA receptors and GluR2 levels in wild type mice.
+GRIA1	drug	cocaine	25268136	In contrast, following repeated <b>cocaine</b> exposure, increased densities of total AMPA receptors, <strong>GluR1</strong> and GluR2 were observed in knock out mice.
+GRIA1	addiction	aversion	25241061	It has also been observed after viral mediated manipulation of <strong>GluR1</strong>, phospholipase Cγ (PLCγ) and cAMP response element binding protein (CREB) expression, with impact on reward and <b>aversion</b> related responses, on anxiety and depression related behaviors and on pain sensitivity.
+GRIA1	addiction	reward	25241061	It has also been observed after viral mediated manipulation of <strong>GluR1</strong>, phospholipase Cγ (PLCγ) and cAMP response element binding protein (CREB) expression, with impact on <b>reward</b> and aversion related responses, on anxiety and depression related behaviors and on pain sensitivity.
+GRIA1	drug	amphetamine	24535653	FR increased <strong>GluA1</strong> in the PSD, and D <b>amphetamine</b> increased p Ser845 <strong>GluA1</strong>, <strong>GluA1</strong>, GluA2, but not GluA3, with a greater effect in FR than AL rats.
+GRIA1	drug	amphetamine	24535653	Results suggest that FR leads to increased synaptic incorporation of <strong>GluA1</strong> homomers to potentiate rewarding effects of appetitive stimuli and, as a maladaptive byproduct, D <b>amphetamine</b>.
+GRIA1	drug	amphetamine	24535653	The D <b>amphetamine</b> induced increase in synaptic p Ser845 <strong>GluA1</strong>, <strong>GluA1</strong>, and GluA2 may contribute to the rewarding effect of D <b>amphetamine</b>, but may also be a mechanism of synaptic strengthening and behavior modification.
+GRIA1	drug	psychedelics	24520403	Also similarly to <b>ketamine</b>, Radix Polygalae appeared to acutely decrease phosphorylation of <strong>GluR1</strong> serine 845 in the hippocampus while leaving the phosphorylation of hippocampal mTOR serine 2448 unchanged.
+GRIA1	addiction	relapse	24469593	mTORC1 inhibition in the nucleus accumbens 'protects' against the expression of drug <b>seeking</b> and '<b>relapse</b>' and is associated with reductions in <strong>GluA1</strong> AMPAR and CAMKIIα levels.
+GRIA1	addiction	relapse	24469593	Rapamycin reduced drug <b>seeking</b> in signaled non drug available periods, PR responding, and cue induced <b>reinstatement</b>, with these effects linked to reduced mTORC1 activity, total CAMKIIα, and <strong>GluA1</strong> AMPAR levels in the NACsh.
+GRIA1	addiction	sensitization	24354924	NAc TrkB BDNF signaling also appeared to be involved in the regulation of <strong>GluA1</strong> in the VTA, as well as in the NAc ΔFosB accumulation that could trigger cross <b>sensitization</b> after social defeat stress.
+GRIA1	drug	amphetamine	24239129	Chronic <b>METH</b> decreased transcript and protein expression of <strong>GluA1</strong> and GluA2 alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid receptor (AMPAR) and GluN1 N methyl D aspartate receptor subunits.
+GRIA1	drug	amphetamine	24239129	Chromatin immunoprecipitation polymerase chain reaction revealed that <b>METH</b> decreased enrichment of acetylated histone H4 on <strong>GluA1</strong>, GluA2, and GluN1 promoters.
+GRIA1	drug	amphetamine	24239129	<b>Methamphetamine</b> exposure also increased repressor element 1 silencing transcription factor (REST) corepressor 1, methylated CpG binding protein 2, and histone deacetylase 2 enrichment, but not of sirtuin 1 or sirtuin 2, onto <strong>GluA1</strong> and GluA2 gene sequences.
+GRIA1	drug	amphetamine	24239129	Surprisingly, methylated DNA immunoprecipitation and hydroxymethylated DNA immunoprecipitation polymerase chain reaction revealed <b>METH</b> induced decreased enrichment of 5 methylcytosine and 5 hydroxymethylcytosine at <strong>GluA1</strong> and GluA2 promoter sequences.
+GRIA1	drug	amphetamine	24231469	Rapid and sustained <strong>GluA1</strong> S845 phosphorylation in synaptic and extrasynaptic locations in the rat forebrain following <b>amphetamine</b> administration.
+GRIA1	drug	amphetamine	24231469	We found that acute injection of <b>amphetamine</b> induced a rapid and relatively sustained increase in <strong>GluA1</strong> S845 phosphorylation at both synaptic and extrasynaptic sites in the striatum.
+GRIA1	drug	amphetamine	24231469	In contrast to S845, <b>amphetamine</b> did not induce a significant change in <strong>GluA1</strong> S831 phosphorylation in synaptic and extrasynaptic pools in the striatum and mPFC.
+GRIA1	drug	amphetamine	24201449	Adaptations in glutamate receptor 1 (<strong>GluR1</strong>) phosphorylation in limbic brain regions have been shown to occur during withdrawal from addictive drugs, such as cocaine, <b>methamphetamine</b>, and heroin.
+GRIA1	drug	cocaine	24201449	Adaptations in glutamate receptor 1 (<strong>GluR1</strong>) phosphorylation in limbic brain regions have been shown to occur during withdrawal from addictive drugs, such as <b>cocaine</b>, methamphetamine, and heroin.
+GRIA1	drug	opioid	24201449	Adaptations in glutamate receptor 1 (<strong>GluR1</strong>) phosphorylation in limbic brain regions have been shown to occur during withdrawal from addictive drugs, such as cocaine, methamphetamine, and <b>heroin</b>.
+GRIA1	addiction	addiction	24201449	Adaptations in glutamate receptor 1 (<strong>GluR1</strong>) phosphorylation in limbic brain regions have been shown to occur during withdrawal from <b>addictive</b> drugs, such as cocaine, methamphetamine, and heroin.
+GRIA1	addiction	withdrawal	24201449	Adaptations in glutamate receptor 1 (<strong>GluR1</strong>) phosphorylation in limbic brain regions have been shown to occur during <b>withdrawal</b> from addictive drugs, such as cocaine, methamphetamine, and heroin.
+GRIA1	drug	opioid	24201449	In our present study, alterations in <strong>GluR1</strong> expression and <strong>GluR1</strong> phosphorylation at serine 845 (Ser845) and serine 831 (Ser831) in multiple limbic brain regions of rats were measured following context induced drug craving after 1 or 10 days of withdrawal from intravenous <b>morphine</b> self administration.
+GRIA1	addiction	relapse	24201449	In our present study, alterations in <strong>GluR1</strong> expression and <strong>GluR1</strong> phosphorylation at serine 845 (Ser845) and serine 831 (Ser831) in multiple limbic brain regions of rats were measured following context induced drug <b>craving</b> after 1 or 10 days of withdrawal from intravenous morphine self administration.
+GRIA1	addiction	withdrawal	24201449	In our present study, alterations in <strong>GluR1</strong> expression and <strong>GluR1</strong> phosphorylation at serine 845 (Ser845) and serine 831 (Ser831) in multiple limbic brain regions of rats were measured following context induced drug craving after 1 or 10 days of <b>withdrawal</b> from intravenous morphine self administration.
+GRIA1	addiction	withdrawal	24201449	Phosphorylation of <strong>GluR1</strong> at Ser845, but not Ser831, increases in the nucleus accumbens and central amygdala from 1 to 10 days of <b>withdrawal</b>, and there were no changes in <strong>GluR1</strong> phosphorylation at Ser845 or Ser831 in the hippocampal CA1 subregion from 1 to 10 days of <b>withdrawal</b>.
+GRIA1	addiction	relapse	24201449	Significant positive correlations between numbers of drug <b>seeking</b> responses and <strong>GluR1</strong> phosphorylation at Ser845 in the nucleus accumbens were found in individual animals.
+GRIA1	drug	opioid	24201449	These results suggest that time dependent and region specific changes in phosphorylation of <strong>GluR1</strong> at Ser845, but not Ser831, are involved in the drug seeking behavior elicited by re exposure to the <b>morphine</b> associated context.
+GRIA1	addiction	relapse	24201449	These results suggest that time dependent and region specific changes in phosphorylation of <strong>GluR1</strong> at Ser845, but not Ser831, are involved in the drug <b>seeking</b> behavior elicited by re exposure to the morphine associated context.
+GRIA1	drug	cocaine	24109187	On the other hand, <b>cocaine</b> self administration and withdrawal increases the surface expression of subunit glutamate receptor 1 (<strong>GluA1</strong>) of alpha amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA) receptors at the level of the NAc.
+GRIA1	addiction	withdrawal	24109187	On the other hand, cocaine self administration and <b>withdrawal</b> increases the surface expression of subunit glutamate receptor 1 (<strong>GluA1</strong>) of alpha amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA) receptors at the level of the NAc.
+GRIA1	drug	cocaine	24079996	Different locomotor sensitization responses to repeated <b>cocaine</b> injections are associated with differential phosphorylation of <strong>GluA1</strong> in the dorsomedial striatum of adult rats.
+GRIA1	addiction	sensitization	24079996	Different locomotor <b>sensitization</b> responses to repeated cocaine injections are associated with differential phosphorylation of <strong>GluA1</strong> in the dorsomedial striatum of adult rats.
+GRIA1	drug	cocaine	24035918	<b>Cocaine</b>/vehicle rats showed elevated stargazin and <strong>GluA1</strong> surface expression on WD7 compared to saline/vehicle rats; the <strong>GluA1</strong> increase was more robust in core, while stargazin increased more robustly in shell.
+GRIA1	drug	cocaine	23786641	Biochemical studies in the ventral striatum show that phosphorylation of DARPP 32(Thr) ( 34) and <strong>GluR1</strong>(Ser) ( 845) is diminished in MC4R null mice after chronic <b>cocaine</b> administration but rescued in MC4R/D1R mice.
+GRIA1	drug	amphetamine	23747591	Regulation of phosphorylation of synaptic and extrasynaptic <strong>GluA1</strong> AMPA receptors in the rat forebrain by <b>amphetamine</b>.
+GRIA1	drug	amphetamine	23747591	We found that acute <b>AMPH</b> administration elevated <strong>GluA1</strong> S845 phosphorylation in the defined synaptic membrane from the striatum in a dose dependent manner.
+GRIA1	drug	amphetamine	23747591	<b>AMPH</b> also induced a comparable increase in S845 phosphorylation in the extrasynaptic fraction of striatal <strong>GluA1</strong>.
+GRIA1	drug	amphetamine	23747591	In contrast, S831 phosphorylation was not altered in synaptic and extrasynaptic <strong>GluA1</strong> in striatal neurons and synaptic <strong>GluA1</strong> in mPFC neurons in response to <b>AMPH</b>, although a moderate increase in S831 phosphorylation was seen in extrasynaptic <strong>GluA1</strong> in the mPFC after an <b>AMPH</b> injection at a high dose.
+GRIA1	drug	amphetamine	23747591	Total synaptic and extrasynaptic <strong>GluA1</strong> expression remained stable in the two regions after <b>AMPH</b> administration.
+GRIA1	drug	amphetamine	23747591	S845 is a primary site where phosphorylation of <strong>GluA1</strong> is upregulated by <b>AMPH</b> in striatal and mPFC neurons at both synaptic and extrasynaptic compartments.
+GRIA1	drug	amphetamine	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (<strong>GluA1</strong>, GluA2) and mGlu5, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated morphine (8 mg/kg) or <b>methamphetamine</b> (1 mg/kg) (treatments producing behavioral sensitization).
+GRIA1	drug	opioid	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (<strong>GluA1</strong>, GluA2) and mGlu5, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated <b>morphine</b> (8 mg/kg) or methamphetamine (1 mg/kg) (treatments producing behavioral sensitization).
+GRIA1	addiction	sensitization	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (<strong>GluA1</strong>, GluA2) and mGlu5, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated morphine (8 mg/kg) or methamphetamine (1 mg/kg) (treatments producing behavioral <b>sensitization</b>).
+GRIA1	drug	opioid	23711322	Acute <b>morphine</b> decreased <strong>GluA1</strong> and GluA2 surface expression in mPFC and <strong>GluA1</strong> in NAc.
+GRIA1	addiction	reward	23603364	MeAM <b>CPP</b> increased surface expression of <strong>GluR1</strong> and GluR2 subunits of AMPA receptor in the BLA.
+GRIA1	drug	cocaine	23598433	Finally, the ability of an A1AR agonist to modulate D1DR induced <b>cocaine</b> seeking and synaptic <strong>GluA1</strong> receptor subunit phosphorylation was explored.
+GRIA1	addiction	relapse	23598433	Finally, the ability of an A1AR agonist to modulate D1DR induced cocaine <b>seeking</b> and synaptic <strong>GluA1</strong> receptor subunit phosphorylation was explored.
+GRIA1	drug	cocaine	23598433	Administration of the A1AR agonist alone decreased synaptic <strong>GluA1</strong> expression, whereas coadministration of the A1AR agonist inhibited both <b>cocaine</b>  and D1DR induced <b>cocaine</b> seeking and reversed D1DR induced AMPA pGluA1(S845).
+GRIA1	addiction	relapse	23598433	Administration of the A1AR agonist alone decreased synaptic <strong>GluA1</strong> expression, whereas coadministration of the A1AR agonist inhibited both cocaine  and D1DR induced cocaine <b>seeking</b> and reversed D1DR induced AMPA pGluA1(S845).
+GRIA1	drug	opioid	23564315	Acute <b>morphine</b> associated alterations in the subcellular location of the AMPA <strong>GluR1</strong> receptor subunit in dendrites of neurons in the mouse central nucleus of the amygdala: comparisons and contrasts with other glutamate receptor subunits.
+GRIA1	drug	opioid	23564315	Although the ultrastructural location of <strong>GluR1</strong> is an important functional feature of this protein, the basal distribution of <strong>GluR1</strong>, as well as its sensitivity to acute <b>morphine</b>, has never been characterized in the mouse central nucleus of the amygdala (CeA).
+GRIA1	drug	opioid	23564315	Electron microscopic immunocytochemistry employing visually distinct gold and peroxidase markers was used to explore the distribution of <strong>GluR1</strong> and its relationship with the mu <b>opioid</b> receptor (µOR) in the mouse CeA under basal conditions and after <b>morphine</b>.
+GRIA1	drug	opioid	23564315	Compared to saline treated animals, mice given <b>morphine</b> showed significant differences in the subcellular location of <strong>GluR1</strong> in dendrites without co expression of µOR.
+GRIA1	drug	cocaine	23499958	Treatment with resveratrol (50μM for 30min) enhanced <b>cocaine</b> induced increases in the phosphorylation of DARPP 32 at Thr34 and <strong>GluA1</strong> at Ser845, postsynaptic substrates for dopamine/D1 receptor/PKA signaling, and a <b>cocaine</b> induced decrease in the phosphorylation of tyrosine hydroxylase at Ser40, a presynaptic substrate for dopamine/D2 receptor signaling.
+GRIA1	drug	cocaine	23461423	We measured the phosphorylation of cAMP response element binding protein (Ser133) and <strong>GluA1</strong> (Ser845) in the dorsomedial (dm) PFC and the presynaptic marker, synapsin I (Ser9, Ser62/67, Ser603), in the NAc after 7 days of abstinence from <b>cocaine</b> SA with or without cue induced <b>cocaine</b> seeking.
+GRIA1	addiction	relapse	23461423	We measured the phosphorylation of cAMP response element binding protein (Ser133) and <strong>GluA1</strong> (Ser845) in the dorsomedial (dm) PFC and the presynaptic marker, synapsin I (Ser9, Ser62/67, Ser603), in the NAc after 7 days of abstinence from cocaine SA with or without cue induced cocaine <b>seeking</b>.
+GRIA1	drug	opioid	23403695	Analysis of the expression and phosphorylation levels of AMPAR subunits (<strong>GluA1</strong>/2/3/4) in homogenates and in postsynaptic density fractions from spinal cord dorsal horns showed an increase in GluA4 expression and phosphorylation in the postsynaptic density after <b>morphine</b>.
+GRIA1	drug	opioid	23396226	Altered phosphorylation of <strong>GluA1</strong> in the striatum is associated with locomotor sensitization induced by exposure to increasing doses of <b>morphine</b>.
+GRIA1	addiction	sensitization	23396226	Altered phosphorylation of <strong>GluA1</strong> in the striatum is associated with locomotor <b>sensitization</b> induced by exposure to increasing doses of morphine.
+GRIA1	drug	opioid	23396226	The results showed a significant increase in pSer845 <strong>GluA1</strong>/<strong>GluA1</strong> ratio in ventral striatum but not dorsal striatum after pretreatment with increasing doses of <b>morphine</b> but not after fixed dose or saline pretreatment.
+GRIA1	drug	opioid	23396226	Importantly, pSer845 <strong>GluA1</strong>/<strong>GluA1</strong> ratio was increased exclusively in dorsal striatum and not ventral striatum following acute <b>morphine</b> challenge specifically paired with increasing dose pretreatment and not fixed dose or saline.
+GRIA1	drug	opioid	23396226	These findings indicate that behavioral sensitization induced by chronic pretreatment with increasing doses of <b>morphine</b> might be more closely associated with the dynamic <strong>GluA1</strong> activity in the striatum rather than the modulation of MAPK signaling.
+GRIA1	addiction	sensitization	23396226	These findings indicate that behavioral <b>sensitization</b> induced by chronic pretreatment with increasing doses of morphine might be more closely associated with the dynamic <strong>GluA1</strong> activity in the striatum rather than the modulation of MAPK signaling.
+GRIA1	addiction	reward	23354537	Rats that expressed a persistent <b>CPP</b> had elevated levels of p ERK1, <strong>GluA1</strong>, and p Ser845 <strong>GluA1</strong> in NAc core, and the latter correlated with <b>CPP</b> expression.
+GRIA1	drug	cocaine	23352852	Acute <b>cocaine</b> increases phosphorylation of CaMKII and <strong>GluA1</strong> in the dorsolateral striatum of drug naïve rats, but not <b>cocaine</b> experienced rats.
+GRIA1	drug	cocaine	23352852	Transport of <strong>GluA1</strong> containing AMPA glutamate receptors to synapses in the nucleus accumbens, a process that involves phosphorylation of key serine residues by CaMKII, is associated with the reinstatement of <b>cocaine</b> seeking behavior.
+GRIA1	addiction	relapse	23352852	Transport of <strong>GluA1</strong> containing AMPA glutamate receptors to synapses in the nucleus accumbens, a process that involves phosphorylation of key serine residues by CaMKII, is associated with the <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+GRIA1	drug	cocaine	23352852	However, the potential role of CaMKII mediated phosphorylation of <strong>GluA1</strong> subunits in the dorsolateral (DL) striatum during <b>cocaine</b> reinstatement has not been examined.
+GRIA1	addiction	relapse	23352852	However, the potential role of CaMKII mediated phosphorylation of <strong>GluA1</strong> subunits in the dorsolateral (DL) striatum during cocaine <b>reinstatement</b> has not been examined.
+GRIA1	drug	cocaine	23352852	These results indicate that acute exposure to <b>cocaine</b> in drug naïve rats increased CaMKII mediated phosphorylation of <strong>GluA1</strong> containing AMPA receptors in the DL striatum, an effect that was not observed during <b>cocaine</b> priming induced reinstatement of drug seeking.
+GRIA1	addiction	relapse	23352852	These results indicate that acute exposure to cocaine in drug naïve rats increased CaMKII mediated phosphorylation of <strong>GluA1</strong> containing AMPA receptors in the DL striatum, an effect that was not observed during cocaine priming induced <b>reinstatement</b> of drug <b>seeking</b>.
+GRIA1	drug	cocaine	23352852	It is possible; therefore, that increased phosphorylation of CaMKII and <strong>GluA1</strong> following acute <b>cocaine</b> is a compensatory mechanism in the DL striatum.
+GRIA1	drug	opioid	23345231	Central amygdala <strong>GluA1</strong> facilitates associative learning of <b>opioid</b> reward.
+GRIA1	addiction	reward	23345231	Central amygdala <strong>GluA1</strong> facilitates associative learning of opioid <b>reward</b>.
+GRIA1	addiction	addiction	23345231	<strong>GluA1</strong> subunits of AMPA glutamate receptors are implicated in the synaptic plasticity induced by drugs of abuse for behaviors of drug <b>addiction</b>, but <strong>GluA1</strong> roles in emotional learning and memories of drug reward in the development of drug <b>addiction</b> remain unclear.
+GRIA1	addiction	reward	23345231	<strong>GluA1</strong> subunits of AMPA glutamate receptors are implicated in the synaptic plasticity induced by drugs of abuse for behaviors of drug addiction, but <strong>GluA1</strong> roles in emotional learning and memories of drug <b>reward</b> in the development of drug addiction remain unclear.
+GRIA1	drug	opioid	23345231	In this study of the central nucleus of the amygdala (CeA), which is critical in emotional learning of drug reward, we investigated how adaptive changes in the expression of <strong>GluA1</strong> subunits affected the learning process of <b>opioid</b> induced context reward association (associative learning) for the acquisition of reward related behavior.
+GRIA1	addiction	reward	23345231	In this study of the central nucleus of the amygdala (CeA), which is critical in emotional learning of drug <b>reward</b>, we investigated how adaptive changes in the expression of <strong>GluA1</strong> subunits affected the learning process of opioid induced context <b>reward</b> association (associative learning) for the acquisition of <b>reward</b> related behavior.
+GRIA1	drug	opioid	23345231	In CeA neurons, we found that CeA <strong>GluA1</strong> expression was significantly increased 2 h after conditioning treatment with <b>morphine</b>, but not 24 h after the conditioning when the behavior of conditioned place reference (CPP) was fully established in rats.
+GRIA1	addiction	reward	23345231	In CeA neurons, we found that CeA <strong>GluA1</strong> expression was significantly increased 2 h after conditioning treatment with morphine, but not 24 h after the conditioning when the behavior of conditioned place reference (<b>CPP</b>) was fully established in rats.
+GRIA1	drug	opioid	23345231	Adenoviral overexpression of <strong>GluA1</strong> subunits in CeA accelerated associative learning, as shown by reduced minimum time of <b>morphine</b> conditioning required for CPP acquisition and by facilitated CPP extinction through extinction training with no <b>morphine</b> involved.
+GRIA1	addiction	reward	23345231	Adenoviral overexpression of <strong>GluA1</strong> subunits in CeA accelerated associative learning, as shown by reduced minimum time of morphine conditioning required for <b>CPP</b> acquisition and by facilitated <b>CPP</b> extinction through extinction training with no morphine involved.
+GRIA1	addiction	reward	23345231	Adenoviral shRNA mediated downregulation of CeA <strong>GluA1</strong> produced opposite effects, inhibiting the processes of both <b>CPP</b> acquisition and <b>CPP</b> extinction.
+GRIA1	addiction	addiction	23345231	These results suggest that increased <strong>GluA1</strong> expression of CeA AMPA receptors facilitates the associative learning of context drug reward, an important process in both development and relapse of drug seeking behaviors in drug <b>addiction</b>.
+GRIA1	addiction	relapse	23345231	These results suggest that increased <strong>GluA1</strong> expression of CeA AMPA receptors facilitates the associative learning of context drug reward, an important process in both development and <b>relapse</b> of drug <b>seeking</b> behaviors in drug addiction.
+GRIA1	addiction	reward	23345231	These results suggest that increased <strong>GluA1</strong> expression of CeA AMPA receptors facilitates the associative learning of context drug <b>reward</b>, an important process in both development and relapse of drug seeking behaviors in drug addiction.
+GRIA1	drug	amphetamine	23345217	<b>Amphetamine</b> exposure transiently increases Ca(2+)/calmodulin dependent protein kinase II (CaMKII) α expression in the nucleus accumbens (NAcc) shell and this persistently increases local <strong>GluA1</strong> S831 phosphorylation and enhances behavioral responding to the drug.
+GRIA1	drug	amphetamine	23345217	Remarkably, this transient inhibition of CaMKII activity produced a long lasting reversal of the increased <strong>GluA1</strong> S831 phosphorylation levels in NAcc shell and persistently blocked the enhanced locomotor response to and self administration of <b>amphetamine</b> normally observed in rats previously exposed to the drug.
+GRIA1	drug	psychedelics	23303054	Cell surface biotinylation studies showed that both GLYX 13 and <b>ketamine</b> led to increases in both NR2B and <strong>GluR1</strong> protein levels, as measured by Western analysis, whereas no changes were seen in mRNA expression (microarray and qRT PCR).
+GRIA1	drug	alcohol	23100433	LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of <b>ethanol</b>, as well as cycles of excessive <b>ethanol</b> consumption and withdrawal, produced a long lasting increase in synaptic localization of the <strong>GluR1</strong> and GluR2 subunits of AMPARs in the DMS.
+GRIA1	addiction	withdrawal	23100433	LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of ethanol, as well as cycles of excessive ethanol consumption and <b>withdrawal</b>, produced a long lasting increase in synaptic localization of the <strong>GluR1</strong> and GluR2 subunits of AMPARs in the DMS.
+GRIA1	drug	cocaine	23085477	Alterations in expression and phosphorylation of <strong>GluA1</strong> receptors following <b>cocaine</b> cue extinction learning.
+GRIA1	drug	cocaine	23085477	Brain regional analyses of total <strong>GluA1</strong> and <strong>GluA1</strong> pSer(845) were used to delineate plasticity of the AMPA receptor in conjunction with <b>cocaine</b> cue extinction learning.
+GRIA1	drug	opioid	23073238	In tissue slices of mPFC, the combined addition of the <b>opioid</b> agonist leu enkephalin and the DA D1 like receptor agonist SKF 81297 produced more than additive increase in the phosphorylation state of AMPA and NMDA receptor subunits <strong>GluR1</strong> and NR1, respectively.
+GRIA1	drug	cocaine	22882295	In the NAc from the stress plus <b>cocaine</b> group we observed a decrease in the phosphorylation of two ABPs, cofilin and cortactin, and an increase in the PSD size and the surface expression of <strong>GluR1</strong>, consistent with a more highly branched actin cytoskeleton.
+GRIA1	drug	cocaine	22882295	This study shows that a history of repeated stress alters the ability of a subsequent <b>cocaine</b> injection to modulate dendritic spine morphology, actin dynamics and <strong>GluR1</strong> expression in the NAc.
+GRIA1	drug	cocaine	22882295	Furthermore, by regulating <strong>GluR1</strong> expression in the NAc, elevated actin cycling contributes to the expression of cross sensitization between stress and <b>cocaine</b>, while stress induced changes in the Pfc were not associated with cross sensitization.
+GRIA1	addiction	sensitization	22882295	Furthermore, by regulating <strong>GluR1</strong> expression in the NAc, elevated actin cycling contributes to the expression of cross <b>sensitization</b> between stress and cocaine, while stress induced changes in the Pfc were not associated with cross <b>sensitization</b>.
+GRIA1	addiction	withdrawal	22830051	FZP <b>withdrawal</b> is correlated with synaptic incorporation of homomeric <strong>GluA1</strong> containing α amino 3 hydroxy 5 methylisoxazole 4 propionic acid receptors (AMPARs) in the proximal stratum radiatum of CA1 neurons.
+GRIA1	addiction	withdrawal	22830051	After 2 days of <b>withdrawal</b>, Ca(2+)/calmodulin dependent protein kinase II (CaMKII) phosphorylates <strong>GluA1</strong> subunits at Ser(831), increasing channel conductance.
+GRIA1	drug	opioid	22675452	Importance of <strong>GluA1</strong> subunit containing AMPA glutamate receptors for <b>morphine</b> state dependency.
+GRIA1	drug	opioid	22675452	Here, mice deficient in AMPA type glutamate receptor <strong>GluA1</strong> subunits were first conditioned to <b>morphine</b> (10 or 20 mg/kg s.c. during eight sessions over four days) using an unbiased procedure, followed by testing for conditioned place preference at <b>morphine</b> states that were the same as or different from the one the mice were conditioned to.
+GRIA1	drug	opioid	22675452	In <strong>GluA1</strong> wildtype littermate mice the same state <b>morphine</b> dose produced the greatest expression of place preference, while in the knockout mice no place preference was then detected.
+GRIA1	drug	opioid	22675452	The results indicate impaired drug induced state dependency in <strong>GluA1</strong> knockout mice, correlating with impaired <b>opioid</b> induced glutamate receptor neuroplasticity.
+GRIA1	drug	alcohol	22666364	Consistent with this, Western blot analysis of the postsynaptic density fraction showed that while there was no change in expression of the AMPA <strong>GluR1</strong> subunit, NMDA NR1 and NRB subunits were significantly increased in CIE exposed mice when examined immediately after the last episode of <b>alcohol</b> exposure.
+GRIA1	drug	cocaine	22655064	Additionally in dSTR, after repeated <b>cocaine</b>, we observed significant increases in total <strong>GluA1</strong>, phosphorylated <strong>GluA1</strong>(Ser 845), and cell surface <strong>GluA1</strong> in all <b>cocaine</b> treated animals vs. controls.
+GRIA1	drug	alcohol	22444953	<b>Alcohol</b> up regulated accumbens Narp levels, concomitant with increases in levels of the <strong>GluR1</strong> AMPA receptor subunit.
+GRIA1	drug	cocaine	22419037	Cav 1.3 L type Ca (2+) channels mediate long term adaptation in dopamine D2L mediated <strong>GluA1</strong> trafficking in the dorsal striatum following <b>cocaine</b> exposure.
+GRIA1	drug	cocaine	22419037	Utilizing <b>cocaine</b> psychomotor sensitization in mice we find that repeated <b>cocaine</b> results in a basal reduction of Ser 845 <strong>GluA1</strong> and cell surface <strong>GluA1</strong> levels in the dorsal striatum (dStr) following a protracted withdrawal period, an adaptation that is dependent on Cav 1.3 channels but not those expressed in the VTA.
+GRIA1	addiction	sensitization	22419037	Utilizing cocaine psychomotor <b>sensitization</b> in mice we find that repeated cocaine results in a basal reduction of Ser 845 <strong>GluA1</strong> and cell surface <strong>GluA1</strong> levels in the dorsal striatum (dStr) following a protracted withdrawal period, an adaptation that is dependent on Cav 1.3 channels but not those expressed in the VTA.
+GRIA1	addiction	withdrawal	22419037	Utilizing cocaine psychomotor sensitization in mice we find that repeated cocaine results in a basal reduction of Ser 845 <strong>GluA1</strong> and cell surface <strong>GluA1</strong> levels in the dorsal striatum (dStr) following a protracted <b>withdrawal</b> period, an adaptation that is dependent on Cav 1.3 channels but not those expressed in the VTA.
+GRIA1	drug	cocaine	22349092	Similarly, alterations in the glutamatergic GluN1 or <strong>GluA1</strong> channels have been implicated in triggering sensitization to other addictive drugs such as <b>cocaine</b>, amphetamines and opiates.
+GRIA1	addiction	addiction	22349092	Similarly, alterations in the glutamatergic GluN1 or <strong>GluA1</strong> channels have been implicated in triggering sensitization to other <b>addictive</b> drugs such as cocaine, amphetamines and opiates.
+GRIA1	addiction	sensitization	22349092	Similarly, alterations in the glutamatergic GluN1 or <strong>GluA1</strong> channels have been implicated in triggering <b>sensitization</b> to other addictive drugs such as cocaine, amphetamines and opiates.
+GRIA1	drug	cocaine	22197517	Expression of AMPA receptor subunits (<strong>GluR1</strong> and GluR2) and CRE binding protein (CREB) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of <b>cocaine</b>, with and without ICSS.
+GRIA1	addiction	reward	22197517	Expression of AMPA receptor subunits (<strong>GluR1</strong> and GluR2) and CRE binding protein (CREB) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of cocaine, with and without <b>ICSS</b>.
+GRIA1	addiction	reward	22197517	<b>ICSS</b> increased <strong>GluR1</strong> in the VTA but not NAc or STR, demonstrating selective changes in protein expression with electrical stimulation of discrete brain structures.
+GRIA1	drug	cocaine	22197517	Repeated <b>cocaine</b> reduced <strong>GluR1</strong>, GluR2 and CREB expression in the NAc, and reductions of <strong>GluR1</strong> and GluR2 but not CREB were further enhanced by ICSS.
+GRIA1	addiction	reward	22197517	Repeated cocaine reduced <strong>GluR1</strong>, GluR2 and CREB expression in the NAc, and reductions of <strong>GluR1</strong> and GluR2 but not CREB were further enhanced by <b>ICSS</b>.
+GRIA1	addiction	reward	22127928	Finally, we found that the levels of PKMζ and GluR2 in the NAc remained unchanged, while the <strong>GluR1</strong> levels were elevated following <b>CPP</b> and fully reversed by ZIP injection.
+GRIA1	drug	opioid	22072679	Hippocampal <strong>GluA1</strong> containing AMPA receptors mediate context dependent sensitization to <b>morphine</b>.
+GRIA1	addiction	sensitization	22072679	Hippocampal <strong>GluA1</strong> containing AMPA receptors mediate context dependent <b>sensitization</b> to morphine.
+GRIA1	addiction	sensitization	22072679	Furthermore, we demonstrated that phosphorylation of <strong>GluA1</strong> AMPAR subunit plays a critical role in the acquisition and expression of context dependent behavioral <b>sensitization</b>, as this behavior is blocked by a viral vector that disrupts <strong>GluA1</strong> phosphorylation.
+GRIA1	drug	cocaine	21940447	Cav1.2 L type Ca²⁺ channels mediate <b>cocaine</b> induced <strong>GluA1</strong> trafficking in the nucleus accumbens, a long term adaptation dependent on ventral tegmental area Ca(v)1.3 channels.
+GRIA1	drug	cocaine	21940447	Utilizing <b>cocaine</b> psychomotor sensitization, we have examined phosphorylation of <strong>GluA1</strong> at key residues serine 845 (S845) and S831, as well as <strong>GluA1</strong> cell surface levels in the nucleus accumbens (NAc) of <b>cocaine</b> preexposed mice and the role of brain specific Ca(v)1.2 and Ca(v)1.3 L type Ca²⁺ channels (LTCCs), therein.
+GRIA1	addiction	sensitization	21940447	Utilizing cocaine psychomotor <b>sensitization</b>, we have examined phosphorylation of <strong>GluA1</strong> at key residues serine 845 (S845) and S831, as well as <strong>GluA1</strong> cell surface levels in the nucleus accumbens (NAc) of cocaine preexposed mice and the role of brain specific Ca(v)1.2 and Ca(v)1.3 L type Ca²⁺ channels (LTCCs), therein.
+GRIA1	drug	cocaine	21940447	We found higher basal levels of S845 phospho <strong>GluA1</strong> (P <strong>GluA1</strong>) and cell surface <strong>GluA1</strong> in the NAc following protracted withdrawal from <b>cocaine</b> exposure, changes that occur independently of LTCCs.
+GRIA1	addiction	withdrawal	21940447	We found higher basal levels of S845 phospho <strong>GluA1</strong> (P <strong>GluA1</strong>) and cell surface <strong>GluA1</strong> in the NAc following protracted <b>withdrawal</b> from cocaine exposure, changes that occur independently of LTCCs.
+GRIA1	drug	cocaine	21940447	In contrast, we found that a <b>cocaine</b> challenge that elicits expression of the <b>cocaine</b> sensitized response increases S831 P <strong>GluA1</strong> that further increases surface <strong>GluA1</strong> beyond the higher basal levels.
+GRIA1	drug	cocaine	21940447	Intra NAc pharmacological manipulations indicate that the Ca(v)1.2 activated CaM kinase II (CaMKII) mediates <b>cocaine</b> induced increase in S831 P <strong>GluA1</strong> and that both Ca(v)1.2 activated CaMKII and extracellular signal regulated kinase 2 (ERK2) mediate the increase in <strong>GluA1</strong> cell surface levels specific to the sensitized response.
+GRIA1	drug	cocaine	21940447	Together, these results identify candidate pathways that mediate <b>cocaine</b> induced AMPAR plasticity in the NAc and provide a mechanism linking LTCCs and <strong>GluA1</strong> plasticity to <b>cocaine</b> induced persistent behavioral changes.
+GRIA1	drug	cocaine	21887497	These behavioural changes were associated to alterations on the expression of metabotropic mGLUR3 glutamate receptors and on the actions of <b>cocaine</b> on the <strong>GLUR1</strong> subunit of AMPA glutamate receptors in the hippocampus of maLPA(1) animals.
+GRIA1	drug	cocaine	21640333	Enhanced <b>cocaine</b> conditioned place preference and associated brain regional levels of BDNF, p ERK1/2 and p Ser845 <strong>GluA1</strong> in food restricted rats.
+GRIA1	drug	cocaine	21640333	On the other hand, FR rats, whether injected with <b>cocaine</b> or vehicle, displayed elevated p ERK1/2 and p Ser845 <strong>GluA1</strong> in dorsal hippocampus.
+GRIA1	drug	cocaine	21640333	The one effect observed exclusively in <b>cocaine</b> treated FR rats was increased p Ser845 <strong>GluA1</strong> in nucleus accumbens.
+GRIA1	drug	cocaine	21613507	Here we show that daily intravenous <b>cocaine</b> self administration, but not passive <b>cocaine</b> administration, induces dynamic upregulation of the AMPA glutamate receptor subunits <strong>GluR1</strong> and GluR2 in the ventral tegmental area (VTA) of rats.
+GRIA1	drug	cocaine	21613507	We investigated the functional significance of <strong>GluR1</strong> upregulation in the VTA on <b>cocaine</b> self administration using localized viral mediated gene transfer.
+GRIA1	drug	cocaine	21613507	In <b>cocaine</b> self administering animals, overexpression of <strong>GluR1</strong>(WT) in the VTA markedly increased the motivation for <b>cocaine</b> injections on a progressive ratio schedule of <b>cocaine</b> reinforcement.
+GRIA1	addiction	reward	21613507	In cocaine self administering animals, overexpression of <strong>GluR1</strong>(WT) in the VTA markedly increased the motivation for cocaine injections on a progressive ratio schedule of cocaine <b>reinforcement</b>.
+GRIA1	drug	cocaine	21613507	In contrast, overexpression of protein kinase A resistant <strong>GluR1</strong>(S845A) in the VTA reduced peak rates of <b>cocaine</b> self administration on a fixed ratio reinforcement schedule.
+GRIA1	addiction	reward	21613507	In contrast, overexpression of protein kinase A resistant <strong>GluR1</strong>(S845A) in the VTA reduced peak rates of cocaine self administration on a fixed ratio <b>reinforcement</b> schedule.
+GRIA1	drug	cocaine	21613507	Neither viral vector altered sucrose self administration, and overexpression of <strong>GluR1</strong>(WT) or <strong>GluR1</strong>(S845A) in the adjacent substantia nigra had no effect on <b>cocaine</b> self administration.
+GRIA1	drug	amphetamine	21564097	Consistent with these findings, preventing <strong>GluR1</strong> phosphorylation with the alanine mutant <strong>GluR1</strong>(S845A) reduces glutamate evoked currents in cultured medium spiny neurons and blocks the locomotor activity produced by NAcc <b>amphetamine</b>.
+GRIA1	drug	cocaine	21490206	Reinstatement of <b>cocaine</b> seeking is thought to require upregulated surface expression of AMPA glutamate receptors, and the inhibitory AKAP peptide reduced the PSD content of protein kinase A (PKA) as well as surface expression of <strong>GluR1</strong> in NAc.
+GRIA1	addiction	relapse	21490206	<b>Reinstatement</b> of cocaine <b>seeking</b> is thought to require upregulated surface expression of AMPA glutamate receptors, and the inhibitory AKAP peptide reduced the PSD content of protein kinase A (PKA) as well as surface expression of <strong>GluR1</strong> in NAc.
+GRIA1	drug	cocaine	21216391	Among them, <strong>GluA1</strong> and GluA3 are preferentially upregulated in their palmitoylation levels by a systemic injection of <b>cocaine</b>.
+GRIA1	drug	cocaine	21215761	However, there is no ultrastructural evidence that the absence of <b>cocaine</b> following repeated administrations affects the critical surface/synaptic availability of AMPAR <strong>GluR1</strong> subunits in either DA or non DA, putative GABAergic neurons within the VTA.
+GRIA1	drug	cocaine	21215761	At each time point, both <b>cocaine</b>  and saline injected mice showed AMPAR <strong>GluR1</strong> immunogold labeling in somatodendritic profiles, many of which contained immunoperoxidase labeling for the DA synthesizing enzyme, tyrosine hydroxylase (TH).
+GRIA1	drug	cocaine	21215761	At 30 min after the last injection, when <b>cocaine</b> was systemically present, only the non TH labeled dendrites showed a significant increase in the synaptic/plasmalemmal density of <strong>GluR1</strong> immunogold particles.
+GRIA1	drug	cocaine	21215761	At 72 h, when systemic <b>cocaine</b> was depleted, synaptic <strong>GluR1</strong> labeling was greatly enhanced in TH containing dendrites throughout the VTA and in non TH dendrites of the limbic associated paranigral VTA.
+GRIA1	drug	cocaine	21215761	Our results demonstrate that systemic <b>cocaine</b> produces <strong>GluR1</strong> trafficking specifically in non DA neurons of the VTA, which may subsequently contribute to the abstinent induced enhancement of AMPA receptor synaptic transmission in mesocorticolimbic DA neurons leading to heightened drug seeking behavior.
+GRIA1	addiction	relapse	21215761	Our results demonstrate that systemic cocaine produces <strong>GluR1</strong> trafficking specifically in non DA neurons of the VTA, which may subsequently contribute to the abstinent induced enhancement of AMPA receptor synaptic transmission in mesocorticolimbic DA neurons leading to heightened drug <b>seeking</b> behavior.
+GRIA1	drug	opioid	21175880	Repeated <b>morphine</b> treatment decreased surface expression of <strong>GluA1</strong> in the medial prefrontal cortex without affecting levels of GluA2.
+GRIA1	drug	cocaine	21126734	In line with the <strong>GluA1</strong> PSD 95 implications of enhanced synaptic plasticity, Homer 1b/c protein expression was increased in both heroin and <b>cocaine</b> users as was its binding partner, dynamin 3.
+GRIA1	drug	opioid	21126734	In line with the <strong>GluA1</strong> PSD 95 implications of enhanced synaptic plasticity, Homer 1b/c protein expression was increased in both <b>heroin</b> and cocaine users as was its binding partner, dynamin 3.
+GRIA1	drug	alcohol	21041654	We further show that the protein expression levels of <strong>GluR1</strong> and Homer, two synaptic proteins whose translation has been shown to be modulated by mTORC1, are up regulated in the NAc of rodents with a history of excessive <b>alcohol</b> consumption.
+GRIA1	drug	cocaine	20942997	Following re exposure to a <b>cocaine</b> paired context, surface expression of the AMPA type glutamate receptor <strong>GluR1</strong> was significantly reduced whereas GluR2 was significantly increased in the dlCPu, independent of Arc antisense ODN infusion.
+GRIA1	drug	cocaine	20868701	Effects of minocycline on <b>cocaine</b> sensitization and phosphorylation of <strong>GluR1</strong> receptors in 5 lipoxygenase deficient mice.
+GRIA1	addiction	sensitization	20868701	Effects of minocycline on cocaine <b>sensitization</b> and phosphorylation of <strong>GluR1</strong> receptors in 5 lipoxygenase deficient mice.
+GRIA1	drug	cocaine	20868701	Locomotor sensitization was induced by 4 daily <b>cocaine</b> injections and the phosphorylation status of <strong>GluR1</strong> glutamate receptors was assayed in brain samples.
+GRIA1	addiction	sensitization	20868701	Locomotor <b>sensitization</b> was induced by 4 daily cocaine injections and the phosphorylation status of <strong>GluR1</strong> glutamate receptors was assayed in brain samples.
+GRIA1	drug	cocaine	20868701	In these mice, neither <b>cocaine</b> nor minocycline 4 day treatment altered <strong>GluR1</strong> phosphorylation.
+GRIA1	drug	cocaine	20868701	In WT mice in which minocycline inhibited development of <b>cocaine</b> sensitization, a 4 day <b>cocaine</b> treatment increased <strong>GluR1</strong> phosphorylation at both Ser831 and Ser845 sites in the frontal cortex but not the striatum; further, this effect was prevented by minocycline.
+GRIA1	addiction	sensitization	20868701	In WT mice in which minocycline inhibited development of cocaine <b>sensitization</b>, a 4 day cocaine treatment increased <strong>GluR1</strong> phosphorylation at both Ser831 and Ser845 sites in the frontal cortex but not the striatum; further, this effect was prevented by minocycline.
+GRIA1	drug	cocaine	20868701	Under basal conditions and in response to a single <b>cocaine</b> injection the levels of <strong>GluR1</strong>, GluR2, and GluR3 AMPA receptor subunits did not differ between WT and 5 LOX deficient mice, but the response of <strong>GluR1</strong> phosphorylation to a single <b>cocaine</b> injection was greater under the 5 LOX deficiency.
+GRIA1	addiction	reward	20864528	In rats, selective activation of D1 D2 heteromers increased grooming behavior and attenuated AMPA receptor <strong>GluR1</strong> phosphorylation by calcium/calmodulin kinase IIα in nucleus accumbens, implying a role in <b>reward</b> pathways.
+GRIA1	drug	benzodiazepine	20853509	<b>Benzodiazepine</b> withdrawal anxiety is associated with enhanced α amino 3 hydroxy 5 methylisoxazole 4 propionic acid receptor (AMPAR) mediated glutamatergic transmission in rat hippocampal CA1 synapses due to enhanced synaptic insertion and phosphorylation of <strong>GluA1</strong> homomers.
+GRIA1	addiction	withdrawal	20853509	Benzodiazepine <b>withdrawal</b> anxiety is associated with enhanced α amino 3 hydroxy 5 methylisoxazole 4 propionic acid receptor (AMPAR) mediated glutamatergic transmission in rat hippocampal CA1 synapses due to enhanced synaptic insertion and phosphorylation of <strong>GluA1</strong> homomers.
+GRIA1	drug	cocaine	20600170	In the ventral tegmental area, <b>cocaine</b> self administration elevated glutamatergic receptor subunits NR1 and <strong>GluR1</strong> and scaffolding protein PSD95, but not GABA(A)β, protein levels.
+GRIA1	drug	cocaine	20553819	Acute and chronic <b>cocaine</b> differentially alter the subcellular distribution of AMPA <strong>GluR1</strong> subunits in region specific neurons within the mouse ventral tegmental area.
+GRIA1	drug	cocaine	20553819	<b>Cocaine</b> administration increases AMPA <strong>GluR1</strong> expression and receptor mediated activation of the ventral tegmental area (VTA).
+GRIA1	drug	cocaine	20553819	To test this hypothesis, we used electron microscopic immunolabeling of AMPA <strong>GluR1</strong> subunits and tyrosine hydroxylase (TH), the enzyme needed for dopamine synthesis, in the cortical associated parabrachial (PB) and in the limbic associated paranigral (PN) VTA of adult male C57BL/6 mice receiving either a single injection (acute) or repeated escalating doses for 14 days (chronic) of <b>cocaine</b>.
+GRIA1	drug	cocaine	20553819	Conversely, TH labeled dendrites within the PN VTA showed greater surface expression of <strong>GluR1</strong> with increases in both synaptic and plasmalemmal <strong>GluR1</strong> immunogold density after a single injection of <b>cocaine</b>.
+GRIA1	drug	cocaine	20553819	In contrast, non TH containing, presumably GABAergic dendrites showed VTA region specific changes only after repeated <b>cocaine</b> administration such that synaptic <strong>GluR1</strong> decreased in the PB, but increased in the PN VTA.
+GRIA1	drug	benzodiazepine	20445501	<b>Benzodiazepine</b> withdrawal anxiety is associated with potentiation of alpha amino 3 hydroxy 5 methyl 4 isoxazolepropionate receptor (AMPAR) currents in hippocampal CA1 pyramidal neurons attributable to increased synaptic incorporation of <strong>GluA1</strong> containing AMPARs.
+GRIA1	addiction	withdrawal	20445501	Benzodiazepine <b>withdrawal</b> anxiety is associated with potentiation of alpha amino 3 hydroxy 5 methyl 4 isoxazolepropionate receptor (AMPAR) currents in hippocampal CA1 pyramidal neurons attributable to increased synaptic incorporation of <strong>GluA1</strong> containing AMPARs.
+GRIA1	drug	benzodiazepine	20445501	Synaptic insertion and subsequent CaMKII alpha mediated Ser(831) phosphorylation of <strong>GluA1</strong> homomers contribute to <b>benzodiazepine</b> withdrawal induced AMPAR potentiation and may represent an important hippocampal pathway mediating both drug induced and activity dependent plasticity.
+GRIA1	addiction	withdrawal	20445501	Synaptic insertion and subsequent CaMKII alpha mediated Ser(831) phosphorylation of <strong>GluA1</strong> homomers contribute to benzodiazepine <b>withdrawal</b> induced AMPAR potentiation and may represent an important hippocampal pathway mediating both drug induced and activity dependent plasticity.
+GRIA1	drug	cocaine	20336176	Consistent with reduced AMPA responsiveness after chronic <b>cocaine</b> in Narp KO mice, <strong>GluR1</strong> was reduced in the postsynaptic density (PSD) fraction of Narp KO mice withdrawn from <b>cocaine</b>.
+GRIA1	drug	opioid	20159947	Immunoblotting studies show that 12 h after <b>morphine</b> treatment, <strong>GluR1</strong> subunits are increased at the postsynaptic density (PSD) and at extrasynaptic sites, whereas GluR3 subunits are only increased at the PSD, and they show how this alters receptor subunit composition.
+GRIA1	drug	cannabinoid	19940171	Discrete disturbances of AMPA <strong>GluR1</strong> and <b>cannabinoid</b> type 1 receptor expression observed in the nucleus accumbens associated with stimulus cue induced heroin seeking were normalized by CBD treatment.
+GRIA1	drug	opioid	19940171	Discrete disturbances of AMPA <strong>GluR1</strong> and cannabinoid type 1 receptor expression observed in the nucleus accumbens associated with stimulus cue induced <b>heroin</b> seeking were normalized by CBD treatment.
+GRIA1	addiction	relapse	19940171	Discrete disturbances of AMPA <strong>GluR1</strong> and cannabinoid type 1 receptor expression observed in the nucleus accumbens associated with stimulus cue induced heroin <b>seeking</b> were normalized by CBD treatment.
+GRIA1	drug	cocaine	19812341	Biochemical assays of isolated mPFC tissue from postnatal rats further showed that <b>cocaine</b> exposure in utero caused a marked reduction in the surface expression of GABA(A) receptor subunits alpha1, beta2, and beta3, but had no effect on glutamate receptor subunit <strong>GluR1</strong>.
+GRIA1	drug	cocaine	19629758	Integrin linked kinase is involved in <b>cocaine</b> sensitization by regulating PSD 95 and synapsin I expression and <strong>GluR1</strong> Ser845 phosphorylation.
+GRIA1	addiction	sensitization	19629758	Integrin linked kinase is involved in cocaine <b>sensitization</b> by regulating PSD 95 and synapsin I expression and <strong>GluR1</strong> Ser845 phosphorylation.
+GRIA1	drug	cocaine	19629758	Under both paradigms, established <b>cocaine</b> sensitization under non silenced conditions was associated with enhanced PSD 95 and synapsin I protein expression as well as enhanced Ser(845) phosphorylation of the <strong>GluR1</strong> subunit on withdrawal day.
+GRIA1	addiction	sensitization	19629758	Under both paradigms, established cocaine <b>sensitization</b> under non silenced conditions was associated with enhanced PSD 95 and synapsin I protein expression as well as enhanced Ser(845) phosphorylation of the <strong>GluR1</strong> subunit on withdrawal day.
+GRIA1	addiction	withdrawal	19629758	Under both paradigms, established cocaine sensitization under non silenced conditions was associated with enhanced PSD 95 and synapsin I protein expression as well as enhanced Ser(845) phosphorylation of the <strong>GluR1</strong> subunit on <b>withdrawal</b> day.
+GRIA1	drug	cocaine	19474322	Furthermore, the increase in <strong>GluR1</strong> and ERK activity was blocked after inhibition of NR2B containing NMDAR during the development of <b>cocaine</b> psychomotor sensitization or when the MEK (mitogen activated protein/ERK kinase) inhibitor was microinjected into the NAc 21 d after withdrawal from <b>cocaine</b>.
+GRIA1	addiction	sensitization	19474322	Furthermore, the increase in <strong>GluR1</strong> and ERK activity was blocked after inhibition of NR2B containing NMDAR during the development of cocaine psychomotor <b>sensitization</b> or when the MEK (mitogen activated protein/ERK kinase) inhibitor was microinjected into the NAc 21 d after withdrawal from cocaine.
+GRIA1	addiction	withdrawal	19474322	Furthermore, the increase in <strong>GluR1</strong> and ERK activity was blocked after inhibition of NR2B containing NMDAR during the development of cocaine psychomotor sensitization or when the MEK (mitogen activated protein/ERK kinase) inhibitor was microinjected into the NAc 21 d after <b>withdrawal</b> from cocaine.
+GRIA1	drug	cocaine	19474322	Enhanced ERK activity drives the increased expression of the <strong>GluR1</strong> subunits, which increases the excitability of NAc neurons after prolonged withdrawal from <b>cocaine</b> and results in enduring expression of psychomotor sensitization.
+GRIA1	addiction	sensitization	19474322	Enhanced ERK activity drives the increased expression of the <strong>GluR1</strong> subunits, which increases the excitability of NAc neurons after prolonged withdrawal from cocaine and results in enduring expression of psychomotor <b>sensitization</b>.
+GRIA1	addiction	withdrawal	19474322	Enhanced ERK activity drives the increased expression of the <strong>GluR1</strong> subunits, which increases the excitability of NAc neurons after prolonged <b>withdrawal</b> from cocaine and results in enduring expression of psychomotor sensitization.
+GRIA1	drug	cocaine	19368820	The effects of extinction following <b>cocaine</b> self administration on the expression and synaptosomal distribution of <strong>GluR1</strong> and NMDAR1 glutamate receptor subunits in the NA shell and core and the dorsolateral striatum were examined.
+GRIA1	drug	cocaine	19368820	These data suggest that extinguished <b>cocaine</b> seeking is associated with changes in <strong>GluR1</strong> and NMDAR1 expression and subcellular distribution that are region specific and consist of both a reversal of <b>cocaine</b> induced adaptations and emergent extinction related alterations that include receptor subunit redistribution and may involve alterations in scaffolding proteins.
+GRIA1	addiction	relapse	19368820	These data suggest that extinguished cocaine <b>seeking</b> is associated with changes in <strong>GluR1</strong> and NMDAR1 expression and subcellular distribution that are region specific and consist of both a reversal of cocaine induced adaptations and emergent extinction related alterations that include receptor subunit redistribution and may involve alterations in scaffolding proteins.
+GRIA1	drug	amphetamine	19183251	In contrast to our previous results in cocaine sensitized rats, we did not observe redistribution of <strong>GluR1</strong> or GluR2 to the cell surface in the NAc after <b>amphetamine</b> withdrawal, although a small increase in total <strong>GluR1</strong> was found in the shell subregion.
+GRIA1	drug	cocaine	19183251	In contrast to our previous results in <b>cocaine</b> sensitized rats, we did not observe redistribution of <strong>GluR1</strong> or GluR2 to the cell surface in the NAc after amphetamine withdrawal, although a small increase in total <strong>GluR1</strong> was found in the shell subregion.
+GRIA1	addiction	withdrawal	19183251	In contrast to our previous results in cocaine sensitized rats, we did not observe redistribution of <strong>GluR1</strong> or GluR2 to the cell surface in the NAc after amphetamine <b>withdrawal</b>, although a small increase in total <strong>GluR1</strong> was found in the shell subregion.
+GRIA1	drug	cocaine	19157986	New molecular and neurochemical adaptations in the glutamatergic system which drive <b>cocaine</b> relapse have been identified, such as the ability of CB1 receptor stimulation to reduce basal glutamate levels and the involvement of the <strong>GluR1</strong> receptor subunit in reinstatement.
+GRIA1	addiction	relapse	19157986	New molecular and neurochemical adaptations in the glutamatergic system which drive cocaine <b>relapse</b> have been identified, such as the ability of CB1 receptor stimulation to reduce basal glutamate levels and the involvement of the <strong>GluR1</strong> receptor subunit in <b>reinstatement</b>.
+GRIA1	addiction	withdrawal	19105975	At 21 days of <b>withdrawal</b>, there was a decrease in the expression of mGluR2/3 protein in core and shell, an increase in <strong>GluR1</strong> and a decrease in Homer1b/c proteins in the nucleus accumbens core tissue.
+GRIA1	drug	opioid	19084907	Phosphorylation of <strong>GluR1</strong>, ERK, and CREB during spontaneous withdrawal from chronic <b>heroin</b> self administration.
+GRIA1	addiction	withdrawal	19084907	Phosphorylation of <strong>GluR1</strong>, ERK, and CREB during spontaneous <b>withdrawal</b> from chronic heroin self administration.
+GRIA1	drug	opioid	19077125	Extinction of <b>morphine</b> dependent conditioned behavior is associated with increased phosphorylation of the <strong>GluR1</strong> subunit of AMPA receptors at hippocampal synapses.
+GRIA1	drug	opioid	19077125	Results showed that <b>morphine</b> dependent CRs did not alter expression or redistribution of <strong>GluR1</strong> or GluR2; however, the unpaired administration of <b>morphine</b> resulted in an increase in the phosphorylation of the <strong>GluR1</strong> subunit at extrasynaptic sites.
+GRIA1	drug	benzodiazepine	18924138	Increased AMPA receptor <strong>GluR1</strong> subunit incorporation in rat hippocampal CA1 synapses during <b>benzodiazepine</b> withdrawal.
+GRIA1	addiction	withdrawal	18924138	Increased AMPA receptor <strong>GluR1</strong> subunit incorporation in rat hippocampal CA1 synapses during benzodiazepine <b>withdrawal</b>.
+GRIA1	addiction	withdrawal	18924138	To test this hypothesis, the postsynaptic incorporation of <strong>GluR1</strong> and GluR2 subunits in CA1 neurons after FZP <b>withdrawal</b> was examined by postembedding immunogold quantitative electron microscopy.
+GRIA1	drug	benzodiazepine	18924138	Taken together with recent functional data from our laboratory, the current study suggests that the enhanced glutamatergic strength at CA1 neuron synapses during <b>benzodiazepine</b> withdrawal is mediated by increased incorporation of <strong>GluR1</strong> containing AMPARs.
+GRIA1	addiction	withdrawal	18924138	Taken together with recent functional data from our laboratory, the current study suggests that the enhanced glutamatergic strength at CA1 neuron synapses during benzodiazepine <b>withdrawal</b> is mediated by increased incorporation of <strong>GluR1</strong> containing AMPARs.
+GRIA1	drug	opioid	18815253	Region specific changes in the subcellular distribution of AMPA receptor <strong>GluR1</strong> subunit in the rat ventral tegmental area after acute or chronic <b>morphine</b> administration.
+GRIA1	drug	opioid	18815253	Indeed, chronic <b>morphine</b> administration is known to increase AMPA receptor glutamate receptor 1 (<strong>GluR1</strong>) subunit in the VTA.
+GRIA1	drug	opioid	18815253	However, there is no ultrastructural evidence that <b>morphine</b> affects the expression or surface availability of <strong>GluR1</strong> subunits in VTA neurons of defined distribution or transmitter phenotype.
+GRIA1	drug	opioid	18815253	Therefore, we examined electron microscopic immunolabeling of <strong>GluR1</strong> and tyrosine hydroxylase (TH) in two VTA regions of rats perfused 1 h after a single injection of <b>morphine</b>, or chronic <b>morphine</b> in intermittent escalating doses for 14 d, and appropriate saline controls.
+GRIA1	drug	opioid	18815253	Acute <b>morphine</b> administration produced a significant increase in <strong>GluR1</strong> immunogold particles at the plasma membrane and postsynaptic densities in both TH  and non TH containing dendrites in the parabrachial VTA, a region that contains mainly prefrontal cortical projecting dopaminergic neurons involved in motivation and drug seeking behavior.
+GRIA1	addiction	relapse	18815253	Acute morphine administration produced a significant increase in <strong>GluR1</strong> immunogold particles at the plasma membrane and postsynaptic densities in both TH  and non TH containing dendrites in the parabrachial VTA, a region that contains mainly prefrontal cortical projecting dopaminergic neurons involved in motivation and drug <b>seeking</b> behavior.
+GRIA1	drug	opioid	18815253	Chronic <b>morphine</b> administration maintained the increased synaptic <strong>GluR1</strong> labeling in the parabrachial VTA, but also increased the number of <strong>GluR1</strong> labeled synapses and TH immunoreactivity in dendrites of the paranigral VTA where substantially more dopaminergic neurons project to limbic structures implicated in locomotor activation and reward.
+GRIA1	addiction	reward	18815253	Chronic morphine administration maintained the increased synaptic <strong>GluR1</strong> labeling in the parabrachial VTA, but also increased the number of <strong>GluR1</strong> labeled synapses and TH immunoreactivity in dendrites of the paranigral VTA where substantially more dopaminergic neurons project to limbic structures implicated in locomotor activation and <b>reward</b>.
+GRIA1	drug	opioid	18815253	These results demonstrate a region  and dose dependent redistribution of <strong>GluR1</strong> containing AMPA receptors, which is consistent with acute <b>morphine</b> activation of cortical projecting VTA neurons and chronic <b>morphine</b> activation of limbic projecting VTA neurons.
+GRIA1	drug	cocaine	18701074	<b>Cocaine</b> strengthens excitatory synapses onto midbrain dopamine neurons through the synaptic delivery of <strong>GluR1</strong> containing AMPA receptors.
+GRIA1	drug	cocaine	18701074	We report that in midbrain slices of <b>cocaine</b> treated mice, synaptic transmission was no longer strengthened when <strong>GluR1</strong> or NR1 was abolished, while in the respective mice the drug still induced normal conditioned place preference and locomotor sensitization.
+GRIA1	addiction	sensitization	18701074	We report that in midbrain slices of cocaine treated mice, synaptic transmission was no longer strengthened when <strong>GluR1</strong> or NR1 was abolished, while in the respective mice the drug still induced normal conditioned place preference and locomotor <b>sensitization</b>.
+GRIA1	addiction	relapse	18701074	In contrast, extinction of drug <b>seeking</b> behavior was absent in mice lacking <strong>GluR1</strong>, while in the NR1 mutant mice <b>reinstatement</b> was abolished.
+GRIA1	drug	cocaine	18640148	<b>Cocaine</b> induced behavioral sensitization in adolescent rats endures until adulthood: lack of association with <strong>GluR1</strong> and NR1 glutamate receptor subunits and tyrosine hydroxylase.
+GRIA1	addiction	sensitization	18640148	Cocaine induced behavioral <b>sensitization</b> in adolescent rats endures until adulthood: lack of association with <strong>GluR1</strong> and NR1 glutamate receptor subunits and tyrosine hydroxylase.
+GRIA1	drug	cocaine	18640148	In <b>cocaine</b> sensitized rats <strong>GluR1</strong> protein was increased in the mPFC on PND37 but not in other ages.
+GRIA1	drug	cocaine	18640148	However, <b>cocaine</b> pretreatment during adolescence induced a transient increase of <strong>GluR1</strong> in the mPFC only when animals were challenged in the same age.
+GRIA1	drug	cocaine	18554320	Enhanced CREB and DARPP 32 phosphorylation in the nucleus accumbens and CREB, ERK, and <strong>GluR1</strong> phosphorylation in the dorsal hippocampus is associated with <b>cocaine</b> conditioned place preference behavior.
+GRIA1	drug	cocaine	18554320	To better understand the mechanism of <b>cocaine</b> conditioned place preference we have used western blot analysis to examine changes in phosphorylation of cAMP response element binding protein (CREB), dopamine  and cyclic AMP regulated phosphoprotein 32 (DARPP 32), extracellular signal regulated kinase (ERK) and <strong>GluR1</strong>, key molecular substrates altered by <b>cocaine</b>, in the nucleus accumbens (NAc) and dorsal hippocampus (DHC) of C57BL/6 mice.
+GRIA1	drug	cocaine	18486119	Contributions of nucleus accumbens core and shell <strong>GluR1</strong> containing AMPA receptors in AMPA  and <b>cocaine</b> primed reinstatement of <b>cocaine</b> seeking behavior.
+GRIA1	addiction	relapse	18486119	Contributions of nucleus accumbens core and shell <strong>GluR1</strong> containing AMPA receptors in AMPA  and cocaine primed <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+GRIA1	drug	cocaine	18486119	We also tested the hypothesis that <strong>GluR1</strong> subunit (<strong>GluR1</strong>) containing alpha amino 3 hydroxy 5 methylisoxazole 4 proprionic acid (AMPA) receptors in the nucleus accumbens core and not the shell regulate reinstatement of previously extinguished <b>cocaine</b> seeking behavior.
+GRIA1	addiction	relapse	18486119	We also tested the hypothesis that <strong>GluR1</strong> subunit (<strong>GluR1</strong>) containing alpha amino 3 hydroxy 5 methylisoxazole 4 proprionic acid (AMPA) receptors in the nucleus accumbens core and not the shell regulate <b>reinstatement</b> of previously extinguished cocaine <b>seeking</b> behavior.
+GRIA1	drug	cocaine	18486119	Administration of antisense oligonucleotides (AS) directed against <strong>GluR1</strong> subunit mRNA into the core and shell disrupted AMPA  and <b>cocaine</b> primed reinstatement  with the most pronounced effects seen in the nucleus accumbens shell.
+GRIA1	addiction	relapse	18486119	Administration of antisense oligonucleotides (AS) directed against <strong>GluR1</strong> subunit mRNA into the core and shell disrupted AMPA  and cocaine primed <b>reinstatement</b>  with the most pronounced effects seen in the nucleus accumbens shell.
+GRIA1	drug	cocaine	18430032	Role of <strong>GluR1</strong> expression in nucleus accumbens neurons in <b>cocaine</b> sensitization and <b>cocaine</b> seeking behavior.
+GRIA1	addiction	relapse	18430032	Role of <strong>GluR1</strong> expression in nucleus accumbens neurons in cocaine sensitization and cocaine <b>seeking</b> behavior.
+GRIA1	addiction	sensitization	18430032	Role of <strong>GluR1</strong> expression in nucleus accumbens neurons in cocaine <b>sensitization</b> and cocaine seeking behavior.
+GRIA1	drug	cocaine	18430032	Transient increases in wt <strong>GluR1</strong> during or after <b>cocaine</b> treatments diminished the development of <b>cocaine</b> sensitization, while pd <strong>GluR1</strong> expression exacerbated <b>cocaine</b> sensitization.
+GRIA1	addiction	sensitization	18430032	Transient increases in wt <strong>GluR1</strong> during or after cocaine treatments diminished the development of cocaine <b>sensitization</b>, while pd <strong>GluR1</strong> expression exacerbated cocaine <b>sensitization</b>.
+GRIA1	drug	cocaine	18430032	As a correlate of the sensitization experiments, we overexpressed wt  or pd <strong>GluR1</strong> in the NAc core during <b>cocaine</b> self administration, and tested the effects on subsequent drug seeking behavior 3 weeks after overexpression declined.
+GRIA1	addiction	relapse	18430032	As a correlate of the sensitization experiments, we overexpressed wt  or pd <strong>GluR1</strong> in the NAc core during cocaine self administration, and tested the effects on subsequent drug <b>seeking</b> behavior 3 weeks after overexpression declined.
+GRIA1	addiction	sensitization	18430032	As a correlate of the <b>sensitization</b> experiments, we overexpressed wt  or pd <strong>GluR1</strong> in the NAc core during cocaine self administration, and tested the effects on subsequent drug seeking behavior 3 weeks after overexpression declined.
+GRIA1	drug	cocaine	18430032	wt <strong>GluR1</strong> overexpression during self administration had no effect on <b>cocaine</b> intake, but subsequently reduced <b>cocaine</b> seeking in extinction and <b>cocaine</b> induced reinstatement, whereas pd <strong>GluR1</strong> facilitated <b>cocaine</b> induced reinstatement.
+GRIA1	addiction	relapse	18430032	wt <strong>GluR1</strong> overexpression during self administration had no effect on cocaine intake, but subsequently reduced cocaine <b>seeking</b> in extinction and cocaine induced <b>reinstatement</b>, whereas pd <strong>GluR1</strong> facilitated cocaine induced <b>reinstatement</b>.
+GRIA1	drug	cocaine	18430032	When overexpressed during reinstatement tests, wt <strong>GluR1</strong> directly attenuated <b>cocaine</b>  and D2 agonist induced reinstatement, while pd <strong>GluR1</strong> enhanced reinstatement.
+GRIA1	addiction	relapse	18430032	When overexpressed during <b>reinstatement</b> tests, wt <strong>GluR1</strong> directly attenuated cocaine  and D2 agonist induced <b>reinstatement</b>, while pd <strong>GluR1</strong> enhanced <b>reinstatement</b>.
+GRIA1	addiction	relapse	18430032	In both experimental procedures, neither wt  nor pd <strong>GluR1</strong> expression affected cue induced <b>reinstatement</b>.
+GRIA1	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (<strong>GluR1</strong>, GluR2, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRIA1	drug	opioid	18294632	Chronic administration of <b>morphine</b> is associated with a decrease in surface AMPA <strong>GluR1</strong> receptor subunit in dopamine D1 receptor expressing neurons in the shell and non D1 receptor expressing neurons in the core of the rat nucleus accumbens.
+GRIA1	drug	opioid	18294632	Immunogold electron microscopy was used to quantify the surface expression of the AMPA <strong>GluR1</strong> subunit in dendritic profiles of neurons in the Acb in response to intermittent 14 day non contingent injections of escalating doses of <b>morphine</b>, a model that parallels <b>opioid</b> self administration.
+GRIA1	drug	opioid	18294632	We provide the first report that chronic <b>morphine</b> administration is associated with a receptor phenotypic decrease in surface trafficking of <strong>GluR1</strong> in Acb subregions.
+GRIA1	drug	opioid	18294632	When compared to saline injected animals, <b>morphine</b> produced a decrease in plasma membrane <strong>GluR1</strong> labeling in medium  and large sized D1R expressing dendritic profiles in the Acb shell.
+GRIA1	drug	opioid	18294632	These results indicate that chronic intermittent injection of escalating doses of <b>morphine</b> is accompanied by ultrastructural plasticity of <strong>GluR1</strong> in neurons that are responsive to glutamate and dopamine induced D1R activation in the Acb shell, and neurons capable of responding to glutamate but not D1R receptor stimulation in the Acb core.
+GRIA1	drug	cocaine	18278040	<b>Cocaine</b> reinstatement is associated with D1 like dopamine receptor dependent increases in accumbens shell CaMKII phosphorylated on Thr286 and glutamate receptor 1 (<strong>GluR1</strong>) phosphorylated on Ser831 (a known CaMKII phosphorylation site), in addition to increases in cell surface expression of <strong>GluR1</strong> containing AMPA receptors in the shell.
+GRIA1	addiction	relapse	18278040	Cocaine <b>reinstatement</b> is associated with D1 like dopamine receptor dependent increases in accumbens shell CaMKII phosphorylated on Thr286 and glutamate receptor 1 (<strong>GluR1</strong>) phosphorylated on Ser831 (a known CaMKII phosphorylation site), in addition to increases in cell surface expression of <strong>GluR1</strong> containing AMPA receptors in the shell.
+GRIA1	drug	cocaine	18278040	Consistent with these findings, <b>cocaine</b> reinstatement is attenuated by intra shell administration of AAV10 <strong>GluR1</strong> C99, a vector that impairs the transport of <strong>GluR1</strong> containing AMPA receptors.
+GRIA1	addiction	relapse	18278040	Consistent with these findings, cocaine <b>reinstatement</b> is attenuated by intra shell administration of AAV10 <strong>GluR1</strong> C99, a vector that impairs the transport of <strong>GluR1</strong> containing AMPA receptors.
+GRIA1	drug	opioid	18265961	Recombinant mu delta <b>opioid</b> receptors (MDOR) and the glutamate receptor 1 (<strong>GluR1</strong>) subunit of amino 3 hydroxy 5 methyl 4 isoxazole propionic acid glutamate receptors are involved in acute and chronic effects of <b>morphine</b>.
+GRIA1	drug	opioid	18265961	Spontaneous home cage activity, novelty induced self grooming and <b>morphine</b> induced hyperactivity were higher in <strong>GluR1</strong> mice compared to Vehicle subjects, whereas MDOR immunization was associated with an increased <b>morphine</b> induced conditioned place preference.
+GRIA1	drug	opioid	18265961	In response to escalating doses of <b>morphine</b> (from 10 to 60 mg/kg i.p., twice daily) and <b>naloxone</b> precipitated withdrawal (1 mg/kg subcutaneous), <strong>GluR1</strong> mice exhibited a more marked stereotyped sniffing behavior and less body tremors compared to Vehicle subjects, whereas less sniffing and teeth chattering were found in MDOR mice.
+GRIA1	addiction	withdrawal	18265961	In response to escalating doses of morphine (from 10 to 60 mg/kg i.p., twice daily) and naloxone precipitated <b>withdrawal</b> (1 mg/kg subcutaneous), <strong>GluR1</strong> mice exhibited a more marked stereotyped sniffing behavior and less body tremors compared to Vehicle subjects, whereas less sniffing and teeth chattering were found in MDOR mice.
+GRIA1	drug	opioid	18265961	These findings indicate an altered response to <b>morphine</b> related reinforcing and aversive effects in MDOR mice and altered coping with the environment in <strong>GluR1</strong> mice.
+GRIA1	addiction	aversion	18265961	These findings indicate an altered response to morphine related reinforcing and <b>aversive</b> effects in MDOR mice and altered coping with the environment in <strong>GluR1</strong> mice.
+GRIA1	addiction	reward	18265961	These findings indicate an altered response to morphine related <b>reinforcing</b> and aversive effects in MDOR mice and altered coping with the environment in <strong>GluR1</strong> mice.
+GRIA1	drug	nicotine	18261852	We investigated the effects of <b>nicotine</b> pre exposure on <b>nicotine</b> preference and levels of <strong>GluR1</strong>/2 and CREB in the mesolimbic system in male mice C57BL/6J and BALB/c inbred mice.
+GRIA1	drug	nicotine	18261852	In addition, alterations in CREB and <strong>GluR1</strong> levels are not sufficient to explain preference for <b>nicotine</b> in a 2 bottle choice paradigm.
+GRIA1	drug	amphetamine	18171924	Intrahippocampal infusion studies with the AMPA specific inhibitor GYKI 52466 [4 (8 methyl 9H 1,3 dioxolo[4,5 h][2,3]benzodiazepin 5 yl) benzenamine hydrochloride], a <strong>GluR1</strong> specific TAT S845 peptide, showed that <strong>GluR1</strong>/2 was essential for the development of manic/hedonic like behaviors such as <b>amphetamine</b> induced hyperactivity.
+GRIA1	addiction	reward	18171924	Intrahippocampal infusion studies with the AMPA specific inhibitor GYKI 52466 [4 (8 methyl 9H 1,3 dioxolo[4,5 h][2,3]benzodiazepin 5 yl) benzenamine hydrochloride], a <strong>GluR1</strong> specific TAT S845 peptide, showed that <strong>GluR1</strong>/2 was essential for the development of manic/<b>hedonic</b> like behaviors such as amphetamine induced hyperactivity.
+GRIA1	drug	cocaine	18160635	To mimic the longer elevation in extracellular DA levels produced by systemic <b>cocaine</b>, cocultures were incubated with DA for 1 h. Synaptic <strong>GluR1</strong> was increased 24 h later, reminiscent of the increased AMPA/NMDA ratio at excitatory synapses onto VTA DA neurons 24 h after <b>cocaine</b> injection (Ungless et al., 2001).
+GRIA1	addiction	relapse	18055123	The nucleus accumbens was dissected immediately after the <b>reinstatement</b> test to examine alterations in <strong>GluR1</strong> and NR1 subunits of glutamatergic receptors.
+GRIA1	addiction	relapse	18055123	<strong>GluR1</strong> levels were decreased on days 1 and 30 but not on day 60 while NR1 levels were unaltered in the <b>reinstatement</b> test.
+GRIA1	drug	amphetamine	18055123	Decreased levels of <strong>GluR1</strong> in the nucleus accumbens might be related to the reinstatement of <b>amphetamine</b> induced conditioning place preference.
+GRIA1	addiction	relapse	18055123	Decreased levels of <strong>GluR1</strong> in the nucleus accumbens might be related to the <b>reinstatement</b> of amphetamine induced conditioning place preference.
+GRIA1	drug	cocaine	17898233	Glutamate receptor 1 (<strong>GluR1</strong>) and GluR2 surface/intracellular (S/I) ratios were increased after 14 d of withdrawal in sensitized rats but were decreased 24 h after challenge with <b>cocaine</b> (which elicited a sensitized locomotor response) or saline (which elicited conditioned locomotion).
+GRIA1	addiction	withdrawal	17898233	Glutamate receptor 1 (<strong>GluR1</strong>) and GluR2 surface/intracellular (S/I) ratios were increased after 14 d of <b>withdrawal</b> in sensitized rats but were decreased 24 h after challenge with cocaine (which elicited a sensitized locomotor response) or saline (which elicited conditioned locomotion).
+GRIA1	drug	cocaine	17898233	JNK phosphorylation also increased after withdrawal, but after <b>cocaine</b> challenge, it was inversely related to <strong>GluR1</strong> and GluR2 S/I ratios.
+GRIA1	addiction	withdrawal	17898233	JNK phosphorylation also increased after <b>withdrawal</b>, but after cocaine challenge, it was inversely related to <strong>GluR1</strong> and GluR2 S/I ratios.
+GRIA1	drug	cocaine	17898233	In summary, surface expression of <strong>GluR1</strong>/2 containing AMPARs increased in the NAc of sensitized rats, but AMPARs internalized after a single reexposure to <b>cocaine</b> or <b>cocaine</b> related cues.
+GRIA1	drug	amphetamine	17762518	In this study, <b>AMPH</b> CPP significantly increased hippocampal <strong>GluR1</strong> receptors, though <b>AMPH</b> CPP was impaired by either blockade of NMDA receptors (AP5) or inhibition of CaMKII (KN 93) during conditioning.
+GRIA1	addiction	reward	17762518	In this study, AMPH <b>CPP</b> significantly increased hippocampal <strong>GluR1</strong> receptors, though AMPH <b>CPP</b> was impaired by either blockade of NMDA receptors (AP5) or inhibition of CaMKII (KN 93) during conditioning.
+GRIA1	drug	cocaine	17680995	Moreover, in sensitized rats acute <b>cocaine</b> administration modified phosphorylation levels of Thr75  and Thr34 DARPP 32, <strong>GluR1</strong>, and NR1 subunits in the nucleus accumbens only at a dose double the efficacious dose in control rats.
+GRIA1	drug	cocaine	17680995	Furthermore, in sensitized rats the acute administration of 6 methyl 2 (phenylethynyl) pyridine, a mGluR5 antagonist, reinstated the phosphorylation levels of Thr75  and Thr34 DARPP 32, <strong>GluR1</strong>, and NR1 to control values, and a subsequent <b>cocaine</b> challenge did not elicit a sensitized response.
+GRIA1	drug	amphetamine	17651730	Western blot analysis of the caudate after <b>methamphetamine</b> revealed little change in Alpha Amino 3 Hydroxy 5 Methyl 4 Isoxazole Propionic Acid (AMPA) <strong>GluR1</strong> or N Methyl d Aspartate (NMDA) NR2B subunits, or their phosphorylation state.
+GRIA1	drug	amphetamine	17651730	However, <b>methamphetamine</b> increased levels of <strong>GluR1</strong> and its phosphorylation state in the prefrontal cortex (PFC), and these increases were attenuated by deprenyl.
+GRIA1	drug	benzodiazepine	17510319	<b>Benzodiazepine</b> withdrawal induced glutamatergic plasticity involves up regulation of <strong>GluR1</strong> containing alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid receptors in Hippocampal CA1 neurons.
+GRIA1	addiction	withdrawal	17510319	Benzodiazepine <b>withdrawal</b> induced glutamatergic plasticity involves up regulation of <strong>GluR1</strong> containing alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid receptors in Hippocampal CA1 neurons.
+GRIA1	drug	benzodiazepine	17510319	As <strong>GluR1</strong> containing AMPARs are critical for activity dependent alterations in excitatory strength, we sought to determine whether changes in <strong>GluR1</strong> subunit distribution in CA1 neurons occurred during <b>benzodiazepine</b> withdrawal.
+GRIA1	addiction	withdrawal	17510319	As <strong>GluR1</strong> containing AMPARs are critical for activity dependent alterations in excitatory strength, we sought to determine whether changes in <strong>GluR1</strong> subunit distribution in CA1 neurons occurred during benzodiazepine <b>withdrawal</b>.
+GRIA1	addiction	withdrawal	17510319	Confocal image analysis revealed that FZP <b>withdrawal</b> promoted <strong>GluR1</strong> subunit incorporation into somatic and proximal dendritic membranes of CA1 neurons without GluR2 subunit alterations.
+GRIA1	addiction	withdrawal	17510319	As with long term potentiation (LTP), the FZP <b>withdrawal</b> induced <strong>GluR1</strong> incorporation into CA1 neuron membranes may require the <strong>GluR1</strong> trafficking protein, synapse associated protein 97, which was also elevated in membrane associated fractions.
+GRIA1	addiction	withdrawal	17510319	Together, our findings provide evidence that during FZP <b>withdrawal</b>, increased membrane incorporation of <strong>GluR1</strong> containing AMPARs and associated up regulation of AMPAR functions in hippocampal CA1 pyramidal neurons share fundamental similarities with the mechanisms underlying LTP.
+GRIA1	drug	cocaine	17439498	Chronic <b>cocaine</b> produced region  and substrate specific tolerance to cAMP dependent protein phosphorylation, including <strong>GluR1</strong>(S845) phosphorylation in striatal and amygdala subregions and NR1(S897) phosphorylation in the CA1 subregion of the hippocampus.
+GRIA1	drug	cocaine	17276011	Importantly, there was an increase in the percentage of cells colabeled with Fos and <strong>GluR1</strong> in the anterior cingulate and nucleus accumbens shell and cells colabeled with Fos and GluR4 in the infralimbic cortex, suggesting that within these regions, a greater, and perhaps even different, population of AMPA receptor subunit expressing neurons is activated in rats engaged in <b>cocaine</b> seeking behavior.
+GRIA1	addiction	relapse	17276011	Importantly, there was an increase in the percentage of cells colabeled with Fos and <strong>GluR1</strong> in the anterior cingulate and nucleus accumbens shell and cells colabeled with Fos and GluR4 in the infralimbic cortex, suggesting that within these regions, a greater, and perhaps even different, population of AMPA receptor subunit expressing neurons is activated in rats engaged in cocaine <b>seeking</b> behavior.
+GRIA1	addiction	reward	17093088	Here, we used herpes simplex virus vectors to examine how transient increases in the expression of <strong>GluR1</strong> or GluR2 protein in the shell component of NAc affect the rewarding impact of electrical stimulation of the medial forebrain bundle, as reflected by intracranial self stimulation (<b>ICSS</b>) thresholds in rats.
+GRIA1	drug	opioid	17093088	We found that elevated <strong>GluR1</strong> in NAc shell increases ICSS thresholds, an effect similar to that caused by treatments that cause anhedonia and dysphoria (prodepressive effects) in rats and humans (e.g., drug withdrawal, kappa <b>opioid</b> agonists).
+GRIA1	addiction	reward	17093088	We found that elevated <strong>GluR1</strong> in NAc shell increases <b>ICSS</b> thresholds, an effect similar to that caused by treatments that cause anhedonia and dysphoria (prodepressive effects) in rats and humans (e.g., drug withdrawal, kappa opioid agonists).
+GRIA1	addiction	withdrawal	17093088	We found that elevated <strong>GluR1</strong> in NAc shell increases ICSS thresholds, an effect similar to that caused by treatments that cause anhedonia and dysphoria (prodepressive effects) in rats and humans (e.g., drug <b>withdrawal</b>, kappa opioid agonists).
+GRIA1	drug	amphetamine	17063155	Dopamine stimulated cAMP production in vitro and phosphorylation of AMPA receptor <strong>GluR1</strong> subunit in response to D <b>amph</b> in vivo were decreased in Gnal+/ , but not Drd1a+/  mice.
+GRIA1	drug	cocaine	16794574	Reversal of <b>cocaine</b> induced behavioral sensitization and associated phosphorylation of the NR2B and <strong>GluR1</strong> subunits of the NMDA and AMPA receptors.
+GRIA1	addiction	sensitization	16794574	Reversal of cocaine induced behavioral <b>sensitization</b> and associated phosphorylation of the NR2B and <strong>GluR1</strong> subunits of the NMDA and AMPA receptors.
+GRIA1	addiction	sensitization	16794574	<b>Sensitization</b> was associated with increased NR2B expression in the accumbens (NAc) shell and decreased Tyr1472 phosphorylation in the NAc core, as well as increased Ser845 phosphorylation of the <strong>GluR1</strong> subunit in prefrontal cortex, NAc core, and shell.
+GRIA1	drug	opioid	16775132	However, the roles of D1 receptors, CREB, and <strong>GluR1</strong> in <b>morphine</b> dependence are not well understood.
+GRIA1	addiction	dependence	16775132	However, the roles of D1 receptors, CREB, and <strong>GluR1</strong> in morphine <b>dependence</b> are not well understood.
+GRIA1	drug	opioid	16775132	Here, we show that somatic signs of <b>naloxone</b> precipitated withdrawal were associated with increased P CREB, but not P <strong>GluR1</strong>, in the NAc of <b>morphine</b> dependent rats.
+GRIA1	addiction	withdrawal	16775132	Here, we show that somatic signs of naloxone precipitated <b>withdrawal</b> were associated with increased P CREB, but not P <strong>GluR1</strong>, in the NAc of morphine dependent rats.
+GRIA1	drug	opioid	16775132	Surprisingly, SKF 82958 increased P <strong>GluR1</strong>, but not P CREB, in the NAc, and <b>naloxone</b> reduced SKF 82958 mediated P <strong>GluR1</strong> induction specifically in <b>morphine</b> dependent rats.
+GRIA1	addiction	dependence	16775132	Furthermore, they suggest a <b>dependence</b> associated shift in the molecular mechanisms that regulate the consequences of D1 receptor stimulation, favoring activation of <strong>GluR1</strong> rather than CREB.
+GRIA1	drug	opioid	16775132	These data raise the possibility that the rewarding effects of SKF 82958 in <b>morphine</b> dependent rats involve increased P <strong>GluR1</strong> in the NAc, although the involvement of other brain regions cannot be ruled out.
+GRIA1	drug	opioid	16687214	We found that repeated administration of <b>morphine</b> significantly elevated aAbs levels to MDOR and to the AMPA <strong>GluR1</strong> subunit, but not to the NMDA NR2 subunit.
+GRIA1	addiction	addiction	16687214	Therefore, together with further investigations on their potential functional consequences, we propose a thorough exploration of aAbs to MDOR and to AMPA <strong>GluR1</strong> subunit as early biomarkers signaling opiate <b>addiction</b>.
+GRIA1	drug	cocaine	16616767	<b>Cocaine</b> withdrawal alters the expression of <strong>GluR1</strong> and GluR2/3 subunits of alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug withdrawal on hippocampus is little known.
+GRIA1	addiction	withdrawal	16616767	Cocaine <b>withdrawal</b> alters the expression of <strong>GluR1</strong> and GluR2/3 subunits of alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug <b>withdrawal</b> on hippocampus is little known.
+GRIA1	drug	opioid	16616767	Here, we have examined the expression of <strong>GluR1</strong> and GluR2/3 in hippocampal membrane and synaptic fractions following repeated <b>morphine</b> exposure and subsequent withdrawal.
+GRIA1	addiction	withdrawal	16616767	Here, we have examined the expression of <strong>GluR1</strong> and GluR2/3 in hippocampal membrane and synaptic fractions following repeated morphine exposure and subsequent <b>withdrawal</b>.
+GRIA1	drug	opioid	16616767	Repeated <b>morphine</b> exposure for 12 d increased <strong>GluR1</strong> and GluR2/3 in synaptosome but not in membrane fraction.
+GRIA1	drug	opioid	16616767	However, during opiate withdrawal, <strong>GluR1</strong> was generally reduced while GluR2/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after withdrawal, but detectably increased in late phase of <b>morphine</b> withdrawal in both fractions.
+GRIA1	addiction	withdrawal	16616767	However, during opiate <b>withdrawal</b>, <strong>GluR1</strong> was generally reduced while GluR2/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after <b>withdrawal</b>, but detectably increased in late phase of morphine <b>withdrawal</b> in both fractions.
+GRIA1	addiction	withdrawal	16616767	These findings indicate that opiate <b>withdrawal</b> induces dynamic expression of <strong>GluR1</strong> and GluR2/3 subunits of AMPA receptors in hippocampal synapses, possibly revealing an adaptive process of the hippocampal functions following opiate <b>withdrawal</b>.
+GRIA1	drug	cocaine	16600521	Both knockout strains displayed increased induction of <strong>GluR1</strong> Ser(845) phosphorylation in response to D1 receptor stimulation in slices, and also displayed enhanced locomotor activation in response to <b>cocaine</b> administration.
+GRIA1	drug	cocaine	16495937	AMPA receptor <strong>GluR1</strong> subunits are involved in the control over behavior by <b>cocaine</b> paired cues.
+GRIA1	drug	cocaine	16495937	Here, we examine the consequences of targeted deletion of the gene encoding GluR1 subunits of AMPA receptors (<strong>gria1</strong> knockouts (KO)) on <b>cocaine</b> self administration and on the ability of <b>cocaine</b> paired cues to affect <b>cocaine</b> seeking in mice.
+GRIA1	addiction	relapse	16495937	Here, we examine the consequences of targeted deletion of the gene encoding GluR1 subunits of AMPA receptors (<strong>gria1</strong> knockouts (KO)) on cocaine self administration and on the ability of cocaine paired cues to affect cocaine <b>seeking</b> in mice.
+GRIA1	drug	cocaine	16495937	Here, we examine the consequences of targeted deletion of the gene encoding <strong>GluR1</strong> subunits of AMPA receptors (<strong>gria1</strong> knockouts (KO)) on <b>cocaine</b> self administration and on the ability of <b>cocaine</b> paired cues to affect <b>cocaine</b> seeking in mice.
+GRIA1	addiction	relapse	16495937	Here, we examine the consequences of targeted deletion of the gene encoding <strong>GluR1</strong> subunits of AMPA receptors (<strong>gria1</strong> knockouts (KO)) on cocaine self administration and on the ability of cocaine paired cues to affect cocaine <b>seeking</b> in mice.
+GRIA1	drug	cocaine	16495937	<b>Cocaine</b> self administration was unaffected by <strong>gria1</strong> deletion, as was the ability of a <b>cocaine</b> paired cue to reinstate responding following extinction, following either a 3 or a 66 day delay.
+GRIA1	drug	cocaine	16495937	These studies indicate that <strong>GluR1</strong> containing AMPA receptors are not involved in <b>cocaine</b> self administration, cue induced reinstatement of <b>cocaine</b> seeking, or incubation of the <b>cocaine</b> seeking response.
+GRIA1	addiction	relapse	16495937	These studies indicate that <strong>GluR1</strong> containing AMPA receptors are not involved in cocaine self administration, cue induced <b>reinstatement</b> of cocaine <b>seeking</b>, or incubation of the cocaine <b>seeking</b> response.
+GRIA1	drug	cocaine	16495937	As with <b>cocaine</b>, there were no effects of <strong>gria1</strong> deletion on food self administration or cue induced reinstatement, and KOs over responded during extinction.
+GRIA1	addiction	relapse	16495937	As with cocaine, there were no effects of <strong>gria1</strong> deletion on food self administration or cue induced <b>reinstatement</b>, and KOs over responded during extinction.
+GRIA1	addiction	reward	16495937	These data indicate that <strong>GluR1</strong> containing AMPA receptors are important in stimulus <b>reward</b> learning, though the method of cue <b>reward</b> association formation, the <b>reward</b> class, and the behavioral end point are critical variables in determining their involvement.
+GRIA1	drug	cocaine	16363995	Statistically significant elevations were observed for NR1, <strong>GluR1</strong>, GluR2/3 and GluR5 (p < 0.05) and a trend towards increased NR1 phosphorylated at serine 896 (p = 0.07) in the NAc but not putamen of monkeys self administering <b>cocaine</b> compared with controls.
+GRIA1	drug	cocaine	16207873	Surface/intracellular (S/I) ratios for glutamate receptor 1 (<strong>GluR1</strong>) and GluR2/3 subunits were increased 21 d after the last injection in <b>cocaine</b> sensitized rats but not rats that failed to sensitize, and the magnitude of the S/I ratio for <b>cocaine</b> sensitized rats was positively correlated with the magnitude of behavioral sensitization.
+GRIA1	addiction	sensitization	16207873	Surface/intracellular (S/I) ratios for glutamate receptor 1 (<strong>GluR1</strong>) and GluR2/3 subunits were increased 21 d after the last injection in cocaine sensitized rats but not rats that failed to sensitize, and the magnitude of the S/I ratio for cocaine sensitized rats was positively correlated with the magnitude of behavioral <b>sensitization</b>.
+GRIA1	drug	cocaine	16046859	Tissue samples of the nucleus accumbens (NAc) and striatum (Str) of all four prenatal treatment groups were examined to determine whether alterations in the transcription factor CREB or glutamate receptor subunit, <strong>GluR1</strong>, induced by prenatal <b>cocaine</b> treatment may have contributed to the altered behavioral responses.
+GRIA1	drug	opioid	16037950	Increased AMPA <strong>GluR1</strong> receptor subunit labeling on the plasma membrane of dendrites in the basolateral amygdala of rats self administering <b>morphine</b>.
+GRIA1	drug	opioid	16037950	High resolution immunogold electron microscopic immunocytochemistry was used to compare surface and intracellular labeling of the calcium sensitive AMPA <strong>GluR1</strong> receptor subunit in the basolateral (BLA) and central (CeA) nuclei of the amygdala in rats self administering escalating doses of <b>morphine</b> or saline.
+GRIA1	drug	opioid	16037950	<b>Morphine</b> self administration was associated with regionally diverse effects on dendritic <strong>GluR1</strong> targeting in the BLA and CeA.
+GRIA1	drug	opioid	16037950	In the BLA of <b>morphine</b> self administering animals, there was a significant increase in the proportion of immunogold particles for <strong>GluR1</strong> on the plasma membrane of dendrites, particularly in association with extrasynaptic sites, which was most prominent in large (2 4 microm) profiles.
+GRIA1	drug	opioid	16037950	In both amygdala regions, <strong>GluR1</strong> and the micro <b>opioid</b> receptor, the major cellular target of <b>morphine</b>, were only infrequently colocalized.
+GRIA1	drug	opioid	16037950	These results indicate that <strong>GluR1</strong> targeting is a dynamic process that can be differentially affected in distinct amygdala regions in response to chronic self administration of <b>morphine</b>.
+GRIA1	addiction	withdrawal	15970947	In the brains of these rats, <b>withdrawal</b> anxiety was accompanied by increased [3H]Ro48 8587 binding in the hippocampus and thalamus, and decreased <strong>GluR1</strong> and GluR2 subunit mRNA expression in the amygdala (<strong>GluR1</strong> and GluR2) and cortex (<strong>GluR1</strong>).
+GRIA1	drug	cocaine	15953359	In the basolateral amygdala, <strong>GluR1</strong> but not GluR2 levels were increased on days 1 and 30, NR2A levels were increased on day 1, and NR2B levels were decreased on day 30 of withdrawal from <b>cocaine</b>.
+GRIA1	addiction	withdrawal	15953359	In the basolateral amygdala, <strong>GluR1</strong> but not GluR2 levels were increased on days 1 and 30, NR2A levels were increased on day 1, and NR2B levels were decreased on day 30 of <b>withdrawal</b> from cocaine.
+GRIA1	drug	cocaine	15953359	In the central amygdala, GluR2 but not <strong>GluR1</strong> levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or NR2B levels were not altered after withdrawal from <b>cocaine</b>.
+GRIA1	addiction	withdrawal	15953359	In the central amygdala, GluR2 but not <strong>GluR1</strong> levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or NR2B levels were not altered after <b>withdrawal</b> from cocaine.
+GRIA1	drug	cocaine	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces <b>cocaine</b> seeking behaviour when reward is withheld, reverses this deficit by up regulating <strong>GluR1</strong> and GluR2/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA1	addiction	relapse	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces cocaine <b>seeking</b> behaviour when reward is withheld, reverses this deficit by up regulating <strong>GluR1</strong> and GluR2/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA1	addiction	reward	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces cocaine seeking behaviour when <b>reward</b> is withheld, reverses this deficit by up regulating <strong>GluR1</strong> and GluR2/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA1	drug	cocaine	15764012	The level of <strong>GluR1</strong> up regulation is positively associated with a reduction in <b>cocaine</b> seeking, suggesting that extinction induced up regulation in AMPA receptors in the NAc opposes motivational influences that maintain <b>cocaine</b> seeking.
+GRIA1	addiction	relapse	15764012	The level of <strong>GluR1</strong> up regulation is positively associated with a reduction in cocaine <b>seeking</b>, suggesting that extinction induced up regulation in AMPA receptors in the NAc opposes motivational influences that maintain cocaine <b>seeking</b>.
+GRIA1	drug	cocaine	15764012	This hypothesis is supported by the finding that over expression of <strong>GluR1</strong> and GluR2 in the NAc facilitates extinction of <b>cocaine</b> self administration.
+GRIA1	drug	cocaine	15764012	Furthermore, a single extinction training session conducted during <strong>GluR1</strong> and GluR2 over expression strongly and selectively attenuates the ability of an environmental stressor to trigger relapse to <b>cocaine</b> seeking long after <strong>GluR1</strong> and GluR2 over expression declines.
+GRIA1	addiction	relapse	15764012	Furthermore, a single extinction training session conducted during <strong>GluR1</strong> and GluR2 over expression strongly and selectively attenuates the ability of an environmental stressor to trigger <b>relapse</b> to cocaine <b>seeking</b> long after <strong>GluR1</strong> and GluR2 over expression declines.
+GRIA1	drug	cocaine	15619119	We investigated the ability of <b>cocaine</b> and food to induce a CPP in mice lacking either the GluR1 or GluR2 subunits of the AMPA receptor [<strong>gria1</strong> or gria2 knockout (KO) mice].
+GRIA1	addiction	reward	15619119	We investigated the ability of cocaine and food to induce a <b>CPP</b> in mice lacking either the GluR1 or GluR2 subunits of the AMPA receptor [<strong>gria1</strong> or gria2 knockout (KO) mice].
+GRIA1	drug	cocaine	15619119	We investigated the ability of <b>cocaine</b> and food to induce a CPP in mice lacking either the <strong>GluR1</strong> or GluR2 subunits of the AMPA receptor [<strong>gria1</strong> or gria2 knockout (KO) mice].
+GRIA1	addiction	reward	15619119	We investigated the ability of cocaine and food to induce a <b>CPP</b> in mice lacking either the <strong>GluR1</strong> or GluR2 subunits of the AMPA receptor [<strong>gria1</strong> or gria2 knockout (KO) mice].
+GRIA1	drug	cocaine	15619119	Following conditioning, <strong>gria1</strong> KOs displayed a significant preference for the food or <b>cocaine</b> paired compartment, and did not differ from wild type (WT) controls.
+GRIA1	addiction	reward	15619119	When the results are considered in relation to our previous findings with <strong>gria1</strong> and gria2 knockout mice, they also raise questions about the <b>CPP</b> paradigm representing a model of conditioned <b>reward</b> over a conditioned approach interpretation.
+GRIA1	drug	cocaine	15548228	A single high dose of <b>cocaine</b> induces behavioural sensitization and modifies mRNA encoding <strong>GluR1</strong> and GAP 43 in rats.
+GRIA1	addiction	sensitization	15548228	A single high dose of cocaine induces behavioural <b>sensitization</b> and modifies mRNA encoding <strong>GluR1</strong> and GAP 43 in rats.
+GRIA1	drug	cocaine	15548228	The present study investigated whether in Sprague Dawley rats a single, behavioural sensitizing dose of <b>cocaine</b> is sufficient to induce changes in the mRNA levels of growth associated protein 43 (GAP 43), an important protein in mediating experience dependent plasticity and synaptic reorganization, and of glutamate receptor 1 (<strong>GluR1</strong>), a subunit of AMPA glutamate receptors, a protein that is up regulated with repeated <b>cocaine</b>.
+GRIA1	drug	cocaine	15548228	Single dose of 20 but not 10 mg/kg <b>cocaine</b> 48 h before scheduled death significantly enhanced <strong>GluR1</strong> and GAP 43 mRNA expression in the nucleus accumbens (NAc), both shell and core subregions, and ventral tegmental area (VTA).
+GRIA1	drug	cocaine	15548228	No changes were found in the levels of mRNA for <strong>GluR1</strong> and GAP 43 in the frontal cortex, caudate putamen, dentate gyrus of hippocampus and basolateral nucleus of the amygdala after the single dose of 20 mg/kg <b>cocaine</b>.
+GRIA1	drug	cocaine	15375209	<b>Cocaine</b> induced potentiation of synaptic strength in dopamine neurons: behavioral correlates in <strong>GluRA</strong>( / ) mice.
+GRIA1	drug	cocaine	15375209	Surprisingly, behavioral sensitization to <b>cocaine</b> was elicited in <strong>GluRA</strong>( / ) mice, indicating that potentiation of excitatory synaptic transmission in DA neurons is not necessary for this form of behavioral plasticity.
+GRIA1	addiction	sensitization	15375209	Surprisingly, behavioral <b>sensitization</b> to cocaine was elicited in <strong>GluRA</strong>( / ) mice, indicating that potentiation of excitatory synaptic transmission in DA neurons is not necessary for this form of behavioral plasticity.
+GRIA1	drug	cocaine	15375209	However, <strong>GluRA</strong>( / ) mice did not exhibit a conditioned locomotor response when placed in a context previously paired with <b>cocaine</b>, nor did they exhibit conditioned place preference in response to <b>cocaine</b>.
+GRIA1	addiction	dependence	15291243	Evidence suggests that the genes for dopamine D4 receptor, phosphodiesterease1B, the AMPA receptor subunit <strong>GluR1</strong>, 5HT1B receptor, protein kinase C and the transcription factor FosB contribute to both <b>dependence</b> susceptibility and comorbid behavioral traits.
+GRIA1	drug	opioid	15287884	The phosphorylation levels of <strong>GluR1</strong> and NR1 subunits decreased in parallel with those of phospho Thr 34 DARPP 32, supporting the hypothesis that <b>morphine</b> challenge elicited a decrease in PKA activity in <b>morphine</b> sensitized rats.
+GRIA1	drug	cannabinoid	15233572	Down regulation of the AMPA glutamate receptor subunits <strong>GluR1</strong> and GluR2/3 in the rat cerebellum following pre  and perinatal delta9 <b>tetrahydrocannabinol</b> exposure.
+GRIA1	drug	cannabinoid	15233572	This paper reports the effects of pre  and perinatal exposure to delta9 <b>tetrahydrocannabinol</b> (<b>THC</b>) on expression levels of specific AMPA glutamate receptor subunits (<strong>GluR1</strong> and GluR2/3) in the cerebellum of male and female rats.
+GRIA1	drug	cannabinoid	15233572	Expression of the <strong>GluR1</strong> and GluR2/3 subunits of AMPA glutamate receptors was analyzed by immunohistochemistry in <b>THC</b> exposed rats at three postnatal ages: PD20 (still exposed to <b>THC</b>) to study the direct effect of drug exposure, and PD30 and PD70 (10 and 50 days following <b>THC</b> withdrawal) to analyze the long term effects of prenatal exposure.
+GRIA1	addiction	withdrawal	15233572	Expression of the <strong>GluR1</strong> and GluR2/3 subunits of AMPA glutamate receptors was analyzed by immunohistochemistry in THC exposed rats at three postnatal ages: PD20 (still exposed to THC) to study the direct effect of drug exposure, and PD30 and PD70 (10 and 50 days following THC <b>withdrawal</b>) to analyze the long term effects of prenatal exposure.
+GRIA1	drug	cannabinoid	15233572	Compared to controls, pre  and perinatal <b>THC</b> exposure decreased the immunoreactivity levels of the <strong>GluR1</strong> subunit in Bergmann glial cells, as well as levels of the GluR2/3 subunit in Purkinje neurons at PD20.
+GRIA1	drug	opioid	15183518	In the core, neuronal apoptotic inhibitory protein (NAIP), GABA A alpha1 subunit, GRIN2C, <strong>GRIA1</strong>, mGluR1, D4 dopamine receptor and PSD 95 were upregulated by <b>morphine</b> administration whereas bax, bcl x, cox 1 and MAP2 were decreased.
+GRIA1	drug	opioid	15183518	Specifically, GABA A alpha1 subunit, <strong>GRIA1</strong> subunit and PSD 95 mRNAs were decreased in the shell but increased in the core following <b>morphine</b> administration.
+GRIA1	drug	amphetamine	15150533	We tested the prediction that an increase in <strong>GluR1</strong> containing AMPA receptors would result in an increase in <strong>GluR1</strong> homomeric receptors at synapses, but were unable to observe any evidence of the predicted rectification in DA neurons from animals treated with <b>amphetamine</b>.
+GRIA1	drug	cocaine	14684464	Opposite effects of <strong>GluR1</strong> and PKA resistant <strong>GluR1</strong> overexpression in the ventral tegmental area on <b>cocaine</b> reinforcement.
+GRIA1	addiction	reward	14684464	Opposite effects of <strong>GluR1</strong> and PKA resistant <strong>GluR1</strong> overexpression in the ventral tegmental area on cocaine <b>reinforcement</b>.
+GRIA1	drug	alcohol	12871650	Neurobehavioral effects of <b>alcohol</b> in AMPA receptor subunit (<strong>GluR1</strong>) deficient mice.
+GRIA1	drug	alcohol	12871650	Using mice deficient in the AMPA receptor subunit <strong>GluR1</strong> (<strong>GluR1</strong> /  mice), we investigated whether the AMPA receptor had a significant role in mediating the effects of <b>ethanol</b>.
+GRIA1	drug	alcohol	12871650	With regard to the effects of <b>ethanol</b> on motor responses, <strong>GluR1</strong> /  mice did not differ significantly from wild type mice in <b>ethanol</b>'s sedative or incoordinating effects.
+GRIA1	drug	alcohol	12871650	However, the <strong>GluR1</strong> /  mice were insensitive to the hypothermic effects of a hypnotic dose of <b>ethanol</b> in contrast to wild types; this effect was dissociable from the hypnotic effects of <b>ethanol</b>.
+GRIA1	drug	alcohol	12871650	Further, tolerance to <b>ethanol</b> developed equally for <strong>GluR1</strong> /  mice versus wild type mice.
+GRIA1	drug	alcohol	12871650	In terms of <b>alcohol</b> drinking behavior, compared to wild types, <strong>GluR1</strong> /  mice differed neither in the acquisition of voluntary <b>ethanol</b> consumption nor in stress induced <b>ethanol</b> drinking, nor in the expression of an <b>alcohol</b> deprivation effect (ADE) which is used as a model of relapse like drinking behavior.
+GRIA1	addiction	relapse	12871650	In terms of alcohol drinking behavior, compared to wild types, <strong>GluR1</strong> /  mice differed neither in the acquisition of voluntary ethanol consumption nor in stress induced ethanol drinking, nor in the expression of an alcohol deprivation effect (ADE) which is used as a model of <b>relapse</b> like drinking behavior.
+GRIA1	drug	alcohol	12871650	In summary, although the loss of a hypothermic effect of <b>ethanol</b> in <strong>GluR1</strong> /  mice indicates a critical role for the AMPA receptors in this effect, the <strong>GluR1</strong> subunit of the AMPA receptor does not seem to play a critical role in the etiology of <b>alcohol</b> dependence.
+GRIA1	addiction	dependence	12871650	In summary, although the loss of a hypothermic effect of ethanol in <strong>GluR1</strong> /  mice indicates a critical role for the AMPA receptors in this effect, the <strong>GluR1</strong> subunit of the AMPA receptor does not seem to play a critical role in the etiology of alcohol <b>dependence</b>.
+GRIA1	drug	cocaine	12787079	In the accumbens of <b>cocaine</b> trained rats, <strong>GluR1</strong> and NMDAR1 levels were increased on days 1 and 90, while GluR2 levels were increased on days 1 and 30, but not day 90; PKA activity levels were increased on days 1 and 30, but not day 90, while AC activity, TH and cdk5 levels were unaltered.
+GRIA1	drug	alcohol	12694947	Despite this augmentation of AMPAR function, no significant changes were found in the sensitivity of AMPA currents to GYKI 52466, cyclothiazide or acute <b>ethanol</b> (100 mM) sensitivity or in the levels of <strong>GluR1</strong>/GluR2 subunit proteins from MS/DB tissue.
+GRIA1	drug	cocaine	12511956	Here we show that extinction training during withdrawal from chronic <b>cocaine</b> self administration induces experience dependent increases in the <strong>GluR1</strong> and GluR2/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in <b>cocaine</b> reward.
+GRIA1	addiction	reward	12511956	Here we show that extinction training during withdrawal from chronic cocaine self administration induces experience dependent increases in the <strong>GluR1</strong> and GluR2/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine <b>reward</b>.
+GRIA1	addiction	withdrawal	12511956	Here we show that extinction training during <b>withdrawal</b> from chronic cocaine self administration induces experience dependent increases in the <strong>GluR1</strong> and GluR2/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine reward.
+GRIA1	drug	cocaine	12511956	Increases in the <strong>GluR1</strong> subunit are positively associated with the level of extinction achieved during training, suggesting that <strong>GluR1</strong> may promote extinction of <b>cocaine</b> seeking.
+GRIA1	addiction	relapse	12511956	Increases in the <strong>GluR1</strong> subunit are positively associated with the level of extinction achieved during training, suggesting that <strong>GluR1</strong> may promote extinction of cocaine <b>seeking</b>.
+GRIA1	drug	cocaine	12511956	Indeed, viral mediated overexpression of both <strong>GluR1</strong> and GluR2 in nucleus accumbens shell neurons facilitates extinction of <b>cocaine</b>  but not sucrose seeking responses.
+GRIA1	addiction	relapse	12511956	Indeed, viral mediated overexpression of both <strong>GluR1</strong> and GluR2 in nucleus accumbens shell neurons facilitates extinction of cocaine  but not sucrose <b>seeking</b> responses.
+GRIA1	addiction	sensitization	12446127	Elevated levels of <strong>GluR1</strong> in the midbrain: a trigger for <b>sensitization</b> to drugs of abuse?
+GRIA1	addiction	sensitization	12446127	Here, we review evidence that the ability of drugs of abuse to elevate levels of the <strong>GluR1</strong> subunit of AMPA glutamate receptors in the ventral tegmental area (VTA) of the midbrain is crucial for the development of <b>sensitization</b>.
+GRIA1	addiction	sensitization	12446127	However, there is ongoing debate over whether elevated levels of <strong>GluR1</strong> in the VTA are a primary cause, or secondary effect, of the neurobiological underpinnings of <b>sensitization</b>.
+GRIA1	drug	cocaine	11801363	Moreover, we observed that rats sensitized to <b>cocaine</b> presented a significant increase in the levels of <strong>GLUR1</strong>, NR1 and NR2B, in the nucleus accumbens, and of NR2B in the hippocampus compared to control animals.
+GRIA1	drug	amphetamine	11751027	<strong>GluR1</strong> immunolabeling was further examined in rats killed 16 18 hrs or 24 hrs after a single injection of <b>amphetamine</b> or repeated injections of saline, <b>amphetamine</b> (5 mg/kg x 5 days) or cocaine (20 mg/kg x 7 days).
+GRIA1	drug	cocaine	11751027	<strong>GluR1</strong> immunolabeling was further examined in rats killed 16 18 hrs or 24 hrs after a single injection of amphetamine or repeated injections of saline, amphetamine (5 mg/kg x 5 days) or <b>cocaine</b> (20 mg/kg x 7 days).
+GRIA1	drug	amphetamine	11751027	Finally, neither repeated <b>amphetamine</b> or cocaine administration significantly altered <strong>GluR1</strong> mRNA levels as quantified by reverse transcriptase polymerase chain reaction.
+GRIA1	drug	cocaine	11751027	Finally, neither repeated amphetamine or <b>cocaine</b> administration significantly altered <strong>GluR1</strong> mRNA levels as quantified by reverse transcriptase polymerase chain reaction.
+GRIA1	drug	alcohol	11696675	Unexpectedly, we found that expression of NR1 (including the expression of NR1 subunits containing the N1, C1, and C2 inserts), NR2A, NR2B, NR2C, <strong>GluR1</strong>, GluR2/3, GluR5, GluR6/7, and KA2 subunits was not altered in hippocampal homogenates from <b>ethanol</b> exposed rats.
+GRIA1	drug	cocaine	11425507	This effect of BSR on <strong>GluR1</strong> expression is opposite of that caused by intermittent exposure to <b>cocaine</b> and morphine, which are known to elevate <strong>GluR1</strong> expression in the VTA.
+GRIA1	drug	opioid	11425507	This effect of BSR on <strong>GluR1</strong> expression is opposite of that caused by intermittent exposure to cocaine and <b>morphine</b>, which are known to elevate <strong>GluR1</strong> expression in the VTA.
+GRIA1	drug	amphetamine	11425507	Considering that elevated <strong>GluR1</strong> expression in the VTA has been associated with increased sensitivity to drug reward, the finding that BSR and drugs of abuse have opposite effects on <strong>GluR1</strong> expression in this region may provide an explanation for why the reward related effects of many drugs (cocaine, morphine, <b>amphetamine</b>, PCP, nicotine) do not sensitize with repeated testing in BSR procedures that quantify reward strength.
+GRIA1	drug	cocaine	11425507	Considering that elevated <strong>GluR1</strong> expression in the VTA has been associated with increased sensitivity to drug reward, the finding that BSR and drugs of abuse have opposite effects on <strong>GluR1</strong> expression in this region may provide an explanation for why the reward related effects of many drugs (<b>cocaine</b>, morphine, amphetamine, PCP, nicotine) do not sensitize with repeated testing in BSR procedures that quantify reward strength.
+GRIA1	drug	nicotine	11425507	Considering that elevated <strong>GluR1</strong> expression in the VTA has been associated with increased sensitivity to drug reward, the finding that BSR and drugs of abuse have opposite effects on <strong>GluR1</strong> expression in this region may provide an explanation for why the reward related effects of many drugs (cocaine, morphine, amphetamine, PCP, <b>nicotine</b>) do not sensitize with repeated testing in BSR procedures that quantify reward strength.
+GRIA1	drug	opioid	11425507	Considering that elevated <strong>GluR1</strong> expression in the VTA has been associated with increased sensitivity to drug reward, the finding that BSR and drugs of abuse have opposite effects on <strong>GluR1</strong> expression in this region may provide an explanation for why the reward related effects of many drugs (cocaine, <b>morphine</b>, amphetamine, PCP, nicotine) do not sensitize with repeated testing in BSR procedures that quantify reward strength.
+GRIA1	addiction	reward	11425507	Considering that elevated <strong>GluR1</strong> expression in the VTA has been associated with increased sensitivity to drug <b>reward</b>, the finding that BSR and drugs of abuse have opposite effects on <strong>GluR1</strong> expression in this region may provide an explanation for why the <b>reward</b> related effects of many drugs (cocaine, morphine, amphetamine, PCP, nicotine) do not sensitize with repeated testing in BSR procedures that quantify <b>reward</b> strength.
+GRIA1	drug	amphetamine	11290405	Repeated <b>amphetamine</b> treatment did not significantly alter <strong>GluR1</strong> 4 levels measured 30 min after the third or tenth <b>amphetamine</b> injection, even though locomotor sensitization was obtained.
+GRIA1	addiction	sensitization	11290405	Repeated amphetamine treatment did not significantly alter <strong>GluR1</strong> 4 levels measured 30 min after the third or tenth amphetamine injection, even though locomotor <b>sensitization</b> was obtained.
+GRIA1	drug	benzodiazepine	11248104	In contrast, dl alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptor <strong>GluR1</strong> subunit mRNA and cognate protein, which are normal during the early phase of <b>diazepam</b> withdrawal, increase by approximately 30% in cortex and hippocampus in association with the appearance of signs of dependence 96 h after <b>diazepam</b> withdrawal.
+GRIA1	addiction	dependence	11248104	In contrast, dl alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptor <strong>GluR1</strong> subunit mRNA and cognate protein, which are normal during the early phase of diazepam withdrawal, increase by approximately 30% in cortex and hippocampus in association with the appearance of signs of <b>dependence</b> 96 h after diazepam withdrawal.
+GRIA1	addiction	withdrawal	11248104	In contrast, dl alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptor <strong>GluR1</strong> subunit mRNA and cognate protein, which are normal during the early phase of diazepam <b>withdrawal</b>, increase by approximately 30% in cortex and hippocampus in association with the appearance of signs of dependence 96 h after diazepam <b>withdrawal</b>.
+GRIA1	addiction	aversion	10684909	Distinct sites of opiate reward and <b>aversion</b> within the midbrain identified using a herpes simplex virus vector expressing <strong>GluR1</strong>.
+GRIA1	addiction	reward	10684909	Distinct sites of opiate <b>reward</b> and aversion within the midbrain identified using a herpes simplex virus vector expressing <strong>GluR1</strong>.
+GRIA1	drug	opioid	10684909	Repeated administration of <b>morphine</b> increases expression of <strong>GluR1</strong> (an AMPA glutamate receptor subunit) in the ventral tegmental area (VTA) of the midbrain, an important neural substrate for the rewarding actions of <b>morphine</b>.
+GRIA1	drug	opioid	10684909	Microinjections of a herpes simplex virus (HSV) vector that causes local overexpression of <strong>GluR1</strong> (HSV <strong>GluR1</strong>) into the VTA can enhance the ability of <b>morphine</b> to establish conditioned place preferences, suggesting that altered <strong>GluR1</strong> expression in this region is directly associated with changes in the rewarding efficacy of <b>morphine</b>.
+GRIA1	drug	opioid	10684909	We now report that in rats given HSV <strong>GluR1</strong> directly into the VTA, <b>morphine</b> is most rewarding when maximal transgene expression is in the rostral VTA, whereas <b>morphine</b> is aversive when maximal transgene expression is in the caudal VTA.
+GRIA1	addiction	aversion	10684909	We now report that in rats given HSV <strong>GluR1</strong> directly into the VTA, morphine is most rewarding when maximal transgene expression is in the rostral VTA, whereas morphine is <b>aversive</b> when maximal transgene expression is in the caudal VTA.
+GRIA1	drug	cocaine	10349849	<strong>GluR1</strong>, GluR2/3, and NMDAR1 subunits of glutamate receptors were quantified from immunoblots in these brain nuclei in rats at 24 h and 3 weeks after discontinuing 1 week of daily <b>cocaine</b> injections.
+GRIA1	addiction	sensitization	10349849	The subjects that developed behavioral <b>sensitization</b> showed a significant increase in <strong>GluR1</strong> levels in the nucleus accumbens at 3 weeks but not at 24 h of withdrawal.
+GRIA1	addiction	withdrawal	10349849	The subjects that developed behavioral sensitization showed a significant increase in <strong>GluR1</strong> levels in the nucleus accumbens at 3 weeks but not at 24 h of <b>withdrawal</b>.
+GRIA1	addiction	withdrawal	10349849	Conversely, sensitized animals showed a significant increase in NMDAR1 and <strong>GluR1</strong> levels in the ventral tegmental area at 1 day but not at 3 weeks of <b>withdrawal</b>.
+GRIA1	addiction	withdrawal	10231131	In the NAc, <strong>GluR1</strong> and GluR2 immunolabeling were unchanged after 3 days of <b>withdrawal</b>, but both were decreased significantly after 14 days of <b>withdrawal</b> (<strong>GluR1</strong>, 85.5+/ 2.6% of control group, P<0.01; GluR2, 79.2+/ 3.2%, P<0.01).
+GRIA1	addiction	withdrawal	10231131	Analysis of core and shell subregions at the 14 day <b>withdrawal</b> time indicated that <strong>GluR1</strong> immunolabeling decreased significantly in shell, while GluR2 immunolabeling decreased significantly in both core and shell.
+GRIA1	addiction	withdrawal	10231131	In the PFC, <strong>GluR1</strong> immunolabeling increased after 3 days of <b>withdrawal</b> (115.3+/ 7.0%, P<0.01) but returned to control levels after 14 days.
+GRIA1	drug	benzodiazepine	9597158	It is believed that the supersensitivity to kainic acid, convulsions and anxiety, and the increased expression of <strong>GLuR1</strong>, R2, and R3 may be parts of the mechanism of <b>diazepam</b> dependence.
+GRIA1	addiction	dependence	9597158	It is believed that the supersensitivity to kainic acid, convulsions and anxiety, and the increased expression of <strong>GLuR1</strong>, R2, and R3 may be parts of the mechanism of diazepam <b>dependence</b>.
+GRIA1	drug	opioid	9242609	It also selectively increases expression of <strong>GluR1</strong> (an AMPA glutamate receptor subunit) in the ventral tegmental area, a midbrain region implicated in <b>morphine</b> action.
+GRIA1	drug	opioid	9242609	By viral mediated gene transfer, a causal relation is shown between these behavioral and biochemical adaptations: <b>Morphine</b>'s stimulant and rewarding properties are intensified after microinjections of a viral vector expressing <strong>GluR1</strong> into the ventral tegmental area.
+GRIA1	drug	amphetamine	9183816	Repeated <b>amphetamine</b> administration decreased levels of <strong>GluR1</strong> and GluR2 but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal.
+GRIA1	addiction	withdrawal	9183816	Repeated amphetamine administration decreased levels of <strong>GluR1</strong> and GluR2 but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day <b>withdrawal</b> time; no changes were observed after 3 days of <b>withdrawal</b>.
+GRIA1	addiction	withdrawal	9183816	In contrast, levels of <strong>GluR1</strong> mRNA in the PFC were increased at 3 but not 14 days of <b>withdrawal</b>, while GluR2 and 3 mRNAs were unchanged.
+GRIA1	drug	cocaine	8613793	By immunoblotting procedures using subunit specific antibodies, we found that repeated, but not acute, <b>cocaine</b> treatment increased the levels of immunoreactivity of <strong>GluR1</strong> (an AMPA receptor subunit) and NMDAR1 (an NMDA receptor subunit) in the ventral tegmental area (VTA), a nucleus containing mesolimbic DA neurons.
+GRIA1	drug	opioid	8613793	Although <b>morphine</b> delivered by subcutaneous pellet implantation had no significant effect on subunit levels, <b>morphine</b> delivered intermittently by subcutaneous injections of escalating doses elevated <strong>GluR1</strong> levels in the VTA.
+GRIA1	drug	cocaine	8613793	Unlike <b>cocaine</b>, morphine, and stress, repeated treatment with other psychotropic drugs (haloperidol, raclopride, sertraline, and desipramine) that lack reinforcing or sensitizing properties did not regulate <strong>GluR1</strong> or NMDAR1 subunit levels in the VTA.
+GRIA1	drug	opioid	8613793	Unlike cocaine, <b>morphine</b>, and stress, repeated treatment with other psychotropic drugs (haloperidol, raclopride, sertraline, and desipramine) that lack reinforcing or sensitizing properties did not regulate <strong>GluR1</strong> or NMDAR1 subunit levels in the VTA.
+GRIA1	addiction	reward	8613793	Unlike cocaine, morphine, and stress, repeated treatment with other psychotropic drugs (haloperidol, raclopride, sertraline, and desipramine) that lack <b>reinforcing</b> or sensitizing properties did not regulate <strong>GluR1</strong> or NMDAR1 subunit levels in the VTA.
+GRIA1	drug	alcohol	8869159	It was found that long term, but not short term, <b>ethanol</b> exposure increased levels of immunoreactivity of the NMDAR1 subunit, an obligatory component of NMDA glutamate receptors, and of the <strong>GluR1</strong> subunit, a component of many AMPA glutamate receptors; but at the same time, long term <b>ethanol</b> exposure decreased immunoreactivity levels of the alpha 1 subunit of the GABAA receptor complex.
+ALDH2	drug	alcohol	32687612	Interaction of <b>Ethanol</b> and Oral ANS 6637, a Selective <strong>ALDH2</strong> Inhibitor in Males: A Randomized, Double Blind, Placebo Controlled, Single Ascending Dose Cohort Study.
+ALDH2	drug	alcohol	32687612	ANS 6637, an orally bioavailable selective and reversible aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) inhibitor, is under development for drug and <b>alcohol</b> use disorders.
+ALDH2	drug	alcohol	32687612	During the elimination of <b>alcohol</b>, <strong>ALDH2</strong> metabolizes acetaldehyde to acetate; inhibiting this enzyme can lead to aversive reactions due to the accumulation of acetaldehyde.
+ALDH2	addiction	aversion	32687612	During the elimination of alcohol, <strong>ALDH2</strong> metabolizes acetaldehyde to acetate; inhibiting this enzyme can lead to <b>aversive</b> reactions due to the accumulation of acetaldehyde.
+ALDH2	drug	alcohol	32127485	Reply to Brewer: Liver targeted <strong>ALDH2</strong> inhibition may reduce <b>alcohol</b> seeking behaviors with limited side effects.
+ALDH2	addiction	relapse	32127485	Reply to Brewer: Liver targeted <strong>ALDH2</strong> inhibition may reduce alcohol <b>seeking</b> behaviors with limited side effects.
+ALDH2	drug	alcohol	32084087	Impacts of interactions between ADH1B and <strong>ALDH2</strong> genotypes on <b>alcohol</b> flushing, <b>alcohol</b> reeking on the day after drinking, and age distribution in Japanese <b>alcohol</b> dependent men.
+ALDH2	drug	alcohol	32084087	The fast metabolizing ADH1B*2(+) genotype (*1/*2 or *2/*2) and the inactive <strong>ALDH2</strong>*2(+) genotype (*1/*2 or *2/*2) affected the multivariate odds ratios for current or former flushing [odds ratio, 95% confidence interval = 2.27 (1.79 2.86) and 23.0 (18.6 28.5), respectively, vs. *2( ) genotype] and for <b>alcohol</b> reeking [0.39 (0.29 0.52) and 1.56 (1.09 2.25), respectively, vs. *2( ) genotype].
+ALDH2	drug	alcohol	32084087	These findings support the protective roles of the ADH1B*2(+) and <strong>ALDH2</strong>*2(+) genotypes against the development of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	32084087	These findings support the protective roles of the ADH1B*2(+) and <strong>ALDH2</strong>*2(+) genotypes against the development of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	32062779	High <b>Ethanol</b> and Acetaldehyde Inhibit Glutamatergic Transmission in the Hippocampus of <strong>Aldh2</strong> Knockout and C57BL/6N Mice: an In Vivo and Ex Vivo Analysis.
+ALDH2	drug	alcohol	32062779	We aimed to investigate whether <b>ethanol</b> (EtOH) and acetaldehyde (AcH) can affect glutamate and its receptors GluN1 and GluA1 in the hippocampus of <strong>Aldh2</strong> knockout (<strong>Aldh2</strong> KO) and C57BL/6N (wild type (WT)) mice.
+ALDH2	drug	alcohol	31870920	To answer these questions, we measured the expression and activity of <b>alcohol</b> dehydrogenase 1 (ADH1) and acetaldehyde dehydrogenase 2 (<strong>ALDH2</strong>) enzymes, <b>ethanol</b> and acetaldehyde levels in vivo, and binge like and preferential drinking behaviors with drinking in the dark and two bottle choice in animal models with liver injury.
+ALDH2	addiction	intoxication	31870920	To answer these questions, we measured the expression and activity of alcohol dehydrogenase 1 (ADH1) and acetaldehyde dehydrogenase 2 (<strong>ALDH2</strong>) enzymes, ethanol and acetaldehyde levels in vivo, and <b>binge</b> like and preferential drinking behaviors with drinking in the dark and two bottle choice in animal models with liver injury.
+ALDH2	drug	alcohol	31845443	To elucidate associations among liver disease, lipid profile, body mass index (BMI), ketonuria, and meal skipping under the influence of <b>alcohol</b> dehydrogenase 1B (ADH1B; rs1229984) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>; rs671) genotypes in men with <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	31845443	To elucidate associations among liver disease, lipid profile, body mass index (BMI), ketonuria, and meal skipping under the influence of alcohol dehydrogenase 1B (ADH1B; rs1229984) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>; rs671) genotypes in men with alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	31792171	Aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), a key enzyme for detoxification the <b>ethanol</b> metabolite acetaldehyde, is recognized as a promising therapeutic target to treat <b>alcohol</b> use disorders (AUDs).
+ALDH2	drug	alcohol	31792171	<b>Disulfiram</b>, a potent <strong>ALDH2</strong> inhibitor, is an approved drug for the treatment of AUD but has clinical limitations due to its side effects.
+ALDH2	drug	alcohol	31792171	This study aims to elucidate the relative contribution of different organs in acetaldehyde clearance through <strong>ALDH2</strong> by using global  (<strong>Aldh2</strong>  / ) and tissue specific <strong>Aldh2</strong> deficient mice, and to examine whether liver specific <strong>ALDH2</strong> inhibition can prevent <b>alcohol</b> seeking behavior.
+ALDH2	addiction	relapse	31792171	This study aims to elucidate the relative contribution of different organs in acetaldehyde clearance through <strong>ALDH2</strong> by using global  (<strong>Aldh2</strong>  / ) and tissue specific <strong>Aldh2</strong> deficient mice, and to examine whether liver specific <strong>ALDH2</strong> inhibition can prevent alcohol <b>seeking</b> behavior.
+ALDH2	drug	alcohol	31792171	<strong>Aldh2</strong>  /  mice showed markedly higher acetaldehyde concentrations than wild type (WT) mice after acute <b>ethanol</b> gavage.
+ALDH2	drug	alcohol	31792171	In the 2 bottle paradigm and the drinking in the dark model, <strong>Aldh2</strong>  /  mice drank negligible volumes from <b>ethanol</b> containing bottles, whereas <strong>Aldh2</strong> Hep /  mice showed reduced <b>alcohol</b> preference at high but not low <b>alcohol</b> concentrations.
+ALDH2	drug	alcohol	31792171	Glial cell  or neuron specific <strong>Aldh2</strong> deficiency did not affect voluntary <b>alcohol</b> consumption.
+ALDH2	drug	alcohol	31792171	Finally, specific liver <strong>Aldh2</strong> knockdown via injection of shAldh2 markedly decreased <b>alcohol</b> preference.
+ALDH2	drug	alcohol	31697578	Introduction: Aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) is a main contributor of the <b>alcohol</b> elimination process.
+ALDH2	drug	alcohol	31697578	Functional polymorphism in the <strong>ALDH2</strong> gene and its inactive form causes unpleasant flushing responses after <b>alcohol</b> consumption and prevents excessive <b>alcohol</b> intake.
+ALDH2	drug	alcohol	31697578	Additionally, <strong>ALDH2</strong> is involved in the elimination of metabolites of neurotransmitters like 3,4 dihydroxyphenylacetaldehyde (DOPAL) and 3,4 dihydroxyphenylglycoaldehyde (DOPGAL) in the central nervous system (CNS).Areas covered: We examine the role of <strong>ALDH2</strong> polymorphism in disease, aging and <b>alcohol</b> addiction and discuss its pharmacological targeting.
+ALDH2	addiction	addiction	31697578	Additionally, <strong>ALDH2</strong> is involved in the elimination of metabolites of neurotransmitters like 3,4 dihydroxyphenylacetaldehyde (DOPAL) and 3,4 dihydroxyphenylglycoaldehyde (DOPGAL) in the central nervous system (CNS).Areas covered: We examine the role of <strong>ALDH2</strong> polymorphism in disease, aging and alcohol <b>addiction</b> and discuss its pharmacological targeting.
+ALDH2	addiction	reward	31550440	Based on the theory that brain acetaldehyde accumulation is associated with the <b>reinforcing</b> properties of EtOH, this study sought to determine brain CAT and <strong>ALDH2</strong> expression in limbic areas of control and Pb exposed animals after voluntary EtOH intake.
+ALDH2	drug	alcohol	31018006	Then, <b>alcohol</b> dehydrogenase (ADH1) and aldehyde dehydrogenase (<strong>ALDH2</strong>) protein levels and enzymatic activities in the livers were quantified.
+ALDH2	drug	alcohol	31018006	The studies show that treatment with fenofibrate not only increased the activity of catalase in the liver of <b>alcohol</b> drinking rats, as reported earlier, but also increased the levels and enzymatic activity of ADH1, while <strong>ALDH2</strong> remained unchanged.
+ALDH2	drug	alcohol	31018006	Tras eso, se midieron los niveles hepáticos y actividades enzimáticas de <b>alcohol</b> deshidrogenasa (ADH1) y de aldehído deshidrogenasa (<strong>ALDH2</strong>).
+ALDH2	drug	alcohol	31018006	Los resultados muestran que el tratamiento con fenofibrato no solo aumenta la actividad de catalasa en el hígado de ratas bebedoras de <b>alcohol</b>, sino que también incrementa los niveles y la actividad de ADH1, sin alterar <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	30931596	Genetic variants in two enzymes involved in the metabolism of <b>ethanol</b>, <b>alcohol</b> dehydrogenase ADH1B *2 and aldehyde dehydrogenase <strong>ALDH2</strong> *2 through increasing the blood level of acetaldehyde, may play a "protective" role against <b>alcoholism</b>.
+ALDH2	drug	alcohol	30852706	Variations in genes affecting <b>alcohol</b> metabolism (ADH1B, <strong>ALDH2</strong>) are protective against both <b>alcohol</b> dependence and excessive consumption, but different variants are found in different populations.
+ALDH2	addiction	dependence	30852706	Variations in genes affecting alcohol metabolism (ADH1B, <strong>ALDH2</strong>) are protective against both alcohol <b>dependence</b> and excessive consumption, but different variants are found in different populations.
+ALDH2	addiction	dependence	30852706	ADH1B and <strong>ALDH2</strong> strongly affect both consumption and <b>dependence</b>.
+ALDH2	drug	alcohol	30629674	Endoscopic screening using esophageal iodine staining and genotypes of ADH1B and <strong>ALDH2</strong> in Japanese <b>alcohol</b> dependent women.
+ALDH2	drug	alcohol	30629674	Several risk factors for DIULs, including genetic polymorphisms of <b>alcohol</b> and aldehyde dehydrogenases (ADH1B, rs1229984; <strong>ALDH2</strong>, rs671), have been demonstrated in Japanese <b>alcohol</b> dependent men.
+ALDH2	drug	alcohol	30629674	The low sensitivity in the present study suggests that a lack of <b>alcohol</b> flushing may play a crucial role in the development of <b>alcohol</b> dependence in women with inactive <strong>ALDH2</strong>.
+ALDH2	addiction	dependence	30629674	The low sensitivity in the present study suggests that a lack of alcohol flushing may play a crucial role in the development of alcohol <b>dependence</b> in women with inactive <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	30629674	No significant differences in age, usual <b>alcohol</b> consumption, or smoking habits were observed according to ADH1B and <strong>ALDH2</strong> genotypes.
+ALDH2	drug	nicotine	30629674	No significant differences in age, usual alcohol consumption, or <b>smoking</b> habits were observed according to ADH1B and <strong>ALDH2</strong> genotypes.
+ALDH2	drug	alcohol	30521820	Activation of mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>) by ALDA 1 reduces both the acquisition and maintenance of <b>ethanol</b> intake in rats: A dual mechanism?
+ALDH2	drug	alcohol	30521820	Recently, it was described that N (1,3 benzodioxol 5 ylmethyl) 2,6 dichlorobenzamide (ALDA 1) activates aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), enzyme that catalyzes the oxidation of <b>ethanol</b> derived acetaldehyde to acetate.
+ALDH2	drug	alcohol	30521820	The study shows that the activation of <strong>ALDH2</strong> by ALDA 1 is effective for inhibiting both the acquisition and the maintenance of chronic <b>ethanol</b> intake by <b>alcohol</b> preferring rats.
+ALDH2	drug	alcohol	30521820	Thus, the activation of brain <strong>ALDH2</strong> may constitute a novel approach in the treatment of <b>alcohol</b> use disorders.
+ALDH2	drug	alcohol	30470859	Gene expression of enzymes involved in the metabolism of <b>ethanol</b>, i.e., Adh1 and <strong>Aldh2</strong>, were altered by hypothyroidism and T4/T3 supplementation.
+ALDH2	drug	alcohol	30121625	<b>Alcohol</b> inhibits T cell glucose metabolism and hepatitis in <strong>ALDH2</strong> deficient mice and humans: roles of acetaldehyde and glucocorticoids.
+ALDH2	drug	alcohol	30121625	Individuals with inactive <strong>ALDH2</strong> accumulate acetaldehyde after <b>alcohol</b> consumption.
+ALDH2	drug	alcohol	30121625	Wild type (WT) and <strong>Aldh2</strong> knockout (<strong>Aldh2</strong>  / ) mice were subjected to chronic <b>ethanol</b> feeding and concanavalin A (ConA) induced T cell hepatitis.
+ALDH2	drug	alcohol	30121625	<b>Ethanol</b> feeding exacerbated ConA induced hepatitis in WT mice but surprisingly attenuated it in <strong>Aldh2</strong>  /  mice despite higher acetaldehyde levels in <strong>Aldh2</strong>  /  mice.
+ALDH2	drug	alcohol	30121625	Elevation of serum cytokines and their downstream signals in the liver post ConA injection was attenuated in <b>ethanol</b> fed <strong>Aldh2</strong>  /  mice compared to WT mice.
+ALDH2	drug	alcohol	30121625	Finally, compared to WT mice, <b>ethanol</b> fed <strong>Aldh2</strong>  /  mice had higher levels of serum corticosterone, a well known factor that inhibits aerobic glycolysis.
+ALDH2	drug	alcohol	30121625	Blockade of corticosterone partially restored ConA mediated hepatitis in <b>ethanol</b> fed <strong>Aldh2</strong>  /  mice.
+ALDH2	drug	alcohol	30121625	Acute <b>alcohol</b> drinking elevated plasma cortisol and corticosterone levels in human subjects with higher levels in those with inactive <strong>ALDH2</strong> than those with active <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	30121625	<strong>ALDH2</strong> deficiency is associated with elevated acetaldehyde and glucocorticoids post <b>alcohol</b> consumption, thereby inhibiting T cell activation and hepatitis.
+ALDH2	drug	alcohol	29779728	The <strong>ALDH2</strong> gene was hypothesized to alter genetic susceptibility to <b>alcohol</b> dependence and <b>alcohol</b> induced liver diseases.
+ALDH2	addiction	dependence	29779728	The <strong>ALDH2</strong> gene was hypothesized to alter genetic susceptibility to alcohol <b>dependence</b> and alcohol induced liver diseases.
+ALDH2	drug	alcohol	29582627	ADH1B, <strong>ALDH2</strong>, GSTM1 and GSTT1 Gene Polymorphic Frequencies among <b>Alcoholics</b> and Controls in the Arcadian Population of Central India Background: Epidemiological research has highlighted the global burden of primary liver cancer cases due to <b>alcohol</b> consumption, even in a low consumption country like India.
+ALDH2	drug	alcohol	29582627	<b>Alcohol</b> detoxification is governed by ADH1B, <strong>ALDH2</strong>, GSTM1 and GSTT1 genes that encode functional enzymes which are coordinated with each other to remove highly toxic metabolites i.e.
+ALDH2	drug	alcohol	29582627	Methods: The aim of this study was to screen the arcadian population of central India in order to investigate and compare the genotype distribution and allele frequencies of <b>alcohol</b> metabolizing genes (ADH1B, <strong>ALDH2</strong>, GSTM1 and GSTT1) in both <b>alcoholic</b> (N=121) and control (N=145) healthy subjects.
+ALDH2	drug	alcohol	29460428	All 3 traits showed genomewide significant association with variants near <strong>ALDH2</strong>, with significance ranging from 2.01 × 10 14 (for flushing; lead single nucleotide polymorphism (SNP) PTPN11* rs143894582) to pmeta = 5.80 × 10 10 (for <b>alcohol</b> dependence criterion count; lead SNP rs149212747).
+ALDH2	addiction	dependence	29460428	All 3 traits showed genomewide significant association with variants near <strong>ALDH2</strong>, with significance ranging from 2.01 × 10 14 (for flushing; lead single nucleotide polymorphism (SNP) PTPN11* rs143894582) to pmeta = 5.80 × 10 10 (for alcohol <b>dependence</b> criterion count; lead SNP rs149212747).
+ALDH2	drug	alcohol	29084628	We evaluated the presence of SNPs in the ADH (ADH1B, ADH1C, and ADH4) and ALDH (<strong>ALDH2</strong>) genes in <b>alcohol</b> users of Goiânia, State of Goiás   Brazil, and then we established a possible relationship with AUD by allelic and genotypic study.
+ALDH2	drug	alcohol	29063269	Slow metabolizing ADH1B and inactive heterozygous <strong>ALDH2</strong> increase vulnerability to fatty liver in Japanese men with <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	29063269	Slow metabolizing ADH1B and inactive heterozygous <strong>ALDH2</strong> increase vulnerability to fatty liver in Japanese men with alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	29063269	Genetic polymorphisms of <b>alcohol</b> dehydrogenase 1B (ADH1B; rs1229984, His48Arg) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>; rs671, Glu504Lys) affect body weight, body fat, and lipid metabolism in individuals with <b>alcohol</b> dependence, and the aim of this study was to identify their determinants in relation to the development of fatty liver.
+ALDH2	addiction	dependence	29063269	Genetic polymorphisms of alcohol dehydrogenase 1B (ADH1B; rs1229984, His48Arg) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>; rs671, Glu504Lys) affect body weight, body fat, and lipid metabolism in individuals with alcohol <b>dependence</b>, and the aim of this study was to identify their determinants in relation to the development of fatty liver.
+ALDH2	drug	alcohol	29063269	We evaluated associations between the presence of fatty liver and ADH1B and <strong>ALDH2</strong> genotypes and other factors in 1604 Japanese men who had been admitted for treatment of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	29063269	We evaluated associations between the presence of fatty liver and ADH1B and <strong>ALDH2</strong> genotypes and other factors in 1604 Japanese men who had been admitted for treatment of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	29063269	Age adjusted usual <b>alcohol</b> intake did not differ according to ADH1B or <strong>ALDH2</strong> genotypes.
+ALDH2	drug	alcohol	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, ADH1C, OPRM1, DRD2, BDNF, and <strong>ALDH2</strong> genes on <b>alcohol</b> dependence in a Caucasian population.
+ALDH2	addiction	dependence	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, ADH1C, OPRM1, DRD2, BDNF, and <strong>ALDH2</strong> genes on alcohol <b>dependence</b> in a Caucasian population.
+ALDH2	drug	alcohol	28750942	A standardized extract of the fruit of Hovenia dulcis alleviated <b>alcohol</b> induced hangover in healthy subjects with heterozygous <strong>ALDH2</strong>: A randomized, controlled, crossover trial.
+ALDH2	drug	alcohol	28750942	Twenty six eligible male adults with heterozygous <strong>ALDH2</strong> (23.7±0.3 years old) consumed 360mL of Korean Soju (50g <b>alcohol</b>) together with HDE (2460mg) or matched placebo with subsequent crossover.
+ALDH2	drug	alcohol	28728635	Among northeast Asians, the variant aldehyde dehydrogenase allele, <strong>ALDH2</strong>*2 (rs671, A/G, minor/major), has been inversely associated with <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	28728635	Among northeast Asians, the variant aldehyde dehydrogenase allele, <strong>ALDH2</strong>*2 (rs671, A/G, minor/major), has been inversely associated with alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	28728635	This study examined <strong>ALDH2</strong> gene status as a moderator of the associations between parental drinking, peer drinking, and acculturation with <b>alcohol</b> use among 222 Chinese American and Korean American college freshmen.
+ALDH2	drug	alcohol	28728635	Negative binomial regressions were used to test the main and interactive effects of <strong>ALDH2</strong> with contextual factors on <b>alcohol</b> frequency (drinking days) and quantity (drinks per drinking day) in the past 3 months.
+ALDH2	drug	alcohol	28728635	<strong>ALDH2</strong>*2 was associated with more subjective flushing symptoms and longer length of flushing but was unrelated to both <b>alcohol</b> frequency and quantity.
+ALDH2	drug	alcohol	28728635	Peer drinking was positively associated with both <b>alcohol</b> frequency and quantity, but neither was moderated by <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	28728635	We observed a nonsignificant trend for the interaction between parental drinking and <strong>ALDH2</strong> on <b>alcohol</b> frequency, where parental drinking was positively associated with <b>alcohol</b> frequency only among participants with <strong>ALDH2</strong>*2.
+ALDH2	drug	alcohol	28728635	We found a significant interaction between acculturation and <strong>ALDH2</strong> on <b>alcohol</b> frequency, where acculturation was positively associated with <b>alcohol</b> frequency only among those with <strong>ALDH2</strong>*2.
+ALDH2	drug	alcohol	28728635	Parental drinking and acculturation may facilitate more frequent drinking among those who have more intense reactions to <b>alcohol</b> (i.e., those with <strong>ALDH2</strong>*2) during the transition from high school to college.
+ALDH2	drug	alcohol	28578603	Most <b>ethanol</b> is broken down in the liver in two steps by <b>alcohol</b> dehydrogenase (ADH) and aldehyde dehydrogenase (<strong>ALDH2</strong>) enzymes, which metabolize down <b>ethanol</b> into acetaldehyde and then acetate.
+ALDH2	drug	alcohol	28578603	These results suggest that gene therapy could be a useful tool for the treatment of <b>alcoholism</b> by knocking down <strong>ALDH2</strong> expression using shRNA technology delivered by AAV vectors.
+ALDH2	drug	alcohol	28485404	We observed the strongest association between the previously reported single nucleotide polymorphism (SNP) rs671 in <strong>ALDH2</strong> and <b>alcohol</b> drinker status (odd ratio (OR)=0.40, P=2.28 × 10 72) in East Asians, and also an effect on drinks/week (beta= 0.17, P=5.42 × 10 4) in the same group.
+ALDH2	drug	alcohol	28485404	Although prior studies reported effects of ADH1B and <strong>ALDH2</strong> on lifetime measures, such as risk of <b>alcohol</b> dependence, our study adds further evidence of the effect of the same genes on a cross sectional measure of average drinking.
+ALDH2	addiction	dependence	28485404	Although prior studies reported effects of ADH1B and <strong>ALDH2</strong> on lifetime measures, such as risk of alcohol <b>dependence</b>, our study adds further evidence of the effect of the same genes on a cross sectional measure of average drinking.
+ALDH2	drug	alcohol	28471244	The <strong>ALDH2</strong>*2 allele (A allele) at rs671 is more commonly carried by Asians and is associated with <b>alcohol</b> related flushing, a strong adverse reaction to <b>alcohol</b> that is protective against drinking.
+ALDH2	drug	alcohol	28471244	This study examined the interplay between <strong>ALDH2</strong>*2, peer drinking, and <b>alcohol</b> consumption in college students.
+ALDH2	drug	alcohol	28471244	We hypothesized that the relationship between <strong>ALDH2</strong>*2 and standard grams of <b>ethanol</b> per month would vary based on the level of peer drinking.
+ALDH2	drug	alcohol	28471244	Main effects of <strong>ALDH2</strong>*2( ) and having more friends who got drunk were associated with greater <b>alcohol</b> consumption.
+ALDH2	drug	alcohol	28471244	The <strong>ALDH2</strong>*2 × peer drunkenness interaction showed a stronger positive association with <b>alcohol</b> consumption for <strong>ALDH2</strong>*2( ) versus <strong>ALDH2</strong>*2(+) at increasing levels of peer drunkenness.
+ALDH2	drug	alcohol	28471244	Follow up comparisons within each peer drunkenness level identified significantly higher <b>alcohol</b> consumption for <strong>ALDH2</strong>*2( ) compared to <strong>ALDH2</strong>*2(+) at the all friends got drunk level.
+ALDH2	drug	alcohol	28471244	There was evidence of a stronger effect for <strong>ALDH2</strong>*2( ) compared to <strong>ALDH2</strong>*2(+) with greater <b>alcohol</b> use when students were more exposed to peer drinking.
+ALDH2	drug	alcohol	28430929	Promoter Polymorphism rs886205 Genotype Interacts With DNA Methylation of the <strong>ALDH2</strong> Regulatory Region in <b>Alcohol</b> Dependence.
+ALDH2	addiction	dependence	28430929	Promoter Polymorphism rs886205 Genotype Interacts With DNA Methylation of the <strong>ALDH2</strong> Regulatory Region in Alcohol <b>Dependence</b>.
+ALDH2	drug	alcohol	28430929	Aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) protects cells from <b>ethanol</b> toxicity by metabolizing acetaldehyde.
+ALDH2	drug	alcohol	28430929	Our results describe a new regulatory role of rs886205 in the methylation of <strong>ALDH2</strong> promoter region and provide additional insight into the complex regulation of <strong>ALDH2</strong> under the condition of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	28430929	Our results describe a new regulatory role of rs886205 in the methylation of <strong>ALDH2</strong> promoter region and provide additional insight into the complex regulation of <strong>ALDH2</strong> under the condition of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	28430929	We investigated the association between the polymorphism rs886205, located on <strong>ALDH2</strong> promoter and methylation kinetics of the neighboring CpG island in <b>alcohol</b> dependent patients.
+ALDH2	drug	alcohol	28109342	The present study sought to interfere with <b>ethanol</b> metabolism by inhibiting <strong>ALDH2</strong> (mitochondrial aldehyde dehydrogenase) activity in both liver and brain from control and Pb exposed rats as a strategy to accumulate ACD, a substance that plays a major role in the drug's reinforcing and/or aversive effects.
+ALDH2	addiction	aversion	28109342	The present study sought to interfere with ethanol metabolism by inhibiting <strong>ALDH2</strong> (mitochondrial aldehyde dehydrogenase) activity in both liver and brain from control and Pb exposed rats as a strategy to accumulate ACD, a substance that plays a major role in the drug's reinforcing and/or <b>aversive</b> effects.
+ALDH2	addiction	reward	28109342	The present study sought to interfere with ethanol metabolism by inhibiting <strong>ALDH2</strong> (mitochondrial aldehyde dehydrogenase) activity in both liver and brain from control and Pb exposed rats as a strategy to accumulate ACD, a substance that plays a major role in the drug's <b>reinforcing</b> and/or aversive effects.
+ALDH2	drug	alcohol	28109342	Systemic CY administration reduced the elevated <b>ethanol</b> intake already reported in the Pb exposed animals (but not in the controls) accompanied by liver (but not brain) <strong>ALDH2</strong> inactivation.
+ALDH2	drug	alcohol	28109342	CY administration enhanced both <b>ethanol</b> intake and locomotor activity accompanied by brain <strong>ALDH2</strong> inactivation in control animals, while an increase in <b>ethanol</b> consumption was also observed in the Pb exposed group, although in the absence of brain <strong>ALDH2</strong> blockade.
+ALDH2	drug	alcohol	28098394	The inactive aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) and highly active <b>alcohol</b> dehydrogenase 1B (ADH1B) genes are protective factors for the development of AUD.
+ALDH2	drug	alcohol	28098394	The inactive <strong>ALDH2</strong> provides its protective effect through the accumulation of acetaldehyde after consuming <b>alcohol</b>, resulting in unpleasant effects, and heightened sensitivity to <b>alcohol</b>.
+ALDH2	addiction	addiction	28052001	Genetic polymorphisms in <strong>ALDH2</strong> are associated with drug <b>addiction</b> in a Chinese Han population.
+ALDH2	drug	alcohol	28052001	We investigated the association between single nucleotide polymorphisms (SNPs) in <strong>ALDH2</strong>, which has been associated with <b>alcohol</b> dependence and several types of diseases, and the risk of drug addiction in a Chinese Han population.
+ALDH2	addiction	addiction	28052001	We investigated the association between single nucleotide polymorphisms (SNPs) in <strong>ALDH2</strong>, which has been associated with alcohol dependence and several types of diseases, and the risk of drug <b>addiction</b> in a Chinese Han population.
+ALDH2	addiction	dependence	28052001	We investigated the association between single nucleotide polymorphisms (SNPs) in <strong>ALDH2</strong>, which has been associated with alcohol <b>dependence</b> and several types of diseases, and the risk of drug addiction in a Chinese Han population.
+ALDH2	addiction	addiction	28052001	Our findings showed that <strong>ALDH2</strong> polymorphisms are significantly associated with the risk of drug <b>addiction</b> in the Chinese Han population.
+ALDH2	drug	alcohol	28032633	PPT enhanced catalase, DPN reduced <strong>ALDH2</strong>, while G1 had no effect on the activity of either enzyme, and none of the agonists influenced <b>alcohol</b> dehydrogenase or CYP2E1 activities in the myocardium.
+ALDH2	drug	alcohol	27991683	We evaluated 989 Japanese <b>alcoholic</b> men to identify the effects of genetic polymorphisms of <b>alcohol</b> dehydrogenase 1B (ADH1B; rs1229984) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>; rs671) on platelet counts during an 8 week in hospital abstinence period.
+ALDH2	drug	alcohol	27991683	In <b>alcoholics</b>, the ADH1B*1/*1 genotype increased the risk of thrombocytopenia upon admission and of a rebound platelet increase 2 weeks thereafter, while the <strong>ALDH2</strong>*1/*1 genotype was associated with lower platelet counts throughout the 8 week hospital stay.
+ALDH2	drug	alcohol	27404720	Acetaldehyde generated from <b>alcohol</b> in the liver is metabolized by the mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>) such that diminishing <strong>ALDH2</strong> activity leads to the aversive effects of blood acetaldehyde upon <b>alcohol</b> intake.
+ALDH2	addiction	aversion	27404720	Acetaldehyde generated from alcohol in the liver is metabolized by the mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>) such that diminishing <strong>ALDH2</strong> activity leads to the <b>aversive</b> effects of blood acetaldehyde upon alcohol intake.
+ALDH2	drug	alcohol	27404720	<b>Ethanol</b> intake was curtailed 47% for 34 days (P < 0.0001), while blood acetaldehyde more than doubled upon <b>ethanol</b> administration and <strong>ALDH2</strong> activity dropped 25% in liver homogenates, not affecting other ALDH isoforms.
+ALDH2	drug	alcohol	27404720	Thus, hairpin ribozymes targeted to 16 nt in the <strong>ALDH2</strong> mRNA provide durable and specific effects in vivo, representing an improvement on previous work and encouraging development of gene therapy for <b>alcoholism</b>.
+ALDH2	drug	alcohol	27338962	Functional missense mutations in ADH1B and <strong>ALDH2</strong> are protective against <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	27338962	Functional missense mutations in ADH1B and <strong>ALDH2</strong> are protective against alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	27186430	A polymorphic mutation in the acetaldehyde dehydrogenase 2 (<strong>ALDH2</strong>) gene has been epidemiologically linked to the high susceptibility to esophageal carcinogenesis for individuals with <b>alcohol</b> use disorders.
+ALDH2	drug	alcohol	27186430	Mice subjected to <b>alcohol</b> drinking show increased oxidative stress and DNA adduct formation in esophageal epithelia where <strong>Aldh2</strong> loss augments <b>alcohol</b> induced genotoxic effects; however, it remains elusive as to how esophageal epithelial cells with dysfunctional <strong>Aldh2</strong> cope with oxidative stress related to <b>alcohol</b> metabolism.
+ALDH2	drug	alcohol	27186430	<strong>Aldh2</strong> deficient cells appeared to be highly susceptible to <b>ethanol</b>  or acetaldehyde mediated toxicity.
+ALDH2	drug	alcohol	27186430	<b>Alcohol</b> dehydrogenase mediated acetaldehyde production was implicated in <b>ethanol</b> induced cell injury in <strong>Aldh2</strong> deficient cells as <b>ethanol</b> induced oxidative stress and cell death was partially inhibited by 4 methylpyrazole.
+ALDH2	drug	alcohol	27186430	Acetaldehyde activated autophagy flux in esophageal keratinocytes where <strong>Aldh2</strong> deficiency increased dependence on autophagy to cope with <b>ethanol</b> induced acetaldehyde mediated oxidative stress.
+ALDH2	addiction	dependence	27186430	Acetaldehyde activated autophagy flux in esophageal keratinocytes where <strong>Aldh2</strong> deficiency increased <b>dependence</b> on autophagy to cope with ethanol induced acetaldehyde mediated oxidative stress.
+ALDH2	drug	alcohol	27186430	Defining autophagymediated cytoprotection against <b>alcohol</b> induced genotoxicity in the context of <strong>Aldh2</strong> deficiency, our study provides mechanistic insights into the tumor suppressor functions of <strong>ALDH2</strong> and autophagy in <b>alcohol</b> related esophageal carcinogenesis.
+ALDH2	drug	alcohol	27163368	Certain genetic variants (i.e., alleles)  particularly the ADH1B*2, ADH1B*3, ADH1C*1, and <strong>ALDH2</strong>*2 alleles  have been associated with lower rates of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	27163368	Certain genetic variants (i.e., alleles)  particularly the ADH1B*2, ADH1B*3, ADH1C*1, and <strong>ALDH2</strong>*2 alleles  have been associated with lower rates of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	26968209	Mortality of SHP( / ) mice after <b>ethanol</b> binge feeding was significantly reduced and their acetaldehyde dehydrogenase (<strong>Aldh2</strong>) mRNA level was higher than that of their WT counterparts.
+ALDH2	addiction	intoxication	26968209	Mortality of SHP( / ) mice after ethanol <b>binge</b> feeding was significantly reduced and their acetaldehyde dehydrogenase (<strong>Aldh2</strong>) mRNA level was higher than that of their WT counterparts.
+ALDH2	drug	alcohol	26848198	Characterization of polymorphisms of genes ADH2, ADH3, <strong>ALDH2</strong> and CYP2E1 and relationship to the <b>alcoholism</b> in a Colombian population.
+ALDH2	drug	alcohol	26848198	Identify and characterize polymorphisms of genes ADH2, ADH3, <strong>ALDH2</strong> and CYP2E1 in a Colombian population residing in the city of Bogotá and determine its possible relationship to the <b>alcoholism</b>.
+ALDH2	drug	alcohol	26848198	ADH2, ADH3, <strong>ALDH2</strong>, and CYP2E1 genotypes a population of 148 individuals with non problematic <b>alcohol</b> and 65 individuals with <b>alcoholism</b> were determined with TaqMan probes and PCR RFLP.
+ALDH2	drug	alcohol	26848198	Since substance dependence requires interaction of multiple genes, the combination of genotypes ADH2 * 2, CYP2E1 * 1 combined with genotype homozygous <strong>ALDH2</strong> * 1 found in this study could be leading to the population to a potential risk to <b>alcoholism</b>.
+ALDH2	addiction	dependence	26848198	Since substance <b>dependence</b> requires interaction of multiple genes, the combination of genotypes ADH2 * 2, CYP2E1 * 1 combined with genotype homozygous <strong>ALDH2</strong> * 1 found in this study could be leading to the population to a potential risk to alcoholism.
+ALDH2	drug	alcohol	26848198	Se determinaron los genotipos ADH2, ADH3, <strong>ALDH2</strong> y CYP2E1 a una población de 148 individuos con un consumo no problemático de <b>alcohol</b> y 65 individuos con alcoholismo.
+ALDH2	drug	alcohol	26842247	Genes in <b>alcohol</b> metabolism pathway, especially ADH1B and <strong>ALDH2</strong>, conferred the major genetic risk for AD in Taiwanese Han population.
+ALDH2	drug	alcohol	26339786	Impaired Regulation of <strong>ALDH2</strong> Protein Expression Revealing a Yet Unknown Epigenetic Impact of rs886205 on Specific Methylation of a Negative Regulatory Promoter Region in <b>Alcohol</b> Dependent Patients.
+ALDH2	drug	alcohol	26339786	Acetaldehyde, the carcinogenic metabolite of <b>ethanol</b> known to provoke aversive symptoms of <b>alcohol</b> consumption, is predominantly eliminated by aldehyde dehydrogenase 2 (<strong>ALDH2</strong>).
+ALDH2	addiction	aversion	26339786	Acetaldehyde, the carcinogenic metabolite of ethanol known to provoke <b>aversive</b> symptoms of alcohol consumption, is predominantly eliminated by aldehyde dehydrogenase 2 (<strong>ALDH2</strong>).
+ALDH2	drug	alcohol	26339786	Reduced <strong>ALDH2</strong> activity correlates with low <b>alcohol</b> tolerance and low risk for <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	26339786	Reduced <strong>ALDH2</strong> activity correlates with low alcohol tolerance and low risk for alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	26339786	On the basis of allele dependent epigenetic effects, we analyzed the rs886205 genotype, methylation rates of cytosine phosphatidyl guanine (CpG) sites within a regulatory promoter region and <strong>ALDH2</strong> protein levels in 82 <b>alcohol</b> dependent patients during a 2 week withdrawal and compared them to 34 matched controls.
+ALDH2	addiction	withdrawal	26339786	On the basis of allele dependent epigenetic effects, we analyzed the rs886205 genotype, methylation rates of cytosine phosphatidyl guanine (CpG) sites within a regulatory promoter region and <strong>ALDH2</strong> protein levels in 82 alcohol dependent patients during a 2 week <b>withdrawal</b> and compared them to 34 matched controls.
+ALDH2	addiction	withdrawal	26339786	Patients without the G allele of rs886205 showed higher methylation of the promoter region than controls and readily adapted epigenetically as well as on protein level during <b>withdrawal</b>, while patients with the G allele displayed retarded methylation readjustment and no change in <strong>ALDH2</strong> protein levels.
+ALDH2	drug	alcohol	26318866	We sought to identify associations between aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), <b>alcohol</b> consumption, and hypertension in Japanese men.
+ALDH2	drug	alcohol	26318866	Multiple regression analysis (stepwise method) for blood pressure according to <strong>ALDH2</strong> genetic polymorphism revealed that the amount of daily <b>alcohol</b> intake affected systolic blood pressure in participants who harbored the <strong>ALDH2</strong> genetic polymorphism *1/*2 or *2/*2.
+ALDH2	drug	alcohol	26318866	The interaction between <b>alcohol</b> intake and <strong>ALDH2</strong> genetic polymorphisms might affect systolic blood pressure in adult male workers.
+ALDH2	drug	alcohol	26266540	In the present study, we used human embryonic stem cell (hESC) derived cortical neurons as in vitro cellular models to investigate <b>alcohol</b> induced expression changes of genes involved in <b>alcohol</b> metabolism (<strong>ALDH2</strong>), anti apoptosis (BCL2 and CCND2), neurotransmission (NMDA receptor subunit genes: GRIN1, GRIN2A, GRIN2B, and GRIN2D), calcium channel activity (ITPR2), or transcriptional repression (JARID2).
+ALDH2	drug	alcohol	26230553	Alleles involved in inefficient (ADH1B2*2 and <strong>ALDH2</strong>*2) or efficient (SNP6, ADH4 gene) <b>alcohol</b> metabolism may influence the risk of <b>alcoholism</b>.
+ALDH2	drug	alcohol	26033520	Comorbid <b>alcohol</b> dependence disorder may be related to aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) and <b>alcohol</b> dehydrogenase 1B (ADH1B) in bipolar II disorder, but only to <strong>ALDH2</strong> in bipolar I disorder, in Han Chinese.
+ALDH2	addiction	dependence	26033520	Comorbid alcohol <b>dependence</b> disorder may be related to aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) and alcohol dehydrogenase 1B (ADH1B) in bipolar II disorder, but only to <strong>ALDH2</strong> in bipolar I disorder, in Han Chinese.
+ALDH2	drug	alcohol	26033520	A polymerase chain reaction and restriction fragment length polymorphism analysis was used to determine genotypes for <b>alcohol</b> dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), two <b>alcohol</b> metabolizing enzymes.
+ALDH2	addiction	relapse	26022266	This review summarizes development of a novel aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) inhibitor that specifically targets unique drug related episodic surges in dopamine (DA), a pathophysiologic mechanism that appears to underlie much of drug <b>seeking</b> behavior.
+ALDH2	drug	alcohol	26022266	We have synthesized highly selective novel <strong>ALDH2</strong> inhibitors (ALDH2i) that block <b>alcohol</b>  and cocaine cue induced surges in nucleus accumbens (NAc) DA and prevent reinstatement of <b>alcohol</b> heavy drinking, cocaine self administration and reinstatement of cocaine relapse like behavior.
+ALDH2	drug	cocaine	26022266	We have synthesized highly selective novel <strong>ALDH2</strong> inhibitors (ALDH2i) that block alcohol  and <b>cocaine</b> cue induced surges in nucleus accumbens (NAc) DA and prevent reinstatement of alcohol heavy drinking, <b>cocaine</b> self administration and reinstatement of <b>cocaine</b> relapse like behavior.
+ALDH2	addiction	relapse	26022266	We have synthesized highly selective novel <strong>ALDH2</strong> inhibitors (ALDH2i) that block alcohol  and cocaine cue induced surges in nucleus accumbens (NAc) DA and prevent <b>reinstatement</b> of alcohol heavy drinking, cocaine self administration and <b>reinstatement</b> of cocaine <b>relapse</b> like behavior.
+ALDH2	addiction	relapse	26022266	Selective inhibition of <strong>ALDH2</strong> appears to have therapeutic potential for treating cue induced drug <b>relapse</b>, a major unmet need for treating addicted subjects.
+ALDH2	drug	alcohol	25713355	Pharmacological recruitment of aldehyde dehydrogenase 3A1 (ALDH3A1) to assist <strong>ALDH2</strong> in acetaldehyde and <b>ethanol</b> metabolism in vivo.
+ALDH2	drug	alcohol	25713355	When given together with the <strong>ALDH2</strong> specific activator, Alda 1, Alda 89 reduced acetaldehyde induced behavioral impairment by causing a rapid reduction in blood <b>ethanol</b> and acetaldehyde levels after acute <b>ethanol</b> intoxication in both wild type and <strong>ALDH2</strong> deficient, <strong>ALDH2</strong>*1/*2, heterozygotic knock in mice.
+ALDH2	addiction	intoxication	25713355	When given together with the <strong>ALDH2</strong> specific activator, Alda 1, Alda 89 reduced acetaldehyde induced behavioral impairment by causing a rapid reduction in blood ethanol and acetaldehyde levels after acute ethanol <b>intoxication</b> in both wild type and <strong>ALDH2</strong> deficient, <strong>ALDH2</strong>*1/*2, heterozygotic knock in mice.
+ALDH2	drug	alcohol	25543082	The present study tested the efficacy of Alda 1, a specific aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) activator, in treating <b>alcoholic</b> liver disease.
+ALDH2	drug	alcohol	25543082	<b>Alcohol</b> feeding for 8 weeks induced hepatic <strong>ALDH2</strong> dysfunction and aldehyde accumulation.
+ALDH2	drug	alcohol	25543082	Pharmacological activation of <strong>ALDH2</strong> by Alda 1 reversed <b>alcoholic</b> steatosis and apoptosis through accelerating aldehyde clearance.
+ALDH2	drug	alcohol	25543082	This study indicates that <strong>ALDH2</strong> is a promising molecular target and Alda 1 has therapeutic potential for treating <b>alcoholic</b> liver disease.
+ALDH2	drug	alcohol	25535445	The genes for <b>alcohol</b> metabolizing enzymes: <b>Alcohol</b> dehydrogenase (ADH2 and ADH3) and aldehyde dehydrogenase (<strong>ALDH2</strong>) exhibit functional polymorphisms.
+ALDH2	drug	alcohol	25535445	To determine whether any association exists between polymorphisms of ADH2, ADH3 and <strong>ALDH2</strong> and <b>alcohol</b> dependence syndrome in a group of Asian Indians.
+ALDH2	addiction	dependence	25535445	To determine whether any association exists between polymorphisms of ADH2, ADH3 and <strong>ALDH2</strong> and alcohol <b>dependence</b> syndrome in a group of Asian Indians.
+ALDH2	drug	alcohol	25419637	No association between the <strong>ALDH2</strong> promoter polymorphism rs886205, <b>alcohol</b> dependence, and risky <b>alcohol</b> consumption in a German population.
+ALDH2	addiction	dependence	25419637	No association between the <strong>ALDH2</strong> promoter polymorphism rs886205, alcohol <b>dependence</b>, and risky alcohol consumption in a German population.
+ALDH2	drug	alcohol	25372623	Association between ADH1C and <strong>ALDH2</strong> polymorphisms and <b>alcoholism</b> in a Turkish sample.
+ALDH2	drug	alcohol	25372623	To evaluate the association between the <b>alcohol</b> dehydrogenase 1C (ADH1C) Ile350Val and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) Glu504Lys polymorphisms and <b>alcohol</b> dependence in a Turkish sample.
+ALDH2	addiction	dependence	25372623	To evaluate the association between the alcohol dehydrogenase 1C (ADH1C) Ile350Val and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) Glu504Lys polymorphisms and alcohol <b>dependence</b> in a Turkish sample.
+ALDH2	drug	alcohol	25372623	235 individuals (115 <b>alcohol</b> dependent patients and 120 controls) were genotyped for ADH1C and <strong>ALDH2</strong> with PCR RFLP (polymerase chain reaction restriction fragment length polymorphism).
+ALDH2	drug	alcohol	25372623	The <strong>ALDH2</strong>  504Lys/Lys or Glu/Lys genotypes were not present in <b>alcohol</b> dependent patients, similar to that seen in European populations and in contrast to the findings in the Asian populations.
+ALDH2	drug	alcohol	25359488	With few exceptions like <strong>ALDH2</strong>*2, the contribution of individual genetic variants to the risk for <b>alcohol</b> related disorders is small.
+ALDH2	drug	alcohol	25354396	Contribution of <strong>ALDH2</strong> polymorphism to <b>alcoholism</b> associated hypertension.
+ALDH2	drug	alcohol	25354396	Although oxidative stress and endothelial injury have been postulated to play a major contributing role to <b>alcoholism</b> induced hypertension, recent evidence depicted a rather unique role for the genotype of the acetaldehyde metabolizing enzyme mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>), which is mainly responsible for detoxifying <b>ethanol</b> consumed, in <b>alcoholism</b> induced elevation of blood pressure.
+ALDH2	drug	alcohol	25354396	Genetic polymorphism of <strong>ALDH2</strong> in human results in altered <b>ethanol</b> pharmacokinetic properties and <b>ethanol</b> metabolism, leading to accumulation of the <b>ethanol</b> metabolite acetaldehyde following <b>alcohol</b> intake.
+ALDH2	drug	alcohol	25354396	The unfavorable consequence of the <strong>ALDH2</strong> variants is believed to be governed by the accumulation of the <b>ethanol</b> metabolite acetaldehyde.
+ALDH2	drug	alcohol	25354396	The aim of this mini review is to summarize the possible contribution of <strong>ALDH2</strong> genetic polymorphism in the onset and development of <b>alcoholism</b> related development of hypertension.
+ALDH2	drug	alcohol	25354396	Furthermore, the double edged sword of <strong>ALDH2</strong> gene and genetic polymorphism in <b>alcoholism</b> and <b>alcoholic</b> tissue damage and relevant patents will be discussed.
+ALDH2	drug	alcohol	25270064	We assessed ancestry admixture and tested for associations between <b>alcohol</b> related phenotypes in the genomic regions around the ADH1 7 and <strong>ALDH2</strong> and ALDH1A1 genes.
+ALDH2	drug	alcohol	25270064	Two significant associations, one in ADH and one in <strong>ALDH2</strong>, were observed with <b>alcohol</b> dependence diagnosis.
+ALDH2	addiction	dependence	25270064	Two significant associations, one in ADH and one in <strong>ALDH2</strong>, were observed with alcohol <b>dependence</b> diagnosis.
+ALDH2	drug	alcohol	24930774	<strong>Aldh2</strong>(+/+) , <strong>Aldh2</strong>(+/ ) , and <strong>Aldh2</strong>( / ) mice were maintained, from 10 weeks of age, on standard solid food, with liquid supplied as <b>ethanol</b> (EtOH) solution at a concentration of 0 to 20% (forced EtOH consumption).
+ALDH2	addiction	dependence	24930774	While multiple regression analysis suggested that the BW and ALT level in <strong>Aldh2</strong>( / ) mice correlated with lifespan, adjustment for EtOH concentration revealed that this correlation was not significant (i.e., reflected EtOH <b>dependence</b>).
+ALDH2	drug	alcohol	24804381	[Relationship among <strong>ALDH2</strong> gene polymorphism, <b>alcohol</b> metabolism and acetaldehyde level in peripheral blood].
+ALDH2	drug	alcohol	24804381	To explore <b>alcohol</b> pharmacokinetics as well as acetaldehyde level in peripheral blood in human subjects with different <strong>ALDH2</strong> genotypes after drinking.
+ALDH2	drug	alcohol	24804381	After the consumption of <b>alcohol</b>, <b>alcohol</b> and acetaldehyde metabolism in blood slow down in <strong>ALDH2</strong>*1/*2 mutation group influenced by the inhibition of enzyme activity, leading to the accumulation of acetaldehyde in peripheral blood, thus reinforcing their effects in the body.
+ALDH2	addiction	reward	24804381	After the consumption of alcohol, alcohol and acetaldehyde metabolism in blood slow down in <strong>ALDH2</strong>*1/*2 mutation group influenced by the inhibition of enzyme activity, leading to the accumulation of acetaldehyde in peripheral blood, thus <b>reinforcing</b> their effects in the body.
+ALDH2	drug	alcohol	24800934	Aldehyde dehydrogenase (<strong>ALDH2</strong>) is an emerging drug target for the treatment of heart disease, cocaine and <b>alcohol</b> dependence, and conditions caused by genetic polymorphisms in <strong>ALDH2</strong>.
+ALDH2	drug	cocaine	24800934	Aldehyde dehydrogenase (<strong>ALDH2</strong>) is an emerging drug target for the treatment of heart disease, <b>cocaine</b> and alcohol dependence, and conditions caused by genetic polymorphisms in <strong>ALDH2</strong>.
+ALDH2	addiction	dependence	24800934	Aldehyde dehydrogenase (<strong>ALDH2</strong>) is an emerging drug target for the treatment of heart disease, cocaine and alcohol <b>dependence</b>, and conditions caused by genetic polymorphisms in <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	24800934	Irreversible inhibition of <strong>ALDH2</strong> activity with <b>disulfiram</b> resulted in a proportional decrease in the amplitude of the acetate resonance.
+ALDH2	drug	alcohol	24800934	(13) C magnetic resonance spectroscopy measurements of hyperpolarized [1 (13) C, U (2) H5 ] <b>ethanol</b> oxidation allow real time assessment of <strong>ALDH2</strong> activity in liver in vivo.
+ALDH2	drug	alcohol	24797321	In the case of acetaldehyde, the AUC0 4 and Cmax of acetaldehyde of ADH1B*2/*2 after administration of 0.25 g/kg <b>alcohol</b> and the AUC0 4 of acetaldehyde of ADH1B*2/*2 at 0.5 g/kg were significantly higher than corresponding values of ADH1B*1/*2 only in the group of <strong>ALDH2</strong>*1/*2.
+ALDH2	drug	alcohol	24749767	Roles of the <strong>ALDH2</strong> and ADH1B genotypes on the association between <b>alcohol</b> intake and serum adiponectin levels among Japanese male workers.
+ALDH2	drug	alcohol	24749767	Two genotypes in the <b>alcohol</b> dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) genes were determined using blood sample.
+ALDH2	drug	alcohol	24661165	Effects of <strong>ALDH2</strong>∗2 on <b>alcohol</b> problem trajectories of Asian American college students.
+ALDH2	drug	alcohol	24661165	The variant aldehyde dehydrogenase allele, <strong>ALDH2</strong>∗2, consistently has been associated with protection against <b>alcohol</b> dependence, but the mechanism underlying this process is not known.
+ALDH2	addiction	dependence	24661165	The variant aldehyde dehydrogenase allele, <strong>ALDH2</strong>∗2, consistently has been associated with protection against alcohol <b>dependence</b>, but the mechanism underlying this process is not known.
+ALDH2	drug	alcohol	24661165	This study examined growth trajectories of <b>alcohol</b> consumption (frequency, average quantity, binge drinking, maximum drinks) and problems over the college years and then tested whether the <strong>ALDH2</strong> genotype mediated or moderated the relationship between <b>alcohol</b> consumption and problems.
+ALDH2	addiction	intoxication	24661165	This study examined growth trajectories of alcohol consumption (frequency, average quantity, <b>binge</b> drinking, maximum drinks) and problems over the college years and then tested whether the <strong>ALDH2</strong> genotype mediated or moderated the relationship between alcohol consumption and problems.
+ALDH2	drug	alcohol	24661165	<b>Alcohol</b> consumption and problems increased over the college years for both those with and without <strong>ALDH2</strong>∗2, but having an <strong>ALDH2</strong>∗2 allele was associated with less of an increase in problems over time.
+ALDH2	addiction	intoxication	24661165	A mediation model was supported, with <strong>ALDH2</strong>∗2 group differences in problems fully accounted for by differences in frequency of <b>binge</b> drinking.
+ALDH2	drug	alcohol	24661165	Findings also supported a moderation hypothesis: All four <b>alcohol</b> consumption variables were significant predictors of subsequent <b>alcohol</b> problems, but these relationships were not as strong in those with <strong>ALDH2</strong>∗2 as in those without <strong>ALDH2</strong>∗2.
+ALDH2	drug	alcohol	24661165	Our findings suggest that the interplay between <strong>ALDH2</strong>∗2 and drinking related problems is complex, involving both mediation and moderation processes that reduce the likelihood of developing problems via reduction of heavy drinking as well as by altering the relationship between <b>alcohol</b> consumption and problems.
+ALDH2	drug	alcohol	24571199	Long term inhibition of <b>ethanol</b> intake by the administration of an aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) coding lentiviral vector into the ventral tegmental area of rats.
+ALDH2	drug	alcohol	24571199	The present studies tested the feasibility of achieving a long term reduction of chronic and post deprivation binge <b>ethanol</b> drinking by a single administration into the brain ventral tegmental area (VTA) of a lentiviral vector that codes for aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), which degrades acetaldehyde.
+ALDH2	addiction	intoxication	24571199	The present studies tested the feasibility of achieving a long term reduction of chronic and post deprivation <b>binge</b> ethanol drinking by a single administration into the brain ventral tegmental area (VTA) of a lentiviral vector that codes for aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), which degrades acetaldehyde.
+ALDH2	drug	alcohol	24571199	The <strong>ALDH2</strong> gene coding vector or a control lentiviral vector were microinjected into the VTA of rats bred for their <b>alcohol</b> preference.
+ALDH2	drug	alcohol	24571199	The single administration of the <strong>ALDH2</strong> coding vector prior to allowing <b>ethanol</b> availability reduced <b>ethanol</b> drinking by 85 90% (P < 0.001) for the 45 days tested.
+ALDH2	addiction	intoxication	24571199	The administration of the <strong>ALDH2</strong> coding vector reduced re access <b>binge</b> drinking by 75 80% (P < 0.001).
+ALDH2	drug	alcohol	24505444	We investigated six variants known to influence nicotine addiction or <b>alcohol</b> metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (<strong>ALDH2</strong>).
+ALDH2	drug	nicotine	24505444	We investigated six variants known to influence <b>nicotine</b> addiction or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (<strong>ALDH2</strong>).
+ALDH2	addiction	addiction	24505444	We investigated six variants known to influence nicotine <b>addiction</b> or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (<strong>ALDH2</strong>).
+ALDH2	drug	alcohol	24277619	<strong>ALDH2</strong> is associated to <b>alcohol</b> dependence and is the major genetic determinant of "daily maximum drinks" in a GWAS study of an isolated rural Chinese sample.
+ALDH2	addiction	dependence	24277619	<strong>ALDH2</strong> is associated to alcohol <b>dependence</b> and is the major genetic determinant of "daily maximum drinks" in a GWAS study of an isolated rural Chinese sample.
+ALDH2	drug	alcohol	24117666	Patients with inactive <strong>ALDH2</strong> significantly sustained abstinence with the use of <b>disulfiram</b> (p = 0.044).
+ALDH2	drug	alcohol	24117666	We indicated the effectiveness of <b>disulfiram</b> for the maintenance of abstinence in patients with inactive <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	23990377	Through linkage analysis, candidate gene approach, and genome wide association studies (GWAS), many genetic susceptibility factors for substance dependence have been discovered such as the <b>alcohol</b> dehydrogenase gene (<strong>ALDH2</strong>) for <b>alcohol</b> dependence (AD) and nicotinic acetylcholine receptor (nAChR) subunit variants on chromosomes 8 and 15 for nicotine dependence (ND).
+ALDH2	drug	nicotine	23990377	Through linkage analysis, candidate gene approach, and genome wide association studies (GWAS), many genetic susceptibility factors for substance dependence have been discovered such as the alcohol dehydrogenase gene (<strong>ALDH2</strong>) for alcohol dependence (AD) and nicotinic acetylcholine receptor (nAChR) subunit variants on chromosomes 8 and 15 for <b>nicotine</b> dependence (ND).
+ALDH2	addiction	dependence	23990377	Through linkage analysis, candidate gene approach, and genome wide association studies (GWAS), many genetic susceptibility factors for substance <b>dependence</b> have been discovered such as the alcohol dehydrogenase gene (<strong>ALDH2</strong>) for alcohol <b>dependence</b> (AD) and nicotinic acetylcholine receptor (nAChR) subunit variants on chromosomes 8 and 15 for nicotine <b>dependence</b> (ND).
+ALDH2	drug	alcohol	23891816	Although DSF's mechanism of action in <b>alcohol</b> abuse is due to the inhibition of liver mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>), its mechanism of action in the treatment of cocaine dependence is unknown.
+ALDH2	drug	cocaine	23891816	Although DSF's mechanism of action in alcohol abuse is due to the inhibition of liver mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>), its mechanism of action in the treatment of <b>cocaine</b> dependence is unknown.
+ALDH2	addiction	dependence	23891816	Although DSF's mechanism of action in alcohol abuse is due to the inhibition of liver mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>), its mechanism of action in the treatment of cocaine <b>dependence</b> is unknown.
+ALDH2	drug	cocaine	23891816	Although inhibition of liver <strong>ALDH2</strong> is the accepted mechanism for DSF's action in treating AUDs, the concurrent changes in DA, GABA, and GLu in the NAc and mPFC after DSF administration suggest that changes in these neurotransmitters as a potential mechanism of action not only for AUDs, but also for <b>cocaine</b> dependence cannot be excluded.
+ALDH2	addiction	dependence	23891816	Although inhibition of liver <strong>ALDH2</strong> is the accepted mechanism for DSF's action in treating AUDs, the concurrent changes in DA, GABA, and GLu in the NAc and mPFC after DSF administration suggest that changes in these neurotransmitters as a potential mechanism of action not only for AUDs, but also for cocaine <b>dependence</b> cannot be excluded.
+ALDH2	addiction	aversion	23847486	Similarly <b>aversive</b> is an increased acetaldehyde level resulting from the inhibition of liver aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) synthesis (by an antisense coding gene against <strong>aldh2</strong> mRNA).
+ALDH2	drug	alcohol	23712313	Some of these genes have been identified, including two genes involved in the metabolism of <b>alcohol</b> (ADH1B and <strong>ALDH2</strong>) that have the strongest known affects on the risk of <b>alcoholism</b>.
+ALDH2	drug	alcohol	23685324	Association between DRD2, 5 HTTLPR, and <strong>ALDH2</strong> genes and specific personality traits in <b>alcohol</b>  and opiate dependent patients.
+ALDH2	drug	alcohol	23685324	We concluded that addicts, both <b>alcohol</b>  and opiate dependent patients, have common genetic variants in DRD2 and 5 HTTLPR but specific for <strong>ALDH2</strong>.
+ALDH2	drug	opioid	23609397	Multiple logistic regression analysis showed significant main effects for novelty seeking (P ≤ 0.001) and harm avoidance (P = 0.001) scores, and a significant interaction effect between novelty seeking and <strong>ALDH2</strong> genotypes (P = 0.016) in <b>heroin</b> dependent patients compared with controls.
+ALDH2	addiction	relapse	23609397	Multiple logistic regression analysis showed significant main effects for novelty <b>seeking</b> (P ≤ 0.001) and harm avoidance (P = 0.001) scores, and a significant interaction effect between novelty <b>seeking</b> and <strong>ALDH2</strong> genotypes (P = 0.016) in heroin dependent patients compared with controls.
+ALDH2	drug	opioid	23609397	When stratified by the <strong>ALDH2</strong> genotypes, only <b>heroin</b> dependent patients with the *1*2 and *2*2 genotypes at <strong>ALDH2</strong> had higher novelty seeking scores than did controls (<b>heroin</b> dependence = 15.94, controls = 12.46; P ≤ 0.001).
+ALDH2	addiction	dependence	23609397	When stratified by the <strong>ALDH2</strong> genotypes, only heroin dependent patients with the *1*2 and *2*2 genotypes at <strong>ALDH2</strong> had higher novelty seeking scores than did controls (heroin <b>dependence</b> = 15.94, controls = 12.46; P ≤ 0.001).
+ALDH2	addiction	relapse	23609397	When stratified by the <strong>ALDH2</strong> genotypes, only heroin dependent patients with the *1*2 and *2*2 genotypes at <strong>ALDH2</strong> had higher novelty <b>seeking</b> scores than did controls (heroin dependence = 15.94, controls = 12.46; P ≤ 0.001).
+ALDH2	drug	opioid	23609397	Our results provide initial evidence that the <strong>ALDH2</strong> gene interacted with novelty seeking in <b>heroin</b> dependent Han Chinese patients in Taiwan.
+ALDH2	addiction	relapse	23609397	Our results provide initial evidence that the <strong>ALDH2</strong> gene interacted with novelty <b>seeking</b> in heroin dependent Han Chinese patients in Taiwan.
+ALDH2	drug	alcohol	23414439	Genetic polymorphisms of <b>alcohol</b> dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) affect susceptibility to <b>alcoholism</b> and may affect body weight via gene associated differences in fuel utilization in <b>alcoholics</b>.
+ALDH2	drug	alcohol	23414439	We evaluated associations between ADH1B/<strong>ALDH2</strong> genotypes and the body weight and body mass index (BMI) of 1,301 Japanese <b>alcoholic</b> men at the time of their first visit to an addiction center.
+ALDH2	addiction	addiction	23414439	We evaluated associations between ADH1B/<strong>ALDH2</strong> genotypes and the body weight and body mass index (BMI) of 1,301 Japanese alcoholic men at the time of their first visit to an <b>addiction</b> center.
+ALDH2	drug	opioid	23266708	The ADH1B and DRD2 gene polymorphism may modify the protective effect of the <strong>ALDH2</strong> gene against <b>heroin</b> dependence.
+ALDH2	addiction	dependence	23266708	The ADH1B and DRD2 gene polymorphism may modify the protective effect of the <strong>ALDH2</strong> gene against heroin <b>dependence</b>.
+ALDH2	drug	alcohol	23266708	Understanding the influences of genes involved in dopamine and serotonin metabolism, such as the aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) and <b>alcohol</b> dehydrogenase 1B (ADH1B) genes, is critical for understanding addictive behavior.
+ALDH2	addiction	addiction	23266708	Understanding the influences of genes involved in dopamine and serotonin metabolism, such as the aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) and alcohol dehydrogenase 1B (ADH1B) genes, is critical for understanding <b>addictive</b> behavior.
+ALDH2	drug	opioid	23266708	Therefore, we investigated the association between the <strong>ALDH2</strong>, ADH1B and DRD2 polymorphisms and <b>heroin</b> dependence.
+ALDH2	addiction	dependence	23266708	Therefore, we investigated the association between the <strong>ALDH2</strong>, ADH1B and DRD2 polymorphisms and heroin <b>dependence</b>.
+ALDH2	drug	opioid	23266708	The frequency of the <strong>ALDH2</strong>*1/*1 genotype was significantly lower in <b>heroin</b> dependent patients than in controls, but the frequency of ADH1B and DRD2 genotypes was not significantly different.
+ALDH2	drug	opioid	23266708	The <strong>ALDH2</strong>*1/*1, ADH1B*1/*1, and ADH1B*1/*2 genotypes may interact and protect their carriers against <b>heroin</b> dependence and the protective effect may be varied by the DRD2 gene polymorphism.
+ALDH2	addiction	dependence	23266708	The <strong>ALDH2</strong>*1/*1, ADH1B*1/*1, and ADH1B*1/*2 genotypes may interact and protect their carriers against heroin <b>dependence</b> and the protective effect may be varied by the DRD2 gene polymorphism.
+ALDH2	drug	opioid	23266708	We conclude that the protective effect of the <strong>ALDH2</strong> polymorphism against <b>heroin</b> dependence may be modified by the ADH1B and DRD2 polymorphism.
+ALDH2	addiction	dependence	23266708	We conclude that the protective effect of the <strong>ALDH2</strong> polymorphism against heroin <b>dependence</b> may be modified by the ADH1B and DRD2 polymorphism.
+ALDH2	drug	alcohol	23134050	Likewise, an <strong>ALDH2</strong> variant with reduced activity results in acetaldehyde buildup and also has a protective effect against <b>alcoholism</b>.
+ALDH2	drug	alcohol	23134043	The key findings of the earlier studies were that variations (i.e., polymorphisms) in the DNA sequences of the genes encoding <b>alcohol</b> dehydrogenase 1B (i.e., the ADH1B gene), aldehyde dehydrogenase 2 (i.e., the <strong>ALDH2</strong> gene), and other <b>alcohol</b> metabolizing enzymes mediate the risk for <b>alcoholism</b>; moreover, these polymorphisms also have an impact on the risk of <b>alcohol</b> related cancers, such as esophageal cancer.
+ALDH2	drug	alcohol	22931071	Associations between <b>alcohol</b> dependence and polymorphisms in ADH1B, ADH1C, and <strong>ALDH2</strong> were compared in a community sample of Native Americans (n 791) living on reservations and Mexican Americans (n 391) living within the same county.
+ALDH2	addiction	dependence	22931071	Associations between alcohol <b>dependence</b> and polymorphisms in ADH1B, ADH1C, and <strong>ALDH2</strong> were compared in a community sample of Native Americans (n 791) living on reservations and Mexican Americans (n 391) living within the same county.
+ALDH2	drug	alcohol	22703173	The most well established genetic factors associated with <b>alcohol</b> dependence are in the genes encoding <b>alcohol</b> dehydrogenase (ADH), which oxidizes <b>alcohol</b> to acetaldehyde, and aldehyde dehydrogenase (<strong>ALDH2</strong>), which oxidizes acetaldehyde to acetate.
+ALDH2	addiction	dependence	22703173	The most well established genetic factors associated with alcohol <b>dependence</b> are in the genes encoding alcohol dehydrogenase (ADH), which oxidizes alcohol to acetaldehyde, and aldehyde dehydrogenase (<strong>ALDH2</strong>), which oxidizes acetaldehyde to acetate.
+ALDH2	drug	alcohol	22640768	A few well validated, specific predictors such as OPRM1, ADH1B, <strong>ALDH2</strong>, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand <b>alcohol</b> related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in nicotine metabolism (CYP26), and, potentially, <b>naltrexone</b> treatment response (OPRM1).
+ALDH2	drug	nicotine	22640768	A few well validated, specific predictors such as OPRM1, ADH1B, <strong>ALDH2</strong>, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand alcohol related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in <b>nicotine</b> metabolism (CYP26), and, potentially, naltrexone treatment response (OPRM1).
+ALDH2	drug	alcohol	22591209	Association of the ALDH1A1*2 promoter polymorphism with <b>alcohol</b> phenotypes in young adults with or without <strong>ALDH2</strong>*2.
+ALDH2	drug	alcohol	22591209	The association of <strong>ALDH2</strong>*2 with reduced <b>alcohol</b> consumption replicates previous findings across numerous studies.
+ALDH2	drug	alcohol	22563891	Developmental trajectory and environmental moderation of the effect of <strong>ALDH2</strong> polymorphism on <b>alcohol</b> use.
+ALDH2	drug	alcohol	22563891	In the aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) gene, the <strong>ALDH2</strong>*2 allele, prevalent in East Asian populations, encodes an enzyme with severely reduced activity, thereby disrupting the normal metabolism of <b>alcohol</b>.
+ALDH2	drug	alcohol	22563891	Possession of the <strong>ALDH2</strong>*2 allele has been repeatedly shown to be associated with lower risk for <b>alcohol</b> dependence and reduced <b>alcohol</b> use.
+ALDH2	addiction	dependence	22563891	Possession of the <strong>ALDH2</strong>*2 allele has been repeatedly shown to be associated with lower risk for alcohol <b>dependence</b> and reduced alcohol use.
+ALDH2	drug	alcohol	22563891	We also sought to determine whether the environmental influences of nonbiological parent and elder sibling <b>alcohol</b> use and misuse, as well as deviant peer behavior, moderated the effect of <strong>ALDH2</strong> genotype upon <b>alcohol</b> use.
+ALDH2	drug	alcohol	22563891	Across all measures of <b>alcohol</b> use, the association between <strong>ALDH2</strong>*2 allele possession and reduced drinking went from negligible to moderate between mid adolescence and early adulthood.
+ALDH2	drug	alcohol	22563891	A combined index of adoptive parent <b>alcohol</b> use and misuse consistently moderated the protective effect of the <strong>ALDH2</strong>*2 allele across the measures of quantity and frequency of <b>alcohol</b> use, and symptomology, such that high parental <b>alcohol</b> use and misuse reduced the protective effect of the <strong>ALDH2</strong>*2 allele, while low parental <b>alcohol</b> use and misuse enhanced the effect of the allele.
+ALDH2	drug	alcohol	22563891	Neither a combined index of elder sibling <b>alcohol</b> use and misuse, nor deviant peer behavior was consistently related to the effect of <strong>ALDH2</strong> genotype.
+ALDH2	drug	alcohol	22563891	The protective effect of the <strong>ALDH2</strong>*2 allele increases over the course of adolescence and young adulthood and is modified by the environmental influence of parental <b>alcohol</b> use and misuse.
+ALDH2	drug	alcohol	22544865	<strong>ALDH2</strong>, as a key enzyme that oxidizes acetaldehyde, is crucial for <b>alcohol</b> metabolism.
+ALDH2	drug	alcohol	22102315	Strong protective effect of the aldehyde dehydrogenase gene (<strong>ALDH2</strong>) 504lys (*2) allele against <b>alcoholism</b> and <b>alcohol</b> induced medical diseases in Asians.
+ALDH2	drug	alcohol	22102315	Individuals heterozygous or homozygous for the lys (A or *2) allele at the single nucleotide polymorphism (SNP) glu504lys (rs671) of <strong>ALDH2</strong> have greatly reduced ability to metabolize acetaldehyde, which greatly decreases their risk for <b>alcohol</b> dependence (AD).
+ALDH2	addiction	dependence	22102315	Individuals heterozygous or homozygous for the lys (A or *2) allele at the single nucleotide polymorphism (SNP) glu504lys (rs671) of <strong>ALDH2</strong> have greatly reduced ability to metabolize acetaldehyde, which greatly decreases their risk for alcohol <b>dependence</b> (AD).
+ALDH2	drug	alcohol	22102315	These findings provide confirmation of the involvement of the human <strong>ALDH2</strong> gene in the pathogenesis of AD as well as <b>alcohol</b> induced medical illnesses in East Asians.
+ALDH2	drug	alcohol	22005600	The aversive characteristics of flushing observed in some populations with an isoform of aldehyde dehydrogenase (<strong>ALDH2</strong>) less active, are the basis for treating <b>alcoholics</b> with <b>disulfiram</b>, an ALDH inhibitor.
+ALDH2	addiction	aversion	22005600	The <b>aversive</b> characteristics of flushing observed in some populations with an isoform of aldehyde dehydrogenase (<strong>ALDH2</strong>) less active, are the basis for treating alcoholics with disulfiram, an ALDH inhibitor.
+ALDH2	drug	alcohol	21848961	Gender differences in the effects of ADH1B and <strong>ALDH2</strong> polymorphisms on <b>alcoholism</b>.
+ALDH2	drug	alcohol	21848961	Polymorphisms of <b>alcohol</b> dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) are strong genetic determinants of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	21848961	Polymorphisms of alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) are strong genetic determinants of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	21848961	This study aimed to clarify gender differences in the effects of ADH1B and <strong>ALDH2</strong> polymorphism on the development of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	21848961	This study aimed to clarify gender differences in the effects of ADH1B and <strong>ALDH2</strong> polymorphism on the development of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	21848961	The onset age of female <b>alcoholics</b> with inactive <strong>ALDH2</strong> genotype was significantly lower than those with active <strong>ALDH2</strong> genotype, but the onset age did not differ between the inactive and active <strong>ALDH2</strong> group in male <b>alcoholics</b>.
+ALDH2	drug	alcohol	21848961	The prevalence of comorbid psychiatric disorders, including major depression, eating disorder, panic disorder, and borderline personality disorder, was significantly higher in female <b>alcoholics</b> with inactive <strong>ALDH2</strong> or superactive ADH1B than in those with active <strong>ALDH2</strong> or normal ADH1B.
+ALDH2	drug	alcohol	21848961	<strong>ALDH2</strong> polymorphism appears to have contrasting effects on the development of <b>alcoholism</b> in women and men.
+ALDH2	drug	alcohol	21848961	One possible reason for this gender difference may be the high prevalence of psychiatric comorbidities in female <b>alcoholics</b> with inactive <strong>ALDH2</strong>.
+ALDH2	addiction	addiction	21723677	Determining the influences of genes involved in metabolizing dopamine and encoding dopamine receptors, such as the aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) and dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1) genes, is critical for understanding <b>addictive</b> behavior.
+ALDH2	drug	opioid	21723677	Therefore, we investigated the association between the <strong>ALDH2</strong> and DRD2/ANKK1 Taq IA polymorphisms and <b>heroin</b> dependence.
+ALDH2	addiction	dependence	21723677	Therefore, we investigated the association between the <strong>ALDH2</strong> and DRD2/ANKK1 Taq IA polymorphisms and heroin <b>dependence</b>.
+ALDH2	drug	opioid	21723677	The frequency of <strong>ALDH2</strong>*1/*2 and *2/*2 genotypes was significantly higher in <b>heroin</b> dependent patients than in controls, but the frequency of DRD2 Taq IA genotypes was not significantly different.
+ALDH2	drug	opioid	21723677	The <strong>ALDH2</strong> polymorphism, but not the DRD2, was associated with <b>heroin</b> dependence.
+ALDH2	addiction	dependence	21723677	The <strong>ALDH2</strong> polymorphism, but not the DRD2, was associated with heroin <b>dependence</b>.
+ALDH2	drug	alcohol	21349255	Activation of <strong>ALDH2</strong> has been shown to benefit cardiovascular outcome following periods of ischemia and renewed interest in specific inhibition of <strong>ALDH2</strong> has application for <b>alcohol</b> aversion therapy, and more recently, in cocaine addiction.
+ALDH2	drug	cocaine	21349255	Activation of <strong>ALDH2</strong> has been shown to benefit cardiovascular outcome following periods of ischemia and renewed interest in specific inhibition of <strong>ALDH2</strong> has application for alcohol aversion therapy, and more recently, in <b>cocaine</b> addiction.
+ALDH2	addiction	addiction	21349255	Activation of <strong>ALDH2</strong> has been shown to benefit cardiovascular outcome following periods of ischemia and renewed interest in specific inhibition of <strong>ALDH2</strong> has application for alcohol aversion therapy, and more recently, in cocaine <b>addiction</b>.
+ALDH2	addiction	aversion	21349255	Activation of <strong>ALDH2</strong> has been shown to benefit cardiovascular outcome following periods of ischemia and renewed interest in specific inhibition of <strong>ALDH2</strong> has application for alcohol <b>aversion</b> therapy, and more recently, in cocaine addiction.
+ALDH2	drug	alcohol	21309949	COMT and <strong>ALDH2</strong> polymorphisms moderate associations of implicit drinking motives with <b>alcohol</b> use.
+ALDH2	drug	alcohol	21309949	The current study examined two polymorphisms with functional significance for <b>alcohol</b> use behavior (COMT Val158Met and <strong>ALDH2</strong>*2) in relation to automatic <b>alcohol</b> cognitions and tested additive and interactive effects of genotype and implicit cognitions on drinking behavior.
+ALDH2	drug	alcohol	21309949	Interaction effects indicated that associations of implicit motives with drinking outcomes were strongest in the context of genetic variants associated with relatively higher risk for <b>alcohol</b> use (COMT Met and <strong>ALDH2</strong>*1).
+ALDH2	drug	alcohol	21118274	Because aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) has been shown to have a great impact on the subjective responses to <b>alcohol</b>, we divided subjects by <strong>ALDH2</strong> genotype for further analyses.
+ALDH2	drug	alcohol	21118274	Subjects with 1 or 2 copies of the more common allele showed greater subjective responses to <b>alcohol</b> than did individuals homozygous for the <b>alcohol</b> dependence associated allele regardless of <strong>ALDH2</strong> genotype.
+ALDH2	addiction	dependence	21118274	Subjects with 1 or 2 copies of the more common allele showed greater subjective responses to alcohol than did individuals homozygous for the alcohol <b>dependence</b> associated allele regardless of <strong>ALDH2</strong> genotype.
+ALDH2	drug	alcohol	21070510	Interaction between <strong>ALDH2</strong>*1*1 and DRD2/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co morbid with <b>alcoholism</b>.
+ALDH2	drug	alcohol	21070510	Previous studies on acetaldehyde dehydrogenase 2 (<strong>ALDH2</strong>) focused on drinking behavior or <b>alcoholism</b> because the <strong>ALDH2</strong>*2 allele protects against the risk of developing <b>alcoholism</b>.
+ALDH2	drug	alcohol	21070510	The interaction of the <strong>ALDH2</strong> gene with neurotransmitters, such as dopamine, is suggested to be related to <b>alcoholism</b>.
+ALDH2	drug	alcohol	20958327	The DNA damage induced by <b>ethanol</b> could be attenuated by <b>alcohol</b> dehydrogenase 1B (ADH1B) or acetaldehyde dehydrogenase 2 (<strong>ALDH2</strong>) inhibitor, and the mRNA expression levels of ADH1B and <strong>ALDH2</strong> were increased markedly by <b>ethanol</b>.
+ALDH2	drug	alcohol	20958327	This study provides direct evidence that <b>ethanol</b> can induce oxidative DNA damage in human peripheral lymphocytes in vitro, and its mechanism may be associated with the metabolism of <b>ethanol</b> by the ADH1B/<strong>ALDH2</strong> pathway.
+ALDH2	drug	alcohol	20714161	We develop a pharmacokinetic model describing how genetic variations in ADH1B, ADH1C, ADH7, <strong>ALDH2</strong>, and TAS2R38 affect consumption behavior, and <b>alcohol</b> and acetaldehyde levels over time in various tissues of individuals with a particular genotype to predict their susceptibility to <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	20714161	We develop a pharmacokinetic model describing how genetic variations in ADH1B, ADH1C, ADH7, <strong>ALDH2</strong>, and TAS2R38 affect consumption behavior, and alcohol and acetaldehyde levels over time in various tissues of individuals with a particular genotype to predict their susceptibility to alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	20700531	Significant interactions were observed between <b>alcohol</b> and ADH1b (rs1229984) with respect to LDL and between <b>alcohol</b> and <strong>ALDH2</strong> (rs886205) with respect to IGT/diabetes.
+ALDH2	drug	alcohol	20652463	Evaluation of a brief web based genetic feedback intervention for reducing <b>alcohol</b> related health risks associated with <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	20652463	The purpose of this study was to evaluate the feasibility, acceptability, and efficacy of a web based <b>alcohol</b> intervention incorporating genetic feedback and risk information specific to <strong>ALDH2</strong> genotype.
+ALDH2	drug	alcohol	20652463	The <strong>ALDH2</strong>*2 variant is associated with partial protection against <b>alcohol</b> dependence but confers significantly increased risk for <b>alcohol</b> related cancers as a function of <b>alcohol</b> exposure.
+ALDH2	addiction	dependence	20652463	The <strong>ALDH2</strong>*2 variant is associated with partial protection against alcohol <b>dependence</b> but confers significantly increased risk for alcohol related cancers as a function of alcohol exposure.
+ALDH2	drug	alcohol	20652463	Results provide initial evidence of the feasibility, acceptability, and brief efficacy of web based genetic feedback for reducing <b>alcohol</b> related health risks associated with <strong>ALDH2</strong> genotype.
+ALDH2	drug	alcohol	20626721	While the rs1800759 and rs1042364 A A haplotype had a potential protective influence on the risk for several AD related phenotypes, this effect is rather small compared to functional variants of other <b>alcohol</b> or acetaldehyde metabolizing enzymes like <strong>ALDH2</strong>*2 or ADH1B*2.
+ALDH2	drug	alcohol	20598484	The genetic variation of ADH1B, <strong>ALDH2</strong>, and CYP2E1 is different among racial populations and cause difference in elimination rates of <b>alcohol</b>.
+ALDH2	drug	alcohol	20598484	This study may be useful in epidemiological studies of the influence of ADH1B, <strong>ALDH2</strong>, CYP2E1*6, and CYP2E1*7B polymorphisms on diseases, including several types of cancer related to <b>alcohol</b> consumption and <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	20598484	This study may be useful in epidemiological studies of the influence of ADH1B, <strong>ALDH2</strong>, CYP2E1*6, and CYP2E1*7B polymorphisms on diseases, including several types of cancer related to alcohol consumption and alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	20518787	Comparison between self reported facial flushing after <b>alcohol</b> consumption and <strong>ALDH2</strong> Glu504Lys polymorphism for risk of upper aerodigestive tract cancer in a Japanese population.
+ALDH2	drug	alcohol	20518787	No significant interaction between facial flushing and <b>alcohol</b> consumption was observed in this study, whereas <strong>ALDH2</strong> Lys allele had significant association with UAT cancer.
+ALDH2	drug	alcohol	20477771	MAOA interacts with the <strong>ALDH2</strong> gene in anxiety depression <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	20477771	MAOA interacts with the <strong>ALDH2</strong> gene in anxiety depression alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	20178264	About half of northeastern Asians lack <strong>ALDH2</strong> (Acetaldehyde Dehydrogenase 2), an enzyme involved in <b>alcohol</b> metabolism.
+ALDH2	drug	alcohol	20178264	People with deficient <strong>ALDH2</strong> often experience facial flushing after drinking a small dose of <b>alcohol</b>.
+ALDH2	drug	nicotine	20093384	We conducted a case control study to examine possible interaction between <b>smoking</b> and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) Glu504Lys polymorphism (rs671) on the risk of lung cancer in Japanese.
+ALDH2	drug	nicotine	20093384	The impact of <b>smoking</b>, <strong>ALDH2</strong> genotype, and their interaction on lung cancer risk were assessed by odds ratio (OR) and 95% confidence interval adjusted for potential confounders.
+ALDH2	drug	nicotine	20093384	Interaction between <strong>ALDH2</strong> genotype (Glu/Glu + Glu/Lys versus Lys/Lys) and cumulative <b>smoking</b> dose was statistically significant (P = 0.036) and was consistently observed in the analysis among never drinkers (interaction P = 0.041).
+ALDH2	drug	nicotine	20093384	These results suggest that <strong>ALDH2</strong> Lys/Lys, a null enzyme activity genotype, modifies the impact of <b>smoking</b> on the risk of lung cancer.
+ALDH2	drug	alcohol	20077761	The genotype frequencies of the ADH2 and <strong>ALDH2</strong> gene polymorphisms as well as the A118G polymorphism of the mu opioid receptor gene (OPRM1) in Korean men and women with <b>alcohol</b> dependence (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for <b>alcoholism</b>.
+ALDH2	drug	opioid	20077761	The genotype frequencies of the ADH2 and <strong>ALDH2</strong> gene polymorphisms as well as the A118G polymorphism of the mu <b>opioid</b> receptor gene (OPRM1) in Korean men and women with alcohol dependence (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for alcoholism.
+ALDH2	addiction	dependence	20077761	The genotype frequencies of the ADH2 and <strong>ALDH2</strong> gene polymorphisms as well as the A118G polymorphism of the mu opioid receptor gene (OPRM1) in Korean men and women with alcohol <b>dependence</b> (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for alcoholism.
+ALDH2	drug	alcohol	20077761	These results suggest that, while the risk of <b>alcoholism</b> in Korean men is predominantly affected by the presence of the <strong>ALDH2</strong> 1/1 genotype, the risk of <b>alcoholism</b> in Korean women is primarily associated with the ADH2 1/1 genotype and G carrier genotype of the OPRM1 A118G polymorphism.
+ALDH2	drug	alcohol	20025435	The association between two functional polymorphisms in <b>alcohol</b> dehydrogenase (ADH2/ADH1B) and aldehyde dehydrogenase (<strong>ALDH2</strong>) genes and <b>alcohol</b> dependence was examined in 182 Chinese and Indian patients undergoing treatment for <b>alcohol</b> dependence and 184 screened control subjects from Singapore.
+ALDH2	addiction	dependence	20025435	The association between two functional polymorphisms in alcohol dehydrogenase (ADH2/ADH1B) and aldehyde dehydrogenase (<strong>ALDH2</strong>) genes and alcohol <b>dependence</b> was examined in 182 Chinese and Indian patients undergoing treatment for alcohol <b>dependence</b> and 184 screened control subjects from Singapore.
+ALDH2	drug	alcohol	20025435	Our results showed that frequencies of ADH1B*2 and <strong>ALDH2</strong>*2 were higher in controls compared to <b>alcohol</b> dependent subjects for both Chinese and Indians.
+ALDH2	drug	alcohol	19942091	This study was designed to evaluate the role of facilitated detoxification of acetaldehyde, the main metabolic product of <b>ethanol</b>, through systemic overexpression of mitochondrial aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) on acute <b>ethanol</b> exposure induced myocardial damage.
+ALDH2	drug	alcohol	19942091	Wild type FVB (friend virus B) and <strong>ALDH2</strong> mice were challenged with <b>ethanol</b> (3 g/kg, intraperitoneally), and cardiac function was assessed 24 h later using the Langendroff and cardiomyocyte edge detection systems.
+ALDH2	drug	alcohol	19942091	<strong>ALDH2</strong> reduced <b>ethanol</b> induced elevation in cardiac acetaldehyde levels.
+ALDH2	drug	alcohol	19942091	Acute <b>ethanol</b> challenge deteriorated myocardial and cardiomyocyte contractile function evidenced by reduction in maximal velocity of pressure development and decline (+/ dP/dt), left ventricular developed pressure, cell shortening, and prolonged relengthening duration, the effects of which were alleviated by <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	19942091	<b>Ethanol</b> treatment dampened phosphorylation of Akt and AMPK associated with up regulated PP2A and PP2C, which was abrogated by <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	19942091	<strong>ALDH2</strong> significantly attenuated <b>ethanol</b> induced decrease in Akt  and AMPK stimulated phosphorylation of Foxo3 at Thr32 and Ser413, respectively.
+ALDH2	drug	alcohol	19942091	Consistently, <strong>ALDH2</strong> rescued <b>ethanol</b> induced myocardial apoptosis, protein damage, and mitochondrial membrane potential depolarization.
+ALDH2	drug	alcohol	19942091	Our results suggest that <strong>ALDH2</strong> is cardioprotective against acute <b>ethanol</b> toxicity, possibly through inhibition of protein phosphatases, leading to enhanced Akt and AMPK activation, and subsequently, inhibition of Foxo3, apoptosis, and mitochondrial dysfunction.
+ALDH2	drug	alcohol	19403456	Association of ADH1B and <strong>ALDH2</strong> gene polymorphisms with <b>alcohol</b> dependence: a pilot study from India.
+ALDH2	addiction	dependence	19403456	Association of ADH1B and <strong>ALDH2</strong> gene polymorphisms with alcohol <b>dependence</b>: a pilot study from India.
+ALDH2	drug	alcohol	19403456	The highlight of the study findings was the uniquely high frequency of the <strong>ALDH2</strong>*2/*2 genotype (among <b>alcohol</b> dependent subjects) being a risk conferring factor for <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	19403456	The highlight of the study findings was the uniquely high frequency of the <strong>ALDH2</strong>*2/*2 genotype (among alcohol dependent subjects) being a risk conferring factor for alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	19393179	The <b>alcohol</b> sensitivity in Orientals is due to a delayed oxidation of acetaldehyde by an atypical aldehyde dehydrogenase ALDH2487Lys, which is resulted from a structural mutation in gene <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	19302089	MAOA uVNTR polymorphism may modify the protective effect of <strong>ALDH2</strong> gene against <b>alcohol</b> dependence in antisocial personality disorder.
+ALDH2	addiction	dependence	19302089	MAOA uVNTR polymorphism may modify the protective effect of <strong>ALDH2</strong> gene against alcohol <b>dependence</b> in antisocial personality disorder.
+ALDH2	drug	alcohol	19302089	Antisocial <b>alcoholism</b> is related to dopamine and serotonin which are catalyzed by monoamine oxidase A (MAOA) and acetaldehyde dehydrogenase 2 (<strong>ALDH2</strong>).
+ALDH2	drug	alcohol	19302089	The objective of this study is to determine whether the interaction between the MAOA and the <strong>ALDH2</strong> genes is associated with subjects with antisocial personality disorder (ASPD) having <b>alcoholism</b>.
+ALDH2	drug	alcohol	19302089	However, the protective effects of the <strong>ALDH2</strong>*2 allele against <b>alcoholism</b> might disappear in subjects with ASPD and carrying MAOA uVNTR 4 repeat allele in the Han Chinese male population.
+ALDH2	drug	alcohol	19298328	Association between personality traits and <strong>ALDH2</strong> polymorphism in Japanese male <b>alcoholics</b>.
+ALDH2	drug	alcohol	19298328	<b>Alcoholics</b> who have developed <b>alcoholism</b> despite a strong negative risk factor, that is, the inactive form of aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), are considered advantageous for studying predisposing factors for <b>alcoholism</b>.
+ALDH2	drug	alcohol	19298328	This study aimed to compare personality profiles and clinical characteristics between <b>alcoholics</b> with active and inactive <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	19298328	<b>Alcoholics</b> with inactive <strong>ALDH2</strong> had significantly higher novelty seeking (NS) and lower harm avoidance (HA) scores compared with those with active <strong>ALDH2</strong>.
+ALDH2	addiction	relapse	19298328	Alcoholics with inactive <strong>ALDH2</strong> had significantly higher novelty <b>seeking</b> (NS) and lower harm avoidance (HA) scores compared with those with active <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	19298328	These results suggest that high NS and low HA scores in <b>alcoholics</b> with inactive <strong>ALDH2</strong> are associated with an increased risk for developing <b>alcoholism</b>, despite a low enzymatic ability to eliminate toxic acetaldehyde in these subjects.
+ALDH2	drug	alcohol	19298328	A study of <b>alcoholics</b> with inactive <strong>ALDH2</strong> is useful for detecting environmental or personality factors related to <b>alcoholism</b>.
+ALDH2	drug	alcohol	19251111	Liver <b>alcohol</b> dehydrogenase oxidizes <b>ethanol</b> to acetaldehyde, which is further oxidized to acetate by aldehyde dehydrogenase 2 (<strong>ALDH2</strong>*1).
+ALDH2	drug	alcohol	19251111	Individuals who carry a low activity <strong>ALDH2</strong> (<strong>ALDH2</strong>*2) display high blood acetaldehyde levels after <b>ethanol</b> consumption, which leads to dysphoric effects, such as facial flushing, nausea, dizziness, and headache ("Asian <b>alcohol</b> phenotype"), which result in an aversion to <b>alcohol</b> and protection against <b>alcohol</b> abuse and <b>alcoholism</b>.
+ALDH2	addiction	aversion	19251111	Individuals who carry a low activity <strong>ALDH2</strong> (<strong>ALDH2</strong>*2) display high blood acetaldehyde levels after ethanol consumption, which leads to dysphoric effects, such as facial flushing, nausea, dizziness, and headache ("Asian alcohol phenotype"), which result in an <b>aversion</b> to alcohol and protection against alcohol abuse and alcoholism.
+ALDH2	drug	alcohol	19251111	This study describes chemically synthesized siRNAs and an endogenously synthesized shRNA, which reduce <strong>ALDH2</strong> activity and constitute tools that should be of value for further <b>alcohol</b> research.
+ALDH2	drug	alcohol	19014920	Functional variant alleles ADH1B*2 and <strong>ALDH2</strong>*2 have been consistently replicated to show protection against developing <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	19014920	Functional variant alleles ADH1B*2 and <strong>ALDH2</strong>*2 have been consistently replicated to show protection against developing alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	19014920	Multiple logistic regression analyses suggest that ADH1B*2 and <strong>ALDH2</strong>*2 may independently influence the risk for <b>alcoholism</b>.
+ALDH2	drug	alcohol	19014920	It has been well documented that homozygosity of <strong>ALDH2</strong>*2 almost fully protects against developing <b>alcoholism</b> and that the heterozygosity only affords a partial protection to varying degrees.
+ALDH2	drug	alcohol	19014920	Correlations of blood <b>ethanol</b> and acetaldehyde concentrations, cardiovascular hemodynamic responses, and subjective perceptions have been investigated in men with different combinatorial ADH1B and <strong>ALDH2</strong> genotypes following challenge with <b>ethanol</b> for a period of 130 min.
+ALDH2	drug	alcohol	19014920	The pharmacokinetic and pharmacodynamic consequences indicate that acetaldehyde, rather than <b>ethanol</b>, is primarily responsible for the observed <b>alcohol</b> sensitivity reactions, suggesting that the full protection by <strong>ALDH2</strong>*2/*2 can be ascribed to the intense unpleasant physiological and psychological reactions caused by persistently elevated blood acetaldehyde after ingesting a small amount of <b>alcohol</b> and that the partial protection by <strong>ALDH2</strong>*1/*2 can be attributed to a faster elimination of acetaldehyde and the lower accumulation in circulation.
+ALDH2	drug	alcohol	19014920	Physiological tolerance or innate insensitivity to acetaldehyde may be crucial for development of <b>alcohol</b> dependence in <b>alcoholics</b> carrying <strong>ALDH2</strong>*2.
+ALDH2	addiction	dependence	19014920	Physiological tolerance or innate insensitivity to acetaldehyde may be crucial for development of alcohol <b>dependence</b> in alcoholics carrying <strong>ALDH2</strong>*2.
+ALDH2	drug	alcohol	18996923	Associations of ADH and <strong>ALDH2</strong> gene variation with self report <b>alcohol</b> reactions, consumption and dependence: an integrated analysis.
+ALDH2	addiction	dependence	18996923	Associations of ADH and <strong>ALDH2</strong> gene variation with self report alcohol reactions, consumption and <b>dependence</b>: an integrated analysis.
+ALDH2	drug	alcohol	18996923	This study tested for associations between nine polymorphisms in <strong>ALDH2</strong> and 41 in the seven ADH genes, and <b>alcohol</b> related flushing, <b>alcohol</b> use and dependence symptom scores in 4597 Australian twins.
+ALDH2	addiction	dependence	18996923	This study tested for associations between nine polymorphisms in <strong>ALDH2</strong> and 41 in the seven ADH genes, and alcohol related flushing, alcohol use and <b>dependence</b> symptom scores in 4597 Australian twins.
+ALDH2	drug	alcohol	18996923	<strong>ALDH2</strong> variation was not associated with flushing or <b>alcohol</b> consumption, but was weakly associated with AD measures.
+ALDH2	addiction	intoxication	18782342	The <strong>ALDH2</strong> promoter variant was associated with <b>binge</b> drinking, and the ALDH1b1 ala69val polymorphism was associated with diastolic blood pressure.
+ALDH2	drug	alcohol	18613661	The <strong>ALDH2</strong>*2 gene encoding the inactive variant form of mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>) protects nearly all carriers of this gene from <b>alcoholism</b>.
+ALDH2	drug	alcohol	18613661	Inhibition of <strong>ALDH2</strong> has hence become a possible strategy to treat <b>alcoholism</b>.
+ALDH2	drug	alcohol	18613661	The natural product 7 O glucosyl 4' hydroxyisoflavone (daidzin), isolated from the kudzu vine (Peruraria lobata), is a specific inhibitor of <strong>ALDH2</strong> and suppresses <b>ethanol</b> consumption.
+ALDH2	drug	alcohol	18613661	Daidzin is the active principle in a herbal remedy for "<b>alcohol</b> addiction" and provides a lead for the design of improved <strong>ALDH2</strong>.
+ALDH2	addiction	addiction	18613661	Daidzin is the active principle in a herbal remedy for "alcohol <b>addiction</b>" and provides a lead for the design of improved <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	18299763	Variant alleles of aldehyde dehydrogenase (<strong>ALDH2</strong>) and <b>alcohol</b> dehydrogenase (ADH1B) genes are prevalent in individuals of Asian heritage and have been associated with an increased level of response to <b>alcohol</b> and a decreased risk for <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	18299763	Variant alleles of aldehyde dehydrogenase (<strong>ALDH2</strong>) and alcohol dehydrogenase (ADH1B) genes are prevalent in individuals of Asian heritage and have been associated with an increased level of response to alcohol and a decreased risk for alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	18299763	The current study examined self report level of response to <b>alcohol</b>, <strong>ALDH2</strong> and ADH1B, country of origin, and family history of <b>alcoholism</b> in 154 Chinese  and 181 Korean American college students.
+ALDH2	drug	alcohol	18299763	This relationship remained significant after considering the effects of gender, height, weight, quantity and frequency of <b>alcohol</b> consumption (over the previous 90 days), <strong>ALDH2</strong> genotype, ADH1B genotype, country of origin, and first degree family history of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	18299763	This relationship remained significant after considering the effects of gender, height, weight, quantity and frequency of alcohol consumption (over the previous 90 days), <strong>ALDH2</strong> genotype, ADH1B genotype, country of origin, and first degree family history of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	18070247	In line with the above, we have tested if inhibiting the expression of the aldehyde dehydrogenase gene (<strong>ALDH2</strong>) by an anti <strong>Aldh2</strong> antisense gene can curtail the drive of <b>alcohol</b> dependent animals to consume <b>alcohol</b>.
+ALDH2	drug	alcohol	18070247	The single intravenous administration of an anti <strong>Aldh2</strong> antisense gene carried by an adenoviral vector reduced liver <strong>ALDH2</strong> activity by 85% (p < 0.002) and inhibited voluntary <b>ethanol</b> intake by 50% (ANOVA p < 0.005) for 34 days.
+ALDH2	drug	alcohol	17980785	The guidelines for <b>Disulfiram</b>, an <strong>ALDH2</strong> inhibitor, provide a set of guidelines for use with the herb Pueraria lobata.
+ALDH2	drug	alcohol	17980785	The recommendations for its use should be similar to those for the <strong>ALDH2</strong> inhibitor, <b>Disulfiram</b>.
+ALDH2	drug	alcohol	17960296	A previous cross sectional study showed that, among individuals of Chinese and Korean descent, possession of <strong>ALDH2</strong>*2 alleles was associated with protection against <b>alcohol</b> dependence, whereas conduct disorder was associated with increased vulnerability to dependence.
+ALDH2	addiction	dependence	17960296	A previous cross sectional study showed that, among individuals of Chinese and Korean descent, possession of <strong>ALDH2</strong>*2 alleles was associated with protection against alcohol <b>dependence</b>, whereas conduct disorder was associated with increased vulnerability to <b>dependence</b>.
+ALDH2	drug	alcohol	17960296	The degree of <b>alcohol</b> consumption observed among participants with <strong>ALDH2</strong>*2 alleles is consistent with previous findings showing that, although their presence may be protective, it does not preclude heavy drinking episodes.
+ALDH2	drug	alcohol	17948892	Due to the documented protective effects against <b>alcoholism</b> of <strong>ALDH2</strong>*1/*2 or *2/*2 genotype among the Han Chinese population, we recruited antisocial non <b>alcoholics</b> from the Han Chinese population in Taiwan to verify Cloninger's hypotheses.
+ALDH2	drug	alcohol	17885622	Pharmacokinetic and pharmacodynamic basis for partial protection against <b>alcoholism</b> in Asians, heterozygous for the variant <strong>ALDH2</strong>*2 gene allele.
+ALDH2	drug	alcohol	17885622	It has been well documented that although homozygosity of the variant aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) gene allele, <strong>ALDH2</strong>*2, in Asians almost fully protects against <b>alcoholism</b>, the heterozygosity only affords a partial protection to varying degrees.
+ALDH2	drug	alcohol	17885622	The subjects were divided into 3 combinatorial genotypic groups of <b>alcohol</b> dehydrogenase (ADH) and ALDH, that is, <strong>ALDH2</strong>*1/*1 ADH1B*1/*1 ADH1C*1/*1 (n=8), <strong>ALDH2</strong>*1/*1 ADH1B*2/*2 ADH1C*1/*1 (n=8), and <strong>ALDH2</strong>*1/*2 ADH1B*2/*2 ADH1C*1/*1 (n=16).
+ALDH2	drug	alcohol	17885622	Heterozygotic <strong>ALDH2</strong>*1/*2 subjects were found to be strikingly responsive to the moderate amount of <b>alcohol</b>, as evidenced by the prominent cardiovascular effects as well as subjective perceptions of general discomfort for as long as 2 h following ingestion.
+ALDH2	drug	alcohol	17718397	Variants of three genes encoding <b>alcohol</b> metabolizing enzymes, the aldehyde dehydrogenase gene <strong>ALDH2</strong> and the <b>alcohol</b> dehydrogenase genes ADH1B and ADH1C, have been associated with reduced rates of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	17718397	Variants of three genes encoding alcohol metabolizing enzymes, the aldehyde dehydrogenase gene <strong>ALDH2</strong> and the alcohol dehydrogenase genes ADH1B and ADH1C, have been associated with reduced rates of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	17673211	We previously reported that mitochondrial <strong>ALDH2</strong> could be inactivated via S nitrosylation in <b>ethanol</b> exposed rats.
+ALDH2	drug	alcohol	17488809	Since the release of NADH from the ADH.NADH complex constitutes the rate limiting step of ADH (but not of <strong>ALDH2</strong>) activity, endogenous NADH oxidizing substrates present at the time of <b>ethanol</b> intake may contribute to the acetaldehyde burst.
+ALDH2	drug	alcohol	17454860	We determined the allele and genotype of ADH2, ADH3 and <strong>ALDH2</strong> in 198 subjects: 57 with <b>alcohol</b> cirrhosis, 44 with <b>alcohol</b> chronic pancreatitis and 43 "healthy <b>alcoholics</b>"; 54 healthy non drinkers served as controls.
+ALDH2	drug	alcohol	17454860	Genetic polymorphism of <strong>ALDH2</strong> shows no correlation with <b>alcohol</b> addiction or <b>alcohol</b> cirrhosis and <b>alcohol</b> chronic pancreatitis.
+ALDH2	addiction	addiction	17454860	Genetic polymorphism of <strong>ALDH2</strong> shows no correlation with alcohol <b>addiction</b> or alcohol cirrhosis and alcohol chronic pancreatitis.
+ALDH2	drug	alcohol	17058263	Measurement of activity and immunoblot results showed that <strong>ALDH2</strong> and ATP synthase were also inhibited through oxidative modification of their cysteine or tyrosine residues in <b>alcoholic</b> fatty livers of rats.
+ALDH2	drug	alcohol	16822169	Meta analyses of <strong>ALDH2</strong> and ADH1B with <b>alcohol</b> dependence in Asians.
+ALDH2	addiction	dependence	16822169	Meta analyses of <strong>ALDH2</strong> and ADH1B with alcohol <b>dependence</b> in Asians.
+ALDH2	drug	alcohol	16822169	Meta analyses were conducted to determine the magnitude of relationships between polymorphisms in 2 genes, <strong>ALDH2</strong> and ADH1B, with <b>alcohol</b> dependence in Asians.
+ALDH2	addiction	dependence	16822169	Meta analyses were conducted to determine the magnitude of relationships between polymorphisms in 2 genes, <strong>ALDH2</strong> and ADH1B, with alcohol <b>dependence</b> in Asians.
+ALDH2	drug	alcohol	16818871	The <strong>ALDH2</strong>*2 allele has been shown to be a protective factor against <b>alcoholism</b> in a normal population owing in part to the elevated blood level of acetaldehyde and its accompanying physiological discomforts after drinking <b>alcohol</b>.
+ALDH2	drug	alcohol	16818871	Despite the well established link between the <strong>ALDH2</strong>*2 allele and the physiological discomforts after drinking, very little is known regarding the psychological expectancies of drinking among persons with <b>alcoholism</b> with different ALDH genotypes.
+ALDH2	drug	alcohol	16818871	To determine whether there are differences in craving, <b>alcohol</b> consumption, and <b>alcohol</b> outcome expectancies between persons with <b>alcoholism</b> who have the <strong>ALDH2</strong>*1/*2 genotype and persons with <b>alcoholism</b> who have the <strong>ALDH2</strong>*1/*1 genotype.
+ALDH2	addiction	relapse	16818871	To determine whether there are differences in <b>craving</b>, alcohol consumption, and alcohol outcome expectancies between persons with alcoholism who have the <strong>ALDH2</strong>*1/*2 genotype and persons with alcoholism who have the <strong>ALDH2</strong>*1/*1 genotype.
+ALDH2	drug	alcohol	16818871	Overall, the <strong>ALDH2</strong>*1/*2 group had lower negative <b>alcohol</b> outcome expectancies (F(4,93) = 2.43, P < or = .05, eta(p)2 = 0.10).
+ALDH2	drug	alcohol	16818871	Moreover, the <strong>ALDH2</strong>*1/*2 group had higher positive <b>alcohol</b> outcome expectancies (F(7,90) = 2.36, P < .05, eta(p)2 = 0.16), and they had more expected positive outcomes in the relaxation and tension reduction domain (P < .05).
+ALDH2	drug	alcohol	16818871	Although the <strong>ALDH2</strong>*2 allele has been associated with negative physiological responses in normal samples in past research, the psychological expectancies of drinking are more positive and less negative for persons with <b>alcoholism</b> who have the <strong>ALDH2</strong>*1/*2 genotype.
+ALDH2	drug	alcohol	16792555	Effects of variation at the <strong>ALDH2</strong> locus on <b>alcohol</b> metabolism, sensitivity, consumption, and dependence in Europeans.
+ALDH2	addiction	dependence	16792555	Effects of variation at the <strong>ALDH2</strong> locus on alcohol metabolism, sensitivity, consumption, and <b>dependence</b> in Europeans.
+ALDH2	drug	alcohol	16792555	The low activity variant of the aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) gene found in East Asian populations leads to the <b>alcohol</b> flush reaction and reduces <b>alcohol</b> consumption and risk of <b>alcohol</b> dependence (AD).
+ALDH2	addiction	dependence	16792555	The low activity variant of the aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) gene found in East Asian populations leads to the alcohol flush reaction and reduces alcohol consumption and risk of alcohol <b>dependence</b> (AD).
+ALDH2	drug	alcohol	16792555	Haplotypes based on 5 single nucleotide polymorphisms (SNPs) were used in tests of the effects of variation in the <strong>ALDH2</strong> gene on <b>alcohol</b> metabolism and <b>alcohol</b>'s effects.
+ALDH2	drug	alcohol	16792555	Significant effects of <strong>ALDH2</strong> haplotype were observed for breath <b>alcohol</b> concentration, with similar but smaller and nonsignificant effects on blood <b>alcohol</b>.
+ALDH2	drug	alcohol	16792555	Genetic variation in <strong>ALDH2</strong> affects <b>alcohol</b> metabolism in Europeans.
+ALDH2	drug	alcohol	16685648	Diplotype trend regression analysis of the ADH gene cluster and the <strong>ALDH2</strong> gene: multiple significant associations with <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	16685648	Diplotype trend regression analysis of the ADH gene cluster and the <strong>ALDH2</strong> gene: multiple significant associations with alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	16679777	We also genotyped a polymorphism, G1510A, in the acetaldehyde dehydrogenase 2 gene (<strong>ALDH2</strong>), in which the A allele causes poor metabolism of acetaldehyde, a major metabolite of <b>alcohol</b>.
+ALDH2	drug	alcohol	16679777	Both OPRM1 118G and <strong>ALDH2</strong> 1510G were significantly associated with <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	16679777	Both OPRM1 118G and <strong>ALDH2</strong> 1510G were significantly associated with alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	16679777	These results suggest that OPRM1 118G in addition to <strong>ALDH2</strong> 1510G might be one of the risk factors for <b>alcohol</b> dependence in Japanese people.
+ALDH2	addiction	dependence	16679777	These results suggest that OPRM1 118G in addition to <strong>ALDH2</strong> 1510G might be one of the risk factors for alcohol <b>dependence</b> in Japanese people.
+ALDH2	drug	alcohol	16679343	There were no significant differences in the genotype frequencies of the DRD2, <strong>ALDH2</strong>, 5 HTTLPR, and COMT polymorphisms between <b>alcoholics</b> with and without ADHD.
+ALDH2	drug	alcohol	16612210	Despite great advances in understanding of genetic vulnerability in <b>alcohol</b> use disorders, only two gene complexes, ADH and <strong>ALDH2</strong>, have been identified as having defined effects on <b>alcohol</b> use and liability to dependence in humans.
+ALDH2	addiction	dependence	16612210	Despite great advances in understanding of genetic vulnerability in alcohol use disorders, only two gene complexes, ADH and <strong>ALDH2</strong>, have been identified as having defined effects on alcohol use and liability to <b>dependence</b> in humans.
+ALDH2	drug	alcohol	21432367	The subjects were 264 men aged 39 to 80 years who were classified into the <strong>ALDH2</strong> deficiency or sufficiency group using the <b>ethanol</b> patch test and the Tokyo University <strong>ALDH2</strong> Phenotype Screening Test.
+ALDH2	drug	nicotine	21432367	Blood pressure and the levels of biochemical markers in groups with <strong>ALDH2</strong> sufficiency, <strong>ALDH2</strong> deficiency and drinking habit were compared using multiple regression models for adjusting age, <b>smoking</b> habit, physical exercising habit and body mass index.
+ALDH2	drug	alcohol	21432367	The levels of serum high density lipoprotein cholesterol, triglycerides, aspartate aminotransferase (AST) and gamma glutamyl transpeptidase (γ GTP) were significantly higher in current drinkers of 20 g of <b>ethanol</b> or more per day than in nondrinkers of the <strong>ALDH2</strong> sufficiency group.
+ALDH2	drug	alcohol	21432367	The levels of serum AST and γ GTP in current drinkers of 20 g of <b>ethanol</b> or more per day, and fasting blood sugar in current drinkers of less than 20 g of <b>ethanol</b> per day were significantly higher than those in nondrinkers of the <strong>ALDH2</strong> deficiency group.
+ALDH2	drug	alcohol	21432367	These results suggest that <b>alcohol</b> consumption increases the levels of serum lipids and liver enzymes in <strong>ALDH2</strong> sufficient individuals and liver enzymes and blood glucose levels in <strong>ALDH2</strong> deficient individuals.
+ALDH2	drug	alcohol	16440674	We analyzed the Kurihama <b>Alcoholism</b> Screening Test (KAST), the Adolescent <b>Alcohol</b> Involvement Scale (AAIS), the Fagerstroem Tolerance Questionnaire (FTQ), the Tokyo University <strong>ALDH2</strong> Phenotype Screening Test (TAST), results of <b>ethanol</b> patch tests, the presence or absence of a smoking habit, and gender by "Hayashi's quantification theory, type II" in 415 senior students (232 males and 183 females) of a dental college between 2000 and 2003, and evaluated their relationships.
+ALDH2	drug	nicotine	16440674	We analyzed the Kurihama Alcoholism Screening Test (KAST), the Adolescent Alcohol Involvement Scale (AAIS), the Fagerstroem Tolerance Questionnaire (FTQ), the Tokyo University <strong>ALDH2</strong> Phenotype Screening Test (TAST), results of ethanol patch tests, the presence or absence of a <b>smoking</b> habit, and gender by "Hayashi's quantification theory, type II" in 415 senior students (232 males and 183 females) of a dental college between 2000 and 2003, and evaluated their relationships.
+ALDH2	drug	alcohol	16404797	Two <b>alcohol</b> dehydrogenase genes (ADHIB and ADH1C on chromosome 4) and one aldehyde dehydrogenase gene (<strong>ALDH2</strong> on chromosome 12) exhibit functional polymorphisms that are associated with lower rates of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	16404797	Two alcohol dehydrogenase genes (ADHIB and ADH1C on chromosome 4) and one aldehyde dehydrogenase gene (<strong>ALDH2</strong> on chromosome 12) exhibit functional polymorphisms that are associated with lower rates of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	16404797	The hypothesized mechanism underlying the associations of the ADH1B and <strong>ALDH2</strong> polymorphisms with <b>alcohol</b> dependence is that the isoenzymes encoded by these alleles lead to an accumulation of acetaldehyde during <b>alcohol</b> metabolism.
+ALDH2	addiction	dependence	16404797	The hypothesized mechanism underlying the associations of the ADH1B and <strong>ALDH2</strong> polymorphisms with alcohol <b>dependence</b> is that the isoenzymes encoded by these alleles lead to an accumulation of acetaldehyde during alcohol metabolism.
+ALDH2	drug	alcohol	16404797	Data are consistent with the hypothesis that elevations in acetaldehyde, increased sensitivity to <b>alcohol</b>, and lower levels of drinking reflect the mechanism by which the <strong>ALDH2</strong>*2 allele reduces risk for <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	16404797	Data are consistent with the hypothesis that elevations in acetaldehyde, increased sensitivity to alcohol, and lower levels of drinking reflect the mechanism by which the <strong>ALDH2</strong>*2 allele reduces risk for alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	16309369	The genotypes of <b>alcohol</b> dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) are related to <b>alcohol</b> dependence and some human disorders.
+ALDH2	addiction	dependence	16309369	The genotypes of alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) are related to alcohol <b>dependence</b> and some human disorders.
+ALDH2	drug	alcohol	16131845	Studies showed that 1) the antisense gene is actively transcribed in the cells and high levels of antisense mRNA are attained, 2) the antisense gene reduced <strong>ALDH2</strong> activity by 65%, and 3) when incubated with 10 mM <b>ethanol</b>, acetaldehyde accumulation by cells increased 8 fold to levels (80 90 microM) known to be aversive to animals and humans.
+ALDH2	addiction	aversion	16131845	Studies showed that 1) the antisense gene is actively transcribed in the cells and high levels of antisense mRNA are attained, 2) the antisense gene reduced <strong>ALDH2</strong> activity by 65%, and 3) when incubated with 10 mM ethanol, acetaldehyde accumulation by cells increased 8 fold to levels (80 90 microM) known to be <b>aversive</b> to animals and humans.
+ALDH2	drug	alcohol	16131845	Data presented show that antialcohol drugs that inhibit <strong>Aldh2</strong> gene expression can be generated endogenously in liver cells infected by an adenoviral vector carrying an antisense coding gene, thus mimicking the high acetaldehyde phenotype that exists in humans carrying the Glu487Lys mutation who are protected against <b>alcoholism</b>.
+ALDH2	drug	alcohol	16125912	One hundred and eleven male patients with <b>alcohol</b> dependence and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 (ADH2), aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), serotonin transporter (5 HTT) and dopamine transporter (DAT1).
+ALDH2	addiction	dependence	16125912	One hundred and eleven male patients with alcohol <b>dependence</b> and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of alcohol dehydrogenase 2 (ADH2), aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), serotonin transporter (5 HTT) and dopamine transporter (DAT1).
+ALDH2	drug	alcohol	16125912	Genotype and allele frequencies of <strong>ALDH2</strong> G1951A SNP in familial or non familial <b>alcoholic</b> patients differ from normal controls.
+ALDH2	drug	alcohol	16046871	Associations between hangover and <strong>ALDH2</strong> genotype, <b>alcohol</b> flushing, and MCV were examined for 251 Japanese workers (139 men, 112 women).
+ALDH2	drug	alcohol	16046871	Inactive <strong>ALDH2</strong>*1/2*2 heterozygotes drank less <b>alcohol</b> than active <strong>ALDH2</strong>*1/2*1 homozygotes (p < 0.0001), but the frequency of hangover did not significantly differ between the two groups for either gender.
+ALDH2	drug	alcohol	16046871	The proportion of men who had hangover three times or more during the past year increased significantly with increased daily <b>alcohol</b> consumption in men with the <strong>ALDH2</strong>*1/2*2 genotype (p = 0.0002) but not in those with the <strong>ALDH2</strong>*1/2*1 genotype.
+ALDH2	drug	alcohol	16046871	For men who usually consumed <44 g of <b>ethanol</b>/day, the median amount of drinking before hangover was significantly lower for <strong>ALDH2</strong>*1/2*2 men than for <strong>ALDH2</strong>*1/2*1 men reporting the same level of consumption.
+ALDH2	drug	alcohol	16046871	Inactive heterozygous <strong>ALDH2</strong>, <b>alcohol</b> flushing, and increased MCV were positively associated with hangover susceptibility in Japanese workers, suggesting that acetaldehyde is etiologically linked to the development of hangover.
+ALDH2	drug	alcohol	15957670	Associations of <strong>ALDH2</strong> and ADH1B genotypes with response to <b>alcohol</b> in Asian Americans.
+ALDH2	drug	alcohol	15957670	Individuals with <b>alcohol</b> dependence are less likely to possess variant alleles of the <b>alcohol</b> metabolizing genes, aldehyde dehydrogenase (<strong>ALDH2</strong>*2) and <b>alcohol</b> dehydrogenase (ADH1B*2), than non <b>alcohol</b> dependent controls.
+ALDH2	addiction	dependence	15957670	Individuals with alcohol <b>dependence</b> are less likely to possess variant alleles of the alcohol metabolizing genes, aldehyde dehydrogenase (<strong>ALDH2</strong>*2) and alcohol dehydrogenase (ADH1B*2), than non alcohol dependent controls.
+ALDH2	drug	alcohol	15957670	Previous research has shown that individuals with <strong>ALDH2</strong>*2 demonstrate enhanced reactions to <b>alcohol</b> compared with those without this genetic variant, but evidence that ADH1B*2 is associated with a greater <b>alcohol</b> response is mixed.
+ALDH2	drug	alcohol	15957670	This study was designed to determine whether the ADH1B genotype is associated with more intense reactions to <b>alcohol</b> after controlling for the <strong>ALDH2</strong> genotype.
+ALDH2	drug	alcohol	15957670	Participants with the <strong>ALDH2</strong>*1/*2 and <strong>ALDH2</strong>*2/*2 genotypes were more likely to experience vomiting following ingestion of the <b>alcohol</b> beverage than those with the <strong>ALDH2</strong>*1/*1 genotype.
+ALDH2	drug	alcohol	15957670	Participants with the <strong>ALDH2</strong>*1/*2 genotype also had greater pulse rate increases, observed flushing ratings, and subjective feelings of intoxication 30 minutes after ingestion of <b>alcohol</b> than participants with the <strong>ALDH2</strong>*1/*1 genotype, despite equivalent blood <b>alcohol</b> concentration (BAC) measurements.
+ALDH2	addiction	intoxication	15957670	Participants with the <strong>ALDH2</strong>*1/*2 genotype also had greater pulse rate increases, observed flushing ratings, and subjective feelings of <b>intoxication</b> 30 minutes after ingestion of alcohol than participants with the <strong>ALDH2</strong>*1/*1 genotype, despite equivalent blood alcohol concentration (BAC) measurements.
+ALDH2	drug	alcohol	15957670	Among participants with the <strong>ALDH2</strong>*1/*1 genotype, there were no additional effects of the ADH1B genotype on any measures of response to <b>alcohol</b>.
+ALDH2	drug	alcohol	15957670	Among participants with the <strong>ALDH2</strong>*1/*2 genotype, those with the ADH1B*2/*2 genotype were more likely to experience <b>alcohol</b> induced vomiting and to report feeling less "great overall" 30 minutes after ingestion of <b>alcohol</b> than those with the ADH1B*1/*2 genotype.
+ALDH2	drug	alcohol	15957670	These findings are consistent with the hypothesis that there is an additional effect of ADH1B*2 on level of response to <b>alcohol</b>, but only among individuals with the <strong>ALDH2</strong>*1/*2 genotype.
+ALDH2	drug	alcohol	15900217	Polymorphisms in the mitochondrial aldehyde dehydrogenase gene (<strong>Aldh2</strong>) determine peak blood acetaldehyde levels and voluntary <b>ethanol</b> consumption in rats.
+ALDH2	drug	alcohol	15900217	Wistar derived rats selectively bred as low <b>alcohol</b> consumers for many generations present an allele (<strong>Aldh2</strong>(2)) of mitochondrial aldehyde dehydrogenase that does not exist in high <b>alcohol</b> consumers, which mostly carry the <strong>Aldh2</strong>(1) allele.
+ALDH2	drug	alcohol	15900217	Data show that, with a mixed genetic background, F2 <strong>Aldh2</strong>(1)/<strong>Aldh2</strong>(1) rats voluntarily consume 65% more <b>alcohol</b> (P<0.01) than F2 <strong>Aldh2</strong>(2)/<strong>Aldh2</strong>(2) rats.
+ALDH2	drug	alcohol	15900217	A major phenotypic difference was a five fold higher (P<0.0025) peak blood acetaldehyde level following <b>ethanol</b> administration in the lower drinker F2 <strong>Aldh2</strong>(2)/<strong>Aldh2</strong>(2) compared to the higher drinker F2 <strong>Aldh2</strong>(1)/<strong>Aldh2</strong>(1) animals, despite the existence of identical steady state levels of blood acetaldehyde in animals of both genotypes.
+ALDH2	drug	alcohol	15900217	Polymorphisms in <strong>Aldh2</strong> play an important role in: (i) determining peak blood acetaldehyde levels and (ii) modulating voluntary <b>ethanol</b> consumption.
+ALDH2	drug	alcohol	15900217	We postulate that the markedly higher peak of blood acetaldehyde generated in <strong>Aldh2</strong>(2)/<strong>Aldh2</strong>(2)(2) animals is aversive, leading to a reduced <b>alcohol</b> intake in <strong>Aldh2</strong>(2)/<strong>Aldh2</strong>(2) versus that in <strong>Aldh2</strong>(1)/<strong>Aldh2</strong>(1) animals.
+ALDH2	addiction	aversion	15900217	We postulate that the markedly higher peak of blood acetaldehyde generated in <strong>Aldh2</strong>(2)/<strong>Aldh2</strong>(2)(2) animals is <b>aversive</b>, leading to a reduced alcohol intake in <strong>Aldh2</strong>(2)/<strong>Aldh2</strong>(2) versus that in <strong>Aldh2</strong>(1)/<strong>Aldh2</strong>(1) animals.
+ALDH2	drug	alcohol	15863807	The authors examined the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 and 3 (ADH2 and ADH3) and aldehyde dehydrogenase (<strong>ALDH2</strong>) in patients diagnosed as having Cloninger's type I or type II <b>alcoholism</b>.
+ALDH2	drug	alcohol	15863807	Seventy two <b>alcoholic</b> men and 38 nonalcoholic, healthy men were tested for the distribution of genotypes and alleles of ADH2, ADH3, and <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	15863807	The frequency of the <strong>ALDH2</strong>*1 allele was significantly higher in men with <b>alcohol</b> dependence than in healthy men.
+ALDH2	addiction	dependence	15863807	The frequency of the <strong>ALDH2</strong>*1 allele was significantly higher in men with alcohol <b>dependence</b> than in healthy men.
+ALDH2	drug	alcohol	15842823	To study the distribution of genotypes about <b>alcohol</b> dehydrogenase 2 (ADH2) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) and its relationship with drinking behaviors in Chinese Han healthy population as to providing a theoretic direction for filtering out high risk and sensitive individuals and taking preventive measures to decrease the <b>alcohol</b> related diseases.
+ALDH2	drug	alcohol	15842823	Correlation between genotypes of ADH2 and <strong>ALDH2</strong> and <b>alcohol</b> related diseases should be more important.
+ALDH2	drug	alcohol	15629893	The possible influence of complex I on <strong>ALDH2</strong> activity and voluntary <b>ethanol</b> intake was investigated.
+ALDH2	drug	alcohol	15542751	<b>Alcohol</b> dehydrogenase (ADH) and aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) play central roles in the metabolism of <b>ethanol</b> and its metabolite, acetaldehyde, in the liver.
+ALDH2	drug	alcohol	15542751	The results revealed that (1) the less active allele of the ADH2 gene (ADH2*1) is associated with an increased risk for <b>alcohol</b> dependence, <b>alcohol</b> induced persistent amnestic disorder, <b>alcohol</b> withdrawal syndrome, and cancer of the upper GI tract; (2) the inactive allele of the <strong>ALDH2</strong> gene (<strong>ALDH2</strong>*2) is associated with a decreased risk for <b>alcohol</b> dependence, and an increased risk for <b>alcoholic</b> polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	15542751	The results revealed that (1) the less active allele of the ADH2 gene (ADH2*1) is associated with an increased risk for alcohol <b>dependence</b>, alcohol induced persistent amnestic disorder, alcohol withdrawal syndrome, and cancer of the upper GI tract; (2) the inactive allele of the <strong>ALDH2</strong> gene (<strong>ALDH2</strong>*2) is associated with a decreased risk for alcohol <b>dependence</b>, and an increased risk for alcoholic polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of alcohol <b>dependence</b>.
+ALDH2	addiction	withdrawal	15542751	The results revealed that (1) the less active allele of the ADH2 gene (ADH2*1) is associated with an increased risk for alcohol dependence, alcohol induced persistent amnestic disorder, alcohol <b>withdrawal</b> syndrome, and cancer of the upper GI tract; (2) the inactive allele of the <strong>ALDH2</strong> gene (<strong>ALDH2</strong>*2) is associated with a decreased risk for alcohol dependence, and an increased risk for alcoholic polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of alcohol dependence.
+ALDH2	drug	alcohol	15122947	<strong>ALDH2</strong> status and conduct disorder mediate the relationship between ethnicity and <b>alcohol</b> dependence in Chinese, Korean, and White American college students.
+ALDH2	addiction	dependence	15122947	<strong>ALDH2</strong> status and conduct disorder mediate the relationship between ethnicity and alcohol <b>dependence</b> in Chinese, Korean, and White American college students.
+ALDH2	drug	alcohol	15122947	This study examined aldehyde dehydrogense (<strong>ALDH2</strong>) gene status, <b>alcohol</b> dehydrogense (ADH2) gene status, conduct disorder, and <b>alcohol</b> dependence in Chinese, Korean, and White American college students.
+ALDH2	addiction	dependence	15122947	This study examined aldehyde dehydrogense (<strong>ALDH2</strong>) gene status, alcohol dehydrogense (ADH2) gene status, conduct disorder, and alcohol <b>dependence</b> in Chinese, Korean, and White American college students.
+ALDH2	drug	alcohol	15122947	The relationship of ethnicity to <b>alcohol</b> dependence was mediated by <strong>ALDH2</strong> status and conduct disorder, although Chinese ethnicity remained significant.
+ALDH2	addiction	dependence	15122947	The relationship of ethnicity to alcohol <b>dependence</b> was mediated by <strong>ALDH2</strong> status and conduct disorder, although Chinese ethnicity remained significant.
+ALDH2	drug	alcohol	15122947	ADH2 status was not related to <b>alcohol</b> dependence with <strong>ALDH2</strong> included, and no interactions were significant.
+ALDH2	addiction	dependence	15122947	ADH2 status was not related to alcohol <b>dependence</b> with <strong>ALDH2</strong> included, and no interactions were significant.
+ALDH2	drug	alcohol	15122947	Results suggest that different rates of risk (e.g., conduct disorder) and protective (e.g., <strong>ALDH2</strong> status) factors partially account for ethnic differences in rates of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	15122947	Results suggest that different rates of risk (e.g., conduct disorder) and protective (e.g., <strong>ALDH2</strong> status) factors partially account for ethnic differences in rates of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	15112932	Mr. Cook's and Dr. Wall's paper adds another dimension to this article by presenting research on both the aldehyde dehydrogenase (<strong>ALDH2</strong>) and <b>alcohol</b> dehydrogenase (ADH2) genetic variants and their association with the <b>alcohol</b> related flushing response that is prevalent in Asian populations.
+ALDH2	drug	alcohol	15084894	In the Han Chinese population, the <b>alcohol</b> dehydrogenase 1B*2/*2 (ADH1B*2/*2) genotype and the aldehyde dehydrogenase 2*2 (<strong>ALDH2</strong>*2) allele have been considered as protective factors against <b>alcohol</b> abuse or dependence.
+ALDH2	addiction	dependence	15084894	In the Han Chinese population, the alcohol dehydrogenase 1B*2/*2 (ADH1B*2/*2) genotype and the aldehyde dehydrogenase 2*2 (<strong>ALDH2</strong>*2) allele have been considered as protective factors against alcohol abuse or <b>dependence</b>.
+ALDH2	drug	alcohol	15084894	We hypothesized that the ADH1B and <strong>ALDH2</strong> genes might interact with the DRD2 gene and that the association between the DRD2 gene and <b>alcohol</b> dependence might be affected by different ADH1B and <strong>ALDH2</strong> genotypes.
+ALDH2	addiction	dependence	15084894	We hypothesized that the ADH1B and <strong>ALDH2</strong> genes might interact with the DRD2 gene and that the association between the DRD2 gene and alcohol <b>dependence</b> might be affected by different ADH1B and <strong>ALDH2</strong> genotypes.
+ALDH2	drug	alcohol	15066702	Mexican Americans have a low frequency of the protective alleles ADH1B(*)2 and <strong>ALDH2</strong>(*)2 and a relatively high frequency of CYP2E1 c2, which is associated with early onset <b>alcoholism</b>.
+ALDH2	drug	alcohol	15041893	Among the multiple factors which influence these variations, genetic factors especially those related to the different alleles of ADH2 and <strong>ALDH2</strong>, are the most well known and are related to the development of <b>alcohol</b> dependence, particularly in some populations such as those of Asian origin.
+ALDH2	addiction	dependence	15041893	Among the multiple factors which influence these variations, genetic factors especially those related to the different alleles of ADH2 and <strong>ALDH2</strong>, are the most well known and are related to the development of alcohol <b>dependence</b>, particularly in some populations such as those of Asian origin.
+ALDH2	drug	alcohol	14691070	We excluded subjects with inactive <strong>ALDH2</strong> and employed the subjects with <strong>ALDH2</strong>*1/2*1 (384 <b>alcoholics</b> and 792 controls).
+ALDH2	addiction	aversion	14690875	), which were not associated with the line difference detected in blood AcH levels, the present study examined the contribution of brain <strong>ALDH2</strong> activity to AcH <b>aversion</b> in UChA and UChB rats.
+ALDH2	addiction	aversion	14690875	In experiment 2, the possibility that the inhibition of the brain <strong>ALDH2</strong> would lower the AcH <b>aversion</b> threshold in both lines was studied by determining the effect of cyanamide (10 mg/kg i.p.)
+ALDH2	addiction	aversion	14690875	pretreatment, an inhibitor of ALDH, on AcH <b>aversion</b>, blood AcH levels and brain <strong>ALDH2</strong> activity.
+ALDH2	addiction	aversion	14690875	The finding that blocking the brain <strong>ALDH2</strong> (52%) by cyanamide can make a non <b>aversive</b> dose of AcH (25 mg/kg) <b>aversive</b> to UChA and UChB rats at blood AcH levels comparable to those induced by a non <b>aversive</b> dose of AcH (100 mg/kg) in control UChB rats indicates that the line difference in AcH <b>aversion</b> is associated more with brain <strong>ALDH2</strong> activity than with liver <strong>ALDH2</strong> activity.
+ALDH2	drug	alcohol	14615012	The objective of the current study was to compare the effect of an intraperitoneal dose of acetaldehyde (50 mg/kg) in high <b>alcohol</b> drinking (UChB) and low <b>alcohol</b> drinking (UChA) rat lines, which differ in the activity of the brain mitochondrial class 2 aldehyde dehydrogenase (<strong>ALDH2</strong>) as a consequence of differences in their <strong>ALDH2</strong> genotypes.
+ALDH2	drug	alcohol	12884000	Allelic variation at <b>alcohol</b> metabolism genes (ADH1B, ADH1C, <strong>ALDH2</strong>) and <b>alcohol</b> dependence in an American Indian population.
+ALDH2	addiction	dependence	12884000	Allelic variation at alcohol metabolism genes (ADH1B, ADH1C, <strong>ALDH2</strong>) and alcohol <b>dependence</b> in an American Indian population.
+ALDH2	drug	alcohol	12884000	Specifically, ADH1B*47His (previously ADH2 2) and <strong>ALDH2</strong> 2 have been shown to confer protection against <b>alcoholism</b>, presumably through accumulation of acetaldehyde in the blood and a resultant 'flushing response' to <b>alcohol</b> consumption.
+ALDH2	drug	alcohol	12884000	In the current study, variants at ADH1B (previously ADH2), ADH1C (previously ADH3), and <strong>ALDH2</strong> were assayed in DNA extracts from participants belonging to a Southwest American Indian tribe (n=490) with a high prevalence of <b>alcoholism</b>.
+ALDH2	drug	alcohol	12824808	In Taiwan, about 70% of the Han Chinese population have the ADH2*2 allele and 50% show <strong>ALDH2</strong>*1/*2 or <strong>ALDH2</strong>*2/*2 genotypes, which offer protection against drinking behavior and the risk of developing <b>alcoholism</b>.
+ALDH2	drug	alcohol	12759156	The drinking behavior, <b>alcohol</b> induced facial flushing and <strong>ALDH2</strong> genotypes were determined in 283 Thai men comprising 85 who were <b>alcohol</b> dependent, 62 hazardous/harmful drinkers and 136 non drinkers or infrequent drinkers.
+ALDH2	drug	alcohol	12759156	The risks of being <b>alcohol</b> dependent and of having hazardous/harmful drinking were lower in individuals with heterozygous <strong>ALDH2</strong>*1/*2, compared with homozygous <strong>ALDH2</strong>*1/*1 [relative probability ratios (95% CI) 0.14 (0.05 0.41) and 0.23 (0.08 0.61), respectively].
+ALDH2	drug	alcohol	12759156	Eighty percent of those who were heterozygous and 28% of those who were homozygous <strong>ALDH2</strong>*1 reported flush symptoms after drinking <b>alcohol</b>.
+ALDH2	drug	alcohol	12759156	Similarly, higher percentages of people drinking beyond the safety limit (>60 g/day) and having <b>alcohol</b> related problems were observed in homozygous <strong>ALDH2</strong>*1 compared with heterozygous individuals: 32% vs. 5% and 27% vs. 12%, respectively.
+ALDH2	drug	alcohol	12759156	Overall, the study supports the role of the mutant <strong>ALDH2</strong>*2 allele in preventing high <b>alcohol</b> consumption and the development of <b>alcohol</b> dependence in a Thai population.
+ALDH2	addiction	dependence	12759156	Overall, the study supports the role of the mutant <strong>ALDH2</strong>*2 allele in preventing high alcohol consumption and the development of alcohol <b>dependence</b> in a Thai population.
+ALDH2	drug	alcohol	12710951	To identify the association between the polymorphisms of genes encoding <b>alcohol</b> metabolizing enzymes and <b>alcoholism</b>, the <b>alcohol</b> dehydrogenase 2 (ADH2), <b>alcohol</b> dehydrogenase 3 (ADH3), aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), and cytochrome P450 2E1 (CYP2E1) genes were studied in 101 male Mexican American <b>alcoholics</b>.
+ALDH2	drug	alcohol	12710951	The allele frequency of ADH2*2 (4.3%) and <strong>ALDH2</strong>*2 (0%), which are considered as protective alleles against <b>alcohol</b> drinking, is very low in Mexican Americans and no association is found between these alleles and <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	12710951	The allele frequency of ADH2*2 (4.3%) and <strong>ALDH2</strong>*2 (0%), which are considered as protective alleles against alcohol drinking, is very low in Mexican Americans and no association is found between these alleles and alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	12604199	At pH 8.8, the second order rate constants for inactivation of the bacterial enzyme was 1 x 10(3) M( 1) s( 1), which compare well with that reported for human liver mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>), the target of DSF inhibition in the aversion therapy of <b>alcoholism</b>.
+ALDH2	addiction	aversion	12604199	At pH 8.8, the second order rate constants for inactivation of the bacterial enzyme was 1 x 10(3) M( 1) s( 1), which compare well with that reported for human liver mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>), the target of DSF inhibition in the <b>aversion</b> therapy of alcoholism.
+ALDH2	drug	alcohol	12505800	Two <b>alcohol</b> dehydrogenase genes (ADH2 and ADH3 on chromosome 4) and one aldehyde dehydrogenase gene (<strong>ALDH2</strong> on chromosome 12) exhibit functional polymorphisms.
+ALDH2	drug	alcohol	12505800	The goal of this study was to determine whether any associations exist between the ADH2, ADH3, and <strong>ALDH2</strong> polymorphisms and <b>alcohol</b> dependence in a group of Native Americans.
+ALDH2	addiction	dependence	12505800	The goal of this study was to determine whether any associations exist between the ADH2, ADH3, and <strong>ALDH2</strong> polymorphisms and alcohol <b>dependence</b> in a group of Native Americans.
+ALDH2	drug	alcohol	12007581	We have previously found the existence of a relation between activity of the brain mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>) and consumption of <b>ethanol</b> in rats of the low <b>alcohol</b> drinking (UChA) and the high <b>alcohol</b> drinking (UChB) strains.
+ALDH2	drug	alcohol	11956970	The use of persons who become <b>alcoholic</b> despite having a well defined negative risk for <b>alcoholism</b> (inactive aldehyde dehydrogenase 2 or <strong>ALDH2</strong>) is advantageous in genetic research because of this population's reduced heterogeneity and possible genetic factors conferring susceptibility to <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	11956970	The use of persons who become alcoholic despite having a well defined negative risk for alcoholism (inactive aldehyde dehydrogenase 2 or <strong>ALDH2</strong>) is advantageous in genetic research because of this population's reduced heterogeneity and possible genetic factors conferring susceptibility to alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	11956970	This investigation of central serotonin neurotransmission, specifically the serotonin 1B (5HT1B) receptor gene and its role in both regulating <b>alcohol</b> consumption and developing <b>alcohol</b> dependence revealed overrepresentation of the C allele of the 861G > C polymorphism of 5HT1B in <b>alcoholics</b> with inactive <strong>ALDH2</strong>, compared with its frequency in nonalcoholic controls.
+ALDH2	addiction	dependence	11956970	This investigation of central serotonin neurotransmission, specifically the serotonin 1B (5HT1B) receptor gene and its role in both regulating alcohol consumption and developing alcohol <b>dependence</b> revealed overrepresentation of the C allele of the 861G > C polymorphism of 5HT1B in alcoholics with inactive <strong>ALDH2</strong>, compared with its frequency in nonalcoholic controls.
+ALDH2	drug	alcohol	11956970	No significant differences in 5HT1B genotype and allele distributions were observed between <b>alcoholics</b> with active <strong>ALDH2</strong> and controls, however.
+ALDH2	drug	alcohol	11925062	Previous studies have shown that Asians who possess a variant aldehyde dehydrogenase allele (<strong>ALDH2</strong>*2) have lower rates of <b>alcohol</b> consumption and dependence.
+ALDH2	addiction	dependence	11925062	Previous studies have shown that Asians who possess a variant aldehyde dehydrogenase allele (<strong>ALDH2</strong>*2) have lower rates of alcohol consumption and <b>dependence</b>.
+ALDH2	drug	alcohol	11925062	Research in Asian men has shown that those with <strong>ALDH2</strong>*2 have greater responses to <b>alcohol</b> than do those without this genetic variant.
+ALDH2	drug	alcohol	11925062	The present study was designed to determine whether similar levels of response to <b>alcohol</b>, using objective and subjective measurements, are seen in men and women with different <strong>ALDH2</strong> genotypes.
+ALDH2	drug	alcohol	11925062	Men and women with <strong>ALDH2</strong>*1/*2 had greater pulse rate increases, greater observed flushing responses and greater subjective feelings of being dizzy, drunk and high compared with <strong>ALDH2</strong>*1/*1 participants, despite having equivalent breath <b>alcohol</b> concentrations.
+ALDH2	addiction	intoxication	11925062	<strong>ALDH2</strong>*1/*2 participants also reported being less likely to drive, following this level of <b>intoxication</b>, compared with <strong>ALDH2</strong>*1/*1 participants.
+ALDH2	drug	alcohol	11925062	This study suggests that low risk for <b>alcoholism</b> based on possession of an <strong>ALDH2</strong>*2 allele relates to greater response to <b>alcohol</b> in both men and women.
+ALDH2	addiction	intoxication	11767261	Studies of Asian college students have found that rates of <b>binge</b> drinking are associated with variation in the aldehyde dehydrogenase (<strong>ALDH2</strong>) gene.
+ALDH2	drug	alcohol	11767261	Chinese and Koreans have different prevalence rates of the <strong>ALDH2</strong>*2 allele, <b>alcohol</b> use, and <b>alcoholism</b>.
+ALDH2	addiction	intoxication	11767261	The association of <strong>ALDH2</strong> status and ethnic group with <b>binge</b> drinking was examined in 328 Chinese, Korean, and White college students.
+ALDH2	addiction	intoxication	11767261	Among Asian participants, <strong>ALDH2</strong> status and ethnicity related to <b>binge</b> drinking in an additive manner.
+ALDH2	addiction	intoxication	11767261	Possessing an <strong>ALDH2</strong>*2 allele and being Chinese were protective factors, and being White and being Korean without an <strong>ALDH2</strong>*2 allele were risk factors for <b>binge</b> drinking.
+ALDH2	addiction	intoxication	11767261	These results suggest that <strong>ALDH2</strong> status, as well as other factors that differ in Koreans and Chinese, but do not interact with <strong>ALDH2</strong>, are associated with <b>binge</b> drinking among Asians.
+ALDH2	drug	alcohol	11545539	In Asians, variation in the <b>alcohol</b> dehydrogenase (ADH2) gene relates to <b>alcohol</b> dependence, <b>alcohol</b> consumption, and reported <b>alcohol</b> related symptoms, even after controlling for variation in the aldehyde dehydrogenase (<strong>ALDH2</strong>) gene.
+ALDH2	addiction	dependence	11545539	In Asians, variation in the alcohol dehydrogenase (ADH2) gene relates to alcohol <b>dependence</b>, alcohol consumption, and reported alcohol related symptoms, even after controlling for variation in the aldehyde dehydrogenase (<strong>ALDH2</strong>) gene.
+ALDH2	drug	alcohol	11535626	A mutation in the gene encoding for the liver mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong> 2), present in some Asian populations, lowers or abolishes the activity of this enzyme and results in elevations in blood acetaldehyde upon <b>ethanol</b> consumption, a phenotype that greatly protects against <b>alcohol</b> abuse and <b>alcoholism</b>.
+ALDH2	drug	alcohol	11535626	Administration of ASO 9 (20 mg/kg/day for 4 d) to rats resulted in a 50% reduction in liver <strong>ALDH2</strong> mRNA, a 40% inhibition in <strong>ALDH2</strong> activity, and a fourfold (P < 0.001) increase in circulating plasma acetaldehyde levels after <b>ethanol</b> (1 g/kg) administration.
+ALDH2	drug	alcohol	11398342	Mitochondrial <strong>ALDH2</strong> is a major enzyme in the oxidation of acetaldehyde derived from <b>ethanol</b> metabolism.
+ALDH2	drug	alcohol	11398342	The catalytic deficiency of <strong>ALDH2</strong> isozyme is responsible for flushing and other vasomotor symptoms caused by higher acetaldehyde levels after <b>alcohol</b> intake.
+ALDH2	drug	alcohol	11398342	Individuals deficient in <strong>ALDH2</strong> activity refrain from excessive drinking of <b>alcohol</b> due to the aversive reactions, leading to protection against <b>alcoholism</b>.
+ALDH2	addiction	aversion	11398342	Individuals deficient in <strong>ALDH2</strong> activity refrain from excessive drinking of alcohol due to the <b>aversive</b> reactions, leading to protection against alcoholism.
+ALDH2	drug	alcohol	11398342	Prevalence of the <strong>ALDH2</strong>*1 allele is associated with <b>alcoholism</b>, and subsequent studies have confirmed the allelic association with <b>alcoholism</b> in different ethnic groups.
+ALDH2	drug	alcohol	11391053	The presentations were (1) Mutations in the exons, exon intron junctions, and promoter regions of human CYP2E1 gene and <b>alcoholism</b>, by Fumio Nomura; (2) Genetic variability in <b>alcohol</b> metabolism and drinking habits in Japanese, by Shoji Harada; (3) Genetic studies of <b>alcohol</b> dependence using <b>alcoholics</b> with inactive <strong>ALDH2</strong>, by Susumu Higuchi; and (4) <b>Alcohol</b> consumption, apolipoprotein polymorphisms, and cardiovascular disorders, by Dharam P. Agarwal.
+ALDH2	addiction	dependence	11391053	The presentations were (1) Mutations in the exons, exon intron junctions, and promoter regions of human CYP2E1 gene and alcoholism, by Fumio Nomura; (2) Genetic variability in alcohol metabolism and drinking habits in Japanese, by Shoji Harada; (3) Genetic studies of alcohol <b>dependence</b> using alcoholics with inactive <strong>ALDH2</strong>, by Susumu Higuchi; and (4) Alcohol consumption, apolipoprotein polymorphisms, and cardiovascular disorders, by Dharam P. Agarwal.
+ALDH2	drug	alcohol	11347517	The aldehyde dehydrogenase allele <strong>ALDH2</strong>*2 has a protective effect against <b>alcoholism</b>.
+ALDH2	drug	alcohol	11261392	Studies of Asian adults have found that <b>alcohol</b> use and <b>alcohol</b> dependence are related to variation in the aldehyde dehydrogenase (<strong>ALDH2</strong>) gene.
+ALDH2	addiction	dependence	11261392	Studies of Asian adults have found that alcohol use and alcohol <b>dependence</b> are related to variation in the aldehyde dehydrogenase (<strong>ALDH2</strong>) gene.
+ALDH2	drug	alcohol	11261392	To investigate the association of <strong>ALDH2</strong> with the development of drug involvement, the authors analyzed retrospective information about the onset and regular use of <b>alcohol</b> and other substances as reported by 180 Asian American college students.
+ALDH2	drug	alcohol	11261392	Possession of an <strong>ALDH2</strong>*2 allele was not related to initiation of <b>alcohol</b> use or having ever been intoxicated, but individuals with <strong>ALDH2</strong>*2 alleles were less likely to be regular drinkers, were less likely to have engaged in a binge drinking episode, reported a lower number of maximum drinks consumed in a 24 hr period, and were less likely to have used tobacco regularly than those without this genetic variant.
+ALDH2	drug	nicotine	11261392	Possession of an <strong>ALDH2</strong>*2 allele was not related to initiation of alcohol use or having ever been intoxicated, but individuals with <strong>ALDH2</strong>*2 alleles were less likely to be regular drinkers, were less likely to have engaged in a binge drinking episode, reported a lower number of maximum drinks consumed in a 24 hr period, and were less likely to have used <b>tobacco</b> regularly than those without this genetic variant.
+ALDH2	addiction	intoxication	11261392	Possession of an <strong>ALDH2</strong>*2 allele was not related to initiation of alcohol use or having ever been intoxicated, but individuals with <strong>ALDH2</strong>*2 alleles were less likely to be regular drinkers, were less likely to have engaged in a <b>binge</b> drinking episode, reported a lower number of maximum drinks consumed in a 24 hr period, and were less likely to have used tobacco regularly than those without this genetic variant.
+ALDH2	drug	alcohol	11261392	These findings suggest that <strong>ALDH2</strong> is associated with the development of not only <b>alcohol</b> related behavior but other substance use behavior as well.
+ALDH2	drug	alcohol	10954050	Dipole estimation of alpha EEG during <b>alcohol</b> ingestion in males genotypes for <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	10954050	Using a dipole tracing method based on the two dipole model, the purpose of the present study was to investigate <b>alcohol</b> induced changes in the alpha band of electroencephalogram (EEG) and its equivalent current dipoles (ECDs) in 12 healthy male volunteers, who were genetically typed for mitochondrial aldehyde dehydrogenase 2 (<strong>ALDH2</strong>).
+ALDH2	drug	alcohol	10954050	The difference in the time course was discussed from the viewpoint of the protective effect of <strong>ALDH2</strong>*2 allele against the risk for <b>alcoholism</b>.
+ALDH2	drug	alcohol	10940605	Fatal acute <b>alcohol</b> intoxication in an <strong>ALDH2</strong> heterozygote: a case report.
+ALDH2	addiction	intoxication	10940605	Fatal acute alcohol <b>intoxication</b> in an <strong>ALDH2</strong> heterozygote: a case report.
+ALDH2	drug	alcohol	10940605	Those who possess the <strong>ALDH2</strong>*2 gene show high concentrations of acetaldehyde (AcH) at even comparatively lower <b>alcohol</b> levels.
+ALDH2	drug	alcohol	10630602	<b>Alcohol</b> metabolism and cardiovascular response in an <b>alcoholic</b> patient homozygous for the <strong>ALDH2</strong>*2 variant gene allele.
+ALDH2	drug	alcohol	10630602	Homozygosity of the variant <strong>ALDH2</strong>*2 allele previously was believed to fully protect East Asian populations against the development of <b>alcoholism</b>.
+ALDH2	drug	alcohol	10630602	An <b>alcohol</b> dependent patient was identified to be <strong>ALDH2</strong>*2/*2, ADH2*2/*2, and ADH3*1/*2.
+ALDH2	drug	alcohol	10630602	During 130 min postingestion, the patient generally displayed similar or even less intense cardiovascular hemodynamic alterations when compared to a previously published study of nonalcoholic individuals with <strong>ALDH2</strong>*2/*2 who had received a lower dose of <b>ethanol</b> (0.2 g/kg).
+ALDH2	drug	alcohol	10630602	Logistic regression analysis of the combinatorial genotypes of ADH2 and <strong>ALDH2</strong> in 420 <b>alcohol</b> dependent and 689 nonalcohol dependent subjects indicated that risk for <b>alcoholism</b> was 100 fold lower for the ADH2*2/*2 <strong>ALDH2</strong>*2/*2 individuals than the ADH2*1/*1 <strong>ALDH2</strong>*1/*1 individuals.
+ALDH2	drug	alcohol	10630602	The gene status of <strong>ALDH2</strong>*2/*2 alone can tremendously but not completely (as thought previously) protect against development of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	10630602	The gene status of <strong>ALDH2</strong>*2/*2 alone can tremendously but not completely (as thought previously) protect against development of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	10630602	Physiological tolerance or innate insensitivity to the accumulation of blood acetaldehyde following <b>alcohol</b> ingestion may be crucial for the development of <b>alcoholism</b> in individuals homozygous for <strong>ALDH2</strong>*2.
+ALDH2	drug	alcohol	10513990	Liver mitochondrial low Km aldehyde dehydrogenase (<strong>ALDH2</strong>, EC 1.2.1.3), the isoform responsible for the conversion of acetaldehyde to acetate, is inhibited by the sulfoxide bioactivation products of Et2NC(O)SMe (from the <b>alcohol</b> aversion drug <b>disulfiram</b>), Pr2NC(O)SEt (the herbicide S ethyl N,N dipropylthiocarbamate), and BuNHC(O)SMe (from the fungicide benomyl).
+ALDH2	addiction	aversion	10513990	Liver mitochondrial low Km aldehyde dehydrogenase (<strong>ALDH2</strong>, EC 1.2.1.3), the isoform responsible for the conversion of acetaldehyde to acetate, is inhibited by the sulfoxide bioactivation products of Et2NC(O)SMe (from the alcohol <b>aversion</b> drug disulfiram), Pr2NC(O)SEt (the herbicide S ethyl N,N dipropylthiocarbamate), and BuNHC(O)SMe (from the fungicide benomyl).
+ALDH2	drug	alcohol	10513990	These findings are of interest relative to selective inhibitors and carbamoylating agents for <strong>ALDH2</strong> and to <b>alcohol</b> aversion upon exposure to herbicides and fungicides.
+ALDH2	addiction	aversion	10513990	These findings are of interest relative to selective inhibitors and carbamoylating agents for <strong>ALDH2</strong> and to alcohol <b>aversion</b> upon exposure to herbicides and fungicides.
+ALDH2	drug	alcohol	10397292	Self reported <b>alcohol</b> associated symptoms and drinking behavior in three <strong>ALDH2</strong> genotypes among Japanese university students.
+ALDH2	drug	alcohol	10397292	Nearly half of the Japanese population is sensitive to <b>alcohol</b> due to a genetic polymorphism in low K(m) aldehyde dehydrogenase (<strong>ALDH2</strong>).
+ALDH2	drug	alcohol	10397292	In the present study, we investigated the effects of the <strong>ALDH2</strong> genotype on both self reported <b>alcohol</b> associated symptoms and <b>alcohol</b> drinking behavior among Japanese university students.
+ALDH2	drug	alcohol	10397292	The frequency of <b>alcohol</b> associated symptoms generally increased in the order <strong>ALDH2</strong>*1/*1, <strong>ALDH2</strong>*1/*2, <strong>ALDH2</strong>*2/*2 among males.
+ALDH2	drug	alcohol	10397292	Mean amounts of <b>alcohol</b> consumption per occasion in the three <strong>ALDH2</strong> genotypes stratified by drinking frequency generally increased significantly in the order <strong>ALDH2</strong>*2/*2, <strong>ALDH2</strong>*1/*2, <strong>ALDH2</strong>*1/*1 in both sexes.
+ALDH2	drug	alcohol	10397292	The proportion of binge drinkers defined by those who drink <b>ethanol</b> of > or = 75 ml per occasion on average also increased in the order <strong>ALDH2</strong>*2/*2 (0.0%), <strong>ALDH2</strong>*1/*2 (9.8%), <strong>ALDH2</strong>*1/*1 (22.1%) among male drinkers (> or = 1 day/month).
+ALDH2	addiction	intoxication	10397292	The proportion of <b>binge</b> drinkers defined by those who drink ethanol of > or = 75 ml per occasion on average also increased in the order <strong>ALDH2</strong>*2/*2 (0.0%), <strong>ALDH2</strong>*1/*2 (9.8%), <strong>ALDH2</strong>*1/*1 (22.1%) among male drinkers (> or = 1 day/month).
+ALDH2	drug	alcohol	10397292	We for the first time demonstrated clear associations between the <strong>ALDH2</strong> genotype, self reported <b>alcohol</b> associated symptoms, and <b>alcohol</b> drinking behavior among Japanese university students.
+ALDH2	drug	alcohol	10355247	[Relationship between <strong>ALDH2</strong> genotypes and choice of <b>alcoholic</b> beverages].
+ALDH2	drug	alcohol	10355247	It has been shown that around half of Japanese show a marked sensitivity to <b>alcoholic</b> beverages because of aversive reactions due to a catalytic deficiency in <strong>ALDH2</strong> isozyme.
+ALDH2	addiction	aversion	10355247	It has been shown that around half of Japanese show a marked sensitivity to alcoholic beverages because of <b>aversive</b> reactions due to a catalytic deficiency in <strong>ALDH2</strong> isozyme.
+ALDH2	drug	alcohol	10355247	Therefore, differences in <strong>ALDH2</strong> genotypes may possibly influence the choice of <b>alcoholic</b> beverages because the individuals possessing the <strong>ALDH2</strong>*2 gene may prefer the <b>alcoholic</b> beverages containing lower concentrations of <b>alcohol</b>.
+ALDH2	drug	alcohol	10355247	A large population survey (320 males, 132 females) was conducted using questionnaires to investigate the relationship between <strong>ALDH2</strong> genotypes and the choice of <b>alcoholic</b> beverages.
+ALDH2	drug	alcohol	10355247	Individuals with the homozygote of <strong>ALDH2</strong>*1 generally showed more preference for <b>alcoholic</b> beverages containing a higher concentration of <b>alcohol</b> than those with the heterozygote or the homozygote of <strong>ALDH2</strong>*2.
+ALDH2	drug	alcohol	10355247	Our data suggested that individuals with <strong>ALDH2</strong>*2 prefer beverages with lower concentrations of <b>alcohol</b> due to an aversive reaction after drinking, and that there are obvious gender differences in the consumption as well as the choice for many <b>alcoholic</b> beverages.
+ALDH2	addiction	aversion	10355247	Our data suggested that individuals with <strong>ALDH2</strong>*2 prefer beverages with lower concentrations of alcohol due to an <b>aversive</b> reaction after drinking, and that there are obvious gender differences in the consumption as well as the choice for many alcoholic beverages.
+ALDH2	drug	alcohol	10235293	The different genotypes at the genes encoding the enzymes involved in <b>alcohol</b> metabolism, class one <b>alcohol</b> dehydrogenase (ADH2 and ADH3) and mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>), have previously been shown to confer different predispositions to the development of <b>alcoholism</b> in Chinese Han males (Thomasson et al., 1991; Chen WJ et al., 1996; Chen CC et al., unpublished data).
+ALDH2	drug	alcohol	10235293	Therefore, association studies of <b>alcoholism</b> in Chinese Han might be more sensitive if controlled for the genotypes of ADH2,ADH3, and <strong>ALDH2</strong>, when other loci, such as DRD2, are examined.
+ALDH2	drug	alcohol	10235293	Several different stratifications by ADH and <strong>ALDH2</strong> genotypes were examined; no genotypes or haplotypes at DRD2 differ between <b>alcoholics</b> and nonalcoholics except for a small number of nominally significant p values which do not constitute significant results given the many tests done, some of which are not independent of one another due to linkage disequilibrium.
+ALDH2	drug	alcohol	10235293	These tests included considering the high risk (ADH2*1/*1; *1/*2; ADH3*1/*2; *2/*2; and <strong>ALDH2</strong>*1/*1) and the low risk (ADH2*2/*2; ADH3*1/*1; and <strong>ALDH2</strong>*1/*2; *2/*2) groups of <b>alcoholics</b>, as well as nonalcoholic controls.
+ALDH2	drug	alcohol	10235293	After stratification by the relevant genotypes of ADH2, ADH3, and <strong>ALDH2</strong> no significant association exists between the genetic variants at the DRD2 locus and <b>alcoholism</b> in the Chinese Han population.
+ALDH2	drug	alcohol	10089015	Approximately 10% of Japanese <b>alcoholics</b> develop their disease despite having an inactive form of aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), known as a genetic deterrent of heavy drinking due to adverse reactions after drinking.
+ALDH2	drug	alcohol	10089015	Examination of the  1438 A/G polymorphism of the serotonin 2A (5HT2A) receptor gene in 225 Japanese <b>alcoholics</b> with inactive <strong>ALDH2</strong> revealed the presence of significantly more of the G allele than was found in 361 control subjects.
+ALDH2	drug	alcohol	10089015	The frequency of the G allele in 282 <b>alcoholics</b> with active <strong>ALDH2</strong> fell between the G allele frequencies of controls and subjects with inactive <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	9862807	The relative sizes of the tunnels also suggest why the bulky <b>alcohol</b> aversive drug <b>disulfiram</b> reacts more rapidly with ALDH1 than <strong>ALDH2</strong>.
+ALDH2	addiction	aversion	9862807	The relative sizes of the tunnels also suggest why the bulky alcohol <b>aversive</b> drug disulfiram reacts more rapidly with ALDH1 than <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	9802521	This high <b>alcohol</b> sensitivity among Orientals has been attributed to a highly prevalent polymorphism in low Km aldehyde dehydrogenase (<strong>ALDH2</strong>).
+ALDH2	drug	alcohol	9802521	In the present study, we attempted to develop a reliable questionnaire method to probe the frequency of <b>alcohol</b> drinking related symptoms to estimate the <strong>ALDH2</strong> genotype.
+ALDH2	drug	alcohol	9752691	2) The percentage of active <strong>ALDH2</strong> was significantly higher in patients with <b>alcohol</b> tolerance than that in those without it (38%).
+ALDH2	drug	alcohol	9752691	3) The estimated amount of <b>alcohol</b> consumption in the past was 506 +/  720 g/week in the active <strong>ALDH2</strong> group, and 156 +/  288 g/week in the inactive <strong>ALDH2</strong> group, showing a significant difference between the two groups.
+ALDH2	addiction	relapse	9752691	However, salt and water <b>craving</b> in dialysis patients may be influenced partially by an active <strong>ALDH2</strong> gene.
+ALDH2	drug	alcohol	26734919	In recent studies involving DNA analysis, it was found that a deficiency of the <strong>ALDH2</strong> isozyme (<strong>ALDH2</strong>*2) was responsible for the flushing symptoms as well as other vasomotor symptoms caused by a higher acetaldehyde level after <b>alcohol</b> consumption.
+ALDH2	drug	alcohol	26734919	Deficiency of <strong>ALDH2</strong> activity has been found prevalently only among people of Mongoloid origin, and the deficiency of <strong>ALDH2</strong> prevents them from developing <b>alcohol</b> dependence due to the unpleasant physical effects of the flushing symptom.
+ALDH2	addiction	dependence	26734919	Deficiency of <strong>ALDH2</strong> activity has been found prevalently only among people of Mongoloid origin, and the deficiency of <strong>ALDH2</strong> prevents them from developing alcohol <b>dependence</b> due to the unpleasant physical effects of the flushing symptom.
+ALDH2	drug	alcohol	26734919	It was reported that Mongoloids such as Japanese and Chinese people carry the enzymatically active (<strong>ALDH2</strong>*1) subunit and/or the inactive (<strong>ALDH2</strong>*2) one, and that a low proportion of <strong>ALDH2</strong> deficiency (<strong>ALDH2</strong>*2 allele frequency) was found in <b>alcoholics</b> compared with healthy controls.
+ALDH2	drug	alcohol	26734919	It was also reported that polymorphism of <strong>ALDH2</strong> and/or CYP2E1 may be associated with the susceptibility to <b>alcohol</b> induced liver injury.
+ALDH2	drug	alcohol	26734919	Concerning blood <b>ethanol</b> elimination kinetics, it was reported that the c2 gene of CYP2E1 and the <strong>ALDH2</strong>*1 gene may have greater effects on <b>ethanol</b> and acetaldehyde elimination than the other genotypes, when the blood <b>ethanol</b> level is below 20 m M.
+ALDH2	drug	alcohol	9605433	S Methyl N,N diethylthiocarbamate (MeDTC) sulfoxide, a potent inhibitor of the target enzyme mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>), is thought to be the principal active metabolite of <b>disulfiram</b> in vivo.
+ALDH2	drug	alcohol	9605433	We examined the effects on recombinant human <strong>ALDH2</strong> of two intermediate metabolites of <b>disulfiram</b>, S methyl N,N diethyldithiocarbamate (MeDDC) sulfoxide and MeDDC sulfine.
+ALDH2	drug	alcohol	9605433	Our results suggest that these newer intermediate metabolites of <b>disulfiram</b>, especially the more potent MeDTC sulfoxide, have the potential to inhibit the target enzyme <strong>ALDH2</strong> in patients receiving <b>disulfiram</b>.
+ALDH2	drug	alcohol	9514293	Multiple logistic regression analysis revealed significant contributions by levels of <b>alcohol</b> consumption, the <strong>ALDH2</strong> genotype, and daily hassles to the prevalence of those with a high KAST score.
+ALDH2	drug	alcohol	9514293	When we analyzed the data for each <strong>ALDH2</strong> genotype, heavier <b>alcohol</b> consumption (> or =28.8 ml/day), older age (> or =40 years old), and very high daily hassles levels (> or =20) significantly increased the prevalence of problem drinkers in <strong>ALDH2</strong>*1/*1.
+ALDH2	drug	alcohol	9514293	On the contrary, no variables other than heavier <b>alcohol</b> consumption influenced the prevalence in <strong>ALDH2</strong>*1/*2.
+ALDH2	drug	alcohol	9514293	Health promotion activities to prevent from <b>alcohol</b> dependence should focus on <strong>ALDH2</strong>*1/*1, especially those of middle age, and should include stress management as a part of their activities.
+ALDH2	addiction	dependence	9514293	Health promotion activities to prevent from alcohol <b>dependence</b> should focus on <strong>ALDH2</strong>*1/*1, especially those of middle age, and should include stress management as a part of their activities.
+ALDH2	drug	alcohol	9383169	We first investigated the relationship of the aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) genotype to <b>alcohol</b> flushing for 53 normal volunteers.
+ALDH2	drug	alcohol	9383169	The first examination of 53 normal volunteers showed that there were differences in the degree of <b>alcohol</b> flushing between the <strong>ALDH2</strong> genotypes (P < 0.01).
+ALDH2	drug	alcohol	9399694	This analysis has 80% power to detect a small to moderate effect of OPRM1 variation on <b>alcohol</b> dependence and 100% power to detect effects of the magnitude of the <strong>ALDH2</strong>*2 variant.
+ALDH2	addiction	dependence	9399694	This analysis has 80% power to detect a small to moderate effect of OPRM1 variation on alcohol <b>dependence</b> and 100% power to detect effects of the magnitude of the <strong>ALDH2</strong>*2 variant.
+ALDH2	drug	alcohol	9195888	The single genetic factor most strongly correlated with reduced <b>alcohol</b> consumption and incidence of <b>alcoholism</b> is a naturally occurring variant of mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>).
+ALDH2	drug	alcohol	9195888	<strong>ALDH2</strong> deficient individuals exhibit an averse response to <b>ethanol</b> consumption, which is probably caused by elevated levels of blood acetaldehyde.
+ALDH2	drug	alcohol	9195888	The structure of <strong>ALDH2</strong> is important for the elucidation of its catalytic mechanism, to gain a clear understanding of the contribution of <strong>ALDH2</strong> to the genetic component of <b>alcoholism</b> and for the development of specific <strong>ALDH2</strong> inhibitors as potential drugs for use in the treatment of <b>alcoholism</b>.
+ALDH2	drug	alcohol	9066994	In this report we determined the genotypes for three genes, ADH2, ADH3, and <strong>ALDH2</strong> among subjects with <b>alcohol</b> dependence (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ALDH2	addiction	dependence	9066994	In this report we determined the genotypes for three genes, ADH2, ADH3, and <strong>ALDH2</strong> among subjects with alcohol <b>dependence</b> (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ALDH2	drug	alcohol	9066994	On a group level, the rare frequencies of <strong>ALDH2</strong>*2, the inactive allele of <strong>ALDH2</strong>, among these aborigines may account partially for their vulnerability to <b>alcohol</b> use disorders.
+ALDH2	drug	alcohol	9118876	A significant difference was observed only in <b>alcohol</b> drinking in subjects classified by aldehyde dehydrogenase 2 isozyme (<strong>ALDH2</strong>) genotype.
+ALDH2	drug	alcohol	9118876	Habitual <b>alcohol</b> intake appeared to increase 8 OHdG in PMN from <strong>ALDH2</strong> deficient subjects.
+ALDH2	drug	alcohol	8837712	Moreover, these frequencies were not altered in <b>alcoholics</b> with inactive aldehyde dehydrogenase 2 (<strong>ALDH2</strong>), a well defined negative risk factor for <b>alcoholism</b>.
+ALDH2	drug	alcohol	8773821	<b>Alcohol</b> metabolising genes and <b>alcoholism</b> among Taiwanese Han men: independent effect of ADH2, ADH3 and <strong>ALDH2</strong>.
+ALDH2	drug	alcohol	8773821	The association of <strong>ALDH2</strong> and ADH2 with the development of <b>alcoholism</b> was found to be independent of each other and has been replicated in different Asian populations, while the effect of ADH3 is less studied.
+ALDH2	drug	alcohol	8773821	Multiple logistic regression was then applied to assess the contribution of ADH3 to <b>alcoholism</b> by controlling the effect of <strong>ALDH2</strong> and ADH2.
+ALDH2	drug	alcohol	8773821	The results of multivariate analyses demonstrated that the odds ratios for an increment of one allele of ADH2*1, ADH3*2 and <strong>ALDH2</strong>*1 in the development of <b>alcoholism</b> were 4.18, 3.82, and 6.89, respectively.
+ALDH2	drug	alcohol	8929946	A point mutation in the aldehyde dehydrogenase 2 gene (<strong>ALDH2</strong>(2) allele) is considered to be a genetic deterrent for <b>alcoholism</b>; however, 80 of 655 Japanese <b>alcoholics</b> had the mutant allele.
+ALDH2	drug	alcohol	8929946	Genotype factors that might increase susceptibility by overriding the deterrent showed a higher frequency of a five repeat allele of the dopamine D4 receptor 48 bp repeat polymorphism in <b>alcoholics</b> with <strong>ALDH2</strong>(2) than in 100 other <b>alcoholics</b> and 144 controls.
+ALDH2	drug	alcohol	8651462	A comparison of the genotypes of <strong>ALDH2</strong>, ADH2, ADH3, and cytochrome P 4502E1 between <b>alcoholics</b> and nonalcoholics.
+ALDH2	drug	alcohol	8651462	We also compared the frequencies of homozygous <strong>ALDH2</strong>*1/1 and heterozygous <strong>ALDH2</strong>*1/2 genotypes in <b>alcoholics</b>.
+ALDH2	drug	alcohol	8651462	Our study revealed differences in the allelic frequencies of the <strong>ALDH2</strong>, ADH2, and ADH3 loci between <b>alcoholics</b> and nonalcoholics.
+ALDH2	drug	alcohol	8651462	For <b>alcoholics</b> with both homozygous <strong>ALDH2</strong>*1/1 and heterozygous <strong>ALDH2</strong>*1/2 genotypes, it was found that ADH2 and ADH3 played important rates.
+ALDH2	drug	alcohol	8651462	<b>Alcoholics</b> with the heterozygous <strong>ALDH2</strong>*1/2 genotype showed a significantly higher frequency of ADH2*1/1 than ones with the homozygous <strong>ALDH2</strong>*1/1 genotype.
+ALDH2	drug	alcohol	8651462	We assume ADH2*1 plays an important role in the development of <b>alcoholism</b> in <b>alcoholics</b> with the heterozygous <strong>ALDH2</strong>*1/2 genotype.
+ALDH2	drug	alcohol	8591846	High incidence of ADH2*1/<strong>ALDH2</strong>*1 genes among Japanese <b>alcohol</b> dependents and patients with <b>alcoholic</b> liver disease.
+ALDH2	drug	alcohol	8591846	Genetic polymorphism of ADH2/<strong>ALDH2</strong> in 66 cases of normal subjects, 90 cases of <b>alcohol</b> dependent, and 31 patients with <b>alcoholic</b> liver disease among Japanese has been analyzed using a polymerase chain reaction assay followed by a direct sequencing method, because <b>ethanol</b> is mainly catabolized by ADH and ALDH and less by cytochrome P450IIE1 and catalase.
+ALDH2	drug	alcohol	8591846	The incidence of both ADH2*1/*1 and <strong>ALDH2</strong>*1/*1 was significantly higher in patients with <b>alcohol</b> dependence and in patients with <b>alcoholic</b> liver disease when compared with that in control subjects.
+ALDH2	addiction	dependence	8591846	The incidence of both ADH2*1/*1 and <strong>ALDH2</strong>*1/*1 was significantly higher in patients with alcohol <b>dependence</b> and in patients with alcoholic liver disease when compared with that in control subjects.
+ALDH2	drug	alcohol	8591846	In addition, the incidence of <strong>ALDH2</strong>*1/*2 and <strong>ALDH2</strong>*2/*2 was significantly reduced in <b>alcoholics</b> compared with control subjects.
+ALDH2	drug	alcohol	8591846	Genetic polymorphism of ADH2/<strong>ALDH2</strong> in patients with <b>alcoholic</b> liver disease was not different from that of <b>alcohol</b> dependents.
+ALDH2	drug	alcohol	8591846	According to these results, not only <strong>ALDH2</strong> gene, often claimed to be responsible for <b>alcohol</b> dependence among Japanese, but also ADH2 gene polymorphism, which modulates the metabolism of <b>ethanol</b>, play important roles in habitual <b>alcohol</b> intake behavior in Japanese patients and in some patients leads to <b>alcoholic</b> liver diseases.
+ALDH2	addiction	dependence	8591846	According to these results, not only <strong>ALDH2</strong> gene, often claimed to be responsible for alcohol <b>dependence</b> among Japanese, but also ADH2 gene polymorphism, which modulates the metabolism of ethanol, play important roles in habitual alcohol intake behavior in Japanese patients and in some patients leads to alcoholic liver diseases.
+ALDH2	drug	alcohol	7573775	CYP2E1 and <strong>ALDH2</strong> genotypes and <b>alcohol</b> dependence in Japanese.
+ALDH2	addiction	dependence	7573775	CYP2E1 and <strong>ALDH2</strong> genotypes and alcohol <b>dependence</b> in Japanese.
+ALDH2	drug	alcohol	7573775	The genotypes of the CYP2E1 and <strong>ALDH2</strong> loci of <b>alcoholic</b> (<b>alcohol</b> dependence) and nonalcoholic (healthy) Japanese were investigated to examine the relationship between the polymorphism of CYP2E1 (C1/C2) and <strong>ALDH2</strong> (<strong>ALDH2</strong>*1/<strong>ALDH2</strong>*2), and the susceptibility to <b>alcoholism</b>.
+ALDH2	addiction	dependence	7573775	The genotypes of the CYP2E1 and <strong>ALDH2</strong> loci of alcoholic (alcohol <b>dependence</b>) and nonalcoholic (healthy) Japanese were investigated to examine the relationship between the polymorphism of CYP2E1 (C1/C2) and <strong>ALDH2</strong> (<strong>ALDH2</strong>*1/<strong>ALDH2</strong>*2), and the susceptibility to alcoholism.
+ALDH2	drug	alcohol	7573775	There was no significant difference in C2 gene frequency between <b>alcoholics</b> (0.19) and nonalcoholics (controls) (0.20), whereas there was a significant difference in <strong>ALDH2</strong> allele frequency, suggesting that, in Japanese, the C2 genotype of CYP2E1 may have nothing to do with the risk of developing <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	7573775	There was no significant difference in C2 gene frequency between alcoholics (0.19) and nonalcoholics (controls) (0.20), whereas there was a significant difference in <strong>ALDH2</strong> allele frequency, suggesting that, in Japanese, the C2 genotype of CYP2E1 may have nothing to do with the risk of developing alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	7573775	However, the <strong>ALDH2</strong>*1 allele may influence drinking behavior and the development of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	7573775	However, the <strong>ALDH2</strong>*1 allele may influence drinking behavior and the development of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	7718681	Heterozygous for <strong>ALDH2</strong> in <b>alcohol</b> dependence: relationship between the <strong>ALDH2</strong> genotype and personality disorder in <b>alcohol</b> dependent patients with the Flushing syndrome.
+ALDH2	addiction	dependence	7718681	Heterozygous for <strong>ALDH2</strong> in alcohol <b>dependence</b>: relationship between the <strong>ALDH2</strong> genotype and personality disorder in alcohol dependent patients with the Flushing syndrome.
+ALDH2	drug	alcohol	7755519	The present study investigates the influence of the <strong>ALDH2</strong> allele and of acculturation in North America on <b>alcohol</b> consumption by Orientals born in Canada or the United States.
+ALDH2	drug	alcohol	7755519	Oriental males carrying the inactive <strong>ALDH2</strong>( ) allele drink two thirds less <b>alcohol</b> (6.1 +/  1.5 vs. 18.2 +/  2.8 drinks/4 weeks; p < 0.001), show one third the prevalence of binge drinking (15.2 vs. 42.2%; p < 0.01), and are three times more likely to be abstainers (39.4 vs. 13.3%; p < 0.01) than Oriental <strong>ALDH2</strong>(+) males carrying the gene for the active enzyme.
+ALDH2	addiction	intoxication	7755519	Oriental males carrying the inactive <strong>ALDH2</strong>( ) allele drink two thirds less alcohol (6.1 +/  1.5 vs. 18.2 +/  2.8 drinks/4 weeks; p < 0.001), show one third the prevalence of <b>binge</b> drinking (15.2 vs. 42.2%; p < 0.01), and are three times more likely to be abstainers (39.4 vs. 13.3%; p < 0.01) than Oriental <strong>ALDH2</strong>(+) males carrying the gene for the active enzyme.
+ALDH2	addiction	intoxication	7755519	There were no significant differences in <b>binge</b> drinking or abstinence rates between <strong>ALDH2</strong>(+) Orientals and Caucasian males.
+ALDH2	drug	alcohol	7755519	It is concluded that a single mutation in the high affinity aldehyde dehydrogenase (<strong>ALDH2</strong>) gene predicts two thirds of the <b>alcohol</b> consumption and excessive <b>alcohol</b> use by Oriental males born in North America.
+ALDH2	drug	alcohol	7943668	Genetic variation at two polymorphic <b>alcohol</b> dehydrogenase loci, ADH2 and ADH3, and at the polymorphic mitochondrial aldehyde dehydrogenase locus, <strong>ALDH2</strong>, may influence the risk of developing <b>alcoholism</b> by modulating the rate of elimination of <b>ethanol</b> and the rate of formation and elimination of acetaldehyde.
+ALDH2	drug	alcohol	7943668	The Atayal with <b>alcohol</b> use disorders also had a lower frequency of <strong>ALDH2</strong>*2 than the controls; this allele is known to be responsible for the <b>alcohol</b> flush reaction among Asians, and thereby deters drinking.
+ALDH2	drug	alcohol	7513575	To study the <b>alcohol</b> consumption pattern and mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>) genotype, a random sample consisting of 170 native males (Chukchee and the Eskimo), residents of 4 Chukotka settlements, was studied.
+ALDH2	drug	alcohol	8290656	About half of Chinese individuals lack mitochondrial aldehyde dehydrogenase 2 (<strong>ALDH2</strong>) activity, which is responsible for the oxidation of acetaldehyde produced during <b>ethanol</b> metabolism.
+ALDH2	drug	alcohol	8290656	The <strong>ALDH2</strong> deficiency in Chinese has been implicated in <b>alcohol</b> flush reaction and reported to be a negative risk factor for development of <b>alcohol</b> dependence.
+ALDH2	addiction	dependence	8290656	The <strong>ALDH2</strong> deficiency in Chinese has been implicated in alcohol flush reaction and reported to be a negative risk factor for development of alcohol <b>dependence</b>.
+ALDH2	drug	alcohol	8464153	All individuals with homozygous atypical <strong>ALDH2</strong>(2)/<strong>ALDH2</strong>(2) and most of those with heterozygous atypical <strong>ALDH2</strong>(1)/<strong>ALDH2</strong>(1) were <b>alcohol</b> flushers, while all of the usual <strong>ALDH2</strong>(1)/<strong>ALDH2</strong>(1) were nonflushers.
+ALDH2	drug	alcohol	8464153	The results indicate that Japanese with the atypical <strong>ALDH2</strong>(2) allele are at a much lower risk in developing <b>alcoholic</b> liver disease than those with usual <strong>ALDH2</strong>(1)/<strong>ALDH2</strong>(1), presumably due to their sensitivity to <b>alcohol</b> intoxication.
+ALDH2	addiction	intoxication	8464153	The results indicate that Japanese with the atypical <strong>ALDH2</strong>(2) allele are at a much lower risk in developing alcoholic liver disease than those with usual <strong>ALDH2</strong>(1)/<strong>ALDH2</strong>(1), presumably due to their sensitivity to alcohol <b>intoxication</b>.
+ALDH2	drug	alcohol	1443441	Subjective feelings of <b>alcohol</b> intoxication in Asians with genetic variations of <strong>ALDH2</strong> alleles.
+ALDH2	addiction	intoxication	1443441	Subjective feelings of alcohol <b>intoxication</b> in Asians with genetic variations of <strong>ALDH2</strong> alleles.
+ALDH2	drug	alcohol	1443441	Asian American men who possess <strong>ALDH2</strong>*2 alleles and who experience a facial flush after consuming <b>alcohol</b> were carefully matched on drinking history and demographic variables with nonflushing Asian males with only <strong>ALDH2</strong>*1 alleles.
+ALDH2	drug	alcohol	1443441	These data suggest that Asians who flush after drinking, particularly those with <strong>ALDH2</strong>*1/2*2 genotype, have a more intense, although not necessarily a more negative, response to <b>alcohol</b> than comparable nonflushing Asians.
+ALDH2	drug	alcohol	3189338	Genetic polymorphisms of two major <b>alcohol</b> metabolizing enzymes i.e., one of the class I <b>alcohol</b> dehydrogenase isozymes (ADH2) and the mitochondrial aldehyde dehydrogenase (<strong>ALDH2</strong>) exist in Japanese and other Orientals but not in Caucasians.
+ALDH2	drug	alcohol	3189338	We determined, by means of hybridization of genomic DNA samples with allele specific synthetic oligonucleotide probes, genotypes of the ADH2 and the <strong>ALDH2</strong> loci of Japanese with <b>alcoholic</b> liver diseases and of control subjects.
+ALDH2	drug	alcohol	3189338	The results indicate that Japanese with the atypical <strong>ALDH2</strong>(2) allele are at a much lower risk in developing the <b>alcoholic</b> liver diseases than are those with homozygous, usual (Caucasian type) ALDH1(2)/ALDH1(2), presumably owing to their sensitivity to <b>alcohol</b> intoxication.
+ALDH2	addiction	intoxication	3189338	The results indicate that Japanese with the atypical <strong>ALDH2</strong>(2) allele are at a much lower risk in developing the alcoholic liver diseases than are those with homozygous, usual (Caucasian type) ALDH1(2)/ALDH1(2), presumably owing to their sensitivity to alcohol <b>intoxication</b>.
+ALDH2	drug	alcohol	7180842	A remarkably higher frequency of acute <b>alcohol</b> intoxication among Orientals than among Caucasians could be related to the absence of the <strong>ALDH2</strong> isozyme, which has a low apparent Km for acetaldehyde.
+ALDH2	addiction	intoxication	7180842	A remarkably higher frequency of acute alcohol <b>intoxication</b> among Orientals than among Caucasians could be related to the absence of the <strong>ALDH2</strong> isozyme, which has a low apparent Km for acetaldehyde.
+MAPK3	drug	alcohol	31845992	Similarly, no changes on the expression of <strong>ERK1</strong>/2, SAPK/JNK, COX 1 or COX 2 were found in the LV during <b>ethanol</b> withdrawal.
+MAPK3	addiction	withdrawal	31845992	Similarly, no changes on the expression of <strong>ERK1</strong>/2, SAPK/JNK, COX 1 or COX 2 were found in the LV during ethanol <b>withdrawal</b>.
+MAPK3	drug	cocaine	31704270	Whereas acute <b>cocaine</b> treated mice showed transient increases in p <strong>ERK1</strong>/2/<strong>ERK1</strong>/2 and p p65/p65 NFκB ratios after <b>cocaine</b> injection, repeated <b>cocaine</b> treated mice showed transient increases in p <strong>ERK1</strong>/2/<strong>ERK1</strong>/2, p p38/p38 MAPK, p NFκB p65/NF κB p65 and p CREB/CREB ratios.
+MAPK3	drug	cocaine	31606593	Interestingly, <b>cocaine</b> exposed serotonin transporter knockout rats showed increased BDNF levels, with no signs of phospho TrkB receptor coupling to phospho Akt and phospho <strong>ERK1</strong>.
+MAPK3	drug	alcohol	31342950	Indeed, an increase in <strong>ERK1</strong>/2 and JNK1/2 activation at PD30 was observed with <b>ethanol</b> consumption.
+MAPK3	drug	opioid	31173210	Electroacupuncture alleviates <b>morphine</b>‑induced hyperalgesia by regulating spinal CB1 receptors and <strong>ERK1</strong>/2 activity.
+MAPK3	drug	cannabinoid	31173210	The current study investigated the effect of EA on intrathecal (IT) morphine‑induced hyperalgesia (MIH) and examined the hypothesis that activation of <b>cannabinoid</b> receptor 1 (CB1) could enhance the antinociceptive effect of EA on MIH via regulation of the extracellular signal‑regulated kinase 1/2 (<strong>ERK1</strong>/2) signaling pathway.
+MAPK3	drug	opioid	31173210	The current study investigated the effect of EA on intrathecal (IT) <b>morphine</b>‑induced hyperalgesia (MIH) and examined the hypothesis that activation of cannabinoid receptor 1 (CB1) could enhance the antinociceptive effect of EA on MIH via regulation of the extracellular signal‑regulated kinase 1/2 (<strong>ERK1</strong>/2) signaling pathway.
+MAPK3	drug	opioid	31173210	The results revealed that chronic IT injections of <b>morphine</b> induced a significant decrease in mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) accompanied with remarkable upregulation of p‑<strong>ERK1</strong>/2 in the spinal cord, which could be attenuated by EA at the ST36‑GB34 acupoints.
+MAPK3	addiction	withdrawal	31173210	The results revealed that chronic IT injections of morphine induced a significant decrease in mechanical <b>withdrawal</b> threshold (MWT) and thermal <b>withdrawal</b> latency (TWL) accompanied with remarkable upregulation of p‑<strong>ERK1</strong>/2 in the spinal cord, which could be attenuated by EA at the ST36‑GB34 acupoints.
+MAPK3	drug	cannabinoid	31173210	In the rat model of MIH, IT injection of WIN 55,212‑2 combined with EA induced a significant increase in MWT and TWL accompanied with a significant decrease in p‑<strong>ERK1</strong>/2 and a significant increase in CB1 protein level compared with EA alone, while <b>SR141716</b> induced the opposite results.
+MAPK3	drug	opioid	31173210	The present study suggests that EA alleviates hyperalgesia induced by IT injection of <b>morphine</b> partially through the inhibition of <strong>ERK1</strong>/2 activation.
+MAPK3	drug	cocaine	31116258	A gene network approach showed that the EHMT1, EHMT2, MAPK1, <strong>MAPK3</strong>, MAP2K1, and HDAC5 genes, which are involved in transcription and chromatin regulation cellular signaling pathways, were also associated with <b>cocaine</b> dependence.
+MAPK3	addiction	dependence	31116258	A gene network approach showed that the EHMT1, EHMT2, MAPK1, <strong>MAPK3</strong>, MAP2K1, and HDAC5 genes, which are involved in transcription and chromatin regulation cellular signaling pathways, were also associated with cocaine <b>dependence</b>.
+MAPK3	drug	amphetamine	31078920	Moreover, phosphorylation of <strong>ERK1</strong>/2 and CREB was increased after <b>METH</b> and LPS exposure but decreased by SCH 23390.
+MAPK3	drug	alcohol	31068789	These results suggest a regulatory role of OEA in short term spatial memory and hippocampal neurogenesis through BDNF/AKT/<strong>ERK1</strong> signaling in response to acute THC in an <b>alcoholic</b> context during adolescence.
+MAPK3	drug	cannabinoid	31068789	These results suggest a regulatory role of OEA in short term spatial memory and hippocampal neurogenesis through BDNF/AKT/<strong>ERK1</strong> signaling in response to acute <b>THC</b> in an alcoholic context during adolescence.
+MAPK3	drug	alcohol	30914307	The extracellular signal regulated kinase (<strong>ERK1</strong>/2) pathway is downstream of mGluR5 and implicated in <b>alcohol</b> addiction; however, its role in sensitization remains unexplored.
+MAPK3	addiction	addiction	30914307	The extracellular signal regulated kinase (<strong>ERK1</strong>/2) pathway is downstream of mGluR5 and implicated in alcohol <b>addiction</b>; however, its role in sensitization remains unexplored.
+MAPK3	addiction	sensitization	30914307	The extracellular signal regulated kinase (<strong>ERK1</strong>/2) pathway is downstream of mGluR5 and implicated in alcohol addiction; however, its role in <b>sensitization</b> remains unexplored.
+MAPK3	drug	alcohol	30914307	We sought to determine if mGluR5 mediated changes in <b>ethanol</b> induced sensitization are associated with changes in <strong>ERK1</strong>/2 phosphorylation (pERK1/2) in specific brain regions.
+MAPK3	addiction	sensitization	30914307	We sought to determine if mGluR5 mediated changes in ethanol induced <b>sensitization</b> are associated with changes in <strong>ERK1</strong>/2 phosphorylation (pERK1/2) in specific brain regions.
+MAPK3	drug	alcohol	30914307	These data indicate that mGluR5 activity is required for the induction of <b>ethanol</b> locomotor sensitization and associated changes in <strong>ERK1</strong>/2 phosphorylation in the AcbSh and LHb, which raises the hypothesis that mGluR5 mediated cell signaling in these brain regions may mediate the induction of sensitization.
+MAPK3	addiction	sensitization	30914307	These data indicate that mGluR5 activity is required for the induction of ethanol locomotor <b>sensitization</b> and associated changes in <strong>ERK1</strong>/2 phosphorylation in the AcbSh and LHb, which raises the hypothesis that mGluR5 mediated cell signaling in these brain regions may mediate the induction of <b>sensitization</b>.
+MAPK3	drug	cocaine	30803445	Neuronal scaffolding protein spinophilin is integral for <b>cocaine</b> induced behavioral sensitization and <strong>ERK1</strong>/2 activation.
+MAPK3	addiction	sensitization	30803445	Neuronal scaffolding protein spinophilin is integral for cocaine induced behavioral <b>sensitization</b> and <strong>ERK1</strong>/2 activation.
+MAPK3	drug	cocaine	30803445	This behavioral alteration in spinophilin knockout mice was accompanied by attenuated c Fos and ∆FosB expression following <b>cocaine</b> administration and blunted <b>cocaine</b> induced phosphorylation of <strong>ERK1</strong>/2 in the striatum, with no change in other relevant signaling molecules.
+MAPK3	drug	cocaine	30803445	Therefore, we suggest spinophilin fulfills an essential role in <b>cocaine</b> induced behavioral sensitization, likely via <strong>ERK1</strong>/2 phosphorylation and induction of c Fos and ∆FosB in the striatum, a mechanism that may underlie specific processes in <b>cocaine</b> addiction.
+MAPK3	addiction	addiction	30803445	Therefore, we suggest spinophilin fulfills an essential role in cocaine induced behavioral sensitization, likely via <strong>ERK1</strong>/2 phosphorylation and induction of c Fos and ∆FosB in the striatum, a mechanism that may underlie specific processes in cocaine <b>addiction</b>.
+MAPK3	addiction	sensitization	30803445	Therefore, we suggest spinophilin fulfills an essential role in cocaine induced behavioral <b>sensitization</b>, likely via <strong>ERK1</strong>/2 phosphorylation and induction of c Fos and ∆FosB in the striatum, a mechanism that may underlie specific processes in cocaine addiction.
+MAPK3	drug	cocaine	30739236	Inhibition of VTA D1R results in increased activation of VTA <strong>ERK1</strong>/2 and in prolonging memory storage of <b>cocaine</b> place association in an ERK dependent manner.
+MAPK3	drug	psychedelics	30700692	Effects of Electroacupuncture on Expression of D1 Receptor (D1R), Phosphorylation of Extracellular Regulated Protein Kinase 1/2 (p <strong>ERK1</strong>/2), and c Fos in the Insular Cortex of <b>Ketamine</b> Addicted Rats.
+MAPK3	drug	psychedelics	30700692	BACKGROUND The aim of this study was to investigate the effects of electroacupuncture (EA) on expression of the D1 receptor (D1R), phosphorylation of extracellular regulated protein kinase 1/2 (p <strong>ERK1</strong>/2) and c Fos in the insular cortex (IC) of <b>ketamine</b> addicted rats.
+MAPK3	drug	psychedelics	30700692	CONCLUSIONS <b>Ketamine</b> addiction induces c Fos overexpression in the IC by increasing the expression of D1R and p <strong>ERK1</strong>/2.
+MAPK3	addiction	addiction	30700692	CONCLUSIONS Ketamine <b>addiction</b> induces c Fos overexpression in the IC by increasing the expression of D1R and p <strong>ERK1</strong>/2.
+MAPK3	drug	opioid	30641110	<b>Heroin</b> based crack induces hyperalgesia through β arrestin 2 redistribution and phosphorylation of <strong>Erk1</strong>/2 and JNK in the periaqueductal gray area.
+MAPK3	drug	opioid	30641110	Furthermore, crack as well as <b>heroin</b> administration increased phosphorylated <strong>Erk1</strong>/2 and JNK in the PAG.
+MAPK3	drug	amphetamine	30544074	Additional experiments showed that expression of brain derived neurotrophic factor (BDNF), phosphorylated tropomyosin receptor kinase B (p TrkB), phosphorylated extracellular signal related kinase 1/2 (p <strong>ERK1</strong>/2) and phosphorylated cAMP response element binding protein (p CREB) were decreased in the hippocampus and prefrontal cortex of mice in <b>METH</b> group and the level of mitogen activated protein kinase phosphatase 1 (MKP 1) was increased.
+MAPK3	drug	amphetamine	30500461	Exposure to FIR protects from <b>methamphetamine</b> (MA) induced memory impairments via phosphorylation of <strong>ERK 1</strong>/2 signaling by positive modulation of protein kinase C δ (PKCδ), M1 muscarinic acetylcholine receptor (M1 mAChR), and nuclear factor E2 related factor 2 (Nrf2) transcription factor.
+MAPK3	drug	alcohol	30445307	Purinergic P2X7 receptor blockade mitigates <b>alcohol</b> induced steatohepatitis and intestinal injury by regulating MEK1/2 <strong>ERK1</strong>/2 signaling and egr 1 activity.
+MAPK3	drug	alcohol	30445307	Furthermore, P2X7R blockade inhibited MEK1/2 <strong>ERK1</strong>/2 phosphorylation and egr 1 expression in both liver and intestine from <b>alcohol</b> fed mice.
+MAPK3	drug	alcohol	30445307	Collectively, P2X7R blockade mitigates <b>alcohol</b> induced steatohepatitis and intestinal injury by inhibiting MEK1/2 <strong>ERK1</strong>/2 signaling and egr 1 expression.
+MAPK3	drug	opioid	30444263	Furthermore, intrathecal injection of a selective <strong>ERK1</strong>/2, p38, or JNK inhibitor blocked pain hypersensitivity induced by chronic <b>morphine</b> treatment.
+MAPK3	drug	opioid	30444263	In addition, co immunoprecipitation assays revealed that NMDARs formed a protein complex with <strong>ERK1</strong>/2, p38, and JNK in the spinal cord and that chronic <b>morphine</b> treatment increased physical interactions of NMDARs with these three MAPKs.
+MAPK3	drug	amphetamine	30433806	The phosphorylated extracellular regulated protein kinase 1/2 (p <strong>ERK1</strong>/2), an important regulator of HCN channels, was also obviously reduced in hippocampus and prefrontal cortex of mice with <b>METH</b> re exposure.
+MAPK3	drug	amphetamine	30433806	Meanwhile, acute <b>METH</b> exposure did not affect the working memory function and the protein expressions of HCN1 channels and p <strong>ERK1</strong>/2.
+MAPK3	drug	amphetamine	30433806	Overall, our data firstly showed the aberrant protein expression of HCN1 channels in <b>METH</b> re exposed mice with enhanced working memory, which was probably related to the down regulation of p <strong>ERK1</strong>/2 protein expression.
+MAPK3	drug	nicotine	30206032	Western blot analysis showed an increased expression of <strong>ERK1</strong>/2 in <b>nicotine</b> treated cultures suggesting <b>nicotine</b> provided neuroprotection in SCG neurons by increasing the expression of <strong>ERK1</strong>/2 through nicotinic receptor dependent mechanisms.
+MAPK3	drug	opioid	30147637	Over expression of CCK1R reversed CREB and <strong>ERK1</strong>/2 activation in HEK293 hMOR cells exposed to <b>morphine</b>.
+MAPK3	drug	opioid	30147637	Our study identifies over expression of CCK1R significantly blocked <b>morphine</b> dependence, which was related with phosphorylation of CREB, and <strong>ERK1</strong>/2 signaling activation.
+MAPK3	addiction	dependence	30147637	Our study identifies over expression of CCK1R significantly blocked morphine <b>dependence</b>, which was related with phosphorylation of CREB, and <strong>ERK1</strong>/2 signaling activation.
+MAPK3	drug	opioid	30147637	While over expression of CCK2R promoted <b>morphine</b> dependence, which was related with phosphorylation of CREB but not <strong>ERK1</strong>/2 signaling activation.
+MAPK3	addiction	dependence	30147637	While over expression of CCK2R promoted morphine <b>dependence</b>, which was related with phosphorylation of CREB but not <strong>ERK1</strong>/2 signaling activation.
+MAPK3	drug	nicotine	30124787	We report that exposure to <b>nicotine</b>, selectively during adolescence, induces profound and long lasting neuronal, molecular and behavioral disturbances involving PFC DA D1R and downstream extracellular signal related kinase 1 2 (<strong>ERK 1</strong> 2) signaling.
+MAPK3	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (Cnr1, Cnr2, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and TRPV1 sensitizing kinases (<strong>Mapk3</strong>, Mapk14, Prkcg, and Prkaca).
+MAPK3	drug	opioid	28971231	Effects of <b>morphine</b> on place conditioning and <strong>ERK1</strong>/2 phosphorylation in the nucleus accumbens of psychogenetically selected Roman low  and high avoidance rats.
+MAPK3	drug	opioid	28971231	Extracellular signal regulated kinase (<strong>ERK1</strong>/2) phosphorylation is critical for neuronal and behavioural functions; in particular, phosphorylated <strong>ERK1</strong>/2 (pERK1/2) expression in the nucleus accumbens (Acb) of the rat is stimulated by addictive drugs with the exception of <b>morphine</b>, which decreases accumbal <strong>ERK1</strong>/2 phosphorylation in the Sprague Dawley and Wistar rats.
+MAPK3	addiction	addiction	28971231	Extracellular signal regulated kinase (<strong>ERK1</strong>/2) phosphorylation is critical for neuronal and behavioural functions; in particular, phosphorylated <strong>ERK1</strong>/2 (pERK1/2) expression in the nucleus accumbens (Acb) of the rat is stimulated by <b>addictive</b> drugs with the exception of morphine, which decreases accumbal <strong>ERK1</strong>/2 phosphorylation in the Sprague Dawley and Wistar rats.
+MAPK3	drug	opioid	28971231	However, the effects of <b>morphine</b> on place conditioning (conditioned place preference (CPP)) and <strong>ERK1</strong>/2 phosphorylation in the Roman lines remain unknown.
+MAPK3	addiction	reward	28971231	However, the effects of morphine on place conditioning (conditioned place preference (<b>CPP</b>)) and <strong>ERK1</strong>/2 phosphorylation in the Roman lines remain unknown.
+MAPK3	drug	opioid	28971231	<b>morphine</b> elicited CPP acquisition) and the relationship between these properties and its effects on <strong>ERK1</strong>/2 phosphorylation in the Acb, the behavioural effects of <b>morphine</b> were evaluated in a place conditioning apparatus and <strong>ERK1</strong>/2 phosphorylation was assessed by immunohistochemistry in the shell and core subregions of the Acb of rats both acutely administered with <b>morphine</b> or undergoing conditioning.
+MAPK3	addiction	reward	28971231	morphine elicited <b>CPP</b> acquisition) and the relationship between these properties and its effects on <strong>ERK1</strong>/2 phosphorylation in the Acb, the behavioural effects of morphine were evaluated in a place conditioning apparatus and <strong>ERK1</strong>/2 phosphorylation was assessed by immunohistochemistry in the shell and core subregions of the Acb of rats both acutely administered with morphine or undergoing conditioning.
+MAPK3	drug	alcohol	28784931	<b>Alcohol</b> disrupted lipopolysaccharide (LPS) TLR4 <strong>ERK1</strong>/2 cyclin D1 signaling and inhibited upregulation of Sca 1 and C/EBPβ expression by lineage negative marrow cells in response to bacteremia.
+MAPK3	drug	alcohol	28616095	<b>Acamprosate</b> in a mouse model of fragile X syndrome: modulation of spontaneous cortical activity, <strong>ERK1</strong>/2 activation, locomotor behavior, and anxiety.
+MAPK3	drug	alcohol	28616095	Additional adult mice were used to assess chronic <b>acamprosate</b> treatment and any potential effects of the calcium moiety using CaCl2 treatment on behavior and nuclear <strong>ERK1</strong>/2 activation.
+MAPK3	drug	alcohol	28616095	<b>Acamprosate</b> attenuated prolonged cortical UP state duration, decreased elevated <strong>ERK1</strong>/2 activation in brain tissue, and reduced nuclear <strong>ERK1</strong>/2 activation in the dentate gyrus in KO mice.
+MAPK3	drug	amphetamine	28597397	Protein Kinase Cδ Gene Depletion Protects Against <b>Methamphetamine</b> Induced Impairments in Recognition Memory and <strong>ERK1</strong>/2 Signaling via Upregulation of Glutathione Peroxidase 1 Gene.
+MAPK3	drug	cocaine	28585320	Distinct SERT dependent gene expression networks triggered by acute and chronic <b>cocaine</b> administration were identified, including PrL Akt and nucleus accumbens <strong>ERK1</strong>/2 signalling.
+MAPK3	drug	cocaine	28432301	Augmenting AMPK activity by intra NAc core infusions of the AMPK activator 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide (AICAR) or adenovirus expressing constitutively active subunits of AMPK decreased cue induced reinstatement of <b>cocaine</b> seeking and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2) pathways.
+MAPK3	addiction	relapse	28432301	Augmenting AMPK activity by intra NAc core infusions of the AMPK activator 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide (AICAR) or adenovirus expressing constitutively active subunits of AMPK decreased cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2) pathways.
+MAPK3	drug	cocaine	28432301	In contrast, inhibition of AMPK activity by intra NAc core infusions of the AMPK inhibitor compound C or adenovirus expressing dominant negative subunits of AMPK increased cue induced reinstatement of <b>cocaine</b> seeking and enhanced mTORC1 and <strong>ERK1</strong>/2 activity.
+MAPK3	addiction	relapse	28432301	In contrast, inhibition of AMPK activity by intra NAc core infusions of the AMPK inhibitor compound C or adenovirus expressing dominant negative subunits of AMPK increased cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and enhanced mTORC1 and <strong>ERK1</strong>/2 activity.
+MAPK3	drug	cocaine	28432301	Altogether, these results indicate that AMPK activity in the NAc core is critical for the cue induced reinstatement of <b>cocaine</b> seeking, which may be mediated by mTORC1 and <strong>ERK1</strong>/2 signaling.
+MAPK3	addiction	relapse	28432301	Altogether, these results indicate that AMPK activity in the NAc core is critical for the cue induced <b>reinstatement</b> of cocaine <b>seeking</b>, which may be mediated by mTORC1 and <strong>ERK1</strong>/2 signaling.
+MAPK3	drug	opioid	28106041	Furthermore, DREADD mediated specific inactivation of the EC dDG pathway or disconnection of the pathway with local postsynaptic GluN2B <strong>ERK1</strong>/2 signaling both decreased context induced reinstatement of <b>heroin</b> seeking.
+MAPK3	addiction	relapse	28106041	Furthermore, DREADD mediated specific inactivation of the EC dDG pathway or disconnection of the pathway with local postsynaptic GluN2B <strong>ERK1</strong>/2 signaling both decreased context induced <b>reinstatement</b> of heroin <b>seeking</b>.
+MAPK3	drug	opioid	28106041	Our results indicate that the EC dDG pathway mediates context induced reinstatement of <b>heroin</b> seeking, via the activation of postsynaptic GluN2B <strong>ERK1</strong>/2 signaling in the dDG.
+MAPK3	addiction	relapse	28106041	Our results indicate that the EC dDG pathway mediates context induced <b>reinstatement</b> of heroin <b>seeking</b>, via the activation of postsynaptic GluN2B <strong>ERK1</strong>/2 signaling in the dDG.
+MAPK3	drug	nicotine	27633557	Acute <b>nicotine</b> enhances both types of memory via L type VGCC blockade and via <strong>ERK1</strong>/2 activation.
+MAPK3	drug	amphetamine	27544406	Ifenprodil attenuates the acquisition and expression of <b>methamphetamine</b> induced behavioral sensitization and activation of Ras <strong>ERK1</strong>/2 cascade in the caudate putamen.
+MAPK3	addiction	sensitization	27544406	Ifenprodil attenuates the acquisition and expression of methamphetamine induced behavioral <b>sensitization</b> and activation of Ras <strong>ERK1</strong>/2 cascade in the caudate putamen.
+MAPK3	drug	amphetamine	27544406	Western blot analysis revealed that pre injection of low dose ifenprodil in the acquisition markedly attenuated <b>METH</b> induced ascent of Ras, pERK1/2/<strong>ERK1</strong>/2, and ΔFosB protein levels in the CPu.
+MAPK3	drug	amphetamine	27544406	Moreover, chronic <b>METH</b> administration increased pERK1/2/<strong>ERK1</strong>/2 level in the NAc.
+MAPK3	drug	opioid	27245230	Role of nucleus accumbens μ <b>opioid</b> receptors in the effects of <b>morphine</b> on <strong>ERK1</strong>/2 phosphorylation.
+MAPK3	drug	opioid	27245230	Despite the critical role attributed to phosphorylated extracellular signal regulated kinase (pERK1/2) in the nucleus accumbens (Acb) in the actions of addictive drugs, the effects of <b>morphine</b> on <strong>ERK1</strong>/2 phosphorylation in this area are still controversial.
+MAPK3	addiction	addiction	27245230	Despite the critical role attributed to phosphorylated extracellular signal regulated kinase (pERK1/2) in the nucleus accumbens (Acb) in the actions of <b>addictive</b> drugs, the effects of morphine on <strong>ERK1</strong>/2 phosphorylation in this area are still controversial.
+MAPK3	drug	opioid	27245230	In order to investigate further this issue, we studied (1) the ability of <b>morphine</b> to affect <strong>ERK1</strong>/2 phosphorylation in the shell (AcbSh) and core (AcbC) of Sprague Dawley and Wistar rats and of CD 1 and C57BL/6J mice and (2) the role of dopamine D1 and μ <b>opioid</b> receptors in Sprague Dawley rats and CD 1 mice.
+MAPK3	drug	opioid	27245230	These findings confirm the differential effects of <b>morphine</b> in rats and mice Acb and that D1 receptors exert a facilitatory role on <strong>ERK1</strong>/2 phosphorylation; furthermore, they indicate that, in rats, removal of the D1 dependent pERK1/2 expression discloses the stimulatory influence of <b>morphine</b> on <strong>ERK1</strong>/2 phosphorylation and that the <b>morphine</b>'s ability to decrease pERK1/2 expression is mediated by Acb μ <b>opioid</b> receptors.
+MAPK3	drug	amphetamine	27138644	However, the mechanism underlying enhanced expression of striatal D1Rs in animals self administering <b>Meth</b> is unknown and is hypothesized to involve maladaptive intracellular signal transduction mechanism via hyperphosphorylation of extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2).
+MAPK3	drug	amphetamine	27138644	We therefore evaluated the effects of extended access <b>Meth</b> self administration on expression of striatal D1Rs, activated <strong>ERK1</strong>/2 and Cav 1.
+MAPK3	drug	amphetamine	27138644	We also report that extended access <b>Meth</b> produces compulsive like unregulated intake of the drug, and these behavioral outcomes are associated with enhanced expression of D1Rs, increased activity of <strong>ERK1</strong>/2, and reduced Cav 1 expression in the dorsal striatum.
+MAPK3	addiction	addiction	27138644	We also report that extended access Meth produces <b>compulsive</b> like unregulated intake of the drug, and these behavioral outcomes are associated with enhanced expression of D1Rs, increased activity of <strong>ERK1</strong>/2, and reduced Cav 1 expression in the dorsal striatum.
+MAPK3	drug	amphetamine	27138644	These data suggest a possible cellular mechanism that involves Cav 1 regulation of D1R expression in response to escalated <b>Meth</b> intake, and how this response of altered D1Rs and enhanced <strong>ERK1</strong>/2 activation to <b>Meth</b> self administration contributes to contingent related processes such as addiction.
+MAPK3	addiction	addiction	27138644	These data suggest a possible cellular mechanism that involves Cav 1 regulation of D1R expression in response to escalated Meth intake, and how this response of altered D1Rs and enhanced <strong>ERK1</strong>/2 activation to Meth self administration contributes to contingent related processes such as <b>addiction</b>.
+MAPK3	drug	cannabinoid	27046127	The results demonstrate that GAT100 is a NAM of the orthosteric CB1R agonist CP55,940 and the <b>endocannabinoids</b> 2 arachidonoylglycerol and anandamide for β arrestin1 recruitment, PLCβ3 and <strong>ERK1</strong>/2 phosphorylation, cAMP accumulation, and CB1R internalization in HEK293A cells overexpressing CB1R and in Neuro2a and STHdh(Q7/Q7) cells endogenously expressing CB1R.
+MAPK3	drug	alcohol	27038596	Ingenuity Pathway Analysis of putative miRNA targets illustrated that miRNAs identified in this study are involved in biological pathways that mediate the effects of <b>alcohol</b>, such as brain derived neurotrophic factor, <strong>ERK1</strong>/2, and PI3K/AKT signaling.
+MAPK3	drug	opioid	26742526	Interestingly, p <strong>ERK 1</strong>/2 levels during chronic <b>morphine</b> and <b>morphine</b> withdrawal correlated RPTPβ/ζ expression.
+MAPK3	addiction	withdrawal	26742526	Interestingly, p <strong>ERK 1</strong>/2 levels during chronic morphine and morphine <b>withdrawal</b> correlated RPTPβ/ζ expression.
+MAPK3	drug	nicotine	26687895	Hippocampal kinases such as cAMP dependent protein kinase (PKA), calcium/calmodulin dependent protein kinases (CAMKs), extracellular signal regulated kinases 1 and 2 (<strong>ERK1</strong>/2), and c jun N terminal kinase 1 (JNK1), and the transcription factor cAMP response element binding protein (CREB) that are activated either directly or indirectly by <b>nicotine</b> may modulate hippocampal plasticity and in parallel hippocampus dependent learning and memory.
+MAPK3	drug	cannabinoid	26664379	The Neuroprotective Effect of Lithium in <b>cannabinoid</b> Dependence is Mediated through Modulation of Cyclic AMP, <strong>ERK1</strong>/2 and GSK 3β Phosphorylation in Cerebellar Granular Neurons of Rat.
+MAPK3	addiction	dependence	26664379	The Neuroprotective Effect of Lithium in cannabinoid <b>Dependence</b> is Mediated through Modulation of Cyclic AMP, <strong>ERK1</strong>/2 and GSK 3β Phosphorylation in Cerebellar Granular Neurons of Rat.
+MAPK3	drug	cannabinoid	26664379	Recent studies indicate the involvement of upstream extracellular signal kinase1/2 (<strong>ERK1</strong>/2) and downstream GSK 3β pathways in the development of <b>cannabinoid</b> induced dependence.
+MAPK3	addiction	dependence	26664379	Recent studies indicate the involvement of upstream extracellular signal kinase1/2 (<strong>ERK1</strong>/2) and downstream GSK 3β pathways in the development of cannabinoid induced <b>dependence</b>.
+MAPK3	drug	cannabinoid	26664379	Accordingly, the present study aimed to investigate the mechanism of modulatory/neuroprotective effects of Li on a <b>cannabinoid</b> agonist (WIN 55,212 2 (WIN)) induced dependence, through quantitative analysis of some involved proteins such as <strong>ERK1</strong>/2, GSK 3β and related signaling pathways including their phosphorylated forms; and cAMP level as the other molecular mechanisms leading to dependence, in CGNs model.
+MAPK3	addiction	dependence	26664379	Accordingly, the present study aimed to investigate the mechanism of modulatory/neuroprotective effects of Li on a cannabinoid agonist (WIN 55,212 2 (WIN)) induced <b>dependence</b>, through quantitative analysis of some involved proteins such as <strong>ERK1</strong>/2, GSK 3β and related signaling pathways including their phosphorylated forms; and cAMP level as the other molecular mechanisms leading to <b>dependence</b>, in CGNs model.
+MAPK3	drug	cannabinoid	26664379	Results further suggested the potential role of Li pretreatment to diminish the development of <b>cannabinoid</b> induced dependence/neuronal injury through possible mechanisms of modulating the cAMP/p <strong>ERK1</strong>/2 cascade independent of p GSK 3β signaling pathway in vitro.
+MAPK3	addiction	dependence	26664379	Results further suggested the potential role of Li pretreatment to diminish the development of cannabinoid induced <b>dependence</b>/neuronal injury through possible mechanisms of modulating the cAMP/p <strong>ERK1</strong>/2 cascade independent of p GSK 3β signaling pathway in vitro.
+MAPK3	drug	opioid	26349634	To examine the effect of various <b>opioids</b> on striatal activation levels of Akt and <strong>ERK1</strong>/2, as well as the signaling responses of D2DRs following <b>opioid</b> exposure.
+MAPK3	drug	opioid	26165762	Inhibition of spinal <strong>ERK1</strong>/2 c JUN signaling pathway counteracts the development of low doses <b>morphine</b> induced hyperalgesia.
+MAPK3	drug	nicotine	26150803	We have demonstrated that HIV 1 transgenic rats exhibit attenuated <b>nicotine</b> mediated locomotor activity, altered cAMP response element binding protein (CREB) and extracellular regulated kinase (<strong>ERK1</strong>/2) signaling in the mesocorticolimbic regions.
+MAPK3	drug	alcohol	26123321	Extracellular signal regulated protein kinase (<strong>ERK1</strong>/2) is activated by <b>ethanol</b> in reward related brain regions.
+MAPK3	addiction	reward	26123321	Extracellular signal regulated protein kinase (<strong>ERK1</strong>/2) is activated by ethanol in <b>reward</b> related brain regions.
+MAPK3	drug	alcohol	26123321	Accordingly, systemic inhibition of <strong>ERK1</strong>/2 potentiates <b>ethanol</b> reinforcement.
+MAPK3	addiction	reward	26123321	Accordingly, systemic inhibition of <strong>ERK1</strong>/2 potentiates ethanol <b>reinforcement</b>.
+MAPK3	drug	alcohol	26123321	This study aims to pharmacologically inhibit <strong>ERK1</strong>/2 in the medial prefrontal cortex (PFC), nucleus accumbens (NAC), and amygdala (AMY) prior to <b>ethanol</b> or sucrose self administration, and evaluate effects of operant <b>ethanol</b> self administration on <strong>ERK1</strong>/2 phosphorylation (pERK1/2).
+MAPK3	addiction	reward	26123321	This study aims to pharmacologically inhibit <strong>ERK1</strong>/2 in the medial prefrontal cortex (PFC), nucleus accumbens (NAC), and amygdala (AMY) prior to ethanol or sucrose self administration, and evaluate effects of <b>operant</b> ethanol self administration on <strong>ERK1</strong>/2 phosphorylation (pERK1/2).
+MAPK3	drug	alcohol	26123321	However, <strong>ERK1</strong>/2 activity only in the PFC mechanistically regulates <b>ethanol</b> self administration.
+MAPK3	drug	alcohol	26123321	These data suggest that <b>ethanol</b> induced activation of <strong>ERK1</strong>/2 in the PFC is a critical pharmacological effect that mediates the reinforcing properties of the drug.
+MAPK3	addiction	reward	26123321	These data suggest that ethanol induced activation of <strong>ERK1</strong>/2 in the PFC is a critical pharmacological effect that mediates the <b>reinforcing</b> properties of the drug.
+MAPK3	addiction	dependence	26096126	Further, our studies established the <b>dependence</b> of the central CB1R mediated pressor response on neuronal nitric oxide synthase (nNOS) and extracellular signal regulated kinase1/2 (<strong>ERK1</strong>/2) phosphorylation in the RVLM.
+MAPK3	drug	alcohol	26044620	Gene network analysis shows immune signaling and <strong>ERK1</strong>/2 as novel genetic markers for multiple addiction phenotypes: <b>alcohol</b>, smoking and opioid addiction.
+MAPK3	drug	nicotine	26044620	Gene network analysis shows immune signaling and <strong>ERK1</strong>/2 as novel genetic markers for multiple addiction phenotypes: alcohol, <b>smoking</b> and opioid addiction.
+MAPK3	drug	opioid	26044620	Gene network analysis shows immune signaling and <strong>ERK1</strong>/2 as novel genetic markers for multiple addiction phenotypes: alcohol, smoking and <b>opioid</b> addiction.
+MAPK3	addiction	addiction	26044620	Gene network analysis shows immune signaling and <strong>ERK1</strong>/2 as novel genetic markers for multiple <b>addiction</b> phenotypes: alcohol, smoking and opioid <b>addiction</b>.
+MAPK3	addiction	addiction	26044620	Using Core Analysis function in Ingenuity Pathway Analysis software, we found that <strong>ERK1</strong>/2 was strongly interconnected across all three <b>addiction</b> networks.
+MAPK3	drug	opioid	25891774	Structure activity relationship studies of functionally selective kappa <b>opioid</b> receptor agonists that modulate <strong>ERK 1</strong>/2 phosphorylation while preserving G protein over βarrestin2 signaling bias.
+MAPK3	drug	alcohol	25837445	<b>Ethanol</b> withdrawal also induced an increase of phospho <strong>ERK1</strong>/2 in both the AcbSh and AcbC, while <b>ethanol</b> re exposure decreased phospho ERK in the AcbSh.
+MAPK3	addiction	withdrawal	25837445	Ethanol <b>withdrawal</b> also induced an increase of phospho <strong>ERK1</strong>/2 in both the AcbSh and AcbC, while ethanol re exposure decreased phospho ERK in the AcbSh.
+MAPK3	drug	alcohol	25703719	<b>Alcohol</b> alters the activation of <strong>ERK1</strong>/2, a functional regulator of binge <b>alcohol</b> drinking in adult C57BL/6J mice.
+MAPK3	addiction	intoxication	25703719	Alcohol alters the activation of <strong>ERK1</strong>/2, a functional regulator of <b>binge</b> alcohol drinking in adult C57BL/6J mice.
+MAPK3	drug	alcohol	25703719	The present experiments were designed to determine the effects of acute <b>alcohol</b> on extracellular signaling related kinases (<strong>ERK1</strong>/2) expression and activity and to determine whether <strong>ERK1</strong>/2 activity functionally regulates binge like <b>alcohol</b> drinking.
+MAPK3	addiction	intoxication	25703719	The present experiments were designed to determine the effects of acute alcohol on extracellular signaling related kinases (<strong>ERK1</strong>/2) expression and activity and to determine whether <strong>ERK1</strong>/2 activity functionally regulates <b>binge</b> like alcohol drinking.
+MAPK3	drug	alcohol	25703719	These findings indicate that <strong>ERK1</strong>/2 MAPK signaling regulates binge like <b>alcohol</b> drinking.
+MAPK3	addiction	intoxication	25703719	These findings indicate that <strong>ERK1</strong>/2 MAPK signaling regulates <b>binge</b> like alcohol drinking.
+MAPK3	drug	opioid	25521224	<b>Buprenorphine</b> did not inhibit AC or stimulate <strong>ERK1</strong>/2 phosphorylation in CHO cells expressing MOPr A6V, but <b>buprenorphine</b> activation of K channels in AtT 20 cells was preserved.
+MAPK3	drug	opioid	25521224	[D Ala2, N MePhe4, Gly ol] enkephalin, <b>morphine</b> and β endorphin inhibition of AC was significantly reduced via MOPr A6V, as was signalling of all <b>opioids</b> to <strong>ERK1</strong>/2.
+MAPK3	drug	opioid	25497384	A pretreatment with the <b>opioid</b> analgesic <b>morphine</b> or the NMDA antagonist MK 801 markedly attenuated <strong>ERK1</strong>/2 phosphorylation in both areas of the pain pathway.
+MAPK3	drug	nicotine	25328101	Effects of environmental enrichment on <strong>ERK1</strong>/2 phosphorylation in the rat prefrontal cortex following <b>nicotine</b> induced sensitization or <b>nicotine</b> self administration.
+MAPK3	addiction	sensitization	25328101	Effects of environmental enrichment on <strong>ERK1</strong>/2 phosphorylation in the rat prefrontal cortex following nicotine induced <b>sensitization</b> or nicotine self administration.
+MAPK3	drug	nicotine	25328101	The current study determined whether environmental enrichment differentially regulates extracellular signal regulated kinase1/2 (<strong>ERK1</strong>/2) activity in the prefrontal cortex in rats following <b>nicotine</b> sensitization or <b>nicotine</b> self administration.
+MAPK3	addiction	sensitization	25328101	The current study determined whether environmental enrichment differentially regulates extracellular signal regulated kinase1/2 (<strong>ERK1</strong>/2) activity in the prefrontal cortex in rats following nicotine <b>sensitization</b> or nicotine self administration.
+MAPK3	drug	cannabinoid	25325202	Lithium attenuates <b>cannabinoid</b> induced dependence in the animal model: involvement of phosphorylated <strong>ERK1</strong>/2 and GSK 3β signaling pathways.
+MAPK3	addiction	dependence	25325202	Lithium attenuates cannabinoid induced <b>dependence</b> in the animal model: involvement of phosphorylated <strong>ERK1</strong>/2 and GSK 3β signaling pathways.
+MAPK3	drug	cannabinoid	25325202	<b>Cannabinoid</b> induced dependence or withdrawal signs are indicated by the result of complex molecular mechanisms including upstream protein kinases (PKs), such as an extracellular signal regulated kinase1/2 (<strong>ERK1</strong>/2) and downstream glycogen synthase kinase 3β (GSK 3β), which lead to neuronal plasticity.
+MAPK3	addiction	dependence	25325202	Cannabinoid induced <b>dependence</b> or withdrawal signs are indicated by the result of complex molecular mechanisms including upstream protein kinases (PKs), such as an extracellular signal regulated kinase1/2 (<strong>ERK1</strong>/2) and downstream glycogen synthase kinase 3β (GSK 3β), which lead to neuronal plasticity.
+MAPK3	addiction	withdrawal	25325202	Cannabinoid induced dependence or <b>withdrawal</b> signs are indicated by the result of complex molecular mechanisms including upstream protein kinases (PKs), such as an extracellular signal regulated kinase1/2 (<strong>ERK1</strong>/2) and downstream glycogen synthase kinase 3β (GSK 3β), which lead to neuronal plasticity.
+MAPK3	drug	cannabinoid	25325202	In this study, we examined the protective effect of lithium (Li) as a potent <strong>ERK1</strong>/2 and GSK 3β modulator to prevent the development of dependence on <b>cannabinoids</b>.
+MAPK3	addiction	dependence	25325202	In this study, we examined the protective effect of lithium (Li) as a potent <strong>ERK1</strong>/2 and GSK 3β modulator to prevent the development of <b>dependence</b> on cannabinoids.
+MAPK3	addiction	withdrawal	25325202	Li and SL pre treatment attenuated the global <b>withdrawal</b> signs in regarding their modulation effect on the up regulation of p <strong>ERK1</strong>/2 cascade enhanced by AM injection.
+MAPK3	drug	cannabinoid	25325202	Therefore, p <strong>ERK1</strong>/2 and p GSK 3β pathways are involved in the <b>cannabinoid</b> induced dependence.
+MAPK3	addiction	dependence	25325202	Therefore, p <strong>ERK1</strong>/2 and p GSK 3β pathways are involved in the cannabinoid induced <b>dependence</b>.
+MAPK3	drug	cannabinoid	25325202	In conclusion, Li neuroprotectionwith regard to <b>cannabinoid</b> abstinence may occur through the regulation of the p <strong>ERK1</strong>/2 cascade inconsequent of p GSK 3β signaling pathways in rats.
+MAPK3	drug	opioid	25196735	Further mechanism studies showed that the opposite effect of <b>morphine</b> and DAMGO on the glutamate release was via the activation of μ receptors, but the downstream signaling pathways of μ receptors were different: DAMGO inhibited the glutamate release via μ receptor Gi protein  PLA2 AA signaling pathway, whereas <b>morphine</b> promoted the glutamate release via μ receptor Gi protein PKC <strong>ERK1</strong>/2 synapsin I signaling pathway.
+MAPK3	addiction	sensitization	24901319	Luteolin inhibits MA induced hyperactivity and behavioral <b>sensitization</b> in mice through the <strong>ERK1</strong>/2/ΔFosB pathway.
+MAPK3	drug	cocaine	24844603	We pioneered the observation that a common feature of addictive drugs is to activate, by a double tyrosine/threonine phosphorylation, the extracellular signal regulated kinases 1 and 2 (<strong>ERK1</strong>/2) in the striatum, which control a plethora of substrates, some of them being critically involved in <b>cocaine</b> mediated molecular and behavioral adaptations.
+MAPK3	addiction	addiction	24844603	We pioneered the observation that a common feature of <b>addictive</b> drugs is to activate, by a double tyrosine/threonine phosphorylation, the extracellular signal regulated kinases 1 and 2 (<strong>ERK1</strong>/2) in the striatum, which control a plethora of substrates, some of them being critically involved in cocaine mediated molecular and behavioral adaptations.
+MAPK3	drug	cocaine	24844603	Herein, we review how the interplay between dopamine and glutamate signaling controls <b>cocaine</b> induced <strong>ERK1</strong>/2 activation in MSNs.
+MAPK3	drug	cocaine	24844603	We emphasize the key role of N methyl D aspartate receptor potentiation by D1 receptor to trigger <strong>ERK1</strong>/2 activation and its subsequent nuclear translocation where it modulates both epigenetic and genetic processes engaged by <b>cocaine</b>.
+MAPK3	drug	cocaine	24844603	We discuss how <b>cocaine</b> induced long term synaptic and structural plasticity of MSNs, as well as behavioral adaptations, are influenced by <strong>ERK1</strong>/2 controlled targets.
+MAPK3	addiction	addiction	24844603	We conclude that a better knowledge of molecular mechanisms underlying <strong>ERK1</strong>/2 activation by drugs of abuse and/or its role in long term neuronal plasticity in the striatum may provide a new route for therapeutic treatment in <b>addiction</b>.
+MAPK3	drug	nicotine	24793809	In a cell line that highly expressed α5 nAChR, the loss of α5 nAChR function by siRNA was used to study whether α5 nAChR is involved in the <b>nicotine</b> induced expression of HIF 1α and VEGF through the activation of the <strong>ERK1</strong>/2 and PI3K/Akt signaling pathways.
+MAPK3	drug	nicotine	24793809	The silencing of α5 nAChR significantly inhibited the <b>nicotine</b> induced cell proliferation compared with the control group and attenuated the <b>nicotine</b> induced upregulation of HIF 1α and VEGF, and these effects required the cooperation of the <strong>ERK1</strong>/2 and PI3K/Akt signaling pathways.
+MAPK3	drug	cocaine	24599455	The <b>cocaine</b> mediated disruption leaves an uninhibited D1 receptor that activates Gs, freely recruits β arrestin, increases p <strong>ERK 1</strong>/2 levels, and induces cell death when over activated.
+MAPK3	drug	opioid	24469921	Furthermore HIV Tat and <b>morphine</b> exposure increased activation of extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2), enhanced levels of p53 and p21, and decreased cyclin D1 and Akt levels in NPCs.
+MAPK3	drug	opioid	24469921	Regulated by <strong>ERK1</strong>/2 and p53, p21 was found to be indispensible for Tat and <b>morphine</b> mediated cell cycle arrest.
+MAPK3	drug	nicotine	24457151	Therefore, the present study examined the effects of <b>nicotine</b> on STM and LTM and the involvement of PKA, <strong>ERK1</strong>/2, and protein synthesis in the <b>nicotine</b> induced enhancement of hippocampus dependent contextual learning in C57BL/6J mice.
+MAPK3	drug	nicotine	24457151	In addition, inhibition of dorsal hippocampal PKA activity blocked the effect of acute <b>nicotine</b> on learning, and <b>nicotine</b> shifted the timing of learning related PKA and <strong>ERK1</strong>/2 activity in the dorsal and ventral hippocampus.
+MAPK3	drug	nicotine	24457151	Thus, the present results suggest that <b>nicotine</b> specifically enhances LTM through altering the timing of PKA and <strong>ERK1</strong>/2 signaling in the hippocampus, and suggests that the timing of PKA and <strong>ERK1</strong>/2 activity could contribute to the strength of memories.
+MAPK3	drug	opioid	24416361	Inhibition of cAMP/PKA and activation of <strong>ERK1</strong>/2 are the possible cellular adaptations to prevent withdrawal induced by chronic <b>morphine</b> use.
+MAPK3	addiction	withdrawal	24416361	Inhibition of cAMP/PKA and activation of <strong>ERK1</strong>/2 are the possible cellular adaptations to prevent <b>withdrawal</b> induced by chronic morphine use.
+MAPK3	drug	opioid	24409147	<b>Morphine</b> withdrawal activates <strong>ERK1</strong>/2 and phosphorylated tyrosine hydroxylase (TH) at Ser31 in the right and left ventricle.
+MAPK3	addiction	withdrawal	24409147	Morphine <b>withdrawal</b> activates <strong>ERK1</strong>/2 and phosphorylated tyrosine hydroxylase (TH) at Ser31 in the right and left ventricle.
+MAPK3	drug	opioid	24409147	The present finding demonstrated that the enhancement of <strong>ERK1</strong>/2 expression and the phosphorylation state of TH at Ser31 during <b>morphine</b> withdrawal are dependent on PKA and suggest cross talk between PKA and <strong>ERK1</strong>/2 transduction pathway mediating <b>morphine</b> withdrawal induced activation of TH.
+MAPK3	addiction	withdrawal	24409147	The present finding demonstrated that the enhancement of <strong>ERK1</strong>/2 expression and the phosphorylation state of TH at Ser31 during morphine <b>withdrawal</b> are dependent on PKA and suggest cross talk between PKA and <strong>ERK1</strong>/2 transduction pathway mediating morphine <b>withdrawal</b> induced activation of TH.
+MAPK3	drug	opioid	24296091	During three phases of <b>morphine</b> induced CPP, the expression levels of <strong>ERK1</strong> and ERK2 mRNA were altered in various brain regions.
+MAPK3	addiction	reward	24296091	During three phases of morphine induced <b>CPP</b>, the expression levels of <strong>ERK1</strong> and ERK2 mRNA were altered in various brain regions.
+MAPK3	drug	opioid	24296091	In the PFC, the expression levels of <strong>ERK1</strong> and ERK2 mRNA were increased after chronic <b>morphine</b> injection (p=0.003, p=0.000), and did not return to the basal level after extinction training (p=0.025, p=0.000), but decreased after a priming injection (p=0.000, p=0.000).
+MAPK3	drug	opioid	24296091	Different from other brain regions, the expression levels of <strong>ERK1</strong> and ERK2 mRNA were decreased in three phases of <b>morphine</b> induced CPP in the hippocampus (<strong>ERK1</strong>: p=0.000, p=0.040, p=0.000; ERK2: p=0.000, p=0.000, p=0.000, respectively).
+MAPK3	addiction	reward	24296091	Different from other brain regions, the expression levels of <strong>ERK1</strong> and ERK2 mRNA were decreased in three phases of morphine induced <b>CPP</b> in the hippocampus (<strong>ERK1</strong>: p=0.000, p=0.040, p=0.000; ERK2: p=0.000, p=0.000, p=0.000, respectively).
+MAPK3	drug	opioid	24296091	These results suggest region specific changes of <strong>ERK1</strong> and ERK2 mRNA expression during <b>morphine</b> induced CPP.
+MAPK3	addiction	reward	24296091	These results suggest region specific changes of <strong>ERK1</strong> and ERK2 mRNA expression during morphine induced <b>CPP</b>.
+MAPK3	drug	amphetamine	24269936	Interestingly, only 2 mg/kg dose of <b>METH</b> induced locomotor sensitization which was accompanied by the activation of <strong>ERK1</strong>/2 in the NAc and CPu in mice.
+MAPK3	addiction	sensitization	24269936	Interestingly, only 2 mg/kg dose of METH induced locomotor <b>sensitization</b> which was accompanied by the activation of <strong>ERK1</strong>/2 in the NAc and CPu in mice.
+MAPK3	drug	amphetamine	24269936	Although l THP (5 and 10 mg/kg) per se did not induce obvious changes in locomotor activities in mice, its co administration with <b>METH</b> could significantly attenuate acute <b>METH</b> induced hyper locomotor activity, the development and expression of <b>METH</b> induced locomotor sensitization, and the accompanying <strong>ERK1</strong>/2 activation in the NAc and CPu.
+MAPK3	addiction	sensitization	24269936	Although l THP (5 and 10 mg/kg) per se did not induce obvious changes in locomotor activities in mice, its co administration with METH could significantly attenuate acute METH induced hyper locomotor activity, the development and expression of METH induced locomotor <b>sensitization</b>, and the accompanying <strong>ERK1</strong>/2 activation in the NAc and CPu.
+MAPK3	drug	amphetamine	24269936	These results suggest that l THP has potential therapeutic effect on <b>METH</b> induced locomotor sensitization, and the underlying molecular mechanism might be related to its inhibitory effect on <strong>ERK1</strong>/2 phosphorylation in the NAc and CPu.
+MAPK3	addiction	sensitization	24269936	These results suggest that l THP has potential therapeutic effect on METH induced locomotor <b>sensitization</b>, and the underlying molecular mechanism might be related to its inhibitory effect on <strong>ERK1</strong>/2 phosphorylation in the NAc and CPu.
+MAPK3	addiction	relapse	24269543	Western blotting results showed that the levels of GLT1, VGLUT2, NR2B, p <strong>ERK1</strong>/2 and p CREB expressions in the mPFC were increased and CaMKII was decreased markedly after the stress priming MAP induced CPP <b>reinstatement</b> test.
+MAPK3	addiction	reward	24269543	Western blotting results showed that the levels of GLT1, VGLUT2, NR2B, p <strong>ERK1</strong>/2 and p CREB expressions in the mPFC were increased and CaMKII was decreased markedly after the stress priming MAP induced <b>CPP</b> reinstatement test.
+MAPK3	addiction	relapse	24269543	In DHC, the levels of VGLUT2, p <strong>ERK1</strong>/2 and CREB expressions were reduced during the stress induced <b>reinstatement</b>, which could be reversed by OT and further abolished by Ato.
+MAPK3	drug	cocaine	23970867	The abundance of surrogate markers of dopamine signaling and plasticity in the dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC) were examined: glycosylated and non glycosylated forms of the dopamine transporter (efficiency of dopamine transport), tyrosine hydroxylase (TH; marker of dopamine synthesis) and phosphorylated TH at Serine 30 and 40 (markers of enzyme activity), extracellular signal regulated kinase 1 and 2 (<strong>ERK1</strong> and ERK 2), and phosphorylated <strong>ERK1</strong> and ERK2 (phosphorylates TH Serine 31; markers of synaptic plasticity), and markers of synaptic integrity, spinophilin and post synaptic density protein 95 (roles in dopamine signaling and response to <b>cocaine</b>).
+MAPK3	drug	opioid	23880531	A pretreatment with the <b>opioid</b> analgesic <b>morphine</b> markedly attenuated <strong>ERK1</strong>/2 phosphorylation.
+MAPK3	drug	opioid	23880531	The present findings indicate that <strong>ERK1</strong>/2 activation in dorsal horn nociceptive neurons may be linked to the development of hyperalgesia, and that <b>opioid</b> analgesics are effective agents to prevent sensitization in the pain pathway at spinal level.
+MAPK3	addiction	sensitization	23880531	The present findings indicate that <strong>ERK1</strong>/2 activation in dorsal horn nociceptive neurons may be linked to the development of hyperalgesia, and that opioid analgesics are effective agents to prevent <b>sensitization</b> in the pain pathway at spinal level.
+MAPK3	drug	opioid	23796752	<b>Morphine</b> mediates a proinflammatory phenotype via μ <b>opioid</b> receptor PKCɛ Akt <strong>ERK1</strong>/2 signaling pathway in activated microglial cells.
+MAPK3	drug	opioid	23796752	The results indicate that <b>morphine</b> increases the LPS induced expression and activation of PKCɛ and stimulates Akt pathway upstream of <strong>ERK1</strong>/2 and iNOS.
+MAPK3	drug	opioid	23682813	Blockade of extracellular regulated protein kinase 1/2 (<strong>ERK1</strong>/2) with its specific inhibitor attenuated <b>naloxone</b> induced CREB phosphorylation.
+MAPK3	drug	opioid	23682813	Pretreatment with NaHS or stimulation of endogenous H2S production also significantly suppressed <b>opioid</b> withdrawal induced <strong>ERK1</strong>/2 activation in mice striatum or SH SY5Y cells.
+MAPK3	addiction	withdrawal	23682813	Pretreatment with NaHS or stimulation of endogenous H2S production also significantly suppressed opioid <b>withdrawal</b> induced <strong>ERK1</strong>/2 activation in mice striatum or SH SY5Y cells.
+MAPK3	drug	nicotine	23587498	<b>Nicotine</b> dependent activation of the Ca(2+)/IP3/<strong>ERK 1</strong>/2 intracellular signalling pathway was also evaluated in normal rat intrahepatic cholangiocyte.
+MAPK3	addiction	reward	23354537	Rats that expressed a persistent <b>CPP</b> had elevated levels of p <strong>ERK1</strong>, GluA1, and p Ser845 GluA1 in NAc core, and the latter correlated with <b>CPP</b> expression.
+MAPK3	drug	cocaine	23232446	We show that the mitogen activated protein kinase (MEK)/<strong>ERK1</strong>/2 inhibitor, U0126 (1.0 μg/0.5 μl/hemisphere), microinfused bilaterally into the BLA  but not the NACc  immediately after brief re exposure to a previously <b>cocaine</b> paired context (that is, <b>cocaine</b> memory reactivation), significantly attenuated subsequent drug context induced <b>cocaine</b> seeking relative to vehicle (VEH).
+MAPK3	addiction	relapse	23232446	We show that the mitogen activated protein kinase (MEK)/<strong>ERK1</strong>/2 inhibitor, U0126 (1.0 μg/0.5 μl/hemisphere), microinfused bilaterally into the BLA  but not the NACc  immediately after brief re exposure to a previously cocaine paired context (that is, cocaine memory reactivation), significantly attenuated subsequent drug context induced cocaine <b>seeking</b> relative to vehicle (VEH).
+MAPK3	drug	cocaine	23232446	This effect in the BLA was associated with a transient inhibition of <strong>ERK1</strong>/2 phosphorylation, and it depended on memory reactivation given that U0126 administered following exposure to a novel context did not alter subsequent <b>cocaine</b> seeking.
+MAPK3	addiction	relapse	23232446	This effect in the BLA was associated with a transient inhibition of <strong>ERK1</strong>/2 phosphorylation, and it depended on memory reactivation given that U0126 administered following exposure to a novel context did not alter subsequent cocaine <b>seeking</b>.
+MAPK3	drug	opioid	23162566	Using the zebrafish as a research model, we discuss the relationship between mir 133b, the dopaminergic system, and <b>morphine</b>, considering: (1) that <b>morphine</b> modulates the expression of miR 133b and of its target transcript Pitx3, (2) the role of the zebrafish mu <b>opioid</b> receptor (zfMOR) in <b>morphine</b> induced regulation of miR 133b, which depends on <strong>ERK1</strong>/2, (3) that <b>morphine</b> regulates miR 133b in hippocampal neurons, and (4) the role of delta <b>opioid</b> receptors in <b>morphine</b> induced regulation of miR 133b.
+MAPK3	drug	nicotine	23149874	These demonstrate that <b>nicotine</b> has ability to induce CRP expression in macrophages through nAChR <strong>ERK1</strong>/2/p38 MAPK NF κB signal pathway, which contributes to better understanding of the pro inflammatory and pro atherosclerotic effects of <b>nicotine</b> in cigarette <b>smokers</b>.
+MAPK3	drug	alcohol	22960015	However, little is known regarding the mechanisms underlying the effects of <b>alcohol</b> exposure, withdrawal, and relapse, particularly with regard to the interaction between CaMKII and <strong>ERK1</strong>/2 signaling in hippocampal subregions.
+MAPK3	addiction	relapse	22960015	However, little is known regarding the mechanisms underlying the effects of alcohol exposure, withdrawal, and <b>relapse</b>, particularly with regard to the interaction between CaMKII and <strong>ERK1</strong>/2 signaling in hippocampal subregions.
+MAPK3	addiction	withdrawal	22960015	However, little is known regarding the mechanisms underlying the effects of alcohol exposure, <b>withdrawal</b>, and relapse, particularly with regard to the interaction between CaMKII and <strong>ERK1</strong>/2 signaling in hippocampal subregions.
+MAPK3	drug	alcohol	22960015	Following chronic <b>alcohol</b> exposure, phospho <strong>ERK1</strong>/2 was significantly decreased in the DG.
+MAPK3	drug	alcohol	22960015	<b>Alcohol</b> withdrawal was associated with an increase of phospho <strong>ERK1</strong>/2 in the CA1 and DG, while <b>alcohol</b> re exposure induced a decrease of phospho <strong>ERK1</strong>/2 in the CA1, CA3, and DG.
+MAPK3	addiction	withdrawal	22960015	Alcohol <b>withdrawal</b> was associated with an increase of phospho <strong>ERK1</strong>/2 in the CA1 and DG, while alcohol re exposure induced a decrease of phospho <strong>ERK1</strong>/2 in the CA1, CA3, and DG.
+MAPK3	drug	alcohol	22960015	The activation of CaMKII (Thr286) correlated with the effects of <b>alcohol</b> on phospho <strong>ERK1</strong>/2.
+MAPK3	drug	alcohol	22960015	Our results indicate that region specific activation CaMKII <strong>ERK1</strong>/2 signaling in the hippocampal CA1 and DG may play an important role in <b>alcohol</b> dependence.
+MAPK3	addiction	dependence	22960015	Our results indicate that region specific activation CaMKII <strong>ERK1</strong>/2 signaling in the hippocampal CA1 and DG may play an important role in alcohol <b>dependence</b>.
+MAPK3	drug	opioid	22776695	Although it has been shown that extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2) activity in the nucleus accumbens (NAc) is modulated by the primary rewarding effect of opiates, little is known as to its role in the <b>morphine</b> associated contextual memory.
+MAPK3	drug	opioid	22776695	In the present study, we investigated the <strong>ERK1</strong>/2 activity indicated by phosphorylated <strong>ERK1</strong>/2 (pERK1/2) levels in rats using a <b>morphine</b> induced conditioned place preference (CPP) procedure.
+MAPK3	addiction	reward	22776695	In the present study, we investigated the <strong>ERK1</strong>/2 activity indicated by phosphorylated <strong>ERK1</strong>/2 (pERK1/2) levels in rats using a morphine induced conditioned place preference (<b>CPP</b>) procedure.
+MAPK3	drug	opioid	22776695	Bilateral injection of an inhibitor of ERK activation into the NAc shell attenuated <strong>ERK1</strong>/2 phosphorylation and prevented the expression of <b>morphine</b> CPP, but injections into the core did not.
+MAPK3	addiction	reward	22776695	Bilateral injection of an inhibitor of ERK activation into the NAc shell attenuated <strong>ERK1</strong>/2 phosphorylation and prevented the expression of morphine <b>CPP</b>, but injections into the core did not.
+MAPK3	addiction	reward	22776695	Selective inhibition of NR2B containing NMDA receptor in the NAc shell by ifenprodil prevented <b>CPP</b> expression and down regulated local <strong>ERK1</strong>/2 phosphorylation.
+MAPK3	drug	opioid	22776695	These findings collectively suggest that recall of <b>morphine</b> associated contextual memory depends specifically upon <strong>ERK1</strong>/2 activation in the NAc shell and that <strong>ERK1</strong>/2 phosphorylation is regulated by the upstream NR2B containing NMDA receptor.
+MAPK3	drug	amphetamine	22530033	Interestingly, a single administration of <b>METH</b> (3 mg/kg) significantly increased the phosphorylation status of <strong>ERK1</strong>/2 in the striatum of WT, but not Srr KO mice.
+MAPK3	drug	amphetamine	22530033	These findings suggest first, that SRR plays a role in the development of behavioral sensitization in mice after repeated administration of <b>METH</b>, and second that phosphorylation of <strong>ERK1</strong>/2 by <b>METH</b> may contribute to the development of this sensitization as seen in WT but not Srr KO mice.
+MAPK3	addiction	sensitization	22530033	These findings suggest first, that SRR plays a role in the development of behavioral <b>sensitization</b> in mice after repeated administration of METH, and second that phosphorylation of <strong>ERK1</strong>/2 by METH may contribute to the development of this <b>sensitization</b> as seen in WT but not Srr KO mice.
+MAPK3	drug	opioid	22428664	In contrast, CB(2) receptor stimulation attenuated <b>morphine</b> induced microglial proinflammatory mediator increases, interfering with <b>morphine</b> action by acting on the Akt <strong>ERK1</strong>/2 signalling pathway.
+MAPK3	drug	alcohol	22269225	Treatment of hepatocytes with <b>ethanol</b> caused increased phosphorylation of p38 MAPK (mitogen activated protein kinase), MSK 1 (mitogen and stress activated kinase) and CREB in the nuclear compartment without activation of <strong>ERK1</strong>/2 (extracellular regulated kinase); whereas angiotensin II induced activation of CREB was accompanied by activation of <strong>ERK1</strong>/2.
+MAPK3	drug	alcohol	22269225	In chronic <b>ethanol</b> binge studies, analysis of the whole cell extracts showed increased phosphorylation of CREB, with no effect on CREB protein levels; increased phospho <strong>ERK1</strong>/2, and decreased phospho p38 MAPK.
+MAPK3	addiction	intoxication	22269225	In chronic ethanol <b>binge</b> studies, analysis of the whole cell extracts showed increased phosphorylation of CREB, with no effect on CREB protein levels; increased phospho <strong>ERK1</strong>/2, and decreased phospho p38 MAPK.
+MAPK3	drug	opioid	22218090	It has been established that mu <b>opioid</b> receptors activate the <strong>ERK1</strong>/2 signaling cascade both in vitro and in vivo.
+MAPK3	drug	opioid	22177524	<strong>ERK1</strong>/2 phosphorylation was rapidly induced by isoproterenol (by 9.5 ± 2.4 fold) and <b>morphine</b> (22 ± 2.2 fold) in G(αs)  transfected cells; mutations of α3/β5 and α4/β6 did not affect the pattern or extent of mitogen activated protein kinase activation.
+MAPK3	drug	opioid	22177524	In addition, G(αs) was required for the rapid phosphorylation of <strong>ERK1</strong>/2 by isoproterenol but not <b>morphine</b>.
+MAPK3	drug	nicotine	22085699	Subsequently, Src, Akt and <strong>ERK1</strong>/2 were phosphorylated at different time points following <b>nicotine</b> treatment.
+MAPK3	drug	nicotine	22085699	We further demonstrated that through Src, the ligation of <b>nicotine</b> with nAChR stimulated the EGFR/<strong>ERK1</strong>/2 pathway for the activation of E2F1 and further cell progression.
+MAPK3	drug	cannabinoid	22034973	Here we used knockout mouse models to examine the regulation of striatal extracellular signal regulated kinases 1 and 2 (<strong>ERK1</strong>/2) signaling by behaviorally relevant doses of <b>cannabinoids</b>.
+MAPK3	drug	cannabinoid	22034973	In C57BL/6J mice, acute administration of the <b>cannabinoid</b> agonists, ( ) 11 hydroxydimethylheptyl Δ8 <b>tetrahydrocannabinol</b> (HU 210) and delta 9 <b>tetrahydrocannabinol</b> (Δ(9)  <b>THC</b>), promoted a dose  and time dependent decrease in the phosphorylation of <strong>ERK1</strong>/2 in dorsal striatum.
+MAPK3	drug	cannabinoid	22034973	Co administration of the CB1 <b>cannabinoid</b> receptor antagonist N (Piperidin 1 yl) 5 (4 iodophenyl) 1 (2,4 dichlorophenyl) 4 methyl 1H pyrazole 3 carboxamide(AM251) with HU 210 prevented <strong>ERK1</strong>/2 inactivation, indicating a requirement for activation of this receptor.
+MAPK3	drug	alcohol	21969878	Chronic <b>ethanol</b> alone had negligible effect on mRNA levels of LDL receptor, or on the levels of nuclear <strong>ERK1</strong>/2 and phospho <strong>ERK1</strong>/2.
+MAPK3	drug	alcohol	21969878	But, chronic <b>ethanol</b> followed by binge caused a decrease in LDL receptor mRNA, and also decreased the levels of <strong>ERK1</strong>/2 and phospho <strong>ERK1</strong>/2 in the nuclear compartment.
+MAPK3	addiction	intoxication	21969878	But, chronic ethanol followed by <b>binge</b> caused a decrease in LDL receptor mRNA, and also decreased the levels of <strong>ERK1</strong>/2 and phospho <strong>ERK1</strong>/2 in the nuclear compartment.
+MAPK3	drug	alcohol	21843598	The present experiments characterized the regulation of three key signaling molecules, DARPP 32 (dopamine and cAMP regulated phosphoprotein, 32kDa), Akt kinase and <strong>ERK1</strong>/2 (extracellular signal regulated kinase 1 and 2) in <b>ethanol</b> preferring AA (Alko, <b>alcohol</b>) and <b>ethanol</b> avoiding ANA (Alko, non <b>alcohol</b>) rat lines.
+MAPK3	drug	cocaine	21813685	We show that the activation of receptors required for I LTD increased <strong>ERK1</strong>/2 phosphorylation and inhibitors of ERK activation blocked I LTD. We further demonstrate that ERK mediates <b>cocaine</b> induced reduction of GABAergic inhibition and facilitation of LTP induction.
+MAPK3	drug	cocaine	21813685	Finally, we show that <b>cocaine</b> conditioned place preference (CPP) training (15 mg/kg; four pairings) increased <strong>ERK1</strong>/2 phosphorylation in the VTA, while bilateral intra VTA injections of a CB(1) antagonist or an inhibitor of ERK activation attenuated <strong>ERK1</strong>/2 phosphorylation and the acquisition, but not the expression, of CPP to <b>cocaine</b>.
+MAPK3	addiction	reward	21813685	Finally, we show that cocaine conditioned place preference (<b>CPP</b>) training (15 mg/kg; four pairings) increased <strong>ERK1</strong>/2 phosphorylation in the VTA, while bilateral intra VTA injections of a CB(1) antagonist or an inhibitor of ERK activation attenuated <strong>ERK1</strong>/2 phosphorylation and the acquisition, but not the expression, of <b>CPP</b> to cocaine.
+MAPK3	drug	cocaine	21812869	Chronic <b>cocaine</b> self administration modulates <strong>ERK1</strong>/2 and CREB responses to dopamine receptor agonists in striatal slices.
+MAPK3	drug	cocaine	21812869	We hypothesized that chronic <b>cocaine</b> self administration could influence dopamine D1 and D2 receptor activation of extracellular signal regulated protein kinase 1 and 2 (<strong>ERK1</strong>/2) and cyclic adenosine monophosphate response element binding protein (CREB) phosphorylation.
+MAPK3	drug	cocaine	21812869	We found that <b>cocaine</b> self administration led to a reduction in the capacity of D1R to activate <strong>ERK1</strong>/2 phosphorylation as compared with control rats.
+MAPK3	drug	cocaine	21812869	D2R induced <strong>ERK1</strong>/2 phosphorylation appeared blunted in striatal slices from <b>cocaine</b> rats.
+MAPK3	drug	alcohol	21790671	Elevated activation of <strong>ERK1</strong> and ERK2 accompany enhanced liver injury following <b>alcohol</b> binge in chronically <b>ethanol</b> fed rats.
+MAPK3	addiction	intoxication	21790671	Elevated activation of <strong>ERK1</strong> and ERK2 accompany enhanced liver injury following alcohol <b>binge</b> in chronically ethanol fed rats.
+MAPK3	drug	alcohol	21790671	Chronic binge group also showed significant increase (compared with chronic <b>ethanol</b> alone) in the phosphorylation of extracellular regulated kinase 1 (<strong>ERK1</strong>), ERK2, and RSK.
+MAPK3	addiction	intoxication	21790671	Chronic <b>binge</b> group also showed significant increase (compared with chronic ethanol alone) in the phosphorylation of extracellular regulated kinase 1 (<strong>ERK1</strong>), ERK2, and RSK.
+MAPK3	addiction	intoxication	21790671	Among other alterations, the activated levels of <strong>ERK1</strong>, and more so ERK2, were remarkably amplified by <b>binge</b> suggesting a role of these isotypes in the <b>binge</b> amplification of the injury.
+MAPK3	drug	alcohol	21790671	This study offers chronic followed by repeat binge as a model for the study of progression of liver injury by <b>ethanol</b> and highlights the involvement of <strong>ERK1</strong> and ERK2 isotypes in the amplification of liver injury by binge <b>ethanol</b>.
+MAPK3	addiction	intoxication	21790671	This study offers chronic followed by repeat <b>binge</b> as a model for the study of progression of liver injury by ethanol and highlights the involvement of <strong>ERK1</strong> and ERK2 isotypes in the amplification of liver injury by <b>binge</b> ethanol.
+MAPK3	drug	amphetamine	21704677	The data clearly suggest that endogenous MK limits <b>amphetamine</b> induced astrocytosis through Fyn , TrkA  and <strong>ERK1</strong>/2 independent mechanisms and identify previously unexpected functional differences between MK and pleiotrophin, the only other member of the MK family of growth factors, in the modulation of effects of drugs of abuse.
+MAPK3	drug	opioid	21681580	We have found that <b>morphine</b> repeated pairing treatment causes a significant preference for compartment paired with <b>morphine</b> after 1 day or 7 days post training, which is associated with increased <strong>ERK1</strong>/2 phosphorylation (p <strong>ERK1</strong>/2, a measure of ERK activity) in the CeA.
+MAPK3	addiction	reward	21681580	The infusion of either MEK inhibitor U0126 or NMDA receptor antagonist MK 801 in the CeA not only suppresses the activation of <strong>ERK1</strong>/2 in the CeA but also abolishes the expression of <b>CPP</b>.
+MAPK3	drug	cocaine	21640333	Enhanced <b>cocaine</b> conditioned place preference and associated brain regional levels of BDNF, p <strong>ERK1</strong>/2 and p Ser845 GluA1 in food restricted rats.
+MAPK3	drug	cocaine	21640333	On the other hand, FR rats, whether injected with <b>cocaine</b> or vehicle, displayed elevated p <strong>ERK1</strong>/2 and p Ser845 GluA1 in dorsal hippocampus.
+MAPK3	drug	cocaine	21640333	FR rats also displayed elevated p <strong>ERK1</strong>/2 in medial prefrontal cortex and elevated p <strong>ERK1</strong> in nucleus accumbens, with further increases produced by <b>cocaine</b>.
+MAPK3	drug	cocaine	21628570	Furthermore, <b>cocaine</b> exposure stimulated the phosphorylation of <strong>Erk1</strong>/2 in ephrinA5 expressing SNr cells in a direct pathway dependent manner.
+MAPK3	drug	opioid	21483469	Extensive studies of mitogen activated protein kinase (MAPK) signaling pathways revealed the involvement of c Jun N terminal kinase (JNK) and extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2) pathways in enhanced toxicity of Tat and <b>morphine</b>.
+MAPK3	drug	alcohol	21315561	In order to explore the neural substrates and the potential mechanism involved in this effect, we examined: 1) the <strong>ERK1</strong>/2 activation in the central (CeA) and basolateral (BLA) nuclei of the amygdala and in the dorsal hippocampus (dHip), 2) the effect of the NMDA receptor antagonist MK 801 on fear conditioning and ERK activation and 3) the effect of the infusion of U0126, a MEK inhibitor, into the BLA on fear memory formation in <b>ethanol</b> withdrawn rats.
+MAPK3	drug	opioid	21088039	The inactivation of brain α(2) adrenoceptors (EEDQ at SW 12 h) further enhanced <b>morphine</b> abstinence intensity and cortical p FADD content at SW 24 h. The disruption of <strong>ERK1</strong>/2 signalling (SL 327 at SW 4 h and SW 8 h) did not alter <b>morphine</b> abstinence at SW 12 h, but it attenuated the behavioural syndrome at SW 24 h. This inhibition of <strong>ERK1</strong>/2, however, did not prevent the up regulation of oligomeric p FADD at SW 12 h and 24 h. These data indicate that cortical oligomeric p FADD, mainly through an interaction with inhibitory α(2) adrenoceptors, plays a functional role in the behavioural expression of <b>morphine</b> abstinence in rats.
+MAPK3	drug	nicotine	21070506	<strong>ERK1</strong>/2 protein and mRNA levels in human blood are linked to <b>smoking</b> behavior.
+MAPK3	drug	alcohol	21070506	From studies in cultured cells and animal models, nicotine and <b>alcohol</b> are known to regulate extracellular signal regulated kinase 1 and 2 (<strong>ERK1</strong>/2).
+MAPK3	drug	nicotine	21070506	From studies in cultured cells and animal models, <b>nicotine</b> and alcohol are known to regulate extracellular signal regulated kinase 1 and 2 (<strong>ERK1</strong>/2).
+MAPK3	drug	nicotine	21070506	Because <strong>ERK1</strong>/2 is known to effect phosphorylation of CREB, the aim of the present study was to further elucidate whether cigarette <b>smoking</b> leads to alterations in terms of <strong>ERK1</strong>/2 in human buffy coat as well.
+MAPK3	drug	nicotine	21070506	In a comparison of 53 <b>smokers</b> with 146 non <b>smoking</b> controls, we found significantly higher levels of <strong>ERK1</strong>/2 protein (P=0.004).
+MAPK3	drug	nicotine	21070506	Multiple regression analysis revealed a significant relation among the number of cigarettes smoked daily (R(2)=0.266, P=0.003), the Fagerström Test for <b>Nicotine</b> Dependence score (R(2)=0.149, P=0.032) and the mRNA expression of <strong>ERK1</strong>.
+MAPK3	addiction	dependence	21070506	Multiple regression analysis revealed a significant relation among the number of cigarettes smoked daily (R(2)=0.266, P=0.003), the Fagerström Test for Nicotine <b>Dependence</b> score (R(2)=0.149, P=0.032) and the mRNA expression of <strong>ERK1</strong>.
+MAPK3	addiction	addiction	21070506	Given that the <strong>ERK1</strong>/2 signaling pathway plays an important role in the physiology and pathophysiology of affective and <b>addictive</b> behavior, our findings provide a rationale basis for additional mechanistic studies that may lead to the development of novel signaling pathway selective therapeutics in humans.
+MAPK3	drug	opioid	21068718	Here we report that chronic <b>morphine</b> withdrawal induced upregulation of glial fibrillary acidic protein (GFAP), tumor necrosis factor alpha (TNFα) and phosphorylation of <strong>ERK1</strong>/2 (pERK1/2) in the caudal ventrolateral PAG (vlPAG).
+MAPK3	addiction	withdrawal	21068718	Here we report that chronic morphine <b>withdrawal</b> induced upregulation of glial fibrillary acidic protein (GFAP), tumor necrosis factor alpha (TNFα) and phosphorylation of <strong>ERK1</strong>/2 (pERK1/2) in the caudal ventrolateral PAG (vlPAG).
+MAPK3	drug	opioid	21068718	Microinjection of HSV vector expressing sTNFR into the PAG also significantly reduced the phosphorylation of both <strong>ERK1</strong>/2 and CREB, and reduced Fos immunoreactivity in neurons of the PAG following <b>naloxone</b> precipitated withdrawal.
+MAPK3	addiction	withdrawal	21068718	Microinjection of HSV vector expressing sTNFR into the PAG also significantly reduced the phosphorylation of both <strong>ERK1</strong>/2 and CREB, and reduced Fos immunoreactivity in neurons of the PAG following naloxone precipitated <b>withdrawal</b>.
+MAPK3	drug	opioid	20519536	<b>Morphine</b> exposure and withdrawal increase phosphorylation of NR1 and NR2B receptors, <strong>ERK1</strong>/2, calmodulin dependent kinase II, and cAMP response element binding proteins; and such phosphorylation is suppressed by either spinal inhibition or targeted mutation of MMP 9.
+MAPK3	addiction	withdrawal	20519536	Morphine exposure and <b>withdrawal</b> increase phosphorylation of NR1 and NR2B receptors, <strong>ERK1</strong>/2, calmodulin dependent kinase II, and cAMP response element binding proteins; and such phosphorylation is suppressed by either spinal inhibition or targeted mutation of MMP 9.
+MAPK3	drug	amphetamine	20486560	Repeated <b>methamphetamine</b> treatment in mice impairs long term recognition memory after withdrawal, which is associated with the dysfunction in dopamine D1 receptor extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2) pathway in the prefrontal cortex.
+MAPK3	addiction	withdrawal	20486560	Repeated methamphetamine treatment in mice impairs long term recognition memory after <b>withdrawal</b>, which is associated with the dysfunction in dopamine D1 receptor extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2) pathway in the prefrontal cortex.
+MAPK3	drug	amphetamine	20486560	Repeated <b>methamphetamine</b> treatment in rats also induces impairment of spatial working memory, which is accompanied by the dysfunction of <strong>ERK1</strong>/2 pathway in the hippocampus.
+MAPK3	drug	amphetamine	20486560	These findings suggest that <strong>ERK1</strong>/2 plays an important role in memory impairments induced by repeated <b>methamphetamine</b> treatment.
+MAPK3	drug	opioid	20359526	Several groups maintain that <b>morphine</b> tolerance and dependence correlate with increased activity of protein kinases <strong>ERK1</strong>/2 and P38 MAPK and PKC as well as elevated levels of the neuropeptides dynorphin (DYN), substance P (sP), and calcitonin gene related peptide (CGRP) in spinal cord dorsal horn (SCDH).
+MAPK3	addiction	dependence	20359526	Several groups maintain that morphine tolerance and <b>dependence</b> correlate with increased activity of protein kinases <strong>ERK1</strong>/2 and P38 MAPK and PKC as well as elevated levels of the neuropeptides dynorphin (DYN), substance P (sP), and calcitonin gene related peptide (CGRP) in spinal cord dorsal horn (SCDH).
+MAPK3	drug	amphetamine	20192945	Interestingly, we found in concomitant in vitro studies that PTN (3 µM) limits <b>amphetamine</b> (1 mM) induced loss of viability of PC12 cell cultures, effect that could be related to the ability of PTN to induce the phosphorylation of Akt and <strong>ERK1</strong>/2.
+MAPK3	drug	amphetamine	20192945	To test this possibility, we used specific Akt and <strong>ERK1</strong>/2 inhibitors uncovering for the first time that PTN induced protective effects against <b>amphetamine</b> induced toxicity in PC12 cells are mediated by the <strong>ERK1</strong>/2 signalling pathway.
+MAPK3	drug	nicotine	20106947	Long term <b>nicotine</b> exposure induced chemoresistance is mediated by activation of Stat3 and downregulation of <strong>ERK1</strong>/2 via nAChR and beta adrenoceptors in human bladder cancer cells.
+MAPK3	drug	nicotine	20106947	Furthermore, <b>nicotine</b> mobilized Stat3 signaling, resulting in the loss of extracellular signal regulated protein kinase 1/2 (<strong>ERK 1</strong>/2) activation and reduced chemosensitivity via nicotinic acetylcholine receptors and beta adrenoceptors.
+MAPK3	drug	opioid	19917879	We hypothesized that activation of extracellular signal regulated kinases 1 and 2 (<strong>ERK1</strong>/2) and the expression of c Fos, prodynorphin (mRNA), and dynorphin in the spinal cord could participate in the molecular mechanisms underlying postoperative <b>opioid</b> induced sensitization.
+MAPK3	addiction	sensitization	19917879	We hypothesized that activation of extracellular signal regulated kinases 1 and 2 (<strong>ERK1</strong>/2) and the expression of c Fos, prodynorphin (mRNA), and dynorphin in the spinal cord could participate in the molecular mechanisms underlying postoperative opioid induced <b>sensitization</b>.
+MAPK3	drug	cannabinoid	19723626	CP55,940 blocks GPR55 internalization, the formation of beta arrestin GPR55 complexes, and the phosphorylation of <strong>ERK1</strong>/2; CP55,940 produces only a slight amount of protein kinase CbetaII membrane recruitment but does not stimulate membrane remodeling like LPI, AM251, or <b>rimonabant</b>.
+MAPK3	drug	opioid	19567779	<b>Naloxone</b> induced <b>morphine</b> withdrawal activates <strong>ERK1</strong>/2 and phosphorylates TH at Ser31 in the right and left ventricle, with an increase in the mean arterial blood pressure and heart rate.
+MAPK3	addiction	withdrawal	19567779	Naloxone induced morphine <b>withdrawal</b> activates <strong>ERK1</strong>/2 and phosphorylates TH at Ser31 in the right and left ventricle, with an increase in the mean arterial blood pressure and heart rate.
+MAPK3	drug	opioid	19567779	When N (2 guanidinoethyl) 5 isoquinolinesulfonamide (HA 1004), a PKA inhibitor, was infused, concomitantly with <b>morphine</b>, it diminished the expression of <strong>ERK1</strong>/2.
+MAPK3	drug	opioid	19567779	In contrast, the infusion of calphostin C (a PKC inhibitor) did not modify the <b>morphine</b> withdrawal induced activation of <strong>ERK1</strong>/2.
+MAPK3	addiction	withdrawal	19567779	In contrast, the infusion of calphostin C (a PKC inhibitor) did not modify the morphine <b>withdrawal</b> induced activation of <strong>ERK1</strong>/2.
+MAPK3	drug	opioid	19567779	The present findings demonstrate that the enhancement of <strong>ERK1</strong>/2 expression and the phosphorylation state of TH at Ser31 during <b>morphine</b> withdrawal are dependent on PKA and suggest cross talk between PKA and <strong>ERK1</strong>/2 transduction pathway mediating <b>morphine</b> withdrawal induced activation (phosphorylation) of TH.
+MAPK3	addiction	withdrawal	19567779	The present findings demonstrate that the enhancement of <strong>ERK1</strong>/2 expression and the phosphorylation state of TH at Ser31 during morphine <b>withdrawal</b> are dependent on PKA and suggest cross talk between PKA and <strong>ERK1</strong>/2 transduction pathway mediating morphine <b>withdrawal</b> induced activation (phosphorylation) of TH.
+MAPK3	drug	amphetamine	19500087	Compared to their respective controls, rats infused with PD98059 or injected with the lentiviral negative <strong>ERK1</strong> construct displayed hyperactivities in multiple tests, exhibited preferentially more open arm activity in the elevated plus maze test, consumed more sweetened liquid in a saccharin preference test, and showed heightened response to <b>amphetamine</b>.
+MAPK3	drug	cocaine	19446794	Finally, we found corresponding changes in <strong>ERK1</strong>/2 activation and in accumulation of FosB/DeltaFosB, a well characterized marker for long term responses to <b>cocaine</b>, in MSN from these animals.
+MAPK3	drug	alcohol	19125235	Increased operant responding for <b>ethanol</b> in male C57BL/6J mice: specific regulation by the <strong>ERK1</strong>/2, but not JNK, MAP kinase pathway.
+MAPK3	addiction	reward	19125235	Increased <b>operant</b> responding for ethanol in male C57BL/6J mice: specific regulation by the <strong>ERK1</strong>/2, but not JNK, MAP kinase pathway.
+MAPK3	drug	alcohol	19053978	Inhibition of p38 mitogen activated protein kinase signaling, but not <strong>ERK1</strong>/2 activity, in MLE 12 cells by acute <b>alcohol</b> is likely an important cause of decreased LIX expression during challenge.
+MAPK3	drug	alcohol	19007447	Furthermore, AA rats showed rapid and transient dephosphorylation of <strong>ERK1</strong>/2 upon acute <b>ethanol</b> challenge in the medial prefrontal cortex (mPFC) and to a lesser degree in the nucleus accumbens; ANA rats were completely non responsive for this mechanism.
+MAPK3	drug	cannabinoid	19004548	Both pharmacological enhancement (with URB597) and attenuation (with naloxone) of this form of endogenous analgesia were associated with reduced expression of phospho <strong>ERK1</strong>/2 in the amygdaloid complex arguing against a causal role for <strong>ERK1</strong>/2 signaling in the amygdala during expression of FCA or its modulation by opioids or <b>cannabinoids</b>.
+MAPK3	drug	opioid	19004548	Both pharmacological enhancement (with URB597) and attenuation (with <b>naloxone</b>) of this form of endogenous analgesia were associated with reduced expression of phospho <strong>ERK1</strong>/2 in the amygdaloid complex arguing against a causal role for <strong>ERK1</strong>/2 signaling in the amygdala during expression of FCA or its modulation by <b>opioids</b> or cannabinoids.
+MAPK3	drug	opioid	18940233	In the present study, we found that compared to the <b>morphine</b> unpaired and saline paired and saline unpaired groups, <b>morphine</b> paired mice showed depressed ERK2 activity in the Frontal Association Cortex (FrA), whereas <strong>ERK1</strong> activity was not changed in the same region.
+MAPK3	drug	cocaine	18940233	In the Accumbens Nucleus (Acb) and Caudate Putamen (CPu) that are associated with <b>cocaine</b> addiction, the activities of <strong>ERK1</strong> and ERK2 among four groups showed no difference.
+MAPK3	addiction	addiction	18940233	In the Accumbens Nucleus (Acb) and Caudate Putamen (CPu) that are associated with cocaine <b>addiction</b>, the activities of <strong>ERK1</strong> and ERK2 among four groups showed no difference.
+MAPK3	drug	opioid	18657552	<b>Opioid</b> receptor agonists enhance the phosphorylation state of Fas associated death domain (FADD) protein in the rat brain: functional interactions with casein kinase Ialpha, Galpha(i) proteins, and <strong>ERK1</strong>/2 signaling.
+MAPK3	drug	opioid	18657552	This study investigated the effects of <b>opioids</b> on p FADD in rat brain, as well as various mechanisms that could link <b>opioid</b> receptors with p FADD, including the modulation of CKIalpha, Galpha(i) proteins and <strong>ERK1</strong>/2 signaling.
+MAPK3	drug	alcohol	18619984	Cue induced reinstatement of <b>alcohol</b> seeking behavior is associated with increased <strong>ERK1</strong>/2 phosphorylation in specific limbic brain regions: blockade by the mGluR5 antagonist MPEP.
+MAPK3	addiction	relapse	18619984	Cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior is associated with increased <strong>ERK1</strong>/2 phosphorylation in specific limbic brain regions: blockade by the mGluR5 antagonist MPEP.
+MAPK3	addiction	addiction	18619984	The extracellular signal regulated kinase (<strong>ERK1</strong>/2) pathway is downstream of mGluR5 and has been implicated in <b>addiction</b>.
+MAPK3	drug	alcohol	18619984	We sought to determine if cue induced reinstatement of <b>alcohol</b> seeking behavior, and its reduction by an mGluR5 antagonist, is associated with changes in <strong>ERK1</strong>/2 activation in reward related limbic brain regions.
+MAPK3	addiction	relapse	18619984	We sought to determine if cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior, and its reduction by an mGluR5 antagonist, is associated with changes in <strong>ERK1</strong>/2 activation in reward related limbic brain regions.
+MAPK3	addiction	reward	18619984	We sought to determine if cue induced reinstatement of alcohol seeking behavior, and its reduction by an mGluR5 antagonist, is associated with changes in <strong>ERK1</strong>/2 activation in <b>reward</b> related limbic brain regions.
+MAPK3	drug	alcohol	18619984	Cue induced reinstatement of <b>alcohol</b> seeking behavior was associated with a three to five fold increase in p <strong>ERK1</strong>/2 IR in the basolateral amygdala and nucleus accumbens shell.
+MAPK3	addiction	relapse	18619984	Cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior was associated with a three to five fold increase in p <strong>ERK1</strong>/2 IR in the basolateral amygdala and nucleus accumbens shell.
+MAPK3	addiction	relapse	18619984	MPEP administration blocked both the <b>relapse</b> like behavior and increase in p <strong>ERK1</strong>/2 IR.
+MAPK3	addiction	relapse	18619984	p <strong>ERK1</strong>/2 IR in the central amygdala and NAcb core was dissociated with the <b>relapse</b> like behavior and the pharmacological effect of mGluR5 blockade.
+MAPK3	drug	alcohol	18619984	These results suggest that exposure to cues previously associated with <b>alcohol</b> self administration is sufficient to produce concomitant increases in relapse like behavior and <strong>ERK1</strong>/2 activation in specific limbic brain regions.
+MAPK3	addiction	relapse	18619984	These results suggest that exposure to cues previously associated with alcohol self administration is sufficient to produce concomitant increases in <b>relapse</b> like behavior and <strong>ERK1</strong>/2 activation in specific limbic brain regions.
+MAPK3	drug	alcohol	18619984	Pharmacological compounds, such as mGluR5 antagonists, that reduce cue induced <strong>ERK1</strong>/2 activation may be useful for treatment of relapse in <b>alcoholics</b> that is triggered by exposure to environmental events.
+MAPK3	addiction	relapse	18619984	Pharmacological compounds, such as mGluR5 antagonists, that reduce cue induced <strong>ERK1</strong>/2 activation may be useful for treatment of <b>relapse</b> in alcoholics that is triggered by exposure to environmental events.
+MAPK3	drug	opioid	18616461	Regulation of <strong>ERK1</strong>/2 phosphorylation by acute and chronic <b>morphine</b>   implications for the role of cAMP responsive element binding factor (CREB) dependent and Ets like protein 1 (Elk 1) dependent transcription; small interfering RNA based strategy.
+MAPK3	drug	opioid	18616461	In this study, we observed a rapid and severe increase in <strong>ERK1</strong>/2 activity after a 5 min <b>morphine</b> treatment of HEK MOR cells (transfected with the rat mu <b>opioid</b> receptor MOR1) expressing mu <b>opioid</b> receptor.
+MAPK3	drug	opioid	18616461	Cellular adaptations to chronic (72 h) <b>morphine</b> treatment were manifested by a slight and sustained increase in <strong>ERK1</strong>/2 activity.
+MAPK3	drug	opioid	18616461	Withdrawal caused by an <b>opioid</b> receptor antagonist   <b>naloxone</b>   attenuated phosphorylation of <strong>ERK1</strong>/2.
+MAPK3	addiction	withdrawal	18616461	<b>Withdrawal</b> caused by an opioid receptor antagonist   naloxone   attenuated phosphorylation of <strong>ERK1</strong>/2.
+MAPK3	drug	opioid	18536752	The PKs PKA and <strong>ERK 1</strong>/2 are involved in phosphorylation of TH at Serine 40 and 31 during <b>morphine</b> withdrawal in rat hearts.
+MAPK3	addiction	withdrawal	18536752	The PKs PKA and <strong>ERK 1</strong>/2 are involved in phosphorylation of TH at Serine 40 and 31 during morphine <b>withdrawal</b> in rat hearts.
+MAPK3	drug	opioid	18536752	In addition, we show that the ability of <b>morphine</b> withdrawal to stimulate phosphorylation at Ser31 was reduced by SL327, an inhibitor of <strong>ERK 1</strong>/2 activation.
+MAPK3	addiction	withdrawal	18536752	In addition, we show that the ability of morphine <b>withdrawal</b> to stimulate phosphorylation at Ser31 was reduced by SL327, an inhibitor of <strong>ERK 1</strong>/2 activation.
+MAPK3	drug	alcohol	18322102	Here, we report that the anxiolytic effects of acute <b>ethanol</b> were associated with increased brain derived neurotrophic factor (BDNF) and tyrosine kinase B (trkB) expression, increased phosphorylation of extracellular signal regulated kinases 1/2 (<strong>Erk1</strong>/2), Elk 1, and cAMP responsive element binding protein (CREB), increased Arc expression, and increased dendritic spine density (DSD) in both the central amygdala (CeA) and medial amygdala (MeA) but not in the basolateral amygdala (BLA) of rats.
+MAPK3	drug	alcohol	18322102	Conversely, the anxiogenic effects of withdrawal after long term <b>ethanol</b> exposure were associated with decreased BDNF and trkB expression, decreased phosphorylation of <strong>Erk1</strong>/2, Elk 1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+MAPK3	addiction	withdrawal	18322102	Conversely, the anxiogenic effects of <b>withdrawal</b> after long term ethanol exposure were associated with decreased BDNF and trkB expression, decreased phosphorylation of <strong>Erk1</strong>/2, Elk 1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+MAPK3	drug	alcohol	18322102	We also showed that BDNF infusion into the CeA normalized phosphorylation of <strong>Erk1</strong>/2, Elk 1, and CREB, and normalized Arc expression, thereby protecting against the onset of <b>ethanol</b> withdrawal related anxiety.
+MAPK3	addiction	withdrawal	18322102	We also showed that BDNF infusion into the CeA normalized phosphorylation of <strong>Erk1</strong>/2, Elk 1, and CREB, and normalized Arc expression, thereby protecting against the onset of ethanol <b>withdrawal</b> related anxiety.
+MAPK3	drug	alcohol	18317950	Differential phosphorylation of translation initiation regulators 4EBP1, S6k1, and <strong>Erk 1</strong>/2 following inhibition of <b>alcohol</b> metabolism in mouse heart.
+MAPK3	drug	alcohol	18317950	Phosphorylation of 4E BP1, S6k1(Thr(389)), and <strong>Erk 1</strong>/2 was reduced 2 h following IP injection of <b>alcohol</b>.
+MAPK3	drug	alcohol	18317950	In contrast, 4 MP prevented the decrease in <strong>Erk 1</strong>/2 phosphorylation observed with acute <b>ethanol</b> intoxication.
+MAPK3	addiction	intoxication	18317950	In contrast, 4 MP prevented the decrease in <strong>Erk 1</strong>/2 phosphorylation observed with acute ethanol <b>intoxication</b>.
+MAPK3	drug	opioid	17957220	In addition, <b>morphine</b> induced <strong>ERK1</strong>/2 phosphorylation was increased in the VTA of both wild type and GKO mice, but only the GKO mice showed increases in <strong>ERK1</strong>/2 and CREB phosphorylation in the amygdala or nucleus accumbens.
+MAPK3	drug	alcohol	17889309	<b>Alcohol</b> exposure did not affect MH S cell nuclear factor kappa beta p65 nuclear localization during challenge, despite dose dependent inhibition of <strong>Erk 1</strong>/2 phosphorylation.
+MAPK3	drug	alcohol	17851539	In the second experiment, reexposure to the <b>ethanol</b> associated context and discrete cues activated both c Jun and extracellular signal regulated kinases (<strong>ERK1</strong>/2) in the basolateral amygdala.
+MAPK3	drug	opioid	17823252	Regulation of serine (Ser) 31 and Ser40 tyrosine hydroxylase phosphorylation during <b>morphine</b> withdrawal in the hypothalamic paraventricular nucleus and nucleus tractus solitarius A2 cell group: role of <strong>ERK1</strong>/2.
+MAPK3	addiction	withdrawal	17823252	Regulation of serine (Ser) 31 and Ser40 tyrosine hydroxylase phosphorylation during morphine <b>withdrawal</b> in the hypothalamic paraventricular nucleus and nucleus tractus solitarius A2 cell group: role of <strong>ERK1</strong>/2.
+MAPK3	drug	nicotine	17638897	Together, the phosphorylation of ERbeta, the dependence on Galphai proteins, the activation of <strong>ERK1</strong>/2, and the preferential targeting of SRE over the classic ERE pathway support a role for nongenomic ERbeta in the development of <b>smoking</b> associated lung cancer.
+MAPK3	addiction	dependence	17638897	Together, the phosphorylation of ERbeta, the <b>dependence</b> on Galphai proteins, the activation of <strong>ERK1</strong>/2, and the preferential targeting of SRE over the classic ERE pathway support a role for nongenomic ERbeta in the development of smoking associated lung cancer.
+MAPK3	drug	cocaine	17610912	The increase of <strong>ERK1</strong>/2 phosphorylation levels in the NAcc by <b>cocaine</b> was completely blocked by CART 55 102 microinjection in this site, while it remains unaffected by inactive CART 1 27 peptide.
+MAPK3	drug	cocaine	17610912	These results suggest that CART 55 102 peptide in the NAcc may play a compensatory inhibitory role in the expression of behavioral sensitization by <b>cocaine</b> and these effects may be mediated by its inhibition of <strong>ERK1</strong>/2 phosphorylation in this site.
+MAPK3	addiction	sensitization	17610912	These results suggest that CART 55 102 peptide in the NAcc may play a compensatory inhibitory role in the expression of behavioral <b>sensitization</b> by cocaine and these effects may be mediated by its inhibition of <strong>ERK1</strong>/2 phosphorylation in this site.
+MAPK3	drug	opioid	17549049	<b>Naloxone</b> induced <b>morphine</b> withdrawal activated <strong>ERK1</strong>/2 and increased c Fos expression in cardiac tissues.
+MAPK3	addiction	withdrawal	17549049	Naloxone induced morphine <b>withdrawal</b> activated <strong>ERK1</strong>/2 and increased c Fos expression in cardiac tissues.
+MAPK3	drug	amphetamine	17514479	In contrast, hyperphosphorylation of <strong>ERK1</strong>/2 was abolished in the hippocampus of rats treated with <b>METH</b>.
+MAPK3	drug	amphetamine	17514479	These findings suggest that repeated <b>METH</b> treatment induces impairment of working memory, which is associated with a dysfunctional <strong>ERK1</strong>/2 pathway in the hippocampus.
+MAPK3	addiction	dependence	17315157	Reverse phase proteomics, Western blot analysis, and immunoprecipitation in immortalized human small airway epithelial cells and in a human PAC cell line in the presence and absence of dominant negative Raf were used to determine Raf <b>dependence</b> of extracellular signal regulated kinase 1 and 2 (<strong>ERK1</strong>/2) activation in response to NNK or isoproterenol.
+MAPK3	drug	cannabinoid	17139682	Treatment with SR141716A after chronic WIN55212 2 resulted in the expected <b>cannabinoid</b> withdrawal syndrome, without concomitant alterations in the phosphorylation state of c Raf 1, MEK1/2, or <strong>ERK1</strong>/2.
+MAPK3	addiction	withdrawal	17139682	Treatment with SR141716A after chronic WIN55212 2 resulted in the expected cannabinoid <b>withdrawal</b> syndrome, without concomitant alterations in the phosphorylation state of c Raf 1, MEK1/2, or <strong>ERK1</strong>/2.
+MAPK3	drug	cocaine	17085074	By contrast, <strong>ERK1</strong> mutation enhances the effects of morphine and <b>cocaine</b>.
+MAPK3	drug	opioid	17085074	By contrast, <strong>ERK1</strong> mutation enhances the effects of <b>morphine</b> and cocaine.
+MAPK3	drug	opioid	16712881	Cross talk between nitric oxide and <strong>ERK1</strong>/2 signaling pathway in the spinal cord mediates <b>naloxone</b> precipitated withdrawal in <b>morphine</b> dependent rats.
+MAPK3	addiction	withdrawal	16712881	Cross talk between nitric oxide and <strong>ERK1</strong>/2 signaling pathway in the spinal cord mediates naloxone precipitated <b>withdrawal</b> in morphine dependent rats.
+MAPK3	drug	opioid	16712881	Our recent study has shown activation of spinal extracellular signal regulated kinase 1 and  2 (<strong>ERK1</strong>/2), a member of the mitogen activated protein kinase (MAPK) family, contributes to <b>naloxone</b> precipitated withdrawal and withdrawal induced spinal neuronal sensitization in <b>morphine</b> dependent rats.
+MAPK3	addiction	sensitization	16712881	Our recent study has shown activation of spinal extracellular signal regulated kinase 1 and  2 (<strong>ERK1</strong>/2), a member of the mitogen activated protein kinase (MAPK) family, contributes to naloxone precipitated withdrawal and withdrawal induced spinal neuronal <b>sensitization</b> in morphine dependent rats.
+MAPK3	addiction	withdrawal	16712881	Our recent study has shown activation of spinal extracellular signal regulated kinase 1 and  2 (<strong>ERK1</strong>/2), a member of the mitogen activated protein kinase (MAPK) family, contributes to naloxone precipitated <b>withdrawal</b> and <b>withdrawal</b> induced spinal neuronal sensitization in morphine dependent rats.
+MAPK3	drug	opioid	16712881	However, the mechanism and significance of the spinal <strong>ERK1</strong>/2 activation during <b>morphine</b> dependence and withdrawal remain unknown.
+MAPK3	addiction	dependence	16712881	However, the mechanism and significance of the spinal <strong>ERK1</strong>/2 activation during morphine <b>dependence</b> and withdrawal remain unknown.
+MAPK3	addiction	withdrawal	16712881	However, the mechanism and significance of the spinal <strong>ERK1</strong>/2 activation during morphine dependence and <b>withdrawal</b> remain unknown.
+MAPK3	drug	opioid	16712881	pretreatment with either the non selective nitric oxide synthase (NOS) inhibitor N(G) nitro L arginine methyl ester (L NAME), neuronal NOS (nNOS) inhibitor 7 nitro indazole (7 NI), or the inducible NOS (iNOS) inhibitor aminoguanidine (AG), could reduce <b>morphine</b> withdrawal induced increase of phospho <strong>ERK1</strong>/2 (pERK1/2) expression in the rat spinal cord.
+MAPK3	addiction	withdrawal	16712881	pretreatment with either the non selective nitric oxide synthase (NOS) inhibitor N(G) nitro L arginine methyl ester (L NAME), neuronal NOS (nNOS) inhibitor 7 nitro indazole (7 NI), or the inducible NOS (iNOS) inhibitor aminoguanidine (AG), could reduce morphine <b>withdrawal</b> induced increase of phospho <strong>ERK1</strong>/2 (pERK1/2) expression in the rat spinal cord.
+MAPK3	drug	opioid	16712881	These findings suggest cross talk between nitric oxide (NO) and the <strong>ERK1</strong>/2 signaling pathway mediates <b>morphine</b> withdrawal and withdrawal induced spinal neuronal sensitization in <b>morphine</b> dependent rats.
+MAPK3	addiction	sensitization	16712881	These findings suggest cross talk between nitric oxide (NO) and the <strong>ERK1</strong>/2 signaling pathway mediates morphine withdrawal and withdrawal induced spinal neuronal <b>sensitization</b> in morphine dependent rats.
+MAPK3	addiction	withdrawal	16712881	These findings suggest cross talk between nitric oxide (NO) and the <strong>ERK1</strong>/2 signaling pathway mediates morphine <b>withdrawal</b> and <b>withdrawal</b> induced spinal neuronal sensitization in morphine dependent rats.
+MAPK3	drug	opioid	16678156	<strong>ERK1</strong>/2 are stimulated by mitogen activated protein kinase kinases (MEK1/2), but little is known about the regulation of MEK activity by <b>opioid</b> drugs.
+MAPK3	drug	alcohol	16410364	gAcrp suppressed LPS stimulated <strong>ERK1</strong>/2 and p38 phosphorylation as well as IkappaB degradation at 100 1,000 ng/ml in Kupffer cells from both pair  and <b>ethanol</b> fed rats.
+MAPK3	drug	alcohol	16410364	Suppression of LPS stimulated <strong>ERK1</strong>/2 signaling by low concentrations of gAcrp was associated with normalization of TNF alpha production by Kupffer cells after chronic <b>ethanol</b> exposure.
+MAPK3	drug	cocaine	16407894	Knockout of <strong>ERK1</strong> enhances <b>cocaine</b> evoked immediate early gene expression and behavioral plasticity.
+MAPK3	drug	cocaine	16407894	We report here that deletion of the <strong>ERK1</strong> isoform, which leads to increased ERK2 stimulus dependent signaling, facilitates the development of <b>cocaine</b> induced psychomotor sensitization and the acquisition of a <b>cocaine</b> conditioned place preference.
+MAPK3	addiction	sensitization	16407894	We report here that deletion of the <strong>ERK1</strong> isoform, which leads to increased ERK2 stimulus dependent signaling, facilitates the development of cocaine induced psychomotor <b>sensitization</b> and the acquisition of a cocaine conditioned place preference.
+MAPK3	drug	cocaine	16407894	Finally, <b>cocaine</b> evoked gene expression in mesocorticolimbic brain regions is potentiated in <strong>ERK1</strong> deficient mice.
+MAPK3	addiction	withdrawal	16158186	The pr ecipitation of <b>withdrawal</b> further decreased the <strong>ERK1</strong>/2 activity.
+MAPK3	drug	amphetamine	16139811	Repeated <b>methamphetamine</b> treatment impairs recognition memory through a failure of novelty induced <strong>ERK1</strong>/2 activation in the prefrontal cortex of mice.
+MAPK3	drug	amphetamine	16139811	Hyperphosphorylation of <strong>ERK1</strong>/2 was found in the prefrontal cortex of mice exposed to the novel objects, but was abolished in mice treated with <b>METH</b>.
+MAPK3	drug	amphetamine	16139811	These results suggest that repeated <b>METH</b> treatment induces cognitive impairment, which is associated with the dysfunction of the <strong>ERK1</strong>/2 pathway in the prefrontal cortex.
+MAPK3	addiction	intoxication	15718389	These findings suggest that EtOH <b>intoxication</b> before burn injury augments Cort release, which suppresses MLN T cell function by inhibiting p38 and <strong>ERK1</strong>/2 activation and promotes bacterial accumulation in MLN after EtOH and burn injury.
+MAPK3	drug	psychedelics	15659598	In dopaminergic neuron like SHSY5Y cells, <b>ibogaine</b> treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, Ret, and the downstream kinase, <strong>ERK1</strong> (extracellular signal regulated kinase 1).
+MAPK3	drug	cocaine	15447670	These results demonstrate direct and indirect regulation of the phosphorylation state of a Cdk5/<strong>ERK1</strong>/2 site on TH and suggest a role for these pathways in the neuroadaptive changes associated with chronic <b>cocaine</b> exposure.
+MAPK3	drug	amphetamine	15329393	Using immunoblot and immunohistochemical analyses, we find that in chronic saline treated rats a challenge injection of <b>amphetamine</b> increases phosphorylation of MAP [extracellular signal regulated kinase 1/2 (<strong>ERK1</strong>/2)] kinase in the VTA that is independent of LTCCs.
+MAPK3	drug	amphetamine	15329393	However, in chronic <b>amphetamine</b> treated rats there is no increase in <b>amphetamine</b> mediated <strong>ERK1</strong>/2 phosphorylation unless LTCCs are blocked, in which case there is robust phosphorylation in VTA dopamine neurons.
+MAPK3	addiction	reward	15102958	Hyperphosphorylation of mitogen activated protein kinase (MAPK) <strong>ERK1</strong>/2, but not p38 and c Jun N terminal kinase/stress activated protein kinase, was found in the nucleus accumbens (NAc) and striatum but not in other brain areas of MAP treated <b>CPP</b>(+) animals.
+MAPK3	addiction	reward	15102958	Both the dopamine D1 receptor antagonist R (+) 7 chloro 8 hydroxy 3 methyl 1 phenyl 2,3,4,5 tetrahydro 1H 3 benzazepine (SCH23390) and the D2 receptor antagonist raclopride inhibited the expression of <b>CPP</b> as well as the activation of <strong>ERK1</strong>/2 in MAP treated <b>CPP</b>(+) animals, when they were injected before the <b>CPP</b> test.
+MAPK3	addiction	reward	15102958	The microinjection of 2' amino 3' methoxyflavone (PD98059), a selective MAPK kinase inhibitor, into the NAc before the test, abolished the MAP induced <strong>ERK1</strong>/2 activation and decreased the expression of MAP induced <b>CPP</b>.
+MAPK3	addiction	reward	15102958	These results suggest the importance of the <strong>ERK1</strong>/2 signaling pathway through activation of dopamine D1 and D2 receptors in the expression of <b>CPP</b> induced by MAP.
+MAPK3	drug	alcohol	12676135	<b>Ethanol</b> significantly reduced carbachol stimulated Ca(2+) signaling, as well as <strong>Erk1</strong>/Erk2, Akt and cyclic AMP response element binding phosphorylations in a dose dependent manner.
+MAPK3	drug	opioid	12535947	<strong>ERK1</strong>/2 activation in rat ventral tegmental area by the mu <b>opioid</b> agonist <b>fentanyl</b>: an in vitro study.
+MAPK3	addiction	reward	12487923	To investigate the effect of <b>reinforcing</b> kidney, replenishing Qi and blood activating prescription (RKRQBAP) on extracellular signal regulating kinase 1 (<strong>ERK 1</strong>) and mitogen activated protein kinase phosphatase 1 (MKP 1) of fetal rats with fetal growth restriction (FGR).
+MAPK3	drug	alcohol	12130710	Finally, blockade of <strong>ERK 1</strong>/2 phosphorylation with the mitogen activated protein kinase (MEK) 1/2 inhibitor SL327 blocked <b>alcohol</b> induced c Fos expression, suggesting that <b>alcohol</b> induces c Fos in Edinger Westphal neurons through activation of the MEK1/2 ERK1/2 Stat3 pathway.
+MAPK3	drug	alcohol	12130710	Finally, blockade of <strong>ERK 1</strong>/2 phosphorylation with the mitogen activated protein kinase (MEK) 1/2 inhibitor SL327 blocked <b>alcohol</b> induced c Fos expression, suggesting that <b>alcohol</b> induces c Fos in Edinger Westphal neurons through activation of the MEK1/2 <strong>ERK1</strong>/2 Stat3 pathway.
+MAPK3	drug	opioid	12062026	Consistently, such activity change is responsible for the hypersensitivity of <strong>ERK1</strong> mutant mice to the rewarding properties of <b>morphine</b>.
+MAPK3	addiction	addiction	12062026	Our results reveal an unexpected complexity of ERK dependent signaling in the brain and a critical regulatory role for <strong>ERK1</strong> in the long term adaptive changes underlying striatum dependent behavioral plasticity and drug <b>addiction</b>.
+MAPK3	drug	benzodiazepine	11923223	Among the proteins, which are tyrosine  nitrated by ammonia, glyceraldehyde 3 phosphate dehydrogenase, the peripheral type <b>benzodiazepine</b> receptor, <strong>Erk 1</strong>, and glutamine synthetase are identified.
+MAPK3	drug	opioid	10737627	Regulation of adenylyl cyclase, <strong>ERK1</strong>/2, and CREB by Gz following acute and chronic activation of the delta <b>opioid</b> receptor.
+MAPK3	drug	opioid	10737627	Both Gi and Gz mediated DPDPE induced activation of <strong>ERK1</strong>/2, but these responses were abolished by chronic <b>opioid</b> treatment.
+MAPK3	drug	opioid	10737627	Collectively, our results show that although Gz mediated <b>opioid</b> induced inhibition of adenylyl cyclase and activation of <strong>ERK1</strong>/2, Gz alone was insufficient to mediate <b>opioid</b> induced adenylyl cyclase supersensitization.
+FAAH1	drug	cannabinoid	32676014	<b>Cannabidiol</b> (CBD), a constituent of the <b>Cannabis</b> Sativa plant, interacts with the <b>endocannabinoid</b> system by inhibiting <strong>fatty acid amide hydrolase</strong> (FAAH) activity (the rate limiting enzyme for anandamide hydrolysis), allosterically modulating CB1 and CB2 receptors, and activating components of the "extended <b>endocannabinoid</b> system."
+FAAH1	drug	cannabinoid	32559067	This Viewpoint aims to highlight positron emission tomography (PET) research studies that have shaped our understanding of the <b>endocannabinoid</b> system (ECS) through radiopharmaceutical targeting of <b>cannabinoid</b> receptors 1 and 2 (CB1 and CB2), and the enzyme <strong>fatty acid amide hydrolase</strong> (FAAH), in several brain health illnesses including addiction, schizophrenia, eating disorders, and post traumatic stress disorder.
+FAAH1	addiction	addiction	32559067	This Viewpoint aims to highlight positron emission tomography (PET) research studies that have shaped our understanding of the endocannabinoid system (ECS) through radiopharmaceutical targeting of cannabinoid receptors 1 and 2 (CB1 and CB2), and the enzyme <strong>fatty acid amide hydrolase</strong> (FAAH), in several brain health illnesses including <b>addiction</b>, schizophrenia, eating disorders, and post traumatic stress disorder.
+FAAH1	addiction	addiction	32425077	Based on current evidence, CB1 receptor neutral antagonists and <strong>fatty acid amide hydrolase</strong> inhibitors demonstrate positive effects in studies assessing several <b>addiction</b> related factors.
+FAAH1	drug	cannabinoid	31960544	<strong>Fatty acid amide hydrolase</strong> is lower in young <b>cannabis</b> users.
+FAAH1	drug	cannabinoid	31960544	We have recently shown that levels of <strong>fatty acid amide hydrolase</strong> (FAAH), the enzyme that metabolizes the <b>endocannabinoid</b> anandamide, are lower in the brains of adult <b>cannabis</b> users (CUs) (34 ± 11 years of age), tested during early abstinence.
+FAAH1	drug	alcohol	31910433	Lower brain <strong>fatty acid amide hydrolase</strong> in treatment seeking patients with <b>alcohol</b> use disorder: a positron emission tomography study with [C 11]CURB.
+FAAH1	addiction	relapse	31910433	Lower brain <strong>fatty acid amide hydrolase</strong> in treatment <b>seeking</b> patients with alcohol use disorder: a positron emission tomography study with [C 11]CURB.
+FAAH1	drug	alcohol	31910433	The endocannabinoid enzyme, <strong>fatty acid amide hydrolase</strong> (FAAH), has been proposed as a therapeutic target for <b>alcohol</b> use disorder (AUD) and co morbid psychiatric illnesses.
+FAAH1	drug	cannabinoid	31910433	The <b>endocannabinoid</b> enzyme, <strong>fatty acid amide hydrolase</strong> (FAAH), has been proposed as a therapeutic target for alcohol use disorder (AUD) and co morbid psychiatric illnesses.
+FAAH1	drug	amphetamine	31789429	The <strong>fatty acid amide hydrolase</strong> (FAAH) gene was involved in the modulation of reward and addiction pathophysiology of illicit drugs abuse, and its polymorphisms might be associated with risk of <b>methamphetamine</b> (<b>METH</b>) dependence.
+FAAH1	addiction	addiction	31789429	The <strong>fatty acid amide hydrolase</strong> (FAAH) gene was involved in the modulation of reward and <b>addiction</b> pathophysiology of illicit drugs abuse, and its polymorphisms might be associated with risk of methamphetamine (METH) dependence.
+FAAH1	addiction	dependence	31789429	The <strong>fatty acid amide hydrolase</strong> (FAAH) gene was involved in the modulation of reward and addiction pathophysiology of illicit drugs abuse, and its polymorphisms might be associated with risk of methamphetamine (METH) <b>dependence</b>.
+FAAH1	addiction	reward	31789429	The <strong>fatty acid amide hydrolase</strong> (FAAH) gene was involved in the modulation of <b>reward</b> and addiction pathophysiology of illicit drugs abuse, and its polymorphisms might be associated with risk of methamphetamine (METH) dependence.
+FAAH1	addiction	addiction	31775159	D3 dopamine receptors and a missense mutation of <strong>fatty acid amide hydrolase</strong> linked in mouse and men: implication for <b>addiction</b>.
+FAAH1	drug	cannabinoid	31775159	We investigated a potential interaction between genetically inherited variation in <strong>fatty acid amide hydrolase</strong> (FAAH, C385A), which metabolizes the <b>cannabis</b> like <b>endocannabinoid</b> anandamide, and dopaminergic system, measured by dopamine receptor levels and mRNA.
+FAAH1	drug	opioid	31712968	A recently discovered fatty acid amide, N oleoylglycine (OlGly), which has been suggested to act as a <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor and as a peroxisome proliferator activated receptor alpha (PPARα) agonist, was previously shown to interfere with a <b>naloxone</b> precipitated MWD induced CPA in rats.
+FAAH1	drug	cannabinoid	31549358	Since then, much research interest has shifted to other <b>cannabinoid</b> based strategies, such as peripheral CB1R antagonists/inverse agonists, neutral CB1R antagonists, allosteric CB1R modulators, CB2R agonists, <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitors, monoacylglycerol lipase (MAGL) inhibitors, fatty acid binding protein (FABP) inhibitors, or nonaddictive phytocannabinoids with CB1R or CB2R binding profiles, as new therapeutics for SUDs.
+FAAH1	addiction	relapse	31292037	Experimental substance use among young people is related to individual factors including personality traits such as impulsivity and sensation <b>seeking</b>, and genetic variations such as single nucleotide polymorphisms (SNPs) in the <strong>fatty acid amide hydrolase</strong> (FAAH) gene.
+FAAH1	drug	cannabinoid	31202911	Conversely, CBD did not affect N methyl d aspartate receptor and gamma aminobutyric acid (GABA) A receptor binding or protein levels of <strong>fatty acid amide hydrolase</strong>, the enzyme that degrades the <b>endocannabinoid</b>, anandamide.
+FAAH1	drug	cannabinoid	31184938	Background: Polymorphisms in <b>cannabinoid</b> receptor type 1 (encoded by CNR1) and <strong>fatty acid amide hydrolase</strong> (encoded by FAAH) have been associated with <b>cannabis</b> dependence, but it remains unknown whether variation within these genes influences <b>cannabis</b>' acute effects on affect.
+FAAH1	addiction	dependence	31184938	Background: Polymorphisms in cannabinoid receptor type 1 (encoded by CNR1) and <strong>fatty acid amide hydrolase</strong> (encoded by FAAH) have been associated with cannabis <b>dependence</b>, but it remains unknown whether variation within these genes influences cannabis' acute effects on affect.
+FAAH1	drug	cannabinoid	31013550	Single nucleotide polymorphisms (SNPs) in the <b>cannabinoid</b> receptor 1 gene (CNR1; rs1049353 and rs806378) and <strong>fatty acid amide hydrolase</strong> (FAAH) gene (rs324420) have been implicated in CUD.
+FAAH1	addiction	dependence	30739035	Brain permeant and impermeant inhibitors of <strong>fatty acid amide hydrolase</strong> suppress the development and maintenance of paclitaxel induced neuropathic pain without producing tolerance or physical <b>dependence</b> in vivo and synergize with paclitaxel to reduce tumor cell line viability in vitro.
+FAAH1	drug	cannabinoid	30739035	Inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the major enzyme catalyzing the degradation of anandamide (AEA), an <b>endocannabinoid</b>, and other fatty acid amides, suppresses pain without unwanted side effects typical of direct CB1 agonists.
+FAAH1	drug	cannabinoid	30578649	Transcriptional regulation of the <b>endocannabinoid</b> system in a rat model of binge eating behavior reveals a selective modulation of the hypothalamic <strong>fatty acid amide hydrolase</strong> gene.
+FAAH1	addiction	intoxication	30578649	Transcriptional regulation of the endocannabinoid system in a rat model of <b>binge</b> eating behavior reveals a selective modulation of the hypothalamic <strong>fatty acid amide hydrolase</strong> gene.
+FAAH1	addiction	intoxication	30578649	We observed a selective down regulation of <strong>fatty acid amide hydrolase</strong> (faah) gene expression in the hypothalamus of rats showing the <b>binge</b> eating behavior with a consistent reduction in histone 3 acetylation at lysine 4 of the gene promoter.
+FAAH1	drug	cannabinoid	30528676	Efficacy and safety of a <strong>fatty acid amide hydrolase</strong> inhibitor (PF 04457845) in the treatment of <b>cannabis</b> withdrawal and dependence in men: a double blind, placebo controlled, parallel group, phase 2a single site randomised controlled trial.
+FAAH1	addiction	dependence	30528676	Efficacy and safety of a <strong>fatty acid amide hydrolase</strong> inhibitor (PF 04457845) in the treatment of cannabis withdrawal and <b>dependence</b> in men: a double blind, placebo controlled, parallel group, phase 2a single site randomised controlled trial.
+FAAH1	addiction	withdrawal	30528676	Efficacy and safety of a <strong>fatty acid amide hydrolase</strong> inhibitor (PF 04457845) in the treatment of cannabis <b>withdrawal</b> and dependence in men: a double blind, placebo controlled, parallel group, phase 2a single site randomised controlled trial.
+FAAH1	drug	cannabinoid	30528676	One approach is to potentiate <b>endocannabinoid</b> signalling by inhibiting <strong>fatty acid amide hydrolase</strong> (FAAH), the enzyme that degrades the <b>endocannabinoid</b> anandamide.
+FAAH1	addiction	relapse	30481332	), an inhibitor of <strong>fatty acid amide hydrolase</strong>, attenuated only cue induced <b>reinstatement</b>.
+FAAH1	drug	amphetamine	30396596	Finally, rats were sacrificed and agouti related peptide (AgRP), neuropeptide Y (NPY), pro opiomelanocortin (POMC) and cocaine  and <b>amphetamine</b> regulated transcript (CART) and <strong>fatty acid amide hydrolase</strong> (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+FAAH1	drug	cocaine	30396596	Finally, rats were sacrificed and agouti related peptide (AgRP), neuropeptide Y (NPY), pro opiomelanocortin (POMC) and <b>cocaine</b>  and amphetamine regulated transcript (CART) and <strong>fatty acid amide hydrolase</strong> (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+FAAH1	drug	cannabinoid	30166624	Although recent efforts have largely focused on evaluating CB1 binding, the synthesis of new radiotracers targeting enzymes involved in <b>endocannabinoid</b> degradation, such as <strong>fatty acid amide hydrolase</strong>, will allow for other facets of <b>endocannabinoid</b> signaling to be evaluated in future studies.
+FAAH1	drug	cannabinoid	30126012	The endogenous <b>cannabinoid</b> anandamide (AEA), an agonist at type 1 <b>cannabinoid</b> (CB1) receptors, is metabolized by <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	addiction	reward	30050084	Enhanced brain levels of anandamide after treatment with inhibitors of <strong>fatty acid amide hydrolase</strong>, the main enzyme responsible for its degradation, seem to affect the rewarding and <b>reinforcing</b> actions of many drugs of abuse.
+FAAH1	drug	cannabinoid	29875385	However, expression patterns of the <b>cannabinoid</b> receptor type 1 (CB1R), the synthesizing enzyme N acyl phosphatidylethanolamine phospholipase D (NAPE PLD), and the degradation enzyme <strong>fatty acid amide hydrolase</strong> (FAAH) in the NAc have not yet been described in non human primates.
+FAAH1	drug	cannabinoid	29863609	Enhancing <b>endocannabinoids</b> by <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitors relieves neuropathic pain and stress induced depressive like behaviors in animal models.
+FAAH1	drug	cannabinoid	29847859	The effects of intra mPFC administration of AM251 [<b>cannabinoid</b> type 1 (CB1) receptor antagonist/inverse agonist], URB597 [<strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor] or URB597 + AM251 on FCA and freezing behaviour were assessed.
+FAAH1	drug	cannabinoid	29842858	We recently found that the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597, which increases anandamide levels by inhibiting its hydrolysis, facilitates memory consolidation through a concurrent activation of both <b>cannabinoid</b> receptor type 1 (CB1) and 2 (CB2).
+FAAH1	drug	alcohol	29748627	Additionally, we evaluated the inhibition of endocannabinoids clearance enzymes [monoacylglycerol lipase (MAGL) and <strong>fatty acid amide hydrolase</strong>] on anxiety like behavior and <b>alcohol</b> consumption in <b>alcohol</b> dependent rats and mice.
+FAAH1	drug	cannabinoid	29748627	Additionally, we evaluated the inhibition of <b>endocannabinoids</b> clearance enzymes [monoacylglycerol lipase (MAGL) and <strong>fatty acid amide hydrolase</strong>] on anxiety like behavior and alcohol consumption in alcohol dependent rats and mice.
+FAAH1	drug	cannabinoid	29457656	Recently, fatty acid binding proteins (FABPs) have been proposed as intracellular transporters of the <b>endocannabinoid</b> anandamide (AEA) as well as other bioactive lipids to their catabolic enzyme, <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	drug	cannabinoid	29403000	<strong>Fatty acid amide hydrolase</strong> (FAAH) represents the primary degradation enzyme of the eCB anandamide (AEA), <b>oleoylethanolamide</b> (OEA) and <b>palmitoylethanolamide</b> (PEA).
+FAAH1	drug	alcohol	29367955	Inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the principal enzyme that degrades the eCB anandamide (AEA), which enhances AEA levels in the brain, significantly increases <b>ethanol</b> consumption and preference.
+FAAH1	drug	alcohol	29186065	Therefore, the current study investigated the effects of neurotoxic, binge like <b>alcohol</b> exposure on components of the endocannabinoid system and related N acylethanolamines (NAEs), and then evaluated the efficacy of <strong>fatty acid amide hydrolase</strong> (FAAH) inhibition on attenuating <b>alcohol</b> induced neurodegeneration.
+FAAH1	drug	cannabinoid	29186065	Therefore, the current study investigated the effects of neurotoxic, binge like alcohol exposure on components of the <b>endocannabinoid</b> system and related N <b>acylethanolamines</b> (NAEs), and then evaluated the efficacy of <strong>fatty acid amide hydrolase</strong> (FAAH) inhibition on attenuating alcohol induced neurodegeneration.
+FAAH1	addiction	intoxication	29186065	Therefore, the current study investigated the effects of neurotoxic, <b>binge</b> like alcohol exposure on components of the endocannabinoid system and related N acylethanolamines (NAEs), and then evaluated the efficacy of <strong>fatty acid amide hydrolase</strong> (FAAH) inhibition on attenuating alcohol induced neurodegeneration.
+FAAH1	drug	alcohol	29071769	Inhibition of <strong>fatty acid amide hydrolase</strong> in the central amygdala alleviates co morbid expression of innate anxiety and excessive <b>alcohol</b> intake.
+FAAH1	drug	cannabinoid	29071769	<strong>Fatty acid amide hydrolase</strong> (FAAH) is an enzyme that prominently degrades the major <b>endocannabinoid</b> N arachidonoylethanolamine (anandamide).
+FAAH1	addiction	dependence	28963903	<strong>Fatty acid amide hydrolase</strong> inhibitor URB597 may protect against kainic acid induced damage to hippocampal neurons: <b>Dependence</b> on the degree of injury.
+FAAH1	drug	cannabinoid	28803323	Effect of footshock stress on place conditioning produced by Δ9 <b>tetrahydrocannabinol</b> and the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor, URB597, in Sprague Dawley rats.
+FAAH1	drug	cannabinoid	28803323	We evaluate the potential of footshock stress to enhance the rewarding effects of <b>THC</b> and the <strong>fatty acid amide hydrolase</strong> inhibitor, URB597, as it has been shown to enhance their anxiolytic effects.
+FAAH1	drug	cannabinoid	28749428	<b>Cannabinoid</b> Receptor 1 and <strong>Fatty Acid Amide Hydrolase</strong> Contribute to Operant Sensation Seeking in Mice.
+FAAH1	addiction	relapse	28749428	Cannabinoid Receptor 1 and <strong>Fatty Acid Amide Hydrolase</strong> Contribute to Operant Sensation <b>Seeking</b> in Mice.
+FAAH1	addiction	reward	28749428	Cannabinoid Receptor 1 and <strong>Fatty Acid Amide Hydrolase</strong> Contribute to <b>Operant</b> Sensation Seeking in Mice.
+FAAH1	drug	cannabinoid	28749428	The purpose of the studies in this report was to begin to explore the role of <b>endocannabinoid</b> signaling in OSS utilizing <b>cannabinoid</b> receptor 1 (CB1R) and <strong>fatty acid amide hydrolase</strong> (FAAH) knock out mice.
+FAAH1	drug	nicotine	28660730	<strong>Fatty acid amide hydrolase</strong> (FAAH) inactivation confers enhanced sensitivity to <b>nicotine</b> induced dopamine release in the mouse nucleus accumbens.
+FAAH1	drug	cannabinoid	28660730	<strong>Fatty acid amide hydrolase</strong> (FAAH) is the main enzyme responsible for the degradation of the <b>endocannabinoid</b> anandamide and other non <b>cannabinoid</b> N <b>acylethanolamines</b>.
+FAAH1	drug	cannabinoid	28570479	Since there is growing evidence that increasing local levels of <b>endocannabinoids</b> can decrease hyperalgesia, we examined the effects of URB597, a <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor, which blocks the hydrolysis of the endogenous <b>cannabinoid</b> anandamide, on hyperalgesia and sensitization of cutaneous nociceptors in a humanized mouse model of SCD.
+FAAH1	addiction	sensitization	28570479	Since there is growing evidence that increasing local levels of endocannabinoids can decrease hyperalgesia, we examined the effects of URB597, a <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor, which blocks the hydrolysis of the endogenous cannabinoid anandamide, on hyperalgesia and <b>sensitization</b> of cutaneous nociceptors in a humanized mouse model of SCD.
+FAAH1	drug	cannabinoid	28192193	We found that expression of morphine CPP was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (<strong>fatty acid amide hydrolase</strong> [FAAH] and monoacylglycerol lipase [MAGL], respectively), but with reductions in <b>cannabinoid</b> 1 receptors (CB1R) and CB2R in dorsal hippocampus following the expression of CPP.
+FAAH1	drug	opioid	28192193	We found that expression of <b>morphine</b> CPP was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (<strong>fatty acid amide hydrolase</strong> [FAAH] and monoacylglycerol lipase [MAGL], respectively), but with reductions in cannabinoid 1 receptors (CB1R) and CB2R in dorsal hippocampus following the expression of CPP.
+FAAH1	addiction	reward	28192193	We found that expression of morphine <b>CPP</b> was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (<strong>fatty acid amide hydrolase</strong> [FAAH] and monoacylglycerol lipase [MAGL], respectively), but with reductions in cannabinoid 1 receptors (CB1R) and CB2R in dorsal hippocampus following the expression of <b>CPP</b>.
+FAAH1	drug	alcohol	28150397	Severity of <b>alcohol</b> dependence is associated with the <strong>fatty acid amide hydrolase</strong> Pro129Thr missense variant.
+FAAH1	addiction	dependence	28150397	Severity of alcohol <b>dependence</b> is associated with the <strong>fatty acid amide hydrolase</strong> Pro129Thr missense variant.
+FAAH1	drug	cannabinoid	28150397	One of the two main <b>endocannabinoid</b> neurotransmitters, anandamide, is metabolized by <strong>fatty acid amide hydrolase</strong>, an enzyme with a functional genetic polymorphism (FAAH Pro129Thr, rs324420).
+FAAH1	drug	cannabinoid	27890700	Biochanin A, a soy isoflavone, has a naturally occurring inhibitor of <strong>fatty acid amide hydrolase</strong> (FAAH) that metabolized <b>endocannabinoids</b>.
+FAAH1	drug	cannabinoid	27890602	Inhibitors of the primary <b>endocannabinoid</b> catabolic enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL) show opioid sparing effects in preclinical models of pain.
+FAAH1	drug	opioid	27890602	Inhibitors of the primary endocannabinoid catabolic enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL) show <b>opioid</b> sparing effects in preclinical models of pain.
+FAAH1	drug	nicotine	27737788	Acute inhibition of anandamide (AEA) degradation efficiently reduces <b>nicotine</b> withdrawal induced affective symptoms in rats and <strong>fatty acid amide hydrolase</strong> (FAAH), the degradation enzyme of AEA, has been proposed as a possible treatment against <b>nicotine</b> addiction.
+FAAH1	addiction	addiction	27737788	Acute inhibition of anandamide (AEA) degradation efficiently reduces nicotine withdrawal induced affective symptoms in rats and <strong>fatty acid amide hydrolase</strong> (FAAH), the degradation enzyme of AEA, has been proposed as a possible treatment against nicotine <b>addiction</b>.
+FAAH1	addiction	withdrawal	27737788	Acute inhibition of anandamide (AEA) degradation efficiently reduces nicotine <b>withdrawal</b> induced affective symptoms in rats and <strong>fatty acid amide hydrolase</strong> (FAAH), the degradation enzyme of AEA, has been proposed as a possible treatment against nicotine addiction.
+FAAH1	drug	cannabinoid	27345297	<strong>Fatty Acid Amide Hydrolase</strong> Binding in Brain of <b>Cannabis</b> Users: Imaging With the Novel Radiotracer [11C]CURB.
+FAAH1	drug	cannabinoid	27345297	One of the major mechanisms for terminating the actions of the <b>endocannabinoid</b> anandamide is hydrolysis by <strong>fatty acid amide hydrolase</strong> (FAAH), and inhibitors of the enzyme were suggested as potential treatment for human <b>cannabis</b> dependence.
+FAAH1	addiction	dependence	27345297	One of the major mechanisms for terminating the actions of the endocannabinoid anandamide is hydrolysis by <strong>fatty acid amide hydrolase</strong> (FAAH), and inhibitors of the enzyme were suggested as potential treatment for human cannabis <b>dependence</b>.
+FAAH1	drug	cannabinoid	27178246	<strong>Fatty acid amide hydrolase</strong> (FAAH) is the major enzyme responsible for degradation of anandamide, an <b>endocannabinoid</b>.
+FAAH1	drug	alcohol	27150075	As endocannabinoids may protect the immature PFC from the harmful effects of high doses of <b>alcohol</b>, this study investigated the effect of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 on oxidative stress induced by acute or chronic binge <b>alcohol</b> intake in adolescent rats.
+FAAH1	drug	cannabinoid	27150075	As <b>endocannabinoids</b> may protect the immature PFC from the harmful effects of high doses of alcohol, this study investigated the effect of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 on oxidative stress induced by acute or chronic binge alcohol intake in adolescent rats.
+FAAH1	addiction	intoxication	27150075	As endocannabinoids may protect the immature PFC from the harmful effects of high doses of alcohol, this study investigated the effect of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 on oxidative stress induced by acute or chronic <b>binge</b> alcohol intake in adolescent rats.
+FAAH1	drug	cannabinoid	27092087	Recent research on the natural lipid ligands of <b>cannabinoid</b> receptors, also known as <b>endocannabinoids</b>, has shed light on the mechanisms of intracellular transport of the <b>endocannabinoid</b> anandamide by fatty acid binding proteins (FABPs) and subsequent catabolism by <strong>fatty acid amide hydrolase</strong>.
+FAAH1	drug	cannabinoid	27091613	The <strong>fatty acid amide hydrolase</strong> inhibitor, URB597, an <b>endocannabinoid</b> enhancing drug, reverses social withdrawal in the sub chronic PCP rat model of schizophrenia, but reduces social interaction (SI) in controls.
+FAAH1	addiction	withdrawal	27091613	The <strong>fatty acid amide hydrolase</strong> inhibitor, URB597, an endocannabinoid enhancing drug, reverses social <b>withdrawal</b> in the sub chronic PCP rat model of schizophrenia, but reduces social interaction (SI) in controls.
+FAAH1	drug	cannabinoid	26864774	The <b>endocannabinoid</b> system is composed of <b>endocannabinoids</b> (such as anandamide), their target receptors (CB1 and CB2 receptors, CB1Rs and CB2Rs), the enzymes that degrade them (<strong>fatty acid amide hydrolase</strong> (FAAH) for anandamide), and an <b>endocannabinoid</b> transporter.
+FAAH1	drug	alcohol	26857901	Involvement of Endocannabinoids in <b>Alcohol</b> "Binge" Drinking: Studies of Mice with Human <strong>Fatty Acid Amide Hydrolase</strong> Genetic Variation and After CB1 Receptor Antagonists.
+FAAH1	drug	cannabinoid	26857901	Involvement of <b>Endocannabinoids</b> in Alcohol "Binge" Drinking: Studies of Mice with Human <strong>Fatty Acid Amide Hydrolase</strong> Genetic Variation and After CB1 Receptor Antagonists.
+FAAH1	addiction	intoxication	26857901	Involvement of Endocannabinoids in Alcohol "<b>Binge</b>" Drinking: Studies of Mice with Human <strong>Fatty Acid Amide Hydrolase</strong> Genetic Variation and After CB1 Receptor Antagonists.
+FAAH1	drug	alcohol	26857901	Inhibition or genetic deletion of <strong>fatty acid amide hydrolase</strong> (FAAH; a key catabolic enzyme for endocannabinoids) leads to increased <b>alcohol</b> consumption and preference in rodent models.
+FAAH1	drug	cannabinoid	26857901	Inhibition or genetic deletion of <strong>fatty acid amide hydrolase</strong> (FAAH; a key catabolic enzyme for <b>endocannabinoids</b>) leads to increased alcohol consumption and preference in rodent models.
+FAAH1	drug	cannabinoid	26811312	These changes resulted in an overall decrease in <b>endocannabinoid</b> synthesis/degradation ratios, especially NAPE PLD/<strong>fatty acid amide hydrolase</strong> and DAGLα/monoacylglycerol lipase, suggesting a reduced <b>endocannabinoid</b> production associated with a compensatory up regulation of CB1 receptor.
+FAAH1	addiction	reward	26803499	Moreover, the <b>reinforcing</b> effects of AM404 were potentiated by the treatment with the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 (0.3 mg/kg) suggesting a major role of anandamide in these effects.
+FAAH1	drug	cannabinoid	26505525	<strong>Fatty acid amide hydrolase</strong> (FAAH) is one of the principle enzymes for metabolizing endogenous <b>cannabinoid</b> neurotransmitters such as anandamide, and thus regulates <b>endocannabinoid</b> (eCB) signaling.
+FAAH1	drug	cannabinoid	26490035	There are two main <b>endocannabinoids</b>: anandamide degraded by <strong>fatty acid amide hydrolase</strong> (FAAH) and 2 arachidonoylglycerol (2 AG) degraded by monoacylglycerol lipase (MAGL).
+FAAH1	drug	alcohol	26483633	We evaluated the protective effects of the selective CB1 receptor agonist ACEA, the selective CB2 receptor agonist JWH133 and the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597, which enhances endocannabinoid receptor activity, on NPC proliferation in rats with forced consumption of <b>ethanol</b> (10%) or sucrose liquid diets for 2 weeks.
+FAAH1	drug	cannabinoid	26483633	We evaluated the protective effects of the selective CB1 receptor agonist ACEA, the selective CB2 receptor agonist JWH133 and the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597, which enhances <b>endocannabinoid</b> receptor activity, on NPC proliferation in rats with forced consumption of ethanol (10%) or sucrose liquid diets for 2 weeks.
+FAAH1	drug	opioid	26274041	<strong>Fatty acid amide hydrolase</strong> inhibitor URB597 prevented tolerance and cognitive deficits induced by chronic <b>morphine</b> administration in rats.
+FAAH1	drug	cannabinoid	26274041	Inhibitors of the <b>endocannabinoid</b> metabolic enzyme <strong>fatty acid amide hydrolase</strong> exert therapeutic effects, but might also be associated with some of the adverse effects of <b>cannabis</b>.
+FAAH1	addiction	dependence	26274041	However, at least one <strong>fatty acid amide hydrolase</strong> inhibitor, URB597, has beneficial effects without signs of abuse or <b>dependence</b>.
+FAAH1	drug	cannabinoid	25933444	Thus, we hypothesized that inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the main enzyme responsible for terminating the actions of the <b>endocannabinoid</b> anandamide, reduces seizures and cell death in the hippocampus in a model of cocaine intoxication.
+FAAH1	drug	cocaine	25933444	Thus, we hypothesized that inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the main enzyme responsible for terminating the actions of the endocannabinoid anandamide, reduces seizures and cell death in the hippocampus in a model of <b>cocaine</b> intoxication.
+FAAH1	addiction	intoxication	25933444	Thus, we hypothesized that inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the main enzyme responsible for terminating the actions of the endocannabinoid anandamide, reduces seizures and cell death in the hippocampus in a model of cocaine <b>intoxication</b>.
+FAAH1	drug	nicotine	25754762	Effects of <strong>Fatty Acid Amide Hydrolase</strong> (FAAH) Inhibitors in Non Human Primate Models of <b>Nicotine</b> Reward and Relapse.
+FAAH1	addiction	relapse	25754762	Effects of <strong>Fatty Acid Amide Hydrolase</strong> (FAAH) Inhibitors in Non Human Primate Models of Nicotine Reward and <b>Relapse</b>.
+FAAH1	addiction	reward	25754762	Effects of <strong>Fatty Acid Amide Hydrolase</strong> (FAAH) Inhibitors in Non Human Primate Models of Nicotine <b>Reward</b> and Relapse.
+FAAH1	drug	nicotine	25754762	Inhibition of the enzyme <strong>fatty acid amide hydrolase</strong> (FAAH) counteracts reward related effects of <b>nicotine</b> in rats, but it has not been tested for this purpose in non human primates.
+FAAH1	addiction	reward	25754762	Inhibition of the enzyme <strong>fatty acid amide hydrolase</strong> (FAAH) counteracts <b>reward</b> related effects of nicotine in rats, but it has not been tested for this purpose in non human primates.
+FAAH1	drug	cannabinoid	25539508	In addition, acute cocaine administration (10 mg/kg) in cocaine sensitized mice (referred to as cocaine priming) induced a selective increase in the <b>endocannabinoid</b> degrading enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL).
+FAAH1	drug	cocaine	25539508	In addition, acute <b>cocaine</b> administration (10 mg/kg) in <b>cocaine</b> sensitized mice (referred to as <b>cocaine</b> priming) induced a selective increase in the endocannabinoid degrading enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL).
+FAAH1	drug	cocaine	25522382	Here, we investigated whether chronic administration during a period of withdrawal of the <strong>fatty acid amide hydrolase</strong> inhibitor URB597, which increases anandamide levels, would decrease the risks of relapse to <b>cocaine</b> seeking.
+FAAH1	addiction	relapse	25522382	Here, we investigated whether chronic administration during a period of withdrawal of the <strong>fatty acid amide hydrolase</strong> inhibitor URB597, which increases anandamide levels, would decrease the risks of <b>relapse</b> to cocaine <b>seeking</b>.
+FAAH1	addiction	withdrawal	25522382	Here, we investigated whether chronic administration during a period of <b>withdrawal</b> of the <strong>fatty acid amide hydrolase</strong> inhibitor URB597, which increases anandamide levels, would decrease the risks of relapse to cocaine seeking.
+FAAH1	drug	cannabinoid	25505113	In this study we determined whether inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), which slows the breakdown of the <b>endocannabinoid</b> anandamide (AEA), reduced sensitization of nociceptors produced by chemotherapy.
+FAAH1	addiction	sensitization	25505113	In this study we determined whether inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), which slows the breakdown of the endocannabinoid anandamide (AEA), reduced <b>sensitization</b> of nociceptors produced by chemotherapy.
+FAAH1	drug	cannabinoid	25479915	Inhibition of <b>endocannabinoid</b> catabolic enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and/or monoacylglycerol lipase (MAGL) reduces somatic morphine withdrawal signs, but its effects on aversive aspects of withdrawal are unknown.
+FAAH1	drug	opioid	25479915	Inhibition of endocannabinoid catabolic enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and/or monoacylglycerol lipase (MAGL) reduces somatic <b>morphine</b> withdrawal signs, but its effects on aversive aspects of withdrawal are unknown.
+FAAH1	addiction	aversion	25479915	Inhibition of endocannabinoid catabolic enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and/or monoacylglycerol lipase (MAGL) reduces somatic morphine withdrawal signs, but its effects on <b>aversive</b> aspects of withdrawal are unknown.
+FAAH1	addiction	withdrawal	25479915	Inhibition of endocannabinoid catabolic enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and/or monoacylglycerol lipase (MAGL) reduces somatic morphine <b>withdrawal</b> signs, but its effects on aversive aspects of <b>withdrawal</b> are unknown.
+FAAH1	drug	cannabinoid	25435020	Disease modifying functions may also complement analgesic and anti spastic effects of <b>cannabis</b>, its constituents, and of '<b>endocannabinoid</b> enhancing' drugs or nutricals like inhibitors of <strong>fatty acid amide hydrolase</strong>.
+FAAH1	drug	cannabinoid	25398241	In this study, we investigated the impact of <b>THC</b> and inhibitors of the <b>endocannabinoid</b> hydrolytic enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL) on operant responding for electrical stimulation of the medial forebrain bundle [intracranial self stimulation (ICSS)], which is known to activate the mesolimbic dopamine system.
+FAAH1	addiction	reward	25398241	In this study, we investigated the impact of THC and inhibitors of the endocannabinoid hydrolytic enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL) on <b>operant</b> responding for electrical stimulation of the medial forebrain bundle [intracranial self stimulation (<b>ICSS</b>)], which is known to activate the mesolimbic dopamine system.
+FAAH1	drug	opioid	25395060	We demonstrated that the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597, which increases eCB levels, facilitates extinction of a <b>naloxone</b> precipitated <b>morphine</b> withdrawal induced conditioned place aversion (CPA).
+FAAH1	addiction	aversion	25395060	We demonstrated that the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597, which increases eCB levels, facilitates extinction of a naloxone precipitated morphine withdrawal induced conditioned place <b>aversion</b> (CPA).
+FAAH1	addiction	withdrawal	25395060	We demonstrated that the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597, which increases eCB levels, facilitates extinction of a naloxone precipitated morphine <b>withdrawal</b> induced conditioned place aversion (CPA).
+FAAH1	drug	cannabinoid	25369747	We highlight the potential of selective inhibitors of <b>endocannabinoid</b> metabolism, directed at <strong>fatty acid amide hydrolase</strong> and monoacylglycerol lipase, to reduce anxiety and stress responses, and discuss novel mechanisms underlying the modulation of the <b>endocannabinoid</b> system, including the attenuation of impulsivity, anxiety, and drug reward by selective CB2 receptor agonists.
+FAAH1	addiction	reward	25369747	We highlight the potential of selective inhibitors of endocannabinoid metabolism, directed at <strong>fatty acid amide hydrolase</strong> and monoacylglycerol lipase, to reduce anxiety and stress responses, and discuss novel mechanisms underlying the modulation of the endocannabinoid system, including the attenuation of impulsivity, anxiety, and drug <b>reward</b> by selective CB2 receptor agonists.
+FAAH1	drug	cannabinoid	25273322	<strong>Fatty acid amide hydrolase</strong> (FAAH), a catabolic enzyme which regulates lipid transmitters in the <b>endocannabinoid</b> system, is an avidly sought therapeutic and positron emission tomography (PET) imaging target for studies involving addiction and neurological disorders.
+FAAH1	addiction	addiction	25273322	<strong>Fatty acid amide hydrolase</strong> (FAAH), a catabolic enzyme which regulates lipid transmitters in the endocannabinoid system, is an avidly sought therapeutic and positron emission tomography (PET) imaging target for studies involving <b>addiction</b> and neurological disorders.
+FAAH1	drug	cannabinoid	25260980	One enzyme responsible for <b>endocannabinoid</b> breakdown is <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	addiction	withdrawal	25260980	In addition to the anti inflammatory effects of URB597, <strong>fatty acid amide hydrolase</strong> (FAAH) inhibition improved both hindlimb weight bearing and von Frey hair <b>withdrawal</b> thresholds.
+FAAH1	drug	cannabinoid	25258021	While blockade of <strong>fatty acid amide hydrolase</strong>, the primary catabolic enzyme of the <b>endocannabinoid</b> arachidonoylethanolamine (anandamide), exacerbates withdrawal responses in nicotine dependent mice, the role of monoacylglycerol lipase (MAGL), the main hydrolytic enzyme of a second <b>endocannabinoid</b> 2 arachidonylglycerol (2 AG), in nicotine withdrawal remains unexplored.
+FAAH1	drug	nicotine	25258021	While blockade of <strong>fatty acid amide hydrolase</strong>, the primary catabolic enzyme of the endocannabinoid arachidonoylethanolamine (anandamide), exacerbates withdrawal responses in <b>nicotine</b> dependent mice, the role of monoacylglycerol lipase (MAGL), the main hydrolytic enzyme of a second endocannabinoid 2 arachidonylglycerol (2 AG), in <b>nicotine</b> withdrawal remains unexplored.
+FAAH1	addiction	withdrawal	25258021	While blockade of <strong>fatty acid amide hydrolase</strong>, the primary catabolic enzyme of the endocannabinoid arachidonoylethanolamine (anandamide), exacerbates <b>withdrawal</b> responses in nicotine dependent mice, the role of monoacylglycerol lipase (MAGL), the main hydrolytic enzyme of a second endocannabinoid 2 arachidonylglycerol (2 AG), in nicotine <b>withdrawal</b> remains unexplored.
+FAAH1	drug	cannabinoid	25083569	The <b>endocannabinoid</b> system comprises the CB1 and CB2 receptors (the targets of the <b>Cannabis</b> sativa compound delta 9 <b>tetrahydrocannabinol</b>), the endogenous ligands (<b>endocannabinoids</b>) arachidonoyl ethanolamide (anandamide) and 2 arachidonoyl glycerol, their synthesizing machinery and membrane transport system, and the hydrolyzing enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL), respectively.
+FAAH1	drug	cannabinoid	25077173	The functional c.385C>A single nucleotide polymorphism (SNP) in the <strong>fatty acid amide hydrolase</strong> (FAAH) gene, one of the major degrading enzymes of <b>endocannabinoids</b>, is reportedly associated with anorexia nervosa (AN).
+FAAH1	drug	alcohol	25041461	The aim of the present study was to assess the state of the CB1 receptor, the enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL), and the extracellular signal regulated kinase (ERK) and cyclic AMP response element binding protein (CREB) in the post mortem prefrontal cortex of <b>alcoholic</b> subjects.
+FAAH1	drug	cannabinoid	24849924	Prolonged monoacylglycerol lipase blockade causes equivalent <b>cannabinoid</b> receptor type 1 receptor mediated adaptations in <strong>fatty acid amide hydrolase</strong> wild type and knockout mice.
+FAAH1	drug	cannabinoid	24849924	Complementary genetic and pharmacological approaches to inhibit monoacylglycerol lipase (MAGL) and <strong>fatty acid amide hydrolase</strong> (FAAH), the primary hydrolytic enzymes of the respective endogenous <b>cannabinoids</b> 2 arachidonoylglycerol (2 AG) and N arachidonoylethanolamine, enable the exploration of potential therapeutic applications and physiologic roles of these enzymes.
+FAAH1	drug	cannabinoid	24788435	Increasing the <b>endocannabinoid</b> anandamide and other fatty acid amides (FAA) by blocking <strong>fatty acid amide hydrolase</strong> (FAAH) has been shown to be antinociceptive in a number of animal models of chronic pain.
+FAAH1	drug	cannabinoid	24583930	<strong>Fatty acid amide hydrolase</strong> (FAAH) inhibitors increase physiological levels of the <b>endocannabinoid</b> anandamide, which may confer improved efficacy and safety relative to direct CBR agonists.
+FAAH1	drug	alcohol	24407958	Risky <b>alcohol</b> consumption in young people is associated with the <strong>fatty acid amide hydrolase</strong> gene polymorphism C385A and affective rating of drug pictures.
+FAAH1	drug	cannabinoid	24247477	Immediately after the memory reactivation session, independent groups of morphine trained rats received a single subcutaneous injection of different doses of <b>cannabinoid</b> CB1 receptor antagonist <b>rimonabant</b>, CB2 selective antagonist AM630, potent CB1/CB2 agonist WIN 55,212 2, inhibitor of enzyme <strong>fatty acid amide hydrolase</strong> URB597, or vehicle.
+FAAH1	drug	opioid	24247477	Immediately after the memory reactivation session, independent groups of <b>morphine</b> trained rats received a single subcutaneous injection of different doses of cannabinoid CB1 receptor antagonist rimonabant, CB2 selective antagonist AM630, potent CB1/CB2 agonist WIN 55,212 2, inhibitor of enzyme <strong>fatty acid amide hydrolase</strong> URB597, or vehicle.
+FAAH1	drug	cannabinoid	24042479	To further understand the human implications of the interaction between these two systems, we investigated the role of the common, functional missense variant Pro129Thr of the gene coding <strong>fatty acid amide hydrolase</strong> (FAAH), the major degrading enzyme of <b>endocannabinoids</b>, on psychophysical and neurotransmitter (dopaminergic, opioid) responses to pain and placebo induced analgesia in humans.
+FAAH1	drug	opioid	24042479	To further understand the human implications of the interaction between these two systems, we investigated the role of the common, functional missense variant Pro129Thr of the gene coding <strong>fatty acid amide hydrolase</strong> (FAAH), the major degrading enzyme of endocannabinoids, on psychophysical and neurotransmitter (dopaminergic, <b>opioid</b>) responses to pain and placebo induced analgesia in humans.
+FAAH1	drug	cannabinoid	23910902	Further, both behavioral and neurochemical cocaine sensitization were facilitated by pharmacological blockade of <b>endocannabinoid</b> metabolism, achieved by inhibiting the <strong>fatty acid amide hydrolase</strong> enzyme.
+FAAH1	drug	cocaine	23910902	Further, both behavioral and neurochemical <b>cocaine</b> sensitization were facilitated by pharmacological blockade of endocannabinoid metabolism, achieved by inhibiting the <strong>fatty acid amide hydrolase</strong> enzyme.
+FAAH1	addiction	sensitization	23910902	Further, both behavioral and neurochemical cocaine <b>sensitization</b> were facilitated by pharmacological blockade of endocannabinoid metabolism, achieved by inhibiting the <strong>fatty acid amide hydrolase</strong> enzyme.
+FAAH1	drug	cannabinoid	23829360	Elements of the ECS, such as <strong>fatty acid amide hydrolase</strong> or the <b>cannabinoid</b> receptors are now considered as promising pharmacological targets for some diseases.
+FAAH1	drug	cannabinoid	23731552	<strong>Fatty acid amide hydrolase</strong> (FAAH) has a significant role in regulating <b>endocannabinoid</b> signaling in the central nervous system.
+FAAH1	drug	cannabinoid	23712084	<strong>Fatty acid amide hydrolase</strong> (FAAH), the enzyme responsible for terminating signaling by the <b>endocannabinoid</b> anandamide, plays an important role in the <b>endocannabinoid</b> system, and FAAH inhibitors are attractive drugs for pain, addiction, and neurological disorders.
+FAAH1	addiction	addiction	23712084	<strong>Fatty acid amide hydrolase</strong> (FAAH), the enzyme responsible for terminating signaling by the endocannabinoid anandamide, plays an important role in the endocannabinoid system, and FAAH inhibitors are attractive drugs for pain, <b>addiction</b>, and neurological disorders.
+FAAH1	drug	cannabinoid	23643692	Furthermore, tissue levels of the <strong>fatty acid amide hydrolase</strong> substrates, AEA, <b>oleoylethanolamide</b> and <b>palmitoylethanolamide</b>, were higher in the hippocampus of VPA exposed rats immediately following social exposure.
+FAAH1	addiction	withdrawal	23587012	Finally, consistent with the behavioral and pharmacological observations, <b>withdrawal</b> from the palatable diet decreased the gene expression of the enzyme <strong>fatty acid amide hydrolase</strong> in the ventromedial hypothalamus while increasing that of CB1 receptors in the dorsal striatum in Chow/Palatable rats, compared to controls.
+FAAH1	drug	cannabinoid	23333350	Inhibitors of <strong>fatty acid amide hydrolase</strong> (FAAH) prevent the breakdown of endogenous ligands for <b>cannabinoid</b> receptors and peroxisome proliferator activated receptors (PPAR), prolonging and enhancing the effects of these ligands when they are naturally released.
+FAAH1	drug	cannabinoid	23303065	Inhibition of the <b>endocannabinoid</b> catabolic enzymes, monoacylglycerol lipase (MAGL) or <strong>fatty acid amide hydrolase</strong> (FAAH) attenuates naloxone precipitated opioid withdrawal signs in mice via activation of CB1 receptors.
+FAAH1	drug	opioid	23303065	Inhibition of the endocannabinoid catabolic enzymes, monoacylglycerol lipase (MAGL) or <strong>fatty acid amide hydrolase</strong> (FAAH) attenuates <b>naloxone</b> precipitated <b>opioid</b> withdrawal signs in mice via activation of CB1 receptors.
+FAAH1	addiction	withdrawal	23303065	Inhibition of the endocannabinoid catabolic enzymes, monoacylglycerol lipase (MAGL) or <strong>fatty acid amide hydrolase</strong> (FAAH) attenuates naloxone precipitated opioid <b>withdrawal</b> signs in mice via activation of CB1 receptors.
+FAAH1	drug	nicotine	23169348	<b>Nicotine</b> exposure had no effect on <strong>fatty acid amide hydrolase</strong> activity in the VTA, suggesting that changes in AEA and OEA signaling result from alterations in their <b>nicotine</b> induced biosynthesis.
+FAAH1	drug	cannabinoid	23072421	The <b>cannabinoid</b> CB₁/CB₂ receptor agonist Δ⁹ <b>tetrahydrocannabinol</b> significantly increased margarine intake selectively in LR rats, while the <strong>fatty acid amide hydrolase</strong> inhibitor URB597 showed no effect.
+FAAH1	drug	cannabinoid	22987804	<strong>Fatty acid amide hydrolase</strong> (FAAH) regulates tissue concentrations of N <b>acylethanolamines</b> (NAEs), including the <b>endocannabinoid</b>, N arachidonylethanolamide (anandamide, AEA).
+FAAH1	addiction	reward	22776995	Investigating emotional motivational dysfunctions as underlying mechanisms, a study in humans revealed that in the C385A polymorphism of the <strong>fatty acid amide hydrolase</strong> (FAAH), the degrading enzyme of the eCB anandamide (AEA), A carriers, who are characterized by increased signaling of AEA as compared to C/C carriers, exhibited reduced brain reactivity towards unpleasant faces and enhanced reactivity towards <b>reward</b>.
+FAAH1	drug	nicotine	22705310	The role of <strong>fatty acid amide hydrolase</strong> inhibition in <b>nicotine</b> reward and dependence.
+FAAH1	addiction	dependence	22705310	The role of <strong>fatty acid amide hydrolase</strong> inhibition in nicotine reward and <b>dependence</b>.
+FAAH1	addiction	reward	22705310	The role of <strong>fatty acid amide hydrolase</strong> inhibition in nicotine <b>reward</b> and dependence.
+FAAH1	drug	cannabinoid	22705310	The endogenous <b>cannabinoid</b> anandamide (AEA) exerts the majority of its effects at CB1 and CB2 receptors and is degraded by <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	drug	cannabinoid	22670561	We used the temporal summation threshold of the nociceptive withdrawal reflex to explore the spinal cord pain processing, and the platelet activity of the enzyme <strong>fatty acid amide hydrolase</strong> to detect the functional state of the <b>endocannabinoid</b> system in 27 medication overuse headache subjects before and 10 and 60 days after a standard withdrawal treatment and compared results with those of 14 controls.
+FAAH1	addiction	withdrawal	22670561	We used the temporal summation threshold of the nociceptive <b>withdrawal</b> reflex to explore the spinal cord pain processing, and the platelet activity of the enzyme <strong>fatty acid amide hydrolase</strong> to detect the functional state of the endocannabinoid system in 27 medication overuse headache subjects before and 10 and 60 days after a standard <b>withdrawal</b> treatment and compared results with those of 14 controls.
+FAAH1	addiction	withdrawal	22670561	A significant <strong>fatty acid amide hydrolase</strong> activity reduction coupled with a significant improvement (reduction) in facilitation of spinal cord pain processing (increase in temporal summation threshold and reduction in related pain sensation) was found in medication overuse headache subjects at both 10 and 60 days after <b>withdrawal</b> treatment when compared with medication overuse headache subjects before <b>withdrawal</b> treatment.
+FAAH1	drug	cannabinoid	22670561	Furthermore, the acute reduction of the <strong>fatty acid amide hydrolase</strong> activity coupled with a reduction of the facilitation in pain processing immediately (10 days) after withdrawal treatment and its persistence 60 days after withdrawal treatment could represent the consequence of a mechanism devoted to acutely reduce the degradation of <b>endocannabinoids</b> and aimed to increase the activity of the <b>endocannabinoid</b> system that results in an antinociceptive effect.
+FAAH1	addiction	withdrawal	22670561	Furthermore, the acute reduction of the <strong>fatty acid amide hydrolase</strong> activity coupled with a reduction of the facilitation in pain processing immediately (10 days) after <b>withdrawal</b> treatment and its persistence 60 days after <b>withdrawal</b> treatment could represent the consequence of a mechanism devoted to acutely reduce the degradation of endocannabinoids and aimed to increase the activity of the endocannabinoid system that results in an antinociceptive effect.
+FAAH1	drug	cannabinoid	22647577	We analysed the effects of inhibition of the two main <b>endocannabinoid</b> degradation enzymes: <strong>fatty acid amide hydrolase</strong> (FAAH), using inhibitor URB597 (1 mg/kg); monoacylglycerol lipase (MAGL), using inhibitor URB602 (10 mg/kg).
+FAAH1	drug	cannabinoid	22242687	Changes of blood <b>endocannabinoids</b> during anaesthesia: a special case for <strong>fatty acid amide hydrolase</strong> inhibition by propofol?
+FAAH1	drug	cannabinoid	22133920	<strong>Fatty acid amide hydrolase</strong> (FAAH) is an enzyme that metabolizes <b>endocannabinoids</b> and fatty acid amides possibly linked to activation of the opioid system.
+FAAH1	drug	opioid	22133920	<strong>Fatty acid amide hydrolase</strong> (FAAH) is an enzyme that metabolizes endocannabinoids and fatty acid amides possibly linked to activation of the <b>opioid</b> system.
+FAAH1	drug	cannabinoid	21937688	The <b>cannabinoid</b> receptor (CNR1) and the <strong>fatty acid amide hydrolase</strong> (FAAH) genes are located on chromosomes 6 and 1 in the 6q15 and 1p33 cytogenetic bands, respectively.
+FAAH1	drug	cannabinoid	21926424	We investigated the effects of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597, which inhibits the catabolism of the <b>endocannabinoid</b> anandamide and related N <b>acylethanolamines</b>, on expression of FCA and fear and pain related behaviour per se in rats.
+FAAH1	drug	opioid	21763761	Behavioral effects of <strong>fatty acid amide hydrolase</strong> inhibition on <b>morphine</b> withdrawal symptoms.
+FAAH1	addiction	withdrawal	21763761	Behavioral effects of <strong>fatty acid amide hydrolase</strong> inhibition on morphine <b>withdrawal</b> symptoms.
+FAAH1	drug	cannabinoid	21763761	The present study examined whether augmentation of the <b>endocannabinoid</b> system by inhibition of <strong>fatty acid amide hydrolase</strong> could suppress the morphine withdrawal syndrome in morphine addicted rats.
+FAAH1	drug	opioid	21763761	The present study examined whether augmentation of the endocannabinoid system by inhibition of <strong>fatty acid amide hydrolase</strong> could suppress the <b>morphine</b> withdrawal syndrome in <b>morphine</b> addicted rats.
+FAAH1	addiction	withdrawal	21763761	The present study examined whether augmentation of the endocannabinoid system by inhibition of <strong>fatty acid amide hydrolase</strong> could suppress the morphine <b>withdrawal</b> syndrome in morphine addicted rats.
+FAAH1	drug	opioid	21763761	The <b>morphine</b> addicted rats received URB597 (1, 0.5, 0.3, 0.1, 0.03 mg/kg), a <strong>fatty acid amide hydrolase</strong> inhibitor, before the precipitation of <b>morphine</b> withdrawal syndromes by <b>naloxone</b>.
+FAAH1	addiction	withdrawal	21763761	The morphine addicted rats received URB597 (1, 0.5, 0.3, 0.1, 0.03 mg/kg), a <strong>fatty acid amide hydrolase</strong> inhibitor, before the precipitation of morphine <b>withdrawal</b> syndromes by naloxone.
+FAAH1	drug	cannabinoid	21719468	The endogenous <b>cannabinoids</b>, N arachidonoylethanolamine (anandamide; AEA) and 2 arachidonylglycerol (2 AG), activate both <b>cannabinoid</b> receptors but are rapidly metabolized by <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL), respectively.
+FAAH1	drug	nicotine	21557729	The <strong>fatty acid amide hydrolase</strong> inhibitor URB597 can reverse the abuse related behavioural and neurochemical effects of <b>nicotine</b> in rats.
+FAAH1	drug	cannabinoid	21557729	<strong>Fatty acid amide hydrolase</strong> inhibitors block the degradation (and thereby magnify and prolong the actions) of the <b>endocannabinoid</b> anandamide (AEA), and also the non <b>cannabinoid</b> fatty acid ethanolamides <b>oleoylethanolamide</b> (OEA) and <b>palmitoylethanolamide</b> (PEA).
+FAAH1	drug	cannabinoid	21549765	The results revealed that intracerebroventricular injections of <b>endocannabinoid</b> analogues, anandamide, a CB(1) agonist (AEA: 1 20 μg/mouse); AM404, an anandamide transport inhibitor (0.1 10 μg/mouse); and URB597, a <strong>fatty acid amide hydrolase</strong> inhibitor (0.05 10 μg/mouse) produced antidepressant like effect dose dependently, whereas influenced the MBB in a biphasic manner (produced a U shaped dose response curve).
+FAAH1	drug	cannabinoid	21524266	Recent pre clinical studies suggest the potential of <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitors such as URB597, <b>endocannabinoid</b> metabolizing enzymes, and nicotinic alpha 7 receptor antagonists such as methyllycaconitine (MLA).Controlled clinical trials are needed to evaluate the clinical efficacy of these medications and to validate the laboratory models being used to study candidate medications.
+FAAH1	drug	nicotine	21501143	Recent studies have shown that the inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH) attenuates reinstatement of <b>nicotine</b> seeking induced by <b>nicotine</b> priming and <b>nicotine</b> associated cues.
+FAAH1	addiction	relapse	21501143	Recent studies have shown that the inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH) attenuates <b>reinstatement</b> of nicotine <b>seeking</b> induced by nicotine priming and nicotine associated cues.
+FAAH1	drug	cannabinoid	21419109	Using in situ hybridization, we compared the expression of the <b>cannabinoid</b> receptor CB1, <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MGL) enzymes in brain regions involved in drug addiction in mice reared in either EE or standard environments (SE) from weaning until adulthood.
+FAAH1	addiction	addiction	21419109	Using in situ hybridization, we compared the expression of the cannabinoid receptor CB1, <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MGL) enzymes in brain regions involved in drug <b>addiction</b> in mice reared in either EE or standard environments (SE) from weaning until adulthood.
+FAAH1	drug	cannabinoid	21300050	The endogenous <b>cannabinoid</b> anandamide shares discriminative stimulus effects with ∆(9) <b>tetrahydrocannabinol</b> in <strong>fatty acid amide hydrolase</strong> knockout mice.
+FAAH1	drug	cannabinoid	21300050	Thus, the goals of this study were to establish AEA as a discriminative stimulus in transgenic mice lacking <strong>fatty acid amide hydrolase</strong> (i.e., FAAH  /  mice unable to rapidly metabolize AEA), evaluate whether <b>THC</b> or oleamide, a fatty acid amide, produced AEA like responding, and assess for CB(1) mediation of AEA's discriminative stimulus.
+FAAH1	drug	opioid	21219293	In the skin and peripheral nerves, potential mediator and receptor therapeutic targets include the H4 histamine receptor, protease activated receptor 2, serine proteases, cathepsin S, peripheral mu  and kappa <b>opioid</b> receptors, interleukin 31, transient receptor potential vanilloid 1 and 3, <strong>fatty acid amide hydrolase</strong>, nerve growth factor and its receptor, acetylcholine, and the Mas related G protein coupled receptors.
+FAAH1	drug	nicotine	20801430	Recent findings indicate that inhibitors of <strong>fatty acid amide hydrolase</strong> (FAAH) counteract the rewarding effects of <b>nicotine</b> in rats.
+FAAH1	drug	cannabinoid	20729846	These data contrast with blockade of <strong>fatty acid amide hydrolase</strong>, an enzyme that degrades the other major <b>endocannabinoid</b> anandamide, which produced sustained analgesia without impairing CB1 receptors.
+FAAH1	drug	cannabinoid	20643159	Reducing <b>endocannabinoid</b> metabolism with the <strong>fatty acid amide hydrolase</strong> inhibitor, URB597, fails to modify reinstatement of morphine induced conditioned floor preference and naloxone precipitated morphine withdrawal induced conditioned floor avoidance.
+FAAH1	drug	opioid	20643159	Reducing endocannabinoid metabolism with the <strong>fatty acid amide hydrolase</strong> inhibitor, URB597, fails to modify reinstatement of <b>morphine</b> induced conditioned floor preference and <b>naloxone</b> precipitated <b>morphine</b> withdrawal induced conditioned floor avoidance.
+FAAH1	addiction	relapse	20643159	Reducing endocannabinoid metabolism with the <strong>fatty acid amide hydrolase</strong> inhibitor, URB597, fails to modify <b>reinstatement</b> of morphine induced conditioned floor preference and naloxone precipitated morphine withdrawal induced conditioned floor avoidance.
+FAAH1	addiction	withdrawal	20643159	Reducing endocannabinoid metabolism with the <strong>fatty acid amide hydrolase</strong> inhibitor, URB597, fails to modify reinstatement of morphine induced conditioned floor preference and naloxone precipitated morphine <b>withdrawal</b> induced conditioned floor avoidance.
+FAAH1	drug	opioid	20643159	The potential of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor, URB597, to modify drug prime induced reinstatement of <b>morphine</b> induced conditioned floor preference or <b>naloxone</b> precipitated <b>morphine</b> withdrawal induced conditioned floor avoidance was evaluated.
+FAAH1	addiction	relapse	20643159	The potential of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor, URB597, to modify drug prime induced <b>reinstatement</b> of morphine induced conditioned floor preference or naloxone precipitated morphine withdrawal induced conditioned floor avoidance was evaluated.
+FAAH1	addiction	withdrawal	20643159	The potential of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor, URB597, to modify drug prime induced reinstatement of morphine induced conditioned floor preference or naloxone precipitated morphine <b>withdrawal</b> induced conditioned floor avoidance was evaluated.
+FAAH1	drug	cocaine	20477753	Effects of <strong>fatty acid amide hydrolase</strong> inhibition on neuronal responses to nicotine, <b>cocaine</b> and morphine in the nucleus accumbens shell and ventral tegmental area: involvement of PPAR alpha nuclear receptors.
+FAAH1	drug	nicotine	20477753	Effects of <strong>fatty acid amide hydrolase</strong> inhibition on neuronal responses to <b>nicotine</b>, cocaine and morphine in the nucleus accumbens shell and ventral tegmental area: involvement of PPAR alpha nuclear receptors.
+FAAH1	drug	opioid	20477753	Effects of <strong>fatty acid amide hydrolase</strong> inhibition on neuronal responses to nicotine, cocaine and <b>morphine</b> in the nucleus accumbens shell and ventral tegmental area: involvement of PPAR alpha nuclear receptors.
+FAAH1	drug	cannabinoid	20477753	We recently demonstrated that inhibition by URB597 of <strong>fatty acid amide hydrolase</strong> (FAAH), the main enzyme that degrades the endogenous <b>cannabinoid</b> N acylethanolamine (NAE) anandamide and the endogenous non <b>cannabinoid</b> NAEs <b>oleoylethanolamide</b> and <b>palmitoylethanolamide</b>, blocks nicotine induced excitation of ventral tegmental area (VTA) dopamine (DA) neurons and DA release in the shell of the nucleus accumbens (ShNAc), as well as nicotine induced drug self administration, conditioned place preference and relapse in rats.
+FAAH1	drug	nicotine	20477753	We recently demonstrated that inhibition by URB597 of <strong>fatty acid amide hydrolase</strong> (FAAH), the main enzyme that degrades the endogenous cannabinoid N acylethanolamine (NAE) anandamide and the endogenous non cannabinoid NAEs oleoylethanolamide and palmitoylethanolamide, blocks <b>nicotine</b> induced excitation of ventral tegmental area (VTA) dopamine (DA) neurons and DA release in the shell of the nucleus accumbens (ShNAc), as well as <b>nicotine</b> induced drug self administration, conditioned place preference and relapse in rats.
+FAAH1	addiction	relapse	20477753	We recently demonstrated that inhibition by URB597 of <strong>fatty acid amide hydrolase</strong> (FAAH), the main enzyme that degrades the endogenous cannabinoid N acylethanolamine (NAE) anandamide and the endogenous non cannabinoid NAEs oleoylethanolamide and palmitoylethanolamide, blocks nicotine induced excitation of ventral tegmental area (VTA) dopamine (DA) neurons and DA release in the shell of the nucleus accumbens (ShNAc), as well as nicotine induced drug self administration, conditioned place preference and <b>relapse</b> in rats.
+FAAH1	drug	cannabinoid	20416378	Inhibitors of monoacylglycerol lipase, <strong>fatty acid amide hydrolase</strong> and <b>endocannabinoid</b> transport differentially suppress capsaicin induced behavioral sensitization through peripheral <b>endocannabinoid</b> mechanisms.
+FAAH1	addiction	sensitization	20416378	Inhibitors of monoacylglycerol lipase, <strong>fatty acid amide hydrolase</strong> and endocannabinoid transport differentially suppress capsaicin induced behavioral <b>sensitization</b> through peripheral endocannabinoid mechanisms.
+FAAH1	drug	cannabinoid	20416378	Monoacylglycerol lipase (MGL) and <strong>fatty acid amide hydrolase</strong> (FAAH) degrade the <b>endocannabinoids</b> 2 arachidonoylglycerol (2 AG) and anandamide (AEA), respectively.
+FAAH1	drug	cannabinoid	20357755	However, the consequences of repeated administration of the <b>endocannabinoid</b> N arachidonoyl ethanolamine (anandamide, AEA) on <b>cannabinoid</b> receptor regulation are unclear because of its rapid metabolism by <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	drug	cannabinoid	20179908	Second, inhibition of anandamide degradation by blockade of <strong>fatty acid amide hydrolase</strong> augmented the <b>THC</b> like effects of quinpirole.
+FAAH1	drug	cannabinoid	20029375	<strong>Fatty acid amide hydrolase</strong> (FAAH) is the main degrading enzyme of the fatty acid ethanolamides anandamide (AEA) and <b>oleoylethanolamide</b> (OEA), which have opposite effects on food intake and energy balance.
+FAAH1	drug	alcohol	20015515	Selective alterations of the CB1 receptors and the <strong>fatty acid amide hydrolase</strong> in the ventral striatum of <b>alcoholics</b> and suicides.
+FAAH1	drug	alcohol	20015515	The levels of CB1 receptors, receptor mediated G protein signaling, and activity and level of the <strong>fatty acid amide hydrolase</strong> (FAAH) were analyzed postmortem in the ventral striatum of <b>alcohol</b> dependent nonsuicides (CA, n=9), <b>alcohol</b> dependent suicides (AS, n=9) and nonpsychiatric controls (C, n=9).
+FAAH1	drug	cannabinoid	20010914	Association of polymorphisms of the <b>cannabinoid</b> receptor (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH) genes with heroin addiction: impact of long repeats of CNR1.
+FAAH1	drug	opioid	20010914	Association of polymorphisms of the cannabinoid receptor (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH) genes with <b>heroin</b> addiction: impact of long repeats of CNR1.
+FAAH1	addiction	addiction	20010914	Association of polymorphisms of the cannabinoid receptor (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH) genes with heroin <b>addiction</b>: impact of long repeats of CNR1.
+FAAH1	drug	cannabinoid	20010914	Alterations in expression of a <b>cannabinoid</b> receptor (CNR1, CB1), and of <strong>fatty acid amide hydrolase</strong> (FAAH) that degrades endogenous ligands of CB1, may contribute to the development of addiction.
+FAAH1	addiction	addiction	20010914	Alterations in expression of a cannabinoid receptor (CNR1, CB1), and of <strong>fatty acid amide hydrolase</strong> (FAAH) that degrades endogenous ligands of CB1, may contribute to the development of <b>addiction</b>.
+FAAH1	drug	cannabinoid	20010552	As previous work has highlighted the significance of the <b>cannabinoid</b> receptor 1 (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH) genes with respect to <b>cannabis</b> dependence (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+FAAH1	addiction	dependence	20010552	As previous work has highlighted the significance of the cannabinoid receptor 1 (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH) genes with respect to cannabis <b>dependence</b> (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+FAAH1	drug	cannabinoid	19918051	Why, however, this full spectrum of activities is not observed upon pharmacological inhibition or genetic deletion of either <strong>fatty acid amide hydrolase</strong> (FAAH) or monoacylglycerol lipase (MAGL), enzymes that regulate the two major <b>endocannabinoids</b> anandamide (AEA) and 2 arachidonoylglycerol (2 AG), respectively, has remained unclear.
+FAAH1	drug	amphetamine	19890266	More aroused, less fatigued: <strong>fatty acid amide hydrolase</strong> gene polymorphisms influence acute response to <b>amphetamine</b>.
+FAAH1	drug	amphetamine	19890266	<b>Amphetamine</b>'s effects are known to be modulated by endogenous cannabinoids, which are degraded by the enzyme <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	drug	cannabinoid	19890266	Amphetamine's effects are known to be modulated by endogenous <b>cannabinoids</b>, which are degraded by the enzyme <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	drug	cocaine	19826190	The effects of <strong>fatty acid amide hydrolase</strong> inhibitors on maintenance of <b>cocaine</b> and food self administration and on reinstatement of <b>cocaine</b> seeking and food taking behavior in rats.
+FAAH1	addiction	relapse	19826190	The effects of <strong>fatty acid amide hydrolase</strong> inhibitors on maintenance of cocaine and food self administration and on <b>reinstatement</b> of cocaine <b>seeking</b> and food taking behavior in rats.
+FAAH1	drug	cannabinoid	19675519	<b>Endocannabinoids</b> are transported into cells by a specific uptake system and degraded by the enzymes <strong>fatty acid amide hydrolase</strong> (FAAH) and monoacylglycerol lipase (MAGL).
+FAAH1	drug	amphetamine	19607756	We also investigated whether systemic application of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 or CB1 receptor blockade by AM251 affected the following PCP induced behavioural deficits reminiscent of schizophrenia like symptoms: (1) working memory impairment (cognitive deficit), (2) social withdrawal (negative symptom), and (3) hyperactivity in response to d <b>amphetamine</b> challenge (positive symptoms).
+FAAH1	addiction	withdrawal	19607756	We also investigated whether systemic application of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 or CB1 receptor blockade by AM251 affected the following PCP induced behavioural deficits reminiscent of schizophrenia like symptoms: (1) working memory impairment (cognitive deficit), (2) social <b>withdrawal</b> (negative symptom), and (3) hyperactivity in response to d amphetamine challenge (positive symptoms).
+FAAH1	addiction	aversion	19524055	<strong>Fatty acid amide hydrolase</strong> (FAAH) knockout mice exhibit enhanced acquisition of an <b>aversive</b>, but not of an appetitive, Barnes maze task.
+FAAH1	drug	cannabinoid	19524055	Consistent with these findings is that genetic deletion or pharmacological inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the primary catabolic enzyme of the endogenous <b>cannabinoid</b> anandamide (AEA), accelerates acquisition as well as extinction in aversive conditioning tasks.
+FAAH1	addiction	aversion	19524055	Consistent with these findings is that genetic deletion or pharmacological inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the primary catabolic enzyme of the endogenous cannabinoid anandamide (AEA), accelerates acquisition as well as extinction in <b>aversive</b> conditioning tasks.
+FAAH1	drug	nicotine	19484221	Inhibition of <strong>fatty acid amide hydrolase</strong> reduces reinstatement of <b>nicotine</b> seeking but not break point for <b>nicotine</b> self administration  comparison with CB(1) receptor blockade.
+FAAH1	addiction	relapse	19484221	Inhibition of <strong>fatty acid amide hydrolase</strong> reduces <b>reinstatement</b> of nicotine <b>seeking</b> but not break point for nicotine self administration  comparison with CB(1) receptor blockade.
+FAAH1	drug	cannabinoid	19484221	The <b>endocannabinoid</b> system consists of <b>endocannabinoids</b> (such as anandamide), their target receptors (mostly <b>cannabinoid</b> CB(1) receptors), and the enzymes that degrade those <b>endocannabinoids</b> (<strong>fatty acid amide hydrolase</strong> (FAAH) for anandamide).
+FAAH1	drug	cannabinoid	19430909	However, new genetic and pharmacological tools are available to increase <b>endocannabinoid</b> levels by targeting <strong>fatty acid amide hydrolase</strong> (FAAH) or monoacylglycerol lipase (MAGL), the enzymes responsible for the degradation of the endogenous <b>cannabinoid</b> ligands anandamide and 2 arachidonoylglycerol, respectively.
+FAAH1	drug	cannabinoid	19259645	<strong>Fatty acid amide hydrolase</strong> (FAAH), the enzyme responsible for degradation of the <b>endocannabinoid</b> anandamide, has emerged as a promising target for anxiety related disorders.
+FAAH1	drug	cannabinoid	19103437	<strong>Fatty acid amide hydrolase</strong> (FAAH) is a key enzyme in regulating <b>endocannabinoid</b> (eCB) signaling.
+FAAH1	drug	cannabinoid	19091987	We discovered that pharmacological inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the enzyme that catabolizes fatty acid ethanolamides, among which the <b>endocannabinoid</b> anandamide (AEA) is the best known, suppressed nicotine induced excitation of dopamine cells.
+FAAH1	drug	nicotine	19091987	We discovered that pharmacological inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the enzyme that catabolizes fatty acid ethanolamides, among which the endocannabinoid anandamide (AEA) is the best known, suppressed <b>nicotine</b> induced excitation of dopamine cells.
+FAAH1	drug	cannabinoid	19004548	Administration of the <strong>fatty acid amide hydrolase</strong> and <b>endocannabinoid</b> catabolism inhibitor, URB597 (0.3 mg/kg, i.p.
+FAAH1	addiction	reward	18814866	<strong>Fatty acid amide hydrolase</strong> inhibition heightens anandamide signaling without producing <b>reinforcing</b> effects in primates.
+FAAH1	drug	cannabinoid	18814866	We investigated the reinforcing effects of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 in monkeys trained to intravenously self administer Delta(9) <b>tetrahydrocannabinol</b> (<b>THC</b>), anandamide, or cocaine and quantified brain <b>endocannabinoid</b> levels using liquid chromatography/mass spectrometry.
+FAAH1	drug	cocaine	18814866	We investigated the reinforcing effects of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 in monkeys trained to intravenously self administer Delta(9) tetrahydrocannabinol (THC), anandamide, or <b>cocaine</b> and quantified brain endocannabinoid levels using liquid chromatography/mass spectrometry.
+FAAH1	addiction	reward	18814866	We investigated the <b>reinforcing</b> effects of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitor URB597 in monkeys trained to intravenously self administer Delta(9) tetrahydrocannabinol (THC), anandamide, or cocaine and quantified brain endocannabinoid levels using liquid chromatography/mass spectrometry.
+FAAH1	drug	cannabinoid	18768763	Inhibiting parabrachial <strong>fatty acid amide hydrolase</strong> activity selectively increases the intake of palatable food via <b>cannabinoid</b> CB1 receptors.
+FAAH1	drug	cannabinoid	18768763	Arachidonoyl serotonin (AA5HT), an inhibitor of the <b>endocannabinoid</b> degradative enzyme, <strong>fatty acid amide hydrolase</strong> (FAAH), was infused into the parabrachial nucleus of male Sprague Dawley rats, and intakes of high fat/sucrose pellets and standard rodent chow were subsequently evaluated under various feeding schedules.
+FAAH1	drug	cannabinoid	18725543	A more functionally selective way to alter <b>endocannabinoid</b> activity is to inhibit <strong>fatty acid amide hydrolase</strong> (FAAH), thereby magnifying and prolonging the effects of the <b>endocannabinoid</b> anandamide only when and where it is synthesized and released on demand.
+FAAH1	drug	cannabinoid	18724387	We have previously demonstrated antinociceptive effects of <strong>fatty acid amide hydrolase</strong> (FAAH) inhibition that were accompanied by increases in the levels of <b>endocannabinoids</b> (ECs) in the hind paw.
+FAAH1	drug	cannabinoid	18705688	<b>Marijuana</b> withdrawal and craving: influence of the <b>cannabinoid</b> receptor 1 (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH) genes.
+FAAH1	addiction	relapse	18705688	Marijuana withdrawal and <b>craving</b>: influence of the cannabinoid receptor 1 (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH) genes.
+FAAH1	addiction	withdrawal	18705688	Marijuana <b>withdrawal</b> and craving: influence of the cannabinoid receptor 1 (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH) genes.
+FAAH1	drug	cannabinoid	18705688	To examine whether withdrawal after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the <b>endocannabinoid</b> system, <b>cannabinoid</b> receptor 1 (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	addiction	relapse	18705688	To examine whether withdrawal after abstinence and cue elicited <b>craving</b> were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, cannabinoid receptor 1 (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	addiction	withdrawal	18705688	To examine whether <b>withdrawal</b> after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, cannabinoid receptor 1 (CNR1) and <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	drug	cannabinoid	18477688	The effect of <b>cannabinoid</b> agonists was mimicked by <b>endocannabinoid</b> uptake or <strong>fatty acid amide hydrolase</strong> inhibitors.
+FAAH1	drug	cannabinoid	18451315	In contrast, genetic deletion, or pharmacological inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the enzyme responsible for catabolism of the <b>endocannabinoid</b> anandamide, enhanced the expression of nicotine CPP.
+FAAH1	drug	nicotine	18451315	In contrast, genetic deletion, or pharmacological inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the enzyme responsible for catabolism of the endocannabinoid anandamide, enhanced the expression of <b>nicotine</b> CPP.
+FAAH1	addiction	reward	18451315	In contrast, genetic deletion, or pharmacological inhibition of <strong>fatty acid amide hydrolase</strong> (FAAH), the enzyme responsible for catabolism of the endocannabinoid anandamide, enhanced the expression of nicotine <b>CPP</b>.
+FAAH1	drug	cannabinoid	18295974	The cDNA 385C to A missense polymorphism of the <b>endocannabinoid</b> degrading enzyme <strong>fatty acid amide hydrolase</strong> (FAAH) is associated with overweight/obesity but not with binge eating disorder in overweight/obese women.
+FAAH1	addiction	intoxication	18295974	The cDNA 385C to A missense polymorphism of the endocannabinoid degrading enzyme <strong>fatty acid amide hydrolase</strong> (FAAH) is associated with overweight/obesity but not with <b>binge</b> eating disorder in overweight/obese women.
+FAAH1	drug	cannabinoid	18295974	Recently, a single nucleotide polymorphism (cDNA 385C to A) of the gene coding for <strong>fatty acid amide hydrolase</strong> (FAAH), the major degrading enzyme of <b>endocannabinoids</b>, has been found to be associated with obesity.
+FAAH1	drug	alcohol	17944864	Manipulation of <strong>fatty acid amide hydrolase</strong> functional activity alters sensitivity and dependence to <b>ethanol</b>.
+FAAH1	addiction	dependence	17944864	Manipulation of <strong>fatty acid amide hydrolase</strong> functional activity alters sensitivity and <b>dependence</b> to ethanol.
+FAAH1	drug	alcohol	17944864	The aim of this study was to examine the role of <strong>fatty acid amide hydrolase</strong> (FAAH) on <b>ethanol</b> sensitivity, preference, and dependence.
+FAAH1	addiction	dependence	17944864	The aim of this study was to examine the role of <strong>fatty acid amide hydrolase</strong> (FAAH) on ethanol sensitivity, preference, and <b>dependence</b>.
+FAAH1	drug	cannabinoid	17904589	The endogenous <b>cannabinoid</b> anandamide has effects on motivation and anxiety that are revealed by <strong>fatty acid amide hydrolase</strong> (FAAH) inhibition.
+FAAH1	drug	alcohol	17621164	Association study between <b>alcoholism</b> and endocannabinoid metabolic enzyme genes encoding <strong>fatty acid amide hydrolase</strong> and monoglyceride lipase in a Japanese population.
+FAAH1	drug	cannabinoid	17621164	Association study between alcoholism and <b>endocannabinoid</b> metabolic enzyme genes encoding <strong>fatty acid amide hydrolase</strong> and monoglyceride lipase in a Japanese population.
+FAAH1	drug	cannabinoid	17621164	<strong>Fatty acid amide hydrolase</strong> (FAAH) and monoglyceride lipase (MGLL) are the major <b>endocannabinoid</b> metabolic enzymes.
+FAAH1	drug	cannabinoid	17290447	The <strong>fatty acid amide hydrolase</strong> C385A (P129T) missense variant in <b>cannabis</b> users: studies of drug use and dependence in Caucasians.
+FAAH1	addiction	dependence	17290447	The <strong>fatty acid amide hydrolase</strong> C385A (P129T) missense variant in cannabis users: studies of drug use and <b>dependence</b> in Caucasians.
+FAAH1	drug	cannabinoid	17258369	Treatment of mice with a <b>cannabinoid</b> receptor agonist (CP55940) or <strong>fatty acid amide hydrolase</strong> inhibitor (URB597) attenuated, while the CB(1) receptor antagonist/inverse agonist, <b>rimonabant</b> (<b>SR141716</b>), enhanced, stress induced decreases in sucrose preference.
+FAAH1	drug	alcohol	17164820	Role of endocannabinoids in <b>alcohol</b> consumption and intoxication: studies of mice lacking <strong>fatty acid amide hydrolase</strong>.
+FAAH1	drug	cannabinoid	17164820	Role of <b>endocannabinoids</b> in alcohol consumption and intoxication: studies of mice lacking <strong>fatty acid amide hydrolase</strong>.
+FAAH1	addiction	intoxication	17164820	Role of endocannabinoids in alcohol consumption and <b>intoxication</b>: studies of mice lacking <strong>fatty acid amide hydrolase</strong>.
+FAAH1	drug	cannabinoid	17164820	<strong>Fatty acid amide hydrolase</strong> (FAAH) is a key membrane protein for metabolism of <b>endocannabinoids</b>, including anandamide, and blockade of FAAH increases the level of anandamide in the brain.
+FAAH1	drug	cannabinoid	17047668	Here, we test the hypothesis that elevating brain levels of the endogenous <b>cannabinoid</b> anandamide through either genetic deletion or pharmacological inhibition of its primary catabolic enzyme <strong>fatty acid amide hydrolase</strong> (FAAH) will potentiate extinction in a fixed platform water maze task.
+FAAH1	addiction	reward	16953388	After brain stimulation <b>reward</b> thresholds stabilized, rats received intraperitoneal injections of the <strong>fatty acid amide hydrolase</strong> (FAAH) inhibitors phenylmethylsulfonyl fluoride (PMSF) (0, 15, 30, and 60 mg/kg) and URB 597 (0, 0.3, 1, and 3 mg/kg) and the selective anandamide reuptake inhibitor OMDM 2 (0, 3, 10, and 30 mg/kg).
+FAAH1	drug	cannabinoid	16805835	Anandamide produced two distinctly different effects on dopamine levels: (1) a rapid, transient increase that was blocked by the <b>cannabinoid</b> CB1 receptor antagonist <b>rimonabant</b>, but not by the vanilloid VR1 receptor antagonist capsazepine, and was magnified and prolonged by the <strong>fatty acid amide hydrolase</strong> (FAAH) enzyme inhibitor, URB597; (2) a smaller delayed and long lasting increase, not sensitive to CB1, VR1 or FAAH blockade.
+FAAH1	drug	cannabinoid	16730696	During test sessions the following drugs were coadministered with saline (substitution studies) or nicotine (0.025 0.4 mg/kg; combination studies): the alpha4beta2 nicotinic acetylcholine receptor subtype antagonist dihydro beta erythroidine (DHbetaE), the non selective nicotinic acetylcholine receptor subtype antagonist mecamylamine, the alpha7 nicotinic acetylcholine receptor subtype antagonist methyllycaconitine (MLA), the alpha4beta2 nicotinic acetylcholine receptor subtype agonist 5 iodo 3 (2(S) azetidinylmethoxy)pyridine (5 IA), the <b>cannabinoid</b> CB1 receptor antagonist/partial agonist <b>rimonabant</b>, the <b>cannabinoid</b> CB2 receptor antagonist N [(1S) endo 1,3,3 trimethylbicyclo [2.2.1]heptan 2 yl]5 (4 chloro 3 methyl phenyl) 1 (4 methybenzyl)pyrazole 3 carboxamide (SR 144528), the <b>cannabinoid</b> CB1/2 receptor agonists ( ) cis 3 [2 hydroxy 4 (1,1 dimethylheptyl) phenyl] trans 4 (3 hydroxy propyl)cyclohexanol (CP 55,940) or R(+) [2,3 dihydro 5 methyl 3 [(morpholinyl)methyl] pyrrolo[1,2,3 de] 1,4 benzoxazin 6 yl] (1 naphthalenyl) methanone mesylate (WIN 55,212 2), the endogenous <b>cannabinoid</b> agonist and non competitive alpha7 nicotinic acetylcholine receptor subtype antagonist anandamide, the anandamide uptake and <strong>fatty acid amide hydrolase</strong> inhibitor N (4 hydroxyphenyl) 5Z,8Z,11Z,14Z eicosatetraenamide (AM 404), the <strong>fatty acid amide hydrolase</strong> inhibitor cyclohexylcarbamic acid 3' carbamoyl biphenyl 3 yl ester (URB 597), AM 404+anandamide or URB 597+anandamide.
+FAAH1	drug	nicotine	16730696	During test sessions the following drugs were coadministered with saline (substitution studies) or <b>nicotine</b> (0.025 0.4 mg/kg; combination studies): the alpha4beta2 nicotinic acetylcholine receptor subtype antagonist dihydro beta erythroidine (DHbetaE), the non selective nicotinic acetylcholine receptor subtype antagonist mecamylamine, the alpha7 nicotinic acetylcholine receptor subtype antagonist methyllycaconitine (MLA), the alpha4beta2 nicotinic acetylcholine receptor subtype agonist 5 iodo 3 (2(S) azetidinylmethoxy)pyridine (5 IA), the cannabinoid CB1 receptor antagonist/partial agonist rimonabant, the cannabinoid CB2 receptor antagonist N [(1S) endo 1,3,3 trimethylbicyclo [2.2.1]heptan 2 yl]5 (4 chloro 3 methyl phenyl) 1 (4 methybenzyl)pyrazole 3 carboxamide (SR 144528), the cannabinoid CB1/2 receptor agonists ( ) cis 3 [2 hydroxy 4 (1,1 dimethylheptyl) phenyl] trans 4 (3 hydroxy propyl)cyclohexanol (CP 55,940) or R(+) [2,3 dihydro 5 methyl 3 [(morpholinyl)methyl] pyrrolo[1,2,3 de] 1,4 benzoxazin 6 yl] (1 naphthalenyl) methanone mesylate (WIN 55,212 2), the endogenous cannabinoid agonist and non competitive alpha7 nicotinic acetylcholine receptor subtype antagonist anandamide, the anandamide uptake and <strong>fatty acid amide hydrolase</strong> inhibitor N (4 hydroxyphenyl) 5Z,8Z,11Z,14Z eicosatetraenamide (AM 404), the <strong>fatty acid amide hydrolase</strong> inhibitor cyclohexylcarbamic acid 3' carbamoyl biphenyl 3 yl ester (URB 597), AM 404+anandamide or URB 597+anandamide.
+FAAH1	drug	cannabinoid	16352709	Here, we show that URB597, a selective inhibitor of the enzyme <strong>fatty acid amide hydrolase</strong>, which catalyzes the intracellular hydrolysis of the <b>endocannabinoid</b> anandamide, exerts potent antidepressant like effects in the mouse tail suspension test and the rat forced swim test.
+FAAH1	drug	opioid	15870833	), an inhibitor of the enzyme <strong>fatty acid amide hydrolase</strong> (FAAH) that degrades anandamide, or their combination, did not increase reinforcing efficacy of <b>heroin</b> at any dose tested.
+FAAH1	addiction	reward	15870833	), an inhibitor of the enzyme <strong>fatty acid amide hydrolase</strong> (FAAH) that degrades anandamide, or their combination, did not increase <b>reinforcing</b> efficacy of heroin at any dose tested.
+FAAH1	drug	cannabinoid	15809662	A naturally occurring missense polymorphism in the gene encoding <strong>fatty acid amide hydrolase</strong> (FAAH), the primary enzyme for inactivation of <b>endocannabinoids</b>, is associated with problem drug use.
+FAAH1	drug	amphetamine	15721218	A nonsynonymous polymorphism in the human <strong>fatty acid amide hydrolase</strong> gene did not associate with either <b>methamphetamine</b> dependence or schizophrenia.
+FAAH1	addiction	dependence	15721218	A nonsynonymous polymorphism in the human <strong>fatty acid amide hydrolase</strong> gene did not associate with either methamphetamine <b>dependence</b> or schizophrenia.
+FAAH1	drug	cannabinoid	15721218	The <strong>fatty acid amide hydrolase</strong> (FAAH) is a primary catabolic enzyme of <b>endocannabinoids</b>.
+FAAH1	drug	cannabinoid	15550444	<b>Endocannabinoids</b> are transported into cells by a specific uptake system and degraded by two well characterized enzymes, the <strong>fatty acid amide hydrolase</strong> and the monoacylglycerol lipase.
+FAAH1	drug	cannabinoid	15254019	Reduced cellular expression and activity of the P129T mutant of human <strong>fatty acid amide hydrolase</strong>: evidence for a link between defects in the <b>endocannabinoid</b> system and problem drug use.
+FAAH1	drug	cannabinoid	15254019	<strong>Fatty acid amide hydrolase</strong> (FAAH) inactivates the endogenous <b>cannabinoid</b> (<b>endocannabinoid</b>) anandamide and related lipid transmitters in vivo.
+FAAH1	drug	cocaine	15100701	The <b>cocaine</b> induced increase in anandamide concentrations was attributable to both stimulation of its synthesis and inhibition of its degradation, as suggested by the ability of <b>cocaine</b> and quinpirole, a D2 like receptor agonist, to enhance the activity of NAPE phospholipase D and to inhibit <strong>fatty acid amide hydrolase</strong>.
+FAAH1	drug	alcohol	12060782	Here, we describe a natural single nucleotide polymorphism in the human gene that encodes the principal endocannabinoid inactivating enzyme, <strong>fatty acid amide hydrolase</strong> (FAAH), that in homozygous form is strongly associated with both street drug use and problem drug/<b>alcohol</b> use.
+FAAH1	drug	cannabinoid	12060782	Here, we describe a natural single nucleotide polymorphism in the human gene that encodes the principal <b>endocannabinoid</b> inactivating enzyme, <strong>fatty acid amide hydrolase</strong> (FAAH), that in homozygous form is strongly associated with both street drug use and problem drug/alcohol use.
+FAAH1	drug	cannabinoid	12052038	The <b>endocannabinoids</b> are widely distributed in brain, they are synthesized and released upon neuronal stimulation, undergo reuptake and are hydrolyzed intracellularly by <strong>fatty acid amide hydrolase</strong> (FAAH).
+FAAH1	drug	cannabinoid	11309246	The endogenous <b>cannabinoid</b> receptor agonist anandamide (AEA) and the related compound <b>palmitoylethanolamide</b> (PEA) are inactivated by transport into cells followed by metabolism by <strong>fatty acid amide hydrolase</strong> (FAAH).
+NPS	drug	psychedelics	32733288	The interview comprised classical substances of abuse, <strong>NPS</strong>, and rarely used substances such as <b>LSD</b>.
+NPS	drug	amphetamine	32671883	However, <strong>NPS</strong> comprise further chiral compound classes such as <b>amphetamine</b> derivatives, ketamines, 2 (aminopropyl)benzofurans, and phenidines.
+NPS	addiction	addiction	32670057	Stimulant drugs, including novel psychoactive substances (<strong>NPS</strong>, formerly "legal highs") have <b>addictive</b> potential which their users may not realize.
+NPS	addiction	reward	32670057	This work aimed to assess the molecular and atomistic mechanisms of stimulant <strong>NPS</strong> actions at DAT, which translate into biological outcomes such as dopamine release in the brain's <b>reward</b> pathway.
+NPS	addiction	addiction	32670057	The present combination of molecular modeling with experimental neurobiological procedures allows for extensive characterization of the mechanisms of drug actions at DAT as the main molecular target of stimulants, and provides an insight into the role of dopamine in the molecular and neurobiological mechanisms of brain responses to stimulant <strong>NPS</strong> that have <b>addictive</b> potential.
+NPS	addiction	addiction	32670057	Such knowledge reveals the risk of <b>addiction</b> related to <strong>NPS</strong> use.
+NPS	drug	nicotine	32650305	The associations between symptoms potentially related to SARS CoV 2 infection and <strong>NPS</strong> results were calculated as adjusted odds ratios with 95% confidence intervals (aOR, 95%CI) by means of multiple logistic regression analysis controlling for age, sex, education, <b>smoking</b> habits, and the number of co morbidities.
+NPS	drug	benzodiazepine	32542312	Flualprazolam is a designer <b>benzodiazepine</b> and novel psychoactive substance (<strong>NPS</strong>) that is increasing in prevalence and appearing in forensic investigations.
+NPS	drug	opioid	32505044	The Comprehensive Addiction and Recovery Act (CARA) of 2016 authorized nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) to obtain a DATA waiver to prescribe <b>buprenorphine</b>.
+NPS	addiction	addiction	32505044	The Comprehensive <b>Addiction</b> and Recovery Act (CARA) of 2016 authorized nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) to obtain a DATA waiver to prescribe buprenorphine.
+NPS	drug	opioid	32505044	From 2017 to 2018, <strong>NPs</strong> (351.9%) and PAs (257.3%) had the largest percent increases in dispensed <b>buprenorphine</b> prescriptions, accounting for 79.6% of the total increase.
+NPS	drug	opioid	32505044	<b>Buprenorphine</b> dispensing rates increased in the US from 2017 to 2018, suggesting the addition of <strong>NPs</strong> and PAs by CARA has contributed to an increase in dispensed <b>buprenorphine</b> prescriptions.
+NPS	addiction	addiction	32144953	Through an analysis of relevant research articles and reviews (particularly those outlining <strong>NPS</strong> neurological and cerebral mechanisms of action and psychopathological consequences arising from <strong>NPS</strong> abuse; research papers more closely focused on chemical/pharmacological aspects have been ruled out), through a systematic analysis of Pubmed, Medline, PsycLIT and EMBASE literature, as well as data released by health care institutions and drug enforcement agencies (among which the World Health Organization, the United Nations Office on Drugs and Crime, the European Monitoring Centre for Drugs and Drug <b>Addiction</b>, Eurojust, the Novel Psychoactive Treatment UK Network, the Court of Justice of the European Union), the authors aimed to elaborate on the most relevant data relative to <strong>NPS</strong> related psychiatric effects, focusing on the conceptual and definition related complexities inherent to <strong>NPS</strong>, clinical management and motivations for <strong>NPS</strong> use; moreover, an effort has been made to highlight the possible measures in order to tackle the unremitting rise of such elusive and potentially harmful substances.
+NPS	drug	opioid	32020187	The growing number of new synthetic <b>opioids</b> (NSO) on the new psychoactive substances (<strong>NPS</strong>) market bears new challenges in toxicology.
+NPS	addiction	reward	31996884	We describe a novel antibiotic delivery system based on magnetic nanoparticles (<strong>NPs</strong>) conjugated to a cell penetrating peptide (<b>CPP</b>).
+NPS	drug	alcohol	31996884	Silica coated iron oxide <strong>NPs</strong> were produced via a co deposition method, and coated by a polyvinyl <b>alcohol</b> (PVA) polymeric network via physicochemical binding.
+NPS	drug	cocaine	31991149	3,4 Methylenedioxypyrovalerone (MDPV) is a new psychoactive substance (<strong>NPS</strong>) considered to be a <b>cocaine</b> like psychostimulant.
+NPS	drug	cocaine	31991149	The substitution of an established illicit drug as <b>cocaine</b> with an <strong>NPS</strong> is a pattern of use reported among drug users.
+NPS	drug	cannabinoid	31942874	It was also found that <strong>NPS</strong> users more often took AMF or <b>cannabinoids</b>, and less frequently benzodiazepines (BDZ) or opioids.
+NPS	drug	opioid	31942874	It was also found that <strong>NPS</strong> users more often took AMF or cannabinoids, and less frequently benzodiazepines (BDZ) or <b>opioids</b>.
+NPS	drug	benzodiazepine	31933443	<strong>NPS</strong> belonging to the <b>benzodiazepine</b> (BZD) class, e.g., 'legal/designer BZDs'/'research chemicals', have recently emerged on the drug (mainly online/virtual) market.
+NPS	drug	opioid	31897505	Silver nanoparticles (Ag <strong>NPs</strong>) in the central amygdala protect the rat conditioned by <b>morphine</b> from withdrawal attack due to <b>naloxone</b> via high level nitric oxide.
+NPS	addiction	withdrawal	31897505	Silver nanoparticles (Ag <strong>NPs</strong>) in the central amygdala protect the rat conditioned by morphine from <b>withdrawal</b> attack due to naloxone via high level nitric oxide.
+NPS	drug	opioid	31897505	We aimed to show the Ag <strong>NPs</strong> protective effect on <b>naloxone</b> (NLX) induced <b>morphine</b> withdrawal in the conditioned rats.
+NPS	addiction	withdrawal	31897505	We aimed to show the Ag <strong>NPs</strong> protective effect on naloxone (NLX) induced morphine <b>withdrawal</b> in the conditioned rats.
+NPS	drug	opioid	31897505	The Ag <strong>NPs</strong> may protect the <b>morphine</b> conditioned rats against the NLX induced withdrawal symptoms due to high level NO in the CeA.
+NPS	addiction	withdrawal	31897505	The Ag <strong>NPs</strong> may protect the morphine conditioned rats against the NLX induced <b>withdrawal</b> symptoms due to high level NO in the CeA.
+NPS	drug	alcohol	31894788	Layered double hydroxide supported Au Cu alloy nanoparticles (<strong>NPs</strong>) were found to be highly efficient catalysts for the oxidative esterification of benzyl <b>alcohol</b> with methanol in the presence of molecular oxygen under visible light irradiation to prepare methyl benzoate.
+NPS	drug	alcohol	31894788	Here, we report that alloying small amounts of copper into gold nanoparticles can increase the ability to activate oxygen molecules to O2˙  radicals and display greater charge heterogeneity to promote the cleavage of the C H bond of benzyl <b>alcohol</b> molecules by reinforcing the coordination of the intermediate with unsaturated metal active sites due to the LSPR effect of alloy <strong>NPs</strong>, which is the rate limiting step of the reaction.
+NPS	addiction	reward	31894788	Here, we report that alloying small amounts of copper into gold nanoparticles can increase the ability to activate oxygen molecules to O2˙  radicals and display greater charge heterogeneity to promote the cleavage of the C H bond of benzyl alcohol molecules by <b>reinforcing</b> the coordination of the intermediate with unsaturated metal active sites due to the LSPR effect of alloy <strong>NPs</strong>, which is the rate limiting step of the reaction.
+NPS	drug	opioid	31850507	The goal of the study was to assess knowledge gaps and practice patterns of US based addiction specialists, primary care physicians (PCPs), nurse practitioners (<strong>NPs</strong>), and physician assistants (PAs) who treat patients with <b>opioid</b> use disorder (OUD).
+NPS	addiction	addiction	31850507	The goal of the study was to assess knowledge gaps and practice patterns of US based <b>addiction</b> specialists, primary care physicians (PCPs), nurse practitioners (<strong>NPs</strong>), and physician assistants (PAs) who treat patients with opioid use disorder (OUD).
+NPS	addiction	addiction	31850507	The surveys were distributed via email between August and September 2017 to a national sample of <b>addiction</b> specialists, PCPs, and <strong>NPs</strong>/PAs that see at least one patient per week and at least 1 percent of their patient population had to be diagnosed with OUD.
+NPS	addiction	addiction	31850507	<b>Addiction</b> specialists saw more patients with OUD than PCPs, <strong>NPs</strong>, or PAs.
+NPS	drug	cannabinoid	31849723	A comprehensive review was conducted using the PubMed/Medline database by combining the search strategy of free text terms and exploding a range of MESH headings relating to the topics of novel psychoactive substances and synthetic/chemical psychoses as follows: {(Novel Psychoactive Substances[Title/Abstract]) AND Psychosis[Title/Abstract])} and for each <strong>NPS</strong> categories as well, focusing on synthetic <b>cannabinoids</b> and cathinones, without time and/or language restrictions.
+NPS	addiction	addiction	31849723	Finally, an overview of the main clinical and psychopathological features between classical versus <strong>NPS</strong> induced chemical/synthetic psychoses is provided for clinicians working with dual disorders and <b>addiction</b> psychiatry.
+NPS	drug	opioid	31799633	The review aims to shed a light on the growing threat caused by <strong>NPS</strong>, and on the dynamics and developments that have led to their spread, including the risk of new adulteration practices which can cause a serious health threat, due to their increased toxicity, e.g., through <b>fentanyl</b> and its analogs.
+NPS	addiction	addiction	31799633	An overview of statistical trends relative to <strong>NPS</strong> use has been provided, in addition to regulatory and legislative approaches in several countries and recommendations and data from International institutions: UN Office on Drugs and Crime, United Nations Commission on Narcotic Drugs, WHO, European Parliament, European Monitoring Centre for Drugs and Drug <b>Addiction</b>, Europol and international collaborative efforts such as the Trans European Drug Information (TEDI) project and the Spanish Energy Control.
+NPS	drug	opioid	31794302	In 2017 the Comprehensive Addiction and Recovery Act enabled nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) to obtain federal waivers allowing them to prescribe <b>buprenorphine</b>, a key medication for <b>opioid</b> use disorder.
+NPS	addiction	addiction	31794302	In 2017 the Comprehensive <b>Addiction</b> and Recovery Act enabled nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) to obtain federal waivers allowing them to prescribe buprenorphine, a key medication for opioid use disorder.
+NPS	drug	opioid	31794302	The rapid growth in the numbers of <strong>NPs</strong> and PAs with <b>buprenorphine</b> waivers is a promising development in improving access to addiction treatment in rural areas.
+NPS	addiction	addiction	31794302	The rapid growth in the numbers of <strong>NPs</strong> and PAs with buprenorphine waivers is a promising development in improving access to <b>addiction</b> treatment in rural areas.
+NPS	addiction	addiction	31766831	An amendment to the Act on Counteracting Drug <b>Addiction</b> issued in July 2018 made it possible for the <strong>NPS</strong> to be considered drugs by law.
+NPS	addiction	addiction	31747318	To date, about 150 SCat have been identified on the clandestine drugs market, which are one of the largest groups of new psychoactive substances (<strong>NPS</strong>) monitored by the United Nations Office on Drugs and Crime and the European Monitoring Center for Drugs and Drug <b>Addiction</b>.
+NPS	drug	cannabinoid	31674690	Within the new psychoactive substances (<strong>NPS</strong>) scenario, several hundred different molecules, mostly including synthetic <b>cannabinoids</b> and cathinones, have been identified so far.
+NPS	drug	cannabinoid	31674690	Most popular <strong>NPS</strong> included: 1265 psychedelic phenethylamines (30.1%; confidence interval [CI] 95%: 28.7 31.5%); 1253 synthetic <b>cannabinoids</b> (29.8%; CI 95%: 28.4 31.2%); 429 synthetic opioids (10.2%; CI 95%: 9.3 10.2%); and 171 synthetic cathinones (4.1%; CI 95% 3.5 4.7%).
+NPS	drug	opioid	31674690	Most popular <strong>NPS</strong> included: 1265 psychedelic phenethylamines (30.1%; confidence interval [CI] 95%: 28.7 31.5%); 1253 synthetic cannabinoids (29.8%; CI 95%: 28.4 31.2%); 429 synthetic <b>opioids</b> (10.2%; CI 95%: 9.3 10.2%); and 171 synthetic cathinones (4.1%; CI 95% 3.5 4.7%).
+NPS	drug	psychedelics	31674690	Most popular <strong>NPS</strong> included: 1265 <b>psychedelic</b> phenethylamines (30.1%; confidence interval [CI] 95%: 28.7 31.5%); 1253 synthetic cannabinoids (29.8%; CI 95%: 28.4 31.2%); 429 synthetic opioids (10.2%; CI 95%: 9.3 10.2%); and 171 synthetic cathinones (4.1%; CI 95% 3.5 4.7%).
+NPS	drug	opioid	31650634	In 2016, the Comprehensive Addiction Recovery Act permitted nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) to obtain a waiver to prescribe <b>buprenorphine</b> to treat <b>opioid</b> use disorder (OUD), with the goal of increasing access to this treatment.
+NPS	addiction	addiction	31650634	In 2016, the Comprehensive <b>Addiction</b> Recovery Act permitted nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) to obtain a waiver to prescribe buprenorphine to treat opioid use disorder (OUD), with the goal of increasing access to this treatment.
+NPS	drug	opioid	31650634	This study's purpose was to describe the <b>buprenorphine</b> prescribing practices of <strong>NPs</strong> and PAs and compare the barriers rural and urban providers face delivering treatment.
+NPS	drug	opioid	31650634	From the October 2018 Drug Enforcement Administration list of providers with the waiver to prescribe <b>buprenorphine</b>, all rural <strong>NPs</strong> and PAs (1,057) and a random sample of 500 urban <strong>NPs</strong> and PAs were surveyed.
+NPS	drug	opioid	31650634	Of the waivered <strong>NPs</strong> and PAs, 80.3% reported having prescribed <b>buprenorphine</b> and 71.1% said they were currently accepting new patients with OUD.
+NPS	drug	opioid	31650634	<strong>NPs</strong> and PAs face many of the same barriers to providing <b>buprenorphine</b> as physicians have reported.
+NPS	drug	cannabinoid	31642644	Additional reference standards were obtained and a multi residue LCMS method was developed to test for 31 benzodiazepines or metabolites in urine including some new benzodiazepines which have been classified as New Psychoactive Substances (<strong>NPS</strong>) which comprise a range of substances, including synthetic <b>cannabinoids</b>, opioids, cathinones and benzodiazepines not covered by international drug controls.
+NPS	drug	opioid	31642644	Additional reference standards were obtained and a multi residue LCMS method was developed to test for 31 benzodiazepines or metabolites in urine including some new benzodiazepines which have been classified as New Psychoactive Substances (<strong>NPS</strong>) which comprise a range of substances, including synthetic cannabinoids, <b>opioids</b>, cathinones and benzodiazepines not covered by international drug controls.
+NPS	drug	alcohol	31602509	While established methods of detection are available for <b>alcohol</b> and classic drugs of abuse, new drugs with potential for abuse (such as methylphenidate, pregabalin) or <strong>NPS</strong>, GHB, GBL, and 4‑BD cannot be detected by conventional methods of immunochemistry in combination with chromatographic methods such as GC MS and HPLC DAD.An improvement in the measurement equipment for specialised laboratories performing such investigations is therefore required in order to be able to adequately care for patients and to clarify criminal offenses.
+NPS	drug	psychedelics	31593907	Mixtures of drugs, such as DOB, 25I <b>NBOMe</b>, <b>MDMA</b> and 25I <b>NBOMe</b> imine were found within the blotters through gas chromatography coupled to mass spectrometry (CGMS); these drugs are classified by international authorities as <strong>NPS</strong> belonging to the phenylethylamines group.
+NPS	drug	amphetamine	31255815	Gold nanoparticles (AuNPs) and Au@Ag <strong>NPs</strong> were synthesized and functionalized with DNA reporter probes (RPs) for <b>METH</b> and cocaine, respectively.
+NPS	drug	cocaine	31255815	Gold nanoparticles (AuNPs) and Au@Ag <strong>NPs</strong> were synthesized and functionalized with DNA reporter probes (RPs) for METH and <b>cocaine</b>, respectively.
+NPS	drug	cannabinoid	31205674	A literature review was undertaken to identify, describe and critically appraise studies investigating <b>cannabinoid</b> use in treating <strong>NPS</strong> in dementia.
+NPS	drug	cannabinoid	31205674	Studies assessing the safety and or effectiveness of <b>cannabinoids</b> in treating <strong>NPS</strong> in dementia in people aged ⩾ 65 years were included.
+NPS	drug	cannabinoid	31097357	Therefore, not only new synthetic opioids but also additional <strong>NPS</strong> including synthetic <b>cannabinoids</b>, new stimulant drugs, and designer benzodiazepines should be included in the routine toxicological screening methods.
+NPS	drug	opioid	31097357	Therefore, not only new synthetic <b>opioids</b> but also additional <strong>NPS</strong> including synthetic cannabinoids, new stimulant drugs, and designer benzodiazepines should be included in the routine toxicological screening methods.
+NPS	drug	psychedelics	30981086	5 (2 ethylaminopropyl)benzofuran (5 EAPB) and 5,6 methylenedioxy 2 aminoindane (MDAI) are two new psychoactive substances (<strong>NPS</strong>) exhibiting <b>MDMA</b> like properties.
+NPS	drug	alcohol	30981086	The cause of death was therefore attributed to the consumption of these <strong>NPS</strong> since screening for other drugs of abuse and for <b>alcohol</b> was negative (oxazepam was found in urine only).
+NPS	drug	benzodiazepine	30981086	The cause of death was therefore attributed to the consumption of these <strong>NPS</strong> since screening for other drugs of abuse and for alcohol was negative (<b>oxazepam</b> was found in urine only).
+NPS	drug	cannabinoid	30907578	In this article, we demonstrate the trace detection of <b>THC</b> in human plasma and saliva solution using a SERS active substrate formed by in situ growth of silver nanoparticles (Ag <strong>NPs</strong>) on diatom frustules.
+NPS	drug	cannabinoid	30850157	Synthetic <b>cannabinoids</b> (SCs) belong to the group of new psychoactive substances (<strong>NPS</strong>) which appear sprayed on herbal mixtures on the "street" drug market and are intended for smoking like <b>marijuana</b>.
+NPS	drug	nicotine	30850157	Synthetic cannabinoids (SCs) belong to the group of new psychoactive substances (<strong>NPS</strong>) which appear sprayed on herbal mixtures on the "street" drug market and are intended for <b>smoking</b> like marijuana.
+NPS	drug	alcohol	30843073	Analyses for classic drugs (opiates, methadone, cocaine, cannabis metabolites, amphetamines, ecstasy and LSD), <b>ethanol</b>, qualitative full screen by gas chromatography mass spectrometry and targeted analysis for 50 <strong>NPS</strong> by liquid chromatography tandem mass spectrometry tested negative; comorbidities were excluded, too.
+NPS	drug	cannabinoid	30843073	Analyses for classic drugs (opiates, methadone, cocaine, <b>cannabis</b> metabolites, amphetamines, ecstasy and LSD), ethanol, qualitative full screen by gas chromatography mass spectrometry and targeted analysis for 50 <strong>NPS</strong> by liquid chromatography tandem mass spectrometry tested negative; comorbidities were excluded, too.
+NPS	drug	cocaine	30843073	Analyses for classic drugs (opiates, methadone, <b>cocaine</b>, cannabis metabolites, amphetamines, ecstasy and LSD), ethanol, qualitative full screen by gas chromatography mass spectrometry and targeted analysis for 50 <strong>NPS</strong> by liquid chromatography tandem mass spectrometry tested negative; comorbidities were excluded, too.
+NPS	drug	opioid	30843073	Analyses for classic drugs (opiates, <b>methadone</b>, cocaine, cannabis metabolites, amphetamines, ecstasy and LSD), ethanol, qualitative full screen by gas chromatography mass spectrometry and targeted analysis for 50 <strong>NPS</strong> by liquid chromatography tandem mass spectrometry tested negative; comorbidities were excluded, too.
+NPS	drug	psychedelics	30843073	Analyses for classic drugs (opiates, methadone, cocaine, cannabis metabolites, amphetamines, <b>ecstasy</b> and <b>LSD</b>), ethanol, qualitative full screen by gas chromatography mass spectrometry and targeted analysis for 50 <strong>NPS</strong> by liquid chromatography tandem mass spectrometry tested negative; comorbidities were excluded, too.
+NPS	addiction	aversion	30657440	A significant association was found between <b>CTA</b> and use of MNPS among the entire sample and among non medical use of prescription stimulants (<strong>NPS</strong>).
+NPS	drug	benzodiazepine	30578721	The number of newly appearing <b>benzodiazepine</b> derivatives on the new psychoactive substances (<strong>NPS</strong>) drug market has increased over the last couple of years totaling 23 'designer benzodiazepines' monitored at the end of 2017 by the European Monitoring Centre for Drugs and Drug Addiction.
+NPS	addiction	addiction	30578721	The number of newly appearing benzodiazepine derivatives on the new psychoactive substances (<strong>NPS</strong>) drug market has increased over the last couple of years totaling 23 'designer benzodiazepines' monitored at the end of 2017 by the European Monitoring Centre for Drugs and Drug <b>Addiction</b>.
+NPS	drug	alcohol	30472966	Platelet monoamine oxidase (MAO) activity, dopamine transporter gene (DAT1) and <strong>neuropeptide S</strong> receptor 1 (NPSR1) gene polymorphisms have been identified as markers of impulsivity, <b>alcohol</b> use and excessive risk taking.
+NPS	drug	opioid	30443678	Today, new psychoactive substances (<strong>NPS</strong>) producers increasingly appear to be targeting new synthetic <b>opioids</b> (NSOs), and the recent emergence of NSOs is causing considerable concern in North America and in Europe.
+NPS	drug	opioid	30443678	For toxicologists, NSO detection in a forensic context presents three additional difficulties to the general <strong>NPS</strong> analytical detection challenge: (i) high frequency of new products, (ii) low concentrations (in μg/L range and under) in biological samples related to their high <b>opioid</b> potency, and (iii) extensive metabolism.
+NPS	drug	opioid	30402728	Graphical abstract Schematic of the mechanism of fluorescence turn on detection of <b>morphine</b> using Au <strong>NPs</strong> (gold nanoparticles) acting asquencher of the fluorescence of fluorescein.
+NPS	drug	psychedelics	30377924	Methoxetamine, one of the <strong>NPS</strong>, was designed as an alternative to <b>ketamine</b> and it was considered an <strong>NPS</strong> candidate owing to its high addictive potential.
+NPS	addiction	addiction	30377924	Methoxetamine, one of the <strong>NPS</strong>, was designed as an alternative to ketamine and it was considered an <strong>NPS</strong> candidate owing to its high <b>addictive</b> potential.
+NPS	drug	opioid	30364252	<b>Fentanyl</b>, <b>fentanyl</b> analogs, and other new synthetic <b>opioids</b> (NSO) have burst onto the illegal drug market as new psychoactive substances (<strong>NPS</strong>).
+NPS	drug	opioid	30364252	This review is focused on the potentially most frequent interactions of <b>opioid</b> <strong>NPS</strong> taking into account the drugs present in the reported cases of poly intoxication, including other illegal drugs of abuse and medication.
+NPS	addiction	intoxication	30364252	This review is focused on the potentially most frequent interactions of opioid <strong>NPS</strong> taking into account the drugs present in the reported cases of poly <b>intoxication</b>, including other illegal drugs of abuse and medication.
+NPS	drug	opioid	30364252	It is crucial that doctors who habitually prescribe <b>opioids</b>, which are often misused by patients and <strong>NPS</strong> users, be aware of designer <b>opioids</b>' potentially life threatening drug drug interactions in order to prevent new cases of intoxication.
+NPS	addiction	intoxication	30364252	It is crucial that doctors who habitually prescribe opioids, which are often misused by patients and <strong>NPS</strong> users, be aware of designer opioids' potentially life threatening drug drug interactions in order to prevent new cases of <b>intoxication</b>.
+NPS	addiction	intoxication	30348014	Occurrence and time course of <strong>NPS</strong> benzodiazepines in Sweden   results from <b>intoxication</b> cases in the STRIDA project.
+NPS	drug	benzodiazepine	30348014	Etizolam (20 cases) was the first detected <strong>NPS</strong> BZD (January 2012), and it was followed by metizolam (four cases), <b>estazolam</b> (two), pyrazolam (33), flubromazepam (33), nifoxipam (five), diclazepam (four), meclonazepam (26), bromazepam (one), flubromazolam (92), deschloroetizolam (one), clonazolam (16), 3 hydroxyphenazepam (eight), ketazolam (one), and phenazepam (one).
+NPS	addiction	intoxication	30348014	An increasing use of <strong>NPS</strong> BZD in Sweden was detected in acute <b>intoxication</b> cases, sometimes leading to intensive care monitoring and support needs.
+NPS	drug	alcohol	30328413	Palladium nanoparticles (Pd <strong>NPs</strong>) supported on Ni single atoms encapsulated in carbon nanotubes (NiSA) show a significantly enhanced electrocatalytic activity for the oxidation reactions of methanol, <b>ethanol</b> and glycerol in alkaline media due to an unusual electron withdrawal effect of NiSA on Pd <strong>NPs</strong>.
+NPS	addiction	withdrawal	30328413	Palladium nanoparticles (Pd <strong>NPs</strong>) supported on Ni single atoms encapsulated in carbon nanotubes (NiSA) show a significantly enhanced electrocatalytic activity for the oxidation reactions of methanol, ethanol and glycerol in alkaline media due to an unusual electron <b>withdrawal</b> effect of NiSA on Pd <strong>NPs</strong>.
+NPS	drug	cannabinoid	30273913	A review on the abuse of three <strong>NPS</strong> (synthetic <b>cannabinoids</b>, kratom, poppers) among youths in Asia.
+NPS	drug	opioid	30273913	A review on the abuse of three <strong>NPS</strong> (synthetic cannabinoids, <b>kratom</b>, poppers) among youths in Asia.
+NPS	drug	cannabinoid	30200549	New Psychoactive Substances (<strong>NPS</strong>) constitute a broad range of hundreds of natural and synthetic drugs, including synthetic opioids, synthetic <b>cannabinoids</b>, synthetic cathinones, and other <strong>NPS</strong> classes, which were not controlled from 1961 to 1971 by the United Nations drug control conventions.
+NPS	drug	opioid	30200549	New Psychoactive Substances (<strong>NPS</strong>) constitute a broad range of hundreds of natural and synthetic drugs, including synthetic <b>opioids</b>, synthetic cannabinoids, synthetic cathinones, and other <strong>NPS</strong> classes, which were not controlled from 1961 to 1971 by the United Nations drug control conventions.
+NPS	addiction	addiction	30194542	The European Monitoring Centre for Drugs and Drug <b>Addiction</b> (EMCDDA) is monitoring more than 670 <strong>NPS</strong> that have appeared on Europe's drug market in the last 20 years, of which almost 90% have appeared in the last decade.
+NPS	drug	opioid	30089426	The Comprehensive Addiction and Recovery Act allows nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) to obtain a Drug Enforcement Administration waiver to prescribe medication assisted treatment (MAT) for <b>opioid</b> use disorder.
+NPS	addiction	addiction	30089426	The Comprehensive <b>Addiction</b> and Recovery Act allows nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) to obtain a Drug Enforcement Administration waiver to prescribe medication assisted treatment (MAT) for opioid use disorder.
+NPS	drug	opioid	30089426	<strong>NPs</strong> and PAs are projected to increase the number of rural patients treated with <b>buprenorphine</b> by 10,777 (15.2%).
+NPS	addiction	addiction	30059368	With the growing trend to avoid the use of opiates to curb potential <b>addiction</b> and increased ED length of stay, <strong>NPs</strong> need to be aware of efficacious, evidence based treatments for acute migraines, a common ED presentation.
+NPS	drug	cannabinoid	29996011	Synthetic <b>cannabinoids</b> are one of the most significant groups within the category new psychoactive substances (<strong>NPS</strong>) and in recent years new compounds have continuously been introduced to the market of recreational drugs.
+NPS	drug	opioid	29923637	To improve access, the Comprehensive Addiction and Recovery Act of 2016 extended the ability to get a Drug Enforcement Administration (DEA) waiver to prescribe <b>buprenorphine</b> to treat OUD to nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs).
+NPS	addiction	addiction	29923637	To improve access, the Comprehensive <b>Addiction</b> and Recovery Act of 2016 extended the ability to get a Drug Enforcement Administration (DEA) waiver to prescribe buprenorphine to treat OUD to nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs).
+NPS	drug	cannabinoid	29855660	New psychoactive substances (<strong>NPS</strong>) are chemical analogues designed to mimic the effects of various classic recreational drugs of abuse including MDMA, LSD, and <b>cannabis</b>.
+NPS	drug	psychedelics	29855660	New psychoactive substances (<strong>NPS</strong>) are chemical analogues designed to mimic the effects of various classic recreational drugs of abuse including <b>MDMA</b>, <b>LSD</b>, and cannabis.
+NPS	addiction	addiction	29855660	<strong>NPS</strong> use is associated with concern about the acute and longer term effects particular substances might have, with abuse and <b>addiction</b> as potential consequences.
+NPS	drug	opioid	29529707	In recent times, structural variants of <b>fentanyl</b> (designer fentanyls) have appeared on the recreational drug market for new psychoactive substances (<strong>NPS</strong>).
+NPS	drug	opioid	29529707	In conclusion, the present results demonstrate that the urinary <b>fentanyl</b> immunoassays are generally useful also for preliminary screening of <b>fentanyl</b> analogs sold as <strong>NPS</strong>.
+NPS	addiction	intoxication	29404633	Consultation with a poison centre is recommended in cases of suspected <b>intoxication</b> with <strong>NPS</strong>.
+NPS	drug	alcohol	29284546	Problem There are uncertainties about the frequencies and severity of intoxications with different types of recreational drugs: <b>ethanol</b>, "classical" illicit party drugs, and new psychoactive substances (<strong>NPS</strong>).
+NPS	drug	opioid	29173157	In vitro Characterization of <strong>NPS</strong> Metabolites Produced by Human Liver Microsomes and the HepaRG Cell Line Using Liquid Chromatographyhigh Resolution Mass Spectrometry (LC HRMS) Analysis: Application to Furanyl <b>Fentanyl</b>.
+NPS	addiction	intoxication	29173157	Identification of metabolites is of importance in the challenge of new psychoactive substances (<strong>NPS</strong>) as it could improve the detection window in biological matrices in clinical and forensic cases of <b>intoxication</b>.
+NPS	drug	opioid	29173157	Considering the numerous and diverse <strong>NPS</strong> reported each year, producers increasingly appear today to be targeting non controlled synthetic <b>opioids</b>, involving <b>fentanyl</b> derivatives such as furanyl <b>fentanyl</b> (Fu F).
+NPS	drug	cannabinoid	29125990	Synthetic <b>cannabinoids</b> are a group of new psychoactive compounds (<strong>NPS</strong>) that act as agonists at the <b>cannabinoid</b> receptor.
+NPS	addiction	addiction	29125990	First reported in 2008, they currently represent one of the largest groups of <strong>NPS</strong> that are monitored by the European Monitoring Centre for Drugs and Drug <b>Addiction</b> (EMCDDA).
+NPS	addiction	addiction	29055747	Overall, females satisfied more <b>addiction</b> like criteria than males, and the same was true for PS rats when compared to <strong>NPS</strong> controls.
+NPS	addiction	intoxication	29045066	Identification of metabolites is of major importance in the context of <strong>NPS</strong> use, as it could improve the detection window in biological matrices in clinical and forensic <b>intoxication</b> cases.
+NPS	drug	amphetamine	28988906	Chemical modifications of existing drugs can generate <strong>NPS</strong> that are not controlled by current legislation, thereby providing legal alternatives to controlled substances such as cocaine or <b>amphetamine</b>.
+NPS	drug	cocaine	28988906	Chemical modifications of existing drugs can generate <strong>NPS</strong> that are not controlled by current legislation, thereby providing legal alternatives to controlled substances such as <b>cocaine</b> or amphetamine.
+NPS	addiction	addiction	28988906	Hence, this study reports for the first time the mode of action for 2 , 3  and 4 FPM and identifies these <strong>NPS</strong> as monoamine releasers with marked potency at catecholamine transporters implicated in abuse and <b>addiction</b>.
+NPS	drug	alcohol	28946499	Poly(vinyl <b>alcohol</b>) (PVA) based nanocomposites (NCs) filled by various weight percent of modified ZrO2 nanoparticles (<strong>NPs</strong>) with vitamin B1 (VB1) up to 7wt% were fabricated via ultrasonication method then was cast to thin films.
+NPS	drug	opioid	28911631	In this review, we briefly discussed the chemistry, pharmacology and toxicology of five common <strong>NPS</strong> of natural origin, i.e., khat, <b>kratom</b>, salvia, magic mushroom and mandrake.
+NPS	addiction	intoxication	28850871	<b>Intoxication</b> cases involving new psychoactive substances (<strong>NPS</strong>) provide several challenges for forensic toxicologists as data on pharmacodynamic and pharmacokinetic properties are lacking, especially on potency and toxicity.
+NPS	drug	cannabinoid	28813207	Use of novel psychoactive substances (<strong>NPS</strong>) such as synthetic <b>cannabinoids</b> (e.g., "Spice," "Serenity") and cathinones (e.g., "bath salts") has proliferated in recent years; however, there is a gap in research examining prevalence among offender samples.
+NPS	drug	alcohol	28813207	<strong>NPS</strong> users reported significantly more past year drug use, including substances not readily detected by standard urine analysis (e.g., hallucinogens, <b>alcohol</b>, and inhalants).
+NPS	addiction	intoxication	28813207	Individuals with higher anxiety symptom counts (OR = 1.07; p < .001) and those who reported drinking to <b>intoxication</b> (OR = 1.30; p < .001) had an increased likelihood of <strong>NPS</strong> use.
+NPS	drug	alcohol	28797805	Age 25 cocaine use, nonmedical use of prescription stimulants (<strong>NPS</strong>), and <b>alcohol</b> use disorder (AUD) risk were significantly associated with trajectory group membership, with Persistent and Intermediate groups exhibiting the highest risk for such outcomes, even accounting for prior substance use and other risk factors.
+NPS	drug	cocaine	28797805	Age 25 <b>cocaine</b> use, nonmedical use of prescription stimulants (<strong>NPS</strong>), and alcohol use disorder (AUD) risk were significantly associated with trajectory group membership, with Persistent and Intermediate groups exhibiting the highest risk for such outcomes, even accounting for prior substance use and other risk factors.
+NPS	drug	cocaine	28797805	Such individuals appear to be at high risk for adverse substance use outcomes, and results suggest possible specificity regarding <b>cocaine</b> use and <strong>NPS</strong>, and AUD risk.
+NPS	addiction	addiction	28713291	By the end of 2015, more than 560 <strong>NPS</strong> had been reported to the European Monitoring Centre for Drugs and Drug <b>Addiction</b>.
+NPS	addiction	intoxication	28659208	Abuse of new psychoactive substances (<strong>NPS</strong>) and the number of patients presenting to the ER with <b>intoxication</b> are increasing.
+NPS	addiction	intoxication	28659208	In this article, we discuss the vital elements of this approach and possible complications of <strong>NPS</strong> <b>intoxication</b>.
+NPS	addiction	intoxication	28659208	This is illustrated by two 20 year old male patients with <strong>NPS</strong> <b>intoxication</b> who presented to our ER as participants in a group <b>intoxication</b>.
+NPS	drug	opioid	28618002	Over the past 5 years, a shift to the use of novel psychoactive substances (<strong>NPS</strong>) has been observed among <b>opioid</b> users.
+NPS	addiction	relapse	28618002	The aim of this study was to assess the potential reasons for <strong>NPS</strong> use among treatment <b>seeking</b> patients receiving opiate substitution therapy.
+NPS	drug	amphetamine	28618002	A series of binary logistic regressions indicated that lifetime <b>amphetamine</b> use (OR = 4.64, 95% CI [2.16, 9.96]) and more severe psychiatric symptoms (OR = 1.89, 95% CI [1.18, 3.04]) may predict <strong>NPS</strong> use.
+NPS	drug	amphetamine	28618002	Synthetic cathinones might still substitute <b>amphetamine</b> derivatives, although these <strong>NPS</strong> are no longer legal.
+NPS	addiction	addiction	28444659	New Psychoactive Substances (<strong>NPS</strong>)   a Challenge for the <b>Addiction</b> Treatment Services.
+NPS	drug	cannabinoid	28444659	Apart from some herbal compounds, <strong>NPS</strong> mainly include synthetic <b>cannabinoids</b> and a range of new synthetic stimulants (e. g., cathinones).
+NPS	addiction	dependence	28419577	New psychoactive substances (<strong>NPS</strong>) have hedonic effects that may lead to <b>dependence</b>.
+NPS	addiction	reward	28419577	New psychoactive substances (<strong>NPS</strong>) have <b>hedonic</b> effects that may lead to dependence.
+NPS	addiction	addiction	28419577	Of the 31 284 episodes of <b>addiction</b> treatment commenced by adults aged 18 to 34 years, 756 (2.4%) were <strong>NPS</strong> related.
+NPS	addiction	addiction	28419577	Over the 2 years after the enactment of prohibition styled legislation targeting <strong>NPS</strong> and headshops, the rate of <strong>NPS</strong> related <b>addiction</b> treatment episodes among young adults declined progressively and substantially.
+NPS	drug	alcohol	28302012	Targeting NPY, CRF/UCNs and <strong>NPS</strong> Neuropeptide Systems to Treat <b>Alcohol</b> Use Disorder (AUD).
+NPS	drug	cannabinoid	28187774	One of the largest groups of <strong>NPS</strong> is synthetic <b>cannabinoids</b> (SCs), which are intended as a replacement to <b>cannabis</b>.
+NPS	drug	cannabinoid	28088088	In Northeast Asia, the most commonly controlled <strong>NPS</strong> were synthetic <b>cannabinoids</b>, synthetic cathinones, and phenethylamines.
+NPS	drug	alcohol	28042935	The nanosecond pulse laser assisted generation of Ni/NiOx core/shell nanoparticles (<strong>NPs</strong>) in water and <b>alcoholic</b> fluids can yield colloidal solutions without surfactants.
+NPS	drug	cocaine	28025810	In addition to well studied and legally controlled compounds like <b>cocaine</b>, new psychoactive substances (<strong>NPS</strong>) are appearing in street drug markets as replacement strategies and legal alternatives.
+NPS	drug	amphetamine	28012094	4 Methyl N methylcathinone (mephedrone) is a popular new psychoactive substance (<strong>NPS</strong>) that is structurally related to the parent compound cathinone, the β keto analogue of <b>amphetamine</b>.
+NPS	addiction	addiction	28012094	More human research is needed to elucidate the safety, toxicity, and <b>addiction</b> potential of mephedrone and related <strong>NPS</strong>.
+NPS	addiction	addiction	28010181	The dominant portrayal of police raids is rarely counterbalanced by voices of active or recovering drug users or professionals in <b>addiction</b> treatment and harm reduction, who could offer a systematic solution to the apparent rapid spread of <strong>NPS</strong> use.
+NPS	drug	psychedelics	27909988	This review examines the currently available evidence from rodent self administration studies of <b>MDMA</b> and two of the new and emerging psychoactive substances (<strong>NPS</strong>) that produce entactogen type neuropharmacological responses   mephedrone (4 methylmethcathinone; 4MMC; "meow meow") and methylone (3,4 methylenedioxymethcathinone).
+NPS	drug	psychedelics	27909988	Overall, the current evidence predicts that these <strong>NPS</strong> entactogens have enhanced abuse liability compared with <b>MDMA</b>.
+NPS	addiction	addiction	27890676	Novel psychoactive substances (<strong>NPS</strong>) are increasingly prevalent world wide although their pharmacological characteristics are largely unknown; those with stimulant properties, due to interactions with the dopamine transporter (DAT), have <b>addictive</b> potential which their users may not realise.
+NPS	drug	cannabinoid	27834146	New Psychoactive Substances (<strong>NPS</strong>) belong to several chemical classes, including phenethylamines, piperazines, synthetic cathinones and synthetic <b>cannabinoids</b>.
+NPS	addiction	intoxication	27834146	Development and validation of analytical methods for the determination of <strong>NPS</strong> both in traditional and alternative matrices is of crucial importance to study drug metabolism and to associate consumption to clinical outcomes and eventual <b>intoxication</b> symptoms.
+NPS	drug	psychedelics	27834144	The traditional 'shamanic style' use of entheogens/plant derived compounds may present with a range of similarities with the 'e psychonauts' use of mostly of hallucinogen/<b>psychedelic</b> <strong>NPS</strong>.
+NPS	drug	opioid	27789102	<strong>NPS</strong> and the <b>methadone</b> queue: Spillages of space and time.
+NPS	drug	opioid	27789102	Between 2008 and 2013, powder stimulants sold by 'head shops' as novel psychoactive substances (<strong>NPS</strong>) or 'legal highs' have displaced <b>heroin</b> among groups of injecting substance users in Bucharest, Romania.
+NPS	drug	opioid	27736030	Increasing numbers of new psychoactive substances (<strong>NPS</strong>) among them <b>fentanyl</b> derivatives has been reported by the European monitoring centre for drugs and drug addiction (EMCDDA).
+NPS	addiction	addiction	27736030	Increasing numbers of new psychoactive substances (<strong>NPS</strong>) among them fentanyl derivatives has been reported by the European monitoring centre for drugs and drug <b>addiction</b> (EMCDDA).
+NPS	addiction	intoxication	27665567	However, data available are very helpful to understand and predict how <strong>NPS</strong> may behave in severe <b>intoxication</b>.
+NPS	drug	alcohol	27639994	The establishment of a regulated legal market for new psychoactive substances (<strong>NPS</strong>, 'legal highs') under New Zealand's Psychoactive Substances Act (PSA) 2013 created a new commercial sector for psychoactive products, previously limited to <b>alcohol</b> and tobacco.
+NPS	drug	nicotine	27639994	The establishment of a regulated legal market for new psychoactive substances (<strong>NPS</strong>, 'legal highs') under New Zealand's Psychoactive Substances Act (PSA) 2013 created a new commercial sector for psychoactive products, previously limited to alcohol and <b>tobacco</b>.
+NPS	drug	cannabinoid	27638057	About a decade ago, synthetic <b>cannabinoids</b> (SC) started to appear as recreational drugs on the new psychoactive substance (<strong>NPS</strong>) market.
+NPS	drug	alcohol	27544812	Tenofovir loaded poly(lactic co glycolic acid) (PLGA)/stearylamine (SA) composite <strong>NPs</strong> with mean diameter of 127nm were obtained with drug association efficiency above 50%, and further incorporated into an approximately 115μm thick, hydroxypropyl methylcellulose/poly(vinyl <b>alcohol</b>) based film.
+NPS	drug	amphetamine	27527499	<strong>NPS</strong> patients were compared with a control group comprising patients with <b>methamphetamine</b> related disorders, using data from the same period.
+NPS	addiction	dependence	27527499	In <strong>NPS</strong> patients, changes were observed in the following three areas between 2012 and 2014: (i) a decrease in the number of employed patients; (ii) an increase in the ratio of patients diagnosed with <b>dependence</b> syndrome; and (iii) a decrease in the ratio of patients diagnosed with psychotic disorder.
+NPS	addiction	dependence	27527499	There is a need to focus future measures against <strong>NPS</strong> <b>dependence</b>: not only on stopping the supply of drugs, but also on reducing the demand for them.
+NPS	drug	amphetamine	27490334	In this paper, a fully validated screening method in blood for the simultaneous detection of 69 substances, including 64 <strong>NPS</strong> (28 synthetic cannabinoids, 19 synthetic cathinones, 5 phenethylamines, 3 indanes, 2 piperazines, 2 tryptamines, 2 phencyclidine, methoxetamine, ketamine and its metabolite) and 5 amphetamines (<b>amphetamine</b>, <b>methamphetamine</b>, MDMA, MDA, 3,4 methylenedioxy N ethylamphetamine   MDEA ) by a dynamic multiple reaction monitoring analysis through liquid chromatography   tandem mass spectrometry (LC MS/MS) is described.
+NPS	drug	cannabinoid	27490334	In this paper, a fully validated screening method in blood for the simultaneous detection of 69 substances, including 64 <strong>NPS</strong> (28 synthetic <b>cannabinoids</b>, 19 synthetic cathinones, 5 phenethylamines, 3 indanes, 2 piperazines, 2 tryptamines, 2 phencyclidine, methoxetamine, ketamine and its metabolite) and 5 amphetamines (amphetamine, methamphetamine, MDMA, MDA, 3,4 methylenedioxy N ethylamphetamine   MDEA ) by a dynamic multiple reaction monitoring analysis through liquid chromatography   tandem mass spectrometry (LC MS/MS) is described.
+NPS	drug	psychedelics	27490334	In this paper, a fully validated screening method in blood for the simultaneous detection of 69 substances, including 64 <strong>NPS</strong> (28 synthetic cannabinoids, 19 synthetic cathinones, 5 phenethylamines, 3 indanes, 2 piperazines, 2 tryptamines, 2 phencyclidine, methoxetamine, <b>ketamine</b> and its metabolite) and 5 amphetamines (amphetamine, methamphetamine, <b>MDMA</b>, MDA, 3,4 methylenedioxy N ethylamphetamine   MDEA ) by a dynamic multiple reaction monitoring analysis through liquid chromatography   tandem mass spectrometry (LC MS/MS) is described.
+NPS	drug	opioid	27476446	Among the new psychoactive substances (<strong>NPS</strong>) that have recently emerged on the market, many of the new synthetic <b>opioids</b> have shown to be particularly harmful.
+NPS	drug	cannabinoid	27466313	The presence of <strong>NPS</strong>, such as synthetic cathinones, <b>cannabinoids</b> and phenethylamines, which are known to be pharmacologically and toxicologically hazardous, has been frequently reported.
+NPS	addiction	reward	27431398	<b>Reinforcing</b> Effects of Cathinone <strong>NPS</strong> in the Intravenous Drug Self Administration Paradigm.
+NPS	addiction	reward	27431398	While the ability of cathinone <strong>NPS</strong> to produce psychotomimetic effects, multiple organ system toxicity, and death in humans is well documented, there has been limited scientific investigation into the <b>reinforcing</b> effects and abuse liability of these drugs.
+NPS	addiction	reward	27431398	In this chapter, we will summarize the existing literature on the <b>reinforcing</b> effects of cathinone <strong>NPS</strong> in rodents using the intravenous self administration (IVSA) paradigm.
+NPS	drug	amphetamine	27431398	We will also compare the ability of cathinone <strong>NPS</strong> to serve as reinforcers to that of classical psychostimulants such as cocaine, <b>methamphetamine</b>, and methylenedioxymethamphetamine (MDMA).
+NPS	drug	cocaine	27431398	We will also compare the ability of cathinone <strong>NPS</strong> to serve as reinforcers to that of classical psychostimulants such as <b>cocaine</b>, methamphetamine, and methylenedioxymethamphetamine (MDMA).
+NPS	drug	psychedelics	27431398	We will also compare the ability of cathinone <strong>NPS</strong> to serve as reinforcers to that of classical psychostimulants such as cocaine, methamphetamine, and <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>).
+NPS	drug	amphetamine	27272068	Additionally, cathinone <strong>NPS</strong> have more dopaminergic vs. serotonergic properties compared with their non β keto <b>amphetamine</b> analogs, suggesting more stimulant and reinforcing properties.
+NPS	addiction	reward	27272068	Additionally, cathinone <strong>NPS</strong> have more dopaminergic vs. serotonergic properties compared with their non β keto amphetamine analogs, suggesting more stimulant and <b>reinforcing</b> properties.
+NPS	drug	alcohol	27235017	<strong>Neuropeptide S</strong> differently modulates <b>alcohol</b> related behaviors in <b>alcohol</b> preferring and non preferring rats.
+NPS	drug	alcohol	27235017	Previous studies performed using Wistar rats demonstrated that <strong>NPS</strong> facilitated <b>alcohol</b> and cocaine seeking but did not affect <b>alcohol</b> or cocaine consumption.
+NPS	drug	cocaine	27235017	Previous studies performed using Wistar rats demonstrated that <strong>NPS</strong> facilitated alcohol and <b>cocaine</b> seeking but did not affect alcohol or <b>cocaine</b> consumption.
+NPS	addiction	relapse	27235017	Previous studies performed using Wistar rats demonstrated that <strong>NPS</strong> facilitated alcohol and cocaine <b>seeking</b> but did not affect alcohol or cocaine consumption.
+NPS	drug	alcohol	27235017	Here, we investigated the effects of <strong>NPS</strong> in Marchigian Sardinian <b>alcohol</b> preferring (msP) rats, a rat strain characterized by excessive <b>alcohol</b> consumption comorbid with heightened anxiety and depressive like phenotypes.
+NPS	drug	alcohol	27235017	Specifically, we evaluated the effect of <strong>NPS</strong> on operant <b>alcohol</b> self administration by msP rats compared to Wistar rats.
+NPS	addiction	reward	27235017	Specifically, we evaluated the effect of <strong>NPS</strong> on <b>operant</b> alcohol self administration by msP rats compared to Wistar rats.
+NPS	drug	alcohol	27235017	The effect of <strong>NPS</strong> on cue induced reinstatement of <b>alcohol</b> seeking in msP rats was also evaluated.
+NPS	addiction	relapse	27235017	The effect of <strong>NPS</strong> on cue induced <b>reinstatement</b> of alcohol <b>seeking</b> in msP rats was also evaluated.
+NPS	drug	alcohol	27235017	<strong>NPS</strong> reduced <b>alcohol</b> self administration but did not affect cue induced reinstatement in the msP rat.
+NPS	addiction	relapse	27235017	<strong>NPS</strong> reduced alcohol self administration but did not affect cue induced <b>reinstatement</b> in the msP rat.
+NPS	drug	alcohol	27235017	In addition, <strong>NPS</strong> induced reinstatement of extinguished <b>alcohol</b> seeking in Wistar rats without affecting <b>alcohol</b> intake.
+NPS	addiction	relapse	27235017	In addition, <strong>NPS</strong> induced <b>reinstatement</b> of extinguished alcohol <b>seeking</b> in Wistar rats without affecting alcohol intake.
+NPS	drug	alcohol	27235017	In Wistar rats, <strong>NPS</strong> acts as a pro arousal agent to promote the reinstatement of <b>alcohol</b> seeking.
+NPS	addiction	relapse	27235017	In Wistar rats, <strong>NPS</strong> acts as a pro arousal agent to promote the <b>reinstatement</b> of alcohol <b>seeking</b>.
+NPS	drug	alcohol	27235017	However, when <b>alcohol</b> drinking is motivated by or associated with a state of pathological anxiety, <strong>NPS</strong> attenuates <b>alcohol</b> consumption and seeking due to its anxiolytic activity.
+NPS	addiction	relapse	27235017	However, when alcohol drinking is motivated by or associated with a state of pathological anxiety, <strong>NPS</strong> attenuates alcohol consumption and <b>seeking</b> due to its anxiolytic activity.
+NPS	addiction	intoxication	27228985	There were only two <strong>NPS</strong> cases; a severe <b>intoxication</b> with paramethoxymethamphetamine (PMMA) in combination with other substances and an <b>intoxication</b> of minor severity with 2,5 dimethoxy 4 propylphenethylamine (2C P).
+NPS	drug	cannabinoid	27227269	The largest group of new psychoactive substances (<strong>NPS</strong>) are synthetic <b>cannabinoids</b> (SC).
+NPS	addiction	addiction	27227269	The recent resurgence of the <strong>NPS</strong> market in Poland resulted in a further amendment to the Drug <b>Addiction</b> Counteraction Act.
+NPS	addiction	reward	27184218	The main <b>incentive</b> for use of <strong>NPS</strong> in general was pleasure and enjoyment.
+NPS	drug	amphetamine	27147945	Neuropharmacology of New Psychoactive Substances (<strong>NPS</strong>): Focus on the Rewarding and Reinforcing Properties of Cannabimimetics and <b>Amphetamine</b> Like Stimulants.
+NPS	addiction	reward	27147945	Neuropharmacology of New Psychoactive Substances (<strong>NPS</strong>): Focus on the Rewarding and <b>Reinforcing</b> Properties of Cannabimimetics and Amphetamine Like Stimulants.
+NPS	drug	alcohol	27147945	The use of <strong>NPS</strong>, mainly consumed along with other drugs of abuse and/or <b>alcohol</b>, has resulted in a significantly growing number of mortality and emergency admissions for overdoses, as reported by several poison centers from all over the world.
+NPS	drug	cannabinoid	27147945	The chemical structure (phenethylamines, piperazines, cathinones, tryptamines, synthetic <b>cannabinoids</b>) of <strong>NPS</strong> and their pharmacological and clinical effects (hallucinogenic, anesthetic, dissociative, depressant) help classify them into different categories.
+NPS	drug	cannabinoid	27147945	In the recent past, 50% of newly identified <strong>NPS</strong> have been classified as synthetic <b>cannabinoids</b> followed by new phenethylamines (17%) (UNODC, 2014b).
+NPS	addiction	addiction	27147945	Besides peripheral toxicological effects, many <strong>NPS</strong> seem to have <b>addictive</b> properties.
+NPS	drug	amphetamine	27147945	This manuscript will review existing literature about the addictive and rewarding properties of the most popular <strong>NPS</strong> classes: cannabimimetics (JWH, HU, CP series) and <b>amphetamine</b> like stimulants (<b>amphetamine</b>, <b>methamphetamine</b>, methcathinone, and MDMA analogs).
+NPS	drug	psychedelics	27147945	This manuscript will review existing literature about the addictive and rewarding properties of the most popular <strong>NPS</strong> classes: cannabimimetics (JWH, HU, CP series) and amphetamine like stimulants (amphetamine, methamphetamine, methcathinone, and <b>MDMA</b> analogs).
+NPS	addiction	addiction	27147945	This manuscript will review existing literature about the <b>addictive</b> and rewarding properties of the most popular <strong>NPS</strong> classes: cannabimimetics (JWH, HU, CP series) and amphetamine like stimulants (amphetamine, methamphetamine, methcathinone, and MDMA analogs).
+NPS	addiction	addiction	27147945	Considering the growing evidence of a widespread use of <strong>NPS</strong>, this review will be useful to understand the new trends in the field of drug reward and drug <b>addiction</b> by revealing the rewarding properties of <strong>NPS</strong>, and will be helpful to gather reliable data regarding the abuse potential of these compounds.
+NPS	addiction	reward	27147945	Considering the growing evidence of a widespread use of <strong>NPS</strong>, this review will be useful to understand the new trends in the field of drug <b>reward</b> and drug addiction by revealing the rewarding properties of <strong>NPS</strong>, and will be helpful to gather reliable data regarding the abuse potential of these compounds.
+NPS	drug	alcohol	26897563	The catalytic activity of the synthesized Au Multipod <strong>NPs</strong> was evaluated in <b>ethanol</b> electrooxidation reaction.
+NPS	addiction	dependence	26810957	One of the most recent compounds to appear on the <strong>NPS</strong> market is the phenmetrazine analog 3 fluorophenmetrazine (3 FPM) which represents one of many phenylmorpholines designed to explore treatment options in areas such as obesity and drug <b>dependence</b>.
+NPS	addiction	addiction	26693960	Using European Monitoring Centre for Drugs and Drug <b>Addiction</b> Internet snapshot methodology, we undertook an English language Internet snapshot survey in May 2015 to gather information on the availability and price of phenibut from Internet <strong>NPS</strong> retailers.
+NPS	addiction	relapse	26680586	Additionally, the involvement of <strong>NPS</strong> in <b>reinstatement</b> of drug <b>seeking</b> behavior has also been reported.
+NPS	drug	amphetamine	26666629	The prevalence of all <strong>NPS</strong> (15.1 17.6%) was similar to <b>amphetamine</b> alone that was detected in 15.1 16.5% of cases.
+NPS	drug	cannabinoid	26666629	<strong>NPS</strong> (one or more) with other conventional drugs (like amphetamines, <b>cannabinoids</b>, cocaine, and benzodiazepines) were detected in most (65%) of the cases.
+NPS	drug	cocaine	26666629	<strong>NPS</strong> (one or more) with other conventional drugs (like amphetamines, cannabinoids, <b>cocaine</b>, and benzodiazepines) were detected in most (65%) of the cases.
+NPS	drug	benzodiazepine	26625894	The extinction facilitating potential of <strong>neuropeptide S</strong>, D cycloserine, and a <b>benzodiazepine</b> was investigated in extinction impaired high anxiety HAB rats and 129S1/SvImJ mice using a classical cued fear conditioning paradigm followed by extinction training and several extinction test sessions to study fear relapse.
+NPS	addiction	relapse	26625894	The extinction facilitating potential of <strong>neuropeptide S</strong>, D cycloserine, and a benzodiazepine was investigated in extinction impaired high anxiety HAB rats and 129S1/SvImJ mice using a classical cued fear conditioning paradigm followed by extinction training and several extinction test sessions to study fear <b>relapse</b>.
+NPS	drug	nicotine	26510313	In the present work, a novel anti <b>nicotine</b> vaccine based on nanohorn supported liposome nanoparticles (NsL <strong>NPs</strong>) was developed.
+NPS	addiction	intoxication	26295489	From July 2013 to March 2015, 1243 cases of suspected <strong>NPS</strong> <b>intoxication</b> originating from ED or ICU were enrolled in the STRIDA project.
+NPS	drug	benzodiazepine	26240749	This review aims to circumscribe a quick moving and growing field, and to categorize <strong>NPS</strong> into five major groups based upon their 'parent' compounds: stimulants similar to cocaine, amphetamines and ecstasy; cannabinoids; <b>benzodiazepine</b> based drugs; dissociatives similar to ketamine and phencyclidine (PCP); and those modelled after classic hallucinogens such as LSD and psilocybin.
+NPS	drug	cannabinoid	26240749	This review aims to circumscribe a quick moving and growing field, and to categorize <strong>NPS</strong> into five major groups based upon their 'parent' compounds: stimulants similar to cocaine, amphetamines and ecstasy; <b>cannabinoids</b>; benzodiazepine based drugs; dissociatives similar to ketamine and phencyclidine (PCP); and those modelled after classic hallucinogens such as LSD and psilocybin.
+NPS	drug	cocaine	26240749	This review aims to circumscribe a quick moving and growing field, and to categorize <strong>NPS</strong> into five major groups based upon their 'parent' compounds: stimulants similar to <b>cocaine</b>, amphetamines and ecstasy; cannabinoids; benzodiazepine based drugs; dissociatives similar to ketamine and phencyclidine (PCP); and those modelled after classic hallucinogens such as LSD and psilocybin.
+NPS	drug	psychedelics	26240749	This review aims to circumscribe a quick moving and growing field, and to categorize <strong>NPS</strong> into five major groups based upon their 'parent' compounds: stimulants similar to cocaine, amphetamines and <b>ecstasy</b>; cannabinoids; benzodiazepine based drugs; dissociatives similar to <b>ketamine</b> and phencyclidine (PCP); and those modelled after classic hallucinogens such as <b>LSD</b> and <b>psilocybin</b>.
+NPS	addiction	intoxication	26240749	Clinicians might encounter <strong>NPS</strong> in various ways: anecdotal reportage; acute <b>intoxication</b>; as part of a substance misuse profile; and as a precipitant or perpetuating factor for longer term physical and psychological ill health.
+NPS	drug	cannabinoid	26216566	<strong>NPS</strong> use was reported by 4.7% of the sample, without significant differences between urban and rural areas; mephedrone (3.3%), synthetic <b>cannabinoids</b> (1.2%) and Salvia divinorum (0.3%) consumption has been identified.
+NPS	addiction	intoxication	26216566	<strong>NPS</strong> use was also predictive of <b>binge</b> drinking behaviours (χ(2) (4) = 929.58, p < .001).
+NPS	addiction	intoxication	26216566	Moreover, the association between <b>binge</b> drinking habits and <strong>NPS</strong> use was really strong.
+NPS	drug	nicotine	26194894	<strong>NPS</strong> users were compared with non users and illicit drug users, who had not used <strong>NPS</strong>, in terms of gender, binge drinking, <b>tobacco</b> use, psychological distress and self efficacy to resist peer pressure.
+NPS	addiction	intoxication	26194894	<strong>NPS</strong> users were compared with non users and illicit drug users, who had not used <strong>NPS</strong>, in terms of gender, <b>binge</b> drinking, tobacco use, psychological distress and self efficacy to resist peer pressure.
+NPS	drug	cannabinoid	26194894	Of the 1126 students, 3% reported having ever tried <strong>NPS</strong>, 2.4% had used synthetic <b>cannabis</b> and 0.4% had used a synthetic stimulant.
+NPS	drug	nicotine	26194894	Analyses revealed that <strong>NPS</strong> users were more likely to have had an episode of binge drinking in the past 6 months, tried <b>tobacco</b> and had higher levels of psychological distress and lower perceived self efficacy to resist peer pressure than non users, but did not significantly differ from users of other illicit drugs.
+NPS	addiction	intoxication	26194894	Analyses revealed that <strong>NPS</strong> users were more likely to have had an episode of <b>binge</b> drinking in the past 6 months, tried tobacco and had higher levels of psychological distress and lower perceived self efficacy to resist peer pressure than non users, but did not significantly differ from users of other illicit drugs.
+NPS	drug	alcohol	26178067	Color controlled spherical Ag nanoparticles (<strong>NPs</strong>) and nanorods, with features that originate from their particle sizes and morphologies, can be synthesized within the mesoporous structure of SBA 15 by the rapid and uniform microwave (MW) assisted <b>alcohol</b> reduction method in the absence or presence of surface modifying organic ligands.
+NPS	drug	opioid	26083809	This report from the Swedish STRIDA project describes analytically confirmed non fatal intoxications involving butyrfentanyl (butyrylfentanyl) or 4 fluorobutyrfentanyl (para fluorobutyrfentanyl), two <b>fentanyl</b> analogues recently introduced as <strong>NPS</strong> <b>opioids</b>.
+NPS	drug	opioid	26083809	Analysis of two "butyrfentanyl" <strong>NPS</strong> products (nasal spray and powder) brought to hospital by patients showed that the 10 fold more potent <b>fentanyl</b> was the main active ingredient (∼7.5 10 fold higher amount) in both.
+NPS	drug	opioid	26083809	The incorrect labelling of butyrfentanyl <strong>NPS</strong> products which instead mainly contained <b>fentanyl</b> is alarming, given the narrow range between a safe and a lethal dose for <b>opioids</b>.
+NPS	drug	cannabinoid	26074742	There are many categories of <strong>NPS</strong>, such as synthetic <b>cannabinoids</b>, synthetic cathinones, phenylethylamines, piperazines, ketamine derivatives and tryptamines.
+NPS	drug	psychedelics	26074742	There are many categories of <strong>NPS</strong>, such as synthetic cannabinoids, synthetic cathinones, phenylethylamines, piperazines, <b>ketamine</b> derivatives and tryptamines.
+NPS	addiction	addiction	26074740	New psychoactive substances (<strong>NPS</strong>) have completely modified the drug scene and the current landscape of <b>addiction</b>.
+NPS	drug	alcohol	26055195	Activation of Hypocretin 1/Orexin A Neurons Projecting to the Bed Nucleus of the Stria Terminalis and Paraventricular Nucleus Is Critical for Reinstatement of <b>Alcohol</b> Seeking by <strong>Neuropeptide S</strong>. Environmental conditioning is a major trigger for relapse in abstinent addicts.
+NPS	addiction	relapse	26055195	Activation of Hypocretin 1/Orexin A Neurons Projecting to the Bed Nucleus of the Stria Terminalis and Paraventricular Nucleus Is Critical for <b>Reinstatement</b> of Alcohol <b>Seeking</b> by <strong>Neuropeptide S</strong>. Environmental conditioning is a major trigger for <b>relapse</b> in abstinent addicts.
+NPS	drug	alcohol	26055195	We showed that activation of the neuropeptide S (<strong>NPS</strong>) system exacerbates reinstatement vulnerability to cocaine and <b>alcohol</b> via stimulation of the hypocretin 1/orexin A (Hcrt 1/Ox A) system.
+NPS	drug	cocaine	26055195	We showed that activation of the neuropeptide S (<strong>NPS</strong>) system exacerbates reinstatement vulnerability to <b>cocaine</b> and alcohol via stimulation of the hypocretin 1/orexin A (Hcrt 1/Ox A) system.
+NPS	addiction	relapse	26055195	We showed that activation of the neuropeptide S (<strong>NPS</strong>) system exacerbates <b>reinstatement</b> vulnerability to cocaine and alcohol via stimulation of the hypocretin 1/orexin A (Hcrt 1/Ox A) system.
+NPS	drug	alcohol	26055195	We showed that activation of the <strong>neuropeptide S</strong> (<strong>NPS</strong>) system exacerbates reinstatement vulnerability to cocaine and <b>alcohol</b> via stimulation of the hypocretin 1/orexin A (Hcrt 1/Ox A) system.
+NPS	drug	cocaine	26055195	We showed that activation of the <strong>neuropeptide S</strong> (<strong>NPS</strong>) system exacerbates reinstatement vulnerability to <b>cocaine</b> and alcohol via stimulation of the hypocretin 1/orexin A (Hcrt 1/Ox A) system.
+NPS	addiction	relapse	26055195	We showed that activation of the <strong>neuropeptide S</strong> (<strong>NPS</strong>) system exacerbates <b>reinstatement</b> vulnerability to cocaine and alcohol via stimulation of the hypocretin 1/orexin A (Hcrt 1/Ox A) system.
+NPS	drug	alcohol	26055195	Combining pharmacologic manipulations with immunohistochemistry techniques, we sought to determine how <strong>NPS</strong> and Hcrt 1/Ox A systems interact to modulate reinstatement of <b>alcohol</b> seeking in rats.
+NPS	addiction	relapse	26055195	Combining pharmacologic manipulations with immunohistochemistry techniques, we sought to determine how <strong>NPS</strong> and Hcrt 1/Ox A systems interact to modulate <b>reinstatement</b> of alcohol <b>seeking</b> in rats.
+NPS	drug	alcohol	26055195	Intrahypothalamic injection of <strong>NPS</strong> facilitated discriminative cue induced reinstatement of <b>alcohol</b> seeking.
+NPS	addiction	relapse	26055195	Intrahypothalamic injection of <strong>NPS</strong> facilitated discriminative cue induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+NPS	drug	alcohol	26055195	Confirming this assumption, intra BNST or PVN Hcrt 1/Ox A injection enhanced <b>alcohol</b> seeking similarly to hypothalamic <strong>NPS</strong> injection but to a lesser degree.
+NPS	addiction	relapse	26055195	Confirming this assumption, intra BNST or PVN Hcrt 1/Ox A injection enhanced alcohol <b>seeking</b> similarly to hypothalamic <strong>NPS</strong> injection but to a lesser degree.
+NPS	addiction	relapse	26055195	Results suggest that the Hcrt 1/Ox A neurocircuitry mediating the facilitation of cue induced <b>reinstatement</b> by <strong>NPS</strong> involves structures critically involved in stress regulation such as the PVN and the BNST.
+NPS	addiction	relapse	26055195	These findings open to the tempting hypothesis of a role of the <strong>NPS</strong> system in modulating the interactions between stress and environmental conditioning factors in drug <b>relapse</b>.
+NPS	drug	opioid	26017246	The two groups comprised drug abusers undergoing <b>opioid</b> maintenance treatment (OMT) or drug withdrawal therapy and routinely visiting a rehabilitation clinic, and drug abusers with irregular attendance at a harm reduction unit (HRU) and suspected of potential <strong>NPS</strong> abuse.
+NPS	addiction	withdrawal	26017246	The two groups comprised drug abusers undergoing opioid maintenance treatment (OMT) or drug <b>withdrawal</b> therapy and routinely visiting a rehabilitation clinic, and drug abusers with irregular attendance at a harm reduction unit (HRU) and suspected of potential <strong>NPS</strong> abuse.
+NPS	drug	cannabinoid	25893495	Among the new psychoactive substances (<strong>NPS</strong>), most frequently synthetic <b>cannabinoids</b> (SCBs) have been found in Europe.
+NPS	addiction	intoxication	25881797	Over a 12 month period from January to December 2014, 750 cases of suspected <strong>NPS</strong> <b>intoxication</b> originating from emergency departments were enrolled in the STRIDA project of which 14 (1.9%) tested positive for diphenidine and 3 (0.4%) tested positive for MXP.
+NPS	drug	alcohol	25881797	Co exposure to several other <strong>NPS</strong> (e.g., 5 /6 (2 aminopropyl)benzofuran, 2 4 bromomethcathinone, butylone, 3,4 dichloromethylphenidate, 5 methoxy N isopropyltryptamine, methiopropamine, and α pyrrolidinopentiothiophenone), also including other dissociative substances (3 /4 methoxyphencyclidine), and classical drugs of abuse (e.g., cannabis and <b>ethanol</b>) was documented in 87% of these cases.
+NPS	drug	cannabinoid	25881797	Co exposure to several other <strong>NPS</strong> (e.g., 5 /6 (2 aminopropyl)benzofuran, 2 4 bromomethcathinone, butylone, 3,4 dichloromethylphenidate, 5 methoxy N isopropyltryptamine, methiopropamine, and α pyrrolidinopentiothiophenone), also including other dissociative substances (3 /4 methoxyphencyclidine), and classical drugs of abuse (e.g., <b>cannabis</b> and ethanol) was documented in 87% of these cases.
+NPS	drug	psychedelics	25881797	The adverse effects noted in analytically confirmed cases of <strong>NPS</strong> intoxication involving diphenidine or MXP were similar to those reported for other dissociative substances such as <b>ketamine</b> and methoxetamine.
+NPS	addiction	intoxication	25881797	The adverse effects noted in analytically confirmed cases of <strong>NPS</strong> <b>intoxication</b> involving diphenidine or MXP were similar to those reported for other dissociative substances such as ketamine and methoxetamine.
+NPS	addiction	intoxication	26946558	[Analysis of <b>intoxication</b> with novel psychoactive substance (<strong>NPS</strong>) in Pomeranian region, from January to July 2015].
+NPS	addiction	intoxication	26946558	Analysis was based on records derived from Electronic Poison Information Database developed and used on a daily basis on Pomeranian Centre of Toxicology (PCT), data obtained from Centre for Monitoring of Adverse Effects of Medicaments and Chemical Substances based in PCT and on information gathered from patients treated in Pomeranian Centre of Toxicology for <strong>NPS</strong> <b>intoxication</b>.
+NPS	drug	psychedelics	26946558	Most dangerous substances found in <strong>NPS</strong> were PMA, PMMA, 25C <b>NBOMe</b> and 251 <b>NBOMe</b>.
+NPS	addiction	intoxication	26946558	There were no deaths of patients treated in PCT because of acute <b>intoxication</b> with <strong>NPS</strong>.
+NPS	drug	cocaine	25220242	Effects of the <strong>neuropeptide S</strong> receptor antagonist RTI 118 on abuse related facilitation of intracranial self stimulation produced by <b>cocaine</b> and methylenedioxypyrovalerone (MDPV) in rats.
+NPS	addiction	reward	25220242	Neuropeptide S (<strong>NPS</strong>) is a neurotransmitter that activates the <strong>NPS</strong> receptor to modulate biological functions including anxiety like behaviors, feeding, and drug <b>reinforcement</b>.
+NPS	addiction	reward	25220242	<strong>Neuropeptide S</strong> (<strong>NPS</strong>) is a neurotransmitter that activates the <strong>NPS</strong> receptor to modulate biological functions including anxiety like behaviors, feeding, and drug <b>reinforcement</b>.
+NPS	drug	cocaine	25220242	RTI 118 is a novel <strong>NPS</strong> receptor antagonist that decreased <b>cocaine</b> self administration in rats at doses that had little or no effect on food maintained responding.
+NPS	drug	cocaine	25220242	These results support further consideration of <strong>NPS</strong> receptor antagonists as candidate treatments for <b>cocaine</b> abuse and provide evidence for differential effects of a candidate treatment on abuse related effects of <b>cocaine</b> and MDPV.
+NPS	drug	opioid	25175898	MT 45 (1 cyclohexyl 4 (1,2 diphenylethyl)piperazine) is an <b>opioid</b> analgesic drug candidate developed in the 1970s that has recently been introduced as a new psychoactive substance (<strong>NPS</strong>) on the "recreational" drug market.
+NPS	drug	alcohol	24754478	<strong>Neuropeptide S</strong> receptor gene variant and environment: contribution to <b>alcohol</b> use disorders and <b>alcohol</b> consumption.
+NPS	drug	alcohol	24754478	The functional polymorphism Asn(107) Ile (rs324981, A > T) of the <strong>neuropeptide S</strong> receptor (NPSR1) gene is involved in the modulation of traits that affect <b>alcohol</b> use.
+NPS	addiction	intoxication	24529166	A number of characteristics of the recreational use of <strong>NPS</strong> may not be well addressed by standard medical clinical trials, including <b>binge</b> use, polydrug use, use by vulnerable groups and high risk modes of administration.
+NPS	drug	alcohol	24529166	If the legal market for <strong>NPS</strong> encourages the use of <strong>NPS</strong>, <b>alcohol</b> and other drugs there may be an increase in drug related harm.
+NPS	drug	amphetamine	24470121	From 2009 to 2012, 24 <strong>NPS</strong> belonging to several chemical classes such as phenethylamines, substituted cathinones, tryptamines, and methoxetamine were identified in 173 samples believed to be MDMA, <b>amphetamine</b>, ketamine, cocaine, mescaline, or <b>methamphetamine</b>.
+NPS	drug	cocaine	24470121	From 2009 to 2012, 24 <strong>NPS</strong> belonging to several chemical classes such as phenethylamines, substituted cathinones, tryptamines, and methoxetamine were identified in 173 samples believed to be MDMA, amphetamine, ketamine, <b>cocaine</b>, mescaline, or methamphetamine.
+NPS	drug	psychedelics	24470121	From 2009 to 2012, 24 <strong>NPS</strong> belonging to several chemical classes such as phenethylamines, substituted cathinones, tryptamines, and methoxetamine were identified in 173 samples believed to be <b>MDMA</b>, amphetamine, <b>ketamine</b>, cocaine, <b>mescaline</b>, or methamphetamine.
+NPS	drug	nicotine	24170619	However, despite consistently higher referrals of <b>tobacco</b> dependent patients for <b>smoking</b> cessation interventions than any other group of healthcare provider, evidence suggests that <strong>NPs</strong> are not adequately trained to treat this addiction.
+NPS	addiction	addiction	24170619	However, despite consistently higher referrals of tobacco dependent patients for smoking cessation interventions than any other group of healthcare provider, evidence suggests that <strong>NPs</strong> are not adequately trained to treat this <b>addiction</b>.
+NPS	drug	nicotine	24170619	This article is a call to action for <strong>NPs</strong> to become familiar with the <b>tobacco</b> cessation policy changes affecting clinical practice, to become experts in <b>tobacco</b> treatment, and to take the lead in this healthcare reform initiative.
+NPS	drug	alcohol	23881888	As described in the 'mismatch theory', the capacity of the human genome to evolve defences against toxins has been outstripped by the pace of cultural change and technological development, such as purposeful fermentation of <b>alcohol</b> and more recently distillation of <b>alcohol</b>; purification and chemical manipulation of plant alkaloids; and the engineering of entirely novel psychoactive substances (<strong>NPS</strong>).
+NPS	drug	alcohol	23761908	A novel brain penetrant <strong>NPS</strong> receptor antagonist, NCGC00185684, blocks <b>alcohol</b> induced ERK phosphorylation in the central amygdala and decreases operant <b>alcohol</b> self administration in rats.
+NPS	addiction	reward	23761908	A novel brain penetrant <strong>NPS</strong> receptor antagonist, NCGC00185684, blocks alcohol induced ERK phosphorylation in the central amygdala and decreases <b>operant</b> alcohol self administration in rats.
+NPS	addiction	addiction	23761908	The <strong>Neuropeptide S</strong> receptor, a Gs/Gq coupled GPCR expressed in brain regions involved in mediating drug reward, has recently emerged as a candidate therapeutic target in <b>addictive</b> disorders.
+NPS	addiction	reward	23761908	The <strong>Neuropeptide S</strong> receptor, a Gs/Gq coupled GPCR expressed in brain regions involved in mediating drug <b>reward</b>, has recently emerged as a candidate therapeutic target in addictive disorders.
+NPS	drug	opioid	23684726	<b>Morphine</b> dependence is associated with changes in <strong>neuropeptide S</strong> receptor expression and function in rat brain.
+NPS	addiction	dependence	23684726	Morphine <b>dependence</b> is associated with changes in <strong>neuropeptide S</strong> receptor expression and function in rat brain.
+NPS	drug	opioid	23684726	Moreover, 7 days after the last <b>morphine</b> dose animals were checked for signs of anxiety and for intracerebroventricular (ICV) <strong>NPS</strong> (0.3 and 1.0 nmol) induced anxiolytic effects by elevated plus maze (EPM).
+NPS	drug	opioid	23684726	These results demonstrated that <b>morphine</b> dependence induction led to (i) changes in NPSR mRNA expression; (ii) increased anxiety; and (iii) more potent anxiolytic like effect of <strong>NPS</strong>.
+NPS	addiction	dependence	23684726	These results demonstrated that morphine <b>dependence</b> induction led to (i) changes in NPSR mRNA expression; (ii) increased anxiety; and (iii) more potent anxiolytic like effect of <strong>NPS</strong>.
+NPS	drug	alcohol	23328431	PLGA <strong>NPs</strong> were formulated with microemulsion method, Polyvinyl <b>alcohol</b> (PVA) was used as surfactant (PVA <strong>NPs</strong>).
+NPS	addiction	withdrawal	23328431	The intracellular level of <strong>NPs</strong> decreased significantly upon the <b>withdrawal</b> of <strong>NPs</strong> in medium.
+NPS	drug	alcohol	23254212	Interviewers assessed <strong>NPS</strong>; Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM IV) cannabis and <b>alcohol</b> use disorders; and frequency of skipping class.
+NPS	drug	cannabinoid	23254212	Interviewers assessed <strong>NPS</strong>; Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM IV) <b>cannabis</b> and alcohol use disorders; and frequency of skipping class.
+NPS	drug	cocaine	23149909	Hypothalamic <strong>neuropeptide S</strong> receptor blockade decreases discriminative cue induced reinstatement of <b>cocaine</b> seeking in the rat.
+NPS	addiction	relapse	23149909	Hypothalamic <strong>neuropeptide S</strong> receptor blockade decreases discriminative cue induced <b>reinstatement</b> of cocaine <b>seeking</b> in the rat.
+NPS	drug	cocaine	23149909	Previous studies have shown that activation of brain <strong>neuropeptide S</strong> receptor (NPSR) facilitates reinstatement of <b>cocaine</b> seeking elicited by environmental cues predictive of drug availability.
+NPS	addiction	relapse	23149909	Previous studies have shown that activation of brain <strong>neuropeptide S</strong> receptor (NPSR) facilitates <b>reinstatement</b> of cocaine <b>seeking</b> elicited by environmental cues predictive of drug availability.
+NPS	drug	cocaine	23149909	To evaluate this hypothesis, we investigated the effect of two newly synthetized NPSR antagonists, namely the quinolinone amide derivative NPSR QA1 and the <strong>NPS</strong> peptidic analogue [D Cys(tBu)⁵]<strong>NPS</strong> on <b>cocaine</b> self administration and on discriminative cue induced relapse to <b>cocaine</b> seeking in the rat.
+NPS	addiction	relapse	23149909	To evaluate this hypothesis, we investigated the effect of two newly synthetized NPSR antagonists, namely the quinolinone amide derivative NPSR QA1 and the <strong>NPS</strong> peptidic analogue [D Cys(tBu)⁵]<strong>NPS</strong> on cocaine self administration and on discriminative cue induced <b>relapse</b> to cocaine <b>seeking</b> in the rat.
+NPS	addiction	relapse	23149909	The NPSR QA1 was injected intraperitoneally and its effect on discriminative cue induced <b>reinstatement</b> was evaluated, while [D Cys(tBut)⁵]<strong>NPS</strong> was injected intracranially, intra lateral hypothalamus, intra perifornical area of the hypothalamus, and intra central amygdala.
+NPS	drug	cocaine	23149909	The efficacy of NPSR antagonism on <b>cocaine</b> seeking was confirmed with [D Cys(tBu)⁵]<strong>NPS</strong> (10 30 nmol/rat) as it markedly inhibited relapse behavior following site specific injection into the lateral hypothalamus and the perifornical area of the hypothalamus but not into the central amygdala.
+NPS	addiction	relapse	23149909	The efficacy of NPSR antagonism on cocaine <b>seeking</b> was confirmed with [D Cys(tBu)⁵]<strong>NPS</strong> (10 30 nmol/rat) as it markedly inhibited <b>relapse</b> behavior following site specific injection into the lateral hypothalamus and the perifornical area of the hypothalamus but not into the central amygdala.
+NPS	drug	cocaine	23149909	The identification of the <strong>NPS</strong>/NPSR system as an important new element involved in the physiopathology of <b>cocaine</b> addiction and the discovery of the anti addictive properties of NPSR antagonists opens the possibility of exploring a new mechanism for <b>cocaine</b> addiction treatment.
+NPS	addiction	addiction	23149909	The identification of the <strong>NPS</strong>/NPSR system as an important new element involved in the physiopathology of cocaine <b>addiction</b> and the discovery of the anti <b>addictive</b> properties of NPSR antagonists opens the possibility of exploring a new mechanism for cocaine <b>addiction</b> treatment.
+NPS	drug	cocaine	22982682	Antagonism of the <strong>neuropeptide S</strong> receptor with RTI 118 decreases <b>cocaine</b> self administration and <b>cocaine</b> seeking behavior in rats.
+NPS	addiction	relapse	22982682	Antagonism of the <strong>neuropeptide S</strong> receptor with RTI 118 decreases cocaine self administration and cocaine <b>seeking</b> behavior in rats.
+NPS	drug	alcohol	22982682	Recent research has found that intracerebroventricular <strong>NPS</strong> can increase cocaine and <b>alcohol</b> self administration in rodents, suggesting a key role in reward related neurocircuitry.
+NPS	drug	cocaine	22982682	Recent research has found that intracerebroventricular <strong>NPS</strong> can increase <b>cocaine</b> and alcohol self administration in rodents, suggesting a key role in reward related neurocircuitry.
+NPS	addiction	reward	22982682	Recent research has found that intracerebroventricular <strong>NPS</strong> can increase cocaine and alcohol self administration in rodents, suggesting a key role in <b>reward</b> related neurocircuitry.
+NPS	drug	cocaine	22982682	It is hypothesized that antagonism of the <strong>NPS</strong> system might represent a novel strategy for the pharmacological treatment of <b>cocaine</b> abuse.
+NPS	drug	cocaine	22982682	These data support the hypothesis that antagonism of the <strong>neuropeptide S</strong> receptor may ultimately show efficacy in reducing <b>cocaine</b> use and relapse.
+NPS	addiction	relapse	22982682	These data support the hypothesis that antagonism of the <strong>neuropeptide S</strong> receptor may ultimately show efficacy in reducing cocaine use and <b>relapse</b>.
+NPS	drug	alcohol	22739468	Chronic <b>ethanol</b> potentiates the effect of <strong>neuropeptide s</strong> in the basolateral amygdala and shows increased anxiolytic and anti depressive effects.
+NPS	drug	alcohol	22739468	We examined whether the <strong>neuropeptide S</strong> receptor (NPSR) was effective at controlling <b>ethanol</b> consumption and the anxiety and depression produced by forced abstinence from <b>ethanol</b>.
+NPS	drug	alcohol	22739468	We found that the anxiolytic and anti depressant effects of <strong>NPS</strong> are enhanced in acute <b>ethanol</b> abstinent mice.
+NPS	drug	alcohol	22739468	In addition, we found that <strong>NPS</strong> reduced <b>ethanol</b> consumption and is not in and of itself rewarding.
+NPS	drug	alcohol	22739468	We also provide evidence that <b>ethanol</b> consumption increases the ability of <strong>NPS</strong> to modulate neuronal activity in the basolateral amygdala.
+NPS	drug	alcohol	22739468	Finally, we found that local injection of <strong>NPS</strong> in the basolateral amygdala promotes anxiolysis after chronic <b>ethanol</b> consumption, thereby providing insight into the molecular mechanism underlying the changes in behavioral response to <strong>NPS</strong>.
+NPS	drug	alcohol	22739468	In light of the improved anxiolytic efficacy and benign side effects of <strong>NPS</strong> in <b>ethanol</b> withdrawn animals, the NPSR may prove a suitable target for reducing relapse in <b>alcoholism</b>.
+NPS	addiction	relapse	22739468	In light of the improved anxiolytic efficacy and benign side effects of <strong>NPS</strong> in ethanol withdrawn animals, the NPSR may prove a suitable target for reducing <b>relapse</b> in alcoholism.
+NPS	drug	cocaine	22580238	The long use of ephedrine, amphetamines, <b>cocaine</b>, LSD and more recently 3,4 methylenedioxy N methylamphetamine (MDMA; "Ecstasy") allows us to predict with some confidence what cardiovascular risks are likely to be associated with novel psychoactive substances (<strong>NPS</strong>).
+NPS	drug	psychedelics	22580238	The long use of ephedrine, amphetamines, cocaine, <b>LSD</b> and more recently 3,4 methylenedioxy N methylamphetamine (<b>MDMA</b>; "<b>Ecstasy</b>") allows us to predict with some confidence what cardiovascular risks are likely to be associated with novel psychoactive substances (<strong>NPS</strong>).
+NPS	drug	benzodiazepine	22248636	In conclusion, the present study indicates that the <strong>NPS</strong>/NPSR system does not tonically control locomotion, sensitivity to <b>diazepam</b>, anxiety, depressive like behaviours, memory and pain transmission in mice.
+NPS	addiction	reward	21575659	Adult male offspring of female rats that received PS or no PS (<strong>nPS</strong>) were implanted with MFB stimulating electrodes, and were then tested in <b>ICSS</b> paradigms.
+NPS	drug	cocaine	21575659	In both <strong>nPS</strong> and PS offspring, acute <b>cocaine</b> injection decreased ICSS thresholds dose dependently.
+NPS	addiction	reward	21575659	In both <strong>nPS</strong> and PS offspring, acute cocaine injection decreased <b>ICSS</b> thresholds dose dependently.
+NPS	drug	cocaine	20974945	<strong>Neuropeptide S</strong> facilitates cue induced relapse to <b>cocaine</b> seeking through activation of the hypothalamic hypocretin system.
+NPS	addiction	relapse	20974945	<strong>Neuropeptide S</strong> facilitates cue induced <b>relapse</b> to cocaine <b>seeking</b> through activation of the hypothalamic hypocretin system.
+NPS	addiction	relapse	20974945	Here we describe a role of the neuropeptide S (<strong>NPS</strong>) system in regulating <b>relapse</b>.
+NPS	addiction	relapse	20974945	Here we describe a role of the <strong>neuropeptide S</strong> (<strong>NPS</strong>) system in regulating <b>relapse</b>.
+NPS	drug	cocaine	20974945	Intracerebroventricular (ICV) injection of <strong>NPS</strong> increased conditioned reinstatement of <b>cocaine</b> seeking, whereas peripheral administration of the <strong>NPS</strong> receptor antagonist SHA 68 reduced it.
+NPS	addiction	relapse	20974945	Intracerebroventricular (ICV) injection of <strong>NPS</strong> increased conditioned <b>reinstatement</b> of cocaine <b>seeking</b>, whereas peripheral administration of the <strong>NPS</strong> receptor antagonist SHA 68 reduced it.
+NPS	drug	cocaine	20974945	Manipulation of the <strong>NPS</strong> receptor system did not modify <b>cocaine</b> self administration.
+NPS	drug	cocaine	20974945	Of note, intra LH and intra PeF administration of <strong>NPS</strong> increased conditioned reinstatement of <b>cocaine</b> responding, an effect that was selectively blocked with the Hcrt 1/Ox A receptor selective antagonist SB334867.
+NPS	addiction	relapse	20974945	Of note, intra LH and intra PeF administration of <strong>NPS</strong> increased conditioned <b>reinstatement</b> of cocaine responding, an effect that was selectively blocked with the Hcrt 1/Ox A receptor selective antagonist SB334867.
+NPS	drug	cocaine	20974945	Finally, results showed that intra LH injection of the <strong>NPS</strong> antagonist [D Cys(tBu) (5)]<strong>NPS</strong> blocked cue induced <b>cocaine</b> seeking, indicating a role for this system in the pathophysiology of drug relapse.
+NPS	addiction	relapse	20974945	Finally, results showed that intra LH injection of the <strong>NPS</strong> antagonist [D Cys(tBu) (5)]<strong>NPS</strong> blocked cue induced cocaine <b>seeking</b>, indicating a role for this system in the pathophysiology of drug <b>relapse</b>.
+NPS	addiction	addiction	20603169	Neuropeptide S (<strong>NPS</strong>), a recently discovered bioactive peptide, was reported to regulate arousal, anxiety, locomotion, feeding behaviors, memory, and drug <b>addiction</b>.
+NPS	addiction	addiction	20603169	<strong>Neuropeptide S</strong> (<strong>NPS</strong>), a recently discovered bioactive peptide, was reported to regulate arousal, anxiety, locomotion, feeding behaviors, memory, and drug <b>addiction</b>.
+NPS	drug	alcohol	19860802	<strong>Neuropeptide S</strong> receptor gene expression in <b>alcohol</b> withdrawal and protracted abstinence in postdependent rats.
+NPS	addiction	withdrawal	19860802	<strong>Neuropeptide S</strong> receptor gene expression in alcohol <b>withdrawal</b> and protracted abstinence in postdependent rats.
+NPS	drug	alcohol	19860802	Recently, it has been shown that neuropeptide S (<strong>NPS</strong>), a newly deorphanized neuropeptide receptor system, facilitates relapse to <b>alcohol</b> seeking in laboratory animals.
+NPS	addiction	relapse	19860802	Recently, it has been shown that neuropeptide S (<strong>NPS</strong>), a newly deorphanized neuropeptide receptor system, facilitates <b>relapse</b> to alcohol <b>seeking</b> in laboratory animals.
+NPS	drug	alcohol	19860802	Recently, it has been shown that <strong>neuropeptide S</strong> (<strong>NPS</strong>), a newly deorphanized neuropeptide receptor system, facilitates relapse to <b>alcohol</b> seeking in laboratory animals.
+NPS	addiction	relapse	19860802	Recently, it has been shown that <strong>neuropeptide S</strong> (<strong>NPS</strong>), a newly deorphanized neuropeptide receptor system, facilitates <b>relapse</b> to alcohol <b>seeking</b> in laboratory animals.
+NPS	drug	alcohol	19860802	Given that a history of <b>ethanol</b> intoxication may increase vulnerability to <b>alcohol</b> addiction, we sought to determine whether <strong>NPS</strong> receptor (NPSR) gene expression is altered during withdrawal.
+NPS	addiction	addiction	19860802	Given that a history of ethanol intoxication may increase vulnerability to alcohol <b>addiction</b>, we sought to determine whether <strong>NPS</strong> receptor (NPSR) gene expression is altered during withdrawal.
+NPS	addiction	intoxication	19860802	Given that a history of ethanol <b>intoxication</b> may increase vulnerability to alcohol addiction, we sought to determine whether <strong>NPS</strong> receptor (NPSR) gene expression is altered during withdrawal.
+NPS	addiction	withdrawal	19860802	Given that a history of ethanol intoxication may increase vulnerability to alcohol addiction, we sought to determine whether <strong>NPS</strong> receptor (NPSR) gene expression is altered during <b>withdrawal</b>.
+NPS	addiction	intoxication	19860802	To investigate the functional significance of NPSR system adaptation following protracted withdrawal 7 days after <b>intoxication</b>, we tested the anxiolytic like properties of <strong>NPS</strong> in nondependent and postdependent rats using the shock probe defensive burying test (DB).
+NPS	addiction	withdrawal	19860802	To investigate the functional significance of NPSR system adaptation following protracted <b>withdrawal</b> 7 days after intoxication, we tested the anxiolytic like properties of <strong>NPS</strong> in nondependent and postdependent rats using the shock probe defensive burying test (DB).
+NPS	addiction	reward	19345242	Neuropeptide S (<strong>NPS</strong>), a recently identified bioactive peptide through reverse pharmacology approach, was reported to regulate arousal, anxiety, locomotor activity, feeding behaviors and drug <b>reward</b>.
+NPS	addiction	reward	19345242	<strong>Neuropeptide S</strong> (<strong>NPS</strong>), a recently identified bioactive peptide through reverse pharmacology approach, was reported to regulate arousal, anxiety, locomotor activity, feeding behaviors and drug <b>reward</b>.
+NPS	addiction	withdrawal	19345242	In the present study, we evaluated the effects of <strong>NPS</strong> in pain modulation at the supraspinal level for the first time, using the tail <b>withdrawal</b> test and hot plate test in mice.
+NPS	drug	opioid	19345242	was not affected by <b>naloxone</b> (i.c.v., 10 nmol co injection or i.p., 10 mg/kg, 10 min prior to <strong>NPS</strong>) in both tail withdrawal test and hot plate test.
+NPS	addiction	withdrawal	19345242	was not affected by naloxone (i.c.v., 10 nmol co injection or i.p., 10 mg/kg, 10 min prior to <strong>NPS</strong>) in both tail <b>withdrawal</b> test and hot plate test.
+NPS	drug	opioid	19345242	These results revealed that <strong>NPS</strong> could produce antinociception through <strong>NPS</strong> receptor, but not <b>opioid</b> receptor, and <strong>NPS</strong> NPSR system could be a potential target for developing new analgesic drugs.
+NPS	drug	cocaine	19339610	<strong>Neuropeptide S</strong> reinstates <b>cocaine</b> seeking behavior and increases locomotor activity through corticotropin releasing factor receptor 1 in mice.
+NPS	addiction	relapse	19339610	<strong>Neuropeptide S</strong> reinstates cocaine <b>seeking</b> behavior and increases locomotor activity through corticotropin releasing factor receptor 1 in mice.
+NPS	drug	cocaine	19339610	Here, we used a self administration paradigm to demonstrate that intracerebroventricular infusion of <strong>NPS</strong> reinstates extinguished <b>cocaine</b> seeking behavior in a dose dependent manner in mice.
+NPS	addiction	relapse	19339610	Here, we used a self administration paradigm to demonstrate that intracerebroventricular infusion of <strong>NPS</strong> reinstates extinguished cocaine <b>seeking</b> behavior in a dose dependent manner in mice.
+NPS	drug	cocaine	19339610	The highest dose of <strong>NPS</strong> (0.45 nM) increased active lever pressing in the absence of <b>cocaine</b> to levels that were equivalent to those observed during self administration.
+NPS	drug	cocaine	19339610	CRF(1) knock out mice did not respond to either the locomotor stimulant or <b>cocaine</b> reinstatement effects of <strong>NPS</strong>, but still responded to its anxiolytic effect.
+NPS	addiction	relapse	19339610	CRF(1) knock out mice did not respond to either the locomotor stimulant or cocaine <b>reinstatement</b> effects of <strong>NPS</strong>, but still responded to its anxiolytic effect.
+NPS	addiction	relapse	19339610	The CRF(1) antagonist antalarmin also blocked the increase in active lever responding in the <b>reinstatement</b> model and the locomotor activating properties of <strong>NPS</strong> without affecting its anxiolytic actions.
+NPS	drug	cocaine	19339610	Our results suggest that <strong>NPS</strong> receptors may be an important target for drug abuse research and treatment and that CRF(1) mediates the <b>cocaine</b> seeking and locomotor stimulant effects of <strong>NPS</strong>, but not its effects on anxiety like behavior.
+NPS	addiction	relapse	19339610	Our results suggest that <strong>NPS</strong> receptors may be an important target for drug abuse research and treatment and that CRF(1) mediates the cocaine <b>seeking</b> and locomotor stimulant effects of <strong>NPS</strong>, but not its effects on anxiety like behavior.
+NPS	drug	alcohol	19322167	Persistent increase of <b>alcohol</b> seeking evoked by <strong>neuropeptide S</strong>: an effect mediated by the hypothalamic hypocretin system.
+NPS	addiction	relapse	19322167	Persistent increase of alcohol <b>seeking</b> evoked by <strong>neuropeptide S</strong>: an effect mediated by the hypothalamic hypocretin system.
+NPS	drug	alcohol	19322167	This study examined in rats the effects of a newly deorphanized neuropeptide receptor and its cognate ligand, Neuropeptide S (<strong>NPS</strong>), on <b>ethanol</b> consumption and reinstatement of <b>ethanol</b> seeking by environmental cues previously associated with <b>ethanol</b> availability.
+NPS	addiction	relapse	19322167	This study examined in rats the effects of a newly deorphanized neuropeptide receptor and its cognate ligand, Neuropeptide S (<strong>NPS</strong>), on ethanol consumption and <b>reinstatement</b> of ethanol <b>seeking</b> by environmental cues previously associated with ethanol availability.
+NPS	drug	alcohol	19322167	This study examined in rats the effects of a newly deorphanized neuropeptide receptor and its cognate ligand, <strong>Neuropeptide S</strong> (<strong>NPS</strong>), on <b>ethanol</b> consumption and reinstatement of <b>ethanol</b> seeking by environmental cues previously associated with <b>ethanol</b> availability.
+NPS	addiction	relapse	19322167	This study examined in rats the effects of a newly deorphanized neuropeptide receptor and its cognate ligand, <strong>Neuropeptide S</strong> (<strong>NPS</strong>), on ethanol consumption and <b>reinstatement</b> of ethanol <b>seeking</b> by environmental cues previously associated with ethanol availability.
+NPS	drug	alcohol	19322167	In the self administration experiments, the stable response rates observed for <b>ethanol</b> reinforcement were not modified by intracerebroventricular (ICV) injection of <strong>NPS</strong> (1.0 and 2.0 nmol per rat).
+NPS	addiction	reward	19322167	In the self administration experiments, the stable response rates observed for ethanol <b>reinforcement</b> were not modified by intracerebroventricular (ICV) injection of <strong>NPS</strong> (1.0 and 2.0 nmol per rat).
+NPS	drug	alcohol	19322167	ICV <strong>NPS</strong> treatment (1.0, 2.0 and 4.0 nmol per rat) resulted in a significant increase of <b>ethanol</b> seeking elicited by <b>ethanol</b> associated cues.
+NPS	addiction	relapse	19322167	ICV <strong>NPS</strong> treatment (1.0, 2.0 and 4.0 nmol per rat) resulted in a significant increase of ethanol <b>seeking</b> elicited by ethanol associated cues.
+NPS	addiction	relapse	19322167	In contrast, <strong>NPS</strong> did not affect the <b>reinstatement</b> of responding to water paired stimuli.
+NPS	drug	alcohol	19322167	Site specific <strong>NPS</strong> injection (0.1 and 0.5 nmol per rat) into the lateral hypothalamus also reinstated extinguished responding to <b>ethanol</b>.
+NPS	drug	alcohol	19322167	These results provide the first demonstration that activation of <strong>NPS</strong> receptors in the LH intensifies relapse to <b>ethanol</b> seeking elicited by environmental conditioning factors.
+NPS	addiction	relapse	19322167	These results provide the first demonstration that activation of <strong>NPS</strong> receptors in the LH intensifies <b>relapse</b> to ethanol <b>seeking</b> elicited by environmental conditioning factors.
+NPS	drug	alcohol	19322167	Based on the present findings, we also predict that antagonism at <strong>NPS</strong> receptors could represent a novel pharmacological approach to <b>alcohol</b> relapse treatment.
+NPS	addiction	relapse	19322167	Based on the present findings, we also predict that antagonism at <strong>NPS</strong> receptors could represent a novel pharmacological approach to alcohol <b>relapse</b> treatment.
+NPS	addiction	intoxication	19120588	To provide an overview of <b>binge</b> drinking in college aged women and to suggest strategies for nurse practitioners (<strong>NPs</strong>) to assist women in preventing the negative consequences associated with this behavior.
+NPS	drug	alcohol	19120588	<strong>NPs</strong> must be aware of this phenomenon and carefully screen women for high risk <b>alcohol</b> use.
+NPS	drug	opioid	18992779	<strong>Neuropeptide S</strong> inhibits the acquisition and the expression of conditioned place preference to <b>morphine</b> in mice.
+NPS	drug	opioid	18992779	In the present study, we examined the influence of <strong>NPS</strong> on the rewarding action of <b>morphine</b>, using the unbiased conditioned place preference (CPP) paradigm.
+NPS	addiction	reward	18992779	In the present study, we examined the influence of <strong>NPS</strong> on the rewarding action of morphine, using the unbiased conditioned place preference (<b>CPP</b>) paradigm.
+NPS	drug	opioid	18992779	For testing the effect of <strong>NPS</strong> on the acquisition of <b>morphine</b> CPP, mice were given the combination of <strong>NPS</strong> and <b>morphine</b> on the conditioning days, and without drug treatment on the followed test day.
+NPS	addiction	reward	18992779	For testing the effect of <strong>NPS</strong> on the acquisition of morphine <b>CPP</b>, mice were given the combination of <strong>NPS</strong> and morphine on the conditioning days, and without drug treatment on the followed test day.
+NPS	drug	opioid	18992779	To study the effect of <strong>NPS</strong> on the expression of <b>morphine</b> CPP, mice received the treatment of saline/<b>morphine</b> on the conditioning days, and <strong>NPS</strong> on the test day, 15 min before the placement in the CPP apparatus.
+NPS	addiction	reward	18992779	To study the effect of <strong>NPS</strong> on the expression of morphine <b>CPP</b>, mice received the treatment of saline/morphine on the conditioning days, and <strong>NPS</strong> on the test day, 15 min before the placement in the <b>CPP</b> apparatus.
+NPS	drug	opioid	18992779	Our results showed that <strong>NPS</strong> (0.3 10 nmol) alone neither induced place preference nor aversion, however, <strong>NPS</strong> (1 and 3 nmol) blocked the acquisition of CPP induced by 3 nmol <b>morphine</b>, and acquisition of 6 nmol <b>morphine</b> induced CPP was also reduced by <strong>NPS</strong> (6 and 10 nmol).
+NPS	addiction	aversion	18992779	Our results showed that <strong>NPS</strong> (0.3 10 nmol) alone neither induced place preference nor <b>aversion</b>, however, <strong>NPS</strong> (1 and 3 nmol) blocked the acquisition of CPP induced by 3 nmol morphine, and acquisition of 6 nmol morphine induced CPP was also reduced by <strong>NPS</strong> (6 and 10 nmol).
+NPS	addiction	reward	18992779	Our results showed that <strong>NPS</strong> (0.3 10 nmol) alone neither induced place preference nor aversion, however, <strong>NPS</strong> (1 and 3 nmol) blocked the acquisition of <b>CPP</b> induced by 3 nmol morphine, and acquisition of 6 nmol morphine induced <b>CPP</b> was also reduced by <strong>NPS</strong> (6 and 10 nmol).
+NPS	drug	opioid	18992779	Moreover, the expression of CPP induced by 6 nmol <b>morphine</b> was also inhibited by <strong>NPS</strong> (0.1, 1 and 10 nmol).
+NPS	addiction	reward	18992779	Moreover, the expression of <b>CPP</b> induced by 6 nmol morphine was also inhibited by <strong>NPS</strong> (0.1, 1 and 10 nmol).
+NPS	drug	opioid	18992779	These results revealed the involvement of <strong>NPS</strong> in rewarding activities of <b>morphine</b>, and demonstrated the interaction between <strong>NPS</strong> system and <b>opioid</b> system for the first time.
+NPS	drug	nicotine	18431218	Data were collected from a written survey of (1) parental <b>smokers</b> accompanying their children to a pediatric ED who consented and were randomized to participate in a <b>tobacco</b> cessation intervention and (2) medical doctors (MDs) or nurse practitioners (<strong>NPs</strong>) caring for their child.
+NPS	drug	nicotine	18431218	Of the MDs/<strong>NPs</strong> participating in this survey, 224 (97.4%) and 206 (89.6%) agreed that the "ED is a good place to screen parents for <b>tobacco</b> use" and that the "ED is a good place to give advice about <b>tobacco</b> cessation," respectively.
+NPS	drug	alcohol	18225963	To define, among a sample of college students, the nature and extent of nonmedical use of prescription stimulants (<strong>NPS</strong>), including both overuse and use of someone else's drug, for attention deficit hyperactivity disorder (ADHD); to characterize <strong>NPS</strong> among individuals not medically using a prescription stimulant for ADHD; and to determine whether <strong>NPS</strong> and overuse of a medically prescribed stimulant for ADHD were independently associated with an increased risk of other illicit drug use and dependence on <b>alcohol</b> and marijuana.
+NPS	drug	cannabinoid	18225963	To define, among a sample of college students, the nature and extent of nonmedical use of prescription stimulants (<strong>NPS</strong>), including both overuse and use of someone else's drug, for attention deficit hyperactivity disorder (ADHD); to characterize <strong>NPS</strong> among individuals not medically using a prescription stimulant for ADHD; and to determine whether <strong>NPS</strong> and overuse of a medically prescribed stimulant for ADHD were independently associated with an increased risk of other illicit drug use and dependence on alcohol and <b>marijuana</b>.
+NPS	addiction	dependence	18225963	To define, among a sample of college students, the nature and extent of nonmedical use of prescription stimulants (<strong>NPS</strong>), including both overuse and use of someone else's drug, for attention deficit hyperactivity disorder (ADHD); to characterize <strong>NPS</strong> among individuals not medically using a prescription stimulant for ADHD; and to determine whether <strong>NPS</strong> and overuse of a medically prescribed stimulant for ADHD were independently associated with an increased risk of other illicit drug use and <b>dependence</b> on alcohol and marijuana.
+NPS	drug	alcohol	18225963	All students completed a 2 hour personal interview to ascertain medical use and overuse of prescription stimulants, <strong>NPS</strong>, nonmedical use of other prescription drugs and illicit drug use, and dependence on <b>alcohol</b> and marijuana.
+NPS	drug	cannabinoid	18225963	All students completed a 2 hour personal interview to ascertain medical use and overuse of prescription stimulants, <strong>NPS</strong>, nonmedical use of other prescription drugs and illicit drug use, and dependence on alcohol and <b>marijuana</b>.
+NPS	addiction	dependence	18225963	All students completed a 2 hour personal interview to ascertain medical use and overuse of prescription stimulants, <strong>NPS</strong>, nonmedical use of other prescription drugs and illicit drug use, and <b>dependence</b> on alcohol and marijuana.
+NPS	drug	alcohol	18225963	Both <strong>NPS</strong> and overuse of prescribed stimulants for ADHD were independently associated with past year use of five drugs, holding constant sociodemographic characteristics; <strong>NPS</strong> was also associated with <b>alcohol</b> and marijuana dependence.
+NPS	drug	cannabinoid	18225963	Both <strong>NPS</strong> and overuse of prescribed stimulants for ADHD were independently associated with past year use of five drugs, holding constant sociodemographic characteristics; <strong>NPS</strong> was also associated with alcohol and <b>marijuana</b> dependence.
+NPS	addiction	dependence	18225963	Both <strong>NPS</strong> and overuse of prescribed stimulants for ADHD were independently associated with past year use of five drugs, holding constant sociodemographic characteristics; <strong>NPS</strong> was also associated with alcohol and marijuana <b>dependence</b>.
+NPS	drug	opioid	17664052	However, federal legislation restricts nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) from prescribing <b>buprenorphine</b>, which may limit its potential for uptake and inhibit the role of these nonphysician providers in delivering drug addiction treatment to patients with HIV.
+NPS	addiction	addiction	17664052	However, federal legislation restricts nurse practitioners (<strong>NPs</strong>) and physician assistants (PAs) from prescribing buprenorphine, which may limit its potential for uptake and inhibit the role of these nonphysician providers in delivering drug <b>addiction</b> treatment to patients with HIV.
+NPS	drug	opioid	17664052	<strong>NPs</strong> and PAs are interested in prescribing <b>buprenorphine</b>.
+NPS	addiction	withdrawal	17469862	Even though the surface of the wafer is placed either vertical or parallel to the monolayer compression direction during the LB transfer, the one dimensional (1D) array of Au <strong>NPs</strong> is observed along the <b>withdrawal</b> direction of the wafer.
+NPS	drug	alcohol	17300536	People struggling with <b>alcohol</b> use are more likely to encounter <strong>NPs</strong>, family doctors, or social workers than counselors specializing in <b>alcohol</b> treatment.
+NPS	drug	nicotine	16499741	To raise awareness among nurse practitioners (<strong>NPs</strong>) about the <b>nicotine</b> inhaler by providing clinical and practical information about the use of the <b>nicotine</b> inhaler as a treatment option for <b>smoking</b> cessation.
+NPS	drug	nicotine	16499741	<strong>NPs</strong> can include the <b>nicotine</b> inhaler in a group of <b>nicotine</b> replacement therapies to ensure that <b>smokers</b> are successful in <b>tobacco</b> cessation.
+NPS	drug	nicotine	15495693	To explore how <b>tobacco</b> dependent nurse practitioners (<strong>NPs</strong>) describe their experiences with health promotion and disease prevention practices with patients who smoke.
+NPS	addiction	relapse	8457763	By developing a standard procedure for identifying patients who smoke, encouraging cessation on each visit, teaching <b>relapse</b> prevention skills, and following up, <strong>NPs</strong> can help ease the withdrawal symptoms that accompany the cessation process.
+NPS	addiction	withdrawal	8457763	By developing a standard procedure for identifying patients who smoke, encouraging cessation on each visit, teaching relapse prevention skills, and following up, <strong>NPs</strong> can help ease the <b>withdrawal</b> symptoms that accompany the cessation process.
+NPS	drug	alcohol	1599627	This relationship is probably not caused by saccharin tasting like <b>alcohol</b> to a rat, because other results indicate that the <strong>NPs</strong> do not have more negative reactions initially to the taste of <b>alcohol</b>, but it might be related to similar mechanisms mediating the reinforcement from sweet tastes and from systemic <b>alcohol</b>.
+NPS	addiction	reward	1599627	This relationship is probably not caused by saccharin tasting like alcohol to a rat, because other results indicate that the <strong>NPs</strong> do not have more negative reactions initially to the taste of alcohol, but it might be related to similar mechanisms mediating the <b>reinforcement</b> from sweet tastes and from systemic alcohol.
+CRHR1	addiction	withdrawal	32450347	At hippocampal level, the <b>withdrawal</b> induced changes in the levels of AMPA receptor GluA1 and GluA2/3 subunits, PSD 95 protein, corticotropin releasing factor (Crf) and Crf receptor 1 (<strong>CrfR1</strong>) mRNA were biphasic: AMPA receptor subunit and PSD95 protein levels initially remained unchanged and decreased after 60 90 days, whereas Crf/<strong>CrfR1</strong> mRNA levels initially increased and then markedly decreased after 60 days.
+CRHR1	drug	alcohol	32059962	In control rats, <b>ethanol</b> mediated inhibition of NMDARs was prevented by <strong>CRF1</strong> receptor (CRFR1) blockade with antalarmin, while CRF/CRFR1 mediated NMDAR blockade was prevented by intracellularly applied inhibitor of phosphatases PP1/PP2A, okadaic acid, but not the selective striatal enriched tyrosine protein phosphatase inhibitor, TC 2153.
+CRHR1	drug	alcohol	32059962	In control rats, <b>ethanol</b> mediated inhibition of NMDARs was prevented by <strong>CRF1</strong> receptor (<strong>CRFR1</strong>) blockade with antalarmin, while CRF/<strong>CRFR1</strong> mediated NMDAR blockade was prevented by intracellularly applied inhibitor of phosphatases PP1/PP2A, okadaic acid, but not the selective striatal enriched tyrosine protein phosphatase inhibitor, TC 2153.
+CRHR1	drug	alcohol	32059962	These findings suggest a cellular mechanism whereby chronic <b>alcohol</b> dysregulates the hormonal and behavioral responses to repetitive stressors by increasing NMDAR function and decreasing <strong>CRFR1</strong> function.
+CRHR1	drug	alcohol	32041742	Within the amygdala, the corticotropin releasing factor (CRF) system has been shown to mediate some of the effects of both stress and <b>ethanol</b>, but the effects of <b>ethanol</b> on specific <strong>CRF1</strong> receptor circuits in the amygdala have not been fully established.
+CRHR1	drug	alcohol	32041742	We used male <strong>CRF1</strong>:GFP reporter mice to characterize <strong>CRF1</strong> expressing (<strong>CRF1</strong>+) and nonexpressing (<strong>CRF1</strong> ) LA neurons and investigate the effects of acute and chronic <b>ethanol</b> exposure on these populations.
+CRHR1	drug	alcohol	32041742	<strong>CRF1</strong>+ neurons exhibited a tonic conductance that was insensitive to acute <b>ethanol</b>.
+CRHR1	drug	alcohol	32041742	<strong>CRF1</strong>  neurons did not display a basal tonic conductance, but the application of acute <b>ethanol</b> induced a δ GABAA receptor subunit dependent tonic conductance and enhanced phasic GABA release onto these cells.
+CRHR1	drug	alcohol	32041742	Chronic <b>ethanol</b> increased <strong>CRF1</strong>+ neuronal excitability but did not significantly alter phasic or tonic GABA signaling in either <strong>CRF1</strong>+ or <strong>CRF1</strong>  cells.
+CRHR1	drug	alcohol	32041742	Together, these results provide the first characterization of the <strong>CRF1</strong>+ population of LA neurons and suggest mechanisms for differential acute <b>ethanol</b> sensitivity within this region.
+CRHR1	drug	alcohol	32028150	We also showed previously that systemic antagonism of corticotropin releasing factor 1 receptors (<strong>CRFR1</strong>) reduced escalation of operant <b>alcohol</b> SA in rats not indexed for avoidance, that corticotropin releasing factor (CRF) infusions into the central amygdala (CeA) produced conditioned place avoidance in stress naïve rats, and that intra CeA infusion of a <strong>CRFR1</strong> antagonist reduced hyperalgesia in Avoiders.
+CRHR1	addiction	addiction	32028150	We also showed previously that systemic antagonism of corticotropin releasing factor 1 receptors (<strong>CRFR1</strong>) reduced <b>escalation</b> of operant alcohol SA in rats not indexed for avoidance, that corticotropin releasing factor (CRF) infusions into the central amygdala (CeA) produced conditioned place avoidance in stress naïve rats, and that intra CeA infusion of a <strong>CRFR1</strong> antagonist reduced hyperalgesia in Avoiders.
+CRHR1	addiction	reward	32028150	We also showed previously that systemic antagonism of corticotropin releasing factor 1 receptors (<strong>CRFR1</strong>) reduced escalation of <b>operant</b> alcohol SA in rats not indexed for avoidance, that corticotropin releasing factor (CRF) infusions into the central amygdala (CeA) produced conditioned place avoidance in stress naïve rats, and that intra CeA infusion of a <strong>CRFR1</strong> antagonist reduced hyperalgesia in Avoiders.
+CRHR1	drug	alcohol	32028150	Finally, we show that intra CeA <strong>CRFR1</strong> antagonism reversed post stress escalation of <b>alcohol</b> SA and reduced avoidance behavior in Avoiders.
+CRHR1	addiction	addiction	32028150	Finally, we show that intra CeA <strong>CRFR1</strong> antagonism reversed post stress <b>escalation</b> of alcohol SA and reduced avoidance behavior in Avoiders.
+CRHR1	drug	alcohol	32028150	Collectively, these findings suggest that elucidation of the mechanisms by which <strong>CRFR1</strong> gated CeA circuits regulate avoidance behavior and <b>alcohol</b> SA may lead to better understanding of the neural mechanisms underlying co morbid PTSD and AUD.
+CRHR1	drug	alcohol	31330967	Corticotropin releasing factor (CRF) signaling via limbic <strong>CRF1</strong> and 2 receptors (CRF1R and CRF2R, respectively) is known to modulate binge like <b>ethanol</b> consumption in rodents.
+CRHR1	addiction	intoxication	31330967	Corticotropin releasing factor (CRF) signaling via limbic <strong>CRF1</strong> and 2 receptors (CRF1R and CRF2R, respectively) is known to modulate <b>binge</b> like ethanol consumption in rodents.
+CRHR1	addiction	aversion	31282111	We used the conditioned place <b>aversion</b> (CPA) paradigm to evaluate the role of corticotropin releasing factor (CRF)/<strong>CRF1</strong> receptor signaling on the BDNF expression and corticosterone plasma levels after CPA expression and extinction.
+CRHR1	drug	opioid	31282111	In addition, the pre treatment with the <strong>CRF1</strong> receptor antagonist CP 154 526 before <b>naloxone</b> conditioning session impaired <b>morphine</b> withdrawal induced aversive memory acquisition, the increased corticosterone plasma levels, and the expression of BDNF observed after CPA expression in the DG and BLA.
+CRHR1	addiction	aversion	31282111	In addition, the pre treatment with the <strong>CRF1</strong> receptor antagonist CP 154 526 before naloxone conditioning session impaired morphine withdrawal induced <b>aversive</b> memory acquisition, the increased corticosterone plasma levels, and the expression of BDNF observed after CPA expression in the DG and BLA.
+CRHR1	addiction	withdrawal	31282111	In addition, the pre treatment with the <strong>CRF1</strong> receptor antagonist CP 154 526 before naloxone conditioning session impaired morphine <b>withdrawal</b> induced aversive memory acquisition, the increased corticosterone plasma levels, and the expression of BDNF observed after CPA expression in the DG and BLA.
+CRHR1	drug	nicotine	31234859	Semen Ziziphi Spinosae (SZS), a prototypical hypnotic sedative herb in Oriental medicine, exhibits anxiolytic effects during <b>nicotine</b> withdrawal by improving amygdaloid CRF/<strong>CRF1</strong> receptor (CRFR1) signaling.
+CRHR1	addiction	withdrawal	31234859	Semen Ziziphi Spinosae (SZS), a prototypical hypnotic sedative herb in Oriental medicine, exhibits anxiolytic effects during nicotine <b>withdrawal</b> by improving amygdaloid CRF/<strong>CRF1</strong> receptor (CRFR1) signaling.
+CRHR1	drug	nicotine	31234859	Semen Ziziphi Spinosae (SZS), a prototypical hypnotic sedative herb in Oriental medicine, exhibits anxiolytic effects during <b>nicotine</b> withdrawal by improving amygdaloid CRF/<strong>CRF1</strong> receptor (<strong>CRFR1</strong>) signaling.
+CRHR1	addiction	withdrawal	31234859	Semen Ziziphi Spinosae (SZS), a prototypical hypnotic sedative herb in Oriental medicine, exhibits anxiolytic effects during nicotine <b>withdrawal</b> by improving amygdaloid CRF/<strong>CRF1</strong> receptor (<strong>CRFR1</strong>) signaling.
+CRHR1	drug	alcohol	31151762	In the European American sample, we identified three additional genome wide significant maximum habitual <b>alcohol</b> consumption loci: on chromosome 17, rs77804065 (p = 1.5 × 10 12), at <strong>CRHR1</strong> (corticotropin releasing hormone receptor 1); the protein product of this gene is involved in stress and immune responses; and on chromosomes 8 and 10.
+CRHR1	drug	alcohol	31151762	In the European American sample, we identified three additional genome wide significant maximum habitual <b>alcohol</b> consumption loci: on chromosome 17, rs77804065 (p = 1.5 × 10 12), at <strong>CRHR1</strong> (<strong>corticotropin releasing hormone receptor 1</strong>); the protein product of this gene is involved in stress and immune responses; and on chromosomes 8 and 10.
+CRHR1	drug	alcohol	31151762	The present study supports five novel <b>alcohol</b> use risk loci, with particularly strong statistical support for <strong>CRHR1</strong>.
+CRHR1	drug	opioid	31071414	<b>Oxycodone</b> CPP males have: a) increases in Bdnf (brain derived neurotrophic factor) expression, which is known to be produced in granule cells, relative to females; b) elevated Mapk1 expression and pMAPK ir in the dentate hilus which harbors newly generated granule cells; and c) increases in <strong>CRHR1</strong> ir in CA3 pyramidal cell soma.
+CRHR1	addiction	reward	31071414	Oxycodone <b>CPP</b> males have: a) increases in Bdnf (brain derived neurotrophic factor) expression, which is known to be produced in granule cells, relative to females; b) elevated Mapk1 expression and pMAPK ir in the dentate hilus which harbors newly generated granule cells; and c) increases in <strong>CRHR1</strong> ir in CA3 pyramidal cell soma.
+CRHR1	addiction	addiction	30886240	Optogenetic dissection of the downstream neuronal pathways demonstrates that the reversal of <b>addiction</b> like behaviors is observed after the inhibition of CeA CRF projections to the bed nucleus of the stria terminalis (BNST) and that inhibition of the CRFCeA BNST pathway is mediated by inhibition of the CRF <strong>CRF1</strong> system and inhibition of BNST cell firing.
+CRHR1	drug	nicotine	30722977	Changes in striatal dopamine release and locomotor activity following acute withdrawal from chronic <b>nicotine</b> are mediated by <strong>CRF1</strong>, but not CRF2, receptors.
+CRHR1	addiction	withdrawal	30722977	Changes in striatal dopamine release and locomotor activity following acute <b>withdrawal</b> from chronic nicotine are mediated by <strong>CRF1</strong>, but not CRF2, receptors.
+CRHR1	drug	nicotine	30722977	The aim of the present study was to investigate the participation of corticotropin releasing factor (CRF) receptors (<strong>CRF1</strong> and CRF2) in the alterations of the dorsal and ventral striatal dopamine release and the vertical and horizontal locomotor activity observed in rats following chronic <b>nicotine</b> treatment and consequent acute withdrawal.
+CRHR1	addiction	withdrawal	30722977	The aim of the present study was to investigate the participation of corticotropin releasing factor (CRF) receptors (<strong>CRF1</strong> and CRF2) in the alterations of the dorsal and ventral striatal dopamine release and the vertical and horizontal locomotor activity observed in rats following chronic nicotine treatment and consequent acute <b>withdrawal</b>.
+CRHR1	drug	nicotine	30722977	The present study demonstrates that the changes of striatal dopamine release and locomotor activity observed following chronic <b>nicotine</b> treatment and consequent acute withdrawal are mediated by <strong>CRF1</strong>, but not CRF2, receptor.
+CRHR1	addiction	withdrawal	30722977	The present study demonstrates that the changes of striatal dopamine release and locomotor activity observed following chronic nicotine treatment and consequent acute <b>withdrawal</b> are mediated by <strong>CRF1</strong>, but not CRF2, receptor.
+CRHR1	drug	opioid	30391476	In the present study, the effect of chronic <b>morphine</b> on the subcellular distribution of mu <b>opioid</b> (MOR) and CRF receptors (<strong>CRFR</strong>) was investigated in the LC of male and female rats using immunoelectron microscopy.
+CRHR1	drug	opioid	30391476	Interestingly, chronic <b>morphine</b> exposure induced <strong>CRFR</strong> recruitment to the plasma membrane of both male and female LC neurons.
+CRHR1	drug	opioid	30391476	These findings provide a potential mechanism by which chronic <b>opioid</b> administration increases stress vulnerability in males and females via an increase in surface availability of <strong>CRFR</strong> in LC neurons.
+CRHR1	drug	cocaine	30355627	Enhanced <strong>CRFR1</strong> Dependent Regulation of a Ventral Tegmental Area to Prelimbic Cortex Projection Establishes Susceptibility to Stress Induced <b>Cocaine</b> Seeking.
+CRHR1	addiction	relapse	30355627	Enhanced <strong>CRFR1</strong> Dependent Regulation of a Ventral Tegmental Area to Prelimbic Cortex Projection Establishes Susceptibility to Stress Induced Cocaine <b>Seeking</b>.
+CRHR1	addiction	relapse	30355627	Both shock induced <b>reinstatement</b> and the prelimbic cortex Fos response were prevented by bilateral intra VTA injections of the CRF receptor 1 (<strong>CRFR1</strong>) antagonist, antalarmin.
+CRHR1	drug	cocaine	30355627	Finally, LgA, but not ShA, <b>cocaine</b> self administration resulted in increased VTA <strong>CRFR1</strong> mRNA levels as measured using in situ hybridization.
+CRHR1	drug	cocaine	30355627	Moreover, we report that this pathway may be recruited as a result of daily <b>cocaine</b> self administration under conditions of extended drug access/heightened drug intake, likely as a result of increased <strong>CRFR1</strong> expression in the VTA, thereby promoting susceptibility to stress induced <b>cocaine</b> seeking.
+CRHR1	addiction	relapse	30355627	Moreover, we report that this pathway may be recruited as a result of daily cocaine self administration under conditions of extended drug access/heightened drug intake, likely as a result of increased <strong>CRFR1</strong> expression in the VTA, thereby promoting susceptibility to stress induced cocaine <b>seeking</b>.
+CRHR1	drug	alcohol	30220589	The center of the emotional universe: <b>Alcohol</b>, stress, and <strong>CRF1</strong> amygdala circuitry.
+CRHR1	drug	alcohol	30220589	Specific intra amygdala circuits and cell type specific subpopulations are emerging as critical targets for stress  and <b>alcohol</b> induced plasticity, chief among them the corticotropin releasing factor (CRF) and CRF receptor 1 (<strong>CRF1</strong>) system.
+CRHR1	drug	alcohol	30220589	CRF and <strong>CRF1</strong> have been implicated in the effects of <b>alcohol</b> in several amygdala nuclei, including the basolateral (BLA) and central amygdala (CeA); however, the precise circuitry involved in these effects and the role of these circuits in stress and anxiety are only beginning to be understood.
+CRHR1	drug	alcohol	29946104	Opposing actions of <strong>CRF R1</strong> and CB1 receptors on VTA GABAergic plasticity following chronic exposure to <b>ethanol</b>.
+CRHR1	drug	alcohol	29946104	In naive animals, activation of <strong>CRF R1</strong> by bath application of CRF or <b>ethanol</b> enhanced GABAA inhibitory postsynaptic currents (IPSCs).
+CRHR1	addiction	sensitization	29857328	Significantly higher <strong>CRF1</strong> and CRF2 receptor levels after <b>sensitization</b> were detected in the Hip.
+CRHR1	drug	opioid	29853227	Association between stress pathway gene (<strong>CRHR1</strong>⧹CRHBP) polymorphisms and <b>heroin</b> dependence.
+CRHR1	addiction	dependence	29853227	Association between stress pathway gene (<strong>CRHR1</strong>⧹CRHBP) polymorphisms and heroin <b>dependence</b>.
+CRHR1	drug	opioid	29853227	To explore the relationship between stress pathway gene (<strong>CRHR1</strong>⧹CRHBP) polymorphisms and <b>heroin</b> dependence, nine tag single nucleotide polymorphisms (<strong>CRHR1</strong> rs12953076, rs4458044, rs242924, rs17689966; CRHBP rs1715751, rs3792738, rs32897, rs10062367, rs1875999) of stress related genes were genotyped by TaqMan SNP genotyping assay for 524 <b>heroin</b> dependent patients who were abstinent and 489 normal controls.
+CRHR1	addiction	dependence	29853227	To explore the relationship between stress pathway gene (<strong>CRHR1</strong>⧹CRHBP) polymorphisms and heroin <b>dependence</b>, nine tag single nucleotide polymorphisms (<strong>CRHR1</strong> rs12953076, rs4458044, rs242924, rs17689966; CRHBP rs1715751, rs3792738, rs32897, rs10062367, rs1875999) of stress related genes were genotyped by TaqMan SNP genotyping assay for 524 heroin dependent patients who were abstinent and 489 normal controls.
+CRHR1	drug	opioid	29780165	Optogenetic inhibition of mPCF neuronal terminals or local infusion of the CRF receptor 1 (<strong>CRFR1</strong>) antagonist in the NAc restored the effects of neuropathic pain on <b>morphine</b> induced CPP behavior, but not in normal mice.
+CRHR1	addiction	reward	29780165	Optogenetic inhibition of mPCF neuronal terminals or local infusion of the CRF receptor 1 (<strong>CRFR1</strong>) antagonist in the NAc restored the effects of neuropathic pain on morphine induced <b>CPP</b> behavior, but not in normal mice.
+CRHR1	drug	opioid	29780165	Local G9a knockdown increased the expression of <strong>CRFR1</strong> and mimicked CCI induced hypersensitivity to acquiring <b>morphine</b> CPP.
+CRHR1	addiction	reward	29780165	Local G9a knockdown increased the expression of <strong>CRFR1</strong> and mimicked CCI induced hypersensitivity to acquiring morphine <b>CPP</b>.
+CRHR1	drug	alcohol	29700576	However, detailed characterization of the specific influences that local neuronal populations exert in mediating <b>alcohol</b> responses is hampered by current limitations in pharmacological and immunohistochemical tools for targeting CRH receptor subtype 1 (<strong>CRHR1</strong>).
+CRHR1	drug	alcohol	29700576	A Cre inducible <strong>Crhr1</strong> expressing adeno associated virus (AAV) was site specifically injected into the CeA of αCaMKII CreERT2 transgenic rats to analyze the role of <strong>CRHR1</strong> in αCaMKII neurons on <b>alcohol</b> self administration and reinstatement behavior.
+CRHR1	addiction	relapse	29700576	A Cre inducible <strong>Crhr1</strong> expressing adeno associated virus (AAV) was site specifically injected into the CeA of αCaMKII CreERT2 transgenic rats to analyze the role of <strong>CRHR1</strong> in αCaMKII neurons on alcohol self administration and <b>reinstatement</b> behavior.
+CRHR1	drug	alcohol	29700576	AAV mediated gene transfer in αCaMKII neurons induced a 24 fold increase of <strong>Crhr1</strong> mRNA in the CeA which had no effect on locomotor activity, <b>alcohol</b> self administration, or cue induced reinstatement.
+CRHR1	addiction	relapse	29700576	AAV mediated gene transfer in αCaMKII neurons induced a 24 fold increase of <strong>Crhr1</strong> mRNA in the CeA which had no effect on locomotor activity, alcohol self administration, or cue induced <b>reinstatement</b>.
+CRHR1	addiction	relapse	29700576	However, rats overexpressing <strong>Crhr1</strong> in the CeA increased responding in the stress induced <b>reinstatement</b> task with yohimbine serving as a pharmacological stressor.
+CRHR1	drug	alcohol	29700576	We demonstrate that <strong>CRHR1</strong> overexpression in CeA αCaMKII neurons is sufficient to mediate increased vulnerability to stress triggered relapse into <b>alcohol</b> seeking.
+CRHR1	addiction	relapse	29700576	We demonstrate that <strong>CRHR1</strong> overexpression in CeA αCaMKII neurons is sufficient to mediate increased vulnerability to stress triggered <b>relapse</b> into alcohol <b>seeking</b>.
+CRHR1	drug	alcohol	29696309	Persistent escalation of <b>alcohol</b> consumption by mice exposed to brief episodes of social defeat stress: suppression by <strong>CRF R1</strong> antagonism.
+CRHR1	addiction	addiction	29696309	Persistent <b>escalation</b> of alcohol consumption by mice exposed to brief episodes of social defeat stress: suppression by <strong>CRF R1</strong> antagonism.
+CRHR1	drug	alcohol	29696309	Mice with a history of episodic social defeat stress were selectively sensitive to the effects of <strong>CRF R1</strong> antagonism, suggesting that <strong>CRF R1</strong> may be a potential target for treating <b>alcohol</b> use disorders in individuals who escalate their drinking after exposure to repeated bouts of psychosocial stress.
+CRHR1	drug	alcohol	29497387	Evaluation of <b>Alcohol</b> Preference and Drinking in msP Rats Bearing a <strong>Crhr1</strong> Promoter Polymorphism.
+CRHR1	drug	alcohol	29497387	The type 1 corticotropin releasing factor (<strong>CRF1</strong>) receptor has received much attention for its putative role in the progression to <b>alcohol</b> dependence, although at present its success in clinical trials has been limited.
+CRHR1	addiction	dependence	29497387	The type 1 corticotropin releasing factor (<strong>CRF1</strong>) receptor has received much attention for its putative role in the progression to alcohol <b>dependence</b>, although at present its success in clinical trials has been limited.
+CRHR1	drug	alcohol	29497387	Two single nucleotide polymorphisms in the rat <strong>Crhr1</strong> promoter have been identified in the Marchigian substrain of Sardinian <b>alcohol</b> preferring (msP) rats.
+CRHR1	drug	alcohol	29497387	Unlike other Wistar derived <b>alcohol</b> preferring lines, nondependent msP rats reduce their <b>alcohol</b> self administration in response to <strong>CRF1</strong> antagonists and show increased brain <strong>CRF1</strong> expression.
+CRHR1	drug	alcohol	29497387	The current study tested the hypotheses that the A alleles in the <strong>Crhr1</strong> promoter polymorphisms are: (1) unique to msP (vs. CRF1 antagonist insensitive) <b>alcohol</b> preferring lines and (2) associate with greater <b>alcohol</b> preference or intake.
+CRHR1	drug	alcohol	29497387	The current study tested the hypotheses that the A alleles in the <strong>Crhr1</strong> promoter polymorphisms are: (1) unique to msP (vs. <strong>CRF1</strong> antagonist insensitive) <b>alcohol</b> preferring lines and (2) associate with greater <b>alcohol</b> preference or intake.
+CRHR1	drug	alcohol	29497387	Two related polymorphisms were observed in which both loci on a given chromosome were either mutant variant (A) or wild type (G) alleles within the distal <strong>Crhr1</strong> promoter of 17/25 msP rats (68%), as compared to 0/23 Indiana P rats, 0/20 Sardinian <b>alcohol</b> preferring rats bred at Scripps (Scr:sP) and 0/21 outbred Wistar rats.
+CRHR1	drug	alcohol	29497387	<b>Alcohol</b> consumption in msP rats did not differ according to the presence of <strong>Crhr1</strong> A alleles, but greater <b>alcohol</b> preference (98%) was observed in A allele homozygous msP rats (AA) compared to msP rats with wild type (GG, 91%) or heterozygous (GA, 91%) genotypes.
+CRHR1	drug	opioid	29407532	The involvement of <strong>CRF1</strong> receptor within the basolateral amygdala and dentate gyrus in the <b>naloxone</b> induced conditioned place aversion in <b>morphine</b> dependent mice.
+CRHR1	addiction	aversion	29407532	The involvement of <strong>CRF1</strong> receptor within the basolateral amygdala and dentate gyrus in the naloxone induced conditioned place <b>aversion</b> in morphine dependent mice.
+CRHR1	addiction	aversion	29407532	However, the involvement of <strong>CRF1</strong> receptor (CRF1R) in <b>aversive</b> memory induced by opiate withdrawal has yet to be elucidated.
+CRHR1	addiction	withdrawal	29407532	However, the involvement of <strong>CRF1</strong> receptor (CRF1R) in aversive memory induced by opiate <b>withdrawal</b> has yet to be elucidated.
+CRHR1	drug	alcohol	29391279	Using quantitative real time polymerase chain reaction, we further confirmed that the expression of genes implicated in <b>alcohol</b> addiction, BDNF, <strong>CRHR1</strong> and OPRM1, was also altered by transplantation of gut microbes from <b>alcohol</b> exposed donors.
+CRHR1	addiction	addiction	29391279	Using quantitative real time polymerase chain reaction, we further confirmed that the expression of genes implicated in alcohol <b>addiction</b>, BDNF, <strong>CRHR1</strong> and OPRM1, was also altered by transplantation of gut microbes from alcohol exposed donors.
+CRHR1	drug	cocaine	29391155	Antagonism of corticotropin releasing factor <strong>CRF1</strong> receptors blocks the enhanced response to <b>cocaine</b> after social stress.
+CRHR1	drug	cocaine	29391155	Blockade of corticotropin releasing factor <strong>CRF1</strong> receptor reversed the increase in <b>cocaine</b> CPP induced by social defeat.
+CRHR1	addiction	reward	29391155	Blockade of corticotropin releasing factor <strong>CRF1</strong> receptor reversed the increase in cocaine <b>CPP</b> induced by social defeat.
+CRHR1	drug	cocaine	29391155	The effect of RSD on <b>cocaine</b> sensitization was again blocked by the corticotropin releasing factor <strong>CRF1</strong> receptor antagonist, while peripheral CRF2 receptor antagonist did not show effect.
+CRHR1	addiction	sensitization	29391155	The effect of RSD on cocaine <b>sensitization</b> was again blocked by the corticotropin releasing factor <strong>CRF1</strong> receptor antagonist, while peripheral CRF2 receptor antagonist did not show effect.
+CRHR1	drug	cocaine	29180955	The ability of many drugs of abuse, including <b>cocaine</b>, to mediate reinforcement and drug seeking behaviors is in part mediated by the corticotropin releasing hormone (CRH) system, in which CRH exerts its effects partly via the CRH receptor subtype 1 (<strong>CRHR1</strong>) in extra hypothalamic areas.
+CRHR1	addiction	relapse	29180955	The ability of many drugs of abuse, including cocaine, to mediate reinforcement and drug <b>seeking</b> behaviors is in part mediated by the corticotropin releasing hormone (CRH) system, in which CRH exerts its effects partly via the CRH receptor subtype 1 (<strong>CRHR1</strong>) in extra hypothalamic areas.
+CRHR1	addiction	reward	29180955	The ability of many drugs of abuse, including cocaine, to mediate <b>reinforcement</b> and drug seeking behaviors is in part mediated by the corticotropin releasing hormone (CRH) system, in which CRH exerts its effects partly via the CRH receptor subtype 1 (<strong>CRHR1</strong>) in extra hypothalamic areas.
+CRHR1	drug	cocaine	29180955	In fact, <strong>CRHR1</strong> expressed in regions of the mesolimbic dopamine (DA) system have been demonstrated to modify <b>cocaine</b> induced DA release and alter <b>cocaine</b> mediated behaviors.
+CRHR1	drug	cocaine	29180955	Here we examined the role of neuronal selectivity of <strong>CRHR1</strong> within the mesolimbic system on <b>cocaine</b> induced behaviors.
+CRHR1	drug	cocaine	29180955	We then studied <b>cocaine</b> sensitization, self administration, and reinstatement in inducible <strong>CRHR1</strong> knockouts using the CreERT2/loxP in either dopamine transporter (DAT) containing neurons (DAT <strong>Crhr1</strong>) or dopamine receptor 1 (D1) containing neurons (D1 <strong>Crhr1</strong>).
+CRHR1	addiction	relapse	29180955	We then studied cocaine sensitization, self administration, and <b>reinstatement</b> in inducible <strong>CRHR1</strong> knockouts using the CreERT2/loxP in either dopamine transporter (DAT) containing neurons (DAT <strong>Crhr1</strong>) or dopamine receptor 1 (D1) containing neurons (D1 <strong>Crhr1</strong>).
+CRHR1	addiction	sensitization	29180955	We then studied cocaine <b>sensitization</b>, self administration, and reinstatement in inducible <strong>CRHR1</strong> knockouts using the CreERT2/loxP in either dopamine transporter (DAT) containing neurons (DAT <strong>Crhr1</strong>) or dopamine receptor 1 (D1) containing neurons (D1 <strong>Crhr1</strong>).
+CRHR1	drug	cocaine	29180955	There were no differences in the acute or sensitized locomotor response to <b>cocaine</b> in DAT <strong>Crhr1</strong> or D1 <strong>Crhr1</strong> mice and their respective controls.
+CRHR1	drug	cocaine	29180955	Furthermore, both DAT <strong>Crhr1</strong> and D1 <strong>Crhr1</strong> mice reliably self administered <b>cocaine</b> at the level of controls.
+CRHR1	addiction	relapse	29180955	However, DAT <strong>Crhr1</strong> mice demonstrated a significant increase in cue induced <b>reinstatement</b> relative to controls, whereas D1 <strong>Crhr1</strong> mice demonstrated a significant decrease in cue induced <b>reinstatement</b> relative to controls.
+CRHR1	drug	cocaine	29180955	These data demonstrate the involvement of <strong>CRHR1</strong> in cue induced reinstatement following <b>cocaine</b> self administration, and implicate a bi directional role of <strong>CRHR1</strong> for <b>cocaine</b> craving.
+CRHR1	addiction	relapse	29180955	These data demonstrate the involvement of <strong>CRHR1</strong> in cue induced <b>reinstatement</b> following cocaine self administration, and implicate a bi directional role of <strong>CRHR1</strong> for cocaine <b>craving</b>.
+CRHR1	drug	alcohol	29118713	After having had continuous access to <b>ethanol</b> (20% weight/volume) for 4 weeks, control and stressed mice had CRF type 1 (<strong>CRFR1</strong>) or type 2 (CRFR2) receptor antagonists infused into the BNST and then had access to <b>ethanol</b> for 24 h. In separate cohorts of control and stressed mice, we assessed mRNA levels of BNST CRF, <strong>CRFR1</strong> and CRFR2.
+CRHR1	drug	alcohol	29118713	The selective blockade of BNST <strong>CRFR1</strong> with CP376,395 effectively reduced <b>alcohol</b> drinking in non stressed mice, whereas the selective CRFR2 antagonist astressin2B produced a dose dependent increase in <b>ethanol</b> consumption in both non stressed controls and stressed mice.
+CRHR1	drug	alcohol	29118713	CRF <strong>CRFR1</strong> signaling in the BNST seems to underlie <b>ethanol</b> intake in non stressed mice, whereas CRFR2 modulates <b>alcohol</b> consumption in both socially defeated and non stressed mice with a history of chronic intake.
+CRHR1	drug	alcohol	29082267	EOD induced <b>alcohol</b> consumption was insensitive to <strong>CRFR1</strong> blockade by antalarmin, but subjects with high CSF levels of CRF were more responsive.
+CRHR1	drug	amphetamine	29064909	Pexacerfont as a <strong>CRF1</strong> antagonist for the treatment of withdrawal symptoms in men with heroin/<b>methamphetamine</b> dependence: a randomized, double blind, placebo controlled clinical trial.
+CRHR1	drug	opioid	29064909	Pexacerfont as a <strong>CRF1</strong> antagonist for the treatment of withdrawal symptoms in men with <b>heroin</b>/methamphetamine dependence: a randomized, double blind, placebo controlled clinical trial.
+CRHR1	addiction	dependence	29064909	Pexacerfont as a <strong>CRF1</strong> antagonist for the treatment of withdrawal symptoms in men with heroin/methamphetamine <b>dependence</b>: a randomized, double blind, placebo controlled clinical trial.
+CRHR1	addiction	withdrawal	29064909	Pexacerfont as a <strong>CRF1</strong> antagonist for the treatment of <b>withdrawal</b> symptoms in men with heroin/methamphetamine dependence: a randomized, double blind, placebo controlled clinical trial.
+CRHR1	addiction	withdrawal	29064909	We assessed the efficacy of pexacerfont, a <strong>CRF1</strong> antagonist, for the treatment of <b>withdrawal</b> symptoms.
+CRHR1	drug	alcohol	28940382	A large body of animal literature implicates CRF acting at type 1 CRF receptors (<strong>CRFR1</strong>) in consumption by <b>alcohol</b> dependent subjects, stress induced reinstatement of <b>alcohol</b> seeking, and possibly binge <b>alcohol</b> consumption.
+CRHR1	addiction	intoxication	28940382	A large body of animal literature implicates CRF acting at type 1 CRF receptors (<strong>CRFR1</strong>) in consumption by alcohol dependent subjects, stress induced reinstatement of alcohol seeking, and possibly <b>binge</b> alcohol consumption.
+CRHR1	addiction	relapse	28940382	A large body of animal literature implicates CRF acting at type 1 CRF receptors (<strong>CRFR1</strong>) in consumption by alcohol dependent subjects, stress induced <b>reinstatement</b> of alcohol <b>seeking</b>, and possibly binge alcohol consumption.
+CRHR1	drug	alcohol	28940382	These studies have encouraged recent pilot studies of <strong>CRFR1</strong> antagonists in humans with <b>alcohol</b> use disorder (AUD).
+CRHR1	drug	alcohol	28833238	<strong>CRF1</strong> Receptor Dependent Increases in Irritability Like Behavior During Abstinence from Chronic Intermittent <b>Ethanol</b> Vapor Exposure.
+CRHR1	drug	alcohol	28833238	The corticotropin releasing factor (CRF) <strong>CRF1</strong> receptor system has been suggested to be critical for the emergence of anxiety like behavior in <b>ethanol</b> dependence, but the role of this system in irritability like behavior has not been characterized.
+CRHR1	addiction	dependence	28833238	The corticotropin releasing factor (CRF) <strong>CRF1</strong> receptor system has been suggested to be critical for the emergence of anxiety like behavior in ethanol <b>dependence</b>, but the role of this system in irritability like behavior has not been characterized.
+CRHR1	drug	alcohol	28833238	Irritability like behavior is a clinically relevant and reliable measure of negative emotional states that is partially mediated by activation of the CRF <strong>CRF1</strong> system and remains elevated during protracted abstinence in <b>ethanol</b> dependent rats.
+CRHR1	drug	alcohol	28807676	Therefore, in this study we used in vitro slice electrophysiology to investigate the effects of CRF and its receptor subtype (<strong>CRF1</strong> and CRF2) antagonists on both evoked and spontaneous action potential independent glutamatergic transmission in the CeA of naive and <b>ethanol</b> dependent Sprague Dawley rats.
+CRHR1	drug	alcohol	28807676	Collectively our data show that CRF primarily acts at presynaptic <strong>CRF1</strong> to produce opposite effects on CeA evoked and spontaneous glutamate release and that the CRF system modulates CeA glutamatergic synapses throughout the development of <b>alcohol</b> dependence.
+CRHR1	addiction	dependence	28807676	Collectively our data show that CRF primarily acts at presynaptic <strong>CRF1</strong> to produce opposite effects on CeA evoked and spontaneous glutamate release and that the CRF system modulates CeA glutamatergic synapses throughout the development of alcohol <b>dependence</b>.
+CRHR1	drug	alcohol	28734867	Here we report that acute <b>alcohol</b> interacts with the CRF/<strong>CRF1</strong> system, such that CRF and <b>alcohol</b> act via presynaptic CRF1s and P/Q type voltage gated calcium channels to promote vesicular GABA release and that both compounds occlude the effects of each other at these synapses.
+CRHR1	drug	alcohol	28734867	Chronic <b>alcohol</b> exposure does not alter P/Q type voltage gated calcium channel membrane abundance or this <strong>CRF1</strong>/P/Q type voltage gated calcium channel mechanism of acute <b>alcohol</b> induced GABA release, indicating that <b>alcohol</b> engages this molecular mechanism at CeA GABAergic synapses throughout the transition to dependence.
+CRHR1	addiction	dependence	28734867	Chronic alcohol exposure does not alter P/Q type voltage gated calcium channel membrane abundance or this <strong>CRF1</strong>/P/Q type voltage gated calcium channel mechanism of acute alcohol induced GABA release, indicating that alcohol engages this molecular mechanism at CeA GABAergic synapses throughout the transition to <b>dependence</b>.
+CRHR1	drug	cocaine	28725939	Repeated infusion of CRF into the VTA persistently alters <b>cocaine</b> valuation and intensifies binge like drug intake in a <strong>CRF R1</strong> dependent manner.
+CRHR1	addiction	intoxication	28725939	Repeated infusion of CRF into the VTA persistently alters cocaine valuation and intensifies <b>binge</b> like drug intake in a <strong>CRF R1</strong> dependent manner.
+CRHR1	drug	cocaine	28698920	Prevention and reversal of social stress escalated <b>cocaine</b> self administration in mice by intra VTA <strong>CRFR1</strong> antagonism.
+CRHR1	drug	cocaine	28698920	The current study examines the roles of CRF and CRF receptor 1 (<strong>CRFR1</strong>) in escalated intravenous <b>cocaine</b> self administration after exposure to social defeat stress in mice.
+CRHR1	drug	cocaine	28698920	To further explore the role of <strong>CRFR1</strong>, CP 376,395 (0.5 and 1 μg/0.2 μl) was infused directly into the VTA before the <b>cocaine</b> self administration session.
+CRHR1	drug	cocaine	28698920	Intra VTA antagonism of <strong>CRFR1</strong> was sufficient to reverse social defeat stress escalated <b>cocaine</b> self administration.
+CRHR1	drug	cocaine	28698920	These findings suggest that CRF and <strong>CRFR1</strong> exert multiple roles in the response to social stress that are relevant to escalated <b>cocaine</b> self administration.
+CRHR1	drug	opioid	28434951	The extent of hyperalgesia was greater in KO versus WT mice, suggesting a role of <strong>CRF1</strong> receptors in the upward modulation of endogenous <b>opioid</b> release.
+CRHR1	addiction	sensitization	28434951	Our results show that CRF/<strong>CRF1</strong> receptors seem to be a protective role in latent pain <b>sensitization</b> induced by surgery and in the local inflammatory response to injury.
+CRHR1	drug	cocaine	28431969	<strong>CRFR1</strong> in the ventromedial caudate putamen modulates acute stress enhanced expression of <b>cocaine</b> locomotor sensitization.
+CRHR1	addiction	sensitization	28431969	<strong>CRFR1</strong> in the ventromedial caudate putamen modulates acute stress enhanced expression of cocaine locomotor <b>sensitization</b>.
+CRHR1	addiction	sensitization	28431969	Moreover, the enhancement in locomotor <b>sensitization</b> was paralleled by a selective increase in the number of the c Fos+ cells, the level of <strong>CRFR1</strong> mRNA in the ventromedial caudate putamen (vmCPu).
+CRHR1	drug	cocaine	28431969	Furthermore, the enhancement was significantly attenuated by <strong>CRFR1</strong> antagonist NBI 27914 into the vmCPu, implying that the up regulation of <strong>CRFR1</strong> in the vmCPu seems to be critical in the acute stress enhanced expression of <b>cocaine</b> locomotor sensitization.
+CRHR1	addiction	sensitization	28431969	Furthermore, the enhancement was significantly attenuated by <strong>CRFR1</strong> antagonist NBI 27914 into the vmCPu, implying that the up regulation of <strong>CRFR1</strong> in the vmCPu seems to be critical in the acute stress enhanced expression of cocaine locomotor <b>sensitization</b>.
+CRHR1	drug	cocaine	28431969	The findings demonstrate that the long term effect of acute stress on the expression of <b>cocaine</b> locomotor sensitization is partially mediated by <strong>CRFR1</strong> in the vmCPu.
+CRHR1	addiction	sensitization	28431969	The findings demonstrate that the long term effect of acute stress on the expression of cocaine locomotor <b>sensitization</b> is partially mediated by <strong>CRFR1</strong> in the vmCPu.
+CRHR1	drug	alcohol	28363981	Collectively, our data indicate that <b>alcohol</b> dependence functionally alters the molecular mechanisms underlying the CeA's response to <b>alcohol</b> (from LTCC  to <strong>CRF1</strong> driven).
+CRHR1	addiction	dependence	28363981	Collectively, our data indicate that alcohol <b>dependence</b> functionally alters the molecular mechanisms underlying the CeA's response to alcohol (from LTCC  to <strong>CRF1</strong> driven).
+CRHR1	addiction	relapse	28265716	We describe potential markers of activation towards individualized treatment, human genetic, and functional data that still implicate <strong>CRF1</strong> systems in emotional disturbance, sex differences, and suggestive clinical findings for <strong>CRF1</strong> antagonists in food <b>craving</b> and CRF driven HPA axis overactivation.
+CRHR1	drug	cocaine	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>), and brain derived neurotrophic factor (BDNF) genes on susceptibility to crack <b>cocaine</b> addiction and BDNF levels.
+CRHR1	addiction	addiction	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>), and brain derived neurotrophic factor (BDNF) genes on susceptibility to crack cocaine <b>addiction</b> and BDNF levels.
+CRHR1	drug	cocaine	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>), and brain derived neurotrophic factor (BDNF) genes on susceptibility to crack <b>cocaine</b> addiction and BDNF levels.
+CRHR1	addiction	addiction	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>), and brain derived neurotrophic factor (BDNF) genes on susceptibility to crack cocaine <b>addiction</b> and BDNF levels.
+CRHR1	drug	cocaine	28237884	This study suggests that SNPs in the NR3C1 and <strong>CRHR1</strong> genes may influence BDNF levels, but this effect is blunted in the context of crack <b>cocaine</b> addiction.
+CRHR1	addiction	addiction	28237884	This study suggests that SNPs in the NR3C1 and <strong>CRHR1</strong> genes may influence BDNF levels, but this effect is blunted in the context of crack cocaine <b>addiction</b>.
+CRHR1	drug	nicotine	28222901	In the present review, we analyze reports studying the role of Corticotropin Releasing Factor (CRF), the principle neuroendocrine mediator of the stress response and its two receptors (<strong>CRF1</strong> and CRF2) in the withdrawal phase as well as in the abstinence from <b>nicotine</b> use.
+CRHR1	addiction	withdrawal	28222901	In the present review, we analyze reports studying the role of Corticotropin Releasing Factor (CRF), the principle neuroendocrine mediator of the stress response and its two receptors (<strong>CRF1</strong> and CRF2) in the <b>withdrawal</b> phase as well as in the abstinence from nicotine use.
+CRHR1	drug	cocaine	28137450	<strong>CRF1</strong> receptor deficiency increases <b>cocaine</b> reward.
+CRHR1	addiction	reward	28137450	<strong>CRF1</strong> receptor deficiency increases cocaine <b>reward</b>.
+CRHR1	drug	cocaine	28137450	Herein, we report that <strong>CRF1</strong> receptor deficient (<strong>CRF1</strong> / ), but not wild type, mice show conditioned place preference (CPP) responses to a relatively low <b>cocaine</b> dose (5 mg/kg, i.p.).
+CRHR1	addiction	reward	28137450	Herein, we report that <strong>CRF1</strong> receptor deficient (<strong>CRF1</strong> / ), but not wild type, mice show conditioned place preference (<b>CPP</b>) responses to a relatively low cocaine dose (5 mg/kg, i.p.).
+CRHR1	drug	cocaine	28137450	Conversely, wild type, but not <strong>CRF1</strong> / , mice display CPP responses to a relatively high <b>cocaine</b> dose (20 mg/kg, i.p.
+CRHR1	addiction	reward	28137450	Conversely, wild type, but not <strong>CRF1</strong> / , mice display <b>CPP</b> responses to a relatively high cocaine dose (20 mg/kg, i.p.
+CRHR1	drug	cocaine	28137450	), indicating that <strong>CRF1</strong> receptor deficiency alters the rewarding effects of <b>cocaine</b>.
+CRHR1	drug	cocaine	28137450	Acute pharmacological antagonism of the <strong>CRF1</strong> receptor by antalarmin also eliminates <b>cocaine</b> reward.
+CRHR1	addiction	reward	28137450	Acute pharmacological antagonism of the <strong>CRF1</strong> receptor by antalarmin also eliminates cocaine <b>reward</b>.
+CRHR1	drug	cocaine	28137450	Nevertheless, <strong>CRF1</strong> /  mice display higher stereotypy responses to <b>cocaine</b> than wild type mice.
+CRHR1	drug	cocaine	28137450	Full rescue of wild type like corticosterone and GR circadian rhythm and level in <strong>CRF1</strong> /  mice by exogenous corticosterone does not affect <strong>CRF1</strong> receptor dependent <b>cocaine</b> reward but induces stereotypy responses to <b>cocaine</b>.
+CRHR1	addiction	reward	28137450	Full rescue of wild type like corticosterone and GR circadian rhythm and level in <strong>CRF1</strong> /  mice by exogenous corticosterone does not affect <strong>CRF1</strong> receptor dependent cocaine <b>reward</b> but induces stereotypy responses to cocaine.
+CRHR1	drug	cocaine	28137450	These results indicate a critical role for the <strong>CRF1</strong> receptor in <b>cocaine</b> reward, independently of the closely related HPA axis activity.
+CRHR1	addiction	reward	28137450	These results indicate a critical role for the <strong>CRF1</strong> receptor in cocaine <b>reward</b>, independently of the closely related HPA axis activity.
+CRHR1	drug	alcohol	27818644	CRF signaling, mostly via <strong>CRF1</strong> receptors, seems to be particularly important in conditions of excessive <b>alcohol</b> taking and seeking, including during early and protracted withdrawal, relapse, as well as during withdrawal induced anxiety and escalated aggression promoted by <b>alcohol</b>.
+CRHR1	addiction	relapse	27818644	CRF signaling, mostly via <strong>CRF1</strong> receptors, seems to be particularly important in conditions of excessive alcohol taking and <b>seeking</b>, including during early and protracted withdrawal, <b>relapse</b>, as well as during withdrawal induced anxiety and escalated aggression promoted by alcohol.
+CRHR1	addiction	withdrawal	27818644	CRF signaling, mostly via <strong>CRF1</strong> receptors, seems to be particularly important in conditions of excessive alcohol taking and seeking, including during early and protracted <b>withdrawal</b>, relapse, as well as during <b>withdrawal</b> induced anxiety and escalated aggression promoted by alcohol.
+CRHR1	drug	alcohol	27818644	Modulation of <strong>CRF1</strong> function seems to exert a less prominent role over low to moderate <b>alcohol</b> intake, or to species typical behaviors.
+CRHR1	drug	alcohol	27235163	We hypothesized that vmPFC CRF <strong>CRFR1</strong> signaling contributes functionally to stress induced avoidance and escalated <b>alcohol</b> self administration.
+CRHR1	drug	alcohol	27235163	In Experiment 3, rats were stressed and indexed, then tested for the effects of intra vmPFC <strong>CRFR1</strong> antagonism on avoidance and <b>alcohol</b> self administration.
+CRHR1	drug	alcohol	27235163	Intra vmPFC CRF infusion produced avoidance of a paired context, and intra vmPFC <strong>CRFR1</strong> antagonism reversed avoidance of a stress paired context, but did not alter post stress <b>alcohol</b> self administration.
+CRHR1	drug	alcohol	27798128	We previously demonstrated that CRF receptor 1 (<strong>CRF1</strong>) neurons comprise a specific component of the CeA microcircuitry that is selectively engaged by acute <b>ethanol</b>.
+CRHR1	drug	alcohol	27798128	To investigate the impact of chronic <b>ethanol</b> exposure on inhibitory signaling in <strong>CRF1</strong>+ CeA neurons, we used <strong>CRF1</strong>:GFP mice subjected to chronic intermittent <b>ethanol</b> (CIE) inhalation and examined changes in local inhibitory control, the effects of acute <b>ethanol</b>, and the output of these neurons from the CeA.
+CRHR1	addiction	withdrawal	27798128	Following CIE, <strong>CRF1</strong>+ neurons displayed decreased phasic inhibition and a complete loss of tonic inhibition that persisted into <b>withdrawal</b>.
+CRHR1	addiction	withdrawal	27798128	<strong>CRF1</strong>  neurons showed a cell type specific upregulation of both phasic and tonic signaling with CIE, the latter of which persists into <b>withdrawal</b> and is likely mediated by δ subunit containing GABAA receptors.
+CRHR1	drug	alcohol	27798128	<strong>CRF1</strong>+ projection neurons displayed an increased baseline firing rate and loss of sensitivity to acute <b>ethanol</b> following CIE.
+CRHR1	drug	alcohol	27798128	These data demonstrate that chronic <b>ethanol</b> exposure produces profound and long lasting changes in local inhibitory control of the CeA, resulting in an increase in the output of the CeA and the <strong>CRF1</strong> receptor system, in particular.
+CRHR1	drug	alcohol	27798128	We showed previously that CRF receptor 1 expressing (<strong>CRF1</strong>+) neurons in the CeA are under tonic inhibitory control and are differentially regulated by acute <b>ethanol</b> (Herman et al., 2013).
+CRHR1	drug	alcohol	27798128	Here we show that the inhibitory control of <strong>CRF1</strong>+ CeA neurons is lost with chronic <b>ethanol</b> exposure, likely by a functional switch in local tonic signaling.
+CRHR1	drug	alcohol	27798128	The loss of tonic inhibition is seen in <strong>CRF1</strong>+ projection neurons, suggesting that a critical consequence of chronic <b>ethanol</b> exposure is an increase in the output of the CeA <strong>CRF1</strong> system, a neuroadaptation that may contribute to the behavioral consequences of <b>alcohol</b> dependence.
+CRHR1	addiction	dependence	27798128	The loss of tonic inhibition is seen in <strong>CRF1</strong>+ projection neurons, suggesting that a critical consequence of chronic ethanol exposure is an increase in the output of the CeA <strong>CRF1</strong> system, a neuroadaptation that may contribute to the behavioral consequences of alcohol <b>dependence</b>.
+CRHR1	drug	nicotine	27461514	In conclusion, the overexpression of CRF in the BNST prevents the dysphoria like state associated with <b>nicotine</b> withdrawal and increases the CRF2/<strong>CRF1</strong> receptor ratio, which may diminish the negative effects of CRF on mood.
+CRHR1	addiction	withdrawal	27461514	In conclusion, the overexpression of CRF in the BNST prevents the dysphoria like state associated with nicotine <b>withdrawal</b> and increases the CRF2/<strong>CRF1</strong> receptor ratio, which may diminish the negative effects of CRF on mood.
+CRHR1	drug	alcohol	27440230	Therefore, in <b>alcohol</b> preferring rats, we examined the effect of bilateral injections into the NI of the <strong>CRF1</strong> receptor antagonist, CP376395 or the CRF2 receptor antagonist, astressin 2B on yohimbine induced reinstatement of <b>alcohol</b> seeking.
+CRHR1	addiction	relapse	27440230	Therefore, in alcohol preferring rats, we examined the effect of bilateral injections into the NI of the <strong>CRF1</strong> receptor antagonist, CP376395 or the CRF2 receptor antagonist, astressin 2B on yohimbine induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+CRHR1	drug	alcohol	27440230	In line with these data, <strong>CRF1</strong> , but not CRF2 , receptor mRNA was upregulated in the NI following chronic <b>ethanol</b> intake.
+CRHR1	drug	alcohol	27440230	These data suggest that NI neurons contribute to reinstatement of <b>alcohol</b> seeking, via an involvement of <strong>CRF1</strong> signalling.
+CRHR1	addiction	relapse	27440230	These data suggest that NI neurons contribute to <b>reinstatement</b> of alcohol <b>seeking</b>, via an involvement of <strong>CRF1</strong> signalling.
+CRHR1	addiction	intoxication	27374820	Dysregulation of the corticotropin releasing factor (CRF) system has been observed in rodent models of <b>binge</b> drinking, with a large focus on CRF receptor 1 (<strong>CRF R1</strong>).
+CRHR1	addiction	reward	27374820	Using in situ hybridization, the regulation of CRF BP, <strong>CRF R1</strong>, and CRF mRNA expression was determined in the stress and <b>reward</b> systems of C57BL/6J mice after repeated cycles of DID.
+CRHR1	drug	alcohol	27374820	We observed a persistent decrease in CRF BP mRNA expression in the mPFC after 3 and 6 DID cycles, which may allow for increased CRF signaling at <strong>CRF R1</strong> and contribute to excessive binge like <b>ethanol</b> consumption.
+CRHR1	addiction	intoxication	27374820	We observed a persistent decrease in CRF BP mRNA expression in the mPFC after 3 and 6 DID cycles, which may allow for increased CRF signaling at <strong>CRF R1</strong> and contribute to excessive <b>binge</b> like ethanol consumption.
+CRHR1	drug	cocaine	27362504	We predicted that LC NE neurons would exhibit Fos activation on ED1, and that blocking <strong>CRF1</strong> signaling would decrease drug seeking on ED1 measured by responding on an active lever previously associated with <b>cocaine</b> self  administration.
+CRHR1	addiction	relapse	27362504	We predicted that LC NE neurons would exhibit Fos activation on ED1, and that blocking <strong>CRF1</strong> signaling would decrease drug <b>seeking</b> on ED1 measured by responding on an active lever previously associated with cocaine self  administration.
+CRHR1	addiction	relapse	27362504	Prior to this Extinction Day 1 (ED1) session, rats were injected with vehicle or the selective <strong>CRF1</strong> antagonist (CP) to measure effects of CRF antagonism on drug <b>seeking</b> during early abstinence.
+CRHR1	addiction	relapse	27316790	Antalarmin, a selective <strong>CRF1</strong> receptor antagonist, Metyrapone, a corticosterone (CORT) synthesis inhibitor and CORT were evaluated for their effects on the <b>reinstatement</b> test in a cue induced <b>relapse</b> model.
+CRHR1	drug	cocaine	27251131	Activation of corticotropin releasing factor type 1 receptors (<strong>CRF R1</strong>) in the ventral tegmental area (VTA) represents a critical mechanism for social defeat to escalate <b>cocaine</b> self administration in adult rats.
+CRHR1	drug	cocaine	27251131	We determined the acute effect of a <strong>CRF R1</strong> antagonist (CP376395) microinfusion into the VTA prior to each episode of social defeat in adolescent rats and determined whether this drug treatment could prevent later escalation of <b>cocaine</b> taking in early adulthood.
+CRHR1	addiction	addiction	27251131	We determined the acute effect of a <strong>CRF R1</strong> antagonist (CP376395) microinfusion into the VTA prior to each episode of social defeat in adolescent rats and determined whether this drug treatment could prevent later <b>escalation</b> of cocaine taking in early adulthood.
+CRHR1	drug	alcohol	27139233	The finding that a <strong>CRF1</strong> receptor antagonist (CRF1RA) minimized CIA withdrawal induced negative affect supported an association of <b>alcohol</b> withdrawal with a stress mechanism.
+CRHR1	addiction	withdrawal	27139233	The finding that a <strong>CRF1</strong> receptor antagonist (CRF1RA) minimized CIA <b>withdrawal</b> induced negative affect supported an association of alcohol <b>withdrawal</b> with a stress mechanism.
+CRHR1	drug	alcohol	27113502	Corticotropin releasing factor (CRF) signaling at the <strong>CRF1</strong> receptor (CRF1R) in the ventral tegmental area (VTA) can modulate <b>ethanol</b> consumption in rodents.
+CRHR1	drug	alcohol	27109623	The <strong>CRF1</strong> Antagonist Verucerfont in Anxious <b>Alcohol</b> Dependent Women: Translation of Neuroendocrine, But not of Anti Craving Effects.
+CRHR1	addiction	relapse	27109623	The <strong>CRF1</strong> Antagonist Verucerfont in Anxious Alcohol Dependent Women: Translation of Neuroendocrine, But not of Anti <b>Craving</b> Effects.
+CRHR1	drug	alcohol	27109623	Blockade of corticotropin releasing factor receptor 1 (<strong>CRF1</strong>) suppresses stress induced <b>alcohol</b> seeking in rodents, but clinical translation remains.
+CRHR1	addiction	relapse	27109623	Blockade of corticotropin releasing factor receptor 1 (<strong>CRF1</strong>) suppresses stress induced alcohol <b>seeking</b> in rodents, but clinical translation remains.
+CRHR1	drug	alcohol	27109623	In contrast to our recent observations with another <strong>CRF1</strong> antagonist, pexacerfont, verucerfont potently blocked the HPA axis response to the dexamethasone CRF test, but left <b>alcohol</b> craving unaffected.
+CRHR1	addiction	relapse	27109623	In contrast to our recent observations with another <strong>CRF1</strong> antagonist, pexacerfont, verucerfont potently blocked the HPA axis response to the dexamethasone CRF test, but left alcohol <b>craving</b> unaffected.
+CRHR1	drug	alcohol	27109623	The findings do not support a clinical efficacy of <strong>CRF1</strong> blockade in stress induced <b>alcohol</b> craving and relapse.
+CRHR1	addiction	relapse	27109623	The findings do not support a clinical efficacy of <strong>CRF1</strong> blockade in stress induced alcohol <b>craving</b> and <b>relapse</b>.
+CRHR1	drug	alcohol	27063791	Candidate genes for mediating the behavioral interaction between <b>ethanol</b> consumption and wheel running include multiple potassium channel genes, Oprm1, Prkcg, Stxbp1, <strong>Crhr1</strong>, Gabra3, Slc6a13, Stx1b, Pomc, Rassf5 and Camta2.
+CRHR1	drug	cocaine	27053215	Intra VTA antagonism of <strong>CRF R1</strong> in the pVTA and CRF R2 in the aVTA during each social defeat prevented escalated <b>cocaine</b> self administration in a 24 h "binge."
+CRHR1	addiction	intoxication	27053215	Intra VTA antagonism of <strong>CRF R1</strong> in the pVTA and CRF R2 in the aVTA during each social defeat prevented escalated cocaine self administration in a 24 h "<b>binge</b>."
+CRHR1	drug	cocaine	27053215	Previously stressed rats continue to express elevated CRF tone within the VTA and antagonism of pVTA <strong>CRF R1</strong> or aVTA CRF R2 reverses <b>cocaine</b> seeking.
+CRHR1	addiction	relapse	27053215	Previously stressed rats continue to express elevated CRF tone within the VTA and antagonism of pVTA <strong>CRF R1</strong> or aVTA CRF R2 reverses cocaine <b>seeking</b>.
+CRHR1	drug	cocaine	27053215	In conclusion, these experiments demonstrate neuroadaptive changes in tonic and phasic CRF with repeated stress, that CRF release during stress may contribute to later escalated <b>cocaine</b> taking, and that persistently elevated CRF tone in the VTA may drive later <b>cocaine</b> seeking through increased activation of pVTA <strong>CRF R1</strong> and aVTA CRF R2.
+CRHR1	addiction	relapse	27053215	In conclusion, these experiments demonstrate neuroadaptive changes in tonic and phasic CRF with repeated stress, that CRF release during stress may contribute to later escalated cocaine taking, and that persistently elevated CRF tone in the VTA may drive later cocaine <b>seeking</b> through increased activation of pVTA <strong>CRF R1</strong> and aVTA CRF R2.
+CRHR1	addiction	intoxication	27023221	To investigate the precise role of these circuits in regulating impulsivity and <b>binge</b> drinking, the <strong>CRF1</strong> receptor antagonist antalarmin and the novel GABA(A) α2 subunit ligand 3 PBC were infused into the central amygdala (CeA) and medial prefrontal cortex (mPFC).
+CRHR1	addiction	withdrawal	26907806	The <strong>CRF1</strong> and the CRF2 receptor mediate recognition memory deficits and vulnerability induced by opiate <b>withdrawal</b>.
+CRHR1	drug	opioid	26907806	In the present study, <strong>CRF1</strong> / , CRF2 /  and their respective wild type mice are injected with escalating doses of <b>morphine</b> and cognitive function assessed by the novel object recognition (NOR) memory task throughout relatively long periods of opiate withdrawal.
+CRHR1	addiction	withdrawal	26907806	In the present study, <strong>CRF1</strong> / , CRF2 /  and their respective wild type mice are injected with escalating doses of morphine and cognitive function assessed by the novel object recognition (NOR) memory task throughout relatively long periods of opiate <b>withdrawal</b>.
+CRHR1	addiction	withdrawal	26907806	Early (2 days) phases of opiate <b>withdrawal</b> impair NOR memory in wild type, <strong>CRF1</strong> /  and CRF2 /  mice.
+CRHR1	addiction	withdrawal	26907806	However, the duration of opiate <b>withdrawal</b> induced NOR memory deficits is prolonged in <strong>CRF1</strong> /  but shortened in CRF2 /  mice, as compared to their respective wild type mice, indicating opposite roles for the two CRF receptor subtypes.
+CRHR1	drug	alcohol	26576941	Social stress escalated intermittent <b>alcohol</b> drinking: modulation by <strong>CRF R1</strong> in the ventral tegmental area and accumbal dopamine in mice.
+CRHR1	drug	alcohol	26576941	<strong>CRF R1</strong> may be a mechanism for balancing the dysregulation of stress and reward in <b>alcohol</b> use disorders.
+CRHR1	addiction	reward	26576941	<strong>CRF R1</strong> may be a mechanism for balancing the dysregulation of stress and <b>reward</b> in alcohol use disorders.
+CRHR1	drug	alcohol	26519902	Here, we examined the effects of <b>ethanol</b>, CRF and a <strong>CRF1</strong> receptor antagonist on spontaneous and evoked glutamatergic transmission in CeA neurons from Wistar and Marchigian Sardinian Preferring (msP) rats, a rodent line genetically selected for excessive <b>alcohol</b> drinking and characterized by heightened activity of the <strong>CRF1</strong> system.
+CRHR1	drug	opioid	26313266	In the present study, we have evaluated the role of <strong>CRF1</strong> receptor (CRF1R) in the rewarding properties of <b>morphine</b> by using the conditioned place preference (CPP) paradigm.
+CRHR1	addiction	reward	26313266	In the present study, we have evaluated the role of <strong>CRF1</strong> receptor (CRF1R) in the rewarding properties of morphine by using the conditioned place preference (<b>CPP</b>) paradigm.
+CRHR1	drug	alcohol	26247973	Most studies with corticotropin releasing factor (CRF) and <b>ethanol</b> (EtOH) consumption have focused on CRF type 1 (<strong>CRF1</strong>) receptors; less is known about other components of the CRF system, such as the CRF type 2 (CRF2) receptors and the CRF binding protein (CRFBP).
+CRHR1	addiction	withdrawal	25898242	Pharmacological blockade of IPN <strong>CRF1</strong> receptors or optogenetic silencing of MHb input reduced IPI activation and alleviated <b>withdrawal</b> induced anxiety; whereas IPN CRF infusion in mice increased anxiety.
+CRHR1	addiction	relapse	25837282	Based on previous work hypothesizing a role for corticotropin releasing factor (CRF) in the IC during <b>craving</b> and <b>relapse</b>, a subsequent experiment found that CRF receptor 1 (<strong>CRF1</strong>) blockade in the AId similarly reduced cued <b>reinstatement</b>.
+CRHR1	drug	cocaine	25837282	Our results suggest that the AId, along with <strong>CRF1</strong> receptors in this region, regulates reinstatement to <b>cocaine</b> seeking, but not food seeking, depending on the type of reinstatement, whereas PIc activity does not influence cue induced reinstatement.
+CRHR1	addiction	relapse	25837282	Our results suggest that the AId, along with <strong>CRF1</strong> receptors in this region, regulates <b>reinstatement</b> to cocaine <b>seeking</b>, but not food <b>seeking</b>, depending on the type of <b>reinstatement</b>, whereas PIc activity does not influence cue induced <b>reinstatement</b>.
+CRHR1	drug	alcohol	25833034	Chronic intermittent <b>ethanol</b> exposure in mice leads to an up regulation of CRH/<strong>CRHR1</strong> signaling.
+CRHR1	drug	opioid	25830629	Sex differences between <strong>CRF1</strong> receptor deficient mice following <b>naloxone</b> precipitated <b>morphine</b> withdrawal in a conditioned place aversion paradigm: implication of HPA axis.
+CRHR1	addiction	aversion	25830629	Sex differences between <strong>CRF1</strong> receptor deficient mice following naloxone precipitated morphine withdrawal in a conditioned place <b>aversion</b> paradigm: implication of HPA axis.
+CRHR1	addiction	withdrawal	25830629	Sex differences between <strong>CRF1</strong> receptor deficient mice following naloxone precipitated morphine <b>withdrawal</b> in a conditioned place aversion paradigm: implication of HPA axis.
+CRHR1	drug	nicotine	25802844	Ethnic specific genetic association of variants in the <strong>corticotropin releasing hormone receptor 1</strong> gene with <b>nicotine</b> dependence.
+CRHR1	addiction	dependence	25802844	Ethnic specific genetic association of variants in the <strong>corticotropin releasing hormone receptor 1</strong> gene with nicotine <b>dependence</b>.
+CRHR1	drug	alcohol	25802844	Variants in the corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) gene have been associated with <b>alcoholism</b> and depression.
+CRHR1	drug	alcohol	25802844	Variants in the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) gene have been associated with <b>alcoholism</b> and depression.
+CRHR1	drug	nicotine	25802844	In this study, we tested five single nucleotide polymorphisms (SNPs) in <strong>CRHR1</strong> for their association with ND, which was assessed by <b>smoking</b> quantity (SQ), the Heaviness of <b>Smoking</b> Index (HSI), and the Fagerström test for ND (FTND) in 2,037 subjects from 602 families of either European American (EA) or African American (AA) ancestry.
+CRHR1	drug	alcohol	25797192	We hypothesized that the corticotropin releasing factor (CRF) system is hyperresponsive in animals with high <b>ethanol</b> intake, which exhibits a reduction of <b>ethanol</b> intake when administered with a <strong>CRF1</strong> receptor antagonist.
+CRHR1	drug	alcohol	25797192	<strong>CRF1</strong> receptor messenger RNA (mRNA) levels in the amygdala and the effect of the <strong>CRF1</strong> receptor antagonist CP 154,526 on <b>ethanol</b> and water intake in the subgroups were studied.
+CRHR1	drug	alcohol	25797192	<strong>CRF1</strong> receptors appear to be involved in <b>ethanol</b> consumption in mice with high <b>ethanol</b> consumption, and CRF system mediated neuroadaptations depend on drinking profiles.
+CRHR1	drug	nicotine	25762751	During <b>nicotine</b> exposure, intact females displayed a decrease in <strong>CRF R1</strong>, CRF R2, Drd3, and Esr2 gene expression and an increase in CRF BP.
+CRHR1	addiction	addiction	25583178	Neuropeptide Y, a powerful anti stress neurotransmitter, has a profile of action on <b>compulsive</b> like responding for drugs similar to a <strong>CRF1</strong> receptor antagonist.
+CRHR1	drug	opioid	25582704	Sympathetic activity induced by <b>naloxone</b> precipitated <b>morphine</b> withdrawal is blocked in genetically engineered mice lacking functional <strong>CRF1</strong> receptor.
+CRHR1	addiction	withdrawal	25582704	Sympathetic activity induced by naloxone precipitated morphine <b>withdrawal</b> is blocked in genetically engineered mice lacking functional <strong>CRF1</strong> receptor.
+CRHR1	drug	opioid	25582704	Here, we performed a series of experiments to characterize the role of <strong>CRF1</strong> receptor (CRF1R) in the stress response induced by <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+CRHR1	addiction	withdrawal	25582704	Here, we performed a series of experiments to characterize the role of <strong>CRF1</strong> receptor (CRF1R) in the stress response induced by naloxone precipitated morphine <b>withdrawal</b>.
+CRHR1	drug	nicotine	25402857	We provide further evidence in rodents that chronic <b>nicotine</b> exposure upregulates Crh mRNA (encoding CRF) in dopaminergic neurons of the posterior VTA, activates local <strong>CRF1</strong> receptors and blocks <b>nicotine</b> induced activation of transient GABAergic input to dopaminergic neurons.
+CRHR1	drug	nicotine	25402857	Local downregulation of Crh mRNA and specific pharmacological blockade of <strong>CRF1</strong> receptors in the VTA reversed the effect of <b>nicotine</b> on GABAergic input to dopaminergic neurons, prevented the aversive effects of <b>nicotine</b> withdrawal and limited the escalation of <b>nicotine</b> intake.
+CRHR1	addiction	addiction	25402857	Local downregulation of Crh mRNA and specific pharmacological blockade of <strong>CRF1</strong> receptors in the VTA reversed the effect of nicotine on GABAergic input to dopaminergic neurons, prevented the aversive effects of nicotine withdrawal and limited the <b>escalation</b> of nicotine intake.
+CRHR1	addiction	aversion	25402857	Local downregulation of Crh mRNA and specific pharmacological blockade of <strong>CRF1</strong> receptors in the VTA reversed the effect of nicotine on GABAergic input to dopaminergic neurons, prevented the <b>aversive</b> effects of nicotine withdrawal and limited the escalation of nicotine intake.
+CRHR1	addiction	withdrawal	25402857	Local downregulation of Crh mRNA and specific pharmacological blockade of <strong>CRF1</strong> receptors in the VTA reversed the effect of nicotine on GABAergic input to dopaminergic neurons, prevented the aversive effects of nicotine <b>withdrawal</b> and limited the escalation of nicotine intake.
+CRHR1	drug	amphetamine	25205625	Saline pre treated rats showed reduced <strong>CRF1</strong> receptor expression in the lateral septum compared to <b>amphetamine</b> pre treated and un treated rats.
+CRHR1	drug	amphetamine	25205625	Overall, these results suggest that central CRF2 antagonism reduces anxiety states during <b>amphetamine</b> withdrawal, and that behavioral effects may be dependent upon the balance of <strong>CRF1</strong> and CRF2 receptor activity in anxiety related regions.
+CRHR1	addiction	withdrawal	25205625	Overall, these results suggest that central CRF2 antagonism reduces anxiety states during amphetamine <b>withdrawal</b>, and that behavioral effects may be dependent upon the balance of <strong>CRF1</strong> and CRF2 receptor activity in anxiety related regions.
+CRHR1	drug	cocaine	25164654	Knockdown of <strong>CRF1</strong> receptors in the ventral tegmental area attenuates cue  and acute food deprivation stress induced <b>cocaine</b> seeking in mice.
+CRHR1	addiction	relapse	25164654	Knockdown of <strong>CRF1</strong> receptors in the ventral tegmental area attenuates cue  and acute food deprivation stress induced cocaine <b>seeking</b> in mice.
+CRHR1	addiction	relapse	25164654	There is controversy, however, concerning the contribution of CRF receptor type 1 (<strong>CRFR1</strong>) to this effect and whether CRF within the VTA is involved in other aspects of reward <b>seeking</b> independent of acute stress.
+CRHR1	addiction	reward	25164654	There is controversy, however, concerning the contribution of CRF receptor type 1 (<strong>CRFR1</strong>) to this effect and whether CRF within the VTA is involved in other aspects of <b>reward</b> seeking independent of acute stress.
+CRHR1	drug	cocaine	25164654	Here we examine the role of <strong>CRFR1</strong> within the VTA in relation to <b>cocaine</b> and natural reward using viral delivery of short hairpin RNAs (lenti shCRFR1) and investigate the effect on operant self administration and motivation to self administer, as well as stress  and cue induced reward seeking in mice.
+CRHR1	addiction	relapse	25164654	Here we examine the role of <strong>CRFR1</strong> within the VTA in relation to cocaine and natural reward using viral delivery of short hairpin RNAs (lenti shCRFR1) and investigate the effect on operant self administration and motivation to self administer, as well as stress  and cue induced reward <b>seeking</b> in mice.
+CRHR1	addiction	reward	25164654	Here we examine the role of <strong>CRFR1</strong> within the VTA in relation to cocaine and natural <b>reward</b> using viral delivery of short hairpin RNAs (lenti shCRFR1) and investigate the effect on <b>operant</b> self administration and motivation to self administer, as well as stress  and cue induced <b>reward</b> seeking in mice.
+CRHR1	drug	cocaine	25164654	While knockdown of <strong>CRFR1</strong> in the VTA had no effect on self administration behavior for either <b>cocaine</b> or sucrose, it effectively blocked acute food deprivation stress induced reinstatement of <b>cocaine</b> seeking.
+CRHR1	addiction	relapse	25164654	While knockdown of <strong>CRFR1</strong> in the VTA had no effect on self administration behavior for either cocaine or sucrose, it effectively blocked acute food deprivation stress induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+CRHR1	drug	cocaine	25164654	We also observed reduced cue induced <b>cocaine</b> seeking assessed in a single extinction session after extended abstinence, but cue induced sucrose seeking was unaffected, suggesting dissociation between the contribution of <strong>CRFR1</strong> in the VTA in <b>cocaine</b> reward and sucrose and <b>cocaine</b> seeking.
+CRHR1	addiction	relapse	25164654	We also observed reduced cue induced cocaine <b>seeking</b> assessed in a single extinction session after extended abstinence, but cue induced sucrose <b>seeking</b> was unaffected, suggesting dissociation between the contribution of <strong>CRFR1</strong> in the VTA in cocaine reward and sucrose and cocaine <b>seeking</b>.
+CRHR1	addiction	reward	25164654	We also observed reduced cue induced cocaine seeking assessed in a single extinction session after extended abstinence, but cue induced sucrose seeking was unaffected, suggesting dissociation between the contribution of <strong>CRFR1</strong> in the VTA in cocaine <b>reward</b> and sucrose and cocaine seeking.
+CRHR1	drug	cocaine	25164654	Further, our data indicate a role for VTA <strong>CRFR1</strong> signaling in <b>cocaine</b> seeking associated with, and independent of, stress potentially involving conditioning and/or salience attribution of <b>cocaine</b> reward related cues.
+CRHR1	addiction	relapse	25164654	Further, our data indicate a role for VTA <strong>CRFR1</strong> signaling in cocaine <b>seeking</b> associated with, and independent of, stress potentially involving conditioning and/or salience attribution of cocaine reward related cues.
+CRHR1	addiction	reward	25164654	Further, our data indicate a role for VTA <strong>CRFR1</strong> signaling in cocaine seeking associated with, and independent of, stress potentially involving conditioning and/or salience attribution of cocaine <b>reward</b> related cues.
+CRHR1	drug	cocaine	25164654	<strong>CRFR1</strong> signaling in the VTA therefore presents a target for convergent effects of both cue  and stress induced <b>cocaine</b> seeking pathways.
+CRHR1	addiction	relapse	25164654	<strong>CRFR1</strong> signaling in the VTA therefore presents a target for convergent effects of both cue  and stress induced cocaine <b>seeking</b> pathways.
+CRHR1	drug	alcohol	25149913	Results also reveal sex differences in the subcellular distribution of the <strong>CRFr</strong> in LC noradrenergic neurons with female subjects exposed to <b>ethanol</b> exhibiting a higher frequency of plasmalemmal CRFrs.
+CRHR1	addiction	addiction	25080599	These studies demonstrate that presynaptic <strong>CRF R1</strong>/R2 tightly regulate glutamate transmission in the VTA via a concerted, heterosynaptic manner that may become altered by stress related pathologies, such as <b>addiction</b>.
+CRHR1	drug	alcohol	24944865	KOR and CRF receptors (<strong>CRF R</strong>) may interact in the production of stress related behaviors but it is not known whether this interaction is involved in reinstatement of <b>alcohol</b> seeking.
+CRHR1	addiction	relapse	24944865	KOR and CRF receptors (<strong>CRF R</strong>) may interact in the production of stress related behaviors but it is not known whether this interaction is involved in <b>reinstatement</b> of alcohol <b>seeking</b>.
+CRHR1	drug	alcohol	24944865	Finally, we determined whether <strong>CRF R1</strong> blockade with antalarmin (10, 20 mg/kg) attenuates <b>alcohol</b> seeking induced by U50,488.
+CRHR1	addiction	relapse	24944865	Finally, we determined whether <strong>CRF R1</strong> blockade with antalarmin (10, 20 mg/kg) attenuates alcohol <b>seeking</b> induced by U50,488.
+CRHR1	drug	alcohol	24944865	These data further support a role for KOR in reinstatement of <b>alcohol</b> seeking under nonstress and stressful conditions and that KOR and <strong>CRF R</strong> interact in these effects.
+CRHR1	addiction	relapse	24944865	These data further support a role for KOR in <b>reinstatement</b> of alcohol <b>seeking</b> under nonstress and stressful conditions and that KOR and <strong>CRF R</strong> interact in these effects.
+CRHR1	drug	opioid	24845178	Nineteen single nucleotide polymorphisms (SNPs) in 9 genes (AVP, AVPR1A, <strong>CRHR1</strong>, CRHR2, FKBP5, GAL, GLRA1, NPY1R and NR3C2) showed nominally significant association with <b>heroin</b> addiction.
+CRHR1	addiction	addiction	24845178	Nineteen single nucleotide polymorphisms (SNPs) in 9 genes (AVP, AVPR1A, <strong>CRHR1</strong>, CRHR2, FKBP5, GAL, GLRA1, NPY1R and NR3C2) showed nominally significant association with heroin <b>addiction</b>.
+CRHR1	drug	cocaine	24806691	This study investigated whether injecting either a <strong>CRFR1</strong> or CRFR2 antagonist directly into the VTA before each social defeat would prevent the development of later (1) locomotor sensitization, (2) dopaminergic sensitization, and (3) escalated <b>cocaine</b> self administration in rats.
+CRHR1	addiction	sensitization	24806691	This study investigated whether injecting either a <strong>CRFR1</strong> or CRFR2 antagonist directly into the VTA before each social defeat would prevent the development of later (1) locomotor <b>sensitization</b>, (2) dopaminergic <b>sensitization</b>, and (3) escalated cocaine self administration in rats.
+CRHR1	drug	cocaine	24806691	Intra VTA antagonism of <strong>CRFR1</strong>, but not CRFR2, inhibited the induction of locomotor cross sensitization to <b>cocaine</b>, whereas both prevented dopaminergic cross sensitization and escalated <b>cocaine</b> self administration during a 24 h "binge."
+CRHR1	addiction	intoxication	24806691	Intra VTA antagonism of <strong>CRFR1</strong>, but not CRFR2, inhibited the induction of locomotor cross sensitization to cocaine, whereas both prevented dopaminergic cross sensitization and escalated cocaine self administration during a 24 h "<b>binge</b>."
+CRHR1	addiction	sensitization	24806691	Intra VTA antagonism of <strong>CRFR1</strong>, but not CRFR2, inhibited the induction of locomotor cross <b>sensitization</b> to cocaine, whereas both prevented dopaminergic cross <b>sensitization</b> and escalated cocaine self administration during a 24 h "binge."
+CRHR1	drug	nicotine	24755994	In conclusion, the overexpression of CRF in the CeA diminishes the dysphoric like state associated with <b>nicotine</b> withdrawal and this might be driven by neuroadaptive changes in <strong>CRF1</strong> and CRF2 receptor gene expression.
+CRHR1	addiction	withdrawal	24755994	In conclusion, the overexpression of CRF in the CeA diminishes the dysphoric like state associated with nicotine <b>withdrawal</b> and this might be driven by neuroadaptive changes in <strong>CRF1</strong> and CRF2 receptor gene expression.
+CRHR1	drug	alcohol	24623788	Indirect effect of <strong>corticotropin releasing hormone receptor 1</strong> gene variation on negative emotionality and <b>alcohol</b> use via right ventrolateral prefrontal cortex.
+CRHR1	drug	alcohol	24623788	Variations in the corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) gene have been found to interact with stress in modulating excessive <b>alcohol</b> consumption.
+CRHR1	drug	alcohol	24623788	Variations in the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) gene have been found to interact with stress in modulating excessive <b>alcohol</b> consumption.
+CRHR1	drug	alcohol	24623788	This study examined the influence of an intronic <strong>CRHR1</strong> gene variant, rs110402, on brain responses to negative emotional words, negative emotional traits, and <b>alcohol</b> use in adolescents and young adults at high risk for <b>alcoholism</b>.
+CRHR1	addiction	addiction	24456850	Drug discovery efforts have yielded brain penetrant <strong>CRF1</strong> antagonists with activity in preclinical models of <b>addiction</b>.
+CRHR1	addiction	addiction	24456850	The results support the hypothesis that brain CRF <strong>CRF1</strong> systems contribute to the etiology and maintenance of <b>addiction</b>.
+CRHR1	drug	opioid	24398105	Furthermore, it studied the efficacy of <strong>CRF1</strong> receptor antagonist, CP 154,526 to prevent the cardiac sympathetic activity induced by <b>morphine</b> withdrawal.
+CRHR1	addiction	withdrawal	24398105	Furthermore, it studied the efficacy of <strong>CRF1</strong> receptor antagonist, CP 154,526 to prevent the cardiac sympathetic activity induced by morphine <b>withdrawal</b>.
+CRHR1	drug	opioid	24398105	Pre treatment with <strong>CRF1</strong> receptor antagonist significantly reduced <b>morphine</b> withdrawal induced increases in plasma adrenocorticotropic hormone (ACTH) levels, NA turnover and TH phosphorylation at Ser31 in the right ventricle.
+CRHR1	addiction	withdrawal	24398105	Pre treatment with <strong>CRF1</strong> receptor antagonist significantly reduced morphine <b>withdrawal</b> induced increases in plasma adrenocorticotropic hormone (ACTH) levels, NA turnover and TH phosphorylation at Ser31 in the right ventricle.
+CRHR1	drug	opioid	24398105	Altogether, these results support the idea that cardiac sympathetic pathways are activated in response to <b>naloxone</b> precipitated <b>morphine</b> withdrawal suggesting that treatment with a <strong>CRF1</strong> receptor antagonist before <b>morphine</b> withdrawal would prevent the development of stress induced behavioural and autonomic dysfunction in <b>opioid</b> addicts.
+CRHR1	addiction	withdrawal	24398105	Altogether, these results support the idea that cardiac sympathetic pathways are activated in response to naloxone precipitated morphine <b>withdrawal</b> suggesting that treatment with a <strong>CRF1</strong> receptor antagonist before morphine <b>withdrawal</b> would prevent the development of stress induced behavioural and autonomic dysfunction in opioid addicts.
+CRHR1	drug	opioid	24330252	Chronic <strong>CRF1</strong> receptor blockade reduces <b>heroin</b> intake escalation and dependence induced hyperalgesia.
+CRHR1	addiction	addiction	24330252	Chronic <strong>CRF1</strong> receptor blockade reduces heroin intake <b>escalation</b> and dependence induced hyperalgesia.
+CRHR1	addiction	dependence	24330252	Chronic <strong>CRF1</strong> receptor blockade reduces heroin intake escalation and <b>dependence</b> induced hyperalgesia.
+CRHR1	drug	opioid	24330252	During acute <b>opioid</b> dependence, systemic administration of the <strong>CRF1</strong> receptor antagonist MPZP (20 mg/kg) alleviated withdrawal induced mechanical hypersensitivity.
+CRHR1	addiction	dependence	24330252	During acute opioid <b>dependence</b>, systemic administration of the <strong>CRF1</strong> receptor antagonist MPZP (20 mg/kg) alleviated withdrawal induced mechanical hypersensitivity.
+CRHR1	addiction	withdrawal	24330252	During acute opioid dependence, systemic administration of the <strong>CRF1</strong> receptor antagonist MPZP (20 mg/kg) alleviated <b>withdrawal</b> induced mechanical hypersensitivity.
+CRHR1	drug	nicotine	24107576	Here, we describe three experiments in which the main hypothesis was that CRF/<strong>CRF1</strong> receptor (CRF1R) signalling in the CeA mediates <b>nicotine</b> withdrawal induced increases in nociceptive sensitivity in rats that are dependent on <b>nicotine</b>.
+CRHR1	addiction	withdrawal	24107576	Here, we describe three experiments in which the main hypothesis was that CRF/<strong>CRF1</strong> receptor (CRF1R) signalling in the CeA mediates nicotine <b>withdrawal</b> induced increases in nociceptive sensitivity in rats that are dependent on nicotine.
+CRHR1	drug	opioid	24055683	Expression levels of BDNF, TrkB and <strong>CRF R1</strong> mRNA were decreased during both <b>morphine</b> exposure and following 7days of withdrawal.
+CRHR1	addiction	withdrawal	24055683	Expression levels of BDNF, TrkB and <strong>CRF R1</strong> mRNA were decreased during both morphine exposure and following 7days of <b>withdrawal</b>.
+CRHR1	drug	alcohol	23914176	Neuropeptide Y, a powerful anti stress neurotransmitter, has a profile of action on compulsive like responding for <b>ethanol</b> similar to a <strong>CRF1</strong> antagonist.
+CRHR1	addiction	addiction	23914176	Neuropeptide Y, a powerful anti stress neurotransmitter, has a profile of action on <b>compulsive</b> like responding for ethanol similar to a <strong>CRF1</strong> antagonist.
+CRHR1	addiction	withdrawal	23895427	To test whether HMGB1 and/or CRF support the CE <b>withdrawal</b> increase in cytokine mRNAs, the HMGB1 antagonists, glycyrrhizin and ethyl pyruvate, and a <strong>CRF1</strong> receptor antagonist (CRF1RA) are administered during 24 hours of CE <b>withdrawal</b>.
+CRHR1	drug	nicotine	23869743	Extended access to <b>nicotine</b> leads to a <strong>CRF1</strong> receptor dependent increase in anxiety like behavior and hyperalgesia in rats.
+CRHR1	drug	nicotine	23869743	Here, we tested the hypothesis that the activation of corticotropin releasing factor 1 (<strong>CRF1</strong>) receptors and emergence of the affective and motivational effects of <b>nicotine</b> abstinence only occur in rats with long access (>21 hours/day, LgA) and not short (1 hour/day, ShA) access to <b>nicotine</b> self administration.
+CRHR1	drug	nicotine	23869743	These findings demonstrate that the model of short access to <b>nicotine</b> self administration has limited validity for <b>tobacco</b> dependence, highlight the translational relevance of the model of extended intermittent access to <b>nicotine</b> self administration for <b>tobacco</b> dependence and demonstrate that activation of <strong>CRF1</strong> receptors is required for the emergence of abstinence induced anxiety like behavior, hyperalgesia and excessive <b>nicotine</b> intake.
+CRHR1	addiction	dependence	23869743	These findings demonstrate that the model of short access to nicotine self administration has limited validity for tobacco <b>dependence</b>, highlight the translational relevance of the model of extended intermittent access to nicotine self administration for tobacco <b>dependence</b> and demonstrate that activation of <strong>CRF1</strong> receptors is required for the emergence of abstinence induced anxiety like behavior, hyperalgesia and excessive nicotine intake.
+CRHR1	addiction	intoxication	23763790	These results were not due to alterations of VTA NMDAR number or function, suggesting that <b>binge</b> drinking may enhance signaling through VTA <strong>CRF1</strong> receptors onto NMDARs.
+CRHR1	addiction	intoxication	23763790	Altered <strong>CRF1</strong> receptor mediated signaling in the VTA promotes <b>binge</b> like EtOH consumption in mice, which supports the idea that <strong>CRF1</strong> receptors may therefore be a promising pharmacological target for reducing <b>binge</b> drinking in humans.
+CRHR1	drug	cocaine	23685321	Repeated <b>cocaine</b> administration (15mg/kg; twice daily for 14 days) suppressed the increase in LS dopamine extracellular levels induced by <strong>CRF R1</strong> activation.
+CRHR1	drug	cocaine	23685321	Interestingly, repeated <b>cocaine</b> administration induces a long term suppression of the <strong>CRF R1</strong> mediated dopamine release and a transient increase in dopamine releasability in the LS.
+CRHR1	drug	alcohol	23630503	Treatment with the <strong>CRF1</strong> R antagonist antalarmin (0, 5, 10, and 20 mg/kg) significantly reduced <b>alcohol</b> reinforced lever pressing in the AA line (10 and 20 mg/kg) while a weaker or no effect was observed in the Wistar and the GG group, respectively.
+CRHR1	drug	alcohol	23630503	In conclusion, these specific SNPs in the <strong>CRF1</strong> R gene do not seem to play a primary role in the expression of the msP excessive drinking phenotype or stress induced drinking but may be associated with a decreased threshold for stress induced <b>alcohol</b> seeking and an increased sensitivity to the effects of pharmacological blockade of <strong>CRF1</strong> R on <b>alcohol</b> drinking.
+CRHR1	addiction	relapse	23630503	In conclusion, these specific SNPs in the <strong>CRF1</strong> R gene do not seem to play a primary role in the expression of the msP excessive drinking phenotype or stress induced drinking but may be associated with a decreased threshold for stress induced alcohol <b>seeking</b> and an increased sensitivity to the effects of pharmacological blockade of <strong>CRF1</strong> R on alcohol drinking.
+CRHR1	drug	opioid	23590881	Both the α 2 adrenergic receptor agonist clonidine (10 μg/kg s.c.) and <strong>CRF1</strong> receptor antagonist N,N bis(2 methoxyethyl) 3 (4 methoxy 2 methylphenyl) 2,5 dimethyl pyrazolo[1,5 a] pyrimidin 7 amine (MPZP; 20 mg/kg s.c.) blocked <b>heroin</b> withdrawal potentiated startle.
+CRHR1	addiction	withdrawal	23590881	Both the α 2 adrenergic receptor agonist clonidine (10 μg/kg s.c.) and <strong>CRF1</strong> receptor antagonist N,N bis(2 methoxyethyl) 3 (4 methoxy 2 methylphenyl) 2,5 dimethyl pyrazolo[1,5 a] pyrimidin 7 amine (MPZP; 20 mg/kg s.c.) blocked heroin <b>withdrawal</b> potentiated startle.
+CRHR1	drug	opioid	23590881	These results suggest that <strong>CRF1</strong> and α 2 receptors play an important role in the heightened anxiety like behaviour observed during acute withdrawal from <b>heroin</b>, possibly via CRF inducing the release of NE in stress related brain regions.
+CRHR1	addiction	withdrawal	23590881	These results suggest that <strong>CRF1</strong> and α 2 receptors play an important role in the heightened anxiety like behaviour observed during acute <b>withdrawal</b> from heroin, possibly via CRF inducing the release of NE in stress related brain regions.
+CRHR1	drug	alcohol	23473364	The <strong>CRHR1</strong> gene, trauma exposure, and <b>alcoholism</b> risk: a test of G × E effects.
+CRHR1	drug	alcohol	23473364	On the basis of the hypothesized effects of <strong>CRHR1</strong> variation on stress reactivity, measures of adulthood traumatic stress exposure were analyzed for their interaction with <strong>CRHR1</strong> haplotypes and single nucleotide polymorphisms (SNPs) in predicting the risk for <b>alcoholism</b>.
+CRHR1	drug	alcohol	23473364	Logistic regression models examined the interaction between <strong>CRHR1</strong> haplotypes/SNPs and adulthood traumatic stress exposure in predicting <b>alcoholism</b> risk.
+CRHR1	drug	alcohol	23473364	This study extends the literature on the interplay between <strong>CRHR1</strong> variation and <b>alcoholism</b>, in the context of exposure to traumatic stress.
+CRHR1	drug	alcohol	23426657	Activation of corticotropin releasing factor type 1 (<strong>CRF1</strong>) receptors in the CeA plays a critical role in the development of <b>ethanol</b> dependence, but these neurons remain uncharacterized.
+CRHR1	addiction	dependence	23426657	Activation of corticotropin releasing factor type 1 (<strong>CRF1</strong>) receptors in the CeA plays a critical role in the development of ethanol <b>dependence</b>, but these neurons remain uncharacterized.
+CRHR1	drug	alcohol	23426657	<b>Ethanol</b> increased the firing discharge of <strong>CRF1</strong> neurons and decreased the firing discharge of unlabeled CeA neurons.
+CRHR1	drug	alcohol	23398267	<strong>CRF1</strong> receptor signaling regulates food and fluid intake in the drinking in the dark model of binge <b>alcohol</b> consumption.
+CRHR1	addiction	intoxication	23398267	<strong>CRF1</strong> receptor signaling regulates food and fluid intake in the drinking in the dark model of <b>binge</b> alcohol consumption.
+CRHR1	drug	alcohol	23398267	Several recent studies implementing the standard "drinking in the dark" (DID) model of short term binge like <b>ethanol</b> (EtOH) intake in C57BL/6J mice highlighted a role for the stress related neuropeptide corticotropin releasing factor (CRF) and its primary binding partner, the CRF type 1 (<strong>CRF1</strong>) receptor.
+CRHR1	addiction	intoxication	23398267	Several recent studies implementing the standard "drinking in the dark" (DID) model of short term <b>binge</b> like ethanol (EtOH) intake in C57BL/6J mice highlighted a role for the stress related neuropeptide corticotropin releasing factor (CRF) and its primary binding partner, the CRF type 1 (<strong>CRF1</strong>) receptor.
+CRHR1	addiction	intoxication	23398267	We evaluated the selectivity of <strong>CRF1</strong> involvement in <b>binge</b> like EtOH intake by interrupting <strong>CRF1</strong> function via pharmacological and genetic methods in a slightly modified 2 bottle choice DID model that allowed calculation of an EtOH preference ratio.
+CRHR1	addiction	intoxication	23398267	Our findings indicate that blockade of <strong>CRF1</strong> receptors does not exert specific effects on EtOH intake in the DID paradigm, and that slight modifications to this procedure, as well as additional consummatory control experiments, may be useful when evaluating the selectivity of pharmacological and genetic manipulations on <b>binge</b> like EtOH intake.
+CRHR1	drug	opioid	23333681	The dynorphin (DYN), μ <b>opioid</b> receptor (mu <b>opioid</b>), neuropeptide Y (NPY), brain derived neurotrophic factor (BDNF), tropomyosin related tyrosine kinase B receptor (TrkB) and corticotropin releasing factor receptor type 1 (<strong>CRF R1</strong>) gene expression were measured by the reverse transcription polymerase chain reaction (RT PCR).
+CRHR1	drug	alcohol	23294766	Functional variants in genes that encode CRF system molecules, including polymorphisms in <strong>Crhr1</strong> (rs110402, rs1876831, rs242938) and Crhbp genes (rs10055255, rs3811939) may promote <b>alcohol</b> seeking and consumption by altering basal or stress induced CRF system activation.
+CRHR1	addiction	relapse	23294766	Functional variants in genes that encode CRF system molecules, including polymorphisms in <strong>Crhr1</strong> (rs110402, rs1876831, rs242938) and Crhbp genes (rs10055255, rs3811939) may promote alcohol <b>seeking</b> and consumption by altering basal or stress induced CRF system activation.
+CRHR1	drug	alcohol	23126554	After stabilization of their intake, both groups were administered 3 pharmacological agents with different mechanisms of action, <b>naltrexone</b> an opioid receptor antagonist, SCH 39166 a dopamine D1 receptor antagonist, and R121919 a Corticotropin Releasing Factor 1 (<strong>CRF1</strong>) receptor antagonist, and their effects on <b>alcohol</b> and water intake were determined.
+CRHR1	drug	opioid	23126554	After stabilization of their intake, both groups were administered 3 pharmacological agents with different mechanisms of action, naltrexone an <b>opioid</b> receptor antagonist, SCH 39166 a dopamine D1 receptor antagonist, and R121919 a Corticotropin Releasing Factor 1 (<strong>CRF1</strong>) receptor antagonist, and their effects on alcohol and water intake were determined.
+CRHR1	drug	opioid	23126554	The Wise procedure in sP rats induces binge like drinking, which appears <b>opioid</b>  and dopamine receptor mediated; the <strong>CRF1</strong> system, on the other hand, does not appear to be involved.
+CRHR1	addiction	intoxication	23126554	The Wise procedure in sP rats induces <b>binge</b> like drinking, which appears opioid  and dopamine receptor mediated; the <strong>CRF1</strong> system, on the other hand, does not appear to be involved.
+CRHR1	drug	opioid	23071721	Since the role of stress in drug addiction is well established, the present study examined the possible involvement of <strong>CRF1</strong> receptor in the interaction between <b>morphine</b> withdrawal and catecholaminergic pathways in the reward system.
+CRHR1	addiction	addiction	23071721	Since the role of stress in drug <b>addiction</b> is well established, the present study examined the possible involvement of <strong>CRF1</strong> receptor in the interaction between morphine withdrawal and catecholaminergic pathways in the reward system.
+CRHR1	addiction	reward	23071721	Since the role of stress in drug addiction is well established, the present study examined the possible involvement of <strong>CRF1</strong> receptor in the interaction between morphine withdrawal and catecholaminergic pathways in the <b>reward</b> system.
+CRHR1	addiction	withdrawal	23071721	Since the role of stress in drug addiction is well established, the present study examined the possible involvement of <strong>CRF1</strong> receptor in the interaction between morphine <b>withdrawal</b> and catecholaminergic pathways in the reward system.
+CRHR1	drug	opioid	23071721	Pretreatment with <strong>CRF1</strong> receptor antagonist resulted in no significant modification of the increased NA turnover at NAc or plasma corticosterone levels that were seen during <b>morphine</b> withdrawal.
+CRHR1	addiction	withdrawal	23071721	Pretreatment with <strong>CRF1</strong> receptor antagonist resulted in no significant modification of the increased NA turnover at NAc or plasma corticosterone levels that were seen during morphine <b>withdrawal</b>.
+CRHR1	drug	opioid	23071721	However, blockade of <strong>CRF1</strong> receptor significantly reduced <b>morphine</b> withdrawal induced increases in plasma adrenocorticotropin (ACTH) levels, DA turnover and TH phosphorylation at Ser40 in the NAc.
+CRHR1	addiction	withdrawal	23071721	However, blockade of <strong>CRF1</strong> receptor significantly reduced morphine <b>withdrawal</b> induced increases in plasma adrenocorticotropin (ACTH) levels, DA turnover and TH phosphorylation at Ser40 in the NAc.
+CRHR1	drug	opioid	23071721	Altogether, these results support the idea that VTA dopaminergic neurons are activated in response to <b>naloxone</b> precipitated <b>morphine</b> withdrawal and suggest that <strong>CRF1</strong> receptors are involved in the activation of dopaminergic pathways which project to NAc.
+CRHR1	addiction	withdrawal	23071721	Altogether, these results support the idea that VTA dopaminergic neurons are activated in response to naloxone precipitated morphine <b>withdrawal</b> and suggest that <strong>CRF1</strong> receptors are involved in the activation of dopaminergic pathways which project to NAc.
+CRHR1	drug	alcohol	22885872	Manipulation of the stress neuropeptide corticotropin releasing factor (CRF), specifically central antagonism of the type 1 receptors (<strong>CRF R1</strong>), effectively reduces <b>alcoholic</b> like <b>ethanol</b> drinking in rodents.
+CRHR1	drug	alcohol	22885872	The current studies investigated the role of <strong>CRF R1</strong> within the VTA and DRN and their relation to escalated <b>ethanol</b> drinking in two species.
+CRHR1	drug	alcohol	22885872	An additional goal was to explore whether high <b>alcohol</b> drinking individuals would be more affected by <strong>CRF R1</strong> antagonism than low <b>alcohol</b> drinking individuals.
+CRHR1	drug	alcohol	22885872	Doses of the <strong>CRF R1</strong> antagonist CP 154,526 (butyl [2,4,6 trimethylphenyl) 7H pyrrolo[2,3 d]pyrimidin 4 yl]ethylamine)) were microinfused to modulate drinking of <b>ethanol</b> and water over the course of 24 h. In both mice and rats, intra VTA CP 154,526 selectively decreased <b>ethanol</b> intake, while identical doses (0.3 and 0.6 μg) infused intra DRN reduced both <b>ethanol</b> and water drinking.
+CRHR1	drug	alcohol	22885872	The current findings confirm previous studies that blockade of <strong>CRF R1</strong> efficaciously reduces escalated drinking while also suggesting that the effects of intermittent access on <b>alcohol</b> consumption may require CRF interaction with dopamine in the VTA.
+CRHR1	addiction	intoxication	22776620	Effects of CB1 and <strong>CRF1</strong> receptor antagonists on <b>binge</b> like eating in rats with limited access to a sweet fat diet: lack of withdrawal like responses.
+CRHR1	addiction	withdrawal	22776620	Effects of CB1 and <strong>CRF1</strong> receptor antagonists on binge like eating in rats with limited access to a sweet fat diet: lack of <b>withdrawal</b> like responses.
+CRHR1	drug	alcohol	22444954	While dependence induced and binge drinking rely on the actions of CRF on <strong>CRFR1</strong> receptors, <b>alcohol</b> consumption in models of these behaviors is inhibited by actions of Ucns on CRFR2.
+CRHR1	addiction	dependence	22444954	While <b>dependence</b> induced and binge drinking rely on the actions of CRF on <strong>CRFR1</strong> receptors, alcohol consumption in models of these behaviors is inhibited by actions of Ucns on CRFR2.
+CRHR1	addiction	intoxication	22444954	While dependence induced and <b>binge</b> drinking rely on the actions of CRF on <strong>CRFR1</strong> receptors, alcohol consumption in models of these behaviors is inhibited by actions of Ucns on CRFR2.
+CRHR1	drug	alcohol	22444954	In contrast, <b>alcohol</b> preference is positively influenced by actions of Ucn1, which is capable of acting on both <strong>CRFR1</strong> and CRFR2.
+CRHR1	drug	nicotine	22182462	Blockade of <strong>CRF1</strong> receptors in the central nucleus of the amygdala attenuates the dysphoria associated with <b>nicotine</b> withdrawal in rats.
+CRHR1	addiction	withdrawal	22182462	Blockade of <strong>CRF1</strong> receptors in the central nucleus of the amygdala attenuates the dysphoria associated with nicotine <b>withdrawal</b> in rats.
+CRHR1	drug	nicotine	22182462	It was investigated if blockade of <strong>CRF1</strong> receptors, blockade of α1 adrenergic receptors, or stimulation of α2 adrenergic receptors in the CeA diminishes the deficit in brain reward function associated with <b>nicotine</b> withdrawal in rats.
+CRHR1	addiction	reward	22182462	It was investigated if blockade of <strong>CRF1</strong> receptors, blockade of α1 adrenergic receptors, or stimulation of α2 adrenergic receptors in the CeA diminishes the deficit in brain <b>reward</b> function associated with nicotine withdrawal in rats.
+CRHR1	addiction	withdrawal	22182462	It was investigated if blockade of <strong>CRF1</strong> receptors, blockade of α1 adrenergic receptors, or stimulation of α2 adrenergic receptors in the CeA diminishes the deficit in brain reward function associated with nicotine <b>withdrawal</b> in rats.
+CRHR1	drug	nicotine	22182462	Intra CeA administration of the <strong>CRF1</strong> receptor antagonist R278995/CRA0450 completely prevented the mecamylamine induced elevations in brain reward thresholds in the <b>nicotine</b> treated rats and did not affect the brain reward thresholds of the saline treated control rats.
+CRHR1	addiction	reward	22182462	Intra CeA administration of the <strong>CRF1</strong> receptor antagonist R278995/CRA0450 completely prevented the mecamylamine induced elevations in brain <b>reward</b> thresholds in the nicotine treated rats and did not affect the brain <b>reward</b> thresholds of the saline treated control rats.
+CRHR1	drug	nicotine	22182462	These studies suggest that <strong>CRF1</strong> receptor antagonists may diminish the dysphoria associated with <b>smoking</b> cessation by blocking <strong>CRF1</strong> receptors in the CeA.
+CRHR1	drug	alcohol	22113086	Brain specific inactivation of the <strong>Crhr1</strong> gene inhibits post dependent and stress induced <b>alcohol</b> intake, but does not affect relapse like drinking.
+CRHR1	addiction	relapse	22113086	Brain specific inactivation of the <strong>Crhr1</strong> gene inhibits post dependent and stress induced alcohol intake, but does not affect <b>relapse</b> like drinking.
+CRHR1	drug	alcohol	22113086	Corticotropin releasing hormone (CRH) and its receptor, CRH receptor 1 (<strong>CRHR1</strong>), have a key role in <b>alcoholism</b>.
+CRHR1	drug	alcohol	22113086	Especially, post dependent and stress induced <b>alcohol</b> intake involve CRH/<strong>CRHR1</strong> signaling within extra hypothalamic structures, but a contribution of the hypothalamic pituitary adrenal (HPA) axis activity might be involved as well.
+CRHR1	drug	alcohol	22113086	Here we examined the role of <strong>CRHR1</strong> in various drinking conditions in relation to HPA and extra HPA sites, and studied relapse like drinking behavior in the <b>alcohol</b> deprivation model (ADE).
+CRHR1	addiction	relapse	22113086	Here we examined the role of <strong>CRHR1</strong> in various drinking conditions in relation to HPA and extra HPA sites, and studied <b>relapse</b> like drinking behavior in the alcohol deprivation model (ADE).
+CRHR1	drug	alcohol	22113086	To dissect CRH/<strong>CRHR1</strong> extra HPA and HPA signaling on a molecular level, a conditional brain specific <strong>Crhr1</strong> knockout (<strong>Crhr1</strong>(NestinCre)) and a global knockout mouse line were studied for basal <b>alcohol</b> drinking, stress induced <b>alcohol</b> consumption, deprivation induced intake, and escalated <b>alcohol</b> consumption in the post dependent state.
+CRHR1	drug	alcohol	22113086	Stress induced augmentation of <b>alcohol</b> intake was lower in <strong>Crhr1</strong>(NestinCre) mice as compared with control animals.
+CRHR1	drug	alcohol	22113086	<strong>Crhr1</strong>(NestinCre) mice were also resistant to escalation of <b>alcohol</b> intake in the post dependent state.
+CRHR1	addiction	addiction	22113086	<strong>Crhr1</strong>(NestinCre) mice were also resistant to <b>escalation</b> of alcohol intake in the post dependent state.
+CRHR1	drug	alcohol	22113086	Contrarily, global <strong>Crhr1</strong> knockouts showed enhanced stress induced <b>alcohol</b> consumption and a more pronounced escalation of intake in the post dependent state than their control littermates.
+CRHR1	addiction	addiction	22113086	Contrarily, global <strong>Crhr1</strong> knockouts showed enhanced stress induced alcohol consumption and a more pronounced <b>escalation</b> of intake in the post dependent state than their control littermates.
+CRHR1	addiction	relapse	22113086	In line with these findings, <strong>CRHR1</strong> antagonists did not affect <b>relapse</b> like drinking after a deprivation period in rats.
+CRHR1	drug	alcohol	22113086	We conclude that CRH/<strong>CRHR1</strong> extra HPA and HPA signaling may have opposing effects on stress related <b>alcohol</b> consumption.
+CRHR1	drug	alcohol	22113086	<strong>CRHR1</strong> does not have a role in basal <b>alcohol</b> intake or relapse like drinking situations with a low stress load.
+CRHR1	addiction	relapse	22113086	<strong>CRHR1</strong> does not have a role in basal alcohol intake or <b>relapse</b> like drinking situations with a low stress load.
+CRHR1	drug	alcohol	22036774	Pharmacological blockade of <strong>corticotropin releasing hormone receptor 1</strong> (CRH1R) reduces voluntary consumption of high <b>alcohol</b> concentrations in non dependent Wistar rats.
+CRHR1	addiction	dependence	21998007	Adverse childhood experiences (ACEs) increase the risk for adult depression and substance <b>dependence</b>, possibly mediated by the corticotropin releasing hormone type 1 receptor (<strong>CRHR1</strong>).
+CRHR1	drug	alcohol	21998007	Other studies have shown a main or moderating effect of SNPs in <strong>CRHR1</strong> on <b>alcohol</b> consumption.
+CRHR1	drug	opioid	21947312	Restricted role of <strong>CRF1</strong> receptor for the activity of brainstem catecholaminergic neurons in the negative state of <b>morphine</b> withdrawal.
+CRHR1	addiction	withdrawal	21947312	Restricted role of <strong>CRF1</strong> receptor for the activity of brainstem catecholaminergic neurons in the negative state of morphine <b>withdrawal</b>.
+CRHR1	drug	alcohol	21895713	Recent studies have shown that CRF receptor type 1 (<strong>CRFR1</strong>) antagonists attenuate <b>alcohol</b> intake in the limited access "drinking in the dark" (DID) model of binge drinking.
+CRHR1	addiction	intoxication	21895713	Recent studies have shown that CRF receptor type 1 (<strong>CRFR1</strong>) antagonists attenuate alcohol intake in the limited access "drinking in the dark" (DID) model of <b>binge</b> drinking.
+CRHR1	drug	alcohol	21895713	To avoid the potential nonspecific effects of antagonists, in this study, we tested <b>alcohol</b> drinking in <strong>CRFR1</strong>, CRFR2, CRF, and urocortin 1 (Ucn1) KO and corresponding wild type (WT) littermates using the DID paradigm.
+CRHR1	drug	alcohol	21895713	On days 1 to 3, the <strong>CRFR1</strong>, CRFR2, Ucn1, and CRF KO mice and their respective WT littermates were provided with 20% <b>ethanol</b> or 10% sucrose for 2 hours with water available at all other times.
+CRHR1	drug	alcohol	21895713	<strong>CRFR1</strong> KO mice had lower <b>alcohol</b> intakes and BECs and higher intakes of sucrose compared with WTs.
+CRHR1	drug	alcohol	21895713	Our results confirm that <strong>CRFR1</strong> plays a key role in binge drinking and identify CRF as the ligand critically involved in excessive <b>alcohol</b> consumption.
+CRHR1	addiction	intoxication	21895713	Our results confirm that <strong>CRFR1</strong> plays a key role in <b>binge</b> drinking and identify CRF as the ligand critically involved in excessive alcohol consumption.
+CRHR1	addiction	relapse	21843515	The essential role of corticotropin releasing factor (CRF) and its type 1 receptor (<strong>CRF1</strong>) in stress induced <b>relapse</b> to drug <b>seeking</b> has been demonstrated.
+CRHR1	drug	cocaine	21843515	The new information involving CRF2 receptors in stress induced relapse to <b>cocaine</b> seeking has generated a need for a reappraisal of the existing anatomical and pharmacological evidence that have been used to support the critical role of <strong>CRF1</strong> receptors.
+CRHR1	addiction	relapse	21843515	The new information involving CRF2 receptors in stress induced <b>relapse</b> to cocaine <b>seeking</b> has generated a need for a reappraisal of the existing anatomical and pharmacological evidence that have been used to support the critical role of <strong>CRF1</strong> receptors.
+CRHR1	addiction	relapse	21843515	In this commentary, the available evidence supporting the role of both <strong>CRF1</strong> and CRF2 receptors in stress induced <b>relapse</b> to drug <b>seeking</b> is reviewed.
+CRHR1	drug	amphetamine	21833501	We previously reported that genetic deletion of the CRF type 2 receptor (CRF R2), but not the CRF type 1 receptor (<strong>CRF R1</strong>) dampened the acute locomotor stimulant response to <b>methamphetamine</b> (1 mg/kg).
+CRHR1	drug	amphetamine	21833501	Since the majority of previous studies focused on cocaine, rather than <b>methamphetamine</b>, we set out to test the hypothesis that these drugs differentially engage <strong>CRF R1</strong> and CRF R2.
+CRHR1	drug	cocaine	21833501	Since the majority of previous studies focused on <b>cocaine</b>, rather than methamphetamine, we set out to test the hypothesis that these drugs differentially engage <strong>CRF R1</strong> and CRF R2.
+CRHR1	drug	amphetamine	21833501	We expanded our earlier findings by first replicating our previous experiments at a higher dose of <b>methamphetamine</b> (2 mg/kg), and by assessing the effects of the <strong>CRF R1</strong> selective antagonist CP 376,395 (10 mg/kg) on <b>methamphetamine</b> induced locomotor activity.
+CRHR1	drug	amphetamine	21833501	While genetic deletion of CRF R2 dampened the locomotor response to <b>methamphetamine</b> (but not cocaine), genetic deletion and pharmacological blockade of <strong>CRF R1</strong> dampened the locomotor response to cocaine (but not <b>methamphetamine</b>).
+CRHR1	drug	cocaine	21833501	While genetic deletion of CRF R2 dampened the locomotor response to methamphetamine (but not <b>cocaine</b>), genetic deletion and pharmacological blockade of <strong>CRF R1</strong> dampened the locomotor response to <b>cocaine</b> (but not methamphetamine).
+CRHR1	addiction	relapse	21813699	In LgA rats, intra VTA CRF induced <b>reinstatement</b> was blocked by administration of the CRF receptor type 1 (<strong>CRF R1</strong>) antagonist antalarmin (500 ng/side) or CP 376395 (500 ng/side), but not the CRF R2 antagonist astressin 2B (500 ng or 1 μg/side) or antisauvagine 30 (ASV 30; 500 ng/side) into the VTA.
+CRHR1	addiction	relapse	21813699	Intra VTA injection of the <strong>CRF R1</strong> selective agonist cortagine (100 ng/side) but not the CRF R2 selective agonist rat urocortin II (rUCN II; 250 ng/side) produced <b>reinstatement</b>.
+CRHR1	drug	cocaine	21813699	These findings reveal that excessive <b>cocaine</b> use increases susceptibility to stressor induced relapse in part by augmenting <strong>CRF R1</strong> dependent regulation of addiction related neurocircuitry in the VTA.
+CRHR1	addiction	addiction	21813699	These findings reveal that excessive cocaine use increases susceptibility to stressor induced relapse in part by augmenting <strong>CRF R1</strong> dependent regulation of <b>addiction</b> related neurocircuitry in the VTA.
+CRHR1	addiction	relapse	21813699	These findings reveal that excessive cocaine use increases susceptibility to stressor induced <b>relapse</b> in part by augmenting <strong>CRF R1</strong> dependent regulation of addiction related neurocircuitry in the VTA.
+CRHR1	drug	alcohol	21752573	[The role of genetic factors on the link between stress and <b>alcohol</b> use: the example of <strong>CRH R1</strong>].
+CRHR1	drug	nicotine	21720754	The aim of the present study was to determine the effect of acute stressor exposure on single trial <b>nicotine</b> conditioned place preference (CPP) in adolescent male rats using a biased CPP procedure and the role of <strong>CRF R1</strong> in this effect.
+CRHR1	addiction	reward	21720754	The aim of the present study was to determine the effect of acute stressor exposure on single trial nicotine conditioned place preference (<b>CPP</b>) in adolescent male rats using a biased <b>CPP</b> procedure and the role of <strong>CRF R1</strong> in this effect.
+CRHR1	drug	nicotine	21720754	Pretreatment with CP 154,526 (20 mg/kg), a selective <strong>CRF R1</strong> antagonist, 30 min before footshock exposure significantly attenuated the effect of prior stress to facilitate <b>nicotine</b> CPP acquisition.
+CRHR1	addiction	reward	21720754	Pretreatment with CP 154,526 (20 mg/kg), a selective <strong>CRF R1</strong> antagonist, 30 min before footshock exposure significantly attenuated the effect of prior stress to facilitate nicotine <b>CPP</b> acquisition.
+CRHR1	drug	nicotine	21720754	CP 154,526 pretreatment had no effect in animals conditioned with a <b>nicotine</b> dose that produced CPP under non stress conditions, suggesting a specific role for <strong>CRF R1</strong> following stress.
+CRHR1	addiction	reward	21720754	CP 154,526 pretreatment had no effect in animals conditioned with a nicotine dose that produced <b>CPP</b> under non stress conditions, suggesting a specific role for <strong>CRF R1</strong> following stress.
+CRHR1	drug	nicotine	21720754	Taken together, the results suggest that during adolescence, <b>nicotine</b> reward is enhanced by recent stressor exposure in a manner that involves signaling at <strong>CRF R1</strong>.
+CRHR1	addiction	reward	21720754	Taken together, the results suggest that during adolescence, nicotine <b>reward</b> is enhanced by recent stressor exposure in a manner that involves signaling at <strong>CRF R1</strong>.
+CRHR1	drug	cocaine	21468623	Prevention of social stress escalated <b>cocaine</b> self administration by <strong>CRF R1</strong> antagonist in the rat VTA.
+CRHR1	drug	cocaine	21468623	The study aims to prevent the effects of intermittently scheduled, brief social defeat stress on subsequent intravenous (IV) <b>cocaine</b> self administration by pretreatment with a CRF receptor subtype 1 (<strong>CRF R1</strong>) antagonist.
+CRHR1	drug	cocaine	21468623	Two experiments examined systemic or intra VTA antagonism of <strong>CRF R1</strong> subtype during stress on the later expression of locomotor sensitization and <b>cocaine</b> self administration during fixed (0.75 mg/kg/infusion) and progressive ratio schedules of reinforcement (0.3 mg/kg/infusion), including a continuous 24 h "binge" (0.3 mg/kg/infusion).
+CRHR1	addiction	intoxication	21468623	Two experiments examined systemic or intra VTA antagonism of <strong>CRF R1</strong> subtype during stress on the later expression of locomotor sensitization and cocaine self administration during fixed (0.75 mg/kg/infusion) and progressive ratio schedules of reinforcement (0.3 mg/kg/infusion), including a continuous 24 h "<b>binge</b>" (0.3 mg/kg/infusion).
+CRHR1	addiction	reward	21468623	Two experiments examined systemic or intra VTA antagonism of <strong>CRF R1</strong> subtype during stress on the later expression of locomotor sensitization and cocaine self administration during fixed (0.75 mg/kg/infusion) and progressive ratio schedules of <b>reinforcement</b> (0.3 mg/kg/infusion), including a continuous 24 h "binge" (0.3 mg/kg/infusion).
+CRHR1	addiction	sensitization	21468623	Two experiments examined systemic or intra VTA antagonism of <strong>CRF R1</strong> subtype during stress on the later expression of locomotor <b>sensitization</b> and cocaine self administration during fixed (0.75 mg/kg/infusion) and progressive ratio schedules of reinforcement (0.3 mg/kg/infusion), including a continuous 24 h "binge" (0.3 mg/kg/infusion).
+CRHR1	drug	cocaine	21468623	In addition, pretreatment with a <strong>CRF R1</strong> antagonist (0.3 μg/0.5 μl/side) into the VTA prior to each social defeat episode prevented stress induced locomotor sensitization to a <b>cocaine</b> challenge and prevented escalated <b>cocaine</b> self administration during a 24 h "binge".
+CRHR1	addiction	intoxication	21468623	In addition, pretreatment with a <strong>CRF R1</strong> antagonist (0.3 μg/0.5 μl/side) into the VTA prior to each social defeat episode prevented stress induced locomotor sensitization to a cocaine challenge and prevented escalated cocaine self administration during a 24 h "<b>binge</b>".
+CRHR1	addiction	sensitization	21468623	In addition, pretreatment with a <strong>CRF R1</strong> antagonist (0.3 μg/0.5 μl/side) into the VTA prior to each social defeat episode prevented stress induced locomotor <b>sensitization</b> to a cocaine challenge and prevented escalated cocaine self administration during a 24 h "binge".
+CRHR1	drug	cocaine	21468623	The current results suggest that <strong>CRF R1</strong> subtype in the VTA is critically involved in the development of stress induced locomotor sensitization which may contribute to escalated <b>cocaine</b> self administration during continuous access in a 24 h "binge".
+CRHR1	addiction	intoxication	21468623	The current results suggest that <strong>CRF R1</strong> subtype in the VTA is critically involved in the development of stress induced locomotor sensitization which may contribute to escalated cocaine self administration during continuous access in a 24 h "<b>binge</b>".
+CRHR1	addiction	sensitization	21468623	The current results suggest that <strong>CRF R1</strong> subtype in the VTA is critically involved in the development of stress induced locomotor <b>sensitization</b> which may contribute to escalated cocaine self administration during continuous access in a 24 h "binge".
+CRHR1	addiction	withdrawal	21377524	To test for a possible interaction between cytokines and CRF, a <strong>CRF1</strong> receptor antagonist (SSR125543) administered prior to the repeated administration of TNFα or MCP 1/CCL2 reduced the magnitude of the <b>withdrawal</b> induced anxiety.
+CRHR1	drug	cocaine	21334600	In particular, behavioral studies point to a serial signaling process initiated by β adrenergic receptors that requires CRF receptor (<strong>CRFR</strong>) dependent signaling in the bed nucleus of the stria terminalis (BNST) to produce stress induced relapse to <b>cocaine</b> seeking.
+CRHR1	addiction	relapse	21334600	In particular, behavioral studies point to a serial signaling process initiated by β adrenergic receptors that requires CRF receptor (<strong>CRFR</strong>) dependent signaling in the bed nucleus of the stria terminalis (BNST) to produce stress induced <b>relapse</b> to cocaine <b>seeking</b>.
+CRHR1	drug	cocaine	21334600	We show that chronic <b>cocaine</b> administration transiently disrupts β(1) adrenergic  and <strong>CRFR1</strong> dependent enhancement of glutamatergic transmission, that this disruption wanes with time, and that it can be reintroduced with a <b>cocaine</b> challenge.
+CRHR1	drug	alcohol	21258618	Previously, we found that both <b>ethanol</b> and corticotropin releasing factor (CRF) increase GABAergic transmission in mouse and rat CeA neurons, in part by enhancing the release of GABA via activation of presynaptic <strong>CRF1</strong> receptors.
+CRHR1	addiction	sensitization	20731720	The present studies addressed the involvement of specific components of the corticotropin releasing factor (CRF) system in locomotor activation and psychomotor <b>sensitization</b> induced by MA (1, 2 mg/kg) by utilizing pharmacological approaches, as well as a series of genetic knockout (KO) mice, each deficient for a single component of the CRF system: <strong>CRF R1</strong>, CRF R2, CRF, or the CRF related peptide Urocortin 1 (Ucn1).
+CRHR1	addiction	sensitization	20731720	<strong>CRF R1</strong> KO mice did not differ from wild type mice in <b>sensitization</b> to MA, and pharmacological blockade of <strong>CRF R1</strong> with CP 154,526 (15, 30 mg/kg) in DBA/2J mice did not selectively attenuate either the acquisition or expression of MA induced <b>sensitization</b>.
+CRHR1	addiction	sensitization	20731720	Deletion of either of the endogenous ligands of <strong>CRF R1</strong> (CRF, Ucn1) either enhanced or had no effect on MA induced <b>sensitization</b>, providing further evidence against a role for <strong>CRF R1</strong> signaling.
+CRHR1	drug	alcohol	20374216	Single nucleotide polymorphisms in corticotropin releasing hormone receptor 1 gene (<strong>CRHR1</strong>) are associated with quantitative trait of event related potential and <b>alcohol</b> dependence.
+CRHR1	addiction	dependence	20374216	Single nucleotide polymorphisms in corticotropin releasing hormone receptor 1 gene (<strong>CRHR1</strong>) are associated with quantitative trait of event related potential and alcohol <b>dependence</b>.
+CRHR1	drug	alcohol	20374216	Single nucleotide polymorphisms in <strong>corticotropin releasing hormone receptor 1</strong> gene (<strong>CRHR1</strong>) are associated with quantitative trait of event related potential and <b>alcohol</b> dependence.
+CRHR1	addiction	dependence	20374216	Single nucleotide polymorphisms in <strong>corticotropin releasing hormone receptor 1</strong> gene (<strong>CRHR1</strong>) are associated with quantitative trait of event related potential and alcohol <b>dependence</b>.
+CRHR1	drug	alcohol	20374216	Recent studies demonstrated a crucial role of corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) in the environmental stress response and <b>ethanol</b> self administration in animal models.
+CRHR1	drug	alcohol	20374216	Recent studies demonstrated a crucial role of <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) in the environmental stress response and <b>ethanol</b> self administration in animal models.
+CRHR1	drug	alcohol	20374216	The aim of the present study was to test the potential associations between single nucleotide polymorphisms (SNPs) in the <strong>CRHR1</strong> gene and the quantitative trait, P3 amplitude during the processing of visual target signals in an oddball paradigm, as well as <b>alcohol</b> dependence diagnosis.
+CRHR1	addiction	dependence	20374216	The aim of the present study was to test the potential associations between single nucleotide polymorphisms (SNPs) in the <strong>CRHR1</strong> gene and the quantitative trait, P3 amplitude during the processing of visual target signals in an oddball paradigm, as well as alcohol <b>dependence</b> diagnosis.
+CRHR1	drug	alcohol	20374216	Significant associations (p < 0.05) were found between the P3 amplitude and <b>alcohol</b> dependence with multiple SNPs in the <strong>CRHR1</strong> gene.
+CRHR1	addiction	dependence	20374216	Significant associations (p < 0.05) were found between the P3 amplitude and alcohol <b>dependence</b> with multiple SNPs in the <strong>CRHR1</strong> gene.
+CRHR1	drug	alcohol	20374216	Our results suggest that <strong>CRHR1</strong> may be involved in modulating the P3 component of the ERP during information processing and in vulnerability to <b>alcoholism</b>.
+CRHR1	drug	alcohol	20201818	The current review provides a comprehensive overview of preclinical evidence from studies involving rodents that when viewed together, suggest a promising role for <strong>CRFR</strong> antagonists in the treatment of <b>alcohol</b> abuse disorders.
+CRHR1	drug	alcohol	20201818	<strong>CRFR</strong> antagonists protect against excessive <b>ethanol</b> intake resulting from <b>ethanol</b> dependence without influencing <b>ethanol</b> intake in non dependent animals.
+CRHR1	addiction	dependence	20201818	<strong>CRFR</strong> antagonists protect against excessive ethanol intake resulting from ethanol <b>dependence</b> without influencing ethanol intake in non dependent animals.
+CRHR1	drug	alcohol	20201818	Similarly, <strong>CRFR</strong> antagonists block excessive binge like <b>ethanol</b> drinking in non dependent mice but do not alter <b>ethanol</b> intake in mice drinking moderate amounts of <b>ethanol</b>.
+CRHR1	addiction	intoxication	20201818	Similarly, <strong>CRFR</strong> antagonists block excessive <b>binge</b> like ethanol drinking in non dependent mice but do not alter ethanol intake in mice drinking moderate amounts of ethanol.
+CRHR1	drug	alcohol	20201818	<strong>CRFR</strong> antagonists also protect against increased <b>ethanol</b> intake and relapse like behaviors precipitated by exposure to a stressful event.
+CRHR1	addiction	relapse	20201818	<strong>CRFR</strong> antagonists also protect against increased ethanol intake and <b>relapse</b> like behaviors precipitated by exposure to a stressful event.
+CRHR1	drug	alcohol	20201818	Additionally, <strong>CRFR</strong> antagonists attenuate the negative emotional responses associated with <b>ethanol</b> withdrawal.
+CRHR1	addiction	withdrawal	20201818	Additionally, <strong>CRFR</strong> antagonists attenuate the negative emotional responses associated with ethanol <b>withdrawal</b>.
+CRHR1	drug	alcohol	20130533	Recent evidence suggests that corticotropin releasing factor (CRF) receptor (<strong>CRFR</strong>) signaling is involved in modulating binge like <b>ethanol</b> consumption in C57BL/6J mice.
+CRHR1	addiction	intoxication	20130533	Recent evidence suggests that corticotropin releasing factor (CRF) receptor (<strong>CRFR</strong>) signaling is involved in modulating <b>binge</b> like ethanol consumption in C57BL/6J mice.
+CRHR1	drug	alcohol	20130533	In this report, a series of experiments were performed to further characterize the role of <strong>CRFR</strong> signaling in binge like <b>ethanol</b> consumption.
+CRHR1	addiction	intoxication	20130533	In this report, a series of experiments were performed to further characterize the role of <strong>CRFR</strong> signaling in <b>binge</b> like ethanol consumption.
+CRHR1	drug	alcohol	20060104	Three <strong>CRF1</strong> receptor (CRF(1)) antagonists decreased basal GABAergic responses and abolished <b>ethanol</b> effects.
+CRHR1	drug	opioid	20052275	<strong>CRF1</strong> R activation of the dynorphin/kappa <b>opioid</b> system in the mouse basolateral amygdala mediates anxiety like behavior.
+CRHR1	drug	alcohol	19878140	An examination of <b>alcohol</b> consumption in adolescents reported a significant genotype x environment (G x E) interaction involving rs1876831, a corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) polymorphism, and negative events.
+CRHR1	drug	alcohol	19878140	An examination of <b>alcohol</b> consumption in adolescents reported a significant genotype x environment (G x E) interaction involving rs1876831, a <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) polymorphism, and negative events.
+CRHR1	addiction	relapse	19800323	The <b>reinstatement</b>, glutamate release, and dopamine release are prevented by VTA infusions of CRF receptor 2 (CRF R2) but not <strong>CRF R1</strong> antagonists.
+CRHR1	drug	cocaine	19800323	Reinstatement is triggered by some but not all CRF R2 agonists and some but not all <strong>CRF R1</strong> agonists; the common denominator of the effective agonists is that they bind to the CRF binding protein (CRF BP), which appears to be essential for the behavioral and VTA effects of stress and CRF in <b>cocaine</b> experienced animals.
+CRHR1	addiction	relapse	19800323	<b>Reinstatement</b> is triggered by some but not all CRF R2 agonists and some but not all <strong>CRF R1</strong> agonists; the common denominator of the effective agonists is that they bind to the CRF binding protein (CRF BP), which appears to be essential for the behavioral and VTA effects of stress and CRF in cocaine experienced animals.
+CRHR1	drug	alcohol	19785977	Variation in the <strong>CRF1</strong> receptor gene has been shown to moderate stress induced <b>alcohol</b> drinking (gene environment interaction) in animals, and this finding was recently extended to humans.
+CRHR1	drug	cocaine	19675537	Stress induced potentiation of <b>cocaine</b> reward: a role for <strong>CRF R1</strong> and CREB.
+CRHR1	addiction	reward	19675537	Stress induced potentiation of cocaine <b>reward</b>: a role for <strong>CRF R1</strong> and CREB.
+CRHR1	drug	opioid	19539724	We used electron microscopy to quantitatively compare immunolabeling of the corticotropin releasing factor receptor (<strong>CRFr</strong>) and CRF in the anterolateral bed nucleus of the stria terminalis (BSTal) of mice injected with saline or <b>morphine</b> in escalating doses for 14 days.
+CRHR1	drug	opioid	19539724	The non injected controls had a significantly lower plasmalemmal density of <strong>CRFr</strong> immunogold particles in dendrites compared with mice receiving saline, but not those receiving <b>morphine</b>, injections.
+CRHR1	drug	opioid	19539724	Compared with saline, however, mice receiving chronic <b>morphine</b> showed a significantly lower plasmalemmal, and greater cytoplasmic, density of <strong>CRFr</strong> immunogold in dendrites.
+CRHR1	drug	opioid	19539724	Within the cytoplasmic compartment of somata and dendrites of the BSTal, the proportion of <strong>CRFr</strong> gold particles associated with mitochondria was three times as great in mice receiving <b>morphine</b> compared with saline.
+CRHR1	drug	opioid	19539724	This subcellular distribution is consistent with <b>morphine</b>,  and <strong>CRFr</strong> associated modulation of intracellular calcium release or oxidative stress.
+CRHR1	drug	opioid	19539724	The between group changes occurred without effect on the total number of dendritic <strong>CRFr</strong> immunogold particles, suggesting that chronic <b>morphine</b> enhances internalization or decreases delivery of the <strong>CRFr</strong> to the plasma membrane, a trafficking effect that is also affected by the stress of daily injections.
+CRHR1	drug	opioid	19539724	In contrast, saline and <b>morphine</b> treatment groups showed no significant differences in the total number of CRF immunoreactive axon terminals, or the frequency with which these terminals contacted <strong>CRFr</strong> containing dendrites.
+CRHR1	drug	nicotine	19217073	Previous research has shown that blockade of corticotropin releasing factor (CRF) receptors with a nonspecific <strong>CRF1</strong>/CRF2 receptor antagonist prevents the deficit in brain reward function associated with <b>nicotine</b> withdrawal and stress induced reinstatement of extinguished <b>nicotine</b> seeking in rats.
+CRHR1	addiction	relapse	19217073	Previous research has shown that blockade of corticotropin releasing factor (CRF) receptors with a nonspecific <strong>CRF1</strong>/CRF2 receptor antagonist prevents the deficit in brain reward function associated with nicotine withdrawal and stress induced <b>reinstatement</b> of extinguished nicotine <b>seeking</b> in rats.
+CRHR1	addiction	reward	19217073	Previous research has shown that blockade of corticotropin releasing factor (CRF) receptors with a nonspecific <strong>CRF1</strong>/CRF2 receptor antagonist prevents the deficit in brain <b>reward</b> function associated with nicotine withdrawal and stress induced reinstatement of extinguished nicotine seeking in rats.
+CRHR1	addiction	withdrawal	19217073	Previous research has shown that blockade of corticotropin releasing factor (CRF) receptors with a nonspecific <strong>CRF1</strong>/CRF2 receptor antagonist prevents the deficit in brain reward function associated with nicotine <b>withdrawal</b> and stress induced reinstatement of extinguished nicotine seeking in rats.
+CRHR1	drug	nicotine	19217073	The aim of these studies was to investigate the role of <strong>CRF1</strong> and CRF2 receptors in the deficit in brain reward function associated with precipitated <b>nicotine</b> withdrawal and stress induced reinstatement of <b>nicotine</b> seeking.
+CRHR1	addiction	relapse	19217073	The aim of these studies was to investigate the role of <strong>CRF1</strong> and CRF2 receptors in the deficit in brain reward function associated with precipitated nicotine withdrawal and stress induced <b>reinstatement</b> of nicotine <b>seeking</b>.
+CRHR1	addiction	reward	19217073	The aim of these studies was to investigate the role of <strong>CRF1</strong> and CRF2 receptors in the deficit in brain <b>reward</b> function associated with precipitated nicotine withdrawal and stress induced reinstatement of nicotine seeking.
+CRHR1	addiction	withdrawal	19217073	The aim of these studies was to investigate the role of <strong>CRF1</strong> and CRF2 receptors in the deficit in brain reward function associated with precipitated nicotine <b>withdrawal</b> and stress induced reinstatement of nicotine seeking.
+CRHR1	drug	nicotine	19217073	The <strong>CRF1</strong> receptor antagonist R278995/CRA0450 but not the CRF2 receptor antagonist astressin 2B prevented the elevations in brain reward thresholds associated with precipitated <b>nicotine</b> withdrawal.
+CRHR1	addiction	reward	19217073	The <strong>CRF1</strong> receptor antagonist R278995/CRA0450 but not the CRF2 receptor antagonist astressin 2B prevented the elevations in brain <b>reward</b> thresholds associated with precipitated nicotine withdrawal.
+CRHR1	addiction	withdrawal	19217073	The <strong>CRF1</strong> receptor antagonist R278995/CRA0450 but not the CRF2 receptor antagonist astressin 2B prevented the elevations in brain reward thresholds associated with precipitated nicotine <b>withdrawal</b>.
+CRHR1	drug	cocaine	19181855	When injected in the acute binge paradigm, <b>cocaine</b> enhanced tPA activity in the amygdala, which required activation of corticotropin releasing factor type 1 (<strong>CRF R1</strong>) receptors.
+CRHR1	addiction	intoxication	19181855	When injected in the acute <b>binge</b> paradigm, cocaine enhanced tPA activity in the amygdala, which required activation of corticotropin releasing factor type 1 (<strong>CRF R1</strong>) receptors.
+CRHR1	drug	opioid	19166913	Thus, in both the CeA and BNST, mu OR and <strong>CRFr</strong> have strategic locations for mediation of CRF and <b>opioid</b> effects on the postsynaptic excitability of single neurons, and on the respective presynaptic release of excitatory and inhibitory neurotransmitters.
+CRHR1	drug	alcohol	19151899	Presynaptic <strong>CRF1</strong> receptors mediate the <b>ethanol</b> enhancement of GABAergic transmission in the mouse central amygdala.
+CRHR1	drug	alcohol	19151899	We recently reported that the <b>ethanol</b> augmentation of GABAergic synaptic transmission in rat CeA involves <strong>CRF1</strong> receptors, because both CRF and <b>ethanol</b> significantly enhanced the amplitude of evoked GABAergic inhibitory postsynaptic currents (IPSCs) in CeA neurons from wild type (WT) and CRF2 knockout (KO) mice, but not in neurons of <strong>CRF1</strong> KO mice.
+CRHR1	drug	alcohol	19151899	A <strong>CRF1</strong> (but not CRF2) KO construct and the <strong>CRF1</strong> selective nonpeptide antagonist NIH 3 (LWH 63) blocked the augmenting effect of both CRF and <b>ethanol</b> on evoked IPSCs.
+CRHR1	drug	alcohol	19151899	The PPF effect of <b>ethanol</b> was abolished in CeA neurons of <strong>CRF1</strong> KO mice.
+CRHR1	drug	alcohol	19151899	The <strong>CRF1</strong> antagonist NIH 3 blocked the CRF  and <b>ethanol</b> induced enhancement of mIPSC frequency in CeA neurons.
+CRHR1	drug	alcohol	19151899	These data indicate that presynaptic <strong>CRF1</strong> receptors play a critical role in permitting or mediating <b>ethanol</b> enhancement of GABAergic synaptic transmission in CeA, via increased vesicular GABA release, and thus may be a rational target for the treatment of <b>alcohol</b> abuse and <b>alcoholism</b>.
+CRHR1	drug	nicotine	19145226	The administration of the nonspecific <strong>CRF1</strong>/2 receptor antagonist D Phe CRF((12 41)) into the CeA and the Nacc shell prevented the mecamylamine induced elevations in brain reward thresholds in the <b>nicotine</b> dependent rats.
+CRHR1	addiction	reward	19145226	The administration of the nonspecific <strong>CRF1</strong>/2 receptor antagonist D Phe CRF((12 41)) into the CeA and the Nacc shell prevented the mecamylamine induced elevations in brain <b>reward</b> thresholds in the nicotine dependent rats.
+CRHR1	drug	nicotine	19145226	Blockade of <strong>CRF1</strong>/2 receptors in the lateral BNST did not prevent the mecamylamine induced elevations in brain reward thresholds in the <b>nicotine</b> dependent rats.
+CRHR1	addiction	reward	19145226	Blockade of <strong>CRF1</strong>/2 receptors in the lateral BNST did not prevent the mecamylamine induced elevations in brain <b>reward</b> thresholds in the nicotine dependent rats.
+CRHR1	drug	cocaine	19091975	Furthermore, we found that both in vivo and ex vivo <b>cocaine</b> induced a dopamine receptor and <strong>CRF R1</strong> dependent enhancement of a form of NMDA receptor dependent short term potentiation in the BNST.
+CRHR1	drug	alcohol	18631323	Effects of <strong>CRF1</strong> receptor and opioid receptor antagonists on dependence induced increases in <b>alcohol</b> drinking by <b>alcohol</b> preferring (P) rats.
+CRHR1	drug	opioid	18631323	Effects of <strong>CRF1</strong> receptor and <b>opioid</b> receptor antagonists on dependence induced increases in alcohol drinking by alcohol preferring (P) rats.
+CRHR1	addiction	dependence	18631323	Effects of <strong>CRF1</strong> receptor and opioid receptor antagonists on <b>dependence</b> induced increases in alcohol drinking by alcohol preferring (P) rats.
+CRHR1	addiction	sensitization	18591672	We posited that <strong>CRF1</strong> signaling pathways are crucial for EtOH induced <b>sensitization</b>.
+CRHR1	addiction	sensitization	18591672	We demonstrate that mice lacking <strong>CRF1</strong> receptors do not show psychomotor <b>sensitization</b> to EtOH, a phenomenon that was also absent in <strong>CRF1</strong> + 2 receptor double knockout mice.
+CRHR1	addiction	sensitization	18591672	The <strong>CRF1</strong> receptor antagonist CP 154,526 attenuated the acquisition and prevented the expression of EtOH induced psychomotor <b>sensitization</b>.
+CRHR1	addiction	sensitization	18591672	Because <strong>CRF1</strong> receptors are also activated by urocortin 1 (Ucn1), we tested Ucn1 knockout mice for EtOH <b>sensitization</b> and found normal <b>sensitization</b> in this genotype.
+CRHR1	addiction	sensitization	18591672	CRF and <strong>CRF1</strong> receptors, therefore, are involved in the neurobiological adaptations that underlie the development and expression of psychomotor <b>sensitization</b> to EtOH.
+CRHR1	addiction	sensitization	18591672	A CRF/<strong>CRF1</strong> mediated mechanism involving the HPA axis is proposed for acquisition, whereas an extrahypothalamic CRF/<strong>CRF1</strong> participation is suggested for expression of <b>sensitization</b> to EtOH.
+CRHR1	addiction	aversion	18184783	CRF induced place <b>aversion</b> was blocked by the CRF2 receptor antagonist antisauvigine 30, but not by the <strong>CRF1</strong> receptor antagonist antalarmin.
+CRHR1	drug	nicotine	17921249	CRF <strong>CRF1</strong> system activation mediates withdrawal induced increases in <b>nicotine</b> self administration in <b>nicotine</b> dependent rats.
+CRHR1	addiction	withdrawal	17921249	CRF <strong>CRF1</strong> system activation mediates <b>withdrawal</b> induced increases in nicotine self administration in nicotine dependent rats.
+CRHR1	addiction	sensitization	17919825	To assess the role of the <strong>CRF1</strong> receptor in the acquisition of behavioral <b>sensitization</b>, mice were pretreated with an i.p.
+CRHR1	drug	alcohol	17919825	To determine the role of the <strong>CRF1</strong> receptor in modulating the expression of <b>ethanol</b> induced sensitization, mice that had previously been sensitized to the locomotor stimulant effects of <b>ethanol</b> were pretreated with CP 154,526 30 min before an i.p.
+CRHR1	addiction	sensitization	17919825	To determine the role of the <strong>CRF1</strong> receptor in modulating the expression of ethanol induced <b>sensitization</b>, mice that had previously been sensitized to the locomotor stimulant effects of ethanol were pretreated with CP 154,526 30 min before an i.p.
+CRHR1	drug	alcohol	17919825	injection of <b>ethanol</b> to determine the combined effects of the <strong>CRF1</strong> receptor antagonist and <b>ethanol</b> on locomotor activity.
+CRHR1	drug	alcohol	17919825	These data provide novel evidence that <strong>CRF1</strong> receptor signaling modulates the expression of <b>ethanol</b> induced locomotor sensitization, and add to a growing literature suggesting a role for neurochemicals and hormones associated with the HPA axis in behavioral sensitization resulting from repeated exposure to drugs of abuse.
+CRHR1	addiction	sensitization	17919825	These data provide novel evidence that <strong>CRF1</strong> receptor signaling modulates the expression of ethanol induced locomotor <b>sensitization</b>, and add to a growing literature suggesting a role for neurochemicals and hormones associated with the HPA axis in behavioral <b>sensitization</b> resulting from repeated exposure to drugs of abuse.
+CRHR1	drug	alcohol	17705061	The <strong>CRF1</strong> receptor antagonist antalarmin attenuates yohimbine induced increases in operant <b>alcohol</b> self administration and reinstatement of <b>alcohol</b> seeking in rats.
+CRHR1	addiction	relapse	17705061	The <strong>CRF1</strong> receptor antagonist antalarmin attenuates yohimbine induced increases in operant alcohol self administration and <b>reinstatement</b> of alcohol <b>seeking</b> in rats.
+CRHR1	addiction	reward	17705061	The <strong>CRF1</strong> receptor antagonist antalarmin attenuates yohimbine induced increases in <b>operant</b> alcohol self administration and reinstatement of alcohol seeking in rats.
+CRHR1	drug	alcohol	17705061	These results suggest that extrahypothalamic <strong>CRF1</strong> receptors are involved in the effect of yohimbine on operant <b>alcohol</b> self administration and on relapse to <b>alcohol</b> seeking and support the notion that <strong>CRF1</strong> receptor antagonists should be considered in <b>alcohol</b> addiction treatment.
+CRHR1	addiction	addiction	17705061	These results suggest that extrahypothalamic <strong>CRF1</strong> receptors are involved in the effect of yohimbine on operant alcohol self administration and on relapse to alcohol seeking and support the notion that <strong>CRF1</strong> receptor antagonists should be considered in alcohol <b>addiction</b> treatment.
+CRHR1	addiction	relapse	17705061	These results suggest that extrahypothalamic <strong>CRF1</strong> receptors are involved in the effect of yohimbine on operant alcohol self administration and on <b>relapse</b> to alcohol <b>seeking</b> and support the notion that <strong>CRF1</strong> receptor antagonists should be considered in alcohol addiction treatment.
+CRHR1	addiction	reward	17705061	These results suggest that extrahypothalamic <strong>CRF1</strong> receptors are involved in the effect of yohimbine on <b>operant</b> alcohol self administration and on relapse to alcohol seeking and support the notion that <strong>CRF1</strong> receptor antagonists should be considered in alcohol addiction treatment.
+CRHR1	drug	opioid	17610870	The <strong>CRF1</strong> receptor antagonist, R121919, attenuates the severity of precipitated <b>morphine</b> withdrawal.
+CRHR1	addiction	withdrawal	17610870	The <strong>CRF1</strong> receptor antagonist, R121919, attenuates the severity of precipitated morphine <b>withdrawal</b>.
+CRHR1	drug	alcohol	17585886	Upregulation of voluntary <b>alcohol</b> intake, behavioral sensitivity to stress, and amygdala <strong>crhr1</strong> expression following a history of dependence.
+CRHR1	addiction	dependence	17585886	Upregulation of voluntary alcohol intake, behavioral sensitivity to stress, and amygdala <strong>crhr1</strong> expression following a history of <b>dependence</b>.
+CRHR1	drug	alcohol	17585886	This persisted 3 months after <b>alcohol</b> exposure and was reversed by the selective <strong>CRH R1</strong> antagonist 3 (4 Chloro 2 morpholin 4 yl thiazol 5 yl) 8 (1 ethylpropyl) 2,6 dimethyl imidazo[1,2 b]pyridazine (MTIP) (10 mg/kg).
+CRHR1	drug	alcohol	17482248	Dependence induced increases in <b>ethanol</b> self administration in mice are blocked by the <strong>CRF1</strong> receptor antagonist antalarmin and by <strong>CRF1</strong> receptor knockout.
+CRHR1	addiction	dependence	17482248	<b>Dependence</b> induced increases in ethanol self administration in mice are blocked by the <strong>CRF1</strong> receptor antagonist antalarmin and by <strong>CRF1</strong> receptor knockout.
+CRHR1	drug	alcohol	17407495	Region specific down regulation of <strong>Crhr1</strong> gene expression in <b>alcohol</b> preferring msP rats following ad lib access to <b>alcohol</b>.
+CRHR1	drug	alcohol	17407495	Corticotropin releasing hormone 1 receptors (<strong>CRH R1</strong>) mediate increased behavioral sensitivity to stress and excessive <b>alcohol</b> self administration following a history of dependence.
+CRHR1	addiction	dependence	17407495	Corticotropin releasing hormone 1 receptors (<strong>CRH R1</strong>) mediate increased behavioral sensitivity to stress and excessive alcohol self administration following a history of <b>dependence</b>.
+CRHR1	drug	alcohol	17407495	It was recently demonstrated that the genetically selected <b>alcohol</b> preferring msP rat line replicates many characteristics of the post dependent state, due to an innate up regulation of the <strong>Crhr1</strong> transcript in several limbic areas related to <b>alcohol</b> drinking motivation.
+CRHR1	drug	alcohol	17407495	Here, we examined whether voluntary <b>alcohol</b> consumption might be able to down regulate <strong>Crhr1</strong> transcript levels in msP rats in brain areas where elevated expression previously has been shown.
+CRHR1	drug	alcohol	17407495	Accumbens, 2 weeks'ad lib access to <b>alcohol</b> led to a highly significant down regulation of the <strong>Crhr1</strong> transcript.
+CRHR1	drug	alcohol	17407495	<b>Alcohol</b> induced <strong>Crhr1</strong> down regulation was not seen in cingulate cortex.
+CRHR1	drug	alcohol	17407495	These data support that recruitment of <strong>CRH R1</strong> signaling within components of the extended amygdala drives excessive <b>alcohol</b> intake, and that <b>alcohol</b> is voluntarily consumed in part for its ability to reduce <strong>CRH R1</strong> activity in this region.
+CRHR1	drug	alcohol	17344409	We describe a novel corticotropin releasing factor receptor 1 (<strong>CRF1</strong>) antagonist with advantageous properties for clinical development, and its in vivo activity in preclinical <b>alcoholism</b> models.
+CRHR1	drug	benzodiazepine	17297634	The <strong>CRF1</strong> receptor antagonist R121919 attenuates the neuroendocrine and behavioral effects of precipitated <b>lorazepam</b> withdrawal.
+CRHR1	addiction	withdrawal	17297634	The <strong>CRF1</strong> receptor antagonist R121919 attenuates the neuroendocrine and behavioral effects of precipitated lorazepam <b>withdrawal</b>.
+CRHR1	addiction	sensitization	17194545	These data provide ultrastructural evidence that <strong>CRFr</strong> and muOR are co localized in LC neurons, a cellular substrate that may underlie opiate induced <b>sensitization</b> of brain noradrenergic neurons to CRF.
+CRHR1	drug	cocaine	17182090	Effects of the <strong>CRF1</strong> antagonist antalarmin on <b>cocaine</b> self administration and discrimination in rhesus monkeys.
+CRHR1	drug	cocaine	17079348	Long term potentiation (LTP) in the central amygdala (CeA) is enhanced after prolonged withdrawal from chronic <b>cocaine</b> and requires <strong>CRF1</strong> receptors.
+CRHR1	addiction	withdrawal	17079348	Long term potentiation (LTP) in the central amygdala (CeA) is enhanced after prolonged <b>withdrawal</b> from chronic cocaine and requires <strong>CRF1</strong> receptors.
+CRHR1	drug	alcohol	17047935	Dissociation between opioid and <strong>CRF1</strong> antagonist sensitive drinking in Sardinian <b>alcohol</b> preferring rats.
+CRHR1	drug	opioid	17047935	Dissociation between <b>opioid</b> and <strong>CRF1</strong> antagonist sensitive drinking in Sardinian alcohol preferring rats.
+CRHR1	drug	alcohol	17015825	Variation at the rat <strong>Crhr1</strong> locus and sensitivity to relapse into <b>alcohol</b> seeking induced by environmental stress.
+CRHR1	addiction	relapse	17015825	Variation at the rat <strong>Crhr1</strong> locus and sensitivity to <b>relapse</b> into alcohol <b>seeking</b> induced by environmental stress.
+CRHR1	drug	alcohol	17015825	An innate up regulation of the <strong>Crhr1</strong> transcript, encoding the corticotropin releasing hormone receptor 1 (CRH R1), was found in several limbic brain areas of msP rats genetically selected for high <b>alcohol</b> preference, was associated with genetic polymorphism of the <strong>Crhr1</strong> promoter, and was accompanied by increased CRH R1 density.
+CRHR1	drug	alcohol	17015825	An innate up regulation of the <strong>Crhr1</strong> transcript, encoding the <strong>corticotropin releasing hormone receptor 1</strong> (CRH R1), was found in several limbic brain areas of msP rats genetically selected for high <b>alcohol</b> preference, was associated with genetic polymorphism of the <strong>Crhr1</strong> promoter, and was accompanied by increased CRH R1 density.
+CRHR1	drug	alcohol	17015825	An innate up regulation of the <strong>Crhr1</strong> transcript, encoding the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRH R1</strong>), was found in several limbic brain areas of msP rats genetically selected for high <b>alcohol</b> preference, was associated with genetic polymorphism of the <strong>Crhr1</strong> promoter, and was accompanied by increased <strong>CRH R1</strong> density.
+CRHR1	drug	alcohol	17015825	A selective <strong>CRH R1</strong> antagonist (antalarmin, 10 20 mg/kg) was devoid of effects on operant <b>alcohol</b> self administration in unselected Wistar rats but significantly suppressed this behavior in the msP line.
+CRHR1	addiction	reward	17015825	A selective <strong>CRH R1</strong> antagonist (antalarmin, 10 20 mg/kg) was devoid of effects on <b>operant</b> alcohol self administration in unselected Wistar rats but significantly suppressed this behavior in the msP line.
+CRHR1	drug	alcohol	17015825	These data demonstrate that <strong>Crhr1</strong> genotype and expression interact with environmental stress to reinstate <b>alcohol</b> seeking behavior.
+CRHR1	addiction	relapse	17015825	These data demonstrate that <strong>Crhr1</strong> genotype and expression interact with environmental stress to reinstate alcohol <b>seeking</b> behavior.
+CRHR1	addiction	withdrawal	17004937	The enhanced CRF induced LTP after 2 weeks of <b>withdrawal</b> was mediated through augmented <strong>CRF1</strong> receptor function, associated with an increased signalling through protein kinase A, and required N methyl D aspartate (NMDA) receptors.
+CRHR1	drug	cocaine	17004937	These results support a role for <strong>CRF1</strong> receptor antagonists as plausible treatment options during withdrawal from chronic <b>cocaine</b> and suggest Ca(V)2.3 blockers as potential candidates for pharmaceutical modulation of CRF systems.
+CRHR1	addiction	withdrawal	17004937	These results support a role for <strong>CRF1</strong> receptor antagonists as plausible treatment options during <b>withdrawal</b> from chronic cocaine and suggest Ca(V)2.3 blockers as potential candidates for pharmaceutical modulation of CRF systems.
+CRHR1	drug	alcohol	16820021	Furthermore, antalarmin, a selective corticotrophin releasing factor type 1 (<strong>CRF1</strong>) receptor antagonist, reduces isolation induced acquisition and maintenance of volitional <b>ethanol</b> consumption in this strain.
+CRHR1	drug	alcohol	16550213	Genetic association of the human corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) with binge drinking and <b>alcohol</b> intake patterns in two independent samples.
+CRHR1	addiction	intoxication	16550213	Genetic association of the human corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) with <b>binge</b> drinking and alcohol intake patterns in two independent samples.
+CRHR1	drug	alcohol	16550213	Genetic association of the human <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) with binge drinking and <b>alcohol</b> intake patterns in two independent samples.
+CRHR1	addiction	intoxication	16550213	Genetic association of the human <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) with <b>binge</b> drinking and alcohol intake patterns in two independent samples.
+CRHR1	drug	alcohol	16550213	To investigate the role of the corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) in patterns of human <b>alcohol</b> drinking and its potential contribution to <b>alcohol</b> dependence, we analysed two independent samples: a sample of adolescents, which consisted of individuals from the 'Mannheim Study of Risk Children' (MARC), who had little previous exposure to <b>alcohol</b>, and a sample of <b>alcohol</b> dependent adults, who met DSM IV criteria of <b>alcohol</b> dependence.
+CRHR1	addiction	dependence	16550213	To investigate the role of the corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) in patterns of human alcohol drinking and its potential contribution to alcohol <b>dependence</b>, we analysed two independent samples: a sample of adolescents, which consisted of individuals from the 'Mannheim Study of Risk Children' (MARC), who had little previous exposure to alcohol, and a sample of alcohol dependent adults, who met DSM IV criteria of alcohol <b>dependence</b>.
+CRHR1	drug	alcohol	16550213	To investigate the role of the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) in patterns of human <b>alcohol</b> drinking and its potential contribution to <b>alcohol</b> dependence, we analysed two independent samples: a sample of adolescents, which consisted of individuals from the 'Mannheim Study of Risk Children' (MARC), who had little previous exposure to <b>alcohol</b>, and a sample of <b>alcohol</b> dependent adults, who met DSM IV criteria of <b>alcohol</b> dependence.
+CRHR1	addiction	dependence	16550213	To investigate the role of the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) in patterns of human alcohol drinking and its potential contribution to alcohol <b>dependence</b>, we analysed two independent samples: a sample of adolescents, which consisted of individuals from the 'Mannheim Study of Risk Children' (MARC), who had little previous exposure to alcohol, and a sample of alcohol dependent adults, who met DSM IV criteria of alcohol <b>dependence</b>.
+CRHR1	drug	alcohol	16550213	The sample of adult <b>alcohol</b> dependent patients showed association of <strong>CRHR1</strong> with high amount of drinking.
+CRHR1	drug	alcohol	16550213	This is the first time that an association of <strong>CRHR1</strong> with specific patterns of <b>alcohol</b> consumption has been reported.
+CRHR1	drug	alcohol	16550213	Our findings support results from animal models, suggesting an importance of <strong>CRHR1</strong> in integrating gene environment effects in <b>alcohol</b> use disorders.
+CRHR1	drug	cocaine	16374599	Systemic injections of the selective corticotropin releasing factor 1 (<strong>CRF1</strong>) receptor antagonist CP 154,526 attenuate footshock stress induced reinstatement of heroin and <b>cocaine</b> seeking and morphine conditioned place preference (CPP).
+CRHR1	drug	opioid	16374599	Systemic injections of the selective corticotropin releasing factor 1 (<strong>CRF1</strong>) receptor antagonist CP 154,526 attenuate footshock stress induced reinstatement of <b>heroin</b> and cocaine seeking and <b>morphine</b> conditioned place preference (CPP).
+CRHR1	addiction	relapse	16374599	Systemic injections of the selective corticotropin releasing factor 1 (<strong>CRF1</strong>) receptor antagonist CP 154,526 attenuate footshock stress induced <b>reinstatement</b> of heroin and cocaine <b>seeking</b> and morphine conditioned place preference (CPP).
+CRHR1	addiction	reward	16374599	Systemic injections of the selective corticotropin releasing factor 1 (<strong>CRF1</strong>) receptor antagonist CP 154,526 attenuate footshock stress induced reinstatement of heroin and cocaine seeking and morphine conditioned place preference (<b>CPP</b>).
+CRHR1	drug	opioid	16374599	We used a CPP version of the reinstatement model to examine the role of <strong>CRF1</strong> receptors in the BNST, amygdala, and nucleus accumbens (NAc) in footshock  or drug priming induced reinstatement of extinguished <b>morphine</b> CPP.
+CRHR1	addiction	relapse	16374599	We used a CPP version of the <b>reinstatement</b> model to examine the role of <strong>CRF1</strong> receptors in the BNST, amygdala, and nucleus accumbens (NAc) in footshock  or drug priming induced <b>reinstatement</b> of extinguished morphine CPP.
+CRHR1	addiction	reward	16374599	We used a <b>CPP</b> version of the reinstatement model to examine the role of <strong>CRF1</strong> receptors in the BNST, amygdala, and nucleus accumbens (NAc) in footshock  or drug priming induced reinstatement of extinguished morphine <b>CPP</b>.
+CRHR1	drug	opioid	16374599	The present results demonstrate dissociable roles of <strong>CRF1</strong> receptors in the BNST, amygdala, and NAc in footshock stress  vs <b>morphine</b> priming induced reinstatement of drug CPP.
+CRHR1	addiction	relapse	16374599	The present results demonstrate dissociable roles of <strong>CRF1</strong> receptors in the BNST, amygdala, and NAc in footshock stress  vs morphine priming induced <b>reinstatement</b> of drug CPP.
+CRHR1	addiction	reward	16374599	The present results demonstrate dissociable roles of <strong>CRF1</strong> receptors in the BNST, amygdala, and NAc in footshock stress  vs morphine priming induced reinstatement of drug <b>CPP</b>.
+CRHR1	addiction	withdrawal	16339307	Here we report that genetic disruption of <strong>CRF1</strong> receptor pathways in mice eliminates the negative affective states of opiate <b>withdrawal</b>.
+CRHR1	addiction	withdrawal	16339307	In particular, neither <strong>CRF1</strong> receptor heterozygous (<strong>CRF1</strong>+/ ) nor homozygous (<strong>CRF1</strong> / ) null mutant mice avoided environmental cues repeatedly paired with the early phase of opiate <b>withdrawal</b>.
+CRHR1	drug	opioid	16339307	These results were not due to altered associative learning processes because <strong>CRF1</strong>+/  and <strong>CRF1</strong> /  mice displayed reliable, conditioned place aversions to environmental cues paired with the kappa <b>opioid</b> receptor agonist U 50,488H.
+CRHR1	addiction	withdrawal	16339307	We also examined the impact of <strong>CRF1</strong> receptor deficiency upon opiate <b>withdrawal</b> induced dynorphin activity in the nucleus accumbens, a brain molecular mechanism thought to underlie the negative affective states of drug <b>withdrawal</b>.
+CRHR1	addiction	withdrawal	16339307	Consistent with the behavioral indices, we found that, during the early phase of opiate <b>withdrawal</b>, neither <strong>CRF1</strong>+/  nor <strong>CRF1</strong> /  showed increased dynorphin mRNA levels in the nucleus accumbens.
+CRHR1	addiction	addiction	16339307	This study reveals a cardinal role for CRF/<strong>CRF1</strong> receptor pathways in the negative affective states of opiate withdrawal and suggests therapeutic strategies for the treatment of opiate <b>addiction</b>.
+CRHR1	addiction	withdrawal	16339307	This study reveals a cardinal role for CRF/<strong>CRF1</strong> receptor pathways in the negative affective states of opiate <b>withdrawal</b> and suggests therapeutic strategies for the treatment of opiate addiction.
+CRHR1	drug	cocaine	16139885	Effects of CP 154,526, a <strong>CRF1</strong> receptor antagonist, on behavioral responses to <b>cocaine</b> in rats.
+CRHR1	drug	cocaine	16139885	The present study implies that <strong>CRF1</strong> receptors control the expression of <b>cocaine</b> hyperactivation and sensitization as well as the <b>cocaine</b> induced relapse behavior, but do not play any role in <b>cocaine</b> discrimination and self administration.
+CRHR1	addiction	relapse	16139885	The present study implies that <strong>CRF1</strong> receptors control the expression of cocaine hyperactivation and sensitization as well as the cocaine induced <b>relapse</b> behavior, but do not play any role in cocaine discrimination and self administration.
+CRHR1	addiction	sensitization	16139885	The present study implies that <strong>CRF1</strong> receptors control the expression of cocaine hyperactivation and <b>sensitization</b> as well as the cocaine induced relapse behavior, but do not play any role in cocaine discrimination and self administration.
+CRHR1	drug	cocaine	16139885	These findings may suggest that <strong>CRF1</strong> receptor antagonists should be considered as possible medications in the treatment of <b>cocaine</b> addiction.
+CRHR1	addiction	addiction	16139885	These findings may suggest that <strong>CRF1</strong> receptor antagonists should be considered as possible medications in the treatment of cocaine <b>addiction</b>.
+CRHR1	drug	alcohol	15992556	Lack of association between single nucleotide polymorphisms in the corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) gene and <b>alcohol</b> dependence.
+CRHR1	addiction	dependence	15992556	Lack of association between single nucleotide polymorphisms in the corticotropin releasing hormone receptor 1 (<strong>CRHR1</strong>) gene and alcohol <b>dependence</b>.
+CRHR1	drug	alcohol	15992556	Lack of association between single nucleotide polymorphisms in the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) gene and <b>alcohol</b> dependence.
+CRHR1	addiction	dependence	15992556	Lack of association between single nucleotide polymorphisms in the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR1</strong>) gene and alcohol <b>dependence</b>.
+CRHR1	drug	alcohol	15992556	While the physiological mechanisms that contribute to the development of <b>alcohol</b> dependence remain unclear, a number of recent studies have indicated a role for the <strong>corticotropin releasing hormone receptor 1</strong> (CRHR 1) in modulating the response of the central nervous system to <b>ethanol</b>.
+CRHR1	addiction	dependence	15992556	While the physiological mechanisms that contribute to the development of alcohol <b>dependence</b> remain unclear, a number of recent studies have indicated a role for the <strong>corticotropin releasing hormone receptor 1</strong> (CRHR 1) in modulating the response of the central nervous system to ethanol.
+CRHR1	drug	alcohol	15992556	While the physiological mechanisms that contribute to the development of <b>alcohol</b> dependence remain unclear, a number of recent studies have indicated a role for the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR</strong> 1) in modulating the response of the central nervous system to <b>ethanol</b>.
+CRHR1	addiction	dependence	15992556	While the physiological mechanisms that contribute to the development of alcohol <b>dependence</b> remain unclear, a number of recent studies have indicated a role for the <strong>corticotropin releasing hormone receptor 1</strong> (<strong>CRHR</strong> 1) in modulating the response of the central nervous system to ethanol.
+CRHR1	drug	alcohol	15992556	Based on these data, the present study aims to identify associations between variations in the <strong>CRHR</strong> 1 gene and <b>alcohol</b> dependence in a population of individuals of European ancestry.
+CRHR1	addiction	dependence	15992556	Based on these data, the present study aims to identify associations between variations in the <strong>CRHR</strong> 1 gene and alcohol <b>dependence</b> in a population of individuals of European ancestry.
+CRHR1	drug	alcohol	15992556	In order to identify such putative associations, five single nucleotide polymorphisms (SNPs) in the <strong>CRHR</strong> 1 gene were analyzed in 120 <b>alcohol</b> dependent and 180 control subjects.
+CRHR1	drug	alcohol	15992556	In comparing both allele and genotype frequencies at these five loci between <b>alcohol</b> dependent and control populations, no significant associations between variations in the <strong>CRHR</strong> 1 gene and <b>alcohol</b> dependence were detected.
+CRHR1	addiction	dependence	15992556	In comparing both allele and genotype frequencies at these five loci between alcohol dependent and control populations, no significant associations between variations in the <strong>CRHR</strong> 1 gene and alcohol <b>dependence</b> were detected.
+CRHR1	drug	alcohol	15992556	The results of this study suggest that polymorphisms in the <strong>CRHR</strong> 1 gene are not major risk factors for the development of <b>alcohol</b> dependence in persons of European ancestry.
+CRHR1	addiction	dependence	15992556	The results of this study suggest that polymorphisms in the <strong>CRHR</strong> 1 gene are not major risk factors for the development of alcohol <b>dependence</b> in persons of European ancestry.
+CRHR1	drug	benzodiazepine	15894069	Other groups of P and SD rats were injected with flumazenil (5 mg/kg), a <b>benzodiazepine</b> (BZD) receptor antagonist, CP 154,526 (10 mg/kg), <strong>CRF1</strong> receptor antagonist, SB243,213, a 5 HT2C receptor inverse agonist, or vehicle during the 1st and 2nd withdrawals but not the third.
+CRHR1	drug	alcohol	15894069	These findings show that <b>alcohol</b> preferring P rats exhibit anxiety like behavior more readily following exposure to <b>ethanol</b> containing diets and that this behavior is counteracted more readily by pretreatment with a <strong>CRF1</strong> receptor antagonist than with BZD or 5 HT2C receptor antagonists.
+CRHR1	drug	cocaine	15784652	Recently, <strong>CRF1</strong> receptor antagonists have been shown to decrease <b>cocaine</b> self administration and inhibit stress induced reinstatement of <b>cocaine</b> seeking behavior.
+CRHR1	addiction	relapse	15784652	Recently, <strong>CRF1</strong> receptor antagonists have been shown to decrease cocaine self administration and inhibit stress induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+CRHR1	addiction	reward	15784652	Based on the large amount of literature demonstrating an association between dopaminergic neurotransmission and <b>reward</b> related behavior, the aim of the present study was to examine the effects of acute versus chronic <strong>CRF1</strong> receptor blockade on mesencephalic dopamine (DA) neuron activity (determined by in vivo extracellular recordings) and extracellular DA levels in the nucleus accumbens (Acb) (using in vivo microdialysis).
+CRHR1	drug	cocaine	15784652	In addition, the effect of <strong>CRF1</strong> receptor antagonism on <b>cocaine</b> induced DA overflow in the Acb was examined and correlated with DA neuron activity in the ventral tegmental area (VTA).
+CRHR1	drug	cocaine	15784652	In addition, both acute and chronic <strong>CRF1</strong> receptor antagonism significantly reduced <b>cocaine</b> stimulated DA overflow in the Acb, and this reduction was correlated with an attenuated <b>cocaine</b> induced inhibition of DA population activity.
+CRHR1	drug	cocaine	15784652	Taken as a whole, these data demonstrate that, although DA neuron population activity exhibits tolerance to chronic <strong>CRF1</strong> receptor antagonism (by CRA 0450), tolerance does not develop to the selective inhibition of <b>cocaine</b> induced DA release (in the Acb) and, as such, may be beneficial in the treatment of <b>cocaine</b> addiction.
+CRHR1	addiction	addiction	15784652	Taken as a whole, these data demonstrate that, although DA neuron population activity exhibits tolerance to chronic <strong>CRF1</strong> receptor antagonism (by CRA 0450), tolerance does not develop to the selective inhibition of cocaine induced DA release (in the Acb) and, as such, may be beneficial in the treatment of cocaine <b>addiction</b>.
+CRHR1	drug	alcohol	15726114	Prior multiple <b>ethanol</b> withdrawals enhance stress induced anxiety like behavior: inhibition by <strong>CRF1</strong>  and benzodiazepine receptor antagonists and a 5 HT1a receptor agonist.
+CRHR1	drug	benzodiazepine	15726114	Prior multiple ethanol withdrawals enhance stress induced anxiety like behavior: inhibition by <strong>CRF1</strong>  and <b>benzodiazepine</b> receptor antagonists and a 5 HT1a receptor agonist.
+CRHR1	drug	benzodiazepine	15726114	Drugs (ie a <strong>CRF1</strong> receptor antagonist, a <b>benzodiazepine</b> receptor antagonist, and a 5 HT1A receptor agonist) previously demonstrated to block the cumulative adaptation, when administered during repeated withdrawals, prevented stress induced anxiety like behavior during abstinence.
+CRHR1	drug	cocaine	15659593	After acute withdrawal from a chronic <b>cocaine</b> administration regimen, <strong>CRF1</strong> activation remained facilitatory, but CRF2 activation facilitated rather than depressed LSMLN EPSCs.
+CRHR1	addiction	withdrawal	15659593	After acute <b>withdrawal</b> from a chronic cocaine administration regimen, <strong>CRF1</strong> activation remained facilitatory, but CRF2 activation facilitated rather than depressed LSMLN EPSCs.
+CRHR1	drug	cocaine	15659593	In saline treated rats, <strong>CRF1</strong> and CRF2 coupled predominantly to protein kinase A signaling pathways, whereas after <b>cocaine</b> withdrawal, protein kinase C activity was more prominent and likely contributed to the CRF2 mediated presynaptic facilitation.
+CRHR1	addiction	withdrawal	15659593	In saline treated rats, <strong>CRF1</strong> and CRF2 coupled predominantly to protein kinase A signaling pathways, whereas after cocaine <b>withdrawal</b>, protein kinase C activity was more prominent and likely contributed to the CRF2 mediated presynaptic facilitation.
+CRHR1	drug	cocaine	15519677	In the anterior pituitary, acute "binge" <b>cocaine</b> or its combinations with either DA antagonist did not alter <strong>CRH R1</strong> receptor or POMC mRNA levels.
+CRHR1	addiction	intoxication	15519677	In the anterior pituitary, acute "<b>binge</b>" cocaine or its combinations with either DA antagonist did not alter <strong>CRH R1</strong> receptor or POMC mRNA levels.
+CRHR1	drug	benzodiazepine	15496666	Previous studies revealed that chronic administration of the anxiolytic <b>alprazolam</b> reduced indices of CRF and <strong>CRF1</strong> receptor function.
+CRHR1	drug	benzodiazepine	15496666	Other indices of CRF <strong>CRF1</strong> and urocortin I CRF2A function, altered by chronic <b>alprazolam</b> treatment as previously described, returned to pretreatment levels over 96 hr.
+CRHR1	drug	opioid	15138444	<b>Buprenorphine</b> and a <strong>CRF1</strong> antagonist block the acquisition of opiate withdrawal induced conditioned place aversion in rats.
+CRHR1	addiction	aversion	15138444	Buprenorphine and a <strong>CRF1</strong> antagonist block the acquisition of opiate withdrawal induced conditioned place <b>aversion</b> in rats.
+CRHR1	addiction	withdrawal	15138444	Buprenorphine and a <strong>CRF1</strong> antagonist block the acquisition of opiate <b>withdrawal</b> induced conditioned place aversion in rats.
+CRHR1	addiction	aversion	15138444	A corticotropin releasing factor 1 (<strong>CRF1</strong>) receptor antagonist (antalarmin) also reversed the place <b>aversion</b> produced by precipitated opiate withdrawal.
+CRHR1	addiction	withdrawal	15138444	A corticotropin releasing factor 1 (<strong>CRF1</strong>) receptor antagonist (antalarmin) also reversed the place aversion produced by precipitated opiate <b>withdrawal</b>.
+CRHR1	addiction	aversion	15138444	In addition, these results suggest that <strong>CRF1</strong> antagonists can block the <b>aversive</b> stimulus effects of opiate withdrawal and may be potential therapeutic targets for opiate dependence.
+CRHR1	addiction	dependence	15138444	In addition, these results suggest that <strong>CRF1</strong> antagonists can block the aversive stimulus effects of opiate withdrawal and may be potential therapeutic targets for opiate <b>dependence</b>.
+CRHR1	addiction	withdrawal	15138444	In addition, these results suggest that <strong>CRF1</strong> antagonists can block the aversive stimulus effects of opiate <b>withdrawal</b> and may be potential therapeutic targets for opiate dependence.
+CRHR1	drug	alcohol	14751471	Modulation of multiple <b>ethanol</b> withdrawal induced anxiety like behavior by CRF and <strong>CRF1</strong> receptors.
+CRHR1	addiction	withdrawal	14751471	Modulation of multiple ethanol <b>withdrawal</b> induced anxiety like behavior by CRF and <strong>CRF1</strong> receptors.
+CRHR1	drug	opioid	14568335	In the present study, we investigated the effect of acute and chronic <b>morphine</b> administration on the level of <strong>CRF1</strong> and melanocortin 4 receptor (MC4 R) mRNAs in the rat amygdala by quantitative real time PCR method.
+CRHR1	drug	cocaine	12747942	The above data suggest that amygdalar CRF system activity is potently activated after administration of morphine and <b>cocaine</b>, and that activation of this system observed at the time of withdrawal from morphine may be responsible for aversion and anxiety related to these states; therefore a <strong>CRF1</strong> receptor may be a target for prospective pharmacotherapies of the withdrawal from abused drugs.
+CRHR1	drug	opioid	12747942	The above data suggest that amygdalar CRF system activity is potently activated after administration of <b>morphine</b> and cocaine, and that activation of this system observed at the time of withdrawal from <b>morphine</b> may be responsible for aversion and anxiety related to these states; therefore a <strong>CRF1</strong> receptor may be a target for prospective pharmacotherapies of the withdrawal from abused drugs.
+CRHR1	addiction	aversion	12747942	The above data suggest that amygdalar CRF system activity is potently activated after administration of morphine and cocaine, and that activation of this system observed at the time of withdrawal from morphine may be responsible for <b>aversion</b> and anxiety related to these states; therefore a <strong>CRF1</strong> receptor may be a target for prospective pharmacotherapies of the withdrawal from abused drugs.
+CRHR1	addiction	withdrawal	12747942	The above data suggest that amygdalar CRF system activity is potently activated after administration of morphine and cocaine, and that activation of this system observed at the time of <b>withdrawal</b> from morphine may be responsible for aversion and anxiety related to these states; therefore a <strong>CRF1</strong> receptor may be a target for prospective pharmacotherapies of the <b>withdrawal</b> from abused drugs.
+CRHR1	drug	cocaine	12652344	In addition, the effect of corticotropin releasing hormone type 1 receptor (<strong>CRH R1</strong>) blockade on <b>cocaine</b> priming induced reinstatement was investigated.
+CRHR1	addiction	relapse	12652344	In addition, the effect of corticotropin releasing hormone type 1 receptor (<strong>CRH R1</strong>) blockade on cocaine priming induced <b>reinstatement</b> was investigated.
+CRHR1	drug	cocaine	12652344	The <strong>CRH R1</strong> antagonist CP 154,526 (10 mg/kg, IV) did not modulate <b>cocaine</b> priming induced reinstatement of drug seeking, but attenuated CRH induced increases in salivary cortisol.
+CRHR1	addiction	relapse	12652344	The <strong>CRH R1</strong> antagonist CP 154,526 (10 mg/kg, IV) did not modulate cocaine priming induced <b>reinstatement</b> of drug <b>seeking</b>, but attenuated CRH induced increases in salivary cortisol.
+CRHR1	drug	alcohol	12614667	The <strong>CRF1</strong> receptor antagonist antalarmin reduces volitional <b>ethanol</b> consumption in isolation reared fawn hooded rats.
+CRHR1	drug	cocaine	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of proopiomelanocortin and <strong>corticotropin releasing hormone receptor 1</strong> mRNAs in the pituitary and hypothalamus of the rat during chronic 'binge' <b>cocaine</b> and withdrawal.
+CRHR1	addiction	intoxication	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of proopiomelanocortin and <strong>corticotropin releasing hormone receptor 1</strong> mRNAs in the pituitary and hypothalamus of the rat during chronic '<b>binge</b>' cocaine and withdrawal.
+CRHR1	addiction	withdrawal	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of proopiomelanocortin and <strong>corticotropin releasing hormone receptor 1</strong> mRNAs in the pituitary and hypothalamus of the rat during chronic 'binge' cocaine and <b>withdrawal</b>.
+CRHR1	drug	cocaine	12576179	In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by <b>cocaine</b> withdrawal may be, at least in part, due to the increased POMC and/or <strong>CRH R1</strong> gene expression observed in the anterior pituitary after chronic 'binge' <b>cocaine</b>.
+CRHR1	addiction	intoxication	12576179	In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part, due to the increased POMC and/or <strong>CRH R1</strong> gene expression observed in the anterior pituitary after chronic '<b>binge</b>' cocaine.
+CRHR1	addiction	withdrawal	12576179	In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine <b>withdrawal</b> may be, at least in part, due to the increased POMC and/or <strong>CRH R1</strong> gene expression observed in the anterior pituitary after chronic 'binge' cocaine.
+CRHR1	drug	benzodiazepine	11713613	The prototypical anxiolytic <b>diazepam</b> was used throughout as a positive control, the antidepressant imipramine was tested in the mouse defense test battery and in both models of predatory exposure, and the selective <strong>CRF1</strong> receptor antagonist antalarmin was used in the cat exposure test in rats.
+CRHR1	drug	opioid	11122350	To investigate the possible role of different <strong>CRFR</strong> antagonists (alpha helical CRF, CP 154,526 and AS 30) in relapse to opiate dependence, the 28 day extinction of <b>morphine</b> conditioned place preference (CPP) was used.
+CRHR1	addiction	dependence	11122350	To investigate the possible role of different <strong>CRFR</strong> antagonists (alpha helical CRF, CP 154,526 and AS 30) in relapse to opiate <b>dependence</b>, the 28 day extinction of morphine conditioned place preference (CPP) was used.
+CRHR1	addiction	relapse	11122350	To investigate the possible role of different <strong>CRFR</strong> antagonists (alpha helical CRF, CP 154,526 and AS 30) in <b>relapse</b> to opiate dependence, the 28 day extinction of morphine conditioned place preference (CPP) was used.
+CRHR1	addiction	reward	11122350	To investigate the possible role of different <strong>CRFR</strong> antagonists (alpha helical CRF, CP 154,526 and AS 30) in relapse to opiate dependence, the 28 day extinction of morphine conditioned place preference (<b>CPP</b>) was used.
+CRHR1	drug	alcohol	11045867	Reduced hypothalamic POMC and anterior pituitary <strong>CRF1</strong> receptor mRNA levels after acute, but not chronic, daily "binge" intragastric <b>alcohol</b> administration.
+CRHR1	addiction	intoxication	11045867	Reduced hypothalamic POMC and anterior pituitary <strong>CRF1</strong> receptor mRNA levels after acute, but not chronic, daily "<b>binge</b>" intragastric alcohol administration.
+CRHR1	drug	alcohol	11045867	Endogenous corticotropin releasing factor (CRF), its pituitary <strong>CRF1</strong> receptor, and proopiomelanocortin (POMC) may be involved in the hypothalamic pituitary adrenal (HPA) responses to <b>alcohol</b>.
+CRHR1	drug	alcohol	11045867	The levels of CRF, <strong>CRF1</strong> receptor, and POMC mRNAs in the hypothalamic pituitary axis were measured after acute (1 day) or chronic (14 days) binge pattern <b>alcohol</b> administration.
+CRHR1	addiction	intoxication	11045867	The levels of CRF, <strong>CRF1</strong> receptor, and POMC mRNAs in the hypothalamic pituitary axis were measured after acute (1 day) or chronic (14 days) <b>binge</b> pattern alcohol administration.
+CRHR1	drug	alcohol	11045867	<strong>CRF1</strong> receptor mRNA levels in the anterior pituitary were decreased significantly after acute administration, with no change after chronic <b>alcohol</b> administration.
+CRHR1	drug	alcohol	11045867	These results suggest that (1) rats exposed to chronic binge <b>alcohol</b> develop tolerance in HPA activity, as shown by no elevation of ACTH and an attenuated corticosterone response to chronic <b>alcohol</b> after initial dramatic elevations by acute <b>alcohol</b> administration; (2) a concurrent acute decrease in <strong>CRF1</strong> receptor mRNA levels in the anterior pituitary is associated with increased HPA activity, and (3) alterations of POMC gene expression in the hypothalamic region may have implications for a molecular understanding of the neuroendocrine response to <b>alcohol</b>.
+CRHR1	addiction	intoxication	11045867	These results suggest that (1) rats exposed to chronic <b>binge</b> alcohol develop tolerance in HPA activity, as shown by no elevation of ACTH and an attenuated corticosterone response to chronic alcohol after initial dramatic elevations by acute alcohol administration; (2) a concurrent acute decrease in <strong>CRF1</strong> receptor mRNA levels in the anterior pituitary is associated with increased HPA activity, and (3) alterations of POMC gene expression in the hypothalamic region may have implications for a molecular understanding of the neuroendocrine response to alcohol.
+CRHR1	drug	opioid	10943688	The possible effect of different corticotropin releasing factor receptor (<strong>CRFR</strong>) antagonists (alpha helical CRF, CP 154,526 and AS 30) on the maintenance and reactivation of <b>morphine</b> conditioned place preference (CPP) induced by <b>morphine</b> or footshock stress, respectively, were investigated in rats.
+CRHR1	addiction	reward	10943688	The possible effect of different corticotropin releasing factor receptor (<strong>CRFR</strong>) antagonists (alpha helical CRF, CP 154,526 and AS 30) on the maintenance and reactivation of morphine conditioned place preference (<b>CPP</b>) induced by morphine or footshock stress, respectively, were investigated in rats.
+CRHR1	drug	opioid	10943688	The results show that <b>morphine</b> induced maintenance of CPP was not affected by pretreatment with any <strong>CRFR</strong> antagonists.
+CRHR1	addiction	reward	10943688	The results show that morphine induced maintenance of <b>CPP</b> was not affected by pretreatment with any <strong>CRFR</strong> antagonists.
+CRHR1	drug	opioid	10943688	The present study demonstrates that <strong>CRFR</strong> type 1, but not <strong>CRFR</strong> type 2, mediates the stress induced maintenance and reactivation of <b>morphine</b> CPP.
+CRHR1	addiction	reward	10943688	The present study demonstrates that <strong>CRFR</strong> type 1, but not <strong>CRFR</strong> type 2, mediates the stress induced maintenance and reactivation of morphine <b>CPP</b>.
+CRHR1	addiction	dependence	10943688	These findings suggest that <strong>CRFR</strong> type 1 antagonists might be of some value in the treatment and prevention of stress induced relapse to drug <b>dependence</b> long after detoxification.
+CRHR1	addiction	relapse	10943688	These findings suggest that <strong>CRFR</strong> type 1 antagonists might be of some value in the treatment and prevention of stress induced <b>relapse</b> to drug dependence long after detoxification.
+CRHR1	addiction	withdrawal	10617121	First, the influence of a selective CRF receptor 1 (<strong>CRF R1</strong>) antagonist, CP 154,526, on opiate <b>withdrawal</b> behavior was examined.
+CRHR1	drug	alcohol	10617121	Pretreatment with the <strong>CRF R1</strong> antagonist significantly attenuated several behavioral signs of <b>naltrexone</b> induced morphine withdrawal, including writhing, chewing, weight loss, lacrimation, salivation, and irritability, measured during the first hour of withdrawal.
+CRHR1	drug	opioid	10617121	Pretreatment with the <strong>CRF R1</strong> antagonist significantly attenuated several behavioral signs of naltrexone induced <b>morphine</b> withdrawal, including writhing, chewing, weight loss, lacrimation, salivation, and irritability, measured during the first hour of withdrawal.
+CRHR1	addiction	withdrawal	10617121	Pretreatment with the <strong>CRF R1</strong> antagonist significantly attenuated several behavioral signs of naltrexone induced morphine <b>withdrawal</b>, including writhing, chewing, weight loss, lacrimation, salivation, and irritability, measured during the first hour of <b>withdrawal</b>.
+CRHR1	addiction	withdrawal	10617121	Next the expression of <strong>CRF R1</strong> was determined as a second measure of the involvement of this receptor in opiate <b>withdrawal</b>.
+CRHR1	drug	alcohol	10617121	<b>Naltrexone</b> induced morphine withdrawal resulted in down regulation of <strong>CRF R1</strong> mRNA in several brain regions, including the frontal cortex, parietal cortex, striatum, nucleus accumbens, and amygdala, but not in the hypothalamus or periaqueductal gray.
+CRHR1	drug	opioid	10617121	Naltrexone induced <b>morphine</b> withdrawal resulted in down regulation of <strong>CRF R1</strong> mRNA in several brain regions, including the frontal cortex, parietal cortex, striatum, nucleus accumbens, and amygdala, but not in the hypothalamus or periaqueductal gray.
+CRHR1	addiction	withdrawal	10617121	Naltrexone induced morphine <b>withdrawal</b> resulted in down regulation of <strong>CRF R1</strong> mRNA in several brain regions, including the frontal cortex, parietal cortex, striatum, nucleus accumbens, and amygdala, but not in the hypothalamus or periaqueductal gray.
+CRHR1	addiction	withdrawal	10617121	Taken together, the behavioral and receptor regulation findings indicate that <strong>CRF R1</strong> is the primary mediator of the actions of the CRF system on opiate <b>withdrawal</b>, although it is possible that CRF R2 contributes to the response.
+CRHR1	drug	cocaine	9630005	Here we examined the effect of a nonpeptide, selective <strong>CRF1</strong> receptor antagonist, CP 154,526, on reinstatement of heroin and <b>cocaine</b> seeking induced by footshock.
+CRHR1	drug	opioid	9630005	Here we examined the effect of a nonpeptide, selective <strong>CRF1</strong> receptor antagonist, CP 154,526, on reinstatement of <b>heroin</b> and cocaine seeking induced by footshock.
+CRHR1	addiction	relapse	9630005	Here we examined the effect of a nonpeptide, selective <strong>CRF1</strong> receptor antagonist, CP 154,526, on <b>reinstatement</b> of heroin and cocaine <b>seeking</b> induced by footshock.
+CRHR1	drug	cocaine	9068125	Due to the many signs of anxiety and responses to stress that are produced by <b>cocaine</b> withdrawal in humans, the present study was designed to assess the effects of chronic <b>cocaine</b> and its withdrawal on regional 125I Tyr oCRF binding to the <strong>CRF1</strong> receptor in brains of male Lewis rats.
+CRHR1	addiction	withdrawal	9068125	Due to the many signs of anxiety and responses to stress that are produced by cocaine <b>withdrawal</b> in humans, the present study was designed to assess the effects of chronic cocaine and its <b>withdrawal</b> on regional 125I Tyr oCRF binding to the <strong>CRF1</strong> receptor in brains of male Lewis rats.
+CRHR1	drug	cocaine	9068125	Tissues were harvested either 15 min after or 10 days after the last <b>cocaine</b> infusion, and the brains were sectioned and prepared for <strong>CRF1</strong> receptor autoradiography.
+CRHR1	addiction	withdrawal	9068125	Neuroendocrine and non neuroendocrine mechanisms associated with <strong>CRF1</strong> receptors do not appear to contribute to long term <b>withdrawal</b> effects.
+NFKB1	drug	opioid	32014377	Stressed mice also showed significant increase in TLR4, Nuclear Factor Kappa B (<strong>NF kB</strong>), inducible nitric oxide synthase (iNOS), dopamine receptor D2 (DRD2), cyclic adenosine monophosphate (cAMP) response element binding protein 1 (CREB 1) and <b>opioid</b> receptor MU 1 (OPRM 1) genes expression compared with control and LPS RS treated stressed mice.
+NFKB1	drug	alcohol	31984446	Western blot testing indicated elevated levels of caspase 3/cleaved caspase 3, <strong>NF kB</strong>, and PKC/pPKC proteins in the cerebella of <b>ethanol</b> treated animals.
+NFKB1	drug	amphetamine	31396089	Ad libitum HRW consumption also had an inhibitory effect on the <b>METH</b> induced increase in the expression of Bax/Bcl 2, cleaved caspase 3, glucose related protein 78 (GRP 78), CCAAT/enhancer binding protein homologous protein (CHOP), and p <strong>NF kB</strong> p65 expression and elevation of interleukin (IL) 6 and tumor necrosis factor (TNF) α levels in the hippocampus.
+NFKB1	drug	alcohol	28848184	<b>Ethanol</b> Decreases Inflammatory Response in Human Lung Epithelial Cells by Inhibiting the Canonical <strong>NF kB</strong> Pathway.
+NFKB1	drug	alcohol	28466267	17β Estradiol via SIRT1/Acetyl p53/<strong>NF kB</strong> Signaling Pathway Rescued Postnatal Rat Brain Against Acute <b>Ethanol</b> Intoxication.
+NFKB1	addiction	intoxication	28466267	17β Estradiol via SIRT1/Acetyl p53/<strong>NF kB</strong> Signaling Pathway Rescued Postnatal Rat Brain Against Acute Ethanol <b>Intoxication</b>.
+NFKB1	addiction	addiction	28043969	The Role of <strong>NFkB</strong> in Drug <b>Addiction</b>: Beyond Inflammation.
+NFKB1	drug	alcohol	28043969	It has recently been demonstrated that <b>alcohol</b> and other drugs of abuse can induce <strong>NFkB</strong> activity and cytokine expression in the brain.
+NFKB1	drug	alcohol	28043969	A number of reviews have been published highlighting this effect of <b>alcohol</b>, and have linked increased <strong>NFkB</strong> function to neuroimmune stimulated toxicity.
+NFKB1	addiction	addiction	28043969	However, in this review we focus on the potentially non immune functions of <strong>NFkB</strong> as possible links between <strong>NFkB</strong> and <b>addiction</b>.
+NFKB1	drug	opioid	28043969	<strong>NFkB</strong> can induce the expression of a diverse set of gene targets besides inflammatory mediators, some of which are involved in addictive processes, such as <b>opioid</b> receptors and neuropeptides.
+NFKB1	addiction	addiction	28043969	<strong>NFkB</strong> can induce the expression of a diverse set of gene targets besides inflammatory mediators, some of which are involved in <b>addictive</b> processes, such as opioid receptors and neuropeptides.
+NFKB1	addiction	reward	28043969	<strong>NFkB</strong> mediates complex behaviors including learning and memory, stress responses, anhedonia and drug <b>reward</b>, processes that may lie outside the role of <strong>NFkB</strong> in the classic neuroimmune response.
+NFKB1	addiction	addiction	28043969	Future studies should focus on these non immune functions of <strong>NFkB</strong> signaling and their association with <b>addiction</b> related processes.
+NFKB1	drug	alcohol	26857094	Oleoylethanolamide prevents neuroimmune HMGB1/TLR4/<strong>NF kB</strong> danger signaling in rat frontal cortex and depressive like behavior induced by <b>ethanol</b> binge administration.
+NFKB1	drug	cannabinoid	26857094	<b>Oleoylethanolamide</b> prevents neuroimmune HMGB1/TLR4/<strong>NF kB</strong> danger signaling in rat frontal cortex and depressive like behavior induced by ethanol binge administration.
+NFKB1	addiction	intoxication	26857094	Oleoylethanolamide prevents neuroimmune HMGB1/TLR4/<strong>NF kB</strong> danger signaling in rat frontal cortex and depressive like behavior induced by ethanol <b>binge</b> administration.
+NFKB1	drug	alcohol	26857094	previous each <b>alcohol</b> gavage blocked the expression of high mobility group box 1 (HMGB1) danger signal and the innate immunity Toll like receptors 4 (TLR4) in frontal cortex, and inhibited the nuclear factor kappa B (<strong>NF kB</strong>) proinflammatory cascade induced by <b>alcohol</b> binge administration.
+NFKB1	addiction	intoxication	26857094	previous each alcohol gavage blocked the expression of high mobility group box 1 (HMGB1) danger signal and the innate immunity Toll like receptors 4 (TLR4) in frontal cortex, and inhibited the nuclear factor kappa B (<strong>NF kB</strong>) proinflammatory cascade induced by alcohol <b>binge</b> administration.
+NFKB1	drug	alcohol	21927955	A testable scheme for this pathway is presented that incorporates recent findings in the <b>alcohol</b> brain literature indicating a role for neuroimmune activation (upregulation of <strong>NF kappaB</strong>, proinflammatory cytokines, and toll like receptors).
+NFKB1	addiction	addiction	20477932	Nuclear factor kappa B (<strong>NFkappaB</strong>) is a sensor of oxidative stress and participates in memory formation that could be involved in drug toxicity and <b>addiction</b> mechanisms.
+NFKB1	drug	cocaine	20477932	Therefore <strong>NFkappaB</strong> activity, oxidative stress, neuronal nitric oxide synthase (nNOS) activity, spatial learning and memory as well as the effect of topiramate, a previously proposed therapy for <b>cocaine</b> addiction, were evaluated in an experimental model of <b>cocaine</b> administration in rats.
+NFKB1	addiction	addiction	20477932	Therefore <strong>NFkappaB</strong> activity, oxidative stress, neuronal nitric oxide synthase (nNOS) activity, spatial learning and memory as well as the effect of topiramate, a previously proposed therapy for cocaine <b>addiction</b>, were evaluated in an experimental model of cocaine administration in rats.
+NFKB1	drug	cocaine	20477932	<strong>NFkappaB</strong> activity was decreased in the frontal cortex of <b>cocaine</b> treated rats, as well as GSH concentration and glutathione peroxidase activity in the hippocampus, whereas nNOS activity in the hippocampus was increased.
+NFKB1	drug	cocaine	20477932	Memory retrieval of experiences acquired prior to <b>cocaine</b> administration was impaired and negatively correlated with <strong>NFkappaB</strong> activity in the frontal cortex.
+NFKB1	drug	cocaine	20477932	These results provide evidence for a possible mechanistic role of oxidative and nitrosative stress and <strong>NFkappaB</strong> in the alterations induced by <b>cocaine</b>.
+NFKB1	drug	alcohol	20388501	Pathway analysis showed that <b>alcohol</b> differentially affected various pathways in a K ras dependent manner   some of which previously shown to be regulated by <b>alcohol</b>   including the insulin/PI3K pathway, the <strong>NF kappaB</strong>, the phosphodiesterases (PDEs) pathway, the Jak/Stat and the adipokine signaling pathways.
+NFKB1	drug	alcohol	20201932	<b>Ethanol</b> exposure increases <strong>NF kappaB</strong> DNA binding in rat brain (Crews et al., 2006) and in brain slice cultures in vitro (Zou and Crews, 2006).
+NFKB1	drug	alcohol	20201932	Using hippocampal entorhinal cortex (HEC) brain slice cultures, we explored the effect of <b>ethanol</b> on <strong>NF kappaB</strong> DNA binding, proinflammatory gene expression, and sensitivity to glutamate neurotoxicity.
+NFKB1	drug	alcohol	20201932	<b>Ethanol</b> treatment results in a progressive increase in <strong>NF kappaB</strong> DNA binding that includes large increases in <strong>NF kappaB</strong> subunit p50 protein DNA binding.
+NFKB1	drug	alcohol	20201932	The expression of <strong>NF kappaB</strong> proinflammatory target genes progressively increased with time of <b>ethanol</b> treatment.
+NFKB1	drug	alcohol	20201932	Blockade of <strong>NF kappaB</strong> by using <strong>NF kappaB</strong> p65 siRNA and BHT reduces <b>ethanol</b> induction of proinflammatory genes.
+NFKB1	drug	alcohol	20201932	These findings indicate that <b>ethanol</b> treatment increases <strong>NF kappaB</strong> DNA binding and proinflammatory gene expression in brain slices.
+NFKB1	drug	alcohol	19765273	However, <strong>NF kappaB</strong> (p65) translocation to the nucleus was not inhibited by <b>ethanol</b>.
+NFKB1	drug	nicotine	19732285	<b>Nicotine</b> suppresses IL 1beta and IL 6 expression at least in part by inhibiting <strong>NFkappaB</strong> activation.
+NFKB1	drug	amphetamine	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (<strong>NFkappaB</strong>)] and Fos (cFos), represent candidates whose expression levels may predict <b>methamphetamine</b> consumption and susceptibility to <b>methamphetamine</b> reward and aversion.
+NFKB1	addiction	aversion	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (<strong>NFkappaB</strong>)] and Fos (cFos), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine reward and <b>aversion</b>.
+NFKB1	addiction	reward	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), Htr3a (serotonin receptor 3A), Rela [nuclear factor kappaB (<strong>NFkappaB</strong>)] and Fos (cFos), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine <b>reward</b> and aversion.
+NFKB1	drug	alcohol	19673747	A functional polymorphism of the <strong>NFKB1</strong> gene increases the risk for <b>alcoholic</b> liver cirrhosis in patients with <b>alcohol</b> dependence.
+NFKB1	addiction	dependence	19673747	A functional polymorphism of the <strong>NFKB1</strong> gene increases the risk for alcoholic liver cirrhosis in patients with alcohol <b>dependence</b>.
+NFKB1	drug	alcohol	19673747	A functional polymorphism of the <strong><strong>NFKB1</strong></strong> gene increases the risk for <b>alcoholic</b> liver cirrhosis in patients with <b>alcohol</b> dependence.
+NFKB1	addiction	dependence	19673747	A functional polymorphism of the <strong><strong>NFKB1</strong></strong> gene increases the risk for alcoholic liver cirrhosis in patients with alcohol <b>dependence</b>.
+NFKB1	drug	alcohol	19673747	Increasing evidence supports a role for the nuclear factor (NF) kappaB, the <strong>NF kappaB</strong> inhibitor alpha (NFKBIA), and the peroxisome proliferator activated receptor (PPAR) gamma in the pathogenesis of <b>alcoholic</b> liver disease, raising the possibility that common polymorphisms in genes encoding these molecules may confer susceptibility to ALC.
+NFKB1	drug	alcohol	19673747	A total of 258 male <b>alcoholics</b> (161 without liver disease and 97 with ALC) and 101 healthy controls were genotyped for the  94ins/delATTG <strong>NFKB1</strong>, 3' UTR+126G>A NFKBIA, and 34C>G PPARG2 polymorphisms.
+NFKB1	drug	alcohol	19673747	A total of 258 male <b>alcoholics</b> (161 without liver disease and 97 with ALC) and 101 healthy controls were genotyped for the  94ins/delATTG <strong><strong>NFKB1</strong></strong>, 3' UTR+126G>A NFKBIA, and 34C>G PPARG2 polymorphisms.
+NFKB1	drug	alcohol	19673747	We found an association between the presence of the deletion allele in <strong>NFKB1</strong> polymorphism and ALC in patients with <b>alcohol</b> dependence.
+NFKB1	addiction	dependence	19673747	We found an association between the presence of the deletion allele in <strong>NFKB1</strong> polymorphism and ALC in patients with alcohol <b>dependence</b>.
+NFKB1	drug	alcohol	19673747	We found an association between the presence of the deletion allele in <strong><strong>NFKB1</strong></strong> polymorphism and ALC in patients with <b>alcohol</b> dependence.
+NFKB1	addiction	dependence	19673747	We found an association between the presence of the deletion allele in <strong><strong>NFKB1</strong></strong> polymorphism and ALC in patients with alcohol <b>dependence</b>.
+NFKB1	drug	alcohol	19561104	In contrast, chronic <b>alcohol</b> decreased IRAK M expression but increased IRAK 1 and IKK kinase activities, <strong>NFkappaB</strong> DNA binding, and <strong>NFkappaB</strong> reporter activity.
+NFKB1	drug	alcohol	19561104	In summary, inhibition of LPS induced <strong>NFkappaB</strong> and ERK activation by acute <b>alcohol</b> leads to hyporesponsiveness of monocytes to LPS due to increased IRAK M. In contrast, chronic <b>alcohol</b> sensitizes monocytes to LPS through decreased IRAK M expression and activation of <strong>NFkappaB</strong> and ERK kinases.
+NFKB1	drug	alcohol	19330277	The expression of important regulators of osteoclast maturation and activity such as <strong>NF kappabeta</strong> (nuclear factor kappabeta) ligand (RANKL) and interleukin 6 were significantly increased (P < 0.05) by binge <b>alcohol</b>, and osteoprotegerin levels were significantly decreased (P < 0.05) in vertebral bone.
+NFKB1	addiction	intoxication	19330277	The expression of important regulators of osteoclast maturation and activity such as <strong>NF kappabeta</strong> (nuclear factor kappabeta) ligand (RANKL) and interleukin 6 were significantly increased (P < 0.05) by <b>binge</b> alcohol, and osteoprotegerin levels were significantly decreased (P < 0.05) in vertebral bone.
+NFKB1	drug	cocaine	19295158	Therefore, we evaluated the role of <strong>NFkappaB</strong> in regulating <b>cocaine</b> induced dendritic spine changes on medium spiny neurons of the NAc and the rewarding effects of <b>cocaine</b>.
+NFKB1	drug	cocaine	19295158	We show that chronic <b>cocaine</b> induces <strong>NFkappaB</strong> dependent transcription in the NAc of <strong>NFkappaB</strong> Lac transgenic mice.
+NFKB1	drug	cocaine	19295158	This induction of <strong>NFkappaB</strong> activity is accompanied by increased expression of several <strong>NFkappaB</strong> genes, the promoters of which show chromatin modifications after chronic <b>cocaine</b> exposure consistent with their transcriptional activation.
+NFKB1	drug	cocaine	19295158	We found that activation of <strong>NFkappaB</strong> by IKKca increases the number of dendritic spines on NAc neurons, whereas inhibition of <strong>NFkappaB</strong> by IKKdn decreases basal dendritic spine number and blocks the increase in dendritic spines after chronic <b>cocaine</b>.
+NFKB1	drug	cocaine	19295158	Moreover, inhibition of <strong>NFkappaB</strong> blocks the rewarding effects of <b>cocaine</b> and the ability of previous <b>cocaine</b> exposure to increase an animal's preference for <b>cocaine</b>.
+NFKB1	drug	cocaine	19295158	Together, these studies establish a direct role for <strong>NFkappaB</strong> pathways in the NAc to regulate structural and behavioral plasticity to <b>cocaine</b>.
+NFKB1	addiction	intoxication	18940959	Drugs that block oxidative stress and <strong>NF kappaB</strong> transcription or increase CREB transcription block <b>binge</b> induced neurodegeneration, inhibition of neurogenesis and proinflammatory enzyme induction.
+NFKB1	drug	nicotine	18262213	We also demonstrate that <b>nicotine</b> treatment induced <strong>NF kB</strong> translocation to the nucleus, phosphorylation of the epidermal growth factor receptor (EGFR), and accumulation of heparin binding EGF in the extracellular medium.
+NFKB1	drug	alcohol	18079108	Association of <strong>NFKB1</strong>, which encodes a subunit of the transcription factor NF kappaB, with <b>alcohol</b> dependence.
+NFKB1	addiction	dependence	18079108	Association of <strong>NFKB1</strong>, which encodes a subunit of the transcription factor NF kappaB, with alcohol <b>dependence</b>.
+NFKB1	drug	alcohol	18079108	Association of <strong>NFKB1</strong>, which encodes a subunit of the transcription factor <strong>NF kappaB</strong>, with <b>alcohol</b> dependence.
+NFKB1	addiction	dependence	18079108	Association of <strong>NFKB1</strong>, which encodes a subunit of the transcription factor <strong>NF kappaB</strong>, with alcohol <b>dependence</b>.
+NFKB1	drug	alcohol	18079108	Association of <strong><strong>NFKB1</strong></strong>, which encodes a subunit of the transcription factor <strong>NF kappaB</strong>, with <b>alcohol</b> dependence.
+NFKB1	addiction	dependence	18079108	Association of <strong><strong>NFKB1</strong></strong>, which encodes a subunit of the transcription factor <strong>NF kappaB</strong>, with alcohol <b>dependence</b>.
+NFKB1	drug	alcohol	18079108	Seeking to identify genes within that region that are associated with <b>alcoholism</b>, we have tested the association of <strong>NFKB1</strong>, located at 4q24, with <b>alcoholism</b>.
+NFKB1	addiction	relapse	18079108	<b>Seeking</b> to identify genes within that region that are associated with alcoholism, we have tested the association of <strong>NFKB1</strong>, located at 4q24, with alcoholism.
+NFKB1	drug	alcohol	18079108	Seeking to identify genes within that region that are associated with <b>alcoholism</b>, we have tested the association of <strong><strong>NFKB1</strong></strong>, located at 4q24, with <b>alcoholism</b>.
+NFKB1	addiction	relapse	18079108	<b>Seeking</b> to identify genes within that region that are associated with alcoholism, we have tested the association of <strong><strong>NFKB1</strong></strong>, located at 4q24, with alcoholism.
+NFKB1	drug	alcohol	18079108	NF kappaB regulates many genes relevant to brain function, and its actions can be potentiated by <b>ethanol</b>; thus, <strong>NFKB1</strong> is an excellent candidate gene for <b>alcoholism</b>.
+NFKB1	drug	alcohol	18079108	<strong>NF kappaB</strong> regulates many genes relevant to brain function, and its actions can be potentiated by <b>ethanol</b>; thus, <strong>NFKB1</strong> is an excellent candidate gene for <b>alcoholism</b>.
+NFKB1	drug	alcohol	18079108	<strong>NF kappaB</strong> regulates many genes relevant to brain function, and its actions can be potentiated by <b>ethanol</b>; thus, <strong><strong>NFKB1</strong></strong> is an excellent candidate gene for <b>alcoholism</b>.
+NFKB1	drug	alcohol	18079108	Nineteen SNPs in and near <strong>NFKB1</strong> were analyzed in a sample of 219 multiplex <b>alcoholic</b> families of European American descent.
+NFKB1	drug	alcohol	18079108	Nineteen SNPs in and near <strong><strong>NFKB1</strong></strong> were analyzed in a sample of 219 multiplex <b>alcoholic</b> families of European American descent.
+NFKB1	drug	alcohol	18079108	Thus, variations in <strong>NFKB1</strong> appear to affect the risk for <b>alcoholism</b>, particularly contributing to an earlier onset of the disease.
+NFKB1	drug	alcohol	18079108	Thus, variations in <strong><strong>NFKB1</strong></strong> appear to affect the risk for <b>alcoholism</b>, particularly contributing to an earlier onset of the disease.
+NFKB1	drug	opioid	18040804	Nuclear factor kappaB (<strong>NF kappaB</strong>), one of the most diverse and critical transcription factors, is one of the downstream molecules that may either directly or indirectly transmit the receptor mediated upstream signals to the nucleus, resulting in the regulation of the <strong>NF kappaB</strong> dependent genes, which are critical for the <b>opioid</b> induced biological responses of neuronal and immune cells.
+NFKB1	drug	opioid	18040804	In this minireview, we focus on current understanding of the involvement of <strong>NF kappaB</strong> signaling in <b>opioid</b> functions and receptor gene expression in cells.
+NFKB1	drug	alcohol	17895971	Neuroadaptations in human chronic <b>alcoholics</b>: dysregulation of the <strong>NF kappaB</strong> system.
+NFKB1	drug	alcohol	17895971	Here we investigated whether transcription factors of Nuclear Factor kappaB (<strong>NF kappaB</strong>) family, controlling neuronal plasticity and neurodegeneration, are involved in these adaptations in human chronic <b>alcoholics</b>.
+NFKB1	drug	alcohol	17895971	Analysis of DNA binding of <strong>NF kappaB</strong> (p65/p50 heterodimer) and the p50 homodimer as well as <strong>NF kappaB</strong> proteins and mRNAs was performed in postmortem human brain samples from 15 chronic <b>alcoholics</b> and 15 control subjects.
+NFKB1	drug	alcohol	17895971	<strong>NF kappaB</strong> and p50 homodimer DNA binding was downregulated, levels of p65 (RELA) mRNA were attenuated, and the stoichiometry of p65/p50 proteins and respective mRNAs was altered in the prefrontal cortex of <b>alcoholics</b>.
+NFKB1	drug	alcohol	17895971	Comparison of a number of p50 homodimer/<strong>NF kappaB</strong> target DNA sites, kappaB elements in 479 genes, down  or upregulated in <b>alcoholics</b> demonstrated that genes with kappaB elements were generally upregulated in <b>alcoholics</b>.
+NFKB1	drug	alcohol	17895971	We suggest that cycles of <b>alcohol</b> intoxication/withdrawal, which may initially activate <strong>NF kappaB</strong>, when repeated over years downregulate RELA expression and <strong>NF kappaB</strong> and p50 homodimer DNA binding.
+NFKB1	addiction	intoxication	17895971	We suggest that cycles of alcohol <b>intoxication</b>/withdrawal, which may initially activate <strong>NF kappaB</strong>, when repeated over years downregulate RELA expression and <strong>NF kappaB</strong> and p50 homodimer DNA binding.
+NFKB1	addiction	withdrawal	17895971	We suggest that cycles of alcohol intoxication/<b>withdrawal</b>, which may initially activate <strong>NF kappaB</strong>, when repeated over years downregulate RELA expression and <strong>NF kappaB</strong> and p50 homodimer DNA binding.
+NFKB1	drug	alcohol	17895971	Alterations in expression of p50 homodimer/<strong>NF kappaB</strong> regulated genes may contribute to neuroplastic adaptation underlying <b>alcoholism</b>.
+NFKB1	drug	alcohol	17127267	Recent findings indicate that low concentrations of <b>ethanol</b> (10 mM) promote inflammatory processes in brain and in glial cells by up regulating cytokines and inflammatory mediators (iNOS, NO, COX 2), and by activating signaling pathways (IKK, MAPKs) and transcriptional factors (<strong>NF kappaB</strong>, AP 1) implicated in inflammatory injury.
+NFKB1	drug	alcohol	17067360	BHT blocks <strong>NF kappaB</strong> activation and <b>ethanol</b> induced brain damage.
+NFKB1	drug	alcohol	17067360	Binge <b>ethanol</b> treatment also caused microglia activation, increased <strong>NF kappaB</strong> DNA binding and COX2 expression.
+NFKB1	addiction	intoxication	17067360	<b>Binge</b> ethanol treatment also caused microglia activation, increased <strong>NF kappaB</strong> DNA binding and COX2 expression.
+NFKB1	addiction	intoxication	17067360	Butylated hydroxytoluene reduced <b>binge</b> induced <strong>NF kappaB</strong> DNA binding and COX2 expression.
+NFKB1	addiction	intoxication	17067360	<b>Binge</b> induced brain damage and activation of <strong>NF kappaB</strong> DNA binding are blocked by BHT.
+NFKB1	drug	alcohol	16385231	Moreover, it was shown that Kupffer cell activation by endotoxin via Toll like receptor (TLR) 4 is involved in <b>alcohol</b> induced liver injury and <b>ethanol</b> induced oxidative stress is important in the regulation of transcription factor <strong>NFkappaB</strong> activation and cytokine production by Kupffer cells.
+NFKB1	drug	alcohol	16385231	In Kupffer cells from mice 1 hr after <b>ethanol</b> treatment, expression of IRAK was decreased, and LPS induced activation of <strong>NFkappaB</strong> was decreased correlatively.
+NFKB1	drug	alcohol	16385231	In contrast, <b>ethanol</b> treatment to mice increased expression of IRAK in Kupffer cells 21hrs later and LPS induced activation of <strong>NFkappaB</strong> was elevated significantly.
+NFKB1	drug	alcohol	16385231	Further, NADPH oxidase plays a pivotal role in the increase in IRAK expression due to <b>ethanol</b> via activation of <strong>NFkappaB</strong> signaling pathway.
+NFKB1	drug	alcohol	16317704	<b>Alcohol</b> administration to ob/ob mice did not increase oxidative stress despite increased CYP2E1, but increased plasma TNF alpha, further increased Hsp70, and profoundly decreased p65 nuclear factor kappaB (<strong>NF kappaB</strong>) protein and DNA binding activity in nuclear extracts.
+NFKB1	drug	alcohol	16317704	Moderate <b>ethanol</b> intoxication does not increase oxidative stress in obese mice, but increases TNF alpha and also decreases nuclear <strong>NF kappaB</strong> activity, thus unleashing the apoptotic effects of TNF alpha.
+NFKB1	addiction	intoxication	16317704	Moderate ethanol <b>intoxication</b> does not increase oxidative stress in obese mice, but increases TNF alpha and also decreases nuclear <strong>NF kappaB</strong> activity, thus unleashing the apoptotic effects of TNF alpha.
+NFKB1	drug	opioid	15183518	In the NAc shell, <b>morphine</b> administration resulted in upregulation of caspace 9, <strong>NF kappaB</strong>, NF H, tau, GABA A delta subunit, FGFR1, Ggamma2, synuclein 1, syntaxin 5 and 13, GRK5, and c fos mRNAs.
+NFKB1	drug	opioid	15048644	We found correspondence between linkage and microarray/candidate gene studies for genes involved with the mitogen activated protein kinase (MAPK) signaling system, nuclear factor kappa B (<strong>NFKB</strong>) complex, neuropeptide Y (NPY) neurotransmission, a nicotinic receptor subunit (CHRNA2), the vesicular monoamine transporter (SLC18A2), genes in pathways implicated in human anxiety (HTR7, TDO2, and the endozepine related protein precursor, DKFZP434A2417), and the micro 1 <b>opioid</b> receptor (OPRM1).
+NFKB1	drug	alcohol	14576487	The injurious effects of <b>ethanol</b> on the pancreas may be mediated through (1) sensitization of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (<strong>NF kappaB</strong>) and activating protein 1 (AP 1); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) sensitization of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+NFKB1	addiction	sensitization	14576487	The injurious effects of ethanol on the pancreas may be mediated through (1) <b>sensitization</b> of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (<strong>NF kappaB</strong>) and activating protein 1 (AP 1); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) <b>sensitization</b> of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+NFKB1	drug	alcohol	12958018	<b>Ethanol</b> differentially regulates <strong>NF kappaB</strong> activation in pancreatic acinar cells through calcium and protein kinase C pathways.
+NFKB1	drug	alcohol	12958018	Previously, we showed that <b>ethanol</b> feeding sensitizes rats to pancreatitis caused by CCK 8, at least in part, by augmenting activation of the proinflammatory transcription factor <strong>NF kappaB</strong>.
+NFKB1	drug	alcohol	12958018	To elucidate the mechanism of sensitization, here we investigate the effect of <b>ethanol</b> on Ca(2+)  and PKC mediated pathways of CCK induced <strong>NF kappaB</strong> activation using an in vitro system of rat pancreatic acini incubated with <b>ethanol</b>.
+NFKB1	addiction	sensitization	12958018	To elucidate the mechanism of <b>sensitization</b>, here we investigate the effect of ethanol on Ca(2+)  and PKC mediated pathways of CCK induced <strong>NF kappaB</strong> activation using an in vitro system of rat pancreatic acini incubated with ethanol.
+NFKB1	drug	alcohol	12958018	<b>Ethanol</b> augmented CCK 8 induced activation of <strong>NF kappaB</strong>, similar to our in vivo findings with <b>ethanol</b> fed rats.
+NFKB1	drug	alcohol	12958018	In contrast, <b>ethanol</b> prevented <strong>NF kappaB</strong> activation caused by thapsigargin, an agent that mobilizes intracellular Ca(2+) bypassing the receptor.
+NFKB1	drug	alcohol	12958018	Pharmacological analysis showed that <strong>NF kappaB</strong> activation by thapsigargin but not by CCK 8 is mediated through the calcineurin pathway and that the inhibitory effect of <b>ethanol</b> on the thapsigargin induced <strong>NF kappaB</strong> activation could be through inhibiting this pathway.
+NFKB1	drug	alcohol	12958018	<b>Ethanol</b> augmented <strong>NF kappaB</strong> activation induced by the phorbol ester PMA, a direct activator of PKC.
+NFKB1	drug	alcohol	12958018	Inhibitory analysis demonstrated that Ca(2+) independent (novel and/or atypical) PKC isoforms are involved in <strong>NF kappaB</strong> activation induced by both CCK 8 and PMA in cells treated and not treated with <b>ethanol</b>.
+NFKB1	drug	alcohol	12958018	The results indicate that <b>ethanol</b> differentially affects the Ca(2+)/calcineurin  and PKC mediated pathways of <strong>NF kappaB</strong> activation in pancreatic acinar cells.
+NFKB1	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for AP 1 in the NAc: the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (<strong>NFkappaB</strong>), without affecting several other proteins examined for comparison.
+NFKB1	drug	amphetamine	12504868	In addition, DNA binding activities of <strong>NF kappaB</strong>, AP 1, and CREB in the frontal cortex and hippocampus were more pronounced in mice injected with Tat plus <b>METH</b> compared to the effects of Tat or <b>METH</b> alone.
+NFKB1	drug	alcohol	12482856	Additionally, overexpression of SOD also blunted <b>ethanol</b> induced activation of redox sensitive transcription factors <strong>NFkappaB</strong> and AP 1 and production of cytokines.
+NFKB1	drug	alcohol	12482856	However, only inhibition of AP 1 with dominant negative TAK1 but not <strong>NFkappaB</strong> by dominant negative IkappaBalpha significantly blunted <b>ethanol</b> induced increases in CD14, suggesting that AP 1 is important for CD14 transcriptional regulation.
+NFKB1	drug	alcohol	12045006	Chronic <b>alcohol</b> intoxication was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of <strong>NF kappaB</strong>, AP 1 and MNP 1 in Kupffer Cells.
+NFKB1	addiction	intoxication	12045006	Chronic alcohol <b>intoxication</b> was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of <strong>NF kappaB</strong>, AP 1 and MNP 1 in Kupffer Cells.
+NFKB1	drug	alcohol	12045006	Chronic <b>ethanol</b> feeding significantly enhanced MNP 1 binding, but not those of <strong>NF kappaB</strong> and AP 1 in endothelial cells.
+NFKB1	drug	alcohol	11994208	<b>Ethanol</b> and LPS modulate <strong>NF kappaB</strong> activation, inducible NO synthase and COX 2 gene expression in rat liver cells in vivo.
+NFKB1	drug	alcohol	11994208	<b>Ethanol</b> and LPS are immunomodulators, whose actions are associated with the activation of the transcription factor, <strong>NF kappaB</strong>, that mediates the expression of a number of rapid response genes involved in the whole body inflammatory response to injury, including transcriptional regulation of iNOS and COX 2.
+NFKB1	drug	alcohol	11994208	We investigated modulation by acute <b>ethanol</b> (EtOH) intoxication, LPS and LPS tolerance of <strong>NF kappaB</strong> activation in hepatocytes, Kupffer cells and sinusoidal endothelial cells (SEC), concurrent regulation of iNOS and COX 2 gene expression and the influence of gender on these mechanisms.
+NFKB1	addiction	intoxication	11994208	We investigated modulation by acute ethanol (EtOH) <b>intoxication</b>, LPS and LPS tolerance of <strong>NF kappaB</strong> activation in hepatocytes, Kupffer cells and sinusoidal endothelial cells (SEC), concurrent regulation of iNOS and COX 2 gene expression and the influence of gender on these mechanisms.
+NFKB1	drug	opioid	11474844	To investigate the role of <strong>NF kB</strong> in the expression of opiate withdrawal, the effects of PDTC, an inhibitor of <strong>NF kB</strong> activation, was studied on acute opiate withdrawal induced by <b>morphine</b> in vitro.
+NFKB1	addiction	withdrawal	11474844	To investigate the role of <strong>NF kB</strong> in the expression of opiate <b>withdrawal</b>, the effects of PDTC, an inhibitor of <strong>NF kB</strong> activation, was studied on acute opiate <b>withdrawal</b> induced by morphine in vitro.
+NFKB1	addiction	withdrawal	11474844	The results of the present study indicate that <strong>NF kB</strong> is involved in the expression of opiate <b>withdrawal</b> thus extending and explaining previous papers performed with dexamethasone and selective arachidonic acid metabolites inhibitors.
+NFKB1	drug	alcohol	11062014	In Kupffer cells from mice treated with <b>ethanol</b> 1 h earlier, LPS induced TNFalpha production, and IRAK expression and activity and <strong>NFkappaB</strong> were decreased 50 60% of control.
+NFKB1	drug	alcohol	11062014	In contrast, in Kupffer cells from mice treated with <b>ethanol</b> 21 h earlier, LPS induced TNFalpha production, expression and activity of IRAK were increased 1.5 fold over controls, while <strong>NFkappaB</strong> was elevated 3 fold.
+NFKB1	drug	alcohol	10611471	To define the molecular basis of <b>ethanol</b> dependence, the changes in gene transcription factor stimulatory protein 1 (SP1) and nuclear factor kB (<strong>NF kB</strong>) DNA binding activities were investigated in the rat cortex and hippocampus during <b>ethanol</b> treatment (15 days) and its withdrawal.
+NFKB1	addiction	dependence	10611471	To define the molecular basis of ethanol <b>dependence</b>, the changes in gene transcription factor stimulatory protein 1 (SP1) and nuclear factor kB (<strong>NF kB</strong>) DNA binding activities were investigated in the rat cortex and hippocampus during ethanol treatment (15 days) and its withdrawal.
+NFKB1	addiction	withdrawal	10611471	To define the molecular basis of ethanol dependence, the changes in gene transcription factor stimulatory protein 1 (SP1) and nuclear factor kB (<strong>NF kB</strong>) DNA binding activities were investigated in the rat cortex and hippocampus during ethanol treatment (15 days) and its <b>withdrawal</b>.
+NFKB1	drug	alcohol	10611471	It was found that both protracted <b>ethanol</b> treatment and its withdrawal (12, 24, or 72 h) had no effect on <strong>NF kB</strong> DNA binding activity in the rat cortex and hippocampus.
+NFKB1	addiction	withdrawal	10611471	It was found that both protracted ethanol treatment and its <b>withdrawal</b> (12, 24, or 72 h) had no effect on <strong>NF kB</strong> DNA binding activity in the rat cortex and hippocampus.
+CHRNA5	drug	nicotine	32738310	Genetic susceptibility to <b>nicotine</b> addiction: Advances and shortcomings in our understanding of the <strong>CHRNA5</strong>/A3/B4 gene cluster contribution.
+CHRNA5	addiction	addiction	32738310	Genetic susceptibility to nicotine <b>addiction</b>: Advances and shortcomings in our understanding of the <strong>CHRNA5</strong>/A3/B4 gene cluster contribution.
+CHRNA5	drug	nicotine	32184221	Human genome wide association studies have linked polymorphisms in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, coding for the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, to <b>nicotine</b> addiction.
+CHRNA5	addiction	addiction	32184221	Human genome wide association studies have linked polymorphisms in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, coding for the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, to nicotine <b>addiction</b>.
+CHRNA5	drug	nicotine	32184221	These data indicate that β4 is a critical modulator of reward related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster and <b>nicotine</b> addiction.
+CHRNA5	addiction	addiction	32184221	These data indicate that β4 is a critical modulator of reward related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster and nicotine <b>addiction</b>.
+CHRNA5	addiction	reward	32184221	These data indicate that β4 is a critical modulator of <b>reward</b> related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster and nicotine addiction.
+CHRNA5	drug	nicotine	31796940	SNPs within <strong>CHRNA5</strong> A3 B4 and CYP2A6/B6, <b>nicotine</b> metabolite concentrations and <b>nicotine</b> dependence treatment success in <b>smokers</b>.
+CHRNA5	addiction	dependence	31796940	SNPs within <strong>CHRNA5</strong> A3 B4 and CYP2A6/B6, nicotine metabolite concentrations and nicotine <b>dependence</b> treatment success in smokers.
+CHRNA5	drug	alcohol	31288250	Profound alteration in reward processing due to a human polymorphism in <strong>CHRNA5</strong>: a role in <b>alcohol</b> dependence and feeding behavior.
+CHRNA5	addiction	dependence	31288250	Profound alteration in reward processing due to a human polymorphism in <strong>CHRNA5</strong>: a role in alcohol <b>dependence</b> and feeding behavior.
+CHRNA5	addiction	reward	31288250	Profound alteration in <b>reward</b> processing due to a human polymorphism in <strong>CHRNA5</strong>: a role in alcohol dependence and feeding behavior.
+CHRNA5	drug	nicotine	31288250	Human genetic variation in the nicotinic receptor gene cluster <strong>CHRNA5</strong>/A3/B4, in particular the non synonymous and frequent <strong>CHRNA5</strong> variant rs16969968 (α5SNP), has an important consequence on <b>smoking</b> behavior in humans.
+CHRNA5	drug	nicotine	31072760	Low <b>Smoking</b> Exposure, the Adolescent Brain, and the Modulating Role of <strong>CHRNA5</strong> Polymorphisms.
+CHRNA5	drug	nicotine	31061854	This article contains data on the allele and genotype frequency for single nucleotide polymorphisms (SNPs) in candidate genes <strong>CHRNA5</strong> (rs16969968, rs17408276, rs680244) CHRNA3 (rs6495307, rs12914385) NRXN1 (rs10865246, rs1882296, rs985919) and HTR2A (rs6311, rs6313) previously evaluated as genetic risk variants for cigarette <b>smoking</b> at an early age and relapse to <b>smoking</b> cessation treatment Pérez Rubio et al., 2018.
+CHRNA5	addiction	relapse	31061854	This article contains data on the allele and genotype frequency for single nucleotide polymorphisms (SNPs) in candidate genes <strong>CHRNA5</strong> (rs16969968, rs17408276, rs680244) CHRNA3 (rs6495307, rs12914385) NRXN1 (rs10865246, rs1882296, rs985919) and HTR2A (rs6311, rs6313) previously evaluated as genetic risk variants for cigarette smoking at an early age and <b>relapse</b> to smoking cessation treatment Pérez Rubio et al., 2018.
+CHRNA5	drug	nicotine	30995302	A common polymorphism, rs16969968, encoded in the α5 nicotinic acetylcholine receptor subunit gene (<strong>CHRNA5</strong>), is a well recognized marker for <b>smoking</b> risk and reduces sensitivity to <b>nicotine</b> aversiveness.
+CHRNA5	drug	nicotine	30829278	Functional polymorphism in nicotinic acetylcholine receptor alpha 5 subunit gene (<strong>CHRNA5</strong> c.1192G>A; rs16969968) is associated with <b>nicotine</b> dependence and risk of lung cancer.
+CHRNA5	addiction	dependence	30829278	Functional polymorphism in nicotinic acetylcholine receptor alpha 5 subunit gene (<strong>CHRNA5</strong> c.1192G>A; rs16969968) is associated with nicotine <b>dependence</b> and risk of lung cancer.
+CHRNA5	drug	nicotine	30543688	Cholinergic Receptor Nicotinic Alpha 5 (<strong>CHRNA5</strong>) is an important susceptibility locus for <b>nicotine</b> addiction and lung cancer.
+CHRNA5	addiction	addiction	30543688	Cholinergic Receptor Nicotinic Alpha 5 (<strong>CHRNA5</strong>) is an important susceptibility locus for nicotine <b>addiction</b> and lung cancer.
+CHRNA5	drug	nicotine	30453884	Combined genetic influence of the nicotinic receptor gene cluster <strong>CHRNA5</strong>/A3/B4 on <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	30453884	Combined genetic influence of the nicotinic receptor gene cluster <strong>CHRNA5</strong>/A3/B4 on nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	30453884	The <strong>CHRNA5</strong>/A3/B4 gene locus is associated with <b>nicotine</b> dependence and other <b>smoking</b> related disorders.
+CHRNA5	addiction	dependence	30453884	The <strong>CHRNA5</strong>/A3/B4 gene locus is associated with nicotine <b>dependence</b> and other smoking related disorders.
+CHRNA5	drug	nicotine	30453884	Searching for variants with evidence of regulatory functions, we have reported interactions between <strong>CHRNA5</strong> and CHRNA3 enhancer variants (tagged by rs880395 and rs1948, respectively) and rs16969968, forming 3 SNP haplotypes and diplotypes that may more accurately reflect the cluster's combined effects on <b>nicotine</b> dependence (Barrie et al., Hum Mutat 38:112 9, 2017).
+CHRNA5	addiction	dependence	30453884	Searching for variants with evidence of regulatory functions, we have reported interactions between <strong>CHRNA5</strong> and CHRNA3 enhancer variants (tagged by rs880395 and rs1948, respectively) and rs16969968, forming 3 SNP haplotypes and diplotypes that may more accurately reflect the cluster's combined effects on nicotine <b>dependence</b> (Barrie et al., Hum Mutat 38:112 9, 2017).
+CHRNA5	drug	nicotine	30453884	These results indicate rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of CHRNA3 and <strong>CHRNA5</strong>, modulates the effect of rs16969968 on <b>nicotine</b> dependence risk.
+CHRNA5	addiction	dependence	30453884	These results indicate rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of CHRNA3 and <strong>CHRNA5</strong>, modulates the effect of rs16969968 on nicotine <b>dependence</b> risk.
+CHRNA5	drug	nicotine	30293722	A Human Polymorphism in <strong>CHRNA5</strong> Is Linked to Relapse to <b>Nicotine</b> Seeking in Transgenic Rats.
+CHRNA5	addiction	relapse	30293722	A Human Polymorphism in <strong>CHRNA5</strong> Is Linked to <b>Relapse</b> to Nicotine <b>Seeking</b> in Transgenic Rats.
+CHRNA5	drug	nicotine	29993116	CHRNA3 rs1051730 and <strong>CHRNA5</strong> rs16969968 polymorphisms are associated with heavy <b>smoking</b>, lung cancer, and chronic obstructive pulmonary disease in a mexican population.
+CHRNA5	drug	nicotine	29993116	Polymorphisms in CHRNA3, <strong>CHRNA5</strong>, and CHRNB4 receptors play a critical role in <b>nicotine</b> dependence, lung cancer (LC) risk, and chronic obstructive pulmonary disease (COPD).
+CHRNA5	addiction	dependence	29993116	Polymorphisms in CHRNA3, <strong>CHRNA5</strong>, and CHRNB4 receptors play a critical role in nicotine <b>dependence</b>, lung cancer (LC) risk, and chronic obstructive pulmonary disease (COPD).
+CHRNA5	drug	nicotine	29993116	This study characterized the CHRNA3 rs1051730 and <strong>CHRNA5</strong> rs16969968 polymorphisms in a Mexican population and its association with <b>nicotine</b> dependence, LC, and COPD.
+CHRNA5	addiction	dependence	29993116	This study characterized the CHRNA3 rs1051730 and <strong>CHRNA5</strong> rs16969968 polymorphisms in a Mexican population and its association with nicotine <b>dependence</b>, LC, and COPD.
+CHRNA5	drug	nicotine	29993116	The <b>smokers</b> were stratified in heavy <b>smokers</b> and moderate/light <b>smokers</b>, and we found in A alleles an OR = 2.86 (P = 0.01) to CHRNA3 rs1051730 and OR = 3.12 (P = 0.03) to <strong>CHRNA5</strong> rs16969968.
+CHRNA5	drug	nicotine	29954848	<strong>Chrna5</strong> Expressing Neurons in the Interpeduncular Nucleus Mediate Aversion Primed by Prior Stimulation or <b>Nicotine</b> Exposure.
+CHRNA5	addiction	aversion	29954848	<strong>Chrna5</strong> Expressing Neurons in the Interpeduncular Nucleus Mediate <b>Aversion</b> Primed by Prior Stimulation or Nicotine Exposure.
+CHRNA5	drug	nicotine	29954848	Genetic studies have shown an association between <b>smoking</b> and variation at the <strong>CHRNA5</strong>/A3/B4 gene locus encoding the α5, α3, and β4 nicotinic receptor subunits.
+CHRNA5	drug	nicotine	29954848	The α5 receptor has been specifically implicated because <b>smoking</b> associated haplotypes contain a coding variant in the <strong>CHRNA5</strong> gene.
+CHRNA5	drug	nicotine	29954848	The <strong>Chrna5</strong>/a3/b4 locus is conserved in rodents and the restricted expression of these subunits suggests neural pathways through which the reinforcing and aversive properties of <b>nicotine</b> may be mediated.
+CHRNA5	addiction	aversion	29954848	The <strong>Chrna5</strong>/a3/b4 locus is conserved in rodents and the restricted expression of these subunits suggests neural pathways through which the reinforcing and <b>aversive</b> properties of nicotine may be mediated.
+CHRNA5	addiction	reward	29954848	The <strong>Chrna5</strong>/a3/b4 locus is conserved in rodents and the restricted expression of these subunits suggests neural pathways through which the <b>reinforcing</b> and aversive properties of nicotine may be mediated.
+CHRNA5	addiction	withdrawal	29954848	Optogenetic stimulation of <strong>Chrna5</strong> expressing IP neurons failed to elicit physical manifestations of <b>withdrawal</b>.
+CHRNA5	drug	nicotine	29954848	These results using mice of both sexes support the idea that the risk allele of <strong>CHRNA5</strong> may increase the drive to smoke via loss of IP mediated <b>nicotine</b> aversion.SIGNIFICANCE STATEMENT Understanding the receptors and neural pathways underlying the reinforcing and aversive effects of <b>nicotine</b> may suggest new treatments for <b>tobacco</b> addiction.
+CHRNA5	addiction	addiction	29954848	These results using mice of both sexes support the idea that the risk allele of <strong>CHRNA5</strong> may increase the drive to smoke via loss of IP mediated nicotine aversion.SIGNIFICANCE STATEMENT Understanding the receptors and neural pathways underlying the reinforcing and aversive effects of nicotine may suggest new treatments for tobacco <b>addiction</b>.
+CHRNA5	addiction	aversion	29954848	These results using mice of both sexes support the idea that the risk allele of <strong>CHRNA5</strong> may increase the drive to smoke via loss of IP mediated nicotine <b>aversion</b>.SIGNIFICANCE STATEMENT Understanding the receptors and neural pathways underlying the reinforcing and <b>aversive</b> effects of nicotine may suggest new treatments for tobacco addiction.
+CHRNA5	addiction	reward	29954848	These results using mice of both sexes support the idea that the risk allele of <strong>CHRNA5</strong> may increase the drive to smoke via loss of IP mediated nicotine aversion.SIGNIFICANCE STATEMENT Understanding the receptors and neural pathways underlying the <b>reinforcing</b> and aversive effects of nicotine may suggest new treatments for tobacco addiction.
+CHRNA5	drug	alcohol	29944862	Interestingly, <strong>Chrna5</strong> gene deletion had no effect on basal <b>ethanol</b> drinking behavior, or <b>ethanol</b> metabolism, but did decrease <b>ethanol</b> intake in the DID paradigm following restraint stress.
+CHRNA5	drug	nicotine	29758381	However, two common variants that were present on the ExomeChip, rs16969968 (p = 2.39 × 10 7) and rs8034191 (p = 6.31 × 10 7) located in <strong>CHRNA5</strong> and AGPHD1 at 15q25.1, showed evidence for association with <b>tobacco</b> use.
+CHRNA5	drug	nicotine	29758381	However, our results confirmed the role of the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster of nicotinic acetylcholine receptor subunit genes in <b>tobacco</b> use.
+CHRNA5	drug	nicotine	29688464	<b>Smoking</b> Interacts With <strong>CHRNA5</strong>, a Nicotinic Acetylcholine Receptor Subunit Gene, to Influence the Risk of IBD Related Surgery.
+CHRNA5	drug	nicotine	29688464	This study evaluated the relationship between <strong>CHRNA5</strong>, a nicotinic receptor subunit gene, and <b>smoking</b> in predicting IBD related surgery as well as the relationship between <strong>CHRNA5</strong> and <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	29688464	This study evaluated the relationship between <strong>CHRNA5</strong>, a nicotinic receptor subunit gene, and smoking in predicting IBD related surgery as well as the relationship between <strong>CHRNA5</strong> and nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	29688464	Participants completed a <b>smoking</b> questionnaire and were genotyped for <strong>CHRNA5</strong> rs16969968.
+CHRNA5	drug	nicotine	29688464	<strong>CHRNA5</strong> genotype, but not <b>smoking</b>, predicted time to surgery in patients with UC (P = 0.007) but not in patients with CD.
+CHRNA5	drug	nicotine	29688464	The <strong>CHRNA5</strong> rs16969968 A variant interacts with <b>smoking</b> to influence IBD related surgery.
+CHRNA5	drug	nicotine	29621993	<strong>Cholinergic receptor nicotinic alpha 5 subunit</strong> polymorphisms are associated with <b>smoking</b> cessation success in women.
+CHRNA5	drug	nicotine	29621993	In the context of personalized medicine, the aims of this study were to evaluate whether cholinergic receptor nicotinic alpha 2 (CHRNA2), cholinergic receptor nicotinic alpha 3 (CHRNA3), cholinergic receptor nicotinic alpha 5 (<strong>CHRNA5</strong>) and cholinergic receptor nicotinic beta 3 (CHRNB3) polymorphisms were associated with <b>nicotine</b> dependence severity, and to investigate possible pharmacogenetics markers of <b>smoking</b> cessation treatment.
+CHRNA5	addiction	dependence	29621993	In the context of personalized medicine, the aims of this study were to evaluate whether cholinergic receptor nicotinic alpha 2 (CHRNA2), cholinergic receptor nicotinic alpha 3 (CHRNA3), cholinergic receptor nicotinic alpha 5 (<strong>CHRNA5</strong>) and cholinergic receptor nicotinic beta 3 (CHRNB3) polymorphisms were associated with nicotine <b>dependence</b> severity, and to investigate possible pharmacogenetics markers of smoking cessation treatment.
+CHRNA5	drug	nicotine	29621993	Females with GA and AA genotypes for <strong>CHRNA5</strong> rs16969968 and rs2036527 polymorphisms had higher success rate in <b>smoking</b> cessation treatment: 44.0% and 56.3% (rs16969968), 41.5% and 56.5% (rs2036527), respectively, compared with carriers of the GG genotypes: 35.7% (rs16969968), 34.8% (rs2036527), (P = 0.03, n = 389; P = 0.01, n = 391).
+CHRNA5	drug	nicotine	29621993	<strong>CHRNA5</strong> rs16969968 and rs2036527 were associated with higher success rate in the <b>smoking</b> cessation treatment in women.
+CHRNA5	drug	nicotine	29573323	The interaction of the <strong>Chrna5</strong> D398N variant with developmental <b>nicotine</b> exposure.
+CHRNA5	drug	nicotine	29573323	A single nucleotide polymorphism (SNP) in <strong>CHRNA5</strong> (rs16969968, change from an aspartic acid [D] to asparagine [N] at position 398 of the human α5 nicotinic acetylcholine receptor subunit) has been associated with increased risk for <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	29573323	A single nucleotide polymorphism (SNP) in <strong>CHRNA5</strong> (rs16969968, change from an aspartic acid [D] to asparagine [N] at position 398 of the human α5 nicotinic acetylcholine receptor subunit) has been associated with increased risk for nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	29438887	To assess its impact, we regressed the lifetime FTND latent variable on well established factors associated with <b>nicotine</b> dependence (quitting <b>smoking</b> and the nicotinic acetylcholine receptor gene [<strong>CHRNA5</strong>] variant rs16969968, separately), and we observed that the regression coefficients were unchanged between models with and without adjustment for measurement non invariance.
+CHRNA5	addiction	dependence	29438887	To assess its impact, we regressed the lifetime FTND latent variable on well established factors associated with nicotine <b>dependence</b> (quitting smoking and the nicotinic acetylcholine receptor gene [<strong>CHRNA5</strong>] variant rs16969968, separately), and we observed that the regression coefficients were unchanged between models with and without adjustment for measurement non invariance.
+CHRNA5	drug	nicotine	29307500	The genes <strong>CHRNA5</strong> and CYP2A6 are strong genomic contributors that alter the risk of heaviness of <b>smoking</b>, <b>tobacco</b> use disorder, and <b>smoking</b> related diseases in humans.
+CHRNA5	drug	nicotine	29302221	Surprisingly, the most convincing association (a nicotinic acetylcholine receptor <strong>CHRNA5</strong> A3 B4 gene cluster in <b>nicotine</b> dependence), with a unique attributable risk of 14%, was detected through a genome wide association study (GWAS) on lung cancer, although lung cancer has a low heritability.
+CHRNA5	addiction	dependence	29302221	Surprisingly, the most convincing association (a nicotinic acetylcholine receptor <strong>CHRNA5</strong> A3 B4 gene cluster in nicotine <b>dependence</b>), with a unique attributable risk of 14%, was detected through a genome wide association study (GWAS) on lung cancer, although lung cancer has a low heritability.
+CHRNA5	drug	nicotine	29302221	Étonnamment, l'association la plus convaincante (gènes <strong>CHRNA5</strong> A3 B4 du récepteur nicotinique à l'acétylcholine dans la dépendance à la <b>nicotine</b>), avec un risque unique attribuable de 14 %, a été détectée grâce à une étude d'association pangénomique (GWAS) sur le cancer du poumon alors que son héritabilité est faible.
+CHRNA5	drug	nicotine	29172281	SNP rs16969968 as a Strong Predictor of <b>Nicotine</b> Dependence and Lung Cancer Risk in a North Indian Population Background: The 15q24 25 loci contain genes (<strong>CHRNA5</strong> and CHRNA3) encoding nicotinic acetylcholine receptor subunits.
+CHRNA5	addiction	dependence	29172281	SNP rs16969968 as a Strong Predictor of Nicotine <b>Dependence</b> and Lung Cancer Risk in a North Indian Population Background: The 15q24 25 loci contain genes (<strong>CHRNA5</strong> and CHRNA3) encoding nicotinic acetylcholine receptor subunits.
+CHRNA5	drug	nicotine	29172281	We here determined for the first time the association of genetic variants rs16969968 and rs3743074 in <strong>CHRNA5</strong> and CHRNA3, respectively, on <b>nicotine</b> dependence and lung cancer risk in a North Indian population by a case control approach.
+CHRNA5	addiction	dependence	29172281	We here determined for the first time the association of genetic variants rs16969968 and rs3743074 in <strong>CHRNA5</strong> and CHRNA3, respectively, on nicotine <b>dependence</b> and lung cancer risk in a North Indian population by a case control approach.
+CHRNA5	drug	nicotine	29172281	Risk allele rs16969968 in <strong>CHRNA5</strong> also showed a significant association with increased lung cancer risk in our cohort, alone (OR= 4.99) and with <b>smoking</b> as a co variable (OR= 4.28).
+CHRNA5	drug	nicotine	29158387	It has been shown that allelic variation in the α5 nicotinic acetylcholine receptor (nAChR) gene <strong>CHRNA5</strong> is associated with higher risk of <b>tobacco</b> dependence.
+CHRNA5	addiction	dependence	29158387	It has been shown that allelic variation in the α5 nicotinic acetylcholine receptor (nAChR) gene <strong>CHRNA5</strong> is associated with higher risk of tobacco <b>dependence</b>.
+CHRNA5	drug	nicotine	28972577	In this largest ever GWAS meta analysis for <b>nicotine</b> dependence and the largest ever cross ancestry GWAS meta analysis for any <b>smoking</b> phenotype, we reconfirmed the well known <strong>CHRNA5</strong> CHRNA3 CHRNB4 genes and further yielded a novel association in the DNA methyltransferase gene DNMT3B.
+CHRNA5	addiction	dependence	28972577	In this largest ever GWAS meta analysis for nicotine <b>dependence</b> and the largest ever cross ancestry GWAS meta analysis for any smoking phenotype, we reconfirmed the well known <strong>CHRNA5</strong> CHRNA3 CHRNB4 genes and further yielded a novel association in the DNA methyltransferase gene DNMT3B.
+CHRNA5	drug	nicotine	28921935	In addition, heaviness of <b>smoking</b> (proxied by a variant in the <strong>CHRNA5</strong> A3 B4 gene cluster) and risk of depression and schizophrenia have been investigated, with no evidence of a causal effect of <b>smoking</b> on depression but some evidence of a causal effect on schizophrenia.
+CHRNA5	drug	nicotine	28520984	The known region of <strong>CHRNA5</strong>, which encodes the α5 cholinergic nicotinic receptor subunit, was associated with heavy <b>smoking</b> at genome wide significance (p ≤ 5 × 10 8) in a comparison of 1929 ever <b>smokers</b> reporting cigarettes per day (CPD) > 10 versus 3156 reporting CPD ≤ 10.
+CHRNA5	drug	nicotine	28520984	Results show that the region of the nicotinic receptor subunit gene <strong>CHRNA5</strong>, which in non Hispanic European ancestry <b>smokers</b> has been associated with heavy <b>smoking</b> as well as cessation and treatment efficacy, is also significantly associated with heavy <b>smoking</b> in this Hispanic/Latino cohort.
+CHRNA5	drug	nicotine	28472521	These Key results involve genetic variants in the nicotinic receptor subunit gene <strong>CHRNA5</strong>, variants in the <b>nicotine</b> metabolism gene CYP2A6, and the <b>nicotine</b> metabolite ratio.
+CHRNA5	addiction	dependence	28368157	Suggestive associations were consistent with previous findings from studies of substance use and <b>dependence</b>, including variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster with cigarettes smoked per day.
+CHRNA5	drug	nicotine	28112735	Recently, genome wide association studies (GWAS) identified single nucleotide polymorphisms (SNPs) in the human <strong>CHRNA5</strong> gene, encoding the α5 nAChR subunit, that increase the risks for both <b>smoking</b> and schizophrenia.
+CHRNA5	drug	nicotine	28069549	SNPs within <strong>CHRNA5</strong> A3 B4 and CYP2A6/B6 are associated with <b>smoking</b> dependence but not with <b>tobacco</b> dependence treatment outcomes in the Czech population.
+CHRNA5	addiction	dependence	28069549	SNPs within <strong>CHRNA5</strong> A3 B4 and CYP2A6/B6 are associated with smoking <b>dependence</b> but not with tobacco <b>dependence</b> treatment outcomes in the Czech population.
+CHRNA5	drug	nicotine	28045487	These studies identify pharmacological tools from two distinct classes of drugs, antagonists and modifiers that are α5 and α5 D398N subtype selective that provide a means to characterize the role of the <strong>CHRNA5</strong>/A3/B4 gene cluster in <b>smoking</b> and cancer.
+CHRNA5	drug	nicotine	27871728	The <strong>CHRNA5</strong> A3 B4 Gene Cluster and <b>Smoking</b>: From Discovery to Therapeutics.
+CHRNA5	drug	nicotine	27871728	Genome wide association studies (GWASs) have identified associations between the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster and <b>smoking</b> heaviness and <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	27871728	Genome wide association studies (GWASs) have identified associations between the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster and smoking heaviness and nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	27871728	GWASs of <b>smoking</b> related health outcomes have also identified this signal in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster.
+CHRNA5	drug	nicotine	27758088	Haplotype/diplotype analysis of rs880395 and rs1948 plus rs16969968 (a nonsynonymous <strong>CHRNA5</strong> risk variant) in GWAS (COGEND, UW TTURC, SAGE) yields a <b>nicotine</b> dependence risk profile only partially captured by rs16969968 alone.
+CHRNA5	addiction	dependence	27758088	Haplotype/diplotype analysis of rs880395 and rs1948 plus rs16969968 (a nonsynonymous <strong>CHRNA5</strong> risk variant) in GWAS (COGEND, UW TTURC, SAGE) yields a nicotine <b>dependence</b> risk profile only partially captured by rs16969968 alone.
+CHRNA5	drug	nicotine	27698409	Increased <b>nicotine</b> response in iPSC derived human neurons carrying the <strong>CHRNA5</strong> N398 allele.
+CHRNA5	addiction	addiction	27698409	Genetic variation in nicotinic receptor alpha 5 (<strong>CHRNA5</strong>) has been associated with increased risk of <b>addiction</b> associated phenotypes in humans yet little is known the underlying neural basis.
+CHRNA5	drug	nicotine	27543155	Genetic Risk Can Be Decreased: Quitting <b>Smoking</b> Decreases and Delays Lung Cancer for <b>Smokers</b> With High and Low <strong>CHRNA5</strong> Risk Genotypes   A Meta Analysis.
+CHRNA5	drug	nicotine	27543155	It is unclear whether <b>smoking</b> cessation confers the same benefits in terms of lung cancer risk reduction for those who possess <strong>CHRNA5</strong> risk variants versus those who do not.
+CHRNA5	drug	nicotine	27543155	The <strong>CHRNA5</strong> rs16969968 risk genotype (AA) was associated with increased risk and earlier diagnosis for lung cancer, but the beneficial effects of <b>smoking</b> cessation were very similar in those with and without the risk genotype.
+CHRNA5	drug	nicotine	27543155	We demonstrate that quitting <b>smoking</b> is highly beneficial in reducing lung cancer risks for <b>smokers</b> regardless of their <strong>CHRNA5</strong> rs16969968 genetic risk status.
+CHRNA5	drug	nicotine	27543155	<b>Smokers</b> with high risk <strong>CHRNA5</strong> genotypes, on average, can largely eliminate their elevated genetic risk for lung cancer by quitting <b>smoking</b>  cutting their risk of lung cancer in half and delaying its onset by 7years for those who develop it.
+CHRNA5	drug	nicotine	27543155	These results: 1) underscore the potential value of <b>smoking</b> cessation for all <b>smokers</b>, 2) suggest that <strong>CHRNA5</strong> rs16969968 genotype affects lung cancer diagnosis through its effects on <b>smoking</b>, and 3) have potential value for framing preventive interventions for those who smoke.
+CHRNA5	drug	nicotine	27428758	In the cholinergic system, regional differences in Chnrb2 and <strong>Chrna5</strong>, sex differences in Chrna4 and <strong>Chrna5</strong>, and <b>nicotine</b> preference effects in the expression of all subunits except α4 were observed.
+CHRNA5	drug	nicotine	27428758	<strong>Chrna5</strong> was lower in maximum than in minimum preferring, and in male than female rats, supporting the inhibitory role of the α5 subunit in <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	27428758	<strong>Chrna5</strong> was lower in maximum than in minimum preferring, and in male than female rats, supporting the inhibitory role of the α5 subunit in nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	27355804	SNPs in NRXN1 and <strong>CHRNA5</strong> are associated to <b>smoking</b> and regulation of GABAergic and glutamatergic pathways.
+CHRNA5	drug	nicotine	27355804	Two SNPs in NRXN1 and two in <strong>CHRNA5</strong> were associated with cigarette consumption, while rs10865246/C (NRXN1) was associated with high <b>nicotine</b> addiction.
+CHRNA5	addiction	addiction	27355804	Two SNPs in NRXN1 and two in <strong>CHRNA5</strong> were associated with cigarette consumption, while rs10865246/C (NRXN1) was associated with high nicotine <b>addiction</b>.
+CHRNA5	drug	nicotine	27327258	Besides the CHRNA4, CHRNB2 and <strong>CHRNA5</strong>/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the CHRNB3 CHRNA6 gene cluster on chromosome 8 in <b>nicotine</b> dependence (ND).
+CHRNA5	addiction	dependence	27327258	Besides the CHRNA4, CHRNB2 and <strong>CHRNA5</strong>/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the CHRNB3 CHRNA6 gene cluster on chromosome 8 in nicotine <b>dependence</b> (ND).
+CHRNA5	drug	nicotine	27302872	Polymorphisms in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster (Chr15q25) have been robustly associated with <b>nicotine</b> dependence, including genome wide studies, as well as with cognitive and neuropsychological measures.
+CHRNA5	addiction	dependence	27302872	Polymorphisms in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster (Chr15q25) have been robustly associated with nicotine <b>dependence</b>, including genome wide studies, as well as with cognitive and neuropsychological measures.
+CHRNA5	drug	nicotine	27302872	Here, we evaluated the effect of polymorphisms in <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster and their interaction with <b>tobacco</b> <b>smoking</b> status on cognition in patients with Attention Deficit/Hyperactivity Disorder (ADHD).
+CHRNA5	drug	nicotine	27208830	Current evidence strongly suggests that genetic variants predict cessation failure and that cessation pharmacotherapy effectiveness is modulated by biomarkers such as nicotinic cholinergic receptor α5 subunit (<strong>CHRNA5</strong>) genotypes or <b>nicotine</b> metabolism ratio (NMR).
+CHRNA5	drug	nicotine	27127891	Association Between CHRNA3 and <strong>CHRNA5</strong> <b>Nicotine</b> Receptor Subunit Gene Variants and <b>Nicotine</b> Dependence in an Isolated Populationof Kashubians in Poland.
+CHRNA5	addiction	dependence	27127891	Association Between CHRNA3 and <strong>CHRNA5</strong> Nicotine Receptor Subunit Gene Variants and Nicotine <b>Dependence</b> in an Isolated Populationof Kashubians in Poland.
+CHRNA5	drug	nicotine	27127891	BACKGROUND Genome wide and allelic association studies have shown the contribution of <strong>CHRNA5</strong> A3 B4 nicotinic receptor subunit gene cluster within chromosome 15 to <b>nicotine</b> dependence (ND).
+CHRNA5	addiction	dependence	27127891	BACKGROUND Genome wide and allelic association studies have shown the contribution of <strong>CHRNA5</strong> A3 B4 nicotinic receptor subunit gene cluster within chromosome 15 to nicotine <b>dependence</b> (ND).
+CHRNA5	drug	nicotine	26997181	<strong>CHRNA5</strong>/A3/B4 Variant rs3743078 and <b>Nicotine</b> Related Phenotypes: Indirect Effects Through <b>Nicotine</b> Craving.
+CHRNA5	addiction	relapse	26997181	<strong>CHRNA5</strong>/A3/B4 Variant rs3743078 and Nicotine Related Phenotypes: Indirect Effects Through Nicotine <b>Craving</b>.
+CHRNA5	drug	nicotine	26997181	The associations between <strong>CHRNA5</strong> CHRNA3 CHRNB4 variants and cigarettes per day (CPD), the Fagerström Test for <b>Nicotine</b> Dependence (FTND), and craving were analyzed in data from 662 lifetime <b>smokers</b> from an Israeli adult Jewish household sample.
+CHRNA5	addiction	dependence	26997181	The associations between <strong>CHRNA5</strong> CHRNA3 CHRNB4 variants and cigarettes per day (CPD), the Fagerström Test for Nicotine <b>Dependence</b> (FTND), and craving were analyzed in data from 662 lifetime smokers from an Israeli adult Jewish household sample.
+CHRNA5	addiction	relapse	26997181	The associations between <strong>CHRNA5</strong> CHRNA3 CHRNB4 variants and cigarettes per day (CPD), the Fagerström Test for Nicotine Dependence (FTND), and <b>craving</b> were analyzed in data from 662 lifetime smokers from an Israeli adult Jewish household sample.
+CHRNA5	drug	nicotine	26952864	The variant also confers risk of several serious <b>smoking</b> related diseases previously shown to be associated with the D398N substitution in <strong>CHRNA5</strong>.
+CHRNA5	drug	nicotine	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 addiction genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to <b>smoking</b> behavior and <b>nicotine</b> metabolism: <strong>CHRNA5</strong> CHRNA3 CHRNB4 and CYP2A6 CYP2B6.
+CHRNA5	addiction	addiction	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 <b>addiction</b> genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to smoking behavior and nicotine metabolism: <strong>CHRNA5</strong> CHRNA3 CHRNB4 and CYP2A6 CYP2B6.
+CHRNA5	drug	nicotine	26771213	Our top result was rs16969968 (P = 1.7 × 10( 14)) in <strong>CHRNA5</strong>, a locus previously associated with COPD susceptibility and <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	26771213	Our top result was rs16969968 (P = 1.7 × 10( 14)) in <strong>CHRNA5</strong>, a locus previously associated with COPD susceptibility and nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	26757861	[Association between genotype and allele frequencies of CYP2A6*12 and rs16969968 in <strong>CHRNA5</strong> variants with <b>smoking</b> and body mass index in young subjects from Northeast Mexico].
+CHRNA5	drug	nicotine	26757861	Several studies have reported that variants rs16969968 G>A of the <strong>CHRNA5</strong> gene and CYP2A6*12 of the CYP2A6 gene are associated with <b>smoking</b> and <b>smoking</b> refusal, respectively.
+CHRNA5	drug	nicotine	26751916	<strong>CHRNA5</strong>/CHRNA3 Locus Associates with Increased Mortality among <b>Smokers</b>.
+CHRNA5	drug	nicotine	26751916	Polymorphisms in the nicotinic acetylcholine receptor gene (<strong>CHRNA5</strong>/CHRNA3 locus) have been associated with several <b>smoking</b> related traits such as <b>nicotine</b> dependence, cigarette consumption, <b>smoking</b> cessation, lung cancer, and COPD.
+CHRNA5	addiction	dependence	26751916	Polymorphisms in the nicotinic acetylcholine receptor gene (<strong>CHRNA5</strong>/CHRNA3 locus) have been associated with several smoking related traits such as nicotine <b>dependence</b>, cigarette consumption, smoking cessation, lung cancer, and COPD.
+CHRNA5	drug	nicotine	26751916	<strong>CHRNA5</strong>/CHRNA3 locus tagged by rs1051730, which has been previously associated with several <b>smoking</b> related diseases was now shown to be associated also with increased all cause mortality among long term <b>smokers</b> with or without clinical COPD further emphasizing the clinical importance of the finding.
+CHRNA5	drug	cocaine	26270548	Our results provide evidence for strong selection in the nicotinic receptor gene cluster on chromosome 8, previously found to be significantly associated with both nicotine and <b>cocaine</b> dependence, as well as evidence selection acting on the region containing the <strong>CHRNA5</strong> nicotinic receptor gene on chromosome 15, that is genome wide significant for risk for nicotine dependence.
+CHRNA5	drug	nicotine	26270548	Our results provide evidence for strong selection in the nicotinic receptor gene cluster on chromosome 8, previously found to be significantly associated with both <b>nicotine</b> and cocaine dependence, as well as evidence selection acting on the region containing the <strong>CHRNA5</strong> nicotinic receptor gene on chromosome 15, that is genome wide significant for risk for <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	26270548	Our results provide evidence for strong selection in the nicotinic receptor gene cluster on chromosome 8, previously found to be significantly associated with both nicotine and cocaine <b>dependence</b>, as well as evidence selection acting on the region containing the <strong>CHRNA5</strong> nicotinic receptor gene on chromosome 15, that is genome wide significant for risk for nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	26239294	Rare, low frequency and common coding variants in <strong>CHRNA5</strong> and their contribution to <b>nicotine</b> dependence in European and African Americans.
+CHRNA5	addiction	dependence	26239294	Rare, low frequency and common coding variants in <strong>CHRNA5</strong> and their contribution to nicotine <b>dependence</b> in European and African Americans.
+CHRNA5	drug	nicotine	26239294	The common nonsynonymous variant rs16969968 in the α5 nicotinic receptor subunit gene (<strong>CHRNA5</strong>) is the strongest genetic risk factor for <b>nicotine</b> dependence in European Americans and contributes to risk in African Americans.
+CHRNA5	addiction	dependence	26239294	The common nonsynonymous variant rs16969968 in the α5 nicotinic receptor subunit gene (<strong>CHRNA5</strong>) is the strongest genetic risk factor for nicotine <b>dependence</b> in European Americans and contributes to risk in African Americans.
+CHRNA5	drug	nicotine	26239294	To comprehensively examine whether other <strong>CHRNA5</strong> coding variation influences <b>nicotine</b> dependence risk, we performed targeted sequencing on 1582 <b>nicotine</b> dependent cases (Fagerström Test for <b>Nicotine</b> Dependence score⩾4) and 1238 non dependent controls, with independent replication of common and low frequency variants using 12 studies with exome chip data.
+CHRNA5	addiction	dependence	26239294	To comprehensively examine whether other <strong>CHRNA5</strong> coding variation influences nicotine <b>dependence</b> risk, we performed targeted sequencing on 1582 nicotine dependent cases (Fagerström Test for Nicotine <b>Dependence</b> score⩾4) and 1238 non dependent controls, with independent replication of common and low frequency variants using 12 studies with exome chip data.
+CHRNA5	drug	nicotine	26239294	Our results indicate that common, low frequency and rare <strong>CHRNA5</strong> coding variants are independently associated with <b>nicotine</b> dependence risk.
+CHRNA5	addiction	dependence	26239294	Our results indicate that common, low frequency and rare <strong>CHRNA5</strong> coding variants are independently associated with nicotine <b>dependence</b> risk.
+CHRNA5	drug	nicotine	26220977	A multiancestry study identifies novel genetic associations with <strong>CHRNA5</strong> methylation in human brain and risk of <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	26220977	A multiancestry study identifies novel genetic associations with <strong>CHRNA5</strong> methylation in human brain and risk of nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	26220977	<b>Nicotine</b> dependence is influenced by chromosome 15q25.1 single nucleotide polymorphisms (SNPs), including the missense SNP rs16969968 that alters function of the α5 nicotinic acetylcholine receptor (<strong>CHRNA5</strong>) and noncoding SNPs that regulate <strong>CHRNA5</strong> mRNA expression.
+CHRNA5	addiction	dependence	26220977	Nicotine <b>dependence</b> is influenced by chromosome 15q25.1 single nucleotide polymorphisms (SNPs), including the missense SNP rs16969968 that alters function of the α5 nicotinic acetylcholine receptor (<strong>CHRNA5</strong>) and noncoding SNPs that regulate <strong>CHRNA5</strong> mRNA expression.
+CHRNA5	drug	nicotine	26220977	Of the eight cis meQTL SNPs, only the intronic CHRNB4 SNP rs11636753 was associated with <strong>CHRNA5</strong> methylation independently of the known SNP effects in prefrontal cortex, and it was the most significantly associated SNP with <b>nicotine</b> dependence across five independent cohorts (total N = 7858 European ancestry and 3238 AA participants): P = 6.7 × 10( 4), odds ratio (OR) [95% confidence interval (CI)] = 1.11 (1.05 1.18).
+CHRNA5	addiction	dependence	26220977	Of the eight cis meQTL SNPs, only the intronic CHRNB4 SNP rs11636753 was associated with <strong>CHRNA5</strong> methylation independently of the known SNP effects in prefrontal cortex, and it was the most significantly associated SNP with nicotine <b>dependence</b> across five independent cohorts (total N = 7858 European ancestry and 3238 AA participants): P = 6.7 × 10( 4), odds ratio (OR) [95% confidence interval (CI)] = 1.11 (1.05 1.18).
+CHRNA5	drug	nicotine	26220977	The rs11636753 major allele (G) was associated with lower <strong>CHRNA5</strong> DNA methylation, lower <strong>CHRNA5</strong> mRNA expression and increased <b>nicotine</b> dependence risk.
+CHRNA5	addiction	dependence	26220977	The rs11636753 major allele (G) was associated with lower <strong>CHRNA5</strong> DNA methylation, lower <strong>CHRNA5</strong> mRNA expression and increased nicotine <b>dependence</b> risk.
+CHRNA5	drug	nicotine	26220977	Our findings identify a novel regulatory SNP association with <b>nicotine</b> dependence and connect, for the first time, previously observed differences in <strong>CHRNA5</strong> mRNA expression and <b>nicotine</b> dependence risk to underlying DNA methylation differences.
+CHRNA5	addiction	dependence	26220977	Our findings identify a novel regulatory SNP association with nicotine <b>dependence</b> and connect, for the first time, previously observed differences in <strong>CHRNA5</strong> mRNA expression and nicotine <b>dependence</b> risk to underlying DNA methylation differences.
+CHRNA5	drug	nicotine	25958762	This approach allowed the identification of the first susceptibility gene in addiction (<b>tobacco</b>), with genes <strong>CHRNA5</strong>, CHRNA3 and CHRNB4 encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for <b>tobacco</b> dependence.
+CHRNA5	addiction	addiction	25958762	This approach allowed the identification of the first susceptibility gene in <b>addiction</b> (tobacco), with genes <strong>CHRNA5</strong>, CHRNA3 and CHRNB4 encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for tobacco dependence.
+CHRNA5	addiction	dependence	25958762	This approach allowed the identification of the first susceptibility gene in addiction (tobacco), with genes <strong>CHRNA5</strong>, CHRNA3 and CHRNB4 encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for tobacco <b>dependence</b>.
+CHRNA5	drug	nicotine	25948103	A <strong>CHRNA5</strong> <b>Smoking</b> Risk Variant Decreases the Aversive Effects of <b>Nicotine</b> in Humans.
+CHRNA5	addiction	aversion	25948103	A <strong>CHRNA5</strong> Smoking Risk Variant Decreases the <b>Aversive</b> Effects of Nicotine in Humans.
+CHRNA5	drug	nicotine	25948103	Genome wide association studies have implicated the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster in risk for heavy <b>smoking</b> and several <b>smoking</b> related disorders.
+CHRNA5	drug	nicotine	25948103	We evaluated the effects of a candidate causal variant in <strong>CHRNA5</strong>, rs16969968, on the acute response to <b>nicotine</b> in European American (EA) and African American (AA) <b>smokers</b> (n=192; 50% AA; 73% male).
+CHRNA5	drug	nicotine	25948103	These findings support differential aversive response to <b>nicotine</b> as one likely mechanism for the association of <strong>CHRNA5</strong> CHRNA3 CHRNB4 with heavy <b>smoking</b>.
+CHRNA5	addiction	aversion	25948103	These findings support differential <b>aversive</b> response to nicotine as one likely mechanism for the association of <strong>CHRNA5</strong> CHRNA3 CHRNB4 with heavy smoking.
+CHRNA5	drug	nicotine	25911614	Neuronal nicotinic acetylcholine receptors (nAChRs) containing the α5 subunit modulate <b>nicotine</b> consumption, and the human <strong>CHRNA5</strong> rs16969968 polymorphism, causing the replacement of the aspartic acid residue at position 398 with an asparagine (α5DN), has recently been associated with increased use of <b>tobacco</b> and higher incidence of lung cancer.
+CHRNA5	drug	nicotine	25745024	By utilizing additional information (i.e., between family information), family U confirmed a previous association of <strong>CHRNA5</strong> with <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	25745024	By utilizing additional information (i.e., between family information), family U confirmed a previous association of <strong>CHRNA5</strong> with nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	25632390	In this study we tested the association of <b>smoking</b> initiation, age at onset of daily <b>smoking</b>, and heaviness of <b>smoking</b> with five single nucleotide polymorphisms (SNPs) within the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster.
+CHRNA5	drug	nicotine	25632390	This study provides strong evidence for the role of the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster in heaviness of <b>nicotine</b> addiction.
+CHRNA5	addiction	addiction	25632390	This study provides strong evidence for the role of the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster in heaviness of nicotine <b>addiction</b>.
+CHRNA5	drug	alcohol	25603899	SNPs in the <b>alcohol</b> metabolizing genes, in the cholinergic gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4, and in the DRD2 and ANNK1 genes, are, to date, the most replicated and significant gene variants associated with <b>alcohol</b>  and nicotine related phenotypes.
+CHRNA5	drug	nicotine	25603899	SNPs in the alcohol metabolizing genes, in the cholinergic gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4, and in the DRD2 and ANNK1 genes, are, to date, the most replicated and significant gene variants associated with alcohol  and <b>nicotine</b> related phenotypes.
+CHRNA5	drug	nicotine	25572450	Selegiline treated <b>smokers</b> with the <strong>CHRNA5</strong> rs680244 GG genotype had lower post quit craving, and unlike placebo treated GG carrying <b>smokers</b>, did not experience a post quit increase in depressive symptoms.
+CHRNA5	addiction	relapse	25572450	Selegiline treated smokers with the <strong>CHRNA5</strong> rs680244 GG genotype had lower post quit <b>craving</b>, and unlike placebo treated GG carrying smokers, did not experience a post quit increase in depressive symptoms.
+CHRNA5	drug	nicotine	25555482	No GWS associations were observed at the chromosome 15 nicotinic receptor gene cluster (<strong>CHRNA5</strong> CHRNA3 CHRNB4) previously associated with <b>nicotine</b> dependence and <b>smoking</b> quantity traits.
+CHRNA5	addiction	dependence	25555482	No GWS associations were observed at the chromosome 15 nicotinic receptor gene cluster (<strong>CHRNA5</strong> CHRNA3 CHRNB4) previously associated with nicotine <b>dependence</b> and smoking quantity traits.
+CHRNA5	drug	nicotine	25555385	<b>Nicotine</b> content of cigarettes was progressively reduced over 6 months and measures of <b>smoking</b> behavior, as well as <b>nicotine</b> metabolites and <b>tobacco</b> smoke toxicant exposure, CYP2A6 and nicotinic <strong>CHRNA5</strong> A3 B4 (rs1051730) genotype were measured.
+CHRNA5	drug	nicotine	27350810	We previously identified common SNPs in a distant regulatory element (DRE) that increase <strong>CHRNA5</strong> mRNA expression in the human prefrontal cortex (PFC) and confer risk for <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	27350810	We previously identified common SNPs in a distant regulatory element (DRE) that increase <strong>CHRNA5</strong> mRNA expression in the human prefrontal cortex (PFC) and confer risk for nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	25498233	As an example of the ability of a natural genetic variant to modify the effect of an engineered mutation, data will be presented that demonstrate that the effect of <strong>Chrna5</strong> deletion on oral <b>nicotine</b> intake is dependent upon naturally occurring variant alleles of Chrna4.
+CHRNA5	drug	nicotine	25476971	This brain area is particularly enriched in nicotinic acetylcholine receptor (nAChR) subunits α5, α3 and β4 encoded by the <strong>CHRNA5</strong> A3 B4 gene cluster, which has been associated with vulnerability to <b>tobacco</b> dependence in human genetics studies.
+CHRNA5	addiction	dependence	25476971	This brain area is particularly enriched in nicotinic acetylcholine receptor (nAChR) subunits α5, α3 and β4 encoded by the <strong>CHRNA5</strong> A3 B4 gene cluster, which has been associated with vulnerability to tobacco <b>dependence</b> in human genetics studies.
+CHRNA5	drug	nicotine	25474695	Stratification by <b>smoking</b> status reveals an association of <strong>CHRNA5</strong> A3 B4 genotype with body mass index in never <b>smokers</b>.
+CHRNA5	drug	nicotine	25474695	We previously used a single nucleotide polymorphism (SNP) in the <strong>CHRNA5</strong> A3 B4 gene cluster associated with heaviness of <b>smoking</b> within <b>smokers</b> to confirm the causal effect of <b>smoking</b> in reducing body mass index (BMI) in a Mendelian randomisation analysis.
+CHRNA5	drug	nicotine	25471942	Contribution of Variants in <strong>CHRNA5</strong>/A3/B4 Gene Cluster on Chromosome 15 to <b>Tobacco</b> <b>Smoking</b>: From Genetic Association to Mechanism.
+CHRNA5	drug	nicotine	25471942	Consistent with this hypothesis, a number of genome wide association studies (GWAS) and subsequent candidate gene based associated studies investigating the genetic variants associated with <b>nicotine</b> dependence (ND) and <b>smoking</b> related phenotypes have shed light on the <strong>CHRNA5</strong>/A3/B4 gene cluster on chromosome 15, which encodes the α5, α3, and β4 nAChR subunits, respectively.
+CHRNA5	addiction	dependence	25471942	Consistent with this hypothesis, a number of genome wide association studies (GWAS) and subsequent candidate gene based associated studies investigating the genetic variants associated with nicotine <b>dependence</b> (ND) and smoking related phenotypes have shed light on the <strong>CHRNA5</strong>/A3/B4 gene cluster on chromosome 15, which encodes the α5, α3, and β4 nAChR subunits, respectively.
+CHRNA5	drug	nicotine	25471942	To gain a better understanding of the function of the highly significant genetic variants identified in this region in controlling <b>smoking</b> related behaviors, in this communication, we provide an up to date review of the progress of studies focusing on the <strong>CHRNA5</strong>/A3/B4 gene cluster and its role in ND.
+CHRNA5	drug	nicotine	25384568	Hippocampal changes produced by overexpression of the human <strong>CHRNA5</strong>/A3/B4 gene cluster may underlie cognitive deficits rescued by <b>nicotine</b> in transgenic mice.
+CHRNA5	drug	nicotine	25384568	Here, we propose that the genetic locus of susceptibility to <b>nicotine</b> addiction, the <strong>CHRNA5</strong>/A3/B4 gene cluster, encoding the α5, α3 and β4 subunits of the nicotinic acetylcholine receptors (nAChRs), may influence <b>nicotine</b> induced neuroadaptations.
+CHRNA5	addiction	addiction	25384568	Here, we propose that the genetic locus of susceptibility to nicotine <b>addiction</b>, the <strong>CHRNA5</strong>/A3/B4 gene cluster, encoding the α5, α3 and β4 subunits of the nicotinic acetylcholine receptors (nAChRs), may influence nicotine induced neuroadaptations.
+CHRNA5	drug	nicotine	25384568	Our results suggest that chronic <b>nicotine</b> treatment may represent a compensatory strategy in individuals with altered expression of the <strong>CHRNA5</strong>/A3/B4 region.
+CHRNA5	drug	nicotine	25297392	An association study on the <strong>CHRNA5</strong>/A3/B4 gene cluster, <b>smoking</b> and psoriasis vulgaris.
+CHRNA5	drug	nicotine	25297392	Genome wide association and large cohort studies have consistently linked several single nucleotide polymorphisms (SNPs) located in the <strong>CHRNA5</strong>/A3/B4 gene cluster to <b>smoking</b> behaviors and <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	25297392	Genome wide association and large cohort studies have consistently linked several single nucleotide polymorphisms (SNPs) located in the <strong>CHRNA5</strong>/A3/B4 gene cluster to smoking behaviors and nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	25297392	Then we conduct the study to examine whether the genetic variations related to <b>smoking</b> behavior located in the <strong>CHRNA5</strong>/A3/B4 gene cluster also predict the risk of psoriasis vulgaris (PV).
+CHRNA5	drug	nicotine	25297392	8 SNPs were selected based on findings from recent studies on <b>smoking</b> and <b>nicotine</b> dependence, all located in the nicotinic acetylcholine receptor subunits <strong>CHRNA5</strong>/A3/B4 gene cluster.
+CHRNA5	addiction	dependence	25297392	8 SNPs were selected based on findings from recent studies on smoking and nicotine <b>dependence</b>, all located in the nicotinic acetylcholine receptor subunits <strong>CHRNA5</strong>/A3/B4 gene cluster.
+CHRNA5	drug	nicotine	25297392	This exploratory study does not provide a relationship between these <b>smoking</b> related SNPs in the <strong>CHRNA5</strong>/A3/B4 gene cluster and PV in Chinese Han population.
+CHRNA5	drug	nicotine	25233467	We evaluated 23 single nucleotide polymorphisms (SNPs) in the five nicotinic receptor related genes (CHRNB3, CHRNA6, and <strong>CHRNA5</strong>/A3/B4) previously reported to be associated with lung cancer risk and <b>smoking</b> behavior and 14 SNPs in the four 'control' genes (TERT, CLPTM1L, CYP1A1, and TP53), which were not reported in the <b>smoking</b> GWA studies.
+CHRNA5	drug	nicotine	25233467	Results show that <b>nicotine</b> dependence is a mediator of the association between lung adenocarcinoma and gene variations in the regions of <strong>CHRNA5</strong>/A3/B4 and accounts for approximately 15% of this relationship.
+CHRNA5	addiction	dependence	25233467	Results show that nicotine <b>dependence</b> is a mediator of the association between lung adenocarcinoma and gene variations in the regions of <strong>CHRNA5</strong>/A3/B4 and accounts for approximately 15% of this relationship.
+CHRNA5	drug	nicotine	25233467	Our findings suggest that <b>nicotine</b> dependence plays an important role between genetic variants in the <strong>CHRNA5</strong>/A3/B4 region, especially CHRNA3, and lung adenocarcinoma.
+CHRNA5	addiction	dependence	25233467	Our findings suggest that nicotine <b>dependence</b> plays an important role between genetic variants in the <strong>CHRNA5</strong>/A3/B4 region, especially CHRNA3, and lung adenocarcinoma.
+CHRNA5	drug	nicotine	25214750	Genomics and personalized medicine: <strong>CHRNA5</strong> CHRNA3 CHRNB4 and <b>smoking</b> cessation treatment.
+CHRNA5	drug	nicotine	25214750	We review the significance of variants in the nicotinic receptor gene cluster (<strong>CHRNA5</strong> CHRNA3 CHRNB4) in the prediction of <b>smoking</b> quantity, <b>smoking</b> cessation, and response to cessation medication in multiple studies of <b>smoking</b> cessation.
+CHRNA5	drug	nicotine	25214750	The genetic variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 region that predict <b>nicotine</b> dependence also predict a later age of <b>smoking</b> cessation in a community based sample.
+CHRNA5	addiction	dependence	25214750	The genetic variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 region that predict nicotine <b>dependence</b> also predict a later age of smoking cessation in a community based sample.
+CHRNA5	drug	nicotine	25072098	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 locus is associated with self reported <b>smoking</b> behavior and also harbors the strongest genetic associations with chronic obstructive pulmonary disease (COPD) and lung cancer.
+CHRNA5	drug	nicotine	25072098	Because the associations with lung disease remain after adjustment for self reported <b>smoking</b> behaviors, it has been asserted that <strong>CHRNA5</strong> CHRNA3 CHRNB4 variants increase COPD and lung cancer susceptibility independently of their effects on <b>smoking</b>.
+CHRNA5	drug	nicotine	25072098	Variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 locus, including rs16969968, a nonsynonymous variant in <strong>CHRNA5</strong>, are genomewide association study significantly associated with CO (β = 2.66; 95% confidence interval [CI], 1.74 3.58; P = 1.65 × 10( 8)), and this association remains strong after adjusting for <b>smoking</b> behavior (β = 2.18; 95% CI, 1.32 3.04; P = 7.47 × 10( 7)).
+CHRNA5	drug	nicotine	24934182	<strong>CHRNA5</strong> variants moderate the effect of <b>nicotine</b> deprivation on a neural index of cognitive control.
+CHRNA5	drug	nicotine	24934182	Minor allele carriers at rs16969968 in the nicotinic acetylcholine receptor α5 subunit gene (<strong>CHRNA5</strong>) have been shown to exhibit both reduced cognitive control and greater <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	24934182	Minor allele carriers at rs16969968 in the nicotinic acetylcholine receptor α5 subunit gene (<strong>CHRNA5</strong>) have been shown to exhibit both reduced cognitive control and greater nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	24934182	We tested the hypothesis that individuals possessing at least one minor allele at rs16969968 in <strong>CHRNA5</strong> would show greater <b>nicotine</b> deprivation induced reductions in P3b and P3a amplitude.
+CHRNA5	drug	nicotine	24934182	Findings indicated that rs16969968 status did not moderate <b>nicotine</b> effects on P3b or P3a, whereas variation in other <strong>CHRNA5</strong> polymorphisms, which are not as well characterized and are not in linkage disequilibrium with rs16969968, predicted <b>nicotine</b> deprivation induced reduction of P3a amplitude: rs588765 (F1,68 = 7.74, P = 0.007) and rs17408276 (F1,67 = 7.34, P = 0.009).
+CHRNA5	drug	nicotine	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the <strong>CHRNA5</strong>, CHRNA3, CHRNB4, CHRNA6 and CHRNB3 genes and found that rare missense variants at conserved residues in CHRNB4 are associated with reduced risk of <b>nicotine</b> dependence among African Americans.
+CHRNA5	addiction	dependence	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the <strong>CHRNA5</strong>, CHRNA3, CHRNB4, CHRNA6 and CHRNB3 genes and found that rare missense variants at conserved residues in CHRNB4 are associated with reduced risk of nicotine <b>dependence</b> among African Americans.
+CHRNA5	addiction	withdrawal	24750073	Mice overexpressing the gene cluster <strong>CHRNA5</strong>/A3/B4 exhibited increased somatic signs of <b>withdrawal</b>.
+CHRNA5	drug	alcohol	24505444	We investigated six variants known to influence nicotine addiction or <b>alcohol</b> metabolism, including rs16969968 (<strong>CHRNA5</strong>), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+CHRNA5	drug	nicotine	24505444	We investigated six variants known to influence <b>nicotine</b> addiction or alcohol metabolism, including rs16969968 (<strong>CHRNA5</strong>), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+CHRNA5	addiction	addiction	24505444	We investigated six variants known to influence nicotine <b>addiction</b> or alcohol metabolism, including rs16969968 (<strong>CHRNA5</strong>), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+CHRNA5	drug	nicotine	24478678	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, encoding the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, has been linked to <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	24478678	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, encoding the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, has been linked to nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	24186853	Distinct loci in the <strong>CHRNA5</strong>/CHRNA3/CHRNB4 gene cluster are associated with onset of regular <b>smoking</b>.
+CHRNA5	drug	nicotine	24186853	Neuronal nicotinic acetylcholine receptor (nAChR) genes (<strong>CHRNA5</strong>/CHRNA3/CHRNB4) have been reproducibly associated with <b>nicotine</b> dependence, <b>smoking</b> behaviors, and lung cancer risk.
+CHRNA5	addiction	dependence	24186853	Neuronal nicotinic acetylcholine receptor (nAChR) genes (<strong>CHRNA5</strong>/CHRNA3/CHRNB4) have been reproducibly associated with nicotine <b>dependence</b>, smoking behaviors, and lung cancer risk.
+CHRNA5	drug	nicotine	24186853	These results provide important insight into the complexity of <b>smoking</b> behavior phenotypes, and suggest that association signals in the <strong>CHRNA5</strong>/A3/B4 gene cluster affecting early <b>smoking</b> behaviors may be different from those affecting the mature <b>nicotine</b> dependence phenotype.
+CHRNA5	addiction	dependence	24186853	These results provide important insight into the complexity of smoking behavior phenotypes, and suggest that association signals in the <strong>CHRNA5</strong>/A3/B4 gene cluster affecting early smoking behaviors may be different from those affecting the mature nicotine <b>dependence</b> phenotype.
+CHRNA5	drug	nicotine	24163739	Large scale, multi cohort GWAS of mainly Caucasian, <b>smoking</b>, populations have identified strong associations for lung cancer mapped to chromosomal regions 15q [nicotinic acetylcholine receptor (nAChR) subunits: CHRNA3, <strong>CHRNA5</strong>], 5p (TERT CLPTM1L locus) and 6p (BAT3 MSH5).
+CHRNA5	drug	nicotine	24163739	GWAS of <b>smoking</b> behaviour have identified risk loci for <b>smoking</b> quantity at 15q (similar genes to lung cancer susceptibility: CHRNA3, <strong>CHRNA5</strong>) and 19q (CYP2A6).
+CHRNA5	drug	nicotine	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster associated with heavy <b>smoking</b> and higher relapse risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster associated with heavy smoking and higher relapse risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of nicotine <b>dependence</b>.
+CHRNA5	addiction	relapse	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster associated with heavy smoking and higher <b>relapse</b> risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of nicotine dependence.
+CHRNA5	drug	nicotine	24065931	We examined genetic polymorphisms within the <strong>CHRNA5</strong> A3 B4 gene cluster (CHRNA3 rs578776, <strong>CHRNA5</strong> rs16969968, LOC123688 rs8034191, and CHRNA3 rs1051730), the ANKK1 gene (rs1800497), and the D2 dopamine receptor gene (DRD2 rs1079597, DRD2 rs1799732) from 104 <b>smokers</b> of European ancestry in a <b>smoking</b> cessation trial.
+CHRNA5	drug	nicotine	24062692	Recently, variants in the nAChR genes CHRNA3, <strong>CHRNA5</strong>, and CHRNB4 have been implicated in <b>nicotine</b> dependence and lung cancer susceptibility.
+CHRNA5	addiction	dependence	24062692	Recently, variants in the nAChR genes CHRNA3, <strong>CHRNA5</strong>, and CHRNB4 have been implicated in nicotine <b>dependence</b> and lung cancer susceptibility.
+CHRNA5	drug	alcohol	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically <b>alcohol</b> and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of <strong>CHRNA5</strong>, CHRNA3, CHRNB4, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of <b>Alcoholism</b> (COGA).
+CHRNA5	drug	cocaine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically alcohol and <b>cocaine</b> dependence, we undertook pooled sequencing of the coding regions and flanking sequence of <strong>CHRNA5</strong>, CHRNA3, CHRNB4, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA5	drug	nicotine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than <b>nicotine</b> dependence, specifically alcohol and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of <strong>CHRNA5</strong>, CHRNA3, CHRNB4, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA5	addiction	dependence	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine <b>dependence</b>, specifically alcohol and cocaine <b>dependence</b>, we undertook pooled sequencing of the coding regions and flanking sequence of <strong>CHRNA5</strong>, CHRNA3, CHRNB4, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA5	drug	nicotine	24055497	Second, genetic variation that modifies noxious responses to <b>nicotine</b> and thereby influences vulnerability to <b>tobacco</b> dependence, in particular variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 nicotinic acetylcholine receptor (nAChR) subunit gene cluster, will be discussed.
+CHRNA5	addiction	dependence	24055497	Second, genetic variation that modifies noxious responses to nicotine and thereby influences vulnerability to tobacco <b>dependence</b>, in particular variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 nicotinic acetylcholine receptor (nAChR) subunit gene cluster, will be discussed.
+CHRNA5	drug	nicotine	24033696	Evidence suggests that both the nicotinic receptor α5 subunit (<strong>CHRNA5</strong>) and Cytochrome P450 2A6 (CYP2A6) genotypes influence <b>smoking</b> cessation success and response to pharmacotherapy.
+CHRNA5	drug	nicotine	24033696	We examine the effect of CYP2A6 genotype on <b>smoking</b> cessation success and response to cessation pharmacotherapy, and combine these effects with those of <strong>CHRNA5</strong> genotypes.
+CHRNA5	drug	nicotine	24033696	The effect of <b>nicotine</b> replacement on continuous abstinence is moderated by the combined genetic risks from CYP2A6 and <strong>CHRNA5</strong> (Wald = 7.44, d.f.
+CHRNA5	drug	nicotine	23958943	Allelic variation in the α5 nicotinic acetylcholine receptor (nAChR) subunit gene, <strong>CHRNA5</strong>, increases vulnerability to <b>tobacco</b> addiction.
+CHRNA5	addiction	addiction	23958943	Allelic variation in the α5 nicotinic acetylcholine receptor (nAChR) subunit gene, <strong>CHRNA5</strong>, increases vulnerability to tobacco <b>addiction</b>.
+CHRNA5	drug	nicotine	23958943	These data suggest that disruption of α5* nAChR signaling greatly expands the range of <b>nicotine</b> doses that facilitate brain reward activity, which may help explain the increased <b>tobacco</b> addiction vulnerability associated with <strong>CHRNA5</strong> risk alleles.
+CHRNA5	addiction	addiction	23958943	These data suggest that disruption of α5* nAChR signaling greatly expands the range of nicotine doses that facilitate brain reward activity, which may help explain the increased tobacco <b>addiction</b> vulnerability associated with <strong>CHRNA5</strong> risk alleles.
+CHRNA5	addiction	reward	23958943	These data suggest that disruption of α5* nAChR signaling greatly expands the range of nicotine doses that facilitate brain <b>reward</b> activity, which may help explain the increased tobacco addiction vulnerability associated with <strong>CHRNA5</strong> risk alleles.
+CHRNA5	drug	alcohol	23875064	Scrutiny of the <strong>CHRNA5</strong> CHRNA3 CHRNB4 smoking behavior locus reveals a novel association with <b>alcohol</b> use in a Finnish population based study.
+CHRNA5	drug	nicotine	23875064	Scrutiny of the <strong>CHRNA5</strong> CHRNA3 CHRNB4 <b>smoking</b> behavior locus reveals a novel association with alcohol use in a Finnish population based study.
+CHRNA5	drug	nicotine	23875064	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster on chromosome 15q25.1 encoding the cholinergic nicotinic receptor subunits is robustly associated with <b>smoking</b> behavior and <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	23875064	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster on chromosome 15q25.1 encoding the cholinergic nicotinic receptor subunits is robustly associated with smoking behavior and nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	23872218	The cluster of human neuronal nicotinic receptor genes (<strong>CHRNA5</strong>/A3/B4) (15q25.1) has been associated with a variety of <b>smoking</b> and drug related behaviors, as well as risk for lung cancer.
+CHRNA5	drug	nicotine	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non <b>smoking</b> adolescents, we aimed to elucidate the impact of genome wide significant <b>smoking</b> associated variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster on reward related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to addiction.
+CHRNA5	addiction	addiction	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non smoking adolescents, we aimed to elucidate the impact of genome wide significant smoking associated variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster on reward related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to <b>addiction</b>.
+CHRNA5	addiction	reward	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non smoking adolescents, we aimed to elucidate the impact of genome wide significant smoking associated variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster on <b>reward</b> related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to addiction.
+CHRNA5	drug	alcohol	23458267	Examination of rare missense variants in the <strong>CHRNA5</strong> A3 B4 gene cluster to level of response to <b>alcohol</b> in the San Diego Sibling Pair study.
+CHRNA5	drug	alcohol	23458267	Common variants in the <strong>CHRNA5</strong> A3 B4 gene cluster have been shown to be associated with nicotine dependence and <b>alcohol</b> use disorders (AUDs) and related traits, including the level of response (LR) to <b>alcohol</b>.
+CHRNA5	drug	nicotine	23458267	Common variants in the <strong>CHRNA5</strong> A3 B4 gene cluster have been shown to be associated with <b>nicotine</b> dependence and alcohol use disorders (AUDs) and related traits, including the level of response (LR) to alcohol.
+CHRNA5	addiction	dependence	23458267	Common variants in the <strong>CHRNA5</strong> A3 B4 gene cluster have been shown to be associated with nicotine <b>dependence</b> and alcohol use disorders (AUDs) and related traits, including the level of response (LR) to alcohol.
+CHRNA5	drug	alcohol	23458267	However, the role of rare variants in the <strong>CHRNA5</strong> A3 B4 gene cluster to the LR to <b>alcohol</b> has not yet been established.
+CHRNA5	drug	alcohol	23458267	To determine whether rare variants in the <strong>CHRNA5</strong> A3 B4 gene cluster contribute to the LR to <b>alcohol</b>, the coding regions of these 3 genes were sequenced in 538 subjects from the San Diego Sibling Pair study.
+CHRNA5	drug	alcohol	23458267	In these analyses, a <strong>CHRNA5</strong> carrier status was significantly associated with the phenotype related to the feeling of intoxication experienced during the <b>alcohol</b> challenge (p = 0.039).
+CHRNA5	addiction	intoxication	23458267	In these analyses, a <strong>CHRNA5</strong> carrier status was significantly associated with the phenotype related to the feeling of <b>intoxication</b> experienced during the alcohol challenge (p = 0.039).
+CHRNA5	drug	alcohol	23458267	These results indicate that rare genetic variation in the <strong>CHRNA5</strong> A3 B4 gene cluster contributes modestly to the LR to <b>alcohol</b> in the San Diego Sibling Pair study and may protect against AUDs.
+CHRNA5	drug	nicotine	23358500	The present study investigated the association of <strong>CHRNA5</strong> polymorphisms and <b>smoking</b> topography in 66 <b>smokers</b> asked to smoke four <b>nicotine</b> containing (<b>nicotine</b> yield=0.60 mg) and four placebo (<b>nicotine</b> yield <0.05 mg) cigarettes, during separate experimental sessions.
+CHRNA5	drug	nicotine	23143843	Indeed, genetic variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to <b>tobacco</b> dependence and <b>smoking</b> associated diseases including lung cancer.
+CHRNA5	addiction	dependence	23143843	Indeed, genetic variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to tobacco <b>dependence</b> and smoking associated diseases including lung cancer.
+CHRNA5	drug	nicotine	23061658	Genome wide association (GWA) studies both in lung cancer and COPD highlighted the same variants (SNPs) on chromosome 15q25 marking the gene cluster CHRNA3 CHRNB4 <strong>CHRNA5</strong> for these <b>smoking</b> related diseases, showing a stimulating connection between this common genetic region and <b>smoking</b> behavior and <b>smoking</b> related illnesses.
+CHRNA5	drug	nicotine	23061658	Moreover variants on the gene cluster CHRNA3 CHRNB4 <strong>CHRNA5</strong> are associated with <b>nicotine</b> addiction antismoking therapy and antismoking therapy side effects.
+CHRNA5	addiction	addiction	23061658	Moreover variants on the gene cluster CHRNA3 CHRNB4 <strong>CHRNA5</strong> are associated with nicotine <b>addiction</b> antismoking therapy and antismoking therapy side effects.
+CHRNA5	drug	nicotine	23029550	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster on 15q25 has consistently been associated with <b>smoking</b> quantity, <b>nicotine</b> dependence and lung cancer.
+CHRNA5	addiction	dependence	23029550	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster on 15q25 has consistently been associated with smoking quantity, nicotine <b>dependence</b> and lung cancer.
+CHRNA5	drug	nicotine	22884254	Association of <b>nicotine</b> dependence susceptibility gene, <strong>CHRNA5</strong>, with Parkinson's disease age at onset: gene and <b>smoking</b> status interaction.
+CHRNA5	addiction	dependence	22884254	Association of nicotine <b>dependence</b> susceptibility gene, <strong>CHRNA5</strong>, with Parkinson's disease age at onset: gene and smoking status interaction.
+CHRNA5	drug	nicotine	22884254	Several genetic variants within the nicotinic cholinergic receptor gene cluster, <strong>CHRNA5</strong> CHRNA3 CHRNB4 have been reported to be associated with <b>nicotine</b> dependence (ND), and this association has been validated in multiple studies.
+CHRNA5	addiction	dependence	22884254	Several genetic variants within the nicotinic cholinergic receptor gene cluster, <strong>CHRNA5</strong> CHRNA3 CHRNB4 have been reported to be associated with nicotine <b>dependence</b> (ND), and this association has been validated in multiple studies.
+CHRNA5	drug	nicotine	22820273	The N398 variant of <strong>CHRNA5</strong> is linked to increased risk for <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	22820273	The N398 variant of <strong>CHRNA5</strong> is linked to increased risk for nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	22648373	Interplay of genetic risk factors (<strong>CHRNA5</strong> CHRNA3 CHRNB4) and cessation treatments in <b>smoking</b> cessation success.
+CHRNA5	drug	nicotine	22648373	This study tested whether variants in the nicotinic receptor gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4 predict age at <b>smoking</b> cessation and relapse after an attempt to quit <b>smoking</b>.
+CHRNA5	addiction	relapse	22648373	This study tested whether variants in the nicotinic receptor gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4 predict age at smoking cessation and <b>relapse</b> after an attempt to quit smoking.
+CHRNA5	drug	nicotine	22648373	In a community based, crosssectional study (N=5,216) and a randomized comparative effectiveness <b>smoking</b> cessation trial (N=1,073), the authors used Cox proportional hazard models and logistic regression to model the relationships of <b>smoking</b> cessation (self reported quit age in the community study and point prevalence abstinence at the end of treatment in the clinical trial) to three common haplotypes in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 region defined by rs16969968 and rs680244.
+CHRNA5	drug	nicotine	22648373	The genetic variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 region that predict <b>nicotine</b> dependence also predicted a later age at <b>smoking</b> cessation in the community sample.
+CHRNA5	addiction	dependence	22648373	The genetic variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 region that predict nicotine <b>dependence</b> also predicted a later age at smoking cessation in the community sample.
+CHRNA5	drug	alcohol	22640768	A few well validated, specific predictors such as OPRM1, ADH1B, ALDH2, <strong>CHRNA5</strong>, and CYP26 have been identified and can provide some specific guidance, for example, to understand <b>alcohol</b> related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in nicotine metabolism (CYP26), and, potentially, <b>naltrexone</b> treatment response (OPRM1).
+CHRNA5	drug	nicotine	22640768	A few well validated, specific predictors such as OPRM1, ADH1B, ALDH2, <strong>CHRNA5</strong>, and CYP26 have been identified and can provide some specific guidance, for example, to understand alcohol related flushing and upper GI cancer risk (ADH1B and AKLDH2), variation in <b>nicotine</b> metabolism (CYP26), and, potentially, naltrexone treatment response (OPRM1).
+CHRNA5	drug	nicotine	22544838	From men to mice: <strong>CHRNA5</strong>/CHRNA3, <b>smoking</b> behavior and disease.
+CHRNA5	drug	alcohol	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster) with <b>alcohol</b> dependence, nicotine dependence and smoking related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNA5	drug	nicotine	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster) with alcohol dependence, <b>nicotine</b> dependence and <b>smoking</b> related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNA5	addiction	dependence	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster) with alcohol <b>dependence</b>, nicotine <b>dependence</b> and smoking related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNA5	drug	alcohol	22438940	To further examine the impact of these genes on the development of substance use disorders, we tested whether variants within and flanking the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster affect the transition to daily smoking (individuals who smoked cigarettes 4 or more days per week) in a cross sectional sample of adolescents and young adults from the COGA (Collaborative Study of the Genetics of <b>Alcoholism</b>) families.
+CHRNA5	drug	nicotine	22438940	To further examine the impact of these genes on the development of substance use disorders, we tested whether variants within and flanking the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster affect the transition to daily <b>smoking</b> (individuals who smoked cigarettes 4 or more days per week) in a cross sectional sample of adolescents and young adults from the COGA (Collaborative Study of the Genetics of Alcoholism) families.
+CHRNA5	drug	alcohol	22382757	The <strong>CHRNA5</strong>/A3/B4 gene cluster and tobacco, <b>alcohol</b>, cannabis, inhalants and other substance use initiation: replication and new findings using mixture analyses.
+CHRNA5	drug	cannabinoid	22382757	The <strong>CHRNA5</strong>/A3/B4 gene cluster and tobacco, alcohol, <b>cannabis</b>, inhalants and other substance use initiation: replication and new findings using mixture analyses.
+CHRNA5	drug	nicotine	22382757	The <strong>CHRNA5</strong>/A3/B4 gene cluster and <b>tobacco</b>, alcohol, cannabis, inhalants and other substance use initiation: replication and new findings using mixture analyses.
+CHRNA5	drug	nicotine	22382757	Multiple studies have provided evidence for genetic associations between single nucleotide polymorphisms (SNPs) located on the <strong>CHRNA5</strong>/A3/B4 gene cluster and various phenotypes related to <b>Nicotine</b> Dependence (Greenbaum et al.
+CHRNA5	addiction	dependence	22382757	Multiple studies have provided evidence for genetic associations between single nucleotide polymorphisms (SNPs) located on the <strong>CHRNA5</strong>/A3/B4 gene cluster and various phenotypes related to Nicotine <b>Dependence</b> (Greenbaum et al.
+CHRNA5	drug	alcohol	22382757	Taken together, our study provides evidence for a general role of the <strong>CHRNA5</strong>/A3/B4 gene cluster in substance use initiation that is not limited to nicotine and <b>alcohol</b>.
+CHRNA5	drug	nicotine	22382757	Taken together, our study provides evidence for a general role of the <strong>CHRNA5</strong>/A3/B4 gene cluster in substance use initiation that is not limited to <b>nicotine</b> and alcohol.
+CHRNA5	drug	nicotine	22380605	Gene association studies in humans have linked the α5 subunit gene <strong>CHRNA5</strong> to an increased risk for <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	22380605	Gene association studies in humans have linked the α5 subunit gene <strong>CHRNA5</strong> to an increased risk for nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	22336398	<b>Nicotine</b> dependence and comorbid psychiatric disorders: examination of specific genetic variants in the <strong>CHRNA5</strong> A3 B4 nicotinic receptor genes.
+CHRNA5	addiction	dependence	22336398	Nicotine <b>dependence</b> and comorbid psychiatric disorders: examination of specific genetic variants in the <strong>CHRNA5</strong> A3 B4 nicotinic receptor genes.
+CHRNA5	drug	nicotine	22336398	The associations between <b>nicotine</b> dependence and specific variants in the nicotinic receptor <strong>CHRNA5</strong> A3 B4 subunit genes are irrefutable with replications in many studies.
+CHRNA5	addiction	dependence	22336398	The associations between nicotine <b>dependence</b> and specific variants in the nicotinic receptor <strong>CHRNA5</strong> A3 B4 subunit genes are irrefutable with replications in many studies.
+CHRNA5	drug	nicotine	22336398	The genetic risks of <b>nicotine</b> dependence associated with the <strong>CHRNA5</strong> A3 B4 subunit genes are specific, and not shared among commonly comorbid psychiatric disorders.
+CHRNA5	addiction	dependence	22336398	The genetic risks of nicotine <b>dependence</b> associated with the <strong>CHRNA5</strong> A3 B4 subunit genes are specific, and not shared among commonly comorbid psychiatric disorders.
+CHRNA5	drug	nicotine	22241830	Analysis of detailed phenotype profiles reveals <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster association with several <b>nicotine</b> dependence traits.
+CHRNA5	addiction	dependence	22241830	Analysis of detailed phenotype profiles reveals <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster association with several nicotine <b>dependence</b> traits.
+CHRNA5	drug	nicotine	22241830	In this study, we included all 15 tagging single nucleotide polymorphisms (SNPs) within the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster and tested associations with 30 <b>smoking</b> related phenotypes.
+CHRNA5	drug	nicotine	22223462	One <strong>CHRNA5</strong> (rs16969968) and two CHRNA3 (rs1051703, rs6495308) SNPs were examined for their ability to predict <b>smokers</b> who "ever" reported ND based on three phenotypic classifications: (1) 25+ CPD, (2) TTF < 10 min, and (3) HSI ≥ 4.
+CHRNA5	drug	nicotine	22102629	CPD is an important simple measure that captures in part the genetic associations of <strong>CHRNA5</strong> and <b>nicotine</b> dependence, even when other more comprehensive measures of <b>smoking</b> behaviors are examined.
+CHRNA5	addiction	dependence	22102629	CPD is an important simple measure that captures in part the genetic associations of <strong>CHRNA5</strong> and nicotine <b>dependence</b>, even when other more comprehensive measures of smoking behaviors are examined.
+CHRNA5	drug	nicotine	22102629	The <strong>CHRNA5</strong> gene is associated with heavy compulsive <b>smoking</b> and craving; this should inform the mission to improve the diagnostic validity of DSM V.
+CHRNA5	addiction	addiction	22102629	The <strong>CHRNA5</strong> gene is associated with heavy <b>compulsive</b> smoking and craving; this should inform the mission to improve the diagnostic validity of DSM V.
+CHRNA5	addiction	relapse	22102629	The <strong>CHRNA5</strong> gene is associated with heavy compulsive smoking and <b>craving</b>; this should inform the mission to improve the diagnostic validity of DSM V.
+CHRNA5	drug	nicotine	22101982	Overexpression of the <strong>CHRNA5</strong>/A3/B4 genomic cluster in mice increases the sensitivity to <b>nicotine</b> and modifies its reinforcing effects.
+CHRNA5	addiction	reward	22101982	Overexpression of the <strong>CHRNA5</strong>/A3/B4 genomic cluster in mice increases the sensitivity to nicotine and modifies its <b>reinforcing</b> effects.
+CHRNA5	drug	nicotine	22101982	Recent genetic studies have highlighted the importance of variants of the <strong>CHRNA5</strong>/A3/B4 genomic cluster in human <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	22101982	Recent genetic studies have highlighted the importance of variants of the <strong>CHRNA5</strong>/A3/B4 genomic cluster in human nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	22101982	Our study provides the first in vivo evidence of the involvement of the <strong>CHRNA5</strong>/A3/B4 genomic cluster in <b>nicotine</b> addiction through modifying the activity of brain regions responsible for the balance between the rewarding and the aversive properties of this drug.
+CHRNA5	addiction	addiction	22101982	Our study provides the first in vivo evidence of the involvement of the <strong>CHRNA5</strong>/A3/B4 genomic cluster in nicotine <b>addiction</b> through modifying the activity of brain regions responsible for the balance between the rewarding and the aversive properties of this drug.
+CHRNA5	addiction	aversion	22101982	Our study provides the first in vivo evidence of the involvement of the <strong>CHRNA5</strong>/A3/B4 genomic cluster in nicotine addiction through modifying the activity of brain regions responsible for the balance between the rewarding and the <b>aversive</b> properties of this drug.
+CHRNA5	drug	nicotine	22071378	Association of the <strong>CHRNA5</strong> A3 B4 gene cluster with heaviness of <b>smoking</b>: a meta analysis.
+CHRNA5	drug	nicotine	22071378	Variation in the <strong>CHRNA5</strong> A3 B4 gene cluster is a promising candidate region for <b>smoking</b> behavior and has been linked to multiple <b>smoking</b> related phenotypes (e.g., <b>nicotine</b> dependence) and diseases (e.g., lung cancer).
+CHRNA5	addiction	dependence	22071378	Variation in the <strong>CHRNA5</strong> A3 B4 gene cluster is a promising candidate region for smoking behavior and has been linked to multiple smoking related phenotypes (e.g., nicotine <b>dependence</b>) and diseases (e.g., lung cancer).
+CHRNA5	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], <strong>CHRNA5</strong> 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CHRNA5	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], <strong>CHRNA5</strong> 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CHRNA5	drug	cannabinoid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (<strong>CHRNA5</strong>), serotoninergic (HTR2A), opioid (OPRM1) or <b>cannabinoid</b> receptors (CNR1).
+CHRNA5	drug	nicotine	22046326	Overall, our results suggest that genetic variants potentially involved in <b>nicotine</b> metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with <b>smoking</b> related phenotypes, as opposed to genetic variants influencing the brain effects of <b>nicotine</b>, e.g., through nicotinic acetylcholine (<strong>CHRNA5</strong>), serotoninergic (HTR2A), opioid (OPRM1) or cannabinoid receptors (CNR1).
+CHRNA5	drug	opioid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (<strong>CHRNA5</strong>), serotoninergic (HTR2A), <b>opioid</b> (OPRM1) or cannabinoid receptors (CNR1).
+CHRNA5	drug	nicotine	22042774	Genome wide association studies have identified common variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 and CHRNA6 CHRNB3 gene clusters that contribute to <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	22042774	Genome wide association studies have identified common variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 and CHRNA6 CHRNB3 gene clusters that contribute to nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the <strong>CHRNA5</strong>, CHRNA3, CHRNB4, CHRNA6 and CHRNB3 genes in African American and European American <b>nicotine</b> dependent <b>smokers</b> and <b>smokers</b> without symptoms of dependence.
+CHRNA5	addiction	dependence	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the <strong>CHRNA5</strong>, CHRNA3, CHRNB4, CHRNA6 and CHRNB3 genes in African American and European American nicotine dependent smokers and smokers without symptoms of <b>dependence</b>.
+CHRNA5	drug	nicotine	22042234	Genetic variation in the <strong>CHRNA5</strong>/CHRNA3/CHRNB4 gene cluster has been associated with early substance experimentation, <b>nicotine</b> dependence, and other drug behaviors.
+CHRNA5	addiction	dependence	22042234	Genetic variation in the <strong>CHRNA5</strong>/CHRNA3/CHRNB4 gene cluster has been associated with early substance experimentation, nicotine <b>dependence</b>, and other drug behaviors.
+CHRNA5	drug	nicotine	22028403	Genetic variants located at 15q25, including those in the cholinergic receptor nicotinic cluster (<strong>CHRNA5</strong>) have been implicated in both lung cancer risk and <b>nicotine</b> dependence in recent genome wide association studies.
+CHRNA5	addiction	dependence	22028403	Genetic variants located at 15q25, including those in the cholinergic receptor nicotinic cluster (<strong>CHRNA5</strong>) have been implicated in both lung cancer risk and nicotine <b>dependence</b> in recent genome wide association studies.
+CHRNA5	drug	nicotine	22012472	Genome wide association studies and rodent models have demonstrated that the α5 nicotinic acetylcholine receptor gene (<strong>CHRNA5</strong>) is important in regulating <b>nicotine</b> intake.
+CHRNA5	drug	nicotine	21968931	The <strong>CHRNA5</strong> A3 B4 gene cluster in <b>nicotine</b> addiction.
+CHRNA5	addiction	addiction	21968931	The <strong>CHRNA5</strong> A3 B4 gene cluster in nicotine <b>addiction</b>.
+CHRNA5	drug	nicotine	21955800	The polymorphism of the <strong>CHRNA5</strong> gene and the strength of <b>nicotine</b> addiction in lung cancer and COPD patients.
+CHRNA5	addiction	addiction	21955800	The polymorphism of the <strong>CHRNA5</strong> gene and the strength of nicotine <b>addiction</b> in lung cancer and COPD patients.
+CHRNA5	drug	nicotine	21955800	A rare variant of chromosomal region 15q25.1, marked by rs16969968 (substitution 1354G>A in <strong>CHRNA5</strong>), was found to be associated with increased lung cancer and <b>nicotine</b> dependence risk.
+CHRNA5	addiction	dependence	21955800	A rare variant of chromosomal region 15q25.1, marked by rs16969968 (substitution 1354G>A in <strong>CHRNA5</strong>), was found to be associated with increased lung cancer and nicotine <b>dependence</b> risk.
+CHRNA5	drug	nicotine	21955800	We attempted to confirm the relationship of the polymorphism of the <strong>CHRNA5</strong> gene and <b>nicotine</b> dependence strength measured by the Fagerström test with the serum cotinine level in lung cancer and chronic obstructive pulmonary disease (COPD) patients and healthy individuals.
+CHRNA5	addiction	dependence	21955800	We attempted to confirm the relationship of the polymorphism of the <strong>CHRNA5</strong> gene and nicotine <b>dependence</b> strength measured by the Fagerström test with the serum cotinine level in lung cancer and chronic obstructive pulmonary disease (COPD) patients and healthy individuals.
+CHRNA5	drug	nicotine	21955800	We report for the first time the relationship between the polymorphism of the <strong>CHRNA5</strong> gene and the strength of <b>nicotine</b> addiction measured by multiple factors including the Fagerström test score.
+CHRNA5	addiction	addiction	21955800	We report for the first time the relationship between the polymorphism of the <strong>CHRNA5</strong> gene and the strength of nicotine <b>addiction</b> measured by multiple factors including the Fagerström test score.
+CHRNA5	drug	nicotine	21858091	Genome wide association studies implicate variations in <strong>CHRNA5</strong> and CHRNA3 as being associated with <b>nicotine</b> addiction (NA).
+CHRNA5	addiction	addiction	21858091	Genome wide association studies implicate variations in <strong>CHRNA5</strong> and CHRNA3 as being associated with nicotine <b>addiction</b> (NA).
+CHRNA5	drug	nicotine	21810735	Single nucleotide polymorphisms in <strong>CHRNA5</strong> rs16969968, CHRNA3 rs578776, and LOC123688 rs8034191 are associated with heaviness of <b>smoking</b> in women in Northeastern Ontario, Canada.
+CHRNA5	drug	nicotine	21810735	Women with the variant AA genotype of <strong>CHRNA5</strong> rs16969968 or variant CC genotype of LOC123688 rs8034191 were at significantly increased risk of heavy <b>smoking</b>, with age adjusted odds ratios (ORs) of 3.2 (95% CI: 1.05 10.0) and 2.8 (95% CI: 1.00 7.91), respectively.
+CHRNA5	drug	nicotine	21764527	Association between <strong>CHRNA5</strong> genetic variation at rs16969968 and brain reactivity to <b>smoking</b> images in <b>nicotine</b> dependent women.
+CHRNA5	drug	nicotine	21764527	Genome wide association studies revealed a relationship between development of <b>nicotine</b> dependence and a single nucleotide polymorphism (SNP, rs16969968) of the <b>nicotine</b> acetylcholine receptor (nAChR) alpha 5 subunit gene (<strong>CHRNA5</strong>).
+CHRNA5	addiction	dependence	21764527	Genome wide association studies revealed a relationship between development of nicotine <b>dependence</b> and a single nucleotide polymorphism (SNP, rs16969968) of the nicotine acetylcholine receptor (nAChR) alpha 5 subunit gene (<strong>CHRNA5</strong>).
+CHRNA5	drug	nicotine	21748402	A twin association study of <b>nicotine</b> dependence with markers in the CHRNA3 and <strong>CHRNA5</strong> genes.
+CHRNA5	addiction	dependence	21748402	A twin association study of nicotine <b>dependence</b> with markers in the CHRNA3 and <strong>CHRNA5</strong> genes.
+CHRNA5	drug	nicotine	21747048	Relationship between CYP2A6 and <strong>CHRNA5</strong> CHRNA3 CHRNB4 variation and <b>smoking</b> behaviors and lung cancer risk.
+CHRNA5	drug	nicotine	21747048	Genetic variations in the CYP2A6 <b>nicotine</b> metabolic gene and the <strong>CHRNA5</strong> CHRNA3 CHRNB4 (<strong>CHRNA5</strong> A3 B4) nicotinic gene cluster have been independently associated with lung cancer.
+CHRNA5	drug	nicotine	21747048	Cigarette consumption (P < .001) and <b>nicotine</b> dependence (P = .036) were the highest in the combined CYP2A6 normal metabolizers and <strong>CHRNA5</strong> A3 B4 AA (tag single nucleotide polymorphism rs1051730 G>A) risk group.
+CHRNA5	addiction	dependence	21747048	Cigarette consumption (P < .001) and nicotine <b>dependence</b> (P = .036) were the highest in the combined CYP2A6 normal metabolizers and <strong>CHRNA5</strong> A3 B4 AA (tag single nucleotide polymorphism rs1051730 G>A) risk group.
+CHRNA5	drug	nicotine	21747048	Variation in CYP2A6 and <strong>CHRNA5</strong> A3 B4 was independently and additively associated with increased cigarette consumption, <b>nicotine</b> dependence, and lung cancer risk.
+CHRNA5	addiction	dependence	21747048	Variation in CYP2A6 and <strong>CHRNA5</strong> A3 B4 was independently and additively associated with increased cigarette consumption, nicotine <b>dependence</b>, and lung cancer risk.
+CHRNA5	drug	nicotine	21747048	CYP2A6 and <strong>CHRNA5</strong> A3 B4 appear to be more strongly associated with <b>smoking</b> behaviors and lung cancer risk, respectively.
+CHRNA5	drug	nicotine	21740894	Consistent with this possibility, human genome wide association studies have shown that genetic variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster located in chromosome region 15q25, which encode the α5, α3 and β4 nAChR subunits, respectively, increases vulnerability to <b>tobacco</b> addiction and <b>smoking</b> related diseases.
+CHRNA5	addiction	addiction	21740894	Consistent with this possibility, human genome wide association studies have shown that genetic variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster located in chromosome region 15q25, which encode the α5, α3 and β4 nAChR subunits, respectively, increases vulnerability to tobacco <b>addiction</b> and smoking related diseases.
+CHRNA5	drug	nicotine	21690317	The rs1051730 genetic variant within the <strong>CHRNA5</strong> A3 B4 gene cluster is associated with heaviness of <b>smoking</b> and has recently been reported to be associated with likelihood of stopping <b>smoking</b>.
+CHRNA5	drug	nicotine	21555077	<b>Nicotine</b> dependence is linked to single nucleotide polymorphisms in the CHRNB4 CHRNA3 <strong>CHRNA5</strong> gene cluster encoding the α3β4α5 nicotinic acetylcholine receptor (nAChR).
+CHRNA5	addiction	dependence	21555077	Nicotine <b>dependence</b> is linked to single nucleotide polymorphisms in the CHRNB4 CHRNA3 <strong>CHRNA5</strong> gene cluster encoding the α3β4α5 nicotinic acetylcholine receptor (nAChR).
+CHRNA5	drug	nicotine	21511889	Common variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene region is robustly associated with <b>smoking</b> quantity.
+CHRNA5	drug	nicotine	21498873	As the physiological effects of <b>nicotine</b> are mediated by nicotinic acetylcholine receptors (nAChRs), we aimed at examining whether single nucleotide polymorphisms (SNPs) residing in nAChR subunit (CHRN) genes, other than CHRNA3/<strong>CHRNA5</strong>/CHRNB4 gene cluster previously showing association in our sample, are associated with <b>smoking</b> quantity or serum cotinine levels.
+CHRNA5	drug	nicotine	21418140	A <strong>CHRNA5</strong> allele related to <b>nicotine</b> addiction and schizophrenia.
+CHRNA5	addiction	addiction	21418140	A <strong>CHRNA5</strong> allele related to nicotine <b>addiction</b> and schizophrenia.
+CHRNA5	drug	nicotine	21418140	A functional <b>smoking</b> related nicotinic acetylcholine receptor α5 subunit gene (<strong>CHRNA5</strong>) nonsynonymous single nucleotide polymorphism (SNP) rs16969968 (Asp398Asn) has recently been discovered and replicated.
+CHRNA5	drug	nicotine	21385908	Association of the <b>nicotine</b> metabolite ratio and <strong>CHRNA5</strong>/CHRNA3 polymorphisms with <b>smoking</b> rate among treatment seeking <b>smokers</b>.
+CHRNA5	addiction	relapse	21385908	Association of the nicotine metabolite ratio and <strong>CHRNA5</strong>/CHRNA3 polymorphisms with smoking rate among treatment <b>seeking</b> smokers.
+CHRNA5	drug	nicotine	21385908	Genome wide association studies have linked single nucleotide polymorphisms (SNPs) in the <strong>CHRNA5</strong>/A3/B4 gene cluster with heaviness of <b>smoking</b>.
+CHRNA5	drug	nicotine	21385908	This study demonstrates the additive and independent association of the NMR and SNPs in the <strong>CHRNA5</strong>/A3/B4 gene cluster with <b>smoking</b> rate in treatment seeking <b>smokers</b>.
+CHRNA5	addiction	relapse	21385908	This study demonstrates the additive and independent association of the NMR and SNPs in the <strong>CHRNA5</strong>/A3/B4 gene cluster with smoking rate in treatment <b>seeking</b> smokers.
+CHRNA5	drug	nicotine	21312287	Using a case control sample of 90 young, Israeli, Jewish female <b>smokers</b> (FTND ≥ 4) and 108 controls (FTND = 0 during heaviest period of <b>smoking</b>), we studied association with ND of 8 COMT tagging SNPs, their interaction with tagging <strong>CHRNA5</strong> A3 SNPs and the role of background, personality, and environmental factors.
+CHRNA5	drug	nicotine	21278726	Genetic variation in <strong>CHRNA5</strong>, the gene encoding the α5 nicotinic acetylcholine receptor subunit, increases vulnerability to <b>tobacco</b> addiction and lung cancer, but the underlying mechanisms are unknown.
+CHRNA5	addiction	addiction	21278726	Genetic variation in <strong>CHRNA5</strong>, the gene encoding the α5 nicotinic acetylcholine receptor subunit, increases vulnerability to tobacco <b>addiction</b> and lung cancer, but the underlying mechanisms are unknown.
+CHRNA5	drug	nicotine	21278726	Here we report markedly increased <b>nicotine</b> intake in mice with a null mutation in <strong>Chrna5</strong>.
+CHRNA5	drug	nicotine	21268243	Markers in the 15q24 nicotinic receptor subunit gene cluster (<strong>CHRNA5</strong> A3 B4) predict severity of <b>nicotine</b> addiction and response to <b>smoking</b> cessation therapy.
+CHRNA5	addiction	addiction	21268243	Markers in the 15q24 nicotinic receptor subunit gene cluster (<strong>CHRNA5</strong> A3 B4) predict severity of nicotine <b>addiction</b> and response to smoking cessation therapy.
+CHRNA5	drug	nicotine	21268243	We focused on eight SNPs in the 15q24 region, which contains the genes for the nicotinic cholinergic receptor subunits <strong>CHRNA5</strong>, CHRNA3, and CHRNB4, and has previously been implicated in <b>nicotine</b> addiction and <b>smoking</b> cessation.
+CHRNA5	addiction	addiction	21268243	We focused on eight SNPs in the 15q24 region, which contains the genes for the nicotinic cholinergic receptor subunits <strong>CHRNA5</strong>, CHRNA3, and CHRNB4, and has previously been implicated in nicotine <b>addiction</b> and smoking cessation.
+CHRNA5	drug	nicotine	21268243	Analyses of baseline <b>smoking</b> quantity (SQ) identified an association between SQ and both the functional <strong>CHRNA5</strong> SNP rs16969968 (D398N) and the CHRNA3 SNP rs1051730 (Y215Y) in a combined cohort containing MT1 and MT2.
+CHRNA5	drug	nicotine	21268243	These results provide further support for the role of the <strong>CHRNA5</strong>/A3/B4 subunits in determining number of cigarettes smoked and response to <b>smoking</b> cessation therapy.
+CHRNA5	drug	nicotine	21248747	Association of a variant in the <strong>CHRNA5</strong> A3 B4 gene cluster region to heavy <b>smoking</b> in the Italian population.
+CHRNA5	drug	nicotine	21248747	One study was the association of single nucleotide polymorphisms (SNPs) in the <strong>CHRNA5</strong> A3 B4 gene cluster to <b>nicotine</b> addiction.
+CHRNA5	addiction	addiction	21248747	One study was the association of single nucleotide polymorphisms (SNPs) in the <strong>CHRNA5</strong> A3 B4 gene cluster to nicotine <b>addiction</b>.
+CHRNA5	drug	nicotine	21228559	An exploratory study on the CHRNA3 <strong>CHRNA5</strong> CHRNB4 cluster, <b>smoking</b>, and Parkinson's disease.
+CHRNA5	drug	nicotine	21228559	Recent genome wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the CHRNA3 <strong>CHRNA5</strong> CHRNB4 cluster on chromosome 15.q25 to <b>smoking</b> behaviors and <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	21228559	Recent genome wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the CHRNA3 <strong>CHRNA5</strong> CHRNB4 cluster on chromosome 15.q25 to smoking behaviors and nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	21228559	Four SNPs in linkage disequilibrium from the CHRNA3 <strong>CHRNA5</strong> CHRNB4 cluster were associated with <b>smoking</b> duration (OR >1.3, p < 0.05).
+CHRNA5	drug	nicotine	21191315	On the basis of known associations with <b>nicotine</b> dependence, we genotyped eight single nucleotide polymorphisms (SNPs) on chromosome 8 (three bins) in the regions of CHRNB3 and CHRNA6, and six SNPs on chromosome 15 (three bins) in the regions of <strong>CHRNA5</strong> and CHRNA3.
+CHRNA5	addiction	dependence	21191315	On the basis of known associations with nicotine <b>dependence</b>, we genotyped eight single nucleotide polymorphisms (SNPs) on chromosome 8 (three bins) in the regions of CHRNB3 and CHRNA6, and six SNPs on chromosome 15 (three bins) in the regions of <strong>CHRNA5</strong> and CHRNA3.
+CHRNA5	drug	nicotine	21168125	TTC12 ANKK1 DRD2 and <strong>CHRNA5</strong> CHRNA3 CHRNB4 influence different pathways leading to <b>smoking</b> behavior from adolescence to mid adulthood.
+CHRNA5	drug	nicotine	21168125	<strong>CHRNA5</strong> CHRNA3 CHRNB4 and TTC12 ANKK1 DRD2 gene clusters influence <b>smoking</b> behavior.
+CHRNA5	drug	nicotine	21168125	In contrast, <strong>CHRNA5</strong> CHRNA3 CHRNB4 is involved in the transition toward heavy <b>smoking</b> in mid adulthood and in <b>smoking</b> persistence.
+CHRNA5	drug	alcohol	21048701	Recent human genetic association studies have implicated the gene cluster CHRNA3 <strong>CHRNA5</strong> CHRNB4 encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop nicotine and <b>alcohol</b> dependence; however, their role in <b>ethanol</b> mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNA5	drug	nicotine	21048701	Recent human genetic association studies have implicated the gene cluster CHRNA3 <strong>CHRNA5</strong> CHRNB4 encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop <b>nicotine</b> and alcohol dependence; however, their role in ethanol mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNA5	addiction	dependence	21048701	Recent human genetic association studies have implicated the gene cluster CHRNA3 <strong>CHRNA5</strong> CHRNB4 encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop nicotine and alcohol <b>dependence</b>; however, their role in ethanol mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNA5	drug	nicotine	20886544	Risk gene variants for <b>nicotine</b> dependence in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster are associated with cognitive performance.
+CHRNA5	addiction	dependence	20886544	Risk gene variants for nicotine <b>dependence</b> in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster are associated with cognitive performance.
+CHRNA5	drug	nicotine	20886544	Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4 with <b>nicotine</b> dependence (ND).
+CHRNA5	addiction	dependence	20886544	Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4 with nicotine <b>dependence</b> (ND).
+CHRNA5	drug	nicotine	20871796	BACKGROUND: Several studies have found replicable associations between <b>nicotine</b> dependence and specific variants in the nicotinic receptor genes <strong>CHRNA5</strong>(rs16969968) and CHRNA3(rs3743078).
+CHRNA5	addiction	dependence	20871796	BACKGROUND: Several studies have found replicable associations between nicotine <b>dependence</b> and specific variants in the nicotinic receptor genes <strong>CHRNA5</strong>(rs16969968) and CHRNA3(rs3743078).
+CHRNA5	drug	nicotine	20840187	Here we test the hypothesis that the nicotinic receptor genes <strong>CHRNA5</strong> (rs16969968), CHRNA3 (rs578776), CHRNB3 (rs13277254) and CHRND (rs12466358) modify the risk for <b>nicotine</b> dependence associated with peer <b>smoking</b>.
+CHRNA5	addiction	dependence	20840187	Here we test the hypothesis that the nicotinic receptor genes <strong>CHRNA5</strong> (rs16969968), CHRNA3 (rs578776), CHRNB3 (rs13277254) and CHRND (rs12466358) modify the risk for nicotine <b>dependence</b> associated with peer smoking.
+CHRNA5	drug	nicotine	20840187	Peer <b>smoking</b> had a substantially lower effect on <b>nicotine</b> dependence among those with the high risk AA genotype at the functional SNP rs16969968 (<strong>CHRNA5</strong>) than among those with lower risk genotypes.
+CHRNA5	addiction	dependence	20840187	Peer smoking had a substantially lower effect on nicotine <b>dependence</b> among those with the high risk AA genotype at the functional SNP rs16969968 (<strong>CHRNA5</strong>) than among those with lower risk genotypes.
+CHRNA5	drug	nicotine	20808433	Associations of variants in <strong>CHRNA5</strong>/A3/B4 gene cluster with <b>smoking</b> behaviors in a Korean population.
+CHRNA5	drug	nicotine	20808433	Multiple genome wide and targeted association studies reveal a significant association of variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 (<strong>CHRNA5</strong>/A3/B4) gene cluster on chromosome 15 with <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	20808433	Multiple genome wide and targeted association studies reveal a significant association of variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 (<strong>CHRNA5</strong>/A3/B4) gene cluster on chromosome 15 with nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	20808433	In this study, we performed comprehensive association and interaction analyses for 32 single nucleotide polymorphisms (SNPs) in <strong>CHRNA5</strong>/A3/B4 with <b>smoking</b> initiation (SI), <b>smoking</b> quantity (SQ), and <b>smoking</b> cessation (SC) in a Korean sample (N = 8,842).
+CHRNA5	drug	nicotine	20808433	A spectrum of haplotypes formed by three consecutive SNPs located between rs16969948 in <strong>CHRNA5</strong> and rs6495316 in the intergenic region downstream from the 5' end of CHRNB4 was associated with these three <b>smoking</b> related phenotypes in both the total and the male sample.
+CHRNA5	drug	nicotine	20808433	Together, our detected associations of variants in the <strong>CHRNA5</strong>/A3/B4 cluster with SI, SQ, and SC in the Korean <b>smoker</b> samples provide strong evidence for the contribution of this cluster to the etiology of SI, ND, and SC in this Asian population.
+CHRNA5	drug	nicotine	20700436	Recently, genetic association findings for <b>nicotine</b> dependence, <b>smoking</b> behavior, and <b>smoking</b> related diseases converged to implicate the chromosome 15q25.1 region, which includes the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cholinergic nicotinic receptor subunit genes.
+CHRNA5	addiction	dependence	20700436	Recently, genetic association findings for nicotine <b>dependence</b>, smoking behavior, and smoking related diseases converged to implicate the chromosome 15q25.1 region, which includes the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cholinergic nicotinic receptor subunit genes.
+CHRNA5	drug	nicotine	20700436	This study is also the first report of association between rs588765 (and correlates) and <b>smoking</b> that achieves genome wide significance; these SNPs have previously been associated with mRNA levels of <strong>CHRNA5</strong> in brain and lung tissue.
+CHRNA5	drug	nicotine	20700147	<strong>CHRNA5</strong>, encoding the nicotinic α5 subunit, is implicated in multiple disorders, including <b>nicotine</b> addiction and lung cancer.
+CHRNA5	addiction	addiction	20700147	<strong>CHRNA5</strong>, encoding the nicotinic α5 subunit, is implicated in multiple disorders, including nicotine <b>addiction</b> and lung cancer.
+CHRNA5	drug	nicotine	20685379	The nicotinic acetylcholine receptor <strong>CHRNA5</strong>/A3/B4 gene cluster: dual role in <b>nicotine</b> addiction and lung cancer.
+CHRNA5	addiction	addiction	20685379	The nicotinic acetylcholine receptor <strong>CHRNA5</strong>/A3/B4 gene cluster: dual role in nicotine <b>addiction</b> and lung cancer.
+CHRNA5	drug	nicotine	20631687	Variation in the nicotinic acetylcholine receptor gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4 and its interaction with recent <b>tobacco</b> use influence cognitive flexibility.
+CHRNA5	drug	nicotine	20631687	Variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster have been associated with <b>nicotine</b> dependence (ND) and ND related traits.
+CHRNA5	addiction	dependence	20631687	Variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster have been associated with nicotine <b>dependence</b> (ND) and ND related traits.
+CHRNA5	drug	nicotine	20631687	These findings suggest that variation in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster influences cognitive flexibility differentially in AAs and EAs and that current <b>smoking</b> moderates this effect.
+CHRNA5	drug	nicotine	20624154	<strong>CHRNA5</strong> exhibited larger effects in later onset <b>smokers</b>, in contrast with a previous report that suggested the opposite interaction (Weiss et al.
+CHRNA5	drug	nicotine	20584212	Several independent studies show that the chromosome 15q25.1 region, which contains the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, harbors variants strongly associated with <b>nicotine</b> dependence, other <b>smoking</b> behaviors, lung cancer and chronic obstructive pulmonary disease.
+CHRNA5	addiction	dependence	20584212	Several independent studies show that the chromosome 15q25.1 region, which contains the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, harbors variants strongly associated with nicotine <b>dependence</b>, other smoking behaviors, lung cancer and chronic obstructive pulmonary disease.
+CHRNA5	drug	nicotine	20581870	From <b>smoking</b> to lung cancer: the <strong>CHRNA5</strong>/A3/B4 connection.
+CHRNA5	drug	nicotine	20564069	Mediating effects of <b>smoking</b> and chronic obstructive pulmonary disease on the relation between the <strong>CHRNA5</strong> A3 genetic locus and lung cancer risk.
+CHRNA5	drug	nicotine	20564069	Recent genome wide association studies of lung cancer have shown that the <strong>CHRNA5</strong> A3 region on chromosome 15q24 25.1 is strongly associated with an increased risk of lung cancer and <b>nicotine</b> dependence, and is thought to be associated with chronic obstructive pulmonary disease as well.
+CHRNA5	addiction	dependence	20564069	Recent genome wide association studies of lung cancer have shown that the <strong>CHRNA5</strong> A3 region on chromosome 15q24 25.1 is strongly associated with an increased risk of lung cancer and nicotine <b>dependence</b>, and is thought to be associated with chronic obstructive pulmonary disease as well.
+CHRNA5	drug	nicotine	20564069	The authors applied a rigorous statistical approach, mediation analysis, to examine the mediating effect of <b>smoking</b> behavior and self reported, physician diagnosed emphysema (chronic obstructive pulmonary disease [COPD]) on the relation between the <strong>CHRNA5</strong> A3 region genetic variant rs1051730 and the risk of lung cancer.
+CHRNA5	drug	alcohol	20496163	This report explores the association between six nAChR subunit genes (Chrna3, Chrna4, Chrnb4, Chrnb2, <strong>Chrna5</strong>, and Chrna7) with <b>alcohol</b> preference (AP) using co segregation of AP with nAChR subunit genotypes in a F(2) population produced from reciprocal crosses of <b>alcohol</b> preferring C57BL/6J (B6) and <b>alcohol</b> avoiding DBA/2J (D2) strains of mice.
+CHRNA5	drug	alcohol	20496163	Further, the Chrnb4 and <strong>Chrna5</strong> genes showed expression differences between B6 and D2 mice, which is compatible with their involvement in AP in mice and, potentially, <b>alcohol</b> abuse in humans.
+CHRNA5	drug	cocaine	20485328	The strongest association signal in either sample was between rs684513 in <strong>CHRNA5</strong> and <b>cocaine</b> dependence (OR=1.43, P=0.0004) in the AA replication set.
+CHRNA5	addiction	dependence	20485328	The strongest association signal in either sample was between rs684513 in <strong>CHRNA5</strong> and cocaine <b>dependence</b> (OR=1.43, P=0.0004) in the AA replication set.
+CHRNA5	drug	alcohol	20485328	We also observed two SNPs associated with <b>alcohol</b> dependence, that is, rs615470 in <strong>CHRNA5</strong> (OR=0.77, P=0.0006) and rs578776 (OR=0.78, P=0.001).
+CHRNA5	addiction	dependence	20485328	We also observed two SNPs associated with alcohol <b>dependence</b>, that is, rs615470 in <strong>CHRNA5</strong> (OR=0.77, P=0.0006) and rs578776 (OR=0.78, P=0.001).
+CHRNA5	drug	alcohol	20438829	Low <b>ethanol</b> concentration alters <strong>CHRNA5</strong> RNA levels during early human development.
+CHRNA5	drug	alcohol	20438829	Substance addiction, which includes <b>alcohol</b>, has been shown to involve the major nicotinic acetylcholine receptor subunit <strong>CHRNA5</strong>.
+CHRNA5	addiction	addiction	20438829	Substance <b>addiction</b>, which includes alcohol, has been shown to involve the major nicotinic acetylcholine receptor subunit <strong>CHRNA5</strong>.
+CHRNA5	drug	alcohol	20438829	Using human embryonic stem cells as a model of early human development, we show that low concentrations of <b>ethanol</b> (20mM) can alter the expression of <strong>CHRNA5</strong>.
+CHRNA5	drug	nicotine	20393456	Recent human genetic studies also imply that <b>tobacco</b> dependence is affected by polymorphisms in the alpha3/alpha5 subunits of the nAChR (CHRNA3/<strong>CHRNA5</strong>) gene cluster.
+CHRNA5	addiction	dependence	20393456	Recent human genetic studies also imply that tobacco <b>dependence</b> is affected by polymorphisms in the alpha3/alpha5 subunits of the nAChR (CHRNA3/<strong>CHRNA5</strong>) gene cluster.
+CHRNA5	drug	nicotine	20124469	Genome wide association studies have implicated the nAChR gene cluster, <strong>CHRNA5</strong>/A3/B4, in <b>nicotine</b> addiction and lung cancer susceptibility.
+CHRNA5	addiction	addiction	20124469	Genome wide association studies have implicated the nAChR gene cluster, <strong>CHRNA5</strong>/A3/B4, in nicotine <b>addiction</b> and lung cancer susceptibility.
+CHRNA5	drug	nicotine	19859904	Association and interaction analysis of variants in <strong>CHRNA5</strong>/CHRNA3/CHRNB4 gene cluster with <b>nicotine</b> dependence in African and European Americans.
+CHRNA5	addiction	dependence	19859904	Association and interaction analysis of variants in <strong>CHRNA5</strong>/CHRNA3/CHRNB4 gene cluster with nicotine <b>dependence</b> in African and European Americans.
+CHRNA5	drug	nicotine	19859904	Several previous genome wide and targeted association studies revealed that variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 (<strong>CHRNA5</strong>/A3/B4) gene cluster on chromosome 15 that encode the alpha5, alpha3, and beta4 subunits of the nicotinic acetylcholine receptors (nAChRs) are associated with <b>nicotine</b> dependence (ND) in European Americans (EAs) or others of European origin.
+CHRNA5	addiction	dependence	19859904	Several previous genome wide and targeted association studies revealed that variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 (<strong>CHRNA5</strong>/A3/B4) gene cluster on chromosome 15 that encode the alpha5, alpha3, and beta4 subunits of the nicotinic acetylcholine receptors (nAChRs) are associated with nicotine <b>dependence</b> (ND) in European Americans (EAs) or others of European origin.
+CHRNA5	drug	nicotine	19859904	We performed a comprehensive association and interaction analysis of the <strong>CHRNA5</strong>/A3/B4 cluster in two ethnic samples to investigate the role of variants in the risk for ND, which was assessed by <b>Smoking</b> Quantity, Heaviness <b>Smoking</b> Index, and Fagerström test for ND.
+CHRNA5	drug	nicotine	19706762	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 nicotinic receptor subunit gene cluster affects risk for <b>nicotine</b> dependence in African Americans and in European Americans.
+CHRNA5	addiction	dependence	19706762	The <strong>CHRNA5</strong> CHRNA3 CHRNB4 nicotinic receptor subunit gene cluster affects risk for nicotine <b>dependence</b> in African Americans and in European Americans.
+CHRNA5	drug	nicotine	19706762	Genetic association studies have shown the importance of variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cholinergic nicotinic receptor subunit gene cluster on chromosome 15q24 25.1 for the risk of <b>nicotine</b> dependence, <b>smoking</b>, and lung cancer in populations of European descent.
+CHRNA5	addiction	dependence	19706762	Genetic association studies have shown the importance of variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cholinergic nicotinic receptor subunit gene cluster on chromosome 15q24 25.1 for the risk of nicotine <b>dependence</b>, smoking, and lung cancer in populations of European descent.
+CHRNA5	drug	nicotine	19706762	The nonsynonymous <strong>CHRNA5</strong> SNP rs16969968 is the most significant SNP associated with <b>nicotine</b> dependence in the full sample of 2,772 subjects [P = 4.49 x 10( 8); odds ratio (OR), 1.42; 95% confidence interval (CI), 1.25 1.61] as well as in African Americans only (P = 0.015; OR, 2.04; 1.15 3.62) and in European Americans only (P = 4.14 x 10( 7); OR, 1.40; 1.23 1.59).
+CHRNA5	addiction	dependence	19706762	The nonsynonymous <strong>CHRNA5</strong> SNP rs16969968 is the most significant SNP associated with nicotine <b>dependence</b> in the full sample of 2,772 subjects [P = 4.49 x 10( 8); odds ratio (OR), 1.42; 95% confidence interval (CI), 1.25 1.61] as well as in African Americans only (P = 0.015; OR, 2.04; 1.15 3.62) and in European Americans only (P = 4.14 x 10( 7); OR, 1.40; 1.23 1.59).
+CHRNA5	drug	nicotine	19706762	Other SNPs that have been shown to affect the mRNA levels of <strong>CHRNA5</strong> in European Americans are associated with <b>nicotine</b> dependence in African Americans but not in European Americans.
+CHRNA5	addiction	dependence	19706762	Other SNPs that have been shown to affect the mRNA levels of <strong>CHRNA5</strong> in European Americans are associated with nicotine <b>dependence</b> in African Americans but not in European Americans.
+CHRNA5	drug	nicotine	19706762	In summary, multiple variants in this gene cluster contribute to <b>nicotine</b> dependence risk, and some are also associated with functional effects on <strong>CHRNA5</strong>.
+CHRNA5	addiction	dependence	19706762	In summary, multiple variants in this gene cluster contribute to nicotine <b>dependence</b> risk, and some are also associated with functional effects on <strong>CHRNA5</strong>.
+CHRNA5	drug	nicotine	19696770	Role of genetic variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster in <b>nicotine</b> dependence risk: importance of gene environment interplay.
+CHRNA5	addiction	dependence	19696770	Role of genetic variants in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 cluster in nicotine <b>dependence</b> risk: importance of gene environment interplay.
+CHRNA5	drug	nicotine	19641473	These findings suggest that SNPs in the CHRNA3 and <strong>CHRNA5</strong> region contribute to lung cancer risk, and while variant alleles are less frequent in African Americans, risk in this group may be greater than in whites and less likely to reflect an indirect effect on lung cancer risk through <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	19641473	These findings suggest that SNPs in the CHRNA3 and <strong>CHRNA5</strong> region contribute to lung cancer risk, and while variant alleles are less frequent in African Americans, risk in this group may be greater than in whites and less likely to reflect an indirect effect on lung cancer risk through nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	19628476	A cluster of three nicotinic acetylcholine receptor genes on chromosome 15 (<strong>CHRNA5</strong>/CHRNA3/CHRNB4) has been shown to be associated with <b>nicotine</b> dependence and <b>smoking</b> quantity.
+CHRNA5	addiction	dependence	19628476	A cluster of three nicotinic acetylcholine receptor genes on chromosome 15 (<strong>CHRNA5</strong>/CHRNA3/CHRNB4) has been shown to be associated with nicotine <b>dependence</b> and smoking quantity.
+CHRNA5	drug	nicotine	19628476	Variation at <strong>CHRNA5</strong>/CHRNA3/CHRNB4 cluster influences <b>nicotine</b> level, measured as cotinine, more strongly than <b>smoking</b> quantity, measured by CPD, and appears thus to be involved in regulation of <b>nicotine</b> levels among <b>smokers</b>.
+CHRNA5	addiction	relapse	19482438	There were possible associations between the temperament trait novelty <b>seeking</b> and CHRNA4 rs1044396, <strong>CHRNA5</strong> rs16969968 and CHRNB2 rs4845378, but these associations were not robust to correction for multiple testing.
+CHRNA5	drug	nicotine	19482438	We conclude that the analysis of polymorphisms in genes coding for four nicotinic acetylcholine receptor subunits (CHRNA4, <strong>CHRNA5</strong>, CHRNB2 and CHRNB3) and several <b>smoking</b> related phenotypes revealed no statistically significant association.
+CHRNA5	drug	nicotine	19443489	Risk for <b>nicotine</b> dependence and lung cancer is conferred by mRNA expression levels and amino acid change in <strong>CHRNA5</strong>.
+CHRNA5	addiction	dependence	19443489	Risk for nicotine <b>dependence</b> and lung cancer is conferred by mRNA expression levels and amino acid change in <strong>CHRNA5</strong>.
+CHRNA5	drug	nicotine	19443489	<b>Nicotine</b> dependence risk and lung cancer risk are associated with variants in a region of chromosome 15 encompassing genes encoding the nicotinic receptor subunits <strong>CHRNA5</strong>, CHRNA3 and CHRNB4.
+CHRNA5	addiction	dependence	19443489	Nicotine <b>dependence</b> risk and lung cancer risk are associated with variants in a region of chromosome 15 encompassing genes encoding the nicotinic receptor subunits <strong>CHRNA5</strong>, CHRNA3 and CHRNB4.
+CHRNA5	drug	nicotine	19443489	Using gene expression and disease association studies, we provide evidence that both <b>nicotine</b> dependence risk and lung cancer risk are influenced by functional variation in <strong>CHRNA5</strong>.
+CHRNA5	addiction	dependence	19443489	Using gene expression and disease association studies, we provide evidence that both nicotine <b>dependence</b> risk and lung cancer risk are influenced by functional variation in <strong>CHRNA5</strong>.
+CHRNA5	drug	nicotine	19443489	When the non risk allele occurs on the background of low mRNA expression of <strong>CHRNA5</strong>, the risk for <b>nicotine</b> dependence and lung cancer is significantly lower compared to those with the higher mRNA expression.
+CHRNA5	addiction	dependence	19443489	When the non risk allele occurs on the background of low mRNA expression of <strong>CHRNA5</strong>, the risk for nicotine <b>dependence</b> and lung cancer is significantly lower compared to those with the higher mRNA expression.
+CHRNA5	drug	nicotine	19443489	We conclude that there are at least two distinct mechanisms conferring risk for <b>nicotine</b> dependence and lung cancer: altered receptor function caused by a D398N amino acid variant in <strong>CHRNA5</strong> (rs16969968) and variability in <strong>CHRNA5</strong> mRNA expression.
+CHRNA5	addiction	dependence	19443489	We conclude that there are at least two distinct mechanisms conferring risk for nicotine <b>dependence</b> and lung cancer: altered receptor function caused by a D398N amino acid variant in <strong>CHRNA5</strong> (rs16969968) and variability in <strong>CHRNA5</strong> mRNA expression.
+CHRNA5	drug	nicotine	19436041	Previous research revealed significant associations between haplotypes in the <strong>CHRNA5</strong> A3 B4 subunit cluster and scores on the Fagerström Test for <b>Nicotine</b> Dependence among individuals reporting daily <b>smoking</b> by age 17.
+CHRNA5	addiction	dependence	19436041	Previous research revealed significant associations between haplotypes in the <strong>CHRNA5</strong> A3 B4 subunit cluster and scores on the Fagerström Test for Nicotine <b>Dependence</b> among individuals reporting daily smoking by age 17.
+CHRNA5	drug	nicotine	19436041	The present study used subsamples of participants from that study to investigate associations between the <strong>CHRNA5</strong> A3 B4 haplotypes and an array of phenotypes not analyzed previously (i.e., withdrawal severity, ability to stop <b>smoking</b>, and specific scales on the Wisconsin Inventory of <b>Smoking</b> Dependence Motives (WISDM 68) that reflect loss of control, strong craving, and heavy <b>smoking</b>.
+CHRNA5	addiction	dependence	19436041	The present study used subsamples of participants from that study to investigate associations between the <strong>CHRNA5</strong> A3 B4 haplotypes and an array of phenotypes not analyzed previously (i.e., withdrawal severity, ability to stop smoking, and specific scales on the Wisconsin Inventory of Smoking <b>Dependence</b> Motives (WISDM 68) that reflect loss of control, strong craving, and heavy smoking.
+CHRNA5	addiction	relapse	19436041	The present study used subsamples of participants from that study to investigate associations between the <strong>CHRNA5</strong> A3 B4 haplotypes and an array of phenotypes not analyzed previously (i.e., withdrawal severity, ability to stop smoking, and specific scales on the Wisconsin Inventory of Smoking Dependence Motives (WISDM 68) that reflect loss of control, strong <b>craving</b>, and heavy smoking.
+CHRNA5	addiction	withdrawal	19436041	The present study used subsamples of participants from that study to investigate associations between the <strong>CHRNA5</strong> A3 B4 haplotypes and an array of phenotypes not analyzed previously (i.e., <b>withdrawal</b> severity, ability to stop smoking, and specific scales on the Wisconsin Inventory of Smoking Dependence Motives (WISDM 68) that reflect loss of control, strong craving, and heavy smoking.
+CHRNA5	drug	nicotine	19436041	The <strong>CHRNA5</strong> A3 B4 haplotypes were significantly associated with the targeted WISDM 68 scales (Tolerance, Craving, Loss of Control) in both samples of participants but only among individuals who began <b>smoking</b> early in life.
+CHRNA5	addiction	relapse	19436041	The <strong>CHRNA5</strong> A3 B4 haplotypes were significantly associated with the targeted WISDM 68 scales (Tolerance, <b>Craving</b>, Loss of Control) in both samples of participants but only among individuals who began smoking early in life.
+CHRNA5	drug	nicotine	19436041	The <strong>CHRNA5</strong> A3 B4 haplotypes are associated with a broad range of <b>nicotine</b> dependence phenotypes, but these associations are not consistently moderated by age at initial <b>smoking</b>.
+CHRNA5	addiction	dependence	19436041	The <strong>CHRNA5</strong> A3 B4 haplotypes are associated with a broad range of nicotine <b>dependence</b> phenotypes, but these associations are not consistently moderated by age at initial smoking.
+CHRNA5	drug	nicotine	19429911	A common genetic variant in the 15q24 nicotinic acetylcholine receptor gene cluster (<strong>CHRNA5</strong> CHRNA3 CHRNB4) is associated with a reduced ability of women to quit <b>smoking</b> in pregnancy.
+CHRNA5	drug	nicotine	19429911	A recent genome wide association study demonstrated an association between a common polymorphism (rs1051730) in the nicotinic acetylcholine receptor gene cluster (<strong>CHRNA5</strong> CHRNA3 CHRNB4) and both <b>smoking</b> quantity and <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	19429911	A recent genome wide association study demonstrated an association between a common polymorphism (rs1051730) in the nicotinic acetylcholine receptor gene cluster (<strong>CHRNA5</strong> CHRNA3 CHRNB4) and both smoking quantity and nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	19247474	In the chr15q25.1 region spanning the nicotinic receptors CHRNA3 and <strong>CHRNA5</strong>, we identified multiple SNPs associated with CPD (p<10( 3)), including rs1051730, which has been associated with <b>nicotine</b> dependence, <b>smoking</b> intensity and lung cancer risk.
+CHRNA5	addiction	dependence	19247474	In the chr15q25.1 region spanning the nicotinic receptors CHRNA3 and <strong>CHRNA5</strong>, we identified multiple SNPs associated with CPD (p<10( 3)), including rs1051730, which has been associated with nicotine <b>dependence</b>, smoking intensity and lung cancer risk.
+CHRNA5	drug	nicotine	19247474	Besides CHRNA3 and <strong>CHRNA5</strong>, MAOA was associated with CPDBI (gene level p<5.4x10( 5)), our analysis provides independent replication of the association between the chr15q25.1 region and <b>smoking</b> intensity and data for multiple other loci associated with <b>smoking</b> behavior that merit further follow up.
+CHRNA5	drug	nicotine	19064933	Genetic association studies indicate that a genetic locus, which includes the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, plays a role in <b>nicotine</b> consumption and dependence.
+CHRNA5	addiction	dependence	19064933	Genetic association studies indicate that a genetic locus, which includes the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster, plays a role in nicotine consumption and <b>dependence</b>.
+CHRNA5	drug	nicotine	19029397	Compared with the most common allele, two separate groups of single nucleotide polymorphisms (SNP) in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster were associated with heavy <b>smoking</b> with a very high statistical significance.
+CHRNA5	drug	nicotine	19029397	One group of eight SNPs, which included a nonsynonymous SNP in the <strong>CHRNA5</strong> gene, was in strong linkage disequilibrium and associated with increased risk of heavy <b>smoking</b>.
+CHRNA5	drug	nicotine	19029397	Our findings identify two loci in the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster that predict <b>smoking</b> behavior and provide strong evidence for the involvement of the alpha5 nicotinic receptor in heavy <b>smoking</b>.
+CHRNA5	drug	nicotine	19010884	A locus at 15q24/15q25.1, which includes the nicotinic acetylcholine receptor A subunits 3 and 5 (CHRNA3 and <strong>CHRNA5</strong>) genes, has recently been associated with lung cancer risk, self reported number of cigarettes smoked per day, and a <b>nicotine</b> dependence scale.
+CHRNA5	addiction	dependence	19010884	A locus at 15q24/15q25.1, which includes the nicotinic acetylcholine receptor A subunits 3 and 5 (CHRNA3 and <strong>CHRNA5</strong>) genes, has recently been associated with lung cancer risk, self reported number of cigarettes smoked per day, and a nicotine <b>dependence</b> scale.
+CHRNA5	drug	nicotine	19010884	We used urinary biomarkers to test whether two linked lung cancer risk variants in CHRNA3 (rs1051730) and <strong>CHRNA5</strong> (rs16969968) are associated with intensity of <b>smoking</b> and exposure to a <b>tobacco</b> specific carcinogenic nitrosamine per cigarette dose.
+CHRNA5	drug	nicotine	19010884	Thus, <b>smokers</b> who carry the CHRNA3 and <strong>CHRNA5</strong> variants are expected to be at increased risk for lung cancer compared with <b>smokers</b> who do not carry these alleles even if they smoked the same number of cigarettes.
+CHRNA5	drug	nicotine	18957677	The <strong>CHRNA5</strong> A3 region on chromosome 15q24 25.1 is a risk factor both for <b>nicotine</b> dependence and for lung cancer.
+CHRNA5	addiction	dependence	18957677	The <strong>CHRNA5</strong> A3 region on chromosome 15q24 25.1 is a risk factor both for nicotine <b>dependence</b> and for lung cancer.
+CHRNA5	drug	nicotine	18957674	Intermediacy and gene environment interaction: the example of <strong>CHRNA5</strong> A3 region, <b>smoking</b>, <b>nicotine</b> dependence, and lung cancer.
+CHRNA5	addiction	dependence	18957674	Intermediacy and gene environment interaction: the example of <strong>CHRNA5</strong> A3 region, smoking, nicotine <b>dependence</b>, and lung cancer.
+CHRNA5	drug	nicotine	18783506	Association of a single nucleotide polymorphism in neuronal acetylcholine receptor subunit alpha 5 (<strong>CHRNA5</strong>) with <b>smoking</b> status and with 'pleasurable buzz' during early experimentation with <b>smoking</b>.
+CHRNA5	drug	nicotine	18783506	To extend the previously identified association between a single nucleotide polymorphism (SNP) in neuronal acetylcholine receptor subunit alpha 5 (<strong>CHRNA5</strong>) and <b>nicotine</b> dependence to current <b>smoking</b> and initial <b>smoking</b> experience phenotypes.
+CHRNA5	addiction	dependence	18783506	To extend the previously identified association between a single nucleotide polymorphism (SNP) in neuronal acetylcholine receptor subunit alpha 5 (<strong>CHRNA5</strong>) and nicotine <b>dependence</b> to current smoking and initial smoking experience phenotypes.
+CHRNA5	drug	nicotine	18783506	A non synonymous coding SNP in <strong>CHRNA5</strong>, rs16969968, was associated with case status [odds ratio (OR) = 1.5, P = 0.01] and, in Caucasians, with experiencing a pleasurable rush or buzz during the first cigarette (OR = 1.6, P = 0.01); these sensations were associated highly with current <b>smoking</b> (OR = 8.2, P = 0.0001).
+CHRNA5	drug	nicotine	18783506	While the ability to test genetic associations was limited by sample size, the polymorphism in the <strong>CHRNA5</strong> subunit was shown to be associated significantly with enhanced pleasurable responses to initial cigarettes in regular <b>smokers</b> in an a priori test.
+CHRNA5	drug	cocaine	18759969	We applied this method to correlated SNPs in the cholinergic nicotinic receptor gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4, in a case control study of <b>cocaine</b> dependence composed of 504 European American and 583 African American samples.
+CHRNA5	addiction	dependence	18759969	We applied this method to correlated SNPs in the cholinergic nicotinic receptor gene cluster <strong>CHRNA5</strong> CHRNA3 CHRNB4, in a case control study of cocaine <b>dependence</b> composed of 504 European American and 583 African American samples.
+CHRNA5	drug	nicotine	18618000	A candidate gene approach identifies the <strong>CHRNA5</strong> A3 B4 region as a risk factor for age dependent <b>nicotine</b> addiction.
+CHRNA5	addiction	addiction	18618000	A candidate gene approach identifies the <strong>CHRNA5</strong> A3 B4 region as a risk factor for age dependent nicotine <b>addiction</b>.
+CHRNA5	drug	nicotine	18618000	In the 2,827 long term <b>smokers</b> examined, common susceptibility and protective haplotypes at the <strong>CHRNA5</strong> A3 B4 locus were associated with <b>nicotine</b> dependence severity (p = 2.0x10( 5); odds ratio = 1.82; 95% confidence interval 1.39 2.39) in subjects who began daily <b>smoking</b> at or before the age of 16, an exposure period that results in a more severe form of adult <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	18618000	In the 2,827 long term smokers examined, common susceptibility and protective haplotypes at the <strong>CHRNA5</strong> A3 B4 locus were associated with nicotine <b>dependence</b> severity (p = 2.0x10( 5); odds ratio = 1.82; 95% confidence interval 1.39 2.39) in subjects who began daily smoking at or before the age of 16, an exposure period that results in a more severe form of adult nicotine <b>dependence</b>.
+CHRNA5	drug	nicotine	18618000	These results establish a strong mechanistic link among early <b>nicotine</b> exposure, common <strong>CHRNA5</strong> A3 B4 haplotypes, and adult <b>nicotine</b> addiction in three independent populations of European origins.
+CHRNA5	addiction	addiction	18618000	These results establish a strong mechanistic link among early nicotine exposure, common <strong>CHRNA5</strong> A3 B4 haplotypes, and adult nicotine <b>addiction</b> in three independent populations of European origins.
+CHRNA5	drug	nicotine	18519524	A recent study provisionally identified numerous genetic variants as risk factors for the transition from <b>smoking</b> to the development of <b>nicotine</b> dependence, including an amino acid change in the alpha5 nicotinic cholinergic receptor (<strong>CHRNA5</strong>).
+CHRNA5	addiction	dependence	18519524	A recent study provisionally identified numerous genetic variants as risk factors for the transition from smoking to the development of nicotine <b>dependence</b>, including an amino acid change in the alpha5 nicotinic cholinergic receptor (<strong>CHRNA5</strong>).
+CHRNA5	drug	nicotine	18519524	The purpose of this study was to replicate these findings in an independent data set and more thoroughly investigate the role of genetic variation in the cluster of physically linked nicotinic receptors, <strong>CHRNA5</strong> CHRNA3 CHRNB4, and the risk of <b>smoking</b>.
+CHRNA5	drug	cocaine	18519132	A risk allele for nicotine dependence in <strong>CHRNA5</strong> is a protective allele for <b>cocaine</b> dependence.
+CHRNA5	drug	nicotine	18519132	A risk allele for <b>nicotine</b> dependence in <strong>CHRNA5</strong> is a protective allele for cocaine dependence.
+CHRNA5	addiction	dependence	18519132	A risk allele for nicotine <b>dependence</b> in <strong>CHRNA5</strong> is a protective allele for cocaine <b>dependence</b>.
+CHRNA5	drug	nicotine	18519132	A nonsynonymous coding polymorphism, rs16969968, of the <strong>CHRNA5</strong> gene that encodes the alpha 5 subunit of the nicotinic acetylcholine receptor (nAChR) has been found to be associated with <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	18519132	A nonsynonymous coding polymorphism, rs16969968, of the <strong>CHRNA5</strong> gene that encodes the alpha 5 subunit of the nicotinic acetylcholine receptor (nAChR) has been found to be associated with nicotine <b>dependence</b>.
+CHRNA5	drug	cocaine	18519132	In the FSCD, there was a significant association between the <strong>CHRNA5</strong> variant and <b>cocaine</b> dependence (odds ratio = .67 per allele, p = .0045, assuming an additive genetic model), but in the reverse direction compared with that previously observed for nicotine dependence.
+CHRNA5	drug	nicotine	18519132	In the FSCD, there was a significant association between the <strong>CHRNA5</strong> variant and cocaine dependence (odds ratio = .67 per allele, p = .0045, assuming an additive genetic model), but in the reverse direction compared with that previously observed for <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	18519132	In the FSCD, there was a significant association between the <strong>CHRNA5</strong> variant and cocaine <b>dependence</b> (odds ratio = .67 per allele, p = .0045, assuming an additive genetic model), but in the reverse direction compared with that previously observed for nicotine <b>dependence</b>.
+CHRNA5	drug	alcohol	18414406	Genetic variation in the <strong>CHRNA5</strong> gene affects mRNA levels and is associated with risk for <b>alcohol</b> dependence.
+CHRNA5	addiction	dependence	18414406	Genetic variation in the <strong>CHRNA5</strong> gene affects mRNA levels and is associated with risk for alcohol <b>dependence</b>.
+CHRNA5	drug	nicotine	18414406	Recently a candidate gene study in <b>nicotine</b> dependent cases and nondependent <b>smoking</b> controls reported strong associations between a missense mutation (rs16969968) in exon 5 of the <strong>CHRNA5</strong> gene and a variant in the 3' UTR of the CHRNA3 gene and <b>nicotine</b> dependence.
+CHRNA5	addiction	dependence	18414406	Recently a candidate gene study in nicotine dependent cases and nondependent smoking controls reported strong associations between a missense mutation (rs16969968) in exon 5 of the <strong>CHRNA5</strong> gene and a variant in the 3' UTR of the CHRNA3 gene and nicotine <b>dependence</b>.
+CHRNA5	drug	alcohol	18414406	In this study we performed a comprehensive association analysis of the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster in the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) families to investigate the role of genetic variants in risk for <b>alcohol</b> dependence.
+CHRNA5	addiction	dependence	18414406	In this study we performed a comprehensive association analysis of the <strong>CHRNA5</strong> CHRNA3 CHRNB4 gene cluster in the Collaborative Study on the Genetics of Alcoholism (COGA) families to investigate the role of genetic variants in risk for alcohol <b>dependence</b>.
+CHRNA5	drug	alcohol	18414406	Using the family based association test, we observed that a different group of polymorphisms, spanning <strong>CHRNA5</strong> CHRNA3, demonstrate association with <b>alcohol</b> dependence defined by Diagnostic and Statistical Manual of Mental Disorders, 4th edn (DSM IV) criteria.
+CHRNA5	addiction	dependence	18414406	Using the family based association test, we observed that a different group of polymorphisms, spanning <strong>CHRNA5</strong> CHRNA3, demonstrate association with alcohol <b>dependence</b> defined by Diagnostic and Statistical Manual of Mental Disorders, 4th edn (DSM IV) criteria.
+CHRNA5	drug	alcohol	18414406	Functional studies in human brain reveal that the variants associated with <b>alcohol</b> dependence are also associated with altered steady state levels of <strong>CHRNA5</strong> mRNA.
+CHRNA5	addiction	dependence	18414406	Functional studies in human brain reveal that the variants associated with alcohol <b>dependence</b> are also associated with altered steady state levels of <strong>CHRNA5</strong> mRNA.
+CHRNA5	drug	nicotine	16314871	For severity of <b>nicotine</b> dependence, two SNPs in CHRNA7 (rs1909884 and rs883473), one SNP in <strong>CHRNA5</strong> (rs680244) and the interaction of a SNP in CHRNA7 (rs2337980) with neuroticism, were included in the model (P=2.24 x 10( 7), Nagelkerke r(2)=0.40).
+CHRNA5	addiction	dependence	16314871	For severity of nicotine <b>dependence</b>, two SNPs in CHRNA7 (rs1909884 and rs883473), one SNP in <strong>CHRNA5</strong> (rs680244) and the interaction of a SNP in CHRNA7 (rs2337980) with neuroticism, were included in the model (P=2.24 x 10( 7), Nagelkerke r(2)=0.40).
+COMT	drug	amphetamine	32739643	<strong>COMT</strong> val158met genotype alters the effects of <b>methamphetamine</b> dependence on dopamine and dopamine related executive function: preliminary findings.
+COMT	addiction	dependence	32739643	<strong>COMT</strong> val158met genotype alters the effects of methamphetamine <b>dependence</b> on dopamine and dopamine related executive function: preliminary findings.
+COMT	drug	amphetamine	32739643	Met carriers may be disproportionately vulnerable to <b>METH</b> related perturbations of DA, yet it is unknown whether <strong>COMT</strong> modulates <b>METH</b> effects on CSF DA biomarkers.
+COMT	drug	amphetamine	32739643	Participants were 75 <b>METH</b>+ and 47 <b>METH</b>  men who underwent neurocognitive testing, <strong>COMT</strong> genotyping, and lumbar puncture.
+COMT	drug	amphetamine	32739643	Separate linear models regressed DA, HVA, and HVA/DA ratios on <strong>COMT</strong>, <b>METH</b> and their interaction.
+COMT	drug	alcohol	32617646	The <strong>catechol O methyltransferase</strong> inhibitor tolcapone modulates <b>alcohol</b> consumption and impulsive choice in <b>alcohol</b> use disorder.
+COMT	drug	alcohol	32617646	To determine if the catechol O methyltransferase (<strong>COMT</strong>) inhibitor tolcapone can attenuate <b>alcohol</b> consumption in individuals with AUD and whether this attenuation correlates with tolcapone induced changes in laboratory based decision making tasks.
+COMT	drug	alcohol	32617646	To determine if the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) inhibitor tolcapone can attenuate <b>alcohol</b> consumption in individuals with AUD and whether this attenuation correlates with tolcapone induced changes in laboratory based decision making tasks.
+COMT	drug	cannabinoid	32398646	Do AKT1, <strong>COMT</strong> and FAAH influence reports of acute <b>cannabis</b> intoxication experiences in patients with first episode psychosis, controls and young adult <b>cannabis</b> users?
+COMT	addiction	intoxication	32398646	Do AKT1, <strong>COMT</strong> and FAAH influence reports of acute cannabis <b>intoxication</b> experiences in patients with first episode psychosis, controls and young adult cannabis users?
+COMT	drug	cannabinoid	32398646	We aimed to determine how variation in AKT1, <strong>COMT</strong> and FAAH genotypes, and their interaction with three different groups (first episode psychosis (FEP) patients (n = 143), controls (n = 92) and young adult (YA) <b>cannabis</b> users n = 485)) influenced <b>cannabis</b> experiences, in those who had used <b>cannabis</b> at least once.
+COMT	drug	cannabinoid	32398646	We investigated the role of AKT1 (rs2494732), <strong>COMT</strong> Val158Met (rs4680) and FAAH (rs324420) on <b>cannabis</b> experiences by combining data from a large case control study of FEP patients, with a naturalistic study of YA <b>cannabis</b> users (n = 720).
+COMT	drug	cannabinoid	32398646	In conclusion, AKT1, <strong>COMT</strong> or FAAH did not modulate specific psychotomimetic response to <b>cannabis</b> and did not interact with group, contrary to previous research.
+COMT	drug	alcohol	32329706	Specific polymorphisms in genes encoding for interleukins 2 and 6, catechol O methyl transferase (<strong>COMT</strong>), monaminooxidase B (MAO B) and several other enzymes were identified as associated with altered risks of <b>alcoholism</b> in humans.
+COMT	addiction	withdrawal	32133633	Hispidulin attenuated social <b>withdrawal</b> by activating D1 receptors indirectly through elevated dopamine levels in the PFC by <strong>COMT</strong> inhibition.
+COMT	drug	amphetamine	31822818	<b>Meth</b> differentially altered dopamine signaling markers (e.g., Dat, <strong>Comt</strong>, and Th) between hBDNFVal/Val and hBDNFMet/Met mice, implicating involvement of BDNF in <b>Meth</b> induced reprogramming of the mesolimbic proteome.
+COMT	drug	amphetamine	31301644	Adverse effect of catechol O methyltransferase (<strong>COMT</strong>) Val158Met met/met genotype in <b>methamphetamine</b> related executive dysfunction.
+COMT	drug	amphetamine	31301644	Adverse effect of <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met met/met genotype in <b>methamphetamine</b> related executive dysfunction.
+COMT	drug	amphetamine	31301644	149 non Hispanic White men, stratified by <b>METH</b> dependence (<b>METH</b>+/ ) and <strong>COMT</strong> (Val/Val, Val/Met, Met/Met), completed three tests of EF: Wisconsin Card Sorting Test (WCST), Stroop Color Word Test (Stroop), and Trail Making Test Part B (Trails B).
+COMT	addiction	dependence	31301644	149 non Hispanic White men, stratified by METH <b>dependence</b> (METH+/ ) and <strong>COMT</strong> (Val/Val, Val/Met, Met/Met), completed three tests of EF: Wisconsin Card Sorting Test (WCST), Stroop Color Word Test (Stroop), and Trail Making Test Part B (Trails B).
+COMT	drug	alcohol	31301644	We examined the interaction of METH and <strong>COMT</strong> on the EF composite and individual test T scores, controlling for premorbid functioning and <b>alcohol</b> use.
+COMT	drug	amphetamine	31301644	We examined the interaction of <b>METH</b> and <strong>COMT</strong> on the EF composite and individual test T scores, controlling for premorbid functioning and alcohol use.
+COMT	drug	opioid	31192519	Substance use, DD, and genotype data (DRD1 rs686 and rs5326, DRD3 rs6280, <strong>COMT</strong> rs4680) were obtained from 106 current <b>heroin</b> users.
+COMT	drug	alcohol	30406194	<strong>COMT</strong> Inhibition Alters Cue Evoked Oscillatory Dynamics during <b>Alcohol</b> Drinking in the Rat.
+COMT	addiction	reward	30406194	Moreover, inhibition of <strong>COMT</strong> within these systems may result in reduced attribution of salience to <b>reward</b> paired stimuli via modulation of stimulus evoked changes to cortical oscillations in genetically susceptible populations.
+COMT	drug	alcohol	30027496	The degree of this improvement positively correlated with subjective measures of stress, depression, and <b>alcohol</b> consumption and was most robust in carriers of the <strong>COMT</strong> Val158 allele.
+COMT	addiction	addiction	30027496	Additional studies should be conducted to determine whether <strong>COMT</strong> inhibitors may be effective in treating decision making disorders and <b>addictive</b> behaviors.
+COMT	drug	alcohol	29684863	After adjustment for covariates, age, <b>alcohol</b> consumption, and the rs4680 AA genotype in the <strong>COMT</strong> gene were associated with suicide attempt.
+COMT	drug	alcohol	29684863	Suicidal behavior in Korean patients with mood disorders may be associated with younger age, <b>alcohol</b> consumption, depressive symptoms, poor social support, less social support seeking coping, and the <strong>COMT</strong> rs4680 Met/Met genotype.
+COMT	addiction	relapse	29684863	Suicidal behavior in Korean patients with mood disorders may be associated with younger age, alcohol consumption, depressive symptoms, poor social support, less social support <b>seeking</b> coping, and the <strong>COMT</strong> rs4680 Met/Met genotype.
+COMT	drug	amphetamine	29383398	In the heart, <b>METH</b> administration induced an increase in soluble (S) <strong>COMT</strong> and membrane bound (MB) <strong>COMT</strong> without changes in phospho (p) TH, Hsp27, or pHsp27.
+COMT	drug	amphetamine	29383398	Similarly, <b>METH</b> withdrawal increased the expression of S  and MB <strong>COMT</strong>.
+COMT	addiction	withdrawal	29383398	Similarly, METH <b>withdrawal</b> increased the expression of S  and MB <strong>COMT</strong>.
+COMT	drug	opioid	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, <strong>COMT</strong>, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+COMT	addiction	dependence	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, <strong>COMT</strong>, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+COMT	drug	opioid	29333880	When the most significant variants associated with dropout rate were analyzed using pairwise analyses, SLC6A4 (5 HTTLPR) and <strong>COMT</strong> (Val158Met; rs4860) had nominally significant associations with dropout rate in <b>methadone</b> patients.
+COMT	addiction	addiction	29333880	Patients with the S/S genotype at 5 HTTLPR in SLC6A4 or the Val/Val genotype at Val158Met in <strong>COMT</strong> may require additional treatment to improve their chances of completing <b>addiction</b> treatment.
+COMT	drug	alcohol	29310047	Differential <strong>COMT</strong> expression and behavioral effects of <strong>COMT</strong> inhibition in male and female Wistar and <b>alcohol</b> preferring rats.
+COMT	drug	alcohol	29310047	Polymorphisms of the catechol O methyl transferase (<strong>COMT</strong>) gene have been associated with <b>alcoholism</b>, suggesting that alterations in the metabolism of catecholamines may be a critical component of the neuropathology of <b>alcoholism</b>.
+COMT	drug	alcohol	29310047	In the current experiments, the <strong>COMT</strong> inhibitor tolcapone was utilized in an operant behavioral model of reinforcer seeking and drinking to determine if this compound was capable of remediating the excessive seeking and drinking phenotype of the <b>alcohol</b> preferring P rat.
+COMT	addiction	relapse	29310047	In the current experiments, the <strong>COMT</strong> inhibitor tolcapone was utilized in an operant behavioral model of reinforcer <b>seeking</b> and drinking to determine if this compound was capable of remediating the excessive <b>seeking</b> and drinking phenotype of the alcohol preferring P rat.
+COMT	addiction	reward	29310047	In the current experiments, the <strong>COMT</strong> inhibitor tolcapone was utilized in an <b>operant</b> behavioral model of reinforcer seeking and drinking to determine if this compound was capable of remediating the excessive seeking and drinking phenotype of the alcohol preferring P rat.
+COMT	addiction	addiction	29310047	These data complement our previous findings in which tolcapone reduced cue evoked responses in P rats and further suggest clinical utility of <strong>COMT</strong> inhibitors in the treatment of <b>addiction</b> disorders, specifically in male high drinkers.
+COMT	drug	opioid	29259946	Genetic Analysis of Mu and Kappa <b>Opioid</b> Receptor and <strong>COMT</strong> Enzyme in Cancer Pain Tunisian Patients Under <b>Opioid</b> Treatment.
+COMT	drug	opioid	29259946	This prospective association study investigated seven variations in the OPRM1, OPRK1 and <strong>COMT</strong> gene, which encode Mu and KAPPA <b>opioid</b> receptors, and Catechol O methyltransferase enzyme respectively, in a cohort of 129 Tunisian cancer pain patients under oral <b>morphine</b> treatment.
+COMT	drug	opioid	29259946	This prospective association study investigated seven variations in the OPRM1, OPRK1 and <strong>COMT</strong> gene, which encode Mu and KAPPA <b>opioid</b> receptors, and <strong>Catechol O methyltransferase</strong> enzyme respectively, in a cohort of 129 Tunisian cancer pain patients under oral <b>morphine</b> treatment.
+COMT	addiction	intoxication	29191570	We found that working memory, verbal and visual memory and sustained attention are more impacted during <b>intoxication</b> in subjects with the Val <strong>COMT</strong> allele.
+COMT	drug	amphetamine	29154367	Moderators predicting <b>AMPH</b> sensitivity were assessed, including the rs4680 single nucleotide polymorphism for catechol O methyltransferase (<strong>COMT</strong>).
+COMT	drug	amphetamine	29154367	Moderators predicting <b>AMPH</b> sensitivity were assessed, including the rs4680 single nucleotide polymorphism for <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>).
+COMT	drug	opioid	29055075	The aim of this study was to investigate if genetic variants of mu, kappa, and delta <b>opioid</b> receptor genes (OPRM1, OPRK1, and OPRD1) and the catechol O methyltransferase gene (<strong>COMT</strong>) influenced the pain phenotype in patients with osteoarthritis.
+COMT	drug	opioid	29055075	The aim of this study was to investigate if genetic variants of mu, kappa, and delta <b>opioid</b> receptor genes (OPRM1, OPRK1, and OPRD1) and the <strong>catechol O methyltransferase</strong> gene (<strong>COMT</strong>) influenced the pain phenotype in patients with osteoarthritis.
+COMT	drug	alcohol	28913946	Facial emotion recognition in schizophrenia: An exploratory study on the role of comorbid <b>alcohol</b> and substance use disorders and <strong>COMT</strong> Val158Met.
+COMT	drug	alcohol	28913946	To explore whether facial emotion recognition (FER), impaired in both schizophrenia and <b>alcohol</b> and substance use disorders (AUDs/SUDs), is additionally compromised among comorbid subjects, also considering the role of catechol O methyltransferase (<strong>COMT</strong>) Val158Met.
+COMT	drug	alcohol	28913946	To explore whether facial emotion recognition (FER), impaired in both schizophrenia and <b>alcohol</b> and substance use disorders (AUDs/SUDs), is additionally compromised among comorbid subjects, also considering the role of <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met.
+COMT	drug	cannabinoid	28822116	Almost consistently, these studies revealed that polymorphisms in <strong>COMT</strong>, BDNF, and FKBP5 genes might interact with early life stress and <b>cannabis</b> abuse or dependence, influencing various outcomes of schizophrenia spectrum disorders and BD.
+COMT	addiction	dependence	28822116	Almost consistently, these studies revealed that polymorphisms in <strong>COMT</strong>, BDNF, and FKBP5 genes might interact with early life stress and cannabis abuse or <b>dependence</b>, influencing various outcomes of schizophrenia spectrum disorders and BD.
+COMT	drug	alcohol	28744152	The objectives of this study were to evaluate the correlation between DRD2, SLC6A3 (DAT) and <strong>COMT</strong> genetic polymorphisms and to investigate their effect on the development of adverse drug reactions in patients with <b>alcohol</b> use disorder who received haloperidol.
+COMT	drug	alcohol	28635556	Executive control in schizophrenia: a preliminary study on the moderating role of <strong>COMT</strong> Val158Met for comorbid <b>alcohol</b> and substance use disorders.
+COMT	drug	alcohol	28635556	A functional polymorphism in the catechol O methyltransferase (<strong>COMT</strong>) gene (Val158Met) appears to influence cognition in people with <b>alcohol</b>/substance use disorders (AUD/SUD) and in those with psychosis.
+COMT	drug	alcohol	28635556	A functional polymorphism in the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene (Val158Met) appears to influence cognition in people with <b>alcohol</b>/substance use disorders (AUD/SUD) and in those with psychosis.
+COMT	drug	cannabinoid	28630452	Remote memories are enhanced by <strong>COMT</strong> activity through dysregulation of the <b>endocannabinoid</b> system in the prefrontal cortex.
+COMT	addiction	aversion	28630452	<strong>COMT</strong> selectively and reversibly modulated the recall of remote memories as silencing <strong>COMT</strong> Val overexpression starting from 30 days after the initial <b>aversive</b> conditioning normalized remote memories.
+COMT	drug	cannabinoid	28630452	<strong>COMT</strong> genetic overactivity produced a selective overdrive of the <b>endocannabinoid</b> system within the PFC, but not in the striatum and hippocampus, which was associated with enhanced remote memories.
+COMT	drug	cannabinoid	28630452	These results demonstrate that <strong>COMT</strong> genetic variations modulate the retrieval of remote memories through the dysregulation of the <b>endocannabinoid</b> system in the PFC.
+COMT	drug	nicotine	28472995	Interaction between cytochrome P450 2A6 and <strong>Catechol O Methyltransferase</strong> genes and their association with <b>smoking</b> risk in young men.
+COMT	drug	nicotine	28472995	Although some effects of gene gene interactions on <b>nicotine</b> dopamine metabolism for <b>smoking</b> behavior have been reported, polymorphisms of cytochrome P450 (CYP) 2A6 and catechol O methyltransferase (<strong>COMT</strong>) have not been studied together to determine their effects on <b>smokers</b>.
+COMT	drug	nicotine	28472995	Although some effects of gene gene interactions on <b>nicotine</b> dopamine metabolism for <b>smoking</b> behavior have been reported, polymorphisms of cytochrome P450 (CYP) 2A6 and <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) have not been studied together to determine their effects on <b>smokers</b>.
+COMT	drug	nicotine	28472995	The aim of this study was to investigate the effects of the interaction between the CYP 2A6 and <strong>COMT</strong> genes on <b>smoking</b> behavior in young Taiwanese men.
+COMT	drug	nicotine	28472995	Polymorphisms of the CYP 2A6 and <strong>COMT</strong> genes as well as urinary <b>nicotine</b> and urinary cotinine levels were determined.
+COMT	drug	nicotine	28472995	The odds ratio for starting <b>smoking</b> was significantly lower in subjects carrying a CYP2A6 low activity/variant <strong>COMT</strong> rs4680 genotype than in those possessing a CYP2A6 wild type/variant <strong>COMT</strong> rs4680 genotype (0.44, 95% confidence interval = 0.19 0.98, P = 0.043).
+COMT	drug	nicotine	28472995	Comparisons of Fagerstrom Test for <b>Nicotine</b> Dependence (FTND), Physiological Cigarette Dependence Scale (PCDS), and Cigarette Withdrawal symptoms (CWS 21) among the <b>smokers</b> with different CYP2A6/<strong>COMT</strong> polymorphisms were not significantly different.
+COMT	addiction	dependence	28472995	Comparisons of Fagerstrom Test for Nicotine <b>Dependence</b> (FTND), Physiological Cigarette <b>Dependence</b> Scale (PCDS), and Cigarette Withdrawal symptoms (CWS 21) among the smokers with different CYP2A6/<strong>COMT</strong> polymorphisms were not significantly different.
+COMT	addiction	withdrawal	28472995	Comparisons of Fagerstrom Test for Nicotine Dependence (FTND), Physiological Cigarette Dependence Scale (PCDS), and Cigarette <b>Withdrawal</b> symptoms (CWS 21) among the smokers with different CYP2A6/<strong>COMT</strong> polymorphisms were not significantly different.
+COMT	drug	nicotine	28472995	These findings suggest that a single nucleotide polymorphism (rs4680) of the <strong>COMT</strong> gene and the interaction between the CYP 2A6 and <strong>COMT</strong> genes affect <b>smoking</b> status in young Taiwanese men.
+COMT	drug	amphetamine	27987399	Association between cerebrospinal fluid dopamine concentrations and <strong>catechol O methyltransferase</strong> gene polymorphisms in forensic autopsy cases of <b>methamphetamine</b> abusers.
+COMT	addiction	intoxication	27987399	Since catechol O methyltransferase (<strong>COMT</strong>) metabolizes catecholamines and mediates adrenergic, noradrenergic, and dopaminergic signaling responses, we investigated the effects of the <strong>COMT</strong> polymorphisms rs4633 and rs4680 on cerebrospinal fluid (CSF) catecholamine concentrations in autopsies of subjects who died of drug <b>intoxication</b>.
+COMT	addiction	intoxication	27987399	Since <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) metabolizes catecholamines and mediates adrenergic, noradrenergic, and dopaminergic signaling responses, we investigated the effects of the <strong>COMT</strong> polymorphisms rs4633 and rs4680 on cerebrospinal fluid (CSF) catecholamine concentrations in autopsies of subjects who died of drug <b>intoxication</b>.
+COMT	drug	alcohol	27898499	<strong>COMT</strong> and BDNF Gene Variants Help to Predict <b>Alcohol</b> Consumption in <b>Alcohol</b> dependent Patients.
+COMT	drug	alcohol	27898499	The relationship between <b>alcohol</b> consumption and single nucleotide polymorphisms, Val66Met in the brain derived neurotrophic factor (BDNF), and Val158Met in the catechol O methyltransferase (<strong>COMT</strong>), was analyzed among 281 <b>alcohol</b> dependent individuals.
+COMT	drug	alcohol	27898499	The relationship between <b>alcohol</b> consumption and single nucleotide polymorphisms, Val66Met in the brain derived neurotrophic factor (BDNF), and Val158Met in the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>), was analyzed among 281 <b>alcohol</b> dependent individuals.
+COMT	drug	alcohol	27898499	Patients carrying both the BDNF Val66Val and <strong>COMT</strong> Met158Met variants had higher <b>alcohol</b> consumption.
+COMT	drug	alcohol	27898499	These effects may be influenced by the effects of BDNF and <strong>COMT</strong> on dopamine responses to <b>alcohol</b>.
+COMT	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of catechol O methyltransferase (<strong>COMT</strong>), dopamine receptor D2 (DRD2) gene score and <b>smoking</b> cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (ANKK1), dopamine transporter (SLC6A3), dopamine receptor D4 (DRD4) gene score and <b>smoking</b> cessation.
+COMT	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>), dopamine receptor D2 (DRD2) gene score and <b>smoking</b> cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (ANKK1), dopamine transporter (SLC6A3), dopamine receptor D4 (DRD4) gene score and <b>smoking</b> cessation.
+COMT	drug	opioid	27288213	Association of the OPRM1 and <strong>COMT</strong> genes' polymorphisms with the efficacy of <b>morphine</b> in Tunisian cancer patients: Impact of the high genetic heterogeneity in Tunisia?
+COMT	drug	opioid	27288213	The aim of the present study was to investigate the possible association of <b>opioid</b> treatment outcome with single nucleotide polymorphisms (SNPs) in the mμ <b>opioid</b> receptor (OPRM1) and catechol o methyltransferase (<strong>COMT</strong>) genes, in Tunisian cancer pain patients.
+COMT	drug	opioid	27288213	The aim of the present study was to investigate the possible association of <b>opioid</b> treatment outcome with single nucleotide polymorphisms (SNPs) in the mμ <b>opioid</b> receptor (OPRM1) and <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>) genes, in Tunisian cancer pain patients.
+COMT	drug	opioid	27288213	We genotyped one hundred and twenty nine cancer patients treated with different doses of <b>morphine</b> for 3 SNPs in OPRM1 gene (rs17174629, rs1799972 and rs1799971) and one in the <strong>COMT</strong> gene (rs4680).
+COMT	drug	opioid	27061230	The ABCB1, rs9282564, AG and TT Genotypes and the <strong>COMT</strong>, rs4680, AA Genotype are Less Frequent in Deceased Patients with <b>Opioid</b> Addiction than in Living Patients with <b>Opioid</b> Addiction.
+COMT	addiction	addiction	27061230	The ABCB1, rs9282564, AG and TT Genotypes and the <strong>COMT</strong>, rs4680, AA Genotype are Less Frequent in Deceased Patients with Opioid <b>Addiction</b> than in Living Patients with Opioid <b>Addiction</b>.
+COMT	drug	opioid	27061230	To examine whether certain genotypes were associated with this, we examined the frequencies of 29 SNPs located in candidate genes related to <b>opioid</b> pharmacology: ABCB1, OPRM1, UGT2B7, CYP3A5, CYP2B6, CYP2C19, CYP2D6, <strong>COMT</strong>, KCNJ6 and SCN9A in 274 deceased patients with OA (DOA), 309 living patients with OA (LOA) and in 394 healthy volunteers (HV).
+COMT	drug	cannabinoid	27052366	<strong>COMT</strong> Val(158)Met genotype and <b>cannabis</b> use in people with an At Risk Mental State for psychosis: Exploring Gene x Environment interactions.
+COMT	drug	cannabinoid	27052366	Epidemiological and retrospective studies suggest a <b>cannabis</b> x catechol O methyltransferase (<strong>COMT</strong>) Val(158)Met interaction effect on development of psychosis.
+COMT	drug	cannabinoid	27052366	Epidemiological and retrospective studies suggest a <b>cannabis</b> x <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val(158)Met interaction effect on development of psychosis.
+COMT	drug	cannabinoid	27052366	<b>Cannabis</b> use and <strong>COMT</strong> Val allele showed an interaction effect in ARMS subjects.
+COMT	drug	cannabinoid	27052366	Our results suggest that the <strong>COMT</strong> Val(158)Met polymorphism moderates the effect of regular <b>cannabis</b> use on severity of subclinical psychotic symptoms.
+COMT	addiction	intoxication	26950642	Epistatic interactions involving DRD2, DRD4, and <strong>COMT</strong> polymorphisms and risk of substance abuse in women with <b>binge</b> purge eating disturbances.
+COMT	addiction	intoxication	26950642	We examined the implications of variations of selected, dopamine relevant polymorphisms (DRD2 Taq1A, DRD4 7R, and <strong>COMT</strong>) for risk of substance abuse in women with <b>binge</b> purge eating syndromes.
+COMT	drug	cannabinoid	26950642	Tests for main and interaction effects of various allele combinations revealed that individuals who carried high function <strong>COMT</strong> and low function DRD4 7R alleles (a combination expected to be associated with higher risk) did indeed show more lifetime substance abuse and, specifically, more <b>cannabis</b> abuse.
+COMT	drug	opioid	26902643	We tested the association between <b>morphine</b> consumption, postoperative pain, and single nucleotide polymorphisms (SNPs) within <b>opioid</b> receptor μ 1 (OPRM1), catechol O methyltransferase (<strong>COMT</strong>), uridine diphosphate glucose glucuronosyltransferase 2B7, and estrogen receptor (ESR1) gene loci to elucidate genetic prediction of <b>opioid</b> consumption.
+COMT	drug	opioid	26902643	We tested the association between <b>morphine</b> consumption, postoperative pain, and single nucleotide polymorphisms (SNPs) within <b>opioid</b> receptor μ 1 (OPRM1), <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>), uridine diphosphate glucose glucuronosyltransferase 2B7, and estrogen receptor (ESR1) gene loci to elucidate genetic prediction of <b>opioid</b> consumption.
+COMT	drug	opioid	26902643	A haplotype of 7 SNPs in OPRM1 showed significant additive effects on <b>opioid</b> consumption (P = .007); a linear regression model including age and 9 SNPs in ESR1, OPRM1, and <strong>COMT</strong> explained the highest proportion of variance of <b>morphine</b> consumption (10.7%; P = .001).
+COMT	drug	opioid	26902643	We found a significant interaction between rs4680 in <strong>COMT</strong> and rs4986936 in ESR1 (P = .007) on <b>opioid</b> consumption.
+COMT	drug	opioid	26902643	Combinations of genetic variants within OPRM1, <strong>COMT</strong>, and ESR1 better explain variability in <b>morphine</b> consumption than single genetic variants.
+COMT	drug	cannabinoid	26882038	Single nucleotide polymorphisms in the AKT1 and catechol O methyltransferase (<strong>COMT</strong>) genes have been implicated in the interaction between <b>cannabis</b>, psychosis and cognition, but no studies have examined their impact on an individual's acute response to smoked <b>cannabis</b>.
+COMT	drug	cannabinoid	26882038	Single nucleotide polymorphisms in the AKT1 and <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) genes have been implicated in the interaction between <b>cannabis</b>, psychosis and cognition, but no studies have examined their impact on an individual's acute response to smoked <b>cannabis</b>.
+COMT	drug	cannabinoid	26882038	Working memory following <b>cannabis</b> acutely was worse in females, with some suggestion of an impact of <strong>COMT</strong> polymorphism on working memory when drug free.
+COMT	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (OPRM1), kappa <b>opioid</b> receptors (OPRK1), catechol O methyltransferase (<strong>COMT</strong>), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (SLC6A3, DAT1) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+COMT	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (OPRM1), kappa <b>opioid</b> receptors (OPRK1), <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (SLC6A3, DAT1) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+COMT	drug	cannabinoid	26572896	Acute effects of cocaine and <b>cannabis</b> on reversal learning as a function of <strong>COMT</strong> and DRD2 genotype.
+COMT	drug	cocaine	26572896	Acute effects of <b>cocaine</b> and cannabis on reversal learning as a function of <strong>COMT</strong> and DRD2 genotype.
+COMT	drug	cannabinoid	26572896	In this study, we aimed to establish the acute effects of administration of <b>cannabis</b> and cocaine on valence dependent reversal learning as a function of DRD2 Taq1A (rs1800497) and <strong>COMT</strong> Val108/158Met (rs4680) genotype.
+COMT	drug	cocaine	26572896	In this study, we aimed to establish the acute effects of administration of cannabis and <b>cocaine</b> on valence dependent reversal learning as a function of DRD2 Taq1A (rs1800497) and <strong>COMT</strong> Val108/158Met (rs4680) genotype.
+COMT	drug	nicotine	26555332	Association between catechol O methyltransferase (<strong>COMT</strong>) Val/Met genotype and <b>smoking</b> cessation treatment with <b>nicotine</b>: a meta analysis.
+COMT	drug	nicotine	26555332	Association between <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val/Met genotype and <b>smoking</b> cessation treatment with <b>nicotine</b>: a meta analysis.
+COMT	drug	nicotine	26555332	Catechol O methyltransferase (<strong>COMT</strong>) is one of the major degradative pathways of dopamine and <strong>COMT</strong> Val/Met polymorphisms are associated with the enzyme activity, which is related to dopamine involvement in the <b>nicotine</b> addiction process.
+COMT	addiction	addiction	26555332	Catechol O methyltransferase (<strong>COMT</strong>) is one of the major degradative pathways of dopamine and <strong>COMT</strong> Val/Met polymorphisms are associated with the enzyme activity, which is related to dopamine involvement in the nicotine <b>addiction</b> process.
+COMT	drug	nicotine	26555332	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) is one of the major degradative pathways of dopamine and <strong>COMT</strong> Val/Met polymorphisms are associated with the enzyme activity, which is related to dopamine involvement in the <b>nicotine</b> addiction process.
+COMT	addiction	addiction	26555332	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) is one of the major degradative pathways of dopamine and <strong>COMT</strong> Val/Met polymorphisms are associated with the enzyme activity, which is related to dopamine involvement in the nicotine <b>addiction</b> process.
+COMT	drug	nicotine	26555332	We reviewed the <b>smoking</b> cessation outcomes among previously reported studies by comparing <strong>COMT</strong> polymorphism.
+COMT	drug	nicotine	26555332	As the results, any significant association between <strong>COMT</strong> polymorphism and <b>smoking</b> cessation were not observed.
+COMT	drug	nicotine	26555332	In the subgroup analysis for evaluating the association between <strong>COMT</strong> polymorphism and <b>smoking</b> cessation therapy, three studies were assessed by comparing two groups (Met/Met vs Val/Met plus Val/Val).
+COMT	drug	nicotine	26555332	A significant association between <strong>COMT</strong> polymorphism and <b>smoking</b> cessation was observed (odds ratio: 1.871 and 95% CI: 1.382 2.534).
+COMT	drug	nicotine	26555332	The <strong>COMT</strong> polymorphisms are associated with the outcomes following <b>smoking</b> cessation treatment with <b>nicotine</b>.
+COMT	drug	opioid	26345603	Predictors of <b>heroin</b> relapse: Personality traits, impulsivity, <strong>COMT</strong> gene Val158met polymorphism in a 5 year prospective study in Shanghai, China.
+COMT	addiction	relapse	26345603	Predictors of heroin <b>relapse</b>: Personality traits, impulsivity, <strong>COMT</strong> gene Val158met polymorphism in a 5 year prospective study in Shanghai, China.
+COMT	drug	opioid	26345603	The aim of this study was to evaluate the effect of personality traits, impulsivity, and <strong>COMT</strong> gene polymorphism (rs4680) on relapse to <b>heroin</b> use during 5 year follow up.
+COMT	addiction	relapse	26345603	The aim of this study was to evaluate the effect of personality traits, impulsivity, and <strong>COMT</strong> gene polymorphism (rs4680) on <b>relapse</b> to heroin use during 5 year follow up.
+COMT	drug	opioid	26345603	Univariate analysis showed that age, having ever been in <b>methadone</b> maintenance treatment (MMT), the total scores and non planning scores of BIS 11, and the <strong>COMT</strong> rs4680 gene variants were different between relapse and abstinent groups.
+COMT	addiction	relapse	26345603	Univariate analysis showed that age, having ever been in methadone maintenance treatment (MMT), the total scores and non planning scores of BIS 11, and the <strong>COMT</strong> rs4680 gene variants were different between <b>relapse</b> and abstinent groups.
+COMT	drug	opioid	26345603	Logistic regression analysis showed higher BIS total score, having ever been in MMT and younger first <b>heroin</b> use age are the predictors of relapse to <b>heroin</b> use during 5 years follow up, and the <strong>COMT</strong> rs4680 gene had an interaction with BIS scores.
+COMT	addiction	relapse	26345603	Logistic regression analysis showed higher BIS total score, having ever been in MMT and younger first heroin use age are the predictors of <b>relapse</b> to heroin use during 5 years follow up, and the <strong>COMT</strong> rs4680 gene had an interaction with BIS scores.
+COMT	drug	opioid	26345603	The <strong>COMT</strong> gene showed a moderational effect in part the relationship of impulsivity with <b>heroin</b> relapse.
+COMT	addiction	relapse	26345603	The <strong>COMT</strong> gene showed a moderational effect in part the relationship of impulsivity with heroin <b>relapse</b>.
+COMT	drug	opioid	26288297	It was genotyped polymorphisms in the following genes: mu <b>opioid</b> receptor (OPRM1), kappa <b>opioid</b> receptor (OPRK1), catechol O methyltransferase (<strong>COMT</strong>), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (DAT1).
+COMT	drug	opioid	26288297	It was genotyped polymorphisms in the following genes: mu <b>opioid</b> receptor (OPRM1), kappa <b>opioid</b> receptor (OPRK1), <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (DAT1).
+COMT	drug	nicotine	26220612	The aim of this study is to examine associations between delay discounting and two a priori loci, rs4680 in <strong>COMT</strong> and rs1800497 in ANKK1, and three exploratory haplotypes proximal to rs1800497 in a sample of daily <b>smokers</b>.
+COMT	drug	opioid	25963335	Statistically significant associations were found between <strong>COMT</strong> rs4633 and rs4680 genotypes and the amount of <b>morphine</b> self administered through a patient controlled analgesia pump.
+COMT	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and <strong>COMT</strong>), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+COMT	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and <strong>COMT</strong>), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+COMT	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and <strong>COMT</strong>), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+COMT	drug	benzodiazepine	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) methadone), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the <b>midazolam</b> test, R,S methadone trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, <strong>COMT</strong>, ABCB1, CYP2B6, CYP3A5, CYP2C19 and CYP2D6 genes.
+COMT	drug	opioid	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) <b>methadone</b>), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the midazolam test, R,S <b>methadone</b> trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, <strong>COMT</strong>, ABCB1, CYP2B6, CYP3A5, CYP2C19 and CYP2D6 genes.
+COMT	drug	alcohol	25491588	Catechol O methyltransferase (<strong>COMT</strong>) plays an important role in dopamine degradation, which is associated with the pathophysiology of Alzheimer's disease (AD) and <b>alcoholism</b>.
+COMT	drug	alcohol	25491588	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) plays an important role in dopamine degradation, which is associated with the pathophysiology of Alzheimer's disease (AD) and <b>alcoholism</b>.
+COMT	drug	alcohol	25491588	A functional <strong>COMT</strong> polymorphism, Val158Met (rs4680 G > A), affects the onset of AD and is associated with <b>alcohol</b> dependence through dopamine receptor sensitivity in the prefrontal cortex.
+COMT	addiction	dependence	25491588	A functional <strong>COMT</strong> polymorphism, Val158Met (rs4680 G > A), affects the onset of AD and is associated with alcohol <b>dependence</b> through dopamine receptor sensitivity in the prefrontal cortex.
+COMT	drug	cannabinoid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ opioid receptor (OPRD1), <b>cannabinoid</b> receptor 1 (CNR1), and catechol o methyltransferase (<strong>COMT</strong>), was strongly associated with overall poor performance.
+COMT	drug	opioid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ <b>opioid</b> receptor (OPRD1), cannabinoid receptor 1 (CNR1), and catechol o methyltransferase (<strong>COMT</strong>), was strongly associated with overall poor performance.
+COMT	drug	cannabinoid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ opioid receptor (OPRD1), <b>cannabinoid</b> receptor 1 (CNR1), and <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>), was strongly associated with overall poor performance.
+COMT	drug	opioid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ <b>opioid</b> receptor (OPRD1), cannabinoid receptor 1 (CNR1), and <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>), was strongly associated with overall poor performance.
+COMT	drug	alcohol	25364629	Caudate Volume in Offspring at Ultra High Risk for <b>Alcohol</b> Dependence: <strong>COMT</strong> Val158Met, DRD2, Externalizing Disorders, and Working Memory.
+COMT	addiction	dependence	25364629	Caudate Volume in Offspring at Ultra High Risk for Alcohol <b>Dependence</b>: <strong>COMT</strong> Val158Met, DRD2, Externalizing Disorders, and Working Memory.
+COMT	drug	alcohol	25257296	Collectively, these data suggest that <strong>COMT</strong> inhibitors may be capable of alleviating the extremely motivating or salient nature of stimuli associated with <b>alcohol</b>.
+COMT	drug	alcohol	25035107	The present study aimed to evaluate the association of <b>alcohol</b> dependence and <b>alcohol</b> dependence related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (<strong>COMT</strong>), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (DRD4) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (DBH) and MAO B intron 13 polymorphisms.
+COMT	addiction	dependence	25035107	The present study aimed to evaluate the association of alcohol <b>dependence</b> and alcohol <b>dependence</b> related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (<strong>COMT</strong>), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (DRD4) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (DBH) and MAO B intron 13 polymorphisms.
+COMT	drug	alcohol	25035107	The present study aimed to evaluate the association of <b>alcohol</b> dependence and <b>alcohol</b> dependence related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (DRD4) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (DBH) and MAO B intron 13 polymorphisms.
+COMT	addiction	dependence	25035107	The present study aimed to evaluate the association of alcohol <b>dependence</b> and alcohol <b>dependence</b> related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (DRD4) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (DBH) and MAO B intron 13 polymorphisms.
+COMT	drug	alcohol	25035107	In addition, we found an increased frequency of the <strong>COMT</strong> Met/Met genotype among suicidal (P=0.002) and patients who attempted suicide (P<0.001) and an increased frequency of <strong>COMT</strong> Val/Val genotype in patients with an early onset of <b>alcohol</b> dependence (P=0.004).
+COMT	addiction	dependence	25035107	In addition, we found an increased frequency of the <strong>COMT</strong> Met/Met genotype among suicidal (P=0.002) and patients who attempted suicide (P<0.001) and an increased frequency of <strong>COMT</strong> Val/Val genotype in patients with an early onset of alcohol <b>dependence</b> (P=0.004).
+COMT	drug	alcohol	25035107	This study provides data from a sample of ethnically homogeneous unrelated Caucasian subjects for future meta analyses and suggests that the increased platelet MAO B activity might be used as independent peripheral indicator of <b>alcohol</b> dependence, while <strong>COMT</strong> Val108/158Met polymorphism is associated with increased suicidality and early onset of <b>alcohol</b> dependence.
+COMT	addiction	dependence	25035107	This study provides data from a sample of ethnically homogeneous unrelated Caucasian subjects for future meta analyses and suggests that the increased platelet MAO B activity might be used as independent peripheral indicator of alcohol <b>dependence</b>, while <strong>COMT</strong> Val108/158Met polymorphism is associated with increased suicidality and early onset of alcohol <b>dependence</b>.
+COMT	drug	cannabinoid	24904437	Individuals with polymorphisms of <strong>COMT</strong> and AKT1 genes may be at increased risk for psychotic disorders in association with <b>cannabinoids</b>, as are individuals with a family history of psychotic disorders or a history of childhood trauma.
+COMT	drug	opioid	24490859	The principal finding of the present study was that plasma ACTH and corticosterone levels, MB <strong>COMT</strong>, S <strong>COMT</strong>, NA turnover, and Hsp27 expression and activation observed during <b>morphine</b> withdrawal were significantly inhibited in the CRF₁ receptor knockout mice.
+COMT	addiction	withdrawal	24490859	The principal finding of the present study was that plasma ACTH and corticosterone levels, MB <strong>COMT</strong>, S <strong>COMT</strong>, NA turnover, and Hsp27 expression and activation observed during morphine <b>withdrawal</b> were significantly inhibited in the CRF₁ receptor knockout mice.
+COMT	drug	nicotine	24444411	Genetic variants in DRD2, DRD4, ANKK1, DAT1, <strong>COMT</strong> and DBH genes show some promise in informing personalized prescribing of <b>smoking</b> cessation pharmacotherapies.
+COMT	drug	alcohol	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), <strong>COMT</strong> (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with <b>alcohol</b>, tobacco and/or cannabis consumption in young individuals (n = 91).
+COMT	drug	cannabinoid	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), <strong>COMT</strong> (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, tobacco and/or <b>cannabis</b> consumption in young individuals (n = 91).
+COMT	drug	nicotine	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), <strong>COMT</strong> (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, <b>tobacco</b> and/or cannabis consumption in young individuals (n = 91).
+COMT	addiction	reward	24273683	We also genotyped the patient using a <b>reward</b> gene panel including (9 genes 18 alleles): DRD 2,3,4; MOA A; <strong>COMT</strong>; DAT1; 5HTTLLR; OPRM1; and GABRA3.
+COMT	drug	opioid	24145159	This study focused on the question whether patients with conventional <b>opioid</b> maintenance treatment (<strong>COMT</strong>) would prefer a switch to <b>heroin</b> maintenance treatment (HMT).
+COMT	addiction	dependence	24145159	All 20 psychiatric hospitals and all 110 physicians' practices in Berlin licensed to offer <strong>COMT</strong> were approached to reach patients under <strong>COMT</strong> and also fulfilling the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) criteria of opiate <b>dependence</b>.
+COMT	drug	opioid	24145159	These patients report more detoxification therapies (P < 0.001), a higher dose of <b>methadone</b> equivalent (P = 0.001), and more often continued use of multiple illegal drugs despite <strong>COMT</strong> (P < 0.001) than patients not preferring HMT.
+COMT	drug	opioid	24145159	The data on the patients' perspective complement the existing clinical studies, showing that previously unresponsive <b>opioid</b> addicted patients especially would switch to HMT, whereas most patients would prefer continuation of <strong>COMT</strong>.
+COMT	drug	opioid	24127930	<strong>Catechol O methyltransferase</strong> genotype modulates <b>opioid</b> release in decision circuitry.
+COMT	drug	alcohol	24127930	Using the selective mu opioid receptor radioligand [¹¹C] carfentanil, we find that, following <b>alcohol</b> consumption, individuals with the <strong>COMT</strong> Val158 allele have greater opioid release in the right NAc but less release in medial orbital frontal cortex (OFC).
+COMT	drug	opioid	24127930	Using the selective mu <b>opioid</b> receptor radioligand [¹¹C] carfentanil, we find that, following alcohol consumption, individuals with the <strong>COMT</strong> Val158 allele have greater <b>opioid</b> release in the right NAc but less release in medial orbital frontal cortex (OFC).
+COMT	drug	alcohol	24118473	Val158Met <strong>COMT</strong> polymorphism and risk of aggression in <b>alcohol</b> dependence.
+COMT	addiction	dependence	24118473	Val158Met <strong>COMT</strong> polymorphism and risk of aggression in alcohol <b>dependence</b>.
+COMT	drug	nicotine	24095246	<b>Smokers</b> were genotyped prospectively for the <strong>COMT</strong> val(158)met polymorphism for exploratory analysis.
+COMT	drug	nicotine	24095246	Data from this proof of concept study do not provide strong support for further evaluation of <strong>COMT</strong> inhibitors as <b>smoking</b> cessation aids.
+COMT	drug	nicotine	24084577	Effect of <strong>COMT</strong> Val(158)Met genotype on <b>nicotine</b> withdrawal related cognitive dysfunction in <b>smokers</b> with and without schizophrenia.
+COMT	addiction	withdrawal	24084577	Effect of <strong>COMT</strong> Val(158)Met genotype on nicotine <b>withdrawal</b> related cognitive dysfunction in smokers with and without schizophrenia.
+COMT	drug	nicotine	23941313	Age, gender, Fagerström Test for <b>Nicotine</b> Dependence, dopamine pathway genotypes (rs1800497 [ANKK1 E713K], rs4680 [<strong>COMT</strong> V158M], DRD4 exon 3 variable number of tandem repeats polymorphism [DRD4 VNTR], SLC6A3,3' VNTR) analyzed both separately and as part of an AGES, time to first lapse and point prevalence abstinence at end of treatment.
+COMT	addiction	dependence	23941313	Age, gender, Fagerström Test for Nicotine <b>Dependence</b>, dopamine pathway genotypes (rs1800497 [ANKK1 E713K], rs4680 [<strong>COMT</strong> V158M], DRD4 exon 3 variable number of tandem repeats polymorphism [DRD4 VNTR], SLC6A3,3' VNTR) analyzed both separately and as part of an AGES, time to first lapse and point prevalence abstinence at end of treatment.
+COMT	drug	opioid	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol O methyl transferase (<strong>COMT</strong>) and dopamine transporter (SLC6A3) genes and <b>heroin</b> dependence in Hungarian patients.
+COMT	addiction	dependence	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol O methyl transferase (<strong>COMT</strong>) and dopamine transporter (SLC6A3) genes and heroin <b>dependence</b> in Hungarian patients.
+COMT	drug	opioid	23840506	303 <b>heroin</b> dependent subjects and 555 healthy controls were genotyped for 7 single nucleotide polymorphisms (SNPs) rs4680 of the <strong>COMT</strong> gene; rs1079597 and rs1800498 of the DRD2 gene; rs1800497 of the ANKK1 gene; rs1800955, rs936462 and rs747302 of the DRD4 gene.
+COMT	drug	nicotine	23828159	Association of abstinence induced alterations in working memory function and <strong>COMT</strong> genotype in <b>smokers</b>.
+COMT	drug	nicotine	23828159	The common methionine (met) for valine (val) at codon 158 (val(158)met) polymorphism in the catechol O methyltransferase (<strong>COMT</strong>) gene has been associated with <b>nicotine</b> dependence, alterations in executive cognitive function, and abstinence induced working memory deficits in <b>smokers</b>.
+COMT	addiction	dependence	23828159	The common methionine (met) for valine (val) at codon 158 (val(158)met) polymorphism in the catechol O methyltransferase (<strong>COMT</strong>) gene has been associated with nicotine <b>dependence</b>, alterations in executive cognitive function, and abstinence induced working memory deficits in smokers.
+COMT	drug	nicotine	23828159	The common methionine (met) for valine (val) at codon 158 (val(158)met) polymorphism in the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene has been associated with <b>nicotine</b> dependence, alterations in executive cognitive function, and abstinence induced working memory deficits in <b>smokers</b>.
+COMT	addiction	dependence	23828159	The common methionine (met) for valine (val) at codon 158 (val(158)met) polymorphism in the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene has been associated with nicotine <b>dependence</b>, alterations in executive cognitive function, and abstinence induced working memory deficits in smokers.
+COMT	drug	nicotine	23828159	The <strong>COMT</strong> val(158)met polymorphism was associated with abstinence related working memory deficits in two independent samples of <b>smokers</b>.
+COMT	drug	opioid	23632726	Single nucleotide polymorphisms (SNPs) in the μ <b>opioid</b> receptor (OPRM1), multidrug resistance (ABCB1), and catechol o methyltransferase (<strong>COMT</strong>) genes are associated with risk for <b>opioid</b> addiction in adults.
+COMT	addiction	addiction	23632726	Single nucleotide polymorphisms (SNPs) in the μ opioid receptor (OPRM1), multidrug resistance (ABCB1), and catechol o methyltransferase (<strong>COMT</strong>) genes are associated with risk for opioid <b>addiction</b> in adults.
+COMT	drug	opioid	23632726	Single nucleotide polymorphisms (SNPs) in the μ <b>opioid</b> receptor (OPRM1), multidrug resistance (ABCB1), and <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>) genes are associated with risk for <b>opioid</b> addiction in adults.
+COMT	addiction	addiction	23632726	Single nucleotide polymorphisms (SNPs) in the μ opioid receptor (OPRM1), multidrug resistance (ABCB1), and <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>) genes are associated with risk for opioid <b>addiction</b> in adults.
+COMT	drug	opioid	23566343	In this study, we aimed to determine whether the catechol O methyl transferase (<strong>COMT</strong>) and <b>opioid</b> receptor μ 1 (OPRM1) common functional polymorphisms rs4680 and rs1799971 were associated with the incidence, intensity, or duration of CPP in patients after lower abdominal surgery.
+COMT	addiction	reward	23566343	In this study, we aimed to determine whether the catechol O methyl transferase (<strong>COMT</strong>) and opioid receptor μ 1 (OPRM1) common functional polymorphisms rs4680 and rs1799971 were associated with the incidence, intensity, or duration of <b>CPP</b> in patients after lower abdominal surgery.
+COMT	addiction	reward	23566343	No combined effect of <strong>COMT</strong>/OPRM1 polymorphisms on <b>CPP</b> phenotypes was observed.
+COMT	addiction	reward	23566343	<strong>COMT</strong> didn't affect <b>CPP</b>, suggesting its potential modality specific effects on human pain.
+COMT	drug	nicotine	23459442	<strong>COMT</strong> Val158Met modulates subjective responses to intravenous <b>nicotine</b> and cognitive performance in abstinent <b>smokers</b>.
+COMT	drug	nicotine	23459442	The catechol O methyltransferase (<strong>COMT</strong>) Val158Met polymorphism may be a risk factor for <b>nicotine</b> addiction.
+COMT	addiction	addiction	23459442	The catechol O methyltransferase (<strong>COMT</strong>) Val158Met polymorphism may be a risk factor for nicotine <b>addiction</b>.
+COMT	drug	nicotine	23459442	The <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met polymorphism may be a risk factor for <b>nicotine</b> addiction.
+COMT	addiction	addiction	23459442	The <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met polymorphism may be a risk factor for nicotine <b>addiction</b>.
+COMT	drug	nicotine	23459442	This study examined the influence of the <strong>COMT</strong> Val158Met polymorphism on subjective, physiological and cognitive effects of intravenous (IV) <b>nicotine</b> use in African Americans (AAs; n=56) and European Americans (EAs; n=68) <b>smokers</b>.
+COMT	drug	nicotine	23459442	These results support the rationale of pharmacologically inhibiting <strong>COMT</strong> to aid with <b>smoking</b> cessation among Val/Val genotype <b>smokers</b>.
+COMT	drug	nicotine	23433232	<b>Nicotine</b> and tonic dopamine (DA) levels [as inferred by catechol O methyl tranferase (<strong>COMT</strong>) Val158Met genotype] interact to affect prefrontal processing.
+COMT	drug	nicotine	23433232	We investigated whether there is a <b>nicotine</b> × <strong>COMT</strong> genotype interaction in brain circuitry during performance feedback of a reward task.
+COMT	addiction	reward	23433232	We investigated whether there is a nicotine × <strong>COMT</strong> genotype interaction in brain circuitry during performance feedback of a <b>reward</b> task.
+COMT	drug	nicotine	23433232	A significant <b>nicotine</b> × <strong>COMT</strong> genotype interaction for BOLD signal during performance feedback in cortico striatal areas was seen.
+COMT	drug	nicotine	23433232	Although these results are preliminary due to small sample size, they suggest a possible neurobiological mechanism underlying the clinical observation that Val/Val homozygotes, presumably with elevated <strong>COMT</strong> activity compared to Met allele carriers and therefore reduced prefrontal DA levels, have poorer outcomes with <b>nicotine</b> replacement therapy.
+COMT	addiction	dependence	23377636	Other candidate genes associated with substance <b>dependence</b> phenotypes in Native Americans include OPRM1, CRN1, <strong>COMT</strong>, GABRA2, MAOA, and HTR3 B.
+COMT	drug	nicotine	23288874	Lack of association of a functional <strong>catechol O methyltransferase</strong> gene polymorphism with risk of <b>tobacco</b> <b>smoking</b>: results from a multicenter case control study.
+COMT	addiction	reward	23288874	The catechol O methyltransferase (<strong>COMT</strong>) modulates dopaminergic neurotransmission in the prefrontal cortex as well as in the mesolimbic <b>reward</b> system.
+COMT	addiction	reward	23288874	The <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) modulates dopaminergic neurotransmission in the prefrontal cortex as well as in the mesolimbic <b>reward</b> system.
+COMT	drug	nicotine	23288874	Since the reward system mediates addictive behavior, the <strong>COMT</strong> gene is a strong candidate gene regarding the pathophysiology of <b>tobacco</b> dependence and <b>smoking</b> behavior.
+COMT	addiction	addiction	23288874	Since the reward system mediates <b>addictive</b> behavior, the <strong>COMT</strong> gene is a strong candidate gene regarding the pathophysiology of tobacco dependence and smoking behavior.
+COMT	addiction	dependence	23288874	Since the reward system mediates addictive behavior, the <strong>COMT</strong> gene is a strong candidate gene regarding the pathophysiology of tobacco <b>dependence</b> and smoking behavior.
+COMT	addiction	reward	23288874	Since the <b>reward</b> system mediates addictive behavior, the <strong>COMT</strong> gene is a strong candidate gene regarding the pathophysiology of tobacco dependence and smoking behavior.
+COMT	drug	nicotine	23288874	Because of rather conflicting results in previous studies, the purpose of the present study was to test for association between a functional genetic variant in the <strong>COMT</strong> gene (single nucleotide polymorphism [SNP] rs4680) and <b>tobacco</b> <b>smoking</b> behavior.
+COMT	drug	nicotine	23288874	Although prefrontal cortical and ventral striatal activity are highly relevant for addictive behavior, and under partial control of <strong>COMT</strong> rs4680 genotype, no association between <strong>COMT</strong> and <b>smoking</b> behavior was observed.
+COMT	addiction	addiction	23288874	Although prefrontal cortical and ventral striatal activity are highly relevant for <b>addictive</b> behavior, and under partial control of <strong>COMT</strong> rs4680 genotype, no association between <strong>COMT</strong> and smoking behavior was observed.
+COMT	drug	opioid	23155402	Pathways to age of onset of <b>heroin</b> use: a structural model approach exploring the relationship of the <strong>COMT</strong> gene, impulsivity and childhood trauma.
+COMT	drug	opioid	23155402	To clarify the impacts and the interactions of the Catechol  O methyltransferase (<strong>COMT</strong>) gene, impulsivity and childhood trauma on the age of onset of <b>heroin</b> use among <b>heroin</b> dependent patients in China.
+COMT	drug	opioid	23155402	The single nucleotide polymorphism (SNP) rs737866 on the <strong>COMT</strong> gene which has previously been associated with <b>heroin</b> abuse, was genotyped using a DNA sequence detection system.
+COMT	drug	opioid	23155402	In structure equation model, both the <strong>COMT</strong> gene and childhood trauma had impacts on the age of onset of <b>heroin</b> use directly or via impulsive personality.
+COMT	drug	opioid	23155402	Our findings indicated that the <strong>COMT</strong> gene, impulsive personality traits and childhood trauma experience were interacted to impact the age of onset of <b>heroin</b> use, which play a critical role in the development of <b>heroin</b> dependence.
+COMT	addiction	dependence	23155402	Our findings indicated that the <strong>COMT</strong> gene, impulsive personality traits and childhood trauma experience were interacted to impact the age of onset of heroin use, which play a critical role in the development of heroin <b>dependence</b>.
+COMT	drug	opioid	23155402	The impact of environmental factor was greater than the <strong>COMT</strong> gene in the development of <b>heroin</b> dependence.
+COMT	addiction	dependence	23155402	The impact of environmental factor was greater than the <strong>COMT</strong> gene in the development of heroin <b>dependence</b>.
+COMT	drug	alcohol	23087644	Associations of Cigarette Smoking and Polymorphisms in Brain Derived Neurotrophic Factor and <strong>Catechol O Methyltransferase</strong> with Neurocognition in <b>Alcohol</b> Dependent Individuals during Early Abstinence.
+COMT	drug	nicotine	23087644	Associations of Cigarette <b>Smoking</b> and Polymorphisms in Brain Derived Neurotrophic Factor and <strong>Catechol O Methyltransferase</strong> with Neurocognition in Alcohol Dependent Individuals during Early Abstinence.
+COMT	drug	nicotine	23087644	Chronic cigarette <b>smoking</b> and polymorphisms in brain derived neurotrophic factor (BDNF) and catechol O methyltransferase (<strong>COMT</strong>) are associated with neurocognition in normal controls and those with various neuropsychiatric conditions.
+COMT	drug	nicotine	23087644	Chronic cigarette <b>smoking</b> and polymorphisms in brain derived neurotrophic factor (BDNF) and <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) are associated with neurocognition in normal controls and those with various neuropsychiatric conditions.
+COMT	drug	alcohol	23087644	The influence of BDNF and <strong>COMT</strong> on neurocognition in <b>alcohol</b> dependence is unclear.
+COMT	addiction	dependence	23087644	The influence of BDNF and <strong>COMT</strong> on neurocognition in alcohol <b>dependence</b> is unclear.
+COMT	drug	alcohol	23087644	The primary goal of this report was to investigate the associations of single nucleotide polymorphisms (SNPs) in BDNF Val66Met (rs6265) and <strong>COMT</strong> Val158Met (rs4680) with neurocognition in a treatment seeking <b>alcohol</b> dependent cohort and determine if neurocognitive differences between non smokers and smokers previously observed in this cohort persist when controlled for these functional SNPs.
+COMT	drug	nicotine	23087644	The primary goal of this report was to investigate the associations of single nucleotide polymorphisms (SNPs) in BDNF Val66Met (rs6265) and <strong>COMT</strong> Val158Met (rs4680) with neurocognition in a treatment seeking alcohol dependent cohort and determine if neurocognitive differences between non <b>smokers</b> and <b>smokers</b> previously observed in this cohort persist when controlled for these functional SNPs.
+COMT	addiction	relapse	23087644	The primary goal of this report was to investigate the associations of single nucleotide polymorphisms (SNPs) in BDNF Val66Met (rs6265) and <strong>COMT</strong> Val158Met (rs4680) with neurocognition in a treatment <b>seeking</b> alcohol dependent cohort and determine if neurocognitive differences between non smokers and smokers previously observed in this cohort persist when controlled for these functional SNPs.
+COMT	drug	nicotine	23087644	After controlling for <strong>COMT</strong> and BDNF genotypes, <b>smoking</b> ALC performed significantly worse than non <b>smoking</b> ALC on the domains of auditory verbal and visuospatial learning and memory, cognitive efficiency, general intelligence, processing speed, and global neurocognition.
+COMT	drug	nicotine	23087644	Results also indicated that the poorer performance of <b>smoking</b> compared to non <b>smoking</b> ALC across multiple neurocognitive domains was not mediated by <strong>COMT</strong> or BDNF genotype.
+COMT	drug	cocaine	23011431	[Effect of <strong>Catechol O methyltransferase</strong> deficiency on reinforcing effects of <b>cocaine</b> (experimental study)].
+COMT	addiction	reward	23011431	[Effect of <strong>Catechol O methyltransferase</strong> deficiency on <b>reinforcing</b> effects of cocaine (experimental study)].
+COMT	addiction	reward	23011431	The literature data suggest that individual differences in <strong>COMT</strong> activity (Val158Met polymorphism) might have indirect downstream effects on the <b>reward</b> system.
+COMT	drug	cocaine	23011431	The aim of the present study was to examine whether <strong>COMT</strong> deletion affects reinforcing effects of <b>cocaine</b> in mice.
+COMT	addiction	reward	23011431	The aim of the present study was to examine whether <strong>COMT</strong> deletion affects <b>reinforcing</b> effects of cocaine in mice.
+COMT	drug	cocaine	23011431	The total <b>cocaine</b> intake did not differ in <strong>COMT</strong> deletion mice and wild type mice.
+COMT	drug	cocaine	23011431	The results of this study suggest that individual differences in <strong>COMT</strong> activity do not affect primary reinforcing effects of <b>cocaine</b> in mice.
+COMT	addiction	reward	23011431	The results of this study suggest that individual differences in <strong>COMT</strong> activity do not affect primary <b>reinforcing</b> effects of cocaine in mice.
+COMT	drug	opioid	22841130	One hundred seven <b>methadone</b> maintenance treatment patients, 36 having an ADHD diagnosis, 176 adult patients with ADHD without SUDs, and 500 healthy controls were genotyped for variants in the DRD4 (exon 3 VNTR), DRD5 (upstream VNTR), HTR1B (rs6296), DBH (rs2519152), <strong>COMT</strong> (rs4680; Val158Met), and OPRM1 (rs1799971; 118A>G) genes.
+COMT	drug	nicotine	22740151	Impact of <strong>COMT</strong> Val 108/158 Met and DRD2 Taq1B gene polymorphisms on vulnerability to cigarette <b>smoking</b> of Thai males.
+COMT	drug	nicotine	22740151	The purposes of this study were to examine the association between two polymorphisms in <strong>COMT</strong> Val (108/158) Met and DRD2 Taq1B and anthropometric biochemical parameters and to ascertain the association between these polymorphisms and cigarette <b>smoking</b>.
+COMT	drug	nicotine	22740151	<b>Smoking</b> status was significantly associated with <strong>COMT</strong> Val (108/158) Met polymorphism, but not associated with DRD2 Taq1B polymorphism.
+COMT	drug	alcohol	22740151	Logistic regression analysis showed that <strong>COMT</strong> Val (108/158) Met gene polymorphism, educational status, parental smoking, and <b>alcohol</b> consumption had statistically significant impacts on cigarette smoking.
+COMT	drug	nicotine	22740151	Logistic regression analysis showed that <strong>COMT</strong> Val (108/158) Met gene polymorphism, educational status, parental <b>smoking</b>, and alcohol consumption had statistically significant impacts on cigarette <b>smoking</b>.
+COMT	drug	nicotine	22740151	The results suggest that <strong>COMT</strong> Val (108/158) Met genetic polymorphisms, but not DRD2 Taq1B, may influence susceptibility to cigarette <b>smoking</b> among Thai males.
+COMT	drug	nicotine	22695756	Association of functional <strong>COMT</strong> Val108/Met polymorphism with <b>smoking</b> cessation in a <b>nicotine</b> replacement therapy.
+COMT	drug	nicotine	22695756	We evaluated the efficacy and safety of sublingual <b>nicotine</b> tablets (SNT) for <b>smoking</b> cessation and the association of catechol O methyltransferase (<strong>COMT</strong>) genotype with efficacy in this <b>smoking</b> cessation trial among Chinese <b>smokers</b>.
+COMT	drug	nicotine	22695756	We evaluated the efficacy and safety of sublingual <b>nicotine</b> tablets (SNT) for <b>smoking</b> cessation and the association of <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) genotype with efficacy in this <b>smoking</b> cessation trial among Chinese <b>smokers</b>.
+COMT	drug	nicotine	22695756	We found that SNT significantly increased <b>smoking</b> abstinence, reduced craving and was well tolerated, and the <strong>COMT</strong> Val/Val genotype was associated with a greater improvement in <b>smoking</b> cessation.
+COMT	addiction	relapse	22695756	We found that SNT significantly increased smoking abstinence, reduced <b>craving</b> and was well tolerated, and the <strong>COMT</strong> Val/Val genotype was associated with a greater improvement in smoking cessation.
+COMT	drug	opioid	22647273	<b>Morphine</b> withdrawn rats showed an increase of NA turnover and <strong>COMT</strong> expression in parallel with an enhancement of adrenocorticotropin and plasma corticosterone concentrations.
+COMT	drug	alcohol	22509987	<strong>COMT</strong> Val158Met modulates the effect of childhood adverse experiences on the risk of <b>alcohol</b> dependence.
+COMT	addiction	dependence	22509987	<strong>COMT</strong> Val158Met modulates the effect of childhood adverse experiences on the risk of alcohol <b>dependence</b>.
+COMT	drug	alcohol	22509987	The <strong>COMT</strong> Val158Met and DRD2/ANKK1 Taq1A genotypes have been suggested to affect both stress sensitivity and the risk for <b>alcohol</b> dependence.
+COMT	addiction	dependence	22509987	The <strong>COMT</strong> Val158Met and DRD2/ANKK1 Taq1A genotypes have been suggested to affect both stress sensitivity and the risk for alcohol <b>dependence</b>.
+COMT	drug	alcohol	22509987	This study tested the hypothesis that genetic variation in <strong>COMT</strong> Val158Met and DRD2/ANKK1 Taq1A interacts with childhood adverse experiences to predict <b>alcohol</b> dependence.
+COMT	addiction	dependence	22509987	This study tested the hypothesis that genetic variation in <strong>COMT</strong> Val158Met and DRD2/ANKK1 Taq1A interacts with childhood adverse experiences to predict alcohol <b>dependence</b>.
+COMT	drug	alcohol	22509987	Male abstinent <b>alcohol</b> dependent patients (n = 110) and age matched healthy male controls (n = 99) were genotyped for the <strong>COMT</strong> Val158Met and the DRD2/ANKK1 Taq1A genotypes.
+COMT	drug	alcohol	22509987	This study provides evidence for a gene environment interaction in <b>alcohol</b> dependence, in which an individual's sensitivity to childhood adverse experience is moderated by the <strong>COMT</strong> genotype.
+COMT	addiction	dependence	22509987	This study provides evidence for a gene environment interaction in alcohol <b>dependence</b>, in which an individual's sensitivity to childhood adverse experience is moderated by the <strong>COMT</strong> genotype.
+COMT	drug	alcohol	22474103	Reduced dopamine receptor sensitivity as an intermediate phenotype in <b>alcohol</b> dependence and the role of the <strong>COMT</strong> Val158Met and DRD2 Taq1A genotypes.
+COMT	addiction	dependence	22474103	Reduced dopamine receptor sensitivity as an intermediate phenotype in alcohol <b>dependence</b> and the role of the <strong>COMT</strong> Val158Met and DRD2 Taq1A genotypes.
+COMT	drug	alcohol	22474103	To test central dopamine receptor sensitivity as an intermediate phenotype for <b>alcohol</b> dependence, specifically evaluating the hypothesis that the dopaminergic genes <strong>COMT</strong> Val158Met and DRD2 Taq1A affect dopamine receptor sensitivity.
+COMT	addiction	dependence	22474103	To test central dopamine receptor sensitivity as an intermediate phenotype for alcohol <b>dependence</b>, specifically evaluating the hypothesis that the dopaminergic genes <strong>COMT</strong> Val158Met and DRD2 Taq1A affect dopamine receptor sensitivity.
+COMT	drug	alcohol	22474103	In a logistic regression analysis, reduced dopamine receptor sensitivity on both measures predicted <b>alcohol</b> dependence, without an additive effect of the <strong>COMT</strong> Val158Met and DRD2 Taq1A genotypes.
+COMT	addiction	dependence	22474103	In a logistic regression analysis, reduced dopamine receptor sensitivity on both measures predicted alcohol <b>dependence</b>, without an additive effect of the <strong>COMT</strong> Val158Met and DRD2 Taq1A genotypes.
+COMT	drug	alcohol	22474103	<strong>COMT</strong> Val158Met and DRD2 Taq1A may confer their risk of <b>alcohol</b> dependence through reduced dopamine receptor sensitivity in the prefrontal cortex and hindbrain, respectively.
+COMT	addiction	dependence	22474103	<strong>COMT</strong> Val158Met and DRD2 Taq1A may confer their risk of alcohol <b>dependence</b> through reduced dopamine receptor sensitivity in the prefrontal cortex and hindbrain, respectively.
+COMT	drug	amphetamine	22455354	Literature review suggests that levamisole might have the advantages of enhancing noradrenergic neurotransmission by inhibiting reuptake, by inhibiting MAO and/or <strong>COMT</strong>, by acting on ganglionic nicotinic receptors and by being partially metabolized into an <b>amphetamine</b> like compound.
+COMT	drug	nicotine	22309446	<b>Nicotine</b> normalizes event related potentials in <strong>COMT</strong> Val tg mice and increases gamma and theta spectral density.
+COMT	drug	nicotine	22309446	Furthermore, <b>smokers</b> who carry the high activity <strong>COMT</strong> Val allele are more prone to cognitive deficits and have an increased risk of <b>smoking</b> relapse.
+COMT	addiction	relapse	22309446	Furthermore, smokers who carry the high activity <strong>COMT</strong> Val allele are more prone to cognitive deficits and have an increased risk of smoking <b>relapse</b>.
+COMT	drug	nicotine	22309446	We also examined the effects of <b>nicotine</b> on these measures to investigate the potential effects of <b>smoking</b> on <strong>COMT</strong> mediated electrophysiological activity.
+COMT	drug	nicotine	22309446	<b>Nicotine</b> restored normal event related activity among <strong>COMT</strong> Val tg mice, suggesting one mechanism through which <b>nicotine</b> may normalize cognitive function among people with the high activity allele.
+COMT	drug	amphetamine	22217949	<strong>COMT</strong> Val158Met, BDNF Val66Met, and OPRM1 Asn40Asp and <b>methamphetamine</b> dependence treatment response: preliminary investigation.
+COMT	addiction	dependence	22217949	<strong>COMT</strong> Val158Met, BDNF Val66Met, and OPRM1 Asn40Asp and methamphetamine <b>dependence</b> treatment response: preliminary investigation.
+COMT	drug	alcohol	22208661	A novel SNP in <strong>COMT</strong> is associated with <b>alcohol</b> dependence but not opiate or nicotine dependence: a case control study.
+COMT	drug	nicotine	22208661	A novel SNP in <strong>COMT</strong> is associated with alcohol dependence but not opiate or <b>nicotine</b> dependence: a case control study.
+COMT	addiction	dependence	22208661	A novel SNP in <strong>COMT</strong> is associated with alcohol <b>dependence</b> but not opiate or nicotine <b>dependence</b>: a case control study.
+COMT	drug	alcohol	22208661	To determine whether <strong>COMT</strong> is important in substance dependence, rs165774 and rs4680 were genotyped and haplotyped in patients with nicotine, <b>alcohol</b> and opiate dependence.
+COMT	drug	nicotine	22208661	To determine whether <strong>COMT</strong> is important in substance dependence, rs165774 and rs4680 were genotyped and haplotyped in patients with <b>nicotine</b>, alcohol and opiate dependence.
+COMT	addiction	dependence	22208661	To determine whether <strong>COMT</strong> is important in substance <b>dependence</b>, rs165774 and rs4680 were genotyped and haplotyped in patients with nicotine, alcohol and opiate <b>dependence</b>.
+COMT	drug	alcohol	22208661	Our study provides further support for the importance of the <strong>COMT</strong> in <b>alcohol</b> dependence in addition to schizophrenia.
+COMT	addiction	dependence	22208661	Our study provides further support for the importance of the <strong>COMT</strong> in alcohol <b>dependence</b> in addition to schizophrenia.
+COMT	drug	alcohol	22208661	It is possible that the rs165774 SNP, in combination with rs4680, results in a common molecular variant of <strong>COMT</strong> that contributes to schizophrenia and <b>alcohol</b> dependence susceptibility.
+COMT	addiction	dependence	22208661	It is possible that the rs165774 SNP, in combination with rs4680, results in a common molecular variant of <strong>COMT</strong> that contributes to schizophrenia and alcohol <b>dependence</b> susceptibility.
+COMT	drug	amphetamine	21934638	A <strong>COMT</strong> gene haplotype associated with <b>methamphetamine</b> abuse.
+COMT	addiction	addiction	21934638	It follows that dopaminergic genes, particularly <strong>COMT</strong> (encoding catechol O methyltransferase) and its val158met polymorphism (rs4680), are natural candidates for susceptibility loci to <b>addiction</b>.
+COMT	addiction	addiction	21934638	It follows that dopaminergic genes, particularly <strong>COMT</strong> (encoding <strong>catechol O methyltransferase</strong>) and its val158met polymorphism (rs4680), are natural candidates for susceptibility loci to <b>addiction</b>.
+COMT	drug	amphetamine	21876500	Lack of association between the Val158Met <strong>catechol O methyltransferase</strong> gene polymorphism and <b>methamphetamine</b> dependence.
+COMT	addiction	dependence	21876500	Lack of association between the Val158Met <strong>catechol O methyltransferase</strong> gene polymorphism and methamphetamine <b>dependence</b>.
+COMT	drug	amphetamine	21876500	Dependence on <b>methamphetamine</b> is markedly related to the brain neurotransmitter dopamine, metabolised by <strong>catechol O methyltransferase</strong> enzyme.
+COMT	addiction	dependence	21876500	<b>Dependence</b> on methamphetamine is markedly related to the brain neurotransmitter dopamine, metabolised by <strong>catechol O methyltransferase</strong> enzyme.
+COMT	drug	amphetamine	21876500	The main aim of the study was to ascertain whether the Val158Met <strong>catechol O methyltransferase</strong> gene polymorphism is associated with <b>methamphetamine</b> dependence in this Central European country.
+COMT	addiction	dependence	21876500	The main aim of the study was to ascertain whether the Val158Met <strong>catechol O methyltransferase</strong> gene polymorphism is associated with methamphetamine <b>dependence</b> in this Central European country.
+COMT	drug	amphetamine	21876500	We did not find any significant association between the Val158Met <strong>catechol O methyltransferase</strong> gene polymorphism and <b>methamphetamine</b> dependence using the population based or family based design (p=0.41 0.66; Chi Square Test or UNPHASED program, Version 3.1.4, respectively).
+COMT	addiction	dependence	21876500	We did not find any significant association between the Val158Met <strong>catechol O methyltransferase</strong> gene polymorphism and methamphetamine <b>dependence</b> using the population based or family based design (p=0.41 0.66; Chi Square Test or UNPHASED program, Version 3.1.4, respectively).
+COMT	addiction	reward	21858957	This document presents evidence supporting the role of the KB220/KB220Z neuroadaptagens consisting of amino acid neurotransmitter precursors and enkephalinase catecholamine methyl transferase (<strong>COMT</strong>) inhibition therapy called Neuroadaptagen Amino Acid Therapy (NAAT) in brain <b>reward</b> function.
+COMT	drug	opioid	21857968	Role of novelty seeking personality traits as mediator of the association between <strong>COMT</strong> and onset age of drug use in Chinese <b>heroin</b> dependent patients.
+COMT	addiction	relapse	21857968	Role of novelty <b>seeking</b> personality traits as mediator of the association between <strong>COMT</strong> and onset age of drug use in Chinese heroin dependent patients.
+COMT	drug	opioid	21857968	Examine the relationships between allelic variants of the catechol O methyltransferase (<strong>COMT</strong>) gene, NS personality traits, and age of onset of drug use in <b>heroin</b> dependent subjects in China.
+COMT	drug	opioid	21857968	Examine the relationships between allelic variants of the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene, NS personality traits, and age of onset of drug use in <b>heroin</b> dependent subjects in China.
+COMT	drug	opioid	21857968	The 478 <b>heroin</b> dependent subjects from four drug rehabilitation centers in Shanghai who were genotyped for eight tagging single nucleotide polymorphisms (SNP) on the <strong>COMT</strong> gene completed the NS subscale from the Temperament and Character Inventory.
+COMT	drug	opioid	21857968	Multivariate analyses were used to assess the potential mediating role of NS personality traits in the association between <strong>COMT</strong> gene variants and the age of onset of <b>heroin</b> use.
+COMT	drug	opioid	21857968	In the univariate analysis the <strong>COMT</strong> rs737866 gene variants were independently associated with both NS and age of onset of drug use: those with the TT genotype had higher NS subscale scores and an earlier onset age of <b>heroin</b> use than individuals with CT or CC genotypes.
+COMT	drug	opioid	21857968	Our findings that <strong>COMT</strong> is associated with both NS personality traits and with the age of onset of <b>heroin</b> use helps to clarify the complex relationship between genetic and psychological factors in the development of substance abuse.
+COMT	drug	cannabinoid	21524266	Results from controlled human laboratory studies and small open label clinical trials suggest that <b>dronabinol</b>, the <strong>COMT</strong> inhibitor entacapone, and lithium may warrant further study.
+COMT	drug	alcohol	21492092	Individuals possessing a paucity of serotonergic and/or dopaminergic receptors and an increased rate of synaptic dopamine catabolism, due to high catabolic genotype of the <strong>COMT</strong> gene, are predisposed to self medicating any substance or behavior that will activate dopamine release including <b>alcohol</b>, opiates, psychostimulants, nicotine, glucose, gambling, sex, and even excessive internet gaming, among others.
+COMT	drug	nicotine	21492092	Individuals possessing a paucity of serotonergic and/or dopaminergic receptors and an increased rate of synaptic dopamine catabolism, due to high catabolic genotype of the <strong>COMT</strong> gene, are predisposed to self medicating any substance or behavior that will activate dopamine release including alcohol, opiates, psychostimulants, <b>nicotine</b>, glucose, gambling, sex, and even excessive internet gaming, among others.
+COMT	drug	nicotine	21312287	VII <strong>COMT</strong> as a risk modifying gene for <b>Nicotine</b> dependence   role of gene gene interaction, personality, and environmental factors.
+COMT	addiction	dependence	21312287	VII <strong>COMT</strong> as a risk modifying gene for Nicotine <b>dependence</b>   role of gene gene interaction, personality, and environmental factors.
+COMT	drug	nicotine	21312287	Catechol O methyltransferase (<strong>COMT</strong>) may be a risk modifying gene for <b>Nicotine</b> dependence (ND) rather than a direct susceptibility gene for this phenotype.
+COMT	addiction	dependence	21312287	Catechol O methyltransferase (<strong>COMT</strong>) may be a risk modifying gene for Nicotine <b>dependence</b> (ND) rather than a direct susceptibility gene for this phenotype.
+COMT	drug	nicotine	21312287	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) may be a risk modifying gene for <b>Nicotine</b> dependence (ND) rather than a direct susceptibility gene for this phenotype.
+COMT	addiction	dependence	21312287	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) may be a risk modifying gene for Nicotine <b>dependence</b> (ND) rather than a direct susceptibility gene for this phenotype.
+COMT	drug	nicotine	21312287	Using a case control sample of 90 young, Israeli, Jewish female <b>smokers</b> (FTND ≥ 4) and 108 controls (FTND = 0 during heaviest period of <b>smoking</b>), we studied association with ND of 8 <strong>COMT</strong> tagging SNPs, their interaction with tagging CHRNA5 A3 SNPs and the role of background, personality, and environmental factors.
+COMT	drug	alcohol	21309949	<strong>COMT</strong> and ALDH2 polymorphisms moderate associations of implicit drinking motives with <b>alcohol</b> use.
+COMT	drug	alcohol	21309949	The current study examined two polymorphisms with functional significance for <b>alcohol</b> use behavior (<strong>COMT</strong> Val158Met and ALDH2*2) in relation to automatic <b>alcohol</b> cognitions and tested additive and interactive effects of genotype and implicit cognitions on drinking behavior.
+COMT	drug	alcohol	21309949	Interaction effects indicated that associations of implicit motives with drinking outcomes were strongest in the context of genetic variants associated with relatively higher risk for <b>alcohol</b> use (<strong>COMT</strong> Met and ALDH2*1).
+COMT	addiction	addiction	21118356	MAO A and <strong>COMT</strong> have a minor role in <b>addiction</b> like behaviour that is further complicated by a sexual dimorphism.
+COMT	addiction	addiction	20975619	Are genetic variants of <strong>COMT</strong> associated with <b>addiction</b>?
+COMT	drug	alcohol	20975619	This article reviews human studies that have explored the association between <strong>COMT</strong> polymorphisms and addiction to drugs, <b>alcohol</b> or tobacco.
+COMT	drug	nicotine	20975619	This article reviews human studies that have explored the association between <strong>COMT</strong> polymorphisms and addiction to drugs, alcohol or <b>tobacco</b>.
+COMT	addiction	addiction	20975619	This article reviews human studies that have explored the association between <strong>COMT</strong> polymorphisms and <b>addiction</b> to drugs, alcohol or tobacco.
+COMT	drug	nicotine	20975619	Although there are reports indicating a positive association with <strong>COMT</strong> polymorphisms and addiction, the majority of the studies failed to detect such a link between them with one exception, <b>smoking</b>.
+COMT	addiction	addiction	20975619	Although there are reports indicating a positive association with <strong>COMT</strong> polymorphisms and <b>addiction</b>, the majority of the studies failed to detect such a link between them with one exception, smoking.
+COMT	addiction	addiction	20975619	Rather, there seems to be a great number of genes that are associated with <b>addiction</b>, among which <strong>COMT</strong> seems to have a minor role.
+COMT	addiction	addiction	20975619	Environmental factors and genetic milieu have a great impact on whether the small effects of <strong>COMT</strong> polymorphisms on risk of <b>addiction</b> can be detected in a given population.
+COMT	drug	alcohol	20860878	Association study of a functional catechol O methyltransferase (<strong>COMT</strong>) Val108/158Met polymorphism and suicide attempts in patients with <b>alcohol</b> dependence.
+COMT	addiction	dependence	20860878	Association study of a functional catechol O methyltransferase (<strong>COMT</strong>) Val108/158Met polymorphism and suicide attempts in patients with alcohol <b>dependence</b>.
+COMT	drug	alcohol	20860878	Association study of a functional <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val108/158Met polymorphism and suicide attempts in patients with <b>alcohol</b> dependence.
+COMT	addiction	dependence	20860878	Association study of a functional <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val108/158Met polymorphism and suicide attempts in patients with alcohol <b>dependence</b>.
+COMT	drug	alcohol	20860878	Our results showed significant (χ2 test with standardized residuals) differences in the frequencies of <strong>COMT</strong> variants in all <b>alcoholics</b>, <b>alcoholics</b> with different comorbid diagnoses, and in male but not in female <b>alcoholics</b>, with or without suicide attempts.
+COMT	drug	cocaine	20801583	Several studies have looked for a link between <b>cocaine</b> addiction and the genes of the dopaminergic system: the genes DRD2, <strong>COMT</strong>, SLC6A3 (coding for the dopamine transporter DAT) and DBH (coding for the dopamine beta hydroxylase) but unfortunately very few well established results.
+COMT	addiction	addiction	20801583	Several studies have looked for a link between cocaine <b>addiction</b> and the genes of the dopaminergic system: the genes DRD2, <strong>COMT</strong>, SLC6A3 (coding for the dopamine transporter DAT) and DBH (coding for the dopamine beta hydroxylase) but unfortunately very few well established results.
+COMT	drug	cocaine	20801583	Several functional alterations caused by different mutations of the genes involved in dopaminergic transmission (principally 1021C>T of the gene DBH, but also Val158Met of the gene <strong>COMT</strong>, TaqI A of the gene DRD2 and VNTR 9 repeat of the DAT) could result in a <b>cocaine</b> induced psychosis prone phenotype.
+COMT	addiction	relapse	20728009	Association between Novelty <b>Seeking</b> of opiate dependent patients and the <strong>catechol O methyltransferase</strong> Val(158)Met polymorphism.
+COMT	drug	amphetamine	20728009	Catechol O methyltransferase (<strong>COMT</strong>) plays a vital role in dopamine inactivation, and the Val(158)Met single nucleotide polymorphism (rs4680) in its gene has been recently associated with the Novelty Seeking (NS) temperament scale of the Temperament and Character Inventory in studies of healthy adults, as well as <b>methamphetamine</b> abusers.
+COMT	addiction	relapse	20728009	Catechol O methyltransferase (<strong>COMT</strong>) plays a vital role in dopamine inactivation, and the Val(158)Met single nucleotide polymorphism (rs4680) in its gene has been recently associated with the Novelty <b>Seeking</b> (NS) temperament scale of the Temperament and Character Inventory in studies of healthy adults, as well as methamphetamine abusers.
+COMT	drug	amphetamine	20728009	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) plays a vital role in dopamine inactivation, and the Val(158)Met single nucleotide polymorphism (rs4680) in its gene has been recently associated with the Novelty Seeking (NS) temperament scale of the Temperament and Character Inventory in studies of healthy adults, as well as <b>methamphetamine</b> abusers.
+COMT	addiction	relapse	20728009	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) plays a vital role in dopamine inactivation, and the Val(158)Met single nucleotide polymorphism (rs4680) in its gene has been recently associated with the Novelty <b>Seeking</b> (NS) temperament scale of the Temperament and Character Inventory in studies of healthy adults, as well as methamphetamine abusers.
+COMT	drug	opioid	20728009	Our goal was to examine the association between temperament dimensions of the Temperament and Character Inventory and the <strong>COMT</strong> Val(158)Met variation in a Hungarian sample of 117 <b>heroin</b> dependent patients and 124 nondependent controls.
+COMT	drug	opioid	20728009	Association of the <strong>COMT</strong> polymorphism and NS temperament scale has been shown for <b>heroin</b> dependent patients and controls regardless of group status.
+COMT	drug	nicotine	20712524	This study evaluates the relationship of six polymorphisms found in the CHRNA3, DRD2 and <strong>COMT</strong> genes with <b>nicotine</b> dependence, the ability to quit <b>smoking</b> and the occurrence of withdrawal symptoms after short term use of <b>nicotine</b> patch in hospitalized patients.
+COMT	addiction	dependence	20712524	This study evaluates the relationship of six polymorphisms found in the CHRNA3, DRD2 and <strong>COMT</strong> genes with nicotine <b>dependence</b>, the ability to quit smoking and the occurrence of withdrawal symptoms after short term use of nicotine patch in hospitalized patients.
+COMT	addiction	withdrawal	20712524	This study evaluates the relationship of six polymorphisms found in the CHRNA3, DRD2 and <strong>COMT</strong> genes with nicotine dependence, the ability to quit smoking and the occurrence of <b>withdrawal</b> symptoms after short term use of nicotine patch in hospitalized patients.
+COMT	drug	alcohol	20517217	[Association study of the Val158Met polymorphism of the <strong>catechol O methyltransferase</strong> gene and <b>alcoholism</b> and heroin dependence: the role of a family history].
+COMT	drug	opioid	20517217	[Association study of the Val158Met polymorphism of the <strong>catechol O methyltransferase</strong> gene and alcoholism and <b>heroin</b> dependence: the role of a family history].
+COMT	addiction	dependence	20517217	[Association study of the Val158Met polymorphism of the <strong>catechol O methyltransferase</strong> gene and alcoholism and heroin <b>dependence</b>: the role of a family history].
+COMT	drug	alcohol	20517217	The aim of this study was to investigate the association the Val158Met polymorphism of the catechol O methyltransferase (<strong>COMT</strong>) gene and predisposition to <b>alcoholism</b> and heroin dependence.
+COMT	drug	opioid	20517217	The aim of this study was to investigate the association the Val158Met polymorphism of the catechol O methyltransferase (<strong>COMT</strong>) gene and predisposition to alcoholism and <b>heroin</b> dependence.
+COMT	addiction	dependence	20517217	The aim of this study was to investigate the association the Val158Met polymorphism of the catechol O methyltransferase (<strong>COMT</strong>) gene and predisposition to alcoholism and heroin <b>dependence</b>.
+COMT	drug	alcohol	20517217	The aim of this study was to investigate the association the Val158Met polymorphism of the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene and predisposition to <b>alcoholism</b> and heroin dependence.
+COMT	drug	opioid	20517217	The aim of this study was to investigate the association the Val158Met polymorphism of the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene and predisposition to alcoholism and <b>heroin</b> dependence.
+COMT	addiction	dependence	20517217	The aim of this study was to investigate the association the Val158Met polymorphism of the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene and predisposition to alcoholism and heroin <b>dependence</b>.
+COMT	drug	alcohol	20517217	The association between the Val158Met <strong>COMT</strong> polymorphism and <b>alcoholism</b> was found in males with high density of family history (two or more blood relatives with <b>alcoholism</b> within the family).
+COMT	addiction	addiction	20517217	The results suggest that the functional Val158Met <strong>COMT</strong> polymorphism is one of the significant markers of genetic predisposition to <b>addiction</b> diseases.
+COMT	drug	amphetamine	20478633	A total of 193 non psychotic males (117 <b>methamphetamine</b> dependent and 76 controls) were genotyped for variants located in six genes (AKT1, ARRB2, BDNF, <strong>COMT</strong>, GSTP1, OPRM1).
+COMT	drug	nicotine	20456288	Genetic variation in D2 type DA receptors and the <strong>catechol O methyltransferase</strong> enzyme appears to moderate cognitive deficits induced by <b>smoking</b> abstinence.
+COMT	drug	opioid	20230086	The purpose of the present investigation was to determine if variation in the catechol O methyltransferase (<strong>COMT</strong>) and mu <b>opioid</b> receptor (OPRM1) genes is associated with pain related positive affective regulation in fibromyalgia (FM).
+COMT	drug	opioid	20230086	The purpose of the present investigation was to determine if variation in the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) and mu <b>opioid</b> receptor (OPRM1) genes is associated with pain related positive affective regulation in fibromyalgia (FM).
+COMT	drug	nicotine	20188797	Association study of a functional <strong>catechol O methyltransferase</strong> polymorphism and <b>smoking</b> in healthy Caucasian subjects.
+COMT	drug	nicotine	20188797	The association of a functional common polymorphism in the catechol o methyltransferase gene (<strong>COMT</strong> Val158Met) with <b>smoking</b> behavior has been extensively studied, but with divergent findings.
+COMT	drug	nicotine	20188797	The association of a functional common polymorphism in the <strong>catechol o methyltransferase</strong> gene (<strong>COMT</strong> Val158Met) with <b>smoking</b> behavior has been extensively studied, but with divergent findings.
+COMT	drug	nicotine	20188797	This significant association between <strong>COMT</strong> Val158Met polymorphism and <b>smoking</b> was not detected in female subjects, due to the small number of women, which represents a limitation of the study.
+COMT	drug	nicotine	20188797	Our results confirmed the significant association between <strong>COMT</strong> variants and <b>smoking</b>, which was due to the higher frequency of Val/Val homozygotes in male <b>smokers</b> compared to male nonsmokers.
+COMT	drug	nicotine	20188797	These results suggest that carriers of the high activity <strong>COMT</strong> variant are more prone to develop a higher level of <b>nicotine</b> dependence, or that they release more dopamine than carriers of Met/Met or Met/Val genotypes.
+COMT	addiction	dependence	20188797	These results suggest that carriers of the high activity <strong>COMT</strong> variant are more prone to develop a higher level of nicotine <b>dependence</b>, or that they release more dopamine than carriers of Met/Met or Met/Val genotypes.
+COMT	drug	nicotine	20070134	Association between <strong>COMT</strong>, PTSD, and increased <b>smoking</b> following hurricane exposure in an epidemiologic sample.
+COMT	drug	nicotine	20070134	Initiation and persistence of cigarette <b>smoking</b> is moderately heritable; two recent investigations have implicated the <strong>COMT</strong> Val158Met (also known as rs4680) polymorphism in <b>smoking</b> age of initiation, dependence, as well as in quantity and frequency of <b>smoking</b>.
+COMT	addiction	dependence	20070134	Initiation and persistence of cigarette smoking is moderately heritable; two recent investigations have implicated the <strong>COMT</strong> Val158Met (also known as rs4680) polymorphism in smoking age of initiation, <b>dependence</b>, as well as in quantity and frequency of smoking.
+COMT	drug	nicotine	20070134	To examine a possible association of <strong>COMT</strong> Val158Met and posttrauma increases in cigarette <b>smoking</b>, we studied 614 adults from the 2004 Florida Hurricane Study who returned saliva DNA samples via mail.
+COMT	drug	nicotine	20070134	Moreover, each <strong>COMT</strong> Val158Met 'Met' allele predicted a 2.10 fold risk of <b>smoking</b> post hurricane, independent of PTSD; follow up analyses revealed that this finding was primarily driven by European American males.
+COMT	drug	amphetamine	20069120	<strong>COMT</strong> Val158Met Polymorphism, Executive Dysfunction, and Sexual Risk Behavior in the Context of HIV Infection and <b>Methamphetamine</b> Dependence.
+COMT	addiction	dependence	20069120	<strong>COMT</strong> Val158Met Polymorphism, Executive Dysfunction, and Sexual Risk Behavior in the Context of HIV Infection and Methamphetamine <b>Dependence</b>.
+COMT	drug	amphetamine	24078782	Impact of <strong>COMT</strong> Val158Met on executive functioning in the context of HIV and <b>methamphetamine</b>.
+COMT	drug	amphetamine	24078782	We sought to determine if the putative relationship between <strong>COMT</strong> and executive dysfunction could be observed among individuals with and without HIV infection and/or <b>METH</b> dependence, and to explore the specificity of this relationship by examining other cognitive domains.
+COMT	addiction	dependence	24078782	We sought to determine if the putative relationship between <strong>COMT</strong> and executive dysfunction could be observed among individuals with and without HIV infection and/or METH <b>dependence</b>, and to explore the specificity of this relationship by examining other cognitive domains.
+COMT	drug	nicotine	21423427	Determination of Methylated CpG Sites in the Promoter Region of Catechol O Methyltransferase (<strong>COMT</strong>) and their Involvement in the Etiology of <b>Tobacco</b> <b>Smoking</b>.
+COMT	drug	nicotine	21423427	Determination of Methylated CpG Sites in the Promoter Region of <strong>Catechol O Methyltransferase</strong> (<strong>COMT</strong>) and their Involvement in the Etiology of <b>Tobacco</b> <b>Smoking</b>.
+COMT	drug	nicotine	21423427	We previously reported that catechol O methyltransferase (<strong>COMT</strong>) is significantly associated with <b>nicotine</b> dependence (ND) in humans.
+COMT	addiction	dependence	21423427	We previously reported that catechol O methyltransferase (<strong>COMT</strong>) is significantly associated with nicotine <b>dependence</b> (ND) in humans.
+COMT	drug	nicotine	21423427	We previously reported that <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) is significantly associated with <b>nicotine</b> dependence (ND) in humans.
+COMT	addiction	dependence	21423427	We previously reported that <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) is significantly associated with nicotine <b>dependence</b> (ND) in humans.
+COMT	drug	nicotine	21423427	In this study, we examined whether there exists any difference in the extent of methylation of CpG dinucleotides in the promoter region of <strong>COMT</strong> in <b>smokers</b> and non <b>smokers</b> by analyzing the methylation status of cytosines at 33 CpG sites through direct sequencing of bisulfite treated DNA (N = 50 per group).
+COMT	drug	nicotine	21423427	Together, our findings provide the first molecular explanation at the epigenetic level for the association of ND with methylation of the <strong>COMT</strong> promoter, implying that methylation plays a role in <b>smoking</b> dependence.
+COMT	addiction	dependence	21423427	Together, our findings provide the first molecular explanation at the epigenetic level for the association of ND with methylation of the <strong>COMT</strong> promoter, implying that methylation plays a role in smoking <b>dependence</b>.
+COMT	drug	cannabinoid	19944543	Because paranoia is a common feature of stimulant abuse and cocaine dependent individuals frequently endorse a history of <b>cannabis</b> abuse, we examined whether early <b>cannabis</b> exposure, in conjunction with polymorphic variation in the catechol O methyl transferase gene (<strong>COMT</strong> Val158Met), influences the risk for cocaine induced paranoia (CIP).
+COMT	drug	cocaine	19944543	Because paranoia is a common feature of stimulant abuse and <b>cocaine</b> dependent individuals frequently endorse a history of cannabis abuse, we examined whether early cannabis exposure, in conjunction with polymorphic variation in the catechol O methyl transferase gene (<strong>COMT</strong> Val158Met), influences the risk for <b>cocaine</b> induced paranoia (CIP).
+COMT	drug	cannabinoid	19944543	Logistic regression and generalized estimating equations' analyses were used to examine the role of adolescent onset <b>cannabis</b> use (< or =15 years of age) on CIP risk, both controlling for previously implicated CIP risk factors and familial relationships, and considering potential interactions with <strong>COMT</strong> Val158Met genotype.
+COMT	drug	cannabinoid	19944543	There were no effects of <strong>COMT</strong> genotype or genotype by early <b>cannabis</b> onset interactions.
+COMT	drug	cannabinoid	19944543	<strong>COMT</strong> genotype and its interaction with early <b>cannabis</b> exposure did not emerge as significant predictors of CIP.
+COMT	addiction	relapse	19940429	This hypothesized mechanism is supported by clinical trials utilizing amino acid neurotransmitter precursors, enkephalinase, and catechol O methyltransferase (<strong>COMT</strong>) enzyme inhibition, which have resulted in attenuated <b>relapse</b> rates in reward deficiency syndrome (RDS) probands.
+COMT	addiction	reward	19940429	This hypothesized mechanism is supported by clinical trials utilizing amino acid neurotransmitter precursors, enkephalinase, and catechol O methyltransferase (<strong>COMT</strong>) enzyme inhibition, which have resulted in attenuated relapse rates in <b>reward</b> deficiency syndrome (RDS) probands.
+COMT	addiction	relapse	19940429	This hypothesized mechanism is supported by clinical trials utilizing amino acid neurotransmitter precursors, enkephalinase, and <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) enzyme inhibition, which have resulted in attenuated <b>relapse</b> rates in reward deficiency syndrome (RDS) probands.
+COMT	addiction	reward	19940429	This hypothesized mechanism is supported by clinical trials utilizing amino acid neurotransmitter precursors, enkephalinase, and <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) enzyme inhibition, which have resulted in attenuated relapse rates in <b>reward</b> deficiency syndrome (RDS) probands.
+COMT	addiction	relapse	19940429	This term couples the mechanism for <b>relapse</b>, which is "deprivation amplification," especially in DRD2 A1 allele carriers with natural D2 agonist therapy utilizing amino acid precursors and <strong>COMT</strong> and enkepalinase inhibition therapy.
+COMT	drug	cannabinoid	19931559	(3) Feeding motivation  and reward related systems (opioids, OPRD1, <b>cannabinoids</b> (anandamide (AEA), <b>THC</b>, CBR1), dopamine, DRD2, DRD3, DRD4, catecholamine O methyl transferase (<strong>COMT</strong>).
+COMT	drug	opioid	19931559	(3) Feeding motivation  and reward related systems (<b>opioids</b>, OPRD1, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, DRD3, DRD4, catecholamine O methyl transferase (<strong>COMT</strong>).
+COMT	addiction	reward	19931559	(3) Feeding motivation  and <b>reward</b> related systems (opioids, OPRD1, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, DRD3, DRD4, catecholamine O methyl transferase (<strong>COMT</strong>).
+COMT	drug	opioid	19827317	In connection with the development of <b>heroin</b> addiction the role of the dopamine D2 and D4 receptors, the dopamine transporter and the <strong>catechol O methyltransferase</strong> genes is discussed.
+COMT	addiction	addiction	19827317	In connection with the development of heroin <b>addiction</b> the role of the dopamine D2 and D4 receptors, the dopamine transporter and the <strong>catechol O methyltransferase</strong> genes is discussed.
+COMT	addiction	relapse	19693267	Novelty <b>seeking</b>, another risk attitude measure from the psychology literature, is associated with several <strong>COMT</strong> (catechol O methyl transferase) SNPs while economic risk attitude measures are associated with several VMAT2 (vesicular monoamine transporter) SNPs, but the significance of these associations did not withstand statistical adjustment for multiple testing and requires larger cohorts.
+COMT	drug	nicotine	19584770	Variants in <strong>COMT</strong> and spontaneous <b>smoking</b> cessation: retrospective cohort analysis of 925 cessation events.
+COMT	drug	nicotine	19584770	Less is known about genetic determinants of <b>smoking</b> cessation, but rs4680 in <strong>COMT</strong> has recently been shown to explain a substantial proportion of the variation in cessation in the general population.
+COMT	drug	amphetamine	19462300	<strong>COMT</strong>, D4 receptor, and BDNF polymorphisms are linked to <b>methamphetamine</b> abuse and psychosis.
+COMT	drug	nicotine	19415821	In this study, we investigated the association and multilocus gene gene interactions of cytochrome P450 2A6 (CYP2A6), dopamine beta hydroxylase (DBH), catechol O methyl transferase (<strong>COMT</strong>), and monoamine oxidase A (MAOA) polymorphisms with <b>smoking</b> behavior in a community based Chinese male population.
+COMT	drug	amphetamine	19259017	A functional polymorphism (<strong>COMT</strong> Val158Met) resulting in increased enzyme activity has been associated with polysubstance abuse and addiction to heroin and <b>methamphetamine</b>.
+COMT	drug	opioid	19259017	A functional polymorphism (<strong>COMT</strong> Val158Met) resulting in increased enzyme activity has been associated with polysubstance abuse and addiction to <b>heroin</b> and methamphetamine.
+COMT	addiction	addiction	19259017	A functional polymorphism (<strong>COMT</strong> Val158Met) resulting in increased enzyme activity has been associated with polysubstance abuse and <b>addiction</b> to heroin and methamphetamine.
+COMT	drug	cannabinoid	19259017	The aim of this study was to examine the relationship between the <strong>COMT</strong> Val158Met polymorphism and use of <b>cannabis</b>.
+COMT	drug	cannabinoid	19259017	There was a difference in genotype frequencies between <b>cannabis</b> users and controls, including the distribution of the <strong>COMT</strong> genotypes (H/H, H/L) (P < 0.001) and alleles (H, L) (P < 0.01), when comparing the patient groups and the control individuals.
+COMT	drug	cannabinoid	19259017	These results suggest a significant association between <strong>COMT</strong> Val158Met polymorphism and susceptibility to <b>cannabis</b> dependence.
+COMT	addiction	dependence	19259017	These results suggest a significant association between <strong>COMT</strong> Val158Met polymorphism and susceptibility to cannabis <b>dependence</b>.
+COMT	drug	amphetamine	19219857	Three genes (<strong>COMT</strong>, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with <b>METH</b> psychosis.
+COMT	addiction	dependence	19219857	Three genes (<strong>COMT</strong>, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.
+COMT	addiction	relapse	19170664	Genetic polymorphisms in several genes (TPH2, SLC6A4, HTR1A, HTR2A, <strong>COMT</strong>, and BDNF) were tested as predictors of <b>relapse</b> (defined as any drinking during follow up) while controlling for baseline measures.
+COMT	addiction	relapse	19170664	Patients with the Val allele in the Val66Met BDNF polymorphism and the Met allele in the Val158Met <strong>COMT</strong> polymorphism were more likely to <b>relapse</b>.
+COMT	drug	nicotine	19160592	The effect of <strong>catechol O methyltransferase</strong> Met/Val functional polymorphism on <b>smoking</b> cessation: retrospective and prospective analyses in a cohort study.
+COMT	drug	nicotine	19160592	The Met/Val functional polymorphism of the gene encoding catechol O methyltransferase (<strong>COMT</strong>) is one of the most widely tested variants for association with different phenotypes of addictive behavior, but replication has been inconsistent for <b>smoking</b> status.
+COMT	addiction	addiction	19160592	The Met/Val functional polymorphism of the gene encoding catechol O methyltransferase (<strong>COMT</strong>) is one of the most widely tested variants for association with different phenotypes of <b>addictive</b> behavior, but replication has been inconsistent for smoking status.
+COMT	drug	nicotine	19160592	The Met/Val functional polymorphism of the gene encoding <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) is one of the most widely tested variants for association with different phenotypes of addictive behavior, but replication has been inconsistent for <b>smoking</b> status.
+COMT	addiction	addiction	19160592	The Met/Val functional polymorphism of the gene encoding <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) is one of the most widely tested variants for association with different phenotypes of <b>addictive</b> behavior, but replication has been inconsistent for smoking status.
+COMT	drug	nicotine	19160592	We investigated the relationship of this <strong>COMT</strong> single nucleotide polymorphism with <b>smoking</b> cessation in elderly persons in retrospective and prospective analyses.
+COMT	drug	nicotine	19160592	In the prospective analyses, we followed 1,195 current <b>smokers</b> up to 12 years and used Cox proportional hazard model to detect the effect of the <strong>COMT</strong> single nucleotide polymorphism on self reported incidence of <b>smoking</b> cessation.
+COMT	drug	nicotine	19160592	The Val/Val genotype of <strong>COMT</strong> had a consistent association with <b>smoking</b> cessation as compared with the Met/Met+Met/Val genotypes in retrospective [odds ratio=0.79, 95% confidence interval (CI): 0.66 0.96, P=0.02] and prospective analyses (hazard ratio=0.80, 95% CI: 0.63 1.01, P=0.06).
+COMT	drug	nicotine	19160592	No sex difference and no effect of the <strong>COMT</strong> polymorphism on <b>smoking</b> initiation were observed.
+COMT	drug	nicotine	19160592	Our results suggest that <strong>COMT</strong> Met/Val polymorphism is strongly associated with <b>smoking</b> cessation.
+COMT	drug	amphetamine	19148623	<b>Amphetamine</b> decreased PPI in SD rats that have relatively low NAC <strong>COMT</strong> gene expression and increased PPI in LE rats that have relatively high NAC <strong>COMT</strong> gene expression.
+COMT	drug	amphetamine	19148623	In rats, the effects of <b>amphetamine</b> on PPI differ significantly in strains with low vs. high NAC <strong>COMT</strong> expression.
+COMT	drug	nicotine	19065145	Effect of abstinence challenge on brain function and cognition in <b>smokers</b> differs by <strong>COMT</strong> genotype.
+COMT	drug	nicotine	19065145	The val allele of the catechol O methyltransferase (<strong>COMT</strong>) val(158)met polymorphism has been linked with <b>nicotine</b> dependence and with cognitive performance in healthy volunteers.
+COMT	addiction	dependence	19065145	The val allele of the catechol O methyltransferase (<strong>COMT</strong>) val(158)met polymorphism has been linked with nicotine <b>dependence</b> and with cognitive performance in healthy volunteers.
+COMT	drug	nicotine	19065145	The val allele of the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) val(158)met polymorphism has been linked with <b>nicotine</b> dependence and with cognitive performance in healthy volunteers.
+COMT	addiction	dependence	19065145	The val allele of the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) val(158)met polymorphism has been linked with nicotine <b>dependence</b> and with cognitive performance in healthy volunteers.
+COMT	drug	nicotine	19065145	Chronic <b>smokers</b> (n=33) were genotyped prospectively for the <strong>COMT</strong> polymorphism for balanced selection of met/met, val/met and val/val groups.
+COMT	drug	nicotine	19065145	These data suggest a novel brain behavior mechanism that may underlie the increased susceptibility to <b>nicotine</b> dependence and <b>smoking</b> relapse associated with the <strong>COMT</strong> val allele.
+COMT	addiction	dependence	19065145	These data suggest a novel brain behavior mechanism that may underlie the increased susceptibility to nicotine <b>dependence</b> and smoking relapse associated with the <strong>COMT</strong> val allele.
+COMT	addiction	relapse	19065145	These data suggest a novel brain behavior mechanism that may underlie the increased susceptibility to nicotine dependence and smoking <b>relapse</b> associated with the <strong>COMT</strong> val allele.
+COMT	drug	nicotine	19065145	Exploration of the effects of <strong>COMT</strong> inhibitors as a possible <b>smoking</b> cessation aid in this group may be warranted.
+COMT	drug	alcohol	19014506	Individuals possessing a paucity of serotonergic and/or dopaminergic receptors, and an increased rate of synaptic DA catabolism due to high catabolic genotype of the <strong>COMT</strong> gene, are predisposed to self medicating any substance or behavior that will activate DA release, including <b>alcohol</b>, opiates, psychostimulants, nicotine, gambling, sex, and even excessive internet gaming.
+COMT	drug	nicotine	19014506	Individuals possessing a paucity of serotonergic and/or dopaminergic receptors, and an increased rate of synaptic DA catabolism due to high catabolic genotype of the <strong>COMT</strong> gene, are predisposed to self medicating any substance or behavior that will activate DA release, including alcohol, opiates, psychostimulants, <b>nicotine</b>, gambling, sex, and even excessive internet gaming.
+COMT	drug	cocaine	18923401	In this issue of Neuropsychopharmacology, several studies are presented supporting a role for <strong>COMT</strong> as a factor in <b>cocaine</b> addiction, brain reward activation, response to tolcapone, distractibility in ADHD, and fMRI bold response.
+COMT	addiction	addiction	18923401	In this issue of Neuropsychopharmacology, several studies are presented supporting a role for <strong>COMT</strong> as a factor in cocaine <b>addiction</b>, brain reward activation, response to tolcapone, distractibility in ADHD, and fMRI bold response.
+COMT	addiction	reward	18923401	In this issue of Neuropsychopharmacology, several studies are presented supporting a role for <strong>COMT</strong> as a factor in cocaine addiction, brain <b>reward</b> activation, response to tolcapone, distractibility in ADHD, and fMRI bold response.
+COMT	drug	opioid	18834357	Stress induced analgesia and <b>morphine</b> responses are changed in <strong>catechol O methyltransferase</strong> deficient male mice.
+COMT	drug	opioid	18834357	Catechol O methyltransferase (<strong>COMT</strong>) polymorphisms modulate pain and <b>opioid</b> analgesia in human beings.
+COMT	drug	opioid	18834357	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) polymorphisms modulate pain and <b>opioid</b> analgesia in human beings.
+COMT	drug	opioid	18834357	In the hot plate test, <b>morphine</b> induced antinociception was significantly greater in the <strong>COMT</strong> knock out mice, compared to the wild type mice.
+COMT	drug	opioid	18834357	In the tail flick test, <b>opioid</b> mediated stress induced analgesia was absent and <b>morphine</b> induced analgesia was decreased in <strong>COMT</strong> knock out mice.
+COMT	drug	opioid	18834357	Our findings show, for the first time, the importance of <strong>COMT</strong> activity in stress  and <b>morphine</b> induced analgesia in mice.
+COMT	drug	nicotine	18781857	Several candidate genes within the dopamine pathway (e.g., DRD2 and <strong>COMT</strong>) have been reported to be associated with the efficacy of bupropion and <b>nicotine</b> replacement therapy, and others (e.g., SLC6A3 and DRD4) have been reported to be associated with <b>smoking</b> cessation independent of pharmacotherapy.
+COMT	drug	cocaine	18704099	Association between the <strong>catechol O methyltransferase</strong> Val158Met polymorphism and <b>cocaine</b> dependence.
+COMT	addiction	dependence	18704099	Association between the <strong>catechol O methyltransferase</strong> Val158Met polymorphism and cocaine <b>dependence</b>.
+COMT	drug	cocaine	18704099	In this study we hypothesize that genetic variation in the <strong>COMT</strong> gene contributes to increased risk for <b>cocaine</b> dependence.
+COMT	addiction	dependence	18704099	In this study we hypothesize that genetic variation in the <strong>COMT</strong> gene contributes to increased risk for cocaine <b>dependence</b>.
+COMT	drug	cocaine	18704099	<b>Cocaine</b> dependent individuals (n=330) and screened unaffected normal controls (n=255) were genotyped for three SNPs in the <strong>COMT</strong> gene (rs737865, rs4680 (Val158Met), rs165599).
+COMT	drug	cocaine	18704099	Results suggest that variation in <strong>COMT</strong> increases risk for <b>cocaine</b> dependence.
+COMT	addiction	dependence	18704099	Results suggest that variation in <strong>COMT</strong> increases risk for cocaine <b>dependence</b>.
+COMT	drug	alcohol	18684228	Increase in free choice oral <b>ethanol</b> self administration in <strong>catechol o methyltransferase</strong> gene disrupted male mice.
+COMT	drug	alcohol	18684228	The effect of catechol O methyltransferase (<strong>Comt</strong>) gene disruption on the voluntary oral consumption of water, <b>ethanol</b> (2.5 20%, v/v) and cocaine (0.1 0.8 mg/ml) was studied in the free choice, two bottle paradigm in male and female mice.
+COMT	drug	cocaine	18684228	The effect of catechol O methyltransferase (<strong>Comt</strong>) gene disruption on the voluntary oral consumption of water, ethanol (2.5 20%, v/v) and <b>cocaine</b> (0.1 0.8 mg/ml) was studied in the free choice, two bottle paradigm in male and female mice.
+COMT	drug	alcohol	18684228	The effect of <strong>catechol O methyltransferase</strong> (<strong>Comt</strong>) gene disruption on the voluntary oral consumption of water, <b>ethanol</b> (2.5 20%, v/v) and cocaine (0.1 0.8 mg/ml) was studied in the free choice, two bottle paradigm in male and female mice.
+COMT	drug	cocaine	18684228	The effect of <strong>catechol O methyltransferase</strong> (<strong>Comt</strong>) gene disruption on the voluntary oral consumption of water, ethanol (2.5 20%, v/v) and <b>cocaine</b> (0.1 0.8 mg/ml) was studied in the free choice, two bottle paradigm in male and female mice.
+COMT	drug	alcohol	18684228	<strong>Catechol O methyltransferase</strong> deficient male mice consumed significantly more <b>ethanol</b> than their wild type male littermates.
+COMT	drug	cocaine	18684228	In female mice, <strong>Comt</strong> genotype was not associated with <b>cocaine</b> consumption.
+COMT	drug	alcohol	18684228	In conclusion, disruption of <strong>Comt</strong> gene influenced <b>ethanol</b> consumption in a gender dependent manner in mice, supporting the hypothesis that low catechol O methyltransferase activity is one of the predisposing factors for high <b>alcohol</b> consumption in males.
+COMT	drug	alcohol	18684228	In conclusion, disruption of <strong>Comt</strong> gene influenced <b>ethanol</b> consumption in a gender dependent manner in mice, supporting the hypothesis that low <strong>catechol O methyltransferase</strong> activity is one of the predisposing factors for high <b>alcohol</b> consumption in males.
+COMT	drug	nicotine	18499348	Thirteen <b>smokers</b> participating in a prior arterial spin labeled (ASL) perfusion MRI study were scanned on two occasions (after >12h abstinence vs. satiety), and were genotyped for variants in the dopamine D2 receptor (DRD2 141 Ins/DelC; DRD2 C957T); a dopamine metabolizing enzyme (<strong>COMT</strong> val(158) met), and the mu opioid receptor (OPRM1 A118G).
+COMT	drug	opioid	18499348	Thirteen smokers participating in a prior arterial spin labeled (ASL) perfusion MRI study were scanned on two occasions (after >12h abstinence vs. satiety), and were genotyped for variants in the dopamine D2 receptor (DRD2 141 Ins/DelC; DRD2 C957T); a dopamine metabolizing enzyme (<strong>COMT</strong> val(158) met), and the mu <b>opioid</b> receptor (OPRM1 A118G).
+COMT	drug	alcohol	18424410	The review focuses on several related genes that control <b>alcohol</b> metabolism such as <b>alcohol</b> dehydrogenase, aldehyde dehydrogenase, cytochrome P450 2E1 and regulate neurotransmission such as <strong>catechol O methyltransferase</strong>, dopamine receptors D2 and D4, and mu opioid receptor.
+COMT	drug	opioid	18424410	The review focuses on several related genes that control alcohol metabolism such as alcohol dehydrogenase, aldehyde dehydrogenase, cytochrome P450 2E1 and regulate neurotransmission such as <strong>catechol O methyltransferase</strong>, dopamine receptors D2 and D4, and mu <b>opioid</b> receptor.
+COMT	addiction	addiction	18270997	Catechol O methyltransferase (<strong>COMT</strong>) gene variants: possible association of the Val158Met variant with opiate <b>addiction</b> in Hispanic women.
+COMT	addiction	addiction	18270997	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) gene variants: possible association of the Val158Met variant with opiate <b>addiction</b> in Hispanic women.
+COMT	addiction	reward	18270997	Catechol O methyltransferase (<strong>COMT</strong>) catalyzes the breakdown of catechol neurotransmitters, including dopamine, which plays a prominent role in drug <b>reward</b>.
+COMT	addiction	reward	18270997	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) catalyzes the breakdown of catechol neurotransmitters, including dopamine, which plays a prominent role in drug <b>reward</b>.
+COMT	drug	opioid	18270997	We sequenced exon IV of <strong>COMT</strong> gene in search for novel polymorphisms and then genotyped four out of five identified by direct sequencing, using TaqMan assay on 266 <b>opioid</b> dependent and 173 control subjects.
+COMT	drug	nicotine	18192898	Association of <strong>COMT</strong> Val108/158Met genotype with <b>smoking</b> cessation.
+COMT	drug	nicotine	18192898	We attempted to extend a previous finding of an association of <strong>COMT</strong> genotype with response to <b>nicotine</b> replacement therapy (NRT), in a larger cohort of treatment seeking <b>smokers</b>, with greater statistical power to detect possible moderating effects of sex.
+COMT	addiction	relapse	18192898	We attempted to extend a previous finding of an association of <strong>COMT</strong> genotype with response to nicotine replacement therapy (NRT), in a larger cohort of treatment <b>seeking</b> smokers, with greater statistical power to detect possible moderating effects of sex.
+COMT	addiction	withdrawal	18192898	We also investigated the association of the <strong>COMT</strong> genotype with <b>withdrawal</b> and mood symptoms, to identify possible mediating mechanisms by which the <strong>COMT</strong> genotype might influence response to NRT.
+COMT	drug	nicotine	18192898	Cox regression analysis indicated a significant effect of the <strong>COMT</strong> genotype on relapse into <b>smoking</b> (P=0.001), with shorter times to relapse being observed among the AG (Val/Met) and GG (Val/Val) genotype groups.
+COMT	addiction	relapse	18192898	Cox regression analysis indicated a significant effect of the <strong>COMT</strong> genotype on <b>relapse</b> into smoking (P=0.001), with shorter times to <b>relapse</b> being observed among the AG (Val/Met) and GG (Val/Val) genotype groups.
+COMT	drug	nicotine	18192898	Our results indicate that the <strong>COMT</strong> genotype is associated with the likelihood of <b>smoking</b> cessation in <b>smokers</b> treated with the NRT transdermal patch.
+COMT	drug	alcohol	18181582	A single nucleotide polymorphism (Val108/158Met) in the catechol O methyl transferase (<strong>COMT</strong>) gene is related to many psychiatric disorders such as schizophrenia, <b>alcoholism</b>, bipolar disorder, and obsessive compulsive disorder.
+COMT	addiction	addiction	18181582	A single nucleotide polymorphism (Val108/158Met) in the catechol O methyl transferase (<strong>COMT</strong>) gene is related to many psychiatric disorders such as schizophrenia, alcoholism, bipolar disorder, and obsessive <b>compulsive</b> disorder.
+COMT	addiction	reward	18160646	Immediate <b>reward</b> bias in humans: fronto parietal networks and a role for the <strong>catechol O methyltransferase</strong> 158(Val/Val) genotype.
+COMT	drug	psychedelics	18074122	Furthermore, interfering in <b>MDMA</b> metabolism using the <strong>catechol O methyltransferase</strong> inhibitor entacapone potentiated the neurotoxicity of <b>MDMA</b>, indicating that metabolites that are substrates for this enzyme may contribute to neurotoxicity.
+COMT	drug	alcohol	17850222	Lack of association of <b>alcohol</b> dependence and habitual smoking with <strong>catechol O methyltransferase</strong>.
+COMT	drug	nicotine	17850222	Lack of association of alcohol dependence and habitual <b>smoking</b> with <strong>catechol O methyltransferase</strong>.
+COMT	addiction	dependence	17850222	Lack of association of alcohol <b>dependence</b> and habitual smoking with <strong>catechol O methyltransferase</strong>.
+COMT	drug	alcohol	17850222	To test whether variation in the gene encoding the enzyme catechol O methyltransferase (<strong>COMT</strong>), which catalyzes the breakdown of dopamine and other catecholamine neurotransmitters, is associated with the risk for <b>alcohol</b> dependence and habitual smoking.
+COMT	drug	nicotine	17850222	To test whether variation in the gene encoding the enzyme catechol O methyltransferase (<strong>COMT</strong>), which catalyzes the breakdown of dopamine and other catecholamine neurotransmitters, is associated with the risk for alcohol dependence and habitual <b>smoking</b>.
+COMT	addiction	dependence	17850222	To test whether variation in the gene encoding the enzyme catechol O methyltransferase (<strong>COMT</strong>), which catalyzes the breakdown of dopamine and other catecholamine neurotransmitters, is associated with the risk for alcohol <b>dependence</b> and habitual smoking.
+COMT	drug	alcohol	17850222	To test whether variation in the gene encoding the enzyme <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>), which catalyzes the breakdown of dopamine and other catecholamine neurotransmitters, is associated with the risk for <b>alcohol</b> dependence and habitual smoking.
+COMT	drug	nicotine	17850222	To test whether variation in the gene encoding the enzyme <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>), which catalyzes the breakdown of dopamine and other catecholamine neurotransmitters, is associated with the risk for alcohol dependence and habitual <b>smoking</b>.
+COMT	addiction	dependence	17850222	To test whether variation in the gene encoding the enzyme <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>), which catalyzes the breakdown of dopamine and other catecholamine neurotransmitters, is associated with the risk for alcohol <b>dependence</b> and habitual smoking.
+COMT	drug	alcohol	17850222	Family based tests of association were performed to evaluate the evidence of association between the 18 SNPs distributed throughout <strong>COMT</strong>, including the functional Val158Met polymorphism, and the phenotypes of <b>alcohol</b> dependence, early onset <b>alcohol</b> dependence, habitual smoking, and comorbid <b>alcohol</b> dependence and habitual smoking.
+COMT	drug	nicotine	17850222	Family based tests of association were performed to evaluate the evidence of association between the 18 SNPs distributed throughout <strong>COMT</strong>, including the functional Val158Met polymorphism, and the phenotypes of alcohol dependence, early onset alcohol dependence, habitual <b>smoking</b>, and comorbid alcohol dependence and habitual <b>smoking</b>.
+COMT	addiction	dependence	17850222	Family based tests of association were performed to evaluate the evidence of association between the 18 SNPs distributed throughout <strong>COMT</strong>, including the functional Val158Met polymorphism, and the phenotypes of alcohol <b>dependence</b>, early onset alcohol <b>dependence</b>, habitual smoking, and comorbid alcohol <b>dependence</b> and habitual smoking.
+COMT	drug	alcohol	17850222	Despite the substantial size of this study, we did not find evidence to support an association between <b>alcohol</b> dependence or habitual smoking and variation in <strong>COMT</strong>.
+COMT	drug	nicotine	17850222	Despite the substantial size of this study, we did not find evidence to support an association between alcohol dependence or habitual <b>smoking</b> and variation in <strong>COMT</strong>.
+COMT	addiction	dependence	17850222	Despite the substantial size of this study, we did not find evidence to support an association between alcohol <b>dependence</b> or habitual smoking and variation in <strong>COMT</strong>.
+COMT	addiction	reward	17497175	Catechol O methyltransferase (<strong>COMT</strong>) is an important modulator in the catabolism of extraneural dopamine, which plays an important role in drug <b>reward</b> mechanisms.
+COMT	addiction	reward	17497175	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) is an important modulator in the catabolism of extraneural dopamine, which plays an important role in drug <b>reward</b> mechanisms.
+COMT	addiction	reward	17497175	It is hypothesized that genetic variations in the <strong>COMT</strong> gene, which can result in a three to fourfold difference in <strong>COMT</strong> enzyme activity, may be associated with several <b>reward</b> motivated behaviors.
+COMT	drug	alcohol	17497175	The aim of our study was to examine the relationship between <strong>COMT</strong> polymorphisms with smoking, obesity and <b>alcohol</b>.
+COMT	drug	nicotine	17497175	The aim of our study was to examine the relationship between <strong>COMT</strong> polymorphisms with <b>smoking</b>, obesity and alcohol.
+COMT	drug	nicotine	17497175	Three single nucleotide polymorphisms (SNPs) in <strong>COMT</strong> were genotyped in 2,371 participants selected randomly from the screening arm of the PLCO Cancer Screening Trial after stratifying by sex, age, and <b>smoking</b> status.
+COMT	drug	alcohol	17497175	We observed no association between any of the <strong>COMT</strong> polymorphisms with smoking behavior or <b>alcohol</b> intake.
+COMT	drug	nicotine	17497175	We observed no association between any of the <strong>COMT</strong> polymorphisms with <b>smoking</b> behavior or alcohol intake.
+COMT	drug	alcohol	17497175	The null association with smoking and <b>alcohol</b> and the pronounced association with increasing BMI among women further implicates <strong>COMT</strong>'s role in estrogen metabolism as a potentially culpable pathway.
+COMT	drug	nicotine	17497175	The null association with <b>smoking</b> and alcohol and the pronounced association with increasing BMI among women further implicates <strong>COMT</strong>'s role in estrogen metabolism as a potentially culpable pathway.
+COMT	addiction	relapse	17467918	Manipulation of catechol O methyl transferase (<strong>COMT</strong>) activity to influence the attenuation of substance <b>seeking</b> behavior, a subtype of Reward Deficiency Syndrome (RDS), is dependent upon gene polymorphisms: a hypothesis.
+COMT	addiction	reward	17467918	Manipulation of catechol O methyl transferase (<strong>COMT</strong>) activity to influence the attenuation of substance seeking behavior, a subtype of <b>Reward</b> Deficiency Syndrome (RDS), is dependent upon gene polymorphisms: a hypothesis.
+COMT	addiction	relapse	17467918	In this regard, based on the current literature we hypothesize that manipulation of catechol O methyl transferase (<strong>COMT</strong>) activity to influence the attenuation of substance <b>seeking</b> behavior, is dependent upon gene polymorphisms.
+COMT	drug	alcohol	17467918	In this regard we hypothesize that carrying the LL genotype with low <strong>COMT</strong> activity should as theorized, increase the reward induced by substance induced dopamine release and may indeed increase the propensity to type 1 <b>alcoholism</b> and possibly other drugs that activate the dopaminergic system.
+COMT	addiction	reward	17467918	In this regard we hypothesize that carrying the LL genotype with low <strong>COMT</strong> activity should as theorized, increase the <b>reward</b> induced by substance induced dopamine release and may indeed increase the propensity to type 1 alcoholism and possibly other drugs that activate the dopaminergic system.
+COMT	drug	alcohol	17467918	Thus when <b>alcohol</b> is present in low <strong>COMT</strong> LL genotype, increasing <strong>COMT</strong> activity, not inhibiting it should assist in the reduction of social consumption or abuse.
+COMT	drug	alcohol	17467918	Thus, in the absence of <b>alcohol</b> or other psychoactive drugs (dopamine releasers), especially during recovery or rehabilitation, decreasing, not increasing <strong>COMT</strong> activity, should result in enhanced synaptic dopamine as physiologically released, thereby proliferating D2 receptors while reducing stress, increasing well being, reducing craving behavior and preventing relapse.
+COMT	addiction	relapse	17467918	Thus, in the absence of alcohol or other psychoactive drugs (dopamine releasers), especially during recovery or rehabilitation, decreasing, not increasing <strong>COMT</strong> activity, should result in enhanced synaptic dopamine as physiologically released, thereby proliferating D2 receptors while reducing stress, increasing well being, reducing <b>craving</b> behavior and preventing <b>relapse</b>.
+COMT	addiction	relapse	17467918	Based on this hypothesis, we believe that adding the <strong>COMT</strong> inhibitor R. rosea (as Rhodimin) to our amino acid and chromium combination in DUI offenders and other illegal drug related crimes, increases the potential for more targeted neurochemical rebalancing and enhanced <b>relapse</b> prevention.
+COMT	addiction	relapse	17467918	Finally, we hypothesize that these data coupled together provide evidence that the combination of enkephalinase inhibition, neurotransmitter precursor loading, brain tryptophan enhancing and <strong>COMT</strong> inhibition as well as DNA analysis of the individual's genome, may be useful as an adjunct to therapy when used in outpatient recovery, specifically to assist in reducing <b>craving</b> behavior and preventing <b>relapse</b>.
+COMT	drug	alcohol	17347351	In addition, a common Met158 variant in the catechol O methyltransferase (<strong>COMT</strong>) gene can confer both risk and resilience to <b>alcoholism</b> in different drinking environments.
+COMT	drug	alcohol	17347351	In addition, a common Met158 variant in the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene can confer both risk and resilience to <b>alcoholism</b> in different drinking environments.
+COMT	drug	nicotine	17206495	Association of functional catechol O methyl transferase (<strong>COMT</strong>) Val108Met polymorphism with <b>smoking</b> severity and age of <b>smoking</b> initiation in Chinese male <b>smokers</b>.
+COMT	drug	nicotine	17206495	Catechol O methyltransferase (<strong>COMT</strong>) is an enzyme involved in the degradation and inactivation of the neurotransmitter dopamine, which is important in mediating drug reward such as <b>nicotine</b> in <b>tobacco</b> smoke.
+COMT	addiction	reward	17206495	Catechol O methyltransferase (<strong>COMT</strong>) is an enzyme involved in the degradation and inactivation of the neurotransmitter dopamine, which is important in mediating drug <b>reward</b> such as nicotine in tobacco smoke.
+COMT	drug	nicotine	17206495	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) is an enzyme involved in the degradation and inactivation of the neurotransmitter dopamine, which is important in mediating drug reward such as <b>nicotine</b> in <b>tobacco</b> smoke.
+COMT	addiction	reward	17206495	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) is an enzyme involved in the degradation and inactivation of the neurotransmitter dopamine, which is important in mediating drug <b>reward</b> such as nicotine in tobacco smoke.
+COMT	drug	nicotine	17206495	Different <strong>COMT</strong> alleles encode enzyme whose activity varies from three  to fourfold that may affect dopamine levels and alter subjective effects of <b>nicotine</b>.
+COMT	drug	nicotine	17206495	Recent evidence also suggests that a <strong>COMT</strong> polymorphism may be especially important in determining an individual's predisposition to developing <b>nicotine</b> dependence.
+COMT	addiction	dependence	17206495	Recent evidence also suggests that a <strong>COMT</strong> polymorphism may be especially important in determining an individual's predisposition to developing nicotine <b>dependence</b>.
+COMT	drug	nicotine	17206495	We studied the <strong>COMT</strong> Val108Met polymorphism in a male population of 203 current <b>smokers</b>, 66 former <b>smokers</b>, and 102 non <b>smokers</b>.
+COMT	drug	nicotine	17206495	The results showed no significant association of the <strong>COMT</strong> Val108Met with initiation, persistent <b>smoking</b>, or <b>smoking</b> cessation.
+COMT	drug	nicotine	17206495	These results suggest that the <strong>COMT</strong> Val108Met polymorphism may not influence <b>smoking</b> status in a Chinese male population but may influence the age at which <b>smoking</b> started and <b>smoking</b> severity among <b>smokers</b>.
+COMT	drug	amphetamine	17187009	The <strong>COMT</strong> Val158Met polymorphism is associated with novelty seeking in Czech <b>methamphetamine</b> abusers: preliminary results.
+COMT	addiction	relapse	17187009	The <strong>COMT</strong> Val158Met polymorphism is associated with novelty <b>seeking</b> in Czech methamphetamine abusers: preliminary results.
+COMT	drug	amphetamine	17187009	The aim of our study was to assess whether the <strong>COMT</strong> gene Val158Met functional polymorphism in patients dependent on <b>methamphetamine</b> is related to their novelty seeking score.
+COMT	addiction	relapse	17187009	The aim of our study was to assess whether the <strong>COMT</strong> gene Val158Met functional polymorphism in patients dependent on methamphetamine is related to their novelty <b>seeking</b> score.
+COMT	addiction	relapse	17187009	We administered the Temperament and Character Inventory (TCI) questionnaire, assessed their novelty <b>seeking</b> score and analysed their DNA samples for <strong>COMT</strong> Val158Met genotype.
+COMT	drug	alcohol	17079080	Family based and case control study of DRD2, DAT, 5HTT, <strong>COMT</strong> genes polymorphisms in <b>alcohol</b> dependence.
+COMT	addiction	dependence	17079080	Family based and case control study of DRD2, DAT, 5HTT, <strong>COMT</strong> genes polymorphisms in alcohol <b>dependence</b>.
+COMT	drug	alcohol	17079080	The paper focuses on such candidate gene polymorphisms that alter <b>alcoholism</b> related intermediate phenotypes including: dopaminergic system polymorphic variants (DRD2  141C Ins/Del in promoter region, exon 8 and DRD2 TaqI A and DAT 40bp VNTR genes polymorphisms) that cause predisposition to severe <b>alcoholism</b> (haplotype Ins/G/A2); <strong>COMT</strong> Val158Met gene polymorphism related to differences in executive cognitive function and 5 HTT gene promoter polymorphism, which alters stress response and affects anxiety and dysphoria.
+COMT	drug	nicotine	16876132	Catechol O methyltransferase (<strong>COMT</strong>) gene variants predict response to bupropion therapy for <b>tobacco</b> dependence.
+COMT	addiction	dependence	16876132	Catechol O methyltransferase (<strong>COMT</strong>) gene variants predict response to bupropion therapy for tobacco <b>dependence</b>.
+COMT	drug	nicotine	16876132	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) gene variants predict response to bupropion therapy for <b>tobacco</b> dependence.
+COMT	addiction	dependence	16876132	<strong>Catechol O methyltransferase</strong> (<strong>COMT</strong>) gene variants predict response to bupropion therapy for tobacco <b>dependence</b>.
+COMT	drug	nicotine	16876132	We investigated variants in the catechol O methyltransferase (<strong>COMT</strong>) gene in a <b>smoking</b> cessation trial of bupropion.
+COMT	drug	nicotine	16876132	We investigated variants in the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene in a <b>smoking</b> cessation trial of bupropion.
+COMT	drug	nicotine	16876132	<strong>COMT</strong> haplotypes at rs737865 and rs165599 may predict a favorable outcome for bupropion treatment for <b>smoking</b> cessation.
+COMT	drug	nicotine	16876132	If study findings are confirmed in additional large studies, <strong>COMT</strong> genotyping could be applied to identify likely responders to bupropion treatment for <b>smoking</b> cessation.
+COMT	drug	alcohol	16679343	There were no significant differences in the genotype frequencies of the DRD2, ALDH2, 5 HTTLPR, and <strong>COMT</strong> polymorphisms between <b>alcoholics</b> with and without ADHD.
+COMT	drug	nicotine	16395295	Significant association of catechol O methyltransferase (<strong>COMT</strong>) haplotypes with <b>nicotine</b> dependence in male and female <b>smokers</b> of two ethnic populations.
+COMT	addiction	dependence	16395295	Significant association of catechol O methyltransferase (<strong>COMT</strong>) haplotypes with nicotine <b>dependence</b> in male and female smokers of two ethnic populations.
+COMT	drug	nicotine	16395295	Significant association of <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) haplotypes with <b>nicotine</b> dependence in male and female <b>smokers</b> of two ethnic populations.
+COMT	addiction	dependence	16395295	Significant association of <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) haplotypes with nicotine <b>dependence</b> in male and female smokers of two ethnic populations.
+COMT	addiction	reward	16395295	The catechol O methyltransferase (<strong>COMT</strong>) gene plays a prominent role in dopaminergic circuits central to drug <b>reward</b>.
+COMT	addiction	reward	16395295	The <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene plays a prominent role in dopaminergic circuits central to drug <b>reward</b>.
+COMT	drug	nicotine	16395295	Allelic variants within the <strong>COMT</strong> gene are therefore potential candidates for examining interindividual differences in vulnerability to <b>nicotine</b> dependence (ND).
+COMT	addiction	dependence	16395295	Allelic variants within the <strong>COMT</strong> gene are therefore potential candidates for examining interindividual differences in vulnerability to nicotine <b>dependence</b> (ND).
+COMT	drug	nicotine	16395295	Further examination of two protective haplotypes, A G T in AAs and T G T in EAs, indicated that the low <strong>COMT</strong> enzyme activity Met allele is protective to become <b>nicotine</b> dependent.
+COMT	drug	nicotine	15941945	In the first study, 342 treatment seeking <b>smokers</b> were genotyped for the Val108Met polymorphism in the functional catechol O methyl transferase (<strong>COMT</strong>) locus.
+COMT	addiction	relapse	15941945	In the first study, 342 treatment <b>seeking</b> smokers were genotyped for the Val108Met polymorphism in the functional catechol O methyl transferase (<strong>COMT</strong>) locus.
+COMT	drug	nicotine	15941945	To validate this initial finding, 443 treatment seeking <b>smokers</b> from an independent <b>smoking</b> cessation clinical trial were genotyped for the <strong>COMT</strong> polymorphism.
+COMT	addiction	relapse	15941945	To validate this initial finding, 443 treatment <b>seeking</b> smokers from an independent smoking cessation clinical trial were genotyped for the <strong>COMT</strong> polymorphism.
+COMT	drug	alcohol	15900232	Association study of <strong>catechol O methyltransferase</strong> gene polymorphism in Korean male <b>alcoholics</b>.
+COMT	drug	alcohol	15900232	The study analyzed the association between the <strong>catechol O methyltransferase</strong> gene polymorphism and <b>alcohol</b> dependence in the Korean population.
+COMT	addiction	dependence	15900232	The study analyzed the association between the <strong>catechol O methyltransferase</strong> gene polymorphism and alcohol <b>dependence</b> in the Korean population.
+COMT	drug	alcohol	15900232	This suggests that the <strong>catechol O methyltransferase</strong> gene polymorphism is not associated with the development of <b>alcohol</b> dependence, but may affect the susceptibility to a clinical heterogeneity of <b>alcohol</b> dependence, at least in the Korean population.
+COMT	addiction	dependence	15900232	This suggests that the <strong>catechol O methyltransferase</strong> gene polymorphism is not associated with the development of alcohol <b>dependence</b>, but may affect the susceptibility to a clinical heterogeneity of alcohol <b>dependence</b>, at least in the Korean population.
+COMT	drug	alcohol	15584875	Functional alleles that alter <b>alcoholism</b> related intermediate phenotypes include common <b>alcohol</b> dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; catechol O methyltransferase (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of <b>naltrexone</b>, a drug used in <b>alcoholism</b> treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+COMT	drug	opioid	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; catechol O methyltransferase (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and <b>opioid</b> function; <b>opioid</b> receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+COMT	addiction	addiction	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; catechol O methyltransferase (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of <b>addiction</b>, and relapse.
+COMT	addiction	aversion	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the <b>aversive</b> flushing reaction; catechol O methyltransferase (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+COMT	addiction	relapse	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; catechol O methyltransferase (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and <b>relapse</b>.
+COMT	drug	alcohol	15584875	Functional alleles that alter <b>alcoholism</b> related intermediate phenotypes include common <b>alcohol</b> dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of <b>naltrexone</b>, a drug used in <b>alcoholism</b> treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+COMT	drug	opioid	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and <b>opioid</b> function; <b>opioid</b> receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+COMT	addiction	addiction	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of <b>addiction</b>, and relapse.
+COMT	addiction	aversion	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the <b>aversive</b> flushing reaction; <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and relapse.
+COMT	addiction	relapse	15584875	Functional alleles that alter alcoholism related intermediate phenotypes include common alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants that cause the aversive flushing reaction; <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) Val158Met leading to differences in three aspects of neurobiology: executive cognitive function, stress/anxiety response, and opioid function; opioid receptor micro1 (OPRM1) Asn40Asp, which may serve as a gatekeeper molecule in the action of naltrexone, a drug used in alcoholism treatment; and HTTLPR, which alters serotonin transporter function and appears to affect stress response and anxiety/dysphoria, which are factors relevant to initial vulnerability, the process of addiction, and <b>relapse</b>.
+COMT	drug	amphetamine	15274053	Association analysis of the DRD4 and <strong>COMT</strong> genes in <b>methamphetamine</b> abuse.
+COMT	drug	amphetamine	15274053	We analyzed two polymorphisms in genes encoding proteins of the dopamine system, the Val158Met polymorphism in the <strong>catechol O methyltransferase</strong> gene and the 120 bp VNTR polymorphism in the promoter of the dopamine D4 receptor gene for association with <b>methamphetamine</b> abuse.
+COMT	drug	opioid	15157710	Loci in the vanilloid receptor subtype 1 gene (TRPV1), delta <b>opioid</b> receptor subtype 1 gene (OPRD1) and catechol O methyltransferase gene (<strong>COMT</strong>) were genotyped using 5' nuclease assays.
+COMT	drug	opioid	15157710	Loci in the vanilloid receptor subtype 1 gene (TRPV1), delta <b>opioid</b> receptor subtype 1 gene (OPRD1) and <strong>catechol O methyltransferase</strong> gene (<strong>COMT</strong>) were genotyped using 5' nuclease assays.
+COMT	drug	psychedelics	14673568	<b>MDMA</b> metabolism is regulated by the levels of CYP2D6 and <strong>COMT</strong> (both exhibit some genetic polymorphism), and range of activity of these enzymes may account for some inter individual differences in terms of toxic responses to the drug.
+COMT	drug	alcohol	12741370	Plasma homovanillic acid: a significant association with <b>alcoholism</b> is independent of a functional polymorphism of the human <strong>catechol O methyltransferase</strong> gene.
+COMT	drug	alcohol	12741370	A functional genetic polymorphism of the enzyme catechol O methyltransferase (<strong>COMT</strong>) that participates in converting dopamine into its final metabolite HVA was investigated for an association with <b>alcoholism</b> or DT during <b>alcohol</b> withdrawal.
+COMT	addiction	withdrawal	12741370	A functional genetic polymorphism of the enzyme catechol O methyltransferase (<strong>COMT</strong>) that participates in converting dopamine into its final metabolite HVA was investigated for an association with alcoholism or DT during alcohol <b>withdrawal</b>.
+COMT	drug	alcohol	12741370	A functional genetic polymorphism of the enzyme <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) that participates in converting dopamine into its final metabolite HVA was investigated for an association with <b>alcoholism</b> or DT during <b>alcohol</b> withdrawal.
+COMT	addiction	withdrawal	12741370	A functional genetic polymorphism of the enzyme <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) that participates in converting dopamine into its final metabolite HVA was investigated for an association with alcoholism or DT during alcohol <b>withdrawal</b>.
+COMT	drug	alcohol	12741370	Plasma HVA concentrations and <strong>COMT</strong> genotypes were determined in 142 German <b>alcoholics</b> and 101 German healthy controls.
+COMT	drug	alcohol	12741370	The functional polymorphism of the human <strong>COMT</strong> gene was neither significantly associated with the diagnosis of <b>alcoholism</b> or DT during <b>alcohol</b> withdrawal nor with plasma HVA concentrations.
+COMT	addiction	withdrawal	12741370	The functional polymorphism of the human <strong>COMT</strong> gene was neither significantly associated with the diagnosis of alcoholism or DT during alcohol <b>withdrawal</b> nor with plasma HVA concentrations.
+COMT	drug	opioid	12673581	[Association study of <b>heroin</b> dependence and <strong>catechol O methyltransferase</strong> gene].
+COMT	addiction	dependence	12673581	[Association study of heroin <b>dependence</b> and <strong>catechol O methyltransferase</strong> gene].
+COMT	drug	opioid	12673581	To detect the relationship between <b>heroin</b> dependence and catechol O methyltransferase (<strong>COMT</strong>) gene.
+COMT	addiction	dependence	12673581	To detect the relationship between heroin <b>dependence</b> and catechol O methyltransferase (<strong>COMT</strong>) gene.
+COMT	drug	opioid	12673581	To detect the relationship between <b>heroin</b> dependence and <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene.
+COMT	addiction	dependence	12673581	To detect the relationship between heroin <b>dependence</b> and <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene.
+COMT	drug	opioid	12673581	Genotype and allele frequencies of 108 val/met and 900 Ins C/Del C polymorphisms of <strong>COMT</strong> gene were examined in 313 <b>heroin</b> dependent subjects and 214 normal controls.
+COMT	drug	opioid	12673581	No differences in genotype and allele frequencies of 108 val/met polymorphism of <strong>COMT</strong> gene were observed between <b>heroin</b> dependent subjects and normal controls (genotype wise: chi square=1.67, P=0.43; allele wise: chi square=1.23, P=0.27).
+COMT	drug	opioid	12673581	No differences in genotype and allele frequencies of 900 Ins C/Del C polymorphism of <strong>COMT</strong> gene were observed between <b>heroin</b> dependent subjects and normal controls (genotype wise: chi square=3.73, P=0.16; allele wise: chi square=0.76, P=0.38).
+COMT	drug	opioid	12673581	The results suggested that neither 108 val/met polymorphism nor 900 Ins C/Del C polymorphism of <strong>COMT</strong> gene was associated with <b>heroin</b> dependence.
+COMT	addiction	dependence	12673581	The results suggested that neither 108 val/met polymorphism nor 900 Ins C/Del C polymorphism of <strong>COMT</strong> gene was associated with heroin <b>dependence</b>.
+COMT	drug	opioid	12627475	Some studies show that a catechol O methyltransferase (<strong>COMT</strong>) polymorphism affecting enzyme activity was associated with personality characteristics and diseases, such as novelty seeking personality, substance abuse, and <b>heroin</b> addiction, whose features are similar to ADHD or are associated with ADHD.
+COMT	addiction	addiction	12627475	Some studies show that a catechol O methyltransferase (<strong>COMT</strong>) polymorphism affecting enzyme activity was associated with personality characteristics and diseases, such as novelty seeking personality, substance abuse, and heroin <b>addiction</b>, whose features are similar to ADHD or are associated with ADHD.
+COMT	addiction	relapse	12627475	Some studies show that a catechol O methyltransferase (<strong>COMT</strong>) polymorphism affecting enzyme activity was associated with personality characteristics and diseases, such as novelty <b>seeking</b> personality, substance abuse, and heroin addiction, whose features are similar to ADHD or are associated with ADHD.
+COMT	drug	opioid	12627475	Some studies show that a <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) polymorphism affecting enzyme activity was associated with personality characteristics and diseases, such as novelty seeking personality, substance abuse, and <b>heroin</b> addiction, whose features are similar to ADHD or are associated with ADHD.
+COMT	addiction	addiction	12627475	Some studies show that a <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) polymorphism affecting enzyme activity was associated with personality characteristics and diseases, such as novelty seeking personality, substance abuse, and heroin <b>addiction</b>, whose features are similar to ADHD or are associated with ADHD.
+COMT	addiction	relapse	12627475	Some studies show that a <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) polymorphism affecting enzyme activity was associated with personality characteristics and diseases, such as novelty <b>seeking</b> personality, substance abuse, and heroin addiction, whose features are similar to ADHD or are associated with ADHD.
+COMT	drug	opioid	12476424	[Association study of <b>heroin</b> dependence and  287 A/G polymorphism of <strong>catechol O methyltransferase</strong> gene].
+COMT	addiction	dependence	12476424	[Association study of heroin <b>dependence</b> and  287 A/G polymorphism of <strong>catechol O methyltransferase</strong> gene].
+COMT	drug	opioid	12476424	To detect the relationship between <b>heroin</b> dependence and  287 A/G polymorphism of catechol O methyltransferase(<strong>COMT</strong>) gene.
+COMT	addiction	dependence	12476424	To detect the relationship between heroin <b>dependence</b> and  287 A/G polymorphism of catechol O methyltransferase(<strong>COMT</strong>) gene.
+COMT	drug	opioid	12476424	To detect the relationship between <b>heroin</b> dependence and  287 A/G polymorphism of <strong>catechol O methyltransferase</strong>(<strong>COMT</strong>) gene.
+COMT	addiction	dependence	12476424	To detect the relationship between heroin <b>dependence</b> and  287 A/G polymorphism of <strong>catechol O methyltransferase</strong>(<strong>COMT</strong>) gene.
+COMT	drug	opioid	12476424	Genotype and allele frequencies of  287 A/G polymorphism of <strong>COMT</strong> gene were examined in 268 <b>heroin</b> dependent subjects and 177 normal controls.
+COMT	drug	opioid	12476424	Weak but significant difference in genotype of  287 A/G polymorphism of <strong>COMT</strong> gene was observed between <b>heroin</b> dependent subjects and controls (chi(2)=7.41, P=0.025), and genotype AA was higher in the former.
+COMT	drug	opioid	12476424	The frequency of allele A of  287 A/G polymorphism of <strong>COMT</strong> gene was also significantly higher in <b>heroin</b> dependent subjects than in the controls (chi(2)=5.69, P=0.017).
+COMT	drug	opioid	12476424	The results suggested that liability to <b>heroin</b> dependence was associated with  287 A/G polymorphism of <strong>COMT</strong> gene.
+COMT	addiction	dependence	12476424	The results suggested that liability to heroin <b>dependence</b> was associated with  287 A/G polymorphism of <strong>COMT</strong> gene.
+COMT	drug	alcohol	11927842	A functional polymorphism (<strong>COMT</strong> 1947A>G) resulting in increased enzyme activity has been associated with <b>alcoholism</b> and polysubstance abuse.
+COMT	drug	nicotine	11927842	We examined the relationship between the <strong>COMT</strong> 1947A>G polymorphism and <b>smoking</b> initiation, <b>smoking</b> persistence and <b>smoking</b> cessation.
+COMT	drug	nicotine	11927842	We genotyped 266 current <b>smokers</b>, 270 ex <b>smokers</b> and 265 lifetime non <b>smokers</b> (never <b>smokers</b>), matched for age and gender, for the <strong>COMT</strong> 1947A>G polymorphism.
+COMT	drug	nicotine	11927842	These data suggest that the <strong>COMT</strong> 1947A>G polymorphism is not associated with <b>smoking</b> initiation, <b>smoking</b> persistence or <b>smoking</b> cessation.
+COMT	drug	alcohol	11900601	Association between catechol O methyltransferase (<strong>COMT</strong>) polymorphism and severe <b>alcoholic</b> withdrawal symptoms in male Japanese <b>alcoholics</b>.
+COMT	addiction	withdrawal	11900601	Association between catechol O methyltransferase (<strong>COMT</strong>) polymorphism and severe alcoholic <b>withdrawal</b> symptoms in male Japanese alcoholics.
+COMT	drug	alcohol	11900601	Association between <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) polymorphism and severe <b>alcoholic</b> withdrawal symptoms in male Japanese <b>alcoholics</b>.
+COMT	addiction	withdrawal	11900601	Association between <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) polymorphism and severe alcoholic <b>withdrawal</b> symptoms in male Japanese alcoholics.
+COMT	drug	alcohol	11900601	The allelic association of a functional polymorphism of the <strong>COMT</strong> gene with the onset, course and clinical characteristics of <b>alcoholism</b> in 91 male Japanese <b>alcoholics</b> and 114 male Japanese controls was examined.
+COMT	drug	alcohol	11900601	The present results suggest that <strong>COMT</strong> activity could partially effect the phenotype of <b>alcoholism</b>, especially the appearance of delirium tremens, in these subjects.
+COMT	drug	alcohol	11204347	A common functional polymorphism that results in a three  to four fold difference in catechol O methyltransferase (<strong>COMT</strong>) enzyme activity has been related to psychiatric disorders such as ultra ultra rapid cycling bipolar disorder, drug abuse and <b>alcoholism</b> (Lachman et al., 1996a; Karayiorgou et al., 1997; Vandenbergh et al., 1997; Papolos et al., 1998; Tiihonen et al., 1999).
+COMT	drug	alcohol	11204347	A common functional polymorphism that results in a three  to four fold difference in <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) enzyme activity has been related to psychiatric disorders such as ultra ultra rapid cycling bipolar disorder, drug abuse and <b>alcoholism</b> (Lachman et al., 1996a; Karayiorgou et al., 1997; Vandenbergh et al., 1997; Papolos et al., 1998; Tiihonen et al., 1999).
+COMT	drug	alcohol	10898913	Lack of association between the functional variant of the catechol o methyltransferase (<strong>COMT</strong>) gene and early onset <b>alcoholism</b> associated with severe antisocial behavior.
+COMT	drug	alcohol	10898913	Lack of association between the functional variant of the <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>) gene and early onset <b>alcoholism</b> associated with severe antisocial behavior.
+COMT	drug	alcohol	10898913	Addictive drugs, including <b>ethanol</b>, increase the brain's dopaminergic transmission, and catechol o methyltransferase (<strong>COMT</strong>) enzyme has a crucial role in dopamine inactivation.
+COMT	addiction	addiction	10898913	<b>Addictive</b> drugs, including ethanol, increase the brain's dopaminergic transmission, and catechol o methyltransferase (<strong>COMT</strong>) enzyme has a crucial role in dopamine inactivation.
+COMT	drug	alcohol	10898913	Addictive drugs, including <b>ethanol</b>, increase the brain's dopaminergic transmission, and <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>) enzyme has a crucial role in dopamine inactivation.
+COMT	addiction	addiction	10898913	<b>Addictive</b> drugs, including ethanol, increase the brain's dopaminergic transmission, and <strong>catechol o methyltransferase</strong> (<strong>COMT</strong>) enzyme has a crucial role in dopamine inactivation.
+COMT	drug	alcohol	10898913	In a previous study, we found an association between type 1 (with late onset but without prominent antisocial behavior) <b>alcoholism</b> and the low activity allele of the <strong>COMT</strong> gene.
+COMT	drug	alcohol	10898913	In this work we analyzed whether the <strong>COMT</strong> polymorphism has any effect on the development of type 2 (with early onset and habitual impulsive violent behavior) <b>alcoholism</b>.
+COMT	drug	alcohol	10898913	The <strong>COMT</strong> genotype was determined in 62 impulsive violent recidivist offenders with early onset (type 2) <b>alcoholism</b>, 123 late onset nonviolent (type 1) <b>alcoholics</b>, and 267 race and gender matched controls.
+COMT	drug	alcohol	10898913	The results suggest that <strong>COMT</strong> genotype has no major role in the development of early onset <b>alcoholism</b> with severe antisocial behavior.
+COMT	drug	alcohol	10551543	Association study between high and low activity polymorphism of <strong>catechol O methyltransferase</strong> gene and <b>alcoholism</b>.
+COMT	drug	alcohol	10551543	Therefore, the <strong>COMT</strong> gene is not likely to play a significant role in <b>alcoholism</b>.
+COMT	drug	alcohol	10395222	Association between the functional variant of the catechol O methyltransferase (<strong>COMT</strong>) gene and type 1 <b>alcoholism</b>.
+COMT	drug	alcohol	10395222	Association between the functional variant of the <strong>catechol O methyltransferase</strong> (<strong>COMT</strong>) gene and type 1 <b>alcoholism</b>.
+COMT	drug	alcohol	10395222	It has been suggested that a common functional genetic polymorphism in the <strong>COMT</strong> gene, which results in 3 to 4 fold difference in <strong>COMT</strong> enzyme activity, may contribute to the etiology of mental disorders such as bipolar disorder and <b>alcoholism</b>.
+COMT	drug	alcohol	10395222	Since <b>ethanol</b> induced euphoria is associated with the rapid release of dopamine in limbic areas, it is conceivable that subjects who inherit the allele encoding the low activity <strong>COMT</strong> variant would have a relatively low dopamine inactivation rate, and therefore would be more vulnerable to the development of <b>ethanol</b> dependence.
+COMT	addiction	dependence	10395222	Since ethanol induced euphoria is associated with the rapid release of dopamine in limbic areas, it is conceivable that subjects who inherit the allele encoding the low activity <strong>COMT</strong> variant would have a relatively low dopamine inactivation rate, and therefore would be more vulnerable to the development of ethanol <b>dependence</b>.
+COMT	drug	alcohol	10395222	The <strong>COMT</strong> polymorphism was determined in two independent male late onset (type 1) <b>alcoholic</b> populations in Turku (n = 67) and Kuopio (n = 56).
+COMT	drug	alcohol	10395222	The results indicate that the <strong>COMT</strong> polymorphism contributes significantly to the development of late onset <b>alcoholism</b>.
+COMT	drug	alcohol	8807664	The identification of a gentic marker associated with significant alterations in enzyme activity will facilitate the analysis of a possible role for the <strong>COMT</strong> gene in neuropsychiatric conditions in which abnormalities in catecholamine neurotransmission are believed to occur, including mood disorders, schizophrenia, obsessive compulsive disorder, <b>alcohol</b> and substance abuse, and attention deficit hyperactivity disorder.
+COMT	addiction	addiction	8807664	The identification of a gentic marker associated with significant alterations in enzyme activity will facilitate the analysis of a possible role for the <strong>COMT</strong> gene in neuropsychiatric conditions in which abnormalities in catecholamine neurotransmission are believed to occur, including mood disorders, schizophrenia, obsessive <b>compulsive</b> disorder, alcohol and substance abuse, and attention deficit hyperactivity disorder.
+COMT	drug	cocaine	2725700	(1) Vasa deferentia obtained from reserpine pretreated rats were exposed to 0.15 mumol l 1 3H ( )noradrenaline (with monoamine oxidase and <strong>catechol O methyltransferase</strong> being inhibited) and initial rates of the neuronal 3H noradrenaline uptake as well as IC50 values for inhibition of uptake by desipramine, <b>cocaine</b> or ( )metaraminol determined at various external Cl  concentrations (0 145 mmol l 1) and a fixed high Na+ concentration (145 mmol l 1).
+COMT	drug	alcohol	2906541	Dopamine content of blood, activity of adenylate  and guanylate cyclases in platelets and lymphocytes, <strong>catechol O methyltransferase</strong> in erythrocytes, dopamine beta hydroxylase in blood plasma, monoamine oxidase in platelets, cAMP and cGMP content of blood, and the intensity of 3H DA uptake by platelets have been investigated in <b>alcoholic</b> patients at different clinical states.
+COMT	drug	alcohol	6641500	Platelet monoamine oxidase and erythrocyte <strong>catechol o methyltransferase</strong> activity in <b>alcoholism</b> and controlled abstinence.
+COMT	drug	alcohol	6641500	Catechol o methyltransferase (<strong>COMT</strong>) activity in erythrocytes of <b>alcoholics</b> did not differ from that of controls.
+COMT	drug	alcohol	6641500	<strong>Catechol o methyltransferase</strong> (<strong>COMT</strong>) activity in erythrocytes of <b>alcoholics</b> did not differ from that of controls.
+COMT	drug	opioid	560969	20 min after precipitation of withdrawal by <b>naloxone</b>, the striatal concentration of 3 methoxytyramine was decreased by about 40%, while the activity of the DA metabolizing enzymes, MAO and <strong>COMT</strong>, remained unchanged.
+COMT	addiction	withdrawal	560969	20 min after precipitation of <b>withdrawal</b> by naloxone, the striatal concentration of 3 methoxytyramine was decreased by about 40%, while the activity of the DA metabolizing enzymes, MAO and <strong>COMT</strong>, remained unchanged.
+CRH	drug	alcohol	32353460	Likewise, genes associated with HPA axis activity were not significantly changed by <b>ethanol</b> drinking [i.e., corticotrophin releasing hormone (<strong>Crh</strong>), adrenocorticotrophic hormone (Acth), and proopiomelanocortin (Pomc)] in these brain regions.
+CRH	drug	opioid	31879737	The effect of <strong>CRH</strong> neurons in CeA on the negative emotions on <b>morphine</b> naïve and withdrawal mice is unclear.
+CRH	addiction	withdrawal	31879737	The effect of <strong>CRH</strong> neurons in CeA on the negative emotions on morphine naïve and <b>withdrawal</b> mice is unclear.
+CRH	drug	opioid	31879737	The results showed that, inhibiting <strong>CRH</strong> neurons of CeA decreased the formation of <b>morphine</b> withdrawal induced CPA, as well as the anxiety level of <strong>CRH</strong> Cre mice.
+CRH	addiction	withdrawal	31879737	The results showed that, inhibiting <strong>CRH</strong> neurons of CeA decreased the formation of morphine <b>withdrawal</b> induced CPA, as well as the anxiety level of <strong>CRH</strong> Cre mice.
+CRH	drug	opioid	31879737	Furthermore, specifically activating <strong>CRH</strong> neurons in CeA evoked CPA and anxiety of <b>morphine</b> naïve mice.
+CRH	drug	opioid	31879737	These results suggest that <strong>CRH</strong> neurons in CeA are involved in the mediation of <b>morphine</b> withdrawal induced negative emotion in mice, providing a theoretical basis for drug addiction and relapse mechanism.
+CRH	addiction	addiction	31879737	These results suggest that <strong>CRH</strong> neurons in CeA are involved in the mediation of morphine withdrawal induced negative emotion in mice, providing a theoretical basis for drug <b>addiction</b> and relapse mechanism.
+CRH	addiction	relapse	31879737	These results suggest that <strong>CRH</strong> neurons in CeA are involved in the mediation of morphine withdrawal induced negative emotion in mice, providing a theoretical basis for drug addiction and <b>relapse</b> mechanism.
+CRH	addiction	withdrawal	31879737	These results suggest that <strong>CRH</strong> neurons in CeA are involved in the mediation of morphine <b>withdrawal</b> induced negative emotion in mice, providing a theoretical basis for drug addiction and relapse mechanism.
+CRH	drug	opioid	31805553	Variation on the <strong>CRH</strong> Gene Determines the Different Performance of <b>Opioid</b> Addicts and Healthy Controls in the IOWA Gambling Task.
+CRH	drug	opioid	31805553	The aim of this study was to investigate the interplay between the HPA axis related genetic variation on corticotropin releasing hormone (<strong>CRH</strong>; secreted from the hypothalamus and constituting the starting point of the HPA axis) gene and <b>opioid</b> addiction, with respect to IGT performance.
+CRH	addiction	addiction	31805553	The aim of this study was to investigate the interplay between the HPA axis related genetic variation on corticotropin releasing hormone (<strong>CRH</strong>; secreted from the hypothalamus and constituting the starting point of the HPA axis) gene and opioid <b>addiction</b>, with respect to IGT performance.
+CRH	drug	opioid	31805553	The aim of this study was to investigate the interplay between the HPA axis related genetic variation on <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>; secreted from the hypothalamus and constituting the starting point of the HPA axis) gene and <b>opioid</b> addiction, with respect to IGT performance.
+CRH	addiction	addiction	31805553	The aim of this study was to investigate the interplay between the HPA axis related genetic variation on <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>; secreted from the hypothalamus and constituting the starting point of the HPA axis) gene and opioid <b>addiction</b>, with respect to IGT performance.
+CRH	drug	opioid	31805553	In total, 138 long term <b>opioid</b> addicts (mean age 38.63 years [SD 9.15]) and 160 healthy controls (mean age 22.57 years [SD 5.86]) performed the IGT and were genotyped for 6 SNPs covering the <strong>CRH</strong> gene and adjacent regions (rs3176921, rs6999780, rs7816410, rs1870393, rs1814583, and rs11996294).
+CRH	drug	alcohol	31666410	This contributes to the development of the pathological craving for <b>alcohol</b> in which <strong>corticotropin releasing hormone</strong> receptors are may be involved.
+CRH	addiction	relapse	31666410	This contributes to the development of the pathological <b>craving</b> for alcohol in which <strong>corticotropin releasing hormone</strong> receptors are may be involved.
+CRH	drug	opioid	31666179	corticotropin releasing hormone (<strong>CRH</strong>), <b>opioids</b>, brain derived neurotrophic factor (BDNF), and the adrenal glucocorticoids.
+CRH	drug	opioid	31666179	<strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), <b>opioids</b>, brain derived neurotrophic factor (BDNF), and the adrenal glucocorticoids.
+CRH	drug	cannabinoid	31193551	Somato dendritically released <b>endocannabinoid</b> acts as a retrograde messenger to suppress excitatory synaptic inputs to <strong>corticotropin releasing hormone</strong> , oxytocin , and vasopressin secreting cells.
+CRH	drug	alcohol	31151762	In the European American sample, we identified three additional genome wide significant maximum habitual <b>alcohol</b> consumption loci: on chromosome 17, rs77804065 (p = 1.5 × 10 12), at CRHR1 (<strong>corticotropin releasing hormone</strong> receptor 1); the protein product of this gene is involved in stress and immune responses; and on chromosomes 8 and 10.
+CRH	drug	cocaine	30844877	Genetic Variant in the <strong>CRH</strong> binding Protein Gene (CRHBP) is Associated With Cessation of <b>Cocaine</b> Use in Methadone Maintenance Patients With Opioid Addiction.
+CRH	drug	opioid	30844877	Genetic Variant in the <strong>CRH</strong> binding Protein Gene (CRHBP) is Associated With Cessation of Cocaine Use in <b>Methadone</b> Maintenance Patients With <b>Opioid</b> Addiction.
+CRH	addiction	addiction	30844877	Genetic Variant in the <strong>CRH</strong> binding Protein Gene (CRHBP) is Associated With Cessation of Cocaine Use in Methadone Maintenance Patients With Opioid <b>Addiction</b>.
+CRH	drug	opioid	29888302	In males, <b>opioid</b>, stress, plasticity and kinase/signaling genes were all down regulated following CIS, except for the gene that codes for <strong>corticotropin releasing hormone</strong>, which was upregulated.
+CRH	drug	alcohol	29700576	Targeted overexpression of <strong>CRH</strong> receptor subtype 1 in central amygdala neurons: effect on <b>alcohol</b> seeking behavior.
+CRH	addiction	relapse	29700576	Targeted overexpression of <strong>CRH</strong> receptor subtype 1 in central amygdala neurons: effect on alcohol <b>seeking</b> behavior.
+CRH	drug	alcohol	29700576	The corticotropin releasing hormone (<strong>CRH</strong>) system is a key mediator of stress induced responses in <b>alcohol</b> seeking behavior.
+CRH	addiction	relapse	29700576	The corticotropin releasing hormone (<strong>CRH</strong>) system is a key mediator of stress induced responses in alcohol <b>seeking</b> behavior.
+CRH	drug	alcohol	29700576	The <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) system is a key mediator of stress induced responses in <b>alcohol</b> seeking behavior.
+CRH	addiction	relapse	29700576	The <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) system is a key mediator of stress induced responses in alcohol <b>seeking</b> behavior.
+CRH	drug	alcohol	29700576	Recent research has identified the central nucleus of the amygdala (CeA), a brain region involved in the regulation of fear and stress induced responses that is especially rich in <strong>CRH</strong> positive neurons, as a key player in mediating excessive <b>alcohol</b> seeking.
+CRH	addiction	relapse	29700576	Recent research has identified the central nucleus of the amygdala (CeA), a brain region involved in the regulation of fear and stress induced responses that is especially rich in <strong>CRH</strong> positive neurons, as a key player in mediating excessive alcohol <b>seeking</b>.
+CRH	drug	alcohol	29700576	However, detailed characterization of the specific influences that local neuronal populations exert in mediating <b>alcohol</b> responses is hampered by current limitations in pharmacological and immunohistochemical tools for targeting <strong>CRH</strong> receptor subtype 1 (CRHR1).
+CRH	addiction	intoxication	29424043	Sex differences in <b>binge</b> like EtOH drinking, <strong>corticotropin releasing hormone</strong> and corticosterone: effects of β endorphin.
+CRH	drug	cocaine	29379100	Examination of hippocampal gene expression revealed in Sub mice, exposure to external stimuli, stress or <b>cocaine</b>, increased <strong>CRH</strong> expression (>100%), which was evoked in Dom mice only by <b>cocaine</b> exposure.
+CRH	drug	cocaine	29180955	Dissociable Role of <strong>Corticotropin Releasing Hormone</strong> Receptor Subtype 1 on Dopaminergic and D1 Dopaminoceptive Neurons in <b>Cocaine</b> Seeking Behavior.
+CRH	addiction	relapse	29180955	Dissociable Role of <strong>Corticotropin Releasing Hormone</strong> Receptor Subtype 1 on Dopaminergic and D1 Dopaminoceptive Neurons in Cocaine <b>Seeking</b> Behavior.
+CRH	drug	cocaine	29180955	The ability of many drugs of abuse, including <b>cocaine</b>, to mediate reinforcement and drug seeking behaviors is in part mediated by the corticotropin releasing hormone (<strong>CRH</strong>) system, in which <strong>CRH</strong> exerts its effects partly via the <strong>CRH</strong> receptor subtype 1 (CRHR1) in extra hypothalamic areas.
+CRH	addiction	relapse	29180955	The ability of many drugs of abuse, including cocaine, to mediate reinforcement and drug <b>seeking</b> behaviors is in part mediated by the corticotropin releasing hormone (<strong>CRH</strong>) system, in which <strong>CRH</strong> exerts its effects partly via the <strong>CRH</strong> receptor subtype 1 (CRHR1) in extra hypothalamic areas.
+CRH	addiction	reward	29180955	The ability of many drugs of abuse, including cocaine, to mediate <b>reinforcement</b> and drug seeking behaviors is in part mediated by the corticotropin releasing hormone (<strong>CRH</strong>) system, in which <strong>CRH</strong> exerts its effects partly via the <strong>CRH</strong> receptor subtype 1 (CRHR1) in extra hypothalamic areas.
+CRH	drug	cocaine	29180955	The ability of many drugs of abuse, including <b>cocaine</b>, to mediate reinforcement and drug seeking behaviors is in part mediated by the <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) system, in which <strong>CRH</strong> exerts its effects partly via the <strong>CRH</strong> receptor subtype 1 (CRHR1) in extra hypothalamic areas.
+CRH	addiction	relapse	29180955	The ability of many drugs of abuse, including cocaine, to mediate reinforcement and drug <b>seeking</b> behaviors is in part mediated by the <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) system, in which <strong>CRH</strong> exerts its effects partly via the <strong>CRH</strong> receptor subtype 1 (CRHR1) in extra hypothalamic areas.
+CRH	addiction	reward	29180955	The ability of many drugs of abuse, including cocaine, to mediate <b>reinforcement</b> and drug seeking behaviors is in part mediated by the <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) system, in which <strong>CRH</strong> exerts its effects partly via the <strong>CRH</strong> receptor subtype 1 (CRHR1) in extra hypothalamic areas.
+CRH	drug	opioid	29129606	In addition, expression of corticotropin releasing hormone (<strong>Crh</strong>) and mu <b>opioid</b> receptor (Oprm1) in the paraventricular nucleus (PVN) were measured using quantitative PCR.
+CRH	drug	opioid	29129606	In addition, expression of <strong>corticotropin releasing hormone</strong> (<strong>Crh</strong>) and mu <b>opioid</b> receptor (Oprm1) in the paraventricular nucleus (PVN) were measured using quantitative PCR.
+CRH	drug	opioid	29129606	Blunted <b>morphine</b> induced corticosterone secretion extended into the MOR F2 generation, as well as effects on <strong>Crh</strong>.
+CRH	drug	alcohol	29082267	We examined the ability of an intermittent access schedule to induce escalation of voluntary <b>alcohol</b> drinking in non human primates and used this model to assess the role of <strong>corticotropin releasing hormone</strong> (CRF) signaling in this process.
+CRH	addiction	addiction	29082267	We examined the ability of an intermittent access schedule to induce <b>escalation</b> of voluntary alcohol drinking in non human primates and used this model to assess the role of <strong>corticotropin releasing hormone</strong> (CRF) signaling in this process.
+CRH	drug	amphetamine	28842817	<b>Methamphetamine</b> Induces TET1  and TET3 Dependent DNA Hydroxymethylation of <strong>Crh</strong> and Avp Genes in the Rat Nucleus Accumbens.
+CRH	drug	amphetamine	28842817	Here, we show that <b>METH</b> administration produced time dependent increases in the expression of corticotropin releasing hormone (<strong>Crh</strong>/Crf), arginine vasopressin (Avp), and cocaine  and <b>amphetamine</b> regulated transcript prepropeptide (Cartpt) mRNAs in the rat nucleus accumbens (NAc).
+CRH	drug	cocaine	28842817	Here, we show that METH administration produced time dependent increases in the expression of corticotropin releasing hormone (<strong>Crh</strong>/Crf), arginine vasopressin (Avp), and <b>cocaine</b>  and amphetamine regulated transcript prepropeptide (Cartpt) mRNAs in the rat nucleus accumbens (NAc).
+CRH	drug	amphetamine	28842817	Here, we show that <b>METH</b> administration produced time dependent increases in the expression of <strong>corticotropin releasing hormone</strong> (<strong>Crh</strong>/Crf), arginine vasopressin (Avp), and cocaine  and <b>amphetamine</b> regulated transcript prepropeptide (Cartpt) mRNAs in the rat nucleus accumbens (NAc).
+CRH	drug	cocaine	28842817	Here, we show that METH administration produced time dependent increases in the expression of <strong>corticotropin releasing hormone</strong> (<strong>Crh</strong>/Crf), arginine vasopressin (Avp), and <b>cocaine</b>  and amphetamine regulated transcript prepropeptide (Cartpt) mRNAs in the rat nucleus accumbens (NAc).
+CRH	drug	amphetamine	28842817	Chromatin immunoprecipitation (ChIP) assays revealed that <b>METH</b> increased the abundance of phosphorylated CREB (pCREB) at the promoter of Cartpt but not at Avp or <strong>Crh</strong> DNA sequences.
+CRH	drug	amphetamine	28842817	In contrast, <b>METH</b> produced DNA hypomethylation at sites near the <strong>Crh</strong> transcription start site (TSS) and at intragenic Avp sequences.
+CRH	drug	amphetamine	28842817	<b>METH</b> also increased DNA hydroxymethylation at the <strong>Crh</strong> TSS and at intragenic Avp sites.
+CRH	drug	amphetamine	28842817	Importantly, <b>METH</b> increased TET1 binding at the <strong>Crh</strong> promoter and increased TET3 binding at Avp intragenic regions.
+CRH	drug	amphetamine	28842817	We further tested the role of TET enzymes in <b>METH</b> induced changes in gene expression by using the TET inhibitor, 1,5 isoquinolinediol (IQD), and found that IQD blocked <b>METH</b> induced increases in <strong>Crh</strong> and Avp mRNA expression.
+CRH	drug	alcohol	28291298	It seems that the most important neuroadaptive changes in progression from occasional <b>alcohol</b> intake to dependence are the down regulation of the dopamine and gamma aminobutyric acid systems, permanent upregulation in the glutamate system and dysregulation in the stress systems (<strong>corticotropin releasing hormone</strong> and serotonin) of the brain.
+CRH	addiction	dependence	28291298	It seems that the most important neuroadaptive changes in progression from occasional alcohol intake to <b>dependence</b> are the down regulation of the dopamine and gamma aminobutyric acid systems, permanent upregulation in the glutamate system and dysregulation in the stress systems (<strong>corticotropin releasing hormone</strong> and serotonin) of the brain.
+CRH	drug	cocaine	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1), and brain derived neurotrophic factor (BDNF) genes on susceptibility to crack <b>cocaine</b> addiction and BDNF levels.
+CRH	addiction	addiction	28237884	This study examined the effects of glucocorticoid receptor (NR3C1), <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1), and brain derived neurotrophic factor (BDNF) genes on susceptibility to crack cocaine <b>addiction</b> and BDNF levels.
+CRH	drug	amphetamine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, AgRP, cocaine  and <b>amphetamine</b> related transcript (CART), corticotropin releasing hormone (<strong>CRH</strong>) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+CRH	drug	cocaine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, AgRP, <b>cocaine</b>  and amphetamine related transcript (CART), corticotropin releasing hormone (<strong>CRH</strong>) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+CRH	drug	amphetamine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, AgRP, cocaine  and <b>amphetamine</b> related transcript (CART), <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+CRH	drug	cocaine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, AgRP, <b>cocaine</b>  and amphetamine related transcript (CART), <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+CRH	drug	cocaine	27870396	Preclinical models have demonstrated increased sensitivity of females to CRF and noradrenergic induced drug reinstatement compared with males, and, consistent with these findings, human laboratory studies have demonstrated greater sensitivity to corticotropin releasing hormone (<strong>CRH</strong>) and noradrenergic stimulation in <b>cocaine</b> dependent women compared with men.
+CRH	addiction	relapse	27870396	Preclinical models have demonstrated increased sensitivity of females to CRF and noradrenergic induced drug <b>reinstatement</b> compared with males, and, consistent with these findings, human laboratory studies have demonstrated greater sensitivity to corticotropin releasing hormone (<strong>CRH</strong>) and noradrenergic stimulation in cocaine dependent women compared with men.
+CRH	drug	cocaine	27870396	Preclinical models have demonstrated increased sensitivity of females to CRF and noradrenergic induced drug reinstatement compared with males, and, consistent with these findings, human laboratory studies have demonstrated greater sensitivity to <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and noradrenergic stimulation in <b>cocaine</b> dependent women compared with men.
+CRH	addiction	relapse	27870396	Preclinical models have demonstrated increased sensitivity of females to CRF and noradrenergic induced drug <b>reinstatement</b> compared with males, and, consistent with these findings, human laboratory studies have demonstrated greater sensitivity to <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and noradrenergic stimulation in cocaine dependent women compared with men.
+CRH	drug	cocaine	27870396	Furthermore, neuroimaging studies have demonstrated increased neural response to stressful stimuli in <b>cocaine</b> dependent women compared with men as well as showing significant sex differences in the sensitivity of brain regions responsible for regulating the response to <strong>CRH</strong>.
+CRH	drug	opioid	27385383	We tested the <b>morphine</b> withdrawal induced negative affective states, such as the aversive (assessed by conditioned place aversion), anxiety (assessed by elevated plus maze), and anhedonic like (assessed by saccharin preference test) behaviors, as well as the mRNA level of corticotropin releasing hormone (<strong>CRH</strong>) via optogenetic inhibition or activation of PV+ interneurons in the CeA.
+CRH	addiction	aversion	27385383	We tested the morphine withdrawal induced negative affective states, such as the <b>aversive</b> (assessed by conditioned place <b>aversion</b>), anxiety (assessed by elevated plus maze), and anhedonic like (assessed by saccharin preference test) behaviors, as well as the mRNA level of corticotropin releasing hormone (<strong>CRH</strong>) via optogenetic inhibition or activation of PV+ interneurons in the CeA.
+CRH	addiction	withdrawal	27385383	We tested the morphine <b>withdrawal</b> induced negative affective states, such as the aversive (assessed by conditioned place aversion), anxiety (assessed by elevated plus maze), and anhedonic like (assessed by saccharin preference test) behaviors, as well as the mRNA level of corticotropin releasing hormone (<strong>CRH</strong>) via optogenetic inhibition or activation of PV+ interneurons in the CeA.
+CRH	drug	opioid	27385383	We tested the <b>morphine</b> withdrawal induced negative affective states, such as the aversive (assessed by conditioned place aversion), anxiety (assessed by elevated plus maze), and anhedonic like (assessed by saccharin preference test) behaviors, as well as the mRNA level of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) via optogenetic inhibition or activation of PV+ interneurons in the CeA.
+CRH	addiction	aversion	27385383	We tested the morphine withdrawal induced negative affective states, such as the <b>aversive</b> (assessed by conditioned place <b>aversion</b>), anxiety (assessed by elevated plus maze), and anhedonic like (assessed by saccharin preference test) behaviors, as well as the mRNA level of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) via optogenetic inhibition or activation of PV+ interneurons in the CeA.
+CRH	addiction	withdrawal	27385383	We tested the morphine <b>withdrawal</b> induced negative affective states, such as the aversive (assessed by conditioned place aversion), anxiety (assessed by elevated plus maze), and anhedonic like (assessed by saccharin preference test) behaviors, as well as the mRNA level of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) via optogenetic inhibition or activation of PV+ interneurons in the CeA.
+CRH	drug	opioid	27385383	Optogenetic inhibition of the CeA PV+ interneurons during the <b>morphine</b> withdrawal significantly attenuated the elevated <strong>CRH</strong> mRNA level in the CeA.
+CRH	addiction	withdrawal	27385383	Optogenetic inhibition of the CeA PV+ interneurons during the morphine <b>withdrawal</b> significantly attenuated the elevated <strong>CRH</strong> mRNA level in the CeA.
+CRH	drug	opioid	27385383	The activation of PV+ interneurons during <b>morphine</b> withdrawal was crucial for the induction of the negative emotion and the up regulation of <strong>CRH</strong> mRNA levels in the CeA.
+CRH	addiction	withdrawal	27385383	The activation of PV+ interneurons during morphine <b>withdrawal</b> was crucial for the induction of the negative emotion and the up regulation of <strong>CRH</strong> mRNA levels in the CeA.
+CRH	drug	cocaine	27181613	Rats that self administered <b>cocaine</b> displayed greater <strong>CRH</strong> expression in the amygdala that was independent of urine exposure.
+CRH	drug	cannabinoid	26821211	Sustained glucocorticoid exposure recruits cortico limbic <strong>CRH</strong> signaling to modulate <b>endocannabinoid</b> function.
+CRH	drug	amphetamine	26433325	We also found that <b>AMPH</b> administration completely blocked the forced swim induced expression of the <strong>corticotropin releasing hormone</strong> (hnCRH) and it partially reduced c fos expression in the paraventricular nucleus of the hypothalamus (PVN).
+CRH	drug	alcohol	26236193	Alterations in <strong>CRH</strong> and AVP following long term <b>ethanol</b> exposure in rodents is well demonstrated, however little is known about the response to <b>ethanol</b> in primates or the mechanisms of adaptation.
+CRH	drug	alcohol	26236193	The presynaptic glutamate density in recurrent (i.e., intra hypothalamic) <strong>CRH</strong> terminals was highly related to <b>ethanol</b> intake, and may be a permissive factor in increased drinking due to stress.
+CRH	drug	cannabinoid	26061727	In enhanced green fluorescent protein expressing <strong>CRH</strong> neurons of the paraventricular nucleus (PVN) and in magnocellular neurons of the PVN and supraoptic nucleus (SON), dexamethasone activated postsynaptic membrane associated receptors and G protein signaling to elicit a rapid suppression of excitatory postsynaptic inputs, which was blocked by genetic deletion of type I <b>cannabinoid</b> receptors and a type I <b>cannabinoid</b> receptor antagonist.
+CRH	drug	alcohol	25833034	Chronic intermittent <b>ethanol</b> exposure in mice leads to an up regulation of <strong>CRH</strong>/CRHR1 signaling.
+CRH	drug	nicotine	25802844	Ethnic specific genetic association of variants in the <strong>corticotropin releasing hormone</strong> receptor 1 gene with <b>nicotine</b> dependence.
+CRH	addiction	dependence	25802844	Ethnic specific genetic association of variants in the <strong>corticotropin releasing hormone</strong> receptor 1 gene with nicotine <b>dependence</b>.
+CRH	drug	alcohol	25802844	Variants in the <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) gene have been associated with <b>alcoholism</b> and depression.
+CRH	drug	alcohol	25409596	The <strong>corticotropin releasing hormone</strong> 1 (CRH1) receptor antagonist pexacerfont in <b>alcohol</b> dependence: a randomized controlled experimental medicine study.
+CRH	addiction	dependence	25409596	The <strong>corticotropin releasing hormone</strong> 1 (CRH1) receptor antagonist pexacerfont in alcohol <b>dependence</b>: a randomized controlled experimental medicine study.
+CRH	drug	alcohol	25409596	The <strong>corticotropin releasing hormone</strong> 1 (<strong>CRH1</strong>) receptor antagonist pexacerfont in <b>alcohol</b> dependence: a randomized controlled experimental medicine study.
+CRH	addiction	dependence	25409596	The <strong>corticotropin releasing hormone</strong> 1 (<strong>CRH1</strong>) receptor antagonist pexacerfont in alcohol <b>dependence</b>: a randomized controlled experimental medicine study.
+CRH	drug	alcohol	25409596	Extensive preclinical data implicate corticotropin releasing hormone (<strong>CRH</strong>), acting through its CRH1 receptor, in stress  and dependence induced <b>alcohol</b> seeking.
+CRH	addiction	dependence	25409596	Extensive preclinical data implicate corticotropin releasing hormone (<strong>CRH</strong>), acting through its CRH1 receptor, in stress  and <b>dependence</b> induced alcohol seeking.
+CRH	addiction	relapse	25409596	Extensive preclinical data implicate corticotropin releasing hormone (<strong>CRH</strong>), acting through its CRH1 receptor, in stress  and dependence induced alcohol <b>seeking</b>.
+CRH	drug	alcohol	25409596	Extensive preclinical data implicate <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), acting through its CRH1 receptor, in stress  and dependence induced <b>alcohol</b> seeking.
+CRH	addiction	dependence	25409596	Extensive preclinical data implicate <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), acting through its CRH1 receptor, in stress  and <b>dependence</b> induced alcohol seeking.
+CRH	addiction	relapse	25409596	Extensive preclinical data implicate <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), acting through its CRH1 receptor, in stress  and dependence induced alcohol <b>seeking</b>.
+CRH	drug	alcohol	25409596	Extensive preclinical data implicate <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), acting through its <strong>CRH1</strong> receptor, in stress  and dependence induced <b>alcohol</b> seeking.
+CRH	addiction	dependence	25409596	Extensive preclinical data implicate <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), acting through its <strong>CRH1</strong> receptor, in stress  and <b>dependence</b> induced alcohol seeking.
+CRH	addiction	relapse	25409596	Extensive preclinical data implicate <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), acting through its <strong>CRH1</strong> receptor, in stress  and dependence induced alcohol <b>seeking</b>.
+CRH	drug	alcohol	25409596	We evaluated pexacerfont, an orally available, brain penetrant <strong>CRH1</strong> antagonist for its ability to suppress stress induced <b>alcohol</b> craving and brain responses in treatment seeking <b>alcohol</b> dependent patients in early abstinence.
+CRH	addiction	relapse	25409596	We evaluated pexacerfont, an orally available, brain penetrant <strong>CRH1</strong> antagonist for its ability to suppress stress induced alcohol <b>craving</b> and brain responses in treatment <b>seeking</b> alcohol dependent patients in early abstinence.
+CRH	drug	alcohol	25409596	Alternatively, the extensive preclinical data on <strong>CRH1</strong> antagonism as a mechanism to suppress <b>alcohol</b> seeking may not translate to humans.
+CRH	addiction	relapse	25409596	Alternatively, the extensive preclinical data on <strong>CRH1</strong> antagonism as a mechanism to suppress alcohol <b>seeking</b> may not translate to humans.
+CRH	drug	nicotine	25402857	We provide further evidence in rodents that chronic <b>nicotine</b> exposure upregulates <strong>Crh</strong> mRNA (encoding CRF) in dopaminergic neurons of the posterior VTA, activates local CRF1 receptors and blocks <b>nicotine</b> induced activation of transient GABAergic input to dopaminergic neurons.
+CRH	drug	nicotine	25402857	Local downregulation of <strong>Crh</strong> mRNA and specific pharmacological blockade of CRF1 receptors in the VTA reversed the effect of <b>nicotine</b> on GABAergic input to dopaminergic neurons, prevented the aversive effects of <b>nicotine</b> withdrawal and limited the escalation of <b>nicotine</b> intake.
+CRH	addiction	addiction	25402857	Local downregulation of <strong>Crh</strong> mRNA and specific pharmacological blockade of CRF1 receptors in the VTA reversed the effect of nicotine on GABAergic input to dopaminergic neurons, prevented the aversive effects of nicotine withdrawal and limited the <b>escalation</b> of nicotine intake.
+CRH	addiction	aversion	25402857	Local downregulation of <strong>Crh</strong> mRNA and specific pharmacological blockade of CRF1 receptors in the VTA reversed the effect of nicotine on GABAergic input to dopaminergic neurons, prevented the <b>aversive</b> effects of nicotine withdrawal and limited the escalation of nicotine intake.
+CRH	addiction	withdrawal	25402857	Local downregulation of <strong>Crh</strong> mRNA and specific pharmacological blockade of CRF1 receptors in the VTA reversed the effect of nicotine on GABAergic input to dopaminergic neurons, prevented the aversive effects of nicotine <b>withdrawal</b> and limited the escalation of nicotine intake.
+CRH	addiction	addiction	25073922	Dopamine and corticotrophin releasing hormone (<strong>CRH</strong>; also known as corticotrophin releasing factor) are key neurotransmitters in the interaction between stress and <b>addiction</b>.
+CRH	drug	cocaine	25073922	Repeated treatment with <b>cocaine</b> potentiates glutamatergic transmission in the rat basolateral amygdala/cortex pathway through a synergistic action of D1  like dopamine receptors and <strong>CRH</strong> type 2α receptors (CRF2 α receptors).
+CRH	addiction	addiction	25073922	D1 /CRF2 α receptor heteromerization might account, at least in part, for the complex physiological interactions established between dopamine and <strong>CRH</strong> in normal and pathological conditions such as <b>addiction</b>, representing a new potential pharmacological target.
+CRH	addiction	relapse	25038175	The most studied peptide in this category is corticotropin releasing hormone (<strong>CRH</strong>), which has been shown to mediate stress induced <b>reinstatement</b> of drug <b>seeking</b>, escalated self administration, and drug withdrawal, but it does not seem to be involved in baseline drug self administration or cue induced <b>reinstatement</b>.
+CRH	addiction	withdrawal	25038175	The most studied peptide in this category is corticotropin releasing hormone (<strong>CRH</strong>), which has been shown to mediate stress induced reinstatement of drug seeking, escalated self administration, and drug <b>withdrawal</b>, but it does not seem to be involved in baseline drug self administration or cue induced reinstatement.
+CRH	addiction	relapse	25038175	The most studied peptide in this category is <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), which has been shown to mediate stress induced <b>reinstatement</b> of drug <b>seeking</b>, escalated self administration, and drug withdrawal, but it does not seem to be involved in baseline drug self administration or cue induced <b>reinstatement</b>.
+CRH	addiction	withdrawal	25038175	The most studied peptide in this category is <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), which has been shown to mediate stress induced reinstatement of drug seeking, escalated self administration, and drug <b>withdrawal</b>, but it does not seem to be involved in baseline drug self administration or cue induced reinstatement.
+CRH	addiction	relapse	25038175	The SP/NK1R system is a major mediator of stress and anxiety, and over the last several years, it has been demonstrated that the SP/NK1R system can have effects similar to those of <strong>CRH</strong> on drug taking and drug <b>seeking</b>.
+CRH	addiction	relapse	24636458	In addition, increased activation of the corticotropin releasing hormone (<strong>CRH</strong>) system within the extended amygdala appears to mediate stress induced <b>relapse</b>.
+CRH	addiction	relapse	24636458	In addition, increased activation of the <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) system within the extended amygdala appears to mediate stress induced <b>relapse</b>.
+CRH	drug	alcohol	24623788	Indirect effect of <strong>corticotropin releasing hormone</strong> receptor 1 gene variation on negative emotionality and <b>alcohol</b> use via right ventrolateral prefrontal cortex.
+CRH	drug	alcohol	24623788	Variations in the <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) gene have been found to interact with stress in modulating excessive <b>alcohol</b> consumption.
+CRH	drug	opioid	24368617	Genetic polymorphisms in the coding or promoter regions of the Mu <b>Opioid</b> Receptor (OPRM1), Corticotropin Releasing Hormone (<strong>CRH</strong>), Monoamine Oxidase A (MAOA), Dopamine D4 Receptor (DRD4), and Serotonin Transporter (SLC6A4) genes have been shown to be functionally similar in humans and rhesus macaques and have been demonstrated to contribute to individual differences in aggression.
+CRH	drug	opioid	24368617	Genetic polymorphisms in the coding or promoter regions of the Mu <b>Opioid</b> Receptor (OPRM1), <strong>Corticotropin Releasing Hormone</strong> (<strong>CRH</strong>), Monoamine Oxidase A (MAOA), Dopamine D4 Receptor (DRD4), and Serotonin Transporter (SLC6A4) genes have been shown to be functionally similar in humans and rhesus macaques and have been demonstrated to contribute to individual differences in aggression.
+CRH	drug	opioid	24048098	At completion of behavioral testing, mu <b>opioid</b> receptor (OPRM1), FosB, cFos, and dopamine receptor mRNA expression was measured in the nucleus accumbens as well as OPRM1 and <strong>corticotropin releasing hormone</strong> mRNA in the paraventricular nucleus.
+CRH	drug	alcohol	23898297	We performed a series of dexamethasone challenges and found that mice undergoing 2 weeks of <b>alcohol</b> abstinence had significantly greater corticosterone and ACTH levels following a DEX <strong>CRH</strong> challenge compared to water controls.
+CRH	drug	alcohol	23898297	Environmental enrichment during <b>alcohol</b> abstinence corrected the abnormal DEX <strong>CRH</strong> corticosterone response despite a further elevation of ACTH levels.
+CRH	drug	opioid	23805290	Chronic <b>morphine</b> exposure or pair feeding did not significantly affect hypothalamic expression of selected stress  and metabolic related neuropeptides   corticotropin releasing hormone (<strong>CRH</strong>), urocortin 2 (UCN2) and proopiomelanocortin (POMC) compared to placebo implanted and pair fed animals.
+CRH	drug	opioid	23805290	Chronic <b>morphine</b> exposure or pair feeding did not significantly affect hypothalamic expression of selected stress  and metabolic related neuropeptides   <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), urocortin 2 (UCN2) and proopiomelanocortin (POMC) compared to placebo implanted and pair fed animals.
+CRH	drug	opioid	23323881	The results indicate that ADAR2 transgenic mice exhibit, (1) a food preference for diets with higher fat content, (2) significantly increased food intake that is non distractible in a competing reward environment, (3) significantly increased messenger RNA (mRNA) expressions of ADAR2, serotonin 2C receptor (5HT2C R), D1, D2 and mu <b>opioid</b> receptors and no change in <strong>corticotropin releasing hormone</strong> mRNAs and significantly reduced ADAR2 protein expression in the hypothalamus, (4) significantly increased D1 receptor and altered bioamines with no change in ADAR2, mu <b>opioid</b> and D2 receptor mRNA expression in the striatum and (5) significantly greater glucose metabolism in the hypothalamus, brain stem, right hippocampus, left and right mid brain regions and suprascapular peripheral tissue than controls.
+CRH	addiction	reward	23323881	The results indicate that ADAR2 transgenic mice exhibit, (1) a food preference for diets with higher fat content, (2) significantly increased food intake that is non distractible in a competing <b>reward</b> environment, (3) significantly increased messenger RNA (mRNA) expressions of ADAR2, serotonin 2C receptor (5HT2C R), D1, D2 and mu opioid receptors and no change in <strong>corticotropin releasing hormone</strong> mRNAs and significantly reduced ADAR2 protein expression in the hypothalamus, (4) significantly increased D1 receptor and altered bioamines with no change in ADAR2, mu opioid and D2 receptor mRNA expression in the striatum and (5) significantly greater glucose metabolism in the hypothalamus, brain stem, right hippocampus, left and right mid brain regions and suprascapular peripheral tissue than controls.
+CRH	drug	opioid	22446386	Polymorphisms of the corticotropin releasing hormone binding protein (<strong>CRH</strong> BP) gene and of the μ <b>opioid</b> receptor (OPRM1) gene were examined as moderators of this relationship.
+CRH	drug	opioid	22446386	Polymorphisms of the <strong>corticotropin releasing hormone</strong> binding protein (<strong>CRH</strong> BP) gene and of the μ <b>opioid</b> receptor (OPRM1) gene were examined as moderators of this relationship.
+CRH	drug	alcohol	22384198	We have previously shown that repeated binge pattern <b>alcohol</b> exposure increased the expression of two critical central regulators of stress and anxiety, corticotrophin releasing hormone (<strong>CRH</strong>) and arginine vasopressin (AVP), in adolescent male rats.
+CRH	addiction	intoxication	22384198	We have previously shown that repeated <b>binge</b> pattern alcohol exposure increased the expression of two critical central regulators of stress and anxiety, corticotrophin releasing hormone (<strong>CRH</strong>) and arginine vasopressin (AVP), in adolescent male rats.
+CRH	drug	alcohol	22384198	Therefore, we tested the hypothesis that 17β estradiol (E(2)), the predominant sex steroid hormone in females, prevents <b>alcohol</b> induced changes in <strong>CRH</strong> and AVP gene expression in the paraventricular nucleus (PVN) of the hypothalamus.
+CRH	drug	alcohol	22384198	Further, repeated binge pattern <b>alcohol</b> exposure significantly decreased <strong>CRH</strong> and AVP mRNA in Ch , but not E(2) treated animals, which was consistent with our previous observations in gonad intact females.
+CRH	addiction	intoxication	22384198	Further, repeated <b>binge</b> pattern alcohol exposure significantly decreased <strong>CRH</strong> and AVP mRNA in Ch , but not E(2) treated animals, which was consistent with our previous observations in gonad intact females.
+CRH	drug	alcohol	22384198	We further tested the effects of E(2) and <b>alcohol</b> treatment on the activity of the wild type <strong>CRH</strong> promoter in a PVN derived neuronal cell line.
+CRH	drug	alcohol	22384198	<b>Alcohol</b> increased <strong>CRH</strong> promoter activity in these cells and concomitant treatment with E(2) completely abolished the effect.
+CRH	drug	alcohol	22384198	Together our data suggest that E(2) regulates the reactivity of the HPA axis to a repeated stressor through modulation of the habituation response and further serves to maintain normal steady state mRNA levels of <strong>CRH</strong> and AVP in the PVN in response to a repeated <b>alcohol</b> stressor.
+CRH	drug	alcohol	22341871	In oil  and estradiol injected <b>ethanol</b> treated females, <strong>CRH</strong> mRNA levels did not change in response to LPS stimulation, whereas those of vasopressin increased, but stayed below control levels.
+CRH	drug	alcohol	22113086	Corticotropin releasing hormone (<strong>CRH</strong>) and its receptor, <strong>CRH</strong> receptor 1 (CRHR1), have a key role in <b>alcoholism</b>.
+CRH	drug	alcohol	22113086	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>) and its receptor, <strong>CRH</strong> receptor 1 (CRHR1), have a key role in <b>alcoholism</b>.
+CRH	drug	alcohol	22113086	Especially, post dependent and stress induced <b>alcohol</b> intake involve <strong>CRH</strong>/CRHR1 signaling within extra hypothalamic structures, but a contribution of the hypothalamic pituitary adrenal (HPA) axis activity might be involved as well.
+CRH	drug	alcohol	22113086	To dissect <strong>CRH</strong>/CRHR1 extra HPA and HPA signaling on a molecular level, a conditional brain specific Crhr1 knockout (Crhr1(NestinCre)) and a global knockout mouse line were studied for basal <b>alcohol</b> drinking, stress induced <b>alcohol</b> consumption, deprivation induced intake, and escalated <b>alcohol</b> consumption in the post dependent state.
+CRH	drug	alcohol	22113086	We conclude that <strong>CRH</strong>/CRHR1 extra HPA and HPA signaling may have opposing effects on stress related <b>alcohol</b> consumption.
+CRH	drug	alcohol	22036774	Pharmacological blockade of <strong>corticotropin releasing hormone</strong> receptor 1 (CRH1R) reduces voluntary consumption of high <b>alcohol</b> concentrations in non dependent Wistar rats.
+CRH	drug	alcohol	22036774	A dysregulation of the corticotropin releasing hormone (<strong>CRH</strong>) system has been implicated in the development of excessive <b>alcohol</b> consumption and dependence.
+CRH	addiction	dependence	22036774	A dysregulation of the corticotropin releasing hormone (<strong>CRH</strong>) system has been implicated in the development of excessive alcohol consumption and <b>dependence</b>.
+CRH	drug	alcohol	22036774	A dysregulation of the <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) system has been implicated in the development of excessive <b>alcohol</b> consumption and dependence.
+CRH	addiction	dependence	22036774	A dysregulation of the <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) system has been implicated in the development of excessive alcohol consumption and <b>dependence</b>.
+CRH	drug	alcohol	22036774	The aim of the present study was to evaluate whether the <strong>CRH</strong> system is also recruited when non dependent Wistar rats escalate to high <b>alcohol</b> intake in the intermittent (alternate days) model of drinking.
+CRH	drug	alcohol	22036774	Pharmacological blockade of CRH1R reduced <b>alcohol</b> drinking when sustained high levels of intake were achieved suggesting that the <strong>CRH</strong> system plays a key role when high doses of <b>ethanol</b> are consumed by non dependent subjects.
+CRH	addiction	dependence	22036774	This supports the notion that <strong>CRH</strong> system not only maintains the dependent state but also engages the transition to <b>dependence</b>.
+CRH	addiction	dependence	21998007	Adverse childhood experiences (ACEs) increase the risk for adult depression and substance <b>dependence</b>, possibly mediated by the <strong>corticotropin releasing hormone</strong> type 1 receptor (CRHR1).
+CRH	drug	alcohol	21934176	Studies using <strong>corticotropin releasing hormone</strong> stimulation and tests after <b>ethanol</b> ingestion revealed inconclusive results.
+CRH	addiction	relapse	21843515	The role of CRF2 receptors in stress induced <b>relapse</b> to drug <b>seeking</b> also opens the question of the putative role of the other peptides of the <strong>CRH</strong> family (urocotin 1, urocortin 2 and urocortin 3) that have high affinity for CRF2 receptors.
+CRH	drug	alcohol	21835193	<b>Ethanol</b> induced stimulation in preweanling rats required the activation of <strong>CRH</strong> 1 receptors.
+CRH	drug	alcohol	21835193	These results are consistent with recent findings indicating that one of the mechanisms by which the <strong>CRH</strong> 1 receptor modulates anxiety depends on sensitization of the 5 HT2 receptor antagonist, and highlight the importance of stress as a modulator of the effects of <b>ethanol</b> during early developmental stages.
+CRH	addiction	sensitization	21835193	These results are consistent with recent findings indicating that one of the mechanisms by which the <strong>CRH</strong> 1 receptor modulates anxiety depends on <b>sensitization</b> of the 5 HT2 receptor antagonist, and highlight the importance of stress as a modulator of the effects of ethanol during early developmental stages.
+CRH	drug	alcohol	21752573	[The role of genetic factors on the link between stress and <b>alcohol</b> use: the example of <strong>CRH</strong> R1].
+CRH	drug	opioid	21706389	Genes at which variation moderates these phenotypes include those encoding monoamine oxidase A (MAOA LPR), the serotonin transporter (HTTLPR), corticotropin releasing hormone (<strong>CRH</strong> 248C/T and  2232 C/G), Neuropeptide Y (NPY 1002 T/G), and the μ <b>opioid</b> receptor (OPRM1 C77G).
+CRH	drug	opioid	21706389	Genes at which variation moderates these phenotypes include those encoding monoamine oxidase A (MAOA LPR), the serotonin transporter (HTTLPR), <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong> 248C/T and  2232 C/G), Neuropeptide Y (NPY 1002 T/G), and the μ <b>opioid</b> receptor (OPRM1 C77G).
+CRH	drug	nicotine	21590390	The narrative is based on experience and considerations made in the course of building these programs, and work on four mechanisms targeted by our libraries: cholinergic <b>nicotine</b> receptors, receptors for corticotropin releasing hormone (<strong>CRH</strong>), neurokinin 1 (NK1) receptors for substance P (SP) and hypocretin/orexin receptors.
+CRH	drug	nicotine	21590390	The narrative is based on experience and considerations made in the course of building these programs, and work on four mechanisms targeted by our libraries: cholinergic <b>nicotine</b> receptors, receptors for <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), neurokinin 1 (NK1) receptors for substance P (SP) and hypocretin/orexin receptors.
+CRH	drug	alcohol	21533237	Our previous studies showed that binge pattern <b>ethanol</b> (EtOH) treatment during pubertal development negatively dysregulated the responsiveness of the hypothalamo pituitary adrenal (HPA) axis, as manifested by alterations in corticotrophin releasing hormone (<strong>CRH</strong>), arginine vasopressin (AVP), and corticosterone (CORT) during this time period.
+CRH	addiction	intoxication	21533237	Our previous studies showed that <b>binge</b> pattern ethanol (EtOH) treatment during pubertal development negatively dysregulated the responsiveness of the hypothalamo pituitary adrenal (HPA) axis, as manifested by alterations in corticotrophin releasing hormone (<strong>CRH</strong>), arginine vasopressin (AVP), and corticosterone (CORT) during this time period.
+CRH	addiction	sensitization	21409840	[The delayed <b>sensitization</b> of <strong>CRH</strong> response developed after chronic variable stress on the acoustic startle reflex].
+CRH	drug	benzodiazepine	21409840	A single treatment with any antidepressant agent had no influence the f ASR while a marked inhibition by a single dose of <b>alprazolam</b>, <strong>CRH1</strong> receptor antagonist, prazosin and propranolol was observed.
+CRH	addiction	sensitization	21409840	The decreased tyrosine hydroxylase activity in the locus coeruleus and the beta adrenoceptor down regulation in the amygdaloid complex might be involved in the inhibiton of the delayed augmentation of f ASR by repeated antidepressant treatment, leading to the possibility that the delayed <b>sensitization</b> of <strong>CRH</strong> response to stress after CVS might contribute to the biological mechanism underlying the formation of pathological states such as anxiety and depressive disorders.
+CRH	drug	alcohol	21376087	<b>Ethanol</b> treatment had no effect on levels of corticotropin releasing hormone (<strong>CRH</strong>) in the hippocampus, striatum, and prefrontal cortex of both groups of rats.
+CRH	drug	alcohol	21376087	<b>Ethanol</b> treatment had no effect on levels of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) in the hippocampus, striatum, and prefrontal cortex of both groups of rats.
+CRH	drug	alcohol	21376087	After <b>ethanol</b> withdrawal, hippocampal levels of mGlu1 receptors were higher in unstressed rats, but lower in PRS rats, whereas NPY and <strong>CRH</strong> levels were similar in the two groups of rats.
+CRH	addiction	withdrawal	21376087	After ethanol <b>withdrawal</b>, hippocampal levels of mGlu1 receptors were higher in unstressed rats, but lower in PRS rats, whereas NPY and <strong>CRH</strong> levels were similar in the two groups of rats.
+CRH	drug	cocaine	21306838	<b>Cocaine</b> use in the 30 days following <strong>CRH</strong> administration was measured.
+CRH	drug	cocaine	21306838	<b>Cocaine</b> dependent individuals also had a greater subjective stress response to <strong>CRH</strong> than controls (p<0.01).
+CRH	drug	cocaine	21306838	Finally, there was a trend for an indirect effect of neuroticism on frequency of <b>cocaine</b> use through subjective reactivity to <strong>CRH</strong>.
+CRH	drug	opioid	21143246	Following experimentwise permutation, markers in the <strong>corticotropin releasing hormone</strong> binding protein (CRHBP) the μ <b>opioid</b> receptor (OPRM1) and the β1 subunit of GABA A (GABA(A)) receptors (GABRB1) met or exceeded the significance threshold.
+CRH	drug	alcohol	21039637	Stress induced and cue induced craving for <b>alcohol</b> in heavy drinkers: Preliminary evidence of genetic moderation by the OPRM1 and <strong>CRH</strong> BP genes.
+CRH	addiction	relapse	21039637	Stress induced and cue induced <b>craving</b> for alcohol in heavy drinkers: Preliminary evidence of genetic moderation by the OPRM1 and <strong>CRH</strong> BP genes.
+CRH	drug	opioid	21039637	This study examines genetic determinants of stress induced and cue induced craving in heavy drinkers by testing single nucleotide polymorphisms (SNPs) of the corticotrophin releasing hormone binding protein (<strong>CRH</strong> BP) gene and the mu <b>opioid</b> receptor (OPRM1) gene.
+CRH	addiction	relapse	21039637	This study examines genetic determinants of stress induced and cue induced <b>craving</b> in heavy drinkers by testing single nucleotide polymorphisms (SNPs) of the corticotrophin releasing hormone binding protein (<strong>CRH</strong> BP) gene and the mu opioid receptor (OPRM1) gene.
+CRH	addiction	relapse	21039637	Analyses, uncorrected for multiple comparisons, revealed that a tag SNP of the <strong>CRH</strong> BP gene (rs10055255) moderated stress induced <b>craving</b> in this sample.
+CRH	drug	alcohol	21039637	These initial results extend recent preclinical and clinical findings implicating the <strong>CRH</strong> BP in stress related <b>alcoholism</b> and confirm the role of the Asp40 allele of the OPRM1 gene in reward driven <b>alcohol</b> phenotypes.
+CRH	addiction	reward	21039637	These initial results extend recent preclinical and clinical findings implicating the <strong>CRH</strong> BP in stress related alcoholism and confirm the role of the Asp40 allele of the OPRM1 gene in <b>reward</b> driven alcohol phenotypes.
+CRH	drug	cocaine	20570051	Influence of <b>cocaine</b> dependence and early life stress on pituitary adrenal axis responses to <strong>CRH</strong> and the Trier social stressor.
+CRH	addiction	dependence	20570051	Influence of cocaine <b>dependence</b> and early life stress on pituitary adrenal axis responses to <strong>CRH</strong> and the Trier social stressor.
+CRH	drug	cocaine	20570051	In this study, the neuroendocrine, physiologic (HR), and subjective responses to corticotropin releasing hormone (<strong>CRH</strong>) and the Trier Social Stress Task (TSST) in individuals with <b>cocaine</b> dependence, with (n=21)/without early life stress (n=21), non dependent individuals with early life stress (n=22), and a control group were examined (n=21).
+CRH	addiction	dependence	20570051	In this study, the neuroendocrine, physiologic (HR), and subjective responses to corticotropin releasing hormone (<strong>CRH</strong>) and the Trier Social Stress Task (TSST) in individuals with cocaine <b>dependence</b>, with (n=21)/without early life stress (n=21), non dependent individuals with early life stress (n=22), and a control group were examined (n=21).
+CRH	drug	cocaine	20570051	In this study, the neuroendocrine, physiologic (HR), and subjective responses to <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and the Trier Social Stress Task (TSST) in individuals with <b>cocaine</b> dependence, with (n=21)/without early life stress (n=21), non dependent individuals with early life stress (n=22), and a control group were examined (n=21).
+CRH	addiction	dependence	20570051	In this study, the neuroendocrine, physiologic (HR), and subjective responses to <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and the Trier Social Stress Task (TSST) in individuals with cocaine <b>dependence</b>, with (n=21)/without early life stress (n=21), non dependent individuals with early life stress (n=22), and a control group were examined (n=21).
+CRH	drug	cocaine	20570051	In response to <strong>CRH</strong>, subjective stress and craving were positively correlated in <b>cocaine</b> dependent subjects regardless of early life stress history, while stress and craving following the TSST were correlated only in <b>cocaine</b> dependent subjects without a history of early life stress.
+CRH	addiction	relapse	20570051	In response to <strong>CRH</strong>, subjective stress and <b>craving</b> were positively correlated in cocaine dependent subjects regardless of early life stress history, while stress and <b>craving</b> following the TSST were correlated only in cocaine dependent subjects without a history of early life stress.
+CRH	drug	alcohol	20374216	Single nucleotide polymorphisms in <strong>corticotropin releasing hormone</strong> receptor 1 gene (CRHR1) are associated with quantitative trait of event related potential and <b>alcohol</b> dependence.
+CRH	addiction	dependence	20374216	Single nucleotide polymorphisms in <strong>corticotropin releasing hormone</strong> receptor 1 gene (CRHR1) are associated with quantitative trait of event related potential and alcohol <b>dependence</b>.
+CRH	drug	alcohol	20374216	Recent studies demonstrated a crucial role of <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) in the environmental stress response and <b>ethanol</b> self administration in animal models.
+CRH	drug	opioid	20113875	Furthermore, genetic variants that alter functioning of the serotonin, endogenous <b>opioid</b>, and <strong>corticotropin releasing hormone</strong> systems are shown to influence both physiological and behavioral outcomes, in some cases interacting with early experience to indicate gene by environment interactions.
+CRH	drug	alcohol	19952347	In this study, we determined the effects of binge <b>ethanol</b> exposure during puberty on two critical central regulators of stress and anxiety behavior: corticotrophin releasing hormone (<strong>CRH</strong>) and arginine vasopressin (AVP).
+CRH	addiction	intoxication	19952347	In this study, we determined the effects of <b>binge</b> ethanol exposure during puberty on two critical central regulators of stress and anxiety behavior: corticotrophin releasing hormone (<strong>CRH</strong>) and arginine vasopressin (AVP).
+CRH	drug	alcohol	19952347	Binge <b>ethanol</b> exposure also significantly increased <strong>CRH</strong> and AVP gene expression in the paraventricular nucleus of males, but not females.
+CRH	addiction	intoxication	19952347	<b>Binge</b> ethanol exposure also significantly increased <strong>CRH</strong> and AVP gene expression in the paraventricular nucleus of males, but not females.
+CRH	drug	alcohol	19913192	Stress related neuropeptides and <b>alcoholism</b>: <strong>CRH</strong>, NPY, and beyond.
+CRH	drug	alcohol	19878140	An examination of <b>alcohol</b> consumption in adolescents reported a significant genotype x environment (G x E) interaction involving rs1876831, a <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) polymorphism, and negative events.
+CRH	drug	alcohol	19799878	However, <b>alcohol</b> consumption was associated with a decrease in the number of vasopressin (VP) neurons only in females and of corticotropin releasing hormone (<strong>CRH</strong>) neurons in males and females.
+CRH	drug	alcohol	19799878	However, <b>alcohol</b> consumption was associated with a decrease in the number of vasopressin (VP) neurons only in females and of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) neurons in males and females.
+CRH	addiction	withdrawal	19799878	Further, the response to <b>withdrawal</b> was sexually dimorphic because in males there was a partial recovery of the number of <strong>CRH</strong> neurons whereas in females there was a further loss of VP and <strong>CRH</strong> neurons.
+CRH	drug	alcohol	19799878	These findings show that the response of <strong>CRH</strong> and VP neurons to excess <b>alcohol</b> is gender specific, with females being more vulnerable during <b>alcohol</b> consumption and, most notably, after withdrawal.
+CRH	addiction	withdrawal	19799878	These findings show that the response of <strong>CRH</strong> and VP neurons to excess alcohol is gender specific, with females being more vulnerable during alcohol consumption and, most notably, after <b>withdrawal</b>.
+CRH	drug	cocaine	19726138	Participants were 53 <b>cocaine</b> dependent individuals who were admitted for a 2 day inpatient stay during which a psychosocial provocation (i.e., the Trier Social Stress Task), a pharmacological provocation (i.e., administration of 1 microg/kg corticotrophin releasing hormone; <strong>CRH</strong>), and a drug cue exposure paradigm were completed.
+CRH	drug	cocaine	19726138	In response to the <strong>CRH</strong> and drug cue exposure, elevated subjective craving and stress were significant predictors of <b>cocaine</b> use during follow up.
+CRH	addiction	relapse	19726138	In response to the <strong>CRH</strong> and drug cue exposure, elevated subjective <b>craving</b> and stress were significant predictors of cocaine use during follow up.
+CRH	drug	cocaine	19717245	<b>Cocaine</b> dependent participants received 1 microg/kg of <strong>corticotropin releasing hormone</strong> intravenously, underwent the Trier Social Stress Task, and were exposed to drug cues and various measures obtained.
+CRH	drug	benzodiazepine	19405150	However, neither the corticosterone receptor antagonist RU486 nor the <strong>CRH</strong> receptor antagonist NBI27914 blocked their poor stress coping, whereas the administration of the GABA(A) receptor allosteric modulator <b>diazepam</b> or the D1 dopamine receptor antagonist SCH23390 prior to restraint stress sessions changed their stress coping response to the stressed AC5(+/+) mouse level.
+CRH	drug	cocaine	19349312	Response to <strong>corticotropin releasing hormone</strong> infusion in <b>cocaine</b> dependent individuals.
+CRH	drug	cocaine	19349312	Corticotropin releasing hormone (<strong>CRH</strong>), through the hypothalamic pituitary adrenal axis and other brain stress systems, is involved in the emotional dysregulation associated with <b>cocaine</b> dependence.
+CRH	addiction	dependence	19349312	Corticotropin releasing hormone (<strong>CRH</strong>), through the hypothalamic pituitary adrenal axis and other brain stress systems, is involved in the emotional dysregulation associated with cocaine <b>dependence</b>.
+CRH	drug	cocaine	19349312	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>), through the hypothalamic pituitary adrenal axis and other brain stress systems, is involved in the emotional dysregulation associated with <b>cocaine</b> dependence.
+CRH	addiction	dependence	19349312	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>), through the hypothalamic pituitary adrenal axis and other brain stress systems, is involved in the emotional dysregulation associated with cocaine <b>dependence</b>.
+CRH	drug	cocaine	19349312	Little is known about the response of <b>cocaine</b> dependent individuals to <strong>CRH</strong> administration.
+CRH	drug	cocaine	19349312	The primary objective was to examine the hypothalamic pituitary adrenal axis and the subjective and physiologic response to <strong>CRH</strong> in <b>cocaine</b> dependent individuals and controls.
+CRH	drug	cocaine	19349312	<b>Cocaine</b> dependent individuals exhibited higher stress (P < .001) and craving for <strong>CRH</strong> compared with controls.
+CRH	addiction	relapse	19349312	Cocaine dependent individuals exhibited higher stress (P < .001) and <b>craving</b> for <strong>CRH</strong> compared with controls.
+CRH	drug	cocaine	19349312	Intravenous <strong>CRH</strong> elevated heart rates in all groups; however, <b>cocaine</b> dependent women demonstrated a significantly higher heart rate at all time points (P = .05).
+CRH	drug	cocaine	19349312	The corticotropin response to <strong>CRH</strong> was independent of sex and <b>cocaine</b> dependence.
+CRH	addiction	dependence	19349312	The corticotropin response to <strong>CRH</strong> was independent of sex and cocaine <b>dependence</b>.
+CRH	drug	cocaine	19349312	There is an increased subjective and heart rate response to <strong>CRH</strong> and a relationship between stress and craving in <b>cocaine</b> dependent individuals.
+CRH	addiction	relapse	19349312	There is an increased subjective and heart rate response to <strong>CRH</strong> and a relationship between stress and <b>craving</b> in cocaine dependent individuals.
+CRH	drug	cocaine	19349312	The lack of difference in hypothalamic pituitary adrenal axis response between the <b>cocaine</b> dependent and control groups suggests that the heart rate and subjective responses in the <b>cocaine</b> group may be mediated by sensitization of nonhypothalamic stress responsive <strong>CRH</strong> systems.
+CRH	addiction	sensitization	19349312	The lack of difference in hypothalamic pituitary adrenal axis response between the cocaine dependent and control groups suggests that the heart rate and subjective responses in the cocaine group may be mediated by <b>sensitization</b> of nonhypothalamic stress responsive <strong>CRH</strong> systems.
+CRH	drug	benzodiazepine	19101875	Also alterations in the expression of neuropeptides like <strong>Corticotropin Releasing Hormone</strong> and Neuropeptide Y are thought to be involved in the development of <b>benzodiazepine</b> dependence.
+CRH	addiction	dependence	19101875	Also alterations in the expression of neuropeptides like <strong>Corticotropin Releasing Hormone</strong> and Neuropeptide Y are thought to be involved in the development of benzodiazepine <b>dependence</b>.
+CRH	drug	opioid	19016181	Sixty <b>heroin</b> dependent patients received either non opiate treatment (NOT) with benzodiazepines and clonidine (n = 30) or <b>methadone</b> stabilization treatment (MT, n = 30), and their serum levels of corticotropin releasing hormone (<strong>CRH</strong>), adrenocorticotropic hormone (ACTH), and cortisol (COR) were measured and compared to those of healthy, nondependent controls.
+CRH	drug	opioid	19016181	Sixty <b>heroin</b> dependent patients received either non opiate treatment (NOT) with benzodiazepines and clonidine (n = 30) or <b>methadone</b> stabilization treatment (MT, n = 30), and their serum levels of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), adrenocorticotropic hormone (ACTH), and cortisol (COR) were measured and compared to those of healthy, nondependent controls.
+CRH	addiction	withdrawal	19016181	Compared with healthy controls, <strong>CRH</strong> was significantly lower (p < .001) while COR was higher (p < .001) during acute <b>withdrawal</b> in the NOT group.
+CRH	drug	opioid	19016181	Our findings suggest that chronic <b>opioid</b> dependence may cause reduced function of the HPA axis, while <b>opioid</b> withdrawal may decrease the response of the pituitary to <strong>CRH</strong> and increase the adrenal response to ACTH.
+CRH	addiction	dependence	19016181	Our findings suggest that chronic opioid <b>dependence</b> may cause reduced function of the HPA axis, while opioid withdrawal may decrease the response of the pituitary to <strong>CRH</strong> and increase the adrenal response to ACTH.
+CRH	addiction	withdrawal	19016181	Our findings suggest that chronic opioid dependence may cause reduced function of the HPA axis, while opioid <b>withdrawal</b> may decrease the response of the pituitary to <strong>CRH</strong> and increase the adrenal response to ACTH.
+CRH	drug	alcohol	18974851	Common genetic origins for EEG, <b>alcoholism</b> and anxiety: the role of <strong>CRH</strong> BP.
+CRH	drug	alcohol	18974851	Moreover, the same SNPs and haplotypes, located within the <strong>CRH</strong> BP haplotype block, were also associated with anxiety disorders in the Plains Indians and <b>alcohol</b> use disorders in the Caucasians.
+CRH	drug	alcohol	18974851	Our results suggest a likely role for <strong>CRH</strong> BP in stress related <b>alcoholism</b> and highlight the use of the resting EEG as an intermediate phenotype for arousal related behaviors such as anxiety and addiction.
+CRH	addiction	addiction	18974851	Our results suggest a likely role for <strong>CRH</strong> BP in stress related alcoholism and highlight the use of the resting EEG as an intermediate phenotype for arousal related behaviors such as anxiety and <b>addiction</b>.
+CRH	drug	alcohol	18678798	<strong>CRH</strong> haplotype as a factor influencing cerebrospinal fluid levels of corticotropin releasing hormone, hypothalamic pituitary adrenal axis activity, temperament, and <b>alcohol</b> consumption in rhesus macaques.
+CRH	drug	alcohol	18678798	<strong>CRH</strong> haplotype as a factor influencing cerebrospinal fluid levels of <strong>corticotropin releasing hormone</strong>, hypothalamic pituitary adrenal axis activity, temperament, and <b>alcohol</b> consumption in rhesus macaques.
+CRH	drug	alcohol	18678798	As such, <strong>CRH</strong> gene variation may influence risk for <b>alcohol</b> use and dependence.
+CRH	addiction	dependence	18678798	As such, <strong>CRH</strong> gene variation may influence risk for alcohol use and <b>dependence</b>.
+CRH	drug	alcohol	18678798	To determine whether <strong>CRH</strong> variation influences relevant intermediate phenotypes, behavior, and <b>alcohol</b> consumption in rhesus macaques.
+CRH	drug	alcohol	18678798	Animals were genotyped for a single nucleotide polymorphism disrupting a glucocorticoid response element, rhCRH  2232 C>G, and the effects of this allele on CSF levels of <strong>CRH</strong>, plasma levels of ACTH, behavior, and <b>ethanol</b> consumption were assessed by analysis of variance.
+CRH	addiction	dependence	18449521	Pathological anxiety responses and the development of substance <b>dependence</b> are both critically mediated through corticotrophin releasing hormone (<strong>CRH</strong>) systems, and the RAS is positioned to interact both with hypothalamic as well as extrahypothalamic <strong>CRH</strong> systems.
+CRH	drug	benzodiazepine	18088080	<b>Benzodiazepine</b> treatment interferes not only with the release of <strong>CRH</strong> but also with the release of NPY and CCK.
+CRH	drug	alcohol	17976860	For <b>ethanol</b> consumption, correlations were found for <strong>CRH</strong> receptors 1 and 2 and vasopressin while strong trends were observed for galanin receptor 1, orexin receptor 1, MCH and adrenoceptor alpha(1B).
+CRH	drug	alcohol	17585886	This persisted 3 months after <b>alcohol</b> exposure and was reversed by the selective <strong>CRH</strong> R1 antagonist 3 (4 Chloro 2 morpholin 4 yl thiazol 5 yl) 8 (1 ethylpropyl) 2,6 dimethyl imidazo[1,2 b]pyridazine (MTIP) (10 mg/kg).
+CRH	drug	alcohol	17407495	Corticotropin releasing hormone 1 receptors (<strong>CRH</strong> R1) mediate increased behavioral sensitivity to stress and excessive <b>alcohol</b> self administration following a history of dependence.
+CRH	addiction	dependence	17407495	Corticotropin releasing hormone 1 receptors (<strong>CRH</strong> R1) mediate increased behavioral sensitivity to stress and excessive alcohol self administration following a history of <b>dependence</b>.
+CRH	drug	alcohol	17407495	<strong>Corticotropin releasing hormone</strong> 1 receptors (<strong>CRH</strong> R1) mediate increased behavioral sensitivity to stress and excessive <b>alcohol</b> self administration following a history of dependence.
+CRH	addiction	dependence	17407495	<strong>Corticotropin releasing hormone</strong> 1 receptors (<strong>CRH</strong> R1) mediate increased behavioral sensitivity to stress and excessive alcohol self administration following a history of <b>dependence</b>.
+CRH	drug	alcohol	17407495	These data support that recruitment of <strong>CRH</strong> R1 signaling within components of the extended amygdala drives excessive <b>alcohol</b> intake, and that <b>alcohol</b> is voluntarily consumed in part for its ability to reduce <strong>CRH</strong> R1 activity in this region.
+CRH	drug	alcohol	17347308	Whether <b>ethanol</b> exposure in developing rats induces beta EP neuronal death and alters their influence on <strong>CRH</strong> neurons in vivo has not been determined.
+CRH	drug	alcohol	17347308	The <b>ethanol</b> treated animals also showed incompetent ability to respond to exogenous beta EP to alter the lipopolysaccharide induced <strong>CRH</strong> mRNA levels.
+CRH	drug	cocaine	17293045	Restraint induced corticosterone secretion and hypothalamic <strong>CRH</strong> mRNA expression are augmented during acute withdrawal from chronic <b>cocaine</b> administration.
+CRH	addiction	withdrawal	17293045	Restraint induced corticosterone secretion and hypothalamic <strong>CRH</strong> mRNA expression are augmented during acute <b>withdrawal</b> from chronic cocaine administration.
+CRH	drug	cocaine	17293045	Basal <strong>CRH</strong> mRNA in the PVN was unaltered as a result of prior <b>cocaine</b> administration.
+CRH	drug	cocaine	17293045	However, a significant increase in <strong>CRH</strong> mRNA was observed 90 min following the termination of restraint in <b>cocaine</b> withdrawn, but not saline treated, rats.
+CRH	drug	opioid	17286593	To reveal secretory, activational and transcriptional changes in the hypothalamus of <b>morphine</b> dependent rats during <b>naloxone</b> precipitated <b>opioid</b> withdrawal, we measured corticosterone secretion, c Fos induction and heteronuclear (hn)RNA levels of corticotropin releasing hormone (<strong>CRH</strong>) and arginine vasopressin (AVP) in naïve and <b>morphine</b> dependent animals injected with saline or 5 mg/kg <b>naloxone</b>.
+CRH	addiction	withdrawal	17286593	To reveal secretory, activational and transcriptional changes in the hypothalamus of morphine dependent rats during naloxone precipitated opioid <b>withdrawal</b>, we measured corticosterone secretion, c Fos induction and heteronuclear (hn)RNA levels of corticotropin releasing hormone (<strong>CRH</strong>) and arginine vasopressin (AVP) in naïve and morphine dependent animals injected with saline or 5 mg/kg naloxone.
+CRH	drug	opioid	17286593	To reveal secretory, activational and transcriptional changes in the hypothalamus of <b>morphine</b> dependent rats during <b>naloxone</b> precipitated <b>opioid</b> withdrawal, we measured corticosterone secretion, c Fos induction and heteronuclear (hn)RNA levels of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and arginine vasopressin (AVP) in naïve and <b>morphine</b> dependent animals injected with saline or 5 mg/kg <b>naloxone</b>.
+CRH	addiction	withdrawal	17286593	To reveal secretory, activational and transcriptional changes in the hypothalamus of morphine dependent rats during naloxone precipitated opioid <b>withdrawal</b>, we measured corticosterone secretion, c Fos induction and heteronuclear (hn)RNA levels of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and arginine vasopressin (AVP) in naïve and morphine dependent animals injected with saline or 5 mg/kg naloxone.
+CRH	drug	opioid	17286593	Using probes complementary to intronic sequences of genes encoding neuropeptides in parvocellular neurosecretory neurons of the PVH, we found robust increases in <strong>CRH</strong> and AVP hnRNAs in <b>morphine</b> dependent rats during <b>naloxone</b> precipitated withdrawal.
+CRH	addiction	withdrawal	17286593	Using probes complementary to intronic sequences of genes encoding neuropeptides in parvocellular neurosecretory neurons of the PVH, we found robust increases in <strong>CRH</strong> and AVP hnRNAs in morphine dependent rats during naloxone precipitated <b>withdrawal</b>.
+CRH	drug	amphetamine	17119930	Previous studies from our laboratory and others have indicated a role for the hypothalamo pituitary adrenal (HPA) axis in the extinction/reinstatement animal model of cocaine relapse This present study was designed to investigate the potential role for the HPA axis in the cue  and <b>methamphetamine</b> induced reinstatement of extinguished <b>methamphetamine</b> seeking behavior by determining the effects of ketoconazole and the <strong>corticotropin releasing hormone</strong> (CRF) type 1 receptor antagonist, CP 154,526, on these behaviors.
+CRH	drug	cocaine	17119930	Previous studies from our laboratory and others have indicated a role for the hypothalamo pituitary adrenal (HPA) axis in the extinction/reinstatement animal model of <b>cocaine</b> relapse This present study was designed to investigate the potential role for the HPA axis in the cue  and methamphetamine induced reinstatement of extinguished methamphetamine seeking behavior by determining the effects of ketoconazole and the <strong>corticotropin releasing hormone</strong> (CRF) type 1 receptor antagonist, CP 154,526, on these behaviors.
+CRH	addiction	relapse	17119930	Previous studies from our laboratory and others have indicated a role for the hypothalamo pituitary adrenal (HPA) axis in the extinction/<b>reinstatement</b> animal model of cocaine <b>relapse</b> This present study was designed to investigate the potential role for the HPA axis in the cue  and methamphetamine induced <b>reinstatement</b> of extinguished methamphetamine <b>seeking</b> behavior by determining the effects of ketoconazole and the <strong>corticotropin releasing hormone</strong> (CRF) type 1 receptor antagonist, CP 154,526, on these behaviors.
+CRH	addiction	reward	17016707	In experiment 2, animals were chronically exposed to <strong>corticotropin releasing hormone</strong> type 1 receptor antagonist, antalarmin, prior to <b>CPP</b> training.
+CRH	drug	alcohol	17015825	An innate up regulation of the Crhr1 transcript, encoding the corticotropin releasing hormone receptor 1 (<strong>CRH</strong> R1), was found in several limbic brain areas of msP rats genetically selected for high <b>alcohol</b> preference, was associated with genetic polymorphism of the Crhr1 promoter, and was accompanied by increased <strong>CRH</strong> R1 density.
+CRH	drug	alcohol	17015825	An innate up regulation of the Crhr1 transcript, encoding the <strong>corticotropin releasing hormone</strong> receptor 1 (<strong>CRH</strong> R1), was found in several limbic brain areas of msP rats genetically selected for high <b>alcohol</b> preference, was associated with genetic polymorphism of the Crhr1 promoter, and was accompanied by increased <strong>CRH</strong> R1 density.
+CRH	drug	alcohol	17015825	A selective <strong>CRH</strong> R1 antagonist (antalarmin, 10 20 mg/kg) was devoid of effects on operant <b>alcohol</b> self administration in unselected Wistar rats but significantly suppressed this behavior in the msP line.
+CRH	addiction	reward	17015825	A selective <strong>CRH</strong> R1 antagonist (antalarmin, 10 20 mg/kg) was devoid of effects on <b>operant</b> alcohol self administration in unselected Wistar rats but significantly suppressed this behavior in the msP line.
+CRH	drug	cocaine	16674926	Apart from activation of the brain reward system, <b>cocaine</b> administration influences the activity of the hypothalamo pituitary adrenal (HPA) axis by affecting <strong>CRH</strong> neurons in the paraventricular nucleus of the hypothalamus (PVN).
+CRH	addiction	reward	16674926	Apart from activation of the brain <b>reward</b> system, cocaine administration influences the activity of the hypothalamo pituitary adrenal (HPA) axis by affecting <strong>CRH</strong> neurons in the paraventricular nucleus of the hypothalamus (PVN).
+CRH	drug	alcohol	16639867	Modified dexamethasone suppression <strong>corticotropin releasing hormone</strong> stimulation test: A pilot study of young healthy volunteers and implications for <b>alcoholism</b> research in adolescents and young adults.
+CRH	drug	alcohol	16639867	Nonalcoholic subjects with a family history of <b>alcoholism</b> exhibit lower plasma ACTH and beta endorphin as well as lower ACTH, cortisol, and beta endorphin responses to psychological stress and <strong>CRH</strong> stimulation.
+CRH	drug	alcohol	16550213	Genetic association of the human <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) with binge drinking and <b>alcohol</b> intake patterns in two independent samples.
+CRH	addiction	intoxication	16550213	Genetic association of the human <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) with <b>binge</b> drinking and alcohol intake patterns in two independent samples.
+CRH	drug	alcohol	16550213	To investigate the role of the <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) in patterns of human <b>alcohol</b> drinking and its potential contribution to <b>alcohol</b> dependence, we analysed two independent samples: a sample of adolescents, which consisted of individuals from the 'Mannheim Study of Risk Children' (MARC), who had little previous exposure to <b>alcohol</b>, and a sample of <b>alcohol</b> dependent adults, who met DSM IV criteria of <b>alcohol</b> dependence.
+CRH	addiction	dependence	16550213	To investigate the role of the <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) in patterns of human alcohol drinking and its potential contribution to alcohol <b>dependence</b>, we analysed two independent samples: a sample of adolescents, which consisted of individuals from the 'Mannheim Study of Risk Children' (MARC), who had little previous exposure to alcohol, and a sample of alcohol dependent adults, who met DSM IV criteria of alcohol <b>dependence</b>.
+CRH	drug	alcohol	16499484	Hypothalamic synthesis and secretion of corticotropin releasing hormone (<strong>CRH</strong>), a putative mediator of various behavioral and physiological responses to <b>ethanol</b> (EtOH), is defective in inbred Lewis (LEW) rats in comparison with their genetically related inbred Fischer 344 (F344) and outbred Sprague Dawley (S D) strains.
+CRH	drug	alcohol	16499484	Hypothalamic synthesis and secretion of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>), a putative mediator of various behavioral and physiological responses to <b>ethanol</b> (EtOH), is defective in inbred Lewis (LEW) rats in comparison with their genetically related inbred Fischer 344 (F344) and outbred Sprague Dawley (S D) strains.
+CRH	drug	alcohol	15992556	Lack of association between single nucleotide polymorphisms in the <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) gene and <b>alcohol</b> dependence.
+CRH	addiction	dependence	15992556	Lack of association between single nucleotide polymorphisms in the <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR1) gene and alcohol <b>dependence</b>.
+CRH	drug	alcohol	15992556	While the physiological mechanisms that contribute to the development of <b>alcohol</b> dependence remain unclear, a number of recent studies have indicated a role for the <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR 1) in modulating the response of the central nervous system to <b>ethanol</b>.
+CRH	addiction	dependence	15992556	While the physiological mechanisms that contribute to the development of alcohol <b>dependence</b> remain unclear, a number of recent studies have indicated a role for the <strong>corticotropin releasing hormone</strong> receptor 1 (CRHR 1) in modulating the response of the central nervous system to ethanol.
+CRH	drug	cocaine	15986362	Effects of <strong>corticotropin releasing hormone</strong> receptor antagonists on <b>cocaine</b> induced dopamine overflow in the medial prefrontal cortex and nucleus accumbens of rats.
+CRH	drug	cocaine	15986362	Recent evidence suggests an important role for corticotropin releasing hormone (<strong>CRH</strong>) and <strong>CRH</strong> receptors in <b>cocaine</b> reinforcement.
+CRH	addiction	reward	15986362	Recent evidence suggests an important role for corticotropin releasing hormone (<strong>CRH</strong>) and <strong>CRH</strong> receptors in cocaine <b>reinforcement</b>.
+CRH	drug	cocaine	15986362	Recent evidence suggests an important role for <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and <strong>CRH</strong> receptors in <b>cocaine</b> reinforcement.
+CRH	addiction	reward	15986362	Recent evidence suggests an important role for <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and <strong>CRH</strong> receptors in cocaine <b>reinforcement</b>.
+CRH	drug	cocaine	15986362	<strong>CRH</strong> receptor antagonists reduce <b>cocaine</b> self administration and attenuate the reinstatement of extinguished <b>cocaine</b> seeking behavior, but little is known about the mechanisms involved.
+CRH	addiction	relapse	15986362	<strong>CRH</strong> receptor antagonists reduce cocaine self administration and attenuate the <b>reinstatement</b> of extinguished cocaine <b>seeking</b> behavior, but little is known about the mechanisms involved.
+CRH	drug	cocaine	15986362	One possible mechanism for these effects may involve the <b>cocaine</b> induced activation of <strong>CRH</strong> located in brain regions outside of the hypothalamus.
+CRH	drug	cocaine	15986362	<strong>CRH</strong> has been shown to increase dopaminergic transmission in regions relevant for <b>cocaine</b> reinforcement, such as the medial prefrontal cortex and the nucleus accumbens.
+CRH	addiction	reward	15986362	<strong>CRH</strong> has been shown to increase dopaminergic transmission in regions relevant for cocaine <b>reinforcement</b>, such as the medial prefrontal cortex and the nucleus accumbens.
+CRH	drug	cocaine	15986362	Here, we report that CP 154,526, a <strong>CRH1</strong> receptor antagonist, actually enhances <b>cocaine</b> induced increases in dopamine overflow in the medial prefrontal cortex, measured using in vivo microdialysis.
+CRH	drug	cocaine	15986362	These data suggest a surprising role for prefrontal cortex dopamine in the ability of <strong>CRH</strong> receptor antagonists to attenuate <b>cocaine</b> seeking in rats.
+CRH	addiction	relapse	15986362	These data suggest a surprising role for prefrontal cortex dopamine in the ability of <strong>CRH</strong> receptor antagonists to attenuate cocaine <b>seeking</b> in rats.
+CRH	drug	alcohol	15834231	Vasoactive intestinal peptide and <strong>corticotropin releasing hormone</strong> increase beta endorphin release and proopiomelanocortin messenger RNA levels in primary cultures of hypothalamic cells: effects of acute and chronic <b>ethanol</b> treatment.
+CRH	drug	alcohol	15834231	Furthermore, the authors studied the effects of acute and chronic treatment with <b>ethanol</b> on the response of beta EP neurons to VIP and <strong>CRH</strong>.
+CRH	drug	alcohol	15834231	Acute treatment with <b>ethanol</b> increased beta EP neuronal gene expression and the secretory response to <strong>CRH</strong> and VIP.
+CRH	drug	alcohol	15834231	However, previous exposure to chronic <b>ethanol</b> reduced the <strong>CRH</strong> and VIP responses of these neurons.
+CRH	drug	alcohol	15834231	These results indicate that VIP and <strong>CRH</strong> stimulate beta EP release from hypothalamic cells in primary cultures and that the stimulatory and adaptive responses of beta EP neurons to <b>ethanol</b> may involve alteration in the responsiveness of beta EP secreting neurons to <strong>CRH</strong> and VIP.
+CRH	drug	cocaine	15519677	Effects of selective D1  or D2 like dopamine receptor antagonists with acute "binge" pattern <b>cocaine</b> on <strong>corticotropin releasing hormone</strong> and proopiomelanocortin mRNA levels in the hypothalamus.
+CRH	addiction	intoxication	15519677	Effects of selective D1  or D2 like dopamine receptor antagonists with acute "<b>binge</b>" pattern cocaine on <strong>corticotropin releasing hormone</strong> and proopiomelanocortin mRNA levels in the hypothalamus.
+CRH	drug	cocaine	15519677	We have previously demonstrated that there are stimulatory effects of acute (1 day) "binge" <b>cocaine</b> on corticotropin releasing hormone (<strong>CRH</strong>) gene expression in the rat hypothalamus and on the stress responsive hypothalamic pituitary adrenal (HPA) activity.
+CRH	addiction	intoxication	15519677	We have previously demonstrated that there are stimulatory effects of acute (1 day) "<b>binge</b>" cocaine on corticotropin releasing hormone (<strong>CRH</strong>) gene expression in the rat hypothalamus and on the stress responsive hypothalamic pituitary adrenal (HPA) activity.
+CRH	drug	cocaine	15519677	We have previously demonstrated that there are stimulatory effects of acute (1 day) "binge" <b>cocaine</b> on <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) gene expression in the rat hypothalamus and on the stress responsive hypothalamic pituitary adrenal (HPA) activity.
+CRH	addiction	intoxication	15519677	We have previously demonstrated that there are stimulatory effects of acute (1 day) "<b>binge</b>" cocaine on <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) gene expression in the rat hypothalamus and on the stress responsive hypothalamic pituitary adrenal (HPA) activity.
+CRH	drug	cocaine	15519677	However, the acute "binge" <b>cocaine</b> induced increase in hypothalamic <strong>CRH</strong> mRNA levels was not found in the rats that received either D1R or D2R antagonist pretreatment.
+CRH	addiction	intoxication	15519677	However, the acute "<b>binge</b>" cocaine induced increase in hypothalamic <strong>CRH</strong> mRNA levels was not found in the rats that received either D1R or D2R antagonist pretreatment.
+CRH	drug	cocaine	15519677	In the anterior pituitary, acute "binge" <b>cocaine</b> or its combinations with either DA antagonist did not alter <strong>CRH</strong> R1 receptor or POMC mRNA levels.
+CRH	addiction	intoxication	15519677	In the anterior pituitary, acute "<b>binge</b>" cocaine or its combinations with either DA antagonist did not alter <strong>CRH</strong> R1 receptor or POMC mRNA levels.
+CRH	drug	cocaine	15519677	These results suggest that both D1R and D2R mediate acute <b>cocaine</b>'s stimulatory effect on HPA axis at the hypothalamic <strong>CRH</strong> level.
+CRH	addiction	relapse	15511714	The most coherent body of data concerns the hypothalamo pituitary adrenocortical (HPA) axis, with low corticotrophin releasing hormone (<strong>CRH</strong>) being associated with more intense <b>craving</b> and increased probability of <b>relapse</b> after acute detoxification.
+CRH	drug	cocaine	15288701	Since the MPC and <strong>CRH</strong> have been implicated in the neurobiology of <b>cocaine</b>, <strong>CRH</strong> induced alterations in dopaminergic neurotransmission may play an important role in this peptide's effects on <b>cocaine</b> responsiveness.
+CRH	drug	cocaine	15288701	Taken together with the results from previous studies, these data suggest that ketoconazole may affect <b>cocaine</b> reward, at least in part, through interactions with dopamine and <strong>CRH</strong> within the MPC.
+CRH	addiction	reward	15288701	Taken together with the results from previous studies, these data suggest that ketoconazole may affect cocaine <b>reward</b>, at least in part, through interactions with dopamine and <strong>CRH</strong> within the MPC.
+CRH	drug	benzodiazepine	15219633	We performed the combined dexamethasone/<strong>CRH</strong> test before <b>benzodiazepine</b> discontinuation (taper off max.
+CRH	drug	benzodiazepine	15219633	Patients with more severe <b>benzodiazepine</b> withdrawal (CIWA B increase > 14 pts; n = 7) showed a significant higher cortisol and ACTH response in the dexamethasone/<strong>CRH</strong> test preceding the discontinuation of benzodiazepines than patients displaying less severe withdrawal symptoms (CIWA B increase <14 pts.
+CRH	addiction	withdrawal	15219633	Patients with more severe benzodiazepine <b>withdrawal</b> (CIWA B increase > 14 pts; n = 7) showed a significant higher cortisol and ACTH response in the dexamethasone/<strong>CRH</strong> test preceding the discontinuation of benzodiazepines than patients displaying less severe <b>withdrawal</b> symptoms (CIWA B increase <14 pts.
+CRH	drug	benzodiazepine	15219633	In view of the GABAergic inhibition of HPA system activity and the anxiogenic effect of <strong>CRH</strong>, <b>benzodiazepine</b> withdrawal symptoms may be partly due to a disinhibition of the HPA system during discontinuation of benzodiazepines.
+CRH	addiction	withdrawal	15219633	In view of the GABAergic inhibition of HPA system activity and the anxiogenic effect of <strong>CRH</strong>, benzodiazepine <b>withdrawal</b> symptoms may be partly due to a disinhibition of the HPA system during discontinuation of benzodiazepines.
+CRH	drug	alcohol	15203442	No association of <strong>CRH1</strong> receptor polymorphism haplotypes, harm avoidance and other personality dimensions in <b>alcohol</b> dependence: results from the Munich gene bank project for <b>alcoholism</b>.
+CRH	addiction	dependence	15203442	No association of <strong>CRH1</strong> receptor polymorphism haplotypes, harm avoidance and other personality dimensions in alcohol <b>dependence</b>: results from the Munich gene bank project for alcoholism.
+CRH	drug	alcohol	15203442	Because corticotrophin releasing hormone (<strong>CRH</strong>) plays a central role in stress regulation, the possible role of CRH1 polymorphism for anxiety related personality variables such as harm avoidance possibly associated with <b>alcoholism</b> was studied.
+CRH	drug	alcohol	15203442	Because corticotrophin releasing hormone (<strong>CRH</strong>) plays a central role in stress regulation, the possible role of <strong>CRH1</strong> polymorphism for anxiety related personality variables such as harm avoidance possibly associated with <b>alcoholism</b> was studied.
+CRH	drug	alcohol	15203442	Based on the examination of 170 <b>alcoholic</b> subjects no association was found between <strong>CRH1</strong> receptor haplotypes of four single nuclotid polymorphisms (SNPs) and low and high temperament traits of harm avoidance, novelty seeking and reward dependence.
+CRH	addiction	dependence	15203442	Based on the examination of 170 alcoholic subjects no association was found between <strong>CRH1</strong> receptor haplotypes of four single nuclotid polymorphisms (SNPs) and low and high temperament traits of harm avoidance, novelty seeking and reward <b>dependence</b>.
+CRH	addiction	relapse	15203442	Based on the examination of 170 alcoholic subjects no association was found between <strong>CRH1</strong> receptor haplotypes of four single nuclotid polymorphisms (SNPs) and low and high temperament traits of harm avoidance, novelty <b>seeking</b> and reward dependence.
+CRH	addiction	reward	15203442	Based on the examination of 170 alcoholic subjects no association was found between <strong>CRH1</strong> receptor haplotypes of four single nuclotid polymorphisms (SNPs) and low and high temperament traits of harm avoidance, novelty seeking and <b>reward</b> dependence.
+CRH	drug	alcohol	15179967	We therefore investigated whether <b>acamprosate</b> normalizes HPA hyperactivity in <b>alcoholics</b> within the first 3 weeks of abstinence, employing a combined dexamethasone/corticotropin releasing hormone (Dex <strong>CRH</strong>) test.
+CRH	drug	alcohol	15179967	We therefore investigated whether <b>acamprosate</b> normalizes HPA hyperactivity in <b>alcoholics</b> within the first 3 weeks of abstinence, employing a combined dexamethasone/<strong>corticotropin releasing hormone</strong> (Dex <strong>CRH</strong>) test.
+CRH	drug	alcohol	15179967	In 15 patients, <b>acamprosate</b>, 1332 1998 mg/day, was administered orally and a second Dex <strong>CRH</strong> test was performed 1 week later.
+CRH	drug	alcohol	15179967	<strong>CRH</strong> stimulated cortisol secretion was significantly increased in both the <b>acamprosate</b> group and the group receiving no anti relapse medication compared to a control group of 15 healthy subjects.
+CRH	addiction	relapse	15179967	<strong>CRH</strong> stimulated cortisol secretion was significantly increased in both the acamprosate group and the group receiving no anti <b>relapse</b> medication compared to a control group of 15 healthy subjects.
+CRH	drug	alcohol	15179967	<b>Acamprosate</b> treatment had no effect on basal or <strong>CRH</strong> stimulated ACTH or cortisol secretion.
+CRH	drug	opioid	15147776	Effect of <b>naloxone</b> precipitated <b>morphine</b> withdrawal on c fos expression in rat <strong>corticotropin releasing hormone</strong> neurons in the paraventricular hypothalamus and extended amygdala.
+CRH	addiction	withdrawal	15147776	Effect of naloxone precipitated morphine <b>withdrawal</b> on c fos expression in rat <strong>corticotropin releasing hormone</strong> neurons in the paraventricular hypothalamus and extended amygdala.
+CRH	addiction	withdrawal	15147776	The 41 amino acid polypeptide corticotropin releasing hormone (<strong>CRH</strong>) is hypothesized to mediate, in part, both the negative affective state and the physical <b>withdrawal</b> syndrome.
+CRH	addiction	withdrawal	15147776	The 41 amino acid polypeptide <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) is hypothesized to mediate, in part, both the negative affective state and the physical <b>withdrawal</b> syndrome.
+CRH	drug	opioid	15147776	Here, by means of dual immunohistochemical methodology, we examined the co expression of the c Fos protein and <strong>CRH</strong> following <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+CRH	addiction	withdrawal	15147776	Here, by means of dual immunohistochemical methodology, we examined the co expression of the c Fos protein and <strong>CRH</strong> following naloxone precipitated morphine <b>withdrawal</b>.
+CRH	drug	opioid	15147776	We found that <b>naloxone</b> precipitated withdrawal of <b>morphine</b> dependent rats increased c Fos immunoreactivity (IR) in <strong>CRH</strong> positive neurons in the paraventricular hypothalamus.
+CRH	addiction	withdrawal	15147776	We found that naloxone precipitated <b>withdrawal</b> of morphine dependent rats increased c Fos immunoreactivity (IR) in <strong>CRH</strong> positive neurons in the paraventricular hypothalamus.
+CRH	drug	opioid	15147776	Withdrawal of <b>morphine</b> dependent rats also increased c Fos IR in the central amygdala and bed nucleus of the stria terminalis, however these were in <strong>CRH</strong> negative neurons.
+CRH	addiction	withdrawal	15147776	<b>Withdrawal</b> of morphine dependent rats also increased c Fos IR in the central amygdala and bed nucleus of the stria terminalis, however these were in <strong>CRH</strong> negative neurons.
+CRH	drug	cocaine	14751291	Effects of chronic <b>cocaine</b> exposure on <strong>corticotropin releasing hormone</strong> binding protein in the central nucleus of the amygdala and bed nucleus of the stria terminalis.
+CRH	drug	cocaine	14751291	The primary objective of the present experiment was to assess whether prior, chronic exposure to <b>cocaine</b> modulates expression of <strong>CRH</strong> BP, and to compare expression of the BP with that of the peptide itself.
+CRH	drug	cocaine	14751291	In the CeA, <b>cocaine</b> pre exposure increased both <strong>CRH</strong> and <strong>CRH</strong> BP mRNA expression 1 day post treatment.
+CRH	drug	cocaine	14751291	In the dorsal BNST, <b>cocaine</b> pre exposure elevated levels of <strong>CRH</strong> BP, but not <strong>CRH</strong>, mRNA 3 days post treatment.
+CRH	drug	cocaine	14751291	Taken together, the results suggest that withdrawal induced changes in the expression of the <strong>CRH</strong> BP, and <strong>CRH</strong> itself, are relatively short lived and that a dysregulation in basal expression of either gene is not likely responsible for long lasting behavioral effects noted with <b>cocaine</b> and other drugs of abuse.
+CRH	addiction	withdrawal	14751291	Taken together, the results suggest that <b>withdrawal</b> induced changes in the expression of the <strong>CRH</strong> BP, and <strong>CRH</strong> itself, are relatively short lived and that a dysregulation in basal expression of either gene is not likely responsible for long lasting behavioral effects noted with cocaine and other drugs of abuse.
+CRH	drug	benzodiazepine	14659475	Specifically, we demonstrate that (1) psychogenic stressors influence the in vivo release of <strong>CRH</strong> at the central nucleus of the amygdala (CeA); (2) although <strong>CRH</strong> changes within the CeA are exquisitely sensitive to stressors, they are also elicited by positive stimuli; and (3) while treatment with <b>diazepam</b> attenuates behavioral signs of anxiety, the <strong>CRH</strong> release associated with a stressor is unaffected by the treatment.
+CRH	addiction	aversion	14659475	We suggest that the <strong>CRH</strong> responses at the CeA may be involved in a preparatory capacity and, as such, may accompany a range of emotionally significant stimuli, be they appetitive or <b>aversive</b>.
+CRH	drug	nicotine	14604602	These effects of <b>nicotine</b> withdrawal were not accompanied by any changes in the expressions of GR and <strong>CRH</strong> mRNA in either hippocampus or PVN.
+CRH	addiction	withdrawal	14604602	These effects of nicotine <b>withdrawal</b> were not accompanied by any changes in the expressions of GR and <strong>CRH</strong> mRNA in either hippocampus or PVN.
+CRH	drug	nicotine	14604602	These results suggest that subsensitivity of the HPA axis to stress during <b>nicotine</b> withdrawal may be implicated in the precipitation of depression during <b>smoking</b> cessation, although GR and <strong>CRH</strong> in the HPA axis do not appear to play a significant role.
+CRH	addiction	withdrawal	14604602	These results suggest that subsensitivity of the HPA axis to stress during nicotine <b>withdrawal</b> may be implicated in the precipitation of depression during smoking cessation, although GR and <strong>CRH</strong> in the HPA axis do not appear to play a significant role.
+CRH	drug	cannabinoid	12968131	Corticotropin releasing hormone (<strong>CRH</strong>) mRNA expression in rat central amygdala in <b>cannabinoid</b> tolerance and withdrawal: evidence for an allostatic shift?
+CRH	addiction	withdrawal	12968131	Corticotropin releasing hormone (<strong>CRH</strong>) mRNA expression in rat central amygdala in cannabinoid tolerance and <b>withdrawal</b>: evidence for an allostatic shift?
+CRH	drug	cannabinoid	12968131	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>) mRNA expression in rat central amygdala in <b>cannabinoid</b> tolerance and withdrawal: evidence for an allostatic shift?
+CRH	addiction	withdrawal	12968131	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>) mRNA expression in rat central amygdala in cannabinoid tolerance and <b>withdrawal</b>: evidence for an allostatic shift?
+CRH	drug	cannabinoid	12968131	Furthermore, <b>cannabinoid</b> antagonist administration precipitates a characteristic withdrawal syndrome in tolerant subjects, accompanied by neuronal activation and enhanced release of corticotropin releasing hormone (<strong>CRH</strong>) in the central amygdala.
+CRH	addiction	withdrawal	12968131	Furthermore, cannabinoid antagonist administration precipitates a characteristic <b>withdrawal</b> syndrome in tolerant subjects, accompanied by neuronal activation and enhanced release of corticotropin releasing hormone (<strong>CRH</strong>) in the central amygdala.
+CRH	drug	cannabinoid	12968131	Furthermore, <b>cannabinoid</b> antagonist administration precipitates a characteristic withdrawal syndrome in tolerant subjects, accompanied by neuronal activation and enhanced release of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) in the central amygdala.
+CRH	addiction	withdrawal	12968131	Furthermore, cannabinoid antagonist administration precipitates a characteristic <b>withdrawal</b> syndrome in tolerant subjects, accompanied by neuronal activation and enhanced release of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) in the central amygdala.
+CRH	drug	cannabinoid	12968131	We examined the role of <b>cannabinoid</b> tolerance and withdrawal for the expression of the <b>cannabinoid</b> 1 (CB1) receptor and of <strong>CRH</strong> in rats.
+CRH	addiction	withdrawal	12968131	We examined the role of cannabinoid tolerance and <b>withdrawal</b> for the expression of the cannabinoid 1 (CB1) receptor and of <strong>CRH</strong> in rats.
+CRH	addiction	withdrawal	12968131	The <strong>CRH</strong> transcript was upregulated in the central amygdala in precipitated <b>withdrawal</b> compared to nonwithdrawn tolerant subjects, suggesting that increased gene expression contributes to the previously reported <strong>CRH</strong> release in <b>withdrawal</b>.
+CRH	addiction	withdrawal	12968131	Most importantly, this increase occurred from a suppressed level in tolerant subjects, and behavioral signs of <b>withdrawal</b>, presumably mediated by <strong>CRH</strong>, were seen at the <strong>CRH</strong> expression that had only returned to normal nontolerant levels.
+CRH	addiction	reward	12798267	In order to investigate whether overproduction of <strong>CRH</strong> alters attentional process, transgenic mice overproducing <strong>CRH</strong> were tested on an <b>operant</b> five choice serial reaction time task, a task which taxes sustained and divided attention.
+CRH	drug	cocaine	12782395	Increased <strong>CRH</strong> mRNA levels in the rat amygdala during short term withdrawal from chronic 'binge' <b>cocaine</b>.
+CRH	addiction	intoxication	12782395	Increased <strong>CRH</strong> mRNA levels in the rat amygdala during short term withdrawal from chronic '<b>binge</b>' cocaine.
+CRH	addiction	withdrawal	12782395	Increased <strong>CRH</strong> mRNA levels in the rat amygdala during short term <b>withdrawal</b> from chronic 'binge' cocaine.
+CRH	addiction	withdrawal	12782395	There is evidence that suggests that increased corticotropin releasing hormone (<strong>CRH</strong>) release in the central nucleus of the amygdala underlies the anxiogenic and stress like consequences of <b>withdrawal</b> that are common in phenomenology to all drugs of abuse.
+CRH	addiction	withdrawal	12782395	There is evidence that suggests that increased <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) release in the central nucleus of the amygdala underlies the anxiogenic and stress like consequences of <b>withdrawal</b> that are common in phenomenology to all drugs of abuse.
+CRH	drug	cocaine	12782395	The present studies were undertaken to determine levels of <strong>CRH</strong> mRNA in the amygdala, and also in the hypothalamus, frontal cortex and brainstem after short term (2 days) and intermediate term (10 days) <b>cocaine</b> withdrawal (with continued saline injections) from chronic (14 days) 'binge' pattern <b>cocaine</b> administration (3 x 15 mg/kg per day at hourly intervals).
+CRH	addiction	intoxication	12782395	The present studies were undertaken to determine levels of <strong>CRH</strong> mRNA in the amygdala, and also in the hypothalamus, frontal cortex and brainstem after short term (2 days) and intermediate term (10 days) cocaine withdrawal (with continued saline injections) from chronic (14 days) '<b>binge</b>' pattern cocaine administration (3 x 15 mg/kg per day at hourly intervals).
+CRH	addiction	withdrawal	12782395	The present studies were undertaken to determine levels of <strong>CRH</strong> mRNA in the amygdala, and also in the hypothalamus, frontal cortex and brainstem after short term (2 days) and intermediate term (10 days) cocaine <b>withdrawal</b> (with continued saline injections) from chronic (14 days) 'binge' pattern cocaine administration (3 x 15 mg/kg per day at hourly intervals).
+CRH	drug	cocaine	12782395	There was also a significant elevation of <strong>CRH</strong> mRNA levels in the amygdala, but not in the hypothalamus, frontal cortex or brainstem after 2 day <b>cocaine</b> withdrawal.
+CRH	addiction	withdrawal	12782395	There was also a significant elevation of <strong>CRH</strong> mRNA levels in the amygdala, but not in the hypothalamus, frontal cortex or brainstem after 2 day cocaine <b>withdrawal</b>.
+CRH	drug	cocaine	12782395	A negative correlation between amygdalar <strong>CRH</strong> mRNA and plasma corticosterone levels was found in the 2 day <b>cocaine</b> withdrawn rats but not in control rats, suggesting that <strong>CRH</strong> neurons in the amygdala may be differentially responsive to glucocorticoids after chronic <b>cocaine</b> exposure and withdrawal.
+CRH	addiction	withdrawal	12782395	A negative correlation between amygdalar <strong>CRH</strong> mRNA and plasma corticosterone levels was found in the 2 day cocaine withdrawn rats but not in control rats, suggesting that <strong>CRH</strong> neurons in the amygdala may be differentially responsive to glucocorticoids after chronic cocaine exposure and <b>withdrawal</b>.
+CRH	drug	cocaine	12782395	There were no changes in either plasma corticosterone or amygdalar <strong>CRH</strong> mRNA levels after 10 day <b>cocaine</b> withdrawal.
+CRH	addiction	withdrawal	12782395	There were no changes in either plasma corticosterone or amygdalar <strong>CRH</strong> mRNA levels after 10 day cocaine <b>withdrawal</b>.
+CRH	drug	cocaine	12782395	Our findings of an increase in amygdalar <strong>CRH</strong> gene expression during early <b>cocaine</b> withdrawal support a potentially important role for amygdalar <strong>CRH</strong> activity in the anxiogenic and aversive consequences of withdrawal from <b>cocaine</b> during a time when humans are most subject to relapse.
+CRH	addiction	aversion	12782395	Our findings of an increase in amygdalar <strong>CRH</strong> gene expression during early cocaine withdrawal support a potentially important role for amygdalar <strong>CRH</strong> activity in the anxiogenic and <b>aversive</b> consequences of withdrawal from cocaine during a time when humans are most subject to relapse.
+CRH	addiction	relapse	12782395	Our findings of an increase in amygdalar <strong>CRH</strong> gene expression during early cocaine withdrawal support a potentially important role for amygdalar <strong>CRH</strong> activity in the anxiogenic and aversive consequences of withdrawal from cocaine during a time when humans are most subject to <b>relapse</b>.
+CRH	addiction	withdrawal	12782395	Our findings of an increase in amygdalar <strong>CRH</strong> gene expression during early cocaine <b>withdrawal</b> support a potentially important role for amygdalar <strong>CRH</strong> activity in the anxiogenic and aversive consequences of <b>withdrawal</b> from cocaine during a time when humans are most subject to relapse.
+CRH	drug	cocaine	12686370	CSF <strong>CRH</strong> in abstinent <b>cocaine</b> dependent patients.
+CRH	drug	cocaine	12686370	Cerebrospinal fluid (CSF) concentrations of corticotropin releasing factor (<strong>CRH</strong>) were determined in 29 abstinent <b>cocaine</b> dependent patients and 66 normal controls.
+CRH	drug	cocaine	12686370	The results showed that there was no significant difference between the abstinent <b>cocaine</b> dependent patients and normal controls for CSF <strong>CRH</strong>.
+CRH	drug	cocaine	12686370	Also, CSF <strong>CRH</strong> concentrations were not related to <b>cocaine</b> craving scores in a cue elicited <b>cocaine</b> craving procedure.
+CRH	addiction	relapse	12686370	Also, CSF <strong>CRH</strong> concentrations were not related to cocaine <b>craving</b> scores in a cue elicited cocaine <b>craving</b> procedure.
+CRH	drug	cocaine	12686370	Thus, these data suggest that after protracted abstinence from <b>cocaine</b> there is no marked dysregulation of <strong>CRH</strong> systems as measured by CSF <strong>CRH</strong> concentrations.
+CRH	drug	cocaine	12652344	In addition, the effect of corticotropin releasing hormone type 1 receptor (<strong>CRH</strong> R1) blockade on <b>cocaine</b> priming induced reinstatement was investigated.
+CRH	addiction	relapse	12652344	In addition, the effect of corticotropin releasing hormone type 1 receptor (<strong>CRH</strong> R1) blockade on cocaine priming induced <b>reinstatement</b> was investigated.
+CRH	drug	cocaine	12652344	In addition, the effect of <strong>corticotropin releasing hormone</strong> type 1 receptor (<strong>CRH</strong> R1) blockade on <b>cocaine</b> priming induced reinstatement was investigated.
+CRH	addiction	relapse	12652344	In addition, the effect of <strong>corticotropin releasing hormone</strong> type 1 receptor (<strong>CRH</strong> R1) blockade on cocaine priming induced <b>reinstatement</b> was investigated.
+CRH	drug	cocaine	12652344	Priming with <strong>corticotropin releasing hormone</strong> (10 and 50 microg/kg), adrenocorticotropic hormone (1 microg/kg), or cortisol (1 10 mg/kg) did not induce significant reinstatement of <b>cocaine</b> seeking.
+CRH	addiction	relapse	12652344	Priming with <strong>corticotropin releasing hormone</strong> (10 and 50 microg/kg), adrenocorticotropic hormone (1 microg/kg), or cortisol (1 10 mg/kg) did not induce significant <b>reinstatement</b> of cocaine <b>seeking</b>.
+CRH	drug	cocaine	12652344	The <strong>CRH</strong> R1 antagonist CP 154,526 (10 mg/kg, IV) did not modulate <b>cocaine</b> priming induced reinstatement of drug seeking, but attenuated <strong>CRH</strong> induced increases in salivary cortisol.
+CRH	addiction	relapse	12652344	The <strong>CRH</strong> R1 antagonist CP 154,526 (10 mg/kg, IV) did not modulate cocaine priming induced <b>reinstatement</b> of drug <b>seeking</b>, but attenuated <strong>CRH</strong> induced increases in salivary cortisol.
+CRH	drug	cocaine	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of proopiomelanocortin and <strong>corticotropin releasing hormone</strong> receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic 'binge' <b>cocaine</b> and withdrawal.
+CRH	addiction	intoxication	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of proopiomelanocortin and <strong>corticotropin releasing hormone</strong> receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic '<b>binge</b>' cocaine and withdrawal.
+CRH	addiction	withdrawal	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of proopiomelanocortin and <strong>corticotropin releasing hormone</strong> receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic 'binge' cocaine and <b>withdrawal</b>.
+CRH	drug	cocaine	12576179	This blunting of HPA axis activity in response to <b>cocaine</b> is associated with a <b>cocaine</b> induced reduction of corticotropin releasing hormone (<strong>CRH</strong>) mRNA level in the hypothalamus.
+CRH	drug	cocaine	12576179	This blunting of HPA axis activity in response to <b>cocaine</b> is associated with a <b>cocaine</b> induced reduction of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) mRNA level in the hypothalamus.
+CRH	drug	cocaine	12576179	In the anterior pituitary, levels of both proopiomelanocortin (POMC) and <strong>CRH</strong> receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic 'binge' <b>cocaine</b> and were at control levels on the 4th day of withdrawal.
+CRH	addiction	intoxication	12576179	In the anterior pituitary, levels of both proopiomelanocortin (POMC) and <strong>CRH</strong> receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic '<b>binge</b>' cocaine and were at control levels on the 4th day of withdrawal.
+CRH	addiction	withdrawal	12576179	In the anterior pituitary, levels of both proopiomelanocortin (POMC) and <strong>CRH</strong> receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic 'binge' cocaine and were at control levels on the 4th day of <b>withdrawal</b>.
+CRH	addiction	withdrawal	12576179	<strong>CRH</strong> mRNA levels in the hypothalamus were not different from saline controls on the 1st and 4th days of <b>withdrawal</b>.
+CRH	drug	cocaine	12576179	In addition to being associated with <strong>CRH</strong> input from the hypothalamus, the activation of the HPA axis by <b>cocaine</b> withdrawal may be, at least in part, due to the increased POMC and/or <strong>CRH</strong> R1 gene expression observed in the anterior pituitary after chronic 'binge' <b>cocaine</b>.
+CRH	addiction	intoxication	12576179	In addition to being associated with <strong>CRH</strong> input from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part, due to the increased POMC and/or <strong>CRH</strong> R1 gene expression observed in the anterior pituitary after chronic '<b>binge</b>' cocaine.
+CRH	addiction	withdrawal	12576179	In addition to being associated with <strong>CRH</strong> input from the hypothalamus, the activation of the HPA axis by cocaine <b>withdrawal</b> may be, at least in part, due to the increased POMC and/or <strong>CRH</strong> R1 gene expression observed in the anterior pituitary after chronic 'binge' cocaine.
+CRH	drug	amphetamine	12542666	Single administration of either IL 1 or <b>amphetamine</b> causes three weeks later a selective decrease in relative DBH innervation density in those subnuclei of the PVN that contain high numbers of corticotrophin releasing hormone (<strong>CRH</strong>) producing neurons: the dorsal parvocellular and medial parvocellular PVN.
+CRH	drug	amphetamine	12542666	We conclude that (1) long lasting sensitization induced by single exposure to IL 1 and <b>amphetamine</b> induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative DBH innervation density in <strong>CRH</strong> rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.
+CRH	addiction	sensitization	12542666	We conclude that (1) long lasting <b>sensitization</b> induced by single exposure to IL 1 and amphetamine induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative DBH innervation density in <strong>CRH</strong> rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.
+CRH	drug	opioid	12431775	Effect of <b>naloxone</b> precipitated <b>morphine</b> withdrawal on <strong>CRH</strong> and vasopressin mRNA expression in the rat hypothalamic paraventricular nucleus.
+CRH	addiction	withdrawal	12431775	Effect of naloxone precipitated morphine <b>withdrawal</b> on <strong>CRH</strong> and vasopressin mRNA expression in the rat hypothalamic paraventricular nucleus.
+CRH	drug	opioid	12431775	Here, by means of in situ hybridization, the changes in <strong>CRH</strong> and vasopressin (AVP) mRNAs have been analysed within the rat hypothalamic paraventricular nucleus (PVN) during <b>morphine</b> dependence and after <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+CRH	addiction	dependence	12431775	Here, by means of in situ hybridization, the changes in <strong>CRH</strong> and vasopressin (AVP) mRNAs have been analysed within the rat hypothalamic paraventricular nucleus (PVN) during morphine <b>dependence</b> and after naloxone precipitated morphine withdrawal.
+CRH	addiction	withdrawal	12431775	Here, by means of in situ hybridization, the changes in <strong>CRH</strong> and vasopressin (AVP) mRNAs have been analysed within the rat hypothalamic paraventricular nucleus (PVN) during morphine dependence and after naloxone precipitated morphine <b>withdrawal</b>.
+CRH	drug	opioid	12431775	<strong>CRH</strong> and AVP mRNA expression were analysed 30 min following administration of saline or <b>naloxone</b> to control groups and to <b>morphine</b> dependent rats.
+CRH	drug	opioid	12431775	The data for in situ hybridization analysis of PVN neurons show that there were no changes in the total size of labelled area for <strong>CRH</strong> or AVP mRNA during <b>morphine</b> withdrawal, indicating that dependence on <b>morphine</b> does not involve alterations in the number of neurons expressing <strong>CRH</strong> or AVP mRNA.
+CRH	addiction	dependence	12431775	The data for in situ hybridization analysis of PVN neurons show that there were no changes in the total size of labelled area for <strong>CRH</strong> or AVP mRNA during morphine withdrawal, indicating that <b>dependence</b> on morphine does not involve alterations in the number of neurons expressing <strong>CRH</strong> or AVP mRNA.
+CRH	addiction	withdrawal	12431775	The data for in situ hybridization analysis of PVN neurons show that there were no changes in the total size of labelled area for <strong>CRH</strong> or AVP mRNA during morphine <b>withdrawal</b>, indicating that dependence on morphine does not involve alterations in the number of neurons expressing <strong>CRH</strong> or AVP mRNA.
+CRH	drug	opioid	12431775	However, levels of mRNA encoding for <strong>CRH</strong> were decreased in the PVN during <b>morphine</b> dependence and withdrawal.
+CRH	addiction	dependence	12431775	However, levels of mRNA encoding for <strong>CRH</strong> were decreased in the PVN during morphine <b>dependence</b> and withdrawal.
+CRH	addiction	withdrawal	12431775	However, levels of mRNA encoding for <strong>CRH</strong> were decreased in the PVN during morphine dependence and <b>withdrawal</b>.
+CRH	drug	alcohol	12393236	Prolonged <b>alcohol</b> intake leads to reversible depression of <strong>corticotropin releasing hormone</strong> and vasopressin immunoreactivity and mRNA levels in the parvocellular neurons of the paraventricular nucleus.
+CRH	drug	alcohol	12393236	Using conventional histological techniques, immunohistochemistry and in situ hybridization, we have examined the medial parvocellular division of the paraventricular nucleus (PVNmp), and the synthesis and expression of corticotropin releasing hormone (<strong>CRH</strong>) and vasopressin (VP) by its constituent neurons, in rats submitted to 6 months of <b>ethanol</b> treatment and to withdrawal (2 months after 6 months of <b>alcohol</b> intake).
+CRH	addiction	withdrawal	12393236	Using conventional histological techniques, immunohistochemistry and in situ hybridization, we have examined the medial parvocellular division of the paraventricular nucleus (PVNmp), and the synthesis and expression of corticotropin releasing hormone (<strong>CRH</strong>) and vasopressin (VP) by its constituent neurons, in rats submitted to 6 months of ethanol treatment and to <b>withdrawal</b> (2 months after 6 months of alcohol intake).
+CRH	drug	alcohol	12393236	Using conventional histological techniques, immunohistochemistry and in situ hybridization, we have examined the medial parvocellular division of the paraventricular nucleus (PVNmp), and the synthesis and expression of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and vasopressin (VP) by its constituent neurons, in rats submitted to 6 months of <b>ethanol</b> treatment and to withdrawal (2 months after 6 months of <b>alcohol</b> intake).
+CRH	addiction	withdrawal	12393236	Using conventional histological techniques, immunohistochemistry and in situ hybridization, we have examined the medial parvocellular division of the paraventricular nucleus (PVNmp), and the synthesis and expression of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and vasopressin (VP) by its constituent neurons, in rats submitted to 6 months of ethanol treatment and to <b>withdrawal</b> (2 months after 6 months of alcohol intake).
+CRH	drug	alcohol	12393236	However, the total number of <strong>CRH</strong>  and VP immunoreactive neurons and the <strong>CRH</strong> mRNA levels were significantly decreased by <b>ethanol</b> treatment.
+CRH	drug	alcohol	12393236	In withdrawn rats, the number of <strong>CRH</strong>  and VP immunostained neurons and the gene expression of <strong>CRH</strong> were increased relative to <b>ethanol</b> treated rats and did not differ from those of controls.
+CRH	drug	alcohol	12393236	These results show that prolonged <b>alcohol</b> intake blunts the expression of <strong>CRH</strong> and VP in the parvocellular neurons of the PVN, and that this effect is, partially at least, reversible by withdrawal.
+CRH	addiction	withdrawal	12393236	These results show that prolonged alcohol intake blunts the expression of <strong>CRH</strong> and VP in the parvocellular neurons of the PVN, and that this effect is, partially at least, reversible by <b>withdrawal</b>.
+CRH	drug	cocaine	12204195	Current therapeutic strategies focus on counteracting the <b>cocaine</b> effects directly on the dopamine transporter, through post synaptic D(1), D(2) or D(3) receptors or through the glutamatergic, serotoninergic, opioid or <strong>corticotropin releasing hormone</strong> systems.
+CRH	drug	opioid	12204195	Current therapeutic strategies focus on counteracting the cocaine effects directly on the dopamine transporter, through post synaptic D(1), D(2) or D(3) receptors or through the glutamatergic, serotoninergic, <b>opioid</b> or <strong>corticotropin releasing hormone</strong> systems.
+CRH	drug	cocaine	12125043	Effects of acute "binge" <b>cocaine</b> on preprodynorphin, preproenkephalin, proopiomelanocortin, and <strong>corticotropin releasing hormone</strong> receptor mRNA levels in the striatum and hypothalamic pituitary adrenal axis of mu opioid receptor knockout mice.
+CRH	drug	opioid	12125043	Effects of acute "binge" cocaine on preprodynorphin, preproenkephalin, proopiomelanocortin, and <strong>corticotropin releasing hormone</strong> receptor mRNA levels in the striatum and hypothalamic pituitary adrenal axis of mu <b>opioid</b> receptor knockout mice.
+CRH	addiction	intoxication	12125043	Effects of acute "<b>binge</b>" cocaine on preprodynorphin, preproenkephalin, proopiomelanocortin, and <strong>corticotropin releasing hormone</strong> receptor mRNA levels in the striatum and hypothalamic pituitary adrenal axis of mu opioid receptor knockout mice.
+CRH	drug	cocaine	12125043	Hypothalamic <strong>CRH</strong>(1) receptor and POMC mRNAs were expressed at similar levels in untreated and in <b>cocaine</b> treated mice of each genotype.
+CRH	drug	cocaine	12125043	However, there were lower basal levels of <strong>CRH</strong>(1) receptor mRNA in the anterior pituitary of the MOR  /  mice than in wild type mice and the MOR  /  mice failed to show the <b>cocaine</b> induced decreases in <strong>CRH</strong>(1) receptor mRNA found in the wild type mice.
+CRH	drug	amphetamine	12079865	The anorexigenic neuropeptides that are upregulated by leptin are alpha MSH (alpha melanocyte stimulating hormone), which acts on MC4R (melanocortin 4 receptor); CART (cocaine and <b>amphetamine</b> regulated transcript); and <strong>CRH</strong> (corticotropin releasing hormone).
+CRH	drug	cocaine	12079865	The anorexigenic neuropeptides that are upregulated by leptin are alpha MSH (alpha melanocyte stimulating hormone), which acts on MC4R (melanocortin 4 receptor); CART (<b>cocaine</b> and amphetamine regulated transcript); and <strong>CRH</strong> (corticotropin releasing hormone).
+CRH	drug	amphetamine	12079865	The anorexigenic neuropeptides that are upregulated by leptin are alpha MSH (alpha melanocyte stimulating hormone), which acts on MC4R (melanocortin 4 receptor); CART (cocaine and <b>amphetamine</b> regulated transcript); and <strong>CRH</strong> (<strong>corticotropin releasing hormone</strong>).
+CRH	drug	cocaine	12079865	The anorexigenic neuropeptides that are upregulated by leptin are alpha MSH (alpha melanocyte stimulating hormone), which acts on MC4R (melanocortin 4 receptor); CART (<b>cocaine</b> and amphetamine regulated transcript); and <strong>CRH</strong> (<strong>corticotropin releasing hormone</strong>).
+CRH	addiction	withdrawal	12074902	Role of <strong>corticotropin releasing hormone</strong> in the amygdala and bed nucleus of the stria terminalis in the behavioral, pain modulatory, and endocrine consequences of opiate <b>withdrawal</b>.
+CRH	addiction	withdrawal	12074902	We used in situ hybridization histochemistry and site specific microinjections of a <strong>CRH</strong> receptor antagonist to study the role of <strong>CRH</strong> in opiate <b>withdrawal</b>.
+CRH	drug	opioid	12074902	In situ hybridization of <strong>CRH</strong> mRNA revealed significant increases in the central nucleus of the amygdala but not in the bed nucleus of the stria terminalis among rats either chronically pre treated with <b>morphine</b>, given an injection of <b>naloxone</b>, or both (precipitated withdrawal).
+CRH	addiction	withdrawal	12074902	In situ hybridization of <strong>CRH</strong> mRNA revealed significant increases in the central nucleus of the amygdala but not in the bed nucleus of the stria terminalis among rats either chronically pre treated with morphine, given an injection of naloxone, or both (precipitated <b>withdrawal</b>).
+CRH	addiction	withdrawal	12074902	An increase of <strong>CRH</strong> mRNA in the paraventricular nucleus of the hypothalamus was specific to rats undergoing <b>withdrawal</b>.
+CRH	addiction	withdrawal	12074902	Intracerebroventricular microinjection of the <strong>CRH</strong> receptor antagonist, alpha(h)<strong>CRH</strong>(9 41), reduced the severity of opiate <b>withdrawal</b>.
+CRH	addiction	withdrawal	12074902	Microinjections of alpha(h)<strong>CRH</strong>(9 41) into the central nucleus of the amygdala also reduced the severity of <b>withdrawal</b> whereas bed nucleus of the stria terminalis microinjections of alpha(h)<strong>CRH</strong>(9 41) were without effect.
+CRH	addiction	dependence	12074902	These experiments provide evidence for a role of amygdala, but not bed nucleus of the stria terminalis, <strong>CRH</strong> in opiate <b>dependence</b>.
+CRH	drug	cocaine	12023504	Corticotropin releasing hormone (<strong>CRH</strong>) seems to play a more prominent role in the maintenance of <b>cocaine</b> self administration and may even be involved in the incentive motivation for the drug.
+CRH	addiction	reward	12023504	Corticotropin releasing hormone (<strong>CRH</strong>) seems to play a more prominent role in the maintenance of cocaine self administration and may even be involved in the <b>incentive</b> motivation for the drug.
+CRH	drug	cocaine	12023504	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>) seems to play a more prominent role in the maintenance of <b>cocaine</b> self administration and may even be involved in the incentive motivation for the drug.
+CRH	addiction	reward	12023504	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>) seems to play a more prominent role in the maintenance of cocaine self administration and may even be involved in the <b>incentive</b> motivation for the drug.
+CRH	drug	cocaine	12023504	Corticosterone and <strong>CRH</strong> are also critical for the stress  and cue induced reinstatement of extinguished <b>cocaine</b> seeking behavior.
+CRH	addiction	relapse	12023504	Corticosterone and <strong>CRH</strong> are also critical for the stress  and cue induced <b>reinstatement</b> of extinguished cocaine <b>seeking</b> behavior.
+CRH	drug	cocaine	11750768	On the other hand, the self administration of doses falling on both the ascending and descending limbs of the <b>cocaine</b> dose response curve can each be attenuated by drugs that block central corticotropin releasing hormone (<strong>CRH</strong>) receptors.
+CRH	drug	cocaine	11750768	On the other hand, the self administration of doses falling on both the ascending and descending limbs of the <b>cocaine</b> dose response curve can each be attenuated by drugs that block central <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) receptors.
+CRH	drug	cocaine	11750768	Finally, corticosterone and <strong>CRH</strong> are also critical for the stress  and cue induced reinstatement of extinguished <b>cocaine</b> seeking behavior, demonstrating an involvement of the HPA axis in the relapse to <b>cocaine</b> use as well.
+CRH	addiction	relapse	11750768	Finally, corticosterone and <strong>CRH</strong> are also critical for the stress  and cue induced <b>reinstatement</b> of extinguished cocaine <b>seeking</b> behavior, demonstrating an involvement of the HPA axis in the <b>relapse</b> to cocaine use as well.
+CRH	drug	cocaine	11734187	Although the role of corticotropin releasing hormone (<strong>CRH</strong>) in stress  and <b>cocaine</b> induced relapse has been reported, its involvement in cue induced behavior has not been established.
+CRH	addiction	relapse	11734187	Although the role of corticotropin releasing hormone (<strong>CRH</strong>) in stress  and cocaine induced <b>relapse</b> has been reported, its involvement in cue induced behavior has not been established.
+CRH	drug	cocaine	11734187	Although the role of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) in stress  and <b>cocaine</b> induced relapse has been reported, its involvement in cue induced behavior has not been established.
+CRH	addiction	relapse	11734187	Although the role of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) in stress  and cocaine induced <b>relapse</b> has been reported, its involvement in cue induced behavior has not been established.
+CRH	addiction	relapse	11734187	Using responding during extinction as a model of cue induced <b>craving</b>, we tested the effects of a selective <strong>CRH1</strong> receptor antagonist, CP 154,526 (butyl ethyl [2,5 dimethyl 7 (2,4,6 trimethyl phenyl) 7H pyrrolo[2,3 d]pyrimidin 4 yl] amine).
+CRH	drug	cocaine	11734187	decreased responding on the <b>cocaine</b> associated lever during extinction, suggesting an involvement of <strong>CRH1</strong> receptors in cue induced craving.
+CRH	addiction	relapse	11734187	decreased responding on the cocaine associated lever during extinction, suggesting an involvement of <strong>CRH1</strong> receptors in cue induced <b>craving</b>.
+CRH	drug	benzodiazepine	11702086	Effect of a <b>benzodiazepine</b> receptor agonist and <strong>corticotropin releasing hormone</strong> receptor antagonists on long term foot shock induced increase in defensive withdrawal behavior.
+CRH	addiction	withdrawal	11702086	Effect of a benzodiazepine receptor agonist and <strong>corticotropin releasing hormone</strong> receptor antagonists on long term foot shock induced increase in defensive <b>withdrawal</b> behavior.
+CRH	drug	opioid	11679056	Differential responsivity of the hypothalamic pituitary adrenal axis to glucocorticoid negative feedback and <strong>corticotropin releasing hormone</strong> in rats undergoing <b>morphine</b> withdrawal: possible mechanisms involved in facilitated and attenuated stress responses.
+CRH	addiction	withdrawal	11679056	Differential responsivity of the hypothalamic pituitary adrenal axis to glucocorticoid negative feedback and <strong>corticotropin releasing hormone</strong> in rats undergoing morphine <b>withdrawal</b>: possible mechanisms involved in facilitated and attenuated stress responses.
+CRH	addiction	withdrawal	11679056	These data suggest that the reduced ACTH responses to stress in 8 day <b>withdrawal</b> rats involved increased sensitivity of negative feedback systems to glucocorticoids as well as reduced <strong>CRH</strong> and/or AVP function in response to stress.
+CRH	drug	cocaine	11597771	Hypothalamic <strong>CRH</strong> mRNA levels are differentially modulated by repeated 'binge' <b>cocaine</b> with or without D(1) dopamine receptor blockade.
+CRH	addiction	intoxication	11597771	Hypothalamic <strong>CRH</strong> mRNA levels are differentially modulated by repeated '<b>binge</b>' cocaine with or without D(1) dopamine receptor blockade.
+CRH	drug	cocaine	11597771	We previously found that there was a rapid stimulatory effect of acute (1 day) 'binge' <b>cocaine</b> on <strong>CRH</strong> mRNA levels in the rat hypothalamus.
+CRH	addiction	intoxication	11597771	We previously found that there was a rapid stimulatory effect of acute (1 day) '<b>binge</b>' cocaine on <strong>CRH</strong> mRNA levels in the rat hypothalamus.
+CRH	drug	cocaine	11597771	In contrast, after 3 days of 'binge' <b>cocaine</b>, there was a modest decrease (12%) in hypothalamic <strong>CRH</strong> mRNA levels, which after 14 days of 'binge' <b>cocaine</b> was greater (32%) and significantly lower than control values.
+CRH	addiction	intoxication	11597771	In contrast, after 3 days of '<b>binge</b>' cocaine, there was a modest decrease (12%) in hypothalamic <strong>CRH</strong> mRNA levels, which after 14 days of '<b>binge</b>' cocaine was greater (32%) and significantly lower than control values.
+CRH	drug	cocaine	11597771	Also, our previous studies found an elevation of <strong>CRH</strong> mRNA in the frontal cortex after 3 days of 'binge' <b>cocaine</b>.
+CRH	addiction	intoxication	11597771	Also, our previous studies found an elevation of <strong>CRH</strong> mRNA in the frontal cortex after 3 days of '<b>binge</b>' cocaine.
+CRH	drug	cocaine	11597771	Small decreases (10 13%) in hypothalamic <strong>CRH</strong> mRNA levels were found again to be induced by 3 days of repeated 'binge' <b>cocaine</b>.
+CRH	addiction	intoxication	11597771	Small decreases (10 13%) in hypothalamic <strong>CRH</strong> mRNA levels were found again to be induced by 3 days of repeated '<b>binge</b>' cocaine.
+CRH	drug	cocaine	11597771	These findings suggest that the inhibitory effect of repeated 'binge' <b>cocaine</b> on the hypothalamic <strong>CRH</strong> mRNA expression is absent when there is D(1), but not D(2), dopamine receptor blockade.
+CRH	addiction	intoxication	11597771	These findings suggest that the inhibitory effect of repeated '<b>binge</b>' cocaine on the hypothalamic <strong>CRH</strong> mRNA expression is absent when there is D(1), but not D(2), dopamine receptor blockade.
+CRH	drug	cocaine	11597771	In the frontal cortex, pretreatment with either SCH23390 or sulpiride did not alter the increases in the <strong>CRH</strong> mRNA levels induced by repeated 'binge' <b>cocaine</b>.
+CRH	addiction	intoxication	11597771	In the frontal cortex, pretreatment with either SCH23390 or sulpiride did not alter the increases in the <strong>CRH</strong> mRNA levels induced by repeated '<b>binge</b>' cocaine.
+CRH	drug	cocaine	11597771	The results suggest that the <b>cocaine</b> induced modulation of hypothalamic <strong>CRH</strong> mRNA expression is secondary to changes in the activity of specific components of dopaminergic systems.
+CRH	addiction	sensitization	11403685	In search of the underlying mechanisms, we studied the temporal pattern of HPA <b>sensitization</b> in relation to (1) the reactivity of noradrenergic projections to the PVN and (2) altered secretagogue production in hypothalamic <strong>CRH</strong> neurons.
+CRH	drug	amphetamine	11403685	<b>Amphetamine</b> induced HPA sensitization was not accompanied by increased costorage of arginine vasopressin (AVP) in <strong>CRH</strong> terminals, as found previously after IL 1 pretreatment.
+CRH	addiction	sensitization	11403685	Amphetamine induced HPA <b>sensitization</b> was not accompanied by increased costorage of arginine vasopressin (AVP) in <strong>CRH</strong> terminals, as found previously after IL 1 pretreatment.
+CRH	drug	amphetamine	11403685	In addition, increased AVP signalling by hypothalamic <strong>CRH</strong> neurons appears to play a role in IL 1 induced, but not in <b>amphetamine</b> induced, HPA sensitization.
+CRH	addiction	sensitization	11403685	In addition, increased AVP signalling by hypothalamic <strong>CRH</strong> neurons appears to play a role in IL 1 induced, but not in amphetamine induced, HPA <b>sensitization</b>.
+CRH	drug	alcohol	11371718	The combined dexamethasone suppression/<strong>CRH</strong> stimulation test in <b>alcoholics</b> during and after acute withdrawal.
+CRH	addiction	withdrawal	11371718	The combined dexamethasone suppression/<strong>CRH</strong> stimulation test in alcoholics during and after acute <b>withdrawal</b>.
+CRH	drug	alcohol	11371718	Patients with <b>alcoholism</b> frequently show nonsuppression in the dexamethasone (Dex) suppression test and also a blunted increase of adrenocorticotropin (ACTH) after injection of <strong>corticotropin releasing hormone</strong> (hCRH).
+CRH	drug	alcohol	11371718	We studied the effect of the combined Dex/<strong>CRH</strong> test in 19 <b>alcoholic</b> inpatients (9 male, 10 female) during and after withdrawal along with 19 healthy controls.
+CRH	addiction	withdrawal	11371718	We studied the effect of the combined Dex/<strong>CRH</strong> test in 19 alcoholic inpatients (9 male, 10 female) during and after <b>withdrawal</b> along with 19 healthy controls.
+CRH	drug	cocaine	11173167	Basal and ovine <strong>corticotropin releasing hormone</strong> (oCRH) stimulated ACTH and cortisol levels were also examined in a subset of 8 healthy and 9 <b>cocaine</b> dependent subjects after 21 days of abstinence.
+CRH	drug	amphetamine	11160452	In both "home" and "novel" <b>amphetamine</b> groups, c fos mRNA in the BSTov and CEA was predominantly expressed in enkephalin containing cells; coexpression with <strong>corticotropin releasing hormone</strong> was rare.
+CRH	drug	cocaine	11027923	Effects of the <strong>CRH</strong> receptor antagonist CP 154,526 on intravenous <b>cocaine</b> self administration in rats.
+CRH	drug	cocaine	11027923	The role for corticotropin releasing hormone (<strong>CRH</strong>) receptors in the maintenance of intravenous <b>cocaine</b> self administration in rats was investigated using the centrally active, small molecule CRH1 receptor antagonist CP 154,526.
+CRH	drug	cocaine	11027923	The role for <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) receptors in the maintenance of intravenous <b>cocaine</b> self administration in rats was investigated using the centrally active, small molecule CRH1 receptor antagonist CP 154,526.
+CRH	drug	cocaine	11027923	The role for <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) receptors in the maintenance of intravenous <b>cocaine</b> self administration in rats was investigated using the centrally active, small molecule <strong>CRH1</strong> receptor antagonist CP 154,526.
+CRH	drug	cocaine	11027923	Furthermore, responding on the <b>cocaine</b> lever following CP 154,526 pretreatment was significantly suppressed, even during the first 15 min of the session, a time when rats typically sample the <b>cocaine</b> lever during extinction, suggesting that <strong>CRH</strong> receptors may also be involved in some of the conditioned effects of <b>cocaine</b> as well.
+CRH	drug	cocaine	11027923	These data are discussed in terms of the role for <strong>CRH</strong> in the neurobehavioral effects of <b>cocaine</b>.
+CRH	drug	opioid	10082881	Finally, a possible relationship between food restriction induced suppression of the kappa <b>opioid</b> mechanism in CeA/BSTLD, local <strong>CRH</strong> function, and sensitization of the neural substrate for incentive motivating effects of abused drugs is discussed.
+CRH	addiction	reward	10082881	Finally, a possible relationship between food restriction induced suppression of the kappa opioid mechanism in CeA/BSTLD, local <strong>CRH</strong> function, and sensitization of the neural substrate for <b>incentive</b> motivating effects of abused drugs is discussed.
+CRH	addiction	sensitization	10082881	Finally, a possible relationship between food restriction induced suppression of the kappa opioid mechanism in CeA/BSTLD, local <strong>CRH</strong> function, and <b>sensitization</b> of the neural substrate for incentive motivating effects of abused drugs is discussed.
+CRH	drug	alcohol	9620773	Corticotropin releasing hormone (<strong>CRH</strong>) is a potent mediator of endocrine, autonomic, behavioural and immune responses to stress, and has been implicated in the stress like and other aversive consequences of drug abuse, such as withdrawal from <b>alcohol</b>.
+CRH	addiction	aversion	9620773	Corticotropin releasing hormone (<strong>CRH</strong>) is a potent mediator of endocrine, autonomic, behavioural and immune responses to stress, and has been implicated in the stress like and other <b>aversive</b> consequences of drug abuse, such as withdrawal from alcohol.
+CRH	addiction	withdrawal	9620773	Corticotropin releasing hormone (<strong>CRH</strong>) is a potent mediator of endocrine, autonomic, behavioural and immune responses to stress, and has been implicated in the stress like and other aversive consequences of drug abuse, such as <b>withdrawal</b> from alcohol.
+CRH	drug	alcohol	9620773	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>) is a potent mediator of endocrine, autonomic, behavioural and immune responses to stress, and has been implicated in the stress like and other aversive consequences of drug abuse, such as withdrawal from <b>alcohol</b>.
+CRH	addiction	aversion	9620773	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>) is a potent mediator of endocrine, autonomic, behavioural and immune responses to stress, and has been implicated in the stress like and other <b>aversive</b> consequences of drug abuse, such as withdrawal from alcohol.
+CRH	addiction	withdrawal	9620773	<strong>Corticotropin releasing hormone</strong> (<strong>CRH</strong>) is a potent mediator of endocrine, autonomic, behavioural and immune responses to stress, and has been implicated in the stress like and other aversive consequences of drug abuse, such as <b>withdrawal</b> from alcohol.
+CRH	drug	opioid	9097397	Prior in vivo <b>morphine</b> treatment also enhanced the stimulatory in vitro effect of corticotropin releasing hormone (<strong>CRH</strong>) on adenylyl cyclase in cultured GABA neurons.
+CRH	drug	opioid	9097397	Prior in vivo <b>morphine</b> treatment also enhanced the stimulatory in vitro effect of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) on adenylyl cyclase in cultured GABA neurons.
+CRH	drug	alcohol	8873112	Cerebrospinal fluid concentrations of corticotropin releasing hormone (<strong>CRH</strong>) and diazepam binding inhibitor (DBI) during <b>alcohol</b> withdrawal and abstinence.
+CRH	drug	benzodiazepine	8873112	Cerebrospinal fluid concentrations of corticotropin releasing hormone (<strong>CRH</strong>) and <b>diazepam</b> binding inhibitor (DBI) during alcohol withdrawal and abstinence.
+CRH	addiction	withdrawal	8873112	Cerebrospinal fluid concentrations of corticotropin releasing hormone (<strong>CRH</strong>) and diazepam binding inhibitor (DBI) during alcohol <b>withdrawal</b> and abstinence.
+CRH	drug	alcohol	8873112	Cerebrospinal fluid concentrations of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and diazepam binding inhibitor (DBI) during <b>alcohol</b> withdrawal and abstinence.
+CRH	drug	benzodiazepine	8873112	Cerebrospinal fluid concentrations of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and <b>diazepam</b> binding inhibitor (DBI) during alcohol withdrawal and abstinence.
+CRH	addiction	withdrawal	8873112	Cerebrospinal fluid concentrations of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) and diazepam binding inhibitor (DBI) during alcohol <b>withdrawal</b> and abstinence.
+CRH	drug	benzodiazepine	8873112	The neuropeptides <b>diazepam</b> binding inhibitor (DBI) and corticotropin releasing hormone (<strong>CRH</strong>) elicit anxietylike symptoms when administered intracerebroventricularly to laboratory animals.
+CRH	drug	benzodiazepine	8873112	The neuropeptides <b>diazepam</b> binding inhibitor (DBI) and <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) elicit anxietylike symptoms when administered intracerebroventricularly to laboratory animals.
+CRH	drug	alcohol	8873112	We therefore measured DBI and <strong>CRH</strong> concentrations in cerebrospinal fluid (CSF) of 15 <b>alcohol</b> dependent patients during acute withdrawal (Day 1) and again at 3 week's abstinence (Day 21).
+CRH	addiction	withdrawal	8873112	We therefore measured DBI and <strong>CRH</strong> concentrations in cerebrospinal fluid (CSF) of 15 alcohol dependent patients during acute <b>withdrawal</b> (Day 1) and again at 3 week's abstinence (Day 21).
+CRH	drug	alcohol	8873112	These tentative findings may implicate <strong>CRH</strong>, but not DBI, in the pathogenesis of <b>alcohol</b> withdrawal.
+CRH	addiction	withdrawal	8873112	These tentative findings may implicate <strong>CRH</strong>, but not DBI, in the pathogenesis of alcohol <b>withdrawal</b>.
+CRH	drug	opioid	8840357	The current study was designed to stimulate hypothalamic <strong>CRH</strong> release using the opiate antagonist <b>naloxone</b> in patients with depression and elevated urinary free cortisols as well as healthy and psychiatric controls.
+CRH	drug	opioid	8840357	We conclude that although <b>naloxone</b> is an effective central stimulant of the hypothalamic <strong>CRH</strong> neuron, stimulation of the hypothalamic <strong>CRH</strong> neuron with <b>naloxone</b> does not provide evidence of dysregulation of the HPA axis in depression.
+CRH	drug	nicotine	8593811	Systemically administered <b>nicotine</b> elicits ACTH release indirectly by acting on neurons in brainstem catecholaminergic regions known to send afferent projections to the paraventricular nucleus of the hypothalamus (PVN), the site of <strong>CRH</strong> neurons involved in initiating ACTH secretion.
+CRH	drug	nicotine	8593811	The results showed that the magnitude of cFos expression was dependent on the dose of <b>nicotine</b> in all regions studied (P < 0.0006); however, at the two lowest doses, only the NTS and <strong>CRH</strong> containing region of the PVN expressed cFos, whereas the LC and the rest of the PVN were activated only by higher doses.
+CRH	drug	alcohol	7586596	Abnormal baseline hypothalamic pituitary adrenal axis function and dexamethasone suppressibility seen in withdrawing <b>alcoholics</b> returns to normal on abstinence, but some studies report blunting of the ACTH response to <strong>CRH</strong> persisting during the early abstinence phase.
+CRH	drug	alcohol	7586596	To evaluate hypothalamic pituitary adrenal axis function in a group of recently abstinent <b>alcoholics</b> using basal hormone data, naloxone (an opioid receptor antagonist), and ovine <strong>CRH</strong>.
+CRH	drug	opioid	7586596	To evaluate hypothalamic pituitary adrenal axis function in a group of recently abstinent alcoholics using basal hormone data, <b>naloxone</b> (an <b>opioid</b> receptor antagonist), and ovine <strong>CRH</strong>.
+CRH	drug	opioid	7586596	Cortisol, ACTH, <strong>CRH</strong> and AVP levels were measured every 20 minutes for 2 hours between 0900 and 1100h Twenty mg <b>naloxone</b> i.v.
+CRH	drug	alcohol	7586596	While reduced levels of central endogenous opioid peptides may be a factor in the blunted ACTH response to naloxone in the <b>alcoholics</b>, it is proposed that the <b>alcoholics</b> have reduced pituitary responsiveness to <strong>CRH</strong>.
+CRH	drug	opioid	7586596	While reduced levels of central endogenous <b>opioid</b> peptides may be a factor in the blunted ACTH response to <b>naloxone</b> in the alcoholics, it is proposed that the alcoholics have reduced pituitary responsiveness to <strong>CRH</strong>.
+CRH	addiction	withdrawal	7695023	In early <b>withdrawal</b>, there was a significant positive correlation between CSF norepinephrine (NE) and corticotropin releasing hormone (<strong>CRH</strong>) concentrations (r = 0.95, p < 0.001).
+CRH	addiction	withdrawal	7695023	In early <b>withdrawal</b>, there was a significant positive correlation between CSF norepinephrine (NE) and <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) concentrations (r = 0.95, p < 0.001).
+CRH	drug	alcohol	7695023	These findings indicate significant perturbations of the noradrenergic neuronal system and a change in <strong>CRH</strong> NE interactions during acute <b>alcohol</b> withdrawal.
+CRH	addiction	withdrawal	7695023	These findings indicate significant perturbations of the noradrenergic neuronal system and a change in <strong>CRH</strong> NE interactions during acute alcohol <b>withdrawal</b>.
+CRH	addiction	withdrawal	7924629	The effects of <strong>Corticotropin Releasing Hormone</strong> infusion on cortisol secretion were significantly enhanced in the acute <b>withdrawal</b> phase in comparison with those occurring when patients were retested and with healthy controls.
+CRH	drug	alcohol	8393888	In study 2, <b>ethanol</b> or placebo was ingested over 15 min, and 1 microgram/kg ovine (o) <strong>CRH</strong> was administered (n = 9).
+CRH	drug	alcohol	8367033	Effects of single and repeated exposures to <b>ethanol</b> on hypothalamic beta endorphin and <strong>CRH</strong> release by the C57BL/6 and DBA/2 strains of mice.
+CRH	drug	alcohol	8367033	Similar to beta EP, an immediate sharp increase of corticotropin releasing hormone (<strong>CRH</strong>) release was induced by <b>ethanol</b> which, however, did not present a spike but was maintained significantly higher than spontaneous release for the duration of <b>ethanol</b> exposure.
+CRH	drug	alcohol	8367033	Similar to beta EP, an immediate sharp increase of <strong>corticotropin releasing hormone</strong> (<strong>CRH</strong>) release was induced by <b>ethanol</b> which, however, did not present a spike but was maintained significantly higher than spontaneous release for the duration of <b>ethanol</b> exposure.
+CRH	drug	alcohol	8367033	Both <b>ethanol</b> induced beta EP and <strong>CRH</strong> release returned to basal levels within 10 min following removal of <b>ethanol</b>.
+CRH	drug	alcohol	8367033	That beta EP levels did not remain elevated for the duration of <b>ethanol</b> exposure was not due to tissue depletion of releasable beta EP pool, since exposure of the hypothalami to 10( 8) M <strong>CRH</strong> for 10 min, immediately after the perifusion with 20 mM <b>ethanol</b>, resulted in a large increase of beta EP release.
+CRH	drug	opioid	1645431	<strong>CRH</strong> mRNA in the PVN was not altered either by <b>naloxone</b> in control rats, or by chronic i.c.v.
+CRH	drug	opioid	1645431	By contrast, <b>naloxone</b> did increase <strong>CRH</strong> mRNA by ca.
+CRH	drug	alcohol	2560222	Human <strong>CRH</strong> stimulation response during acute withdrawal and after medium term abstention from <b>alcohol</b> abuse.
+CRH	addiction	withdrawal	2560222	Human <strong>CRH</strong> stimulation response during acute <b>withdrawal</b> and after medium term abstention from alcohol abuse.
+CRH	drug	alcohol	2560222	These findings support an altered corticotrophic <strong>CRH</strong> receptor function in detoxified sober <b>alcoholics</b>.
+CRH	drug	alcohol	2840977	Response of ACTH and cortisol to human <strong>corticotropin releasing hormone</strong> after short term abstention from <b>alcohol</b> abuse.
+CRH	drug	alcohol	2840977	The authors administered 100 micrograms human corticotropin releasing hormone (h <strong>CRH</strong>) to <b>alcohol</b> dependent subjects after short term abstention from <b>alcohol</b> abuse and observed that these patients released significantly less adrenocorticotrophic hormone (ACTH) than a control group.
+CRH	drug	alcohol	2840977	The authors administered 100 micrograms human <strong>corticotropin releasing hormone</strong> (h <strong>CRH</strong>) to <b>alcohol</b> dependent subjects after short term abstention from <b>alcohol</b> abuse and observed that these patients released significantly less adrenocorticotrophic hormone (ACTH) than a control group.
+CRH	drug	alcohol	2825572	Pituitary responsiveness to <strong>corticotropin releasing hormone</strong>, which is a central regulator of stress responses and increases the firing rate of brain noradrenergic neurons, is altered during <b>alcohol</b> withdrawal.
+CRH	addiction	withdrawal	2825572	Pituitary responsiveness to <strong>corticotropin releasing hormone</strong>, which is a central regulator of stress responses and increases the firing rate of brain noradrenergic neurons, is altered during alcohol <b>withdrawal</b>.
+PDYN	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous opioid peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), prodynorphin (<strong>Pdyn</strong>) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+PDYN	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous <b>opioid</b> peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), prodynorphin (<strong>Pdyn</strong>) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+PDYN	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous opioid peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), <strong>prodynorphin</strong> (<strong>Pdyn</strong>) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+PDYN	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous <b>opioid</b> peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), <strong>prodynorphin</strong> (<strong>Pdyn</strong>) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+PDYN	drug	cocaine	32730947	In the CPu, <b>cocaine</b> self administration significantly increased the mRNA levels of Penk and <strong>Pdyn</strong> and abolished the mRNA levels of Pomc.
+PDYN	drug	cocaine	32730947	In the PFC, <b>cocaine</b> self administration only increased <strong>Pdyn</strong> mRNA levels without changing the mRNA levels of Pomc and Penk.
+PDYN	drug	alcohol	32692311	Exposure to predator odor during protracted withdrawal from intermittent <b>alcohol</b> drinking resulted in enhanced prefrontal cortex (PFC) driven excitation of <strong>prodynorphin</strong> containing neurons in the BNST.
+PDYN	addiction	withdrawal	32692311	Exposure to predator odor during protracted <b>withdrawal</b> from intermittent alcohol drinking resulted in enhanced prefrontal cortex (PFC) driven excitation of <strong>prodynorphin</strong> containing neurons in the BNST.
+PDYN	drug	alcohol	32692311	Furthermore, deletion of <strong>prodynorphin</strong> in the BNST and chemogenetic inhibition of the PFC BNST pathway restored abnormal responses to predator odor in <b>alcohol</b> exposed mice.
+PDYN	drug	opioid	32487735	Since then, ~20 peptides with <b>opioid</b> receptor activity have been discovered, all of which are generated from three precursors (proenkephalin, <strong>prodynorphin</strong>, and proopiomelanocortin) by sequential proteolytic processing by prohormone convertases and carboxypeptidase E. Each of these peptides bind to all three of the <b>opioid</b> receptor types (mu, delta, kappa), albeit with differing affinities.
+PDYN	drug	opioid	32393639	It is generally thought that the three types of <b>opioid</b> receptors (μ, δ, κ) are activated by endogenous peptides derived from three different precursors: Proopiomelanocortin, proenkephalin, and <strong>prodynorphin</strong>.
+PDYN	drug	alcohol	32099099	Conditional gene knockout resulted in sex specific responses wherein <strong>PDYN</strong> knockout decreased <b>alcohol</b> drinking in both male and female mice, whereas KOR knockout decreased drinking in males only.
+PDYN	drug	alcohol	32099099	We also found that neither <strong>PDYN</strong> nor KOR knockout protected against anxiety caused by <b>alcohol</b> drinking.
+PDYN	drug	alcohol	32099099	Lastly, a history of <b>alcohol</b> drinking did not alter synaptic transmission in <strong>PDYN</strong> neurons in the CeA of either sex, but excitability of <strong>PDYN</strong> neurons was increased in male mice only.
+PDYN	drug	alcohol	32099099	Taken together, our findings indicate that <strong>PDYN</strong> and KOR signaling in the CeA plays an important role in regulating excessive <b>alcohol</b> consumption and highlight the need for future studies to examine how this is mediated through downstream effector regions.
+PDYN	drug	opioid	31510971	Association between <strong>prodynorphin</strong> gene polymorphisms and <b>opioid</b> dependence susceptibility: a meta analysis.
+PDYN	addiction	dependence	31510971	Association between <strong>prodynorphin</strong> gene polymorphisms and opioid <b>dependence</b> susceptibility: a meta analysis.
+PDYN	drug	opioid	31510971	Prodynorphin (<strong>PDYN</strong>) gene polymorphisms have been linked with <b>opioid</b> dependence (OD) with conflicting outcomes, the aim of this study is to synthesize the existing evidence of the association between <strong>PDYN</strong> polymorphisms and OD susceptibility.
+PDYN	addiction	dependence	31510971	Prodynorphin (<strong>PDYN</strong>) gene polymorphisms have been linked with opioid <b>dependence</b> (OD) with conflicting outcomes, the aim of this study is to synthesize the existing evidence of the association between <strong>PDYN</strong> polymorphisms and OD susceptibility.
+PDYN	drug	opioid	31510971	<strong>Prodynorphin</strong> (<strong>PDYN</strong>) gene polymorphisms have been linked with <b>opioid</b> dependence (OD) with conflicting outcomes, the aim of this study is to synthesize the existing evidence of the association between <strong>PDYN</strong> polymorphisms and OD susceptibility.
+PDYN	addiction	dependence	31510971	<strong>Prodynorphin</strong> (<strong>PDYN</strong>) gene polymorphisms have been linked with opioid <b>dependence</b> (OD) with conflicting outcomes, the aim of this study is to synthesize the existing evidence of the association between <strong>PDYN</strong> polymorphisms and OD susceptibility.
+PDYN	drug	alcohol	31339663	nPE1 /  had lower basal Pomc and <strong>Pdyn</strong> (prodynorphin) levels compared to nPE1+/+ , coupled with increased basal Oprm1 and Oprk1 (kappa opioid receptor) levels, and low <b>alcohol</b> drinking increased Pomc and <strong>Pdyn</strong> to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and Oprk1.
+PDYN	drug	opioid	31339663	nPE1 /  had lower basal Pomc and <strong>Pdyn</strong> (prodynorphin) levels compared to nPE1+/+ , coupled with increased basal Oprm1 and Oprk1 (kappa <b>opioid</b> receptor) levels, and low alcohol drinking increased Pomc and <strong>Pdyn</strong> to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and Oprk1.
+PDYN	drug	alcohol	31339663	nPE1 /  had lower basal Pomc and <strong>Pdyn</strong> (<strong>prodynorphin</strong>) levels compared to nPE1+/+ , coupled with increased basal Oprm1 and Oprk1 (kappa opioid receptor) levels, and low <b>alcohol</b> drinking increased Pomc and <strong>Pdyn</strong> to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and Oprk1.
+PDYN	drug	opioid	31339663	nPE1 /  had lower basal Pomc and <strong>Pdyn</strong> (<strong>prodynorphin</strong>) levels compared to nPE1+/+ , coupled with increased basal Oprm1 and Oprk1 (kappa <b>opioid</b> receptor) levels, and low alcohol drinking increased Pomc and <strong>Pdyn</strong> to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and Oprk1.
+PDYN	drug	alcohol	31339663	In nPE1+/+ , excessive <b>alcohol</b> intake increased Pomc and Oprm1, with no effect on <strong>Pdyn</strong> or Oprk1.
+PDYN	drug	opioid	31166231	In addition, we sought to determine whether these behaviors were influenced by kappa <b>opioid</b> receptor signaling and measured expression of <strong>prodynorphin</strong> messenger RNA in the nucleus accumbens and medial prefrontal cortex after conditioning and before reinstatement with <b>morphine</b> and incisional injury.
+PDYN	addiction	relapse	31166231	In addition, we sought to determine whether these behaviors were influenced by kappa opioid receptor signaling and measured expression of <strong>prodynorphin</strong> messenger RNA in the nucleus accumbens and medial prefrontal cortex after conditioning and before <b>reinstatement</b> with morphine and incisional injury.
+PDYN	drug	opioid	31166231	<strong>Prodynorphin</strong> expression was greatly enhanced in the nucleus accumbens and medial prefrontal cortex of mice with incisional injury and <b>morphine</b> conditioning and remained elevated up to drug primed reinstatement.
+PDYN	addiction	relapse	31166231	<strong>Prodynorphin</strong> expression was greatly enhanced in the nucleus accumbens and medial prefrontal cortex of mice with incisional injury and morphine conditioning and remained elevated up to drug primed <b>reinstatement</b>.
+PDYN	drug	opioid	30936032	Association of variants of <strong>prodynorphin</strong> promoter 68 bp repeats in caucasians with <b>opioid</b> dependence diagnosis: Effect on age trajectory of <b>heroin</b> use.
+PDYN	addiction	dependence	30936032	Association of variants of <strong>prodynorphin</strong> promoter 68 bp repeats in caucasians with opioid <b>dependence</b> diagnosis: Effect on age trajectory of heroin use.
+PDYN	drug	opioid	30936032	Exposure to mu <b>opioid</b> receptor agonists such as <b>heroin</b> increases expression of the prodynorphin gene (<strong>PDYN</strong>) in the brain.
+PDYN	drug	opioid	30936032	Exposure to mu <b>opioid</b> receptor agonists such as <b>heroin</b> increases expression of the <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) in the brain.
+PDYN	drug	opioid	30936032	In this study in a Caucasian cohort, we examined the association of the functional <strong>PDYN</strong> 68 bp repeat polymorphism with <b>opioid</b> use disorders.
+PDYN	drug	opioid	30936032	In this case control study, 554 subjects with Caucasian ancestry (142 healthy controls, 153 <b>opioid</b> exposed, but never <b>opioid</b> dependent, NOD, and 259 with an <b>opioid</b> dependence diagnosis, OD) were examined for association of the <strong>PDYN</strong> 68 bp repeats with the diagnosis of <b>opioid</b> dependence (DSM IV criteria), with a dimensional measure of <b>heroin</b> exposure (KMSK scale), and age trajectory parameters of <b>heroin</b> use (age of <b>heroin</b> first use, and age of onset of heaviest use).
+PDYN	addiction	dependence	30936032	In this case control study, 554 subjects with Caucasian ancestry (142 healthy controls, 153 opioid exposed, but never opioid dependent, NOD, and 259 with an opioid <b>dependence</b> diagnosis, OD) were examined for association of the <strong>PDYN</strong> 68 bp repeats with the diagnosis of opioid <b>dependence</b> (DSM IV criteria), with a dimensional measure of heroin exposure (KMSK scale), and age trajectory parameters of heroin use (age of heroin first use, and age of onset of heaviest use).
+PDYN	drug	opioid	30936032	The <strong>PDYN</strong> 68 bp repeat genotype (classified as: "short short" [SS], "long long" [LL], and "short long" [SL], based on the number of repeats) was not associated with categorical <b>opioid</b> dependence diagnoses.
+PDYN	addiction	dependence	30936032	The <strong>PDYN</strong> 68 bp repeat genotype (classified as: "short short" [SS], "long long" [LL], and "short long" [SL], based on the number of repeats) was not associated with categorical opioid <b>dependence</b> diagnoses.
+PDYN	drug	opioid	30936032	This suggests that the functional <strong>PDYN</strong> 68 bp repeat genotype is associated with the age of first use of <b>heroin</b> in Caucasians diagnosed with <b>opioid</b> dependence.
+PDYN	addiction	dependence	30936032	This suggests that the functional <strong>PDYN</strong> 68 bp repeat genotype is associated with the age of first use of heroin in Caucasians diagnosed with opioid <b>dependence</b>.
+PDYN	drug	opioid	30818133	After short  (PND45) or long term (PND90) abstinence, prodynorphin κ <b>opioid</b> receptor (<strong>pDYN</strong> KOP) and pronociceptin nociceptin receptor (pN/OFQ NOP) gene expression were evaluated in the nucleus accumbens (NAc) and hippocampus (Hip) together with the analysis of BDNF signaling pathways.
+PDYN	drug	opioid	30818133	After short  (PND45) or long term (PND90) abstinence, <strong>prodynorphin</strong> κ <b>opioid</b> receptor (<strong>pDYN</strong> KOP) and pronociceptin nociceptin receptor (pN/OFQ NOP) gene expression were evaluated in the nucleus accumbens (NAc) and hippocampus (Hip) together with the analysis of BDNF signaling pathways.
+PDYN	drug	cocaine	30818133	Our results indicate that the short term withdrawal from adolescent <b>cocaine</b> exposure is characterized by a parallel <strong>pDYN</strong> mRNA and BDNF signaling increase in the NAc.
+PDYN	addiction	withdrawal	30818133	Our results indicate that the short term <b>withdrawal</b> from adolescent cocaine exposure is characterized by a parallel <strong>pDYN</strong> mRNA and BDNF signaling increase in the NAc.
+PDYN	drug	opioid	30418215	Postfracture expression levels of several genes previously associated with <b>opioid</b> induced hyperalgesia, including brain derived neurotrophic factor and <strong>prodynorphin</strong>, were unchanged, but neuroinflammation involving Toll like receptor 4 receptor expressing microglia was observed (6.8 ± 1.5 [mean ± SD] cells per high power field for fracture + vehicle vs. 12 ± 2.8 fracture + <b>morphine</b>, P < 0.001, n = 8 per /group).
+PDYN	drug	opioid	30138645	Prodynorphin (<strong>PDYN</strong>) binds to k <b>opioid</b> receptors (KOPr; encoded by OPRK1) and is known to regulate dopaminergic tone, making this system important for drugs addiction.
+PDYN	addiction	addiction	30138645	Prodynorphin (<strong>PDYN</strong>) binds to k opioid receptors (KOPr; encoded by OPRK1) and is known to regulate dopaminergic tone, making this system important for drugs <b>addiction</b>.
+PDYN	drug	opioid	30138645	<strong>Prodynorphin</strong> (<strong>PDYN</strong>) binds to k <b>opioid</b> receptors (KOPr; encoded by OPRK1) and is known to regulate dopaminergic tone, making this system important for drugs addiction.
+PDYN	addiction	addiction	30138645	<strong>Prodynorphin</strong> (<strong>PDYN</strong>) binds to k opioid receptors (KOPr; encoded by OPRK1) and is known to regulate dopaminergic tone, making this system important for drugs <b>addiction</b>.
+PDYN	drug	alcohol	30075159	The current experiments were designed to assess dysregulation of the BNST DYN/KOR system by evaluating <b>alcohol</b> dependence induced changes in DYN/KOR gene expression (<strong>Pdyn</strong> and Oprk1, respectively), and the sensitivity of <b>alcohol</b> self administration, negative affective like behavior and physiological withdrawal to intra BNST KOR antagonism during acute withdrawal.
+PDYN	addiction	dependence	30075159	The current experiments were designed to assess dysregulation of the BNST DYN/KOR system by evaluating alcohol <b>dependence</b> induced changes in DYN/KOR gene expression (<strong>Pdyn</strong> and Oprk1, respectively), and the sensitivity of alcohol self administration, negative affective like behavior and physiological withdrawal to intra BNST KOR antagonism during acute withdrawal.
+PDYN	addiction	withdrawal	30075159	The current experiments were designed to assess dysregulation of the BNST DYN/KOR system by evaluating alcohol dependence induced changes in DYN/KOR gene expression (<strong>Pdyn</strong> and Oprk1, respectively), and the sensitivity of alcohol self administration, negative affective like behavior and physiological <b>withdrawal</b> to intra BNST KOR antagonism during acute <b>withdrawal</b>.
+PDYN	addiction	dependence	30075159	BNST micropunches from air  and vapor exposed animals were analyzed using RT qPCR to quantify <b>dependence</b> induced changes in <strong>Pdyn</strong> and Oprk1 mRNA expression.
+PDYN	drug	opioid	29925858	Prodynorphin (<strong>PDYN</strong>) gives rise to dynorphin (DYNs) <b>opioid</b> peptides which target kappa <b>opioid</b> receptor (KOR).
+PDYN	drug	opioid	29925858	<strong>Prodynorphin</strong> (<strong>PDYN</strong>) gives rise to dynorphin (DYNs) <b>opioid</b> peptides which target kappa <b>opioid</b> receptor (KOR).
+PDYN	drug	alcohol	29925858	We addressed this hypothesis by comparing the expression levels and co expression (transcriptionally coordinated) patterns of <strong>PDYN</strong> and KOR (OPRK1) genes in dorsolateral prefrontal cortex (dlPFC) between human <b>alcoholics</b> and controls.
+PDYN	drug	alcohol	29925858	<strong>PDYN</strong> was found to be downregulated in dlPFC of <b>alcoholics</b>, while OPRK1 transcription was not altered.
+PDYN	drug	alcohol	29925858	<strong>PDYN</strong> downregulation was confined to subgroup of subjects carrying C, a high risk allele of <strong>PDYN</strong> promoter SNP rs1997794 associated with <b>alcoholism</b>.
+PDYN	drug	alcohol	29925858	Changes in <strong>PDYN</strong> expression did not depend on the decline in neuronal proportion in <b>alcoholics</b>, and thereby may be attributed to transcriptional adaptations in <b>alcoholic</b> brain.
+PDYN	drug	alcohol	29925858	Absolute expression levels of <strong>PDYN</strong> were lower compared to those of OPRK1, suggesting that <strong>PDYN</strong> expression is a limiting factor in the DYN/KOR signaling, and that the <strong>PDYN</strong> downregulation diminishes efficacy of DYN/KOR signaling in dlPFC of human <b>alcoholics</b>.
+PDYN	drug	opioid	29911117	Evaluation of <strong>prodynorphin</strong> gene polymorphisms and their association with <b>heroin</b> addiction in a sample of the southeast Iranian population.
+PDYN	addiction	addiction	29911117	Evaluation of <strong>prodynorphin</strong> gene polymorphisms and their association with heroin <b>addiction</b> in a sample of the southeast Iranian population.
+PDYN	drug	opioid	29911117	This study aims at investigating the effect of rs2281285, rs2235749, rs910080 and 68bp VNTR polymorphisms of prodynorphin (<strong>PDYN</strong>) gene on <b>heroin</b> dependence risk in a sample of the southeast Iranian population.
+PDYN	addiction	dependence	29911117	This study aims at investigating the effect of rs2281285, rs2235749, rs910080 and 68bp VNTR polymorphisms of prodynorphin (<strong>PDYN</strong>) gene on heroin <b>dependence</b> risk in a sample of the southeast Iranian population.
+PDYN	drug	opioid	29911117	This study aims at investigating the effect of rs2281285, rs2235749, rs910080 and 68bp VNTR polymorphisms of <strong>prodynorphin</strong> (<strong>PDYN</strong>) gene on <b>heroin</b> dependence risk in a sample of the southeast Iranian population.
+PDYN	addiction	dependence	29911117	This study aims at investigating the effect of rs2281285, rs2235749, rs910080 and 68bp VNTR polymorphisms of <strong>prodynorphin</strong> (<strong>PDYN</strong>) gene on heroin <b>dependence</b> risk in a sample of the southeast Iranian population.
+PDYN	drug	opioid	29911117	The findings showed that <strong>PDYN</strong> rs910080 T>C variant significantly increased the risk of <b>heroin</b> dependence (OR=7.91, 95%CI=3.36 18.61, P<0.0001, CC vs TT; OR=7.53, 95%CI=3.30 17.16, P<0.0001, CC vs TT+TC; OR=1.75, 95%CI=1.33 2.32, p<0.0001, C vs T).
+PDYN	addiction	dependence	29911117	The findings showed that <strong>PDYN</strong> rs910080 T>C variant significantly increased the risk of heroin <b>dependence</b> (OR=7.91, 95%CI=3.36 18.61, P<0.0001, CC vs TT; OR=7.53, 95%CI=3.30 17.16, P<0.0001, CC vs TT+TC; OR=1.75, 95%CI=1.33 2.32, p<0.0001, C vs T).
+PDYN	drug	opioid	29911117	The rs2235749 C>T, rs2281285 A>G and 68bp VNTR variants of <strong>PDYN</strong> gene were not associated with <b>heroin</b> dependence.
+PDYN	addiction	dependence	29911117	The rs2235749 C>T, rs2281285 A>G and 68bp VNTR variants of <strong>PDYN</strong> gene were not associated with heroin <b>dependence</b>.
+PDYN	drug	opioid	29911117	Altogether, our results provide an association between rs910080 polymorphism of <strong>PDYN</strong> gene and risk of <b>heroin</b> dependence in a sample of the southeast Iranian population.
+PDYN	addiction	dependence	29911117	Altogether, our results provide an association between rs910080 polymorphism of <strong>PDYN</strong> gene and risk of heroin <b>dependence</b> in a sample of the southeast Iranian population.
+PDYN	drug	opioid	29852138	Prodynorphin (<strong>Pdyn</strong>) expression was upregulated in the ipsilateral dorsal domains by each the left and right side SNL, while changes in expression of μ <b>opioid</b> receptor (Oprm1) and proenkephalin (Penk) genes were dependent on the SNL side.
+PDYN	drug	opioid	29852138	<strong>Prodynorphin</strong> (<strong>Pdyn</strong>) expression was upregulated in the ipsilateral dorsal domains by each the left and right side SNL, while changes in expression of μ <b>opioid</b> receptor (Oprm1) and proenkephalin (Penk) genes were dependent on the SNL side.
+PDYN	drug	opioid	29852138	Changes in expression of the <strong>Pdyn</strong> and κ <b>opioid</b> receptor (Oprk1) genes were coordinated between the ipsi  and contralateral sides.
+PDYN	addiction	withdrawal	29852138	<b>Withdrawal</b> response thresholds, indicators of mechanical allodynia correlated negatively with <strong>Pdyn</strong> expression in the right ventral domain after right side SNL.
+PDYN	drug	cannabinoid	29713172	Gender specific association of functional <strong>prodynorphin</strong> 68 bp repeats with <b>cannabis</b> exposure in an African American cohort.
+PDYN	drug	cannabinoid	29713172	In this case control study of adult African Americans (n=476; 206 females, 270 males), we examined the association of the functional prodynorphin 68 bp (<strong>PDYN</strong> 68 bp) promoter repeats with categorical diagnoses of <b>cannabis</b> dependence (Diagnostic and Statistical Manual of Mental Disorders IV criteria), as well as with a rapid dimensional measure of maximum lifetime <b>cannabis</b> exposure (the Kreek McHugh Schluger Kellogg <b>cannabis</b> scale).
+PDYN	addiction	dependence	29713172	In this case control study of adult African Americans (n=476; 206 females, 270 males), we examined the association of the functional prodynorphin 68 bp (<strong>PDYN</strong> 68 bp) promoter repeats with categorical diagnoses of cannabis <b>dependence</b> (Diagnostic and Statistical Manual of Mental Disorders IV criteria), as well as with a rapid dimensional measure of maximum lifetime cannabis exposure (the Kreek McHugh Schluger Kellogg cannabis scale).
+PDYN	drug	cannabinoid	29713172	In this case control study of adult African Americans (n=476; 206 females, 270 males), we examined the association of the functional <strong>prodynorphin</strong> 68 bp (<strong>PDYN</strong> 68 bp) promoter repeats with categorical diagnoses of <b>cannabis</b> dependence (Diagnostic and Statistical Manual of Mental Disorders IV criteria), as well as with a rapid dimensional measure of maximum lifetime <b>cannabis</b> exposure (the Kreek McHugh Schluger Kellogg <b>cannabis</b> scale).
+PDYN	addiction	dependence	29713172	In this case control study of adult African Americans (n=476; 206 females, 270 males), we examined the association of the functional <strong>prodynorphin</strong> 68 bp (<strong>PDYN</strong> 68 bp) promoter repeats with categorical diagnoses of cannabis <b>dependence</b> (Diagnostic and Statistical Manual of Mental Disorders IV criteria), as well as with a rapid dimensional measure of maximum lifetime cannabis exposure (the Kreek McHugh Schluger Kellogg cannabis scale).
+PDYN	drug	cannabinoid	29713172	The <strong>PDYN</strong> 68 bp genotype (examined as short short [SS], short long [SL], or long long [LL], based on the number of repeats) was not significantly associated with categorical <b>cannabis</b> dependence diagnoses, either in males or in females.
+PDYN	addiction	dependence	29713172	The <strong>PDYN</strong> 68 bp genotype (examined as short short [SS], short long [SL], or long long [LL], based on the number of repeats) was not significantly associated with categorical cannabis <b>dependence</b> diagnoses, either in males or in females.
+PDYN	drug	cannabinoid	29713172	However, in males, the <strong>PDYN</strong> 68 bp SS+SL genotype was associated with both greater odds of any use of <b>cannabis</b> (p<0.05) and earlier age of first <b>cannabis</b> use, compared to the LL genotype (ie, 15 versus 16.5 years of age; p<0.045).
+PDYN	drug	cannabinoid	29713172	This study provides the first data on how the <strong>PDYN</strong> 68 bp genotype is associated with gender specific patterns of exposure to <b>cannabis</b>.
+PDYN	drug	cannabinoid	29713172	Overall, this study shows that <strong>PDYN</strong> 68 bp polymorphisms affect behaviors involved in early stages of nonmedical <b>cannabis</b> use and potentially lead to increasing self exposure.
+PDYN	drug	opioid	29678771	We measured brain mRNA levels of prodynorphin (<strong>PDYN</strong>), κ <b>opioid</b> receptors (KOR), the nociceptin/orphanin FQ <b>opioid</b> peptide precursor prepronociceptin (ppN/OFQ) and nociceptine/orphanin FQ receptors (NOR).
+PDYN	drug	opioid	29678771	We measured brain mRNA levels of <strong>prodynorphin</strong> (<strong>PDYN</strong>), κ <b>opioid</b> receptors (KOR), the nociceptin/orphanin FQ <b>opioid</b> peptide precursor prepronociceptin (ppN/OFQ) and nociceptine/orphanin FQ receptors (NOR).
+PDYN	drug	alcohol	29678771	Prenatal <b>ethanol</b> exposure upregulated <strong>PDYN</strong> and KOR mRNA levels in the ventral tegmental area (VTA) in infant and adolescent rats and KOR mRNA levels in the prefrontal cortex in infant rats.
+PDYN	drug	opioid	29430855	The present study aimed to investigate whether neuropathic pain is accompanied by prodynorphin (<strong>Pdyn</strong>) and κ <b>opioid</b> receptor (Oprk1) gene expression alterations in selected mouse brain areas.
+PDYN	drug	opioid	29430855	The present study aimed to investigate whether neuropathic pain is accompanied by <strong>prodynorphin</strong> (<strong>Pdyn</strong>) and κ <b>opioid</b> receptor (Oprk1) gene expression alterations in selected mouse brain areas.
+PDYN	drug	alcohol	29383684	We here analyzed post mortem NAc samples of human <b>alcoholics</b> to assess changes in prodynorphin (<strong>PDYN</strong>) and KOR (OPRK1) gene expression and co expression (transcriptionally coordinated) patterns.
+PDYN	drug	alcohol	29383684	We here analyzed post mortem NAc samples of human <b>alcoholics</b> to assess changes in <strong>prodynorphin</strong> (<strong>PDYN</strong>) and KOR (OPRK1) gene expression and co expression (transcriptionally coordinated) patterns.
+PDYN	drug	alcohol	29383684	No significant differences in <strong>PDYN</strong> and OPRK1 gene expression levels between <b>alcoholics</b> and controls were evident.
+PDYN	drug	alcohol	29383684	However, <strong>PDYN</strong> and OPRK1 showed transcriptionally coordinated pattern that was significantly different between <b>alcoholics</b> and controls.
+PDYN	drug	opioid	28968778	The prodynorphin gene (<strong>PDYN</strong>) gives rise to dynorphin <b>opioid</b> peptides mediating depression and substance dependence.
+PDYN	addiction	dependence	28968778	The prodynorphin gene (<strong>PDYN</strong>) gives rise to dynorphin opioid peptides mediating depression and substance <b>dependence</b>.
+PDYN	drug	opioid	28968778	The <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) gives rise to dynorphin <b>opioid</b> peptides mediating depression and substance dependence.
+PDYN	addiction	dependence	28968778	The <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) gives rise to dynorphin opioid peptides mediating depression and substance <b>dependence</b>.
+PDYN	drug	opioid	28656735	Drug addiction is a novelty seeking personality trait that is associated with the candidate genes OPRD1 (<b>opioid</b> delta receptors), OPRK1 (<b>opioid</b> kappa receptors) and <strong>PDYN</strong> (prodynorphin).
+PDYN	addiction	addiction	28656735	Drug <b>addiction</b> is a novelty seeking personality trait that is associated with the candidate genes OPRD1 (opioid delta receptors), OPRK1 (opioid kappa receptors) and <strong>PDYN</strong> (prodynorphin).
+PDYN	addiction	relapse	28656735	Drug addiction is a novelty <b>seeking</b> personality trait that is associated with the candidate genes OPRD1 (opioid delta receptors), OPRK1 (opioid kappa receptors) and <strong>PDYN</strong> (prodynorphin).
+PDYN	drug	opioid	28656735	Drug addiction is a novelty seeking personality trait that is associated with the candidate genes OPRD1 (<b>opioid</b> delta receptors), OPRK1 (<b>opioid</b> kappa receptors) and <strong>PDYN</strong> (<strong>prodynorphin</strong>).
+PDYN	addiction	addiction	28656735	Drug <b>addiction</b> is a novelty seeking personality trait that is associated with the candidate genes OPRD1 (opioid delta receptors), OPRK1 (opioid kappa receptors) and <strong>PDYN</strong> (<strong>prodynorphin</strong>).
+PDYN	addiction	relapse	28656735	Drug addiction is a novelty <b>seeking</b> personality trait that is associated with the candidate genes OPRD1 (opioid delta receptors), OPRK1 (opioid kappa receptors) and <strong>PDYN</strong> (<strong>prodynorphin</strong>).
+PDYN	addiction	relapse	28656735	However, associations between single nucleotide polymorphisms (SNPs) rs1042114 (80G>T) of the OPRD1 gene, rs702764 (843 A>G) of the OPRK1 gene, and rs910080 (3' UTR _743T>C), rs1997794 (5' UTR  381A>G) and rs1022563 (3' UTR) of the <strong>PDYN</strong> gene and novelty <b>seeking</b> remain controversial as reported results have not been reproducible.
+PDYN	drug	opioid	28656735	A significant association between <b>opioid</b> dependence and SNP rs910080 of <strong>PDYN</strong> (P=.0217) was detected, but there was no association for SNPs rs199774 and rs1022563.
+PDYN	addiction	dependence	28656735	A significant association between opioid <b>dependence</b> and SNP rs910080 of <strong>PDYN</strong> (P=.0217) was detected, but there was no association for SNPs rs199774 and rs1022563.
+PDYN	drug	nicotine	28509375	Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>) derived opioid peptides are proposed as important mediators of <b>nicotine</b> reward.
+PDYN	drug	opioid	28509375	Delta and kappa <b>opioid</b> receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>) derived <b>opioid</b> peptides are proposed as important mediators of nicotine reward.
+PDYN	addiction	reward	28509375	Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>) derived opioid peptides are proposed as important mediators of nicotine <b>reward</b>.
+PDYN	drug	nicotine	28509375	Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) derived opioid peptides are proposed as important mediators of <b>nicotine</b> reward.
+PDYN	drug	opioid	28509375	Delta and kappa <b>opioid</b> receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) derived <b>opioid</b> peptides are proposed as important mediators of nicotine reward.
+PDYN	addiction	reward	28509375	Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) derived opioid peptides are proposed as important mediators of nicotine <b>reward</b>.
+PDYN	drug	nicotine	28509375	This study investigated the regulatory effect of chronic <b>nicotine</b> treatment on the gene expression of DOR, KOR, PENK and <strong>PDYN</strong> in the mesocorticolimbic system.
+PDYN	drug	nicotine	28509375	Conversely, <strong>PDYN</strong> mRNA was reduced in the LHA with 0.6 mg/kg <b>nicotine</b> and in the AMG with 0.4 mg/kg <b>nicotine</b>.
+PDYN	drug	alcohol	28336495	Genetic variation and epigenetic modification of the <strong>prodynorphin</strong> gene in peripheral blood cells in <b>alcoholism</b>.
+PDYN	drug	alcohol	28336495	<b>Alcohol</b> induced changes in the <strong>prodynorphin</strong> gene expression may be influenced by both gene polymorphisms and epigenetic modifications.
+PDYN	drug	alcohol	28336495	The present study of human <b>alcoholics</b> aims to evaluate DNA methylation patterns in the prodynorphin gene (<strong>PDYN</strong>) promoter and to identify single nucleotide polymorphisms (SNPs) associated with <b>alcohol</b> dependence and with altered DNA methylation.
+PDYN	addiction	dependence	28336495	The present study of human alcoholics aims to evaluate DNA methylation patterns in the prodynorphin gene (<strong>PDYN</strong>) promoter and to identify single nucleotide polymorphisms (SNPs) associated with alcohol <b>dependence</b> and with altered DNA methylation.
+PDYN	drug	alcohol	28336495	The present study of human <b>alcoholics</b> aims to evaluate DNA methylation patterns in the <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) promoter and to identify single nucleotide polymorphisms (SNPs) associated with <b>alcohol</b> dependence and with altered DNA methylation.
+PDYN	addiction	dependence	28336495	The present study of human alcoholics aims to evaluate DNA methylation patterns in the <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) promoter and to identify single nucleotide polymorphisms (SNPs) associated with alcohol <b>dependence</b> and with altered DNA methylation.
+PDYN	drug	alcohol	28336495	Genomic DNA was isolated from peripheral blood cells of <b>alcoholics</b> and healthy controls, and DNA methylation was studied in the <strong>PDYN</strong> promoter by bisulfite pyrosequencing.
+PDYN	drug	alcohol	28336495	Association with <b>alcoholism</b> was observed for rs2235751 and the presence of the minor allele G was associated with reduced DNA methylation at <strong>PDYN</strong> promoter in females and younger subjects.
+PDYN	drug	alcohol	28336495	Genetic and epigenetic factors within <strong>PDYN</strong> are related to risk for <b>alcoholism</b>, providing further evidence of its involvement on <b>ethanol</b> effects.
+PDYN	drug	psychedelics	27989838	Chromatin immunoprecipitation assays revealed that acute <b>MDMA</b> increased me3H3K4 at the pN/OFQ, <strong>pDYN</strong> and NOP promoters.
+PDYN	drug	amphetamine	27841313	Increased expression of proenkephalin and <strong>prodynorphin</strong> mRNAs in the nucleus accumbens of compulsive <b>methamphetamine</b> taking rats.
+PDYN	addiction	addiction	27841313	Increased expression of proenkephalin and <strong>prodynorphin</strong> mRNAs in the nucleus accumbens of <b>compulsive</b> methamphetamine taking rats.
+PDYN	drug	amphetamine	27841313	Because <strong>PDYN</strong> and PENK are expressed in dopamine D1  and D2 containing NAc neurons, respectively, these findings suggest that mechanisms, which impact both cell types may play a role in the regulation of compulsive <b>methamphetamine</b> taking by rats.
+PDYN	addiction	addiction	27841313	Because <strong>PDYN</strong> and PENK are expressed in dopamine D1  and D2 containing NAc neurons, respectively, these findings suggest that mechanisms, which impact both cell types may play a role in the regulation of <b>compulsive</b> methamphetamine taking by rats.
+PDYN	drug	nicotine	27430399	Repeated <b>nicotine</b> exposure modulates <strong>prodynorphin</strong> and pronociceptin levels in the reward pathway.
+PDYN	addiction	reward	27430399	Repeated nicotine exposure modulates <strong>prodynorphin</strong> and pronociceptin levels in the <b>reward</b> pathway.
+PDYN	addiction	sensitization	27430399	A significant positive effect of <b>sensitization</b> on <strong>pdyn</strong> mRNA levels was detected in the CPu.
+PDYN	drug	nicotine	27430399	Moreover, chronic but not acute <b>nicotine</b> treatment significantly decreased <strong>pdyn</strong> mRNA levels in the NAc and increased expression in the PFCx.
+PDYN	drug	nicotine	27430399	While several pnoc and <strong>pdyn</strong> changes were associated to <b>nicotine</b> administration, the only significant effect of sensitization was a significant increase in <strong>pdyn</strong> in the CPu.
+PDYN	addiction	sensitization	27430399	While several pnoc and <strong>pdyn</strong> changes were associated to nicotine administration, the only significant effect of <b>sensitization</b> was a significant increase in <strong>pdyn</strong> in the CPu.
+PDYN	drug	amphetamine	27275252	Association between VNTR Polymorphism in Promoter Region of Prodynorphin (<strong>PDYN</strong>) Gene and <b>Methamphetamine</b> Dependence.
+PDYN	addiction	dependence	27275252	Association between VNTR Polymorphism in Promoter Region of Prodynorphin (<strong>PDYN</strong>) Gene and Methamphetamine <b>Dependence</b>.
+PDYN	drug	amphetamine	27275252	Association between VNTR Polymorphism in Promoter Region of <strong>Prodynorphin</strong> (<strong>PDYN</strong>) Gene and <b>Methamphetamine</b> Dependence.
+PDYN	addiction	dependence	27275252	Association between VNTR Polymorphism in Promoter Region of <strong>Prodynorphin</strong> (<strong>PDYN</strong>) Gene and Methamphetamine <b>Dependence</b>.
+PDYN	drug	amphetamine	27275252	The present study revealed no association between the VNTR polymorphism in the promoter region of the <strong>PDYN</strong> gene and <b>methamphetamine</b> dependence risk.
+PDYN	addiction	dependence	27275252	The present study revealed no association between the VNTR polymorphism in the promoter region of the <strong>PDYN</strong> gene and methamphetamine <b>dependence</b> risk.
+PDYN	drug	opioid	27094549	The expression of Bdnf and <strong>Pdyn</strong> (qPCR) was increased after <b>morphine</b> treatment and incision.
+PDYN	drug	opioid	27094549	Chromatin immunoprecipitation assays demonstrated that the <strong>Pdyn</strong> and Bdnf promoters were more strongly associated with acetylated H3K9 after <b>morphine</b> plus incision than in the <b>morphine</b> or incision alone groups.
+PDYN	drug	opioid	27094549	Spinal epigenetic changes involving Bdnf and <strong>Pdyn</strong> may contribute to the enhanced postoperative nociceptive sensitization and analgesic tolerance observed after continuous <b>opioid</b> exposure.
+PDYN	addiction	sensitization	27094549	Spinal epigenetic changes involving Bdnf and <strong>Pdyn</strong> may contribute to the enhanced postoperative nociceptive <b>sensitization</b> and analgesic tolerance observed after continuous opioid exposure.
+PDYN	addiction	relapse	27074815	A Functional 3'UTR Polymorphism (rs2235749) of <strong>Prodynorphin</strong> Alters microRNA 365 Binding in Ventral Striatonigral Neurons to Influence Novelty <b>Seeking</b> and Positive Reward Traits.
+PDYN	addiction	reward	27074815	A Functional 3'UTR Polymorphism (rs2235749) of <strong>Prodynorphin</strong> Alters microRNA 365 Binding in Ventral Striatonigral Neurons to Influence Novelty Seeking and Positive <b>Reward</b> Traits.
+PDYN	addiction	reward	27074815	Our multidisciplinary approach revealed that the single nucleotide polymorphism (SNP) rs2235749 (in high linkage disequilibrium with rs910080) modifies striatal <strong>PDYN</strong> expression via impaired binding of miR 365, a microRNA that targets the <strong>PDYN</strong> 3' untranslated region (3'UTR), and is significantly associated to novelty  and <b>reward</b> related behavioral traits in humans and translational animal models.
+PDYN	addiction	relapse	27074815	Using lentiviral miRZip 365 constructs selectively expressed in <strong>Pdyn</strong> neurons of the NAcSh, we demonstrated that the <strong>Pdyn</strong> miR365 interaction in the NAcSh directly influences novelty <b>seeking</b> exploratory behavior and facilitates self administration of natural reward.
+PDYN	addiction	reward	27074815	Using lentiviral miRZip 365 constructs selectively expressed in <strong>Pdyn</strong> neurons of the NAcSh, we demonstrated that the <strong>Pdyn</strong> miR365 interaction in the NAcSh directly influences novelty seeking exploratory behavior and facilitates self administration of natural <b>reward</b>.
+PDYN	addiction	relapse	27074815	Overall, this translational study suggests that genetically determined miR 365 mediated epigenetic regulation of <strong>PDYN</strong> expression in mesolimbic striatonigral/striatomesencephalic circuits possibly contributes to novelty <b>seeking</b> and positive reinforcement traits.
+PDYN	addiction	reward	27074815	Overall, this translational study suggests that genetically determined miR 365 mediated epigenetic regulation of <strong>PDYN</strong> expression in mesolimbic striatonigral/striatomesencephalic circuits possibly contributes to novelty seeking and positive <b>reinforcement</b> traits.
+PDYN	drug	cocaine	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, Penk, <strong>Pdyn</strong>) and cognate receptors (Oprm, Oprk and Oprd) in reward related brain regions, after exposure to either <b>cocaine</b> self administration or yoked saline, in the aforementioned translational paradigm.
+PDYN	drug	opioid	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous <b>opioid</b> peptides (Pomc, Penk, <strong>Pdyn</strong>) and cognate receptors (Oprm, Oprk and Oprd) in reward related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+PDYN	addiction	reward	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, Penk, <strong>Pdyn</strong>) and cognate receptors (Oprm, Oprk and Oprd) in <b>reward</b> related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+PDYN	drug	cocaine	26777278	Moreover, gene expression level of <strong>Pdyn</strong>, Penk, Oprk, and Oprm in the DS was significantly correlated with <b>cocaine</b> intake only in Fischer rats.
+PDYN	drug	opioid	26733781	We will highlight evidence that the function of DYN KOR systems is influenced in a sex dependent manner by: polymorphisms in the prodynorphin (<strong>pDYN</strong>) gene, genetic linkage with the melanocortin 1 receptor (MC1R), heterodimerization of KORs and mu <b>opioid</b> receptors (MORs), and gonadal hormones.
+PDYN	drug	opioid	26733781	We will highlight evidence that the function of DYN KOR systems is influenced in a sex dependent manner by: polymorphisms in the <strong>prodynorphin</strong> (<strong>pDYN</strong>) gene, genetic linkage with the melanocortin 1 receptor (MC1R), heterodimerization of KORs and mu <b>opioid</b> receptors (MORs), and gonadal hormones.
+PDYN	drug	alcohol	26502829	Associations of <strong>prodynorphin</strong> sequence variation with <b>alcohol</b> dependence and related traits are phenotype specific and sex dependent.
+PDYN	addiction	dependence	26502829	Associations of <strong>prodynorphin</strong> sequence variation with alcohol <b>dependence</b> and related traits are phenotype specific and sex dependent.
+PDYN	drug	alcohol	26502829	We previously demonstrated that prodynorphin (<strong>PDYN</strong>) haplotypes and single nucleotide polymorphism (SNP) rs2281285 are associated with <b>alcohol</b> dependence and the propensity to drink in negative emotional states, and recent studies suggest that <strong>PDYN</strong> gene effects on substance dependence risk may be sex related.
+PDYN	addiction	dependence	26502829	We previously demonstrated that prodynorphin (<strong>PDYN</strong>) haplotypes and single nucleotide polymorphism (SNP) rs2281285 are associated with alcohol <b>dependence</b> and the propensity to drink in negative emotional states, and recent studies suggest that <strong>PDYN</strong> gene effects on substance <b>dependence</b> risk may be sex related.
+PDYN	drug	alcohol	26502829	We previously demonstrated that <strong>prodynorphin</strong> (<strong>PDYN</strong>) haplotypes and single nucleotide polymorphism (SNP) rs2281285 are associated with <b>alcohol</b> dependence and the propensity to drink in negative emotional states, and recent studies suggest that <strong>PDYN</strong> gene effects on substance dependence risk may be sex related.
+PDYN	addiction	dependence	26502829	We previously demonstrated that <strong>prodynorphin</strong> (<strong>PDYN</strong>) haplotypes and single nucleotide polymorphism (SNP) rs2281285 are associated with alcohol <b>dependence</b> and the propensity to drink in negative emotional states, and recent studies suggest that <strong>PDYN</strong> gene effects on substance <b>dependence</b> risk may be sex related.
+PDYN	drug	alcohol	26502829	We examined sex dependent associations of <strong>PDYN</strong> variation with <b>alcohol</b> dependence and related phenotypes, including negative craving, time until relapse after treatment and the length of sobriety episodes before seeking treatment, in discovery and validation cohorts of European ancestry.
+PDYN	addiction	dependence	26502829	We examined sex dependent associations of <strong>PDYN</strong> variation with alcohol <b>dependence</b> and related phenotypes, including negative craving, time until relapse after treatment and the length of sobriety episodes before seeking treatment, in discovery and validation cohorts of European ancestry.
+PDYN	addiction	relapse	26502829	We examined sex dependent associations of <strong>PDYN</strong> variation with alcohol dependence and related phenotypes, including negative <b>craving</b>, time until <b>relapse</b> after treatment and the length of sobriety episodes before <b>seeking</b> treatment, in discovery and validation cohorts of European ancestry.
+PDYN	drug	alcohol	26502829	Our findings suggest that sex dependent effects of <strong>PDYN</strong> variants in <b>alcohol</b> dependence are phenotype specific.
+PDYN	addiction	dependence	26502829	Our findings suggest that sex dependent effects of <strong>PDYN</strong> variants in alcohol <b>dependence</b> are phenotype specific.
+PDYN	drug	opioid	26341936	Therefore, the current study investigated the potential link between the functional <b>opioid</b> peptide prodynorphin (<strong>PDYN</strong>) 68 bp VNTR genetic polymorphism and neuronal correlates of performance monitoring.
+PDYN	drug	opioid	26341936	Therefore, the current study investigated the potential link between the functional <b>opioid</b> peptide <strong>prodynorphin</strong> (<strong>PDYN</strong>) 68 bp VNTR genetic polymorphism and neuronal correlates of performance monitoring.
+PDYN	drug	opioid	26169942	Spinocerebellar ataxia type 23 is caused by mutations in <strong>PDYN</strong>, which encodes the <b>opioid</b> neuropeptide precursor protein, prodynorphin.
+PDYN	drug	opioid	26169942	Spinocerebellar ataxia type 23 is caused by mutations in <strong>PDYN</strong>, which encodes the <b>opioid</b> neuropeptide precursor protein, <strong>prodynorphin</strong>.
+PDYN	drug	opioid	26169942	<strong>Prodynorphin</strong> is processed into the <b>opioid</b> peptides, α neoendorphin, and dynorphins A and B, that normally exhibit <b>opioid</b> receptor mediated actions in pain signalling and addiction.
+PDYN	addiction	addiction	26169942	<strong>Prodynorphin</strong> is processed into the opioid peptides, α neoendorphin, and dynorphins A and B, that normally exhibit opioid receptor mediated actions in pain signalling and <b>addiction</b>.
+PDYN	drug	opioid	26049060	<strong>Prodynorphin</strong> mRNA and protein levels were increased in the nucleus accumbens (NAc) after four weeks of <b>morphine</b> withdrawal.
+PDYN	addiction	withdrawal	26049060	<strong>Prodynorphin</strong> mRNA and protein levels were increased in the nucleus accumbens (NAc) after four weeks of morphine <b>withdrawal</b>.
+PDYN	drug	alcohol	26029055	We compared the levels of prodynorphin (<strong>PDYN</strong>) and proenkephalin (PENK) mRNAs (by qRT PCR), and dynorphins and enkephalins (by radioimmunoassay) in the caudate nucleus and putamen between <b>alcoholics</b> and control subjects.
+PDYN	drug	alcohol	26029055	We compared the levels of <strong>prodynorphin</strong> (<strong>PDYN</strong>) and proenkephalin (PENK) mRNAs (by qRT PCR), and dynorphins and enkephalins (by radioimmunoassay) in the caudate nucleus and putamen between <b>alcoholics</b> and control subjects.
+PDYN	drug	alcohol	26029055	We also evaluated whether <strong>PDYN</strong> promoter variant rs1997794 associated with <b>alcoholism</b> affects <strong>PDYN</strong> expression.
+PDYN	drug	alcohol	26029055	<strong>PDYN</strong> mRNA and Met enkephalin Arg Phe, a marker of PENK were downregulated in the caudate of <b>alcoholics</b>, while <strong>PDYN</strong> mRNA and Leu enkephalin Arg, a marker of <strong>PDYN</strong> were decreased in the putamen of <b>alcoholics</b> carrying high risk rs1997794 C allele.
+PDYN	drug	opioid	25854026	The mRNA expressions of µ <b>opioid</b> receptor (MOR), κ <b>opioid</b> receptor (KOR), δ <b>opioid</b> receptor (DOR), proopiomelanocortin (POMC) and prodynorphin (<strong>PDYN</strong>) in dorsal root ganglion (DRG) and lumbar spinal cord dorsal horn (SCDH) of L4 L6 of the affected side were detected by PCR method.
+PDYN	drug	opioid	25854026	The mRNA expressions of µ <b>opioid</b> receptor (MOR), κ <b>opioid</b> receptor (KOR), δ <b>opioid</b> receptor (DOR), proopiomelanocortin (POMC) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) in dorsal root ganglion (DRG) and lumbar spinal cord dorsal horn (SCDH) of L4 L6 of the affected side were detected by PCR method.
+PDYN	drug	opioid	25722510	In the immunohistochemistry study, pro dynorphine (<strong>PDYN</strong>) expression was increased after <b>morphine</b> administration in both amygdala and nucleus accumbens (NAcc).
+PDYN	drug	opioid	25722510	On exposure to <b>morphine</b>, in CRF OE mice the <strong>PDYN</strong> protein expression was increased as compared to WT mice in the amygdala and NAcc.
+PDYN	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and <strong>Pdyn</strong>.
+PDYN	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and <strong>Pdyn</strong>.
+PDYN	drug	alcohol	25177835	A molecular prospective provides new insights into implication of <strong>PDYN</strong> and OPRK1 genes in <b>alcohol</b> dependence.
+PDYN	addiction	dependence	25177835	A molecular prospective provides new insights into implication of <strong>PDYN</strong> and OPRK1 genes in alcohol <b>dependence</b>.
+PDYN	drug	alcohol	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for <b>alcohol</b> dependence by remodeling DNA protein interaction patterns in prodynorphin (<strong>PDYN</strong>) and the κ opioid receptor (OPRK1) genes.
+PDYN	drug	opioid	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for alcohol dependence by remodeling DNA protein interaction patterns in prodynorphin (<strong>PDYN</strong>) and the κ <b>opioid</b> receptor (OPRK1) genes.
+PDYN	addiction	dependence	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for alcohol <b>dependence</b> by remodeling DNA protein interaction patterns in prodynorphin (<strong>PDYN</strong>) and the κ opioid receptor (OPRK1) genes.
+PDYN	drug	alcohol	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for <b>alcohol</b> dependence by remodeling DNA protein interaction patterns in <strong>prodynorphin</strong> (<strong>PDYN</strong>) and the κ opioid receptor (OPRK1) genes.
+PDYN	drug	opioid	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for alcohol dependence by remodeling DNA protein interaction patterns in <strong>prodynorphin</strong> (<strong>PDYN</strong>) and the κ <b>opioid</b> receptor (OPRK1) genes.
+PDYN	addiction	dependence	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for alcohol <b>dependence</b> by remodeling DNA protein interaction patterns in <strong>prodynorphin</strong> (<strong>PDYN</strong>) and the κ opioid receptor (OPRK1) genes.
+PDYN	drug	alcohol	25177835	In order to elaborate the underlying molecular mechanism behind these susceptibility differences we used bioinformatics tools to retrieve differential DNA protein interactions at <strong>PDYN</strong> and OPRK1 SNPs significantly associated with <b>alcohol</b> dependence.
+PDYN	addiction	dependence	25177835	In order to elaborate the underlying molecular mechanism behind these susceptibility differences we used bioinformatics tools to retrieve differential DNA protein interactions at <strong>PDYN</strong> and OPRK1 SNPs significantly associated with alcohol <b>dependence</b>.
+PDYN	drug	alcohol	25177835	In a nutshell, transition of a single nucleotide may modify differential DNA protein interactions at OPRK1 and <strong>PDYN</strong>׳s SNPs, significantly associated with pathology that may lead to altered individual vulnerability for <b>alcohol</b> dependence.
+PDYN	addiction	dependence	25177835	In a nutshell, transition of a single nucleotide may modify differential DNA protein interactions at OPRK1 and <strong>PDYN</strong>׳s SNPs, significantly associated with pathology that may lead to altered individual vulnerability for alcohol <b>dependence</b>.
+PDYN	drug	opioid	25048760	Association between VNTR polymorphism in promoter region of prodynorphin (<strong>PDYN</strong>) gene and <b>heroin</b> dependence.
+PDYN	addiction	dependence	25048760	Association between VNTR polymorphism in promoter region of prodynorphin (<strong>PDYN</strong>) gene and heroin <b>dependence</b>.
+PDYN	drug	opioid	25048760	Association between VNTR polymorphism in promoter region of <strong>prodynorphin</strong> (<strong>PDYN</strong>) gene and <b>heroin</b> dependence.
+PDYN	addiction	dependence	25048760	Association between VNTR polymorphism in promoter region of <strong>prodynorphin</strong> (<strong>PDYN</strong>) gene and heroin <b>dependence</b>.
+PDYN	drug	cocaine	24966820	This enhanced <b>cocaine</b> seeking response was associated with increased levels of activity regulated transcripts and <strong>prodynorphin</strong>.
+PDYN	addiction	relapse	24966820	This enhanced cocaine <b>seeking</b> response was associated with increased levels of activity regulated transcripts and <strong>prodynorphin</strong>.
+PDYN	drug	cocaine	24943644	We have used genetically modified mice to evaluate the involvement of μ opioid receptor (MOR) and δ opioid receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>), in the reinstatement of <b>cocaine</b> seeking behavior.
+PDYN	drug	opioid	24943644	We have used genetically modified mice to evaluate the involvement of μ <b>opioid</b> receptor (MOR) and δ <b>opioid</b> receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>), in the reinstatement of cocaine seeking behavior.
+PDYN	addiction	relapse	24943644	We have used genetically modified mice to evaluate the involvement of μ opioid receptor (MOR) and δ opioid receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>), in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+PDYN	drug	cocaine	24943644	We have used genetically modified mice to evaluate the involvement of μ opioid receptor (MOR) and δ opioid receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>), in the reinstatement of <b>cocaine</b> seeking behavior.
+PDYN	drug	opioid	24943644	We have used genetically modified mice to evaluate the involvement of μ <b>opioid</b> receptor (MOR) and δ <b>opioid</b> receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>), in the reinstatement of cocaine seeking behavior.
+PDYN	addiction	relapse	24943644	We have used genetically modified mice to evaluate the involvement of μ opioid receptor (MOR) and δ opioid receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>), in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+PDYN	drug	cocaine	24943644	Constitutive knockout mice of MOR, DOR, PENK, and <strong>PDYN</strong>, and their wild type littermates were trained to self administer <b>cocaine</b> or to seek for palatable food, followed by a period of extinction and finally tested on a cue induced reinstatement of seeking behavior.
+PDYN	addiction	relapse	24943644	Constitutive knockout mice of MOR, DOR, PENK, and <strong>PDYN</strong>, and their wild type littermates were trained to self administer cocaine or to seek for palatable food, followed by a period of extinction and finally tested on a cue induced <b>reinstatement</b> of <b>seeking</b> behavior.
+PDYN	addiction	relapse	24943644	In contrast, <strong>PDYN</strong> knockout mice showed a slower extinction and increased <b>relapse</b> than wild type littermates.
+PDYN	drug	cocaine	24943644	Our results indicate that MOR, DOR, and <strong>PDYN</strong> have a differential role in cue induced reinstatement of <b>cocaine</b> seeking behavior.
+PDYN	addiction	relapse	24943644	Our results indicate that MOR, DOR, and <strong>PDYN</strong> have a differential role in cue induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+PDYN	drug	cocaine	24816773	Virus mediated shRNA knockdown of <strong>prodynorphin</strong> in the rat nucleus accumbens attenuates depression like behavior and <b>cocaine</b> locomotor sensitization.
+PDYN	addiction	sensitization	24816773	Virus mediated shRNA knockdown of <strong>prodynorphin</strong> in the rat nucleus accumbens attenuates depression like behavior and cocaine locomotor <b>sensitization</b>.
+PDYN	drug	opioid	24816773	Dynorphins, endogenous <b>opioid</b> peptides that arise from the precursor protein prodynorphin (<strong>Pdyn</strong>), are hypothesized to be involved in the regulation of mood states and the neuroplasticity associated with addiction.
+PDYN	addiction	addiction	24816773	Dynorphins, endogenous opioid peptides that arise from the precursor protein prodynorphin (<strong>Pdyn</strong>), are hypothesized to be involved in the regulation of mood states and the neuroplasticity associated with <b>addiction</b>.
+PDYN	drug	opioid	24816773	Dynorphins, endogenous <b>opioid</b> peptides that arise from the precursor protein <strong>prodynorphin</strong> (<strong>Pdyn</strong>), are hypothesized to be involved in the regulation of mood states and the neuroplasticity associated with addiction.
+PDYN	addiction	addiction	24816773	Dynorphins, endogenous opioid peptides that arise from the precursor protein <strong>prodynorphin</strong> (<strong>Pdyn</strong>), are hypothesized to be involved in the regulation of mood states and the neuroplasticity associated with <b>addiction</b>.
+PDYN	drug	cocaine	24816773	More specifically, we examined whether knockdown of <strong>Pdyn</strong> within the NAcc in rats would alter the expression of depressive like and anxiety like behavior, as well as <b>cocaine</b> locomotor sensitization.
+PDYN	addiction	sensitization	24816773	More specifically, we examined whether knockdown of <strong>Pdyn</strong> within the NAcc in rats would alter the expression of depressive like and anxiety like behavior, as well as cocaine locomotor <b>sensitization</b>.
+PDYN	drug	cocaine	24816773	<strong>Pdyn</strong> knockdown did not alter baseline locomotor behavior, the locomotor response to acute <b>cocaine</b>, or the initial sensitization of the locomotor response to <b>cocaine</b> over the first 4 <b>cocaine</b> treatment days.
+PDYN	addiction	sensitization	24816773	<strong>Pdyn</strong> knockdown did not alter baseline locomotor behavior, the locomotor response to acute cocaine, or the initial <b>sensitization</b> of the locomotor response to cocaine over the first 4 cocaine treatment days.
+PDYN	addiction	addiction	24587148	These findings provide first evidence in humans that the <strong>PDYN</strong> polymorphism modulates neural processes associated with the anticipation of rewards, which ultimately may help to explain differences between genotypes with respect to <b>addiction</b> and drug abuse.
+PDYN	drug	opioid	24305833	Immunohistochemical analysis showed <strong>prodynorphin</strong> content increased in the nucleus accumbens core in all <b>heroin</b> exposed rats, but selectively increased in the nucleus accumbens shell in long access rats.
+PDYN	addiction	addiction	24231353	Impaired periamygdaloid cortex <strong>prodynorphin</strong> is characteristic of opiate <b>addiction</b> and depression.
+PDYN	drug	opioid	24231353	Here, we found reduced <strong>PDYN</strong> mRNA expression in the postmortem human amygdala nucleus of the periamygdaloid cortex (PAC) in both <b>heroin</b> abusers and MDD subjects.
+PDYN	drug	opioid	24231353	Similar to humans, rats that chronically self administered <b>heroin</b> had reduced <strong>Pdyn</strong> mRNA expression in the PAC at a time point associated with a negative affective state.
+PDYN	addiction	addiction	24231353	Altogether, our translational study supports a functional role for impaired <strong>Pdyn</strong> in the PAC in opiate abuse through activation of the stress and negative affect neurocircuitry implicated in <b>addiction</b> vulnerability.
+PDYN	addiction	relapse	24223163	The aim of this study was to replicate a previously reported association of the <strong>PDYN</strong> rs2281285 variant with negative <b>craving</b> using a different phenotyping approach.
+PDYN	addiction	relapse	24223163	Despite the use of a different phenotyping approach to the measurement of negative <b>craving</b>, our results confirm the association between negative <b>craving</b> and <strong>PDYN</strong> rs2281285.
+PDYN	drug	cocaine	24184686	<b>Cocaine</b> induces neurochemical changes of endogenous prodynorphin kappa opioid receptor (<strong>pDYN</strong> KOP) and pronociceptin/orphaninFQ nociceptin receptor (pN/OFQ NOP) systems.
+PDYN	drug	opioid	24184686	Cocaine induces neurochemical changes of endogenous prodynorphin kappa <b>opioid</b> receptor (<strong>pDYN</strong> KOP) and pronociceptin/orphaninFQ nociceptin receptor (pN/OFQ NOP) systems.
+PDYN	drug	cocaine	24184686	<b>Cocaine</b> induces neurochemical changes of endogenous <strong>prodynorphin</strong> kappa opioid receptor (<strong>pDYN</strong> KOP) and pronociceptin/orphaninFQ nociceptin receptor (pN/OFQ NOP) systems.
+PDYN	drug	opioid	24184686	Cocaine induces neurochemical changes of endogenous <strong>prodynorphin</strong> kappa <b>opioid</b> receptor (<strong>pDYN</strong> KOP) and pronociceptin/orphaninFQ nociceptin receptor (pN/OFQ NOP) systems.
+PDYN	drug	cocaine	24184686	Results showed that <b>cocaine</b> induced <strong>pDYN</strong> gene expression up regulation in the NA and lCPu, and its down regulation in the mCPu, whereas KOP mRNA levels were unchanged.
+PDYN	drug	cocaine	24184686	The present findings contribute to better define the role of endogenous <strong>pDYN</strong> KOP and pN/OFQ NOP systems in neuroplasticity mechanisms following chronic <b>cocaine</b> treatment.
+PDYN	drug	opioid	24035914	This neuromodulator system is composed of three receptors, mu, delta and kappa, interacting with a family of <b>opioid</b> peptides derived from POMC (β endorphin), preproenkephalin (pEnk) and preprodynorphin (<strong>pDyn</strong>) precursors.
+PDYN	drug	cannabinoid	24035914	The kappa receptor mainly interacts with <strong>pDyn</strong> peptides to limit drug reward, and mediate dysphoric effects of <b>cannabinoids</b> and nicotine.
+PDYN	drug	nicotine	24035914	The kappa receptor mainly interacts with <strong>pDyn</strong> peptides to limit drug reward, and mediate dysphoric effects of cannabinoids and <b>nicotine</b>.
+PDYN	addiction	reward	24035914	The kappa receptor mainly interacts with <strong>pDyn</strong> peptides to limit drug <b>reward</b>, and mediate dysphoric effects of cannabinoids and nicotine.
+PDYN	drug	alcohol	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (OPRK1) opioid receptors and precursors of their ligands   proopiomelanocortin (POMC), coding for beta endorphin and prodynorphin (<strong>PDYN</strong>) coding for dynorphins, were analyzed in a case control study that included 354 male <b>alcohol</b> dependent and 357 male control subjects from Croatian population.
+PDYN	drug	opioid	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (OPRK1) <b>opioid</b> receptors and precursors of their ligands   proopiomelanocortin (POMC), coding for beta endorphin and prodynorphin (<strong>PDYN</strong>) coding for dynorphins, were analyzed in a case control study that included 354 male alcohol dependent and 357 male control subjects from Croatian population.
+PDYN	drug	alcohol	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (OPRK1) opioid receptors and precursors of their ligands   proopiomelanocortin (POMC), coding for beta endorphin and <strong>prodynorphin</strong> (<strong>PDYN</strong>) coding for dynorphins, were analyzed in a case control study that included 354 male <b>alcohol</b> dependent and 357 male control subjects from Croatian population.
+PDYN	drug	opioid	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (OPRK1) <b>opioid</b> receptors and precursors of their ligands   proopiomelanocortin (POMC), coding for beta endorphin and <strong>prodynorphin</strong> (<strong>PDYN</strong>) coding for dynorphins, were analyzed in a case control study that included 354 male alcohol dependent and 357 male control subjects from Croatian population.
+PDYN	drug	alcohol	24035285	Thus, the data obtained suggest no association of the selected polymorphisms of the genes OPRM1/POMC and OPRK1/<strong>PDYN</strong> with <b>alcoholism</b> in Croatian population.
+PDYN	drug	opioid	24008352	The effects of acid were also examined on mRNA expression for prodynorphin (<strong>PDYN</strong>) and κ <b>opioid</b> receptors (KORs) in mesocorticolimbic brain regions.
+PDYN	drug	opioid	24008352	The effects of acid were also examined on mRNA expression for <strong>prodynorphin</strong> (<strong>PDYN</strong>) and κ <b>opioid</b> receptors (KORs) in mesocorticolimbic brain regions.
+PDYN	drug	opioid	23448472	KORs are widely distributed in the central and peripheral nervous systems, and are specifically activated by endogenous <b>opioids</b> derived from <strong>prodynorphin</strong>.
+PDYN	drug	opioid	23346966	Finally, we assessed the expression of the genes proopiomelanocortin (POMC), pro dynorphin (<strong>PDyn</strong>) and pro enkephalin (PEnk), coding for the <b>opioids</b> peptides in the NAcc and the mPFC in both groups.
+PDYN	drug	cocaine	23164614	<strong>Pdyn</strong> mRNA levels were higher in the <b>cocaine</b> groups than in controls.
+PDYN	drug	alcohol	23101464	Association of the <strong>PDYN</strong> gene with <b>alcohol</b> dependence and the propensity to drink in negative emotional states.
+PDYN	addiction	dependence	23101464	Association of the <strong>PDYN</strong> gene with alcohol <b>dependence</b> and the propensity to drink in negative emotional states.
+PDYN	drug	alcohol	23101464	Synthetic κ opioid receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (OPRK1) and prodynorphin (<strong>PDYN</strong>) genes have been shown to be associated with <b>alcohol</b> dependence.
+PDYN	drug	opioid	23101464	Synthetic κ <b>opioid</b> receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (OPRK1) and prodynorphin (<strong>PDYN</strong>) genes have been shown to be associated with alcohol dependence.
+PDYN	addiction	dependence	23101464	Synthetic κ opioid receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (OPRK1) and prodynorphin (<strong>PDYN</strong>) genes have been shown to be associated with alcohol <b>dependence</b>.
+PDYN	drug	alcohol	23101464	Synthetic κ opioid receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (OPRK1) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) genes have been shown to be associated with <b>alcohol</b> dependence.
+PDYN	drug	opioid	23101464	Synthetic κ <b>opioid</b> receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (OPRK1) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) genes have been shown to be associated with alcohol dependence.
+PDYN	addiction	dependence	23101464	Synthetic κ opioid receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (OPRK1) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) genes have been shown to be associated with alcohol <b>dependence</b>.
+PDYN	drug	alcohol	23101464	We genotyped 23 single nucleotide polymorphisms (SNPs) in the <strong>PDYN</strong> and OPRK1 genes in 816 <b>alcohol</b> dependent subjects and investigated their association with: (1) negative craving measured by a subscale of the Inventory of Drug Taking Situations; (2) a self reported history of depression; (3) the intensity of depressive symptoms measured by the Beck Depression Inventory II.
+PDYN	addiction	relapse	23101464	We genotyped 23 single nucleotide polymorphisms (SNPs) in the <strong>PDYN</strong> and OPRK1 genes in 816 alcohol dependent subjects and investigated their association with: (1) negative <b>craving</b> measured by a subscale of the Inventory of Drug Taking Situations; (2) a self reported history of depression; (3) the intensity of depressive symptoms measured by the Beck Depression Inventory II.
+PDYN	drug	alcohol	23101464	In addition, 13 of the 23 <strong>PDYN</strong> and OPRK1 SNPs, which were previously genotyped in a set of 1248 controls, were used to evaluate association with <b>alcohol</b> dependence.
+PDYN	addiction	dependence	23101464	In addition, 13 of the 23 <strong>PDYN</strong> and OPRK1 SNPs, which were previously genotyped in a set of 1248 controls, were used to evaluate association with alcohol <b>dependence</b>.
+PDYN	drug	alcohol	23101464	Analysis of a haplotype spanning the <strong>PDYN</strong> gene (rs6045784, rs910080, rs2235751, rs2281285) revealed significant association with <b>alcohol</b> dependence (p = 0.00079) and with negative craving (p = 0.0499).
+PDYN	addiction	dependence	23101464	Analysis of a haplotype spanning the <strong>PDYN</strong> gene (rs6045784, rs910080, rs2235751, rs2281285) revealed significant association with alcohol <b>dependence</b> (p = 0.00079) and with negative craving (p = 0.0499).
+PDYN	addiction	relapse	23101464	Analysis of a haplotype spanning the <strong>PDYN</strong> gene (rs6045784, rs910080, rs2235751, rs2281285) revealed significant association with alcohol dependence (p = 0.00079) and with negative <b>craving</b> (p = 0.0499).
+PDYN	drug	alcohol	23101464	A candidate haplotype containing the <strong>PDYN</strong> rs2281285 rs1997794 SNPs that was previously associated with <b>alcohol</b> dependence was also associated with negative craving (p = 0.024) and <b>alcohol</b> dependence (p = 0.0008) in this study.
+PDYN	addiction	dependence	23101464	A candidate haplotype containing the <strong>PDYN</strong> rs2281285 rs1997794 SNPs that was previously associated with alcohol <b>dependence</b> was also associated with negative craving (p = 0.024) and alcohol <b>dependence</b> (p = 0.0008) in this study.
+PDYN	addiction	relapse	23101464	A candidate haplotype containing the <strong>PDYN</strong> rs2281285 rs1997794 SNPs that was previously associated with alcohol dependence was also associated with negative <b>craving</b> (p = 0.024) and alcohol dependence (p = 0.0008) in this study.
+PDYN	drug	alcohol	23101464	These findings support the hypothesis that sequence variation in the <strong>PDYN</strong> gene contributes to both <b>alcohol</b> dependence and the induction of negative craving in <b>alcohol</b> dependent subjects.
+PDYN	addiction	dependence	23101464	These findings support the hypothesis that sequence variation in the <strong>PDYN</strong> gene contributes to both alcohol <b>dependence</b> and the induction of negative craving in alcohol dependent subjects.
+PDYN	addiction	relapse	23101464	These findings support the hypothesis that sequence variation in the <strong>PDYN</strong> gene contributes to both alcohol dependence and the induction of negative <b>craving</b> in alcohol dependent subjects.
+PDYN	drug	opioid	23031399	Additionally, SP dependent upregulation of <strong>prodynorphin</strong>, NMDA1 and NK1 receptor expression in spinal cord was seen after <b>morphine</b> treatment and incision.
+PDYN	drug	cocaine	22709632	κ Opioid receptors (KOPr; encoded by OPRK1), and their endogenous agonists, the dynorphins (encoded by <strong>PDYN</strong>), have counter modulatory effects on reward caused by <b>cocaine</b> or MOPr agonist exposure, and exhibit plasticity in addictive like states.
+PDYN	drug	opioid	22709632	κ <b>Opioid</b> receptors (KOPr; encoded by OPRK1), and their endogenous agonists, the dynorphins (encoded by <strong>PDYN</strong>), have counter modulatory effects on reward caused by cocaine or MOPr agonist exposure, and exhibit plasticity in addictive like states.
+PDYN	addiction	addiction	22709632	κ Opioid receptors (KOPr; encoded by OPRK1), and their endogenous agonists, the dynorphins (encoded by <strong>PDYN</strong>), have counter modulatory effects on reward caused by cocaine or MOPr agonist exposure, and exhibit plasticity in <b>addictive</b> like states.
+PDYN	addiction	reward	22709632	κ Opioid receptors (KOPr; encoded by OPRK1), and their endogenous agonists, the dynorphins (encoded by <strong>PDYN</strong>), have counter modulatory effects on <b>reward</b> caused by cocaine or MOPr agonist exposure, and exhibit plasticity in addictive like states.
+PDYN	addiction	addiction	22709632	Vulnerability and resilience can be due to pre existing (e.g., genetic) factors, or epigenetic modifications of the OPRK1 or <strong>PDYN</strong> genes during the <b>addiction</b> cycle.
+PDYN	drug	alcohol	22684622	<b>Ethanol</b> induces epigenetic modulation of <strong>prodynorphin</strong> and pronociceptin gene expression in the rat amygdala complex.
+PDYN	drug	alcohol	22684622	Recently, we reported that binge intragastric administration of <b>ethanol</b> induces selective alterations of pronociceptin and <strong>prodynorphin</strong> gene expression in the rat amygdala complex depending on the days of exposures and on the development of tolerance and dependence.
+PDYN	addiction	dependence	22684622	Recently, we reported that binge intragastric administration of ethanol induces selective alterations of pronociceptin and <strong>prodynorphin</strong> gene expression in the rat amygdala complex depending on the days of exposures and on the development of tolerance and <b>dependence</b>.
+PDYN	addiction	intoxication	22684622	Recently, we reported that <b>binge</b> intragastric administration of ethanol induces selective alterations of pronociceptin and <strong>prodynorphin</strong> gene expression in the rat amygdala complex depending on the days of exposures and on the development of tolerance and dependence.
+PDYN	drug	alcohol	22684622	We found a linkage between gene expression alterations and epigenetic modulation at pronociceptin and <strong>prodynorphin</strong> promoters following <b>alcohol</b> treatment.
+PDYN	drug	opioid	22479578	Data obtained from different strains of prodynorphin (<strong>Pdyn</strong>)  and kappa <b>opioid</b> receptor (KOP) deficient mice do not provide a consistent picture of the functions of Dyn/KOP in anxiety, suggesting the influence of testing conditions and/or genetic background.
+PDYN	drug	opioid	22479578	Data obtained from different strains of <strong>prodynorphin</strong> (<strong>Pdyn</strong>)  and kappa <b>opioid</b> receptor (KOP) deficient mice do not provide a consistent picture of the functions of Dyn/KOP in anxiety, suggesting the influence of testing conditions and/or genetic background.
+PDYN	drug	cocaine	22443215	Genetic association analyses of <strong>PDYN</strong> polymorphisms with heroin and <b>cocaine</b> addiction.
+PDYN	drug	opioid	22443215	Genetic association analyses of <strong>PDYN</strong> polymorphisms with <b>heroin</b> and cocaine addiction.
+PDYN	addiction	addiction	22443215	Genetic association analyses of <strong>PDYN</strong> polymorphisms with heroin and cocaine <b>addiction</b>.
+PDYN	drug	opioid	22443215	Dynorphin peptides, derived from the prodynorphin (<strong>PDYN</strong>) precursor, bind to <b>opioid</b> receptors, preferentially the kappa <b>opioid</b> receptor, and may mediate the aversive effects of drugs of abuse.
+PDYN	addiction	aversion	22443215	Dynorphin peptides, derived from the prodynorphin (<strong>PDYN</strong>) precursor, bind to opioid receptors, preferentially the kappa opioid receptor, and may mediate the <b>aversive</b> effects of drugs of abuse.
+PDYN	drug	opioid	22443215	Dynorphin peptides, derived from the <strong>prodynorphin</strong> (<strong>PDYN</strong>) precursor, bind to <b>opioid</b> receptors, preferentially the kappa <b>opioid</b> receptor, and may mediate the aversive effects of drugs of abuse.
+PDYN	addiction	aversion	22443215	Dynorphin peptides, derived from the <strong>prodynorphin</strong> (<strong>PDYN</strong>) precursor, bind to opioid receptors, preferentially the kappa opioid receptor, and may mediate the <b>aversive</b> effects of drugs of abuse.
+PDYN	drug	cocaine	22443215	<b>Cocaine</b> and heroin have both been shown to increase expression of <strong>PDYN</strong> in brain regions relevant for drug reward and use.
+PDYN	drug	opioid	22443215	Cocaine and <b>heroin</b> have both been shown to increase expression of <strong>PDYN</strong> in brain regions relevant for drug reward and use.
+PDYN	addiction	reward	22443215	Cocaine and heroin have both been shown to increase expression of <strong>PDYN</strong> in brain regions relevant for drug <b>reward</b> and use.
+PDYN	addiction	addiction	22443215	Polymorphisms in <strong>PDYN</strong> are therefore hypothesized to increase risk for <b>addiction</b> to drugs of abuse.
+PDYN	drug	cocaine	22443215	In this study, 3 polymorphisms in <strong>PDYN</strong> (rs1022563, rs910080 and rs1997794) were genotyped in opioid addicted [248 African Americans (AAs) and 1040 European Americans (EAs)], <b>cocaine</b> addicted (1248 AAs and 336 EAs) and control individuals (674 AAs and 656 EAs).
+PDYN	drug	opioid	22443215	In this study, 3 polymorphisms in <strong>PDYN</strong> (rs1022563, rs910080 and rs1997794) were genotyped in <b>opioid</b> addicted [248 African Americans (AAs) and 1040 European Americans (EAs)], cocaine addicted (1248 AAs and 336 EAs) and control individuals (674 AAs and 656 EAs).
+PDYN	drug	opioid	22443215	Sex specific analyses were also performed as a previous study identified <strong>PDYN</strong> polymorphisms to be more significantly associated with female <b>opioid</b> addicts.
+PDYN	drug	opioid	22443215	These data show that polymorphisms in <strong>PDYN</strong> are associated with <b>opioid</b> addiction in EAs and provide further evidence that these risk variants may be more relevant in females.
+PDYN	addiction	addiction	22443215	These data show that polymorphisms in <strong>PDYN</strong> are associated with opioid <b>addiction</b> in EAs and provide further evidence that these risk variants may be more relevant in females.
+PDYN	drug	cocaine	22387539	As TOP can be implicated in the processing of many neuropeptides, and previous studies have shown that <b>cocaine</b> also alters the gene expression of proenkephalin and <strong>prodynorphin</strong> in the striatum, the present findings suggest that TOP changes in the brain could play important role in the balance of neuropeptide level correlated with <b>cocaine</b> effects.
+PDYN	drug	opioid	22205946	Using real time PCR gene expression analysis, we also showed that mitragynine reduces the mRNA expression of corticotropin releasing factor receptors and <strong>prodynorphin</strong> in zebrafish brain during <b>morphine</b> withdrawal phase, revealing for the first time a possible link between mitragynine's ability to attenuate anxiety during opiate withdrawal with the stress related corticotropin pathway.
+PDYN	addiction	withdrawal	22205946	Using real time PCR gene expression analysis, we also showed that mitragynine reduces the mRNA expression of corticotropin releasing factor receptors and <strong>prodynorphin</strong> in zebrafish brain during morphine <b>withdrawal</b> phase, revealing for the first time a possible link between mitragynine's ability to attenuate anxiety during opiate <b>withdrawal</b> with the stress related corticotropin pathway.
+PDYN	drug	nicotine	22086359	CREB involvement in the regulation of striatal <strong>prodynorphin</strong> by <b>nicotine</b>.
+PDYN	addiction	addiction	22086359	Dynorphin (Dyn) contributes to the <b>addictive</b> process and its precursor gene <strong>prodynorphin</strong> (PD) is regulated by CREB.
+PDYN	drug	alcohol	21966993	Increased <b>ethanol</b> intake in <strong>prodynorphin</strong> knockout mice is associated to changes in opioid receptor function and dopamine transmission.
+PDYN	drug	opioid	21966993	Increased ethanol intake in <strong>prodynorphin</strong> knockout mice is associated to changes in <b>opioid</b> receptor function and dopamine transmission.
+PDYN	drug	alcohol	21966993	The purpose of this study was to examine the role of the <strong>prodynorphin</strong> gene in <b>alcohol</b> sensitivity, preference and vulnerability to <b>alcohol</b> consumption.
+PDYN	drug	alcohol	21966993	Handling induced convulsion (HIC) associated to <b>alcohol</b>, <b>alcohol</b> induced loss of righting reflex (LORR), hypothermic effects in response to acute <b>ethanol</b> challenge, blood <b>ethanol</b> levels (BELs), conditioned place preference, voluntary <b>ethanol</b> consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and µ , δ  and κ opioid agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (<strong>PDYN</strong> KO) and wild type (WT) mice.
+PDYN	drug	opioid	21966993	Handling induced convulsion (HIC) associated to alcohol, alcohol induced loss of righting reflex (LORR), hypothermic effects in response to acute ethanol challenge, blood ethanol levels (BELs), conditioned place preference, voluntary ethanol consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and µ , δ  and κ <b>opioid</b> agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (<strong>PDYN</strong> KO) and wild type (WT) mice.
+PDYN	drug	alcohol	21966993	Handling induced convulsion (HIC) associated to <b>alcohol</b>, <b>alcohol</b> induced loss of righting reflex (LORR), hypothermic effects in response to acute <b>ethanol</b> challenge, blood <b>ethanol</b> levels (BELs), conditioned place preference, voluntary <b>ethanol</b> consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and µ , δ  and κ opioid agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in <strong>prodynorphin</strong> knockout (<strong>PDYN</strong> KO) and wild type (WT) mice.
+PDYN	drug	opioid	21966993	Handling induced convulsion (HIC) associated to alcohol, alcohol induced loss of righting reflex (LORR), hypothermic effects in response to acute ethanol challenge, blood ethanol levels (BELs), conditioned place preference, voluntary ethanol consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and proenkephalin (PENK) gene expression, and µ , δ  and κ <b>opioid</b> agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in <strong>prodynorphin</strong> knockout (<strong>PDYN</strong> KO) and wild type (WT) mice.
+PDYN	drug	alcohol	21966993	There were no differences in HIC, LORR or the decrease in body temperature in response to acute <b>ethanol</b> challenge between <strong>PDYN</strong> KO and WT mice.
+PDYN	drug	alcohol	21966993	<strong>PDYN</strong> KO mice presented higher BEL, higher <b>ethanol</b> conditioned place preference and more <b>ethanol</b> consumption and preference in a two bottle choice paradigm than WT mice.
+PDYN	drug	opioid	21966993	The functional activity of the µ <b>opioid</b> receptor was lower in the CPu, AcbC, AcbSh and cingulate cortex (Cg) of <strong>PDYN</strong> KO mice.
+PDYN	drug	opioid	21966993	In contrast, δ  and κ <b>opioid</b> receptor binding autoradiographies were increased in the CPu and Cg (δ), and in the CPu, AcbC and Cg (κ) of <strong>PDYN</strong> KO.
+PDYN	drug	alcohol	21966993	These results suggest that deletion of the <strong>PDYN</strong> gene increased vulnerability for <b>ethanol</b> consumption by altering, at least in part, PENK, TH and DAT gene expression, and µ , δ  and κ opioid receptor functional activity in brain areas closely related to <b>ethanol</b> reinforcement.
+PDYN	drug	opioid	21966993	These results suggest that deletion of the <strong>PDYN</strong> gene increased vulnerability for ethanol consumption by altering, at least in part, PENK, TH and DAT gene expression, and µ , δ  and κ <b>opioid</b> receptor functional activity in brain areas closely related to ethanol reinforcement.
+PDYN	addiction	reward	21966993	These results suggest that deletion of the <strong>PDYN</strong> gene increased vulnerability for ethanol consumption by altering, at least in part, PENK, TH and DAT gene expression, and µ , δ  and κ opioid receptor functional activity in brain areas closely related to ethanol <b>reinforcement</b>.
+PDYN	drug	alcohol	21955155	<strong>Prodynorphin</strong> mRNA and dynorphins in dl PFC, κ opioid receptor mRNA in OFC and dynorphins in hippocampus were up regulated in <b>alcoholics</b>.
+PDYN	drug	opioid	21955155	<strong>Prodynorphin</strong> mRNA and dynorphins in dl PFC, κ <b>opioid</b> receptor mRNA in OFC and dynorphins in hippocampus were up regulated in alcoholics.
+PDYN	drug	alcohol	21820648	Maternal cigarette use was associated with reduced NAc <strong>prodynorphin</strong> messenger RNA expression, and <b>alcohol</b> exposure induced broad alterations primarily in the dorsal striatum of most genes.
+PDYN	drug	amphetamine	21738744	Furthermore, Western blot analysis and quantitative real time reverse transcription polymerase chain reaction demonstrated that ICER overexpression abolished the <b>METH</b> induced increase in CREB expression and repressed cocaine  and <b>amphetamine</b> regulated transcript (CART) and prodynorphin (<strong>Pdyn</strong>) expression in mice.
+PDYN	drug	cocaine	21738744	Furthermore, Western blot analysis and quantitative real time reverse transcription polymerase chain reaction demonstrated that ICER overexpression abolished the METH induced increase in CREB expression and repressed <b>cocaine</b>  and amphetamine regulated transcript (CART) and prodynorphin (<strong>Pdyn</strong>) expression in mice.
+PDYN	drug	amphetamine	21738744	Furthermore, Western blot analysis and quantitative real time reverse transcription polymerase chain reaction demonstrated that ICER overexpression abolished the <b>METH</b> induced increase in CREB expression and repressed cocaine  and <b>amphetamine</b> regulated transcript (CART) and <strong>prodynorphin</strong> (<strong>Pdyn</strong>) expression in mice.
+PDYN	drug	cocaine	21738744	Furthermore, Western blot analysis and quantitative real time reverse transcription polymerase chain reaction demonstrated that ICER overexpression abolished the METH induced increase in CREB expression and repressed <b>cocaine</b>  and amphetamine regulated transcript (CART) and <strong>prodynorphin</strong> (<strong>Pdyn</strong>) expression in mice.
+PDYN	drug	amphetamine	21738744	The decreased CART and <strong>Pdyn</strong> mRNA expression levels in vivo may underlie the inhibitory role of ICER in <b>METH</b> induced locomotor sensitization.
+PDYN	addiction	sensitization	21738744	The decreased CART and <strong>Pdyn</strong> mRNA expression levels in vivo may underlie the inhibitory role of ICER in METH induced locomotor <b>sensitization</b>.
+PDYN	drug	alcohol	21736916	<b>Alcohol</b> dependence, disinhibited behavior and variation in the <strong>prodynorphin</strong> gene.
+PDYN	addiction	dependence	21736916	Alcohol <b>dependence</b>, disinhibited behavior and variation in the <strong>prodynorphin</strong> gene.
+PDYN	drug	alcohol	21736916	Fifteen percent (n=151) of the sample met DSM IV criteria for <b>alcohol</b> dependence and while results did not support an association between the <strong>PDYN</strong> polymorphism and the diagnosis of <b>alcohol</b> dependence, we did observe an association between the "low" expressing L allele of the <strong>PDYN</strong> gene and a preference for engaging in disinhibited behavior.
+PDYN	addiction	dependence	21736916	Fifteen percent (n=151) of the sample met DSM IV criteria for alcohol <b>dependence</b> and while results did not support an association between the <strong>PDYN</strong> polymorphism and the diagnosis of alcohol <b>dependence</b>, we did observe an association between the "low" expressing L allele of the <strong>PDYN</strong> gene and a preference for engaging in disinhibited behavior.
+PDYN	drug	alcohol	21521424	<strong>Prodynorphin</strong> CpG SNPs associated with <b>alcohol</b> dependence: elevated methylation in the brain of human <b>alcoholics</b>.
+PDYN	addiction	dependence	21521424	<strong>Prodynorphin</strong> CpG SNPs associated with alcohol <b>dependence</b>: elevated methylation in the brain of human alcoholics.
+PDYN	drug	alcohol	21521424	We addressed this hypothesis by analyzing methylation of prodynorphin (<strong>PDYN</strong>) CpG SNPs associated with <b>alcohol</b> dependence, in human <b>alcoholics</b>.
+PDYN	addiction	dependence	21521424	We addressed this hypothesis by analyzing methylation of prodynorphin (<strong>PDYN</strong>) CpG SNPs associated with alcohol <b>dependence</b>, in human alcoholics.
+PDYN	drug	alcohol	21521424	We addressed this hypothesis by analyzing methylation of <strong>prodynorphin</strong> (<strong>PDYN</strong>) CpG SNPs associated with <b>alcohol</b> dependence, in human <b>alcoholics</b>.
+PDYN	addiction	dependence	21521424	We addressed this hypothesis by analyzing methylation of <strong>prodynorphin</strong> (<strong>PDYN</strong>) CpG SNPs associated with alcohol <b>dependence</b>, in human alcoholics.
+PDYN	drug	alcohol	21521424	Three <strong>PDYN</strong> CpG SNPs associated with <b>alcoholism</b> were found to be differently methylated in the human brain.
+PDYN	drug	alcohol	21521424	The findings suggest a causal link between <b>alcoholism</b> associated <strong>PDYN</strong> 3' UTR CpG SNP methylation, activation of <strong>PDYN</strong> transcription and vulnerability of individuals with the C, non risk allele(s) to develop <b>alcohol</b> dependence.
+PDYN	addiction	dependence	21521424	The findings suggest a causal link between alcoholism associated <strong>PDYN</strong> 3' UTR CpG SNP methylation, activation of <strong>PDYN</strong> transcription and vulnerability of individuals with the C, non risk allele(s) to develop alcohol <b>dependence</b>.
+PDYN	drug	opioid	21507157	In the amygdala, an up regulation of <strong>prodynorphin</strong> and pronociceptin was observed in the 1 day group; moreover, pronociceptin and the kappa <b>opioid</b> receptor mRNAs in the 5 day group and both peptide precursors in the 1 day withdrawal group were also up regulated.
+PDYN	addiction	withdrawal	21507157	In the amygdala, an up regulation of <strong>prodynorphin</strong> and pronociceptin was observed in the 1 day group; moreover, pronociceptin and the kappa opioid receptor mRNAs in the 5 day group and both peptide precursors in the 1 day <b>withdrawal</b> group were also up regulated.
+PDYN	drug	opioid	21382455	Association between <b>heroin</b> dependence and <strong>prodynorphin</strong> gene polymorphisms.
+PDYN	addiction	dependence	21382455	Association between heroin <b>dependence</b> and <strong>prodynorphin</strong> gene polymorphisms.
+PDYN	drug	opioid	21382455	This study examined potential association between <b>heroin</b> dependence and four single nucleotide polymorphisms (SNPs) of prodynorphin (<strong>PDYN</strong>) gene (rs35286281 in promoter region and rs1022563, rs2235749, rs910080 in 3'UTR).
+PDYN	addiction	dependence	21382455	This study examined potential association between heroin <b>dependence</b> and four single nucleotide polymorphisms (SNPs) of prodynorphin (<strong>PDYN</strong>) gene (rs35286281 in promoter region and rs1022563, rs2235749, rs910080 in 3'UTR).
+PDYN	drug	opioid	21382455	This study examined potential association between <b>heroin</b> dependence and four single nucleotide polymorphisms (SNPs) of <strong>prodynorphin</strong> (<strong>PDYN</strong>) gene (rs35286281 in promoter region and rs1022563, rs2235749, rs910080 in 3'UTR).
+PDYN	addiction	dependence	21382455	This study examined potential association between heroin <b>dependence</b> and four single nucleotide polymorphisms (SNPs) of <strong>prodynorphin</strong> (<strong>PDYN</strong>) gene (rs35286281 in promoter region and rs1022563, rs2235749, rs910080 in 3'UTR).
+PDYN	drug	opioid	21382455	The analysis indicated a significant higher frequency of the <strong>PDYN</strong> 68bp VNTR (rs35286281) H allele in <b>heroin</b> dependent subjects than in controls (p=0.002 after Bonferroni correction).
+PDYN	drug	opioid	21382455	These findings support the important role of <strong>PDYN</strong> polymorphism in <b>heroin</b> dependence, and may guide future studies to identify genetic risk factors for <b>heroin</b> dependence.
+PDYN	addiction	dependence	21382455	These findings support the important role of <strong>PDYN</strong> polymorphism in heroin <b>dependence</b>, and may guide future studies to identify genetic risk factors for heroin <b>dependence</b>.
+PDYN	drug	alcohol	21338584	<strong>Prodynorphin</strong> promoter SNP associated with <b>alcohol</b> dependence forms noncanonical AP 1 binding site that may influence gene expression in human brain.
+PDYN	addiction	dependence	21338584	<strong>Prodynorphin</strong> promoter SNP associated with alcohol <b>dependence</b> forms noncanonical AP 1 binding site that may influence gene expression in human brain.
+PDYN	drug	alcohol	21338584	Single nucleotide polymorphism (rs1997794) in promoter of the prodynorphin gene (<strong>PDYN</strong>) associated with <b>alcohol</b> dependence may impact <strong>PDYN</strong> transcription in human brain.
+PDYN	addiction	dependence	21338584	Single nucleotide polymorphism (rs1997794) in promoter of the prodynorphin gene (<strong>PDYN</strong>) associated with alcohol <b>dependence</b> may impact <strong>PDYN</strong> transcription in human brain.
+PDYN	drug	alcohol	21338584	Single nucleotide polymorphism (rs1997794) in promoter of the <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) associated with <b>alcohol</b> dependence may impact <strong>PDYN</strong> transcription in human brain.
+PDYN	addiction	dependence	21338584	Single nucleotide polymorphism (rs1997794) in promoter of the <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) associated with alcohol <b>dependence</b> may impact <strong>PDYN</strong> transcription in human brain.
+PDYN	drug	alcohol	21338584	To address this hypothesis we analyzed <strong>PDYN</strong> mRNA levels in the dorsolateral prefrontal cortex (dl PFC) and hippocampus, both involved in cognitive control of addictive behavior and <strong>PDYN</strong> promoter SNP genotype in <b>alcohol</b> dependent and control human subjects.
+PDYN	addiction	addiction	21338584	To address this hypothesis we analyzed <strong>PDYN</strong> mRNA levels in the dorsolateral prefrontal cortex (dl PFC) and hippocampus, both involved in cognitive control of <b>addictive</b> behavior and <strong>PDYN</strong> promoter SNP genotype in alcohol dependent and control human subjects.
+PDYN	drug	alcohol	21338584	The principal component analysis suggested that <strong>PDYN</strong> expression in the dl PFC may be related to <b>alcoholism</b>, while in the hippocampus may depend on the genotype.
+PDYN	drug	alcohol	21338584	The impact of genetic variations on <strong>PDYN</strong> transcription may be relevant for diverse adaptive responses of this gene to <b>alcohol</b>.
+PDYN	drug	amphetamine	21229349	Chronic <b>METH</b> exposure also caused significant decreases in preprotachykinin, but not in <strong>prodynorphin</strong>, mRNA levels.
+PDYN	addiction	relapse	21161187	A down regulation of <strong>prodynorphin</strong> mRNA was found in the dorsal striatum and nucleus accumbens after the acquisition, extinction, and <b>reinstatement</b> of the operant behavior.
+PDYN	addiction	reward	21161187	A down regulation of <strong>prodynorphin</strong> mRNA was found in the dorsal striatum and nucleus accumbens after the acquisition, extinction, and reinstatement of the <b>operant</b> behavior.
+PDYN	addiction	relapse	21161187	An up regulation of <strong>PDYN</strong> mRNA expression was found in the hypothalamus after extinction and <b>reinstatement</b>.
+PDYN	drug	alcohol	21106935	<b>Ethanol</b> and acetaldehyde exposure induces specific epigenetic modifications in the <strong>prodynorphin</strong> gene promoter in a human neuroblastoma cell line.
+PDYN	drug	alcohol	21106935	The results demonstrated a temporal relationship between selective chromatin modifications induced by <b>ethanol</b> and acetaldehyde and changes in <strong>prodynorphin</strong> gene expression quantitated by real time qPCR.
+PDYN	drug	alcohol	21106935	A link has been observed between gene expression alterations and selective epigenetic modulation in the <strong>prodynorphin</strong> promoter region, demonstrating a specificity of the changes induced by <b>ethanol</b> and acetaldehyde.
+PDYN	drug	opioid	21035104	<strong>PDYN</strong> is the precursor protein for the <b>opioid</b> neuropeptides, α neoendorphin, and dynorphins A and B (Dyn A and B).
+PDYN	drug	opioid	21035104	The fourth mutation was located in the nonopioid <strong>PDYN</strong> domain and was associated with altered expression of components of the <b>opioid</b> and glutamate system, as evident from analysis of SCA23 autopsy tissue.
+PDYN	drug	opioid	21035104	The fourth mutation was located in the nonopioid <strong>PDYN</strong> domain and was associated with altered expression of components of the <b>opioid</b> and glutamate system, as evident from analysis of <strong>SCA23</strong> autopsy tissue.
+PDYN	drug	alcohol	20962231	We also showed, using triple label immunofluorescence, that the majority of PVT projecting extinction neurons express <strong>prodynorphin</strong>, suggesting that actions at κ opioid receptors (KORs) in PVT may be critical for inhibiting <b>alcoholic</b> beer seeking.
+PDYN	drug	opioid	20962231	We also showed, using triple label immunofluorescence, that the majority of PVT projecting extinction neurons express <strong>prodynorphin</strong>, suggesting that actions at κ <b>opioid</b> receptors (KORs) in PVT may be critical for inhibiting alcoholic beer seeking.
+PDYN	addiction	relapse	20962231	We also showed, using triple label immunofluorescence, that the majority of PVT projecting extinction neurons express <strong>prodynorphin</strong>, suggesting that actions at κ opioid receptors (KORs) in PVT may be critical for inhibiting alcoholic beer <b>seeking</b>.
+PDYN	drug	opioid	20683583	Amidino TAPA injected subcutaneously produced an extremely potent and longer lasting antinociception than <b>morphine</b> in ddY mice, <strong>prodynorphin</strong> knockout mice, and wild type C57BL/6J mice.
+PDYN	drug	opioid	20651230	Moreover, Tat expression widely disrupted the endogenous <b>opioid</b> system, altering mu and kappa, but not delta, <b>opioid</b> receptor and proopiomelanocortin, proenkephalin, and <strong>prodynorphin</strong> transcript levels in cortex, hippocampus, and striatum.
+PDYN	drug	alcohol	20401606	Male C57Bl/6J mice were tested in a biased <b>ethanol</b> conditioned place preference (CPP) procedure, and both C57Bl/6J and <strong>prodynorphin</strong> gene disrupted (Dyn  / ) mice were used in two bottle free choice (TBC) assays, with or without exposure to FSS.
+PDYN	addiction	reward	20401606	Male C57Bl/6J mice were tested in a biased ethanol conditioned place preference (<b>CPP</b>) procedure, and both C57Bl/6J and <strong>prodynorphin</strong> gene disrupted (Dyn  / ) mice were used in two bottle free choice (TBC) assays, with or without exposure to FSS.
+PDYN	drug	opioid	20201854	In addition, we provide the first evidence of a cis acting polymorphism and a functional haplotype in the <strong>PDYN</strong> gene, of significantly higher DNA methylation rate of the OPRM1 gene in the lymphocytes of <b>heroin</b> addicts, and significant differences in genotype frequencies of three single nucleotide polymorphisms of the P glycoprotein gene (ABCB1) between "higher" and "lower" <b>methadone</b> doses in <b>methadone</b> maintained patients.
+PDYN	drug	nicotine	20170672	Thus, endogenous enkephalins and beta endorphins acting on mu opioid receptors are involved in <b>nicotine</b> rewarding effects, whereas opioid peptides derived from <strong>prodynorphin</strong> participate in <b>nicotine</b> aversive responses.
+PDYN	drug	opioid	20170672	Thus, endogenous enkephalins and beta endorphins acting on mu <b>opioid</b> receptors are involved in nicotine rewarding effects, whereas <b>opioid</b> peptides derived from <strong>prodynorphin</strong> participate in nicotine aversive responses.
+PDYN	addiction	aversion	20170672	Thus, endogenous enkephalins and beta endorphins acting on mu opioid receptors are involved in nicotine rewarding effects, whereas opioid peptides derived from <strong>prodynorphin</strong> participate in nicotine <b>aversive</b> responses.
+PDYN	drug	opioid	19997907	Forebrain PENK and <strong>PDYN</strong> gene expression levels in three inbred strains of mice and their relationship to genotype dependent <b>morphine</b> reward sensitivity.
+PDYN	addiction	reward	19997907	Forebrain PENK and <strong>PDYN</strong> gene expression levels in three inbred strains of mice and their relationship to genotype dependent morphine <b>reward</b> sensitivity.
+PDYN	addiction	addiction	19997907	Proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>) gene expression was measured by in situ hybridization in brain regions implicated in <b>addiction</b>.
+PDYN	addiction	addiction	19997907	Proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) gene expression was measured by in situ hybridization in brain regions implicated in <b>addiction</b>.
+PDYN	drug	opioid	19997907	The influence of the kappa <b>opioid</b> receptor antagonist nor binaltorphimine (nor BNI), which attenuates effects of endogenous <strong>PDYN</strong> derived peptides, on rewarding actions of <b>morphine</b> was studied using the conditioned place preference (CPP) paradigm.
+PDYN	addiction	reward	19997907	The influence of the kappa opioid receptor antagonist nor binaltorphimine (nor BNI), which attenuates effects of endogenous <strong>PDYN</strong> derived peptides, on rewarding actions of morphine was studied using the conditioned place preference (<b>CPP</b>) paradigm.
+PDYN	drug	opioid	19997907	Our results demonstrate that inter strain differences in PENK and <strong>PDYN</strong> genes expression in the nucleus accumbens parallel sensitivity of the selected mouse strains to rewarding effects of <b>morphine</b>.
+PDYN	addiction	reward	19997907	They suggest that high expression of <strong>PDYN</strong> may protect against drug abuse by limiting drug produced <b>reward</b>, which may be due to dynorphin mediated modulation of dopamine release in the nucleus accumbens.
+PDYN	drug	opioid	19917879	We hypothesized that activation of extracellular signal regulated kinases 1 and 2 (ERK1/2) and the expression of c Fos, <strong>prodynorphin</strong> (mRNA), and dynorphin in the spinal cord could participate in the molecular mechanisms underlying postoperative <b>opioid</b> induced sensitization.
+PDYN	addiction	sensitization	19917879	We hypothesized that activation of extracellular signal regulated kinases 1 and 2 (ERK1/2) and the expression of c Fos, <strong>prodynorphin</strong> (mRNA), and dynorphin in the spinal cord could participate in the molecular mechanisms underlying postoperative opioid induced <b>sensitization</b>.
+PDYN	drug	opioid	19789384	The <b>opioid</b> system consists of three receptors, mu, delta, and kappa, which are activated by endogenous <b>opioid</b> peptides processed from three protein precursors, proopiomelanocortin, proenkephalin, and <strong>prodynorphin</strong>.
+PDYN	drug	alcohol	19588333	state.vt.su/adap/cork], <b>Alcohol</b> and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF VIC) [www.adf.org.au], Centre for Education and Information on Drugs and <b>Alcohol</b> (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug Dependence Inc. proceedings, the reference lists of all identified studies and published reviews; authors of identified RCTs were asked about other published or unpublished relevant RCTs.
+PDYN	addiction	dependence	19588333	state.vt.su/adap/cork], Alcohol and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF VIC) [www.adf.org.au], Centre for Education and Information on Drugs and Alcohol (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug <b>Dependence</b> Inc. proceedings, the reference lists of all identified studies and published reviews; authors of identified RCTs were asked about other published or unpublished relevant RCTs.
+PDYN	addiction	sensitization	19559544	<strong>Prodynorphin</strong> gene deficiency potentiates nalbuphine induced behavioral <b>sensitization</b> and withdrawal syndrome in mice.
+PDYN	addiction	withdrawal	19559544	<strong>Prodynorphin</strong> gene deficiency potentiates nalbuphine induced behavioral sensitization and <b>withdrawal</b> syndrome in mice.
+PDYN	addiction	sensitization	19559544	<strong>Pdyn</strong> gene deficiency potentiates nalbuphine induced behavioral <b>sensitization</b> of locomotor activity and accumbal c Fos expression.
+PDYN	drug	opioid	19559544	In addition, <strong>Pdyn</strong> ( / ) mice were more vulnerable to the <b>naloxone</b> precipitated withdrawal syndrome (i.e., teeth chattering, wet dog shakes, forepaw tremors, jumping, weight loss, and global withdrawal score) after repeated treatment with nalbuphine than the WT mice.
+PDYN	addiction	withdrawal	19559544	In addition, <strong>Pdyn</strong> ( / ) mice were more vulnerable to the naloxone precipitated <b>withdrawal</b> syndrome (i.e., teeth chattering, wet dog shakes, forepaw tremors, jumping, weight loss, and global <b>withdrawal</b> score) after repeated treatment with nalbuphine than the WT mice.
+PDYN	drug	opioid	19559544	Consistently, nor binaltorphimine, a kappa <b>opioid</b> receptor antagonist, significantly potentiated nalbuphine induced behavioral effects in WT mice, whereas U 50488H, a kappa <b>opioid</b> receptor agonist, significantly attenuated these changes in <strong>Pdyn</strong> ( / ) mice in a dose dependent manner.
+PDYN	drug	opioid	19481570	Besides actions of peptides from all three classical <b>opioid</b> precursors (proenkephalin, <strong>prodynorphin</strong>, proopiomelanocortin) on the three classical <b>opioid</b> receptors (delta, mu and kappa), dynorphins were also shown to exert non <b>opioid</b> effects mainly through direct effects on NMDA receptors.
+PDYN	drug	opioid	19481570	In recent years, the generation of <strong>prodynorphin</strong>  and <b>opioid</b> receptor deficient mice has provided the tools to investigate open questions on network effects of endogenous dynorphins.
+PDYN	drug	opioid	19298317	An association of <strong>prodynorphin</strong> polymorphisms and <b>opioid</b> dependence in females in a Chinese population.
+PDYN	addiction	dependence	19298317	An association of <strong>prodynorphin</strong> polymorphisms and opioid <b>dependence</b> in females in a Chinese population.
+PDYN	drug	opioid	19298317	Prodynorphin (<strong>PDYN</strong>) binds to kappa <b>opioid</b> receptors and is known to regulate dopaminergic tone, making this system important for the reinforcing and rewarding properties of drugs of abuse such as <b>opioids</b>.
+PDYN	addiction	reward	19298317	Prodynorphin (<strong>PDYN</strong>) binds to kappa opioid receptors and is known to regulate dopaminergic tone, making this system important for the <b>reinforcing</b> and rewarding properties of drugs of abuse such as opioids.
+PDYN	drug	opioid	19298317	<strong>Prodynorphin</strong> (<strong>PDYN</strong>) binds to kappa <b>opioid</b> receptors and is known to regulate dopaminergic tone, making this system important for the reinforcing and rewarding properties of drugs of abuse such as <b>opioids</b>.
+PDYN	addiction	reward	19298317	<strong>Prodynorphin</strong> (<strong>PDYN</strong>) binds to kappa opioid receptors and is known to regulate dopaminergic tone, making this system important for the <b>reinforcing</b> and rewarding properties of drugs of abuse such as opioids.
+PDYN	drug	opioid	19298317	We were interested to analyse a possible gender specificity of dynorphin effects in humans and to this end three single nucleotide polymorphisms (SNPs) in <strong>PDYN</strong> were genotyped in a Chinese population of 484 <b>opioid</b> dependents and 374 controls.
+PDYN	drug	opioid	19298317	Chi squared tests for association revealed that the genotype distributions of SNPs rs1997794 (P = 0.019) and rs1022563 (P = 0.006) in the promoter and 3' region of <strong>PDYN</strong>, respectively, were found to be associated with <b>opioid</b> dependence.
+PDYN	addiction	dependence	19298317	Chi squared tests for association revealed that the genotype distributions of SNPs rs1997794 (P = 0.019) and rs1022563 (P = 0.006) in the promoter and 3' region of <strong>PDYN</strong>, respectively, were found to be associated with opioid <b>dependence</b>.
+PDYN	drug	opioid	19298317	Therefore, SNPs in <strong>PDYN</strong> are significantly associated with the risk of developing <b>opioid</b> dependence; however, this effect may only be seen in females.
+PDYN	addiction	dependence	19298317	Therefore, SNPs in <strong>PDYN</strong> are significantly associated with the risk of developing opioid <b>dependence</b>; however, this effect may only be seen in females.
+PDYN	drug	opioid	19298317	These data suggest that <strong>PDYN</strong> polymorphisms should be studied in additional female <b>opioid</b> dependent populations with an emphasis on the promoter and 3' regions of the gene.
+PDYN	drug	amphetamine	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, <strong>PDYN</strong>, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with <b>METH</b> psychosis.
+PDYN	addiction	dependence	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, <strong>PDYN</strong>, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.
+PDYN	drug	amphetamine	19116947	This study examined the effects of chronic, escalating doses of D <b>AMPH</b> followed by 24 h of withdrawal on the expression of <strong>prodynorphin</strong> (PD) and c fos mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and SERT mRNA expression in the dorsal raphe nucleus (DRN).
+PDYN	addiction	withdrawal	19116947	This study examined the effects of chronic, escalating doses of D AMPH followed by 24 h of <b>withdrawal</b> on the expression of <strong>prodynorphin</strong> (PD) and c fos mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and SERT mRNA expression in the dorsal raphe nucleus (DRN).
+PDYN	drug	opioid	19100723	Alterations of <strong>prodynorphin</strong> gene expression in the rat mesocorticolimbic system during <b>heroin</b> self administration.
+PDYN	drug	opioid	19100723	Opiate induced alterations in the gene expression of the <b>opioid</b> propeptides prodynorphin (<strong>PDYN</strong>) and proenkephalin (PENK) in the brain have previously been described.
+PDYN	drug	opioid	19100723	Opiate induced alterations in the gene expression of the <b>opioid</b> propeptides <strong>prodynorphin</strong> (<strong>PDYN</strong>) and proenkephalin (PENK) in the brain have previously been described.
+PDYN	drug	opioid	19100723	In our study, using in situ hybridization, we measured <strong>PDYN</strong> and PENK mRNA levels in the dorsal striatum, central nucleus of amygdala (CEA), and nucleus accumbens (NAcc) shell and core in rats after 6 weeks of <b>heroin</b> self administration (fixed ratio 5, 0.02 mg/kg/infusion of <b>heroin</b> i.v.)
+PDYN	drug	opioid	19100723	Our results show an increase in the <strong>PDYN</strong> mRNA level in the CEA and NAcc shell and no changes of PENK gene expression after <b>heroin</b> self administration.
+PDYN	drug	opioid	19100723	In addition, to dissociate pharmacological effects of <b>heroin</b> from those produced by motivational processes driving active <b>heroin</b> intake on the <strong>PDYN</strong> and PENK gene expression, we compared effects of response dependent (contingent) and response independent (noncontingent  "yoked" <b>heroin</b> control) <b>heroin</b> administration.
+PDYN	drug	opioid	19100723	In conclusion, our results indicate neuroadaptations in the <strong>PDYN</strong> but not PENK gene expression in rat limbic forebrain during <b>heroin</b> self administration.
+PDYN	drug	nicotine	18937881	<strong>Prodynorphin</strong> gene disruption increases the sensitivity to <b>nicotine</b> self administration in mice.
+PDYN	drug	nicotine	18937881	The aim of the study was to determine the contribution of the endogenous peptides derived from <strong>prodynorphin</strong> in acute and chronic <b>nicotine</b> responses, mainly those related to its addictive properties.
+PDYN	addiction	addiction	18937881	The aim of the study was to determine the contribution of the endogenous peptides derived from <strong>prodynorphin</strong> in acute and chronic nicotine responses, mainly those related to its <b>addictive</b> properties.
+PDYN	drug	nicotine	18937881	Locomotion and nociception were evaluated after acute <b>nicotine</b> administration in <strong>prodynorphin</strong> knockout mice.
+PDYN	drug	nicotine	18937881	However, a shift to the left in the percentage of acquisition of intravenous <b>nicotine</b> self administration was observed in <strong>prodynorphin</strong> KO mice.
+PDYN	drug	nicotine	18937881	These findings reveal a specific role of endogenous peptides derived from <strong>prodynorphin</strong> in <b>nicotine</b> self administration, probably through the modulation of its aversive effects.
+PDYN	addiction	aversion	18937881	These findings reveal a specific role of endogenous peptides derived from <strong>prodynorphin</strong> in nicotine self administration, probably through the modulation of its <b>aversive</b> effects.
+PDYN	drug	cocaine	18923396	A functional haplotype implicated in vulnerability to develop <b>cocaine</b> dependence is associated with reduced <strong>PDYN</strong> expression in human brain.
+PDYN	addiction	dependence	18923396	A functional haplotype implicated in vulnerability to develop cocaine <b>dependence</b> is associated with reduced <strong>PDYN</strong> expression in human brain.
+PDYN	drug	alcohol	18923396	We tested polymorphisms of the prodynorphin gene (<strong>PDYN</strong>) for association with cocaine dependence and cocaine/<b>alcohol</b> codependence.
+PDYN	drug	cocaine	18923396	We tested polymorphisms of the prodynorphin gene (<strong>PDYN</strong>) for association with <b>cocaine</b> dependence and <b>cocaine</b>/alcohol codependence.
+PDYN	addiction	dependence	18923396	We tested polymorphisms of the prodynorphin gene (<strong>PDYN</strong>) for association with cocaine <b>dependence</b> and cocaine/alcohol codependence.
+PDYN	drug	alcohol	18923396	We tested polymorphisms of the <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) for association with cocaine dependence and cocaine/<b>alcohol</b> codependence.
+PDYN	drug	cocaine	18923396	We tested polymorphisms of the <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) for association with <b>cocaine</b> dependence and <b>cocaine</b>/alcohol codependence.
+PDYN	addiction	dependence	18923396	We tested polymorphisms of the <strong>prodynorphin</strong> gene (<strong>PDYN</strong>) for association with cocaine <b>dependence</b> and cocaine/alcohol codependence.
+PDYN	drug	alcohol	18923396	This study provides evidence that a 3'UTR <strong>PDYN</strong> haplotype, implicated in vulnerability to develop cocaine addiction and/or cocaine/<b>alcohol</b> codependence, is related to lower mRNA expression of the <strong>PDYN</strong> gene in human dorsal and ventral striatum.
+PDYN	drug	cocaine	18923396	This study provides evidence that a 3'UTR <strong>PDYN</strong> haplotype, implicated in vulnerability to develop <b>cocaine</b> addiction and/or <b>cocaine</b>/alcohol codependence, is related to lower mRNA expression of the <strong>PDYN</strong> gene in human dorsal and ventral striatum.
+PDYN	addiction	addiction	18923396	This study provides evidence that a 3'UTR <strong>PDYN</strong> haplotype, implicated in vulnerability to develop cocaine <b>addiction</b> and/or cocaine/alcohol codependence, is related to lower mRNA expression of the <strong>PDYN</strong> gene in human dorsal and ventral striatum.
+PDYN	drug	nicotine	18807250	Acute <b>nicotine</b> changes dynorphin and <strong>prodynorphin</strong> mRNA in the striatum.
+PDYN	drug	opioid	18575850	Stress induced reinstatement did not occur for mice pretreated with the kappa <b>opioid</b> receptor antagonist norbinaltorphimine (10 mg/kg) and did not occur in mice lacking either kappa <b>opioid</b> receptors (KOR  / ) or <strong>prodynorphin</strong> (Dyn  / ).
+PDYN	addiction	relapse	18575850	Stress induced <b>reinstatement</b> did not occur for mice pretreated with the kappa opioid receptor antagonist norbinaltorphimine (10 mg/kg) and did not occur in mice lacking either kappa opioid receptors (KOR  / ) or <strong>prodynorphin</strong> (Dyn  / ).
+PDYN	drug	nicotine	18361441	Dynorphin and <strong>prodynorphin</strong> mRNA changes in the striatum during <b>nicotine</b> withdrawal.
+PDYN	addiction	withdrawal	18361441	Dynorphin and <strong>prodynorphin</strong> mRNA changes in the striatum during nicotine <b>withdrawal</b>.
+PDYN	drug	nicotine	18361441	Mice were administered <b>nicotine</b>, 2 mg/kg, s.c., four times daily for 14 days, and Dyn and <strong>prodynorphin</strong> (PD) mRNA estimated in selective brain regions at various times (30 min to 96 h) following drug discontinuation.
+PDYN	drug	opioid	18184800	We examined polymorphisms of proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>) genes in relation to <b>heroin</b> abuse and gene expression in the human striatum and the relevance of genetic dopaminergic tone, critical for drug reward and striatal function.
+PDYN	addiction	reward	18184800	We examined polymorphisms of proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>) genes in relation to heroin abuse and gene expression in the human striatum and the relevance of genetic dopaminergic tone, critical for drug <b>reward</b> and striatal function.
+PDYN	drug	opioid	18184800	We examined polymorphisms of proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) genes in relation to <b>heroin</b> abuse and gene expression in the human striatum and the relevance of genetic dopaminergic tone, critical for drug reward and striatal function.
+PDYN	addiction	reward	18184800	We examined polymorphisms of proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) genes in relation to heroin abuse and gene expression in the human striatum and the relevance of genetic dopaminergic tone, critical for drug <b>reward</b> and striatal function.
+PDYN	drug	opioid	18184800	In contrast to PENK, no association was detected between <strong>PDYN</strong> genotype (68 bp repeat element containing one to four copies of AP 1 binding sites in the promoter region) and <b>heroin</b> abuse, although there was a clear functional association with striatal <strong>PDYN</strong> mRNA expression: an increased number of inducible repeats (three and four) correlated with higher <strong>PDYN</strong> levels than adult or fetal subjects with noninducible (one and two) alleles.
+PDYN	drug	amphetamine	18093743	The expression patterns of nerve growth factor inducible clone A (NGFI A), secretogranin, post synaptic density protein of 95 Kd (PSD 95), <strong>prodynorphin</strong> and proenkephalin mRNA were also analyzed using in situ hybridization, after the challenge with <b>amphetamine</b>.
+PDYN	drug	opioid	17934066	We observed a significant decrease in the expression of <b>opioid</b> peptide precursors (proopiomelanocortin, proenkephalin, and <strong>prodynorphin</strong>) and of the kappa <b>opioid</b> receptor after 48 and 72 h of EtOH exposure (10 and 40 mM).
+PDYN	drug	opioid	17934066	We observed the same pattern of changes for <strong>prodynorphin</strong>, proenkephalin, and the kappa <b>opioid</b> receptor as after 72 h exposure to EtOH.
+PDYN	drug	opioid	17619861	Cotreatment with the kappa <b>opioid</b> agonist U69593 enhances locomotor sensitization to the D2/D3 dopamine agonist quinpirole and alters dopamine D2 receptor and <strong>prodynorphin</strong> mRNA expression in rats.
+PDYN	addiction	sensitization	17619861	Cotreatment with the kappa opioid agonist U69593 enhances locomotor <b>sensitization</b> to the D2/D3 dopamine agonist quinpirole and alters dopamine D2 receptor and <strong>prodynorphin</strong> mRNA expression in rats.
+PDYN	drug	opioid	17619861	Gene expression of D1 and D2 receptors (D1R and D2R), the DA transporter, as well as the endogenous <b>opioid</b> <strong>prodynorphin</strong> (DYN), in the basal ganglia was examined by in situ hybridization in rats after one or ten drug injections.
+PDYN	drug	alcohol	17559549	<strong>Prodynorphin</strong> gene promoter repeat associated with cocaine/<b>alcohol</b> codependence.
+PDYN	drug	cocaine	17559549	<strong>Prodynorphin</strong> gene promoter repeat associated with <b>cocaine</b>/alcohol codependence.
+PDYN	drug	alcohol	17503481	In an earlier study, we reported that variation in the genes encoding the kappa opioid receptor (OPRK1) and its peptide ligand (<strong>PDYN</strong>) were associated with the risk for <b>alcoholism</b>.
+PDYN	drug	opioid	17503481	In an earlier study, we reported that variation in the genes encoding the kappa <b>opioid</b> receptor (OPRK1) and its peptide ligand (<strong>PDYN</strong>) were associated with the risk for alcoholism.
+PDYN	drug	opioid	17493673	Therefore, in the present study, we assessed activity levels, emotionality, sensitivity to the effects of <b>morphine</b>, as well as expression of proenkephalin and <strong>prodynorphin</strong> in several brain regions in 35 and 90 day old male mice, subjected to postnatal manipulation consisting in brief exposures to clean bedding (CB).
+PDYN	drug	opioid	17467916	In contrast gene deletion of either proenkephalin or <strong>prodynorphin</strong> <b>opioids</b> did not block the effects of pSNL.
+PDYN	drug	cocaine	17055175	It has been shown that chronic <b>cocaine</b> increases <strong>prodynorphin</strong> mRNA in the caudate putamen and decreases it in the hypothalamus.
+PDYN	drug	opioid	17055175	In addition, treatment with a kappa <b>opioid</b> receptor agonist produced the opposite effect on <strong>prodynorphin</strong> gene expression in these brain regions and also evoked a decrease in the hippocampus.
+PDYN	drug	opioid	17055175	The serotonin system has also been shown to regulate dynorphin gene expression and a continuous infusion of fluoxetine induced <strong>prodynorphin</strong> gene expression in the same pattern as the kappa <b>opioid</b> agonist (+)(5a,7a,8b) N methyl N [7 (1 pyrrolidinyl) 1 oxaspiro[4.5]dec 8 yl] benzeneacetamide (U 69593) in the brain regions investigated.
+PDYN	drug	cocaine	17055175	To determine whether serotonin plays a role in the regulation of <strong>prodynorphin</strong> mRNA by kappa opioid agonists or <b>cocaine</b>, rats were treated with the serotonin depleter parachloroamphetamine (PCA).
+PDYN	drug	opioid	17055175	To determine whether serotonin plays a role in the regulation of <strong>prodynorphin</strong> mRNA by kappa <b>opioid</b> agonists or cocaine, rats were treated with the serotonin depleter parachloroamphetamine (PCA).
+PDYN	drug	cocaine	17055175	Beginning 24 h later, rats were treated with the selective kappa opioid agonist U 69593 for 5 days or continuously with <b>cocaine</b> for 7 days and <strong>prodynorphin</strong> mRNA was measured.
+PDYN	drug	opioid	17055175	Beginning 24 h later, rats were treated with the selective kappa <b>opioid</b> agonist U 69593 for 5 days or continuously with cocaine for 7 days and <strong>prodynorphin</strong> mRNA was measured.
+PDYN	drug	cocaine	17055175	Subsequent to PCA administration the effects of U 69593 or <b>cocaine</b> on <strong>prodynorphin</strong> mRNA were differentially affected across brain regions.
+PDYN	drug	cocaine	17055175	In contrast, in the hippocampus, the decrease in <strong>prodynorphin</strong> mRNA produced by U 69593 was no longer evident after PCA and <b>cocaine</b>, which previously had no effect, now increased it in the serotonin depleted group.
+PDYN	drug	cocaine	17055175	These findings suggest that serotonin is necessary to maintain normal levels of dynorphin mRNA in all of the investigated brain areas and that the regulation of <strong>prodynorphin</strong> mRNA expression by chronic treatment with a kappa opioid receptor agonist or <b>cocaine</b> requires serotonin in the hippocampus, but not in the hypothalamus or caudate putamen.
+PDYN	drug	opioid	17055175	These findings suggest that serotonin is necessary to maintain normal levels of dynorphin mRNA in all of the investigated brain areas and that the regulation of <strong>prodynorphin</strong> mRNA expression by chronic treatment with a kappa <b>opioid</b> receptor agonist or cocaine requires serotonin in the hippocampus, but not in the hypothalamus or caudate putamen.
+PDYN	drug	alcohol	16924269	We genotyped SNPs throughout OPRK1, encoding the kappa opioid receptor, and <strong>PDYN</strong>, which encodes its ligand prodynorphin, in a group of 1860 European American individuals from 219 multiplex <b>alcohol</b> dependent families.
+PDYN	drug	opioid	16924269	We genotyped SNPs throughout OPRK1, encoding the kappa <b>opioid</b> receptor, and <strong>PDYN</strong>, which encodes its ligand prodynorphin, in a group of 1860 European American individuals from 219 multiplex alcohol dependent families.
+PDYN	drug	alcohol	16924269	We genotyped SNPs throughout OPRK1, encoding the kappa opioid receptor, and <strong>PDYN</strong>, which encodes its ligand <strong>prodynorphin</strong>, in a group of 1860 European American individuals from 219 multiplex <b>alcohol</b> dependent families.
+PDYN	drug	opioid	16924269	We genotyped SNPs throughout OPRK1, encoding the kappa <b>opioid</b> receptor, and <strong>PDYN</strong>, which encodes its ligand <strong>prodynorphin</strong>, in a group of 1860 European American individuals from 219 multiplex alcohol dependent families.
+PDYN	drug	alcohol	16924269	Family based analyses demonstrated associations between <b>alcohol</b> dependence and multiple SNPs in the promoter and 3' end of <strong>PDYN</strong>, and in intron 2 of OPRK1.
+PDYN	addiction	dependence	16924269	Family based analyses demonstrated associations between alcohol <b>dependence</b> and multiple SNPs in the promoter and 3' end of <strong>PDYN</strong>, and in intron 2 of OPRK1.
+PDYN	drug	alcohol	16924269	Thus, variations in the genes encoding both the kappa opioid receptor and its ligand, OPRK1 and <strong>PDYN</strong>, are associated with the risk for <b>alcohol</b> dependence; this makes biological sense as variations in either should affect signaling through the kappa opioid system.
+PDYN	drug	opioid	16924269	Thus, variations in the genes encoding both the kappa <b>opioid</b> receptor and its ligand, OPRK1 and <strong>PDYN</strong>, are associated with the risk for alcohol dependence; this makes biological sense as variations in either should affect signaling through the kappa <b>opioid</b> system.
+PDYN	addiction	dependence	16924269	Thus, variations in the genes encoding both the kappa opioid receptor and its ligand, OPRK1 and <strong>PDYN</strong>, are associated with the risk for alcohol <b>dependence</b>; this makes biological sense as variations in either should affect signaling through the kappa opioid system.
+PDYN	drug	opioid	16861108	Alterations in <strong>prodynorphin</strong> gene expression and dynorphin levels in different brain regions after chronic administration of 14 methoxymetopon and <b>oxycodone</b> 6 oxime.
+PDYN	drug	opioid	16861108	It was also reported that <b>morphine</b> decreased the <strong>prodynorphin</strong> gene expression in the rat hippocampus, striatum and hypothalamus.
+PDYN	drug	opioid	16861108	In this study, we determined the <strong>prodynorphin</strong> gene expression and dynorphin levels in selected brain regions of <b>opioid</b> tolerant rats.
+PDYN	drug	opioid	16861108	We found that in the striatum <b>morphine</b> decreased, while <b>oxycodone</b> 6 oxime increased and 14 methoxymetopon did not alter the <strong>prodynorphin</strong> gene expression.
+PDYN	drug	opioid	16861108	In the nucleus accumbens, <b>morphine</b> and <b>oxycodone</b> 6 oxime did not change, while 14 methoxymetopon increased the <strong>prodynorphin</strong> gene expression.
+PDYN	drug	opioid	16861108	In the hippocampus both <b>oxycodone</b> 6 oxime and 14 methoxymetopon enhanced, whereas <b>morphine</b> did not alter the <strong>prodynorphin</strong> gene expression.
+PDYN	drug	opioid	16861108	In the rat striatum only <b>oxycodone</b> 6 oxime increased dynorphin levels significantly in accordance with the <strong>prodynorphin</strong> mRNA changes.
+PDYN	drug	opioid	16861108	In the hippocampus both <b>opioid</b> agonists increased the dynorphin levels significantly similarly to the augmented <strong>prodynorphin</strong> gene expression.
+PDYN	drug	opioid	16861108	Since the endogenous <strong>prodynorphin</strong> system may play a modulatory role in the development of <b>opioid</b> tolerance, the elevated supraspinal dynorphin levels appear to be partly responsible for the reduced degree of tolerance induced by the investigated <b>opioids</b>.
+PDYN	drug	amphetamine	16529859	Genetic variant of <strong>prodynorphin</strong> gene is risk factor for <b>methamphetamine</b> dependence.
+PDYN	addiction	dependence	16529859	Genetic variant of <strong>prodynorphin</strong> gene is risk factor for methamphetamine <b>dependence</b>.
+PDYN	drug	opioid	16529859	Prodynorphin (<strong>PDYN</strong>) is an <b>opioid</b> peptide precursor that yields dynorphins, endogenous kappa <b>opioid</b> receptor agonists that play important roles in substance abuse.
+PDYN	drug	opioid	16529859	<strong>Prodynorphin</strong> (<strong>PDYN</strong>) is an <b>opioid</b> peptide precursor that yields dynorphins, endogenous kappa <b>opioid</b> receptor agonists that play important roles in substance abuse.
+PDYN	drug	amphetamine	16529859	We analyzed this polymorphism of the <strong>PDYN</strong> gene by a case control association study in 143 patients with <b>methamphetamine</b> dependence and 209 healthy controls in the Japanese population.
+PDYN	addiction	dependence	16529859	We analyzed this polymorphism of the <strong>PDYN</strong> gene by a case control association study in 143 patients with methamphetamine <b>dependence</b> and 209 healthy controls in the Japanese population.
+PDYN	drug	amphetamine	16529859	A 3  or 4 repeat allele in the <strong>PDYN</strong> gene promoter was found significantly more frequently in patients with <b>methamphetamine</b> dependence than in controls (chi(2)=9.45, p=0.0021).
+PDYN	addiction	dependence	16529859	A 3  or 4 repeat allele in the <strong>PDYN</strong> gene promoter was found significantly more frequently in patients with methamphetamine <b>dependence</b> than in controls (chi(2)=9.45, p=0.0021).
+PDYN	drug	amphetamine	16529859	A 3  or 4 repeat allele in the <strong>PDYN</strong> gene promoter, which was shown to produce significantly higher transcription activity of the <strong>PDYN</strong> gene than a 1  or 2 repeat allele, is a genetic risk factor for development of <b>methamphetamine</b> dependence (odds ratio: 1.83, 95% CI=1.24 2.68).
+PDYN	addiction	dependence	16529859	A 3  or 4 repeat allele in the <strong>PDYN</strong> gene promoter, which was shown to produce significantly higher transcription activity of the <strong>PDYN</strong> gene than a 1  or 2 repeat allele, is a genetic risk factor for development of methamphetamine <b>dependence</b> (odds ratio: 1.83, 95% CI=1.24 2.68).
+PDYN	drug	cocaine	16412997	Contingency does not contribute to the effects of <b>cocaine</b> self administration on <strong>prodynorphin</strong> and proenkephalin gene expression in the rat forebrain.
+PDYN	drug	opioid	16412997	Although regulation of the gene expression of the <b>opioid</b> propeptides proenkephalin (PENK) and prodynorphin (<strong>PDYN</strong>) by psychostimulants has previously been described, little attention has been paid to dissociating effects of pharmacological actions of the drugs from those produced by motivational processes driving active drug intake in self administration paradigms.
+PDYN	drug	opioid	16412997	Although regulation of the gene expression of the <b>opioid</b> propeptides proenkephalin (PENK) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) by psychostimulants has previously been described, little attention has been paid to dissociating effects of pharmacological actions of the drugs from those produced by motivational processes driving active drug intake in self administration paradigms.
+PDYN	drug	cocaine	16412997	In the present study, effects of response dependent (contingent) and response independent (noncontingent) <b>cocaine</b> administration on the PENK and <strong>PDYN</strong> gene expression in the rat forebrain have been directly compared using the "yoked" self administration procedure.
+PDYN	drug	cocaine	16412997	In situ hybridization analysis revealed that levels of the <strong>PDYN</strong> mRNA were significantly increased in the caudate/putamen, to the same extent in rats self administering <b>cocaine</b> as in animals receiving noncontingent injections of the drug at the same frequency and dosage.
+PDYN	drug	cocaine	16412997	The obtained data indicate that up regulation of the <strong>PDYN</strong> gene expression in the caudate/putamen results from direct pharmacological actions of <b>cocaine</b> rather than from the motivational and cognitive processes underlying active self administration of the drug.
+PDYN	drug	opioid	16314761	A functional <strong>prodynorphin</strong> promoter polymorphism and <b>opioid</b> dependence.
+PDYN	addiction	dependence	16314761	A functional <strong>prodynorphin</strong> promoter polymorphism and opioid <b>dependence</b>.
+PDYN	drug	opioid	16314761	These data suggest that the <strong>PDYN</strong> repeat polymorphism should be studied in additional <b>opioid</b> dependent populations.
+PDYN	drug	opioid	16289352	We studied the effects of single and repeated 3,4 methylenedioxy N methylamphetamine ('Ecstasy') on the gene expression of the <b>opioid</b> precursor <strong>prodynorphin</strong>, and on the levels of peptide dynorphin A in the rat brain.
+PDYN	drug	psychedelics	16289352	We studied the effects of single and repeated 3,4 methylenedioxy N methylamphetamine ('<b>Ecstasy</b>') on the gene expression of the opioid precursor <strong>prodynorphin</strong>, and on the levels of peptide dynorphin A in the rat brain.
+PDYN	drug	cocaine	16184603	Confirmation of the association between a polymorphism in the promoter region of the <strong>prodynorphin</strong> gene and <b>cocaine</b> dependence.
+PDYN	addiction	dependence	16184603	Confirmation of the association between a polymorphism in the promoter region of the <strong>prodynorphin</strong> gene and cocaine <b>dependence</b>.
+PDYN	drug	cocaine	16184603	It has recently been reported that the variable nucleotide tandem repeat (VNTR) polymorphism in the 5' promoter region of the <strong>prodynorphin</strong> gene, which encodes the precursor for three endogenous opioid peptides, is associated with the <b>cocaine</b> dependent phenotype.
+PDYN	drug	opioid	16184603	It has recently been reported that the variable nucleotide tandem repeat (VNTR) polymorphism in the 5' promoter region of the <strong>prodynorphin</strong> gene, which encodes the precursor for three endogenous <b>opioid</b> peptides, is associated with the cocaine dependent phenotype.
+PDYN	drug	cocaine	16184603	In order to confirm this finding, we genotyped the <strong>prodynorphin</strong> promoter polymorphism in <b>cocaine</b> dependent (n = 167) and control (n = 88) individuals of African descent.
+PDYN	drug	cocaine	16184603	The results from this experiment indicate a statistically significant (chi2 = 5.64, OR = 1.59, P = 0.018) association between the <strong>prodynorphin</strong> promoter VNTR polymorphism and the <b>cocaine</b> dependent phenotype.
+PDYN	drug	cocaine	16184603	In contrast to previous work showing increased risk conferred by one or two copies of the <strong>prodynorphin</strong> VNTR, the genotyping results from this study indicate that persons with three or four copies of this polymorphism are more likely to become <b>cocaine</b> dependent.
+PDYN	drug	cocaine	16184603	This disparity suggests that the <strong>prodynorphin</strong> promoter VNTR may not be the functional polymorphism associating with the <b>cocaine</b> dependent phenotype.
+PDYN	drug	opioid	16123746	Previous studies have demonstrated that repeated forced swim stress induced behaviors (including analgesia, immobility, and increased drug reward) were mediated by the release of endogenous <strong>prodynorphin</strong> derived <b>opioid</b> peptides and subsequent activation of the kappa <b>opioid</b> receptor (KOR).
+PDYN	addiction	reward	16123746	Previous studies have demonstrated that repeated forced swim stress induced behaviors (including analgesia, immobility, and increased drug <b>reward</b>) were mediated by the release of endogenous <strong>prodynorphin</strong> derived opioid peptides and subsequent activation of the kappa opioid receptor (KOR).
+PDYN	drug	cocaine	16123746	Consistent with this result, mice lacking the <strong>prodynorphin</strong> gene did not show stress induced potentiation of <b>cocaine</b> CPP, whereas wild type littermates did.
+PDYN	addiction	reward	16123746	Consistent with this result, mice lacking the <strong>prodynorphin</strong> gene did not show stress induced potentiation of cocaine <b>CPP</b>, whereas wild type littermates did.
+PDYN	drug	opioid	15976090	In addition, we examined two genes (<strong>prodynorphin</strong> and FK506 binding protein 5) that are strongly regulated by chronic <b>morphine</b> or <b>morphine</b> withdrawal in the LC for their role in regulating withdrawal associated behaviors.
+PDYN	addiction	withdrawal	15976090	In addition, we examined two genes (<strong>prodynorphin</strong> and FK506 binding protein 5) that are strongly regulated by chronic morphine or morphine <b>withdrawal</b> in the LC for their role in regulating <b>withdrawal</b> associated behaviors.
+PDYN	addiction	withdrawal	15869750	Previous data demonstrated significant increases in whole brain prodynorphin (<strong>Pdyn</strong>) mRNA in WSP mice only during EtOH <b>withdrawal</b>.
+PDYN	addiction	withdrawal	15869750	Previous data demonstrated significant increases in whole brain <strong>prodynorphin</strong> (<strong>Pdyn</strong>) mRNA in WSP mice only during EtOH <b>withdrawal</b>.
+PDYN	addiction	withdrawal	15869750	The present study characterized <strong>Pdyn</strong> mRNA and the KOP R in WSP and WSR mice during EtOH <b>withdrawal</b> using in situ hybridization (ISH) and KOP R autoradiography.
+PDYN	addiction	withdrawal	15869750	ISH analyses confirmed previous findings; EtOH <b>withdrawal</b> increased <strong>Pdyn</strong> mRNA in multiple brain regions of WSP mice, but not WSR.
+PDYN	drug	cocaine	15869520	The results also demonstrate that <b>cocaine</b> administration increases the expression of MC4 R in the nucleus accumbens and striatum, and that MC4 R is co localized with <strong>prodynorphin</strong> in medium spiny neurons in the nucleus accumbens.
+PDYN	drug	cocaine	15857718	Second, we examined the effects of repeated <b>cocaine</b> administration on locomotor activity, dopamine overflow and striatal <strong>prodynorphin</strong> mRNA expression.
+PDYN	drug	cocaine	15857718	Postmortem analyses of striatal <strong>prodynorphin</strong> mRNA expression (using in situ hybridization histochemistry) revealed a differentiated response to the <b>cocaine</b> exposure.
+PDYN	drug	cocaine	15857718	In contrast to control FRL rats, the FSL rats showed no typical <b>cocaine</b> evoked elevation of <strong>prodynorphin</strong> mRNA levels in rostral subregions of the striatum whereas both strains expressed increased <strong>prodynorphin</strong> mRNA levels in the caudal striatum after <b>cocaine</b> administration.
+PDYN	drug	alcohol	15266465	state.vt.su/adap/cork], <b>Alcohol</b> and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF  VIC) [www.adf.org.au], Centre for Education and Information on Drugs and <b>Alcohol</b> (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug Dependence Inc. proceedings, the reference lists of all identified studies and published reviews and authors of identified RCT's were asked about any other published or unpublished relevant RCT.
+PDYN	addiction	dependence	15266465	state.vt.su/adap/cork], Alcohol and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF  VIC) [www.adf.org.au], Centre for Education and Information on Drugs and Alcohol (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug <b>Dependence</b> Inc. proceedings, the reference lists of all identified studies and published reviews and authors of identified RCT's were asked about any other published or unpublished relevant RCT.
+PDYN	drug	opioid	15182311	DREAM (downstream regulatory element antagonistic modulator) is a novel transcriptional repressor for the <strong>prodynorphin</strong> gene, and genetic deletion of DREAM in mice results in a phenotype of ongoing analgesia by virtue of its effect on <b>opioid</b> gene expression.
+PDYN	drug	opioid	14525992	Cloning and characterization of Xen dorphin prohormone from Xenopus laevis: a new <b>opioid</b> like prohormone distinct from proenkephalin and <strong>prodynorphin</strong>.
+PDYN	drug	opioid	12843270	Kappa <b>opioid</b> receptor antagonism and <strong>prodynorphin</strong> gene disruption block stress induced behavioral responses.
+PDYN	drug	opioid	12843270	Previous studies have demonstrated that stress may increase <strong>prodynorphin</strong> gene expression, and kappa <b>opioid</b> agonists suppress drug reward.
+PDYN	addiction	reward	12843270	Previous studies have demonstrated that stress may increase <strong>prodynorphin</strong> gene expression, and kappa opioid agonists suppress drug <b>reward</b>.
+PDYN	drug	cocaine	12843270	Consistent with this result, mice lacking the <strong>prodynorphin</strong> gene did not show a stress induced potentiation of <b>cocaine</b> CPP, whereas wild type littermates did.
+PDYN	addiction	reward	12843270	Consistent with this result, mice lacking the <strong>prodynorphin</strong> gene did not show a stress induced potentiation of cocaine <b>CPP</b>, whereas wild type littermates did.
+PDYN	drug	alcohol	12804430	state.vt.su/adap/cork], <b>Alcohol</b> and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF VIC) [www.adf.org.au], Centre for Education and Information on Drugs and <b>Alcohol</b> (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug Dependence Inc. proceedings, the reference lists of all identified studies and published reviews; authors of identified RCTs were asked about other published or unpublished relevant RCTs.
+PDYN	addiction	dependence	12804430	state.vt.su/adap/cork], Alcohol and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF VIC) [www.adf.org.au], Centre for Education and Information on Drugs and Alcohol (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug <b>Dependence</b> Inc. proceedings, the reference lists of all identified studies and published reviews; authors of identified RCTs were asked about other published or unpublished relevant RCTs.
+PDYN	drug	alcohol	12804429	state.vt.su/adap/cork], <b>Alcohol</b> and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF  VIC) [www.adf.org.au], Centre for Education and Information on Drugs and <b>Alcohol</b> (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug Dependence Inc. proceedings, the reference lists of all identified studies and published reviews and authors of identified RCT's were asked about any other published or unpublished relevant RCT.
+PDYN	addiction	dependence	12804429	state.vt.su/adap/cork], Alcohol and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF  VIC) [www.adf.org.au], Centre for Education and Information on Drugs and Alcohol (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug <b>Dependence</b> Inc. proceedings, the reference lists of all identified studies and published reviews and authors of identified RCT's were asked about any other published or unpublished relevant RCT.
+PDYN	drug	cocaine	12786988	Temporal upregulation of <strong>prodynorphin</strong> mRNA in the primate striatum after <b>cocaine</b> self administration.
+PDYN	drug	cocaine	12786988	In the current study, prodynorphin (<strong>PDYN</strong>) mRNA expression was examined in monkeys at initial and chronic phases of <b>cocaine</b> self administration.
+PDYN	drug	cocaine	12786988	In the current study, <strong>prodynorphin</strong> (<strong>PDYN</strong>) mRNA expression was examined in monkeys at initial and chronic phases of <b>cocaine</b> self administration.
+PDYN	drug	cocaine	12786988	Moreover, <b>cocaine</b> self administration failed to alter the <strong>PDYN</strong> mRNA expression in high  or low expressing <strong>PDYN</strong> cell populations in the nucleus accumbens during any condition studied.
+PDYN	addiction	dependence	12786988	In addition, the temporal nature of the changes in <strong>PDYN</strong> gene expression within the striatal compartments could reflect a change in drug responsivity that occurs during the transition to drug <b>dependence</b>.
+PDYN	drug	cocaine	12581184	In this study we have compared the time course of striatal FosB/DeltaFosB like immunoreactivity and <strong>prodynorphin</strong> mRNA expression after discontinuation of chronic <b>cocaine</b> treatment to intact rats and chronic L DOPA treatment to unilaterally 6 hydroxydopamine (6 OHDA) lesioned rats.
+PDYN	drug	cocaine	12581184	The concomitant upregulation of <strong>prodynorphin</strong> mRNA, a target of DeltaFosB, paralleled the time course of DeltaFosB like immunoreactivity in the 6 OHDA lesion/L DOPA model, but was more transient in animals treated with <b>cocaine</b>.
+PDYN	drug	amphetamine	12542667	In contrast, it suppressed the increase in <strong>prodynorphin</strong> and substance P mRNA expression induced by <b>methamphetamine</b>.
+PDYN	drug	amphetamine	12523490	Effect of cocaine and <b>amphetamine</b> on biosynthesis of proenkephalin and <strong>prodynorphin</strong> in some regions of the rat limbic system.
+PDYN	drug	cocaine	12523490	Effect of <b>cocaine</b> and amphetamine on biosynthesis of proenkephalin and <strong>prodynorphin</strong> in some regions of the rat limbic system.
+PDYN	drug	amphetamine	12523490	The goal of the present study was to investigate the influence of acutely and chronically administered drugs of abuse, cocaine and <b>amphetamine</b> on biosynthesis of <strong>prodynorphin</strong> and proenkephalin in the rat amygdala, the structure involved in the mechanism of drug addiction.
+PDYN	drug	cocaine	12523490	The goal of the present study was to investigate the influence of acutely and chronically administered drugs of abuse, <b>cocaine</b> and amphetamine on biosynthesis of <strong>prodynorphin</strong> and proenkephalin in the rat amygdala, the structure involved in the mechanism of drug addiction.
+PDYN	addiction	addiction	12523490	The goal of the present study was to investigate the influence of acutely and chronically administered drugs of abuse, cocaine and amphetamine on biosynthesis of <strong>prodynorphin</strong> and proenkephalin in the rat amygdala, the structure involved in the mechanism of drug <b>addiction</b>.
+PDYN	drug	cocaine	12523490	In contrast, the level of <strong>prodynorphin</strong> mRNA was significantly increased in this structure after <b>cocaine</b>.
+PDYN	drug	cocaine	12523490	Repeated <b>cocaine</b> administration (20 mg/kg ip every hour for 3 h, for 5 days) had no effect on the proenkephalin and <strong>prodynorphin</strong> mRNA in the central nucleus of the amygdala.
+PDYN	drug	amphetamine	12523490	Chronic <b>amphetamine</b> (2.5 mg/kg twice daily for 5 days) administration decreased proenkephalin and increased <strong>prodynorphin</strong> mRNA level in the central nucleus of the amygdala (at 24 and 48 h).
+PDYN	drug	amphetamine	12523490	Moreover, significant increase in <strong>prodynorphin</strong> mRNA level was observed in the hippocampal dentate gyrus after acute (cocaine) and chronic (cocaine, <b>amphetamine</b>) administration of the psychostimulants.
+PDYN	drug	cocaine	12523490	Moreover, significant increase in <strong>prodynorphin</strong> mRNA level was observed in the hippocampal dentate gyrus after acute (<b>cocaine</b>) and chronic (<b>cocaine</b>, amphetamine) administration of the psychostimulants.
+PDYN	drug	alcohol	12519570	state.vt.su/adap/cork], <b>Alcohol</b> and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF VIC) [www.adf.org.au], Centre for Education and Information on Drugs and <b>Alcohol</b> (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug Dependence Inc. proceedings, the reference lists of all identified studies and published reviews; authors of identified RCTs were asked about other published or unpublished relevant RCTs.
+PDYN	addiction	dependence	12519570	state.vt.su/adap/cork], Alcohol and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF VIC) [www.adf.org.au], Centre for Education and Information on Drugs and Alcohol (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug <b>Dependence</b> Inc. proceedings, the reference lists of all identified studies and published reviews; authors of identified RCTs were asked about other published or unpublished relevant RCTs.
+PDYN	drug	alcohol	12519569	state.vt.su/adap/cork], <b>Alcohol</b> and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF  VIC) [www.adf.org.au], Centre for Education and Information on Drugs and <b>Alcohol</b> (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug Dependence Inc. proceedings, the reference lists of all identified studies and published reviews and authors of identified RCT's were asked about any other published or unpublished relevant RCT.
+PDYN	addiction	dependence	12519569	state.vt.su/adap/cork], Alcohol and Drug Council of Australia (<strong>ADCA</strong>) [www.<strong>adca</strong>.org.au], Australian Drug Foundation (ADF  VIC) [www.adf.org.au], Centre for Education and Information on Drugs and Alcohol (CEIDA) [www.ceida.net.au], Australian Bibliographic Network (ABN), and Library of Congress databases, available NIDA monographs and the College on Problems of Drug <b>Dependence</b> Inc. proceedings, the reference lists of all identified studies and published reviews and authors of identified RCT's were asked about any other published or unpublished relevant RCT.
+PDYN	drug	opioid	12015197	The endogenous <b>opioid</b> system consists of three <b>opioid</b> peptide precursor genes encoding enkephalins (preproenkephalin, Penk), dynorphins (preprodynorphin, <strong>Pdyn</strong>) and beta endorphin (betaend), proopiomelanocortin (POMC) and three receptor genes encoding mu opiod receptor (MOR), delta opiod receptor (DOR) and kappa opiod receptor (KOR).
+PDYN	drug	cocaine	11992566	Potentially functional polymorphism in the promoter region of <strong>prodynorphin</strong> gene may be associated with protection against <b>cocaine</b> dependence or abuse.
+PDYN	addiction	dependence	11992566	Potentially functional polymorphism in the promoter region of <strong>prodynorphin</strong> gene may be associated with protection against cocaine <b>dependence</b> or abuse.
+PDYN	drug	cocaine	11992566	Our results suggest that this allelic variation at the promoter region of the <strong>prodynorphin</strong> gene (alleles with three or four repeats), which may result in enhanced transcription of the gene, may contribute to relative protection and decrease individual vulnerability to develop <b>cocaine</b> dependence or abuse.
+PDYN	addiction	dependence	11992566	Our results suggest that this allelic variation at the promoter region of the <strong>prodynorphin</strong> gene (alleles with three or four repeats), which may result in enhanced transcription of the gene, may contribute to relative protection and decrease individual vulnerability to develop cocaine <b>dependence</b> or abuse.
+PDYN	drug	cannabinoid	11717384	The involvement of dynorphin on Delta 9 <b>tetrahydrocannabinol</b> (<b>THC</b>) and morphine responses has been investigated by using mice with a targeted inactivation of the prodynorphin (<strong>Pdyn</strong>) gene.
+PDYN	drug	opioid	11717384	The involvement of dynorphin on Delta 9 tetrahydrocannabinol (THC) and <b>morphine</b> responses has been investigated by using mice with a targeted inactivation of the prodynorphin (<strong>Pdyn</strong>) gene.
+PDYN	drug	cannabinoid	11717384	The involvement of dynorphin on Delta 9 <b>tetrahydrocannabinol</b> (<b>THC</b>) and morphine responses has been investigated by using mice with a targeted inactivation of the <strong>prodynorphin</strong> (<strong>Pdyn</strong>) gene.
+PDYN	drug	opioid	11717384	The involvement of dynorphin on Delta 9 tetrahydrocannabinol (THC) and <b>morphine</b> responses has been investigated by using mice with a targeted inactivation of the <strong>prodynorphin</strong> (<strong>Pdyn</strong>) gene.
+PDYN	drug	alcohol	10871698	Elevated <strong>prodynorphin</strong> expression associated with <b>ethanol</b> withdrawal convulsions.
+PDYN	addiction	withdrawal	10871698	Elevated <strong>prodynorphin</strong> expression associated with ethanol <b>withdrawal</b> convulsions.
+PDYN	drug	alcohol	10871698	The data revealed significantly increased levels of <strong>prodynorphin</strong> mRNA expression in mice susceptible to <b>ethanol</b> withdrawal convulsions after withdrawal, with no corresponding increase in <strong>prodynorphin</strong> steady state levels in mice resistant to <b>ethanol</b> withdrawal convulsions.
+PDYN	addiction	withdrawal	10871698	The data revealed significantly increased levels of <strong>prodynorphin</strong> mRNA expression in mice susceptible to ethanol <b>withdrawal</b> convulsions after <b>withdrawal</b>, with no corresponding increase in <strong>prodynorphin</strong> steady state levels in mice resistant to ethanol <b>withdrawal</b> convulsions.
+PDYN	drug	alcohol	10871698	These results extend our understanding of <strong>prodynorphin</strong>'s role in generalized seizure activity to include <b>ethanol</b> withdrawal induced convulsions.
+PDYN	addiction	withdrawal	10871698	These results extend our understanding of <strong>prodynorphin</strong>'s role in generalized seizure activity to include ethanol <b>withdrawal</b> induced convulsions.
+PDYN	drug	alcohol	10871698	Our findings suggest that <strong>prodynorphin</strong> expression is modulated during <b>ethanol</b> withdrawal convulsions, or alternatively, <strong>prodynorphin</strong> may mediate the severity of <b>ethanol</b> withdrawal convulsions.
+PDYN	addiction	withdrawal	10871698	Our findings suggest that <strong>prodynorphin</strong> expression is modulated during ethanol <b>withdrawal</b> convulsions, or alternatively, <strong>prodynorphin</strong> may mediate the severity of ethanol <b>withdrawal</b> convulsions.
+PDYN	addiction	addiction	10821116	In situ hybridization was used to compare the content of proopiomelanocortin, proenkephalin and <strong>prodynorphin</strong> mRNA in distinct brain regions known to be involved in the reinforcing properties of <b>addictive</b> drugs, between rats from each line.
+PDYN	addiction	reward	10821116	In situ hybridization was used to compare the content of proopiomelanocortin, proenkephalin and <strong>prodynorphin</strong> mRNA in distinct brain regions known to be involved in the <b>reinforcing</b> properties of addictive drugs, between rats from each line.
+PDYN	drug	opioid	10646497	<strong>Prodynorphin</strong>, the precursor of the dynorphin <b>opioid</b> peptides, has been shown to play an important role in several aspects of human diseases and complex traits, e.g., drug abuse, epilepsy, and mood disorders.
+PDYN	addiction	addiction	10646497	Dynorphin was found to be involved in many pathophysiological processes so that the described <strong>prodynorphin</strong> alleles may correlate with the occurrence of several diseases, for example, drug <b>addiction</b>.
+PDYN	drug	opioid	10646497	However, <strong>prodynorphin</strong> allelic distributions were not significantly different in <b>heroin</b> addicts and control subjects.
+PDYN	drug	cocaine	10415667	We have used the techniques of in vivo microdialysis to measure and manipulate extracellular concentrations of dopamine in animals that self administer <b>cocaine</b>, and in situ hybridization to study mRNA expression levels of <strong>prodynorphin</strong> and dopamine receptors.
+PDYN	drug	cocaine	10415667	It is clear from these studies that different stages of the <b>cocaine</b> use cycle are characterized by distinct patterns of <strong>prodynorphin</strong> and dopamine D1 mRNA expression levels.
+PDYN	drug	amphetamine	9988101	<b>Methamphetamine</b> alters <strong>prodynorphin</strong> gene expression and dynorphin A levels in rat hypothalamus.
+PDYN	drug	amphetamine	9988101	To better understand the possible existence of common neuronal pathways shared by different classes of drugs of abuse, we studied the effects of <b>methamphetamine</b> on the gene expression of the opioid precursor <strong>prodynorphin</strong> and on the levels of peptide dynorphin A in the rat brain.
+PDYN	drug	opioid	9988101	To better understand the possible existence of common neuronal pathways shared by different classes of drugs of abuse, we studied the effects of methamphetamine on the gene expression of the <b>opioid</b> precursor <strong>prodynorphin</strong> and on the levels of peptide dynorphin A in the rat brain.
+PDYN	drug	amphetamine	9988101	for 15 days) <b>methamphetamine</b> markedly raised <strong>prodynorphin</strong> mRNA levels in the hypothalamus, whereas no effect was observed in the hippocampus.
+PDYN	drug	amphetamine	9988101	These results indicate that <b>methamphetamine</b> affects <strong>prodynorphin</strong> gene expression in the hypothalamus, which may be an important site (also for its relevant neuroendocrine correlates) for opioidergic mechanisms activated by addictive drugs.
+PDYN	addiction	addiction	9988101	These results indicate that methamphetamine affects <strong>prodynorphin</strong> gene expression in the hypothalamus, which may be an important site (also for its relevant neuroendocrine correlates) for opioidergic mechanisms activated by <b>addictive</b> drugs.
+PDYN	drug	opioid	9681945	Effects of repeated psychostimulant administration on the <strong>prodynorphin</strong> system activity and kappa <b>opioid</b> receptor density in the rat brain.
+PDYN	drug	amphetamine	9681945	To elucidate the activity of the endogenous <strong>prodynorphin</strong> system upon treatment with psychostimulants, we investigated the effect of single and repeated cocaine and <b>amphetamine</b> on the <strong>prodynorphin</strong> messenger RNA level, the <strong>prodynorphin</strong> derived peptide alpha neoendorphin tissue level, and its in vitro release in the nucleus accumbens and striatum of rats.
+PDYN	drug	cocaine	9681945	To elucidate the activity of the endogenous <strong>prodynorphin</strong> system upon treatment with psychostimulants, we investigated the effect of single and repeated <b>cocaine</b> and amphetamine on the <strong>prodynorphin</strong> messenger RNA level, the <strong>prodynorphin</strong> derived peptide alpha neoendorphin tissue level, and its in vitro release in the nucleus accumbens and striatum of rats.
+PDYN	drug	cocaine	9681945	As shown by an in situ hybridization study, the <strong>prodynorphin</strong> messenger RNA levels in the nucleus accumbens and striatum were raised following single (at 3 h) and chronic (at 3 and 24 h) <b>cocaine</b> administration.
+PDYN	drug	amphetamine	9681945	The <strong>prodynorphin</strong> messenger RNA level in the nucleus accumbens was markedly elevated after single or repeated <b>amphetamine</b> administration.
+PDYN	drug	amphetamine	9681945	The above data indicate that the <b>amphetamine</b> induced changes were more abundant than those caused by cocaine; only treatment with <b>amphetamine</b> markedly enhanced the release of <strong>prodynorphin</strong> derived peptide.
+PDYN	drug	cocaine	9681945	The above data indicate that the amphetamine induced changes were more abundant than those caused by <b>cocaine</b>; only treatment with amphetamine markedly enhanced the release of <strong>prodynorphin</strong> derived peptide.
+PDYN	drug	opioid	9681945	Furthermore, the psychostimulant induced enhancement of biosynthetic activity of <strong>prodynorphin</strong> neurons was correlated with a marked and persistent decrease in the kappa <b>opioid</b> receptor density at a late withdrawal time.
+PDYN	addiction	withdrawal	9681945	Furthermore, the psychostimulant induced enhancement of biosynthetic activity of <strong>prodynorphin</strong> neurons was correlated with a marked and persistent decrease in the kappa opioid receptor density at a late <b>withdrawal</b> time.
+PDYN	drug	cocaine	9602109	Specific reductions of striatal <strong>prodynorphin</strong> and D1 dopamine receptor messenger RNAs during <b>cocaine</b> abstinence.
+PDYN	drug	opioid	9602109	In the present study, the mRNA expression of the dopamine receptors, D1 and D2, and the <b>opioid</b> peptides, <strong>prodynorphin</strong> and proenkephalin, were analyzed in the rat striatum using in situ hybridization histochemistry.
+PDYN	drug	cocaine	9602109	Acute and intermittent <b>cocaine</b> administration elevated the <strong>prodynorphin</strong> mRNA expression in the dorsal striatum, consistent with previous reports, while the abstinent phase resulted in a significant reduction of <strong>prodynorphin</strong> mRNA levels in the ventrorostral striatum.
+PDYN	drug	cocaine	9602109	These results show long term suppression on <strong>prodynorphin</strong> and D1 receptor systems in specific striatal populations localized mainly in rostral areas during withdrawal from <b>cocaine</b>.
+PDYN	addiction	withdrawal	9602109	These results show long term suppression on <strong>prodynorphin</strong> and D1 receptor systems in specific striatal populations localized mainly in rostral areas during <b>withdrawal</b> from cocaine.
+PDYN	drug	alcohol	9464643	<b>Ethanol</b> withdrawal enhances the <strong>prodynorphin</strong> system activity in the rat nucleus accumbens.
+PDYN	addiction	withdrawal	9464643	Ethanol <b>withdrawal</b> enhances the <strong>prodynorphin</strong> system activity in the rat nucleus accumbens.
+PDYN	drug	alcohol	9464643	An in situ hybridization study showed an increase in the <strong>prodynorphin</strong> mRNA level at 24 and 48 h (by 189 and 146%, respectively) after <b>ethanol</b> withdrawal, whereas the proenkephalin mRNA level remained unchanged.
+PDYN	addiction	withdrawal	9464643	An in situ hybridization study showed an increase in the <strong>prodynorphin</strong> mRNA level at 24 and 48 h (by 189 and 146%, respectively) after ethanol <b>withdrawal</b>, whereas the proenkephalin mRNA level remained unchanged.
+PDYN	addiction	withdrawal	9464643	Furthermore, after a 48 h <b>withdrawal</b> period, the level of alpha neoendorphin (alphaNEO), a <strong>prodynorphin</strong> derived peptide, was significantly decreased (by 48%), that effect being associated with the enhancement of the K+ stimulated release of that peptide from nucleus accumbens slices.
+PDYN	drug	alcohol	9464643	Our data indicate that after 48 h of <b>ethanol</b> withdrawal, <strong>prodynorphin</strong> neurons are highly activated.
+PDYN	addiction	withdrawal	9464643	Our data indicate that after 48 h of ethanol <b>withdrawal</b>, <strong>prodynorphin</strong> neurons are highly activated.
+PDYN	drug	alcohol	9394118	The objective of the present studies was to investigate the presence of differences in (a) the density of kappa opioid binding sites, (b) the content of <strong>prodynorphin</strong> mRNA, and (c) the content of dynorphin peptides in distinct brain regions between the C57BL/6 (<b>ethanol</b> preferring) and the DBA/2 (<b>ethanol</b> avoiding) mice.
+PDYN	drug	opioid	9394118	The objective of the present studies was to investigate the presence of differences in (a) the density of kappa <b>opioid</b> binding sites, (b) the content of <strong>prodynorphin</strong> mRNA, and (c) the content of dynorphin peptides in distinct brain regions between the C57BL/6 (ethanol preferring) and the DBA/2 (ethanol avoiding) mice.
+PDYN	drug	opioid	9394118	Results indicated that the C57BL/6 mice have a higher content of kappa <b>opioid</b> binding sites and dynorphin A 1 13 in the amygdala, and dynorphin A 1 8 in the ventral tegmental area, whereas the DBA/2 mice presented a significantly higher content of kappa <b>opioid</b> binding sites, <strong>prodynorphin</strong> mRNA, as well as dynorphin A 1 13 and dynorphin A 1 8 peptides in the nucleus accumbens and septum.
+PDYN	drug	opioid	9308024	Effects of <b>morphine</b> treatment on <strong>prodynorphin</strong> peptide levels were evaluated and compared with previous findings in decapitated rats.
+PDYN	drug	opioid	9308024	These results indicate tissue specific metabolism of <strong>prodynorphin</strong> peptides and show that metabolism of <b>opioid</b> peptides occurs during the dissection procedure after decapitation of the rat even though precautions are taken to minimize degradation.
+PDYN	drug	cocaine	9030708	<strong>Prodynorphin</strong>, proenkephalin and kappa opioid receptor mRNA responses to acute "binge" <b>cocaine</b>.
+PDYN	drug	opioid	9030708	<strong>Prodynorphin</strong>, proenkephalin and kappa <b>opioid</b> receptor mRNA responses to acute "binge" cocaine.
+PDYN	addiction	intoxication	9030708	<strong>Prodynorphin</strong>, proenkephalin and kappa opioid receptor mRNA responses to acute "<b>binge</b>" cocaine.
+PDYN	drug	opioid	8947935	Using in vitro autoradiography, radioimmunoassays and a solution hybridization mRNA assay, brain regional mu and kappa <b>opioid</b> receptor binding, levels of <strong>prodynorphin</strong> derived peptides, and <strong>prodynorphin</strong> mRNA, respectively, were measured in food restricted and diabetic rats.
+PDYN	addiction	reward	8947935	Changes that could plausibly be involved in <b>reward</b> sensitization are discussed, with emphasis on the increased dynorphin A1 3 and <strong>prodynorphin</strong> mRNA levels in lateral hypothalamic neurons that innervate the pontine parabrachial nucleus, where mu binding decreased and kappa binding increased.
+PDYN	addiction	sensitization	8947935	Changes that could plausibly be involved in reward <b>sensitization</b> are discussed, with emphasis on the increased dynorphin A1 3 and <strong>prodynorphin</strong> mRNA levels in lateral hypothalamic neurons that innervate the pontine parabrachial nucleus, where mu binding decreased and kappa binding increased.
+PDYN	drug	opioid	9157322	Using in situ hybridization histochemistry, the messenger RNA expression of the <b>opioid</b> precursors, <strong>prodynorphin</strong> and proenkephalin, was studied in whole hemisphere human brain tissue.
+PDYN	drug	opioid	9157322	The marked anatomical dissociation between the expression of these two <b>opioid</b> peptide genes, seen clearly in whole hemisphere sections, indicates that distinct functions must be subserved by the <strong>prodynorphin</strong> and proenkephalin systems in the human brain.
+PDYN	drug	opioid	9045086	The effect of single and repeated <b>morphine</b> administration on the <strong>prodynorphin</strong> system activity in the nucleus accumbens and striatum of the rat.
+PDYN	drug	opioid	9045086	Pharmacological data indicate that <strong>prodynorphin</strong> peptides and exogenous kappa agonists affect <b>opioid</b> tolerance and dependence.
+PDYN	addiction	dependence	9045086	Pharmacological data indicate that <strong>prodynorphin</strong> peptides and exogenous kappa agonists affect opioid tolerance and <b>dependence</b>.
+PDYN	drug	opioid	9045086	In order to elucidate the activity of the endogenous <strong>prodynorphin</strong> system during opiate tolerance and dependence, we investigated the effect of single and repeated <b>morphine</b> administration on the alpha neoendorphin tissue level, its in vitro release, and the <strong>prodynorphin</strong> messenger RNA level in the nucleus accumbens and striatum of the rat.
+PDYN	addiction	dependence	9045086	In order to elucidate the activity of the endogenous <strong>prodynorphin</strong> system during opiate tolerance and <b>dependence</b>, we investigated the effect of single and repeated morphine administration on the alpha neoendorphin tissue level, its in vitro release, and the <strong>prodynorphin</strong> messenger RNA level in the nucleus accumbens and striatum of the rat.
+PDYN	drug	opioid	9045086	The <strong>prodynorphin</strong> messenger RNA hybridization signal in the nucleus accumbens was enhanced at 3 h after acute <b>morphine</b> injection, whereas repeated <b>morphine</b> administration decreased the messenger RNA level at that time point.
+PDYN	drug	opioid	9045086	Upon late chronic <b>morphine</b> withdrawal (at 24 and 48 h), the <strong>prodynorphin</strong> messenger RNA level in that tissue was significantly elevated.
+PDYN	addiction	withdrawal	9045086	Upon late chronic morphine <b>withdrawal</b> (at 24 and 48 h), the <strong>prodynorphin</strong> messenger RNA level in that tissue was significantly elevated.
+PDYN	drug	opioid	9045086	In the striatum, single <b>morphine</b> administration had no effect on the alpha neoendorphin tissue level, release of the peptide, and <strong>prodynorphin</strong> messenger RNA level.
+PDYN	drug	opioid	9045086	Repeated <b>morphine</b> administration elevated the striatal <strong>prodynorphin</strong> messenger RNA level at 24 and 48 h after the drug withdrawal.
+PDYN	addiction	withdrawal	9045086	Repeated morphine administration elevated the striatal <strong>prodynorphin</strong> messenger RNA level at 24 and 48 h after the drug <b>withdrawal</b>.
+PDYN	drug	opioid	9045086	The present study indicates that withdrawal of chronic <b>morphine</b> leads to enhancement of the <strong>prodynorphin</strong> neurons activity in the nucleus accumbens and striatum of the rat.
+PDYN	addiction	withdrawal	9045086	The present study indicates that <b>withdrawal</b> of chronic morphine leads to enhancement of the <strong>prodynorphin</strong> neurons activity in the nucleus accumbens and striatum of the rat.
+PDYN	addiction	reward	7583238	In the present study, the effects of streptozotocin induced diabetes on levels of three immunoreactive (ir) <strong>prodynorphin</strong> derived peptides, ir dynorphin A1 17 (A1 17), ir dynorphin A1 8 (A1 8) and ir dynorphin B1 13 (B1 13), were determined in eleven brain regions known to be involved in appetite, taste and <b>reward</b>.
+PDYN	drug	opioid	7552341	Leu enkephalin, which derives from both <strong>prodynorphin</strong> and proenkephalin, and Met enkephalin, which derives from proenkephalin, were affected by chronic <b>morphine</b> mainly in Fischer rats, increasing levels in most of the brain areas examined.
+PDYN	drug	opioid	7552341	The results in this study show (1) strain differences in basal levels of <strong>prodynorphin</strong> derived <b>opioid</b> peptides, (2) the <strong>prodynorphin</strong> system to be differently influenced by <b>morphine</b> in Lewis rats than in Fischer rats and 3) the proenkephalin system to be influenced by chronic <b>morphine</b> in brain areas related to reward processes only in Fischer rats.
+PDYN	addiction	reward	7552341	The results in this study show (1) strain differences in basal levels of <strong>prodynorphin</strong> derived opioid peptides, (2) the <strong>prodynorphin</strong> system to be differently influenced by morphine in Lewis rats than in Fischer rats and 3) the proenkephalin system to be influenced by chronic morphine in brain areas related to <b>reward</b> processes only in Fischer rats.
+PDYN	drug	amphetamine	7718243	Neuronal adaptation to <b>amphetamine</b> and dopamine: molecular mechanisms of <strong>prodynorphin</strong> gene regulation in rat striatum.
+PDYN	addiction	aversion	7718243	Induction of <strong>prodynorphin</strong> gene expression by psychostimulant drugs may represent a compensatory adaptation to excessive dopamine stimulation and may contribute to the <b>aversive</b> aspects of withdrawal.
+PDYN	addiction	withdrawal	7718243	Induction of <strong>prodynorphin</strong> gene expression by psychostimulant drugs may represent a compensatory adaptation to excessive dopamine stimulation and may contribute to the aversive aspects of <b>withdrawal</b>.
+PDYN	drug	opioid	7568625	The effect of <b>morphine</b> tolerance and withdrawal on <strong>prodynorphin</strong> peptides was studied in relevant brain areas and in the pituitary gland of male Sprague Dawley rats, and compared with effects on the proenkephalin derived peptide Met enkephalin.
+PDYN	addiction	withdrawal	7568625	The effect of morphine tolerance and <b>withdrawal</b> on <strong>prodynorphin</strong> peptides was studied in relevant brain areas and in the pituitary gland of male Sprague Dawley rats, and compared with effects on the proenkephalin derived peptide Met enkephalin.
+PDYN	drug	opioid	7752808	In this study, we completed the localization on mouse chromosomes of the genes encoding mu (Oprm) and kappa (Oprk) receptors, as well as the genes for the <b>opioid</b> propeptides proenkephalin (Penk) and prodynorphin (<strong>Pdyn</strong>).
+PDYN	drug	opioid	7752808	In this study, we completed the localization on mouse chromosomes of the genes encoding mu (Oprm) and kappa (Oprk) receptors, as well as the genes for the <b>opioid</b> propeptides proenkephalin (Penk) and <strong>prodynorphin</strong> (<strong>Pdyn</strong>).
+PDYN	addiction	reward	7895045	In the present study, the effect of chronic food restriction on levels of three <strong>prodynorphin</strong> derived peptides, namely dynorphin A1 17 (A1 17), dynorphin A1 8 (A1 8) and dynorphin B1 13 (B1 13) were measured in eleven brain regions known to be involved in appetite, taste and <b>reward</b>.
+PDYN	drug	opioid	7895045	The present results suggest that food restriction alters posttranslational processing within the dynorphin A domain of the <strong>prodynorphin</strong> precursor, possibly leading to a change in the balance between kappa and non kappa <b>opioid</b> receptor stimulation in specific brain regions.
+PDYN	drug	alcohol	7847619	Differences between <b>alcohol</b> preferring (AA) and <b>alcohol</b> avoiding (ANA) rats in the <strong>prodynorphin</strong> and proenkephalin systems.
+PDYN	drug	alcohol	7847619	<b>Alcohol</b> drinking caused MEAP levels in the accumbens to rise, but had no effect on <strong>prodynorphin</strong> peptides.
+PDYN	drug	alcohol	7969792	In situ hybridization and specific radioimmunoassays were used to study the influence of <b>ethanol</b> on proopiomelanocortin (POMC) and prodynorphin (<strong>PDYN</strong>) biosynthesis in the rat pituitary.
+PDYN	drug	alcohol	7969792	In situ hybridization and specific radioimmunoassays were used to study the influence of <b>ethanol</b> on proopiomelanocortin (POMC) and <strong>prodynorphin</strong> (<strong>PDYN</strong>) biosynthesis in the rat pituitary.
+PDYN	addiction	withdrawal	7969792	In contrast, the <strong>PDYN</strong> mRNA level was found to be decreased in the anterior lobe during the <b>withdrawal</b> (by about 43%).
+PDYN	drug	alcohol	7969792	The <strong>PDYN</strong> mRNA level in the intermediate lobe and the alpha neoendorphin level in the neurointermediate lobe were unchanged after <b>ethanol</b>, as well as during the withdrawal period.
+PDYN	addiction	withdrawal	7969792	The <strong>PDYN</strong> mRNA level in the intermediate lobe and the alpha neoendorphin level in the neurointermediate lobe were unchanged after ethanol, as well as during the <b>withdrawal</b> period.
+PDYN	drug	alcohol	7969792	On the other hand, acute <b>ethanol</b> had no effect on the POMC and <strong>PDYN</strong> mRNA levels, nor did it affect the alpha neoendorphin concentration in the pituitary.
+PDYN	drug	opioid	7908338	We investigated the changes in the levels of mRNA of proenkephalin (PPE) and <strong>prodynorphin</strong> (DYN) and the stimulatory G protein alpha subunit (G alpha s) in adult <b>morphine</b> tolerant rats.
+PDYN	drug	cocaine	7694032	'Binge' <b>cocaine</b> administration induces a sustained increase of <strong>prodynorphin</strong> mRNA in rat caudate putamen.
+PDYN	addiction	intoxication	7694032	'<b>Binge</b>' cocaine administration induces a sustained increase of <strong>prodynorphin</strong> mRNA in rat caudate putamen.
+PDYN	drug	cocaine	7694032	Using a quantitative solution hybridization protection assay for mRNA, we detected a significant increase in the concentration of <strong>prodynorphin</strong> mRNA in caudate putamen extracts of rats injected with <b>cocaine</b> following a 'binge' administration pattern designed to mimic human <b>cocaine</b> abuse.
+PDYN	addiction	intoxication	7694032	Using a quantitative solution hybridization protection assay for mRNA, we detected a significant increase in the concentration of <strong>prodynorphin</strong> mRNA in caudate putamen extracts of rats injected with cocaine following a '<b>binge</b>' administration pattern designed to mimic human cocaine abuse.
+PDYN	drug	cocaine	7694032	Increased <strong>prodynorphin</strong> mRNA was observed at the earliest time point studied (50 h) and the lowest dose (10 mg/kg/day) of <b>cocaine</b> tested and persisted through the 14 day period studied.
+GRIA2	drug	opioid	32717192	Conditioned place preference (CPP) was used to evaluate the rewarding effects of <b>morphine</b> and Western blot immunoreactive assays were used to evaluate <b>morphine</b> induced changes in dopamine D2 receptor and GluA1 AMPA receptor and <strong>GluA2</strong> AMPA receptor expression in the brain of rats.
+GRIA2	addiction	reward	32717192	Conditioned place preference (<b>CPP</b>) was used to evaluate the rewarding effects of morphine and Western blot immunoreactive assays were used to evaluate morphine induced changes in dopamine D2 receptor and GluA1 AMPA receptor and <strong>GluA2</strong> AMPA receptor expression in the brain of rats.
+GRIA2	drug	opioid	32717192	We then examined the expression of dopamine D2 receptor and GluA1 AMPA receptor and <strong>GluA2</strong> AMPA receptor subunit expression in rats after acquisition of <b>morphine</b> induced CPP.
+GRIA2	addiction	reward	32717192	We then examined the expression of dopamine D2 receptor and GluA1 AMPA receptor and <strong>GluA2</strong> AMPA receptor subunit expression in rats after acquisition of morphine induced <b>CPP</b>.
+GRIA2	drug	alcohol	32599136	Our findings demonstrate that developmental <b>alcohol</b> exposure enhances <b>alcohol</b> intake during adolescence, which is associated with a decrease in the pCREB/CREB ratio in the hippocampus, prefrontal cortex and striatum, while the GluR1/<strong>GluR2</strong> ratio showed a decrease in the hippocampus.
+GRIA2	drug	alcohol	32599136	Our findings demonstrate that developmental <b>alcohol</b> exposure enhances <b>alcohol</b> intake during adolescence, which is associated with a decrease in the pCREB/CREB ratio in the hippocampus, prefrontal cortex and striatum, while the GluR1/<strong><strong>GluR2</strong></strong> ratio showed a decrease in the hippocampus.
+GRIA2	addiction	withdrawal	32450347	At hippocampal level, the <b>withdrawal</b> induced changes in the levels of AMPA receptor GluA1 and <strong>GluA2</strong>/3 subunits, PSD 95 protein, corticotropin releasing factor (Crf) and Crf receptor 1 (CrfR1) mRNA were biphasic: AMPA receptor subunit and PSD95 protein levels initially remained unchanged and decreased after 60 90 days, whereas Crf/CrfR1 mRNA levels initially increased and then markedly decreased after 60 days.
+GRIA2	drug	cocaine	32329565	We also investigated the subsequent alterations on <strong>GluR2</strong>, GluR1, cAMP response element binding (CREB), and CREB phosphorylation (pCREB) in ventral tegmental area (VTA) and nucleus accumbens (NAc) induced by both MSEW and <b>cocaine</b> SA.
+GRIA2	drug	cocaine	32329565	We also investigated the subsequent alterations on <strong><strong>GluR2</strong></strong>, GluR1, cAMP response element binding (CREB), and CREB phosphorylation (pCREB) in ventral tegmental area (VTA) and nucleus accumbens (NAc) induced by both MSEW and <b>cocaine</b> SA.
+GRIA2	drug	cocaine	32102661	Our study provides an initial characterisation of a new mouse model for studying the role of unedited <strong>GluA2</strong>(Q) in synaptic and dendritic spine plasticity in disorders where unedited <strong>GluA2</strong>(Q), synapse loss, neurodegeneration, behavioural impairments and/or seizures are observed, such as ischemia, seizures and epilepsy, Huntington's disease, amyotrophic lateral sclerosis, astrocytoma, <b>cocaine</b> seeking behaviour and Alzheimer's disease.
+GRIA2	addiction	relapse	32102661	Our study provides an initial characterisation of a new mouse model for studying the role of unedited <strong>GluA2</strong>(Q) in synaptic and dendritic spine plasticity in disorders where unedited <strong>GluA2</strong>(Q), synapse loss, neurodegeneration, behavioural impairments and/or seizures are observed, such as ischemia, seizures and epilepsy, Huntington's disease, amyotrophic lateral sclerosis, astrocytoma, cocaine <b>seeking</b> behaviour and Alzheimer's disease.
+GRIA2	drug	cocaine	31918976	Moreover, we evaluated the effects of <b>cocaine</b> SA in both sexes during adulthood, and the possible changes in GluA1, <strong>GluA2</strong>, pCREB and CREB expressions.
+GRIA2	drug	cocaine	31805281	Protein interacting with C kinase 1 (PICK1) regulates intra cellular trafficking of <strong>GluA2</strong> containing AMPA receptors, a process known to play a critical role in <b>cocaine</b> seeking behavior.
+GRIA2	addiction	relapse	31805281	Protein interacting with C kinase 1 (PICK1) regulates intra cellular trafficking of <strong>GluA2</strong> containing AMPA receptors, a process known to play a critical role in cocaine <b>seeking</b> behavior.
+GRIA2	drug	alcohol	31705540	Furthermore, alterations in glutamatergic excitability (GluA1/<strong>GluA2</strong> ratio) and ΔFosB expression were found in the prefrontal cortex and the striatum of <b>alcohol</b> exposed mice after cocaine primed reinstatement.
+GRIA2	drug	cocaine	31705540	Furthermore, alterations in glutamatergic excitability (GluA1/<strong>GluA2</strong> ratio) and ΔFosB expression were found in the prefrontal cortex and the striatum of alcohol exposed mice after <b>cocaine</b> primed reinstatement.
+GRIA2	addiction	relapse	31705540	Furthermore, alterations in glutamatergic excitability (GluA1/<strong>GluA2</strong> ratio) and ΔFosB expression were found in the prefrontal cortex and the striatum of alcohol exposed mice after cocaine primed <b>reinstatement</b>.
+GRIA2	drug	alcohol	31503067	Pharmacological inhibition of glycogen synthase kinase 3 increases operant <b>alcohol</b> self administration in a manner associated with altered pGSK 3β, protein interacting with C kinase and <strong>GluA2</strong> protein expression in the reward pathway of male C57BL/6J mice.
+GRIA2	addiction	reward	31503067	Pharmacological inhibition of glycogen synthase kinase 3 increases <b>operant</b> alcohol self administration in a manner associated with altered pGSK 3β, protein interacting with C kinase and <strong>GluA2</strong> protein expression in the <b>reward</b> pathway of male C57BL/6J mice.
+GRIA2	drug	alcohol	31503067	Given prior results showing that AMPA receptor activity regulates <b>alcohol</b> self administration, we propose that signaling through the GSK 3/PICK1/<strong>GluA2</strong> molecular pathway drives the positive reinforcing effects of the drug, which are required for abuse liability.
+GRIA2	addiction	reward	31503067	Given prior results showing that AMPA receptor activity regulates alcohol self administration, we propose that signaling through the GSK 3/PICK1/<strong>GluA2</strong> molecular pathway drives the positive <b>reinforcing</b> effects of the drug, which are required for abuse liability.
+GRIA2	drug	cocaine	31364211	<b>Cocaine</b> significantly increased the binding of phosphorylated BRD4 (pBRD4) at the promoter of <strong>Gria2</strong> and Bdnf genes in the NAc.
+GRIA2	drug	cocaine	31364211	(+)JQ1, a selective BRD4 inhibitor, markedly reduced the reinforcement and reinstatement of <b>cocaine</b> seeking behaviors, which was accompanied by the decreased expressions of <strong>GRIA2</strong> and BDNF.
+GRIA2	addiction	relapse	31364211	(+)JQ1, a selective BRD4 inhibitor, markedly reduced the reinforcement and <b>reinstatement</b> of cocaine <b>seeking</b> behaviors, which was accompanied by the decreased expressions of <strong>GRIA2</strong> and BDNF.
+GRIA2	addiction	reward	31364211	(+)JQ1, a selective BRD4 inhibitor, markedly reduced the <b>reinforcement</b> and reinstatement of cocaine seeking behaviors, which was accompanied by the decreased expressions of <strong>GRIA2</strong> and BDNF.
+GRIA2	drug	cocaine	31364211	Furthermore, chromatin immunoprecipitation assay showed that (+)JQ1 clearly attenuated <b>cocaine</b> enhanced binding of pBRD4 at the promotor of <strong>Gria2</strong> and Bdnf genes.
+GRIA2	drug	alcohol	31339221	The increase in <b>ethanol</b> self administration was associated with (a) reductions in levels of the endocannabinoids N arachidonoylethanolomine and 2 arachidonoylglycerol in the CeA, (b) increased amygdalar gene expression of cannabinoid type 1 receptor (CB1), N acyl phosphatidylethanolamine phospholipase D (Nape pld), fatty acid amid hydrolase (Faah), (c) decreased amygdalar gene expression of ionotropic AMPA (<strong>GluA2</strong> and GluA4) and metabotropic (mGlu3) glutamate receptors, and (d) increased glutamatergic receptor function.
+GRIA2	drug	cannabinoid	31339221	The increase in ethanol self administration was associated with (a) reductions in levels of the <b>endocannabinoids</b> N arachidonoylethanolomine and 2 arachidonoylglycerol in the CeA, (b) increased amygdalar gene expression of <b>cannabinoid</b> type 1 receptor (CB1), N acyl phosphatidylethanolamine phospholipase D (Nape pld), fatty acid amid hydrolase (Faah), (c) decreased amygdalar gene expression of ionotropic AMPA (<strong>GluA2</strong> and GluA4) and metabotropic (mGlu3) glutamate receptors, and (d) increased glutamatergic receptor function.
+GRIA2	drug	opioid	31209728	Results showed that membrane expression of GluA1 and <strong>GluA2</strong> in the vmPFC was decreased following the recent retrieval, while the membrane expression of GluA1 and <strong>GluA2</strong> in the vmPFC was increased following the remote retrieval of <b>morphine</b> associated memory.
+GRIA2	drug	opioid	31209728	Furthermore, the microinfusion of Tat <strong>GluA2</strong> 3Y, a <strong>GluA2</strong> endocytosis inhibitor, into the vmPFC impaired the recent retrieval of <b>morphine</b> associated memory.
+GRIA2	drug	cocaine	31201496	Following abstinence, an acute drug re exposure produced a rapid and enduring endocytosis of <strong>GluA2</strong> containing AMPARs at D1 MSNs in the shell, that when blocked by an intra NAc shell infusion of the Tat GluA23Y peptide, increased reinstatement of morphine place preference a phenomenon distinctly different than effects previously found with <b>cocaine</b>.
+GRIA2	drug	opioid	31201496	Following abstinence, an acute drug re exposure produced a rapid and enduring endocytosis of <strong>GluA2</strong> containing AMPARs at D1 MSNs in the shell, that when blocked by an intra NAc shell infusion of the Tat GluA23Y peptide, increased reinstatement of <b>morphine</b> place preference a phenomenon distinctly different than effects previously found with cocaine.
+GRIA2	addiction	relapse	31201496	Following abstinence, an acute drug re exposure produced a rapid and enduring endocytosis of <strong>GluA2</strong> containing AMPARs at D1 MSNs in the shell, that when blocked by an intra NAc shell infusion of the Tat GluA23Y peptide, increased <b>reinstatement</b> of morphine place preference a phenomenon distinctly different than effects previously found with cocaine.
+GRIA2	drug	amphetamine	31146278	Here, for <b>methamphetamine</b>, we observed no significant change in surface or total GluA1 (<strong>GluA2</strong> and GluA3 were also unchanged).
+GRIA2	drug	cocaine	31056833	From the nucleus to the cytosol, HMGB1 binds to glutamate receptor subunits (<strong>GluA2</strong>/GluN2B) on the membrane, which regulates <b>cocaine</b> induced synaptic adaptation and the formation of <b>cocaine</b> related memory.
+GRIA2	drug	cocaine	30948476	These data support a model in which mGluR5 mediated reduction in <strong>GluA2</strong> containing AMPARs at NAc shell synapses receiving input from the infralimbic cortex is a critical factor in triggering reinstatement of <b>cocaine</b> primed conditioned approach behavior.SIGNIFICANCE STATEMENT These studies identified a sequence of neural events whereby reexposure to <b>cocaine</b> activates a signaling cascade that alters synaptic strength in the NAc shell and triggers a behavioral response driven by a drug associated memory.
+GRIA2	addiction	relapse	30948476	These data support a model in which mGluR5 mediated reduction in <strong>GluA2</strong> containing AMPARs at NAc shell synapses receiving input from the infralimbic cortex is a critical factor in triggering <b>reinstatement</b> of cocaine primed conditioned approach behavior.SIGNIFICANCE STATEMENT These studies identified a sequence of neural events whereby reexposure to cocaine activates a signaling cascade that alters synaptic strength in the NAc shell and triggers a behavioral response driven by a drug associated memory.
+GRIA2	addiction	withdrawal	30773388	At the end of e CIG or CIG exposure and during <b>withdrawal</b>, the mice also had a higher AMPA receptors GluA1/<strong>GluA2</strong> 3 ratio in the NAc.
+GRIA2	addiction	withdrawal	30733663	We then analyzed the expression levels of presynaptic (vGlut1, vGlut2, CB1 receptor, synaptophysin) and postsynaptic (PSD95, GluN1, GluN2A, GluN2B, GluA1, <strong>GluA2</strong>, mGluR1 and mGluR5) proteins after 7 days EtOH incubation or after EtOH <b>withdrawal</b>.
+GRIA2	drug	alcohol	30692226	Following chronic <b>alcohol</b> experience, <strong>GluA2</strong> lacking AMPARs, which are Ca permeable, were inserted into vHipp to D1 MSN synapses.
+GRIA2	drug	cocaine	30654007	We tested the specific role of soluble TNF in MS induced <strong>GluA2</strong> loss and <b>cocaine</b> induced CPP with biologic disruption of TNF signaling.
+GRIA2	addiction	reward	30654007	We tested the specific role of soluble TNF in MS induced <strong>GluA2</strong> loss and cocaine induced <b>CPP</b> with biologic disruption of TNF signaling.
+GRIA2	drug	cocaine	30498893	Here, we show that <b>cocaine</b> SA decreased PrL NA core spine head diameter, nuclear Fos IR and pCREB IR, and GluA1 IR and <strong>GluA2</strong> IR in putative mushroom type spines 2 h after the end of <b>cocaine</b> SA, whereas the opposite occurred following 1 week of abstinence.
+GRIA2	drug	cocaine	30144237	In <b>cocaine</b> naïve animals, SERT removal led to reduced baseline Hb mRNA levels of critical determinants of glutamate transmission, such as SLC1A2, the main glutamate transporter and N methyl D aspartate (Grin1, Grin2A and Grin2B) as well as α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (Gria1 and <strong>Gria2</strong>) receptor subunits, with no changes in the scaffolding protein Dlg4.
+GRIA2	drug	amphetamine	29931627	Assessment of two targets of ΔFosB regulated transcription revealed (1) increased dopamine D1 receptor (D1R) immunoreactivity in the NA shell of Tg <b>meth</b> rats versus saline Tg controls, but (2) no changes in the AMPA receptor subunit, <strong>GluA2</strong>.
+GRIA2	drug	cocaine	29622268	We compared basal overall translation and its regulation by metabotropic glutamate receptor 1 (mGlu1), mGlu5, and N methyl D aspartate receptors (NMDARs) in drug naïve, saline control, and <b>cocaine</b> rats, and we compared GluA1 and <strong>GluA2</strong> translation by immunoprecipitating puromycin labeled proteins.
+GRIA2	drug	cocaine	29622268	<b>Cocaine</b>/late withdrawal rats exhibited greater translation of GluA1 (but not <strong>GluA2</strong>), which was not further affected by NMDAR blockade.
+GRIA2	addiction	withdrawal	29622268	Cocaine/late <b>withdrawal</b> rats exhibited greater translation of GluA1 (but not <strong>GluA2</strong>), which was not further affected by NMDAR blockade.
+GRIA2	drug	amphetamine	29338492	Genotyping of GRIA1 rs1428920, <strong>GRIA2</strong> rs3813296, GRIA3 rs3761554, rs502434 and rs989638 was performed in 102 male Thai controls and 100 <b>METH</b> dependent subjects (53 with <b>METH</b> dependent psychosis).
+GRIA2	drug	amphetamine	29338492	We observed no evidence of association with <b>METH</b> dependence and <b>METH</b> dependent psychosis in the GRIA1 and <strong>GRIA2</strong> polymorphisms, nor with single polymorphisms rs3761554 and rs989638 in GRIA3.
+GRIA2	addiction	dependence	29338492	We observed no evidence of association with METH <b>dependence</b> and METH dependent psychosis in the GRIA1 and <strong>GRIA2</strong> polymorphisms, nor with single polymorphisms rs3761554 and rs989638 in GRIA3.
+GRIA2	drug	opioid	29134962	We showed that context induced reinstatement of <b>heroin</b> seeking caused selective activation of the vCA1 IL but not vCA1 PL glutamatergic projections, decreased synaptosomal <strong>GluA2</strong> expression in the IL, impaired basal synaptic transmission, and facilitation of long term depression (LTD) in the vCA1 IL pathway.
+GRIA2	addiction	relapse	29134962	We showed that context induced <b>reinstatement</b> of heroin <b>seeking</b> caused selective activation of the vCA1 IL but not vCA1 PL glutamatergic projections, decreased synaptosomal <strong>GluA2</strong> expression in the IL, impaired basal synaptic transmission, and facilitation of long term depression (LTD) in the vCA1 IL pathway.
+GRIA2	drug	cocaine	29029785	Compared with saline pretreated mice, AMPAR mediated excitatory postsynaptic currents (EPSCs) of <b>cocaine</b> pretreated mice showed a marked inward rectification, demonstrating the insertion of <strong>GluR2</strong> lacking AMPARs to plasma membrane.
+GRIA2	drug	cocaine	29029785	Compared with saline pretreated mice, AMPAR mediated excitatory postsynaptic currents (EPSCs) of <b>cocaine</b> pretreated mice showed a marked inward rectification, demonstrating the insertion of <strong><strong>GluR2</strong></strong> lacking AMPARs to plasma membrane.
+GRIA2	drug	alcohol	28890345	We further demonstrate that Prosapip1 is required for <b>alcohol</b> dependent synaptic localization of <strong>GluA2</strong> lacking AMPA receptors in NAc shell MSNs.
+GRIA2	drug	cocaine	28668281	Exposure to both <b>cocaine</b> and stress can lead to alterations in protein kinase C mediated phosphorylation of <strong>GluA2</strong> AMPA subunits and thus alter the trafficking of <strong>GluA2</strong> containing AMPARs.
+GRIA2	drug	cocaine	28668281	Although no differences were seen in the response to a forced swim stress in naïve mice, <strong>GluA2</strong> K882A knock in mice exhibited an increased stress response following <b>cocaine</b> self administration.
+GRIA2	drug	cocaine	28668281	Furthermore, we demonstrated that disrupting <strong>GluA2</strong> phosphorylation increases vulnerability to stress induced reinstatement of both <b>cocaine</b> seeking and <b>cocaine</b> conditioned reward.
+GRIA2	addiction	relapse	28668281	Furthermore, we demonstrated that disrupting <strong>GluA2</strong> phosphorylation increases vulnerability to stress induced <b>reinstatement</b> of both cocaine <b>seeking</b> and cocaine conditioned reward.
+GRIA2	addiction	reward	28668281	Furthermore, we demonstrated that disrupting <strong>GluA2</strong> phosphorylation increases vulnerability to stress induced reinstatement of both cocaine seeking and cocaine conditioned <b>reward</b>.
+GRIA2	drug	cocaine	28668281	Taken together these results indicate that disrupting <strong>GluA2</strong> phosphorylation leads to increased responsivity to acute stress following <b>cocaine</b> exposure and increased vulnerability to chronic stress.
+GRIA2	addiction	relapse	28495973	Intra NAc xCT knockdown prevented ceftriaxone from attenuating <b>reinstatement</b> and from upregulating GLT 1 and resulted in increased surface expression of AMPA receptor subunits GluA1 and <strong>GluA2</strong>.
+GRIA2	addiction	relapse	28495973	Intra NAc GLT 1 knockdown also prevented ceftriaxone from attenuating <b>reinstatement</b> and from upregulating xCT expression, without affecting GluA1 and <strong>GluA2</strong> expression.
+GRIA2	drug	cocaine	28495973	In the absence of <b>cocaine</b> or ceftriaxone treatment, xCT knockdown in the NAc increased the expression of both GluA1 and <strong>GluA2</strong> without affecting GLT 1 expression while GLT 1 knockdown had no effect.
+GRIA2	drug	amphetamine	28223211	Using protein cross linking, biochemical, subcellular fractionation, and slice electrophysiological approaches in the NAcc, we found that, unlike cocaine, previous exposure to <b>amphetamine</b> did not increase cell surface levels of either GluA1 or <strong>GluA2</strong> AMPA receptor subunits, redistribution of these subunits to the synaptic or perisynaptic cellular membrane domains, protein protein associations required to support the accumulation and retention of AMPA receptors in the PSD, or the peak amplitude of AMPA receptor mediated mEPSCs recorded in NAcc slices.
+GRIA2	drug	cocaine	28223211	Using protein cross linking, biochemical, subcellular fractionation, and slice electrophysiological approaches in the NAcc, we found that, unlike <b>cocaine</b>, previous exposure to amphetamine did not increase cell surface levels of either GluA1 or <strong>GluA2</strong> AMPA receptor subunits, redistribution of these subunits to the synaptic or perisynaptic cellular membrane domains, protein protein associations required to support the accumulation and retention of AMPA receptors in the PSD, or the peak amplitude of AMPA receptor mediated mEPSCs recorded in NAcc slices.
+GRIA2	drug	cocaine	27993521	However, <strong>GluA2</strong> lacking, Ca2+ permeable AMPA receptors (CP AMPARs) accumulate after prolonged withdrawal from extended access <b>cocaine</b> self administration and thereafter their activation is required for the intensified (incubated) cue induced <b>cocaine</b> craving that characterizes prolonged withdrawal from such regimens.
+GRIA2	addiction	relapse	27993521	However, <strong>GluA2</strong> lacking, Ca2+ permeable AMPA receptors (CP AMPARs) accumulate after prolonged withdrawal from extended access cocaine self administration and thereafter their activation is required for the intensified (incubated) cue induced cocaine <b>craving</b> that characterizes prolonged withdrawal from such regimens.
+GRIA2	addiction	withdrawal	27993521	However, <strong>GluA2</strong> lacking, Ca2+ permeable AMPA receptors (CP AMPARs) accumulate after prolonged <b>withdrawal</b> from extended access cocaine self administration and thereafter their activation is required for the intensified (incubated) cue induced cocaine craving that characterizes prolonged <b>withdrawal</b> from such regimens.
+GRIA2	addiction	reward	27881347	The protein expressions of TH, NR2B and <strong>GLUR2</strong> in the brain of zebrafish with <b>CPP</b> were detected with Western blotting.
+GRIA2	addiction	reward	27881347	The protein expressions of TH, NR2B and <strong><strong>GLUR2</strong></strong> in the brain of zebrafish with <b>CPP</b> were detected with Western blotting.
+GRIA2	drug	amphetamine	27881347	Compared with the control group, zebrafish in <b>methamphetamine</b> group showed significant variations in the staying time and swimming distance in the drug box after conditioning (P<0.05) with obvious alterations of NR2B, TH and <strong>GLUR2</strong> expressions in the brain (P<0.05).
+GRIA2	drug	amphetamine	27881347	Compared with the control group, zebrafish in <b>methamphetamine</b> group showed significant variations in the staying time and swimming distance in the drug box after conditioning (P<0.05) with obvious alterations of NR2B, TH and <strong><strong>GLUR2</strong></strong> expressions in the brain (P<0.05).
+GRIA2	drug	amphetamine	27881347	Treatment of <b>methamphetamine</b> dependent zebrafish with high dose rhynchophylline significantly reduced the variations in the staying time and swimming distance in the drug box (P<0.05) and in the expressions of NR2B, TH and <strong>GLUR2</strong> in the brain (P<0.05).
+GRIA2	drug	amphetamine	27881347	Treatment of <b>methamphetamine</b> dependent zebrafish with high dose rhynchophylline significantly reduced the variations in the staying time and swimming distance in the drug box (P<0.05) and in the expressions of NR2B, TH and <strong><strong>GLUR2</strong></strong> in the brain (P<0.05).
+GRIA2	drug	amphetamine	27881347	Rhynchophylline can inhibit <b>methamphetamine</b> dependence in zebrafish, the mechanism of which may involve the expressions of TH, NR2B and <strong>GLUR2</strong> proteins in the brain.
+GRIA2	addiction	dependence	27881347	Rhynchophylline can inhibit methamphetamine <b>dependence</b> in zebrafish, the mechanism of which may involve the expressions of TH, NR2B and <strong>GLUR2</strong> proteins in the brain.
+GRIA2	drug	amphetamine	27881347	Rhynchophylline can inhibit <b>methamphetamine</b> dependence in zebrafish, the mechanism of which may involve the expressions of TH, NR2B and <strong><strong>GLUR2</strong></strong> proteins in the brain.
+GRIA2	addiction	dependence	27881347	Rhynchophylline can inhibit methamphetamine <b>dependence</b> in zebrafish, the mechanism of which may involve the expressions of TH, NR2B and <strong><strong>GLUR2</strong></strong> proteins in the brain.
+GRIA2	drug	cocaine	27622930	Disrupting <strong>GluA2</strong> phosphorylation potentiates reinstatement of <b>cocaine</b> seeking.
+GRIA2	addiction	relapse	27622930	Disrupting <strong>GluA2</strong> phosphorylation potentiates <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRIA2	drug	cocaine	27622930	Exposure to <b>cocaine</b> can lead to protein kinase C mediated phosphorylation of <strong>GluA2</strong> AMPA subunits and this phosphorylation event leads to the internalization of <strong>GluA2</strong> containing AMPARs, which are calcium impermeable.
+GRIA2	drug	cocaine	27622930	Utilizing a mouse with a point mutation within the <strong>GluA2</strong> subunit c terminus, the current study demonstrates that disrupting PKC mediated <strong>GluA2</strong> phosphorylation potentiates reinstatement of both cue induced <b>cocaine</b> seeking and <b>cocaine</b> conditioned reward without affecting operant learning, food self administration or <b>cocaine</b> sensitization.
+GRIA2	addiction	relapse	27622930	Utilizing a mouse with a point mutation within the <strong>GluA2</strong> subunit c terminus, the current study demonstrates that disrupting PKC mediated <strong>GluA2</strong> phosphorylation potentiates <b>reinstatement</b> of both cue induced cocaine <b>seeking</b> and cocaine conditioned reward without affecting operant learning, food self administration or cocaine sensitization.
+GRIA2	addiction	reward	27622930	Utilizing a mouse with a point mutation within the <strong>GluA2</strong> subunit c terminus, the current study demonstrates that disrupting PKC mediated <strong>GluA2</strong> phosphorylation potentiates reinstatement of both cue induced cocaine seeking and cocaine conditioned <b>reward</b> without affecting <b>operant</b> learning, food self administration or cocaine sensitization.
+GRIA2	addiction	sensitization	27622930	Utilizing a mouse with a point mutation within the <strong>GluA2</strong> subunit c terminus, the current study demonstrates that disrupting PKC mediated <strong>GluA2</strong> phosphorylation potentiates reinstatement of both cue induced cocaine seeking and cocaine conditioned reward without affecting operant learning, food self administration or cocaine <b>sensitization</b>.
+GRIA2	drug	cocaine	27622930	In support of this increase in <strong>GluA2</strong> activity mediating the augmented <b>cocaine</b> reinstatement, we found that accumbal overexpression of <strong>GluA2</strong> recapitulated this behavioral effect in wildtype mice while not altering reinstatement behavior in the <strong>GluA2</strong> K882A knock in mice.
+GRIA2	addiction	relapse	27622930	In support of this increase in <strong>GluA2</strong> activity mediating the augmented cocaine <b>reinstatement</b>, we found that accumbal overexpression of <strong>GluA2</strong> recapitulated this behavioral effect in wildtype mice while not altering <b>reinstatement</b> behavior in the <strong>GluA2</strong> K882A knock in mice.
+GRIA2	drug	cocaine	27622930	In addition, disrupting <strong>GluA2</strong> phosphorylation was associated with blunted long term depression in the nucleus accumbens, mimicking the anaplasticity seen following <b>cocaine</b> self administration.
+GRIA2	drug	cocaine	27622930	Taken together these results indicate that disrupting <strong>GluA2</strong> phosphorylation and increasing <strong>GluA2</strong> mediated transmission in the nucleus accumbens leads to increased vulnerability to <b>cocaine</b> relapse.
+GRIA2	addiction	relapse	27622930	Taken together these results indicate that disrupting <strong>GluA2</strong> phosphorylation and increasing <strong>GluA2</strong> mediated transmission in the nucleus accumbens leads to increased vulnerability to cocaine <b>relapse</b>.
+GRIA2	addiction	addiction	27622930	Further, these results indicate that modulating <strong>GluA2</strong> containing AMPAR trafficking can contribute to <b>addictive</b> phenotypes in the absence of alterations in <strong>GluA2</strong> lacking receptors.
+GRIA2	drug	cocaine	27622930	These results highlight the <strong>GluA2</strong> phosphorylation site as a novel target for the development of <b>cocaine</b> addiction therapeutics.
+GRIA2	addiction	addiction	27622930	These results highlight the <strong>GluA2</strong> phosphorylation site as a novel target for the development of cocaine <b>addiction</b> therapeutics.
+GRIA2	drug	cocaine	27494187	Further, we show that potential ΔFosB transcriptional targets, including <strong>GluA2</strong>, are also downregulated in the HPC but not PFC of <b>cocaine</b> addicts.
+GRIA2	drug	opioid	27225765	Using a protein cross linking approach, we found that the surface/intracellular ratio of NAc GluA1, but not <strong>GluA2</strong>, increased with <b>morphine</b> treatment, suggesting postsynaptic insertion of <strong>GluA2</strong> lacking AMPARs.
+GRIA2	drug	opioid	27225765	Consistent with this, 1 naphthylacetyl spermine trihydrochloride (NASPM), an antagonist of <strong>GluA2</strong> lacking AMPARs, attenuated <b>naloxone</b> induced decreases in sensitivity to brain stimulation reward.
+GRIA2	addiction	reward	27225765	Consistent with this, 1 naphthylacetyl spermine trihydrochloride (NASPM), an antagonist of <strong>GluA2</strong> lacking AMPARs, attenuated naloxone induced decreases in sensitivity to brain stimulation <b>reward</b>.
+GRIA2	drug	cocaine	27122037	Previous studies have shown that a single <b>cocaine</b> exposure in vivo leads to an increase in <strong>GluA2</strong> lacking AMPARs in dopamine neurons of the ventral tegmental area (VTA).
+GRIA2	drug	cocaine	27122037	We report that a single <b>cocaine</b> injection in vivo in wild type mice leads to inward rectification of EPSCs and renders EPSCs sensitive to a <strong>GluA2</strong> lacking AMPAR blocker in VTA dopamine neurons.
+GRIA2	drug	cocaine	27122037	The <b>cocaine</b> induced increase in <strong>GluA2</strong> lacking AMPARs was absent in Epac2 deficient mice but not in Epac1 deficient mice.
+GRIA2	drug	cocaine	27122037	In addition, activation of Epac with the selective Epac agonist 8 CPT 2Me cAMP (8 CPT) recapitulated the <b>cocaine</b> induced increase in <strong>GluA2</strong> lacking AMPARs, and the effects of 8 CPT were mediated by Epac2.
+GRIA2	addiction	withdrawal	27038592	Incubation with chronic EtOH for 7 days and its removal from the medium induced a significant decrease in GluA1 and <strong>GluA2</strong> expression levels; a significant reduction in the expression of synaptophysin and GluN2A was observed only after EtOH <b>withdrawal</b>.
+GRIA2	drug	opioid	26924808	<strong>GluR2</strong> 3Y Inhibits the Acquisition and Reinstatement of <b>Morphine</b> Induced Conditioned Place Preference in Rats.
+GRIA2	addiction	relapse	26924808	<strong>GluR2</strong> 3Y Inhibits the Acquisition and <b>Reinstatement</b> of Morphine Induced Conditioned Place Preference in Rats.
+GRIA2	drug	opioid	26924808	<strong><strong>GluR2</strong></strong> 3Y Inhibits the Acquisition and Reinstatement of <b>Morphine</b> Induced Conditioned Place Preference in Rats.
+GRIA2	addiction	relapse	26924808	<strong><strong>GluR2</strong></strong> 3Y Inhibits the Acquisition and <b>Reinstatement</b> of Morphine Induced Conditioned Place Preference in Rats.
+GRIA2	addiction	addiction	26924808	However, the role of AMPARs containing the <strong>GluR2</strong> subunit in opiate <b>addiction</b> is still unclear.
+GRIA2	addiction	addiction	26924808	However, the role of AMPARs containing the <strong><strong>GluR2</strong></strong> subunit in opiate <b>addiction</b> is still unclear.
+GRIA2	drug	opioid	26924808	In this study, we explored the effect of intravenous injection of <strong>GluR2</strong> 3Y on the acquisition, expression, and reinstatement of <b>morphine</b> induced conditioned place preference (mCPP) in rats.
+GRIA2	addiction	relapse	26924808	In this study, we explored the effect of intravenous injection of <strong>GluR2</strong> 3Y on the acquisition, expression, and <b>reinstatement</b> of morphine induced conditioned place preference (mCPP) in rats.
+GRIA2	drug	opioid	26924808	In this study, we explored the effect of intravenous injection of <strong><strong>GluR2</strong></strong> 3Y on the acquisition, expression, and reinstatement of <b>morphine</b> induced conditioned place preference (mCPP) in rats.
+GRIA2	addiction	relapse	26924808	In this study, we explored the effect of intravenous injection of <strong><strong>GluR2</strong></strong> 3Y on the acquisition, expression, and <b>reinstatement</b> of morphine induced conditioned place preference (mCPP) in rats.
+GRIA2	drug	opioid	26924808	We found that infusion of <strong>GluR2</strong> 3Y (1.5 nmol/g) one hour before <b>morphine</b> during the conditioning phase inhibited the acquisition of mCPP, while an identical injection one hour before the post conditioning test had no influence on the expression of mCPP.
+GRIA2	drug	opioid	26924808	We found that infusion of <strong><strong>GluR2</strong></strong> 3Y (1.5 nmol/g) one hour before <b>morphine</b> during the conditioning phase inhibited the acquisition of mCPP, while an identical injection one hour before the post conditioning test had no influence on the expression of mCPP.
+GRIA2	drug	opioid	26924808	Injection of <strong>GluR2</strong> 3Y (1.5 nmol/g) after mCPP extinction blocked the <b>morphine</b> induced reinstatement of mCPP.
+GRIA2	addiction	relapse	26924808	Injection of <strong>GluR2</strong> 3Y (1.5 nmol/g) after mCPP extinction blocked the morphine induced <b>reinstatement</b> of mCPP.
+GRIA2	drug	opioid	26924808	Injection of <strong><strong>GluR2</strong></strong> 3Y (1.5 nmol/g) after mCPP extinction blocked the <b>morphine</b> induced reinstatement of mCPP.
+GRIA2	addiction	relapse	26924808	Injection of <strong><strong>GluR2</strong></strong> 3Y (1.5 nmol/g) after mCPP extinction blocked the morphine induced <b>reinstatement</b> of mCPP.
+GRIA2	drug	cocaine	26881139	Surface biotinylation analysis of protein expression in the dlSTR revealed that, in <b>cocaine</b> animals, intra dlSTR MTEP administration decreased mGlu5 surface expression and prevented changes in Arc and GluA1/<strong>GluA2</strong> observed in their vehicle counterparts.
+GRIA2	drug	opioid	26840481	Chronic <b>morphine</b> exposure selectively potentiates excitatory transmission between the paraventricular nucleus of the thalamus and D2 receptor expressing medium spiny neurons via synaptic insertion of <strong>GluA2</strong> lacking AMPA receptors.
+GRIA2	drug	amphetamine	26748780	At the molecular level, we discovered that prolonged extinction training reversed the <b>METH</b> conditioned place preference induced increase in surface expression of <strong>GluA2</strong> and alpha amino 3 hydroxy 5 methylisoxazole 4 propionate (AMPA)/NMDA ratio in the basolateral amygdala.
+GRIA2	drug	amphetamine	26748780	At the molecular level, we discovered that extensive extinction (EE) reversed the <b>METH</b> CPP induced increase in surface expression of <strong>GluA2</strong> and AMPA/NMDA ratio.
+GRIA2	addiction	reward	26748780	At the molecular level, we discovered that extensive extinction (EE) reversed the METH <b>CPP</b> induced increase in surface expression of <strong>GluA2</strong> and AMPA/NMDA ratio.
+GRIA2	drug	opioid	26739562	Here, we find that repeated <b>morphine</b> potentiates excitatory transmission and increases <strong>GluA2</strong> lacking AMPA receptor expression in D1R MSNs, while reducing signaling in D2 MSNs following 10 14 d of forced abstinence.
+GRIA2	addiction	relapse	26706696	Here we investigated the effects of ceftriaxone (100 and 200 mg/kg) on context primed <b>relapse</b> following abstinence without extinction training and examined the effects of ceftriaxone on GluA1, <strong>GluA2</strong> and GLT 1 expression.
+GRIA2	drug	cocaine	26706696	GluA1 was reduced in the NAc by both doses of ceftriaxone while <strong>GluA2</strong> expression was unchanged, indicating that ceftriaxone altered AMPA subunit composition following <b>cocaine</b>.
+GRIA2	drug	cocaine	26585289	Cell Type Specific Insertion of <strong>GluA2</strong> Lacking AMPARs with <b>Cocaine</b> Exposure Leading to Sensitization, Cue Induced Seeking, and Incubation of Craving.
+GRIA2	addiction	relapse	26585289	Cell Type Specific Insertion of <strong>GluA2</strong> Lacking AMPARs with Cocaine Exposure Leading to Sensitization, Cue Induced <b>Seeking</b>, and Incubation of <b>Craving</b>.
+GRIA2	addiction	sensitization	26585289	Cell Type Specific Insertion of <strong>GluA2</strong> Lacking AMPARs with Cocaine Exposure Leading to <b>Sensitization</b>, Cue Induced Seeking, and Incubation of Craving.
+GRIA2	drug	cocaine	26585289	In D1 MSN, we found the presence of <strong>GluA2</strong> lacking α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid receptors (AMPARs) after single or chronic non contingent exposure to <b>cocaine</b> as well as after <b>cocaine</b> self administration (SA).
+GRIA2	drug	cocaine	26585289	Remarkably, insertion of <strong>GluA2</strong> lacking AMPARs was also detected in D2 MSN after SA of a high dose of <b>cocaine</b> but not regular dose (1.5 vs 0.75 mg/kg), which was the only condition where incubation of <b>cocaine</b> craving was observed in this study.
+GRIA2	addiction	relapse	26585289	Remarkably, insertion of <strong>GluA2</strong> lacking AMPARs was also detected in D2 MSN after SA of a high dose of cocaine but not regular dose (1.5 vs 0.75 mg/kg), which was the only condition where incubation of cocaine <b>craving</b> was observed in this study.
+GRIA2	addiction	withdrawal	26248656	Intra PAG injection of 0.15, 1.5, 7.5, and 15 pmol of <strong>GluA2</strong> 3y induced dose dependent increases in hindpaw <b>withdrawal</b> latencies to noxious thermal and mechanical stimuli in intact rats, suggesting that <strong>GluA2</strong> cell surface trafficking in the PAG is involved in pain modulation.
+GRIA2	drug	opioid	26248656	Interestingly, the intra PAG injection of 15 pmol <strong>GluA2</strong> 3y had an analgesic effect similar to 10 μg (35 nmol) <b>morphine</b> in rats with neuropathic pain.
+GRIA2	addiction	reward	25589145	In experiment 1, <b>CPP</b> expression in AL rats was associated with elevated pSer845 GluA1, GluA1, and <strong>GluA2</strong> in NAc.
+GRIA2	drug	cocaine	25349168	ADAR2 dependent <strong>GluA2</strong> editing regulates <b>cocaine</b> seeking.
+GRIA2	addiction	relapse	25349168	ADAR2 dependent <strong>GluA2</strong> editing regulates cocaine <b>seeking</b>.
+GRIA2	drug	cocaine	25349168	However, the role of <strong>GluA2</strong> Q/R site editing and ADAR2 in <b>cocaine</b> seeking is unclear.
+GRIA2	addiction	relapse	25349168	However, the role of <strong>GluA2</strong> Q/R site editing and ADAR2 in cocaine <b>seeking</b> is unclear.
+GRIA2	drug	cocaine	25349168	In the present study, we investigated the effects of forced <b>cocaine</b> abstinence on <strong>GluA2</strong> Q/R site editing and ADAR2 expression in the nucleus accumbens.
+GRIA2	drug	cocaine	25349168	Our results demonstrate that 7 days of <b>cocaine</b> abstinence is associated with decreased <strong>GluA2</strong> Q/R site editing and reduced ADAR2 expression in the accumbens shell, but not core, of <b>cocaine</b> experienced rats compared with yoked saline controls.
+GRIA2	drug	cocaine	25349168	To examine the functional significance of ADAR2 and <strong>GluA2</strong> Q/R site editing in <b>cocaine</b> seeking, we used viral mediated gene delivery to overexpress ADAR2b in the accumbens shell.
+GRIA2	addiction	relapse	25349168	To examine the functional significance of ADAR2 and <strong>GluA2</strong> Q/R site editing in cocaine <b>seeking</b>, we used viral mediated gene delivery to overexpress ADAR2b in the accumbens shell.
+GRIA2	drug	cocaine	25349168	Increased ADAR2b expression in the shell attenuated <b>cocaine</b> priming induced reinstatement of drug seeking and was associated with increased <strong>GluA2</strong> Q/R site editing and surface expression of <strong>GluA2</strong> containing AMPARs.
+GRIA2	addiction	relapse	25349168	Increased ADAR2b expression in the shell attenuated cocaine priming induced <b>reinstatement</b> of drug <b>seeking</b> and was associated with increased <strong>GluA2</strong> Q/R site editing and surface expression of <strong>GluA2</strong> containing AMPARs.
+GRIA2	drug	cocaine	25349168	Taken together, these findings support the novel hypothesis that an increased contribution of accumbens shell CP AMPARs containing unedited <strong>GluA2</strong>(Q) promotes <b>cocaine</b> seeking.
+GRIA2	addiction	relapse	25349168	Taken together, these findings support the novel hypothesis that an increased contribution of accumbens shell CP AMPARs containing unedited <strong>GluA2</strong>(Q) promotes cocaine <b>seeking</b>.
+GRIA2	drug	cocaine	25349168	Therefore, CP AMPARs containing unedited <strong>GluA2</strong>(Q) represent a novel target for <b>cocaine</b> addiction pharmacotherapies.
+GRIA2	addiction	addiction	25349168	Therefore, CP AMPARs containing unedited <strong>GluA2</strong>(Q) represent a novel target for cocaine <b>addiction</b> pharmacotherapies.
+GRIA2	drug	cocaine	25268136	After repeated <b>cocaine</b> exposure, the density of GluR1 was increased, but there was no change in total AMPA receptors and <strong>GluR2</strong> levels in wild type mice.
+GRIA2	drug	cocaine	25268136	After repeated <b>cocaine</b> exposure, the density of GluR1 was increased, but there was no change in total AMPA receptors and <strong><strong>GluR2</strong></strong> levels in wild type mice.
+GRIA2	drug	cocaine	25268136	In contrast, following repeated <b>cocaine</b> exposure, increased densities of total AMPA receptors, GluR1 and <strong>GluR2</strong> were observed in knock out mice.
+GRIA2	drug	cocaine	25268136	In contrast, following repeated <b>cocaine</b> exposure, increased densities of total AMPA receptors, GluR1 and <strong><strong>GluR2</strong></strong> were observed in knock out mice.
+GRIA2	drug	alcohol	24872560	Whereas CDPPB treatment did not alter the amplitude of PrL or IfL AMPA currents, it did promote the expression of IfL calcium permeable <strong>GluR2</strong> lacking receptors in both abstinence  and extinction trained rats, but had no effect in <b>ethanol</b> naive rats.
+GRIA2	drug	alcohol	24872560	Whereas CDPPB treatment did not alter the amplitude of PrL or IfL AMPA currents, it did promote the expression of IfL calcium permeable <strong><strong>GluR2</strong></strong> lacking receptors in both abstinence  and extinction trained rats, but had no effect in <b>ethanol</b> naive rats.
+GRIA2	drug	cocaine	24599450	Interactions between N ethylmaleimide sensitive factor and <strong>GluR2</strong> in the nucleus accumbens contribute to the expression of locomotor sensitization to <b>cocaine</b>.
+GRIA2	addiction	sensitization	24599450	Interactions between N ethylmaleimide sensitive factor and <strong>GluR2</strong> in the nucleus accumbens contribute to the expression of locomotor <b>sensitization</b> to cocaine.
+GRIA2	drug	cocaine	24599450	Interactions between N ethylmaleimide sensitive factor and <strong><strong>GluR2</strong></strong> in the nucleus accumbens contribute to the expression of locomotor sensitization to <b>cocaine</b>.
+GRIA2	addiction	sensitization	24599450	Interactions between N ethylmaleimide sensitive factor and <strong><strong>GluR2</strong></strong> in the nucleus accumbens contribute to the expression of locomotor <b>sensitization</b> to cocaine.
+GRIA2	addiction	sensitization	24599450	We demonstrated that the expression of behavioral <b>sensitization</b> was negatively controlled by N ethylmaleimide sensitive factor (NSF) <strong>GluR2</strong> interactions in the NAc.
+GRIA2	addiction	sensitization	24599450	We demonstrated that the expression of behavioral <b>sensitization</b> was negatively controlled by N ethylmaleimide sensitive factor (NSF) <strong><strong>GluR2</strong></strong> interactions in the NAc.
+GRIA2	drug	cocaine	24599450	The upregulation of NSF <strong>GluR2</strong> interactions, which may be resulted by the increase in NSF S nitrosylation after withdrawal from <b>cocaine</b>, was associated with the changes in the expression of behavioral sensitization.
+GRIA2	addiction	sensitization	24599450	The upregulation of NSF <strong>GluR2</strong> interactions, which may be resulted by the increase in NSF S nitrosylation after withdrawal from cocaine, was associated with the changes in the expression of behavioral <b>sensitization</b>.
+GRIA2	addiction	withdrawal	24599450	The upregulation of NSF <strong>GluR2</strong> interactions, which may be resulted by the increase in NSF S nitrosylation after <b>withdrawal</b> from cocaine, was associated with the changes in the expression of behavioral sensitization.
+GRIA2	drug	cocaine	24599450	The upregulation of NSF <strong><strong>GluR2</strong></strong> interactions, which may be resulted by the increase in NSF S nitrosylation after withdrawal from <b>cocaine</b>, was associated with the changes in the expression of behavioral sensitization.
+GRIA2	addiction	sensitization	24599450	The upregulation of NSF <strong><strong>GluR2</strong></strong> interactions, which may be resulted by the increase in NSF S nitrosylation after withdrawal from cocaine, was associated with the changes in the expression of behavioral <b>sensitization</b>.
+GRIA2	addiction	withdrawal	24599450	The upregulation of NSF <strong><strong>GluR2</strong></strong> interactions, which may be resulted by the increase in NSF S nitrosylation after <b>withdrawal</b> from cocaine, was associated with the changes in the expression of behavioral sensitization.
+GRIA2	drug	cocaine	24599450	Disruption of NSF <strong>GluR2</strong> interactions in the NAc with a specific peptide, TAT pep R845A, increased the locomotor response of rats to <b>cocaine</b> by decreasing <strong>GluR2</strong> surface insertion.
+GRIA2	drug	cocaine	24599450	Disruption of NSF <strong><strong>GluR2</strong></strong> interactions in the NAc with a specific peptide, TAT pep R845A, increased the locomotor response of rats to <b>cocaine</b> by decreasing <strong><strong>GluR2</strong></strong> surface insertion.
+GRIA2	addiction	sensitization	24599450	In contrast, prevention of <strong>GluR2</strong> containing AMPARs removal from synapses with Pep2 EVKI attenuated the expression of behavioral <b>sensitization</b>.
+GRIA2	addiction	sensitization	24599450	In contrast, prevention of <strong><strong>GluR2</strong></strong> containing AMPARs removal from synapses with Pep2 EVKI attenuated the expression of behavioral <b>sensitization</b>.
+GRIA2	addiction	sensitization	24599450	Similarly, treatment with the nitric oxide donor, S Nitroso N acetyl DL penicillamine (SNAP), attenuated the expression of locomotor <b>sensitization</b> by promoting <strong>GluR2</strong> surface expression.
+GRIA2	addiction	sensitization	24599450	Similarly, treatment with the nitric oxide donor, S Nitroso N acetyl DL penicillamine (SNAP), attenuated the expression of locomotor <b>sensitization</b> by promoting <strong><strong>GluR2</strong></strong> surface expression.
+GRIA2	drug	cocaine	24599450	Thus, these results indicate that increased NSF <strong>GluR2</strong> interactions in the NAc after withdrawal from <b>cocaine</b> attenuated the expression of behavioral sensitization and serves as a negative regulatory mechanism in drug exposed individuals.
+GRIA2	addiction	sensitization	24599450	Thus, these results indicate that increased NSF <strong>GluR2</strong> interactions in the NAc after withdrawal from cocaine attenuated the expression of behavioral <b>sensitization</b> and serves as a negative regulatory mechanism in drug exposed individuals.
+GRIA2	addiction	withdrawal	24599450	Thus, these results indicate that increased NSF <strong>GluR2</strong> interactions in the NAc after <b>withdrawal</b> from cocaine attenuated the expression of behavioral sensitization and serves as a negative regulatory mechanism in drug exposed individuals.
+GRIA2	drug	cocaine	24599450	Thus, these results indicate that increased NSF <strong><strong>GluR2</strong></strong> interactions in the NAc after withdrawal from <b>cocaine</b> attenuated the expression of behavioral sensitization and serves as a negative regulatory mechanism in drug exposed individuals.
+GRIA2	addiction	sensitization	24599450	Thus, these results indicate that increased NSF <strong><strong>GluR2</strong></strong> interactions in the NAc after withdrawal from cocaine attenuated the expression of behavioral <b>sensitization</b> and serves as a negative regulatory mechanism in drug exposed individuals.
+GRIA2	addiction	withdrawal	24599450	Thus, these results indicate that increased NSF <strong><strong>GluR2</strong></strong> interactions in the NAc after <b>withdrawal</b> from cocaine attenuated the expression of behavioral sensitization and serves as a negative regulatory mechanism in drug exposed individuals.
+GRIA2	drug	amphetamine	24535653	FR increased GluA1 in the PSD, and D <b>amphetamine</b> increased p Ser845 GluA1, GluA1, <strong>GluA2</strong>, but not GluA3, with a greater effect in FR than AL rats.
+GRIA2	drug	amphetamine	24535653	The D <b>amphetamine</b> induced increase in synaptic p Ser845 GluA1, GluA1, and <strong>GluA2</strong> may contribute to the rewarding effect of D <b>amphetamine</b>, but may also be a mechanism of synaptic strengthening and behavior modification.
+GRIA2	drug	alcohol	24523671	Out of the 16 glutamate receptor subunits, mRNAs encoding two AMPA [2 amino 3 (3 hydroxy 5 methyl isoxazol 4 yl)propanoic acid] receptor subunits <strong>GluA2</strong> and GluA3; three kainate receptor subunits GluK2, GluK3 and GluK5 and five NMDA (N methyl D aspartate) receptor subunits GluN1, GluN2A, GluN2C, GluN2D, and GluN3A were significantly increased in the HP DG region in <b>alcoholics</b>.
+GRIA2	addiction	sensitization	24290077	The present study uses an "interference" peptide, Tat <strong>GluA2</strong>(3Y), that blocks long term depression (LTD) at glutamatergic synapses by disrupting the endocytosis of α  amino 3 hydroxy 5 methylisoxazole 4 propionic acid receptors (AMPARs), to explore the role of this form of synaptic plasticity in the induction and maintenance of <b>sensitization</b>.
+GRIA2	drug	amphetamine	24290077	Tat <strong>GluA2</strong>(3Y), was administered by 2 different routes (intravenously and intracerebrally to the ventral tegmental area [VTA] or to the NAcc) before each injection of d <b>AMPH</b>.
+GRIA2	addiction	sensitization	24290077	Systemic administration of Tat <strong>GluA2</strong>(3Y) during the induction phase blocked maintenance of behavioural <b>sensitization</b> and attenuated the maintenance of neurochemical <b>sensitization</b>.
+GRIA2	drug	amphetamine	24290077	Intra VTA infusion of Tat <strong>GluA2</strong>(3Y) before each administration of d <b>AMPH</b> did not affect induction, but inhibited maintenance and subsequent expression of sensitization, whereas intra NAcc infusion of the peptide did not affect induction or maintenance of sensitization.
+GRIA2	addiction	sensitization	24290077	Intra VTA infusion of Tat <strong>GluA2</strong>(3Y) before each administration of d AMPH did not affect induction, but inhibited maintenance and subsequent expression of <b>sensitization</b>, whereas intra NAcc infusion of the peptide did not affect induction or maintenance of <b>sensitization</b>.
+GRIA2	addiction	sensitization	24290077	Furthermore, the unique ability of Tat <strong>GluA2</strong>(3Y) to block maintenance of behavioural <b>sensitization</b> implicates LTD in the consolidation of essential associative memories.
+GRIA2	addiction	relapse	24290077	Tat <strong>GluA2</strong>(3Y) has the unique ability to disrupt functional neuroadaptations triggered by repeated psychostimulant exposure and therefore may protect against the development of <b>craving</b> and drug <b>seeking</b> behaviours.
+GRIA2	drug	cocaine	24262606	We found that surface Hcrtr 2 levels remain unchanged following 14, 25 or 48 days of withdrawal from <b>cocaine</b>, a time period in which high conductance <strong>GluA2</strong> lacking AMPA receptors progressively emerge in the NAc.
+GRIA2	addiction	withdrawal	24262606	We found that surface Hcrtr 2 levels remain unchanged following 14, 25 or 48 days of <b>withdrawal</b> from cocaine, a time period in which high conductance <strong>GluA2</strong> lacking AMPA receptors progressively emerge in the NAc.
+GRIA2	drug	amphetamine	24239129	Chronic <b>METH</b> decreased transcript and protein expression of GluA1 and <strong>GluA2</strong> alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid receptor (AMPAR) and GluN1 N methyl D aspartate receptor subunits.
+GRIA2	drug	amphetamine	24239129	Chromatin immunoprecipitation polymerase chain reaction revealed that <b>METH</b> decreased enrichment of acetylated histone H4 on GluA1, <strong>GluA2</strong>, and GluN1 promoters.
+GRIA2	drug	amphetamine	24239129	<b>Methamphetamine</b> exposure also increased repressor element 1 silencing transcription factor (REST) corepressor 1, methylated CpG binding protein 2, and histone deacetylase 2 enrichment, but not of sirtuin 1 or sirtuin 2, onto GluA1 and <strong>GluA2</strong> gene sequences.
+GRIA2	drug	amphetamine	24239129	Surprisingly, methylated DNA immunoprecipitation and hydroxymethylated DNA immunoprecipitation polymerase chain reaction revealed <b>METH</b> induced decreased enrichment of 5 methylcytosine and 5 hydroxymethylcytosine at GluA1 and <strong>GluA2</strong> promoter sequences.
+GRIA2	drug	amphetamine	24231469	<strong>GluA2</strong> S880 phosphorylation in synaptic and extrasynaptic fractions in the two brain regions also remained stable in response to <b>amphetamine</b>.
+GRIA2	drug	cocaine	24126453	Glutamate receptor interacting protein (GRIP) is a neuronal scaffolding protein that stabilizes <strong>GluA2</strong> AMPARs at synapses but its role in <b>cocaine</b> addiction has not been examined.
+GRIA2	addiction	addiction	24126453	Glutamate receptor interacting protein (GRIP) is a neuronal scaffolding protein that stabilizes <strong>GluA2</strong> AMPARs at synapses but its role in cocaine <b>addiction</b> has not been examined.
+GRIA2	drug	cocaine	24109187	Also, <b>cocaine</b> self administration and withdrawal induce the formation of subunit glutamate receptor 2 (<strong>GluA2</strong>), lacking the Ca(2+) permeable AMPA receptors (CP AMPARs) at the level of the NAc.
+GRIA2	addiction	withdrawal	24109187	Also, cocaine self administration and <b>withdrawal</b> induce the formation of subunit glutamate receptor 2 (<strong>GluA2</strong>), lacking the Ca(2+) permeable AMPA receptors (CP AMPARs) at the level of the NAc.
+GRIA2	drug	cocaine	23986250	<b>Cocaine</b> seeking previously was linked to increased phosphorylation of <strong>GluA2</strong> at Ser880, a PKC phosphorylation site, which promotes the endocytosis of <strong>GluA2</strong> containing AMPA receptors via interactions with Protein Associated with C Kinase (PICK1).
+GRIA2	addiction	relapse	23986250	Cocaine <b>seeking</b> previously was linked to increased phosphorylation of <strong>GluA2</strong> at Ser880, a PKC phosphorylation site, which promotes the endocytosis of <strong>GluA2</strong> containing AMPA receptors via interactions with Protein Associated with C Kinase (PICK1).
+GRIA2	drug	cocaine	23986250	Moreover, the endocytosis of shell <strong>GluA2</strong> containing AMPARs during <b>cocaine</b> seeking may depend on interactions with PKCγ and PICK1.
+GRIA2	addiction	relapse	23986250	Moreover, the endocytosis of shell <strong>GluA2</strong> containing AMPARs during cocaine <b>seeking</b> may depend on interactions with PKCγ and PICK1.
+GRIA2	drug	amphetamine	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (GluA1, <strong>GluA2</strong>) and mGlu5, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated morphine (8 mg/kg) or <b>methamphetamine</b> (1 mg/kg) (treatments producing behavioral sensitization).
+GRIA2	drug	opioid	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (GluA1, <strong>GluA2</strong>) and mGlu5, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated <b>morphine</b> (8 mg/kg) or methamphetamine (1 mg/kg) (treatments producing behavioral sensitization).
+GRIA2	addiction	sensitization	23711322	STEP61 levels, and cellular distribution/expression of AMPAR subunits (GluA1, <strong>GluA2</strong>) and mGlu5, were evaluated via a protein cross linking assay in medial prefrontal cortex (mPFC), nucleus accumbens (NAc), and ventral pallidum (VP) harvested 1 day after acute, or fourteen days after repeated morphine (8 mg/kg) or methamphetamine (1 mg/kg) (treatments producing behavioral <b>sensitization</b>).
+GRIA2	drug	opioid	23711322	Acute <b>morphine</b> decreased GluA1 and <strong>GluA2</strong> surface expression in mPFC and GluA1 in NAc.
+GRIA2	drug	amphetamine	23711322	In mPFC, mGlu5 were unaltered; however, after <b>methamphetamine</b>, STEP61 levels decreased and <strong>GluA2</strong> surface expression increased.
+GRIA2	drug	amphetamine	23711322	Pre treatment with a mGlu5 selective negative allosteric modulator, blocked <b>methamphetamine</b> induced behavioral sensitization and changes in mPFC <strong>GluA2</strong> and STEP61 .
+GRIA2	addiction	sensitization	23711322	Pre treatment with a mGlu5 selective negative allosteric modulator, blocked methamphetamine induced behavioral <b>sensitization</b> and changes in mPFC <strong>GluA2</strong> and STEP61 .
+GRIA2	drug	amphetamine	23711322	These data reveal (i) region specific distinctions in glutamate receptor trafficking between acute and repeated treatments of morphine and <b>methamphetamine</b>, and (ii) that mGlu5 is necessary for <b>methamphetamine</b> induced alterations in mPFC <strong>GluA2</strong> and STEP61 .
+GRIA2	drug	opioid	23711322	These data reveal (i) region specific distinctions in glutamate receptor trafficking between acute and repeated treatments of <b>morphine</b> and methamphetamine, and (ii) that mGlu5 is necessary for methamphetamine induced alterations in mPFC <strong>GluA2</strong> and STEP61 .
+GRIA2	addiction	reward	23603364	MeAM <b>CPP</b> increased surface expression of GluR1 and <strong>GluR2</strong> subunits of AMPA receptor in the BLA.
+GRIA2	addiction	reward	23603364	MeAM <b>CPP</b> increased surface expression of GluR1 and <strong><strong>GluR2</strong></strong> subunits of AMPA receptor in the BLA.
+GRIA2	drug	opioid	23564315	We also looked at the effect of <b>morphine</b> on other glutamate receptor subunits, including AMPA <strong>GluR2</strong> (<strong>GluR2</strong>) and NMDA NR1 (NR1).
+GRIA2	drug	opioid	23564315	We also looked at the effect of <b>morphine</b> on other glutamate receptor subunits, including AMPA <strong><strong>GluR2</strong></strong> (<strong><strong>GluR2</strong></strong>) and NMDA NR1 (NR1).
+GRIA2	drug	nicotine	23518606	In addition, relapse to <b>nicotine</b> seeking increased the phosphorylation levels of <strong>GluR2</strong> Ser880, NR1 Ser890, and p38 MAPK in the nucleus accumbens (NAc), but not in the prefrontal cortex.
+GRIA2	addiction	relapse	23518606	In addition, <b>relapse</b> to nicotine <b>seeking</b> increased the phosphorylation levels of <strong>GluR2</strong> Ser880, NR1 Ser890, and p38 MAPK in the nucleus accumbens (NAc), but not in the prefrontal cortex.
+GRIA2	drug	nicotine	23518606	In addition, relapse to <b>nicotine</b> seeking increased the phosphorylation levels of <strong><strong>GluR2</strong></strong> Ser880, NR1 Ser890, and p38 MAPK in the nucleus accumbens (NAc), but not in the prefrontal cortex.
+GRIA2	addiction	relapse	23518606	In addition, <b>relapse</b> to nicotine <b>seeking</b> increased the phosphorylation levels of <strong><strong>GluR2</strong></strong> Ser880, NR1 Ser890, and p38 MAPK in the nucleus accumbens (NAc), but not in the prefrontal cortex.
+GRIA2	drug	nicotine	23518606	The intra accumbens infusion of the protein kinase C (PKC) inhibitor NPC 15437 reduced <b>nicotine</b> seeking behavior elicited by drug paired cues consistent with the PKC dependent phosphorylations of <strong>GluR2</strong> Ser880 and NR1 Ser890.
+GRIA2	addiction	relapse	23518606	The intra accumbens infusion of the protein kinase C (PKC) inhibitor NPC 15437 reduced nicotine <b>seeking</b> behavior elicited by drug paired cues consistent with the PKC dependent phosphorylations of <strong>GluR2</strong> Ser880 and NR1 Ser890.
+GRIA2	drug	nicotine	23518606	The intra accumbens infusion of the protein kinase C (PKC) inhibitor NPC 15437 reduced <b>nicotine</b> seeking behavior elicited by drug paired cues consistent with the PKC dependent phosphorylations of <strong><strong>GluR2</strong></strong> Ser880 and NR1 Ser890.
+GRIA2	addiction	relapse	23518606	The intra accumbens infusion of the protein kinase C (PKC) inhibitor NPC 15437 reduced nicotine <b>seeking</b> behavior elicited by drug paired cues consistent with the PKC dependent phosphorylations of <strong><strong>GluR2</strong></strong> Ser880 and NR1 Ser890.
+GRIA2	drug	opioid	23403695	We have recently reported that repeated <b>morphine</b> administration triggers an insertion of <strong>GluA2</strong> lacking (Ca(2+) permeable) α amino 3 hydroxy 5 methyl 4 isoxazole propionic acid receptors (AMPAR) in the hippocampus.
+GRIA2	drug	psychedelics	23352746	Individual and combined effects of rhynchophylline and <b>ketamine</b> on proliferation, NMDAR1 and <strong>GluA2</strong>/3 protein expression in PC12 cells.
+GRIA2	drug	psychedelics	23352746	The individual and combined effects of rhynchophylline and <b>ketamine</b> on proliferation and GluN1 and <strong>GluA2</strong>/3 protein expression in PC12 cells were investigated.
+GRIA2	drug	psychedelics	23352746	While <strong>GluA2</strong>/3 protein expression was upregulated by <b>ketamine</b>, it was not influenced by rhynchophylline.
+GRIA2	drug	psychedelics	23352746	These findings demonstrate that rhynchophylline suppresses <strong>GluA2</strong>/3 expression in <b>ketamine</b> induced PC12 cells and downregulates GluN1 expression.
+GRIA2	addiction	reward	23345231	Adenoviral knockdown of CeA <strong>GluA2</strong> subunits facilitated <b>CPP</b> acquisition, but did not alter <b>CPP</b> extinction.
+GRIA2	addiction	reward	23303053	We also found that lactacystin infusion into the NAc core but not into the shell immediately after extinction training sessions inhibited <b>CPP</b> extinction and reversed the extinction training induced decrease in NSF and <strong>GluR2</strong> in the synaptosomal membrane fraction in the NAc core.
+GRIA2	addiction	reward	23303053	We also found that lactacystin infusion into the NAc core but not into the shell immediately after extinction training sessions inhibited <b>CPP</b> extinction and reversed the extinction training induced decrease in NSF and <strong><strong>GluR2</strong></strong> in the synaptosomal membrane fraction in the NAc core.
+GRIA2	drug	alcohol	23100433	LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of <b>ethanol</b>, as well as cycles of excessive <b>ethanol</b> consumption and withdrawal, produced a long lasting increase in synaptic localization of the GluR1 and <strong>GluR2</strong> subunits of AMPARs in the DMS.
+GRIA2	addiction	withdrawal	23100433	LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of ethanol, as well as cycles of excessive ethanol consumption and <b>withdrawal</b>, produced a long lasting increase in synaptic localization of the GluR1 and <strong>GluR2</strong> subunits of AMPARs in the DMS.
+GRIA2	drug	alcohol	23100433	LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of <b>ethanol</b>, as well as cycles of excessive <b>ethanol</b> consumption and withdrawal, produced a long lasting increase in synaptic localization of the GluR1 and <strong><strong>GluR2</strong></strong> subunits of AMPARs in the DMS.
+GRIA2	addiction	withdrawal	23100433	LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of ethanol, as well as cycles of excessive ethanol consumption and <b>withdrawal</b>, produced a long lasting increase in synaptic localization of the GluR1 and <strong><strong>GluR2</strong></strong> subunits of AMPARs in the DMS.
+GRIA2	drug	cocaine	22956853	As a consequence, a protocol pairing presynaptic glutamate release with somatic hyperpolarization, to increase the efficiency of <strong>GluA2</strong> lacking AMPA receptors, elicited a long term potentiation in neurons only from <b>cocaine</b> treated mice.
+GRIA2	addiction	aversion	22933785	We further demonstrated that Arc/Arg3.1 regulated AMPAR endocytosis was <strong>GluR2</strong> dependent, as intra amygdala injection of Tat <strong>GluR2</strong>(3Y), a <strong>GluR2</strong> derived peptide that has been shown to specifically block regulated, but not constitutive, AMPAR endocytosis, prevented AMPAR endocytosis, LTD induction, and <b>aversive</b> memory formation.
+GRIA2	addiction	aversion	22933785	We further demonstrated that Arc/Arg3.1 regulated AMPAR endocytosis was <strong><strong>GluR2</strong></strong> dependent, as intra amygdala injection of Tat <strong><strong>GluR2</strong></strong>(3Y), a <strong><strong>GluR2</strong></strong> derived peptide that has been shown to specifically block regulated, but not constitutive, AMPAR endocytosis, prevented AMPAR endocytosis, LTD induction, and <b>aversive</b> memory formation.
+GRIA2	drug	cocaine	22860224	In <b>cocaine</b> treated mice, C2 significantly elevates mRNA levels of the AMPA glutamate receptor <strong>GluR2</strong> subunit with specificity, a known target gene of ΔFosB that plays a role in drug addiction and endogenous resilience mechanisms.
+GRIA2	addiction	addiction	22860224	In cocaine treated mice, C2 significantly elevates mRNA levels of the AMPA glutamate receptor <strong>GluR2</strong> subunit with specificity, a known target gene of ΔFosB that plays a role in drug <b>addiction</b> and endogenous resilience mechanisms.
+GRIA2	drug	cocaine	22860224	In <b>cocaine</b> treated mice, C2 significantly elevates mRNA levels of the AMPA glutamate receptor <strong><strong>GluR2</strong></strong> subunit with specificity, a known target gene of ΔFosB that plays a role in drug addiction and endogenous resilience mechanisms.
+GRIA2	addiction	addiction	22860224	In cocaine treated mice, C2 significantly elevates mRNA levels of the AMPA glutamate receptor <strong><strong>GluR2</strong></strong> subunit with specificity, a known target gene of ΔFosB that plays a role in drug <b>addiction</b> and endogenous resilience mechanisms.
+GRIA2	drug	cocaine	22754497	This plasticity is rapid in onset (hours), <strong>GluA2</strong> dependent, and can be observed with a single <b>cocaine</b> injection.
+GRIA2	drug	cocaine	22721675	We used regional analyses of c Fos and <strong>GluR2</strong> protein expression to delineate neural activity and plasticity that may be associated with <b>cocaine</b> cue extinction learning.
+GRIA2	drug	cocaine	22721675	We used regional analyses of c Fos and <strong><strong>GluR2</strong></strong> protein expression to delineate neural activity and plasticity that may be associated with <b>cocaine</b> cue extinction learning.
+GRIA2	drug	cocaine	22721675	Findings suggest that basolateral amygdala and prelimbic prefrontal cortex neurons are activated during acquisition of <b>cocaine</b> cue extinction learning, a process that is independent of changes in <strong>GluR2</strong> abundance.
+GRIA2	drug	cocaine	22721675	Findings suggest that basolateral amygdala and prelimbic prefrontal cortex neurons are activated during acquisition of <b>cocaine</b> cue extinction learning, a process that is independent of changes in <strong><strong>GluR2</strong></strong> abundance.
+GRIA2	drug	opioid	22633960	Facilitated extinction of <b>morphine</b> conditioned place preference with Tat <strong>GluA2</strong>(3Y) interference peptide.
+GRIA2	drug	opioid	22633960	In this study, Tat <strong>GluA2</strong>(3Y) was used to assess the role of LTD in the induction, expression, extinction and reinstatement of <b>morphine</b> induced conditioned place preference (CPP).
+GRIA2	addiction	relapse	22633960	In this study, Tat <strong>GluA2</strong>(3Y) was used to assess the role of LTD in the induction, expression, extinction and <b>reinstatement</b> of morphine induced conditioned place preference (CPP).
+GRIA2	addiction	reward	22633960	In this study, Tat <strong>GluA2</strong>(3Y) was used to assess the role of LTD in the induction, expression, extinction and reinstatement of morphine induced conditioned place preference (<b>CPP</b>).
+GRIA2	addiction	reward	22633960	), scrambled peptide (Tat <strong>GluA2</strong>(Sc)), or vehicle was administered during the acquisition phase or prior to the test for <b>CPP</b>.
+GRIA2	drug	opioid	22633960	Tat <strong>GluA2</strong>(3Y) had no effect on the induction or initial expression of <b>morphine</b> induced CPP.
+GRIA2	addiction	reward	22633960	Tat <strong>GluA2</strong>(3Y) had no effect on the induction or initial expression of morphine induced <b>CPP</b>.
+GRIA2	drug	opioid	22633960	Rats that received Tat <strong>GluA2</strong>(3Y) or Tat <strong>GluA2</strong>(Sc) during acquisition were subsequently tested for 11 consecutive days in order to extinguish <b>morphine</b> CPP.
+GRIA2	addiction	reward	22633960	Rats that received Tat <strong>GluA2</strong>(3Y) or Tat <strong>GluA2</strong>(Sc) during acquisition were subsequently tested for 11 consecutive days in order to extinguish morphine <b>CPP</b>.
+GRIA2	drug	opioid	22633960	Co administration of <b>morphine</b> and Tat <strong>GluA2</strong>(3Y) during acquisition greatly facilitated extinction of CPP without affecting <b>morphine</b> induced reinstatement of CPP.
+GRIA2	addiction	relapse	22633960	Co administration of morphine and Tat <strong>GluA2</strong>(3Y) during acquisition greatly facilitated extinction of CPP without affecting morphine induced <b>reinstatement</b> of CPP.
+GRIA2	addiction	reward	22633960	Co administration of morphine and Tat <strong>GluA2</strong>(3Y) during acquisition greatly facilitated extinction of <b>CPP</b> without affecting morphine induced reinstatement of <b>CPP</b>.
+GRIA2	addiction	reward	22633960	Using an intermittent retest schedule with bi weekly tests to measure the maintenance of <b>CPP</b>, Tat <strong>GluA2</strong>(3Y) during the acquisition phase had no effect on the maintenance of <b>CPP</b>.
+GRIA2	drug	opioid	22633960	We propose that co administration of Tat <strong>GluA2</strong>(3Y) with <b>morphine</b> during acquisition of CPP weakens the association between <b>morphine</b> and contextual cues leading to rapid extinction of <b>morphine</b> CPP with repeated daily testing.
+GRIA2	addiction	reward	22633960	We propose that co administration of Tat <strong>GluA2</strong>(3Y) with morphine during acquisition of <b>CPP</b> weakens the association between morphine and contextual cues leading to rapid extinction of morphine <b>CPP</b> with repeated daily testing.
+GRIA2	drug	alcohol	22291662	<strong>GRIA2</strong> flop mRNA levels in this region were positively correlated with daily <b>ethanol</b> intake and BEC averaged over the 6 months prior to necropsy.
+GRIA2	drug	cocaine	22197517	Expression of AMPA receptor subunits (GluR1 and <strong>GluR2</strong>) and CRE binding protein (CREB) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of <b>cocaine</b>, with and without ICSS.
+GRIA2	addiction	reward	22197517	Expression of AMPA receptor subunits (GluR1 and <strong>GluR2</strong>) and CRE binding protein (CREB) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of cocaine, with and without <b>ICSS</b>.
+GRIA2	drug	cocaine	22197517	Expression of AMPA receptor subunits (GluR1 and <strong><strong>GluR2</strong></strong>) and CRE binding protein (CREB) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of <b>cocaine</b>, with and without ICSS.
+GRIA2	addiction	reward	22197517	Expression of AMPA receptor subunits (GluR1 and <strong><strong>GluR2</strong></strong>) and CRE binding protein (CREB) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of cocaine, with and without <b>ICSS</b>.
+GRIA2	drug	cocaine	22197517	Repeated <b>cocaine</b> reduced GluR1, <strong>GluR2</strong> and CREB expression in the NAc, and reductions of GluR1 and <strong>GluR2</strong> but not CREB were further enhanced by ICSS.
+GRIA2	addiction	reward	22197517	Repeated cocaine reduced GluR1, <strong>GluR2</strong> and CREB expression in the NAc, and reductions of GluR1 and <strong>GluR2</strong> but not CREB were further enhanced by <b>ICSS</b>.
+GRIA2	drug	cocaine	22197517	Repeated <b>cocaine</b> reduced GluR1, <strong><strong>GluR2</strong></strong> and CREB expression in the NAc, and reductions of GluR1 and <strong><strong>GluR2</strong></strong> but not CREB were further enhanced by ICSS.
+GRIA2	addiction	reward	22197517	Repeated cocaine reduced GluR1, <strong><strong>GluR2</strong></strong> and CREB expression in the NAc, and reductions of GluR1 and <strong><strong>GluR2</strong></strong> but not CREB were further enhanced by <b>ICSS</b>.
+GRIA2	addiction	reward	22127928	Finally, we found that the levels of PKMζ and <strong>GluR2</strong> in the NAc remained unchanged, while the GluR1 levels were elevated following <b>CPP</b> and fully reversed by ZIP injection.
+GRIA2	addiction	reward	22127928	Finally, we found that the levels of PKMζ and <strong><strong>GluR2</strong></strong> in the NAc remained unchanged, while the GluR1 levels were elevated following <b>CPP</b> and fully reversed by ZIP injection.
+GRIA2	drug	cocaine	22072669	Finally, reduced surface expression of the <strong>GluR2</strong> subunit of the AMPA receptor is associated with <b>cocaine</b> seeking, and daily RGD microinjections during self administration training normalized the surface expression of <strong>GluR2</strong>.
+GRIA2	addiction	relapse	22072669	Finally, reduced surface expression of the <strong>GluR2</strong> subunit of the AMPA receptor is associated with cocaine <b>seeking</b>, and daily RGD microinjections during self administration training normalized the surface expression of <strong>GluR2</strong>.
+GRIA2	drug	cocaine	22072669	Finally, reduced surface expression of the <strong><strong>GluR2</strong></strong> subunit of the AMPA receptor is associated with <b>cocaine</b> seeking, and daily RGD microinjections during self administration training normalized the surface expression of <strong><strong>GluR2</strong></strong>.
+GRIA2	addiction	relapse	22072669	Finally, reduced surface expression of the <strong><strong>GluR2</strong></strong> subunit of the AMPA receptor is associated with cocaine <b>seeking</b>, and daily RGD microinjections during self administration training normalized the surface expression of <strong><strong>GluR2</strong></strong>.
+GRIA2	drug	cocaine	22072669	Together, these data indicate that the regulation integrins may contribute to <b>cocaine</b> reinstated drug seeking, in part by promoting reduced <strong>GluR2</strong> surface expression.
+GRIA2	addiction	relapse	22072669	Together, these data indicate that the regulation integrins may contribute to cocaine reinstated drug <b>seeking</b>, in part by promoting reduced <strong>GluR2</strong> surface expression.
+GRIA2	drug	cocaine	22072669	Together, these data indicate that the regulation integrins may contribute to <b>cocaine</b> reinstated drug seeking, in part by promoting reduced <strong><strong>GluR2</strong></strong> surface expression.
+GRIA2	addiction	relapse	22072669	Together, these data indicate that the regulation integrins may contribute to cocaine reinstated drug <b>seeking</b>, in part by promoting reduced <strong><strong>GluR2</strong></strong> surface expression.
+GRIA2	drug	cocaine	21613507	Here we show that daily intravenous <b>cocaine</b> self administration, but not passive <b>cocaine</b> administration, induces dynamic upregulation of the AMPA glutamate receptor subunits GluR1 and <strong>GluR2</strong> in the ventral tegmental area (VTA) of rats.
+GRIA2	drug	cocaine	21613507	Here we show that daily intravenous <b>cocaine</b> self administration, but not passive <b>cocaine</b> administration, induces dynamic upregulation of the AMPA glutamate receptor subunits GluR1 and <strong><strong>GluR2</strong></strong> in the ventral tegmental area (VTA) of rats.
+GRIA2	drug	cocaine	21490215	However, synaptic incorporation of <strong>GluA2</strong> lacking/Ca(2+) permeable AMPARs (CP AMPARs) was observed after longer withdrawal (WD35) from repeated noncontingent <b>cocaine</b> injections in young mice (Mameli et al., 2009).
+GRIA2	addiction	withdrawal	21490215	However, synaptic incorporation of <strong>GluA2</strong> lacking/Ca(2+) permeable AMPARs (CP AMPARs) was observed after longer <b>withdrawal</b> (WD35) from repeated noncontingent cocaine injections in young mice (Mameli et al., 2009).
+GRIA2	drug	opioid	21471379	Accumbens core injections of Tat <strong>GluR2</strong>(3Y), which inhibits <strong>GluR2</strong> dependent AMPA receptor endocytosis, prevented the impairment in <b>morphine</b> CPP induced by local ZIP injections, indicating that the persistent effect of PKMζ is on <strong>GluR2</strong> containing AMPA receptors.
+GRIA2	addiction	reward	21471379	Accumbens core injections of Tat <strong>GluR2</strong>(3Y), which inhibits <strong>GluR2</strong> dependent AMPA receptor endocytosis, prevented the impairment in morphine <b>CPP</b> induced by local ZIP injections, indicating that the persistent effect of PKMζ is on <strong>GluR2</strong> containing AMPA receptors.
+GRIA2	drug	opioid	21471379	Accumbens core injections of Tat <strong><strong>GluR2</strong></strong>(3Y), which inhibits <strong><strong>GluR2</strong></strong> dependent AMPA receptor endocytosis, prevented the impairment in <b>morphine</b> CPP induced by local ZIP injections, indicating that the persistent effect of PKMζ is on <strong><strong>GluR2</strong></strong> containing AMPA receptors.
+GRIA2	addiction	reward	21471379	Accumbens core injections of Tat <strong><strong>GluR2</strong></strong>(3Y), which inhibits <strong><strong>GluR2</strong></strong> dependent AMPA receptor endocytosis, prevented the impairment in morphine <b>CPP</b> induced by local ZIP injections, indicating that the persistent effect of PKMζ is on <strong><strong>GluR2</strong></strong> containing AMPA receptors.
+GRIA2	drug	opioid	21459090	With an emphasis on a recent publication describing the anatomical relationship between the μ <b>opioid</b> receptor (MOR) and the AMPA <strong>GluR2</strong> subunit (Beckerman, M. A., and Glass, M. J., 2011.
+GRIA2	drug	opioid	21459090	With an emphasis on a recent publication describing the anatomical relationship between the μ <b>opioid</b> receptor (MOR) and the AMPA <strong><strong>GluR2</strong></strong> subunit (Beckerman, M. A., and Glass, M. J., 2011.
+GRIA2	drug	opioid	21459090	Ultrastructural relationship between the AMPA <strong>GluR2</strong> receptor subunit and the mu <b>opioid</b> receptor in the mouse central nucleus of the amygdala.
+GRIA2	drug	opioid	21459090	Ultrastructural relationship between the AMPA <strong><strong>GluR2</strong></strong> receptor subunit and the mu <b>opioid</b> receptor in the mouse central nucleus of the amygdala.
+GRIA2	drug	cocaine	21336270	We found that <b>cocaine</b> reduced NMDA receptor excitatory postsynaptic currents and inserted <strong>GluA2</strong> lacking AMPA receptors in dopamine neurons of mice.
+GRIA2	drug	cocaine	21209835	<b>Cocaine</b> for example drives insertion of <strong>GluA2</strong> lacking AMPA receptors (AMPARs) at glutamatergic synapes in DA neurons.
+GRIA2	drug	cocaine	21209835	Finally, activating DA VTA neurons optogenetically is sufficient to drive insertion of <strong>GluA2</strong> lacking AMPARs, mimicking the changes observed after a single injection of morphine, nicotine or <b>cocaine</b>.
+GRIA2	drug	nicotine	21209835	Finally, activating DA VTA neurons optogenetically is sufficient to drive insertion of <strong>GluA2</strong> lacking AMPARs, mimicking the changes observed after a single injection of morphine, <b>nicotine</b> or cocaine.
+GRIA2	drug	opioid	21209835	Finally, activating DA VTA neurons optogenetically is sufficient to drive insertion of <strong>GluA2</strong> lacking AMPARs, mimicking the changes observed after a single injection of <b>morphine</b>, nicotine or cocaine.
+GRIA2	drug	cannabinoid	21187978	Here we show in rats that chronic <b>cannabinoid</b> exposure activates VTA <b>cannabinoid</b> CB1 receptors to induce transient neurotransmission depression at VTA local Glu DA synapses through activation of NMDA receptors and subsequent endocytosis of AMPA receptor <strong>GluR2</strong> subunits.
+GRIA2	drug	cannabinoid	21187978	Here we show in rats that chronic <b>cannabinoid</b> exposure activates VTA <b>cannabinoid</b> CB1 receptors to induce transient neurotransmission depression at VTA local Glu DA synapses through activation of NMDA receptors and subsequent endocytosis of AMPA receptor <strong><strong>GluR2</strong></strong> subunits.
+GRIA2	drug	cannabinoid	21187978	A <strong>GluR2</strong> derived peptide blocks <b>cannabinoid</b> induced VTA synaptic depression and conditioned place preference, i.e., learning to associate drug exposure with environmental cues.
+GRIA2	drug	cannabinoid	21187978	A <strong><strong>GluR2</strong></strong> derived peptide blocks <b>cannabinoid</b> induced VTA synaptic depression and conditioned place preference, i.e., learning to associate drug exposure with environmental cues.
+GRIA2	drug	cannabinoid	21187978	These data not only provide the first evidence, to our knowledge, that NMDA receptor dependent synaptic depression at VTA dopamine circuitry requires <strong>GluR2</strong> endocytosis, but also suggest an essential contribution of such synaptic depression to <b>cannabinoid</b> associated addictive learning, in addition to pointing to novel pharmacological strategies for the treatment of <b>cannabis</b> addiction.
+GRIA2	addiction	addiction	21187978	These data not only provide the first evidence, to our knowledge, that NMDA receptor dependent synaptic depression at VTA dopamine circuitry requires <strong>GluR2</strong> endocytosis, but also suggest an essential contribution of such synaptic depression to cannabinoid associated <b>addictive</b> learning, in addition to pointing to novel pharmacological strategies for the treatment of cannabis <b>addiction</b>.
+GRIA2	drug	cannabinoid	21187978	These data not only provide the first evidence, to our knowledge, that NMDA receptor dependent synaptic depression at VTA dopamine circuitry requires <strong><strong>GluR2</strong></strong> endocytosis, but also suggest an essential contribution of such synaptic depression to <b>cannabinoid</b> associated addictive learning, in addition to pointing to novel pharmacological strategies for the treatment of <b>cannabis</b> addiction.
+GRIA2	addiction	addiction	21187978	These data not only provide the first evidence, to our knowledge, that NMDA receptor dependent synaptic depression at VTA dopamine circuitry requires <strong><strong>GluR2</strong></strong> endocytosis, but also suggest an essential contribution of such synaptic depression to cannabinoid associated <b>addictive</b> learning, in addition to pointing to novel pharmacological strategies for the treatment of cannabis <b>addiction</b>.
+GRIA2	drug	opioid	21175880	Repeated <b>morphine</b> treatment decreased surface expression of GluA1 in the medial prefrontal cortex without affecting levels of <strong>GluA2</strong>.
+GRIA2	drug	opioid	20970421	Ultrastructural relationship between the AMPA <strong>GluR2</strong> receptor subunit and the mu <b>opioid</b> receptor in the mouse central nucleus of the amygdala.
+GRIA2	drug	opioid	20970421	Ultrastructural relationship between the AMPA <strong><strong>GluR2</strong></strong> receptor subunit and the mu <b>opioid</b> receptor in the mouse central nucleus of the amygdala.
+GRIA2	drug	opioid	20970421	Activation of <strong>GluR2</strong> expressing non calcium permeable AMPA type glutamate receptors in the central nucleus of the amygdala (CeA) may play an important role in integrating emotion and memory with goal directed behaviors involved in <b>opioid</b> addiction.
+GRIA2	addiction	addiction	20970421	Activation of <strong>GluR2</strong> expressing non calcium permeable AMPA type glutamate receptors in the central nucleus of the amygdala (CeA) may play an important role in integrating emotion and memory with goal directed behaviors involved in opioid <b>addiction</b>.
+GRIA2	drug	opioid	20970421	Activation of <strong><strong>GluR2</strong></strong> expressing non calcium permeable AMPA type glutamate receptors in the central nucleus of the amygdala (CeA) may play an important role in integrating emotion and memory with goal directed behaviors involved in <b>opioid</b> addiction.
+GRIA2	addiction	addiction	20970421	Activation of <strong><strong>GluR2</strong></strong> expressing non calcium permeable AMPA type glutamate receptors in the central nucleus of the amygdala (CeA) may play an important role in integrating emotion and memory with goal directed behaviors involved in opioid <b>addiction</b>.
+GRIA2	addiction	addiction	20970421	The presence of <strong>GluR2</strong> in dendritic profiles receiving asymmetric synapses suggests that activation of the non calcium permeable AMPA receptor plays a role in the postsynaptic modulation of excitatory signaling involving CeA neuronal circuits that coordinate sensory, affective, and behavioral processes involved in drug <b>addiction</b>.
+GRIA2	addiction	addiction	20970421	The presence of <strong><strong>GluR2</strong></strong> in dendritic profiles receiving asymmetric synapses suggests that activation of the non calcium permeable AMPA receptor plays a role in the postsynaptic modulation of excitatory signaling involving CeA neuronal circuits that coordinate sensory, affective, and behavioral processes involved in drug <b>addiction</b>.
+GRIA2	drug	cocaine	20942997	Following re exposure to a <b>cocaine</b> paired context, surface expression of the AMPA type glutamate receptor GluR1 was significantly reduced whereas <strong>GluR2</strong> was significantly increased in the dlCPu, independent of Arc antisense ODN infusion.
+GRIA2	drug	cocaine	20942997	Following re exposure to a <b>cocaine</b> paired context, surface expression of the AMPA type glutamate receptor GluR1 was significantly reduced whereas <strong><strong>GluR2</strong></strong> was significantly increased in the dlCPu, independent of Arc antisense ODN infusion.
+GRIA2	drug	cocaine	20868701	Under basal conditions and in response to a single <b>cocaine</b> injection the levels of GluR1, <strong>GluR2</strong>, and GluR3 AMPA receptor subunits did not differ between WT and 5 LOX deficient mice, but the response of GluR1 phosphorylation to a single <b>cocaine</b> injection was greater under the 5 LOX deficiency.
+GRIA2	drug	cocaine	20868701	Under basal conditions and in response to a single <b>cocaine</b> injection the levels of GluR1, <strong><strong>GluR2</strong></strong>, and GluR3 AMPA receptor subunits did not differ between WT and 5 LOX deficient mice, but the response of GluR1 phosphorylation to a single <b>cocaine</b> injection was greater under the 5 LOX deficiency.
+GRIA2	drug	cocaine	20534838	In contrast, activation of glutamate afferents onto the same DA neurons via stimulation within the VTA evoked EPSCs mediated by <strong>GluR2</strong> lacking AMPARs that demonstrated LTD or EPSCs mediated by <strong>GluR2</strong> containing AMPA receptors that did not express LTD. Twenty four hours after single <b>cocaine</b> injections to rats, <strong>GluR2</strong> lacking AMPARs were increased at both PPN and local VTA projections, and this permitted LTD expression in both pathways.
+GRIA2	drug	cocaine	20534838	In contrast, activation of glutamate afferents onto the same DA neurons via stimulation within the VTA evoked EPSCs mediated by <strong><strong>GluR2</strong></strong> lacking AMPARs that demonstrated LTD or EPSCs mediated by <strong><strong>GluR2</strong></strong> containing AMPA receptors that did not express LTD. Twenty four hours after single <b>cocaine</b> injections to rats, <strong><strong>GluR2</strong></strong> lacking AMPARs were increased at both PPN and local VTA projections, and this permitted LTD expression in both pathways.
+GRIA2	drug	cannabinoid	20534838	Single injections with the main psychoactive ingredient of <b>marijuana</b>, Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>), increased <strong>GluR2</strong> lacking AMPA receptors and permitted LTD in only the PPN pathway, and these effects were prevented by in vivo pretreatment with the <b>cannabinoid</b> CB1 receptor antagonist AM251.
+GRIA2	drug	cannabinoid	20534838	Single injections with the main psychoactive ingredient of <b>marijuana</b>, Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>), increased <strong><strong>GluR2</strong></strong> lacking AMPA receptors and permitted LTD in only the PPN pathway, and these effects were prevented by in vivo pretreatment with the <b>cannabinoid</b> CB1 receptor antagonist AM251.
+GRIA2	drug	cannabinoid	20534838	These results demonstrate that cocaine more globally increases <strong>GluR2</strong> lacking AMPA receptors at all glutamate synapses on VTA dopamine neurons, whereas Delta(9) <b>THC</b> selectively increased <strong>GluR2</strong> lacking AMPA receptors at subcortical PPN synapses.
+GRIA2	drug	cocaine	20534838	These results demonstrate that <b>cocaine</b> more globally increases <strong>GluR2</strong> lacking AMPA receptors at all glutamate synapses on VTA dopamine neurons, whereas Delta(9) THC selectively increased <strong>GluR2</strong> lacking AMPA receptors at subcortical PPN synapses.
+GRIA2	drug	cannabinoid	20534838	These results demonstrate that cocaine more globally increases <strong><strong>GluR2</strong></strong> lacking AMPA receptors at all glutamate synapses on VTA dopamine neurons, whereas Delta(9) <b>THC</b> selectively increased <strong><strong>GluR2</strong></strong> lacking AMPA receptors at subcortical PPN synapses.
+GRIA2	drug	cocaine	20534838	These results demonstrate that <b>cocaine</b> more globally increases <strong><strong>GluR2</strong></strong> lacking AMPA receptors at all glutamate synapses on VTA dopamine neurons, whereas Delta(9) THC selectively increased <strong><strong>GluR2</strong></strong> lacking AMPA receptors at subcortical PPN synapses.
+GRIA2	addiction	withdrawal	20445501	mEPSC inhibition by 1 naphthyl acetyl spermine and the negative shift in rectification index at both <b>withdrawal</b> time points were consistent with functional incorporation of <strong>GluA2</strong> lacking AMPARs.
+GRIA2	drug	opioid	20159947	In addition, we provide electrophysiological evidence that AMPARs are switched to Ca(2+) permeable (<strong>GluR2</strong> lacking) at the synapse 12 h after repeated <b>morphine</b> treatment, affecting the magnitude of long term depression at hippocampal neurons.
+GRIA2	drug	opioid	20159947	In addition, we provide electrophysiological evidence that AMPARs are switched to Ca(2+) permeable (<strong><strong>GluR2</strong></strong> lacking) at the synapse 12 h after repeated <b>morphine</b> treatment, affecting the magnitude of long term depression at hippocampal neurons.
+GRIA2	drug	alcohol	20153402	The decreased expression of GLAST, GLT 1 and <strong>GluR2</strong> in the <b>alcoholic</b> patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug seeking and chronic relapse.
+GRIA2	addiction	relapse	20153402	The decreased expression of GLAST, GLT 1 and <strong>GluR2</strong> in the alcoholic patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug <b>seeking</b> and chronic <b>relapse</b>.
+GRIA2	drug	alcohol	20153402	The decreased expression of GLAST, GLT 1 and <strong><strong>GluR2</strong></strong> in the <b>alcoholic</b> patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug seeking and chronic relapse.
+GRIA2	addiction	relapse	20153402	The decreased expression of GLAST, GLT 1 and <strong><strong>GluR2</strong></strong> in the alcoholic patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug <b>seeking</b> and chronic <b>relapse</b>.
+GRIA2	drug	amphetamine	19183251	In contrast to our previous results in cocaine sensitized rats, we did not observe redistribution of GluR1 or <strong>GluR2</strong> to the cell surface in the NAc after <b>amphetamine</b> withdrawal, although a small increase in total GluR1 was found in the shell subregion.
+GRIA2	drug	cocaine	19183251	In contrast to our previous results in <b>cocaine</b> sensitized rats, we did not observe redistribution of GluR1 or <strong>GluR2</strong> to the cell surface in the NAc after amphetamine withdrawal, although a small increase in total GluR1 was found in the shell subregion.
+GRIA2	addiction	withdrawal	19183251	In contrast to our previous results in cocaine sensitized rats, we did not observe redistribution of GluR1 or <strong>GluR2</strong> to the cell surface in the NAc after amphetamine <b>withdrawal</b>, although a small increase in total GluR1 was found in the shell subregion.
+GRIA2	drug	amphetamine	19183251	In contrast to our previous results in cocaine sensitized rats, we did not observe redistribution of GluR1 or <strong><strong>GluR2</strong></strong> to the cell surface in the NAc after <b>amphetamine</b> withdrawal, although a small increase in total GluR1 was found in the shell subregion.
+GRIA2	drug	cocaine	19183251	In contrast to our previous results in <b>cocaine</b> sensitized rats, we did not observe redistribution of GluR1 or <strong><strong>GluR2</strong></strong> to the cell surface in the NAc after amphetamine withdrawal, although a small increase in total GluR1 was found in the shell subregion.
+GRIA2	addiction	withdrawal	19183251	In contrast to our previous results in cocaine sensitized rats, we did not observe redistribution of GluR1 or <strong><strong>GluR2</strong></strong> to the cell surface in the NAc after amphetamine <b>withdrawal</b>, although a small increase in total GluR1 was found in the shell subregion.
+GRIA2	drug	opioid	19160503	Here we show in a rat self administration model that reexposure to cues previously associated with <b>heroin</b> results in downregulation of AMPA receptor subunit <strong>GluR2</strong> and concomitant upregulation of clathrin coat assembly protein AP2ml in synaptic membranes of the medial prefrontal cortex (mPFC).
+GRIA2	drug	opioid	19160503	Here we show in a rat self administration model that reexposure to cues previously associated with <b>heroin</b> results in downregulation of AMPA receptor subunit <strong><strong>GluR2</strong></strong> and concomitant upregulation of clathrin coat assembly protein AP2ml in synaptic membranes of the medial prefrontal cortex (mPFC).
+GRIA2	drug	opioid	19160503	Systemic or ventral (but not dorsal) mPFC injections of a peptide inhibiting <strong>GluR2</strong> endocytosis attenuated both the rectification index and cue induced relapse to <b>heroin</b> seeking, without affecting sucrose seeking.
+GRIA2	addiction	relapse	19160503	Systemic or ventral (but not dorsal) mPFC injections of a peptide inhibiting <strong>GluR2</strong> endocytosis attenuated both the rectification index and cue induced <b>relapse</b> to heroin <b>seeking</b>, without affecting sucrose <b>seeking</b>.
+GRIA2	drug	opioid	19160503	Systemic or ventral (but not dorsal) mPFC injections of a peptide inhibiting <strong><strong>GluR2</strong></strong> endocytosis attenuated both the rectification index and cue induced relapse to <b>heroin</b> seeking, without affecting sucrose seeking.
+GRIA2	addiction	relapse	19160503	Systemic or ventral (but not dorsal) mPFC injections of a peptide inhibiting <strong><strong>GluR2</strong></strong> endocytosis attenuated both the rectification index and cue induced <b>relapse</b> to heroin <b>seeking</b>, without affecting sucrose <b>seeking</b>.
+GRIA2	drug	opioid	19160503	We conclude that <strong>GluR2</strong> receptor endocytosis and the resulting synaptic depression in ventral mPFC are crucial for cue induced relapse to <b>heroin</b> seeking.
+GRIA2	addiction	relapse	19160503	We conclude that <strong>GluR2</strong> receptor endocytosis and the resulting synaptic depression in ventral mPFC are crucial for cue induced <b>relapse</b> to heroin <b>seeking</b>.
+GRIA2	drug	opioid	19160503	We conclude that <strong><strong>GluR2</strong></strong> receptor endocytosis and the resulting synaptic depression in ventral mPFC are crucial for cue induced relapse to <b>heroin</b> seeking.
+GRIA2	addiction	relapse	19160503	We conclude that <strong><strong>GluR2</strong></strong> receptor endocytosis and the resulting synaptic depression in ventral mPFC are crucial for cue induced <b>relapse</b> to heroin <b>seeking</b>.
+GRIA2	drug	opioid	19160503	As reexposure to conditioned stimuli is a major cause for <b>heroin</b> relapse, inhibition of <strong>GluR2</strong> endocytosis may provide a new target for the treatment of <b>heroin</b> addiction.
+GRIA2	addiction	addiction	19160503	As reexposure to conditioned stimuli is a major cause for heroin relapse, inhibition of <strong>GluR2</strong> endocytosis may provide a new target for the treatment of heroin <b>addiction</b>.
+GRIA2	addiction	relapse	19160503	As reexposure to conditioned stimuli is a major cause for heroin <b>relapse</b>, inhibition of <strong>GluR2</strong> endocytosis may provide a new target for the treatment of heroin addiction.
+GRIA2	drug	opioid	19160503	As reexposure to conditioned stimuli is a major cause for <b>heroin</b> relapse, inhibition of <strong><strong>GluR2</strong></strong> endocytosis may provide a new target for the treatment of <b>heroin</b> addiction.
+GRIA2	addiction	addiction	19160503	As reexposure to conditioned stimuli is a major cause for heroin relapse, inhibition of <strong><strong>GluR2</strong></strong> endocytosis may provide a new target for the treatment of heroin <b>addiction</b>.
+GRIA2	addiction	relapse	19160503	As reexposure to conditioned stimuli is a major cause for heroin <b>relapse</b>, inhibition of <strong><strong>GluR2</strong></strong> endocytosis may provide a new target for the treatment of heroin addiction.
+GRIA2	drug	opioid	19077125	Results showed that <b>morphine</b> dependent CRs did not alter expression or redistribution of GluR1 or <strong>GluR2</strong>; however, the unpaired administration of <b>morphine</b> resulted in an increase in the phosphorylation of the GluR1 subunit at extrasynaptic sites.
+GRIA2	drug	opioid	19077125	Results showed that <b>morphine</b> dependent CRs did not alter expression or redistribution of GluR1 or <strong><strong>GluR2</strong></strong>; however, the unpaired administration of <b>morphine</b> resulted in an increase in the phosphorylation of the GluR1 subunit at extrasynaptic sites.
+GRIA2	drug	opioid	18957577	It is surprising that continuous subcutaneous infusion of the <strong>GluR2</strong>/GluR5 preferring antagonist LY293558 [(3S,4aR,6R,8aR) 6 [2 (1(2)H tetrazole 5 yl)ethyl]decahydroisoquinoline 3 carboxylic acid] decreased the number of <b>naloxone</b> precipitated jumps to a similar extent in WT and GluR5 KO mice.
+GRIA2	drug	opioid	18957577	It is surprising that continuous subcutaneous infusion of the <strong><strong>GluR2</strong></strong>/GluR5 preferring antagonist LY293558 [(3S,4aR,6R,8aR) 6 [2 (1(2)H tetrazole 5 yl)ethyl]decahydroisoquinoline 3 carboxylic acid] decreased the number of <b>naloxone</b> precipitated jumps to a similar extent in WT and GluR5 KO mice.
+GRIA2	drug	cocaine	18945913	Phosphorylation dependent trafficking of <strong>GluR2</strong> containing AMPA receptors in the nucleus accumbens plays a critical role in the reinstatement of <b>cocaine</b> seeking.
+GRIA2	addiction	relapse	18945913	Phosphorylation dependent trafficking of <strong>GluR2</strong> containing AMPA receptors in the nucleus accumbens plays a critical role in the <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRIA2	drug	cocaine	18945913	Phosphorylation dependent trafficking of <strong><strong>GluR2</strong></strong> containing AMPA receptors in the nucleus accumbens plays a critical role in the reinstatement of <b>cocaine</b> seeking.
+GRIA2	addiction	relapse	18945913	Phosphorylation dependent trafficking of <strong><strong>GluR2</strong></strong> containing AMPA receptors in the nucleus accumbens plays a critical role in the <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRIA2	drug	cocaine	18945913	<b>Cocaine</b> priming induced reinstatement of <b>cocaine</b> seeking also was associated with increases in <strong>GluR2</strong> pSer880 in the nucleus accumbens shell.
+GRIA2	addiction	relapse	18945913	Cocaine priming induced <b>reinstatement</b> of cocaine <b>seeking</b> also was associated with increases in <strong>GluR2</strong> pSer880 in the nucleus accumbens shell.
+GRIA2	drug	cocaine	18945913	<b>Cocaine</b> priming induced reinstatement of <b>cocaine</b> seeking also was associated with increases in <strong><strong>GluR2</strong></strong> pSer880 in the nucleus accumbens shell.
+GRIA2	addiction	relapse	18945913	Cocaine priming induced <b>reinstatement</b> of cocaine <b>seeking</b> also was associated with increases in <strong><strong>GluR2</strong></strong> pSer880 in the nucleus accumbens shell.
+GRIA2	drug	cocaine	18945913	The current results showed that administration of a cell permeable peptide that disrupts <strong>GluR2</strong> trafficking (Pep2 EVKI) into either the accumbens core or shell attenuated <b>cocaine</b> induced reinstatement of drug seeking.
+GRIA2	addiction	relapse	18945913	The current results showed that administration of a cell permeable peptide that disrupts <strong>GluR2</strong> trafficking (Pep2 EVKI) into either the accumbens core or shell attenuated cocaine induced <b>reinstatement</b> of drug <b>seeking</b>.
+GRIA2	drug	cocaine	18945913	The current results showed that administration of a cell permeable peptide that disrupts <strong><strong>GluR2</strong></strong> trafficking (Pep2 EVKI) into either the accumbens core or shell attenuated <b>cocaine</b> induced reinstatement of drug seeking.
+GRIA2	addiction	relapse	18945913	The current results showed that administration of a cell permeable peptide that disrupts <strong><strong>GluR2</strong></strong> trafficking (Pep2 EVKI) into either the accumbens core or shell attenuated cocaine induced <b>reinstatement</b> of drug <b>seeking</b>.
+GRIA2	drug	cocaine	18945913	The present results also demonstrate that the reinstatement of <b>cocaine</b> seeking is associated with increases in the phosphorylation dependent trafficking of <strong>GluR2</strong> containing AMPA receptors in the nucleus accumbens.
+GRIA2	addiction	relapse	18945913	The present results also demonstrate that the <b>reinstatement</b> of cocaine <b>seeking</b> is associated with increases in the phosphorylation dependent trafficking of <strong>GluR2</strong> containing AMPA receptors in the nucleus accumbens.
+GRIA2	drug	cocaine	18945913	The present results also demonstrate that the reinstatement of <b>cocaine</b> seeking is associated with increases in the phosphorylation dependent trafficking of <strong><strong>GluR2</strong></strong> containing AMPA receptors in the nucleus accumbens.
+GRIA2	addiction	relapse	18945913	The present results also demonstrate that the <b>reinstatement</b> of cocaine <b>seeking</b> is associated with increases in the phosphorylation dependent trafficking of <strong><strong>GluR2</strong></strong> containing AMPA receptors in the nucleus accumbens.
+GRIA2	addiction	withdrawal	18924138	To test this hypothesis, the postsynaptic incorporation of GluR1 and <strong>GluR2</strong> subunits in CA1 neurons after FZP <b>withdrawal</b> was examined by postembedding immunogold quantitative electron microscopy.
+GRIA2	addiction	withdrawal	18924138	To test this hypothesis, the postsynaptic incorporation of GluR1 and <strong><strong>GluR2</strong></strong> subunits in CA1 neurons after FZP <b>withdrawal</b> was examined by postembedding immunogold quantitative electron microscopy.
+GRIA2	drug	opioid	18671727	Decreased AMPA <strong>GluR2</strong>, but not GluR3, mRNA expression in rat amygdala and dorsal hippocampus following <b>morphine</b> induced behavioural sensitization.
+GRIA2	addiction	sensitization	18671727	Decreased AMPA <strong>GluR2</strong>, but not GluR3, mRNA expression in rat amygdala and dorsal hippocampus following morphine induced behavioural <b>sensitization</b>.
+GRIA2	drug	opioid	18671727	Decreased AMPA <strong><strong>GluR2</strong></strong>, but not GluR3, mRNA expression in rat amygdala and dorsal hippocampus following <b>morphine</b> induced behavioural sensitization.
+GRIA2	addiction	sensitization	18671727	Decreased AMPA <strong><strong>GluR2</strong></strong>, but not GluR3, mRNA expression in rat amygdala and dorsal hippocampus following morphine induced behavioural <b>sensitization</b>.
+GRIA2	drug	opioid	18671727	In order to evaluate the mechanism underlying the behavioural responses, quantitative real time reverse transcription polymerase chain reaction was used to evaluate mRNA expression of the AMPA receptor subunits <strong>GluR2</strong> and GluR3 in the striatum, prefrontal cortex, hippocampus, hypothalamus and amygdala of animals treated repeatedly with <b>morphine</b>.
+GRIA2	drug	opioid	18671727	In order to evaluate the mechanism underlying the behavioural responses, quantitative real time reverse transcription polymerase chain reaction was used to evaluate mRNA expression of the AMPA receptor subunits <strong><strong>GluR2</strong></strong> and GluR3 in the striatum, prefrontal cortex, hippocampus, hypothalamus and amygdala of animals treated repeatedly with <b>morphine</b>.
+GRIA2	drug	opioid	18671727	In addition, repeated <b>morphine</b> treatment followed by 7 days (but not 24 h) washout decreased <strong>GluR2</strong> mRNA expression in both the amygdala (by 50%) and hippocampus (by 35%).
+GRIA2	drug	opioid	18671727	In addition, repeated <b>morphine</b> treatment followed by 7 days (but not 24 h) washout decreased <strong><strong>GluR2</strong></strong> mRNA expression in both the amygdala (by 50%) and hippocampus (by 35%).
+GRIA2	addiction	sensitization	18671727	The decreases in <strong>GluR2</strong> mRNA expression in the amygdala and hippocampus may result in the formation of calcium permeable AMPA receptors, which are believed to play an important role in behavioural <b>sensitization</b>.
+GRIA2	addiction	sensitization	18671727	The decreases in <strong><strong>GluR2</strong></strong> mRNA expression in the amygdala and hippocampus may result in the formation of calcium permeable AMPA receptors, which are believed to play an important role in behavioural <b>sensitization</b>.
+GRIA2	drug	cocaine	18500330	Formation of accumbens <strong>GluR2</strong> lacking AMPA receptors mediates incubation of <b>cocaine</b> craving.
+GRIA2	addiction	relapse	18500330	Formation of accumbens <strong>GluR2</strong> lacking AMPA receptors mediates incubation of cocaine <b>craving</b>.
+GRIA2	drug	cocaine	18500330	Formation of accumbens <strong><strong>GluR2</strong></strong> lacking AMPA receptors mediates incubation of <b>cocaine</b> craving.
+GRIA2	addiction	relapse	18500330	Formation of accumbens <strong><strong>GluR2</strong></strong> lacking AMPA receptors mediates incubation of cocaine <b>craving</b>.
+GRIA2	drug	cocaine	18500330	Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged withdrawal from <b>cocaine</b> self administration by the addition of new AMPA receptors lacking glutamate receptor 2 (<strong>GluR2</strong>).
+GRIA2	addiction	withdrawal	18500330	Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged <b>withdrawal</b> from cocaine self administration by the addition of new AMPA receptors lacking glutamate receptor 2 (<strong>GluR2</strong>).
+GRIA2	drug	cocaine	18500330	Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged withdrawal from <b>cocaine</b> self administration by the addition of new AMPA receptors lacking glutamate receptor 2 (<strong><strong>GluR2</strong></strong>).
+GRIA2	addiction	withdrawal	18500330	Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged <b>withdrawal</b> from cocaine self administration by the addition of new AMPA receptors lacking glutamate receptor 2 (<strong><strong>GluR2</strong></strong>).
+GRIA2	drug	cocaine	18500330	Our results indicate that <strong>GluR2</strong> lacking AMPA receptors could be a new target for drug development for the treatment of <b>cocaine</b> addiction.
+GRIA2	addiction	addiction	18500330	Our results indicate that <strong>GluR2</strong> lacking AMPA receptors could be a new target for drug development for the treatment of cocaine <b>addiction</b>.
+GRIA2	drug	cocaine	18500330	Our results indicate that <strong><strong>GluR2</strong></strong> lacking AMPA receptors could be a new target for drug development for the treatment of <b>cocaine</b> addiction.
+GRIA2	addiction	addiction	18500330	Our results indicate that <strong><strong>GluR2</strong></strong> lacking AMPA receptors could be a new target for drug development for the treatment of cocaine <b>addiction</b>.
+GRIA2	drug	cocaine	18500330	We propose that after prolonged withdrawal from <b>cocaine</b>, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong>GluR2</strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to <b>cocaine</b> related cues, leading to an intensification of drug craving and relapse.
+GRIA2	addiction	relapse	18500330	We propose that after prolonged withdrawal from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong>GluR2</strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine related cues, leading to an intensification of drug <b>craving</b> and <b>relapse</b>.
+GRIA2	addiction	withdrawal	18500330	We propose that after prolonged <b>withdrawal</b> from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong>GluR2</strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine related cues, leading to an intensification of drug craving and relapse.
+GRIA2	drug	cocaine	18500330	We propose that after prolonged withdrawal from <b>cocaine</b>, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong><strong>GluR2</strong></strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to <b>cocaine</b> related cues, leading to an intensification of drug craving and relapse.
+GRIA2	addiction	relapse	18500330	We propose that after prolonged withdrawal from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong><strong>GluR2</strong></strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine related cues, leading to an intensification of drug <b>craving</b> and <b>relapse</b>.
+GRIA2	addiction	withdrawal	18500330	We propose that after prolonged <b>withdrawal</b> from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong><strong>GluR2</strong></strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine related cues, leading to an intensification of drug craving and relapse.
+GRIA2	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, <strong>GluR2</strong>, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRIA2	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, <strong><strong>GluR2</strong></strong>, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRIA2	drug	nicotine	18261852	Voluntary oral <b>nicotine</b> intake in mice down regulates <strong>GluR2</strong> but does not modulate depression like behaviors.
+GRIA2	drug	nicotine	18261852	Voluntary oral <b>nicotine</b> intake in mice down regulates <strong><strong>GluR2</strong></strong> but does not modulate depression like behaviors.
+GRIA2	drug	nicotine	18261852	There were few behavioral changes in mice subjected to chronic <b>nicotine</b> exposure, but there was a marked regulation of <strong>GluR2</strong> in the mesolimbic system.
+GRIA2	drug	nicotine	18261852	There were few behavioral changes in mice subjected to chronic <b>nicotine</b> exposure, but there was a marked regulation of <strong><strong>GluR2</strong></strong> in the mesolimbic system.
+GRIA2	drug	cocaine	17898233	Glutamate receptor 1 (GluR1) and <strong>GluR2</strong> surface/intracellular (S/I) ratios were increased after 14 d of withdrawal in sensitized rats but were decreased 24 h after challenge with <b>cocaine</b> (which elicited a sensitized locomotor response) or saline (which elicited conditioned locomotion).
+GRIA2	addiction	withdrawal	17898233	Glutamate receptor 1 (GluR1) and <strong>GluR2</strong> surface/intracellular (S/I) ratios were increased after 14 d of <b>withdrawal</b> in sensitized rats but were decreased 24 h after challenge with cocaine (which elicited a sensitized locomotor response) or saline (which elicited conditioned locomotion).
+GRIA2	drug	cocaine	17898233	Glutamate receptor 1 (GluR1) and <strong><strong>GluR2</strong></strong> surface/intracellular (S/I) ratios were increased after 14 d of withdrawal in sensitized rats but were decreased 24 h after challenge with <b>cocaine</b> (which elicited a sensitized locomotor response) or saline (which elicited conditioned locomotion).
+GRIA2	addiction	withdrawal	17898233	Glutamate receptor 1 (GluR1) and <strong><strong>GluR2</strong></strong> surface/intracellular (S/I) ratios were increased after 14 d of <b>withdrawal</b> in sensitized rats but were decreased 24 h after challenge with cocaine (which elicited a sensitized locomotor response) or saline (which elicited conditioned locomotion).
+GRIA2	drug	cocaine	17898233	JNK phosphorylation also increased after withdrawal, but after <b>cocaine</b> challenge, it was inversely related to GluR1 and <strong>GluR2</strong> S/I ratios.
+GRIA2	addiction	withdrawal	17898233	JNK phosphorylation also increased after <b>withdrawal</b>, but after cocaine challenge, it was inversely related to GluR1 and <strong>GluR2</strong> S/I ratios.
+GRIA2	drug	cocaine	17898233	JNK phosphorylation also increased after withdrawal, but after <b>cocaine</b> challenge, it was inversely related to GluR1 and <strong><strong>GluR2</strong></strong> S/I ratios.
+GRIA2	addiction	withdrawal	17898233	JNK phosphorylation also increased after <b>withdrawal</b>, but after cocaine challenge, it was inversely related to GluR1 and <strong><strong>GluR2</strong></strong> S/I ratios.
+GRIA2	addiction	withdrawal	17510319	Confocal image analysis revealed that FZP <b>withdrawal</b> promoted GluR1 subunit incorporation into somatic and proximal dendritic membranes of CA1 neurons without <strong>GluR2</strong> subunit alterations.
+GRIA2	addiction	withdrawal	17510319	Confocal image analysis revealed that FZP <b>withdrawal</b> promoted GluR1 subunit incorporation into somatic and proximal dendritic membranes of CA1 neurons without <strong><strong>GluR2</strong></strong> subunit alterations.
+GRIA2	addiction	reward	17093088	Here, we used herpes simplex virus vectors to examine how transient increases in the expression of GluR1 or <strong>GluR2</strong> protein in the shell component of NAc affect the rewarding impact of electrical stimulation of the medial forebrain bundle, as reflected by intracranial self stimulation (<b>ICSS</b>) thresholds in rats.
+GRIA2	addiction	reward	17093088	Here, we used herpes simplex virus vectors to examine how transient increases in the expression of GluR1 or <strong><strong>GluR2</strong></strong> protein in the shell component of NAc affect the rewarding impact of electrical stimulation of the medial forebrain bundle, as reflected by intracranial self stimulation (<b>ICSS</b>) thresholds in rats.
+GRIA2	addiction	reward	17093088	In contrast, elevated <strong>GluR2</strong> decreases <b>ICSS</b> thresholds, an effect similar to that caused by rewarding treatments (e.g., drugs of abuse).
+GRIA2	addiction	reward	17093088	In contrast, elevated <strong><strong>GluR2</strong></strong> decreases <b>ICSS</b> thresholds, an effect similar to that caused by rewarding treatments (e.g., drugs of abuse).
+GRIA2	drug	cocaine	16616767	<b>Cocaine</b> withdrawal alters the expression of GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug withdrawal on hippocampus is little known.
+GRIA2	addiction	withdrawal	16616767	Cocaine <b>withdrawal</b> alters the expression of GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug <b>withdrawal</b> on hippocampus is little known.
+GRIA2	drug	cocaine	16616767	<b>Cocaine</b> withdrawal alters the expression of GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug withdrawal on hippocampus is little known.
+GRIA2	addiction	withdrawal	16616767	Cocaine <b>withdrawal</b> alters the expression of GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug <b>withdrawal</b> on hippocampus is little known.
+GRIA2	drug	opioid	16616767	Here, we have examined the expression of GluR1 and <strong>GluR2</strong>/3 in hippocampal membrane and synaptic fractions following repeated <b>morphine</b> exposure and subsequent withdrawal.
+GRIA2	addiction	withdrawal	16616767	Here, we have examined the expression of GluR1 and <strong>GluR2</strong>/3 in hippocampal membrane and synaptic fractions following repeated morphine exposure and subsequent <b>withdrawal</b>.
+GRIA2	drug	opioid	16616767	Here, we have examined the expression of GluR1 and <strong><strong>GluR2</strong></strong>/3 in hippocampal membrane and synaptic fractions following repeated <b>morphine</b> exposure and subsequent withdrawal.
+GRIA2	addiction	withdrawal	16616767	Here, we have examined the expression of GluR1 and <strong><strong>GluR2</strong></strong>/3 in hippocampal membrane and synaptic fractions following repeated morphine exposure and subsequent <b>withdrawal</b>.
+GRIA2	drug	opioid	16616767	Repeated <b>morphine</b> exposure for 12 d increased GluR1 and <strong>GluR2</strong>/3 in synaptosome but not in membrane fraction.
+GRIA2	drug	opioid	16616767	Repeated <b>morphine</b> exposure for 12 d increased GluR1 and <strong><strong>GluR2</strong></strong>/3 in synaptosome but not in membrane fraction.
+GRIA2	drug	opioid	16616767	However, during opiate withdrawal, GluR1 was generally reduced while <strong>GluR2</strong>/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after withdrawal, but detectably increased in late phase of <b>morphine</b> withdrawal in both fractions.
+GRIA2	addiction	withdrawal	16616767	However, during opiate <b>withdrawal</b>, GluR1 was generally reduced while <strong>GluR2</strong>/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after <b>withdrawal</b>, but detectably increased in late phase of morphine <b>withdrawal</b> in both fractions.
+GRIA2	drug	opioid	16616767	However, during opiate withdrawal, GluR1 was generally reduced while <strong><strong>GluR2</strong></strong>/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after withdrawal, but detectably increased in late phase of <b>morphine</b> withdrawal in both fractions.
+GRIA2	addiction	withdrawal	16616767	However, during opiate <b>withdrawal</b>, GluR1 was generally reduced while <strong><strong>GluR2</strong></strong>/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after <b>withdrawal</b>, but detectably increased in late phase of morphine <b>withdrawal</b> in both fractions.
+GRIA2	addiction	withdrawal	16616767	Importantly, the opiate <b>withdrawal</b> induced increase in <strong>GluR2</strong>/3 was dependent on the activation of glucocorticoid receptors and NMDA receptors, as it was prevented by the glucocorticoid receptor antagonist RU38486, or intrahippocampal injection of the NMDA receptor antagonist AP 5 or the antagonist to NR2B containing NMDA receptors, Ro25 6981.
+GRIA2	addiction	withdrawal	16616767	Importantly, the opiate <b>withdrawal</b> induced increase in <strong><strong>GluR2</strong></strong>/3 was dependent on the activation of glucocorticoid receptors and NMDA receptors, as it was prevented by the glucocorticoid receptor antagonist RU38486, or intrahippocampal injection of the NMDA receptor antagonist AP 5 or the antagonist to NR2B containing NMDA receptors, Ro25 6981.
+GRIA2	addiction	withdrawal	16616767	These findings indicate that opiate <b>withdrawal</b> induces dynamic expression of GluR1 and <strong>GluR2</strong>/3 subunits of AMPA receptors in hippocampal synapses, possibly revealing an adaptive process of the hippocampal functions following opiate <b>withdrawal</b>.
+GRIA2	addiction	withdrawal	16616767	These findings indicate that opiate <b>withdrawal</b> induces dynamic expression of GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of AMPA receptors in hippocampal synapses, possibly revealing an adaptive process of the hippocampal functions following opiate <b>withdrawal</b>.
+GRIA2	drug	cocaine	16582902	Using an 'ex vivo' approach in mice, we show that a single injection of <b>cocaine</b> caused strong rectification and conferred sensitivity to the polyamine Joro spider toxin (JST) of AMPAR mediated excitatory postsynaptic currents (AMPAR EPSCs), indicating the recruitment of receptors that lack <strong>GluR2</strong>.
+GRIA2	drug	cocaine	16582902	Using an 'ex vivo' approach in mice, we show that a single injection of <b>cocaine</b> caused strong rectification and conferred sensitivity to the polyamine Joro spider toxin (JST) of AMPAR mediated excitatory postsynaptic currents (AMPAR EPSCs), indicating the recruitment of receptors that lack <strong><strong>GluR2</strong></strong>.
+GRIA2	drug	cocaine	16363995	Statistically significant elevations were observed for NR1, GluR1, <strong>GluR2</strong>/3 and GluR5 (p < 0.05) and a trend towards increased NR1 phosphorylated at serine 896 (p = 0.07) in the NAc but not putamen of monkeys self administering <b>cocaine</b> compared with controls.
+GRIA2	drug	cocaine	16363995	Statistically significant elevations were observed for NR1, GluR1, <strong><strong>GluR2</strong></strong>/3 and GluR5 (p < 0.05) and a trend towards increased NR1 phosphorylated at serine 896 (p = 0.07) in the NAc but not putamen of monkeys self administering <b>cocaine</b> compared with controls.
+GRIA2	drug	amphetamine	16311338	Systemic or intra NAc infusion of the membrane permeable <strong>GluR2</strong> peptide prevented the expression of <b>amphetamine</b> induced behavioral sensitization in the rat.
+GRIA2	addiction	sensitization	16311338	Systemic or intra NAc infusion of the membrane permeable <strong>GluR2</strong> peptide prevented the expression of amphetamine induced behavioral <b>sensitization</b> in the rat.
+GRIA2	drug	amphetamine	16311338	Systemic or intra NAc infusion of the membrane permeable <strong><strong>GluR2</strong></strong> peptide prevented the expression of <b>amphetamine</b> induced behavioral sensitization in the rat.
+GRIA2	addiction	sensitization	16311338	Systemic or intra NAc infusion of the membrane permeable <strong><strong>GluR2</strong></strong> peptide prevented the expression of amphetamine induced behavioral <b>sensitization</b> in the rat.
+GRIA2	drug	cocaine	16207873	Surface/intracellular (S/I) ratios for glutamate receptor 1 (GluR1) and <strong>GluR2</strong>/3 subunits were increased 21 d after the last injection in <b>cocaine</b> sensitized rats but not rats that failed to sensitize, and the magnitude of the S/I ratio for <b>cocaine</b> sensitized rats was positively correlated with the magnitude of behavioral sensitization.
+GRIA2	addiction	sensitization	16207873	Surface/intracellular (S/I) ratios for glutamate receptor 1 (GluR1) and <strong>GluR2</strong>/3 subunits were increased 21 d after the last injection in cocaine sensitized rats but not rats that failed to sensitize, and the magnitude of the S/I ratio for cocaine sensitized rats was positively correlated with the magnitude of behavioral <b>sensitization</b>.
+GRIA2	drug	cocaine	16207873	Surface/intracellular (S/I) ratios for glutamate receptor 1 (GluR1) and <strong><strong>GluR2</strong></strong>/3 subunits were increased 21 d after the last injection in <b>cocaine</b> sensitized rats but not rats that failed to sensitize, and the magnitude of the S/I ratio for <b>cocaine</b> sensitized rats was positively correlated with the magnitude of behavioral sensitization.
+GRIA2	addiction	sensitization	16207873	Surface/intracellular (S/I) ratios for glutamate receptor 1 (GluR1) and <strong><strong>GluR2</strong></strong>/3 subunits were increased 21 d after the last injection in cocaine sensitized rats but not rats that failed to sensitize, and the magnitude of the S/I ratio for cocaine sensitized rats was positively correlated with the magnitude of behavioral <b>sensitization</b>.
+GRIA2	addiction	withdrawal	15970947	In the brains of these rats, <b>withdrawal</b> anxiety was accompanied by increased [3H]Ro48 8587 binding in the hippocampus and thalamus, and decreased GluR1 and <strong>GluR2</strong> subunit mRNA expression in the amygdala (GluR1 and <strong>GluR2</strong>) and cortex (GluR1).
+GRIA2	addiction	withdrawal	15970947	In the brains of these rats, <b>withdrawal</b> anxiety was accompanied by increased [3H]Ro48 8587 binding in the hippocampus and thalamus, and decreased GluR1 and <strong><strong>GluR2</strong></strong> subunit mRNA expression in the amygdala (GluR1 and <strong><strong>GluR2</strong></strong>) and cortex (GluR1).
+GRIA2	drug	cocaine	15953359	In the basolateral amygdala, GluR1 but not <strong>GluR2</strong> levels were increased on days 1 and 30, NR2A levels were increased on day 1, and NR2B levels were decreased on day 30 of withdrawal from <b>cocaine</b>.
+GRIA2	addiction	withdrawal	15953359	In the basolateral amygdala, GluR1 but not <strong>GluR2</strong> levels were increased on days 1 and 30, NR2A levels were increased on day 1, and NR2B levels were decreased on day 30 of <b>withdrawal</b> from cocaine.
+GRIA2	drug	cocaine	15953359	In the basolateral amygdala, GluR1 but not <strong><strong>GluR2</strong></strong> levels were increased on days 1 and 30, NR2A levels were increased on day 1, and NR2B levels were decreased on day 30 of withdrawal from <b>cocaine</b>.
+GRIA2	addiction	withdrawal	15953359	In the basolateral amygdala, GluR1 but not <strong><strong>GluR2</strong></strong> levels were increased on days 1 and 30, NR2A levels were increased on day 1, and NR2B levels were decreased on day 30 of <b>withdrawal</b> from cocaine.
+GRIA2	drug	cocaine	15953359	In the central amygdala, <strong>GluR2</strong> but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or NR2B levels were not altered after withdrawal from <b>cocaine</b>.
+GRIA2	addiction	withdrawal	15953359	In the central amygdala, <strong>GluR2</strong> but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or NR2B levels were not altered after <b>withdrawal</b> from cocaine.
+GRIA2	drug	cocaine	15953359	In the central amygdala, <strong><strong>GluR2</strong></strong> but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or NR2B levels were not altered after withdrawal from <b>cocaine</b>.
+GRIA2	addiction	withdrawal	15953359	In the central amygdala, <strong><strong>GluR2</strong></strong> but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or NR2B levels were not altered after <b>withdrawal</b> from cocaine.
+GRIA2	drug	cocaine	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces <b>cocaine</b> seeking behaviour when reward is withheld, reverses this deficit by up regulating GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA2	addiction	relapse	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces cocaine <b>seeking</b> behaviour when reward is withheld, reverses this deficit by up regulating GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA2	addiction	reward	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces cocaine seeking behaviour when <b>reward</b> is withheld, reverses this deficit by up regulating GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA2	drug	cocaine	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces <b>cocaine</b> seeking behaviour when reward is withheld, reverses this deficit by up regulating GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA2	addiction	relapse	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces cocaine <b>seeking</b> behaviour when reward is withheld, reverses this deficit by up regulating GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA2	addiction	reward	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces cocaine seeking behaviour when <b>reward</b> is withheld, reverses this deficit by up regulating GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRIA2	drug	cocaine	15764012	This hypothesis is supported by the finding that over expression of GluR1 and <strong>GluR2</strong> in the NAc facilitates extinction of <b>cocaine</b> self administration.
+GRIA2	drug	cocaine	15764012	This hypothesis is supported by the finding that over expression of GluR1 and <strong><strong>GluR2</strong></strong> in the NAc facilitates extinction of <b>cocaine</b> self administration.
+GRIA2	drug	cocaine	15764012	Furthermore, a single extinction training session conducted during GluR1 and <strong>GluR2</strong> over expression strongly and selectively attenuates the ability of an environmental stressor to trigger relapse to <b>cocaine</b> seeking long after GluR1 and <strong>GluR2</strong> over expression declines.
+GRIA2	addiction	relapse	15764012	Furthermore, a single extinction training session conducted during GluR1 and <strong>GluR2</strong> over expression strongly and selectively attenuates the ability of an environmental stressor to trigger <b>relapse</b> to cocaine <b>seeking</b> long after GluR1 and <strong>GluR2</strong> over expression declines.
+GRIA2	drug	cocaine	15764012	Furthermore, a single extinction training session conducted during GluR1 and <strong><strong>GluR2</strong></strong> over expression strongly and selectively attenuates the ability of an environmental stressor to trigger relapse to <b>cocaine</b> seeking long after GluR1 and <strong><strong>GluR2</strong></strong> over expression declines.
+GRIA2	addiction	relapse	15764012	Furthermore, a single extinction training session conducted during GluR1 and <strong><strong>GluR2</strong></strong> over expression strongly and selectively attenuates the ability of an environmental stressor to trigger <b>relapse</b> to cocaine <b>seeking</b> long after GluR1 and <strong><strong>GluR2</strong></strong> over expression declines.
+GRIA2	drug	cocaine	15619119	We investigated the ability of <b>cocaine</b> and food to induce a CPP in mice lacking either the GluR1 or GluR2 subunits of the AMPA receptor [gria1 or <strong>gria2</strong> knockout (KO) mice].
+GRIA2	addiction	reward	15619119	We investigated the ability of cocaine and food to induce a <b>CPP</b> in mice lacking either the GluR1 or GluR2 subunits of the AMPA receptor [gria1 or <strong>gria2</strong> knockout (KO) mice].
+GRIA2	drug	cocaine	15619119	We investigated the ability of <b>cocaine</b> and food to induce a CPP in mice lacking either the GluR1 or <strong>GluR2</strong> subunits of the AMPA receptor [gria1 or <strong>gria2</strong> knockout (KO) mice].
+GRIA2	addiction	reward	15619119	We investigated the ability of cocaine and food to induce a <b>CPP</b> in mice lacking either the GluR1 or <strong>GluR2</strong> subunits of the AMPA receptor [gria1 or <strong>gria2</strong> knockout (KO) mice].
+GRIA2	drug	cocaine	15619119	We investigated the ability of <b>cocaine</b> and food to induce a CPP in mice lacking either the GluR1 or <strong><strong>GluR2</strong></strong> subunits of the AMPA receptor [gria1 or <strong>gria2</strong> knockout (KO) mice].
+GRIA2	addiction	reward	15619119	We investigated the ability of cocaine and food to induce a <b>CPP</b> in mice lacking either the GluR1 or <strong><strong>GluR2</strong></strong> subunits of the AMPA receptor [gria1 or <strong>gria2</strong> knockout (KO) mice].
+GRIA2	drug	cocaine	15619119	However, <strong>gria2</strong> knockouts displayed a preference for a <b>cocaine</b> paired compartment, but not a food paired compartment, indicating a specific deficit in place preference conditioning to food.
+GRIA2	addiction	reward	15619119	When the results are considered in relation to our previous findings with gria1 and <strong>gria2</strong> knockout mice, they also raise questions about the <b>CPP</b> paradigm representing a model of conditioned <b>reward</b> over a conditioned approach interpretation.
+GRIA2	drug	nicotine	15343057	As for vulnerability to addictive behaviour, <b>nicotine</b> exposure during adolescence dose dependently down regulated levels of AMPA <strong>GluR2</strong>/3 subunits in the striatum, suggesting a reduced neurobehavioural plasticity in adult subjects.
+GRIA2	addiction	addiction	15343057	As for vulnerability to <b>addictive</b> behaviour, nicotine exposure during adolescence dose dependently down regulated levels of AMPA <strong>GluR2</strong>/3 subunits in the striatum, suggesting a reduced neurobehavioural plasticity in adult subjects.
+GRIA2	drug	nicotine	15343057	As for vulnerability to addictive behaviour, <b>nicotine</b> exposure during adolescence dose dependently down regulated levels of AMPA <strong><strong>GluR2</strong></strong>/3 subunits in the striatum, suggesting a reduced neurobehavioural plasticity in adult subjects.
+GRIA2	addiction	addiction	15343057	As for vulnerability to <b>addictive</b> behaviour, nicotine exposure during adolescence dose dependently down regulated levels of AMPA <strong><strong>GluR2</strong></strong>/3 subunits in the striatum, suggesting a reduced neurobehavioural plasticity in adult subjects.
+GRIA2	drug	cannabinoid	15233572	Down regulation of the AMPA glutamate receptor subunits GluR1 and <strong>GluR2</strong>/3 in the rat cerebellum following pre  and perinatal delta9 <b>tetrahydrocannabinol</b> exposure.
+GRIA2	drug	cannabinoid	15233572	Down regulation of the AMPA glutamate receptor subunits GluR1 and <strong><strong>GluR2</strong></strong>/3 in the rat cerebellum following pre  and perinatal delta9 <b>tetrahydrocannabinol</b> exposure.
+GRIA2	drug	cannabinoid	15233572	This paper reports the effects of pre  and perinatal exposure to delta9 <b>tetrahydrocannabinol</b> (<b>THC</b>) on expression levels of specific AMPA glutamate receptor subunits (GluR1 and <strong>GluR2</strong>/3) in the cerebellum of male and female rats.
+GRIA2	drug	cannabinoid	15233572	This paper reports the effects of pre  and perinatal exposure to delta9 <b>tetrahydrocannabinol</b> (<b>THC</b>) on expression levels of specific AMPA glutamate receptor subunits (GluR1 and <strong><strong>GluR2</strong></strong>/3) in the cerebellum of male and female rats.
+GRIA2	drug	cannabinoid	15233572	Expression of the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA glutamate receptors was analyzed by immunohistochemistry in <b>THC</b> exposed rats at three postnatal ages: PD20 (still exposed to <b>THC</b>) to study the direct effect of drug exposure, and PD30 and PD70 (10 and 50 days following <b>THC</b> withdrawal) to analyze the long term effects of prenatal exposure.
+GRIA2	addiction	withdrawal	15233572	Expression of the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA glutamate receptors was analyzed by immunohistochemistry in THC exposed rats at three postnatal ages: PD20 (still exposed to THC) to study the direct effect of drug exposure, and PD30 and PD70 (10 and 50 days following THC <b>withdrawal</b>) to analyze the long term effects of prenatal exposure.
+GRIA2	drug	cannabinoid	15233572	Expression of the GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of AMPA glutamate receptors was analyzed by immunohistochemistry in <b>THC</b> exposed rats at three postnatal ages: PD20 (still exposed to <b>THC</b>) to study the direct effect of drug exposure, and PD30 and PD70 (10 and 50 days following <b>THC</b> withdrawal) to analyze the long term effects of prenatal exposure.
+GRIA2	addiction	withdrawal	15233572	Expression of the GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of AMPA glutamate receptors was analyzed by immunohistochemistry in THC exposed rats at three postnatal ages: PD20 (still exposed to THC) to study the direct effect of drug exposure, and PD30 and PD70 (10 and 50 days following THC <b>withdrawal</b>) to analyze the long term effects of prenatal exposure.
+GRIA2	drug	cannabinoid	15233572	Compared to controls, pre  and perinatal <b>THC</b> exposure decreased the immunoreactivity levels of the GluR1 subunit in Bergmann glial cells, as well as levels of the <strong>GluR2</strong>/3 subunit in Purkinje neurons at PD20.
+GRIA2	drug	cannabinoid	15233572	Compared to controls, pre  and perinatal <b>THC</b> exposure decreased the immunoreactivity levels of the GluR1 subunit in Bergmann glial cells, as well as levels of the <strong><strong>GluR2</strong></strong>/3 subunit in Purkinje neurons at PD20.
+GRIA2	addiction	intoxication	15140200	In the NAc, <strong>GluR2</strong>/3 levels were increased following withdrawal compared with <b>binge</b> access, and were the only changes observed in this region.
+GRIA2	addiction	withdrawal	15140200	In the NAc, <strong>GluR2</strong>/3 levels were increased following <b>withdrawal</b> compared with binge access, and were the only changes observed in this region.
+GRIA2	addiction	intoxication	15140200	In the NAc, <strong><strong>GluR2</strong></strong>/3 levels were increased following withdrawal compared with <b>binge</b> access, and were the only changes observed in this region.
+GRIA2	addiction	withdrawal	15140200	In the NAc, <strong><strong>GluR2</strong></strong>/3 levels were increased following <b>withdrawal</b> compared with binge access, and were the only changes observed in this region.
+GRIA2	addiction	addiction	14666123	At 2 months after pretreatment, we measured levels of AMPA <strong>GluR2</strong>/3 subunits, thought to be involved in the control of <b>addictive</b> behaviors.
+GRIA2	addiction	addiction	14666123	At 2 months after pretreatment, we measured levels of AMPA <strong><strong>GluR2</strong></strong>/3 subunits, thought to be involved in the control of <b>addictive</b> behaviors.
+GRIA2	addiction	reward	14573529	Involvement of AMPA receptor GluR2 subunits in stimulus <b>reward</b> learning: evidence from glutamate receptor <strong>gria2</strong> knock out mice.
+GRIA2	addiction	reward	14573529	Involvement of AMPA receptor <strong>GluR2</strong> subunits in stimulus <b>reward</b> learning: evidence from glutamate receptor <strong>gria2</strong> knock out mice.
+GRIA2	addiction	reward	14573529	Involvement of AMPA receptor <strong><strong>GluR2</strong></strong> subunits in stimulus <b>reward</b> learning: evidence from glutamate receptor <strong>gria2</strong> knock out mice.
+GRIA2	addiction	reward	14573529	We investigated whether mice lacking the GluR2 subunit [<strong>gria2</strong> knock out (KO) mice] displayed impairments in learning stimulus <b>reward</b> associations, and the subsequent ability of <b>reward</b> paired cues to control motivated behavior.
+GRIA2	addiction	reward	14573529	We investigated whether mice lacking the <strong>GluR2</strong> subunit [<strong>gria2</strong> knock out (KO) mice] displayed impairments in learning stimulus <b>reward</b> associations, and the subsequent ability of <b>reward</b> paired cues to control motivated behavior.
+GRIA2	addiction	reward	14573529	We investigated whether mice lacking the <strong><strong>GluR2</strong></strong> subunit [<strong>gria2</strong> knock out (KO) mice] displayed impairments in learning stimulus <b>reward</b> associations, and the subsequent ability of <b>reward</b> paired cues to control motivated behavior.
+GRIA2	addiction	reward	14573529	Subsequently, the cues also served to reinforce an <b>operant</b> response in both KO and WT mice (conditioned <b>reinforcement</b>), although response rates were greater in <strong>gria2</strong> KOs.
+GRIA2	addiction	reward	14573529	The ability of the cues to elicit approach behavior (conditioned approach) and to enhance responding for the <b>reward</b> (pavlovian to instrumental transfer; PIT) were also impaired in <strong>gria2</strong> KO mice.
+GRIA2	addiction	reward	14573529	These results suggest that <strong>GluR2</strong> containing AMPA receptors, possibly within the CeA, are critical for the formation of stimulus <b>reward</b> associations necessary for PIT and conditioned approach, but are not involved in the plastic processes underlying the attribution of motivational value to the conditioned stimulus (CS).
+GRIA2	addiction	reward	14573529	These results suggest that <strong><strong>GluR2</strong></strong> containing AMPA receptors, possibly within the CeA, are critical for the formation of stimulus <b>reward</b> associations necessary for PIT and conditioned approach, but are not involved in the plastic processes underlying the attribution of motivational value to the conditioned stimulus (CS).
+GRIA2	drug	cocaine	12787079	In the accumbens of <b>cocaine</b> trained rats, GluR1 and NMDAR1 levels were increased on days 1 and 90, while <strong>GluR2</strong> levels were increased on days 1 and 30, but not day 90; PKA activity levels were increased on days 1 and 30, but not day 90, while AC activity, TH and cdk5 levels were unaltered.
+GRIA2	drug	cocaine	12787079	In the accumbens of <b>cocaine</b> trained rats, GluR1 and NMDAR1 levels were increased on days 1 and 90, while <strong><strong>GluR2</strong></strong> levels were increased on days 1 and 30, but not day 90; PKA activity levels were increased on days 1 and 30, but not day 90, while AC activity, TH and cdk5 levels were unaltered.
+GRIA2	drug	cocaine	12787079	In the VTA of <b>cocaine</b> trained rats, NMDAR1 levels were increased for up to 90 days, while <strong>GluR2</strong> levels were increased only on day 1; TH and Cdk5 levels were increased only on day 1, while PKA and AC activity levels were unaltered.
+GRIA2	drug	cocaine	12787079	In the VTA of <b>cocaine</b> trained rats, NMDAR1 levels were increased for up to 90 days, while <strong><strong>GluR2</strong></strong> levels were increased only on day 1; TH and Cdk5 levels were increased only on day 1, while PKA and AC activity levels were unaltered.
+GRIA2	drug	cocaine	12716423	Array analysis revealed significant up regulation of numerous transcripts in the VTA, but not in the l SN, of <b>cocaine</b> overdose victims including NMDAR1, <strong>GluR2</strong>, GluR5 and KA2 receptor mRNA (p < 0.05).
+GRIA2	drug	cocaine	12716423	Array analysis revealed significant up regulation of numerous transcripts in the VTA, but not in the l SN, of <b>cocaine</b> overdose victims including NMDAR1, <strong><strong>GluR2</strong></strong>, GluR5 and KA2 receptor mRNA (p < 0.05).
+GRIA2	drug	cocaine	12716423	Correspondingly, western blot analysis revealed VTA selective up regulation of CREB (p < 0.01), NMDAR1 (p < 0.01), <strong>GluR2</strong> (p < 0.05), GluR5 (p < 0.01) and KA2 (p < 0.05) protein levels of <b>cocaine</b> overdose victims.
+GRIA2	drug	cocaine	12716423	Correspondingly, western blot analysis revealed VTA selective up regulation of CREB (p < 0.01), NMDAR1 (p < 0.01), <strong><strong>GluR2</strong></strong> (p < 0.05), GluR5 (p < 0.01) and KA2 (p < 0.05) protein levels of <b>cocaine</b> overdose victims.
+GRIA2	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for AP 1 in the NAc: the AMPA glutamate receptor subunit <strong>GluR2</strong>, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+GRIA2	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for AP 1 in the NAc: the AMPA glutamate receptor subunit <strong><strong>GluR2</strong></strong>, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+GRIA2	drug	alcohol	12694947	Despite this augmentation of AMPAR function, no significant changes were found in the sensitivity of AMPA currents to GYKI 52466, cyclothiazide or acute <b>ethanol</b> (100 mM) sensitivity or in the levels of GluR1/<strong>GluR2</strong> subunit proteins from MS/DB tissue.
+GRIA2	drug	alcohol	12694947	Despite this augmentation of AMPAR function, no significant changes were found in the sensitivity of AMPA currents to GYKI 52466, cyclothiazide or acute <b>ethanol</b> (100 mM) sensitivity or in the levels of GluR1/<strong><strong>GluR2</strong></strong> subunit proteins from MS/DB tissue.
+GRIA2	drug	cocaine	12687634	Acute "binge" <b>cocaine</b> also increased mRNA levels for glutamate receptor <strong>GluR2</strong>, dopamine receptor D1, and a number of phosphatases.
+GRIA2	addiction	intoxication	12687634	Acute "<b>binge</b>" cocaine also increased mRNA levels for glutamate receptor <strong>GluR2</strong>, dopamine receptor D1, and a number of phosphatases.
+GRIA2	drug	cocaine	12687634	Acute "binge" <b>cocaine</b> also increased mRNA levels for glutamate receptor <strong><strong>GluR2</strong></strong>, dopamine receptor D1, and a number of phosphatases.
+GRIA2	addiction	intoxication	12687634	Acute "<b>binge</b>" cocaine also increased mRNA levels for glutamate receptor <strong><strong>GluR2</strong></strong>, dopamine receptor D1, and a number of phosphatases.
+GRIA2	drug	cocaine	12511956	Here we show that extinction training during withdrawal from chronic <b>cocaine</b> self administration induces experience dependent increases in the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in <b>cocaine</b> reward.
+GRIA2	addiction	reward	12511956	Here we show that extinction training during withdrawal from chronic cocaine self administration induces experience dependent increases in the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine <b>reward</b>.
+GRIA2	addiction	withdrawal	12511956	Here we show that extinction training during <b>withdrawal</b> from chronic cocaine self administration induces experience dependent increases in the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine reward.
+GRIA2	drug	cocaine	12511956	Here we show that extinction training during withdrawal from chronic <b>cocaine</b> self administration induces experience dependent increases in the GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in <b>cocaine</b> reward.
+GRIA2	addiction	reward	12511956	Here we show that extinction training during withdrawal from chronic cocaine self administration induces experience dependent increases in the GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine <b>reward</b>.
+GRIA2	addiction	withdrawal	12511956	Here we show that extinction training during <b>withdrawal</b> from chronic cocaine self administration induces experience dependent increases in the GluR1 and <strong><strong>GluR2</strong></strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine reward.
+GRIA2	drug	cocaine	12511956	Indeed, viral mediated overexpression of both GluR1 and <strong>GluR2</strong> in nucleus accumbens shell neurons facilitates extinction of <b>cocaine</b>  but not sucrose seeking responses.
+GRIA2	addiction	relapse	12511956	Indeed, viral mediated overexpression of both GluR1 and <strong>GluR2</strong> in nucleus accumbens shell neurons facilitates extinction of cocaine  but not sucrose <b>seeking</b> responses.
+GRIA2	drug	cocaine	12511956	Indeed, viral mediated overexpression of both GluR1 and <strong><strong>GluR2</strong></strong> in nucleus accumbens shell neurons facilitates extinction of <b>cocaine</b>  but not sucrose seeking responses.
+GRIA2	addiction	relapse	12511956	Indeed, viral mediated overexpression of both GluR1 and <strong><strong>GluR2</strong></strong> in nucleus accumbens shell neurons facilitates extinction of cocaine  but not sucrose <b>seeking</b> responses.
+GRIA2	drug	alcohol	11696675	Unexpectedly, we found that expression of NR1 (including the expression of NR1 subunits containing the N1, C1, and C2 inserts), NR2A, NR2B, NR2C, GluR1, <strong>GluR2</strong>/3, GluR5, GluR6/7, and KA2 subunits was not altered in hippocampal homogenates from <b>ethanol</b> exposed rats.
+GRIA2	drug	alcohol	11696675	Unexpectedly, we found that expression of NR1 (including the expression of NR1 subunits containing the N1, C1, and C2 inserts), NR2A, NR2B, NR2C, GluR1, <strong><strong>GluR2</strong></strong>/3, GluR5, GluR6/7, and KA2 subunits was not altered in hippocampal homogenates from <b>ethanol</b> exposed rats.
+GRIA2	drug	cocaine	10349849	GluR1, <strong>GluR2</strong>/3, and NMDAR1 subunits of glutamate receptors were quantified from immunoblots in these brain nuclei in rats at 24 h and 3 weeks after discontinuing 1 week of daily <b>cocaine</b> injections.
+GRIA2	drug	cocaine	10349849	GluR1, <strong><strong>GluR2</strong></strong>/3, and NMDAR1 subunits of glutamate receptors were quantified from immunoblots in these brain nuclei in rats at 24 h and 3 weeks after discontinuing 1 week of daily <b>cocaine</b> injections.
+GRIA2	drug	cocaine	10349849	None of these increases occurred in the rats exposed to daily <b>cocaine</b> that did not develop behavioral sensitization (<20% increase in motor activity), and no changes were measured in the level of <strong>GluR2</strong>/3 in any treatment group.
+GRIA2	addiction	sensitization	10349849	None of these increases occurred in the rats exposed to daily cocaine that did not develop behavioral <b>sensitization</b> (<20% increase in motor activity), and no changes were measured in the level of <strong>GluR2</strong>/3 in any treatment group.
+GRIA2	drug	cocaine	10349849	None of these increases occurred in the rats exposed to daily <b>cocaine</b> that did not develop behavioral sensitization (<20% increase in motor activity), and no changes were measured in the level of <strong><strong>GluR2</strong></strong>/3 in any treatment group.
+GRIA2	addiction	sensitization	10349849	None of these increases occurred in the rats exposed to daily cocaine that did not develop behavioral <b>sensitization</b> (<20% increase in motor activity), and no changes were measured in the level of <strong><strong>GluR2</strong></strong>/3 in any treatment group.
+GRIA2	addiction	withdrawal	10231131	In the NAc, GluR1 and <strong>GluR2</strong> immunolabeling were unchanged after 3 days of <b>withdrawal</b>, but both were decreased significantly after 14 days of <b>withdrawal</b> (GluR1, 85.5+/ 2.6% of control group, P<0.01; <strong>GluR2</strong>, 79.2+/ 3.2%, P<0.01).
+GRIA2	addiction	withdrawal	10231131	In the NAc, GluR1 and <strong><strong>GluR2</strong></strong> immunolabeling were unchanged after 3 days of <b>withdrawal</b>, but both were decreased significantly after 14 days of <b>withdrawal</b> (GluR1, 85.5+/ 2.6% of control group, P<0.01; <strong><strong>GluR2</strong></strong>, 79.2+/ 3.2%, P<0.01).
+GRIA2	addiction	withdrawal	10231131	Analysis of core and shell subregions at the 14 day <b>withdrawal</b> time indicated that GluR1 immunolabeling decreased significantly in shell, while <strong>GluR2</strong> immunolabeling decreased significantly in both core and shell.
+GRIA2	addiction	withdrawal	10231131	Analysis of core and shell subregions at the 14 day <b>withdrawal</b> time indicated that GluR1 immunolabeling decreased significantly in shell, while <strong><strong>GluR2</strong></strong> immunolabeling decreased significantly in both core and shell.
+GRIA2	addiction	withdrawal	10231131	No changes in <strong>GluR2</strong>/3, <strong>GluR2</strong>/4, or GluR4 immunolabeling in NAc were found at either <b>withdrawal</b> time.
+GRIA2	addiction	withdrawal	10231131	No changes in <strong><strong>GluR2</strong></strong>/3, <strong><strong>GluR2</strong></strong>/4, or GluR4 immunolabeling in NAc were found at either <b>withdrawal</b> time.
+GRIA2	addiction	dependence	9390995	Differential <b>dependence</b> on <strong>GluR2</strong> expression of three characteristic features of AMPA receptors.
+GRIA2	addiction	dependence	9390995	Differential <b>dependence</b> on <strong><strong>GluR2</strong></strong> expression of three characteristic features of AMPA receptors.
+GRIA2	drug	opioid	9390995	The physiological effects of a moderate change in <strong>GluR2</strong> relative abundance, such as occurs after ischemia or seizures or after chronic exposure to <b>morphine</b>, thus will be dependent on the ambient <strong>GluR2</strong> level in a cell specific manner.
+GRIA2	drug	opioid	9390995	The physiological effects of a moderate change in <strong><strong>GluR2</strong></strong> relative abundance, such as occurs after ischemia or seizures or after chronic exposure to <b>morphine</b>, thus will be dependent on the ambient <strong><strong>GluR2</strong></strong> level in a cell specific manner.
+GRIA2	drug	amphetamine	9183816	Repeated <b>amphetamine</b> administration decreased levels of GluR1 and <strong>GluR2</strong> but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal.
+GRIA2	addiction	withdrawal	9183816	Repeated amphetamine administration decreased levels of GluR1 and <strong>GluR2</strong> but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day <b>withdrawal</b> time; no changes were observed after 3 days of <b>withdrawal</b>.
+GRIA2	drug	amphetamine	9183816	Repeated <b>amphetamine</b> administration decreased levels of GluR1 and <strong><strong>GluR2</strong></strong> but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal.
+GRIA2	addiction	withdrawal	9183816	Repeated amphetamine administration decreased levels of GluR1 and <strong><strong>GluR2</strong></strong> but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day <b>withdrawal</b> time; no changes were observed after 3 days of <b>withdrawal</b>.
+GRIA2	addiction	withdrawal	9183816	In contrast, levels of GluR1 mRNA in the PFC were increased at 3 but not 14 days of <b>withdrawal</b>, while <strong>GluR2</strong> and 3 mRNAs were unchanged.
+GRIA2	addiction	withdrawal	9183816	In contrast, levels of GluR1 mRNA in the PFC were increased at 3 but not 14 days of <b>withdrawal</b>, while <strong><strong>GluR2</strong></strong> and 3 mRNAs were unchanged.
+GRIA2	drug	cocaine	8613793	In contrast, chronic <b>cocaine</b> treatment did not alter levels of <strong>GluR2</strong> (an AMPA receptor subunit), NMDA2A/B (NMDA receptor subunits), or GluR6/7 (kainate receptor subunits) in this brain region.
+GRIA2	drug	cocaine	8613793	In contrast, chronic <b>cocaine</b> treatment did not alter levels of <strong><strong>GluR2</strong></strong> (an AMPA receptor subunit), NMDA2A/B (NMDA receptor subunits), or GluR6/7 (kainate receptor subunits) in this brain region.
+GRIA2	drug	alcohol	8133290	In contrast, <b>ethanol</b> did not alter the levels of glutamate receptor subunit (GLUR) 1 or <strong>GLUR2</strong> protein, subunits that make up the alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid glutamate receptor, in the hippocampus.
+GRIA2	drug	alcohol	8133290	In contrast, <b>ethanol</b> did not alter the levels of glutamate receptor subunit (GLUR) 1 or <strong><strong>GLUR2</strong></strong> protein, subunits that make up the alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid glutamate receptor, in the hippocampus.
+HTR1B	drug	alcohol	32088264	The 5 HT1A and <strong>5 HT1B</strong> serotonin receptors are abundantly expressed in the CNS and constitute validated as well as putative drug targets in a variety of psychiatric and cognitive disorders, <b>alcoholism</b>/addiction, pain and migraine.
+HTR1B	addiction	addiction	32088264	The 5 HT1A and <strong>5 HT1B</strong> serotonin receptors are abundantly expressed in the CNS and constitute validated as well as putative drug targets in a variety of psychiatric and cognitive disorders, alcoholism/<b>addiction</b>, pain and migraine.
+HTR1B	drug	psychedelics	31927606	Here, we aimed to provide a platform for investigating mechanisms underlying anti OCD effects of <b>ketamine</b> treatment by assessing whether <b>ketamine</b> pretreatment could alleviate <strong>5 HT1B</strong> receptor (5 HT1BR) induced OCD like behavior in mice.
+HTR1B	drug	psychedelics	31826983	<b>MDMA</b>'s prosocial effect requires <strong>5 HT1b</strong> receptor activation and is mimicked by d fenfluramine, a selective serotonin releasing compound.
+HTR1B	drug	amphetamine	31042352	Neural Circuits Associated with <strong>5 HT1B</strong> Receptor Agonist Inhibition of <b>Methamphetamine</b> Seeking in the Conditioned Place Preference Model.
+HTR1B	addiction	relapse	31042352	Neural Circuits Associated with <strong>5 HT1B</strong> Receptor Agonist Inhibition of Methamphetamine <b>Seeking</b> in the Conditioned Place Preference Model.
+HTR1B	addiction	reward	31042352	<strong>5 HT1B</strong> receptors (5 HT1BRs) modulate psychostimulant <b>reward</b> and <b>incentive</b> motivation in rodents.
+HTR1B	drug	alcohol	30774345	The association between <strong>HTR1B</strong> gene rs13212041 polymorphism and onset of <b>alcohol</b> abuse.
+HTR1B	drug	alcohol	30774345	Serotonergic changes have been associated with <b>alcoholism</b>, while serotonin receptors type 1B (<strong>5 HT1B</strong>) play an important role in regulating serotonergic neurotransmission.
+HTR1B	drug	alcohol	30774345	This study examined the association of platelet serotonin (5 HT) and <strong>HTR1B</strong> gene with the onset of <b>alcohol</b> abuse in <b>alcohol</b> dependent subjects.
+HTR1B	drug	alcohol	30774345	Determination of platelet 5 HT concentration and genotyping of rs13212041 <strong>HTR1B</strong> gene polymorphism were performed in 613 <b>alcohol</b> dependent patients, subdivided according to early/late onset (before/after 25 years of age) of <b>alcohol</b> abuse.
+HTR1B	drug	alcohol	30774345	Besides <strong>HTR1B</strong> genotype, age and gender, but not platelet 5 HT, were major variables associated with the onset of <b>alcohol</b> abuse.
+HTR1B	drug	alcohol	30774345	Platelet 5 HT concentration was not significantly different between patients with early and late onset of <b>alcohol</b> abuse, or patients carrying various <strong>HTR1B</strong> genotypes.
+HTR1B	drug	alcohol	30774345	These findings support potential involvement of <strong>5 HT1B</strong> receptors in the onset of <b>alcohol</b> abuse and development of <b>alcohol</b> dependence.
+HTR1B	addiction	dependence	30774345	These findings support potential involvement of <strong>5 HT1B</strong> receptors in the onset of alcohol abuse and development of alcohol <b>dependence</b>.
+HTR1B	drug	cocaine	30464742	Addendum: Effects of a <strong>5 HT1B</strong> Receptor Agonist on Locomotion and Reinstatement of <b>Cocaine</b> Conditioned Place Preference after Abstinence from Repeated Injections in Mice.
+HTR1B	addiction	relapse	30464742	Addendum: Effects of a <strong>5 HT1B</strong> Receptor Agonist on Locomotion and <b>Reinstatement</b> of Cocaine Conditioned Place Preference after Abstinence from Repeated Injections in Mice.
+HTR1B	drug	amphetamine	30168018	<b>Amphetamine</b> Self Administration and Its Extinction Alter the <strong>5 HT1B</strong> Receptor Protein Levels in Designated Structures of the Rat Brain.
+HTR1B	drug	amphetamine	30168018	Focus of this study was to examine changes in <strong>5 HT1B</strong> receptor protein expression in several brain structures linked to substance drug disorder in different stages of <b>amphetamine</b> addiction single session of <b>amphetamine</b> self administration, 20 consecutive days of <b>amphetamine</b> self administration, and 3 and 14 days of extinction from chronic drug intake.
+HTR1B	addiction	addiction	30168018	Focus of this study was to examine changes in <strong>5 HT1B</strong> receptor protein expression in several brain structures linked to substance drug disorder in different stages of amphetamine <b>addiction</b> single session of amphetamine self administration, 20 consecutive days of amphetamine self administration, and 3 and 14 days of extinction from chronic drug intake.
+HTR1B	drug	amphetamine	30168018	Single <b>amphetamine</b> session decreased the amount of <strong>5 HT1B</strong> receptors in SN, VTA, and HIP in active and yoked rats.
+HTR1B	drug	amphetamine	30168018	On the contrary, 20 days of chronic <b>amphetamine</b> exposure triggered elevation of <strong>5 HT1B</strong> receptors exclusively in animals that voluntarily administered the drug in NAc core, GP ventral, and HIP.
+HTR1B	drug	amphetamine	30168018	Furthermore, 14 day (but not 3 day) extinction from <b>amphetamine</b> increased the <strong>5 HT1B</strong> receptor expression in ventral and lateral GP, HIP, and SN.
+HTR1B	drug	amphetamine	30168018	This study is the first to demonstrate that exposure to <b>amphetamine</b> and its extinction alter the expression of <strong>5 HT1B</strong> receptors in various rat brain regions, and those changes seem to be transient and region specific.
+HTR1B	drug	amphetamine	30168018	Importantly, since increased expression of <strong>5 HT1B</strong> receptor after chronic <b>amphetamine</b> self administration was limited only to active group of animals, we suggest that <strong>5 HT1B</strong> receptor is linked to motivational aspect of addiction.
+HTR1B	addiction	addiction	30168018	Importantly, since increased expression of <strong>5 HT1B</strong> receptor after chronic amphetamine self administration was limited only to active group of animals, we suggest that <strong>5 HT1B</strong> receptor is linked to motivational aspect of <b>addiction</b>.
+HTR1B	drug	cocaine	29949237	Another Larry's major contributions are the studies on 5 HT and 5 HT receptors' role in <b>cocaine</b> stimulant actions, which resulted in the identification of <strong>5 HT1B</strong> receptors as a critical substrate of <b>cocaine</b> reinforcement.
+HTR1B	addiction	reward	29949237	Another Larry's major contributions are the studies on 5 HT and 5 HT receptors' role in cocaine stimulant actions, which resulted in the identification of <strong>5 HT1B</strong> receptors as a critical substrate of cocaine <b>reinforcement</b>.
+HTR1B	drug	cocaine	29660439	Activation of <strong>5 HT1B</strong> receptors in the Lateral Habenula attenuates the anxiogenic effects of <b>cocaine</b>.
+HTR1B	drug	cocaine	29660439	Intra LHb pretreatment with the <strong>5 HT1B</strong> agonist CP 94,253 (0, 0.1, or 0.25 μg/side) attenuated the development of approach/avoidance "retreat" behaviors known to be a consequence of <b>cocaine</b>'s dual rewarding (approach) and anxiogenic (avoidance) properties.
+HTR1B	drug	cocaine	29660439	These data suggest that <strong>5 HT1B</strong> signaling within the LHb contributes to the anxiogenic effects of <b>cocaine</b>.
+HTR1B	drug	cocaine	29066957	Effects of a <strong>5 HT1B</strong> Receptor Agonist on Locomotion and Reinstatement of <b>Cocaine</b> Conditioned Place Preference after Abstinence from Repeated Injections in Mice.
+HTR1B	addiction	relapse	29066957	Effects of a <strong>5 HT1B</strong> Receptor Agonist on Locomotion and <b>Reinstatement</b> of Cocaine Conditioned Place Preference after Abstinence from Repeated Injections in Mice.
+HTR1B	drug	cocaine	29066957	<strong>5 HT1B</strong> receptors (5 HT1BRs) modulate behavioral effects of <b>cocaine</b>.
+HTR1B	drug	psychedelics	28890736	This 25B <b>NBOMe</b> induced rhabdomyolysis was inhibited by the 5 HT2A receptor antagonists ritanserin and aripirazole, but not by the 5 HT1A + <strong>5 HT1B</strong> receptor antagonist propranolol and the 5 HT3 receptor antagonist granisetron, indicating 5 HT2A dependent rhabdomyolysis.
+HTR1B	drug	cocaine	28720013	There is evidence that the <strong>5 HT1B</strong> serotonin receptor subtype mediates some of the <b>cocaine</b> induced gene regulation.
+HTR1B	drug	cocaine	28444326	<strong>5 HT1B</strong> receptor agonists enhance <b>cocaine</b> intake during daily self administration sessions but decrease <b>cocaine</b> intake when tested after prolonged abstinence.
+HTR1B	drug	amphetamine	28444326	We examined if <strong>5 HT1B</strong> receptor agonists produce similar abstinence dependent effects on <b>methamphetamine</b> intake.
+HTR1B	drug	amphetamine	28444326	Rats were then tested for the effects of the selective <strong>5 HT1B</strong> receptor agonist, CP 94,253 (5.6 or 10 mg/kg), or the less selective but clinically available <strong>5 HT1B</strong>/1D receptor agonist, zolmitriptan (10 mg/kg), on <b>methamphetamine</b> self administration both before and after a 21 day forced abstinence period during which the rats remained in their home cages.
+HTR1B	drug	amphetamine	28444326	The CP 94,253 induced decrease in <b>methamphetamine</b> intake was replicated in rats tested on a variable ratio 5 schedule, and the <strong>5 HT1B</strong> receptor antagonist SB 224,289 (10 mg/kg) reversed this effect.
+HTR1B	drug	amphetamine	28444326	Unlike the abstinence dependent effect of <strong>5 HT1B</strong> receptor agonists on cocaine intake reported previously, both CP 94,253 and zolmitriptan decreased <b>methamphetamine</b> intake regardless of abstinence.
+HTR1B	drug	cocaine	28444326	Unlike the abstinence dependent effect of <strong>5 HT1B</strong> receptor agonists on <b>cocaine</b> intake reported previously, both CP 94,253 and zolmitriptan decreased methamphetamine intake regardless of abstinence.
+HTR1B	drug	cocaine	27888284	Attenuation of the anxiogenic effects of <b>cocaine</b> by <strong>5 HT1B</strong> autoreceptor stimulation in the bed nucleus of the stria terminalis of rats.
+HTR1B	drug	cocaine	27888284	Intra BNST infusions of the <strong>5 HT1B</strong> autoreceptor agonist attenuated the anxiogenic effects of <b>cocaine</b> as reflected by a decrease in runway approach avoidance conflict behavior.
+HTR1B	drug	cocaine	27888284	Inhibition of <strong>5 HT1B</strong> signaling within the BNST selectively attenuated the anxiogenic effects of <b>cocaine</b>, while leaving unaffected the positive incentive properties of the drug.
+HTR1B	addiction	reward	27888284	Inhibition of <strong>5 HT1B</strong> signaling within the BNST selectively attenuated the anxiogenic effects of cocaine, while leaving unaffected the positive <b>incentive</b> properties of the drug.
+HTR1B	drug	psychedelics	27264435	Doses of the 5 HT1A antagonist, WAY 100635 (0.1 1.0mg/kg), <strong>5 HT1B</strong> antagonist, GR 127935 (1.0 3.0mg/kg), and the 5 HT2A antagonist, ketanserin (1.0 3.0mg/kg) that have previously been shown to decrease self administration of other psychostimulants and that decreased <b>MDMA</b> produced hyperactivity in the present study did not alter <b>MDMA</b> self administration.
+HTR1B	drug	psychedelics	27264435	The 5 HT1A agonist, 8 OH DPAT (0.1 1.0mg/kg), but not the <strong>5 HT1B</strong>/1A agonist, RU 24969 (0.3 3.0mg/kg), decreased drug seeking produced by the reintroduction of a light stimulus that had been paired with self administered <b>MDMA</b> infusions.
+HTR1B	addiction	relapse	27264435	The 5 HT1A agonist, 8 OH DPAT (0.1 1.0mg/kg), but not the <strong>5 HT1B</strong>/1A agonist, RU 24969 (0.3 3.0mg/kg), decreased drug <b>seeking</b> produced by the reintroduction of a light stimulus that had been paired with self administered MDMA infusions.
+HTR1B	drug	psychedelics	27264435	These findings suggest a limited role of activation of 5 HT1A, <strong>5 HT1B</strong> or 5 HT2 receptor mechanisms in <b>MDMA</b> self administration or in <b>MDMA</b> produced drug seeking following extinction.
+HTR1B	addiction	relapse	27264435	These findings suggest a limited role of activation of 5 HT1A, <strong>5 HT1B</strong> or 5 HT2 receptor mechanisms in MDMA self administration or in MDMA produced drug <b>seeking</b> following extinction.
+HTR1B	drug	cocaine	26990537	Here we examined the role of the protein p11, which recruits serotonin <strong>5HT1B</strong> and 5HT4 receptors to the cell surface, in <b>cocaine</b> reward.
+HTR1B	addiction	reward	26990537	Here we examined the role of the protein p11, which recruits serotonin <strong>5HT1B</strong> and 5HT4 receptors to the cell surface, in cocaine <b>reward</b>.
+HTR1B	addiction	reward	26856853	The 5 HT1A and <strong>5 HT1B</strong> receptors are both well localized to regulate dopamine (DA) release, and have been implicated in modulating the <b>reinforcing</b> effects of many drugs of abuse, but a role in acquisition of self administration has not been determined.
+HTR1B	drug	psychedelics	26856853	This study was designed to determine the effect of pharmacological manipulation of 5 HT1A and <strong>5 HT1B</strong> receptor mechanisms on the acquisition of <b>MDMA</b> self administration.
+HTR1B	drug	psychedelics	26856853	These data suggest that the initial reinforcing effects of <b>MDMA</b> are modulated by 5 HT1A and/or <strong>5 HT1B</strong> receptor mechanisms.
+HTR1B	addiction	reward	26856853	These data suggest that the initial <b>reinforcing</b> effects of MDMA are modulated by 5 HT1A and/or <strong>5 HT1B</strong> receptor mechanisms.
+HTR1B	drug	cannabinoid	26465930	The Efficacy of Eslicarbazepine Acetate in Models of Trigeminal, Neuropathic, and Visceral Pain: The Involvement of <strong>5 HT1B</strong>/1D Serotonergic and CB1/CB2 <b>Cannabinoid</b> Receptors.
+HTR1B	drug	cannabinoid	26465930	The influence of <strong>5 HT1B</strong>/1D serotonin receptor (GR 127935) and CB1 (AM251) and CB2 <b>cannabinoid</b> receptor (AM630) antagonists on the antinociceptive effect of ESL was tested in the model of trigeminal pain.
+HTR1B	drug	cannabinoid	26465930	In the trigeminal pain model, the antinociceptive effect of ESL is, at least in part, mediated by <strong>5 HT1B</strong>/1D serotonin and CB1/CB2 <b>cannabinoid</b> receptors.
+HTR1B	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, <strong>HTR1B</strong>, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+HTR1B	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, <strong>HTR1B</strong>, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+HTR1B	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, <strong>HTR1B</strong>, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+HTR1B	drug	amphetamine	25485646	The present experiments examined serotonergic roles in <b>METH</b> induced locomotor sensitization by assessing: (a) the effect of serotonin transporter (SERT; Slc6A4) knockout (KO) on <b>METH</b> induced locomotor sensitization; (b) extracellular monoamine levels in <b>METH</b> treated animals as determined by in vivo microdialysis; and (c) effects of serotonin (5 HT) receptor antagonists on <b>METH</b> induced behavioral sensitization, with focus on effects of the <strong>5 HT1B</strong> receptor antagonist SB 216641 and a comparison with the 5 HT2 receptor antagonist ketanserin.
+HTR1B	addiction	sensitization	25485646	The present experiments examined serotonergic roles in METH induced locomotor <b>sensitization</b> by assessing: (a) the effect of serotonin transporter (SERT; Slc6A4) knockout (KO) on METH induced locomotor <b>sensitization</b>; (b) extracellular monoamine levels in METH treated animals as determined by in vivo microdialysis; and (c) effects of serotonin (5 HT) receptor antagonists on METH induced behavioral <b>sensitization</b>, with focus on effects of the <strong>5 HT1B</strong> receptor antagonist SB 216641 and a comparison with the 5 HT2 receptor antagonist ketanserin.
+HTR1B	drug	amphetamine	25485646	The selective <strong>5 HT1B</strong> antagonist receptor SB 216641 restored <b>METH</b> induced locomotor sensitization in SERT /  mice, whereas ketanserin was ineffective.
+HTR1B	addiction	sensitization	25485646	The selective <strong>5 HT1B</strong> antagonist receptor SB 216641 restored METH induced locomotor <b>sensitization</b> in SERT /  mice, whereas ketanserin was ineffective.
+HTR1B	drug	amphetamine	25485646	These experiments demonstrate that 5 HT actions, including those at <strong>5 HT1B</strong> receptors, contribute to <b>METH</b> induced locomotor sensitization.
+HTR1B	addiction	sensitization	25485646	These experiments demonstrate that 5 HT actions, including those at <strong>5 HT1B</strong> receptors, contribute to METH induced locomotor <b>sensitization</b>.
+HTR1B	drug	amphetamine	25485646	Modulation of <strong>5 HT1B</strong> receptors might aid therapeutic approaches to the sequelae of chronic <b>METH</b> use.
+HTR1B	drug	cocaine	25442058	Reductions of p11 and <strong>5 HT1B</strong> receptor availability in limbic brain regions in <b>cocaine</b> dependence.
+HTR1B	addiction	dependence	25442058	Reductions of p11 and <strong>5 HT1B</strong> receptor availability in limbic brain regions in cocaine <b>dependence</b>.
+HTR1B	addiction	addiction	25218038	Given that <strong>5 HT1B</strong> receptors are known to facilitate <b>addiction</b> related gene regulation and behavior, our results suggest that SSRIs may enhance the <b>addiction</b> liability of methylphenidate by increasing <strong>5 HT1B</strong> receptor signaling.
+HTR1B	drug	cannabinoid	24688470	Altogether, our findings suggest that a depressive like state may alter <b>cannabinoid</b> CB1 receptor agonist induced brain reward function and that a dopaminergic rather than a <strong>5 HT1B</strong> mechanism is likely to underlie enhanced WIN self administration in OBX rats.
+HTR1B	addiction	reward	24688470	Altogether, our findings suggest that a depressive like state may alter cannabinoid CB1 receptor agonist induced brain <b>reward</b> function and that a dopaminergic rather than a <strong>5 HT1B</strong> mechanism is likely to underlie enhanced WIN self administration in OBX rats.
+HTR1B	drug	cocaine	24433854	Reductions in brain <strong>5 HT1B</strong> receptor availability in primarily <b>cocaine</b> dependent humans.
+HTR1B	drug	cocaine	24433854	Preclinical evidence implicates the serotonin receptor 5 hydroxytryptamine 1B (<strong>5 HT1B</strong>) in the effects of <b>cocaine</b>.
+HTR1B	drug	cocaine	24433854	This study explores <strong>5 HT1B</strong> in humans by examining receptor availability in vivo in subjects whose primary addiction is <b>cocaine</b> dependence (CD) using positron emission tomography.
+HTR1B	addiction	addiction	24433854	This study explores <strong>5 HT1B</strong> in humans by examining receptor availability in vivo in subjects whose primary <b>addiction</b> is cocaine dependence (CD) using positron emission tomography.
+HTR1B	addiction	dependence	24433854	This study explores <strong>5 HT1B</strong> in humans by examining receptor availability in vivo in subjects whose primary addiction is cocaine <b>dependence</b> (CD) using positron emission tomography.
+HTR1B	drug	cocaine	24369697	Pharmacological evidence for an abstinence induced switch in <strong>5 HT1B</strong> receptor modulation of <b>cocaine</b> self administration and <b>cocaine</b> seeking behavior.
+HTR1B	addiction	relapse	24369697	Pharmacological evidence for an abstinence induced switch in <strong>5 HT1B</strong> receptor modulation of cocaine self administration and cocaine <b>seeking</b> behavior.
+HTR1B	drug	cocaine	24369697	Studies examining serotonin 1B (<strong>5 HT1B</strong>) receptor manipulations on <b>cocaine</b> self administration and <b>cocaine</b> seeking behavior initially seemed discrepant.
+HTR1B	addiction	relapse	24369697	Studies examining serotonin 1B (<strong>5 HT1B</strong>) receptor manipulations on cocaine self administration and cocaine <b>seeking</b> behavior initially seemed discrepant.
+HTR1B	drug	cocaine	24369697	However, we recently suggested based on viral mediated <strong>5 HT1B</strong> receptor gene transfer that the discrepancies are likely due to differences in the length of abstinence from <b>cocaine</b> prior to testing.
+HTR1B	drug	cocaine	24369697	To further validate our findings pharmacologically, we examined the effects of the selective <strong>5 HT1B</strong> receptor agonist CP 94,253 (5.6 mg/kg, s.c.) on <b>cocaine</b> self administration during maintenance and after a period of protracted abstinence with or without daily extinction training.
+HTR1B	drug	cocaine	24369697	The attenuating effects of CP 94,253 on the descending limb of the <b>cocaine</b> dose effect function were blocked by the selective <strong>5 HT1B</strong> receptor antagonist SB 224289 (5 mg/kg, i.p.)
+HTR1B	drug	cocaine	24369697	The results support a switch in <strong>5 HT1B</strong> receptor modulation of <b>cocaine</b> reinforcement from facilitatory during self administration maintenance to inhibitory during protracted abstinence.
+HTR1B	addiction	reward	24369697	The results support a switch in <strong>5 HT1B</strong> receptor modulation of cocaine <b>reinforcement</b> from facilitatory during self administration maintenance to inhibitory during protracted abstinence.
+HTR1B	drug	cocaine	24369697	These findings suggest that the <strong>5 HT1B</strong> receptor may be a novel target for developing medication for treating <b>cocaine</b> dependence.
+HTR1B	addiction	dependence	24369697	These findings suggest that the <strong>5 HT1B</strong> receptor may be a novel target for developing medication for treating cocaine <b>dependence</b>.
+HTR1B	drug	amphetamine	24145075	To substantiate a role for those receptors in incentive motivation for <b>amphetamine</b>, we used the extinction/reinstatement model to examine the effects of the <strong>5 HT1B</strong> receptor ligands on the reinstatement of extinguished <b>amphetamine</b> seeking behavior.
+HTR1B	addiction	relapse	24145075	To substantiate a role for those receptors in incentive motivation for amphetamine, we used the extinction/<b>reinstatement</b> model to examine the effects of the <strong>5 HT1B</strong> receptor ligands on the <b>reinstatement</b> of extinguished amphetamine <b>seeking</b> behavior.
+HTR1B	addiction	reward	24145075	To substantiate a role for those receptors in <b>incentive</b> motivation for amphetamine, we used the extinction/reinstatement model to examine the effects of the <strong>5 HT1B</strong> receptor ligands on the reinstatement of extinguished amphetamine seeking behavior.
+HTR1B	drug	amphetamine	24145075	The <strong>5 HT1B</strong> receptor antagonist SB 216641 (5 7.5 mg/kg) attenuated the <b>amphetamine</b> (1.5 mg/kg)  and the <b>amphetamine</b> associated cue combined with the threshold dose of <b>amphetamine</b> (0.5 mg/kg) induced reinstatement of <b>amphetamine</b> seeking behavior.
+HTR1B	addiction	relapse	24145075	The <strong>5 HT1B</strong> receptor antagonist SB 216641 (5 7.5 mg/kg) attenuated the amphetamine (1.5 mg/kg)  and the amphetamine associated cue combined with the threshold dose of amphetamine (0.5 mg/kg) induced <b>reinstatement</b> of amphetamine <b>seeking</b> behavior.
+HTR1B	drug	amphetamine	24145075	The <strong>5 HT1B</strong> receptor agonist CP 94253 (1.25 5 mg/kg) also inhibited the <b>amphetamine</b> seeking behavior induced by <b>amphetamine</b> (1.5 mg/kg) but not by the cue combined with the threshold dose of <b>amphetamine</b>.
+HTR1B	addiction	relapse	24145075	The <strong>5 HT1B</strong> receptor agonist CP 94253 (1.25 5 mg/kg) also inhibited the amphetamine <b>seeking</b> behavior induced by amphetamine (1.5 mg/kg) but not by the cue combined with the threshold dose of amphetamine.
+HTR1B	drug	amphetamine	24145075	The inhibitory effect of CP94253 on <b>amphetamine</b> seeking behavior remained unaffected by the <strong>5 HT1B</strong> receptor antagonist.
+HTR1B	addiction	relapse	24145075	The inhibitory effect of CP94253 on amphetamine <b>seeking</b> behavior remained unaffected by the <strong>5 HT1B</strong> receptor antagonist.
+HTR1B	drug	amphetamine	24145075	Our results indicate that tonic activation of <strong>5 HT1B</strong> receptors is involved in <b>amphetamine</b>  and cue induced reinstatement of <b>amphetamine</b> seeking behavior and that the inhibitory effects of <strong>5 HT1B</strong> receptor antagonists on these phenomena are directly related to the motivational aspects of <b>amphetamine</b> abuse.
+HTR1B	addiction	relapse	24145075	Our results indicate that tonic activation of <strong>5 HT1B</strong> receptors is involved in amphetamine  and cue induced <b>reinstatement</b> of amphetamine <b>seeking</b> behavior and that the inhibitory effects of <strong>5 HT1B</strong> receptor antagonists on these phenomena are directly related to the motivational aspects of amphetamine abuse.
+HTR1B	drug	amphetamine	24145075	The inhibitory effect of CP 94253 on <b>amphetamine</b> seeking behavior seems to be unrelated to <strong>5 HT1B</strong> receptor activation and may result from a general reduction of motivation.
+HTR1B	addiction	relapse	24145075	The inhibitory effect of CP 94253 on amphetamine <b>seeking</b> behavior seems to be unrelated to <strong>5 HT1B</strong> receptor activation and may result from a general reduction of motivation.
+HTR1B	drug	cocaine	24075973	Differential effect of viral overexpression of nucleus accumbens shell <strong>5 HT1B</strong> receptors on stress  and <b>cocaine</b> priming induced reinstatement of <b>cocaine</b> seeking.
+HTR1B	addiction	relapse	24075973	Differential effect of viral overexpression of nucleus accumbens shell <strong>5 HT1B</strong> receptors on stress  and cocaine priming induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+HTR1B	addiction	relapse	24075973	While interactions between NAccSh <strong>5 HT1B</strong> receptors and stress have been reported in early stages of psychostimulant induced neuroadaptations, specifically psychomotor sensitization, the effect of this interaction on later stages of drug <b>seeking</b> is currently unknown.
+HTR1B	addiction	sensitization	24075973	While interactions between NAccSh <strong>5 HT1B</strong> receptors and stress have been reported in early stages of psychostimulant induced neuroadaptations, specifically psychomotor <b>sensitization</b>, the effect of this interaction on later stages of drug seeking is currently unknown.
+HTR1B	drug	cocaine	24075973	Here, we examined the effect of herpes simplex virus (HSV) mediated overexpression of NAccSh <strong>5 HT1B</strong> receptors on reinstatement of <b>cocaine</b> seeking induced by exposure to stress or a <b>cocaine</b> prime.
+HTR1B	addiction	relapse	24075973	Here, we examined the effect of herpes simplex virus (HSV) mediated overexpression of NAccSh <strong>5 HT1B</strong> receptors on <b>reinstatement</b> of cocaine <b>seeking</b> induced by exposure to stress or a cocaine prime.
+HTR1B	drug	cocaine	24075973	The effect of <strong>5 HT1B</strong> receptor overexpression was assessed on reinstatement induced by intermittent footshock (0.5 mA for 15 min) or a <b>cocaine</b> prime (10mg/kg, ip).
+HTR1B	addiction	relapse	24075973	The effect of <strong>5 HT1B</strong> receptor overexpression was assessed on <b>reinstatement</b> induced by intermittent footshock (0.5 mA for 15 min) or a cocaine prime (10mg/kg, ip).
+HTR1B	drug	cocaine	24075973	Results indicate that NAccSh <strong>5 HT1B</strong> receptor overexpression had no effect on footshock reinstatement while significantly decreasing <b>cocaine</b> priming induced reinstatement.
+HTR1B	addiction	relapse	24075973	Results indicate that NAccSh <strong>5 HT1B</strong> receptor overexpression had no effect on footshock <b>reinstatement</b> while significantly decreasing cocaine priming induced <b>reinstatement</b>.
+HTR1B	drug	cocaine	24075973	These results suggest that the efficacy of pharmacological agents targeting <strong>5 HT1B</strong> receptors for the treatment of <b>cocaine</b> relapse will depend largely on the nature of the reinstating stimulus.
+HTR1B	addiction	relapse	24075973	These results suggest that the efficacy of pharmacological agents targeting <strong>5 HT1B</strong> receptors for the treatment of cocaine <b>relapse</b> will depend largely on the nature of the reinstating stimulus.
+HTR1B	drug	cocaine	23452061	Our results reveal a novel <strong>5 HT1B</strong> receptor mediated LTD in the NAc and suggest that <b>cocaine</b> exposure may result in elevated phosphorylation of presynaptic proteins involved in regulating glutamate release, which counteracts the presynaptic depressant effects of <strong>5 HT1B</strong> receptors and thereby impairs the induction of LTD by 5 HT.
+HTR1B	drug	alcohol	23335468	Associations of the 5 hydroxytryptamine (serotonin) receptor 1B gene (<strong>HTR1B</strong>) with <b>alcohol</b>, cocaine, and heroin abuse.
+HTR1B	drug	cocaine	23335468	Associations of the 5 hydroxytryptamine (serotonin) receptor 1B gene (<strong>HTR1B</strong>) with alcohol, <b>cocaine</b>, and heroin abuse.
+HTR1B	drug	opioid	23335468	Associations of the 5 hydroxytryptamine (serotonin) receptor 1B gene (<strong>HTR1B</strong>) with alcohol, cocaine, and <b>heroin</b> abuse.
+HTR1B	drug	alcohol	23335468	To clarify the roles of commonly reported single nucleotide polymorphisms (SNPs) of the <strong>HTR1B</strong> gene underlying <b>alcohol</b> and drug dependence (abuse), we performed a meta analysis based on the available genotype data from individual candidate gene based association studies.
+HTR1B	addiction	dependence	23335468	To clarify the roles of commonly reported single nucleotide polymorphisms (SNPs) of the <strong>HTR1B</strong> gene underlying alcohol and drug <b>dependence</b> (abuse), we performed a meta analysis based on the available genotype data from individual candidate gene based association studies.
+HTR1B	drug	alcohol	23335468	This meta analysis supports the associations of <strong>HTR1B</strong>  261T>G and  161A>T with <b>alcohol</b> and drug abuse and further investigations are warranted in larger samples.
+HTR1B	drug	nicotine	23177301	In line with genetic and pharmacological studies suggesting that neurotransmitter pathways play a role in <b>nicotine</b> dependence, research was conducted in connection with 4 genetic polymorphisms: OPRM1, TPH1, ADRA2A and <strong>HTR1B</strong>.
+HTR1B	addiction	dependence	23177301	In line with genetic and pharmacological studies suggesting that neurotransmitter pathways play a role in nicotine <b>dependence</b>, research was conducted in connection with 4 genetic polymorphisms: OPRM1, TPH1, ADRA2A and <strong>HTR1B</strong>.
+HTR1B	drug	alcohol	23118018	Role of 5 hydroxytryptamine 1B (<strong>5 HT1B</strong>) receptors in the regulation of <b>ethanol</b> intake in rodents.
+HTR1B	drug	alcohol	23118018	Among serotonin receptors, 5 hydroxytryptamine 1B (<strong>5 HT1B</strong>) receptors have been associated with drug abuse including <b>alcohol</b>.
+HTR1B	drug	alcohol	23118018	In this review, the neurocircuitry involving <strong>5 HT1B</strong> receptors in central reward brain regions related to <b>alcohol</b> intake are discussed in detail.
+HTR1B	addiction	reward	23118018	In this review, the neurocircuitry involving <strong>5 HT1B</strong> receptors in central <b>reward</b> brain regions related to alcohol intake are discussed in detail.
+HTR1B	drug	alcohol	23118018	Emphasis has been placed on the pharmacological manipulations of <strong>5 HT1B</strong> receptor mediated <b>alcohol</b> intake.
+HTR1B	drug	alcohol	23118018	Furthermore, <strong>5 HT1B</strong> auto  and hetero receptors regulate <b>alcohol</b> intake through the regulatory mechanism involving release of 5 HT, gamma aminobutyric acid (GABA), dopamine, and glutamate is evaluated.
+HTR1B	drug	alcohol	23118018	Thus, interactions between <strong>5 HT1B</strong> receptors and these neurotransmitter systems are suggested to modulate <b>alcohol</b> drinking behavior.
+HTR1B	drug	alcohol	23118018	This review on the role of <strong>5 HT1B</strong> receptors in neurotransmitter release and consequent <b>alcohol</b> intake provides important information about the potential therapeutic role of <strong>5 HT1B</strong> receptors for the treatment of <b>alcohol</b> dependence.
+HTR1B	addiction	dependence	23118018	This review on the role of <strong>5 HT1B</strong> receptors in neurotransmitter release and consequent alcohol intake provides important information about the potential therapeutic role of <strong>5 HT1B</strong> receptors for the treatment of alcohol <b>dependence</b>.
+HTR1B	drug	opioid	22841130	One hundred seven <b>methadone</b> maintenance treatment patients, 36 having an ADHD diagnosis, 176 adult patients with ADHD without SUDs, and 500 healthy controls were genotyped for variants in the DRD4 (exon 3 VNTR), DRD5 (upstream VNTR), <strong>HTR1B</strong> (rs6296), DBH (rs2519152), COMT (rs4680; Val158Met), and OPRM1 (rs1799971; 118A>G) genes.
+HTR1B	addiction	addiction	22358079	Role of serotonin <strong>5 HT1B</strong> receptors in psychostimulant <b>addiction</b>.
+HTR1B	drug	amphetamine	22227331	The effect of serotonin <strong>5HT1B</strong> receptor ligands on <b>amphetamine</b> self administration in rats.
+HTR1B	addiction	addiction	22064162	Genes that have been previously associated with depression, AD, or other <b>addiction</b> related phenotypes   such as CDH13, CSMD2, GRID1, and <strong>HTR1B</strong>   were implicated by nominally significant SNPs.
+HTR1B	drug	nicotine	22028400	Among committed never <b>smokers</b> (N = 872), three genes (OPRM1, SNAP25, <strong>HTR1B</strong>) were associated with experimentation as were all psychosocial factors.
+HTR1B	drug	alcohol	22005095	A haplotype analysis is consistent with the role of functional <strong>HTR1B</strong> variants in <b>alcohol</b> dependence.
+HTR1B	addiction	dependence	22005095	A haplotype analysis is consistent with the role of functional <strong>HTR1B</strong> variants in alcohol <b>dependence</b>.
+HTR1B	drug	alcohol	22005095	Association studies between the <strong>HTR1B</strong> gene variants and <b>alcoholism</b> have found significant results.
+HTR1B	drug	alcohol	22005095	The aim of this study is to investigate the role of the most relevant variants (rs11568817, rs130058, rs6296 and rs13212041) of the <strong>HTR1B</strong> gene in the susceptibility to <b>alcohol</b> dependence.
+HTR1B	addiction	dependence	22005095	The aim of this study is to investigate the role of the most relevant variants (rs11568817, rs130058, rs6296 and rs13212041) of the <strong>HTR1B</strong> gene in the susceptibility to alcohol <b>dependence</b>.
+HTR1B	drug	alcohol	22005095	In conclusion, our findings point to an association between functional variants in the promoter region of the <strong>HTR1B</strong> gene and <b>alcohol</b> dependence, supporting previous neurobiological evidences of the involvement of <strong>HTR1B</strong> variations in <b>alcohol</b> related phenotypes.
+HTR1B	addiction	dependence	22005095	In conclusion, our findings point to an association between functional variants in the promoter region of the <strong>HTR1B</strong> gene and alcohol <b>dependence</b>, supporting previous neurobiological evidences of the involvement of <strong>HTR1B</strong> variations in alcohol related phenotypes.
+HTR1B	drug	alcohol	21906503	Case control genetic analyses were conducted for the association between <strong>HTR1B</strong>, SLC6A4, DRD2, and OPRμ1 genes and subgroups of <b>alcohol</b> dependence using a sample of 530 controls screened for <b>alcohol</b> problems.
+HTR1B	addiction	dependence	21906503	Case control genetic analyses were conducted for the association between <strong>HTR1B</strong>, SLC6A4, DRD2, and OPRμ1 genes and subgroups of alcohol <b>dependence</b> using a sample of 530 controls screened for alcohol problems.
+HTR1B	drug	alcohol	21906503	In addition, markers in the <strong>HTR1B</strong> and OPRμ1 genes showed genetic associations with subgroups of <b>alcohol</b> dependence (ORs = 1.5 2.4).
+HTR1B	addiction	dependence	21906503	In addition, markers in the <strong>HTR1B</strong> and OPRμ1 genes showed genetic associations with subgroups of alcohol <b>dependence</b> (ORs = 1.5 2.4).
+HTR1B	drug	amphetamine	21886584	Association Between <strong>5HT1b</strong> Receptor Gene and <b>Methamphetamine</b> Dependence.
+HTR1B	addiction	dependence	21886584	Association Between <strong>5HT1b</strong> Receptor Gene and Methamphetamine <b>Dependence</b>.
+HTR1B	drug	alcohol	21886584	Mice with a knock out of the 5HT1b receptor gene (<strong>HTR1B</strong>) displayed increased locomotor response to cocaine and elevated motivation to self administer cocaine and <b>alcohol</b>.
+HTR1B	drug	cocaine	21886584	Mice with a knock out of the 5HT1b receptor gene (<strong>HTR1B</strong>) displayed increased locomotor response to <b>cocaine</b> and elevated motivation to self administer <b>cocaine</b> and alcohol.
+HTR1B	drug	alcohol	21886584	Mice with a knock out of the <strong>5HT1b</strong> receptor gene (<strong>HTR1B</strong>) displayed increased locomotor response to cocaine and elevated motivation to self administer cocaine and <b>alcohol</b>.
+HTR1B	drug	cocaine	21886584	Mice with a knock out of the <strong>5HT1b</strong> receptor gene (<strong>HTR1B</strong>) displayed increased locomotor response to <b>cocaine</b> and elevated motivation to self administer <b>cocaine</b> and alcohol.
+HTR1B	drug	alcohol	21886584	Previous genetic studies showed significant associations of <strong>HTR1B</strong> with <b>alcohol</b> dependence and substance abuse, but were followed by inconsistent results.
+HTR1B	addiction	dependence	21886584	Previous genetic studies showed significant associations of <strong>HTR1B</strong> with alcohol <b>dependence</b> and substance abuse, but were followed by inconsistent results.
+HTR1B	drug	amphetamine	21886584	We examined a case control genetic association study of <strong>HTR1B</strong> with <b>methamphetamine</b> dependence patients in a Japanese population.
+HTR1B	addiction	dependence	21886584	We examined a case control genetic association study of <strong>HTR1B</strong> with methamphetamine <b>dependence</b> patients in a Japanese population.
+HTR1B	drug	amphetamine	21886584	Genetic associations of <strong>HTR1B</strong> were tested with several clinical phenotypes of <b>methamphetamine</b> dependence and/or psychosis, such as age at first abuse, duration of latency from the first abuse to onset of psychosis, prognosis of psychosis after therapy, and complication of spontaneous relapse of psychotic state.
+HTR1B	addiction	dependence	21886584	Genetic associations of <strong>HTR1B</strong> were tested with several clinical phenotypes of methamphetamine <b>dependence</b> and/or psychosis, such as age at first abuse, duration of latency from the first abuse to onset of psychosis, prognosis of psychosis after therapy, and complication of spontaneous relapse of psychotic state.
+HTR1B	addiction	relapse	21886584	Genetic associations of <strong>HTR1B</strong> were tested with several clinical phenotypes of methamphetamine dependence and/or psychosis, such as age at first abuse, duration of latency from the first abuse to onset of psychosis, prognosis of psychosis after therapy, and complication of spontaneous <b>relapse</b> of psychotic state.
+HTR1B	drug	amphetamine	21886584	The present findings may indicate that <strong>HTR1B</strong> does not play a major role in individual susceptibility to <b>methamphetamine</b> dependence or development of <b>methamphetamine</b> induced psychosis.
+HTR1B	addiction	dependence	21886584	The present findings may indicate that <strong>HTR1B</strong> does not play a major role in individual susceptibility to methamphetamine <b>dependence</b> or development of methamphetamine induced psychosis.
+HTR1B	drug	alcohol	21172311	Association between the 5 <strong>HTR1B</strong> gene polymorphisms and <b>alcohol</b> dependence in a Han Chinese population.
+HTR1B	addiction	dependence	21172311	Association between the 5 <strong>HTR1B</strong> gene polymorphisms and alcohol <b>dependence</b> in a Han Chinese population.
+HTR1B	drug	alcohol	21172311	Previous research has suggested that the genetic variation of the <strong>HTR1B</strong> gene may confer susceptibility to <b>alcoholism</b> or some subtypes of <b>alcohol</b> dependence, but the evidence has been inconsistent.
+HTR1B	addiction	dependence	21172311	Previous research has suggested that the genetic variation of the <strong>HTR1B</strong> gene may confer susceptibility to alcoholism or some subtypes of alcohol <b>dependence</b>, but the evidence has been inconsistent.
+HTR1B	drug	alcohol	21172311	The aim of the present study is to examine whether polymorphic variants of the <strong>HTR1B</strong> gene are associated with <b>alcohol</b> dependence subtypes or drinking related behaviors in Chinese Han population.
+HTR1B	addiction	dependence	21172311	The aim of the present study is to examine whether polymorphic variants of the <strong>HTR1B</strong> gene are associated with alcohol <b>dependence</b> subtypes or drinking related behaviors in Chinese Han population.
+HTR1B	drug	alcohol	21172311	<b>Alcohol</b> dependent (AD) male patients (n=135) and controls (n=143) were genotyped for two polymorphisms: A161T in the promoter region and the synonymous variation G861C in the coding region of <strong>HTR1B</strong>.
+HTR1B	drug	alcohol	21172311	These findings confirm <strong>HTR1B</strong> as a susceptibility gene for <b>alcohol</b> dependence in the sample of Chinese Han population.
+HTR1B	addiction	dependence	21172311	These findings confirm <strong>HTR1B</strong> as a susceptibility gene for alcohol <b>dependence</b> in the sample of Chinese Han population.
+HTR1B	drug	alcohol	21172311	The <strong>HTR1B</strong> A 161T polymorphism may be particularly valuable as a functional genetic marker for <b>alcoholism</b> and merits additional study.
+HTR1B	drug	alcohol	19519719	Several studies have suggested that the serotonin receptor 1B gene (<strong>5HT1B</strong>) may be important in the pathogenesis of <b>alcohol</b> dependence (<b>alcoholism</b>; ALC; AD).
+HTR1B	addiction	dependence	19519719	Several studies have suggested that the serotonin receptor 1B gene (<strong>5HT1B</strong>) may be important in the pathogenesis of alcohol <b>dependence</b> (alcoholism; ALC; AD).
+HTR1B	drug	alcohol	19519719	We further explored correlation of this <strong>5HT1B</strong> gene variant between anxiety depression <b>alcoholism</b> (ANX/DEP ALC) and antisocial <b>alcoholism</b> (antisocial ALC) subgroups because of the high comorbidity of anxiety depression, antisocial personality disorder, and AD.
+HTR1B	drug	psychedelics	18812013	<strong>5 HT1B</strong> receptor density and G protein coupling were higher in <b>MDMA</b> treated S100B mutant mice than in saline treated mutant mice and <b>MDMA</b> treated wild type mice in the medial globus pallidus.
+HTR1B	addiction	addiction	18406571	The serotonin1B receptor knockout (<strong>5 HT1B</strong> KO) mouse is a valuable animal model of <b>addiction</b> to psychostimulants.
+HTR1B	drug	opioid	18406571	<strong>5 HT1B</strong> KO showed selective decreases in G protein coupling to mu <b>opioid</b> receptors in the paraventricular thalamic nucleus, and to GABAB receptors in the basolateral nucleus of amygdala.
+HTR1B	addiction	addiction	18406571	It is likely that these latter changes underlie some aspects of the <b>addictive</b> behavior of the <strong>5 HT1B</strong> KO mouse.
+HTR1B	drug	amphetamine	18048951	Modulatory role of <strong>5 HT1B</strong> receptors in the discriminative signal of <b>amphetamine</b> in the conditioned taste aversion paradigm.
+HTR1B	addiction	aversion	18048951	Modulatory role of <strong>5 HT1B</strong> receptors in the discriminative signal of amphetamine in the conditioned taste <b>aversion</b> paradigm.
+HTR1B	drug	amphetamine	18048951	We examined the role of <strong>5 HT1B</strong> receptors on the discriminative stimulus properties of <b>AMPH</b> using conditioned taste aversion (CTA) as the drug discrimination procedure.
+HTR1B	addiction	aversion	18048951	We examined the role of <strong>5 HT1B</strong> receptors on the discriminative stimulus properties of AMPH using conditioned taste <b>aversion</b> (<b>CTA</b>) as the drug discrimination procedure.
+HTR1B	drug	amphetamine	18048951	In generalization and combination tests, the training dose of <b>AMPH</b> was substituted by <strong>5 HT1B</strong> receptor ligands RU24969 (<strong>5 HT1B</strong> agonist: 0.1, 0.3 and 1.0 mg/kg), CP94253 (<strong>5 HT1B</strong> agonist: 1.0, 3.0 and 5.6 mg/kg) and GR127935 (<strong>5 HT1B</strong> antagonist: 0.3, 1.0 and 3.0 mg/kg) or a combination of RU24969 (0.1, 0.3 and 1.0 mg/kg), CP94253 (1.0, 3.0 and 5.6 mg/kg) or GR127935 (0.3, 1.0 and 3.0 mg/kg) with <b>AMPH</b> (0.3 mg/kg) or GR127935 (0.3, 1.0 and 3.0 mg/kg) and CP94253 (5.6 mg/kg) with <b>AMPH</b> (0.3 mg/kg).
+HTR1B	drug	amphetamine	18048951	The results showed that <strong>5 HT1B</strong> agonists RU24969 and CP94253 produced partial generalization of 48% and 60%, respectively, and the <strong>5 HT1B</strong> antagonist GR127935 neither substituted for <b>AMPH</b> nor affected the discriminative cue of <b>AMPH</b>; however, when RU24969 or CP94253 were administrated in combination with <b>AMPH</b>, they increased the discriminative cue of <b>AMPH</b>.
+HTR1B	drug	amphetamine	18048951	These data suggest that <strong>5 HT1B</strong> receptors play a modulatory role in the discriminative cue of <b>AMPH</b>.
+HTR1B	drug	cocaine	17291490	Effects of serotonin <strong>5 HT1B</strong> receptor ligands on the <b>cocaine</b>  and food maintained self administration in rats.
+HTR1B	drug	cocaine	17291490	In order to substantiate the concept that <b>cocaine</b> behavioral effects may be influenced by serotonin (5 HT)1B receptors, male Wistar rats were trained to self administer <b>cocaine</b> intravenously (0.5 mg/kg/injection), and were systemically pretreated with the selective <strong>5 HT1B</strong> receptor antagonist N [3 [3 (dimethylamine)ethoxy] 4 methoxyphenyl] 2' methyl 4' (5 methyl 1,2,4 oxadiazol 3 yl) [1,1' biphenyl] 4 carboxamide hydrochloride (SB 216641), or with the agonist 5 propoxy 3(1,2,3,6 tetrahydro 4 pyridinyl) 1H pyrrolo[3,2 b]pyridine hydrochloride (CP 94253) before test session during the maintenance phase.
+HTR1B	drug	cocaine	17291490	Our present findings extend previous observations that tonic activation of <strong>5 HT1B</strong> receptors is not required for <b>cocaine</b> reinforcement while pharmacological stimulation of <strong>5 HT1B</strong> receptors enhances such a property of the psychostimulant.
+HTR1B	addiction	reward	17291490	Our present findings extend previous observations that tonic activation of <strong>5 HT1B</strong> receptors is not required for cocaine <b>reinforcement</b> while pharmacological stimulation of <strong>5 HT1B</strong> receptors enhances such a property of the psychostimulant.
+HTR1B	drug	cocaine	17291490	Furthermore, we demonstrated that <strong>5 HT1B</strong> receptor agonist induced enhancement of <b>cocaine</b> reward was independent of an alteration in natural reinforcement.
+HTR1B	addiction	reward	17291490	Furthermore, we demonstrated that <strong>5 HT1B</strong> receptor agonist induced enhancement of cocaine <b>reward</b> was independent of an alteration in natural <b>reinforcement</b>.
+HTR1B	drug	alcohol	17217931	Some studies have associated <b>alcohol</b> dependence (AD) with the human serotonin (5 HT)(1B) receptor (<strong>HTR1B</strong>).
+HTR1B	addiction	dependence	17217931	Some studies have associated alcohol <b>dependence</b> (AD) with the human serotonin (5 HT)(1B) receptor (<strong>HTR1B</strong>).
+HTR1B	drug	cocaine	17074068	Biphasic alterations in serotonin 1B (<strong>5 HT1B</strong>) receptor function during abstinence from extended <b>cocaine</b> self administration.
+HTR1B	drug	cocaine	17074068	Alterations in <strong>5 HT1B</strong> receptor function during <b>cocaine</b> abstinence were evaluated in rats given either limited  or extended access (LA and EA, respectively) to <b>cocaine</b> self administration.
+HTR1B	drug	cocaine	17074068	The locomotor response to the <strong>5 HT1B</strong>/1A agonist RU24969 was significantly reduced in <b>cocaine</b> experienced animals relative to <b>cocaine</b> naïve controls following 6 h of abstinence but became sensitized over the subsequent 14 days of abstinence.
+HTR1B	drug	cocaine	17074068	Collectively these findings demonstrate that <strong>5 HT1B</strong> receptor function is persistently altered by <b>cocaine</b> self administration.
+HTR1B	drug	cocaine	17059838	<b>Cocaine</b> increases <strong>5 HT1B</strong> mRNA in rat nucleus accumbens shell neurons.
+HTR1B	drug	cocaine	17059838	Therefore, we examined the effect of binge <b>cocaine</b> administration on <strong>5 HT1B</strong> mRNA expression in rat brain.
+HTR1B	addiction	intoxication	17059838	Therefore, we examined the effect of <b>binge</b> cocaine administration on <strong>5 HT1B</strong> mRNA expression in rat brain.
+HTR1B	drug	alcohol	16839853	Increased expression of <strong>5 HT1B</strong> receptors in rat nucleus accumbens via virally mediated gene transfer increases voluntary <b>alcohol</b> consumption.
+HTR1B	drug	opioid	16344719	Association analysis of polymorphisms in serotonin 1B receptor (<strong>HTR1B</strong>) gene with <b>heroin</b> addiction: a comparison of molecular and statistically estimated haplotypes.
+HTR1B	addiction	addiction	16344719	Association analysis of polymorphisms in serotonin 1B receptor (<strong>HTR1B</strong>) gene with heroin <b>addiction</b>: a comparison of molecular and statistically estimated haplotypes.
+HTR1B	drug	alcohol	16344719	5 Hydroxytryptamine (serotonin) 1B receptors (<strong>HTR1B</strong>) may play an important role in psychiatric disorders and drug and <b>alcohol</b> dependence.
+HTR1B	addiction	dependence	16344719	5 Hydroxytryptamine (serotonin) 1B receptors (<strong>HTR1B</strong>) may play an important role in psychiatric disorders and drug and alcohol <b>dependence</b>.
+HTR1B	drug	opioid	16344719	In this study we report on genotype, molecular haplotype and statistically estimated haplotype analyses of previously identified polymorphisms in positions  261T>G,  161A>T, 129C>T, 861G>C and 1180A>G of the <strong>HTR1B</strong> gene in ethnically diverse populations (African Americans, Caucasians, Hispanics and Asians) including 235 former <b>heroin</b> addicts and 161 control subjects from New York City.
+HTR1B	drug	opioid	16344719	The objectives were to test for an association of molecular and statistically estimated haplotypes and genotypes in <strong>HTR1B</strong> gene with <b>heroin</b> addiction and to compare results provided by molecular and statistically estimated haplotyping methods.
+HTR1B	addiction	addiction	16344719	The objectives were to test for an association of molecular and statistically estimated haplotypes and genotypes in <strong>HTR1B</strong> gene with heroin <b>addiction</b> and to compare results provided by molecular and statistically estimated haplotyping methods.
+HTR1B	drug	alcohol	16212943	Involvement of <strong>5 HT1B</strong> receptors within the ventral tegmental area in <b>ethanol</b> induced increases in mesolimbic dopaminergic transmission.
+HTR1B	drug	alcohol	16212943	Evidence suggests that 5 hydroxytriptamine 1B (<strong>5 HT1B</strong>) receptors play a role in modifying <b>ethanol</b>'s reinforcing effects and voluntary intake, and that <strong>5 HT1B</strong> receptors within the ventral tegmental area (VTA) are involved in regulation of mesolimbic dopaminergic neuronal activity.
+HTR1B	addiction	reward	16212943	Evidence suggests that 5 hydroxytriptamine 1B (<strong>5 HT1B</strong>) receptors play a role in modifying ethanol's <b>reinforcing</b> effects and voluntary intake, and that <strong>5 HT1B</strong> receptors within the ventral tegmental area (VTA) are involved in regulation of mesolimbic dopaminergic neuronal activity.
+HTR1B	drug	alcohol	16212943	Since increased mesolimbic dopaminergic transmission has been implicated in <b>ethanol</b>'s reinforcing properties, this study was designed to assess the involvement of VTA <strong>5 HT1B</strong> receptors in mediating the stimulatory effects of <b>ethanol</b> on VTA dopaminergic neurons.
+HTR1B	addiction	reward	16212943	Since increased mesolimbic dopaminergic transmission has been implicated in ethanol's <b>reinforcing</b> properties, this study was designed to assess the involvement of VTA <strong>5 HT1B</strong> receptors in mediating the stimulatory effects of ethanol on VTA dopaminergic neurons.
+HTR1B	drug	alcohol	16212943	The results also showed that intra tegmental infusion of CP 94253, a <strong>5 HT1B</strong> receptor agonist, significantly prolonged the effects of <b>ethanol</b> on NACC DA.
+HTR1B	drug	alcohol	16212943	The results suggest that blockade and activation of VTA <strong>5 HT1B</strong> receptors attenuates and potentiates the neurochemical effects of <b>ethanol</b>, respectively, and support the suggestion that VTA 5 HT(1B) receptors may be involved in part in mediating the activating effects of <b>ethanol</b> on mesolimbic DA neurons.
+HTR1B	drug	cocaine	15885246	<b>Cocaine</b> facilitates dopamine transmission from ventral tegmental area (VTA) neurons that project to nucleus accumbens (NAcc), and previous experiments suggest that serotonin 1B (<strong>5 HT1B</strong>) receptors are involved in this effect.
+HTR1B	drug	cocaine	15885246	Specifically, activation of <strong>5 HT1B</strong> receptors in VTA during <b>cocaine</b> exposure increases dopamine release in NAcc and enhances <b>cocaine</b> induced locomotor activity, reward, and reinforcement.
+HTR1B	addiction	reward	15885246	Specifically, activation of <strong>5 HT1B</strong> receptors in VTA during cocaine exposure increases dopamine release in NAcc and enhances cocaine induced locomotor activity, <b>reward</b>, and <b>reinforcement</b>.
+HTR1B	drug	cocaine	15885246	This experiment gives evidence that <strong>5 HT1B</strong> antagonists may reduce some of the behavioral effects of <b>cocaine</b>, but may have negative effects on anxiety as well.
+HTR1B	drug	cocaine	15680183	Stimulation of <strong>5 HT1B</strong> receptors decreases <b>cocaine</b>  and sucrose seeking behavior.
+HTR1B	addiction	relapse	15680183	Stimulation of <strong>5 HT1B</strong> receptors decreases cocaine  and sucrose <b>seeking</b> behavior.
+HTR1B	drug	alcohol	15581469	The <strong>5 HT1B</strong> could be more interesting as being located in a locus linked to <b>alcohol</b> preference in rodents, and associated with antisocial <b>alcoholism</b> in two human studies.
+HTR1B	drug	alcohol	15578608	<strong>5 HT1B</strong> knockout mice display hyperactivity, increased exploratory activity and aggression, reduced anxiety, increased vulnerability to cocaine self administration, and elevated <b>alcohol</b> consumption.
+HTR1B	drug	cocaine	15578608	<strong>5 HT1B</strong> knockout mice display hyperactivity, increased exploratory activity and aggression, reduced anxiety, increased vulnerability to <b>cocaine</b> self administration, and elevated alcohol consumption.
+HTR1B	addiction	dependence	15291243	Evidence suggests that the genes for dopamine D4 receptor, phosphodiesterease1B, the AMPA receptor subunit GluR1, <strong>5HT1B</strong> receptor, protein kinase C and the transcription factor FosB contribute to both <b>dependence</b> susceptibility and comorbid behavioral traits.
+HTR1B	drug	cocaine	15056481	Effects of <strong>5 HT1B</strong> receptor ligands microinjected into the ventral tegmental area on the locomotor and sensitizating effects of <b>cocaine</b> in rats.
+HTR1B	drug	alcohol	14714219	Association of <strong>5 HT1B</strong> receptor gene and antisocial behavior in <b>alcoholism</b>.
+HTR1B	drug	alcohol	14714219	The <strong>5 HT1B</strong> receptor gene has been postulated to play a modulatory role in <b>alcohol</b> consumption and <b>alcohol</b> dependence, and was considered a candidate gene for <b>alcoholism</b>.
+HTR1B	addiction	dependence	14714219	The <strong>5 HT1B</strong> receptor gene has been postulated to play a modulatory role in alcohol consumption and alcohol <b>dependence</b>, and was considered a candidate gene for alcoholism.
+HTR1B	drug	alcohol	14714219	Based on the examination of 164 <b>alcoholic</b> subjects, an association was found between a lower frequency of the <strong>5 HT 1B</strong> 861C allele, antisocial personality traits and conduct disorder in <b>alcohol</b> dependent subjects.
+HTR1B	drug	cocaine	14623133	Withdrawal from chronic <b>cocaine</b> up regulates <strong>5 HT1B</strong> receptors in the rat brain.
+HTR1B	addiction	withdrawal	14623133	<b>Withdrawal</b> from chronic cocaine up regulates <strong>5 HT1B</strong> receptors in the rat brain.
+HTR1B	drug	cocaine	12486179	Elevated expression of <strong>5 HT1B</strong> receptors in nucleus accumbens efferents sensitizes animals to <b>cocaine</b>.
+HTR1B	drug	cocaine	12486179	For example, serotonin actions at <strong>5 HT1B</strong> receptors in the ventral tegmental area (VTA) modulate <b>cocaine</b> induced dopamine release in the nucleus accumbens (NAcc) and alter the rewarding and stimulant properties of <b>cocaine</b>.
+HTR1B	drug	cocaine	12486179	HA1B GFP injection induced elevated expression of <strong>5 HT1B</strong> receptors in neuronal fibers in VTA and increased <b>cocaine</b> induced locomotor hyperactivity without affecting baseline locomotion.
+HTR1B	drug	cocaine	12486179	Overexpression of <strong>5 HT1B</strong> receptors also shifted the dose response curve for <b>cocaine</b> conditioned place preference to the left, indicating alterations in the rewarding effects of <b>cocaine</b>.
+HTR1B	drug	cocaine	12486179	Thus, increased expression of <strong>5 HT1B</strong> receptors in NAcc efferents, probably in the terminals of medium spiny neurons projecting to the VTA, may contribute to psychomotor sensitization and offer an important target for regulating the addictive effects of <b>cocaine</b>.
+HTR1B	addiction	addiction	12486179	Thus, increased expression of <strong>5 HT1B</strong> receptors in NAcc efferents, probably in the terminals of medium spiny neurons projecting to the VTA, may contribute to psychomotor sensitization and offer an important target for regulating the <b>addictive</b> effects of cocaine.
+HTR1B	addiction	sensitization	12486179	Thus, increased expression of <strong>5 HT1B</strong> receptors in NAcc efferents, probably in the terminals of medium spiny neurons projecting to the VTA, may contribute to psychomotor <b>sensitization</b> and offer an important target for regulating the addictive effects of cocaine.
+HTR1B	addiction	addiction	12437478	From the three reported family based case control studies of <strong>HTR1B</strong> to various disorders, one provides preliminary evidence for association of G861C with obsessive <b>compulsive</b> disorder.
+HTR1B	drug	alcohol	12022963	Because the linkage of antisocial <b>alcoholism</b> to the <strong>HTR1B</strong> gene was recently reported in two populations, it was of interest to identify genetic variants at the <strong>HTR1B</strong> locus and study their association with <b>alcoholism</b> in the Taiwanese Han population.
+HTR1B	drug	alcohol	12022963	We sequenced DNA from Taiwanese Han to screen for genetic variation in the coding, promoter, and partial 3' untranslated regions of the <strong>HTR1B</strong> locus of 158 <b>alcohol</b> dependent cases with withdrawal symptoms and 149 control subjects, who either never drank or drank only occasionally and in low quantities.
+HTR1B	addiction	withdrawal	12022963	We sequenced DNA from Taiwanese Han to screen for genetic variation in the coding, promoter, and partial 3' untranslated regions of the <strong>HTR1B</strong> locus of 158 alcohol dependent cases with <b>withdrawal</b> symptoms and 149 control subjects, who either never drank or drank only occasionally and in low quantities.
+HTR1B	drug	alcohol	12022963	Our results support an association between <strong>HTR1B</strong> and <b>alcohol</b> dependence.
+HTR1B	addiction	dependence	12022963	Our results support an association between <strong>HTR1B</strong> and alcohol <b>dependence</b>.
+HTR1B	drug	alcohol	11956970	This investigation of central serotonin neurotransmission, specifically the serotonin 1B (<strong>5HT1B</strong>) receptor gene and its role in both regulating <b>alcohol</b> consumption and developing <b>alcohol</b> dependence revealed overrepresentation of the C allele of the 861G > C polymorphism of <strong>5HT1B</strong> in <b>alcoholics</b> with inactive ALDH2, compared with its frequency in nonalcoholic controls.
+HTR1B	addiction	dependence	11956970	This investigation of central serotonin neurotransmission, specifically the serotonin 1B (<strong>5HT1B</strong>) receptor gene and its role in both regulating alcohol consumption and developing alcohol <b>dependence</b> revealed overrepresentation of the C allele of the 861G > C polymorphism of <strong>5HT1B</strong> in alcoholics with inactive ALDH2, compared with its frequency in nonalcoholic controls.
+HTR1B	drug	alcohol	11956970	No significant differences in <strong>5HT1B</strong> genotype and allele distributions were observed between <b>alcoholics</b> with active ALDH2 and controls, however.
+HTR1B	drug	alcohol	11956970	Taken together with recent observations, these results suggest that genetic variability of the <strong>5HT1B</strong> receptor is involved in the development of some type of <b>alcohol</b> dependence.
+HTR1B	addiction	dependence	11956970	Taken together with recent observations, these results suggest that genetic variability of the <strong>5HT1B</strong> receptor is involved in the development of some type of alcohol <b>dependence</b>.
+HTR1B	addiction	dependence	11751038	Polymorphism of the 5 HT1B receptor gene (<strong>HTR1B</strong>): strong within locus linkage disequilibrium without association to antisocial substance <b>dependence</b>.
+HTR1B	addiction	dependence	11751038	Polymorphism of the <strong>5 HT1B</strong> receptor gene (<strong>HTR1B</strong>): strong within locus linkage disequilibrium without association to antisocial substance <b>dependence</b>.
+HTR1B	drug	alcohol	11751038	found evidence for linkage of antisocial <b>alcoholism</b> to <strong>HTR1B</strong> (the locus encoding the 5 HT1B receptor) in both Finns and Southwestern American Indians, and of allelic association of a G861C polymorphism at that locus with antisocial <b>alcoholism</b> in Finns.
+HTR1B	drug	alcohol	11751038	found evidence for linkage of antisocial <b>alcoholism</b> to <strong>HTR1B</strong> (the locus encoding the <strong>5 HT1B</strong> receptor) in both Finns and Southwestern American Indians, and of allelic association of a G861C polymorphism at that locus with antisocial <b>alcoholism</b> in Finns.
+HTR1B	drug	alcohol	11751038	The present study evaluated LD across three polymorphic systems at <strong>HTR1B</strong> and haplotype frequencies and allelic association of these systems with both SD generally and <b>alcohol</b> dependence (AD) specifically, with or without a comorbid antisocial diagnosis.
+HTR1B	addiction	dependence	11751038	The present study evaluated LD across three polymorphic systems at <strong>HTR1B</strong> and haplotype frequencies and allelic association of these systems with both SD generally and alcohol <b>dependence</b> (AD) specifically, with or without a comorbid antisocial diagnosis.
+HTR1B	addiction	dependence	11751038	Despite no evidence in this study for allelic association of <strong>HTR1B</strong> to antisocial substance <b>dependence</b>, further evaluation of the hypothesized association is warranted in other population groups.
+HTR1B	drug	alcohol	11605102	Oral drug self administration in the home cage of mice: <b>alcohol</b> heightened aggression and inhibition by the <strong>5 HT1B</strong> agonist anpirtoline.
+HTR1B	drug	alcohol	11605102	In order to model heightened aggression after <b>alcohol</b> consumption and to study the inhibitory influence of <strong>5 HT1B</strong> receptors on drinking and fighting, an experimental procedure should enable self administration of precise amounts of <b>alcohol</b> in a limited period of time before an aggressive confrontation.
+HTR1B	drug	alcohol	11605102	To design a new device that can reinforce operant responding by the delivery of sweet <b>alcohol</b> in the resident mouse home cage, where aggressive behavior toward an intruder can subsequently be examined, and to demonstrate inhibition of <b>alcohol</b> heightened aggression by <strong>5 HT1B</strong> receptor agonist treatment.
+HTR1B	addiction	reward	11605102	To design a new device that can reinforce <b>operant</b> responding by the delivery of sweet alcohol in the resident mouse home cage, where aggressive behavior toward an intruder can subsequently be examined, and to demonstrate inhibition of alcohol heightened aggression by <strong>5 HT1B</strong> receptor agonist treatment.
+HTR1B	drug	alcohol	11605102	The effective inhibition of high levels of aggressive behavior due to <b>alcohol</b> consumption after anpirtoline treatment confirm the <strong>5 HT1B</strong> receptor as a critical site in the termination of aggression.
+HTR1B	drug	cocaine	11396515	The present study was designed to determine how <strong>5 HT1B</strong> receptor ligands affected the development or the expression phase of sensitization to the <b>cocaine</b> induced locomotor response in rats.
+HTR1B	addiction	sensitization	11396515	The present study was designed to determine how <strong>5 HT1B</strong> receptor ligands affected the development or the expression phase of <b>sensitization</b> to the cocaine induced locomotor response in rats.
+HTR1B	drug	cocaine	11396515	In Experiment 1, rats were treated repeatedly (for 5 days) with <b>cocaine</b> (10 mg/kg) in combination with either saline, GR 127935 (<strong>5 HT1B</strong> antagonist), CP 94,253 (<strong>5 HT1B</strong> agonist) or GR 127935 + CP 94,253.
+HTR1B	drug	cocaine	11396515	Our results indicate that <strong>5 HT1B</strong> receptors are involved in neither the development nor the expression of sensitization to <b>cocaine</b> induced locomotor hyperactivity.
+HTR1B	addiction	sensitization	11396515	Our results indicate that <strong>5 HT1B</strong> receptors are involved in neither the development nor the expression of <b>sensitization</b> to cocaine induced locomotor hyperactivity.
+HTR1B	drug	cocaine	11396515	On the other hand, they also show that pharmacological activation of <strong>5 HT1B</strong> receptors enhances both phases of this phenomenon, and that repeated administration of <b>cocaine</b> leads to an increased functional reactivity of these receptors.
+HTR1B	drug	cocaine	11374326	The mice lacking the <strong>5 HT1B</strong> receptor have also been reported to exhibit an increased vulnerability to <b>cocaine</b>.
+HTR1B	drug	alcohol	11198050	Results showed that the 5 HT releaser d fenfluramine, the selective serotonin reuptake inhibitor fluoxetine, the 5 HT1A receptor agonist 8 hydroxy 2[di n propylamino]tetralin, the partial 5 HT1A receptor agonist buspirone, and the <strong>5 HT1B</strong>/5 HT2C receptor agonist 1 (3 trifluoromethylphenyl)piperazine, but not the 5 HT2A/5 HT2C receptor agonist 1 (2,5 dimethoxy 4 iodophenylaminopropane) 2, selectively reduced responding on a lever leading to presentation of an <b>ethanol</b> paired conditioned stimulus.
+HTR1B	drug	alcohol	11198050	Results are consistent with involvement of the dopaminergic and 5 HT systems, in particular activation of 5 HT1A and <strong>5 HT1B</strong> receptor subtypes, in mediation of the conditioned or secondary reinforcing properties of <b>ethanol</b>.
+HTR1B	addiction	reward	11198050	Results are consistent with involvement of the dopaminergic and 5 HT systems, in particular activation of 5 HT1A and <strong>5 HT1B</strong> receptor subtypes, in mediation of the conditioned or secondary <b>reinforcing</b> properties of ethanol.
+HTR1B	drug	cocaine	11164086	Modulation of the effects of <b>cocaine</b> by <strong>5 HT1B</strong> receptors: a comparison of knockouts and antagonists.
+HTR1B	drug	cocaine	11164086	To evaluate the role of the <strong>5 HT1B</strong> receptor in mediating the actions of <b>cocaine</b>, we used two model systems: knockout (KO) mice lacking the <strong>5 HT1B</strong> receptor and an acute treatment with the <strong>5 HT1B</strong>/1D antagonist GR127935.
+HTR1B	drug	cocaine	11164086	In contrast, as demonstrated previously, the <strong>5 HT1B</strong> receptor KO mice showed a heightened locomotor response to <b>cocaine</b>, as well as an increased propensity to self administer <b>cocaine</b>.
+HTR1B	drug	cocaine	11164086	Thus, an acute pharmacological blockade of the <strong>5 HT1B</strong> receptor decreases some effects of <b>cocaine</b>, while a constitutive genetic KO of the same receptor has opposite effects.
+HTR1B	drug	cocaine	11164086	These results suggest that compensatory changes have taken place during the development of the <strong>5 HT1B</strong> KO mice, which may have rendered these mice more vulnerable to <b>cocaine</b>.
+HTR1B	drug	cocaine	10837864	This study investigated the involvement of the serotonin 1B (<strong>5 HT1B</strong>) receptor in modulating <b>cocaine</b> induced place conditioning by comparing the response of <strong>5 HT1B</strong> receptor gene knock out mice with wild type 129/Sv ter mice.
+HTR1B	drug	cocaine	10837864	Results clearly show that <strong>5 HT1B</strong> receptor knock out mice failed to display a conditioned place preference for stimuli paired with <b>cocaine</b> while wild type mice exhibited a conditioned place preference for the compartment paired with <b>cocaine</b> (5 and 20 mg/kg).
+HTR1B	drug	cocaine	10837864	As other studies showed that <strong>5 HT1B</strong> knock out mice self administer <b>cocaine</b>, these results suggest a dissociation between the psychologic state linked to self administration and the one measured in conditioned place preference.
+HTR1B	drug	amphetamine	10780831	RU 24969 disrupts d <b>amphetamine</b> self administration and responding for conditioned reward via stimulation of <strong>5 HT1B</strong> receptors.
+HTR1B	addiction	reward	10780831	RU 24969 disrupts d amphetamine self administration and responding for conditioned <b>reward</b> via stimulation of <strong>5 HT1B</strong> receptors.
+HTR1B	drug	amphetamine	10780831	The suppressant actions of RU 24969 on <b>amphetamine</b> self administration and CR responding involve stimulation of <strong>5 HT1B</strong> receptors, since they were reversed by the <strong>5 HT1B</strong>/1D antagonist GR 127935 (3 mg/kg), but not by the 5 HT1A antagonist WAY 100635 (1 mg/kg).
+HTR1B	addiction	reward	10780831	Rather, global activation of <strong>5 HT1B</strong> receptors appear to exert a general disruptive effect on <b>operant</b> responding.
+HTR1B	drug	alcohol	20575831	Evaluation of an allelic association of the serotonin <strong>5 HT1B</strong> G681C polymorphism with antisocial <b>alcoholism</b> in the German population.
+HTR1B	drug	alcohol	20575831	Our study tested whether an association of the 861C allele of the serotonin 5 HT1B gene (<strong>HTR1B</strong>) with antisocial <b>alcoholism</b> exists in the German population.
+HTR1B	drug	alcohol	20575831	Our study tested whether an association of the 861C allele of the serotonin <strong>5 HT1B</strong> gene (<strong>HTR1B</strong>) with antisocial <b>alcoholism</b> exists in the German population.
+HTR1B	drug	alcohol	20575831	The <strong>HTR1B</strong> G861C polymorphism was genotyped in 588 subjects of German descent, comprising 250 non <b>alcoholic</b> controls and 338 <b>alcohol</b> dependent subjects, of whom 56 exhibited a dissocial personality disorder (DSPD).
+HTR1B	drug	cocaine	10414358	The <strong>5 HT1B</strong> receptor knockout mice show a phenotype of increased vulnerability to drugs of abuse such as <b>cocaine</b>.
+HTR1B	drug	cocaine	10414358	However, pharmacological studies suggest that <strong>5 HT1B</strong> stimulation enhances the effects of <b>cocaine</b>, while <strong>5 HT1B</strong> blockade can attenuate some of the effects of <b>cocaine</b>.
+HTR1B	drug	alcohol	10403028	Oral operant <b>ethanol</b> self administration in <strong>5 HT1b</strong> knockout mice.
+HTR1B	addiction	reward	10403028	Oral <b>operant</b> ethanol self administration in <strong>5 HT1b</strong> knockout mice.
+HTR1B	drug	alcohol	10403028	The present experiment examined oral <b>ethanol</b> self administration in <strong>5 HT1b</strong> knockout (KO) mice and <strong>5 HT1b</strong> wide type (WT) control mice using a continuous access operant procedure.
+HTR1B	addiction	reward	10403028	The present experiment examined oral ethanol self administration in <strong>5 HT1b</strong> knockout (KO) mice and <strong>5 HT1b</strong> wide type (WT) control mice using a continuous access <b>operant</b> procedure.
+HTR1B	drug	alcohol	10403028	After lever press training, adult <strong>5 HT1b</strong> KO and <strong>5 HT1b</strong> WT mice were placed in operant chambers on a 23 h per day basis with access to food (FR1), 10% v/v <b>ethanol</b> (FR4), and water from a sipper tube.
+HTR1B	addiction	reward	10403028	After lever press training, adult <strong>5 HT1b</strong> KO and <strong>5 HT1b</strong> WT mice were placed in <b>operant</b> chambers on a 23 h per day basis with access to food (FR1), 10% v/v ethanol (FR4), and water from a sipper tube.
+HTR1B	drug	alcohol	10403028	Since KO mice showed greater levels of <b>ethanol</b> responding only for unsweetened 10% v/v <b>ethanol</b>, and showed modest <b>ethanol</b> self administration overall, the present results are not consistent with the notion that <strong>5 HT1b</strong> KO have a generally greater preference for <b>ethanol</b> than <strong>5 HT1b</strong> WT mice.
+HTR1B	drug	alcohol	10334495	The present study evaluated the effects of the selective serotonin (5 hydroxyhyptamine; 5 HT) reuptake inhibitor, fluoxetine, the <strong>5 HT1B</strong> receptor agonist, tetrahydro 4 pyridyl[3,2 b]pyridine, CP 94,253 the preferential 5 HT2A receptor agonist, 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane, DOI and the mixed 5 HT2C/1B receptor agonist, 1 (3 chlorophenyl)piperazine, mCPP, on oral <b>ethanol</b> (10% v/v) self administration in a two lever, fixed ratio:1, water vs. <b>ethanol</b> choice procedure in the rat.
+HTR1B	drug	alcohol	10334495	These findings suggest that operant <b>ethanol</b> self administration can be suppressed in a specific manner by activation of 5 HT2A and, possibly, 5 HT2C receptors, and in a nonselective manner by activation of <strong>5 HT1B</strong> receptors.
+HTR1B	addiction	reward	10334495	These findings suggest that <b>operant</b> ethanol self administration can be suppressed in a specific manner by activation of 5 HT2A and, possibly, 5 HT2C receptors, and in a nonselective manner by activation of <strong>5 HT1B</strong> receptors.
+HTR1B	drug	alcohol	10334495	As fluoxetine indirectly stimulates these receptors and its behavioral profile resembles more that of a <strong>5 HT1B</strong> receptor agonist, activation of <strong>5 HT1B</strong> receptors may underlie its effects on operant <b>ethanol</b> self administration.
+HTR1B	addiction	reward	10334495	As fluoxetine indirectly stimulates these receptors and its behavioral profile resembles more that of a <strong>5 HT1B</strong> receptor agonist, activation of <strong>5 HT1B</strong> receptors may underlie its effects on <b>operant</b> ethanol self administration.
+HTR1B	drug	amphetamine	10102769	Activation of <strong>5 HT1B</strong> receptors in the nucleus accumbens reduces <b>amphetamine</b> induced enhancement of responding for conditioned reward.
+HTR1B	addiction	reward	10102769	Activation of <strong>5 HT1B</strong> receptors in the nucleus accumbens reduces amphetamine induced enhancement of responding for conditioned <b>reward</b>.
+HTR1B	drug	amphetamine	10102769	The effect of CP93,129, the most selective of the <strong>5 HT1B</strong> agonists, to inhibit the response potentiating effect of d <b>amphetamine</b> was reversed by the 5 HT(1B/1D) antagonist GR127935 (3 mg/kg).
+HTR1B	addiction	reward	10027505	RU 24969, a 5 HT1A/1B agonist, elevates brain stimulation <b>reward</b> thresholds: an effect reversed by GR 127935, a <strong>5 HT1B</strong>/1D antagonist.
+HTR1B	addiction	reward	10027505	Recent studies suggest that serotonergic neurotransmission through the serotonin 1B (<strong>5 HT1B</strong>) receptor is involved in <b>reward</b> processes.
+HTR1B	addiction	reward	10027505	However, pretreatment with an intermediate dose of GR 127935 (3 mg/kg), which was previously without effect on <b>ICSS</b> behavior, reversed the threshold elevating effects of RU 24969 (1 mg/kg), suggesting the involvement of the <strong>5 HT1B</strong> receptor in this effect of RU 24969 administration.
+HTR1B	drug	psychedelics	9928242	Likewise, the serotonin releasing compounds <b>MDMA</b>(+), MBDB(+/ ), and alpha ethyltryptamine (AET) have no effect on PPI in wild type mice, but increase PPI in <strong>5 HT1B</strong> knockout mice.
+HTR1B	drug	cocaine	9822762	The effects of serotonin1B [5 hydroxytryptamine1B (<strong>5 HT1B</strong>)] receptor activation on <b>cocaine</b> reinforcement were investigated using intravenous <b>cocaine</b> self administration by rats.
+HTR1B	addiction	reward	9822762	The effects of serotonin1B [5 hydroxytryptamine1B (<strong>5 HT1B</strong>)] receptor activation on cocaine <b>reinforcement</b> were investigated using intravenous cocaine self administration by rats.
+HTR1B	drug	cocaine	9822762	In addition, each of these <strong>5 HT1B</strong> agonists lowered the threshold dose of <b>cocaine</b> that supported self administration.
+HTR1B	drug	cocaine	9822762	These results are consistent with a <strong>5 HT1B</strong> agonist induced potentiation of <b>cocaine</b> reinforcement.
+HTR1B	addiction	reward	9822762	These results are consistent with a <strong>5 HT1B</strong> agonist induced potentiation of cocaine <b>reinforcement</b>.
+HTR1B	drug	cocaine	9822762	Self administration behavior was not maintained when either RU 24969 or CP 94,253 was substituted for <b>cocaine</b>, indicating that these <strong>5 HT1B</strong> agonists do not produce significant reinforcing effects alone.
+HTR1B	addiction	reward	9822762	Self administration behavior was not maintained when either RU 24969 or CP 94,253 was substituted for cocaine, indicating that these <strong>5 HT1B</strong> agonists do not produce significant <b>reinforcing</b> effects alone.
+HTR1B	drug	cocaine	9822762	Together, these findings indicate that <strong>5 HT1B</strong> receptor stimulation facilitates the reinforcing properties of <b>cocaine</b>.
+HTR1B	addiction	reward	9822762	Together, these findings indicate that <strong>5 HT1B</strong> receptor stimulation facilitates the <b>reinforcing</b> properties of cocaine.
+HTR1B	drug	alcohol	9744857	These results demonstrate that, under the present experimental conditions, activation of central 5 HT1A, <strong>5 HT1B</strong>, and 5 HT2 receptors reduced <b>ethanol</b> intake and reinforced behaviour in an operant paradigm.
+HTR1B	addiction	reward	9744857	These results demonstrate that, under the present experimental conditions, activation of central 5 HT1A, <strong>5 HT1B</strong>, and 5 HT2 receptors reduced ethanol intake and reinforced behaviour in an <b>operant</b> paradigm.
+HTR1B	drug	alcohol	9694030	These studies thus confirm the potential for decreasing <b>ethanol</b> consumption and <b>ethanol</b> preference of 5 HT1A agonists and 5 HT3 antagonists, but failed to find any selective effects for agents acting at <strong>5 HT1B</strong> or 5 HT2 receptors.
+HTR1B	addiction	reward	9616795	We explore the concept of impulsivity and its relation with the neurotransmitter serotonin in the context of aggressive behavior and behavior associated with positive <b>reinforcement</b> using a knockout mouse that lacks one of the serotonin receptors, the <strong>5 HT1B</strong> receptor.
+HTR1B	drug	cocaine	9603521	Here we examine the effects of <b>cocaine</b> in mice lacking one of the serotonin receptor subtypes, the <strong>5 HT1B</strong> receptor.
+HTR1B	drug	cocaine	9603521	We show that mice lacking <strong>5 HT1B</strong> display increased locomotor responses to <b>cocaine</b> and that they are more motivated to self administer <b>cocaine</b>.
+HTR1B	drug	cocaine	9603521	We propose that even drug naive <strong>5 HT1B</strong> knockout mice are in a behavioural and biochemical state that resembles that of wild type mice sensitized to <b>cocaine</b> by repeated exposure to the drug.
+HTR1B	addiction	dependence	9453273	Intensity <b>dependence</b> of the cortical auditory evoked potentials as a surrogate marker of central nervous system serotonin transmission in man: demonstration of a central effect for the <strong>5HT1B</strong>/1D agonist zolmitriptan (311C90, Zomig).
+HTR1B	drug	cocaine	9218264	Intravenous <b>cocaine</b> self administration in mice lacking <strong>5 HT1B</strong> receptors.
+HTR1B	drug	cocaine	9218264	The present experiment tested the hypothesis that <strong>5 HT1B</strong> receptors are involved in the reinforcing effects of <b>cocaine</b>.
+HTR1B	addiction	reward	9218264	The present experiment tested the hypothesis that <strong>5 HT1B</strong> receptors are involved in the <b>reinforcing</b> effects of cocaine.
+HTR1B	drug	cocaine	9218264	Transgenic mice lacking <strong>5 HT1B</strong> receptors were used as subjects and compared with wild type mice for the acquisition and maintenance of intravenous (IV) <b>cocaine</b> self administration.
+HTR1B	drug	cocaine	9218264	Male 129/Sv ter and <strong>5 HT1B</strong> minus 129/Sv ter inbred mice (Columbia University, New York) were initially trained to press a lever under a fixed ratio schedule 2, first for sweetened condensed milk as reinforcer and subsequently for <b>cocaine</b> (2.0 mg/kg/infusion).
+HTR1B	drug	cocaine	9218264	These results suggest that the <strong>5 HT1B</strong> receptors may be implicated in the propensity to self administer <b>cocaine</b>, but other mechanisms might be involved in the maintenance of <b>cocaine</b> self administration.
+HTR1B	addiction	reward	9200507	The 5 HT1 agonist 5 carboxamidotryptamine (19 and 38 nanomol) and the <strong>5 HT1B</strong> agonist, CGS 12066B (1.12 and 2.24 nanomol), but not the non selective 5 HT agonist m <b>CPP</b> (41 to 164 nanomol), 5 HT2 agonist alpha methylserotonin (36 and 72 nanomol) and 5 HT3 agonist 2 methylserotonin (36 and 72 nanomol), produced a dose dependent antinociceptive effect.
+HTR1B	drug	opioid	9200507	These results indicate that the antinociceptive effects of <b>opioid</b> or serotonergic agonists microinjected into the APtN depend on drug interaction with local mu or <strong>5 HT1B</strong> receptors, respectively.
+HTR1B	addiction	reward	8956376	The effect of <strong>5 HT1B</strong> receptor stimulation on dopamine mediated <b>reinforcement</b> in rats was investigated using intravenous self administration of the selective dopamine uptake inhibitor GBR 12909 on an FR5 schedule of <b>reinforcement</b>.
+HTR1B	drug	cocaine	8956376	Finally, CGS 12066B pretreatment (1 10 mg/kg, IP) did not alter the self administration of <b>cocaine</b> (0.03 0.5 mg/injection), suggesting that the simultaneous stimulation of multiple 5 HT receptor subtypes by the indirect 5 HT agonist properties of <b>cocaine</b> may mask the effect of <strong>5 HT1B</strong> receptor stimulation on DA mediated reinforcement.
+HTR1B	addiction	reward	8956376	Finally, CGS 12066B pretreatment (1 10 mg/kg, IP) did not alter the self administration of cocaine (0.03 0.5 mg/injection), suggesting that the simultaneous stimulation of multiple 5 HT receptor subtypes by the indirect 5 HT agonist properties of cocaine may mask the effect of <strong>5 HT1B</strong> receptor stimulation on DA mediated <b>reinforcement</b>.
+HTR1B	drug	alcohol	8947316	Reduced sensitivity to <b>ethanol</b> reward, but not <b>ethanol</b> aversion, in mice lacking <strong>5 HT1B</strong> receptors.
+HTR1B	addiction	aversion	8947316	Reduced sensitivity to ethanol reward, but not ethanol <b>aversion</b>, in mice lacking <strong>5 HT1B</strong> receptors.
+HTR1B	addiction	reward	8947316	Reduced sensitivity to ethanol <b>reward</b>, but not ethanol aversion, in mice lacking <strong>5 HT1B</strong> receptors.
+HTR1B	drug	alcohol	8947316	This experiment characterized the acquisition of <b>ethanol</b> induced conditioned taste aversion and <b>ethanol</b> induced conditioned place reference in mutant knockout mice lacking <strong>5 HT1b</strong> receptors.
+HTR1B	addiction	aversion	8947316	This experiment characterized the acquisition of ethanol induced conditioned taste <b>aversion</b> and ethanol induced conditioned place reference in mutant knockout mice lacking <strong>5 HT1b</strong> receptors.
+HTR1B	drug	alcohol	8947316	These results are generally consistent with an important role for serotonergic systems in <b>ethanol</b> reward and specifically indicate that <strong>5 HT1b</strong> receptors are important for <b>ethanol</b>'s rewarding effects but not for <b>ethanol</b>'s aversive effects.
+HTR1B	addiction	aversion	8947316	These results are generally consistent with an important role for serotonergic systems in ethanol reward and specifically indicate that <strong>5 HT1b</strong> receptors are important for ethanol's rewarding effects but not for ethanol's <b>aversive</b> effects.
+HTR1B	addiction	reward	8947316	These results are generally consistent with an important role for serotonergic systems in ethanol <b>reward</b> and specifically indicate that <strong>5 HT1b</strong> receptors are important for ethanol's rewarding effects but not for ethanol's aversive effects.
+HTR1B	drug	alcohol	8782828	Elevated <b>alcohol</b> consumption in null mutant mice lacking <strong>5 HT1B</strong> serotonin receptors.
+HTR1B	drug	alcohol	8782828	Our results suggest that the <strong>5 HT1B</strong> receptor participates in the regulation of <b>ethanol</b> drinking, and demonstrate that serotonergic manipulations lead to reduced responsiveness to certain ataxic effects of <b>ethanol</b> without affecting dependence.
+HTR1B	addiction	dependence	8782828	Our results suggest that the <strong>5 HT1B</strong> receptor participates in the regulation of ethanol drinking, and demonstrate that serotonergic manipulations lead to reduced responsiveness to certain ataxic effects of ethanol without affecting <b>dependence</b>.
+HTR1B	drug	alcohol	8842634	Alterations in serotonin1B (<strong>5HT1B</strong>) receptor subtypes in the brain of <b>ethanol</b> treated rats.
+HTR1B	drug	alcohol	8842634	The effects of acute or chronic <b>ethanol</b> treatment and of withdrawal (24 h) after chronic <b>ethanol</b> treatment on <strong>5HT1B</strong> receptor subtypes in different regions of the rat brain were investigated.
+HTR1B	addiction	withdrawal	8842634	The effects of acute or chronic ethanol treatment and of <b>withdrawal</b> (24 h) after chronic ethanol treatment on <strong>5HT1B</strong> receptor subtypes in different regions of the rat brain were investigated.
+HTR1B	drug	alcohol	8842634	It was observed that acute <b>ethanol</b> treatment had no significant effect on the maximum number of binding sites (Bmax) or the apparent dissociation constant (KD) of <strong>5HT1B</strong> receptor binding sites in the various brain regions.
+HTR1B	drug	alcohol	8842634	On the other hand, chronic <b>ethanol</b> treatment produced a significant increase in Bmax of 125I CYP binding to <strong>5HT1B</strong> receptors in the rat cortex and hippocampus, which remained increased after 24 h of <b>ethanol</b> withdrawal.
+HTR1B	addiction	withdrawal	8842634	On the other hand, chronic ethanol treatment produced a significant increase in Bmax of 125I CYP binding to <strong>5HT1B</strong> receptors in the rat cortex and hippocampus, which remained increased after 24 h of ethanol <b>withdrawal</b>.
+HTR1B	drug	alcohol	8842634	In contrast, in the striatum and the cerebellum of chronic <b>ethanol</b> treated and withdrawn rats, the <strong>5HT1B</strong> binding parameters (Bmax and KD) were unchanged.
+HTR1B	drug	alcohol	8842634	These results suggest the possible involvement of cortical and hippocampal <strong>5HT1B</strong> receptors in <b>ethanol</b> dependence.
+HTR1B	addiction	dependence	8842634	These results suggest the possible involvement of cortical and hippocampal <strong>5HT1B</strong> receptors in ethanol <b>dependence</b>.
+HTR1B	addiction	withdrawal	8521905	The expression of central 5 HT1A and <strong>5 HT1B</strong> receptors was studied in several brain areas of rats subjected to a 2 week period of chronic alcoholization, followed by 18 h <b>withdrawal</b>.
+HTR1B	drug	alcohol	8521905	These data suggest that altered sensitivity of chronically alcoholized rats to 5 HT1A and <strong>5 HT1B</strong> receptor ligands may result from <b>alcohol</b> induced changes in the transcription of the genes encoding these receptors.
+HTR1B	drug	opioid	7733277	The stimulatory effect of <b>morphine</b>, dexmedetomidine (an alpha 2 adrenoceptor agonist), 1 (3 chlorophenyl) piperazine (m CPP, a <strong>5 HT1B</strong> agonist), U 50488H (a kappa <b>opioid</b> receptor agonist), pimozide (a dopamine antagonist), and restraint stress on prolactin and growth hormone (GH) secretion was compared during cold exposure (4 degrees C) and under basal conditions (30 degrees C) in male rats.
+HTR1B	addiction	reward	7733277	The stimulatory effect of morphine, dexmedetomidine (an alpha 2 adrenoceptor agonist), 1 (3 chlorophenyl) piperazine (m <b>CPP</b>, a <strong>5 HT1B</strong> agonist), U 50488H (a kappa opioid receptor agonist), pimozide (a dopamine antagonist), and restraint stress on prolactin and growth hormone (GH) secretion was compared during cold exposure (4 degrees C) and under basal conditions (30 degrees C) in male rats.
+HTR1B	drug	psychedelics	7898613	The long lasting effect of <b>ibogaine</b> on serotonergic functioning, in particular, its blocking of the <strong>5HT1B</strong> agonist mediated increase in dopamine efflux, may have significance in the mediation of its anti addictive properties.
+HTR1B	addiction	addiction	7898613	The long lasting effect of ibogaine on serotonergic functioning, in particular, its blocking of the <strong>5HT1B</strong> agonist mediated increase in dopamine efflux, may have significance in the mediation of its anti <b>addictive</b> properties.
+HTR1B	drug	cocaine	8332619	Overall, the results indicate that, at least in the present behavioral paradigm, the effects of chronic <b>cocaine</b> administration are mediated by changes in 5 HT1A receptor sensitivity but not by changes in <strong>5 HT1B</strong> receptor sensitivity.
+HTR1B	drug	alcohol	7748340	This is indicated by (a) lower contents of DA and 5 HT; (b) fewer 5 HT immunostained fibers; (c) lower densities of <strong>5 HT1B</strong>, 5 HT2 and D2 receptors; and (d) higher densities of 5 HT1A receptors in the CNS of P rats compared to the <b>alcohol</b> nonpreferring NP line of rats.
+HTR1B	addiction	reward	1532259	Metachlorophenylpiperazine (mCPP) 2.5 mg/kg IP, an agonist at <strong>5 HT1B</strong> and 5 HT1C receptors, and d fenfluramine (DF) 1.25 mg/kg IP, a releaser of 5 HT from nerve terminals and inhibitor of 5 HT uptake, increased the percentage of omissions and the latency to respond correctly or to collect the <b>reinforcement</b> with no effects on the correct responses.
+HTR1B	drug	alcohol	1839497	[3H]Ketanserin binding to 5 HT2 receptors in the cortex, ( )[125I] iodo cyanopindolol [(125I]CYP) binding to <strong>5 HT1b</strong> receptors in the striatum and hypothalamus, and [3H] 8 OH DPAT binding in the cortex were not affected by chronic <b>ethanol</b> administration.
+HTR1B	addiction	reward	1975107	5 HT agonists selective for other receptor subtypes, such as the <strong>5 HT1B</strong>/1C agonist m <b>CPP</b> (5 mg/kg) and the 5 HT2/1C agonist DOB (1 mg/kg), were not effective in this behavioral test.
+HTR1B	addiction	reward	2746512	It is likely that the hypoactivity and PRL responses of m <b>CPP</b> are mediated by <strong>5 HT1B</strong> receptors, and the cardiodepressive effects by 5 HT1A receptors.
+HTR1B	drug	opioid	2566495	8 Hydroxy 2 (di n propylamino)tetralin (8 OH DPAT) and RU 24969 have been used to investigate whether 5 HT1A and <strong>5 HT1B</strong> receptors are involved in the <b>naloxone</b> induced jumping behaviour of the chronically <b>morphine</b> dependent mouse.
+HTR1B	drug	alcohol	2648491	In addition, administration of a <strong>5 HT1B</strong> agonist also attenuated the oral intake of <b>ethanol</b> by P rats.
+HTR1B	drug	alcohol	3228486	The cross generalization between <b>ethanol</b> and THBC is, thus, indicated and relates to previous evidence in which both <b>ethanol</b>  and THBC trained rats generalize to a common agent, TFMPP, a putatively specific <strong>5HT1B</strong> receptor agonist.
+FOSB	drug	cocaine	32742260	Cytoplasmic Polyadenylation Element Binding Proteins CPEB1 and CPEB3 Regulate the Translation of <strong>FosB</strong> and Are Required for Maintaining Addiction Like Behaviors Induced by <b>Cocaine</b>.
+FOSB	addiction	addiction	32742260	Cytoplasmic Polyadenylation Element Binding Proteins CPEB1 and CPEB3 Regulate the Translation of <strong>FosB</strong> and Are Required for Maintaining <b>Addiction</b> Like Behaviors Induced by Cocaine.
+FOSB	drug	cocaine	32742260	Finally, we found that (1) CPEB is reduced in transgenic mice following <b>cocaine</b> injections and that (2) <strong>FosB</strong>, known for its contribution to establishing the addictive phenotype, when its expression in the striatum is increased by drug administration, is a novel target of CPEBs molecules.
+FOSB	addiction	addiction	32742260	Finally, we found that (1) CPEB is reduced in transgenic mice following cocaine injections and that (2) <strong>FosB</strong>, known for its contribution to establishing the <b>addictive</b> phenotype, when its expression in the striatum is increased by drug administration, is a novel target of CPEBs molecules.
+FOSB	drug	cocaine	32457073	We identified 133 genes differentially expressed between CUD case patients and <b>cocaine</b> free control subjects, including previously implicated candidates for <b>cocaine</b> use/addiction (<strong>FOSB</strong>, ARC, KCNJ9/GIRK3, NR4A2, JUNB, and MECP2).
+FOSB	addiction	addiction	32457073	We identified 133 genes differentially expressed between CUD case patients and cocaine free control subjects, including previously implicated candidates for cocaine use/<b>addiction</b> (<strong>FOSB</strong>, ARC, KCNJ9/GIRK3, NR4A2, JUNB, and MECP2).
+FOSB	drug	amphetamine	31952958	Furthermore, sensitized behavioral responding to and for <b>amphetamine</b> following exposure to uncertainty is accompanied by increased levels of Ca2+/calmodulin dependent protein kinase II (CaMKII) and protein kinase C (PKC) phosphorylation as well as altered protein levels of the transcription factor ∆<strong>FosB</strong> (increased) and glutamate transporter 1 (GLT1; decreased) in NAcc tissues.
+FOSB	addiction	relapse	31952958	Increased ∆<strong>FosB</strong> and decreased GLT1 levels are observed following psychostimulant exposure, are associated with increased drug taking and <b>seeking</b>, and are known to modulate AMPA receptors and extracellular glutamate levels respectively.
+FOSB	drug	cocaine	31477569	Epigenetic Regulation of Hippocampal <strong>Fosb</strong> Expression Controls Behavioral Responses to <b>Cocaine</b>.
+FOSB	drug	cocaine	31477569	Further, we characterize changes in histone modifications at the <strong>FosB</strong> promoter in hippocampus in response to chronic <b>cocaine</b> and found that locus specific epigenetic modification is essential for <strong>FosB</strong> induction and multiple hippocampus dependent behaviors, including <b>cocaine</b> place preference.
+FOSB	drug	cocaine	31477569	Collectively, these findings suggest that exposure to <b>cocaine</b> induces histone modification at the hippocampal <strong>FosB</strong> gene promoter to cause ΔFosB induction critical for <b>cocaine</b> related learning.SIGNIFICANCE STATEMENT Although <b>cocaine</b> addiction is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which <b>cocaine</b> alters hippocampal gene expression to drive formation of these associations is poorly understood.
+FOSB	addiction	addiction	31477569	Collectively, these findings suggest that exposure to cocaine induces histone modification at the hippocampal <strong>FosB</strong> gene promoter to cause ΔFosB induction critical for cocaine related learning.SIGNIFICANCE STATEMENT Although cocaine <b>addiction</b> is driven in part by the formation of indelible associations between the drug and the environment, paraphernalia, and circumstances of use, and although this type of associative learning is dependent upon changes in gene expression in a brain region called the hippocampus, the mechanisms by which cocaine alters hippocampal gene expression to drive formation of these associations is poorly understood.
+FOSB	drug	cocaine	31477569	Here, we demonstrate that chronic <b>cocaine</b> engages locus specific changes in the epigenetic profile of the <strong>FosB</strong> gene in the hippocampus, and that these alterations are required for <b>cocaine</b> dependent gene expression and <b>cocaine</b> environment associations.
+FOSB	drug	opioid	31442272	H3K4 dimethylation at <strong>FosB</strong> promoter in the striatum of chronic stressed rats promotes <b>morphine</b> induced conditioned place preference.
+FOSB	addiction	addiction	31442272	Expression of <strong>FosB</strong> gene in striatum is essential in <b>addiction</b> establishment.
+FOSB	addiction	addiction	31442272	Therefore, elevation of <strong>FosB</strong> expression in striatum serves as one mechanism by which stress increases risk for <b>addiction</b>.
+FOSB	addiction	addiction	31442272	In this study, adult male Sprague Dawley rats were used to investigate whether chronic stress result in histone modifications at <strong>FosB</strong> gene promoter in striatum and how these histone modifications affect <strong>FosB</strong> expression and the establishment of <b>addiction</b> behavior after administration of drugs of abuse.
+FOSB	drug	opioid	31442272	Before and after <b>morphine</b> administration, <strong>FosB</strong> mRNA in striatum was quantified by real time RT PCR.
+FOSB	drug	opioid	31442272	Levels of histone H3/H4 acetylation and histone H3K4 dimethylation at <strong>FosB</strong> promoter in striatum after <b>morphine</b> administration were measured by using chromatin immunoprecipitation (ChIP) plus real time PCR.
+FOSB	drug	opioid	31442272	EFS group had stronger place preference to <b>morphine</b> and had significantly higher level of <strong>FosB</strong> mRNA in striatum than the other two groups.
+FOSB	drug	opioid	31442272	Mifepristone administration before EFS decreased histone H3K4 dimethylation and <strong>FosB</strong> mRNA in striatum, and also diminished <b>morphine</b> induced conditioned place preference.
+FOSB	drug	opioid	31442272	Altogether, increased level of H3K4 dimethylation at <strong>FosB</strong> promoter in striatum is partially dependent on the activation of GR and responsible for the elevated level of <b>morphine</b> induced <strong>FosB</strong> mRNA in chronic stressed animals.
+FOSB	drug	psychedelics	31373119	Regional changes in ∆<strong>FosB</strong> expression in rat brain following <b>MDMA</b> self administration predict increased sensitivity to effects of locally infused <b>MDMA</b>.
+FOSB	drug	psychedelics	31373119	The effects of extensive 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>) self administration on immunohistochemical measurements of ∆<strong>FosB</strong> accumulation in 12 brain regions was compared with a matched, drug naive, control group.
+FOSB	drug	psychedelics	31373119	Other groups were pretreated with <b>MDMA</b> (0.0 or 10.0 mg/kg, ip, once daily for 5 days), and the locomotor activating effect of <b>MDMA</b> (200 μg/side) microinjected bilaterally into brain regions selected on the basis of the ∆<strong>FosB</strong> results was subsequently determined.
+FOSB	drug	psychedelics	31373119	<b>MDMA</b> self administration significantly increased ∆<strong>FosB</strong> expression in the nucleus accumbens core, ventromedial and dorsomedial caudate putamen, anterior cingulate, prelimbic, infralimbic, and orbitofrontal cortex, and both the central and basolateral amygdala, but not in the ventrolateral or dorsolateral caudate putamen.
+FOSB	drug	psychedelics	31373119	<b>MDMA</b> pretreatment enhanced <b>MDMA</b> produced hyperactivity only when administered into the nucleus accumbens or the medial, but not the lateral, caudate putamen, mirroring the ∆<strong>FosB</strong> results.
+FOSB	drug	cocaine	31043484	RNA sequencing revealed five genes upregulated in <b>cocaine</b> relative to food self administering mice: <strong>Fosb</strong>, Npas4, Vgf, Nptx2, and Pmepa1, which reflect known and novel <b>cocaine</b> plasticity associated genes.
+FOSB	drug	amphetamine	30967896	FOS and <strong>FOSB</strong>, which are implicated in the <b>amphetamine</b> addiction pathway, were up regulated in schizophrenia fibroblast samples.
+FOSB	addiction	addiction	30967896	FOS and <strong>FOSB</strong>, which are implicated in the amphetamine <b>addiction</b> pathway, were up regulated in schizophrenia fibroblast samples.
+FOSB	drug	cocaine	30963104	<strong>Fosb</strong> Induction in Nucleus Accumbens by <b>Cocaine</b> Is Regulated by E2F3a.
+FOSB	drug	cocaine	30963104	We further conclude that ΔFosB expression is regulated specifically by E2F3a, not E2F3b, that E2f3a expression is specific to D1 receptor expressing medium spiny neurons, and that E2F3a overexpression in NAc recapitulates the induction of <strong>Fosb</strong> and ΔFosb mRNA expression observed after chronic <b>cocaine</b> exposure.
+FOSB	drug	cocaine	30803445	This behavioral alteration in spinophilin knockout mice was accompanied by attenuated c Fos and ∆<strong>FosB</strong> expression following <b>cocaine</b> administration and blunted <b>cocaine</b> induced phosphorylation of ERK1/2 in the striatum, with no change in other relevant signaling molecules.
+FOSB	drug	cocaine	30803445	Therefore, we suggest spinophilin fulfills an essential role in <b>cocaine</b> induced behavioral sensitization, likely via ERK1/2 phosphorylation and induction of c Fos and ∆<strong>FosB</strong> in the striatum, a mechanism that may underlie specific processes in <b>cocaine</b> addiction.
+FOSB	addiction	addiction	30803445	Therefore, we suggest spinophilin fulfills an essential role in cocaine induced behavioral sensitization, likely via ERK1/2 phosphorylation and induction of c Fos and ∆<strong>FosB</strong> in the striatum, a mechanism that may underlie specific processes in cocaine <b>addiction</b>.
+FOSB	addiction	sensitization	30803445	Therefore, we suggest spinophilin fulfills an essential role in cocaine induced behavioral <b>sensitization</b>, likely via ERK1/2 phosphorylation and induction of c Fos and ∆<strong>FosB</strong> in the striatum, a mechanism that may underlie specific processes in cocaine addiction.
+FOSB	drug	opioid	30632799	<b>Tramadol</b> induces changes in Δ <strong>FosB</strong>, µ <b>opioid</b> receptor, and p CREB level in the nucleus accumbens and prefrontal cortex of male Wistar rat.
+FOSB	drug	opioid	30632088	Interestingly, <b>morphine</b> induced elevations of <strong>FosB</strong>/ΔFosB+ cells were suppressed by TMCA (50, 100 mg/kg) in the nucleus accumbens sub shell region of mice.
+FOSB	addiction	relapse	30405417	The genic expression of <strong>FosB</strong> seems to be modified after long time exposure to drugs of abuse and these changes may be involved in <b>craving</b> and addicted behavior.
+FOSB	drug	cocaine	30030395	Using primary striatal cultures, we show that transcription of Dnmt3a2, but not that of Dnmt3a1, is activated by dopamine D1 receptor signaling and that knockdown of Dnmt3a2 using viral vector mediated expression of Dnmt3a2 specific shRNAs impairs induction of the IEGs, Arc, <strong>FosB</strong>, and Egr2 Acute <b>cocaine</b> administration increases expression of Dnmt3a2 but not that of Dnmt3a1 in the NAc shell.
+FOSB	drug	cocaine	30030395	shRNA mediated knockdown of Dnmt3a2 in vivo impairs the induction of IEGs, including Egr2 and <strong>FosB</strong> indicating that Dnmt3a2 regulates <b>cocaine</b> dependent expression of plasticity genes in the rat NAc shell.
+FOSB	drug	cocaine	29740282	Immediate early gene (IEG) expression (cFos and <strong>FosB</strong>) induced by repeated <b>cocaine</b> injections was significantly increased in the forebrain of M4R D1RCre mice, whereas it remained normal in the M4R ChATCre mice.
+FOSB	drug	alcohol	29306704	At transcriptional level, <b>ethanol</b> reduced the upregulation of a subset of IEGs encoding for transcription factors such as Atf3, c Fos, <strong>FosB</strong>, Egr1, Egr3 and Npas4 but did not affect the upregulation of others (e.g.
+FOSB	addiction	reward	29093669	Gene expression analysis after <b>CPP</b> test revealed specific up regulation in the CAF COC group of Drd1a, cFos, and <strong>FosB</strong> in the NAc, and cFos, Egr1, and Npas4 in the mPFC.
+FOSB	drug	cocaine	28963688	However, the functional consequences of regulated expression patterns of <strong>Fosb</strong> and Crem (cAMP response element modulator) in both brain regions in response to volitional intake of <b>cocaine</b> in social environment is yet to be explored.
+FOSB	drug	cocaine	28963688	These changes were accompanied by hypomethylation or hypermethylation in the promoters of <strong>Fosb</strong> and Crem genes in the PFC and HPC of the <b>cocaine</b> experienced mice, respectively.
+FOSB	drug	cocaine	28963688	Furthermore, our data delineate the molecular response of Crem and <strong>Fosb</strong> to oral <b>cocaine</b> in group housed mice and demonstrates differential regulation of activities within the substrate brain regions studied.
+FOSB	drug	cocaine	28710498	In particular, we identified an <strong>AP 1</strong> regulated transcriptional network in dlPFC neurons associated with <b>cocaine</b> use disorder that contains several differentially expressed hub genes.
+FOSB	drug	cocaine	27957784	Following CPP, we tested if DCS were able to reduce <strong>FosB</strong>/∆<strong>FosB</strong> protein expression, a molecular switch for <b>cocaine</b> seeking behaviour.
+FOSB	addiction	relapse	27957784	Following CPP, we tested if DCS were able to reduce <strong>FosB</strong>/∆<strong>FosB</strong> protein expression, a molecular switch for cocaine <b>seeking</b> behaviour.
+FOSB	addiction	reward	27957784	Following <b>CPP</b>, we tested if DCS were able to reduce <strong>FosB</strong>/∆<strong>FosB</strong> protein expression, a molecular switch for cocaine seeking behaviour.
+FOSB	drug	cocaine	27815415	We used mice expressing the eGFP protein in D1 receptor positive (D1R(+)) neurons to determine whether Δ <strong>FosB</strong> induced by enriched environment or <b>cocaine</b> injections (5×15 mg/kg) would occur in selective subpopulations of neurons in several subregions of the striatum and prefrontal cortex.
+FOSB	drug	cocaine	27815415	We found that: (1) exposure to enriched environment reduces <b>cocaine</b> induced locomotor activation, confirming our previous findings; (2) exposure to enriched environment by itself increases the accumulation of Δ <strong>FosB</strong> mostly in D1R( ) cells in the shell part of the nucleus accumbens and dorsal striatum, whereas in the nucleus accumbens core, Δ <strong>FosB</strong> accumulates in both D1R(+) and D1R( ) neurons; (3) in standard environment mice, <b>cocaine</b> induces accumulation of Δ <strong>FosB</strong> selectively in D1R(+) cells in the nucleus accumbens, dorsal striatum, and infralimbic cortex; and (4) the effects of enriched environments and <b>cocaine</b> on accumulation of Δ <strong>FosB</strong> were reciprocally blocked by their combination.
+FOSB	drug	cocaine	27664298	ERK (extracellular regulated kinase), CREB (cAMP responsive element binding protein), <strong>FosB</strong> and ΔFosB proteins were of particular interest due to their involvement in <b>cocaine</b> reward and in synaptic plasticity underlying learning and memory.
+FOSB	addiction	reward	27664298	ERK (extracellular regulated kinase), CREB (cAMP responsive element binding protein), <strong>FosB</strong> and ΔFosB proteins were of particular interest due to their involvement in cocaine <b>reward</b> and in synaptic plasticity underlying learning and memory.
+FOSB	drug	cocaine	27664298	We also show that <b>cocaine</b> induced increases in Caudate Putamen (CPu) <strong>FosB</strong> and ΔFosB levels are decreased after MK 801 pre treatment during conditioning.
+FOSB	addiction	addiction	27494187	Differential Expression of <strong>FosB</strong> Proteins and Potential Target Genes in Select Brain Regions of <b>Addiction</b> and Depression Patients.
+FOSB	drug	cocaine	27494187	Here, we use biochemistry to examine the expression of the <strong>FosB</strong> family of transcription factors and their potential gene targets in PFC and HPC postmortem samples from depressed patients and <b>cocaine</b> addicts.
+FOSB	drug	cocaine	27494187	Thus, we provide the first evidence of <strong>FosB</strong> gene expression in human HPC and PFC in these psychiatric disorders, and in light of recent findings demonstrating the critical role of HPC ΔFosB in rodent models of learning and memory, these data suggest that reduced ΔFosB in HPC could potentially underlie cognitive deficits accompanying chronic <b>cocaine</b> abuse or depression.
+FOSB	drug	amphetamine	27339870	Ifenprodil Attenuates <b>Methamphetamine</b> Induced Behavioral Sensitization and Activation of Ras ERK ∆<strong>FosB</strong> Pathway in the Caudate Putamen.
+FOSB	addiction	sensitization	27339870	Ifenprodil Attenuates Methamphetamine Induced Behavioral <b>Sensitization</b> and Activation of Ras ERK ∆<strong>FosB</strong> Pathway in the Caudate Putamen.
+FOSB	drug	amphetamine	27339870	Further results of western blot experiments showed that repeated administration of <b>METH</b> caused the increases in the levels of Ras, pERK/ERK and ∆<strong>FosB</strong> in the CPu, and these changes were inhibited by only the 2.5 mg/kg dose of ifenprodil.
+FOSB	drug	amphetamine	27339870	Moreover, GluN2B containing NMDARs and their downstream Ras ERK ∆<strong>FosB</strong> signaling pathway in the CPu might be involved in <b>METH</b> induced behavioral sensitization.
+FOSB	addiction	sensitization	27339870	Moreover, GluN2B containing NMDARs and their downstream Ras ERK ∆<strong>FosB</strong> signaling pathway in the CPu might be involved in METH induced behavioral <b>sensitization</b>.
+FOSB	drug	opioid	26988162	These findings indicate that the integrity of the insular cortex is essential to motivational aversion associated with <b>morphine</b> withdrawal, and that this kind of aversion induces neuroadaptation, observed as the increase of <strong>FosB</strong>/deltaFosB expression, in the insular cortex.
+FOSB	addiction	aversion	26988162	These findings indicate that the integrity of the insular cortex is essential to motivational <b>aversion</b> associated with morphine withdrawal, and that this kind of <b>aversion</b> induces neuroadaptation, observed as the increase of <strong>FosB</strong>/deltaFosB expression, in the insular cortex.
+FOSB	addiction	withdrawal	26988162	These findings indicate that the integrity of the insular cortex is essential to motivational aversion associated with morphine <b>withdrawal</b>, and that this kind of aversion induces neuroadaptation, observed as the increase of <strong>FosB</strong>/deltaFosB expression, in the insular cortex.
+FOSB	drug	alcohol	26686767	Using wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with <b>ethanol</b> (3g/kg) for 2 weeks, we showed that binge like <b>ethanol</b> treatment in adolescent mice promotes short  and long term alterations in synaptic plasticity and epigenetic changes in the promoter region of bdnf and <strong>fosb</strong>, which increased their expression in the mPFC of young adult animals.
+FOSB	addiction	intoxication	26686767	Using wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with ethanol (3g/kg) for 2 weeks, we showed that <b>binge</b> like ethanol treatment in adolescent mice promotes short  and long term alterations in synaptic plasticity and epigenetic changes in the promoter region of bdnf and <strong>fosb</strong>, which increased their expression in the mPFC of young adult animals.
+FOSB	drug	opioid	26655477	Expression and colocalization of NMDA receptor and <strong>FosB</strong>/ΔFosB in sensitive brain regions in rats after chronic <b>morphine</b> exposure.
+FOSB	drug	opioid	26655477	In addition, increased levels of <strong>FosB</strong> like proteins (<strong>FosB</strong>/ΔFosB) were found to be related to <b>morphine</b> withdrawal behaviors.
+FOSB	addiction	withdrawal	26655477	In addition, increased levels of <strong>FosB</strong> like proteins (<strong>FosB</strong>/ΔFosB) were found to be related to morphine <b>withdrawal</b> behaviors.
+FOSB	drug	opioid	26655477	However, the relationship between NMDAR and <strong>FosB</strong>/ΔFosB in sensitive brain regions during <b>morphine</b> withdrawal is largely unknown.
+FOSB	addiction	withdrawal	26655477	However, the relationship between NMDAR and <strong>FosB</strong>/ΔFosB in sensitive brain regions during morphine <b>withdrawal</b> is largely unknown.
+FOSB	drug	opioid	26655477	In this study, we aimed to investigate NMDAR dynamics and <strong>FosB</strong>/ΔFosB levels in multiple brain regions and whether they are related in sensitive brain regions during <b>morphine</b> abstinence.
+FOSB	drug	opioid	26655477	Quantitative immunohistochemistry was adopted to test NMDAR and <strong>FosB</strong>/ΔfosB levels during <b>morphine</b> withdrawal in rats.
+FOSB	addiction	withdrawal	26655477	Quantitative immunohistochemistry was adopted to test NMDAR and <strong>FosB</strong>/ΔfosB levels during morphine <b>withdrawal</b> in rats.
+FOSB	drug	cocaine	26598422	Increased expression after <b>cocaine</b> self administration was found for 6 IEGs in dorsal and ventral striatum (c fos, Mkp1, <strong>Fosb</strong>/ΔFosb, Egr2, Egr4, and Arc) and 10 IEGs in mPFC (same 6 IEGs as in striatum, plus Bdnf, Homer1, Sgk1 and Rgs2).
+FOSB	drug	cocaine	26598422	Importantly, no major differences were found between IEG expression patterns after 10 or 60 days of <b>cocaine</b> self administration, except <strong>Fosb</strong>/ΔFosb in dorsal striatum and Egr2 in mPFC, whereas the amount of <b>cocaine</b> obtained per session was comparable for short term and long term self administration.
+FOSB	addiction	relapse	25855177	Context induced <b>reinstatement</b> was associated with increased expression of the immediate early genes Fos and <strong>FosB</strong> and the NMDA receptor subunit gene Grin2a in only Fos positive neurons.
+FOSB	drug	cocaine	25522720	Caudate Putamen (CPu) pERK and <strong>FosB</strong> protein levels increased after re exposure to the <b>cocaine</b> chamber only after conditioning with the higher <b>cocaine</b> dose.
+FOSB	drug	cocaine	25522720	Conversely, the higher <b>cocaine</b> dose, independent of environment, resulted in increased NAc <strong>FosB</strong>, ΔFosB and phosphorylated CREB (pCREB) protein levels compared to those conditioned with 5mg/kg <b>cocaine</b> (non CPP expressing).
+FOSB	addiction	reward	25522720	Conversely, the higher cocaine dose, independent of environment, resulted in increased NAc <strong>FosB</strong>, ΔFosB and phosphorylated CREB (pCREB) protein levels compared to those conditioned with 5mg/kg cocaine (non <b>CPP</b> expressing).
+FOSB	drug	cocaine	25522720	Additionally, we show distinct patterns of intracellular responses in the NAc and CPu indicating a region specific role for pERK/pCREB/<strong>FosB</strong> intracellular signaling in the retrieval of <b>cocaine</b> context associations.
+FOSB	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, <strong>Fosb</strong>, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+FOSB	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, <strong>Fosb</strong>, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+FOSB	addiction	reward	25143625	Of particular interest is the transcription factor ΔFosB, a truncated and stable <strong>FosB</strong> gene product whose expression in nucleus accumbens (NAc), a key <b>reward</b> region, is induced by chronic exposure to virtually all drugs of abuse and regulates their psychomotor and rewarding effects.
+FOSB	addiction	reward	24718372	Finally, presentation of a conditioned <b>reward</b> cue was found to induce striatal <strong>FosB</strong>/ΔFosB expression in WT mice, but not in KO mice, indicating a reduced stimulation of <b>reward</b> related brain regions in conditioned KO mice by odor presentation.
+FOSB	drug	alcohol	24355551	Withdrawal induces distinct patterns of <strong>FosB</strong>/∆<strong>FosB</strong> expression in outbred Swiss mice classified as susceptible and resistant to <b>ethanol</b> induced locomotor sensitization.
+FOSB	addiction	sensitization	24355551	Withdrawal induces distinct patterns of <strong>FosB</strong>/∆<strong>FosB</strong> expression in outbred Swiss mice classified as susceptible and resistant to ethanol induced locomotor <b>sensitization</b>.
+FOSB	addiction	withdrawal	24355551	<b>Withdrawal</b> induces distinct patterns of <strong>FosB</strong>/∆<strong>FosB</strong> expression in outbred Swiss mice classified as susceptible and resistant to ethanol induced locomotor sensitization.
+FOSB	addiction	addiction	24355551	Although increases in <strong>FosB</strong>/DeltaFosB expression constitute one of the most important forms of neuronal plasticity in drug <b>addiction</b>, it is unclear whether they represent functional or pathological plasticity.
+FOSB	addiction	withdrawal	24355551	On the 5th day of <b>withdrawal</b>, we could observe increased <strong>FosB</strong>/DeltaFosB expression in the EtOH_High group (in the motor cortex), in the EtOH_Low group (in the ventral tegmental area), and in both groups (in the striatum).
+FOSB	addiction	withdrawal	24355551	Furthermore, distinct patterns of <strong>FosB</strong>/DeltaFosB expression detected in sensitized and non sensitized mice seem to be more related to <b>withdrawal</b> period rather than to chronic drug exposure.
+FOSB	addiction	withdrawal	24355551	Finally, increases in <strong>FosB</strong>/DeltaFosB expression during <b>withdrawal</b> period could be considered as being due to both functional and pathological plasticity.
+FOSB	drug	opioid	24048098	At completion of behavioral testing, mu <b>opioid</b> receptor (OPRM1), <strong>FosB</strong>, cFos, and dopamine receptor mRNA expression was measured in the nucleus accumbens as well as OPRM1 and corticotropin releasing hormone mRNA in the paraventricular nucleus.
+FOSB	drug	amphetamine	23895375	<b>Methamphetamine</b> induced 3 20 fold increases of immediate early genes arc, homer 2, c fos, <strong>fosB</strong>, and its isoforms (ΔfosB and a novel isoform ΔfosB 2) in Fos positive but not Fos negative neurons.
+FOSB	drug	amphetamine	23726845	<b>METH</b> self administration caused increases in mRNA expression of the transcription factors, c fos and <strong>fosb</strong>, the neurotrophic factor, Bdnf, and the synaptic protein, synaptophysin (Syp) in the dorsal striatum.
+FOSB	drug	amphetamine	23726845	Importantly, ChIP PCR showed that <b>METH</b> self administration caused enrichment of phosphorylated CREB (pCREB), but not of histone H3 trimethylated at lysine 4 (H3K4me3), on promoters of c fos, <strong>fosb</strong>, Bdnf and Syp at 2h after cessation of drug intake.
+FOSB	drug	cocaine	23665060	CPP scores were positively correlated to NAc pERK, HIP pERK and CPu <strong>FosB</strong> protein levels, suggesting that similar to males, the ERK/CREB intracellular pathway in mesocorticolimbic regions undergoes <b>cocaine</b> induced neuroplasticity in female rats.
+FOSB	addiction	reward	23665060	<b>CPP</b> scores were positively correlated to NAc pERK, HIP pERK and CPu <strong>FosB</strong> protein levels, suggesting that similar to males, the ERK/CREB intracellular pathway in mesocorticolimbic regions undergoes cocaine induced neuroplasticity in female rats.
+FOSB	drug	amphetamine	23562942	Chronic exposure to either nicotine or <b>METH</b> caused significant decreases in the expression of <strong>fosb</strong>, fra1, and fra2 in the nucleus accumbens (NAc) but not in the dorsal striatum whereas the drug combination increased fra2 expression in both structures.
+FOSB	drug	nicotine	23562942	Chronic exposure to either <b>nicotine</b> or METH caused significant decreases in the expression of <strong>fosb</strong>, fra1, and fra2 in the nucleus accumbens (NAc) but not in the dorsal striatum whereas the drug combination increased fra2 expression in both structures.
+FOSB	drug	cocaine	23447367	<strong>FosB</strong>/ΔFosB expression was increased in all groups and regions after repeated <b>cocaine</b> administration, although it reached lower expression levels in PA19 rats.
+FOSB	drug	cocaine	23319622	To determine the behavioral consequences of cell type specific actions of ∆<strong>FosB</strong>, we selectively overexpressed ∆<strong>FosB</strong> in D1 direct or D2 indirect MSNs in NAc in vivo and found that direct (but not indirect) pathway MSN expression enhances behavioral responses to <b>cocaine</b>.
+FOSB	addiction	reward	23319622	These results reveal that ∆<strong>FosB</strong> in NAc differentially modulates synaptic properties and <b>reward</b> related behaviors in a cell type  and subregion specific fashion.
+FOSB	drug	opioid	23274705	The effect of electroacupuncture on extinction responding of <b>heroin</b> seeking behavior and <strong>FosB</strong> expression in the nucleus accumbens core.
+FOSB	addiction	relapse	23274705	The effect of electroacupuncture on extinction responding of heroin <b>seeking</b> behavior and <strong>FosB</strong> expression in the nucleus accumbens core.
+FOSB	drug	opioid	23185589	This study examined the role of GC in regulation of <strong>FosB</strong>/ΔFosB in both hypothalamic and extrahypothalamic brain stress systems during <b>morphine</b> dependence.
+FOSB	addiction	dependence	23185589	This study examined the role of GC in regulation of <strong>FosB</strong>/ΔFosB in both hypothalamic and extrahypothalamic brain stress systems during morphine <b>dependence</b>.
+FOSB	drug	opioid	23185589	For that, expression of <strong>FosB</strong>/ΔFosB was measured in control (sham operated) and adrenalectomized (ADX) rats that were made opiate dependent after ten days of <b>morphine</b> treatment.
+FOSB	drug	opioid	23185589	In sham operated rats, <strong>FosB</strong>/ΔFosB was induced after chronic <b>morphine</b> administration in all the brain stress areas investigated: nucleus accumbens(shell) (NAc), bed nucleus of the stria terminalis (BNST), central amygdala (CeA), hypothalamic paraventricular nucleus (PVN) and nucleus of the solitary tract noradrenergic cell group (NTS A(2)).
+FOSB	drug	opioid	23185589	Adrenalectomy attenuated the increased production of <strong>FosB</strong>/ΔFosB observed after chronic <b>morphine</b> exposure in NAc, CeA, and NTS.
+FOSB	addiction	addiction	23185589	These data suggest that neuroadaptation (estimated as accumulation of <strong>FosB</strong>/ΔFosB) to opiates in brain areas associated with stress is modulated by GC, supporting the evidence of a link between brain stress hormones and <b>addiction</b>.
+FOSB	drug	alcohol	23020045	Chronic cocaine and <b>alcohol</b> treatment activate and repress many genes such as <strong>FosB</strong>, Cdk5, and Bdnf, where their dysregulation, at the chromatin level, contribute to the development and maintenance of addiction.
+FOSB	drug	cocaine	23020045	Chronic <b>cocaine</b> and alcohol treatment activate and repress many genes such as <strong>FosB</strong>, Cdk5, and Bdnf, where their dysregulation, at the chromatin level, contribute to the development and maintenance of addiction.
+FOSB	addiction	addiction	23020045	Chronic cocaine and alcohol treatment activate and repress many genes such as <strong>FosB</strong>, Cdk5, and Bdnf, where their dysregulation, at the chromatin level, contribute to the development and maintenance of <b>addiction</b>.
+FOSB	drug	cocaine	22836260	ΔFosB, a <strong>Fosb</strong> gene product, is induced in nucleus accumbens (NAc) and caudate putamen (CPu) by repeated exposure to drugs of abuse such as <b>cocaine</b>.
+FOSB	drug	cocaine	22836260	Here, we assessed whether a remote history of <b>cocaine</b> exposure in rats might alter inducibility of the <strong>Fosb</strong> gene elicited by subsequent drug exposure.
+FOSB	drug	cocaine	22836260	We show that prior chronic <b>cocaine</b> administration, followed by extended withdrawal, increases inducibility of <strong>Fosb</strong> in NAc, as evidenced by greater acute induction of ΔFosB mRNA and faster accumulation of ΔFosB protein after repeated <b>cocaine</b> reexposure.
+FOSB	addiction	withdrawal	22836260	We show that prior chronic cocaine administration, followed by extended <b>withdrawal</b>, increases inducibility of <strong>Fosb</strong> in NAc, as evidenced by greater acute induction of ΔFosB mRNA and faster accumulation of ΔFosB protein after repeated cocaine reexposure.
+FOSB	drug	cocaine	22836260	Prior chronic <b>cocaine</b> administration induces a long lasting increase in RNA polymerase II (Pol II) binding at the <strong>Fosb</strong> promoter in NAc only, suggesting that Pol II "stalling" primes <strong>Fosb</strong> for induction in this region upon reexposure to <b>cocaine</b>.
+FOSB	drug	cocaine	22836260	A <b>cocaine</b> challenge then triggers the release of Pol II from the gene promoter, allowing for more rapid <strong>Fosb</strong> transcription.
+FOSB	drug	cocaine	22836260	A <b>cocaine</b> challenge also decreases repressive histone modifications at the <strong>Fosb</strong> promoter in NAc, but increases such repressive marks and decreases activating marks in CPu.
+FOSB	drug	cocaine	22836260	These results provide new insight into the chromatin dynamics at the <strong>Fosb</strong> promoter and reveal a novel mechanism for primed <strong>Fosb</strong> induction in NAc upon reexposure to <b>cocaine</b>.
+FOSB	drug	alcohol	22792289	Electroacupuncture decreases excessive <b>alcohol</b> consumption involving reduction of <strong>FosB</strong>/ΔFosB levels in reward related brain regions.
+FOSB	addiction	reward	22792289	Electroacupuncture decreases excessive alcohol consumption involving reduction of <strong>FosB</strong>/ΔFosB levels in <b>reward</b> related brain regions.
+FOSB	drug	alcohol	22792289	ΔFosB and <strong>FosB</strong> are members of the Fos family of transcription factors implicated in neural plasticity in drug addiction; a connection between electroacupuncture's treatment of <b>alcohol</b> abuse and the Fos family has not been established.
+FOSB	addiction	addiction	22792289	ΔFosB and <strong>FosB</strong> are members of the Fos family of transcription factors implicated in neural plasticity in drug <b>addiction</b>; a connection between electroacupuncture's treatment of alcohol abuse and the Fos family has not been established.
+FOSB	addiction	reward	22792289	The level of <strong>FosB</strong>/ΔFosB in <b>reward</b> related brain regions was assessed by immunohistochemistry.
+FOSB	drug	alcohol	22792289	Additionally, <strong>FosB</strong>/ΔFosB levels in the prefrontal cortex, striatal region and the posterior region of ventral tegmental area were increased following excessive <b>ethanol</b> consumption, but were reduced after six day 100 Hz electroacupuncture.
+FOSB	addiction	reward	22792289	This effect of electroacupuncture may be mediated by down regulation of <strong>FosB</strong>/ΔFosB in <b>reward</b> related brain regions.
+FOSB	drug	cocaine	22649236	CREB and SRF are both activated in NAc by <b>cocaine</b> and bind to the <strong>fosB</strong> gene promoter.
+FOSB	drug	opioid	22569574	Additionally, the expression of <strong>FosB</strong> like proteins, transcription factors associated with behavioral alterations, in the nucleus accumbens of the brain was attenuated in <b>morphine</b> administered mice treated by ZnE.
+FOSB	drug	cocaine	22403532	Preventive role of social interaction for <b>cocaine</b> conditioned place preference: correlation with <strong>FosB</strong>/DeltaFosB and pCREB expression in rat mesocorticolimbic areas.
+FOSB	drug	cocaine	22403532	Here we show that social interaction during extinction of <b>cocaine</b> CPP also reduced <b>cocaine</b> CPP stimulated <strong>FosB</strong> expression in the nucleus accumbens shell and core.
+FOSB	addiction	reward	22403532	Here we show that social interaction during extinction of cocaine <b>CPP</b> also reduced cocaine <b>CPP</b> stimulated <strong>FosB</strong> expression in the nucleus accumbens shell and core.
+FOSB	drug	cocaine	22403532	Our results show that <strong>FosB</strong> and pCREB may be implicated in the protective effect of social interaction against <b>cocaine</b> induced reinstatement of CPP.
+FOSB	addiction	relapse	22403532	Our results show that <strong>FosB</strong> and pCREB may be implicated in the protective effect of social interaction against cocaine induced <b>reinstatement</b> of CPP.
+FOSB	addiction	reward	22403532	Our results show that <strong>FosB</strong> and pCREB may be implicated in the protective effect of social interaction against cocaine induced reinstatement of <b>CPP</b>.
+FOSB	drug	alcohol	22349397	After treating juvenile and adult rats with intermittent <b>ethanol</b> administration, we found that <b>ethanol</b> treatment upregulates histone acetyl transferase (HAT) activity in adolescent prefrontal cortex and increases histone (H3 or H4) acetylation and H3(K4) dimethylation in the promoter region of cFos, Cdk5 and <strong>FosB</strong>.
+FOSB	drug	alcohol	22349397	Inhibition of histone deacetylase by sodium butyrate before <b>ethanol</b> injection enhances both up regulation of HAT activity and histone acetylation of cFos, Cdk5 and <strong>FosB</strong>.
+FOSB	drug	amphetamine	22266344	Regional c Fos and <strong>FosB</strong>/ΔFosB expression associated with chronic <b>methamphetamine</b> self administration and <b>methamphetamine</b> seeking behavior in rats.
+FOSB	addiction	relapse	22266344	Regional c Fos and <strong>FosB</strong>/ΔFosB expression associated with chronic methamphetamine self administration and methamphetamine <b>seeking</b> behavior in rats.
+FOSB	drug	amphetamine	22266344	The regional expression of the transcription factors c Fos and <strong>FosB</strong>/ΔFosB was examined in rats given acute exposure to intravenous <b>methamphetamine</b> (<b>METH</b>) or repeated intravenous <b>METH</b> self administration.
+FOSB	drug	amphetamine	22266344	<strong>FosB</strong>/ΔFosB was elevated in the lateral hypothalamus, posterior ventral tegmental area, central amygdala, and dorsal raphe of all the rats with a history of <b>METH</b> self administration.
+FOSB	drug	amphetamine	22266344	This occurred regardless of whether they received <b>METH</b> on test day, suggesting presence of the long lived <strong>FosB</strong> isoform, ΔFosB.
+FOSB	drug	amphetamine	22266344	Overall, these results show persistent upregulated regional brain Fos and <strong>FosB</strong>/ΔFosB expression with chronic <b>METH</b> self administration and indicate a role for the lateral hypothalamus and lateral septum in <b>METH</b> seeking behavior.
+FOSB	addiction	relapse	22266344	Overall, these results show persistent upregulated regional brain Fos and <strong>FosB</strong>/ΔFosB expression with chronic METH self administration and indicate a role for the lateral hypothalamus and lateral septum in METH <b>seeking</b> behavior.
+FOSB	drug	cocaine	22049069	Nicotine primed the response to <b>cocaine</b> by enhancing its ability to induce transcriptional activation of the <strong>FosB</strong> gene through inhibition of histone deacetylase, which caused global histone acetylation in the striatum.
+FOSB	drug	nicotine	22049069	<b>Nicotine</b> primed the response to cocaine by enhancing its ability to induce transcriptional activation of the <strong>FosB</strong> gene through inhibition of histone deacetylase, which caused global histone acetylation in the striatum.
+FOSB	drug	cocaine	22049069	We tested this conclusion further and found that a histone deacetylase inhibitor simulated the actions of nicotine by priming the response to <b>cocaine</b> and enhancing <strong>FosB</strong> gene expression and LTP depression in the nucleus accumbens.
+FOSB	drug	nicotine	22049069	We tested this conclusion further and found that a histone deacetylase inhibitor simulated the actions of <b>nicotine</b> by priming the response to cocaine and enhancing <strong>FosB</strong> gene expression and LTP depression in the nucleus accumbens.
+FOSB	drug	alcohol	22020770	To our surprise, the impairment of <strong>AP 1</strong> activation was sufficient to mediate a severe and dose dependent phenotype in human monocytes in vitro at <b>alcohol</b> concentrations as low as 0.16% (or 26 mM).
+FOSB	drug	opioid	21967557	Agmatine could reduce the cyclic 3', 5' adenosine monophosphate (cAMP) overshoot at the concentration of 0.01 10 µM in the primary cultured rat hippocampal neurons and attenuated the withdrawal signals and the elevation of <strong>FosB</strong> and ΔFosB at the dose of 5 mg/kg in the <b>morphine</b> dependent mice.
+FOSB	addiction	withdrawal	21967557	Agmatine could reduce the cyclic 3', 5' adenosine monophosphate (cAMP) overshoot at the concentration of 0.01 10 µM in the primary cultured rat hippocampal neurons and attenuated the <b>withdrawal</b> signals and the elevation of <strong>FosB</strong> and ΔFosB at the dose of 5 mg/kg in the morphine dependent mice.
+FOSB	addiction	sensitization	21886798	Opiate <b>sensitization</b> induces <strong>FosB</strong>/ΔFosB expression in prefrontal cortical, striatal and amygdala brain regions.
+FOSB	addiction	addiction	21886798	ΔFosB and <strong>FosB</strong> are members of the Fos family of transcription factors that are implicated in neural plasticity in <b>addiction</b>.
+FOSB	drug	opioid	21886798	This study examined the effects of intermittent <b>morphine</b> treatment, associated with motor sensitization, on <strong>FosB</strong>/ΔFosB levels using quantitative immunohistochemistry.
+FOSB	addiction	sensitization	21886798	This study examined the effects of intermittent morphine treatment, associated with motor <b>sensitization</b>, on <strong>FosB</strong>/ΔFosB levels using quantitative immunohistochemistry.
+FOSB	drug	opioid	21886798	Intermittent <b>morphine</b> pre treatment on these six pre treatment days produced a significant induction of <strong>FosB</strong>/ΔFosB, measured on day 16, in multiple brain regions including prelimbic (PL) and infralimbic (IL) cortex, nucleus accumbens (NAc) core, dorsomedial caudate putamen (CPU), basolateral amygdala (BLA) and central nucleus of the amygdala (CNA) but not in a motor cortex control region.
+FOSB	drug	opioid	21782156	Thus, c Fos, <strong>FosB</strong>/ΔFosB and P CREB immunoreactive profiles were quantified in the rat CPu after either acute or continuous (6 day) administration of <b>morphine</b> and/or PD168,077.
+FOSB	drug	opioid	21782156	Interestingly, at some time points, combined treatment with <b>morphine</b> and PD168,077 substantially increased c Fos, <strong>FosB</strong>/ΔFosB and P CREB expression.
+FOSB	drug	alcohol	21338584	Prodynorphin promoter SNP associated with <b>alcohol</b> dependence forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+FOSB	addiction	dependence	21338584	Prodynorphin promoter SNP associated with alcohol <b>dependence</b> forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+FOSB	drug	amphetamine	21229349	Acute injection of <b>METH</b> increased c fos, <strong>fosB</strong>, fra2, junB, Egr1 3, Nr4a1 (Nur77), and Nr4a3 (Nor 1) mRNA levels in the striatum of saline pretreated rats.
+FOSB	drug	amphetamine	20974185	Association between striatal accumulation of <strong>FosB</strong>/ΔFosB and long term psychomotor sensitization to <b>amphetamine</b> in mice depends on the genetic background.
+FOSB	addiction	sensitization	20974185	Association between striatal accumulation of <strong>FosB</strong>/ΔFosB and long term psychomotor <b>sensitization</b> to amphetamine in mice depends on the genetic background.
+FOSB	drug	amphetamine	20974185	Previous results demonstrated association between increased <strong>FosB</strong>/ΔFosB immunostaining in the ventromedial striatum and behavioral sensitization to <b>amphetamine</b> promoted by repeated stress or by repeated pairings of the psychostimulant and the testing cage in mice of the C57BL/6J strain.
+FOSB	addiction	sensitization	20974185	Previous results demonstrated association between increased <strong>FosB</strong>/ΔFosB immunostaining in the ventromedial striatum and behavioral <b>sensitization</b> to amphetamine promoted by repeated stress or by repeated pairings of the psychostimulant and the testing cage in mice of the C57BL/6J strain.
+FOSB	addiction	sensitization	20974185	Instead, mice of the genetically unrelated DBA/2J inbred strain expressing robust <b>sensitization</b> in the same protocol did not show changes in <strong>FosB</strong>/ΔFosB immunostaining throughout the striatal complex.
+FOSB	drug	amphetamine	20974185	Lack of effects in <strong>FosB</strong>/ΔFosB immunostaining was also observed in DBA/2J mice behaviorally sensitized by repeated pairings of <b>amphetamine</b> with the test cage.
+FOSB	drug	cocaine	20720536	In contrast, acute and repeated <b>cocaine</b> administrations induced hypomethylation and decreased binding of MeCP2 at the <strong>fosB</strong> promoter, and these are associated with transcriptional upregulation of <strong>fosB</strong> in NAc.
+FOSB	drug	cocaine	20633205	Striatal regulation of ΔFosB, <strong>FosB</strong>, and cFos during <b>cocaine</b> self administration and withdrawal.
+FOSB	addiction	withdrawal	20633205	Striatal regulation of ΔFosB, <strong>FosB</strong>, and cFos during cocaine self administration and <b>withdrawal</b>.
+FOSB	drug	cocaine	20633205	The present study examined regulation of the Fos family of transcription factors, specifically cFos, <strong>FosB</strong>, and ΔFosB, in striatal subregions during and after chronic intravenous <b>cocaine</b> administration in self administering and yoked rats.
+FOSB	drug	cocaine	20633205	We found that cFos, <strong>FosB</strong>, and ΔFosB exhibit regionally and temporally distinct expression patterns, with greater accumulation of ΔFosB protein in the nucleus accumbens (NAc) shell and core after chronic <b>cocaine</b> administration, whereas ΔFosB increases in the caudate putamen (CPu) remained similar with either acute or chronic administration.
+FOSB	drug	cocaine	20633205	Interestingly, tolerance to <b>cocaine</b> induced cFos induction was dependent on volitional control of <b>cocaine</b> intake in ventral but not dorsal striatal regions, whereas regulation of <strong>FosB</strong> and ΔFosB was similar in <b>cocaine</b> self administering and yoked animals.
+FOSB	drug	opioid	20438612	Induction of <strong>FosB</strong>/DeltaFosB in the brain stress system related structures during <b>morphine</b> dependence and withdrawal.
+FOSB	addiction	dependence	20438612	Induction of <strong>FosB</strong>/DeltaFosB in the brain stress system related structures during morphine <b>dependence</b> and withdrawal.
+FOSB	addiction	withdrawal	20438612	Induction of <strong>FosB</strong>/DeltaFosB in the brain stress system related structures during morphine dependence and <b>withdrawal</b>.
+FOSB	drug	opioid	20438612	This study was designed to evaluate the possible modifications in <strong>FosB</strong>/DeltaFosB expression in both hypothalamic and extrahypothalamic brain stress system during <b>morphine</b> dependence and withdrawal.
+FOSB	addiction	dependence	20438612	This study was designed to evaluate the possible modifications in <strong>FosB</strong>/DeltaFosB expression in both hypothalamic and extrahypothalamic brain stress system during morphine <b>dependence</b> and withdrawal.
+FOSB	addiction	withdrawal	20438612	This study was designed to evaluate the possible modifications in <strong>FosB</strong>/DeltaFosB expression in both hypothalamic and extrahypothalamic brain stress system during morphine dependence and <b>withdrawal</b>.
+FOSB	drug	opioid	20438612	Using immunohistochemistry and western blot, the expression of <strong>FosB</strong>/DeltaFosB, tyrosine hydroxylase (TH), corticotropin releasing factor (CRF) and pro dynorphin (DYN) was measured in different nuclei from the brain stress system in <b>morphine</b> dependent rats and after <b>morphine</b> withdrawal.
+FOSB	addiction	withdrawal	20438612	Using immunohistochemistry and western blot, the expression of <strong>FosB</strong>/DeltaFosB, tyrosine hydroxylase (TH), corticotropin releasing factor (CRF) and pro dynorphin (DYN) was measured in different nuclei from the brain stress system in morphine dependent rats and after morphine <b>withdrawal</b>.
+FOSB	drug	opioid	20438612	<strong>FosB</strong>/DeltaFosB was induced after chronic <b>morphine</b> administration in the parvocellular part of the hypothalamic paraventricular nucleus (PVN), NAc shell, bed nucleus of the stria terminalis, central amygdala and A(2) noradrenergic part of the nucleus tractus solitarius (NTS A(2)).
+FOSB	drug	opioid	20438612	<b>Morphine</b> dependence and withdrawal evoked an increase in <strong>FosB</strong>/DeltaFosB TH and <strong>FosB</strong>/DeltaFosB CRF double labelling in NTS A(2) and PVN, respectively, besides an increase in TH levels in NTS A(2) and CRF expression in PVN.
+FOSB	addiction	dependence	20438612	Morphine <b>dependence</b> and withdrawal evoked an increase in <strong>FosB</strong>/DeltaFosB TH and <strong>FosB</strong>/DeltaFosB CRF double labelling in NTS A(2) and PVN, respectively, besides an increase in TH levels in NTS A(2) and CRF expression in PVN.
+FOSB	addiction	withdrawal	20438612	Morphine dependence and <b>withdrawal</b> evoked an increase in <strong>FosB</strong>/DeltaFosB TH and <strong>FosB</strong>/DeltaFosB CRF double labelling in NTS A(2) and PVN, respectively, besides an increase in TH levels in NTS A(2) and CRF expression in PVN.
+FOSB	addiction	addiction	20438612	These data indicate that neuroadaptation to <b>addictive</b> substances, observed as accumulation of <strong>FosB</strong>/DeltaFosB, is not limited to the reward circuits but may also manifest in other brain regions, such as the brain stress system, which have been proposed to be directly related to <b>addiction</b>.
+FOSB	addiction	reward	20438612	These data indicate that neuroadaptation to addictive substances, observed as accumulation of <strong>FosB</strong>/DeltaFosB, is not limited to the <b>reward</b> circuits but may also manifest in other brain regions, such as the brain stress system, which have been proposed to be directly related to addiction.
+FOSB	drug	alcohol	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after <b>ethanol</b> withdrawal.
+FOSB	addiction	withdrawal	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after ethanol <b>withdrawal</b>.
+FOSB	addiction	reward	19566711	Delta <strong>FosB</strong> overexpression in the nucleus accumbens enhances sexual <b>reward</b> in female Syrian hamsters.
+FOSB	addiction	reward	19566711	Animals with AAV mediated overexpression of Delta <strong>FosB</strong> in the NAc showed evidence of sexual <b>reward</b> in a conditioned place preference paradigm under conditions in which control animals receiving an injection of AAV green fluorescent protein (GFP) into the NAc did not.
+FOSB	drug	alcohol	19523044	<strong>FOSB</strong> proteins in the orbitofrontal and dorsolateral prefrontal cortices of human <b>alcoholics</b>.
+FOSB	drug	alcohol	19523044	To address this hypothesis in the context of substance dependence in humans, we compared the immunoreactivities of <strong>FOSB</strong> proteins in the orbitofrontal and dorsolateral prefrontal cortices (OFC and DLPFC respectively) between controls and <b>alcoholics</b> using semiquantitative immunoblotting.
+FOSB	addiction	dependence	19523044	To address this hypothesis in the context of substance <b>dependence</b> in humans, we compared the immunoreactivities of <strong>FOSB</strong> proteins in the orbitofrontal and dorsolateral prefrontal cortices (OFC and DLPFC respectively) between controls and alcoholics using semiquantitative immunoblotting.
+FOSB	drug	cocaine	19478136	During this period, under a protocol that typically induces <strong>FosB</strong> expression in the caudate nucleus, these rats and unprotected controls given only empty vector or saline were subjected to repeated twice daily injections of <b>cocaine</b> (30 mg/kg i.p.).
+FOSB	drug	cocaine	19478136	Immunohistochemistry of the neostriatum on day 7 showed many <strong>FosB</strong> reactive nuclei in unprotected rats but few if any in rats pretreated with active vector, which resembled rats never exposed to <b>cocaine</b>.
+FOSB	drug	cocaine	19478136	In contrast there was a more localized protection against <b>cocaine</b> elicited <strong>FosB</strong> induction when hydrolase vector was injected directly into the ventral striatum, which generated high transgene expression in many neurons of the target area.
+FOSB	drug	cocaine	19446794	Finally, we found corresponding changes in ERK1/2 activation and in accumulation of <strong>FosB</strong>/DeltaFosB, a well characterized marker for long term responses to <b>cocaine</b>, in MSN from these animals.
+FOSB	drug	alcohol	19324071	Differences in basal and morphine induced <strong>FosB</strong>/DeltaFosB and pCREB immunoreactivities in dopaminergic brain regions of <b>alcohol</b> preferring AA and <b>alcohol</b> avoiding ANA rats.
+FOSB	drug	opioid	19324071	Differences in basal and <b>morphine</b> induced <strong>FosB</strong>/DeltaFosB and pCREB immunoreactivities in dopaminergic brain regions of alcohol preferring AA and alcohol avoiding ANA rats.
+FOSB	drug	opioid	19324071	These findings suggest that enhanced sensitivity of AA rats to <b>morphine</b> is related to augmented <b>morphine</b> induced expression of <strong>FosB</strong>/DeltaFosB and <b>morphine</b> induced reduction of pCREB levels.
+FOSB	drug	cocaine	18991842	We found that the composition of <strong>AP 1</strong> transcription complexes and expression levels of <strong>AP 1</strong> complexes, and several transcription factors, neurotransmitter receptors as well as intracellular signaling molecules following repeated <b>cocaine</b> administration are altered in Fos deficient brains.
+FOSB	drug	amphetamine	18848971	Repeated treatment with <b>amphetamine</b> produced HDACi like effects: enhanced global histone H4 acetylation level by Western blot as well as specific histone H4 acetylation associated with <strong>fosB</strong> promoter by chromatin immunoprecipitation in the striatum.
+FOSB	drug	cocaine	18822274	In this study, we show that a single <b>cocaine</b> administration (30 mg/kg) time dependently increases ERK phosphorylation, c Fos and <strong>FosB</strong> protein expression, and MKP 1 phosphorylation (p MKP 1), in the caudate putamen (CPu) and nucleus accumbens (NAc) of Fischer rats.
+FOSB	drug	cocaine	18822274	In the CPu, 1 h after <b>cocaine</b> injection, the increase in c Fos and <strong>FosB</strong> protein expressions is totally abolished by pre administration of DA D1 receptor antagonist, SCH23390.
+FOSB	drug	amphetamine	18632938	Delta <strong>FosB</strong> mediates epigenetic desensitization of the c fos gene after chronic <b>amphetamine</b> exposure.
+FOSB	drug	opioid	18474394	Increased analgesic tolerance to acute <b>morphine</b> in <strong>fosB</strong> knock out mice: a gender study.
+FOSB	drug	opioid	18474394	We used both male and female mice lacking <strong>fosB</strong> gene to study its contribution to <b>morphine</b> effects.
+FOSB	drug	opioid	18474394	<strong>FosB</strong>  /  mice, as compared to <strong>fosB</strong> +/+ mice, developed enhanced tolerance to <b>morphine</b> induced analgesia.
+FOSB	drug	opioid	18474394	These results suggest that <strong>fosB</strong> may be involved in the development of tolerance to <b>morphine</b> analgesia but not hypothermia.
+FOSB	drug	opioid	18474394	The gender study implicates that lack of <strong>FosB</strong> proteins in female <strong>fosB</strong>  /  mice enhanced <b>morphine</b> analgesic potency.
+FOSB	drug	opioid	18474394	In conclusion, we show that <strong>fosB</strong> gene is important to analgesia but not hypothermia phenotype indicating its role in <b>morphine</b> effects.
+FOSB	drug	opioid	18460772	[Effect of electroacupuncture on drug seeking behaviors induced by <b>heroin</b> priming and <strong>FosB</strong> expression in relevant brain regions].
+FOSB	addiction	relapse	18460772	[Effect of electroacupuncture on drug <b>seeking</b> behaviors induced by heroin priming and <strong>FosB</strong> expression in relevant brain regions].
+FOSB	drug	opioid	18460772	To explore the effect of electroacupuncture on <b>heroin</b> seeking behavior and <strong>FosB</strong> expression in relevant brain regions.
+FOSB	addiction	relapse	18460772	To explore the effect of electroacupuncture on heroin <b>seeking</b> behavior and <strong>FosB</strong> expression in relevant brain regions.
+FOSB	drug	opioid	18460772	Continuous acupuncture and needle retention attentuate the reinstatement of <b>heroin</b> seeking behaviors induced by <b>heroin</b> priming, and the inhibitory effect may be mediated partially by the expression of <strong>FosB</strong> in relevant regions which are involved in the process of <b>heroin</b> addiction.
+FOSB	addiction	addiction	18460772	Continuous acupuncture and needle retention attentuate the reinstatement of heroin seeking behaviors induced by heroin priming, and the inhibitory effect may be mediated partially by the expression of <strong>FosB</strong> in relevant regions which are involved in the process of heroin <b>addiction</b>.
+FOSB	addiction	relapse	18460772	Continuous acupuncture and needle retention attentuate the <b>reinstatement</b> of heroin <b>seeking</b> behaviors induced by heroin priming, and the inhibitory effect may be mediated partially by the expression of <strong>FosB</strong> in relevant regions which are involved in the process of heroin addiction.
+FOSB	drug	opioid	18407360	Role of <strong>fosB</strong> in behaviours related to <b>morphine</b> reward and spatial memory.
+FOSB	addiction	reward	18407360	Role of <strong>fosB</strong> in behaviours related to morphine <b>reward</b> and spatial memory.
+FOSB	drug	opioid	18407360	Rewarding effects of <b>morphine</b> in <strong>fosB</strong>  /  mice were abolished whereas spatial learning was impaired.
+FOSB	drug	opioid	18407360	In summary, our results indicate that mice lacking <strong>fosB</strong> are less sensitive to rewarding properties of <b>morphine</b> and display spatial memory impairment and suggest involvement of <strong>fosB</strong> and its proteins in motivational aspects of reinforcers as well as in learning and memory processes.
+FOSB	drug	cocaine	18355967	These results indicate that <strong>AP 1</strong> suppresses this behavioral response to <b>cocaine</b>.
+FOSB	drug	cocaine	18342839	In the present study, chronic mild food restriction was used as a stressor to investigate its effect on the locomotor simulant effects of <b>cocaine</b> as well as <strong>FosB</strong> expression in the nucleus accumbens and caudate putamen.
+FOSB	drug	opioid	18184800	In contrast to PENK, no association was detected between PDYN genotype (68 bp repeat element containing one to four copies of <strong>AP 1</strong> binding sites in the promoter region) and <b>heroin</b> abuse, although there was a clear functional association with striatal PDYN mRNA expression: an increased number of inducible repeats (three and four) correlated with higher PDYN levels than adult or fetal subjects with noninducible (one and two) alleles.
+FOSB	drug	amphetamine	18184321	To test whether the behavioral phenotype is also accompanied by similar neuroplastic adaptations, the present study evaluated changes in Fos and <strong>FosB</strong>/DeltaFosB transcription factors induced in the brain of C57BL/6J mice behaviorally sensitized by repeated <b>amphetamine</b> or repeated restraint stress.
+FOSB	drug	cocaine	18093170	Although only 2% of striatal neurons were <strong>FosB</strong> labeled, 87% of these <strong>FosB</strong> labeled neurons were co labeled with c fos when <b>cocaine</b> was injected in the <b>cocaine</b> paired environment.
+FOSB	drug	opioid	17935891	These results demonstrate that a deficient nutritional status during the perinatal period results in adult subjects having neural alterations, leading to an increased responsiveness to <b>morphine</b> and/or enhanced reinforcement effects, which correlates with an overexpression of <strong>FosB</strong> in selective brain areas related to the rewarding network.
+FOSB	addiction	reward	17935891	These results demonstrate that a deficient nutritional status during the perinatal period results in adult subjects having neural alterations, leading to an increased responsiveness to morphine and/or enhanced <b>reinforcement</b> effects, which correlates with an overexpression of <strong>FosB</strong> in selective brain areas related to the rewarding network.
+FOSB	drug	alcohol	17851539	<b>Alcohol</b> relapse induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+FOSB	addiction	relapse	17851539	Alcohol <b>relapse</b> induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+FOSB	drug	opioid	17592519	Microinjection of M(5) muscarinic receptor antisense oligonucleotide into VTA inhibits <strong>FosB</strong> expression in the NAc and the hippocampus of <b>heroin</b> sensitized rats.
+FOSB	drug	opioid	17592519	To investigate the effect of M(5) muscarinic receptor subtype on the locomotor sensitization induced by <b>heroin</b> priming, and it's effect on the <strong>FosB</strong> expression in the nucleus accumbens (NAc) and the hippocampus in the <b>heroin</b> sensitized rats.
+FOSB	addiction	sensitization	17592519	To investigate the effect of M(5) muscarinic receptor subtype on the locomotor <b>sensitization</b> induced by heroin priming, and it's effect on the <strong>FosB</strong> expression in the nucleus accumbens (NAc) and the hippocampus in the heroin sensitized rats.
+FOSB	drug	opioid	17592519	Meanwhile, the expression of <strong>FosB</strong> positive neurons in either the NAc or the dentate gyrus (DG) of the hippocampus increased in <b>heroin</b> induced locomotor sensitized rats.
+FOSB	drug	opioid	17592519	The enhancement of <strong>FosB</strong> positive neurons in the NAc or DG could be inhibited by microinjection of M(5) muscarinic receptor AS ONs into the VTA before the <b>heroin</b> induced locomotor sensitization was performed.
+FOSB	addiction	sensitization	17592519	The enhancement of <strong>FosB</strong> positive neurons in the NAc or DG could be inhibited by microinjection of M(5) muscarinic receptor AS ONs into the VTA before the heroin induced locomotor <b>sensitization</b> was performed.
+FOSB	drug	opioid	17592519	In contrast, microinjection of M(5) muscarinic receptor sense oligonucleotide (S ONs) into the VTA did not block the expression of behavioral sensitization or the expression of <strong>FosB</strong> in the NAc or DG in the <b>heroin</b> sensitized rats.
+FOSB	addiction	sensitization	17592519	In contrast, microinjection of M(5) muscarinic receptor sense oligonucleotide (S ONs) into the VTA did not block the expression of behavioral <b>sensitization</b> or the expression of <strong>FosB</strong> in the NAc or DG in the heroin sensitized rats.
+FOSB	drug	opioid	17592519	Blocking M(5) muscarinic receptor in the VTA inhibits the expression of <b>heroin</b> induced locomotor sensitization, which is associated with the regulation of <strong>FosB</strong> expression in the NAc and hippocampus neurons.
+FOSB	addiction	sensitization	17592519	Blocking M(5) muscarinic receptor in the VTA inhibits the expression of heroin induced locomotor <b>sensitization</b>, which is associated with the regulation of <strong>FosB</strong> expression in the NAc and hippocampus neurons.
+FOSB	drug	alcohol	17572394	Accumbal <strong>FosB</strong>/DeltaFosB immunoreactivity and conditioned place preference in <b>alcohol</b> preferring AA rats and <b>alcohol</b> avoiding ANA rats treated repeatedly with cocaine.
+FOSB	drug	cocaine	17572394	Accumbal <strong>FosB</strong>/DeltaFosB immunoreactivity and conditioned place preference in alcohol preferring AA rats and alcohol avoiding ANA rats treated repeatedly with <b>cocaine</b>.
+FOSB	drug	cocaine	17572394	<b>Cocaine</b> treatment increased the <strong>FosB</strong>/DeltaFosB immunoreactivity (IR) in the nucleus accumbens of AA rats but not in ANA rats.
+FOSB	drug	cocaine	17572394	In the caudate putamen <b>cocaine</b> significantly increased <strong>FosB</strong>/DeltaFosB IR, but no differences were found between the rats of two lines.
+FOSB	drug	cocaine	17572394	In conclusion, our findings show that AA rats are more sensitive to <b>cocaine</b> than ANA rats, and suggest that one possible mediator for this increased sensitivity could be the increased expression of <strong>fosB</strong> derived proteins in the nucleus accumbens of AA rats.
+FOSB	drug	cocaine	17560044	Elevations of <strong>FosB</strong> in the nucleus accumbens during forced <b>cocaine</b> abstinence correlate with divergent changes in reward function.
+FOSB	addiction	reward	17560044	Elevations of <strong>FosB</strong> in the nucleus accumbens during forced cocaine abstinence correlate with divergent changes in <b>reward</b> function.
+FOSB	addiction	withdrawal	17560044	At the earliest <b>withdrawal</b> period, these behavioral changes were accompanied by elevations in <strong>FosB</strong> like immunoreactive staining in the basolateral amygdala (BLA) and nucleus accumbens shell (NAc Sh) and core (NAc C).
+FOSB	drug	cocaine	17560044	<strong>FosB</strong> staining in all three brain areas correlated positively with <b>cocaine</b> preference, but negatively with novelty preference.
+FOSB	drug	cocaine	17560044	After 5 weeks of withdrawal, <strong>FosB</strong> staining was only elevated in the NAc Sh and again correlated positively with elevated <b>cocaine</b> preference but negatively with decreased novelty preference.
+FOSB	addiction	withdrawal	17560044	After 5 weeks of <b>withdrawal</b>, <strong>FosB</strong> staining was only elevated in the NAc Sh and again correlated positively with elevated cocaine preference but negatively with decreased novelty preference.
+FOSB	drug	cocaine	17560044	These data indicate that alterations in the expression of <strong>FosB</strong> like transcription factors in the NAc can predict the dysregulation of hedonic processing that occurs during protracted withdrawal from <b>cocaine</b>.
+FOSB	addiction	reward	17560044	These data indicate that alterations in the expression of <strong>FosB</strong> like transcription factors in the NAc can predict the dysregulation of <b>hedonic</b> processing that occurs during protracted withdrawal from cocaine.
+FOSB	addiction	withdrawal	17560044	These data indicate that alterations in the expression of <strong>FosB</strong> like transcription factors in the NAc can predict the dysregulation of hedonic processing that occurs during protracted <b>withdrawal</b> from cocaine.
+FOSB	drug	nicotine	17468183	Pleiotropic impact of constitutive <strong>fosB</strong> inactivation on <b>nicotine</b> induced behavioral alterations and stress related traits in mice.
+FOSB	drug	cocaine	17468183	Previous rodent studies have shown that many addictive substances and stressful stimuli increase the expression of the transcription factor <strong>FosB</strong> in limbic and associated regions and that the protein products of <strong>fosB</strong> contribute to certain behavioral effects of <b>cocaine</b> and morphine.
+FOSB	drug	opioid	17468183	Previous rodent studies have shown that many addictive substances and stressful stimuli increase the expression of the transcription factor <strong>FosB</strong> in limbic and associated regions and that the protein products of <strong>fosB</strong> contribute to certain behavioral effects of cocaine and <b>morphine</b>.
+FOSB	addiction	addiction	17468183	Previous rodent studies have shown that many <b>addictive</b> substances and stressful stimuli increase the expression of the transcription factor <strong>FosB</strong> in limbic and associated regions and that the protein products of <strong>fosB</strong> contribute to certain behavioral effects of cocaine and morphine.
+FOSB	drug	nicotine	17468183	We tested the hypothesis that a constitutive level of <strong>FosB</strong> affects <b>nicotine</b> regulated behaviors and comorbid behavioral traits using constitutive <strong>fosB</strong> knockout (KO) mice.
+FOSB	drug	nicotine	17468183	In wild type mice, repeated <b>nicotine</b> injections, but not a single acute injection, increased the expression of <strong>FosB</strong> and its truncated variant DeltaFosB in the targets but not at the origins of the mesolimbic and nigrostriatal dopamine pathways; no detectable level of <strong>FosB</strong>/DeltaFosB was found in KO mice.
+FOSB	drug	nicotine	17468183	Our results suggest that the constitutive absence of <strong>fosB</strong> has a pleiotropic influence on the behavioral effects of repeated or prolonged <b>nicotine</b> administration and on stress related behavioral traits in mice.
+FOSB	drug	nicotine	17333132	<b>Nicotine</b> increases <strong>FosB</strong> expression within a subset of reward  and memory related brain regions during both peri  and post adolescence.
+FOSB	addiction	reward	17333132	Nicotine increases <strong>FosB</strong> expression within a subset of <b>reward</b>  and memory related brain regions during both peri  and post adolescence.
+FOSB	drug	nicotine	17333132	To begin to identify brain regions that may be altered by developmental <b>nicotine</b> exposure, we have measured expression of a transcription factor, <strong>FosB</strong>, within a series of reward  and memory related brain regions of Sprague Dawley rats.
+FOSB	addiction	reward	17333132	To begin to identify brain regions that may be altered by developmental nicotine exposure, we have measured expression of a transcription factor, <strong>FosB</strong>, within a series of <b>reward</b>  and memory related brain regions of Sprague Dawley rats.
+FOSB	drug	nicotine	17333132	Our results demonstrate that <strong>FosB</strong> is increased within nucleus accumbens and also the granule cell layer of hippocampal dentate gyrus after both peri  and post adolescent <b>nicotine</b> exposure (0.4 mg kg( 1) day( 1) from days 34 to 43 and 60 to 69, respectively).
+FOSB	drug	opioid	17165513	[Effects of electroacupuncture of low frequency on <b>heroin</b> seeking behavior and <strong>FosB</strong> protein expression in relative brain regions].
+FOSB	addiction	relapse	17165513	[Effects of electroacupuncture of low frequency on heroin <b>seeking</b> behavior and <strong>FosB</strong> protein expression in relative brain regions].
+FOSB	drug	opioid	17165513	To observe effects of electroacupuncture (EA) of low frequency on <b>heroin</b> seeking behavior and <strong>FosB</strong> protein expression in relative brain regions so as to explore the mechanism of EA.
+FOSB	addiction	relapse	17165513	To observe effects of electroacupuncture (EA) of low frequency on heroin <b>seeking</b> behavior and <strong>FosB</strong> protein expression in relative brain regions so as to explore the mechanism of EA.
+FOSB	drug	opioid	17165513	<b>Heroin</b> seeking behavior was elicited by conditional clue and small dose of <b>heroin</b>; <strong>FosB</strong> protein expression was investigated with immunohistochemical technique.
+FOSB	addiction	relapse	17165513	Heroin <b>seeking</b> behavior was elicited by conditional clue and small dose of heroin; <strong>FosB</strong> protein expression was investigated with immunohistochemical technique.
+FOSB	drug	opioid	17165513	After treatment, the <b>heroin</b> seeking behavior induced by conditional clue decreased in the needle retention control group and the weak EA group, and the <b>heroin</b> seeking behavior induced by small dose of <b>heroin</b> in the weak EA group significantly reduced as compared with the control group, and <strong>FosB</strong> protein expression in the nucleus accumbens septi, globus pallidus, basolateral amygdaloid nucleus significantly decreased in the weak EA group, and did not significantly change in the strong EA group; the activity induced by <b>heroin</b> increased as compared with those in the control group and the weak EA group.
+FOSB	addiction	relapse	17165513	After treatment, the heroin <b>seeking</b> behavior induced by conditional clue decreased in the needle retention control group and the weak EA group, and the heroin <b>seeking</b> behavior induced by small dose of heroin in the weak EA group significantly reduced as compared with the control group, and <strong>FosB</strong> protein expression in the nucleus accumbens septi, globus pallidus, basolateral amygdaloid nucleus significantly decreased in the weak EA group, and did not significantly change in the strong EA group; the activity induced by heroin increased as compared with those in the control group and the weak EA group.
+FOSB	drug	alcohol	17127267	Recent findings indicate that low concentrations of <b>ethanol</b> (10 mM) promote inflammatory processes in brain and in glial cells by up regulating cytokines and inflammatory mediators (iNOS, NO, COX 2), and by activating signaling pathways (IKK, MAPKs) and transcriptional factors (NF kappaB, <strong>AP 1</strong>) implicated in inflammatory injury.
+FOSB	drug	amphetamine	16713106	Habituation to the test cage influences <b>amphetamine</b> induced locomotion and Fos expression and increases <strong>FosB</strong>/DeltaFosB like immunoreactivity in mice.
+FOSB	drug	amphetamine	16713106	The present experiments tested the effects of repeated exposure to a test cage (1 h daily for four consecutive days) on <b>amphetamine</b> induced locomotion and Fos expression as well as on <strong>FosB</strong>/DeltaFosB like immunoreactivity in mice of the C57BL/6J and DBA/2J inbred strains that differ for the response to <b>amphetamine</b>, stress and novelty.
+FOSB	drug	cocaine	16674926	Acute and repeated <b>cocaine</b> induces alterations in <strong>FosB</strong>/DeltaFosB expression in the paraventricular nucleus of the hypothalamus.
+FOSB	drug	cocaine	16674926	In order to find a molecular mechanism of <b>cocaine</b> evoked effects in the PVN, in the present study, we investigated the impact of <b>cocaine</b> on the expression of <strong>FosB</strong>/DeltaFosB transcription factors in the PVN.
+FOSB	drug	cocaine	16674926	Using an immunohistochemical method, we found that acute <b>cocaine</b> treatment (25 mg/kg) induced a relatively long lasting (at least 72 h) expression of <strong>FosB</strong>/DeltaFosB in the PVN, whereas repeated <b>cocaine</b> administration (25 mg/kg, once daily for 5 consecutive days) caused accumulation of <strong>FosB</strong>/DeltaFosB in the PVN.
+FOSB	drug	cocaine	16674926	Using a double labeling immunofluorescent method, it was established that <strong>FosB</strong>/DeltaFosB proteins induced by repeated <b>cocaine</b> treatment were present in a small population of CRF immunoreactive neurons of the PVN.
+FOSB	drug	cocaine	16674926	Furthermore, it was found that pretreatment with the specific antagonist of dopamine D1 like receptors SCH 23390 (1 mg/kg) attenuated the expression and accumulation of <strong>FosB</strong>/DeltaFosB in the PVN, evoked by repeated <b>cocaine</b> administration.
+FOSB	drug	cocaine	16674926	Although functional consequences of the above effects for the process of addiction remain to be established, the obtained results indicate that <b>cocaine</b> administration can produce relatively long lasting changes in the expression of <strong>FosB</strong>/DeltaFosB transcription factors in PVN neurons (in some populations of CRF immunoreactive neurons, among others) and that dopamine D1 like receptors are involved in the above effects.
+FOSB	addiction	addiction	16674926	Although functional consequences of the above effects for the process of <b>addiction</b> remain to be established, the obtained results indicate that cocaine administration can produce relatively long lasting changes in the expression of <strong>FosB</strong>/DeltaFosB transcription factors in PVN neurons (in some populations of CRF immunoreactive neurons, among others) and that dopamine D1 like receptors are involved in the above effects.
+FOSB	drug	nicotine	16631212	Effects of chronic <b>nicotine</b> administration and its withdrawal on striatal <strong>FosB</strong>/DeltaFosB and c Fos expression in rats and mice.
+FOSB	addiction	withdrawal	16631212	Effects of chronic nicotine administration and its <b>withdrawal</b> on striatal <strong>FosB</strong>/DeltaFosB and c Fos expression in rats and mice.
+FOSB	drug	nicotine	16631212	In mice neither 2  nor 7 week oral <b>nicotine</b> treatment induced expression of long lived DeltaFosB isoforms although during the treatment in the NAcc <strong>FosB</strong>/DeltaFosB expression was increased as was c Fos in the CPu.
+FOSB	drug	nicotine	16631212	In rats given <b>nicotine</b> subcutaneously once daily for 5days <strong>FosB</strong>/DeltaFosB expression was elevated in the NAcc still after 24 h withdrawal suggesting accumulation of DeltaFosB but in the CPu neither <strong>FosB</strong>/DeltaFosB nor c Fos expression was altered.
+FOSB	addiction	withdrawal	16631212	In rats given nicotine subcutaneously once daily for 5days <strong>FosB</strong>/DeltaFosB expression was elevated in the NAcc still after 24 h <b>withdrawal</b> suggesting accumulation of DeltaFosB but in the CPu neither <strong>FosB</strong>/DeltaFosB nor c Fos expression was altered.
+FOSB	drug	nicotine	16631212	However, in mice given <b>nicotine</b> via drinking fluid although striatal <strong>fosB</strong> and c fos were activated by <b>nicotine</b> even after 7 week treatment no evidence of accumulation of long lived DeltaFosB was found suggesting perhaps a species difference or more likely a role for the manner of administration.
+FOSB	drug	cocaine	16380431	CREB binding protein controls response to <b>cocaine</b> by acetylating histones at the <strong>fosB</strong> promoter in the mouse striatum.
+FOSB	drug	cocaine	16380431	Here, we show that histone acetylation by the cAMP response element binding protein (CREB) binding protein (CBP) mediates sensitivity to <b>cocaine</b> by regulating expression of the <strong>fosB</strong> gene and its splice variant, DeltafosB, a transcription factor previously implicated in addiction.
+FOSB	addiction	addiction	16380431	Here, we show that histone acetylation by the cAMP response element binding protein (CREB) binding protein (CBP) mediates sensitivity to cocaine by regulating expression of the <strong>fosB</strong> gene and its splice variant, DeltafosB, a transcription factor previously implicated in <b>addiction</b>.
+FOSB	drug	cocaine	16380431	Using the chromatin immunoprecipitation assay with antibodies against histone H4 or CBP, we find that CBP is recruited to the <strong>fosB</strong> promoter to acetylate histone H4 in response to acute exposure to <b>cocaine</b>.
+FOSB	drug	cocaine	16380431	We show that mutant mice that lack one allele of the CBP gene and have normal levels of <strong>fosB</strong> expression are less sensitive to chronic (10 day) administration of <b>cocaine</b> than are wild type mice.
+FOSB	drug	cocaine	16263220	It has also been shown that extracellular signal regulated kinase activation can regulate <b>cocaine</b> induced expression of c Fos and <strong>FosB</strong>, two possible components of activator protein 1.
+FOSB	drug	cocaine	16263220	SL327 pre treatment, however, reduces the DNA binding activity of the activator protein 1 complex induced six hours after an acute <b>cocaine</b> treatment as well as one hour after the last of the chronic <b>cocaine</b> injections, a phenomenon that results from the concomitant reduction of all <b>cocaine</b> induced proteins (c Fos, <strong>FosB</strong>, deltaFosB, JunB).
+FOSB	addiction	intoxication	15987270	At the end of the experiment, 6 month period, or acute <b>intoxication</b> associated with SE induction, animals were deeply anesthetized and had their brains subjected to histologic processing for Nissl and delta <strong>FosB</strong>.
+FOSB	drug	opioid	15899480	Furthermore, agmatine inhibited the increased expression of <strong>FosB</strong> in the nucleus accumbens caused by chronic <b>morphine</b>.
+FOSB	drug	opioid	15899480	All these results suggest that agmatine could inhibit <b>morphine</b> induced psychological dependence and relapses by affecting the expression of transcription factor <strong>FosB</strong>.
+FOSB	addiction	dependence	15899480	All these results suggest that agmatine could inhibit morphine induced psychological <b>dependence</b> and relapses by affecting the expression of transcription factor <strong>FosB</strong>.
+FOSB	drug	amphetamine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of <b>amphetamine</b> or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+FOSB	drug	cocaine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or <b>cocaine</b> (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+FOSB	addiction	addiction	15814102	In order to approach the astroglial implication of <b>addictive</b> and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+FOSB	addiction	dependence	15814102	Because astrocytes interact extensively with the neurons in the brain, our data led us to conclude that oxidation regulated <strong>AP 1</strong> target genes may represent one of the molecular mechanisms underlying neuronal adaptation associated with psychostimulant <b>dependence</b>.
+FOSB	drug	cocaine	15770241	These results suggest that genes encoding certain extracellular factors, membrane receptors and modulators, and intracellular signaling molecules, among others, are regulated by <b>cocaine</b> via the D1 receptor, and these <strong>AP 1</strong> transcription complex regulated genes might contribute to persistent <b>cocaine</b> induced behavioral changes.
+FOSB	drug	amphetamine	15680202	Ginsenosides attenuate <b>methamphetamine</b> induced behavioral side effects in mice via activation of adenosine A2A receptors: possible involvements of the striatal reduction in <strong>AP 1</strong> DNA binding activity and proenkephalin gene expression.
+FOSB	drug	cocaine	15464827	<b>Cocaine</b> induced behavioral effects (hyperlocomotion and CPP) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+FOSB	addiction	reward	15464827	Cocaine induced behavioral effects (hyperlocomotion and <b>CPP</b>) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+FOSB	addiction	dependence	15291243	Evidence suggests that the genes for dopamine D4 receptor, phosphodiesterease1B, the AMPA receptor subunit GluR1, 5HT1B receptor, protein kinase C and the transcription factor <strong>FosB</strong> contribute to both <b>dependence</b> susceptibility and comorbid behavioral traits.
+FOSB	drug	opioid	15287893	Activation of <strong>AP 1</strong> and CRE dependent gene expression via mu <b>opioid</b> receptor.
+FOSB	drug	opioid	15287893	Transcription factors Ca2+/cAMP responsive element binding protein (CREB) and activator protein 1 (<strong>AP 1</strong>) may constitute a direct link between the <b>opioid</b> regulated signal transduction pathways and modulation of gene expression.
+FOSB	drug	opioid	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during withdrawal from the <b>opioid</b>.
+FOSB	addiction	withdrawal	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during <b>withdrawal</b> from the opioid.
+FOSB	drug	alcohol	15276803	Dissociation of <b>ethanol</b> and saccharin preference in <strong>fosB</strong> knockout mice.
+FOSB	drug	alcohol	15276803	The purpose of the present study was to evaluate the role of the <strong>fosB</strong> gene in two bottle choice <b>ethanol</b> self administration.
+FOSB	drug	alcohol	15276803	For this aim, <b>ethanol</b> (2 8% v/v) intake and preference was assessed in <strong>fosB</strong> mutant (n=17) and wild type (WT) mice (n=16).
+FOSB	drug	alcohol	15276803	The present results suggest that permanent elimination of <strong>fosB</strong> gene products does not alter <b>ethanol</b> intake but may enhance preference for sweet solutions in mice.
+FOSB	drug	alcohol	14576487	The injurious effects of <b>ethanol</b> on the pancreas may be mediated through (1) sensitization of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) sensitization of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+FOSB	addiction	sensitization	14576487	The injurious effects of ethanol on the pancreas may be mediated through (1) <b>sensitization</b> of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) <b>sensitization</b> of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+FOSB	addiction	reward	14566342	DeltaFosB (a truncated form of <strong>FosB</strong>) and CREB (cAMP response element binding protein) are transcription factors induced in the brain's <b>reward</b> pathways after chronic exposure to drugs of abuse.
+FOSB	drug	amphetamine	12726824	<b>Amphetamine</b> withdrawal modulates <strong>FosB</strong> expression in mesolimbic dopaminergic target nuclei: effects of different schedules of administration.
+FOSB	addiction	withdrawal	12726824	Amphetamine <b>withdrawal</b> modulates <strong>FosB</strong> expression in mesolimbic dopaminergic target nuclei: effects of different schedules of administration.
+FOSB	drug	amphetamine	12726824	escalating (ESC) <b>AMPH</b> injections, for the effects of these treatments on numbers of <strong>FosB</strong> positive nuclei and monoamine utilization in dopaminergic target areas.
+FOSB	drug	amphetamine	12726824	Withdrawal from <b>AMPH</b> pretreatment according to the ESC schedule markedly increased <strong>FosB</strong> expression in the nucleus accumbens shell and basolateral amygdala.
+FOSB	addiction	withdrawal	12726824	<b>Withdrawal</b> from AMPH pretreatment according to the ESC schedule markedly increased <strong>FosB</strong> expression in the nucleus accumbens shell and basolateral amygdala.
+FOSB	drug	amphetamine	12726824	In contrast, withdrawal from INT <b>AMPH</b> administration did not increase <strong>FosB</strong> expression in any of the regions examined.
+FOSB	addiction	withdrawal	12726824	In contrast, <b>withdrawal</b> from INT AMPH administration did not increase <strong>FosB</strong> expression in any of the regions examined.
+FOSB	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for <strong>AP 1</strong> in the NAc: the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+FOSB	drug	cocaine	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying <b>cocaine</b> addiction.
+FOSB	addiction	addiction	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying cocaine <b>addiction</b>.
+FOSB	drug	cocaine	12581184	In this study we have compared the time course of striatal <strong>FosB</strong>/DeltaFosB like immunoreactivity and prodynorphin mRNA expression after discontinuation of chronic <b>cocaine</b> treatment to intact rats and chronic L DOPA treatment to unilaterally 6 hydroxydopamine (6 OHDA) lesioned rats.
+FOSB	addiction	withdrawal	12581184	In both treatment paradigms, the drug induced <strong>FosB</strong>/DeltaFosB immunoreactivity remained significantly elevated in the caudate putamen even at the longest <b>withdrawal</b> period examined.
+FOSB	drug	amphetamine	12504868	In addition, DNA binding activities of NF kappaB, <strong>AP 1</strong>, and CREB in the frontal cortex and hippocampus were more pronounced in mice injected with Tat plus <b>METH</b> compared to the effects of Tat or <b>METH</b> alone.
+FOSB	drug	alcohol	12482856	Up regulation of CD14 in liver caused by acute <b>ethanol</b> involves oxidant dependent <strong>AP 1</strong> pathway.
+FOSB	drug	alcohol	12482856	Additionally, overexpression of SOD also blunted <b>ethanol</b> induced activation of redox sensitive transcription factors NFkappaB and <strong>AP 1</strong> and production of cytokines.
+FOSB	drug	alcohol	12482856	However, only inhibition of <strong>AP 1</strong> with dominant negative TAK1 but not NFkappaB by dominant negative IkappaBalpha significantly blunted <b>ethanol</b> induced increases in CD14, suggesting that <strong>AP 1</strong> is important for CD14 transcriptional regulation.
+FOSB	drug	amphetamine	12112395	Similarly, in the second experiment it was found that the D1R dependent induction by <b>AMPH</b> of Fos, <strong>FosB</strong>, and JunB, but not NGFI A, in the NAc was enhanced in rats exposed 1 week earlier to repeated VTA <b>AMPH</b>.
+FOSB	drug	alcohol	12045006	Chronic <b>alcohol</b> intoxication was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+FOSB	addiction	intoxication	12045006	Chronic alcohol <b>intoxication</b> was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+FOSB	drug	alcohol	12045006	Chronic <b>ethanol</b> feeding significantly enhanced MNP 1 binding, but not those of NF kappaB and <strong>AP 1</strong> in endothelial cells.
+FOSB	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induces c fos and junB expression and elevates <strong>AP 1</strong> mediated transcriptional activities via the mitogen activated protein kinase cascade.
+FOSB	drug	alcohol	11164784	Expression of inducible transcription factors (ITFs) c Fos and <strong>FosB</strong> was investigated during acquisition of <b>alcohol</b> drinking in C57BL/6J mice.
+FOSB	drug	cocaine	11032893	<strong>FosB</strong> induction was measured to confirm that repeated <b>cocaine</b> exposure influenced protein expression, as previously reported.
+FOSB	drug	cocaine	10986339	The suppressive effects of pentobarbital were not specific to c Fos, such that pentobarbital also suppressed expression of ITFs <strong>FosB</strong> and Egr1 in the striatum of <b>cocaine</b> treated rats.
+FOSB	drug	alcohol	10575084	Furthermore, <strong>FosB</strong> expression in the CeMPV and the EW was also significantly higher in the <b>alcohol</b> consuming animals vs. water controls.
+FOSB	drug	nicotine	10555165	The influence of <b>nicotine</b> on the expression of Fos family proteins, which specifically formed complexes with the <strong>AP 1</strong> sequence, was assessed.
+FOSB	addiction	addiction	10491599	<b>Addictive</b> drugs induce a truncated form of <strong>fosB</strong> in the striatum.
+FOSB	drug	alcohol	10443996	In this study, immunohistochemical expression analysis of immediate early genes c fos, <strong>fosB</strong>, and zif268 was performed in brain of C57BL/6J mice after voluntary <b>alcohol</b> consumption.
+FOSB	drug	alcohol	10443996	Consumption of the <b>ethanol</b>/sucrose solution also significantly reduced <strong>FosB</strong> expression in the basolateral amygdala and lateral hypothalamus, and Zif268 expression in the CA1 region of the hippocampus of stressed animals.
+FOSB	drug	nicotine	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during <b>nicotine</b> dependence.
+FOSB	addiction	dependence	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during nicotine <b>dependence</b>.
+FOSB	drug	nicotine	10320004	The effects of acute and chronic <b>nicotine</b> treatment on activator protein 1 (<strong>AP 1</strong>) gene transcription factor binding activity in the rat cortex were investigated.
+FOSB	drug	nicotine	10320004	It was observed that 1 h after acute <b>nicotine</b> treatment (single injection) <strong>AP 1</strong> DNA binding activity was significantly increased in the rat cortex.
+FOSB	drug	nicotine	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of <b>nicotine</b> withdrawal after repeated <b>nicotine</b> treatment (10 days).
+FOSB	addiction	withdrawal	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of nicotine <b>withdrawal</b> after repeated nicotine treatment (10 days).
+FOSB	drug	nicotine	10320004	However, at 18 and 24 h of <b>nicotine</b> withdrawal after 10 days of <b>nicotine</b> treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+FOSB	addiction	withdrawal	10320004	However, at 18 and 24 h of nicotine <b>withdrawal</b> after 10 days of nicotine treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+FOSB	drug	nicotine	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to <b>nicotine</b> dependence.
+FOSB	addiction	dependence	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to nicotine <b>dependence</b>.
+FOSB	drug	amphetamine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered Fos like proteins in brain by chronic cocaine and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on <b>methamphetamine</b> induced stereotypy in mice, Jpn.
+FOSB	drug	cocaine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered Fos like proteins in brain by chronic <b>cocaine</b> and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on methamphetamine induced stereotypy in mice, Jpn.
+FOSB	drug	alcohol	9918601	This investigation examined the effects of acute and chronic <b>ethanol</b> exposure and its withdrawal on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+FOSB	addiction	withdrawal	9918601	This investigation examined the effects of acute and chronic ethanol exposure and its <b>withdrawal</b> on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+FOSB	drug	alcohol	9918601	It was observed that acute <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+FOSB	addiction	withdrawal	9918601	It was observed that acute ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+FOSB	drug	alcohol	9918601	It was also found that chronic <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+FOSB	addiction	withdrawal	9918601	It was also found that chronic ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+FOSB	drug	alcohol	9835277	Repeated <b>alcohol</b> administration differentially affects c Fos and <strong>FosB</strong> protein immunoreactivity in DBA/2J mice.
+FOSB	drug	alcohol	9835277	To identify <b>alcohol</b> responsive brain areas, we have immunohistochemically analyzed expression of c Fos, <strong>FosB</strong>, and other Fos related antigens in the brain of inbred DBA/2J mice after a single or repeated injection of <b>alcohol</b> (4 g/kg).
+FOSB	drug	alcohol	9835277	In contrast to c Fos, <strong>FosB</strong> expression was found to be elevated significantly higher after repeated than after acute treatment with <b>alcohol</b> in several brain areas, including the shell of nucleus accumbens.
+FOSB	drug	alcohol	9835277	In contrast to previous c Fos studies, our studies confirm that <b>alcohol</b> administration indeed activates the reward circuits, including the basal ganglia, and suggest that <strong>FosB</strong> could serve as a more sensitive marker for this activation.
+FOSB	addiction	reward	9835277	In contrast to previous c Fos studies, our studies confirm that alcohol administration indeed activates the <b>reward</b> circuits, including the basal ganglia, and suggest that <strong>FosB</strong> could serve as a more sensitive marker for this activation.
+FOSB	drug	cocaine	9668659	<b>Cocaine</b> and the <strong>AP 1</strong> transcription factor complex.
+FOSB	drug	cocaine	9668659	Interestingly, repeated <b>cocaine</b> administration induces novel delta <strong>FosB</strong> related proteins (called chronic Fos related antigens (Fras)) in the NAc and Str that replace the downregulated isoforms of Fos.
+FOSB	drug	cocaine	9668659	Unlike the acutely induced, short lasting isoforms of Fos and <strong>FosB</strong>, the chronic Fras persist long after the last <b>cocaine</b> administration.
+FOSB	drug	cocaine	9668659	We presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain
+FOSB	drug	cocaine	29090793	<b>Cocaine</b> and the <strong>AP 1</strong> Transcription Factor Complex.
+FOSB	drug	cocaine	29090793	Interestingly, repeated <b>cocaine</b> administration induces novel delta <strong>FosB</strong> related proteins (called chronic Fos related antigens (Fras)) in the NAc and Str that replace the downregulated isoforms of Fos.
+FOSB	drug	cocaine	29090793	Unlike the acutely induced, short lasting isoforms of Fos and <strong>FosB</strong>, the chronic Fras persist long after the last <b>cocaine</b> administration.
+FOSB	drug	cocaine	29090793	We are presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain.
+FOSB	drug	cocaine	9294222	<strong>FosB</strong> mutant mice: loss of chronic <b>cocaine</b> induction of Fos related proteins and heightened sensitivity to <b>cocaine</b>'s psychomotor and rewarding effects.
+FOSB	drug	cocaine	9294222	This deficiency was associated with enhanced behavioral responses to <b>cocaine</b>: <strong>fosB</strong> mutant mice showed exaggerated locomotor activation in response to initial <b>cocaine</b> exposures as well as robust conditioned place preference to a lower dose of <b>cocaine</b>, compared with wild type littermates.
+FOSB	drug	cocaine	9294222	These results establish the long lasting Fos related proteins as products of the <strong>fosB</strong> gene (specifically DeltaFosB isoforms) and suggest that transcriptional regulation by <strong>fosB</strong> gene products plays a critical role in <b>cocaine</b> induced behavioral responses.
+FOSB	drug	cocaine	9294222	This finding demonstrates that a Fos family member protein plays a functional role in behavioral responses to drugs of abuse and implicates <strong>fosB</strong> gene products as important determinants of <b>cocaine</b> abuse.
+FOSB	drug	alcohol	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during <b>ethanol</b> withdrawal.
+FOSB	addiction	withdrawal	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during ethanol <b>withdrawal</b>.
+FOSB	drug	alcohol	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during <b>ethanol</b> withdrawal.
+FOSB	addiction	withdrawal	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during ethanol <b>withdrawal</b>.
+FOSB	addiction	withdrawal	9202324	The AP 1 DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of <strong>FosB</strong>, c Jun, JunB, and JunD.
+FOSB	addiction	withdrawal	9202324	The <strong>AP 1</strong> DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of <strong>FosB</strong>, c Jun, JunB, and JunD.
+FOSB	addiction	withdrawal	9202324	<b>Withdrawal</b> severity did not affect the composition of the <strong>AP 1</strong> DNA binding activities.
+FOSB	drug	amphetamine	9070635	Thus, <b>amphetamine</b> sensitization is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+FOSB	addiction	sensitization	9070635	Thus, amphetamine <b>sensitization</b> is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+FOSB	drug	cocaine	8959019	However, the induction of the chronic <strong>AP 1</strong> complex and the chronic Fras provides a mechanism capable of underlying long lasting alterations in gene expression following chronic <b>cocaine</b> treatment.
+FOSB	drug	opioid	8843097	A mu receptor <b>opioid</b> agonist induces <strong>AP 1</strong> and NF kappa B transcription factor activity in primary cultures of rat cortical neurons.
+FOSB	drug	opioid	8843097	The specific mu receptor <b>opioid</b> agonist, Tyr, D Ala2, Gly, N Me Phe4, Gly ol5 (DAMGO), was found to increase <strong>AP 1</strong> and NF kappa B activity in primary cultures of neurons from rat cerebral cortex.
+FOSB	drug	opioid	8843097	Acute (2 h, 4 h) and long term (72 h) treatment with DAMGO time dependently increased the DNA binding activity of both <strong>AP 1</strong> and NF kappa B and the stimulation could be abolished or inhibited by concurrent incubation with <b>naloxone</b>.
+FOSB	drug	opioid	8843097	However, acute <b>naloxone</b> precipitated withdrawal did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+FOSB	addiction	withdrawal	8843097	However, acute naloxone precipitated <b>withdrawal</b> did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+FOSB	drug	opioid	8843097	These results indicate a mu <b>opioid</b> receptor related co induction of <strong>AP 1</strong> and NF kappa B transcription factors in cultured cortical neurons.
+FOSB	drug	opioid	8609891	After 5 days of <b>morphine</b> treatment, we observed increased levels of the chronic Fras and of <strong>AP 1</strong> binding activity in rat striatum and nucleus accumbens, effects that were not seen in most other brain regions that we studied.
+FOSB	drug	alcohol	8609891	Withdrawal studies demonstrated robust induction of several known acute Fras, including c Fos, <strong>FosB</strong>, Fra 1, Fra 2, and delta <strong>FosB</strong>, at 6 hr after <b>naltrexone</b> precipitation of withdrawal in the striatum, nucleus accumbens, and several other brain regions.
+FOSB	addiction	withdrawal	8609891	<b>Withdrawal</b> studies demonstrated robust induction of several known acute Fras, including c Fos, <strong>FosB</strong>, Fra 1, Fra 2, and delta <strong>FosB</strong>, at 6 hr after naltrexone precipitation of <b>withdrawal</b> in the striatum, nucleus accumbens, and several other brain regions.
+FOSB	drug	opioid	7838131	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal, a model of <b>opioid</b> dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+FOSB	addiction	dependence	7838131	Naloxone precipitated morphine withdrawal, a model of opioid <b>dependence</b>, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+FOSB	addiction	withdrawal	7838131	Naloxone precipitated morphine <b>withdrawal</b>, a model of opioid dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+FOSB	addiction	withdrawal	7838131	<strong>AP 1</strong> DNA binding activity and dimer composition also exhibited regulation after <b>withdrawal</b>, presumably as a result of both transcriptional and post translational events.
+FOSB	drug	opioid	7838131	Thus, <b>morphine</b> dependence results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+FOSB	addiction	dependence	7838131	Thus, morphine <b>dependence</b> results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+FOSB	drug	cocaine	7969045	One early cellular response to <b>cocaine</b> administration is a brain region specific alteration in the transcriptional pattern of immediate early genes belonging to the Fos/Jun family of nucleotide sequence specific [activator protein 1 (<strong>AP 1</strong>)] DNA binding proteins.
+FOSB	drug	cocaine	7969045	The work described here compares <b>cocaine</b> induced transcriptional regulation of immediate early gene mRNA levels, as well as <strong>AP 1</strong> DNA binding activity, within the striatum and cerebellum.
+FOSB	drug	cocaine	7969045	Gel retention analysis using antibodies to the various Fos and Jun proteins was used to characterize <b>cocaine</b> dependent alterations in the composition of striatal and cerebellar <strong>AP 1</strong> DNA binding complexes.
+FOSB	drug	cocaine	7969045	In striatum, <b>cocaine</b> increases the relative levels of c Fos, Fos B, Jun B, and Jun D proteins that bind the <strong>AP 1</strong> DNA sequence element, whereas in the cerebellum only c Fos and Jun D binding activities are increased.
+FOSB	drug	opioid	8078918	SCH23390 attenuated <b>morphine</b> induction of <strong>AP 1</strong> binding in striatum, suggesting that c fos and junB contribute to <strong>AP 1</strong> binding.
+FOSB	drug	amphetamine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with <b>methamphetamine</b>, cocaine and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of <b>methamphetamine</b> and cocaine, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+FOSB	drug	cocaine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, <b>cocaine</b> and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and <b>cocaine</b>, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+FOSB	drug	opioid	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, cocaine and <b>morphine</b>: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and cocaine, 2) CRE binding activity was decreased by chronic <b>morphine</b> treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic <b>morphine</b> treatment in the mouse cerebellum.
+FOSB	drug	alcohol	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during <b>ethanol</b> withdrawal.
+FOSB	addiction	withdrawal	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during ethanol <b>withdrawal</b>.
+FOSB	drug	alcohol	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing <b>ethanol</b> withdrawal.
+FOSB	addiction	withdrawal	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing ethanol <b>withdrawal</b>.
+FOSB	drug	alcohol	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>ethanol</b> withdrawal.
+FOSB	addiction	withdrawal	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after ethanol <b>withdrawal</b>.
+FOSB	drug	alcohol	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of <b>ethanol</b> withdrawal.
+FOSB	addiction	withdrawal	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of ethanol <b>withdrawal</b>.
+FOSB	addiction	withdrawal	8974322	Gel shift assays indicated the formation of <strong>AP 1</strong> binding factors in nuclear extracts of the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>withdrawal</b>.
+FOSB	drug	cocaine	1631058	Regulation of immediate early gene expression and <strong>AP 1</strong> binding in the rat nucleus accumbens by chronic <b>cocaine</b>.
+FOSB	drug	cocaine	1631058	We therefore examined changes in the mRNA levels for the IEGs c fos, c jun, <strong>fosB</strong>, junB, and zif268 in the NAc of rats treated acutely and chronically with <b>cocaine</b>.
+FOSB	drug	cocaine	1631058	As would be expected from the RNA data and immunohistochemistry, acute <b>cocaine</b> administration increased <strong>AP 1</strong> binding activity in the NAc, an effect that reverted completely to control levels within 8 12 hr.
+FOSB	drug	cocaine	1631058	In contrast, <strong>AP 1</strong> binding activity in the NAc of animals treated chronically with <b>cocaine</b> remained elevated at acute levels 18 hr after the last chronic injection, a time at which c fos and c jun mRNA levels and Fos like immunoreactivity had returned to control values.
+FOSB	drug	cocaine	1631058	An additional acute <b>cocaine</b> challenge did not further increase <strong>AP 1</strong> binding.
+FOSB	drug	cocaine	1631058	The data suggest that chronic <b>cocaine</b> treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of <b>cocaine</b> addiction.
+FOSB	addiction	addiction	1631058	The data suggest that chronic cocaine treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of cocaine <b>addiction</b>.
+HTR2C	drug	alcohol	32477119	The spontaneous chronic consumption of either <b>alcohol</b> or cocaine under a 3 week free choice progressive paradigm of <b>alcohol</b> (3/6/10%) or cocaine (0.2/0.4/0.6 mg/ml), was assessed in VGV transgenic mice, having full <strong>5 HT2C</strong> receptor editing and displaying PTSD like behaviors.
+HTR2C	drug	cocaine	32477119	The spontaneous chronic consumption of either alcohol or <b>cocaine</b> under a 3 week free choice progressive paradigm of alcohol (3/6/10%) or <b>cocaine</b> (0.2/0.4/0.6 mg/ml), was assessed in VGV transgenic mice, having full <strong>5 HT2C</strong> receptor editing and displaying PTSD like behaviors.
+HTR2C	drug	cocaine	32477119	Regarding <b>cocaine</b>, in contrast to WT mice, VGV mice did not increase their drug consumption along with increasing doses, an effect that might be related with enhanced drug stimuli discrimination via increased <strong>5 HT2C</strong> receptors.
+HTR2C	drug	opioid	31980285	Lorcaserin, a high affinity <strong>5 HT2C</strong> receptor agonist approved for treating obesity, decreased self administration of <b>oxycodone</b> and cue induced reinstatement of drug seeking behavior in preclinical studies.
+HTR2C	addiction	relapse	31980285	Lorcaserin, a high affinity <strong>5 HT2C</strong> receptor agonist approved for treating obesity, decreased self administration of oxycodone and cue induced <b>reinstatement</b> of drug <b>seeking</b> behavior in preclinical studies.
+HTR2C	drug	alcohol	31968217	Fluoxetine improves behavioural deficits induced by chronic <b>alcohol</b> treatment by alleviating RNA editing of <strong>5 HT2C</strong> receptors.
+HTR2C	drug	alcohol	31778691	Anxiety during <b>alcohol</b> withdrawal involves <strong>5 HT2C</strong> receptors and M channels in the lateral habenula.
+HTR2C	addiction	withdrawal	31778691	Anxiety during alcohol <b>withdrawal</b> involves <strong>5 HT2C</strong> receptors and M channels in the lateral habenula.
+HTR2C	drug	nicotine	31470021	Acute and chronic interactive treatments of serotonin <strong>5HT2C</strong> and dopamine D1 receptor systems for decreasing <b>nicotine</b> self administration in female rats.
+HTR2C	drug	nicotine	31470021	In the current study, we tested the interactions of the D1 antagonist SCH 23390 and the serotonin <strong>5HT2c</strong> agonist lorcaserin, both of which we have previously shown to significantly reduce <b>nicotine</b> self administration.
+HTR2C	drug	benzodiazepine	31196061	A hydroalcoholic, thujone free extract from freshly harvested Salvia officinalis leaves (A.Vogel Menosan®) was investigated in an acetylcholinesterase enzyme assay and several receptor binding assays (adrenergic alpha 2A, GABA (<b>benzodiazepine</b> site), GABAB; muscarinic M3, μ opioid, serotonin 5 HT1A, serotonin 5 HT2B, serotonin <strong>5 HT2C</strong> and serotonin transporter).
+HTR2C	drug	opioid	31196061	A hydroalcoholic, thujone free extract from freshly harvested Salvia officinalis leaves (A.Vogel Menosan®) was investigated in an acetylcholinesterase enzyme assay and several receptor binding assays (adrenergic alpha 2A, GABA (benzodiazepine site), GABAB; muscarinic M3, μ <b>opioid</b>, serotonin 5 HT1A, serotonin 5 HT2B, serotonin <strong>5 HT2C</strong> and serotonin transporter).
+HTR2C	drug	amphetamine	30989246	Effect of coadministration of the GABAB agonist baclofen and the <strong>5 HT2C</strong> agonist Ro60 0175 on the expression of <b>amphetamine</b> induced locomotor sensitization.
+HTR2C	addiction	sensitization	30989246	Effect of coadministration of the GABAB agonist baclofen and the <strong>5 HT2C</strong> agonist Ro60 0175 on the expression of amphetamine induced locomotor <b>sensitization</b>.
+HTR2C	drug	amphetamine	30989246	Therefore, the objective of this study was to evaluate the effects of joint administration of an intermediate dose of the GABAB agonist baclofen (3.0 mg/kg) with different doses of the <strong>5HT2C</strong> agonist Ro60 0175 (0.3, 1.0, and 3.0 mg/kg) on the locomotor sensitization expression induced by the repeated administration of <b>amphetamine</b> (1.0 mg/kg).
+HTR2C	addiction	sensitization	30989246	Therefore, the objective of this study was to evaluate the effects of joint administration of an intermediate dose of the GABAB agonist baclofen (3.0 mg/kg) with different doses of the <strong>5HT2C</strong> agonist Ro60 0175 (0.3, 1.0, and 3.0 mg/kg) on the locomotor <b>sensitization</b> expression induced by the repeated administration of amphetamine (1.0 mg/kg).
+HTR2C	drug	cocaine	30952156	Eight day withdrawal from high <b>cocaine</b> escalation was associated, respectively, with increased and decreased dopamine receptor D2 (DRD2) and serotonin receptor 2C (<strong>HTR2C</strong>) expression in the ventral striatum compared with controls.
+HTR2C	addiction	addiction	30952156	Eight day withdrawal from high cocaine <b>escalation</b> was associated, respectively, with increased and decreased dopamine receptor D2 (DRD2) and serotonin receptor 2C (<strong>HTR2C</strong>) expression in the ventral striatum compared with controls.
+HTR2C	addiction	withdrawal	30952156	Eight day <b>withdrawal</b> from high cocaine escalation was associated, respectively, with increased and decreased dopamine receptor D2 (DRD2) and serotonin receptor 2C (<strong>HTR2C</strong>) expression in the ventral striatum compared with controls.
+HTR2C	drug	psychedelics	30629611	In the binding (radioligand displacement) studies some of these compounds exhibited only modest selectivity for either 5 HT2A or <strong>5 HT2C</strong> receptors suggesting that a few of them, with affinities in the 10 100 nanomolar range for 5 HT2A receptors, might presumably be <b>psychedelic</b>.
+HTR2C	drug	cocaine	30578419	Serotonin transporter inhibition and <strong>5 HT2C</strong> receptor activation drive loss of <b>cocaine</b> induced locomotor activation in DAT Val559 mice.
+HTR2C	drug	cocaine	30578419	Furthermore, genetic elimination of high affinity <b>cocaine</b> interactions at SERT in DAT Val559 mice, or specific inhibition of <strong>5 HT2C</strong> receptors in these animals, restored <b>cocaine</b> induced locomotion, but did not restore <b>cocaine</b> induced elevations of extracellular DA.
+HTR2C	drug	cocaine	30578419	Our findings reveal a significant serotonergic plasticity arising in the DAT Val559 model that involves enhanced <strong>5 HT2C</strong> signaling, acting independently of striatal DA release, capable of suppressing the activity of <b>cocaine</b> sensitive motor circuits.
+HTR2C	drug	amphetamine	30469095	In the present study, we investigated the effects of the selective 5HT2A receptor antagonist M100907 alone or in combination with the selective <strong>5HT2C</strong> agonist WAY 163909 on intravenous <b>methamphetamine</b> self administration in rhesus macaques (N = 3).
+HTR2C	drug	amphetamine	30469095	Combination approaches with sub threshold doses of 5 HT2A receptor antagonists and <strong>5 HT2C</strong> receptor agonists, on the other hand, do not seem to be effective in decreasing <b>methamphetamine</b> reinforcement.
+HTR2C	addiction	reward	30469095	Combination approaches with sub threshold doses of 5 HT2A receptor antagonists and <strong>5 HT2C</strong> receptor agonists, on the other hand, do not seem to be effective in decreasing methamphetamine <b>reinforcement</b>.
+HTR2C	drug	nicotine	30419272	Persistent attenuation of <b>nicotine</b> self administration in rats by co administration of chronic <b>nicotine</b> infusion with the dopamine D1 receptor antagonist SCH 23390 or the serotonin <strong>5 HT2C</strong> agonist lorcaserin.
+HTR2C	drug	alcohol	30419272	Serotonin through its actions on <strong>5 HT2C</strong> receptors has been shown to play a key role in modulating the reinforcement of addictive drugs, including nicotine and <b>alcohol</b>.
+HTR2C	drug	nicotine	30419272	Serotonin through its actions on <strong>5 HT2C</strong> receptors has been shown to play a key role in modulating the reinforcement of addictive drugs, including <b>nicotine</b> and alcohol.
+HTR2C	addiction	addiction	30419272	Serotonin through its actions on <strong>5 HT2C</strong> receptors has been shown to play a key role in modulating the reinforcement of <b>addictive</b> drugs, including nicotine and alcohol.
+HTR2C	addiction	reward	30419272	Serotonin through its actions on <strong>5 HT2C</strong> receptors has been shown to play a key role in modulating the <b>reinforcement</b> of addictive drugs, including nicotine and alcohol.
+HTR2C	drug	nicotine	30419272	These studies were conducted to evaluate combination therapies utilizing <b>nicotine</b> replacement therapy in conjunction with either a dopamine D1 receptor antagonist SCH 23390 or a serotonin <strong>5 HT2C</strong> receptor agonist, lorcaserin.
+HTR2C	drug	nicotine	30419272	<strong>5HT2C</strong> agonist treatment had additive effects with chronic <b>nicotine</b> infusion for significantly lowering <b>nicotine</b> self administration.
+HTR2C	drug	psychedelics	30261175	25D <b>NBOMe</b>, 25E <b>NBOMe</b>, 25H <b>NBOMe</b>, 25I NBOH and 25N <b>NBOMe</b> had very high affinity for, and full efficacy at, 5 HT2A and <strong>5 HT2C</strong> receptors.
+HTR2C	drug	psychedelics	30261175	At the <strong>5 HT2C</strong> receptor, four had very high potencies, similar to <b>LSD</b> and serotonin, while 25H <b>NBOMe</b> had lower potency.
+HTR2C	addiction	addiction	30233224	The present review will evaluate the lorcaserin clinical studies (obesity, diabetes, and <b>addiction</b>), XR bioequivalence studies, pharmacogenomics of the serotonin (<strong>5HT2c</strong>) system, and adherence data in once daily versus twice daily medications.
+HTR2C	addiction	aversion	30072053	Numerous studies describe how various epigenetic phenomena, mainly histone acetylation, histone methylation, DNA methylation, but also other less known epigenetic phenomena such as histone poly[ADP] ribosylation and <strong>5 HT2C</strong> receptor pre mRNA editing, exert significant regulatory roles in <b>aversion</b> memory and fear extinction memory formation.
+HTR2C	drug	amphetamine	29715538	Age  and sex dependent effects of <b>methamphetamine</b> on cognitive flexibility and <strong>5 HT2C</strong> receptor localization in the orbitofrontal cortex of Sprague Dawley rats.
+HTR2C	addiction	reward	29715538	After all rats reached adulthood, they were tested in an <b>operant</b> strategy shifting task and their brains were subsequently analyzed using immunofluorescence to quantify co localization of <strong>5 HT2C</strong> receptors with parvalbumin interneurons in the OFC.
+HTR2C	drug	cocaine	29620897	An impaired signaling capacity of the serotonin (5 HT) <strong>5 HT2C</strong> receptor (5 HT2CR) has been implicated in the neurobehavioral processes that promote relapse vulnerability in <b>cocaine</b> use disorder (CUD).
+HTR2C	addiction	relapse	29620897	An impaired signaling capacity of the serotonin (5 HT) <strong>5 HT2C</strong> receptor (5 HT2CR) has been implicated in the neurobehavioral processes that promote <b>relapse</b> vulnerability in cocaine use disorder (CUD).
+HTR2C	drug	amphetamine	29555337	In the present study, we investigated whether the <strong>5 HT2C</strong> receptors control <b>amphetamine</b> evoked locomotor activity and regulate food consumption.
+HTR2C	drug	amphetamine	29555337	Localized microinjections into the VTA or the ARC were used to assess the effects of a highly selective <strong>5 HT2C</strong> receptor agonist, AR231630, on the locomotor stimulant effect of <b>amphetamine</b> as well as on food intake.
+HTR2C	addiction	reward	29555337	We can conclude that <strong>5 HT2C</strong> receptor in the VTA, but not in the ARC, participates in both homeostatic and <b>hedonic</b> food intake and brain <b>reward</b> function.
+HTR2C	addiction	reward	29545208	To investigate the effects and mechanisms of YYO reversing the anxiety induced by <strong>5 HT2C</strong> receptor agonist 1 (3 chlorophenyl) piperazine (m <b>CPP</b>).
+HTR2C	drug	nicotine	29498158	Preclinical evidence for combining the <strong>5 HT2C</strong> receptor agonist lorcaserin and varenicline as a treatment for <b>nicotine</b> dependence.
+HTR2C	addiction	dependence	29498158	Preclinical evidence for combining the <strong>5 HT2C</strong> receptor agonist lorcaserin and varenicline as a treatment for nicotine <b>dependence</b>.
+HTR2C	drug	cocaine	29217539	Inhibition of <b>Cocaine</b> and 3,4 Methylenedioxypyrovalerone (MDPV) Self Administration by Lorcaserin Is Mediated by <strong>5 HT2C</strong> Receptors in Rats.
+HTR2C	drug	cocaine	29217539	Although this effect is partially inhibited by a <strong>5 HT2C</strong> receptor antagonist (SB242084), lorcaserin also has effects at 5 HT2A and 5 HT1A receptors, and the relative contribution of these receptors to its anti <b>cocaine</b> effects has not been investigated.
+HTR2C	drug	cocaine	29217539	Antagonism of <strong>5 HT2C</strong> (but not 5 HT1A or 5 HT2A) receptors blocked the effects of lorcaserin on <b>cocaine</b> and MDPV self administration.
+HTR2C	drug	nicotine	29040827	Accumulating evidence suggests that the FDA approved serotonin <strong>5 HT2C</strong> receptor agonist, lorcaserin (Belviq®), may be a promising candidate for the management of substance use disorders, including <b>nicotine</b> addiction.
+HTR2C	addiction	addiction	29040827	Accumulating evidence suggests that the FDA approved serotonin <strong>5 HT2C</strong> receptor agonist, lorcaserin (Belviq®), may be a promising candidate for the management of substance use disorders, including nicotine <b>addiction</b>.
+HTR2C	drug	nicotine	28668504	Some studies show that the 5 HT2A, <strong>5 HT2C</strong>, and 5 HT3 receptors have a central role in the induction and expression of <b>nicotine</b> induced locomotor sensitization.
+HTR2C	addiction	sensitization	28668504	Some studies show that the 5 HT2A, <strong>5 HT2C</strong>, and 5 HT3 receptors have a central role in the induction and expression of nicotine induced locomotor <b>sensitization</b>.
+HTR2C	drug	amphetamine	28588509	The effects of fluoxetine, but not of d <b>amphetamine</b>, were prevented by the selective <strong>5 HT2C</strong> receptor antagonist SB242084.
+HTR2C	drug	amphetamine	28584928	The aim of the present study was to evaluate the effects of the selective serotonin <strong>5 HT2C</strong> receptor agonist WAY163909 on the behavioral neuropharmacology of cocaine and <b>methamphetamine</b> in adult rhesus macaques.
+HTR2C	drug	cocaine	28584928	The aim of the present study was to evaluate the effects of the selective serotonin <strong>5 HT2C</strong> receptor agonist WAY163909 on the behavioral neuropharmacology of <b>cocaine</b> and methamphetamine in adult rhesus macaques.
+HTR2C	addiction	relapse	28584928	Our data indicate that selective <strong>5 HT2C</strong> receptor activation decreases drug intake and drug <b>seeking</b> behavior in nonhuman primate models of psychostimulant abuse through neurochemical mechanisms involved in the modulation of mesolimbic dopamine.
+HTR2C	addiction	addiction	28265714	A short history of the <strong>5 HT2C</strong> receptor: from the choroid plexus to depression, obesity and <b>addiction</b> treatment.
+HTR2C	drug	opioid	28107783	Serotonin (5 HT) neurotransmission, particularly through the <strong>5 HT2C</strong> receptor (5 HT2CR), regulates psychostimulant reward and cue reactivity, and in the present experiments, we investigated the hypothesis that the selective 5 HT2CR agonist lorcaserin, which is approved by the United States Food and Drug Administration (FDA) for the treatment of obesity, will suppress <b>oxycodone</b> self administration and <b>oxycodone</b> associated cue reactivity in rats.
+HTR2C	addiction	reward	28107783	Serotonin (5 HT) neurotransmission, particularly through the <strong>5 HT2C</strong> receptor (5 HT2CR), regulates psychostimulant <b>reward</b> and cue reactivity, and in the present experiments, we investigated the hypothesis that the selective 5 HT2CR agonist lorcaserin, which is approved by the United States Food and Drug Administration (FDA) for the treatment of obesity, will suppress oxycodone self administration and oxycodone associated cue reactivity in rats.
+HTR2C	drug	amphetamine	27986974	Thus, we examined the effects of a <strong>5 HT2C</strong> receptor agonist, WAY163909, and a 5 HT2A receptor antagonist, M100907, given alone and in combination, on actigraphy based sleep parameters disrupted by <b>methamphetamine</b> self administration in non human primates.
+HTR2C	addiction	addiction	27903793	The serotonin <strong>5 HT2C</strong> receptor and the non <b>addictive</b> nature of classic hallucinogens.
+HTR2C	addiction	addiction	27903793	However, many preclinical studies show that <strong>5 HT2C</strong> agonists counteract the <b>addictive</b> effects of drugs from several classes, suggesting this pharmacological property of classic hallucinogens may be significant.
+HTR2C	addiction	reward	27903793	<strong>5 HT2C</strong> agonists work, in part, by modulating dopamine neuron activity in the ventral tegmental area nucleus accumbens (NAc) <b>reward</b> pathway.
+HTR2C	drug	cocaine	27903793	Together with experiments that show that addictive drugs, such as <b>cocaine</b>, potentiate Kv1.x channels, thereby suppressing NAc shell GABAergic activity, this hypothesis provides a mechanism by which classic hallucinogen mediated stimulation of <strong>5 HT2C</strong> receptors could thwart addiction.
+HTR2C	addiction	addiction	27903793	Together with experiments that show that <b>addictive</b> drugs, such as cocaine, potentiate Kv1.x channels, thereby suppressing NAc shell GABAergic activity, this hypothesis provides a mechanism by which classic hallucinogen mediated stimulation of <strong>5 HT2C</strong> receptors could thwart <b>addiction</b>.
+HTR2C	drug	cocaine	27857126	Repeated 7 Day Treatment with the <strong>5 HT2C</strong> Agonist Lorcaserin or the 5 HT2A Antagonist Pimavanserin Alone or in Combination Fails to Reduce <b>Cocaine</b> vs Food Choice in Male Rhesus Monkeys.
+HTR2C	drug	cocaine	27857126	Therefore, the present study aim was to determine whether repeated 7 day treatment with the <strong>5 HT2C</strong> agonist lorcaserin (0.1 1.0 mg/kg per day, intramuscular; 0.032 0.1 mg/kg/h, intravenous) or the 5 HT2A inverse agonist/antagonist pimavanserin (0.32 10 mg/kg per day, intramuscular) attenuated <b>cocaine</b> reinforcement under a concurrent 'choice' schedule of <b>cocaine</b> and food availability in rhesus monkeys.
+HTR2C	addiction	reward	27857126	Therefore, the present study aim was to determine whether repeated 7 day treatment with the <strong>5 HT2C</strong> agonist lorcaserin (0.1 1.0 mg/kg per day, intramuscular; 0.032 0.1 mg/kg/h, intravenous) or the 5 HT2A inverse agonist/antagonist pimavanserin (0.32 10 mg/kg per day, intramuscular) attenuated cocaine <b>reinforcement</b> under a concurrent 'choice' schedule of cocaine and food availability in rhesus monkeys.
+HTR2C	drug	cocaine	27857126	These results suggest that neither <strong>5 HT2C</strong> receptor activation nor 5 HT2A receptor blockade are sufficient to produce a therapeutic like decrease in <b>cocaine</b> choice and a complementary increase in food choice.
+HTR2C	drug	cocaine	27857126	Overall, these results do not support the clinical utility of <strong>5 HT2C</strong> agonists and 5 HT2A inverse agonists/antagonists alone or in combination as candidate anti <b>cocaine</b> use disorder pharmacotherapies.
+HTR2C	addiction	reward	27815511	To our knowledge, this is the first demonstration in humans of a potential role of <strong>5 HT2C</strong> agonism in the modulation of central neurological circuits involved with <b>reward</b>.
+HTR2C	drug	cocaine	27650954	The serotonin2C [5 hydroxytryptamine2C (<strong>5 HT2C</strong>)] receptor agonist lorcaserin decreases some abuse related effects of <b>cocaine</b> in monkeys and might be useful for treating stimulant abuse.
+HTR2C	drug	amphetamine	26011513	In the hypothalamus, PRS increased ERα and ERβ estrogen receptor and CARTP (cocaine and <b>amphetamine</b> receptor transcript peptide) mRNA levels in males, and <strong>5 HT2C</strong> receptor mRNA levels in females.
+HTR2C	drug	cocaine	26011513	In the hypothalamus, PRS increased ERα and ERβ estrogen receptor and CARTP (<b>cocaine</b> and amphetamine receptor transcript peptide) mRNA levels in males, and <strong>5 HT2C</strong> receptor mRNA levels in females.
+HTR2C	drug	cocaine	26926963	Incubation of <b>cocaine</b> cue reactivity associates with neuroadaptations in the cortical serotonin (5 HT) <strong>5 HT2C</strong> receptor (5 HT2CR) system.
+HTR2C	drug	cocaine	26926963	We tested the hypothesis that incubation of cue reactivity during abstinence from <b>cocaine</b> self administration is accompanied by lower potency and/or efficacy of the selective serotonin (5 HT) <strong>5 HT2C</strong>​ receptor (5 HT2CR) agonist WAY163909 to suppress cue reactivity and a shift in the subcellular localization profile of the mPFC 5 HT2CR protein.
+HTR2C	drug	nicotine	26704812	We have found in the rat model that the H1 histamine antagonist pyrilamine and the serotonin <strong>5HT2C</strong> agonist lorcaserin also significantly reduce <b>nicotine</b> self administration.
+HTR2C	drug	cannabinoid	26464979	These include the dopamine 1 receptor (D1R), the dopamine 2 receptor (D2R), the melanocortin 3 receptor (MC3R), the serotonin 2C receptor (<strong>5 HT2C</strong>), and possibly the <b>cannabinoid</b> type 1 receptor (CB1).
+HTR2C	addiction	relapse	26375926	Pharmacological activation of <strong>5 HT2C</strong> receptors (5 HT2CRs) suppresses psychostimulant induced drug <b>seeking</b> and behavioral sensitization.
+HTR2C	addiction	sensitization	26375926	Pharmacological activation of <strong>5 HT2C</strong> receptors (5 HT2CRs) suppresses psychostimulant induced drug seeking and behavioral <b>sensitization</b>.
+HTR2C	drug	psychedelics	26068050	The results showed that chronic <b>MDMA</b> caused hippocampal protein deficits in adolescent and young adult rats at different levels: (1) impaired serotonergic (5 HT2A and <strong>5 HT2C</strong> post synaptic receptors) and GABAergic (GAD2 enzyme) signaling, and (2) decreased structural cytoskeletal neurofilament proteins (NF H, NF M and NF L).
+HTR2C	drug	psychedelics	26041338	The aim of this study is to investigate whether <strong>5 HT2C</strong> receptor activation is necessary for rate decreasing effects produced in an ICSS procedure in rats by the 5 HT selective monoamine releaser fenfluramine and the non selective releasers napthylisopropylamine (PAL 287) and (+) 3,4 <b>methylenedioxymethamphetamine</b> ((+) <b>MDMA</b>).
+HTR2C	addiction	reward	26041338	The aim of this study is to investigate whether <strong>5 HT2C</strong> receptor activation is necessary for rate decreasing effects produced in an <b>ICSS</b> procedure in rats by the 5 HT selective monoamine releaser fenfluramine and the non selective releasers napthylisopropylamine (PAL 287) and (+) 3,4 methylenedioxymethamphetamine ((+) MDMA).
+HTR2C	drug	psychedelics	26041338	Effectiveness of the <strong>5 HT2C</strong> antagonist SB 242,084 was evaluated to block rate decreasing effects produced by (1) the <strong>5 HT2C</strong> agonist Ro 60 0175, (2) the 5 HT selective releaser fenfluramine, and (3) the mixed action dopamine (DA)/norepinephrine (NE)/5 HT releasers PAL 287 (1.0 5.6 mg/kg) and (+) <b>MDMA</b> (1.0 3.2 mg/kg).
+HTR2C	addiction	reward	26041338	These data suggest that <strong>5 HT2C</strong> receptor activation contributes to rate decreasing effects that are produced by selective and mixed action 5 HT releasers in rats and that may oppose and limit the expression of abuse related <b>ICSS</b> facilitation by these compounds.
+HTR2C	drug	nicotine	26031442	Discovering the mechanisms underlying serotonin (5 HT)2A and <strong>5 HT2C</strong> receptor regulation following <b>nicotine</b> withdrawal in rats.
+HTR2C	addiction	withdrawal	26031442	Discovering the mechanisms underlying serotonin (5 HT)2A and <strong>5 HT2C</strong> receptor regulation following nicotine <b>withdrawal</b> in rats.
+HTR2C	drug	nicotine	26031442	These results show that the reduction in the 5 HT2A receptor transcript level may be an auto regulatory response to the increased receptor density in the hippocampus and ventral tegmental area during <b>nicotine</b> withdrawal, while decreased <strong>5 HT2C</strong> receptor mRNA editing may explain the reduction in receptor labeling in the hippocampus.
+HTR2C	addiction	withdrawal	26031442	These results show that the reduction in the 5 HT2A receptor transcript level may be an auto regulatory response to the increased receptor density in the hippocampus and ventral tegmental area during nicotine <b>withdrawal</b>, while decreased <strong>5 HT2C</strong> receptor mRNA editing may explain the reduction in receptor labeling in the hippocampus.
+HTR2C	drug	nicotine	26031442	Here, we show that the reduction in 5 HT2A receptor transcript level may be an auto regulatory response to the increased receptor number in the hippocampus and ventral tegmental area during <b>nicotine</b> withdrawal, while attenuated <strong>5 HT2C</strong> receptor mRNA editing in the hippocampus might explain reduced inverse agonist binding to <strong>5 HT2C</strong> receptor and suggest a shift toward a population of more active receptors.
+HTR2C	addiction	withdrawal	26031442	Here, we show that the reduction in 5 HT2A receptor transcript level may be an auto regulatory response to the increased receptor number in the hippocampus and ventral tegmental area during nicotine <b>withdrawal</b>, while attenuated <strong>5 HT2C</strong> receptor mRNA editing in the hippocampus might explain reduced inverse agonist binding to <strong>5 HT2C</strong> receptor and suggest a shift toward a population of more active receptors.
+HTR2C	drug	nicotine	25933953	Context controlled <b>nicotine</b> induced changes in the labeling of serotonin (5 HT)2A and <strong>5 HT2C</strong> receptors in the rat brain.
+HTR2C	drug	nicotine	25933953	We have previously demonstrated that serotonin (5 HT)2A and <strong>5 HT2C</strong> receptor ligands modulate the sensitizing effects of <b>nicotine</b>.
+HTR2C	drug	nicotine	25933953	In the present study we used male rats to verify the hypothesis that the binding pattern of 5 HT2A and <strong>5 HT2C</strong> receptors in the brain is altered by chronic <b>nicotine</b> treatment in different environments.
+HTR2C	drug	nicotine	25933953	Repeated treatment with <b>nicotine</b> in home cages evoked significant increases in [(3)H]ketanserin binding to 5 HT2A receptors in the prefrontal cortex, striatal subregions and ventral tegmental area as well as reductions in [(3)H]mesulergine binding to <strong>5 HT2C</strong> receptors in subregions of the prefrontal cortex.
+HTR2C	drug	nicotine	25933953	In contrast, <b>nicotine</b> paired with environmental context produced robust increases in 5 HT2A receptor labeling in the infralimbic cortex and decreased [(3)H]ketanserin binding in striatal subregions and ventral tegmental area; <strong>5 HT2C</strong> receptor labeling in the prefrontal cortex fell.
+HTR2C	drug	nicotine	25933953	The present data indicate that chronic <b>nicotine</b> administration in home cages induces bi directional neuroplastic changes within 5 HT2A and <strong>5 HT2C</strong> receptors in the prefrontal cortex.
+HTR2C	drug	cocaine	25877746	Attenuation of <b>cocaine</b> induced reinstatement of drug seeking in squirrel monkeys by direct and indirect activation of <strong>5 HT2C</strong> receptors.
+HTR2C	addiction	relapse	25877746	Attenuation of cocaine induced <b>reinstatement</b> of drug <b>seeking</b> in squirrel monkeys by direct and indirect activation of <strong>5 HT2C</strong> receptors.
+HTR2C	drug	cocaine	25877746	5 Hydroxytryptamine (5 HT) transport inhibitors can attenuate the abuse related effects of <b>cocaine</b>, and the mechanisms underlying this attenuation may involve activation of <strong>5 HT2C</strong> receptors.
+HTR2C	drug	cocaine	25877746	The objective of this study was to investigate the consequences of direct and indirect pharmacological activation of <strong>5 HT2C</strong> receptors on reinstatement of <b>cocaine</b> seeking behavior induced by <b>cocaine</b> priming and a <b>cocaine</b> paired stimulus.
+HTR2C	addiction	relapse	25877746	The objective of this study was to investigate the consequences of direct and indirect pharmacological activation of <strong>5 HT2C</strong> receptors on <b>reinstatement</b> of cocaine <b>seeking</b> behavior induced by cocaine priming and a cocaine paired stimulus.
+HTR2C	drug	cocaine	25877746	Pretreatment with either the 5 HT transport inhibitor fluoxetine (5.6 mg/kg) or the <strong>5 HT2C</strong> receptor agonist Ro 60 0175 (1 mg/kg) attenuated reinstatement of drug seeking by <b>cocaine</b> priming.
+HTR2C	addiction	relapse	25877746	Pretreatment with either the 5 HT transport inhibitor fluoxetine (5.6 mg/kg) or the <strong>5 HT2C</strong> receptor agonist Ro 60 0175 (1 mg/kg) attenuated <b>reinstatement</b> of drug <b>seeking</b> by cocaine priming.
+HTR2C	addiction	relapse	25877746	The <b>reinstatement</b> attenuating effects of both drugs were reversed by the <strong>5 HT2C</strong> receptor antagonist SB 242084 (0.03 0.56 mg/kg).
+HTR2C	drug	cocaine	25877746	<strong>5 HT2C</strong> receptor mechanisms play a key role in the modulation of <b>cocaine</b> induced reinstatement by fluoxetine and Ro 60 0175.
+HTR2C	addiction	relapse	25877746	<strong>5 HT2C</strong> receptor mechanisms play a key role in the modulation of cocaine induced <b>reinstatement</b> by fluoxetine and Ro 60 0175.
+HTR2C	drug	cocaine	25877746	Direct activation of <strong>5 HT2C</strong> receptors may offer a novel, tolerance free therapeutic strategy for the prevention of <b>cocaine</b> relapse.
+HTR2C	addiction	relapse	25877746	Direct activation of <strong>5 HT2C</strong> receptors may offer a novel, tolerance free therapeutic strategy for the prevention of cocaine <b>relapse</b>.
+HTR2C	addiction	addiction	25870913	Therapeutic Potential of <strong>5 HT2C</strong> Receptor Agonists for <b>Addictive</b> Disorders.
+HTR2C	drug	alcohol	25870913	This review examines evidence to support the use of selective <strong>5 HT2C</strong> receptor agonists as treatments for conditions beyond obesity, including substance abuse (particularly nicotine, psychostimulant, and <b>alcohol</b> dependence), obsessive compulsive, and excessive gambling disorder.
+HTR2C	drug	nicotine	25870913	This review examines evidence to support the use of selective <strong>5 HT2C</strong> receptor agonists as treatments for conditions beyond obesity, including substance abuse (particularly <b>nicotine</b>, psychostimulant, and alcohol dependence), obsessive compulsive, and excessive gambling disorder.
+HTR2C	addiction	addiction	25870913	This review examines evidence to support the use of selective <strong>5 HT2C</strong> receptor agonists as treatments for conditions beyond obesity, including substance abuse (particularly nicotine, psychostimulant, and alcohol dependence), obsessive <b>compulsive</b>, and excessive gambling disorder.
+HTR2C	addiction	dependence	25870913	This review examines evidence to support the use of selective <strong>5 HT2C</strong> receptor agonists as treatments for conditions beyond obesity, including substance abuse (particularly nicotine, psychostimulant, and alcohol <b>dependence</b>), obsessive compulsive, and excessive gambling disorder.
+HTR2C	addiction	reward	25870913	We then highlight the critical involvement of the <strong>5 HT2C</strong> receptor in mediating the effect of (dex)fenfluramine on feeding and body weight gain and the evidence that <strong>5 HT2C</strong> receptor agonists reduce measures of drug <b>reward</b> and impulsivity.
+HTR2C	drug	nicotine	25870913	A recent report of lorcaserin efficacy in a <b>smoking</b> cessation trial further strengthens the idea that <strong>5 HT2C</strong> receptor agonists may have potential as a treatment for addiction.
+HTR2C	addiction	addiction	25870913	A recent report of lorcaserin efficacy in a smoking cessation trial further strengthens the idea that <strong>5 HT2C</strong> receptor agonists may have potential as a treatment for <b>addiction</b>.
+HTR2C	addiction	reward	25781911	We previously suggested that <strong>5 HT2C</strong> receptor agonists affect <b>reward</b> processes and reduce the rewarding effects of drugs of abuse.
+HTR2C	drug	cocaine	25656481	The serotonin system is intimately linked to both the mediation of anxiety and long term effects of <b>cocaine</b>, potentially through interaction of inhibitory <strong>5 HT2C</strong> receptor and gamma aminobutyric acid (GABA) networks.
+HTR2C	drug	cocaine	25656481	This study characterized the function of the dorsal raphe (DR) <strong>5 HT2C</strong> receptor and GABA network in anxiety produced by chronic <b>cocaine</b> withdrawal.
+HTR2C	addiction	withdrawal	25656481	This study characterized the function of the dorsal raphe (DR) <strong>5 HT2C</strong> receptor and GABA network in anxiety produced by chronic cocaine <b>withdrawal</b>.
+HTR2C	drug	cocaine	25656481	In a separate cohort of <b>cocaine</b> injected mice at 25 h of withdrawal, both global and intra DR blockade of <strong>5 HT2C</strong> receptors prior to elevated plus maze testing attenuated anxiety like behavior.
+HTR2C	addiction	withdrawal	25656481	In a separate cohort of cocaine injected mice at 25 h of <b>withdrawal</b>, both global and intra DR blockade of <strong>5 HT2C</strong> receptors prior to elevated plus maze testing attenuated anxiety like behavior.
+HTR2C	drug	cocaine	25656481	This study demonstrates that DR <strong>5 HT2C</strong> receptor blockade prevents anxiety like behavior produced by <b>cocaine</b> withdrawal, potentially through attenuation of heightened GABA activity, supporting a role for the <strong>5 HT2C</strong> receptor in mediating anxiety produced by <b>cocaine</b> withdrawal.
+HTR2C	addiction	withdrawal	25656481	This study demonstrates that DR <strong>5 HT2C</strong> receptor blockade prevents anxiety like behavior produced by cocaine <b>withdrawal</b>, potentially through attenuation of heightened GABA activity, supporting a role for the <strong>5 HT2C</strong> receptor in mediating anxiety produced by cocaine <b>withdrawal</b>.
+HTR2C	drug	cocaine	25505168	However, the 5 HT2A and <strong>5 HT2C</strong> receptors in particular have been implicated as likely candidates for mediating the influence of 5 HT in <b>cocaine</b> abuse as well as to traits (e.g., impulsivity) that contribute to the development of <b>cocaine</b> use disorder and relapse in humans.
+HTR2C	addiction	relapse	25505168	However, the 5 HT2A and <strong>5 HT2C</strong> receptors in particular have been implicated as likely candidates for mediating the influence of 5 HT in cocaine abuse as well as to traits (e.g., impulsivity) that contribute to the development of cocaine use disorder and <b>relapse</b> in humans.
+HTR2C	drug	amphetamine	25417553	Critical involvement of <strong>5 HT2C</strong> receptor function in <b>amphetamine</b> induced 50 kHz ultrasonic vocalizations in rats.
+HTR2C	drug	amphetamine	25417553	Because 50 kHz USV emission is, at least in part, dopamine (DA) dependent and <strong>5 HT2C</strong> agonists inhibit DA neurotransmission, we hypothesized that <b>AMPH</b> induced 50 kHz USV can be attenuated by pretreatment with a <strong>5 HT2C</strong> agonist.
+HTR2C	drug	amphetamine	25417553	In experiment III, rats were pretreated with the <strong>5 HT2C</strong> agonist CP 809,101 (0.0, 0.3, 1.0, 3.0, and 10 mg/kg), while in experiment IV, CP 809,101 (3.0 mg/kg), the <strong>5 HT2C</strong> antagonist SB 242084 (1.0 mg/kg), or the combination of the two, was applied before <b>AMPH</b> administration (2.0 mg/kg).
+HTR2C	drug	amphetamine	25417553	The <strong>5 HT2C</strong> agonist CP 809,101 dose dependently blocked <b>AMPH</b> induced 50 kHz USV, most notably trills, a call subtype that is considered to exclusively reflect a positive affective state, while the <strong>5 HT2C</strong> antagonist SB 242084 induced opposite effects.
+HTR2C	drug	amphetamine	25417553	<strong>5 HT2C</strong> receptors are critically involved in <b>AMPH</b> induced 50 kHz USV, with <strong>5 HT2C</strong> antagonism resulting in a stimulant like effect.
+HTR2C	addiction	relapse	25417553	Attenuation of drug wanting/<b>craving</b> and/or liking by coadministration of a <strong>5 HT2C</strong> agonist could be a translational pharmacodynamic biomarker.
+HTR2C	drug	alcohol	25382408	The serotonin <strong>5 HT2C</strong> receptor has shown promise in vivo as a pharmacotherapeutic target for <b>alcoholism</b>.
+HTR2C	drug	alcohol	25382408	For example, recently, a novel 4 phenyl 2 N,N dimethylaminotetralin (PAT) drug candidate, that demonstrates <strong>5 HT2C</strong> receptor agonist activity together with 5 HT2A/2B receptor inverse agonist activity, was shown to reduce operant responding for <b>ethanol</b> after peripheral administration to rats.
+HTR2C	addiction	reward	25382408	For example, recently, a novel 4 phenyl 2 N,N dimethylaminotetralin (PAT) drug candidate, that demonstrates <strong>5 HT2C</strong> receptor agonist activity together with 5 HT2A/2B receptor inverse agonist activity, was shown to reduce <b>operant</b> responding for ethanol after peripheral administration to rats.
+HTR2C	drug	alcohol	25382408	Thus, in contrast to results reported for the VTA, current results suggest <strong>5 HT2C</strong> receptor agonists decrease stimulated GABA release in the NAcc, and provide a possible mechanism of action for 5HT2C  mediated negative modulation of <b>ethanol</b> self administration.
+HTR2C	drug	alcohol	25382408	Thus, in contrast to results reported for the VTA, current results suggest <strong>5 HT2C</strong> receptor agonists decrease stimulated GABA release in the NAcc, and provide a possible mechanism of action for <strong>5HT2C</strong>  mediated negative modulation of <b>ethanol</b> self administration.
+HTR2C	drug	amphetamine	25229719	Nucleus accumbens shell excitability is decreased by <b>methamphetamine</b> self administration and increased by <strong>5 HT2C</strong> receptor inverse agonism and agonism.
+HTR2C	addiction	relapse	25229719	One therapeutic target showing preclinical promise at attenuating psychostimulant <b>seeking</b> is <strong>5 HT2C</strong> receptors; however, the effects of <strong>5 HT2C</strong> receptor ligands on neuronal physiology are unclear.
+HTR2C	drug	amphetamine	25229719	<strong>5 HT2C</strong> receptor agonism decreases psychostimulant mediated behaviors, and the putative <strong>5 HT2C</strong> receptor inverse agonist, SB 206553, attenuates <b>methamphetamine</b> seeking in rats.
+HTR2C	addiction	relapse	25229719	<strong>5 HT2C</strong> receptor agonism decreases psychostimulant mediated behaviors, and the putative <strong>5 HT2C</strong> receptor inverse agonist, SB 206553, attenuates methamphetamine <b>seeking</b> in rats.
+HTR2C	drug	amphetamine	25229719	To ascertain the effects of <b>methamphetamine</b>, and <strong>5 HT2C</strong> receptor inverse agonism and agonism, on neuronal function in the nucleus accumbens, we evaluated <b>methamphetamine</b>, SB 206553, and the <strong>5 HT2C</strong> receptor agonist and Ro 60 0175, on neuronal excitability within the accumbens shell subregion using whole cell current clamp recordings in forebrain slices ex vivo.
+HTR2C	drug	amphetamine	25229719	These findings demonstrate that <b>methamphetamine</b> induced decreases in excitability of neurons within the nucleus accumbens shell were abrogated by both <strong>5 HT2C</strong> inverse agonism and agonism, and this effect likely involved activation of Gq mediated signaling pathways.
+HTR2C	drug	alcohol	25229718	<b>Ethanol</b> induced adaptations in <strong>5 HT2c</strong> receptor signaling in the bed nucleus of the stria terminalis: implications for anxiety during <b>ethanol</b> withdrawal.
+HTR2C	addiction	withdrawal	25229718	Ethanol induced adaptations in <strong>5 HT2c</strong> receptor signaling in the bed nucleus of the stria terminalis: implications for anxiety during ethanol <b>withdrawal</b>.
+HTR2C	drug	alcohol	25229718	Using a model of chronic intermittent <b>ethanol</b> (CIE) vapor in mice, we investigated the role of serotonin2c receptor (<strong>5HT2c</strong> R) signaling in the BNST as a neural substrate underlying <b>ethanol</b> induced anxiety during withdrawal.
+HTR2C	addiction	withdrawal	25229718	Using a model of chronic intermittent ethanol (CIE) vapor in mice, we investigated the role of serotonin2c receptor (<strong>5HT2c</strong> R) signaling in the BNST as a neural substrate underlying ethanol induced anxiety during <b>withdrawal</b>.
+HTR2C	addiction	withdrawal	25229718	Using immunohistochemistry and whole cell patch clamp electrophysiology, we also found that CIE increased FOS IR and enhanced neuronal excitability in the ventral BNST (vBNST) 24 h into <b>withdrawal</b> in a <strong>5HT2c</strong> R dependent manner.
+HTR2C	drug	nicotine	25158104	In this study, we assessed roles for dopamine (DA) D1 or D2 receptors, and two serotonin (5 HT) receptor subtypes known to modulate DA activity, the <strong>5 HT2C</strong> or 5 HT2A subtypes, on <b>nicotine</b> enhanced responding for a conditioned reinforcer.
+HTR2C	drug	nicotine	25158104	To examine potential roles for dopamine (DA) and serotonin (5 HT) receptors in this effect, separate groups of animals were used to assess the impact of administering the D1 receptor antagonist SCH 23390, D2 receptor antagonist eticlopride, <strong>5 HT2C</strong> receptor agonist Ro 60 0175, or 5 HT2A receptor antagonist M100907 on <b>nicotine</b> enhanced responding for conditioned reinforcement.
+HTR2C	addiction	reward	25158104	To examine potential roles for dopamine (DA) and serotonin (5 HT) receptors in this effect, separate groups of animals were used to assess the impact of administering the D1 receptor antagonist SCH 23390, D2 receptor antagonist eticlopride, <strong>5 HT2C</strong> receptor agonist Ro 60 0175, or 5 HT2A receptor antagonist M100907 on nicotine enhanced responding for conditioned <b>reinforcement</b>.
+HTR2C	drug	alcohol	25109272	The purpose of this study was to evaluate the efficacy of a novel <strong>5 HT2c</strong> receptor agonist, lorcaserin for reducing <b>alcohol</b> consumption in <b>alcohol</b> preferring (P) rats.
+HTR2C	drug	alcohol	25109272	These results show the efficacy of lorcaserin in reducing <b>alcohol</b> intake without a significant effect on water intake and locomotion suggesting the involvement of <strong>5 HT2c</strong> receptors in <b>alcohol</b> seeking behavior.
+HTR2C	addiction	relapse	25109272	These results show the efficacy of lorcaserin in reducing alcohol intake without a significant effect on water intake and locomotion suggesting the involvement of <strong>5 HT2c</strong> receptors in alcohol <b>seeking</b> behavior.
+HTR2C	drug	cocaine	24984080	Effects of the <strong>5 HT2C</strong> receptor agonist CP809101 in the amygdala on reinstatement of <b>cocaine</b> seeking behavior and anxiety like behavior.
+HTR2C	addiction	relapse	24984080	Effects of the <strong>5 HT2C</strong> receptor agonist CP809101 in the amygdala on <b>reinstatement</b> of cocaine <b>seeking</b> behavior and anxiety like behavior.
+HTR2C	drug	nicotine	24953434	In the current study, using the operant licking <b>nicotine</b> self administration model with young adult Sprague Dawley rats (0.03mg/kg/infusion of <b>nicotine</b>), we tested the effect of antagonists of H1 histamine receptors pyrilamine, serotonin (5HT) type 2 receptors ketanserin and N methyl d aspartate (NMDA) glutamate receptors with d cycloserine as well as an agonist of <strong>5HT2c</strong> receptors lorcaserin, in dose ranges that we have found in previous studies to significantly reduce IV <b>nicotine</b> self administration with the operant lever press operand.
+HTR2C	addiction	reward	24953434	In the current study, using the <b>operant</b> licking nicotine self administration model with young adult Sprague Dawley rats (0.03mg/kg/infusion of nicotine), we tested the effect of antagonists of H1 histamine receptors pyrilamine, serotonin (5HT) type 2 receptors ketanserin and N methyl d aspartate (NMDA) glutamate receptors with d cycloserine as well as an agonist of <strong>5HT2c</strong> receptors lorcaserin, in dose ranges that we have found in previous studies to significantly reduce IV nicotine self administration with the <b>operant</b> lever press operand.
+HTR2C	drug	nicotine	24953434	The <strong>5HT2C</strong> agonist lorcaserin significantly decreased <b>nicotine</b> self administration in the licking paradigm at the same dose threshold as with lever press responding.
+HTR2C	addiction	intoxication	24763081	Furthermore, MA <b>binge</b> exposure increased 5 HT2A and decreased mGlu2 receptor expression in the medial frontal cortex, whereas <strong>5 HT2C</strong> and 5 HT1A receptors were unaffected.
+HTR2C	drug	cocaine	24618688	In the present translational study, we investigated the contribution of variation in the serotonin (5 HT) <strong>5 HT2C</strong> receptor (5 HT2CR) system in individual differences in <b>cocaine</b> cue reactivity in humans and rodents.
+HTR2C	drug	cocaine	24618688	We found that <b>cocaine</b> dependent subjects carrying a single nucleotide polymorphism (SNP) in the <strong>HTR2C</strong> gene that encodes for the conversion of cysteine to serine at codon 23 (Ser23 variant) exhibited significantly higher attentional bias to <b>cocaine</b> cues in the <b>cocaine</b> word Stroop task than those carrying the Cys23 variant.
+HTR2C	drug	alcohol	24041931	Serotonin (5 HT) <strong>5 HT2C</strong> receptor agonists have shown promise as novel <b>alcoholism</b> pharmacotherapies, but developing selective agonists has been problematic.
+HTR2C	addiction	reward	24041931	<strong>5 HT2C</strong> receptor modulators (Ro60 0175, SB242,084, and ( ) trans PAT) were administered before <b>operant</b> sessions.
+HTR2C	drug	alcohol	24041931	As a control for the effects of <strong>5 HT2C</strong> receptor agonism on caloric intake, drugs were also tested using non <b>ethanol</b> containing gelatin.
+HTR2C	drug	alcohol	24041931	Ro60 0175, a 5 HT2 family receptor agonist, decreased both <b>ethanol</b> and vehicle responding while ( ) trans PAT, a <strong>5 HT2C</strong> receptor agonist with 5 HT2A 2B receptor inverse agonist activity, selectively reduced only <b>ethanol</b> responding.
+HTR2C	drug	alcohol	24041931	The effect of <strong>5 HT2C</strong> receptor agonists on self administration after reinstatement of <b>ethanol</b> after a three week deprivation was also determined.
+HTR2C	addiction	relapse	24041931	The effect of <strong>5 HT2C</strong> receptor agonists on self administration after <b>reinstatement</b> of ethanol after a three week deprivation was also determined.
+HTR2C	drug	nicotine	24041919	The availability of selective <strong>5 HT2C</strong> agonists provides an opportunity to evaluate their potential as treatments for <b>nicotine</b> dependence or psychostimulant abuse, conditions for which there is significant medical need but only limited available treatment options.
+HTR2C	addiction	dependence	24041919	The availability of selective <strong>5 HT2C</strong> agonists provides an opportunity to evaluate their potential as treatments for nicotine <b>dependence</b> or psychostimulant abuse, conditions for which there is significant medical need but only limited available treatment options.
+HTR2C	drug	cocaine	23939424	Functional status of the serotonin <strong>5 HT2C</strong> receptor (5 HT2CR) drives interlocked phenotypes that precipitate relapse like behaviors in <b>cocaine</b> dependence.
+HTR2C	addiction	dependence	23939424	Functional status of the serotonin <strong>5 HT2C</strong> receptor (5 HT2CR) drives interlocked phenotypes that precipitate relapse like behaviors in cocaine <b>dependence</b>.
+HTR2C	addiction	relapse	23939424	Functional status of the serotonin <strong>5 HT2C</strong> receptor (5 HT2CR) drives interlocked phenotypes that precipitate <b>relapse</b> like behaviors in cocaine dependence.
+HTR2C	drug	cocaine	23748692	This review provides an overview of the role of central serotonin2C (<strong>5 HT2C</strong>) receptors in drug addiction, specifically focusing on their impact on the neurochemical and behavioral effects of <b>cocaine</b>, one of the most worldwide abused drug.
+HTR2C	addiction	addiction	23748692	This review provides an overview of the role of central serotonin2C (<strong>5 HT2C</strong>) receptors in drug <b>addiction</b>, specifically focusing on their impact on the neurochemical and behavioral effects of cocaine, one of the most worldwide abused drug.
+HTR2C	addiction	dependence	23748692	First, we described the neurochemical and electrophysiological mechanisms underlying the interaction between <strong>5 HT2C</strong> receptors and the mesocorticolimbic dopaminergic network, in keeping with the key role of this system in drug abuse and <b>dependence</b>.
+HTR2C	drug	cocaine	23748692	Thereafter, we focused on the role of <strong>5 HT2C</strong> receptors in the effects of <b>cocaine</b> in various preclinical behavioral models used in drug addiction research, such as locomotor hyperactivity, locomotor sensitization, drug discrimination, and self administration, to end with an overview of the neurochemical mechanisms underlying the interactions between <strong>5 HT2C</strong> receptors, mesocorticolimbic dopamine system, and <b>cocaine</b>.
+HTR2C	addiction	addiction	23748692	Thereafter, we focused on the role of <strong>5 HT2C</strong> receptors in the effects of cocaine in various preclinical behavioral models used in drug <b>addiction</b> research, such as locomotor hyperactivity, locomotor sensitization, drug discrimination, and self administration, to end with an overview of the neurochemical mechanisms underlying the interactions between <strong>5 HT2C</strong> receptors, mesocorticolimbic dopamine system, and cocaine.
+HTR2C	addiction	sensitization	23748692	Thereafter, we focused on the role of <strong>5 HT2C</strong> receptors in the effects of cocaine in various preclinical behavioral models used in drug addiction research, such as locomotor hyperactivity, locomotor <b>sensitization</b>, drug discrimination, and self administration, to end with an overview of the neurochemical mechanisms underlying the interactions between <strong>5 HT2C</strong> receptors, mesocorticolimbic dopamine system, and cocaine.
+HTR2C	drug	cocaine	23748692	On their whole, the presented data provide compelling preclinical evidence that <strong>5 HT2C</strong> receptor agonists may have efficacy in the treatment of <b>cocaine</b> abuse and dependence, thereby underlying the need for additional clinical studies to ascertain whether preclinical data translate to the human.
+HTR2C	addiction	dependence	23748692	On their whole, the presented data provide compelling preclinical evidence that <strong>5 HT2C</strong> receptor agonists may have efficacy in the treatment of cocaine abuse and <b>dependence</b>, thereby underlying the need for additional clinical studies to ascertain whether preclinical data translate to the human.
+HTR2C	drug	cocaine	23632436	<b>Cocaine</b> modulation of frontostriatal expression of Zif268, D2, and <strong>5 HT2c</strong> receptors in high and low impulsive rats.
+HTR2C	drug	cocaine	23632436	We used in situ hybridization to map brain expression of two major genes implicated in impulsivity, encoding the dopamine D2 receptor (DA D2R) and the <strong>5 HT2c</strong> receptor (5 HT2cR), and an immediate early gene associated with neuronal plasticity, zif268, in groups of rats selected for HI and low impulsivity (LI) on a 5 choice serial reaction time task (5 CSRTT) immediately after 5 CSRTT training, and following 10 or 50 days of <b>cocaine</b> self administration.
+HTR2C	drug	opioid	23323881	The results indicate that ADAR2 transgenic mice exhibit, (1) a food preference for diets with higher fat content, (2) significantly increased food intake that is non distractible in a competing reward environment, (3) significantly increased messenger RNA (mRNA) expressions of ADAR2, serotonin 2C receptor (<strong>5HT2C</strong> R), D1, D2 and mu <b>opioid</b> receptors and no change in corticotropin releasing hormone mRNAs and significantly reduced ADAR2 protein expression in the hypothalamus, (4) significantly increased D1 receptor and altered bioamines with no change in ADAR2, mu <b>opioid</b> and D2 receptor mRNA expression in the striatum and (5) significantly greater glucose metabolism in the hypothalamus, brain stem, right hippocampus, left and right mid brain regions and suprascapular peripheral tissue than controls.
+HTR2C	addiction	reward	23323881	The results indicate that ADAR2 transgenic mice exhibit, (1) a food preference for diets with higher fat content, (2) significantly increased food intake that is non distractible in a competing <b>reward</b> environment, (3) significantly increased messenger RNA (mRNA) expressions of ADAR2, serotonin 2C receptor (<strong>5HT2C</strong> R), D1, D2 and mu opioid receptors and no change in corticotropin releasing hormone mRNAs and significantly reduced ADAR2 protein expression in the hypothalamus, (4) significantly increased D1 receptor and altered bioamines with no change in ADAR2, mu opioid and D2 receptor mRNA expression in the striatum and (5) significantly greater glucose metabolism in the hypothalamus, brain stem, right hippocampus, left and right mid brain regions and suprascapular peripheral tissue than controls.
+HTR2C	addiction	reward	23192316	Food restricted <strong>5 HT2C</strong> receptor null mutant and wild type (WT) mice were trained on the 5 CSRT test in which subjects detect and correctly respond to brief light stimuli for food <b>reinforcement</b>.
+HTR2C	drug	nicotine	23184281	The primary aim was to evaluate the highly selective <strong>5 HT2C</strong> agonist, CP 809101, against food motivated (operant FR5 and progressive ratio schedules, palatability induced feeding) and <b>nicotine</b> motivated (intravenous self administration, drug discrimination) behaviours in rats and to compare with equivalent findings for the structurally distinct <strong>5 HT2C</strong> receptor agonists lorcaserin and Ro 60 0175.
+HTR2C	addiction	reward	23184281	The primary aim was to evaluate the highly selective <strong>5 HT2C</strong> agonist, CP 809101, against food motivated (<b>operant</b> FR5 and progressive ratio schedules, palatability induced feeding) and nicotine motivated (intravenous self administration, drug discrimination) behaviours in rats and to compare with equivalent findings for the structurally distinct <strong>5 HT2C</strong> receptor agonists lorcaserin and Ro 60 0175.
+HTR2C	drug	nicotine	23184281	These studies support the utility of <strong>5 HT2C</strong> agonists as a therapeutic approach to treat <b>nicotine</b> dependence.
+HTR2C	addiction	dependence	23184281	These studies support the utility of <strong>5 HT2C</strong> agonists as a therapeutic approach to treat nicotine <b>dependence</b>.
+HTR2C	drug	cocaine	22763621	Depleting forebrain serotonin induced compulsive <b>cocaine</b> seeking in rats with a limited <b>cocaine</b> taking history; this was reversed by systemic treatment with a 5 hydroxytryptamine (<strong>5 HT2C</strong>) receptor agonist and mimicked by systemic treatment with a <strong>5 HT2C</strong> receptor antagonist in intact animals.
+HTR2C	addiction	addiction	22763621	Depleting forebrain serotonin induced <b>compulsive</b> cocaine seeking in rats with a limited cocaine taking history; this was reversed by systemic treatment with a 5 hydroxytryptamine (<strong>5 HT2C</strong>) receptor agonist and mimicked by systemic treatment with a <strong>5 HT2C</strong> receptor antagonist in intact animals.
+HTR2C	addiction	relapse	22763621	Depleting forebrain serotonin induced compulsive cocaine <b>seeking</b> in rats with a limited cocaine taking history; this was reversed by systemic treatment with a 5 hydroxytryptamine (<strong>5 HT2C</strong>) receptor agonist and mimicked by systemic treatment with a <strong>5 HT2C</strong> receptor antagonist in intact animals.
+HTR2C	drug	amphetamine	22697313	SB 206553, a putative <strong>5 HT2C</strong> inverse agonist, attenuates <b>methamphetamine</b> seeking in rats.
+HTR2C	addiction	relapse	22697313	SB 206553, a putative <strong>5 HT2C</strong> inverse agonist, attenuates methamphetamine <b>seeking</b> in rats.
+HTR2C	drug	amphetamine	22697313	To help distinguish the roles for antagonism vs. inverse agonism, here we explored the ability of a more selective <strong>5 HT2C</strong> inverse agonist, SB 206553 to attenuate <b>meth</b> seeking behavior, and compared its effects to those obtained with <strong>5 HT2C</strong> antagonists, SDZ Ser 082 and SB 242084.
+HTR2C	addiction	relapse	22697313	To help distinguish the roles for antagonism vs. inverse agonism, here we explored the ability of a more selective <strong>5 HT2C</strong> inverse agonist, SB 206553 to attenuate meth <b>seeking</b> behavior, and compared its effects to those obtained with <strong>5 HT2C</strong> antagonists, SDZ Ser 082 and SB 242084.
+HTR2C	drug	amphetamine	22697313	Motor function was largely unaltered by the <strong>5 HT2C</strong> ligands; however, SB 206553, at the highest dose tested (10.0 mg/kg), attenuated <b>meth</b> induced rearing behavior.
+HTR2C	drug	amphetamine	22697313	The lack of effect by <strong>5 HT2C</strong> antagonists suggests that <b>meth</b> seeking and <b>meth</b> evoked motor activity are independent of endogenous 5 HT acting at <strong>5 HT2C</strong> receptors.
+HTR2C	addiction	relapse	22697313	The lack of effect by <strong>5 HT2C</strong> antagonists suggests that meth <b>seeking</b> and meth evoked motor activity are independent of endogenous 5 HT acting at <strong>5 HT2C</strong> receptors.
+HTR2C	drug	amphetamine	22697313	While SB 206553 dramatically impacted <b>meth</b> evoked behaviors it is unclear whether the observed effects were <strong>5 HT2C</strong> receptor mediated.
+HTR2C	drug	nicotine	22342986	Effects of the <strong>5 HT2C</strong> receptor agonist Ro60 0175 and the 5 HT2A receptor antagonist M100907 on <b>nicotine</b> self administration and reinstatement.
+HTR2C	addiction	relapse	22342986	Effects of the <strong>5 HT2C</strong> receptor agonist Ro60 0175 and the 5 HT2A receptor antagonist M100907 on nicotine self administration and <b>reinstatement</b>.
+HTR2C	drug	nicotine	22189292	The <strong>5 HT2C</strong> receptor agonist lorcaserin reduces <b>nicotine</b> self administration, discrimination, and reinstatement: relationship to feeding behavior and impulse control.
+HTR2C	addiction	relapse	22189292	The <strong>5 HT2C</strong> receptor agonist lorcaserin reduces nicotine self administration, discrimination, and <b>reinstatement</b>: relationship to feeding behavior and impulse control.
+HTR2C	drug	cocaine	21989806	Individual differences in the improvement of <b>cocaine</b> induced place preference response by the <strong>5 HT2C</strong> receptor antagonist SB242084 in rats.
+HTR2C	drug	alcohol	21658435	Administration of the <strong>5 HT2C</strong> receptor antagonist SB 242084 into the nucleus accumbens blocks the expression of <b>ethanol</b> induced behavioral sensitization in Albino Swiss mice.
+HTR2C	addiction	sensitization	21658435	Administration of the <strong>5 HT2C</strong> receptor antagonist SB 242084 into the nucleus accumbens blocks the expression of ethanol induced behavioral <b>sensitization</b> in Albino Swiss mice.
+HTR2C	drug	nicotine	21636655	Lorcaserin, a <strong>5 HT2C</strong> agonist, decreases <b>nicotine</b> self administration in female rats.
+HTR2C	drug	alcohol	20974231	We previously demonstrated that <b>ethanol</b> enhances GABA release onto VTA DA neurons via activation of <strong>5 HT2C</strong> receptors and subsequent release of calcium from intracellular stores.
+HTR2C	drug	cocaine	20814782	Blockade of nucleus accumbens 5 HT2A and <strong>5 HT2C</strong> receptors prevents the expression of <b>cocaine</b> induced behavioral and neurochemical sensitization in rats.
+HTR2C	addiction	sensitization	20814782	Blockade of nucleus accumbens 5 HT2A and <strong>5 HT2C</strong> receptors prevents the expression of cocaine induced behavioral and neurochemical <b>sensitization</b> in rats.
+HTR2C	addiction	reward	20624416	Genetic and pharmacological evidence that <strong>5 HT2C</strong> receptor activation, but not inhibition, affects motivation to feed under a progressive ratio schedule of <b>reinforcement</b>.
+HTR2C	drug	cocaine	20577718	Role of serotonin 5 HT2A and <strong>5 HT2C</strong> receptors on brain stimulation reward and the reward facilitating effect of <b>cocaine</b>.
+HTR2C	addiction	reward	20577718	Role of serotonin 5 HT2A and <strong>5 HT2C</strong> receptors on brain stimulation <b>reward</b> and the <b>reward</b> facilitating effect of cocaine.
+HTR2C	addiction	reward	20177374	Acquisition session length modulates consolidation effects produced by <strong>5 HT2C</strong> ligands in a mouse autoshaping <b>operant</b> procedure.
+HTR2C	addiction	reward	20177374	In this study, <strong>5 HT2C</strong> receptor ligands of varying relative intrinsic efficacies were tested in a mouse learning and memory model called autoshaping <b>operant</b>.
+HTR2C	addiction	reward	20177374	Day 1 injection of the <strong>5 HT2C</strong> inverse agonist mianserin produced greater retrieval impairments of the autoshaped <b>operant</b> response on day 2 than any other agent tested.
+HTR2C	drug	benzodiazepine	19066419	Responsiveness of <strong>5 HT2C</strong> receptors in repeatedly <b>diazepam</b> injected rats: a behavioral and neurochemical study.
+HTR2C	drug	benzodiazepine	19066419	In view of the withdrawal anxiety associated with repeated <b>diazepam</b> intake, the present study concerns the efficacy of <strong>5 HT2C</strong> receptors in rats treated with <b>diazepam</b>.
+HTR2C	addiction	withdrawal	19066419	In view of the <b>withdrawal</b> anxiety associated with repeated diazepam intake, the present study concerns the efficacy of <strong>5 HT2C</strong> receptors in rats treated with diazepam.
+HTR2C	drug	benzodiazepine	19066419	The behavioral and neurochemical effects of 1 (m chlorophenyl)piperazine (m CPP) (3 mg/kg), a <strong>5 HT2C</strong> agonist, were monitored following withdrawal (three days) from two weeks of <b>diazepam</b> administration.
+HTR2C	addiction	reward	19066419	The behavioral and neurochemical effects of 1 (m chlorophenyl)piperazine (m <b>CPP</b>) (3 mg/kg), a <strong>5 HT2C</strong> agonist, were monitored following withdrawal (three days) from two weeks of diazepam administration.
+HTR2C	addiction	withdrawal	19066419	The behavioral and neurochemical effects of 1 (m chlorophenyl)piperazine (m CPP) (3 mg/kg), a <strong>5 HT2C</strong> agonist, were monitored following <b>withdrawal</b> (three days) from two weeks of diazepam administration.
+HTR2C	addiction	withdrawal	19066419	Results are discussed in the context of the role of <strong>5 HT2C</strong> receptors in the precipitation of <b>withdrawal</b> anxiety.
+HTR2C	drug	nicotine	18950618	Ketanserin, a 5 HT2a and <strong>5 HT2c</strong> receptor antagonist, significantly attenuates <b>nicotine</b> effects on attention and memory.
+HTR2C	drug	nicotine	18805442	Differential effects of <strong>5 HT2C</strong> receptor activation by WAY 161503 on <b>nicotine</b> induced place conditioning and locomotor activity in rats.
+HTR2C	addiction	addiction	18772044	PTEN <strong>5 HT2C</strong> coupling: a new target for treating drug <b>addiction</b>.
+HTR2C	drug	cannabinoid	18571742	We recently found that the interfering peptide Tat 3L4F is able not only to disrupt the protein protein interaction of PTEN (phosphatase and tensin homologue deleted on chromosome 10) with the serotonin <strong>5 HT2C</strong> receptor in the rat ventral tegmental area (VTA) but also to suppress the conditioned place preference induced by <b>cannabinoid</b> and nicotine without significant effects on anxiety, feeding behavior and motor activity.
+HTR2C	drug	nicotine	18571742	We recently found that the interfering peptide Tat 3L4F is able not only to disrupt the protein protein interaction of PTEN (phosphatase and tensin homologue deleted on chromosome 10) with the serotonin <strong>5 HT2C</strong> receptor in the rat ventral tegmental area (VTA) but also to suppress the conditioned place preference induced by cannabinoid and <b>nicotine</b> without significant effects on anxiety, feeding behavior and motor activity.
+HTR2C	drug	alcohol	18311688	Despite the small differences in endocrine and subjective responses between <b>alcoholic</b> patients and controls, the effect of SSRI on endocrine response with respect to <strong>5HT2C</strong> functional alleles deserves further investigation in larger samples to clarify whether this genetic variant constitutes a potential risk factor for changes in neuroendocrine functioning and subsequent psychiatric disorders.
+HTR2C	addiction	withdrawal	18262506	Currently, there is limited information available about the mechanism by which MPDZ influences drug <b>withdrawal</b> and/or other CNS hyperexcitability states, but may involve its interaction with <strong>5 HT2C</strong> and/or GABAB receptors.
+HTR2C	drug	alcohol	18262506	Our results are consistent with the hypothesis that Mpdz's effects on CNS hyperexcitability, including <b>alcohol</b> and barbiturate withdrawal, involve MPDZ interaction with <strong>5 HT2C</strong> and/or GABAB receptors.
+HTR2C	addiction	withdrawal	18262506	Our results are consistent with the hypothesis that Mpdz's effects on CNS hyperexcitability, including alcohol and barbiturate <b>withdrawal</b>, involve MPDZ interaction with <strong>5 HT2C</strong> and/or GABAB receptors.
+HTR2C	drug	cocaine	17989517	Stimulation of <strong>5 HT2C</strong> receptors attenuates cue and <b>cocaine</b> primed reinstatement of <b>cocaine</b> seeking behavior in rats.
+HTR2C	addiction	relapse	17989517	Stimulation of <strong>5 HT2C</strong> receptors attenuates cue and cocaine primed <b>reinstatement</b> of cocaine <b>seeking</b> behavior in rats.
+HTR2C	drug	cocaine	17989517	The extinction/reinstatement model has been used in this study to examine the role of <strong>5 HT2C</strong> receptors in <b>cocaine</b> seeking behavior elicited by <b>cocaine</b> associated cues and <b>cocaine</b> priming injections.
+HTR2C	addiction	relapse	17989517	The extinction/<b>reinstatement</b> model has been used in this study to examine the role of <strong>5 HT2C</strong> receptors in cocaine <b>seeking</b> behavior elicited by cocaine associated cues and cocaine priming injections.
+HTR2C	drug	cocaine	17899022	It has been suggested that the increase in serotonin transmission induced by indirect agonists such as fenfluramine and fluoxetine attenuates cue elicited reinstatement of <b>cocaine</b> seeking in rats through a <strong>5 HT2C</strong> receptor dependent mechanism.
+HTR2C	addiction	relapse	17899022	It has been suggested that the increase in serotonin transmission induced by indirect agonists such as fenfluramine and fluoxetine attenuates cue elicited <b>reinstatement</b> of cocaine <b>seeking</b> in rats through a <strong>5 HT2C</strong> receptor dependent mechanism.
+HTR2C	drug	cocaine	17899022	These findings, provided they can be extrapolated to abstinent human addicts, suggest therapeutic potential for the selective <strong>5 HT2C</strong> agonist in preventing cue controlled <b>cocaine</b> seeking and relapse.
+HTR2C	addiction	relapse	17899022	These findings, provided they can be extrapolated to abstinent human addicts, suggest therapeutic potential for the selective <strong>5 HT2C</strong> agonist in preventing cue controlled cocaine <b>seeking</b> and <b>relapse</b>.
+HTR2C	drug	amphetamine	17805311	Moreover, we show that the effects of SCH23390, a D1 receptor antagonist known to inhibit development of d <b>amphetamine</b> behavioral sensitization, are due to its <strong>5 HT2C</strong> receptor agonist property.
+HTR2C	addiction	sensitization	17805311	Moreover, we show that the effects of SCH23390, a D1 receptor antagonist known to inhibit development of d amphetamine behavioral <b>sensitization</b>, are due to its <strong>5 HT2C</strong> receptor agonist property.
+HTR2C	drug	amphetamine	17805311	SCH23390 blocks <b>amphetamine</b> induced release of norepinephrine and RS102221, a <strong>5 HT2C</strong> antagonist, can reverse this inhibition as well as inhibition of noradrenergic sensitization and development of behavioral sensitization induced by repeated d <b>amphetamine</b>.
+HTR2C	addiction	sensitization	17805311	SCH23390 blocks amphetamine induced release of norepinephrine and RS102221, a <strong>5 HT2C</strong> antagonist, can reverse this inhibition as well as inhibition of noradrenergic <b>sensitization</b> and development of behavioral <b>sensitization</b> induced by repeated d amphetamine.
+HTR2C	drug	cocaine	17653111	The <strong>5 HT2C</strong> receptor agonist Ro60 0175 reduces <b>cocaine</b> self administration and reinstatement induced by the stressor yohimbine, and contextual cues.
+HTR2C	addiction	relapse	17653111	The <strong>5 HT2C</strong> receptor agonist Ro60 0175 reduces cocaine self administration and <b>reinstatement</b> induced by the stressor yohimbine, and contextual cues.
+HTR2C	drug	cocaine	17653111	Previously, we showed that the <strong>5 HT2C</strong> receptor agonist Ro60 0175 reduces <b>cocaine</b> self administration, and the ability of <b>cocaine</b> to reinstate responding after extinction of drug seeking behavior.
+HTR2C	addiction	relapse	17653111	Previously, we showed that the <strong>5 HT2C</strong> receptor agonist Ro60 0175 reduces cocaine self administration, and the ability of cocaine to reinstate responding after extinction of drug <b>seeking</b> behavior.
+HTR2C	drug	cocaine	17653111	Thus, Ro60 0175, acting via <strong>5 HT2C</strong> receptors, reduces <b>cocaine</b> self administration and <b>cocaine</b> seeking triggered by a stressor and by drug associated cues.
+HTR2C	addiction	relapse	17653111	Thus, Ro60 0175, acting via <strong>5 HT2C</strong> receptors, reduces cocaine self administration and cocaine <b>seeking</b> triggered by a stressor and by drug associated cues.
+HTR2C	drug	opioid	17105947	The possibility that a serotonin <strong>5 HT2c</strong> receptor modulating compound, AP 267, will influence spontaneous <b>morphine</b> withdrawal symptoms and the alterations in the brain fluid microenvironment was examined in a rat model.
+HTR2C	addiction	withdrawal	17105947	The possibility that a serotonin <strong>5 HT2c</strong> receptor modulating compound, AP 267, will influence spontaneous morphine <b>withdrawal</b> symptoms and the alterations in the brain fluid microenvironment was examined in a rat model.
+HTR2C	addiction	withdrawal	17105947	Taken together, these observations suggest that (a) stress associated with the <b>withdrawal</b> symptoms are sufficient enough to induce breakdown of the BBB function, and (b) modulation of serotonin <strong>5 HT2c</strong> receptors may have some protective influence on the stress symptoms and the BBB disruption.
+HTR2C	drug	benzodiazepine	17074317	Anxiolytic activity of a novel potent serotonin <strong>5 HT2C</strong> receptor antagonist FR260010: a comparison with <b>diazepam</b> and buspirone.
+HTR2C	addiction	dependence	17017968	Serotonin 5 HT2A and <strong>5 HT2C</strong> receptors as potential targets for modulation of psychostimulant use and <b>dependence</b>.
+HTR2C	drug	cocaine	17017968	Two key modulators of DA output are the serotonin (5 HT)2A receptor (5 HT2A R) and the <strong>5 HT2C</strong> R. These receptors are known to control the neurochemical and behavioral effects of psychostimulants, and in particular, the in vivo effects of <b>cocaine</b>.
+HTR2C	drug	cocaine	17017968	Preclinical studies indicate that 5 HT2A R antagonists and/or <strong>5 HT2C</strong> R agonists may effectively reduce craving and/or relapse, and likewise, enhance abstinence, while <strong>5 HT2C</strong> R agonists may also effectively reduce <b>cocaine</b> intake in active <b>cocaine</b> users.
+HTR2C	addiction	relapse	17017968	Preclinical studies indicate that 5 HT2A R antagonists and/or <strong>5 HT2C</strong> R agonists may effectively reduce <b>craving</b> and/or <b>relapse</b>, and likewise, enhance abstinence, while <strong>5 HT2C</strong> R agonists may also effectively reduce cocaine intake in active cocaine users.
+HTR2C	drug	cocaine	17017968	At present, the progression of studies to probe the effectiveness of 5 HT2A R and <strong>5 HT2C</strong> R ligands in the clinical setting is hindered by a lack of available selective 5 HT2A R antagonists or <strong>5 HT2C</strong> R agonists for use in human <b>cocaine</b> abusers.
+HTR2C	drug	alcohol	16767411	Reduction in repeated <b>ethanol</b> withdrawal induced anxiety like behavior by site selective injections of 5 HT1A and <strong>5 HT2C</strong> ligands.
+HTR2C	addiction	withdrawal	16767411	Reduction in repeated ethanol <b>withdrawal</b> induced anxiety like behavior by site selective injections of 5 HT1A and <strong>5 HT2C</strong> ligands.
+HTR2C	drug	alcohol	16767411	Anxiety like behavior resulting from repeated withdrawals from chronic <b>ethanol</b> diets is counteracted by systemic administration of a <strong>5 HT2C</strong> receptor antagonist or a 5 HT1A receptor partial agonist.
+HTR2C	drug	alcohol	16767411	These results are consistent with the involvement of <strong>5 HT2C</strong> receptors in the amygdala and 5 HT1A autoreceptors in the dorsal raphe nucleus in repeated <b>ethanol</b> withdrawal induced sensitization of anxiety like behavior.
+HTR2C	addiction	sensitization	16767411	These results are consistent with the involvement of <strong>5 HT2C</strong> receptors in the amygdala and 5 HT1A autoreceptors in the dorsal raphe nucleus in repeated ethanol withdrawal induced <b>sensitization</b> of anxiety like behavior.
+HTR2C	addiction	withdrawal	16767411	These results are consistent with the involvement of <strong>5 HT2C</strong> receptors in the amygdala and 5 HT1A autoreceptors in the dorsal raphe nucleus in repeated ethanol <b>withdrawal</b> induced sensitization of anxiety like behavior.
+HTR2C	drug	cocaine	16146672	Serotonin2C receptors (<strong>5 HT2C</strong> R) control expression of <b>cocaine</b> induced conditioned hyperactivity.
+HTR2C	drug	cocaine	16146672	The <strong>5 HT2C</strong> receptor (<strong>5 HT2C</strong> R) has been shown to control the behavioral effects of acute <b>cocaine</b> administration and, in the present study, we investigated the role of this receptor in the expression of <b>cocaine</b> induced conditioned hyperactivity.
+HTR2C	drug	cocaine	16146672	These results suggest that the <strong>5 HT2C</strong> R controls expression of <b>cocaine</b> induced conditioned hyperactivity and suggest that such ligands may be useful in preventing relapse and promoting abstinence in <b>cocaine</b> dependent individuals.
+HTR2C	addiction	relapse	16146672	These results suggest that the <strong>5 HT2C</strong> R controls expression of cocaine induced conditioned hyperactivity and suggest that such ligands may be useful in preventing <b>relapse</b> and promoting abstinence in cocaine dependent individuals.
+HTR2C	drug	benzodiazepine	15894069	Other groups of P and SD rats were injected with flumazenil (5 mg/kg), a <b>benzodiazepine</b> (BZD) receptor antagonist, CP 154,526 (10 mg/kg), CRF1 receptor antagonist, SB243,213, a <strong>5 HT2C</strong> receptor inverse agonist, or vehicle during the 1st and 2nd withdrawals but not the third.
+HTR2C	drug	alcohol	15894069	These findings show that <b>alcohol</b> preferring P rats exhibit anxiety like behavior more readily following exposure to <b>ethanol</b> containing diets and that this behavior is counteracted more readily by pretreatment with a CRF1 receptor antagonist than with BZD or <strong>5 HT2C</strong> receptor antagonists.
+HTR2C	addiction	addiction	15866558	Reinforced spatial alternation as an animal model of obsessive <b>compulsive</b> disorder (OCD): investigation of <strong>5 HT2C</strong> and 5 HT1D receptor involvement in OCD pathophysiology.
+HTR2C	drug	psychedelics	15841107	Administration of SCH 23390 into the medial prefrontal cortex blocks the expression of <b>MDMA</b> induced behavioral sensitization in rats: an effect mediated by <strong>5 HT2C</strong> receptor stimulation and not by D1 receptor blockade.
+HTR2C	addiction	sensitization	15841107	Administration of SCH 23390 into the medial prefrontal cortex blocks the expression of MDMA induced behavioral <b>sensitization</b> in rats: an effect mediated by <strong>5 HT2C</strong> receptor stimulation and not by D1 receptor blockade.
+HTR2C	drug	alcohol	15570522	We investigated phenotype and 5 HTT/<strong>5 HT2c</strong> allelic characteristics in 314 <b>alcoholics</b> of German descent.
+HTR2C	drug	alcohol	15570522	There was no significant difference in 5 HTT  or <strong>5 HT2c</strong> allele distribution between <b>alcoholics</b> and matched controls or between <b>alcoholics</b> with or without ADHD.
+HTR2C	drug	alcohol	15570522	In our sample the functional relevant 5 HTT promoter and the <strong>5 HT2c</strong> receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and <b>alcohol</b> dependence.
+HTR2C	addiction	dependence	15570522	In our sample the functional relevant 5 HTT promoter and the <strong>5 HT2c</strong> receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and alcohol <b>dependence</b>.
+HTR2C	drug	nicotine	15565434	After characterizing a dose response curve for <b>nicotine</b>, we tested the ability of the 5HT(2A/2C) agonists (+/ ) 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane HCL (DOI; 0.18 1.0 mg/kg) and 1 (4 bromo 2, 5 dimethoxyphenyl) 2 aminopropane (DOB; 0.1 1.0 mg/kg), the <strong>5HT2C</strong> agonist 6 chloro 2 (1 piperazinyl)pyrazine hydrochloride (MK 212; 0.1 mg/kg 1.0 mg/kg), and the 5HT1A agonist (+/ ) 8 hydroxy 2 (di n propylamino)tetralin hydrobromide (8 OH DPAT; 0.01 mg/kg 1.0 mg/kg) to modulate <b>nicotine</b>'s discriminative stimulus effects.
+HTR2C	drug	alcohol	15304380	To examine whether polymorphic variants of the <strong>HTR2C</strong> gene are associated with diagnosis of <b>alcohol</b> dependence.
+HTR2C	addiction	dependence	15304380	To examine whether polymorphic variants of the <strong>HTR2C</strong> gene are associated with diagnosis of alcohol <b>dependence</b>.
+HTR2C	drug	alcohol	15304380	We compared allele frequencies of five <strong>HTR2C</strong> promoter polymorphisms in a Nordic population of <b>alcohol</b> dependent individuals (Males: n = 309; Females: n = 127) and ethnically matched controls (Males: n = 83; Females: n = 190) in whom <b>alcohol</b> dependence was established, or any diagnosis of substance disorder was excluded, respectively.
+HTR2C	addiction	dependence	15304380	We compared allele frequencies of five <strong>HTR2C</strong> promoter polymorphisms in a Nordic population of alcohol dependent individuals (Males: n = 309; Females: n = 127) and ethnically matched controls (Males: n = 83; Females: n = 190) in whom alcohol <b>dependence</b> was established, or any diagnosis of substance disorder was excluded, respectively.
+HTR2C	drug	alcohol	15304380	We suggest that a follow up study with larger sample numbers should be performed to improve the power to detect the genetic influences of <strong>HTR2C</strong> in <b>alcohol</b> dependence.
+HTR2C	addiction	dependence	15304380	We suggest that a follow up study with larger sample numbers should be performed to improve the power to detect the genetic influences of <strong>HTR2C</strong> in alcohol <b>dependence</b>.
+HTR2C	drug	cocaine	14666118	Injection of the <strong>5 HT2C</strong> receptor agonist Ro60 0175 into the ventral tegmental area reduces <b>cocaine</b> induced locomotor activity and <b>cocaine</b> self administration.
+HTR2C	drug	alcohol	14574222	We investigated phenotype and 5 HTT/<strong>5 HT2c</strong> genotype characteristics in 314 <b>alcoholics</b> of German descent.
+HTR2C	drug	alcohol	14574222	There was no significant difference in 5 HTT genotype or <strong>5 HT2c</strong> allele distribution between <b>alcoholics</b> and matched controls.
+HTR2C	drug	alcohol	14574222	There were no differences in 5 HTT genotype or <strong>5 HT2c</strong> allele distribution between the ADHD+ subgroups and <b>alcoholics</b> without comorbidity and matched controls, respectively.
+HTR2C	drug	alcohol	14574222	In our sample, the functional relevant 5 HTT promoter and the <strong>5 HT2c</strong> receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and <b>alcohol</b> dependence.
+HTR2C	addiction	dependence	14574222	In our sample, the functional relevant 5 HTT promoter and the <strong>5 HT2c</strong> receptor Cys23Ser polymorphism do not contribute to the supposed common genetic predisposition of ADHD and alcohol <b>dependence</b>.
+HTR2C	drug	alcohol	12895679	NPI 031G (puerarin) reduces anxiogenic effects of <b>alcohol</b> withdrawal or benzodiazepine inverse or <strong>5 HT2C</strong> agonists.
+HTR2C	drug	benzodiazepine	12895679	NPI 031G (puerarin) reduces anxiogenic effects of alcohol withdrawal or <b>benzodiazepine</b> inverse or <strong>5 HT2C</strong> agonists.
+HTR2C	addiction	withdrawal	12895679	NPI 031G (puerarin) reduces anxiogenic effects of alcohol <b>withdrawal</b> or benzodiazepine inverse or <strong>5 HT2C</strong> agonists.
+HTR2C	drug	cocaine	12757964	Medications such as olanzapine, which block dopamine D2 receptors, as well as serotonin receptors 5HT2A and <strong>5HT2C</strong> may be able to reduce <b>cocaine</b> use in <b>cocaine</b> dependent patients by reducing the euphoric effects of <b>cocaine</b> and attenuating <b>cocaine</b> craving.
+HTR2C	addiction	relapse	12757964	Medications such as olanzapine, which block dopamine D2 receptors, as well as serotonin receptors 5HT2A and <strong>5HT2C</strong> may be able to reduce cocaine use in cocaine dependent patients by reducing the euphoric effects of cocaine and attenuating cocaine <b>craving</b>.
+HTR2C	drug	alcohol	12677355	A 5 HT1A agonist and a <strong>5 HT2c</strong> antagonist reduce social interaction deficit induced by multiple <b>ethanol</b> withdrawals in rats.
+HTR2C	drug	cocaine	12427861	A line of mutant mice devoid of <strong>5 HT2C</strong> receptors was used to examine the contribution of this receptor subtype to the serotonergic modulation of <b>cocaine</b> responses.
+HTR2C	drug	cocaine	12427861	These findings strongly implicate <strong>5 HT2C</strong> receptors in the serotonergic suppression of DA mediated behavioral responses to <b>cocaine</b> and as a potential therapeutic target for <b>cocaine</b> abuse.
+HTR2C	drug	psychedelics	11705117	It appears that 5 HT2A, <strong>5 HT2C</strong>, and sigma 2 receptors are involved in mediating the stimulus effects of <b>ibogaine</b>.
+HTR2C	drug	psychedelics	11705117	<b>Ibogaine</b>'s hallucinogenic effects may be explained by its interactions with 5 HT2A and <strong>5 HT2C</strong> receptors, while its putative antiaddictive properties may result from its interactions with sigma 2 and opiate receptors.
+HTR2C	addiction	withdrawal	11489455	SB 243213; a selective <strong>5 HT2C</strong> receptor inverse agonist with improved anxiolytic profile: lack of tolerance and <b>withdrawal</b> anxiety.
+HTR2C	addiction	reward	11239674	In addition, the effects of the anxiogenic Serotonin 2C (<strong>5 HT2C</strong>) receptor agonist, m chlorophenylpiperazine (m <b>CPP</b>), were studied.
+HTR2C	drug	alcohol	11198050	Results showed that the 5 HT releaser d fenfluramine, the selective serotonin reuptake inhibitor fluoxetine, the 5 HT1A receptor agonist 8 hydroxy 2[di n propylamino]tetralin, the partial 5 HT1A receptor agonist buspirone, and the 5 HT1B/<strong>5 HT2C</strong> receptor agonist 1 (3 trifluoromethylphenyl)piperazine, but not the 5 HT2A/<strong>5 HT2C</strong> receptor agonist 1 (2,5 dimethoxy 4 iodophenylaminopropane) 2, selectively reduced responding on a lever leading to presentation of an <b>ethanol</b> paired conditioned stimulus.
+HTR2C	drug	alcohol	10994642	We genotyped patients with <b>alcohol</b> dependence, panic disorder without agoraphobia, generalized anxiety disorder, narcolepsy and normal healthy volunteers for the <strong>5 HT2C</strong> Cys23Ser polymorphism.
+HTR2C	addiction	dependence	10994642	We genotyped patients with alcohol <b>dependence</b>, panic disorder without agoraphobia, generalized anxiety disorder, narcolepsy and normal healthy volunteers for the <strong>5 HT2C</strong> Cys23Ser polymorphism.
+HTR2C	drug	alcohol	10994642	<strong>5 HT2C</strong> Cys23Ser allele frequencies and genotypes did not differ among patients with <b>alcohol</b> dependence, panic disorder, generalized anxiety disorder, narcolepsy and normal healthy volunteers.
+HTR2C	addiction	dependence	10994642	<strong>5 HT2C</strong> Cys23Ser allele frequencies and genotypes did not differ among patients with alcohol <b>dependence</b>, panic disorder, generalized anxiety disorder, narcolepsy and normal healthy volunteers.
+HTR2C	drug	alcohol	10334495	The present study evaluated the effects of the selective serotonin (5 hydroxyhyptamine; 5 HT) reuptake inhibitor, fluoxetine, the 5 HT1B receptor agonist, tetrahydro 4 pyridyl[3,2 b]pyridine, CP 94,253 the preferential 5 HT2A receptor agonist, 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane, DOI and the mixed <strong>5 HT2C</strong>/1B receptor agonist, 1 (3 chlorophenyl)piperazine, mCPP, on oral <b>ethanol</b> (10% v/v) self administration in a two lever, fixed ratio:1, water vs. <b>ethanol</b> choice procedure in the rat.
+HTR2C	drug	alcohol	10334495	These findings suggest that operant <b>ethanol</b> self administration can be suppressed in a specific manner by activation of 5 HT2A and, possibly, <strong>5 HT2C</strong> receptors, and in a nonselective manner by activation of 5 HT1B receptors.
+HTR2C	addiction	reward	10334495	These findings suggest that <b>operant</b> ethanol self administration can be suppressed in a specific manner by activation of 5 HT2A and, possibly, <strong>5 HT2C</strong> receptors, and in a nonselective manner by activation of 5 HT1B receptors.
+HTR2C	drug	alcohol	10206230	Our results suggest that the common Cys23Ser substitution polymorphism of the human <strong>5 HT2c</strong> receptor gene does not confer susceptibility to neuronal hyperexcitability in either idiopathic generalized epilepsy or <b>alcohol</b> withdrawal seizure or delirium.
+HTR2C	addiction	withdrawal	10206230	Our results suggest that the common Cys23Ser substitution polymorphism of the human <strong>5 HT2c</strong> receptor gene does not confer susceptibility to neuronal hyperexcitability in either idiopathic generalized epilepsy or alcohol <b>withdrawal</b> seizure or delirium.
+HTR2C	drug	alcohol	10088053	Selective genotyping for the role of 5 HT2A, <strong>5 HT2C</strong>, and GABA alpha 6 receptors and the serotonin transporter in the level of response to <b>alcohol</b>: a pilot study.
+HTR2C	drug	alcohol	10088053	There was no evidence that two polymorphisms of the 5 HT2A receptor gene and one of the <strong>5 HT2C</strong> receptor gene were related to LR or <b>alcoholism</b> in this sample.
+HTR2C	drug	psychedelics	9924841	Most <b>psychedelic</b> drugs are potent agonists at 5 HT2A and <strong>5 HT2C</strong> receptors and their binding potency to these receptors is strongly correlated with their human potency as hallucinogens.
+HTR2C	drug	alcohol	9887443	It appears from the literature that PKC plays an important role in the modulation of the function of various neurotransmitter receptors (e.g., gamma aminobutyrate type A [GABAA], N methyl D aspartate [NMDA], serotonin2A [5 HT2A], and <strong>5 HT2C</strong>, and muscarinic [m1] receptors) resulting from <b>ethanol</b> exposure.
+HTR2C	addiction	aversion	9716307	Dose dependent increases in threshold for operant fear/escape responses of rats submitted to <b>aversive</b> stimulation of the dorsolateral periaqueductal gray (dPAG) were recorded following intraperitoneal injection of three chemically unrelated but selective <strong>5HT2C</strong> receptor agonists (Ro 60 0175, Org 12962 and Ro 60 0332) and fluoxetine.
+HTR2C	addiction	reward	9716307	Dose dependent increases in threshold for <b>operant</b> fear/escape responses of rats submitted to aversive stimulation of the dorsolateral periaqueductal gray (dPAG) were recorded following intraperitoneal injection of three chemically unrelated but selective <strong>5HT2C</strong> receptor agonists (Ro 60 0175, Org 12962 and Ro 60 0332) and fluoxetine.
+HTR2C	drug	benzodiazepine	9716307	In this paradigm which has been validated as a simulation of acute anxiety with relevance to panic disorder, the selective activation of <strong>5HT2C</strong> receptors by Ro 60 0175, Org 12962 or Ro 60 0332 induces effects analogous to those observed following <b>benzodiazepine</b> receptor activation by antipanic agents such as <b>clonazepam</b> or <b>alprazolam</b> or following non selective and indirect 5HT receptor activation by fluoxetine.
+HTR2C	drug	benzodiazepine	9716307	Potency and efficacy of <strong>5HT2C</strong> receptor agonists were intermediate between those of <b>clonazepam</b> and fluoxetine, indicating authentic antiaversive properties and suggesting antipanic potential for these <strong>5HT2C</strong> receptor agonists.
+HTR2C	drug	benzodiazepine	9716307	It is also speculated that serotonin/<b>benzodiazepine</b> interactions existing in the brain may functionally involve the <strong>5HT2C</strong> receptor subtypes and that the anxiogenic action reported under certain circumstances for 5HT mimetics are not mediated by <strong>5HT2C</strong> receptor subtypes.
+HTR2C	drug	psychedelics	9566028	In substitution tests, D lysergic acid diethylamide (<b>LSD</b>, 0.02 and 0.04 mg/kg) and quipazine (0.5, 1.5 and 3 mg/kg), 5 HT2A/2C agonists, evoked dose related responses to the (+/ )DOI appropriate lever, while the non selective 5 HT agonist 1 (3 chlorophenyl)piperazine (m CPP, 0.1, 0.5 and 1 mg/kg), which has the highest binding affinity for <strong>5 HT2C</strong> receptors, failed to show substitution.
+HTR2C	addiction	reward	9566028	In substitution tests, D lysergic acid diethylamide (LSD, 0.02 and 0.04 mg/kg) and quipazine (0.5, 1.5 and 3 mg/kg), 5 HT2A/2C agonists, evoked dose related responses to the (+/ )DOI appropriate lever, while the non selective 5 HT agonist 1 (3 chlorophenyl)piperazine (m <b>CPP</b>, 0.1, 0.5 and 1 mg/kg), which has the highest binding affinity for <strong>5 HT2C</strong> receptors, failed to show substitution.
+HTR2C	drug	alcohol	9403358	In humans, a bolus dose of mCPP can cause <b>alcohol</b> craving (in abstinent <b>alcoholics</b>) and migraine (in susceptible persons), suggesting that there is a <strong>5 HT2C</strong> receptor hyperresponsiveness in these conditions also.
+HTR2C	addiction	relapse	9403358	In humans, a bolus dose of mCPP can cause alcohol <b>craving</b> (in abstinent alcoholics) and migraine (in susceptible persons), suggesting that there is a <strong>5 HT2C</strong> receptor hyperresponsiveness in these conditions also.
+HTR2C	drug	alcohol	8988963	Furthermore, <b>alcoholics</b> may have reduced sensitivity of <strong>5 HT2C</strong> receptors in comparison with healthy subjects.
+HTR2C	drug	alcohol	8788509	On the other hand, chronic <b>ethanol</b> treatment (60 days) significantly increased <strong>5 HT2C</strong> receptors and 5 HT stimulated PI hydrolysis in the rat choroid plexus.
+HTR2C	addiction	reward	8587903	The results show that agents acting as full or partial agonists at 5 HT1A receptors and blockers of postsynaptic <strong>5 HT2C</strong> receptors have anxiolytic like effects in a model of punished <b>operant</b> responding, whereas antagonists at 5 HT1A and 5 HT3 receptors have no such effect.
+HTR2C	addiction	reward	8539344	The <strong>5 HT2C</strong>/1B receptor agonist m <b>CPP</b>, the inverse BZD receptor agonists FG 7142 and DMCM, and the alpha 2 adrenoceptor antagonist yohimbine, to all of which putative anxiogenic effects have been ascribed, had no effect on SAP directed towards the prod.
+HTR2C	drug	cocaine	7965077	The actions of both 5 HT and <b>cocaine</b> were attenuated by the <strong>5 HT1C</strong>/D antagonist metergoline.
+HTR2C	addiction	reward	7846211	Four non selective <strong>5 HT2C</strong>/5 HT2A receptor antagonists, mianserin (2 8 mg/kg), 1 naphthyl piperazine (1 NP) (0.5 1 mg/kg), ICI 169,369 (20 mg/kg) and LY 53857 (5 mg/kg), increased punished responding for a food <b>reward</b> in the rat Geller Seifter test 30 min after subcutaneous (SC) administration.
+HTR2C	addiction	relapse	8032167	Ritanserin is a potent, centrally acting, highly selective <strong>5 HT1C</strong>/2 antagonist which, in addition to having a sleep regulating and anti depression/anti axiety effect, displays a unique pharmacological action in several animal paradigms of substance abuse which assess drug <b>craving</b>.
+HTR2C	drug	benzodiazepine	7902543	Co administration of buspirone (5 HT1A agonist) or ondansetron (5 HT3 antagonist), but not mianserin (<strong>5 HT1C</strong> antagonist) or ketanserin (5 HT2 antagonist) with <b>diazepam</b> potentiated the hypersensitivity to FG 7142 following chronic treatment with <b>diazepam</b>.
+HTR2C	drug	alcohol	8258364	Modulation of <strong>5 HT1C</strong> receptors and phosphoinositide system by <b>ethanol</b> consumption in rat brain and choroid plexus.
+HTR2C	drug	alcohol	8258364	The effect of chronic <b>ethanol</b> consumption (60 days) on <strong>5 HT1C</strong> receptors as measured by [3H]mesulergine binding in the hippocampus, cortex, and choroid plexus of rats was investigated.
+HTR2C	drug	alcohol	8258364	It was observed that chronic <b>ethanol</b> treatment significantly increased the 5 HT stimulated [3H]inositol 1 phosphate ([3H]IP1) formation, as well as the density (Bmax) of <strong>5 HT1C</strong> receptors without causing a significant change in affinity (KD) of [3H]mesulergine binding in rat choroid plexus.
+HTR2C	drug	alcohol	8258364	It was also observed that chronic <b>ethanol</b> consumption had no significant effect on the Bmax or KD of <strong>5 HT1C</strong> receptor binding sites in the hippocampus and cortex brain regions of rats.
+HTR2C	drug	alcohol	8258364	These results thus suggest that chronic <b>ethanol</b> consumption causes an up regulation of both <strong>5 HT1C</strong> receptors and <strong>5 HT1C</strong> receptor mediated phosphoinositide hydrolysis in rat choroid plexus but has no significant effects on the <strong>5 HT1C</strong> receptors in brain.
+HTR2C	drug	alcohol	8258364	These results also suggest that <strong>5 HT1C</strong> receptors and their functional response may be involved in the pathogenesis of <b>alcohol</b> dependence.
+HTR2C	addiction	dependence	8258364	These results also suggest that <strong>5 HT1C</strong> receptors and their functional response may be involved in the pathogenesis of alcohol <b>dependence</b>.
+HTR2C	drug	alcohol	8397879	Sensitization to <strong>5 HT1C</strong> receptor agonist in rats observed following withdrawal from chronic <b>ethanol</b>.
+HTR2C	addiction	sensitization	8397879	<b>Sensitization</b> to <strong>5 HT1C</strong> receptor agonist in rats observed following withdrawal from chronic ethanol.
+HTR2C	addiction	withdrawal	8397879	Sensitization to <strong>5 HT1C</strong> receptor agonist in rats observed following <b>withdrawal</b> from chronic ethanol.
+HTR2C	drug	alcohol	8397879	Anxiogenic action of m chlorophenylpiperazine (mCPP), a <strong>5 HT1C</strong> receptor agonist, was studied in naive rats and in <b>ethanol</b> tolerant rats following withdrawal from chronic <b>ethanol</b> administration.
+HTR2C	addiction	withdrawal	8397879	Anxiogenic action of m chlorophenylpiperazine (mCPP), a <strong>5 HT1C</strong> receptor agonist, was studied in naive rats and in ethanol tolerant rats following <b>withdrawal</b> from chronic ethanol administration.
+HTR2C	drug	alcohol	8397879	A shift of the mCPP dose response curve to the left following withdrawal from chronic <b>ethanol</b> may indicate that <strong>5 HT1C</strong> receptor sites are more sensitive to the activation by an agonist.
+HTR2C	addiction	withdrawal	8397879	A shift of the mCPP dose response curve to the left following <b>withdrawal</b> from chronic ethanol may indicate that <strong>5 HT1C</strong> receptor sites are more sensitive to the activation by an agonist.
+HTR2C	drug	alcohol	8397879	This effect may be exploited in developing specific <strong>5 HT1C</strong> receptor antagonists for the treatment of <b>ethanol</b> withdrawal symptoms.
+HTR2C	addiction	withdrawal	8397879	This effect may be exploited in developing specific <strong>5 HT1C</strong> receptor antagonists for the treatment of ethanol <b>withdrawal</b> symptoms.
+HTR2C	drug	alcohol	8488986	Potential role of <strong>5HT1C</strong> and/or 5HT2 receptors in the mianserin induced prevention of anxiogenic behaviors occurring during <b>ethanol</b> withdrawal.
+HTR2C	addiction	withdrawal	8488986	Potential role of <strong>5HT1C</strong> and/or 5HT2 receptors in the mianserin induced prevention of anxiogenic behaviors occurring during ethanol <b>withdrawal</b>.
+HTR2C	drug	alcohol	8488986	A single dose of mianserin (a <strong>5HT1C</strong>/5HT2 antagonist), administered 1 hr, 48 hr, or 7 days before testing, was evaluated for its efficacy in alleviating or preventing the occurrence of anxiogenic behaviors observed during <b>ethanol</b> withdrawal.
+HTR2C	addiction	withdrawal	8488986	A single dose of mianserin (a <strong>5HT1C</strong>/5HT2 antagonist), administered 1 hr, 48 hr, or 7 days before testing, was evaluated for its efficacy in alleviating or preventing the occurrence of anxiogenic behaviors observed during ethanol <b>withdrawal</b>.
+HTR2C	drug	alcohol	8488986	In contrast, the <strong>5HT1C</strong>/5HT2 receptor agonist (+/ ) 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane HCl (DOl) did not affect behaviors in the EPM in <b>ethanol</b> naive rats, nor in those undergoing <b>ethanol</b> withdrawal.
+HTR2C	addiction	withdrawal	8488986	In contrast, the <strong>5HT1C</strong>/5HT2 receptor agonist (+/ ) 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane HCl (DOl) did not affect behaviors in the EPM in ethanol naive rats, nor in those undergoing ethanol <b>withdrawal</b>.
+HTR2C	drug	benzodiazepine	1356807	It is concluded that the reduction in aversive responding caused by pharmacological manipulation at the <b>benzodiazepine</b>, 5 HT receptor subtypes 5 HT1A, <strong>5 HT1C</strong>/5 HT2 and 5 HT3 (but not at the cholecystokin CCKA or angiotensin receptors or inhibition of angiotensin converting enzyme) can be inhibited by R(+) and S( ) zacopride.
+HTR2C	addiction	aversion	1356807	It is concluded that the reduction in <b>aversive</b> responding caused by pharmacological manipulation at the benzodiazepine, 5 HT receptor subtypes 5 HT1A, <strong>5 HT1C</strong>/5 HT2 and 5 HT3 (but not at the cholecystokin CCKA or angiotensin receptors or inhibition of angiotensin converting enzyme) can be inhibited by R(+) and S( ) zacopride.
+HTR2C	drug	psychedelics	1532259	The effects of <b>LSD</b> and quipazine were reversed by 1 2 mg/kg ritanserin, a potent 5 HT2 and <strong>5 HT1C</strong> receptor antagonist.
+HTR2C	addiction	reward	1532259	Metachlorophenylpiperazine (mCPP) 2.5 mg/kg IP, an agonist at 5 HT1B and <strong>5 HT1C</strong> receptors, and d fenfluramine (DF) 1.25 mg/kg IP, a releaser of 5 HT from nerve terminals and inhibitor of 5 HT uptake, increased the percentage of omissions and the latency to respond correctly or to collect the <b>reinforcement</b> with no effects on the correct responses.
+HTR2C	drug	alcohol	1775600	The present investigation was a pilot study to determine whether a single dose of mianserin, which produces long term down regulation of serotonin1C (<strong>5 HT1c</strong>) and 5 HT2 receptors, would prevent anxiogenic behaviors occurring during <b>ethanol</b> withdrawal as evaluated in the elevated plus maze.
+HTR2C	addiction	withdrawal	1775600	The present investigation was a pilot study to determine whether a single dose of mianserin, which produces long term down regulation of serotonin1C (<strong>5 HT1c</strong>) and 5 HT2 receptors, would prevent anxiogenic behaviors occurring during ethanol <b>withdrawal</b> as evaluated in the elevated plus maze.
+HTR2C	addiction	reward	1771219	m <b>CPP</b> (1 (3 chlorophenyl)piperazine) and DOI [+/ ) 1 (2,5 dimethoxy 4 iodophenyl) 2 aminopropane), drugs with putative actions at <strong>5HT1C</strong> and 5HT2 receptor sites both decreased calling but differed according to their effects on motor activity.
+HTR2C	addiction	reward	2746512	The catecholamine responses to m <b>CPP</b> appear to be partially mediated by <strong>5 HT1C</strong> receptors and also by nonserotonergic mechanisms.
+ARC	drug	cocaine	32457073	We identified 133 genes differentially expressed between CUD case patients and <b>cocaine</b> free control subjects, including previously implicated candidates for <b>cocaine</b> use/addiction (FOSB, <strong>ARC</strong>, KCNJ9/GIRK3, NR4A2, JUNB, and MECP2).
+ARC	addiction	addiction	32457073	We identified 133 genes differentially expressed between CUD case patients and cocaine free control subjects, including previously implicated candidates for cocaine use/<b>addiction</b> (FOSB, <strong>ARC</strong>, KCNJ9/GIRK3, NR4A2, JUNB, and MECP2).
+ARC	drug	alcohol	31783685	The results show that <b>alcohol</b> dependence is related to lower absolute, relative, and residualized body measurements for height and weight, head circumference, bitragion head <strong>arc</strong>, lip chin distance, hip, thigh, and calf circumference, and foot length and breadth.
+ARC	addiction	dependence	31783685	The results show that alcohol <b>dependence</b> is related to lower absolute, relative, and residualized body measurements for height and weight, head circumference, bitragion head <strong>arc</strong>, lip chin distance, hip, thigh, and calf circumference, and foot length and breadth.
+ARC	drug	alcohol	31778848	<strong>ARC</strong> scores varied according to primary substance (Kruskal Wallis χ2 = 101.10, df = 6, p < 0.001); <b>alcohol</b> and marijuana showed the highest scores and heroin the lowest.
+ARC	drug	cannabinoid	31778848	<strong>ARC</strong> scores varied according to primary substance (Kruskal Wallis χ2 = 101.10, df = 6, p < 0.001); alcohol and <b>marijuana</b> showed the highest scores and heroin the lowest.
+ARC	drug	opioid	31778848	<strong>ARC</strong> scores varied according to primary substance (Kruskal Wallis χ2 = 101.10, df = 6, p < 0.001); alcohol and marijuana showed the highest scores and <b>heroin</b> the lowest.
+ARC	drug	cocaine	31682894	The activity regulated cytoskeleton associated protein, <strong>Arc</strong>/Arg3.1, influences mouse <b>cocaine</b> self administration.
+ARC	drug	cocaine	31682894	The <strong>activity regulated cytoskeleton associated protein</strong>, <strong>Arc</strong>/Arg3.1, influences mouse <b>cocaine</b> self administration.
+ARC	drug	cocaine	31682894	The <strong>activity regulated cytoskeleton associated protein</strong>, <strong>Arc</strong>/<strong>Arg3.1</strong>, influences mouse <b>cocaine</b> self administration.
+ARC	drug	cocaine	31682894	The activity regulated cytoskeleton associated protein (<strong>Arc</strong>, also known as Arg3.1), an immediate early gene and synaptic regulator, is upregulated following a single <b>cocaine</b> exposure.
+ARC	drug	cocaine	31682894	The <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>, also known as Arg3.1), an immediate early gene and synaptic regulator, is upregulated following a single <b>cocaine</b> exposure.
+ARC	drug	cocaine	31682894	The <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>, also known as <strong>Arg3.1</strong>), an immediate early gene and synaptic regulator, is upregulated following a single <b>cocaine</b> exposure.
+ARC	addiction	addiction	31682894	However, there is not much known regarding <strong>Arc</strong>/Arg3.1's potential contribution to <b>addiction</b> relevant behaviors.
+ARC	addiction	addiction	31682894	However, there is not much known regarding <strong>Arc</strong>/<strong>Arg3.1</strong>'s potential contribution to <b>addiction</b> relevant behaviors.
+ARC	drug	cocaine	31682894	Despite known learning and memory deficits in contextual fear and water maze reversal learning tasks, we find that mice lacking <strong>Arc</strong>/Arg3.1 perform conditioned place preference and operant conditioning involving positive reinforcers (food and <b>cocaine</b>) with little to no impairment.
+ARC	addiction	reward	31682894	Despite known learning and memory deficits in contextual fear and water maze reversal learning tasks, we find that mice lacking <strong>Arc</strong>/Arg3.1 perform conditioned place preference and <b>operant</b> conditioning involving positive reinforcers (food and cocaine) with little to no impairment.
+ARC	drug	cocaine	31682894	Despite known learning and memory deficits in contextual fear and water maze reversal learning tasks, we find that mice lacking <strong>Arc</strong>/<strong>Arg3.1</strong> perform conditioned place preference and operant conditioning involving positive reinforcers (food and <b>cocaine</b>) with little to no impairment.
+ARC	addiction	reward	31682894	Despite known learning and memory deficits in contextual fear and water maze reversal learning tasks, we find that mice lacking <strong>Arc</strong>/<strong>Arg3.1</strong> perform conditioned place preference and <b>operant</b> conditioning involving positive reinforcers (food and cocaine) with little to no impairment.
+ARC	drug	cocaine	31682894	Importantly, <strong>Arc</strong>/Arg3.1 KO and WT mice behave comparably on an increasing cost task (FR1 FR3; acquisition dose), providing evidence that both groups find <b>cocaine</b> reinforcing.
+ARC	addiction	reward	31682894	Importantly, <strong>Arc</strong>/Arg3.1 KO and WT mice behave comparably on an increasing cost task (FR1 FR3; acquisition dose), providing evidence that both groups find cocaine <b>reinforcing</b>.
+ARC	drug	cocaine	31682894	Importantly, <strong>Arc</strong>/<strong>Arg3.1</strong> KO and WT mice behave comparably on an increasing cost task (FR1 FR3; acquisition dose), providing evidence that both groups find <b>cocaine</b> reinforcing.
+ARC	addiction	reward	31682894	Importantly, <strong>Arc</strong>/<strong>Arg3.1</strong> KO and WT mice behave comparably on an increasing cost task (FR1 FR3; acquisition dose), providing evidence that both groups find cocaine <b>reinforcing</b>.
+ARC	addiction	addiction	31682894	Our data suggest that <strong>Arc</strong>/Arg3.1 may contribute to <b>addiction</b> as a regulator of drug taking vulnerability under different drug availability conditions.
+ARC	addiction	addiction	31682894	Our data suggest that <strong>Arc</strong>/<strong>Arg3.1</strong> may contribute to <b>addiction</b> as a regulator of drug taking vulnerability under different drug availability conditions.
+ARC	drug	cocaine	31653935	Consistent with this in vivo observation, we found that lack of Rhes in mice caused a greater increase in striatal <b>cocaine</b> dependent D1R/cAMP/PKA signaling, along with considerable enhancement of <strong>Arc</strong>, zif268, and Homer1 mRNA expression.
+ARC	drug	alcohol	31517050	A withdrawal associated impairment in β endorphin neurotransmission in the arcuate nucleus (<strong>ARC</strong>) of the hypothalamus is associated with <b>alcohol</b> dependence characterized by a chronic relapsing disorder.
+ARC	addiction	dependence	31517050	A withdrawal associated impairment in β endorphin neurotransmission in the arcuate nucleus (<strong>ARC</strong>) of the hypothalamus is associated with alcohol <b>dependence</b> characterized by a chronic relapsing disorder.
+ARC	addiction	withdrawal	31517050	A <b>withdrawal</b> associated impairment in β endorphin neurotransmission in the arcuate nucleus (<strong>ARC</strong>) of the hypothalamus is associated with alcohol dependence characterized by a chronic relapsing disorder.
+ARC	drug	alcohol	31517050	Although acupuncture activates β endorphin neurons in the <strong>ARC</strong> projecting to the nucleus accumbens (NAc), a role for <strong>ARC</strong> β endorphin neurons in <b>alcohol</b> dependence and acupuncture effects has not been examined.
+ARC	addiction	dependence	31517050	Although acupuncture activates β endorphin neurons in the <strong>ARC</strong> projecting to the nucleus accumbens (NAc), a role for <strong>ARC</strong> β endorphin neurons in alcohol <b>dependence</b> and acupuncture effects has not been examined.
+ARC	drug	alcohol	31517050	Here, we show that acupuncture at Shenmen (HT7) points attenuates behavioral manifestation of <b>alcohol</b> dependence by activating endorphinergic input to the NAc from the <strong>ARC</strong>.
+ARC	addiction	dependence	31517050	Here, we show that acupuncture at Shenmen (HT7) points attenuates behavioral manifestation of alcohol <b>dependence</b> by activating endorphinergic input to the NAc from the <strong>ARC</strong>.
+ARC	drug	alcohol	31517050	Acupuncture also reversed the decreased β endorphin levels in the NAc and a reduction of neuronal activity in the <strong>ARC</strong> during <b>ethanol</b> withdrawal.
+ARC	addiction	withdrawal	31517050	Acupuncture also reversed the decreased β endorphin levels in the NAc and a reduction of neuronal activity in the <strong>ARC</strong> during ethanol <b>withdrawal</b>.
+ARC	drug	opioid	31376054	NGF, BDNF and <strong>Arc</strong> mRNA Expression in the Hippocampus of Rats After Administration of <b>Morphine</b>.
+ARC	drug	opioid	31376054	<b>Morphine</b> can influence immediate early genes (IEG) of activity regulated cytoskeletal associated protein (<strong>Arc</strong>) and brain derived neurotrophic factor (BDNF) which are activated in response to physiological stimuli during learning, as well as the nerve growth factor (NGF) gene which increases the expression of several IEGs for memory formation.
+ARC	drug	opioid	31376054	The purpose of the current study was first to evaluate the effect of acute (1 day) and subchronic (15 days) <b>morphine</b> administration on memory retrieval of rats and second to determine the hippocampal expression of NGF, BDNF and <strong>Arc</strong> genes as potential contributors in the observed effects in each setting.
+ARC	drug	opioid	31376054	We did not detect a significant change in the hippocampal expression of <strong>Arc</strong>, BDNF or NGF genes after a single episode of <b>morphine</b> treatment.
+ARC	drug	opioid	31376054	However, subchronic <b>morphine</b> administration (15 and 20 mg/kg) increased the expression of <strong>Arc</strong> and BDNF genes in a dose dependent manner.
+ARC	drug	opioid	31376054	We hypothesize that the subchronic effects were <b>morphine</b> induced behavioral sensitization which may have been enhanced through increased hippocampal <strong>Arc</strong> expression.
+ARC	addiction	sensitization	31376054	We hypothesize that the subchronic effects were morphine induced behavioral <b>sensitization</b> which may have been enhanced through increased hippocampal <strong>Arc</strong> expression.
+ARC	drug	opioid	31071414	<b>Oxycodone</b> CPP females have: a) increases in <strong>ARC</strong> (activity regulated cytoskeletal associated protein) immunoreactivity (ir) in CA3 pyramidal cells; b) decreases in Npy (neuropeptide Y) gene expression in the medial hippocampus but higher numbers of NPY containing hilar interneurons compared to males; c) increases in Crhr2 (corticotropin releasing factor receptor 2) expression in CA2/3; d) increases in Akt1 (AKT serine/threonine kinase 1) expression in medial hippocampus; and e) decreases in phosphorylated MAPK (mitogen activated protein kinase) ir in CA1 and dentate gyrus.
+ARC	addiction	reward	31071414	Oxycodone <b>CPP</b> females have: a) increases in <strong>ARC</strong> (activity regulated cytoskeletal associated protein) immunoreactivity (ir) in CA3 pyramidal cells; b) decreases in Npy (neuropeptide Y) gene expression in the medial hippocampus but higher numbers of NPY containing hilar interneurons compared to males; c) increases in Crhr2 (corticotropin releasing factor receptor 2) expression in CA2/3; d) increases in Akt1 (AKT serine/threonine kinase 1) expression in medial hippocampus; and e) decreases in phosphorylated MAPK (mitogen activated protein kinase) ir in CA1 and dentate gyrus.
+ARC	drug	cocaine	30946882	Further, we found that dysregulated metabolic activity and mGlu5 receptor signaling in the PrL of <b>cocaine</b> rats correlated with past working memory performance and/or drug seeking, as indicated by the analysis of cytochrome oxidase reactivity, mGlu5 and Homer 1b/c protein expression, as well as <strong>Arc</strong> mRNA expression in mGlu5 positive cells.
+ARC	addiction	relapse	30946882	Further, we found that dysregulated metabolic activity and mGlu5 receptor signaling in the PrL of cocaine rats correlated with past working memory performance and/or drug <b>seeking</b>, as indicated by the analysis of cytochrome oxidase reactivity, mGlu5 and Homer 1b/c protein expression, as well as <strong>Arc</strong> mRNA expression in mGlu5 positive cells.
+ARC	drug	opioid	30801002	Using retrograde labeling, immunohistochemical, and optogenetic approaches, we found that, although BLA neurons projecting to the prelimbic cortex (PrL) played an important role in conditioned context induced retrieval of <b>morphine</b> withdrawal memory, they do not exhibit increased expression of the neuronal plasticity marker <strong>Arc</strong>.
+ARC	addiction	withdrawal	30801002	Using retrograde labeling, immunohistochemical, and optogenetic approaches, we found that, although BLA neurons projecting to the prelimbic cortex (PrL) played an important role in conditioned context induced retrieval of morphine <b>withdrawal</b> memory, they do not exhibit increased expression of the neuronal plasticity marker <strong>Arc</strong>.
+ARC	addiction	addiction	30763873	Positive psychological states in the <strong>arc</strong> from mindfulness to self transcendence: extensions of the Mindfulness to Meaning Theory and applications to <b>addiction</b> and chronic pain treatment.
+ARC	drug	opioid	30550948	Distinct regulation pattern of Egr 1, BDNF and <strong>Arc</strong> during <b>morphine</b> withdrawal conditioned place aversion paradigm: Role of glucocorticoids.
+ARC	addiction	aversion	30550948	Distinct regulation pattern of Egr 1, BDNF and <strong>Arc</strong> during morphine withdrawal conditioned place <b>aversion</b> paradigm: Role of glucocorticoids.
+ARC	addiction	withdrawal	30550948	Distinct regulation pattern of Egr 1, BDNF and <strong>Arc</strong> during morphine <b>withdrawal</b> conditioned place aversion paradigm: Role of glucocorticoids.
+ARC	addiction	aversion	30550948	qPCR was employed to detect the expression of brain derived neurotrophic factor (Bdnf) and the immediate early genes (IEG) early growth response 1 (Egr 1) and activity regulated cytoskeletal associated protein (<strong>Arc</strong>) mRNAs in the VTA and mPFC at different time points of the conditioned place <b>aversion</b> (CPA) paradigm: after the conditioning phase and after the test phase.
+ARC	drug	opioid	30550948	Egr 1 and <strong>Arc</strong> were induced in the VTA and mPFC after <b>morphine</b> withdrawal conditioning phase.
+ARC	addiction	withdrawal	30550948	Egr 1 and <strong>Arc</strong> were induced in the VTA and mPFC after morphine <b>withdrawal</b> conditioning phase.
+ARC	drug	cocaine	30421552	<strong>ARC</strong> and BDNF expression after <b>cocaine</b> self administration or cue induced reinstatement of <b>cocaine</b> seeking in adolescent and adult male rats.
+ARC	addiction	relapse	30421552	<strong>ARC</strong> and BDNF expression after cocaine self administration or cue induced <b>reinstatement</b> of cocaine <b>seeking</b> in adolescent and adult male rats.
+ARC	drug	cocaine	30421552	Two neuroplasticity related genes, activity regulated cytoskeletal associated gene (<strong>Arc</strong>) and brain derived neurotrophic factor (Bdnf), influence <b>cocaine</b> self administration and cue induced reinstatement.
+ARC	addiction	relapse	30421552	Two neuroplasticity related genes, activity regulated cytoskeletal associated gene (<strong>Arc</strong>) and brain derived neurotrophic factor (Bdnf), influence cocaine self administration and cue induced <b>reinstatement</b>.
+ARC	addiction	relapse	30421552	These data partially support the hypothesis that higher levels of <strong>Arc</strong> and/or Bdnf gene expression in reinforcement related brain regions of younger animals contribute to lower rates of extinction responding and/or <b>reinstatement</b>.
+ARC	addiction	reward	30421552	These data partially support the hypothesis that higher levels of <strong>Arc</strong> and/or Bdnf gene expression in <b>reinforcement</b> related brain regions of younger animals contribute to lower rates of extinction responding and/or reinstatement.
+ARC	drug	cocaine	30421552	Future studies should include mechanistic analysis of <strong>Arc</strong>, Bdnf, and their signaling pathways in age dependent effects of <b>cocaine</b>.
+ARC	drug	opioid	30342963	Key determinants for <b>morphine</b> withdrawal conditioned context induced increase in <strong>Arc</strong> expression in anterior cingulate cortex and withdrawal memory retrieval.
+ARC	addiction	withdrawal	30342963	Key determinants for morphine <b>withdrawal</b> conditioned context induced increase in <strong>Arc</strong> expression in anterior cingulate cortex and <b>withdrawal</b> memory retrieval.
+ARC	drug	opioid	30342963	In this paper, using immunohistochemical and single cell microinjection techniques, combining behavioral assay, we found that (1) contextual withdrawal conditioning increases the expression of c Fos, but not <strong>Arc</strong>, in the ACC in <b>morphine</b> withdrawal mice; (2) at the first day after conditioning, conditioned context has no influence on the expression of c Fos and <strong>Arc</strong> in the ACC in <b>morphine</b> withdrawal mice; (3) at the 14th day after conditioning, conditioned context increases the expression of both c Fos and <strong>Arc</strong> in the ACC in <b>morphine</b> withdrawal mice; (4) the inhibition of dendritic spines of the ACC or projection neurons from the CA3 of the hippocampus to the ACC attenuates the conditioned context induced increase of <strong>Arc</strong> expression in the ACC and abolishes the retrieval of withdrawal memory at the 14th day after conditioning.
+ARC	addiction	withdrawal	30342963	In this paper, using immunohistochemical and single cell microinjection techniques, combining behavioral assay, we found that (1) contextual <b>withdrawal</b> conditioning increases the expression of c Fos, but not <strong>Arc</strong>, in the ACC in morphine <b>withdrawal</b> mice; (2) at the first day after conditioning, conditioned context has no influence on the expression of c Fos and <strong>Arc</strong> in the ACC in morphine <b>withdrawal</b> mice; (3) at the 14th day after conditioning, conditioned context increases the expression of both c Fos and <strong>Arc</strong> in the ACC in morphine <b>withdrawal</b> mice; (4) the inhibition of dendritic spines of the ACC or projection neurons from the CA3 of the hippocampus to the ACC attenuates the conditioned context induced increase of <strong>Arc</strong> expression in the ACC and abolishes the retrieval of <b>withdrawal</b> memory at the 14th day after conditioning.
+ARC	addiction	withdrawal	30342963	These results suggest that the ACC may exhibit a change in neuroplasticity at the 14th day after conditioning, and the dendritic spines of the ACC and the projection neurons from the CA3 of the hippocampus to the ACC are key determinants for conditioned context induced increase in <strong>Arc</strong> expression in the ACC and the retrieval of <b>withdrawal</b> memory at the 14th day after conditioning.
+ARC	drug	cocaine	30321610	Increased expression of <strong>Arc</strong>, CDK5 and TH, and decrease in DAT protein levels persisted longer after withdrawal, pointing to a neuroplastic lasting effect similar to that involved in <b>cocaine</b> addiction.
+ARC	addiction	addiction	30321610	Increased expression of <strong>Arc</strong>, CDK5 and TH, and decrease in DAT protein levels persisted longer after withdrawal, pointing to a neuroplastic lasting effect similar to that involved in cocaine <b>addiction</b>.
+ARC	addiction	withdrawal	30321610	Increased expression of <strong>Arc</strong>, CDK5 and TH, and decrease in DAT protein levels persisted longer after <b>withdrawal</b>, pointing to a neuroplastic lasting effect similar to that involved in cocaine addiction.
+ARC	drug	cocaine	30030395	Using primary striatal cultures, we show that transcription of Dnmt3a2, but not that of Dnmt3a1, is activated by dopamine D1 receptor signaling and that knockdown of Dnmt3a2 using viral vector mediated expression of Dnmt3a2 specific shRNAs impairs induction of the IEGs, <strong>Arc</strong>, FosB, and Egr2 Acute <b>cocaine</b> administration increases expression of Dnmt3a2 but not that of Dnmt3a1 in the NAc shell.
+ARC	drug	alcohol	29800622	The presence of an <b>alcohol</b> use disorder was associated with greater improvement in <b>alcohol</b> use in UC + CALM <strong>ARC</strong> compared to UC.
+ARC	addiction	withdrawal	29800622	Higher opiate related <b>withdrawal</b> symptoms and the presence of more SUDs were associated with greater improvement in drug use outcomes in UC + CALM <strong>ARC</strong> compared to UC.
+ARC	drug	amphetamine	29555337	Localized microinjections into the VTA or the <strong>ARC</strong> were used to assess the effects of a highly selective 5 HT2C receptor agonist, AR231630, on the locomotor stimulant effect of <b>amphetamine</b> as well as on food intake.
+ARC	drug	amphetamine	29555337	AR231630 injected into the VTA, but not into the <strong>ARC</strong>, dose dependently reduced locomotor activity elicited by <b>amphetamine</b>.
+ARC	addiction	reward	29555337	We can conclude that 5 HT2C receptor in the VTA, but not in the <strong>ARC</strong>, participates in both homeostatic and <b>hedonic</b> food intake and brain <b>reward</b> function.
+ARC	drug	alcohol	29097439	We analysed frequency, phenotype, transcriptional regulation and function of blood MAIT cells in severe <b>alcoholic</b> hepatitis (SAH), <b>alcohol</b> related cirrhosis (<strong>ARC</strong>) and healthy controls (HC).
+ARC	drug	amphetamine	28653356	Gene expression of neuropeptide Y, agouti related peptide, cocaine  and <b>amphetamine</b> regulated transcript, pro opiomelanocortin, long form leptin receptor and suppressor of cytokine signalling 3 in the hypothalamic arcuate nucleus (<strong>ARC</strong>), as well as enkephalin, dynorphin, dopamine 2 receptor and dopamine 3 receptor in the nucleus accumbens (NAcc) in the forebrain, were measured by in situ hybridisation.
+ARC	drug	cocaine	28653356	Gene expression of neuropeptide Y, agouti related peptide, <b>cocaine</b>  and amphetamine regulated transcript, pro opiomelanocortin, long form leptin receptor and suppressor of cytokine signalling 3 in the hypothalamic arcuate nucleus (<strong>ARC</strong>), as well as enkephalin, dynorphin, dopamine 2 receptor and dopamine 3 receptor in the nucleus accumbens (NAcc) in the forebrain, were measured by in situ hybridisation.
+ARC	addiction	intoxication	28653356	The effects of feeding regime on <strong>ARC</strong> gene expression were emphasised by significant positive or negative correlations with body weight gain, fat mass and blood leptin, although they did not appear to be related to feeding behaviour in the schedule fed groups (ie, the large, <b>binge</b> type meals) and did not reveal any potential candidates for the regulation of these meals.
+ARC	drug	opioid	28630256	Here, we report that extinction of conditioned place aversion (CPA) to <b>naloxone</b> precipitated opiate withdrawal in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (<strong>Arc</strong>) through facilitating actin polymerization.
+ARC	addiction	aversion	28630256	Here, we report that extinction of conditioned place <b>aversion</b> (CPA) to naloxone precipitated opiate withdrawal in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (<strong>Arc</strong>) through facilitating actin polymerization.
+ARC	addiction	withdrawal	28630256	Here, we report that extinction of conditioned place aversion (CPA) to naloxone precipitated opiate <b>withdrawal</b> in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (<strong>Arc</strong>) through facilitating actin polymerization.
+ARC	drug	opioid	28630256	Here, we report that extinction of conditioned place aversion (CPA) to <b>naloxone</b> precipitated opiate withdrawal in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>) through facilitating actin polymerization.
+ARC	addiction	aversion	28630256	Here, we report that extinction of conditioned place <b>aversion</b> (CPA) to naloxone precipitated opiate withdrawal in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>) through facilitating actin polymerization.
+ARC	addiction	withdrawal	28630256	Here, we report that extinction of conditioned place aversion (CPA) to naloxone precipitated opiate <b>withdrawal</b> in male rats activates Rho GTPase Rac1 in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>) through facilitating actin polymerization.
+ARC	addiction	aversion	28630256	Thus, the present study provides first evidence that Rac1 dependent GABAAR endocytosis plays a crucial role in extinction of <b>aversive</b> memories and reveals the sequence of molecular events that contribute to learning experience modulation of synaptic GABAAR endocytosis.SIGNIFICANCE STATEMENT This study reveals that Rac1 dependent GABAAR endocytosis plays a crucial role in extinction of <b>aversive</b> memories associated with drug withdrawal and identifies <strong>Arc</strong> as a downstream effector of Rac1 regulations of synaptic plasticity as well as learning and memory, thereby suggesting therapeutic targets to promote extinction of the unwanted memories.
+ARC	addiction	withdrawal	28630256	Thus, the present study provides first evidence that Rac1 dependent GABAAR endocytosis plays a crucial role in extinction of aversive memories and reveals the sequence of molecular events that contribute to learning experience modulation of synaptic GABAAR endocytosis.SIGNIFICANCE STATEMENT This study reveals that Rac1 dependent GABAAR endocytosis plays a crucial role in extinction of aversive memories associated with drug <b>withdrawal</b> and identifies <strong>Arc</strong> as a downstream effector of Rac1 regulations of synaptic plasticity as well as learning and memory, thereby suggesting therapeutic targets to promote extinction of the unwanted memories.
+ARC	addiction	sensitization	28608416	Allergic rhino conjunctivitis (<strong>ARC</strong>) was used as a marker for allergic <b>sensitization</b> to define allergic asthma.
+ARC	drug	nicotine	28560653	Analysis of epidemiological factors revealed that age (P < 0.001), cast of subjects (P = 0.001), diabetes (P < 0.001), hypertension (P = 0.001), <b>smoking</b> habit (P = 0.01), drug abuse (P < 0.05), steroid use (P = 0.001) and body weight (P < 0.001) can influence the incidence of <strong>ARC</strong> in enrolled subjects.
+ARC	addiction	addiction	28441678	In 2014, the authors developed and launched the <b>Addiction</b> Recovery Clinic (<strong>ARC</strong>) to address this educational gap while also providing outpatient clinical services to patients with substance use disorders.
+ARC	addiction	addiction	28441678	The <strong>ARC</strong> is embedded within the residency primary care practice and is staffed by three to four internal medicine residents, two board certified <b>addiction</b> medicine specialists, one chief resident, and one psychologist.
+ARC	addiction	withdrawal	27730515	Moreover, our results support the idea that targeting <strong>Arc</strong> and Egr 1 in the DG may provide important insights into the role of these signaling cascades in <b>withdrawal</b> context memory re consolidation.
+ARC	addiction	aversion	27728875	Interestingly, we observed that GCs were only increased in sham dependent rodents during <b>aversive</b> withdrawal memory consolidation, and that GR expression correlated with phosphorylated cAMP response element binding (pCREB) protein, early growth response 1 (Egr 1) and activity regulated cytoskeletal associated (<strong>Arc</strong>) mRNA induction in this experimental group.
+ARC	addiction	withdrawal	27728875	Interestingly, we observed that GCs were only increased in sham dependent rodents during aversive <b>withdrawal</b> memory consolidation, and that GR expression correlated with phosphorylated cAMP response element binding (pCREB) protein, early growth response 1 (Egr 1) and activity regulated cytoskeletal associated (<strong>Arc</strong>) mRNA induction in this experimental group.
+ARC	drug	opioid	27728875	Importantly, memory retrieval elicited increased pCREB levels in sham+<b>morphine</b> animals (not in ADX+<b>morphine</b> group), which were directly correlated with enhanced <strong>Arc</strong> mRNA/protein expression mainly in glutamatergic neurons.
+ARC	addiction	aversion	27728875	Moreover, dysregulation of CREB signaling, in part through <strong>Arc</strong> expression, may enhance reconsolidation, resulting in the maintenance of excessive <b>aversive</b> states.
+ARC	drug	cocaine	27567310	<strong>Activity Regulated Cytoskeleton Associated Protein</strong> Accumulates in the Nucleus in Response to <b>Cocaine</b> and Acts as a Brake on Chromatin Remodeling and Long Term Behavioral Alterations.
+ARC	drug	cocaine	27567310	Molecular and behavioral adaptations to <b>cocaine</b> were studied from <strong>Arc</strong> deficient mice and their wild type littermates.
+ARC	drug	cocaine	27567310	<strong>Arc</strong> messenger RNA and proteins are rapidly induced in the striatum after acute <b>cocaine</b> administration, via an extracellular signal regulated kinase dependent de novo protein synthesis.
+ARC	drug	cocaine	27567310	<b>Cocaine</b> induces the rapid induction of <strong>Arc</strong> and its nuclear accumulation in striatal neurons.
+ARC	drug	cocaine	27567310	These original observations posit <strong>Arc</strong> as a major homeostatic modulator of molecular and behavioral responses to <b>cocaine</b>.
+ARC	addiction	addiction	27567310	Thus, modulating <strong>Arc</strong> levels may provide promising therapeutic approaches in drug <b>addiction</b>.
+ARC	drug	opioid	27038750	This group had higher POMC in the arcuate nucleus (<strong>ARC</strong>), higher tyrosine hydroxylase (TH) in the VTA, higher dopa decarboxylase (DDc), higher D2R and μu <b>opioid</b> receptor in the NAc.
+ARC	drug	cocaine	26881139	Surface biotinylation analysis of protein expression in the dlSTR revealed that, in <b>cocaine</b> animals, intra dlSTR MTEP administration decreased mGlu5 surface expression and prevented changes in <strong>Arc</strong> and GluA1/GluA2 observed in their vehicle counterparts.
+ARC	drug	alcohol	26708208	Localized brain differences in <strong>Arc</strong> expression between mice showing low vs. high propensity to <b>ethanol</b> sensitization.
+ARC	addiction	sensitization	26708208	Localized brain differences in <strong>Arc</strong> expression between mice showing low vs. high propensity to ethanol <b>sensitization</b>.
+ARC	addiction	sensitization	26708208	We examined regional brain expression of the immediate early gene activity regulated cytoskeleton associated protein (<strong>Arc</strong>) in order to identify brain areas in which neuroplastic changes may contribute to the development and expression of EtOH <b>sensitization</b>.
+ARC	addiction	sensitization	26708208	We examined regional brain expression of the immediate early gene <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>) in order to identify brain areas in which neuroplastic changes may contribute to the development and expression of EtOH <b>sensitization</b>.
+ARC	addiction	sensitization	26708208	In both LS and HS mice sacrificed after the last <b>sensitization</b> injection, <strong>Arc</strong> expression was decreased throughout the brain in comparison to SAL animals.
+ARC	addiction	sensitization	26708208	The observation that HS mice do not show increases in <strong>Arc</strong> expression with an EtOH challenge suggests the possibility that increased tolerance to the <strong>Arc</strong> inducing effects of EtOH may be a factor in behavioral <b>sensitization</b>.
+ARC	drug	cocaine	26598422	Increased expression after <b>cocaine</b> self administration was found for 6 IEGs in dorsal and ventral striatum (c fos, Mkp1, Fosb/ΔFosb, Egr2, Egr4, and <strong>Arc</strong>) and 10 IEGs in mPFC (same 6 IEGs as in striatum, plus Bdnf, Homer1, Sgk1 and Rgs2).
+ARC	drug	amphetamine	26496011	We detected six downregulated genes in the frontal cortex and the hippocampus of chronic <b>METH</b> treated mice, including five IEGs (<strong>Arc</strong>, Egr2, Fos, Klf10, and Nr4a1) and one neuronal receptor gene (Grm1), compared with normal saline treated group, but only four genes (<strong>Arc</strong>, Egr2, Fos, and Nr4a1) were confirmed to be different.
+ARC	drug	amphetamine	26496011	Furthermore, we found several CpG sites of the <strong>Arc</strong> and the Fos that had significant changes in DNA methylation status in the frontal cortex of chronic <b>METH</b> treated mice, while the klf10 and the Nr4a1 that had significant changes in the hippocampus.
+ARC	drug	opioid	26418560	The present study used passive leg movement (PLM) and intrathecal injection of <b>fentanyl</b> to blunt the afferent portion of this reflex <strong>arc</strong> to better understand the role of the mechanoreflex on central and peripheral hemodynamics in HF.
+ARC	drug	nicotine	26219213	Here we evaluated whether maternal exposure to <b>nicotine</b> during lactation causes changes in dopamine and leptin signaling pathways at the end of exposure and after 5days of withdrawal in the: VTA, NAc, arcuate nucleus (<strong>ARC</strong>) and dorsal striatum (DS).
+ARC	addiction	withdrawal	26219213	Here we evaluated whether maternal exposure to nicotine during lactation causes changes in dopamine and leptin signaling pathways at the end of exposure and after 5days of <b>withdrawal</b> in the: VTA, NAc, arcuate nucleus (<strong>ARC</strong>) and dorsal striatum (DS).
+ARC	drug	amphetamine	26031216	We also matched the predicted targets of <b>METH</b> regulated miRNAs with the NAc messenger RNA expression profile, revealing eight putative <b>METH</b> regulated target genes (<strong>Arc</strong>, Capn9, Gbp5, Lefty1, Patl2, Pde4c, Strc, and Vmn1r58).
+ARC	drug	cannabinoid	26008155	Pre binge treatment with <b>rimonabant</b>, a drug recommended for the treatment of BE, produced anorexia, increased CART expression in <strong>ARC</strong> and LH, but not in AcbSh and PVT.
+ARC	addiction	intoxication	26008155	Pre <b>binge</b> treatment with rimonabant, a drug recommended for the treatment of BE, produced anorexia, increased CART expression in <strong>ARC</strong> and LH, but not in AcbSh and PVT.
+ARC	addiction	reward	26008155	We conclude that CART bearing <strong>ARC</strong> LH PVT AcbSh <b>reward</b> circuit may override the satiety signaling in <strong>ARC</strong> PVN pathway in BE rats.
+ARC	drug	cocaine	25982833	Neuronal reactivity was analyzed through the expression of two immediate early genes (<strong>Arc</strong> and c Fos) to decipher cellular responses to STN HFS and <b>cocaine</b>.
+ARC	drug	cocaine	25982833	Interestingly, and despite some differential effects on <strong>Arc</strong> and c Fos expression, STN HFS diminished the c Fos response induced by acute <b>cocaine</b> in the striatum.
+ARC	drug	alcohol	25929272	The rats conditioned to self administer <b>ethanol</b> showed significant increase in the population of NPY immunoreactive cells and fibres in the AcbSh, central nucleus of amygdala (CeA), hypothalamic arcuate nucleus (<strong>ARC</strong>) and lateral part of bed nucleus of stria terminalis as compared with that in the naïve rats.
+ARC	drug	alcohol	25929272	As NPY and dopamine systems in reward areas are known to interact, we suggest that NPY inputs from <strong>ARC</strong> and CeA may play an important role in modulation of the dopaminergic system in the AcbSh and consequently influence the <b>ethanol</b> induced reward and addiction.
+ARC	addiction	addiction	25929272	As NPY and dopamine systems in reward areas are known to interact, we suggest that NPY inputs from <strong>ARC</strong> and CeA may play an important role in modulation of the dopaminergic system in the AcbSh and consequently influence the ethanol induced reward and <b>addiction</b>.
+ARC	addiction	reward	25929272	As NPY and dopamine systems in <b>reward</b> areas are known to interact, we suggest that NPY inputs from <strong>ARC</strong> and CeA may play an important role in modulation of the dopaminergic system in the AcbSh and consequently influence the ethanol induced <b>reward</b> and addiction.
+ARC	drug	alcohol	25814047	AIE also induced anxiety like behaviors and enhanced <b>ethanol</b> intake in adulthood, which was attenuated by TSA treatment via normalization of deficits in histone H3 acetylation of BDNF and <strong>Arc</strong> genes.
+ARC	drug	opioid	25746394	NAc Shell <strong>Arc</strong>/Arg3.1 Protein Mediates Reconsolidation of <b>Morphine</b> CPP by Increased GluR1 Cell Surface Expression: Activation of ERK Coupled CREB is Required.
+ARC	addiction	reward	25746394	NAc Shell <strong>Arc</strong>/Arg3.1 Protein Mediates Reconsolidation of Morphine <b>CPP</b> by Increased GluR1 Cell Surface Expression: Activation of ERK Coupled CREB is Required.
+ARC	drug	opioid	25746394	NAc Shell <strong>Arc</strong>/<strong>Arg3.1</strong> Protein Mediates Reconsolidation of <b>Morphine</b> CPP by Increased GluR1 Cell Surface Expression: Activation of ERK Coupled CREB is Required.
+ARC	addiction	reward	25746394	NAc Shell <strong>Arc</strong>/<strong>Arg3.1</strong> Protein Mediates Reconsolidation of Morphine <b>CPP</b> by Increased GluR1 Cell Surface Expression: Activation of ERK Coupled CREB is Required.
+ARC	drug	opioid	25746394	<b>Morphine</b> conditioned place preference (CPP) was used to assess activity regulated cytoskeleton associated protein (<strong>Arc</strong>/Arg3.1) and correlative molecule expression in the Nucleus accumbens (NAc) shell during the reconsolidation of <b>morphine</b> CPP.
+ARC	addiction	reward	25746394	Morphine conditioned place preference (<b>CPP</b>) was used to assess activity regulated cytoskeleton associated protein (<strong>Arc</strong>/Arg3.1) and correlative molecule expression in the Nucleus accumbens (NAc) shell during the reconsolidation of morphine <b>CPP</b>.
+ARC	drug	opioid	25746394	<b>Morphine</b> conditioned place preference (CPP) was used to assess <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>/Arg3.1) and correlative molecule expression in the Nucleus accumbens (NAc) shell during the reconsolidation of <b>morphine</b> CPP.
+ARC	addiction	reward	25746394	Morphine conditioned place preference (<b>CPP</b>) was used to assess <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>/Arg3.1) and correlative molecule expression in the Nucleus accumbens (NAc) shell during the reconsolidation of morphine <b>CPP</b>.
+ARC	drug	opioid	25746394	<b>Morphine</b> conditioned place preference (CPP) was used to assess <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>/<strong>Arg3.1</strong>) and correlative molecule expression in the Nucleus accumbens (NAc) shell during the reconsolidation of <b>morphine</b> CPP.
+ARC	addiction	reward	25746394	Morphine conditioned place preference (<b>CPP</b>) was used to assess <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>/<strong>Arg3.1</strong>) and correlative molecule expression in the Nucleus accumbens (NAc) shell during the reconsolidation of morphine <b>CPP</b>.
+ARC	drug	opioid	25746394	The retrieval of <b>morphine</b> CPP in rats specifically increased the <strong>Arc</strong>/Arg3.1 protein level in the NAc shell, accompanied simultaneously by increases in the phosphorylation of extracellular signal regulated kinase1/2 (pERK1/2), the phosphorylation of Cyclic Adenosine monophosphate (cAMP) response element binding (pCREB), and the up regulation of the membrane α amino 3 hydroxy 5 methyl 4 isoxazole propionate (AMPA) receptors GluR1 subunit level.
+ARC	addiction	reward	25746394	The retrieval of morphine <b>CPP</b> in rats specifically increased the <strong>Arc</strong>/Arg3.1 protein level in the NAc shell, accompanied simultaneously by increases in the phosphorylation of extracellular signal regulated kinase1/2 (pERK1/2), the phosphorylation of Cyclic Adenosine monophosphate (cAMP) response element binding (pCREB), and the up regulation of the membrane α amino 3 hydroxy 5 methyl 4 isoxazole propionate (AMPA) receptors GluR1 subunit level.
+ARC	drug	opioid	25746394	The retrieval of <b>morphine</b> CPP in rats specifically increased the <strong>Arc</strong>/<strong>Arg3.1</strong> protein level in the NAc shell, accompanied simultaneously by increases in the phosphorylation of extracellular signal regulated kinase1/2 (pERK1/2), the phosphorylation of Cyclic Adenosine monophosphate (cAMP) response element binding (pCREB), and the up regulation of the membrane α amino 3 hydroxy 5 methyl 4 isoxazole propionate (AMPA) receptors GluR1 subunit level.
+ARC	addiction	reward	25746394	The retrieval of morphine <b>CPP</b> in rats specifically increased the <strong>Arc</strong>/<strong>Arg3.1</strong> protein level in the NAc shell, accompanied simultaneously by increases in the phosphorylation of extracellular signal regulated kinase1/2 (pERK1/2), the phosphorylation of Cyclic Adenosine monophosphate (cAMP) response element binding (pCREB), and the up regulation of the membrane α amino 3 hydroxy 5 methyl 4 isoxazole propionate (AMPA) receptors GluR1 subunit level.
+ARC	drug	opioid	25746394	Intra NAc shell infusion U0126, an inhibitor of the Mitogen activated protein kinase kinase (MEK), prevented the retrieval induced up regulation of pERK1/2, pCREB, <strong>Arc</strong>/Arg3.1, and membrane GluR1 immediately after retrieval of <b>morphine</b> CPP.
+ARC	addiction	reward	25746394	Intra NAc shell infusion U0126, an inhibitor of the Mitogen activated protein kinase kinase (MEK), prevented the retrieval induced up regulation of pERK1/2, pCREB, <strong>Arc</strong>/Arg3.1, and membrane GluR1 immediately after retrieval of morphine <b>CPP</b>.
+ARC	drug	opioid	25746394	Intra NAc shell infusion U0126, an inhibitor of the Mitogen activated protein kinase kinase (MEK), prevented the retrieval induced up regulation of pERK1/2, pCREB, <strong>Arc</strong>/<strong>Arg3.1</strong>, and membrane GluR1 immediately after retrieval of <b>morphine</b> CPP.
+ARC	addiction	reward	25746394	Intra NAc shell infusion U0126, an inhibitor of the Mitogen activated protein kinase kinase (MEK), prevented the retrieval induced up regulation of pERK1/2, pCREB, <strong>Arc</strong>/<strong>Arg3.1</strong>, and membrane GluR1 immediately after retrieval of morphine <b>CPP</b>.
+ARC	drug	opioid	25746394	Furthermore, the specific knockdown of <strong>Arc</strong>/Arg3.1 in the NAc shell decreased the membrane GluR1 level, and impaired both the reconsolidation and the reinstatement of <b>morphine</b> CPP.
+ARC	addiction	relapse	25746394	Furthermore, the specific knockdown of <strong>Arc</strong>/Arg3.1 in the NAc shell decreased the membrane GluR1 level, and impaired both the reconsolidation and the <b>reinstatement</b> of morphine CPP.
+ARC	addiction	reward	25746394	Furthermore, the specific knockdown of <strong>Arc</strong>/Arg3.1 in the NAc shell decreased the membrane GluR1 level, and impaired both the reconsolidation and the reinstatement of morphine <b>CPP</b>.
+ARC	drug	opioid	25746394	Furthermore, the specific knockdown of <strong>Arc</strong>/<strong>Arg3.1</strong> in the NAc shell decreased the membrane GluR1 level, and impaired both the reconsolidation and the reinstatement of <b>morphine</b> CPP.
+ARC	addiction	relapse	25746394	Furthermore, the specific knockdown of <strong>Arc</strong>/<strong>Arg3.1</strong> in the NAc shell decreased the membrane GluR1 level, and impaired both the reconsolidation and the <b>reinstatement</b> of morphine CPP.
+ARC	addiction	reward	25746394	Furthermore, the specific knockdown of <strong>Arc</strong>/<strong>Arg3.1</strong> in the NAc shell decreased the membrane GluR1 level, and impaired both the reconsolidation and the reinstatement of morphine <b>CPP</b>.
+ARC	drug	opioid	25746394	<strong>Arc</strong>/Arg3.1 in the NAc shell mediates the reconsolidation of <b>morphine</b> associated context memory via up regulating the level of membrane of GluR1, for which the local activation of the ERK CREB signal pathway, as an upstream mechanism of <strong>Arc</strong>/Arg3.1, is required.
+ARC	drug	opioid	25746394	<strong>Arc</strong>/<strong>Arg3.1</strong> in the NAc shell mediates the reconsolidation of <b>morphine</b> associated context memory via up regulating the level of membrane of GluR1, for which the local activation of the ERK CREB signal pathway, as an upstream mechanism of <strong>Arc</strong>/<strong>Arg3.1</strong>, is required.
+ARC	addiction	addiction	25646592	There is recent evidence of microRNA (miRNA) associated posttranscriptional suppression of <strong>Arc</strong> and animal models of <b>addiction</b> have identified a key role for miRNA in the regulation of <b>addiction</b> relevant genes.
+ARC	addiction	addiction	25646592	In further support of this link, we identified several differentially expressed miRNA with the potential to influence <b>addiction</b> relevant plasticity genes, including <strong>Arc</strong>.
+ARC	addiction	addiction	25590549	Nonetheless, some people consider themselves cyberdependent and request treatment services in the <b>addiction</b> rehabilitation centers (<strong>ARC</strong>) of the province of Quebec.
+ARC	drug	alcohol	25590549	1) Describe the socio demographical characteristics of cyberdependent individuals receiving treatment in the <strong>ARC</strong>; 2) Document their associated problems, such as problems related to <b>alcohol</b> and drug abuse, gambling, self esteem, and symptoms of depression and anxiety.
+ARC	addiction	addiction	25590549	To participate in this study, individuals had to be 18 years or older, identify themselves as cyberdependent, and request help for an Internet <b>addiction</b> problem in a public <strong>ARC</strong>.
+ARC	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, <strong>Arc</strong>, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+ARC	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, <strong>Arc</strong>, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+ARC	drug	opioid	25290009	To better dissect the time course of <b>opioid</b> produced IEG induction, we used in situ hybridization to examine the expression of the IEGs c fos, zif268 and <strong>arc</strong> in the mouse forebrain at several time points after acute <b>morphine</b> injection.
+ARC	drug	cocaine	25225165	Retrieval induced NMDA receptor dependent <strong>Arc</strong> expression in two models of <b>cocaine</b> cue memory.
+ARC	drug	cocaine	25225165	First, we directly compared, in a consistent setting, the involvement of cortical and subcortical brain regions in <b>cocaine</b> cue memory retrieval by quantifying activity regulated cytoskeletal associated (<strong>Arc</strong>) protein expression in both the CPP and CA models.
+ARC	addiction	reward	25225165	First, we directly compared, in a consistent setting, the involvement of cortical and subcortical brain regions in cocaine cue memory retrieval by quantifying activity regulated cytoskeletal associated (<strong>Arc</strong>) protein expression in both the <b>CPP</b> and CA models.
+ARC	addiction	reward	25225165	In both the <b>CPP</b> and CA models, drug paired animals showed significant increases in <strong>Arc</strong> immunoreactivity in regions of the frontal cortex and amygdala compared to unpaired controls.
+ARC	drug	cocaine	25225165	The enhanced <strong>Arc</strong> expression evident in a subset of corticolimbic regions after retrieval of a <b>cocaine</b> context memory, observed in both the CPP and CA paradigms, likely signifies that these regions: (i) are activated during retrieval of these memories irrespective of preference based decisions, and (ii) undergo neuroplasticity in order to update information about cues previously associated with <b>cocaine</b>.
+ARC	addiction	reward	25225165	The enhanced <strong>Arc</strong> expression evident in a subset of corticolimbic regions after retrieval of a cocaine context memory, observed in both the <b>CPP</b> and CA paradigms, likely signifies that these regions: (i) are activated during retrieval of these memories irrespective of preference based decisions, and (ii) undergo neuroplasticity in order to update information about cues previously associated with cocaine.
+ARC	drug	cocaine	25225165	Overall, these results demonstrate the utility of the CA model for studies of <b>cocaine</b> context memory and suggest the involvement of an NMDA receptor dependent <strong>Arc</strong> induction pathway in drug cue memory interference.
+ARC	drug	cocaine	24912888	The objective of the present study was to discern if acute or repeated regimens of daily <b>cocaine</b> (10 mg/kg) lead to reliable changes in the expression of some protein markers for neural plasticity such as synaptophysin, p21 <strong>Arc</strong>, alpha tubulin (α tubulin), and stathmin, in the mesolimbic dopaminergic circuit.
+ARC	drug	cocaine	24912888	The findings revealed that sensitizing regimen of <b>cocaine</b> increases stathmin levels within the nucleus accumbens at day 18 of treatment, not day 8, without changes of synaptophysin, p21 <strong>Arc</strong>, or α tubulin.
+ARC	drug	nicotine	24440829	In immunohistochemical study, <b>nicotine</b> decreased NPY immunoreactivity in nucleus accumbens shell (AcbSh), bed nucleus of stria terminalis, lateral part (BNSTl), arcuate nucleus (<strong>ARC</strong>) and paraventricular nucleus (PVN).
+ARC	drug	alcohol	24103311	Reversal of deficits in dendritic spines, BDNF and <strong>Arc</strong> expression in the amygdala during <b>alcohol</b> dependence by HDAC inhibitor treatment.
+ARC	addiction	dependence	24103311	Reversal of deficits in dendritic spines, BDNF and <strong>Arc</strong> expression in the amygdala during alcohol <b>dependence</b> by HDAC inhibitor treatment.
+ARC	drug	alcohol	24103311	Development of anxiety like behaviours during <b>ethanol</b> withdrawal has been correlated with increased histone deacetylase (HDAC) activity and decreased brain derived neurotrophic factor (BDNF) and activity regulated cytoskeleton associated protein (<strong>Arc</strong>) gene expression in the amygdala.
+ARC	addiction	withdrawal	24103311	Development of anxiety like behaviours during ethanol <b>withdrawal</b> has been correlated with increased histone deacetylase (HDAC) activity and decreased brain derived neurotrophic factor (BDNF) and activity regulated cytoskeleton associated protein (<strong>Arc</strong>) gene expression in the amygdala.
+ARC	drug	alcohol	24103311	Development of anxiety like behaviours during <b>ethanol</b> withdrawal has been correlated with increased histone deacetylase (HDAC) activity and decreased brain derived neurotrophic factor (BDNF) and <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>) gene expression in the amygdala.
+ARC	addiction	withdrawal	24103311	Development of anxiety like behaviours during ethanol <b>withdrawal</b> has been correlated with increased histone deacetylase (HDAC) activity and decreased brain derived neurotrophic factor (BDNF) and <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>) gene expression in the amygdala.
+ARC	drug	alcohol	24103311	In this study we used the HDAC inhibitor trichostatin A (TSA) to determine whether HDAC inhibition could prevent <b>ethanol</b> withdrawal induced deficits in dendritic spine density (DSD), BDNF or <strong>Arc</strong> expression in the amygdala of rats.
+ARC	addiction	withdrawal	24103311	In this study we used the HDAC inhibitor trichostatin A (TSA) to determine whether HDAC inhibition could prevent ethanol <b>withdrawal</b> induced deficits in dendritic spine density (DSD), BDNF or <strong>Arc</strong> expression in the amygdala of rats.
+ARC	drug	alcohol	24103311	It was found that decreased BDNF and <strong>Arc</strong> expression in the central (CeA) and medial nucleus of amygdala (MeA), observed during withdrawal after chronic <b>ethanol</b> exposure, were normalized following acute TSA treatment.
+ARC	addiction	withdrawal	24103311	It was found that decreased BDNF and <strong>Arc</strong> expression in the central (CeA) and medial nucleus of amygdala (MeA), observed during <b>withdrawal</b> after chronic ethanol exposure, were normalized following acute TSA treatment.
+ARC	drug	alcohol	24103311	Taken together, these findings demonstrate that correcting the deficits in histone acetylation through TSA treatment also amends downstream synaptic plasticity related deficits such as BDNF and <strong>Arc</strong> expression, and DSD in the CeA and MeA as well as attenuates anxiety like behaviours in rats during withdrawal after chronic <b>ethanol</b> exposure.
+ARC	addiction	withdrawal	24103311	Taken together, these findings demonstrate that correcting the deficits in histone acetylation through TSA treatment also amends downstream synaptic plasticity related deficits such as BDNF and <strong>Arc</strong> expression, and DSD in the CeA and MeA as well as attenuates anxiety like behaviours in rats during <b>withdrawal</b> after chronic ethanol exposure.
+ARC	addiction	relapse	24069163	After extinction training and <b>reinstatement</b> testing, where both cues were presented in separate sessions, rats were sacrificed and processed for cellular analysis of temporal activity by fluorescent in situ hybridization (CatFISH) for activity regulated cytoskeleton associated protein (<strong>Arc</strong>) mRNA and for radioactive in situ hybridization for <strong>Arc</strong> and zif268 mRNAs.
+ARC	addiction	relapse	24069163	After extinction training and <b>reinstatement</b> testing, where both cues were presented in separate sessions, rats were sacrificed and processed for cellular analysis of temporal activity by fluorescent in situ hybridization (CatFISH) for <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>) mRNA and for radioactive in situ hybridization for <strong>Arc</strong> and zif268 mRNAs.
+ARC	addiction	relapse	24069163	We have shown that while rats reinstate drug <b>seeking</b> in response to temporally discrete presentations of distinct drug associated cues, such <b>reinstatement</b> is not associated with increased transcriptional activation of <strong>Arc</strong> or zif268 mRNAs, suggesting that expression of these genes may not be necessary for cue induced <b>reinstatement</b> of drug <b>seeking</b> behavior.
+ARC	drug	amphetamine	23895375	<b>Methamphetamine</b> induced 3 20 fold increases of immediate early genes <strong>arc</strong>, homer 2, c fos, fosB, and its isoforms (ΔfosB and a novel isoform ΔfosB 2) in Fos positive but not Fos negative neurons.
+ARC	drug	alcohol	23792540	We found that binge like <b>ethanol</b> exposure during adolescence significantly reduced basal α MSH IR in the central nucleus of the amygdala (CeA), the arcuate nucleus (<strong>Arc</strong>) and the paraventricular nucleus of the hypothalamus (PVN) during adulthood.
+ARC	addiction	intoxication	23792540	We found that <b>binge</b> like ethanol exposure during adolescence significantly reduced basal α MSH IR in the central nucleus of the amygdala (CeA), the arcuate nucleus (<strong>Arc</strong>) and the paraventricular nucleus of the hypothalamus (PVN) during adulthood.
+ARC	drug	alcohol	23792540	Additionally, acute <b>ethanol</b> elicited AgRP IR in the <strong>Arc</strong>.
+ARC	drug	opioid	23708554	Immunohistochemical assay was used to quantify <strong>Arc</strong> protein expression in the medial prefrontal cortex (mPFC), the nucleus accumbens (NAc), the dorsomedial striatum (DMS) and the ventrolateral striatum (VLS) in response to chronic self administration of <b>heroin</b> or milk tablets.
+ARC	drug	opioid	23708554	Runway training with <b>heroin</b> resulted in robust enhancement of <strong>Arc</strong> expression in the mPFC, the NAc and the DMS on d 1, 7, and 15, and in the VLS on d 1 and d 7.
+ARC	drug	opioid	23708554	Both <b>heroin</b> seeking behavior and <strong>Arc</strong> protein expression were blocked by MK801 or SCH23390 administration.
+ARC	addiction	relapse	23708554	Both heroin <b>seeking</b> behavior and <strong>Arc</strong> protein expression were blocked by MK801 or SCH23390 administration.
+ARC	addiction	relapse	23708554	The NMDA  and D1 receptor dependent <strong>Arc</strong> expression is important in drug <b>seeking</b> behavior.
+ARC	addiction	reward	23511250	NPY immunoreactivity in the AcbSh, arcuate nucleus (<strong>ARC</strong>) and lateral part of bed nucleus of stria terminalis (BNSTl) was significantly more in the <b>operant</b> conditioned rats than in naïve control.
+ARC	drug	opioid	23511250	Since the role of <b>morphine</b> in modulation of mesolimbic dopaminergic pathway is well established, we suggest that NPY system in AcbSh, <strong>ARC</strong> and BNSTl, perhaps acting via Y1 receptor system, may be an important component of the mesolimbic AcbSh reward circuitry triggered by endogenous <b>opioids</b>.
+ARC	addiction	reward	23511250	Since the role of morphine in modulation of mesolimbic dopaminergic pathway is well established, we suggest that NPY system in AcbSh, <strong>ARC</strong> and BNSTl, perhaps acting via Y1 receptor system, may be an important component of the mesolimbic AcbSh <b>reward</b> circuitry triggered by endogenous opioids.
+ARC	drug	alcohol	23485013	Acute <b>ethanol</b> exposure decreased amygdaloid HDAC activity and HDAC2 protein levels, increased global and gene (Bdnf and <strong>Arc</strong>) specific histone acetylation, and attenuated anxiety like behaviors in P rats but had no effects in NP rats.
+ARC	drug	alcohol	23485013	The HDAC2 knockdown in the CeA attenuated anxiety like behaviors and voluntary <b>alcohol</b> but not sucrose consumption in P rats and increased histone acetylation of Bdnf and <strong>Arc</strong> with a resultant increase in protein levels that correlated with increased dendritic spine density.
+ARC	drug	opioid	23337531	After 12 h withdrawal, <b>heroin</b> treated mice showed lower signal intensity of POMC EGFP positive cells in the <strong>ARC</strong>, higher levels of POMC mRNA in the amygdala but lower levels in the hippocampus than saline controls.
+ARC	addiction	withdrawal	23337531	After 12 h <b>withdrawal</b>, heroin treated mice showed lower signal intensity of POMC EGFP positive cells in the <strong>ARC</strong>, higher levels of POMC mRNA in the amygdala but lower levels in the hippocampus than saline controls.
+ARC	drug	opioid	23238466	Among them, a cluster of 8 genes, including 6 inducible transcription factors (c fos, fra 2, junB, zif268 (egr1), egr2, NGFI B) and 2 effector IEG (<strong>arc</strong> and mkp1) seemed to be regulated in concert in response to <b>morphine</b>.
+ARC	addiction	reward	23194408	or with daily 2 h scheduled access and standard pellet available for 22 h. Energy balance gene expression in the hypothalamic arcuate nucleus (<strong>ARC</strong>) and nucleus accumbens (NAcc) <b>reward</b> gene expression were assessed by in situ hybridisation.
+ARC	drug	amphetamine	23194408	on any of the palatable diets were heavier, fatter and had higher blood leptin than controls, and had reduced NPY and increased cocaine  and <b>amphetamine</b> regulated transcript mRNA in the <strong>ARC</strong>.
+ARC	drug	cocaine	23194408	on any of the palatable diets were heavier, fatter and had higher blood leptin than controls, and had reduced NPY and increased <b>cocaine</b>  and amphetamine regulated transcript mRNA in the <strong>ARC</strong>.
+ARC	drug	amphetamine	22945419	The purposes of the present study were: (1) to determine if the retrieval of contextual memories would induce <strong>Arc</strong> in hippocampal and amygdalar neurons; (2) use unbiased stereology at the ultrastructural level to quantify synapses contacting <strong>Arc</strong> labeled (<strong>Arc</strong>+) and unlabeled (<strong>Arc</strong> ) postsynaptic structures in brain regions in which the amount of <strong>Arc</strong> integrated density (ID) correlated strongly with the degree of <b>amphetamine</b> conditioned place preference (<b>AMPH</b> CPP).
+ARC	addiction	reward	22945419	The purposes of the present study were: (1) to determine if the retrieval of contextual memories would induce <strong>Arc</strong> in hippocampal and amygdalar neurons; (2) use unbiased stereology at the ultrastructural level to quantify synapses contacting <strong>Arc</strong> labeled (<strong>Arc</strong>+) and unlabeled (<strong>Arc</strong> ) postsynaptic structures in brain regions in which the amount of <strong>Arc</strong> integrated density (ID) correlated strongly with the degree of amphetamine conditioned place preference (AMPH <b>CPP</b>).
+ARC	drug	amphetamine	22945419	Stereological quantification of <strong>Arc</strong>+ and <strong>Arc</strong>  synapses in the basolateral nucleus of the amygdala (BLA) was undertaken because the strongest relationship between the amount of <strong>Arc</strong> ID and <b>AMPH</b> CPP was observed in the BLA.
+ARC	addiction	reward	22945419	Stereological quantification of <strong>Arc</strong>+ and <strong>Arc</strong>  synapses in the basolateral nucleus of the amygdala (BLA) was undertaken because the strongest relationship between the amount of <strong>Arc</strong> ID and AMPH <b>CPP</b> was observed in the BLA.
+ARC	addiction	aversion	22933785	Actin polymerization dependent increase in synaptic <strong>Arc</strong>/Arg3.1 expression in the amygdala is crucial for the expression of <b>aversive</b> memory associated with drug withdrawal.
+ARC	addiction	withdrawal	22933785	Actin polymerization dependent increase in synaptic <strong>Arc</strong>/Arg3.1 expression in the amygdala is crucial for the expression of aversive memory associated with drug <b>withdrawal</b>.
+ARC	addiction	aversion	22933785	Actin polymerization dependent increase in synaptic <strong>Arc</strong>/<strong>Arg3.1</strong> expression in the amygdala is crucial for the expression of <b>aversive</b> memory associated with drug withdrawal.
+ARC	addiction	withdrawal	22933785	Actin polymerization dependent increase in synaptic <strong>Arc</strong>/<strong>Arg3.1</strong> expression in the amygdala is crucial for the expression of aversive memory associated with drug <b>withdrawal</b>.
+ARC	addiction	aversion	22933785	Increased synaptic <strong>Arc</strong>/Arg3.1 expression contributed to <b>aversive</b> memory formation by regulating synaptic AMPA receptor (AMPAR) endocytosis, as in vivo knockdown of amygdalar <strong>Arc</strong>/Arg3.1 with <strong>Arc</strong>/Arg3.1 shRNA prevented both AMPAR endocytosis and CPA formation.
+ARC	addiction	aversion	22933785	Increased synaptic <strong>Arc</strong>/<strong>Arg3.1</strong> expression contributed to <b>aversive</b> memory formation by regulating synaptic AMPA receptor (AMPAR) endocytosis, as in vivo knockdown of amygdalar <strong>Arc</strong>/<strong>Arg3.1</strong> with <strong>Arc</strong>/<strong>Arg3.1</strong> shRNA prevented both AMPAR endocytosis and CPA formation.
+ARC	addiction	aversion	22933785	We further demonstrated that <strong>Arc</strong>/Arg3.1 regulated AMPAR endocytosis was GluR2 dependent, as intra amygdala injection of Tat GluR2(3Y), a GluR2 derived peptide that has been shown to specifically block regulated, but not constitutive, AMPAR endocytosis, prevented AMPAR endocytosis, LTD induction, and <b>aversive</b> memory formation.
+ARC	addiction	aversion	22933785	We further demonstrated that <strong>Arc</strong>/<strong>Arg3.1</strong> regulated AMPAR endocytosis was GluR2 dependent, as intra amygdala injection of Tat GluR2(3Y), a GluR2 derived peptide that has been shown to specifically block regulated, but not constitutive, AMPAR endocytosis, prevented AMPAR endocytosis, LTD induction, and <b>aversive</b> memory formation.
+ARC	addiction	aversion	22933785	Therefore, this study extends previous studies on the role of actin polymerization in synaptic plasticity and memory formation by revealing the critical molecular events involved in <b>aversive</b> memory formation as well as LTD induction, and by showing that <strong>Arc</strong>/Arg3.1 is a crucial mediator for actin polymerization functions, and, thus, underscores the unknown details of how actin polymerization mediates synaptic plasticity and memory.
+ARC	addiction	aversion	22933785	Therefore, this study extends previous studies on the role of actin polymerization in synaptic plasticity and memory formation by revealing the critical molecular events involved in <b>aversive</b> memory formation as well as LTD induction, and by showing that <strong>Arc</strong>/<strong>Arg3.1</strong> is a crucial mediator for actin polymerization functions, and, thus, underscores the unknown details of how actin polymerization mediates synaptic plasticity and memory.
+ARC	drug	benzodiazepine	22759216	Impact of contextual cues in the expression of the memory associated with <b>diazepam</b> withdrawal: involvement of hippocampal PKMζ in vivo, and <strong>Arc</strong> expression and LTP in vitro.
+ARC	addiction	withdrawal	22759216	Impact of contextual cues in the expression of the memory associated with diazepam <b>withdrawal</b>: involvement of hippocampal PKMζ in vivo, and <strong>Arc</strong> expression and LTP in vitro.
+ARC	addiction	withdrawal	22759216	We found that the context was relevant for the expression of <b>withdrawal</b> signs as changes in contextual cues prevented the expression of the anxiety like behavior observed during plus maze (PM) re exposure, the associated enhanced synaptic plasticity and the increase in <strong>Arc</strong> expression.
+ARC	drug	cocaine	21976515	Consequently, TDE altered <b>cocaine</b> induced regulation of genes bearing SRE site(s) in their promoters, including c fos, zif268, ΔFosB, and <strong>arc</strong>/arg3.1 (activity regulated cytoskeleton associated protein).
+ARC	drug	cocaine	21976515	Consequently, TDE altered <b>cocaine</b> induced regulation of genes bearing SRE site(s) in their promoters, including c fos, zif268, ΔFosB, and <strong>arc</strong>/arg3.1 (<strong>activity regulated cytoskeleton associated protein</strong>).
+ARC	drug	cocaine	21976515	Consequently, TDE altered <b>cocaine</b> induced regulation of genes bearing SRE site(s) in their promoters, including c fos, zif268, ΔFosB, and <strong>arc</strong>/<strong>arg3.1</strong> (<strong>activity regulated cytoskeleton associated protein</strong>).
+ARC	drug	alcohol	21895716	<b>Ethanol</b> induced loss of righting response during <b>ethanol</b> withdrawal in male and female rats: associations with alterations in <strong>Arc</strong> labeling.
+ARC	addiction	withdrawal	21895716	Ethanol induced loss of righting response during ethanol <b>withdrawal</b> in male and female rats: associations with alterations in <strong>Arc</strong> labeling.
+ARC	drug	alcohol	21895716	<strong>Arc</strong> protein levels in motor cortex and preoptic nuclei significantly increased at 1 day EW across all sex conditions, suggestive of an association with the reduced <b>ethanol</b> induced sleep times during EW.
+ARC	drug	cocaine	21590283	Stress and <b>cocaine</b> interact to modulate <strong>Arc</strong>/Arg3.1 expression in rat brain.
+ARC	drug	cocaine	21590283	Stress and <b>cocaine</b> interact to modulate <strong>Arc</strong>/<strong>Arg3.1</strong> expression in rat brain.
+ARC	drug	cocaine	21590283	This research aims to study the modulation of <strong>Arc</strong>/Arg3.1 expression as a marker of neuronal changes associated with exposure to stress and <b>cocaine</b>.
+ARC	drug	cocaine	21590283	This research aims to study the modulation of <strong>Arc</strong>/<strong>Arg3.1</strong> expression as a marker of neuronal changes associated with exposure to stress and <b>cocaine</b>.
+ARC	drug	cocaine	21590283	In the prefrontal cortex, acute stress potentiated <b>cocaine</b> induced <strong>Arc</strong>/Arg3.1 mRNA elevation, whereas prolonged stress attenuated the response to <b>cocaine</b>.
+ARC	drug	cocaine	21590283	In the prefrontal cortex, acute stress potentiated <b>cocaine</b> induced <strong>Arc</strong>/<strong>Arg3.1</strong> mRNA elevation, whereas prolonged stress attenuated the response to <b>cocaine</b>.
+ARC	drug	cocaine	21590283	In the hypothalamus, although markedly reduced by acute stress, <strong>Arc</strong>/Arg3.1 gene expression was still increased by <b>cocaine</b>.
+ARC	drug	cocaine	21590283	In the hypothalamus, although markedly reduced by acute stress, <strong>Arc</strong>/<strong>Arg3.1</strong> gene expression was still increased by <b>cocaine</b>.
+ARC	drug	cocaine	21590283	Notably, <b>cocaine</b> induced <strong>Arc</strong>/Arg3.1 mRNA levels were not influenced by stress in striatum and hippocampus.
+ARC	drug	cocaine	21590283	Notably, <b>cocaine</b> induced <strong>Arc</strong>/<strong>Arg3.1</strong> mRNA levels were not influenced by stress in striatum and hippocampus.
+ARC	drug	cocaine	21590283	In our experimental model, stress interacted with <b>cocaine</b> to alter <strong>Arc</strong>/Arg3.1 expression in a regionally selective fashion and in a way that depended on whether stress was acute or repeated.
+ARC	drug	cocaine	21590283	In our experimental model, stress interacted with <b>cocaine</b> to alter <strong>Arc</strong>/<strong>Arg3.1</strong> expression in a regionally selective fashion and in a way that depended on whether stress was acute or repeated.
+ARC	drug	cocaine	21590283	These results point to <strong>Arc</strong>/Arg3.1 as a potential molecular target modulated by stress to alter cellular sensitivity to <b>cocaine</b>.
+ARC	drug	cocaine	21590283	These results point to <strong>Arc</strong>/<strong>Arg3.1</strong> as a potential molecular target modulated by stress to alter cellular sensitivity to <b>cocaine</b>.
+ARC	drug	opioid	21549764	Expression of activity regulated cytoskeleton associated protein (<strong>Arc</strong>/Arg3.1) in the nucleus accumbens is critical for the acquisition, expression and reinstatement of <b>morphine</b> induced conditioned place preference.
+ARC	addiction	relapse	21549764	Expression of activity regulated cytoskeleton associated protein (<strong>Arc</strong>/Arg3.1) in the nucleus accumbens is critical for the acquisition, expression and <b>reinstatement</b> of morphine induced conditioned place preference.
+ARC	drug	opioid	21549764	Expression of <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>/Arg3.1) in the nucleus accumbens is critical for the acquisition, expression and reinstatement of <b>morphine</b> induced conditioned place preference.
+ARC	addiction	relapse	21549764	Expression of <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>/Arg3.1) in the nucleus accumbens is critical for the acquisition, expression and <b>reinstatement</b> of morphine induced conditioned place preference.
+ARC	drug	opioid	21549764	Expression of <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>/<strong>Arg3.1</strong>) in the nucleus accumbens is critical for the acquisition, expression and reinstatement of <b>morphine</b> induced conditioned place preference.
+ARC	addiction	relapse	21549764	Expression of <strong>activity regulated cytoskeleton associated protein</strong> (<strong>Arc</strong>/<strong>Arg3.1</strong>) in the nucleus accumbens is critical for the acquisition, expression and <b>reinstatement</b> of morphine induced conditioned place preference.
+ARC	addiction	reward	21549764	Although the <strong>Arc</strong>/Arg3.1 gene has been shown to be induced by a variety of abused drugs and its protein has been implicated in diverse forms of long term memory, relatively little is known about its role in drug induced <b>reward</b> memory.
+ARC	addiction	reward	21549764	Although the <strong>Arc</strong>/<strong>Arg3.1</strong> gene has been shown to be induced by a variety of abused drugs and its protein has been implicated in diverse forms of long term memory, relatively little is known about its role in drug induced <b>reward</b> memory.
+ARC	drug	opioid	21549764	In this study, we investigated the potential role of <strong>Arc</strong>/Arg3.1 protein expression in reward related associative learning and memory using <b>morphine</b> induced conditioned place preference (CPP) in rats.
+ARC	addiction	reward	21549764	In this study, we investigated the potential role of <strong>Arc</strong>/Arg3.1 protein expression in <b>reward</b> related associative learning and memory using morphine induced conditioned place preference (<b>CPP</b>) in rats.
+ARC	drug	opioid	21549764	In this study, we investigated the potential role of <strong>Arc</strong>/<strong>Arg3.1</strong> protein expression in reward related associative learning and memory using <b>morphine</b> induced conditioned place preference (CPP) in rats.
+ARC	addiction	reward	21549764	In this study, we investigated the potential role of <strong>Arc</strong>/<strong>Arg3.1</strong> protein expression in <b>reward</b> related associative learning and memory using morphine induced conditioned place preference (<b>CPP</b>) in rats.
+ARC	drug	opioid	21549764	injection of <b>morphine</b> (10mg/kg) increased <strong>Arc</strong>/Arg3.1 protein levels after 2h in the NAc core but not in the NAc shell.
+ARC	drug	opioid	21549764	injection of <b>morphine</b> (10mg/kg) increased <strong>Arc</strong>/<strong>Arg3.1</strong> protein levels after 2h in the NAc core but not in the NAc shell.
+ARC	drug	opioid	21549764	(2) In CPP experiments, <strong>Arc</strong>/Arg3.1 protein was increased in the NAc shell of rats following both <b>morphine</b> conditioning and the CPP expression test compared to rats that received the conditioning without the test or those that did not receive <b>morphine</b> conditioning.
+ARC	addiction	reward	21549764	(2) In <b>CPP</b> experiments, <strong>Arc</strong>/Arg3.1 protein was increased in the NAc shell of rats following both morphine conditioning and the <b>CPP</b> expression test compared to rats that received the conditioning without the test or those that did not receive morphine conditioning.
+ARC	drug	opioid	21549764	(2) In CPP experiments, <strong>Arc</strong>/<strong>Arg3.1</strong> protein was increased in the NAc shell of rats following both <b>morphine</b> conditioning and the CPP expression test compared to rats that received the conditioning without the test or those that did not receive <b>morphine</b> conditioning.
+ARC	addiction	reward	21549764	(2) In <b>CPP</b> experiments, <strong>Arc</strong>/<strong>Arg3.1</strong> protein was increased in the NAc shell of rats following both morphine conditioning and the <b>CPP</b> expression test compared to rats that received the conditioning without the test or those that did not receive morphine conditioning.
+ARC	drug	opioid	21549764	(3) Microinjection of <strong>Arc</strong>/Arg3.1 antisense oligodeoxynucleotide (AS) into the NAc core inhibited the acquisition, expression and reinstatement of <b>morphine</b> CPP; however, intra NAc shell infusions of the AS only blocked the expression of CPP.
+ARC	addiction	relapse	21549764	(3) Microinjection of <strong>Arc</strong>/Arg3.1 antisense oligodeoxynucleotide (AS) into the NAc core inhibited the acquisition, expression and <b>reinstatement</b> of morphine CPP; however, intra NAc shell infusions of the AS only blocked the expression of CPP.
+ARC	addiction	reward	21549764	(3) Microinjection of <strong>Arc</strong>/Arg3.1 antisense oligodeoxynucleotide (AS) into the NAc core inhibited the acquisition, expression and reinstatement of morphine <b>CPP</b>; however, intra NAc shell infusions of the AS only blocked the expression of <b>CPP</b>.
+ARC	drug	opioid	21549764	(3) Microinjection of <strong>Arc</strong>/<strong>Arg3.1</strong> antisense oligodeoxynucleotide (AS) into the NAc core inhibited the acquisition, expression and reinstatement of <b>morphine</b> CPP; however, intra NAc shell infusions of the AS only blocked the expression of CPP.
+ARC	addiction	relapse	21549764	(3) Microinjection of <strong>Arc</strong>/<strong>Arg3.1</strong> antisense oligodeoxynucleotide (AS) into the NAc core inhibited the acquisition, expression and <b>reinstatement</b> of morphine CPP; however, intra NAc shell infusions of the AS only blocked the expression of CPP.
+ARC	addiction	reward	21549764	(3) Microinjection of <strong>Arc</strong>/<strong>Arg3.1</strong> antisense oligodeoxynucleotide (AS) into the NAc core inhibited the acquisition, expression and reinstatement of morphine <b>CPP</b>; however, intra NAc shell infusions of the AS only blocked the expression of <b>CPP</b>.
+ARC	drug	opioid	21549764	These findings suggest that expression of the <strong>Arc</strong>/Arg3.1 protein in the NAc core is required for the acquisition, context induced retrieval and reinstatement of <b>morphine</b> associated reward memory, whereas <strong>Arc</strong>/Arg3.1 protein expression in the NAc shell is only critical for the context induced retrieval of memory.
+ARC	addiction	relapse	21549764	These findings suggest that expression of the <strong>Arc</strong>/Arg3.1 protein in the NAc core is required for the acquisition, context induced retrieval and <b>reinstatement</b> of morphine associated reward memory, whereas <strong>Arc</strong>/Arg3.1 protein expression in the NAc shell is only critical for the context induced retrieval of memory.
+ARC	addiction	reward	21549764	These findings suggest that expression of the <strong>Arc</strong>/Arg3.1 protein in the NAc core is required for the acquisition, context induced retrieval and reinstatement of morphine associated <b>reward</b> memory, whereas <strong>Arc</strong>/Arg3.1 protein expression in the NAc shell is only critical for the context induced retrieval of memory.
+ARC	drug	opioid	21549764	These findings suggest that expression of the <strong>Arc</strong>/<strong>Arg3.1</strong> protein in the NAc core is required for the acquisition, context induced retrieval and reinstatement of <b>morphine</b> associated reward memory, whereas <strong>Arc</strong>/<strong>Arg3.1</strong> protein expression in the NAc shell is only critical for the context induced retrieval of memory.
+ARC	addiction	relapse	21549764	These findings suggest that expression of the <strong>Arc</strong>/<strong>Arg3.1</strong> protein in the NAc core is required for the acquisition, context induced retrieval and <b>reinstatement</b> of morphine associated reward memory, whereas <strong>Arc</strong>/<strong>Arg3.1</strong> protein expression in the NAc shell is only critical for the context induced retrieval of memory.
+ARC	addiction	reward	21549764	These findings suggest that expression of the <strong>Arc</strong>/<strong>Arg3.1</strong> protein in the NAc core is required for the acquisition, context induced retrieval and reinstatement of morphine associated <b>reward</b> memory, whereas <strong>Arc</strong>/<strong>Arg3.1</strong> protein expression in the NAc shell is only critical for the context induced retrieval of memory.
+ARC	addiction	relapse	21549764	As a result, <strong>Arc</strong>/Arg3.1 may be a potential therapeutic target for the prevention of drug abuse or the <b>relapse</b> of drug use.
+ARC	addiction	relapse	21549764	As a result, <strong>Arc</strong>/<strong>Arg3.1</strong> may be a potential therapeutic target for the prevention of drug abuse or the <b>relapse</b> of drug use.
+ARC	drug	cocaine	21318636	Regulation of the immediate early genes <strong>arc</strong> and zif268 in a mouse operant model of <b>cocaine</b> seeking reinstatement.
+ARC	addiction	relapse	21318636	Regulation of the immediate early genes <strong>arc</strong> and zif268 in a mouse operant model of cocaine <b>seeking</b> <b>reinstatement</b>.
+ARC	addiction	reward	21318636	Regulation of the immediate early genes <strong>arc</strong> and zif268 in a mouse <b>operant</b> model of cocaine seeking reinstatement.
+ARC	drug	cocaine	21318636	The aim of the present study was to assess regional brain activation, as measured by induction of the immediate early genes (IEG) <strong>arc</strong> and zif268, during priming  or cue elicited reinstatement of <b>cocaine</b> seeking using this new mouse model and the in situ hybridization technique.
+ARC	addiction	relapse	21318636	The aim of the present study was to assess regional brain activation, as measured by induction of the immediate early genes (IEG) <strong>arc</strong> and zif268, during priming  or cue elicited <b>reinstatement</b> of cocaine <b>seeking</b> using this new mouse model and the in situ hybridization technique.
+ARC	drug	amphetamine	21229349	In contrast, the <b>METH</b> challenge caused significant but blunted increases in Nr4a3 and <strong>Arc</strong> expression in <b>METH</b> pretreated rats.
+ARC	drug	nicotine	21147173	Acute <b>nicotine</b> treatment caused a significant increase above control in the CART immunoreactive cells and fibers in the hypothalamic paraventricular (PVN) and fibers in the arcuate (<strong>ARC</strong>) nuclei.
+ARC	drug	nicotine	21147173	However, chronic <b>nicotine</b> administration had no effect on the CART immunoreactivity in the PVN and <strong>ARC</strong>.
+ARC	drug	nicotine	21147173	While <b>nicotine</b> withdrawal reduced the population of CART immunoreactive cells and fibers in the PVN, the immunoreactivity in the <strong>ARC</strong> fibers was increased.
+ARC	addiction	withdrawal	21147173	While nicotine <b>withdrawal</b> reduced the population of CART immunoreactive cells and fibers in the PVN, the immunoreactivity in the <strong>ARC</strong> fibers was increased.
+ARC	drug	cocaine	20942997	Re exposure to an operant chamber previously associated with <b>cocaine</b>, but not yoked saline, increases activity regulated cytoskeleton associated (<strong>Arc</strong>) gene mRNA expression within the dorsolateral (dl) CPu following prolonged abstinence.
+ARC	addiction	reward	20942997	Re exposure to an <b>operant</b> chamber previously associated with cocaine, but not yoked saline, increases activity regulated cytoskeleton associated (<strong>Arc</strong>) gene mRNA expression within the dorsolateral (dl) CPu following prolonged abstinence.
+ARC	drug	cocaine	20942997	In this study, we tested the hypothesis that antisense gene knockdown of <strong>Arc</strong> within the dlCPu would alter <b>cocaine</b> seeking.
+ARC	addiction	relapse	20942997	In this study, we tested the hypothesis that antisense gene knockdown of <strong>Arc</strong> within the dlCPu would alter cocaine <b>seeking</b>.
+ARC	drug	cocaine	20942997	Initial studies showed that a single infusion of <strong>Arc</strong> antisense oligodeoxynucleotide (ODN) into the dlCPu significantly attenuated the induction of <strong>Arc</strong> mRNA and <strong>Arc</strong> protein by a single <b>cocaine</b> exposure (20 mg/kg i.p.)
+ARC	drug	cocaine	20942997	In <b>cocaine</b> self administering rats, infusion of <strong>Arc</strong> antisense ODN into the dlCPu 3 h prior to a test of context driven drug seeking significantly attenuated <strong>Arc</strong> protein induction, but failed to alter responding during testing, suggesting striatal <strong>Arc</strong> does not facilitate context induced drug seeking following prolonged abstinence.
+ARC	addiction	relapse	20942997	In cocaine self administering rats, infusion of <strong>Arc</strong> antisense ODN into the dlCPu 3 h prior to a test of context driven drug <b>seeking</b> significantly attenuated <strong>Arc</strong> protein induction, but failed to alter responding during testing, suggesting striatal <strong>Arc</strong> does not facilitate context induced drug <b>seeking</b> following prolonged abstinence.
+ARC	drug	cocaine	20942997	Following re exposure to a <b>cocaine</b> paired context, surface expression of the AMPA type glutamate receptor GluR1 was significantly reduced whereas GluR2 was significantly increased in the dlCPu, independent of <strong>Arc</strong> antisense ODN infusion.
+ARC	addiction	relapse	20942997	Together, these findings indicate an important role for <strong>Arc</strong> in neuroadaptations within brain regions responsible for drug <b>seeking</b> after abstinence and direct attention to changes occurring within striatal circuitry that are necessary to break down the habitual behaviour that leads to <b>relapse</b>.
+ARC	drug	cocaine	20654701	In this study, the expression patterns of zif268 and activity regulated cytoskeleton associated gene (<strong>arc</strong>) were investigated in the basolateral amygdala (BLA) and dorsal hippocampal (dHPC) subregions during context induced drug seeking following 22 h or 15 d abstinence from <b>cocaine</b> self administration.
+ARC	addiction	relapse	20654701	In this study, the expression patterns of zif268 and activity regulated cytoskeleton associated gene (<strong>arc</strong>) were investigated in the basolateral amygdala (BLA) and dorsal hippocampal (dHPC) subregions during context induced drug <b>seeking</b> following 22 h or 15 d abstinence from cocaine self administration.
+ARC	drug	cocaine	20654701	<strong>Arc</strong> and zif/268 mRNA in BLA and dHPC increased after re exposure to the <b>cocaine</b> paired chamber at both timepoints; however, only the BLA increases (with one exception see below) were differentially affected by the presence or absence of the <b>cocaine</b> paired lever in the chamber.
+ARC	drug	cocaine	20654701	Following 22 h of abstinence, <strong>arc</strong> mRNA was significantly increased in the BLA of <b>cocaine</b> treated rats re exposed to the chamber only with levers extended, whereas following 15 d of abstinence, <strong>arc</strong> mRNA in the BLA was increased in <b>cocaine</b> treated rats returned to the chamber with or without levers extended.
+ARC	drug	cocaine	20654701	In the dentate gyrus (DG) following 22 h of abstinence, zif268 mRNA was greater in rats returned to the chamber where levers were absent regardless of drug treatment whereas <strong>arc</strong> mRNA was increased in CA1 (cell bodies and dendrites) and CA3 only in <b>cocaine</b> treated groups.
+ARC	drug	cocaine	20654701	Following 15 d of abstinence, <strong>arc</strong> mRNA was significantly greater in CA1 and CA3 of both <b>cocaine</b> treated groups returned to the chamber than in those placed into a familiar, non salient alternate environment; however, only in CA1 cell bodies the <b>cocaine</b> context induced increases significantly greater than in yoked saline controls.
+ARC	drug	cocaine	20654701	These data suggest that the temporal dynamics of <strong>arc</strong> and zif268 gene expression in the BLA and dHPC encode different key elements of drug context induced <b>cocaine</b> seeking.
+ARC	addiction	relapse	20654701	These data suggest that the temporal dynamics of <strong>arc</strong> and zif268 gene expression in the BLA and dHPC encode different key elements of drug context induced cocaine <b>seeking</b>.
+ARC	drug	alcohol	20102560	Results indicated that acute <b>ethanol</b> administration triggered a dose dependent increase in AgRP immunoreactivity in the arcuate (<strong>ARC</strong>) of C57BL/6J mice, an effect that was not evident in the 129/SvJ strain.
+ARC	drug	alcohol	20102560	Although acute administration of <b>ethanol</b> did not influence alpha MSH immunoreactivity, C57BL/6J mice had significantly greater overall alpha MSH immunoreactivity in the <strong>ARC</strong>, dorsomedial, and lateral regions of the hypothalamus relative to the 129/SvJ strain.
+ARC	drug	opioid	19793983	In addition, we found that conditioned <b>morphine</b> withdrawal also increased activity regulated cytoskeletal associated protein (<strong>Arc</strong>) expression in the amygdala but not in the DH, although actin rearrangements were observed in both areas.
+ARC	addiction	withdrawal	19793983	In addition, we found that conditioned morphine <b>withdrawal</b> also increased activity regulated cytoskeletal associated protein (<strong>Arc</strong>) expression in the amygdala but not in the DH, although actin rearrangements were observed in both areas.
+ARC	addiction	aversion	19793983	Therefore, our findings reveal that actin rearrangements in the amygdala and the DH are required for the acquisition and consolidation of the <b>aversive</b> memories of drug withdrawal and that the beta noradrenergic system within the amygdala modulates <b>aversive</b> memory consolidation by regulating actin rearrangements but not <strong>Arc</strong> protein expression in the DH, which is distinct from its role in modulation of inhibitory avoidance memory.
+ARC	addiction	withdrawal	19793983	Therefore, our findings reveal that actin rearrangements in the amygdala and the DH are required for the acquisition and consolidation of the aversive memories of drug <b>withdrawal</b> and that the beta noradrenergic system within the amygdala modulates aversive memory consolidation by regulating actin rearrangements but not <strong>Arc</strong> protein expression in the DH, which is distinct from its role in modulation of inhibitory avoidance memory.
+ARC	drug	alcohol	19756388	Study of the downstream effectors of CREB have identified several important CREB related genes, such as neuropeptide Y, brain derived neurotrophic factor, <strong>activity regulated cytoskeleton associated protein</strong>, and corticotrophin releasing factor, that may play a crucial role in the behavioral effects of <b>ethanol</b> and molecular changes in the specific neurocircuitry that underlie both <b>alcohol</b> addiction and a genetic predisposition to <b>alcoholism</b>.
+ARC	addiction	addiction	19756388	Study of the downstream effectors of CREB have identified several important CREB related genes, such as neuropeptide Y, brain derived neurotrophic factor, <strong>activity regulated cytoskeleton associated protein</strong>, and corticotrophin releasing factor, that may play a crucial role in the behavioral effects of ethanol and molecular changes in the specific neurocircuitry that underlie both alcohol <b>addiction</b> and a genetic predisposition to alcoholism.
+ARC	addiction	withdrawal	19728364	Furthermore, we studied the hippocampal synaptic plasticity and anatomical expression of <strong>Arc</strong> protein during <b>withdrawal</b> and the re exposure to the context associated with anxiety expression (characteristic sign of benzodiazepines <b>withdrawal</b>).
+ARC	addiction	withdrawal	19728364	An overexpression of <strong>Arc</strong> protein in the dorsal dentate gyrus and CA1 on the first day of <b>withdrawal</b> in the dependent animals was observed.
+ARC	drug	opioid	19262551	Expression pattern of neural synaptic plasticity marker <strong>Arc</strong> in different brain regions induced by conditioned drug withdrawal from acute <b>morphine</b> dependent rats.
+ARC	addiction	withdrawal	19262551	Expression pattern of neural synaptic plasticity marker <strong>Arc</strong> in different brain regions induced by conditioned drug <b>withdrawal</b> from acute morphine dependent rats.
+ARC	drug	opioid	19262551	In the present study, we examined the expression of <strong>Arc</strong> protein induced by conditioned <b>naloxone</b> precipitated drug withdrawal in different brain regions of acute <b>morphine</b> dependent rats.
+ARC	addiction	withdrawal	19262551	In the present study, we examined the expression of <strong>Arc</strong> protein induced by conditioned naloxone precipitated drug <b>withdrawal</b> in different brain regions of acute morphine dependent rats.
+ARC	addiction	aversion	19262551	An immunohistochemical method was employed to detect the expression of <strong>Arc</strong>, which was used as a plasticity marker to trace the brain areas that contribute to the formation of the place <b>aversion</b>.
+ARC	drug	cocaine	19025723	Single session of <b>cocaine</b> intravenous self administration shapes goal oriented behaviours and up regulates <strong>Arc</strong> mRNA levels in rat medial prefrontal cortex.
+ARC	drug	cocaine	19025723	self administration is sufficient to shape rat behaviour towards goal directed behaviours and selectively up regulate <strong>Arc</strong> expression in mPFC (of SA animals), providing the first evidence that the mPFC's function is already profoundly influenced by the first voluntary <b>cocaine</b> exposure.
+ARC	drug	alcohol	18823957	However, the profile of CART immunoreactive cells and/or fibers in the periventricular area (PeA), arcuate nucleus (<strong>ARC</strong>), perifornical area inclusive of lateral hypothalamus (LH) and tuber cinereum (TC), dorsomedial (DMH), and ventromedial (VMH) hypothalamus at the 0 h <b>ethanol</b> withdrawal time point was quite similar to that in the pair fed control rats.
+ARC	addiction	withdrawal	18823957	However, the profile of CART immunoreactive cells and/or fibers in the periventricular area (PeA), arcuate nucleus (<strong>ARC</strong>), perifornical area inclusive of lateral hypothalamus (LH) and tuber cinereum (TC), dorsomedial (DMH), and ventromedial (VMH) hypothalamus at the 0 h ethanol <b>withdrawal</b> time point was quite similar to that in the pair fed control rats.
+ARC	drug	alcohol	18823957	While significant reduction in CART immunoreactivity was noticed in the PVN, PeA, <strong>ARC</strong> and VMH at 48 h, immunoreactive profile was restored to normal by 72 h post <b>ethanol</b> withdrawal.
+ARC	addiction	withdrawal	18823957	While significant reduction in CART immunoreactivity was noticed in the PVN, PeA, <strong>ARC</strong> and VMH at 48 h, immunoreactive profile was restored to normal by 72 h post ethanol <b>withdrawal</b>.
+ARC	drug	alcohol	18499089	Acute <b>ethanol</b> significantly reduced the alpha MSH immunoreactivity in the cells and fibers of <strong>ARC</strong>, and fibers in the PVN, DMNd, DMNv and CeA.
+ARC	drug	cocaine	18488248	Using an animal model of relapse to <b>cocaine</b> seeking, the present study investigated the expression patterns of three different activity related genes (c fos, zif/268, and <strong>arc</strong>) in cortical and striatal brain regions implicated in compulsive drug seeking in order to determine the neuroadaptations that occur during context induced relapse following brief or prolonged abstinence from <b>cocaine</b> self administration.
+ARC	addiction	addiction	18488248	Using an animal model of relapse to cocaine seeking, the present study investigated the expression patterns of three different activity related genes (c fos, zif/268, and <strong>arc</strong>) in cortical and striatal brain regions implicated in <b>compulsive</b> drug seeking in order to determine the neuroadaptations that occur during context induced relapse following brief or prolonged abstinence from cocaine self administration.
+ARC	addiction	relapse	18488248	Using an animal model of <b>relapse</b> to cocaine <b>seeking</b>, the present study investigated the expression patterns of three different activity related genes (c fos, zif/268, and <strong>arc</strong>) in cortical and striatal brain regions implicated in compulsive drug <b>seeking</b> in order to determine the neuroadaptations that occur during context induced <b>relapse</b> following brief or prolonged abstinence from cocaine self administration.
+ARC	drug	cocaine	18488248	Re exposure to the environment previously associated with <b>cocaine</b> self administration following 22 h or 15 days of abstinence produced a significant increase in zif/268 and <strong>arc</strong>, but not c fos mRNA, in the caudate putamen and nucleus accumbens.
+ARC	drug	cocaine	18488248	With the exception of <strong>arc</strong> mRNA levels following 15 days of abstinence, all three genes were increased in the anterior cingulate cortex of animals with a <b>cocaine</b> history when they were re exposed to the operant chamber.
+ARC	addiction	reward	18488248	With the exception of <strong>arc</strong> mRNA levels following 15 days of abstinence, all three genes were increased in the anterior cingulate cortex of animals with a cocaine history when they were re exposed to the <b>operant</b> chamber.
+ARC	drug	opioid	18466961	<strong>Arc</strong> expression increased following the extinction session only in rats with a history of <b>heroin</b> self administration and only when tested following 1, but not 14, days of abstinence.
+ARC	drug	cocaine	18361437	Upregulation of <strong>Arc</strong> mRNA expression in the prefrontal cortex following cue induced reinstatement of extinguished <b>cocaine</b> seeking behavior.
+ARC	addiction	relapse	18361437	Upregulation of <strong>Arc</strong> mRNA expression in the prefrontal cortex following cue induced <b>reinstatement</b> of extinguished cocaine <b>seeking</b> behavior.
+ARC	drug	cocaine	18361437	Here we examine the hypothesis that neuronal processes associated with incentive motivational effects of <b>cocaine</b> cues involve increased expression of the plasticity associated gene, <strong>Arc</strong>.
+ARC	addiction	reward	18361437	Here we examine the hypothesis that neuronal processes associated with <b>incentive</b> motivational effects of cocaine cues involve increased expression of the plasticity associated gene, <strong>Arc</strong>.
+ARC	drug	cocaine	18361437	Cues elicited reinstatement of <b>cocaine</b> seeking behavior and were accompanied by increased <strong>Arc</strong> mRNA levels in the orbitofrontal, prelimbic, and anterior cingulate cortices, suggesting <strong>Arc</strong> involvement in conditioned plasticity associated with incentive motivational effects of <b>cocaine</b> cues.
+ARC	addiction	relapse	18361437	Cues elicited <b>reinstatement</b> of cocaine <b>seeking</b> behavior and were accompanied by increased <strong>Arc</strong> mRNA levels in the orbitofrontal, prelimbic, and anterior cingulate cortices, suggesting <strong>Arc</strong> involvement in conditioned plasticity associated with incentive motivational effects of cocaine cues.
+ARC	addiction	reward	18361437	Cues elicited reinstatement of cocaine seeking behavior and were accompanied by increased <strong>Arc</strong> mRNA levels in the orbitofrontal, prelimbic, and anterior cingulate cortices, suggesting <strong>Arc</strong> involvement in conditioned plasticity associated with <b>incentive</b> motivational effects of cocaine cues.
+ARC	drug	cocaine	18361437	Additionally, rats with a history of <b>cocaine</b> self administration and extinction exhibited upregulation of <strong>Arc</strong> expression in several limbic and cortical regions relative to saline yoked controls regardless of cue exposure condition, suggesting persistent neuroadaptations involving <strong>Arc</strong> within these regions.
+ARC	drug	alcohol	18322102	Effector immediate early gene <strong>arc</strong> in the amygdala plays a critical role in <b>alcoholism</b>.
+ARC	drug	alcohol	18322102	However, the role of <strong>Arc</strong> in <b>alcoholism</b> is unknown.
+ARC	drug	alcohol	18322102	Here, we report that the anxiolytic effects of acute <b>ethanol</b> were associated with increased brain derived neurotrophic factor (BDNF) and tyrosine kinase B (trkB) expression, increased phosphorylation of extracellular signal regulated kinases 1/2 (Erk1/2), Elk 1, and cAMP responsive element binding protein (CREB), increased <strong>Arc</strong> expression, and increased dendritic spine density (DSD) in both the central amygdala (CeA) and medial amygdala (MeA) but not in the basolateral amygdala (BLA) of rats.
+ARC	drug	alcohol	18322102	Conversely, the anxiogenic effects of withdrawal after long term <b>ethanol</b> exposure were associated with decreased BDNF and trkB expression, decreased phosphorylation of Erk1/2, Elk 1, and CREB, decreased <strong>Arc</strong> expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+ARC	addiction	withdrawal	18322102	Conversely, the anxiogenic effects of <b>withdrawal</b> after long term ethanol exposure were associated with decreased BDNF and trkB expression, decreased phosphorylation of Erk1/2, Elk 1, and CREB, decreased <strong>Arc</strong> expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+ARC	drug	alcohol	18322102	We also showed that BDNF infusion into the CeA normalized phosphorylation of Erk1/2, Elk 1, and CREB, and normalized <strong>Arc</strong> expression, thereby protecting against the onset of <b>ethanol</b> withdrawal related anxiety.
+ARC	addiction	withdrawal	18322102	We also showed that BDNF infusion into the CeA normalized phosphorylation of Erk1/2, Elk 1, and CREB, and normalized <strong>Arc</strong> expression, thereby protecting against the onset of ethanol <b>withdrawal</b> related anxiety.
+ARC	drug	alcohol	18322102	We further demonstrated that arresting <strong>Arc</strong> expression in the CeA decreased DSD, thereby increasing anxiety like and <b>alcohol</b> drinking behaviors in control rats.
+ARC	drug	alcohol	18322102	These results revealed that BDNF <strong>Arc</strong> signaling and the associated DSD in the CeA, and possibly in the MeA, may be involved in the molecular processes of <b>alcohol</b> dependence and comorbidity of anxiety and <b>alcohol</b> drinking behaviors.
+ARC	addiction	dependence	18322102	These results revealed that BDNF <strong>Arc</strong> signaling and the associated DSD in the CeA, and possibly in the MeA, may be involved in the molecular processes of alcohol <b>dependence</b> and comorbidity of anxiety and alcohol drinking behaviors.
+ARC	drug	cocaine	18311559	Rats self administered <b>cocaine</b> or received yoked saline for 2 h/day for 10 days followed by 22 h or 2 weeks of abstinence when they were re exposed to the self administration chamber with or without levers available to press for 1 h. Brains were harvested and sections through the prefrontal cortex were processed for in situ hybridization using radioactive oligonucleotide probes encoding c fos, zif/268, <strong>arc</strong>, and bdnf.
+ARC	drug	opioid	18157469	The present study was undertaken to investigate the effect of melatonin on the content of β endorphin (β EP) in the hypothalamic arcuate nucleus (<strong>Arc</strong>) and periaqueductal grey (PAG) of midbrain in <b>morphine</b> withdrawal mice.
+ARC	addiction	withdrawal	18157469	The present study was undertaken to investigate the effect of melatonin on the content of β endorphin (β EP) in the hypothalamic arcuate nucleus (<strong>Arc</strong>) and periaqueductal grey (PAG) of midbrain in morphine <b>withdrawal</b> mice.
+ARC	drug	opioid	18157469	The results suggest that MEL increases the content of β EP in the PAG of midbrain, decrease the content of β EP in the <strong>Arc</strong> in <b>morphine</b> withdrawal mice.
+ARC	addiction	withdrawal	18157469	The results suggest that MEL increases the content of β EP in the PAG of midbrain, decrease the content of β EP in the <strong>Arc</strong> in morphine <b>withdrawal</b> mice.
+ARC	addiction	relapse	17959795	Arcuate nucleus (<strong>Arc</strong>) injections of PYY3 36 (0.4 microg per side) decreased pellet priming induced <b>reinstatement</b>.
+ARC	addiction	relapse	17959795	The attenuation of pellet priming induced <b>reinstatement</b> by systemic PYY3 36 was reversed by systemic (2 mg/kg) but not <strong>Arc</strong> (0.5 microg per side) injections of the Y2 receptor antagonist BIIE0246.
+ARC	addiction	relapse	17959795	<strong>Arc</strong> PYY3 36 injections did not decrease pellet cue induced <b>reinstatement</b>.
+ARC	addiction	relapse	17959795	These data identify an effect of systemic PYY3 36 on <b>relapse</b> to food <b>seeking</b> that is independent of Y2 receptor activation in <strong>Arc</strong> and suggest that PYY3 36 should be considered for the treatment of <b>relapse</b> to maladaptive food taking habits during dieting.
+ARC	drug	opioid	17600376	The galanin induced increases in HWLs were inhibited by injection of 10 microg of the <b>opioid</b> receptor antagonist <b>naloxone</b> or 1 nmol of the mu <b>opioid</b> receptor antagonist beta funaltrexamine (beta FNA) into PAG, suggesting that the antinociceptive effects induced by intra <strong>ARC</strong> injection of galanin occur via the neural pathway from <strong>ARC</strong> to PAG.
+ARC	drug	amphetamine	17499349	Effects of SKF 38393, a dopamine D1 receptor agonist on expression of <b>amphetamine</b> induced behavioral sensitization and expression of immediate early gene <strong>arc</strong> in prefrontal cortex of rats.
+ARC	addiction	sensitization	17499349	Effects of SKF 38393, a dopamine D1 receptor agonist on expression of amphetamine induced behavioral <b>sensitization</b> and expression of immediate early gene <strong>arc</strong> in prefrontal cortex of rats.
+ARC	drug	amphetamine	17499349	We examined whether a dopamine D1 agonist can reverse behavioral sensitization once established by repeated <b>amphetamine</b> (AMP) administrations and determined the mRNA expression levels of the D1 and D2 receptors, metabotropic glutamate receptor 1 (mGluR1), and activity regulated cytoskeleton associated protein (<strong>arc</strong>) in rats.
+ARC	addiction	sensitization	17499349	We examined whether a dopamine D1 agonist can reverse behavioral <b>sensitization</b> once established by repeated amphetamine (AMP) administrations and determined the mRNA expression levels of the D1 and D2 receptors, metabotropic glutamate receptor 1 (mGluR1), and activity regulated cytoskeleton associated protein (<strong>arc</strong>) in rats.
+ARC	drug	amphetamine	17499349	We examined whether a dopamine D1 agonist can reverse behavioral sensitization once established by repeated <b>amphetamine</b> (AMP) administrations and determined the mRNA expression levels of the D1 and D2 receptors, metabotropic glutamate receptor 1 (mGluR1), and <strong>activity regulated cytoskeleton associated protein</strong> (<strong>arc</strong>) in rats.
+ARC	addiction	sensitization	17499349	We examined whether a dopamine D1 agonist can reverse behavioral <b>sensitization</b> once established by repeated amphetamine (AMP) administrations and determined the mRNA expression levels of the D1 and D2 receptors, metabotropic glutamate receptor 1 (mGluR1), and <strong>activity regulated cytoskeleton associated protein</strong> (<strong>arc</strong>) in rats.
+ARC	addiction	sensitization	17499349	There was no significant difference in <strong>arc</strong> expression level between the saline and SKF treatment groups after the AMP challenge, suggesting that <strong>arc</strong> expression level is not involved in the reversal effects of SKF in AMP <b>sensitization</b>.
+ARC	drug	amphetamine	17049170	Neurotoxic <b>AMPH</b> pretreatment resulted in significantly diminished <b>AMPH</b> challenge induced mRNA increases of activity regulated cytoskeletal protein (<strong>ARC</strong>), nerve growth factor inducible protein A (NGFI A), and nerve growth factor inducible protein B (NGFI B) in the parietal cortex while neither saline pretreatment nor non neurotoxic <b>AMPH</b> pretreatment did.
+ARC	drug	amphetamine	17049170	In the striatum, there were no differences between saline, neurotoxic <b>AMPH</b>, and non neurotoxic <b>AMPH</b> pretreatments on <strong>ARC</strong>, NGFI A or NGFI B expression elicited by the <b>AMPH</b> challenge.
+ARC	drug	amphetamine	16218999	Withdrawal of the obesogenic diets decreased gene expression for cocaine and <b>amphetamine</b> regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (<strong>ARC</strong>), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas neuropeptide Y (NPY) gene expression in the <strong>ARC</strong> was increased.
+ARC	drug	cocaine	16218999	Withdrawal of the obesogenic diets decreased gene expression for <b>cocaine</b> and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (<strong>ARC</strong>), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas neuropeptide Y (NPY) gene expression in the <strong>ARC</strong> was increased.
+ARC	addiction	withdrawal	16218999	<b>Withdrawal</b> of the obesogenic diets decreased gene expression for cocaine and amphetamine regulated transcript (CART) and dynorphin (DYN) in the arcuate nucleus (<strong>ARC</strong>), and DYN and brain derived neurotrophic factor (BDNF) in the VMH, whereas neuropeptide Y (NPY) gene expression in the <strong>ARC</strong> was increased.
+ARC	drug	opioid	16211563	<b>Morphine</b> activates <strong>Arc</strong> expression in the mouse striatum and in mouse neuroblastoma Neuro2A MOR1A cells expressing mu <b>opioid</b> receptors.
+ARC	drug	opioid	16211563	In the present experiments, the influence of <b>morphine</b> on <strong>Arc</strong> expression was assessed by quantitative reverse transcription real time PCR and Western blotting in vivo in the mouse striatum/nucleus accumbens and, in vitro, in the mouse Neuro2A MOR1A cell line, expressing mu <b>opioid</b> receptor.
+ARC	drug	opioid	16211563	An acute administration of <b>morphine</b> produced a marked increase in <strong>Arc</strong> mRNA and protein level in the mouse striatum/nucleus accumbens complex.
+ARC	drug	opioid	16211563	After prolonged opiate treatment, tolerance to the stimulatory effect of <b>morphine</b> on <strong>Arc</strong> expression developed.
+ARC	drug	opioid	16211563	No changes in the striatal <strong>Arc</strong> mRNA levels were observed during spontaneous or <b>opioid</b> antagonist precipitated <b>morphine</b> withdrawal.
+ARC	addiction	withdrawal	16211563	No changes in the striatal <strong>Arc</strong> mRNA levels were observed during spontaneous or opioid antagonist precipitated morphine <b>withdrawal</b>.
+ARC	drug	opioid	16211563	In Neuro2A MOR1A cells, acute, but not prolonged, <b>morphine</b> treatment elevated <strong>Arc</strong> mRNA level by activation of mu <b>opioid</b> receptor.
+ARC	drug	opioid	16211563	Inhibition experiments revealed that <b>morphine</b> induced <strong>Arc</strong> expression in Neuro2A MOR1A cells via intracellular signaling pathways involving mitogen activated protein (MAP) kinases and protein kinase C. These results lend further support to the notion that stimulation of <b>opioid</b> receptors may exert an activating influence on some intracellular pathways and leads to induction of immediate early genes.
+ARC	drug	opioid	16211563	They also demonstrate that <strong>Arc</strong> is induced in the brain in vivo after <b>morphine</b> administration and thus may play a role in neuroadaptations produced by the drug.
+ARC	drug	cocaine	16123776	Consistent with these behavioral findings, we found that <b>cocaine</b> regulation of gene expression in striatum, including the acute induction of the immediate early genes c fos and <strong>arc</strong> (activity regulated cytoskeletal associated gene), was abolished in DARPP 32 Thr 34 mutants, but not in Thr 75 mutants.
+ARC	drug	nicotine	16084664	Differential expression of <strong>arc</strong> mRNA and other plasticity related genes induced by <b>nicotine</b> in adolescent rat forebrain.
+ARC	drug	nicotine	16084664	To investigate this question, we examined the expression of a number of early response genes (<strong>arc</strong>, c fos and NGFI B) that have been implicated in synaptic plasticity and addiction, following acute <b>nicotine</b> in adolescent and adult rats.
+ARC	addiction	addiction	16084664	To investigate this question, we examined the expression of a number of early response genes (<strong>arc</strong>, c fos and NGFI B) that have been implicated in synaptic plasticity and <b>addiction</b>, following acute nicotine in adolescent and adult rats.
+ARC	drug	nicotine	16084664	Following acute <b>nicotine</b> treatment (0.1, 0.4mg/kg), we found a marked induction of <strong>arc</strong> mRNA in the prefrontal cortex of <b>nicotine</b> treated adolescents compared with a less pronounced increase of <strong>arc</strong> in the adult.
+ARC	drug	nicotine	16084664	In contrast, <b>nicotine</b> induced less <strong>arc</strong>, c fos, and NGFI B expression in the somatosensory cortex of adolescents compared with adults.
+ARC	drug	cannabinoid	15901756	The present study sought to determine whether <b>cannabinoids</b> modulate A type K(+) currents (I(A)) in neurons of the hypothalamic arcuate nucleus (<strong>ARC</strong>).
+ARC	drug	cannabinoid	15901756	Collectively, these data reveal that guinea pig <strong>ARC</strong> neurons, including proopiomelanocortin neurons, express a prominent I(A) that is positively modulated by <b>cannabinoids</b> in a sex specific way by altering the voltage dependence of its inactivation.
+ARC	addiction	dependence	15901756	Collectively, these data reveal that guinea pig <strong>ARC</strong> neurons, including proopiomelanocortin neurons, express a prominent I(A) that is positively modulated by cannabinoids in a sex specific way by altering the voltage <b>dependence</b> of its inactivation.
+ARC	drug	opioid	15849022	Recent gene expression profiling studies reveal additional clusters of <b>morphine</b> responsive genes: whereas single dose administration has been shown to predominantly reduce expression of genes involved in metabolic function, ascending <b>morphine</b> doses leading to <b>morphine</b> tolerance revealed induction of genes which alter patterns of synaptic connectivity such as <strong>arc</strong> or ania 3.
+ARC	drug	nicotine	15705350	We found that increasing the rate of intravenous <b>nicotine</b> infusion potentiated its ability to produce locomotor sensitization, and to induce c fos and <strong>arc</strong> mRNA expression in mesocorticolimbic structures.
+ARC	addiction	sensitization	15705350	We found that increasing the rate of intravenous nicotine infusion potentiated its ability to produce locomotor <b>sensitization</b>, and to induce c fos and <strong>arc</strong> mRNA expression in mesocorticolimbic structures.
+ARC	drug	opioid	15544839	We showed that the antinociceptive effect induced by intra <strong>ARC</strong> injection of galanin was dose dependently attenuated by the following intra <strong>ARC</strong> injection of <b>naloxone</b>.
+ARC	drug	opioid	15544839	Furthermore, intra <strong>ARC</strong> administration of the selective mu <b>opioid</b> receptor antagonist beta funaltrexamine (beta FNA) attenuated the increased HWL induced by intra <strong>ARC</strong> injection of galanin in a dose dependent manner, while the delta <b>opioid</b> receptor antagonist naltrindole or the kappa <b>opioid</b> receptor antagonist nor binaltorphimine (nor BNI) did not.
+ARC	drug	opioid	15544839	Moreover, intra <strong>ARC</strong> injection of a galanin receptor antagonist galantide attenuated intraperitoneal <b>morphine</b> induced increases in HWLs.
+ARC	drug	opioid	15544839	These results demonstrate that the antinociceptive effect of galanin was related to the <b>opioid</b> system, especially mu <b>opioid</b> receptor was involved in, and that systemic <b>morphine</b> induced antinociception involves galanin in the <strong>ARC</strong>.
+ARC	drug	cocaine	15254092	Rapid infusions potentiated the ability of <b>cocaine</b> to block DA reuptake, to induce c fos and <strong>arc</strong> mRNA expression, especially in mesocorticolimbic regions, and to produce psychomotor sensitization.
+ARC	addiction	sensitization	15254092	Rapid infusions potentiated the ability of cocaine to block DA reuptake, to induce c fos and <strong>arc</strong> mRNA expression, especially in mesocorticolimbic regions, and to produce psychomotor <b>sensitization</b>.
+ARC	drug	amphetamine	12890524	When given in a novel test environment <b>amphetamine</b> produces greater levels of c fos and <strong>arc</strong> mRNA expression in many brain regions relative to when it is given in the home cage.
+ARC	drug	opioid	12855314	Intra <strong>ARC</strong> injection of <b>naloxone</b> had no significant influence on the HWL to thermal and mechanical stimulation in intact rats.
+ARC	drug	opioid	12855314	The HWL decreased significantly after intra <strong>ARC</strong> injection of 1 or 10 microg of <b>naloxone</b> in rats with inflammation, but not with 0.1 microg of <b>naloxone</b>.
+ARC	drug	opioid	12855314	Furthermore, intra <strong>ARC</strong> administration of the selective mu <b>opioid</b> receptor antagonist beta funaltrexamine (beta FNA) decreased the nociceptive response latencies to both stimulation in a dose dependent manner in rats with inflammation, while intra <strong>ARC</strong> administration of the selective delta <b>opioid</b> receptor antagonist naltrindole or the selective kappa <b>opioid</b> receptor antagonist nor binaltorphimine (nor BNI) showed no influences on the nociceptive response latency.
+ARC	drug	opioid	12855314	The results indicate that endogenous beta endorphin in the <strong>ARC</strong> plays an important role in the endogenous antinociceptive system in rats with inflammation, and that its effect is predominantly mediated by the mu <b>opioid</b> receptor.
+ARC	addiction	withdrawal	12784103	In contrast, <strong>Arc</strong>, another 'effector' IEG, was not induced by opiate <b>withdrawal</b>.
+ARC	drug	amphetamine	12774298	Differential regulation by stimulants of neocortical expression of mrt1, <strong>arc</strong>, and homer1a mRNA in the rats treated with repeated <b>methamphetamine</b>.
+ARC	drug	cocaine	12774298	In contrast, the basal expression of other stimulant inducible and plasticity related genes <strong>arc</strong> and homer1a and the ability of MAP or <b>cocaine</b> challenge to augment the amounts of their transcripts were not affected by the repeated MAP regimen in the cortical area.
+ARC	addiction	sensitization	12774298	These findings suggest the differential regulation by stimulant of neocortical mrt1, <strong>arc</strong>, and homer1a expression in the behaviorally sensitized animals and supports the view that stimulant induction of mrt1 may be involved in the early molecular signalings for stimulant <b>sensitization</b>.
+ARC	drug	cocaine	12687634	Many genes upregulated in the CPu by <b>cocaine</b> were immediate early genes for transcription factors and for "effector" proteins (e.g., vesl/Homer1a, <strong>Arc</strong>, synaptotagmin IV).
+ARC	addiction	sensitization	12642909	synaptophysin, stathmin and <strong>arc</strong>), synaptogenesis, neuritic sprouting and elongation must develop during behavioral <b>sensitization</b>.
+ARC	drug	amphetamine	12638131	Using these criteria, the mRNA for three immediate early genes (IEGs), coding for activity regulated cytoskeletal associated protein (<strong>Arc</strong>), nerve growth factor induced protein A (NGFI A; early growth response protein 1) and nerve growth factor induced protein B (NGFI B), were upregulated 1 and 3 h after <b>amphetamine</b> as previously described.
+ARC	drug	alcohol	12130710	No effects were seen in <b>alcohol</b> induced c Fos after the pretreatment of 20 mg/kg propranolol (beta adrenoceptor antagonist), 10 mg/kg 2 (2 (4 (2 methoxyphenyl)piperazin 1 yl) ethy) 4,4 dimethyl 1,3 (2H,4H) isoquinolindione dihydrochloride (<strong>ARC</strong> 239) (alpha(2B/C) adrenoceptor antagonist), or 30 mg/kg <b>naltrexone</b> (opioid antagonist).
+ARC	drug	opioid	12130710	No effects were seen in alcohol induced c Fos after the pretreatment of 20 mg/kg propranolol (beta adrenoceptor antagonist), 10 mg/kg 2 (2 (4 (2 methoxyphenyl)piperazin 1 yl) ethy) 4,4 dimethyl 1,3 (2H,4H) isoquinolindione dihydrochloride (<strong>ARC</strong> 239) (alpha(2B/C) adrenoceptor antagonist), or 30 mg/kg naltrexone (<b>opioid</b> antagonist).
+ARC	drug	cocaine	12117546	Protein levels of protein tyrosine kinase 2 (PYK2), activity regulated cytoskeletal protein (<strong>ARC</strong>), as well as an antigen related to nerve growth factor I B (NGFI B RA) were shown to be significantly induced after <b>cocaine</b> administration.
+ARC	drug	amphetamine	12105085	The mRNA of <strong>arc</strong>, an activity regulated protein associated with cytoskeleton, but not of alpha tubulin, as markers for neuritic elongation, showed robust increases in the striatum, hippocampus, and cortices after a single dose of <b>methamphetamine</b>.
+ARC	drug	amphetamine	12105085	Synaptophysin and stathmin mRNAs did not increase again after chronic <b>methamphetamine</b> administration, whereas the increases in <strong>arc</strong>, MKP 1, and MKP 3 mRNAs persisted in the brain regions after chronic <b>methamphetamine</b> administration.
+ARC	drug	amphetamine	11879792	The ability of <b>amphetamine</b> to evoke <strong>arc</strong> (Arg 3.1) mRNA expression in the caudate, nucleus accumbens and neocortex is modulated by environmental context.
+ARC	drug	amphetamine	11879792	The purpose of this study was to determine if environmental context has a similar effect on the ability of <b>amphetamine</b> to induce the expression of <strong>arc</strong> (also known as Arg 3.1), an "effector" immediate early gene (IEG) thought to play a direct role in cellular plasticity.
+ARC	drug	amphetamine	11879792	In the prefrontal cortex, caudate putamen and core of the nucleus accumbens, <b>amphetamine</b> significantly increased <strong>arc</strong> mRNA expression under both conditions, but the level of expression was significantly enhanced when <b>amphetamine</b> was given in a distinct environment.
+ARC	drug	amphetamine	11879792	In the shell of the nucleus accumbens <b>amphetamine</b> significantly increased the expression of <strong>arc</strong> mRNA only when it was administered in the distinct environment.
+ARC	drug	amphetamine	11879792	Thus, the ability of <b>amphetamine</b> to induce the expression of <strong>arc</strong> varies as a function of the environmental context in which it is administered.
+ARC	drug	amphetamine	11400323	<strong>Arc</strong> protein is an "effector protein" and markedly induced by convulsion or <b>methamphetamine</b>.
+ARC	addiction	sensitization	11233297	2) Research on neural plasticity related <b>sensitization</b> revealed the involvement of several molecules such as tissue plasminogen activator, <strong>arc</strong> (activity regulated, cytoskeleton associated), synaptophysin and stathmin.
+ARC	drug	amphetamine	9689478	A robust increase in expression of <strong>arc</strong> gene, an effector immediate early gene, in the rat brain after acute and chronic <b>methamphetamine</b> administration.
+ARC	drug	amphetamine	9689478	The effect of acute and chronic administration of <b>methamphetamine</b> (<b>METH</b>) on the levels of activity regulated cytoskeleton associated protein (<strong>arc</strong>), an effector immediate early gene, mRNA has been investigated in rat brain using in situ hybridization.
+ARC	drug	amphetamine	9689478	The effect of acute and chronic administration of <b>methamphetamine</b> (<b>METH</b>) on the levels of <strong>activity regulated cytoskeleton associated protein</strong> (<strong>arc</strong>), an effector immediate early gene, mRNA has been investigated in rat brain using in situ hybridization.
+ARC	drug	amphetamine	9689478	Levels of <strong>arc</strong> mRNAs in the brain regions examined increased significantly from 0.5 1 h after an acute <b>METH</b> (4 mg/kg) administration compared with basal levels.
+ARC	drug	amphetamine	9689478	The increase in <strong>arc</strong> mRNA continued by 3 h, and then subsided to basal levels by 6 h. The degree of increase in <strong>arc</strong> mRNA and the peak time after <b>METH</b> administration varied according to brain area.
+ARC	drug	amphetamine	9689478	<strong>Arc</strong> mRNA in cerebral cortices showed robust increase 1 h after <b>METH</b> administration.
+ARC	drug	amphetamine	9689478	Microscopic examination revealed that the <b>METH</b> induced <strong>arc</strong> mRNAs in the parietal cortex were enriched in layers IV and VI, and those in the striatum existed mainly in the medium sized neuron.
+ARC	drug	amphetamine	9689478	Pretreatment with either 0.5 mg/kg SCH23390 or 0.25 mg/kg MK 801 almost completely blocked the enhanced striatal <strong>arc</strong> mRNA levels induced by acute <b>METH</b> administration, whereas such pretreatments only partially reduced the effect of <b>METH</b> in the cerebral cortical regions.
+ARC	drug	amphetamine	9689478	In the chronic treatment experiment, the <strong>arc</strong> mRNA levels of the group that received chronic treatment with <b>METH</b> followed by a <b>METH</b> challenge showed an increase like seen after acute <b>METH</b> administration.
+ARC	drug	amphetamine	9689478	Since previous studies proposed that <strong>arc</strong> is one of cytoskeleton associated proteins and is selectively localized in neural dendrites, the results of the present study suggested that <strong>arc</strong> may play an important role in the synaptic plasticity underlying <b>METH</b> induced adaptational changes including behavioral sensitization.
+ARC	addiction	sensitization	9689478	Since previous studies proposed that <strong>arc</strong> is one of cytoskeleton associated proteins and is selectively localized in neural dendrites, the results of the present study suggested that <strong>arc</strong> may play an important role in the synaptic plasticity underlying METH induced adaptational changes including behavioral <b>sensitization</b>.
+ARC	drug	alcohol	9584966	'Craving is generally considered a significant factor in opiate addiction that is associated with drug dependence and in relapse to drug use after treatment' <strong>ARC</strong> expert consensus (Pickens and Johanson, Drug and <b>Alcohol</b> Dependence 30: 127 131).
+ARC	addiction	addiction	9584966	'Craving is generally considered a significant factor in opiate <b>addiction</b> that is associated with drug dependence and in relapse to drug use after treatment' <strong>ARC</strong> expert consensus (Pickens and Johanson, Drug and Alcohol Dependence 30: 127 131).
+ARC	addiction	dependence	9584966	'Craving is generally considered a significant factor in opiate addiction that is associated with drug <b>dependence</b> and in relapse to drug use after treatment' <strong>ARC</strong> expert consensus (Pickens and Johanson, Drug and Alcohol <b>Dependence</b> 30: 127 131).
+ARC	addiction	relapse	9584966	'<b>Craving</b> is generally considered a significant factor in opiate addiction that is associated with drug dependence and in <b>relapse</b> to drug use after treatment' <strong>ARC</strong> expert consensus (Pickens and Johanson, Drug and Alcohol Dependence 30: 127 131).
+ARC	drug	opioid	9472985	Supported by studies using an <b>opioid</b> receptor agonist (<b>morphine</b>) and antagonist (<b>naloxone</b>), these observations demonstrate that <strong>ARC</strong> derived (beta END) neurons modulate the responses of PVN neurons to DEX.
+ARC	drug	opioid	8613967	The membrane hyperpolarization to DAMGO ([D Ala2, N Me Phe4, Gly ol5] enkephalin) in beta endorphin and other arcuate (<strong>ARC</strong>) neurons was investigated in hypothalamic slices from control and <b>morphine</b> treated, ovariectomized guinea pigs.
+ARC	drug	opioid	8613967	Chronic <b>morphine</b> treatment caused both a decreased potency (EC50 220 +/  10 nM vs. 64 +/  3 nM in controls) and a decreased efficacy (Vmax:  7.1 +/  1.1 mV vs.  10.7 +/  0.6 mV in controls) of DAMGO in a population of <strong>ARC</strong> neurons including beta endorphin neurons.
+ARC	drug	opioid	8613967	In another population of <strong>ARC</strong> neurons from <b>morphine</b> treated animals, DAMGO was less potent (EC50: 110 +/  4 nm) than in controls (EC50: 64 +/  3nM), but there was not a significant change in the efficacy of DAMGO.
+ARC	drug	opioid	8613967	The density of mu <b>opioid</b> receptors labeled with the antagonist radioligand [3H]diprenorphine was found to be significantly decreased in the <strong>ARC</strong> and surrounding mediobasal hypothalamus after <b>morphine</b> treatment (Bmax: 217 +/  9 vs. 276 +/  16 fmol/mg protein in controls), which is consistent with the altered response in beta endorphin neurons.
+ARC	drug	opioid	8613967	In summary, chronic <b>morphine</b> treatment decreases mu <b>opioid</b> receptor density and the functional coupling of mu <b>opioid</b> receptors to K+ channels in <strong>ARC</strong> neurons.
+ARC	drug	opioid	8613967	This expression of <b>morphine</b> tolerance by beta endorphin (<strong>ARC</strong>) neurons may serve as a homeostatic mechanism to maintain <b>opioid</b> control of a variety of systems ranging from reproduction to motivation and reward.
+ARC	addiction	reward	8613967	This expression of morphine tolerance by beta endorphin (<strong>ARC</strong>) neurons may serve as a homeostatic mechanism to maintain opioid control of a variety of systems ranging from reproduction to motivation and <b>reward</b>.
+ARC	drug	alcohol	8491503	The site of action of <b>alcohol</b> could reside anywhere within the baroreceptor reflex <strong>arc</strong>.
+ARC	addiction	addiction	8510191	Relationships were explored among the frequencies of use of various drugs by a sample of drug abusing clients of the <b>Addiction</b> Research Foundation (ARF) in Toronto and by drug abusers volunteering to participate in research at the <b>Addiction</b> Research Center (<strong>ARC</strong>) in Baltimore.
+ARC	drug	alcohol	8510191	Those from ARF were admitted primarily for diagnosis and possible treatment for <b>alcohol</b> and non opioid drug problems, whereas those from the <strong>ARC</strong> were admitted for participation in research on other drugs of abuse, primarily involving opioids.
+ARC	drug	opioid	8510191	Those from ARF were admitted primarily for diagnosis and possible treatment for alcohol and non <b>opioid</b> drug problems, whereas those from the <strong>ARC</strong> were admitted for participation in research on other drugs of abuse, primarily involving <b>opioids</b>.
+ARC	drug	opioid	1436012	Background and design of a controlled clinical trial (<strong>ARC</strong> 090) for the treatment of <b>opioid</b> dependence.
+ARC	addiction	dependence	1436012	Background and design of a controlled clinical trial (<strong>ARC</strong> 090) for the treatment of opioid <b>dependence</b>.
+ARC	drug	opioid	2913859	The effect of lumbar intrathecal <b>fentanyl</b> on reported pain, nociceptive flexor withdrawal reflexes, a monosynaptic motor <strong>arc</strong> (H reflex), and supraspinal effects such as miosis, nausea, respiratory depression was evaluated.
+ARC	addiction	withdrawal	2913859	The effect of lumbar intrathecal fentanyl on reported pain, nociceptive flexor <b>withdrawal</b> reflexes, a monosynaptic motor <strong>arc</strong> (H reflex), and supraspinal effects such as miosis, nausea, respiratory depression was evaluated.
+CNR1	drug	alcohol	32738384	We have closely monitored the critical indicators reflecting changes of ECS during the whole process from <b>alcohol</b> absorption to its metabolization after acute <b>alcohol</b> (4.5 g/kg) intake by intragastric administration, including two key endocannabinoids (AEA and 2 AG) and their hydrolytic enzymes (FAAH and MAGL), as well as two crucial receptors (<strong>CB1R</strong> and CB2R) of ECS in blood and three brain regions.
+CNR1	drug	cannabinoid	32738384	We have closely monitored the critical indicators reflecting changes of ECS during the whole process from alcohol absorption to its metabolization after acute alcohol (4.5 g/kg) intake by intragastric administration, including two key <b>endocannabinoids</b> (AEA and 2 AG) and their hydrolytic enzymes (FAAH and MAGL), as well as two crucial receptors (<strong>CB1R</strong> and CB2R) of ECS in blood and three brain regions.
+CNR1	drug	alcohol	32738384	The levels of <strong>CB1R</strong> and CB2R in striatum showed similar tendency of increasing at 4h, which was consistent with the peak time of non oxidative <b>ethanol</b> metabolite.
+CNR1	drug	alcohol	32738384	The expression of <strong>CB1R</strong> and CB2R in prefrontal cortex were elevated after <b>alcohol</b> consumption.
+CNR1	drug	alcohol	32710885	The present study assessed the reinforcing properties of a <strong>cannabinoid receptor 1</strong> (CB1) agonist self administered directly into the nucleus accumbens shell (AcbSh) in female Wistar and <b>alcohol</b> preferring (P) rats.
+CNR1	drug	cannabinoid	32710885	The present study assessed the reinforcing properties of a <strong><b>cannabinoid</b> receptor 1</strong> (CB1) agonist self administered directly into the nucleus accumbens shell (AcbSh) in female Wistar and alcohol preferring (P) rats.
+CNR1	addiction	reward	32710885	The present study assessed the <b>reinforcing</b> properties of a <strong>cannabinoid receptor 1</strong> (CB1) agonist self administered directly into the nucleus accumbens shell (AcbSh) in female Wistar and alcohol preferring (P) rats.
+CNR1	drug	cannabinoid	32433545	<b>Cannabinoid</b> receptor <strong>CNR1</strong> expression and DNA methylation in human prefrontal cortex, hippocampus and caudate in brain development and schizophrenia.
+CNR1	drug	cannabinoid	32433545	The type 1 <b>cannabinoid</b> receptor (CB1), encoded by the <strong>CNR1</strong> gene, is a key component of the <b>endocannabinoid</b> system.
+CNR1	drug	alcohol	32433545	THC or <b>ethanol</b> are each significantly associated with dysregulated expression of <strong>CNR1</strong> in the PFC of patients with affective disorder, and the expression of <strong>CNR1</strong> is significantly upregulated in the PFC of schizophrenia patients who completed suicide.
+CNR1	drug	cannabinoid	32433545	<b>THC</b> or ethanol are each significantly associated with dysregulated expression of <strong>CNR1</strong> in the PFC of patients with affective disorder, and the expression of <strong>CNR1</strong> is significantly upregulated in the PFC of schizophrenia patients who completed suicide.
+CNR1	drug	cannabinoid	32414087	<b>Cannabis</b> Constituents and Acetylcholinesterase Interaction: Molecular Docking, In Vitro Studies and Association with <strong>CNR1</strong> rs806368 and ACHE rs17228602.
+CNR1	drug	cannabinoid	32414087	Further, genetic predisposition to <b>cannabis</b> addiction was investigated by association analysis of <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) single nucleotide polymorphism (SNP) rs806368 and ACHE rs17228602 using restriction fragment length polymorphism (RFLP) method.
+CNR1	addiction	addiction	32414087	Further, genetic predisposition to cannabis <b>addiction</b> was investigated by association analysis of cannabinoid receptor 1 (<strong>CNR1</strong>) single nucleotide polymorphism (SNP) rs806368 and ACHE rs17228602 using restriction fragment length polymorphism (RFLP) method.
+CNR1	drug	cannabinoid	32414087	Further, genetic predisposition to <b>cannabis</b> addiction was investigated by association analysis of <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) single nucleotide polymorphism (SNP) rs806368 and ACHE rs17228602 using restriction fragment length polymorphism (RFLP) method.
+CNR1	addiction	addiction	32414087	Further, genetic predisposition to cannabis <b>addiction</b> was investigated by association analysis of <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) single nucleotide polymorphism (SNP) rs806368 and ACHE rs17228602 using restriction fragment length polymorphism (RFLP) method.
+CNR1	drug	cannabinoid	32308209	It interacts with the <b>endocannabinoid</b> signaling, especially through the activation of <b>cannabinoid</b> receptors 1 <strong>CB1R</strong>, which can lead to abnormal neurodevelopmental processes and neuronal circuits functions.
+CNR1	drug	alcohol	32150428	<b>Alcohol</b> preferring and nonpreferring rodents exhibit differences in CB1 receptor expression (<strong>CB1R</strong>; Hansson et al., 2007; Hungund & Basavarajappa, 2000), but whether dorsal striatal CB1Rs are important for other <b>alcohol</b> related behaviors such as attentional set shifting tasks remains unclear.
+CNR1	drug	alcohol	32150428	This study assesses whether selectively bred high (HAP) versus low <b>alcohol</b> preferring mice differ in an operant attentional set shifting task or <strong>CB1R</strong> levels in the dorsal striatum and whether a history of voluntary <b>alcohol</b> consumption in crossed HAP mice exacerbates inflexibility.
+CNR1	addiction	reward	32150428	This study assesses whether selectively bred high (HAP) versus low alcohol preferring mice differ in an <b>operant</b> attentional set shifting task or <strong>CB1R</strong> levels in the dorsal striatum and whether a history of voluntary alcohol consumption in crossed HAP mice exacerbates inflexibility.
+CNR1	drug	alcohol	32150428	However, high <b>alcohol</b> preferring mice 3 mice showed reduced levels of dorsal striatal <strong>CB1R</strong> compared with low <b>alcohol</b> preferring 3 mice, suggesting that genetic differences in <b>alcohol</b> consumption may be mediated in part by striatal <strong>CB1R</strong>.
+CNR1	drug	cannabinoid	32095523	Using a genetic knock in mouse model (FAAHC/A) that biologically recapitulates the human polymorphism associated with problematic drug use, we find that in adolescent female mice, but not male mice, this FAAH polymorphism enhances the mesolimbic dopamine circuitry projecting from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) and alters <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) levels at inhibitory and excitatory terminals in the VTA.
+CNR1	drug	cannabinoid	32095523	Using a genetic knock in mouse model (FAAHC/A) that biologically recapitulates the human polymorphism associated with problematic drug use, we find that in adolescent female mice, but not male mice, this FAAH polymorphism enhances the mesolimbic dopamine circuitry projecting from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) and alters <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) levels at inhibitory and excitatory terminals in the VTA.
+CNR1	drug	cannabinoid	32093166	Targeting Peripherally Restricted <strong><b>Cannabinoid</b> Receptor 1</strong>, <b>Cannabinoid</b> Receptor 2, and <b>Endocannabinoid</b> Degrading Enzymes for the Treatment of Neuropathic Pain Including Neuropathic Orofacial Pain.
+CNR1	drug	cannabinoid	31973708	It has been hypothesized that heteromers of adenosine A2A receptors (A2AR) and <b>cannabinoid</b> CB1 receptors (<strong>CB1R</strong>) localized in glutamatergic nerve terminals mediate the integration of adenosine and <b>endocannabinoid</b> signaling involved in the modulation of striatal excitatory neurotransmission.
+CNR1	addiction	dependence	31973708	A <b>dependence</b> of A2AR signaling for the Gi protein mediated <strong>CB1R</strong> signaling was described as one of its main biochemical characteristics.
+CNR1	drug	cannabinoid	31973708	We demonstrate that the well established <b>cannabinoid</b> induced inhibition of striatal glutamate release can mostly be explained by a <strong>CB1R</strong> mediated counteraction of the A2AR mediated constitutive activation of adenylyl cyclase in the A2AR <strong>CB1R</strong> heteromer.
+CNR1	drug	cannabinoid	31733097	Loss of LTD was accompanied by desensitization of <strong><b>cannabinoid</b> receptor 1</strong> (CB1R).
+CNR1	drug	cannabinoid	31733097	Loss of LTD was accompanied by desensitization of <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>).
+CNR1	drug	cannabinoid	31733097	These data implicate NAcore <strong>CB1R</strong> as critical regulators of metaplasticity induced by <b>cannabis</b> self administration and the cues predicting <b>cannabis</b> availability.
+CNR1	drug	cannabinoid	31667531	The <b>endocannabinoid</b> system, comprising the <b>cannabinoid</b> receptors (<strong>CB1R</strong> and CB2R), the <b>endocannabinoids</b>, and their metabolizing enzymes, modulates the mesolimbic dopaminergic pathway and represents a potential target for the treatment of addiction.
+CNR1	addiction	addiction	31667531	The endocannabinoid system, comprising the cannabinoid receptors (<strong>CB1R</strong> and CB2R), the endocannabinoids, and their metabolizing enzymes, modulates the mesolimbic dopaminergic pathway and represents a potential target for the treatment of <b>addiction</b>.
+CNR1	drug	cocaine	31667531	Male Swiss mice received injections of AM251 (<strong>CB1R</strong> antagonist; 0.3 10 mg/kg) or JWH133 (CB2R agonist; 1 10 mg/kg) before acquisition or expression of <b>cocaine</b> (20 mg/kg) induced sensitization and CPP.
+CNR1	addiction	reward	31667531	Male Swiss mice received injections of AM251 (<strong>CB1R</strong> antagonist; 0.3 10 mg/kg) or JWH133 (CB2R agonist; 1 10 mg/kg) before acquisition or expression of cocaine (20 mg/kg) induced sensitization and <b>CPP</b>.
+CNR1	addiction	sensitization	31667531	Male Swiss mice received injections of AM251 (<strong>CB1R</strong> antagonist; 0.3 10 mg/kg) or JWH133 (CB2R agonist; 1 10 mg/kg) before acquisition or expression of cocaine (20 mg/kg) induced <b>sensitization</b> and CPP.
+CNR1	drug	cocaine	31667531	<strong>CB1R</strong> and CB2R have opposite roles in modulating <b>cocaine</b> induced sensitization and CPP, possibly by preventing neuronal activation in the hippocampus.
+CNR1	addiction	reward	31667531	<strong>CB1R</strong> and CB2R have opposite roles in modulating cocaine induced sensitization and <b>CPP</b>, possibly by preventing neuronal activation in the hippocampus.
+CNR1	addiction	sensitization	31667531	<strong>CB1R</strong> and CB2R have opposite roles in modulating cocaine induced <b>sensitization</b> and CPP, possibly by preventing neuronal activation in the hippocampus.
+CNR1	drug	cannabinoid	31634502	<strong><b>Cannabinoid</b> receptor 1</strong> (CB1R) is a GPCR expressed widely in the brain as well as in peripheral metabolic organs.
+CNR1	drug	cannabinoid	31634502	<strong><b>Cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) is a GPCR expressed widely in the brain as well as in peripheral metabolic organs.
+CNR1	drug	nicotine	31634502	Although pharmacological blockade of <strong>CB1R</strong> has been effective for the treatment of obesity and <b>tobacco</b> addiction, precise distribution of <strong>CB1R</strong> within the brain and potential changes by obesity or <b>nicotine</b> exposure have not been thoroughly addressed.
+CNR1	addiction	addiction	31634502	Although pharmacological blockade of <strong>CB1R</strong> has been effective for the treatment of obesity and tobacco <b>addiction</b>, precise distribution of <strong>CB1R</strong> within the brain and potential changes by obesity or nicotine exposure have not been thoroughly addressed.
+CNR1	drug	nicotine	31634502	To address the effect of <b>nicotine</b> on food intake and body weight, and on potential changes of <strong>CB1R</strong> levels in the hypothalamus, mice kept on a high fat diet (HFD) for four weeks were challenged with <b>nicotine</b> intraperitoneally.
+CNR1	drug	nicotine	31634502	Neither HFD nor <b>nicotine</b> alone altered <strong>CB1R</strong> levels in any nucleus tested.
+CNR1	drug	nicotine	31634502	By contrast, treatment of HFD fed mice with <b>nicotine</b> led to a significant increase in <strong>CB1R</strong> levels in the arcuate, paraventricular and lateral nuclei.
+CNR1	drug	nicotine	31634502	The expression of <strong>CB1R</strong> was augmented only when mice were treated with HFD and <b>nicotine</b> in combination.
+CNR1	drug	alcohol	31568767	Opposed cannabinoid 1 receptor (<strong>CB1R</strong>) expression in the prefrontal cortex vs. nucleus accumbens is associated with <b>alcohol</b> consumption in male rats.
+CNR1	drug	cannabinoid	31568767	Opposed <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) expression in the prefrontal cortex vs. nucleus accumbens is associated with alcohol consumption in male rats.
+CNR1	drug	alcohol	31568767	There is extensive literature indicating that cannabinoid 1 receptor (<strong>CB1R</strong>) plays a crucial role in mediating <b>alcohol</b>'s reward effects.
+CNR1	drug	cannabinoid	31568767	There is extensive literature indicating that <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) plays a crucial role in mediating alcohol's reward effects.
+CNR1	addiction	reward	31568767	There is extensive literature indicating that cannabinoid 1 receptor (<strong>CB1R</strong>) plays a crucial role in mediating alcohol's <b>reward</b> effects.
+CNR1	drug	alcohol	31568767	The present study researched whether anxiety like behaviors and the level of motivation for a natural reward, and <strong>CB1R</strong> expression in the prefrontal cortex (PFC) and nucleus accumbens (NAcc) can predict <b>alcohol</b> consumption in non MCD and MCD male rats.
+CNR1	addiction	reward	31568767	The present study researched whether anxiety like behaviors and the level of motivation for a natural <b>reward</b>, and <strong>CB1R</strong> expression in the prefrontal cortex (PFC) and nucleus accumbens (NAcc) can predict alcohol consumption in non MCD and MCD male rats.
+CNR1	drug	alcohol	31568767	Hence, both higher anxiety like behaviors and higher <strong>CB1R</strong> expression in the NAcc and lower <strong>CB1R</strong> expression in the PFC are associated with higher <b>alcohol</b> intake.
+CNR1	drug	cannabinoid	31549358	Significant progress was made with the discovery of <b>rimonabant</b>, a selective CB1 receptor (<strong>CB1R</strong>) antagonist (also an inverse agonist), as a promising therapeutic for SUDs and obesity.
+CNR1	drug	cannabinoid	31549358	However, serious adverse effects such as depression and suicidality led to the withdrawal of <b>rimonabant</b> (and almost all other <strong>CB1R</strong> antagonists/inverse agonists) from clinical trials worldwide in 2008.
+CNR1	addiction	withdrawal	31549358	However, serious adverse effects such as depression and suicidality led to the <b>withdrawal</b> of rimonabant (and almost all other <strong>CB1R</strong> antagonists/inverse agonists) from clinical trials worldwide in 2008.
+CNR1	drug	cannabinoid	31549358	Since then, much research interest has shifted to other <b>cannabinoid</b> based strategies, such as peripheral <strong>CB1R</strong> antagonists/inverse agonists, neutral <strong>CB1R</strong> antagonists, allosteric <strong>CB1R</strong> modulators, CB2R agonists, fatty acid amide hydrolase (FAAH) inhibitors, monoacylglycerol lipase (MAGL) inhibitors, fatty acid binding protein (FABP) inhibitors, or nonaddictive phytocannabinoids with <strong>CB1R</strong> or CB2R binding profiles, as new therapeutics for SUDs.
+CNR1	drug	cannabinoid	31549358	As evidence continues to accumulate, neutral <strong>CB1R</strong> antagonists (such as AM4113), CB2R agonists (JWH133, Xie2 64), and nonselective phytocannabinoids (<b>cannabidiol</b>, β caryophyllene, ∆9 <b>tetrahydrocannabivarin</b>) have shown great therapeutic potential for SUDs, as shown in experimental animals.
+CNR1	drug	alcohol	31524960	Cannabinoids and their principle psychoactive target, the cannabinoid type 1 receptor (<strong>CB1R</strong>), impact a number of <b>alcohol</b> related properties, and although <b>alcohol</b> and cannabis are often co used, particularly in adolescence, few animal models of this phenomenon exist.
+CNR1	drug	cannabinoid	31524960	<b>Cannabinoids</b> and their principle psychoactive target, the <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>), impact a number of alcohol related properties, and although alcohol and <b>cannabis</b> are often co used, particularly in adolescence, few animal models of this phenomenon exist.
+CNR1	drug	cannabinoid	31524960	The remaining mice were assessed for tolerance to <b>THC</b> induced hypothermia, and whole brain <strong>CB1R</strong> expression was assessed in all mice.
+CNR1	drug	cannabinoid	31515283	<strong><b>Cannabinoid</b> receptor 1</strong> (CB1) is a potential therapeutic target for the treatment of pain, obesity and obesity related metabolic disorders, and addiction.
+CNR1	addiction	addiction	31515283	<strong>Cannabinoid receptor 1</strong> (CB1) is a potential therapeutic target for the treatment of pain, obesity and obesity related metabolic disorders, and <b>addiction</b>.
+CNR1	drug	cannabinoid	31506004	<strong><b>Cannabinoid</b> receptor 1</strong> (CB1) antagonist AM251 (0.5, 1.0 or 2.0 mg/kg, i.p.)
+CNR1	drug	cannabinoid	31467080	We have previously reported that <b>tetrahydrocannabinol</b> mediated cognitive impairment arises from homo  or heterooligomerization between the GPCRs <b>cannabinoid</b> receptor type 1 (<strong>CB1R</strong>) and 5 hydroxytryptamine 2A (5 HT2AR) receptors.
+CNR1	drug	cannabinoid	31464475	When the <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>) antagonist, <b>rimonabant</b>, was administered prior to the most effective <b>THC</b> heroin combination, <b>rimonabant</b> blocked the <b>THC</b> enhancement of heroin antinociception.
+CNR1	drug	opioid	31464475	When the cannabinoid type 1 receptor (<strong>CB1R</strong>) antagonist, rimonabant, was administered prior to the most effective THC <b>heroin</b> combination, rimonabant blocked the THC enhancement of <b>heroin</b> antinociception.
+CNR1	drug	cannabinoid	31464475	Heroin produced both dose  and temperature dependent thermal antinociception in nonhuman primates and <b>THC</b> produced opioid enhancing effects in a <strong>CB1R</strong> dependent manner.
+CNR1	drug	opioid	31464475	<b>Heroin</b> produced both dose  and temperature dependent thermal antinociception in nonhuman primates and THC produced <b>opioid</b> enhancing effects in a <strong>CB1R</strong> dependent manner.
+CNR1	drug	alcohol	31445429	Disruption of an enhancer associated with addictive behaviour within the <strong>cannabinoid receptor 1</strong> gene suggests a possible role in <b>alcohol</b> intake, cannabinoid response and anxiety related behaviour.
+CNR1	drug	cannabinoid	31445429	Disruption of an enhancer associated with addictive behaviour within the <strong><b>cannabinoid</b> receptor 1</strong> gene suggests a possible role in alcohol intake, <b>cannabinoid</b> response and anxiety related behaviour.
+CNR1	addiction	addiction	31445429	Disruption of an enhancer associated with <b>addictive</b> behaviour within the <strong>cannabinoid receptor 1</strong> gene suggests a possible role in alcohol intake, cannabinoid response and anxiety related behaviour.
+CNR1	drug	cannabinoid	31445429	The combination of comparative genomics and CRISPR/CAS9 disruption used in our study to determine the functional effects of genetic and epigenetic changes on the activity of tissue specific regulatory elements at the <strong>CNR1</strong> locus represent an important first step in gaining a mechanistic understanding of <b>cannabinoid</b> regulatory pharmacogenetics.
+CNR1	drug	cannabinoid	31372820	Data reveal inhibitory control deficits in female Tat(+) mice (p = .048) and an upregulation of <b>cannabinoid</b> type 1 receptors (<strong>CB1R</strong>) in the infralimbic (IL) cortex in the same female Tat(+) group (p < .05).
+CNR1	drug	cannabinoid	31372820	The demonstrated inhibitory control deficits appear to be associated with an upregulation of <b>cannabinoid</b> type 1 receptors (<strong>CB1R</strong>) in the infralimbic (IL) cortex in the same female Tat(+) group.
+CNR1	drug	cannabinoid	31332736	The majority of studies on these receptors have been conducted in the past two and half decades after the identification of the molecular constituents of the <b>endocannabinoid</b> (eCB) system that started with the characterization of <strong>CB1R</strong>.
+CNR1	drug	alcohol	31332736	Several preclinical studies have provided evidence that <strong>CB1R</strong> significantly contributes to the motivational and reinforcing properties of <b>ethanol</b> and that the chronic consumption of <b>ethanol</b> alters eCB transmitters and <strong>CB1R</strong> expression in the brain nuclei associated with addiction pathways.
+CNR1	addiction	addiction	31332736	Several preclinical studies have provided evidence that <strong>CB1R</strong> significantly contributes to the motivational and reinforcing properties of ethanol and that the chronic consumption of ethanol alters eCB transmitters and <strong>CB1R</strong> expression in the brain nuclei associated with <b>addiction</b> pathways.
+CNR1	addiction	reward	31332736	Several preclinical studies have provided evidence that <strong>CB1R</strong> significantly contributes to the motivational and <b>reinforcing</b> properties of ethanol and that the chronic consumption of ethanol alters eCB transmitters and <strong>CB1R</strong> expression in the brain nuclei associated with addiction pathways.
+CNR1	drug	cannabinoid	31284863	The <b>Cannabinoid</b> CB1 Receptor (<strong>CB1R</strong>) is involved in a variety of physiological pathways and has long been considered a golden target for therapeutic manipulation.
+CNR1	addiction	addiction	31284863	A large body of evidence in both animal and human studies suggests that <strong>CB1R</strong> antagonism is highly effective for the treatment of obesity, metabolic disorders and drug <b>addiction</b>.
+CNR1	drug	cannabinoid	31284863	However, the first in class <strong>CB1R</strong> antagonist/inverse agonist, <b>rimonabant</b>, though demonstrating effectiveness for obesity treatment and smoking cessation, displays serious psychiatric side effects, including anxiety, depression and even suicidal ideation, resulting in its eventual withdrawal from the European market.
+CNR1	drug	nicotine	31284863	However, the first in class <strong>CB1R</strong> antagonist/inverse agonist, rimonabant, though demonstrating effectiveness for obesity treatment and <b>smoking</b> cessation, displays serious psychiatric side effects, including anxiety, depression and even suicidal ideation, resulting in its eventual withdrawal from the European market.
+CNR1	addiction	withdrawal	31284863	However, the first in class <strong>CB1R</strong> antagonist/inverse agonist, rimonabant, though demonstrating effectiveness for obesity treatment and smoking cessation, displays serious psychiatric side effects, including anxiety, depression and even suicidal ideation, resulting in its eventual <b>withdrawal</b> from the European market.
+CNR1	drug	cannabinoid	31250073	by blocking the <b>cannabinoid</b> type 1 receptor (<strong>CB1r</strong>).
+CNR1	addiction	aversion	31250073	Taken together, these results suggest that <strong>CB1r</strong> antagonism induces social deficits without increasing anxiety levels and impairs the extinction of <b>aversive</b> memories.
+CNR1	drug	cannabinoid	31202911	Therefore, the <b>endocannabinoid</b> system could represent a therapeutic target for schizophrenia as a regulator of glutamate and GABA release via the CB1 receptor (<strong>CB1R</strong>).
+CNR1	drug	cannabinoid	31184938	<strong>CNR1</strong> and FAAH variation and affective states induced by <b>marijuana</b> smoking.
+CNR1	drug	nicotine	31184938	<strong>CNR1</strong> and FAAH variation and affective states induced by marijuana <b>smoking</b>.
+CNR1	drug	cannabinoid	31184938	Background: Polymorphisms in <b>cannabinoid</b> receptor type 1 (encoded by <strong>CNR1</strong>) and fatty acid amide hydrolase (encoded by FAAH) have been associated with <b>cannabis</b> dependence, but it remains unknown whether variation within these genes influences <b>cannabis</b>' acute effects on affect.
+CNR1	addiction	dependence	31184938	Background: Polymorphisms in cannabinoid receptor type 1 (encoded by <strong>CNR1</strong>) and fatty acid amide hydrolase (encoded by FAAH) have been associated with cannabis <b>dependence</b>, but it remains unknown whether variation within these genes influences cannabis' acute effects on affect.
+CNR1	drug	cannabinoid	31184938	Objective: Conduct a secondary data analysis study to determine whether previously observed acute effects of <b>tetrahydrocannabinol</b> (<b>THC</b>) on mood was dependent upon variation in <strong>CNR1</strong> and FAAH.
+CNR1	drug	cannabinoid	31184938	Results: <b>THC</b> increased levels of POMS Tension Anxiety and Confusion Bewilderment over and above the effects of variation in <strong>CNR1</strong> and FAAH.
+CNR1	drug	cannabinoid	31173210	The current study investigated the effect of EA on intrathecal (IT) morphine‑induced hyperalgesia (MIH) and examined the hypothesis that activation of <strong><b>cannabinoid</b> receptor 1</strong> (CB1) could enhance the antinociceptive effect of EA on MIH via regulation of the extracellular signal‑regulated kinase 1/2 (ERK1/2) signaling pathway.
+CNR1	drug	opioid	31173210	The current study investigated the effect of EA on intrathecal (IT) <b>morphine</b>‑induced hyperalgesia (MIH) and examined the hypothesis that activation of <strong>cannabinoid receptor 1</strong> (CB1) could enhance the antinociceptive effect of EA on MIH via regulation of the extracellular signal‑regulated kinase 1/2 (ERK1/2) signaling pathway.
+CNR1	addiction	aversion	31116971	<strong>CB1R</strong> mediates oleamide's reward while 5HT2cR mediates <b>aversion</b> in the nucleus accumbens shell of rats.
+CNR1	addiction	reward	31116971	<strong>CB1R</strong> mediates oleamide's <b>reward</b> while 5HT2cR mediates aversion in the nucleus accumbens shell of rats.
+CNR1	drug	cannabinoid	31116971	We sought to determine if CPP occurs via <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) and CPA via serontoninergic 2c receptor (5HT2cR).
+CNR1	addiction	reward	31116971	We sought to determine if <b>CPP</b> occurs via <strong>cannabinoid receptor 1</strong> (CB1R) and CPA via serontoninergic 2c receptor (5HT2cR).
+CNR1	drug	cannabinoid	31116971	We sought to determine if CPP occurs via <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) and CPA via serontoninergic 2c receptor (5HT2cR).
+CNR1	addiction	reward	31116971	We sought to determine if <b>CPP</b> occurs via <strong>cannabinoid receptor 1</strong> (<strong>CB1R</strong>) and CPA via serontoninergic 2c receptor (5HT2cR).
+CNR1	addiction	reward	31116971	AM251 (<strong>CB1R</strong> inverse agonist) prevented <b>CPP</b> induced with 1 μg; while SB242084 (5HT2cR antagonist) not only prevented CPA induced with 10 μg but caused a switch to <b>CPP</b>.
+CNR1	addiction	aversion	31116971	These results suggest that oleamide at low doses promotes reward through <strong>CB1R</strong>, and <b>aversion</b> at high doses via 5HT2cR.
+CNR1	addiction	reward	31116971	These results suggest that oleamide at low doses promotes <b>reward</b> through <strong>CB1R</strong>, and aversion at high doses via 5HT2cR.
+CNR1	drug	alcohol	31105045	Endocannabinoids acting on the cannabinoid 1 receptor (<strong>CB1R</strong>) or ghrelin acting on its receptor (GHS R1A) both promote <b>alcohol</b> seeking behavior, but an interaction between the two signaling systems has not been explored.
+CNR1	drug	cannabinoid	31105045	<b>Endocannabinoids</b> acting on the <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) or ghrelin acting on its receptor (GHS R1A) both promote alcohol seeking behavior, but an interaction between the two signaling systems has not been explored.
+CNR1	addiction	relapse	31105045	Endocannabinoids acting on the cannabinoid 1 receptor (<strong>CB1R</strong>) or ghrelin acting on its receptor (GHS R1A) both promote alcohol <b>seeking</b> behavior, but an interaction between the two signaling systems has not been explored.
+CNR1	drug	alcohol	31105045	Here, we report that the peripheral <strong>CB1R</strong> inverse agonist JD5037 reduces <b>ethanol</b> drinking in wild type mice but not in mice lacking <strong>CB1R</strong>, ghrelin peptide or GHS R1A.
+CNR1	drug	alcohol	31105045	Blocking gastric vagal afferents abrogated the ability of either <strong>CB1R</strong> or GHS R1A blockade to reduce <b>ethanol</b> drinking.
+CNR1	drug	alcohol	31105045	We conclude that blocking <strong>CB1R</strong> in ghrelin producing cells reduces <b>alcohol</b> drinking by inhibiting the formation of active ghrelin and its signaling via gastric vagal afferents.
+CNR1	drug	alcohol	31105045	Thus, peripheral <strong>CB1R</strong> blockade may have therapeutic potential in the treatment of <b>alcoholism</b>.
+CNR1	drug	cannabinoid	31013550	Single nucleotide polymorphisms (SNPs) in the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>; rs1049353 and rs806378) and fatty acid amide hydrolase (FAAH) gene (rs324420) have been implicated in CUD.
+CNR1	drug	cannabinoid	31013550	Results indicated that <strong>CNR1</strong> rs1049353 GG carriers showed increased state satiety after <b>THC</b>/<b>THC</b> + CBD administration in comparison with placebo and reduced the salience of appetitive cues after <b>THC</b> in comparison with CBD administration; A carriers did not vary on either of these measures indicative of a vulnerability to CUD.
+CNR1	drug	cannabinoid	30965351	Remarkably, <b>THC</b> consumption by adolescent male rats and not female rats led to impaired Pavlovian reward predictive cue behaviors in adulthood consistent with a male specific loss of <strong>CB1R</strong> expressing vGlut 1 synaptic terminals in the ventral tegmental area (VTA).
+CNR1	addiction	reward	30965351	Remarkably, THC consumption by adolescent male rats and not female rats led to impaired Pavlovian <b>reward</b> predictive cue behaviors in adulthood consistent with a male specific loss of <strong>CB1R</strong> expressing vGlut 1 synaptic terminals in the ventral tegmental area (VTA).
+CNR1	drug	cannabinoid	30945071	Role of <strong><b>cannabinoid</b> receptor 1</strong> and the peroxisome proliferator activated receptor α in mediating anti nociceptive effects of synthetic <b>cannabinoids</b> and a <b>cannabinoid</b> like compound.
+CNR1	drug	cannabinoid	30945071	The aim of this study is to evaluate the anti nociceptive effects of synthetic <b>cannabinoids</b> (WIN 55,212 and HU210) and the <b>cannabinoid</b> like compound <b>palmitoylethanolamide</b> (PEA) in rat models of OA and to assess the role of <strong><b>cannabinoid</b> receptor 1</strong> (CB1) and the peroxisome proliferator activated receptor α (PPARα) in mediating these effects.
+CNR1	drug	cannabinoid	30763598	Experimental data suggest that RES induces peripheral antinociception through μOR and <strong>CB1R</strong> activation by endogenous opioid and <b>endocannabinoid</b> releasing.
+CNR1	drug	opioid	30763598	Experimental data suggest that RES induces peripheral antinociception through μOR and <strong>CB1R</strong> activation by endogenous <b>opioid</b> and endocannabinoid releasing.
+CNR1	drug	cannabinoid	30664203	In addition, kininogen 1, lysophosphatidic acid receptor 5, formyl peptide receptor (FPR) 2, adenylate cyclase 2, γ‑aminobutyric acid type B receptor subunit 2, FPR1, hydroxycarboxylic acid receptor 1, prostaglandin E receptor 3, <strong><b>cannabinoid</b> receptor 1</strong> and proenkephalin were identified as the top 10 hub genes.
+CNR1	drug	cannabinoid	30659912	In the present study, we have evaluated the existence of functional interaction between orexin 2 receptor (OX2R) and <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) in the nucleus accumbens core (NAcc), in nicotine induced conditioned place preference (CPP) of Wistar male rat.
+CNR1	drug	nicotine	30659912	In the present study, we have evaluated the existence of functional interaction between orexin 2 receptor (OX2R) and cannabinoid 1 receptor (<strong>CB1R</strong>) in the nucleus accumbens core (NAcc), in <b>nicotine</b> induced conditioned place preference (CPP) of Wistar male rat.
+CNR1	addiction	reward	30659912	In the present study, we have evaluated the existence of functional interaction between orexin 2 receptor (OX2R) and cannabinoid 1 receptor (<strong>CB1R</strong>) in the nucleus accumbens core (NAcc), in nicotine induced conditioned place preference (<b>CPP</b>) of Wistar male rat.
+CNR1	drug	nicotine	30659912	Intra NAcc administration of ineffective and effective doses of TCS OX2 29 (2 and 6 ng/rat), a selective OX2R antagonist and AM251 (10 and 50 ng/rat), a selective <strong>CB1R</strong> antagonist, showed a significant interaction between OX2R and <strong>CB1R</strong> in the acquisition of <b>nicotine</b> induced CPP (p < 0.01), and the locomotor activity (p < 0.05).
+CNR1	addiction	reward	30659912	Intra NAcc administration of ineffective and effective doses of TCS OX2 29 (2 and 6 ng/rat), a selective OX2R antagonist and AM251 (10 and 50 ng/rat), a selective <strong>CB1R</strong> antagonist, showed a significant interaction between OX2R and <strong>CB1R</strong> in the acquisition of nicotine induced <b>CPP</b> (p < 0.01), and the locomotor activity (p < 0.05).
+CNR1	drug	nicotine	30659912	Our findings provide insight into the possible interaction of OX2R and <strong>CB1R</strong> of the NAcc in <b>nicotine</b> addiction.
+CNR1	addiction	addiction	30659912	Our findings provide insight into the possible interaction of OX2R and <strong>CB1R</strong> of the NAcc in nicotine <b>addiction</b>.
+CNR1	drug	cannabinoid	30643290	Here, in mice, we identified that BLA cholecystokinin (CCK) glutamatergic neurons mediated negative reinforcement via D2 medium spiny neurons (MSNs) in the nucleus accumbens (NAc) and that chronic social defeat selectively potentiated excitatory transmission of the CCKBLA D2NAc circuit in susceptible mice via reduction of presynaptic <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>).
+CNR1	addiction	reward	30643290	Here, in mice, we identified that BLA cholecystokinin (CCK) glutamatergic neurons mediated negative <b>reinforcement</b> via D2 medium spiny neurons (MSNs) in the nucleus accumbens (NAc) and that chronic social defeat selectively potentiated excitatory transmission of the CCKBLA D2NAc circuit in susceptible mice via reduction of presynaptic cannabinoid type 1 receptor (<strong>CB1R</strong>).
+CNR1	drug	cannabinoid	30635160	The most well established finding is the down regulation of <b>cannabinoid</b> CB1 receptors (<strong>CB1R</strong>) after chronic and recent <b>cannabis</b> exposure, but it remains uncertain whether this effect is present in <b>cannabis</b> users with schizophrenia.
+CNR1	drug	cannabinoid	30564071	The results showed that pre training intra CA1 microinjection of ACPA, the <b>cannabinoid</b> type 1 receptor (<strong>CB1r</strong>) agonist, at doses of 0.001, 0.01 or 1 µg/rat, or AM251, the <b>cannabinoid</b> type 1 receptor (<strong>CB1r</strong>) antagonist, at doses of 1, 10 or 100 ng/rat, increased escape latency and traveled distance to the platform, suggesting a spatial learning impairment, whereas intraperitoneal administration of lithium (0.5, 1 or 5 mg/kg) had no effect on spatial learning.
+CNR1	drug	cannabinoid	30546300	The Impact of <strong><b>Cannabinoid</b> Receptor 1</strong> Gene on Gambling Tasks.
+CNR1	drug	cannabinoid	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>), because it is related to addictive behavior and reward processing.
+CNR1	addiction	addiction	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the cannabinoid receptor 1 (<strong>CNR1</strong>), because it is related to <b>addictive</b> behavior and reward processing.
+CNR1	addiction	reward	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the cannabinoid receptor 1 (<strong>CNR1</strong>), because it is related to addictive behavior and <b>reward</b> processing.
+CNR1	drug	cannabinoid	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>), because it is related to addictive behavior and reward processing.
+CNR1	addiction	addiction	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>), because it is related to <b>addictive</b> behavior and reward processing.
+CNR1	addiction	reward	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>), because it is related to addictive behavior and <b>reward</b> processing.
+CNR1	drug	cannabinoid	30300803	Assessment of <b>rimonabant</b> like adverse effects of purported <strong>CB1R</strong> neutral antagonist / CB2R agonist aminoalkylindole derivatives in mice.
+CNR1	drug	cannabinoid	30300803	<b>Cannabinoids</b> may be useful in the treatment of CNS disorders including drug abuse and addiction, where both <strong>CB1R</strong> antagonists / inverse agonists and CB2R agonists have shown preclinical efficacy.
+CNR1	addiction	addiction	30300803	Cannabinoids may be useful in the treatment of CNS disorders including drug abuse and <b>addiction</b>, where both <strong>CB1R</strong> antagonists / inverse agonists and CB2R agonists have shown preclinical efficacy.
+CNR1	drug	alcohol	30300803	TV 5 249 and TV 6 41, two novel aminoalkylindoles with dual action as neutral <strong>CB1R</strong> antagonists and CB2R agonists, previously attenuated abuse related effects of <b>ethanol</b> in mice.
+CNR1	drug	cannabinoid	30300803	To further characterize these drugs, TV 5 249 and TV 6 41 were compared with the <strong>CB1R</strong> antagonist / inverse agonist <b>rimonabant</b> in assays relevant to adverse effects and <b>cannabinoid</b> withdrawal.
+CNR1	addiction	withdrawal	30300803	To further characterize these drugs, TV 5 249 and TV 6 41 were compared with the <strong>CB1R</strong> antagonist / inverse agonist rimonabant in assays relevant to adverse effects and cannabinoid <b>withdrawal</b>.
+CNR1	drug	cannabinoid	30300803	The <b>cannabinoid</b> tetrad confirmed that TV 5 249 and TV 6 41 were devoid of <strong>CB1R</strong> agonist effects at behaviorally relevant doses, and neither of the novel drugs induced <b>rimonabant</b> like scratching.
+CNR1	drug	cannabinoid	30300803	Schedule controlled responding and observation of somatic signs were used to assess withdrawal like effects precipitated by <b>rimonabant</b> or TV 6 41 in mice previously treated with the high efficacy <strong>CB1R</strong> agonist JWH 018 or vehicle.
+CNR1	addiction	withdrawal	30300803	Schedule controlled responding and observation of somatic signs were used to assess <b>withdrawal</b> like effects precipitated by rimonabant or TV 6 41 in mice previously treated with the high efficacy <strong>CB1R</strong> agonist JWH 018 or vehicle.
+CNR1	drug	cannabinoid	30300803	These findings suggest differences in both direct adverse effects and withdrawal related effects elicited by <b>rimonabant</b>, TV 5 249, and TV 6 41, which could relate to neutral <strong>CB1R</strong> antagonism, CB2R agonism, or a combination of both.
+CNR1	addiction	withdrawal	30300803	These findings suggest differences in both direct adverse effects and <b>withdrawal</b> related effects elicited by rimonabant, TV 5 249, and TV 6 41, which could relate to neutral <strong>CB1R</strong> antagonism, CB2R agonism, or a combination of both.
+CNR1	drug	cannabinoid	30296558	Many of these effects are mediated via the <b>cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) subtype.
+CNR1	drug	cannabinoid	30273593	Repeated <b>Cannabidiol</b> treatment reduces cocaine intake and modulates neural proliferation and <strong>CB1R</strong> expression in the mouse hippocampus.
+CNR1	drug	cocaine	30273593	Repeated Cannabidiol treatment reduces <b>cocaine</b> intake and modulates neural proliferation and <strong>CB1R</strong> expression in the mouse hippocampus.
+CNR1	drug	cannabinoid	30257184	In this study, we have established a CPP method to investigate the effects of modulating astroglial glutamate transporters in <b>cannabinoid</b> dependence using a <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) agonist, CP 55,940 (CP).
+CNR1	addiction	dependence	30257184	In this study, we have established a CPP method to investigate the effects of modulating astroglial glutamate transporters in cannabinoid <b>dependence</b> using a <strong>cannabinoid receptor 1</strong> (CB1R) agonist, CP 55,940 (CP).
+CNR1	addiction	reward	30257184	In this study, we have established a <b>CPP</b> method to investigate the effects of modulating astroglial glutamate transporters in cannabinoid dependence using a <strong>cannabinoid receptor 1</strong> (CB1R) agonist, CP 55,940 (CP).
+CNR1	drug	cannabinoid	30257184	In this study, we have established a CPP method to investigate the effects of modulating astroglial glutamate transporters in <b>cannabinoid</b> dependence using a <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) agonist, CP 55,940 (CP).
+CNR1	addiction	dependence	30257184	In this study, we have established a CPP method to investigate the effects of modulating astroglial glutamate transporters in cannabinoid <b>dependence</b> using a <strong>cannabinoid receptor 1</strong> (<strong>CB1R</strong>) agonist, CP 55,940 (CP).
+CNR1	addiction	reward	30257184	In this study, we have established a <b>CPP</b> method to investigate the effects of modulating astroglial glutamate transporters in cannabinoid dependence using a <strong>cannabinoid receptor 1</strong> (<strong>CB1R</strong>) agonist, CP 55,940 (CP).
+CNR1	drug	cannabinoid	30204109	We measured nociceptive thermal paw withdrawal latencies and mechanical thresholds monolaterally in rats following microinjections of NSAIDs (diclofenac, ketoprofen, xefocam), saline or the <strong><b>cannabinoid</b> receptor 1</strong> (CB1) antagonist (AM 251) in the ACC.
+CNR1	addiction	withdrawal	30204109	We measured nociceptive thermal paw <b>withdrawal</b> latencies and mechanical thresholds monolaterally in rats following microinjections of NSAIDs (diclofenac, ketoprofen, xefocam), saline or the <strong>cannabinoid receptor 1</strong> (CB1) antagonist (AM 251) in the ACC.
+CNR1	drug	cannabinoid	30166624	Most studies employed radiotracers targeting <strong><b>cannabinoid</b> receptor 1</strong> (CB1).
+CNR1	drug	cannabinoid	30151725	These <b>THC</b> effects were prevented by administration of Ro 61 8048 or the <strong>CB1R</strong> antagonist, <b>rimonabant</b>.
+CNR1	drug	cannabinoid	30109373	<strong><b>Cannabinoid</b> receptor 1</strong> signaling contributions to sign tracking and conditioned reinforcement in rats.
+CNR1	addiction	reward	30109373	<strong>Cannabinoid receptor 1</strong> signaling contributions to sign tracking and conditioned <b>reinforcement</b> in rats.
+CNR1	drug	cannabinoid	30109373	<b>Endocannabinoids</b> (eCBs) are critical gatekeepers of dopaminergic signaling, and disrupting <strong><b>cannabinoid</b> receptor 1</strong> (CB1) signaling alters DA dynamics to attenuate cue motivated behaviors.
+CNR1	drug	cannabinoid	30077609	Synthesis and pharmacological characterization of functionalized 6 piperazin 1 yl purines as <strong><b>cannabinoid</b> receptor 1</strong> (CB1) inverse agonists.
+CNR1	drug	alcohol	30063884	The pharmacological manipulation of cannabinoid CB1 receptor (<strong>CB1r</strong>) in <b>alcoholic</b> patients provided discouraging results, so researchers have recently turned their attention to the cannabinoid CB2 receptor (CB2r).
+CNR1	drug	cannabinoid	30063884	The pharmacological manipulation of <b>cannabinoid</b> CB1 receptor (<strong>CB1r</strong>) in alcoholic patients provided discouraging results, so researchers have recently turned their attention to the <b>cannabinoid</b> CB2 receptor (CB2r).
+CNR1	drug	opioid	30063884	By means of real time polymerase chain reaction (PCR), we also analysed relative gene expression of tyrosine hydroxylase (TH) in the ventral tegmental area (VTA), and of mu <b>opioid</b> receptor (OPRM1), <strong>CNR1</strong> and CNR2 in the nucleus accumbens (NAcc).
+CNR1	drug	cannabinoid	30054391	Blocking NMDA receptors or nitric oxide synthase strongly attenuated LTD, whereas a <strong><b>cannabinoid</b> receptor 1</strong> antagonist had no effect.
+CNR1	drug	cannabinoid	30026011	Chronic direct activation of <b>cannabinoid</b> CB1 receptors (<strong>CB1r</strong>) may lead to downregulation of <strong>CB1r</strong> which may in turn result in a depression like phenotype in certain individuals.
+CNR1	drug	cannabinoid	30026011	We examined the effects of chronic <b>cannabinoid</b> receptor activation before exposure to an emotional traumatic event on <strong>CB1r</strong> expression in the basolateral amygdala (BLA) and CA1 and on protracted anxiety  and depression like behaviors.
+CNR1	addiction	withdrawal	30026011	Chronic treatment with WIN55,212 2 was found to down regulate <strong>CB1r</strong> protein levels in the BLA in the 10 days <b>withdrawal</b> condition, and to upregulate <strong>CB1r</strong> protein levels in the 24 hrs condition.
+CNR1	drug	cannabinoid	30019168	Moreover, mice maintained on a high fat diet (HFD) expressed higher levels of fibrinogen, whereas <b>cannabinoid</b> receptor type 1 (<strong>CB1R</strong>) KO mice fed an HFD had nearly normal fibrinogen levels.
+CNR1	drug	cannabinoid	29981335	Co administration with selective <b>cannabinoid</b> receptor subtype blockers revealed that PrNMI's anti allodynic effects are mediated by CB1 receptor (<strong>CB1R</strong>) activation.
+CNR1	drug	cannabinoid	29967454	However, clinical trials with SR141716A (<b>rimonabant</b>, a selective <strong>CB1R</strong> antagonist/inverse agonist) for the treatment of obesity and smoking cessation failed due to unwanted side effects, such as depression, anxiety, and suicidal tendencies.
+CNR1	drug	nicotine	29967454	However, clinical trials with SR141716A (rimonabant, a selective <strong>CB1R</strong> antagonist/inverse agonist) for the treatment of obesity and <b>smoking</b> cessation failed due to unwanted side effects, such as depression, anxiety, and suicidal tendencies.
+CNR1	drug	nicotine	29967454	Recent preclinical studies suggest that the neutral <strong>CB1R</strong> antagonist AM4113 may retain the therapeutic anti addictive effects of SR141716A in <b>nicotine</b> self administration models and possibly has fewer unwanted side effects.
+CNR1	addiction	addiction	29967454	Recent preclinical studies suggest that the neutral <strong>CB1R</strong> antagonist AM4113 may retain the therapeutic anti <b>addictive</b> effects of SR141716A in nicotine self administration models and possibly has fewer unwanted side effects.
+CNR1	drug	opioid	29967454	Together, these findings show that neutral <strong>CB1R</strong> antagonists such as AM4113 deserve further research as a new class of <strong>CB1R</strong> based medications for the treatment of <b>opioid</b> addiction without SR141716A like aversive effects.
+CNR1	addiction	addiction	29967454	Together, these findings show that neutral <strong>CB1R</strong> antagonists such as AM4113 deserve further research as a new class of <strong>CB1R</strong> based medications for the treatment of opioid <b>addiction</b> without SR141716A like aversive effects.
+CNR1	addiction	aversion	29967454	Together, these findings show that neutral <strong>CB1R</strong> antagonists such as AM4113 deserve further research as a new class of <strong>CB1R</strong> based medications for the treatment of opioid addiction without SR141716A like <b>aversive</b> effects.
+CNR1	drug	cannabinoid	29875385	However, expression patterns of the <b>cannabinoid</b> receptor type 1 (<strong>CB1R</strong>), the synthesizing enzyme N acyl phosphatidylethanolamine phospholipase D (NAPE PLD), and the degradation enzyme fatty acid amide hydrolase (FAAH) in the NAc have not yet been described in non human primates.
+CNR1	addiction	addiction	29778010	The most abundant receptor of the eCB system in the central nervous system is the CB1 receptor (<strong>CB1R</strong>), which is predominantly expressed in areas involved in drug <b>addiction</b>, such as the nucleus accumbens, the ventral tegmental area, the substantia nigra and the raphe nucleus.
+CNR1	drug	cannabinoid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the opioid μ receptor (Oprm1), <b>cannabinoid</b> CB1 receptor (<strong>Cnr1</strong>) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+CNR1	drug	opioid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the <b>opioid</b> μ receptor (Oprm1), cannabinoid CB1 receptor (<strong>Cnr1</strong>) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+CNR1	drug	cannabinoid	29450258	The purpose of this research was to investigate the antinociceptive and anti inflammatory effects of <b>cannabinoids</b> with reported actions at <b>cannabinoid</b> 1 (<strong>CB1R</strong>) and <b>cannabinoid</b> 2 (CB2R) receptors and/or noncannabinoid receptors in an experimental model of corneal hyperalgesia.
+CNR1	drug	cannabinoid	29450258	Cauterized eyes were treated topically with the phytocannabinoids Δ8 <b>tetrahydrocannabinol</b> (Δ8THC) or <b>cannabidiol</b> (CBD), or the CBD derivative HU 308, in the presence or absence of the <strong>CB1R</strong> antagonist AM251 (2.0 mg/kg i.p.
+CNR1	drug	cannabinoid	29450258	The antinociceptive and anti inflammatory actions of Δ8THC, but not CBD, were blocked by the <strong>CB1R</strong> antagonist AM251, but were still apparent, for both <b>cannabinoids</b>, in CB2R /  mice.
+CNR1	drug	cannabinoid	29450258	The antinociceptive and anti inflammatory effects of Δ8THC are mediated primarily via <strong>CB1R</strong>, whereas that of the <b>cannabinoids</b> CBD and HU 308, involve activation of 5 HT1A receptors and CB2Rs, respectively.
+CNR1	drug	cannabinoid	29417597	), <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) or <b>cannabinoid</b> 2 receptor (CB2R) agonists, as well as selective <b>cannabinoid</b> (CB) antagonists, alone or combined.
+CNR1	drug	cannabinoid	29417597	Treatment with 2 different <strong>CB1R</strong> antagonists (AM251 or <b>SR141716</b>) reversed both <strong>CB1R</strong> agonist and EtOH inhibition of adult neurogenesis.
+CNR1	drug	cannabinoid	29417597	Together, these findings suggest that acute <strong>CB1R</strong> <b>cannabinoid</b> receptor activation and binge EtOH treatment reduce neurogenesis through mechanisms involving <strong>CB1R</strong>.
+CNR1	addiction	intoxication	29417597	Together, these findings suggest that acute <strong>CB1R</strong> cannabinoid receptor activation and <b>binge</b> EtOH treatment reduce neurogenesis through mechanisms involving <strong>CB1R</strong>.
+CNR1	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (<strong>Cnr1</strong>, Cnr2, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and TRPV1 sensitizing kinases (Mapk3, Mapk14, Prkcg, and Prkaca).
+CNR1	drug	cannabinoid	29355038	Allosteric modulation of the type 1 <b>cannabinoid</b> receptor (<strong>CB1R</strong>) holds great therapeutic potential.
+CNR1	addiction	dependence	29355038	Consequently, <strong>CB1R</strong> allosteric modulators have an effect ceiling which allows for the tempering of <strong>CB1R</strong> signaling without the desensitization, tolerance, <b>dependence</b>, and psychoactivity associated with orthosteric compounds.
+CNR1	drug	cannabinoid	29355030	Allosteric modulators of <strong><b>cannabinoid</b> receptor 1</strong>: developing compounds for improved specificity.
+CNR1	drug	cannabinoid	29355030	The <strong><b>cannabinoid</b> receptor 1</strong> (CB1) is a G protein coupled receptor (GPCR) that is located primarily in the central nervous system.
+CNR1	drug	cannabinoid	29113897	<b>Cannabinoid</b> administration modulates dopamine transmission via an indirect, multisynaptic mechanism that includes the activation of <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>).
+CNR1	drug	cannabinoid	29113897	The present study evaluated in rodents, the effects of acute and chronic (20 days) WIN55,212 2 administration, a non selective <strong>CB1R</strong> agonist, on dopamine uptake and synthesis in the mesolimbic and nigrostriatal dopaminergic pathways and associate them to its effects on the <b>endocannabinoid</b> system.
+CNR1	drug	cannabinoid	29113897	Furthermore, after chronic agonist treatment, we observed reduced <strong>CB1R</strong> binding and mRNA levels in SN and striatum, providing evidence for a possible regulatory role of the <b>endocannabinoid</b> system on dopaminergic function.
+CNR1	drug	cannabinoid	29100630	Corticosterone application attenuated inhibitory synaptic transmission in the PL via <b>cannabinoid</b> receptor type 1 (<strong>CB1R</strong>)  and 2 arachidonoylglycerol dependent inhibition of gamma aminobutyric acid release without altering postsynaptic responses.
+CNR1	drug	cocaine	29100630	The ability of systemic stress level corticosterone treatment to potentiate <b>cocaine</b> primed reinstatement was recapitulated by intra PL injection of corticosterone, the <strong>CB1R</strong> agonist WIN 55,212 2, or the monoacylglycerol lipase inhibitor URB602.
+CNR1	addiction	relapse	29100630	The ability of systemic stress level corticosterone treatment to potentiate cocaine primed <b>reinstatement</b> was recapitulated by intra PL injection of corticosterone, the <strong>CB1R</strong> agonist WIN 55,212 2, or the monoacylglycerol lipase inhibitor URB602.
+CNR1	addiction	relapse	29100630	Corticosterone effects on <b>reinstatement</b> were attenuated by intra PL injections of either the <strong>CB1R</strong> antagonist, AM251, or the diacylglycerol lipase inhibitor, DO34.
+CNR1	drug	cocaine	29100630	These findings suggest that stress induced increases in corticosterone promote <b>cocaine</b> seeking by mobilizing 2 arachidonoylglycerol in the PL, resulting in <strong>CB1R</strong> mediated attenuation of inhibitory transmission in this brain region.
+CNR1	addiction	relapse	29100630	These findings suggest that stress induced increases in corticosterone promote cocaine <b>seeking</b> by mobilizing 2 arachidonoylglycerol in the PL, resulting in <strong>CB1R</strong> mediated attenuation of inhibitory transmission in this brain region.
+CNR1	drug	cannabinoid	29038246	A novel CB1 dependent LTD was induced in GABA cells that was dependent on metabotropic glutamate receptor 5, and <strong><b>cannabinoid</b> receptor 1</strong> (CB1).
+CNR1	drug	cannabinoid	29022083	Here, we examine persistent effects of ACRS with the <strong><b>cannabinoid</b> receptor 1</strong>/2 specific agonist WIN55 212,2 (WIN; 1.2 mg/kg/day, postnatal day (PD) 30 43), on natural reward seeking behaviors and ECB system function in adult male Long Evans rats (PD 60+).
+CNR1	addiction	relapse	29022083	Here, we examine persistent effects of ACRS with the <strong>cannabinoid receptor 1</strong>/2 specific agonist WIN55 212,2 (WIN; 1.2 mg/kg/day, postnatal day (PD) 30 43), on natural reward <b>seeking</b> behaviors and ECB system function in adult male Long Evans rats (PD 60+).
+CNR1	addiction	reward	29022083	Here, we examine persistent effects of ACRS with the <strong>cannabinoid receptor 1</strong>/2 specific agonist WIN55 212,2 (WIN; 1.2 mg/kg/day, postnatal day (PD) 30 43), on natural <b>reward</b> seeking behaviors and ECB system function in adult male Long Evans rats (PD 60+).
+CNR1	drug	cannabinoid	28930056	Developmentally Specific Associations Between <strong>CNR1</strong> Genotype and <b>Cannabis</b> Use Across Emerging Adulthood.
+CNR1	drug	cannabinoid	28930056	Previous studies have found preliminary evidence for associations between common single nucleotide polymorphisms (SNPs) in the <b>cannabinoid</b> receptor gene <strong>CNR1</strong> and <b>cannabis</b> use and dependence.
+CNR1	addiction	dependence	28930056	Previous studies have found preliminary evidence for associations between common single nucleotide polymorphisms (SNPs) in the cannabinoid receptor gene <strong>CNR1</strong> and cannabis use and <b>dependence</b>.
+CNR1	drug	cannabinoid	28930056	The present study examined a set of eight independent SNPs in or near <strong>CNR1</strong> in relation to <b>cannabis</b> use measured longitudinally across emerging adulthood.
+CNR1	drug	cannabinoid	28930056	Using latent growth curve modeling of 10 waves of longitudinal data spanning mean ages 18.4 23.8 years in a sample of non Hispanic White individuals (n = 334), we tested if genotype at each <strong>CNR1</strong> SNP was associated with both level and growth of <b>cannabis</b> use over time.
+CNR1	drug	cannabinoid	28825421	As E2 has been implicated in <b>endocannabinoid</b> mobilization, which can disinhibit PrL PFC projection neurons, we investigated whether <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>) activation is necessary for E2 to potentiate reinstatement.
+CNR1	addiction	relapse	28825421	As E2 has been implicated in endocannabinoid mobilization, which can disinhibit PrL PFC projection neurons, we investigated whether cannabinoid type 1 receptor (<strong>CB1R</strong>) activation is necessary for E2 to potentiate <b>reinstatement</b>.
+CNR1	drug	cocaine	28825421	The <strong>CB1R</strong> antagonist AM251 (1 or 3 mg/kg, i.p., 30 min pretreatment) administered prior to E2 and <b>cocaine</b> suppressed reinstatement in a dose dependent manner.
+CNR1	addiction	relapse	28825421	The <strong>CB1R</strong> antagonist AM251 (1 or 3 mg/kg, i.p., 30 min pretreatment) administered prior to E2 and cocaine suppressed <b>reinstatement</b> in a dose dependent manner.
+CNR1	addiction	relapse	28825421	Together, these results suggest that E2 can augment reactivity to an ordinarily subthreshold <b>relapse</b> trigger in a PrL PFC <strong>CB1R</strong> activation dependent manner.
+CNR1	drug	cannabinoid	28750808	Design and Synthesis of <b>Cannabinoid</b> 1 Receptor (<strong>CB1R</strong>) Allosteric Modulators: Drug Discovery Applications.
+CNR1	drug	cannabinoid	28750808	Also expressed in various peripheral tissues, the type 1 <b>cannabinoid</b> receptor (<strong>CB1R</strong>) is the predominant G protein coupled receptor (GPCR) in brain, where it is responsible for retrograde control of neurotransmitter release.
+CNR1	drug	cannabinoid	28749428	<strong><b>Cannabinoid</b> Receptor 1</strong> and Fatty Acid Amide Hydrolase Contribute to Operant Sensation Seeking in Mice.
+CNR1	addiction	relapse	28749428	<strong>Cannabinoid Receptor 1</strong> and Fatty Acid Amide Hydrolase Contribute to Operant Sensation <b>Seeking</b> in Mice.
+CNR1	addiction	reward	28749428	<strong>Cannabinoid Receptor 1</strong> and Fatty Acid Amide Hydrolase Contribute to <b>Operant</b> Sensation Seeking in Mice.
+CNR1	drug	cannabinoid	28749428	The purpose of the studies in this report was to begin to explore the role of <b>endocannabinoid</b> signaling in OSS utilizing <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) and fatty acid amide hydrolase (FAAH) knock out mice.
+CNR1	drug	cannabinoid	28749428	The purpose of the studies in this report was to begin to explore the role of <b>endocannabinoid</b> signaling in OSS utilizing <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) and fatty acid amide hydrolase (FAAH) knock out mice.
+CNR1	drug	cannabinoid	28669034	<b>Cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) transmission modulates VTA dopamine (DA) neuron activity and previous reports demonstrate anatomically segregated effects of <strong>CB1R</strong> transmission in the VTA.
+CNR1	addiction	aversion	28669034	In contrast, intra NAc DA receptor blockade selectively blocked the <b>aversive</b> effects of pVTA <strong>CB1R</strong> antagonism.
+CNR1	addiction	aversion	28669034	Activation vs. blockade of <strong>CB1R</strong> transmission in the posterior VTA produces bivalent rewarding or <b>aversive</b> effects through separate mu vs. kappa opiate receptor substrates.
+CNR1	drug	cannabinoid	28642081	<b>Cannabis</b> and agonists of the brain <b>cannabinoid</b> receptor (<strong>CB1R</strong>) produce acute memory impairments in humans.
+CNR1	drug	amphetamine	28642068	We used chloramphenicol (CAP, a protein synthesis inhibitor), to evaluate its effects on <b>amphetamine</b> (<b>amph</b>) seeking behavior, on <strong>CB1R</strong> expression and on protein synthesis in general, in specific areas of the brain.
+CNR1	addiction	relapse	28642068	We used chloramphenicol (CAP, a protein synthesis inhibitor), to evaluate its effects on amphetamine (amph) <b>seeking</b> behavior, on <strong>CB1R</strong> expression and on protein synthesis in general, in specific areas of the brain.
+CNR1	addiction	reward	28642068	Once <b>CPP</b> was evaluated rats were sacrificed and the prefrontal cortex (PFC), the nucleus accumbens (NAcc) and the hippocampus (Hipp) were isolated and prepared for <strong>CB1R</strong> Western blot analysis.
+CNR1	addiction	reward	28642068	Results indicate that group 1 developed <b>CPP</b> while increasing <strong>CB1R</strong> expression in the NAcc.
+CNR1	drug	amphetamine	28642068	Group 2 did not develop CPP, had lower <strong>CB1R</strong> expression in the PFC and lacked the <strong>CB1R</strong> increase in the NAcc observed in the <b>amph</b>+veh group.
+CNR1	addiction	reward	28642068	Group 2 did not develop <b>CPP</b>, had lower <strong>CB1R</strong> expression in the PFC and lacked the <strong>CB1R</strong> increase in the NAcc observed in the amph+veh group.
+CNR1	drug	amphetamine	28642068	These results support the notion that among the underlying mechanisms for <b>amph</b> seeking reward is an increase in <strong>CB1R</strong>, further supporting an interaction between dopamine/endocannabinoids in CPP learning.
+CNR1	drug	cannabinoid	28642068	These results support the notion that among the underlying mechanisms for amph seeking reward is an increase in <strong>CB1R</strong>, further supporting an interaction between dopamine/<b>endocannabinoids</b> in CPP learning.
+CNR1	addiction	relapse	28642068	These results support the notion that among the underlying mechanisms for amph <b>seeking</b> reward is an increase in <strong>CB1R</strong>, further supporting an interaction between dopamine/endocannabinoids in CPP learning.
+CNR1	addiction	reward	28642068	These results support the notion that among the underlying mechanisms for amph seeking <b>reward</b> is an increase in <strong>CB1R</strong>, further supporting an interaction between dopamine/endocannabinoids in <b>CPP</b> learning.
+CNR1	drug	cannabinoid	28592614	GW405833, widely accepted as a <b>cannabinoid</b> receptor 2 (CB2) agonist, suppresses pathologic pain in preclinical models without the unwanted central side effects of <strong><b>cannabinoid</b> receptor 1</strong> (CB1) agonists; however, recent in vitro studies have suggested that GW405833 may also behave as a noncompetitive CB1 antagonist, suggesting that its pharmacology is more complex than initially appreciated.
+CNR1	drug	cannabinoid	28579186	In light of recent advances and complexity in the field, we review <b>cannabinoid</b> based therapeutic strategies for the treatment of obesity and how peripheral restriction of <strong>CB1R</strong> antagonists may provide a different mechanism of weight loss without the central adverse effects.
+CNR1	drug	cannabinoid	28564576	The <strong><b>cannabinoid</b> receptor 1</strong> (CB1) inverse agonist <b>rimonabant</b> showed promising effects for smoking cessation but also caused psychiatric side effects and currently lacks regulatory approval.
+CNR1	drug	nicotine	28564576	The <strong>cannabinoid receptor 1</strong> (CB1) inverse agonist rimonabant showed promising effects for <b>smoking</b> cessation but also caused psychiatric side effects and currently lacks regulatory approval.
+CNR1	drug	cannabinoid	28492437	<b>Cannabinoid</b> receptors (<strong>CB1R</strong>/CB2R) are known to play important roles in pain transmission.
+CNR1	drug	opioid	28492416	After the extinction of CPP, a priming dose of <b>morphine</b> was sufficient to reinstate <b>morphine</b> CPP and was associated with the elevated <strong>CB1R</strong> levels compared with saline control groups, suggesting upregulation of <strong>CB1R</strong> pathway in the hippocampus contribute to the reinstatement of <b>morphine</b> CPP.
+CNR1	addiction	relapse	28492416	After the extinction of CPP, a priming dose of morphine was sufficient to reinstate morphine CPP and was associated with the elevated <strong>CB1R</strong> levels compared with saline control groups, suggesting upregulation of <strong>CB1R</strong> pathway in the hippocampus contribute to the <b>reinstatement</b> of morphine CPP.
+CNR1	addiction	reward	28492416	After the extinction of <b>CPP</b>, a priming dose of morphine was sufficient to reinstate morphine <b>CPP</b> and was associated with the elevated <strong>CB1R</strong> levels compared with saline control groups, suggesting upregulation of <strong>CB1R</strong> pathway in the hippocampus contribute to the reinstatement of morphine <b>CPP</b>.
+CNR1	drug	opioid	28492416	By using a pharmacological inhibitor of <strong>CB1R</strong> administered into the dorsal hippocampus, we showed that blockade of <strong>CB1R</strong> signaling did not alter the <b>morphine</b> CPP acquisition but inhibited the reinstatement of <b>morphine</b> CPP.
+CNR1	addiction	relapse	28492416	By using a pharmacological inhibitor of <strong>CB1R</strong> administered into the dorsal hippocampus, we showed that blockade of <strong>CB1R</strong> signaling did not alter the morphine CPP acquisition but inhibited the <b>reinstatement</b> of morphine CPP.
+CNR1	addiction	reward	28492416	By using a pharmacological inhibitor of <strong>CB1R</strong> administered into the dorsal hippocampus, we showed that blockade of <strong>CB1R</strong> signaling did not alter the morphine <b>CPP</b> acquisition but inhibited the reinstatement of morphine <b>CPP</b>.
+CNR1	drug	opioid	28492416	In addition, no effects were induced upon <strong>CB1R</strong> blockade in the prefrontal cortex on reinstatement of <b>morphine</b> CPP.
+CNR1	addiction	relapse	28492416	In addition, no effects were induced upon <strong>CB1R</strong> blockade in the prefrontal cortex on <b>reinstatement</b> of morphine CPP.
+CNR1	addiction	reward	28492416	In addition, no effects were induced upon <strong>CB1R</strong> blockade in the prefrontal cortex on reinstatement of morphine <b>CPP</b>.
+CNR1	drug	opioid	28492416	These studies reveal region specific effects of hippocampal blockade of <strong>CB1R</strong> signaling pathway on the reinstatement of <b>morphine</b> CPP.
+CNR1	addiction	relapse	28492416	These studies reveal region specific effects of hippocampal blockade of <strong>CB1R</strong> signaling pathway on the <b>reinstatement</b> of morphine CPP.
+CNR1	addiction	reward	28492416	These studies reveal region specific effects of hippocampal blockade of <strong>CB1R</strong> signaling pathway on the reinstatement of morphine <b>CPP</b>.
+CNR1	drug	cannabinoid	28457972	After the SA procedure, HFB mice exhibited reduced levels of the mu opioid receptor (MOr) and increased <b>cannabinoid</b> 1 receptor (<strong>CB1r</strong>) gene expression in the nucleus accumbens (N Acc), and decreased of tyrosine hydroxylase (TH) gene expression in the ventral tegmental area (VTA).
+CNR1	drug	opioid	28457972	After the SA procedure, HFB mice exhibited reduced levels of the mu <b>opioid</b> receptor (MOr) and increased cannabinoid 1 receptor (<strong>CB1r</strong>) gene expression in the nucleus accumbens (N Acc), and decreased of tyrosine hydroxylase (TH) gene expression in the ventral tegmental area (VTA).
+CNR1	drug	cannabinoid	28364110	[Role of <strong><b>cannabinoid</b> receptor 1</strong> mediated synaptic plasticity in neuropathic pain and associated depression].
+CNR1	drug	cannabinoid	28364110	<strong><b>Cannabinoid</b> receptor 1</strong> (CB1R) of <b>endocannabinoid</b> system modulates synaptic transmission, regulates synaptic plasticity, inhibits central sensitization, and thus attenuates neuropathic pain.
+CNR1	addiction	sensitization	28364110	<strong>Cannabinoid receptor 1</strong> (CB1R) of endocannabinoid system modulates synaptic transmission, regulates synaptic plasticity, inhibits central <b>sensitization</b>, and thus attenuates neuropathic pain.
+CNR1	drug	cannabinoid	28364110	<strong><b>Cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) of <b>endocannabinoid</b> system modulates synaptic transmission, regulates synaptic plasticity, inhibits central sensitization, and thus attenuates neuropathic pain.
+CNR1	addiction	sensitization	28364110	<strong>Cannabinoid receptor 1</strong> (<strong>CB1R</strong>) of endocannabinoid system modulates synaptic transmission, regulates synaptic plasticity, inhibits central <b>sensitization</b>, and thus attenuates neuropathic pain.
+CNR1	drug	cannabinoid	28255675	In the present study, we investigated the cellular sites for interactions between the <b>cannabinoid</b> receptor type 1 (<strong>CB1r</strong>) and CRF in the LC.
+CNR1	drug	cannabinoid	28192193	We found that expression of morphine CPP was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (fatty acid amide hydrolase [FAAH] and monoacylglycerol lipase [MAGL], respectively), but with reductions in <b>cannabinoid</b> 1 receptors (<strong>CB1R</strong>) and CB2R in dorsal hippocampus following the expression of CPP.
+CNR1	drug	opioid	28192193	We found that expression of <b>morphine</b> CPP was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (fatty acid amide hydrolase [FAAH] and monoacylglycerol lipase [MAGL], respectively), but with reductions in cannabinoid 1 receptors (<strong>CB1R</strong>) and CB2R in dorsal hippocampus following the expression of CPP.
+CNR1	addiction	reward	28192193	We found that expression of morphine <b>CPP</b> was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (fatty acid amide hydrolase [FAAH] and monoacylglycerol lipase [MAGL], respectively), but with reductions in cannabinoid 1 receptors (<strong>CB1R</strong>) and CB2R in dorsal hippocampus following the expression of <b>CPP</b>.
+CNR1	drug	opioid	28192193	However, our results indicated that decreased in MAGL and increased <strong>CB1R</strong> mRNA levels were accompanied with <b>morphine</b> CPP reinstatement.
+CNR1	addiction	relapse	28192193	However, our results indicated that decreased in MAGL and increased <strong>CB1R</strong> mRNA levels were accompanied with morphine CPP <b>reinstatement</b>.
+CNR1	addiction	reward	28192193	However, our results indicated that decreased in MAGL and increased <strong>CB1R</strong> mRNA levels were accompanied with morphine <b>CPP</b> reinstatement.
+CNR1	drug	cannabinoid	28103441	The <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) is one of the most widely expressed metabotropic G protein coupled receptors in brain, and its participation in various (patho)physiological processes has made <strong>CB1R</strong> activation a viable therapeutic modality.
+CNR1	drug	cannabinoid	27875353	<b>Endocannabinoids</b> may limit intestinal inflammation through <strong><b>cannabinoid</b> receptor 1</strong> and/or 2 (CB1, CB2).
+CNR1	drug	cannabinoid	27810775	With the help of HTDocking program, we predicted four novel targets for salvinorin A, including muscarinic acetylcholine receptor 2, <strong><b>cannabinoid</b> receptor 1</strong>, <b>cannabinoid</b> receptor 2 and dopamine receptor 2.
+CNR1	drug	cannabinoid	27737762	Memory impairment during nicotine withdrawal was blocked by the <strong>CB1R</strong> antagonist <b>rimonabant</b> or the genetic deletion of <strong>CB1R</strong> in forebrain gamma aminobutyric acidergic (GABAergic) neurons (GABA <strong>CB1R</strong>).
+CNR1	drug	nicotine	27737762	Memory impairment during <b>nicotine</b> withdrawal was blocked by the <strong>CB1R</strong> antagonist rimonabant or the genetic deletion of <strong>CB1R</strong> in forebrain gamma aminobutyric acidergic (GABAergic) neurons (GABA <strong>CB1R</strong>).
+CNR1	addiction	withdrawal	27737762	Memory impairment during nicotine <b>withdrawal</b> was blocked by the <strong>CB1R</strong> antagonist rimonabant or the genetic deletion of <strong>CB1R</strong> in forebrain gamma aminobutyric acidergic (GABAergic) neurons (GABA <strong>CB1R</strong>).
+CNR1	drug	cannabinoid	27737762	Interestingly, these structural plasticity alterations were normalized in GABA <strong>CB1R</strong> conditional knockout mice and after subchronic treatment with <b>rimonabant</b>.
+CNR1	drug	nicotine	27737762	These findings underline the interest of <strong>CB1R</strong> as a target to improve cognitive performance during early <b>nicotine</b> withdrawal.
+CNR1	addiction	withdrawal	27737762	These findings underline the interest of <strong>CB1R</strong> as a target to improve cognitive performance during early nicotine <b>withdrawal</b>.
+CNR1	drug	cannabinoid	27461790	<b>Cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) is highly expressed in the mesocorticolimbic system and associated with drug craving and relapse.
+CNR1	addiction	relapse	27461790	Cannabinoid CB1 receptor (<strong>CB1R</strong>) is highly expressed in the mesocorticolimbic system and associated with drug <b>craving</b> and <b>relapse</b>.
+CNR1	addiction	addiction	27461790	Clinical trials suggest that <strong>CB1R</strong> antagonists may represent new therapies for drug <b>addiction</b>.
+CNR1	drug	opioid	27461790	In the present study, we investigated the relationship between <strong>CB1R</strong> and the extracellular signal regulated kinase (ERK), cAMP response element binding protein (CREB), brain derived neurotrophic factor (BDNF) signaling in the nucleus accumbens (NAc) and hippocampus in <b>morphine</b> induced conditioned place preference (CPP), which is used to assess the <b>morphine</b> induced reward memory.
+CNR1	addiction	reward	27461790	In the present study, we investigated the relationship between <strong>CB1R</strong> and the extracellular signal regulated kinase (ERK), cAMP response element binding protein (CREB), brain derived neurotrophic factor (BDNF) signaling in the nucleus accumbens (NAc) and hippocampus in morphine induced conditioned place preference (<b>CPP</b>), which is used to assess the morphine induced <b>reward</b> memory.
+CNR1	addiction	reward	27461790	Additionally, a <strong>CB1R</strong> antagonist, AM251, was used to study whether blockade of <strong>CB1R</strong> altered the <b>CPP</b> and above mentioned molecules.
+CNR1	drug	opioid	27461790	We found an increase of <strong>CB1R</strong> expression in the NAc and hippocampus of the mice following <b>morphine</b> CPP, but not those after repeated <b>morphine</b> in home cage without context exposure (NO CPP).
+CNR1	addiction	reward	27461790	We found an increase of <strong>CB1R</strong> expression in the NAc and hippocampus of the mice following morphine <b>CPP</b>, but not those after repeated morphine in home cage without context exposure (NO <b>CPP</b>).
+CNR1	drug	opioid	27461790	Furthermore, pretreatment with AM251 before <b>morphine</b> attenuated the CPP acquisition and <strong>CB1R</strong> expression as well as the activation of ERK CREB BDNF cascade.
+CNR1	addiction	reward	27461790	Furthermore, pretreatment with AM251 before morphine attenuated the <b>CPP</b> acquisition and <strong>CB1R</strong> expression as well as the activation of ERK CREB BDNF cascade.
+CNR1	drug	opioid	27461790	Collectively, these findings demonstrate that (1) Repeated <b>morphine</b> with context exposures but not merely the pharmacological effects of <b>morphine</b> increased <strong>CB1R</strong> expression both in the NAc and hippocampus.
+CNR1	drug	opioid	27461790	(2) <strong>CB1R</strong> antagonist mediated blockade of ERK CREB BDNF signaling activation in the NAc and hippocampus may be an important mechanism underlying the attenuation of <b>morphine</b> CPP.
+CNR1	addiction	reward	27461790	(2) <strong>CB1R</strong> antagonist mediated blockade of ERK CREB BDNF signaling activation in the NAc and hippocampus may be an important mechanism underlying the attenuation of morphine <b>CPP</b>.
+CNR1	drug	cannabinoid	27453054	<b>Cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during nicotine withdrawal.
+CNR1	drug	nicotine	27453054	Cannabinoid receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during <b>nicotine</b> withdrawal.
+CNR1	addiction	withdrawal	27453054	Cannabinoid receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during nicotine <b>withdrawal</b>.
+CNR1	drug	cannabinoid	27453054	<strong><b>Cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during nicotine withdrawal.
+CNR1	drug	nicotine	27453054	<strong>Cannabinoid receptor 1</strong> (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during <b>nicotine</b> withdrawal.
+CNR1	addiction	withdrawal	27453054	<strong>Cannabinoid receptor 1</strong> (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during nicotine <b>withdrawal</b>.
+CNR1	drug	cannabinoid	27453054	Variation on the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) has been related to nicotine dependence, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	drug	nicotine	27453054	Variation on the cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been related to <b>nicotine</b> dependence, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	addiction	dependence	27453054	Variation on the cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been related to nicotine <b>dependence</b>, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	drug	cannabinoid	27453054	Variation on the <strong><b>cannabinoid</b> receptor 1</strong> gene (<strong>CNR1</strong>) has been related to nicotine dependence, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	drug	nicotine	27453054	Variation on the <strong>cannabinoid receptor 1</strong> gene (<strong>CNR1</strong>) has been related to <b>nicotine</b> dependence, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	addiction	dependence	27453054	Variation on the <strong>cannabinoid receptor 1</strong> gene (<strong>CNR1</strong>) has been related to nicotine <b>dependence</b>, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	drug	nicotine	27453054	We targeted <strong>CNR1</strong> variants as moderators of a validated neural marker of <b>nicotine</b> withdrawal related cognitive disruption.
+CNR1	addiction	withdrawal	27453054	We targeted <strong>CNR1</strong> variants as moderators of a validated neural marker of nicotine <b>withdrawal</b> related cognitive disruption.
+CNR1	drug	cannabinoid	27404285	Here, we measured <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) availability using positron emission tomography (PET) with [(18)F]MK 9470 in 54 patients with food intake disorders (FID) covering a wide body mass index (BMI) range (anorexia nervosa, bulimia nervosa, functional dyspepsia with weight loss and obesity; BMI range=12.5 40.6 kg/m(2)) and 26 age , gender  and average BMI matched healthy subjects (BMI range=18.5 26.6 kg/m(2)).
+CNR1	addiction	reward	27404285	The association between regional <strong>CB1R</strong> availability and BMI was assessed within predefined homeostatic and <b>reward</b> related regions of interest using voxel based linear regression analyses.
+CNR1	addiction	reward	27404285	However, in FID patients, <strong>CB1R</strong> availability was also negatively correlated with BMI throughout the mesolimbic <b>reward</b> system (midbrain, striatum, insula, amygdala and orbitofrontal cortex), which constitutes the key circuit implicated in processing appetitive motivation and <b>hedonic</b> value of perceived food rewards.
+CNR1	addiction	reward	27404285	Our results indicate that the cerebral homeostatic <strong>CB1R</strong> system is inextricably linked to BMI, with additional involvement of <b>reward</b> areas under conditions of disordered body weight.
+CNR1	drug	cannabinoid	27394933	Five genes known to play a role in the <b>endocannabinoid</b> system and CUDs were examined in a community sample of young adult Mexican Americans (MAs): <strong>CNR1</strong>, MGLL, FAAH, DAGLA, and DAGLB.
+CNR1	drug	cannabinoid	27266915	Here we investigate whether <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) activation is a part of the mechanism whereby estradiol influences behavioral and synaptic correlates of addiction.
+CNR1	addiction	addiction	27266915	Here we investigate whether cannabinoid 1 receptor (<strong>CB1R</strong>) activation is a part of the mechanism whereby estradiol influences behavioral and synaptic correlates of <b>addiction</b>.
+CNR1	drug	cannabinoid	27230434	In the BLA, inhibitory GABAergic substrates are inhibited by <b>cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) activation and can modulate BLA projections to various limbic regions, including the NAc.
+CNR1	drug	opioid	27230434	We report that intra BLA <strong>CB1R</strong> activation switches normally rewarding effects of <b>morphine</b> into strongly aversive effects.
+CNR1	addiction	aversion	27230434	We report that intra BLA <strong>CB1R</strong> activation switches normally rewarding effects of morphine into strongly <b>aversive</b> effects.
+CNR1	drug	opioid	27230434	In contrast, <strong>CB1R</strong> blockade strongly potentiates normally subreward threshold effects of <b>morphine</b>.
+CNR1	addiction	aversion	27230434	Finally, using multi unit, in vivo electrophysiological recordings in the NASh, we report that the ability of intra BLA <strong>CB1R</strong> modulation to control opiate reward salience and motivational valence is associated with distinct reward or <b>aversion</b> neuronal activity patterns and bi directional regulation of intra NASh fast spiking interneurons versus medium spiny neurons.
+CNR1	addiction	reward	27230434	Finally, using multi unit, in vivo electrophysiological recordings in the NASh, we report that the ability of intra BLA <strong>CB1R</strong> modulation to control opiate <b>reward</b> salience and motivational valence is associated with distinct <b>reward</b> or aversion neuronal activity patterns and bi directional regulation of intra NASh fast spiking interneurons versus medium spiny neurons.
+CNR1	drug	cannabinoid	27208730	Strikingly, this anti insulin action of dexamethasone was also blocked by two CB1 <b>cannabinoid</b> receptor (<strong>CB1R</strong>) antagonists, O 2050 (500nM) and SR141716A (500nM), as well as by tetrahydrolipstatin (10μM), an inhibitor of diacylglycerol lipases the enzymes responsible for the synthesis of the <b>endocannabinoid</b>, 2 arachidonoyl glycerol (2 AG).
+CNR1	drug	alcohol	27186643	Impaired <b>Ethanol</b> Induced Sensitization and Decreased <strong>Cannabinoid Receptor 1</strong> in a Model of Posttraumatic Stress Disorder.
+CNR1	drug	cannabinoid	27186643	Impaired Ethanol Induced Sensitization and Decreased <strong><b>Cannabinoid</b> Receptor 1</strong> in a Model of Posttraumatic Stress Disorder.
+CNR1	addiction	sensitization	27186643	Impaired Ethanol Induced <b>Sensitization</b> and Decreased <strong>Cannabinoid Receptor 1</strong> in a Model of Posttraumatic Stress Disorder.
+CNR1	drug	alcohol	27186643	<strong>Cannabinoid receptor 1</strong> (CB1) is sensitive to the effects of <b>ethanol</b> (EtOH) and traumatic stress, and is a critical regulator of striatal plasticity.
+CNR1	drug	cannabinoid	27186643	<strong><b>Cannabinoid</b> receptor 1</strong> (CB1) is sensitive to the effects of ethanol (EtOH) and traumatic stress, and is a critical regulator of striatal plasticity.
+CNR1	drug	cannabinoid	27071101	POMC neurons receive orexin A (OX A) expressing inputs and express both OX A receptor type 1 (OX 1R) and <b>cannabinoid</b> receptor type 1 (<strong>CB1R</strong>) on the plasma membrane.
+CNR1	drug	cannabinoid	27071101	OX A is crucial for the control of wakefulness and energy homeostasis and promotes, in OX 1R expressing cells, the biosynthesis of the endogenous counterpart of <b>marijuana</b>'s psychotropic and appetite inducing component Δ(9) <b>tetrahydrocannabinol</b>, i.e., the <b>endocannabinoid</b> 2 arachidonoylglycerol (2 AG), which acts at <strong>CB1R</strong>.
+CNR1	drug	cannabinoid	27046127	One of the most abundant G protein coupled receptors (GPCRs) in brain, the <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>), is a tractable therapeutic target for treating diverse psychobehavioral and somatic disorders.
+CNR1	drug	cannabinoid	27046127	The results demonstrate that GAT100 is a NAM of the orthosteric <strong>CB1R</strong> agonist CP55,940 and the <b>endocannabinoids</b> 2 arachidonoylglycerol and anandamide for β arrestin1 recruitment, PLCβ3 and ERK1/2 phosphorylation, cAMP accumulation, and <strong>CB1R</strong> internalization in HEK293A cells overexpressing <strong>CB1R</strong> and in Neuro2a and STHdh(Q7/Q7) cells endogenously expressing <strong>CB1R</strong>.
+CNR1	drug	cannabinoid	27012427	Enkephalin levels and the number of neuropeptide Y containing interneurons in the hippocampus are decreased in female <strong><b>cannabinoid</b> receptor 1</strong> knock out mice.
+CNR1	drug	cannabinoid	27012427	This was achieved by quantitatively analyzing the immunoperoxidase labeling for each of these neuropeptide in the dorsal hippocampus of female wild type (CB1+/+) and <strong><b>cannabinoid</b> receptor 1</strong> knockout (CB1 / ) C57/BL6 mice.
+CNR1	drug	nicotine	26864774	FAAH inhibition has been recently identified as having a critical involvement in behaviors related to <b>nicotine</b> addiction and has been shown to reduce the effect of <b>nicotine</b> on the mesolimbic dopaminergic system via <strong>CB1R</strong> and peroxisome proliferator activated receptor alpha (PPARα).
+CNR1	addiction	addiction	26864774	FAAH inhibition has been recently identified as having a critical involvement in behaviors related to nicotine <b>addiction</b> and has been shown to reduce the effect of nicotine on the mesolimbic dopaminergic system via <strong>CB1R</strong> and peroxisome proliferator activated receptor alpha (PPARα).
+CNR1	drug	nicotine	26864774	The study aims to explore the mechanism of action of the inhibitor of FAAH activity, URB597, on relapse to <b>nicotine</b> seeking by evaluating the effect of the <strong>CB1R</strong>, CB2R, and PPARα antagonists on the attenuating effect of URB597 on cue induced reinstatement of <b>nicotine</b> seeking in rats.
+CNR1	addiction	relapse	26864774	The study aims to explore the mechanism of action of the inhibitor of FAAH activity, URB597, on <b>relapse</b> to nicotine <b>seeking</b> by evaluating the effect of the <strong>CB1R</strong>, CB2R, and PPARα antagonists on the attenuating effect of URB597 on cue induced <b>reinstatement</b> of nicotine <b>seeking</b> in rats.
+CNR1	drug	cannabinoid	26864774	URB597 reduced cue induced reinstatement of nicotine seeking, an effect that was reversed by the <strong>CB1R</strong> antagonist <b>rimonabant</b>, but not by the CB2R or PPARα antagonists AM630 and MK886, respectively.
+CNR1	drug	nicotine	26864774	URB597 reduced cue induced reinstatement of <b>nicotine</b> seeking, an effect that was reversed by the <strong>CB1R</strong> antagonist rimonabant, but not by the CB2R or PPARα antagonists AM630 and MK886, respectively.
+CNR1	addiction	relapse	26864774	URB597 reduced cue induced <b>reinstatement</b> of nicotine <b>seeking</b>, an effect that was reversed by the <strong>CB1R</strong> antagonist rimonabant, but not by the CB2R or PPARα antagonists AM630 and MK886, respectively.
+CNR1	drug	cannabinoid	26858993	The widespread use of <b>cannabis</b>, the increasing legalization of "medical" <b>cannabis</b>, the increasing potency of <b>cannabis</b> and the growing recreational use of synthetic <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) full agonists underscores the importance of elucidating the effects of <b>cannabinoids</b> on the <strong>CB1R</strong> system.
+CNR1	drug	cannabinoid	26858993	Exposure to <b>cannabinoids</b> is known to result in <strong>CB1R</strong> downregulation.
+CNR1	drug	cannabinoid	26858993	However, the precise time course of changes in <strong>CB1R</strong> availability in <b>cannabis</b> dependent subjects (CDs) following short and intermediate term abstinence has not been determined.
+CNR1	drug	cannabinoid	26858993	However, these group differences in <strong>CB1R</strong> availability were no longer evident after just 2 days of monitored abstinence from <b>cannabis</b>.
+CNR1	addiction	withdrawal	26858993	There was a robust negative correlation between <strong>CB1R</strong> availability and <b>withdrawal</b> symptoms after 2 days of abstinence.
+CNR1	drug	cannabinoid	26858993	<b>Cannabis</b> dependence is associated with <strong>CB1R</strong> downregulation, which begins to reverse surprisingly rapidly upon termination of <b>cannabis</b> use and may continue to increase over time.
+CNR1	addiction	dependence	26858993	Cannabis <b>dependence</b> is associated with <strong>CB1R</strong> downregulation, which begins to reverse surprisingly rapidly upon termination of cannabis use and may continue to increase over time.
+CNR1	drug	cannabinoid	26833047	An Information Theoretical Study of the Epistasis Between the <strong>CNR1</strong> 1359 G/A Polymorphism and the Taq1A and Taq1B DRD2 Polymorphisms: Assessing the Susceptibility to <b>Cannabis</b> Addiction in a Turkish Population.
+CNR1	addiction	addiction	26833047	An Information Theoretical Study of the Epistasis Between the <strong>CNR1</strong> 1359 G/A Polymorphism and the Taq1A and Taq1B DRD2 Polymorphisms: Assessing the Susceptibility to Cannabis <b>Addiction</b> in a Turkish Population.
+CNR1	drug	cannabinoid	26833047	In this study, we discuss the interaction between the 1359 G/A polymorphism of the <strong>CNR1</strong> gene and the DRD2 gene polymorphisms and the net effect of any possible epistasis on the <b>cannabis</b> addiction phenotype in a Turkish population.
+CNR1	addiction	addiction	26833047	In this study, we discuss the interaction between the 1359 G/A polymorphism of the <strong>CNR1</strong> gene and the DRD2 gene polymorphisms and the net effect of any possible epistasis on the cannabis <b>addiction</b> phenotype in a Turkish population.
+CNR1	drug	cannabinoid	26833047	We hypothesize that overlapping expressions of CB1 and D2R is the cause of CB1 D2R interactions in cases of substance abuse and the different polymorphisms of <strong>CNR1</strong> and DRD2 genes may have decisive roles in the nature of these interactions in terms of promoting or alleviating the <b>cannabis</b> addiction risk factor of the individual.
+CNR1	addiction	addiction	26833047	We hypothesize that overlapping expressions of CB1 and D2R is the cause of CB1 D2R interactions in cases of substance abuse and the different polymorphisms of <strong>CNR1</strong> and DRD2 genes may have decisive roles in the nature of these interactions in terms of promoting or alleviating the cannabis <b>addiction</b> risk factor of the individual.
+CNR1	drug	cannabinoid	26803309	The basolateral amygdala (BLA) is rich of CB1 <b>cannabinoid</b> receptors (<strong>CB1R</strong>) and has reciprocal connections with the nucleus accumbens (NAc) which is involved in opioid sensitization.
+CNR1	drug	opioid	26803309	The basolateral amygdala (BLA) is rich of CB1 cannabinoid receptors (<strong>CB1R</strong>) and has reciprocal connections with the nucleus accumbens (NAc) which is involved in <b>opioid</b> sensitization.
+CNR1	addiction	sensitization	26803309	The basolateral amygdala (BLA) is rich of CB1 cannabinoid receptors (<strong>CB1R</strong>) and has reciprocal connections with the nucleus accumbens (NAc) which is involved in opioid <b>sensitization</b>.
+CNR1	drug	opioid	26803309	In this study, effects of intra BLA administration of <strong>CB1R</strong> agonist on sensitization to antinociceptive effect of <b>morphine</b> and changes in the levels of μ <b>opioid</b> receptor (MOR), p CREB, and c fos in the NAc were investigated.
+CNR1	addiction	sensitization	26803309	In this study, effects of intra BLA administration of <strong>CB1R</strong> agonist on <b>sensitization</b> to antinociceptive effect of morphine and changes in the levels of μ opioid receptor (MOR), p CREB, and c fos in the NAc were investigated.
+CNR1	addiction	sensitization	26803309	Animals received intra BLA microinjection of <strong>CB1R</strong> agonist (WIN55,212 2) once daily for 3 days consecutively (<b>sensitization</b> period).
+CNR1	drug	cannabinoid	26757949	Importantly, many of its metabolic actions are mediated through the <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>), whose hyperactivation is associated with obesity and impaired metabolic function.
+CNR1	drug	cannabinoid	26757949	Herein, we explored the effects of administering <b>rimonabant</b>, a selective <strong>CB1R</strong> inverse agonist, upon key metabolic parameters in young (4 month old) and aged (17 month old) adult male C57BL/6 mice.
+CNR1	drug	cannabinoid	26756393	The association between young adult patterns of <b>cannabis</b> use or <b>cannabis</b> abuse/dependence was tested with genetic variation in the <b>cannabinoid</b> gene, <strong>CNR1</strong>, the ANKK1 DRD2 gene, and childhood developmental trajectories of P300.
+CNR1	addiction	dependence	26756393	The association between young adult patterns of cannabis use or cannabis abuse/<b>dependence</b> was tested with genetic variation in the cannabinoid gene, <strong>CNR1</strong>, the ANKK1 DRD2 gene, and childhood developmental trajectories of P300.
+CNR1	drug	cannabinoid	26756393	Although <strong>CNR1</strong> variation overall was not significantly associated with these patterns, among individuals with <b>cannabis</b> abuse/dependence the presence of one or both copies of the rs806368 A > G minor allele conferred a 5.4 fold increase (P = 0.003) in the likelihood that they would be in the frequent and persistent use group rather than the declining use group.
+CNR1	addiction	dependence	26756393	Although <strong>CNR1</strong> variation overall was not significantly associated with these patterns, among individuals with cannabis abuse/<b>dependence</b> the presence of one or both copies of the rs806368 A > G minor allele conferred a 5.4 fold increase (P = 0.003) in the likelihood that they would be in the frequent and persistent use group rather than the declining use group.
+CNR1	drug	cannabinoid	29560896	The widespread use of <b>cannabis</b>, the increasing legalization of "medical" <b>cannabis</b>, the increasing potency of <b>cannabis</b>, and the growing recreational use of synthetic <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) full agonists all underscore the importance of elucidating the effects of <b>cannabinoids</b> on the <strong>CB1R</strong> system.
+CNR1	drug	cannabinoid	29560896	Exposure to <b>cannabinoids</b> is known to result in <strong>CB1R</strong> downregulation.
+CNR1	drug	cannabinoid	29560896	However, the precise time course of changes in <strong>CB1R</strong> availability in <b>cannabis</b> dependent (CD) subjects after short term and intermediate term abstinence has not been determined.
+CNR1	drug	cannabinoid	29560896	However, these group differences in <strong>CB1R</strong> availability were no longer evident after just 2 days of monitored abstinence from <b>cannabis</b>.
+CNR1	addiction	withdrawal	29560896	There was a robust negative correlation between <strong>CB1R</strong> availability and <b>withdrawal</b> symptoms after 2 days of abstinence.
+CNR1	drug	cannabinoid	29560896	<b>Cannabis</b> dependence is associated with <strong>CB1R</strong> downregulation, which begins to reverse rapidly on termination of <b>cannabis</b> use and may continue to increase over time.
+CNR1	addiction	dependence	29560896	Cannabis <b>dependence</b> is associated with <strong>CB1R</strong> downregulation, which begins to reverse rapidly on termination of cannabis use and may continue to increase over time.
+CNR1	drug	cocaine	28861476	Targeting the allosteric site on <strong>CB1R</strong>, new families structurally based on urea and on 3 phenyltropane analogs of <b>cocaine</b> have been discovered as <strong>CB1R</strong> negative allosteric modulators (NAMs), respectively, by Prosidion and by the Research Triangle Park.
+CNR1	drug	cannabinoid	28861476	Curiously, the peroxisome proliferator activated receptor γ agonist fenofibrate or polypeptides such as pepcan 12 have been shown to act on the <b>endocannabinoid</b> system through <strong>CB1R</strong> allosteric modulation.
+CNR1	addiction	dependence	28861476	Therefore, further understanding of the chemical features required for allosteric modulation as well as their orthosteric probe <b>dependence</b> may broaden novel approaches for fine tuning the signaling pathways of the <strong>CB1R</strong>.
+CNR1	drug	cannabinoid	26684509	Sex dependence of anxiety like behavior in <b>cannabinoid</b> receptor 1 (<strong>Cnr1</strong>) knockout mice.
+CNR1	addiction	dependence	26684509	Sex <b>dependence</b> of anxiety like behavior in cannabinoid receptor 1 (<strong>Cnr1</strong>) knockout mice.
+CNR1	drug	cannabinoid	26684509	Sex dependence of anxiety like behavior in <strong><b>cannabinoid</b> receptor 1</strong> (<strong>Cnr1</strong>) knockout mice.
+CNR1	addiction	dependence	26684509	Sex <b>dependence</b> of anxiety like behavior in <strong>cannabinoid receptor 1</strong> (<strong>Cnr1</strong>) knockout mice.
+CNR1	drug	cannabinoid	26684509	We observe greater anxiety like behavior in male mice with global knockout of the <b>cannabinoid</b> 1 receptor (<strong>Cnr1</strong>) compared to male, wild type controls as measured by percent open arm entries on an elevated plus maze test.
+CNR1	drug	cannabinoid	26681496	Using an integrative combination of in vivo electrophysiological recordings and behavioral pharmacologic assays in rats, we tested whether activation of <b>cannabinoid</b> type 1 receptors (<strong>CB1R</strong>) in the vHipp may modulate neuronal activity in the shell subregion of the nucleus accumbens (NASh).
+CNR1	addiction	aversion	26681496	We next examined how vHipp <strong>CB1R</strong> signaling may control the salience of rewarding or <b>aversive</b> emotional memory formation and social interaction/recognition behaviors via intra NASh glutamatergic transmission.
+CNR1	addiction	aversion	26681496	We demonstrate for the first time that vHipp <strong>CB1R</strong> transmission can potently modulate NASh neuronal activity and can differentially control the formation of context dependent and context independent forms of rewarding or <b>aversion</b> related emotional associative memories.
+CNR1	drug	cannabinoid	26681496	Together, these findings demonstrate a critical role for hippocampal <b>cannabinoid</b> signaling in the modulation of mesolimbic neuronal activity states and suggest that dysregulation of <strong>CB1R</strong> transmission in the vHipp→NASh circuit may underlie hippocampal mediated affective and social behavioral disturbances present in neuropsychiatric disorders.
+CNR1	drug	cannabinoid	26664379	This is mediated through <strong><b>cannabinoid</b> receptor 1</strong> (CB1) enriched in cerebellar granular neurons (CGNs).
+CNR1	drug	cannabinoid	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism: MGLL, FAAH; binding: <strong>CNR1</strong>; SNPs N = 65) and childhood sexual abuse (CSA) predict <b>cannabis</b> dependence symptoms.
+CNR1	addiction	dependence	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism: MGLL, FAAH; binding: <strong>CNR1</strong>; SNPs N = 65) and childhood sexual abuse (CSA) predict cannabis <b>dependence</b> symptoms.
+CNR1	drug	cannabinoid	26468198	Here, we hypothesize that the <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>) may play a critical role in mediating adolescent behavior because enhanced <b>endocannabinoid</b> (eCB) signaling has been suggested to occur transiently during adolescence.
+CNR1	drug	cannabinoid	26468198	We present the first rodent model with a gain of function mutation in the <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>).
+CNR1	drug	cannabinoid	26455361	The objective of this study was to test the hypothesis that <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>) signaling is required for stress potentiated reinstatement of cocaine seeking in rats.
+CNR1	drug	cocaine	26455361	The objective of this study was to test the hypothesis that cannabinoid type 1 receptor (<strong>CB1R</strong>) signaling is required for stress potentiated reinstatement of <b>cocaine</b> seeking in rats.
+CNR1	addiction	relapse	26455361	The objective of this study was to test the hypothesis that cannabinoid type 1 receptor (<strong>CB1R</strong>) signaling is required for stress potentiated <b>reinstatement</b> of cocaine <b>seeking</b> in rats.
+CNR1	drug	cannabinoid	26455361	These findings demonstrate that footshock stress increases prefrontal cortical <b>endocannabinoids</b> and stress potentiated reinstatement is <strong>CB1R</strong> dependent, suggesting that <strong>CB1R</strong> is a potential therapeutic target for relapse prevention, particularly in individuals whose cocaine use is stress related.
+CNR1	drug	cocaine	26455361	These findings demonstrate that footshock stress increases prefrontal cortical endocannabinoids and stress potentiated reinstatement is <strong>CB1R</strong> dependent, suggesting that <strong>CB1R</strong> is a potential therapeutic target for relapse prevention, particularly in individuals whose <b>cocaine</b> use is stress related.
+CNR1	addiction	relapse	26455361	These findings demonstrate that footshock stress increases prefrontal cortical endocannabinoids and stress potentiated <b>reinstatement</b> is <strong>CB1R</strong> dependent, suggesting that <strong>CB1R</strong> is a potential therapeutic target for <b>relapse</b> prevention, particularly in individuals whose cocaine use is stress related.
+CNR1	drug	cannabinoid	26427583	Audiograms, gap detection thresholds, and frequency difference limens in <strong><b>cannabinoid</b> receptor 1</strong> knockout mice.
+CNR1	drug	cannabinoid	26427583	The <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) is found at several stages in the auditory pathway, but its role in hearing is unknown.
+CNR1	drug	cannabinoid	26427583	The <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) is found at several stages in the auditory pathway, but its role in hearing is unknown.
+CNR1	drug	cannabinoid	26412490	We found that <b>cannabinoid</b> type 1 receptors (<strong>CB1R</strong>), key regulators of aversive responses, are present at presynaptic terminals of MHb neurons in the IPN.
+CNR1	addiction	aversion	26412490	We found that cannabinoid type 1 receptors (<strong>CB1R</strong>), key regulators of <b>aversive</b> responses, are present at presynaptic terminals of MHb neurons in the IPN.
+CNR1	addiction	aversion	26412490	Conditional deletion of <strong>CB1R</strong> from MHb neurons reduces fear conditioned freezing and abolishes conditioned odor <b>aversion</b> in mice, without affecting neutral or appetitively motivated memories.
+CNR1	addiction	aversion	26412490	Thus, presynaptic <strong>CB1R</strong> control expression of <b>aversive</b> memories by selectively modulating cholinergic transmission at MHb synapses in the IPN.
+CNR1	drug	cannabinoid	26342856	Reduced avoidance behaviour was associated with lower telencepahalic gene expression levels of <b>cannabinoid</b> receptor 1 (<strong>cnr1</strong>) and higher gene expression levels of corticotropin releasing factor (crf).
+CNR1	drug	cannabinoid	26331953	A <strong><b>cannabinoid</b> receptor 1</strong> polymorphism is protective against major depressive disorder in methadone maintained outpatients.
+CNR1	drug	opioid	26331953	A <strong>cannabinoid receptor 1</strong> polymorphism is protective against major depressive disorder in <b>methadone</b> maintained outpatients.
+CNR1	drug	cannabinoid	26331953	Given the preclinical and clinical evidence regarding the associations between <b>cannabinoid</b> systems and both opiate dependence and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the <b>cannabinoid</b> receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable methadone treatment.
+CNR1	drug	opioid	26331953	Given the preclinical and clinical evidence regarding the associations between cannabinoid systems and both opiate dependence and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the cannabinoid receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable <b>methadone</b> treatment.
+CNR1	addiction	dependence	26331953	Given the preclinical and clinical evidence regarding the associations between cannabinoid systems and both opiate <b>dependence</b> and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the cannabinoid receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable methadone treatment.
+CNR1	drug	cannabinoid	26223500	In this study, the authors provide evidence that congenitally enhanced <b>endocannabinoid</b> levels in the neuronal circuits underlying anxiety like behavioral states (mainly medial prefrontal cortex, amygdala and hippocampus) lead to <strong>CB1R</strong> desenistization and anxiety and depression.
+CNR1	drug	cannabinoid	26223500	These findings may have potential relevance to the understanding of the neurochemical effects of chronic <strong>CB1R</strong> overstimulation in <b>cannabis</b> abusers.
+CNR1	drug	cannabinoid	26191005	During this time, the four groups for each age (i.e., intact/saline, intact/<b>THC</b>, OVX/saline, and OVX/<b>THC</b>) were trained in a learning and performance procedure and dose effect curves were established for Δ(9) <b>THC</b> (0.56 56 mg/kg) and the <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>) antagonist <b>rimonabant</b> (0.32 10 mg/kg).
+CNR1	drug	cannabinoid	26191005	Hippocampal protein expression of <strong>CB1R</strong>, AHA1 (a co chaperone of <strong>CB1R</strong>) and HSP90β (a molecular chaperone modulated by AHA 1) was affected more by OVX than chronic Δ(9) <b>THC</b>; striatal protein expression was not consistently affected by either manipulation.
+CNR1	drug	alcohol	26123153	For example, chronic exposure to <b>ethanol</b>, in either cell culture or preclinical rodent models, causes an increase in endocannabinoid levels that results in down regulation of the <strong>cannabinoid receptor 1</strong> (CB1) and uncoupling of this receptor from downstream G protein signaling pathways.
+CNR1	drug	cannabinoid	26123153	For example, chronic exposure to ethanol, in either cell culture or preclinical rodent models, causes an increase in <b>endocannabinoid</b> levels that results in down regulation of the <strong><b>cannabinoid</b> receptor 1</strong> (CB1) and uncoupling of this receptor from downstream G protein signaling pathways.
+CNR1	drug	cannabinoid	26096126	A pivotal role for enhanced brainstem Orexin receptor 1 signaling in the central <strong><b>cannabinoid</b> receptor 1</strong> mediated pressor response in conscious rats.
+CNR1	drug	cannabinoid	26096126	Orexin receptor 1 (OX1R) signaling is implicated in <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) modulation of feeding.
+CNR1	drug	cannabinoid	26096126	Orexin receptor 1 (OX1R) signaling is implicated in <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) modulation of feeding.
+CNR1	addiction	dependence	26096126	Further, our studies established the <b>dependence</b> of the central <strong>CB1R</strong> mediated pressor response on neuronal nitric oxide synthase (nNOS) and extracellular signal regulated kinase1/2 (ERK1/2) phosphorylation in the RVLM.
+CNR1	drug	cannabinoid	25979787	(2) The effect of propofol was blocked by prior administration of the <strong><b>cannabinoid</b> receptor 1</strong> antagonist AM 251.
+CNR1	drug	cannabinoid	25942289	Here, we reported that a single in vivo morphine exposure (SM) did not affect inhibitory long term depression (I LTD) in the hippocampus, compared with saline control; while repeated morphine exposure (RM) abolished this I LTD. Interestingly, opioid withdrawal for 3 5 days after repeated (RMW), but not a single morphine exposure (SMW), largely enhanced I LTD. More importantly, the I LTD in single morphine treatment is dependent on presynaptic mechanism since it can be blocked by AM251, a selective <strong><b>cannabinoid</b> receptor 1</strong> antagonist.
+CNR1	drug	opioid	25942289	Here, we reported that a single in vivo <b>morphine</b> exposure (SM) did not affect inhibitory long term depression (I LTD) in the hippocampus, compared with saline control; while repeated <b>morphine</b> exposure (RM) abolished this I LTD. Interestingly, <b>opioid</b> withdrawal for 3 5 days after repeated (RMW), but not a single <b>morphine</b> exposure (SMW), largely enhanced I LTD. More importantly, the I LTD in single <b>morphine</b> treatment is dependent on presynaptic mechanism since it can be blocked by AM251, a selective <strong>cannabinoid receptor 1</strong> antagonist.
+CNR1	addiction	withdrawal	25942289	Here, we reported that a single in vivo morphine exposure (SM) did not affect inhibitory long term depression (I LTD) in the hippocampus, compared with saline control; while repeated morphine exposure (RM) abolished this I LTD. Interestingly, opioid <b>withdrawal</b> for 3 5 days after repeated (RMW), but not a single morphine exposure (SMW), largely enhanced I LTD. More importantly, the I LTD in single morphine treatment is dependent on presynaptic mechanism since it can be blocked by AM251, a selective <strong>cannabinoid receptor 1</strong> antagonist.
+CNR1	drug	cannabinoid	25772338	The objective of this study is to introduce an animal model to study <b>cannabinoid</b> dependence by incorporating traditional methodologies and profiling novel <b>cannabinoid</b> ligands with distinct pharmacological properties/modes of action by evaluating their pharmacological effects on CB1 receptor (<strong>CB1R</strong>) related physiological/behavioral endpoints.
+CNR1	addiction	dependence	25772338	The objective of this study is to introduce an animal model to study cannabinoid <b>dependence</b> by incorporating traditional methodologies and profiling novel cannabinoid ligands with distinct pharmacological properties/modes of action by evaluating their pharmacological effects on CB1 receptor (<strong>CB1R</strong>) related physiological/behavioral endpoints.
+CNR1	drug	cannabinoid	25772338	These findings suggest <b>cannabinoid</b> precipitated withdrawal may not be ascribed to the inverse properties of <b>rimonabant</b>, but rather to rapid competition with the agonist at the <strong>CB1R</strong>.
+CNR1	addiction	withdrawal	25772338	These findings suggest cannabinoid precipitated <b>withdrawal</b> may not be ascribed to the inverse properties of rimonabant, but rather to rapid competition with the agonist at the <strong>CB1R</strong>.
+CNR1	addiction	withdrawal	25772338	This <b>withdrawal</b> syndrome is likely centrally mediated, since only the centrally acting <strong>CB1R</strong> antagonists elicited <b>withdrawal</b>, i.e., such responses were absent after the purported peripherally selective <strong>CB1R</strong> antagonist AM6545.
+CNR1	drug	cannabinoid	25747605	Nevertheless, the pharmacological actions of MAM 2201 on <b>cannabinoid</b> receptor type 1 (<strong>CB1R</strong>) and neuronal functions have not been elucidated.
+CNR1	drug	cannabinoid	25747605	The reduction of neurotransmitter release from <strong>CB1R</strong> containing synapses could contribute to some of the symptoms of synthetic <b>cannabinoid</b> intoxication including impairments in cerebellum dependent motor coordination and motor learning.
+CNR1	addiction	intoxication	25747605	The reduction of neurotransmitter release from <strong>CB1R</strong> containing synapses could contribute to some of the symptoms of synthetic cannabinoid <b>intoxication</b> including impairments in cerebellum dependent motor coordination and motor learning.
+CNR1	drug	cannabinoid	25529106	During test days, the rats received local injections of either vehicle or ACEA, a <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>) agonist in the ACC or OFC.
+CNR1	addiction	reward	25529106	We showed that <strong>CB1R</strong> activation in the ACC impaired decision making such that rats were less willing to invest physical effort to gain high <b>reward</b>.
+CNR1	drug	cannabinoid	25510937	Disturbances in <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>) signaling have been linked to emotional and cognitive deficits characterizing neuropsychiatric disorders, including schizophrenia.
+CNR1	addiction	reward	25510937	Furthermore, using a conditioned place preference procedure and a social interaction test, we report that intra vHipp <strong>CB1R</strong> activation potentiates the <b>reward</b> salience of normally sub threshold conditioning doses of opiates and induces deficits in natural sociability and social recognition behaviors.
+CNR1	addiction	reward	25510937	Collectively, these findings identify hippocampal <strong>CB1R</strong> transmission as a critical modulator of the mesolimbic DA pathway and in the processing of <b>reward</b> and social related behavioral phenomena.
+CNR1	drug	cannabinoid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ opioid receptor (OPRD1), <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+CNR1	drug	opioid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ <b>opioid</b> receptor (OPRD1), cannabinoid receptor 1 (<strong>CNR1</strong>), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+CNR1	drug	cannabinoid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ opioid receptor (OPRD1), <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+CNR1	drug	opioid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ <b>opioid</b> receptor (OPRD1), <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+CNR1	drug	cannabinoid	25361428	<strong><b>Cannabinoid</b> receptor 1</strong> antagonist treatment induces glucagon release and shows an additive therapeutic effect with GLP 1 agonist in diet induced obese mice.
+CNR1	drug	cannabinoid	25258300	Upstream open reading frames regulate <strong><b>cannabinoid</b> receptor 1</strong> expression under baseline conditions and during cellular stress.
+CNR1	drug	cannabinoid	25258300	The <b>cannabinoid</b> receptor subtype 1 gene <strong>CNR1</strong> is not only associated with phenotypes such as cognitive performance, addiction and anxiety, but is also known to be crucially involved in responses to acute and chronic psychological and cellular stress conditions.
+CNR1	addiction	addiction	25258300	The cannabinoid receptor subtype 1 gene <strong>CNR1</strong> is not only associated with phenotypes such as cognitive performance, <b>addiction</b> and anxiety, but is also known to be crucially involved in responses to acute and chronic psychological and cellular stress conditions.
+CNR1	drug	opioid	25252306	[Association study of <strong>CNR1</strong>, GAD1 and BDNF polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan].
+CNR1	addiction	dependence	25252306	[Association study of <strong>CNR1</strong>, GAD1 and BDNF polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan].
+CNR1	drug	cannabinoid	25252306	In order to analyze the association of <strong>CNR1</strong>(<b>Cannabinoid</b> receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	drug	opioid	25252306	In order to analyze the association of <strong>CNR1</strong>(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	addiction	dependence	25252306	In order to analyze the association of <strong>CNR1</strong>(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	drug	cannabinoid	25252306	In order to analyze the association of <strong>CNR1</strong>(<strong><b>Cannabinoid</b> receptor 1</strong>), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	drug	opioid	25252306	In order to analyze the association of <strong>CNR1</strong>(<strong>Cannabinoid receptor 1</strong>), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	addiction	dependence	25252306	In order to analyze the association of <strong>CNR1</strong>(<strong>Cannabinoid receptor 1</strong>), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	drug	opioid	25252306	A case control study was performed with 8 SNPs from <strong>CNR1</strong>, GAD1, and BDNF genes in 165 <b>heroin</b> dependent males and 170 healthy males of the Dai population.
+CNR1	drug	opioid	25252306	Furthermore, polymorphisms in <strong>CNR1</strong> (rs1049353), GAD1 (rs1978340 and rs11542313), and BDNF (rs6265 and rs13306221) were associated with <b>heroin</b> dependence in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be <b>heroin</b> dependent.
+CNR1	addiction	dependence	25252306	Furthermore, polymorphisms in <strong>CNR1</strong> (rs1049353), GAD1 (rs1978340 and rs11542313), and BDNF (rs6265 and rs13306221) were associated with heroin <b>dependence</b> in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be heroin dependent.
+CNR1	drug	cannabinoid	25251035	<b>Marijuana</b>, which acts within the <b>endocannabinoid</b> (eCB) system as an agonist of the <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>), exhibits addictive properties and has powerful actions on the state of arousal of an organism.
+CNR1	addiction	addiction	25251035	Marijuana, which acts within the endocannabinoid (eCB) system as an agonist of the cannabinoid type 1 receptor (<strong>CB1R</strong>), exhibits <b>addictive</b> properties and has powerful actions on the state of arousal of an organism.
+CNR1	drug	cannabinoid	25231848	Expression and localization of <strong><b>cannabinoid</b> receptor 1</strong> in rats' brain treated with acute and repeated morphine.
+CNR1	drug	opioid	25231848	Expression and localization of <strong>cannabinoid receptor 1</strong> in rats' brain treated with acute and repeated <b>morphine</b>.
+CNR1	drug	cannabinoid	25231848	The <strong><b>cannabinoid</b> receptor 1</strong> (CB1 R) is one of the receptors that mediate the actions of <b>cannabinoids</b> and <b>endocannabinoids</b> in the CNS.
+CNR1	drug	cannabinoid	25088915	In the present study, we investigated whether treatment with the selective <strong><b>cannabinoid</b> receptor 1</strong> (CB1) agonist arachidonyl 2' chloroethylamide (ACEA) affects NGF induced sensitization of TRPV1 in adult mouse dorsal root ganglion (DRG) afferent neurons.
+CNR1	addiction	sensitization	25088915	In the present study, we investigated whether treatment with the selective <strong>cannabinoid receptor 1</strong> (CB1) agonist arachidonyl 2' chloroethylamide (ACEA) affects NGF induced <b>sensitization</b> of TRPV1 in adult mouse dorsal root ganglion (DRG) afferent neurons.
+CNR1	drug	cannabinoid	25081244	Since type 1 <b>cannabinoid</b> receptors (CB1Rs), expressed in many brain areas including the mPFC, can modulate excitatory and inhibitory neurotransmission, we aimed to determine whether <strong>CB1R</strong> activation results in modifications of the E/I balance.
+CNR1	drug	cannabinoid	25081244	By decomposing the synaptic response evoked by layer I stimulation into its excitatory and inhibitory components, we show that in vitro <strong>CB1R</strong> activation with the <b>cannabinoid</b> receptor agonists WIN55,212 2 (WIN) and CP 55940 (CP) modulates the balance between excitation and inhibition (E/I balance) of layer II/III pyramidal neurons.
+CNR1	drug	cannabinoid	25081244	This modulation of the E/I balance by CB1Rs may thus be fundamental in the regulation of local PL cortical network excitability and could be the mechanism through which excessive <strong>CB1R</strong> activation (<b>cannabis</b> abuse) affects cognitive functions.
+CNR1	drug	cannabinoid	25064144	On the contrary, while the <strong>CB1R</strong> antagonist <b>SR141716</b> per se did not affect the population spike, it did worsen KA induced bursts, confirming increased eCB tone upon KA treatment.
+CNR1	drug	cannabinoid	24980155	Research investigating the impact of genetic variants in the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) and of early rearing conditions has demonstrated that both factors contribute to the prediction of impulsivity related phenotypes.
+CNR1	drug	cannabinoid	24853387	Chronic <b>cannabinoid</b> receptor 2 activation reverses paclitaxel neuropathy without tolerance or <strong><b>cannabinoid</b> receptor 1</strong> dependent withdrawal.
+CNR1	addiction	withdrawal	24853387	Chronic cannabinoid receptor 2 activation reverses paclitaxel neuropathy without tolerance or <strong>cannabinoid receptor 1</strong> dependent <b>withdrawal</b>.
+CNR1	drug	cannabinoid	24853387	Mixed <strong><b>cannabinoid</b> receptor 1</strong> and 2 (CB1 and CB2) agonists such as Δ(9) <b>tetrahydrocannabinol</b> (Δ(9) <b>THC</b>) can produce tolerance, physical withdrawal, and unwanted CB1 mediated central nervous system side effects.
+CNR1	addiction	withdrawal	24853387	Mixed <strong>cannabinoid receptor 1</strong> and 2 (CB1 and CB2) agonists such as Δ(9) tetrahydrocannabinol (Δ(9) THC) can produce tolerance, physical <b>withdrawal</b>, and unwanted CB1 mediated central nervous system side effects.
+CNR1	drug	cannabinoid	24836296	Commercially available <b>cannabinoids</b> are subject to psychotomimetic and addiction (cannabinomimetic) adverse effects largely through activation of the <b>cannabinoid</b> 1 receptor (<strong>CB1r</strong>).
+CNR1	addiction	addiction	24836296	Commercially available cannabinoids are subject to psychotomimetic and <b>addiction</b> (cannabinomimetic) adverse effects largely through activation of the cannabinoid 1 receptor (<strong>CB1r</strong>).
+CNR1	drug	cannabinoid	24836296	Recently developed peripherally restricted <b>cannabinoids</b>, regionally administered <b>cannabinoids</b>, bifunctional <b>cannabinoid</b> ligands and <b>cannabinoid</b> enzyme inhibitors, <b>endocannabinoids</b>, which do not interact with classic <b>cannabinoid</b> receptors (<strong>CB1r</strong> and CB2r), <b>cannabinoid</b> receptor antagonists and selective <strong>CB1r</strong> agonists hold promise as analgesics.
+CNR1	drug	cannabinoid	24719095	Mutation of putative GRK phosphorylation sites in the <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) confers resistance to <b>cannabinoid</b> tolerance and hypersensitivity to <b>cannabinoids</b> in mice.
+CNR1	drug	cannabinoid	24719095	Mutation of putative GRK phosphorylation sites in the <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) confers resistance to <b>cannabinoid</b> tolerance and hypersensitivity to <b>cannabinoids</b> in mice.
+CNR1	drug	cannabinoid	24719095	For many G protein coupled receptors (GPCRs), including <strong><b>cannabinoid</b> receptor 1</strong> (CB1R), desensitization has been proposed as a principal mechanism driving initial tolerance to agonists.
+CNR1	drug	cannabinoid	24719095	For many G protein coupled receptors (GPCRs), including <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>), desensitization has been proposed as a principal mechanism driving initial tolerance to agonists.
+CNR1	drug	cannabinoid	24719095	<strong>CB1R</strong> desensitization in the periaqueductal gray and spinal cord following 7 d of treatment with Δ(9) <b>THC</b> was absent in S426A/S430A mutants.
+CNR1	drug	cannabinoid	24719095	Δ(9) <b>THC</b> induced downregulation of <strong>CB1R</strong> in the spinal cord was also absent in S426A/S430A mutants.
+CNR1	drug	cannabinoid	24607771	F344 rats displayed higher levels of <b>cannabinoid</b> receptor binding in the lateral globus pallidus and weaker <strong>CNR1</strong> gene expression in the prefrontal cortex (PFc) than LEW rats.
+CNR1	drug	alcohol	24553924	Involvement of the type 1 cannabinoid receptor (<strong>CB1R</strong>) in the effects of <b>alcohol</b> on the brain is supported by animal experiments, but how in vivo <strong>CB1R</strong> levels are altered in <b>alcoholic</b> patients is still unclear.
+CNR1	drug	cannabinoid	24553924	Involvement of the type 1 <b>cannabinoid</b> receptor (<strong>CB1R</strong>) in the effects of alcohol on the brain is supported by animal experiments, but how in vivo <strong>CB1R</strong> levels are altered in alcoholic patients is still unclear.
+CNR1	drug	alcohol	24553924	To assess the short time effects of a binge drinking episode on <strong>CB1R</strong> availability, 20 healthy social drinkers underwent [(18)F]MK 9470 positron emission tomography (PET) at baseline and after intravenous <b>ethanol</b> administration (ALC ACU).
+CNR1	addiction	intoxication	24553924	To assess the short time effects of a <b>binge</b> drinking episode on <strong>CB1R</strong> availability, 20 healthy social drinkers underwent [(18)F]MK 9470 positron emission tomography (PET) at baseline and after intravenous ethanol administration (ALC ACU).
+CNR1	drug	alcohol	24553924	Moreover, 26 <b>alcoholic</b> patients underwent sequential <strong>CB1R</strong> PET after chronic heavy drinking (ALC CHR) and after 1 month of abstinence (ALC ABST).
+CNR1	drug	alcohol	24553924	In conclusion, whereas the acute <b>alcohol</b> effect is an increase in <strong>CB1R</strong> availability, chronic heavy drinking leads to reduced <strong>CB1R</strong> availability that is not reversible after 1 month of abstinence.
+CNR1	drug	alcohol	24553924	An enhanced <strong>CB1R</strong> signaling may offer a new therapeutic direction for treatment of the negative affective state produced by <b>alcohol</b> withdrawal and abstinence, which is critical for the maintenance of <b>alcohol</b> addiction.
+CNR1	addiction	addiction	24553924	An enhanced <strong>CB1R</strong> signaling may offer a new therapeutic direction for treatment of the negative affective state produced by alcohol withdrawal and abstinence, which is critical for the maintenance of alcohol <b>addiction</b>.
+CNR1	addiction	withdrawal	24553924	An enhanced <strong>CB1R</strong> signaling may offer a new therapeutic direction for treatment of the negative affective state produced by alcohol <b>withdrawal</b> and abstinence, which is critical for the maintenance of alcohol addiction.
+CNR1	drug	cannabinoid	24518035	were comparable in wild type and knockout <b>cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) mice, indicating that previously reported CB1 allosteric effects do not decrease cocaine like effects of RTI 371.
+CNR1	drug	cocaine	24518035	were comparable in wild type and knockout cannabinoid CB1 receptor (<strong>CB1R</strong>) mice, indicating that previously reported CB1 allosteric effects do not decrease <b>cocaine</b> like effects of RTI 371.
+CNR1	drug	cannabinoid	24494683	The inhibitory effect of 2 AG on fear related behaviour, but not pain related behaviour, was blocked by co administration of the <strong><b>cannabinoid</b> receptor 1</strong> (CB1) antagonist/inverse agonist <b>rimonabant</b>.
+CNR1	drug	cannabinoid	24445195	Here we analyzed whether repeatedly administered <b>cannabinoid</b> type 1 receptor (<strong>CB1r</strong>) agonist WIN 55 212,2 (WIN) or antagonist AM 251 (AM) induce effects per se and if concurrent pre treatments affect cocaine induced changes in marmoset behavior.
+CNR1	drug	cocaine	24445195	Here we analyzed whether repeatedly administered cannabinoid type 1 receptor (<strong>CB1r</strong>) agonist WIN 55 212,2 (WIN) or antagonist AM 251 (AM) induce effects per se and if concurrent pre treatments affect <b>cocaine</b> induced changes in marmoset behavior.
+CNR1	drug	cocaine	24445195	However, when given as a pre treatment to <b>cocaine</b>, <strong>CB1r</strong> blockade enhanced the former׳s hypervigilance effect and potentially conditioned this response to the exposure context.
+CNR1	drug	cocaine	24445195	Enhancement may have resulted from AM׳s inhibition of eCB potentiated <b>cocaine</b> induced anxiogenesis and/or its action independent of the eCB system, or even <strong>CB1r</strong> mediated changes in synaptic plasticity involved in <b>cocaine</b> reward learning.
+CNR1	addiction	reward	24445195	Enhancement may have resulted from AM׳s inhibition of eCB potentiated cocaine induced anxiogenesis and/or its action independent of the eCB system, or even <strong>CB1r</strong> mediated changes in synaptic plasticity involved in cocaine <b>reward</b> learning.
+CNR1	drug	cocaine	24445195	Thus, changes in <strong>CB1r</strong> function   alone and in combination with <b>cocaine</b>   affected stereotyped vigilance related behaviors in this NHP, further implicating the eCB system in the neurobiological mechanisms of <b>cocaine</b> addiction.
+CNR1	addiction	addiction	24445195	Thus, changes in <strong>CB1r</strong> function   alone and in combination with cocaine   affected stereotyped vigilance related behaviors in this NHP, further implicating the eCB system in the neurobiological mechanisms of cocaine <b>addiction</b>.
+CNR1	drug	alcohol	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with <b>alcohol</b>, tobacco and/or cannabis consumption in young individuals (n = 91).
+CNR1	drug	cannabinoid	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, tobacco and/or <b>cannabis</b> consumption in young individuals (n = 91).
+CNR1	drug	nicotine	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, <b>tobacco</b> and/or cannabis consumption in young individuals (n = 91).
+CNR1	drug	cannabinoid	24152087	One of the single nucleotide polymorphisms (SNP) of the <strong>CNR1</strong> gene, which codes for <b>cannabinoid</b> receptor 1 (CB1R), is the rs2180619, located in a regulatory region of this gene (6q14 q15).
+CNR1	drug	cannabinoid	24152087	One of the single nucleotide polymorphisms (SNP) of the <strong>CNR1</strong> gene, which codes for <b>cannabinoid</b> receptor 1 (<strong>CB1R</strong>), is the rs2180619, located in a regulatory region of this gene (6q14 q15).
+CNR1	drug	cannabinoid	24152087	Our results suggest that, although the performance of GG subjects was at normal levels, a lower efficiency of the <b>endocannabinoid</b> system, probably due to a lowered expression of <strong>CB1R</strong>, produced a reduction in the performance of these subjects when attentional control and working memory processing is challenged.
+CNR1	drug	cocaine	24138924	Here, we investigated whether impulsive behavior observed following <b>cocaine</b> exposure requires <strong>CB1R</strong> activation.
+CNR1	drug	cannabinoid	24132958	We investigated whether escalating doses of the <strong><b>cannabinoid</b> receptor 1</strong> (CB1 R) agonist, HU 210, in adolescence would affect adult hippocampal neurogenesis and behavioral processes putatively modulated by hippocampal neurogenesis, in adult male and female Sprague Dawley rats.
+CNR1	drug	cannabinoid	24084047	Studies reviewed will indicate that in contrast to partial agonist properties of Δ(9) <b>THC</b> typically observed in vitro, SCBs in K2 products act as full <b>cannabinoid</b> receptor type 1 (<strong>CB1R</strong>) and type 2 (CB2R) agonists in both cellular assays and animal studies.
+CNR1	drug	cannabinoid	24063277	These drugs, which include JWH 018, JWH 073 and CP 47,497, bind and activate the <b>cannabinoid</b> receptors <strong>CB1R</strong> and CB2R with remarkable potency and efficacy.
+CNR1	drug	alcohol	24060590	Therefore, we studied the expression of <strong>CNR1</strong> and CNR2, and the novel cannabinoid G protein coupled receptor (GPCR) 55 (GPR55) in human monocyte derived dendritic cells (MDDCs) from <b>alcohol</b> users.
+CNR1	drug	cannabinoid	24060590	Therefore, we studied the expression of <strong>CNR1</strong> and CNR2, and the novel <b>cannabinoid</b> G protein coupled receptor (GPCR) 55 (GPR55) in human monocyte derived dendritic cells (MDDCs) from alcohol users.
+CNR1	drug	cannabinoid	23959891	Here, we first examined the effects of chronic EtOH on DLS neuronal morphology, synaptic plasticity, and <b>endocannabinoid</b> <strong>CB1R</strong> signaling.
+CNR1	drug	cannabinoid	23916480	This study examined the role of <b>cannabinoid</b> CB1 receptors (<strong>CB1r</strong>) in aggressive behavior.
+CNR1	drug	cannabinoid	23911834	Increased expression of <strong><b>cannabinoid</b> receptor 1</strong> in the nucleus accumbens core in a rat model with morphine withdrawal.
+CNR1	drug	opioid	23911834	Increased expression of <strong>cannabinoid receptor 1</strong> in the nucleus accumbens core in a rat model with <b>morphine</b> withdrawal.
+CNR1	addiction	withdrawal	23911834	Increased expression of <strong>cannabinoid receptor 1</strong> in the nucleus accumbens core in a rat model with morphine <b>withdrawal</b>.
+CNR1	drug	cannabinoid	23911834	To reveal the mechanism that underlies this finding, we examined the expression pattern of the <strong><b>cannabinoid</b> receptor 1</strong> (CB1 R) in the NAcc of SD rats that had been undergoing morphine withdrawal (MW) for 1 day, 3 days and 3 weeks (acute, latent and chronic phases, respectively).
+CNR1	drug	opioid	23911834	To reveal the mechanism that underlies this finding, we examined the expression pattern of the <strong>cannabinoid receptor 1</strong> (CB1 R) in the NAcc of SD rats that had been undergoing <b>morphine</b> withdrawal (MW) for 1 day, 3 days and 3 weeks (acute, latent and chronic phases, respectively).
+CNR1	addiction	withdrawal	23911834	To reveal the mechanism that underlies this finding, we examined the expression pattern of the <strong>cannabinoid receptor 1</strong> (CB1 R) in the NAcc of SD rats that had been undergoing morphine <b>withdrawal</b> (MW) for 1 day, 3 days and 3 weeks (acute, latent and chronic phases, respectively).
+CNR1	drug	benzodiazepine	23820739	In this study, we investigated the effects of N methyl D aspartic acid receptor (NMDAR) antagonists, protein synthesis inhibitors, cannabinoid receptor type 1 (<strong>CB1R</strong>) antagonists, and <b>benzodiazepine</b> on reinstatement of conditioned fear in mice.
+CNR1	drug	cannabinoid	23820739	In this study, we investigated the effects of N methyl D aspartic acid receptor (NMDAR) antagonists, protein synthesis inhibitors, <b>cannabinoid</b> receptor type 1 (<strong>CB1R</strong>) antagonists, and benzodiazepine on reinstatement of conditioned fear in mice.
+CNR1	addiction	relapse	23820739	In this study, we investigated the effects of N methyl D aspartic acid receptor (NMDAR) antagonists, protein synthesis inhibitors, cannabinoid receptor type 1 (<strong>CB1R</strong>) antagonists, and benzodiazepine on <b>reinstatement</b> of conditioned fear in mice.
+CNR1	drug	benzodiazepine	23820739	<strong>CB1R</strong> antagonists, SR141716, and a <b>benzodiazepine</b>, <b>diazepam</b>, had no effect on fear reinstatement.
+CNR1	drug	cannabinoid	23820739	<strong>CB1R</strong> antagonists, <b>SR141716</b>, and a benzodiazepine, diazepam, had no effect on fear reinstatement.
+CNR1	addiction	relapse	23820739	<strong>CB1R</strong> antagonists, SR141716, and a benzodiazepine, diazepam, had no effect on fear <b>reinstatement</b>.
+CNR1	drug	cannabinoid	23801678	In vitro drug drug interactions were assessed using competition receptor binding assays employing mouse brain homogenates and <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) mediated inhibition of adenylyl cyclase activity in Neuro2A wild type cells.
+CNR1	drug	alcohol	23740372	Using [(18)F]MK 9470 small animal PET imaging, our primary objective was to evaluate in vivo type 1 cannabinoid receptor (<strong>CB1R</strong>) binding changes in rats subjected to several <b>ethanol</b> conditions: (1) at baseline, (2) after acute intraperitoneal administration of <b>ethanol</b> (4 g/kg) or saline, (3) after 7 days of forced chronic <b>ethanol</b> consumption, and (4) after abstinence for 7 and 14 days.
+CNR1	drug	cannabinoid	23740372	Using [(18)F]MK 9470 small animal PET imaging, our primary objective was to evaluate in vivo type 1 <b>cannabinoid</b> receptor (<strong>CB1R</strong>) binding changes in rats subjected to several ethanol conditions: (1) at baseline, (2) after acute intraperitoneal administration of ethanol (4 g/kg) or saline, (3) after 7 days of forced chronic ethanol consumption, and (4) after abstinence for 7 and 14 days.
+CNR1	drug	alcohol	23740372	Acute <b>ethanol</b> administration increased relative <strong>CB1R</strong> binding in the NAcc that was positively correlated with the change in AEA levels of that region.
+CNR1	drug	alcohol	23740372	Chronic <b>ethanol</b> consumption decreased relative <strong>CB1R</strong> binding in the hippocampus and caudate putamen, whereas same regions showed increased relative <strong>CB1R</strong> binding after 7 and 14 days of abstinence compared to the baseline condition.
+CNR1	drug	alcohol	23740372	This study provides in vivo evidence that acute <b>ethanol</b> consumption is associated with enhanced endocannabinoid signalling in the NAcc, indicated by an increased <strong>CB1R</strong> binding and AEA content.
+CNR1	drug	cannabinoid	23740372	This study provides in vivo evidence that acute ethanol consumption is associated with enhanced <b>endocannabinoid</b> signalling in the NAcc, indicated by an increased <strong>CB1R</strong> binding and AEA content.
+CNR1	drug	alcohol	23740372	In addition, chronic <b>ethanol</b> exposure leads to regional dysfunctions in <strong>CB1R</strong> levels, involving the hippocampus and caudate putamen that are reversible within 2 weeks in this animal model.
+CNR1	drug	cocaine	23680694	Sex dependent changes in brain <strong>CB1R</strong> expression and functionality and immune CB2R expression as a consequence of maternal deprivation and adolescent <b>cocaine</b> exposure.
+CNR1	drug	cocaine	23680694	Present findings provide evidence for changes in brain <strong>CB1R</strong> expression and functionality and immune CB2R expression as a consequence of early life stress and adolescent <b>cocaine</b> exposure, and indicate functional interactions between both treatments, which in many regions differ between males and females.
+CNR1	drug	alcohol	23647533	This study investigated possible differential expression of cannabinoid receptors CB1 (<strong>CB1R</strong>) and CB2 (CB2R) in an outbred mice strain displaying behavioral variability to <b>ethanol</b> (EtOH) induced locomotor sensitization.
+CNR1	drug	cannabinoid	23647533	This study investigated possible differential expression of <b>cannabinoid</b> receptors CB1 (<strong>CB1R</strong>) and CB2 (CB2R) in an outbred mice strain displaying behavioral variability to ethanol (EtOH) induced locomotor sensitization.
+CNR1	addiction	sensitization	23647533	This study investigated possible differential expression of cannabinoid receptors CB1 (<strong>CB1R</strong>) and CB2 (CB2R) in an outbred mice strain displaying behavioral variability to ethanol (EtOH) induced locomotor <b>sensitization</b>.
+CNR1	addiction	withdrawal	23647533	Temporal analysis of <strong>CB1R</strong> and CB2R immunoreactivity was performed in 3 different occasions: (i) at the end of chronic EtOH treatment, (ii) on the fifth day of EtOH <b>withdrawal</b>, and (iii) after EtOH challenge.
+CNR1	addiction	withdrawal	23647533	On the fifth day of <b>withdrawal</b>, only EtOH_High mice presented increase in <strong>CB1R</strong>.
+CNR1	addiction	sensitization	23647533	We hypothesize that CB2R down regulation might be related to resilience to develop locomotor <b>sensitization</b>, while <strong>CB1R</strong> up regulation relates to withdrawal aspects in sensitized mice.
+CNR1	addiction	withdrawal	23647533	We hypothesize that CB2R down regulation might be related to resilience to develop locomotor sensitization, while <strong>CB1R</strong> up regulation relates to <b>withdrawal</b> aspects in sensitized mice.
+CNR1	drug	cannabinoid	23644187	Because anandamide (AEA) activation of <b>cannabinoid</b> type 1 receptors (<strong>CB1R</strong>) on nociceptors reduces nociception, manipulation of AEA metabolism in the periphery may be an effective alternative or adjuvant therapy in the management of cancer pain.
+CNR1	drug	cannabinoid	23640247	Irrespective of its psychiatric side effects, <b>rimonabant</b> through blocking <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) induces an increase in whole body insulin sensitivity.
+CNR1	drug	alcohol	23631463	Attenuation of increased endocannabinoid signaling with a <strong>CB1R</strong> neutral antagonist might offer a new therapeutic direction for treatment of <b>alcohol</b> abuse.
+CNR1	drug	cannabinoid	23631463	Attenuation of increased <b>endocannabinoid</b> signaling with a <strong>CB1R</strong> neutral antagonist might offer a new therapeutic direction for treatment of alcohol abuse.
+CNR1	drug	alcohol	23631463	Similar to the <strong>CB1R</strong> antagonist/inverse agonist rimonabant, analogues 27 and 30 decrease oral <b>alcohol</b> self administration without affecting total fluid intake and block the development of <b>alcohol</b> conditioned place preference.
+CNR1	drug	cannabinoid	23631463	Similar to the <strong>CB1R</strong> antagonist/inverse agonist <b>rimonabant</b>, analogues 27 and 30 decrease oral alcohol self administration without affecting total fluid intake and block the development of alcohol conditioned place preference.
+CNR1	drug	alcohol	23631463	Collectively, these initial findings suggest that design and systematic modification of aminoalkylindoles such as 3 may lead to development of novel cannabinoid ligands with dual <strong>CB1R</strong> antagonist/CB2R agonist activity with potential for use as treatments of <b>alcohol</b> abuse.
+CNR1	drug	cannabinoid	23631463	Collectively, these initial findings suggest that design and systematic modification of aminoalkylindoles such as 3 may lead to development of novel <b>cannabinoid</b> ligands with dual <strong>CB1R</strong> antagonist/CB2R agonist activity with potential for use as treatments of alcohol abuse.
+CNR1	drug	cannabinoid	23466226	Compound 13 had the highest selectivity of all the compounds examined, and represents a potent <b>cannabinoid</b> ligand with 34 times greater selectivity for CB2R over <strong>CB1R</strong>.
+CNR1	drug	cannabinoid	23291357	The eCB receptor name <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) is expressed in the EP in GABAergic terminals.
+CNR1	drug	cannabinoid	23291357	The eCB receptor name <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) is expressed in the EP in GABAergic terminals.
+CNR1	drug	cannabinoid	23246480	Animals were sacrificed on PND 68 75 and levels of serotonin (5 HT) and its metabolite 5 hydroxyindole acetic acid were measured in the striatum, hippocampus and cortex, while the expression of hippocampal CB1 <b>cannabinoid</b> receptor (<strong>CB1R</strong>) and circulating levels of corticosterone and leptin were also measured.
+CNR1	drug	psychedelics	23246480	A reduction in striatal and cortical 5 HT levels, increased expression of hippocampal <strong>CB1R</strong> and a marked trend towards higher circulating leptin levels were observed in <b>MDMA</b> treated MD males.
+CNR1	addiction	aversion	23227007	The influence of CB1 receptors on the <b>aversion</b> driven spatial learning in the Morris water maze test is strongly age dependent: mice with genetic deletion of CB1 receptors (<strong>Cnr1</strong>( / )) show superior learning when young but inferior learning when old compared to age matched wild type mice.
+CNR1	drug	cannabinoid	23190435	Participants with at least one copy of the minor allele for SNPs in synaptosomal associated protein 25 gene (SNAP25; rs363035 OR = 0.53; P = 0.005) and <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>; rs6454672 OR = 0.62; P = 0.022) have decreased likelihood of meeting PA recommendations.
+CNR1	drug	cannabinoid	23070073	The <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) was put forward as a promising drug target for antiobesity medication.
+CNR1	drug	cannabinoid	23070073	However, the first marketed <strong>CB1R</strong> antagonist/inverse agonist <b>rimonabant</b> was discontinued, as its use was occasionally associated with negative affect and suicidality.
+CNR1	drug	cannabinoid	23070073	We show that <strong>CB1R</strong> inverse agonists like <b>rimonabant</b> suppress the constitutive <strong>CB1R</strong> activity in such regions, and cause anxiety and reduced motivation for reward.
+CNR1	addiction	reward	23070073	We show that <strong>CB1R</strong> inverse agonists like rimonabant suppress the constitutive <strong>CB1R</strong> activity in such regions, and cause anxiety and reduced motivation for <b>reward</b>.
+CNR1	drug	cannabinoid	23012412	<strong><b>Cannabinoid</b> receptor 1</strong> expressing neurons in the nucleus accumbens.
+CNR1	drug	cannabinoid	23012412	<b>Endocannabinoid</b> signaling critically regulates emotional and motivational states via activation of <strong><b>cannabinoid</b> receptor 1</strong> (CB1) in the brain.
+CNR1	drug	cannabinoid	22959963	Nicotine induced anxiety like behavior in a rat model of the novelty seeking phenotype is associated with long lasting neuropeptidergic and neuroplastic adaptations in the amygdala: effects of the <strong><b>cannabinoid</b> receptor 1</strong> antagonist AM251.
+CNR1	drug	nicotine	22959963	<b>Nicotine</b> induced anxiety like behavior in a rat model of the novelty seeking phenotype is associated with long lasting neuropeptidergic and neuroplastic adaptations in the amygdala: effects of the <strong>cannabinoid receptor 1</strong> antagonist AM251.
+CNR1	addiction	relapse	22959963	Nicotine induced anxiety like behavior in a rat model of the novelty <b>seeking</b> phenotype is associated with long lasting neuropeptidergic and neuroplastic adaptations in the amygdala: effects of the <strong>cannabinoid receptor 1</strong> antagonist AM251.
+CNR1	drug	cannabinoid	22959963	Furthermore, treatment with the <strong><b>cannabinoid</b> receptor 1</strong> antagonist, AM251 (5 mg/kg) during a short (1 wk) abstinence is ineffective in reversing nicotine induced anxiety, fluctuations in BDNF and spinophilin mRNAs, and the neuropeptidergic dysregulations in the amygdala; although this treatment is effective in reversing the expression of locomotor sensitization to challenge nicotine even after a long abstinence.
+CNR1	drug	nicotine	22959963	Furthermore, treatment with the <strong>cannabinoid receptor 1</strong> antagonist, AM251 (5 mg/kg) during a short (1 wk) abstinence is ineffective in reversing <b>nicotine</b> induced anxiety, fluctuations in BDNF and spinophilin mRNAs, and the neuropeptidergic dysregulations in the amygdala; although this treatment is effective in reversing the expression of locomotor sensitization to challenge <b>nicotine</b> even after a long abstinence.
+CNR1	addiction	sensitization	22959963	Furthermore, treatment with the <strong>cannabinoid receptor 1</strong> antagonist, AM251 (5 mg/kg) during a short (1 wk) abstinence is ineffective in reversing nicotine induced anxiety, fluctuations in BDNF and spinophilin mRNAs, and the neuropeptidergic dysregulations in the amygdala; although this treatment is effective in reversing the expression of locomotor <b>sensitization</b> to challenge nicotine even after a long abstinence.
+CNR1	drug	cannabinoid	22913292	SA daily treatment significantly reduced mechanical allodynia in KOR and <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) sensitive manner.
+CNR1	drug	cannabinoid	22913292	SA daily treatment significantly reduced mechanical allodynia in KOR and <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) sensitive manner.
+CNR1	drug	cannabinoid	22863674	The <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) is present in Acb neurons expressing each of these peptides, but its location in the VP is not known.
+CNR1	addiction	reward	22863674	To address this question, we used electron microscopic dual immunolabeling of the <strong>CB1R</strong> and either dynorphin 1 8 (Dyn) or Met(5) enkephalin (ME) in the VP of C57BL/6J mice, a species in which <strong>CB1R</strong> gene deletion produces a <b>reward</b> deficit.
+CNR1	drug	cannabinoid	22850347	MAPK14 and <strong>CNR1</strong> gene variant interactions: effects on brain volume deficits in schizophrenia patients with <b>marijuana</b> misuse.
+CNR1	drug	cannabinoid	22850347	We previously reported that <b>marijuana</b> misuse in conjunction with specific <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) genetic variants (rs12720071 G allele carriers) contributed to white matter (WM) brain volume deficits in schizophrenia patients.
+CNR1	drug	cannabinoid	22850347	In this study, we assessed the influence of another <b>cannabinoid</b> related gene, mitogen activated protein kinase 14 (MAPK14), and potential MAPK14 <strong>CNR1</strong> gene gene interactions in conferring brain volume abnormalities among schizophrenia patients with <b>marijuana</b> abuse/dependence.
+CNR1	addiction	dependence	22850347	In this study, we assessed the influence of another cannabinoid related gene, mitogen activated protein kinase 14 (MAPK14), and potential MAPK14 <strong>CNR1</strong> gene gene interactions in conferring brain volume abnormalities among schizophrenia patients with marijuana abuse/<b>dependence</b>.
+CNR1	drug	cannabinoid	22850347	There were significant main effects of the MAPK14 <strong>CNR1</strong> diplotype and diplotype × <b>marijuana</b> interaction on WM brain volumes, with both genetic variants having additive contributions to WM volume deficits only in patients with <b>marijuana</b> misuse.
+CNR1	drug	cannabinoid	22850347	Given that <strong>CNR1</strong> induced apoptosis is preceded by increased MAPK phosphorylation, our study suggests that potential MAPK14 <strong>CNR1</strong> gene gene interactions may mediate brain morphometric features in schizophrenia patients with heavy <b>marijuana</b> use.
+CNR1	drug	cannabinoid	22700585	Fasting induces CART down regulation in the zebrafish nervous system in a <strong><b>cannabinoid</b> receptor 1</strong> dependent manner.
+CNR1	drug	cannabinoid	22669173	Associations between <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) variation and hippocampus and amygdala volumes in heavy <b>cannabis</b> users.
+CNR1	drug	cannabinoid	22669173	A single nucleotide polymorphism in the <b>cannabis</b> receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced withdrawal, cue elicited craving, and parahippocampal activation to <b>cannabis</b> cues.
+CNR1	addiction	relapse	22669173	A single nucleotide polymorphism in the cannabis receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced withdrawal, cue elicited <b>craving</b>, and parahippocampal activation to cannabis cues.
+CNR1	addiction	withdrawal	22669173	A single nucleotide polymorphism in the cannabis receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced <b>withdrawal</b>, cue elicited craving, and parahippocampal activation to cannabis cues.
+CNR1	drug	cannabinoid	22669173	These data replicate previous findings of reduced hippocampal and amygdalar volume among heavy <b>cannabis</b> users, and suggest that <strong>CNR1</strong> rs2023239 variation may predispose smaller hippocampal volume after heavy <b>cannabis</b> use.
+CNR1	drug	cannabinoid	22646861	Associated increases in <b>cannabinoid</b> 1 G protein coupled receptor (<strong>CB1R</strong>) activity/expression further exacerbate food consumption and the metabolic shift toward fat production and accumulation.
+CNR1	drug	cannabinoid	22646861	The role of <strong>CB1R</strong> activity in hyperphagia and weight gain spurred the development of <b>rimonabant</b> (<b>SR141716</b>; Acomplia), the first in class <strong>CB1R</strong> antagonist/inverse agonist weight loss drug.
+CNR1	drug	cannabinoid	22646861	<b>Rimonabant</b> and similar <strong>CB1R</strong> inverse agonists also exert pleiotropic actions in addition to weight loss effects that help correct obesity related metabolic derangements and reduce cardiovascular risk in humans.
+CNR1	drug	cannabinoid	22646861	Laboratory studies demonstrate that <strong>CB1R</strong> neutral antagonists   whether readily accessible to the central nervous system or not (i.e., 'periphero neutral' antagonists)   retain the salient therapeutic effects of <strong>CB1R</strong> inverse agonists on hyperphagia, weight gain, and obesity driven metabolic abnormalities with the distinct advantage of being associated with significantly less preclinical adverse events than are conventional <strong>CB1R</strong> inverse agonists such as <b>rimonabant</b>.
+CNR1	drug	alcohol	22613131	<strong>CB1R</strong> play a role in <b>alcohol</b> withdrawal and in some effects of acupuncture.
+CNR1	addiction	withdrawal	22613131	<strong>CB1R</strong> play a role in alcohol <b>withdrawal</b> and in some effects of acupuncture.
+CNR1	drug	alcohol	22613131	Here, we investigated electroacupuncture (EA) effects during <b>ethanol</b> withdrawal on <strong>CB1R</strong> immunoreactivity.
+CNR1	addiction	withdrawal	22613131	Here, we investigated electroacupuncture (EA) effects during ethanol <b>withdrawal</b> on <strong>CB1R</strong> immunoreactivity.
+CNR1	drug	alcohol	22613131	Therefore, EA inhibits <strong>CB1R</strong> upregulation seen in <b>ethanol</b> withdrawn mice.
+CNR1	drug	cannabinoid	22362764	Allele specific differences in activity of a novel <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene intronic enhancer in hypothalamus, dorsal root ganglia, and hippocampus.
+CNR1	drug	cannabinoid	22362764	Polymorphisms within intron 2 of the <strong>CNR1</strong> gene, which encodes <b>cannabinoid</b> receptor 1 (CB(1)), have been associated with addiction, obesity, and brain volume deficits.
+CNR1	addiction	addiction	22362764	Polymorphisms within intron 2 of the <strong>CNR1</strong> gene, which encodes cannabinoid receptor 1 (CB(1)), have been associated with <b>addiction</b>, obesity, and brain volume deficits.
+CNR1	drug	cannabinoid	22362764	Polymorphisms within intron 2 of the <strong>CNR1</strong> gene, which encodes <strong><b>cannabinoid</b> receptor 1</strong> (CB(1)), have been associated with addiction, obesity, and brain volume deficits.
+CNR1	addiction	addiction	22362764	Polymorphisms within intron 2 of the <strong>CNR1</strong> gene, which encodes <strong>cannabinoid receptor 1</strong> (CB(1)), have been associated with <b>addiction</b>, obesity, and brain volume deficits.
+CNR1	drug	cannabinoid	22335400	<b>Cannabinoid</b> 1 receptor (<strong>CB1R</strong>) blockers as medicines: beyond obesity and cardiometabolic disorders to substance abuse/drug addiction with <strong>CB1R</strong> neutral antagonists.
+CNR1	addiction	addiction	22335400	Cannabinoid 1 receptor (<strong>CB1R</strong>) blockers as medicines: beyond obesity and cardiometabolic disorders to substance abuse/drug <b>addiction</b> with <strong>CB1R</strong> neutral antagonists.
+CNR1	drug	cannabinoid	22335400	Signal transmission through the <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) in the central nervous system (CNS) modulates neurotransmitters/neuronal pathways contributing to the rewarding properties and hedonic effects of certain nondrug stimuli (e.g., food) and many prototypical addictive drugs, promoting excessive intake and its pathological consequences.
+CNR1	addiction	addiction	22335400	Signal transmission through the cannabinoid 1 receptor (<strong>CB1R</strong>) in the central nervous system (CNS) modulates neurotransmitters/neuronal pathways contributing to the rewarding properties and hedonic effects of certain nondrug stimuli (e.g., food) and many prototypical <b>addictive</b> drugs, promoting excessive intake and its pathological consequences.
+CNR1	addiction	reward	22335400	Signal transmission through the cannabinoid 1 receptor (<strong>CB1R</strong>) in the central nervous system (CNS) modulates neurotransmitters/neuronal pathways contributing to the rewarding properties and <b>hedonic</b> effects of certain nondrug stimuli (e.g., food) and many prototypical addictive drugs, promoting excessive intake and its pathological consequences.
+CNR1	addiction	addiction	22335400	This mini review calls attention to the proposition that <strong>CB1R</strong> neutral antagonists offer attractive opportunities for pharmacotherapeutic exploitation in the substance abuse/drug <b>addiction</b> space, whereas the restricted CNS accessibility of peripherally biased <strong>CB1R</strong> inverse agonists circumscribes their therapeutic utility for this indication.
+CNR1	addiction	addiction	22335400	The unique preclinical pharmacology, efficacy profiles, and reduced adverse event risk of <strong>CB1R</strong> neutral antagonists make them worthy of translational study for their potential therapeutic application beyond obesity/cardiometabolic disease to include substance abuse/drug <b>addiction</b> disorders.
+CNR1	drug	cannabinoid	22260337	In laboratory and clinical studies, the <strong><b>cannabinoid</b> receptor 1</strong> agonist oral Δ9tetrahydrocannabinol (<b>THC</b>; <b>dronabinol</b>) has been shown to decrease <b>marijuana</b> withdrawal but not relapse.
+CNR1	addiction	relapse	22260337	In laboratory and clinical studies, the <strong>cannabinoid receptor 1</strong> agonist oral Δ9tetrahydrocannabinol (THC; dronabinol) has been shown to decrease marijuana withdrawal but not <b>relapse</b>.
+CNR1	addiction	withdrawal	22260337	In laboratory and clinical studies, the <strong>cannabinoid receptor 1</strong> agonist oral Δ9tetrahydrocannabinol (THC; dronabinol) has been shown to decrease marijuana <b>withdrawal</b> but not relapse.
+CNR1	drug	cannabinoid	22119710	Long term effects of juvenile nicotine exposure on abstinence related social anxiety like behavior and amygdalar <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) mRNA expression in the novelty seeking phenotype.
+CNR1	drug	nicotine	22119710	Long term effects of juvenile <b>nicotine</b> exposure on abstinence related social anxiety like behavior and amygdalar <strong>cannabinoid receptor 1</strong> (CB1R) mRNA expression in the novelty seeking phenotype.
+CNR1	addiction	relapse	22119710	Long term effects of juvenile nicotine exposure on abstinence related social anxiety like behavior and amygdalar <strong>cannabinoid receptor 1</strong> (CB1R) mRNA expression in the novelty <b>seeking</b> phenotype.
+CNR1	drug	cannabinoid	22119710	Long term effects of juvenile nicotine exposure on abstinence related social anxiety like behavior and amygdalar <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) mRNA expression in the novelty seeking phenotype.
+CNR1	drug	nicotine	22119710	Long term effects of juvenile <b>nicotine</b> exposure on abstinence related social anxiety like behavior and amygdalar <strong>cannabinoid receptor 1</strong> (<strong>CB1R</strong>) mRNA expression in the novelty seeking phenotype.
+CNR1	addiction	relapse	22119710	Long term effects of juvenile nicotine exposure on abstinence related social anxiety like behavior and amygdalar <strong>cannabinoid receptor 1</strong> (<strong>CB1R</strong>) mRNA expression in the novelty <b>seeking</b> phenotype.
+CNR1	drug	cannabinoid	22119710	Present study investigates implication of <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) in the basolateral (BLA) and the central (CeA) nuclei of amygdala in behaviorally sensitizing effects of nicotine and accompanying social anxiety following juvenile nicotine training and a 1  or 3 wk injection free period in the novelty seeking phenotype.
+CNR1	drug	nicotine	22119710	Present study investigates implication of <strong>cannabinoid receptor 1</strong> (CB1R) in the basolateral (BLA) and the central (CeA) nuclei of amygdala in behaviorally sensitizing effects of <b>nicotine</b> and accompanying social anxiety following juvenile <b>nicotine</b> training and a 1  or 3 wk injection free period in the novelty seeking phenotype.
+CNR1	addiction	relapse	22119710	Present study investigates implication of <strong>cannabinoid receptor 1</strong> (CB1R) in the basolateral (BLA) and the central (CeA) nuclei of amygdala in behaviorally sensitizing effects of nicotine and accompanying social anxiety following juvenile nicotine training and a 1  or 3 wk injection free period in the novelty <b>seeking</b> phenotype.
+CNR1	drug	cannabinoid	22119710	Present study investigates implication of <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) in the basolateral (BLA) and the central (CeA) nuclei of amygdala in behaviorally sensitizing effects of nicotine and accompanying social anxiety following juvenile nicotine training and a 1  or 3 wk injection free period in the novelty seeking phenotype.
+CNR1	drug	nicotine	22119710	Present study investigates implication of <strong>cannabinoid receptor 1</strong> (<strong>CB1R</strong>) in the basolateral (BLA) and the central (CeA) nuclei of amygdala in behaviorally sensitizing effects of <b>nicotine</b> and accompanying social anxiety following juvenile <b>nicotine</b> training and a 1  or 3 wk injection free period in the novelty seeking phenotype.
+CNR1	addiction	relapse	22119710	Present study investigates implication of <strong>cannabinoid receptor 1</strong> (<strong>CB1R</strong>) in the basolateral (BLA) and the central (CeA) nuclei of amygdala in behaviorally sensitizing effects of nicotine and accompanying social anxiety following juvenile nicotine training and a 1  or 3 wk injection free period in the novelty <b>seeking</b> phenotype.
+CNR1	drug	nicotine	22119710	Decreased <strong>CB1R</strong> mRNA levels in both compartments of the amygdala were also observed following <b>nicotine</b> challenge in saline pre trained HRs after a 3 wk injection free period compared to HRs after a 1 wk injection free period.
+CNR1	drug	nicotine	22119710	These findings show robust, long lasting expression of behavioral sensitization to <b>nicotine</b> in HRs associated with changes in amygdalar <strong>CB1R</strong> mRNA as a potential substrate for abstinence related anxiety.
+CNR1	addiction	sensitization	22119710	These findings show robust, long lasting expression of behavioral <b>sensitization</b> to nicotine in HRs associated with changes in amygdalar <strong>CB1R</strong> mRNA as a potential substrate for abstinence related anxiety.
+CNR1	drug	alcohol	22085192	<strong>Cannabinoid receptor 1</strong> gene is associated with <b>alcohol</b> dependence.
+CNR1	drug	cannabinoid	22085192	<strong><b>Cannabinoid</b> receptor 1</strong> gene is associated with alcohol dependence.
+CNR1	addiction	dependence	22085192	<strong>Cannabinoid receptor 1</strong> gene is associated with alcohol <b>dependence</b>.
+CNR1	drug	cannabinoid	22085192	Given the potential role of <b>endocannabinoid</b> system in AD, polymorphisms within <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) have been potentially associated with susceptibility to this disease.
+CNR1	drug	alcohol	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with dependence to <b>alcohol</b> and other substances and emphasizes the relevance of endocannabinoid system in AD.
+CNR1	drug	cannabinoid	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with dependence to alcohol and other substances and emphasizes the relevance of <b>endocannabinoid</b> system in AD.
+CNR1	addiction	dependence	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with <b>dependence</b> to alcohol and other substances and emphasizes the relevance of endocannabinoid system in AD.
+CNR1	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], <strong>CNR1</strong> 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CNR1	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], <strong>CNR1</strong> 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CNR1	drug	cannabinoid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (OPRM1) or <b>cannabinoid</b> receptors (<strong>CNR1</strong>).
+CNR1	drug	nicotine	22046326	Overall, our results suggest that genetic variants potentially involved in <b>nicotine</b> metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with <b>smoking</b> related phenotypes, as opposed to genetic variants influencing the brain effects of <b>nicotine</b>, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (OPRM1) or cannabinoid receptors (<strong>CNR1</strong>).
+CNR1	drug	opioid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), <b>opioid</b> (OPRM1) or cannabinoid receptors (<strong>CNR1</strong>).
+CNR1	drug	cannabinoid	22034972	As striatal DA signalling modulates the <b>endocannabinoid</b> system (ECS), the present study was aimed at investigating <b>cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) function in a model of ADHD obtained by triple point mutation in the dopamine transporter (DAT) gene in mice, making them insensitive to cocaine [DAT cocaine insensitive (DAT CI) mice].
+CNR1	drug	cocaine	22034972	As striatal DA signalling modulates the endocannabinoid system (ECS), the present study was aimed at investigating cannabinoid CB1 receptor (<strong>CB1R</strong>) function in a model of ADHD obtained by triple point mutation in the dopamine transporter (DAT) gene in mice, making them insensitive to <b>cocaine</b> [DAT <b>cocaine</b> insensitive (DAT CI) mice].
+CNR1	drug	cocaine	22034972	In DAT CI mice, the blockade of <strong>CB1R</strong>((GABA)) function was complete even after <b>cocaine</b> or environmental manipulations activating the endogenous DA dependent reward system, which are known to sensitize these receptors in control animals.
+CNR1	addiction	reward	22034972	In DAT CI mice, the blockade of <strong>CB1R</strong>((GABA)) function was complete even after cocaine or environmental manipulations activating the endogenous DA dependent <b>reward</b> system, which are known to sensitize these receptors in control animals.
+CNR1	drug	cannabinoid	21989802	To characterize the novel, high affinity <strong><b>cannabinoid</b> receptor 1</strong> (CB(1)R) HHC ligand AM2389 [9β hydroxy 3 (1 hexyl cyclobut 1 yl) hexahydrocannabinol in two rodent pre clinical assays.
+CNR1	drug	cannabinoid	21982932	Analyses were focused a priori on the orbitofrontal cortex, anterior cingulate cortex, striatum, amygdala, hippocampus, and cerebellum, regions implicated in substance dependence and/or with high <strong><b>cannabinoid</b> receptor 1</strong> concentrations.
+CNR1	addiction	dependence	21982932	Analyses were focused a priori on the orbitofrontal cortex, anterior cingulate cortex, striatum, amygdala, hippocampus, and cerebellum, regions implicated in substance <b>dependence</b> and/or with high <strong>cannabinoid receptor 1</strong> concentrations.
+CNR1	drug	cannabinoid	21937688	The <b>cannabinoid</b> receptor (<strong>CNR1</strong>) and the fatty acid amide hydrolase (FAAH) genes are located on chromosomes 6 and 1 in the 6q15 and 1p33 cytogenetic bands, respectively.
+CNR1	addiction	addiction	21937688	However, many works have repeatedly associated polymorphisms in the <strong>CNR1</strong> and FAAH genes with drug related behaviours; this suggests that these genes should be examined in further genetic studies focusing on drug <b>addiction</b> and other psychiatric disorders.
+CNR1	drug	amphetamine	21886587	Association Study of Two Cannabinoid Receptor Genes, <strong>CNR1</strong> and CNR2, with <b>Methamphetamine</b> Dependence.
+CNR1	drug	cannabinoid	21886587	Association Study of Two <b>Cannabinoid</b> Receptor Genes, <strong>CNR1</strong> and CNR2, with Methamphetamine Dependence.
+CNR1	addiction	dependence	21886587	Association Study of Two Cannabinoid Receptor Genes, <strong>CNR1</strong> and CNR2, with Methamphetamine <b>Dependence</b>.
+CNR1	drug	amphetamine	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode cannabinoid receptors CB1 and CB2, with <b>methamphetamine</b> dependence, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+CNR1	drug	cannabinoid	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode <b>cannabinoid</b> receptors CB1 and CB2, with methamphetamine dependence, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+CNR1	addiction	dependence	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode cannabinoid receptors CB1 and CB2, with methamphetamine <b>dependence</b>, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+CNR1	drug	amphetamine	21886587	Rs806379 of the <strong>CNR1</strong> gene showed a significant association with the phenotype of latency of psychosis after the first consumption of <b>methamphetamine</b>.
+CNR1	drug	amphetamine	21886587	The present study suggests a possibility that genetic variants of the <strong>CNR1</strong> gene may produce a liability to the complication of psychotic state after abuse of <b>methamphetamine</b>; however, our findings need to be confirmed by future replications.
+CNR1	drug	cannabinoid	21821098	This D1R+D2R mediated firing increase required CB1Rs, since it was prevented by the <strong>CB1R</strong> antagonists AM251 and <b>Rimonabant</b>.
+CNR1	drug	cannabinoid	21808284	rs806365 in <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) had a significant male specific gene treatment interaction at 6 month follow up (adjusted P = 3.9 × 10( 5)); within males using nasal spray, rs806365 was associated with a decrease in odds of abstinence (OR = 0.04; 95% CI: 0.01 0.2).
+CNR1	drug	nicotine	21808284	While the role of <strong>CNR1</strong> in substance abuse has been well studied, we report EPB41 for the first time in the <b>nicotine</b> literature.
+CNR1	drug	cocaine	21790903	Further evidence for association of polymorphisms in the <strong>CNR1</strong> gene with <b>cocaine</b> addiction: confirmation in an independent sample and meta analysis.
+CNR1	addiction	addiction	21790903	Further evidence for association of polymorphisms in the <strong>CNR1</strong> gene with cocaine <b>addiction</b>: confirmation in an independent sample and meta analysis.
+CNR1	drug	cannabinoid	21790903	The <b>cannabinoid</b> receptor 1 protein regulates both the <b>endocannabinoid</b> and dopaminergic neurobiological systems, and polymorphisms in the <b>cannabinoid</b> receptor gene, <strong>CNR1</strong>, have been associated previously with substance dependence.
+CNR1	addiction	dependence	21790903	The cannabinoid receptor 1 protein regulates both the endocannabinoid and dopaminergic neurobiological systems, and polymorphisms in the cannabinoid receptor gene, <strong>CNR1</strong>, have been associated previously with substance <b>dependence</b>.
+CNR1	drug	cannabinoid	21790903	The <strong><b>cannabinoid</b> receptor 1</strong> protein regulates both the <b>endocannabinoid</b> and dopaminergic neurobiological systems, and polymorphisms in the <b>cannabinoid</b> receptor gene, <strong>CNR1</strong>, have been associated previously with substance dependence.
+CNR1	addiction	dependence	21790903	The <strong>cannabinoid receptor 1</strong> protein regulates both the endocannabinoid and dopaminergic neurobiological systems, and polymorphisms in the cannabinoid receptor gene, <strong>CNR1</strong>, have been associated previously with substance <b>dependence</b>.
+CNR1	drug	cocaine	21790903	<b>Cocaine</b> addicted individuals (n=860) and unaffected controls (n=334) of African descent were genotyped for two single nucleotide polymorphisms (SNPs) in <strong>CNR1</strong> (rs6454674, rs806368).
+CNR1	drug	cocaine	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance dependence or are specific to <b>cocaine</b> addiction.
+CNR1	addiction	addiction	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance dependence or are specific to cocaine <b>addiction</b>.
+CNR1	addiction	dependence	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance <b>dependence</b> or are specific to cocaine addiction.
+CNR1	drug	cocaine	21785434	We found that systemic, intranasal or intra accumbens local administration of JWH133, a selective CB(2) receptor agonist, dose dependently inhibited intravenous <b>cocaine</b> self administration, <b>cocaine</b> enhanced locomotion, and <b>cocaine</b> enhanced accumbens extracellular dopamine in wild type and CB(1) receptor knockout (CB(1)( / ), also known as <strong>Cnr1</strong>( / )) mice, but not in CB(2)( / ) (Cnr2( / )) mice.
+CNR1	drug	cannabinoid	21777606	Adolescent <b>cannabinoid</b> exposure attenuates adult female sexual motivation but does not alter adulthood <strong>CB1R</strong> expression or estrous cyclicity.
+CNR1	drug	cannabinoid	21749491	Blocking <strong><b>cannabinoid</b> receptor 1</strong> (CB(1)) reduced mGluR1 LTP in the saline treated but not cocaine withdrawn group.
+CNR1	drug	cocaine	21749491	Blocking <strong>cannabinoid receptor 1</strong> (CB(1)) reduced mGluR1 LTP in the saline treated but not <b>cocaine</b> withdrawn group.
+CNR1	drug	cannabinoid	21718968	We used positron emission tomography to investigate the type 1 <b>cannabinoid</b> receptor (<strong>CB1R</strong>) in bulimic and anorectic patients.
+CNR1	drug	cannabinoid	21718968	Global <strong>CB1R</strong> upregulation in AN patients is a possible long term compensatory mechanism to an underactive <b>endocannabinoid</b> system in anorectic conditions.
+CNR1	addiction	reward	21718968	There is a similarity in <strong>CB1R</strong> dysregulation both in AN and BN in the insular cortex, which is involved in the integration of interoceptive information, gustatory information, <b>reward</b>, and emotion processing.
+CNR1	drug	cannabinoid	21714860	Variation in the human <b>cannabinoid</b> receptor <strong>CNR1</strong> gene modulates gaze duration for happy faces.
+CNR1	drug	cannabinoid	21714860	In this study, we tested whether variations in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene are associated with gaze duration towards happy faces.
+CNR1	drug	cannabinoid	21714860	This gene was selected because <strong>CNR1</strong> is a key component of the <b>endocannabinoid</b> system, which is involved in processing reward, and in our previous functional magnetic resonance imaging (fMRI) study, we found that variations in <strong>CNR1</strong> modulate the striatal response to happy (but not disgust) faces.
+CNR1	addiction	reward	21714860	This gene was selected because <strong>CNR1</strong> is a key component of the endocannabinoid system, which is involved in processing <b>reward</b>, and in our previous functional magnetic resonance imaging (fMRI) study, we found that variations in <strong>CNR1</strong> modulate the striatal response to happy (but not disgust) faces.
+CNR1	addiction	reward	21714860	These results suggest that <strong>CNR1</strong> variations modulate the striatal function that underlies the perception of signals of social <b>reward</b>, such as happy faces.
+CNR1	drug	cannabinoid	21696342	As neural mechanism underlying these changes, an interaction between the <b>cannabinoid</b> system, especially <strong><b>cannabinoid</b> receptor 1</strong>, and the serotonergic and dopaminergic system in the prefrontal cortex, nucleus accumbens, and hippocampus is suggested.
+CNR1	drug	cannabinoid	21585053	[Effects of repeated electroacupuncture on gene expression of <strong><b>cannabinoid</b> receptor 1</strong> and dopamine 1 receptor in nucleus accumbens caudate nucleus region in inflammatory pain rats].
+CNR1	drug	cannabinoid	21585053	To observe the effect of repeated electroacupuncture (EA) on the expression of <strong><b>cannabinoid</b> receptor 1</strong> (CB 1) mrRNA and dopamine 1 receptor (D 1) mRNA in Nucleus Accumbens (NAC) Caudate Nucleus (CN) region in inflammatory pain rats, so as to study its underlying mechanism in analgesia.
+CNR1	drug	cannabinoid	21513772	Association between a <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism and <b>cannabinoid</b> induced alterations of the auditory event related P300 potential.
+CNR1	drug	cannabinoid	21513772	Recently, an (AAT)n triplet repeat polymorphism within the <b>cannabinoid</b> receptor gene <strong>CNR1</strong> has been found to be associated with both schizophrenia and substance dependence, and to modulate the P300 potential.
+CNR1	addiction	dependence	21513772	Recently, an (AAT)n triplet repeat polymorphism within the cannabinoid receptor gene <strong>CNR1</strong> has been found to be associated with both schizophrenia and substance <b>dependence</b>, and to modulate the P300 potential.
+CNR1	drug	cannabinoid	21513772	Moreover, it appears that variations within <strong>CNR1</strong> may differentially alter the sensitivity to the acute effects of <b>cannabinoids</b> on P300 generation in healthy subjects.
+CNR1	drug	cannabinoid	21497918	We summarize <b>endocannabinoid</b> signaling in pathways related to anxiety and depression, identify the serotonergic system as the most likely candidate to mediate the side effects of CB₁ receptor antagonists, and propose that poloymorphisms in <strong>CNR1</strong>, SLC6A4 and certain CYP 450 enzymes could help to identify individuals who may benefit from treatment with CB₁ receptor antagonist without psychiatric side effects.
+CNR1	drug	cannabinoid	21466769	Study II is a cross sectional study to establish the expression of <strong><b>cannabinoid</b> receptor 1</strong> from various adipose tissue depots of lean and obese persons.
+CNR1	drug	cannabinoid	21441120	<b>THC</b> based drug design of a less academic nature, however, has led to the marketing of "synthetic <b>marijuana</b>," labeled as K2 or "Spice," among other terms, which elicits psychotropic actions via <strong>CB1R</strong> activation.
+CNR1	drug	cannabinoid	21420833	<strong><b>Cannabinoid</b> receptor 1</strong> gene polymorphisms and <b>marijuana</b> misuse interactions on white matter and cognitive deficits in schizophrenia.
+CNR1	drug	cannabinoid	21420833	<b>Cannabinoid</b> receptor 1 (CB1/<strong>CNR1</strong>) is the principal brain receptor mediating <b>marijuana</b> effects.
+CNR1	drug	cannabinoid	21420833	No study to date has systematically investigated the impact of <strong>CNR1</strong> on quantitative phenotypic features in schizophrenia and inter relationships with <b>marijuana</b> misuse.
+CNR1	drug	alcohol	21420833	Effects of <strong>CNR1</strong> tSNPs and marijuana abuse/dependence on brain volumes and neurocognition were assessed using ANCOVA, including co morbid <b>alcohol</b>/non marijuana illicit drug misuse as covariates.
+CNR1	drug	cannabinoid	21420833	Effects of <strong>CNR1</strong> tSNPs and <b>marijuana</b> abuse/dependence on brain volumes and neurocognition were assessed using ANCOVA, including co morbid alcohol/non <b>marijuana</b> illicit drug misuse as covariates.
+CNR1	addiction	dependence	21420833	Effects of <strong>CNR1</strong> tSNPs and marijuana abuse/<b>dependence</b> on brain volumes and neurocognition were assessed using ANCOVA, including co morbid alcohol/non marijuana illicit drug misuse as covariates.
+CNR1	drug	cannabinoid	21420833	Our findings suggest that heavy <b>cannabis</b> use in the context of specific <strong>CNR1</strong> genotypes may contribute to greater WM volume deficits and cognitive impairment, which could in turn increase schizophrenia risk.
+CNR1	addiction	intoxication	21406230	In order to gain further insights on the potential role of <strong>CB1R</strong> in HD physiopathology, we evaluated the pathophysiological consequences of a genetic deletion of <strong>CB1R</strong> in the N171 82Q transgenic model and following 3 nitropropionic (3NP) <b>intoxication</b>.
+CNR1	drug	cannabinoid	21341382	In M. mulatta, the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) mRNA was expressed in the all tissues; in contrast, the <b>cannabinoid</b> receptor 2 (CNR2) mRNA was only present in the spleen.
+CNR1	drug	cannabinoid	21324836	The effects of the <b>endocannabinoid</b> transport inhibitor AM404 and the <strong><b>cannabinoid</b> receptor 1</strong> antagonist AM251 in a nicotine dependent rodent model were investigated.
+CNR1	drug	nicotine	21324836	The effects of the endocannabinoid transport inhibitor AM404 and the <strong>cannabinoid receptor 1</strong> antagonist AM251 in a <b>nicotine</b> dependent rodent model were investigated.
+CNR1	drug	cannabinoid	21251919	Activation of presynaptic <b>cannabinoid</b> 1 receptors (<strong>CB1R</strong>) with WIN55,212 2 (250 nM, 1 μM) significantly modulated PS amplitude in slices from age matched control rats while slices from EtOH consuming rats remained unaffected, indicating that eCB signaling is inhibited at a level that is downstream from <strong>CB1R</strong> activation.
+CNR1	drug	alcohol	21251919	Intermittent <b>alcohol</b> intake for seven weeks might thus be sufficient to modulate a presynaptic mechanism that needs to be synergized with <strong>CB1R</strong> activation for induction of long term depression (LTD).
+CNR1	drug	cannabinoid	21094647	Attenuation of food intake in chicks by an inverse agonist of <strong><b>cannabinoid</b> receptor 1</strong> administered by either injection or ingestion in hydrocolloid carriers.
+CNR1	drug	alcohol	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in <b>ethanol</b>'s reinforcing and addictive properties prompted us to study the levels and distribution of CB1R after chronic <b>ethanol</b> intake, in the presence and absence of DRD2.
+CNR1	drug	cannabinoid	20958329	The anatomical proximity of the <b>cannabinoid</b> type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and addictive properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	addiction	addiction	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and <b>addictive</b> properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	addiction	reward	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's <b>reinforcing</b> and addictive properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	drug	alcohol	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/<strong>CB1R</strong>) and the dopamine D2 receptors (DRD2), their ability to form <strong>CB1R</strong> DRD2 heteromers, their opposing roles in locomotion, and their involvement in <b>ethanol</b>'s reinforcing and addictive properties prompted us to study the levels and distribution of <strong>CB1R</strong> after chronic <b>ethanol</b> intake, in the presence and absence of DRD2.
+CNR1	drug	cannabinoid	20958329	The anatomical proximity of the <b>cannabinoid</b> type 1 (<strong>CNR1</strong>/<strong>CB1R</strong>) and the dopamine D2 receptors (DRD2), their ability to form <strong>CB1R</strong> DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and addictive properties prompted us to study the levels and distribution of <strong>CB1R</strong> after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	addiction	addiction	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/<strong>CB1R</strong>) and the dopamine D2 receptors (DRD2), their ability to form <strong>CB1R</strong> DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and <b>addictive</b> properties prompted us to study the levels and distribution of <strong>CB1R</strong> after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	addiction	reward	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/<strong>CB1R</strong>) and the dopamine D2 receptors (DRD2), their ability to form <strong>CB1R</strong> DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's <b>reinforcing</b> and addictive properties prompted us to study the levels and distribution of <strong>CB1R</strong> after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	drug	alcohol	20958329	We monitored the drinking patterns and locomotor activity of Drd2+/+ and Drd2 /  mice consuming either water or a 20% (v/v) <b>ethanol</b> solution (forced <b>ethanol</b> intake) for 6 months and used the selective CB1 receptor antagonist [³H]SR141716A to quantify <strong>CB1R</strong> levels in different brain regions with in vitro receptor autoradiography.
+CNR1	drug	alcohol	20958329	We found that the lack of DRD2 leads to a marked upregulation (approximately 2 fold increase) of <strong>CB1R</strong> in the cerebral cortex, the caudate putamen, and the nucleus accumbens, which was reversed by chronic <b>ethanol</b> intake.
+CNR1	drug	cannabinoid	20457524	In this context, it is important to recognize the utility of <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) agonists, natural as Delta(9) <b>tetrahydrocannabinol</b> (<b>THC</b>) or synthetic as <b>Nabilone</b> as useful drugs to alleviate this kind of patients' suffering.
+CNR1	drug	cannabinoid	20457524	In this context, it is important to recognize the utility of <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) agonists, natural as Delta(9) <b>tetrahydrocannabinol</b> (<b>THC</b>) or synthetic as <b>Nabilone</b> as useful drugs to alleviate this kind of patients' suffering.
+CNR1	drug	cannabinoid	20353780	This finding is corroborated by the evidence that <b>endocannabinoids</b> inhibit, through a <b>cannabinoid</b> type 1 receptor (<strong>CB1R</strong>) dependent retrograde mechanism, the release of neurotransmitters controlling nociceptive inputs and that the levels of these lipids are high in those regions (such as sensory terminals, skin, dorsal root ganglia) known to be involved in transmission and modulation of pain signals.
+CNR1	addiction	addiction	20192949	<strong>CNR1</strong> gene polymorphisms in <b>addictive</b> disorders: a systematic review and a meta analysis.
+CNR1	drug	cannabinoid	20192949	The aim of the present work was to systematically review all association studies of <b>cannabis</b> receptor 1 (<strong>CNR1</strong>) polymorphisms with dependence syndrome and to perform a meta analysis.
+CNR1	addiction	dependence	20192949	The aim of the present work was to systematically review all association studies of cannabis receptor 1 (<strong>CNR1</strong>) polymorphisms with <b>dependence</b> syndrome and to perform a meta analysis.
+CNR1	addiction	dependence	20192949	In line with the polygenic model, our meta analysis supports a minor implication for <strong>CNR1</strong> AAT polymorphism in illicit substance <b>dependence</b> vulnerability.
+CNR1	drug	cannabinoid	20010914	Association of polymorphisms of the <b>cannabinoid</b> receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with heroin addiction: impact of long repeats of <strong>CNR1</strong>.
+CNR1	drug	opioid	20010914	Association of polymorphisms of the cannabinoid receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with <b>heroin</b> addiction: impact of long repeats of <strong>CNR1</strong>.
+CNR1	addiction	addiction	20010914	Association of polymorphisms of the cannabinoid receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with heroin <b>addiction</b>: impact of long repeats of <strong>CNR1</strong>.
+CNR1	drug	cannabinoid	20010914	Alterations in expression of a <b>cannabinoid</b> receptor (<strong>CNR1</strong>, CB1), and of fatty acid amide hydrolase (FAAH) that degrades endogenous ligands of CB1, may contribute to the development of addiction.
+CNR1	addiction	addiction	20010914	Alterations in expression of a cannabinoid receptor (<strong>CNR1</strong>, CB1), and of fatty acid amide hydrolase (FAAH) that degrades endogenous ligands of CB1, may contribute to the development of <b>addiction</b>.
+CNR1	drug	opioid	20010914	The 385C>A in the FAAH gene and six polymorphisms of <strong>CNR1</strong> were genotyped in former <b>heroin</b> addicts and control subjects (247 Caucasians, 161 Hispanics, 179 African Americans and 19 Asians).
+CNR1	drug	cannabinoid	20010552	Individual and additive effects of the <strong>CNR1</strong> and FAAH genes on brain response to <b>marijuana</b> cues.
+CNR1	drug	cannabinoid	20010552	As previous work has highlighted the significance of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with respect to <b>cannabis</b> dependence (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+CNR1	addiction	dependence	20010552	As previous work has highlighted the significance of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with respect to cannabis <b>dependence</b> (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+CNR1	drug	cannabinoid	20010552	As previous work has highlighted the significance of the <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with respect to <b>cannabis</b> dependence (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+CNR1	addiction	dependence	20010552	As previous work has highlighted the significance of the <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with respect to cannabis <b>dependence</b> (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+CNR1	drug	cannabinoid	20010552	Between group comparisons showed that carriers of the <strong>CNR1</strong> rs2023239 G allele had significantly greater activity in reward related areas of the brain, such as the orbitofrontal cortex (OFC), inferior frontal gyrus (IFG), and anterior cingulate gyrus (ACG), during exposure to <b>marijuana</b> cues, as compared with those with the A/A genotype for this SNP.
+CNR1	addiction	reward	20010552	Between group comparisons showed that carriers of the <strong>CNR1</strong> rs2023239 G allele had significantly greater activity in <b>reward</b> related areas of the brain, such as the orbitofrontal cortex (OFC), inferior frontal gyrus (IFG), and anterior cingulate gyrus (ACG), during exposure to marijuana cues, as compared with those with the A/A genotype for this SNP.
+CNR1	drug	cannabinoid	20010552	These findings are in accord with earlier reported associations between <strong>CNR1</strong> and FAAH and CD intermediate phenotypes, and suggest that the underlying mechanism of these genetic effects may be enhanced neural response in reward areas of the brain in carriers of the <strong>CNR1</strong> G allele and FAAH C/C genotype in response to <b>marijuana</b> cues.
+CNR1	addiction	reward	20010552	These findings are in accord with earlier reported associations between <strong>CNR1</strong> and FAAH and CD intermediate phenotypes, and suggest that the underlying mechanism of these genetic effects may be enhanced neural response in <b>reward</b> areas of the brain in carriers of the <strong>CNR1</strong> G allele and FAAH C/C genotype in response to marijuana cues.
+CNR1	drug	cannabinoid	19886064	The implication of <strong>CNR1</strong> gene's polymorphisms in the modulation of <b>endocannabinoid</b> system effects.
+CNR1	drug	cannabinoid	19886064	It is composed of <b>cannabinoid</b> receptors CB1 and CB2, and their genes (<strong>CNR1</strong> and CNR2), their endogenous ligands and the enzymes which mediate endogenous ligands' biosynthesis and degradation.
+CNR1	drug	alcohol	19860799	Taken together, these results revealed that blockade of cannabinoid CB1 receptors (<strong>CB1r</strong>) decreased voluntary <b>ethanol</b> intake in <b>ethanol</b> habituated rats by normalizing the neurochemical alterations induced by <b>ethanol</b>.
+CNR1	drug	cannabinoid	19860799	Taken together, these results revealed that blockade of <b>cannabinoid</b> CB1 receptors (<strong>CB1r</strong>) decreased voluntary ethanol intake in ethanol habituated rats by normalizing the neurochemical alterations induced by ethanol.
+CNR1	drug	cannabinoid	19723626	The <strong><b>cannabinoid</b> receptor 1</strong> (CB(1)) and CB(2) <b>cannabinoid</b> receptors, associated with drugs of abuse, may provide a means to treat pain, mood, and addiction disorders affecting widespread segments of society.
+CNR1	addiction	addiction	19723626	The <strong>cannabinoid receptor 1</strong> (CB(1)) and CB(2) cannabinoid receptors, associated with drugs of abuse, may provide a means to treat pain, mood, and <b>addiction</b> disorders affecting widespread segments of society.
+CNR1	drug	cannabinoid	19675519	The <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) is distributed in brain areas associated with motor control, emotional responses, motivated behaviour and energy homeostasis.
+CNR1	drug	cannabinoid	19675519	The <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) is distributed in brain areas associated with motor control, emotional responses, motivated behaviour and energy homeostasis.
+CNR1	drug	cannabinoid	19443135	The association between <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) and <b>cannabis</b> dependence symptoms in adolescents and young adults.
+CNR1	addiction	dependence	19443135	The association between cannabinoid receptor 1 gene (<strong>CNR1</strong>) and cannabis <b>dependence</b> symptoms in adolescents and young adults.
+CNR1	drug	cannabinoid	19443135	The association between <strong><b>cannabinoid</b> receptor 1</strong> gene (<strong>CNR1</strong>) and <b>cannabis</b> dependence symptoms in adolescents and young adults.
+CNR1	addiction	dependence	19443135	The association between <strong>cannabinoid receptor 1</strong> gene (<strong>CNR1</strong>) and cannabis <b>dependence</b> symptoms in adolescents and young adults.
+CNR1	drug	cannabinoid	19443135	This study examined the genetic association between variation in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene and <b>cannabis</b> dependence symptoms.
+CNR1	addiction	dependence	19443135	This study examined the genetic association between variation in the cannabinoid receptor 1 (<strong>CNR1</strong>) gene and cannabis <b>dependence</b> symptoms.
+CNR1	drug	cannabinoid	19443135	This study examined the genetic association between variation in the <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) gene and <b>cannabis</b> dependence symptoms.
+CNR1	addiction	dependence	19443135	This study examined the genetic association between variation in the <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) gene and cannabis <b>dependence</b> symptoms.
+CNR1	drug	cannabinoid	19443135	Additional family based studies are needed to clarify the role of the <strong>CNR1</strong> gene, and its various SNPs, in the development of <b>cannabis</b> use disorders.
+CNR1	drug	cannabinoid	19367507	Since the discovery of the <b>cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) in 1988, and subsequently of the CB2 receptor (CB2R) in 1993, there has been an exponential growth of research investigating the functions of the <b>endocannabinoid</b> system.
+CNR1	drug	cannabinoid	19367507	With the identification of the selective <strong>CB1R</strong> antagonist, <b>rimonabant</b>, in 1994, and subsequently of other <strong>CB1R</strong> antagonists, there has been a rapid expansion of research investigating their ability to modulate the effects of the drugs of abuse.
+CNR1	drug	cannabinoid	19344705	In the same conditions, the <strong><b>cannabinoid</b> receptor 1</strong> (CB(1)) agonist, WIN55,212 2 (0.1 micromol/kg) reduced pain responses leading to a hypoalgesic state.
+CNR1	drug	cannabinoid	19335651	Gene association studies are presented for (a) genes posited to have specific influences on <b>cannabis</b> use disorders: <strong>CNR1</strong>, CB2, FAAH, MGLL, TRPV1 and GPR55 and (b) genes from various neurotransmitter systems that are likely to exert a non specific influence on risk of <b>cannabis</b> use disorders, e.g.
+CNR1	drug	cannabinoid	19231809	Excellent enrichment factors were obtained in both cases: For the <strong><b>cannabinoid</b> receptor 1</strong> (CB1), SeleX CS outperformed the best single score and afforded an enrichment factor of 41 at 1% of the screening library compared with the best single score value of 15 (GOLD_Fitness).
+CNR1	drug	cannabinoid	19188542	Positron emission tomography using fluorine 18 labeled MK 9470 now enables quantification of type 1 <b>cannabinoid</b> receptors (<strong>CB1R</strong>) in the brain.
+CNR1	addiction	relapse	19188542	Novelty <b>seeking</b> was inversely correlated with global <strong>CB1R</strong> availability (r =  0.33, P = .02), with the most significant correlation in the left amygdala (r =  0.41, P = .005).
+CNR1	addiction	relapse	19188542	Low baseline cerebral <strong>CB1R</strong> availability is related to a high novelty <b>seeking</b> personality, in particular to extravagance, most pronounced in the amygdala.
+CNR1	addiction	addiction	19188542	Further investigation of the functional role of the <strong>CB1R</strong> is warranted in pathological behavior known to be strongly related to novelty seeking, such as <b>addiction</b> and eating disorders.
+CNR1	addiction	relapse	19188542	Further investigation of the functional role of the <strong>CB1R</strong> is warranted in pathological behavior known to be strongly related to novelty <b>seeking</b>, such as addiction and eating disorders.
+CNR1	drug	cocaine	19052543	Interaction between two independent <strong>CNR1</strong> variants increases risk for <b>cocaine</b> dependence in European Americans: a replication study in family based sample and population based sample.
+CNR1	addiction	dependence	19052543	Interaction between two independent <strong>CNR1</strong> variants increases risk for cocaine <b>dependence</b> in European Americans: a replication study in family based sample and population based sample.
+CNR1	drug	cannabinoid	19052543	We recently reported that, in a European American (EA) sample, the interaction between two <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug dependence (DD), including cocaine dependence (CD).
+CNR1	drug	cocaine	19052543	We recently reported that, in a European American (EA) sample, the interaction between two cannabinoid receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug dependence (DD), including <b>cocaine</b> dependence (CD).
+CNR1	addiction	dependence	19052543	We recently reported that, in a European American (EA) sample, the interaction between two cannabinoid receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug <b>dependence</b> (DD), including cocaine <b>dependence</b> (CD).
+CNR1	drug	cannabinoid	19052543	We recently reported that, in a European American (EA) sample, the interaction between two <strong><b>cannabinoid</b> receptor 1</strong> gene (<strong>CNR1</strong>) variants significantly increased risk for drug dependence (DD), including cocaine dependence (CD).
+CNR1	drug	cocaine	19052543	We recently reported that, in a European American (EA) sample, the interaction between two <strong>cannabinoid receptor 1</strong> gene (<strong>CNR1</strong>) variants significantly increased risk for drug dependence (DD), including <b>cocaine</b> dependence (CD).
+CNR1	addiction	dependence	19052543	We recently reported that, in a European American (EA) sample, the interaction between two <strong>cannabinoid receptor 1</strong> gene (<strong>CNR1</strong>) variants significantly increased risk for drug <b>dependence</b> (DD), including cocaine <b>dependence</b> (CD).
+CNR1	drug	cannabinoid	19016476	Evidence for association between polymorphisms in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene and <b>cannabis</b> dependence.
+CNR1	addiction	dependence	19016476	Evidence for association between polymorphisms in the cannabinoid receptor 1 (<strong>CNR1</strong>) gene and cannabis <b>dependence</b>.
+CNR1	drug	cannabinoid	19016476	Evidence for association between polymorphisms in the <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) gene and <b>cannabis</b> dependence.
+CNR1	addiction	dependence	19016476	Evidence for association between polymorphisms in the <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) gene and cannabis <b>dependence</b>.
+CNR1	drug	cannabinoid	19016476	The <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) on chromosome 6q14 15 is an excellent candidate gene for <b>cannabis</b> dependence due to the important role of the G protein coupled receptor encoded by this gene in the rewarding effects of Delta9 <b>tetrahydrocannabinol</b>.
+CNR1	addiction	dependence	19016476	The cannabinoid receptor 1 gene (<strong>CNR1</strong>) on chromosome 6q14 15 is an excellent candidate gene for cannabis <b>dependence</b> due to the important role of the G protein coupled receptor encoded by this gene in the rewarding effects of Delta9 tetrahydrocannabinol.
+CNR1	drug	cannabinoid	19016476	The <strong><b>cannabinoid</b> receptor 1</strong> gene (<strong>CNR1</strong>) on chromosome 6q14 15 is an excellent candidate gene for <b>cannabis</b> dependence due to the important role of the G protein coupled receptor encoded by this gene in the rewarding effects of Delta9 <b>tetrahydrocannabinol</b>.
+CNR1	addiction	dependence	19016476	The <strong>cannabinoid receptor 1</strong> gene (<strong>CNR1</strong>) on chromosome 6q14 15 is an excellent candidate gene for cannabis <b>dependence</b> due to the important role of the G protein coupled receptor encoded by this gene in the rewarding effects of Delta9 tetrahydrocannabinol.
+CNR1	drug	cannabinoid	19016476	We investigate the association between 9 SNPs spanning <strong>CNR1</strong> and <b>cannabis</b> dependence in 1,923 individuals.
+CNR1	addiction	dependence	19016476	We investigate the association between 9 SNPs spanning <strong>CNR1</strong> and cannabis <b>dependence</b> in 1,923 individuals.
+CNR1	drug	cannabinoid	19016476	These results suggest a role for the <strong><b>cannabinoid</b> receptor 1</strong> gene in <b>cannabis</b> dependence.
+CNR1	addiction	dependence	19016476	These results suggest a role for the <strong>cannabinoid receptor 1</strong> gene in cannabis <b>dependence</b>.
+CNR1	drug	alcohol	18977415	These <b>alcohol</b> related behaviors are linked to differential changes in <strong>CNR1</strong> and NR1 subunit mRNA transcripts.
+CNR1	drug	cannabinoid	18977415	In conclusion, pharmacological inactivation of the glycine binding site of NMDA receptors may control <b>cannabinoid</b> induced relapse like drinking, which is associated with altered expression of <strong>CNR1</strong> and NR1 gene expression as observed after WIN treatment.
+CNR1	addiction	relapse	18977415	In conclusion, pharmacological inactivation of the glycine binding site of NMDA receptors may control cannabinoid induced <b>relapse</b> like drinking, which is associated with altered expression of <strong>CNR1</strong> and NR1 gene expression as observed after WIN treatment.
+CNR1	drug	cannabinoid	18782581	Systemic and intracranial administration of HU210, a <b>cannabinoid</b> <strong>CB1R</strong> agonist, into the nucleus accumbens core (NAC) and prelimbic cortex (PrC) reinstated MAP seeking behavior.
+CNR1	addiction	relapse	18782581	Systemic and intracranial administration of HU210, a cannabinoid <strong>CB1R</strong> agonist, into the nucleus accumbens core (NAC) and prelimbic cortex (PrC) reinstated MAP <b>seeking</b> behavior.
+CNR1	drug	cannabinoid	18782581	The reinstatement caused by the systemic HU210 treatment was attenuated by intracranial administration of AM251, a <b>cannabinoid</b> <strong>CB1R</strong> antagonist, into each region mentioned above.
+CNR1	addiction	relapse	18782581	The <b>reinstatement</b> caused by the systemic HU210 treatment was attenuated by intracranial administration of AM251, a cannabinoid <strong>CB1R</strong> antagonist, into each region mentioned above.
+CNR1	drug	cannabinoid	18705688	<b>Marijuana</b> withdrawal and craving: influence of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	addiction	relapse	18705688	Marijuana withdrawal and <b>craving</b>: influence of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	addiction	withdrawal	18705688	Marijuana <b>withdrawal</b> and craving: influence of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	drug	cannabinoid	18705688	<b>Marijuana</b> withdrawal and craving: influence of the <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	addiction	relapse	18705688	Marijuana withdrawal and <b>craving</b>: influence of the <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	addiction	withdrawal	18705688	Marijuana <b>withdrawal</b> and craving: influence of the <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	drug	cannabinoid	18705688	To examine whether withdrawal after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the <b>endocannabinoid</b> system, <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	addiction	relapse	18705688	To examine whether withdrawal after abstinence and cue elicited <b>craving</b> were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	addiction	withdrawal	18705688	To examine whether <b>withdrawal</b> after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	drug	cannabinoid	18705688	To examine whether withdrawal after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the <b>endocannabinoid</b> system, <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	addiction	relapse	18705688	To examine whether withdrawal after abstinence and cue elicited <b>craving</b> were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	addiction	withdrawal	18705688	To examine whether <b>withdrawal</b> after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	drug	cannabinoid	18705688	Two single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> (rs2023239) and FAAH (rs324420) genes, associated previously with substance abuse and functional changes in <b>cannabinoid</b> regulation, were examined in a sample of daily <b>marijuana</b> smokers.
+CNR1	drug	nicotine	18705688	Two single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> (rs2023239) and FAAH (rs324420) genes, associated previously with substance abuse and functional changes in cannabinoid regulation, were examined in a sample of daily marijuana <b>smokers</b>.
+CNR1	addiction	relapse	18705688	The <strong>CNR1</strong> SNP displayed a significant abstinence x genotype interaction on withdrawal, as well as a main effect on overall levels of <b>craving</b>, while the FAAH SNP displayed a significant abstinence x genotype interaction on <b>craving</b>.
+CNR1	addiction	withdrawal	18705688	The <strong>CNR1</strong> SNP displayed a significant abstinence x genotype interaction on <b>withdrawal</b>, as well as a main effect on overall levels of craving, while the FAAH SNP displayed a significant abstinence x genotype interaction on craving.
+CNR1	drug	cannabinoid	18640150	We examined open field effects in rats of the <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) agonist WIN55,212 2 (WIN; 3 mg/kg) and its interaction with the <strong>CB1R</strong> putative neutral antagonist AM4113 (0.3 to 3 mg/kg).
+CNR1	drug	cannabinoid	18640150	Unlike the <strong>CB1R</strong> antagonist <b>rimonabant</b>, in vitro (e.g., [Sink K.S., McLaughlin P.J., Wood J.A., Brown C., Fan P., Vemuri V.K., Pang Y., Olzewska T., Thakur G.A., Makriyannis A., Parker L.A., Salamone J.D.
+CNR1	drug	cannabinoid	18640150	Yet, unlike the inverse agonists <b>rimonabant</b> and AM251, the putative neutral <strong>CB1R</strong> antagonist AM4113 did not produce signs of nausea in ferrets and rats ([Chambers A.P., Vemuri V.K., Peng Y., Wood J.T., Olszewska T., Pittman Q.J., Makriyannis A., Sharkey K.A.
+CNR1	drug	alcohol	18606956	The incentive salience of <b>alcohol</b>: translating the effects of genetic variant in <strong>CNR1</strong>.
+CNR1	addiction	reward	18606956	The <b>incentive</b> salience of alcohol: translating the effects of genetic variant in <strong>CNR1</strong>.
+CNR1	drug	alcohol	18606956	The gene that codes for cannabinoid receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of <b>alcohol</b> dependence.
+CNR1	drug	cannabinoid	18606956	The gene that codes for <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of alcohol dependence.
+CNR1	addiction	dependence	18606956	The gene that codes for cannabinoid receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of alcohol <b>dependence</b>.
+CNR1	drug	alcohol	18606956	The gene that codes for <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of <b>alcohol</b> dependence.
+CNR1	drug	cannabinoid	18606956	The gene that codes for <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of alcohol dependence.
+CNR1	addiction	dependence	18606956	The gene that codes for <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of alcohol <b>dependence</b>.
+CNR1	drug	alcohol	18606956	To achieve a better understanding of the role of the <strong>CNR1</strong> gene in the etiology and treatment of <b>alcohol</b> dependence.
+CNR1	addiction	dependence	18606956	To achieve a better understanding of the role of the <strong>CNR1</strong> gene in the etiology and treatment of alcohol <b>dependence</b>.
+CNR1	drug	cannabinoid	18606954	<strong><b>Cannabinoid</b> receptor 1</strong> gene association with nicotine dependence.
+CNR1	drug	nicotine	18606954	<strong>Cannabinoid receptor 1</strong> gene association with <b>nicotine</b> dependence.
+CNR1	addiction	dependence	18606954	<strong>Cannabinoid receptor 1</strong> gene association with nicotine <b>dependence</b>.
+CNR1	drug	cannabinoid	18606954	The <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene is 1 of the 2 receptors expressed in the brain.
+CNR1	drug	nicotine	18606954	To test the hypothesis that the <strong>CNR1</strong> gene is associated with <b>nicotine</b> dependence.
+CNR1	addiction	dependence	18606954	To test the hypothesis that the <strong>CNR1</strong> gene is associated with nicotine <b>dependence</b>.
+CNR1	drug	nicotine	18606954	Variants and haplotypes in the <strong>CNR1</strong> gene may alter the risk for <b>nicotine</b> dependence, and the associations are likely sex specific.
+CNR1	addiction	dependence	18606954	Variants and haplotypes in the <strong>CNR1</strong> gene may alter the risk for nicotine <b>dependence</b>, and the associations are likely sex specific.
+CNR1	drug	cannabinoid	18579347	<b>Cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene: impact on antidepressant treatment response and emotion processing in major depression.
+CNR1	drug	cannabinoid	18579347	Therefore, the impact of <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) variants rs1049353 and rs12720071 on antidepressant treatment response was evaluated in 256 Caucasian patients with Major Depression.
+CNR1	addiction	reward	18579347	This analysis provides preliminary support for a role of <strong>CNR1</strong> gene variation in depression and anxiety, potentially mediated by subcortical hypo responsiveness to social <b>reward</b> stimuli.
+CNR1	drug	cannabinoid	18519829	For DSM IV <b>cannabis</b> dependence, a modest LOD score on chromosome 6 (1.42) near <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) was identified.
+CNR1	addiction	dependence	18519829	For DSM IV cannabis <b>dependence</b>, a modest LOD score on chromosome 6 (1.42) near cannabinoid receptor 1 (<strong>CNR1</strong>) was identified.
+CNR1	drug	cannabinoid	18519829	For DSM IV <b>cannabis</b> dependence, a modest LOD score on chromosome 6 (1.42) near <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CNR1</strong>) was identified.
+CNR1	addiction	dependence	18519829	For DSM IV cannabis <b>dependence</b>, a modest LOD score on chromosome 6 (1.42) near <strong>cannabinoid receptor 1</strong> (<strong>CNR1</strong>) was identified.
+CNR1	drug	cannabinoid	18519829	Genes such as ELTD1 on chromosome 1, in addition to genes on chromosomes 4 (eg, GABRA2) and 6 (eg, <strong>CNR1</strong>), may be associated with the genetic risk for <b>cannabis</b> use disorders.
+CNR1	drug	cannabinoid	18493584	<b>Cannabinoids</b>, the active components of <b>marijuana</b>, stimulate appetite, and <strong><b>cannabinoid</b> receptor 1</strong> (CB1 R) antagonists suppress appetite and promote weight loss.
+CNR1	drug	alcohol	18480689	<strong>Cannabinoid receptor 1</strong> blocker rimonabant (SR 141716) for treatment of <b>alcohol</b> dependence: results from a placebo controlled, double blind trial.
+CNR1	drug	cannabinoid	18480689	<strong><b>Cannabinoid</b> receptor 1</strong> blocker <b>rimonabant</b> (SR 141716) for treatment of alcohol dependence: results from a placebo controlled, double blind trial.
+CNR1	addiction	dependence	18480689	<strong>Cannabinoid receptor 1</strong> blocker rimonabant (SR 141716) for treatment of alcohol <b>dependence</b>: results from a placebo controlled, double blind trial.
+CNR1	drug	alcohol	18480689	In addition, in animal models, the <strong>cannabinoid receptor 1</strong> blocker rimonabant was found to decrease <b>alcohol</b> consumption, possibly by indirect modulation of dopaminergic neurotransmission.
+CNR1	drug	cannabinoid	18480689	In addition, in animal models, the <strong><b>cannabinoid</b> receptor 1</strong> blocker <b>rimonabant</b> was found to decrease alcohol consumption, possibly by indirect modulation of dopaminergic neurotransmission.
+CNR1	drug	alcohol	18480689	This was a 12 week double blind, placebo controlled, proof of concept study to assess the possible efficacy of the <strong>cannabinoid receptor 1</strong> antagonist rimonabant 20 mg/d (2 x 10 mg) in the prevention of relapse to <b>alcohol</b> in recently detoxified <b>alcohol</b> dependent patients.
+CNR1	drug	cannabinoid	18480689	This was a 12 week double blind, placebo controlled, proof of concept study to assess the possible efficacy of the <strong><b>cannabinoid</b> receptor 1</strong> antagonist <b>rimonabant</b> 20 mg/d (2 x 10 mg) in the prevention of relapse to alcohol in recently detoxified alcohol dependent patients.
+CNR1	addiction	relapse	18480689	This was a 12 week double blind, placebo controlled, proof of concept study to assess the possible efficacy of the <strong>cannabinoid receptor 1</strong> antagonist rimonabant 20 mg/d (2 x 10 mg) in the prevention of <b>relapse</b> to alcohol in recently detoxified alcohol dependent patients.
+CNR1	drug	alcohol	18446329	A major clinical concern with the use of <strong>cannabinoid receptor 1</strong> (CB1) direct agonists is that these compounds increase <b>alcohol</b> drinking and drug abuse related behaviours.
+CNR1	drug	cannabinoid	18446329	A major clinical concern with the use of <strong><b>cannabinoid</b> receptor 1</strong> (CB1) direct agonists is that these compounds increase alcohol drinking and drug abuse related behaviours.
+CNR1	drug	cannabinoid	18377702	We have shown that <b>cannabinoid</b> agonists lack reinforcing/rewarding properties in the intracranial self stimulation (ICSS) paradigm and that the CB1 receptor (<strong>CB1R</strong>) agonist WIN55,212 2 attenuates the reward facilitating actions of cocaine.
+CNR1	drug	cocaine	18377702	We have shown that cannabinoid agonists lack reinforcing/rewarding properties in the intracranial self stimulation (ICSS) paradigm and that the CB1 receptor (<strong>CB1R</strong>) agonist WIN55,212 2 attenuates the reward facilitating actions of <b>cocaine</b>.
+CNR1	addiction	reward	18377702	We have shown that cannabinoid agonists lack <b>reinforcing</b>/rewarding properties in the intracranial self stimulation (<b>ICSS</b>) paradigm and that the CB1 receptor (<strong>CB1R</strong>) agonist WIN55,212 2 attenuates the <b>reward</b> facilitating actions of cocaine.
+CNR1	drug	cocaine	18377702	AM 404 (10 mg/kg) attenuated this action of <b>cocaine</b>, an effect which was reversed by pretreatment with the selective <strong>CB1R</strong> antagonist SR141716A.
+CNR1	drug	cannabinoid	17979719	<b>Endocannabinoids</b> like anandamide and 2 arachidonoylglycerol bind and activate type 1 (<strong>CB1R</strong>) and type 2 (CB2R) <b>cannabinoid</b> receptors, two inhibitory G protein coupled receptors (GPCRs) that are localized in the central nervous system and in peripheral tissues.
+CNR1	drug	cannabinoid	17950256	Locomotion, body temperature, and anxiogenic like responses were evaluated after acute MDMA administration in CB(1) <strong><b>cannabinoid</b> receptor 1</strong> knockout mice.
+CNR1	drug	psychedelics	17950256	Locomotion, body temperature, and anxiogenic like responses were evaluated after acute <b>MDMA</b> administration in CB(1) <strong>cannabinoid receptor 1</strong> knockout mice.
+CNR1	drug	cannabinoid	17945506	Human studies show that <b>marijuana</b> dependence is frequently associated with cocaine dependence, and that the <b>cannabinoid</b> receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine addiction.
+CNR1	drug	cocaine	17945506	Human studies show that marijuana dependence is frequently associated with <b>cocaine</b> dependence, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to <b>cocaine</b> addiction.
+CNR1	addiction	addiction	17945506	Human studies show that marijuana dependence is frequently associated with cocaine dependence, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine <b>addiction</b>.
+CNR1	addiction	dependence	17945506	Human studies show that marijuana <b>dependence</b> is frequently associated with cocaine <b>dependence</b>, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine addiction.
+CNR1	drug	cannabinoid	17606273	At these synapses exogenous <strong><b>cannabinoid</b> receptor 1</strong> (CB1R) agonists reversibly inhibit excitatory transmission, and the sustained release of endogenous <b>cannabinoids</b> (eCB) following prolonged cortical stimulation leads to long term depression (LTD).
+CNR1	drug	cannabinoid	17606273	At these synapses exogenous <strong><b>cannabinoid</b> receptor 1</strong> (<strong>CB1R</strong>) agonists reversibly inhibit excitatory transmission, and the sustained release of endogenous <b>cannabinoids</b> (eCB) following prolonged cortical stimulation leads to long term depression (LTD).
+CNR1	drug	cannabinoid	17553010	Here we show that the <strong><b>cannabinoid</b> receptor 1</strong> (CB1) plays differential roles in acquisition, extinction and reconsolidation of conditioned taste aversion (CTA) memory in the rat insular cortex, which contains the taste cortex.
+CNR1	addiction	aversion	17553010	Here we show that the <strong>cannabinoid receptor 1</strong> (CB1) plays differential roles in acquisition, extinction and reconsolidation of conditioned taste <b>aversion</b> (<b>CTA</b>) memory in the rat insular cortex, which contains the taste cortex.
+CNR1	drug	alcohol	17509535	<strong>CNR1</strong> variation modulates risk for drug and <b>alcohol</b> dependence.
+CNR1	addiction	dependence	17509535	<strong>CNR1</strong> variation modulates risk for drug and alcohol <b>dependence</b>.
+CNR1	drug	cannabinoid	17509535	Human <b>cannabinoid</b> receptor 1 (CB1), which is encoded by the <strong>CNR1</strong> gene, may play a role in the development of substance dependence (SD).
+CNR1	addiction	dependence	17509535	Human cannabinoid receptor 1 (CB1), which is encoded by the <strong>CNR1</strong> gene, may play a role in the development of substance <b>dependence</b> (SD).
+CNR1	drug	cannabinoid	17509535	Human <strong><b>cannabinoid</b> receptor 1</strong> (CB1), which is encoded by the <strong>CNR1</strong> gene, may play a role in the development of substance dependence (SD).
+CNR1	addiction	dependence	17509535	Human <strong>cannabinoid receptor 1</strong> (CB1), which is encoded by the <strong>CNR1</strong> gene, may play a role in the development of substance <b>dependence</b> (SD).
+CNR1	drug	alcohol	17508995	Polymorphisms of the dopamine D4 receptor gene (DRD4 VNTR) and cannabinoid CB1 receptor gene (<strong>CNR1</strong>) are not strongly related to cue reactivity after <b>alcohol</b> exposure.
+CNR1	drug	cannabinoid	17508995	Polymorphisms of the dopamine D4 receptor gene (DRD4 VNTR) and <b>cannabinoid</b> CB1 receptor gene (<strong>CNR1</strong>) are not strongly related to cue reactivity after alcohol exposure.
+CNR1	drug	alcohol	17508995	Polymorphisms in the D4 dopamine receptor gene (DRD4) and the CB1 cannabinoid receptor gene (<strong>CNR1</strong>) have been associated with a differential response to <b>alcohol</b> after consumption.
+CNR1	drug	cannabinoid	17508995	Polymorphisms in the D4 dopamine receptor gene (DRD4) and the CB1 <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) have been associated with a differential response to alcohol after consumption.
+CNR1	drug	alcohol	17508995	As weekly <b>alcohol</b> consumption increased, the <strong>CNR1</strong> C allele group tended to report more craving for <b>alcohol</b> during the <b>alcohol</b> exposure than the T allele group.
+CNR1	addiction	relapse	17508995	As weekly alcohol consumption increased, the <strong>CNR1</strong> C allele group tended to report more <b>craving</b> for alcohol during the alcohol exposure than the T allele group.
+CNR1	drug	alcohol	17508995	The DRD4 and <strong>CNR1</strong> polymorphisms do not appear to strongly moderate cue reactivity after <b>alcohol</b> cue exposure, in male heavy drinkers.
+CNR1	drug	cannabinoid	17419755	This study examines the effect of intravenous self administration (SA) of either heroin or the <b>cannabinoid</b> receptor agonist WIN 55,212 2 on levels and functionality of mu opioid (MOR) and CB1 <b>cannabinoid</b> receptors (<strong>CB1R</strong>) in reward related brain areas, such as the prefrontal cortex (PFC), nucleus accumbens (NAc), caudate putamen (CP), hippocampus (Hippo), amygdala (Amy), hypothalamus (Hypo) and ventral tegmental area (VTA).
+CNR1	drug	opioid	17419755	This study examines the effect of intravenous self administration (SA) of either <b>heroin</b> or the cannabinoid receptor agonist WIN 55,212 2 on levels and functionality of mu <b>opioid</b> (MOR) and CB1 cannabinoid receptors (<strong>CB1R</strong>) in reward related brain areas, such as the prefrontal cortex (PFC), nucleus accumbens (NAc), caudate putamen (CP), hippocampus (Hippo), amygdala (Amy), hypothalamus (Hypo) and ventral tegmental area (VTA).
+CNR1	addiction	reward	17419755	This study examines the effect of intravenous self administration (SA) of either heroin or the cannabinoid receptor agonist WIN 55,212 2 on levels and functionality of mu opioid (MOR) and CB1 cannabinoid receptors (<strong>CB1R</strong>) in <b>reward</b> related brain areas, such as the prefrontal cortex (PFC), nucleus accumbens (NAc), caudate putamen (CP), hippocampus (Hippo), amygdala (Amy), hypothalamus (Hypo) and ventral tegmental area (VTA).
+CNR1	drug	opioid	17419755	With respect to control groups, which displayed very similar values, rats SA <b>heroin</b> showed increased MOR binding in the NAc (+174%), CP (+165%), Hippo (+121%), VTA (+175%), an enhanced <strong>CB1R</strong> density localized in the Amy (+147%) and VTA (+37%), and a widespread increased CB1 receptor functionality in the PFC (+95%), NAc (+313%), CP (+265%), Hippo (+38%), Amy (+221%).
+CNR1	drug	cannabinoid	17419755	In turn, <b>cannabinoid</b> SA differently modulates <strong>CB1R</strong> binding in the Amy (+47%), Hypo (+94%), Hippo ( 23%), VTA ( 15%), and increases MOR levels (PFC: +124%; NAc: +68%; CP: +80%; Hippo: +73%; Amy: +99%) and efficiency (Hippo: +518%; Amy: +173%; Hypo: +188%).
+CNR1	drug	cannabinoid	17401783	[<b>Endocannabinoid</b> system and <strong>CNR1</strong> gene polymorphisms in schizophrenia and addictive disorders].
+CNR1	addiction	addiction	17401783	[Endocannabinoid system and <strong>CNR1</strong> gene polymorphisms in schizophrenia and <b>addictive</b> disorders].
+CNR1	drug	cannabinoid	17386072	We measured the levels of <b>cannabinoid</b> 1 receptor (<strong>CB1R</strong>) protein (Western blot using a C terminal directed antibody), <strong>CB1R</strong> mRNA (real time RT PCR), <strong>CB1R</strong> localization (immunocytochemistry), tissue levels of the <b>endocannabinoids</b> N arachidonoylethanolamine/anandamide (AEA) and 2 arachidonoylglycerol (2 AG), and function (patch clamp recordings of depolarization induced suppression of inhibition (DSI), as well as effects of <strong>CB1R</strong> agonist WIN 55,212 2 on inhibitory currents) in the hippocampus of CIE rats and their saline treated controls.
+CNR1	drug	alcohol	17386072	The data further suggest that the effectiveness of <strong>CB1R</strong> blockade in decreasing <b>alcohol</b> consumption may be greater after protracted abstinence from <b>alcohol</b>.
+CNR1	drug	cannabinoid	16917946	<b>Cannabis</b> is a major substance of abuse, and the gene encoding for the central <b>cannabinoid</b> receptor (<strong>CNR1</strong>) is a logical candidate gene for vulnerability toward developing symptoms of <b>cannabis</b> dependence.
+CNR1	addiction	dependence	16917946	Cannabis is a major substance of abuse, and the gene encoding for the central cannabinoid receptor (<strong>CNR1</strong>) is a logical candidate gene for vulnerability toward developing symptoms of cannabis <b>dependence</b>.
+CNR1	drug	cannabinoid	16917946	We studied four single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> gene for association with having one or more symptoms of <b>cannabis</b> dependence in 541 adolescent subjects who had all tried <b>cannabis</b> five or more times.
+CNR1	addiction	dependence	16917946	We studied four single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> gene for association with having one or more symptoms of cannabis <b>dependence</b> in 541 adolescent subjects who had all tried cannabis five or more times.
+CNR1	drug	cannabinoid	16917946	Univariate (single marker) association tests demonstrated that SNP rs806380, located in intron 2 of the <strong>CNR1</strong> gene, was significantly associated with developing one or more <b>cannabis</b> dependence symptoms, with the G allele having a protective effect (P < 0.02).
+CNR1	addiction	dependence	16917946	Univariate (single marker) association tests demonstrated that SNP rs806380, located in intron 2 of the <strong>CNR1</strong> gene, was significantly associated with developing one or more cannabis <b>dependence</b> symptoms, with the G allele having a protective effect (P < 0.02).
+CNR1	drug	cannabinoid	16917946	Our findings provide evidence suggesting that a common <strong>CNR1</strong> haplotype is associated with developing fewer <b>cannabis</b> dependence symptoms among adolescents who have experimented with <b>cannabis</b>.
+CNR1	addiction	dependence	16917946	Our findings provide evidence suggesting that a common <strong>CNR1</strong> haplotype is associated with developing fewer cannabis <b>dependence</b> symptoms among adolescents who have experimented with cannabis.
+CNR1	drug	cannabinoid	16850116	WIN 55,212 2, a potent <strong><b>cannabinoid</b> receptor 1</strong> agonist, is self administered by animals to evaluate abuse liability of <b>cannabinoids</b>, but to date no information is yet available about its effects on dopaminergic transmission during active response contingent administration.
+CNR1	drug	cannabinoid	16788767	(AAT)n repeat in the <b>cannabinoid</b> receptor gene, <strong>CNR1</strong>: association with schizophrenia in a Spanish population.
+CNR1	drug	cannabinoid	16788767	The <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) has been associated with addictive disorders and schizophrenia in different studies.
+CNR1	addiction	addiction	16788767	The cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been associated with <b>addictive</b> disorders and schizophrenia in different studies.
+CNR1	drug	cannabinoid	16788767	The <strong><b>cannabinoid</b> receptor 1</strong> gene (<strong>CNR1</strong>) has been associated with addictive disorders and schizophrenia in different studies.
+CNR1	addiction	addiction	16788767	The <strong>cannabinoid receptor 1</strong> gene (<strong>CNR1</strong>) has been associated with <b>addictive</b> disorders and schizophrenia in different studies.
+CNR1	addiction	dependence	16741937	Association study of the <strong>CNR1</strong> gene exon 3 alternative promoter region polymorphisms and substance <b>dependence</b>.
+CNR1	drug	cannabinoid	16741937	An alternative promoter producing a novel 5' untranslated region of <b>cannabinoid</b> receptor mRNA has recently been described in <strong>CNR1</strong>, the gene encoding the <b>cannabinoid</b> receptor protein.
+CNR1	drug	alcohol	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., <b>alcohol</b>, cocaine, and opioids), as well as with polysubstance dependence.
+CNR1	drug	cocaine	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., alcohol, <b>cocaine</b>, and opioids), as well as with polysubstance dependence.
+CNR1	drug	opioid	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., alcohol, cocaine, and <b>opioids</b>), as well as with polysubstance dependence.
+CNR1	addiction	dependence	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance <b>dependence</b> diagnoses (i.e., alcohol, cocaine, and opioids), as well as with polysubstance <b>dependence</b>.
+CNR1	drug	cannabinoid	16723539	There is substantial evidence of cerebellar <strong>CB1R</strong> molecular adaptation and modifications in receptor signaling after prolonged <b>cannabinoid</b> exposure.
+CNR1	drug	cannabinoid	16723539	In <b>THC</b> tolerant mice, an increase of the basal release probability was found at PF PC synapses, in parallel with a facilitation of slow mGluR1 (metabotropic glutamate receptor type 1) mediated excitatory postsynaptic currents and a reduced sensitivity to the inhibitory effects of the <strong>CB1R</strong> agonist CP55,940 [( ) cis 3 [2 hydroxy 4 (1,1 dimethylheptyl)phenyl] trans 4 (3 hydroxypropyl)cyclohexanol].
+CNR1	drug	cannabinoid	16623851	Variations in the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene modulate striatal responses to happy faces.
+CNR1	drug	cannabinoid	16623851	The <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) is the best characterized molecule of the <b>endocannabinoid</b> system, involved in processing rewards.
+CNR1	addiction	reward	16623851	This suggests a role for the variations of the <strong>CNR1</strong> gene in underlying social <b>reward</b> responsivity.
+CNR1	drug	cannabinoid	16570102	These data clearly suggest that the observed beneficial effects of CB1 (<strong><b>cannabinoid</b> receptor 1</strong>) receptor antagonists on obesity may be related to the central <b>endocannabinoid</b> system.
+CNR1	drug	cannabinoid	16487916	This review discusses the role of <b>rimonabant</b>, a <strong><b>cannabinoid</b> receptor 1</strong> blocker, which has undergone Phase III clinical testing, in the treatment of obesity and tobacco dependence.
+CNR1	drug	nicotine	16487916	This review discusses the role of rimonabant, a <strong>cannabinoid receptor 1</strong> blocker, which has undergone Phase III clinical testing, in the treatment of obesity and <b>tobacco</b> dependence.
+CNR1	addiction	dependence	16487916	This review discusses the role of rimonabant, a <strong>cannabinoid receptor 1</strong> blocker, which has undergone Phase III clinical testing, in the treatment of obesity and tobacco <b>dependence</b>.
+CNR1	addiction	reward	16364907	Here, we show that depolarization of perifornical lateral hypothalamus (LH) neurons elicits a <strong>CB1R</strong> mediated suppression of inhibition in local circuits thought to be involved in appetite and "natural <b>reward</b>."
+CNR1	drug	cannabinoid	16354920	Using biochemical and electrophysiological approaches, we now report that 1 week of repeated in vivo <b>THC</b> treatment reduces the coupling efficiency of <b>cannabinoid</b> CB1 receptors (CB1Rs) to G(i/o) transduction proteins, as well as <strong>CB1R</strong> mediated inhibition of excitatory synaptic transmission at the excitatory synapses between the prefrontal cortex and the nucleus accumbens (NAc).
+CNR1	drug	cannabinoid	16314880	(AAT)n repeat in the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>): association with cocaine addiction in an African Caribbean population.
+CNR1	drug	cocaine	16314880	(AAT)n repeat in the cannabinoid receptor gene (<strong>CNR1</strong>): association with <b>cocaine</b> addiction in an African Caribbean population.
+CNR1	addiction	addiction	16314880	(AAT)n repeat in the cannabinoid receptor gene (<strong>CNR1</strong>): association with cocaine <b>addiction</b> in an African Caribbean population.
+CNR1	drug	cannabinoid	16314880	We examined the (AAT)n triplet repeat polymorphism nearby the <strong>CNR1</strong> gene, which encodes human <b>cannabinoid</b> (CB1) receptor, in a male Afro Caribbean population.
+CNR1	drug	cocaine	16314880	Our results support that the (AAT)n polymorphism nearby the <strong>CNR1</strong> gene could be associated with predisposition to <b>cocaine</b> dependency.
+CNR1	drug	cannabinoid	16301180	Here we show that LTD induction is blocked by a <b>cannabinoid</b> receptor (<strong>CB1R</strong>) antagonist, by inhibiting the synthesis of the <b>endocannabinoid</b> 2 arachidonyl glycerol (2 AG), and is absent in mice lacking the <strong>CB1R</strong>.
+CNR1	drug	cannabinoid	16148435	Current evidence supporting a role of <b>cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) antagonists as potential pharmacotherapies for drug abuse disorders.
+CNR1	drug	cannabinoid	16148435	Since the discovery of the <b>cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) in 1988, and subsequently of the CB2 receptor (CB2R) in 1993, there has been an exponential growth of research investigating the functions of the <b>endocannabinoid</b> system.
+CNR1	drug	cannabinoid	16148435	With the identification of the selective <strong>CB1R</strong> antagonist, <b>SR141716</b>, in 1994, and its subsequent widespread availability, there has been a rapid expansion of research investigating its ability to modulate the effects of drugs of abuse.
+CNR1	drug	cannabinoid	16148435	This report critically reviews preclinical and clinical studies involving the ability of <strong>CB1R</strong> antagonists to attenuate the effects of drugs of abuse, while providing an overview of the neuroanatomical and neurochemical points of contact between the <b>endocannabinoid</b> system and systems mediating abuse related effects.
+CNR1	drug	cannabinoid	15740726	To this end, male <b>cannabinoid</b> CB1 receptor deficient mice (<strong>CB1R</strong> / ) and their wild type littermate controls (<strong>CB1R</strong>+/+) were trained in an appetitively motivated operant conditioning task, in which food deprived animals received a food reward on nose poking into an illuminated hole.
+CNR1	addiction	reward	15740726	To this end, male cannabinoid CB1 receptor deficient mice (<strong>CB1R</strong> / ) and their wild type littermate controls (<strong>CB1R</strong>+/+) were trained in an appetitively motivated <b>operant</b> conditioning task, in which food deprived animals received a food <b>reward</b> on nose poking into an illuminated hole.
+CNR1	drug	cocaine	15295029	Both <strong>CB1R</strong> and mGluR5 are involved in <b>cocaine</b> related behaviors; however, the impact of in vivo <b>cocaine</b> exposure on eCB mediated retrograde synaptic plasticity remains unknown.
+CNR1	drug	cannabinoid	15289816	Human <strong><b>cannabinoid</b> receptor 1</strong>: 5' exons, candidate regulatory regions, polymorphisms, haplotypes and association with polysubstance abuse.
+CNR1	addiction	addiction	15289816	A number of lines of evidence make the gene that encodes the G protein coupled CB1/<strong>Cnr1</strong> receptor a strong candidate to harbor variants that might contribute to individual differences in human <b>addiction</b> vulnerability.
+CNR1	drug	cannabinoid	15289816	The CB1/<strong>Cnr1</strong> receptor is the major brain site at which <b>cannabinoid</b> <b>marijuana</b> constituents are psychoactive as well as the principal brain receptor for endogenous anandamide ligands.
+CNR1	addiction	addiction	15289816	CB1/ <strong>Cnr1</strong> genomic variation thus appears to play roles in human <b>addiction</b> vulnerability.
+CNR1	drug	cannabinoid	14969571	Animal studies provide promising evidence for the use of <strong><b>cannabinoid</b> receptor 1</strong> agonists, by showing potent inhibition of TLOSRs in the dog, thus opening a new route for clinical investigation in humans.
+CNR1	drug	cannabinoid	14724049	<b>Cannabinoid</b> CB1 receptor (<strong>CB1R</strong>) inverse agonists reduce appetite and body weight (BW) gain in various species.
+CNR1	drug	alcohol	14714115	The aim of this study is to test the potential influence of a bi allelic cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe <b>alcohol</b> withdrawal syndromes.
+CNR1	drug	cannabinoid	14714115	The aim of this study is to test the potential influence of a bi allelic <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe alcohol withdrawal syndromes.
+CNR1	addiction	withdrawal	14714115	The aim of this study is to test the potential influence of a bi allelic cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe alcohol <b>withdrawal</b> syndromes.
+CNR1	drug	alcohol	14714115	After correcting for multiple testing, no association of the A  or G allele of <strong>CNR1</strong> polymorphism with a history of <b>alcohol</b> withdrawal induced seizures was detected.
+CNR1	addiction	withdrawal	14714115	After correcting for multiple testing, no association of the A  or G allele of <strong>CNR1</strong> polymorphism with a history of alcohol <b>withdrawal</b> induced seizures was detected.
+CNR1	drug	alcohol	12657705	Furthermore, foot shock stress had no affect on <b>alcohol</b> preference in <strong>Cnr1</strong> /  mice, although it induced a dramatic increase in <strong>Cnr1</strong>+/+ animals.
+CNR1	drug	alcohol	12538878	Endocannabinoid signaling via <strong>cannabinoid receptor 1</strong> is involved in <b>ethanol</b> preference and its age dependent decline in mice.
+CNR1	drug	cannabinoid	12538878	<b>Endocannabinoid</b> signaling via <strong><b>cannabinoid</b> receptor 1</strong> is involved in ethanol preference and its age dependent decline in mice.
+CNR1	drug	alcohol	12538878	The high <b>ethanol</b> preference of young (6 10 weeks) C57BL6J mice is reduced by the <strong>cannabinoid receptor 1</strong> (CB1) antagonist SR141716A to levels observed in their CB1 knockout littermates or in old (26 48 weeks) wild type mice, in both of which <b>ethanol</b> preference is unaffected by SR141716A.
+CNR1	drug	cannabinoid	12538878	The high ethanol preference of young (6 10 weeks) C57BL6J mice is reduced by the <strong><b>cannabinoid</b> receptor 1</strong> (CB1) antagonist SR141716A to levels observed in their CB1 knockout littermates or in old (26 48 weeks) wild type mice, in both of which ethanol preference is unaffected by SR141716A.
+CNR1	drug	cannabinoid	12152079	The <strong><b>cannabinoid</b> receptor 1</strong> (CB1) and <b>endocannabinoids</b> are present in memory related brain areas and modulate memory.
+CNR1	drug	alcohol	11841893	Association of a CB1 cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism with severe <b>alcohol</b> dependence.
+CNR1	drug	cannabinoid	11841893	Association of a CB1 <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism with severe alcohol dependence.
+CNR1	addiction	dependence	11841893	Association of a CB1 cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism with severe alcohol <b>dependence</b>.
+CNR1	drug	alcohol	11841893	Due to the involvement of the endogenous cannabinoid system in brain reward mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human cannabinoid receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian <b>alcoholics</b> and 136 most likely non <b>alcoholic</b> controls.
+CNR1	drug	cannabinoid	11841893	Due to the involvement of the endogenous <b>cannabinoid</b> system in brain reward mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian alcoholics and 136 most likely non alcoholic controls.
+CNR1	addiction	reward	11841893	Due to the involvement of the endogenous cannabinoid system in brain <b>reward</b> mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human cannabinoid receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian alcoholics and 136 most likely non alcoholic controls.
+CNR1	drug	alcohol	11841893	This finding suggests that the homozygous genotype <strong>CNR1</strong> 1359A/A confers vulnerability to <b>alcohol</b> withdrawal delirium.
+CNR1	addiction	withdrawal	11841893	This finding suggests that the homozygous genotype <strong>CNR1</strong> 1359A/A confers vulnerability to alcohol <b>withdrawal</b> delirium.
+CNR1	drug	cannabinoid	11605080	We tested the effects of five doses of the <strong><b>cannabinoid</b> receptor 1</strong> (CB1) antagonist <b>SR141716</b> [0, 0.3, 1, 3 and 10 mg/kg intraperitoneal (IP)] on intracranial self stimulation at the level of the median forebrain bundle (MFB).
+CNR1	drug	cannabinoid	11526463	Association study of <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) alleles and drug dependence.
+CNR1	addiction	dependence	11526463	Association study of cannabinoid receptor gene (<strong>CNR1</strong>) alleles and drug <b>dependence</b>.
+CNR1	drug	cannabinoid	11457579	The reinforcing properties of the <b>cannabinoid</b> agonist were fully antagonised by pretreatment with the brain <strong><b>cannabinoid</b> receptor 1</strong> (CB(1)) antagonist, [N piperidino 5 (4 chlorophenyl) 1 (2,4 dichloro phenyl) 4 methyl pyrazole 3 carboxamide hydrochloride] (SR 141716A) and naloxone.
+CNR1	drug	opioid	11457579	The reinforcing properties of the cannabinoid agonist were fully antagonised by pretreatment with the brain <strong>cannabinoid receptor 1</strong> (CB(1)) antagonist, [N piperidino 5 (4 chlorophenyl) 1 (2,4 dichloro phenyl) 4 methyl pyrazole 3 carboxamide hydrochloride] (SR 141716A) and <b>naloxone</b>.
+CNR1	addiction	reward	11457579	The <b>reinforcing</b> properties of the cannabinoid agonist were fully antagonised by pretreatment with the brain <strong>cannabinoid receptor 1</strong> (CB(1)) antagonist, [N piperidino 5 (4 chlorophenyl) 1 (2,4 dichloro phenyl) 4 methyl pyrazole 3 carboxamide hydrochloride] (SR 141716A) and naloxone.
+CNR1	drug	cannabinoid	11341859	The <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) is not affected in German i.v.
+CNR1	drug	cannabinoid	11341859	The aim of the study was to investigate a possible contribution of the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) to the development of i.v.
+CNR1	drug	cannabinoid	10441206	A frequent polymorphism in the coding exon of the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene.
+CNR1	drug	cannabinoid	10441206	The cloning of the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene facilitates molecular genetic studies in disorders like Gilles de la Tourette syndrome (GTS), obsessive compulsive disorder (OCD), Parkinsons disease, Alzheimers disease or other neuro psychiatric or neurological diseases, which may be predisposed or influenced by mutations or variants in the <strong>CNR1</strong> gene.
+CNR1	addiction	addiction	10441206	The cloning of the human cannabinoid receptor (<strong>CNR1</strong>) gene facilitates molecular genetic studies in disorders like Gilles de la Tourette syndrome (GTS), obsessive <b>compulsive</b> disorder (OCD), Parkinsons disease, Alzheimers disease or other neuro psychiatric or neurological diseases, which may be predisposed or influenced by mutations or variants in the <strong>CNR1</strong> gene.
+CNR1	drug	cannabinoid	9106243	Association between the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) and the P300 event related potential.
+CNR1	drug	cannabinoid	9106243	In our prior study we observed a significant association between homozygosity for the > or = alleles of a microsatellite polymorphism of <b>cannabinoid</b> receptor genes (<strong>CNR1</strong>) and drug dependence.
+CNR1	addiction	dependence	9106243	In our prior study we observed a significant association between homozygosity for the > or = alleles of a microsatellite polymorphism of cannabinoid receptor genes (<strong>CNR1</strong>) and drug <b>dependence</b>.
+CNR1	drug	alcohol	9106243	Since marijuana intoxication has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 <b>alcohol</b> and drug addicts, by MANOVA.
+CNR1	drug	cannabinoid	9106243	Since <b>marijuana</b> intoxication has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 alcohol and drug addicts, by MANOVA.
+CNR1	addiction	intoxication	9106243	Since marijuana <b>intoxication</b> has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 alcohol and drug addicts, by MANOVA.
+CNR1	drug	cannabinoid	9106242	<b>Cannabinoid</b> receptor gene (<strong>CNR1</strong>): association with i.v.
+CNR1	drug	cannabinoid	9106242	A microsatellite polymorphism (AAT)n at the <b>cannabinoid</b> CB1 (brain) receptor gene (<strong>CNR1</strong>) consists of 9 alleles.
+CNR1	drug	alcohol	9106242	Since the cannabinoid system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to <b>alcohol</b> or drug dependence.
+CNR1	drug	cannabinoid	9106242	Since the <b>cannabinoid</b> system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug dependence.
+CNR1	addiction	dependence	9106242	Since the cannabinoid system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug <b>dependence</b>.
+CNR1	addiction	reward	9106242	Since the cannabinoid system is part of the <b>reward</b> pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug dependence.
+FAM3B	drug	opioid	28799847	Results showed positive willingness to use a SIF was independently associated with use of <b>heroin</b> as main substance (odds ratio [OR]: 5.47; 95% confidence interval [CI]: 1.9 15.4; P = .0004), public injection (OR: 5.09; 95% CI: 1.8 14.3; P = .002), history of seeking substance use disorder (SUD) treatment (OR: 4.99; 95% CI: 1.<strong>2 21</strong>.1; P = .05), having heard of SIF (OR: 4.80; 95% CI: 1.6 14.8; P = .004), Hispanic ethnicity (OR: 4.22; 95% CI: 0.9 18.8; P = .04), frequent NEP use (OR: 4.18; 95% CI: 1.2 14.7; P = .02), current desire for SUD treatment (OR: 4.15; 95% CI: 1.2 14.7; P = .03), hepatitis C diagnosis (OR: 3.68; 95% CI: 1.2 10.1; P = .02), posttraumatic stress disorder (PTSD) diagnosis (OR: 3.27; 95% CI: 1.3 8.4; P = .01), report of at least 1 chronic medical diagnosis (hepatitis C, human immunodeficiency virus [HIV], hypertension, or diabetes) (OR: 3.27; 95% CI: 1.2 8.9; P = .02), and comorbid medical and mental health diagnoses (OR: 2.93; 95% CI: 1.2 7.4; P = .02).
+FAM3B	addiction	relapse	28799847	Results showed positive willingness to use a SIF was independently associated with use of heroin as main substance (odds ratio [OR]: 5.47; 95% confidence interval [CI]: 1.9 15.4; P = .0004), public injection (OR: 5.09; 95% CI: 1.8 14.3; P = .002), history of <b>seeking</b> substance use disorder (SUD) treatment (OR: 4.99; 95% CI: 1.<strong>2 21</strong>.1; P = .05), having heard of SIF (OR: 4.80; 95% CI: 1.6 14.8; P = .004), Hispanic ethnicity (OR: 4.22; 95% CI: 0.9 18.8; P = .04), frequent NEP use (OR: 4.18; 95% CI: 1.2 14.7; P = .02), current desire for SUD treatment (OR: 4.15; 95% CI: 1.2 14.7; P = .03), hepatitis C diagnosis (OR: 3.68; 95% CI: 1.2 10.1; P = .02), posttraumatic stress disorder (PTSD) diagnosis (OR: 3.27; 95% CI: 1.3 8.4; P = .01), report of at least 1 chronic medical diagnosis (hepatitis C, human immunodeficiency virus [HIV], hypertension, or diabetes) (OR: 3.27; 95% CI: 1.2 8.9; P = .02), and comorbid medical and mental health diagnoses (OR: 2.93; 95% CI: 1.2 7.4; P = .02).
+FAM3B	drug	nicotine	23901338	The multivariate model showed that anemia (AOR: 19.8, 95% CI: 5.6 35.5), positive sputum smear (AOR: 13.4, 95% CI: 6.8 33.6), <b>smoking</b> (AOR: 12.9, 95% CI: 3.9 27.3), drug hepatitis (AOR: 12.3, 95% CI: 6.7 24.7), diabetes mellitus (AOR: 9.7, 95% CI: 2.9 32.0), drug use (AOR: 7.8, 95% CI: 2.4 25.5), and history of previous TB (AOR: 6.8, 95% CI: 2.<strong>2 21</strong>.3) were major risk factors for death in TB patients.
+FAM3B	drug	alcohol	8679015	Multivariate analysis showed a strong relationship between a parental history of <b>alcoholism</b> and the presence of a neuropathy, when the severity of the <b>alcoholic</b> disease was taken into account (adjusted OR = 6.8, IC95% [2.<strong>2 21</strong>.6], P < 0.001).
+FAM3B	drug	opioid	8451267	Two parallel experiments in rats <strong>2 21</strong> days of age investigated the onset and characteristics of <b>morphine</b> induced antinociception.
+FAM3B	drug	opioid	4040881	The dose of <b>morphine</b> to produce equi analgesia increased <strong>2 21</strong>.8 times during 1 8 days treatment with <b>morphine</b> in S rat.
+JUN	drug	alcohol	31262967	Hepatic phospho extracellular signal regulated kinase 1/2 and phosph p38 mitogen activated protein kinase levels were lower in females compared with males after binge <b>alcohol</b>, but no differences were found in the phospho C <strong>jun</strong> N terminal kinase levels.
+JUN	addiction	intoxication	31262967	Hepatic phospho extracellular signal regulated kinase 1/2 and phosph p38 mitogen activated protein kinase levels were lower in females compared with males after <b>binge</b> alcohol, but no differences were found in the phospho C <strong>jun</strong> N terminal kinase levels.
+JUN	drug	alcohol	30321699	Dysregulation of c <strong>Jun</strong> N terminal kinase phosphorylation in <b>alcohol</b> dependence.
+JUN	addiction	dependence	30321699	Dysregulation of c <strong>Jun</strong> N terminal kinase phosphorylation in alcohol <b>dependence</b>.
+JUN	drug	alcohol	30321699	As a key negative regulator of GR mediated signaling, the current study first measured c <strong>Jun</strong> N terminal kinase (JNK) phosphorylation in animals following an acute <b>alcohol</b> challenge.
+JUN	drug	opioid	29916183	Chronic <b>morphine</b> pretreatment alone elevated both c <strong>Jun</strong> protein and miR 139 5p expression levels, while dramatically artificial elevation of miR 139 5p inhibited c <strong>Jun</strong> at the translational level.
+JUN	drug	opioid	29916183	These findings suggested that miR 139 5p was involved in regulating chronic <b>morphine</b> induced, <b>naloxone</b> precipitated cAMP overshoot in a negative feedback manner through its target c <strong>Jun</strong>, which extends our understanding of neurobiological mechanisms underlying <b>morphine</b> dependence and addiction.
+JUN	addiction	addiction	29916183	These findings suggested that miR 139 5p was involved in regulating chronic morphine induced, naloxone precipitated cAMP overshoot in a negative feedback manner through its target c <strong>Jun</strong>, which extends our understanding of neurobiological mechanisms underlying morphine dependence and <b>addiction</b>.
+JUN	addiction	dependence	29916183	These findings suggested that miR 139 5p was involved in regulating chronic morphine induced, naloxone precipitated cAMP overshoot in a negative feedback manner through its target c <strong>Jun</strong>, which extends our understanding of neurobiological mechanisms underlying morphine <b>dependence</b> and addiction.
+JUN	drug	alcohol	29863389	Reports an error in "Initiation and retention in couples outpatient treatment for parents with drug and <b>alcohol</b> use disorders" by Abby L. Braitman and Michelle L. Kelley (Experimental and Clinical Psychopharmacology, 2016[<strong>Jun</strong>], Vol 24[3], 174 184).
+JUN	drug	alcohol	29404485	Furthermore, cell death rates were elevated when primary hepatocytes or human hepatoma cells were exposed to EVs from <b>alcohol</b> exposed rodents and patients with <b>alcoholism</b>, demonstrating that EVs from <b>alcohol</b> exposed rats and patients with <b>alcoholism</b> are functional and can promote cell death by activating the apoptosis signaling pathway, including phospho c <strong>Jun</strong> N terminal kinase, proapoptotic Bax, and activated caspase 3.
+JUN	drug	cocaine	28710498	In particular, we identified an <strong>AP 1</strong> regulated transcriptional network in dlPFC neurons associated with <b>cocaine</b> use disorder that contains several differentially expressed hub genes.
+JUN	drug	alcohol	28466267	A single subcutaneous injection of <b>ethanol</b> induced oxidative stress triggered phospho c <strong>jun</strong> N terminal kinase (p JNK) and phospho mammalian target of rapamycin (p mTOR) accompanied by neuroinflammation and widespread neurodegeneration.
+JUN	drug	alcohol	28369910	In addition, we found that <b>ethanol</b> induced autophagy and cardiac injury largely via the sequential triggering of reactive oxygen species (ROS) accumulation, activation of c <strong>Jun</strong> NH2 terminal kinase (JNK), phosphorylation of Bcl 2, and dissociation of the Beclin 1/Bcl 2 complex.
+JUN	drug	opioid	27495086	We first measured the transcript level of 13 genes (RASA1, PRKCB, PDK1, <strong>JUN</strong>, CEBPG, CD74, CEBPB, AUTS2, ENO2, IMPDH2, HAT1, MBD1, and RGS3) in lymphoblastoid cell lines in a sample of 124 male <b>heroin</b> addicts and 124 male control subjects using real time quantitative PCR.
+JUN	drug	opioid	27495086	Further analysis using 3 statistical methods including logistic regression analysis, support vector machine learning analysis, and a computer software BIASLESS revealed that a set of 4 genes (<strong>JUN</strong>, CEBPB, PRKCB, ENO2, or CEBPG) could predict the diagnosis of <b>heroin</b> addiction with the accuracy rate around 85% in our dataset.
+JUN	addiction	addiction	27495086	Further analysis using 3 statistical methods including logistic regression analysis, support vector machine learning analysis, and a computer software BIASLESS revealed that a set of 4 genes (<strong>JUN</strong>, CEBPB, PRKCB, ENO2, or CEBPG) could predict the diagnosis of heroin <b>addiction</b> with the accuracy rate around 85% in our dataset.
+JUN	addiction	withdrawal	27430907	Extracellular signal regulated kinase (ERK), but neither p38 nor c <strong>Jun</strong> N terminal kinase (JNK), was activated by budesonide <b>withdrawal</b>, and the activation was blocked by Pinellia ternata treatment.
+JUN	drug	alcohol	27278235	We have previously shown that PS1 interacts with a mitogen activated protein kinase [(MAPK) <strong>jun</strong> NH2 terminal kinase], and another MAPK (p38) is activated by <b>ethanol</b> withdrawal (EW), abrupt termination from chronic <b>ethanol</b> exposure.
+JUN	addiction	withdrawal	27278235	We have previously shown that PS1 interacts with a mitogen activated protein kinase [(MAPK) <strong>jun</strong> NH2 terminal kinase], and another MAPK (p38) is activated by ethanol <b>withdrawal</b> (EW), abrupt termination from chronic ethanol exposure.
+JUN	drug	nicotine	27235579	c <strong>Jun</strong> N terminal kinase 1 is necessary for <b>nicotine</b> induced enhancement of contextual fear conditioning.
+JUN	drug	nicotine	27235579	The effects of <b>nicotine</b> on learning may involve recruitment of signaling through the c <strong>Jun</strong> N terminal kinase family (JNK 1 3).
+JUN	drug	nicotine	26687895	Hippocampal kinases such as cAMP dependent protein kinase (PKA), calcium/calmodulin dependent protein kinases (CAMKs), extracellular signal regulated kinases 1 and 2 (ERK1/2), and c <strong>jun</strong> N terminal kinase 1 (JNK1), and the transcription factor cAMP response element binding protein (CREB) that are activated either directly or indirectly by <b>nicotine</b> may modulate hippocampal plasticity and in parallel hippocampus dependent learning and memory.
+JUN	drug	opioid	26339395	The overall objective of this study was to investigate neuronal apoptosis and expression of apoptosis related proteins (c <strong>jun</strong>, cytc and Bax) in the cerebellum of rates with <b>heroin</b> addiction.
+JUN	addiction	addiction	26339395	The overall objective of this study was to investigate neuronal apoptosis and expression of apoptosis related proteins (c <strong>jun</strong>, cytc and Bax) in the cerebellum of rates with heroin <b>addiction</b>.
+JUN	drug	opioid	26339395	Compared with the control group, the proportion of apoptotic neurons increased significantly in the <b>heroin</b> addiction groups (10 d, 20 d, 30 d, 40 d) (P < 0.05), also accompanied by markedly increased expressions of c <strong>jun</strong>, cytc and Bax (P < 0.05) depending on doses of <b>heroin</b> in the cerebellum.
+JUN	addiction	addiction	26339395	Compared with the control group, the proportion of apoptotic neurons increased significantly in the heroin <b>addiction</b> groups (10 d, 20 d, 30 d, 40 d) (P < 0.05), also accompanied by markedly increased expressions of c <strong>jun</strong>, cytc and Bax (P < 0.05) depending on doses of heroin in the cerebellum.
+JUN	drug	opioid	26339395	Long term use of <b>heroin</b> may induce neuronal apoptosis in the cerebellum by raising the expressions of pro apoptotic c <strong>jun</strong>, cytc and Bax, which might be one of mechanisms underlying the <b>heroin</b> induced cerebellum neuronal damage.
+JUN	drug	alcohol	26219600	As such, <b>acamprosate</b> mediated reduction of calpain activity resulted in decreased degradation of p35, increased abundance of the pro survival factor STAT6, and reduced N terminal <strong>Jun</strong> kinase activation.
+JUN	drug	opioid	26165762	Inhibition of spinal ERK1/2 c <strong>JUN</strong> signaling pathway counteracts the development of low doses <b>morphine</b> induced hyperalgesia.
+JUN	drug	opioid	26165762	<b>Morphine</b> exposure increased phosphorylation of c <strong>JUN</strong>, that was prevented by the inhibition of ERK pathway.
+JUN	drug	opioid	26165762	These data suggest that ERK contributes to the <b>morphine</b> induced hyperalgesia by regulating the activation of c <strong>JUN</strong>.
+JUN	drug	opioid	25848832	<b>Heroin</b> activates ATF3 and CytC via c <strong>Jun</strong> N terminal kinase pathways to mediate neuronal apoptosis.
+JUN	drug	opioid	25848832	RESULTS We found that <b>heroin</b> induces the apoptosis of primary cultured cerebellar granule cells (CGCS) and that the c <strong>Jun</strong> N terminal kinase (JNK) pathway was activated under <b>heroin</b> treatment and stimulated obvious increases in the levels of C <strong>jun</strong>, Cytc, and ATF3mRNA.
+JUN	drug	opioid	25848832	The results suggested that SP600125 of JNK/C <strong>jun</strong> can inhibit <b>heroin</b> induced apoptosis of neurons.
+JUN	drug	opioid	25806604	<b>Morphine</b> elevated spinal JNK1, JNK2, and c <strong>Jun</strong> phosphorylation.
+JUN	drug	opioid	25806604	Pretreatment with a PKC inhibitor prevented <b>morphine</b> hyperalgesia and JNK and c <strong>Jun</strong> overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by <b>morphine</b>.
+JUN	drug	alcohol	25666017	Sustained c <strong>Jun</strong> N terminal kinase (JNK) activation by saturated fatty acids plays a role in lipotoxicity and the pathogenesis of non <b>alcoholic</b> steatohepatitis (NASH).
+JUN	drug	cocaine	25658879	On the other hand, chemokine C C motif ligand 2 and <strong>jun</strong> proto oncogene expression were unaffected in <b>cocaine</b> abusing subjects dying of gunshot wounds, in contrast to the differential expression previously reported in <b>cocaine</b> related fatalities.
+JUN	drug	nicotine	25637801	<b>Nicotine</b> stimulated expression of the pro inflammatory signal transduction proteins phosphorylated extracellular signal regulated kinase (p ERK), phosphorylated c <strong>Jun</strong> N terminal kinase (p JNK), and protein kinase A (PKA) in the spinal trigeminal nucleus.
+JUN	drug	nicotine	25430056	Both cFos and phosphorylated <strong>cJun</strong> (p <strong>cJun</strong>) were immediately increased in the nucleus, together with an increase of calmodulin kinase (CaMK) IV but not CaMKII expression after <b>nicotine</b> exposure.
+JUN	drug	nicotine	25430056	Both cFos and phosphorylated <strong><strong>cJun</strong></strong> (p <strong><strong>cJun</strong></strong>) were immediately increased in the nucleus, together with an increase of calmodulin kinase (CaMK) IV but not CaMKII expression after <b>nicotine</b> exposure.
+JUN	drug	nicotine	25430056	A nonselective inhibitor of CaMKs, KN 93, and a calcium chelating regent, BAPTA AM, completely suppressed the expression of cFos and p <strong>cJun</strong> in the nucleus as well as the <b>nicotine</b> induced IP3 R 1 upregulation.
+JUN	drug	nicotine	25430056	A nonselective inhibitor of CaMKs, KN 93, and a calcium chelating regent, BAPTA AM, completely suppressed the expression of cFos and p <strong><strong>cJun</strong></strong> in the nucleus as well as the <b>nicotine</b> induced IP3 R 1 upregulation.
+JUN	drug	nicotine	25430056	These results indicate that nAChR activation by <b>nicotine</b> upregulates IP3 R 1 via increase of activator protein 1, which is a cFos and <strong>cJun</strong> dimmer, in the nucleus, with activation of Ca(2+) signaling transduction processes.
+JUN	drug	nicotine	25430056	These results indicate that nAChR activation by <b>nicotine</b> upregulates IP3 R 1 via increase of activator protein 1, which is a cFos and <strong><strong>cJun</strong></strong> dimmer, in the nucleus, with activation of Ca(2+) signaling transduction processes.
+JUN	drug	opioid	25134609	An <strong>jun</strong> ning, a traditional herbal formula, attenuates spontaneous withdrawal symptoms via modulation of the dopamine system in <b>morphine</b> dependent rats.
+JUN	addiction	withdrawal	25134609	An <strong>jun</strong> ning, a traditional herbal formula, attenuates spontaneous <b>withdrawal</b> symptoms via modulation of the dopamine system in morphine dependent rats.
+JUN	drug	opioid	25134609	This study aimed to investigate the effects of An <strong>jun</strong> ning (AJN), a commercial traditional Chinese medicine formula used for the treatment of <b>opioid</b> addiction, on the dopamine system in <b>morphine</b> dependent rats and to explore the possible mechanism underlying its therapeutic effects.
+JUN	addiction	addiction	25134609	This study aimed to investigate the effects of An <strong>jun</strong> ning (AJN), a commercial traditional Chinese medicine formula used for the treatment of opioid <b>addiction</b>, on the dopamine system in morphine dependent rats and to explore the possible mechanism underlying its therapeutic effects.
+JUN	drug	alcohol	25126745	Herein, we examined whether the decrease in IFN γ is resulted from altered expression of miRNA155 and transcription factors  NFAT, Tbx21, <strong>Jun</strong> and Fos  in T cells following <b>ethanol</b> and burn injury.
+JUN	drug	alcohol	25126745	We observed a significant decrease in miRNA155, NFAT, Tbx21, <strong>Jun</strong> and Fos expression as well as IFN γ release in T cells cultured with anti CD3 following <b>ethanol</b> and burn injury compared with shams.
+JUN	drug	cocaine	24970755	The inhibition of c <strong>Jun</strong> N terminal kinase (JNK) also attenuated the renewed <b>cocaine</b> challenge induced increase in BiP expression.
+JUN	drug	opioid	24950452	<b>Morphine</b> exposure also increased phosphorylation of cortical c <strong>Jun</strong> whereas levels of phosphorylated cAMP response element binding protein (CREB) remained unmodified.
+JUN	drug	opioid	23485395	Inhibition of c <strong>Jun</strong> NH2 terminal kinase stimulates mu <b>opioid</b> receptor expression via p38 MAPK mediated nuclear NF κB activation in neuronal and non neuronal cells.
+JUN	drug	opioid	23485395	Several in vivo and in vitro studies have shown that the c <strong>Jun</strong> NH2 terminal kinase (JNK) pathway is closely associated with neuropathic hyperalgesia, which closely resembles the neuroplastic changes observed with <b>morphine</b> antinociceptive tolerance.
+JUN	drug	opioid	23262244	<b>Heroin</b> activates Bim via c <strong>Jun</strong> N terminal kinase/c <strong>Jun</strong> pathway to mediate neuronal apoptosis.
+JUN	drug	opioid	23262244	Meanwhile, c <strong>Jun</strong> N terminal kinase (JNK)/c <strong>Jun</strong> pathway was activated in <b>heroin</b> induced apoptosis.
+JUN	drug	opioid	23262244	These results indicate that Bim plays a critical role in the neurotoxic process by <b>heroin</b> and JNK/c <strong>Jun</strong> pathway acts upstream of Bim in regulating <b>heroin</b> induced neuronal death.
+JUN	drug	opioid	22491351	One of the cascades that could be regulated by β arrestin 2 is <strong>cJun</strong> N terminal kinase (JNK), which binds with β arrestin 2 and modulates the analgesic effects of <b>morphine</b>.
+JUN	drug	opioid	22491351	One of the cascades that could be regulated by β arrestin 2 is <strong><strong>cJun</strong></strong> N terminal kinase (JNK), which binds with β arrestin 2 and modulates the analgesic effects of <b>morphine</b>.
+JUN	drug	opioid	22491351	Using neurons lacking β arrestin 2 (β arr2 / ) to examine this interaction, we found that β arr2 /  neurons show altered intracellular distribution of JNK and <strong>cJun</strong>, and that <b>morphine</b>, but not <b>fentanyl</b>, increased the nuclear localization of the phosphorylated, therefore activated, form of <strong>cJun</strong>, a JNK target in dorsal root ganglia neurons.
+JUN	drug	opioid	22491351	Using neurons lacking β arrestin 2 (β arr2 / ) to examine this interaction, we found that β arr2 /  neurons show altered intracellular distribution of JNK and <strong><strong>cJun</strong></strong>, and that <b>morphine</b>, but not <b>fentanyl</b>, increased the nuclear localization of the phosphorylated, therefore activated, form of <strong><strong>cJun</strong></strong>, a JNK target in dorsal root ganglia neurons.
+JUN	drug	amphetamine	22426312	<b>Methamphetamine</b> induced a transient activation of stress kinases c <strong>Jun</strong> N terminal kinase 1/2 and p38 in the brain parenchyma and increased intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 expression on cerebral microvessels without inducing loss of tight junction proteins and without inducing IgG extravasation.
+JUN	drug	amphetamine	22426312	Elevated expression of ApoE was noted in the brain parenchyma by <b>methamphetamine</b>, activating ApoE receptor 2 on brain capillaries, deactivating c <strong>Jun</strong> N terminal kinase 1/2 and c <strong>Jun</strong>, and regulating ABCB1 and ABCC1 expression.
+JUN	drug	amphetamine	22426312	Acute exposure to <b>methamphetamine</b> at doses comparable to those consumed in drug addiction does not induce tight junction breakdown but differentially regulates adenosine triphosphate binding cassette transporters through the ApoE/ApoE receptor 2/c <strong>Jun</strong> N terminal kinase 1/2 pathway.
+JUN	addiction	addiction	22426312	Acute exposure to methamphetamine at doses comparable to those consumed in drug <b>addiction</b> does not induce tight junction breakdown but differentially regulates adenosine triphosphate binding cassette transporters through the ApoE/ApoE receptor 2/c <strong>Jun</strong> N terminal kinase 1/2 pathway.
+JUN	drug	alcohol	22020770	To our surprise, the impairment of <strong>AP 1</strong> activation was sufficient to mediate a severe and dose dependent phenotype in human monocytes in vitro at <b>alcohol</b> concentrations as low as 0.16% (or 26 mM).
+JUN	drug	alcohol	22020770	The nuclear factor κB signaling cascade and the p38/c <strong>Jun</strong> N terminal kinase modules of the mitogen activated protein kinase pathway were <b>alcohol</b> insensitive.
+JUN	addiction	intoxication	21790671	Phosphorylation of c <strong>Jun</strong> N terminal kinase (JNK) and p38 MAPK did not increase by the <b>binge</b>.
+JUN	drug	opioid	21483469	Extensive studies of mitogen activated protein kinase (MAPK) signaling pathways revealed the involvement of c <strong>Jun</strong> N terminal kinase (JNK) and extracellular signal regulated kinase 1/2 (ERK1/2) pathways in enhanced toxicity of Tat and <b>morphine</b>.
+JUN	drug	alcohol	21338584	Prodynorphin promoter SNP associated with <b>alcohol</b> dependence forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+JUN	addiction	dependence	21338584	Prodynorphin promoter SNP associated with alcohol <b>dependence</b> forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+JUN	addiction	reward	21168475	Activation of ERK and CaMKIIα, but not the c <strong>Jun</strong> N terminal kinase and p38, in the nucleus accumbens, amygdala and prefrontal cortex is also potentiated in D3 receptor mutant mice compared to that in wild type mice following <b>CPP</b> expression.
+JUN	addiction	reward	20456009	Moreover, ERK, but not the c <strong>jun</strong> N terminal kinase and p38, is activated in wild type and D3 receptor mutant mice but not in D1 receptor mutant mice following <b>CPP</b> acquisition.
+JUN	drug	alcohol	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after <b>ethanol</b> withdrawal.
+JUN	addiction	withdrawal	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after ethanol <b>withdrawal</b>.
+JUN	drug	nicotine	19776730	Involvement of hippocampal <strong>jun</strong> N terminal kinase pathway in the enhancement of learning and memory by <b>nicotine</b>.
+JUN	drug	nicotine	19776730	Transcriptional upregulation of hippocampal <strong>jun</strong> N terminal kinase 1 (JNK1) mRNA was found in mice that learned contextual fear conditioning (FC) in the presence of <b>nicotine</b>, whereas neither learning alone nor <b>nicotine</b> administration alone exerted an effect.
+JUN	drug	opioid	19468867	There is substantial evidence indicating that mitogen activated protein kinase (MAPK), a family including extracellular signal regulated protein kinase, p38 MAPK, and c <strong>Jun</strong> N terminal kinase, can be activated by chronic <b>morphine</b> treatment in the central and peripheral nervous systems and that application of a MAPK inhibitor reduces <b>morphine</b> tolerance and dependence.
+JUN	addiction	dependence	19468867	There is substantial evidence indicating that mitogen activated protein kinase (MAPK), a family including extracellular signal regulated protein kinase, p38 MAPK, and c <strong>Jun</strong> N terminal kinase, can be activated by chronic morphine treatment in the central and peripheral nervous systems and that application of a MAPK inhibitor reduces morphine tolerance and <b>dependence</b>.
+JUN	addiction	sensitization	19445931	C <strong>Jun</strong> N terminal kinase (JNK) has been implicated in tumor growth and neuropathic pain <b>sensitization</b>.
+JUN	drug	cocaine	18991842	We found that the composition of <strong>AP 1</strong> transcription complexes and expression levels of <strong>AP 1</strong> complexes, and several transcription factors, neurotransmitter receptors as well as intracellular signaling molecules following repeated <b>cocaine</b> administration are altered in Fos deficient brains.
+JUN	drug	alcohol	18402055	<b>Ethanol</b> induces c <strong>Jun</strong> N terminal kinase (JNK) activation leading to cell death in hepatocytes.
+JUN	drug	cocaine	18355967	These results indicate that <strong>AP 1</strong> suppresses this behavioral response to <b>cocaine</b>.
+JUN	drug	opioid	18184800	In contrast to PENK, no association was detected between PDYN genotype (68 bp repeat element containing one to four copies of <strong>AP 1</strong> binding sites in the promoter region) and <b>heroin</b> abuse, although there was a clear functional association with striatal PDYN mRNA expression: an increased number of inducible repeats (three and four) correlated with higher PDYN levels than adult or fetal subjects with noninducible (one and two) alleles.
+JUN	addiction	addiction	17898233	Because MAPKs (mitogen activated protein kinases) regulate AMPAR trafficking and are implicated in <b>addiction</b>, we also evaluated phosphorylation of extracellular signal regulated kinase (ERK), c <strong>Jun</strong> N terminal kinase (JNK), and p38.
+JUN	drug	alcohol	17851539	<b>Alcohol</b> relapse induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+JUN	addiction	relapse	17851539	Alcohol <b>relapse</b> induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+JUN	drug	alcohol	17851539	In the second experiment, c Fos activation after reinstatement of <b>ethanol</b> seeking induced by discrete cues was compared with the activation pattern of its putative partner (c <strong>Jun</strong>) and regulators (extracellular signal regulated kinases and c <strong>Jun</strong> N terminal kinases).
+JUN	addiction	relapse	17851539	In the second experiment, c Fos activation after <b>reinstatement</b> of ethanol <b>seeking</b> induced by discrete cues was compared with the activation pattern of its putative partner (c <strong>Jun</strong>) and regulators (extracellular signal regulated kinases and c <strong>Jun</strong> N terminal kinases).
+JUN	drug	alcohol	17851539	In the second experiment, reexposure to the <b>ethanol</b> associated context and discrete cues activated both c <strong>Jun</strong> and extracellular signal regulated kinases (ERK1/2) in the basolateral amygdala.
+JUN	drug	opioid	17702750	Long acting kappa <b>opioid</b> antagonists disrupt receptor signaling and produce noncompetitive effects by activating c <strong>Jun</strong> N terminal kinase.
+JUN	drug	alcohol	17127267	Recent findings indicate that low concentrations of <b>ethanol</b> (10 mM) promote inflammatory processes in brain and in glial cells by up regulating cytokines and inflammatory mediators (iNOS, NO, COX 2), and by activating signaling pathways (IKK, MAPKs) and transcriptional factors (NF kappaB, <strong>AP 1</strong>) implicated in inflammatory injury.
+JUN	drug	amphetamine	17049170	This effect was specific to these genes as tissue plasminogen activator (t PA), neuropeptide Y (NPY) and c <strong>jun</strong> expression in response to <b>AMPH</b> challenge was unaltered or enhanced by <b>amphetamine</b> pretreatments.
+JUN	drug	alcohol	16343492	Acute <b>ethanol</b> loading causes oxidative stress to activate cell death signaling via c <strong>Jun</strong> NH2 terminal kinase (JNK) in livers.
+JUN	drug	cocaine	16179556	In the present study, we evaluated the effect of increasing doses of <b>cocaine</b> on the expression of immediate early genes (IEGs), c fos and c <strong>jun</strong>, and closely related transcription factors, SP 1 and NF kbeta, at 24 h after the exposure to <b>cocaine</b> (50, 100, 200, 500, 1000, 2500 microM) in NGF differentiated PC12 cells.
+JUN	drug	cocaine	16179556	<b>Cocaine</b> (50 500 microM) resulted in significant induction of the expression of c fos, c <strong>jun</strong>, SP 1, and NF kbeta.
+JUN	drug	cocaine	15879001	In the present study, the effects of <b>cocaine</b> and BD1063 on the expression of six fos and <strong>jun</strong> genes were evaluated in mouse brains using cDNA microarrays.
+JUN	drug	amphetamine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of <b>amphetamine</b> or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUN	drug	cocaine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or <b>cocaine</b> (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUN	addiction	addiction	15814102	In order to approach the astroglial implication of <b>addictive</b> and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUN	addiction	dependence	15814102	Because astrocytes interact extensively with the neurons in the brain, our data led us to conclude that oxidation regulated <strong>AP 1</strong> target genes may represent one of the molecular mechanisms underlying neuronal adaptation associated with psychostimulant <b>dependence</b>.
+JUN	drug	cocaine	15770241	These results suggest that genes encoding certain extracellular factors, membrane receptors and modulators, and intracellular signaling molecules, among others, are regulated by <b>cocaine</b> via the D1 receptor, and these <strong>AP 1</strong> transcription complex regulated genes might contribute to persistent <b>cocaine</b> induced behavioral changes.
+JUN	drug	amphetamine	15680202	Ginsenosides attenuate <b>methamphetamine</b> induced behavioral side effects in mice via activation of adenosine A2A receptors: possible involvements of the striatal reduction in <strong>AP 1</strong> DNA binding activity and proenkephalin gene expression.
+JUN	drug	cocaine	15464827	<b>Cocaine</b> induced behavioral effects (hyperlocomotion and CPP) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+JUN	addiction	reward	15464827	Cocaine induced behavioral effects (hyperlocomotion and <b>CPP</b>) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+JUN	addiction	reward	15301601	The c <strong>Jun</strong> N terminal kinase (JNK) inhibitor SP600125 (1.0 2.5 microg) failed to block the <b>CPP</b> effect.
+JUN	drug	opioid	15287893	Activation of <strong>AP 1</strong> and CRE dependent gene expression via mu <b>opioid</b> receptor.
+JUN	drug	opioid	15287893	Transcription factors Ca2+/cAMP responsive element binding protein (CREB) and activator protein 1 (<strong>AP 1</strong>) may constitute a direct link between the <b>opioid</b> regulated signal transduction pathways and modulation of gene expression.
+JUN	drug	opioid	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during withdrawal from the <b>opioid</b>.
+JUN	addiction	withdrawal	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during <b>withdrawal</b> from the opioid.
+JUN	addiction	withdrawal	15176483	Whereas earlier studies have primarily demonstrated an early and transient transcriptional activation of members of the Fos, <strong>Jun</strong>, and Krox families, recent microarray studies investigating the delayed response could additionally identify several transcriptional repressors such as cAMP response element modulator (CREM), IkappaB, silencer factor B, helix loop helix proteins, or glucocorticoid induced leucine zipper, indicating the attempt of the brain to re establish homeostasis after <b>withdrawal</b> induced excitation.
+JUN	addiction	reward	15102958	Hyperphosphorylation of mitogen activated protein kinase (MAPK) ERK1/2, but not p38 and c <strong>Jun</strong> N terminal kinase/stress activated protein kinase, was found in the nucleus accumbens (NAc) and striatum but not in other brain areas of MAP treated <b>CPP</b>(+) animals.
+JUN	drug	opioid	14643766	Chronic <b>morphine</b> treatment and withdrawal induce up regulation of c <strong>Jun</strong> N terminal kinase 3 gene expression in rat brain.
+JUN	addiction	withdrawal	14643766	Chronic morphine treatment and <b>withdrawal</b> induce up regulation of c <strong>Jun</strong> N terminal kinase 3 gene expression in rat brain.
+JUN	drug	alcohol	14576487	The injurious effects of <b>ethanol</b> on the pancreas may be mediated through (1) sensitization of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) sensitization of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+JUN	addiction	sensitization	14576487	The injurious effects of ethanol on the pancreas may be mediated through (1) <b>sensitization</b> of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) <b>sensitization</b> of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+JUN	drug	cocaine	12706249	Inducible, brain region specific expression of a dominant negative mutant of c <strong>Jun</strong> in transgenic mice decreases sensitivity to <b>cocaine</b>.
+JUN	drug	cocaine	12706249	Expression of Deltac <strong>Jun</strong> in the striatum and certain other brain regions of adult mice decreases their development of <b>cocaine</b> induced conditioned place preference, suggesting reduced sensitivity to the rewarding effects of <b>cocaine</b>.
+JUN	drug	cocaine	12706249	In contrast, Deltac <strong>Jun</strong> expression had no effect on <b>cocaine</b> induced locomotor activity or sensitization.
+JUN	addiction	sensitization	12706249	In contrast, Deltac <strong>Jun</strong> expression had no effect on cocaine induced locomotor activity or <b>sensitization</b>.
+JUN	drug	cocaine	12706249	However, expression of Deltac <strong>Jun</strong> in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for AP 1 in the NAc: the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+JUN	drug	cocaine	12706249	However, expression of Deltac <strong>Jun</strong> in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for <strong>AP 1</strong> in the NAc: the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+JUN	drug	cocaine	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying <b>cocaine</b> addiction.
+JUN	addiction	addiction	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying cocaine <b>addiction</b>.
+JUN	drug	amphetamine	12504868	In addition, DNA binding activities of NF kappaB, <strong>AP 1</strong>, and CREB in the frontal cortex and hippocampus were more pronounced in mice injected with Tat plus <b>METH</b> compared to the effects of Tat or <b>METH</b> alone.
+JUN	drug	alcohol	12482856	Up regulation of CD14 in liver caused by acute <b>ethanol</b> involves oxidant dependent <strong>AP 1</strong> pathway.
+JUN	drug	alcohol	12482856	Additionally, overexpression of SOD also blunted <b>ethanol</b> induced activation of redox sensitive transcription factors NFkappaB and <strong>AP 1</strong> and production of cytokines.
+JUN	drug	alcohol	12482856	However, only inhibition of <strong>AP 1</strong> with dominant negative TAK1 but not NFkappaB by dominant negative IkappaBalpha significantly blunted <b>ethanol</b> induced increases in CD14, suggesting that <strong>AP 1</strong> is important for CD14 transcriptional regulation.
+JUN	drug	amphetamine	12125044	To determine if D(2) dopamine receptor mediated nuclear signaling is altered during the development of <b>amphetamine</b> sensitization, we examined the expression of immediate early gene (IEG) products, Fos, <strong>Jun</strong>, and Fos related antigen (FRA), in both controls and <b>amphetamine</b> sensitized rats after a challenge with the D(2) antagonist haloperidol.
+JUN	addiction	sensitization	12125044	To determine if D(2) dopamine receptor mediated nuclear signaling is altered during the development of amphetamine <b>sensitization</b>, we examined the expression of immediate early gene (IEG) products, Fos, <strong>Jun</strong>, and Fos related antigen (FRA), in both controls and amphetamine sensitized rats after a challenge with the D(2) antagonist haloperidol.
+JUN	drug	amphetamine	12125044	In contrast, more <strong>Jun</strong> and 35 kDa FRA were expressed in the ventral striatum of the <b>amphetamine</b> treated group than in the controls when haloperidol was given at w10.
+JUN	drug	amphetamine	12125044	Conversely, the increase in <strong>Jun</strong> immunoreactive neurons in <b>amphetamine</b> treated rats at w10 was observed in the dorsolateral caudate/putamen; in the case of the FRAs, the increase was observed in the nucleus accumbens shell.
+JUN	drug	alcohol	12045006	Chronic <b>alcohol</b> intoxication was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+JUN	addiction	intoxication	12045006	Chronic alcohol <b>intoxication</b> was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+JUN	drug	alcohol	12045006	Chronic <b>ethanol</b> feeding significantly enhanced MNP 1 binding, but not those of NF kappaB and <strong>AP 1</strong> in endothelial cells.
+JUN	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induces c fos and junB expression and elevates <strong>AP 1</strong> mediated transcriptional activities via the mitogen activated protein kinase cascade.
+JUN	drug	cocaine	11299316	fos and <strong>jun</strong> proteins, and cyclic AMP response element binding protein) previously shown to be relevant to <b>cocaine</b>'s behavioral actions.
+JUN	drug	nicotine	10555165	The influence of <b>nicotine</b> on the expression of Fos family proteins, which specifically formed complexes with the <strong>AP 1</strong> sequence, was assessed.
+JUN	drug	nicotine	10555165	mRNA for c Fos, c <strong>jun</strong> and <strong>jun</strong> B were up regulated at 0.5 h after <b>nicotine</b> treatment, elevated c Fos also being apparent after withdrawal.
+JUN	addiction	withdrawal	10555165	mRNA for c Fos, c <strong>jun</strong> and <strong>jun</strong> B were up regulated at 0.5 h after nicotine treatment, elevated c Fos also being apparent after <b>withdrawal</b>.
+JUN	drug	nicotine	10555165	These results indicate that <b>nicotine</b> treatment may affect the transcriptional activity of many genes through c Fos and c <strong>Jun</strong> protein expression in neural cells, and that Fra 1 protein may make a contribution.
+JUN	drug	opioid	10415375	Previous studies from this laboratory have demonstrated that acute, systemic administration of <b>morphine</b> results in an induction of the immediate early gene (IEG) proteins, c Fos and <strong>Jun</strong> B, in the dorsomedial portion of the rat caudate putamen (CPu).
+JUN	addiction	withdrawal	10415375	An increase in the IEG protein, <strong>Jun</strong> B, was also seen following 7 but not 14 days of <b>withdrawal</b> in both the dorsomedial and dorsolateral CPu.
+JUN	drug	amphetamine	10336889	In addition, we observed pronounced induction of cell stress associated transcription factor c <strong>jun</strong> and translation initiation inhibitor p97 after <b>amphetamine</b> treatment.
+JUN	drug	nicotine	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during <b>nicotine</b> dependence.
+JUN	addiction	dependence	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during nicotine <b>dependence</b>.
+JUN	drug	nicotine	10320004	The effects of acute and chronic <b>nicotine</b> treatment on activator protein 1 (<strong>AP 1</strong>) gene transcription factor binding activity in the rat cortex were investigated.
+JUN	drug	nicotine	10320004	It was observed that 1 h after acute <b>nicotine</b> treatment (single injection) <strong>AP 1</strong> DNA binding activity was significantly increased in the rat cortex.
+JUN	drug	nicotine	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of <b>nicotine</b> withdrawal after repeated <b>nicotine</b> treatment (10 days).
+JUN	addiction	withdrawal	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of nicotine <b>withdrawal</b> after repeated nicotine treatment (10 days).
+JUN	drug	nicotine	10320004	However, at 18 and 24 h of <b>nicotine</b> withdrawal after 10 days of <b>nicotine</b> treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+JUN	addiction	withdrawal	10320004	However, at 18 and 24 h of nicotine <b>withdrawal</b> after 10 days of nicotine treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+JUN	drug	nicotine	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to <b>nicotine</b> dependence.
+JUN	addiction	dependence	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to nicotine <b>dependence</b>.
+JUN	drug	amphetamine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered Fos like proteins in brain by chronic cocaine and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on <b>methamphetamine</b> induced stereotypy in mice, Jpn.
+JUN	drug	cocaine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered Fos like proteins in brain by chronic <b>cocaine</b> and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on methamphetamine induced stereotypy in mice, Jpn.
+JUN	drug	alcohol	9918601	This investigation examined the effects of acute and chronic <b>ethanol</b> exposure and its withdrawal on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+JUN	addiction	withdrawal	9918601	This investigation examined the effects of acute and chronic ethanol exposure and its <b>withdrawal</b> on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+JUN	drug	alcohol	9918601	It was observed that acute <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+JUN	addiction	withdrawal	9918601	It was observed that acute ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+JUN	drug	alcohol	9918601	It was also found that chronic <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+JUN	addiction	withdrawal	9918601	It was also found that chronic ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+JUN	drug	cocaine	9668659	<b>Cocaine</b> and the <strong>AP 1</strong> transcription factor complex.
+JUN	drug	cocaine	9668659	We presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain
+JUN	drug	nicotine	9600337	<b>Nicotine</b> appears to have no effect on the activities of c <strong>jun</strong> NH2 terminal protein kinase (JNK) and p38 MAP kinases, which have also been shown to be involved in apoptosis.
+JUN	drug	cocaine	29090793	<b>Cocaine</b> and the <strong>AP 1</strong> Transcription Factor Complex.
+JUN	drug	cocaine	29090793	We are presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain.
+JUN	drug	alcohol	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during <b>ethanol</b> withdrawal.
+JUN	addiction	withdrawal	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during ethanol <b>withdrawal</b>.
+JUN	drug	alcohol	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during <b>ethanol</b> withdrawal.
+JUN	addiction	withdrawal	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during ethanol <b>withdrawal</b>.
+JUN	addiction	withdrawal	9202324	The AP 1 DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of FosB, c <strong>Jun</strong>, JunB, and JunD.
+JUN	addiction	withdrawal	9202324	The <strong>AP 1</strong> DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of FosB, c <strong>Jun</strong>, JunB, and JunD.
+JUN	addiction	withdrawal	9202324	<b>Withdrawal</b> severity did not affect the composition of the <strong>AP 1</strong> DNA binding activities.
+JUN	drug	amphetamine	9070635	Thus, <b>amphetamine</b> sensitization is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+JUN	addiction	sensitization	9070635	Thus, amphetamine <b>sensitization</b> is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+JUN	addiction	sensitization	9403355	During the "central <b>sensitization</b>" phenomenon, noxious stimuli lead to expression of IEGs (c fos, c <strong>jun</strong>, krox 24); their proteic products have been postulated to convert short term stimulations into long lasting responses in dorsal horn neurons.
+JUN	drug	opioid	9346391	<b>Morphine</b> also enhanced mRNA expression for c <strong>jun</strong> and c myc on RMIC.
+JUN	drug	cocaine	8959019	However, the induction of the chronic <strong>AP 1</strong> complex and the chronic Fras provides a mechanism capable of underlying long lasting alterations in gene expression following chronic <b>cocaine</b> treatment.
+JUN	drug	opioid	8843097	A mu receptor <b>opioid</b> agonist induces <strong>AP 1</strong> and NF kappa B transcription factor activity in primary cultures of rat cortical neurons.
+JUN	drug	opioid	8843097	The specific mu receptor <b>opioid</b> agonist, Tyr, D Ala2, Gly, N Me Phe4, Gly ol5 (DAMGO), was found to increase <strong>AP 1</strong> and NF kappa B activity in primary cultures of neurons from rat cerebral cortex.
+JUN	drug	opioid	8843097	Acute (2 h, 4 h) and long term (72 h) treatment with DAMGO time dependently increased the DNA binding activity of both <strong>AP 1</strong> and NF kappa B and the stimulation could be abolished or inhibited by concurrent incubation with <b>naloxone</b>.
+JUN	drug	opioid	8843097	However, acute <b>naloxone</b> precipitated withdrawal did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+JUN	addiction	withdrawal	8843097	However, acute naloxone precipitated <b>withdrawal</b> did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+JUN	drug	opioid	8843097	These results indicate a mu <b>opioid</b> receptor related co induction of <strong>AP 1</strong> and NF kappa B transcription factors in cultured cortical neurons.
+JUN	drug	cocaine	8755486	Network level changes in expression of inducible Fos <strong>Jun</strong> proteins in the striatum during chronic <b>cocaine</b> treatment and withdrawal.
+JUN	addiction	withdrawal	8755486	Network level changes in expression of inducible Fos <strong>Jun</strong> proteins in the striatum during chronic cocaine treatment and <b>withdrawal</b>.
+JUN	drug	opioid	8609891	After 5 days of <b>morphine</b> treatment, we observed increased levels of the chronic Fras and of <strong>AP 1</strong> binding activity in rat striatum and nucleus accumbens, effects that were not seen in most other brain regions that we studied.
+JUN	drug	amphetamine	21359726	Examples of pharmacological stimuli that lead to long term changes are the highly addictive psychostimulant drugs, <b>amphetamine</b> and cocaine These drugs produce a robust activation of IEGs (e.g., c fos, <strong>jun</strong> B, egr 1) in areas of the brain that are believed to be part of the neural substrates of addiction (4 8) In animal models of epileptogenesis or memory, such as kindling and long term potentiation (LTP), respectively, electrical stimuli produce activation of IEGs within the brain structures thought to underlie the long lasting changes associated with these experimental procedures (9 16).
+JUN	drug	cocaine	21359726	Examples of pharmacological stimuli that lead to long term changes are the highly addictive psychostimulant drugs, amphetamine and <b>cocaine</b> These drugs produce a robust activation of IEGs (e.g., c fos, <strong>jun</strong> B, egr 1) in areas of the brain that are believed to be part of the neural substrates of addiction (4 8) In animal models of epileptogenesis or memory, such as kindling and long term potentiation (LTP), respectively, electrical stimuli produce activation of IEGs within the brain structures thought to underlie the long lasting changes associated with these experimental procedures (9 16).
+JUN	addiction	addiction	21359726	Examples of pharmacological stimuli that lead to long term changes are the highly <b>addictive</b> psychostimulant drugs, amphetamine and cocaine These drugs produce a robust activation of IEGs (e.g., c fos, <strong>jun</strong> B, egr 1) in areas of the brain that are believed to be part of the neural substrates of <b>addiction</b> (4 8) In animal models of epileptogenesis or memory, such as kindling and long term potentiation (LTP), respectively, electrical stimuli produce activation of IEGs within the brain structures thought to underlie the long lasting changes associated with these experimental procedures (9 16).
+JUN	drug	alcohol	8749800	The present study examined fetal <b>alcohol</b> effects (FAE) on the induction of the immediate early genes (IEGs) c fos, <strong>jun</strong> B, c <strong>jun</strong>, and zif268 mRNAs in the prefrontal cortex, hippocampus, and other brain regions after testing in an alternation task.
+JUN	drug	opioid	8532189	The expression of immediate early genes (IEG)s c fos, c <strong>jun</strong> and zif/268 was studied during <b>naloxone</b> precipitated <b>morphine</b> withdrawal in various organs of the rat.
+JUN	addiction	withdrawal	8532189	The expression of immediate early genes (IEG)s c fos, c <strong>jun</strong> and zif/268 was studied during naloxone precipitated morphine <b>withdrawal</b> in various organs of the rat.
+JUN	drug	opioid	8532189	Increased levels of c fos and c <strong>jun</strong> mRNA were observed in the spinal cord at 40 min of <b>morphine</b> withdrawal.
+JUN	addiction	withdrawal	8532189	Increased levels of c fos and c <strong>jun</strong> mRNA were observed in the spinal cord at 40 min of morphine <b>withdrawal</b>.
+JUN	drug	amphetamine	7784961	This study illustrates how a 2 week, twice daily 7.5 mg/kg d <b>amphetamine</b> or saline regimen alters rat brain regional expression of transcription factor genes, including c fos, fos B, <strong>jun</strong> B, c <strong>jun</strong>, and zif 268, and seeks potential correlations between those changes and alterations in neurotransmitter levels and behavioral novelty responses.
+JUN	drug	opioid	8555277	Grouping the monthly data into birth trimesters (Oct Jan; Feb May; <strong>Jun</strong> Sep) clearly shows this difference: <b>opioid</b> dependent persons  38.5/29.8/31.8%; normals  33.4/32.0/34.7%.
+JUN	drug	opioid	7838131	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal, a model of <b>opioid</b> dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUN	addiction	dependence	7838131	Naloxone precipitated morphine withdrawal, a model of opioid <b>dependence</b>, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUN	addiction	withdrawal	7838131	Naloxone precipitated morphine <b>withdrawal</b>, a model of opioid dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUN	addiction	dependence	7838131	Rapid increases in c fos, fos B, <strong>jun</strong> B, and c <strong>jun</strong> mRNA levels accompany withdrawal, with the relative level of induction correlating with the severity of physical <b>dependence</b>.
+JUN	addiction	withdrawal	7838131	Rapid increases in c fos, fos B, <strong>jun</strong> B, and c <strong>jun</strong> mRNA levels accompany <b>withdrawal</b>, with the relative level of induction correlating with the severity of physical dependence.
+JUN	addiction	withdrawal	7838131	<strong>AP 1</strong> DNA binding activity and dimer composition also exhibited regulation after <b>withdrawal</b>, presumably as a result of both transcriptional and post translational events.
+JUN	drug	opioid	7838131	Thus, <b>morphine</b> dependence results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+JUN	addiction	dependence	7838131	Thus, morphine <b>dependence</b> results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+JUN	drug	cocaine	7969045	One early cellular response to <b>cocaine</b> administration is a brain region specific alteration in the transcriptional pattern of immediate early genes belonging to the Fos/<strong>Jun</strong> family of nucleotide sequence specific [activator protein 1 (AP 1)] DNA binding proteins.
+JUN	drug	cocaine	7969045	One early cellular response to <b>cocaine</b> administration is a brain region specific alteration in the transcriptional pattern of immediate early genes belonging to the Fos/<strong>Jun</strong> family of nucleotide sequence specific [activator protein 1 (<strong>AP 1</strong>)] DNA binding proteins.
+JUN	drug	cocaine	7969045	The work described here compares <b>cocaine</b> induced transcriptional regulation of immediate early gene mRNA levels, as well as <strong>AP 1</strong> DNA binding activity, within the striatum and cerebellum.
+JUN	drug	cocaine	7969045	In the striatum, acute <b>cocaine</b> administration increases cellular levels of c fos and <strong>jun</strong> B mRNA, whereas transcriptional effects in the cerebellum are limited to c fos mRNA.
+JUN	drug	cocaine	7969045	Gel retention analysis using antibodies to the various Fos and <strong>Jun</strong> proteins was used to characterize <b>cocaine</b> dependent alterations in the composition of striatal and cerebellar AP 1 DNA binding complexes.
+JUN	drug	cocaine	7969045	Gel retention analysis using antibodies to the various Fos and <strong>Jun</strong> proteins was used to characterize <b>cocaine</b> dependent alterations in the composition of striatal and cerebellar <strong>AP 1</strong> DNA binding complexes.
+JUN	drug	cocaine	7969045	In striatum, <b>cocaine</b> increases the relative levels of c Fos, Fos B, <strong>Jun</strong> B, and <strong>Jun</strong> D proteins that bind the AP 1 DNA sequence element, whereas in the cerebellum only c Fos and <strong>Jun</strong> D binding activities are increased.
+JUN	drug	cocaine	7969045	In striatum, <b>cocaine</b> increases the relative levels of c Fos, Fos B, <strong>Jun</strong> B, and <strong>Jun</strong> D proteins that bind the <strong>AP 1</strong> DNA sequence element, whereas in the cerebellum only c Fos and <strong>Jun</strong> D binding activities are increased.
+JUN	drug	opioid	8078918	SCH23390 attenuated <b>morphine</b> induction of <strong>AP 1</strong> binding in striatum, suggesting that c fos and junB contribute to <strong>AP 1</strong> binding.
+JUN	drug	amphetamine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with <b>methamphetamine</b>, cocaine and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of <b>methamphetamine</b> and cocaine, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+JUN	drug	cocaine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, <b>cocaine</b> and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and <b>cocaine</b>, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+JUN	drug	opioid	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, cocaine and <b>morphine</b>: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and cocaine, 2) CRE binding activity was decreased by chronic <b>morphine</b> treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic <b>morphine</b> treatment in the mouse cerebellum.
+JUN	drug	alcohol	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during <b>ethanol</b> withdrawal.
+JUN	addiction	withdrawal	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during ethanol <b>withdrawal</b>.
+JUN	drug	alcohol	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing <b>ethanol</b> withdrawal.
+JUN	addiction	withdrawal	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing ethanol <b>withdrawal</b>.
+JUN	drug	alcohol	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>ethanol</b> withdrawal.
+JUN	addiction	withdrawal	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after ethanol <b>withdrawal</b>.
+JUN	drug	alcohol	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of <b>ethanol</b> withdrawal.
+JUN	addiction	withdrawal	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of ethanol <b>withdrawal</b>.
+JUN	drug	alcohol	8974322	The expression of the proteins (C FOS and C <strong>JUN</strong>) encoded by the immediate early genes c fos and c <strong>jun</strong> was investigated in the brains of rats undergoing <b>ethanol</b> withdrawal.
+JUN	addiction	withdrawal	8974322	The expression of the proteins (C FOS and C <strong>JUN</strong>) encoded by the immediate early genes c fos and c <strong>jun</strong> was investigated in the brains of rats undergoing ethanol <b>withdrawal</b>.
+JUN	addiction	withdrawal	8974322	Both proteins were induced in the cerebral cortex, the piriform cortex, the olfactory bulb, the inferior colliculus, the granular cell layer of the cerebellum and in the brain stem, but only C <strong>JUN</strong> was induced in the hippocampus of animals undergoing <b>withdrawal</b> without overt seizures.
+JUN	addiction	withdrawal	8974322	Maximal C FOS expression occurred 15 hr after <b>withdrawal</b> while C <strong>JUN</strong> was maximal at 24 hr.
+JUN	addiction	withdrawal	8974322	Gel shift assays indicated the formation of <strong>AP 1</strong> binding factors in nuclear extracts of the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>withdrawal</b>.
+JUN	addiction	withdrawal	19912955	A large, transient increase in the expression of whole brain c fos, c <strong>jun</strong>, and zif/268 mRNA was observed 12 h after <b>withdrawal</b>, and expression of their protein products was detected 15 to 24 h after <b>withdrawal</b>.
+JUN	addiction	withdrawal	19912955	All three proteins were present in the cerebral cortex, the olfactory bulb, the inferior colliculus, the granular cell layer of the cerebellum, and in the brain stem, but only C <strong>JUN</strong> and ZIF/268 were detected in the hippocampus of animals undergoing <b>withdrawal</b> without overt seizures.
+JUN	drug	cocaine	8385579	The investigations have focused on the Fos <strong>Jun</strong> family of immediate early gene transcription factors, and the CREB family of transcription factors, as possible mediators of the effects of chronic opiate and <b>cocaine</b> exposure on regulation of neuronal gene expression.
+JUN	drug	cocaine	1631058	Regulation of immediate early gene expression and <strong>AP 1</strong> binding in the rat nucleus accumbens by chronic <b>cocaine</b>.
+JUN	drug	cocaine	1631058	We therefore examined changes in the mRNA levels for the IEGs c fos, c <strong>jun</strong>, fosB, junB, and zif268 in the NAc of rats treated acutely and chronically with <b>cocaine</b>.
+JUN	drug	cocaine	1631058	As would be expected from the RNA data and immunohistochemistry, acute <b>cocaine</b> administration increased <strong>AP 1</strong> binding activity in the NAc, an effect that reverted completely to control levels within 8 12 hr.
+JUN	drug	cocaine	1631058	In contrast, AP 1 binding activity in the NAc of animals treated chronically with <b>cocaine</b> remained elevated at acute levels 18 hr after the last chronic injection, a time at which c fos and c <strong>jun</strong> mRNA levels and Fos like immunoreactivity had returned to control values.
+JUN	drug	cocaine	1631058	In contrast, <strong>AP 1</strong> binding activity in the NAc of animals treated chronically with <b>cocaine</b> remained elevated at acute levels 18 hr after the last chronic injection, a time at which c fos and c <strong>jun</strong> mRNA levels and Fos like immunoreactivity had returned to control values.
+JUN	drug	cocaine	1631058	An additional acute <b>cocaine</b> challenge did not further increase <strong>AP 1</strong> binding.
+JUN	drug	cocaine	1631058	The data suggest that chronic <b>cocaine</b> treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of <b>cocaine</b> addiction.
+JUN	addiction	addiction	1631058	The data suggest that chronic cocaine treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of cocaine <b>addiction</b>.
+JUN	addiction	withdrawal	1701330	In the LC and some other brain regions, induction of c fos during opiate <b>withdrawal</b> was associated with a parallel induction of c <strong>jun</strong>, another nuclear proto oncogene, which, like c fos, is expressed rapidly in brain in response to certain extracellular stimuli.
+CASP3	drug	opioid	32524520	The <b>morphine</b> induced increases of apoptosis, neuron death, OS, lipid peroxidation, <strong>caspase 3</strong> and caspase 9, neuroinflammatory cytokines (IL 1β, TNF α, IL 6), and Ca2+ levels in the hippocampal neuron of TRPM2 WT mouse were decreased by the L NAME, ACA, and 2 APB treatments, although cell viability, neuron count, and reduced glutathione and glutathione peroxidase levels were increased by the treatments.
+CASP3	drug	amphetamine	32450188	Inhibition of circHomer1 expression indeed alleviated <b>METH</b> induced neurotoxicity, with lower apoptosis rate via flow cytometry and cleaved <strong>Caspase3</strong> protein level.
+CASP3	drug	amphetamine	32120831	Moreover, diminished expression of anti apoptotic proteins, including Bcl 2, <strong>Caspase3</strong>, Caspase7, and Caspase8 in <b>METH</b> exposed SH SY5y cells, was significantly recovered by treatment with lupenone.
+CASP3	drug	amphetamine	32086884	In addition, to explore <b>METH</b> induced neurotoxicity, we measured the level of Parkin and the phosphorylation levels of α syn, Polo like kinase 2 (PLK2), the proteasome activity marker CD3δ, and the apoptosis related proteins <strong>Caspase 3</strong> and PARP.
+CASP3	drug	amphetamine	32035215	Results further showed that luteolin pretreatment significantly repressed the <b>METH</b> induced increases of PI3K, Akt, p Akt, p53, Bax, <strong>caspase 3</strong>, normalized the ratio of p Akt/Akt, and autophagy related proteins (Beclin1, Atg5 and LC3 II) expression.
+CASP3	drug	alcohol	31984446	Western blot testing indicated elevated levels of <strong>caspase 3</strong>/cleaved <strong>caspase 3</strong>, NF kB, and PKC/pPKC proteins in the cerebella of <b>ethanol</b> treated animals.
+CASP3	drug	amphetamine	31928234	FIHMI significantly attenuated the <b>METH</b> caused cell damage in 661W cells, evidenced by increasing cell viability and mitochondrial membrane potential, decreasing cytochrome c release and DNA fragmentation, inhibiting activities of <strong>caspase 3</strong>/9, and changing expression of apoptosis related protein.
+CASP3	drug	nicotine	31911195	Of the altered proteins, <strong>CASP3</strong>, LCMT2, GRIN2D, CCNT2, FADS3 and MRPS18B were inversely changed in response to <b>nicotine</b> and withdrawal, coincidence with the change of body weight.
+CASP3	addiction	withdrawal	31911195	Of the altered proteins, <strong>CASP3</strong>, LCMT2, GRIN2D, CCNT2, FADS3 and MRPS18B were inversely changed in response to nicotine and <b>withdrawal</b>, coincidence with the change of body weight.
+CASP3	drug	nicotine	31911195	Further Western blot and RT qPCR analyses confirmed that the levels of the 4 proteins <strong>CASP3</strong>, LCMT2, GRIN2D and CCNT2, instead of their mRNA transcripts, altered in response to <b>nicotine</b> and withdrawal.
+CASP3	addiction	withdrawal	31911195	Further Western blot and RT qPCR analyses confirmed that the levels of the 4 proteins <strong>CASP3</strong>, LCMT2, GRIN2D and CCNT2, instead of their mRNA transcripts, altered in response to nicotine and <b>withdrawal</b>.
+CASP3	drug	nicotine	31911195	Through TMT based proteomic analysis, this study identified differential hypothalamic protein profiles in response to <b>nicotine</b> treatment and its withdrawal, and 4 <b>nicotine</b>  and withdrawal induced contrary proteins <strong>CASP3</strong>, LCMT2, GRIN2D and CCNT2 are involved in several enriched GO terms and KEGG pathways, which are associated with cell apoptosis, neurotransmission and metabolism.
+CASP3	addiction	withdrawal	31911195	Through TMT based proteomic analysis, this study identified differential hypothalamic protein profiles in response to nicotine treatment and its <b>withdrawal</b>, and 4 nicotine  and <b>withdrawal</b> induced contrary proteins <strong>CASP3</strong>, LCMT2, GRIN2D and CCNT2 are involved in several enriched GO terms and KEGG pathways, which are associated with cell apoptosis, neurotransmission and metabolism.
+CASP3	drug	amphetamine	31396089	Ad libitum HRW consumption also had an inhibitory effect on the <b>METH</b> induced increase in the expression of Bax/Bcl 2, cleaved <strong>caspase 3</strong>, glucose related protein 78 (GRP 78), CCAAT/enhancer binding protein homologous protein (CHOP), and p NF kB p65 expression and elevation of interleukin (IL) 6 and tumor necrosis factor (TNF) α levels in the hippocampus.
+CASP3	drug	amphetamine	31228610	These effects preceded the activation of cleaved <strong>caspase 3</strong> in dopamine cell bodies, as well as decreases in tyrosine hydroxylase (TH) immunoreactivity in the substantia nigra and dopamine transporter (DAT) immunoreactivity in the striatum measured at 7 days after <b>Meth</b>.
+CASP3	drug	amphetamine	31228610	Intervention with a selective COX 2 inhibitor during EtOH drinking prevented the changes in microglia, and attenuated the increase in cleaved <strong>caspase 3</strong>, and decreases in TH and DAT after <b>Meth</b> administration.
+CASP3	drug	alcohol	31105269	<b>Alcohol</b> increased IL 17A production and pro apoptotic signaling evidenced by Bax, Bim, <strong>caspase 3</strong>, and caspase 8 increases via endoplasmic reticulum (ER) stress indicated by C/EBP homologous protein (CHOP) upregulation; this was prevented by the ER stress inhibitor, 4 PBA, in isolated crypts in vitro and in vivo.
+CASP3	drug	alcohol	31068789	OEA restored <b>ethanol</b>/THC related decreases in both short term spatial memory (spontaneous alternation by Y maze) and circulating levels of BDNF, reduced cell proliferation (Mki67 and IdU+ cells) and maturation (Dcx, Calb1), and improved cell survival (<strong>Casp3</strong> and BrdU+ cells) in the dorsal hippocampus.
+CASP3	drug	cannabinoid	31068789	OEA restored ethanol/<b>THC</b> related decreases in both short term spatial memory (spontaneous alternation by Y maze) and circulating levels of BDNF, reduced cell proliferation (Mki67 and IdU+ cells) and maturation (Dcx, Calb1), and improved cell survival (<strong>Casp3</strong> and BrdU+ cells) in the dorsal hippocampus.
+CASP3	drug	nicotine	30504847	Using western blot, we confirmed downregulation of SIRT1 and increased cleaved <strong>caspase 3</strong> expression in the brains of <b>nicotine</b> exposed female rats and no change in expression levels in the other groups.
+CASP3	drug	amphetamine	30456731	Seven days after <b>METH</b> injection, the brains were removed for biochemical assessments, glial fibrillary acidic protein (GFAP), and <strong>caspase 3</strong> immunohistochemistry staining.
+CASP3	drug	amphetamine	30456731	Moreover, H2S could significantly decrease <strong>caspase 3</strong> and GFAP positive cells in the CA1 region of the hippocampus (P < 0.01) compared to the <b>METH</b> group.
+CASP3	drug	nicotine	30358437	<b>Nicotine</b> also caused a dose dependent increase in epithelial cell death and an increase in <strong>caspase 3</strong>/7 activities.
+CASP3	drug	amphetamine	30259275	Seven days after <b>METH</b> injection, the rats' brains were removed for biochemical assessment using the ELISA technique, and immunohistochemistry staining was used for <strong>caspase 3</strong> and glial fibrillary acidic protein (GFAP) detection.
+CASP3	drug	nicotine	30217256	It is worthy to note that <b>nicotine</b> toxicity induced significant increments in the protein expression levels of nuclear factor kappa B as well as <strong>caspase 3</strong>.
+CASP3	addiction	intoxication	30069273	Another biological evidence on <b>binge</b> drinking effect include inflammatory response, oxidative stress, formation of toxic ceramides, activation of <strong>caspase 3</strong>, and secretion of corticoliberin.
+CASP3	drug	nicotine	29906478	Increased oxidative stress by tramadol and/or <b>nicotine</b> sequentially augmented nuclear factor kappa B and the proinflammatory cytokine tumor necrosis factor α with the induction of apoptosis evident by the increased <strong>caspase 3</strong> immunoreactivity.
+CASP3	drug	opioid	29906478	Increased oxidative stress by <b>tramadol</b> and/or nicotine sequentially augmented nuclear factor kappa B and the proinflammatory cytokine tumor necrosis factor α with the induction of apoptosis evident by the increased <strong>caspase 3</strong> immunoreactivity.
+CASP3	drug	alcohol	29404485	Furthermore, cell death rates were elevated when primary hepatocytes or human hepatoma cells were exposed to EVs from <b>alcohol</b> exposed rodents and patients with <b>alcoholism</b>, demonstrating that EVs from <b>alcohol</b> exposed rats and patients with <b>alcoholism</b> are functional and can promote cell death by activating the apoptosis signaling pathway, including phospho c Jun N terminal kinase, proapoptotic Bax, and activated <strong>caspase 3</strong>.
+CASP3	drug	alcohol	29205963	The α syn and <strong>caspase 3</strong> were detected by immunohistochemical staining and imaging analysis at 1 h, 3 h, 6 h and 12 h after acute <b>alcoholism</b>.
+CASP3	drug	alcohol	29205963	The number of α syn positive cell and average optical density in brain cortex of acute <b>alcoholism</b> rat increased significantly and peaked at 6 hour with a following slight decrease at 12 h, but still higher than the groups at 1 h and 3 h. Within 12 hours after poisoning, the number of <strong>caspase 3</strong> positive cell and average optical density in brain cortex of rats gradually increased.
+CASP3	drug	alcohol	28784931	<b>Alcohol</b> administration inhibited this activation of lin  c kit+ <strong>Sca 1</strong>+ cells.
+CASP3	drug	alcohol	28784931	<b>Alcohol</b> disrupted lipopolysaccharide (LPS) TLR4 ERK1/2 cyclin D1 signaling and inhibited upregulation of <strong>Sca 1</strong> and C/EBPβ expression by lineage negative marrow cells in response to bacteremia.
+CASP3	drug	nicotine	28691127	Western blotting showed marked significant elevation in <strong>caspase 3</strong> activities against <b>nicotine</b>.
+CASP3	drug	amphetamine	28552341	<b>Meth</b>/gp120 activated <strong>caspase 3</strong> and increased <strong>caspase 3</strong>/7 activity in microglia and inhibition of <strong>caspase 3</strong> by its specific inhibitor significantly decreased microglial production of TNF α and iNOS and attenuated microglia associated neurotoxic activity.
+CASP3	drug	amphetamine	28552341	Moreover, blockage of KV1.3 by specific blockers attenuated <b>Meth</b>/gp120 enhancement of <strong>caspase 3</strong>/7 activity.
+CASP3	drug	amphetamine	28552341	Taking together, these results suggest an involvement of microglial KV1.3 in the mediation of <b>Meth</b>/gp120 co morbid effect on microglial neurotoxic activity via <strong>caspase 3</strong> signaling.
+CASP3	drug	alcohol	27826748	Biochemical analyses revealed that <b>ethanol</b> administration induced an increase in the production of reactive oxygen species and the activity of <strong>caspase 3</strong> in PACAP KO mice in an age independent manner.
+CASP3	drug	alcohol	27665770	Acetaminophen and <b>ethanol</b>, which are also hepatotoxicants but do not induce idiosyncratic DILI, did not affect the OCR or <strong>caspase 3</strong>/7 activity.
+CASP3	drug	alcohol	27628528	Moreover, bilateral microinjections of <b>ethanol</b> did not change the expression of either pro apoptotic (<strong>caspase 3</strong> and Bax) or anti apoptotic (Bcl 2) proteins, suggesting that the dose was safe and validating the method used in the current study.
+CASP3	drug	alcohol	27565756	Additionally, we also observed increased activated <strong>caspase3</strong> staining in hippocampal cells 24 h after <b>ethanol</b> withdrawal.
+CASP3	addiction	withdrawal	27565756	Additionally, we also observed increased activated <strong>caspase3</strong> staining in hippocampal cells 24 h after ethanol <b>withdrawal</b>.
+CASP3	drug	opioid	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, Bax, Bcl 2 and <strong>Caspase 3</strong>, of prefrontal cortex neurons in <b>morphine</b> relapse rats, an effective, successful <b>morphine</b> relapse rat model using the conditioned place preference (CPP) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+CASP3	addiction	relapse	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, Bax, Bcl 2 and <strong>Caspase 3</strong>, of prefrontal cortex neurons in morphine <b>relapse</b> rats, an effective, successful morphine <b>relapse</b> rat model using the conditioned place preference (CPP) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+CASP3	addiction	reward	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, Bax, Bcl 2 and <strong>Caspase 3</strong>, of prefrontal cortex neurons in morphine relapse rats, an effective, successful morphine relapse rat model using the conditioned place preference (<b>CPP</b>) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+CASP3	drug	opioid	27544013	The results showed that the expression of Bcl 2 was very weak and those of Bax and <strong>Caspase 3</strong> were hardly seen in group normal saline; the expressions of Bax and <strong>Caspase 3</strong> were strong and that of Bcl 2 was weak in group <b>morphine</b> and compared to group normal saline, there were significant differences (P<0.05); the expressions of Bax, <strong>Caspase 3</strong> and the ratios of Bax/Bcl 2 have a gradually decreased trend in the sequence of group 0.01μg, group 0.1μg and group 1.0μg, but the expression of Bcl 2 has an opposite trend in the same sequence, and compared to group <b>morphine</b>, there were significant differences (P<0.05) excluding group 0.01μg.
+CASP3	drug	opioid	27544013	So we draw a conclusion that CCK 8 (0.1 and 1.0μg, i.c.v) could protect neurons of prefrontal cortex through up regulating the expression of Bcl 2, down regulating those of Bax and <strong>Caspase 3</strong> and reducing Bax/Bcl 2 ratio in the model of <b>morphine</b> relapse rats.
+CASP3	addiction	relapse	27544013	So we draw a conclusion that CCK 8 (0.1 and 1.0μg, i.c.v) could protect neurons of prefrontal cortex through up regulating the expression of Bcl 2, down regulating those of Bax and <strong>Caspase 3</strong> and reducing Bax/Bcl 2 ratio in the model of morphine <b>relapse</b> rats.
+CASP3	drug	alcohol	27527870	<b>Ethanol</b> caused both apoptotic and necrotic cell death which was demonstrated by the increase in active <strong>caspase 3</strong>, caspase 8, cleaved PARP, cleaved CK 18 and the secretion of high mobility group protein B1 (HMGB1).
+CASP3	drug	nicotine	26909550	This effect correlated with the induction of Bcl 2, Bax, Survivin and <strong>Caspase 3</strong> by <b>nicotine</b> in gastric cell lines.
+CASP3	drug	alcohol	26857094	OEA also prevented <b>ethanol</b> induced lipid peroxidation, caspase 8 and pro apoptotic <strong>caspase 3</strong> activation in frontal cortex.
+CASP3	drug	alcohol	26805422	Binge <b>ethanol</b> treated rats demonstrated a significant increase in KLF11, both MAO isoforms, protein oxidation and <strong>caspase 3</strong>, as well as a reduction in BDNF expression in the frontal cortex compared to control rats.
+CASP3	addiction	intoxication	26805422	<b>Binge</b> ethanol treated rats demonstrated a significant increase in KLF11, both MAO isoforms, protein oxidation and <strong>caspase 3</strong>, as well as a reduction in BDNF expression in the frontal cortex compared to control rats.
+CASP3	drug	cocaine	26790673	Levels of MDA and TNFα in PFC, and levels of MDA, SOD, GSH, IL 6, IL 1β, TNFα, <strong>caspase 3</strong> and BAX in HP, but not SIRT1 expression in both regions were significantly changed during <b>cocaine</b> withdrawal period.
+CASP3	addiction	withdrawal	26790673	Levels of MDA and TNFα in PFC, and levels of MDA, SOD, GSH, IL 6, IL 1β, TNFα, <strong>caspase 3</strong> and BAX in HP, but not SIRT1 expression in both regions were significantly changed during cocaine <b>withdrawal</b> period.
+CASP3	drug	psychedelics	25937004	24h following washout of the specific drug, a significant elevation of the pro apoptotic marker BAX, as well as activated <strong>Caspase 3</strong> positive neurons, could be detected in cultures exposed to 100μM MK801 and 25μM S(+) <b>ketamine</b>.
+CASP3	drug	opioid	25846801	Various regimens of <b>morphine</b> reduced TWI, cortisol levels, Bax activity, <strong>caspase 3</strong>, caspase 9, TNF α, and IL 1β and lipid peroxidation.
+CASP3	drug	opioid	25712644	The results showed that <b>morphine</b> significantly increased lipid peroxidation, mitochondrial GSH level, concentration of Bax; <strong>caspase 3</strong> and caspase 9 activities while decreasing Bcl 2 concentration.
+CASP3	drug	amphetamine	25631491	In addition, blocking caspase 11 expression inhibited <b>METH</b> induced activation of <strong>caspase 3</strong> and PARP in vitro and in vivo, suggesting that caspase 11/<strong>caspase 3</strong> signal pathway is involved in <b>METH</b> induced neurotoxicity.
+CASP3	drug	opioid	25597171	Group II also exhibited a significantly reduced epididymal perm count (P < 0.05) and remarkably upregulated expressions of Bax and <strong>Caspase 3</strong> in comparison with group I. <b>Morphine</b> might increase testicular cell apoptosis and reduce sperm concentration by upregulating the expressions of Bax and <strong>Caspase 3</strong> in the rat model of <b>morphine</b> tolerance.
+CASP3	drug	alcohol	25556946	In adolescent animals, <b>alcohol</b> decreased the expression of genes involved in the repair and protection of oxidative DNA damage such as atr, gpx7, or nudt15 and increased the expression of proapoptotic genes such as <strong>casp3</strong>.
+CASP3	drug	amphetamine	25260424	Proliferation of progenitors via Ki 67 labeling and apoptosis via activated <strong>caspase 3</strong> labeling were studied in rats that intravenously self administered <b>methamphetamine</b> in a limited access (1h/day: short access (ShA)) or extended access (6h/day: long access (LgA)) paradigm over 4, 13, 22 or 42 sessions, and in rats that experienced 22 sessions and were withdrawn from self administration for a period of 4weeks.
+CASP3	drug	opioid	24959978	In this study, we investigated the effects of <b>morphine</b> induced conditioned place preference (CPP) in the presence and absence of stress on the changes of apoptotic factors (Bax/Bcl 2 ratio, <strong>caspase 3</strong> activation and PARP degradation) in the MCL system.
+CASP3	addiction	reward	24959978	In this study, we investigated the effects of morphine induced conditioned place preference (<b>CPP</b>) in the presence and absence of stress on the changes of apoptotic factors (Bax/Bcl 2 ratio, <strong>caspase 3</strong> activation and PARP degradation) in the MCL system.
+CASP3	drug	opioid	24959978	In the <b>morphine</b> treated animals, AS and SS increased apoptotic factors remarkably (except for the Bax/Bcl 2 ratio after AS and SS in the Str and <strong>caspase 3</strong> activation after AS in the NAc) and also decreased conditioning scores.
+CASP3	drug	alcohol	24625836	Several fold increases for cytochrome P450 2E1, caspase 8 and <strong>caspase 3</strong> found in the lungs of <b>ethanol</b> fed mice as compared to pair fed controls suggest role of oxidative stress in <b>ethanol</b> induced lung injury.
+CASP3	drug	alcohol	24507877	The <b>alcohol</b> injections on PD 7 produced average peak blood <b>alcohol</b> concentrations of 472 mg/dL and evoked typical patterns of activated <strong>caspase 3</strong> positive neurons in the cortex, hippocampal formation, and striatum 6 h after the last injection.
+CASP3	drug	cocaine	24409127	Additionally, we measured cell apoptosis (as monitored by the expression of cleaved <strong>caspase 3</strong>) and glial activation [by analyzing the expression of glial fibrillary acidic protein (GFAP) and Iba 1] in the striatum and hippocampus during acute and repeated (4 days) <b>cocaine</b> administration (20 mg/kg).
+CASP3	drug	cannabinoid	24409127	Both acute and repeated cocaine exposure increased the number of cleaved <strong>caspase 3</strong> , GFAP  and Iba1 ir cells in the hippocampus, and this effect was counteracted by AM630 or <b>Rimonabant</b>, which increased the number of BrdU , GFAP , and Iba1 ir cells in the hippocampus.
+CASP3	drug	cocaine	24409127	Both acute and repeated <b>cocaine</b> exposure increased the number of cleaved <strong>caspase 3</strong> , GFAP  and Iba1 ir cells in the hippocampus, and this effect was counteracted by AM630 or Rimonabant, which increased the number of BrdU , GFAP , and Iba1 ir cells in the hippocampus.
+CASP3	drug	opioid	24096212	In the NAc, <b>morphine</b> significantly increased the Bax/Bcl 2 ratio, <strong>caspase3</strong> and PARP in the lowest dose (0.5mg/kg) but in the PFC considerable increase was seen in dose of 5mg/kg.
+CASP3	drug	opioid	23936592	This study aimed to investigate neuronal apoptosis and expression of apoptosis related proteins (Fas, <strong>Caspase 3</strong> and Bcl 2) in the brain of rates with <b>morphine</b> addiction.
+CASP3	addiction	addiction	23936592	This study aimed to investigate neuronal apoptosis and expression of apoptosis related proteins (Fas, <strong>Caspase 3</strong> and Bcl 2) in the brain of rates with morphine <b>addiction</b>.
+CASP3	addiction	addiction	23936592	When compared with the control group, the proportion of apoptotic neurons increased significantly in the <b>addiction</b> group and the abstinence group (P<0.01), accompanied by significantly increased expressions of Fas and <strong>Caspase 3</strong> (P<0.01) and markedly decreased Bcl 2 expression (P<0.01) in the hippocampuse.
+CASP3	drug	opioid	23936592	Long term use of <b>morphine</b> can induce neuronal apoptosis in the brain by increasing the expressions of pro apoptotic Fas and <strong>Caspase 3</strong> and decreasing the anti apoptotic Bcl 2 expression, which might be one of mechanisms underlying the opiate induced neuronal damage.
+CASP3	drug	alcohol	23567812	Quantitative analyses of immunoreactivity revealed a significant reduction in measures of neurogenesis, progenitor proliferation, as indexed by doublecortin (DCX), Ki67, and increased markers of cell death as indexed by cleaved <strong>caspase 3</strong>, and Fluoro Jade at 72 days, and decreases in DCX, and increases in cleaved <strong>caspase 3</strong> at 114 days in the <b>ethanol</b> vapor exposed rats.
+CASP3	drug	alcohol	23396011	In addition, it appears that increased dimethylation of H3K9 makes it susceptible to proteolytic degradation by <strong>caspase 3</strong> in conditions in which <b>ethanol</b> induces neurodegeneration.
+CASP3	drug	opioid	23319379	Bax and cleaved <strong>caspase 3</strong> were positive only in the <b>heroin</b> subjects.
+CASP3	addiction	reward	27385959	In this study, the effects of acute and subchronic stress on the changes in apoptotic factors (Bax/Bcl 2 ratio, <strong>caspase 3</strong> activation and PARP degradation) in the HYP and HIP during conditioned place preference (<b>CPP</b>) paradigm were evaluated.
+CASP3	drug	opioid	27385959	<strong>Caspase 3</strong> and PARP increased during AS and SS in saline  or <b>morphine</b> treated animals.
+CASP3	drug	opioid	27385959	For example, <strong>caspase 3</strong> increased during AS and SS in <b>morphine</b> treated animals by 2.4 folds and PARP (89 KDa) increased by 3.1 and 3.5 folds, respectively.
+CASP3	drug	alcohol	23102656	Collaborating on studies of subchronic daily intoxication in juvenile and adult rats, we examined whether the repetitive <b>ethanol</b> treatments at these two life stages altered levels of key neuroinflammation associated proteins aquaporin 4 (AQP4), certain phospholipase A2 (PLA2) enzymes, PARP 1 and <strong>caspase 3</strong> in hippocampus (HC) and entorhinal cortex (EC).
+CASP3	addiction	intoxication	23102656	Collaborating on studies of subchronic daily <b>intoxication</b> in juvenile and adult rats, we examined whether the repetitive ethanol treatments at these two life stages altered levels of key neuroinflammation associated proteins aquaporin 4 (AQP4), certain phospholipase A2 (PLA2) enzymes, PARP 1 and <strong>caspase 3</strong> in hippocampus (HC) and entorhinal cortex (EC).
+CASP3	drug	alcohol	23102656	Furthermore, the robust PARP 1 elevations accompanied by negligible <strong>caspase 3</strong> activation indicate that repetitive <b>ethanol</b> intoxication may be potentiating non apoptotic neurodegenerative processes such as parthanatos.
+CASP3	addiction	intoxication	23102656	Furthermore, the robust PARP 1 elevations accompanied by negligible <strong>caspase 3</strong> activation indicate that repetitive ethanol <b>intoxication</b> may be potentiating non apoptotic neurodegenerative processes such as parthanatos.
+CASP3	addiction	intoxication	22404759	Acute apoptotic Pcell death 10 hours after a moderate dose <b>binge</b> EtOH exposure from postnatal days (PDs) 0 to 10 was assessed using active <strong>caspase 3</strong> immunolabeling.
+CASP3	drug	alcohol	22238460	In this study, we investigated the role of <strong>Sca 1</strong> in promoting ERK dependent myeloid lineage proliferation and the effects of <b>alcohol</b> on this process.
+CASP3	drug	opioid	22210043	Protein expression of cleaved <strong>caspase 3</strong> and Bax decreased, whereas Bcl 2 protein levels in hippocampus increased with exogenous H(2)S. Exogenous H(2)S alleviated <b>heroin</b> induced rat hippocampal damage through antioxidant and antiapoptosis effects.
+CASP3	addiction	dependence	23983323	These effects showed a time <b>dependence</b> over 48 hours of incubation, with high doses of SFE extracts eliminating viable cells by necrosis, depleting ATP levels and decreasing <strong>caspase 3</strong>/ 7 activity (p< 0.001).
+CASP3	drug	cocaine	21925237	Chronic exposure to <b>cocaine</b> in rats, including withdrawal for 3 days, did not alter Fas FADD receptor complex, cytochrome c, <strong>caspase 3</strong>/fragments, AIF, PARP 1 cleavage, and associated signaling in the cerebral cortex.
+CASP3	addiction	withdrawal	21925237	Chronic exposure to cocaine in rats, including <b>withdrawal</b> for 3 days, did not alter Fas FADD receptor complex, cytochrome c, <strong>caspase 3</strong>/fragments, AIF, PARP 1 cleavage, and associated signaling in the cerebral cortex.
+CASP3	drug	alcohol	21803053	After 4h, a single dose of <b>ethanol</b> induced upregulation of Bax, release of mitochondrial cytochrome c into the cytosol, activation of <strong>caspase 3</strong> and cleavage of poly (ADP ribose) polymerase (PARP 1), all of which promote apoptosis.
+CASP3	drug	alcohol	21664448	These structures showed activation of <strong>caspase 3</strong> and 9 but not of caspase 8 suggesting that <b>alcohol</b> induced apoptosis could occur by the intrinsic pathway.
+CASP3	drug	opioid	21483469	Enhanced toxicity by Tat and <b>morphine</b> was accompanied by increased numbers of TUNEL positive apoptotic neurons, elevated <strong>caspase 3</strong> levels and decreased ratio of anti  and pro apoptotic proteins, Bcl2/Bax.
+CASP3	drug	alcohol	20870739	Cultured rat PSCs were exposed to 10 mM <b>ethanol</b> 6 1 mg/ml LPS for 48 or 72 h and apoptosis was assessed (Annexin V, <strong>caspase 3</strong> and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL)).
+CASP3	drug	opioid	20711699	Although minocycline did not change the level of <strong>caspase 3</strong> at the doses used with <b>morphine</b> but the minocycline treated rats showed a significantly lower increase in <strong>caspase 3</strong> activity than did in the control.
+CASP3	drug	opioid	20600172	In this study, we show that <b>morphine</b> induces microglia apoptosis and <strong>caspase 3</strong> activation in an <b>opioid</b> receptor dependent manner.
+CASP3	drug	opioid	20600172	In addition, inhibition of p38 MAPK by its specific inhibitor SB203580 significantly inhibited <b>morphine</b> induced apoptosis and <strong>caspase 3</strong> activation.
+CASP3	drug	psychedelics	20526188	After intrathecal injection of <b>ketamine</b> at P3, 7, or 21, spinal cords were examined for apoptosis (Fluoro Jade C and activated <strong>caspase 3</strong>), histopathologic change, and glial responses (ionized calcium binding adapter molecule 1 and glial fibrillary acid protein).
+CASP3	drug	alcohol	20090911	Myocardium from <b>ethanol</b> treated mice displayed enhanced Bax, <strong>Caspase 3</strong> and decreased Bcl 2 expression, the effect of which with the exception of <strong>Caspase 3</strong> was augmented by ADH.
+CASP3	drug	amphetamine	19663261	Furthermore, high concentration of <b>METH</b>, but not MPH, reduced MAP2a/b positive cells and activated the immunoreactivity of the cleaved <strong>caspase 3</strong> in primary cultured limbic neurons, whereas MPH had no such effect.
+CASP3	drug	psychedelics	19580862	Although a few <strong>caspase 3</strong>  and Fluoro Jade C positive neuronal profiles were observed in some additional brain areas including the hippocampus, thalamus, striatum and amygdala, no significant differences were detected between <b>ketamine</b> treated and control monkeys in these areas after 3, 9 or 24h of exposure.
+CASP3	drug	alcohol	19155505	Acute <b>alcohol</b> intoxication inhibits the lineage  c kit+ <strong>Sca 1</strong>+ cell response to Escherichia coli bacteremia.
+CASP3	addiction	intoxication	19155505	Acute alcohol <b>intoxication</b> inhibits the lineage  c kit+ <strong>Sca 1</strong>+ cell response to Escherichia coli bacteremia.
+CASP3	drug	alcohol	19155505	Acute <b>alcohol</b> intoxication inhibited the increase in the number of lin( )c kit(+)<strong>Sca 1</strong>(+) cells in the bone marrow after E. coli infection.
+CASP3	addiction	intoxication	19155505	Acute alcohol <b>intoxication</b> inhibited the increase in the number of lin( )c kit(+)<strong>Sca 1</strong>(+) cells in the bone marrow after E. coli infection.
+CASP3	drug	alcohol	19155505	<b>Alcohol</b> impeded the increase in BrdU incorporation into marrow lin( )c kit(+)<strong>Sca 1</strong>(+) cells in response to bacteremia.
+CASP3	drug	alcohol	19155505	<b>Alcohol</b> also suppressed the plasma TNF alpha response to bacteremia and inhibited TNF alpha induced phenotypic inversion of lin( )c kit(+)<strong>Sca 1</strong>(+)<strong>Sca 1</strong>( ) cells in vitro.
+CASP3	drug	alcohol	19073235	The investigation of downstream signaling pathways involving NAP neuroprotection revealed that this peptide significantly prevented <b>alcohol</b> induced increase in the concentrations of <strong>caspase 3</strong> in E13 fetal brains.
+CASP3	drug	opioid	18782518	[Effects of <b>heroin</b> exposure on the expression of <strong>caspase 3</strong> in prefrontal lobe cortex, hippocampus and nucleus accumbens].
+CASP3	drug	opioid	18782518	To investigate the expression of <strong>caspase 3</strong> in the brain regions related to addiction, learning and memory in mice prenatally exposed to <b>heroin</b> and to ascertain whether postnatal apoptotic mechanism participates in neurobehavioral teratogenicity induced by maternal <b>heroin</b> abuse.
+CASP3	addiction	addiction	18782518	To investigate the expression of <strong>caspase 3</strong> in the brain regions related to <b>addiction</b>, learning and memory in mice prenatally exposed to heroin and to ascertain whether postnatal apoptotic mechanism participates in neurobehavioral teratogenicity induced by maternal heroin abuse.
+CASP3	drug	opioid	18782518	E8 E18 prenatal exposure to <b>heroin</b> can induce apoptosis through <strong>caspase 3</strong> activation in brain regions related to addiction, learning and memory, which indicates that apoptotic mechanism may be involved in neurobehavioral teratogenicity by <b>heroin</b> exposure in uterus.
+CASP3	addiction	addiction	18782518	E8 E18 prenatal exposure to heroin can induce apoptosis through <strong>caspase 3</strong> activation in brain regions related to <b>addiction</b>, learning and memory, which indicates that apoptotic mechanism may be involved in neurobehavioral teratogenicity by heroin exposure in uterus.
+CASP3	drug	opioid	18676827	<b>Methadone</b> inhibited proliferation in leukemia cells and induced cell death through apoptosis induction and activated apoptosis pathways through the activation of caspase 9 and <strong>caspase 3</strong>, down regulation of Bcl x(L) and X chromosome linked inhibitor of apoptosis, and cleavage of poly(ADP ribose) polymerase.
+CASP3	addiction	withdrawal	18486243	This was not accompanied by enhanced neurotoxicity or reactive gliosis as demonstrated by the immunohistological analysis using the apoptotic marker activated <strong>Caspase 3</strong> and GFAP (glial fibrillary acidic protein; a marker for astrocytes) following both short  and long term <b>withdrawal</b> periods.
+CASP3	drug	psychedelics	17920787	Stereologic quantification of silver stained nuclear and linear profiles as well as activated <strong>caspase 3</strong> labeling was used to address: (1) whether or not <b>ketamine</b> increases excitotoxic and apoptotic cell death in hippocampal CA3 and (2) whether or not <b>ketamine</b> induced cell death varies by genetic background.
+CASP3	drug	psychedelics	17920787	Neither silver staining nor activated <strong>caspase 3</strong> labeling varied by strain, nor was there an interaction between <b>ketamine</b> induced cell death and strain.
+CASP3	drug	alcohol	17706724	An increase in the <strong>caspase 3</strong> activity in PC12 cells deprived of serum was observed that was further increased by <b>ethanol</b> exposure.
+CASP3	drug	amphetamine	17647000	Using methods employed and confirmed in traumatic brain injury (TBI) studies, rat brain tissues were examined, 24 and 48 h after <b>Meth</b> and MDMA exposure, for the activation of calpain 1 and <strong>caspase 3</strong>, and their subsequent alphaII spectrin cleavage breakdown products (SBDPs), SBDP145, and SBDP120, respectively.
+CASP3	drug	psychedelics	17647000	Using methods employed and confirmed in traumatic brain injury (TBI) studies, rat brain tissues were examined, 24 and 48 h after Meth and <b>MDMA</b> exposure, for the activation of calpain 1 and <strong>caspase 3</strong>, and their subsequent alphaII spectrin cleavage breakdown products (SBDPs), SBDP145, and SBDP120, respectively.
+CASP3	drug	psychedelics	17426105	<b>Ketamine</b> (24 h infusion) produced a significant increase in the number of <strong>caspase 3</strong> , Fluoro Jade C  and silver stain positive cells in the cortex of gestational and PND 5 animals but not in PND 35 animals.
+CASP3	drug	opioid	17250679	Ionotropic glutamate receptors, <b>opioid</b> receptors and oxidative stress were not involved in <strong>caspase 3</strong> activation.
+CASP3	drug	opioid	17250679	Pure <b>heroin</b> hydrochloride similarly decreased metabolic viability but only slightly activated <strong>caspase 3</strong>.
+CASP3	drug	amphetamine	17161385	Moreover, there was <b>METH</b> induced expression of activated <strong>caspase 3</strong> in TH positive cells.
+CASP3	drug	amphetamine	16622715	Immunohistochemical investigation of dopaminergic terminal markers and <strong>caspase 3</strong> activation in the striatum of human <b>methamphetamine</b> users.
+CASP3	drug	amphetamine	16622715	In this study, we examined the suitability of the immunohistochemical detection of tyrosine hydroxylase (TH), dopamine transporter (DAT), and vesicular monoamine transporter 2 (VMAT2) levels, and <strong>caspase 3</strong> activation in the striatum to diagnose <b>METH</b> abuse.
+CASP3	drug	amphetamine	16622715	On the other hand, we observed little <strong>caspase 3</strong> activation, indicative of apoptosis, in the striatal neurons of chronic <b>METH</b> users.
+CASP3	addiction	dependence	16555300	Results show that Ca(2+) activation of the transcription factor cAMP responsive element binding protein (CREB) and Ca(2+) induced alterations in the level of the apoptotic enzyme <strong>caspase 3</strong> show both dose and age <b>dependence</b> in the early developing Purkinje neurons.
+CASP3	drug	alcohol	16555300	Exposure to <b>ethanol</b> altered Ca(2+) activation of pCREB in an age dependent manner but did not alter Ca(2+) regulation of <strong>caspase 3</strong> or calbindin levels.
+CASP3	drug	opioid	16496378	After a single dose of <b>morphine</b>, no apoptotic cells were detected by TUNEL or active <strong>caspase 3</strong> immunocytochemistry.
+CASP3	drug	alcohol	16317704	In lean mice, these moderate <b>ethanol</b> doses did not increase plasma TNF alpha and hepatic <strong>caspase 3</strong> activity, but triggered some apoptotic hepatocytes.
+CASP3	addiction	intoxication	15654300	Vitamin E also failed to protect against increases in <strong>caspase 3</strong> active subunit expression induced by acute <b>binge</b> EtOH exposure on PD 4.
+CASP3	drug	opioid	15628595	Indices of oxidative stress, nitric oxide (NO) metabolism as well as the activity of <strong>caspase 3</strong>, an important enzyme of apoptotic cell death, were measured during the <b>morphine</b> withdrawal syndrome in liver and thymus of rats.
+CASP3	addiction	withdrawal	15628595	Indices of oxidative stress, nitric oxide (NO) metabolism as well as the activity of <strong>caspase 3</strong>, an important enzyme of apoptotic cell death, were measured during the morphine <b>withdrawal</b> syndrome in liver and thymus of rats.
+CASP3	drug	alcohol	15550790	Activity of <strong>caspase 3</strong> was higher in <b>ethanol</b> treated groups (P < 0.05).
+CASP3	drug	opioid	15217373	Moreover, the increased cell death is mediated by mu <b>opioid</b> receptors and accompanied by the activation of <strong>caspase 3</strong>.
+CASP3	drug	alcohol	14741756	c fos and cleaved <strong>caspase 3</strong> expression after perinatal exposure to <b>ethanol</b>, cocaine, or the combination of both drugs.
+CASP3	drug	cocaine	14741756	c fos and cleaved <strong>caspase 3</strong> expression after perinatal exposure to ethanol, <b>cocaine</b>, or the combination of both drugs.
+CASP3	drug	alcohol	14741756	Increased cleaved <strong>caspase 3</strong> expression was observed at the 24 h time point for both <b>ethanol</b>  and cocaine exposed brains, most notably in the septum, retrosplenial cortex, and the hippocampus.
+CASP3	drug	cocaine	14741756	Increased cleaved <strong>caspase 3</strong> expression was observed at the 24 h time point for both ethanol  and <b>cocaine</b> exposed brains, most notably in the septum, retrosplenial cortex, and the hippocampus.
+CASP3	drug	alcohol	14741756	Concurrent <b>ethanol</b> and cocaine exposure did not elevate cleaved <strong>caspase 3</strong> expression beyond that of either drug alone.
+CASP3	drug	cocaine	14741756	Concurrent ethanol and <b>cocaine</b> exposure did not elevate cleaved <strong>caspase 3</strong> expression beyond that of either drug alone.
+CASP3	drug	alcohol	14741756	These results indicate that both prenatal cocaine and prenatal <b>ethanol</b> exposure increase Fos and cleaved <strong>caspase 3</strong> expression in the developing brain in a time  and region dependent manner, but that the combination of low dose, chronic <b>ethanol</b>, and binge cocaine does not cause greater apoptosis.
+CASP3	drug	cocaine	14741756	These results indicate that both prenatal <b>cocaine</b> and prenatal ethanol exposure increase Fos and cleaved <strong>caspase 3</strong> expression in the developing brain in a time  and region dependent manner, but that the combination of low dose, chronic ethanol, and binge <b>cocaine</b> does not cause greater apoptosis.
+CASP3	addiction	intoxication	14741756	These results indicate that both prenatal cocaine and prenatal ethanol exposure increase Fos and cleaved <strong>caspase 3</strong> expression in the developing brain in a time  and region dependent manner, but that the combination of low dose, chronic ethanol, and <b>binge</b> cocaine does not cause greater apoptosis.
+CASP3	drug	alcohol	14724834	<b>Ethanol</b> binge increased <strong>caspase 3</strong> and caspase 8 activity, the expression of Fas ligand, and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling in fa/fa rats.
+CASP3	addiction	intoxication	14724834	Ethanol <b>binge</b> increased <strong>caspase 3</strong> and caspase 8 activity, the expression of Fas ligand, and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling in fa/fa rats.
+CASP3	drug	alcohol	14615011	Results also showed that <b>ethanol</b> withdrawn rats had more <strong>caspase 3</strong> positive cells than observed for the dextrin diet fed group in a manner reversed by E(2) and exacerbated by bicuculline.
+CASP3	drug	alcohol	14615010	These findings support the suggestion that E(2) protects against cerebellar neuronal damage in <b>ethanol</b> withdrawn rats by inhibition of DNA fragmentation and <strong>caspase 3</strong> activation, and that reduced PKC activity may be involved in the protection.
+CASP3	drug	alcohol	14502238	The cell death process occurs over a 6 16 h period following <b>ethanol</b> administration, is accompanied by a robust display of <strong>caspase 3</strong> enzyme activation, and meets ultrastructural criteria for apoptosis.
+CASP3	drug	alcohol	14502238	We also found that <b>ethanol</b> triggers robust <strong>caspase 3</strong> activation and apoptotic neurodegeneration in C57BL/6 wildtype mice, but induces neither phenomenon in homozygous Bax deficient mice.
+CASP3	drug	alcohol	14502238	Therefore, it appears that <b>ethanol</b> induced neuroapoptosis is an intrinsic pathway mediated phenomenon involving Bax induced disruption of mitochondrial membranes and cytochrome c release as early events leading to <strong>caspase 3</strong> activation.
+CASP3	drug	cocaine	12821377	Blockade of D1 dopaminergic transmission alleviates c fos induction and cleaved <strong>caspase 3</strong> expression in the brains of rat pups exposed to prenatal <b>cocaine</b> or perinatal asphyxia.
+CASP3	drug	cocaine	12821377	We used immediate early gene and cleaved <strong>caspase 3</strong> expression patterns to monitor fetal brain regions affected by intrauterine hypoxia and prenatal <b>cocaine</b> and pretreatment with the D1 dopamine receptor antagonist SCH 23390 to determine how much of the induction observed was due to dopamine.
+CASP3	drug	cocaine	12821377	Cells immunoreactive for cleaved <strong>caspase 3</strong> expression were more numerous after perinatal asphyxia than after prenatal <b>cocaine</b> exposure in most brain regions 24 h after C section.
+CASP3	addiction	intoxication	12603597	In addition, <b>binge</b> drinking induced the cleavage of <strong>caspase 3</strong>, suggesting activation of <strong>caspase 3</strong> in T cells.
+CASP3	drug	cannabinoid	12427829	Oligodendrocyte progenitors undergo apoptosis with the withdrawal of trophic support, as determined by TUNEL assay and <strong>caspase 3</strong> activation, and both the selective CB1 agonist arachidonyl 2' chloroethylamide/(all Z) N (2 cycloethyl) 5,8,11,14 eicosatetraenamide (ACEA) and the nonselective <b>cannabinoid</b> agonists HU210 and (+) Win 55212 2 enhanced cell survival.
+CASP3	addiction	withdrawal	12427829	Oligodendrocyte progenitors undergo apoptosis with the <b>withdrawal</b> of trophic support, as determined by TUNEL assay and <strong>caspase 3</strong> activation, and both the selective CB1 agonist arachidonyl 2' chloroethylamide/(all Z) N (2 cycloethyl) 5,8,11,14 eicosatetraenamide (ACEA) and the nonselective cannabinoid agonists HU210 and (+) Win 55212 2 enhanced cell survival.
+CASP3	drug	alcohol	11895372	<b>Ethanol</b> induced <strong>caspase 3</strong> activation in the in vivo developing mouse brain.
+CASP3	drug	alcohol	11895372	In the present study, using immunocytochemical methods, we document that <b>ethanol</b> intoxication of 7 day old infant mice causes a widespread pattern of <strong>caspase 3</strong> activation corresponding to the pattern of apoptotic neurodegeneration that is occurring simultaneously.
+CASP3	addiction	intoxication	11895372	In the present study, using immunocytochemical methods, we document that ethanol <b>intoxication</b> of 7 day old infant mice causes a widespread pattern of <strong>caspase 3</strong> activation corresponding to the pattern of apoptotic neurodegeneration that is occurring simultaneously.
+CASP3	drug	nicotine	11682702	This study examined the effects and the mechanisms of action of <b>nicotine</b> on dexamethasone (DEX) induced apoptosis in murine immune cells by examining the expression of levels of the 17 kDa active <strong>caspase 3</strong>, a marker of apoptosis.
+CASP3	drug	nicotine	11682702	The data showed that <b>nicotine</b> significantly blocked the formation of the DEX induced 17 kDa <strong>caspase 3</strong> subunit expression.
+CASP3	drug	nicotine	11682702	Addition of d tubocurarine chloride (dTC), a general nicotinic receptor antagonist, inhibited <b>nicotine</b> downregulation of the DEX induced active <strong>caspase 3</strong> expression, providing evidence that this action of <b>nicotine</b> was receptor mediated.
+CASP3	drug	alcohol	11438480	<b>Ethanol</b> induced apoptosis in mouse liver: Fas  and cytochrome c mediated <strong>caspase 3</strong> activation pathway.
+CASP3	drug	alcohol	11438480	This study was undertaken to examine specifically the involvement of the upstream signals, Fas and cytochrome c, in <b>alcohol</b> induced <strong>caspase 3</strong> activation and apoptosis in the liver.
+CASP3	drug	alcohol	11438480	The results thus demonstrate that Fas/Fas ligand system mediated <strong>caspase 3</strong> activation plays a central role in the <b>ethanol</b> induced hepatic apoptosis.
+CASP3	drug	alcohol	10607886	Inclusion of <b>ethanol</b> during the serum deprivation augmented Ac DEVD amc cleavage without further increasing the amount of active <strong>caspase 3</strong>.
+CASP3	drug	alcohol	10607886	The ability of <b>ethanol</b> to promote apoptosis involves an increase in caspase activity, but this does not entail an increase in the proteolytic activation of <strong>caspase 3</strong>.
+CASP3	addiction	withdrawal	10602513	The activity of <strong>caspase 3</strong> detected in K562 Tat cells after serum <b>withdrawal</b> paralleled with the mitochondria permeability transition.
+CASP3	drug	opioid	10534122	In addition, <b>morphine</b> treated Jurkat cells showed activation of <strong>caspase 3</strong>.
+CASP3	addiction	dependence	10212287	NMDA treatment reduced <strong>caspase 3</strong> like activity in cerebellar granule neurons, and the time course and concentration <b>dependence</b> of the protective effect of NMDA mirrored the ability of NMDA to induce brain derived neurotrophic factor (BDNF) expression.
+NGF	drug	opioid	32652238	To quantify preferences for attributes of potential analgesic treatments for moderate to severe pain associated with osteoarthritis (OA) and/or chronic low back pain (CLBP) as relevant to injectable nerve growth factor (<strong>NGF</strong>) inhibitors, nonsteroidal anti inflammatory drugs (NSAIDs), and <b>opioids</b>.
+NGF	drug	opioid	32652238	To quantify preferences for attributes of potential analgesic treatments for moderate to severe pain associated with osteoarthritis (OA) and/or chronic low back pain (CLBP) as relevant to injectable <strong>nerve growth factor</strong> (<strong>NGF</strong>) inhibitors, nonsteroidal anti inflammatory drugs (NSAIDs), and <b>opioids</b>.
+NGF	drug	amphetamine	31564117	Cocaine  and <b>amphetamine</b> regulated transcript promoter regulated by nicotine in <strong>nerve growth factor</strong> treated PC12 cells.
+NGF	drug	cocaine	31564117	<b>Cocaine</b>  and amphetamine regulated transcript promoter regulated by nicotine in <strong>nerve growth factor</strong> treated PC12 cells.
+NGF	drug	nicotine	31564117	Cocaine  and amphetamine regulated transcript promoter regulated by <b>nicotine</b> in <strong>nerve growth factor</strong> treated PC12 cells.
+NGF	drug	nicotine	31564117	This study investigated the regulatory effect of <b>nicotine</b> on promoter activity of the CART gene in PC12 cells, which were differentiated into a neuronal phenotype by nerve growth factor (<strong>NGF</strong>) treatment.
+NGF	drug	nicotine	31564117	This study investigated the regulatory effect of <b>nicotine</b> on promoter activity of the CART gene in PC12 cells, which were differentiated into a neuronal phenotype by <strong>nerve growth factor</strong> (<strong>NGF</strong>) treatment.
+NGF	drug	opioid	31376054	<strong>NGF</strong>, BDNF and Arc mRNA Expression in the Hippocampus of Rats After Administration of <b>Morphine</b>.
+NGF	drug	opioid	31376054	<b>Morphine</b> can influence immediate early genes (IEG) of activity regulated cytoskeletal associated protein (Arc) and brain derived neurotrophic factor (BDNF) which are activated in response to physiological stimuli during learning, as well as the nerve growth factor (<strong>NGF</strong>) gene which increases the expression of several IEGs for memory formation.
+NGF	drug	opioid	31376054	<b>Morphine</b> can influence immediate early genes (IEG) of activity regulated cytoskeletal associated protein (Arc) and brain derived neurotrophic factor (BDNF) which are activated in response to physiological stimuli during learning, as well as the <strong>nerve growth factor</strong> (<strong>NGF</strong>) gene which increases the expression of several IEGs for memory formation.
+NGF	drug	opioid	31376054	The purpose of the current study was first to evaluate the effect of acute (1 day) and subchronic (15 days) <b>morphine</b> administration on memory retrieval of rats and second to determine the hippocampal expression of <strong>NGF</strong>, BDNF and Arc genes as potential contributors in the observed effects in each setting.
+NGF	drug	opioid	31376054	We did not detect a significant change in the hippocampal expression of Arc, BDNF or <strong>NGF</strong> genes after a single episode of <b>morphine</b> treatment.
+NGF	drug	cannabinoid	31158702	This study investigated whether local intramuscular injection of non psychoactive <b>cannabinoids</b>, <b>cannabidiol</b> (CBD), <b>cannabinol</b> (CBN), <b>cannabichromene</b> (CBC) and their combinations can decrease nerve growth factor (<strong>NGF</strong>) induced masticatory muscle sensitization in female rats.
+NGF	addiction	sensitization	31158702	This study investigated whether local intramuscular injection of non psychoactive cannabinoids, cannabidiol (CBD), cannabinol (CBN), cannabichromene (CBC) and their combinations can decrease nerve growth factor (<strong>NGF</strong>) induced masticatory muscle <b>sensitization</b> in female rats.
+NGF	drug	cannabinoid	31158702	This study investigated whether local intramuscular injection of non psychoactive <b>cannabinoids</b>, <b>cannabidiol</b> (CBD), <b>cannabinol</b> (CBN), <b>cannabichromene</b> (CBC) and their combinations can decrease <strong>nerve growth factor</strong> (<strong>NGF</strong>) induced masticatory muscle sensitization in female rats.
+NGF	addiction	sensitization	31158702	This study investigated whether local intramuscular injection of non psychoactive cannabinoids, cannabidiol (CBD), cannabinol (CBN), cannabichromene (CBC) and their combinations can decrease <strong>nerve growth factor</strong> (<strong>NGF</strong>) induced masticatory muscle <b>sensitization</b> in female rats.
+NGF	drug	cannabinoid	31158702	In awake rats, changes in mechanical sensitivity induced by intramuscular injection of <strong>NGF</strong> and <b>cannabinoids</b> were measured by applying an electronic von Frey hair over the masseter muscle to measure the withdrawal response.
+NGF	addiction	withdrawal	31158702	In awake rats, changes in mechanical sensitivity induced by intramuscular injection of <strong>NGF</strong> and cannabinoids were measured by applying an electronic von Frey hair over the masseter muscle to measure the <b>withdrawal</b> response.
+NGF	addiction	sensitization	31158702	In behavioral experiments, CBD (5 mg/ml) or CBN (1 mg/ml) decreased <strong>NGF</strong> induced mechanical <b>sensitization</b>.
+NGF	drug	psychedelics	30890941	Although previous reports have shown <b>ibogaine</b>'s ability to induce GDNF expression in rat midbrain, there are no studies addressing its effect on the expression of GDNF and other neurotrophic factors (NFs) such as Brain Derived Neurotrophic Factor (BDNF) or Nerve Growth Factor (<strong>NGF</strong>) in distinct brain regions containing dopaminergic neurons.
+NGF	drug	psychedelics	30890941	Although previous reports have shown <b>ibogaine</b>'s ability to induce GDNF expression in rat midbrain, there are no studies addressing its effect on the expression of GDNF and other neurotrophic factors (NFs) such as Brain Derived Neurotrophic Factor (BDNF) or <strong>Nerve Growth Factor</strong> (<strong>NGF</strong>) in distinct brain regions containing dopaminergic neurons.
+NGF	drug	amphetamine	30699853	BDNF, <strong>NGF</strong>, and GDNF levels were decreased, while NT 3 and NT 4 levels were increased in brains after d <b>AMPH</b> sensitization.
+NGF	addiction	sensitization	30699853	BDNF, <strong>NGF</strong>, and GDNF levels were decreased, while NT 3 and NT 4 levels were increased in brains after d AMPH <b>sensitization</b>.
+NGF	drug	amphetamine	30488612	Functional enrichment analysis for this subnetwork revealed that the gene enrichment involved primarily <strong>nerve growth factor</strong> pathways, and cocaine and <b>amphetamine</b> addiction.
+NGF	drug	cocaine	30488612	Functional enrichment analysis for this subnetwork revealed that the gene enrichment involved primarily <strong>nerve growth factor</strong> pathways, and <b>cocaine</b> and amphetamine addiction.
+NGF	addiction	addiction	30488612	Functional enrichment analysis for this subnetwork revealed that the gene enrichment involved primarily <strong>nerve growth factor</strong> pathways, and cocaine and amphetamine <b>addiction</b>.
+NGF	drug	nicotine	30206032	Therefore we determined the effect of <b>nicotine</b> exposure on survival of SCG neurons during <strong>NGF</strong> withdrawal in a well established cell culture system.
+NGF	addiction	withdrawal	30206032	Therefore we determined the effect of nicotine exposure on survival of SCG neurons during <strong>NGF</strong> <b>withdrawal</b> in a well established cell culture system.
+NGF	drug	nicotine	30206032	<strong>NGF</strong> was withdrawn in rat neonatal SCG neuron cultures which were then treated with either 10 μM <b>nicotine</b> alone or with nAChR antagonists 0.1 μM α bungarotoxin (antagonist for α7 subunit bearing nAChR) and 10 μM mecamylamine (non specific antagonist for ganglionic nAChR) for 48 h. Apoptotic death was determined by TUNEL staining.
+NGF	drug	nicotine	30206032	Our results showed that exposure to 10 μM <b>nicotine</b> significantly reduced apoptotic cell death in SCG neurons resulting from <strong>NGF</strong> withdrawal as shown by fewer TUNEL positive cells.
+NGF	addiction	withdrawal	30206032	Our results showed that exposure to 10 μM nicotine significantly reduced apoptotic cell death in SCG neurons resulting from <strong>NGF</strong> <b>withdrawal</b> as shown by fewer TUNEL positive cells.
+NGF	drug	nicotine	30206032	The MTS assay results also revealed that 10 μM <b>nicotine</b> concentration significantly increased cell survival thus indicating neuroprotective effect of <b>nicotine</b> against cell death resulting from <strong>NGF</strong> withdrawal.
+NGF	addiction	withdrawal	30206032	The MTS assay results also revealed that 10 μM nicotine concentration significantly increased cell survival thus indicating neuroprotective effect of nicotine against cell death resulting from <strong>NGF</strong> <b>withdrawal</b>.
+NGF	drug	opioid	30070410	<strong>NGF</strong> gene polymorphisms are not associated with <b>heroin</b> dependence in a Taiwanese male population.
+NGF	addiction	dependence	30070410	<strong>NGF</strong> gene polymorphisms are not associated with heroin <b>dependence</b> in a Taiwanese male population.
+NGF	addiction	reward	30070410	Nerve growth factor (<strong>NGF</strong>) is a crucial modulator in the neurodevelopment, and may be a key mediator of <b>reward</b> processes in HD.
+NGF	addiction	reward	30070410	<strong>Nerve growth factor</strong> (<strong>NGF</strong>) is a crucial modulator in the neurodevelopment, and may be a key mediator of <b>reward</b> processes in HD.
+NGF	drug	cocaine	29426863	We differentiated the cells with 0.1 μg/ml nerve growth factor (<strong>NGF</strong>) for 5 days, followed by treatment with <b>cocaine</b> for 48 h at in vivo and in vitro concentrations.
+NGF	drug	cocaine	29426863	We differentiated the cells with 0.1 μg/ml <strong>nerve growth factor</strong> (<strong>NGF</strong>) for 5 days, followed by treatment with <b>cocaine</b> for 48 h at in vivo and in vitro concentrations.
+NGF	drug	opioid	29224006	Epigenetic Regulation of the Promotor Region of Vascular Endothelial Growth Factor A and <strong>Nerve Growth Factor</strong> in <b>Opioid</b> Maintained Patients.
+NGF	drug	opioid	29224006	The aim of the study was to identify differences in the regulation of both neuropeptides via the DNA methylation status of the promotor regions of <strong>NGF</strong> and VEGF A in different forms of maintenance therapy for <b>opioid</b> dependence and the related stress regulation via the hypothalamic pituitary adrenal axis.
+NGF	addiction	dependence	29224006	The aim of the study was to identify differences in the regulation of both neuropeptides via the DNA methylation status of the promotor regions of <strong>NGF</strong> and VEGF A in different forms of maintenance therapy for opioid <b>dependence</b> and the related stress regulation via the hypothalamic pituitary adrenal axis.
+NGF	drug	amphetamine	29165617	Selective Activation of Striatal <strong>NGF</strong> TrkA/p75NTR/MAPK Intracellular Signaling in Rats That Show Suppression of <b>Methamphetamine</b> Intake 30 Days following Drug Abstinence.
+NGF	drug	amphetamine	29165617	These findings support the notion that animals with distinct phenotypes for <b>methamphetamine</b> intake in the presence of adverse consequences also display differential changes in an intracellular signaling cascade activated by <strong>nerve growth factor</strong> TrkA/p75NTR interactions.
+NGF	drug	amphetamine	29165617	Thus, the development of pharmacological agents that can activate <strong>nerve growth factor</strong> dependent pathways may be a promising therapeutic approach to combat <b>methamphetamine</b> addiction.
+NGF	addiction	addiction	29165617	Thus, the development of pharmacological agents that can activate <strong>nerve growth factor</strong> dependent pathways may be a promising therapeutic approach to combat methamphetamine <b>addiction</b>.
+NGF	drug	alcohol	28847297	<strong>NGF</strong> and BDNF Alterations by Prenatal <b>Alcohol</b> Exposure.
+NGF	drug	alcohol	28847297	Neurotrophins, in particular nerve growth factor (<strong>NGF</strong>) and brain derived neurotrophic factor (BDNF), are molecules playing a pivotal role in the survival, development and function of the peripheral and central nervous systems but also in the pathogenesis of developmental defects caused by <b>alcohol</b> exposure.
+NGF	drug	alcohol	28847297	Neurotrophins, in particular <strong>nerve growth factor</strong> (<strong>NGF</strong>) and brain derived neurotrophic factor (BDNF), are molecules playing a pivotal role in the survival, development and function of the peripheral and central nervous systems but also in the pathogenesis of developmental defects caused by <b>alcohol</b> exposure.
+NGF	drug	alcohol	28847297	<strong>NGF</strong> and BDNF changes play a subtle role in short  and long lasting effects of <b>alcohol</b> in <b>ethanol</b> target tissues, including neuronal cell death and severe cognitive and physiological deficits in the newborns.
+NGF	drug	opioid	28847022	This study was aimed to investigate the attenuation effect of Cerebrolysin, a mixture of potent growth factors (BDNF, GDNF, <strong>NGF</strong>, CNTF etc,), on the development of <b>Morphine</b> induced dependence and tolerance.
+NGF	addiction	dependence	28847022	This study was aimed to investigate the attenuation effect of Cerebrolysin, a mixture of potent growth factors (BDNF, GDNF, <strong>NGF</strong>, CNTF etc,), on the development of Morphine induced <b>dependence</b> and tolerance.
+NGF	drug	opioid	28722336	Thermal hyperalgesia (tail flick) induced by nerve growth factor (<strong>NGF</strong>, a neurotrophic compound) and mechanical hyperalgesia (von Frey) induced by dynorphin A (1 17) (<b>opioid</b> compound) each correlated with the per cent of thalamic mast cells that were degranulated.
+NGF	drug	opioid	28722336	Thermal hyperalgesia (tail flick) induced by <strong>nerve growth factor</strong> (<strong>NGF</strong>, a neurotrophic compound) and mechanical hyperalgesia (von Frey) induced by dynorphin A (1 17) (<b>opioid</b> compound) each correlated with the per cent of thalamic mast cells that were degranulated.
+NGF	drug	cannabinoid	28722246	This study investigated whether intramuscular injection of delta 9 <b>tetrahydrocannabinol</b> (<b>THC</b>), by acting on peripheral <b>cannabinoid</b> (CB) receptors, could decrease nerve growth factor (<strong>NGF</strong>) induced sensitization in female rat masseter muscle; a model which mimics the symptoms of myofascial temporomandibular disorders.
+NGF	addiction	sensitization	28722246	This study investigated whether intramuscular injection of delta 9 tetrahydrocannabinol (THC), by acting on peripheral cannabinoid (CB) receptors, could decrease nerve growth factor (<strong>NGF</strong>) induced <b>sensitization</b> in female rat masseter muscle; a model which mimics the symptoms of myofascial temporomandibular disorders.
+NGF	drug	cannabinoid	28722246	This study investigated whether intramuscular injection of delta 9 <b>tetrahydrocannabinol</b> (<b>THC</b>), by acting on peripheral <b>cannabinoid</b> (CB) receptors, could decrease <strong>nerve growth factor</strong> (<strong>NGF</strong>) induced sensitization in female rat masseter muscle; a model which mimics the symptoms of myofascial temporomandibular disorders.
+NGF	addiction	sensitization	28722246	This study investigated whether intramuscular injection of delta 9 tetrahydrocannabinol (THC), by acting on peripheral cannabinoid (CB) receptors, could decrease <strong>nerve growth factor</strong> (<strong>NGF</strong>) induced <b>sensitization</b> in female rat masseter muscle; a model which mimics the symptoms of myofascial temporomandibular disorders.
+NGF	drug	cannabinoid	28722246	In behavioural experiments, intramuscular injection (10 μL) of <b>THC</b> (1 mg/mL) attenuated <strong>NGF</strong> induced mechanical sensitization.
+NGF	addiction	sensitization	28722246	In behavioural experiments, intramuscular injection (10 μL) of THC (1 mg/mL) attenuated <strong>NGF</strong> induced mechanical <b>sensitization</b>.
+NGF	drug	cannabinoid	28722246	These results suggest that reduced inhibitory input from the peripheral <b>cannabinoid</b> system may contribute to <strong>NGF</strong> induced local myofascial sensitization of mechanoreceptors.
+NGF	addiction	sensitization	28722246	These results suggest that reduced inhibitory input from the peripheral cannabinoid system may contribute to <strong>NGF</strong> induced local myofascial <b>sensitization</b> of mechanoreceptors.
+NGF	drug	alcohol	28430931	In this study we investigated a possible association between alterations in the methylation of the BDNF IV/<strong>NGF</strong> I gene promoter and the cytokines tumor necrosis factor α (TNF α) and interleukin 6 (IL 6) in 55 male <b>alcohol</b> dependent patients.
+NGF	addiction	withdrawal	28430931	Moreover, mean methylation of the <strong>NGF</strong> I promoter was significantly associated with the IL 6 serum levels and STAI I score during <b>withdrawal</b> (P < 0.001).
+NGF	drug	alcohol	28430931	Our results suggest an association between the epigenetic regulation of both neurotrophins, BDNF and <strong>NGF</strong>, cytokine release and the symptomatology of <b>alcohol</b> dependence.
+NGF	addiction	dependence	28430931	Our results suggest an association between the epigenetic regulation of both neurotrophins, BDNF and <strong>NGF</strong>, cytokine release and the symptomatology of alcohol <b>dependence</b>.
+NGF	drug	alcohol	27090822	Effects of chronic <b>alcohol</b> consumption, withdrawal and <strong>nerve growth factor</strong> on neuropeptide Y expression and cholinergic innervation of the rat dentate hilus.
+NGF	addiction	withdrawal	27090822	Effects of chronic alcohol consumption, <b>withdrawal</b> and <strong>nerve growth factor</strong> on neuropeptide Y expression and cholinergic innervation of the rat dentate hilus.
+NGF	drug	alcohol	27090822	In addition, because <b>alcohol</b> consumption and withdrawal are associated with impaired nerve growth factor (<strong>NGF</strong>) trophic support and the administration of exogenous <strong>NGF</strong> alters the effects of those conditions on various cholinergic markers, we have also estimated the same morphological parameters in withdrawn rats infused intracerebroventricularly with <strong>NGF</strong>.
+NGF	addiction	withdrawal	27090822	In addition, because alcohol consumption and <b>withdrawal</b> are associated with impaired nerve growth factor (<strong>NGF</strong>) trophic support and the administration of exogenous <strong>NGF</strong> alters the effects of those conditions on various cholinergic markers, we have also estimated the same morphological parameters in withdrawn rats infused intracerebroventricularly with <strong>NGF</strong>.
+NGF	drug	alcohol	27090822	In addition, because <b>alcohol</b> consumption and withdrawal are associated with impaired <strong>nerve growth factor</strong> (<strong>NGF</strong>) trophic support and the administration of exogenous <strong>NGF</strong> alters the effects of those conditions on various cholinergic markers, we have also estimated the same morphological parameters in withdrawn rats infused intracerebroventricularly with <strong>NGF</strong>.
+NGF	addiction	withdrawal	27090822	In addition, because alcohol consumption and <b>withdrawal</b> are associated with impaired <strong>nerve growth factor</strong> (<strong>NGF</strong>) trophic support and the administration of exogenous <strong>NGF</strong> alters the effects of those conditions on various cholinergic markers, we have also estimated the same morphological parameters in withdrawn rats infused intracerebroventricularly with <strong>NGF</strong>.
+NGF	addiction	withdrawal	27090822	NPY expression increased after <b>withdrawal</b> and returned to control values after <strong>NGF</strong> treatment.
+NGF	drug	alcohol	26792039	This study aims to reveal the relationship of depression with growth factors such as brain derived neurotrophic factor (BDNF), nerve growth factor (<strong>NGF</strong>), and insulin like growth factor 1 (IGF 1) in inpatients diagnosed with <b>alcohol</b> dependence, and to identify candidate growth factors as biological markers to indicate the comorbid of <b>alcohol</b> dependence and depression.
+NGF	addiction	dependence	26792039	This study aims to reveal the relationship of depression with growth factors such as brain derived neurotrophic factor (BDNF), nerve growth factor (<strong>NGF</strong>), and insulin like growth factor 1 (IGF 1) in inpatients diagnosed with alcohol <b>dependence</b>, and to identify candidate growth factors as biological markers to indicate the comorbid of alcohol <b>dependence</b> and depression.
+NGF	drug	alcohol	26792039	This study aims to reveal the relationship of depression with growth factors such as brain derived neurotrophic factor (BDNF), <strong>nerve growth factor</strong> (<strong>NGF</strong>), and insulin like growth factor 1 (IGF 1) in inpatients diagnosed with <b>alcohol</b> dependence, and to identify candidate growth factors as biological markers to indicate the comorbid of <b>alcohol</b> dependence and depression.
+NGF	addiction	dependence	26792039	This study aims to reveal the relationship of depression with growth factors such as brain derived neurotrophic factor (BDNF), <strong>nerve growth factor</strong> (<strong>NGF</strong>), and insulin like growth factor 1 (IGF 1) in inpatients diagnosed with alcohol <b>dependence</b>, and to identify candidate growth factors as biological markers to indicate the comorbid of alcohol <b>dependence</b> and depression.
+NGF	drug	alcohol	26792039	BDNF and <strong>NGF</strong> showed no significant difference between <b>alcohol</b> dependent patients with and without depression, but IGF 1 was significantly higher in those with than in those without depression.
+NGF	drug	opioid	26440527	<strong>NGF</strong> expression was unaffected in <b>morphine</b> withdrawal but significantly decreased during <b>oxycodone</b> withdrawal.
+NGF	addiction	withdrawal	26440527	<strong>NGF</strong> expression was unaffected in morphine <b>withdrawal</b> but significantly decreased during oxycodone <b>withdrawal</b>.
+NGF	drug	opioid	26440527	A decrease in <strong>NGF</strong> expression in <b>oxycodone</b>  but not in <b>morphine</b> treated mice could be due to mechanistic differences in <b>oxycodone</b> and <b>morphine</b>.
+NGF	addiction	dependence	26354917	However, in contrast to prior studies of priming induced by receptor mediated (i.e., TNFα, <strong>NGF</strong>, or IL 6 receptor) or direct activation of protein kinase Cε (PKCε), the pronociceptive effects of PGE2 in DAMGO treated rats demonstrated the following: (1) rapid induction (4 h compared with 3 d); (2) protein kinase A (PKA), rather than PKCε, <b>dependence</b>; (3) prolongation of hyperalgesia induced by an activator of PKA, 8 bromo cAMP; (4) failure to be reversed by a protein translation inhibitor; (5) priming in females as well as in males; and (6) lack of <b>dependence</b> on the isolectin B4 positive nociceptor.
+NGF	drug	opioid	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of <b>morphine</b> dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (<strong>NGF</strong>), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous <b>morphine</b> withdrawal in dependent animals.
+NGF	addiction	dependence	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine <b>dependence</b> on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (<strong>NGF</strong>), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine withdrawal in dependent animals.
+NGF	addiction	withdrawal	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (<strong>NGF</strong>), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine <b>withdrawal</b> in dependent animals.
+NGF	drug	opioid	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of <b>morphine</b> dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), <strong>nerve growth factor</strong> (<strong>NGF</strong>), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous <b>morphine</b> withdrawal in dependent animals.
+NGF	addiction	dependence	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine <b>dependence</b> on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), <strong>nerve growth factor</strong> (<strong>NGF</strong>), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine withdrawal in dependent animals.
+NGF	addiction	withdrawal	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), <strong>nerve growth factor</strong> (<strong>NGF</strong>), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine <b>withdrawal</b> in dependent animals.
+NGF	drug	opioid	26346883	The expression of the BDNF, GDNF, <strong>NGF</strong>, IGF1, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after <b>morphine</b> withdrawal.
+NGF	addiction	withdrawal	26346883	The expression of the BDNF, GDNF, <strong>NGF</strong>, IGF1, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after morphine <b>withdrawal</b>.
+NGF	drug	cannabinoid	25974242	Ultramicronized <b>palmitoylethanolamide</b> treated vs placebo treated rats showed significantly lower number, duration and complexity of ureteral crises, shorter duration of uterine pain, and smaller cyst diameter (0.0001 < P < 0.004); a significantly higher percentage of expelled stones (P < 0.0001); significantly lower MC number (P < 0.01), vessel number (P < 0.01), chymase (P < 0.05), <strong>NGF</strong> (P < 0.05), VEGF (P < 0.01), and Flk 1 (P < 0.01) expression in cysts and <strong>NGF</strong> expression in DRG (P < 0.01).
+NGF	drug	alcohol	25940002	Paternal <b>alcohol</b> exposure in mice alters brain <strong>NGF</strong> and BDNF and increases <b>ethanol</b> elicited preference in male offspring.
+NGF	drug	alcohol	25940002	DAT was affected in the olfactory lobes in PAE animals treated with 0.5 g/kg of <b>ethanol</b> while no differences were found on D1/D2 receptors and for pro <strong>NGF</strong> or pro BDNF.
+NGF	drug	alcohol	25940002	In conclusion, this study shows that: PAE affects <strong>NGF</strong> and BDNF expression in the mouse brain; PAE may induce <b>ethanol</b> intake preference in the male offspring.
+NGF	addiction	sensitization	25846624	However, in addition to broadly overlapping mediators of itch and pain, there is also evidence for overlapping functions in primary afferents: nociceptive primary afferents can provoke itch when activated very locally in the epidermis, and <b>sensitization</b> of both nociceptors and pruriceptors has been found following local <strong>nerve growth factor</strong> application in volunteers.
+NGF	drug	cannabinoid	25846611	Such topics are the concept of hyperalgesic priming, the role of voltage gated sodium channels and nerve growth factor (<strong>NGF</strong>) in different inflammatory and neuropathic pain states, the hyperalgesic effects of <strong>NGF</strong> in different tissues, the contribution of proteinase activated receptors (PARs) to the development of pain in several chronic pain conditions, the role of spinal NO and of glial cell activation in the generation and maintenance of inflammatory and neuropathic pain, the potential role of spinal inhibitory interneurons, the endogenous <b>endocannabinoid</b> system, and the importance of nonneuronal immune mechanisms in opioid signaling in the control of pain, the influence of spinal mechanisms on the expression of peripheral inflammation, the role of the amygdala and their connections to the medial prefrontal cortex in pain states, the experimental methods to test central sensitization of the nociceptive system in humans, and differences and similarities of the neuronal systems of pain and itch.
+NGF	drug	opioid	25846611	Such topics are the concept of hyperalgesic priming, the role of voltage gated sodium channels and nerve growth factor (<strong>NGF</strong>) in different inflammatory and neuropathic pain states, the hyperalgesic effects of <strong>NGF</strong> in different tissues, the contribution of proteinase activated receptors (PARs) to the development of pain in several chronic pain conditions, the role of spinal NO and of glial cell activation in the generation and maintenance of inflammatory and neuropathic pain, the potential role of spinal inhibitory interneurons, the endogenous endocannabinoid system, and the importance of nonneuronal immune mechanisms in <b>opioid</b> signaling in the control of pain, the influence of spinal mechanisms on the expression of peripheral inflammation, the role of the amygdala and their connections to the medial prefrontal cortex in pain states, the experimental methods to test central sensitization of the nociceptive system in humans, and differences and similarities of the neuronal systems of pain and itch.
+NGF	addiction	sensitization	25846611	Such topics are the concept of hyperalgesic priming, the role of voltage gated sodium channels and nerve growth factor (<strong>NGF</strong>) in different inflammatory and neuropathic pain states, the hyperalgesic effects of <strong>NGF</strong> in different tissues, the contribution of proteinase activated receptors (PARs) to the development of pain in several chronic pain conditions, the role of spinal NO and of glial cell activation in the generation and maintenance of inflammatory and neuropathic pain, the potential role of spinal inhibitory interneurons, the endogenous endocannabinoid system, and the importance of nonneuronal immune mechanisms in opioid signaling in the control of pain, the influence of spinal mechanisms on the expression of peripheral inflammation, the role of the amygdala and their connections to the medial prefrontal cortex in pain states, the experimental methods to test central <b>sensitization</b> of the nociceptive system in humans, and differences and similarities of the neuronal systems of pain and itch.
+NGF	drug	cannabinoid	25846611	Such topics are the concept of hyperalgesic priming, the role of voltage gated sodium channels and <strong>nerve growth factor</strong> (<strong>NGF</strong>) in different inflammatory and neuropathic pain states, the hyperalgesic effects of <strong>NGF</strong> in different tissues, the contribution of proteinase activated receptors (PARs) to the development of pain in several chronic pain conditions, the role of spinal NO and of glial cell activation in the generation and maintenance of inflammatory and neuropathic pain, the potential role of spinal inhibitory interneurons, the endogenous <b>endocannabinoid</b> system, and the importance of nonneuronal immune mechanisms in opioid signaling in the control of pain, the influence of spinal mechanisms on the expression of peripheral inflammation, the role of the amygdala and their connections to the medial prefrontal cortex in pain states, the experimental methods to test central sensitization of the nociceptive system in humans, and differences and similarities of the neuronal systems of pain and itch.
+NGF	drug	opioid	25846611	Such topics are the concept of hyperalgesic priming, the role of voltage gated sodium channels and <strong>nerve growth factor</strong> (<strong>NGF</strong>) in different inflammatory and neuropathic pain states, the hyperalgesic effects of <strong>NGF</strong> in different tissues, the contribution of proteinase activated receptors (PARs) to the development of pain in several chronic pain conditions, the role of spinal NO and of glial cell activation in the generation and maintenance of inflammatory and neuropathic pain, the potential role of spinal inhibitory interneurons, the endogenous endocannabinoid system, and the importance of nonneuronal immune mechanisms in <b>opioid</b> signaling in the control of pain, the influence of spinal mechanisms on the expression of peripheral inflammation, the role of the amygdala and their connections to the medial prefrontal cortex in pain states, the experimental methods to test central sensitization of the nociceptive system in humans, and differences and similarities of the neuronal systems of pain and itch.
+NGF	addiction	sensitization	25846611	Such topics are the concept of hyperalgesic priming, the role of voltage gated sodium channels and <strong>nerve growth factor</strong> (<strong>NGF</strong>) in different inflammatory and neuropathic pain states, the hyperalgesic effects of <strong>NGF</strong> in different tissues, the contribution of proteinase activated receptors (PARs) to the development of pain in several chronic pain conditions, the role of spinal NO and of glial cell activation in the generation and maintenance of inflammatory and neuropathic pain, the potential role of spinal inhibitory interneurons, the endogenous endocannabinoid system, and the importance of nonneuronal immune mechanisms in opioid signaling in the control of pain, the influence of spinal mechanisms on the expression of peripheral inflammation, the role of the amygdala and their connections to the medial prefrontal cortex in pain states, the experimental methods to test central <b>sensitization</b> of the nociceptive system in humans, and differences and similarities of the neuronal systems of pain and itch.
+NGF	drug	alcohol	25638740	A comparison of dexmedetomidine and placebo on the plasma concentrations of <strong>NGF</strong>, BDNF, GDNF, and epinephrine during severe <b>alcohol</b> withdrawal.
+NGF	addiction	withdrawal	25638740	A comparison of dexmedetomidine and placebo on the plasma concentrations of <strong>NGF</strong>, BDNF, GDNF, and epinephrine during severe alcohol <b>withdrawal</b>.
+NGF	drug	alcohol	25638740	<b>Alcohol</b> withdrawal and therapies may affect nerve growth factor (<strong>NGF</strong>), brain derived neurotrophic growth factor (BDNF), glial derived neurotrophic growth factor (GDNF), and epinephrine (EPI).
+NGF	addiction	withdrawal	25638740	Alcohol <b>withdrawal</b> and therapies may affect nerve growth factor (<strong>NGF</strong>), brain derived neurotrophic growth factor (BDNF), glial derived neurotrophic growth factor (GDNF), and epinephrine (EPI).
+NGF	drug	alcohol	25638740	<b>Alcohol</b> withdrawal and therapies may affect <strong>nerve growth factor</strong> (<strong>NGF</strong>), brain derived neurotrophic growth factor (BDNF), glial derived neurotrophic growth factor (GDNF), and epinephrine (EPI).
+NGF	addiction	withdrawal	25638740	Alcohol <b>withdrawal</b> and therapies may affect <strong>nerve growth factor</strong> (<strong>NGF</strong>), brain derived neurotrophic growth factor (BDNF), glial derived neurotrophic growth factor (GDNF), and epinephrine (EPI).
+NGF	drug	alcohol	25638740	This study evaluated dexmedetomidine (DEX) on <strong>NGF</strong>, BDNF, GDNF, and EPI in severe <b>alcohol</b> withdrawal and related their plasma concentrations to DEX concentrations.
+NGF	addiction	withdrawal	25638740	This study evaluated dexmedetomidine (DEX) on <strong>NGF</strong>, BDNF, GDNF, and EPI in severe alcohol <b>withdrawal</b> and related their plasma concentrations to DEX concentrations.
+NGF	drug	alcohol	25638740	In summary, the plasma concentrations of <strong>NGF</strong>, BDNF, GDNF, and EPI during <b>alcohol</b> withdrawal are variable and the effects of DEX were marginal.
+NGF	addiction	withdrawal	25638740	In summary, the plasma concentrations of <strong>NGF</strong>, BDNF, GDNF, and EPI during alcohol <b>withdrawal</b> are variable and the effects of DEX were marginal.
+NGF	drug	alcohol	25623403	The aim of this study was to investigate the alterations in serum neurotrophin levels (brain derived neurotrophic factor [BDNF], glial derived neurotrophic factor [GDNF], and nerve growth factor [<strong>NGF</strong>]) in <b>alcohol</b> use disorder in a young population, and thus possibly representing the early stages of the illness.
+NGF	drug	alcohol	25623403	The aim of this study was to investigate the alterations in serum neurotrophin levels (brain derived neurotrophic factor [BDNF], glial derived neurotrophic factor [GDNF], and <strong>nerve growth factor</strong> [<strong>NGF</strong>]) in <b>alcohol</b> use disorder in a young population, and thus possibly representing the early stages of the illness.
+NGF	drug	alcohol	25419139	Decreased serum level of <strong>NGF</strong> in <b>alcohol</b> dependent patients with declined executive function.
+NGF	drug	alcohol	25419139	The purpose of this study was to investigate the relationship between decreased <strong>NGF</strong> levels and cognitive decline in <b>alcohol</b> dependent patients.
+NGF	drug	alcohol	25419139	The serum concentration of <strong>NGF</strong> was measured in 38 patients with chronic <b>alcohol</b> dependence, and several neuropsychological tests were also performed for cognitive function assessment.
+NGF	addiction	dependence	25419139	The serum concentration of <strong>NGF</strong> was measured in 38 patients with chronic alcohol <b>dependence</b>, and several neuropsychological tests were also performed for cognitive function assessment.
+NGF	drug	alcohol	25419139	This finding may imply a protective role of <strong>NGF</strong> in preventing neuron damage among patients with <b>alcohol</b> dependence.
+NGF	addiction	dependence	25419139	This finding may imply a protective role of <strong>NGF</strong> in preventing neuron damage among patients with alcohol <b>dependence</b>.
+NGF	addiction	sensitization	25088915	Activation of CB1 inhibits <strong>NGF</strong> induced <b>sensitization</b> of TRPV1 in adult mouse afferent neurons.
+NGF	addiction	sensitization	25088915	Exposure to nerve growth factor (<strong>NGF</strong>) rapidly increases TRPV1 activity (<b>sensitization</b>).
+NGF	addiction	sensitization	25088915	Exposure to <strong>nerve growth factor</strong> (<strong>NGF</strong>) rapidly increases TRPV1 activity (<b>sensitization</b>).
+NGF	drug	cannabinoid	25088915	In the present study, we investigated whether treatment with the selective <b>cannabinoid</b> receptor 1 (CB1) agonist arachidonyl 2' chloroethylamide (ACEA) affects <strong>NGF</strong> induced sensitization of TRPV1 in adult mouse dorsal root ganglion (DRG) afferent neurons.
+NGF	addiction	sensitization	25088915	In the present study, we investigated whether treatment with the selective cannabinoid receptor 1 (CB1) agonist arachidonyl 2' chloroethylamide (ACEA) affects <strong>NGF</strong> induced <b>sensitization</b> of TRPV1 in adult mouse dorsal root ganglion (DRG) afferent neurons.
+NGF	addiction	sensitization	25088915	Our results indicate that the analgesic effect of CB1 activation may in part be due to inhibition of <strong>NGF</strong> induced <b>sensitization</b> of TRPV1 and also that the effect of CB1 activation is at least partly mediated by attenuation of <strong>NGF</strong> induced increased PI3 signaling.
+NGF	drug	psychedelics	25064020	Serum brain derived neurotrophic factor and <strong>nerve growth factor</strong> decreased in chronic <b>ketamine</b> abusers.
+NGF	drug	psychedelics	25064020	This study investigated the serum levels of brain derived neurotrophic factor (BDNF) and nerve growth factor (<strong>NGF</strong>) in a group of chronic <b>ketamine</b> abusers in comparison to healthy controls.
+NGF	drug	psychedelics	25064020	This study investigated the serum levels of brain derived neurotrophic factor (BDNF) and <strong>nerve growth factor</strong> (<strong>NGF</strong>) in a group of chronic <b>ketamine</b> abusers in comparison to healthy controls.
+NGF	drug	psychedelics	25064020	The correlations between the serum BDNF, <strong>NGF</strong> level with the subjects' demographic, pattern of <b>ketamine</b> use were also examined.
+NGF	drug	psychedelics	25064020	Both serum levels of BDNF and <strong>NGF</strong> were significant lower in the <b>ketamine</b> users compared to the healthy control subjects (9.50±6.68 versus 14.37±6.07 ng/ml, p=0.019 for BDNF; 1.93±0.80 versus 2.60±1.07 ng/ml, p=0.011 for <strong>NGF</strong>).
+NGF	drug	psychedelics	25064020	Both BDNF and <strong>NGF</strong> serum concentrations were significantly lower among chronic <b>ketamine</b> users than among health controls.
+NGF	drug	psychedelics	24942641	Furthermore, when <strong>NGF</strong> differentiated PC12 cells were pretreated with the compounds, a significant increase in binding of [(3)H]epibatidine was found for (R) <b>MDMA</b>, indicating up regulation of heteromeric nAChR in the cell surface.
+NGF	drug	alcohol	24893293	This study investigated the relationship between chronic <b>alcohol</b> consumption and subsequent withdrawal and the expression of NPY and acetylcholine in the NAc, and the possible involvement of nerve growth factor (<strong>NGF</strong>) in mediating the effects of <b>ethanol</b>.
+NGF	addiction	withdrawal	24893293	This study investigated the relationship between chronic alcohol consumption and subsequent <b>withdrawal</b> and the expression of NPY and acetylcholine in the NAc, and the possible involvement of nerve growth factor (<strong>NGF</strong>) in mediating the effects of ethanol.
+NGF	drug	alcohol	24893293	This study investigated the relationship between chronic <b>alcohol</b> consumption and subsequent withdrawal and the expression of NPY and acetylcholine in the NAc, and the possible involvement of <strong>nerve growth factor</strong> (<strong>NGF</strong>) in mediating the effects of <b>ethanol</b>.
+NGF	addiction	withdrawal	24893293	This study investigated the relationship between chronic alcohol consumption and subsequent <b>withdrawal</b> and the expression of NPY and acetylcholine in the NAc, and the possible involvement of <strong>nerve growth factor</strong> (<strong>NGF</strong>) in mediating the effects of ethanol.
+NGF	drug	amphetamine	24407463	<b>Methamphetamine</b> reversed maternal separation induced decrease in <strong>nerve growth factor</strong> in the ventral hippocampus.
+NGF	drug	amphetamine	24407463	The purpose of the present study was to investigate the individual effects of MS and <b>methamphetamine</b> administration during adolescence and the combined effects of both stressors on brain derived neurotrophic factor (BDNF) and nerve growth factor (<strong>NGF</strong>) levels in the dorsal and ventral hippocampus (HC) in adulthood.
+NGF	drug	amphetamine	24407463	The purpose of the present study was to investigate the individual effects of MS and <b>methamphetamine</b> administration during adolescence and the combined effects of both stressors on brain derived neurotrophic factor (BDNF) and <strong>nerve growth factor</strong> (<strong>NGF</strong>) levels in the dorsal and ventral hippocampus (HC) in adulthood.
+NGF	drug	amphetamine	24407463	MS decreased <strong>NGF</strong> levels in the ventral HC which was restored by <b>methamphetamine</b> administration in adolescence.
+NGF	drug	amphetamine	24407463	We propose that the restoration of <strong>NGF</strong> levels in the ventral HC may reflect a possible compensatory mechanism in response to <b>methamphetamine</b> exposure in adolescence following the early life stress of MS.
+NGF	drug	alcohol	24061482	Our primary interest is the examination of how regions that receive BF cholinergic projections are influenced by short term <b>ethanol</b> exposure through alterations in the mRNA levels of neurotrophic factors [<strong>nerve growth factor</strong>/TrkA, brain derived neurotrophic factor/TrkB, and glial derived neurotrophic factor (GDNF)/GDNF family receptor α1].
+NGF	drug	cannabinoid	23850608	CB1 <b>cannabinoid</b> receptor agonist prevents <strong>NGF</strong> induced sensitization of TRPV1 in sensory neurons.
+NGF	addiction	sensitization	23850608	CB1 cannabinoid receptor agonist prevents <strong>NGF</strong> induced <b>sensitization</b> of TRPV1 in sensory neurons.
+NGF	drug	cannabinoid	23850608	We tested the hypothesis that activation of the CB1 receptor by <b>cannabinoids</b> attenuates <strong>NGF</strong> induced TRPV1 sensitization.
+NGF	addiction	sensitization	23850608	We tested the hypothesis that activation of the CB1 receptor by cannabinoids attenuates <strong>NGF</strong> induced TRPV1 <b>sensitization</b>.
+NGF	drug	cannabinoid	23850608	When the <b>cannabinoid</b> agonist ACEA (arachidonoyl 2' chloroethylamide; 10nM) was given before <strong>NGF</strong>, only 10.8% of cells (4 of 37) were sensitized (p<0.05).
+NGF	addiction	sensitization	23850608	Neither this rate, nor the magnitude of the <b>sensitization</b> (198 ± 63% of baseline) were different from that seen in cells not treated with <strong>NGF</strong> (3 of 25 cells sensitized (12.0%), 253 ± 70% of baseline).
+NGF	addiction	sensitization	23850608	Pretreatment with the CB1 antagonist AM 251 (100 nM) prevented the effect of ACEA on <strong>NGF</strong> induced <b>sensitization</b>.
+NGF	drug	cannabinoid	23850608	These results support the hypothesis that <b>cannabinoids</b>, acting through CB1 receptors, may produce analgesia in part by preventing <strong>NGF</strong> induced sensitization of TRPV1 in afferent nociceptor nerve endings.
+NGF	addiction	sensitization	23850608	These results support the hypothesis that cannabinoids, acting through CB1 receptors, may produce analgesia in part by preventing <strong>NGF</strong> induced <b>sensitization</b> of TRPV1 in afferent nociceptor nerve endings.
+NGF	drug	alcohol	23128606	Serum brain derived neurotrophic factor and <strong>nerve growth factor</strong> concentrations change after <b>alcohol</b> withdrawal: preliminary data of a case control comparison.
+NGF	addiction	withdrawal	23128606	Serum brain derived neurotrophic factor and <strong>nerve growth factor</strong> concentrations change after alcohol <b>withdrawal</b>: preliminary data of a case control comparison.
+NGF	drug	alcohol	23128606	In this study, we addressed the question whether BDNF and <strong>NGF</strong> serum concentrations change during subacute <b>alcohol</b> withdrawal in patients with <b>alcohol</b> dependence compared to healthy controls.
+NGF	addiction	dependence	23128606	In this study, we addressed the question whether BDNF and <strong>NGF</strong> serum concentrations change during subacute alcohol withdrawal in patients with alcohol <b>dependence</b> compared to healthy controls.
+NGF	addiction	withdrawal	23128606	In this study, we addressed the question whether BDNF and <strong>NGF</strong> serum concentrations change during subacute alcohol <b>withdrawal</b> in patients with alcohol dependence compared to healthy controls.
+NGF	drug	alcohol	23128606	Mean BDNF levels (7.8 ng/ml, IQR = 4.4 10.7 vs. 16.5 ng/ml, IQR = 13.9 25.6; Z =  3.8, p < 0.0001) and <strong>NGF</strong> levels (5.8 pg/ml, IQR = 3.8 13.0 vs. 18.4 pg/ml, IQR = 10.9 25.1; Z =  2.5, p = 0.012) were significantly decreased in <b>alcohol</b> dependent subjects when compared to healthy matched controls.
+NGF	drug	alcohol	23128606	Decreased <strong>NGF</strong> and BDNF concentrations in patients suffering from <b>alcohol</b> dependence, which stabilize after physical withdrawal, are in line with withdrawal symptoms and neurological risk factors.
+NGF	addiction	dependence	23128606	Decreased <strong>NGF</strong> and BDNF concentrations in patients suffering from alcohol <b>dependence</b>, which stabilize after physical withdrawal, are in line with withdrawal symptoms and neurological risk factors.
+NGF	addiction	withdrawal	23128606	Decreased <strong>NGF</strong> and BDNF concentrations in patients suffering from alcohol dependence, which stabilize after physical <b>withdrawal</b>, are in line with <b>withdrawal</b> symptoms and neurological risk factors.
+NGF	drug	amphetamine	23076832	The present study aims to evaluate the effects of TMX on biochemical targets of Li, such as glycogen synthase kinase 3β (GSK 3β), PKC, PKA, CREB, BDNF and <strong>NGF</strong>, in the brain of rats subjected to an animal model of mania induced by d <b>amphetamine</b> (d <b>AMPH</b>).
+NGF	drug	amphetamine	23076832	Western blot showed that d <b>AMPH</b> significantly increased GSK 3 and PKC levels, and decreased pGSK 3, PKA, <strong>NGF</strong>, BDNF and CREB levels in the structures analyzed.
+NGF	drug	opioid	23031399	However, chronic <b>morphine</b> treatment greatly exacerbated increases in skin <strong>nerve growth factor</strong> levels after incision, an effect entirely dependent upon intact SP signaling.
+NGF	drug	opioid	23031399	These studies show that SP signaling modulates enhanced <strong>nerve growth factor</strong> production and changes in neuronal gene expression seen after incision in mice previously exposed to <b>morphine</b>.
+NGF	drug	opioid	22871918	Upregulation of <strong>nerve growth factor</strong> in central amygdala increases sensitivity to <b>opioid</b> reward.
+NGF	addiction	reward	22871918	Upregulation of <strong>nerve growth factor</strong> in central amygdala increases sensitivity to opioid <b>reward</b>.
+NGF	drug	opioid	22871918	We report here that <b>morphine</b> that induced reward sensitization, as demonstrated by reinstatement of the behavior of conditioned place preference (CPP) with sub threshold priming <b>morphine</b>, epigenetically upregulated the output activity of <strong>Ngf</strong> encoding the nerve growth factor (<strong>NGF</strong>) by increasing histone H4 acetylation in the rat central nucleus of the amygdala (CeA).
+NGF	addiction	relapse	22871918	We report here that morphine that induced reward sensitization, as demonstrated by <b>reinstatement</b> of the behavior of conditioned place preference (CPP) with sub threshold priming morphine, epigenetically upregulated the output activity of <strong>Ngf</strong> encoding the nerve growth factor (<strong>NGF</strong>) by increasing histone H4 acetylation in the rat central nucleus of the amygdala (CeA).
+NGF	addiction	reward	22871918	We report here that morphine that induced <b>reward</b> sensitization, as demonstrated by reinstatement of the behavior of conditioned place preference (<b>CPP</b>) with sub threshold priming morphine, epigenetically upregulated the output activity of <strong>Ngf</strong> encoding the nerve growth factor (<strong>NGF</strong>) by increasing histone H4 acetylation in the rat central nucleus of the amygdala (CeA).
+NGF	addiction	sensitization	22871918	We report here that morphine that induced reward <b>sensitization</b>, as demonstrated by reinstatement of the behavior of conditioned place preference (CPP) with sub threshold priming morphine, epigenetically upregulated the output activity of <strong>Ngf</strong> encoding the nerve growth factor (<strong>NGF</strong>) by increasing histone H4 acetylation in the rat central nucleus of the amygdala (CeA).
+NGF	drug	opioid	22871918	We report here that <b>morphine</b> that induced reward sensitization, as demonstrated by reinstatement of the behavior of conditioned place preference (CPP) with sub threshold priming <b>morphine</b>, epigenetically upregulated the output activity of <strong>Ngf</strong> encoding the <strong>nerve growth factor</strong> (<strong>NGF</strong>) by increasing histone H4 acetylation in the rat central nucleus of the amygdala (CeA).
+NGF	addiction	relapse	22871918	We report here that morphine that induced reward sensitization, as demonstrated by <b>reinstatement</b> of the behavior of conditioned place preference (CPP) with sub threshold priming morphine, epigenetically upregulated the output activity of <strong>Ngf</strong> encoding the <strong>nerve growth factor</strong> (<strong>NGF</strong>) by increasing histone H4 acetylation in the rat central nucleus of the amygdala (CeA).
+NGF	addiction	reward	22871918	We report here that morphine that induced <b>reward</b> sensitization, as demonstrated by reinstatement of the behavior of conditioned place preference (<b>CPP</b>) with sub threshold priming morphine, epigenetically upregulated the output activity of <strong>Ngf</strong> encoding the <strong>nerve growth factor</strong> (<strong>NGF</strong>) by increasing histone H4 acetylation in the rat central nucleus of the amygdala (CeA).
+NGF	addiction	sensitization	22871918	We report here that morphine that induced reward <b>sensitization</b>, as demonstrated by reinstatement of the behavior of conditioned place preference (CPP) with sub threshold priming morphine, epigenetically upregulated the output activity of <strong>Ngf</strong> encoding the <strong>nerve growth factor</strong> (<strong>NGF</strong>) by increasing histone H4 acetylation in the rat central nucleus of the amygdala (CeA).
+NGF	drug	opioid	22871918	<strong>NGF</strong> locally infused into the CeA mimicked the <b>morphine</b> effect in inducing new functional delta <b>opioid</b> receptor (DOR) that was required for the reward sensitization, and <b>morphine</b> induced reward sensitization was inhibited by blocking <strong>NGF</strong> receptor signaling in the CeA.
+NGF	addiction	reward	22871918	<strong>NGF</strong> locally infused into the CeA mimicked the morphine effect in inducing new functional delta opioid receptor (DOR) that was required for the <b>reward</b> sensitization, and morphine induced <b>reward</b> sensitization was inhibited by blocking <strong>NGF</strong> receptor signaling in the CeA.
+NGF	addiction	sensitization	22871918	<strong>NGF</strong> locally infused into the CeA mimicked the morphine effect in inducing new functional delta opioid receptor (DOR) that was required for the reward <b>sensitization</b>, and morphine induced reward <b>sensitization</b> was inhibited by blocking <strong>NGF</strong> receptor signaling in the CeA.
+NGF	addiction	reward	22871918	Histone deacetylase inhibitors that increased the acetylation level at the <strong>Ngf</strong> promoter and <strong>NGF</strong> expression in the CeA also induced <b>reward</b> sensitization in a CeA <strong>NGF</strong> signaling  and DOR dependent manner.
+NGF	addiction	sensitization	22871918	Histone deacetylase inhibitors that increased the acetylation level at the <strong>Ngf</strong> promoter and <strong>NGF</strong> expression in the CeA also induced reward <b>sensitization</b> in a CeA <strong>NGF</strong> signaling  and DOR dependent manner.
+NGF	drug	opioid	22871918	Furthermore, CeA applied <strong>NGF</strong> substituted prior <b>morphine</b> to induce reward sensitization in naive rats and also substituted priming <b>morphine</b> to reinstate the CPP induced by prior <b>morphine</b>.
+NGF	addiction	reward	22871918	Furthermore, CeA applied <strong>NGF</strong> substituted prior morphine to induce <b>reward</b> sensitization in naive rats and also substituted priming morphine to reinstate the <b>CPP</b> induced by prior morphine.
+NGF	addiction	sensitization	22871918	Furthermore, CeA applied <strong>NGF</strong> substituted prior morphine to induce reward <b>sensitization</b> in naive rats and also substituted priming morphine to reinstate the CPP induced by prior morphine.
+NGF	drug	opioid	22871918	Thus, epigenetic upregulation of <strong>NGF</strong> activity in the CeA may promote the behavior of <b>opioid</b> reward and increase the sensitivity to the rewarding effect of subsequent <b>opioids</b>, a potentially important mechanism in drug addiction.
+NGF	addiction	addiction	22871918	Thus, epigenetic upregulation of <strong>NGF</strong> activity in the CeA may promote the behavior of opioid reward and increase the sensitivity to the rewarding effect of subsequent opioids, a potentially important mechanism in drug <b>addiction</b>.
+NGF	addiction	reward	22871918	Thus, epigenetic upregulation of <strong>NGF</strong> activity in the CeA may promote the behavior of opioid <b>reward</b> and increase the sensitivity to the rewarding effect of subsequent opioids, a potentially important mechanism in drug addiction.
+NGF	drug	nicotine	22827868	The role of endogenous opioids on the development of pain and other important substances such as serotonin, nerve growth factor (<strong>NGF</strong>) and <b>nicotine</b> are mentioned.
+NGF	drug	opioid	22827868	The role of endogenous <b>opioids</b> on the development of pain and other important substances such as serotonin, nerve growth factor (<strong>NGF</strong>) and nicotine are mentioned.
+NGF	drug	nicotine	22827868	The role of endogenous opioids on the development of pain and other important substances such as serotonin, <strong>nerve growth factor</strong> (<strong>NGF</strong>) and <b>nicotine</b> are mentioned.
+NGF	drug	opioid	22827868	The role of endogenous <b>opioids</b> on the development of pain and other important substances such as serotonin, <strong>nerve growth factor</strong> (<strong>NGF</strong>) and nicotine are mentioned.
+NGF	drug	cocaine	22832183	Companions reverse stressor induced decreases in neurogenesis and <b>cocaine</b> conditioning possibly by restoring BDNF and <strong>NGF</strong> levels in dentate gyrus.
+NGF	drug	cocaine	22832183	Intra ventricular infusion with K252a, a mixed TrkA and TrkB antagonist, did not affect the protective effects of companions on local <strong>NGF</strong>, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and <b>cocaine</b> induced CPP.
+NGF	addiction	reward	22832183	Intra ventricular infusion with K252a, a mixed TrkA and TrkB antagonist, did not affect the protective effects of companions on local <strong>NGF</strong>, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and cocaine induced <b>CPP</b>.
+NGF	drug	cocaine	22832183	These results, taken together, indicate that stressor decreased <strong>NGF</strong> and BDNF levels in DG could be involved in the stressor decreased DG neurogenesis and <b>cocaine</b> conditioning.
+NGF	drug	cocaine	22832183	The presence of companions reverses the stressor decreased DG neurogenesis and <b>cocaine</b> conditioning possibly by restoring BDNF and <strong>NGF</strong> levels in DG.
+NGF	addiction	dependence	22517242	Association of <strong>nerve growth factor</strong> and vascular endothelial growth factor A with psychometric measurements of opiate <b>dependence</b>: results of a pilot study in patients participating in a structured diamorphine maintenance program.
+NGF	addiction	addiction	22517242	Preclinical study results suggest that neurotrophic peptides like nerve growth factor (<strong>NGF</strong>) and vascular endothelial growth factor A (VEGF A) may be associated with symptoms of <b>addictive</b> behavior like withdrawal symptoms and rewarding effects.
+NGF	addiction	withdrawal	22517242	Preclinical study results suggest that neurotrophic peptides like nerve growth factor (<strong>NGF</strong>) and vascular endothelial growth factor A (VEGF A) may be associated with symptoms of addictive behavior like <b>withdrawal</b> symptoms and rewarding effects.
+NGF	addiction	addiction	22517242	Preclinical study results suggest that neurotrophic peptides like <strong>nerve growth factor</strong> (<strong>NGF</strong>) and vascular endothelial growth factor A (VEGF A) may be associated with symptoms of <b>addictive</b> behavior like withdrawal symptoms and rewarding effects.
+NGF	addiction	withdrawal	22517242	Preclinical study results suggest that neurotrophic peptides like <strong>nerve growth factor</strong> (<strong>NGF</strong>) and vascular endothelial growth factor A (VEGF A) may be associated with symptoms of addictive behavior like <b>withdrawal</b> symptoms and rewarding effects.
+NGF	drug	opioid	22517242	We investigated alterations in <strong>NGF</strong> and VEGF A serum levels in opiate dependent patients (25 male patients), who received diamorphine (DAM, <b>heroin</b>) treatment within a structured opiate maintenance program, and compared the results with the <strong>NGF</strong> and VEGF A serum levels of healthy controls (23 male controls).
+NGF	drug	opioid	22517242	<strong>NGF</strong> and VEGF A serum levels were assessed before and after DAM administration twice a day (in the morning (16 h after last application  t1) and in the afternoon (7 h after last application  t3)) in order to detect a possible immediate or summative (in the afternoon) <b>heroin</b> effect on these two neuropeptides.
+NGF	drug	opioid	22517242	We found a significant positive association between the <strong>NGF</strong> serum levels and several items of the short opiate withdrawal scale as well as a negative association between self reported mood (measured by visual analogue scale) and mood before <b>heroin</b> application (in the morning as in the afternoon).
+NGF	addiction	withdrawal	22517242	We found a significant positive association between the <strong>NGF</strong> serum levels and several items of the short opiate <b>withdrawal</b> scale as well as a negative association between self reported mood (measured by visual analogue scale) and mood before heroin application (in the morning as in the afternoon).
+NGF	drug	opioid	22517242	Moreover, we found a significant positive association between the <strong>NGF</strong> serum levels (t1 and t3) and the self reported craving for <b>methadone</b>.
+NGF	addiction	relapse	22517242	Moreover, we found a significant positive association between the <strong>NGF</strong> serum levels (t1 and t3) and the self reported <b>craving</b> for methadone.
+NGF	addiction	dependence	22517242	In conclusion, the results of this pilot study show that there might be an association between symptoms of opiate <b>dependence</b> and withdrawal and serum levels of VEGF A and <strong>NGF</strong>.
+NGF	addiction	withdrawal	22517242	In conclusion, the results of this pilot study show that there might be an association between symptoms of opiate dependence and <b>withdrawal</b> and serum levels of VEGF A and <strong>NGF</strong>.
+NGF	drug	alcohol	22497026	Functional <strong>nerve growth factor</strong> and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic <b>ethanol</b> exposure and withdrawal.
+NGF	addiction	withdrawal	22497026	Functional <strong>nerve growth factor</strong> and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and <b>withdrawal</b>.
+NGF	drug	amphetamine	21907308	The results indicated that respiratory electron transport chain, synaptic transmission, mitochondrial electron transport, signal transduction, locomotory behavior, response to <b>amphetamine</b>, negative regulation of cell migration, glucose regulation of insulin secretion, signaling by <strong>NGF</strong>, diabetes pathways, integration of energy metabolism, dopamine receptors may play an important role in drug addiction.
+NGF	addiction	addiction	21907308	The results indicated that respiratory electron transport chain, synaptic transmission, mitochondrial electron transport, signal transduction, locomotory behavior, response to amphetamine, negative regulation of cell migration, glucose regulation of insulin secretion, signaling by <strong>NGF</strong>, diabetes pathways, integration of energy metabolism, dopamine receptors may play an important role in drug <b>addiction</b>.
+NGF	drug	opioid	21886595	Since activation of pain pathways result in exhaustion of growth factors, we examined the influence of cerebrolysin, a mixture of potent growth factors (BDNF, GDNF, <strong>NGF</strong>, CNTF etc,) on <b>morphine</b> induced HSP expression.
+NGF	addiction	sensitization	21623686	Anti <strong>NGF</strong> antibody therapy may be particularly effective in blocking bone cancer pain because <strong>NGF</strong> appears to be integrally involved in the upregulation, <b>sensitization</b> and disinhibition of multiple neurotransmitters, ion channels and receptors in the primary afferent nerve.
+NGF	drug	alcohol	21392176	Epigenetic down regulation of <strong>nerve growth factor</strong> during <b>alcohol</b> withdrawal.
+NGF	addiction	withdrawal	21392176	Epigenetic down regulation of <strong>nerve growth factor</strong> during alcohol <b>withdrawal</b>.
+NGF	drug	alcohol	21392176	We investigated the Cytosin phosphatidyl Guanin (CpG) island promoter methylation (mean and methylation of individual CpG sites) of the nerve growth factor (<strong>NGF</strong>) gene in the blood of <b>alcohol</b> dependent patients (57 male patients) during withdrawal (days 1, 7 and 14).
+NGF	addiction	withdrawal	21392176	We investigated the Cytosin phosphatidyl Guanin (CpG) island promoter methylation (mean and methylation of individual CpG sites) of the nerve growth factor (<strong>NGF</strong>) gene in the blood of alcohol dependent patients (57 male patients) during <b>withdrawal</b> (days 1, 7 and 14).
+NGF	drug	alcohol	21392176	We investigated the Cytosin phosphatidyl Guanin (CpG) island promoter methylation (mean and methylation of individual CpG sites) of the <strong>nerve growth factor</strong> (<strong>NGF</strong>) gene in the blood of <b>alcohol</b> dependent patients (57 male patients) during withdrawal (days 1, 7 and 14).
+NGF	addiction	withdrawal	21392176	We investigated the Cytosin phosphatidyl Guanin (CpG) island promoter methylation (mean and methylation of individual CpG sites) of the <strong>nerve growth factor</strong> (<strong>NGF</strong>) gene in the blood of alcohol dependent patients (57 male patients) during <b>withdrawal</b> (days 1, 7 and 14).
+NGF	drug	alcohol	21392176	These results imply an epigenetic regulation of the <strong>NGF</strong> gene during <b>alcohol</b> withdrawal.
+NGF	addiction	withdrawal	21392176	These results imply an epigenetic regulation of the <strong>NGF</strong> gene during alcohol <b>withdrawal</b>.
+NGF	drug	opioid	21358750	<strong>Nerve growth factor</strong> β polypeptide (NGFB) genetic variability: association with the <b>methadone</b> dose required for effective maintenance treatment.
+NGF	drug	opioid	21358750	<strong>Nerve growth factor</strong> β polypeptide (<strong>NGFB</strong>) genetic variability: association with the <b>methadone</b> dose required for effective maintenance treatment.
+NGF	drug	opioid	21358750	This study explores the effects of polymorphisms in the <strong>nerve growth factor</strong> (β polypeptide) gene, NGFB, on the <b>methadone</b> doses required for successful maintenance treatment for <b>heroin</b> addiction.
+NGF	addiction	addiction	21358750	This study explores the effects of polymorphisms in the <strong>nerve growth factor</strong> (β polypeptide) gene, NGFB, on the methadone doses required for successful maintenance treatment for heroin <b>addiction</b>.
+NGF	drug	opioid	21358750	This study explores the effects of polymorphisms in the <strong>nerve growth factor</strong> (β polypeptide) gene, <strong>NGFB</strong>, on the <b>methadone</b> doses required for successful maintenance treatment for <b>heroin</b> addiction.
+NGF	addiction	addiction	21358750	This study explores the effects of polymorphisms in the <strong>nerve growth factor</strong> (β polypeptide) gene, <strong>NGFB</strong>, on the methadone doses required for successful maintenance treatment for heroin <b>addiction</b>.
+NGF	drug	opioid	21358750	Genotypes of 14 <strong>NGFB</strong> polymorphisms were analyzed for association with the stabilizing <b>methadone</b> dose in 72 former severe <b>heroin</b> addicts with no major co medications.
+NGF	drug	opioid	21358750	There was significant difference in <b>methadone</b> doses required by subjects with different genotypes of the <strong>NGFB</strong> intronic single nucleotide polymorphism rs2239622 (P=0.0002).
+NGF	drug	opioid	21219293	In the skin and peripheral nerves, potential mediator and receptor therapeutic targets include the H4 histamine receptor, protease activated receptor 2, serine proteases, cathepsin S, peripheral mu  and kappa <b>opioid</b> receptors, interleukin 31, transient receptor potential vanilloid 1 and 3, fatty acid amide hydrolase, <strong>nerve growth factor</strong> and its receptor, acetylcholine, and the Mas related G protein coupled receptors.
+NGF	addiction	sensitization	21208378	They interact with keratinocytes, inflammatory cells such as T lymphocytes, eosinophils and basophils which have been shown to release multiple pruritogenic mediators (e.g., <strong>nerve growth factor</strong>, interleukin 31) which lead to activation, <b>sensitization</b> and sprouting of skin nerves.
+NGF	addiction	sensitization	21182491	The experimental pain tests (phasic pain, <b>sensitization</b>) involved pressure at the tibial bone, cutaneous electrical and thermal stimulation, intramuscular <strong>nerve growth factor</strong>, UVB light burn injury model and intradermal capsaicin induced hyperalgesia.
+NGF	drug	opioid	21182491	Compared with placebo, <b>buprenorphine</b>, but not <b>fentanyl</b>, significantly attenuated pressure at the tibial bone as well as pressure pain in the primary hyperalgesic area induced by UVB light The two drugs were equipotent and better than placebo against cutaneous thermal pain stimulation), but failed to show significant analgesic effect to cutaneous electrical stimulation, <strong>nerve growth factor</strong> induced muscle soreness and to capsaicin induced hyperalgesia.
+NGF	drug	psychedelics	20519846	Thus, the present study examined the effect of recreational drugs, such as <b>MDMA</b>, 3,4 methylenedioxyamphetamine (MDA) and diphenylprolinol, a novel recreational drug with a similar chemical structure as that of psychoactive agent pipradrol, on nerve growth factor (<strong>NGF</strong>) induced neurite outgrowth.
+NGF	drug	psychedelics	20519846	Thus, the present study examined the effect of recreational drugs, such as <b>MDMA</b>, 3,4 methylenedioxyamphetamine (MDA) and diphenylprolinol, a novel recreational drug with a similar chemical structure as that of psychoactive agent pipradrol, on <strong>nerve growth factor</strong> (<strong>NGF</strong>) induced neurite outgrowth.
+NGF	drug	psychedelics	20519846	To examine the effects of these recreational drugs on <strong>NGF</strong> induced neurite outgrowth, PC12 cells were treated with <strong>NGF</strong> together with <b>MDMA</b>, MDA, S diphenylprolinol or R diphenylprolinol at low toxic concentrations.
+NGF	drug	alcohol	20472139	<strong>NGF</strong> in the other hand is thought to be involved in aggression and <b>alcohol</b> dependence.
+NGF	addiction	dependence	20472139	<strong>NGF</strong> in the other hand is thought to be involved in aggression and alcohol <b>dependence</b>.
+NGF	drug	alcohol	20382450	The aim of this study was to investigate changes in nerve growth factor (<strong>NGF</strong>), brain derived neurotrophic factor (BDNF), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF) in brain areas, liver, and kidney of 18 mo old male mice exposed perinatally to <b>ethanol</b> at 11% vol or to red wine at the same <b>ethanol</b> concentration.
+NGF	drug	alcohol	20382450	The aim of this study was to investigate changes in <strong>nerve growth factor</strong> (<strong>NGF</strong>), brain derived neurotrophic factor (BDNF), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF) in brain areas, liver, and kidney of 18 mo old male mice exposed perinatally to <b>ethanol</b> at 11% vol or to red wine at the same <b>ethanol</b> concentration.
+NGF	drug	alcohol	20382450	The authors found that <b>ethanol</b> per se elevated <strong>NGF</strong>, BDNF, HGF, and VEGF measured by ELISA in brain limbic system areas.
+NGF	drug	alcohol	19861148	Short term exposure to <b>ethanol</b> causes a differential response between <strong>nerve growth factor</strong> and brain derived neurotrophic factor ligand/receptor systems in the mouse cerebellum.
+NGF	drug	alcohol	19861148	We found that exposure to <b>ethanol</b> resulted in elevated levels of nerve growth factor (<strong>NGF</strong>) and TrkA mRNA expression but a decreased level of brain derived neurotrophic factor (BDNF) mRNA expression.
+NGF	drug	alcohol	19861148	We found that exposure to <b>ethanol</b> resulted in elevated levels of <strong>nerve growth factor</strong> (<strong>NGF</strong>) and TrkA mRNA expression but a decreased level of brain derived neurotrophic factor (BDNF) mRNA expression.
+NGF	drug	alcohol	19560628	Relation between plasma brain derived neurotrophic factor and <strong>nerve growth factor</strong> in the male patients with <b>alcohol</b> dependence.
+NGF	addiction	dependence	19560628	Relation between plasma brain derived neurotrophic factor and <strong>nerve growth factor</strong> in the male patients with alcohol <b>dependence</b>.
+NGF	drug	alcohol	19560628	Our aim was to verify the changes in human plasma BDNF and <strong>NGF</strong> concentrations induced by chronic <b>alcohol</b> use.
+NGF	drug	alcohol	19560628	Mean plasma <strong>NGF</strong> level was also significantly higher in patients with <b>alcohol</b> dependence (137.64+/ 32.7 pg/mL) than in healthy subjects (112.61+/ 90.2 pg/mL) (P=.012).
+NGF	addiction	dependence	19560628	Mean plasma <strong>NGF</strong> level was also significantly higher in patients with alcohol <b>dependence</b> (137.64+/ 32.7 pg/mL) than in healthy subjects (112.61+/ 90.2 pg/mL) (P=.012).
+NGF	drug	alcohol	19560628	Plasma BDNF and <strong>NGF</strong> levels showed significant negative correlation in <b>alcohol</b> dependence group (r= 0.388, P=.012).
+NGF	addiction	dependence	19560628	Plasma BDNF and <strong>NGF</strong> levels showed significant negative correlation in alcohol <b>dependence</b> group (r= 0.388, P=.012).
+NGF	drug	alcohol	19560628	Increased plasma BDNF and <strong>NGF</strong> with negative correlation in <b>alcohol</b> dependent patients may have some role in the regeneration of damage done by chronic <b>alcohol</b> use.
+NGF	drug	opioid	19150465	This article begins with the peripheral actions of <b>opioids</b>, turns to a discussion of the effects of adrenergic co adjuvants, and then moves on to a discussion of pro inflammatory mechanisms focusing on TRP channels and <strong>nerve growth factor</strong>, their signaling pathways and arising therapeutic perspectives.
+NGF	drug	opioid	19114089	Accumulating evidence suggests that the nerve growth factor (<strong>NGF</strong>) family of neurotrophins may have an important modulatory role in the induction of <b>opioid</b> analgesia and <b>opioid</b> addiction.
+NGF	addiction	addiction	19114089	Accumulating evidence suggests that the nerve growth factor (<strong>NGF</strong>) family of neurotrophins may have an important modulatory role in the induction of opioid analgesia and opioid <b>addiction</b>.
+NGF	drug	opioid	19114089	Accumulating evidence suggests that the <strong>nerve growth factor</strong> (<strong>NGF</strong>) family of neurotrophins may have an important modulatory role in the induction of <b>opioid</b> analgesia and <b>opioid</b> addiction.
+NGF	addiction	addiction	19114089	Accumulating evidence suggests that the <strong>nerve growth factor</strong> (<strong>NGF</strong>) family of neurotrophins may have an important modulatory role in the induction of opioid analgesia and opioid <b>addiction</b>.
+NGF	drug	cannabinoid	18765135	These features include the <strong>nerve growth factor</strong> actions and failure of the <b>endocannabinoid</b> system.
+NGF	drug	alcohol	18639986	<strong>NGF</strong> plasma levels increase due to <b>alcohol</b> intoxication and decrease during withdrawal.
+NGF	addiction	intoxication	18639986	<strong>NGF</strong> plasma levels increase due to alcohol <b>intoxication</b> and decrease during withdrawal.
+NGF	addiction	withdrawal	18639986	<strong>NGF</strong> plasma levels increase due to alcohol intoxication and decrease during <b>withdrawal</b>.
+NGF	drug	alcohol	18639986	Recent studies show that <b>alcohol</b> dependence is associated with alterations in plasma levels of nerve growth factor (<strong>NGF</strong>).
+NGF	addiction	dependence	18639986	Recent studies show that alcohol <b>dependence</b> is associated with alterations in plasma levels of nerve growth factor (<strong>NGF</strong>).
+NGF	drug	alcohol	18639986	Recent studies show that <b>alcohol</b> dependence is associated with alterations in plasma levels of <strong>nerve growth factor</strong> (<strong>NGF</strong>).
+NGF	addiction	dependence	18639986	Recent studies show that alcohol <b>dependence</b> is associated with alterations in plasma levels of <strong>nerve growth factor</strong> (<strong>NGF</strong>).
+NGF	drug	alcohol	18639986	The aim of this study was to further elucidate reported alterations in <strong>NGF</strong> plasma levels during <b>alcohol</b> intoxication and withdrawal.
+NGF	addiction	intoxication	18639986	The aim of this study was to further elucidate reported alterations in <strong>NGF</strong> plasma levels during alcohol <b>intoxication</b> and withdrawal.
+NGF	addiction	withdrawal	18639986	The aim of this study was to further elucidate reported alterations in <strong>NGF</strong> plasma levels during alcohol intoxication and <b>withdrawal</b>.
+NGF	drug	alcohol	18639986	Therefore, we assessed <strong>NGF</strong> plasma levels by enzyme linked immunosorbent assay (ELISA) on admission (day 0) and day 7 of <b>alcohol</b> withdrawal in male <b>alcohol</b> dependent patients (n=75) in comparison to healthy controls (n=44).
+NGF	addiction	withdrawal	18639986	Therefore, we assessed <strong>NGF</strong> plasma levels by enzyme linked immunosorbent assay (ELISA) on admission (day 0) and day 7 of alcohol <b>withdrawal</b> in male alcohol dependent patients (n=75) in comparison to healthy controls (n=44).
+NGF	drug	alcohol	18639986	We found significant higher (U=1005.0, p<0.001) <strong>NGF</strong> plasma levels in the <b>alcohol</b> dependent patients.
+NGF	drug	alcohol	18639986	Subgroup analysis showed significant higher (U= 2.934, p=0.003) <strong>NGF</strong> plasma levels in patients suffering from acute <b>alcohol</b> intoxication (group A) than in early abstinent patients (group B).
+NGF	addiction	intoxication	18639986	Subgroup analysis showed significant higher (U= 2.934, p=0.003) <strong>NGF</strong> plasma levels in patients suffering from acute alcohol <b>intoxication</b> (group A) than in early abstinent patients (group B).
+NGF	drug	alcohol	18639986	From day 0 to day 7 of <b>alcohol</b> withdrawal <strong>NGF</strong> plasma levels decreased significantly in both groups (group A: Z= 3.118, p=0.002, group B: Z= 2.103, p=0.035).
+NGF	addiction	withdrawal	18639986	From day 0 to day 7 of alcohol <b>withdrawal</b> <strong>NGF</strong> plasma levels decreased significantly in both groups (group A: Z= 3.118, p=0.002, group B: Z= 2.103, p=0.035).
+NGF	drug	alcohol	18639986	Our results suggest that acute <b>alcohol</b> intoxication is associated with an increase in <strong>NGF</strong> plasma levels, which decrease during <b>alcohol</b> withdrawal.
+NGF	addiction	intoxication	18639986	Our results suggest that acute alcohol <b>intoxication</b> is associated with an increase in <strong>NGF</strong> plasma levels, which decrease during alcohol withdrawal.
+NGF	addiction	withdrawal	18639986	Our results suggest that acute alcohol intoxication is associated with an increase in <strong>NGF</strong> plasma levels, which decrease during alcohol <b>withdrawal</b>.
+NGF	drug	alcohol	18639986	These results suggest that <strong>NGF</strong> plasma levels increase as part of a regulation mechanism that counteracts <b>alcohol</b> intoxication.
+NGF	addiction	intoxication	18639986	These results suggest that <strong>NGF</strong> plasma levels increase as part of a regulation mechanism that counteracts alcohol <b>intoxication</b>.
+NGF	drug	alcohol	18427989	In search for the substrate of <b>naltrexone</b> and <b>acamprosate</b> action on <b>alcohol</b> craving, we investigated the effects of <b>ethanol</b> alone and combined with <b>naltrexone</b> or <b>acamprosate</b> on expression of <strong>nerve growth factor</strong> inducible clone A (NGFI A; zif268).
+NGF	addiction	relapse	18427989	In search for the substrate of naltrexone and acamprosate action on alcohol <b>craving</b>, we investigated the effects of ethanol alone and combined with naltrexone or acamprosate on expression of <strong>nerve growth factor</strong> inducible clone A (NGFI A; zif268).
+NGF	addiction	withdrawal	18333964	The TSPO ligand Ro5 4864 rescued cultured neonatal DRG neurons from <strong>nerve growth factor</strong> <b>withdrawal</b> induced apoptosis and protected neonatal spinal cord motor neurons from death due to sciatic nerve axotomy.
+NGF	drug	amphetamine	18093743	The expression patterns of <strong>nerve growth factor</strong> inducible clone A (NGFI A), secretogranin, post synaptic density protein of 95 Kd (PSD 95), prodynorphin and proenkephalin mRNA were also analyzed using in situ hybridization, after the challenge with <b>amphetamine</b>.
+NGF	drug	cocaine	17715210	Chronic heroin and <b>cocaine</b> abuse is associated with decreased serum concentrations of the <strong>nerve growth factor</strong> and brain derived neurotrophic factor.
+NGF	drug	opioid	17715210	Chronic <b>heroin</b> and cocaine abuse is associated with decreased serum concentrations of the <strong>nerve growth factor</strong> and brain derived neurotrophic factor.
+NGF	drug	cocaine	17715210	In the present study, we measured by enzyme linked immunosorbent assay (ELISA) the <strong>NGF</strong> and BDNF levels in serum of three groups of subjects: heroin dependent patients, <b>cocaine</b> dependent patients and healthy volunteers.
+NGF	drug	opioid	17715210	In the present study, we measured by enzyme linked immunosorbent assay (ELISA) the <strong>NGF</strong> and BDNF levels in serum of three groups of subjects: <b>heroin</b> dependent patients, cocaine dependent patients and healthy volunteers.
+NGF	drug	cocaine	17715210	BDNF was decreased in heroin users whereas <strong>NGF</strong> was decreased in both heroin and <b>cocaine</b> users.
+NGF	drug	opioid	17715210	BDNF was decreased in <b>heroin</b> users whereas <strong>NGF</strong> was decreased in both <b>heroin</b> and cocaine users.
+NGF	addiction	addiction	17715210	These findings indicate that <strong>NGF</strong> and BDNF may play a role in the neurotoxicity and <b>addiction</b> induced by these drugs.
+NGF	addiction	sensitization	17693023	As the anti <strong>NGF</strong> antibody does not appreciably cross the blood brain barrier, the present data suggest that the anti hyperalgesic action of anti <strong>NGF</strong> therapy results from blockade of activation and/or <b>sensitization</b> of the CGRP/trkA positive fibers that normally constitute the majority of sensory fibers that innervate the bone.
+NGF	drug	amphetamine	17614110	<b>METH</b> and MDMA displaced [(3)H]methyllycaconitine and [(3)H]epibatidine binding in membranes from <strong>NGF</strong> differentiated PC 12 cells and mouse brain, with K(i) values in the micromolar range, MDMA revealing a greater affinity than <b>METH</b>.
+NGF	drug	psychedelics	17614110	METH and <b>MDMA</b> displaced [(3)H]methyllycaconitine and [(3)H]epibatidine binding in membranes from <strong>NGF</strong> differentiated PC 12 cells and mouse brain, with K(i) values in the micromolar range, <b>MDMA</b> revealing a greater affinity than METH.
+NGF	drug	amphetamine	17434716	Chronic <b>amphetamine</b> treatment reduces <strong>NGF</strong> and BDNF in the rat brain.
+NGF	drug	amphetamine	17434716	In this study in order to investigate the mechanism of <b>amphetamine</b> induced neurotoxicity and further elucidate the role of neurotrophins in the pathogenesis of schizophrenia we administered intraperitoneally d <b>amphetamine</b> for 8 days to rats and measured the levels of neurotrophins <strong>NGF</strong> and BDNF in selected brain regions by ELISA.
+NGF	drug	amphetamine	17434716	<b>Amphetamine</b> reduced <strong>NGF</strong> levels in the hippocampus, occipital cortex and hypothalamus and of BDNF in the occipital cortex and hypothalamus.
+NGF	drug	amphetamine	17434716	Thus the present data indicate that chronic <b>amphetamine</b> can reduce the levels of <strong>NGF</strong> and BDNF in selected brain regions.
+NGF	drug	alcohol	17434673	<strong>Nerve growth factor</strong> in serum is a marker of the stage of <b>alcohol</b> disease.
+NGF	drug	alcohol	17434673	We examined patients in different stages of <b>alcohol</b> disease and measured their <strong>NGF</strong> serum concentrations based on the hypothesis that these reflect the state of disease.
+NGF	drug	alcohol	17434673	<strong>NGF</strong> serum levels were significantly elevated in <b>alcohol</b> dependent patients, more so in those with prior delirium.
+NGF	drug	alcohol	17434673	In accordance with this hypothesis, <strong>NGF</strong> values are "normal" in patients with persistent <b>alcohol</b> related cognitive decline.
+NGF	drug	alcohol	17316397	Functional <strong>nerve growth factor</strong> and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic <b>ethanol</b> exposure and withdrawal.
+NGF	addiction	withdrawal	17316397	Functional <strong>nerve growth factor</strong> and trkA autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and <b>withdrawal</b>.
+NGF	drug	alcohol	17316397	As <b>ethanol</b> (Et) can induce cortical nerve growth factor (<strong>NGF</strong>) expression, adult rats were challenged with Et on three consecutive days per week for 6 weeks.
+NGF	drug	alcohol	17316397	As <b>ethanol</b> (Et) can induce cortical <strong>nerve growth factor</strong> (<strong>NGF</strong>) expression, adult rats were challenged with Et on three consecutive days per week for 6 weeks.
+NGF	drug	amphetamine	17049170	Neurotoxic <b>AMPH</b> pretreatment resulted in significantly diminished <b>AMPH</b> challenge induced mRNA increases of activity regulated cytoskeletal protein (ARC), <strong>nerve growth factor</strong> inducible protein A (NGFI A), and <strong>nerve growth factor</strong> inducible protein B (NGFI B) in the parietal cortex while neither saline pretreatment nor non neurotoxic <b>AMPH</b> pretreatment did.
+NGF	drug	alcohol	16737466	Possible role of <strong>nerve growth factor</strong> in the pathogenesis of <b>alcohol</b> dependence.
+NGF	addiction	dependence	16737466	Possible role of <strong>nerve growth factor</strong> in the pathogenesis of alcohol <b>dependence</b>.
+NGF	drug	alcohol	16737466	Recent studies have raised the possibility that nerve growth factor (<strong>NGF</strong>) is abnormally regulated in the central nervous system (CNS) of animal models of chronic <b>ethanol</b> treatment.
+NGF	drug	alcohol	16737466	Recent studies have raised the possibility that <strong>nerve growth factor</strong> (<strong>NGF</strong>) is abnormally regulated in the central nervous system (CNS) of animal models of chronic <b>ethanol</b> treatment.
+NGF	drug	alcohol	16737466	The goals of this study were to determine whether prolonged <b>alcohol</b> consumption is associated with the plasma <strong>NGF</strong> levels and to assess the effect of a positive family history of <b>alcohol</b> dependence on plasma <strong>NGF</strong> levels in the <b>alcohol</b> dependent patients.
+NGF	addiction	dependence	16737466	The goals of this study were to determine whether prolonged alcohol consumption is associated with the plasma <strong>NGF</strong> levels and to assess the effect of a positive family history of alcohol <b>dependence</b> on plasma <strong>NGF</strong> levels in the alcohol dependent patients.
+NGF	drug	alcohol	16737466	We used the enzyme linked immunosorbent assay (ELISA) to determine the concentrations of peripheral <strong>NGF</strong> in patients with <b>alcohol</b> dependence and in a control group.
+NGF	addiction	dependence	16737466	We used the enzyme linked immunosorbent assay (ELISA) to determine the concentrations of peripheral <strong>NGF</strong> in patients with alcohol <b>dependence</b> and in a control group.
+NGF	drug	alcohol	16737466	The plasma <strong>NGF</strong> concentrations in the <b>alcohol</b> dependent patients were significantly lower than in the controls (71.9 vs 110.5 pg/mL, respectively).
+NGF	drug	alcohol	16737466	Moreover, the <b>alcohol</b> dependent patients with positive family histories showed a greater decrease in their <strong>NGF</strong> levels than those subjects with negative family histories (64.7 vs 83.3 pg/mL, respectively).
+NGF	drug	alcohol	16737466	Our study suggests that the <strong>NGF</strong> levels may be a trait marker for the development of <b>alcohol</b> dependence.
+NGF	addiction	dependence	16737466	Our study suggests that the <strong>NGF</strong> levels may be a trait marker for the development of alcohol <b>dependence</b>.
+NGF	drug	alcohol	16252071	Chronic <b>alcohol</b> intoxication in rats leads to a strong but transient increase in <strong>NGF</strong> levels in distinct brain regions.
+NGF	addiction	intoxication	16252071	Chronic alcohol <b>intoxication</b> in rats leads to a strong but transient increase in <strong>NGF</strong> levels in distinct brain regions.
+NGF	drug	alcohol	16252071	In this study <strong>NGF</strong> protein levels were determined in areas of the basal forebrain cholinergic system, its projection areas as well as the striatum and the cerebellum after long term exposure (6 and 9 months) to <b>ethanol</b> and a phase of withdrawal in male Sprague Dawley rats.
+NGF	addiction	withdrawal	16252071	In this study <strong>NGF</strong> protein levels were determined in areas of the basal forebrain cholinergic system, its projection areas as well as the striatum and the cerebellum after long term exposure (6 and 9 months) to ethanol and a phase of <b>withdrawal</b> in male Sprague Dawley rats.
+NGF	drug	alcohol	16252071	6 month <b>alcohol</b> treatment led to an increase of <strong>NGF</strong> to 650 850% of controls in the basal forebrain and the septum and to a 210 485% increase in the cholinergic projection areas (anterior cortex, hippocampus and olfactory bulb).
+NGF	drug	alcohol	16252071	After 9 months exposure to <b>ethanol</b>, a decrease of <strong>NGF</strong> by 16% in the frontal cortex was observed compared to controls.
+NGF	drug	cocaine	16179556	In the present study, we evaluated the effect of increasing doses of <b>cocaine</b> on the expression of immediate early genes (IEGs), c fos and c jun, and closely related transcription factors, SP 1 and NF kbeta, at 24 h after the exposure to <b>cocaine</b> (50, 100, 200, 500, 1000, 2500 microM) in <strong>NGF</strong> differentiated PC12 cells.
+NGF	addiction	sensitization	15836976	Anti <strong>NGF</strong> therapy profoundly reduces bone cancer pain and the accompanying increase in markers of peripheral and central <b>sensitization</b>.
+NGF	drug	opioid	15836976	As nerve growth factor (<strong>NGF</strong>) has been shown to modulate inflammatory and neuropathic pain states, we focused on a novel <strong>NGF</strong> sequestering antibody and demonstrated that two administrations of this therapy in a mouse model of bone cancer pain produces a profound reduction in both ongoing and movement evoked bone cancer pain related behaviors that was greater than that achieved with acute administration of 10 or 30 mg/kg of <b>morphine</b>.
+NGF	drug	opioid	15836976	As <strong>nerve growth factor</strong> (<strong>NGF</strong>) has been shown to modulate inflammatory and neuropathic pain states, we focused on a novel <strong>NGF</strong> sequestering antibody and demonstrated that two administrations of this therapy in a mouse model of bone cancer pain produces a profound reduction in both ongoing and movement evoked bone cancer pain related behaviors that was greater than that achieved with acute administration of 10 or 30 mg/kg of <b>morphine</b>.
+NGF	addiction	sensitization	15836976	Mechanistically, the great majority of sensory fibers that innervate the bone are CGRP/TrkA expressing fibers, and if the <b>sensitization</b> and activation of these fibers is blocked by anti <strong>NGF</strong> therapy there would not be another population of nociceptors, such as the non peptidergic IB4/RET IR nerve fibers, to take their place in signaling nociceptive events.
+NGF	drug	alcohol	15520530	The effects of <strong>nerve growth factor</strong> upon the neuropeptide content of the suprachiasmatic nucleus of rats withdrawn from <b>ethanol</b> are mediated by the nucleus basalis magnocellularis.
+NGF	drug	alcohol	15520530	It has been previously shown that withdrawal from <b>alcohol</b> decreases the synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (VIP) in the suprachiasmatic nucleus (SCN), and that the infusion of <strong>NGF</strong> over 1 month completely restores these changes.
+NGF	addiction	withdrawal	15520530	It has been previously shown that <b>withdrawal</b> from alcohol decreases the synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (VIP) in the suprachiasmatic nucleus (SCN), and that the infusion of <strong>NGF</strong> over 1 month completely restores these changes.
+NGF	drug	alcohol	15520530	For this purpose we destroyed, with quinolinic acid, the NBM of rats withdrawn from <b>ethanol</b> and later infused them with <strong>NGF</strong> over a period of 13 days.
+NGF	drug	alcohol	15296847	The parietal cortex was susceptible to <b>ethanol</b> exposure, <strong>NGF</strong> and BDNF content increased, and NT 3 content fell, whereas no changes were detectable in the entorhinal cortex.
+NGF	drug	alcohol	15296847	Neurotrophin content in the two segments of the basal forebrain was affected; <strong>NGF</strong> and NT 3 content in the basal forebrain was reduced and <strong>NGF</strong> and BDNF content in the septal nuclei was increased by <b>ethanol</b> exposure.
+NGF	drug	alcohol	15246696	<b>Ethanol</b> exposure during this vulnerable window induces rapid apoptotic Purkinje cell death that is hypothesized to result from <b>ethanol</b> inhibition in brain derived <strong>nerve growth factor</strong> (BDNF) TrkB neurotrophic signaling that results in loss of apoptotic suppression.
+NGF	drug	nicotine	15066159	Additionally, neonatal quinpirole produced a significant decrease in hippocampal <strong>NGF</strong> content compared to controls, however, <b>nicotine</b> failed to alleviate this decrease in <strong>NGF</strong>.
+NGF	drug	benzodiazepine	15009662	In wild type animals, <b>diazepam</b> reduced the expression levels of the alpha subunit of the calcium/calmodulin dependent protein kinase II, as well as brain derived neurotrophic factor, MAP kinase phosphatase, transcription factor GIF, c fos and <strong>nerve growth factor</strong> induced gene A.
+NGF	drug	cocaine	14973246	A single intra VTA infusion of BDNF, but not <strong>NGF</strong>, induced long lasting enhancement of <b>cocaine</b> seeking for up to 30 d, an effect reversed by U0126.
+NGF	addiction	relapse	14973246	A single intra VTA infusion of BDNF, but not <strong>NGF</strong>, induced long lasting enhancement of cocaine <b>seeking</b> for up to 30 d, an effect reversed by U0126.
+NGF	drug	cannabinoid	14639155	A novel neuroimmune mechanism in <b>cannabinoid</b> mediated attenuation of <strong>nerve growth factor</strong> induced hyperalgesia.
+NGF	drug	cannabinoid	14639155	The effects of administration of the <b>cannabinoid</b> anandamide and the cannabimimetic <b>palmitoylethanolamide</b> on an <strong>NGF</strong> induced hyperalgesia and neutrophil accumulation were examined in this study.
+NGF	addiction	withdrawal	14639155	Baseline hind limb <b>withdrawal</b> latencies to a noxious heat stimulus were recorded before intraplantar administration of <strong>NGF</strong> (1 microg in 0.05 ml) to the hind paw of 75 male Wistar rats.
+NGF	drug	cannabinoid	14639155	Anandamide or <b>palmitoylethanolamide</b> (a substance that has <b>cannabinoid</b> like actions but little affinity for <b>cannabinoid</b> receptors) at doses of 10 and 25 mg/kg were given (intraperitoneally) immediately after <strong>NGF</strong>.
+NGF	drug	cannabinoid	14639155	<strong>NGF</strong> induced a thermal hyperalgesia that was attenuated by anandamide and <b>palmitoylethanolamide</b>.
+NGF	drug	nicotine	14500754	Differential regulation of nicotinic acetylcholine receptors in PC12 cells by <b>nicotine</b> and <strong>nerve growth factor</strong>.
+NGF	drug	nicotine	14500754	Two subtypes of receptors labeled by [3H]epibatidine were found: one that was increased about 4 fold in cells grown for 2 to 4 days in the presence of <b>nicotine</b> and one that was increased 5 fold in cells grown for 2 to 4 days in the presence of nerve growth factor (<strong>NGF</strong>).
+NGF	drug	nicotine	14500754	Two subtypes of receptors labeled by [3H]epibatidine were found: one that was increased about 4 fold in cells grown for 2 to 4 days in the presence of <b>nicotine</b> and one that was increased 5 fold in cells grown for 2 to 4 days in the presence of <strong>nerve growth factor</strong> (<strong>NGF</strong>).
+NGF	drug	nicotine	14500754	The pharmacology of the binding sites in the <b>nicotine</b>  and <strong>NGF</strong> treated cells was compared with the pharmacology of defined alpha3beta2 and alpha3beta4 nicotinic acetylcholine receptor (nAChR) subtypes heterologously expressed in human embryonic kidney 293 cells.
+NGF	drug	nicotine	14500754	<b>Nicotine</b> treatment predominantly increased a receptor with characteristics of an alpha3beta2 subtype, whereas the <strong>NGF</strong> treatment exclusively increased a receptor with characteristics of an alpha3beta4 subtype.
+NGF	drug	nicotine	14500754	Receptor function measured with the [3H]norepinephrine release assay was measurable in both <b>nicotine</b> treated and <strong>NGF</strong> treated cells; however, cytisine stimulated [3H]norepinephrine release indicated that <b>nicotine</b> treatment increased an nAChR containing beta2 subunits, whereas <strong>NGF</strong> increased a receptor containing beta4 subunits.
+NGF	drug	nicotine	14500754	<strong>NGF</strong> treatment increased mRNA only for beta4 subunits in these cells, whereas <b>nicotine</b> treatment did not affect mRNA for any of the subunits measured.
+NGF	drug	nicotine	14500754	After withdrawal of the treatments, the receptors increased by <b>nicotine</b> were much less stable than those increased by <strong>NGF</strong>.
+NGF	addiction	withdrawal	14500754	After <b>withdrawal</b> of the treatments, the receptors increased by nicotine were much less stable than those increased by <strong>NGF</strong>.
+NGF	drug	nicotine	12970390	<b>Nicotine</b> (1 1000 muM) produced a concentration dependent increase in cell viability in differentiated PC 12 cells that underwent <strong>nerve growth factor</strong> withdrawal for 24 h. Cell viability was maintained near 100% by 100 muM <b>nicotine</b>.
+NGF	addiction	withdrawal	12970390	Nicotine (1 1000 muM) produced a concentration dependent increase in cell viability in differentiated PC 12 cells that underwent <strong>nerve growth factor</strong> <b>withdrawal</b> for 24 h. Cell viability was maintained near 100% by 100 muM nicotine.
+NGF	drug	alcohol	12914967	<strong>NGF</strong> and NT 3 exert differential effects on the expression of neuropeptides in the suprachiasmatic nucleus of rats withdrawn from <b>ethanol</b> treatment.
+NGF	drug	alcohol	12914967	It was also recently shown that <strong>NGF</strong>, infused over 1 month, offsets the decreased synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (VIP) in the suprachiasmatic nucleus (SCN) of rats submitted to chronic <b>ethanol</b> treatment and withdrawal.
+NGF	addiction	withdrawal	12914967	It was also recently shown that <strong>NGF</strong>, infused over 1 month, offsets the decreased synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (VIP) in the suprachiasmatic nucleus (SCN) of rats submitted to chronic ethanol treatment and <b>withdrawal</b>.
+NGF	drug	alcohol	12831864	<strong>Nerve growth factor</strong> prevents cell death and induces hypertrophy of basal forebrain cholinergic neurons in rats withdrawn from prolonged <b>ethanol</b> intake.
+NGF	drug	alcohol	12831864	Because neurons in these nuclei are vulnerable to <b>ethanol</b> consumption and withdrawal we thought of interest to investigate, in withdrawn rats previously submitted to a prolonged period of <b>ethanol</b> intake, the effects of intraventricular delivery of <strong>NGF</strong> upon the MS/VDB cholinergic neurons.
+NGF	addiction	withdrawal	12831864	Because neurons in these nuclei are vulnerable to ethanol consumption and <b>withdrawal</b> we thought of interest to investigate, in withdrawn rats previously submitted to a prolonged period of ethanol intake, the effects of intraventricular delivery of <strong>NGF</strong> upon the MS/VDB cholinergic neurons.
+NGF	addiction	withdrawal	12831864	<strong>NGF</strong> treatment prevented the <b>withdrawal</b> associated loss, and induced hypertrophy, of cholinergic neurons.
+NGF	addiction	withdrawal	12831864	These findings show that exogenous <strong>NGF</strong> protects the phenotype and prevents the <b>withdrawal</b> induced degeneration of cholinergic neurons in the MS/VDB.
+NGF	drug	alcohol	12763581	<strong>Nerve growth factor</strong> and chronic <b>ethanol</b> treatment alter calcium homeostasis in developing rat septal neurons.
+NGF	addiction	withdrawal	12763581	PCET CET decreased and acute EtOH <b>withdrawal</b> increased overall K(+) stimulated changes in [Ca(2+)](i), but only in +<strong>NGF</strong> PCET neurons.
+NGF	addiction	withdrawal	12763581	<strong>NGF</strong> reduced overall K(+) stimulated changes in [Ca(2+)](i) in PCET neurons during EtOH <b>withdrawal</b> and during AET with 200 mg % EtOH and increased overall K(+) stimulated changes in [Ca(2+)](i) during AET with 400 and 800 mg % EtOH.
+NGF	drug	amphetamine	12638131	Using these criteria, the mRNA for three immediate early genes (IEGs), coding for activity regulated cytoskeletal associated protein (Arc), <strong>nerve growth factor</strong> induced protein A (NGFI A; early growth response protein 1) and <strong>nerve growth factor</strong> induced protein B (NGFI B), were upregulated 1 and 3 h after <b>amphetamine</b> as previously described.
+NGF	drug	cocaine	12629527	Transgenic (TG) mice expressing an antisense mRNA against the glucocorticoid receptor (GR), which partially blocks GR expression, were used to assess the role of GR dysfunction on <b>cocaine</b> (COC) induced c fos and <strong>Nerve Growth Factor</strong> Inducible B (NGFI B, or Nur77) gene expression.
+NGF	addiction	reward	12574402	Other rats were killed without testing on days 1, 30, and 90 of <b>reward</b> withdrawal, and BDNF and nerve growth factor (<strong>NGF</strong>) protein levels were measured in the ventral tegmental area (VTA), accumbens, and amygdala.
+NGF	addiction	withdrawal	12574402	Other rats were killed without testing on days 1, 30, and 90 of reward <b>withdrawal</b>, and BDNF and nerve growth factor (<strong>NGF</strong>) protein levels were measured in the ventral tegmental area (VTA), accumbens, and amygdala.
+NGF	addiction	reward	12574402	Other rats were killed without testing on days 1, 30, and 90 of <b>reward</b> withdrawal, and BDNF and <strong>nerve growth factor</strong> (<strong>NGF</strong>) protein levels were measured in the ventral tegmental area (VTA), accumbens, and amygdala.
+NGF	addiction	withdrawal	12574402	Other rats were killed without testing on days 1, 30, and 90 of reward <b>withdrawal</b>, and BDNF and <strong>nerve growth factor</strong> (<strong>NGF</strong>) protein levels were measured in the ventral tegmental area (VTA), accumbens, and amygdala.
+NGF	drug	cocaine	12574402	BDNF, but not <strong>NGF</strong>, levels in the VTA, accumbens, and amygdala progressively increased after <b>cocaine</b>, but not sucrose, withdrawal.
+NGF	addiction	withdrawal	12574402	BDNF, but not <strong>NGF</strong>, levels in the VTA, accumbens, and amygdala progressively increased after cocaine, but not sucrose, <b>withdrawal</b>.
+NGF	drug	alcohol	12478399	<strong>Nerve growth factor</strong> improves spatial learning and restores hippocampal cholinergic fibers in rats withdrawn from chronic treatment with <b>ethanol</b>.
+NGF	drug	alcohol	12478399	We hypothesized that exogenous supply of nerve growth factor (<strong>NGF</strong>), known to serve as a trophic substance for septal cholinergic neurons, can revert the <b>ethanol</b> induced changes in the septohippocampal cholinergic system.
+NGF	drug	alcohol	12478399	We hypothesized that exogenous supply of <strong>nerve growth factor</strong> (<strong>NGF</strong>), known to serve as a trophic substance for septal cholinergic neurons, can revert the <b>ethanol</b> induced changes in the septohippocampal cholinergic system.
+NGF	drug	alcohol	12478399	During the first 4 weeks after the animals were withdrawn from <b>ethanol</b>, they were intraventricularly infused with either <strong>NGF</strong> or vehicle alone via implanted osmotic minipumps.
+NGF	drug	alcohol	12478399	These data provide support to the notion that <strong>NGF</strong> is capable of ameliorating memory deficits and restoring septohippocampal cholinergic projections following chronic treatment with <b>ethanol</b>.
+NGF	drug	amphetamine	12231455	Neither <strong>NGF</strong> antibody nor DA receptor antagonists blocked <b>AMPH</b> induced neurite outgrowth, demonstrating that <b>AMPH</b> induced neurite outgrowth is not dependent on endogenous <strong>NGF</strong> release or DA receptors.
+NGF	drug	amphetamine	12223225	Differentiation of the cells with <strong>nerve growth factor</strong> did not alter the <b>amphetamine</b> mediated dopamine release in control cells or the development of enhanced release in <b>amphetamine</b> treated cells.
+NGF	drug	cocaine	12117546	Protein levels of protein tyrosine kinase 2 (PYK2), activity regulated cytoskeletal protein (ARC), as well as an antigen related to <strong>nerve growth factor</strong> I B (NGFI B RA) were shown to be significantly induced after <b>cocaine</b> administration.
+NGF	drug	nicotine	11925315	<strong>Nerve growth factor</strong> and <b>smoking</b> cessation.
+NGF	drug	alcohol	11709626	<strong>Nerve growth factor</strong> restores mRNA levels and the expression of neuropeptides in the suprachiasmatic nucleus of rats submitted to chronic <b>ethanol</b> treatment and withdrawal.
+NGF	addiction	withdrawal	11709626	<strong>Nerve growth factor</strong> restores mRNA levels and the expression of neuropeptides in the suprachiasmatic nucleus of rats submitted to chronic ethanol treatment and <b>withdrawal</b>.
+NGF	drug	alcohol	11709626	To test this possibility, nerve growth factor (<strong>NGF</strong>) was delivered intraventricularly, over a 4 week period, to rats submitted to <b>ethanol</b> treatment for 6 months and to withdrawn rats.
+NGF	drug	alcohol	11709626	To test this possibility, <strong>nerve growth factor</strong> (<strong>NGF</strong>) was delivered intraventricularly, over a 4 week period, to rats submitted to <b>ethanol</b> treatment for 6 months and to withdrawn rats.
+NGF	drug	alcohol	11709626	In <b>ethanol</b> treated and withdrawn rats, <strong>NGF</strong> produced increases in the number of AVP  and VIP immunostained neurons to values identical to those of controls.
+NGF	drug	alcohol	11709626	These findings show that <strong>NGF</strong> can correct the changes induced by chronic <b>ethanol</b> treatment and withdrawal in the gene expression and protein content of the neuropeptides synthesized by suprachiasmatic neurons.
+NGF	addiction	withdrawal	11709626	These findings show that <strong>NGF</strong> can correct the changes induced by chronic ethanol treatment and <b>withdrawal</b> in the gene expression and protein content of the neuropeptides synthesized by suprachiasmatic neurons.
+NGF	drug	opioid	10810245	The mechanism of these effects is unknown, but may involve changes in the expression of <strong>nerve growth factor</strong>, which is reduced by <b>opioid</b> exposure.
+NGF	drug	opioid	10727796	<b>Opioid</b> mechanisms, which are likely of dorsal horn origin, do not fall under the direct influence of <strong>nerve growth factor</strong> mechanisms and therefore the intriguing possibility is raised that <b>opioid</b> mechanisms in the spinal cord are regulated at least in part by substance P related mechanisms.
+NGF	drug	cocaine	10564376	Intravenous <b>cocaine</b> self administration in mice was studied to find correlates of the acquisition of <b>cocaine</b> oriented operant behaviour in the expression of <strong>nerve growth factor</strong> induced clone A (NGFI A), c fos and secretogranin II mRNAs.
+NGF	addiction	reward	10564376	Intravenous cocaine self administration in mice was studied to find correlates of the acquisition of cocaine oriented <b>operant</b> behaviour in the expression of <strong>nerve growth factor</strong> induced clone A (NGFI A), c fos and secretogranin II mRNAs.
+NGF	addiction	addiction	10407052	<b>Addiction</b> prone Lewis but not Fischer rats develop <b>compulsive</b> running that coincides with downregulation of <strong>nerve growth factor</strong> inducible B and neuron derived orphan receptor 1.
+NGF	addiction	sensitization	10384257	<strong>Nerve growth factor</strong> inducer, 4 methyl catechol, potentiates central <b>sensitization</b> associated with acceleration of spinal glutamate release after mustard oil paw injection in rats.
+NGF	addiction	sensitization	10384257	These data also suggest a possible involvement of <strong>NGF</strong> in the development of central <b>sensitization</b> after acute peripheral nociceptive stimulation.
+NGF	drug	alcohol	10372659	<strong>NGF</strong> differentiated and undifferentiated PC12 cells vary in induction of apoptosis by <b>ethanol</b>.
+NGF	drug	alcohol	9541742	Brain derived neurotrophic factor (BDNF) and nerve growth factor (<strong>NGF</strong>) have previously been shown to ameliorate <b>ethanol</b> , hypoglycemia  and hypoxia induced neurotoxicity.
+NGF	drug	alcohol	9541742	Brain derived neurotrophic factor (BDNF) and <strong>nerve growth factor</strong> (<strong>NGF</strong>) have previously been shown to ameliorate <b>ethanol</b> , hypoglycemia  and hypoxia induced neurotoxicity.
+NGF	drug	alcohol	9541742	<strong>NGF</strong> treatment provided the most extensive neuroprotection, being effective against <b>ethanol</b> (200 and 400 mg/dl), gwHG, and aHP, alone and combined.
+NGF	drug	alcohol	8727238	Changes in human plasma <strong>nerve growth factor</strong> level after chronic <b>alcohol</b> consumption and withdrawal.
+NGF	addiction	withdrawal	8727238	Changes in human plasma <strong>nerve growth factor</strong> level after chronic alcohol consumption and <b>withdrawal</b>.
+NGF	drug	alcohol	8727238	In the present study, we demonstrated that withdrawal from chronic consumption of either <b>ethanol</b> or heroin causes a significant increase in plasma <strong>nerve growth factor</strong>, suggesting that the resulting anxiety condition triggers the release of this molecule.
+NGF	drug	opioid	8727238	In the present study, we demonstrated that withdrawal from chronic consumption of either ethanol or <b>heroin</b> causes a significant increase in plasma <strong>nerve growth factor</strong>, suggesting that the resulting anxiety condition triggers the release of this molecule.
+NGF	addiction	withdrawal	8727238	In the present study, we demonstrated that <b>withdrawal</b> from chronic consumption of either ethanol or heroin causes a significant increase in plasma <strong>nerve growth factor</strong>, suggesting that the resulting anxiety condition triggers the release of this molecule.
+NGF	drug	opioid	8545003	<strong>Nerve growth factor</strong> alone had no effect on tyrosine hydroxylase or glial fibrillary acidic protein levels and did not affect <b>morphine</b>'s ability to induce these proteins.
+NGF	drug	opioid	3437467	This activity is not due to <b>morphine</b> itself and is not due to an increase in the <strong>nerve growth factor</strong> as antibodies to <strong>nerve growth factor</strong> fail to block the response.
+TLR4	drug	opioid	32733481	Toll Like Receptor 4 (<strong>TLR4</strong>)/<b>Opioid</b> Receptor Pathway Crosstalk and Impact on <b>Opioid</b> Analgesia, Immune Function, and Gastrointestinal Motility.
+TLR4	drug	opioid	32733481	<strong>Toll Like Receptor 4</strong> (<strong>TLR4</strong>)/<b>Opioid</b> Receptor Pathway Crosstalk and Impact on <b>Opioid</b> Analgesia, Immune Function, and Gastrointestinal Motility.
+TLR4	drug	opioid	32733481	This review summarizes the following types of <strong>TLR4</strong>/<b>opioid</b> receptor pathway crosstalk: (a) <b>Opioid</b> receptor agonists non stereoselectively activate the <strong>TLR4</strong> signaling pathway in the central nervous system (CNS), in the absence of lipopolysaccharide (LPS).
+TLR4	drug	opioid	32733481	<b>Opioids</b> bind to <strong>TLR4</strong>, in a manner parallel to LPS, activating <strong>TLR4</strong> signaling, which leads to nuclear factor kappa light chain enhancer of activated B cells (NF κB) expression and the production of the pro inflammatory cytokines tumor necrosis factor (TNF) α, interleukin (IL) 1β, and IL 6.
+TLR4	drug	opioid	32733481	(b) <b>Opioid</b> receptor agonists inhibit the LPS induced <strong>TLR4</strong> signaling pathway in peripheral immune cells.
+TLR4	drug	opioid	32733481	It is apparent that <strong>TLR4</strong>/<b>opioid</b> receptor pathway crosstalk varies dependent on the cell type and activating stimulus.
+TLR4	drug	opioid	32733481	(c) Both the <strong>TLR4</strong> and <b>opioid</b> receptor pathways activate the mitogen activated protein kinase (MAPK) pathway.
+TLR4	drug	opioid	32733481	This crosstalk is located downstream of the <strong>TLR4</strong> and <b>opioid</b> receptor signaling pathways.
+TLR4	drug	opioid	32733481	(d) <b>Opioid</b> receptor agonists induce the production of high mobility group box 1 (HMGB1), an endogenous <strong>TLR4</strong> agonist, supporting intercellular (neuron to glia or glia to neuron) interactions.
+TLR4	drug	opioid	32733481	This review also summarizes the potential effects of <strong>TLR4</strong>/<b>opioid</b> receptor pathway crosstalk on <b>opioid</b> analgesia, immune function, and gastrointestinal motility.
+TLR4	drug	opioid	32733481	<b>Opioids</b> non stereoselectively activate the <strong>TLR4</strong> pathway, and together with the subsequent release of pro inflammatory cytokines such as IL 1 by glia, this <strong>TLR4</strong> signaling initiates the central immune signaling response and modifies <b>opioid</b> pharmacodynamics.
+TLR4	drug	opioid	32733481	To explain <b>morphine</b> induced persistent sensitization, a positive feedback loop has been proposed; this involves an initial <b>morphine</b> induced amplified release of IL 1β and a subsequent exacerbated release of DAMPs, which increases the activation of <strong>TLR4</strong> and the purinergic receptor P2X7R.
+TLR4	addiction	sensitization	32733481	To explain morphine induced persistent <b>sensitization</b>, a positive feedback loop has been proposed; this involves an initial morphine induced amplified release of IL 1β and a subsequent exacerbated release of DAMPs, which increases the activation of <strong>TLR4</strong> and the purinergic receptor P2X7R.
+TLR4	drug	opioid	32733481	The intracellular <strong>TLR4</strong>/<b>opioid</b> receptor signaling pathway crosstalk induces the formation of the β arrestin 2/TNF receptor associated factor 6 (TRAF6) complex, which contributes to <b>morphine</b> induced inhibition of LPS induced TNF α secretion in mast cells.
+TLR4	drug	opioid	32733481	A possible molecular mechanism is that the <strong>TLR4</strong> pathway initially triggers the formation of the β arrestin 2/TRAF6 complex, which is amplified by <b>opioid</b> receptor signaling, suggesting that β arrestin 2 acts as a functional component of the <strong>TLR4</strong> pathway.
+TLR4	drug	opioid	32590120	Subsequently the discovery of <strong>TLR 4</strong> capacity to bind to <b>opioids</b> on glial cells revealed that they shared the same neuroinflammatory mechanisms underlying cancer and non cancer pain, and could also worsen pain for which they were used.
+TLR4	drug	cocaine	32278944	Consistently, we found elevated protein levels of Iba1, CCL2, <strong>TLR4</strong> and mature IL1β in the striatum, not in the mPFc of <b>cocaine</b> receiving mice.
+TLR4	drug	alcohol	32233400	We have particularly focused on the discovery of <strong>TLR4</strong> antagonists and have assessed their great potential in the clinical treatment of drug addiction and <b>alcohol</b> use disorders.
+TLR4	addiction	addiction	32233400	We have particularly focused on the discovery of <strong>TLR4</strong> antagonists and have assessed their great potential in the clinical treatment of drug <b>addiction</b> and alcohol use disorders.
+TLR4	drug	alcohol	32014377	Role of <strong>toll like receptor 4</strong> antagonist Lipopolysaccharide Rhodobacter sphaeroides on acute stress induced voluntary <b>ethanol</b> preference and drinking behaviour: In vivo Swiss Albino mouse model.
+TLR4	drug	alcohol	32014377	The present study focused on investigating the effect of toll like receptor 4 (<strong>TLR4</strong>) antagonist Lipopolysaccharide Rhodobacter sphaeroides(LPS RS) on acute, stress induced voluntary <b>ethanol</b> preference and drinking behaviour, neuronal components activation, and gene expression associated with stress and addictive behaviour.
+TLR4	addiction	addiction	32014377	The present study focused on investigating the effect of toll like receptor 4 (<strong>TLR4</strong>) antagonist Lipopolysaccharide Rhodobacter sphaeroides(LPS RS) on acute, stress induced voluntary ethanol preference and drinking behaviour, neuronal components activation, and gene expression associated with stress and <b>addictive</b> behaviour.
+TLR4	drug	alcohol	32014377	The present study focused on investigating the effect of <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) antagonist Lipopolysaccharide Rhodobacter sphaeroides(LPS RS) on acute, stress induced voluntary <b>ethanol</b> preference and drinking behaviour, neuronal components activation, and gene expression associated with stress and addictive behaviour.
+TLR4	addiction	addiction	32014377	The present study focused on investigating the effect of <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) antagonist Lipopolysaccharide Rhodobacter sphaeroides(LPS RS) on acute, stress induced voluntary ethanol preference and drinking behaviour, neuronal components activation, and gene expression associated with stress and <b>addictive</b> behaviour.
+TLR4	drug	alcohol	32014377	<strong>TLR4</strong> antagonist LPS RS treated stressed mice showed a significant decrease in <b>ethanol</b> drinking compared with stressed mice.
+TLR4	drug	opioid	32014377	Stressed mice also showed significant increase in <strong>TLR4</strong>, Nuclear Factor Kappa B (NF kB), inducible nitric oxide synthase (iNOS), dopamine receptor D2 (DRD2), cyclic adenosine monophosphate (cAMP) response element binding protein 1 (CREB 1) and <b>opioid</b> receptor MU 1 (OPRM 1) genes expression compared with control and LPS RS treated stressed mice.
+TLR4	addiction	addiction	32014377	As a conclusion, the antagonism of <strong>TLR4</strong> could provide therapeutic value in the treatment of stress induced <b>addiction</b>.
+TLR4	drug	amphetamine	31935095	Exploring <b>Methamphetamine</b> Nonenantioselectively Targeting <strong>Toll like Receptor 4</strong>/Myeloid Differentiation Protein 2 by in Silico Simulations and Wet Lab Techniques.
+TLR4	drug	amphetamine	31935095	<b>Methamphetamine</b> (<b>METH</b>) is one of the highly addictive nonopioid psychostimulants, acting as a xenobiotic associated molecular pattern (XAMP) to target <strong>TLR4</strong> and activate microglia.
+TLR4	addiction	addiction	31935095	Methamphetamine (METH) is one of the highly <b>addictive</b> nonopioid psychostimulants, acting as a xenobiotic associated molecular pattern (XAMP) to target <strong>TLR4</strong> and activate microglia.
+TLR4	drug	amphetamine	31935095	However, the molecule recognition of <b>METH</b> by innate immune receptor <strong>TLR4</strong>/MD 2 is not well understood.
+TLR4	drug	amphetamine	31935095	<b>METH</b> exists in two enantiomeric forms, and it is unclear whether the <strong>TLR4</strong> innate immune recognition with <b>METH</b> is stereoselective.
+TLR4	drug	amphetamine	31935095	Herein, molecular dynamics (MDs) simulations were performed to dissect the recognition of (+) <b>METH</b> and ( ) <b>METH</b> by <strong>TLR4</strong>/MD 2 at the atomic level.
+TLR4	drug	amphetamine	31935095	Computational simulations indicate that <b>METH</b> binds into the interaction interface between MD 2 as well as <strong>TLR4</strong>* that is from the adjacent copy of <strong>TLR4</strong> MD 2, therefore stabilizing the active heterotetramer (<strong>TLR4</strong>/MD 2)2 complex.
+TLR4	drug	amphetamine	31935095	The calculated binding free energies and potential of mean force (PMF) values show that ( ) <b>METH</b> and (+) <b>METH</b> have similar <strong>TLR4</strong>/MD 2 binding affinity.
+TLR4	drug	amphetamine	31935095	Further dynamics analyses of bindings with <strong>TLR4</strong>/MD 2 indicate that ( ) <b>METH</b> and (+) <b>METH</b> behave similarly.
+TLR4	drug	amphetamine	31935095	Unlike the stereoselective neuron stimulating activities of <b>METH</b>, no enantioselectivity was observed for <b>METH</b> interacting with <strong>TLR4</strong>/MD 2 complex as well as activating <strong>TLR4</strong> signaling.
+TLR4	drug	amphetamine	31935095	Compared to <b>METH</b>, <b>AMPH</b> showed much weaker interactions with <strong>TLR4</strong>/MD 2, indicating that the substituted methyl group is critical in the molecular recognition of <b>METH</b> by <strong>TLR4</strong>/MD 2.
+TLR4	drug	amphetamine	31935095	In all, this study provides molecular insight into the innate immune recognition of <b>METH</b>, which demonstrates that <b>METH</b> could be nonenantioselectively sensed by <strong>TLR4</strong>/MD 2.
+TLR4	drug	opioid	31921165	Beginning with a paper published in 2005, evidence was presented that <b>morphine</b> is immune stimulating via binding to MD2, a molecule associated with Toll like Receptor 4 (<strong>TLR4</strong>), the receptor for bacterial lipopolysaccharide (LPS).
+TLR4	drug	opioid	31921165	Beginning with a paper published in 2005, evidence was presented that <b>morphine</b> is immune stimulating via binding to MD2, a molecule associated with <strong>Toll like Receptor 4</strong> (<strong>TLR4</strong>), the receptor for bacterial lipopolysaccharide (LPS).
+TLR4	drug	opioid	31921165	Since engagement of <strong>TLR4</strong> is universally accepted to result in immune activation by up regulation of NF κB, if <b>morphine</b> were binding to <strong>TLR4</strong>, it would be predicted that <b>opioids</b> would have been found to be pro inflammatory, which they were not.
+TLR4	drug	opioid	31921165	Further, <b>morphine</b> is immunosuppressive in mice with a defective <strong>TLR4</strong> receptor.
+TLR4	drug	opioid	31921165	It is proposed that an occult variable in experiments where <b>morphine</b> is being proposed to activate <strong>TLR4</strong> is actually underlying sepsis induced by the <b>opioid</b>.
+TLR4	drug	opioid	31879851	<b>morphine</b> exposure led to increased expression of HMGB1, Toll like receptor 4 (<strong>TLR4</strong>), and receptor for advanced glycation end products (RAGE) and their mRNAs in the dorsal horn.
+TLR4	drug	opioid	31879851	<b>morphine</b> exposure led to increased expression of HMGB1, <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>), and receptor for advanced glycation end products (RAGE) and their mRNAs in the dorsal horn.
+TLR4	drug	opioid	31879851	<b>Morphine</b> challenge also promoted HMGB1 expression and release in cultured spinal neurons, but these effects were inhibited by TAK 242, <b>naloxone</b> (antagonists of <strong>TLR4</strong>), and <strong>TLR4</strong> siRNA.
+TLR4	drug	opioid	31879851	Together, these results suggest that <b>morphine</b> mediated upregulation of spinal HMGB1 contributes to analgesic tolerance and hyperalgesia via activation of <strong>TLR4</strong>/NF κB signaling, and the HMGB1 inhibitor might be a promising adjuvant to <b>morphine</b> in the treatment of intractable pain in the clinic.
+TLR4	drug	opioid	31775878	The methylation of genes coding for the Toll like receptor 4 (<strong>TLR4</strong>) as a major mediator of glial contributions to persistent pain or for the μ <b>opioid</b> receptor (OPRM1) was analyzed and its association with the pain phenotype was compared with that conferred by global genome wide DNA methylation assessed via quantification of the methylation in the retrotransposon LINE1.
+TLR4	drug	opioid	31775878	The methylation of genes coding for the <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) as a major mediator of glial contributions to persistent pain or for the μ <b>opioid</b> receptor (OPRM1) was analyzed and its association with the pain phenotype was compared with that conferred by global genome wide DNA methylation assessed via quantification of the methylation in the retrotransposon LINE1.
+TLR4	drug	alcohol	31666409	The effects of acute (single) and chronic <b>ethanol</b> administration on the level of pro inflammatory cytokines (IL 1β and TNF α), as well as on the level of mRNA NF κB, <strong>TLR4</strong> and its endogenous agonist, HMGB1 protein, were investigated in rats.
+TLR4	drug	alcohol	31666409	The <b>ethanol</b> withdrawal after prolonged administration resulted in dysregulation of cytokine levels, <strong>TLR4</strong> and HMGB1.
+TLR4	addiction	withdrawal	31666409	The ethanol <b>withdrawal</b> after prolonged administration resulted in dysregulation of cytokine levels, <strong>TLR4</strong> and HMGB1.
+TLR4	drug	opioid	31433351	By contrast, the blockade of <strong>TLR4</strong> had no effect on the induction of <b>opioid</b> withdrawal LTP.
+TLR4	addiction	withdrawal	31433351	By contrast, the blockade of <strong>TLR4</strong> had no effect on the induction of opioid <b>withdrawal</b> LTP.
+TLR4	drug	amphetamine	31282647	<b>Methamphetamine</b> Activates <strong>Toll Like Receptor 4</strong> to Induce Central Immune Signaling within the Ventral Tegmental Area and Contributes to Extracellular Dopamine Increase in the Nucleus Accumbens Shell.
+TLR4	drug	amphetamine	31282647	Herein, we provide direct evidence that <b>METH</b> creates neuroinflammation, at least in part, via the activation of the innate immune Toll like receptor 4 (<strong>TLR4</strong>).
+TLR4	drug	amphetamine	31282647	Herein, we provide direct evidence that <b>METH</b> creates neuroinflammation, at least in part, via the activation of the innate immune <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>).
+TLR4	drug	amphetamine	31282647	Biophysical studies revealed that <b>METH</b> bound to MD 2, the key coreceptor of <strong>TLR4</strong>.
+TLR4	drug	amphetamine	31282647	Molecular dynamics simulations showed <b>METH</b> binding stabilized the active heterotetramer (<strong>TLR4</strong>/MD 2)2 conformation.
+TLR4	drug	amphetamine	31282647	Classic <strong>TLR4</strong> antagonists LPS RS and TAK 242 attenuated <b>METH</b> induced NF κB activation of microglia, whereas added MD 2 protein boosted <b>METH</b> induced NF κB activation.
+TLR4	drug	amphetamine	31282647	Systemic administration of a nonopioid, blood brain barrier permeable <strong>TLR4</strong> antagonist (+) naloxone inhibited <b>METH</b> induced activation of microglia and IL 6 mRNA overexpression in VTA.
+TLR4	drug	opioid	31282647	Systemic administration of a nonopioid, blood brain barrier permeable <strong>TLR4</strong> antagonist (+) <b>naloxone</b> inhibited METH induced activation of microglia and IL 6 mRNA overexpression in VTA.
+TLR4	drug	amphetamine	31282647	<b>METH</b> was found to increase conditioned place preference (CPP) as well as extracellular dopamine concentrations in the NAc, with both effects suppressed by the nonopioid <strong>TLR4</strong> antagonist (+) naloxone.
+TLR4	drug	opioid	31282647	METH was found to increase conditioned place preference (CPP) as well as extracellular dopamine concentrations in the NAc, with both effects suppressed by the nonopioid <strong>TLR4</strong> antagonist (+) <b>naloxone</b>.
+TLR4	addiction	reward	31282647	METH was found to increase conditioned place preference (<b>CPP</b>) as well as extracellular dopamine concentrations in the NAc, with both effects suppressed by the nonopioid <strong>TLR4</strong> antagonist (+) naloxone.
+TLR4	drug	amphetamine	31282647	Taken together, this series of studies demonstrate that <b>METH</b> induced neuroinflammation is, at least in part, mediated by <strong>TLR4</strong> IL6 signaling within the VTA, which has the downstream effect of elevating dopamine in the NAc shell.
+TLR4	drug	alcohol	31268779	<b>Alcohol</b> induced adipose tissue macrophage phenotypic switching is independent of myeloid <strong>Toll like receptor 4</strong> expression.
+TLR4	drug	alcohol	31268779	Here, we sought to determine the role of the innate immune receptor Toll like receptor 4 (<strong>TLR4</strong>) in <b>alcohol</b> induced adipose tissue inflammation.
+TLR4	drug	alcohol	31268779	Here, we sought to determine the role of the innate immune receptor <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) in <b>alcohol</b> induced adipose tissue inflammation.
+TLR4	drug	alcohol	31268779	Using a model of chronic, multiple binge <b>alcohol</b> exposure, we showed that <b>alcohol</b> mediated accumulation of proinflammatory adipose tissue macrophages was absent in global <strong>TLR4</strong> knockout mice.
+TLR4	addiction	intoxication	31268779	Using a model of chronic, multiple <b>binge</b> alcohol exposure, we showed that alcohol mediated accumulation of proinflammatory adipose tissue macrophages was absent in global <strong>TLR4</strong> knockout mice.
+TLR4	drug	alcohol	31268779	Proinflammatory macrophage accumulation did not depend on macrophage <strong>TLR4</strong> expression; LysMCre driven deletion of <strong>Tlr4</strong> from myeloid cells did not affect circulating endotoxin or the accumulation of M1 macrophages in adipose tissue following <b>alcohol</b> exposure.
+TLR4	drug	alcohol	31268779	Finally, the levels of other adipose immune cells, such as dendritic cells, neutrophils, B cells, and T cells, were modulated by chronic, multiple binge <b>alcohol</b> and the presence of <strong>TLR4</strong>.
+TLR4	addiction	intoxication	31268779	Finally, the levels of other adipose immune cells, such as dendritic cells, neutrophils, B cells, and T cells, were modulated by chronic, multiple <b>binge</b> alcohol and the presence of <strong>TLR4</strong>.
+TLR4	drug	alcohol	31268779	Together, these data indicate that <strong>TLR4</strong> expression on cells, other than myeloid cells, is important for the <b>alcohol</b> induced increase in proinflammatory adipose tissue macrophages.
+TLR4	addiction	intoxication	31265902	The <b>binge</b> group showed increased expression of CCR5 and PD 1 in NKCs, respective to the LR group, and decreased expression of <strong>TLR4</strong>, along with fewer CCR4+ cells.
+TLR4	addiction	addiction	31162938	Deregulation of innate immune <strong>TLR4</strong> signaling contributes to various diseases including neuropathic pain and drug <b>addiction</b>.
+TLR4	drug	alcohol	31162938	<b>Naltrexone</b> is one of the rare <strong>TLR4</strong> antagonists with good blood brain barrier permeability and showing no stereoselectivity for <strong>TLR4</strong>.
+TLR4	drug	alcohol	31162938	Interestingly, (+) norbinaltorphimine [(+) 1] showed ∼25 times better <strong>TLR4</strong> antagonist activity than <b>naltrexone</b> in microglial BV 2 cell line, whereas ( ) norbinaltorphimine [( ) 1] lost <strong>TLR4</strong> activity.
+TLR4	drug	alcohol	31096703	Natural Dietary Supplementation of Curcumin Protects Mice Brains against <b>Ethanol</b> Induced Oxidative Stress Mediated Neurodegeneration and Memory Impairment via Nrf2/<strong>TLR4</strong>/RAGE Signaling.
+TLR4	drug	alcohol	31096703	Moreover, curcumin regulated the expression of the glial cell markers in <b>ethanol</b> treated mice brains, as analyzed by the relative expression <strong>TLR4</strong> (Toll like Receptor 4), RAGE (Receptor for Advanced Glycations End products), GFAP (Glial fibrillary acidic protein), and Iba 1 (Ionized calcium binding adaptor molecule 1), through Western blot and confocal microscopic analysis.
+TLR4	drug	alcohol	31096703	Moreover, curcumin regulated the expression of the glial cell markers in <b>ethanol</b> treated mice brains, as analyzed by the relative expression <strong>TLR4</strong> (<strong>Toll like Receptor 4</strong>), RAGE (Receptor for Advanced Glycations End products), GFAP (Glial fibrillary acidic protein), and Iba 1 (Ionized calcium binding adaptor molecule 1), through Western blot and confocal microscopic analysis.
+TLR4	drug	alcohol	31030249	In this review, we discuss our findings designed to elucidate the potential contribution of the activated <strong>TLR4</strong> signal located in neurons, on impulsivity and the predisposition to initiate <b>alcohol</b> drinking (binge drinking).
+TLR4	addiction	intoxication	31030249	In this review, we discuss our findings designed to elucidate the potential contribution of the activated <strong>TLR4</strong> signal located in neurons, on impulsivity and the predisposition to initiate alcohol drinking (<b>binge</b> drinking).
+TLR4	drug	alcohol	31030249	Our findings indicate that the <strong>TLR4</strong> signal is innately activated in neurons from <b>alcohol</b> preferring subjects, identifying a genetic contribution to the regulation of impulsivity and the <b>alcohol</b> seeking propensity.
+TLR4	addiction	relapse	31030249	Our findings indicate that the <strong>TLR4</strong> signal is innately activated in neurons from alcohol preferring subjects, identifying a genetic contribution to the regulation of impulsivity and the alcohol <b>seeking</b> propensity.
+TLR4	addiction	intoxication	31030249	Focus is on the effect of <strong>TLR4</strong> signal activation on the balance between pro  and anti inflammatory chemokines [chemokine (C C motif) ligand 2 (CCL2)/chemokine (C X3 C motif) ligand 1 (CX3CL1)] and its effect on <b>binge</b> drinking.
+TLR4	addiction	intoxication	31030249	They indicate that the balance between pro  and anti inflammatory <strong>TLR4</strong> signaling plays a major role in <b>binge</b> drinking.
+TLR4	drug	opioid	30890355	<b>Morphine</b> affects glia by binding to the innate immune receptor toll like receptor 4 (<strong>TLR4</strong>), leading to the release of proinflammatory cytokines and opposition of <b>morphine</b> analgesia.
+TLR4	drug	opioid	30890355	<b>Morphine</b> affects glia by binding to the innate immune receptor <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), leading to the release of proinflammatory cytokines and opposition of <b>morphine</b> analgesia.
+TLR4	drug	opioid	30890355	This review attempts to summarize what is known regarding the role of vlPAG glia and <strong>TLR4</strong> in the development of <b>morphine</b> tolerance.
+TLR4	drug	alcohol	30836218	While, the PUE+SIL treatment showed the most effective protection, which was associated with reducing <b>alcohol</b> induced hepatic steatosis via upregulating LKB1/AMPK/ACC signaling, and inhibiting hepatic inflammation via LPS triggered <strong>TLR4</strong> mediated NF κB signaling pathway.
+TLR4	drug	opioid	30741729	A further assessment of a role for <strong>Toll like receptor 4</strong> in the reinforcing and reinstating effects of <b>opioids</b>.
+TLR4	addiction	reward	30741729	A further assessment of a role for <strong>Toll like receptor 4</strong> in the <b>reinforcing</b> and reinstating effects of opioids.
+TLR4	drug	alcohol	30741729	The Toll like receptor 4 (<strong>TLR4</strong>) antagonists, (+) naloxone and (+) <b>naltrexone</b>, have been reported to decrease self administration of opioids in rats and to reduce other preclinical indicators of abuse potential.
+TLR4	drug	opioid	30741729	The Toll like receptor 4 (<strong>TLR4</strong>) antagonists, (+) <b>naloxone</b> and (+) naltrexone, have been reported to decrease self administration of <b>opioids</b> in rats and to reduce other preclinical indicators of abuse potential.
+TLR4	drug	alcohol	30741729	The <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) antagonists, (+) naloxone and (+) <b>naltrexone</b>, have been reported to decrease self administration of opioids in rats and to reduce other preclinical indicators of abuse potential.
+TLR4	drug	opioid	30741729	The <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) antagonists, (+) <b>naloxone</b> and (+) naltrexone, have been reported to decrease self administration of <b>opioids</b> in rats and to reduce other preclinical indicators of abuse potential.
+TLR4	drug	opioid	30741729	However, under the self administration conditions studied, the effects of <strong>TLR4</strong> antagonists were not reinforcer selective, questioning the involvement of those receptors and their mediated inflammatory response specifically in <b>opioid</b> abuse.
+TLR4	drug	opioid	30741729	The objectives of the current study were to further characterize the reinforcer specificity of <strong>TLR4</strong> antagonism in <b>opioid</b> self administration and to explore its effects in a preclinical model of craving/relapse.
+TLR4	addiction	relapse	30741729	The objectives of the current study were to further characterize the reinforcer specificity of <strong>TLR4</strong> antagonism in opioid self administration and to explore its effects in a preclinical model of <b>craving</b>/<b>relapse</b>.
+TLR4	drug	alcohol	30741729	The <strong>TLR4</strong> antagonist (+) <b>naltrexone</b> decreased responding in rats trained to self administer the µ opioid receptor agonist remifentanil, but with a potency that was not significantly different from that observed in another group of subjects in which responding was maintained by food reinforcement.
+TLR4	drug	opioid	30741729	The <strong>TLR4</strong> antagonist (+) naltrexone decreased responding in rats trained to self administer the µ <b>opioid</b> receptor agonist remifentanil, but with a potency that was not significantly different from that observed in another group of subjects in which responding was maintained by food reinforcement.
+TLR4	addiction	reward	30741729	The <strong>TLR4</strong> antagonist (+) naltrexone decreased responding in rats trained to self administer the µ opioid receptor agonist remifentanil, but with a potency that was not significantly different from that observed in another group of subjects in which responding was maintained by food <b>reinforcement</b>.
+TLR4	drug	alcohol	30741729	Responding reinstated by heroin injection was decreased by (+) <b>naltrexone</b>; however, a similar reduction was not reproduced with the administration of another <strong>TLR4</strong> antagonist, lipopolysaccharide from Rhodobacter sphaeroides, administered into the NAcc shell.
+TLR4	drug	opioid	30741729	Responding reinstated by <b>heroin</b> injection was decreased by (+) naltrexone; however, a similar reduction was not reproduced with the administration of another <strong>TLR4</strong> antagonist, lipopolysaccharide from Rhodobacter sphaeroides, administered into the NAcc shell.
+TLR4	drug	alcohol	30741729	Thus, <strong>TLR4</strong> antagonists lacked reinforcer selectivity in reducing opioid self administration and were not uniformly effective in a model of craving/relapse, suggesting limitations on the development of (+) <b>naltrexone</b> or <strong>TLR4</strong> antagonists as treatments for opioid abuse.
+TLR4	drug	opioid	30741729	Thus, <strong>TLR4</strong> antagonists lacked reinforcer selectivity in reducing <b>opioid</b> self administration and were not uniformly effective in a model of craving/relapse, suggesting limitations on the development of (+) naltrexone or <strong>TLR4</strong> antagonists as treatments for <b>opioid</b> abuse.
+TLR4	addiction	relapse	30741729	Thus, <strong>TLR4</strong> antagonists lacked reinforcer selectivity in reducing opioid self administration and were not uniformly effective in a model of <b>craving</b>/<b>relapse</b>, suggesting limitations on the development of (+) naltrexone or <strong>TLR4</strong> antagonists as treatments for opioid abuse.
+TLR4	drug	amphetamine	30701618	We examined a novel adjuvant, E6020, a Toll like receptor 4 (<strong>TLR 4</strong>) agonist combined with tetanus toxoid conjugated to succinyl <b>methamphetamine</b> (TT SMA) adsorbed on aluminum hydroxide (alum).
+TLR4	drug	amphetamine	30701618	We examined a novel adjuvant, E6020, a <strong>Toll like receptor 4</strong> (<strong>TLR 4</strong>) agonist combined with tetanus toxoid conjugated to succinyl <b>methamphetamine</b> (TT SMA) adsorbed on aluminum hydroxide (alum).
+TLR4	drug	alcohol	30687006	<b>Alcohol</b> abuse is characterized by induction of peripheral inflammation and neuroinflammation, which hallmark is the activation of innate immunity toll like receptors 4 (<strong>TLR4</strong>).
+TLR4	drug	alcohol	30687006	Exogenous administration of OEA blocks the <b>alcohol</b> induced <strong>TLR4</strong> mediated pro inflammatory cascade, reducing the release of proinflammatory cytokines and chemokines, oxidative and nitrosative stress, and ultimately, preventing the neural damage in frontal cortex of rodents.
+TLR4	drug	alcohol	30687006	Clinical evidences will be highlighted, including the OEA release and the correlation of plasma OEA levels with <strong>TLR4</strong> dependent peripheral inflammatory markers in <b>alcohol</b> abusers.
+TLR4	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol <strong>TLR4</strong> Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+TLR4	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol <strong>TLR4</strong> <strong>Toll like receptor 4</strong> TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+TLR4	drug	opioid	30418215	Postfracture expression levels of several genes previously associated with <b>opioid</b> induced hyperalgesia, including brain derived neurotrophic factor and prodynorphin, were unchanged, but neuroinflammation involving <strong>Toll like receptor 4</strong> receptor expressing microglia was observed (6.8 ± 1.5 [mean ± SD] cells per high power field for fracture + vehicle vs. 12 ± 2.8 fracture + <b>morphine</b>, P < 0.001, n = 8 per /group).
+TLR4	drug	opioid	30418215	Treatment with a <strong>Toll like receptor 4</strong> antagonist TAK242 improved nociceptive sensitization for about 2 weeks in <b>morphine</b> treated fracture mice (F(1, 198) = 73.36, P < 0.001, fracture + <b>morphine</b> + TAK242 vs. fracture + <b>morphine</b>, n = 10 per group).
+TLR4	addiction	sensitization	30418215	Treatment with a <strong>Toll like receptor 4</strong> antagonist TAK242 improved nociceptive <b>sensitization</b> for about 2 weeks in morphine treated fracture mice (F(1, 198) = 73.36, P < 0.001, fracture + morphine + TAK242 vs. fracture + morphine, n = 10 per group).
+TLR4	drug	opioid	30418215	Measures preventing glial activation through <strong>Toll like receptor 4</strong> signaling may reduce the adverse consequences of postoperative <b>opioid</b> administration.
+TLR4	addiction	intoxication	30400371	These findings suggested that GOPs have a significant protective effect on <b>binge</b> drinking induced liver injury, and the mechanism possibly mediated by the partial inhibition of lipopolysaccharide <strong>toll like receptor 4</strong> nuclear factor κB p65 signaling in the liver.
+TLR4	drug	alcohol	30248186	Colonic tissues showed signs of inflammation, and activation of innate (<strong>Toll like receptor 4</strong>) and adaptive (IgA) immune systems and TJ proteins (occludin and claudin 3) were decreased after <b>ethanol</b> binges.
+TLR4	drug	opioid	30044299	Furthermore, spinal cord <strong>toll like receptor 4</strong> levels 3 weeks after fracture were higher in fracture mice given <b>morphine</b> than those given oliceridine.
+TLR4	drug	cocaine	30029767	In humans, <b>cocaine</b> modulated <strong>toll like receptor 4</strong> mediated innate immunity, an effect that was enhanced in those addicted to <b>cocaine</b> who had experienced a difficult childhood.
+TLR4	drug	alcohol	29982285	Interactions between <strong>TLR4</strong> methylation and <b>alcohol</b> consumption on subjective responses to an <b>alcohol</b> infusion.
+TLR4	drug	alcohol	29982285	Converging evidence has implicated perturbed inflammatory signaling in <b>alcohol</b> use disorders (AUDs), and both animal and human studies suggest that <b>alcohol</b> induced inflammatory signaling is mediated by Toll Like Receptor 4 (<strong>TLR4</strong>).
+TLR4	drug	alcohol	29982285	Converging evidence has implicated perturbed inflammatory signaling in <b>alcohol</b> use disorders (AUDs), and both animal and human studies suggest that <b>alcohol</b> induced inflammatory signaling is mediated by <strong>Toll Like Receptor 4</strong> (<strong>TLR4</strong>).
+TLR4	drug	alcohol	29982285	Examining the relationship between <strong>TLR4</strong> methylation and subjective <b>alcohol</b> responses could shed light on the role of <strong>TLR4</strong> in promoting AUDs, thereby highlighting its potential as a treatment target.
+TLR4	drug	alcohol	29982285	Significant interactions were demonstrated between Toll like Receptor 4 (<strong>TLR4</strong>) methylation and human <b>alcohol</b> consumption patterns, such that greater methylation was associated with decreased positive and negative self reported arousal during an <b>alcohol</b> infusion among light to moderate drinkers, but increased self reported positive arousal and physiological arousal (i.e.
+TLR4	drug	alcohol	29982285	Significant interactions were demonstrated between <strong>Toll like Receptor 4</strong> (<strong>TLR4</strong>) methylation and human <b>alcohol</b> consumption patterns, such that greater methylation was associated with decreased positive and negative self reported arousal during an <b>alcohol</b> infusion among light to moderate drinkers, but increased self reported positive arousal and physiological arousal (i.e.
+TLR4	drug	alcohol	29982285	Latent growth models were used to examine the relationship between <strong>TLR4</strong> methylation and subjective responses and physiological measures of arousal during an <b>alcohol</b> infusion across 222 drinkers.
+TLR4	drug	alcohol	29982285	We observed significant interactions of <strong>TLR4</strong> methylation and <b>alcohol</b> use (drinks per week) on intercepts for self report and physiological arousal measures.
+TLR4	drug	alcohol	29982285	Findings suggest that the relationship between <strong>TLR4</strong> methylation and subjective and physiological arousal during acute <b>alcohol</b> intoxication depends upon on self reported <b>alcohol</b> use.
+TLR4	addiction	intoxication	29982285	Findings suggest that the relationship between <strong>TLR4</strong> methylation and subjective and physiological arousal during acute alcohol <b>intoxication</b> depends upon on self reported alcohol use.
+TLR4	drug	alcohol	29982285	These data demonstrate the influence of <strong>TLR4</strong> on subjective responses to <b>alcohol</b>, thereby supporting the need for further research on its potential as a pharmacological treatment target.
+TLR4	drug	alcohol	29884546	Hepatocyte <strong>toll like receptor 4</strong> deficiency protects against <b>alcohol</b> induced fatty liver disease.
+TLR4	drug	alcohol	29884546	Recent studies have suggested a critical role for toll like receptor 4 (<strong>TLR4</strong>) in the development of <b>alcoholic</b> liver disease.
+TLR4	drug	alcohol	29884546	Recent studies have suggested a critical role for <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) in the development of <b>alcoholic</b> liver disease.
+TLR4	drug	alcohol	29884546	As <strong>TLR4</strong> is widely expressed throughout the body, it is unclear which <strong>TLR4</strong> expressing cell types contribute to <b>alcohol</b> induced liver damage.
+TLR4	drug	alcohol	29884546	We found that selective hepatocyte <strong>TLR4</strong> deletion protected mice from chronic <b>alcohol</b> induced liver injury and fatty liver.
+TLR4	drug	alcohol	29884546	Furthermore, in an acute <b>alcohol</b> binge model, hepatocyte <strong>TLR4</strong> deficient mice had significantly decreased plasma alanine transaminase (ALT) levels and attenuated hepatic triglyceride content compared to their <b>alcohol</b> gavaged control mice.
+TLR4	addiction	intoxication	29884546	Furthermore, in an acute alcohol <b>binge</b> model, hepatocyte <strong>TLR4</strong> deficient mice had significantly decreased plasma alanine transaminase (ALT) levels and attenuated hepatic triglyceride content compared to their alcohol gavaged control mice.
+TLR4	drug	alcohol	29884546	In contrast, deleting <strong>TLR4</strong> in myeloid cells did not affect the development of chronic <b>alcohol</b> induced fatty liver, despite the finding that mice lacking myeloid cell <strong>TLR4</strong> had significantly reduced circulating ALT concentrations.
+TLR4	drug	alcohol	29884546	These findings suggest that hepatocyte <strong>TLR4</strong> plays an important role in regulating <b>alcohol</b> induced liver damage and fatty liver disease.
+TLR4	drug	alcohol	29864452	Binge like <b>ethanol</b> treatment in adolescence impairs autophagy and hinders synaptic maturation: Role of <strong>TLR4</strong>.
+TLR4	addiction	intoxication	29864452	<b>Binge</b> like ethanol treatment in adolescence impairs autophagy and hinders synaptic maturation: Role of <strong>TLR4</strong>.
+TLR4	drug	alcohol	29864452	<b>Alcohol</b> is a neurotoxic compound whose abuse in adolescence causes <strong>TLR4</strong> response activation by triggering neuroinflammation, neural damage and behavioral alterations.
+TLR4	drug	alcohol	29864452	We therefore evaluated whether binge <b>ethanol</b> drinking alters autophagy pathways by contributing to adolescent synaptic dysfunctions, and if the immune receptor <strong>TLR4</strong> response participates in these events.
+TLR4	addiction	intoxication	29864452	We therefore evaluated whether <b>binge</b> ethanol drinking alters autophagy pathways by contributing to adolescent synaptic dysfunctions, and if the immune receptor <strong>TLR4</strong> response participates in these events.
+TLR4	drug	alcohol	29864452	With wild type (WT) and <strong>TLR4</strong> deficient (<strong>TLR4</strong> KO) adolescent mice treated intermittently with <b>ethanol</b> (3.0 g/kg) for 2 weeks, we show that binge like <b>ethanol</b> exposure in adolescence impairs autophagy machinery by increasing autophagy inhibitor mTOR by lowering LC3 II levels and accumulating p62.
+TLR4	addiction	intoxication	29864452	With wild type (WT) and <strong>TLR4</strong> deficient (<strong>TLR4</strong> KO) adolescent mice treated intermittently with ethanol (3.0 g/kg) for 2 weeks, we show that <b>binge</b> like ethanol exposure in adolescence impairs autophagy machinery by increasing autophagy inhibitor mTOR by lowering LC3 II levels and accumulating p62.
+TLR4	drug	alcohol	29864452	Elimination of the <strong>TLR4</strong> receptors using <strong>TLR4</strong> KO mice prevents autophagy dysfunctions and reduces the number or size of the synaptic connections induced by <b>ethanol</b>.
+TLR4	drug	alcohol	29864452	These results suggest the role of autophagy dysfunctions in the structural synaptic plasticity alterations induced by binge <b>alcohol</b> in adolescence, and support the participation of the <strong>TLR4</strong> response in these events.
+TLR4	addiction	intoxication	29864452	These results suggest the role of autophagy dysfunctions in the structural synaptic plasticity alterations induced by <b>binge</b> alcohol in adolescence, and support the participation of the <strong>TLR4</strong> response in these events.
+TLR4	drug	opioid	29723521	Maintenance of this <b>morphine</b> induced persistent sensitization was dependent on microglial reactivity and <strong>Toll like receptor 4</strong> signaling.
+TLR4	addiction	sensitization	29723521	Maintenance of this morphine induced persistent <b>sensitization</b> was dependent on microglial reactivity and <strong>Toll like receptor 4</strong> signaling.
+TLR4	drug	alcohol	29690521	The GABAA Receptor α2 Subunit Activates a Neuronal <strong>TLR4</strong> Signal in the Ventral Tegmental Area that Regulates <b>Alcohol</b> and Nicotine Abuse.
+TLR4	drug	nicotine	29690521	The GABAA Receptor α2 Subunit Activates a Neuronal <strong>TLR4</strong> Signal in the Ventral Tegmental Area that Regulates Alcohol and <b>Nicotine</b> Abuse.
+TLR4	drug	alcohol	29690521	The predisposition of non <b>alcohol</b> exposed subjects to initiate binge drinking is controlled by neuroimmune signaling that includes an innately activated neuronal Toll like receptor 4 (<strong>TLR4</strong>) signal.
+TLR4	addiction	intoxication	29690521	The predisposition of non alcohol exposed subjects to initiate <b>binge</b> drinking is controlled by neuroimmune signaling that includes an innately activated neuronal Toll like receptor 4 (<strong>TLR4</strong>) signal.
+TLR4	drug	alcohol	29690521	The predisposition of non <b>alcohol</b> exposed subjects to initiate binge drinking is controlled by neuroimmune signaling that includes an innately activated neuronal <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) signal.
+TLR4	addiction	intoxication	29690521	The predisposition of non alcohol exposed subjects to initiate <b>binge</b> drinking is controlled by neuroimmune signaling that includes an innately activated neuronal <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) signal.
+TLR4	drug	alcohol	29690521	The signal is activated through α2/<strong>TLR4</strong> interaction, as evidenced by co immunoprecipitation, and it is present in the VTA from drug untreated <b>alcohol</b> preferring P rats.
+TLR4	drug	alcohol	29690521	VTA infusion of neurotropic herpes simplex virus (HSV) vectors for α2 (pHSVsiLA2) or <strong>TLR4</strong> (pHSVsiTLR4) but not scrambled (pHSVsiNC) siRNA inhibits signal activation and both binge <b>alcohol</b> drinking and nicotine sensitization, suggesting that the α2 activated <strong>TLR4</strong> signal contributes to the regulation of both <b>alcohol</b> and nicotine abuse.
+TLR4	drug	nicotine	29690521	VTA infusion of neurotropic herpes simplex virus (HSV) vectors for α2 (pHSVsiLA2) or <strong>TLR4</strong> (pHSVsiTLR4) but not scrambled (pHSVsiNC) siRNA inhibits signal activation and both binge alcohol drinking and <b>nicotine</b> sensitization, suggesting that the α2 activated <strong>TLR4</strong> signal contributes to the regulation of both alcohol and <b>nicotine</b> abuse.
+TLR4	addiction	intoxication	29690521	VTA infusion of neurotropic herpes simplex virus (HSV) vectors for α2 (pHSVsiLA2) or <strong>TLR4</strong> (pHSVsiTLR4) but not scrambled (pHSVsiNC) siRNA inhibits signal activation and both <b>binge</b> alcohol drinking and nicotine sensitization, suggesting that the α2 activated <strong>TLR4</strong> signal contributes to the regulation of both alcohol and nicotine abuse.
+TLR4	addiction	sensitization	29690521	VTA infusion of neurotropic herpes simplex virus (HSV) vectors for α2 (pHSVsiLA2) or <strong>TLR4</strong> (pHSVsiTLR4) but not scrambled (pHSVsiNC) siRNA inhibits signal activation and both binge alcohol drinking and nicotine <b>sensitization</b>, suggesting that the α2 activated <strong>TLR4</strong> signal contributes to the regulation of both alcohol and nicotine abuse.
+TLR4	drug	opioid	29651005	<b>Morphine</b> slowed movement of ingested content in WT but this retardation effect was attenuated in <strong>TLR4</strong>  /  and TLR2/4  /  .
+TLR4	drug	alcohol	29576702	EALT supplementation prevented <b>alcoholic</b> liver injury through attenuation of inflammatory mediators such as <strong>toll like receptor 4</strong>, cytochrome P4502E1, and cyclooxygenase 2, and inflammatory cytokine interleukin 6.
+TLR4	drug	alcohol	29518316	Dissecting the Innate Immune Recognition of Opioid Inactive Isomer (+) <b>Naltrexone</b> Derived Toll like Receptor 4 (<strong>TLR4</strong>) Antagonists.
+TLR4	drug	opioid	29518316	Dissecting the Innate Immune Recognition of <b>Opioid</b> Inactive Isomer (+) Naltrexone Derived Toll like Receptor 4 (<strong>TLR4</strong>) Antagonists.
+TLR4	drug	alcohol	29518316	Dissecting the Innate Immune Recognition of Opioid Inactive Isomer (+) <b>Naltrexone</b> Derived <strong>Toll like Receptor 4</strong> (<strong>TLR4</strong>) Antagonists.
+TLR4	drug	opioid	29518316	Dissecting the Innate Immune Recognition of <b>Opioid</b> Inactive Isomer (+) Naltrexone Derived <strong>Toll like Receptor 4</strong> (<strong>TLR4</strong>) Antagonists.
+TLR4	drug	alcohol	29518316	The opioid inactive isomer (+) <b>naltrexone</b> is one of the rare Toll like receptor 4 (<strong>TLR4</strong>) antagonists with good blood brain barrier (BBB) permeability, which is a lead with promising potential for treating neuropathic pain and drug addiction.
+TLR4	drug	opioid	29518316	The <b>opioid</b> inactive isomer (+) naltrexone is one of the rare Toll like receptor 4 (<strong>TLR4</strong>) antagonists with good blood brain barrier (BBB) permeability, which is a lead with promising potential for treating neuropathic pain and drug addiction.
+TLR4	addiction	addiction	29518316	The opioid inactive isomer (+) naltrexone is one of the rare Toll like receptor 4 (<strong>TLR4</strong>) antagonists with good blood brain barrier (BBB) permeability, which is a lead with promising potential for treating neuropathic pain and drug <b>addiction</b>.
+TLR4	drug	alcohol	29518316	The opioid inactive isomer (+) <b>naltrexone</b> is one of the rare <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) antagonists with good blood brain barrier (BBB) permeability, which is a lead with promising potential for treating neuropathic pain and drug addiction.
+TLR4	drug	opioid	29518316	The <b>opioid</b> inactive isomer (+) naltrexone is one of the rare <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) antagonists with good blood brain barrier (BBB) permeability, which is a lead with promising potential for treating neuropathic pain and drug addiction.
+TLR4	addiction	addiction	29518316	The opioid inactive isomer (+) naltrexone is one of the rare <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) antagonists with good blood brain barrier (BBB) permeability, which is a lead with promising potential for treating neuropathic pain and drug <b>addiction</b>.
+TLR4	drug	alcohol	29518316	(+) <b>Naltrexone</b> targets the lipopolysaccharides (LPS) binding pocket of myeloid differentiation protein 2 (MD 2) and blocks innate immune <strong>TLR4</strong> signaling.
+TLR4	drug	alcohol	29518316	The calculated binding free energies of (+) <b>naltrexone</b> and its derivatives in complex with MD 2 correlated well with their experimental binding affinities and <strong>TLR4</strong> antagonistic activities.
+TLR4	drug	alcohol	29518316	Hydrophobic residues in the MD 2 cavity interacted directly with these (+) <b>naltrexone</b> based <strong>TLR4</strong> antagonists and principally participated in ligand binding.
+TLR4	drug	alcohol	29518316	Molecular dynamics (MD) simulations showed the binding of (+) <b>naltrexone</b> or its derivatives to MD 2 stabilized the "collapsed" conformation of MD 2, consequently blocking the binding and signaling of <strong>TLR4</strong>.
+TLR4	drug	alcohol	29518316	Thermodynamics and dynamic analysis showed the topology of substituted group at N 17 of (+) <b>naltrexone</b> affected the binding with MD 2 and <strong>TLR4</strong> antagonistic activity.
+TLR4	drug	opioid	29518316	This study provides a molecular insight into the innate immune recognition of <b>opioid</b> inactive (+) isomers, which would be of great help for the development of next generation of (+) <b>opioid</b> based <strong>TLR4</strong> antagonists.
+TLR4	drug	alcohol	29445009	Human Binge <b>Alcohol</b> Intake Inhibits <strong>TLR4</strong> MyD88 and <strong>TLR4</strong> TRIF Responses but Not the TLR3 TRIF Pathway: HspA1A and PP1 Play Selective Regulatory Roles.
+TLR4	addiction	intoxication	29445009	Human <b>Binge</b> Alcohol Intake Inhibits <strong>TLR4</strong> MyD88 and <strong>TLR4</strong> TRIF Responses but Not the TLR3 TRIF Pathway: HspA1A and PP1 Play Selective Regulatory Roles.
+TLR4	drug	alcohol	29445009	Binge/moderate <b>alcohol</b> suppresses <strong>TLR4</strong> MyD88 proinflammatory cytokines; however, <b>alcohol</b>'s effects on TLR TRIF signaling, especially after in vivo exposure in humans, are unclear.
+TLR4	addiction	intoxication	29445009	<b>Binge</b>/moderate alcohol suppresses <strong>TLR4</strong> MyD88 proinflammatory cytokines; however, alcohol's effects on TLR TRIF signaling, especially after in vivo exposure in humans, are unclear.
+TLR4	drug	alcohol	29445009	We performed a comparative analysis of the <strong>TLR4</strong> MyD88, <strong>TLR4</strong> TRIF, and TLR3 TRIF pathways in human monocytes following binge <b>alcohol</b> exposure.
+TLR4	addiction	intoxication	29445009	We performed a comparative analysis of the <strong>TLR4</strong> MyD88, <strong>TLR4</strong> TRIF, and TLR3 TRIF pathways in human monocytes following <b>binge</b> alcohol exposure.
+TLR4	drug	alcohol	29445009	Two approaches for <b>alcohol</b> exposure were used: in vivo exposure of primary monocytes in binge <b>alcohol</b> consuming human volunteers or in vitro exposure of human monocytes/murine macrophages to physiological <b>alcohol</b> concentrations (25 50 mM <b>ethanol</b>), followed by LPS (<strong>TLR4</strong>) or polyinosinic polycytidylic acid (TLR3) stimulation ex vivo.
+TLR4	addiction	intoxication	29445009	Two approaches for alcohol exposure were used: in vivo exposure of primary monocytes in <b>binge</b> alcohol consuming human volunteers or in vitro exposure of human monocytes/murine macrophages to physiological alcohol concentrations (25 50 mM ethanol), followed by LPS (<strong>TLR4</strong>) or polyinosinic polycytidylic acid (TLR3) stimulation ex vivo.
+TLR4	drug	alcohol	29445009	In vivo and in vitro binge <b>alcohol</b> exposure significantly inhibited the <strong>TLR4</strong> MyD88 cytokines TNF α and IL 6, as well as the <strong>TLR4</strong> TRIF cytokines/chemokines IFN β, IP 10, and RANTES, in human monocytes, but not TLR3 TRIF induced cytokines/chemokines, as detected by quantitative PCR and ELISA.
+TLR4	addiction	intoxication	29445009	In vivo and in vitro <b>binge</b> alcohol exposure significantly inhibited the <strong>TLR4</strong> MyD88 cytokines TNF α and IL 6, as well as the <strong>TLR4</strong> TRIF cytokines/chemokines IFN β, IP 10, and RANTES, in human monocytes, but not TLR3 TRIF induced cytokines/chemokines, as detected by quantitative PCR and ELISA.
+TLR4	drug	alcohol	29445009	Mechanistic analyses revealed TBK 1 independent inhibition of the <strong>TLR4</strong> TRIF effector IRF3 in <b>alcohol</b> treated macrophages.
+TLR4	drug	alcohol	29445009	<b>Alcohol</b> induced HspA1A was required for inhibition of <strong>TLR4</strong> MyD88 signaling but not <strong>TLR4</strong> TRIF cytokines in macrophages.
+TLR4	drug	alcohol	29445009	In contrast, inhibition of PP1 prevented <b>alcohol</b> mediated <strong>TLR4</strong> TRIF tolerance in macrophages.
+TLR4	drug	alcohol	29445009	Collectively, our results demonstrate that in vivo and in vitro binge <b>alcohol</b> exposure in humans suppresses <strong>TLR4</strong> MyD88 and <strong>TLR4</strong> TRIF, but not TLR3 TRIF, responses.
+TLR4	addiction	intoxication	29445009	Collectively, our results demonstrate that in vivo and in vitro <b>binge</b> alcohol exposure in humans suppresses <strong>TLR4</strong> MyD88 and <strong>TLR4</strong> TRIF, but not TLR3 TRIF, responses.
+TLR4	drug	alcohol	29445009	Whereas <b>alcohol</b> mediated effects on the PP1 IRF3 axis inhibit the <strong>TLR4</strong> TRIF pathway, HspA1A selectively suppresses the <strong>TLR4</strong> MyD88 pathway in monocytes/macrophages.
+TLR4	drug	alcohol	29377216	It is hypothesized that lower than standard doses of <b>naltrexone</b> inhibit cellular proliferation of T and B cells and block <strong>Toll like receptor 4</strong>, resulting in an analgesic and antiinflammatory effect.
+TLR4	drug	alcohol	29339456	We now find in 4 day binged HEC slice cultures (100 mM <b>ethanol</b>) that PARP1 elevations after two overnight binges precede PAR, cPLA2, and sPLA2 enhancements by 1 day and high mobility group box 1 (HMGB1), an <b>ethanol</b> responsive alarmin that augments proinflammatory cytokines via toll like receptor 4 (<strong>TLR4</strong>), by 2 days.
+TLR4	drug	alcohol	29339456	We now find in 4 day binged HEC slice cultures (100 mM <b>ethanol</b>) that PARP1 elevations after two overnight binges precede PAR, cPLA2, and sPLA2 enhancements by 1 day and high mobility group box 1 (HMGB1), an <b>ethanol</b> responsive alarmin that augments proinflammatory cytokines via <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), by 2 days.
+TLR4	drug	alcohol	29339456	Also, PJ34 and olaparib blocked <b>ethanol</b> induced HMGB1 elevations, linking brain PARP induction to <strong>TLR4</strong> activation.
+TLR4	drug	alcohol	29339456	The results provide evidence in adult brains that induction of PARP1 may mediate dual neuroinflammatory pathways (PLA2→phospholipid→ARA and HMGB1→<strong>TLR4</strong>→proinflammatory cytokines) that are complicit in binge <b>ethanol</b> induced neurodegeneration.
+TLR4	addiction	intoxication	29339456	The results provide evidence in adult brains that induction of PARP1 may mediate dual neuroinflammatory pathways (PLA2→phospholipid→ARA and HMGB1→<strong>TLR4</strong>→proinflammatory cytokines) that are complicit in <b>binge</b> ethanol induced neurodegeneration.
+TLR4	drug	alcohol	29214654	Special emphasis is given to the actions of <b>ethanol</b> in the innate immune receptor toll like receptor 4 (<strong>TLR4</strong>), since recent studies have demonstrated that by activating the inflammatory <strong>TLR4</strong>/NFκB signaling response in glial cells, binge drinking of <b>ethanol</b> triggers the release of cytokines/chemokines and free radicals, which exacerbate the immune response that causes neuroinflammation/neural damage as well as short  and long term neurophysiological, cognitive, and behavioral dysfunction.
+TLR4	addiction	intoxication	29214654	Special emphasis is given to the actions of ethanol in the innate immune receptor toll like receptor 4 (<strong>TLR4</strong>), since recent studies have demonstrated that by activating the inflammatory <strong>TLR4</strong>/NFκB signaling response in glial cells, <b>binge</b> drinking of ethanol triggers the release of cytokines/chemokines and free radicals, which exacerbate the immune response that causes neuroinflammation/neural damage as well as short  and long term neurophysiological, cognitive, and behavioral dysfunction.
+TLR4	drug	alcohol	29214654	Special emphasis is given to the actions of <b>ethanol</b> in the innate immune receptor <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), since recent studies have demonstrated that by activating the inflammatory <strong>TLR4</strong>/NFκB signaling response in glial cells, binge drinking of <b>ethanol</b> triggers the release of cytokines/chemokines and free radicals, which exacerbate the immune response that causes neuroinflammation/neural damage as well as short  and long term neurophysiological, cognitive, and behavioral dysfunction.
+TLR4	addiction	intoxication	29214654	Special emphasis is given to the actions of ethanol in the innate immune receptor <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), since recent studies have demonstrated that by activating the inflammatory <strong>TLR4</strong>/NFκB signaling response in glial cells, <b>binge</b> drinking of ethanol triggers the release of cytokines/chemokines and free radicals, which exacerbate the immune response that causes neuroinflammation/neural damage as well as short  and long term neurophysiological, cognitive, and behavioral dysfunction.
+TLR4	drug	alcohol	29178411	We found that during abstinence, <b>alcohol</b> binge drinkers had elevated plasma levels of oleoylethanolamide, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (<strong>TLR4</strong>), pro inflammatory cytokines/chemokines interleukin 1 beta, interleukin 6 and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+TLR4	drug	cannabinoid	29178411	We found that during abstinence, alcohol binge drinkers had elevated plasma levels of <b>oleoylethanolamide</b>, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (<strong>TLR4</strong>), pro inflammatory cytokines/chemokines interleukin 1 beta, interleukin 6 and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+TLR4	addiction	intoxication	29178411	We found that during abstinence, alcohol <b>binge</b> drinkers had elevated plasma levels of oleoylethanolamide, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (<strong>TLR4</strong>), pro inflammatory cytokines/chemokines interleukin 1 beta, interleukin 6 and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+TLR4	drug	alcohol	29178411	Additionally, plasma oleoylethanolamide positively correlated with plasma levels of high mobility group box 1, which is a danger associated molecular pattern and an endogenous <strong>TLR4</strong> agonist, specifically in female <b>alcohol</b> binge drinkers.
+TLR4	drug	cannabinoid	29178411	Additionally, plasma <b>oleoylethanolamide</b> positively correlated with plasma levels of high mobility group box 1, which is a danger associated molecular pattern and an endogenous <strong>TLR4</strong> agonist, specifically in female alcohol binge drinkers.
+TLR4	addiction	intoxication	29178411	Additionally, plasma oleoylethanolamide positively correlated with plasma levels of high mobility group box 1, which is a danger associated molecular pattern and an endogenous <strong>TLR4</strong> agonist, specifically in female alcohol <b>binge</b> drinkers.
+TLR4	drug	alcohol	29146239	We have previously shown that a neuronal Toll like receptor 4 (<strong>TLR4</strong>) signal located in the central amygdala (CeA) and ventral tegmental area (VTA) controls the initiation of binge drinking in <b>alcohol</b> preferring P rats, and <strong>TLR4</strong> expression is upregulated by <b>alcohol</b> induced corticotropin releasing factor (CRF) at these sites.
+TLR4	addiction	intoxication	29146239	We have previously shown that a neuronal Toll like receptor 4 (<strong>TLR4</strong>) signal located in the central amygdala (CeA) and ventral tegmental area (VTA) controls the initiation of <b>binge</b> drinking in alcohol preferring P rats, and <strong>TLR4</strong> expression is upregulated by alcohol induced corticotropin releasing factor (CRF) at these sites.
+TLR4	drug	alcohol	29146239	We have previously shown that a neuronal <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) signal located in the central amygdala (CeA) and ventral tegmental area (VTA) controls the initiation of binge drinking in <b>alcohol</b> preferring P rats, and <strong>TLR4</strong> expression is upregulated by <b>alcohol</b> induced corticotropin releasing factor (CRF) at these sites.
+TLR4	addiction	intoxication	29146239	We have previously shown that a neuronal <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) signal located in the central amygdala (CeA) and ventral tegmental area (VTA) controls the initiation of <b>binge</b> drinking in alcohol preferring P rats, and <strong>TLR4</strong> expression is upregulated by alcohol induced corticotropin releasing factor (CRF) at these sites.
+TLR4	addiction	relapse	29146239	However, the function of the <strong>TLR4</strong> signal in the nucleus accumbens shell (NAc shell), a site implicated in the control of reward, drug <b>seeking</b> behavior and impulsivity and the contribution of other signal associated genes, are still poorly understood.
+TLR4	addiction	reward	29146239	However, the function of the <strong>TLR4</strong> signal in the nucleus accumbens shell (NAc shell), a site implicated in the control of <b>reward</b>, drug seeking behavior and impulsivity and the contribution of other signal associated genes, are still poorly understood.
+TLR4	drug	alcohol	29146239	Here we report that P rats have an innately activated <strong>TLR4</strong> signal in NAc shell neurons that co express the α2 GABAA receptor subunit and CRF prior to <b>alcohol</b> exposure.
+TLR4	drug	alcohol	29142263	Hyaluronic acid 35 normalizes <strong>TLR4</strong> signaling in Kupffer cells from <b>ethanol</b> fed rats via regulation of microRNA291b and its target Tollip.
+TLR4	drug	alcohol	29142263	<strong>TLR4</strong> signaling in hepatic macrophages is increased after chronic <b>ethanol</b> feeding.
+TLR4	drug	alcohol	29142263	Treatment of hepatic macrophages after chronic <b>ethanol</b> feeding with small specific sized hyaluronic acid 35 (HA35) normalizes <strong>TLR4</strong> signaling; however, the mechanisms for HA35 action are not completely understood.
+TLR4	drug	alcohol	29142263	Here we used Next Generation Sequencing of microRNAs to identify negative regulators of <strong>TLR4</strong> signaling reciprocally modulated by <b>ethanol</b> and HA35 in hepatic macrophages.
+TLR4	drug	alcohol	29142263	Tollip expression was decreased in hepatic macrophages from <b>ethanol</b> fed rats, but treatment with HA35 or transfection with a miR291b hairpin inhibitor restored Tollip expression and normalized <strong>TLR4</strong> stimulated TNFα expression.
+TLR4	drug	alcohol	29142263	Normalization of the miR291b → Tollip pathway by HA35 ameliorated <b>ethanol</b> induced sensitization of <strong>TLR4</strong> signaling in macrophages/monocytes, suggesting that HA35 may be a novel therapeutic agent in the treatment of ALD.
+TLR4	addiction	sensitization	29142263	Normalization of the miR291b → Tollip pathway by HA35 ameliorated ethanol induced <b>sensitization</b> of <strong>TLR4</strong> signaling in macrophages/monocytes, suggesting that HA35 may be a novel therapeutic agent in the treatment of ALD.
+TLR4	drug	alcohol	29113896	Excessive <b>alcohol</b> intake induces an inflammatory response in the brain, via TNFα, <strong>TLR4</strong> and NF κB signaling pathways.
+TLR4	drug	alcohol	28947376	Antagonising <strong>TLR4</strong> TRIF signalling before or after a low dose <b>alcohol</b> binge during adolescence prevents <b>alcohol</b> drinking but not seeking behaviour in adulthood.
+TLR4	addiction	intoxication	28947376	Antagonising <strong>TLR4</strong> TRIF signalling before or after a low dose alcohol <b>binge</b> during adolescence prevents alcohol drinking but not seeking behaviour in adulthood.
+TLR4	addiction	relapse	28947376	Antagonising <strong>TLR4</strong> TRIF signalling before or after a low dose alcohol binge during adolescence prevents alcohol drinking but not <b>seeking</b> behaviour in adulthood.
+TLR4	drug	alcohol	28947376	Therefore, the aims of this project were to develop a more relevant animal model of adolescent <b>alcohol</b> exposure and to characterise its effects on <strong>TLR4</strong> signalling and <b>alcohol</b> related behaviours later life.
+TLR4	drug	alcohol	28947376	Subsequent analysis of nucleus accumbal mRNA, revealed increased expression of <strong>TLR4</strong> related mRNAs in mice who received <b>alcohol</b> during adolescence.
+TLR4	drug	alcohol	28947376	To further elucidate the role of <strong>TLR4</strong>, (+) <b>Naltrexone</b>, a biased <strong>TLR4</strong> antagonist was administered 30 min before or after the adolescent binge paradigm.
+TLR4	addiction	intoxication	28947376	To further elucidate the role of <strong>TLR4</strong>, (+) Naltrexone, a biased <strong>TLR4</strong> antagonist was administered 30 min before or after the adolescent <b>binge</b> paradigm.
+TLR4	drug	alcohol	28947376	This study highlights that even a small amount of <b>alcohol</b>, when given during a critical neurodevelopmental period, can potentiate <b>alcohol</b> related behaviours and <strong>TLR4</strong> activation later in life.
+TLR4	drug	alcohol	28947376	Interestingly, attenuation of <strong>TLR4</strong> before or after adolescent <b>alcohol</b> exposure reduced only binge <b>alcohol</b> intake in adulthood.
+TLR4	addiction	intoxication	28947376	Interestingly, attenuation of <strong>TLR4</strong> before or after adolescent alcohol exposure reduced only <b>binge</b> alcohol intake in adulthood.
+TLR4	addiction	dependence	28878132	Nonetheless, there are several disease specific molecular signaling pathways, such as differential pathway activation downstream of <strong>TLR4</strong> (MyD88 <b>dependence</b> in NASH versus MyD88 independence in ASH), inflammasome activation and IL 1β signaling in ASH, insulin resistance and lipotoxicity in NASH, and dysregulation of different microRNAs, which clearly highlight that ASH and NASH are two distinct biological entities.
+TLR4	addiction	reward	28864261	While the role of the immune system, specifically, Toll like receptor 4 (<strong>TLR4</strong>, an innate immune receptor) in drug induced <b>reward</b> is becoming increasingly appreciated, it is unclear whether its effects vary according to light cycle.
+TLR4	addiction	reward	28864261	While the role of the immune system, specifically, <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>, an innate immune receptor) in drug induced <b>reward</b> is becoming increasingly appreciated, it is unclear whether its effects vary according to light cycle.
+TLR4	drug	alcohol	28864261	Administration of (+) <b>Naltrexone</b>, a <strong>TLR4</strong> antagonist, reduced immune related gene mRNA expression and <b>alcohol</b> preference with its effects most pronounced during the dark cycle.
+TLR4	drug	alcohol	28864261	However, (+) <b>Naltrexone</b>, like other <strong>TLR4</strong> antagonists exhibited off target side effects, with a significant reduction in overall saccharin intake   an effect likely attributable to a reduction in tyrosine hydroxylase (Th) mRNA expression levels.
+TLR4	drug	alcohol	28864261	Collectively, the study highlights a link between a time of day dependent influence of <strong>TLR4</strong> on natural and <b>alcohol</b> reward like behaviour in mice.
+TLR4	addiction	reward	28864261	Collectively, the study highlights a link between a time of day dependent influence of <strong>TLR4</strong> on natural and alcohol <b>reward</b> like behaviour in mice.
+TLR4	drug	opioid	28860068	We conclude that after peripheral nerve injury, <b>morphine</b> treatment results in persistent DAMP release via <strong>TLR4</strong>, P2X7R and caspase 1, which are involved in formation/activation of NLRP3 inflammasomes.
+TLR4	drug	alcohol	28840951	Compared with controls, young <b>alcohol</b> binge drinkers had elevated levels of blood endotoxin and upregulated markers of the <strong>toll like receptor 4</strong>/NF κB inflammatory pathway in peripheral blood mononuclear cells, together with pro inflammatory cytokine/chemokine release, oxidative stress and lipid peroxidation.
+TLR4	addiction	intoxication	28840951	Compared with controls, young alcohol <b>binge</b> drinkers had elevated levels of blood endotoxin and upregulated markers of the <strong>toll like receptor 4</strong>/NF κB inflammatory pathway in peripheral blood mononuclear cells, together with pro inflammatory cytokine/chemokine release, oxidative stress and lipid peroxidation.
+TLR4	addiction	intoxication	28840951	Finally, higher levels of inflammatory markers, mainly monocyte chemoattractant protein 1, as well as LPS, high mobility group box 1, <strong>toll like receptor 4</strong>, IL 6 and ciclooxygenase 2, correlated with worse scores on episodic memory and executive functioning tasks in female <b>binge</b> drinkers but not in male <b>binge</b> drinkers.
+TLR4	drug	opioid	28827130	Activation of <strong>TLR4</strong>/STAT3 signaling in VTA contributes to the acquisition and maintenance of <b>morphine</b> induced conditioned place preference.
+TLR4	drug	opioid	28827130	The present study showed that intra VTA microinjection of <strong>TLR4</strong> antagonist LPS RS prevented the acquisition and maintenance, but not the expression, of <b>morphine</b> induced CPP in rats.
+TLR4	addiction	reward	28827130	The present study showed that intra VTA microinjection of <strong>TLR4</strong> antagonist LPS RS prevented the acquisition and maintenance, but not the expression, of morphine induced <b>CPP</b> in rats.
+TLR4	drug	opioid	28827130	Importantly, the <strong>TLR4</strong> expression is colocalized with p STAT3 positive cell in VTA, and repeated injection of LPS RS significantly attenuated the STAT3 activation in VTA induced by chronic <b>morphine</b> treatment.
+TLR4	drug	opioid	28827130	Collectively, these data suggest that <strong>TLR4</strong>/STAT3 signaling pathway in VTA might play a critical role in the acquisition and maintenance of <b>morphine</b> CPP, and provides new evidence that <strong>TLR4</strong>/STAT3 signaling pathway might be a potential target for treatment of <b>morphine</b> addiction.
+TLR4	addiction	addiction	28827130	Collectively, these data suggest that <strong>TLR4</strong>/STAT3 signaling pathway in VTA might play a critical role in the acquisition and maintenance of morphine CPP, and provides new evidence that <strong>TLR4</strong>/STAT3 signaling pathway might be a potential target for treatment of morphine <b>addiction</b>.
+TLR4	addiction	reward	28827130	Collectively, these data suggest that <strong>TLR4</strong>/STAT3 signaling pathway in VTA might play a critical role in the acquisition and maintenance of morphine <b>CPP</b>, and provides new evidence that <strong>TLR4</strong>/STAT3 signaling pathway might be a potential target for treatment of morphine addiction.
+TLR4	drug	cocaine	28813640	Here, we used a rodent model of <b>cocaine</b> addiction to investigate the role of <strong>TLR4</strong> in the ventral tegmental area (VTA) in <b>cocaine</b> seeking.
+TLR4	addiction	addiction	28813640	Here, we used a rodent model of cocaine <b>addiction</b> to investigate the role of <strong>TLR4</strong> in the ventral tegmental area (VTA) in cocaine seeking.
+TLR4	addiction	relapse	28813640	Here, we used a rodent model of cocaine addiction to investigate the role of <strong>TLR4</strong> in the ventral tegmental area (VTA) in cocaine <b>seeking</b>.
+TLR4	drug	cocaine	28813640	Pharmacological antagonism of <strong>TLR4</strong> in the VTA using lipopolysaccharide from the bacterium Rhodobacter sphaeroides (LPS RS) significantly reduced <b>cocaine</b> primed reinstatement of drug seeking but had no effect on sucrose seeking.
+TLR4	addiction	relapse	28813640	Pharmacological antagonism of <strong>TLR4</strong> in the VTA using lipopolysaccharide from the bacterium Rhodobacter sphaeroides (LPS RS) significantly reduced cocaine primed <b>reinstatement</b> of drug <b>seeking</b> but had no effect on sucrose <b>seeking</b>.
+TLR4	drug	cocaine	28813640	<strong>TLR4</strong> activation within the VTA using the <strong>TLR4</strong> activator, lipopolysaccharide, was sufficient to moderately reinstate <b>cocaine</b> seeking.
+TLR4	addiction	relapse	28813640	<strong>TLR4</strong> activation within the VTA using the <strong>TLR4</strong> activator, lipopolysaccharide, was sufficient to moderately reinstate cocaine <b>seeking</b>.
+TLR4	drug	alcohol	28784931	<b>Alcohol</b> disrupted lipopolysaccharide (LPS) <strong>TLR4</strong> ERK1/2 cyclin D1 signaling and inhibited upregulation of Sca 1 and C/EBPβ expression by lineage negative marrow cells in response to bacteremia.
+TLR4	addiction	reward	28760987	<strong>Toll like receptor 4</strong> deficiency alters nucleus accumbens synaptic physiology and drug <b>reward</b> behavior.
+TLR4	addiction	reward	28760987	Consistent with altered NAc LTD, <strong>TLR4</strong>.KO animals exhibit an attenuation in drug <b>reward</b> learning.
+TLR4	addiction	reward	28760987	These results suggest that <strong>TLR4</strong> influences NAc MSN synaptic physiology and drug <b>reward</b> learning and behavior.
+TLR4	drug	alcohol	28669901	Behavioural effects were associated with an upregulation of pro inflammatory signalling (<strong>Toll like receptor 4</strong>, nuclear factor kappa B p65, NOD like receptor protein 3, caspase 1, and interleukin 1β), gliosis, neuronal cell death and a reduction in several structural myelin proteins (myelin associated glycoprotein, myelin basic protein, myelin proteolipid protein and myelin regulatory factor) in both the prefrontal cortex and hippocampus of adult mice exposed to <b>alcohol</b>.
+TLR4	drug	opioid	28623271	Decoy peptide targeted to Toll IL 1R domain inhibits LPS and <strong>TLR4</strong> active metabolite <b>morphine</b> 3 glucuronide sensitization of sensory neurons.
+TLR4	addiction	sensitization	28623271	Decoy peptide targeted to Toll IL 1R domain inhibits LPS and <strong>TLR4</strong> active metabolite morphine 3 glucuronide <b>sensitization</b> of sensory neurons.
+TLR4	drug	opioid	28623271	In this study we investigated the degree to which TLR TIR decoy peptide modified to include a TAT sequence (Trans Activator of Transcription gene in HIV; TAT 4BB) affected LPS induced intracellular calcium flux and excitation in sensory neurons, and behavioral changes due to <strong>TLR4</strong> active metabolite, <b>morphine</b> 3 glucuronide (M3G) exposure in vivo.
+TLR4	drug	alcohol	28493563	Nalmefene Prevents <b>Alcohol</b> Induced Neuroinflammation and <b>Alcohol</b> Drinking Preference in Adolescent Female Mice: Role of <strong>TLR4</strong>.
+TLR4	drug	alcohol	28493563	We previously showed that, by activating innate immune receptors Toll like 4 (<strong>TLR4</strong>), adolescent intermittent <b>ethanol</b> (EtOH) exposure causes neuroinflammation, myelin damage, and behavioral dysfunctions.
+TLR4	drug	alcohol	28493563	Recent findings reveal that clinically used opioid antagonists <b>naltrexone</b> (NT) and naloxone (NX) inhibit opioid induced <strong>TLR4</strong> signaling and that NT, NX, and nalmefene (NF), the 6 methylene derivative of NX, are able to reduce <b>alcohol</b> drinking escalation.
+TLR4	drug	opioid	28493563	Recent findings reveal that clinically used <b>opioid</b> antagonists naltrexone (NT) and <b>naloxone</b> (NX) inhibit <b>opioid</b> induced <strong>TLR4</strong> signaling and that NT, NX, and nalmefene (NF), the 6 methylene derivative of NX, are able to reduce alcohol drinking escalation.
+TLR4	addiction	addiction	28493563	Recent findings reveal that clinically used opioid antagonists naltrexone (NT) and naloxone (NX) inhibit opioid induced <strong>TLR4</strong> signaling and that NT, NX, and nalmefene (NF), the 6 methylene derivative of NX, are able to reduce alcohol drinking <b>escalation</b>.
+TLR4	drug	alcohol	28493563	The effect of NF on <b>alcohol</b> drinking preference was evaluated in both the wild type and <strong>TLR4</strong> knockout (KO) adolescent mice.
+TLR4	drug	alcohol	28493563	NF also abolishes EtOH induced escalation of <b>alcohol</b> preference/consumption, but has no effect when administered to <strong>TLR4</strong> KO mice.
+TLR4	addiction	addiction	28493563	NF also abolishes EtOH induced <b>escalation</b> of alcohol preference/consumption, but has no effect when administered to <strong>TLR4</strong> KO mice.
+TLR4	drug	alcohol	28493563	These results suggest that NF prevents neuroinflammation and brain damage by blocking the <strong>TLR4</strong> response and also support the role of central pro inflammatory immune signaling in the modulation of <b>alcohol</b> consumption/addiction.
+TLR4	addiction	addiction	28493563	These results suggest that NF prevents neuroinflammation and brain damage by blocking the <strong>TLR4</strong> response and also support the role of central pro inflammatory immune signaling in the modulation of alcohol consumption/<b>addiction</b>.
+TLR4	drug	alcohol	28400259	Preclinical studies have largely supported that <b>alcohol</b> consumption induces the development of an important neuro inflammation and this neuro inflammation contributes to <b>alcohol</b> drinking behaviors, notably through <strong>TLR4</strong> and LPS related mechanisms.
+TLR4	drug	opioid	28306133	Injection of <strong>Toll like receptor 4</strong> siRNA into the ventrolateral periaqueductal gray attenuates withdrawal syndrome in <b>morphine</b> dependent rats.
+TLR4	addiction	withdrawal	28306133	Injection of <strong>Toll like receptor 4</strong> siRNA into the ventrolateral periaqueductal gray attenuates <b>withdrawal</b> syndrome in morphine dependent rats.
+TLR4	drug	opioid	28306133	We assessed the role of the Toll like receptor 4 (<strong>TLR4</strong>) gene in the ventrolateral periaqueductal gray (vlPAG) region of <b>morphine</b> dependent rats on attenuating withdrawal syndrome, and regulating glutamic acid decarboxylase (GAD67), glutamic acid (Glu), and gamma aminobutyric acid (GABA).
+TLR4	addiction	withdrawal	28306133	We assessed the role of the Toll like receptor 4 (<strong>TLR4</strong>) gene in the ventrolateral periaqueductal gray (vlPAG) region of morphine dependent rats on attenuating <b>withdrawal</b> syndrome, and regulating glutamic acid decarboxylase (GAD67), glutamic acid (Glu), and gamma aminobutyric acid (GABA).
+TLR4	drug	opioid	28306133	We assessed the role of the <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) gene in the ventrolateral periaqueductal gray (vlPAG) region of <b>morphine</b> dependent rats on attenuating withdrawal syndrome, and regulating glutamic acid decarboxylase (GAD67), glutamic acid (Glu), and gamma aminobutyric acid (GABA).
+TLR4	addiction	withdrawal	28306133	We assessed the role of the <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) gene in the ventrolateral periaqueductal gray (vlPAG) region of morphine dependent rats on attenuating <b>withdrawal</b> syndrome, and regulating glutamic acid decarboxylase (GAD67), glutamic acid (Glu), and gamma aminobutyric acid (GABA).
+TLR4	addiction	withdrawal	28306133	After siRNA mediated downregulation of <strong>TLR4</strong>, changes were observed in <b>withdrawal</b> behavior and downstream signaling molecules.
+TLR4	drug	opioid	28306133	Rats were injected into the vlPAG with <strong>TLR4</strong> siRNA, followed by intraperitoneal injection of <b>morphine</b> for 5 consecutive days, and then <b>naloxone</b>, and the behavioral indices of <b>morphine</b> withdrawal were observed.
+TLR4	addiction	withdrawal	28306133	Rats were injected into the vlPAG with <strong>TLR4</strong> siRNA, followed by intraperitoneal injection of morphine for 5 consecutive days, and then naloxone, and the behavioral indices of morphine <b>withdrawal</b> were observed.
+TLR4	drug	nicotine	28284355	<strong>TLR4</strong> gene polymorphism associated with lifetime cigarette <b>smoking</b> in bipolar disorder.
+TLR4	drug	nicotine	28284355	Toll like receptor 4, a sensor of pathogens and of products of cellular stress and damage, is a major innate immune molecule and logical candidate gene for <b>tobacco</b> dependence in BD because (i) the involvement of <strong>TLR4</strong> molecules in several substance use disorders has been suggested, (ii) and the association between the <strong>TLR4</strong> gene and BD.
+TLR4	addiction	dependence	28284355	Toll like receptor 4, a sensor of pathogens and of products of cellular stress and damage, is a major innate immune molecule and logical candidate gene for tobacco <b>dependence</b> in BD because (i) the involvement of <strong>TLR4</strong> molecules in several substance use disorders has been suggested, (ii) and the association between the <strong>TLR4</strong> gene and BD.
+TLR4	drug	nicotine	28284355	<strong>Toll like receptor 4</strong>, a sensor of pathogens and of products of cellular stress and damage, is a major innate immune molecule and logical candidate gene for <b>tobacco</b> dependence in BD because (i) the involvement of <strong>TLR4</strong> molecules in several substance use disorders has been suggested, (ii) and the association between the <strong>TLR4</strong> gene and BD.
+TLR4	addiction	dependence	28284355	<strong>Toll like receptor 4</strong>, a sensor of pathogens and of products of cellular stress and damage, is a major innate immune molecule and logical candidate gene for tobacco <b>dependence</b> in BD because (i) the involvement of <strong>TLR4</strong> molecules in several substance use disorders has been suggested, (ii) and the association between the <strong>TLR4</strong> gene and BD.
+TLR4	drug	nicotine	28284355	We analysed herein the potential association between six <strong>TLR4</strong> polymorphisms and lifetime <b>tobacco</b> <b>smoking</b> in 514 BD patients.
+TLR4	drug	nicotine	28284355	Our results suggest that <strong>TLR4</strong> gene polymorphism may act as an intermediate factor for the association between <b>tobacco</b> <b>smoking</b> addiction and BD.
+TLR4	addiction	addiction	28284355	Our results suggest that <strong>TLR4</strong> gene polymorphism may act as an intermediate factor for the association between tobacco smoking <b>addiction</b> and BD.
+TLR4	drug	alcohol	28257601	MicroRNA 181b 3p and its target importin α5 regulate <strong>toll like receptor 4</strong> signaling in Kupffer cells and liver injury in mice in response to <b>ethanol</b>.
+TLR4	drug	alcohol	28257601	Toll like receptor 4 (<strong>TLR4</strong>) mediated signaling was assessed in primary cultures of Kupffer cells from <b>ethanol</b>  and pair fed rats after treatment with HA35.
+TLR4	drug	alcohol	28257601	<strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) mediated signaling was assessed in primary cultures of Kupffer cells from <b>ethanol</b>  and pair fed rats after treatment with HA35.
+TLR4	drug	alcohol	28257601	<strong>TLR4</strong> signaling was increased in Kupffer cells by <b>ethanol</b>; this sensitization was normalized by ex vivo treatment with HA35.
+TLR4	addiction	sensitization	28257601	<strong>TLR4</strong> signaling was increased in Kupffer cells by ethanol; this <b>sensitization</b> was normalized by ex vivo treatment with HA35.
+TLR4	drug	cocaine	28070538	Lack of Effects of <strong>Toll Like Receptor 4</strong> Antagonists on the Reinforcing Effects of <b>Cocaine</b> and Remifentanil.
+TLR4	addiction	reward	28070538	Lack of Effects of <strong>Toll Like Receptor 4</strong> Antagonists on the <b>Reinforcing</b> Effects of Cocaine and Remifentanil.
+TLR4	addiction	withdrawal	28062186	We attempted to verify <b>withdrawal</b> regulation of induced nitric oxide synthase (iNOS), astroglia marker, glial fibrillary acidic protein (GFAP), ionized calcium binding protein (Iba1), a microglia activation marker, a pro inflammatory mediator, tumor necrosis alpha (TNF α) and immune receptor, toll like receptor 4 (<strong>TLR 4</strong>) genes by real time polymerase chain reaction (RT PCR).
+TLR4	addiction	withdrawal	28062186	We attempted to verify <b>withdrawal</b> regulation of induced nitric oxide synthase (iNOS), astroglia marker, glial fibrillary acidic protein (GFAP), ionized calcium binding protein (Iba1), a microglia activation marker, a pro inflammatory mediator, tumor necrosis alpha (TNF α) and immune receptor, <strong>toll like receptor 4</strong> (<strong>TLR 4</strong>) genes by real time polymerase chain reaction (RT PCR).
+TLR4	drug	alcohol	27986929	Genetic and Pharmacologic Manipulation of <strong>TLR4</strong> Has Minimal Impact on <b>Ethanol</b> Consumption in Rodents.
+TLR4	drug	alcohol	27986929	Toll like receptor 4 (<strong>TLR4</strong>) is a critical component of innate immune signaling and has been implicated in <b>alcohol</b> responses in preclinical and clinical models.
+TLR4	drug	alcohol	27986929	<strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) is a critical component of innate immune signaling and has been implicated in <b>alcohol</b> responses in preclinical and clinical models.
+TLR4	drug	alcohol	27986929	Members of the Integrative Neuroscience Initiative on <b>Alcoholism</b> (INIA Neuroimmune) consortium tested the hypothesis that <strong>TLR4</strong> mediates excessive <b>ethanol</b> drinking using the following models: (1) <strong>Tlr4</strong> knock out (KO) rats, (2) selective knockdown of <strong>Tlr4</strong> mRNA in mouse nucleus accumbens (NAc), and (3) injection of the <strong>TLR4</strong> antagonist (+) naloxone in mice.
+TLR4	drug	opioid	27986929	Members of the Integrative Neuroscience Initiative on Alcoholism (INIA Neuroimmune) consortium tested the hypothesis that <strong>TLR4</strong> mediates excessive ethanol drinking using the following models: (1) <strong>Tlr4</strong> knock out (KO) rats, (2) selective knockdown of <strong>Tlr4</strong> mRNA in mouse nucleus accumbens (NAc), and (3) injection of the <strong>TLR4</strong> antagonist (+) <b>naloxone</b> in mice.
+TLR4	drug	alcohol	27986929	Lipopolysaccharide (LPS) decreased food/water intake and body weight in <b>ethanol</b> naive and <b>ethanol</b> trained wild type (WT), but not <strong>Tlr4</strong> KO rats.
+TLR4	drug	alcohol	27986929	Using different species and sexes, different methods to inhibit <strong>TLR4</strong> signaling, and different <b>ethanol</b> consumption tests, our comprehensive studies indicate that <strong>TLR4</strong> may play a role in <b>ethanol</b> induced sedation and GABAA receptor function, but does not regulate excessive drinking directly and would not be an effective therapeutic target.
+TLR4	drug	alcohol	27986929	Toll like receptor 4 (<strong>TLR4</strong>) is a key mediator of innate immune signaling and has been implicated in <b>alcohol</b> responses in animal models and human <b>alcoholics</b>.
+TLR4	drug	alcohol	27986929	<strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) is a key mediator of innate immune signaling and has been implicated in <b>alcohol</b> responses in animal models and human <b>alcoholics</b>.
+TLR4	drug	alcohol	27986929	Members of the Integrative Neuroscience Initiative on <b>Alcoholism</b> (INIA Neuroimmune) consortium participated in the first comprehensive study across multiple laboratories to test the hypothesis that <strong>TLR4</strong> regulates excessive <b>alcohol</b> consumption in different species and different models of chronic, dependence driven, and binge like drinking.
+TLR4	addiction	dependence	27986929	Members of the Integrative Neuroscience Initiative on Alcoholism (INIA Neuroimmune) consortium participated in the first comprehensive study across multiple laboratories to test the hypothesis that <strong>TLR4</strong> regulates excessive alcohol consumption in different species and different models of chronic, <b>dependence</b> driven, and binge like drinking.
+TLR4	addiction	intoxication	27986929	Members of the Integrative Neuroscience Initiative on Alcoholism (INIA Neuroimmune) consortium participated in the first comprehensive study across multiple laboratories to test the hypothesis that <strong>TLR4</strong> regulates excessive alcohol consumption in different species and different models of chronic, dependence driven, and <b>binge</b> like drinking.
+TLR4	drug	alcohol	27986929	Although <strong>TLR4</strong> was not a critical determinant of excessive drinking, it was important in the acute sedative effects of <b>alcohol</b>.
+TLR4	drug	alcohol	27834881	Salidroside Regulates Inflammatory Response in Raw 264.7 Macrophages via <strong>TLR4</strong>/TAK1 and Ameliorates Inflammation in <b>Alcohol</b> Binge Drinking Induced Liver Injury.
+TLR4	addiction	intoxication	27834881	Salidroside Regulates Inflammatory Response in Raw 264.7 Macrophages via <strong>TLR4</strong>/TAK1 and Ameliorates Inflammation in Alcohol <b>Binge</b> Drinking Induced Liver Injury.
+TLR4	drug	alcohol	27650785	It also reviews findings that indicate the role of <strong>TLR4</strong> dependent signaling immune molecules in <b>alcohol</b> consumption, reward, and addiction.
+TLR4	addiction	addiction	27650785	It also reviews findings that indicate the role of <strong>TLR4</strong> dependent signaling immune molecules in alcohol consumption, reward, and <b>addiction</b>.
+TLR4	addiction	reward	27650785	It also reviews findings that indicate the role of <strong>TLR4</strong> dependent signaling immune molecules in alcohol consumption, <b>reward</b>, and addiction.
+TLR4	drug	alcohol	27650785	The research data suggest that overactivation of <strong>TLR4</strong> or NLRs increases pro inflammatory cytokines and mediators to cause neural damage in the cerebral cortex and hippocampus, while modest <strong>TLR4</strong> activation, along with the generation of certain cytokines and chemokines in specific brain areas (e.g., amygdala, ventral tegmental area), modulate neurotransmission, <b>alcohol</b> drinking, and <b>alcohol</b> rewards.
+TLR4	drug	alcohol	27699959	The present study aims to assess plasma cytokine and chemokine levels in male and female adolescents and young adults during acute <b>alcohol</b> intoxication and to correlate these results with the toll like receptor 4 (<strong>TLR4</strong>) response.
+TLR4	addiction	intoxication	27699959	The present study aims to assess plasma cytokine and chemokine levels in male and female adolescents and young adults during acute alcohol <b>intoxication</b> and to correlate these results with the toll like receptor 4 (<strong>TLR4</strong>) response.
+TLR4	drug	alcohol	27699959	The present study aims to assess plasma cytokine and chemokine levels in male and female adolescents and young adults during acute <b>alcohol</b> intoxication and to correlate these results with the <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) response.
+TLR4	addiction	intoxication	27699959	The present study aims to assess plasma cytokine and chemokine levels in male and female adolescents and young adults during acute alcohol <b>intoxication</b> and to correlate these results with the <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) response.
+TLR4	drug	alcohol	27699959	The potential role of the <strong>TLR4</strong> signaling response was also assessed in plasma and prefrontal cortex (PFC) of adolescent wild type and <strong>TLR4</strong> knockout male and female mice with binge <b>ethanol</b> treatment.
+TLR4	addiction	intoxication	27699959	The potential role of the <strong>TLR4</strong> signaling response was also assessed in plasma and prefrontal cortex (PFC) of adolescent wild type and <strong>TLR4</strong> knockout male and female mice with <b>binge</b> ethanol treatment.
+TLR4	drug	alcohol	27699959	The results showed that <b>alcohol</b> intoxication increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of <strong>TLR4</strong> mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+TLR4	addiction	intoxication	27699959	The results showed that alcohol <b>intoxication</b> increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of <strong>TLR4</strong> mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+TLR4	drug	alcohol	27699959	No changes in serum or prefrontal cortex cytokine and chemokine levels were noted in <b>ethanol</b> treated male or female <strong>TLR4</strong> knockout mice.
+TLR4	drug	alcohol	27699959	Our findings revealed that females are more vulnerable than males to inflammatory effects of binge <b>ethanol</b> drinking and suggested that <strong>TLR4</strong> is an important target of <b>ethanol</b> induced inflammation and neuroinflammation in adolescence.
+TLR4	addiction	intoxication	27699959	Our findings revealed that females are more vulnerable than males to inflammatory effects of <b>binge</b> ethanol drinking and suggested that <strong>TLR4</strong> is an important target of ethanol induced inflammation and neuroinflammation in adolescence.
+TLR4	drug	alcohol	27659607	Markers of steatosis, intestinal barrier function, activation of <strong>toll like receptor 4</strong> signaling cascades, lipid peroxidation and lipogenesis were determined in liver, small intestine and plasma 2 h and 12 h after acute <b>alcohol</b> ingestion.
+TLR4	drug	alcohol	27627966	<strong>Tlr4</strong> mutant mice are resistant to acute <b>alcohol</b> induced sterol regulatory element binding protein activation and hepatic lipid accumulation.
+TLR4	drug	alcohol	27627966	The present study showed that acute <b>alcohol</b> intoxication caused hepatic lipid accumulation in <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	addiction	intoxication	27627966	The present study showed that acute alcohol <b>intoxication</b> caused hepatic lipid accumulation in <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	drug	alcohol	27627966	Hepatic sterol regulatory element binding protein (SREBP) 1, a transcription factor regulating fatty acid and triglyceride (TG) synthesis, was activated in <b>alcohol</b> treated <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	drug	alcohol	27627966	Hepatic Fas, Acc, Scd 1 and Dgat 2, the key genes for fatty acid and TG synthesis, were up regulated in <b>alcohol</b> treated <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	drug	alcohol	27627966	Additional experiment showed that hepatic MyD88 was elevated in <b>alcohol</b> treated <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	drug	alcohol	27627966	Hepatic NF κB was activated in <b>alcohol</b> treated <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	drug	alcohol	27627966	Moreover, hepatic GSH content was reduced and hepatic MDA level was elevated in <b>alcohol</b> treated <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	drug	alcohol	27627966	Hepatic CYP2E1 was elevated in <b>alcohol</b> treated <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	drug	alcohol	27627966	Hepatic p67phox and gp91phox, two NADPH oxidase subunits, were up regulated in <b>alcohol</b> treated <strong>Tlr4</strong> wild type mice but not in <strong>Tlr4</strong> mutant mice.
+TLR4	drug	alcohol	27627966	In conclusion, <strong>Tlr4</strong> mutant mice are resistant to acute <b>alcohol</b> induced hepatic SREBP 1 activation and hepatic lipid accumulation.
+TLR4	drug	opioid	27461080	<strong>Toll like Receptor 4</strong> Mediates <b>Morphine</b> Induced Neuroinflammation and Tolerance via Soluble Tumor Necrosis Factor Signaling.
+TLR4	drug	opioid	27461080	Immune signaling contributes to the decreased efficacy of <b>opioids</b>, and we recently demonstrated that Toll like receptor 4 (<strong>TLR4</strong>) mediated neuroinflammation in the periaqueductal gray (PAG) drives tolerance.
+TLR4	drug	opioid	27461080	Immune signaling contributes to the decreased efficacy of <b>opioids</b>, and we recently demonstrated that <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) mediated neuroinflammation in the periaqueductal gray (PAG) drives tolerance.
+TLR4	drug	opioid	27461080	Tumor necrosis factor (TNF), a product of <strong>TLR4</strong> signaling, promotes inflammation and facilitates glutamatergic signaling, key components of <b>opioid</b> tolerance.
+TLR4	drug	opioid	27461080	Therefore, we hypothesize that <strong>TLR4</strong> mediated <b>opioid</b> tolerance requires TNF signaling.
+TLR4	drug	opioid	27461080	By expression of a dominant negative TNF peptide via lentiviral vector injection in rat PAG to sequester soluble TNF (solTNF), we demonstrate that solTNF mediates <b>morphine</b> tolerance induced by <strong>TLR4</strong> signaling, stimulates neuroinflammation (increased IL 1β and <strong>TLR4</strong> mRNA), and disrupts glutamate reuptake (decreased GLT 1 and GLAST mRNA).
+TLR4	drug	alcohol	27296151	Recently, the (+) enantiomers of naloxone and <b>naltrexone</b>, <strong>TLR4</strong> antagonists, have been reported to attenuate preclinical indicators of both opioid and stimulant abuse.
+TLR4	drug	opioid	27296151	Recently, the (+) enantiomers of <b>naloxone</b> and naltrexone, <strong>TLR4</strong> antagonists, have been reported to attenuate preclinical indicators of both <b>opioid</b> and stimulant abuse.
+TLR4	drug	alcohol	27296151	Furthermore, although an attenuation of either cocaine or remifentanil self administration was obtained at the highest doses of (+) naloxone and (+) <b>naltrexone</b>, those doses also attenuated rates of food maintained behaviors, indicating a lack of selectivity of <strong>TLR4</strong> antagonist effects for behaviors reinforced with drug injections.
+TLR4	drug	cocaine	27296151	Furthermore, although an attenuation of either <b>cocaine</b> or remifentanil self administration was obtained at the highest doses of (+) naloxone and (+) naltrexone, those doses also attenuated rates of food maintained behaviors, indicating a lack of selectivity of <strong>TLR4</strong> antagonist effects for behaviors reinforced with drug injections.
+TLR4	drug	opioid	27296151	Furthermore, although an attenuation of either cocaine or remifentanil self administration was obtained at the highest doses of (+) <b>naloxone</b> and (+) naltrexone, those doses also attenuated rates of food maintained behaviors, indicating a lack of selectivity of <strong>TLR4</strong> antagonist effects for behaviors reinforced with drug injections.
+TLR4	drug	alcohol	27296151	The present studies demonstrate that under a wide range of doses and experimental conditions, the <strong>TLR4</strong> antagonists, (+) naloxone and (+) <b>naltrexone</b>, did not specifically block neurochemical or behavioral abuse related effects of cocaine or opioid agonists.
+TLR4	drug	cocaine	27296151	The present studies demonstrate that under a wide range of doses and experimental conditions, the <strong>TLR4</strong> antagonists, (+) naloxone and (+) naltrexone, did not specifically block neurochemical or behavioral abuse related effects of <b>cocaine</b> or opioid agonists.
+TLR4	drug	opioid	27296151	The present studies demonstrate that under a wide range of doses and experimental conditions, the <strong>TLR4</strong> antagonists, (+) <b>naloxone</b> and (+) naltrexone, did not specifically block neurochemical or behavioral abuse related effects of cocaine or <b>opioid</b> agonists.
+TLR4	drug	opioid	27278234	Toll like receptor 4 (<strong>TLR4</strong>) signaling is implied in <b>opioid</b> reinforcement, reward, and withdrawal.
+TLR4	addiction	reward	27278234	Toll like receptor 4 (<strong>TLR4</strong>) signaling is implied in opioid <b>reinforcement</b>, <b>reward</b>, and withdrawal.
+TLR4	addiction	withdrawal	27278234	Toll like receptor 4 (<strong>TLR4</strong>) signaling is implied in opioid reinforcement, reward, and <b>withdrawal</b>.
+TLR4	drug	opioid	27278234	<strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) signaling is implied in <b>opioid</b> reinforcement, reward, and withdrawal.
+TLR4	addiction	reward	27278234	<strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) signaling is implied in opioid <b>reinforcement</b>, <b>reward</b>, and withdrawal.
+TLR4	addiction	withdrawal	27278234	<strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) signaling is implied in opioid reinforcement, reward, and <b>withdrawal</b>.
+TLR4	drug	opioid	27278234	Here, we explored whether <strong>TLR4</strong> signaling is involved in the acute psychomotor stimulating effects of <b>heroin</b>, 6 acetylmorphine (6 AM), and <b>morphine</b> as well as whether there are differences between the three <b>opioids</b> regarding <strong>TLR4</strong> signaling.
+TLR4	drug	opioid	27278234	To address this, we examined how pretreatment with (+) <b>naloxone</b>, a <strong>TLR4</strong> active but <b>opioid</b> receptor (OR) inactive antagonist, affected the acute increase in locomotor activity induced by <b>heroin</b>, 6 AM, or <b>morphine</b> in mice.
+TLR4	drug	opioid	27278234	We also assessed the effect of pretreatment with ( ) <b>naloxone</b>, a <strong>TLR4</strong> and OR active antagonist, as well as the pharmacokinetic profiles of (+) and ( ) <b>naloxone</b> in the blood and brain.
+TLR4	drug	opioid	27278234	By contrast, (+) <b>naloxone</b>, administered in doses assumed to antagonize <strong>TLR4</strong> but not ORs, did not affect acute locomotor activity induced by <b>heroin</b>, 6 AM, or <b>morphine</b>.
+TLR4	drug	opioid	27278234	Our results underpin the importance of OR activation and do not indicate an apparent role of <strong>TLR4</strong> signaling in acute <b>opioid</b> induced psychomotor stimulation in mice.
+TLR4	drug	opioid	27278234	Furthermore, there were no marked differences between <b>heroin</b>, 6 AM, and <b>morphine</b> regarding involvement of OR or <strong>TLR4</strong> signaling.
+TLR4	drug	alcohol	27187237	We have previously shown that <b>alcohol</b> preferring P rats have innately elevated levels of a neuronal Toll like receptor 4 (<strong>TLR4</strong>) signal in the ventral tegmental area (VTA) that controls the initiation of excessive <b>alcohol</b> drinking.
+TLR4	drug	alcohol	27187237	We have previously shown that <b>alcohol</b> preferring P rats have innately elevated levels of a neuronal <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) signal in the ventral tegmental area (VTA) that controls the initiation of excessive <b>alcohol</b> drinking.
+TLR4	drug	alcohol	27187237	The data suggest that <strong>TLR4</strong> signaling in VTA dopaminergic neurons controls impulsivity related to the regulation of TH expression, likely contributing to the initiation of <b>alcohol</b> drinking and its transition to <b>alcohol</b> dependence.
+TLR4	addiction	dependence	27187237	The data suggest that <strong>TLR4</strong> signaling in VTA dopaminergic neurons controls impulsivity related to the regulation of TH expression, likely contributing to the initiation of alcohol drinking and its transition to alcohol <b>dependence</b>.
+TLR4	drug	amphetamine	27156126	The effects of D3R on <strong>TLR4</strong> signaling involved in the regulation of <b>METH</b> mediated mast cells activation.
+TLR4	drug	amphetamine	27156126	Furthermore, we explored the effects of D3R on <b>METH</b> mediated <strong>TLR4</strong> and downstream MAPK and NF κB signaling induced by LPS in mouse BMMCs.
+TLR4	drug	amphetamine	27156126	D3R was also involved in <b>METH</b> mediated modulation of LPS induced expression of <strong>TLR4</strong> and downstream MAPK and NF κB signaling molecules in mouse BMMCs.
+TLR4	drug	amphetamine	27156126	Taken together, our findings demonstrate that the effect of D3R on <strong>TLR4</strong> signaling may be implicated in the regulation of <b>METH</b> mediated MCs activation induced by LPS.
+TLR4	drug	alcohol	27151970	Evaluation of <strong>TLR4</strong> Inhibitor, T5342126, in Modulation of <b>Ethanol</b> Drinking Behavior in <b>Alcohol</b> Dependent Mice.
+TLR4	drug	alcohol	27151970	Several lines of evidence support a critical role of <strong>TLR4</strong> in the neuroimmune responses associated with <b>alcohol</b> disorders and propose inhibitors of <strong>TLR4</strong> signaling as potential treatments for <b>alcoholism</b>.
+TLR4	drug	alcohol	27151970	In this work, we investigated the effect of T5342126 compound, a selective <strong>TLR4</strong> inhibitor, on excessive drinking and microglial activation associated with <b>ethanol</b> dependence.
+TLR4	addiction	dependence	27151970	In this work, we investigated the effect of T5342126 compound, a selective <strong>TLR4</strong> inhibitor, on excessive drinking and microglial activation associated with ethanol <b>dependence</b>.
+TLR4	drug	alcohol	27151970	Collectively, our data suggest that T5342126, via blocking <strong>TLR4</strong> activation, contributes to the reduction of <b>ethanol</b> drinking and <b>ethanol</b> induced neuroimmune responses.
+TLR4	drug	alcohol	27151970	T5342126, an experimental <strong>TLR4</strong> inhibitor, is effective in reducing <b>ethanol</b> drinking and inhibiting the activation and proliferation of microglia in both <b>ethanol</b> dependent and non dependent mice.
+TLR4	drug	cocaine	27112496	Critically, following a period of abstinence, a weak <strong>TLR4</strong> agonist can reactivate microglia, increase TNF α production, depress striatal synaptic strength, and suppress <b>cocaine</b> induced sensitization.
+TLR4	addiction	sensitization	27112496	Critically, following a period of abstinence, a weak <strong>TLR4</strong> agonist can reactivate microglia, increase TNF α production, depress striatal synaptic strength, and suppress cocaine induced <b>sensitization</b>.
+TLR4	drug	alcohol	26949123	Disruption of blood brain barrier integrity in postmortem <b>alcoholic</b> brain: preclinical evidence of <strong>TLR4</strong> involvement from a binge like drinking model.
+TLR4	addiction	intoxication	26949123	Disruption of blood brain barrier integrity in postmortem alcoholic brain: preclinical evidence of <strong>TLR4</strong> involvement from a <b>binge</b> like drinking model.
+TLR4	drug	alcohol	26949123	Because there is evidence that <b>ethanol</b> (EtOH) induces release of free radicals, cytokines and inflammatory mediators we examined BBB integrity and matrix metalloproteinase (MMP) activity in postmortem human <b>alcoholic</b> brain and investigated the role of <strong>TLR4</strong> signaling in BBB permeability in <strong>TLR4</strong> knockout mice under a binge like EtOH drinking protocol.
+TLR4	addiction	intoxication	26949123	Because there is evidence that ethanol (EtOH) induces release of free radicals, cytokines and inflammatory mediators we examined BBB integrity and matrix metalloproteinase (MMP) activity in postmortem human alcoholic brain and investigated the role of <strong>TLR4</strong> signaling in BBB permeability in <strong>TLR4</strong> knockout mice under a <b>binge</b> like EtOH drinking protocol.
+TLR4	drug	opioid	26898358	We will discuss about experimental evidences reported for several potential <b>opioid</b> adjuvants, including N methyl D aspartate receptor antagonists, 5 HT7 agonists, sigma 1 antagonists, I2 R ligands, cholecystokinin antagonists, neuropeptide FF R antagonists and <strong>toll like receptor 4</strong> antagonists.
+TLR4	drug	alcohol	26857094	Oleoylethanolamide prevents neuroimmune HMGB1/<strong>TLR4</strong>/NF kB danger signaling in rat frontal cortex and depressive like behavior induced by <b>ethanol</b> binge administration.
+TLR4	drug	cannabinoid	26857094	<b>Oleoylethanolamide</b> prevents neuroimmune HMGB1/<strong>TLR4</strong>/NF kB danger signaling in rat frontal cortex and depressive like behavior induced by ethanol binge administration.
+TLR4	addiction	intoxication	26857094	Oleoylethanolamide prevents neuroimmune HMGB1/<strong>TLR4</strong>/NF kB danger signaling in rat frontal cortex and depressive like behavior induced by ethanol <b>binge</b> administration.
+TLR4	drug	alcohol	26857094	previous each <b>alcohol</b> gavage blocked the expression of high mobility group box 1 (HMGB1) danger signal and the innate immunity Toll like receptors 4 (<strong>TLR4</strong>) in frontal cortex, and inhibited the nuclear factor kappa B (NF kB) proinflammatory cascade induced by <b>alcohol</b> binge administration.
+TLR4	addiction	intoxication	26857094	previous each alcohol gavage blocked the expression of high mobility group box 1 (HMGB1) danger signal and the innate immunity Toll like receptors 4 (<strong>TLR4</strong>) in frontal cortex, and inhibited the nuclear factor kappa B (NF kB) proinflammatory cascade induced by alcohol <b>binge</b> administration.
+TLR4	drug	alcohol	26773297	In ALD, chronic <b>ethanol</b> exposure sensitizes Kupffer cells to activation by lipopolysaccharides through Toll like receptors, e.g., <strong>Toll like receptor 4</strong>.
+TLR4	drug	alcohol	26695754	<b>Ethanol</b> exposure activates signaling pathways featuring high mobility group box 1 and Toll like receptor 4 (<strong>TLR4</strong>), resulting in induction of the transcription factor nuclear factor kappa light chain enhancer of activated B cells, which regulates expression of several cytokine genes involved in innate immunity, and its target genes.
+TLR4	drug	alcohol	26695754	<b>Ethanol</b> exposure activates signaling pathways featuring high mobility group box 1 and <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>), resulting in induction of the transcription factor nuclear factor kappa light chain enhancer of activated B cells, which regulates expression of several cytokine genes involved in innate immunity, and its target genes.
+TLR4	drug	alcohol	26686767	Involvement of <strong>TLR4</strong> in the long term epigenetic changes, rewarding and anxiety effects induced by intermittent <b>ethanol</b> treatment in adolescence.
+TLR4	drug	alcohol	26686767	Although the mechanisms that participate in these effects are largely unknown, we have shown that <b>ethanol</b> by activating innate immune receptors, toll like receptor 4 (<strong>TLR4</strong>), induces neuroinflammation, impairs myelin proteins and causes cognitive dysfunctions in adolescent mice.
+TLR4	drug	alcohol	26686767	Although the mechanisms that participate in these effects are largely unknown, we have shown that <b>ethanol</b> by activating innate immune receptors, <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), induces neuroinflammation, impairs myelin proteins and causes cognitive dysfunctions in adolescent mice.
+TLR4	drug	alcohol	26686767	Using wild type (WT) and <strong>TLR4</strong> deficient (<strong>TLR4</strong> KO) adolescent mice treated intermittently with <b>ethanol</b> (3g/kg) for 2 weeks, we showed that binge like <b>ethanol</b> treatment in adolescent mice promotes short  and long term alterations in synaptic plasticity and epigenetic changes in the promoter region of bdnf and fosb, which increased their expression in the mPFC of young adult animals.
+TLR4	addiction	intoxication	26686767	Using wild type (WT) and <strong>TLR4</strong> deficient (<strong>TLR4</strong> KO) adolescent mice treated intermittently with ethanol (3g/kg) for 2 weeks, we showed that <b>binge</b> like ethanol treatment in adolescent mice promotes short  and long term alterations in synaptic plasticity and epigenetic changes in the promoter region of bdnf and fosb, which increased their expression in the mPFC of young adult animals.
+TLR4	drug	alcohol	26686767	Our results further showed the participation of neuroimmune system activation and the <strong>TLR4</strong> signaling response since deficient mice in <strong>TLR4</strong> (<strong>TLR4</strong> KO) are protected against molecular and behavioral alterations of <b>ethanol</b> in the adolescent brain.
+TLR4	drug	alcohol	26603732	Pharmacological characterization of the opioid inactive isomers (+) <b>naltrexone</b> and (+) naloxone as antagonists of <strong>toll like receptor 4</strong>.
+TLR4	drug	opioid	26603732	Pharmacological characterization of the <b>opioid</b> inactive isomers (+) naltrexone and (+) <b>naloxone</b> as antagonists of <strong>toll like receptor 4</strong>.
+TLR4	addiction	reward	26603732	The toll like receptor <strong>TLR4</strong> is involved in neuropathic pain and in drug <b>reward</b> and <b>reinforcement</b>.
+TLR4	drug	alcohol	26603732	The opioid inactive isomers (+) <b>naltrexone</b> and (+) naloxone act as <strong>TLR4</strong> antagonists, reversing neuropathic pain and reducing opioid and cocaine reward and reinforcement.
+TLR4	drug	cocaine	26603732	The opioid inactive isomers (+) naltrexone and (+) naloxone act as <strong>TLR4</strong> antagonists, reversing neuropathic pain and reducing opioid and <b>cocaine</b> reward and reinforcement.
+TLR4	drug	opioid	26603732	The <b>opioid</b> inactive isomers (+) naltrexone and (+) <b>naloxone</b> act as <strong>TLR4</strong> antagonists, reversing neuropathic pain and reducing <b>opioid</b> and cocaine reward and reinforcement.
+TLR4	addiction	reward	26603732	The opioid inactive isomers (+) naltrexone and (+) naloxone act as <strong>TLR4</strong> antagonists, reversing neuropathic pain and reducing opioid and cocaine <b>reward</b> and <b>reinforcement</b>.
+TLR4	drug	alcohol	26603732	Here, we have elucidated the molecular mechanism of (+) <b>naltrexone</b> and (+) naloxone on <strong>TLR4</strong> signalling.
+TLR4	drug	opioid	26603732	Here, we have elucidated the molecular mechanism of (+) naltrexone and (+) <b>naloxone</b> on <strong>TLR4</strong> signalling.
+TLR4	drug	alcohol	26603732	Effects were measured using Western blotting, luciferase reporter assays, fluorescence microscopy and ELISA KEY RESULTS: (+) <b>Naltrexone</b> and (+) naloxone were equi potent inhibitors of the LPS induced <strong>TLR4</strong> downstream signalling and induction of the pro inflammatory factors NO and TNF α.
+TLR4	drug	opioid	26603732	Effects were measured using Western blotting, luciferase reporter assays, fluorescence microscopy and ELISA KEY RESULTS: (+) Naltrexone and (+) <b>naloxone</b> were equi potent inhibitors of the LPS induced <strong>TLR4</strong> downstream signalling and induction of the pro inflammatory factors NO and TNF α.
+TLR4	drug	alcohol	26603732	(+) <b>Naltrexone</b> and (+) naloxone were TRIF IFN regulatory factor 3 axis biased <strong>TLR4</strong> antagonists.
+TLR4	drug	opioid	26603732	(+) Naltrexone and (+) <b>naloxone</b> were TRIF IFN regulatory factor 3 axis biased <strong>TLR4</strong> antagonists.
+TLR4	addiction	intoxication	26151816	The <b>Binge</b> drinking group showed increased γGT together with increased expression of CD69 and reduced expression of <strong>TLR4</strong>, PD1, CCR2 and CXCR4 in peripheral CD8 cells.
+TLR4	drug	alcohol	26151816	PCA established 3 factors associated with <b>alcohol</b> consumption: "Early Activation" represented by CD69 and <strong>TLR4</strong> expression in the CD8 population; "Effector Activation" by CD69 expression in CD8 CD127(+)CD137(+) and CD8 CD25(+) CD137(+); and Trafficking by CXCR4 expression on total CD8 and CD8 GB(+)CXCR4(+), and CCR2 expression on total CD8.
+TLR4	drug	alcohol	26151816	<b>Alcohol</b> consumption affects the immune phenotype of CD8 cells since binge drinking pattern was found to be associated with high CD69 and low <strong>TLR4</strong>, CXCR4 and CCR2 expression, which suggest recent activation, decreased sensitivity to LPS and lower migration capacity in response to chemokines SDF 1 and MCP 1.
+TLR4	addiction	intoxication	26151816	Alcohol consumption affects the immune phenotype of CD8 cells since <b>binge</b> drinking pattern was found to be associated with high CD69 and low <strong>TLR4</strong>, CXCR4 and CCR2 expression, which suggest recent activation, decreased sensitivity to LPS and lower migration capacity in response to chemokines SDF 1 and MCP 1.
+TLR4	drug	opioid	26136385	Recent studies have revealed that <strong>TLR4</strong> activation is a significant trigger of signal transmission pathways in the nervous system, which could result in chronic pain as well as <b>opioid</b> tolerance and dependence.
+TLR4	addiction	dependence	26136385	Recent studies have revealed that <strong>TLR4</strong> activation is a significant trigger of signal transmission pathways in the nervous system, which could result in chronic pain as well as opioid tolerance and <b>dependence</b>.
+TLR4	addiction	reward	26022268	These glial products of <strong>TLR4</strong> activation enhance neuronal excitability within brain <b>reward</b> circuitry, thereby enhancing their rewarding and <b>reinforcing</b> effects.
+TLR4	drug	alcohol	26022268	Indeed, selective pharmacological blockade of <strong>TLR4</strong> activation, such as with the non opioid <strong>TLR4</strong> antagonist (+) <b>naltrexone</b>, suppresses a number of indices of drug reward/reinforcement.
+TLR4	drug	opioid	26022268	Indeed, selective pharmacological blockade of <strong>TLR4</strong> activation, such as with the non <b>opioid</b> <strong>TLR4</strong> antagonist (+) naltrexone, suppresses a number of indices of drug reward/reinforcement.
+TLR4	addiction	reward	26022268	Indeed, selective pharmacological blockade of <strong>TLR4</strong> activation, such as with the non opioid <strong>TLR4</strong> antagonist (+) naltrexone, suppresses a number of indices of drug <b>reward</b>/<b>reinforcement</b>.
+TLR4	drug	alcohol	26010811	Structure Activity Relationships of (+) <b>Naltrexone</b> Inspired Toll like Receptor 4 (<strong>TLR4</strong>) Antagonists.
+TLR4	drug	alcohol	26010811	Structure Activity Relationships of (+) <b>Naltrexone</b> Inspired <strong>Toll like Receptor 4</strong> (<strong>TLR4</strong>) Antagonists.
+TLR4	drug	alcohol	26010811	(+) <b>Naltrexone</b> acts as a Toll like receptor 4 (<strong>TLR4</strong>) antagonist and has been shown to reverse neuropathic pain in rat studies.
+TLR4	drug	alcohol	26010811	(+) <b>Naltrexone</b> acts as a <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) antagonist and has been shown to reverse neuropathic pain in rat studies.
+TLR4	drug	alcohol	26010811	We designed and synthesized compounds based on (+) <b>naltrexone</b> and (+) noroxymorphone and evaluated their <strong>TLR4</strong> antagonist activities by their effects on inhibiting lipopolysaccharide (LPS) induced <strong>TLR4</strong> downstream nitric oxide (NO) production in microglia BV 2 cells.
+TLR4	drug	alcohol	26010811	The most promising analog, (+) N phenethylnoroxymorphone ((4S,4aR,7aS,12bR) 4a,9 dihydroxy 3 phenethyl 2,3,4,4a,5,6 hexahydro 1H 4,12 methanobenzofuro[3,2 e]isoquinolin 7(7aH) one, 1j) showed ∼75 times better <strong>TLR 4</strong> antagonist activity than (+) <b>naltrexone</b>, and the ratio of its cell viability IC50, a measure of its toxicity, to <strong>TLR 4</strong> antagonist activity (140 μM/1.4 μM) was among the best of the new analogs.
+TLR4	drug	alcohol	25999437	Markers of steatosis, lipogenesis, activation of the <strong>toll like receptor 4</strong> signaling cascade and lipid export in liver and tight junction proteins in duodenum were measured 6 and 12 h after acute <b>ethanol</b> or beer intake.
+TLR4	drug	alcohol	25930080	Although previous studies reported the involvement of the <strong>TLR4</strong> TRIF pathway in <b>alcohol</b> induced liver injury, the role of TLR2 and TLR9 signaling in <b>alcohol</b> mediated neutrophil infiltration and liver injury has not been elucidated.
+TLR4	addiction	reward	25896879	Another accumbal <b>reward</b> marker, <strong>Tlr4</strong> mRNA, was elevated in females by high fat feeding.
+TLR4	drug	opioid	25850855	<b>Morphine</b> potentiates LPS induced autophagy initiation but inhibits autophagosomal maturation through distinct <strong>TLR4</strong> dependent and independent pathways.
+TLR4	drug	opioid	25850855	<b>Morphine</b> modulation of LPS induced autophagosome maturation visualized using co localization of GFP mcherry LC3 was <strong>TLR4</strong> independent, but mediated through μ <b>opioid</b> receptor signalling.
+TLR4	drug	cocaine	25644383	DAT isn't all that: <b>cocaine</b> reward and reinforcement require <strong>Toll like receptor 4</strong> signaling.
+TLR4	addiction	reward	25644383	DAT isn't all that: cocaine <b>reward</b> and <b>reinforcement</b> require <strong>Toll like receptor 4</strong> signaling.
+TLR4	drug	cocaine	25644383	Here we demonstrate that <b>cocaine</b> also interacts with the immunosurveillance receptor complex, Toll like receptor 4 (<strong>TLR4</strong>), on microglial cells to initiate central innate immune signaling.
+TLR4	drug	cocaine	25644383	Here we demonstrate that <b>cocaine</b> also interacts with the immunosurveillance receptor complex, <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>), on microglial cells to initiate central innate immune signaling.
+TLR4	drug	cocaine	25644383	Disruption of <b>cocaine</b> signaling at <strong>TLR4</strong> suppresses <b>cocaine</b> induced extracellular dopamine in the NAc, as well as <b>cocaine</b> conditioned place preference and <b>cocaine</b> self administration.
+TLR4	drug	alcohol	25567426	CRF amplified neuronal <strong>TLR4</strong>/MCP 1 signaling regulates <b>alcohol</b> self administration.
+TLR4	drug	alcohol	25567426	We report that <b>alcohol</b> preferring P rats have innately elevated levels of Toll like receptor 4 (<strong>TLR4</strong>) and monocyte chemotactic protein 1 (MCP 1) that colocalize in neurons from the central nucleus of the amygdala (CeA) and ventral tegmental area (VTA).
+TLR4	drug	alcohol	25567426	We report that <b>alcohol</b> preferring P rats have innately elevated levels of <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) and monocyte chemotactic protein 1 (MCP 1) that colocalize in neurons from the central nucleus of the amygdala (CeA) and ventral tegmental area (VTA).
+TLR4	addiction	intoxication	25567426	Infusion of amplicons for <strong>TLR4</strong> or MCP 1 siRNA into the CeA or VTA from the P rats inhibited target gene expression and blunted <b>binge</b> drinking.
+TLR4	drug	alcohol	25567426	A similarly delivered amplicon for scrambled siRNA did not inhibit <strong>TLR4</strong> or MCP 1 expression nor reduce binge drinking, identifying a neuronal <strong>TLR4</strong>/MCP 1 signal that regulates the initiation of voluntary <b>alcohol</b> self administration.
+TLR4	addiction	intoxication	25567426	A similarly delivered amplicon for scrambled siRNA did not inhibit <strong>TLR4</strong> or MCP 1 expression nor reduce <b>binge</b> drinking, identifying a neuronal <strong>TLR4</strong>/MCP 1 signal that regulates the initiation of voluntary alcohol self administration.
+TLR4	drug	alcohol	25567426	The signal was sustained during <b>alcohol</b> drinking by increased expression of corticotropin releasing factor and its feedback regulation of <strong>TLR4</strong> expression, likely contributing to the transition to <b>alcohol</b> dependence.
+TLR4	addiction	dependence	25567426	The signal was sustained during alcohol drinking by increased expression of corticotropin releasing factor and its feedback regulation of <strong>TLR4</strong> expression, likely contributing to the transition to alcohol <b>dependence</b>.
+TLR4	drug	alcohol	25486089	<strong>TLR4</strong> elimination prevents synaptic and myelin alterations and long term cognitive dysfunctions in adolescent mice with intermittent <b>ethanol</b> treatment.
+TLR4	drug	alcohol	25486089	Although the mechanisms of these effects are largely unknown, we demonstrated that <b>ethanol</b> by activating innate immune receptors toll like receptor 4 (<strong>TLR4</strong>), induces neuroinflammation and brain damage in adult mice.
+TLR4	drug	alcohol	25486089	Although the mechanisms of these effects are largely unknown, we demonstrated that <b>ethanol</b> by activating innate immune receptors <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), induces neuroinflammation and brain damage in adult mice.
+TLR4	drug	alcohol	25486089	The present study aims to evaluate whether intermittent <b>ethanol</b> treatment in adolescence promotes <strong>TLR4</strong> dependent pro inflammatory processes, leading to myelin and synaptic dysfunctions, and long term cognitive impairments.
+TLR4	drug	alcohol	25486089	Using wild type (WT) and <strong>TLR4</strong> deficient (<strong>TLR4</strong> KO) adolescent mice treated intermittently with <b>ethanol</b> (3.0g/kg) for 2weeks, we show that binge like <b>ethanol</b> treatment activates <strong>TLR4</strong> signaling pathways (MAPK, NFκB) leading to the up regulation of cytokines and pro inflammatory mediators (COX 2, iNOS, HMGB1), impairing synaptic and myelin protein levels and causing ultrastructural alterations.
+TLR4	addiction	intoxication	25486089	Using wild type (WT) and <strong>TLR4</strong> deficient (<strong>TLR4</strong> KO) adolescent mice treated intermittently with ethanol (3.0g/kg) for 2weeks, we show that <b>binge</b> like ethanol treatment activates <strong>TLR4</strong> signaling pathways (MAPK, NFκB) leading to the up regulation of cytokines and pro inflammatory mediators (COX 2, iNOS, HMGB1), impairing synaptic and myelin protein levels and causing ultrastructural alterations.
+TLR4	drug	alcohol	25486089	These results support the role of the neuroimmune response and <strong>TLR4</strong> signaling in the neurotoxic and behavioral effects of <b>ethanol</b> in adolescence.
+TLR4	drug	opioid	25446875	<strong>Toll like receptor 4</strong> mediated nuclear factor κB activation in spinal cord contributes to chronic <b>morphine</b> induced analgesic tolerance and hyperalgesia in rats.
+TLR4	drug	opioid	25446875	Meanwhile, intrathecal pretreatment with lipopolysaccharide from Rhodobacter sphaeroides, an antagonist of toll like receptor 4 (<strong>TLR4</strong>), blocked the activation of NF κB, and prevented the development of <b>morphine</b> tolerance and withdrawal induced abnormal pain.
+TLR4	addiction	withdrawal	25446875	Meanwhile, intrathecal pretreatment with lipopolysaccharide from Rhodobacter sphaeroides, an antagonist of toll like receptor 4 (<strong>TLR4</strong>), blocked the activation of NF κB, and prevented the development of morphine tolerance and <b>withdrawal</b> induced abnormal pain.
+TLR4	drug	opioid	25446875	Meanwhile, intrathecal pretreatment with lipopolysaccharide from Rhodobacter sphaeroides, an antagonist of <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), blocked the activation of NF κB, and prevented the development of <b>morphine</b> tolerance and withdrawal induced abnormal pain.
+TLR4	addiction	withdrawal	25446875	Meanwhile, intrathecal pretreatment with lipopolysaccharide from Rhodobacter sphaeroides, an antagonist of <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), blocked the activation of NF κB, and prevented the development of morphine tolerance and <b>withdrawal</b> induced abnormal pain.
+TLR4	drug	opioid	25446875	These data indicated that <strong>TLR4</strong> mediated NF κB activation in the spinal cord is involved in the development and maintenance of <b>morphine</b> analgesic tolerance and withdrawal induced pain hypersensitivity.
+TLR4	addiction	withdrawal	25446875	These data indicated that <strong>TLR4</strong> mediated NF κB activation in the spinal cord is involved in the development and maintenance of morphine analgesic tolerance and <b>withdrawal</b> induced pain hypersensitivity.
+TLR4	drug	opioid	25241065	Activation of adult rat CNS endothelial cells by <b>opioid</b> induced toll like receptor 4 (<strong>TLR4</strong>) signaling induces proinflammatory, biochemical, morphological, and behavioral sequelae.
+TLR4	drug	opioid	25241065	Activation of adult rat CNS endothelial cells by <b>opioid</b> induced <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) signaling induces proinflammatory, biochemical, morphological, and behavioral sequelae.
+TLR4	drug	opioid	25241065	Such effects are mediated by <b>opioid</b> signaling at toll like receptor 4 (<strong>TLR4</strong>), presumptively of glial origin.
+TLR4	drug	opioid	25241065	Such effects are mediated by <b>opioid</b> signaling at <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), presumptively of glial origin.
+TLR4	drug	opioid	25241065	These studies examined adult primary rat CNS endothelial cell responses to ( ) <b>morphine</b> or its mu <b>opioid</b> receptor (MOR) inactive metabolite <b>morphine</b> 3 glucuronide (M3G), both known <strong>TLR4</strong> agonists.
+TLR4	drug	opioid	25241065	( ) <b>Morphine</b> induced upregulation of TNFα mRNA and PGE2 release were unmasked by pre treatment with nalmefene, a MOR antagonist without <strong>TLR4</strong> activity (unlike CTAP, shown to have both MOR  and <strong>TLR4</strong> activity), suggestive of an interplay between MOR and <strong>TLR4</strong> co activation by ( ) <b>morphine</b>.
+TLR4	drug	opioid	25241065	In support, MOR dependent Protein Kinase A (PKA) opposed <strong>TLR4</strong> signaling, as PKA inhibition (H 89) also unmasked ( ) <b>morphine</b> induced TNFα and COX2 mRNA upregulation.
+TLR4	drug	opioid	25241065	These data indicate that ( ) <b>morphine</b> and M3G can activate CNS endothelial cells via <strong>TLR4</strong>, inducing proinflammatory, biochemical, morphological, and behavioral sequelae.
+TLR4	drug	opioid	25241065	CNS endothelial cells may have previously unanticipated roles in <b>opioid</b> induced effects, in phenomena blocked by presumptive glial inhibitors, as well as <strong>TLR4</strong> mediated phenomena more broadly.
+TLR4	drug	alcohol	25175868	In addition, HMGB1 <strong>TLR4</strong> and innate immune NF κB target genes are increased leading to persistent and sensitized neuroimmune responses to <b>ethanol</b> and other agents that release HMGB1 or directly stimulate TLR receptors and/or NMDA receptors.
+TLR4	drug	opioid	25175864	Discovery of a novel site of <b>opioid</b> action at the innate immune pattern recognition receptor <strong>TLR4</strong> and its role in addiction.
+TLR4	addiction	addiction	25175864	Discovery of a novel site of opioid action at the innate immune pattern recognition receptor <strong>TLR4</strong> and its role in <b>addiction</b>.
+TLR4	drug	opioid	25175864	Evidence suggests an innate immune pattern recognition receptor (<strong>toll like receptor 4</strong>) as an integral component underlying <b>opioid</b> induced glial activation.
+TLR4	drug	alcohol	25109571	'Translational potential of naloxone and <b>naltrexone</b> as <strong>TLR4</strong> antagonists'.
+TLR4	drug	opioid	25109571	'Translational potential of <b>naloxone</b> and naltrexone as <strong>TLR4</strong> antagonists'.
+TLR4	drug	opioid	25103966	Glial <strong>TLR4</strong> signaling does not contribute to <b>opioid</b> induced depression of respiration.
+TLR4	drug	opioid	25103966	<b>Opioids</b> activate glia in the central nervous system in part by activating the toll like receptor 4 (<strong>TLR4</strong>)/myeloid differentiation 2 (MD2) complex.
+TLR4	drug	opioid	25103966	<b>Opioids</b> activate glia in the central nervous system in part by activating the <strong>toll like receptor 4</strong> (<strong>TLR4</strong>)/myeloid differentiation 2 (MD2) complex.
+TLR4	drug	opioid	25103966	<strong>TLR4</strong>/MD2 mediated activation of glia by <b>opioids</b> compromises their analgesic actions.
+TLR4	drug	opioid	25103966	We tested the contribution of <strong>TLR4</strong> to <b>opioid</b> induced respiratory depression using rhythmically active medullary slices that contain the pre Bötzinger Complex (preBötC, an important site of respiratory rhythm generation) and adult rats in vivo.
+TLR4	drug	opioid	25103966	This DAMGO mediated frequency inhibition was unaffected by preapplication of lipopolysaccharides from Rhodobacter sphaeroides (a <strong>TLR4</strong> antagonist, 2,000 ng/ml) or (+)<b>naloxone</b> (1 10 μM, a <strong>TLR4</strong> antagonist).
+TLR4	drug	opioid	25103966	Bath application of ( )<b>naloxone</b> (500 nM; a <strong>TLR4</strong> and μ <b>opioid</b> antagonist), however, rapidly reversed the <b>opioid</b> mediated frequency decrease.
+TLR4	drug	opioid	25103966	These data indicate that neither activation of microglia in preBötC nor <strong>TLR4</strong>/MD2 activation contribute to <b>opioid</b> induced respiratory depression.
+TLR4	drug	alcohol	25024384	In this study, we show that cellular stress proteins HSF1 and hsp70 play a mechanistic role in <b>alcohol</b> mediated inhibition of the <strong>TLR4</strong>/MyD88 pathway.
+TLR4	drug	alcohol	25024384	Our data suggest that <b>alcohol</b> mediated activation of HSF1 and induction of hsp70 inhibit <strong>TLR4</strong> MyD88 signaling and are required for <b>alcohol</b> induced endotoxin tolerance.
+TLR4	drug	opioid	24824631	<strong>Toll like receptor 4</strong> mutant and null mice retain <b>morphine</b> induced tolerance, hyperalgesia, and physical dependence.
+TLR4	addiction	dependence	24824631	<strong>Toll like receptor 4</strong> mutant and null mice retain morphine induced tolerance, hyperalgesia, and physical <b>dependence</b>.
+TLR4	drug	opioid	24824631	The innate immune system modulates <b>opioid</b> induced effects within the central nervous system and one target that has received considerable attention is the toll like receptor 4 (<strong>TLR4</strong>).
+TLR4	drug	opioid	24824631	The innate immune system modulates <b>opioid</b> induced effects within the central nervous system and one target that has received considerable attention is the <strong>toll like receptor 4</strong> (<strong>TLR4</strong>).
+TLR4	drug	opioid	24824631	Here, we examined the contribution of <strong>TLR4</strong> in the development of <b>morphine</b> tolerance, hyperalgesia, and physical dependence in two inbred mouse strains: C3H/HeJ mice which have a dominant negative point mutation in the <strong>Tlr4</strong> gene rendering the receptor non functional, and B10ScNJ mice which are <strong>TLR4</strong> null mutants.
+TLR4	addiction	dependence	24824631	Here, we examined the contribution of <strong>TLR4</strong> in the development of morphine tolerance, hyperalgesia, and physical <b>dependence</b> in two inbred mouse strains: C3H/HeJ mice which have a dominant negative point mutation in the <strong>Tlr4</strong> gene rendering the receptor non functional, and B10ScNJ mice which are <strong>TLR4</strong> null mutants.
+TLR4	drug	opioid	24824631	We found that neither acute antinociceptive response to a single dose of <b>morphine</b>, nor the development of analgesic tolerance to repeated <b>morphine</b> treatment, was affected by <strong>TLR4</strong> genotype.
+TLR4	drug	opioid	24824631	Likewise, <b>opioid</b> induced hyperalgesia and <b>opioid</b> physical dependence (assessed by <b>naloxone</b> precipitated withdrawal) were not altered in <strong>TLR4</strong> mutant or null mice.
+TLR4	addiction	dependence	24824631	Likewise, opioid induced hyperalgesia and opioid physical <b>dependence</b> (assessed by naloxone precipitated withdrawal) were not altered in <strong>TLR4</strong> mutant or null mice.
+TLR4	addiction	withdrawal	24824631	Likewise, opioid induced hyperalgesia and opioid physical dependence (assessed by naloxone precipitated <b>withdrawal</b>) were not altered in <strong>TLR4</strong> mutant or null mice.
+TLR4	drug	opioid	24824631	We also examined the behavioural consequence of two stereoisomers of <b>naloxone</b>: ( ) <b>naloxone</b>, an <b>opioid</b> receptor antagonist, and (+) <b>naloxone</b>, a purported antagonist of <strong>TLR4</strong>.
+TLR4	drug	opioid	24824631	Both stereoisomers of <b>naloxone</b> suppressed <b>opioid</b> induced hyperalgesia in wild type control, <strong>TLR4</strong> mutant, and <strong>TLR4</strong> null mice.
+TLR4	drug	opioid	24824631	Collectively, our data suggest that <strong>TLR4</strong> is not required for <b>opioid</b> induced analgesic tolerance, hyperalgesia, or physical dependence.
+TLR4	addiction	dependence	24824631	Collectively, our data suggest that <strong>TLR4</strong> is not required for opioid induced analgesic tolerance, hyperalgesia, or physical <b>dependence</b>.
+TLR4	drug	alcohol	24675033	Excessive <b>ethanol</b> drinking in rodent models may involve activation of the innate immune system, especially toll like receptor 4 (<strong>TLR4</strong>) signaling pathways.
+TLR4	drug	alcohol	24675033	Excessive <b>ethanol</b> drinking in rodent models may involve activation of the innate immune system, especially <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) signaling pathways.
+TLR4	drug	alcohol	24675033	We used intracellular recording of evoked GABAergic inhibitory postsynaptic potentials (eIPSPs) in central amygdala (CeA) neurons to examine the role of <strong>TLR4</strong> activation by lipopolysaccharide (LPS) and deletion of its adapter protein CD14 in acute <b>ethanol</b> effects on the GABAergic system.
+TLR4	drug	alcohol	24675033	Furthermore, (+) naloxone, a <strong>TLR4</strong> MD 2 complex inhibitor, blocked LPS effects on eIPSPs in WT mice and delayed the <b>ethanol</b> induced potentiation of GABAergic transmission.
+TLR4	drug	opioid	24675033	Furthermore, (+) <b>naloxone</b>, a <strong>TLR4</strong> MD 2 complex inhibitor, blocked LPS effects on eIPSPs in WT mice and delayed the ethanol induced potentiation of GABAergic transmission.
+TLR4	drug	alcohol	24675033	In summary, our results indicate that <strong>TLR4</strong> and CD14 signaling play an important role in the acute <b>ethanol</b> effects on GABAergic transmission in the CeA and support the idea that CD14 and <strong>TLR4</strong> may be therapeutic targets for treatment of <b>alcohol</b> abuse.
+TLR4	drug	alcohol	24551070	<b>Ethanol</b> and HMGB1 treatment increased mRNA expression of proinflammatory cytokines TNFα and IL 1β as well as toll like receptor 4 (<strong>TLR4</strong>).
+TLR4	drug	alcohol	24551070	<b>Ethanol</b> and HMGB1 treatment increased mRNA expression of proinflammatory cytokines TNFα and IL 1β as well as <strong>toll like receptor 4</strong> (<strong>TLR4</strong>).
+TLR4	drug	alcohol	24551070	Targeting HMGB1 or microglial <strong>TLR4</strong> by using siRNAs to HMGB1 and <strong>TLR4</strong>, HMGB1 neutralizing antibody, HMGB1 inhibitor glycyrrhizin and <strong>TLR4</strong> antagonist as well as inhibitor of microglial activation all blocked <b>ethanol</b> induced expression of proinflammatory cytokines TNFα and IL 1β.
+TLR4	drug	alcohol	24551070	These results support the hypothesis that <b>ethanol</b> alters HDACs that regulate HMGB1 release and that danger signal HMGB1 as endogenous ligand for <strong>TLR4</strong> mediates <b>ethanol</b> induced brain neuroimmune signaling through activation of microglial <strong>TLR4</strong>.
+TLR4	drug	alcohol	24217958	Binge like <b>ethanol</b> administration to adolescent rats increased the gene expression of <strong>TLR4</strong> and TLR2 in the prefrontal cortex (PFC), as well as inflammatory cytokines TNFα and IL 1β.
+TLR4	addiction	intoxication	24217958	<b>Binge</b> like ethanol administration to adolescent rats increased the gene expression of <strong>TLR4</strong> and TLR2 in the prefrontal cortex (PFC), as well as inflammatory cytokines TNFα and IL 1β.
+TLR4	drug	opioid	24121451	In this study we investigated the neurodegenerative effects of <b>morphine</b> through its effects on Toll Like Receptor 4 (<strong>TLR4</strong>) in the male rat hippocampus and evaluated the level of Interleukin 1 beta (IL 1β).
+TLR4	drug	opioid	24121451	In this study we investigated the neurodegenerative effects of <b>morphine</b> through its effects on <strong>Toll Like Receptor 4</strong> (<strong>TLR4</strong>) in the male rat hippocampus and evaluated the level of Interleukin 1 beta (IL 1β).
+TLR4	drug	opioid	24121451	Then we compared the difference between inhibitory effects on mu <b>opioid</b> receptors (by β Funaltrexamine, β FNA) and <strong>TLR4</strong> (by Ibudilast).
+TLR4	drug	alcohol	23895427	Recently, dysregulation of the neuroimmune system by chronic <b>ethanol</b> (CE) has implicated Toll like receptor 4 (<strong>TLR4</strong>) activation.
+TLR4	drug	alcohol	23895427	Recently, dysregulation of the neuroimmune system by chronic <b>ethanol</b> (CE) has implicated <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) activation.
+TLR4	addiction	withdrawal	23895427	Therefore, the hypothesis is tested that release of an endogenous <strong>TLR4</strong> agonist, high mobility group box 1 (HMGB1) and/or corticotropin releasing factor (CRF) during CE <b>withdrawal</b> are responsible for CE protocols increasing cytokine mRNAs.
+TLR4	drug	alcohol	23867237	Adolescent intermittent <b>ethanol</b> exposure also increased <strong>TLR4</strong> and HMGB1 expression at P56 that persisted into young adulthood (P80).
+TLR4	drug	alcohol	23867237	Together, these human and animal data support the hypothesis that an early age of drinking onset upregulates RAGE/<strong>TLR4</strong> HMGB1 and other neuroimmune genes that persist into young adulthood and could contribute to risk of <b>alcoholism</b> or other brain diseases associated with neuroinflammation.
+TLR4	drug	opioid	23764149	Additionally, in the case of <b>opioids</b>, these hypotheses have advanced through to the discovery of the novel site of <b>opioid</b> action at the innate immune pattern recognition receptor <strong>Toll like receptor 4</strong> as the necessary triggering event that engages this reward facilitating central immune signaling.
+TLR4	addiction	reward	23764149	Additionally, in the case of opioids, these hypotheses have advanced through to the discovery of the novel site of opioid action at the innate immune pattern recognition receptor <strong>Toll like receptor 4</strong> as the necessary triggering event that engages this <b>reward</b> facilitating central immune signaling.
+TLR4	drug	alcohol	23428594	Acute <b>ethanol</b> administration inhibits <strong>Toll like receptor 4</strong> signaling pathway in rat intestinal epithelia.
+TLR4	drug	alcohol	23428594	<b>Alcohol</b> impairs macrophage function by suppression of the Toll like receptor 4 (<strong>TLR4</strong>) pathway.
+TLR4	drug	alcohol	23428594	<b>Alcohol</b> impairs macrophage function by suppression of the <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) pathway.
+TLR4	drug	alcohol	23428594	This study investigated the effects of acute <b>ethanol</b> intake on the <strong>TLR4</strong> pathway in rat intestinal epithelia, which usually encounters luminal antigens at first and participates in the development of intestinal immunity.
+TLR4	drug	alcohol	23428594	LPS levels increased in peripheral and portal venous plasma (p < 0.05), but mucosal <strong>TLR4</strong>, TBK1, nuclear NF κB, IFN γ and TNF α were unchanged in the <b>ethanol</b> group.
+TLR4	drug	alcohol	23428594	LPS treatment in vitro up regulated the level of <strong>TLR4</strong>, TBK1 and nuclear NF κB as well as the production of IFN γ and TNF α in isolated intestinal epithelia in the control (p < 0.05), but not the <b>ethanol</b> group.
+TLR4	drug	alcohol	23428594	These findings suggest the hyposensitivity of intestinal epithelial <strong>TLR4</strong> to LPS induced by acute <b>alcohol</b> abuse probably through <b>ethanol</b> per se and <b>ethanol</b> enhanced intestinal mucosal SST pathway may be a novel mechanism for increased susceptibility to intestinal pathogens.
+TLR4	drug	opioid	23392901	The present study was designed to assess the role of <strong>TLR4</strong> in cancer induced bone pain (CIBP) by intrathecal administration of <strong>TLR4</strong> signaling pathway blocker <b>naloxone</b> or lipopolysaccharide Rhodobacter sphaeroides (LPS RS).
+TLR4	drug	alcohol	23384483	Effect of chronic delivery of the <strong>Toll like receptor 4</strong> antagonist (+) <b>naltrexone</b> on incubation of heroin craving.
+TLR4	drug	opioid	23384483	Effect of chronic delivery of the <strong>Toll like receptor 4</strong> antagonist (+) naltrexone on incubation of <b>heroin</b> craving.
+TLR4	addiction	relapse	23384483	Effect of chronic delivery of the <strong>Toll like receptor 4</strong> antagonist (+) naltrexone on incubation of heroin <b>craving</b>.
+TLR4	drug	opioid	23384483	Recent evidence implicates toll like receptor 4 (<strong>TLR4</strong>) in <b>opioid</b> analgesia, tolerance, conditioned place preference, and self administration.
+TLR4	drug	opioid	23384483	Recent evidence implicates <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) in <b>opioid</b> analgesia, tolerance, conditioned place preference, and self administration.
+TLR4	drug	alcohol	23384483	Here, we determined the effect of the <strong>TLR4</strong> antagonist (+) <b>naltrexone</b> (a μ opioid receptor inactive isomer) on the time dependent increases in cue induced heroin seeking after withdrawal (incubation of heroin craving).
+TLR4	drug	opioid	23384483	Here, we determined the effect of the <strong>TLR4</strong> antagonist (+) naltrexone (a μ <b>opioid</b> receptor inactive isomer) on the time dependent increases in cue induced <b>heroin</b> seeking after withdrawal (incubation of <b>heroin</b> craving).
+TLR4	addiction	relapse	23384483	Here, we determined the effect of the <strong>TLR4</strong> antagonist (+) naltrexone (a μ opioid receptor inactive isomer) on the time dependent increases in cue induced heroin <b>seeking</b> after withdrawal (incubation of heroin <b>craving</b>).
+TLR4	addiction	withdrawal	23384483	Here, we determined the effect of the <strong>TLR4</strong> antagonist (+) naltrexone (a μ opioid receptor inactive isomer) on the time dependent increases in cue induced heroin seeking after <b>withdrawal</b> (incubation of heroin craving).
+TLR4	drug	amphetamine	23384483	The present results suggest a critical role of <strong>TLR4</strong> in the development of incubation of heroin, but not <b>methamphetamine</b>, craving.
+TLR4	drug	opioid	23384483	The present results suggest a critical role of <strong>TLR4</strong> in the development of incubation of <b>heroin</b>, but not methamphetamine, craving.
+TLR4	addiction	relapse	23384483	The present results suggest a critical role of <strong>TLR4</strong> in the development of incubation of heroin, but not methamphetamine, <b>craving</b>.
+TLR4	drug	alcohol	23348028	Glucuronic acid and the <b>ethanol</b> metabolite ethyl glucuronide cause <strong>toll like receptor 4</strong> activation and enhanced pain.
+TLR4	drug	opioid	23348028	We have previously observed that the non <b>opioid</b> <b>morphine</b> metabolite, <b>morphine</b> 3 glucuronide, enhances pain via a toll like receptor 4 (<strong>TLR4</strong>) dependent mechanism.
+TLR4	drug	opioid	23348028	We have previously observed that the non <b>opioid</b> <b>morphine</b> metabolite, <b>morphine</b> 3 glucuronide, enhances pain via a <strong>toll like receptor 4</strong> (<strong>TLR4</strong>) dependent mechanism.
+TLR4	drug	alcohol	23348028	In silico modeling predicted that glucuronic acid alone and ethyl glucuronide, a minor but long lasting <b>ethanol</b> metabolite, would dock to the same MD 2 portion of the <strong>TLR4</strong> receptor complex previously characterized as the docking site for morphine 3 glucuronide.
+TLR4	drug	opioid	23348028	In silico modeling predicted that glucuronic acid alone and ethyl glucuronide, a minor but long lasting ethanol metabolite, would dock to the same MD 2 portion of the <strong>TLR4</strong> receptor complex previously characterized as the docking site for <b>morphine</b> 3 glucuronide.
+TLR4	drug	alcohol	23348028	Glucuronic acid, ethyl glucuronide and <b>ethanol</b> all caused an increase in <strong>TLR4</strong> dependent reporter protein expression in a cell line transfected with <strong>TLR4</strong> and associated co signaling molecules.
+TLR4	drug	alcohol	23348028	Glucuronic acid , ethyl glucuronide , and <b>ethanol</b> induced increases in <strong>TLR4</strong> signaling were blocked by the <strong>TLR4</strong> antagonists LPS RS and (+) naloxone.
+TLR4	drug	opioid	23348028	Glucuronic acid , ethyl glucuronide , and ethanol induced increases in <strong>TLR4</strong> signaling were blocked by the <strong>TLR4</strong> antagonists LPS RS and (+) <b>naloxone</b>.
+TLR4	drug	alcohol	23348028	The finding that ethyl glucuronide can cause <strong>TLR4</strong> dependent pain could have implications for human conditions such as hangover headache and <b>alcohol</b> withdrawal hyperalgesia, as well as suggesting that other classes of glucuronide metabolites could have similar effects.
+TLR4	addiction	withdrawal	23348028	The finding that ethyl glucuronide can cause <strong>TLR4</strong> dependent pain could have implications for human conditions such as hangover headache and alcohol <b>withdrawal</b> hyperalgesia, as well as suggesting that other classes of glucuronide metabolites could have similar effects.
+TLR4	drug	opioid	23325235	Thus, we examined the role of microglia within the nucleus accumbens of these rats and determined that rats exposed to <b>morphine</b> during adolescence had a significant increase in Toll like receptor 4 (<strong>TLR4</strong>) mRNA and protein expression specifically on microglia.
+TLR4	drug	opioid	23325235	Thus, we examined the role of microglia within the nucleus accumbens of these rats and determined that rats exposed to <b>morphine</b> during adolescence had a significant increase in <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) mRNA and protein expression specifically on microglia.
+TLR4	drug	opioid	23325235	<b>Morphine</b> binds to <strong>TLR4</strong> directly, and this increase in <strong>TLR4</strong> was associated with exaggerated <b>morphine</b> induced <strong>TLR4</strong> signaling and microglial activation in rats previously exposed to <b>morphine</b> during adolescence.
+TLR4	drug	alcohol	23206318	We investigated expression of HMGB1, TLR2, TLR3, and <strong>TLR4</strong> in chronic <b>ethanol</b> treated mouse brain, postmortem human <b>alcoholic</b> brain, and rat brain slice culture to test the hypothesis that neuroimmune activation in <b>alcoholic</b> brain involves <b>ethanol</b> activation of HMGB1/TLR danger signaling.
+TLR4	drug	alcohol	23206318	<b>Ethanol</b> treatment of mice increased brain mRNA and +IR protein expression of HMGB1, TLR2, TLR3, and <strong>TLR4</strong>.
+TLR4	drug	alcohol	23206318	Postmortem human <b>alcoholic</b> brain also showed increased HMGB1, TLR2, TLR3, and <strong>TLR4</strong> +IR cells that correlated with lifetime <b>alcohol</b> consumption, as well as each other.
+TLR4	drug	alcohol	23206318	Neutralizing antibodies to HMGB1 and small inhibitory mRNA to HMGB1 or <strong>TLR4</strong> blunted <b>ethanol</b> induction of IL 1β.
+TLR4	drug	alcohol	23206318	Increased expression of HMGB1, TLR2, TLR3, and <strong>TLR4</strong> in <b>alcoholic</b> brain and in mice treated with <b>ethanol</b> suggests that chronic <b>alcohol</b> induced brain neuroimmune activation occurs through HMGB1/TLR signaling.
+TLR4	drug	opioid	23144180	Recent evidence indicates that chronic <b>opioid</b> administration may exacerbate pain in the long term by activating <strong>toll like receptor 4</strong> on glial cells, resulting in a pro inflammatory state that manifests clinically as increased pain.
+TLR4	drug	opioid	22902523	Prior <b>morphine</b> elevated IL 1β mRNA at both sites, MHC II and <strong>TLR4</strong> in the trigeminal nucleus caudalis but not spinal cord, but not glial activation markers at either site.
+TLR4	drug	opioid	22895704	<b>Opioid</b> activation of <strong>toll like receptor 4</strong> contributes to drug reinforcement.
+TLR4	addiction	reward	22895704	Opioid activation of <strong>toll like receptor 4</strong> contributes to drug <b>reinforcement</b>.
+TLR4	drug	opioid	22895704	Here, we present evidence for an additional novel contributor to <b>opioid</b> reward: the innate immune pattern recognition receptor, toll like receptor 4 (<strong>TLR4</strong>), and its MyD88 dependent signaling.
+TLR4	addiction	reward	22895704	Here, we present evidence for an additional novel contributor to opioid <b>reward</b>: the innate immune pattern recognition receptor, toll like receptor 4 (<strong>TLR4</strong>), and its MyD88 dependent signaling.
+TLR4	drug	opioid	22895704	Here, we present evidence for an additional novel contributor to <b>opioid</b> reward: the innate immune pattern recognition receptor, <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), and its MyD88 dependent signaling.
+TLR4	addiction	reward	22895704	Here, we present evidence for an additional novel contributor to opioid <b>reward</b>: the innate immune pattern recognition receptor, <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), and its MyD88 dependent signaling.
+TLR4	drug	opioid	22895704	Blockade of <strong>TLR4</strong>/MD2 by administration of the nonopioid, unnatural isomer of <b>naloxone</b>, (+) <b>naloxone</b> (rats), or two independent genetic knock outs of MyD88 <strong>TLR4</strong> dependent signaling (mice), suppressed <b>opioid</b> induced conditioned place preference.
+TLR4	drug	opioid	22895704	Moreover, pharmacological blockade of <b>morphine</b> <strong>TLR4</strong>/MD2 activity potently reduced <b>morphine</b> induced elevations of extracellular dopamine in rat nucleus accumbens, a region critical for <b>opioid</b> reinforcement.
+TLR4	addiction	reward	22895704	Moreover, pharmacological blockade of morphine <strong>TLR4</strong>/MD2 activity potently reduced morphine induced elevations of extracellular dopamine in rat nucleus accumbens, a region critical for opioid <b>reinforcement</b>.
+TLR4	drug	opioid	22895704	Importantly, <b>opioid</b> <strong>TLR4</strong> actions are not a unidirectional influence on <b>opioid</b> pharmacodynamics, since <strong>TLR4</strong>( / ) mice had reduced <b>oxycodone</b> induced p38 and JNK phosphorylation, while displaying potentiated analgesia.
+TLR4	drug	opioid	22895704	Similar to our recent reports of <b>morphine</b> <strong>TLR4</strong>/MD2 binding, here we provide a combination of in silico and biophysical data to support (+) <b>naloxone</b> and remifentanil binding to <strong>TLR4</strong>/MD2.
+TLR4	drug	opioid	22895704	Collectively, these data indicate that the actions of <b>opioids</b> at classical <b>opioid</b> receptors, together with their newly identified <strong>TLR4</strong>/MD2 actions, affect the mesolimbic dopamine system that amplifies <b>opioid</b> induced elevations in extracellular dopamine levels, therefore possibly explaining altered <b>opioid</b> reward behaviors.
+TLR4	addiction	reward	22895704	Collectively, these data indicate that the actions of opioids at classical opioid receptors, together with their newly identified <strong>TLR4</strong>/MD2 actions, affect the mesolimbic dopamine system that amplifies opioid induced elevations in extracellular dopamine levels, therefore possibly explaining altered opioid <b>reward</b> behaviors.
+TLR4	drug	opioid	22895704	Thus, the discovery of <strong>TLR4</strong>/MD2 recognition of <b>opioids</b> as foreign xenobiotic substances adds to the existing hypothesized neuronal reinforcement mechanisms, identifies a new drug target in <strong>TLR4</strong>/MD2 for the treatment of addictions, and provides further evidence supporting a role for central proinflammatory immune signaling in drug reward.
+TLR4	addiction	reward	22895704	Thus, the discovery of <strong>TLR4</strong>/MD2 recognition of opioids as foreign xenobiotic substances adds to the existing hypothesized neuronal <b>reinforcement</b> mechanisms, identifies a new drug target in <strong>TLR4</strong>/MD2 for the treatment of addictions, and provides further evidence supporting a role for central proinflammatory immune signaling in drug <b>reward</b>.
+TLR4	drug	alcohol	22782967	Induction of Bcl 3 by acute binge <b>alcohol</b> results in <strong>toll like receptor 4</strong>/LPS tolerance.
+TLR4	addiction	intoxication	22782967	Induction of Bcl 3 by acute <b>binge</b> alcohol results in <strong>toll like receptor 4</strong>/LPS tolerance.
+TLR4	drug	alcohol	22782967	Acute <b>alcohol</b> binge results in immunosuppression and impaired production of proinflammatory cytokines, including TNF α. TNF α production is induced by LPS, a <strong>TLR4</strong> ligand, and is tightly regulated at various levels of the signaling cascade, including the NF κB transcription factor.
+TLR4	addiction	intoxication	22782967	Acute alcohol <b>binge</b> results in immunosuppression and impaired production of proinflammatory cytokines, including TNF α. TNF α production is induced by LPS, a <strong>TLR4</strong> ligand, and is tightly regulated at various levels of the signaling cascade, including the NF κB transcription factor.
+TLR4	drug	alcohol	22782967	Here, we hypothesized that acute <b>alcohol</b> induces <strong>TLR4</strong>/LPS tolerance via Bcl 3, a nuclear protein and member of the NF κB family.
+TLR4	drug	alcohol	22782967	We found that acute <b>alcohol</b> pretreatment resulted in the same attenuating effect as LPS pretreatment on <strong>TLR4</strong> induced TNF α production in human monocytes and murine RAW 264.7 macrophages.
+TLR4	drug	alcohol	22782967	In summary, our novel data suggest that acute <b>alcohol</b> treatment in vitro and in vivo induces molecular signatures of <strong>TLR4</strong>/LPS tolerance through the induction of Bcl 3, a negative regulator of TNF α transcription via its association with NF κB p50/p50 dimers.
+TLR4	drug	alcohol	21657944	However, in both adult and adolescent brains, <b>alcohol</b> damages specific brain areas through mechanisms involving excitotoxicity, free radical formation and neuroinflammatory damage resulting from activation of the innate immune system mediated by <strong>TLR4</strong> receptors.
+TLR4	drug	opioid	21447380	Such <b>opioid</b> induced glial activation occurs, at least in part, through a non classical <b>opioid</b> mechanism involving Toll like receptor 4 (<strong>TLR4</strong>).
+TLR4	drug	opioid	21447380	Such <b>opioid</b> induced glial activation occurs, at least in part, through a non classical <b>opioid</b> mechanism involving <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>).
+TLR4	drug	opioid	21447380	Among the immune factors released following the <b>opioid</b> glia <strong>TLR4</strong> interaction, interleukin 1β (IL 1β) plays a prominent role.
+TLR4	drug	opioid	21447380	Chronic <b>morphine</b> induced tolerance and dependence were assessed in 3 inbred wild type mouse strains (Balb/c, CBA, and C57BL/6) and 2 knockout strains (<strong>TLR4</strong> and MyD88).
+TLR4	addiction	dependence	21447380	Chronic morphine induced tolerance and <b>dependence</b> were assessed in 3 inbred wild type mouse strains (Balb/c, CBA, and C57BL/6) and 2 knockout strains (<strong>TLR4</strong> and MyD88).
+TLR4	addiction	dependence	21447380	Gene sequence differences of IL   1β and <strong>TLR4</strong> genes alone did not explain the heterogeneity of <b>dependence</b> behavior between mouse strains.
+TLR4	drug	alcohol	21368176	Binge <b>alcohol</b> drinking is associated with GABAA alpha2 regulated Toll like receptor 4 (<strong>TLR4</strong>) expression in the central amygdala.
+TLR4	addiction	intoxication	21368176	<b>Binge</b> alcohol drinking is associated with GABAA alpha2 regulated Toll like receptor 4 (<strong>TLR4</strong>) expression in the central amygdala.
+TLR4	drug	alcohol	21368176	Binge <b>alcohol</b> drinking is associated with GABAA alpha2 regulated <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) expression in the central amygdala.
+TLR4	addiction	intoxication	21368176	<b>Binge</b> alcohol drinking is associated with GABAA alpha2 regulated <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>) expression in the central amygdala.
+TLR4	drug	alcohol	21368176	We report that a GABA(A) α2 siRNA vector (pHSVsiLA2) infused into the central nucleus of the amygdala (CeA) of <b>alcohol</b> preferring (P) rats caused profound and selective reduction of binge drinking associated with inhibition of α2 expression, decreased GABA(A) receptor density, and inhibition of Toll like receptor 4 (<strong>TLR4</strong>).
+TLR4	addiction	intoxication	21368176	We report that a GABA(A) α2 siRNA vector (pHSVsiLA2) infused into the central nucleus of the amygdala (CeA) of alcohol preferring (P) rats caused profound and selective reduction of <b>binge</b> drinking associated with inhibition of α2 expression, decreased GABA(A) receptor density, and inhibition of Toll like receptor 4 (<strong>TLR4</strong>).
+TLR4	drug	alcohol	21368176	We report that a GABA(A) α2 siRNA vector (pHSVsiLA2) infused into the central nucleus of the amygdala (CeA) of <b>alcohol</b> preferring (P) rats caused profound and selective reduction of binge drinking associated with inhibition of α2 expression, decreased GABA(A) receptor density, and inhibition of <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>).
+TLR4	addiction	intoxication	21368176	We report that a GABA(A) α2 siRNA vector (pHSVsiLA2) infused into the central nucleus of the amygdala (CeA) of alcohol preferring (P) rats caused profound and selective reduction of <b>binge</b> drinking associated with inhibition of α2 expression, decreased GABA(A) receptor density, and inhibition of <strong>Toll like receptor 4</strong> (<strong>TLR4</strong>).
+TLR4	addiction	intoxication	21368176	CeA infusion of a <strong>TLR4</strong> siRNA vector (pHSVsiLTLR4a) also inhibited <b>binge</b> drinking, but neither vector functioned when infused into the ventral pallidum.
+TLR4	addiction	intoxication	21368176	<b>Binge</b> drinking was inhibited by a GABA(A) α1 siRNA vector (pHSVsiLA1) infused into the ventral pallidum, unrelated to <strong>TLR4</strong>.
+TLR4	addiction	intoxication	21368176	The data indicate that GABA(A) α2 regulated <strong>TLR4</strong> expression in the CeA contributes to <b>binge</b> drinking and may be a key early neuroadaptation in excessive drinking.
+TLR4	drug	alcohol	21352907	Impact of <strong>TLR4</strong> on behavioral and cognitive dysfunctions associated with <b>alcohol</b> induced neuroinflammatory damage.
+TLR4	drug	alcohol	21352907	Our recent results have demonstrated that <b>ethanol</b> is capable of activating glial <strong>TLR4</strong> receptors and that the elimination of these receptors in mice protects against <b>ethanol</b> induced glial activation, induction of inflammatory mediators and apoptosis.
+TLR4	drug	alcohol	21352907	This study was designed to assess whether <b>ethanol</b> induced inflammatory damage causes behavioral and cognitive consequences, and if behavioral alterations are dependent of <strong>TLR4</strong> functions.
+TLR4	drug	alcohol	21352907	Mice lacking <strong>TLR4</strong> receptors are protected against <b>ethanol</b> induced inflammatory damage, and behavioral associated effects.
+TLR4	drug	alcohol	21352907	These results provide the first evidence of the role that <strong>TLR4</strong> functions play in the behavioral consequences of <b>alcohol</b> induced inflammatory damage and suggest that the epigenetic modifications mediated by <strong>TLR4</strong> could contribute to short  or long term <b>alcohol</b> induced behavioral or cognitive dysfunctions.
+TLR4	drug	psychedelics	21269783	<b>MDMA</b> could limit the IL 27 response of HV 68 infected or LPS exposed macrophages and dendritic cells in vitro and in vivo, demonstrating the ability of this drug to alter normal cytokine responses in the context of a viral infection and/or a <strong>TLR4</strong> agonist.
+TLR4	drug	alcohol	21091930	Chronic <b>ethanol</b> exposure sensitizes Kupffer cells to activation by lipopolysaccharides via <strong>toll like receptor 4</strong>.
+TLR4	drug	alcohol	20870739	<b>Alcohol</b> and LPS significantly inhibited PSC apoptosis in vitro, and the effect of LPS on PSC apoptosis could be blocked by <strong>Toll like receptor 4</strong> small interfering RNA.
+TLR4	drug	alcohol	20624996	Thus, the effects of <b>ethanol</b> responsible for lethal outcome in sepsis are not dependent on inhibition of <strong>TLR4</strong> signaling, as we and others had previously suspected.
+TLR4	drug	alcohol	20608903	Decreased pulmonary inflammation following <b>ethanol</b> and burn injury in mice deficient in <strong>TLR4</strong> but not TLR2 signaling.
+TLR4	drug	alcohol	20608903	Wild type, TLR2, and <strong>TLR4</strong> knockout mice were treated with vehicle or a single binge dose of <b>ethanol</b> (1.11 g/kg) and subsequently given a sham or burn injury.
+TLR4	addiction	intoxication	20608903	Wild type, TLR2, and <strong>TLR4</strong> knockout mice were treated with vehicle or a single <b>binge</b> dose of ethanol (1.11 g/kg) and subsequently given a sham or burn injury.
+TLR4	drug	alcohol	20608903	Consistent with these findings, pulmonary levels of KC and IL 6 were increased in wild type mice following burn and <b>ethanol</b> compared to burn injury alone as well as to their <strong>TLR4</strong> knockout counterparts.
+TLR4	drug	alcohol	20608903	These data suggest that <strong>TLR4</strong> signaling is a crucial contributory component in the exuberant inflammation after <b>ethanol</b> and burn injury.
+TLR4	drug	alcohol	20238399	Chronic <b>ethanol</b> exposure sensitizes Kupffer cells to activation by lipopolysaccharide via <strong>Toll like receptor 4</strong>.
+TLR4	drug	alcohol	21525758	For example, we showed that in <b>alcoholic</b> liver disease, the MyD88 independent, IRF3 dependent <strong>TLR4</strong> cascade plays a role in steatosis and inflammation.
+TLR4	drug	alcohol	19765273	Considering evidence that signaling can be very different in vitro and in vivo, the present study was conducted to determine if effects of <b>ethanol</b> on <strong>TLR4</strong> signaling reported for cells in culture or cells removed from <b>ethanol</b> treated mice and stimulated in culture also occur when <b>ethanol</b> treatment and <strong>TLR4</strong> activation occur in vivo.
+TLR4	drug	alcohol	19765273	<b>Ethanol</b> suppressed production of most pro inflammatory cytokines to a similar degree as it inhibited key <strong>TLR4</strong> signaling events.
+TLR4	drug	opioid	19762094	Such effects can occur, not via classical <b>opioid</b> receptors, but rather via non stereoselective activation of toll like receptor 4 (<strong>TLR4</strong>), a recently recognized key glial receptor participating in neuropathic pain as well.
+TLR4	drug	opioid	19762094	Such effects can occur, not via classical <b>opioid</b> receptors, but rather via non stereoselective activation of <strong>toll like receptor 4</strong> (<strong>TLR4</strong>), a recently recognized key glial receptor participating in neuropathic pain as well.
+TLR4	drug	opioid	19762094	This discovery identifies a means for separating the beneficial actions of <b>opioids</b> (<b>opioid</b> receptor mediated) from the unwanted side effects (<strong>TLR4</strong>/glial mediated) by pharmacologically targeting <strong>TLR4</strong>.
+TLR4	drug	opioid	19679181	Evidence that <b>opioids</b> may have <strong>toll like receptor 4</strong> and MD 2 effects.
+TLR4	drug	opioid	19679181	<b>Morphine</b> non stereoselectively induced <strong>TLR4</strong> signaling in vitro, blocked by a classical <strong>TLR4</strong> antagonist and non stereoselectively by <b>naloxone</b>.
+TLR4	drug	opioid	19679181	Pharmacological blockade of <strong>TLR4</strong> signaling in vivo potentiated acute intrathecal <b>morphine</b> analgesia, attenuated development of analgesic tolerance, hyperalgesia, and <b>opioid</b> withdrawal behaviors.
+TLR4	addiction	withdrawal	19679181	Pharmacological blockade of <strong>TLR4</strong> signaling in vivo potentiated acute intrathecal morphine analgesia, attenuated development of analgesic tolerance, hyperalgesia, and opioid <b>withdrawal</b> behaviors.
+TLR4	drug	opioid	19679181	<strong>TLR4</strong> opposition to <b>opioid</b> actions was supported by <b>morphine</b> treatment of <strong>TLR4</strong> knockout mice, which revealed a significant threefold leftward shift in the analgesia dose response function, versus wildtype mice.
+TLR4	drug	opioid	19679181	A range of structurally diverse clinically employed <b>opioid</b> analgesics was found to be capable of activating <strong>TLR4</strong> signaling in vitro.
+TLR4	drug	opioid	19679181	Selectivity in the response was identified since <b>morphine</b> 3 glucuronide, a <b>morphine</b> metabolite with no <b>opioid</b> receptor activity, displayed significant <strong>TLR4</strong> activity, whilst the <b>opioid</b> receptor active metabolite, <b>morphine</b> 6 glucuronide, was devoid of such properties.
+TLR4	drug	opioid	19679181	These data provide evidence that select <b>opioids</b> may non stereoselectively influence <strong>TLR4</strong> signaling and have behavioral consequences resulting, in part, via <strong>TLR4</strong> signaling.
+TLR4	drug	alcohol	18958703	Different effects of acute and chronic <b>ethanol</b> on LPS induced cytokine production and <strong>TLR4</strong> receptor behavior in mouse peritoneal macrophages.
+TLR4	drug	opioid	17982582	Here we demonstrate that selective acute antagonism of <strong>TLR4</strong> results in reversal of neuropathic pain as well as potentiation of <b>opioid</b> analgesia.
+TLR4	drug	opioid	17982582	Moreover, a novel antagonism of <strong>TLR4</strong> by (+)  and ( ) isomer <b>opioid</b> antagonists has now been characterized, and both antiallodynic and <b>morphine</b> analgesia potentiating activity shown.
+TLR4	drug	opioid	17982582	<b>Opioid</b> agonists were found to also possess <strong>TLR4</strong> agonistic activity, predictive of glial activation.
+TLR4	drug	alcohol	17127267	<b>Ethanol</b> intake enhances inflammatory mediators in brain: role of glial cells and <strong>TLR4</strong>/IL 1RI receptors.
+TLR4	drug	alcohol	17127267	<strong>TLR4</strong>/IL 1RI receptors may be involved in <b>ethanol</b> mediated inflammatory signaling, since blocking these receptors abolishes the production of <b>ethanol</b> induced inflammatory mediators and cell death.
+TLR4	drug	alcohol	17127267	We propose that at low physiologically relevant concentrations, <b>ethanol</b> facilitates <strong>TLR4</strong>/IL 1RI recruitment into lipid rafts microdomains, leading to the activation and signaling of these receptors.
+TLR4	drug	alcohol	17127267	In summary, current results suggest that <strong>TLR4</strong>/ IL 1RI are important targets of <b>ethanol</b> induced inflammatory brain damage.
+TLR4	drug	alcohol	16385231	Here, we show that IRAK, one of signaling molecules of <strong>TLR 4</strong>, regulates tolerance and sensitization to LPS and acute <b>ethanol</b> increases in IRAK expression through a mechanism dependent upon oxidant production.
+TLR4	addiction	sensitization	16385231	Here, we show that IRAK, one of signaling molecules of <strong>TLR 4</strong>, regulates tolerance and <b>sensitization</b> to LPS and acute ethanol increases in IRAK expression through a mechanism dependent upon oxidant production.
+TLR4	drug	alcohol	16126318	Additional experiment showed that chronic <b>ethanol</b> exposure significantly increased plasma endotoxin level and hepatic CD14 and <strong>TLR 4</strong> mRNA expression, all of which were blocked by elimination of Gram negative bacteria and endotoxin with antibiotics.
+TLR4	drug	alcohol	15528012	It has been reported that acute administration of <b>ethanol</b> suppresses responses mediated through TLR3 and <strong>TLR4</strong>.
+IL10	drug	opioid	32113469	Furthermore, spinal cinobufagin induced mechanical antiallodynia was inhibited by the pretreatment with intrathecal injection of the microglial inhibitor minocycline, <strong>IL 10</strong> antibody, β endorphin antiserum and specific μ <b>opioid</b> receptor antagonist CTAP.
+IL10	addiction	withdrawal	31589333	After 1 day of <b>withdrawal</b>, IL 18 was reduced, and IP 10 was elevated, whereas both IP 10 and <strong>IL 10</strong> were elevated at 28 days following <b>withdrawal</b>.
+IL10	addiction	withdrawal	31589333	In the frontal cortex, adolescent EtOH exposure induced an increase in IL 1β at day 35, and 28 days of <b>withdrawal</b>, and <strong>IL 10</strong> was increased after 28 days of <b>withdrawal</b>.
+IL10	drug	amphetamine	30793820	The aim of this study was to assess whether CBD prevents reinstatement of <b>METH</b> through change of gene expression of cytokines such as interleukin 1β, interleukin 6, <strong>interleukin 10</strong>, and tumor necrosis factor α (TNF α) in extinguished rats.
+IL10	addiction	relapse	30793820	The aim of this study was to assess whether CBD prevents <b>reinstatement</b> of METH through change of gene expression of cytokines such as interleukin 1β, interleukin 6, <strong>interleukin 10</strong>, and tumor necrosis factor α (TNF α) in extinguished rats.
+IL10	addiction	intoxication	30625475	<b>Binge</b> like consumption resulted in a 67% decrease in <strong>IL 10</strong> immunoreactivity but had no effect on IL 4 or IL 6 compared with the water drinking control group.
+IL10	addiction	intoxication	30485380	Pulmonary cytokine expression (TNF α, GM CSF) decreased, while splenic cytokine (<strong>IL 10</strong>) increased in <b>binge</b> drunk mice.
+IL10	drug	alcohol	29733875	We measured the acute concentrations and dynamics of lipoxins LxA4 and LxB4 and the interleukins IL 4, IL 5, IL 9, <strong>IL 10</strong>, and IL 13 in the serum of patients treated with methyl <b>alcohol</b> poisoning and the follow up concentrations in survivors two years after discharge from the hospital.
+IL10	drug	alcohol	29656414	Symptom severity, <b>alcohol</b> use, cytokine (plasma tumor necrosis factor α and C reactive protein [CRP], transforming growth factor β1 [TGF β1], interleukin 8 [IL 8], <strong>IL 10</strong>), and plasma BDNF levels were regularly assessed.
+IL10	drug	alcohol	29500107	Among people with only an <b>alcohol</b> use disorder, IL 6 was positively associated with depression and psychological distress scores, and <strong>IL 10</strong> was negatively associated with anxiety score.
+IL10	drug	alcohol	29163491	On the contrary, iNKT cell deficient Jα18 /  or interleukin 10 (<strong>IL 10</strong>) /  mice showed fewer <b>alcoholic</b> steatosis, along with the recovered number and IFN γ release of hepatic NK cells, and exogenous <strong>IL 10</strong> injection was sufficient to compensate for iNKT cell deficiency.
+IL10	drug	alcohol	29163491	On the contrary, iNKT cell deficient Jα18 /  or <strong>interleukin 10</strong> (<strong>IL 10</strong>) /  mice showed fewer <b>alcoholic</b> steatosis, along with the recovered number and IFN γ release of hepatic NK cells, and exogenous <strong>IL 10</strong> injection was sufficient to compensate for iNKT cell deficiency.
+IL10	drug	alcohol	29163491	Importantly, adoptive transfer of iNKT cells purified from normal but not <strong>IL 10</strong> /  mice resulted in suppression of the number and functions of NK cells and aggravated <b>alcoholic</b> liver injury in Jα18 /  mice, indicating that <strong>IL 10</strong> producing iNKT (NKT10) cells are the regulators on NK cells.
+IL10	drug	opioid	28697991	In the <b>morphine</b> abuser, a decrease in pain threshold, an increase in IL 6 and a decrease in <strong>IL 10</strong> levels were evident compared with non abuser subjects.
+IL10	drug	alcohol	28675117	The <b>alcohol</b> group demonstrated decreased basal <strong>IL 10</strong> compared with controls particularly following exposure to <b>alcohol</b> cue.
+IL10	drug	alcohol	28669319	Our aim is to describe changes in serum concentration for the pro inflammatory factors TNF α, IFN γ, IL 1β, IL 8, IL 6, <strong>IL 10</strong>, IL 12 and MCP 1, for the satiety factor leptin and for factors associated with neuronal changes, neuron specific enolase (NSE) and glial activation S100 beta protein (S100 β), and explore their association with abstinence in <b>alcohol</b> dependent subjects after withdrawal.
+IL10	addiction	withdrawal	28669319	Our aim is to describe changes in serum concentration for the pro inflammatory factors TNF α, IFN γ, IL 1β, IL 8, IL 6, <strong>IL 10</strong>, IL 12 and MCP 1, for the satiety factor leptin and for factors associated with neuronal changes, neuron specific enolase (NSE) and glial activation S100 beta protein (S100 β), and explore their association with abstinence in alcohol dependent subjects after <b>withdrawal</b>.
+IL10	drug	amphetamine	28621212	RAW264.7 macrophages tended to switch to the M1 phenotype, releasing more nitric oxide and proinflammatory cytokines, including tumor necrosis factor α (TNFα), interleukin (IL) 12, and IL 1β, while decreasing the release of anti inflammatory cytokine <strong>IL 10</strong> after treatment with <b>Meth</b>.
+IL10	drug	amphetamine	28621212	<b>Meth</b> upregulated the gene expression of IL 6, IL 1β, and TNFα and downregulated the expression of Arg 1, <strong>IL 10</strong>, and KLF4.
+IL10	drug	alcohol	28568647	Besides, <b>alcohol</b> treatment increased brain derived neurotrophic factor and <strong>interleukin 10</strong> levels in prefrontal cortex, which was not reverted by P. incarnata.
+IL10	drug	opioid	28436446	<b>Opioid</b> Self Administration is Attenuated by Early Life Experience and Gene Therapy for Anti Inflammatory <strong>IL 10</strong> in the Nucleus Accumbens of Male Rats.
+IL10	drug	opioid	28436446	Previous work has shown that a neonatal handling procedure in rats (which promotes enriched maternal care) attenuates <b>morphine</b> conditioning, reduces <b>morphine</b> induced glial activation, and increases microglial expression of the anti inflammatory cytokine interleukin 10 (<strong>IL 10</strong>).
+IL10	drug	opioid	28436446	Previous work has shown that a neonatal handling procedure in rats (which promotes enriched maternal care) attenuates <b>morphine</b> conditioning, reduces <b>morphine</b> induced glial activation, and increases microglial expression of the anti inflammatory cytokine <strong>interleukin 10</strong> (<strong>IL 10</strong>).
+IL10	drug	opioid	28436446	Moreover, manipulation of the <strong>IL 10</strong> signaling pathway represents a novel approach for influencing <b>opioid</b> reinforcement.
+IL10	addiction	reward	28436446	Moreover, manipulation of the <strong>IL 10</strong> signaling pathway represents a novel approach for influencing opioid <b>reinforcement</b>.
+IL10	drug	alcohol	28386694	Although the exercise bout increased LPS stimulated production of TNF α (%change from PRE: 5 h POST 109%; 24 h POST 49%; 48 h POST 40%) and decreased LPS stimulated production of IL 8 (5 h POST  40%; 24 h POST  50%; 48 h POST:  43%) and <strong>IL 10</strong> (5 h POST:  37%; 24 h POST  32%; 48 h POST  31%), consuming <b>alcohol</b> after exercise did not affect this response.
+IL10	drug	alcohol	27640210	Modulation of Binge like <b>Ethanol</b> Consumption by <strong>IL 10</strong> Signaling in the Basolateral Amygdala.
+IL10	addiction	intoxication	27640210	Modulation of <b>Binge</b> like Ethanol Consumption by <strong>IL 10</strong> Signaling in the Basolateral Amygdala.
+IL10	drug	alcohol	27640210	The current study furthers this research by determining the impact of excessive <b>ethanol</b> consumption on interleukin 10 (<strong>IL 10</strong>) and interleukin 4 (IL 4) activity in a model of non dependent binge consumption called the "drinking in the dark" (DID) paradigm.
+IL10	addiction	intoxication	27640210	The current study furthers this research by determining the impact of excessive ethanol consumption on interleukin 10 (<strong>IL 10</strong>) and interleukin 4 (IL 4) activity in a model of non dependent <b>binge</b> consumption called the "drinking in the dark" (DID) paradigm.
+IL10	drug	alcohol	27640210	The current study furthers this research by determining the impact of excessive <b>ethanol</b> consumption on <strong>interleukin 10</strong> (<strong>IL 10</strong>) and interleukin 4 (IL 4) activity in a model of non dependent binge consumption called the "drinking in the dark" (DID) paradigm.
+IL10	addiction	intoxication	27640210	The current study furthers this research by determining the impact of excessive ethanol consumption on <strong>interleukin 10</strong> (<strong>IL 10</strong>) and interleukin 4 (IL 4) activity in a model of non dependent <b>binge</b> consumption called the "drinking in the dark" (DID) paradigm.
+IL10	drug	alcohol	27640210	Furthermore, the ability of <strong>IL 10</strong> to modulate <b>ethanol</b> consumption was tested using site directed pharmacology.
+IL10	drug	alcohol	27640210	Immunohistochemistry analyses determined that <b>ethanol</b> decreased <strong>IL 10</strong> by 50 % in the basolateral amygdala (BLA) but had no effect on IL 4.
+IL10	drug	alcohol	27640210	Finally, bilateral infusions of <strong>IL 10</strong> into the BLA, but not CeA, reduced binge like drinking and corresponding blood <b>ethanol</b> concentrations without impacting either locomotor activity or anxiety like behavioral correlates.
+IL10	addiction	intoxication	27640210	Finally, bilateral infusions of <strong>IL 10</strong> into the BLA, but not CeA, reduced <b>binge</b> like drinking and corresponding blood ethanol concentrations without impacting either locomotor activity or anxiety like behavioral correlates.
+IL10	drug	alcohol	27640210	Together, these data support the idea that <b>alcohol</b> abuse dysregulates specific anti inflammatory cytokines; however, ameliorating <b>alcohol</b> induced effects on cytokines, like <strong>IL 10</strong>, may prove to be an effective therapy in curbing excessive consumption.
+IL10	addiction	intoxication	27455577	It was established in experiments on noninbred albino rats that the acute <b>intoxication</b> with methanol (1.0 LD50) decreased cellular and humoral immune responses, Th2 lymphocyte activity (to a greater extent as compared to the function of Th1 cells), reduced the blood concentration of immunoregulatory (IFN g, IL 2, IL 4) and proinflammatory (TNF, IL 1b, IL 6) cytokines on the average by 36.5% (p < 0.05), and did not affect the content of anti inflammatory cytokines (<strong>IL 10</strong>, IL 13).
+IL10	drug	alcohol	27016017	Role of interleukin 10 (<strong>IL 10</strong>) in regulation of GABAergic transmission and acute response to <b>ethanol</b>.
+IL10	drug	alcohol	27016017	Role of <strong>interleukin 10</strong> (<strong>IL 10</strong>) in regulation of GABAergic transmission and acute response to <b>ethanol</b>.
+IL10	addiction	withdrawal	27016017	Recent evidence suggests that interleukin 10 (<strong>IL 10</strong>), an anti inflammatory cytokine, is upregulated during <b>withdrawal</b> from chronic EtOH exposure.
+IL10	addiction	withdrawal	27016017	Recent evidence suggests that <strong>interleukin 10</strong> (<strong>IL 10</strong>), an anti inflammatory cytokine, is upregulated during <b>withdrawal</b> from chronic EtOH exposure.
+IL10	addiction	intoxication	27016017	These results suggest that EtOH causes an early release of <strong>IL 10</strong> in the brain, which may contribute to neuronal hyperexcitability as well as disturbed sleep seen after <b>binge</b> exposure to EtOH.
+IL10	drug	alcohol	27016017	These results also identify <strong>IL 10</strong> signaling as a potential therapeutic target in <b>alcohol</b> use disorders and other CNS disorders where GABAergic transmission is altered.
+IL10	drug	amphetamine	26322025	In addition, the serum pro inflammatory (TNF, IL12 p70, IL1β, IL 6, and KC GRO) and Th2 (IL 2, <strong>IL 10</strong>, and IL 4) cytokine profiles were also altered in the presence of <b>METH</b>.
+IL10	drug	alcohol	26013579	Protracted <b>alcohol</b> abstinence induces analgesia in rats: Possible relationships with BDNF and <strong>interleukin 10</strong>.
+IL10	drug	alcohol	26013579	In addition, we evaluated BDNF and interleukin 10 (<strong>IL 10</strong>) in the cerebral prefrontal cortex, brainstem and hippocampus of rats after protracted <b>alcohol</b> abstinence.
+IL10	drug	alcohol	26013579	In addition, we evaluated BDNF and <strong>interleukin 10</strong> (<strong>IL 10</strong>) in the cerebral prefrontal cortex, brainstem and hippocampus of rats after protracted <b>alcohol</b> abstinence.
+IL10	drug	alcohol	26013579	In addition, <b>alcohol</b> withdrawal induced a significant increase in the hippocampus, prefrontal cortex and brainstem <strong>IL 10</strong> levels compared with control group.
+IL10	addiction	withdrawal	26013579	In addition, alcohol <b>withdrawal</b> induced a significant increase in the hippocampus, prefrontal cortex and brainstem <strong>IL 10</strong> levels compared with control group.
+IL10	addiction	sensitization	25960750	Farnesol supplementation significantly (P < 0.05) restored the cytokine secretion ability of peritoneal macrophages that was suppressed as a result of OVA <b>sensitization</b> and challenge and slightly decreased tumor necrosis factor (TNF α)/<strong>IL 10</strong> cytokine secretion ratios.
+IL10	drug	cocaine	25762940	The plasma concentrations of interleukin 1 beta (IL 1β), IL 6, <strong>IL 10</strong>, and tumor necrosis factor alpha (TNFα) were affected by history of <b>cocaine</b> addiction and sex.
+IL10	addiction	addiction	25762940	The plasma concentrations of interleukin 1 beta (IL 1β), IL 6, <strong>IL 10</strong>, and tumor necrosis factor alpha (TNFα) were affected by history of cocaine <b>addiction</b> and sex.
+IL10	drug	alcohol	25716995	Our data show that acute <b>alcohol</b> binge drinking in healthy volunteers results in increased frequency of CD16(+) and CD68(+) and M2 type (CD206(+), dendritic cell [DC] SIGN(+) expressing and <strong>IL 10</strong> secreting) circulating CD14(+) monocytes.
+IL10	addiction	intoxication	25716995	Our data show that acute alcohol <b>binge</b> drinking in healthy volunteers results in increased frequency of CD16(+) and CD68(+) and M2 type (CD206(+), dendritic cell [DC] SIGN(+) expressing and <strong>IL 10</strong> secreting) circulating CD14(+) monocytes.
+IL10	drug	alcohol	25716995	The functional role of miR 27a in macrophage polarization was demonstrated by transfecting monocytes with an miR 27a inhibitor that resulted in reduced <b>alcohol</b>  and HCV  mediated monocyte activation (CD14 and CD68 expression), polarization (CD206 and DC SIGN expression), and <strong>IL 10</strong> secretion.
+IL10	drug	opioid	25660662	We tested the cytokine production of IL 1β, IL 6, IL 8, <strong>IL 10</strong> and tumor necrosis factor (TNF) α from a group of <b>heroin</b> addicts (n=34) and healthy controls (n=20).
+IL10	addiction	sensitization	25524712	Prior studies have shown that exposure to lead is associated with atopic <b>sensitization</b> and modulation of several cytokines (eg, interleukin [IL] 12, <strong>IL 10</strong>, interferon [IFN] γ, and IL 4 production) and with T cell dysregulation and bias toward T helper 2 (Th2) activity.
+IL10	drug	alcohol	25446642	Effect of repeated <b>alcohol</b> exposure during the third trimester equivalent on messenger RNA levels for interleukin 1β, chemokine (C C motif) ligand 2, and <strong>interleukin 10</strong> in the developing rat brain after injection of lipopolysaccharide.
+IL10	drug	alcohol	25446642	Conversely, LPS only minimally affected <strong>IL 10</strong> mRNA expression and there were no significant differences between air  and <b>alcohol</b> exposed rats.
+IL10	addiction	relapse	24712338	Mucosal gene therapy using a pseudotyped lentivirus vector encoding murine <strong>interleukin 10</strong> (mIL 10) suppresses the development and <b>relapse</b> of experimental murine colitis.
+IL10	addiction	relapse	24712338	This study investigates the safety and therapeutic benefit of a locally administered lentiviral vector encoding murine <strong>interleukin 10</strong> in altering the onset and <b>relapse</b> of dextran sodium sulfate induced murine colitis.
+IL10	drug	alcohol	24712338	Lentiviral vectors encoding the reporter genes firefly luciferase and murine <strong>interleukin 10</strong> were administered by intrarectal instillation, either once or twice following an <b>ethanol</b> enema to facilitate mucosal uptake, on Days 3 and 20 in Balb/c mice with acute and relapsing colitis induced with dextran sulfate sodium (DSS).
+IL10	drug	opioid	24643510	Serum <strong>IL 10</strong> involved in <b>morphine</b> tolerance development during adjuvant induced arthritis.
+IL10	drug	opioid	24643510	This study was aimed to assess the role of serum <strong>IL 10</strong> in <b>morphine</b> tolerance development during adjuvant induced arthritis.
+IL10	drug	opioid	24643510	Moreover, there was a significant difference in <b>morphine</b> tolerance induction between the AA and control rats, and our results also demonstrated that <strong>IL 10</strong> played an important role in tolerance induction process.
+IL10	drug	opioid	24643510	On the other hand, it seems that increased level of serum <strong>IL 10</strong> may affect <b>morphine</b> tolerance development during inflammation.
+IL10	drug	cannabinoid	25812351	These effects of morphine and <b>cannabinoids</b> T cell suppression were accompanied by elevation of <strong>IL 10</strong> level and concomitant reduction in IL 17 secretion from cultured CD4+ T cells.
+IL10	drug	opioid	25812351	These effects of <b>morphine</b> and cannabinoids T cell suppression were accompanied by elevation of <strong>IL 10</strong> level and concomitant reduction in IL 17 secretion from cultured CD4+ T cells.
+IL10	drug	nicotine	23749933	<strong>IL10</strong> induction by cigarette <b>smoking</b> plays a role in <b>smoking</b> related lung tumor progression.
+IL10	addiction	relapse	23749933	We therefore expected to find a difference in impact of <strong>IL10</strong> haplotypes on overall survival (OS) and <b>relapse</b> free survival (RFS) between squamous cell carcinomas (SCC) and adenocarcinomas (ADC) of lung.
+IL10	addiction	relapse	23749933	The <strong>IL10</strong> haplotype may independently predict survival and <b>relapse</b> in patients with surgically resected SCC, but not ADC.
+IL10	drug	benzodiazepine	24617047	However, subchronic doses of <b>clonazepam</b> increased the production of <strong>IL 10</strong> in both treated groups.
+IL10	addiction	relapse	23118878	Differential impact of <strong>IL 10</strong> expression on survival and <b>relapse</b> between HPV16 positive and  negative oral squamous cell carcinomas.
+IL10	addiction	relapse	23118878	Kaplan Meier and Cox regression analysis indicated that the prognostic significance of <strong>IL 10</strong> mRNA on overall survival and <b>relapse</b> free survival was only observed in HPV positive OSCC, but not in HPV negative OSCC.
+IL10	addiction	relapse	23118878	Therefore, we suggest that <strong>IL 10</strong> induced by E6 promotes cell growth and migration capability and consequent poor survival and <b>relapse</b> in HPV positive OSCC.
+IL10	drug	opioid	23047422	Using blood from preterm (≤ 30 weeks gestational age (GA), n=7) and full term (≥ 37 weeks GA, n=19) infants, we investigated the changes in cytokine profile (IL 1β, IL 6, IL 8, <strong>IL 10</strong>, IL 12p70 and TNF α), cyclic adenosine monophosphate (cAMP) levels and μ , δ  and κ  <b>opioid</b> receptor (OPR) gene and protein expression, following in vitro exposure to <b>morphine</b>, <b>methadone</b>, <b>fentanyl</b> or clonidine at increasing concentrations ranging from 0 to 1 mM.
+IL10	drug	amphetamine	23026442	Elevated levels of IL 4, but decreased levels of <strong>IL 10</strong> were also found in samples of lung explants after <b>AMPH</b> treatment.
+IL10	drug	amphetamine	23026442	<b>AMPH</b> also abrogates the release of the anti inflammatory cytokine <strong>IL 10</strong>.
+IL10	drug	alcohol	23023014	Activation of toll like receptor 3 attenuates <b>alcoholic</b> liver injury by stimulating Kupffer cells and stellate cells to produce <strong>interleukin 10</strong> in mice.
+IL10	drug	alcohol	23023014	Finally, the protective effects of poly I:C on <b>alcoholic</b> liver injury were diminished in TLR3( / ) and <strong>IL 10</strong>( / ) mice.
+IL10	drug	alcohol	23023014	TLR3 activation ameliorates <b>alcoholic</b> liver injury via the stimulation of <strong>IL 10</strong> production in HSCs and Kupffer cells.
+IL10	drug	opioid	23022502	Using immunohistochemical staining, we demonstrated the administration of MC4R during the induction of <b>morphine</b> tolerance inhibited the activation of astrocytes; reduced the expression of proinflammatory cytokines interleukin 1β, IL 6, and tumor necrosis factor α; upregulated the expression of anti inflammatory cytokines <strong>IL 10</strong> at the L5 lumbar spinal cord.
+IL10	drug	alcohol	22981868	High <strong>IL10</strong> expression in OSCC patients was significantly associated with male gender (P<0.001), smoking (P=0.015), <b>alcohol</b> consumption (P=0.018), betel quid chewing (P=0.003), poor relapse free survival (P=0.012), and poor overall survival (P=0.001).
+IL10	drug	nicotine	22981868	High <strong>IL10</strong> expression in OSCC patients was significantly associated with male gender (P<0.001), <b>smoking</b> (P=0.015), alcohol consumption (P=0.018), betel quid chewing (P=0.003), poor relapse free survival (P=0.012), and poor overall survival (P=0.001).
+IL10	addiction	relapse	22981868	High <strong>IL10</strong> expression in OSCC patients was significantly associated with male gender (P<0.001), smoking (P=0.015), alcohol consumption (P=0.018), betel quid chewing (P=0.003), poor <b>relapse</b> free survival (P=0.012), and poor overall survival (P=0.001).
+IL10	drug	alcohol	22803049	Experiments of outbred albino rats showed that chronic <b>ethanol</b> intoxication (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1 cells, increased blood corticosterone concentration, reduced T lymphocyte acetylcholinesterase activity, blood concentrations of IFN γ, IL 2, IL 4, <strong>IL 10</strong>, and increased IL 6 level.
+IL10	addiction	intoxication	22803049	Experiments of outbred albino rats showed that chronic ethanol <b>intoxication</b> (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1 cells, increased blood corticosterone concentration, reduced T lymphocyte acetylcholinesterase activity, blood concentrations of IFN γ, IL 2, IL 4, <strong>IL 10</strong>, and increased IL 6 level.
+IL10	drug	alcohol	22782967	In a mouse model of binge <b>alcohol</b>, an increase in Bcl 3 and a concomitant decrease in TNF α but no change in <strong>IL 10</strong> production were found in mice that received <b>alcohol</b> followed by LPS challenge.
+IL10	addiction	intoxication	22782967	In a mouse model of <b>binge</b> alcohol, an increase in Bcl 3 and a concomitant decrease in TNF α but no change in <strong>IL 10</strong> production were found in mice that received alcohol followed by LPS challenge.
+IL10	drug	alcohol	22521198	Participants were assessed for gut permeability, systemic inflammation (LPS, TNFα, IL 6, <strong>IL 10</strong>, hsCRP) and for depression, anxiety, <b>alcohol</b> craving and selective attention.
+IL10	addiction	relapse	22521198	Participants were assessed for gut permeability, systemic inflammation (LPS, TNFα, IL 6, <strong>IL 10</strong>, hsCRP) and for depression, anxiety, alcohol <b>craving</b> and selective attention.
+IL10	addiction	relapse	22521198	At T2 however, the anti inflammatory cytokine <strong>IL 10</strong> was negatively correlated with depression, anxiety and <b>craving</b>.
+IL10	drug	cocaine	22389080	<b>Cocaine</b> abusers demonstrated decreased basal <strong>IL 10</strong> compared with social drinkers.
+IL10	drug	opioid	22366510	Moreover, the administration of LXA4ME during the induction of <b>morphine</b> tolerance inhibited the activation of microglia and astrocytes; reduced the expression of proinflammatory cytokines interleukin 1β (IL 1β), IL 6, and tumor necrosis factor α (TNF α); upregulated the expression of anti inflammatory cytokines <strong>IL 10</strong> and transforming growth factor β1 (TGF β1); and inhibited nuclear factor kappa B (NF κB) activation at the L5 lumbar spinal cord.
+IL10	drug	opioid	22159099	Early life experience decreases drug induced reinstatement of <b>morphine</b> CPP in adulthood via microglial specific epigenetic programming of anti inflammatory <strong>IL 10</strong> expression.
+IL10	addiction	relapse	22159099	Early life experience decreases drug induced <b>reinstatement</b> of morphine CPP in adulthood via microglial specific epigenetic programming of anti inflammatory <strong>IL 10</strong> expression.
+IL10	addiction	reward	22159099	Early life experience decreases drug induced reinstatement of morphine <b>CPP</b> in adulthood via microglial specific epigenetic programming of anti inflammatory <strong>IL 10</strong> expression.
+IL10	drug	opioid	22159099	A neonatal handling paradigm that increases the quantity and quality of maternal care significantly increases baseline expression of the anti inflammatory cytokine <strong>IL 10</strong> within the NAcc, attenuates <b>morphine</b> induced glial activation, and prevents the subsequent reinstatement of <b>morphine</b> CPP in adulthood.
+IL10	addiction	relapse	22159099	A neonatal handling paradigm that increases the quantity and quality of maternal care significantly increases baseline expression of the anti inflammatory cytokine <strong>IL 10</strong> within the NAcc, attenuates morphine induced glial activation, and prevents the subsequent <b>reinstatement</b> of morphine CPP in adulthood.
+IL10	addiction	reward	22159099	A neonatal handling paradigm that increases the quantity and quality of maternal care significantly increases baseline expression of the anti inflammatory cytokine <strong>IL 10</strong> within the NAcc, attenuates morphine induced glial activation, and prevents the subsequent reinstatement of morphine <b>CPP</b> in adulthood.
+IL10	drug	opioid	22159099	<strong>IL 10</strong> expression within the NAcc and reinstatement of CPP are negatively correlated, suggesting a protective role for this specific cytokine against <b>morphine</b> induced glial reactivity and drug induced reinstatement of <b>morphine</b> CPP.
+IL10	addiction	relapse	22159099	<strong>IL 10</strong> expression within the NAcc and <b>reinstatement</b> of CPP are negatively correlated, suggesting a protective role for this specific cytokine against morphine induced glial reactivity and drug induced <b>reinstatement</b> of morphine CPP.
+IL10	addiction	reward	22159099	<strong>IL 10</strong> expression within the NAcc and reinstatement of <b>CPP</b> are negatively correlated, suggesting a protective role for this specific cytokine against morphine induced glial reactivity and drug induced reinstatement of morphine <b>CPP</b>.
+IL10	drug	opioid	22159099	The effect of neonatal handling is mimicked by pharmacological modulation of glia in adulthood with ibudilast, which increases <strong>IL 10</strong> expression, inhibits <b>morphine</b> induced glial activation within the NAcc, and prevents reinstatement of <b>morphine</b> CPP.
+IL10	addiction	relapse	22159099	The effect of neonatal handling is mimicked by pharmacological modulation of glia in adulthood with ibudilast, which increases <strong>IL 10</strong> expression, inhibits morphine induced glial activation within the NAcc, and prevents <b>reinstatement</b> of morphine CPP.
+IL10	addiction	reward	22159099	The effect of neonatal handling is mimicked by pharmacological modulation of glia in adulthood with ibudilast, which increases <strong>IL 10</strong> expression, inhibits morphine induced glial activation within the NAcc, and prevents reinstatement of morphine <b>CPP</b>.
+IL10	addiction	withdrawal	21802933	Sputum was also analysed for mRNA levels of haemoxygenase 1, tumour necrosis factor α, RANTES, interleukin 5(IL 5), <strong>IL 10</strong>, IL 12, IL 13, transforming growth factor β, and interferon γ. Cox regression analyses were performed using time to exacerbation as outcome variable to identify significant hazards for a COPD exacerbation after ICS <b>withdrawal</b>.
+IL10	drug	opioid	21788320	The intrathecally administered kappa 2 <b>opioid</b> agonist GR89696 and <strong>interleukin 10</strong> attenuate bone cancer induced pain through synergistic interaction.
+IL10	addiction	withdrawal	21788320	Ten days later, a paw <b>withdrawal</b> threshold to mechanical stimulus by von Frey hairs was measured using the up down method, after intrathecal administration of GR89696 and <strong>IL 10</strong>.
+IL10	addiction	withdrawal	21788320	Intrathecal GR89696 and <strong>IL 10</strong> significantly increased the paw <b>withdrawal</b> threshold of the cancer cell implanted rat, in a dose dependent manner, with 50% effective dose values (95% confidence interval) of 50.78 μg (31.80 80.07μg) and 0.83 μg (0.59 1.15 μg), respectively.
+IL10	drug	opioid	21788320	These results raise the intriguing possibility of κ(2) <b>opioid</b> receptor agonists and <strong>IL 10</strong> as a new therapeutic approach for the management of bone cancer associated pain.
+IL10	drug	alcohol	21508281	Binge <b>alcohol</b> treatment prior to injury significantly suppressed the increase in serum levels of interleukin (IL) 6, white blood cells, IL 2, <strong>IL 10</strong>, and C reactive protein after the fracture.
+IL10	addiction	intoxication	21508281	<b>Binge</b> alcohol treatment prior to injury significantly suppressed the increase in serum levels of interleukin (IL) 6, white blood cells, IL 2, <strong>IL 10</strong>, and C reactive protein after the fracture.
+IL10	drug	alcohol	21421450	<b>Alcoholics</b> admitted for programmed withdrawal showed higher IL 6, IFN γ, <strong>IL 10</strong>, Il 4 and ICAM 1 serum levels than healthy controls.
+IL10	addiction	withdrawal	21421450	Alcoholics admitted for programmed <b>withdrawal</b> showed higher IL 6, IFN γ, <strong>IL 10</strong>, Il 4 and ICAM 1 serum levels than healthy controls.
+IL10	drug	alcohol	21254593	It was established in experiments on noninbred rats that their <b>ethanol</b> intoxication (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, IL 2, IL 4, <strong>IL 10</strong>, increases the concentration of IL 6, suppresses the immune responses, and reduces the interrelation IFNgamma/IL 4 in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes.
+IL10	addiction	intoxication	21254593	It was established in experiments on noninbred rats that their ethanol <b>intoxication</b> (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, IL 2, IL 4, <strong>IL 10</strong>, increases the concentration of IL 6, suppresses the immune responses, and reduces the interrelation IFNgamma/IL 4 in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes.
+IL10	drug	alcohol	21143255	Human PBMCs were cultured in the presence of 100 mM <b>ethanol</b> and/or 100 ng/ml LPS for various time periods (1, 3, 8, and 24 hours) and analyzed for the kinetics of gene expression by quantitative real time PCR of selected transcription factors (T bet, GATA3, Foxp3, and RORγt) and cytokines (TNF α, IL 6, <strong>IL 10</strong>, and IFN γ).
+IL10	drug	alcohol	21143255	Markers of inflammation including TNF α and IL 1β in supernatant of PBMCs were significantly decreased, while levels of <strong>IL 10</strong> and IL 6 remained unchanged following <b>ethanol</b> exposure.
+IL10	drug	alcohol	20238399	Anti inflammatory pathways and <b>alcoholic</b> liver disease: role of an adiponectin/<strong>interleukin 10</strong>/heme oxygenase 1 pathway.
+IL10	drug	alcohol	20238399	Recent studies have identified an adiponectin/<strong>interleukin 10</strong>/heme oxygenase 1 (HO 1) pathway that is profoundly effective in dampening the enhanced activation of innate immune responses in primary cultures of Kupffer cells, as well as in an in vivo mouse model of chronic <b>ethanol</b> feeding.
+IL10	addiction	relapse	20203531	The animals were scored clinically throughout the experiment, and axonal degeneration, demyelination, T cells, microglia/macrophages, TNF alpha, IL 12, IFN gamma, <strong>IL 10</strong> and the T(H)17 response were estimated at the peak of the first <b>relapse</b>.
+IL10	drug	alcohol	20052772	Here we tested the hypothesis that adiponectin mediated suppression of LPS signaling in Kupffer cells is mediated via an interleukin 10 (<strong>IL 10</strong>)/heme oxygenase 1 (HO 1) pathway after chronic <b>ethanol</b> feeding.
+IL10	drug	alcohol	20052772	Here we tested the hypothesis that adiponectin mediated suppression of LPS signaling in Kupffer cells is mediated via an <strong>interleukin 10</strong> (<strong>IL 10</strong>)/heme oxygenase 1 (HO 1) pathway after chronic <b>ethanol</b> feeding.
+IL10	drug	alcohol	20052772	gAcrp increased <strong>IL 10</strong> mRNA and protein expression, as well as expression of the <strong>IL 10</strong> inducible gene, HO 1; expression was higher in Kupffer cells from <b>ethanol</b> fed rats compared with pair fed controls.
+IL10	drug	alcohol	20052772	Although <strong>IL 10</strong> receptor surface expression on Kupffer cells was not affected by <b>ethanol</b> feeding, <strong>IL 10</strong> mediated phosphorylation of STAT3 and expression of HO 1 was higher in Kupffer cells after <b>ethanol</b> feeding.
+IL10	drug	alcohol	20052772	Kupffer cells from <b>ethanol</b> fed rats are highly sensitive to the anti inflammatory effects of gAcrp; this sensitivity is associated with both increased expression and sensitivity to <strong>IL 10</strong>.
+IL10	drug	cocaine	18719314	After 10 days withdrawal from <b>cocaine</b>, reinstatement of <b>cocaine</b> seeking behavior induced either by a priming dose of the drug (unconditioned stimulus), by cue previously associated with <b>cocaine</b> self administration (conditioned stimuli), or by both these stimuli evoked similar changes in several immunological parameters, for example, a decrease in relative spleen weight, proliferative activity of splenocytes, and their ability to produce <strong>IL 10</strong>.
+IL10	addiction	relapse	18719314	After 10 days withdrawal from cocaine, <b>reinstatement</b> of cocaine <b>seeking</b> behavior induced either by a priming dose of the drug (unconditioned stimulus), by cue previously associated with cocaine self administration (conditioned stimuli), or by both these stimuli evoked similar changes in several immunological parameters, for example, a decrease in relative spleen weight, proliferative activity of splenocytes, and their ability to produce <strong>IL 10</strong>.
+IL10	addiction	withdrawal	18719314	After 10 days <b>withdrawal</b> from cocaine, reinstatement of cocaine seeking behavior induced either by a priming dose of the drug (unconditioned stimulus), by cue previously associated with cocaine self administration (conditioned stimuli), or by both these stimuli evoked similar changes in several immunological parameters, for example, a decrease in relative spleen weight, proliferative activity of splenocytes, and their ability to produce <strong>IL 10</strong>.
+IL10	drug	alcohol	18436572	<strong>Interleukin 10</strong> gene polymorphism is associated with <b>alcoholism</b> but not with <b>alcoholic</b> liver disease.
+IL10	drug	alcohol	18436572	To determine whether the functional polymorphism  592C>A of the interleukin (IL) 10 gene (<strong>IL10</strong>) influences the development of <b>alcoholic</b> liver disease or <b>alcoholism</b> in <b>alcoholic</b> Spanish subjects.
+IL10	drug	alcohol	18436572	The  592C>A <strong>IL10</strong> polymorphism was analyzed by the polymerase chain reaction and digestion with restriction enzymes in 257 male <b>alcoholics</b> [161 without <b>alcoholic</b> liver disease and 96 with <b>alcoholic</b> liver cirrhosis (ALC)] and 100 male healthy controls.
+IL10	drug	opioid	17993452	This study was performed to investigate the in vitro production of interferon gamma and <strong>interleukin 10</strong> after antigenic stimulation of cells using whole blood from <b>opioid</b> addicts.
+IL10	drug	opioid	17993452	The results demonstrated a significant decrease in interferon gamma production and an increase in <strong>interleukin 10</strong> secretion in <b>heroin</b> addicts, relative to the control group (35.9+/ 26.3 versus 110.2+/ 60.3 pg/mL, p<0.01 and 71.8+/ 28.4 versus 17.1+/ 13.5 pg/mL, p<0.01, respectively), however the changes in these values in opium addicts were not significant compared to healthy individuals.
+IL10	drug	opioid	17974159	However, <strong>IL 10</strong> production was significantly increased in both groups accompanied by a significant suppression of <strong>IL 10</strong> secretion in the presence of <b>naloxone</b>.
+IL10	drug	alcohol	17855333	Serum insulin like growth factor 1 (IGF 1), interleukin (IL) 6, IL 8, <strong>IL 10</strong>, TNF alpha, PTH, estradiol, free testosterone, and corticosterone were measured in 36 <b>alcoholics</b>, ten of them cirrhotics, who also underwent brain CT, which recorded the presence of cortical atrophy or cerebellar atrophy, Evan's, Huckmann's, cella media, bicaudate, cortical atrophy, bifrontal, and ventricular indices, and diameter of the third ventricle; subjective nutritional assessment, midarm anthropometry, and evaluation of liver function.
+IL10	drug	alcohol	17374050	While T x Hem did not prevent LPS induced release of TNF alpha, IL 1alpha, IL 6, or <strong>IL 10</strong> at 6 or 24 hours, <b>alcohol</b> binge suppressed TNF alpha, IL 1 and IL 6 release, without altering <strong>IL 10</strong> response in cells isolated from blood and pleural compartment.
+IL10	addiction	intoxication	17374050	While T x Hem did not prevent LPS induced release of TNF alpha, IL 1alpha, IL 6, or <strong>IL 10</strong> at 6 or 24 hours, alcohol <b>binge</b> suppressed TNF alpha, IL 1 and IL 6 release, without altering <strong>IL 10</strong> response in cells isolated from blood and pleural compartment.
+IL10	drug	opioid	17201885	Leukocyte subpopulation NK, CD4+, CD8+ and some cytokines Th1 (IFNgamma, interleukin [IL]2) and Th2 (IL 6, <strong>IL 10</strong>) were evaluated prior to, during and after <b>methadone</b> treatment.
+IL10	drug	alcohol	16792568	The role of <strong>IL 10</strong> in <b>alcohol</b> mediated suppression of AM IL 23 p19 mRNA expression was assessed using wild type (WT) and <strong>IL 10</strong> knock out (KO) mice.
+IL10	addiction	intoxication	16792568	Acute <b>intoxication</b> increases lung and BAL cell <strong>IL 10</strong> mRNA expression 2 hours after in vivo infection and, in vitro, recombinant <strong>IL 10</strong> inhibits AM IL 23 expression.
+IL10	drug	alcohol	16792568	However, <b>alcohol</b> impairs IL 23 similarly in AM harvested from both WT and <strong>IL 10</strong> KO mice.
+IL10	drug	alcohol	16792568	Acute <b>alcohol</b> intoxication inhibits the pulmonary IL 23 response to K. pneumoniae infection both in vivo and in vitro, an effect independent of <strong>IL 10</strong> induction.
+IL10	addiction	intoxication	16792568	Acute alcohol <b>intoxication</b> inhibits the pulmonary IL 23 response to K. pneumoniae infection both in vivo and in vitro, an effect independent of <strong>IL 10</strong> induction.
+IL10	drug	nicotine	15710343	The present study aimed at investigating the effect of <b>nicotine</b> on TGF beta1, <strong>IL 10</strong>, IL 12, and TNF alpha production in Cpn infected human peripheral blood mononuclear cells (PBMCs).
+IL10	drug	nicotine	15710343	<b>Nicotine</b> treatment of the Cpn infected cells up regulated <strong>IL 10</strong>, but not TNF alpha and IL 12, and also resulted in significant down regulation of TGF beta1 production which was marked in the Cpn infected control cells.
+IL10	drug	alcohol	15528012	<b>Ethanol</b> significantly affected the concentration of at least one of the cytokines evaluated in serum or peritoneal lavage fluid [interleukin (IL) 6, <strong>IL 10</strong>, and IL 12 p40 subunit] induced by all TLR ligands tested.
+IL10	drug	alcohol	15469574	The anti inflammatory parameters <strong>IL 10</strong> and tumour necrosis factor receptors I and II did not differ between <b>alcoholic</b> and nonalcoholic patients.
+IL10	drug	alcohol	15289211	In 36 <b>alcoholics</b> without liver disease, at the point of commencing withdrawal from <b>alcohol</b>, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, IL1RA, IL4, IL6, IL8, <strong>IL10</strong> and IL12).
+IL10	addiction	withdrawal	15289211	In 36 alcoholics without liver disease, at the point of commencing <b>withdrawal</b> from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, IL1RA, IL4, IL6, IL8, <strong>IL10</strong> and IL12).
+IL10	drug	alcohol	15282117	In the current study, our aim was to evaluate and investigate the influence of heavy <b>alcohol</b> intake on serum interleukin (IL) 6, IL 8, <strong>IL 10</strong>, IL 12, and tumor necrosis factor alpha (TNF alpha) concentrations.
+IL10	drug	psychedelics	15056370	Specifically, <b>MDMA</b> suppresses neutrophil phagocytosis, suppresses production of the pro inflammatory cytokines tumour necrosis factor alpha (TNF alpha) and interleukin (IL) 1beta, and increases production of the endogenous immunosuppressive cytokine (<strong>IL 10</strong>), thereby promoting an immunosuppressive cytokine phenotype.
+IL10	drug	opioid	15055740	Similarly, production of IL 2, <strong>IL 10</strong> and IFNgamma was higher in the group of <b>heroin</b> addicts than in healthy controls.
+IL10	drug	alcohol	12821046	Chronic <b>alcohol</b> exposure sensitizes mice to galactosamine induced liver injury through enhanced keratinocyte chemoattractant and defective <strong>IL 10</strong> production.
+IL10	drug	alcohol	12821046	In GAL+<b>ethanol</b> treated mice, <strong>IL 10</strong> treatment reduced ALT release, KC and MCP 1 serum and hepatic mRNA levels, and improved liver inflammation.
+IL10	drug	alcohol	12821046	Enhancement of GAL induced liver injury by <b>ethanol</b> is associated with an imbalance between proinflammatory cytokines and the anti inflammatory cytokine <strong>IL 10</strong> and depends on gut bacterial flora.
+IL10	drug	alcohol	11956381	<b>Alcohol</b> blunted the hemorrhage induced rise in plasma TNF alpha (142 +/  48 pg/mL) and enhanced the hemorrhage induced increase in <strong>IL 10</strong> (678 +/  187 pg/mL).
+IL10	drug	alcohol	11956381	<b>Alcohol</b> exacerbated the hemorrhage induced increase in lung TNF alpha, and did not alter the IL 1alpha, IL 6, and <strong>IL 10</strong> lung responses.
+IL10	drug	alcohol	11821657	A role for <strong>interleukin 10</strong> in <b>alcohol</b> induced liver sensitization to bacterial lipopolysaccharide.
+IL10	addiction	sensitization	11821657	A role for <strong>interleukin 10</strong> in alcohol induced liver <b>sensitization</b> to bacterial lipopolysaccharide.
+IL10	drug	alcohol	11821657	<strong>IL 10</strong> knock out and their C57BL/6J counterpart wild type mice were fed <b>alcohol</b> in drinking water for 7 weeks.
+IL10	drug	alcohol	11821657	In the <strong>IL 10</strong> knock out mice, LPS alone increased aspartate aminotransferase and alanine aminotransferase enzyme activity, and this was potentiated by <b>alcohol</b>.
+IL10	drug	alcohol	11821657	Proinflammatory cytokine levels were increased by LPS and further enhanced by <b>alcohol</b> treatment, particularly in the <strong>IL 10</strong> knock out mice.
+IL10	drug	alcohol	11821657	<strong>IL 10</strong> plasma levels in the wild type animals were down regulated by <b>alcohol</b>.
+IL10	drug	alcohol	11821657	<b>Alcohol</b> induced liver sensitization to LPS in wild type mice may involve down regulation of <strong>IL 10</strong>.
+IL10	addiction	sensitization	11821657	Alcohol induced liver <b>sensitization</b> to LPS in wild type mice may involve down regulation of <strong>IL 10</strong>.
+IL10	drug	alcohol	11821657	<strong>IL 10</strong> may also limit <b>alcohol</b> induced liver damage by counteracting the effects of proinflammatory cytokines.
+IL10	drug	alcohol	11505051	No difference was observed regarding <strong>IL 10</strong>, IL 12, and IL 13 production between <b>alcoholics</b> and controls.
+IL10	addiction	relapse	11293664	The mRNA for cytokines IL 1beta, IL 6, <strong>IL 10</strong> and the chemokines CINC, MIP 1alpha, MCP 1 were significantly (P < 0.05) elevated and persisted for 2 weeks, decreased in 6 weeks and increased again during <b>relapse</b>.
+IL10	drug	alcohol	10976010	Influence of acute <b>alcohol</b> intake and <b>alcohol</b> withdrawal on circulating levels of IL 6, IL 8, <strong>IL 10</strong> and IL 12.
+IL10	addiction	withdrawal	10976010	Influence of acute alcohol intake and alcohol <b>withdrawal</b> on circulating levels of IL 6, IL 8, <strong>IL 10</strong> and IL 12.
+IL10	drug	alcohol	10976010	The present study was aimed to evaluate the influence of both acute <b>alcohol</b> abstinence (in <b>alcoholics</b>) and acute <b>alcohol</b> intake (in healthy subjects) on serum IL 6, IL 8, <strong>IL 10</strong>, and IL 12 levels.
+IL10	drug	alcohol	10976010	Increased serum levels of IL 6, <strong>IL 10</strong> and, to a lesser extent IL 8, declined in the few days after <b>alcohol</b> abstinence in patients with <b>alcohol</b> withdrawal syndrome.
+IL10	addiction	withdrawal	10976010	Increased serum levels of IL 6, <strong>IL 10</strong> and, to a lesser extent IL 8, declined in the few days after alcohol abstinence in patients with alcohol <b>withdrawal</b> syndrome.
+IL10	drug	alcohol	10798594	Decreased natural killer cell responses and altered interleukin 6 and <strong>interleukin 10</strong> production in <b>alcoholism</b>: an interaction between <b>alcohol</b> dependence and African American ethnicity.
+IL10	addiction	dependence	10798594	Decreased natural killer cell responses and altered interleukin 6 and <strong>interleukin 10</strong> production in alcoholism: an interaction between alcohol <b>dependence</b> and African American ethnicity.
+IL10	drug	alcohol	10798594	This study compared NK activity, interleukin (IL) 2 stimulated NK activity, and concanavalin A stimulated peripheral blood mononuclear cell production of Th1 (IL 12 and IL 2), Th2 (<strong>IL 10</strong>), and proinflammatory (IL 6) cytokines in 31 hospitalized chronic <b>alcoholic</b> patients and 31 age matched controls who were stratified on the basis of ethnicity.
+IL10	drug	alcohol	10798594	Compared with the other three groups, African American <b>alcoholics</b> also showed lower levels of IL 6 (F = 7.2;p < 0.01) and higher levels of <strong>IL 10</strong> (F = 4.9;p < 0.05).
+IL10	drug	alcohol	10798594	Regression analyses showed that <b>alcohol</b> dependence and ethnicity predicted NK activity, whereas the interaction between <b>alcohol</b> dependence and ethnicity predicted levels of IL 6 and <strong>IL 10</strong>.
+IL10	addiction	dependence	10798594	Regression analyses showed that alcohol <b>dependence</b> and ethnicity predicted NK activity, whereas the interaction between alcohol <b>dependence</b> and ethnicity predicted levels of IL 6 and <strong>IL 10</strong>.
+IL10	drug	alcohol	9895030	This study examines i) the activity of serum prolyl endopeptidase (PEP) and dipeptidlyl peptidase IV (DPP IV) in detoxified <b>alcohol</b> dependent patients without liver disease versus normal controls, and ii) the relationships between serum DPP IV and PEP activity and the production of cytokines or cytokine receptors, such as interleukin 6 (IL 6), tumor necrosis factor alpha (TNF alpha), interferon y (IFN y), IL 1 receptor antagonist (IL 1RA), and <strong>IL 10</strong>, and granulocyte macrophage colony stimulatory factor (GM CSF).
+ADH1B	drug	alcohol	32084087	Impacts of interactions between <strong>ADH1B</strong> and ALDH2 genotypes on <b>alcohol</b> flushing, <b>alcohol</b> reeking on the day after drinking, and age distribution in Japanese <b>alcohol</b> dependent men.
+ADH1B	drug	alcohol	32084087	The fast metabolizing <strong>ADH1B</strong>*2(+) genotype (*1/*2 or *2/*2) and the inactive ALDH2*2(+) genotype (*1/*2 or *2/*2) affected the multivariate odds ratios for current or former flushing [odds ratio, 95% confidence interval = 2.27 (1.79 2.86) and 23.0 (18.6 28.5), respectively, vs. *2( ) genotype] and for <b>alcohol</b> reeking [0.39 (0.29 0.52) and 1.56 (1.09 2.25), respectively, vs. *2( ) genotype].
+ADH1B	drug	alcohol	32084087	These findings support the protective roles of the <strong>ADH1B</strong>*2(+) and ALDH2*2(+) genotypes against the development of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	32084087	These findings support the protective roles of the <strong>ADH1B</strong>*2(+) and ALDH2*2(+) genotypes against the development of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	31989819	Native <b>ethanol</b> dehydrogenase <strong>ADH2</strong> and acetaldehyde dehydrogenase ADA from Dickeya zeae were further overexpressed, which enhanced the capability to utilize <b>ethanol</b> for squalene synthesis and endowed the engineered strain with greater adaptability to high <b>ethanol</b> concentrations.
+ADH1B	drug	alcohol	31845443	To elucidate associations among liver disease, lipid profile, body mass index (BMI), ketonuria, and meal skipping under the influence of <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>; rs1229984) and aldehyde dehydrogenase 2 (ALDH2; rs671) genotypes in men with <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	31845443	To elucidate associations among liver disease, lipid profile, body mass index (BMI), ketonuria, and meal skipping under the influence of alcohol dehydrogenase 1B (<strong>ADH1B</strong>; rs1229984) and aldehyde dehydrogenase 2 (ALDH2; rs671) genotypes in men with alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	31090166	Genome wide association studies (GWAS) of <b>alcohol</b> dependence (AD) have reliably identified variation within <b>alcohol</b> metabolizing genes (eg, <strong>ADH1B</strong>) but have inconsistently located other signals, which may be partially attributable to symptom heterogeneity underlying the disorder.
+ADH1B	addiction	dependence	31090166	Genome wide association studies (GWAS) of alcohol <b>dependence</b> (AD) have reliably identified variation within alcohol metabolizing genes (eg, <strong>ADH1B</strong>) but have inconsistently located other signals, which may be partially attributable to symptom heterogeneity underlying the disorder.
+ADH1B	drug	alcohol	31055022	The primary outcomes were daily <b>alcohol</b> consumption, binge drinking, problem drinking (CAGE score 2+) and smoking status in relation to tagging variants within the FTO and <strong>ADH1B</strong> genes.
+ADH1B	drug	nicotine	31055022	The primary outcomes were daily alcohol consumption, binge drinking, problem drinking (CAGE score 2+) and <b>smoking</b> status in relation to tagging variants within the FTO and <strong>ADH1B</strong> genes.
+ADH1B	addiction	intoxication	31055022	The primary outcomes were daily alcohol consumption, <b>binge</b> drinking, problem drinking (CAGE score 2+) and smoking status in relation to tagging variants within the FTO and <strong>ADH1B</strong> genes.
+ADH1B	drug	nicotine	31055022	In women, the combination of the FTO/<strong>ADH1B</strong> GG/+A genotypes doubled the risk of binge drinking (OR 2.10, 95% CI 1.19 3.71, p < 0.05), and the risk was further increased among <b>smoking</b> women (OR 4.10, 95% CI 1.64 10.24, p = 0.008).
+ADH1B	addiction	intoxication	31055022	In women, the combination of the FTO/<strong>ADH1B</strong> GG/+A genotypes doubled the risk of <b>binge</b> drinking (OR 2.10, 95% CI 1.19 3.71, p < 0.05), and the risk was further increased among smoking women (OR 4.10, 95% CI 1.64 10.24, p = 0.008).
+ADH1B	drug	nicotine	31055022	In this large population study, the FTO gene appeared associated with binge and problem drinking, and the associations were modified by sex, <b>smoking</b> status and the <strong>ADH1B</strong> polymorphism.
+ADH1B	addiction	intoxication	31055022	In this large population study, the FTO gene appeared associated with <b>binge</b> and problem drinking, and the associations were modified by sex, smoking status and the <strong>ADH1B</strong> polymorphism.
+ADH1B	drug	alcohol	31011876	The prevalence of <strong>ADH1B</strong> and OPRM1 alleles predisposing for <b>alcohol</b> consumption are increased in the Hungarian psoriasis population.
+ADH1B	drug	alcohol	30994927	We also examined the extent to which an single nucleotide polymorphism (rs1229984) in <strong>ADH1B</strong>, which is strongly associated with both <b>alcohol</b> consumption and dependence, contributed to the polygenic association with these phenotypes and whether PRS interacted with sex, age, or family history of <b>alcoholism</b> to predict <b>alcohol</b> related outcomes.
+ADH1B	addiction	dependence	30994927	We also examined the extent to which an single nucleotide polymorphism (rs1229984) in <strong>ADH1B</strong>, which is strongly associated with both alcohol consumption and <b>dependence</b>, contributed to the polygenic association with these phenotypes and whether PRS interacted with sex, age, or family history of alcoholism to predict alcohol related outcomes.
+ADH1B	drug	alcohol	30994927	The inclusion of rs1229984 attenuated the effects of the <b>alcohol</b> consumption PRS, particularly for DSM4AD and DSM5AUDSX, but the PRS continued to exert an independent effect for all 5 <b>alcohol</b> measures (Δmarginal R2 after controlling for <strong>ADH1B</strong> = 0.14 to 1.22%).
+ADH1B	drug	alcohol	30931596	Genetic variants in two enzymes involved in the metabolism of <b>ethanol</b>, <b>alcohol</b> dehydrogenase <strong>ADH1B</strong> *2 and aldehyde dehydrogenase ALDH2 *2 through increasing the blood level of acetaldehyde, may play a "protective" role against <b>alcoholism</b>.
+ADH1B	drug	alcohol	30852706	Variations in genes affecting <b>alcohol</b> metabolism (<strong>ADH1B</strong>, ALDH2) are protective against both <b>alcohol</b> dependence and excessive consumption, but different variants are found in different populations.
+ADH1B	addiction	dependence	30852706	Variations in genes affecting alcohol metabolism (<strong>ADH1B</strong>, ALDH2) are protective against both alcohol <b>dependence</b> and excessive consumption, but different variants are found in different populations.
+ADH1B	addiction	dependence	30852706	<strong>ADH1B</strong> and ALDH2 strongly affect both consumption and <b>dependence</b>.
+ADH1B	drug	alcohol	30629674	Endoscopic screening using esophageal iodine staining and genotypes of <strong>ADH1B</strong> and ALDH2 in Japanese <b>alcohol</b> dependent women.
+ADH1B	drug	alcohol	30629674	Several risk factors for DIULs, including genetic polymorphisms of <b>alcohol</b> and aldehyde dehydrogenases (<strong>ADH1B</strong>, rs1229984; ALDH2, rs671), have been demonstrated in Japanese <b>alcohol</b> dependent men.
+ADH1B	drug	alcohol	30629674	No significant differences in age, usual <b>alcohol</b> consumption, or smoking habits were observed according to <strong>ADH1B</strong> and ALDH2 genotypes.
+ADH1B	drug	nicotine	30629674	No significant differences in age, usual alcohol consumption, or <b>smoking</b> habits were observed according to <strong>ADH1B</strong> and ALDH2 genotypes.
+ADH1B	drug	alcohol	30483881	Because <b>alcohol</b> dehydrogenase is one of the most important <b>alcohol</b> detoxification enzymes, we tried to replicate a putative association of the risk of developing PD with two missense gene variations affecting the <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) gene (one of them related with aversive effects to <b>alcohol</b>).
+ADH1B	addiction	aversion	30483881	Because alcohol dehydrogenase is one of the most important alcohol detoxification enzymes, we tried to replicate a putative association of the risk of developing PD with two missense gene variations affecting the alcohol dehydrogenase 1B (<strong>ADH1B</strong>) gene (one of them related with <b>aversive</b> effects to alcohol).
+ADH1B	drug	alcohol	30320893	A functional variant in <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) is protective in people of European and Asian descent, and a different functional variant in the same gene is protective in those of African descent.
+ADH1B	drug	alcohol	30209858	The rs1229984 (<strong>ADH1B</strong>) was genotyped; <b>alcohol</b> consumption, hay fever and asthma were self reported.
+ADH1B	drug	alcohol	29582627	<strong>ADH1B</strong>, ALDH2, GSTM1 and GSTT1 Gene Polymorphic Frequencies among <b>Alcoholics</b> and Controls in the Arcadian Population of Central India Background: Epidemiological research has highlighted the global burden of primary liver cancer cases due to <b>alcohol</b> consumption, even in a low consumption country like India.
+ADH1B	drug	alcohol	29582627	<b>Alcohol</b> detoxification is governed by <strong>ADH1B</strong>, ALDH2, GSTM1 and GSTT1 genes that encode functional enzymes which are coordinated with each other to remove highly toxic metabolites i.e.
+ADH1B	drug	alcohol	29582627	Methods: The aim of this study was to screen the arcadian population of central India in order to investigate and compare the genotype distribution and allele frequencies of <b>alcohol</b> metabolizing genes (<strong>ADH1B</strong>, ALDH2, GSTM1 and GSTT1) in both <b>alcoholic</b> (N=121) and control (N=145) healthy subjects.
+ADH1B	drug	alcohol	29084628	We evaluated the presence of SNPs in the ADH (<strong>ADH1B</strong>, ADH1C, and ADH4) and ALDH (ALDH2) genes in <b>alcohol</b> users of Goiânia, State of Goiás   Brazil, and then we established a possible relationship with AUD by allelic and genotypic study.
+ADH1B	drug	alcohol	29063269	Slow metabolizing <strong>ADH1B</strong> and inactive heterozygous ALDH2 increase vulnerability to fatty liver in Japanese men with <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	29063269	Slow metabolizing <strong>ADH1B</strong> and inactive heterozygous ALDH2 increase vulnerability to fatty liver in Japanese men with alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	29063269	Genetic polymorphisms of <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>; rs1229984, His48Arg) and aldehyde dehydrogenase 2 (ALDH2; rs671, Glu504Lys) affect body weight, body fat, and lipid metabolism in individuals with <b>alcohol</b> dependence, and the aim of this study was to identify their determinants in relation to the development of fatty liver.
+ADH1B	addiction	dependence	29063269	Genetic polymorphisms of alcohol dehydrogenase 1B (<strong>ADH1B</strong>; rs1229984, His48Arg) and aldehyde dehydrogenase 2 (ALDH2; rs671, Glu504Lys) affect body weight, body fat, and lipid metabolism in individuals with alcohol <b>dependence</b>, and the aim of this study was to identify their determinants in relation to the development of fatty liver.
+ADH1B	drug	alcohol	29063269	We evaluated associations between the presence of fatty liver and <strong>ADH1B</strong> and ALDH2 genotypes and other factors in 1604 Japanese men who had been admitted for treatment of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	29063269	We evaluated associations between the presence of fatty liver and <strong>ADH1B</strong> and ALDH2 genotypes and other factors in 1604 Japanese men who had been admitted for treatment of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	29063269	Age adjusted usual <b>alcohol</b> intake did not differ according to <strong>ADH1B</strong> or ALDH2 genotypes.
+ADH1B	drug	alcohol	29045753	We have aimed to establish the possible association between two common single nucleotide polymorphisms (SNPs) in the <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) gene and the risk for RLS.
+ADH1B	drug	alcohol	28921935	The relationship between <b>alcohol</b> consumption (proxied by a variant in the <strong>ADH1B</strong> gene) and cardiovascular risk has been investigated, finding that <b>alcohol</b> consumption increases risk, with no evidence of a cardioprotective effect at moderate consumption levels.
+ADH1B	drug	alcohol	28805974	Effect of single nucleotide polymorphisms in <strong>ADH1B</strong>, ADH4, ADH1C, OPRM1, DRD2, BDNF, and ALDH2 genes on <b>alcohol</b> dependence in a Caucasian population.
+ADH1B	addiction	dependence	28805974	Effect of single nucleotide polymorphisms in <strong>ADH1B</strong>, ADH4, ADH1C, OPRM1, DRD2, BDNF, and ALDH2 genes on alcohol <b>dependence</b> in a Caucasian population.
+ADH1B	drug	alcohol	28485404	We also observed a genome wide significant association in non Hispanic whites between the previously reported SNP rs1229984 in <strong>ADH1B</strong> and both <b>alcohol</b> consumption phenotypes (OR=0.79, P=2.47 × 10 20 for drinker status and beta= 0.19, P=1.91 × 10 35 for drinks/week), which replicated in Hispanic/Latinos (OR=0.72, P=4.35 × 10 7 and beta= 0.21, P=2.58 × 10 6, respectively).
+ADH1B	drug	alcohol	28485404	Although prior studies reported effects of <strong>ADH1B</strong> and ALDH2 on lifetime measures, such as risk of <b>alcohol</b> dependence, our study adds further evidence of the effect of the same genes on a cross sectional measure of average drinking.
+ADH1B	addiction	dependence	28485404	Although prior studies reported effects of <strong>ADH1B</strong> and ALDH2 on lifetime measures, such as risk of alcohol <b>dependence</b>, our study adds further evidence of the effect of the same genes on a cross sectional measure of average drinking.
+ADH1B	drug	alcohol	28361821	With respect to the 5 hydroxytryptamine (5HT) transporter long promoter region (5HTTLPR), cholinergic receptor muscarinic (CHRM2) and <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) genes, there was no significant difference between the cases and the controls.
+ADH1B	drug	alcohol	28098394	The inactive aldehyde dehydrogenase 2 (ALDH2) and highly active <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) genes are protective factors for the development of AUD.
+ADH1B	drug	alcohol	27991683	We evaluated 989 Japanese <b>alcoholic</b> men to identify the effects of genetic polymorphisms of <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>; rs1229984) and aldehyde dehydrogenase 2 (ALDH2; rs671) on platelet counts during an 8 week in hospital abstinence period.
+ADH1B	drug	alcohol	27991683	In <b>alcoholics</b>, the <strong>ADH1B</strong>*1/*1 genotype increased the risk of thrombocytopenia upon admission and of a rebound platelet increase 2 weeks thereafter, while the ALDH2*1/*1 genotype was associated with lower platelet counts throughout the 8 week hospital stay.
+ADH1B	drug	alcohol	27338962	Functional missense mutations in <strong>ADH1B</strong> and ALDH2 are protective against <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	27338962	Functional missense mutations in <strong>ADH1B</strong> and ALDH2 are protective against alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	27172571	Both religious involvement and <strong>ADH1B</strong> rs1229984 were negatively associated with the number of maximum drinks consumed and the number of lifetime <b>alcohol</b> dependence symptoms endorsed.
+ADH1B	addiction	dependence	27172571	Both religious involvement and <strong>ADH1B</strong> rs1229984 were negatively associated with the number of maximum drinks consumed and the number of lifetime alcohol <b>dependence</b> symptoms endorsed.
+ADH1B	drug	alcohol	27172571	The interactions of religious involvement with <strong>ADH1B</strong> rs2066702, ADH1C rs698, and ADH4 rs1042364 were significantly associated with maximum drinks and <b>alcohol</b> dependence symptoms.
+ADH1B	addiction	dependence	27172571	The interactions of religious involvement with <strong>ADH1B</strong> rs2066702, ADH1C rs698, and ADH4 rs1042364 were significantly associated with maximum drinks and alcohol <b>dependence</b> symptoms.
+ADH1B	drug	alcohol	27163368	Certain genetic variants (i.e., alleles)  particularly the <strong>ADH1B</strong>*2, <strong>ADH1B</strong>*3, ADH1C*1, and ALDH2*2 alleles  have been associated with lower rates of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	27163368	Certain genetic variants (i.e., alleles)  particularly the <strong>ADH1B</strong>*2, <strong>ADH1B</strong>*3, ADH1C*1, and ALDH2*2 alleles  have been associated with lower rates of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	26848198	Characterization of polymorphisms of genes <strong>ADH2</strong>, ADH3, ALDH2 and CYP2E1 and relationship to the <b>alcoholism</b> in a Colombian population.
+ADH1B	drug	alcohol	26848198	Identify and characterize polymorphisms of genes <strong>ADH2</strong>, ADH3, ALDH2 and CYP2E1 in a Colombian population residing in the city of Bogotá and determine its possible relationship to the <b>alcoholism</b>.
+ADH1B	drug	alcohol	26848198	<strong>ADH2</strong>, ADH3, ALDH2, and CYP2E1 genotypes a population of 148 individuals with non problematic <b>alcohol</b> and 65 individuals with <b>alcoholism</b> were determined with TaqMan probes and PCR RFLP.
+ADH1B	drug	alcohol	26848198	Since substance dependence requires interaction of multiple genes, the combination of genotypes <strong>ADH2</strong> * 2, CYP2E1 * 1 combined with genotype homozygous ALDH2 * 1 found in this study could be leading to the population to a potential risk to <b>alcoholism</b>.
+ADH1B	addiction	dependence	26848198	Since substance <b>dependence</b> requires interaction of multiple genes, the combination of genotypes <strong>ADH2</strong> * 2, CYP2E1 * 1 combined with genotype homozygous ALDH2 * 1 found in this study could be leading to the population to a potential risk to alcoholism.
+ADH1B	drug	alcohol	26848198	Se determinaron los genotipos <strong>ADH2</strong>, ADH3, ALDH2 y CYP2E1 a una población de 148 individuos con un consumo no problemático de <b>alcohol</b> y 65 individuos con alcoholismo.
+ADH1B	drug	alcohol	26842247	Genes in <b>alcohol</b> metabolism pathway, especially <strong>ADH1B</strong> and ALDH2, conferred the major genetic risk for AD in Taiwanese Han population.
+ADH1B	drug	alcohol	26036284	The results provide further support that <strong>ADH1B</strong> modulates <b>alcohol</b> consumption.
+ADH1B	drug	alcohol	26033520	Comorbid <b>alcohol</b> dependence disorder may be related to aldehyde dehydrogenase 2 (ALDH2) and <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) in bipolar II disorder, but only to ALDH2 in bipolar I disorder, in Han Chinese.
+ADH1B	addiction	dependence	26033520	Comorbid alcohol <b>dependence</b> disorder may be related to aldehyde dehydrogenase 2 (ALDH2) and alcohol dehydrogenase 1B (<strong>ADH1B</strong>) in bipolar II disorder, but only to ALDH2 in bipolar I disorder, in Han Chinese.
+ADH1B	drug	alcohol	26033520	A polymerase chain reaction and restriction fragment length polymorphism analysis was used to determine genotypes for <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) and aldehyde dehydrogenase 2 (ALDH2), two <b>alcohol</b> metabolizing enzymes.
+ADH1B	drug	alcohol	25958762	Variants of <strong>ADH1B</strong> and ADH1C genes encoding <b>alcohol</b> dehydrogenases enzymes have also been consistently associated, this time with <b>alcohol</b> dependence (AD).
+ADH1B	addiction	dependence	25958762	Variants of <strong>ADH1B</strong> and ADH1C genes encoding alcohol dehydrogenases enzymes have also been consistently associated, this time with alcohol <b>dependence</b> (AD).
+ADH1B	drug	alcohol	25828809	Which <b>alcohol</b> use disorder criteria contribute to the association of <strong>ADH1B</strong> with <b>alcohol</b> dependence?
+ADH1B	addiction	dependence	25828809	Which alcohol use disorder criteria contribute to the association of <strong>ADH1B</strong> with alcohol <b>dependence</b>?
+ADH1B	drug	alcohol	25828809	In a genome wide association study (GWAS), we identified highly significant associations between two population specific functional variants in the <b>alcohol</b> dehydrogenase 1B gene (<strong>ADH1B</strong>) and AD in African Americans (AAs; rs2066702) and European Americans (EAs; rs1229984).
+ADH1B	drug	alcohol	25828809	Both <strong>ADH1B</strong> variants were associated with MaxDrinks, a measure of innate tolerance, and MaxDrinks mediated the associations between <strong>ADH1B</strong> and <b>alcohol</b> outcomes.
+ADH1B	drug	alcohol	25535445	The genes for <b>alcohol</b> metabolizing enzymes: <b>Alcohol</b> dehydrogenase (<strong>ADH2</strong> and ADH3) and aldehyde dehydrogenase (ALDH2) exhibit functional polymorphisms.
+ADH1B	drug	alcohol	25535445	To determine whether any association exists between polymorphisms of <strong>ADH2</strong>, ADH3 and ALDH2 and <b>alcohol</b> dependence syndrome in a group of Asian Indians.
+ADH1B	addiction	dependence	25535445	To determine whether any association exists between polymorphisms of <strong>ADH2</strong>, ADH3 and ALDH2 and alcohol <b>dependence</b> syndrome in a group of Asian Indians.
+ADH1B	drug	alcohol	25535445	Allele frequencies of <strong>ADH2</strong>*2 (0.50), ADH3*1 (0.67) and ALSH2*2 (0.09) were significantly low in the <b>alcohol</b> dependent subjects.
+ADH1B	drug	alcohol	25410943	The joint effects of <strong>ADH1B</strong> variants and childhood adversity on <b>alcohol</b> related phenotypes in African American and European American women and men.
+ADH1B	drug	alcohol	25410943	The <strong>ADH1B</strong> gene has consistently been implicated in problem drinking, but rarely incorporated into gene by environment investigations of <b>alcohol</b> phenotypes.
+ADH1B	drug	alcohol	25410943	This study examined the joint effects of variation in <strong>ADH1B</strong> and childhood adversity a well documented risk factor for <b>alcohol</b> problems and moderator of genetic liability to psychiatric outcomes on maximum drinks consumed in a 24 hour period (maxdrinks) and <b>alcohol</b> use disorder (AUD) symptoms.
+ADH1B	drug	alcohol	25410943	We tested the most significant <strong>ADH1B</strong> single nucleotide polymorphisms for <b>alcohol</b> dependence from a genomewide association study with this sample, <strong>ADH1B</strong> rs1229984 (Arg48His) and <strong>ADH1B</strong> rs2066702 (Arg370Cys), in EA and AA subsamples, respectively.
+ADH1B	addiction	dependence	25410943	We tested the most significant <strong>ADH1B</strong> single nucleotide polymorphisms for alcohol <b>dependence</b> from a genomewide association study with this sample, <strong>ADH1B</strong> rs1229984 (Arg48His) and <strong>ADH1B</strong> rs2066702 (Arg370Cys), in EA and AA subsamples, respectively.
+ADH1B	drug	alcohol	25257461	The functional variant rs1229984 in <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) has been associated at a genome wide level with <b>alcohol</b> use disorders in diverse adult populations.
+ADH1B	drug	alcohol	25208201	Regular male drinkers without <b>alcohol</b> dependence (n = 112) ages 18 25 years participated in <b>alcohol</b> challenge sessions consisting of placebo and two doses of <b>alcohol</b> (target BrAC: 0 g/dl for placebo, .04 g/dl low dose, and .08 g/dl high dose) and genotyped for variants in <strong>ADH1B</strong>*3 and ADH1C*2.
+ADH1B	addiction	dependence	25208201	Regular male drinkers without alcohol <b>dependence</b> (n = 112) ages 18 25 years participated in alcohol challenge sessions consisting of placebo and two doses of alcohol (target BrAC: 0 g/dl for placebo, .04 g/dl low dose, and .08 g/dl high dose) and genotyped for variants in <strong>ADH1B</strong>*3 and ADH1C*2.
+ADH1B	drug	alcohol	25208201	Higher responses on the SHAS items muddle/confused and nauseated were significantly associated with the presence of at least one <strong>ADH1B</strong>*3 allele following the high dose of <b>alcohol</b> in Afro T. Indo T with at least one ADH1C*2 allele displayed significantly different Drug × Time interactions for the SHAS item effects of <b>alcohol</b> at the low dose and for the SHAS items clumsy, muddle/confused, effects of <b>alcohol</b>, floating, drunk, and total at the high dose from Indo T with two ADH1C*1 alleles.
+ADH1B	drug	alcohol	25208201	In Afro T, having at least one <strong>ADH1B</strong>*3 allele appears to exert a protective effect by enhancing the unpleasant effects of <b>alcohol</b>, such as nausea and confusion.
+ADH1B	drug	alcohol	25085997	A multivariate analysis by the proportional odds model showed that the odds ratio (95% confidence interval) for an increase in ketosis by one category was 0.94 (0.84 1.06) per 10 year increase in age, 0.93 (0.89 0.97) per 1 day increase in interval since the last drink, 1.78 (1.41 2.26) in the presence of slow metabolizing <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>*1/*1), 1.61 (1.10 2.36) and 1.30 (1.03 1.65) when the beverage of choice was whiskey and shochu, respectively (distilled no carbohydrate beverages vs. the other beverages), 2.05 (1.27 3.32) in the presence of hypoglycemia <80 mg/dl, 0.91 (0.88 0.94) per 1 kg/m(2) increase in body mass index (BMI), 1.09 (1.00 1.18) per +10 cigarettes smoked, and 2.78 (2.05 3.75) when the serum total bilirubin level was ≥2.0 mg/dl, and 1.97 (1.47 2.66) when the serum AST level was ≥200 IU/l.
+ADH1B	drug	alcohol	25085997	Ketosis was a very common complication and frequently accompanied by <b>alcoholic</b> liver injury in our Japanese male <b>alcoholic</b> population, in which <strong>ADH1B</strong>*1/*1 genotype, consumption of whiskey or shochu, hypoglycemia, lower BMI and smoking were significant determinants of the development of ketosis.
+ADH1B	drug	nicotine	25085997	Ketosis was a very common complication and frequently accompanied by alcoholic liver injury in our Japanese male alcoholic population, in which <strong>ADH1B</strong>*1/*1 genotype, consumption of whiskey or shochu, hypoglycemia, lower BMI and <b>smoking</b> were significant determinants of the development of ketosis.
+ADH1B	drug	alcohol	25011450	To use the rs1229984 variant in the <b>alcohol</b> dehydrogenase 1B gene (<strong>ADH1B</strong>) as an instrument to investigate the causal role of <b>alcohol</b> in cardiovascular disease.
+ADH1B	drug	alcohol	25011450	Data were available on <strong>ADH1B</strong> rs1229984 variant, <b>alcohol</b> phenotypes, and cardiovascular biomarkers.
+ADH1B	drug	alcohol	25011450	Odds ratio for coronary heart disease and stroke associated with the <strong>ADH1B</strong> variant in all individuals and by categories of <b>alcohol</b> consumption.
+ADH1B	drug	alcohol	25011450	Carriers of the A allele of <strong>ADH1B</strong> rs1229984 consumed 17.2% fewer units of <b>alcohol</b> per week (95% confidence interval 15.6% to 18.9%), had a lower prevalence of binge drinking (odds ratio 0.78 (95% CI 0.73 to 0.84)), and had higher abstention (odds ratio 1.27 (1.21 to 1.34)) than non carriers.
+ADH1B	addiction	intoxication	25011450	Carriers of the A allele of <strong>ADH1B</strong> rs1229984 consumed 17.2% fewer units of alcohol per week (95% confidence interval 15.6% to 18.9%), had a lower prevalence of <b>binge</b> drinking (odds ratio 0.78 (95% CI 0.73 to 0.84)), and had higher abstention (odds ratio 1.27 (1.21 to 1.34)) than non carriers.
+ADH1B	drug	alcohol	25011450	The protective association of the <strong>ADH1B</strong> rs1229984 A allele variant remained the same across all categories of <b>alcohol</b> consumption (P=0.83 for heterogeneity).
+ADH1B	drug	alcohol	24797321	Effect of the allelic variant of <b>alcohol</b> dehydrogenase <strong>ADH1B</strong>*2 on <b>ethanol</b> metabolism.
+ADH1B	drug	alcohol	24797321	It has been known that <strong>ADH1B</strong>*2 allele has a protective effect against the development of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	24797321	It has been known that <strong>ADH1B</strong>*2 allele has a protective effect against the development of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	24797321	We investigated whether <strong>ADH1B</strong> gene polymorphism affects <b>ethanol</b> (EtOH) metabolism.
+ADH1B	drug	alcohol	24797321	In the case of acetaldehyde, the AUC0 4 and Cmax of acetaldehyde of <strong>ADH1B</strong>*2/*2 after administration of 0.25 g/kg <b>alcohol</b> and the AUC0 4 of acetaldehyde of <strong>ADH1B</strong>*2/*2 at 0.5 g/kg were significantly higher than corresponding values of <strong>ADH1B</strong>*1/*2 only in the group of ALDH2*1/*2.
+ADH1B	drug	alcohol	24797321	To our knowledge, this is the first report to demonstrate the association of <strong>ADH1B</strong>*2 allele with blood EtOH and acetaldehyde levels in humans, and these results suggest that higher blood EtOH and acetaldehyde concentrations in <strong>ADH1B</strong>*2/*2 may constitute the mechanism of protection against <b>alcoholism</b> by <strong>ADH1B</strong>*2/*2.
+ADH1B	drug	alcohol	24749767	Roles of the ALDH2 and <strong>ADH1B</strong> genotypes on the association between <b>alcohol</b> intake and serum adiponectin levels among Japanese male workers.
+ADH1B	drug	alcohol	24749767	Two genotypes in the <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) and aldehyde dehydrogenase 2 (ALDH2) genes were determined using blood sample.
+ADH1B	drug	alcohol	24749767	When we performed analyses separately for each genotype, high <b>alcohol</b> consumption was negatively associated with T Ad, HMW Ad, and LMW Ad levels only in those with <strong>ADH1B</strong> *2/*2.
+ADH1B	drug	alcohol	24749767	High <b>alcohol</b> consumption was inversely associated with T Ad, HMW Ad, and LMW Ad levels in those with <strong>ADH1B</strong> *2/*2 genotype, but not in those with the other <strong>ADH1B</strong> genotypes.
+ADH1B	drug	alcohol	24735490	Genetic variants in or near <strong>ADH1B</strong> and ADH1C affect susceptibility to <b>alcohol</b> dependence in a British and Irish population.
+ADH1B	addiction	dependence	24735490	Genetic variants in or near <strong>ADH1B</strong> and ADH1C affect susceptibility to alcohol <b>dependence</b> in a British and Irish population.
+ADH1B	drug	alcohol	24553426	We genotyped the rs1229984 G→A variant of the <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) gene, which is associated with lower prevalence of <b>alcohol</b> abuse and dependence.
+ADH1B	addiction	dependence	24553426	We genotyped the rs1229984 G→A variant of the alcohol dehydrogenase 1B (<strong>ADH1B</strong>) gene, which is associated with lower prevalence of alcohol abuse and <b>dependence</b>.
+ADH1B	drug	alcohol	24505444	We investigated six variants known to influence nicotine addiction or <b>alcohol</b> metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (<strong>ADH1B</strong>), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+ADH1B	drug	nicotine	24505444	We investigated six variants known to influence <b>nicotine</b> addiction or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (<strong>ADH1B</strong>), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+ADH1B	addiction	addiction	24505444	We investigated six variants known to influence nicotine <b>addiction</b> or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (<strong>ADH1B</strong>), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+ADH1B	drug	alcohol	24166409	We confirmed well known risk loci mapped to <b>alcohol</b> metabolizing enzyme genes, notably <strong>ADH1B</strong> (EAs: Arg48His, P=1.17 × 10( 31); AAs: Arg369Cys, P=6.33 × 10( 17)) and ADH1C in AAs (Thr151Thr, P=4.94 × 10( 10)), and identified novel risk loci mapping to the ADH gene cluster on chromosome 4 and extending centromerically beyond it to include GWS associations at LOC100507053 in AAs (P=2.63 × 10( 11)), PDLIM5 in EAs (P=2.01 × 10( 8)), and METAP in AAs (P=3.35 × 10( 8)).
+ADH1B	drug	alcohol	24018899	The triangular association of <strong>ADH1B</strong> genetic polymorphism, <b>alcohol</b> consumption and the risk of depression in older men.
+ADH1B	drug	alcohol	24018899	Given the logistic and ethical constraints that would be associated with a trial of <b>alcohol</b> use to prevent depression, we aimed to complete a Mendelian randomization study to determine if a genetic polymorphism associated with <b>alcohol</b> abuse and dependence (<strong>ADH1B</strong> rs1229984 G  >A) contributed to modulate the risk of depression in a community derived cohort of older men.
+ADH1B	addiction	dependence	24018899	Given the logistic and ethical constraints that would be associated with a trial of alcohol use to prevent depression, we aimed to complete a Mendelian randomization study to determine if a genetic polymorphism associated with alcohol abuse and <b>dependence</b> (<strong>ADH1B</strong> rs1229984 G  >A) contributed to modulate the risk of depression in a community derived cohort of older men.
+ADH1B	drug	alcohol	23794556	A Mendelian randomization approach was used to estimate the association between maternal genotype and offspring balance using the non synonymous variant rs1229984*A (<strong>ADH1B</strong>) to proxy for lower maternal <b>alcohol</b> consumption; no strong associations were found between this genotype/proxy and offspring balance.
+ADH1B	drug	alcohol	23712313	Some of these genes have been identified, including two genes involved in the metabolism of <b>alcohol</b> (<strong>ADH1B</strong> and ALDH2) that have the strongest known affects on the risk of <b>alcoholism</b>.
+ADH1B	drug	alcohol	23468174	Humans express at least seven <b>alcohol</b> dehydrogenase (ADH) isoforms that are encoded by ADH gene cluster (ADH7 ADH1C <strong>ADH1B</strong> ADH1A ADH6 ADH4 ADH5) at chromosome 4.
+ADH1B	drug	alcohol	23414439	Genetic polymorphisms of <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) and aldehyde dehydrogenase 2 (ALDH2) affect susceptibility to <b>alcoholism</b> and may affect body weight via gene associated differences in fuel utilization in <b>alcoholics</b>.
+ADH1B	drug	alcohol	23414439	We evaluated associations between <strong>ADH1B</strong>/ALDH2 genotypes and the body weight and body mass index (BMI) of 1,301 Japanese <b>alcoholic</b> men at the time of their first visit to an addiction center.
+ADH1B	addiction	addiction	23414439	We evaluated associations between <strong>ADH1B</strong>/ALDH2 genotypes and the body weight and body mass index (BMI) of 1,301 Japanese alcoholic men at the time of their first visit to an <b>addiction</b> center.
+ADH1B	drug	nicotine	23414439	The body weight and BMI values showed that the <strong>ADH1B</strong>*2/*2 and *1/*2 carriers (n = 939) were significantly leaner than the <strong>ADH1B</strong>*1/*1 carriers (n = 362) irrespective of age, drinking, <b>smoking</b>, and dietary habits.
+ADH1B	drug	alcohol	23414439	A multivariate analysis showed that BMI decreased by 0.35 per 10 year increase in age, by 1.73 in the presence of the <strong>ADH1B</strong>*2 allele, by 1.55 when the preferred beverage was whiskey, and by 0.19 per +10 cigarettes/d and that it increased by 0.10 per +22 g <b>ethanol</b> (EtOH)/d and by 0.41 per increase in category of frequency of milk intake (every day, occasionally, rarely, and never).
+ADH1B	drug	alcohol	23414439	The increase in BMI as <b>alcohol</b> consumption increased was significantly smaller in the <strong>ADH1B</strong>*2 group than in the <strong>ADH1B</strong>*1/*1 group (p = 0.002).
+ADH1B	drug	alcohol	23414439	<strong>ADH1B</strong> genotype was a strong determinant of body weight in the <b>alcoholics</b>.
+ADH1B	drug	alcohol	23414439	The more rapid EtOH elimination associated with the <strong>ADH1B</strong>*2 allele may result in less efficient utilization of EtOH as an energy source in <b>alcoholics</b>.
+ADH1B	drug	opioid	23266708	The <strong>ADH1B</strong> and DRD2 gene polymorphism may modify the protective effect of the ALDH2 gene against <b>heroin</b> dependence.
+ADH1B	addiction	dependence	23266708	The <strong>ADH1B</strong> and DRD2 gene polymorphism may modify the protective effect of the ALDH2 gene against heroin <b>dependence</b>.
+ADH1B	drug	alcohol	23266708	Understanding the influences of genes involved in dopamine and serotonin metabolism, such as the aldehyde dehydrogenase 2 (ALDH2) and <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) genes, is critical for understanding addictive behavior.
+ADH1B	addiction	addiction	23266708	Understanding the influences of genes involved in dopamine and serotonin metabolism, such as the aldehyde dehydrogenase 2 (ALDH2) and alcohol dehydrogenase 1B (<strong>ADH1B</strong>) genes, is critical for understanding <b>addictive</b> behavior.
+ADH1B	drug	opioid	23266708	Therefore, we investigated the association between the ALDH2, <strong>ADH1B</strong> and DRD2 polymorphisms and <b>heroin</b> dependence.
+ADH1B	addiction	dependence	23266708	Therefore, we investigated the association between the ALDH2, <strong>ADH1B</strong> and DRD2 polymorphisms and heroin <b>dependence</b>.
+ADH1B	drug	opioid	23266708	The frequency of the ALDH2*1/*1 genotype was significantly lower in <b>heroin</b> dependent patients than in controls, but the frequency of <strong>ADH1B</strong> and DRD2 genotypes was not significantly different.
+ADH1B	drug	opioid	23266708	The ALDH2*1/*1, <strong>ADH1B</strong>*1/*1, and <strong>ADH1B</strong>*1/*2 genotypes may interact and protect their carriers against <b>heroin</b> dependence and the protective effect may be varied by the DRD2 gene polymorphism.
+ADH1B	addiction	dependence	23266708	The ALDH2*1/*1, <strong>ADH1B</strong>*1/*1, and <strong>ADH1B</strong>*1/*2 genotypes may interact and protect their carriers against heroin <b>dependence</b> and the protective effect may be varied by the DRD2 gene polymorphism.
+ADH1B	drug	opioid	23266708	We conclude that the protective effect of the ALDH2 polymorphism against <b>heroin</b> dependence may be modified by the <strong>ADH1B</strong> and DRD2 polymorphism.
+ADH1B	addiction	dependence	23266708	We conclude that the protective effect of the ALDH2 polymorphism against heroin <b>dependence</b> may be modified by the <strong>ADH1B</strong> and DRD2 polymorphism.
+ADH1B	drug	alcohol	23134050	For example, certain <strong>ADH1B</strong> and ADH1C variants that are commonly found in East Asian populations lead to more rapid <b>ethanol</b> breakdown and acetaldehyde accumulation in the body.
+ADH1B	drug	alcohol	23134043	The key findings of the earlier studies were that variations (i.e., polymorphisms) in the DNA sequences of the genes encoding <b>alcohol</b> dehydrogenase 1B (i.e., the <strong>ADH1B</strong> gene), aldehyde dehydrogenase 2 (i.e., the ALDH2 gene), and other <b>alcohol</b> metabolizing enzymes mediate the risk for <b>alcoholism</b>; moreover, these polymorphisms also have an impact on the risk of <b>alcohol</b> related cancers, such as esophageal cancer.
+ADH1B	drug	alcohol	23019235	<strong>ADH1B</strong>*2, <strong>ADH1B</strong>*3 and ADH1C*2) that significantly affect the risk of <b>alcohol</b> dependence are rare variants in most populations.
+ADH1B	addiction	dependence	23019235	<strong>ADH1B</strong>*2, <strong>ADH1B</strong>*3 and ADH1C*2) that significantly affect the risk of alcohol <b>dependence</b> are rare variants in most populations.
+ADH1B	drug	alcohol	22931071	Associations between <b>alcohol</b> dependence and polymorphisms in <strong>ADH1B</strong>, ADH1C, and ALDH2 were compared in a community sample of Native Americans (n 791) living on reservations and Mexican Americans (n 391) living within the same county.
+ADH1B	addiction	dependence	22931071	Associations between alcohol <b>dependence</b> and polymorphisms in <strong>ADH1B</strong>, ADH1C, and ALDH2 were compared in a community sample of Native Americans (n 791) living on reservations and Mexican Americans (n 391) living within the same county.
+ADH1B	drug	alcohol	22931071	Presence of at least one <strong>ADH1B</strong>*2 allele was found in 7% of the Native Americans and 13% of the Mexican Americans, but was only associated with protection against <b>alcohol</b> dependence in the Mexican Americans.
+ADH1B	addiction	dependence	22931071	Presence of at least one <strong>ADH1B</strong>*2 allele was found in 7% of the Native Americans and 13% of the Mexican Americans, but was only associated with protection against alcohol <b>dependence</b> in the Mexican Americans.
+ADH1B	drug	alcohol	22931071	Presence of at least one <strong>ADH1B</strong>*3 allele was found in 4% of the Native Americans and 2% of the Mexican Americans, but was associated with protection against <b>alcohol</b> dependence only in the Native Americans.
+ADH1B	addiction	dependence	22931071	Presence of at least one <strong>ADH1B</strong>*3 allele was found in 4% of the Native Americans and 2% of the Mexican Americans, but was associated with protection against alcohol <b>dependence</b> only in the Native Americans.
+ADH1B	drug	alcohol	22931071	Polymorphisms in <strong>ADH1B</strong> are protective against <b>alcoholism</b> in these two populations; however, these findings do not explain the high prevalence of <b>alcoholism</b> in these populations.
+ADH1B	drug	alcohol	22640768	A few well validated, specific predictors such as OPRM1, <strong>ADH1B</strong>, ALDH2, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand <b>alcohol</b> related flushing and upper GI cancer risk (<strong>ADH1B</strong> and AKLDH2), variation in nicotine metabolism (CYP26), and, potentially, <b>naltrexone</b> treatment response (OPRM1).
+ADH1B	drug	nicotine	22640768	A few well validated, specific predictors such as OPRM1, <strong>ADH1B</strong>, ALDH2, CHRNA5, and CYP26 have been identified and can provide some specific guidance, for example, to understand alcohol related flushing and upper GI cancer risk (<strong>ADH1B</strong> and AKLDH2), variation in <b>nicotine</b> metabolism (CYP26), and, potentially, naltrexone treatment response (OPRM1).
+ADH1B	drug	alcohol	22331481	For the <strong>ADH1B</strong> gene, there were statistically significant associations between all levels of <b>alcohol</b> intake and risk of breast cancer (all OR > 1.34 and all lower CI > 1.01), while for women with the GA or AA genotype, there were no significant associations between <b>alcohol</b> intake and risk of breast cancer.
+ADH1B	drug	alcohol	22150722	<strong>ADH1B</strong> polymorphism, <b>alcohol</b> consumption, and binge drinking in Slavic Caucasians: results from the Czech HAPIEE study.
+ADH1B	addiction	intoxication	22150722	<strong>ADH1B</strong> polymorphism, alcohol consumption, and <b>binge</b> drinking in Slavic Caucasians: results from the Czech HAPIEE study.
+ADH1B	drug	alcohol	22150722	We have analyzed the effect of the Arg47His (rs1229984) variant within the <b>alcohol</b> dehydrogenase (<strong>ADH1B</strong>) gene on a range of drinking related variables in a large Eastern European Slavic population (Czech HAPIEE study), which recruited random samples of men and women aged 45 69 years in 7 Czech towns (3,016 males and 3,481 females with complete data).
+ADH1B	addiction	intoxication	22150722	The <strong>ADH1B</strong> genotype was associated with the frequency and volume of drinking but its associations with <b>binge</b> drinking and problem drinking were less consistent.
+ADH1B	drug	alcohol	22048268	Combined effect of <strong>ADH1B</strong> RS1229984, RS2066702 and ADH1C RS1693482/ RS698 alleles on <b>alcoholism</b> and chronic liver diseases.
+ADH1B	drug	alcohol	22048268	The aim of this study was to analyze the combined effect of the most frequent <b>alcohol</b> dehydrogenase polymorphisms (Arg48His and Arg370Cys in <strong>ADH1B</strong>, Arg272Gln and Ile350Val in ADH1C) on the <b>alcohol</b> use habits, <b>alcohol</b> dependence and chronic liver diseases in Hungary.
+ADH1B	addiction	dependence	22048268	The aim of this study was to analyze the combined effect of the most frequent alcohol dehydrogenase polymorphisms (Arg48His and Arg370Cys in <strong>ADH1B</strong>, Arg272Gln and Ile350Val in ADH1C) on the alcohol use habits, alcohol <b>dependence</b> and chronic liver diseases in Hungary.
+ADH1B	drug	alcohol	21968928	<strong>ADH1B</strong> is associated with <b>alcohol</b> dependence and <b>alcohol</b> consumption in populations of European and African ancestry.
+ADH1B	addiction	dependence	21968928	<strong>ADH1B</strong> is associated with alcohol <b>dependence</b> and alcohol consumption in populations of European and African ancestry.
+ADH1B	drug	alcohol	21968928	A coding variant in <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) (rs1229984) that leads to the replacement of Arg48 with His48 is common in Asian populations and reduces their risk for <b>alcoholism</b>, but because of very low allele frequencies the effects in European or African populations have been difficult to detect.
+ADH1B	drug	alcohol	21848961	Gender differences in the effects of <strong>ADH1B</strong> and ALDH2 polymorphisms on <b>alcoholism</b>.
+ADH1B	drug	alcohol	21848961	Polymorphisms of <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) and aldehyde dehydrogenase 2 (ALDH2) are strong genetic determinants of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	21848961	Polymorphisms of alcohol dehydrogenase 1B (<strong>ADH1B</strong>) and aldehyde dehydrogenase 2 (ALDH2) are strong genetic determinants of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	21848961	This study aimed to clarify gender differences in the effects of <strong>ADH1B</strong> and ALDH2 polymorphism on the development of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	21848961	This study aimed to clarify gender differences in the effects of <strong>ADH1B</strong> and ALDH2 polymorphism on the development of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	21848961	The prevalence of comorbid psychiatric disorders, including major depression, eating disorder, panic disorder, and borderline personality disorder, was significantly higher in female <b>alcoholics</b> with inactive ALDH2 or superactive <strong>ADH1B</strong> than in those with active ALDH2 or normal <strong>ADH1B</strong>.
+ADH1B	drug	alcohol	21635275	No evidence for association with the <b>alcohol</b> dependence diagnosis was observed, but an SNP in exon 9 of <strong>ADH1B</strong> (rs2066702; <strong>ADH1B</strong>*3) and an SNP at the 5' end of ADH4 (rs3762894) showed significant evidence of association with the presence of withdrawal symptoms (p = 0.0018 and 0.0012, respectively).
+ADH1B	addiction	dependence	21635275	No evidence for association with the alcohol <b>dependence</b> diagnosis was observed, but an SNP in exon 9 of <strong>ADH1B</strong> (rs2066702; <strong>ADH1B</strong>*3) and an SNP at the 5' end of ADH4 (rs3762894) showed significant evidence of association with the presence of withdrawal symptoms (p = 0.0018 and 0.0012, respectively).
+ADH1B	addiction	withdrawal	21635275	No evidence for association with the alcohol dependence diagnosis was observed, but an SNP in exon 9 of <strong>ADH1B</strong> (rs2066702; <strong>ADH1B</strong>*3) and an SNP at the 5' end of ADH4 (rs3762894) showed significant evidence of association with the presence of <b>withdrawal</b> symptoms (p = 0.0018 and 0.0012, respectively).
+ADH1B	drug	alcohol	21635275	These results suggest that variants in the <strong>ADH1B</strong> and ADH4 genes may be protective against the development of some symptoms associated with <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	21635275	These results suggest that variants in the <strong>ADH1B</strong> and ADH4 genes may be protective against the development of some symptoms associated with alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	21497796	Strong association of the <b>alcohol</b> dehydrogenase 1B gene (<strong>ADH1B</strong>) with <b>alcohol</b> dependence and <b>alcohol</b> induced medical diseases.
+ADH1B	addiction	dependence	21497796	Strong association of the alcohol dehydrogenase 1B gene (<strong>ADH1B</strong>) with alcohol <b>dependence</b> and alcohol induced medical diseases.
+ADH1B	drug	alcohol	21497796	The <b>alcohol</b> dehydrogenase 1B gene (<strong>ADH1B</strong>) is hypothesized to affect predisposition to <b>alcohol</b> dependence (AD) and abuse.
+ADH1B	addiction	dependence	21497796	The alcohol dehydrogenase 1B gene (<strong>ADH1B</strong>) is hypothesized to affect predisposition to alcohol <b>dependence</b> (AD) and abuse.
+ADH1B	drug	alcohol	21497796	A variant of the <strong>ADH1B</strong> gene (rs1229984 or Arg48His; previously referred to as Arg [*1] and His [*1]) has been reported to be associated with reduced rates of <b>alcohol</b> and drug dependence.
+ADH1B	addiction	dependence	21497796	A variant of the <strong>ADH1B</strong> gene (rs1229984 or Arg48His; previously referred to as Arg [*1] and His [*1]) has been reported to be associated with reduced rates of alcohol and drug <b>dependence</b>.
+ADH1B	drug	alcohol	21497796	Our findings provide further strong evidence for the involvement of the <strong>ADH1B</strong> gene in the pathogenesis of <b>alcohol</b> dependence and abuse as well as for some <b>alcohol</b> induced medical diseases in the multiple ethnic populations  in particular, certain Asian populations.
+ADH1B	addiction	dependence	21497796	Our findings provide further strong evidence for the involvement of the <strong>ADH1B</strong> gene in the pathogenesis of alcohol <b>dependence</b> and abuse as well as for some alcohol induced medical diseases in the multiple ethnic populations  in particular, certain Asian populations.
+ADH1B	drug	alcohol	20958327	The DNA damage induced by <b>ethanol</b> could be attenuated by <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) or acetaldehyde dehydrogenase 2 (ALDH2) inhibitor, and the mRNA expression levels of <strong>ADH1B</strong> and ALDH2 were increased markedly by <b>ethanol</b>.
+ADH1B	drug	alcohol	20958327	This study provides direct evidence that <b>ethanol</b> can induce oxidative DNA damage in human peripheral lymphocytes in vitro, and its mechanism may be associated with the metabolism of <b>ethanol</b> by the <strong>ADH1B</strong>/ALDH2 pathway.
+ADH1B	drug	alcohol	20714161	We develop a pharmacokinetic model describing how genetic variations in <strong>ADH1B</strong>, ADH1C, ADH7, ALDH2, and TAS2R38 affect consumption behavior, and <b>alcohol</b> and acetaldehyde levels over time in various tissues of individuals with a particular genotype to predict their susceptibility to <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	20714161	We develop a pharmacokinetic model describing how genetic variations in <strong>ADH1B</strong>, ADH1C, ADH7, ALDH2, and TAS2R38 affect consumption behavior, and alcohol and acetaldehyde levels over time in various tissues of individuals with a particular genotype to predict their susceptibility to alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	20700531	Significant interactions were observed between <b>alcohol</b> and <strong>ADH1b</strong> (rs1229984) with respect to LDL and between <b>alcohol</b> and ALDH2 (rs886205) with respect to IGT/diabetes.
+ADH1B	drug	alcohol	20626721	While the rs1800759 and rs1042364 A A haplotype had a potential protective influence on the risk for several AD related phenotypes, this effect is rather small compared to functional variants of other <b>alcohol</b> or acetaldehyde metabolizing enzymes like ALDH2*2 or <strong>ADH1B</strong>*2.
+ADH1B	drug	alcohol	20598484	The genetic variation of <strong>ADH1B</strong>, ALDH2, and CYP2E1 is different among racial populations and cause difference in elimination rates of <b>alcohol</b>.
+ADH1B	drug	alcohol	20598484	This study may be useful in epidemiological studies of the influence of <strong>ADH1B</strong>, ALDH2, CYP2E1*6, and CYP2E1*7B polymorphisms on diseases, including several types of cancer related to <b>alcohol</b> consumption and <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	20598484	This study may be useful in epidemiological studies of the influence of <strong>ADH1B</strong>, ALDH2, CYP2E1*6, and CYP2E1*7B polymorphisms on diseases, including several types of cancer related to alcohol consumption and alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	20477764	<strong>ADH1B</strong>*3 and response to <b>alcohol</b> in African Americans.
+ADH1B	drug	alcohol	20477764	One variant, <strong>ADH1B</strong>*3, is observed almost exclusively in populations of African ancestry and has been shown to be associated with reduced rates of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	20477764	One variant, <strong>ADH1B</strong>*3, is observed almost exclusively in populations of African ancestry and has been shown to be associated with reduced rates of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	20477764	We conducted an <b>alcohol</b> challenge study to test whether <strong>ADH1B</strong>*3 is associated with differences in subjective and physiological response to <b>alcohol</b>.
+ADH1B	drug	alcohol	20477764	Participants were genotyped for <strong>ADH1B</strong>, as well as additional polymorphisms that might contribute to <b>alcohol</b> response.
+ADH1B	drug	alcohol	20477764	<strong>ADH1B</strong>*3 was associated with higher levels of sedation and a sharper increase in pulse rate immediately following <b>alcohol</b> consumption.
+ADH1B	drug	alcohol	20477764	These findings suggest that the lower rates of <b>alcohol</b> dependence in those with <strong>ADH1B</strong>*3 alleles may be because of differences in <b>alcohol</b> response, particularly increased sedation.
+ADH1B	addiction	dependence	20477764	These findings suggest that the lower rates of alcohol <b>dependence</b> in those with <strong>ADH1B</strong>*3 alleles may be because of differences in alcohol response, particularly increased sedation.
+ADH1B	drug	alcohol	20401433	The purpose of this study was to investigate the differences, if present, in the allele and genotype frequency of <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>), ADH1C and the microsomal <b>ethanol</b> oxidizing system (MEOS/CYP2E1) between <b>alcohol</b> dependent individuals and controls and also to determine if these genotypes cause a difference in the age at which the patients become <b>alcohol</b> dependent.
+ADH1B	drug	alcohol	20401433	The allele and genotype frequencies of <strong>ADH1B</strong>, ADH1C, and CYP2E1 were determined in 204 <b>alcohol</b> dependent men and 172 healthy volunteers who do not drink <b>alcohol</b> (control group).
+ADH1B	drug	alcohol	20401433	<strong>ADH1B</strong>*1 (99.3%) and ADH1C*1 (62.5%) alleles and <strong>ADH1B</strong>*1/*1 (N = 201) and ADH1C*1/*1 (N = 85) genotypes were statistically more frequent among <b>alcohol</b> dependent subjects than among controls (99.3 and 62.5%, N = 201 and 85 vs 94.5 and 40.7%, N = 153 and 32, respectively).
+ADH1B	drug	alcohol	20401433	In the Polish men examined, ADH1C*1 and <strong>ADH1B</strong>*1 alleles and ADH1C*1/*1 and <strong>ADH1B</strong>*1/*1 genotypes favor <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	20401433	In the Polish men examined, ADH1C*1 and <strong>ADH1B</strong>*1 alleles and ADH1C*1/*1 and <strong>ADH1B</strong>*1/*1 genotypes favor alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	20401433	The <strong>ADH1B</strong>*2 allele may protect from <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	20401433	The <strong>ADH1B</strong>*2 allele may protect from alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	20357489	The fast metabolizing allele of the <strong>ADH1b</strong> polymorphism was significantly associated with CCD sensitization in <b>alcohol</b> drinkers.
+ADH1B	addiction	sensitization	20357489	The fast metabolizing allele of the <strong>ADH1b</strong> polymorphism was significantly associated with CCD <b>sensitization</b> in alcohol drinkers.
+ADH1B	drug	alcohol	20357489	The observed association between the <strong>ADH1b</strong> polymorphism and CCD sensitization may support that <b>alcohol</b> is causally related to the risk of CCD sensitization.
+ADH1B	addiction	sensitization	20357489	The observed association between the <strong>ADH1b</strong> polymorphism and CCD <b>sensitization</b> may support that alcohol is causally related to the risk of CCD <b>sensitization</b>.
+ADH1B	drug	alcohol	20077761	The genotype frequencies of the <strong>ADH2</strong> and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu opioid receptor gene (OPRM1) in Korean men and women with <b>alcohol</b> dependence (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for <b>alcoholism</b>.
+ADH1B	drug	opioid	20077761	The genotype frequencies of the <strong>ADH2</strong> and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu <b>opioid</b> receptor gene (OPRM1) in Korean men and women with alcohol dependence (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for alcoholism.
+ADH1B	addiction	dependence	20077761	The genotype frequencies of the <strong>ADH2</strong> and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu opioid receptor gene (OPRM1) in Korean men and women with alcohol <b>dependence</b> (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for alcoholism.
+ADH1B	drug	alcohol	20077761	These results suggest that, while the risk of <b>alcoholism</b> in Korean men is predominantly affected by the presence of the ALDH2 1/1 genotype, the risk of <b>alcoholism</b> in Korean women is primarily associated with the <strong>ADH2</strong> 1/1 genotype and G carrier genotype of the OPRM1 A118G polymorphism.
+ADH1B	drug	alcohol	20025435	The association between two functional polymorphisms in <b>alcohol</b> dehydrogenase (ADH2/<strong>ADH1B</strong>) and aldehyde dehydrogenase (ALDH2) genes and <b>alcohol</b> dependence was examined in 182 Chinese and Indian patients undergoing treatment for <b>alcohol</b> dependence and 184 screened control subjects from Singapore.
+ADH1B	addiction	dependence	20025435	The association between two functional polymorphisms in alcohol dehydrogenase (ADH2/<strong>ADH1B</strong>) and aldehyde dehydrogenase (ALDH2) genes and alcohol <b>dependence</b> was examined in 182 Chinese and Indian patients undergoing treatment for alcohol <b>dependence</b> and 184 screened control subjects from Singapore.
+ADH1B	drug	alcohol	20025435	The association between two functional polymorphisms in <b>alcohol</b> dehydrogenase (<strong>ADH2</strong>/<strong>ADH1B</strong>) and aldehyde dehydrogenase (ALDH2) genes and <b>alcohol</b> dependence was examined in 182 Chinese and Indian patients undergoing treatment for <b>alcohol</b> dependence and 184 screened control subjects from Singapore.
+ADH1B	addiction	dependence	20025435	The association between two functional polymorphisms in alcohol dehydrogenase (<strong>ADH2</strong>/<strong>ADH1B</strong>) and aldehyde dehydrogenase (ALDH2) genes and alcohol <b>dependence</b> was examined in 182 Chinese and Indian patients undergoing treatment for alcohol <b>dependence</b> and 184 screened control subjects from Singapore.
+ADH1B	drug	alcohol	20025435	Our results showed that frequencies of <strong>ADH1B</strong>*2 and ALDH2*2 were higher in controls compared to <b>alcohol</b> dependent subjects for both Chinese and Indians.
+ADH1B	drug	alcohol	19403456	Association of <strong>ADH1B</strong> and ALDH2 gene polymorphisms with <b>alcohol</b> dependence: a pilot study from India.
+ADH1B	addiction	dependence	19403456	Association of <strong>ADH1B</strong> and ALDH2 gene polymorphisms with alcohol <b>dependence</b>: a pilot study from India.
+ADH1B	drug	alcohol	19193628	Alleles of ADH7 SNPs were associated with the early stages of <b>alcohol</b> metabolism, with additional effects in the ADH1A, <strong>ADH1B</strong> and ADH4 regions.
+ADH1B	drug	alcohol	19014920	Functional variant alleles <strong>ADH1B</strong>*2 and ALDH2*2 have been consistently replicated to show protection against developing <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	19014920	Functional variant alleles <strong>ADH1B</strong>*2 and ALDH2*2 have been consistently replicated to show protection against developing alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	19014920	Multiple logistic regression analyses suggest that <strong>ADH1B</strong>*2 and ALDH2*2 may independently influence the risk for <b>alcoholism</b>.
+ADH1B	drug	alcohol	19014920	Correlations of blood <b>ethanol</b> and acetaldehyde concentrations, cardiovascular hemodynamic responses, and subjective perceptions have been investigated in men with different combinatorial <strong>ADH1B</strong> and ALDH2 genotypes following challenge with <b>ethanol</b> for a period of 130 min.
+ADH1B	addiction	dependence	18996923	There were study wide significant associations (P<2.3 x 10( 4)) between <strong>ADH1B</strong> Arg48His (rs1229984) and flushing and consumption, but only nominally significant associations (P<0.01) with <b>dependence</b>.
+ADH1B	drug	alcohol	18996923	After controlling for rs1229984, an independent association was observed between rs1042026 (<strong>ADH1B</strong>) and <b>alcohol</b> intake (P=4.7 x 10( 5)) and suggestive associations (P<0.001) between <b>alcohol</b> consumption phenotypes and rs1693482 (ADH1C), rs1230165 (ADH5) and rs3762894 (ADH4).
+ADH1B	drug	alcohol	18996923	These results bridge the gap between DNA sequence variation and <b>alcohol</b> related behavior, confirming that the <strong>ADH1B</strong> Arg48His polymorphism affects both <b>alcohol</b> related flushing in Europeans and <b>alcohol</b> intake.
+ADH1B	drug	alcohol	18299763	Variant alleles of aldehyde dehydrogenase (ALDH2) and <b>alcohol</b> dehydrogenase (<strong>ADH1B</strong>) genes are prevalent in individuals of Asian heritage and have been associated with an increased level of response to <b>alcohol</b> and a decreased risk for <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	18299763	Variant alleles of aldehyde dehydrogenase (ALDH2) and alcohol dehydrogenase (<strong>ADH1B</strong>) genes are prevalent in individuals of Asian heritage and have been associated with an increased level of response to alcohol and a decreased risk for alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	18299763	The current study examined self report level of response to <b>alcohol</b>, ALDH2 and <strong>ADH1B</strong>, country of origin, and family history of <b>alcoholism</b> in 154 Chinese  and 181 Korean American college students.
+ADH1B	drug	alcohol	18299763	This relationship remained significant after considering the effects of gender, height, weight, quantity and frequency of <b>alcohol</b> consumption (over the previous 90 days), ALDH2 genotype, <strong>ADH1B</strong> genotype, country of origin, and first degree family history of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	18299763	This relationship remained significant after considering the effects of gender, height, weight, quantity and frequency of alcohol consumption (over the previous 90 days), ALDH2 genotype, <strong>ADH1B</strong> genotype, country of origin, and first degree family history of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	17885622	The subjects were divided into 3 combinatorial genotypic groups of <b>alcohol</b> dehydrogenase (ADH) and ALDH, that is, ALDH2*1/*1 <strong>ADH1B</strong>*1/*1 ADH1C*1/*1 (n=8), ALDH2*1/*1 <strong>ADH1B</strong>*2/*2 ADH1C*1/*1 (n=8), and ALDH2*1/*2 <strong>ADH1B</strong>*2/*2 ADH1C*1/*1 (n=16).
+ADH1B	drug	alcohol	17718398	Studies have demonstrated that a certain variant of the gene encoding <strong>ADH1B</strong> (<strong>ADH1B</strong>*3) is associated with a reduced risk of <b>alcoholism</b> in Afro Trinidadians, as is a variant of the gene encoding ADH1C (i.e., ADH1C*1) in Indo Trinidadians.
+ADH1B	drug	alcohol	17718397	Variants of three genes encoding <b>alcohol</b> metabolizing enzymes, the aldehyde dehydrogenase gene ALDH2 and the <b>alcohol</b> dehydrogenase genes <strong>ADH1B</strong> and ADH1C, have been associated with reduced rates of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	17718397	Variants of three genes encoding alcohol metabolizing enzymes, the aldehyde dehydrogenase gene ALDH2 and the alcohol dehydrogenase genes <strong>ADH1B</strong> and ADH1C, have been associated with reduced rates of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	17454860	We determined the allele and genotype of <strong>ADH2</strong>, ADH3 and ALDH2 in 198 subjects: 57 with <b>alcohol</b> cirrhosis, 44 with <b>alcohol</b> chronic pancreatitis and 43 "healthy <b>alcoholics</b>"; 54 healthy non drinkers served as controls.
+ADH1B	drug	alcohol	17454860	The <strong>ADH2</strong>*1 and the ADH3*1 alleles were statistically more common among patients who abuse <b>alcohol</b> in comparison with the controls.
+ADH1B	drug	alcohol	17454860	The <strong>ADH2</strong>*2 allele was not detected in any of the patients with chronic <b>alcohol</b> pancreatitis.
+ADH1B	drug	alcohol	17454860	The <strong>ADH2</strong>*1/*1 and the ADH3*1/*1 genotypes were statistically significantly more common among the patients who abuse <b>alcohol</b> than in the control group.
+ADH1B	drug	alcohol	17250612	Two of the class I <b>alcohol</b> dehydrogenase (ADH) genes located on chromosome 4 (<strong>ADH1B</strong> and ADH1C) encode for multiple isozymes that differ in their kinetic properties.
+ADH1B	drug	alcohol	17250612	<strong>ADH1B</strong>(*)2 (found mostly in individuals of East Asian and Jewish descent) and <strong>ADH1B</strong>(*)3 (found mostly in individuals of African decent) alleles encode for a more active enzyme variants than <strong>ADH1B</strong>(*)1 and the presence of these alleles has been associated with protection from <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	17250612	<strong>ADH1B</strong>(*)2 (found mostly in individuals of East Asian and Jewish descent) and <strong>ADH1B</strong>(*)3 (found mostly in individuals of African decent) alleles encode for a more active enzyme variants than <strong>ADH1B</strong>(*)1 and the presence of these alleles has been associated with protection from alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	17250612	The specific aim of the study was to investigate the associations between <strong>ADH1B</strong> alleles and <b>alcohol</b> dependence, drinking history, and liver function in individuals from the 2 major ethnic groups of Trinidad (individuals of African and East Indian ancestry).
+ADH1B	addiction	dependence	17250612	The specific aim of the study was to investigate the associations between <strong>ADH1B</strong> alleles and alcohol <b>dependence</b>, drinking history, and liver function in individuals from the 2 major ethnic groups of Trinidad (individuals of African and East Indian ancestry).
+ADH1B	drug	alcohol	17250612	African participants with at least 1 <strong>ADH1B</strong>(*)3 allele were found to be significantly less likely to be <b>alcohol</b> dependent (p<0.018), and to have lower <b>alcohol</b> consumption levels (p<0.05).
+ADH1B	drug	alcohol	17250612	Among those participants who were <b>alcohol</b> dependent, <strong>ADH1B</strong>(*)3 was associated with significantly higher levels of ALT (p<0.05).
+ADH1B	drug	alcohol	17250612	This study suggests, in this sample of Trinidadians, that the <strong>ADH1B</strong>(*)3 allele is associated with protection from the development of <b>alcoholism</b> but is also associated with enhanced risk for elevated serum ALT levels in those individuals who do become <b>alcohol</b> dependent.
+ADH1B	drug	alcohol	17180580	Previous studies have found that a variant of the <b>alcohol</b> dehydrogenase (ADH) gene (<strong>ADH1B</strong>*47His) is associated with protection against <b>alcohol</b> dependence in Māori.
+ADH1B	addiction	dependence	17180580	Previous studies have found that a variant of the alcohol dehydrogenase (ADH) gene (<strong>ADH1B</strong>*47His) is associated with protection against alcohol <b>dependence</b> in Māori.
+ADH1B	drug	alcohol	17180580	We analysed nine single nucleotide polymorphisms (SNPs) spanning a 500 kb region on chromosome 4q surrounding the <strong>ADH1B</strong> variant and several other <b>alcohol</b> metabolising genes (ADH 4, 5, 6, 7).
+ADH1B	drug	alcohol	17134660	This study sought to determine whether an association exists between ADH (ADH1C previously ADH3, <strong>ADH1B</strong>*2 previously ADH2*2) genotypes, <b>alcohol</b> dependence, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH1B	addiction	dependence	17134660	This study sought to determine whether an association exists between ADH (ADH1C previously ADH3, <strong>ADH1B</strong>*2 previously ADH2*2) genotypes, alcohol <b>dependence</b>, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH1B	drug	alcohol	17134660	This study sought to determine whether an association exists between ADH (ADH1C previously ADH3, <strong>ADH1B</strong>*2 previously <strong>ADH2</strong>*2) genotypes, <b>alcohol</b> dependence, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH1B	addiction	dependence	17134660	This study sought to determine whether an association exists between ADH (ADH1C previously ADH3, <strong>ADH1B</strong>*2 previously <strong>ADH2</strong>*2) genotypes, alcohol <b>dependence</b>, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH1B	drug	alcohol	17134660	Only three individuals had an <strong>ADH1B</strong>*2 allele (one Indo TT <b>alcohol</b> dependent, two Indo TT controls).
+ADH1B	drug	alcohol	16930209	Variations in the <strong>ADH1B</strong> and ADH1C genes may influence the LR to <b>alcohol</b> by increasing levels of acetaldehyde during <b>alcohol</b> metabolism, although most data on this question come from Asian populations.
+ADH1B	drug	alcohol	16930209	Participants with the <strong>ADH1B</strong>*1/*2 genotype had a higher LR to <b>alcohol</b> early in the <b>alcohol</b> challenge (i.e., 30, 60, and 90 minutes after drinking) as measured by both <b>alcohol</b> related changes in subjective feelings of intoxication and body sway, even when controlling for sex and Russian/Eastern European ancestry.
+ADH1B	addiction	intoxication	16930209	Participants with the <strong>ADH1B</strong>*1/*2 genotype had a higher LR to alcohol early in the alcohol challenge (i.e., 30, 60, and 90 minutes after drinking) as measured by both alcohol related changes in subjective feelings of <b>intoxication</b> and body sway, even when controlling for sex and Russian/Eastern European ancestry.
+ADH1B	drug	alcohol	16930209	These findings suggest that studies searching for genes relating to the LR to <b>alcohol</b> as a vulnerability factor for AUDs should consider controlling for <strong>ADH1B</strong> genotype, as the <strong>ADH1B</strong>*2 allele could obscure the impact of other genetic polymorphisms.
+ADH1B	drug	alcohol	16822169	Meta analyses of ALDH2 and <strong>ADH1B</strong> with <b>alcohol</b> dependence in Asians.
+ADH1B	addiction	dependence	16822169	Meta analyses of ALDH2 and <strong>ADH1B</strong> with alcohol <b>dependence</b> in Asians.
+ADH1B	drug	alcohol	16822169	Meta analyses were conducted to determine the magnitude of relationships between polymorphisms in 2 genes, ALDH2 and <strong>ADH1B</strong>, with <b>alcohol</b> dependence in Asians.
+ADH1B	addiction	dependence	16822169	Meta analyses were conducted to determine the magnitude of relationships between polymorphisms in 2 genes, ALDH2 and <strong>ADH1B</strong>, with alcohol <b>dependence</b> in Asians.
+ADH1B	drug	alcohol	16600530	Carriage of genotypes containing the <strong>ADH1B</strong>*2 mutant allele significantly protected against <b>alcoholism</b> [odds ratio (OR)=0.00; 95% confidence interval (95% CI): 0.00 0.94; p=0.02] but was associated with an increased risk for <b>alcoholic</b> liver disease among <b>alcohol</b> dependent women [OR=0.43; 95% CI: 0.18 0.41; p=0.004].
+ADH1B	drug	alcohol	16600530	In Caucasian Spanish women the <strong>ADH1B</strong>*2 allele modulates the risk for <b>alcohol</b> dependence and for <b>alcoholic</b> liver disease.
+ADH1B	addiction	dependence	16600530	In Caucasian Spanish women the <strong>ADH1B</strong>*2 allele modulates the risk for alcohol <b>dependence</b> and for alcoholic liver disease.
+ADH1B	drug	alcohol	16571603	Haplotype tag SNPs were selected for the block in the ADH4 gene that provided evidence of association and subsequently used in association analysis; the haplotype was significantly associated with <b>alcoholism</b> (P=0.01) There was weaker evidence that variations in ADH1A and <strong>ADH1B</strong> might also play a role in modifying risk.
+ADH1B	drug	alcohol	16404797	The <strong>ADH1B</strong>*2, <strong>ADH1B</strong>*3, and ADHlC*i alleles, found in varying prevalence in different ethnic groups, have also been associated with lower rates of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	16404797	The <strong>ADH1B</strong>*2, <strong>ADH1B</strong>*3, and ADHlC*i alleles, found in varying prevalence in different ethnic groups, have also been associated with lower rates of alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	16404797	The hypothesized mechanism underlying the associations of the <strong>ADH1B</strong> and ALDH2 polymorphisms with <b>alcohol</b> dependence is that the isoenzymes encoded by these alleles lead to an accumulation of acetaldehyde during <b>alcohol</b> metabolism.
+ADH1B	addiction	dependence	16404797	The hypothesized mechanism underlying the associations of the <strong>ADH1B</strong> and ALDH2 polymorphisms with alcohol <b>dependence</b> is that the isoenzymes encoded by these alleles lead to an accumulation of acetaldehyde during alcohol metabolism.
+ADH1B	drug	alcohol	16309369	The genotypes of <b>alcohol</b> dehydrogenase 1B (<strong>ADH1B</strong>) and aldehyde dehydrogenase 2 (ALDH2) are related to <b>alcohol</b> dependence and some human disorders.
+ADH1B	addiction	dependence	16309369	The genotypes of alcohol dehydrogenase 1B (<strong>ADH1B</strong>) and aldehyde dehydrogenase 2 (ALDH2) are related to alcohol <b>dependence</b> and some human disorders.
+ADH1B	drug	alcohol	16184481	Genetic time series analysis identifies a major QTL for in vivo <b>alcohol</b> metabolism not predicted by in vitro studies of structural protein polymorphism at the <strong>ADH1B</strong> or ADH1C loci.
+ADH1B	drug	alcohol	16125912	One hundred and eleven male patients with <b>alcohol</b> dependence and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 (<strong>ADH2</strong>), aldehyde dehydrogenase 2 (ALDH2), serotonin transporter (5 HTT) and dopamine transporter (DAT1).
+ADH1B	addiction	dependence	16125912	One hundred and eleven male patients with alcohol <b>dependence</b> and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of alcohol dehydrogenase 2 (<strong>ADH2</strong>), aldehyde dehydrogenase 2 (ALDH2), serotonin transporter (5 HTT) and dopamine transporter (DAT1).
+ADH1B	drug	alcohol	16125912	There were significant differences in genotype frequencies of <strong>ADH2</strong> C992G and A13543G SNPs between <b>alcoholic</b> patients with family history of <b>alcohol</b> dependence (familial) and <b>alcoholic</b> patients without family history (non familial).
+ADH1B	addiction	dependence	16125912	There were significant differences in genotype frequencies of <strong>ADH2</strong> C992G and A13543G SNPs between alcoholic patients with family history of alcohol <b>dependence</b> (familial) and alcoholic patients without family history (non familial).
+ADH1B	drug	alcohol	23105541	Subtypes of <strong>ADH2</strong> gene in <b>alcoholics</b>.
+ADH1B	drug	alcohol	23105541	In the present study, genetic variation was detected in the subtypes of gene, coding for the <b>alcohol</b> metabolizing enzyme <b>Alcohol</b> Dehydrogenase 2 (<strong>ADH2</strong>).
+ADH1B	drug	alcohol	23105541	Blood samples were collected from the <b>alcoholic</b> and non <b>alcoholic</b> subjects and genotyping was performed using PCR RFLP (Polymerase Chain Reaction Restriction Fragment Length Polymorphism), analysis to determine genetic polymorphisms in the <strong>ADH2</strong> gene subtypes.
+ADH1B	drug	alcohol	23105541	The three subtypes of <strong>ADH2</strong> gene (<strong>ADH2</strong>.1, <strong>ADH2</strong>.2 and <strong>ADH2</strong>.3) were found in both <b>alcoholics</b> (Family History Positive and Family History Negative) as well as non <b>alcoholics</b>.
+ADH1B	drug	alcohol	15957670	Associations of ALDH2 and <strong>ADH1B</strong> genotypes with response to <b>alcohol</b> in Asian Americans.
+ADH1B	drug	alcohol	15957670	Individuals with <b>alcohol</b> dependence are less likely to possess variant alleles of the <b>alcohol</b> metabolizing genes, aldehyde dehydrogenase (ALDH2*2) and <b>alcohol</b> dehydrogenase (<strong>ADH1B</strong>*2), than non <b>alcohol</b> dependent controls.
+ADH1B	addiction	dependence	15957670	Individuals with alcohol <b>dependence</b> are less likely to possess variant alleles of the alcohol metabolizing genes, aldehyde dehydrogenase (ALDH2*2) and alcohol dehydrogenase (<strong>ADH1B</strong>*2), than non alcohol dependent controls.
+ADH1B	drug	alcohol	15957670	Previous research has shown that individuals with ALDH2*2 demonstrate enhanced reactions to <b>alcohol</b> compared with those without this genetic variant, but evidence that <strong>ADH1B</strong>*2 is associated with a greater <b>alcohol</b> response is mixed.
+ADH1B	drug	alcohol	15957670	This study was designed to determine whether the <strong>ADH1B</strong> genotype is associated with more intense reactions to <b>alcohol</b> after controlling for the ALDH2 genotype.
+ADH1B	drug	alcohol	15957670	Among participants with the ALDH2*1/*1 genotype, there were no additional effects of the <strong>ADH1B</strong> genotype on any measures of response to <b>alcohol</b>.
+ADH1B	drug	alcohol	15957670	Among participants with the ALDH2*1/*2 genotype, those with the <strong>ADH1B</strong>*2/*2 genotype were more likely to experience <b>alcohol</b> induced vomiting and to report feeling less "great overall" 30 minutes after ingestion of <b>alcohol</b> than those with the <strong>ADH1B</strong>*1/*2 genotype.
+ADH1B	drug	alcohol	15957670	These findings are consistent with the hypothesis that there is an additional effect of <strong>ADH1B</strong>*2 on level of response to <b>alcohol</b>, but only among individuals with the ALDH2*1/*2 genotype.
+ADH1B	drug	alcohol	15863807	The authors examined the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 and 3 (<strong>ADH2</strong> and ADH3) and aldehyde dehydrogenase (ALDH2) in patients diagnosed as having Cloninger's type I or type II <b>alcoholism</b>.
+ADH1B	drug	alcohol	15863807	Seventy two <b>alcoholic</b> men and 38 nonalcoholic, healthy men were tested for the distribution of genotypes and alleles of <strong>ADH2</strong>, ADH3, and ALDH2.
+ADH1B	drug	alcohol	15863807	The frequencies of <strong>ADH2</strong>*1 and ADH3*2 alleles were significantly higher in men with type II <b>alcoholism</b> than in men with type I <b>alcoholism</b> and healthy men.
+ADH1B	drug	alcohol	15842823	To study the distribution of genotypes about <b>alcohol</b> dehydrogenase 2 (<strong>ADH2</strong>) and aldehyde dehydrogenase 2 (ALDH2) and its relationship with drinking behaviors in Chinese Han healthy population as to providing a theoretic direction for filtering out high risk and sensitive individuals and taking preventive measures to decrease the <b>alcohol</b> related diseases.
+ADH1B	drug	alcohol	15842823	Correlation between genotypes of <strong>ADH2</strong> and ALDH2 and <b>alcohol</b> related diseases should be more important.
+ADH1B	drug	alcohol	15542751	The results revealed that (1) the less active allele of the <strong>ADH2</strong> gene (<strong>ADH2</strong>*1) is associated with an increased risk for <b>alcohol</b> dependence, <b>alcohol</b> induced persistent amnestic disorder, <b>alcohol</b> withdrawal syndrome, and cancer of the upper GI tract; (2) the inactive allele of the ALDH2 gene (ALDH2*2) is associated with a decreased risk for <b>alcohol</b> dependence, and an increased risk for <b>alcoholic</b> polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	15542751	The results revealed that (1) the less active allele of the <strong>ADH2</strong> gene (<strong>ADH2</strong>*1) is associated with an increased risk for alcohol <b>dependence</b>, alcohol induced persistent amnestic disorder, alcohol withdrawal syndrome, and cancer of the upper GI tract; (2) the inactive allele of the ALDH2 gene (ALDH2*2) is associated with a decreased risk for alcohol <b>dependence</b>, and an increased risk for alcoholic polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of alcohol <b>dependence</b>.
+ADH1B	addiction	withdrawal	15542751	The results revealed that (1) the less active allele of the <strong>ADH2</strong> gene (<strong>ADH2</strong>*1) is associated with an increased risk for alcohol dependence, alcohol induced persistent amnestic disorder, alcohol <b>withdrawal</b> syndrome, and cancer of the upper GI tract; (2) the inactive allele of the ALDH2 gene (ALDH2*2) is associated with a decreased risk for alcohol dependence, and an increased risk for alcoholic polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of alcohol dependence.
+ADH1B	drug	alcohol	15122947	This study examined aldehyde dehydrogense (ALDH2) gene status, <b>alcohol</b> dehydrogense (<strong>ADH2</strong>) gene status, conduct disorder, and <b>alcohol</b> dependence in Chinese, Korean, and White American college students.
+ADH1B	addiction	dependence	15122947	This study examined aldehyde dehydrogense (ALDH2) gene status, alcohol dehydrogense (<strong>ADH2</strong>) gene status, conduct disorder, and alcohol <b>dependence</b> in Chinese, Korean, and White American college students.
+ADH1B	drug	alcohol	15122947	<strong>ADH2</strong> status was not related to <b>alcohol</b> dependence with ALDH2 included, and no interactions were significant.
+ADH1B	addiction	dependence	15122947	<strong>ADH2</strong> status was not related to alcohol <b>dependence</b> with ALDH2 included, and no interactions were significant.
+ADH1B	drug	alcohol	15112932	Mr. Cook's and Dr. Wall's paper adds another dimension to this article by presenting research on both the aldehyde dehydrogenase (ALDH2) and <b>alcohol</b> dehydrogenase (<strong>ADH2</strong>) genetic variants and their association with the <b>alcohol</b> related flushing response that is prevalent in Asian populations.
+ADH1B	drug	alcohol	15084894	In the Han Chinese population, the <b>alcohol</b> dehydrogenase 1B*2/*2 (<strong>ADH1B</strong>*2/*2) genotype and the aldehyde dehydrogenase 2*2 (ALDH2*2) allele have been considered as protective factors against <b>alcohol</b> abuse or dependence.
+ADH1B	addiction	dependence	15084894	In the Han Chinese population, the alcohol dehydrogenase 1B*2/*2 (<strong>ADH1B</strong>*2/*2) genotype and the aldehyde dehydrogenase 2*2 (ALDH2*2) allele have been considered as protective factors against alcohol abuse or <b>dependence</b>.
+ADH1B	drug	alcohol	15084894	We hypothesized that the <strong>ADH1B</strong> and ALDH2 genes might interact with the DRD2 gene and that the association between the DRD2 gene and <b>alcohol</b> dependence might be affected by different <strong>ADH1B</strong> and ALDH2 genotypes.
+ADH1B	addiction	dependence	15084894	We hypothesized that the <strong>ADH1B</strong> and ALDH2 genes might interact with the DRD2 gene and that the association between the DRD2 gene and alcohol <b>dependence</b> might be affected by different <strong>ADH1B</strong> and ALDH2 genotypes.
+ADH1B	drug	alcohol	15066702	Mexican Americans have a low frequency of the protective alleles <strong>ADH1B</strong>(*)2 and ALDH2(*)2 and a relatively high frequency of CYP2E1 c2, which is associated with early onset <b>alcoholism</b>.
+ADH1B	drug	alcohol	15041893	Among the multiple factors which influence these variations, genetic factors especially those related to the different alleles of <strong>ADH2</strong> and ALDH2, are the most well known and are related to the development of <b>alcohol</b> dependence, particularly in some populations such as those of Asian origin.
+ADH1B	addiction	dependence	15041893	Among the multiple factors which influence these variations, genetic factors especially those related to the different alleles of <strong>ADH2</strong> and ALDH2, are the most well known and are related to the development of alcohol <b>dependence</b>, particularly in some populations such as those of Asian origin.
+ADH1B	drug	alcohol	14745297	There is growing evidence of a functional role of the <strong>ADH2</strong>*2 allele in <b>alcohol</b> drinking patterns among Jews, who have traditionally exhibited low rates of <b>alcoholism</b> and <b>alcohol</b> related problems.
+ADH1B	drug	alcohol	14745297	This study examined the effect of <strong>ADH2</strong>*2 on <b>alcohol</b> elimination rates (AER) under experimental conditions.
+ADH1B	drug	alcohol	14745297	The rate of <b>alcohol</b> elimination is significantly associated with the <strong>ADH2</strong> genotype of Jewish males.
+ADH1B	drug	alcohol	12884000	Allelic variation at <b>alcohol</b> metabolism genes (<strong>ADH1B</strong>, ADH1C, ALDH2) and <b>alcohol</b> dependence in an American Indian population.
+ADH1B	addiction	dependence	12884000	Allelic variation at alcohol metabolism genes (<strong>ADH1B</strong>, ADH1C, ALDH2) and alcohol <b>dependence</b> in an American Indian population.
+ADH1B	drug	alcohol	12884000	Specifically, <strong>ADH1B</strong>*47His (previously ADH2 2) and ALDH2 2 have been shown to confer protection against <b>alcoholism</b>, presumably through accumulation of acetaldehyde in the blood and a resultant 'flushing response' to <b>alcohol</b> consumption.
+ADH1B	drug	alcohol	12884000	Specifically, <strong>ADH1B</strong>*47His (previously <strong>ADH2</strong> 2) and ALDH2 2 have been shown to confer protection against <b>alcoholism</b>, presumably through accumulation of acetaldehyde in the blood and a resultant 'flushing response' to <b>alcohol</b> consumption.
+ADH1B	drug	alcohol	12884000	In the current study, variants at <strong>ADH1B</strong> (previously ADH2), ADH1C (previously ADH3), and ALDH2 were assayed in DNA extracts from participants belonging to a Southwest American Indian tribe (n=490) with a high prevalence of <b>alcoholism</b>.
+ADH1B	drug	alcohol	12884000	In the current study, variants at <strong>ADH1B</strong> (previously <strong>ADH2</strong>), ADH1C (previously ADH3), and ALDH2 were assayed in DNA extracts from participants belonging to a Southwest American Indian tribe (n=490) with a high prevalence of <b>alcoholism</b>.
+ADH1B	drug	alcohol	12824808	In Taiwan, about 70% of the Han Chinese population have the <strong>ADH2</strong>*2 allele and 50% show ALDH2*1/*2 or ALDH2*2/*2 genotypes, which offer protection against drinking behavior and the risk of developing <b>alcoholism</b>.
+ADH1B	drug	alcohol	12710951	To identify the association between the polymorphisms of genes encoding <b>alcohol</b> metabolizing enzymes and <b>alcoholism</b>, the <b>alcohol</b> dehydrogenase 2 (<strong>ADH2</strong>), <b>alcohol</b> dehydrogenase 3 (ADH3), aldehyde dehydrogenase 2 (ALDH2), and cytochrome P450 2E1 (CYP2E1) genes were studied in 101 male Mexican American <b>alcoholics</b>.
+ADH1B	drug	alcohol	12710951	The allele frequency of <strong>ADH2</strong>*2 (4.3%) and ALDH2*2 (0%), which are considered as protective alleles against <b>alcohol</b> drinking, is very low in Mexican Americans and no association is found between these alleles and <b>alcohol</b> dependence.
+ADH1B	addiction	dependence	12710951	The allele frequency of <strong>ADH2</strong>*2 (4.3%) and ALDH2*2 (0%), which are considered as protective alleles against alcohol drinking, is very low in Mexican Americans and no association is found between these alleles and alcohol <b>dependence</b>.
+ADH1B	drug	alcohol	12505800	Two <b>alcohol</b> dehydrogenase genes (<strong>ADH2</strong> and ADH3 on chromosome 4) and one aldehyde dehydrogenase gene (ALDH2 on chromosome 12) exhibit functional polymorphisms.
+ADH1B	drug	alcohol	12505800	The goal of this study was to determine whether any associations exist between the <strong>ADH2</strong>, ADH3, and ALDH2 polymorphisms and <b>alcohol</b> dependence in a group of Native Americans.
+ADH1B	addiction	dependence	12505800	The goal of this study was to determine whether any associations exist between the <strong>ADH2</strong>, ADH3, and ALDH2 polymorphisms and alcohol <b>dependence</b> in a group of Native Americans.
+ADH1B	drug	alcohol	12505800	A significant difference in the <strong>ADH2</strong> allele distributions was found between <b>alcohol</b> dependent and non <b>alcohol</b> dependent participants.
+ADH1B	drug	alcohol	12505800	Those with <b>alcohol</b> dependence were significantly less likely to have the <strong>ADH2</strong>*3 allele (odds ratio=0.28) and significantly more likely to have the <strong>ADH2</strong>*1 allele (odds ratio=2.00) than those who were not <b>alcohol</b> dependent.
+ADH1B	addiction	dependence	12505800	Those with alcohol <b>dependence</b> were significantly less likely to have the <strong>ADH2</strong>*3 allele (odds ratio=0.28) and significantly more likely to have the <strong>ADH2</strong>*1 allele (odds ratio=2.00) than those who were not alcohol dependent.
+ADH1B	drug	alcohol	12505800	These results are consistent with genetic linkage studies showing protective associations for <b>alcohol</b> dependence and related behavior on chromosome 4 and suggest that <strong>ADH2</strong> polymorphisms may account for these findings.
+ADH1B	addiction	dependence	12505800	These results are consistent with genetic linkage studies showing protective associations for alcohol <b>dependence</b> and related behavior on chromosome 4 and suggest that <strong>ADH2</strong> polymorphisms may account for these findings.
+ADH1B	drug	alcohol	12500100	All participants completed the Time Line Follow Back, had blood drawn for genotyping at the <b>alcohol</b> dehydrogenase locus <strong>ADH2</strong>, and reported their religious affiliation and the number of religious services attended in the past year.
+ADH1B	drug	alcohol	12500100	In the total sample, individuals who possessed a variant <b>alcohol</b> dehydrogenase allele <strong>ADH2</strong>*2 were approximately half as likely to binge drink as those who did not possess this allele.
+ADH1B	addiction	intoxication	12500100	In the total sample, individuals who possessed a variant alcohol dehydrogenase allele <strong>ADH2</strong>*2 were approximately half as likely to <b>binge</b> drink as those who did not possess this allele.
+ADH1B	drug	alcohol	12351924	The <strong>ADH2</strong>*2 allele of the <b>alcohol</b> dehydrogenase 2 (<strong>ADH2</strong>) gene protects against <b>alcoholism</b> in Asians and is found in approximately 20% of Jews.
+ADH1B	addiction	dependence	12351924	We studied the relationship of <strong>ADH2</strong>*2 to DSM IV <b>dependence</b> severity in a random community sample of Israeli Ashkenazis, recent Russian immigrants (also Ashkenazis), and Sephardics.
+ADH1B	drug	alcohol	12351924	Controlling for group and other potentially confounding factors, <strong>ADH2</strong>*2 was associated with a lower lifetime DSM IV <b>alcohol</b> dependence severity, although this differed somewhat within groups.
+ADH1B	addiction	dependence	12351924	Controlling for group and other potentially confounding factors, <strong>ADH2</strong>*2 was associated with a lower lifetime DSM IV alcohol <b>dependence</b> severity, although this differed somewhat within groups.
+ADH1B	addiction	dependence	12351924	<strong>ADH2</strong>*2 protects against <b>dependence</b> severity in Jewish samples.
+ADH1B	drug	alcohol	12351924	Future work in larger samples should address genetic and environmental factors that affect the relationship of <strong>ADH2</strong>*2 to <b>alcohol</b> consumption and dependence.
+ADH1B	addiction	dependence	12351924	Future work in larger samples should address genetic and environmental factors that affect the relationship of <strong>ADH2</strong>*2 to alcohol consumption and <b>dependence</b>.
+ADH1B	drug	alcohol	11900616	<b>Alcohol</b> dehydrogenase <strong>ADH2</strong> 1 and <strong>ADH2</strong> 2 allelic isoforms in the Russian population correlate with type of <b>alcoholic</b> disease.
+ADH1B	drug	alcohol	11900616	The frequency <strong>ADH2</strong> 2 allele in the Moscow urban population and a correlation between the <strong>ADH2</strong> 2 allele, <b>alcoholic</b> dependence without cirrhosis, symptomatic <b>alcoholic</b> cirrhosis and status on hepatitis B and C infection have been studied.
+ADH1B	addiction	dependence	11900616	The frequency <strong>ADH2</strong> 2 allele in the Moscow urban population and a correlation between the <strong>ADH2</strong> 2 allele, alcoholic <b>dependence</b> without cirrhosis, symptomatic alcoholic cirrhosis and status on hepatitis B and C infection have been studied.
+ADH1B	drug	alcohol	11900616	There is a negative correlation between the <strong>ADH2</strong> 2 allele and <b>alcohol</b> misuse (both <b>alcoholic</b> dependence and <b>alcoholic</b> cirrhosis).
+ADH1B	addiction	dependence	11900616	There is a negative correlation between the <strong>ADH2</strong> 2 allele and alcohol misuse (both alcoholic <b>dependence</b> and alcoholic cirrhosis).
+ADH1B	drug	alcohol	11900616	In spite of the possession of the <strong>ADH2</strong> 2 allele (or genotype <strong>ADH2</strong> 1/2), <b>alcohol</b> misuse increases the risk of cirrhosis.
+ADH1B	drug	alcohol	11900616	At the same time, positive status for active hepatitis B, C or combined infection B + C (replication markers HBV DNA or HCV RNA) increases the risk for symptomatic <b>alcoholic</b> cirrhosis in <b>alcohol</b> abusing patients, independently of <strong>ADH2</strong> genotype.
+ADH1B	drug	alcohol	11584143	In view of this association and the known genetic influences on both <b>alcohol</b> pharmacokinetics and <b>alcohol</b> dependence, it is probable that part of the heritability of dependence is mediated by genes (other than the known <strong>ADH2</strong> and ADH3 polymorphisms) affecting <b>alcohol</b> metabolism.
+ADH1B	addiction	dependence	11584143	In view of this association and the known genetic influences on both alcohol pharmacokinetics and alcohol <b>dependence</b>, it is probable that part of the heritability of <b>dependence</b> is mediated by genes (other than the known <strong>ADH2</strong> and ADH3 polymorphisms) affecting alcohol metabolism.
+ADH1B	drug	alcohol	11545539	<strong>ADH2</strong> and <b>alcohol</b> related phenotypes in Ashkenazic Jewish American college students.
+ADH1B	drug	alcohol	11545539	In Asians, variation in the <b>alcohol</b> dehydrogenase (<strong>ADH2</strong>) gene relates to <b>alcohol</b> dependence, <b>alcohol</b> consumption, and reported <b>alcohol</b> related symptoms, even after controlling for variation in the aldehyde dehydrogenase (ALDH2) gene.
+ADH1B	addiction	dependence	11545539	In Asians, variation in the alcohol dehydrogenase (<strong>ADH2</strong>) gene relates to alcohol <b>dependence</b>, alcohol consumption, and reported alcohol related symptoms, even after controlling for variation in the aldehyde dehydrogenase (ALDH2) gene.
+ADH1B	drug	alcohol	11545539	The association of <strong>ADH2</strong> polymorphisms with <b>alcohol</b> related behavior, however, has not been well characterized in non Asians.
+ADH1B	drug	alcohol	11545539	<strong>ADH2</strong>*2, however, was not related to <b>alcohol</b> use disorders, <b>alcohol</b> induced flushing and associated symptoms, number of binge drinking episodes in the past 90 days, maximum number of drinks ever consumed, or self reported levels of response to <b>alcohol</b>.
+ADH1B	addiction	intoxication	11545539	<strong>ADH2</strong>*2, however, was not related to alcohol use disorders, alcohol induced flushing and associated symptoms, number of <b>binge</b> drinking episodes in the past 90 days, maximum number of drinks ever consumed, or self reported levels of response to alcohol.
+ADH1B	drug	alcohol	11545539	Results suggest that Ashkenazic Jewish Americans with <strong>ADH2</strong>*2 alleles drink less frequently, which might contribute, in part, to the overall lower rates of <b>alcoholism</b> in this population.
+ADH1B	drug	alcohol	11315223	In men, effects of <b>alcohol</b> dehydrogenase <strong>ADH2</strong>*1/*2 genotype or high <b>alcohol</b> sensitivity (risk decreasing), and of history of childhood conduct disorder, or having monozygotic co twin or twin sister with AlcD (risk increasing) were significant and comparable in magnitude.
+ADH1B	drug	alcohol	10630602	An <b>alcohol</b> dependent patient was identified to be ALDH2*2/*2, <strong>ADH2</strong>*2/*2, and ADH3*1/*2.
+ADH1B	drug	alcohol	10630602	Logistic regression analysis of the combinatorial genotypes of <strong>ADH2</strong> and ALDH2 in 420 <b>alcohol</b> dependent and 689 nonalcohol dependent subjects indicated that risk for <b>alcoholism</b> was 100 fold lower for the <strong>ADH2</strong>*2/*2 ALDH2*2/*2 individuals than the <strong>ADH2</strong>*1/*1 ALDH2*1/*1 individuals.
+ADH1B	drug	alcohol	10235293	The different genotypes at the genes encoding the enzymes involved in <b>alcohol</b> metabolism, class one <b>alcohol</b> dehydrogenase (<strong>ADH2</strong> and ADH3) and mitochondrial aldehyde dehydrogenase (ALDH2), have previously been shown to confer different predispositions to the development of <b>alcoholism</b> in Chinese Han males (Thomasson et al., 1991; Chen WJ et al., 1996; Chen CC et al., unpublished data).
+ADH1B	drug	alcohol	10235293	Therefore, association studies of <b>alcoholism</b> in Chinese Han might be more sensitive if controlled for the genotypes of <strong>ADH2</strong>,ADH3, and ALDH2, when other loci, such as DRD2, are examined.
+ADH1B	drug	alcohol	10235293	These tests included considering the high risk (<strong>ADH2</strong>*1/*1; *1/*2; ADH3*1/*2; *2/*2; and ALDH2*1/*1) and the low risk (<strong>ADH2</strong>*2/*2; ADH3*1/*1; and ALDH2*1/*2; *2/*2) groups of <b>alcoholics</b>, as well as nonalcoholic controls.
+ADH1B	drug	alcohol	10235293	After stratification by the relevant genotypes of <strong>ADH2</strong>, ADH3, and ALDH2 no significant association exists between the genetic variants at the DRD2 locus and <b>alcoholism</b> in the Chinese Han population.
+ADH1B	addiction	dependence	9802529	<strong>ADH2</strong> genotype had significant effects on both consumption and <b>dependence</b> in the men, but not in the women.
+ADH1B	drug	alcohol	9509496	Men with an <strong>ADH2</strong> x 3 allele had significantly higher amplitude P3 components at placebo and also demonstrated more <b>alcohol</b> induced reductions in P3 amplitude than men with <strong>ADH2</strong> x 1 alleles only.
+ADH1B	drug	alcohol	9373704	The purpose of this paper is to assemble and evaluate existing data on the effect of genetic variation in <strong>ADH2</strong> and ADH3 on the risk of <b>alcohol</b> dependence, and on the risk of <b>alcoholic</b> liver disease.
+ADH1B	addiction	dependence	9373704	The purpose of this paper is to assemble and evaluate existing data on the effect of genetic variation in <strong>ADH2</strong> and ADH3 on the risk of alcohol <b>dependence</b>, and on the risk of alcoholic liver disease.
+ADH1B	drug	alcohol	9373704	It is clear that possession of the <strong>ADH2</strong> 2 allele decreases the risk of <b>alcohol</b> dependence, but it increases the risk of <b>alcoholic</b> liver disease among <b>alcoholics</b>.
+ADH1B	addiction	dependence	9373704	It is clear that possession of the <strong>ADH2</strong> 2 allele decreases the risk of alcohol <b>dependence</b>, but it increases the risk of alcoholic liver disease among alcoholics.
+ADH1B	drug	alcohol	9373704	ADH3 variation also has significant effects on <b>alcohol</b> dependence, which may be due to linkage to <strong>ADH2</strong>; the ADH3 effect differs significantly between Asian and European subjects.
+ADH1B	addiction	dependence	9373704	ADH3 variation also has significant effects on alcohol <b>dependence</b>, which may be due to linkage to <strong>ADH2</strong>; the ADH3 effect differs significantly between Asian and European subjects.
+ADH1B	drug	alcohol	9066994	In this report we determined the genotypes for three genes, <strong>ADH2</strong>, ADH3, and ALDH2 among subjects with <b>alcohol</b> dependence (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ADH1B	addiction	dependence	9066994	In this report we determined the genotypes for three genes, <strong>ADH2</strong>, ADH3, and ALDH2 among subjects with alcohol <b>dependence</b> (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ADH1B	drug	alcohol	9066994	On an individual level, however, the genotypes controlling <b>alcohol</b> metabolism did not account for intragroup differences in vulnerability to <b>alcoholism</b> except in the case of <strong>ADH2</strong> for the Ami ethnic group.
+ADH1B	drug	alcohol	8904964	The influences of estimated body water, recent drinking history, recent smoking history, polymorphism at the <strong>ADH2</strong> and ADH3 loci, family history of <b>alcoholism</b>, and percentage Native American heritage on <b>alcohol</b> elimination rate were determined using multiple regression analyses.
+ADH1B	drug	nicotine	8904964	The influences of estimated body water, recent drinking history, recent <b>smoking</b> history, polymorphism at the <strong>ADH2</strong> and ADH3 loci, family history of alcoholism, and percentage Native American heritage on alcohol elimination rate were determined using multiple regression analyses.
+ADH1B	drug	alcohol	8904964	There was also a nonsignificant trend for subjects with an <strong>ADH2</strong>*3 allele (n = 6) to have faster rates of <b>alcohol</b> elimination than those with <strong>ADH2</strong>*1 alleles only (n = 33).
+ADH1B	drug	alcohol	8773821	<b>Alcohol</b> metabolising genes and <b>alcoholism</b> among Taiwanese Han men: independent effect of <strong>ADH2</strong>, ADH3 and ALDH2.
+ADH1B	drug	alcohol	8773821	The association of ALDH2 and <strong>ADH2</strong> with the development of <b>alcoholism</b> was found to be independent of each other and has been replicated in different Asian populations, while the effect of ADH3 is less studied.
+ADH1B	drug	alcohol	8773821	Multiple logistic regression was then applied to assess the contribution of ADH3 to <b>alcoholism</b> by controlling the effect of ALDH2 and <strong>ADH2</strong>.
+ADH1B	drug	alcohol	8773821	The results of multivariate analyses demonstrated that the odds ratios for an increment of one allele of <strong>ADH2</strong>*1, ADH3*2 and ALDH2*1 in the development of <b>alcoholism</b> were 4.18, 3.82, and 6.89, respectively.
+ADH1B	drug	alcohol	8651462	A comparison of the genotypes of ALDH2, <strong>ADH2</strong>, ADH3, and cytochrome P 4502E1 between <b>alcoholics</b> and nonalcoholics.
+ADH1B	drug	alcohol	8651462	Our study revealed differences in the allelic frequencies of the ALDH2, <strong>ADH2</strong>, and ADH3 loci between <b>alcoholics</b> and nonalcoholics.
+ADH1B	drug	alcohol	8651462	For <b>alcoholics</b> with both homozygous ALDH2*1/1 and heterozygous ALDH2*1/2 genotypes, it was found that <strong>ADH2</strong> and ADH3 played important rates.
+ADH1B	drug	alcohol	8651462	<b>Alcoholics</b> with the heterozygous ALDH2*1/2 genotype showed a significantly higher frequency of <strong>ADH2</strong>*1/1 than ones with the homozygous ALDH2*1/1 genotype.
+ADH1B	drug	alcohol	8651462	We assume <strong>ADH2</strong>*1 plays an important role in the development of <b>alcoholism</b> in <b>alcoholics</b> with the heterozygous ALDH2*1/2 genotype.
+ADH1B	drug	alcohol	8591846	High incidence of <strong>ADH2</strong>*1/ALDH2*1 genes among Japanese <b>alcohol</b> dependents and patients with <b>alcoholic</b> liver disease.
+ADH1B	drug	alcohol	8591846	Genetic polymorphism of <strong>ADH2</strong>/ALDH2 in 66 cases of normal subjects, 90 cases of <b>alcohol</b> dependent, and 31 patients with <b>alcoholic</b> liver disease among Japanese has been analyzed using a polymerase chain reaction assay followed by a direct sequencing method, because <b>ethanol</b> is mainly catabolized by ADH and ALDH and less by cytochrome P450IIE1 and catalase.
+ADH1B	drug	alcohol	8591846	The incidence of both <strong>ADH2</strong>*1/*1 and ALDH2*1/*1 was significantly higher in patients with <b>alcohol</b> dependence and in patients with <b>alcoholic</b> liver disease when compared with that in control subjects.
+ADH1B	addiction	dependence	8591846	The incidence of both <strong>ADH2</strong>*1/*1 and ALDH2*1/*1 was significantly higher in patients with alcohol <b>dependence</b> and in patients with alcoholic liver disease when compared with that in control subjects.
+ADH1B	drug	alcohol	8591846	Genetic polymorphism of <strong>ADH2</strong>/ALDH2 in patients with <b>alcoholic</b> liver disease was not different from that of <b>alcohol</b> dependents.
+ADH1B	drug	alcohol	8591846	According to these results, not only ALDH2 gene, often claimed to be responsible for <b>alcohol</b> dependence among Japanese, but also <strong>ADH2</strong> gene polymorphism, which modulates the metabolism of <b>ethanol</b>, play important roles in habitual <b>alcohol</b> intake behavior in Japanese patients and in some patients leads to <b>alcoholic</b> liver diseases.
+ADH1B	addiction	dependence	8591846	According to these results, not only ALDH2 gene, often claimed to be responsible for alcohol <b>dependence</b> among Japanese, but also <strong>ADH2</strong> gene polymorphism, which modulates the metabolism of ethanol, play important roles in habitual alcohol intake behavior in Japanese patients and in some patients leads to alcoholic liver diseases.
+ADH1B	drug	alcohol	7943668	Low frequency of the <strong>ADH2</strong>*2 allele among Atayal natives of Taiwan with <b>alcohol</b> use disorders.
+ADH1B	drug	alcohol	7943668	Genetic variation at two polymorphic <b>alcohol</b> dehydrogenase loci, <strong>ADH2</strong> and ADH3, and at the polymorphic mitochondrial aldehyde dehydrogenase locus, ALDH2, may influence the risk of developing <b>alcoholism</b> by modulating the rate of elimination of <b>ethanol</b> and the rate of formation and elimination of acetaldehyde.
+ADH1B	drug	alcohol	7943668	Among the Atayal, the group with <b>alcohol</b> use disorders (<b>alcohol</b> dependence and <b>alcohol</b> abuse) had a significantly lower frequency of the <strong>ADH2</strong>*2 allele (0.82) than those without <b>alcohol</b> use disorders (0.91).
+ADH1B	addiction	dependence	7943668	Among the Atayal, the group with alcohol use disorders (alcohol <b>dependence</b> and alcohol abuse) had a significantly lower frequency of the <strong>ADH2</strong>*2 allele (0.82) than those without alcohol use disorders (0.91).
+ADH1B	drug	alcohol	7943668	The <strong>ADH2</strong>*2 allele encodes the beta 2 subunit; isozymes containing beta 2 subunits oxidize <b>alcohol</b> faster in vitro than the beta 1 beta 1 isozyme encoded by <strong>ADH2</strong>*1.
+ADH1B	drug	alcohol	3189338	Genetic polymorphisms of two major <b>alcohol</b> metabolizing enzymes i.e., one of the class I <b>alcohol</b> dehydrogenase isozymes (<strong>ADH2</strong>) and the mitochondrial aldehyde dehydrogenase (ALDH2) exist in Japanese and other Orientals but not in Caucasians.
+ADH1B	drug	alcohol	3189338	We determined, by means of hybridization of genomic DNA samples with allele specific synthetic oligonucleotide probes, genotypes of the <strong>ADH2</strong> and the ALDH2 loci of Japanese with <b>alcoholic</b> liver diseases and of control subjects.
+ADH1B	drug	alcohol	6321953	Seven cis dominant mutations leading to the overproduction of the glucose repressible <b>alcohol</b> dehydrogenase isozyme ADHII (structural gene, <strong>ADH2</strong>) in Saccharomyces cerevisiae have previously been shown to be due to insertion of a transposable element, Ty, in the 5' regulatory region of the <strong>ADH2</strong> gene.
+CYP2A6	drug	nicotine	32573327	Higher activity of the <strong>CYP2A6</strong> enzyme is associated with <b>nicotine</b> dependence, but no research has addressed the PSE effects on the <strong>CYP2A6</strong> gene or its mouse homologue Cyp2a5.
+CYP2A6	addiction	dependence	32573327	Higher activity of the <strong>CYP2A6</strong> enzyme is associated with nicotine <b>dependence</b>, but no research has addressed the PSE effects on the <strong>CYP2A6</strong> gene or its mouse homologue Cyp2a5.
+CYP2A6	drug	nicotine	31796940	SNPs within CHRNA5 A3 B4 and <strong>CYP2A6</strong>/B6, <b>nicotine</b> metabolite concentrations and <b>nicotine</b> dependence treatment success in <b>smokers</b>.
+CYP2A6	addiction	dependence	31796940	SNPs within CHRNA5 A3 B4 and <strong>CYP2A6</strong>/B6, nicotine metabolite concentrations and nicotine <b>dependence</b> treatment success in smokers.
+CYP2A6	drug	nicotine	31796940	Although <strong>CYP2A6</strong> and EGLN2 polymorphisms were associated with <b>nicotine</b> metabolism ratios, neither these polymorphisms nor the ratios were associated with abstinence rates.
+CYP2A6	drug	nicotine	31628204	The Novel <strong>CYP2A6</strong> Inhibitor, DLCI 1, Decreases <b>Nicotine</b> Self Administration in Mice.
+CYP2A6	drug	nicotine	31628204	During <b>tobacco</b> and e cigarette use, <b>nicotine</b> is mainly metabolized in the human liver by cytochrome P450 2A6 (<strong>CYP2A6</strong>).
+CYP2A6	drug	nicotine	31628204	Given that a slower <strong>CYP2A6</strong> metabolism has been associated with less vulnerability to develop <b>nicotine</b> dependence, the current studies sought to validate a novel <strong>CYP2A6</strong> inhibitor, (5 (4 ethylpyridin 3 yl)thiophen 2 yl)methanamine (DLCI 1), for its effects on intravenous <b>nicotine</b> self administration.
+CYP2A6	addiction	dependence	31628204	Given that a slower <strong>CYP2A6</strong> metabolism has been associated with less vulnerability to develop nicotine <b>dependence</b>, the current studies sought to validate a novel <strong>CYP2A6</strong> inhibitor, (5 (4 ethylpyridin 3 yl)thiophen 2 yl)methanamine (DLCI 1), for its effects on intravenous nicotine self administration.
+CYP2A6	drug	nicotine	31578905	While the liver specific <strong>CYP2A6</strong> is associated with the <b>nicotine</b> clearance and <b>smoking</b> addiction, the metabolic activation of the <b>tobacco</b> specific nitrosamine by lung specific CYP2A13 can lead to lung tumorigenesis.It has been reported that inhibition of <strong>CYP2A6</strong> and CYP2A13 enzymes by flavonoids constituents could be an aids in <b>smoking</b> cessation.
+CYP2A6	addiction	addiction	31578905	While the liver specific <strong>CYP2A6</strong> is associated with the nicotine clearance and smoking <b>addiction</b>, the metabolic activation of the tobacco specific nitrosamine by lung specific CYP2A13 can lead to lung tumorigenesis.It has been reported that inhibition of <strong>CYP2A6</strong> and CYP2A13 enzymes by flavonoids constituents could be an aids in smoking cessation.
+CYP2A6	drug	nicotine	31521954	Differences were not statistically significant when adjusted for age, BMI, sex and <strong>CYP2A6</strong> genotype or the <b>nicotine</b> metabolite ratio (NMR), and no evidence of significant correlations were found between melanin (facultative or constitutive) and the pharmacokinetic parameters of <b>nicotine</b> or cotinine or <b>tobacco</b> dependence measures.
+CYP2A6	addiction	dependence	31521954	Differences were not statistically significant when adjusted for age, BMI, sex and <strong>CYP2A6</strong> genotype or the nicotine metabolite ratio (NMR), and no evidence of significant correlations were found between melanin (facultative or constitutive) and the pharmacokinetic parameters of nicotine or cotinine or tobacco <b>dependence</b> measures.
+CYP2A6	drug	nicotine	31241144	Pharmacogenomics of <b>Nicotine</b> Metabolism: Novel <strong>CYP2A6</strong> and CYP2B6 Genetic Variation Patterns in Alaska Native and American Indian Populations.
+CYP2A6	drug	nicotine	31241144	Diverse <strong>CYP2A6</strong> and CYP2B6 variation among the subgroups highlight the need for comprehensive pharmacogenetic testing to guide <b>tobacco</b> cessation therapy for AN/AI populations.
+CYP2A6	drug	nicotine	31241144	<b>Nicotine</b> metabolism is largely determined by <strong>CYP2A6</strong> genotype, and variation in <strong>CYP2A6</strong> activity has altered the treatment success in other populations.
+CYP2A6	drug	nicotine	30815984	The <b>nicotine</b> metabolite ratio (NMR; 3 hydroxycotinine/cotinine) is an index of <strong>CYP2A6</strong> activity.
+CYP2A6	drug	nicotine	30815984	<strong>CYP2A6</strong> is responsible for <b>nicotine</b>'s metabolic inactivation and variation in the NMR/<strong>CYP2A6</strong> is associated with several <b>smoking</b> behaviors.
+CYP2A6	drug	nicotine	30815984	The wGRS was compared with a previous <strong>CYP2A6</strong> gene scoring approach designed for an alternative phenotype (C2/N2; cotinine d2/(<b>nicotine</b> d2 + cotinine d2)).
+CYP2A6	drug	nicotine	30242831	<strong>CYP2A6</strong> normal (n = 82) and reduced (n = 42) genotype predicted plasma <b>nicotine</b> concentrations but not withdrawal symptoms.
+CYP2A6	addiction	withdrawal	30242831	<strong>CYP2A6</strong> normal (n = 82) and reduced (n = 42) genotype predicted plasma nicotine concentrations but not <b>withdrawal</b> symptoms.
+CYP2A6	drug	nicotine	29875862	The Role of <strong>CYP2A6</strong> Genetic Polymorphism in <b>Nicotine</b> Dependence and <b>Tobacco</b> Consumption among Bataknese Male <b>Smokers</b>.
+CYP2A6	addiction	dependence	29875862	The Role of <strong>CYP2A6</strong> Genetic Polymorphism in Nicotine <b>Dependence</b> and Tobacco Consumption among Bataknese Male Smokers.
+CYP2A6	drug	nicotine	29875862	This research aimed to analyse the relationship between <strong>CYP2A6</strong> gene polymorphism with <b>nicotine</b> dependence and its relation to the number of cigarette consumption among Bataknese <b>smokers</b>.
+CYP2A6	addiction	dependence	29875862	This research aimed to analyse the relationship between <strong>CYP2A6</strong> gene polymorphism with nicotine <b>dependence</b> and its relation to the number of cigarette consumption among Bataknese smokers.
+CYP2A6	drug	alcohol	29568101	Hepatic <strong>CYP2A6</strong> expression is increased in patients with non <b>alcoholic</b> fatty liver disease (NAFLD).
+CYP2A6	drug	alcohol	29404485	The number of EVs and the amounts of EV CYP2E1, <strong>CYP2A</strong>, CYP1A1/2, and CYP4B proteins were markedly elevated in both patients with <b>alcoholism</b> and <b>alcohol</b> exposed rats and mice.
+CYP2A6	drug	nicotine	29307500	The genes CHRNA5 and <strong>CYP2A6</strong> are strong genomic contributors that alter the risk of heaviness of <b>smoking</b>, <b>tobacco</b> use disorder, and <b>smoking</b> related diseases in humans.
+CYP2A6	drug	nicotine	29048184	Our objective was to study the influence of <b>nicotine</b> metabolite ratio, <strong>CYP2A6</strong> genotype and sex on the response to <b>nicotine</b> replacement therapy and varenicline.
+CYP2A6	drug	nicotine	29048184	The hazard ratio of relapsing was estimated in multivariate Cox regression models including the sex and the <b>nicotine</b> metabolism determined by the phenotype or by <strong>CYP2A6</strong> genotyping (rs1801272 and rs28399433).
+CYP2A6	drug	nicotine	28971126	Data on polymorphisms in <strong>CYP2A6</strong> associated to risk and predispose to <b>smoking</b> related variables.
+CYP2A6	drug	nicotine	28971126	This article contains data on the single nucleotide polymorphisms (SNPs) rs1137115, rs1801272 and rs28399433 rs4105144 in <strong>CYP2A6</strong> associated to <b>smoking</b> related variables in Mexican Mestizo <b>smokers</b> (Pérez Rubio et al., 2017) [1].
+CYP2A6	drug	nicotine	28921760	The activity of <strong>CYP2A6</strong>, the major <b>nicotine</b> inactivating enzyme, is measurable in <b>smokers</b> using the <b>nicotine</b> metabolite ratio (NMR; 3'hydroxycotinine/cotinine).
+CYP2A6	drug	nicotine	28734893	Genetic polymorphisms in <strong>CYP2A6</strong> are associated with a risk of cigarette <b>smoking</b> and predispose to <b>smoking</b> at younger ages.
+CYP2A6	drug	nicotine	28734893	The <strong>CYP2A6</strong> gene encodes the main enzyme responsible for <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	28734893	Depending on the study population, different genetic variants of <strong>CYP2A6</strong> associated with cigarette <b>smoking</b> have been described.
+CYP2A6	drug	nicotine	28734893	Therefore, we evaluated the possible association between SNPs in <strong>CYP2A6</strong> with cigarette <b>smoking</b> and <b>nicotine</b> addiction related variables in Mexican mestizo <b>smokers</b>.
+CYP2A6	addiction	addiction	28734893	Therefore, we evaluated the possible association between SNPs in <strong>CYP2A6</strong> with cigarette smoking and nicotine <b>addiction</b> related variables in Mexican mestizo smokers.
+CYP2A6	drug	nicotine	28734893	We found that the A allele of rs1137115 (OR=1.41) in exon 1 of <strong>CYP2A6</strong> and the T allele of rs4105144 (OR=1.32) in the 5' UTR of the gene are associated with the risk of cigarette <b>smoking</b> (p<0.05); rs1137115 affects the level of alternative splicing, resulting in a <strong>CYP2A6</strong> isoform with low enzymatic activity, whereas rs4105144 is likely to be in a binding site for the transcription factor for glucocorticoids receptor (GR) and regulates the expression of <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	28683421	Individual differences in the rate of <b>nicotine</b> metabolism contribute to differences in <b>tobacco</b> use, dependence, and efficacy of <b>smoking</b> cessation treatments and can be assessed using the <b>nicotine</b> metabolite ratio (NMR), a validated biomarker for <strong>CYP2A6</strong> activity.
+CYP2A6	addiction	dependence	28683421	Individual differences in the rate of nicotine metabolism contribute to differences in tobacco use, <b>dependence</b>, and efficacy of smoking cessation treatments and can be assessed using the nicotine metabolite ratio (NMR), a validated biomarker for <strong>CYP2A6</strong> activity.
+CYP2A6	drug	nicotine	28583088	Finally, we found that liver specific CHRNA4 transcription was highly correlated with genes involved in the <b>nicotine</b> metabolism, including <strong>CYP2A6</strong>, UGT2B7, and FMO3.
+CYP2A6	drug	nicotine	28542511	Association of <strong>CYP2A6</strong> activity with lung cancer incidence in <b>smokers</b>: The multiethnic cohort study.
+CYP2A6	drug	nicotine	28542511	In most <b>smokers</b>, cytochrome P450 2A6 (<strong>CYP2A6</strong>) catalyzed C oxidation accounts for >75% of <b>nicotine</b> metabolism, and the activity of this enzyme has been shown to correlate with the amount of <b>nicotine</b> and carcinogens drawn from cigarettes.
+CYP2A6	drug	nicotine	28542511	We prospectively evaluated the association of urinary biomarkers of <b>nicotine</b> uptake (total <b>nicotine</b> equivalents [TNE]) and <strong>CYP2A6</strong> activity (ratio of urinary total trans 3' hydroxycotinine to cotinine) with lung cancer risk among 2,309 Multiethnic Cohort Study participants who were current <b>smokers</b> at time of urine collection; 92 cases were diagnosed during a mean follow up of 9.5 years.
+CYP2A6	drug	nicotine	28542511	We found that higher <strong>CYP2A6</strong> activity and TNE was associated with increased lung cancer risk after adjusting for age, sex, race/ethnicity, body mass index, <b>smoking</b> duration, and urinary creatinine (p's = 0.002).
+CYP2A6	drug	nicotine	28542511	These findings suggest that <strong>CYP2A6</strong> activity provides information on lung cancer risk that is not captured by <b>smoking</b> history or a (short term) biomarker of dose.
+CYP2A6	drug	nicotine	28542511	<strong>CYP2A6</strong> activity should be further studied as a risk biomarker for <b>smoking</b> related lung cancer.
+CYP2A6	drug	nicotine	28507465	Distribution of polymorphic variants of <strong>CYP2A6</strong> and their involvement in <b>nicotine</b> addiction.
+CYP2A6	addiction	addiction	28507465	Distribution of polymorphic variants of <strong>CYP2A6</strong> and their involvement in nicotine <b>addiction</b>.
+CYP2A6	drug	nicotine	28507465	<strong>CYP2A6</strong> has been identified as the main gene that codifies the enzyme that metabolizes <b>nicotine</b>.
+CYP2A6	drug	nicotine	28507465	Many alleles have been identified after the discovery of <strong>CYP2A6</strong>, suggesting a wide interethnic variability and a diverse <b>smoking</b> behavior of the allele carrying individuals.
+CYP2A6	drug	nicotine	28507465	The main purpose of this review is to update and highlight the effects of the <strong>CYP2A6</strong> gene variability related to <b>tobacco</b> consumption reported from diverse human populations.
+CYP2A6	drug	nicotine	28507465	The review further aims to consider <strong>CYP2A6</strong> in future studies as a possible genetic marker for the prevention and treatment of <b>nicotine</b> addiction.
+CYP2A6	addiction	addiction	28507465	The review further aims to consider <strong>CYP2A6</strong> in future studies as a possible genetic marker for the prevention and treatment of nicotine <b>addiction</b>.
+CYP2A6	drug	nicotine	28472995	The odds ratio for starting <b>smoking</b> was significantly lower in subjects carrying a <strong>CYP2A6</strong> low activity/variant COMT rs4680 genotype than in those possessing a <strong>CYP2A6</strong> wild type/variant COMT rs4680 genotype (0.44, 95% confidence interval = 0.19 0.98, P = 0.043).
+CYP2A6	drug	nicotine	28472995	Comparisons of Fagerstrom Test for <b>Nicotine</b> Dependence (FTND), Physiological Cigarette Dependence Scale (PCDS), and Cigarette Withdrawal symptoms (CWS 21) among the <b>smokers</b> with different <strong>CYP2A6</strong>/COMT polymorphisms were not significantly different.
+CYP2A6	addiction	dependence	28472995	Comparisons of Fagerstrom Test for Nicotine <b>Dependence</b> (FTND), Physiological Cigarette <b>Dependence</b> Scale (PCDS), and Cigarette Withdrawal symptoms (CWS 21) among the smokers with different <strong>CYP2A6</strong>/COMT polymorphisms were not significantly different.
+CYP2A6	addiction	withdrawal	28472995	Comparisons of Fagerstrom Test for Nicotine Dependence (FTND), Physiological Cigarette Dependence Scale (PCDS), and Cigarette <b>Withdrawal</b> symptoms (CWS 21) among the smokers with different <strong>CYP2A6</strong>/COMT polymorphisms were not significantly different.
+CYP2A6	drug	nicotine	28472521	These Key results involve genetic variants in the nicotinic receptor subunit gene CHRNA5, variants in the <b>nicotine</b> metabolism gene <strong>CYP2A6</strong>, and the <b>nicotine</b> metabolite ratio.
+CYP2A6	drug	nicotine	28290528	<strong>CYP2A6</strong>, the primary hepatic <b>nicotine</b> metabolism gene, is robustly associated with cigarette consumption but other enzymes contribute to <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	28290528	The polymorphism rs2266780 (E308G) was associated with N oxidation of both orally administered and ad libitum smoked <b>nicotine</b> (P⩽3.3 × 10 5 controlling for <strong>CYP2A6</strong> genotype).
+CYP2A6	drug	nicotine	28290528	As N oxidation accounts for only a small percentage of hepatic <b>nicotine</b> metabolism we hypothesized that FMO3 genotype affects <b>nicotine</b> metabolism in the brain (unlike <strong>CYP2A6</strong>, FMO3 is expressed in human brain) or that <b>nicotine</b> N oxide itself has pharmacological activity.
+CYP2A6	drug	nicotine	28092945	<b>Nicotine</b> is the primary addictive agent in <b>tobacco</b>, and P450 2A6 (gene name: <strong>CYP2A6</strong>) is the primary catalyst of <b>nicotine</b> metabolism.
+CYP2A6	addiction	addiction	28092945	Nicotine is the primary <b>addictive</b> agent in tobacco, and P450 2A6 (gene name: <strong>CYP2A6</strong>) is the primary catalyst of nicotine metabolism.
+CYP2A6	drug	nicotine	28092945	Numerous studies have reported that <b>smokers</b> who carry reduced activity or null <strong>CYP2A6</strong> alleles do smoke less.
+CYP2A6	drug	nicotine	28092945	Yet only in Asian populations, both Japanese and Chinese, which have a high prevalence of genetic variants, has a link between <strong>CYP2A6</strong>, <b>smoking</b> dose, and lung cancer been established.
+CYP2A6	drug	nicotine	28069549	SNPs within CHRNA5 A3 B4 and <strong>CYP2A6</strong>/B6 are associated with <b>smoking</b> dependence but not with <b>tobacco</b> dependence treatment outcomes in the Czech population.
+CYP2A6	addiction	dependence	28069549	SNPs within CHRNA5 A3 B4 and <strong>CYP2A6</strong>/B6 are associated with smoking <b>dependence</b> but not with tobacco <b>dependence</b> treatment outcomes in the Czech population.
+CYP2A6	drug	nicotine	28069549	We confirmed the association between variants within genes that code nicotinic acetylcholine receptors ( A3,  A5 and  B3), <strong>CYP2A6</strong>/B6 and <b>tobacco</b> dependence development in the Czech population.
+CYP2A6	addiction	dependence	28069549	We confirmed the association between variants within genes that code nicotinic acetylcholine receptors ( A3,  A5 and  B3), <strong>CYP2A6</strong>/B6 and tobacco <b>dependence</b> development in the Czech population.
+CYP2A6	drug	nicotine	28032407	<strong>CYP2A6</strong> metabolism in the development of <b>smoking</b> behaviors in young adults.
+CYP2A6	drug	nicotine	28032407	Cytochrome P450 2A6 (<strong>CYP2A6</strong>) encodes the enzyme responsible for the majority of <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	28032407	Previous studies support that slow metabolizers smoke fewer cigarettes once <b>nicotine</b> dependent but provide conflicting results on the role of <strong>CYP2A6</strong> in the development of dependence.
+CYP2A6	addiction	dependence	28032407	Previous studies support that slow metabolizers smoke fewer cigarettes once nicotine dependent but provide conflicting results on the role of <strong>CYP2A6</strong> in the development of <b>dependence</b>.
+CYP2A6	drug	nicotine	28032407	By focusing on the critical period of young adulthood, this study examines the relationship of <strong>CYP2A6</strong> variation and <b>smoking</b> milestones.
+CYP2A6	drug	alcohol	28032407	A total of 1209 European American young adults enrolled in the Collaborative Study on the Genetics of <b>Alcoholism</b> were genotyped for <strong>CYP2A6</strong> variants to calculate a previously well validated metric that estimates nicotine metabolism.
+CYP2A6	drug	nicotine	28032407	A total of 1209 European American young adults enrolled in the Collaborative Study on the Genetics of Alcoholism were genotyped for <strong>CYP2A6</strong> variants to calculate a previously well validated metric that estimates <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	28032407	These findings highlight the complex role of <strong>CYP2A6</strong> variation across different developmental stages of <b>smoking</b> behaviors.
+CYP2A6	drug	nicotine	27865452	<strong>CYP2A6</strong> Genetic Variation Alters Striatal Cingulate Circuits, Network Hubs, and Executive Processing in <b>Smokers</b>.
+CYP2A6	drug	nicotine	27865452	Variation in the <strong>CYP2A6</strong> gene alters the rate of <b>nicotine</b> metabolic inactivation and is associated with <b>smoking</b> behaviors and cessation success rates.
+CYP2A6	drug	nicotine	27865452	A significant <strong>CYP2A6</strong> genotype × <b>smoking</b> effect was found in the dorsal anterior cingulate cortex and ventral striatum, such that the normal (vs. slow) genotype individuals showed greater functional connectivity strength among <b>smokers</b> but not nonsmokers.
+CYP2A6	drug	nicotine	27865452	Because the <strong>CYP2A6</strong> effect was seen only in <b>smokers</b>, these data suggest that the rate of <b>nicotine</b> metabolism and thus the concentration of <b>nicotine</b> presented to the brain over the course of <b>nicotine</b> addiction shapes brain circuits that, among other functions, compute reward and impulsivity processes.
+CYP2A6	addiction	addiction	27865452	Because the <strong>CYP2A6</strong> effect was seen only in smokers, these data suggest that the rate of nicotine metabolism and thus the concentration of nicotine presented to the brain over the course of nicotine <b>addiction</b> shapes brain circuits that, among other functions, compute reward and impulsivity processes.
+CYP2A6	addiction	reward	27865452	Because the <strong>CYP2A6</strong> effect was seen only in smokers, these data suggest that the rate of nicotine metabolism and thus the concentration of nicotine presented to the brain over the course of nicotine addiction shapes brain circuits that, among other functions, compute <b>reward</b> and impulsivity processes.
+CYP2A6	drug	nicotine	27106177	<b>Nicotine</b> is a substrate of <strong>CYP2A6</strong>, which is induced by oestrogen, resulting in lower concentrations of <b>nicotine</b> in females than in males, especially in females taking oral contraceptives.
+CYP2A6	drug	nicotine	27338962	<b>Nicotine</b> use disorders are associated with polymorphisms in a cluster of nicotinic acetylcholine receptors on chromosome 15q24, and mutations that reduce the enzymatic activity of <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	27180107	Rate of <b>nicotine</b> metabolism has been identified as an important factor influencing <b>nicotine</b> intake and can be estimated using the <b>nicotine</b> metabolite ratio (NMR), a validated biomarker of <strong>CYP2A6</strong> enzyme activity.
+CYP2A6	drug	nicotine	27180107	Overall there was a greater step down, linear type relationship between NMR groups and cotinine or cotinine/cigarette in African Americans, which is consistent with the idea that differences in blood cotinine levels between the African American NMR groups were primarily due to differences in <strong>CYP2A6</strong> enzyme activity without titration of <b>nicotine</b> intake among faster <b>nicotine</b> metabolizers.
+CYP2A6	drug	nicotine	27113016	This meta GWAS of the NMR identifies <strong>CYP2A6</strong> variants, replicates the top ranked single nucleotide polymorphism from a recent Finnish meta GWAS of the NMR, identifies functional mechanisms, and provides pan continental population biomarkers for <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	27113016	We replicate the top ranking single nucleotide polymorphism from a recent GWAS of the NMR in Finnish <b>smokers</b>, identify a functional mechanism for this intronic variant from in silico analyses of RNA seq data that is consistent with <strong>CYP2A6</strong> expression measured in postmortem lung and liver, and provide additional support for the intergenic region between <strong>CYP2A6</strong> and CYP2A7.
+CYP2A6	drug	nicotine	27080866	Hepatic cytochrome P 450 2A6 (<strong>CYP2A6</strong>) is involved in the 70 80 % of the initial metabolism of <b>nicotine</b> and its co metabolites.
+CYP2A6	drug	nicotine	27080866	As this metabolism is slowed by inhibitors of <strong>CYP2A6</strong>, this kind of enzymatic inhibition has been proposed as a novel target for <b>smoking</b> cessation.
+CYP2A6	drug	nicotine	27080866	This study revealed that three <strong>CYP2A6</strong> inhibitors: two furanocoumarins, xanthotoxin (15 mg/kg) and bergapten (25 mg/kg), and the simple coumarin umbelliferone (25 mg/kg), prolonged the antidepressive and procognitive effects of <b>nicotine</b>.
+CYP2A6	drug	nicotine	27035242	Disposition kinetics and metabolism of <b>nicotine</b> and cotinine in African American <b>smokers</b>: impact of <strong>CYP2A6</strong> genetic variation and enzymatic activity.
+CYP2A6	drug	nicotine	27035242	The rate of <b>nicotine</b> metabolism, determined primarily by <strong>CYP2A6</strong> activity, influences <b>tobacco</b> dependence and <b>smoking</b> induced disease risk.
+CYP2A6	addiction	dependence	27035242	The rate of nicotine metabolism, determined primarily by <strong>CYP2A6</strong> activity, influences tobacco <b>dependence</b> and smoking induced disease risk.
+CYP2A6	drug	nicotine	27035242	We studied <b>nicotine</b> disposition kinetics and metabolism by the <strong>CYP2A6</strong> genotype and enzymatic activity, as measured by the <b>nicotine</b> metabolite ratio (NMR), in African American <b>smokers</b>.
+CYP2A6	drug	nicotine	27035242	<strong>CYP2A6</strong> genotype, NMR, and <b>nicotine</b> pharmacokinetic data may inform studies of individual differences in <b>smoking</b> behavior and biomarkers of <b>nicotine</b> exposure.
+CYP2A6	drug	nicotine	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 addiction genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to <b>smoking</b> behavior and <b>nicotine</b> metabolism: CHRNA5 CHRNA3 CHRNB4 and <strong>CYP2A6</strong> CYP2B6.
+CYP2A6	addiction	addiction	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 <b>addiction</b> genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to smoking behavior and nicotine metabolism: CHRNA5 CHRNA3 CHRNB4 and <strong>CYP2A6</strong> CYP2B6.
+CYP2A6	drug	nicotine	26921259	In a genome wide association analysis of the <b>nicotine</b> metabolite ratio in 315 individuals participating in <b>nicotine</b> metabolism laboratory studies, we identified genome wide significant variants in the <strong>CYP2A6</strong> region (min p = 9.10E 15).
+CYP2A6	drug	nicotine	26757861	[Association between genotype and allele frequencies of <strong>CYP2A6</strong>*12 and rs16969968 in CHRNA5 variants with <b>smoking</b> and body mass index in young subjects from Northeast Mexico].
+CYP2A6	drug	nicotine	26757861	Several studies have reported that variants rs16969968 G>A of the CHRNA5 gene and <strong>CYP2A6</strong>*12 of the <strong>CYP2A6</strong> gene are associated with <b>smoking</b> and <b>smoking</b> refusal, respectively.
+CYP2A6	drug	nicotine	26670214	<strong>CYP2A6</strong> genotyping is of clinical importance  <strong>CYP2A6</strong> gene variants influence <b>nicotine</b> metabolism and are associated with <b>nicotine</b> dependence, cigarettes per day, <b>smoking</b> cessation and the risk for <b>tobacco</b> associated cancers.
+CYP2A6	addiction	dependence	26670214	<strong>CYP2A6</strong> genotyping is of clinical importance  <strong>CYP2A6</strong> gene variants influence nicotine metabolism and are associated with nicotine <b>dependence</b>, cigarettes per day, smoking cessation and the risk for tobacco associated cancers.
+CYP2A6	drug	nicotine	26648056	Administering chemical inhibitors of <strong>CYP2A6</strong> has been shown to slow down the elimination of <b>nicotine</b> with consequent reduction in number of cigarettes smoked.
+CYP2A6	drug	nicotine	26644138	Variation in <strong>CYP2A6</strong> and <b>tobacco</b> dependence throughout adolescence and in young adult <b>smokers</b>.
+CYP2A6	addiction	dependence	26644138	Variation in <strong>CYP2A6</strong> and tobacco <b>dependence</b> throughout adolescence and in young adult smokers.
+CYP2A6	drug	nicotine	26644138	<b>Smoking</b> is influenced by genetic factors including variation in <strong>CYP2A6</strong> and CYP2B6, which encode <b>nicotine</b> metabolizing enzymes.
+CYP2A6	drug	nicotine	26644138	In early adolescence, <strong>CYP2A6</strong> slow <b>nicotine</b> metabolism was associated with higher dependence acquisition, but reduced cigarette consumption.
+CYP2A6	addiction	dependence	26644138	In early adolescence, <strong>CYP2A6</strong> slow nicotine metabolism was associated with higher <b>dependence</b> acquisition, but reduced cigarette consumption.
+CYP2A6	drug	nicotine	26644138	Here we extend this work by examining associations of <strong>CYP2A6</strong> and CYP2B6 with <b>tobacco</b> dependence acquisition in a larger sample of <b>smokers</b> followed throughout adolescence.
+CYP2A6	addiction	dependence	26644138	Here we extend this work by examining associations of <strong>CYP2A6</strong> and CYP2B6 with tobacco <b>dependence</b> acquisition in a larger sample of smokers followed throughout adolescence.
+CYP2A6	drug	nicotine	26644138	Cox's proportional hazards models compared the risk of ICD 10 <b>tobacco</b> dependence acquisition (score 3+) for <strong>CYP2A6</strong> and CYP2B6 metabolism groups.
+CYP2A6	addiction	dependence	26644138	Cox's proportional hazards models compared the risk of ICD 10 tobacco <b>dependence</b> acquisition (score 3+) for <strong>CYP2A6</strong> and CYP2B6 metabolism groups.
+CYP2A6	addiction	dependence	26644138	In those who initiated inhalation during follow up, <strong>CYP2A6</strong> slow (vs. normal) metabolizers were at greater risk of <b>dependence</b> (hazards ratio (HR)=2.3; 95% CI=1.1, 4.8); CYP2B6 slow (vs. normal) metabolizers had non significantly greater risk (HR=1.5; 95% CI=0.8, 2.6).
+CYP2A6	drug	nicotine	26644138	Variation in <strong>CYP2A6</strong> or CYP2B6 was not significantly associated with early <b>smoking</b> symptoms or cigarette consumption at end of follow up.
+CYP2A6	drug	nicotine	26644138	Our findings extend previous work indicating that slow <b>nicotine</b> metabolism mediated by <strong>CYP2A6</strong>, and perhaps CYP2B6, increases risk for <b>tobacco</b> dependence throughout adolescence.
+CYP2A6	addiction	dependence	26644138	Our findings extend previous work indicating that slow nicotine metabolism mediated by <strong>CYP2A6</strong>, and perhaps CYP2B6, increases risk for tobacco <b>dependence</b> throughout adolescence.
+CYP2A6	drug	nicotine	26416825	Three hundred sixty four Mexican Mestizo Mexico City residents from 87 families with at least one <b>smoker</b> were assessed for association of 12 gene variants of six candidate genes (CHRNA4, CHRNB2, DRD2, ANKK1, SLC6A3, and <strong>CYP2A6</strong>) with cigarette consumption, age of initiation and <b>smoking</b> duration.
+CYP2A6	drug	nicotine	26416825	Our results indicate effects of the rs2072658 CHRNB2 and rs28399433 <strong>CYP2A6</strong> gene variants on AO, SS and PD in Mexican Mestizo <b>smokers</b>.
+CYP2A6	drug	nicotine	26370685	EFFECT OF <strong>CYP2A6</strong>*4 GENETIC POLYMORPHISMS ON <b>SMOKING</b> BEHAVIORS AND <b>NICOTINE</b> DEPENDENCE IN A GENERAL POPULATION OF JAPANESE MEN.
+CYP2A6	addiction	dependence	26370685	EFFECT OF <strong>CYP2A6</strong>*4 GENETIC POLYMORPHISMS ON SMOKING BEHAVIORS AND NICOTINE <b>DEPENDENCE</b> IN A GENERAL POPULATION OF JAPANESE MEN.
+CYP2A6	drug	nicotine	26370685	<b>Nicotine</b> in cigarettes is metabolized primarily by <strong>CYP2A6</strong> catalyzed oxidation.
+CYP2A6	drug	nicotine	26370685	The aim of this study was to examine the effects of <strong>CYP2A6</strong>*4 genetic polymorphism on <b>smoking</b> behavior and <b>nicotine</b> dependence in a general population of Japanese men.
+CYP2A6	addiction	dependence	26370685	The aim of this study was to examine the effects of <strong>CYP2A6</strong>*4 genetic polymorphism on smoking behavior and nicotine <b>dependence</b> in a general population of Japanese men.
+CYP2A6	drug	nicotine	26370685	<strong>CYP2A6</strong>*4 genetic polymorphisms may not strongly affect <b>smoking</b> behavior but may possibly have an effect on <b>nicotine</b> dependence.
+CYP2A6	addiction	dependence	26370685	<strong>CYP2A6</strong>*4 genetic polymorphisms may not strongly affect smoking behavior but may possibly have an effect on nicotine <b>dependence</b>.
+CYP2A6	drug	nicotine	26272810	The <b>nicotine</b> metabolite ratio (NMR), a stable measure of hepatic <b>nicotine</b> metabolism via the <strong>CYP2A6</strong> pathway and total <b>nicotine</b> clearance, is a predictive biomarker of response to <b>nicotine</b> replacement therapy, with increased quit rates in slower metabolizers.
+CYP2A6	drug	nicotine	26100465	In humans, <b>nicotine</b> is metabolized primarily by hepatic <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	26100465	When <strong>CYP2A6</strong> is substantially inhibited, <b>nicotine</b> clearance is delayed and <b>nicotine</b> withdrawal symptoms are attenuated.
+CYP2A6	addiction	withdrawal	26100465	When <strong>CYP2A6</strong> is substantially inhibited, nicotine clearance is delayed and nicotine <b>withdrawal</b> symptoms are attenuated.
+CYP2A6	drug	nicotine	26100465	Behavioral and pharmacokinetic e cig studies should be interpreted with attention to likely levels of nicotyrine delivery: e cig studies may need to routinely measure nicotyrine exposure, assess <strong>CYP2A6</strong> activity, confirm <b>nicotine</b> delivery, or deliberately compare unoxidized and oxidized e liquids.
+CYP2A6	drug	nicotine	26100465	<strong>CYP2A</strong> inhibitors like nicotyrine may be useful for future <b>smoking</b> cessation therapy.
+CYP2A6	drug	nicotine	26081405	A Meta analysis was performed to assess the association of defective hepatic cytochrome P450 2A6 (<strong>CYP2A6</strong>) gene with <b>smoking</b> behaviors.
+CYP2A6	drug	nicotine	26081405	All eligible studies published up to 2014 were searched out from PubMed, China National Knowledge Internet (CNKI), ISI Web of knowledge (ISI), vip citation databases (VIP), Chinese BioMedical Literature (CBM) and Elsevier Science Direct, searching words were "smok*","<b>nicotine</b> dependence","<strong>CYP2A6</strong>","cytochrome P450 2A6","polymorphism","mut*"and"varia*", while 436 articles were concluded.
+CYP2A6	addiction	dependence	26081405	All eligible studies published up to 2014 were searched out from PubMed, China National Knowledge Internet (CNKI), ISI Web of knowledge (ISI), vip citation databases (VIP), Chinese BioMedical Literature (CBM) and Elsevier Science Direct, searching words were "smok*","nicotine <b>dependence</b>","<strong>CYP2A6</strong>","cytochrome P450 2A6","polymorphism","mut*"and"varia*", while 436 articles were concluded.
+CYP2A6	drug	nicotine	26081405	We didn't find a significant effect of defective <strong>CYP2A6</strong> gene on <b>smoking</b> initiation (fixed effect model (FEM): OR = 0.90, 95%CI: 0.78 1.03, I(2) = 25.8%), <b>smoking</b> persistence (random effect model (REM): OR = 0.85, 95%CI: 0.59 1.23, I(2) = 66.3%) and <b>smoking</b> cessation (REM: OR = 0.89, 95%CI: 0.57 1.40, I(2) = 67.1%).
+CYP2A6	drug	nicotine	26081405	But it showed a significant protective effect of <strong>CYP2A6</strong>*4 on <b>smoking</b> initiation (FEM: OR = 0.78, 95%CI: 0.61 0.99, I(2) = 28.2%), <b>smoking</b> persistence (FEM: OR = 0.53, 95%CI: 0.36 0.77, I(2) = 41.0%) and <b>smoking</b> cessation (REM: OR = 0.49, 95%CI: 0.31 0.80, I(2) = 0.0%).
+CYP2A6	drug	nicotine	26081405	This Meta analysis suggested that there was not a protective effect of defective <strong>CYP2A6</strong> gene against <b>smoking</b> behaviors.
+CYP2A6	drug	nicotine	26081405	But <b>smokers</b> with whole <strong>CYP2A6</strong> gene deletion would be less likely to start <b>smoking</b>, less <b>smoking</b> persistence and more likely to quit <b>smoking</b> successful than <b>smokers</b> with wild <strong>CYP2A6</strong> gene.
+CYP2A6	drug	nicotine	26069034	Inter individual differences in <b>smoking</b> behavior result, in part, from variation in the rate of <strong>CYP2A6</strong> mediated <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	26069034	A phenotypic measure of <strong>CYP2A6</strong> activity is the <b>nicotine</b> metabolite ratio (NMR), the ratio of 3'hydroxycotinine/cotinine.
+CYP2A6	drug	nicotine	26060595	<strong>CYP2A6</strong> Polymorphisms May Strengthen Individualized Treatment for <b>Nicotine</b> Dependence.
+CYP2A6	addiction	dependence	26060595	<strong>CYP2A6</strong> Polymorphisms May Strengthen Individualized Treatment for Nicotine <b>Dependence</b>.
+CYP2A6	drug	nicotine	26060595	Each <strong>CYP2A6</strong> gene variant metabolizes <b>nicotine</b> differently depending on its enzymatic activities.
+CYP2A6	drug	nicotine	26060595	The normal <b>nicotine</b> metabolizer <strong>CYP2A6</strong>(*)1A is associated with high scores of <b>nicotine</b> dependence (5 10) on the Fagerström Test for <b>Nicotine</b> Dependence (FTND) scale because it encodes for enzymes that catalyze <b>nicotine</b> 100%.
+CYP2A6	addiction	dependence	26060595	The normal nicotine metabolizer <strong>CYP2A6</strong>(*)1A is associated with high scores of nicotine <b>dependence</b> (5 10) on the Fagerström Test for Nicotine <b>Dependence</b> (FTND) scale because it encodes for enzymes that catalyze nicotine 100%.
+CYP2A6	drug	nicotine	26060595	Slow <b>nicotine</b> metabolizers (i.e., <strong>CYP2A6</strong>(*)1H, <strong>CYP2A6</strong>(*)4A, <strong>CYP2A6</strong>(*)9, and <strong>CYP2A6</strong>(*)12A) are associated with underrated <b>nicotine</b> metabolizing activity (50% 75%), linking them to low scores for <b>nicotine</b> dependence (0 4) on the FTND scale.
+CYP2A6	addiction	dependence	26060595	Slow nicotine metabolizers (i.e., <strong>CYP2A6</strong>(*)1H, <strong>CYP2A6</strong>(*)4A, <strong>CYP2A6</strong>(*)9, and <strong>CYP2A6</strong>(*)12A) are associated with underrated nicotine metabolizing activity (50% 75%), linking them to low scores for nicotine <b>dependence</b> (0 4) on the FTND scale.
+CYP2A6	drug	nicotine	26060595	An overview of <strong>CYP2A6</strong> polymorphism enzymatic activities in <b>nicotine</b> dependence etiology and treatment revealed that slow <b>nicotine</b> metabolizers may strengthen the individualized treatment of <b>nicotine</b> dependence.
+CYP2A6	addiction	dependence	26060595	An overview of <strong>CYP2A6</strong> polymorphism enzymatic activities in nicotine <b>dependence</b> etiology and treatment revealed that slow nicotine metabolizers may strengthen the individualized treatment of nicotine <b>dependence</b>.
+CYP2A6	drug	nicotine	25862079	The <strong>CYP2A6</strong>*4 allele, characterized as the whole deletion of this gene, is closely associated with <b>nicotine</b> dependence, cancer susceptibility, and drug responsiveness.
+CYP2A6	addiction	dependence	25862079	The <strong>CYP2A6</strong>*4 allele, characterized as the whole deletion of this gene, is closely associated with nicotine <b>dependence</b>, cancer susceptibility, and drug responsiveness.
+CYP2A6	drug	nicotine	25862079	This work greatly expanded our understanding of the distribution of <strong>CYP2A6</strong>*4 in Chinese population and provided more information of different ethnic population's <b>smoking</b> behavior and also in disease susceptibility and drug response.
+CYP2A6	drug	nicotine	25857233	The human cytochrome P450 2A6 (<strong>CYP2A6</strong>) and monoamine oxidases (MAO A and MAO B), catalyzing <b>nicotine</b> and dopamine metabolisms, respectively, are two therapeutic targets of <b>nicotine</b> dependence.
+CYP2A6	addiction	dependence	25857233	The human cytochrome P450 2A6 (<strong>CYP2A6</strong>) and monoamine oxidases (MAO A and MAO B), catalyzing nicotine and dopamine metabolisms, respectively, are two therapeutic targets of nicotine <b>dependence</b>.
+CYP2A6	addiction	dependence	25857233	Flavonoids possessed strong inhibitory effect on <strong>CYP2A6</strong> in reversible mode, while inhibition by hirsutinolides was mechanism based (NADPH , concentration , and time <b>dependence</b>) and irreversible.
+CYP2A6	drug	nicotine	25744963	<strong>CYP2A6</strong> Longitudinal Effects in Young <b>Smokers</b>.
+CYP2A6	drug	nicotine	25744963	The present study sought to identify time dependent within participant effects of <strong>CYP2A6</strong> genotypes on <b>smoking</b> frequency and <b>nicotine</b> dependence in young <b>smokers</b>.
+CYP2A6	addiction	dependence	25744963	The present study sought to identify time dependent within participant effects of <strong>CYP2A6</strong> genotypes on smoking frequency and nicotine <b>dependence</b> in young smokers.
+CYP2A6	drug	nicotine	25744963	Predicted <b>nicotine</b> metabolic rate based on <strong>CYP2A6</strong> diplotypes (<strong>CYP2A6</strong> diplotype predicted rate [CDPR]) was partitioned into Normal, Intermediate, and Slow categories using a metabolism metric.
+CYP2A6	drug	nicotine	25744963	Reduced metabolism <strong>CYP2A6</strong> genotypes are associated with both risk and protective effects in novice <b>smokers</b>.
+CYP2A6	drug	nicotine	25683822	There was also a significant difference of age of <b>smoking</b> initiation between normal and intermediate metabolizers of <strong>CYP2A6</strong> gene (FEM: SMD = 0.216, 95%CI: 0.056 0.377).
+CYP2A6	drug	nicotine	25683822	No significant difference of <b>tobacco</b> dependence between normal and reduced metabolizers of <strong>CYP2A6</strong> gene was found (FEM: SMD = 0.185, 95%CI =  0.001 to 0.371).
+CYP2A6	addiction	dependence	25683822	No significant difference of tobacco <b>dependence</b> between normal and reduced metabolizers of <strong>CYP2A6</strong> gene was found (FEM: SMD = 0.185, 95%CI =  0.001 to 0.371).
+CYP2A6	drug	nicotine	25655887	<b>Nicotine</b>, the major psychoactive compound in cigarette smoke, is metabolized by a number of enzymes, including <strong>CYP2A6</strong>, CYP2B6, FMOs, and UGTs, among others.
+CYP2A6	drug	nicotine	25655887	Variation in the genes encoding these enzymes, in particular <strong>CYP2A6</strong>, can alter the rate of <b>nicotine</b> metabolism and <b>smoking</b> behaviors.
+CYP2A6	drug	nicotine	25555385	<b>Nicotine</b> content of cigarettes was progressively reduced over 6 months and measures of <b>smoking</b> behavior, as well as <b>nicotine</b> metabolites and <b>tobacco</b> smoke toxicant exposure, <strong>CYP2A6</strong> and nicotinic CHRNA5 A3 B4 (rs1051730) genotype were measured.
+CYP2A6	drug	nicotine	25555385	Neither rate of <b>nicotine</b> metabolism, nor <strong>CYP2A6</strong> or nicotinic receptor genotype, had an effect on the outcome variables of interest.
+CYP2A6	drug	nicotine	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (ANKK1), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (SLC6A3) and cytochrome P450 2A6 (<strong>CYP2A6</strong>) genes influence <b>smoking</b> cessation and <b>nicotine</b> dependence in a Japanese population.
+CYP2A6	addiction	dependence	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (ANKK1), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (SLC6A3) and cytochrome P450 2A6 (<strong>CYP2A6</strong>) genes influence smoking cessation and nicotine <b>dependence</b> in a Japanese population.
+CYP2A6	drug	nicotine	25526961	In 96 current and former <b>smokers</b>, genotyping frequencies for the ANKK1/DRD2 TaqIA, SLC6A3 VNTR, and <strong>CYP2A6</strong> polymorphisms were subjected to chi square analysis, and regression analyses were used to determine the association of the genotypes of current <b>smokers</b> with a Heavy <b>Smoking</b> Index, in addition to evaluating the effect of the subjects' <b>smoking</b> history on the association.
+CYP2A6	drug	nicotine	25526961	Genotyping results suggested that <b>nicotine</b> dependence among current <b>smokers</b> homozygous for the SLC6A3 10r allele was lower than that of <b>smokers</b> carrying the minor alleles, and that the <strong>CYP2A6</strong> polymorphism might mediate this association.
+CYP2A6	addiction	dependence	25526961	Genotyping results suggested that nicotine <b>dependence</b> among current smokers homozygous for the SLC6A3 10r allele was lower than that of smokers carrying the minor alleles, and that the <strong>CYP2A6</strong> polymorphism might mediate this association.
+CYP2A6	drug	nicotine	25446842	The <strong>CYP2A6</strong>*4 allele, characterized as the whole deletion of this gene, is closely associated with <b>nicotine</b> dependence, cancer susceptibility, and drug responsiveness.
+CYP2A6	addiction	dependence	25446842	The <strong>CYP2A6</strong>*4 allele, characterized as the whole deletion of this gene, is closely associated with nicotine <b>dependence</b>, cancer susceptibility, and drug responsiveness.
+CYP2A6	drug	nicotine	25012994	The ratio of 3'hydroxycotinine to cotinine, or <b>nicotine</b> metabolite ratio (NMR), is strongly associated with <strong>CYP2A6</strong> genotype, <strong>CYP2A6</strong> mediated <b>nicotine</b> and cotinine metabolism, and <b>nicotine</b> clearance.
+CYP2A6	drug	nicotine	24859605	Metabolism of <b>nicotine</b> to inactive cotinine by hepatic enzyme <strong>CYP2A6</strong> is the principal pathway by which active <b>nicotine</b> is removed from circulation.
+CYP2A6	drug	nicotine	24859605	We therefore hypothesized that inhibition of mouse CYP2A5, the ortolog of human <strong>CYP2A6</strong>, by methoxsalen (8 methoxypsoralen) alter dependence related behaviors of <b>nicotine</b> in the mouse.
+CYP2A6	addiction	dependence	24859605	We therefore hypothesized that inhibition of mouse CYP2A5, the ortolog of human <strong>CYP2A6</strong>, by methoxsalen (8 methoxypsoralen) alter <b>dependence</b> related behaviors of nicotine in the mouse.
+CYP2A6	drug	nicotine	24859605	Combining <strong>CYP2A6</strong> inhibitors with low dose <b>nicotine</b> replacement therapies may have a beneficial role in <b>smoking</b> cessation because it will decrease the drug elimination rate and maintain plasma and brain <b>nicotine</b> levels.
+CYP2A6	drug	nicotine	24527722	The chimeric system was also successfully used to demonstrate the inhibition of the electrochemical activity of the immobilized <strong>CYP2A6</strong> FLD, toward both coumarin and <b>nicotine</b> substrates, by tranylcypromine, a potent and selective <strong>CYP2A6</strong> inhibitor.
+CYP2A6	drug	nicotine	24305170	Novel <strong>CYP2A6</strong> variants identified in African Americans are associated with slow <b>nicotine</b> metabolism in vitro and in vivo.
+CYP2A6	drug	nicotine	24305170	<b>Nicotine</b>, the main addictive ingredient in <b>tobacco</b>, is metabolically inactivated to cotinine primarily by the hepatic enzyme <strong>CYP2A6</strong>.
+CYP2A6	addiction	addiction	24305170	Nicotine, the main <b>addictive</b> ingredient in tobacco, is metabolically inactivated to cotinine primarily by the hepatic enzyme <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	24305170	Considerable genetic variation in the <strong>CYP2A6</strong> gene results in large variation in the rates of <b>nicotine</b> metabolism, which in turn alters <b>smoking</b> behaviours (e.g.
+CYP2A6	drug	nicotine	24305170	The <strong>CYP2A6</strong> gene from African American phenotypically slow <b>nicotine</b> metabolizers was sequenced and seven novel variants were identified [<strong>CYP2A6</strong>*39 (V68M), <strong>CYP2A6</strong>*40 (I149M), <strong>CYP2A6</strong>*41 (R265Q), <strong>CYP2A6</strong>*42 (I268T), <strong>CYP2A6</strong>*43 (T303I), <strong>CYP2A6</strong>*44 (E390K), <strong>CYP2A6</strong>*44 (L462P)].
+CYP2A6	drug	nicotine	24305170	Variants were introduced into a bi cistronic cDNA expression construct containing <strong>CYP2A6</strong> and P450 oxidoreductase and assessed for protein expression, enzymatic activity and stability as evaluated using western blotting and <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	24163739	GWAS of <b>smoking</b> behaviour have identified risk loci for <b>smoking</b> quantity at 15q (similar genes to lung cancer susceptibility: CHRNA3, CHRNA5) and 19q (<strong>CYP2A6</strong>).
+CYP2A6	drug	nicotine	24127329	Are serotonergic system genes associated to <b>smoking</b> cessation therapy success in addition to <strong>CYP2A6</strong>?
+CYP2A6	drug	nicotine	24127329	The aim of this study was to evaluate the association between the effectiveness of treatment with <b>nicotine</b> or bupropion in heavy <b>smokers</b> (n=70), and 6 candidate polymorphisms in <strong>CYP2A6</strong>, 5 HTT and HTR2A genes.
+CYP2A6	drug	nicotine	24127329	Analysis revealed a significant association between "favourable" genotype combination carriers (<strong>CYP2A6</strong> "slow metabolizer" or 5HTT L allele or HTR2A 1438GG) and <b>nicotine</b> treatment outcome (OR=2.69, 95% CI=1.28 5.64).
+CYP2A6	drug	nicotine	24127329	Genetic variations in <strong>CYP2A6</strong> gene or genotypes associated with reduced synaptic serotonin activity may influence the success of <b>smoking</b> cessation treatment.
+CYP2A6	drug	nicotine	24045616	Variants in two adjacent genes, EGLN2 and <strong>CYP2A6</strong>, influence <b>smoking</b> behavior related to disease risk via different mechanisms.
+CYP2A6	drug	nicotine	24045616	Genome wide significant associations with cigarettes per day (CPD) and risk for lung cancer and chronic obstructive pulmonary disease (COPD) were previously reported in a region of 19q13, including <strong>CYP2A6</strong> (<b>nicotine</b> metabolism enzyme) and EGLN2 (hypoxia response).
+CYP2A6	drug	nicotine	24045616	Here, we demonstrate that when <strong>CYP2A6</strong> and EGLN2 genotypes are analyzed together, the key EGLN2 variant, rs3733829, is not associated with <b>nicotine</b> metabolism independent of <strong>CYP2A6</strong>, but is nevertheless independently associated with CPD, and with breath carbon monoxide (CO), a phenotype associated with cigarette consumption and relevant to hypoxia.
+CYP2A6	drug	nicotine	24045421	Impact of <b>nicotine</b> metabolism on <b>nicotine</b>'s pharmacological effects and behavioral responses: insights from a <strong>Cyp2a</strong>(4/5)bgs null mouse.
+CYP2A6	drug	nicotine	24045421	As a key step toward testing this hypothesis, we have studied <b>nicotine</b> metabolism and <b>nicotine</b>'s pharmacological and behavioral effects in a novel knockout mouse model [named <strong>Cyp2a</strong>(4/5)bgs null] lacking a number of cytochrome P450 genes known to be or possibly involved in <b>nicotine</b> metabolism, including two <strong>Cyp2a</strong> and all Cyp2b genes.
+CYP2A6	drug	nicotine	24045421	We found that, compared with wild type mice, the <strong>Cyp2a</strong>(4/5)bgs null mice showed >90% decreases in hepatic microsomal <b>nicotine</b> oxidase activity in vitro, and in rates of systemic <b>nicotine</b> clearance in vivo.
+CYP2A6	drug	nicotine	24045421	Further comparisons of <b>nicotine</b> metabolism between <strong>Cyp2a</strong>(4/5)bgs null and Cyp2a5 null mice revealed significant roles of both CYP2A5 and CYP2B enzymes in <b>nicotine</b> clearance.
+CYP2A6	drug	nicotine	24045421	Compared with the behavioral responses in wild type mice, the decreases in <b>nicotine</b> metabolism in the <strong>Cyp2a</strong>(4/5)bgs null mice led to prolonged <b>nicotine</b> induced acute pharmacological effects, in that null mice showed enhanced <b>nicotine</b> hypothermia and antinociception.
+CYP2A6	drug	nicotine	24045421	Furthermore, we found that the <strong>Cyp2a</strong>(4/5)bgs null mice developed a preference for <b>nicotine</b> in a conditioned place preference test, a commonly used test of <b>nicotine</b>'s rewarding effects, at a <b>nicotine</b> dose that was 4 fold lower than what was required by wild type mice.
+CYP2A6	drug	nicotine	24045421	Thus, <strong>CYP2A</strong>/2B catalyzed <b>nicotine</b> clearance affects <b>nicotine</b>'s behavioral response as well as its acute pharmacological effects in mice.
+CYP2A6	drug	nicotine	24033696	Pharmacotherapy effects on <b>smoking</b> cessation vary with <b>nicotine</b> metabolism gene (<strong>CYP2A6</strong>).
+CYP2A6	drug	nicotine	24033696	Evidence suggests that both the nicotinic receptor α5 subunit (CHRNA5) and Cytochrome P450 2A6 (<strong>CYP2A6</strong>) genotypes influence <b>smoking</b> cessation success and response to pharmacotherapy.
+CYP2A6	drug	nicotine	24033696	We examine the effect of <strong>CYP2A6</strong> genotype on <b>smoking</b> cessation success and response to cessation pharmacotherapy, and combine these effects with those of CHRNA5 genotypes.
+CYP2A6	drug	nicotine	24033696	Survival analysis was used to model time to relapse using <b>nicotine</b> metabolism derived from <strong>CYP2A6</strong> genotype based estimates.
+CYP2A6	addiction	relapse	24033696	Survival analysis was used to model time to <b>relapse</b> using nicotine metabolism derived from <strong>CYP2A6</strong> genotype based estimates.
+CYP2A6	drug	nicotine	24033696	<strong>CYP2A6</strong> defined <b>nicotine</b> metabolic function moderated the effect of <b>smoking</b> cessation pharmacotherapy on <b>smoking</b> relapse over 90 days [hazard ratio (HR) = 2.81, 95% confidence interval (CI) = 1.32 5.99, P = 0.0075], with pharmacotherapy significantly slowing relapse in fast (HR = 0.39, 95% CI = 0.28 0.55, P = 1.97 × 10( 8)), but not slow metabolizers (HR = 1.09, 95% CI = 0.55 2.17, P = 0.80).
+CYP2A6	addiction	relapse	24033696	<strong>CYP2A6</strong> defined nicotine metabolic function moderated the effect of smoking cessation pharmacotherapy on smoking <b>relapse</b> over 90 days [hazard ratio (HR) = 2.81, 95% confidence interval (CI) = 1.32 5.99, P = 0.0075], with pharmacotherapy significantly slowing <b>relapse</b> in fast (HR = 0.39, 95% CI = 0.28 0.55, P = 1.97 × 10( 8)), but not slow metabolizers (HR = 1.09, 95% CI = 0.55 2.17, P = 0.80).
+CYP2A6	drug	nicotine	24033696	Further, only the effect of <b>nicotine</b> replacement, and not bupropion, varies with <strong>CYP2A6</strong> defined metabolic function.
+CYP2A6	drug	nicotine	24033696	The effect of <b>nicotine</b> replacement on continuous abstinence is moderated by the combined genetic risks from <strong>CYP2A6</strong> and CHRNA5 (Wald = 7.44, d.f.
+CYP2A6	drug	nicotine	24033696	<b>Nicotine</b> replacement therapy is effective among individuals with fast, but not slow, <strong>CYP2A6</strong> defined <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	24033696	The effect of bupropion on relapse likelihood is unlikely to be affected by <b>nicotine</b> metabolism as estimated from <strong>CYP2A6</strong> genotype.
+CYP2A6	addiction	relapse	24033696	The effect of bupropion on <b>relapse</b> likelihood is unlikely to be affected by nicotine metabolism as estimated from <strong>CYP2A6</strong> genotype.
+CYP2A6	drug	nicotine	23933970	Sixty never <b>smokers</b>, balanced for gender and race (white, black, and Asian), wore 7 mg <b>nicotine</b> skin patches for up to 8 h. Serial plasma <b>nicotine</b> concentrations and subjective and cardiovascular effects were measured, and genetic variation in the <strong>CYP2A6</strong> gene, encoding the primary enzyme responsible for <b>nicotine</b> metabolism, was assessed.
+CYP2A6	drug	nicotine	23933970	Toxicity and subjective and cardiovascular effects of <b>nicotine</b> were associated with the presence of reduced function <strong>CYP2A6</strong> alleles, presumably reflecting slow <b>nicotine</b> metabolic inactivation.
+CYP2A6	drug	alcohol	22935730	Differential effects of nicotine treatment and <b>ethanol</b> self administration on <strong>CYP2A6</strong>, CYP2B6 and nicotine pharmacokinetics in African green monkeys.
+CYP2A6	drug	nicotine	22935730	Differential effects of <b>nicotine</b> treatment and ethanol self administration on <strong>CYP2A6</strong>, CYP2B6 and <b>nicotine</b> pharmacokinetics in African green monkeys.
+CYP2A6	drug	nicotine	22935730	In primates, <b>nicotine</b> is metabolically inactivated in the liver by <strong>CYP2A6</strong> and possibly CYP2B6.
+CYP2A6	drug	nicotine	22935730	s.c.) on hepatic <strong>CYP2A6</strong> and CYP2B6 levels (mRNA, protein, and enzymatic activity), in vitro <b>nicotine</b> metabolism, and in vivo <b>nicotine</b> pharmacokinetics in monkeys.
+CYP2A6	drug	alcohol	22935730	<strong>CYP2A6</strong> mRNA and protein levels and in vitro coumarin (selective <strong>CYP2A6</strong> substrate) and nicotine metabolism were decreased by nicotine treatment but unaffected by <b>ethanol</b>.
+CYP2A6	drug	nicotine	22935730	<strong>CYP2A6</strong> mRNA and protein levels and in vitro coumarin (selective <strong>CYP2A6</strong> substrate) and <b>nicotine</b> metabolism were decreased by <b>nicotine</b> treatment but unaffected by ethanol.
+CYP2A6	drug	alcohol	22935730	Combined <b>ethanol</b> and nicotine exposure decreased <strong>CYP2A6</strong> mRNA and protein levels, as well as in vitro coumarin and nicotine metabolism, and increased CYP2B6 protein levels and in vitro bupropion metabolism, with no change in CYP2B6 mRNA levels.
+CYP2A6	drug	nicotine	22935730	Combined ethanol and <b>nicotine</b> exposure decreased <strong>CYP2A6</strong> mRNA and protein levels, as well as in vitro coumarin and <b>nicotine</b> metabolism, and increased CYP2B6 protein levels and in vitro bupropion metabolism, with no change in CYP2B6 mRNA levels.
+CYP2A6	drug	nicotine	22935730	Chronic <b>nicotine</b> resulted in higher <b>nicotine</b> plasma levels achieved after <b>nicotine</b> administration, consistent with decreased <strong>CYP2A6</strong>.
+CYP2A6	drug	alcohol	22935730	Thus, nicotine can decrease hepatic <strong>CYP2A6</strong>, reducing the metabolism of its substrates, including nicotine, whereas <b>ethanol</b> can increase hepatic CYP2B6, increasing the metabolism of CYP2B6 substrates.
+CYP2A6	drug	nicotine	22935730	Thus, <b>nicotine</b> can decrease hepatic <strong>CYP2A6</strong>, reducing the metabolism of its substrates, including <b>nicotine</b>, whereas ethanol can increase hepatic CYP2B6, increasing the metabolism of CYP2B6 substrates.
+CYP2A6	drug	nicotine	22869927	<strong>CYP2A6</strong>  and CYP2A13 catalyzed metabolism of the <b>nicotine</b> Δ5'(1')iminium ion.
+CYP2A6	drug	nicotine	22869927	<b>Nicotine</b>, the major addictive agent in <b>tobacco</b>, is metabolized primarily by <strong>CYP2A6</strong> catalyzed oxidation.
+CYP2A6	addiction	addiction	22869927	Nicotine, the major <b>addictive</b> agent in tobacco, is metabolized primarily by <strong>CYP2A6</strong> catalyzed oxidation.
+CYP2A6	drug	nicotine	22869927	We reported previously that both <strong>CYP2A6</strong> and the closely related extrahepatic enzyme CYP2A13 were inactivated during <b>nicotine</b> metabolism; however, inactivation occurred after metabolism was complete.
+CYP2A6	drug	nicotine	22869927	In the studies presented here, we confirm that the <b>nicotine</b> Δ5'(1')iminium ion is an inactivator of both <strong>CYP2A6</strong> and CYP2A13, and inactivation depends on time, concentration, and the presence of NADPH.
+CYP2A6	drug	nicotine	22869927	These data are consistent with the characterization of the <b>nicotine</b> Δ5'(1')iminium ion as a mechanism based inactivator of both CYP2A13 and <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	22869927	We also confirm that both <strong>CYP2A6</strong> and CYP2A13 catalyze the metabolism of the <b>nicotine</b> Δ5'(1')iminium ion to cotinine and provide evidence that both enzymes catalyze the sequential metabolism of the <b>nicotine</b> Δ5'(1')iminium ion.
+CYP2A6	drug	nicotine	22854688	[Relation of genetic variants of <strong>CYP2A6</strong> with <b>tobacco</b> dependence and <b>smoking</b> habit in Chilean subjects.
+CYP2A6	addiction	dependence	22854688	[Relation of genetic variants of <strong>CYP2A6</strong> with tobacco <b>dependence</b> and smoking habit in Chilean subjects.
+CYP2A6	drug	nicotine	22854688	To assess the prevalence of allelic and genotype variants of <strong>CYP2A6</strong> in a sample of Chilean subjects and to evaluate their relationship with <b>smoking</b> and <b>tobacco</b> dependence.
+CYP2A6	addiction	dependence	22854688	To assess the prevalence of allelic and genotype variants of <strong>CYP2A6</strong> in a sample of Chilean subjects and to evaluate their relationship with smoking and tobacco <b>dependence</b>.
+CYP2A6	drug	nicotine	22854688	The association between the presence of allelic variants of <strong>CYP2A6</strong> and <b>smoking</b> and <b>tobacco</b> dependence was evaluated with chi square test.
+CYP2A6	addiction	dependence	22854688	The association between the presence of allelic variants of <strong>CYP2A6</strong> and smoking and tobacco <b>dependence</b> was evaluated with chi square test.
+CYP2A6	drug	nicotine	22854688	No significant association was observed between being a carrier of a variant genotype of <strong>CYP2A6</strong> and <b>smoking</b> or <b>tobacco</b> dependence.
+CYP2A6	addiction	dependence	22854688	No significant association was observed between being a carrier of a variant genotype of <strong>CYP2A6</strong> and smoking or tobacco <b>dependence</b>.
+CYP2A6	drug	nicotine	22854688	In this sample of Chilean individuals we did not find a relation between any <strong>CYP2A6</strong> genotype with <b>smoking</b> or <b>tobacco</b> dependence.
+CYP2A6	addiction	dependence	22854688	In this sample of Chilean individuals we did not find a relation between any <strong>CYP2A6</strong> genotype with smoking or tobacco <b>dependence</b>.
+CYP2A6	drug	nicotine	22700965	X ray structures of <b>nicotine</b> complexes with CYP2A13 (2.5 Å) and <strong>CYP2A6</strong> (2.3 Å) yield a structural rationale for the preferential binding of <b>nicotine</b> to CYP2A13.
+CYP2A6	drug	nicotine	22696418	Most compounds evaluated [tryptamine, 4 dimethylaminobenzaldehyde, phenethyl isothiocyanate, β nicotyrine, (S) <b>nicotine</b>, and pilocarpine] demonstrated only moderate or no preference for inhibition of one <strong>CYP2A</strong> enzyme over the other.
+CYP2A6	addiction	relapse	22696418	This information is useful to inform reinterpretation of previous data with these inhibitors and to guide future studies <b>seeking</b> to determine which human <strong>CYP2A</strong> enzyme is responsible for the in vivo metabolism of compounds in human tissues expressing both enzymes.
+CYP2A6	drug	nicotine	22486895	<b>Nicotine</b> is the primary addictive agent in <b>tobacco</b> products and is metabolized in humans by <strong>CYP2A6</strong>.
+CYP2A6	addiction	addiction	22486895	Nicotine is the primary <b>addictive</b> agent in tobacco products and is metabolized in humans by <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	22486895	Decreased <strong>CYP2A6</strong> activity has been associated with decreased <b>smoking</b>.
+CYP2A6	drug	nicotine	22486895	The extrahepatic enzyme, CYP2A13 (94% identical to <strong>CYP2A6</strong>) also catalyzes the metabolism of <b>nicotine</b>, but is most noted for its role in the metabolic activation of the <b>tobacco</b> specific lung carcinogen, 4 (methylnitrosamino) 1 (3 pyridyl) 1 butanone (NNK).
+CYP2A6	drug	nicotine	22486895	In this study, the inhibition and potential inactivation of <strong>CYP2A6</strong> and CYP2A13 by two <b>tobacco</b> constituents, 1 methyl 4 (3 pyridinyl) pyrrole (β nicotyrine) and ( ) menthol were characterized and compared to the potent mechanism based inactivator of <strong>CYP2A6</strong>, menthofuran.
+CYP2A6	drug	nicotine	22451501	Previous investigations of the relationship between Cytochrome P450 2A6 (<strong>CYP2A6</strong>) genotype and <b>smoking</b> phenotypes made comparisons by dividing subjects into broad categories based on assumptions that simplify the range of function of different <strong>CYP2A6</strong> alleles, their numerous possible diplotype combinations and non additive allele effects.
+CYP2A6	drug	nicotine	22451501	<strong>CYP2A6</strong> genotype is not associated with <b>nicotine</b> dependence, as defined by the Fagerström Test of <b>Nicotine</b> Dependence, demonstrating that cigarettes smoked per day (CPD) and <b>nicotine</b> dependence have distinct genetic correlates.
+CYP2A6	addiction	dependence	22451501	<strong>CYP2A6</strong> genotype is not associated with nicotine <b>dependence</b>, as defined by the Fagerström Test of Nicotine <b>Dependence</b>, demonstrating that cigarettes smoked per day (CPD) and nicotine <b>dependence</b> have distinct genetic correlates.
+CYP2A6	drug	nicotine	22342802	Genetic variation in <strong>CYP2A6</strong> predicts neural reactivity to <b>smoking</b> cues as measured using fMRI.
+CYP2A6	drug	nicotine	22342802	<b>Nicotine</b> metabolism, mediated by the enzyme <strong>CYP2A6</strong>, also influences <b>smoking</b> behavior.
+CYP2A6	drug	nicotine	22342802	In this study, we investigated how <b>nicotine</b> metabolism and genetic variation in <strong>CYP2A6</strong> influence the neural response to <b>smoking</b> cues in humans using functional magnetic resonance imaging (fMRI).
+CYP2A6	drug	nicotine	22342802	We screened 169 <b>smokers</b> for their rate of <b>nicotine</b> metabolism and <strong>CYP2A6</strong> genotype, and selected 31 <b>smokers</b> with the fastest and slowest rates for fMRI, matched for daily cigarette intake.
+CYP2A6	drug	nicotine	22290489	There are reproducible and clinically significant associations of genotypic and phenotypic measures of <strong>CYP2A6</strong> enzyme activity and <b>nicotine</b> metabolic rate with <b>smoking</b> cessation as well as response to <b>nicotine</b> replacement therapies and bupropion.
+CYP2A6	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: <strong>CYP2A6</strong>*1×2, <strong>CYP2A6</strong>*2 (1799T>A) [rs1801272], <strong>CYP2A6</strong>*9 ( 48T>G) [rs28399433], <strong>CYP2A6</strong>*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CYP2A6	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: <strong>CYP2A6</strong>*1×2, <strong>CYP2A6</strong>*2 (1799T>A) [rs1801272], <strong>CYP2A6</strong>*9 ( 48T>G) [rs28399433], <strong>CYP2A6</strong>*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CYP2A6	drug	nicotine	22046326	Compared with carriers of variant alleles, the odds ratio (OR) for being a non <b>smoker</b> in individuals with the wild type genotype of <strong>CYP2A6</strong>*12 and DRD2 ANKK1 2137G>A (Taq1A) polymorphisms was 3.60 (95%CI: 1.75, 7.44) and 2.63 (95%CI: 1.41, 4.89) respectively.
+CYP2A6	drug	nicotine	22046326	Compared with the wild type genotype, the OR for being a non <b>smoker</b> in carriers of the minor <strong>CYP2A6</strong>*2 allele was 1.80 (95%CI: 1.24, 2.65).
+CYP2A6	drug	nicotine	22046326	We found a significant genotype effect (all P≤0.017) for the following <b>smoking</b> related phenotypes: (i) cigarettes smoked per day and CYP2A13*3; (ii) pack years smoked and <strong>CYP2A6</strong>*2, <strong>CYP2A6</strong>*1×2, CYP2A13*7, CYP2B6*4 and DRD2 ANKK1 2137G>A (Taq1A); (iii) <b>nicotine</b> dependence (assessed with the Fagestrom test) and <strong>CYP2A6</strong>*9.
+CYP2A6	addiction	dependence	22046326	We found a significant genotype effect (all P≤0.017) for the following smoking related phenotypes: (i) cigarettes smoked per day and CYP2A13*3; (ii) pack years smoked and <strong>CYP2A6</strong>*2, <strong>CYP2A6</strong>*1×2, CYP2A13*7, CYP2B6*4 and DRD2 ANKK1 2137G>A (Taq1A); (iii) nicotine <b>dependence</b> (assessed with the Fagestrom test) and <strong>CYP2A6</strong>*9.
+CYP2A6	drug	cannabinoid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, <strong>CYP2A6</strong> polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (OPRM1) or <b>cannabinoid</b> receptors (CNR1).
+CYP2A6	drug	nicotine	22046326	Overall, our results suggest that genetic variants potentially involved in <b>nicotine</b> metabolization (mainly, <strong>CYP2A6</strong> polymorphisms) are those showing the strongest association with <b>smoking</b> related phenotypes, as opposed to genetic variants influencing the brain effects of <b>nicotine</b>, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (OPRM1) or cannabinoid receptors (CNR1).
+CYP2A6	drug	opioid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, <strong>CYP2A6</strong> polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), <b>opioid</b> (OPRM1) or cannabinoid receptors (CNR1).
+CYP2A6	drug	nicotine	22019468	The human <strong>CYP2A6</strong> enzyme metabolises several xenobiotics including <b>nicotine</b>, the addictive component in <b>tobacco</b>.
+CYP2A6	addiction	addiction	22019468	The human <strong>CYP2A6</strong> enzyme metabolises several xenobiotics including nicotine, the <b>addictive</b> component in tobacco.
+CYP2A6	drug	nicotine	22019468	Reduced activity of <strong>CYP2A6</strong>, either for genetic reasons or by administering inhibitors of <strong>CYP2A6</strong>, reduces <b>tobacco</b> <b>smoking</b>.
+CYP2A6	drug	nicotine	21747048	Relationship between <strong>CYP2A6</strong> and CHRNA5 CHRNA3 CHRNB4 variation and <b>smoking</b> behaviors and lung cancer risk.
+CYP2A6	drug	nicotine	21747048	Genetic variations in the <strong>CYP2A6</strong> <b>nicotine</b> metabolic gene and the CHRNA5 CHRNA3 CHRNB4 (CHRNA5 A3 B4) nicotinic gene cluster have been independently associated with lung cancer.
+CYP2A6	drug	nicotine	21747048	Cigarette consumption (P < .001) and <b>nicotine</b> dependence (P = .036) were the highest in the combined <strong>CYP2A6</strong> normal metabolizers and CHRNA5 A3 B4 AA (tag single nucleotide polymorphism rs1051730 G>A) risk group.
+CYP2A6	addiction	dependence	21747048	Cigarette consumption (P < .001) and nicotine <b>dependence</b> (P = .036) were the highest in the combined <strong>CYP2A6</strong> normal metabolizers and CHRNA5 A3 B4 AA (tag single nucleotide polymorphism rs1051730 G>A) risk group.
+CYP2A6	drug	nicotine	21747048	Variation in <strong>CYP2A6</strong> and CHRNA5 A3 B4 was independently and additively associated with increased cigarette consumption, <b>nicotine</b> dependence, and lung cancer risk.
+CYP2A6	addiction	dependence	21747048	Variation in <strong>CYP2A6</strong> and CHRNA5 A3 B4 was independently and additively associated with increased cigarette consumption, nicotine <b>dependence</b>, and lung cancer risk.
+CYP2A6	drug	nicotine	21747048	<strong>CYP2A6</strong> and CHRNA5 A3 B4 appear to be more strongly associated with <b>smoking</b> behaviors and lung cancer risk, respectively.
+CYP2A6	drug	alcohol	21362114	Thus far, the most promising results were obtained for polymorphisms in the OPRM1 and <strong>CYP2A6</strong> genes, which have been effective in predicting clinical response to <b>naltrexone</b> in <b>alcoholism</b> and nicotine replacement therapy in smoking, respectively.
+CYP2A6	drug	nicotine	21362114	Thus far, the most promising results were obtained for polymorphisms in the OPRM1 and <strong>CYP2A6</strong> genes, which have been effective in predicting clinical response to naltrexone in alcoholism and <b>nicotine</b> replacement therapy in <b>smoking</b>, respectively.
+CYP2A6	drug	nicotine	21266057	Participants responded to survey items and provided blood samples for evaluation of phenotype and genotype of <strong>CYP2A6</strong> and CYP2B6 enzymes involved in <b>nicotine</b> and bupropion metabolism.
+CYP2A6	drug	nicotine	21266057	KIS III is the first study designed to examine both <b>nicotine</b> and bupropion metabolism, evaluating <strong>CYP2A6</strong> and CYP2B6 phenotype and genotype in conjunction with psychosocial factors, in the context of treatment of African American light <b>smokers</b>.
+CYP2A6	drug	nicotine	21208832	The ratio of another <b>nicotine</b> metabolite, trans 3' hydroxycotinine, to cotinine in biofluids is highly correlated with the rate of <b>nicotine</b> metabolism, which is catalyzed mainly by cytochrome P450 2A6 (<strong>CYP2A6</strong>).
+CYP2A6	drug	nicotine	21208832	Consequently, this <b>nicotine</b> metabolite ratio is being used to phenotype individuals for <strong>CYP2A6</strong> activity and to individualize pharmacotherapies for <b>tobacco</b> addiction.
+CYP2A6	addiction	addiction	21208832	Consequently, this nicotine metabolite ratio is being used to phenotype individuals for <strong>CYP2A6</strong> activity and to individualize pharmacotherapies for tobacco <b>addiction</b>.
+CYP2A6	drug	alcohol	21161757	AD and ND are among the most prevalent addictive disorders worldwide, are among the best studied, and are also associated globally with the largest socioeconomic impact.We describe different mechanisms through which genes can have an impact on the addictive behaviors, distinguishing between the genes that inscribe the proteins affecting the metabolism of the addictive substance (e.g., ADH/ALDH for <b>alcohol</b> or <strong>CYP2A6</strong> for nicotine) and genes that code for the brain transmitter systems, such as genes involved in cerebral neurotransmission thought to be involved in addiction (e.g., brain reward system, mood regulation, opioid system).
+CYP2A6	drug	nicotine	21161757	AD and ND are among the most prevalent addictive disorders worldwide, are among the best studied, and are also associated globally with the largest socioeconomic impact.We describe different mechanisms through which genes can have an impact on the addictive behaviors, distinguishing between the genes that inscribe the proteins affecting the metabolism of the addictive substance (e.g., ADH/ALDH for alcohol or <strong>CYP2A6</strong> for <b>nicotine</b>) and genes that code for the brain transmitter systems, such as genes involved in cerebral neurotransmission thought to be involved in addiction (e.g., brain reward system, mood regulation, opioid system).
+CYP2A6	drug	opioid	21161757	AD and ND are among the most prevalent addictive disorders worldwide, are among the best studied, and are also associated globally with the largest socioeconomic impact.We describe different mechanisms through which genes can have an impact on the addictive behaviors, distinguishing between the genes that inscribe the proteins affecting the metabolism of the addictive substance (e.g., ADH/ALDH for alcohol or <strong>CYP2A6</strong> for nicotine) and genes that code for the brain transmitter systems, such as genes involved in cerebral neurotransmission thought to be involved in addiction (e.g., brain reward system, mood regulation, <b>opioid</b> system).
+CYP2A6	addiction	addiction	21161757	AD and ND are among the most prevalent <b>addictive</b> disorders worldwide, are among the best studied, and are also associated globally with the largest socioeconomic impact.We describe different mechanisms through which genes can have an impact on the <b>addictive</b> behaviors, distinguishing between the genes that inscribe the proteins affecting the metabolism of the <b>addictive</b> substance (e.g., ADH/ALDH for alcohol or <strong>CYP2A6</strong> for nicotine) and genes that code for the brain transmitter systems, such as genes involved in cerebral neurotransmission thought to be involved in <b>addiction</b> (e.g., brain reward system, mood regulation, opioid system).
+CYP2A6	addiction	reward	21161757	AD and ND are among the most prevalent addictive disorders worldwide, are among the best studied, and are also associated globally with the largest socioeconomic impact.We describe different mechanisms through which genes can have an impact on the addictive behaviors, distinguishing between the genes that inscribe the proteins affecting the metabolism of the addictive substance (e.g., ADH/ALDH for alcohol or <strong>CYP2A6</strong> for nicotine) and genes that code for the brain transmitter systems, such as genes involved in cerebral neurotransmission thought to be involved in addiction (e.g., brain <b>reward</b> system, mood regulation, opioid system).
+CYP2A6	drug	nicotine	20418888	Sequence variants at CHRNB3 CHRNA6 and <strong>CYP2A6</strong> affect <b>smoking</b> behavior.
+CYP2A6	drug	nicotine	20418888	Among the genes at the two newly associated loci are genes encoding <b>nicotine</b> metabolizing enzymes (<strong>CYP2A6</strong> and CYP2B6) and nicotinic acetylcholine receptor subunits (CHRNB3 and CHRNA6), all of which have been highlighted in previous studies of <b>smoking</b> and <b>nicotine</b> dependence.
+CYP2A6	addiction	dependence	20418888	Among the genes at the two newly associated loci are genes encoding nicotine metabolizing enzymes (<strong>CYP2A6</strong> and CYP2B6) and nicotinic acetylcholine receptor subunits (CHRNB3 and CHRNA6), all of which have been highlighted in previous studies of smoking and nicotine <b>dependence</b>.
+CYP2A6	drug	nicotine	19415821	Gene gene interactions of <strong>CYP2A6</strong> and MAOA polymorphisms on <b>smoking</b> behavior in Chinese male population.
+CYP2A6	drug	nicotine	19415821	In this study, we investigated the association and multilocus gene gene interactions of cytochrome P450 2A6 (<strong>CYP2A6</strong>), dopamine beta hydroxylase (DBH), catechol O methyl transferase (COMT), and monoamine oxidase A (MAOA) polymorphisms with <b>smoking</b> behavior in a community based Chinese male population.
+CYP2A6	drug	nicotine	19415821	Statistically significant trends were shown for increased risk of <b>smoking</b> initiation in participants with <strong>CYP2A6</strong>*1B/<strong>CYP2A6</strong>*1B genotypes compared with those with <strong>CYP2A6</strong>*1A/<strong>CYP2A6</strong>*1A genotypes [odds ratio (OR)=3.5, 95% confidence interval (CI)= 1.5 8.1], and participants with <strong>CYP2A6</strong>*1/<strong>CYP2A6</strong>*1 genotypes were at higher risk of <b>smoking</b> initiation (OR=2.4, 95% CI=1.2 4.5) and <b>smoking</b> persistence (OR=4.0, 95% CI=1.5 10.3) than those who have <strong>CYP2A6</strong>*4C genotypes.
+CYP2A6	drug	nicotine	19415821	Moreover, the best model involved a gene gene interaction between MAOA and <strong>CYP2A6</strong> was characterized by the multifactor dimensionality reduction method (64.11% accuracy, P<0.001), and indicated that carriers of the combined 1460 T/O genotype for MAOA EcoRV and <strong>CYP2A6</strong>*1/<strong>CYP2A6</strong>*1 genotypes were at higher risk of <b>smoking</b> (OR=15.4, 95% CI=4.5 52.5).
+CYP2A6	drug	nicotine	19415821	These findings suggested a substantial influence of <strong>CYP2A6</strong> polymorphism as well as the interaction with MAOA resulting in risk modulation on <b>smoking</b> behavior in Chinese male population.
+CYP2A6	drug	nicotine	19279561	Association of <b>nicotine</b> metabolite ratio and <strong>CYP2A6</strong> genotype with <b>smoking</b> cessation treatment in African American light <b>smokers</b>.
+CYP2A6	drug	nicotine	19279561	Cytochrome P450 2A6 (<strong>CYP2A6</strong>) is the main <b>nicotine</b> (NIC) metabolizing enzyme in humans.
+CYP2A6	drug	nicotine	19279561	We investigated the relationships between <strong>CYP2A6</strong> genotype, baseline plasma trans  3' hydroxycotinine/cotinine (3HC/COT) (a phenotypic marker of <strong>CYP2A6</strong> activity), and <b>smoking</b> behavior in African American light <b>smokers</b>.
+CYP2A6	addiction	dependence	19279561	Cigarette consumption, age of initiation, and <b>dependence</b> scores did not differ among 3HC/COT quartiles or <strong>CYP2A6</strong> genotype groups.
+CYP2A6	drug	nicotine	19279561	The determination of the 3HC/COT ratio, and possibly <strong>CYP2A6</strong> genotype, may be useful in the future for personalizing the choice of <b>smoking</b> cessation treatment in African American light <b>smokers</b>.
+CYP2A6	drug	nicotine	19251795	Recently, it has been shown that genetic variants in the dopaminergic system, opioid receptors, the bupropion metabolising enzyme CYP2B6 and the <b>nicotine</b> metabolising enzyme <strong>CYP2A6</strong> may play an important role in predicting <b>smoking</b> cessation responses to <b>nicotine</b> replacement therapy and bupropion treatment.
+CYP2A6	drug	opioid	19251795	Recently, it has been shown that genetic variants in the dopaminergic system, <b>opioid</b> receptors, the bupropion metabolising enzyme CYP2B6 and the nicotine metabolising enzyme <strong>CYP2A6</strong> may play an important role in predicting smoking cessation responses to nicotine replacement therapy and bupropion treatment.
+CYP2A6	drug	nicotine	19184652	Genetic studies have demonstrated that polymorphisms in <strong>CYP2A6</strong>, the primary enzyme responsible for <b>nicotine</b> breakdown, make a sizable contribution to the wide range of <b>nicotine</b> metabolic capacity observed in humans.
+CYP2A6	drug	nicotine	19184652	Thus, special attention will be given to <strong>CYP2A6</strong>, because slower <b>nicotine</b> metabolism requires less frequent self administration, and accordingly influences <b>smoking</b> behaviors.
+CYP2A6	drug	nicotine	19184645	<b>Nicotine</b> is metabolized primarily by the liver enzymes <strong>CYP2A6</strong>, UDPglucuronosyltransferase (UGT), and flavin containing monooxygenase (FMO).
+CYP2A6	drug	nicotine	19169923	<b>Nicotine</b> metabolism is mediated primarily by cytochrome P450 2A6 (<strong>CYP2A6</strong>).
+CYP2A6	drug	nicotine	19169923	Genetic variation in the <strong>CYP2A6</strong> gene has been linked with several <b>smoking</b> behavior phenotypes.
+CYP2A6	drug	nicotine	19169923	Individuals who carry null or reduced activity alleles for <strong>CYP2A6</strong> smoke fewer cigarettes per day, are less dependent on <b>nicotine</b>, and may have an easier time quitting <b>smoking</b>.
+CYP2A6	drug	nicotine	19169923	A phenotypic measure of <strong>CYP2A6</strong> enzyme activity, defined as the ratio of the <b>nicotine</b> metabolites 3'hydroxycotinine/cotinine, also predicts successful quitting with the transdermal <b>nicotine</b> patch, and counseling alone.
+CYP2A6	drug	nicotine	19169923	Inhibition of the <strong>CYP2A6</strong> enzyme to slow <b>nicotine</b> metabolism is a promising approach to increase <b>nicotine</b> availability and potentially reduce harm from <b>tobacco</b> <b>smoking</b>.
+CYP2A6	drug	nicotine	19018727	<strong>CYP2A6</strong> polymorphisms and risk for <b>tobacco</b> related cancers.
+CYP2A6	drug	nicotine	19018727	The psychoactive compound responsible for <b>tobacco</b> addiction, <b>nicotine</b> and the potent carcinogens present at high concentrations either in cigarette mainstream smoke or in smokeless <b>tobacco</b> products, 4 (methylnitrosamino) 1 (3 pyridyl) butanone (NNK) and N nitrosonornicotine (NNN) can be metabolized by <strong>CYP2A6</strong>.
+CYP2A6	addiction	addiction	19018727	The psychoactive compound responsible for tobacco <b>addiction</b>, nicotine and the potent carcinogens present at high concentrations either in cigarette mainstream smoke or in smokeless tobacco products, 4 (methylnitrosamino) 1 (3 pyridyl) butanone (NNK) and N nitrosonornicotine (NNN) can be metabolized by <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	19018727	The <strong>CYP2A6</strong> gene is highly polymorphic and <strong>CYP2A6</strong> alleles coding for enzymes with altered expression or metabolic capacity produce alterations in <b>nicotine</b> metabolism in vivo and seem to influence <b>smoking</b> behavior.
+CYP2A6	drug	nicotine	19018727	However, to date only a few and inconclusive studies have addressed the risk that a given <strong>CYP2A6</strong> polymorphism presents for the development of <b>tobacco</b> related tumors.
+CYP2A6	drug	nicotine	19018727	Finally, the interaction between polymorphisms of genes that code for <strong>CYP2A6</strong>, CYP2A13 and other potent carcinogen metabolizing CYP enzymes may help to determine individuals that are at higher risk of developing tumors associated with <b>tobacco</b> consumption.
+CYP2A6	drug	nicotine	18976031	Genetic polymorphism of <strong>CYP2A6</strong> gene is a major causal factor in the large interindividual differences in <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	18666753	The idea that the liver enzyme cytochrome P450 2A6 (<strong>CYP2A6</strong>), known also as <b>nicotine</b> C oxidase, is one of the determinants of <b>smoking</b> addiction and <b>smoking</b> behavior is primarily based on its role in <b>nicotine</b> metabolism and disposition.
+CYP2A6	addiction	addiction	18666753	The idea that the liver enzyme cytochrome P450 2A6 (<strong>CYP2A6</strong>), known also as nicotine C oxidase, is one of the determinants of smoking <b>addiction</b> and smoking behavior is primarily based on its role in nicotine metabolism and disposition.
+CYP2A6	drug	nicotine	18666753	The results of studies linking the <strong>CYP2A6</strong> genetic polymorphism with <b>smoking</b> dependence and <b>smoking</b> behavior however remain controversial.
+CYP2A6	addiction	dependence	18666753	The results of studies linking the <strong>CYP2A6</strong> genetic polymorphism with smoking <b>dependence</b> and smoking behavior however remain controversial.
+CYP2A6	drug	nicotine	18666753	In the present review, we summarize research findings on biological significance of <strong>CYP2A6</strong> and gene polymorphisms together with a discussion on <strong>CYP2A6</strong> inhibitors that hold the promise of uses in <b>smoking</b> cessation.
+CYP2A6	drug	nicotine	18666753	In addition, we provide the phenotype/genotype information derived from our systematic investigation on the relationship between <strong>CYP2A6</strong> genotypes, <b>smoking</b> habits and coumarin metabolism phenotypes in a group of 393 normal adults (197 women and 196 men), 16 to 60 years of age, whose exposure to cadmium and lead were also determined, enabling us to assess the <strong>CYP2A6</strong> phenotypic variability associated with <strong>CYP2A6</strong> genotypes and environmental exposure.
+CYP2A6	drug	nicotine	18666753	The results indicate that the phenotype of <strong>CYP2A6</strong> enzyme in liver is an outcome of interactions between the <strong>CYP2A6</strong> gene, cadmium, <b>nicotine</b> and possibly its metabolites.
+CYP2A6	drug	nicotine	18305452	<b>Nicotine</b> is metabolized primarily by <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	17978975	Sections 3 and 4 describe enzymes involved in <b>nicotine</b> metabolism, with section 3 focusing on the major <b>nicotine</b> to cotinine metabolizing enzyme, <strong>CYP2A6</strong>, and how genetically differing rates of metabolic inactivation of <b>nicotine</b> alter <b>smoking</b>.
+CYP2A6	drug	nicotine	18041664	<b>Smoking</b> behavior and related cancers: the role of <strong>CYP2A6</strong> polymorphisms.
+CYP2A6	drug	nicotine	18041664	The absorbed <b>nicotine</b> is rapidly and extensively metabolized to inactive cotinine by <strong>CYP2A6</strong> in human livers, which has a major impact on <b>nicotine</b> clearance.
+CYP2A6	drug	nicotine	18041664	Progress has been made in understanding the relationship between the inter individual variability in <b>nicotine</b> metabolism and genetic polymorphisms of <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	18041664	Recent findings have increased our knowledge concerning ethnic differences in the allele frequencies of the <strong>CYP2A6</strong> variants, <b>nicotine</b> metabolism, and cancer risk.
+CYP2A6	drug	nicotine	18041664	In this review, the potential associations between the <strong>CYP2A6</strong> polymorphisms and <b>smoking</b> behavior or the risk of cancer are also discussed.
+CYP2A6	drug	nicotine	18004205	Gene gene interactions between CYP2B6 and <strong>CYP2A6</strong> in <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	18004205	<strong>CYP2A6</strong> is the major enzyme involved in <b>nicotine</b> metabolism, yet large interindividual variations in the rate of <b>nicotine</b> metabolism exist within groups of individuals having the same <strong>CYP2A6</strong> genotype.
+CYP2A6	drug	nicotine	18004205	We investigated the influence of genetic variation in another potential <b>nicotine</b> metabolizing enzyme, CYP2B6, and its interaction with <strong>CYP2A6</strong>, on the metabolism of <b>nicotine</b>.
+CYP2A6	drug	nicotine	18004205	We observed that the CYP2B6*6 haplotype (defined as having both Q172 H and K262R variants) was associated with faster <b>nicotine</b> and cotinine clearance, and that such associations were more prominent among individuals having decreased activity <strong>CYP2A6</strong> genotypes.
+CYP2A6	drug	nicotine	18004205	Statistically significant interactions between CYP2B6 and <strong>CYP2A6</strong> genotypes were observed (P<0.003 for <b>nicotine</b> clearance and P<0.002 for cotinine clearance).
+CYP2A6	drug	nicotine	18004205	Our results indicate that CYP2B6 genetic variation is associated with the metabolism of <b>nicotine</b> and cotinine among individuals with decreased <strong>CYP2A6</strong> activity.
+CYP2A6	drug	nicotine	18004205	Further investigation of the roles of CYP2B6 and the interaction between CYP2B6 and <strong>CYP2A6</strong> genotypes in mediating <b>nicotine</b> dependence and <b>tobacco</b> related diseases is merited.
+CYP2A6	addiction	dependence	18004205	Further investigation of the roles of CYP2B6 and the interaction between CYP2B6 and <strong>CYP2A6</strong> genotypes in mediating nicotine <b>dependence</b> and tobacco related diseases is merited.
+CYP2A6	drug	nicotine	17979512	Genetic variability in <strong>CYP2A6</strong> and the pharmacokinetics of <b>nicotine</b>.
+CYP2A6	drug	nicotine	17979512	This article reviews <strong>CYP2A6</strong> genetic variation and its impact on in vivo <b>nicotine</b> kinetics, including a description of the individual variants, different phenotyping approaches for assessing in vivo <strong>CYP2A6</strong> activity and other sources of variation in <b>nicotine</b> metabolism such as gender.
+CYP2A6	drug	nicotine	17979512	In addition, the effect of <strong>CYP2A6</strong> polymorphisms on <b>smoking</b> behavior and <b>tobacco</b> related lung cancer risk are briefly described.
+CYP2A6	drug	nicotine	17934923	<strong>CYP2A6</strong> gene polymorphism and personality traits for NEO FFI on the <b>smoking</b> behavior of youths.
+CYP2A6	drug	nicotine	17934923	We performed a survey on the relationship between <b>nicotine</b> dependence and psychological (the personality traits using neuroticism extroversion openess five factor inventory (NEO FFI)/<b>nicotine</b> metabolism (the <strong>CYP2A6</strong> gene polymorphism) factors among Japanese young students to elucidate the mechanism of the development of <b>nicotine</b> dependence.
+CYP2A6	addiction	dependence	17934923	We performed a survey on the relationship between nicotine <b>dependence</b> and psychological (the personality traits using neuroticism extroversion openess five factor inventory (NEO FFI)/nicotine metabolism (the <strong>CYP2A6</strong> gene polymorphism) factors among Japanese young students to elucidate the mechanism of the development of nicotine <b>dependence</b>.
+CYP2A6	drug	nicotine	17934923	As a result, the frequency of the <strong>CYP2A6</strong>*4C gene (enzyme activity deficit) was significantly (p<0.05) higher among nonsmokers than <b>smokers</b>, and the Openness score by NEO FFI was higher among <b>smokers</b> than nonsmokers.
+CYP2A6	drug	nicotine	17934923	We conclude that the <strong>CYP2A6</strong>*4C gene and the Openness personality trait may affect the development of the <b>smoking</b> behavior of youth.
+CYP2A6	drug	nicotine	17923852	Identification of inhibitors of the <b>nicotine</b> metabolising <strong>CYP2A6</strong> enzyme  an in silico approach.
+CYP2A6	drug	nicotine	17923852	<b>Nicotine</b> is eliminated by metabolism through the cytochrome P450 2A6 (<strong>CYP2A6</strong>) enzyme in liver.
+CYP2A6	drug	nicotine	17923852	Inhibition of <strong>CYP2A6</strong> by chemical compounds may represent a potential supplement to anti <b>smoking</b> therapy.
+CYP2A6	drug	nicotine	17923852	This compound can be used as a lead in the design of <strong>CYP2A6</strong> inhibitor drugs to combat <b>nicotine</b> addiction.
+CYP2A6	addiction	addiction	17923852	This compound can be used as a lead in the design of <strong>CYP2A6</strong> inhibitor drugs to combat nicotine <b>addiction</b>.
+CYP2A6	drug	nicotine	17454707	An association of <strong>CYP2A6</strong> genotype and <b>smoking</b> topography.
+CYP2A6	drug	nicotine	17454707	<b>Nicotine</b> is metabolized into biologically inactive cotinine primarily by the cytochrome P450 enzyme <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	17454707	<strong>CYP2A6</strong> also is involved in the metabolic activation of <b>tobacco</b> specific procarcinogenic nitrosamines, such as 4 (methyl nitrosamino) 1 (3 pyridyl) 1 butanone (NNK) and 4 (methyl nitrosamino) 1 (3 pyridyl) 1 butanol (NNAL).
+CYP2A6	drug	nicotine	17454707	The present study investigated the association of <strong>CYP2A6</strong> genotype with <b>smoking</b> topography, a quantifiable measure of <b>smoking</b> behavior, in a sample of treatment seeking <b>smokers</b> prior to treatment.
+CYP2A6	addiction	relapse	17454707	The present study investigated the association of <strong>CYP2A6</strong> genotype with smoking topography, a quantifiable measure of smoking behavior, in a sample of treatment <b>seeking</b> smokers prior to treatment.
+CYP2A6	drug	nicotine	17454707	<b>Smokers</b> having <strong>CYP2A6</strong> variants resulting in low activity metabolize <b>nicotine</b> more slowly, and convert procarcinogen nitrosamines to carcinogens more slowly, than do normal metabolizers.
+CYP2A6	drug	nicotine	17372541	Some variants of the cytochrome P450 seem to be more frequent among dependent <b>smokers</b> than controls or ever <b>smokers</b> (<strong>CYP2A6</strong>) and heavier <b>smokers</b> (CYP2D6).
+CYP2A6	drug	nicotine	17130279	The role of <strong>CYP2A6</strong> in the emergence of <b>nicotine</b> dependence in adolescents.
+CYP2A6	addiction	dependence	17130279	The role of <strong>CYP2A6</strong> in the emergence of nicotine <b>dependence</b> in adolescents.
+CYP2A6	drug	nicotine	17130279	Latent growth curve modeling indicated that normal metabolizers (individuals with no detected <strong>CYP2A6</strong> variants) progressed in <b>nicotine</b> dependence at a faster rate and that these increases in <b>nicotine</b> dependence leveled off more slowly compared with slower metabolizers (individuals with <strong>CYP2A6</strong> variants).
+CYP2A6	addiction	dependence	17130279	Latent growth curve modeling indicated that normal metabolizers (individuals with no detected <strong>CYP2A6</strong> variants) progressed in nicotine <b>dependence</b> at a faster rate and that these increases in nicotine <b>dependence</b> leveled off more slowly compared with slower metabolizers (individuals with <strong>CYP2A6</strong> variants).
+CYP2A6	drug	nicotine	17130279	Initial <b>smoking</b> experiences did not account for how <strong>CYP2A6</strong> genetic variation impacts <b>nicotine</b> dependence.
+CYP2A6	addiction	dependence	17130279	Initial smoking experiences did not account for how <strong>CYP2A6</strong> genetic variation impacts nicotine <b>dependence</b>.
+CYP2A6	drug	nicotine	17037346	[The relationship between <b>smoking</b> behavior in young people and <strong>CYP2A6</strong> gene polymorphisms, between them and personality traits assessed by NEO FFI].
+CYP2A6	drug	nicotine	17037346	Samples were taken from young students of which 87 were <b>smokers</b> and 142 were non <b>smokers</b> and we tried to clarify the relationship between the <b>nicotine</b> metabolizing ability (<strong>CYP2A6</strong>), personality, and <b>smoking</b> behavior.
+CYP2A6	drug	nicotine	17037346	As a result, the frequency of the <strong>CYP2A6</strong>*4C gene was significantly higher among non <b>smokers</b> than <b>smokers</b>, and the Openness score by NEO FFI was higher among <b>smokers</b> than non <b>smokers</b>.
+CYP2A6	drug	nicotine	17037346	We concluded that the <strong>CYP2A6</strong>*4C gene and the Openness personality trait may be a cause of <b>smoking</b> among the young <b>smokers</b>.
+CYP2A6	drug	nicotine	17037346	Therefore, there is a possibility that <b>smoking</b> behavior in youths may be affected not only by the <strong>CYP2A6</strong> gene but also by the Openness personality trait.
+CYP2A6	drug	nicotine	17021260	Studies were undertaken to examine whether methoxsalen (9 methoxyfuro[3,2 g][1]benzopyran 7 one), a specific and relatively selective inhibitor of human <strong>CYP2A6</strong>, inhibited CYP2A5 mediated <b>nicotine</b> metabolism in vitro.
+CYP2A6	drug	nicotine	17015050	However, known alleles of <strong>CYP2A6</strong> associated with fast or slow metabolism are relatively uncommon, and there remains considerable variation in metabolic activity among those with presumed wild type <strong>CYP2A6</strong> alleles, suggesting that other genetic or environmental factors also influence the rate of <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	17015050	The ratio of the <b>nicotine</b> metabolite trans 3' hydroxycotinine to cotinine in plasma was used as an index of <strong>CYP2A6</strong> activity and thus as a marker of the rate of <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	17015050	The <b>nicotine</b> metabolite ratio was associated with sex (P < .0001), <strong>CYP2A6</strong> genotype (*1B, *2, *4, *9, and *12) (P < .0001), CYP2B6 haplotype (*4 dominant) (P = .02), plasma <b>nicotine</b> concentration (P < .0001), and age (P = .02) but was not associated with dependence score (P > .20).
+CYP2A6	addiction	dependence	17015050	The nicotine metabolite ratio was associated with sex (P < .0001), <strong>CYP2A6</strong> genotype (*1B, *2, *4, *9, and *12) (P < .0001), CYP2B6 haplotype (*4 dominant) (P = .02), plasma nicotine concentration (P < .0001), and age (P = .02) but was not associated with <b>dependence</b> score (P > .20).
+CYP2A6	drug	nicotine	17015050	In this cohort the rate of <b>nicotine</b> metabolism is related to age, sex, <strong>CYP2A6</strong> genotype, and CYP2B6 genotype and may affect the level of <b>tobacco</b> consumption.
+CYP2A6	drug	nicotine	16952495	Comprehensive evaluation of variability in <b>nicotine</b> metabolism and <strong>CYP2A6</strong> polymorphic alleles in four ethnic populations.
+CYP2A6	drug	nicotine	16952495	However, there are few data on the ethnic influences of the <strong>CYP2A6</strong> <b>nicotine</b> metabolism relationship, particularly with regard to black subjects.
+CYP2A6	drug	nicotine	16952495	We determined the <b>nicotine</b> metabolism and <strong>CYP2A6</strong> genotype in 176 white subjects and 160 black subjects, comparing them with our previous data from 209 Korean subjects and 92 Japanese subjects.
+CYP2A6	drug	nicotine	16952495	These <strong>CYP2A6</strong> alleles were associated with reduced <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	16952495	This comprehensive study of 4 populations extends our understanding of <b>nicotine</b> metabolism and the impact of genetic polymorphisms of the <strong>CYP2A6</strong> gene.
+CYP2A6	drug	nicotine	16872570	Within subject variation of the salivary 3HC/COT ratio in regular daily <b>smokers</b>: prospects for estimating <strong>CYP2A6</strong> enzyme activity in large scale surveys of <b>nicotine</b> metabolic rate.
+CYP2A6	drug	nicotine	16872570	The 3HC/COT ratio measured in the saliva of <b>smokers</b> is highly correlated with the intrinsic hepatic clearance of <b>nicotine</b> and, therefore, may be a useful non invasive marker of <strong>CYP2A6</strong> activity and metabolic rate of <b>nicotine</b>.
+CYP2A6	drug	nicotine	16872570	These findings should be useful for designing large scale population surveys to assess the variation in the metabolic rate of <b>nicotine</b> (via <strong>CYP2A6</strong>) in <b>smokers</b>.
+CYP2A6	drug	opioid	16785264	Candidate genes include those involved in central mechanisms (such as genes encoding the nicotinic acetylcholine receptors, dopamine receptors, dopamine transporters and <b>opioid</b> receptors) and peripheral mechanisms (such as genes encoding the drug metabolizing enzymes <strong>CYP2A6</strong> and CYP2B6).
+CYP2A6	drug	nicotine	16765148	Assessments included demographics, <b>smoking</b> history, body mass index, and plasma <b>nicotine</b>, cotinine, and 3 HC concentrations, as well as <strong>CYP2A6</strong> genotypes.
+CYP2A6	drug	nicotine	16720336	<b>Smoking</b> cessation program and <strong>CYP2A6</strong> polymorphism.
+CYP2A6	drug	nicotine	16720336	The relationship between <strong>CYP2A6</strong> genotype and <b>smoking</b> status remains unclear although several studies have been reported.
+CYP2A6	drug	nicotine	16720336	In this study, we have investigated the significance of <strong>CYP2A6</strong> genotype on <b>smoking</b> habit and treatment of <b>nicotine</b> patch.
+CYP2A6	drug	nicotine	16485141	Cyp2a5, the mouse homologue of human <strong>CYP2A6</strong>, encodes for the enzyme responsible for the primary metabolism of <b>nicotine</b>.
+CYP2A6	drug	nicotine	16485141	Variation in human <strong>CYP2A6</strong> activity can alter the amount smoked such as number of cigarettes smoked per day and <b>smoking</b> intensity.
+CYP2A6	drug	nicotine	16402128	Impact of <strong>CYP2A6</strong> genotype on pretreatment <b>smoking</b> behaviour and <b>nicotine</b> levels from and usage of <b>nicotine</b> replacement therapy.
+CYP2A6	drug	nicotine	16402128	We investigated the effect of slow metabolism of <b>nicotine</b>, predicted by <strong>CYP2A6</strong> genotypes resulting in less than or equal to 50% activity, on baseline <b>smoking</b> behaviours and treatment variables in an open label <b>nicotine</b> replacement therapy (NRT) clinical trial.
+CYP2A6	drug	nicotine	16402128	Caucasian <b>smokers</b> with <strong>CYP2A6</strong> slow vs normal metabolism had lower metabolic activity, indicated by the 3 hydroxycotinine/cotinine ratio (0.23+/ 0.17 vs 0.45+/ 0.22, P<0.01, respectively).
+CYP2A6	drug	nicotine	16402128	These findings indicate that <strong>CYP2A6</strong> genotype influences <b>smoking</b> behaviour in a Caucasian treatment seeking population and that <strong>CYP2A6</strong> genotype affects plasma levels obtained from, and usage of, NRT.
+CYP2A6	addiction	relapse	16402128	These findings indicate that <strong>CYP2A6</strong> genotype influences smoking behaviour in a Caucasian treatment <b>seeking</b> population and that <strong>CYP2A6</strong> genotype affects plasma levels obtained from, and usage of, NRT.
+CYP2A6	drug	nicotine	16402086	<strong>CYP2A6</strong> polymorphisms are associated with <b>nicotine</b> dependence and influence withdrawal symptoms in <b>smoking</b> cessation.
+CYP2A6	addiction	dependence	16402086	<strong>CYP2A6</strong> polymorphisms are associated with nicotine <b>dependence</b> and influence withdrawal symptoms in smoking cessation.
+CYP2A6	addiction	withdrawal	16402086	<strong>CYP2A6</strong> polymorphisms are associated with nicotine dependence and influence <b>withdrawal</b> symptoms in smoking cessation.
+CYP2A6	drug	nicotine	16402086	<strong>CYP2A6</strong> is the main enzyme that catalyzes <b>nicotine</b> into cotinine.
+CYP2A6	drug	nicotine	16402086	Interindividual differences in <b>nicotine</b> metabolism result at least partially from polymorphic variation of <strong>CYP2A6</strong> gene.
+CYP2A6	drug	nicotine	16402086	In this study, we evaluated the influence of <strong>CYP2A6</strong> polymorphisms on clinical phenotypes of <b>smoking</b>, such as <b>smoking</b> habit and withdrawal symptoms.
+CYP2A6	addiction	withdrawal	16402086	In this study, we evaluated the influence of <strong>CYP2A6</strong> polymorphisms on clinical phenotypes of smoking, such as smoking habit and <b>withdrawal</b> symptoms.
+CYP2A6	drug	nicotine	16402086	Japanese <b>smokers</b> (n = 107) were genotyped for <strong>CYP2A6</strong>*1, *4 and *9.
+CYP2A6	drug	nicotine	16402086	Consistent with the previous reports, <strong>CYP2A6</strong> genotypes have a tendency to correlate with the number of cigarettes per day and with daily intake of <b>nicotine</b>.
+CYP2A6	drug	nicotine	16402086	Interestingly, <strong>CYP2A6</strong> high activity group (<strong>CYP2A6</strong>*1/*1, *1/*9, *1/*4, *9/*9) smoked the first cigarette of the day earlier than low activity group (<strong>CYP2A6</strong>*4/*9, *4/*4), indicating more remarkable <b>nicotine</b> dependence.
+CYP2A6	addiction	dependence	16402086	Interestingly, <strong>CYP2A6</strong> high activity group (<strong>CYP2A6</strong>*1/*1, *1/*9, *1/*4, *9/*9) smoked the first cigarette of the day earlier than low activity group (<strong>CYP2A6</strong>*4/*9, *4/*4), indicating more remarkable nicotine <b>dependence</b>.
+CYP2A6	drug	nicotine	16402086	Furthermore, <b>nicotine</b> withdrawal symptoms were more serious in <b>smoking</b> cessation in <strong>CYP2A6</strong> high activity group.
+CYP2A6	addiction	withdrawal	16402086	Furthermore, nicotine <b>withdrawal</b> symptoms were more serious in smoking cessation in <strong>CYP2A6</strong> high activity group.
+CYP2A6	drug	nicotine	16402086	Collectively, <strong>CYP2A6</strong> genotypes are related with <b>nicotine</b> dependence, influencing <b>smoking</b> habits and withdrawal symptoms in quitting <b>smoking</b>.
+CYP2A6	addiction	dependence	16402086	Collectively, <strong>CYP2A6</strong> genotypes are related with nicotine <b>dependence</b>, influencing smoking habits and withdrawal symptoms in quitting smoking.
+CYP2A6	addiction	withdrawal	16402086	Collectively, <strong>CYP2A6</strong> genotypes are related with nicotine dependence, influencing smoking habits and <b>withdrawal</b> symptoms in quitting smoking.
+CYP2A6	drug	nicotine	16402086	It is proposed that individualized <b>smoking</b> cessation program could be designed based on <strong>CYP2A6</strong> genotypes.
+CYP2A6	drug	nicotine	16272956	<strong>CYP2A6</strong>, MAOA, DBH, DRD4, and 5HT2A genotypes, <b>smoking</b> behaviour and cotinine levels in 1518 UK adolescents.
+CYP2A6	drug	nicotine	16272956	Mutations in <strong>CYP2A6</strong> slow metabolism of <b>nicotine</b> to cotinine.
+CYP2A6	drug	nicotine	16272956	1518 subjects from the Ten Towns Heart Health Study were genotyped for <strong>CYP2A6</strong> alleles *1A, *1B, *2, *4, *5, *9 and *12 to classify predicted <b>nicotine</b> metabolism rate.
+CYP2A6	drug	nicotine	16272956	At age 18, haploinsufficiency (HI) for <strong>CYP2A6</strong> was associated with a higher odds of being a current <b>smoker</b> compared with the *1B carriers (WT1B) (OR = 2.23 (1.16, 4.27) for current versus ex); *1A homozygotes (WT1A) were also at slightly higher risk (OR = 1.44 (1.01, 2.06)).
+CYP2A6	drug	nicotine	16272956	<strong>CYP2A6</strong> haploinsufficiency increases likelihood of continuing <b>smoking</b> in teenagers.
+CYP2A6	drug	nicotine	16188955	Inactivation of <strong>CYP2A6</strong> and CYP2A13 during <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	16188955	The primary catalyst of <b>nicotine</b> metabolism in humans is <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	16188955	Here we report that both <strong>CYP2A6</strong> and CYP2A13 were inactivated during <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	16141602	A major pathway of <b>nicotine</b> metabolism is C oxidation to cotinine, which is catalyzed by <strong>CYP2A6</strong> in human livers.
+CYP2A6	drug	nicotine	16141602	Since the genetic polymorphisms of the <strong>CYP2A6</strong> gene have a major impact on <b>nicotine</b> clearance, its relationships with <b>smoking</b> behavior or the risk of lung cancer have been suggested.
+CYP2A6	drug	nicotine	15735610	Our objective was to evaluate the effect of the phase of the menstrual cycle on the activity of <strong>CYP2A6</strong> and the cardiovascular effects of <b>nicotine</b>.
+CYP2A6	drug	nicotine	15735610	<strong>CYP2A6</strong> activity is not affected by menstrual cycle phase, and it is unlikely that menstrual cycle related <b>smoking</b> habits of women are determined by changes in <b>nicotine</b> pharmacokinetics.
+CYP2A6	drug	nicotine	15735609	Implications of <strong>CYP2A6</strong> genetic variation for <b>smoking</b> behaviors and <b>nicotine</b> dependence.
+CYP2A6	addiction	dependence	15735609	Implications of <strong>CYP2A6</strong> genetic variation for smoking behaviors and nicotine <b>dependence</b>.
+CYP2A6	drug	nicotine	15735609	In humans <b>nicotine</b> is mainly inactivated to cotinine and <strong>CYP2A6</strong> mediates approximately 90% of this conversion.
+CYP2A6	drug	nicotine	15735609	Some, but not all, studies suggest that genetic variation in <strong>CYP2A6</strong> may play a role in <b>smoking</b>.
+CYP2A6	drug	nicotine	15735609	We review some of the recent findings on the influence of <strong>CYP2A6</strong> genetic polymorphisms on <b>nicotine</b> kinetics, <b>smoking</b> behaviors, and how the gene appears to exert differential effects during various stages of <b>smoking</b> (eg, initiation, conversion to dependence, amount smoked during dependence, and quitting).
+CYP2A6	addiction	dependence	15735609	We review some of the recent findings on the influence of <strong>CYP2A6</strong> genetic polymorphisms on nicotine kinetics, smoking behaviors, and how the gene appears to exert differential effects during various stages of smoking (eg, initiation, conversion to <b>dependence</b>, amount smoked during <b>dependence</b>, and quitting).
+CYP2A6	drug	nicotine	15734728	<b>Nicotine</b> is of importance as the addictive chemical in <b>tobacco</b>, pharmacotherapy for <b>smoking</b> cessation, a potential medication for several diseases, and a useful probe drug for phenotyping cytochrome P450 2A6 (<strong>CYP2A6</strong>).
+CYP2A6	addiction	addiction	15734728	Nicotine is of importance as the <b>addictive</b> chemical in tobacco, pharmacotherapy for smoking cessation, a potential medication for several diseases, and a useful probe drug for phenotyping cytochrome P450 2A6 (<strong>CYP2A6</strong>).
+CYP2A6	drug	nicotine	15734728	Due to the significance of the <strong>CYP2A6</strong> enzyme in <b>nicotine</b> clearance, special emphasis is given to the effects and population distributions of <strong>CYP2A6</strong> alleles and the regulation of <strong>CYP2A6</strong> enzyme.
+CYP2A6	drug	nicotine	15564629	Genetically decreased <strong>CYP2A6</strong> and the risk of <b>tobacco</b> dependence: a prospective study of novice <b>smokers</b>.
+CYP2A6	addiction	dependence	15564629	Genetically decreased <strong>CYP2A6</strong> and the risk of tobacco <b>dependence</b>: a prospective study of novice smokers.
+CYP2A6	drug	nicotine	15564629	Case control studies in adults suggest that defective alleles in the gene that codes for the hepatic cytochrome P450 2A6 (<strong>CYP2A6</strong>) protect against <b>nicotine</b> dependence (ND) and higher levels of cigarette consumption.
+CYP2A6	addiction	dependence	15564629	Case control studies in adults suggest that defective alleles in the gene that codes for the hepatic cytochrome P450 2A6 (<strong>CYP2A6</strong>) protect against nicotine <b>dependence</b> (ND) and higher levels of cigarette consumption.
+CYP2A6	addiction	dependence	15564629	The association between metabolic activity, represented by <strong>CYP2A6</strong> genotype, and conversion to <b>dependence</b> was analysed using Cox's proportional hazards model.
+CYP2A6	addiction	dependence	15564629	Relative to <strong>CYP2A6</strong>*1/*1, having 1 2 copies of the inactive <strong>CYP2A6</strong>*2 or *4 variant was a strong risk factor for developing <b>dependence</b> (hazard ratio 2.8, 95% confidence 1.3 to 6.3).
+CYP2A6	drug	nicotine	15534625	<strong>CYP2A6</strong> genetic polymorphisms and correlation with <b>smoking</b> status in Brazilians.
+CYP2A6	drug	nicotine	15534625	We investigated polymorphisms of cytochrome P450 2A6 (<strong>CYP2A6</strong>) and its association with <b>smoking</b> habits in 412 healthy Brazilians, self recognized as white (n=147), black (n=123) and intermediate (n=142), and classified as <b>smokers</b> (n=205, including 61 ex <b>smokers</b>) and nonsmokers (n=207).
+CYP2A6	drug	nicotine	15534625	An association between <strong>CYP2A6</strong> genotype and <b>smoking</b> dependence was detected, which could not be explained by the expected phenotypic activity of <strong>CYP2A6</strong>.
+CYP2A6	addiction	dependence	15534625	An association between <strong>CYP2A6</strong> genotype and smoking <b>dependence</b> was detected, which could not be explained by the expected phenotypic activity of <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	15534625	In white and intermediate persons, the odds ratio (OR) of being <b>smokers</b> vs nonsmokers was 0.07 (95% CI 0.02 0.20; P<0.001) and 0.27 (95% CI 0.12 0.61; P<0.001), respectively, for genotypes including allele <strong>CYP2A6</strong>(*)1B, as compared to wild type homozygous.
+CYP2A6	drug	nicotine	15534625	These data suggest that the <strong>CYP2A6</strong>(*)1B is associated with <b>smoking</b> dependence in white and intermediate, but not black Brazilians.
+CYP2A6	addiction	dependence	15534625	These data suggest that the <strong>CYP2A6</strong>(*)1B is associated with smoking <b>dependence</b> in white and intermediate, but not black Brazilians.
+CYP2A6	drug	nicotine	15475735	Ethnic variation in <strong>CYP2A6</strong> and association of genetically slow <b>nicotine</b> metabolism and <b>smoking</b> in adult Caucasians.
+CYP2A6	drug	nicotine	15475735	Genetically variable <strong>CYP2A6</strong> is the primary enzyme that inactivates <b>nicotine</b> to cotinine.
+CYP2A6	drug	nicotine	15475735	Adult Caucasian non <b>smokers</b> (n = 224) (1 99 cigarettes/lifetime) and <b>smokers</b> (n = 375) (> or = 100 cigarettes/lifetime) were assessed for demographics, <b>tobacco</b>/drug use history and DSM IV dependence and genotyped for <strong>CYP2A6</strong> alleles associated with decreased <b>nicotine</b> metabolism (<strong>CYP2A6</strong>*2, <strong>CYP2A6</strong>*4, <strong>CYP2A6</strong>*9, <strong>CYP2A6</strong>*12).
+CYP2A6	addiction	dependence	15475735	Adult Caucasian non smokers (n = 224) (1 99 cigarettes/lifetime) and smokers (n = 375) (> or = 100 cigarettes/lifetime) were assessed for demographics, tobacco/drug use history and DSM IV <b>dependence</b> and genotyped for <strong>CYP2A6</strong> alleles associated with decreased nicotine metabolism (<strong>CYP2A6</strong>*2, <strong>CYP2A6</strong>*4, <strong>CYP2A6</strong>*9, <strong>CYP2A6</strong>*12).
+CYP2A6	drug	nicotine	15229465	Our objective was to evaluate the use of oral <b>nicotine</b> with measurement of the trans 3' hydroxycotinine (3HC)/cotinine (COT) metabolite ratio as a noninvasive probe of <strong>CYP2A6</strong> activity.
+CYP2A6	drug	nicotine	15229465	The ratio appears to be a useful noninvasive marker of the rate of <b>nicotine</b> metabolism (which is important in studying <b>nicotine</b> addiction and <b>smoking</b> behavior), as well as a general marker of <strong>CYP2A6</strong> activity (which is important in studying drug and toxin metabolism).
+CYP2A6	addiction	addiction	15229465	The ratio appears to be a useful noninvasive marker of the rate of nicotine metabolism (which is important in studying nicotine <b>addiction</b> and smoking behavior), as well as a general marker of <strong>CYP2A6</strong> activity (which is important in studying drug and toxin metabolism).
+CYP2A6	drug	nicotine	15203795	A meta analytic review of the <strong>CYP2A6</strong> genotype and <b>smoking</b> behavior.
+CYP2A6	drug	nicotine	15203795	Individuals who carry variant alleles of the <strong>CYP2A6</strong> gene are poor metabolizers of <b>nicotine</b> and are believed to be more sensitive to <b>nicotine</b>'s aversive effects than those with normal alleles.
+CYP2A6	addiction	aversion	15203795	Individuals who carry variant alleles of the <strong>CYP2A6</strong> gene are poor metabolizers of nicotine and are believed to be more sensitive to nicotine's <b>aversive</b> effects than those with normal alleles.
+CYP2A6	drug	nicotine	15203795	Although early studies found an association between variant <strong>CYP2A6</strong> alleles and <b>smoking</b> behavior, more recent studies have not.
+CYP2A6	drug	nicotine	15203795	A literature search produced 11 studies providing information on <strong>CYP2A6</strong> genotyping in <b>smokers</b> or nonsmoking control subjects.
+CYP2A6	drug	nicotine	15203795	Participants were classified as <b>smokers</b> (ever <b>smokers</b> or current <b>smokers</b>) or nonsmokers (former or never <b>smokers</b>), and as carrying normal <strong>CYP2A6</strong> genes or one or more variant alleles.
+CYP2A6	drug	nicotine	15203795	This analysis failed to find any empirical evidence of a relationship between variant <strong>CYP2A6</strong> alleles and <b>smoking</b> status (n=4091) or cigarette consumption (n=1537).
+CYP2A6	drug	nicotine	15203795	Although these results suggest the <strong>CYP2A6</strong> gene is not associated with <b>smoking</b> behavior, the use of broad <b>smoking</b> status classifications (e.g., ever  vs. never <b>smoking</b>), which fail to account for the complex nature of gene expression (e.g., gene gene interactions), may have obscured the relatively modest genetic influences that might have been present.
+CYP2A6	drug	nicotine	15203795	What role, if any, the <strong>CYP2A6</strong> gene plays in <b>smoking</b> behavior will be understood only if future research addresses these methodological concerns.
+CYP2A6	drug	nicotine	14668073	We studied the effect of inhibiting <strong>CYP2A6</strong> on <b>smoking</b> behavior and metabolism of the procarcinogen NNK.
+CYP2A6	drug	nicotine	14668073	In study 1, abstinent <b>smokers</b> (n=7) received methoxsalen (a potent <strong>CYP2A6</strong> inhibitor), 30 50 mg orally, one half hour before three subcutaneous <b>nicotine</b> injections (31 microg/kg) were given at hourly intervals.
+CYP2A6	drug	nicotine	14668073	Thus, treatment with the <strong>CYP2A6</strong> inhibitor methoxsalen in vivo increases the routing of NNK to the inactive NNAL glucuronide and decreases <b>smoking</b>.
+CYP2A6	drug	nicotine	14668073	<strong>CYP2A6</strong> inhibition may have potential as an exposure reduction or cessation strategy in <b>tobacco</b> dependence.
+CYP2A6	addiction	dependence	14668073	<strong>CYP2A6</strong> inhibition may have potential as an exposure reduction or cessation strategy in tobacco <b>dependence</b>.
+CYP2A6	drug	nicotine	14577978	<b>Nicotine</b> is metabolized extensively by the liver enzyme <strong>CYP2A6</strong>, primarily to cotinine.
+CYP2A6	drug	nicotine	12832682	Association of <strong>CYP2A6</strong> deletion polymorphism with <b>smoking</b> habit and development of pulmonary emphysema.
+CYP2A6	drug	nicotine	12832682	<b>Nicotine</b> is responsible for <b>smoking</b> dependence and is mainly metabolised by <strong>CYP2A6</strong>.
+CYP2A6	addiction	dependence	12832682	Nicotine is responsible for smoking <b>dependence</b> and is mainly metabolised by <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	12832682	Several types of genetic polymorphism of <strong>CYP2A6</strong> have been reported, but their relation to <b>smoking</b> habit and chronic obstructive pulmonary disease (COPD) phenotypes has not been fully clarified.
+CYP2A6	drug	nicotine	12818518	Decreasing <b>smoking</b> behaviour and risk through <strong>CYP2A6</strong> inhibition.
+CYP2A6	drug	nicotine	12818518	Current treatments are outlined and we highlight new strategies that are based on the manipulation of cytochrome P450 2A6 (<strong>CYP2A6</strong>) activity, which is responsible for the metabolism of <b>nicotine</b>.
+CYP2A6	drug	nicotine	12818518	The clinical implications of <strong>CYP2A6</strong> polymorphisms have been linked to a decreased risk of <b>tobacco</b> dependence, a decrease in number of cigarettes smoked and reduced risk of <b>tobacco</b> related cancers.
+CYP2A6	addiction	dependence	12818518	The clinical implications of <strong>CYP2A6</strong> polymorphisms have been linked to a decreased risk of tobacco <b>dependence</b>, a decrease in number of cigarettes smoked and reduced risk of tobacco related cancers.
+CYP2A6	drug	nicotine	12749606	Association of <strong>CYP2A6</strong> gene deletion with cigarette <b>smoking</b> status in Japanese adults.
+CYP2A6	drug	nicotine	12749606	Genetic variation of <strong>CYP2A6</strong> is shown to alter <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	12749606	This study was developed to investigate the genetic influence of the whole deletion allele of <strong>CYP2A6</strong> on active and passive <b>smoking</b> behavior.
+CYP2A6	drug	nicotine	12749606	Genetic influence of <strong>CYP2A6</strong> polymorphism on <b>smoking</b> behavior was evaluated using the Mantel extension test.
+CYP2A6	drug	nicotine	12749606	Furthermore, <strong>CYP2A6</strong> genotypes were correlated neither with the number of cigarettes smoked per day nor with the age at starting <b>smoking</b> (p = 0.364 and 0.880, respectively).
+CYP2A6	drug	nicotine	12749606	Among never <b>smokers</b>, <strong>CYP2A6</strong> genotypes were not correlated with exposure to passive <b>smoking</b> at home or in the workplace (p = 0.623 and 0.484, respectively).
+CYP2A6	drug	nicotine	12749606	Despite the possible protection against active <b>smoking</b> behavior in subjects homozygous for the deletion allele, the <strong>CYP2A6</strong> polymorphism has only a limited impact on public health because no protective effect was found in heterozygous subjects.
+CYP2A6	drug	nicotine	11805739	Genetic variation in <strong>CYP2A6</strong> mediated <b>nicotine</b> metabolism alters <b>smoking</b> behavior.
+CYP2A6	drug	nicotine	11805739	The genetically polymorphic <strong>CYP2A6</strong> enzyme is responsible for the majority of the metabolic inactivation of <b>nicotine</b> to cotinine (12 14).
+CYP2A6	drug	nicotine	11805739	<strong>CYP2A6</strong> is genetically polymorphic, individuals carrying inactive <strong>CYP2A6</strong> alleles have decreased <b>nicotine</b> metabolism, are less likely to become <b>smokers</b> and if they do, they smoke fewer cigarettes per day (13,18,19).
+CYP2A6	drug	nicotine	11805739	A duplication variant in the <strong>CYP2A6</strong> gene locus has been identified which increases <b>nicotine</b> inactivation and increases <b>smoking</b> (19).
+CYP2A6	drug	nicotine	11805739	<strong>CYP2A6</strong> can also activate <b>tobacco</b> smoke procarcinogens (e.g.
+CYP2A6	drug	nicotine	11805739	Kinetic studies in humans indicated that selective <strong>CYP2A6</strong> inhibitors decrease the metabolic removal of <b>nicotine</b>.
+CYP2A6	drug	nicotine	11805739	It was also shown that inhibiting <strong>CYP2A6</strong> in vivo (phenocopying, or mimicking the genetic defect) in <b>smokers</b> results in decreased <b>smoking</b>, making <b>nicotine</b> orally bioavailable, and the rerouting of procarcinogens to detoxifying pathways (20 22).
+CYP2A6	drug	nicotine	11768189	<strong>CYP2A6</strong> is the enzyme responsible for the majority of the inactivation of <b>nicotine</b> in humans.
+CYP2A6	drug	nicotine	11768189	This paper outlines how genetic variation in the <strong>CYP2A6</strong> gene may protect individuals from becoming <b>nicotine</b> dependent <b>smokers</b>, and if dependent, how impairment of the <strong>CYP2A6</strong> gene function decreases the number of cigarettes consumed by <b>smokers</b> (Pianezza M, Sellers EM, Tyndale RF.
+CYP2A6	drug	nicotine	11768189	We also discuss recent findings which suggest that mimicking this gene defect by inhibiting <strong>CYP2A6</strong> decreases <b>nicotine</b> metabolism and <b>smoking</b>.
+CYP2A6	drug	nicotine	11768189	Further research is needed in order to improve our understanding of how genetic variation in <strong>CYP2A6</strong> alters the risk for <b>nicotine</b> dependence and lowers <b>nicotine</b> consumption.
+CYP2A6	addiction	dependence	11768189	Further research is needed in order to improve our understanding of how genetic variation in <strong>CYP2A6</strong> alters the risk for nicotine <b>dependence</b> and lowers nicotine consumption.
+CYP2A6	drug	nicotine	11768189	This includes a better understanding of how the genetic variants alter <b>nicotine</b> metabolism in vivo in males and females as well as the role of <strong>CYP2A6</strong> genetic variation in risk for <b>tobacco</b> related cancers.
+CYP2A6	drug	nicotine	11259349	Variable <strong>CYP2A6</strong> mediated <b>nicotine</b> metabolism alters <b>smoking</b> behavior and risk.
+CYP2A6	drug	nicotine	11259349	In humans, 70 to 80% of <b>nicotine</b> is metabolized to the inactive metabolite cotinine by the enzyme <strong>CYP2A6</strong>.
+CYP2A6	drug	nicotine	11259349	<strong>CYP2A6</strong> can also activate <b>tobacco</b> smoke procarcinogens [e.g., NNK, 4 (methylnitrosamino) 1 (3 pyridyl) 1 butanone].
+CYP2A6	drug	nicotine	11259349	In initial studies we found that there was an under representation of individuals carrying defective <strong>CYP2A6</strong> alleles in a <b>tobacco</b> dependent population, and that among <b>smokers</b>, those with deficient <b>nicotine</b> metabolism smoked fewer cigarettes.
+CYP2A6	drug	nicotine	11259349	We have since reproduced this data in a prospective <b>smoking</b> study (400 male and female, heavy and light <b>smokers</b>) examining the role of the <strong>CYP2A6</strong> genotype on carbon monoxide levels, plasma and urine <b>nicotine</b> and cotinine levels, and cigarette counts.
+CYP2A6	drug	nicotine	11259349	We have also recently identified deletion and duplication variants in the <strong>CYP2A6</strong> gene locus and have examined their impact on <b>smoking</b>.
+CYP2A6	drug	nicotine	11259349	Both kinetic and behavioral experiments in human <b>smokers</b> demonstrated that inhibiting <strong>CYP2A6</strong> in vivo decreased <b>nicotine</b> metabolism and <b>smoking</b> behavior.
+CYP2A6	drug	nicotine	11207029	Cytochrome P450 2A6 (<strong>CYP2A6</strong>) is involved in the C oxidation of <b>nicotine</b> and in the metabolic activation of <b>tobacco</b> nitrosamines.
+CYP2A6	drug	nicotine	11207029	Recent data have suggested that <strong>CYP2A6</strong> genetic polymorphisms might play a role in <b>tobacco</b> dependence and consumption as well as in lung cancer risk.
+CYP2A6	addiction	dependence	11207029	Recent data have suggested that <strong>CYP2A6</strong> genetic polymorphisms might play a role in tobacco <b>dependence</b> and consumption as well as in lung cancer risk.
+CYP2A6	drug	nicotine	11207029	In this Caucasian population, we found neither a relation between genetically impaired <b>nicotine</b> metabolism and cigarette consumption, nor any modification of lung cancer risk related to the presence of defective <strong>CYP2A6</strong> alleles (odds ratio = 1.1, 95% confidence interval = 0.7 1.9).
+CYP2A6	drug	nicotine	11054771	Functional variants at <strong>CYP2A6</strong>: new genotyping methods, population genetics, and relevance to studies of <b>tobacco</b> dependence.
+CYP2A6	addiction	dependence	11054771	Functional variants at <strong>CYP2A6</strong>: new genotyping methods, population genetics, and relevance to studies of tobacco <b>dependence</b>.
+CYP2A6	drug	nicotine	11054771	Cytochrome P450CYP2A6 (<strong>CYP2A6</strong>) is the predominant enzyme responsible for the metabolism of <b>nicotine</b> to cotinine.
+CYP2A6	drug	nicotine	10945314	Individuals with genetically deficient <strong>CYP2A6</strong> <b>nicotine</b> metabolism are at lower risk to become <b>smokers</b> and, if dependent, will smoke fewer cigarettes.
+CYP2A6	drug	nicotine	10945314	Hepatic <strong>CYP2A6</strong> accounts for <b>nicotine</b>'s low systemic bioavailability, precluding oral <b>nicotine</b> replacement to treat dependence.
+CYP2A6	addiction	dependence	10945314	Hepatic <strong>CYP2A6</strong> accounts for nicotine's low systemic bioavailability, precluding oral nicotine replacement to treat <b>dependence</b>.
+CYP2A6	drug	nicotine	10945314	We sought to determine whether <strong>CYP2A6</strong> inhibition via oral methoxsalen decreases <b>nicotine</b> clearance, increases <b>nicotine</b> bioavailability, and decreases <b>smoking</b>.
+CYP2A6	drug	nicotine	10945314	Placebo plus <b>nicotine</b> 4 mg orally increased the mean 3 hour plasma <b>nicotine</b> level by 4 ng/mL over residual baseline <b>nicotine</b> level, whereas methoxsalen 10 or 30 mg plus <b>nicotine</b> increased it by 9 ng/mL (P<.01), demonstrating in vivo inhibition of <strong>CYP2A6</strong> <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	10945314	<strong>CYP2A6</strong> inhibitors may have an important role in <b>smoking</b> cessation and <b>tobacco</b> exposure reduction.
+CYP2A6	drug	benzodiazepine	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes CYP2D6 (codeine, amphetamines, dextromethorphan), <strong>CYP2A6</strong> (nicotine) and CYP2C19 (<b>flunitrazepam</b>).
+CYP2A6	drug	nicotine	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes CYP2D6 (codeine, amphetamines, dextromethorphan), <strong>CYP2A6</strong> (<b>nicotine</b>) and CYP2C19 (flunitrazepam).
+CYP2A6	drug	opioid	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes CYP2D6 (<b>codeine</b>, amphetamines, dextromethorphan), <strong>CYP2A6</strong> (nicotine) and CYP2C19 (flunitrazepam).
+CYP2A6	drug	nicotine	10911933	In epidemiologic studies CYP2D6 and <strong>CYP2A6</strong> null mutations protect individuals from becoming codeine and <b>tobacco</b> dependent, respectively.
+CYP2A6	drug	opioid	10911933	In epidemiologic studies CYP2D6 and <strong>CYP2A6</strong> null mutations protect individuals from becoming <b>codeine</b> and tobacco dependent, respectively.
+CYP2A6	drug	nicotine	10544257	Identification and characterisation of novel polymorphisms in the <strong>CYP2A</strong> locus: implications for <b>nicotine</b> metabolism.
+CYP2A6	drug	nicotine	10544257	The polymorphic human cytochrome P450 2A6 (<strong>CYP2A6</strong>) metabolises a number of drugs, activates a variety of precarcinogens and constitutes the major <b>nicotine</b> C oxidase.
+CYP2A6	drug	nicotine	10544257	A relationship between <strong>CYP2A6</strong> genotype and <b>smoking</b> habits, as well as incidence of lung cancer, has been proposed.
+CYP2A6	drug	nicotine	10544257	Among Caucasians, an additional defective and frequently distributed allele (<strong>CYP2A6</strong>*3) has been suggested to play a protective role against <b>nicotine</b> addiction and cigarette consumption.
+CYP2A6	addiction	addiction	10544257	Among Caucasians, an additional defective and frequently distributed allele (<strong>CYP2A6</strong>*3) has been suggested to play a protective role against nicotine <b>addiction</b> and cigarette consumption.
+TRPV1	addiction	addiction	32534009	Red hot chili receptors: A systematic review of <strong>TRPV1</strong> antagonism in animal models of psychiatric disorders and <b>addiction</b>.
+TRPV1	drug	cannabinoid	32534009	<strong>TRPV1</strong> receptors are distributed in several brain areas and interact with important neurotransmitter systems linked to mental disorders, such as <b>endocannabinoid</b> and opioid systems.
+TRPV1	drug	opioid	32534009	<strong>TRPV1</strong> receptors are distributed in several brain areas and interact with important neurotransmitter systems linked to mental disorders, such as endocannabinoid and <b>opioid</b> systems.
+TRPV1	drug	amphetamine	32534009	The results, still limited to preclinical studies, suggest that <strong>TRPV1</strong> antagonism could represent a potential mechanism for the treatment of depression and anxiety, as well as for opioids, <b>methamphetamine</b> and cocaine addiction.
+TRPV1	drug	cocaine	32534009	The results, still limited to preclinical studies, suggest that <strong>TRPV1</strong> antagonism could represent a potential mechanism for the treatment of depression and anxiety, as well as for opioids, methamphetamine and <b>cocaine</b> addiction.
+TRPV1	drug	opioid	32534009	The results, still limited to preclinical studies, suggest that <strong>TRPV1</strong> antagonism could represent a potential mechanism for the treatment of depression and anxiety, as well as for <b>opioids</b>, methamphetamine and cocaine addiction.
+TRPV1	addiction	addiction	32534009	The results, still limited to preclinical studies, suggest that <strong>TRPV1</strong> antagonism could represent a potential mechanism for the treatment of depression and anxiety, as well as for opioids, methamphetamine and cocaine <b>addiction</b>.
+TRPV1	addiction	addiction	32534009	Single studies report the effectiveness of <strong>TRPV1</strong> antagonists in animal models of obsessive <b>compulsive</b> disorder and fibromyalgia.
+TRPV1	drug	opioid	31998461	The role of locus coeruleus nucleus <strong>TRPV1</strong> receptors in the development and expression of <b>morphine</b> dependence.
+TRPV1	addiction	dependence	31998461	The role of locus coeruleus nucleus <strong>TRPV1</strong> receptors in the development and expression of morphine <b>dependence</b>.
+TRPV1	drug	opioid	31998461	This study investigated the role of locus coeruleus (LC) nucleus <strong>TRPV1</strong> receptors (TRPV1r) in the expression and development of <b>morphine</b> physical dependence by intra LC administration of AMG9810 (selective TRPV1r antagonist) in male Wistar rats.
+TRPV1	addiction	dependence	31998461	This study investigated the role of locus coeruleus (LC) nucleus <strong>TRPV1</strong> receptors (TRPV1r) in the expression and development of morphine physical <b>dependence</b> by intra LC administration of AMG9810 (selective TRPV1r antagonist) in male Wistar rats.
+TRPV1	drug	opioid	31760085	Blockade of peripheral nociceptive inputs prevented chronic <b>morphine</b> induced increases in spinal SP, NR1, and <strong>TRPV1</strong> and a rightward shift of the <b>morphine</b> dose response curve in the CCI model.
+TRPV1	drug	opioid	31655852	Antinociceptive and genotoxic assessments of the antagonist <strong>TRPV1</strong> receptor SB 366791 on <b>morphine</b> induced tolerance in mice.
+TRPV1	addiction	sensitization	31551772	<strong>TRPV1</strong> contributes to peripheral <b>sensitization</b> and hyperalgesia, in part, via triggering the release of proinflammatory peptides, such as calcitonin gene related peptide (CGRP), both locally and at the dorsal horn of the spinal cord.
+TRPV1	drug	opioid	31551772	Blocking <strong>TRPV1</strong>, but not <b>opioid</b> receptors, attenuated the onset of analgesia and capsaicin induced CGRP release.
+TRPV1	drug	opioid	31551772	These findings indicate that phytochemicals in the E. bicolor latex induce hyperalgesia followed by peripheral, non <b>opioid</b> analgesia in both male and female rats, which occurs in part via <strong>TRPV1</strong> and may provide novel, non <b>opioid</b> peripheral analgesics that warrant further examination.
+TRPV1	drug	cannabinoid	31437433	<b>Cannabidiol</b> attenuates the rewarding effects of cocaine in rats by CB2, 5 HT1A and <strong>TRPV1</strong> receptor mechanisms.
+TRPV1	drug	cocaine	31437433	Cannabidiol attenuates the rewarding effects of <b>cocaine</b> in rats by CB2, 5 HT1A and <strong>TRPV1</strong> receptor mechanisms.
+TRPV1	drug	cannabinoid	31437433	Strikingly, this reduction in both cocaine self administration and BSR was blocked by AM630 (a <b>cannabinoid</b> CB2 receptor antagonist), WAY100135 (a 5 HT1A receptor antagonist), or capsazepine (a <strong>TRPV1</strong> channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a GPR55 antagonist), or naloxone (an opioid receptor antagonist), suggesting the involvement of CB2, 5 HT1A, and <strong>TRPV1</strong> receptors in CBD action.
+TRPV1	drug	cocaine	31437433	Strikingly, this reduction in both <b>cocaine</b> self administration and BSR was blocked by AM630 (a cannabinoid CB2 receptor antagonist), WAY100135 (a 5 HT1A receptor antagonist), or capsazepine (a <strong>TRPV1</strong> channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a GPR55 antagonist), or naloxone (an opioid receptor antagonist), suggesting the involvement of CB2, 5 HT1A, and <strong>TRPV1</strong> receptors in CBD action.
+TRPV1	drug	opioid	31437433	Strikingly, this reduction in both cocaine self administration and BSR was blocked by AM630 (a cannabinoid CB2 receptor antagonist), WAY100135 (a 5 HT1A receptor antagonist), or capsazepine (a <strong>TRPV1</strong> channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a GPR55 antagonist), or <b>naloxone</b> (an <b>opioid</b> receptor antagonist), suggesting the involvement of CB2, 5 HT1A, and <strong>TRPV1</strong> receptors in CBD action.
+TRPV1	drug	cocaine	31432769	However, no study has yet examined the mechanism of <strong>TRPV1</strong> in the NAc on <b>cocaine</b> reinstatement.
+TRPV1	addiction	relapse	31432769	However, no study has yet examined the mechanism of <strong>TRPV1</strong> in the NAc on cocaine <b>reinstatement</b>.
+TRPV1	drug	cocaine	31432769	We investigated the mechanism of <strong>TRPV1</strong> in NAc on <b>cocaine</b> reinstatement using the conditioned place preference (CPP) test in mice.
+TRPV1	addiction	relapse	31432769	We investigated the mechanism of <strong>TRPV1</strong> in NAc on cocaine <b>reinstatement</b> using the conditioned place preference (CPP) test in mice.
+TRPV1	addiction	reward	31432769	We investigated the mechanism of <strong>TRPV1</strong> in NAc on cocaine reinstatement using the conditioned place preference (<b>CPP</b>) test in mice.
+TRPV1	drug	cocaine	31432769	), and genetic deletion of <strong>TRPV1</strong> on the reinstatement of <b>cocaine</b> induced CPP (15 mg/kg, administered i.p.).
+TRPV1	addiction	relapse	31432769	), and genetic deletion of <strong>TRPV1</strong> on the <b>reinstatement</b> of cocaine induced CPP (15 mg/kg, administered i.p.).
+TRPV1	addiction	reward	31432769	), and genetic deletion of <strong>TRPV1</strong> on the reinstatement of cocaine induced <b>CPP</b> (15 mg/kg, administered i.p.).
+TRPV1	drug	cocaine	31432769	The expression of <strong>TRPV1</strong> and Ca2+/calmodulin mediated kinase II (CaMKII) in the NAc were determined after <b>cocaine</b> reinstatement.
+TRPV1	addiction	relapse	31432769	The expression of <strong>TRPV1</strong> and Ca2+/calmodulin mediated kinase II (CaMKII) in the NAc were determined after cocaine <b>reinstatement</b>.
+TRPV1	drug	cocaine	31432769	Microinjection of SB366791 (0.2 ng, a selective <strong>TRPV1</strong> antagonist) in the NAc was assessed on SKF 81297 (1 µg, D1 like dopamine (DA) receptor agonist) primed <b>cocaine</b> reinstatement.
+TRPV1	addiction	relapse	31432769	Microinjection of SB366791 (0.2 ng, a selective <strong>TRPV1</strong> antagonist) in the NAc was assessed on SKF 81297 (1 µg, D1 like dopamine (DA) receptor agonist) primed cocaine <b>reinstatement</b>.
+TRPV1	drug	cocaine	31432769	In addition, genetic deletion of <strong>TRPV1</strong> inhibited <b>cocaine</b> priming reinstatement.
+TRPV1	addiction	relapse	31432769	In addition, genetic deletion of <strong>TRPV1</strong> inhibited cocaine priming <b>reinstatement</b>.
+TRPV1	drug	cocaine	31432769	<b>Cocaine</b> reinstatement was mediated by increased <strong>TRPV1</strong> expression in the NAc, which involves CaMKII.
+TRPV1	addiction	relapse	31432769	Cocaine <b>reinstatement</b> was mediated by increased <strong>TRPV1</strong> expression in the NAc, which involves CaMKII.
+TRPV1	drug	cocaine	31432769	These findings suggest that activation of <strong>TRPV1</strong> mediates the stimulation of D1 like DA receptors and CaMKII in the NAc, resulting in the facilitation of <b>cocaine</b> reinstatement behaviors.
+TRPV1	addiction	relapse	31432769	These findings suggest that activation of <strong>TRPV1</strong> mediates the stimulation of D1 like DA receptors and CaMKII in the NAc, resulting in the facilitation of cocaine <b>reinstatement</b> behaviors.
+TRPV1	addiction	relapse	31432769	Thus, our findings reveal a previously unknown <strong>TRPV1</strong> mechanism in the <b>reinstatement</b> to drugs of abuse.
+TRPV1	drug	alcohol	31412038	Mice avoided water sources surrounded by both volatile <strong>TRPV1</strong> (cyclohexanone) and TRPA1 (allyl isothiocyanate) irritants and the aversion to cyclohexanone was mitigated when combined with a pure odorant (rose fragrance, phenylethyl <b>alcohol</b>, PEA).
+TRPV1	addiction	aversion	31412038	Mice avoided water sources surrounded by both volatile <strong>TRPV1</strong> (cyclohexanone) and TRPA1 (allyl isothiocyanate) irritants and the <b>aversion</b> to cyclohexanone was mitigated when combined with a pure odorant (rose fragrance, phenylethyl alcohol, PEA).
+TRPV1	drug	cannabinoid	31294469	Recent studies indicated the two nociceptive receptors, <b>cannabinoid</b> receptor (CB) and transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) channel, are co expressed in bone cells and play important role in the metabolism of bone cells, suggesting that dualtargeting these 2 receptors/channel may provide a novel approach for osteoporotic pain.
+TRPV1	drug	cannabinoid	31096838	Diverse <strong>TRPV1</strong> responses to <b>cannabinoids</b>.
+TRPV1	drug	cannabinoid	31096838	Here, we explore and compare a suite of <b>cannabinoids</b> for their impact upon the physiology of <strong>TRPV1</strong>.
+TRPV1	drug	cannabinoid	31096838	<b>Cannabinoid</b> activation of <strong>TRPV1</strong> displays significant dependence on internal and external calcium levels.
+TRPV1	addiction	dependence	31096838	Cannabinoid activation of <strong>TRPV1</strong> displays significant <b>dependence</b> on internal and external calcium levels.
+TRPV1	drug	cannabinoid	31096838	<b>Cannabinoid</b> activation of <strong>TRPV1</strong> does not appear to induce the highly permeant, pore dilated channel state seen with Capsaicin, even at high current amplitudes.
+TRPV1	drug	cannabinoid	31096838	Finally, we analyzed <b>cannabinoid</b> responses at nociceptive channels other than <strong>TRPV1</strong> (TRPV2, TRPM8, and TRPA1), and report that <b>cannabinoids</b> differentially activate these channels.
+TRPV1	addiction	sensitization	30706780	On the basis of their anatomic location, transient receptor potential ion channels (<strong>TRPV1</strong>, TRPV2 and TRPM8), Piezo 2, acid sensing ion channels (ASICs), purinergic (P2X and P2Y), bradykinin (B1 and B2), α amino 3 hydroxy 5  methylisoxazole 4 propionate (AMPA), N methyl D aspartate (NMDA), metabotropic glutamate (mGlu), neurokinin 1 (NK1) and calcitonin gene related peptide (CGRP) receptors are activated during pain <b>sensitization</b>.
+TRPV1	drug	alcohol	30676422	In vivo, local administration of <strong>TRPV1</strong> antagonists into the lateral habenula attenuated hyperalgesia, anxiety, and relapse like drinking in rats who chronically consumed <b>alcohol</b>.The data suggest that enhanced <strong>TRPV1</strong> channel function during withdrawal may contribute to aberrant behavior that promotes relapse <b>alcohol</b> consumption.
+TRPV1	addiction	relapse	30676422	In vivo, local administration of <strong>TRPV1</strong> antagonists into the lateral habenula attenuated hyperalgesia, anxiety, and <b>relapse</b> like drinking in rats who chronically consumed alcohol.The data suggest that enhanced <strong>TRPV1</strong> channel function during withdrawal may contribute to aberrant behavior that promotes <b>relapse</b> alcohol consumption.
+TRPV1	addiction	withdrawal	30676422	In vivo, local administration of <strong>TRPV1</strong> antagonists into the lateral habenula attenuated hyperalgesia, anxiety, and relapse like drinking in rats who chronically consumed alcohol.The data suggest that enhanced <strong>TRPV1</strong> channel function during <b>withdrawal</b> may contribute to aberrant behavior that promotes relapse alcohol consumption.
+TRPV1	drug	alcohol	30676422	<strong>TRPV1</strong>, a vanilloid receptor expressed in the habenula, is involved in pain, <b>alcohol</b> dependence, and glutamatergic transmission.
+TRPV1	addiction	dependence	30676422	<strong>TRPV1</strong>, a vanilloid receptor expressed in the habenula, is involved in pain, alcohol <b>dependence</b>, and glutamatergic transmission.
+TRPV1	drug	alcohol	30676422	The authors therefore hypothesized that <strong>TRPV1</strong> contributes to the changes in both the behavioral phenotypes and the habenula activity in <b>alcohol</b> withdrawn rats.
+TRPV1	drug	alcohol	30676422	The primary outcome was the change in <b>alcohol</b> related behaviors and lateral habenula activity induced by pharmacologic manipulation of <strong>TRPV1</strong> activity.
+TRPV1	drug	alcohol	30676422	In Withdrawn rats, intra habenula infusion of <strong>TRPV1</strong> antagonists attenuated hyperalgesia and anxiety like behaviors, decreased <b>alcohol</b> consumption upon resuming drinking, and elicited a conditioned place preference.
+TRPV1	drug	alcohol	30676422	Enhanced <strong>TRPV1</strong> function may contribute to increased glutamatergic transmission and activity of lateral habenula neurons, resulting in the aberrant behaviors during <b>ethanol</b> withdrawal.
+TRPV1	addiction	withdrawal	30676422	Enhanced <strong>TRPV1</strong> function may contribute to increased glutamatergic transmission and activity of lateral habenula neurons, resulting in the aberrant behaviors during ethanol <b>withdrawal</b>.
+TRPV1	drug	cannabinoid	30589475	We found that administration of the <b>endocannabinoid</b> transport inhibitor AM404 reduced habitual responding for food and that antagonism of <b>cannabinoid</b> receptor type 1 (CB1), but not transient receptor potential cation subfamily V (<strong>TRPV1</strong>), receptors produced a similar reduction in habitual responding.
+TRPV1	drug	opioid	30292787	<strong>TRPV1</strong> modulates <b>morphine</b> self administration via activation of the CaMKII CREB pathway in the nucleus accumbens.
+TRPV1	drug	opioid	30292787	We have previously shown that <strong>TRPV1</strong> plays a critical role in <b>morphine</b> addiction using a self administration paradigm in rats, and the current study evaluates the effects of the <strong>TRPV1</strong> signaling pathway on <b>morphine</b> self administration (SA).
+TRPV1	addiction	addiction	30292787	We have previously shown that <strong>TRPV1</strong> plays a critical role in morphine <b>addiction</b> using a self administration paradigm in rats, and the current study evaluates the effects of the <strong>TRPV1</strong> signaling pathway on morphine self administration (SA).
+TRPV1	drug	opioid	30292787	We found that treatment with a selective <strong>TRPV1</strong> antagonist, SB366791, significantly decreased the <b>morphine</b> SA induced activation of Ca2+/calmodulin dependent protein kinase II (CaMKII), Akt and the cAMP response element binding protein (CREB) in the nucleus accumbens (NAc).
+TRPV1	drug	opioid	30292787	Taken together, our findings highlight that <strong>TRPV1</strong> plays an important role in <b>morphine</b> addiction, likely via activation of the CaMKII CREB pathway in the NAc.
+TRPV1	addiction	addiction	30292787	Taken together, our findings highlight that <strong>TRPV1</strong> plays an important role in morphine <b>addiction</b>, likely via activation of the CaMKII CREB pathway in the NAc.
+TRPV1	drug	cannabinoid	30026689	<b>Endocannabinoid</b> LTP Mediated by CB1 and <strong>TRPV1</strong> Receptors Encodes for Limited Occurrences of Coincident Activity in Neocortex.
+TRPV1	drug	cannabinoid	30026689	This tLTP was not mediated by NMDA receptor activation but requires CB1 receptors and transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) activated by <b>endocannabinoids</b> (eCBs).
+TRPV1	drug	cannabinoid	29991708	Despite the apparent abundance of ligand gated transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) and possible cross talk between the <b>endocannabinoid</b> and endovanilloid systems in the central nervous system (CNS), it is unclear what role <strong>TRPV1</strong> receptor activation in CNS plays in neurobehavioral development.
+TRPV1	drug	cannabinoid	29596901	In the present work, we investigated the interplay between the vanilloid <strong>TRPV1</strong> and <b>cannabinoid</b> CB1 receptors in the NMDA dlPAG defensive response and in subsequent aversive learning.
+TRPV1	addiction	aversion	29596901	In the present work, we investigated the interplay between the vanilloid <strong>TRPV1</strong> and cannabinoid CB1 receptors in the NMDA dlPAG defensive response and in subsequent <b>aversive</b> learning.
+TRPV1	addiction	aversion	29596901	The results showed that immediate defensive responses rely on NMDA receptors, and <b>aversive</b> learning on the fine tuning of <strong>TRPV1</strong>, CB1, metabotropic glutamate and AMPA receptors located in pre  and postsynaptic membranes.
+TRPV1	addiction	aversion	29596901	In conclusion, the activity of the dlPAG determines core affective aspects of <b>aversive</b> memory formation controlled by local <strong>TRPV1</strong>/CB1 balance.
+TRPV1	addiction	sensitization	29430557	It has been shown in rat models that repeated exposure to acrolein induces trigeminovascular <b>sensitization</b> to both TRPA1 and TRP vanilloid 1 (<strong>TRPV1</strong>) agonists, a phenomenon linked to headache.
+TRPV1	addiction	sensitization	29430557	In this study, we test the hypothesis that the <b>sensitization</b> of trigeminovascular responses in rats after acrolein exposure via inhalation is associated with changes in levels of endogenous lipids, including <strong>TRPV1</strong> agonists, in the trigeminal ganglia, trigeminal nucleus, and cerebellum.
+TRPV1	drug	cannabinoid	29430557	After chronic acrolein exposure, levels of all 6 N acyl ethanolamines in the screening library, including the endogenous <b>cannabinoid</b> and <strong>TRPV1</strong> agonist, N arachidonoyl ethanolamine, were elevated in trigeminal tissue and in the cerebellum.
+TRPV1	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (Cnr1, Cnr2, and <strong>Trpv1</strong>), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and <strong>TRPV1</strong> sensitizing kinases (Mapk3, Mapk14, Prkcg, and Prkaca).
+TRPV1	drug	amphetamine	29343767	Blockade of <strong>TRPV1</strong> Inhibits <b>Methamphetamine</b> induced Rewarding Effects.
+TRPV1	addiction	addiction	29343767	Recent studies have identified the distribution of <strong>TRPV1</strong> in several brain regions that are related to drug <b>addiction</b>, including nucleus accumbens (NAc) and dorsal striatum (DSt).
+TRPV1	addiction	reward	29343767	We found that both CPZ and SB significantly inhibited MAP induced <b>CPP</b> and self administration; in contrast, <strong>TRPV1</strong> knock out (KO) mice did not develop MAP induced <b>CPP</b>.
+TRPV1	addiction	reward	29343767	Real time RT PCR, Western blot and quantitative autoradiographic tests showed up regulation of <strong>TRPV1</strong> mRNA and protein expression in the NAc and/or DSt regions of mice exhibiting MAP induced <b>CPP</b>.
+TRPV1	addiction	addiction	29343767	Together, these data suggest that <strong>TRPV1</strong> plays an important role in MAP reward via the modulation of DA release and DAT density, thereby providing a novel therapeutic target for MAP <b>addiction</b>.
+TRPV1	addiction	reward	29343767	Together, these data suggest that <strong>TRPV1</strong> plays an important role in MAP <b>reward</b> via the modulation of DA release and DAT density, thereby providing a novel therapeutic target for MAP addiction.
+TRPV1	drug	cannabinoid	29338068	<b>Cannabinoid</b> withdrawal signs were assessed following precipitated withdrawal by acute administration of the CB1 receptor antagonist <b>SR141716</b>, the 5 HT1A receptor antagonist WAY100635, the <strong>TRPV1</strong> receptor antagonist capsazepine or the adenosine A2A receptor antagonist SCH58261.
+TRPV1	addiction	withdrawal	29338068	Cannabinoid <b>withdrawal</b> signs were assessed following precipitated <b>withdrawal</b> by acute administration of the CB1 receptor antagonist SR141716, the 5 HT1A receptor antagonist WAY100635, the <strong>TRPV1</strong> receptor antagonist capsazepine or the adenosine A2A receptor antagonist SCH58261.
+TRPV1	drug	nicotine	29247491	The hydrophilic <b>nicotine</b> was ineffective unless applied unprotonated in alkaline (pH9) solution, activating TRPA1 and <strong>TRPV1</strong>.
+TRPV1	drug	opioid	29103813	Corrigendum to "<strong>TRPV1</strong> modulates <b>morphine</b> induced conditioned place preference via p38 MAPK in the nucleus accumbens" [Behav.
+TRPV1	drug	opioid	28930716	Antinociceptive Effect of Ghrelin in a Rat Model of Irritable Bowel Syndrome Involves <strong>TRPV1</strong>/<b>Opioid</b> Systems.
+TRPV1	drug	opioid	28930716	Expression of transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) and µ and κ <b>opioid</b> receptors (MOR and KOR) in colon, dorsal root ganglion (DRG) and cerebral cortex tissues were detected by western blotting, quantitative real time polymerase chain reaction (qRT PCR), immunohistochemical analyses and immunofluorescence.
+TRPV1	drug	opioid	28930716	Ghrelin treatment increased expression of <b>opioid</b> receptors and inhibited expression of <strong>TRPV1</strong> in colon, dorsal root ganglion (DRG) and cerebral cortex.
+TRPV1	drug	opioid	28930716	The results indicate that ghrelin exerted an antinociceptive effect, which was mediated via <strong>TRPV1</strong>/<b>opioid</b> systems, in IBS induced visceral hypersensitivity.
+TRPV1	drug	opioid	28901432	Whether coadministration of a CB2 receptor agonist and <b>morphine</b> could reduce <strong>TRPV1</strong> expression in <b>morphine</b>‑induced antinociception and tolerance in cancer pain is unclear.
+TRPV1	drug	opioid	28901432	Therefore, we investigated the effects of coadministration of a CB2 receptor agonist AM1241 and <b>morphine</b> on <strong>TRPV1</strong> expression and tolerance in cancer pain.
+TRPV1	drug	opioid	28901432	Repeated <b>morphine</b> treatment for a period of 8 days induced upregulation of the <strong>TRPV1</strong> protein expression levels in the DRG in the tumor‑bearing rats, although no change in mRNA expression.
+TRPV1	drug	opioid	28901432	Pretreatment with AM1241 reduced this <b>morphine</b>‑induced upregulation of <strong>TRPV1</strong> and the effect was reversed by the CB2 receptor antagonist AM630.
+TRPV1	drug	opioid	28901432	Our findings suggest that coadministration of a CB2 receptor agonist AM1241 and <b>morphine</b> reduced <b>morphine</b> tolerance possibly through regulation of <strong>TRPV1</strong> protein expression in the DRG in cancer pain.
+TRPV1	drug	cannabinoid	28821005	Here we tested the hypothesis that CBD anticonvulsant mechanisms are prevented by <b>cannabinoid</b> (CB1 and CB2) and vanilloid (<strong>TRPV1</strong>) receptor blockers.
+TRPV1	drug	cannabinoid	28821005	In conclusion, the robust anticonvulsant effects of CBD may result from multiple pharmacological mechanisms, including facilitation of <b>endocannabinoid</b> signaling and <strong>TRPV1</strong> mechanisms.
+TRPV1	drug	opioid	28734766	<strong>TRPV1</strong> modulates <b>morphine</b> induced conditioned place preference via p38 MAPK in the nucleus accumbens.
+TRPV1	drug	cocaine	28734766	Emerging evidence suggests that the transient receptor potential vanilloid type 1 channel (<strong>TRPV1</strong>) is a novel target for the treatment of drug addiction, such as <b>cocaine</b> and morphine.
+TRPV1	drug	opioid	28734766	Emerging evidence suggests that the transient receptor potential vanilloid type 1 channel (<strong>TRPV1</strong>) is a novel target for the treatment of drug addiction, such as cocaine and <b>morphine</b>.
+TRPV1	addiction	addiction	28734766	Emerging evidence suggests that the transient receptor potential vanilloid type 1 channel (<strong>TRPV1</strong>) is a novel target for the treatment of drug <b>addiction</b>, such as cocaine and morphine.
+TRPV1	drug	opioid	28734766	Previously we reported that <strong>TRPV1</strong> inhibition reduced <b>morphine</b> reward in the dorsal striatum (DSt) of mice and <b>morphine</b> self administration through a decrease in accumbal activity in rats.
+TRPV1	addiction	reward	28734766	Previously we reported that <strong>TRPV1</strong> inhibition reduced morphine <b>reward</b> in the dorsal striatum (DSt) of mice and morphine self administration through a decrease in accumbal activity in rats.
+TRPV1	drug	opioid	28734766	However, the role of <strong>TRPV1</strong> on <b>morphine</b> conditioned reward in addiction related brain regions, such as the nucleus accumbens (NAc), has not been previously established.
+TRPV1	addiction	addiction	28734766	However, the role of <strong>TRPV1</strong> on morphine conditioned reward in <b>addiction</b> related brain regions, such as the nucleus accumbens (NAc), has not been previously established.
+TRPV1	addiction	reward	28734766	However, the role of <strong>TRPV1</strong> on morphine conditioned <b>reward</b> in addiction related brain regions, such as the nucleus accumbens (NAc), has not been previously established.
+TRPV1	drug	opioid	28734766	Here, we investigated the effects of <strong>TRPV1</strong> on <b>morphine</b> conditioned place preference (CPP) and intracellular mechanisms of <strong>TRPV1</strong> using Western blot analysis and immunohistochemistry (IHC) in <b>morphine</b> administered mice.
+TRPV1	addiction	reward	28734766	Here, we investigated the effects of <strong>TRPV1</strong> on morphine conditioned place preference (<b>CPP</b>) and intracellular mechanisms of <strong>TRPV1</strong> using Western blot analysis and immunohistochemistry (IHC) in morphine administered mice.
+TRPV1	drug	opioid	28734766	<strong>TRPV1</strong> knockout mice did not exhibit <b>morphine</b> reward responses, and both i.p.
+TRPV1	addiction	reward	28734766	<strong>TRPV1</strong> knockout mice did not exhibit morphine <b>reward</b> responses, and both i.p.
+TRPV1	drug	opioid	28734766	and intra NAc injections of SB366791, a selective <strong>TRPV1</strong> antagonist, reduced <b>morphine</b> induced CPP in wild type mice.
+TRPV1	addiction	reward	28734766	and intra NAc injections of SB366791, a selective <strong>TRPV1</strong> antagonist, reduced morphine induced <b>CPP</b> in wild type mice.
+TRPV1	drug	opioid	28734766	To determine the molecular mechanisms of the <strong>TRPV1</strong>/p38 MAPK pathway in <b>morphine</b> CPP, we investigated the expression of adenylyl cyclase type 1 (AC1) and phospho p38 mitogen activated protein kinase (MAPK) and nuclear factor kappa B (NF κB) in the NAc.
+TRPV1	addiction	reward	28734766	To determine the molecular mechanisms of the <strong>TRPV1</strong>/p38 MAPK pathway in morphine <b>CPP</b>, we investigated the expression of adenylyl cyclase type 1 (AC1) and phospho p38 mitogen activated protein kinase (MAPK) and nuclear factor kappa B (NF κB) in the NAc.
+TRPV1	drug	opioid	28734766	Taken together, our findings suggest that <strong>TRPV1</strong> may modulate <b>morphine</b> induced conditioned reward effects via the p38 MAPK signaling pathway in the NAc.
+TRPV1	addiction	reward	28734766	Taken together, our findings suggest that <strong>TRPV1</strong> may modulate morphine induced conditioned <b>reward</b> effects via the p38 MAPK signaling pathway in the NAc.
+TRPV1	drug	opioid	28734766	Therefore, blockade of <strong>TRPV1</strong> may provide a novel therapeutic approach for the prevention and treatment of <b>opioid</b> addiction.
+TRPV1	addiction	addiction	28734766	Therefore, blockade of <strong>TRPV1</strong> may provide a novel therapeutic approach for the prevention and treatment of opioid <b>addiction</b>.
+TRPV1	drug	cannabinoid	28680405	Also, recent studies point to a complex <b>endocannabinoid</b> endovanilloid interplay, including the influence of anandamide (endogenous CB1 and <strong>TRPV1</strong> agonist) on cognitive variables, such as aversive memory extinction.
+TRPV1	addiction	aversion	28680405	Also, recent studies point to a complex endocannabinoid endovanilloid interplay, including the influence of anandamide (endogenous CB1 and <strong>TRPV1</strong> agonist) on cognitive variables, such as <b>aversive</b> memory extinction.
+TRPV1	drug	cannabinoid	28583049	N arachidonoyl serotonin, a dual FAAH and <strong>TRPV1</strong> blocker, inhibits the retrieval of contextual fear memory: Role of the <b>cannabinoid</b> CB1 receptor in the dorsal hippocampus.
+TRPV1	addiction	aversion	28583049	At high concentrations, however, anandamide may exert pro <b>aversive</b> activities mediated by the transient receptor potential vanilloid type 1 channel (<strong>TRPV1</strong>).
+TRPV1	drug	opioid	28188777	Enhanced ability of <strong>TRPV1</strong> channels in regulating glutamatergic transmission after repeated <b>morphine</b> exposure in the nucleus accumbens of rat.
+TRPV1	drug	opioid	28188777	In the present study, whole cell patch clamp recordings were adopted to examine the activity of <strong>TRPV1</strong> Channels in regulating glutamate mediated excitatory postsynaptic currents (EPSCs) in NAc of rat during <b>morphine</b> withdrawal for 3days and 3weeks.
+TRPV1	addiction	withdrawal	28188777	In the present study, whole cell patch clamp recordings were adopted to examine the activity of <strong>TRPV1</strong> Channels in regulating glutamate mediated excitatory postsynaptic currents (EPSCs) in NAc of rat during morphine <b>withdrawal</b> for 3days and 3weeks.
+TRPV1	drug	opioid	28188777	The data showed that the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) and the amplitudes of evoked excitatory postsynaptic currents (eEPSCs) were increased during <b>morphine</b> withdrawal after applied with capsaicin (<strong>TRPV1</strong> agonist).
+TRPV1	addiction	withdrawal	28188777	The data showed that the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) and the amplitudes of evoked excitatory postsynaptic currents (eEPSCs) were increased during morphine <b>withdrawal</b> after applied with capsaicin (<strong>TRPV1</strong> agonist).
+TRPV1	drug	cannabinoid	28188777	Additionally, In the presence of AM251 (CB1 receptor antagonist), depolarization induced release of endogenous <b>cannabinoids</b> activated <strong>TRPV1</strong> channels to enhance glutamatergic neurotransmission during morphine withdrawal.
+TRPV1	drug	opioid	28188777	Additionally, In the presence of AM251 (CB1 receptor antagonist), depolarization induced release of endogenous cannabinoids activated <strong>TRPV1</strong> channels to enhance glutamatergic neurotransmission during <b>morphine</b> withdrawal.
+TRPV1	addiction	withdrawal	28188777	Additionally, In the presence of AM251 (CB1 receptor antagonist), depolarization induced release of endogenous cannabinoids activated <strong>TRPV1</strong> channels to enhance glutamatergic neurotransmission during morphine <b>withdrawal</b>.
+TRPV1	drug	opioid	28188777	Our findings demonstrate the ability of <strong>TRPV1</strong> in regulating excitatory glutamatergic transmission is enhanced during <b>morphine</b> withdrawal in NAc, which would deepen our understanding of glutamatergic modulation during <b>opioids</b> withdrawal.
+TRPV1	addiction	withdrawal	28188777	Our findings demonstrate the ability of <strong>TRPV1</strong> in regulating excitatory glutamatergic transmission is enhanced during morphine <b>withdrawal</b> in NAc, which would deepen our understanding of glutamatergic modulation during opioids <b>withdrawal</b>.
+TRPV1	addiction	sensitization	28126501	The prevention of this hyperalgesia by diclofenac (1 10μg), the inhibitors of COX 1 SC 560 (0.1 1μg) or COX 2 celecoxib (1 5μg), the <strong>TRPV1</strong> antagonist capsazepine (0.03 0.3μg) or the TRPA1 antagonist HC030031 (10 50μg) demonstrates the involvement of prostaglandin synthesis and TRP <b>sensitization</b> in CCL5 evoked hyperalgesia.
+TRPV1	drug	cannabinoid	27062913	These results indicate that AEA modulates the pro aversive effects of intra VMHdm bicuculline treatment, recruiting CB1 <b>cannabinoid</b> receptors and the <strong>TRPV1</strong> channel is involved in the AM251 related potentiation of bicuculline effects on non oriented escape behaviour.
+TRPV1	addiction	aversion	27062913	These results indicate that AEA modulates the pro <b>aversive</b> effects of intra VMHdm bicuculline treatment, recruiting CB1 cannabinoid receptors and the <strong>TRPV1</strong> channel is involved in the AM251 related potentiation of bicuculline effects on non oriented escape behaviour.
+TRPV1	drug	cannabinoid	27737792	URB597 (0.1, 0.3, 1mg/kg; inhibitor of anandamide hydrolysis), WIN55,212 2 (0.1, 0.3, 1mg/kg; synthetic <b>cannabinoid</b>), arachidonoyl serotonin (1, 2.5, 5mg/kg; dual <strong>TRPV1</strong> and anandamide hydrolysis inhibitor), and <b>cannabidiol</b> (5, 10, 20, 40mg/kg; a <b>phytocannabinoid</b>) did not decrease escape duration.
+TRPV1	drug	opioid	27730727	We previously demonstrated that <strong>TRPV1</strong> in the dorsal striatum significantly contributes to <b>morphine</b> reward by using the conditioned place preference paradigm in mice; however, it is unknown whether <strong>TRPV1</strong> has the same effect in other reward models.
+TRPV1	addiction	reward	27730727	We previously demonstrated that <strong>TRPV1</strong> in the dorsal striatum significantly contributes to morphine <b>reward</b> by using the conditioned place preference paradigm in mice; however, it is unknown whether <strong>TRPV1</strong> has the same effect in other <b>reward</b> models.
+TRPV1	drug	opioid	27730727	In this study, we investigated the role of <strong>TRPV1</strong> in <b>morphine</b> reward by using a self administration paradigm in rats.
+TRPV1	addiction	reward	27730727	In this study, we investigated the role of <strong>TRPV1</strong> in morphine <b>reward</b> by using a self administration paradigm in rats.
+TRPV1	drug	opioid	27730727	We found that treatment with a selective <strong>TRPV1</strong> antagonist, SB366791, significantly decreased <b>morphine</b> self administration on a fixed ratio 1 schedule or a progressive ratio schedule of reinforcement.
+TRPV1	addiction	reward	27730727	We found that treatment with a selective <strong>TRPV1</strong> antagonist, SB366791, significantly decreased morphine self administration on a fixed ratio 1 schedule or a progressive ratio schedule of <b>reinforcement</b>.
+TRPV1	drug	opioid	27730727	In addition, treatment with another selective <strong>TRPV1</strong> antagonist, AMG9810, not only significantly prevented <b>morphine</b> self administration but also prevented <b>morphine</b> induced c fos expression in the nucleus accumbens.
+TRPV1	drug	opioid	27730727	Taken together, our findings suggest that blockade of <strong>TRPV1</strong> receptors could provide an approach to limiting <b>morphine</b> addiction.
+TRPV1	addiction	addiction	27730727	Taken together, our findings suggest that blockade of <strong>TRPV1</strong> receptors could provide an approach to limiting morphine <b>addiction</b>.
+TRPV1	drug	cannabinoid	27531838	The LTD induced by muscimol likely involved <b>endocannabinoids</b>, metabotropic glutamate receptors (mGluRs), but not <strong>TRPV1</strong> receptors.
+TRPV1	drug	cannabinoid	27531838	This LTD was mediated by <b>endocannabinoids</b> but did not involve mGluRs or <strong>TRPV1</strong> receptors.
+TRPV1	addiction	sensitization	27178246	When central <b>sensitization</b> was established, FAAH KO mice displayed elevated levels of anandamide, other fatty acid amides, and endogenous <strong>TRPV1</strong> agonists in both paw skin and lumbar spinal cord relative to wild type mice.
+TRPV1	addiction	addiction	27167081	Considering both transient receptor potential cation channel, subfamily V, member 1 (<strong>TRPV1</strong>) and N Methyl d aspartate (NMDA) receptors contribute to pathophysiology of mood and <b>addictive</b> disorders, in this study, we investigated the role of <strong>TRPV1</strong> and NMDA receptors in mediating depressive like behaviors following AW in male mice.
+TRPV1	drug	cannabinoid	26884754	<strong>TRPV1</strong> receptors function as homotetramers that also respond to heat, proinflammatory substances, lipoxygenase products, resiniferatoxin, <b>endocannabinoids</b>, protons, and peptide toxins.
+TRPV1	addiction	sensitization	26480812	Human and animal studies indicate a critical role for oxidative stress and activation of transient receptor potential (TRP) cation channel subfamily members <strong>TRPV1</strong> and TRPA1 on pancreatic nociceptors in <b>sensitization</b> mechanisms that result in pain.
+TRPV1	drug	opioid	26411768	The <strong>TRPV1</strong> channel also plays a function in <b>morphine</b> tolerance and hyperalgesia.
+TRPV1	drug	alcohol	26411768	Some drugs such as cocaine and methamphetamine also seem to have an important role in <b>alcohol</b> addiction and substance abuse via activation of the <strong>TRPV1</strong> channel.
+TRPV1	drug	amphetamine	26411768	Some drugs such as cocaine and <b>methamphetamine</b> also seem to have an important role in alcohol addiction and substance abuse via activation of the <strong>TRPV1</strong> channel.
+TRPV1	drug	cocaine	26411768	Some drugs such as <b>cocaine</b> and methamphetamine also seem to have an important role in alcohol addiction and substance abuse via activation of the <strong>TRPV1</strong> channel.
+TRPV1	addiction	addiction	26411768	Some drugs such as cocaine and methamphetamine also seem to have an important role in alcohol <b>addiction</b> and substance abuse via activation of the <strong>TRPV1</strong> channel.
+TRPV1	drug	opioid	26176938	The mechanism of μ <b>opioid</b> receptor (MOR) <strong>TRPV1</strong> crosstalk in <strong>TRPV1</strong> activation involves <b>morphine</b> anti nociception, tolerance and dependence.
+TRPV1	addiction	dependence	26176938	The mechanism of μ opioid receptor (MOR) <strong>TRPV1</strong> crosstalk in <strong>TRPV1</strong> activation involves morphine anti nociception, tolerance and <b>dependence</b>.
+TRPV1	drug	opioid	26176938	Recent reports suggest that <b>opioid</b> or <strong>TRPV1</strong> receptor agonist exposure has contrasting consequences for anti nociception, tolerance and dependence.
+TRPV1	addiction	dependence	26176938	Recent reports suggest that opioid or <strong>TRPV1</strong> receptor agonist exposure has contrasting consequences for anti nociception, tolerance and <b>dependence</b>.
+TRPV1	drug	opioid	26176938	Chronic <b>morphine</b> exposure modulates <strong>TRPV1</strong> activation and induces the anti nociception effects of <b>morphine</b>.
+TRPV1	drug	opioid	26176938	Additional factors also include capsaicin treatment blocking the anti nociception effects of <b>morphine</b> in rats, as well as <b>opioid</b> modulation of <strong>TRPV1</strong> responses through the cAMP dependent PKA pathway and MAPK signaling pathways.
+TRPV1	drug	opioid	26176938	Here, we review new insights concerning the mechanism underlying MOR <strong>TRPV1</strong> crosstalk and signaling pathways and discuss the potential mechanisms of <b>morphine</b> induced anti nociception, tolerance and dependence associated with the <strong>TRPV1</strong> signaling pathway and highlight how understanding these mechanisms might help find therapeutic targets for the treatment of <b>morphine</b> induced antinociception, tolerance and dependence.
+TRPV1	addiction	dependence	26176938	Here, we review new insights concerning the mechanism underlying MOR <strong>TRPV1</strong> crosstalk and signaling pathways and discuss the potential mechanisms of morphine induced anti nociception, tolerance and <b>dependence</b> associated with the <strong>TRPV1</strong> signaling pathway and highlight how understanding these mechanisms might help find therapeutic targets for the treatment of morphine induced antinociception, tolerance and <b>dependence</b>.
+TRPV1	addiction	sensitization	25708385	Our data revealed specific signaling pathways, leading to bone cancer pain, including the activation of PAR2, downstream PKCε/PKA, <strong>TRPV1</strong> and resultant <b>sensitization</b> of MOR.
+TRPV1	drug	alcohol	25447051	Herein, we evaluated the role of signaling through <strong>TRPV1</strong> in an experimental animal model of <b>alcoholic</b> liver disease (ALD).
+TRPV1	drug	alcohol	25447051	Genetic depletion of <strong>TRPV1</strong> did not blunt hepatic steatosis caused by <b>ethanol</b>, but prevented hepatic injury.
+TRPV1	drug	alcohol	25447051	<strong>TRPV1</strong> depletion markedly blunted <b>ethanol</b> mediated induction of plasminogen activator inhibitor 1, an important <b>alcohol</b> induced hepatic inflammation mediator, via fibrin accumulation.
+TRPV1	drug	alcohol	25421513	<b>Ethanol</b> attenuation of long term depression in the nucleus accumbens can be overcome by activation of <strong>TRPV1</strong> receptors.
+TRPV1	addiction	dependence	25421513	These findings demonstrate a novel form of <strong>TRPV1</strong> dependent LTD in the NAc shell that may be critical for EtOH <b>dependence</b>.
+TRPV1	drug	opioid	25118895	Blocking <strong>TRPV1</strong> in nucleus accumbens inhibits persistent <b>morphine</b> conditioned place preference expression in rats.
+TRPV1	drug	opioid	25118895	Based on the general role of <strong>TRPV1</strong> antagonist in blocking neural over excitability by both pre  and post synaptic mechanisms, <strong>TRPV1</strong> antagonist capsazepine (CPZ) was tested for its ability to prohibit persistent <b>opioid</b> craving in rats.
+TRPV1	addiction	relapse	25118895	Based on the general role of <strong>TRPV1</strong> antagonist in blocking neural over excitability by both pre  and post synaptic mechanisms, <strong>TRPV1</strong> antagonist capsazepine (CPZ) was tested for its ability to prohibit persistent opioid <b>craving</b> in rats.
+TRPV1	drug	opioid	25118895	In the present study, we assessed the expression of <strong>TRPV1</strong> in nucleus accumbens and investigated the effect of CPZ in bilateral nucleus accumbens on persistent <b>morphine</b> conditioned place preference (mCPP) in rats.
+TRPV1	drug	opioid	25118895	We found that <b>morphine</b> conditioned place preference increased the <strong>TRPV1</strong> expression and CPZ attenuated <b>morphine</b> conditioned place preference in a dose dependent and target specific manner after both short  and long term spontaneous withdrawal, reflected by the reduction of the increased time in <b>morphine</b> paired side.
+TRPV1	addiction	withdrawal	25118895	We found that morphine conditioned place preference increased the <strong>TRPV1</strong> expression and CPZ attenuated morphine conditioned place preference in a dose dependent and target specific manner after both short  and long term spontaneous <b>withdrawal</b>, reflected by the reduction of the increased time in morphine paired side.
+TRPV1	drug	opioid	25118895	Collectively, these results indicated that injection of <strong>TRPV1</strong> antagonist in nucleus accumbens is capable of attenuating persistent <b>morphine</b> conditioned place preference without affecting normal activity.
+TRPV1	drug	opioid	25118895	Thus, <strong>TRPV1</strong> antagonist is one of the promising therapeutic drugs for the treatment of <b>opioid</b> addiction.
+TRPV1	addiction	addiction	25118895	Thus, <strong>TRPV1</strong> antagonist is one of the promising therapeutic drugs for the treatment of opioid <b>addiction</b>.
+TRPV1	addiction	sensitization	25088915	Activation of CB1 inhibits NGF induced <b>sensitization</b> of <strong>TRPV1</strong> in adult mouse afferent neurons.
+TRPV1	addiction	sensitization	25088915	Exposure to nerve growth factor (NGF) rapidly increases <strong>TRPV1</strong> activity (<b>sensitization</b>).
+TRPV1	drug	cannabinoid	25088915	In the present study, we investigated whether treatment with the selective <b>cannabinoid</b> receptor 1 (CB1) agonist arachidonyl 2' chloroethylamide (ACEA) affects NGF induced sensitization of <strong>TRPV1</strong> in adult mouse dorsal root ganglion (DRG) afferent neurons.
+TRPV1	addiction	sensitization	25088915	In the present study, we investigated whether treatment with the selective cannabinoid receptor 1 (CB1) agonist arachidonyl 2' chloroethylamide (ACEA) affects NGF induced <b>sensitization</b> of <strong>TRPV1</strong> in adult mouse dorsal root ganglion (DRG) afferent neurons.
+TRPV1	addiction	sensitization	25088915	Our results indicate that the analgesic effect of CB1 activation may in part be due to inhibition of NGF induced <b>sensitization</b> of <strong>TRPV1</strong> and also that the effect of CB1 activation is at least partly mediated by attenuation of NGF induced increased PI3 signaling.
+TRPV1	drug	opioid	25085415	β arrestin 2 biased agonism of delta <b>opioid</b> receptors sensitizes transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) in primary sensory neurons.
+TRPV1	drug	opioid	25085415	Additionally, chronic activation of MOPr results in pain hypersensitivity known as <b>opioid</b> induced hyperalgesia (OIH), and we have shown recently that recruitment of β arrestin2 to MOPr, away from transient potential vanilloid eceptor type 1 (<strong>TRPV1</strong>) in primary sensory neurons contributes to this phenomenon.
+TRPV1	addiction	sensitization	25085415	Here we report that chronic activation of DOPr by the DOPr selective agonist, SNC80, results in the <b>sensitization</b> of <strong>TRPV1</strong> and behavioral signs of OIH via β arrestin2 recruitment to DOPr and away from <strong>TRPV1</strong>.
+TRPV1	drug	opioid	24850983	<b>Morphine</b> Reduces Expression of <strong>TRPV1</strong> Receptors in the Amygdala but not in the Hippocampus of Male Rats.
+TRPV1	drug	opioid	24850983	The aim of this study was to evaluate the effect of <b>morphine</b> dependence on the expression of <strong>TRPV1</strong> receptors in the amygdala and CA1 region of the hippocampus.
+TRPV1	addiction	dependence	24850983	The aim of this study was to evaluate the effect of morphine <b>dependence</b> on the expression of <strong>TRPV1</strong> receptors in the amygdala and CA1 region of the hippocampus.
+TRPV1	drug	opioid	24850983	The results showed a significant decrease in <strong>TRPV1</strong> gene expression in the amygdala (P<0.05) but not the CA1 region of <b>morphine</b> dependent rats.
+TRPV1	drug	opioid	24850983	<strong>TRPV1</strong> receptors may be involved in <b>morphine</b> induced dependence.
+TRPV1	addiction	dependence	24850983	<strong>TRPV1</strong> receptors may be involved in morphine induced <b>dependence</b>.
+TRPV1	drug	opioid	24732880	<strong>TRPV1</strong> involvement in <b>morphine</b> induced antinociception, tolerance, and withdrawal symptoms has been previously reported.
+TRPV1	addiction	withdrawal	24732880	<strong>TRPV1</strong> involvement in morphine induced antinociception, tolerance, and <b>withdrawal</b> symptoms has been previously reported.
+TRPV1	addiction	addiction	24732880	Emerging evidence indicates that <strong>TRPV1</strong> may be related to both the cellular and behavioral effects of <b>addictive</b> drugs.
+TRPV1	drug	opioid	24732880	In the present study, we investigated the role of <strong>TRPV1</strong> in <b>morphine</b> reward using the conditioned place preference (CPP) paradigm in mice.
+TRPV1	addiction	reward	24732880	In the present study, we investigated the role of <strong>TRPV1</strong> in morphine <b>reward</b> using the conditioned place preference (<b>CPP</b>) paradigm in mice.
+TRPV1	drug	opioid	24732880	Repeated <b>morphine</b> treatments upregulated <strong>TRPV1</strong> expression in the dorsal striatum (DSt).
+TRPV1	drug	opioid	24732880	Treatment with a <strong>TRPV1</strong> agonist potentiated <b>morphine</b> reward, and pretreatment with <strong>TRPV1</strong> antagonists attenuated these effects.
+TRPV1	addiction	reward	24732880	Treatment with a <strong>TRPV1</strong> agonist potentiated morphine <b>reward</b>, and pretreatment with <strong>TRPV1</strong> antagonists attenuated these effects.
+TRPV1	drug	opioid	24732880	Microinjection of a selective <strong>TRPV1</strong> antagonist into the DSt significantly inhibited <b>morphine</b> CPP.
+TRPV1	addiction	reward	24732880	Microinjection of a selective <strong>TRPV1</strong> antagonist into the DSt significantly inhibited morphine <b>CPP</b>.
+TRPV1	drug	opioid	24732880	In addition, treatment with a <strong>TRPV1</strong> antagonist suppressed <b>morphine</b> induced increases in μ <b>opioid</b> receptor binding, adenylyl cyclase 1 (AC1), p38 mitogen activated protein kinase (p38 MAPK), and nuclear factor kappa B (NF κB) expression in the DSt.
+TRPV1	drug	opioid	24732880	Administering a p38 inhibitor not only prevented <b>morphine</b> CPP, but also prevented <b>morphine</b> induced NF κB and <strong>TRPV1</strong> activation in the DSt.
+TRPV1	addiction	reward	24732880	Administering a p38 inhibitor not only prevented morphine <b>CPP</b>, but also prevented morphine induced NF κB and <strong>TRPV1</strong> activation in the DSt.
+TRPV1	drug	opioid	24732880	Our findings suggest that <strong>TRPV1</strong> in the DSt contribute to <b>morphine</b> reward via AC1, p38 MAPK, and NF κB.
+TRPV1	addiction	reward	24732880	Our findings suggest that <strong>TRPV1</strong> in the DSt contribute to morphine <b>reward</b> via AC1, p38 MAPK, and NF κB.
+TRPV1	drug	opioid	24732880	Brain <strong>TRPV1</strong> may serve as a novel therapeutic target to treat <b>morphine</b> addictive disorders.
+TRPV1	addiction	addiction	24732880	Brain <strong>TRPV1</strong> may serve as a novel therapeutic target to treat morphine <b>addictive</b> disorders.
+TRPV1	addiction	sensitization	24434730	In contrast, <strong>Trpv1</strong> /  mice, which are generally unresponsive to noxious thermal stimuli at lower power settings, exhibit withdrawal responses and inflammation induced <b>sensitization</b> using high power, short duration Aδ stimuli.
+TRPV1	addiction	withdrawal	24434730	In contrast, <strong>Trpv1</strong> /  mice, which are generally unresponsive to noxious thermal stimuli at lower power settings, exhibit <b>withdrawal</b> responses and inflammation induced sensitization using high power, short duration Aδ stimuli.
+TRPV1	drug	opioid	24434730	The qualitative intensity of Aδ responses, the leftward shift of the stimulus response curve, the increased guarding behaviors during carrageenan inflammation or after incision, and the reduction of Aδ responses with <b>morphine</b> suggest multiple roles for <strong>TRPV1</strong>+ Aδ fibers in nociceptive processes and their modulation of pathological pain conditions.
+TRPV1	drug	cannabinoid	23956775	Selective ionotropic <b>cannabinoids</b> may also produce cross desensitization of the TRPA1 <strong>TRPV1</strong> heteromeric nociceptor channels by being negative allosteric modulators of these channels leading to antinociception and antihyperalgesia.
+TRPV1	drug	cannabinoid	23948212	Given that AEA may bind to <b>cannabinoid</b> type 1 (CB1) receptors as well as to postsynaptic ionotropic Transient Receptor Potential Vanilloid type 1 (<strong>TRPV1</strong>) channels, particular attention was paid in determining how the increased AEA tone influenced fear responses.
+TRPV1	drug	cannabinoid	23929722	qRT PCR analysis of 1 μM nonivamide treated SH SY5Y cells revealed gene regulation of the receptors dopamine D1 and D2, serotonin HTR1A, 1B and 2A, <b>cannabinoid</b> 1, and <strong>TRPV1</strong>.
+TRPV1	drug	opioid	23880531	The pain pathway in the rat following noxious thermal stimulation: effect of <b>morphine</b> on pERK1/2 and <strong>TRPV1</strong> at the dorsal horn level, and on hyperalgesia.
+TRPV1	drug	opioid	23880531	The protein content of <strong>TRPV1</strong> in the lumbar dorsal spinal cord was not significantly altered at 1 and 4 h after the thermal hind paw stimulation and by the <b>morphine</b> pretreatment.
+TRPV1	drug	cannabinoid	23850608	CB1 <b>cannabinoid</b> receptor agonist prevents NGF induced sensitization of <strong>TRPV1</strong> in sensory neurons.
+TRPV1	addiction	sensitization	23850608	CB1 cannabinoid receptor agonist prevents NGF induced <b>sensitization</b> of <strong>TRPV1</strong> in sensory neurons.
+TRPV1	drug	cannabinoid	23850608	We tested the hypothesis that activation of the CB1 receptor by <b>cannabinoids</b> attenuates NGF induced <strong>TRPV1</strong> sensitization.
+TRPV1	addiction	sensitization	23850608	We tested the hypothesis that activation of the CB1 receptor by cannabinoids attenuates NGF induced <strong>TRPV1</strong> <b>sensitization</b>.
+TRPV1	drug	cannabinoid	23850608	These results support the hypothesis that <b>cannabinoids</b>, acting through CB1 receptors, may produce analgesia in part by preventing NGF induced sensitization of <strong>TRPV1</strong> in afferent nociceptor nerve endings.
+TRPV1	addiction	sensitization	23850608	These results support the hypothesis that cannabinoids, acting through CB1 receptors, may produce analgesia in part by preventing NGF induced <b>sensitization</b> of <strong>TRPV1</strong> in afferent nociceptor nerve endings.
+TRPV1	drug	cannabinoid	23831917	Presynaptic <strong>TRPV1</strong> vanilloid receptor function is age  but not CB1 <b>cannabinoid</b> receptor dependent in the rodent forebrain.
+TRPV1	addiction	aversion	23474373	Antagonism of <strong>TRPV1</strong> with capsazepine injected into the dlPAG reduced the defense response induced by local NMDA injection, suggesting an anti <b>aversive</b> effect.
+TRPV1	drug	opioid	23398938	<strong>TRPV1</strong> can be inhibited via μ <b>opioid</b> receptor (MOR) mediated reduced activity of adenylyl cyclases (ACs) and decreased cyclic adenosine monophosphate (cAMP) levels.
+TRPV1	drug	opioid	23398938	Here we investigated (1) whether an increase in cAMP during <b>opioid</b> withdrawal increases the activity of <strong>TRPV1</strong> and (2) how <b>opioid</b> withdrawal modulates capsaicin induced nocifensive behavior in rats.
+TRPV1	addiction	withdrawal	23398938	Here we investigated (1) whether an increase in cAMP during opioid <b>withdrawal</b> increases the activity of <strong>TRPV1</strong> and (2) how opioid <b>withdrawal</b> modulates capsaicin induced nocifensive behavior in rats.
+TRPV1	drug	opioid	23398938	<b>Opioid</b> withdrawal significantly increased cAMP levels and capsaicin induced <strong>TRPV1</strong> activity in both transfected human embryonic kidney 293 cells and dissociated dorsal root ganglion (DRG) neurons.
+TRPV1	addiction	withdrawal	23398938	Opioid <b>withdrawal</b> significantly increased cAMP levels and capsaicin induced <strong>TRPV1</strong> activity in both transfected human embryonic kidney 293 cells and dissociated dorsal root ganglion (DRG) neurons.
+TRPV1	drug	opioid	23398938	In summary, our results demonstrate an increased activity of <strong>TRPV1</strong> in DRG neurons as a new mechanism contributing to <b>opioid</b> withdrawal induced hyperalgesia.
+TRPV1	addiction	withdrawal	23398938	In summary, our results demonstrate an increased activity of <strong>TRPV1</strong> in DRG neurons as a new mechanism contributing to opioid <b>withdrawal</b> induced hyperalgesia.
+TRPV1	drug	cannabinoid	23337417	The mechanism of analgesic action of topical propofol is not clear, but may involve desensitization of <strong>TRPV1</strong> or TRPA1 receptors expressed in peripheral nociceptive nerve endings, engagement of <b>endocannabinoids</b>, or activation of peripheral γ aminobutyric acid A receptors.
+TRPV1	drug	opioid	22998799	To explore alternatives to <b>opioid</b> based analgesia, the present study investigates a novel allosteric pharmacological approach operating through the cation channel <strong>TRPV1</strong>.
+TRPV1	addiction	withdrawal	22998799	An infrared diode laser was used to stimulate <strong>TRPV1</strong> expressing nerve terminals and the latency and intensity of paw <b>withdrawal</b> responses were recorded.
+TRPV1	addiction	withdrawal	22998799	However, rats treated with the combination of capsaicin and MRS1477 exhibited increased <b>withdrawal</b> latency and decreased response intensity consistent with agonist potentiation and inactivation or lesion of <strong>TRPV1</strong> containing nerve terminals.
+TRPV1	drug	cannabinoid	22705310	AEA and these other substrates activate non <b>cannabinoid</b> receptor systems, including <strong>TRPV1</strong> and PPAR α receptors.
+TRPV1	addiction	aversion	22394688	The results indicate that AEA can modulate in a dual way the pro <b>aversive</b> effects of NO in the dlPAG by activating CB1 or <strong>TRPV1</strong> receptors.
+TRPV1	drug	alcohol	22378825	Fetal <b>ethanol</b> exposure attenuates aversive oral effects of <strong>TrpV1</strong>, but not TrpA1 agonists in rats.
+TRPV1	addiction	aversion	22378825	Fetal ethanol exposure attenuates <b>aversive</b> oral effects of <strong>TrpV1</strong>, but not TrpA1 agonists in rats.
+TRPV1	addiction	aversion	22378825	We focused on two excitatory ligand gated ion channels, <strong>TrpV1</strong> and TrpA1, which are expressed in oral trigeminal neurons and mediate the <b>aversive</b> orosensory response to many chemical irritants.
+TRPV1	drug	alcohol	22378825	Moreover, the increased acceptability of <b>ethanol</b> was directly related to the reduced aversiveness of the <strong>TrpV1</strong> mediated orosensory input.
+TRPV1	drug	cannabinoid	22325096	The effects of <b>cannabinoid</b> CB1, CB2 and vanilloid <strong>TRPV1</strong> receptor antagonists on cocaine addictive behavior in rats.
+TRPV1	drug	cocaine	22325096	The effects of cannabinoid CB1, CB2 and vanilloid <strong>TRPV1</strong> receptor antagonists on <b>cocaine</b> addictive behavior in rats.
+TRPV1	addiction	addiction	22325096	The effects of cannabinoid CB1, CB2 and vanilloid <strong>TRPV1</strong> receptor antagonists on cocaine <b>addictive</b> behavior in rats.
+TRPV1	drug	cannabinoid	22325096	To further explore the importance of other <b>endocannabinoid</b> related receptors in an animal model of cocaine addiction, the present paper examines <b>cannabinoid</b> CB2 receptor antagonist N ((1S) endo 1,3,3 trimethylbicyclo(2.2.1)heptan 2 yl) 5 (4 chloro 3 methylphenyl) 1 (4 methylbenzyl) pyrazole 3 carboxamide (<b>SR144528</b>) and the transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) receptor antagonist N (3 methoxyphenyl) 4 chlorocinnamide (SB366791) on intravenous (i.v.)
+TRPV1	drug	cocaine	22325096	To further explore the importance of other endocannabinoid related receptors in an animal model of <b>cocaine</b> addiction, the present paper examines cannabinoid CB2 receptor antagonist N ((1S) endo 1,3,3 trimethylbicyclo(2.2.1)heptan 2 yl) 5 (4 chloro 3 methylphenyl) 1 (4 methylbenzyl) pyrazole 3 carboxamide (SR144528) and the transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) receptor antagonist N (3 methoxyphenyl) 4 chlorocinnamide (SB366791) on intravenous (i.v.)
+TRPV1	addiction	addiction	22325096	To further explore the importance of other endocannabinoid related receptors in an animal model of cocaine <b>addiction</b>, the present paper examines cannabinoid CB2 receptor antagonist N ((1S) endo 1,3,3 trimethylbicyclo(2.2.1)heptan 2 yl) 5 (4 chloro 3 methylphenyl) 1 (4 methylbenzyl) pyrazole 3 carboxamide (SR144528) and the transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) receptor antagonist N (3 methoxyphenyl) 4 chlorocinnamide (SB366791) on intravenous (i.v.)
+TRPV1	drug	cocaine	22325096	In conclusion, our results indicate for the first time, that tonic activation of CB2 or <strong>TRPV1</strong> receptors is involved in <b>cocaine</b> induced reinstatement of <b>cocaine</b> seeking behavior, but their activity is not necessary for the rewarding effect of this psychostimulant.
+TRPV1	addiction	relapse	22325096	In conclusion, our results indicate for the first time, that tonic activation of CB2 or <strong>TRPV1</strong> receptors is involved in cocaine induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior, but their activity is not necessary for the rewarding effect of this psychostimulant.
+TRPV1	drug	cocaine	22325096	In contrast to CB1 receptors, neither CB2 nor <strong>TRPV1</strong> receptors play a role in cue induced reinstatement of <b>cocaine</b> seeking behavior.
+TRPV1	addiction	relapse	22325096	In contrast to CB1 receptors, neither CB2 nor <strong>TRPV1</strong> receptors play a role in cue induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+TRPV1	drug	cannabinoid	22300746	Indications for <b>endocannabinoid</b> catabolism inhibitors in psychiatric disorders, that might be CB1 receptor independent and might involve <strong>TRPV1</strong> receptors, are also discussed.
+TRPV1	drug	cannabinoid	22248639	<b>Endocannabinoid</b> analogues exacerbate marble burying behavior in mice via <strong>TRPV1</strong> receptor.
+TRPV1	addiction	addiction	22248639	Conversely, at higher doses (40 or 20 μg/mouse) these compounds increased MBB similar to capsaicin (<strong>TRPV1</strong> agonist, 100 μg/mouse) exhibiting a pro <b>compulsive</b> effect.
+TRPV1	addiction	addiction	22248639	Pretreatment with AM251 (CB(1) antagonist, 1 μg/mouse) antagonized the anticompulsive effect of these compounds, while their pro <b>compulsive</b> effect at higher doses was attenuated by inactive dose of capsazepine (<strong>TRPV1</strong> antagonist, 10 μg/mouse).
+TRPV1	addiction	sensitization	22171045	Transient receptor potential subtype vanilloid 1 (<strong>TRPV1</strong>) and TRP ankyryn 1 (TRPA1) contribute importantly to the genesis of inflammatory pain via both peripheral mechanisms (peripheral <b>sensitization</b>) and spinal cord mechanisms (central <b>sensitization</b>).
+TRPV1	drug	cannabinoid	21554718	Also, <strong>TRPV1</strong> positive fibers were found to co express CB1, supporting the hypothesis of a direct action of the <b>cannabinoid</b> agonist on nociceptive afferents.
+TRPV1	drug	cannabinoid	21439272	<b>Endocannabinoids</b> are also known to activate transient receptor potential vanilloid (<strong>TRPV1</strong>) receptors, but PAG microinjection of a <strong>TRPV1</strong> receptor antagonist (capsazepine) did not affect post ictal analgesia in GEPRs.
+TRPV1	drug	cannabinoid	21106058	Calcium imaging showed significantly enhanced capsaicin (<strong>TRPV1</strong> agonist), responses after acute 20 μg/ml oxaliplatin treatment where the second of paired capsaicin responses increased from 80.7 ± 0.6% without oxaliplatin, to 171.26 ± 29% with oxaliplatin, (n = 6 paired t test, P < 0.05); this was reduced to 81.42 ± 8.1% (P < 0.05), by pretreatment with the <b>cannabinoid</b> CB2 receptor agonist GW 833972.
+TRPV1	drug	cannabinoid	21076424	Using bacterial artificial chromosome transgenic mice, we found that synaptic activation of group I metabotropic glutamate receptors in NAc MSNs in the indirect, but not direct, pathway led to the production of <b>endocannabinoids</b>, which activated presynaptic CB1 receptors to trigger <b>endocannabinoid</b> mediated long term depression (eCB LTD) as well as postsynaptic transient receptor potential vanilloid 1 (<strong>TRPV1</strong>) channels to trigger a form of LTD resulting from endocytosis of AMPA receptors.
+TRPV1	drug	cannabinoid	21076424	These results reveal a previously unknown action of <strong>TRPV1</strong> channels and indicate that the postsynaptic generation of <b>endocannabinoids</b> can modulate synaptic strength in a cell type specific fashion by activating distinct pre  and postsynaptic targets.
+TRPV1	drug	opioid	20719804	Repeated <b>morphine</b> treatment has been shown to induce transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) expression in the spinal cord, dorsal root ganglion (DRG), and sciatic nerve of a rat model.
+TRPV1	drug	opioid	20719804	Increased <strong>TRPV1</strong> expression may therefore play a role in <b>morphine</b> tolerance.
+TRPV1	drug	opioid	20719804	We investigated whether blockage of <strong>TRPV1</strong> by capsazepine, a <strong>TRPV1</strong> antagonist, affected antinociception, development of tolerance, and physical dependence on <b>morphine</b> in mice.
+TRPV1	addiction	dependence	20719804	We investigated whether blockage of <strong>TRPV1</strong> by capsazepine, a <strong>TRPV1</strong> antagonist, affected antinociception, development of tolerance, and physical <b>dependence</b> on morphine in mice.
+TRPV1	drug	opioid	20719804	Our results suggest that <strong>TRPV1</strong> antagonists can be used adjunctively to <b>morphine</b> treatment because they strengthen <b>morphine</b> antinociception and prevent the development of tolerance, and also physical dependence, on <b>morphine</b>.
+TRPV1	addiction	dependence	20719804	Our results suggest that <strong>TRPV1</strong> antagonists can be used adjunctively to morphine treatment because they strengthen morphine antinociception and prevent the development of tolerance, and also physical <b>dependence</b>, on morphine.
+TRPV1	drug	amphetamine	20122992	Repeated <b>methamphetamine</b> treatment increases expression of <strong>TRPV1</strong> mRNA in the frontal cortex but not in the striatum or hippocampus of mice.
+TRPV1	addiction	addiction	20122992	The powerful rewarding properties of MAP are attributed to multiple pharmacological actions, but the mechanistic association between <strong>TRPV1</strong> expression and MAP induced drug <b>addiction</b> has not established.
+TRPV1	addiction	addiction	20122992	These data support a potential role for <strong>TRPV1</strong> in the treatment of MAP induced drug <b>addiction</b>.
+TRPV1	drug	alcohol	19705551	Deletion of vanilloid receptor (<strong>TRPV1</strong>) in mice alters behavioral effects of <b>ethanol</b>.
+TRPV1	drug	alcohol	19705551	The vanilloid receptor <strong>TRPV1</strong> is activated by <b>ethanol</b> and this may be important for some of the central and peripheral actions of <b>ethanol</b>.
+TRPV1	drug	alcohol	19705551	To determine if this receptor has a role in <b>ethanol</b> mediated behaviors, we studied null mutant mice in which the <strong>Trpv1</strong> gene was deleted.
+TRPV1	drug	alcohol	19705551	Two behavioral phenotypes (decreased sensitivity to <b>ethanol</b> induced sedation and faster recovery from <b>ethanol</b> induced motor incoordination) seen in null mutant mice were reproduced in wild type mice by injection of a <strong>TRPV1</strong> antagonist, capsazepine (10 mg/kg).
+TRPV1	drug	alcohol	19705551	These two <b>ethanol</b> behaviors were changed in the opposite direction after injection of capsaicin, a selective <strong>TRPV1</strong> agonist, in wild type mice.
+TRPV1	drug	alcohol	19705551	The studies provide the first evidence that <strong>TRPV1</strong> is important for specific behavioral actions of <b>ethanol</b>.
+TRPV1	drug	opioid	19633705	<strong>TRPV1</strong> plays a crucial role in the transmission of pain signals, especially under inflammation and the neoplasm conditions, and it can also modulate nociceptive afferents by reinforcing <b>morphine</b> tolerance.
+TRPV1	addiction	reward	19633705	<strong>TRPV1</strong> plays a crucial role in the transmission of pain signals, especially under inflammation and the neoplasm conditions, and it can also modulate nociceptive afferents by <b>reinforcing</b> morphine tolerance.
+TRPV1	addiction	sensitization	19473241	<strong>TRPV1</strong> controls acid  and heat induced calcitonin gene related peptide release and <b>sensitization</b> by bradykinin in the isolated mouse trachea.
+TRPV1	addiction	sensitization	19473241	<strong>TRPV1</strong> knockout mice were employed to assess the <strong>TRPV1</strong> contribution to tracheal responsiveness and <b>sensitization</b>.
+TRPV1	drug	alcohol	19473241	This heat response was facilitated by the <strong>TRPV1</strong> agonist <b>ethanol</b> and the <strong>TRPV1</strong> 3 agonist 2 aminoethoxydiphenyl borate, effects that were reduced or absent in <strong>TRPV1</strong>( / ), respectively.
+TRPV1	addiction	sensitization	19473241	The data suggest that tracheal acid sensing mainly involves <strong>TRPV1</strong> but not acid sensing ion channels, whereas noxious heat responsiveness partly depends and (inflammatory) <b>sensitization</b> to heat largely depends on the capsaicin receptor in tracheal nerve endings.
+TRPV1	drug	opioid	19371406	High concentrations of <b>morphine</b> sensitize and activate mouse dorsal root ganglia via <strong>TRPV1</strong> and TRPA1 receptors.
+TRPV1	drug	opioid	19371406	To study a possible involvement of TRP receptors in the pro nociceptive effects of <b>morphine</b> (0.3   10 mM), two models of nociception were employed using C57BL/6 mice and genetically related <strong>TRPV1</strong> and TRPA1 knockout animals, which were crossed and generated double knockouts.
+TRPV1	drug	opioid	19371406	<b>Morphine</b> activated HEK293t cells transfected with <strong>TRPV1</strong> or TRPA1.
+TRPV1	drug	opioid	19371406	In neurons from <strong>TRPV1</strong> and TRPA1 knockout animals activation by <b>morphine</b> was markedly reduced, in the <strong>TRPV1</strong>/A1 double knockout animals this <b>morphine</b> effect was abrogated.
+TRPV1	drug	opioid	19371406	Nociceptor activation and sensitization by <b>morphine</b> is conveyed by <strong>TRPV1</strong> and TRPA1.
+TRPV1	addiction	sensitization	19371406	Nociceptor activation and <b>sensitization</b> by morphine is conveyed by <strong>TRPV1</strong> and TRPA1.
+TRPV1	drug	cannabinoid	19335651	Gene association studies are presented for (a) genes posited to have specific influences on <b>cannabis</b> use disorders: CNR1, CB2, FAAH, MGLL, <strong>TRPV1</strong> and GPR55 and (b) genes from various neurotransmitter systems that are likely to exert a non specific influence on risk of <b>cannabis</b> use disorders, e.g.
+TRPV1	drug	cannabinoid	19131477	Anandamide (AEA), an arachidonic acid derivative produced during inflammatory conditions, is an endogenous agonist of both transient receptor potential vanilloid 1 (<strong>TRPV1</strong>) receptors and <b>cannabinoid</b> CB1 receptors.
+TRPV1	drug	cannabinoid	20203492	In the isolated vagus nerve, representing visceral innervation, the endovanilloid/<b>endocannabinoid</b> anandamide induced or sensitized calcitonin gene related peptide release by activation of <strong>TRPV1</strong>.
+TRPV1	drug	cannabinoid	19096514	The same was observed with the transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) antagonist capsazepine and with <b>cannabidiol</b>, a nonpsychotomimetic <b>phytocannabinoid</b> that produces anxiolytic like effects after systemic administration in humans and laboratory animals.
+TRPV1	drug	cannabinoid	19064314	The <b>endocannabinoid</b> anandamide is a possible agonist at the Transient Receptor Potential Vanilloid Type 1 (<strong>TRPV1</strong>) channel, in addition to its agonist activity at <b>cannabinoid</b> type 1 (CB1) receptor.
+TRPV1	addiction	aversion	19064314	Altogether, our data suggest that, while CB1 receptors seem to inhibit <b>aversive</b> responses in the dlPAG, <strong>TRPV1</strong> could facilitate them.
+TRPV1	drug	cannabinoid	19015836	Since anandamide is a ligand for not only <b>cannabinoid</b> receptors but also transient receptor potential vanilloid 1 (<strong>TRPV1</strong>) receptors, and as recently suggested, peroxisome proliferator activated nuclear receptor alpha (PPARalpha), we also determined whether anandamide's effects in this task were mediated by each of these receptors.
+TRPV1	drug	cannabinoid	19015836	These effects were blocked by the <strong>TRPV1</strong> antagonist capsazepine, but not by the <b>cannabinoid</b> receptor antagonist <b>rimonabant</b> or the PPARalpha antagonist MK886.
+TRPV1	drug	alcohol	18839303	<b>Ethanol</b> is a known oral trigeminal stimulant and recent data indicate that these effects are mediated in part by transient receptor potential channel vanilloid receptor 1 (<strong>TRPV1</strong>).
+TRPV1	drug	alcohol	18839303	Here, we compared orosensory responding to <b>ethanol</b> in <strong>TRPV1</strong> deficient and wild type mice in a brief access paradigm that assesses orosensory influences by measuring immediate licking responses to small stimulus volumes.
+TRPV1	drug	alcohol	18839303	<strong>TRPV1</strong>( / ) and control mice were tested with six concentrations of <b>ethanol</b> (3, 5, 10, 15, 25, 40%), capsaicin (0.003, 0.01, 0.03, 0.1, 0.3, 1 mM), sucrose (0.003, 0.01, 0.03, 0.1, 0.3, 1 M), and quinine (0.01, 0.03, 0.1, 0.3, 1, 3 mM) and psychophysical concentration response functions were generated for each genotype and stimulus.
+TRPV1	drug	alcohol	18839303	<strong>TRPV1</strong> knockouts displayed reduced oral avoidance responses to <b>ethanol</b> regardless of concentration, insensitivity to capsaicin, and little to no difference in sweet or bitter taste responding relative to wild type mice.
+TRPV1	drug	alcohol	18839303	These data indicate that the <strong>TRPV1</strong> channel plays a role in orosensory mediated <b>ethanol</b> avoidance, but that other receptor mechanisms likely also contribute to aversive oral responses to <b>alcohol</b>.
+TRPV1	addiction	aversion	18839303	These data indicate that the <strong>TRPV1</strong> channel plays a role in orosensory mediated ethanol avoidance, but that other receptor mechanisms likely also contribute to <b>aversive</b> oral responses to alcohol.
+TRPV1	addiction	reward	18828909	Characterization of mouse orofacial pain and the effects of lesioning <strong>TRPV1</strong> expressing neurons on <b>operant</b> behavior.
+TRPV1	addiction	reward	18828909	In the current study, we used an <b>operant</b> model based on a <b>reward</b> conflict paradigm to assess nociceptive responses in three strains of mice (SKH1 Hrhr, C57BL/6J, <strong>TRPV1</strong> knockout).
+TRPV1	addiction	reward	18828909	Additionally, we evaluated the effects on <b>operant</b> behaviors of mice manipulated genetically (e.g., <strong>TRPV1</strong> k.o.)
+TRPV1	addiction	reward	18828909	As the temperature of the thermal stimulus became noxiously hot, <b>reward</b> licking events in SKH1 Hrhr and C57BL/6J mice declined while licking events in <strong>TRPV1</strong> k.o.
+TRPV1	addiction	sensitization	18755744	<strong>TRPV1</strong> receptors on unmyelinated C fibres mediate colitis induced <b>sensitization</b> of pelvic afferent nerve fibres in rats.
+TRPV1	addiction	sensitization	18755744	The aim of the current study was to investigate the role of transient receptor potential of the vanilloid type 1 (<strong>TRPV1</strong>) receptors in the pathophysiology of colitis induced pelvic afferent nerve <b>sensitization</b>.
+TRPV1	addiction	sensitization	18755744	<strong>TRPV1</strong> signalling mediates the colitis induced <b>sensitization</b> of pelvic afferent C fibres to CRD, while Adelta fibres are neither sensitized by colitis nor affected by <strong>TRPV1</strong> inhibition.
+TRPV1	drug	opioid	18579164	Removing <strong>TRPV1</strong> expressing primary afferent neurons potentiates the spinal analgesic effect of delta <b>opioid</b> agonists on mechano nociception.
+TRPV1	drug	opioid	18579164	In this study, we determined the role of delta <b>opioid</b> receptors expressed on <strong>TRPV1</strong> sensory neurons in the antinociceptive effect of the delta <b>opioid</b> receptor agonists [D Pen(2),D Pen(5)] enkephalin and [D Ala(2),Glu(4)] deltorphin.
+TRPV1	drug	opioid	18579164	In RTX treated rats, the delta <b>opioid</b> receptor on <strong>TRPV1</strong> immunoreactive dorsal root ganglion neurons and afferent terminals in the spinal cord was diminished.
+TRPV1	drug	opioid	18579164	These findings indicate that loss of <strong>TRPV1</strong> expressing afferent neurons leads to a substantial reduction in presynaptic delta <b>opioid</b> receptors in the spinal dorsal horn.
+TRPV1	drug	opioid	18579164	However, the effect of delta <b>opioid</b> agonists on mechano nociception is paradoxically potentiated in the absence of <strong>TRPV1</strong> expressing sensory neurons.
+TRPV1	addiction	sensitization	18482991	<b>Sensitization</b> of <strong>TRPV1</strong> responses by cAMP dependent PKA crucially contributes to the development of inflammatory hyperalgesia.
+TRPV1	drug	opioid	18482991	Using HEK cells stably expressing <strong>TRPV1</strong> and the mu <b>opioid</b> receptor, we demonstrated that treatment with the adenylate cyclase activator forskolin significantly increased the multimeric <strong>TRPV1</strong> species.
+TRPV1	drug	opioid	18482991	Pretreatment with the mu <b>opioid</b> receptor agonist <b>morphine</b> reversed this increased <strong>TRPV1</strong> multimerization.
+TRPV1	drug	opioid	18482991	Treatment with forskolin also caused an increase in <strong>TRPV1</strong> expression on the plasma membrane not resulting from increased <strong>TRPV1</strong> expression, and this rapid <strong>TRPV1</strong> translocation was inhibited by treatment with <b>morphine</b>.
+TRPV1	addiction	sensitization	18065157	The <b>sensitization</b> to heat appears unusually resistant against pharmacological interventions and does not involve <strong>TRPV1</strong>.
+TRPV1	drug	alcohol	17977563	Involvement of peripheral <strong>TRPV1</strong> in TMJ hyperalgesia induced by <b>ethanol</b> withdrawal.
+TRPV1	addiction	withdrawal	17977563	Involvement of peripheral <strong>TRPV1</strong> in TMJ hyperalgesia induced by ethanol <b>withdrawal</b>.
+TRPV1	drug	alcohol	17977563	Little is known about the neurological basis for hyperalgesia induced by <b>ethanol</b> withdrawal, but it has been reported that <b>ethanol</b> can potentiate the response of transient receptor potential vanilloid receptor 1 (<strong>TRPV1</strong>) in superficial tissues.
+TRPV1	addiction	withdrawal	17977563	Little is known about the neurological basis for hyperalgesia induced by ethanol <b>withdrawal</b>, but it has been reported that ethanol can potentiate the response of transient receptor potential vanilloid receptor 1 (<strong>TRPV1</strong>) in superficial tissues.
+TRPV1	drug	alcohol	17977563	The present study was designed to test the hypothesis that peripheral <strong>TRPV1</strong> could be involved on nociceptive behavioral responses induced by the injection of formalin into the TMJ region of rats exposed to chronic <b>ethanol</b> administration and <b>ethanol</b> withdrawal.
+TRPV1	addiction	withdrawal	17977563	The present study was designed to test the hypothesis that peripheral <strong>TRPV1</strong> could be involved on nociceptive behavioral responses induced by the injection of formalin into the TMJ region of rats exposed to chronic ethanol administration and ethanol <b>withdrawal</b>.
+TRPV1	drug	alcohol	17977563	These results indicate that the peripheral <strong>TRPV1</strong> can contribute to the hyperalgesia induced by <b>ethanol</b> withdrawal on deep pain conditions.
+TRPV1	addiction	withdrawal	17977563	These results indicate that the peripheral <strong>TRPV1</strong> can contribute to the hyperalgesia induced by ethanol <b>withdrawal</b> on deep pain conditions.
+TRPV1	drug	opioid	17239544	Deletion of transient receptor potential vanilloid type 1 (<strong>TRPV1</strong>) expressing afferent neurons reduces presynaptic mu <b>opioid</b> receptors but paradoxically potentiates the analgesic efficacy of mu <b>opioid</b> agonists.
+TRPV1	drug	opioid	17239544	In this study, we determined if removal of <strong>TRPV1</strong> expressing afferent neurons by resiniferatoxin (RTX), an ultrapotent capsaicin analog, influences the development of <b>opioid</b> analgesic tolerance.
+TRPV1	drug	opioid	17239544	These findings suggest that loss of <strong>TRPV1</strong> expressing sensory neurons attenuates the development of <b>morphine</b> analgesic tolerance possibly by reducing mu <b>opioid</b> receptor desensitization through protein kinase Cgamma in the spinal cord.
+TRPV1	drug	opioid	17239544	These data also suggest that the function of presynaptic mu <b>opioid</b> receptors on <strong>TRPV1</strong> expressing sensory neurons is particularly sensitive to down regulation by mu <b>opioid</b> agonists during <b>opioid</b> tolerance development.
+TRPV1	addiction	withdrawal	16962719	Intraplantar capsaicin produced dose related SMH (enhanced paw <b>withdrawal</b> response to von Frey monofilament stimulation at an area away from injection site) that lasted for over 4 h. While pretreatment with a potent selective transient receptor potential vanilloid receptor 1 (<strong>TRPV1</strong>) antagonist A 425619 (1 isoquinolin 5 yl 3 (4 trifluoromethyl benzyl) urea) prevented development of acute nocifensive (flinching) behavior immediately following capsaicin injection (ED(50)=4.9 mg/kg), the compound failed to attenuate the SMH when administered 2 h following capsaicin (10 microg/10 microl).
+TRPV1	drug	opioid	16467418	Loss of <strong>TRPV1</strong> expressing sensory neurons reduces spinal mu <b>opioid</b> receptors but paradoxically potentiates <b>opioid</b> analgesia.
+TRPV1	drug	opioid	16467418	In this study, we determined how loss of <strong>TRPV1</strong> expressing sensory neurons alters the antinociceptive effect of mu <b>opioids</b> and mu <b>opioid</b> receptors in the spinal cord.
+TRPV1	drug	opioid	16467418	However, RTX treatment did not affect the dorsal horn neurons labeled with both <strong>TRPV1</strong>  and mu <b>opioid</b> receptor immunoreactivity.
+TRPV1	drug	opioid	16467418	This study provides novel information that loss of <strong>TRPV1</strong> afferent neurons eliminates presynaptic mu <b>opioid</b> receptors present on <strong>TRPV1</strong> expressing afferent neurons but paradoxically potentiates the analgesic effect of mu <b>opioid</b> agonists.
+TRPV1	drug	opioid	16467418	Mechano nociception, transmitted through non <strong>TRPV1</strong> sensory neurons, is subject to potent modulation by mu <b>opioid</b> agonists.
+TRPV1	drug	opioid	15288402	Finally, <strong>TRPV1</strong> does not appear to be under tonic <b>opioid</b> receptor control since the <b>opioid</b> antagonist <b>naloxone</b> does not change CAP induced excitation and does not effect OCT induced inhibition of CAP responses.
+TRPV1	drug	opioid	15157710	Loci in the vanilloid receptor subtype 1 gene (<strong>TRPV1</strong>), delta <b>opioid</b> receptor subtype 1 gene (OPRD1) and catechol O methyltransferase gene (COMT) were genotyped using 5' nuclease assays.
+TRPV1	addiction	withdrawal	15157710	Female European Americans with the <strong>TRPV1</strong> Val(585) Val allele and males with low harm avoidance showed longer cold <b>withdrawal</b> times based on the classification and regression tree (CART) analysis.
+TRPV1	drug	alcohol	15128291	In addition, this mechanism links <strong>TRPV1</strong> to intracellular signaling by various important endogenous as well as exogenous substances such as bradykinin, <b>ethanol</b>, nicotin and insulin.
+GRM2	drug	alcohol	32599136	Our findings demonstrate that developmental <b>alcohol</b> exposure enhances <b>alcohol</b> intake during adolescence, which is associated with a decrease in the pCREB/CREB ratio in the hippocampus, prefrontal cortex and striatum, while the GluR1/<strong>GluR2</strong> ratio showed a decrease in the hippocampus.
+GRM2	drug	alcohol	32416868	Positive allosteric modulators (PAMs) of <strong>mGlu2</strong> and negative allosteric modulators of mGlu5 show particular promise for reducing <b>alcohol</b> intake and/or preventing relapse.
+GRM2	addiction	relapse	32416868	Positive allosteric modulators (PAMs) of <strong>mGlu2</strong> and negative allosteric modulators of mGlu5 show particular promise for reducing alcohol intake and/or preventing <b>relapse</b>.
+GRM2	drug	cocaine	32329565	We also investigated the subsequent alterations on <strong>GluR2</strong>, GluR1, cAMP response element binding (CREB), and CREB phosphorylation (pCREB) in ventral tegmental area (VTA) and nucleus accumbens (NAc) induced by both MSEW and <b>cocaine</b> SA.
+GRM2	drug	amphetamine	32179027	Environmental enrichment and a selective metabotropic glutamate receptor2/3 (<strong>mGluR2</strong>/3) agonist suppress <b>amphetamine</b> self administration: Characterizing baseline differences.
+GRM2	drug	amphetamine	32179027	However, the ability for <strong>mGluR2</strong>/3 activation to suppress <b>amphetamine</b> (AMP) SA in differentially reared rats is not determined.
+GRM2	drug	cocaine	31705165	Effects of the <strong>mGluR2</strong>/3 receptor agonist LY379268 on the reinforcing strength of <b>cocaine</b> in rhesus monkeys.
+GRM2	addiction	reward	31705165	Effects of the <strong>mGluR2</strong>/3 receptor agonist LY379268 on the <b>reinforcing</b> strength of cocaine in rhesus monkeys.
+GRM2	drug	cocaine	31705165	The present study examined the effects of the <strong>mGluR2</strong>/3 receptor selective agonist, ( ) 2 oxa 4 aminobicylco hexane 4,6 dicarboxylic acid (LY379268), in male rhesus monkeys self administering <b>cocaine</b> under two procedures that assess the strength of <b>cocaine</b> as a reinforcer.
+GRM2	drug	alcohol	31233806	Loss of <strong>mGlu2</strong> function has recently been associated with increased <b>ethanol</b> seeking and consumption, but the ability of <b>alcohol</b> to produce adaptations in <strong>mGlu2</strong> function in the DLS has not been investigated.
+GRM2	addiction	relapse	31233806	Loss of <strong>mGlu2</strong> function has recently been associated with increased ethanol <b>seeking</b> and consumption, but the ability of alcohol to produce adaptations in <strong>mGlu2</strong> function in the DLS has not been investigated.
+GRM2	drug	alcohol	31233806	We exposed male C57Bl/6J mice to a 2 week chronic intermittent <b>ethanol</b> (CIE) paradigm followed by a brief withdrawal period, then used whole cell patch clamp recordings of glutamatergic transmission in the striatum to assess CIE effects on <strong>mGlu2</strong> mediated synaptic plasticity.
+GRM2	addiction	withdrawal	31233806	We exposed male C57Bl/6J mice to a 2 week chronic intermittent ethanol (CIE) paradigm followed by a brief <b>withdrawal</b> period, then used whole cell patch clamp recordings of glutamatergic transmission in the striatum to assess CIE effects on <strong>mGlu2</strong> mediated synaptic plasticity.
+GRM2	drug	alcohol	31233806	Interestingly, CIE induced impairment of <strong>mGlu2</strong> LTD in the dorsolateral striatum is only observed when <b>alcohol</b> exposure occurs during adolescence.
+GRM2	drug	alcohol	31233806	In contrast to the 2 week CIE paradigm, acute exposure of striatal slices to <b>ethanol</b> concentrations that mimic <b>ethanol</b> levels during CIE exposure fails to disrupt <strong>mGlu2</strong> LTD. We did not observe a reduction of <strong>mGlu2</strong> mRNA or protein levels following CIE exposure, suggesting that <b>alcohol</b> effects on <strong>mGlu2</strong> occur at the functional level.
+GRM2	drug	alcohol	31233806	Our findings contribute to growing evidence that adolescents are uniquely vulnerable to certain <b>alcohol</b> induced neuroadaptations, and identify enhancement of <strong>mGlu2</strong> activity as a strategy to reverse the effects of adolescent <b>alcohol</b> exposure on DLS physiology.
+GRM2	drug	cannabinoid	31202811	The <b>cannabinoid</b> CB1 receptor antagonist <b>rimonabant</b> and the <strong>mGlu2</strong>/3 receptor agonist LY379268 also selectively reduced reinstatement.
+GRM2	addiction	relapse	31202811	The cannabinoid CB1 receptor antagonist rimonabant and the <strong>mGlu2</strong>/3 receptor agonist LY379268 also selectively reduced <b>reinstatement</b>.
+GRM2	addiction	relapse	30471010	In addition, group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) were found to be implicated in <b>relapse</b> <b>seeking</b> behavior.
+GRM2	drug	amphetamine	30471010	These findings suggest that these glutamate transporters and <strong>mGluR2</strong>/3 might be potential therapeutic targets for the attenuation of reinstatement to <b>METH</b> seeking.
+GRM2	addiction	relapse	30471010	These findings suggest that these glutamate transporters and <strong>mGluR2</strong>/3 might be potential therapeutic targets for the attenuation of <b>reinstatement</b> to METH <b>seeking</b>.
+GRM2	drug	opioid	30315852	Downregulation of <strong>mGluR2</strong>/3 receptors during <b>morphine</b> withdrawal in rats impairs <strong>mGluR2</strong>/3  and NMDA receptor dependent long term depression in the nucleus accumbens.
+GRM2	addiction	withdrawal	30315852	Downregulation of <strong>mGluR2</strong>/3 receptors during morphine <b>withdrawal</b> in rats impairs <strong>mGluR2</strong>/3  and NMDA receptor dependent long term depression in the nucleus accumbens.
+GRM2	drug	opioid	30315852	The expression of <strong>mGluR2</strong>/3 was downregulated during withdrawal from repeated <b>morphine</b> exposure (10 days after the last injection), resulting in impaired low frequency stimulation induced LTD.
+GRM2	addiction	withdrawal	30315852	The expression of <strong>mGluR2</strong>/3 was downregulated during <b>withdrawal</b> from repeated morphine exposure (10 days after the last injection), resulting in impaired low frequency stimulation induced LTD.
+GRM2	drug	opioid	30315852	These results indicate that withdrawal induced <strong>mGluR2</strong>/3 downregulation alters neural plasticity after <b>morphine</b> exposure, which may be a mechanism contributing to drug addiction.
+GRM2	addiction	addiction	30315852	These results indicate that withdrawal induced <strong>mGluR2</strong>/3 downregulation alters neural plasticity after morphine exposure, which may be a mechanism contributing to drug <b>addiction</b>.
+GRM2	addiction	withdrawal	30315852	These results indicate that <b>withdrawal</b> induced <strong>mGluR2</strong>/3 downregulation alters neural plasticity after morphine exposure, which may be a mechanism contributing to drug addiction.
+GRM2	addiction	addiction	30283001	Recent studies suggest that the type 2 metabotropic glutamate receptor (<strong>mGluR2</strong>) is critically involved in substance abuse and <b>addiction</b>.
+GRM2	drug	opioid	30283001	In the present study, we evaluated whether low <strong>mGluR2</strong> expression may represent a risk factor for the development of <b>opioid</b> abuse and addiction using transgenic <strong>mGluR2</strong> knockout (<strong>mGluR2</strong> KO) rats.
+GRM2	addiction	addiction	30283001	In the present study, we evaluated whether low <strong>mGluR2</strong> expression may represent a risk factor for the development of opioid abuse and <b>addiction</b> using transgenic <strong>mGluR2</strong> knockout (<strong>mGluR2</strong> KO) rats.
+GRM2	drug	opioid	30283001	Compared to wild type controls, <strong>mGluR2</strong> KO rats exhibited higher nucleus accumbens (NAc) dopamine (DA) and locomotor responses to <b>heroin</b>, higher <b>heroin</b> self administration and <b>heroin</b> intake, more potent <b>morphine</b> induced analgesia and more severe <b>naloxone</b> precipitated withdrawal symptoms.
+GRM2	addiction	withdrawal	30283001	Compared to wild type controls, <strong>mGluR2</strong> KO rats exhibited higher nucleus accumbens (NAc) dopamine (DA) and locomotor responses to heroin, higher heroin self administration and heroin intake, more potent morphine induced analgesia and more severe naloxone precipitated <b>withdrawal</b> symptoms.
+GRM2	drug	opioid	30283001	In contrast, <strong>mGluR2</strong> KO rats displayed lower motivation for <b>heroin</b> self administration under high price progressive ratio (PR) reinforcement conditions.
+GRM2	addiction	reward	30283001	In contrast, <strong>mGluR2</strong> KO rats displayed lower motivation for heroin self administration under high price progressive ratio (PR) <b>reinforcement</b> conditions.
+GRM2	drug	opioid	30283001	Taken together, these findings suggest that <strong>mGluR2</strong> may play an inhibitory role in <b>opioid</b> action, such that deletion of this receptor results in an increase in brain DA responses to <b>heroin</b> and in acute <b>opioid</b> reward and analgesia.
+GRM2	addiction	reward	30283001	Taken together, these findings suggest that <strong>mGluR2</strong> may play an inhibitory role in opioid action, such that deletion of this receptor results in an increase in brain DA responses to heroin and in acute opioid <b>reward</b> and analgesia.
+GRM2	drug	opioid	30283001	Low <strong>mGluR2</strong> expression in the brain may therefore be a risk factor for the initial development of <b>opioid</b> abuse and addiction.
+GRM2	addiction	addiction	30283001	Low <strong>mGluR2</strong> expression in the brain may therefore be a risk factor for the initial development of opioid abuse and <b>addiction</b>.
+GRM2	drug	amphetamine	30240581	Chronic <b>methamphetamine</b> self administration dysregulates 5 HT2A and <strong>mGlu2</strong> receptor expression in the rat prefrontal and perirhinal cortex: Comparison to chronic phencyclidine and MK 801.
+GRM2	drug	amphetamine	30240581	Therefore, in the present study we examined the effects of chronic exposure to three different drugs known to produce persistent deficits in sensorimotor gating and cognition [<b>meth</b>, phencyclidine (PCP) and MK 801] on the expression of 5 HT2A and <strong>mGlu2</strong> within the rat medial prefrontal cortex (mPFC), dorsal hippocampus (dHPC) and perirhinal cortex (PRh).
+GRM2	drug	amphetamine	30240581	We found that despite different pharmacological mechanism of action, chronic <b>meth</b>, PCP, and MK 801 similarly dysregulated 5 HT2A and <strong>mGlu2</strong>, as indicated by an increase in the 5 HT2A/<strong>mGlu2</strong> expression ratio in the mPFC (all three tested drugs), PRh (<b>meth</b> and PCP), and dHPC (MK 801 only).
+GRM2	drug	amphetamine	30240581	In summary, these data suggest that a shift towards increased availability (and G protein coupling) of cortical 5 HT2A vs. <strong>mGlu2</strong> receptors may represent a common neurobiological mechanism underlying the emergence of psychosis and cognitive deficits observed in subjects with <b>meth</b> use disorder and schizophrenia.
+GRM2	drug	cannabinoid	30238023	Based on quality of evidence to date, promising first tier neurochemical receptor targets include: noradrenergic (α1 and β antagonist, α2 agonist), kappa opioid antagonist, nociceptin antagonist, orexin 1 antagonist, and <b>endocannabinoid</b> modulation (e.g., <b>cannabidiol</b>, FAAH inhibition); second tier candidates may include corticotropin releasing factor 1 antagonists, serotonergic agents (e.g., 5 HT reuptake inhibitors, 5 HT3 antagonists), glutamatergic agents (e.g., <strong>mGluR2</strong>/3 agonist/positive allosteric modulator, mGluR5 antagonist/negative allosteric modulator), GABA promoters (e.g., pregabalin, tiagabine), vasopressin 1b antagonist, NK 1 antagonist, and PPAR γ agonist (e.g., pioglitazone).
+GRM2	drug	opioid	30238023	Based on quality of evidence to date, promising first tier neurochemical receptor targets include: noradrenergic (α1 and β antagonist, α2 agonist), kappa <b>opioid</b> antagonist, nociceptin antagonist, orexin 1 antagonist, and endocannabinoid modulation (e.g., cannabidiol, FAAH inhibition); second tier candidates may include corticotropin releasing factor 1 antagonists, serotonergic agents (e.g., 5 HT reuptake inhibitors, 5 HT3 antagonists), glutamatergic agents (e.g., <strong>mGluR2</strong>/3 agonist/positive allosteric modulator, mGluR5 antagonist/negative allosteric modulator), GABA promoters (e.g., pregabalin, tiagabine), vasopressin 1b antagonist, NK 1 antagonist, and PPAR γ agonist (e.g., pioglitazone).
+GRM2	addiction	relapse	29566161	The <strong>mGlu2</strong>/3 antagonist LY 341495 reversed oxytocin's ability to attenuate cued <b>reinstatement</b>.
+GRM2	drug	opioid	29462112	Microinjection of the <strong>mGluR2</strong>/3 agonist, LY379268, into the nucleus accumbens attenuates extinction latencies and the reinstatement of <b>morphine</b> induced conditioned place preference in rats.
+GRM2	addiction	relapse	29462112	Microinjection of the <strong>mGluR2</strong>/3 agonist, LY379268, into the nucleus accumbens attenuates extinction latencies and the <b>reinstatement</b> of morphine induced conditioned place preference in rats.
+GRM2	drug	opioid	29462112	Previous studies indicate that metabotropic glutamate receptor type 2/3 (<strong>mGluR2</strong>/3) has a key role in the rewarding properties of <b>morphine</b> induced conditioning place preference (CPP).
+GRM2	addiction	reward	29462112	Previous studies indicate that metabotropic glutamate receptor type 2/3 (<strong>mGluR2</strong>/3) has a key role in the rewarding properties of morphine induced conditioning place preference (<b>CPP</b>).
+GRM2	addiction	addiction	29462112	Group II <strong>mGluR2</strong>/3 agonists are offered as a drug <b>addiction</b> treatment.
+GRM2	drug	opioid	29462112	In this study, we evaluated the effects of <strong>mGluR2</strong>/3 agonist, LY379268, on the extinction and reinstatement of <b>morphine</b> induced CPP, following its microinjection into the NAc.
+GRM2	addiction	relapse	29462112	In this study, we evaluated the effects of <strong>mGluR2</strong>/3 agonist, LY379268, on the extinction and <b>reinstatement</b> of morphine induced CPP, following its microinjection into the NAc.
+GRM2	addiction	reward	29462112	In this study, we evaluated the effects of <strong>mGluR2</strong>/3 agonist, LY379268, on the extinction and reinstatement of morphine induced <b>CPP</b>, following its microinjection into the NAc.
+GRM2	drug	opioid	29462112	The intra accumbal injection of the <strong>mGluR2</strong>/3 agonist, LY379268, significantly decreased the extinction latencies and reinstatement of <b>morphine</b> induced CPP at higher doses.
+GRM2	addiction	relapse	29462112	The intra accumbal injection of the <strong>mGluR2</strong>/3 agonist, LY379268, significantly decreased the extinction latencies and <b>reinstatement</b> of morphine induced CPP at higher doses.
+GRM2	addiction	reward	29462112	The intra accumbal injection of the <strong>mGluR2</strong>/3 agonist, LY379268, significantly decreased the extinction latencies and reinstatement of morphine induced <b>CPP</b> at higher doses.
+GRM2	addiction	relapse	29462112	It seems that the NAc might be a functional region for <strong>mGluR2</strong>/3 to play a regulatory role for decreasing drug <b>seeking</b> behavior in rats.
+GRM2	addiction	relapse	29462112	Furthermore, it can be said that <strong>mGluR2</strong>/3 agonists have a potential role in the treatment of drug <b>seeking</b> behaviors.
+GRM2	drug	amphetamine	29363229	Acupuncture inhibition of <b>METH</b> induced NAc temperature was prevented by pre treatment with a group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) antagonist EGLU into the NAc or mimicked by injection of an <strong>mGluR2</strong>/3 agonist DCG IV into the NAc.
+GRM2	drug	amphetamine	29363229	These results suggest that acupuncture reduces extracellular DA release and metabolic neuronal activity in the NAc through activation of <strong>mGluR2</strong>/3 and suppresses <b>METH</b> induced affective states and locomotor behavior.
+GRM2	drug	nicotine	29301614	Accumulating evidence suggests the critical role of <strong>mGluR2</strong>/3 in different aspects of <b>nicotine</b> addiction, including acquisition and maintenance of <b>nicotine</b> taking, <b>nicotine</b> withdrawal, and persistent <b>nicotine</b> seeking even after prolonged abstinence.
+GRM2	addiction	addiction	29301614	Accumulating evidence suggests the critical role of <strong>mGluR2</strong>/3 in different aspects of nicotine <b>addiction</b>, including acquisition and maintenance of nicotine taking, nicotine withdrawal, and persistent nicotine seeking even after prolonged abstinence.
+GRM2	addiction	relapse	29301614	Accumulating evidence suggests the critical role of <strong>mGluR2</strong>/3 in different aspects of nicotine addiction, including acquisition and maintenance of nicotine taking, nicotine withdrawal, and persistent nicotine <b>seeking</b> even after prolonged abstinence.
+GRM2	addiction	withdrawal	29301614	Accumulating evidence suggests the critical role of <strong>mGluR2</strong>/3 in different aspects of nicotine addiction, including acquisition and maintenance of nicotine taking, nicotine <b>withdrawal</b>, and persistent nicotine seeking even after prolonged abstinence.
+GRM2	drug	nicotine	29301614	The involvement of <strong>mGluR2</strong>/3 in other neuropsychiatric conditions, such as anxiety, depression, schizophrenia, Alzheimer's disease, Parkinson's disease, and pain, provides convincing evidence suggesting that <strong>mGluR2</strong>/3 may provide an effective therapeutic approach for comorbidity of <b>smoking</b> and these conditions.
+GRM2	drug	nicotine	29301614	This focused review article highlights that <strong>mGluR2</strong>/3 provide a promising target in the search for <b>smoking</b> cessation medication with novel mechanisms of actions that differ from those of currently U.S. Food and Drug Administration approved pharmacotherapies.
+GRM2	drug	alcohol	29294238	Additionally, the effects of VU 29 on expression of mGlu5 and <strong>mGlu2</strong> receptor proteins in the hippocampus, prefrontal cortex, and striatum were determined 48 h after <b>ethanol</b> withdrawal.
+GRM2	addiction	withdrawal	29294238	Additionally, the effects of VU 29 on expression of mGlu5 and <strong>mGlu2</strong> receptor proteins in the hippocampus, prefrontal cortex, and striatum were determined 48 h after ethanol <b>withdrawal</b>.
+GRM2	drug	alcohol	29294238	Our ELISA results show that VU 29 normalized <b>ethanol</b> withdrawal induced increase in expression of mGlu5 receptor protein in the hippocampus, prefrontal cortex, and striatum, as well as expression of <strong>mGlu2</strong> receptor protein in the hippocampus.
+GRM2	addiction	withdrawal	29294238	Our ELISA results show that VU 29 normalized ethanol <b>withdrawal</b> induced increase in expression of mGlu5 receptor protein in the hippocampus, prefrontal cortex, and striatum, as well as expression of <strong>mGlu2</strong> receptor protein in the hippocampus.
+GRM2	drug	alcohol	29294238	Moreover, mGlu5 (hippocampus, prefrontal cortex, and striatum) and <strong>mGlu2</strong> (hippocampus) receptors play an important role in the <b>ethanol</b> induced recognition memory impairment induced by <b>ethanol</b> withdrawal.
+GRM2	addiction	withdrawal	29294238	Moreover, mGlu5 (hippocampus, prefrontal cortex, and striatum) and <strong>mGlu2</strong> (hippocampus) receptors play an important role in the ethanol induced recognition memory impairment induced by ethanol <b>withdrawal</b>.
+GRM2	drug	alcohol	29220747	Previous studies suggest that group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) are involved in regulating <b>ethanol</b> seeking and consumption.
+GRM2	addiction	relapse	29220747	Previous studies suggest that group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) are involved in regulating ethanol <b>seeking</b> and consumption.
+GRM2	drug	alcohol	29220747	The mGluR2/3 agonist LY379268 (LY37) and selective mGluR2 positive allosteric modulator biphenyl‑indanone A (BINA) were used to investigate the relative contribution of <strong>mGlu2</strong> and mGlu3 receptors on <b>ethanol</b>  and sucrose seeking and consumption.
+GRM2	addiction	relapse	29220747	The mGluR2/3 agonist LY379268 (LY37) and selective mGluR2 positive allosteric modulator biphenyl‑indanone A (BINA) were used to investigate the relative contribution of <strong>mGlu2</strong> and mGlu3 receptors on ethanol  and sucrose <b>seeking</b> and consumption.
+GRM2	drug	alcohol	29220747	The <strong>mGluR2</strong>/3 agonist LY379268 (LY37) and selective <strong>mGluR2</strong> positive allosteric modulator biphenyl‑indanone A (BINA) were used to investigate the relative contribution of <strong>mGlu2</strong> and mGlu3 receptors on <b>ethanol</b>  and sucrose seeking and consumption.
+GRM2	addiction	relapse	29220747	The <strong>mGluR2</strong>/3 agonist LY379268 (LY37) and selective <strong>mGluR2</strong> positive allosteric modulator biphenyl‑indanone A (BINA) were used to investigate the relative contribution of <strong>mGlu2</strong> and mGlu3 receptors on ethanol  and sucrose <b>seeking</b> and consumption.
+GRM2	drug	alcohol	29220747	A microinjection study was then performed to examine the role of nucleus accumbens (NAc) core <strong>mGluR2</strong>/3 on <b>ethanol</b> seeking.
+GRM2	addiction	relapse	29220747	A microinjection study was then performed to examine the role of nucleus accumbens (NAc) core <strong>mGluR2</strong>/3 on ethanol <b>seeking</b>.
+GRM2	drug	alcohol	29220747	Systemic administration of the <strong>mGluR2</strong>/3 agonist LY37 significantly reduced <b>ethanol</b>  and sucrose seeking.
+GRM2	addiction	relapse	29220747	Systemic administration of the <strong>mGluR2</strong>/3 agonist LY37 significantly reduced ethanol  and sucrose <b>seeking</b>.
+GRM2	drug	alcohol	29220747	Systemic administration of the selective <strong>mGluR2</strong> PAM BINA, however, had no effect on either seeking or consumption of <b>ethanol</b> or sucrose.
+GRM2	addiction	relapse	29220747	Systemic administration of the selective <strong>mGluR2</strong> PAM BINA, however, had no effect on either <b>seeking</b> or consumption of ethanol or sucrose.
+GRM2	addiction	relapse	29220747	These findings suggest that systemic <strong>mGluR2</strong>/3 agonism, but not allosteric modulation of <strong>mGluR2</strong>, reduces reinforcer <b>seeking</b>.
+GRM2	addiction	relapse	29061508	For testing, rats were microinjected with vehicle, 20 mM of the <strong>mGlu2</strong>/3 agonist LY379268 (to lower endogenous glutamate), or 300 μM of the excitatory amino acid transporter inhibitor threo β benzyloxyaspartate (TBOA; to raise endogenous glutamate) into either the IL or PL (0.5 μl/side) and then given a 30 min test for cue reinforced drug <b>seeking</b>.
+GRM2	drug	cocaine	29029785	Compared with saline pretreated mice, AMPAR mediated excitatory postsynaptic currents (EPSCs) of <b>cocaine</b> pretreated mice showed a marked inward rectification, demonstrating the insertion of <strong>GluR2</strong> lacking AMPARs to plasma membrane.
+GRM2	drug	cocaine	28988614	Neuroadaptive changes in metabotropic glutamate <strong>mGlu2</strong>/3R expression during different phases of <b>cocaine</b> addiction in rats.
+GRM2	addiction	addiction	28988614	Neuroadaptive changes in metabotropic glutamate <strong>mGlu2</strong>/3R expression during different phases of cocaine <b>addiction</b> in rats.
+GRM2	addiction	addiction	28988614	In this respect, among glutamatergic receptors special attention is paid to the group II of metabotropic glutamatergic receptors (<strong>mGlu2</strong>/3R) which are involved in the transition from drug use to drug <b>addiction</b> including the relapse mechanisms.
+GRM2	addiction	relapse	28988614	In this respect, among glutamatergic receptors special attention is paid to the group II of metabotropic glutamatergic receptors (<strong>mGlu2</strong>/3R) which are involved in the transition from drug use to drug addiction including the <b>relapse</b> mechanisms.
+GRM2	drug	cocaine	28988614	The present study employed radioligand binding and Western blot assays to study <strong>mGlu2</strong>/3R density, affinity and protein expression in selected rat brain areas after <b>cocaine</b> self administration, extinction training and <b>cocaine</b> induced reinstatement.
+GRM2	addiction	relapse	28988614	The present study employed radioligand binding and Western blot assays to study <strong>mGlu2</strong>/3R density, affinity and protein expression in selected rat brain areas after cocaine self administration, extinction training and cocaine induced <b>reinstatement</b>.
+GRM2	drug	cocaine	28988614	<b>Cocaine</b> self administration and yoked <b>cocaine</b> delivery resulted in a significant increase in the <strong>mGlu2</strong>/3R density in the prefrontal cortex and the dorsal striatum, while 10 day extinction training provoked a reduction in the prefrontal cortex and the nucleus accumbens.
+GRM2	drug	cocaine	28988614	<b>Cocaine</b> abstinence also enhanced an increase in the [3H]ligand binding to <strong>mGlu2</strong>/3R in the prefrontal cortex.
+GRM2	drug	cocaine	28988614	During reinstatement the <b>cocaine</b> challenge dose (10mg/kg, ip) led to important elevation in the <strong>mGlu2</strong>/3R density in the prefrontal cortex.
+GRM2	addiction	relapse	28988614	During <b>reinstatement</b> the cocaine challenge dose (10mg/kg, ip) led to important elevation in the <strong>mGlu2</strong>/3R density in the prefrontal cortex.
+GRM2	drug	cocaine	28988614	Our study demonstrated the role of <strong>mGlu2</strong>/3R localized in the prefrontal cortex striatum pathways to <b>cocaine</b> repeated exposure.
+GRM2	addiction	sensitization	28919158	In a separate cohort, the <strong>mGlu2</strong>/3 agonist LY354740 (10mg/kg), given prior to the EtOH challenge, abolished the expression of <b>sensitization</b>.
+GRM2	drug	amphetamine	28870523	Antagonism of <strong>mGlu2</strong>/3 receptors in the nucleus accumbens prevents oxytocin from reducing cued <b>methamphetamine</b> seeking in male and female rats.
+GRM2	addiction	relapse	28870523	Antagonism of <strong>mGlu2</strong>/3 receptors in the nucleus accumbens prevents oxytocin from reducing cued methamphetamine <b>seeking</b> in male and female rats.
+GRM2	addiction	relapse	28870523	Before <b>reinstatement</b> sessions, rats received LY341495, an <strong>mGluR2</strong>/3 antagonist, or its vehicle followed by a second infusion/injection of oxytocin or saline.
+GRM2	drug	amphetamine	28870523	Overall, we report that oxytocin reduced responding to <b>meth</b> associated cues and blocking presynaptic <strong>mGluR2</strong>/3 reversed this effect.
+GRM2	drug	opioid	28831734	A range of agonists or positive allosteric modulators (PAMs) for mostly Gi/o coupled receptors, including metabotropic glutamate2 (<strong>mGlu2</strong>), adenosine A1, or μ <b>opioid</b> receptors, suppress these effects of 5 HT2A receptor stimulation.
+GRM2	addiction	relapse	28726801	However, glutamate release probability is negatively regulated by presynaptic <strong>mGluR2</strong>/3, and sucrose <b>reinstatement</b> was potentiated following <strong>mGluR2</strong>/3 blockade.
+GRM2	addiction	relapse	28726801	Potentiated sucrose <b>reinstatement</b> by <strong>mGluR2</strong>/3 blockade was reversed by antagonizing mGluR5, but reinstated sucrose <b>seeking</b> in the absence of <strong>mGluR2</strong>/3 blockade was not affected by blocking mGluR5.
+GRM2	drug	cocaine	28726801	In <b>cocaine</b> trained rodents mGluR5 stimulation reinstates drug seeking by activating nNOS, but activating mGluR5 did not promote reinstated sucrose seeking, nor was potentiated reinstatement after <strong>mGluR2</strong>/3 blockade reduced by blocking nNOS.
+GRM2	addiction	relapse	28726801	In cocaine trained rodents mGluR5 stimulation reinstates drug <b>seeking</b> by activating nNOS, but activating mGluR5 did not promote reinstated sucrose <b>seeking</b>, nor was potentiated <b>reinstatement</b> after <strong>mGluR2</strong>/3 blockade reduced by blocking nNOS.
+GRM2	addiction	relapse	28726801	These data indicate that dysregulated presynaptic <strong>mGluR2</strong>/3 signaling is a possible site of shared signaling in drug <b>seeking</b> and potentiated reinstated sucrose <b>seeking</b>, but that downregulated glutamate transport and subsequent activation of nNOS by synaptic glutamate spillover is not shared.
+GRM2	drug	cocaine	28700935	<b>Cocaine</b> users show reduced expression of the metabotropic glutamate receptor (<strong>mGluR2</strong>), but it is not clear whether this is a predisposing trait for addiction or a consequence of drug exposure.
+GRM2	addiction	addiction	28700935	Cocaine users show reduced expression of the metabotropic glutamate receptor (<strong>mGluR2</strong>), but it is not clear whether this is a predisposing trait for <b>addiction</b> or a consequence of drug exposure.
+GRM2	drug	cocaine	28700935	In this study, we found that a nonsense mutation at the <strong>mGluR2</strong> gene decreased <strong>mGluR2</strong> expression and altered the seeking and taking of <b>cocaine</b>.
+GRM2	addiction	relapse	28700935	In this study, we found that a nonsense mutation at the <strong>mGluR2</strong> gene decreased <strong>mGluR2</strong> expression and altered the <b>seeking</b> and taking of cocaine.
+GRM2	drug	cocaine	28700935	<strong>mGluR2</strong> mutant rats show reduced sensitivity to <b>cocaine</b> reward, requiring more <b>cocaine</b> to reach satiation when it was freely available and ceasing their drug seeking behavior sooner than controls when the response requirement was increased.
+GRM2	addiction	relapse	28700935	<strong>mGluR2</strong> mutant rats show reduced sensitivity to cocaine reward, requiring more cocaine to reach satiation when it was freely available and ceasing their drug <b>seeking</b> behavior sooner than controls when the response requirement was increased.
+GRM2	addiction	reward	28700935	<strong>mGluR2</strong> mutant rats show reduced sensitivity to cocaine <b>reward</b>, requiring more cocaine to reach satiation when it was freely available and ceasing their drug seeking behavior sooner than controls when the response requirement was increased.
+GRM2	drug	cocaine	28700935	<strong>mGluR2</strong> mutant rats also show a lower propensity to relapse after a period of <b>cocaine</b> abstinence, an effect associated with reduced <b>cocaine</b> induced dopamine and glutamate overflow in the nucleus accumbens.
+GRM2	addiction	relapse	28700935	<strong>mGluR2</strong> mutant rats also show a lower propensity to <b>relapse</b> after a period of cocaine abstinence, an effect associated with reduced cocaine induced dopamine and glutamate overflow in the nucleus accumbens.
+GRM2	drug	cocaine	28700935	These findings suggest that <strong>mGluR2</strong> polymorphisms or reduced availability of <strong>mGluR2</strong> might be risk factors for the initial development of <b>cocaine</b> use but could actually protect against addiction by reducing sensitivity to <b>cocaine</b> reward.
+GRM2	addiction	addiction	28700935	These findings suggest that <strong>mGluR2</strong> polymorphisms or reduced availability of <strong>mGluR2</strong> might be risk factors for the initial development of cocaine use but could actually protect against <b>addiction</b> by reducing sensitivity to cocaine reward.
+GRM2	addiction	reward	28700935	These findings suggest that <strong>mGluR2</strong> polymorphisms or reduced availability of <strong>mGluR2</strong> might be risk factors for the initial development of cocaine use but could actually protect against addiction by reducing sensitivity to cocaine <b>reward</b>.
+GRM2	drug	opioid	28534263	Activation of presynaptic group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) inhibits drug reward and drug seeking behavior, but the role of N acetylaspartylglutamate (NAAG), an agonist of endogenous <strong>mGluR2</strong>/3, in <b>heroin</b> reward and <b>heroin</b> seeking behavior remained unclear.
+GRM2	addiction	relapse	28534263	Activation of presynaptic group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) inhibits drug reward and drug <b>seeking</b> behavior, but the role of N acetylaspartylglutamate (NAAG), an agonist of endogenous <strong>mGluR2</strong>/3, in heroin reward and heroin <b>seeking</b> behavior remained unclear.
+GRM2	addiction	reward	28534263	Activation of presynaptic group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) inhibits drug <b>reward</b> and drug seeking behavior, but the role of N acetylaspartylglutamate (NAAG), an agonist of endogenous <strong>mGluR2</strong>/3, in heroin <b>reward</b> and heroin seeking behavior remained unclear.
+GRM2	drug	opioid	28534263	), an antagonist of <strong>mGluR2</strong>/3, on day 11 and the effects of NAAG on <b>heroin</b> self administration under FR1 were recorded for 3 consecutive days.
+GRM2	drug	opioid	28534263	These results demonstrated that NAAG, via activation of presynaptic <strong>mGluR2</strong>/3, attenuated the <b>heroin</b> reinforcement, <b>heroin</b> motivational value, and <b>heroin</b> seeking behavior, suggesting that it may be used as an adjunct treatment for <b>heroin</b> addiction.
+GRM2	addiction	addiction	28534263	These results demonstrated that NAAG, via activation of presynaptic <strong>mGluR2</strong>/3, attenuated the heroin reinforcement, heroin motivational value, and heroin seeking behavior, suggesting that it may be used as an adjunct treatment for heroin <b>addiction</b>.
+GRM2	addiction	relapse	28534263	These results demonstrated that NAAG, via activation of presynaptic <strong>mGluR2</strong>/3, attenuated the heroin reinforcement, heroin motivational value, and heroin <b>seeking</b> behavior, suggesting that it may be used as an adjunct treatment for heroin addiction.
+GRM2	addiction	reward	28534263	These results demonstrated that NAAG, via activation of presynaptic <strong>mGluR2</strong>/3, attenuated the heroin <b>reinforcement</b>, heroin motivational value, and heroin seeking behavior, suggesting that it may be used as an adjunct treatment for heroin addiction.
+GRM2	addiction	withdrawal	28326943	This effect also persisted for two weeks after drug <b>withdrawal</b> and was associated with increased levels of acetylated histone H3 bound to the <strong>Grm2</strong> gene promoter in the dorsal root ganglia.
+GRM2	drug	alcohol	28285415	2 PMPA also moderated the effect of <b>ethanol</b> on short term memory in <strong>mGluR2</strong> ko mice but failed to do so in mGluR3 ko mice.
+GRM2	addiction	addiction	28251297	Metabotropic glutamate 2 and 3 (<strong>mGluR2</strong>/3) receptors are implicated in drug <b>addiction</b> as they limit excessive glutamate release during relapse.
+GRM2	addiction	relapse	28251297	Metabotropic glutamate 2 and 3 (<strong>mGluR2</strong>/3) receptors are implicated in drug addiction as they limit excessive glutamate release during <b>relapse</b>.
+GRM2	drug	alcohol	28242339	Among the glutamate receptors involved in <b>alcohol</b> drinking behavior are the metabotropic receptors such as mGluR1/5, <strong>mGluR2</strong>/3, and mGluR7, as well as the ionotropic receptors, NMDA and AMPA.
+GRM2	addiction	relapse	28213190	An optimal dose for <b>relapse</b> prevention may be one that restores extrasynaptic glutamate to physiological levels and predominantly activates <strong>mGluR2</strong> and 3, but not mGluR5 receptors, which are linked to <b>relapse</b>.
+GRM2	drug	cocaine	28137451	Intermittent intake of rapid <b>cocaine</b> injections promotes robust psychomotor sensitization, increased incentive motivation for the drug and <strong>mGlu2</strong>/3 receptor dysregulation.
+GRM2	addiction	reward	28137451	Intermittent intake of rapid cocaine injections promotes robust psychomotor sensitization, increased <b>incentive</b> motivation for the drug and <strong>mGlu2</strong>/3 receptor dysregulation.
+GRM2	addiction	sensitization	28137451	Intermittent intake of rapid cocaine injections promotes robust psychomotor <b>sensitization</b>, increased incentive motivation for the drug and <strong>mGlu2</strong>/3 receptor dysregulation.
+GRM2	addiction	addiction	28137451	This <b>addiction</b> relevant phenotype was accompanied by enhanced functional activity of metabotropic glutamate group II receptors (<strong>mGluR2</strong>/3s) in the prelimbic cortex and nucleus accumbens.
+GRM2	drug	cocaine	28137451	Pharmacological activation of <strong>mGluR2</strong>/3s with LY379268 also preferentially decreased the motivation to take <b>cocaine</b> in rats previously exposed to rapid drug injections.
+GRM2	addiction	addiction	27995279	This paper provides an overview of the role of type 2 metabotropic glutamate receptors (<strong>mGluR2</strong>) in <b>addiction</b> and behaviors reflecting <b>addictive</b> processes.
+GRM2	addiction	reward	27881347	The protein expressions of TH, NR2B and <strong>GLUR2</strong> in the brain of zebrafish with <b>CPP</b> were detected with Western blotting.
+GRM2	drug	amphetamine	27881347	Compared with the control group, zebrafish in <b>methamphetamine</b> group showed significant variations in the staying time and swimming distance in the drug box after conditioning (P<0.05) with obvious alterations of NR2B, TH and <strong>GLUR2</strong> expressions in the brain (P<0.05).
+GRM2	drug	amphetamine	27881347	Treatment of <b>methamphetamine</b> dependent zebrafish with high dose rhynchophylline significantly reduced the variations in the staying time and swimming distance in the drug box (P<0.05) and in the expressions of NR2B, TH and <strong>GLUR2</strong> in the brain (P<0.05).
+GRM2	drug	amphetamine	27881347	Rhynchophylline can inhibit <b>methamphetamine</b> dependence in zebrafish, the mechanism of which may involve the expressions of TH, NR2B and <strong>GLUR2</strong> proteins in the brain.
+GRM2	addiction	dependence	27881347	Rhynchophylline can inhibit methamphetamine <b>dependence</b> in zebrafish, the mechanism of which may involve the expressions of TH, NR2B and <strong>GLUR2</strong> proteins in the brain.
+GRM2	drug	nicotine	27558879	<strong>mGluR2</strong>/3 mediates short term control of <b>nicotine</b> seeking by acute systemic N acetylcysteine.
+GRM2	addiction	relapse	27558879	<strong>mGluR2</strong>/3 mediates short term control of nicotine <b>seeking</b> by acute systemic N acetylcysteine.
+GRM2	drug	nicotine	27558879	Restoring basal concentrations of extracellular Glu, thereby increasing tonic activation of the presynaptic group II metabotropic Glu receptors (<strong>mGluR2</strong>/3) with N acetylcysteine (N AC), might offer a valid therapeutic approach for maintaining <b>smoking</b> abstinence.
+GRM2	drug	nicotine	27558879	Although N AC modulates <b>nicotine</b> seeking behavior by drug associated stimuli in abstinent rats, it is still unclear whether it occurs through activation of <strong>mGluR2</strong>/3.
+GRM2	addiction	relapse	27558879	Although N AC modulates nicotine <b>seeking</b> behavior by drug associated stimuli in abstinent rats, it is still unclear whether it occurs through activation of <strong>mGluR2</strong>/3.
+GRM2	drug	nicotine	27558879	The finding that N AC prevents cue induced <b>nicotine</b> seeking by stimulating <strong>mGluR2</strong>/3 might indicate a therapeutic opportunity for acute cue controlled <b>nicotine</b> seeking.
+GRM2	addiction	relapse	27558879	The finding that N AC prevents cue induced nicotine <b>seeking</b> by stimulating <strong>mGluR2</strong>/3 might indicate a therapeutic opportunity for acute cue controlled nicotine <b>seeking</b>.
+GRM2	drug	cocaine	27394931	The individual and combined effects of phenmetrazine and <strong>mgluR2</strong>/3 agonist LY379268 on the motivation to self administer <b>cocaine</b>.
+GRM2	drug	alcohol	27339394	The <strong>mGluR2</strong> Positive Allosteric Modulator, AZD8529, and Cue Induced Relapse to <b>Alcohol</b> Seeking in Rats.
+GRM2	addiction	relapse	27339394	The <strong>mGluR2</strong> Positive Allosteric Modulator, AZD8529, and Cue Induced <b>Relapse</b> to Alcohol <b>Seeking</b> in Rats.
+GRM2	drug	alcohol	27339394	Group II metabotropic glutamate receptors (<strong>mGluR2</strong> and mGluR3) may control relapse of <b>alcohol</b> seeking, but previously available Group II agonists were unable to discriminate between <strong>mGluR2</strong> and mGluR3.
+GRM2	addiction	relapse	27339394	Group II metabotropic glutamate receptors (<strong>mGluR2</strong> and mGluR3) may control <b>relapse</b> of alcohol <b>seeking</b>, but previously available Group II agonists were unable to discriminate between <strong>mGluR2</strong> and mGluR3.
+GRM2	drug	alcohol	27339394	Here we use AZD8529, a novel positive allosteric <strong>mGluR2</strong> modulator, to determine the role of this receptor for <b>alcohol</b> related behaviors in rats.
+GRM2	drug	alcohol	27339394	More importantly, cue  but not stress induced <b>alcohol</b> seeking was blocked by the <strong>mGluR2</strong> positive allosteric modulator.
+GRM2	addiction	relapse	27339394	More importantly, cue  but not stress induced alcohol <b>seeking</b> was blocked by the <strong>mGluR2</strong> positive allosteric modulator.
+GRM2	drug	alcohol	27339394	Our findings provide evidence for a causal role of <strong>mGluR2</strong> in cue induced relapse to <b>alcohol</b> seeking.
+GRM2	addiction	relapse	27339394	Our findings provide evidence for a causal role of <strong>mGluR2</strong> in cue induced <b>relapse</b> to alcohol <b>seeking</b>.
+GRM2	addiction	relapse	27339394	They contribute support for the notion that positive allosteric modulators of <strong>mGluR2</strong> block <b>relapse</b> like behavior across different drug categories.
+GRM2	drug	alcohol	27207718	No change in metabotropic glutamate receptor 2/3 (<strong>mGlu2</strong>/3) function was detected as bath application of the <strong>mGlu2</strong>/3 agonist LY379268 decreased spontaneous and miniature EPSC frequency in slices from both control and <b>ethanol</b> consuming rats.
+GRM2	drug	alcohol	27207718	Taken together, these findings indicate that the increase in basal extracellular glutamate occurring after chronic <b>ethanol</b> consumption is not mediated by an increase in action potential dependent glutamate release or a failure of <strong>mGlu2</strong>/3 autoreceptors to regulate such release.
+GRM2	drug	psychedelics	27189960	The Rapidly Acting Antidepressant <b>Ketamine</b> and the <strong>mGlu2</strong>/3 Receptor Antagonist LY341495 Rapidly Engage Dopaminergic Mood Circuits.
+GRM2	drug	psychedelics	27189960	Preclinical data suggest that blockade of metabotropic glutamate (<strong>mGlu2</strong>/3) receptors shares many overlapping features and mechanisms with <b>ketamine</b> and may also provide rapid efficacy for TRD patients.
+GRM2	drug	psychedelics	27189960	Herein, we evaluated the changes in dopaminergic neurotransmission after acute administration of <b>ketamine</b> and the <strong>mGlu2</strong>/3 receptor antagonist LY341495 [(2S) 2 amino 2 [(1S,2S) 2 carboxycycloprop 1 yl] 3 (xanth 9 yl) propanoic acid ] in preclinical models using electrophysiologic, neurochemical, and behavioral endpoints.
+GRM2	drug	psychedelics	27189960	These findings provide another overlapping mechanism of action of <b>ketamine</b> and <strong>mGlu2</strong>/3 receptor antagonism that differentiates them from conventional antidepressants and thus support the potential rapidly acting antidepressant actions of <strong>mGlu2</strong>/3 receptor antagonism in patients.
+GRM2	drug	opioid	26924808	<strong>GluR2</strong> 3Y Inhibits the Acquisition and Reinstatement of <b>Morphine</b> Induced Conditioned Place Preference in Rats.
+GRM2	addiction	relapse	26924808	<strong>GluR2</strong> 3Y Inhibits the Acquisition and <b>Reinstatement</b> of Morphine Induced Conditioned Place Preference in Rats.
+GRM2	addiction	addiction	26924808	However, the role of AMPARs containing the <strong>GluR2</strong> subunit in opiate <b>addiction</b> is still unclear.
+GRM2	drug	opioid	26924808	In this study, we explored the effect of intravenous injection of <strong>GluR2</strong> 3Y on the acquisition, expression, and reinstatement of <b>morphine</b> induced conditioned place preference (mCPP) in rats.
+GRM2	addiction	relapse	26924808	In this study, we explored the effect of intravenous injection of <strong>GluR2</strong> 3Y on the acquisition, expression, and <b>reinstatement</b> of morphine induced conditioned place preference (mCPP) in rats.
+GRM2	drug	opioid	26924808	We found that infusion of <strong>GluR2</strong> 3Y (1.5 nmol/g) one hour before <b>morphine</b> during the conditioning phase inhibited the acquisition of mCPP, while an identical injection one hour before the post conditioning test had no influence on the expression of mCPP.
+GRM2	drug	opioid	26924808	Injection of <strong>GluR2</strong> 3Y (1.5 nmol/g) after mCPP extinction blocked the <b>morphine</b> induced reinstatement of mCPP.
+GRM2	addiction	relapse	26924808	Injection of <strong>GluR2</strong> 3Y (1.5 nmol/g) after mCPP extinction blocked the morphine induced <b>reinstatement</b> of mCPP.
+GRM2	drug	nicotine	26873083	Attenuation of <b>nicotine</b> taking and <b>nicotine</b> seeking behavior by the <strong>mGlu2</strong> receptor positive allosteric modulators AZD8418 and AZD8529 in rats.
+GRM2	addiction	relapse	26873083	Attenuation of nicotine taking and nicotine <b>seeking</b> behavior by the <strong>mGlu2</strong> receptor positive allosteric modulators AZD8418 and AZD8529 in rats.
+GRM2	drug	nicotine	26873083	However, the relative contribution of <strong>mGlu2</strong> receptors in <b>nicotine</b> dependence is still unknown.
+GRM2	addiction	dependence	26873083	However, the relative contribution of <strong>mGlu2</strong> receptors in nicotine <b>dependence</b> is still unknown.
+GRM2	drug	nicotine	26873083	The present study evaluated the role of <strong>mGlu2</strong> receptors in <b>nicotine</b> taking and <b>nicotine</b> seeking behavior using the novel, relatively selective <strong>mGlu2</strong> positive allosteric modulators (PAMs) AZD8418 and AZD8529.
+GRM2	addiction	relapse	26873083	The present study evaluated the role of <strong>mGlu2</strong> receptors in nicotine taking and nicotine <b>seeking</b> behavior using the novel, relatively selective <strong>mGlu2</strong> positive allosteric modulators (PAMs) AZD8418 and AZD8529.
+GRM2	drug	nicotine	26873083	These findings indicate an important role for <strong>mGlu2</strong> receptors in the reinforcing properties of self administered <b>nicotine</b> and the motivational impact of cues that were previously associated with <b>nicotine</b> administration (i.e., cue induced reinstatement of <b>nicotine</b> seeking behavior).
+GRM2	addiction	relapse	26873083	These findings indicate an important role for <strong>mGlu2</strong> receptors in the reinforcing properties of self administered nicotine and the motivational impact of cues that were previously associated with nicotine administration (i.e., cue induced <b>reinstatement</b> of nicotine <b>seeking</b> behavior).
+GRM2	addiction	reward	26873083	These findings indicate an important role for <strong>mGlu2</strong> receptors in the <b>reinforcing</b> properties of self administered nicotine and the motivational impact of cues that were previously associated with nicotine administration (i.e., cue induced reinstatement of nicotine seeking behavior).
+GRM2	drug	nicotine	26873083	Thus, <strong>mGlu2</strong> PAMs may be useful medications to assist people to quit <b>tobacco</b> <b>smoking</b> and prevent relapse.
+GRM2	addiction	relapse	26873083	Thus, <strong>mGlu2</strong> PAMs may be useful medications to assist people to quit tobacco smoking and prevent <b>relapse</b>.
+GRM2	drug	alcohol	26449720	Reversal of <b>alcohol</b> dependence induced deficits in cue guided behavior via <strong>mGluR2</strong>/3 signaling in mice.
+GRM2	addiction	dependence	26449720	Reversal of alcohol <b>dependence</b> induced deficits in cue guided behavior via <strong>mGluR2</strong>/3 signaling in mice.
+GRM2	drug	alcohol	26449720	In the present study, we examined the effects of chronic intermittent <b>ethanol</b> exposure (CIE) on the use of reward paired cues to guide consummatory behaviors in a mouse model, and further, how manipulations of <strong>mGluR2</strong>/3 signaling known to be dysregulated after chronic <b>alcohol</b> exposure may alter the expression of this behavior.
+GRM2	addiction	reward	26449720	In the present study, we examined the effects of chronic intermittent ethanol exposure (CIE) on the use of <b>reward</b> paired cues to guide consummatory behaviors in a mouse model, and further, how manipulations of <strong>mGluR2</strong>/3 signaling known to be dysregulated after chronic alcohol exposure may alter the expression of this behavior.
+GRM2	addiction	reward	26449720	In addition, systemic administration of an <strong>mGluR2</strong>/3 agonist restored the use of <b>reward</b> paired cues in CIE exposed animals without impacting behavior in air controls.
+GRM2	addiction	reward	26449720	Conversely, administration of an <strong>mGluR2</strong>/3 antagonist mimicked the effects of CIE on cue guided licking behavior, indicating that <strong>mGluR2</strong>/3 signaling can bidirectionally regulate the ability to use <b>reward</b> paired cues to guide behavior.
+GRM2	drug	alcohol	26449720	Together, these data suggest that chronic <b>ethanol</b> exposure drives impairments in the ability to use reward paired cues to adaptively regulate behavior and that <strong>mGluR2</strong>/3 receptors represent a therapeutic target for restoration of these deficits in behavioral control in the <b>alcoholic</b>.
+GRM2	addiction	reward	26449720	Together, these data suggest that chronic ethanol exposure drives impairments in the ability to use <b>reward</b> paired cues to adaptively regulate behavior and that <strong>mGluR2</strong>/3 receptors represent a therapeutic target for restoration of these deficits in behavioral control in the alcoholic.
+GRM2	addiction	relapse	26149611	Group II metabotropic glutamate receptors (<strong>mGluR2</strong> and mGluR3) have been suggested to play an important role in mediation of drug reinforced behaviors, as well as in the mechanisms underlying <b>relapse</b> in abstinent subjects.
+GRM2	drug	amphetamine	26149611	The prototypical <strong>mGluR2</strong>/3 agonist, LY379268, has been shown to attenuate nicotine reinforcement and cue induced reinstatement of drug seeking in rats, as well as reinstatement induced by drug associated stimuli and contexts across different drugs of abuse (i.e., cocaine, heroin, and <b>methamphetamine</b>).
+GRM2	drug	cocaine	26149611	The prototypical <strong>mGluR2</strong>/3 agonist, LY379268, has been shown to attenuate nicotine reinforcement and cue induced reinstatement of drug seeking in rats, as well as reinstatement induced by drug associated stimuli and contexts across different drugs of abuse (i.e., <b>cocaine</b>, heroin, and methamphetamine).
+GRM2	drug	nicotine	26149611	The prototypical <strong>mGluR2</strong>/3 agonist, LY379268, has been shown to attenuate <b>nicotine</b> reinforcement and cue induced reinstatement of drug seeking in rats, as well as reinstatement induced by drug associated stimuli and contexts across different drugs of abuse (i.e., cocaine, heroin, and methamphetamine).
+GRM2	drug	opioid	26149611	The prototypical <strong>mGluR2</strong>/3 agonist, LY379268, has been shown to attenuate nicotine reinforcement and cue induced reinstatement of drug seeking in rats, as well as reinstatement induced by drug associated stimuli and contexts across different drugs of abuse (i.e., cocaine, <b>heroin</b>, and methamphetamine).
+GRM2	addiction	relapse	26149611	The prototypical <strong>mGluR2</strong>/3 agonist, LY379268, has been shown to attenuate nicotine reinforcement and cue induced <b>reinstatement</b> of drug <b>seeking</b> in rats, as well as <b>reinstatement</b> induced by drug associated stimuli and contexts across different drugs of abuse (i.e., cocaine, heroin, and methamphetamine).
+GRM2	addiction	reward	26149611	The prototypical <strong>mGluR2</strong>/3 agonist, LY379268, has been shown to attenuate nicotine <b>reinforcement</b> and cue induced reinstatement of drug seeking in rats, as well as reinstatement induced by drug associated stimuli and contexts across different drugs of abuse (i.e., cocaine, heroin, and methamphetamine).
+GRM2	drug	cocaine	26149611	To explore the therapeutic potential of <strong>mGluR2</strong>/3 agonists, we compared the effects of LY379268 (0.03 1.0 mg/kg) on nicotine, <b>cocaine</b>, and food self administration under a fixed ratio (FR10) schedule in three separate groups of squirrel monkeys.
+GRM2	drug	nicotine	26149611	To explore the therapeutic potential of <strong>mGluR2</strong>/3 agonists, we compared the effects of LY379268 (0.03 1.0 mg/kg) on <b>nicotine</b>, cocaine, and food self administration under a fixed ratio (FR10) schedule in three separate groups of squirrel monkeys.
+GRM2	drug	nicotine	26149611	The present findings provide strong support for the potential utility of <strong>mGlu2</strong>/3 receptor agonists for the treatment of <b>nicotine</b> dependence and suggest their utility for prevention of relapse induced by environmental cues associated with drug taking.
+GRM2	addiction	dependence	26149611	The present findings provide strong support for the potential utility of <strong>mGlu2</strong>/3 receptor agonists for the treatment of nicotine <b>dependence</b> and suggest their utility for prevention of relapse induced by environmental cues associated with drug taking.
+GRM2	addiction	relapse	26149611	The present findings provide strong support for the potential utility of <strong>mGlu2</strong>/3 receptor agonists for the treatment of nicotine dependence and suggest their utility for prevention of <b>relapse</b> induced by environmental cues associated with drug taking.
+GRM2	addiction	reward	26071679	<strong>mGlu2</strong>/3 glutamate receptors in the NAc have important roles in the <b>reward</b> pathway.
+GRM2	drug	opioid	26071679	In this study, we examined the effects of bilateral intra accumbal administration of LY379268, an <strong>mGlu2</strong>/3 receptor agonist on the acquisition and expression of <b>morphine</b> induced CPP in rats.
+GRM2	addiction	reward	26071679	In this study, we examined the effects of bilateral intra accumbal administration of LY379268, an <strong>mGlu2</strong>/3 receptor agonist on the acquisition and expression of morphine induced <b>CPP</b> in rats.
+GRM2	drug	opioid	26071679	Our findings suggest that activation of <strong>mGlu2</strong>/3 receptors in the NAc dose dependently blocked both the establishment and the maintenance of <b>morphine</b> induced CPP and confirmed the role of this system as a potential therapeutic target for addiction.
+GRM2	addiction	addiction	26071679	Our findings suggest that activation of <strong>mGlu2</strong>/3 receptors in the NAc dose dependently blocked both the establishment and the maintenance of morphine induced CPP and confirmed the role of this system as a potential therapeutic target for <b>addiction</b>.
+GRM2	addiction	reward	26071679	Our findings suggest that activation of <strong>mGlu2</strong>/3 receptors in the NAc dose dependently blocked both the establishment and the maintenance of morphine induced <b>CPP</b> and confirmed the role of this system as a potential therapeutic target for addiction.
+GRM2	drug	cocaine	26022263	In vivo microdialysis results indicated that a nucleus accumbens ventral pallidum γ aminobutyric acid ergic mechanism may underlie AMN082 induced antagonism of the reinforcing effects of <b>cocaine</b>, whereas a glutamate <strong>mGlu2</strong>/3 receptor mechanism underlies the AMN082 induced blockade of <b>cocaine</b> seeking.
+GRM2	addiction	relapse	26022263	In vivo microdialysis results indicated that a nucleus accumbens ventral pallidum γ aminobutyric acid ergic mechanism may underlie AMN082 induced antagonism of the reinforcing effects of cocaine, whereas a glutamate <strong>mGlu2</strong>/3 receptor mechanism underlies the AMN082 induced blockade of cocaine <b>seeking</b>.
+GRM2	addiction	reward	26022263	In vivo microdialysis results indicated that a nucleus accumbens ventral pallidum γ aminobutyric acid ergic mechanism may underlie AMN082 induced antagonism of the <b>reinforcing</b> effects of cocaine, whereas a glutamate <strong>mGlu2</strong>/3 receptor mechanism underlies the AMN082 induced blockade of cocaine seeking.
+GRM2	addiction	addiction	25802079	Based on rodent studies, group II metabotropic glutamate receptors (<strong>mGluR2</strong> and mGluR3) were suggested as targets for <b>addiction</b> treatment.
+GRM2	drug	nicotine	25802079	Here, we determined the effects of AZD8529, a selective positive allosteric modulator of <strong>mGluR2</strong>, on abuse related effects of <b>nicotine</b> in squirrel monkeys and rats.
+GRM2	drug	nicotine	25802079	These results provide evidence for efficacy of positive allosteric modulators of <strong>mGluR2</strong> in nonhuman primate models of <b>nicotine</b> reinforcement and relapse.
+GRM2	addiction	relapse	25802079	These results provide evidence for efficacy of positive allosteric modulators of <strong>mGluR2</strong> in nonhuman primate models of nicotine reinforcement and <b>relapse</b>.
+GRM2	addiction	reward	25802079	These results provide evidence for efficacy of positive allosteric modulators of <strong>mGluR2</strong> in nonhuman primate models of nicotine <b>reinforcement</b> and relapse.
+GRM2	drug	alcohol	25425009	In rodents, <strong>mGluR2</strong>/3 agonists attenuate the reinstatement of <b>alcohol</b> seeking behavior.
+GRM2	addiction	relapse	25425009	In rodents, <strong>mGluR2</strong>/3 agonists attenuate the <b>reinstatement</b> of alcohol <b>seeking</b> behavior.
+GRM2	drug	alcohol	25425009	Linking possible alterations of the <strong>mGluR2</strong>/3 system to the etiology and type of <b>alcoholism</b> could provide valuable information for the development of novel <strong>mGluR2</strong>/3 function modulating therapies in addiction treatment.
+GRM2	addiction	addiction	25425009	Linking possible alterations of the <strong>mGluR2</strong>/3 system to the etiology and type of alcoholism could provide valuable information for the development of novel <strong>mGluR2</strong>/3 function modulating therapies in <b>addiction</b> treatment.
+GRM2	drug	alcohol	25425009	To date, <strong>mGluR2</strong>/3 binding density has not been studied in human <b>alcoholics</b>.
+GRM2	drug	alcohol	25425009	We aimed to investigate the possible differences in <strong>mGluR2</strong>/3 binding between Cloninger type 1 anxiety prone and type 2 impulsive <b>alcoholics</b> and controls.
+GRM2	drug	alcohol	25425009	We performed a post mortem whole hemisphere autoradiography to study the <strong>mGluR2</strong>/3 binding density of 9 type 1 <b>alcoholics</b>, 8 type 2 <b>alcoholics</b> and 10 controls.
+GRM2	drug	alcohol	25425009	This preliminary study suggests that impulsive type 2 <b>alcoholics</b> might have alterations in the <strong>mGluR2</strong>/3 function in the pACC, a brain area presumed to be involved in the control of drug seeking behaviors and self control.
+GRM2	addiction	relapse	25425009	This preliminary study suggests that impulsive type 2 alcoholics might have alterations in the <strong>mGluR2</strong>/3 function in the pACC, a brain area presumed to be involved in the control of drug <b>seeking</b> behaviors and self control.
+GRM2	drug	cocaine	25268136	After repeated <b>cocaine</b> exposure, the density of GluR1 was increased, but there was no change in total AMPA receptors and <strong>GluR2</strong> levels in wild type mice.
+GRM2	drug	cocaine	25268136	In contrast, following repeated <b>cocaine</b> exposure, increased densities of total AMPA receptors, GluR1 and <strong>GluR2</strong> were observed in knock out mice.
+GRM2	drug	alcohol	24872560	Whereas CDPPB treatment did not alter the amplitude of PrL or IfL AMPA currents, it did promote the expression of IfL calcium permeable <strong>GluR2</strong> lacking receptors in both abstinence  and extinction trained rats, but had no effect in <b>ethanol</b> naive rats.
+GRM2	addiction	intoxication	24763081	Furthermore, MA <b>binge</b> exposure increased 5 HT2A and decreased <strong>mGlu2</strong> receptor expression in the medial frontal cortex, whereas 5 HT2C and 5 HT1A receptors were unaffected.
+GRM2	drug	cocaine	24735492	Design and synthesis of systemically active metabotropic glutamate subtype 2 and  3 (<strong>mGlu2</strong>/3) receptor positive allosteric modulators (PAMs): pharmacological characterization and assessment in a rat model of <b>cocaine</b> dependence.
+GRM2	addiction	dependence	24735492	Design and synthesis of systemically active metabotropic glutamate subtype 2 and  3 (<strong>mGlu2</strong>/3) receptor positive allosteric modulators (PAMs): pharmacological characterization and assessment in a rat model of cocaine <b>dependence</b>.
+GRM2	drug	cocaine	24599450	Interactions between N ethylmaleimide sensitive factor and <strong>GluR2</strong> in the nucleus accumbens contribute to the expression of locomotor sensitization to <b>cocaine</b>.
+GRM2	addiction	sensitization	24599450	Interactions between N ethylmaleimide sensitive factor and <strong>GluR2</strong> in the nucleus accumbens contribute to the expression of locomotor <b>sensitization</b> to cocaine.
+GRM2	addiction	sensitization	24599450	We demonstrated that the expression of behavioral <b>sensitization</b> was negatively controlled by N ethylmaleimide sensitive factor (NSF) <strong>GluR2</strong> interactions in the NAc.
+GRM2	drug	cocaine	24599450	The upregulation of NSF <strong>GluR2</strong> interactions, which may be resulted by the increase in NSF S nitrosylation after withdrawal from <b>cocaine</b>, was associated with the changes in the expression of behavioral sensitization.
+GRM2	addiction	sensitization	24599450	The upregulation of NSF <strong>GluR2</strong> interactions, which may be resulted by the increase in NSF S nitrosylation after withdrawal from cocaine, was associated with the changes in the expression of behavioral <b>sensitization</b>.
+GRM2	addiction	withdrawal	24599450	The upregulation of NSF <strong>GluR2</strong> interactions, which may be resulted by the increase in NSF S nitrosylation after <b>withdrawal</b> from cocaine, was associated with the changes in the expression of behavioral sensitization.
+GRM2	drug	cocaine	24599450	Disruption of NSF <strong>GluR2</strong> interactions in the NAc with a specific peptide, TAT pep R845A, increased the locomotor response of rats to <b>cocaine</b> by decreasing <strong>GluR2</strong> surface insertion.
+GRM2	addiction	sensitization	24599450	In contrast, prevention of <strong>GluR2</strong> containing AMPARs removal from synapses with Pep2 EVKI attenuated the expression of behavioral <b>sensitization</b>.
+GRM2	addiction	sensitization	24599450	Similarly, treatment with the nitric oxide donor, S Nitroso N acetyl DL penicillamine (SNAP), attenuated the expression of locomotor <b>sensitization</b> by promoting <strong>GluR2</strong> surface expression.
+GRM2	drug	cocaine	24599450	Thus, these results indicate that increased NSF <strong>GluR2</strong> interactions in the NAc after withdrawal from <b>cocaine</b> attenuated the expression of behavioral sensitization and serves as a negative regulatory mechanism in drug exposed individuals.
+GRM2	addiction	sensitization	24599450	Thus, these results indicate that increased NSF <strong>GluR2</strong> interactions in the NAc after withdrawal from cocaine attenuated the expression of behavioral <b>sensitization</b> and serves as a negative regulatory mechanism in drug exposed individuals.
+GRM2	addiction	withdrawal	24599450	Thus, these results indicate that increased NSF <strong>GluR2</strong> interactions in the NAc after <b>withdrawal</b> from cocaine attenuated the expression of behavioral sensitization and serves as a negative regulatory mechanism in drug exposed individuals.
+GRM2	drug	amphetamine	24467371	The effects of <strong>mGluR2</strong>/3 activation on acute and repeated <b>amphetamine</b> induced locomotor activity in differentially reared male rats.
+GRM2	drug	amphetamine	24467371	The current study investigated the effects of the Group 2 metabotropic glutamate receptor (<strong>mGluR2</strong>/3) agonist, LY 379268 (0.5, 1.0 mg/kg), on acute and repeated <b>amphetamine</b> induced locomotor activity in differentially reared male rats.
+GRM2	drug	alcohol	24082084	By genomic sequencing, linkage analysis, and functional validation, we identified that genetic variation of <strong>Grm2</strong>, which encodes metabotropic glutamate receptor 2 (mGluR2), alters <b>alcohol</b> preference in animal models.
+GRM2	drug	alcohol	24082084	By genomic sequencing, linkage analysis, and functional validation, we identified that genetic variation of <strong>Grm2</strong>, which encodes metabotropic glutamate receptor 2 (<strong>mGluR2</strong>), alters <b>alcohol</b> preference in animal models.
+GRM2	drug	alcohol	24082084	Selectively bred <b>alcohol</b> preferring (P) rats are homozygous for a <strong>Grm2</strong> stop codon (<strong>Grm2</strong> *407) that leads to largely uncompensated loss of mGluR2.
+GRM2	drug	alcohol	24082084	Selectively bred <b>alcohol</b> preferring (P) rats are homozygous for a <strong>Grm2</strong> stop codon (<strong>Grm2</strong> *407) that leads to largely uncompensated loss of <strong>mGluR2</strong>.
+GRM2	drug	alcohol	24082084	<strong>Grm2</strong> *407 was linked to increased <b>alcohol</b> consumption and preference in F2 rats generated by intercrossing inbred P and nonpreferring rats.
+GRM2	drug	alcohol	24082084	Pharmacologic blockade of <strong>mGluR2</strong> escalated <b>alcohol</b> self administration in Wistar rats, the parental strain of P and nonpreferring rats.
+GRM2	drug	alcohol	24082084	The causal role of mGluR2 in altered <b>alcohol</b> preference was further supported by elevated <b>alcohol</b> consumption in <strong>Grm2</strong> ( / ) mice.
+GRM2	drug	alcohol	24082084	The causal role of <strong>mGluR2</strong> in altered <b>alcohol</b> preference was further supported by elevated <b>alcohol</b> consumption in <strong>Grm2</strong> ( / ) mice.
+GRM2	drug	alcohol	24082084	Together, these data point to <strong>mGluR2</strong> as an origin of <b>alcohol</b> preference and a potential therapeutic target.
+GRM2	drug	alcohol	23995381	Blocking mGluR5 potently affects various <b>alcohol</b> related behaviors in rodents, and <strong>mGluR2</strong>/3 agonism also suppresses <b>alcohol</b> consumption.
+GRM2	addiction	addiction	23624743	The <strong>mGluR2</strong>/3 agonist LY379268 induced anti reinstatement effects in rats exhibiting <b>addiction</b> like behavior.
+GRM2	addiction	relapse	23624743	The <strong>mGluR2</strong>/3 agonist LY379268 induced anti <b>reinstatement</b> effects in rats exhibiting addiction like behavior.
+GRM2	drug	cocaine	23624743	We therefore hypothesized that <b>cocaine</b> seeking in addict like rats could be treated with an <strong>mGluR2</strong>/3 agonist.
+GRM2	addiction	relapse	23624743	We therefore hypothesized that cocaine <b>seeking</b> in addict like rats could be treated with an <strong>mGluR2</strong>/3 agonist.
+GRM2	drug	cocaine	23624743	Indeed, addict like rats that were treated systemically with the <strong>mGluR2</strong>/3 agonist LY379268 (0, 0.3, and 3 mg/kg) showed a pronounced reduction in cue induced reinstatement of <b>cocaine</b> seeking.
+GRM2	addiction	relapse	23624743	Indeed, addict like rats that were treated systemically with the <strong>mGluR2</strong>/3 agonist LY379268 (0, 0.3, and 3 mg/kg) showed a pronounced reduction in cue induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM2	drug	cocaine	23624743	In an attempt to dissect the role played by <strong>mGluR2</strong> and mGluR3 in cue induced reinstatement, we analyzed the mRNA expression patterns in several relevant brain areas but did not find any significant differences between <b>cocaine</b> addict like and non addict like rats, suggesting that the behavioral differences observed are due to translational rather than transcriptional regulation.
+GRM2	addiction	relapse	23624743	In an attempt to dissect the role played by <strong>mGluR2</strong> and mGluR3 in cue induced <b>reinstatement</b>, we analyzed the mRNA expression patterns in several relevant brain areas but did not find any significant differences between cocaine addict like and non addict like rats, suggesting that the behavioral differences observed are due to translational rather than transcriptional regulation.
+GRM2	addiction	addiction	23624743	Another possibility to study the contributions of <strong>mGluR2</strong> and mGluR3 in mediating <b>addictive</b> like behavior is the use of knockout models.
+GRM2	addiction	reward	23624743	Because <strong>mGluR2</strong> knockouts cannot be used in <b>operant</b> procedures due to motoric impairment, we only tested mGluR3 knockouts.
+GRM2	addiction	addiction	23624743	These mice did not differ from controls in reinstatement, suggesting that <strong>mGluR2</strong> receptors are critical in mediating <b>addictive</b> like behavior.
+GRM2	addiction	relapse	23624743	These mice did not differ from controls in <b>reinstatement</b>, suggesting that <strong>mGluR2</strong> receptors are critical in mediating addictive like behavior.
+GRM2	drug	alcohol	23623810	mGluR5 selective antagonist, MTEP (3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]pyridine hydrochloride) and <strong>mGluR2</strong>/3 agonist, LY354740 (1S,2S,5R,6S) 2 aminobicyclo[3.1.0]hexane 2,6 dicarboxylic acid), caused effects similar to <b>acamprosate</b> at doses 1.25 5mg/kg and 2.5 5mg/kg, respectively.
+GRM2	addiction	reward	23603364	MeAM <b>CPP</b> increased surface expression of GluR1 and <strong>GluR2</strong> subunits of AMPA receptor in the BLA.
+GRM2	drug	opioid	23564315	We also looked at the effect of <b>morphine</b> on other glutamate receptor subunits, including AMPA <strong>GluR2</strong> (<strong>GluR2</strong>) and NMDA NR1 (NR1).
+GRM2	drug	nicotine	23518606	In addition, relapse to <b>nicotine</b> seeking increased the phosphorylation levels of <strong>GluR2</strong> Ser880, NR1 Ser890, and p38 MAPK in the nucleus accumbens (NAc), but not in the prefrontal cortex.
+GRM2	addiction	relapse	23518606	In addition, <b>relapse</b> to nicotine <b>seeking</b> increased the phosphorylation levels of <strong>GluR2</strong> Ser880, NR1 Ser890, and p38 MAPK in the nucleus accumbens (NAc), but not in the prefrontal cortex.
+GRM2	drug	nicotine	23518606	The intra accumbens infusion of the protein kinase C (PKC) inhibitor NPC 15437 reduced <b>nicotine</b> seeking behavior elicited by drug paired cues consistent with the PKC dependent phosphorylations of <strong>GluR2</strong> Ser880 and NR1 Ser890.
+GRM2	addiction	relapse	23518606	The intra accumbens infusion of the protein kinase C (PKC) inhibitor NPC 15437 reduced nicotine <b>seeking</b> behavior elicited by drug paired cues consistent with the PKC dependent phosphorylations of <strong>GluR2</strong> Ser880 and NR1 Ser890.
+GRM2	drug	amphetamine	23473878	Effect of an <strong>mGlu2</strong>/3 receptor antagonist on depressive behavior induced by withdrawal from chronic treatment with <b>methamphetamine</b>.
+GRM2	addiction	withdrawal	23473878	Effect of an <strong>mGlu2</strong>/3 receptor antagonist on depressive behavior induced by <b>withdrawal</b> from chronic treatment with methamphetamine.
+GRM2	drug	amphetamine	23473878	In the present study, we investigated the effect of an <strong>mGlu2</strong>/3 receptor antagonist, LY341495, on the depressive behavior induced by withdrawal from chronic treatment with a psychostimulant, <b>methamphetamine</b> (MAP) (5.0mg/kg/day×5 days).
+GRM2	addiction	withdrawal	23473878	In the present study, we investigated the effect of an <strong>mGlu2</strong>/3 receptor antagonist, LY341495, on the depressive behavior induced by <b>withdrawal</b> from chronic treatment with a psychostimulant, methamphetamine (MAP) (5.0mg/kg/day×5 days).
+GRM2	addiction	withdrawal	23473878	Taken together, the present results suggested that the blockade of the <strong>mGlu2</strong>/3 receptor may prevent the depressive symptoms induced by <b>withdrawal</b> from a psychostimulant and that the blockade of the <strong>mGlu2</strong>/3 receptor in the NAc may contribute to the antidepressant like effects of the <strong>mGlu2</strong>/3 receptor antagonist in this test.
+GRM2	drug	alcohol	23407939	Rescue of infralimbic <strong>mGluR2</strong> deficit restores control over drug seeking behavior in <b>alcohol</b> dependence.
+GRM2	addiction	dependence	23407939	Rescue of infralimbic <strong>mGluR2</strong> deficit restores control over drug seeking behavior in alcohol <b>dependence</b>.
+GRM2	addiction	relapse	23407939	Rescue of infralimbic <strong>mGluR2</strong> deficit restores control over drug <b>seeking</b> behavior in alcohol dependence.
+GRM2	drug	benzodiazepine	23392308	The mRNA expression levels of <strong>mGluR2</strong> and mGluR3 were lowered in the cerebral cortex of mice pretreated with <b>diazepam</b> or <b>alprazolam</b>.
+GRM2	addiction	reward	23303053	We also found that lactacystin infusion into the NAc core but not into the shell immediately after extinction training sessions inhibited <b>CPP</b> extinction and reversed the extinction training induced decrease in NSF and <strong>GluR2</strong> in the synaptosomal membrane fraction in the NAc core.
+GRM2	drug	alcohol	23100433	LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of <b>ethanol</b>, as well as cycles of excessive <b>ethanol</b> consumption and withdrawal, produced a long lasting increase in synaptic localization of the GluR1 and <strong>GluR2</strong> subunits of AMPARs in the DMS.
+GRM2	addiction	withdrawal	23100433	LTP is mediated by the insertion of AMPAR subunits into the synaptic membrane, and we found that repeated systemic administration of ethanol, as well as cycles of excessive ethanol consumption and <b>withdrawal</b>, produced a long lasting increase in synaptic localization of the GluR1 and <strong>GluR2</strong> subunits of AMPARs in the DMS.
+GRM2	drug	cocaine	23017017	Modafinil (300 mg/kg, intraperitoneal) inhibited reinstated <b>cocaine</b> seeking (but did not alter extinction responding by itself), and this effect was prevented by pre treatment with bilateral microinjections of the <strong>mGluR2</strong>/3 antagonist LY 341495 (LY) into nucleus accumbens core.
+GRM2	addiction	relapse	23017017	Modafinil (300 mg/kg, intraperitoneal) inhibited reinstated cocaine <b>seeking</b> (but did not alter extinction responding by itself), and this effect was prevented by pre treatment with bilateral microinjections of the <strong>mGluR2</strong>/3 antagonist LY 341495 (LY) into nucleus accumbens core.
+GRM2	drug	cocaine	23017017	We conclude that modafinil increases extracellular glutamate in nucleus accumbens from glial and neuronal sources in <b>cocaine</b> exposed rats, which may be important for its <strong>mGluR2</strong>/3 mediated antirelapse properties.
+GRM2	addiction	aversion	22933785	We further demonstrated that Arc/Arg3.1 regulated AMPAR endocytosis was <strong>GluR2</strong> dependent, as intra amygdala injection of Tat <strong>GluR2</strong>(3Y), a <strong>GluR2</strong> derived peptide that has been shown to specifically block regulated, but not constitutive, AMPAR endocytosis, prevented AMPAR endocytosis, LTD induction, and <b>aversive</b> memory formation.
+GRM2	drug	cocaine	22860224	In <b>cocaine</b> treated mice, C2 significantly elevates mRNA levels of the AMPA glutamate receptor <strong>GluR2</strong> subunit with specificity, a known target gene of ΔFosB that plays a role in drug addiction and endogenous resilience mechanisms.
+GRM2	addiction	addiction	22860224	In cocaine treated mice, C2 significantly elevates mRNA levels of the AMPA glutamate receptor <strong>GluR2</strong> subunit with specificity, a known target gene of ΔFosB that plays a role in drug <b>addiction</b> and endogenous resilience mechanisms.
+GRM2	drug	cocaine	22721675	We used regional analyses of c Fos and <strong>GluR2</strong> protein expression to delineate neural activity and plasticity that may be associated with <b>cocaine</b> cue extinction learning.
+GRM2	drug	cocaine	22721675	Findings suggest that basolateral amygdala and prelimbic prefrontal cortex neurons are activated during acquisition of <b>cocaine</b> cue extinction learning, a process that is independent of changes in <strong>GluR2</strong> abundance.
+GRM2	drug	amphetamine	22659409	Attenuation of <b>methamphetamine</b> seeking by the <strong>mGluR2</strong>/3 agonist LY379268 in rats with histories of restricted and escalated self administration.
+GRM2	addiction	relapse	22659409	Attenuation of methamphetamine <b>seeking</b> by the <strong>mGluR2</strong>/3 agonist LY379268 in rats with histories of restricted and escalated self administration.
+GRM2	drug	cocaine	22546614	In addition, elevated extracellular glutamate activated presynaptic <strong>mGlu2</strong>/3 autoreceptors which in turn inhibited <b>cocaine</b> priming  or cue induced enhancement of glutamate release and reinstatement of drug seeking behavior.
+GRM2	addiction	relapse	22546614	In addition, elevated extracellular glutamate activated presynaptic <strong>mGlu2</strong>/3 autoreceptors which in turn inhibited cocaine priming  or cue induced enhancement of glutamate release and <b>reinstatement</b> of drug <b>seeking</b> behavior.
+GRM2	drug	amphetamine	22479593	Extinction dependent alterations in corticostriatal <strong>mGluR2</strong>/3 and mGluR7 receptors following chronic <b>methamphetamine</b> self administration in rats.
+GRM2	drug	amphetamine	22479593	Extended access to <b>meth</b> self administration followed by abstinence decreased surface and total levels of <strong>mGluR2</strong>/3 receptors in the NAc and dSTR, while in the PFC, only a loss of surface <strong>mGluR2</strong>/3 and mGluR7 receptors was detected.
+GRM2	drug	amphetamine	22479593	Daily extinction trials reversed the downregulation of <strong>mGluR2</strong>/3 receptors in the NAc and dSTR and mGluR7 in the PFC, but downregulation of surface <strong>mGluR2</strong>/3 receptors in the PFC was present regardless of post <b>meth</b> experience.
+GRM2	drug	opioid	22388870	The function of the presynaptic group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) was downregulated, enhancing the probability of glutamate release on synaptic terminals during chronic <b>morphine</b> withdrawal.
+GRM2	addiction	withdrawal	22388870	The function of the presynaptic group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) was downregulated, enhancing the probability of glutamate release on synaptic terminals during chronic morphine <b>withdrawal</b>.
+GRM2	drug	opioid	22388870	These results suggest that chronic <b>morphine</b> withdrawal downregulates <strong>mGluR2</strong>/3 to induce potentiation of MSN glutamatergic synapse via increased glutamate release, leading to potentiation of intrinsic excitability.
+GRM2	addiction	withdrawal	22388870	These results suggest that chronic morphine <b>withdrawal</b> downregulates <strong>mGluR2</strong>/3 to induce potentiation of MSN glutamatergic synapse via increased glutamate release, leading to potentiation of intrinsic excitability.
+GRM2	drug	cocaine	22197517	Expression of AMPA receptor subunits (GluR1 and <strong>GluR2</strong>) and CRE binding protein (CREB) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of <b>cocaine</b>, with and without ICSS.
+GRM2	addiction	reward	22197517	Expression of AMPA receptor subunits (GluR1 and <strong>GluR2</strong>) and CRE binding protein (CREB) was measured in the ventral tegmental area (VTA), dorsolateral striatum (STR) and nucleus accumbens (NAc) before and after a sensitizing regimen of cocaine, with and without <b>ICSS</b>.
+GRM2	drug	cocaine	22197517	Repeated <b>cocaine</b> reduced GluR1, <strong>GluR2</strong> and CREB expression in the NAc, and reductions of GluR1 and <strong>GluR2</strong> but not CREB were further enhanced by ICSS.
+GRM2	addiction	reward	22197517	Repeated cocaine reduced GluR1, <strong>GluR2</strong> and CREB expression in the NAc, and reductions of GluR1 and <strong>GluR2</strong> but not CREB were further enhanced by <b>ICSS</b>.
+GRM2	addiction	relapse	22137594	Here, we examine the effects of NAC applied directly to the NAcore on <b>relapse</b> and neurotransmission in PFC NAcore synapses, as well as the involvement of the metabotropic glutamate receptors 2/3 (<strong>mGluR2</strong>/3) and 5 (mGluR5).
+GRM2	drug	cocaine	22137594	The effect of NAC on relapse to <b>cocaine</b> seeking depends on the balance between stimulating <strong>mGluR2</strong>/3 and mGluR5 in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting mGluR5.
+GRM2	addiction	relapse	22137594	The effect of NAC on <b>relapse</b> to cocaine <b>seeking</b> depends on the balance between stimulating <strong>mGluR2</strong>/3 and mGluR5 in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting mGluR5.
+GRM2	addiction	reward	22127928	Finally, we found that the levels of PKMζ and <strong>GluR2</strong> in the NAc remained unchanged, while the GluR1 levels were elevated following <b>CPP</b> and fully reversed by ZIP injection.
+GRM2	drug	cocaine	22072669	Finally, reduced surface expression of the <strong>GluR2</strong> subunit of the AMPA receptor is associated with <b>cocaine</b> seeking, and daily RGD microinjections during self administration training normalized the surface expression of <strong>GluR2</strong>.
+GRM2	addiction	relapse	22072669	Finally, reduced surface expression of the <strong>GluR2</strong> subunit of the AMPA receptor is associated with cocaine <b>seeking</b>, and daily RGD microinjections during self administration training normalized the surface expression of <strong>GluR2</strong>.
+GRM2	drug	cocaine	22072669	Together, these data indicate that the regulation integrins may contribute to <b>cocaine</b> reinstated drug seeking, in part by promoting reduced <strong>GluR2</strong> surface expression.
+GRM2	addiction	relapse	22072669	Together, these data indicate that the regulation integrins may contribute to cocaine reinstated drug <b>seeking</b>, in part by promoting reduced <strong>GluR2</strong> surface expression.
+GRM2	drug	cocaine	21881873	Given the important role of group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3s) in regulating glutamate release from the glutamatergic terminals, this study aimed to test whether activation of <strong>mGluR2</strong>/3s in the VTA can inhibit <b>cocaine</b> induced reinstatement of <b>cocaine</b> seeking behavior, a model of relapse to drug seeking behavior.
+GRM2	addiction	relapse	21881873	Given the important role of group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3s) in regulating glutamate release from the glutamatergic terminals, this study aimed to test whether activation of <strong>mGluR2</strong>/3s in the VTA can inhibit cocaine induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior, a model of <b>relapse</b> to drug <b>seeking</b> behavior.
+GRM2	drug	cocaine	21881873	Then the dose response effects of a selective <strong>mGluR2</strong>/3 agonist LY 379268 microinjected into the VTA on <b>cocaine</b> induced reinstatement of <b>cocaine</b> seeking behavior were assessed.
+GRM2	addiction	relapse	21881873	Then the dose response effects of a selective <strong>mGluR2</strong>/3 agonist LY 379268 microinjected into the VTA on cocaine induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior were assessed.
+GRM2	drug	cocaine	21881873	Our data support the idea that glutamate release in the VTA is critically involved in <b>cocaine</b> induced reinstatement and indicate that loss of <strong>mGluR2</strong>/3 mediated regulation of glutamate release in the VTA may critically contribute to the risk of relapse.
+GRM2	addiction	relapse	21881873	Our data support the idea that glutamate release in the VTA is critically involved in cocaine induced <b>reinstatement</b> and indicate that loss of <strong>mGluR2</strong>/3 mediated regulation of glutamate release in the VTA may critically contribute to the risk of <b>relapse</b>.
+GRM2	drug	amphetamine	21832989	<strong>GRM2</strong>/3( / ) mice were also hypoactive in response to <b>amphetamine</b>.
+GRM2	drug	cocaine	21790902	The present study was designed to examine whether antagonizing mGluR5 or activating <strong>mGluR2</strong>/3 prevents stress induced reinstatement of <b>cocaine</b> seeking.
+GRM2	addiction	relapse	21790902	The present study was designed to examine whether antagonizing mGluR5 or activating <strong>mGluR2</strong>/3 prevents stress induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM2	drug	cocaine	21790902	Both the selective mGluR5 antagonist 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]piperidine (MTEP) (0 3 mg/kg, intraperitoneally) and the selective <strong>mGluR2</strong>/3 agonist ( ) 2 oxa 4 aminobicylco[3.1.0]hexane 4,6 dicarboxylic acid (LY379268) (0 3 mg/kg, subcutaneously) prevented <b>cocaine</b> seeking induced by footshock stress following the same dose response function.
+GRM2	addiction	relapse	21790902	Both the selective mGluR5 antagonist 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl]piperidine (MTEP) (0 3 mg/kg, intraperitoneally) and the selective <strong>mGluR2</strong>/3 agonist ( ) 2 oxa 4 aminobicylco[3.1.0]hexane 4,6 dicarboxylic acid (LY379268) (0 3 mg/kg, subcutaneously) prevented cocaine <b>seeking</b> induced by footshock stress following the same dose response function.
+GRM2	addiction	relapse	21790902	The data show that although <strong>mGluR2</strong>/3 and mGluR5 are differentially located on synaptic compartments, both LY379268 and MTEP produced the same behavioral effects in reducing stress induced <b>reinstatement</b>.
+GRM2	addiction	relapse	21790902	These results are important because they demonstrate that a reduction in glutamate mediated neural excitability (albeit via different mechanisms of action) reverses footshock induced <b>reinstatement</b> and suggest that pharmacological manipulations of <strong>mGluR2</strong>/3 and mGluR5 can prevent the effects of stress, a major precipitating factor for <b>relapse</b>.
+GRM2	addiction	relapse	21790902	These findings further confirm that <strong>mGluR2</strong>/3 or mGluR5 are promising targets for <b>relapse</b> prevention.
+GRM2	drug	alcohol	21734651	Metabotropic glutamate receptor subtypes (<strong>mGlu2</strong>/3) regulate a variety of <b>alcohol</b> associated behaviors, including <b>alcohol</b> reinforcement, and relapse like behavior.
+GRM2	addiction	relapse	21734651	Metabotropic glutamate receptor subtypes (<strong>mGlu2</strong>/3) regulate a variety of alcohol associated behaviors, including alcohol reinforcement, and <b>relapse</b> like behavior.
+GRM2	addiction	reward	21734651	Metabotropic glutamate receptor subtypes (<strong>mGlu2</strong>/3) regulate a variety of alcohol associated behaviors, including alcohol <b>reinforcement</b>, and relapse like behavior.
+GRM2	drug	alcohol	21734651	To date, the role of <strong>mGlu2</strong>/3 receptors in modulating the discriminative stimulus effects of <b>alcohol</b> has not been examined.
+GRM2	drug	alcohol	21734651	Given that the discriminative stimulus effects of drugs are determinants of abuse liability and can influence drug seeking, we examined the contributions of <strong>mGlu2</strong>/3 receptors in modulating the discriminative stimulus effects of <b>alcohol</b>.
+GRM2	addiction	relapse	21734651	Given that the discriminative stimulus effects of drugs are determinants of abuse liability and can influence drug <b>seeking</b>, we examined the contributions of <strong>mGlu2</strong>/3 receptors in modulating the discriminative stimulus effects of alcohol.
+GRM2	drug	alcohol	21734651	In male Long Evans rats trained to discriminate between <b>alcohol</b> (1 g/kg, IG) and water, the <strong>mGlu2</strong>/3 agonist LY379268 (0.3 10 mg/kg) did not produce <b>alcohol</b> like stimulus effects.
+GRM2	drug	alcohol	21734651	Intra amygdala activation of <strong>mGlu2</strong>/3 receptors by LY379268 (6 μg) inhibited the discriminative stimulus effects of <b>alcohol</b>, without altering response rate.
+GRM2	drug	alcohol	21734651	These data suggest that amygdala <strong>mGlu2</strong>/3 receptors have a functional role in modulating the discriminative stimulus properties of <b>alcohol</b> and demonstrate differential motor sensitivity to activation of <strong>mGlu2</strong>/3 receptors in the amygdala and the accumbens.
+GRM2	drug	nicotine	21654734	The metabotropic glutamate 2/3 (<strong>mGlu2</strong>/3) receptor agonist LY379268 ([ ] 2 oxa 4 aminobicyclo [3.1.0] hexane 4,6 dicarboxylate) attenuates both <b>nicotine</b> self administration and cue induced <b>nicotine</b> seeking in rats.
+GRM2	addiction	relapse	21654734	The metabotropic glutamate 2/3 (<strong>mGlu2</strong>/3) receptor agonist LY379268 ([ ] 2 oxa 4 aminobicyclo [3.1.0] hexane 4,6 dicarboxylate) attenuates both nicotine self administration and cue induced nicotine <b>seeking</b> in rats.
+GRM2	drug	nicotine	21654734	These intriguing findings suggest that activation of <strong>mGlu2</strong>/3 receptors negatively modulates the combined effects of <b>nicotine</b> and <b>nicotine</b> associated contexts/cues on NAcc dopamine.
+GRM2	drug	nicotine	21654734	Thus, these data highlight a critical role for <strong>mGlu2</strong>/3 receptors in context/cue induced drug seeking behavior and suggest a neurochemical mechanism by which <strong>mGlu2</strong>/3 receptor agonists may promote <b>smoking</b> cessation by preventing relapse induced by the combination of <b>nicotine</b> and <b>nicotine</b> associated contexts and cues.
+GRM2	addiction	relapse	21654734	Thus, these data highlight a critical role for <strong>mGlu2</strong>/3 receptors in context/cue induced drug <b>seeking</b> behavior and suggest a neurochemical mechanism by which <strong>mGlu2</strong>/3 receptor agonists may promote smoking cessation by preventing <b>relapse</b> induced by the combination of nicotine and nicotine associated contexts and cues.
+GRM2	drug	cocaine	21613507	Here we show that daily intravenous <b>cocaine</b> self administration, but not passive <b>cocaine</b> administration, induces dynamic upregulation of the AMPA glutamate receptor subunits GluR1 and <strong>GluR2</strong> in the ventral tegmental area (VTA) of rats.
+GRM2	drug	opioid	21471379	Accumbens core injections of Tat <strong>GluR2</strong>(3Y), which inhibits <strong>GluR2</strong> dependent AMPA receptor endocytosis, prevented the impairment in <b>morphine</b> CPP induced by local ZIP injections, indicating that the persistent effect of PKMζ is on <strong>GluR2</strong> containing AMPA receptors.
+GRM2	addiction	reward	21471379	Accumbens core injections of Tat <strong>GluR2</strong>(3Y), which inhibits <strong>GluR2</strong> dependent AMPA receptor endocytosis, prevented the impairment in morphine <b>CPP</b> induced by local ZIP injections, indicating that the persistent effect of PKMζ is on <strong>GluR2</strong> containing AMPA receptors.
+GRM2	drug	opioid	21459090	With an emphasis on a recent publication describing the anatomical relationship between the μ <b>opioid</b> receptor (MOR) and the AMPA <strong>GluR2</strong> subunit (Beckerman, M. A., and Glass, M. J., 2011.
+GRM2	drug	opioid	21459090	Ultrastructural relationship between the AMPA <strong>GluR2</strong> receptor subunit and the mu <b>opioid</b> receptor in the mouse central nucleus of the amygdala.
+GRM2	drug	cannabinoid	21187978	Here we show in rats that chronic <b>cannabinoid</b> exposure activates VTA <b>cannabinoid</b> CB1 receptors to induce transient neurotransmission depression at VTA local Glu DA synapses through activation of NMDA receptors and subsequent endocytosis of AMPA receptor <strong>GluR2</strong> subunits.
+GRM2	drug	cannabinoid	21187978	A <strong>GluR2</strong> derived peptide blocks <b>cannabinoid</b> induced VTA synaptic depression and conditioned place preference, i.e., learning to associate drug exposure with environmental cues.
+GRM2	drug	cannabinoid	21187978	These data not only provide the first evidence, to our knowledge, that NMDA receptor dependent synaptic depression at VTA dopamine circuitry requires <strong>GluR2</strong> endocytosis, but also suggest an essential contribution of such synaptic depression to <b>cannabinoid</b> associated addictive learning, in addition to pointing to novel pharmacological strategies for the treatment of <b>cannabis</b> addiction.
+GRM2	addiction	addiction	21187978	These data not only provide the first evidence, to our knowledge, that NMDA receptor dependent synaptic depression at VTA dopamine circuitry requires <strong>GluR2</strong> endocytosis, but also suggest an essential contribution of such synaptic depression to cannabinoid associated <b>addictive</b> learning, in addition to pointing to novel pharmacological strategies for the treatment of cannabis <b>addiction</b>.
+GRM2	drug	cocaine	21155570	Design and synthesis of an orally active metabotropic glutamate receptor subtype 2 (<strong>mGluR2</strong>) positive allosteric modulator (PAM) that decreases <b>cocaine</b> self administration in rats.
+GRM2	drug	cocaine	21155570	The benzisothiazol 3 one derivative 14 decreased <b>cocaine</b> self administration in rats, providing proof of concept for the use of <strong>mGluR2</strong> PAMs for the treatment of <b>cocaine</b> dependence.
+GRM2	addiction	dependence	21155570	The benzisothiazol 3 one derivative 14 decreased cocaine self administration in rats, providing proof of concept for the use of <strong>mGluR2</strong> PAMs for the treatment of cocaine <b>dependence</b>.
+GRM2	drug	opioid	20970421	Ultrastructural relationship between the AMPA <strong>GluR2</strong> receptor subunit and the mu <b>opioid</b> receptor in the mouse central nucleus of the amygdala.
+GRM2	drug	opioid	20970421	Activation of <strong>GluR2</strong> expressing non calcium permeable AMPA type glutamate receptors in the central nucleus of the amygdala (CeA) may play an important role in integrating emotion and memory with goal directed behaviors involved in <b>opioid</b> addiction.
+GRM2	addiction	addiction	20970421	Activation of <strong>GluR2</strong> expressing non calcium permeable AMPA type glutamate receptors in the central nucleus of the amygdala (CeA) may play an important role in integrating emotion and memory with goal directed behaviors involved in opioid <b>addiction</b>.
+GRM2	addiction	addiction	20970421	The presence of <strong>GluR2</strong> in dendritic profiles receiving asymmetric synapses suggests that activation of the non calcium permeable AMPA receptor plays a role in the postsynaptic modulation of excitatory signaling involving CeA neuronal circuits that coordinate sensory, affective, and behavioral processes involved in drug <b>addiction</b>.
+GRM2	drug	cocaine	20942997	Following re exposure to a <b>cocaine</b> paired context, surface expression of the AMPA type glutamate receptor GluR1 was significantly reduced whereas <strong>GluR2</strong> was significantly increased in the dlCPu, independent of Arc antisense ODN infusion.
+GRM2	drug	cocaine	20868701	Under basal conditions and in response to a single <b>cocaine</b> injection the levels of GluR1, <strong>GluR2</strong>, and GluR3 AMPA receptor subunits did not differ between WT and 5 LOX deficient mice, but the response of GluR1 phosphorylation to a single <b>cocaine</b> injection was greater under the 5 LOX deficiency.
+GRM2	addiction	addiction	20631691	In addition, group II metabotropic glutamate receptors (<strong>mGlu2</strong>/3R) have been suggested as a new therapeutic target for drug <b>addiction</b>.
+GRM2	drug	opioid	20631691	Here, we investigated the ability of modafinil to prevent the acute <b>morphine</b> to promote reinstatement of extinguished preference for <b>morphine</b>, and the involvement of <strong>mGlu2</strong>/3Rs in this effect.
+GRM2	addiction	relapse	20631691	Here, we investigated the ability of modafinil to prevent the acute morphine to promote <b>reinstatement</b> of extinguished preference for morphine, and the involvement of <strong>mGlu2</strong>/3Rs in this effect.
+GRM2	addiction	relapse	20631691	The anti <b>reinstatement</b> effect of modafinil was completely prevented by pretreatment with the selective <strong>mGlu2</strong>/3 antagonist LY341495.
+GRM2	addiction	addiction	20631691	These data reveal a novel mechanism for modafinil actions, a role for <strong>mGlu2</strong>/3 receptors in reinstatement of opiate seeking, and a new therapeutic option to treat relapse in opiate <b>addiction</b>.
+GRM2	addiction	relapse	20631691	These data reveal a novel mechanism for modafinil actions, a role for <strong>mGlu2</strong>/3 receptors in <b>reinstatement</b> of opiate <b>seeking</b>, and a new therapeutic option to treat <b>relapse</b> in opiate addiction.
+GRM2	drug	cocaine	20555310	The <strong>mGluR2</strong> positive allosteric modulator BINA decreases <b>cocaine</b> self administration and cue induced <b>cocaine</b> seeking and counteracts <b>cocaine</b> induced enhancement of brain reward function in rats.
+GRM2	addiction	relapse	20555310	The <strong>mGluR2</strong> positive allosteric modulator BINA decreases cocaine self administration and cue induced cocaine <b>seeking</b> and counteracts cocaine induced enhancement of brain reward function in rats.
+GRM2	addiction	reward	20555310	The <strong>mGluR2</strong> positive allosteric modulator BINA decreases cocaine self administration and cue induced cocaine seeking and counteracts cocaine induced enhancement of brain <b>reward</b> function in rats.
+GRM2	drug	cocaine	20555310	Metabotropic glutamate receptor 2/3 (<strong>mGluR2</strong>/3) agonists were shown previously to nonselectively decrease both <b>cocaine</b>  and food maintained responding in rats.
+GRM2	drug	cocaine	20555310	We analyzed the effects of the selective, brain penetrant, and systemically active <strong>mGluR2</strong> PAM potassium 3' ([(2 cyclopentyl 6 7 dimethyl 1 oxo 2,3 dihydro 1H inden 5 yl)oxy]methyl)biphenyl l 4 carboxylate (BINA) and the <strong>mGluR2</strong>/3 agonist LY379268 on intravenous <b>cocaine</b> self administration and <b>cocaine</b> seeking behavior in rats that had short (1 h, ShA) or long (6 h, LgA) access to <b>cocaine</b>.
+GRM2	addiction	relapse	20555310	We analyzed the effects of the selective, brain penetrant, and systemically active <strong>mGluR2</strong> PAM potassium 3' ([(2 cyclopentyl 6 7 dimethyl 1 oxo 2,3 dihydro 1H inden 5 yl)oxy]methyl)biphenyl l 4 carboxylate (BINA) and the <strong>mGluR2</strong>/3 agonist LY379268 on intravenous cocaine self administration and cocaine <b>seeking</b> behavior in rats that had short (1 h, ShA) or long (6 h, LgA) access to cocaine.
+GRM2	drug	cocaine	20555310	The higher selectivity of BINA compared with an <strong>mGluR2</strong>/3 agonist for drug  vs food motivated behaviors suggests a therapeutic role for <strong>mGluR2</strong> PAMs for the treatment of <b>cocaine</b> addiction and possibly other drugs of abuse.
+GRM2	addiction	addiction	20555310	The higher selectivity of BINA compared with an <strong>mGluR2</strong>/3 agonist for drug  vs food motivated behaviors suggests a therapeutic role for <strong>mGluR2</strong> PAMs for the treatment of cocaine <b>addiction</b> and possibly other drugs of abuse.
+GRM2	drug	cocaine	20534838	In contrast, activation of glutamate afferents onto the same DA neurons via stimulation within the VTA evoked EPSCs mediated by <strong>GluR2</strong> lacking AMPARs that demonstrated LTD or EPSCs mediated by <strong>GluR2</strong> containing AMPA receptors that did not express LTD. Twenty four hours after single <b>cocaine</b> injections to rats, <strong>GluR2</strong> lacking AMPARs were increased at both PPN and local VTA projections, and this permitted LTD expression in both pathways.
+GRM2	drug	cannabinoid	20534838	Single injections with the main psychoactive ingredient of <b>marijuana</b>, Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>), increased <strong>GluR2</strong> lacking AMPA receptors and permitted LTD in only the PPN pathway, and these effects were prevented by in vivo pretreatment with the <b>cannabinoid</b> CB1 receptor antagonist AM251.
+GRM2	drug	cannabinoid	20534838	These results demonstrate that cocaine more globally increases <strong>GluR2</strong> lacking AMPA receptors at all glutamate synapses on VTA dopamine neurons, whereas Delta(9) <b>THC</b> selectively increased <strong>GluR2</strong> lacking AMPA receptors at subcortical PPN synapses.
+GRM2	drug	cocaine	20534838	These results demonstrate that <b>cocaine</b> more globally increases <strong>GluR2</strong> lacking AMPA receptors at all glutamate synapses on VTA dopamine neurons, whereas Delta(9) THC selectively increased <strong>GluR2</strong> lacking AMPA receptors at subcortical PPN synapses.
+GRM2	drug	cocaine	20534005	Activation of mGluR7s inhibits <b>cocaine</b> induced reinstatement of drug seeking behavior by a nucleus accumbens glutamate <strong>mGluR2</strong>/3 mechanism in rats.
+GRM2	addiction	relapse	20534005	Activation of mGluR7s inhibits cocaine induced <b>reinstatement</b> of drug <b>seeking</b> behavior by a nucleus accumbens glutamate <strong>mGluR2</strong>/3 mechanism in rats.
+GRM2	drug	cocaine	20534005	Pre treatment with AMN082 dose dependently blocked both <b>cocaine</b> enhanced NAc glutamate and <b>cocaine</b> induced reinstatement, an effect that was blocked by MMPIP or LY341497 (a selective <strong>mGluR2</strong>/3 antagonist).
+GRM2	addiction	relapse	20534005	Pre treatment with AMN082 dose dependently blocked both cocaine enhanced NAc glutamate and cocaine induced <b>reinstatement</b>, an effect that was blocked by MMPIP or LY341497 (a selective <strong>mGluR2</strong>/3 antagonist).
+GRM2	drug	cocaine	20534005	These data suggest that mGluR7 activation inhibits <b>cocaine</b> induced reinstatement of drug seeking behavior by a glutamate <strong>mGluR2</strong>/3 mechanism in the NAc.
+GRM2	addiction	relapse	20534005	These data suggest that mGluR7 activation inhibits cocaine induced <b>reinstatement</b> of drug <b>seeking</b> behavior by a glutamate <strong>mGluR2</strong>/3 mechanism in the NAc.
+GRM2	drug	cocaine	20416862	Rats with 1 hour daily <b>cocaine</b> access (short access [ShA]) versus 6 hour access (long access [LgA]) were tested for differences in the effects of the metabotropic glutamate receptor 2/3 (<strong>mGluR2</strong>/3) agonist ( ) 2 oxa 4 aminobicylco(3.1.0)hexane 4,6 dicarboxylic acid (LY379268) and the metabotropic glutamate receptor 5 (mGluR5) antagonist 3 [(2 methyl 1,3 thiazol 4 yl)ethynyl] pyridine (MTEP) on <b>cocaine</b> reinforced progressive ratio responding and differences in expression levels and functional activity of <strong>mGluR2</strong>/3 and mGluR5.
+GRM2	drug	cocaine	20416862	Consistent with this behavioral effect, functional <strong>mGluR2</strong>/3 activity was significantly elevated following LgA <b>cocaine</b> exposure.
+GRM2	drug	cocaine	20416862	Functional upregulation of <strong>mGluR2</strong>/3 and downregulation of mGluR5 are likely factors in the transition to <b>cocaine</b> dependence.
+GRM2	addiction	dependence	20416862	Functional upregulation of <strong>mGluR2</strong>/3 and downregulation of mGluR5 are likely factors in the transition to cocaine <b>dependence</b>.
+GRM2	drug	cocaine	20416862	The differential behavioral effects of LY379268 and MTEP in rats with a history of long access to <b>cocaine</b> have implications for the treatment target potential of <strong>mGluR2</strong>/3 and mGluR5.
+GRM2	drug	alcohol	20189165	Effects of the <strong>mGlu2</strong>/3 agonist LY379268 and the mGlu5 antagonist MTEP on <b>ethanol</b> seeking and reinforcement are differentially altered in rats with a history of <b>ethanol</b> dependence.
+GRM2	addiction	dependence	20189165	Effects of the <strong>mGlu2</strong>/3 agonist LY379268 and the mGlu5 antagonist MTEP on ethanol seeking and reinforcement are differentially altered in rats with a history of ethanol <b>dependence</b>.
+GRM2	addiction	relapse	20189165	Effects of the <strong>mGlu2</strong>/3 agonist LY379268 and the mGlu5 antagonist MTEP on ethanol <b>seeking</b> and reinforcement are differentially altered in rats with a history of ethanol dependence.
+GRM2	addiction	reward	20189165	Effects of the <strong>mGlu2</strong>/3 agonist LY379268 and the mGlu5 antagonist MTEP on ethanol seeking and <b>reinforcement</b> are differentially altered in rats with a history of ethanol dependence.
+GRM2	drug	alcohol	20189165	To extend the understanding of the role of mGluRs in the addiction relevant effects of <b>ethanol</b> as well as of the treatment target potential of these receptors for <b>alcohol</b> abuse, the effects of a selective <strong>mGlu2</strong>/3 agonist (LY379268) and a selective mGlu5 antagonist (MTEP) were tested on two processes central to <b>alcohol</b> addiction: <b>ethanol</b> reinforcement and stress induced reinstatement of <b>ethanol</b> seeking in rats with a history of <b>ethanol</b> dependence.
+GRM2	addiction	addiction	20189165	To extend the understanding of the role of mGluRs in the <b>addiction</b> relevant effects of ethanol as well as of the treatment target potential of these receptors for alcohol abuse, the effects of a selective <strong>mGlu2</strong>/3 agonist (LY379268) and a selective mGlu5 antagonist (MTEP) were tested on two processes central to alcohol <b>addiction</b>: ethanol reinforcement and stress induced reinstatement of ethanol seeking in rats with a history of ethanol dependence.
+GRM2	addiction	dependence	20189165	To extend the understanding of the role of mGluRs in the addiction relevant effects of ethanol as well as of the treatment target potential of these receptors for alcohol abuse, the effects of a selective <strong>mGlu2</strong>/3 agonist (LY379268) and a selective mGlu5 antagonist (MTEP) were tested on two processes central to alcohol addiction: ethanol reinforcement and stress induced reinstatement of ethanol seeking in rats with a history of ethanol <b>dependence</b>.
+GRM2	addiction	relapse	20189165	To extend the understanding of the role of mGluRs in the addiction relevant effects of ethanol as well as of the treatment target potential of these receptors for alcohol abuse, the effects of a selective <strong>mGlu2</strong>/3 agonist (LY379268) and a selective mGlu5 antagonist (MTEP) were tested on two processes central to alcohol addiction: ethanol reinforcement and stress induced <b>reinstatement</b> of ethanol <b>seeking</b> in rats with a history of ethanol dependence.
+GRM2	addiction	reward	20189165	To extend the understanding of the role of mGluRs in the addiction relevant effects of ethanol as well as of the treatment target potential of these receptors for alcohol abuse, the effects of a selective <strong>mGlu2</strong>/3 agonist (LY379268) and a selective mGlu5 antagonist (MTEP) were tested on two processes central to alcohol addiction: ethanol <b>reinforcement</b> and stress induced reinstatement of ethanol seeking in rats with a history of ethanol dependence.
+GRM2	drug	alcohol	20189165	These findings suggest that neuroadaptation associated with chronic <b>ethanol</b> exposure or withdrawal alters the sensitivity of <strong>mGlu2</strong>/3 receptors, with implications for the understanding of the neural basis of <b>alcohol</b> dependence and the treatment target potential of these receptors.
+GRM2	addiction	dependence	20189165	These findings suggest that neuroadaptation associated with chronic ethanol exposure or withdrawal alters the sensitivity of <strong>mGlu2</strong>/3 receptors, with implications for the understanding of the neural basis of alcohol <b>dependence</b> and the treatment target potential of these receptors.
+GRM2	addiction	withdrawal	20189165	These findings suggest that neuroadaptation associated with chronic ethanol exposure or <b>withdrawal</b> alters the sensitivity of <strong>mGlu2</strong>/3 receptors, with implications for the understanding of the neural basis of alcohol dependence and the treatment target potential of these receptors.
+GRM2	drug	cannabinoid	20167255	The objectives of the present study were (i) to discern the CPP effects of in vivo gene silencing of accumbal CB(1) receptors by means of lentiviruses containing siRNAs; (ii) to discern the CPP effects of intra accumbens infusions of the <b>cannabinoid</b> CB(1)R ligand <b>rimonabant</b>, and to evaluate whether effects are due to receptor blockade or inverse agonism; (iii) to discern the role of CB(1)R located within the nucleus accumbens shell in the rewarding effects of cocaine, by means of local infusions of <b>rimonabant</b>, and (iv) to discern the role of glutamate receptors (AMPAR, NMDAR, <strong>mGluR2</strong>/3) in <b>rimonabant</b> induced effects on CPP in cocaine treated rats.
+GRM2	drug	cocaine	20167255	The objectives of the present study were (i) to discern the CPP effects of in vivo gene silencing of accumbal CB(1) receptors by means of lentiviruses containing siRNAs; (ii) to discern the CPP effects of intra accumbens infusions of the cannabinoid CB(1)R ligand rimonabant, and to evaluate whether effects are due to receptor blockade or inverse agonism; (iii) to discern the role of CB(1)R located within the nucleus accumbens shell in the rewarding effects of <b>cocaine</b>, by means of local infusions of rimonabant, and (iv) to discern the role of glutamate receptors (AMPAR, NMDAR, <strong>mGluR2</strong>/3) in rimonabant induced effects on CPP in <b>cocaine</b> treated rats.
+GRM2	addiction	reward	20167255	The objectives of the present study were (i) to discern the <b>CPP</b> effects of in vivo gene silencing of accumbal CB(1) receptors by means of lentiviruses containing siRNAs; (ii) to discern the <b>CPP</b> effects of intra accumbens infusions of the cannabinoid CB(1)R ligand rimonabant, and to evaluate whether effects are due to receptor blockade or inverse agonism; (iii) to discern the role of CB(1)R located within the nucleus accumbens shell in the rewarding effects of cocaine, by means of local infusions of rimonabant, and (iv) to discern the role of glutamate receptors (AMPAR, NMDAR, <strong>mGluR2</strong>/3) in rimonabant induced effects on <b>CPP</b> in cocaine treated rats.
+GRM2	drug	cannabinoid	20167255	Glutamate receptors participate in <b>rimonabant</b> mediated place preference because it was abolished after blocking AMPA glutamate receptors, but not NMDAR or <strong>mGluR2</strong>/3.
+GRM2	drug	cannabinoid	20167255	Finally, in cocaine treated rats, local <b>rimonabant</b> induced place aversion to the drug (not place preference), and this effect was mediated by glutamate neurotransmission because it was abolished after blockade of AMPA, NMDA or <strong>mGlu2</strong>/3 receptors, even though only the blockade of <strong>mGlu2</strong>/3 autoreceptors restored the emergence of place preference to cocaine.
+GRM2	drug	cocaine	20167255	Finally, in <b>cocaine</b> treated rats, local rimonabant induced place aversion to the drug (not place preference), and this effect was mediated by glutamate neurotransmission because it was abolished after blockade of AMPA, NMDA or <strong>mGlu2</strong>/3 receptors, even though only the blockade of <strong>mGlu2</strong>/3 autoreceptors restored the emergence of place preference to <b>cocaine</b>.
+GRM2	addiction	aversion	20167255	Finally, in cocaine treated rats, local rimonabant induced place <b>aversion</b> to the drug (not place preference), and this effect was mediated by glutamate neurotransmission because it was abolished after blockade of AMPA, NMDA or <strong>mGlu2</strong>/3 receptors, even though only the blockade of <strong>mGlu2</strong>/3 autoreceptors restored the emergence of place preference to cocaine.
+GRM2	drug	opioid	20159947	In addition, we provide electrophysiological evidence that AMPARs are switched to Ca(2+) permeable (<strong>GluR2</strong> lacking) at the synapse 12 h after repeated <b>morphine</b> treatment, affecting the magnitude of long term depression at hippocampal neurons.
+GRM2	drug	alcohol	20153402	The decreased expression of GLAST, GLT 1 and <strong>GluR2</strong> in the <b>alcoholic</b> patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug seeking and chronic relapse.
+GRM2	addiction	relapse	20153402	The decreased expression of GLAST, GLT 1 and <strong>GluR2</strong> in the alcoholic patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug <b>seeking</b> and chronic <b>relapse</b>.
+GRM2	drug	alcohol	19897175	This study sought to evaluate the functional role of Group I (mGluR5) and Group II (<strong>mGluR2</strong>/3) in mesocorticolimbic brain regions in <b>ethanol</b> self administration.
+GRM2	drug	cocaine	19895667	Inhibition of NAALADase by 2 PMPA attenuates <b>cocaine</b> induced relapse in rats: a NAAG <strong>mGluR2</strong>/3 mediated mechanism.
+GRM2	addiction	relapse	19895667	Inhibition of NAALADase by 2 PMPA attenuates cocaine induced <b>relapse</b> in rats: a NAAG <strong>mGluR2</strong>/3 mediated mechanism.
+GRM2	drug	cocaine	19895667	Pharmacological activation of group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) inhibits <b>cocaine</b> self administration and reinstatement of drug seeking behavior, suggesting a possible use of <strong>mGluR2</strong>/3 agonists in the treatment of <b>cocaine</b> dependence.
+GRM2	addiction	dependence	19895667	Pharmacological activation of group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) inhibits cocaine self administration and reinstatement of drug seeking behavior, suggesting a possible use of <strong>mGluR2</strong>/3 agonists in the treatment of cocaine <b>dependence</b>.
+GRM2	addiction	relapse	19895667	Pharmacological activation of group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) inhibits cocaine self administration and <b>reinstatement</b> of drug <b>seeking</b> behavior, suggesting a possible use of <strong>mGluR2</strong>/3 agonists in the treatment of cocaine dependence.
+GRM2	drug	cocaine	19895667	In this study, we investigated whether elevation of the endogenous <strong>mGluR2</strong>/3 ligand N acetyl aspartatylglutamate (NAAG) levels by the N acetylated alpha linked acidic dipeptidase inhibitor 2 (phosphonomethyl)pentanedioic acid (2 PMPA) attenuates <b>cocaine</b> self administration and <b>cocaine</b> induced reinstatement of drug seeking.
+GRM2	addiction	relapse	19895667	In this study, we investigated whether elevation of the endogenous <strong>mGluR2</strong>/3 ligand N acetyl aspartatylglutamate (NAAG) levels by the N acetylated alpha linked acidic dipeptidase inhibitor 2 (phosphonomethyl)pentanedioic acid (2 PMPA) attenuates cocaine self administration and cocaine induced <b>reinstatement</b> of drug <b>seeking</b>.
+GRM2	drug	cocaine	19895667	Microinjections of 2 PMPA (3 5 microg/side) or NAAG (3 5 microg/side) into the nucleus accumbens (NAc), but not into the dorsal striatum, also inhibited <b>cocaine</b> induced reinstatement, an effect that was blocked by intra NAc injection of LY341495, a selective <strong>mGluR2</strong>/3 antagonist.
+GRM2	addiction	relapse	19895667	Microinjections of 2 PMPA (3 5 microg/side) or NAAG (3 5 microg/side) into the nucleus accumbens (NAc), but not into the dorsal striatum, also inhibited cocaine induced <b>reinstatement</b>, an effect that was blocked by intra NAc injection of LY341495, a selective <strong>mGluR2</strong>/3 antagonist.
+GRM2	drug	cocaine	19895667	These findings suggest that 2 PMPA is effective in attenuating <b>cocaine</b> induced reinstatement of drug seeking behavior, likely by attenuating <b>cocaine</b> induced increases in NAc DA and glutamate via pre synaptic <strong>mGluR2</strong>/3s.
+GRM2	addiction	relapse	19895667	These findings suggest that 2 PMPA is effective in attenuating cocaine induced <b>reinstatement</b> of drug <b>seeking</b> behavior, likely by attenuating cocaine induced increases in NAc DA and glutamate via pre synaptic <strong>mGluR2</strong>/3s.
+GRM2	drug	cocaine	19887067	We have recently reported that the endogenous <strong>mGlu2</strong>/3 agonist N acetylaspartylglutamate (NAAG) and the N acetylated alpha linked acidic dipeptidase (NAALADase, a NAAG degradation enzyme) inhibitor 2 PMPA significantly inhibit <b>cocaine</b> self administration and <b>cocaine</b> induced reinstatement of drug seeking behavior by attenuating <b>cocaine</b> enhanced extracellular dopamine and glutamate in the nucleus accumbens.
+GRM2	addiction	relapse	19887067	We have recently reported that the endogenous <strong>mGlu2</strong>/3 agonist N acetylaspartylglutamate (NAAG) and the N acetylated alpha linked acidic dipeptidase (NAALADase, a NAAG degradation enzyme) inhibitor 2 PMPA significantly inhibit cocaine self administration and cocaine induced <b>reinstatement</b> of drug <b>seeking</b> behavior by attenuating cocaine enhanced extracellular dopamine and glutamate in the nucleus accumbens.
+GRM2	drug	cocaine	19703487	Interactions between the <strong>mGluR2</strong>/3 agonist, LY379268, and <b>cocaine</b> on in vivo neurochemistry and behavior in squirrel monkeys.
+GRM2	drug	cocaine	19703487	Recent evidence indicates that group II metabotropic glutamate receptors (<strong>mGluR2</strong> and mGluR3) may play a role in the pathology of <b>cocaine</b> addiction.
+GRM2	addiction	addiction	19703487	Recent evidence indicates that group II metabotropic glutamate receptors (<strong>mGluR2</strong> and mGluR3) may play a role in the pathology of cocaine <b>addiction</b>.
+GRM2	drug	cocaine	19703487	The purpose of the current study was to determine the effects of the <strong>mGluR2</strong>/3 agonist, LY379268, on <b>cocaine</b> induced changes in DA neurochemistry in nonhuman primates.
+GRM2	drug	cocaine	19559037	Pharmacological activation of group II metabotropic glutamate (<strong>mGlu2</strong> and mGlu3) receptors inhibits reward seeking behavior and/or rewarding efficacy induced by drugs (<b>cocaine</b>, nicotine) or natural rewards (food, sucrose).
+GRM2	drug	nicotine	19559037	Pharmacological activation of group II metabotropic glutamate (<strong>mGlu2</strong> and mGlu3) receptors inhibits reward seeking behavior and/or rewarding efficacy induced by drugs (cocaine, <b>nicotine</b>) or natural rewards (food, sucrose).
+GRM2	addiction	relapse	19559037	Pharmacological activation of group II metabotropic glutamate (<strong>mGlu2</strong> and mGlu3) receptors inhibits reward <b>seeking</b> behavior and/or rewarding efficacy induced by drugs (cocaine, nicotine) or natural rewards (food, sucrose).
+GRM2	addiction	reward	19559037	Pharmacological activation of group II metabotropic glutamate (<strong>mGlu2</strong> and mGlu3) receptors inhibits <b>reward</b> seeking behavior and/or rewarding efficacy induced by drugs (cocaine, nicotine) or natural rewards (food, sucrose).
+GRM2	drug	cocaine	19559037	These findings suggest that systemic administration of 2 PMPA or intranasal administration of NAAG inhibits <b>cocaine</b>'s rewarding efficacy and <b>cocaine</b> enhanced NAc DA   likely by activation of presynaptic <strong>mGlu2</strong>/3 receptors in the NAc.
+GRM2	drug	amphetamine	19183251	In contrast to our previous results in cocaine sensitized rats, we did not observe redistribution of GluR1 or <strong>GluR2</strong> to the cell surface in the NAc after <b>amphetamine</b> withdrawal, although a small increase in total GluR1 was found in the shell subregion.
+GRM2	drug	cocaine	19183251	In contrast to our previous results in <b>cocaine</b> sensitized rats, we did not observe redistribution of GluR1 or <strong>GluR2</strong> to the cell surface in the NAc after amphetamine withdrawal, although a small increase in total GluR1 was found in the shell subregion.
+GRM2	addiction	withdrawal	19183251	In contrast to our previous results in cocaine sensitized rats, we did not observe redistribution of GluR1 or <strong>GluR2</strong> to the cell surface in the NAc after amphetamine <b>withdrawal</b>, although a small increase in total GluR1 was found in the shell subregion.
+GRM2	drug	opioid	19160503	Here we show in a rat self administration model that reexposure to cues previously associated with <b>heroin</b> results in downregulation of AMPA receptor subunit <strong>GluR2</strong> and concomitant upregulation of clathrin coat assembly protein AP2ml in synaptic membranes of the medial prefrontal cortex (mPFC).
+GRM2	drug	opioid	19160503	Systemic or ventral (but not dorsal) mPFC injections of a peptide inhibiting <strong>GluR2</strong> endocytosis attenuated both the rectification index and cue induced relapse to <b>heroin</b> seeking, without affecting sucrose seeking.
+GRM2	addiction	relapse	19160503	Systemic or ventral (but not dorsal) mPFC injections of a peptide inhibiting <strong>GluR2</strong> endocytosis attenuated both the rectification index and cue induced <b>relapse</b> to heroin <b>seeking</b>, without affecting sucrose <b>seeking</b>.
+GRM2	drug	opioid	19160503	We conclude that <strong>GluR2</strong> receptor endocytosis and the resulting synaptic depression in ventral mPFC are crucial for cue induced relapse to <b>heroin</b> seeking.
+GRM2	addiction	relapse	19160503	We conclude that <strong>GluR2</strong> receptor endocytosis and the resulting synaptic depression in ventral mPFC are crucial for cue induced <b>relapse</b> to heroin <b>seeking</b>.
+GRM2	drug	opioid	19160503	As reexposure to conditioned stimuli is a major cause for <b>heroin</b> relapse, inhibition of <strong>GluR2</strong> endocytosis may provide a new target for the treatment of <b>heroin</b> addiction.
+GRM2	addiction	addiction	19160503	As reexposure to conditioned stimuli is a major cause for heroin relapse, inhibition of <strong>GluR2</strong> endocytosis may provide a new target for the treatment of heroin <b>addiction</b>.
+GRM2	addiction	relapse	19160503	As reexposure to conditioned stimuli is a major cause for heroin <b>relapse</b>, inhibition of <strong>GluR2</strong> endocytosis may provide a new target for the treatment of heroin addiction.
+GRM2	drug	cocaine	19128205	The <strong>mGluR2</strong>/3 agonist LY379268 is effective in inhibiting <b>cocaine</b> seeking in preclinical animal models and could decrease stress induced relapse due to its anxiolytic effects.
+GRM2	addiction	relapse	19128205	The <strong>mGluR2</strong>/3 agonist LY379268 is effective in inhibiting cocaine <b>seeking</b> in preclinical animal models and could decrease stress induced <b>relapse</b> due to its anxiolytic effects.
+GRM2	addiction	withdrawal	19105975	At 21 days of <b>withdrawal</b>, there was a decrease in the expression of <strong>mGluR2</strong>/3 protein in core and shell, an increase in GluR1 and a decrease in Homer1b/c proteins in the nucleus accumbens core tissue.
+GRM2	drug	cocaine	19084053	By using experimental values for <b>cocaine</b> induced reductions in cystine glutamate exchange and <strong>mGluR2</strong>/3 signaling, and by predicting the down regulation of glutamate transporters, the computational model successfully represented the experimentally observed increase in glutamate that is seen in rats during <b>cocaine</b> seeking.
+GRM2	addiction	relapse	19084053	By using experimental values for cocaine induced reductions in cystine glutamate exchange and <strong>mGluR2</strong>/3 signaling, and by predicting the down regulation of glutamate transporters, the computational model successfully represented the experimentally observed increase in glutamate that is seen in rats during cocaine <b>seeking</b>.
+GRM2	drug	opioid	19077125	Results showed that <b>morphine</b> dependent CRs did not alter expression or redistribution of GluR1 or <strong>GluR2</strong>; however, the unpaired administration of <b>morphine</b> resulted in an increase in the phosphorylation of the GluR1 subunit at extrasynaptic sites.
+GRM2	drug	opioid	18957577	It is surprising that continuous subcutaneous infusion of the <strong>GluR2</strong>/GluR5 preferring antagonist LY293558 [(3S,4aR,6R,8aR) 6 [2 (1(2)H tetrazole 5 yl)ethyl]decahydroisoquinoline 3 carboxylic acid] decreased the number of <b>naloxone</b> precipitated jumps to a similar extent in WT and GluR5 KO mice.
+GRM2	drug	cocaine	18945913	Phosphorylation dependent trafficking of <strong>GluR2</strong> containing AMPA receptors in the nucleus accumbens plays a critical role in the reinstatement of <b>cocaine</b> seeking.
+GRM2	addiction	relapse	18945913	Phosphorylation dependent trafficking of <strong>GluR2</strong> containing AMPA receptors in the nucleus accumbens plays a critical role in the <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM2	drug	cocaine	18945913	<b>Cocaine</b> priming induced reinstatement of <b>cocaine</b> seeking also was associated with increases in <strong>GluR2</strong> pSer880 in the nucleus accumbens shell.
+GRM2	addiction	relapse	18945913	Cocaine priming induced <b>reinstatement</b> of cocaine <b>seeking</b> also was associated with increases in <strong>GluR2</strong> pSer880 in the nucleus accumbens shell.
+GRM2	drug	cocaine	18945913	The current results showed that administration of a cell permeable peptide that disrupts <strong>GluR2</strong> trafficking (Pep2 EVKI) into either the accumbens core or shell attenuated <b>cocaine</b> induced reinstatement of drug seeking.
+GRM2	addiction	relapse	18945913	The current results showed that administration of a cell permeable peptide that disrupts <strong>GluR2</strong> trafficking (Pep2 EVKI) into either the accumbens core or shell attenuated cocaine induced <b>reinstatement</b> of drug <b>seeking</b>.
+GRM2	drug	cocaine	18945913	The present results also demonstrate that the reinstatement of <b>cocaine</b> seeking is associated with increases in the phosphorylation dependent trafficking of <strong>GluR2</strong> containing AMPA receptors in the nucleus accumbens.
+GRM2	addiction	relapse	18945913	The present results also demonstrate that the <b>reinstatement</b> of cocaine <b>seeking</b> is associated with increases in the phosphorylation dependent trafficking of <strong>GluR2</strong> containing AMPA receptors in the nucleus accumbens.
+GRM2	addiction	withdrawal	18924138	To test this hypothesis, the postsynaptic incorporation of GluR1 and <strong>GluR2</strong> subunits in CA1 neurons after FZP <b>withdrawal</b> was examined by postembedding immunogold quantitative electron microscopy.
+GRM2	drug	opioid	18671727	Decreased AMPA <strong>GluR2</strong>, but not GluR3, mRNA expression in rat amygdala and dorsal hippocampus following <b>morphine</b> induced behavioural sensitization.
+GRM2	addiction	sensitization	18671727	Decreased AMPA <strong>GluR2</strong>, but not GluR3, mRNA expression in rat amygdala and dorsal hippocampus following morphine induced behavioural <b>sensitization</b>.
+GRM2	drug	opioid	18671727	In order to evaluate the mechanism underlying the behavioural responses, quantitative real time reverse transcription polymerase chain reaction was used to evaluate mRNA expression of the AMPA receptor subunits <strong>GluR2</strong> and GluR3 in the striatum, prefrontal cortex, hippocampus, hypothalamus and amygdala of animals treated repeatedly with <b>morphine</b>.
+GRM2	drug	opioid	18671727	In addition, repeated <b>morphine</b> treatment followed by 7 days (but not 24 h) washout decreased <strong>GluR2</strong> mRNA expression in both the amygdala (by 50%) and hippocampus (by 35%).
+GRM2	addiction	sensitization	18671727	The decreases in <strong>GluR2</strong> mRNA expression in the amygdala and hippocampus may result in the formation of calcium permeable AMPA receptors, which are believed to play an important role in behavioural <b>sensitization</b>.
+GRM2	drug	opioid	18520992	We examined the effects of chronic <b>morphine</b> treatment and withdrawal on the expression of metabotropic glutamate (mGlu)1, mGlu5, and <strong>mGlu2</strong>/3 receptors in the nucleus accumbens and caudate putamen.
+GRM2	addiction	withdrawal	18520992	We examined the effects of chronic morphine treatment and <b>withdrawal</b> on the expression of metabotropic glutamate (mGlu)1, mGlu5, and <strong>mGlu2</strong>/3 receptors in the nucleus accumbens and caudate putamen.
+GRM2	addiction	withdrawal	18520992	In contrast, <strong>mGlu2</strong>/3 receptors in the nucleus accumbens, but not in the caudate putamen, increased at day 1, 3, and 14 of <b>withdrawal</b>.
+GRM2	drug	opioid	18520992	We suggest that an increased expression of <strong>mGlu2</strong>/3 receptors in the nucleus accumbens might contribute to the symptoms of <b>morphine</b> withdrawal.
+GRM2	addiction	withdrawal	18520992	We suggest that an increased expression of <strong>mGlu2</strong>/3 receptors in the nucleus accumbens might contribute to the symptoms of morphine <b>withdrawal</b>.
+GRM2	drug	cocaine	18500330	Formation of accumbens <strong>GluR2</strong> lacking AMPA receptors mediates incubation of <b>cocaine</b> craving.
+GRM2	addiction	relapse	18500330	Formation of accumbens <strong>GluR2</strong> lacking AMPA receptors mediates incubation of cocaine <b>craving</b>.
+GRM2	drug	cocaine	18500330	Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged withdrawal from <b>cocaine</b> self administration by the addition of new AMPA receptors lacking glutamate receptor 2 (<strong>GluR2</strong>).
+GRM2	addiction	withdrawal	18500330	Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged <b>withdrawal</b> from cocaine self administration by the addition of new AMPA receptors lacking glutamate receptor 2 (<strong>GluR2</strong>).
+GRM2	drug	cocaine	18500330	Our results indicate that <strong>GluR2</strong> lacking AMPA receptors could be a new target for drug development for the treatment of <b>cocaine</b> addiction.
+GRM2	addiction	addiction	18500330	Our results indicate that <strong>GluR2</strong> lacking AMPA receptors could be a new target for drug development for the treatment of cocaine <b>addiction</b>.
+GRM2	drug	cocaine	18500330	We propose that after prolonged withdrawal from <b>cocaine</b>, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong>GluR2</strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to <b>cocaine</b> related cues, leading to an intensification of drug craving and relapse.
+GRM2	addiction	relapse	18500330	We propose that after prolonged withdrawal from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong>GluR2</strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine related cues, leading to an intensification of drug <b>craving</b> and <b>relapse</b>.
+GRM2	addiction	withdrawal	18500330	We propose that after prolonged <b>withdrawal</b> from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of <strong>GluR2</strong> lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine related cues, leading to an intensification of drug craving and relapse.
+GRM2	drug	alcohol	18420113	Effects of the <strong>mGluR2</strong>/3 agonist LY379268 and the mGluR5 antagonist MPEP on handling induced convulsions during <b>ethanol</b> withdrawal in mice.
+GRM2	addiction	withdrawal	18420113	Effects of the <strong>mGluR2</strong>/3 agonist LY379268 and the mGluR5 antagonist MPEP on handling induced convulsions during ethanol <b>withdrawal</b> in mice.
+GRM2	drug	alcohol	18420113	Therefore, the present study was designed to determine the effects the <strong>mGluR2</strong>/3 agonist LY379268 and the mGluR5 antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) on <b>ethanol</b> withdrawal induced seizure activity.
+GRM2	addiction	withdrawal	18420113	Therefore, the present study was designed to determine the effects the <strong>mGluR2</strong>/3 agonist LY379268 and the mGluR5 antagonist 2 methyl 6 (phenylethynyl) pyridine (MPEP) on ethanol <b>withdrawal</b> induced seizure activity.
+GRM2	drug	alcohol	18420113	These results suggest that inhibition of glutamate transmission by <strong>mGluR2</strong>/3 agonists or mGluR5 antagonists does not alter HIC activity during withdrawal from repeated <b>ethanol</b> exposure, and as such these compounds may have limited usefulness in the treatment of central nervous system hyperexcitability during <b>alcohol</b> withdrawal.
+GRM2	addiction	withdrawal	18420113	These results suggest that inhibition of glutamate transmission by <strong>mGluR2</strong>/3 agonists or mGluR5 antagonists does not alter HIC activity during <b>withdrawal</b> from repeated ethanol exposure, and as such these compounds may have limited usefulness in the treatment of central nervous system hyperexcitability during alcohol <b>withdrawal</b>.
+GRM2	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, <strong>GluR2</strong>, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRM2	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, <strong>GluR2</strong>, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, <strong>mGluR2</strong>, mGluR3, mGluR5) in six different brain regions.
+GRM2	drug	nicotine	18261852	Voluntary oral <b>nicotine</b> intake in mice down regulates <strong>GluR2</strong> but does not modulate depression like behaviors.
+GRM2	drug	nicotine	18261852	There were few behavioral changes in mice subjected to chronic <b>nicotine</b> exposure, but there was a marked regulation of <strong>GluR2</strong> in the mesolimbic system.
+GRM2	drug	cocaine	17898233	Glutamate receptor 1 (GluR1) and <strong>GluR2</strong> surface/intracellular (S/I) ratios were increased after 14 d of withdrawal in sensitized rats but were decreased 24 h after challenge with <b>cocaine</b> (which elicited a sensitized locomotor response) or saline (which elicited conditioned locomotion).
+GRM2	addiction	withdrawal	17898233	Glutamate receptor 1 (GluR1) and <strong>GluR2</strong> surface/intracellular (S/I) ratios were increased after 14 d of <b>withdrawal</b> in sensitized rats but were decreased 24 h after challenge with cocaine (which elicited a sensitized locomotor response) or saline (which elicited conditioned locomotion).
+GRM2	drug	cocaine	17898233	JNK phosphorylation also increased after withdrawal, but after <b>cocaine</b> challenge, it was inversely related to GluR1 and <strong>GluR2</strong> S/I ratios.
+GRM2	addiction	withdrawal	17898233	JNK phosphorylation also increased after <b>withdrawal</b>, but after cocaine challenge, it was inversely related to GluR1 and <strong>GluR2</strong> S/I ratios.
+GRM2	addiction	relapse	17895914	Metabotropic glutamate 2/3 receptors (<strong>mGluR2</strong>/3) are emerging targets for the reduction of stress that contributes to drug <b>relapse</b>.
+GRM2	drug	cocaine	17895914	The effect of a history of <b>cocaine</b> escalation on stress reactivity during abstinence and the role of <strong>mGlu2</strong>/3 receptors in stress in these animals were tested.
+GRM2	addiction	addiction	17895914	The effect of a history of cocaine <b>escalation</b> on stress reactivity during abstinence and the role of <strong>mGlu2</strong>/3 receptors in stress in these animals were tested.
+GRM2	drug	cocaine	17895914	The anxiolytic like effects of LY379268 identify <strong>mGlu2</strong>/3 receptors as targets for ameliorating stress associated relapse risk, and point toward the possibility that a history of <b>cocaine</b> escalation in rats may modify glutamatergic function.
+GRM2	addiction	addiction	17895914	The anxiolytic like effects of LY379268 identify <strong>mGlu2</strong>/3 receptors as targets for ameliorating stress associated relapse risk, and point toward the possibility that a history of cocaine <b>escalation</b> in rats may modify glutamatergic function.
+GRM2	addiction	relapse	17895914	The anxiolytic like effects of LY379268 identify <strong>mGlu2</strong>/3 receptors as targets for ameliorating stress associated <b>relapse</b> risk, and point toward the possibility that a history of cocaine escalation in rats may modify glutamatergic function.
+GRM2	drug	nicotine	17715344	We found that acute systemic, as well as intra VTA or intra NAc, administration of the <strong>mGlu2</strong>/3 receptor agonist LY379268 [( ) 2 oxa 4 aminobicyclo[3.1.0]hexane 4,6 dicarboxylate] decreased <b>nicotine</b>, but not food, self administration in rats.
+GRM2	drug	nicotine	17715344	In addition, <b>nicotine</b> self administration downregulated <strong>mGlu2</strong>/3 receptor function in corticolimbic rat brain sites including the VTA and the NAc, demonstrated by decreased coupling of <strong>mGlu2</strong>/3 receptors to G proteins in the [35S]GTPgammaS binding assay.
+GRM2	drug	nicotine	17715344	Together, these findings indicate an important role for <strong>mGlu2</strong>/3 receptors in the posterior VTA and the NAc shell in the mediation of the rewarding effects of <b>nicotine</b> and potentially in cue induced <b>nicotine</b> seeking behavior.
+GRM2	addiction	relapse	17715344	Together, these findings indicate an important role for <strong>mGlu2</strong>/3 receptors in the posterior VTA and the NAc shell in the mediation of the rewarding effects of nicotine and potentially in cue induced nicotine <b>seeking</b> behavior.
+GRM2	drug	nicotine	17601493	In laboratory animals, the <strong>mGlu2</strong>/3 receptor agonist LY379268 has been previously shown to decrease intravenous <b>nicotine</b> self administration and cue induced reinstatement of <b>nicotine</b> seeking behavior.
+GRM2	addiction	relapse	17601493	In laboratory animals, the <strong>mGlu2</strong>/3 receptor agonist LY379268 has been previously shown to decrease intravenous nicotine self administration and cue induced <b>reinstatement</b> of nicotine <b>seeking</b> behavior.
+GRM2	drug	nicotine	17601493	Such <strong>mGlu2</strong>/3 receptor agonists may therefore be useful medications to assist people in <b>smoking</b> cessation.
+GRM2	drug	nicotine	17601493	Because of the demonstrated preclinical efficacy of <strong>mGlu2</strong>/3 receptor agonists in decreasing the primary rewarding and conditioned effects of <b>nicotine</b> in rats, we wished to examine whether such compounds could potentially influence additional aspects of <b>nicotine</b> dependence, such as <b>nicotine</b> withdrawal.
+GRM2	addiction	dependence	17601493	Because of the demonstrated preclinical efficacy of <strong>mGlu2</strong>/3 receptor agonists in decreasing the primary rewarding and conditioned effects of nicotine in rats, we wished to examine whether such compounds could potentially influence additional aspects of nicotine <b>dependence</b>, such as nicotine withdrawal.
+GRM2	addiction	withdrawal	17601493	Because of the demonstrated preclinical efficacy of <strong>mGlu2</strong>/3 receptor agonists in decreasing the primary rewarding and conditioned effects of nicotine in rats, we wished to examine whether such compounds could potentially influence additional aspects of nicotine dependence, such as nicotine <b>withdrawal</b>.
+GRM2	drug	nicotine	17601493	We hypothesized that an <strong>mGlu2</strong>/3 receptor agonist would have negative effects on <b>nicotine</b> withdrawal because <strong>mGlu2</strong>/3 receptor antagonists have previously been shown to attenuate <b>nicotine</b> withdrawal induced reward deficits, while an <strong>mGlu2</strong>/3 receptor agonist precipitated withdrawal like reward deficits in rats dependent on <b>nicotine</b>.
+GRM2	addiction	reward	17601493	We hypothesized that an <strong>mGlu2</strong>/3 receptor agonist would have negative effects on nicotine withdrawal because <strong>mGlu2</strong>/3 receptor antagonists have previously been shown to attenuate nicotine withdrawal induced <b>reward</b> deficits, while an <strong>mGlu2</strong>/3 receptor agonist precipitated withdrawal like <b>reward</b> deficits in rats dependent on nicotine.
+GRM2	addiction	withdrawal	17601493	We hypothesized that an <strong>mGlu2</strong>/3 receptor agonist would have negative effects on nicotine <b>withdrawal</b> because <strong>mGlu2</strong>/3 receptor antagonists have previously been shown to attenuate nicotine <b>withdrawal</b> induced reward deficits, while an <strong>mGlu2</strong>/3 receptor agonist precipitated <b>withdrawal</b> like reward deficits in rats dependent on nicotine.
+GRM2	drug	nicotine	17601493	To test this hypothesis, we assessed the effects of the <strong>mGlu2</strong>/3 receptor agonist LY379268 on brain reward deficits associated with spontaneous <b>nicotine</b> withdrawal in rats.
+GRM2	addiction	reward	17601493	To test this hypothesis, we assessed the effects of the <strong>mGlu2</strong>/3 receptor agonist LY379268 on brain <b>reward</b> deficits associated with spontaneous nicotine withdrawal in rats.
+GRM2	addiction	withdrawal	17601493	To test this hypothesis, we assessed the effects of the <strong>mGlu2</strong>/3 receptor agonist LY379268 on brain reward deficits associated with spontaneous nicotine <b>withdrawal</b> in rats.
+GRM2	drug	nicotine	17601493	Thus, this <strong>mGlu2</strong>/3 agonist does not appear to significantly influence the affective depression like aspects of <b>nicotine</b> withdrawal.
+GRM2	addiction	withdrawal	17601493	Thus, this <strong>mGlu2</strong>/3 agonist does not appear to significantly influence the affective depression like aspects of nicotine <b>withdrawal</b>.
+GRM2	addiction	relapse	17537525	Systemic and central amygdala injections of the <strong>mGluR2</strong>/3 agonist LY379268 attenuate the expression of incubation of sucrose <b>craving</b> in rats.
+GRM2	addiction	withdrawal	17510319	Confocal image analysis revealed that FZP <b>withdrawal</b> promoted GluR1 subunit incorporation into somatic and proximal dendritic membranes of CA1 neurons without <strong>GluR2</strong> subunit alterations.
+GRM2	drug	nicotine	17113075	Interactive effects of the mGlu5 receptor antagonist MPEP and the <strong>mGlu2</strong>/3 receptor antagonist LY341495 on <b>nicotine</b> self administration and reward deficits associated with <b>nicotine</b> withdrawal in rats.
+GRM2	addiction	reward	17113075	Interactive effects of the mGlu5 receptor antagonist MPEP and the <strong>mGlu2</strong>/3 receptor antagonist LY341495 on nicotine self administration and <b>reward</b> deficits associated with nicotine withdrawal in rats.
+GRM2	addiction	withdrawal	17113075	Interactive effects of the mGlu5 receptor antagonist MPEP and the <strong>mGlu2</strong>/3 receptor antagonist LY341495 on nicotine self administration and reward deficits associated with nicotine <b>withdrawal</b> in rats.
+GRM2	drug	nicotine	17113075	Because both presynaptic inhibitory <strong>mGlu2</strong>/3 and postsynaptic excitatory mGlu5 receptors provide potential targets for treatment of aspects of <b>nicotine</b> dependence, we examined interacting effects of mGlu5 (2 methyl 6 (phenylethynyl) pyridine, MPEP) and <strong>mGlu2</strong>/3 (LY341495) receptor antagonists on <b>nicotine</b> self administration and brain reward threshold elevations associated with spontaneous <b>nicotine</b> withdrawal in rats.
+GRM2	addiction	dependence	17113075	Because both presynaptic inhibitory <strong>mGlu2</strong>/3 and postsynaptic excitatory mGlu5 receptors provide potential targets for treatment of aspects of nicotine <b>dependence</b>, we examined interacting effects of mGlu5 (2 methyl 6 (phenylethynyl) pyridine, MPEP) and <strong>mGlu2</strong>/3 (LY341495) receptor antagonists on nicotine self administration and brain reward threshold elevations associated with spontaneous nicotine withdrawal in rats.
+GRM2	addiction	reward	17113075	Because both presynaptic inhibitory <strong>mGlu2</strong>/3 and postsynaptic excitatory mGlu5 receptors provide potential targets for treatment of aspects of nicotine dependence, we examined interacting effects of mGlu5 (2 methyl 6 (phenylethynyl) pyridine, MPEP) and <strong>mGlu2</strong>/3 (LY341495) receptor antagonists on nicotine self administration and brain <b>reward</b> threshold elevations associated with spontaneous nicotine withdrawal in rats.
+GRM2	addiction	withdrawal	17113075	Because both presynaptic inhibitory <strong>mGlu2</strong>/3 and postsynaptic excitatory mGlu5 receptors provide potential targets for treatment of aspects of nicotine dependence, we examined interacting effects of mGlu5 (2 methyl 6 (phenylethynyl) pyridine, MPEP) and <strong>mGlu2</strong>/3 (LY341495) receptor antagonists on nicotine self administration and brain reward threshold elevations associated with spontaneous nicotine <b>withdrawal</b> in rats.
+GRM2	drug	nicotine	17113075	We hypothesized that increasing glutamate transmission by blocking presynaptic inhibitory <strong>mGlu2</strong>/3 autoreceptors would antagonize MPEP induced decreases in <b>nicotine</b> self administration.
+GRM2	drug	nicotine	17113075	We also hypothesized that blocking postsynaptic actions of glutamate on mGlu5 receptors would exacerbate <b>nicotine</b> withdrawal induced reward deficits, and that this effect would be attenuated by co administration of the <strong>mGlu2</strong>/3 receptor antagonist LY341495.
+GRM2	addiction	reward	17113075	We also hypothesized that blocking postsynaptic actions of glutamate on mGlu5 receptors would exacerbate nicotine withdrawal induced <b>reward</b> deficits, and that this effect would be attenuated by co administration of the <strong>mGlu2</strong>/3 receptor antagonist LY341495.
+GRM2	addiction	withdrawal	17113075	We also hypothesized that blocking postsynaptic actions of glutamate on mGlu5 receptors would exacerbate nicotine <b>withdrawal</b> induced reward deficits, and that this effect would be attenuated by co administration of the <strong>mGlu2</strong>/3 receptor antagonist LY341495.
+GRM2	drug	nicotine	17113075	Thus, increasing glutamate transmission via <strong>mGlu2</strong>/3 autoreceptor blockade reduces the effects of mGlu5 receptor blockade on <b>nicotine</b> self administration and MPEP induced exacerbation of brain reward deficits associated with <b>nicotine</b> withdrawal.
+GRM2	addiction	reward	17113075	Thus, increasing glutamate transmission via <strong>mGlu2</strong>/3 autoreceptor blockade reduces the effects of mGlu5 receptor blockade on nicotine self administration and MPEP induced exacerbation of brain <b>reward</b> deficits associated with nicotine withdrawal.
+GRM2	addiction	withdrawal	17113075	Thus, increasing glutamate transmission via <strong>mGlu2</strong>/3 autoreceptor blockade reduces the effects of mGlu5 receptor blockade on nicotine self administration and MPEP induced exacerbation of brain reward deficits associated with nicotine <b>withdrawal</b>.
+GRM2	addiction	reward	17093088	Here, we used herpes simplex virus vectors to examine how transient increases in the expression of GluR1 or <strong>GluR2</strong> protein in the shell component of NAc affect the rewarding impact of electrical stimulation of the medial forebrain bundle, as reflected by intracranial self stimulation (<b>ICSS</b>) thresholds in rats.
+GRM2	addiction	reward	17093088	In contrast, elevated <strong>GluR2</strong> decreases <b>ICSS</b> thresholds, an effect similar to that caused by rewarding treatments (e.g., drugs of abuse).
+GRM2	drug	cocaine	16914679	Blockade of NAc metabotropic glutamate <strong>mGluR2</strong>/3 receptors by LY341495 [(2S) 2 amino 2 [(1S,2S) 2 carboxycycloprop 1 yl] 3 (xanth 9 yl) propanoic acid] slightly facilitated <b>cocaine</b> enhanced glutamate release but blocked the antagonism of <b>cocaine</b> induced reinstatement by AM251.
+GRM2	addiction	relapse	16914679	Blockade of NAc metabotropic glutamate <strong>mGluR2</strong>/3 receptors by LY341495 [(2S) 2 amino 2 [(1S,2S) 2 carboxycycloprop 1 yl] 3 (xanth 9 yl) propanoic acid] slightly facilitated cocaine enhanced glutamate release but blocked the antagonism of cocaine induced <b>reinstatement</b> by AM251.
+GRM2	drug	cocaine	16914679	These data suggest the following: (1) CB1 receptors exert tonic inhibition over NAc glutamate release under <b>cocaine</b> extinction conditions; (2) blockade of CB1 receptors by AM251 inhibits <b>cocaine</b> enhanced NAc glutamate release and <b>cocaine</b> triggered reinstatement; and (3) these effects appear to be mediated by activation of presynaptic <strong>mGluR2</strong>/3 autoreceptors secondary to AM251 induced increase (disinhibition) of NAc glutamate release.
+GRM2	addiction	relapse	16914679	These data suggest the following: (1) CB1 receptors exert tonic inhibition over NAc glutamate release under cocaine extinction conditions; (2) blockade of CB1 receptors by AM251 inhibits cocaine enhanced NAc glutamate release and cocaine triggered <b>reinstatement</b>; and (3) these effects appear to be mediated by activation of presynaptic <strong>mGluR2</strong>/3 autoreceptors secondary to AM251 induced increase (disinhibition) of NAc glutamate release.
+GRM2	drug	cocaine	16893525	Here, we further explored the role of central amygdala glutamate in the incubation of <b>cocaine</b> craving by determining the effect of systemic or central amygdala injections of the <strong>mGluR2</strong>/3 agonist LY379268 (which decreases glutamate release) on cue induced <b>cocaine</b> seeking during early and late withdrawal.
+GRM2	addiction	relapse	16893525	Here, we further explored the role of central amygdala glutamate in the incubation of cocaine <b>craving</b> by determining the effect of systemic or central amygdala injections of the <strong>mGluR2</strong>/3 agonist LY379268 (which decreases glutamate release) on cue induced cocaine <b>seeking</b> during early and late withdrawal.
+GRM2	addiction	withdrawal	16893525	Here, we further explored the role of central amygdala glutamate in the incubation of cocaine craving by determining the effect of systemic or central amygdala injections of the <strong>mGluR2</strong>/3 agonist LY379268 (which decreases glutamate release) on cue induced cocaine seeking during early and late <b>withdrawal</b>.
+GRM2	addiction	relapse	16834996	The <strong>mGluR2</strong>/3 agonist LY379268 attenuates context  and discrete cue induced <b>reinstatement</b> of sucrose <b>seeking</b> but not sucrose self administration in rats.
+GRM2	addiction	addiction	16703399	Group II metabotropic glutamate receptor (<strong>mGluR2</strong>/3) agonists are proposed to serve as potential treatment for <b>addiction</b>.
+GRM2	drug	cocaine	16703399	The present study examined the hypothesis that <strong>mGluR2</strong>/3 agonists exert inhibitory effects on <b>cocaine</b> induced reinstatement of <b>cocaine</b> seeking.
+GRM2	addiction	relapse	16703399	The present study examined the hypothesis that <strong>mGluR2</strong>/3 agonists exert inhibitory effects on cocaine induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+GRM2	drug	cocaine	16703399	These results support a potential therapeutic role for <strong>mGluR2</strong>/3 agonists on relapse of <b>cocaine</b> seeking.
+GRM2	addiction	relapse	16703399	These results support a potential therapeutic role for <strong>mGluR2</strong>/3 agonists on <b>relapse</b> of cocaine <b>seeking</b>.
+GRM2	addiction	relapse	16703399	In addition, the NAc core is one site of action where the <strong>mGluR2</strong>/3 agonists elicit effects on reward <b>seeking</b> behavior.
+GRM2	addiction	reward	16703399	In addition, the NAc core is one site of action where the <strong>mGluR2</strong>/3 agonists elicit effects on <b>reward</b> seeking behavior.
+GRM2	drug	alcohol	16678921	The objective of this study was to assess the effects of the <strong>mGlu2</strong>/3 receptor agonist LY404039 (LY) on operant <b>ethanol</b> (EtOH) self administration during <b>alcohol</b> seeking (pavlovian spontaneous recovery, PSR), <b>alcohol</b> relapse (<b>alcohol</b> deprivation effect, ADE), and maintenance responding for <b>alcohol</b>.
+GRM2	addiction	relapse	16678921	The objective of this study was to assess the effects of the <strong>mGlu2</strong>/3 receptor agonist LY404039 (LY) on operant ethanol (EtOH) self administration during alcohol <b>seeking</b> (pavlovian spontaneous recovery, PSR), alcohol <b>relapse</b> (alcohol deprivation effect, ADE), and maintenance responding for alcohol.
+GRM2	addiction	reward	16678921	The objective of this study was to assess the effects of the <strong>mGlu2</strong>/3 receptor agonist LY404039 (LY) on <b>operant</b> ethanol (EtOH) self administration during alcohol seeking (pavlovian spontaneous recovery, PSR), alcohol relapse (alcohol deprivation effect, ADE), and maintenance responding for alcohol.
+GRM2	drug	alcohol	16678921	The results of this study demonstrate that activating <strong>mGlu2</strong>/3 receptors inhibits the expression of <b>alcohol</b> seeking and relapse behavior without altering <b>alcohol</b> self administration behavior.
+GRM2	addiction	relapse	16678921	The results of this study demonstrate that activating <strong>mGlu2</strong>/3 receptors inhibits the expression of alcohol <b>seeking</b> and <b>relapse</b> behavior without altering alcohol self administration behavior.
+GRM2	drug	cocaine	16616767	<b>Cocaine</b> withdrawal alters the expression of GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug withdrawal on hippocampus is little known.
+GRM2	addiction	withdrawal	16616767	Cocaine <b>withdrawal</b> alters the expression of GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methylisoxazole 4 propionic acid (AMPA) receptors in nucleus accumbens or amygdala, but the influence of drug <b>withdrawal</b> on hippocampus is little known.
+GRM2	drug	opioid	16616767	Here, we have examined the expression of GluR1 and <strong>GluR2</strong>/3 in hippocampal membrane and synaptic fractions following repeated <b>morphine</b> exposure and subsequent withdrawal.
+GRM2	addiction	withdrawal	16616767	Here, we have examined the expression of GluR1 and <strong>GluR2</strong>/3 in hippocampal membrane and synaptic fractions following repeated morphine exposure and subsequent <b>withdrawal</b>.
+GRM2	drug	opioid	16616767	Repeated <b>morphine</b> exposure for 12 d increased GluR1 and <strong>GluR2</strong>/3 in synaptosome but not in membrane fraction.
+GRM2	drug	opioid	16616767	However, during opiate withdrawal, GluR1 was generally reduced while <strong>GluR2</strong>/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after withdrawal, but detectably increased in late phase of <b>morphine</b> withdrawal in both fractions.
+GRM2	addiction	withdrawal	16616767	However, during opiate <b>withdrawal</b>, GluR1 was generally reduced while <strong>GluR2</strong>/3 was prominently increased in both fractions; pCaMKIIalpha was strongly decreased immediately after <b>withdrawal</b>, but detectably increased in late phase of morphine <b>withdrawal</b> in both fractions.
+GRM2	addiction	withdrawal	16616767	Importantly, the opiate <b>withdrawal</b> induced increase in <strong>GluR2</strong>/3 was dependent on the activation of glucocorticoid receptors and NMDA receptors, as it was prevented by the glucocorticoid receptor antagonist RU38486, or intrahippocampal injection of the NMDA receptor antagonist AP 5 or the antagonist to NR2B containing NMDA receptors, Ro25 6981.
+GRM2	addiction	withdrawal	16616767	These findings indicate that opiate <b>withdrawal</b> induces dynamic expression of GluR1 and <strong>GluR2</strong>/3 subunits of AMPA receptors in hippocampal synapses, possibly revealing an adaptive process of the hippocampal functions following opiate <b>withdrawal</b>.
+GRM2	drug	cocaine	16582902	Using an 'ex vivo' approach in mice, we show that a single injection of <b>cocaine</b> caused strong rectification and conferred sensitivity to the polyamine Joro spider toxin (JST) of AMPAR mediated excitatory postsynaptic currents (AMPAR EPSCs), indicating the recruitment of receptors that lack <strong>GluR2</strong>.
+GRM2	drug	cannabinoid	16545872	These include the <b>cannabinoid</b> CB1 receptor, receptors modulating glutamatergic transmission (<strong>mGluR2</strong>, 3 and 5), and receptors for stress related neuropeptides corticotropin releasing factor (CRF), neuropeptide Y (NPY) and nociceptin.
+GRM2	drug	cocaine	16363995	Statistically significant elevations were observed for NR1, GluR1, <strong>GluR2</strong>/3 and GluR5 (p < 0.05) and a trend towards increased NR1 phosphorylated at serine 896 (p = 0.07) in the NAc but not putamen of monkeys self administering <b>cocaine</b> compared with controls.
+GRM2	drug	cannabinoid	16354920	The present data show that, in <b>THC</b> treated mice, long term depression is expressed because a presynaptic <strong>mGluR2</strong>/3 (metabotropic glutamate receptor 2/3) dependent mechanism replaces the impaired <b>endocannabinoid</b> system.
+GRM2	drug	opioid	16341024	In an initial pharmacological characterization, we found that the <strong>mGluR2</strong>/3 agonist LY379268, which acts centrally to reduce evoked glutamate release, attenuates context induced reinstatement of <b>heroin</b> seeking when injected systemically or into the ventral tegmental area, the cell body region of the mesolimbic dopamine system.
+GRM2	addiction	relapse	16341024	In an initial pharmacological characterization, we found that the <strong>mGluR2</strong>/3 agonist LY379268, which acts centrally to reduce evoked glutamate release, attenuates context induced <b>reinstatement</b> of heroin <b>seeking</b> when injected systemically or into the ventral tegmental area, the cell body region of the mesolimbic dopamine system.
+GRM2	drug	alcohol	16324694	Suppression of <b>alcohol</b> self administration and cue induced reinstatement of <b>alcohol</b> seeking by the <strong>mGlu2</strong>/3 receptor agonist LY379268 and the mGlu8 receptor agonist (S) 3,4 DCPG.
+GRM2	addiction	relapse	16324694	Suppression of alcohol self administration and cue induced <b>reinstatement</b> of alcohol <b>seeking</b> by the <strong>mGlu2</strong>/3 receptor agonist LY379268 and the mGlu8 receptor agonist (S) 3,4 DCPG.
+GRM2	drug	amphetamine	16311338	Systemic or intra NAc infusion of the membrane permeable <strong>GluR2</strong> peptide prevented the expression of <b>amphetamine</b> induced behavioral sensitization in the rat.
+GRM2	addiction	sensitization	16311338	Systemic or intra NAc infusion of the membrane permeable <strong>GluR2</strong> peptide prevented the expression of amphetamine induced behavioral <b>sensitization</b> in the rat.
+GRM2	drug	alcohol	16292590	Effects of mGluR1, <strong>mGluR2</strong>/3, and mGluR5 antagonists were then tested on parameters of <b>ethanol</b> self administration behavior.
+GRM2	drug	cocaine	16207873	Surface/intracellular (S/I) ratios for glutamate receptor 1 (GluR1) and <strong>GluR2</strong>/3 subunits were increased 21 d after the last injection in <b>cocaine</b> sensitized rats but not rats that failed to sensitize, and the magnitude of the S/I ratio for <b>cocaine</b> sensitized rats was positively correlated with the magnitude of behavioral sensitization.
+GRM2	addiction	sensitization	16207873	Surface/intracellular (S/I) ratios for glutamate receptor 1 (GluR1) and <strong>GluR2</strong>/3 subunits were increased 21 d after the last injection in cocaine sensitized rats but not rats that failed to sensitize, and the magnitude of the S/I ratio for cocaine sensitized rats was positively correlated with the magnitude of behavioral <b>sensitization</b>.
+GRM2	addiction	relapse	16000629	It was hypothesized that the activation of xc  prevents drug <b>seeking</b> by increasing glutamatergic tone on presynaptic group II metabotropic glutamate receptors (<strong>mGluR2</strong>/3) and thereby inhibiting excitatory transmission.
+GRM2	drug	cocaine	16000629	In the second experiment, blocking <strong>mGluR2</strong>/3 prevented the ability of N acetylcystine to inhibit the reinstatement of drug seeking in rats trained to self administer <b>cocaine</b>.
+GRM2	addiction	relapse	16000629	In the second experiment, blocking <strong>mGluR2</strong>/3 prevented the ability of N acetylcystine to inhibit the <b>reinstatement</b> of drug <b>seeking</b> in rats trained to self administer cocaine.
+GRM2	addiction	withdrawal	15970947	In the brains of these rats, <b>withdrawal</b> anxiety was accompanied by increased [3H]Ro48 8587 binding in the hippocampus and thalamus, and decreased GluR1 and <strong>GluR2</strong> subunit mRNA expression in the amygdala (GluR1 and <strong>GluR2</strong>) and cortex (GluR1).
+GRM2	drug	cocaine	15953359	In the basolateral amygdala, GluR1 but not <strong>GluR2</strong> levels were increased on days 1 and 30, NR2A levels were increased on day 1, and NR2B levels were decreased on day 30 of withdrawal from <b>cocaine</b>.
+GRM2	addiction	withdrawal	15953359	In the basolateral amygdala, GluR1 but not <strong>GluR2</strong> levels were increased on days 1 and 30, NR2A levels were increased on day 1, and NR2B levels were decreased on day 30 of <b>withdrawal</b> from cocaine.
+GRM2	drug	cocaine	15953359	In the central amygdala, <strong>GluR2</strong> but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or NR2B levels were not altered after withdrawal from <b>cocaine</b>.
+GRM2	addiction	withdrawal	15953359	In the central amygdala, <strong>GluR2</strong> but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or NR2B levels were not altered after <b>withdrawal</b> from cocaine.
+GRM2	drug	opioid	15931079	The novel <strong>mGluR2</strong>/3 agonist LY379268 attenuates cue induced reinstatement of <b>heroin</b> seeking.
+GRM2	addiction	relapse	15931079	The novel <strong>mGluR2</strong>/3 agonist LY379268 attenuates cue induced <b>reinstatement</b> of heroin <b>seeking</b>.
+GRM2	drug	opioid	15931079	Here, we determined the effect of LY379268, an <strong>mGluR2</strong>/3 agonist that decreases evoked glutamate release, on cue induced reinstatement of <b>heroin</b> seeking.
+GRM2	addiction	relapse	15931079	Here, we determined the effect of LY379268, an <strong>mGluR2</strong>/3 agonist that decreases evoked glutamate release, on cue induced <b>reinstatement</b> of heroin <b>seeking</b>.
+GRM2	drug	opioid	15931079	Results indicate that glutamate plays an important role in cue induced reinstatement of <b>heroin</b> seeking and suggest that <strong>mGluR2</strong>/3 agonists should be considered for the treatment of opiate relapse.
+GRM2	addiction	relapse	15931079	Results indicate that glutamate plays an important role in cue induced <b>reinstatement</b> of heroin <b>seeking</b> and suggest that <strong>mGluR2</strong>/3 agonists should be considered for the treatment of opiate <b>relapse</b>.
+GRM2	drug	cocaine	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces <b>cocaine</b> seeking behaviour when reward is withheld, reverses this deficit by up regulating GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRM2	addiction	relapse	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces cocaine <b>seeking</b> behaviour when reward is withheld, reverses this deficit by up regulating GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRM2	addiction	reward	15764012	We previously reported that extinction training, a form of inhibitory learning that progressively reduces cocaine seeking behaviour when <b>reward</b> is withheld, reverses this deficit by up regulating GluR1 and <strong>GluR2</strong>/3 subunits of alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid (AMPA) glutamate receptors in the NAc.
+GRM2	drug	cocaine	15764012	This hypothesis is supported by the finding that over expression of GluR1 and <strong>GluR2</strong> in the NAc facilitates extinction of <b>cocaine</b> self administration.
+GRM2	drug	cocaine	15764012	Furthermore, a single extinction training session conducted during GluR1 and <strong>GluR2</strong> over expression strongly and selectively attenuates the ability of an environmental stressor to trigger relapse to <b>cocaine</b> seeking long after GluR1 and <strong>GluR2</strong> over expression declines.
+GRM2	addiction	relapse	15764012	Furthermore, a single extinction training session conducted during GluR1 and <strong>GluR2</strong> over expression strongly and selectively attenuates the ability of an environmental stressor to trigger <b>relapse</b> to cocaine <b>seeking</b> long after GluR1 and <strong>GluR2</strong> over expression declines.
+GRM2	drug	cocaine	15753323	They showed a significant increase in locomotor sensitization and conditioned place preference in association with repeated <b>cocaine</b> administration, indicating that <strong>mGluR2</strong> contributes to behavioral responses implicated in reinforcement and addiction of <b>cocaine</b>.
+GRM2	addiction	addiction	15753323	They showed a significant increase in locomotor sensitization and conditioned place preference in association with repeated cocaine administration, indicating that <strong>mGluR2</strong> contributes to behavioral responses implicated in reinforcement and <b>addiction</b> of cocaine.
+GRM2	addiction	reward	15753323	They showed a significant increase in locomotor sensitization and conditioned place preference in association with repeated cocaine administration, indicating that <strong>mGluR2</strong> contributes to behavioral responses implicated in <b>reinforcement</b> and addiction of cocaine.
+GRM2	addiction	sensitization	15753323	They showed a significant increase in locomotor <b>sensitization</b> and conditioned place preference in association with repeated cocaine administration, indicating that <strong>mGluR2</strong> contributes to behavioral responses implicated in reinforcement and addiction of cocaine.
+GRM2	drug	cocaine	15753323	Upon in vivo microdialysis analysis after <b>cocaine</b> administration, not only did extracellular levels of dopamine increase but also the response pattern of glutamate release markedly changed in the nucleus accumbens of <strong>mGluR2</strong> /  KO mice.
+GRM2	drug	alcohol	15717208	After the establishment of operant <b>ethanol</b> self administration, subjects were treated with various metabotropic glutamate receptor (mGluR) subtype antagonists immediately prior to experimental sessions: the mGluR5 antagonist MPEP (1, 3, and 10 mg/kg); the <strong>mGluR2</strong>  3 antagonist LY 341495 (1, 3, and 10 mg/kg); and the mGluR1 antagonist CPCCOEt (1, 3, and 10 mg/kg).
+GRM2	addiction	reward	15717208	After the establishment of <b>operant</b> ethanol self administration, subjects were treated with various metabotropic glutamate receptor (mGluR) subtype antagonists immediately prior to experimental sessions: the mGluR5 antagonist MPEP (1, 3, and 10 mg/kg); the <strong>mGluR2</strong>  3 antagonist LY 341495 (1, 3, and 10 mg/kg); and the mGluR1 antagonist CPCCOEt (1, 3, and 10 mg/kg).
+GRM2	drug	cocaine	15619119	We investigated the ability of <b>cocaine</b> and food to induce a CPP in mice lacking either the GluR1 or <strong>GluR2</strong> subunits of the AMPA receptor [gria1 or gria2 knockout (KO) mice].
+GRM2	addiction	reward	15619119	We investigated the ability of cocaine and food to induce a <b>CPP</b> in mice lacking either the GluR1 or <strong>GluR2</strong> subunits of the AMPA receptor [gria1 or gria2 knockout (KO) mice].
+GRM2	drug	nicotine	15343057	As for vulnerability to addictive behaviour, <b>nicotine</b> exposure during adolescence dose dependently down regulated levels of AMPA <strong>GluR2</strong>/3 subunits in the striatum, suggesting a reduced neurobehavioural plasticity in adult subjects.
+GRM2	addiction	addiction	15343057	As for vulnerability to <b>addictive</b> behaviour, nicotine exposure during adolescence dose dependently down regulated levels of AMPA <strong>GluR2</strong>/3 subunits in the striatum, suggesting a reduced neurobehavioural plasticity in adult subjects.
+GRM2	drug	cannabinoid	15233572	Down regulation of the AMPA glutamate receptor subunits GluR1 and <strong>GluR2</strong>/3 in the rat cerebellum following pre  and perinatal delta9 <b>tetrahydrocannabinol</b> exposure.
+GRM2	drug	cannabinoid	15233572	This paper reports the effects of pre  and perinatal exposure to delta9 <b>tetrahydrocannabinol</b> (<b>THC</b>) on expression levels of specific AMPA glutamate receptor subunits (GluR1 and <strong>GluR2</strong>/3) in the cerebellum of male and female rats.
+GRM2	drug	cannabinoid	15233572	Expression of the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA glutamate receptors was analyzed by immunohistochemistry in <b>THC</b> exposed rats at three postnatal ages: PD20 (still exposed to <b>THC</b>) to study the direct effect of drug exposure, and PD30 and PD70 (10 and 50 days following <b>THC</b> withdrawal) to analyze the long term effects of prenatal exposure.
+GRM2	addiction	withdrawal	15233572	Expression of the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA glutamate receptors was analyzed by immunohistochemistry in THC exposed rats at three postnatal ages: PD20 (still exposed to THC) to study the direct effect of drug exposure, and PD30 and PD70 (10 and 50 days following THC <b>withdrawal</b>) to analyze the long term effects of prenatal exposure.
+GRM2	drug	cannabinoid	15233572	Compared to controls, pre  and perinatal <b>THC</b> exposure decreased the immunoreactivity levels of the GluR1 subunit in Bergmann glial cells, as well as levels of the <strong>GluR2</strong>/3 subunit in Purkinje neurons at PD20.
+GRM2	drug	cocaine	15152032	The present study sought to determine whether group II mGluR activation by the potent <strong>mGlu2</strong>/3 receptor agonist, ( ) 2 oxa 4 aminobicylco hexane 4,6 dicarboxylic acid (LY379268), antagonizes reinstatement of <b>cocaine</b> seeking induced by <b>cocaine</b> related stimuli and whether this effect extends to behavior induced by stimuli conditioned to a potent conventional reinforcer, sweetened condensed milk (SCM).
+GRM2	addiction	relapse	15152032	The present study sought to determine whether group II mGluR activation by the potent <strong>mGlu2</strong>/3 receptor agonist, ( ) 2 oxa 4 aminobicylco hexane 4,6 dicarboxylic acid (LY379268), antagonizes <b>reinstatement</b> of cocaine <b>seeking</b> induced by cocaine related stimuli and whether this effect extends to behavior induced by stimuli conditioned to a potent conventional reinforcer, sweetened condensed milk (SCM).
+GRM2	addiction	intoxication	15140200	In the NAc, <strong>GluR2</strong>/3 levels were increased following withdrawal compared with <b>binge</b> access, and were the only changes observed in this region.
+GRM2	addiction	withdrawal	15140200	In the NAc, <strong>GluR2</strong>/3 levels were increased following <b>withdrawal</b> compared with binge access, and were the only changes observed in this region.
+GRM2	drug	opioid	14996539	The selective <strong>mGlu2</strong>/3 receptor antagonist LY341495 exacerbates behavioral signs of <b>morphine</b> withdrawal and <b>morphine</b> withdrawal induced activation of locus coeruleus neurons.
+GRM2	addiction	withdrawal	14996539	The selective <strong>mGlu2</strong>/3 receptor antagonist LY341495 exacerbates behavioral signs of morphine <b>withdrawal</b> and morphine <b>withdrawal</b> induced activation of locus coeruleus neurons.
+GRM2	drug	opioid	14996539	Previous research has demonstrated that <strong>mGlu2</strong>/3 agonists can decrease many behavioral signs and the activation of locus coeruleus (LC) neurons observed during <b>morphine</b> withdrawal.
+GRM2	addiction	withdrawal	14996539	Previous research has demonstrated that <strong>mGlu2</strong>/3 agonists can decrease many behavioral signs and the activation of locus coeruleus (LC) neurons observed during morphine <b>withdrawal</b>.
+GRM2	drug	opioid	14996539	However, it is not known if <strong>mGlu2</strong>/3 receptors are activated during <b>morphine</b> withdrawal by endogenous glutamate.
+GRM2	addiction	withdrawal	14996539	However, it is not known if <strong>mGlu2</strong>/3 receptors are activated during morphine <b>withdrawal</b> by endogenous glutamate.
+GRM2	drug	alcohol	14996539	Therefore, we investigated the effect of a novel metabotropic glutamate 2, 3 (<strong>mGlu2</strong>/3) receptor antagonist (LY341495) on <b>naltrexone</b> precipitated behavioral signs of morphine withdrawal and withdrawal induced activation of LC neurons.
+GRM2	drug	opioid	14996539	Therefore, we investigated the effect of a novel metabotropic glutamate 2, 3 (<strong>mGlu2</strong>/3) receptor antagonist (LY341495) on naltrexone precipitated behavioral signs of <b>morphine</b> withdrawal and withdrawal induced activation of LC neurons.
+GRM2	addiction	withdrawal	14996539	Therefore, we investigated the effect of a novel metabotropic glutamate 2, 3 (<strong>mGlu2</strong>/3) receptor antagonist (LY341495) on naltrexone precipitated behavioral signs of morphine <b>withdrawal</b> and <b>withdrawal</b> induced activation of LC neurons.
+GRM2	drug	opioid	14996539	These results indicate that endogenous activation of <strong>mGlu2</strong>/3 receptors during <b>morphine</b> withdrawal acts to reduce the severity of <b>morphine</b> withdrawal and demonstrates that <strong>mGlu2</strong>/3 receptors are activated under a physiologically relevant, pathological condition.
+GRM2	addiction	withdrawal	14996539	These results indicate that endogenous activation of <strong>mGlu2</strong>/3 receptors during morphine <b>withdrawal</b> acts to reduce the severity of morphine <b>withdrawal</b> and demonstrates that <strong>mGlu2</strong>/3 receptors are activated under a physiologically relevant, pathological condition.
+GRM2	addiction	addiction	14666123	At 2 months after pretreatment, we measured levels of AMPA <strong>GluR2</strong>/3 subunits, thought to be involved in the control of <b>addictive</b> behaviors.
+GRM2	addiction	reward	14573529	Involvement of AMPA receptor <strong>GluR2</strong> subunits in stimulus <b>reward</b> learning: evidence from glutamate receptor gria2 knock out mice.
+GRM2	addiction	reward	14573529	We investigated whether mice lacking the <strong>GluR2</strong> subunit [gria2 knock out (KO) mice] displayed impairments in learning stimulus <b>reward</b> associations, and the subsequent ability of <b>reward</b> paired cues to control motivated behavior.
+GRM2	addiction	reward	14573529	These results suggest that <strong>GluR2</strong> containing AMPA receptors, possibly within the CeA, are critical for the formation of stimulus <b>reward</b> associations necessary for PIT and conditioned approach, but are not involved in the plastic processes underlying the attribution of motivational value to the conditioned stimulus (CS).
+GRM2	drug	cocaine	12787079	In the accumbens of <b>cocaine</b> trained rats, GluR1 and NMDAR1 levels were increased on days 1 and 90, while <strong>GluR2</strong> levels were increased on days 1 and 30, but not day 90; PKA activity levels were increased on days 1 and 30, but not day 90, while AC activity, TH and cdk5 levels were unaltered.
+GRM2	drug	cocaine	12787079	In the VTA of <b>cocaine</b> trained rats, NMDAR1 levels were increased for up to 90 days, while <strong>GluR2</strong> levels were increased only on day 1; TH and Cdk5 levels were increased only on day 1, while PKA and AC activity levels were unaltered.
+GRM2	drug	cocaine	12716423	Array analysis revealed significant up regulation of numerous transcripts in the VTA, but not in the l SN, of <b>cocaine</b> overdose victims including NMDAR1, <strong>GluR2</strong>, GluR5 and KA2 receptor mRNA (p < 0.05).
+GRM2	drug	cocaine	12716423	Correspondingly, western blot analysis revealed VTA selective up regulation of CREB (p < 0.01), NMDAR1 (p < 0.01), <strong>GluR2</strong> (p < 0.05), GluR5 (p < 0.01) and KA2 (p < 0.05) protein levels of <b>cocaine</b> overdose victims.
+GRM2	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for AP 1 in the NAc: the AMPA glutamate receptor subunit <strong>GluR2</strong>, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+GRM2	drug	alcohol	12694947	Despite this augmentation of AMPAR function, no significant changes were found in the sensitivity of AMPA currents to GYKI 52466, cyclothiazide or acute <b>ethanol</b> (100 mM) sensitivity or in the levels of GluR1/<strong>GluR2</strong> subunit proteins from MS/DB tissue.
+GRM2	drug	cocaine	12687634	Acute "binge" <b>cocaine</b> also increased mRNA levels for glutamate receptor <strong>GluR2</strong>, dopamine receptor D1, and a number of phosphatases.
+GRM2	addiction	intoxication	12687634	Acute "<b>binge</b>" cocaine also increased mRNA levels for glutamate receptor <strong>GluR2</strong>, dopamine receptor D1, and a number of phosphatases.
+GRM2	drug	cocaine	12511956	Here we show that extinction training during withdrawal from chronic <b>cocaine</b> self administration induces experience dependent increases in the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in <b>cocaine</b> reward.
+GRM2	addiction	reward	12511956	Here we show that extinction training during withdrawal from chronic cocaine self administration induces experience dependent increases in the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine <b>reward</b>.
+GRM2	addiction	withdrawal	12511956	Here we show that extinction training during <b>withdrawal</b> from chronic cocaine self administration induces experience dependent increases in the GluR1 and <strong>GluR2</strong>/3 subunits of AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine reward.
+GRM2	drug	cocaine	12511956	Indeed, viral mediated overexpression of both GluR1 and <strong>GluR2</strong> in nucleus accumbens shell neurons facilitates extinction of <b>cocaine</b>  but not sucrose seeking responses.
+GRM2	addiction	relapse	12511956	Indeed, viral mediated overexpression of both GluR1 and <strong>GluR2</strong> in nucleus accumbens shell neurons facilitates extinction of cocaine  but not sucrose <b>seeking</b> responses.
+GRM2	drug	opioid	12473091	Because presynaptic <strong>mGlu2</strong>/3 functions are augmented in the ventral tegmental area of <b>morphine</b> withdrawn rats, we have evaluated the consequences of opiate treatment on <strong>mGlu2</strong>/3 LTD at prelimbic NAc glutamatergic synapses.
+GRM2	drug	opioid	12473091	Here we report that <strong>mGlu2</strong>/3 LTD is abolished after 1 week of withdrawal from chronic <b>morphine</b> treatment; in the <b>morphine</b> withdrawn group LTD measured 5.99 +/  4.84% (P < 0.05) compared with 21.13 +/  5.42% in the sham group.
+GRM2	addiction	withdrawal	12473091	Here we report that <strong>mGlu2</strong>/3 LTD is abolished after 1 week of <b>withdrawal</b> from chronic morphine treatment; in the morphine withdrawn group LTD measured 5.99 +/  4.84% (P < 0.05) compared with 21.13 +/  5.42% in the sham group.
+GRM2	drug	opioid	12473091	In contrast, chronic <b>morphine</b> treatment did not alter the mechanisms normally underlying <strong>mGlu2</strong>/3 LTD, such as the cAMP/PKA pathway or P/Q type Ca2+ channels.
+GRM2	drug	cocaine	12388642	Group II metabotropic glutamate autoreceptors (<strong>mGluR2</strong>/3) regulate glutamate release, and this study investigates whether repeated <b>cocaine</b> injection produces long lasting alterations in <strong>mGluR2</strong>/3 content, phosphorylation, and physiology.
+GRM2	drug	cocaine	12388642	Rats were administered <b>cocaine</b> daily for 1 week, and 3 weeks after the last injection, <strong>mGluR2</strong>/3 protein levels were altered in the accumbens and prefrontal cortex (PFC) but not in the dorsal striatum or ventral tegmental area.
+GRM2	drug	cocaine	12388642	The capacity of the <strong>mGluR2</strong>/3 agonist 2R,4R 4 aminopyrrolidine 2,4 dicarboxylate (APDC) to inhibit [(35)S]cystine uptake via cystine/glutamate antiporter in accumbens tissue slices was reduced by repeated <b>cocaine</b>.
+GRM2	drug	cocaine	12388642	Together, these data demonstrate that repeated <b>cocaine</b> produces an enduring reduction in <strong>mGluR2</strong>/3 function in the nucleus accumbens.
+GRM2	drug	amphetamine	12117587	The <strong>mGlu2</strong>/3 receptor agonist LY379268 blocks the expression of locomotor sensitization by <b>amphetamine</b>.
+GRM2	addiction	sensitization	12117587	The <strong>mGlu2</strong>/3 receptor agonist LY379268 blocks the expression of locomotor <b>sensitization</b> by amphetamine.
+GRM2	drug	alcohol	11696675	Unexpectedly, we found that expression of NR1 (including the expression of NR1 subunits containing the N1, C1, and C2 inserts), NR2A, NR2B, NR2C, GluR1, <strong>GluR2</strong>/3, GluR5, GluR6/7, and KA2 subunits was not altered in hippocampal homogenates from <b>ethanol</b> exposed rats.
+GRM2	drug	cocaine	10349849	GluR1, <strong>GluR2</strong>/3, and NMDAR1 subunits of glutamate receptors were quantified from immunoblots in these brain nuclei in rats at 24 h and 3 weeks after discontinuing 1 week of daily <b>cocaine</b> injections.
+GRM2	drug	cocaine	10349849	None of these increases occurred in the rats exposed to daily <b>cocaine</b> that did not develop behavioral sensitization (<20% increase in motor activity), and no changes were measured in the level of <strong>GluR2</strong>/3 in any treatment group.
+GRM2	addiction	sensitization	10349849	None of these increases occurred in the rats exposed to daily cocaine that did not develop behavioral <b>sensitization</b> (<20% increase in motor activity), and no changes were measured in the level of <strong>GluR2</strong>/3 in any treatment group.
+GRM2	addiction	withdrawal	10231131	In the NAc, GluR1 and <strong>GluR2</strong> immunolabeling were unchanged after 3 days of <b>withdrawal</b>, but both were decreased significantly after 14 days of <b>withdrawal</b> (GluR1, 85.5+/ 2.6% of control group, P<0.01; <strong>GluR2</strong>, 79.2+/ 3.2%, P<0.01).
+GRM2	addiction	withdrawal	10231131	Analysis of core and shell subregions at the 14 day <b>withdrawal</b> time indicated that GluR1 immunolabeling decreased significantly in shell, while <strong>GluR2</strong> immunolabeling decreased significantly in both core and shell.
+GRM2	addiction	withdrawal	10231131	No changes in <strong>GluR2</strong>/3, <strong>GluR2</strong>/4, or GluR4 immunolabeling in NAc were found at either <b>withdrawal</b> time.
+GRM2	drug	opioid	10218862	The selective <strong>mGlu2</strong>/3 receptor agonist LY354740 attenuates <b>morphine</b> withdrawal induced activation of locus coeruleus neurons and behavioral signs of <b>morphine</b> withdrawal.
+GRM2	addiction	withdrawal	10218862	The selective <strong>mGlu2</strong>/3 receptor agonist LY354740 attenuates morphine <b>withdrawal</b> induced activation of locus coeruleus neurons and behavioral signs of morphine <b>withdrawal</b>.
+GRM2	drug	opioid	10218862	These results indicate <strong>mGlu2</strong>/3 receptor agonists: (1) can attenuate the <b>morphine</b> withdrawal induced activation of LC neurons and many behavioral signs of <b>morphine</b> withdrawal; and (2) may have therapeutic effects in man for the treatment of opiate withdrawal.
+GRM2	addiction	withdrawal	10218862	These results indicate <strong>mGlu2</strong>/3 receptor agonists: (1) can attenuate the morphine <b>withdrawal</b> induced activation of LC neurons and many behavioral signs of morphine <b>withdrawal</b>; and (2) may have therapeutic effects in man for the treatment of opiate <b>withdrawal</b>.
+GRM2	addiction	dependence	9390995	Differential <b>dependence</b> on <strong>GluR2</strong> expression of three characteristic features of AMPA receptors.
+GRM2	drug	opioid	9390995	The physiological effects of a moderate change in <strong>GluR2</strong> relative abundance, such as occurs after ischemia or seizures or after chronic exposure to <b>morphine</b>, thus will be dependent on the ambient <strong>GluR2</strong> level in a cell specific manner.
+GRM2	drug	amphetamine	9183816	Repeated <b>amphetamine</b> administration decreased levels of GluR1 and <strong>GluR2</strong> but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal.
+GRM2	addiction	withdrawal	9183816	Repeated amphetamine administration decreased levels of GluR1 and <strong>GluR2</strong> but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day <b>withdrawal</b> time; no changes were observed after 3 days of <b>withdrawal</b>.
+GRM2	addiction	withdrawal	9183816	In contrast, levels of GluR1 mRNA in the PFC were increased at 3 but not 14 days of <b>withdrawal</b>, while <strong>GluR2</strong> and 3 mRNAs were unchanged.
+GRM2	drug	cocaine	8613793	In contrast, chronic <b>cocaine</b> treatment did not alter levels of <strong>GluR2</strong> (an AMPA receptor subunit), NMDA2A/B (NMDA receptor subunits), or GluR6/7 (kainate receptor subunits) in this brain region.
+GRM2	drug	alcohol	8133290	In contrast, <b>ethanol</b> did not alter the levels of glutamate receptor subunit (GLUR) 1 or <strong>GLUR2</strong> protein, subunits that make up the alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid glutamate receptor, in the hippocampus.
+DRD4	drug	nicotine	31903031	The purpose of this study is to investigate the relationship between the variable number tandem repeat (VNTR) variant in exon III of the Dopamine D4 receptor (<strong>DRD4</strong>) gene and genetic predisposition of <b>smoking</b> status in a Turkish population.
+DRD4	drug	nicotine	31903031	There was a significant difference between <b>smoker</b> and non <b>smoker</b> groups regarding the distribution of the alleles and genotypes of the <strong>DRD4</strong> gene (p=0.000, p=0.000, respectively).
+DRD4	drug	nicotine	31903031	When the number of repeat alleles (48 bp) are accepted as short (S) if six or less, and as long (L) if seven or more, it was found that the frequency of S/S genotype of the <strong>DRD4</strong> VNTR variant was lower in the <b>smoker</b> group and S/L genotype was higher in the <b>smoker</b> group (p=0.006, p=0.006, respectively).
+DRD4	drug	nicotine	31903031	The results indicated that the subjects carrying <strong>DRD4</strong> exon III VNTR S/L genotype have a risk for <b>smoking</b> status in a Turkish population.
+DRD4	drug	alcohol	31149768	Parsing out the role of dopamine D4 receptor gene (<strong>DRD4</strong>) on <b>alcohol</b> related phenotypes: A meta analysis and systematic review.
+DRD4	drug	alcohol	31149768	To date, no quantitative synthesis of the published literature on the effects of <strong>DRD4</strong> VNTR variation on <b>alcohol</b> related phenotypes has been conducted.
+DRD4	addiction	relapse	31149768	It was not possible to conduct a meta analysis of the <b>craving</b> data, but a systematic review of this literature found mixed results on <strong>DRD4</strong> VNTR genotype effect.
+DRD4	drug	alcohol	31149768	The present meta analysis suggests <strong>DRD4</strong> VNTR variation may be a risk factor for problematic <b>alcohol</b> use.
+DRD4	addiction	relapse	30797855	Dopamine D4 receptor (<strong>DRD4</strong>) dysregulation is associated with a variety of behaviors including novelty <b>seeking</b>, approach avoidance, and ADHD.
+DRD4	drug	cocaine	30797855	The present study sought to examine the role of <strong>DRD4</strong> on <b>cocaine</b> seeking behavior in the conditioned place preference (CPP) test and determine its effects on extinction and reinstatement in adult wild type (WT), heterozygous (HT), and knockout (KO) mice.
+DRD4	addiction	relapse	30797855	The present study sought to examine the role of <strong>DRD4</strong> on cocaine <b>seeking</b> behavior in the conditioned place preference (CPP) test and determine its effects on extinction and <b>reinstatement</b> in adult wild type (WT), heterozygous (HT), and knockout (KO) mice.
+DRD4	addiction	reward	30797855	The present study sought to examine the role of <strong>DRD4</strong> on cocaine seeking behavior in the conditioned place preference (<b>CPP</b>) test and determine its effects on extinction and reinstatement in adult wild type (WT), heterozygous (HT), and knockout (KO) mice.
+DRD4	drug	cocaine	30797855	Female <strong>DRD4</strong> KO mice failed to extinguish their preference for the <b>cocaine</b> paired chamber following the extinction period.
+DRD4	drug	cocaine	30797855	The observed effects illustrate the role <strong>DRD4</strong> gene expression has on extinction and reinstatement, but not acquisition, of <b>cocaine</b> seeking behavior.
+DRD4	addiction	relapse	30797855	The observed effects illustrate the role <strong>DRD4</strong> gene expression has on extinction and <b>reinstatement</b>, but not acquisition, of cocaine <b>seeking</b> behavior.
+DRD4	drug	cocaine	30367264	Effects of DRD2 splicing regulatory polymorphism and <strong>DRD4</strong> 48 bp VNTR on crack <b>cocaine</b> addiction.
+DRD4	addiction	addiction	30367264	Effects of DRD2 splicing regulatory polymorphism and <strong>DRD4</strong> 48 bp VNTR on crack cocaine <b>addiction</b>.
+DRD4	drug	cocaine	30367264	The influence of DRD2 rs2283265 and <strong>DRD4</strong> 48 bp VNTR in exon 3 variants, as well as their interaction on crack <b>cocaine</b> addiction susceptibility and severity were evaluated in women and men separately.
+DRD4	addiction	addiction	30367264	The influence of DRD2 rs2283265 and <strong>DRD4</strong> 48 bp VNTR in exon 3 variants, as well as their interaction on crack cocaine <b>addiction</b> susceptibility and severity were evaluated in women and men separately.
+DRD4	drug	cocaine	30367264	In this same group, interaction analysis demonstrated that the presence of DRD2 T allele and concomitant absence of <strong>DRD4</strong> 7R allele were associated with risk for crack <b>cocaine</b> addiction.
+DRD4	addiction	addiction	30367264	In this same group, interaction analysis demonstrated that the presence of DRD2 T allele and concomitant absence of <strong>DRD4</strong> 7R allele were associated with risk for crack cocaine <b>addiction</b>.
+DRD4	addiction	addiction	30367264	No influence of DRD2 and <strong>DRD4</strong> variants was observed in men regarding <b>addiction</b> severity.
+DRD4	drug	opioid	30268777	<strong>DRD4</strong> mRNA level increased only in the amygdala of <b>opioid</b> abusers.
+DRD4	drug	alcohol	30192917	The current candidate gene and environment interaction (cGxE) study examined whether the effects of an experimentally manipulated psychosocial stressor on self reported drinking urge and implicit attentional bias for <b>alcohol</b> cues differ as a function of a cumulative genetic score of 5 HTTLPR, MAO A, <strong>DRD4</strong>, DAT1 and DRD2 genotypes.
+DRD4	addiction	addiction	29434815	<strong>Dopamine receptor D4</strong> promoter hypermethylation increases the risk of drug <b>addiction</b>.
+DRD4	addiction	addiction	29434815	Dopamine receptor D4 (<strong>DRD4</strong>), a key receptor in the dopaminergic system, may facilitate the development of drug <b>addiction</b>.
+DRD4	addiction	addiction	29434815	<strong>Dopamine receptor D4</strong> (<strong>DRD4</strong>), a key receptor in the dopaminergic system, may facilitate the development of drug <b>addiction</b>.
+DRD4	addiction	addiction	29434815	The aim of the present study was to investigate the association between the promoter methylation level of <strong>DRD4</strong> gene and drug <b>addiction</b>.
+DRD4	drug	amphetamine	29434815	Significantly higher levels of <strong>DRD4</strong> CpG1 and CpG4 methylation were detected in <b>METH</b> and heroin drug addicts compared with controls (P<0.05).
+DRD4	drug	opioid	29434815	Significantly higher levels of <strong>DRD4</strong> CpG1 and CpG4 methylation were detected in METH and <b>heroin</b> drug addicts compared with controls (P<0.05).
+DRD4	drug	amphetamine	29434815	Male <b>METH</b> addicts exhibited significantly higher <strong>DRD4</strong> CpG1, CpG2 and CpG4 methylation levels compared with sex matched controls (P<0.05).
+DRD4	drug	opioid	29434815	In <b>heroin</b> addicts, a positive correlation was observed between depression dejection and <strong>DRD4</strong> CpG5 methylation (r=0.537, P=0.039) whereas there was a negative correlation between drug usage frequency and CpG1 methylation (r= 0.632, P=0.011).
+DRD4	addiction	addiction	29434815	The results of the present study suggest that DNA methylation of <strong>DRD4</strong> may be responsible for the pathophysiology of drug <b>addiction</b>.
+DRD4	drug	alcohol	29395188	This secondary data analysis examined whether and how the dopamine receptor D4 gene (<strong>DRD4</strong>) influenced <b>naltrexone</b> treatment responsiveness in a randomized clinical trial.
+DRD4	drug	alcohol	29395188	This secondary data analysis examined whether and how the <strong>dopamine receptor D4</strong> gene (<strong>DRD4</strong>) influenced <b>naltrexone</b> treatment responsiveness in a randomized clinical trial.
+DRD4	drug	alcohol	29395188	We leveraged intensive experience sampling methods to test the hypothesis that craving recorded at drinking and non drinking moments would mediate <b>naltrexone</b> effects on the likelihood of heavy drinking, but only among carriers of the <strong>DRD4</strong> long (<strong>DRD4</strong> L) allele.
+DRD4	addiction	relapse	29395188	We leveraged intensive experience sampling methods to test the hypothesis that <b>craving</b> recorded at drinking and non drinking moments would mediate naltrexone effects on the likelihood of heavy drinking, but only among carriers of the <strong>DRD4</strong> long (<strong>DRD4</strong> L) allele.
+DRD4	drug	alcohol	29395188	Moderated mediation multilevel structural equation models showed that craving during non drinking moments mediated the treatment effect of <b>naltrexone</b> on heavy drinking but only among carriers of the <strong>DRD4</strong> L allele.
+DRD4	addiction	relapse	29395188	Moderated mediation multilevel structural equation models showed that <b>craving</b> during non drinking moments mediated the treatment effect of naltrexone on heavy drinking but only among carriers of the <strong>DRD4</strong> L allele.
+DRD4	drug	alcohol	29395188	Findings provide the first in vivo evidence that, among carriers of the <strong>DRD4</strong> L allele, <b>naltrexone</b> blunts craving in real world settings, and this effect in turn reduces the likelihood of heavy drinking.
+DRD4	addiction	relapse	29395188	Findings provide the first in vivo evidence that, among carriers of the <strong>DRD4</strong> L allele, naltrexone blunts <b>craving</b> in real world settings, and this effect in turn reduces the likelihood of heavy drinking.
+DRD4	drug	nicotine	29379551	Aerobic and concentration training and allele 7 in the dopamine receptor D4 (<strong>D4DR</strong>) gene increase chances of <b>smoking</b> cessation in young Polish women.
+DRD4	drug	nicotine	29379551	Aerobic and concentration training and allele 7 in the <strong>dopamine receptor D4</strong> (<strong>D4DR</strong>) gene increase chances of <b>smoking</b> cessation in young Polish women.
+DRD4	drug	nicotine	29379551	The goal of the study was to evaluate the effectiveness of health training for <b>smoking</b> cessation by young women in connection with the dopamine receptor gene (<strong>D4DR</strong>) in their genetic profile.
+DRD4	drug	nicotine	29379551	Individuals with allele 7 in the <strong>dopamine receptor D4</strong> gene have two times greater chances (OR = 2.13: 95% CI: 0.91 4.96) of quitting <b>smoking</b> than individuals without allele 7.
+DRD4	drug	cannabinoid	28448718	<b>Cannabis</b> use by women during pregnancy does not influence infant DNA methylation of the dopamine receptor <strong>DRD4</strong>.
+DRD4	drug	cannabinoid	28448718	To determine whether maternal <b>cannabis</b> use is associated with methylation of the dopamine receptor gene <strong>DRD4</strong> promoter in infants.
+DRD4	drug	cannabinoid	28448718	Of 19 cytosine phosphate guanine dinucleotides (CpG) units tested in <strong>DRD4</strong>, gestational <b>cannabis</b> use was associated with offspring methylation at 1 CpG unit in multivariate models (β + 1.48, CI: 0.02 to 2.93, and p = 0.047).
+DRD4	drug	cannabinoid	28448718	There is no strong evidence that maternal <b>cannabis</b> use in pregnancy is associated with offspring <strong>DRD4</strong> methylation.
+DRD4	drug	nicotine	28103253	Polymorphisms in HTR2A and <strong>DRD4</strong> Predispose to <b>Smoking</b> and <b>Smoking</b> Quantity.
+DRD4	drug	nicotine	28103253	To identify genetic variants in the promoter regions and exons of the <strong>DRD4</strong> and HTR2A genes associated with <b>tobacco</b> <b>smoking</b> and the degree of <b>nicotine</b> addiction in Mexican mestizos.
+DRD4	addiction	addiction	28103253	To identify genetic variants in the promoter regions and exons of the <strong>DRD4</strong> and HTR2A genes associated with tobacco smoking and the degree of nicotine <b>addiction</b> in Mexican mestizos.
+DRD4	drug	nicotine	28103253	The C allele of rs1800955 in <strong>DRD4</strong> was found to be associated with cigarette <b>smoking</b> in the HS vs. NS and LS vs. NS comparisons (p = 2.34E 03 and p = 1.13E 03, respectively); the association was maintained in the homozygous CC genotype (p = 5.00E 04 and p = 2.00E 04, respectively).
+DRD4	drug	nicotine	28103253	Among Mexican mestizos, the C allele of rs1800955 in the <strong>DRD4</strong> gene and the A allele of rs6311 in the HTR2A gene are associated with cigarette <b>smoking</b>, whereas the T allele of rs6313 in HTR2A is associated with cigarette <b>smoking</b> and the degree of <b>nicotine</b> addiction.
+DRD4	addiction	addiction	28103253	Among Mexican mestizos, the C allele of rs1800955 in the <strong>DRD4</strong> gene and the A allele of rs6311 in the HTR2A gene are associated with cigarette smoking, whereas the T allele of rs6313 in HTR2A is associated with cigarette smoking and the degree of nicotine <b>addiction</b>.
+DRD4	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of catechol O methyltransferase (COMT), dopamine receptor D2 (DRD2) gene score and <b>smoking</b> cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (ANKK1), dopamine transporter (SLC6A3), dopamine receptor D4 (<strong>DRD4</strong>) gene score and <b>smoking</b> cessation.
+DRD4	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of catechol O methyltransferase (COMT), dopamine receptor D2 (DRD2) gene score and <b>smoking</b> cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (ANKK1), dopamine transporter (SLC6A3), <strong>dopamine receptor D4</strong> (<strong>DRD4</strong>) gene score and <b>smoking</b> cessation.
+DRD4	addiction	intoxication	26950642	Epistatic interactions involving DRD2, <strong>DRD4</strong>, and COMT polymorphisms and risk of substance abuse in women with <b>binge</b> purge eating disturbances.
+DRD4	addiction	intoxication	26950642	We examined the implications of variations of selected, dopamine relevant polymorphisms (DRD2 Taq1A, <strong>DRD4</strong> 7R, and COMT) for risk of substance abuse in women with <b>binge</b> purge eating syndromes.
+DRD4	drug	cannabinoid	26950642	Tests for main and interaction effects of various allele combinations revealed that individuals who carried high function COMT and low function <strong>DRD4</strong> 7R alleles (a combination expected to be associated with higher risk) did indeed show more lifetime substance abuse and, specifically, more <b>cannabis</b> abuse.
+DRD4	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (OPRM1), kappa <b>opioid</b> receptors (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (<strong>DRD4</strong>), dopamine beta hydroxylase, and dopamine transporter (SLC6A3, DAT1) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+DRD4	addiction	relapse	28300812	Regardless of treatment several polymorphisms were associated with high risk of <b>relapse</b>: allele Т (rs510769) OPRM1 (р=0.053), allele А (rs1799971, A118G) OPRM1 (р=0.056), allele S exon III 48 bp <strong>DRD4</strong> VNTR (р=0.001; HR=3.1 (ДИ 95% 1.57 6.18); genotype combinations: <strong>DRD4</strong>   521 С/Т (ТТ) + DRD2 Nco I (TT), р=0.026; <strong>DRD4</strong>  521 С/Т (ТТ) + DRD2  141 С (II), р=0.011; <strong>DRD4</strong>   521 С/Т (ТТ) + OPRM1 A118G (rs1799971) (AA), р=0.011; DRD2 Nco I(ТТ) + ADRA2A (СС), р=0.012; DRD2 Nco I(ТТ) + OPRM1 A118G (AA), р=0.02.
+DRD4	addiction	relapse	28300812	The effects dependent on the treatment group were as follows: 1) in the N+G group, patients with the <strong>DRD4</strong>  521 С/Т TT genotype had higher probability of completion of treatment program in comparison with other genotypes (CC and CT) (log rank test: p=0.002); 2) in NP + GP group, patients with the OPRM1 rs510769 T allele had higher risk of <b>relapse</b> compared to the genotype GG (p=0.008) (FDR p<0.0125).
+DRD4	drug	alcohol	28300812	Pharmacological effects of <b>naltrexone</b> and guanfacine were associated with genetic variants of the <strong>DRD4</strong>   521C/T polymorphism, since its effect was shown only in the N+G group.
+DRD4	addiction	addiction	26688118	The variable number tandem repeats (VNTR) polymorphism of the dopamine D4 receptor gene (<strong>DRD4</strong>) has received considerable attention as a potential genetic contributor to <b>addiction</b>.
+DRD4	drug	alcohol	26621272	The results indicate that <b>alcohol</b> dependence is associated with high expression of SNCA and <strong>DRD4</strong> (signifi cantly higher than in the control group) and is not associated with changes in the work of NR4A2 and DRD3 genes.
+DRD4	addiction	dependence	26621272	The results indicate that alcohol <b>dependence</b> is associated with high expression of SNCA and <strong>DRD4</strong> (signifi cantly higher than in the control group) and is not associated with changes in the work of NR4A2 and DRD3 genes.
+DRD4	drug	alcohol	26621272	The expression of SNCA and <strong>DRD4</strong> genes can serve as an important peripheral marker of <b>alcohol</b> dependence development, which is essential for antipsychotic therapy.
+DRD4	addiction	dependence	26621272	The expression of SNCA and <strong>DRD4</strong> genes can serve as an important peripheral marker of alcohol <b>dependence</b> development, which is essential for antipsychotic therapy.
+DRD4	drug	alcohol	26595480	Interactions between <strong>DRD4</strong> and developmentally specific environments in <b>alcohol</b> dependence symptoms.
+DRD4	addiction	dependence	26595480	Interactions between <strong>DRD4</strong> and developmentally specific environments in alcohol <b>dependence</b> symptoms.
+DRD4	drug	alcohol	26581567	Polymorphisms in the dopamine D4 receptor (<strong>DRD4</strong>) have previously been shown to associate with a variety of human behavioral phenotypes, including ADHD pathology, <b>alcohol</b> and tobacco craving, financial risk taking in males, and broader personality traits such as novelty seeking.
+DRD4	drug	nicotine	26581567	Polymorphisms in the dopamine D4 receptor (<strong>DRD4</strong>) have previously been shown to associate with a variety of human behavioral phenotypes, including ADHD pathology, alcohol and <b>tobacco</b> craving, financial risk taking in males, and broader personality traits such as novelty seeking.
+DRD4	addiction	relapse	26581567	Polymorphisms in the dopamine D4 receptor (<strong>DRD4</strong>) have previously been shown to associate with a variety of human behavioral phenotypes, including ADHD pathology, alcohol and tobacco <b>craving</b>, financial risk taking in males, and broader personality traits such as novelty <b>seeking</b>.
+DRD4	drug	nicotine	26497691	We examined whether this polymorphism along with three <strong>DRD4</strong> single nucleotide polymorphisms (SNPs: rs936460, rs936461, and rs12280580) moderate the influence of <b>nicotine</b> on subjective responses to cigarettes.
+DRD4	drug	nicotine	26497691	Although <strong>DRD4</strong> VNTR variation did not moderate overall <b>nicotine</b> response, there was a moderation of <b>nicotine</b> response over successive cigarettes.
+DRD4	drug	nicotine	26497691	<b>Smokers</b> with fewer than seven repeats for the <strong>DRD4</strong> VNTR reported markedly reduced craving, increased satisfaction, and a greater calming effect in response to earlier smoked <b>nicotine</b> cigarettes, whereas those with seven or more repeats did not.
+DRD4	addiction	relapse	26497691	Smokers with fewer than seven repeats for the <strong>DRD4</strong> VNTR reported markedly reduced <b>craving</b>, increased satisfaction, and a greater calming effect in response to earlier smoked nicotine cigarettes, whereas those with seven or more repeats did not.
+DRD4	drug	nicotine	26497691	In addition, minor carriers for all three <strong>DRD4</strong> SNPs displayed blunted overall response to <b>nicotine</b>.
+DRD4	drug	nicotine	26497691	These findings provide support for <strong>DRD4</strong> variation as an informative predictor of subjective responses to <b>nicotine</b>.
+DRD4	drug	nicotine	26449981	Parental smoke exposure and the development of <b>nicotine</b> craving in adolescent novice <b>smokers</b>: the roles of DRD2, <strong>DRD4</strong>, and OPRM1 genotypes.
+DRD4	addiction	relapse	26449981	Parental smoke exposure and the development of nicotine <b>craving</b> in adolescent novice smokers: the roles of DRD2, <strong>DRD4</strong>, and OPRM1 genotypes.
+DRD4	drug	nicotine	26449981	The aim of this study was to identify specific genetic (i.e., DRD2 Taq1A, <strong>DRD4</strong> 48 bp VNTR, and OPRM1 A118G polymorphisms) and environmental mechanisms that underlie the emergence of both cue induced and cognitive craving among adolescent novice <b>smokers</b>.
+DRD4	addiction	relapse	26449981	The aim of this study was to identify specific genetic (i.e., DRD2 Taq1A, <strong>DRD4</strong> 48 bp VNTR, and OPRM1 A118G polymorphisms) and environmental mechanisms that underlie the emergence of both cue induced and cognitive <b>craving</b> among adolescent novice smokers.
+DRD4	addiction	reward	26307243	The dopamine receptor D4 gene (<strong>DRD4</strong>) is a potential candidate gene that may influence adolescents' susceptibility to their peer environment due to the role dopamine plays in <b>reward</b> sensation during social interaction.
+DRD4	addiction	reward	26307243	The <strong>dopamine receptor D4</strong> gene (<strong>DRD4</strong>) is a potential candidate gene that may influence adolescents' susceptibility to their peer environment due to the role dopamine plays in <b>reward</b> sensation during social interaction.
+DRD4	drug	alcohol	26307243	We hypothesized that <strong>DRD4</strong> genotype status would moderate the impact of 7th grade antisocial peer pressure on 12th grade lifetime <b>alcohol</b> use (n = 414; 58.7% female; 92.8% White).
+DRD4	drug	alcohol	26307243	The results revealed significant main effects for antisocial peer pressure, but no main effects for <strong>DRD4</strong> genotype on lifetime <b>alcohol</b> use.
+DRD4	drug	alcohol	26307243	Adolescent <strong>DRD4</strong> genotype moderated the association between peer pressure and lifetime <b>alcohol</b> use.
+DRD4	drug	alcohol	26307243	For individuals who carried at least one copy of the <strong>DRD4</strong> 7 repeat allele (7+), antisocial peer pressure was associated with increased lifetime <b>alcohol</b> use.
+DRD4	drug	opioid	26288297	It was genotyped polymorphisms in the following genes: mu <b>opioid</b> receptor (OPRM1), kappa <b>opioid</b> receptor (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (<strong>DRD4</strong>), dopamine beta hydroxylase, and dopamine transporter (DAT1).
+DRD4	addiction	relapse	26288297	Regardless of treatment several polymorphisms of these genes were associated with high risk of <b>relapse</b>: an allele L (2R) <strong>DRD4</strong> 120bp (p=0.05; OR (95% CI)=3.3(1.1 10.1)); an allele С DRD2 NcoI (р=0,051; OR (95% CI)=2,86 (1,09 7,52)); the genotype 9.9 DAT VNTR 40bp (р=0,04; OR (95% CI)=1,4 (1,3 1,5)); on the contrary, (СС+СТ) (ТТ)) variants of OPRK1 DRD2Ncol increased a chance to complete treatment program (р=0,004; OR (95% CI)=7.4 (1.8 30.4)), Kaplan Meier survival analysis (р=0,016).
+DRD4	drug	alcohol	26146874	Polymorphisms of the DRD2, ANKK1, DAT1, DBH, and <strong>DRD4</strong> genes have been found to moderate the effects of pharmacotherapy of <b>alcohol</b>, opioid, and cocaine use disorders.
+DRD4	drug	cocaine	26146874	Polymorphisms of the DRD2, ANKK1, DAT1, DBH, and <strong>DRD4</strong> genes have been found to moderate the effects of pharmacotherapy of alcohol, opioid, and <b>cocaine</b> use disorders.
+DRD4	drug	opioid	26146874	Polymorphisms of the DRD2, ANKK1, DAT1, DBH, and <strong>DRD4</strong> genes have been found to moderate the effects of pharmacotherapy of alcohol, <b>opioid</b>, and cocaine use disorders.
+DRD4	drug	alcohol	26092968	Influence of the A118G Polymorphism of the OPRM1 Gene and Exon 3 VNTR Polymorphism of the <strong>DRD4</strong> Gene on Cigarette Craving After <b>Alcohol</b> Administration.
+DRD4	addiction	relapse	26092968	Influence of the A118G Polymorphism of the OPRM1 Gene and Exon 3 VNTR Polymorphism of the <strong>DRD4</strong> Gene on Cigarette <b>Craving</b> After Alcohol Administration.
+DRD4	drug	alcohol	26092968	The current study examined whether the presence of the G allele of the A118G polymorphism of the OPRM1 gene (rs1799971) and the long allele of exon 3 VNTR polymorphism of the <strong>DRD4</strong> gene moderate the effect of <b>alcohol</b> administration on urge to smoke.
+DRD4	drug	alcohol	25914336	We hypothesized that: (1) mice with low (<strong>Drd4</strong>(+/ )) or deficient (<strong>Drd4</strong>( / )) in D4 receptors would show enhanced <b>ethanol</b> consumption compared with control mice (<strong>Drd4</strong>(+/+)), and (2) a specific phenotype in these mice is associated with future vulnerability for <b>alcohol</b> consumption.
+DRD4	drug	alcohol	25914336	Correlation analyses showed that in male <strong>Drd4</strong>( / ) mice (relative to <strong>Drd4</strong>(+/+) controls), anxiolytic behavior was significantly correlated with increased <b>alcohol</b> consumption.
+DRD4	drug	alcohol	25914336	Also, in male <strong>Drd4</strong>( / ) mice, there was a significant positive correlation between increased exploratory behavior and increased <b>alcohol</b> consumption.
+DRD4	drug	alcohol	25660313	Meta analysis of six genes (BDNF, DRD1, DRD3, <strong>DRD4</strong>, GRIN2B and MAOA) involved in neuroplasticity and the risk for <b>alcohol</b> dependence.
+DRD4	addiction	dependence	25660313	Meta analysis of six genes (BDNF, DRD1, DRD3, <strong>DRD4</strong>, GRIN2B and MAOA) involved in neuroplasticity and the risk for alcohol <b>dependence</b>.
+DRD4	drug	alcohol	27087792	We sought to explore the association between a dopamine D4 receptor gene (<strong>DRD4</strong>), a genetic marker associated with natural variations in rewarding behaviors, and self reported <b>alcohol</b> use and sexual risk behaviors, while controlling for other known correlates of risk taking such as impulsivity, sensation seeking, and peer norms among a group of high risk African American female adolescents to evaluate whether this biological factor enhances our understanding of patterns of risk in this vulnerable group.
+DRD4	addiction	relapse	27087792	We sought to explore the association between a dopamine D4 receptor gene (<strong>DRD4</strong>), a genetic marker associated with natural variations in rewarding behaviors, and self reported alcohol use and sexual risk behaviors, while controlling for other known correlates of risk taking such as impulsivity, sensation <b>seeking</b>, and peer norms among a group of high risk African American female adolescents to evaluate whether this biological factor enhances our understanding of patterns of risk in this vulnerable group.
+DRD4	drug	alcohol	25212749	Ondansetron and sertraline may interact with 5 HTTLPR and <strong>DRD4</strong> polymorphisms to reduce drinking in non treatment seeking <b>alcohol</b> dependent women: exploratory findings.
+DRD4	addiction	relapse	25212749	Ondansetron and sertraline may interact with 5 HTTLPR and <strong>DRD4</strong> polymorphisms to reduce drinking in non treatment <b>seeking</b> alcohol dependent women: exploratory findings.
+DRD4	drug	alcohol	25212749	The purpose of this exploratory study was to examine the interaction of 5 HTTLPR and <strong>DRD4</strong> exon III polymorphisms with gender in non treatment seeking <b>alcohol</b> dependent (AD) individuals while alternately taking ondansetron and sertraline.
+DRD4	addiction	relapse	25212749	The purpose of this exploratory study was to examine the interaction of 5 HTTLPR and <strong>DRD4</strong> exon III polymorphisms with gender in non treatment <b>seeking</b> alcohol dependent (AD) individuals while alternately taking ondansetron and sertraline.
+DRD4	drug	alcohol	25035107	The present study aimed to evaluate the association of <b>alcohol</b> dependence and <b>alcohol</b> dependence related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (COMT), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (<strong>DRD4</strong>) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (DBH) and MAO B intron 13 polymorphisms.
+DRD4	addiction	dependence	25035107	The present study aimed to evaluate the association of alcohol <b>dependence</b> and alcohol <b>dependence</b> related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (COMT), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (<strong>DRD4</strong>) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (DBH) and MAO B intron 13 polymorphisms.
+DRD4	drug	alcohol	25035107	The present study aimed to evaluate the association of <b>alcohol</b> dependence and <b>alcohol</b> dependence related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (COMT), variable number of tandem repeats (VNTR) in the third exon of <strong>dopamine receptor D4</strong> (<strong>DRD4</strong>) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (DBH) and MAO B intron 13 polymorphisms.
+DRD4	addiction	dependence	25035107	The present study aimed to evaluate the association of alcohol <b>dependence</b> and alcohol <b>dependence</b> related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (COMT), variable number of tandem repeats (VNTR) in the third exon of <strong>dopamine receptor D4</strong> (<strong>DRD4</strong>) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (DBH) and MAO B intron 13 polymorphisms.
+DRD4	drug	opioid	24755993	SNPs in the genes for brain derived neurotrophic factor (BDNF), the muscarinic acetylcholine receptor M2 (CHRM2), the dopamine receptor D4 (<strong>DRD4</strong>) and the μ1 <b>opioid</b> receptor (OPRM1) significantly moderated the impact of treatment condition over time on PA. Genetic variation in the genes for CHRM2 and OPRM1 specifically had an impact on the level of PA following MBCT.
+DRD4	drug	opioid	24755993	SNPs in the genes for brain derived neurotrophic factor (BDNF), the muscarinic acetylcholine receptor M2 (CHRM2), the <strong>dopamine receptor D4</strong> (<strong>DRD4</strong>) and the μ1 <b>opioid</b> receptor (OPRM1) significantly moderated the impact of treatment condition over time on PA. Genetic variation in the genes for CHRM2 and OPRM1 specifically had an impact on the level of PA following MBCT.
+DRD4	drug	nicotine	24659022	Effects of <b>nicotine</b> deprivation and replacement on BOLD fMRI response to <b>smoking</b> cues as a function of <strong>DRD4</strong> VNTR genotype.
+DRD4	drug	nicotine	24659022	Reactivity to <b>smoking</b> cues is an important factor in the motivation to smoke and has been associated with the dopamine receptor 4 variable number tandem repeat (<strong>DRD4</strong> exon III VNTR) polymorphism.
+DRD4	drug	nicotine	24659022	Non treatment seeking Caucasian <b>smokers</b> completed overnight abstinence and viewed <b>smoking</b> and neutral cues during 2 separate functional magnetic resonance imaging scans while wearing either a <b>nicotine</b> or placebo patch (order randomized) and were genotyped for the <strong>DRD4</strong> VNTR.
+DRD4	addiction	relapse	24659022	Non treatment <b>seeking</b> Caucasian smokers completed overnight abstinence and viewed smoking and neutral cues during 2 separate functional magnetic resonance imaging scans while wearing either a nicotine or placebo patch (order randomized) and were genotyped for the <strong>DRD4</strong> VNTR.
+DRD4	drug	nicotine	24659022	We conducted mixed effects repeated measures analyses of variance (within subject factor: <b>nicotine</b> or placebo patch; between subject factor: <strong>DRD4</strong> long [L: ≥ 1 copy of ≥ 7 repeats] or short [S: 2 copies ≤ 6 repeats] genotype) of 6 a priori regions of interest.
+DRD4	addiction	relapse	24659022	A patch × <strong>DRD4</strong> interaction was observed in the left amygdala, an area associated with appetitive reinforcement and <b>relapse</b> risk, such that S allele carriers demonstrated greater activation on active patch than on placebo patch.
+DRD4	addiction	reward	24659022	A patch × <strong>DRD4</strong> interaction was observed in the left amygdala, an area associated with appetitive <b>reinforcement</b> and relapse risk, such that S allele carriers demonstrated greater activation on active patch than on placebo patch.
+DRD4	drug	nicotine	24659022	Brain systems associated with reward salience may become primed and overreactive at <b>nicotine</b> replacement doses intended for the first step of <b>smoking</b> cessation and may become inhibited during <b>nicotine</b> withdrawal in <strong>DRD4</strong> S but not in <strong>DRD4</strong> L carriers.
+DRD4	addiction	reward	24659022	Brain systems associated with <b>reward</b> salience may become primed and overreactive at nicotine replacement doses intended for the first step of smoking cessation and may become inhibited during nicotine withdrawal in <strong>DRD4</strong> S but not in <strong>DRD4</strong> L carriers.
+DRD4	addiction	withdrawal	24659022	Brain systems associated with reward salience may become primed and overreactive at nicotine replacement doses intended for the first step of smoking cessation and may become inhibited during nicotine <b>withdrawal</b> in <strong>DRD4</strong> S but not in <strong>DRD4</strong> L carriers.
+DRD4	drug	nicotine	24659022	These findings are consistent with the role of these regions in drug reinforcement and suggest a differential influence of <b>nicotine</b> replacement on amygdala activation in the association of incentive salience with <b>smoking</b> stimuli across <strong>DRD4</strong> genotypes.
+DRD4	addiction	reward	24659022	These findings are consistent with the role of these regions in drug <b>reinforcement</b> and suggest a differential influence of nicotine replacement on amygdala activation in the association of <b>incentive</b> salience with smoking stimuli across <strong>DRD4</strong> genotypes.
+DRD4	drug	nicotine	24446757	We investigated the role of exposure to <b>smoking</b> (by parents, siblings, and peers) and reward related candidate gene polymorphisms (OPRM1 A118G, DRD2 TaqlA and <strong>DRD4</strong> bp VNTR) in adolescents' responses to initial <b>smoking</b>.
+DRD4	addiction	reward	24446757	We investigated the role of exposure to smoking (by parents, siblings, and peers) and <b>reward</b> related candidate gene polymorphisms (OPRM1 A118G, DRD2 TaqlA and <strong>DRD4</strong> bp VNTR) in adolescents' responses to initial smoking.
+DRD4	drug	nicotine	24444411	Genetic variants in DRD2, <strong>DRD4</strong>, ANKK1, DAT1, COMT and DBH genes show some promise in informing personalized prescribing of <b>smoking</b> cessation pharmacotherapies.
+DRD4	drug	opioid	24368617	Genetic polymorphisms in the coding or promoter regions of the Mu <b>Opioid</b> Receptor (OPRM1), Corticotropin Releasing Hormone (CRH), Monoamine Oxidase A (MAOA), Dopamine D4 Receptor (<strong>DRD4</strong>), and Serotonin Transporter (SLC6A4) genes have been shown to be functionally similar in humans and rhesus macaques and have been demonstrated to contribute to individual differences in aggression.
+DRD4	drug	alcohol	24135011	Statistically significant associations of polymorphisms in DRD1 and <strong>DRD4</strong> with <b>alcoholism</b> were found.
+DRD4	drug	nicotine	23941313	Age, gender, Fagerström Test for <b>Nicotine</b> Dependence, dopamine pathway genotypes (rs1800497 [ANKK1 E713K], rs4680 [COMT V158M], <strong>DRD4</strong> exon 3 variable number of tandem repeats polymorphism [<strong>DRD4</strong> VNTR], SLC6A3,3' VNTR) analyzed both separately and as part of an AGES, time to first lapse and point prevalence abstinence at end of treatment.
+DRD4	addiction	dependence	23941313	Age, gender, Fagerström Test for Nicotine <b>Dependence</b>, dopamine pathway genotypes (rs1800497 [ANKK1 E713K], rs4680 [COMT V158M], <strong>DRD4</strong> exon 3 variable number of tandem repeats polymorphism [<strong>DRD4</strong> VNTR], SLC6A3,3' VNTR) analyzed both separately and as part of an AGES, time to first lapse and point prevalence abstinence at end of treatment.
+DRD4	drug	opioid	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (<strong>DRD4</strong>), catechol O methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and <b>heroin</b> dependence in Hungarian patients.
+DRD4	addiction	dependence	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (<strong>DRD4</strong>), catechol O methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and heroin <b>dependence</b> in Hungarian patients.
+DRD4	drug	opioid	23840506	303 <b>heroin</b> dependent subjects and 555 healthy controls were genotyped for 7 single nucleotide polymorphisms (SNPs) rs4680 of the COMT gene; rs1079597 and rs1800498 of the DRD2 gene; rs1800497 of the ANKK1 gene; rs1800955, rs936462 and rs747302 of the <strong>DRD4</strong> gene.
+DRD4	drug	alcohol	23818181	Association between DRD2/<strong>DRD4</strong> interaction and conduct disorder: a potential developmental pathway to <b>alcohol</b> dependence.
+DRD4	addiction	dependence	23818181	Association between DRD2/<strong>DRD4</strong> interaction and conduct disorder: a potential developmental pathway to alcohol <b>dependence</b>.
+DRD4	drug	nicotine	23522492	Lack of association of <strong>DRD4</strong> exon 3 VNTR genotype with reactivity to dynamic <b>smoking</b> cues in movies.
+DRD4	drug	nicotine	23522492	The objective of the present study was first to examine whether dynamic <b>smoking</b> cues in movies trigger craving, and second to explore whether the <strong>DRD4</strong> 48 bp variable number of tandem repeat (VNTR) exon 3 genotype modifies this relationship.
+DRD4	addiction	relapse	23522492	The objective of the present study was first to examine whether dynamic smoking cues in movies trigger <b>craving</b>, and second to explore whether the <strong>DRD4</strong> 48 bp variable number of tandem repeat (VNTR) exon 3 genotype modifies this relationship.
+DRD4	addiction	relapse	23522492	The results did not indicate any evidence of a three way interaction between movie condition, the <strong>DRD4</strong> VNTR polymorphism and time and no evidence of a main effect of condition on <b>craving</b>.
+DRD4	drug	nicotine	23522492	The results found evidence of a main effect of the <strong>DRD4</strong> VNTR polymorphism on craving (p=.03), indicating that <b>smokers</b> carrying the <strong>DRD4</strong> 7 repeat allele showed higher levels of craving compared with <b>smokers</b> without the <strong>DRD4</strong> 7 repeat allele.
+DRD4	addiction	relapse	23522492	The results found evidence of a main effect of the <strong>DRD4</strong> VNTR polymorphism on <b>craving</b> (p=.03), indicating that smokers carrying the <strong>DRD4</strong> 7 repeat allele showed higher levels of <b>craving</b> compared with smokers without the <strong>DRD4</strong> 7 repeat allele.
+DRD4	drug	nicotine	23522492	Dynamic <b>smoking</b> cues in movies do not affect <b>smokers</b>' craving and this is not modified by <strong>DRD4</strong> genotype.
+DRD4	addiction	relapse	23522492	Dynamic smoking cues in movies do not affect smokers' <b>craving</b> and this is not modified by <strong>DRD4</strong> genotype.
+DRD4	drug	nicotine	23522492	<b>Smokers</b> carrying the <strong>DRD4</strong> 7 repeat allele developed higher levels of craving in the context of watching a movie than non carriers.
+DRD4	addiction	relapse	23522492	Smokers carrying the <strong>DRD4</strong> 7 repeat allele developed higher levels of <b>craving</b> in the context of watching a movie than non carriers.
+DRD4	addiction	reward	23336089	Likewise, voting, voting turnout and attachment to a particular political ideology is differentially related to various <b>reward</b> genes (e.g., 5HTT, MOA, DRD2, and <strong>DRD4</strong>), possibly predicting liberalism or conservatism.
+DRD4	addiction	intoxication	23298155	Fibrosis progression in HCV carriers with mild hepatitis who possess the high repetition variant of the <strong>DRD4</strong> gene, a genetic marker for <b>binge</b> drinking and risk seeking behavior: a longitudinal study.
+DRD4	addiction	relapse	23298155	Fibrosis progression in HCV carriers with mild hepatitis who possess the high repetition variant of the <strong>DRD4</strong> gene, a genetic marker for binge drinking and risk <b>seeking</b> behavior: a longitudinal study.
+DRD4	drug	alcohol	23298155	We hypothesized that carriage of high repetition variants (HRV) of the variable number of tandem repeats (VNTR) in exon III of the <strong>dopamine receptor D4</strong> gene, linked to binge drinking and risk seeking behavior, might be a proxy measure of <b>alcohol</b> consumption, and aimed to verify whether it may affect histologic outcome.
+DRD4	addiction	intoxication	23298155	We hypothesized that carriage of high repetition variants (HRV) of the variable number of tandem repeats (VNTR) in exon III of the <strong>dopamine receptor D4</strong> gene, linked to <b>binge</b> drinking and risk seeking behavior, might be a proxy measure of alcohol consumption, and aimed to verify whether it may affect histologic outcome.
+DRD4	addiction	relapse	23298155	We hypothesized that carriage of high repetition variants (HRV) of the variable number of tandem repeats (VNTR) in exon III of the <strong>dopamine receptor D4</strong> gene, linked to binge drinking and risk <b>seeking</b> behavior, might be a proxy measure of alcohol consumption, and aimed to verify whether it may affect histologic outcome.
+DRD4	drug	alcohol	23262301	anxiety, family history and onset of <b>alcoholism</b>, and D4 dopamine receptor (<strong>DRD4</strong>) and 5 HTTLPR polymorphisms.
+DRD4	drug	alcohol	23262301	As for the exploratory analyses, baclofen's effects to increase <b>alcohol</b> sedation and to reduce <b>alcohol</b> consumption were limited to those individuals with <strong>DRD4</strong> ≥7 repeats (DRD4L).
+DRD4	drug	nicotine	23212438	<strong>DRD4</strong> Exon III Variable Number of Tandem Repeat (VNTR) variation was found to interact with bupropion to influence prospective <b>smoking</b> abstinence, in a recently published longitudinal analyses of N = 331 individuals from a randomized double blind placebo controlled trial of bupropion and intensive cognitive behavioral mood management therapy.
+DRD4	drug	opioid	22841130	One hundred seven <b>methadone</b> maintenance treatment patients, 36 having an ADHD diagnosis, 176 adult patients with ADHD without SUDs, and 500 healthy controls were genotyped for variants in the <strong>DRD4</strong> (exon 3 VNTR), DRD5 (upstream VNTR), HTR1B (rs6296), DBH (rs2519152), COMT (rs4680; Val158Met), and OPRM1 (rs1799971; 118A>G) genes.
+DRD4	drug	nicotine	22609848	Lack of association between <strong>dopamine receptor D4</strong> variable numbers of tandem repeats gene polymorphism and <b>smoking</b>.
+DRD4	drug	nicotine	22609848	Literature data showed not only an association, but also a lack of association between variable number of tandem repeats (VNTR) polymorphism located in the third exon of dopamine D4 receptor (<strong>DRD4</strong>) gene and <b>smoking</b>.
+DRD4	drug	nicotine	22609848	The aim of this study was to determine the association between VNTR in <strong>DRD4</strong> gene and present <b>smoking</b> status in ethnically homogenous Caucasian population from the Eastern European (Croatian) origin.
+DRD4	drug	nicotine	22609848	Logistic regression analyses, adjusted for age and sex, revealed the lack of significant (p>0.05) effect of the 4/4, 4/7 and 7/7 genotypes, or carriers of the long and short allele, or all genotypes of the <strong>DRD4</strong> VNTR on <b>smoking</b> status.
+DRD4	drug	nicotine	22609848	The results of this study failed to confirm the hypothesis that long allele of the <strong>DRD4</strong> VNTR is associated with <b>smoking</b> status in Caucasian subjects.
+DRD4	drug	alcohol	22587755	Variation in the <strong>DRD4</strong> gene, which encodes the dopamine D(4) receptor, may predict better response to <b>naltrexone</b> and olanzapine.
+DRD4	drug	alcohol	22565782	DRD2/<strong>DRD4</strong> heteromerization may influence genetic susceptibility to <b>alcohol</b> dependence.
+DRD4	addiction	dependence	22565782	DRD2/<strong>DRD4</strong> heteromerization may influence genetic susceptibility to alcohol <b>dependence</b>.
+DRD4	drug	alcohol	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, DRD2, DRD3, <strong>DRD4</strong>) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of craving, as well as alpha synuclein (SNCA), which has been previously found to be associated with craving, were associated with <b>alcohol</b> craving in this sample.
+DRD4	addiction	relapse	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, DRD2, DRD3, <strong>DRD4</strong>) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of <b>craving</b>, as well as alpha synuclein (SNCA), which has been previously found to be associated with <b>craving</b>, were associated with alcohol <b>craving</b> in this sample.
+DRD4	drug	alcohol	22436571	The effect of the OPRM1 and <strong>DRD4</strong> polymorphisms on the relation between attentional bias and <b>alcohol</b> use in adolescence and young adulthood.
+DRD4	drug	alcohol	22436571	The effect of the OPRM1 c.118A>G polymorphism, associated with liking and wanting, and the <strong>DRD4</strong> VNTR polymorphism, related to wanting, on the relation between attentional bias and <b>alcohol</b> use was investigated.
+DRD4	drug	alcohol	22347363	<strong>DRD4</strong> polymorphism moderates the effect of <b>alcohol</b> consumption on social bonding.
+DRD4	drug	alcohol	22347363	We employed a 3 (group beverage condition) ×2 (genotype) design (N = 422) to test the moderating influence of the dopamine D4 receptor gene (<strong>DRD4</strong> VNTR) polymorphism on the effects of <b>alcohol</b> on social bonding.
+DRD4	drug	alcohol	22347363	These data converge with other recent gene environment interaction findings implicating the <strong>DRD4</strong> polymorphism in the development of <b>alcohol</b> use disorders, and results suggest a specific pathway by which social factors may increase risk for problematic drinking among 7 repeat carriers.
+DRD4	drug	alcohol	22232964	[The influence of parents personality and <strong>DRD4</strong> and 5HTT genes polymorphisms on predisposition to <b>alcohol</b> dependence in their sons].
+DRD4	addiction	dependence	22232964	[The influence of parents personality and <strong>DRD4</strong> and 5HTT genes polymorphisms on predisposition to alcohol <b>dependence</b> in their sons].
+DRD4	addiction	addiction	22232964	Also the possibility of recognising their genotypes <strong>DRD4</strong> (Gene ID: 1815A) and 5HTT (Gene ID: 6532) could be helpful in predicting predisposition to <b>addiction</b>.
+DRD4	drug	alcohol	22126256	To investigate the combined effect of an exon III variable number tandem repeat in the dopamine receptor gene (<strong>DRD4</strong>) and insecure attachment style on risk for tobacco, cannabis and <b>alcohol</b> use problems in young adulthood.
+DRD4	drug	cannabinoid	22126256	To investigate the combined effect of an exon III variable number tandem repeat in the dopamine receptor gene (<strong>DRD4</strong>) and insecure attachment style on risk for tobacco, <b>cannabis</b> and alcohol use problems in young adulthood.
+DRD4	drug	nicotine	22126256	To investigate the combined effect of an exon III variable number tandem repeat in the dopamine receptor gene (<strong>DRD4</strong>) and insecure attachment style on risk for <b>tobacco</b>, cannabis and alcohol use problems in young adulthood.
+DRD4	drug	nicotine	22030716	It has been reported that polymorphism of the <strong>DRD4</strong> gene in humans is associated with reactivity to cues related to <b>tobacco</b> <b>smoking</b>.
+DRD4	drug	nicotine	22030716	However, the role of <strong>DRD4</strong> in animal models of <b>nicotine</b> addiction has seldom been explored.
+DRD4	addiction	addiction	22030716	However, the role of <strong>DRD4</strong> in animal models of nicotine <b>addiction</b> has seldom been explored.
+DRD4	drug	nicotine	22030716	Effects of the selective <strong>DRD4</strong> antagonist L 745,870 were evaluated on <b>nicotine</b> self administration behavior and on reinstatement of extinguished <b>nicotine</b> seeking behavior induced by <b>nicotine</b> associated cues or by priming injections of <b>nicotine</b>.
+DRD4	addiction	relapse	22030716	Effects of the selective <strong>DRD4</strong> antagonist L 745,870 were evaluated on nicotine self administration behavior and on <b>reinstatement</b> of extinguished nicotine <b>seeking</b> behavior induced by nicotine associated cues or by priming injections of nicotine.
+DRD4	drug	nicotine	22030716	In addition, the selective <strong>DRD4</strong> agonist PD 168,077 was tested for its ability to reinstate extinguished <b>nicotine</b> seeking behavior.
+DRD4	addiction	relapse	22030716	In addition, the selective <strong>DRD4</strong> agonist PD 168,077 was tested for its ability to reinstate extinguished nicotine <b>seeking</b> behavior.
+DRD4	drug	nicotine	22030716	As <strong>DRD4</strong> blockade by L 745,870 selectively attenuated both cue  and <b>nicotine</b> induced reinstatement of <b>nicotine</b> seeking behavior, without affecting cue  or food induced reinstatement of food seeking behavior, <strong>DRD4</strong> antagonists are potential therapeutic agents against <b>tobacco</b> <b>smoking</b> relapse.
+DRD4	addiction	relapse	22030716	As <strong>DRD4</strong> blockade by L 745,870 selectively attenuated both cue  and nicotine induced <b>reinstatement</b> of nicotine <b>seeking</b> behavior, without affecting cue  or food induced <b>reinstatement</b> of food <b>seeking</b> behavior, <strong>DRD4</strong> antagonists are potential therapeutic agents against tobacco smoking <b>relapse</b>.
+DRD4	drug	opioid	21714067	Association between polymorphisms of DRD2 and <strong>DRD4</strong> and <b>opioid</b> dependence: evidence from the current studies.
+DRD4	addiction	dependence	21714067	Association between polymorphisms of DRD2 and <strong>DRD4</strong> and opioid <b>dependence</b>: evidence from the current studies.
+DRD4	drug	opioid	21714067	Several studies have assessed the association between genetic polymorphisms of DRD2 and <strong>DRD4</strong> genes and <b>opioid</b> dependence risk, while the results were inconsistent.
+DRD4	addiction	dependence	21714067	Several studies have assessed the association between genetic polymorphisms of DRD2 and <strong>DRD4</strong> genes and opioid <b>dependence</b> risk, while the results were inconsistent.
+DRD4	drug	opioid	21714067	We performed a meta analysis, including 6,846 <b>opioid</b> dependence cases and 4,187 controls from 22 individual studies, to evaluate the roles of four variants (DRD2  141ins/delC, rs1799732; DRD2 311 Ser > Cys, rs1801028; DRD2 related TaqI A, rs1800497 and <strong>DRD4</strong> exon III VNTR) in <b>opioid</b> dependence for the first time.
+DRD4	addiction	dependence	21714067	We performed a meta analysis, including 6,846 opioid <b>dependence</b> cases and 4,187 controls from 22 individual studies, to evaluate the roles of four variants (DRD2  141ins/delC, rs1799732; DRD2 311 Ser > Cys, rs1801028; DRD2 related TaqI A, rs1800497 and <strong>DRD4</strong> exon III VNTR) in opioid <b>dependence</b> for the first time.
+DRD4	drug	opioid	21714067	Moreover, long allele (≥5 repeat) and 7 repeat allele of <strong>DRD4</strong> exon III VNTR were found to be associated with significantly increased <b>opioid</b> dependence risk (OR, 1.50; 95% CI, 1.24 1.80 and OR, 1.57; 95%, 1.18 2.09, respectively).
+DRD4	addiction	dependence	21714067	Moreover, long allele (≥5 repeat) and 7 repeat allele of <strong>DRD4</strong> exon III VNTR were found to be associated with significantly increased opioid <b>dependence</b> risk (OR, 1.50; 95% CI, 1.24 1.80 and OR, 1.57; 95%, 1.18 2.09, respectively).
+DRD4	drug	opioid	21714067	In conclusion, our results suggested that DRD2  141ins/delC, DRD2 related TaqI A and <strong>DRD4</strong> exon III VNTR polymorphisms might play important roles in the development of <b>opioid</b> dependence.
+DRD4	addiction	dependence	21714067	In conclusion, our results suggested that DRD2  141ins/delC, DRD2 related TaqI A and <strong>DRD4</strong> exon III VNTR polymorphisms might play important roles in the development of opioid <b>dependence</b>.
+DRD4	drug	alcohol	21381802	Interaction between the <strong>DRD4</strong> VNTR polymorphism and proximal and distal environments in <b>alcohol</b> dependence during emerging and young adulthood.
+DRD4	addiction	dependence	21381802	Interaction between the <strong>DRD4</strong> VNTR polymorphism and proximal and distal environments in alcohol <b>dependence</b> during emerging and young adulthood.
+DRD4	drug	alcohol	21381802	Taking a developmental approach, we characterized interaction between the dopamine receptor 4 variable number tandem repeat (<strong>DRD4</strong> VNTR) polymorphism and developmentally specific environmental factors (childhood adversity, college/Greek organization involvement, and delayed adult role transition) on <b>alcohol</b> dependence during emerging and young adulthood.
+DRD4	addiction	dependence	21381802	Taking a developmental approach, we characterized interaction between the dopamine receptor 4 variable number tandem repeat (<strong>DRD4</strong> VNTR) polymorphism and developmentally specific environmental factors (childhood adversity, college/Greek organization involvement, and delayed adult role transition) on alcohol <b>dependence</b> during emerging and young adulthood.
+DRD4	drug	alcohol	21381802	We accounted for those <b>alcohol</b> dependence factors by modeling 3 two way interaction effects between the <strong>DRD4</strong> VNTR polymorphism and the 3 developmentally specific environment factors.
+DRD4	addiction	dependence	21381802	We accounted for those alcohol <b>dependence</b> factors by modeling 3 two way interaction effects between the <strong>DRD4</strong> VNTR polymorphism and the 3 developmentally specific environment factors.
+DRD4	drug	alcohol	21381802	Carriers of the <strong>DRD4</strong> long allele showed greater susceptibility to environmental effects; they showed more persistent symptoms of <b>alcohol</b> dependence as childhood adversity increased and more <b>alcohol</b> dependence symptoms limited to emerging adulthood as college/Greek organization involvement increased.
+DRD4	addiction	dependence	21381802	Carriers of the <strong>DRD4</strong> long allele showed greater susceptibility to environmental effects; they showed more persistent symptoms of alcohol <b>dependence</b> as childhood adversity increased and more alcohol <b>dependence</b> symptoms limited to emerging adulthood as college/Greek organization involvement increased.
+DRD4	drug	nicotine	21127031	A role for the <strong>DRD4</strong> exon III VNTR in modifying the association between <b>nicotine</b> dependence and neuroticism.
+DRD4	addiction	dependence	21127031	A role for the <strong>DRD4</strong> exon III VNTR in modifying the association between nicotine <b>dependence</b> and neuroticism.
+DRD4	drug	nicotine	21127031	The purpose of this study was to examine association between both <b>smoking</b> initiation (SI) and progression to ND by young adulthood and (a) history of neuroticism during adolescence, (b) <strong>DRD4</strong> 7R+, and (c) interaction between neuroticism and <strong>DRD4</strong> 7R+.
+DRD4	drug	opioid	20801104	Association study of polymorphisms in the promoter region of <strong>DRD4</strong> with schizophrenia, depression, and <b>heroin</b> addiction.
+DRD4	addiction	addiction	20801104	Association study of polymorphisms in the promoter region of <strong>DRD4</strong> with schizophrenia, depression, and heroin <b>addiction</b>.
+DRD4	drug	opioid	20801104	This study investigated the possible association between three functional polymorphisms in the promoter region of the dopamine D4 receptor (<strong>DRD4</strong>) gene and schizophrenia, depression, and <b>heroin</b> addiction.
+DRD4	addiction	addiction	20801104	This study investigated the possible association between three functional polymorphisms in the promoter region of the dopamine D4 receptor (<strong>DRD4</strong>) gene and schizophrenia, depression, and heroin <b>addiction</b>.
+DRD4	drug	opioid	20801104	These observations strongly suggest that the  120 bp duplication polymorphism of <strong>DRD4</strong> is associated with schizophrenia and that the  521 C/T polymorphism is associated with <b>heroin</b> addiction.
+DRD4	addiction	addiction	20801104	These observations strongly suggest that the  120 bp duplication polymorphism of <strong>DRD4</strong> is associated with schizophrenia and that the  521 C/T polymorphism is associated with heroin <b>addiction</b>.
+DRD4	drug	opioid	20482509	We consider four neurotransmitter systems: opioidergic, dopaminergic, GABAergic, and glutamatergic and focus on one receptor protein in each: OPRM1 (the &#micro; <b>opioid</b> receptor gene), <strong>DRD4</strong> (the D(4) dopamine receptor gene), GABRA2 (GABA(A) receptor alpha 2 subunit gene), and GRIK1 (the kainite receptor GluR5 subunit gene).
+DRD4	drug	alcohol	20482509	Promising findings include the observations that a polymorphism in GABRA2 predicts the response to specific psychotherapies; a polymorphism in <strong>DRD4</strong> predicts the effects of the antipsychotic olanzapine on craving for <b>alcohol</b> and drinking behavior; and a polymorphism in GRIKI predicts adverse events resulting from treatment with the anticonvulsant topiramate.
+DRD4	addiction	relapse	20482509	Promising findings include the observations that a polymorphism in GABRA2 predicts the response to specific psychotherapies; a polymorphism in <strong>DRD4</strong> predicts the effects of the antipsychotic olanzapine on <b>craving</b> for alcohol and drinking behavior; and a polymorphism in GRIKI predicts adverse events resulting from treatment with the anticonvulsant topiramate.
+DRD4	drug	opioid	20218801	Association of VNTR polymorphisms in the MAOA promoter and <strong>DRD4</strong> exon 3 with <b>heroin</b> dependence in male Chinese addicts.
+DRD4	addiction	dependence	20218801	Association of VNTR polymorphisms in the MAOA promoter and <strong>DRD4</strong> exon 3 with heroin <b>dependence</b> in male Chinese addicts.
+DRD4	drug	opioid	20218801	To explore the involvement of variable number tandem repeat (VNTR) polymorphisms in the monoamine oxidase A (MAOA) promoter and exon 3 of the dopamine D4 receptor (<strong>DRD4</strong>) gene in <b>heroin</b> addiction modulate the vulnerability of individuals to <b>heroin</b> addiction.
+DRD4	addiction	addiction	20218801	To explore the involvement of variable number tandem repeat (VNTR) polymorphisms in the monoamine oxidase A (MAOA) promoter and exon 3 of the dopamine D4 receptor (<strong>DRD4</strong>) gene in heroin <b>addiction</b> modulate the vulnerability of individuals to heroin <b>addiction</b>.
+DRD4	drug	opioid	20218801	The geno distribution of the <strong>DRD4</strong> exon 3 VNTR polymorphism in controls was in Hardy Weinberg equilibrium (HWEchi(2)=0.925), but the distribution in <b>heroin</b> addicts was not (HWEchi(2)=28.35).
+DRD4	drug	opioid	20218801	The long repeat alleles of the <strong>DRD4</strong> exon 3 VNTR polymorphism were found more frequently in the <b>heroin</b> addicts (P=0.019).
+DRD4	drug	opioid	20218801	The long repeat allelic variants (>4 repeats) and 2 repeat allele of the <strong>DRD4</strong> exon 3 VNTR polymorphism might be risk alleles for individual vulnerability to <b>heroin</b> addiction in Chinese men, but the MAOA promoter VNTR polymorphism does not mean that the partial dominant inherited mode might involved in the genetics of <b>heroin</b> dependence.
+DRD4	addiction	addiction	20218801	The long repeat allelic variants (>4 repeats) and 2 repeat allele of the <strong>DRD4</strong> exon 3 VNTR polymorphism might be risk alleles for individual vulnerability to heroin <b>addiction</b> in Chinese men, but the MAOA promoter VNTR polymorphism does not mean that the partial dominant inherited mode might involved in the genetics of heroin dependence.
+DRD4	addiction	dependence	20218801	The long repeat allelic variants (>4 repeats) and 2 repeat allele of the <strong>DRD4</strong> exon 3 VNTR polymorphism might be risk alleles for individual vulnerability to heroin addiction in Chinese men, but the MAOA promoter VNTR polymorphism does not mean that the partial dominant inherited mode might involved in the genetics of heroin <b>dependence</b>.
+DRD4	drug	alcohol	20141248	Polymorphisms of the mu opioid receptor (OPRM1) and dopamine D4 receptor (<strong>DRD4</strong>) genes are associated with subjective responses to <b>alcohol</b> and urge to drink under laboratory conditions.
+DRD4	drug	opioid	20141248	Polymorphisms of the mu <b>opioid</b> receptor (OPRM1) and dopamine D4 receptor (<strong>DRD4</strong>) genes are associated with subjective responses to alcohol and urge to drink under laboratory conditions.
+DRD4	drug	alcohol	20141248	Effects of OPRM1 and <strong>DRD4</strong> variable number of tandem repeats genotypes appear to be <b>alcohol</b> dose dependent.
+DRD4	drug	alcohol	20141248	Specifically, carriers of the <strong>DRD4</strong> L allele reported slight decreases in urge to drink at higher levels of estimated blood <b>alcohol</b> concentration (eBAC), and Asp40 carriers reported decreases in vigor and increases in negative mood as eBAC rose, as compared to carriers of the major allele for each gene.
+DRD4	drug	cannabinoid	19931559	(3) Feeding motivation  and reward related systems (opioids, OPRD1, <b>cannabinoids</b> (anandamide (AEA), <b>THC</b>, CBR1), dopamine, DRD2, DRD3, <strong>DRD4</strong>, catecholamine O methyl transferase (COMT).
+DRD4	drug	opioid	19931559	(3) Feeding motivation  and reward related systems (<b>opioids</b>, OPRD1, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, DRD3, <strong>DRD4</strong>, catecholamine O methyl transferase (COMT).
+DRD4	addiction	reward	19931559	(3) Feeding motivation  and <b>reward</b> related systems (opioids, OPRD1, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, DRD3, <strong>DRD4</strong>, catecholamine O methyl transferase (COMT).
+DRD4	addiction	relapse	19298319	Therefore, the objectives of this study were: (1) to test whether a single session of MET increased motivation to reduce drinking and drinking outcomes; and (2) to examine whether genetic dopamine D(4) receptor L (<strong>DRD4</strong> L) and individual personality risk factors (impulsivity and novelty <b>seeking</b>) moderated the effects of the MET.
+DRD4	addiction	relapse	19298319	Follow up data indicated that only individuals who were low in impulsivity, novelty <b>seeking</b> and/or who had the short <strong>DRD4</strong> variable number of tandem repeats genotype evidenced differentially increased behavior change (taking steps toward reducing drinking) following the MET.
+DRD4	drug	amphetamine	19275926	To test this hypothesis, 6 putatively functional polymorphisms of D2 like receptors,  141C Ins/Del, Ser311Cys and TaqIA of the DRD2 gene, Ser9Gly of the DRD3 gene, and  521C>T and a variable number of tandem repeats in exon 3 of the <strong>DRD4</strong> gene, were analyzed in 202 patients with <b>methamphetamine</b> dependence and/or psychosis and 243 healthy controls in a Japanese population.
+DRD4	addiction	dependence	19275926	To test this hypothesis, 6 putatively functional polymorphisms of D2 like receptors,  141C Ins/Del, Ser311Cys and TaqIA of the DRD2 gene, Ser9Gly of the DRD3 gene, and  521C>T and a variable number of tandem repeats in exon 3 of the <strong>DRD4</strong> gene, were analyzed in 202 patients with methamphetamine <b>dependence</b> and/or psychosis and 243 healthy controls in a Japanese population.
+DRD4	drug	amphetamine	19275926	These findings revealed that genetic variants of DRD2, but not DRD3 or <strong>DRD4</strong>, confer individual risks for rapid onset, prolonged duration, and spontaneous relapse of <b>methamphetamine</b> psychosis.
+DRD4	addiction	relapse	19275926	These findings revealed that genetic variants of DRD2, but not DRD3 or <strong>DRD4</strong>, confer individual risks for rapid onset, prolonged duration, and spontaneous <b>relapse</b> of methamphetamine psychosis.
+DRD4	drug	amphetamine	19219857	Three genes (COMT, <strong>DRD4</strong>, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with <b>METH</b> psychosis.
+DRD4	addiction	dependence	19219857	Three genes (COMT, <strong>DRD4</strong>, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.
+DRD4	addiction	addiction	19179847	Here, we will review the information collected implicating the receptors of the D1 family (DRD1 and DRD5) and of the D2 family (DRD2, DRD3 and <strong>DRD4</strong>) in drug <b>addiction</b>.
+DRD4	drug	cannabinoid	19084357	In nonsmokers, impulsive personality, prior <b>marijuana</b> use, and DRD2 and <strong>DRD4</strong> genotypes may moderate nicotine responses in men but apparently not in women.
+DRD4	drug	nicotine	19084357	In nonsmokers, impulsive personality, prior marijuana use, and DRD2 and <strong>DRD4</strong> genotypes may moderate <b>nicotine</b> responses in men but apparently not in women.
+DRD4	drug	nicotine	19084357	However, the <strong>DRD4</strong> gene may alter <b>smoking</b> reinforcement in response to negative mood in women but not men, a finding that could help explain <b>smoking</b> persistence in low SES women.
+DRD4	addiction	reward	19084357	However, the <strong>DRD4</strong> gene may alter smoking <b>reinforcement</b> in response to negative mood in women but not men, a finding that could help explain smoking persistence in low SES women.
+DRD4	drug	opioid	18991844	<strong>Dopamine receptor D4</strong> gene  521C/T polymorphism is associated with <b>opioid</b> dependence through cold pain responses.
+DRD4	addiction	dependence	18991844	<strong>Dopamine receptor D4</strong> gene  521C/T polymorphism is associated with opioid <b>dependence</b> through cold pain responses.
+DRD4	drug	opioid	18991844	The dopamine receptor D4 gene (<strong>DRD4</strong>) is associated with <b>heroin</b> dependence; one of its polymorphisms is a C/T variation 521 bp upstream to the gene ( 521C/T).
+DRD4	addiction	dependence	18991844	The dopamine receptor D4 gene (<strong>DRD4</strong>) is associated with heroin <b>dependence</b>; one of its polymorphisms is a C/T variation 521 bp upstream to the gene ( 521C/T).
+DRD4	drug	opioid	18991844	The <strong>dopamine receptor D4</strong> gene (<strong>DRD4</strong>) is associated with <b>heroin</b> dependence; one of its polymorphisms is a C/T variation 521 bp upstream to the gene ( 521C/T).
+DRD4	addiction	dependence	18991844	The <strong>dopamine receptor D4</strong> gene (<strong>DRD4</strong>) is associated with heroin <b>dependence</b>; one of its polymorphisms is a C/T variation 521 bp upstream to the gene ( 521C/T).
+DRD4	drug	opioid	18991844	The data suggest that <strong>DRD4</strong> 521C/T plays an important role in <b>opioid</b> dependence through modulating cold pain responses.
+DRD4	addiction	dependence	18991844	The data suggest that <strong>DRD4</strong> 521C/T plays an important role in opioid <b>dependence</b> through modulating cold pain responses.
+DRD4	drug	nicotine	18781857	Several candidate genes within the dopamine pathway (e.g., DRD2 and COMT) have been reported to be associated with the efficacy of bupropion and <b>nicotine</b> replacement therapy, and others (e.g., SLC6A3 and <strong>DRD4</strong>) have been reported to be associated with <b>smoking</b> cessation independent of pharmacotherapy.
+DRD4	drug	alcohol	18715282	The dopamine D Receptor (<strong>DRD4</strong>) gene exon III polymorphism, problematic <b>alcohol</b> use and novelty seeking: direct and mediated genetic effects.
+DRD4	addiction	relapse	18715282	The dopamine D Receptor (<strong>DRD4</strong>) gene exon III polymorphism, problematic alcohol use and novelty <b>seeking</b>: direct and mediated genetic effects.
+DRD4	addiction	relapse	18715282	The present study sought to integrate convergent lines of research on the associations among the dopamine D(4) receptor (<strong>DRD4</strong>) gene, novelty <b>seeking</b> and drinking behaviors with the overall goal of elucidating genetic influences on problematic drinking in young adulthood.
+DRD4	drug	alcohol	18715282	Specifically, this study tested a model in which novelty seeking mediated the relationship between <strong>DRD4</strong> variable number of tandem repeats (VNTR) genotype and problematic <b>alcohol</b> use.
+DRD4	addiction	relapse	18715282	Specifically, this study tested a model in which novelty <b>seeking</b> mediated the relationship between <strong>DRD4</strong> variable number of tandem repeats (VNTR) genotype and problematic alcohol use.
+DRD4	drug	alcohol	18715282	Analyses using a structural equation modeling framework suggested that the significant direct path between <strong>DRD4</strong> VNTR genotype and problematic <b>alcohol</b> use was reduced to a trend level in the context of a model that included novelty seeking as a mediator, thereby suggesting that the effects of <strong>DRD4</strong> VNTR genotype on problematic <b>alcohol</b> use among heavy drinking young adults were partially mediated by novelty seeking.
+DRD4	addiction	relapse	18715282	Analyses using a structural equation modeling framework suggested that the significant direct path between <strong>DRD4</strong> VNTR genotype and problematic alcohol use was reduced to a trend level in the context of a model that included novelty <b>seeking</b> as a mediator, thereby suggesting that the effects of <strong>DRD4</strong> VNTR genotype on problematic alcohol use among heavy drinking young adults were partially mediated by novelty <b>seeking</b>.
+DRD4	drug	alcohol	18715282	These results extend recent findings of the association between this polymorphism of the <strong>DRD4</strong> receptor gene, problematic <b>alcohol</b> use and novelty seeking.
+DRD4	addiction	relapse	18715282	These results extend recent findings of the association between this polymorphism of the <strong>DRD4</strong> receptor gene, problematic alcohol use and novelty <b>seeking</b>.
+DRD4	drug	nicotine	18690118	The increase in <b>smoking</b> amount owing to negative mood was associated with: dopamine D2 receptor (DRD2) C957T (CC>TT or CT), SLC6A3 (presence of 9 repeat>absence of 9), and among those given a <b>nicotine</b> cigarette, <strong>DRD4</strong> (presence of 7 repeat>absence of 7) and DRD2/ANKK1 TaqIA (TT or CT>CC).
+DRD4	drug	nicotine	18690117	For the dopamine D4 receptor [<strong>DRD4</strong> variable number of tandem repeats (VNTR)], presence of the 7 repeat allele was associated with greater aversive responses to <b>nicotine</b> (decreases in 'vigor', positive affect, and rapid information processing; increased cortisol) and reduced <b>nicotine</b> choice.
+DRD4	addiction	aversion	18690117	For the dopamine D4 receptor [<strong>DRD4</strong> variable number of tandem repeats (VNTR)], presence of the 7 repeat allele was associated with greater <b>aversive</b> responses to nicotine (decreases in 'vigor', positive affect, and rapid information processing; increased cortisol) and reduced nicotine choice.
+DRD4	drug	alcohol	19899572	The aim of this study was to evaluate the role of dopamine D4 receptor (<strong>DRD4</strong>) exon 3 polymorphisms (48 bp VNTR) in the pathogenesis of <b>alcoholism</b>.
+DRD4	drug	alcohol	19899572	The results of this study suggest that inherited short variants of <strong>DRD4</strong> alleles may play role in pathogenesis of <b>alcohol</b> dependence.
+DRD4	addiction	dependence	19899572	The results of this study suggest that inherited short variants of <strong>DRD4</strong> alleles may play role in pathogenesis of alcohol <b>dependence</b>.
+DRD4	drug	nicotine	18434921	<b>Smoking</b> initiation was related to allelic variation in the dopamine D4 receptor gene (<strong>DRD4</strong>), whereas <b>smoking</b> continuation and dependence showed association with the dopamine D2 receptor gene (DRD2).
+DRD4	addiction	dependence	18434921	Smoking initiation was related to allelic variation in the dopamine D4 receptor gene (<strong>DRD4</strong>), whereas smoking continuation and <b>dependence</b> showed association with the dopamine D2 receptor gene (DRD2).
+DRD4	drug	nicotine	18434921	Adolescents with the seven repeat allele of the common <strong>DRD4</strong> exon 3 polymorphism had rates of ever <b>smoking</b> that were significantly higher than in those with other genotypes.
+DRD4	drug	nicotine	18331372	<b>Smoking</b> status moderates the association of the dopamine D4 receptor (<strong>DRD4</strong>) gene VNTR polymorphism with selective processing of <b>smoking</b> related cues.
+DRD4	drug	nicotine	18331372	Recently, a variable number of tandem repeats (VNTR) polymorphism in the dopamine D4 receptor (<strong>DRD4</strong>) gene has been reported to be associated with greater craving and more attention to <b>smoking</b> cues, following a cue elicited craving procedure.
+DRD4	addiction	relapse	18331372	Recently, a variable number of tandem repeats (VNTR) polymorphism in the dopamine D4 receptor (<strong>DRD4</strong>) gene has been reported to be associated with greater <b>craving</b> and more attention to smoking cues, following a cue elicited <b>craving</b> procedure.
+DRD4	drug	nicotine	18331372	We investigated whether the <strong>DRD4</strong> VNTR 7 repeat polymorphism is associated with selective processing of <b>smoking</b> related stimuli, using a modified Stroop task, and whether <b>smoking</b> status moderates this association.
+DRD4	drug	nicotine	18331372	The experimental design included two between subjects factors of <b>smoking</b> status (current <b>smoker</b>, ex <b>smoker</b>) and <strong>DRD4</strong> genotype (short, long).
+DRD4	drug	nicotine	18331372	The <strong>DRD4</strong> VNTR polymorphism was associated with selective processing of <b>smoking</b> related stimuli in ex <b>smokers</b> but not in current <b>smokers</b>.
+DRD4	drug	alcohol	18028530	Polymorphisms in the D4 dopamine receptor (<strong>DRD4</strong>) gene and the mu opiate receptor (OPRM1) gene, family history of <b>alcohol</b> problems, age of onset of <b>alcoholism</b> and gender were explored as potential moderators of NTX's effects.
+DRD4	drug	alcohol	18028530	<b>Naltrexone</b> reduced percentage drinking days in all participants and reduced percent heavy drinking days in <strong>DRD4</strong> L individuals; NTX decreased urge levels in participants with younger age of <b>alcoholism</b> onset; NTX increased time between drinks in participants who had more relatives with <b>alcohol</b> problems; and NTX reduced the stimulating effects of <b>alcohol</b> in women.
+DRD4	drug	cocaine	17671965	Polymorphisms TaqI A of the DRD2, BalI of the DRD3, exon III repeat of the <strong>DRD4</strong>, and 3' UTR VNTR of the DAT: association with childhood ADHD in male African Caribbean <b>cocaine</b> dependents?
+DRD4	drug	cocaine	17671965	The potential association of the variants TaqI A of the DRD2, BalI of the DRD3, exon III repeat of the <strong>DRD4</strong>, and 3' UTR VNTR of the DAT was examined in African Caribbean males, smoked <b>cocaine</b> dependents.
+DRD4	drug	nicotine	17611740	<strong>DRD4</strong> VNTR polymorphism is associated with transient fMRI BOLD responses to <b>smoking</b> cues.
+DRD4	drug	nicotine	17611740	A dopamine receptor 4 variable number tandem repeat (<strong>DRD4</strong> VNTR) polymorphism has been related to reactivity to <b>smoking</b> cues among <b>smokers</b>, but the effect of this genetic variation on brain responses to <b>smoking</b> cues has not been evaluated.
+DRD4	drug	nicotine	17611740	The present study evaluated the relationship between carrying the <strong>DRD4</strong> VNTR 7 repeat allele and transient functional magnetic resonance imaging (fMRI) blood oxygen level dependent responses to <b>smoking</b> cues among adult dependent cigarette <b>smokers</b>.
+DRD4	drug	nicotine	17611740	Contrasts in brain cue reactivity (<b>smoking</b> minus control cues) between <strong>DRD4</strong> groups were conducted using SPM2.
+DRD4	drug	nicotine	17611740	Exposure to <b>smoking</b> cues resulted in greater activation of right superior frontal gyrus (BA 10) and right insula in <strong>DRD4</strong> L compared to <strong>DRD4</strong> S individuals.
+DRD4	drug	nicotine	17611740	By contrast, exposure to <b>smoking</b> cues among <strong>DRD4</strong> S individuals resulted in no significant increases in activation compared to <strong>DRD4</strong> L individuals.
+DRD4	drug	nicotine	17611740	These brain imaging results suggest that <strong>DRD4</strong> VNTR polymorphism is related to transient brain responses to <b>smoking</b> cues in regions subserving executive and somatosensory processes.
+DRD4	drug	alcohol	17508995	Polymorphisms of the dopamine D4 receptor gene (<strong>DRD4</strong> VNTR) and cannabinoid CB1 receptor gene (CNR1) are not strongly related to cue reactivity after <b>alcohol</b> exposure.
+DRD4	drug	cannabinoid	17508995	Polymorphisms of the dopamine D4 receptor gene (<strong>DRD4</strong> VNTR) and <b>cannabinoid</b> CB1 receptor gene (CNR1) are not strongly related to cue reactivity after alcohol exposure.
+DRD4	drug	alcohol	17508995	Polymorphisms in the D4 dopamine receptor gene (<strong>DRD4</strong>) and the CB1 cannabinoid receptor gene (CNR1) have been associated with a differential response to <b>alcohol</b> after consumption.
+DRD4	drug	cannabinoid	17508995	Polymorphisms in the D4 dopamine receptor gene (<strong>DRD4</strong>) and the CB1 <b>cannabinoid</b> receptor gene (CNR1) have been associated with a differential response to alcohol after consumption.
+DRD4	drug	alcohol	17508995	Unexpectedly, the <strong>DRD4</strong> L participants reported, on average, less craving for <b>alcohol</b> and more subjective arousal during cue exposure, compared with the <strong>DRD4</strong> S participants.
+DRD4	addiction	relapse	17508995	Unexpectedly, the <strong>DRD4</strong> L participants reported, on average, less <b>craving</b> for alcohol and more subjective arousal during cue exposure, compared with the <strong>DRD4</strong> S participants.
+DRD4	drug	alcohol	17508995	The <strong>DRD4</strong> and CNR1 polymorphisms do not appear to strongly moderate cue reactivity after <b>alcohol</b> cue exposure, in male heavy drinkers.
+DRD4	drug	nicotine	17407504	Dopamine receptor genes (DRD2, DRD3 and <strong>DRD4</strong>) and gene gene interactions associated with <b>smoking</b> related behaviors.
+DRD4	drug	nicotine	17407504	Cigarette <b>smoking</b>, like many addictive behaviors, has a genetic component, and the dopamine D2 like receptor genes (DRD2, DRD3 and <strong>DRD4</strong>) are candidates for contributing to these behaviors.
+DRD4	addiction	addiction	17407504	Cigarette smoking, like many <b>addictive</b> behaviors, has a genetic component, and the dopamine D2 like receptor genes (DRD2, DRD3 and <strong>DRD4</strong>) are candidates for contributing to these behaviors.
+DRD4	addiction	relapse	17407504	There was a trend for <strong>DRD4</strong> long alleles of the variable number of tandem repeats polymorphism to be associated with reduced severity of three withdrawal symptoms [desire/<b>craving</b> (P = 0.054); anger/irritability (P = 0.10); and trouble sleeping (P = 0.068)].
+DRD4	addiction	withdrawal	17407504	There was a trend for <strong>DRD4</strong> long alleles of the variable number of tandem repeats polymorphism to be associated with reduced severity of three <b>withdrawal</b> symptoms [desire/craving (P = 0.054); anger/irritability (P = 0.10); and trouble sleeping (P = 0.068)].
+DRD4	drug	nicotine	17387332	Genetic variation in the dopamine D4 receptor (<strong>DRD4</strong>) gene and <b>smoking</b> cessation: follow up of a randomised clinical trial of transdermal <b>nicotine</b> patch.
+DRD4	drug	nicotine	17387332	<b>Smokers</b> of European ancestry (n=720) who participated in a double blind, randomised, placebo controlled trial of transdermal <b>nicotine</b> replacement therapy, were genotyped for two functional polymorphisms (variable number of tandem repeats (VNTR) and a C to T transition at position  521 (C 521T)) in the dopamine D4 receptor gene (<strong>DRD4</strong>) gene.
+DRD4	drug	nicotine	17387332	For the <strong>DRD4</strong> VNTR models, the main effect of treatment was significant at both 12 week (P=0.001) and 26 week (P=0.006) follow ups, indicating an increased likelihood of successful cessation on active <b>nicotine</b> replacement therapy transdermal patch relative to placebo.
+DRD4	drug	alcohol	17309802	Effects of craving and <strong>DRD4</strong> VNTR genotype on the relative value of <b>alcohol</b>: an initial human laboratory study.
+DRD4	addiction	relapse	17309802	Effects of <b>craving</b> and <strong>DRD4</strong> VNTR genotype on the relative value of alcohol: an initial human laboratory study.
+DRD4	addiction	relapse	17309802	In addition, based on previous evidence of its role in the expression of <b>craving</b>, the influence of <strong>DRD4</strong> VNTR genotype (<strong>DRD4</strong> L vs. <strong>DRD4</strong> S) was also examined.
+DRD4	drug	alcohol	17309802	Thirty five heavy drinkers (54% male; 31% <strong>DRD4</strong> L) were randomly assigned to receive either a craving induction (exposure to personally relevant <b>alcohol</b> cues) or a control induction (exposure to neutral cues), which was followed by an <b>alcohol</b> money choice task.
+DRD4	addiction	relapse	17309802	Thirty five heavy drinkers (54% male; 31% <strong>DRD4</strong> L) were randomly assigned to receive either a <b>craving</b> induction (exposure to personally relevant alcohol cues) or a control induction (exposure to neutral cues), which was followed by an alcohol money choice task.
+DRD4	addiction	relapse	17309802	Factorial analyses including <strong>DRD4</strong> VNTR genotype of did not suggest an influence on reactivity to the <b>craving</b> induction, although this analysis was substantially compromised by small cell sample sizes.
+DRD4	drug	alcohol	17309802	Continuous analyses revealed that craving was significantly associated with the relative value of <b>alcohol</b> (p < .05) and possession of the <strong>DRD4</strong> L allele further amplified this relationship (p < .001).
+DRD4	addiction	relapse	17309802	Continuous analyses revealed that <b>craving</b> was significantly associated with the relative value of alcohol (p < .05) and possession of the <strong>DRD4</strong> L allele further amplified this relationship (p < .001).
+DRD4	drug	alcohol	17309802	These results are interpreted as generally supporting Loewenstein's visceral theory of craving and evidence of a functional role of <strong>DRD4</strong> VNTR genotype in the expression of craving for <b>alcohol</b>.
+DRD4	addiction	relapse	17309802	These results are interpreted as generally supporting Loewenstein's visceral theory of <b>craving</b> and evidence of a functional role of <strong>DRD4</strong> VNTR genotype in the expression of <b>craving</b> for alcohol.
+DRD4	drug	alcohol	16945348	The aim of this study was to examine whether allelic variants of the dopamine D4 receptor gene (<strong>DRD4</strong>) are associated with <b>alcohol</b> use in adolescents and to determine the extent to which these links are mediated by NS.
+DRD4	drug	alcohol	16945348	Male participants carrying the 7 repeat allele of <strong>DRD4</strong> drank higher maximum amounts of <b>alcohol</b> per occasion and had greater lifetime rates of heavy drinking than male participants without this allele.
+DRD4	addiction	relapse	16899031	Polymorphisms in the D4 dopamine receptor (<strong>DRD4</strong>) gene and mu opiate receptor gene (OPRM1) may moderate NTX's effects on <b>craving</b>.
+DRD4	drug	alcohol	16899031	The non treatment seeking male and female heavy drinkers (62% <b>alcohol</b> dependent) were genotyped for the variable number of tandem repeats polymorphism in the <strong>DRD4</strong> gene [L=7 or more (n=34), S=less than 7 (n=56)] and Asn40Asp single nucleotide polymorphism in the OPRM1 gene [29 aspartate (Asp) carriers and 59 asparagine (Asn) homozygotes].
+DRD4	addiction	relapse	16899031	The non treatment <b>seeking</b> male and female heavy drinkers (62% alcohol dependent) were genotyped for the variable number of tandem repeats polymorphism in the <strong>DRD4</strong> gene [L=7 or more (n=34), S=less than 7 (n=56)] and Asn40Asp single nucleotide polymorphism in the OPRM1 gene [29 aspartate (Asp) carriers and 59 asparagine (Asn) homozygotes].
+DRD4	drug	alcohol	16819620	The present study was designed to examine the influence of the DA D4 receptor (<strong>DRD4</strong>) and the serotonin transporter (5 HTT) genotype and their interaction on adolescent <b>alcohol</b> and tobacco experimentation.
+DRD4	drug	nicotine	16819620	The present study was designed to examine the influence of the DA D4 receptor (<strong>DRD4</strong>) and the serotonin transporter (5 HTT) genotype and their interaction on adolescent alcohol and <b>tobacco</b> experimentation.
+DRD4	drug	nicotine	16819620	The <strong>DRD4</strong> 7 repeat allele was associated with greater <b>smoking</b> and drinking involvement in boys.
+DRD4	drug	nicotine	16819620	Girls without the <strong>DRD4</strong> 7 repeat allele and who were homozygous for the long allele of 5 HTTLPR displayed the highest <b>smoking</b> and drinking activity.
+DRD4	drug	opioid	16703401	The objective of this study was to test the hypothesis that <b>heroin</b> addicts carrying D4 dopamine receptor gene (<strong>DRD4</strong>) variable number tandem repeat (VNTR) long type allele would have higher craving after exposure to a <b>heroin</b> related cue.
+DRD4	addiction	relapse	16703401	The objective of this study was to test the hypothesis that heroin addicts carrying D4 dopamine receptor gene (<strong>DRD4</strong>) variable number tandem repeat (VNTR) long type allele would have higher <b>craving</b> after exposure to a heroin related cue.
+DRD4	drug	opioid	16703401	Significantly stronger cue elicited <b>heroin</b> craving was found in individuals carrying <strong>DRD4</strong> VNTR long type allele than the non carriers (F=31.040, p<0.001).
+DRD4	addiction	relapse	16703401	Significantly stronger cue elicited heroin <b>craving</b> was found in individuals carrying <strong>DRD4</strong> VNTR long type allele than the non carriers (F=31.040, p<0.001).
+DRD4	drug	opioid	16703401	The results of our study suggest that <strong>DRD4</strong> VNTR polymorphism contributes to cue elicited craving in <b>heroin</b> dependence, indicating <strong>DRD4</strong> VNTR represents one of potential genetic risk factors for cue induced craving.
+DRD4	addiction	dependence	16703401	The results of our study suggest that <strong>DRD4</strong> VNTR polymorphism contributes to cue elicited craving in heroin <b>dependence</b>, indicating <strong>DRD4</strong> VNTR represents one of potential genetic risk factors for cue induced craving.
+DRD4	addiction	relapse	16703401	The results of our study suggest that <strong>DRD4</strong> VNTR polymorphism contributes to cue elicited <b>craving</b> in heroin dependence, indicating <strong>DRD4</strong> VNTR represents one of potential genetic risk factors for cue induced <b>craving</b>.
+DRD4	drug	nicotine	16526060	<b>Smoking</b> cessation, weight gain, and <strong>DRD4</strong>  521 genotype.
+DRD4	drug	nicotine	16526060	We did not observe an interaction between <b>smoking</b> status and <strong>DRD4</strong> genotype.
+DRD4	drug	nicotine	16526060	However, independently of the weight gain among those who stopped <b>smoking</b> during the course of the study, <strong>DRD4</strong> genotype was significantly associated with BMI, with possession of the  521 C allele associated with increased BMI.
+DRD4	drug	nicotine	16272956	CYP2A6, MAOA, DBH, <strong>DRD4</strong>, and 5HT2A genotypes, <b>smoking</b> behaviour and cotinine levels in 1518 UK adolescents.
+DRD4	drug	nicotine	16272956	No significant associations were identified for DBH, MAOA, <strong>DRD4</strong> and 5HT2A markers, with <b>smoking</b> status or cotinine level at either age.
+DRD4	drug	alcohol	16237394	Previous studies have indicated that olanzapine decreases craving after a priming dose of <b>alcohol</b>, that craving after a priming dose of <b>alcohol</b> is greater among individuals with the seven repeat allele of the <strong>DRD4</strong> variable number of tandem repeats (VNTR) polymorphism, and that the effect of olanzapine (a D2/D4 antagonist) is more pronounced among individuals with this allele.
+DRD4	addiction	relapse	16237394	Previous studies have indicated that olanzapine decreases <b>craving</b> after a priming dose of alcohol, that <b>craving</b> after a priming dose of alcohol is greater among individuals with the seven repeat allele of the <strong>DRD4</strong> variable number of tandem repeats (VNTR) polymorphism, and that the effect of olanzapine (a D2/D4 antagonist) is more pronounced among individuals with this allele.
+DRD4	drug	alcohol	16237394	The results suggested that participants who were homozygous or heterozygous for the seven (or longer) repeat allele of the <strong>DRD4</strong> VNTR responded to olanzapine with reductions in cue elicited craving as well as reductions in <b>alcohol</b> consumption over the course of the 12 week trial, whereas individuals with the shorter alleles did not respond favorably to olanzapine.
+DRD4	addiction	relapse	16237394	The results suggested that participants who were homozygous or heterozygous for the seven (or longer) repeat allele of the <strong>DRD4</strong> VNTR responded to olanzapine with reductions in cue elicited <b>craving</b> as well as reductions in alcohol consumption over the course of the 12 week trial, whereas individuals with the shorter alleles did not respond favorably to olanzapine.
+DRD4	drug	alcohol	16182111	We found associations between the <strong>DRD4</strong> long allele and increased systolic BP (P = .031), diastolic BP (P = .034), and a history of regular <b>alcohol</b> use (P = .008).
+DRD4	addiction	dependence	16167465	Dopamine D4 receptor (<strong>DRD4</strong>) and serotonin transporter (SERT) gene polymorphisms were studied, as possible genetic risk factors for substance <b>dependence</b>.
+DRD4	drug	opioid	16167465	Association between the  521 C/T SNP of the <strong>DRD4</strong> promoter region and substance dependence was significant in the subgroup of <b>heroin</b> dependents (p = 0.044).
+DRD4	addiction	dependence	16167465	Association between the  521 C/T SNP of the <strong>DRD4</strong> promoter region and substance <b>dependence</b> was significant in the subgroup of heroin dependents (p = 0.044).
+DRD4	addiction	relapse	15900228	Recent meta analyses have questioned the association between the dopamine receptor D4 (<strong>DRD4</strong>) gene polymorphism and the temperament trait of novelty <b>seeking</b>, and proposed an interaction between the polymorphism and other factors.
+DRD4	addiction	relapse	15900228	Recent meta analyses have questioned the association between the <strong>dopamine receptor D4</strong> (<strong>DRD4</strong>) gene polymorphism and the temperament trait of novelty <b>seeking</b>, and proposed an interaction between the polymorphism and other factors.
+DRD4	drug	alcohol	15900228	We wanted to test whether parental <b>alcohol</b> use during childhood moderated the effect of an offspring dopamine receptor gene (<strong>DRD4</strong>) polymorphism on the temperament trait of novelty seeking in adulthood.
+DRD4	addiction	relapse	15900228	We wanted to test whether parental alcohol use during childhood moderated the effect of an offspring dopamine receptor gene (<strong>DRD4</strong>) polymorphism on the temperament trait of novelty <b>seeking</b> in adulthood.
+DRD4	addiction	relapse	15900228	In 1997, study participants completed the Temperament and Character Inventory for the novelty <b>seeking</b> temperament trait, and a subsample (n=150) was genotyped for the <strong>DRD4</strong> exon III polymorphism.
+DRD4	drug	alcohol	15900228	For the participants with the father, but not the mother, reporting more frequent <b>alcohol</b> consumption or drunkenness in examinations 17 and/or 14 years before the novelty seeking assessment, an association between the short (two  or five repeat) alleles of the <strong>DRD4</strong> gene and extremely high novelty seeking scores was observed.
+DRD4	addiction	relapse	15900228	For the participants with the father, but not the mother, reporting more frequent alcohol consumption or drunkenness in examinations 17 and/or 14 years before the novelty <b>seeking</b> assessment, an association between the short (two  or five repeat) alleles of the <strong>DRD4</strong> gene and extremely high novelty <b>seeking</b> scores was observed.
+DRD4	addiction	relapse	15900228	These results provide preliminary information on gene environment interaction on the temperament trait of novelty <b>seeking</b> and may partly explain the heterogeneity of findings concerning the association between <strong>DRD4</strong> polymorphisms and novelty <b>seeking</b>.
+DRD4	addiction	relapse	15876472	Results also suggest that the <strong>DRD4</strong> VNTR polymorphism influences cue elicited <b>craving</b> for food, although the influence of the <strong>DRD4</strong> may depend on the population under study.
+DRD4	drug	nicotine	15843770	Association of the <strong>DRD4</strong> exon III polymorphism with <b>smoking</b> in fifteen year olds: a mediating role for novelty seeking?
+DRD4	addiction	relapse	15843770	Association of the <strong>DRD4</strong> exon III polymorphism with smoking in fifteen year olds: a mediating role for novelty <b>seeking</b>?
+DRD4	drug	nicotine	15843770	This study was designed to examine the role of DNA variants of the dopamine D4 receptor gene (<strong>DRD4</strong>) in <b>smoking</b> experimentation in adolescents and to determine the extent to which novelty seeking (NS) could account for a possible effect of <strong>DRD4</strong> on <b>tobacco</b> use.
+DRD4	addiction	relapse	15843770	This study was designed to examine the role of DNA variants of the dopamine D4 receptor gene (<strong>DRD4</strong>) in smoking experimentation in adolescents and to determine the extent to which novelty <b>seeking</b> (NS) could account for a possible effect of <strong>DRD4</strong> on tobacco use.
+DRD4	drug	nicotine	15843770	<strong>DRD4</strong> was associated with <b>smoking</b> status and NS in males but not in females.
+DRD4	drug	nicotine	15843770	Multiple regression analyses revealed that NS mediated the relationship between <strong>DRD4</strong> and <b>smoking</b> in males.
+DRD4	addiction	relapse	15318029	There is no support for linkage of novelty <b>seeking</b> or HA to the regions around <strong>DRD4</strong> and 5HTT, respectively.
+DRD4	drug	opioid	15288384	3 (1997) 251] showed that the 7 repeat allele of the <strong>DRD4</strong> receptor is significantly overpresented in the <b>opioid</b> dependent cohort and confers a relative risk of 2.46.
+DRD4	drug	amphetamine	15274053	Association analysis of the <strong>DRD4</strong> and COMT genes in <b>methamphetamine</b> abuse.
+DRD4	addiction	relapse	15048656	Association of a duplicated repeat polymorphism in the 5' untranslated region of the <strong>DRD4</strong> gene with novelty <b>seeking</b>.
+DRD4	drug	nicotine	14982687	Dopamine receptor D(3) (DRD3) and D(4) (<strong>DRD4</strong>) mRNA expression in PBLs was measured by real time polymerase chain reaction in <b>smokers</b> (n=26) and former <b>smokers</b> (n=14), compared with nonsmoking control subjects (n=35).
+DRD4	drug	alcohol	14681925	Effects of <strong>dopamine receptor D4</strong> variation on <b>alcohol</b> and tobacco use and on novelty seeking: multivariate linkage and association analysis.
+DRD4	drug	nicotine	14681925	Effects of <strong>dopamine receptor D4</strong> variation on alcohol and <b>tobacco</b> use and on novelty seeking: multivariate linkage and association analysis.
+DRD4	addiction	relapse	14681925	Effects of <strong>dopamine receptor D4</strong> variation on alcohol and tobacco use and on novelty <b>seeking</b>: multivariate linkage and association analysis.
+DRD4	drug	alcohol	14681925	In this study we have assessed the linkage and association of <strong>DRD4</strong> genotype with novelty seeking, <b>alcohol</b> use, and smoking in a sample of 377 dizygotic twin pairs and 15 single twins recruited from the Australian Twin Registry (ATR).
+DRD4	drug	nicotine	14681925	In this study we have assessed the linkage and association of <strong>DRD4</strong> genotype with novelty seeking, alcohol use, and <b>smoking</b> in a sample of 377 dizygotic twin pairs and 15 single twins recruited from the Australian Twin Registry (ATR).
+DRD4	addiction	relapse	14681925	In this study we have assessed the linkage and association of <strong>DRD4</strong> genotype with novelty <b>seeking</b>, alcohol use, and smoking in a sample of 377 dizygotic twin pairs and 15 single twins recruited from the Australian Twin Registry (ATR).
+DRD4	addiction	relapse	14681925	Specifically, it has been suggested that the <strong>DRD4</strong> 7 repeat allele is associated with increased novelty <b>seeking</b> in males but we found no evidence for this, despite considerable power to do so.
+DRD4	drug	alcohol	14681925	We conclude that <strong>DRD4</strong> variation does not have an effect on use of <b>alcohol</b> and the problems that arise from it, on smoking, or on novelty seeking behavior.
+DRD4	drug	nicotine	14681925	We conclude that <strong>DRD4</strong> variation does not have an effect on use of alcohol and the problems that arise from it, on <b>smoking</b>, or on novelty seeking behavior.
+DRD4	addiction	relapse	14681925	We conclude that <strong>DRD4</strong> variation does not have an effect on use of alcohol and the problems that arise from it, on smoking, or on novelty <b>seeking</b> behavior.
+DRD4	drug	alcohol	12898574	For this study, homogeneous population consisting of 243 young <b>alcohol</b>  and drug naive Koreans who were blood unrelated with a mean age (+/ SD) of 13.87 (+/ 0.30) years old was analyzed for the <strong>DRD4</strong> and the DRD2 polymorphisms with their personality trait by Temperament and character inventory (TCI).
+DRD4	addiction	relapse	12898574	The association between Novelty <b>seeking</b> (NS) score and <strong>DRD4</strong> long alleles was only observed among the female subjects (t = 2.11, P = 0.037), but not in the male counter part.
+DRD4	addiction	reward	12898574	These results, thus, confirmed the previous findings in which the long repeats of the <strong>DRD4</strong> exon III polymorphism are related to NS personality trait, and also suggested that the DRD2 less frequent alleles were also associated with the <b>reward</b> dependent trait.
+DRD4	drug	alcohol	12888781	Olanzapine reduces craving for <b>alcohol</b>: a <strong>DRD4</strong> VNTR polymorphism by pharmacotherapy interaction.
+DRD4	addiction	relapse	12888781	Olanzapine reduces <b>craving</b> for alcohol: a <strong>DRD4</strong> VNTR polymorphism by pharmacotherapy interaction.
+DRD4	drug	alcohol	12888781	Separate investigations have suggested that olanzapine, a D4 antagonist, decreases craving after a priming dose of <b>alcohol</b> and that the <strong>DRD4</strong> variable number of tandem repeats (VNTR) polymorphism influences the expression of craving after a priming dose of <b>alcohol</b>.
+DRD4	addiction	relapse	12888781	Separate investigations have suggested that olanzapine, a D4 antagonist, decreases <b>craving</b> after a priming dose of alcohol and that the <strong>DRD4</strong> variable number of tandem repeats (VNTR) polymorphism influences the expression of <b>craving</b> after a priming dose of alcohol.
+DRD4	addiction	relapse	12888781	The present study tested the hypothesis that olanzapine may be differentially effective at reducing cue elicited <b>craving</b> based on individual differences in <strong>DRD4</strong> VNTR in a sample of heavy social drinkers.
+DRD4	drug	alcohol	12888781	Participants who were homozygous or heterozygous for the 7 (or longer) repeat allele of the <strong>DRD4</strong> VNTR were classified as <strong>DRD4</strong> L, while the other participants were classified as <strong>DRD4</strong> S. The findings indicated that olanzapine reduces craving for <b>alcohol</b> at baseline for both <strong>DRD4</strong> S and <strong>DRD4</strong> L individuals, but only reduces craving after exposure to <b>alcohol</b> cues and after a priming dose of <b>alcohol</b> for <strong>DRD4</strong> L individuals.
+DRD4	addiction	relapse	12888781	Participants who were homozygous or heterozygous for the 7 (or longer) repeat allele of the <strong>DRD4</strong> VNTR were classified as <strong>DRD4</strong> L, while the other participants were classified as <strong>DRD4</strong> S. The findings indicated that olanzapine reduces <b>craving</b> for alcohol at baseline for both <strong>DRD4</strong> S and <strong>DRD4</strong> L individuals, but only reduces <b>craving</b> after exposure to alcohol cues and after a priming dose of alcohol for <strong>DRD4</strong> L individuals.
+DRD4	addiction	relapse	12393313	These findings are in line with a number of more recent studies questioning the association between novelty <b>seeking</b> and <strong>DRD4</strong> dopamine receptor gene polymorphism.
+DRD4	drug	alcohol	11950104	The <strong>DRD4</strong> VNTR polymorphism moderates craving after <b>alcohol</b> consumption.
+DRD4	addiction	relapse	11950104	The <strong>DRD4</strong> VNTR polymorphism moderates <b>craving</b> after alcohol consumption.
+DRD4	drug	alcohol	11950104	Because the D4 dopamine receptor gene, variable numbers of tandem repeats (<strong>DRD4</strong> VNTR) polymorphism putatively expresses functional differences in dopamine receptors, the present study tested whether this polymorphism influences the effects of a priming dose of <b>alcohol</b> on craving.
+DRD4	addiction	relapse	11950104	Because the D4 dopamine receptor gene, variable numbers of tandem repeats (<strong>DRD4</strong> VNTR) polymorphism putatively expresses functional differences in dopamine receptors, the present study tested whether this polymorphism influences the effects of a priming dose of alcohol on <b>craving</b>.
+DRD4	drug	alcohol	11950104	Participants who were homozygous or heterozygous for the 7 (or longer) repeat allele were classified as <strong>DRD4</strong> L, whereas the other participants were classified as <strong>DRD4</strong> S. Results suggested that <strong>DRD4</strong> L participants demonstrated significantly higher craving after consumption of <b>alcohol</b> as compared with the control beverage.
+DRD4	addiction	relapse	11950104	Participants who were homozygous or heterozygous for the 7 (or longer) repeat allele were classified as <strong>DRD4</strong> L, whereas the other participants were classified as <strong>DRD4</strong> S. Results suggested that <strong>DRD4</strong> L participants demonstrated significantly higher <b>craving</b> after consumption of alcohol as compared with the control beverage.
+DRD4	addiction	reward	11901357	The D2 and D4 dopamine receptors (DRD2 and <strong>DRD4</strong>) play major roles in the central effects of psychostimulants and in the <b>reward</b> system.
+DRD4	addiction	dependence	11901357	Previous studies, although not all, have demonstrated associations between the DRD2 TaqI and the <strong>DRD4</strong> exon III variable number tandem repeat (VNTR) polymorphisms and substance <b>dependence</b>.
+DRD4	addiction	dependence	11901357	No significant difference was demonstrated for genotype or allele frequency when comparing MAP dependent and control cases for the DRD2 TaqI and the <strong>DRD4</strong> gene exon III VNTR polymorphisms, suggesting that these two polymorphisms do not play major roles in MAP <b>dependence</b> for our sample of Chinese males.
+DRD4	drug	nicotine	11866166	The <strong>DRD4</strong> VNTR polymorphism influences reactivity to <b>smoking</b> cues.
+DRD4	drug	nicotine	11866166	Given the potential role of dopamine in cue elicited craving, the authors examined whether the <strong>DRD4</strong> VNTR polymorphism is associated with cue elicited craving for <b>tobacco</b>.
+DRD4	addiction	relapse	11866166	Given the potential role of dopamine in cue elicited <b>craving</b>, the authors examined whether the <strong>DRD4</strong> VNTR polymorphism is associated with cue elicited <b>craving</b> for tobacco.
+DRD4	drug	nicotine	11866166	Participants who were homozygous or heterozygous for the 7 repeat (or longer) allele were classified as <strong>DRD4</strong> L, and all other participants were classified as <strong>DRD4</strong> S. Participants were exposed to <b>smoking</b> cues before <b>smoking</b> either high <b>nicotine</b> cigarettes or control cigarettes.
+DRD4	drug	alcohol	11347517	More than 80% of <b>alcoholics</b> smoke cigarettes in the U.S.A. Other genetic methods such as linkage analysis, allele sharing methods, association studies and analysis of inbred, transgenic and gene knockout rodents, have partially agreed in showing that the 5HT 1B serotonin receptor and the DRD1, DRD2 and <strong>DRD4</strong> dopamine receptors, as well as the dopamine transporter DAT, play an important role in behaviors related to <b>alcoholism</b> and substance abuse.
+DRD4	drug	alcohol	11347517	Two whole genome linkage studies have shown linkage to chromosomal regions that are in the proximity of the <strong>DRD4</strong> dopamine receptor, the GABA receptor gene cluster and the <b>alcohol</b> dehydrogenase gene cluster.
+DRD4	drug	alcohol	11244477	<strong>DRD4</strong> and DAT1 as modifying genes in <b>alcoholism</b>: interaction with novelty seeking on level of <b>alcohol</b> consumption.
+DRD4	addiction	relapse	11244477	<strong>DRD4</strong> and DAT1 as modifying genes in alcoholism: interaction with novelty <b>seeking</b> on level of alcohol consumption.
+DRD4	drug	opioid	11054768	Association analysis of polymorphisms in the <strong>DRD4</strong> gene and <b>heroin</b> abuse in Chinese subjects.
+DRD4	drug	opioid	11054768	When we compared the <b>heroin</b> abuse group with controls, we found no significant difference between the patients and controls for either polymorphism in the <strong>DRD4</strong> gene or their haplotypes.
+DRD4	drug	opioid	11054768	We were also unable to replicate our earlier association between "long" <strong>DRD4</strong> alleles and <b>heroin</b> abuse.
+DRD4	addiction	relapse	11054768	The association we observed between inhalers and the <strong>DRD4</strong> polymorphism is difficult to interpret, although it is possible that the association is explained by different levels of novelty <b>seeking</b> between the two subgroups.
+DRD4	drug	alcohol	20575866	No significant association between the polymorphism at <strong>DRD4</strong> and opiate or <b>alcohol</b> abuse was found.
+DRD4	addiction	dependence	20575866	This study suggests that the <strong>DRD4</strong> gene does not directly influence vulnerability to substance <b>dependence</b>, but that possession of the LL genotype significantly increases severity of <b>dependence</b>.
+DRD4	drug	alcohol	20575843	Susceptibility for <b>alcoholism</b>: <strong>DRD4</strong> exon III polymorphism: a case control and a family based association approach.
+DRD4	drug	alcohol	20575843	Using a classical case control approach we first compared <strong>DRD4</strong> exon III VNTR frequencies between <b>alcoholics</b> and ethnically matched controls (sample I).
+DRD4	drug	alcohol	20575843	The impact of the <strong>DRD4</strong> exon III polymorphism on susceptibility to addictive behaviour putatively plays only a minor role in our sample of <b>alcohol</b> dependent patients, since we were not able to replicate our findings by the family based association approach.
+DRD4	addiction	addiction	20575843	The impact of the <strong>DRD4</strong> exon III polymorphism on susceptibility to <b>addictive</b> behaviour putatively plays only a minor role in our sample of alcohol dependent patients, since we were not able to replicate our findings by the family based association approach.
+DRD4	drug	opioid	10673776	<strong>DRD4</strong> exon III VNTR polymorphism susceptibility factor for <b>heroin</b> dependence?
+DRD4	addiction	dependence	10673776	<strong>DRD4</strong> exon III VNTR polymorphism susceptibility factor for heroin <b>dependence</b>?
+DRD4	drug	opioid	10673776	Dopaminergic abnormalities are implicated in the pathogenesis of substance abuse.1 Recently, two reports have been published suggesting an association between <b>opioid</b> dependence and presence of long alleles of the dopamine D4 receptor (<strong>DRD4</strong>) gene exon III VNTR.2, 3 We have attempted to replicate this finding using a two tiered strategy employing independent case control and family based association samples.
+DRD4	addiction	dependence	10673776	Dopaminergic abnormalities are implicated in the pathogenesis of substance abuse.1 Recently, two reports have been published suggesting an association between opioid <b>dependence</b> and presence of long alleles of the dopamine D4 receptor (<strong>DRD4</strong>) gene exon III VNTR.2, 3 We have attempted to replicate this finding using a two tiered strategy employing independent case control and family based association samples.
+DRD4	drug	opioid	10673776	We found long alleles of the <strong>DRD4</strong> exon III VNTR in similar frequency among 285 <b>heroin</b> addicts and 197 controls.
+DRD4	drug	opioid	10673776	Our results, therefore, do not support the hypothesis that alleles of the <strong>DRD4</strong> exon III VNTR are susceptibility factors for <b>opioid</b> dependence in man.
+DRD4	addiction	dependence	10673776	Our results, therefore, do not support the hypothesis that alleles of the <strong>DRD4</strong> exon III VNTR are susceptibility factors for opioid <b>dependence</b> in man.
+DRD4	addiction	relapse	10551544	The presence of the seven repeat allele of the VNTR in the exon 3 of the dopamine D4 receptor gene (<strong>DRD4</strong>) has been associated in healthy subjects to the personality trait of novelty <b>seeking</b>.
+DRD4	addiction	relapse	10551544	The lack of association between novelty <b>seeking</b> and the <strong>DRD4</strong> exon 3 polymorphism is further corroborated by the fact that the comorbid antisocial personality disorder is not associated to the presence of the seven repeat allele.
+DRD4	drug	alcohol	10490712	To determine the role of genes in the chromosomal regions 11p15 and 4p12 in the development of <b>alcohol</b> dependence, a sample of <b>alcoholics</b> (n = 133) and normal controls (n = 89) were screened using polymorphisms in the dopamine D4 receptor (<strong>DRD4</strong>), tyrosine hydroxylase (TH), and GABA receptor beta1 (GABRbeta1) genes.
+DRD4	addiction	dependence	10490712	To determine the role of genes in the chromosomal regions 11p15 and 4p12 in the development of alcohol <b>dependence</b>, a sample of alcoholics (n = 133) and normal controls (n = 89) were screened using polymorphisms in the dopamine D4 receptor (<strong>DRD4</strong>), tyrosine hydroxylase (TH), and GABA receptor beta1 (GABRbeta1) genes.
+DRD4	drug	alcohol	10490712	The allele distributions of the polymorphisms in the <strong>DRD4</strong> and TH genes in <b>alcoholics</b> and normal controls were similar and their differences were not significant.
+DRD4	drug	alcohol	10490712	Results with TH and <strong>DRD4</strong> genes indicate that these two genes may not play major roles in the development of <b>alcoholism</b>.
+DRD4	addiction	relapse	10379515	Recent reports suggest that DNA variants of the dopamine D4 receptor gene (<strong>DRD4</strong>) are associated with the personality trait of novelty <b>seeking</b>; however, others fail to replicate this finding.
+DRD4	drug	alcohol	10379515	We provide a critical analysis of genetic studies of <strong>DRD4</strong> variants with novelty seeking, <b>alcoholism</b>, drug abuse, and attention deficit hyperactivity disorder.
+DRD4	addiction	relapse	10379515	We provide a critical analysis of genetic studies of <strong>DRD4</strong> variants with novelty <b>seeking</b>, alcoholism, drug abuse, and attention deficit hyperactivity disorder.
+DRD4	addiction	relapse	10379515	Evidence for the role of <strong>DRD4</strong> in novelty <b>seeking</b> is inconclusive, with a number of methodological concerns.
+DRD4	drug	alcohol	20575787	These results, together with those available in the literature for other ethnic groups, suggest a minor role, if any, of the <strong>DRD4</strong> gene in the susceptibility to <b>alcoholism</b>.
+DRD4	drug	opioid	26735123	Additional evidence for an association between the dopamine D4 receptor (<strong>D4DR</strong>) exon III seven repeat allele and substance abuse in <b>opioid</b> dependent subjects: relationship of treatment retention to genotype and personality.
+DRD4	addiction	relapse	26735123	The long form of the dopamine D4 receptor (<strong>D4DR</strong>) exon III repeat polymorphism has been linked in some but not all studies to impulsive, extravagant and novelty <b>seeking</b> personality traits that are prominent in affiliated behaviours such as attention deficit disorder and substance abuse.
+DRD4	drug	opioid	26735123	In order to further substantiate the role of <strong>D4DR</strong> in contributing to <b>heroin</b> addiction we have genotyped an additional, smaller cohort of <b>opioid</b> dependent subjects.
+DRD4	addiction	addiction	26735123	In order to further substantiate the role of <strong>D4DR</strong> in contributing to heroin <b>addiction</b> we have genotyped an additional, smaller cohort of opioid dependent subjects.
+DRD4	drug	alcohol	9603615	The relationship of various dimensions of temperament, measured by the Tridimensional Personality Questionnaire (TPQ), to polymorphisms of the D2 dopamine receptor (DRD2) and D4 dopamine receptor (<strong>DRD4</strong>) genes was determined in 119 healthy Caucasian boys who had not yet begun to consume <b>alcohol</b> and other drugs of abuse.
+DRD4	addiction	relapse	9603615	Boys with the <strong>DRD4</strong> 7 repeat (7R) allele also had a significantly higher Novelty <b>Seeking</b> score than those without this allele.
+DRD4	addiction	relapse	9603615	However, the greatest difference in Novelty <b>Seeking</b> score was found when boys having all three minor DRD2 alleles and the <strong>DRD4</strong> 7R allele were contrasted to those without any of these alleles.
+DRD4	addiction	dependence	9603615	Whereas subjects having all three minor DRD2 alleles had a significantly higher Reward <b>Dependence</b> 2 (Persistence) score than subjects without any of these alleles, no significant difference in this personality score was found between subjects with and without the <strong>DRD4</strong> 7R allele.
+DRD4	addiction	reward	9603615	Whereas subjects having all three minor DRD2 alleles had a significantly higher <b>Reward</b> Dependence 2 (Persistence) score than subjects without any of these alleles, no significant difference in this personality score was found between subjects with and without the <strong>DRD4</strong> 7R allele.
+DRD4	addiction	relapse	9603615	In conclusion, DRD2 and <strong>DRD4</strong> polymorphisms individually associate with Novelty <b>Seeking</b> behavior.
+DRD4	addiction	relapse	9433345	No association between novelty <b>seeking</b> and the type 4 dopamine receptor gene (<strong>DRD4</strong>) in two New Zealand samples.
+DRD4	addiction	relapse	9433345	Two widely reported studies found significant associations between novelty <b>seeking</b> and the type 4 dopamine receptor gene (<strong>DRD4</strong>), although a more recent study did not.
+DRD4	addiction	relapse	9433345	Novelty <b>seeking</b> and <strong>DRD4</strong> were not statistically associated.
+DRD4	addiction	relapse	9433345	In these samples, there was no suggestion that the <strong>DRD4</strong> polymorphism contributed to individual differences in the behavioral trait of novelty <b>seeking</b>.
+DRD4	addiction	relapse	9342196	Recently, a significant association between the seven repeat allele (<strong>DRD4</strong>*7R) of a 16 amino acid motif in the third exon of the dopamine D4 receptor gene (<strong>DRD4</strong>) and the personality trait of novelty <b>seeking</b> has been reported.
+DRD4	drug	alcohol	9342196	Our population based association study tested the hypothesis that the <strong>DRD4</strong>*7R variant predisposes to high levels of novelty seeking, which may underlie <b>alcohol</b> seeking behavior.
+DRD4	addiction	relapse	9342196	Our population based association study tested the hypothesis that the <strong>DRD4</strong>*7R variant predisposes to high levels of novelty <b>seeking</b>, which may underlie alcohol <b>seeking</b> behavior.
+DRD4	drug	alcohol	9342196	The genotypes of the expressed <strong>DRD4</strong> exon III polymorphism were determined in 197 German controls and 252 German <b>alcohol</b> dependent males, of whom 92 <b>alcoholics</b> completed the tridimensional personality questionnaire.
+DRD4	drug	alcohol	9342196	We found no significant differences in the <strong>DRD4</strong>*7R frequencies between controls and <b>alcoholics</b>, including two subgroups (56 <b>alcoholics</b> with dissocial personality disorder according to ICD 10 and 89 <b>alcoholics</b> with severe withdrawal symptoms) with a high level of novelty seeking.
+DRD4	addiction	relapse	9342196	We found no significant differences in the <strong>DRD4</strong>*7R frequencies between controls and alcoholics, including two subgroups (56 alcoholics with dissocial personality disorder according to ICD 10 and 89 alcoholics with severe withdrawal symptoms) with a high level of novelty <b>seeking</b>.
+DRD4	addiction	withdrawal	9342196	We found no significant differences in the <strong>DRD4</strong>*7R frequencies between controls and alcoholics, including two subgroups (56 alcoholics with dissocial personality disorder according to ICD 10 and 89 alcoholics with severe <b>withdrawal</b> symptoms) with a high level of novelty seeking.
+DRD4	drug	alcohol	9342196	The present results do not provide evidence that the <strong>DRD4</strong>*7R allele contributes a common and relevant effect to <b>alcohol</b> seeking behavior in our sample of <b>alcoholics</b>.
+DRD4	addiction	relapse	9342196	The present results do not provide evidence that the <strong>DRD4</strong>*7R allele contributes a common and relevant effect to alcohol <b>seeking</b> behavior in our sample of alcoholics.
+DRD4	addiction	relapse	9322237	Substance abuse is associated with novelty <b>seeking</b>, a heritable human personality trait which may be influenced by alleles of the dopamine D4 (<strong>DRD4</strong>) gene exon III VNTR.
+DRD4	drug	opioid	9322237	We conclude that our findings support the hypothesis that alleles of the <strong>DRD4</strong> exon III VNTR are susceptibility factors for <b>heroin</b> abuse.
+DRD4	drug	opioid	9152990	Excess dopamine D4 receptor (<strong>D4DR</strong>) exon III seven repeat allele in <b>opioid</b> dependent subjects.
+DRD4	addiction	relapse	9152990	In addition, we recently reported an association between a human personality trait, Novelty <b>Seeking</b> and the long alleles (represented chiefly by the 7 repeat) of the D4 dopamine receptor (<strong>D4DR</strong>) exon III polymorphism.
+DRD4	drug	opioid	9152990	The twin role of dopamine receptors in mediating Novelty Seeking and drugreinforcement prompted us to examine a group of Israeli <b>heroin</b> addicts for prevalence of the <strong>D4DR</strong> repeat polymorphism.
+DRD4	addiction	relapse	9152990	The twin role of dopamine receptors in mediating Novelty <b>Seeking</b> and drugreinforcement prompted us to examine a group of Israeli heroin addicts for prevalence of the <strong>D4DR</strong> repeat polymorphism.
+DRD4	drug	alcohol	9034534	The dopamine D4 receptor gene (<strong>DRD4</strong>) is not associated with <b>alcoholism</b> in three Taiwanese populations: six polymorphisms tested separately and as haplotypes.
+DRD4	drug	alcohol	9034534	Especially because the powerful, multi site haplotype analysis was not statistically significant in any of the population samples, we conclude that there is no association of the <strong>DRD4</strong> locus with <b>alcoholism</b> in Taiwanese populations.
+DRD4	addiction	relapse	9154232	The association between the dopamine D4 receptor (<strong>D4DR</strong>) 16 amino acid repeat polymorphism and novelty <b>seeking</b>.
+DRD4	addiction	relapse	9154232	Ebstein and colleagues have recently reported a significant association between the 7 repeat allele of the dopamine D4 receptor (<strong>D4DR</strong>) 16 amino acid repeat polymorphism and the personality trait of Novelty <b>Seeking</b> (NS) in 124 Israeli subjects.
+DRD4	drug	alcohol	9154232	We have determined <strong>D4DR</strong> genotypes in two groups of Finnish subjects; 193 psychiatrically screened normal controls and 138 <b>alcoholic</b> offenders and assessed NS with the Tridimensional Personality Questionnaire (TPQ).
+DRD4	drug	alcohol	7573171	<strong>DRD4</strong> dopamine receptor genotype and CSF monoamine metabolites in Finnish <b>alcoholics</b> and controls.
+DRD4	drug	alcohol	7573171	Thus far, these <strong>DRD4</strong> alleles have been investigated for association with schizophrenia, bipolar disorder, Parkinson's disease, and chronic <b>alcoholism</b>, and all have been largely negative for a direct association.
+DRD4	drug	alcohol	7573171	We evaluated the <strong>DRD4</strong> genotype in 226 Finish adult males, 113 of whom were <b>alcoholics</b>, many of the early onset type with features of impulsivity and antisocial traits.
+DRD4	drug	alcohol	7573171	No association was found between a particular <strong>DRD4</strong> dopamine receptor allele and <b>alcoholism</b>.
+DRD4	drug	alcohol	7573171	This study of the <strong>DRD4</strong> dopamine receptor in <b>alcoholics</b> is the first to be conducted in a clinically and ethnically homogeneous population and to relate the <strong>DRD4</strong> genotype to CSF monoamine concentrations.
+DRD4	drug	alcohol	7573171	The results indicate that there is no association of the <strong>DRD4</strong> receptor with <b>alcoholism</b>.
+DBH	drug	opioid	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (TH), DOPA decarboxylase (DDC), solute carrier family 6 member 3 (SLC6A3) and DA beta hydroxylase (<strong>DBH</strong>), with six important phenotypes of <b>heroin</b> dependence.
+DBH	addiction	dependence	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (TH), DOPA decarboxylase (DDC), solute carrier family 6 member 3 (SLC6A3) and DA beta hydroxylase (<strong>DBH</strong>), with six important phenotypes of heroin <b>dependence</b>.
+DBH	drug	opioid	32736537	We found that <strong>DBH</strong> rs1611114 TT genotype had a protective effect on memory impairment after <b>heroin</b> dependence (P = 0.002, OR = 0.610).
+DBH	addiction	dependence	32736537	We found that <strong>DBH</strong> rs1611114 TT genotype had a protective effect on memory impairment after heroin <b>dependence</b> (P = 0.002, OR = 0.610).
+DBH	drug	alcohol	32070787	Another major aspect of the hypothesis is that phenol or polyphenol molecules, found in various plants, may combine with particular fats or even <b>ethanol</b> to form dopamine, which can then be converted to norepinephrine through the already established step involving the enzyme <strong>dopamine beta hydroxylase</strong>.
+DBH	drug	cocaine	31247269	Finally, using immunostaining, we demonstrated dopamine β hydroxylase (<strong>DBH</strong>) positive afferents in the VTA of <b>cocaine</b> abstinent rats, providing a neuroanatomical substrate for the α1 AR mechanism.
+DBH	drug	alcohol	29963872	<b>Disulfiram</b> (<b>Antabuse</b>), an acetaldehyde dehydrogenase and <strong>dopamine beta hydroxylase</strong> inhibitor, has shown promise in preclinical and clinical studies as a pharmacotherapy for cocaine addiction.
+DBH	drug	cocaine	29963872	Disulfiram (Antabuse), an acetaldehyde dehydrogenase and <strong>dopamine beta hydroxylase</strong> inhibitor, has shown promise in preclinical and clinical studies as a pharmacotherapy for <b>cocaine</b> addiction.
+DBH	addiction	addiction	29963872	Disulfiram (Antabuse), an acetaldehyde dehydrogenase and <strong>dopamine beta hydroxylase</strong> inhibitor, has shown promise in preclinical and clinical studies as a pharmacotherapy for cocaine <b>addiction</b>.
+DBH	drug	cocaine	28392265	<b>Cocaine</b> primed reinstatement can also be attenuated by systemic administration of dopamine β hydroxylase (<strong>DBH</strong>) inhibitors, which prevent norepinephrine (NE) synthesis, or by α1 adrenergic receptor (α1AR) antagonists, indicating functional modulation by the noradrenergic system.
+DBH	addiction	relapse	28392265	Cocaine primed <b>reinstatement</b> can also be attenuated by systemic administration of dopamine β hydroxylase (<strong>DBH</strong>) inhibitors, which prevent norepinephrine (NE) synthesis, or by α1 adrenergic receptor (α1AR) antagonists, indicating functional modulation by the noradrenergic system.
+DBH	drug	cocaine	28392265	We found that while intracerebroventricular infusion of the α1AR agonist phenylephrine did not induce reinstatement on its own, it did overcome the blockade of <b>cocaine</b> primed reinstatement by the <strong>DBH</strong> inhibitor nepicastat.
+DBH	addiction	relapse	28392265	We found that while intracerebroventricular infusion of the α1AR agonist phenylephrine did not induce <b>reinstatement</b> on its own, it did overcome the blockade of cocaine primed <b>reinstatement</b> by the <strong>DBH</strong> inhibitor nepicastat.
+DBH	drug	alcohol	28139629	[Combination of DAT and <strong>DBH</strong> gene polymorphisms with a family history of <b>alcohol</b> use disorders increases the risk of withdrawal seizures and delirium tremens during <b>alcohol</b> withdrawal in <b>alcohol</b> dependent men].
+DBH	addiction	withdrawal	28139629	[Combination of DAT and <strong>DBH</strong> gene polymorphisms with a family history of alcohol use disorders increases the risk of <b>withdrawal</b> seizures and delirium tremens during alcohol <b>withdrawal</b> in alcohol dependent men].
+DBH	drug	alcohol	28139629	To explore the genetic influence of a family history of <b>alcohol</b> use disorders and the dopamine transporter SLC6A3 (DAT1) and dopamine beta hydroxylase (<strong>DBH</strong>) gene polymorphisms on the risk of severe complications (withdrawal seizures (AWS) and delirium tremens (DT)) during <b>alcohol</b> withdrawal in <b>alcohol</b> dependent men.
+DBH	addiction	withdrawal	28139629	To explore the genetic influence of a family history of alcohol use disorders and the dopamine transporter SLC6A3 (DAT1) and dopamine beta hydroxylase (<strong>DBH</strong>) gene polymorphisms on the risk of severe complications (<b>withdrawal</b> seizures (AWS) and delirium tremens (DT)) during alcohol <b>withdrawal</b> in alcohol dependent men.
+DBH	drug	alcohol	28139629	To explore the genetic influence of a family history of <b>alcohol</b> use disorders and the dopamine transporter SLC6A3 (DAT1) and <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) gene polymorphisms on the risk of severe complications (withdrawal seizures (AWS) and delirium tremens (DT)) during <b>alcohol</b> withdrawal in <b>alcohol</b> dependent men.
+DBH	addiction	withdrawal	28139629	To explore the genetic influence of a family history of alcohol use disorders and the dopamine transporter SLC6A3 (DAT1) and <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) gene polymorphisms on the risk of severe complications (<b>withdrawal</b> seizures (AWS) and delirium tremens (DT)) during alcohol <b>withdrawal</b> in alcohol dependent men.
+DBH	drug	alcohol	28139629	We investigated the effects of 3 previously reported candidate genetic variations: 40 bp variable number tandem repeat (VNTR) polymorphism and C/T exon 15 (rs27072) in the 3' untranslated region (3' UTR) of the SLC6A3(DAT1) gene, and  1021 C/T (rs1611115) of <strong>DBH</strong> gene in 266 <b>alcohol</b> dependent Russian male inpatients in two groups by presence (SC group: AWS, DT, AWS+DT, n=130) or absence (n=136) of severe complications diagnosed by ICD 10 during current <b>alcohol</b> withdrawal.
+DBH	addiction	withdrawal	28139629	We investigated the effects of 3 previously reported candidate genetic variations: 40 bp variable number tandem repeat (VNTR) polymorphism and C/T exon 15 (rs27072) in the 3' untranslated region (3' UTR) of the SLC6A3(DAT1) gene, and  1021 C/T (rs1611115) of <strong>DBH</strong> gene in 266 alcohol dependent Russian male inpatients in two groups by presence (SC group: AWS, DT, AWS+DT, n=130) or absence (n=136) of severe complications diagnosed by ICD 10 during current alcohol <b>withdrawal</b>.
+DBH	drug	alcohol	28139629	According to an analysis of total cohort of patients, the T variant of <strong>DBH</strong> (rs1611115) is associated with any kind of manifestation of delirium in <b>alcohol</b> dependent men (p=0.039).
+DBH	drug	alcohol	28139629	This study demonstrate the genetic influence of a family history of <b>alcohol</b> use disorders and DAT and <strong>DBH</strong> gene polymorphisms on the risk of withdrawal seizures and delirium tremens.
+DBH	addiction	withdrawal	28139629	This study demonstrate the genetic influence of a family history of alcohol use disorders and DAT and <strong>DBH</strong> gene polymorphisms on the risk of <b>withdrawal</b> seizures and delirium tremens.
+DBH	addiction	addiction	27194378	Dopamine beta hydroxylase (<strong>DBH</strong>) converts dopamine to norepinephrine; the T allele of a functional single nucleotide polymorphism rs1611115 (C 1021T) in the <strong>DBH</strong> gene is associated with less <strong>DBH</strong> activity and has been linked to emotional processes and <b>addiction</b>.
+DBH	addiction	addiction	27194378	<strong>Dopamine beta hydroxylase</strong> (<strong>DBH</strong>) converts dopamine to norepinephrine; the T allele of a functional single nucleotide polymorphism rs1611115 (C 1021T) in the <strong>DBH</strong> gene is associated with less <strong>DBH</strong> activity and has been linked to emotional processes and <b>addiction</b>.
+DBH	drug	cocaine	27194378	Analyses focused on brain activation differences related to <strong>DBH</strong> genotype (CC/T carrier [i.e., CT and TT]) and condition (sad/gambling/<b>cocaine</b>).
+DBH	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (OPRM1), kappa <b>opioid</b> receptors (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), <strong>dopamine beta hydroxylase</strong>, and dopamine transporter (SLC6A3, DAT1) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+DBH	drug	cannabinoid	26667034	<b>Cannabis</b> and cocaine decrease cognitive impulse control and functional corticostriatal connectivity in drug users with low activity <strong>DBH</strong> genotypes.
+DBH	drug	cocaine	26667034	Cannabis and <b>cocaine</b> decrease cognitive impulse control and functional corticostriatal connectivity in drug users with low activity <strong>DBH</strong> genotypes.
+DBH	drug	cannabinoid	26667034	We hypothesized that individuals with low activity <strong>DBH</strong> genotypes (rs1611115 CT/TT) are more sensitive to the influence of <b>cannabis</b> and cocaine on cognitive impulse control and functional connectivity in the limbic 'reward' circuit because they experience a drug induced hyperdopaminergic state compared to individuals with high activity <strong>DBH</strong> genotypes (rs1611115 CC).
+DBH	drug	cocaine	26667034	We hypothesized that individuals with low activity <strong>DBH</strong> genotypes (rs1611115 CT/TT) are more sensitive to the influence of cannabis and <b>cocaine</b> on cognitive impulse control and functional connectivity in the limbic 'reward' circuit because they experience a drug induced hyperdopaminergic state compared to individuals with high activity <strong>DBH</strong> genotypes (rs1611115 CC).
+DBH	addiction	reward	26667034	We hypothesized that individuals with low activity <strong>DBH</strong> genotypes (rs1611115 CT/TT) are more sensitive to the influence of cannabis and cocaine on cognitive impulse control and functional connectivity in the limbic '<b>reward</b>' circuit because they experience a drug induced hyperdopaminergic state compared to individuals with high activity <strong>DBH</strong> genotypes (rs1611115 CC).
+DBH	drug	cannabinoid	26667034	The influence of <b>cannabis</b> and cocaine on impulsivity and functional connectivity significantly interacted with <strong>DBH</strong> genotype.
+DBH	drug	cocaine	26667034	The influence of cannabis and <b>cocaine</b> on impulsivity and functional connectivity significantly interacted with <strong>DBH</strong> genotype.
+DBH	drug	cannabinoid	26667034	It is concluded that interference of <b>cannabis</b> and cocaine with cognitive impulse control and functional corticostriatal connectivity depends on <strong>DBH</strong> genotype.
+DBH	drug	cocaine	26667034	It is concluded that interference of cannabis and <b>cocaine</b> with cognitive impulse control and functional corticostriatal connectivity depends on <strong>DBH</strong> genotype.
+DBH	addiction	relapse	26667034	The present data provide a neural substrate and behavioral mechanism by which drug users can progress to drug <b>seeking</b> and may also offer a rationale for targeted pharmacotherapy in chronic drug users with high risk <strong>DBH</strong> genotypes.
+DBH	drug	alcohol	26664087	Presence of <b>alcohol</b> withdrawal seizures (50%), DSF induced hypertension (HTN) (37.5%), psychosis (12.5%) were noted, that may suggest common neurobiological underpinnings like <strong>dopamine beta hydroxylase</strong> inhibition.
+DBH	addiction	withdrawal	26664087	Presence of alcohol <b>withdrawal</b> seizures (50%), DSF induced hypertension (HTN) (37.5%), psychosis (12.5%) were noted, that may suggest common neurobiological underpinnings like <strong>dopamine beta hydroxylase</strong> inhibition.
+DBH	drug	alcohol	26516613	<b>Disulfiram</b> has been claimed to be useful in cocaine addiction therapy, its efficacy being attributed to dopamine beta hydroxylase (<strong>DBH</strong>) inhibition.
+DBH	drug	cocaine	26516613	Disulfiram has been claimed to be useful in <b>cocaine</b> addiction therapy, its efficacy being attributed to dopamine beta hydroxylase (<strong>DBH</strong>) inhibition.
+DBH	addiction	addiction	26516613	Disulfiram has been claimed to be useful in cocaine <b>addiction</b> therapy, its efficacy being attributed to dopamine beta hydroxylase (<strong>DBH</strong>) inhibition.
+DBH	drug	alcohol	26516613	<b>Disulfiram</b> has been claimed to be useful in cocaine addiction therapy, its efficacy being attributed to <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) inhibition.
+DBH	drug	cocaine	26516613	Disulfiram has been claimed to be useful in <b>cocaine</b> addiction therapy, its efficacy being attributed to <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) inhibition.
+DBH	addiction	addiction	26516613	Disulfiram has been claimed to be useful in cocaine <b>addiction</b> therapy, its efficacy being attributed to <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) inhibition.
+DBH	drug	alcohol	26516613	Our previous results indicate that <b>disulfiram</b> and the selective <strong>DBH</strong> inhibitor nepicastat increase extracellular dopamine (DA) in the rat medial prefrontal cortex (mPFC), and markedly potentiated cocaine induced increase.
+DBH	drug	cocaine	26516613	Our previous results indicate that disulfiram and the selective <strong>DBH</strong> inhibitor nepicastat increase extracellular dopamine (DA) in the rat medial prefrontal cortex (mPFC), and markedly potentiated <b>cocaine</b> induced increase.
+DBH	addiction	relapse	26410615	<strong>DBH</strong> was also significantly associated with Automaticity, <b>Craving</b>, and Tolerance; Automaticity and Tolerance also served as mediators of the <strong>DBH</strong> ND relationship.
+DBH	drug	alcohol	26356164	[The 444G/A and  1021 C/T polymorphisms of the <strong>dopamine beta hydroxylase</strong> gene modulate the trajectory of <b>alcohol</b> dependence development].
+DBH	addiction	dependence	26356164	[The 444G/A and  1021 C/T polymorphisms of the <strong>dopamine beta hydroxylase</strong> gene modulate the trajectory of alcohol <b>dependence</b> development].
+DBH	drug	alcohol	26356164	To study the influence of 444 G/A (rs 1108580) and  1021 C/T (rs 1611115) polymorphisms of the dopamine beta hydroxylase (<strong>DBH</strong>) gene on clinical parameters of the trajectory of <b>alcohol</b> dependence.
+DBH	addiction	dependence	26356164	To study the influence of 444 G/A (rs 1108580) and  1021 C/T (rs 1611115) polymorphisms of the dopamine beta hydroxylase (<strong>DBH</strong>) gene on clinical parameters of the trajectory of alcohol <b>dependence</b>.
+DBH	drug	alcohol	26356164	To study the influence of 444 G/A (rs 1108580) and  1021 C/T (rs 1611115) polymorphisms of the <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) gene on clinical parameters of the trajectory of <b>alcohol</b> dependence.
+DBH	addiction	dependence	26356164	To study the influence of 444 G/A (rs 1108580) and  1021 C/T (rs 1611115) polymorphisms of the <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) gene on clinical parameters of the trajectory of alcohol <b>dependence</b>.
+DBH	drug	alcohol	26356164	The effects of <strong>DBH</strong> * 444 G/A on the rate of formation of <b>alcohol</b> withdrawal syndrome (AWS), and <strong>DBH</strong> * 1021C/T on the age of onset of <b>alcohol</b> abuse with significant role of the age of first <b>alcohol</b> use were identified.
+DBH	addiction	withdrawal	26356164	The effects of <strong>DBH</strong> * 444 G/A on the rate of formation of alcohol <b>withdrawal</b> syndrome (AWS), and <strong>DBH</strong> * 1021C/T on the age of onset of alcohol abuse with significant role of the age of first alcohol use were identified.
+DBH	drug	alcohol	26313930	The association of polymorphisms in DAT (40 bp VNTR, C>T 3'UTR) and <strong>DBH</strong> ( 1021 C/T) genes with the severe complications of <b>alcohol</b> withdrawal state.
+DBH	addiction	withdrawal	26313930	The association of polymorphisms in DAT (40 bp VNTR, C>T 3'UTR) and <strong>DBH</strong> ( 1021 C/T) genes with the severe complications of alcohol <b>withdrawal</b> state.
+DBH	drug	opioid	26288297	It was genotyped polymorphisms in the following genes: mu <b>opioid</b> receptor (OPRM1), kappa <b>opioid</b> receptor (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), <strong>dopamine beta hydroxylase</strong>, and dopamine transporter (DAT1).
+DBH	drug	alcohol	26146874	Polymorphisms of the DRD2, ANKK1, DAT1, <strong>DBH</strong>, and DRD4 genes have been found to moderate the effects of pharmacotherapy of <b>alcohol</b>, opioid, and cocaine use disorders.
+DBH	drug	cocaine	26146874	Polymorphisms of the DRD2, ANKK1, DAT1, <strong>DBH</strong>, and DRD4 genes have been found to moderate the effects of pharmacotherapy of alcohol, opioid, and <b>cocaine</b> use disorders.
+DBH	drug	opioid	26146874	Polymorphisms of the DRD2, ANKK1, DAT1, <strong>DBH</strong>, and DRD4 genes have been found to moderate the effects of pharmacotherapy of alcohol, <b>opioid</b>, and cocaine use disorders.
+DBH	drug	nicotine	25450229	We also observed a significant excess of rare nonsynonymous variants exclusive to EA <b>smokers</b> in NRXN1, CHRNA9, TAS2R38, GRIN3A, <strong>DBH</strong>, ANKK1/DRD2, NRXN3 and CDH13 with WSS P values between 3.5 × 10( 5) and 1 × 10( 6).
+DBH	drug	alcohol	25135633	Previous investigations indicate that the dopamine β hydroxylase (<strong>DBH</strong>) inhibitors <b>disulfiram</b> and nepicastat suppress cocaine primed reinstatement of cocaine self administration behaviour.
+DBH	drug	cocaine	25135633	Previous investigations indicate that the dopamine β hydroxylase (<strong>DBH</strong>) inhibitors disulfiram and nepicastat suppress <b>cocaine</b> primed reinstatement of <b>cocaine</b> self administration behaviour.
+DBH	addiction	relapse	25135633	Previous investigations indicate that the dopamine β hydroxylase (<strong>DBH</strong>) inhibitors disulfiram and nepicastat suppress cocaine primed <b>reinstatement</b> of cocaine self administration behaviour.
+DBH	drug	cocaine	25135633	This study was aimed to clarify if the suppressant effect of <strong>DBH</strong> inhibitors on <b>cocaine</b> reinstatement was mediated by the high extracellular dopamine in the rat mPFC leading to a supra maximal stimulation of D1 receptors in the dorsal division of mPFC, an area critical for reinstatement of <b>cocaine</b> seeking behaviour.
+DBH	addiction	relapse	25135633	This study was aimed to clarify if the suppressant effect of <strong>DBH</strong> inhibitors on cocaine <b>reinstatement</b> was mediated by the high extracellular dopamine in the rat mPFC leading to a supra maximal stimulation of D1 receptors in the dorsal division of mPFC, an area critical for <b>reinstatement</b> of cocaine <b>seeking</b> behaviour.
+DBH	drug	cocaine	25135633	In line with previous microdialysis studies in drug naïve animals, both <strong>DBH</strong> inhibitors potentiated <b>cocaine</b> induced dopamine release in the mPFC, in the same animals in which they also suppressed reinstatement of <b>cocaine</b> seeking.
+DBH	addiction	relapse	25135633	In line with previous microdialysis studies in drug naïve animals, both <strong>DBH</strong> inhibitors potentiated cocaine induced dopamine release in the mPFC, in the same animals in which they also suppressed <b>reinstatement</b> of cocaine <b>seeking</b>.
+DBH	drug	cocaine	25135633	Similar to the <strong>DBH</strong> inhibitors, L DOPA potentiated <b>cocaine</b> induced dopamine release in the mPFC and suppressed <b>cocaine</b> induced reinstatement of <b>cocaine</b> seeking behaviour.
+DBH	addiction	relapse	25135633	Similar to the <strong>DBH</strong> inhibitors, L DOPA potentiated cocaine induced dopamine release in the mPFC and suppressed cocaine induced <b>reinstatement</b> of cocaine <b>seeking</b> behaviour.
+DBH	drug	cocaine	25135633	These results suggest that stimulation of D1 receptors in the dorsal mPFC plays a crucial role in <b>cocaine</b> induced reinstatement of <b>cocaine</b> seeking, whereas the suppressant effect of <strong>DBH</strong> inhibitors and L DOPA on drug induced reinstatement is mediated by a supra maximal stimulation of D1 receptors leading to their inactivation.
+DBH	addiction	relapse	25135633	These results suggest that stimulation of D1 receptors in the dorsal mPFC plays a crucial role in cocaine induced <b>reinstatement</b> of cocaine <b>seeking</b>, whereas the suppressant effect of <strong>DBH</strong> inhibitors and L DOPA on drug induced <b>reinstatement</b> is mediated by a supra maximal stimulation of D1 receptors leading to their inactivation.
+DBH	drug	cocaine	25123018	Chronic inhibition of dopamine β hydroxylase (<strong>DBH</strong>), which converts DA to NE, increases the aversive effects of <b>cocaine</b> and reduces <b>cocaine</b> use in humans, and produces behavioral hypersensitivity to <b>cocaine</b> and D2 agonism in rodents, but the underlying mechanism is unknown.
+DBH	addiction	aversion	25123018	Chronic inhibition of dopamine β hydroxylase (<strong>DBH</strong>), which converts DA to NE, increases the <b>aversive</b> effects of cocaine and reduces cocaine use in humans, and produces behavioral hypersensitivity to cocaine and D2 agonism in rodents, but the underlying mechanism is unknown.
+DBH	drug	cocaine	25123018	We found a decrease in β arrestin2 (βArr2) in the nucleus accumbens (NAc) following chronic genetic or pharmacological <strong>DBH</strong> inhibition, and overexpression of βArr2 in the NAc normalized <b>cocaine</b> induced locomotion in <strong>DBH</strong> knockout (<strong>Dbh</strong>  / ) mice.
+DBH	drug	alcohol	25035107	The present study aimed to evaluate the association of <b>alcohol</b> dependence and <b>alcohol</b> dependence related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (COMT), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (DRD4) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (<strong>DBH</strong>) and MAO B intron 13 polymorphisms.
+DBH	addiction	dependence	25035107	The present study aimed to evaluate the association of alcohol <b>dependence</b> and alcohol <b>dependence</b> related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (COMT), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (DRD4) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of dopamine beta hydroxylase (<strong>DBH</strong>) and MAO B intron 13 polymorphisms.
+DBH	drug	alcohol	25035107	The present study aimed to evaluate the association of <b>alcohol</b> dependence and <b>alcohol</b> dependence related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (COMT), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (DRD4) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) and MAO B intron 13 polymorphisms.
+DBH	addiction	dependence	25035107	The present study aimed to evaluate the association of alcohol <b>dependence</b> and alcohol <b>dependence</b> related phenotypes with platelet monoamine oxidase type B (MAO B) activity, Val108/158Met of catechol o methyltransferase (COMT), variable number of tandem repeats (VNTR) in the third exon of dopamine receptor D4 (DRD4) gene, VNTR in the 3' untranslated region of dopamine transporter (DAT) gene,  1021C/T of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) and MAO B intron 13 polymorphisms.
+DBH	drug	alcohol	24817036	One of many biochemical actions of <b>disulfiram</b> is inhibition of dopamine β hydroxylase (<strong>DBH</strong>), the enzyme that converts dopamine (DA) to norepinephrine (NE) in noradrenergic neurons.
+DBH	drug	alcohol	24817036	In rats, both <b>disulfiram</b> and the selective <strong>DBH</strong> inhibitor nepicastat block cocaine primed reinstatement, a paradigm which is thought to model some aspects of drug relapse.
+DBH	drug	cocaine	24817036	In rats, both disulfiram and the selective <strong>DBH</strong> inhibitor nepicastat block <b>cocaine</b> primed reinstatement, a paradigm which is thought to model some aspects of drug relapse.
+DBH	addiction	relapse	24817036	In rats, both disulfiram and the selective <strong>DBH</strong> inhibitor nepicastat block cocaine primed <b>reinstatement</b>, a paradigm which is thought to model some aspects of drug <b>relapse</b>.
+DBH	drug	cocaine	24817036	This is consistent with some clinical results and supports the use of <strong>DBH</strong> inhibitors for the treatment of <b>cocaine</b> dependence.
+DBH	addiction	dependence	24817036	This is consistent with some clinical results and supports the use of <strong>DBH</strong> inhibitors for the treatment of cocaine <b>dependence</b>.
+DBH	drug	cocaine	24817036	Neither <strong>DBH</strong> inhibitor altered <b>cocaine</b> induced reinstatement.
+DBH	addiction	relapse	24817036	Neither <strong>DBH</strong> inhibitor altered cocaine induced <b>reinstatement</b>.
+DBH	drug	cocaine	24817036	Both <strong>DBH</strong> inhibitors attenuated <b>cocaine</b> induced DA overflow in the NAc.
+DBH	addiction	relapse	24817036	Overall, the reported behavioral effects of <strong>DBH</strong> inhibition in rodent models of <b>relapse</b> did not extend to nonhuman primates under the conditions used in the current studies.
+DBH	drug	cocaine	24809448	Seventy one <b>cocaine</b> dependent patients who participated in a 12 week randomized double blind placebo controlled trial of levodopa/carbidopa were genotyped for the DβH gene (<strong>DBH</strong>) polymorphism rs1611115.
+DBH	drug	alcohol	24724887	<strong>DBH</strong> interacted with <b>naltrexone</b> on the primary outcome of abstinence from heavy drinking (χ(2) (1) = 5.23, p = .02).
+DBH	drug	alcohol	24724887	Also, <strong>DBH</strong> genotype interacted with disulfram (F(1,17) = 7.52, p = .01) on drinks per drinking day with less drinking for subjects with the "CC" genotype than for T allele carriers on <b>disulfiram</b>.
+DBH	drug	alcohol	24724887	<strong>DBH</strong>*rs1611115*T associated with better response to <b>naltrexone</b>, while for those on <b>disulfiram</b> that drank, "CC" subjects drank less than T carriers.
+DBH	drug	nicotine	24667010	SNP × <b>nicotine</b> dependence interactions reached region wide significance for several SNPs in the Dopamine Beta Hydroxylase (<strong>DBH</strong>) locus (0.0005<Adjusted P<0.05), including rs1541333, which reached system wide significance for predicting end of treatment (EOT) abstinence (Adjusted P=0.0004).
+DBH	addiction	dependence	24667010	SNP × nicotine <b>dependence</b> interactions reached region wide significance for several SNPs in the Dopamine Beta Hydroxylase (<strong>DBH</strong>) locus (0.0005<Adjusted P<0.05), including rs1541333, which reached system wide significance for predicting end of treatment (EOT) abstinence (Adjusted P=0.0004).
+DBH	drug	nicotine	24667010	SNP × <b>nicotine</b> dependence interactions reached region wide significance for several SNPs in the <strong>Dopamine Beta Hydroxylase</strong> (<strong>DBH</strong>) locus (0.0005<Adjusted P<0.05), including rs1541333, which reached system wide significance for predicting end of treatment (EOT) abstinence (Adjusted P=0.0004).
+DBH	addiction	dependence	24667010	SNP × nicotine <b>dependence</b> interactions reached region wide significance for several SNPs in the <strong>Dopamine Beta Hydroxylase</strong> (<strong>DBH</strong>) locus (0.0005<Adjusted P<0.05), including rs1541333, which reached system wide significance for predicting end of treatment (EOT) abstinence (Adjusted P=0.0004).
+DBH	drug	nicotine	24667010	A haplotype including 6 <strong>DBH</strong> SNPs predicted abstinence at EOT (OR=1.7, P=0.001) and 6 month follow up (OR=1.6, P=0.008) in those with high <b>nicotine</b> dependence (n=526) but not in those with low dependence (n=227).
+DBH	addiction	dependence	24667010	A haplotype including 6 <strong>DBH</strong> SNPs predicted abstinence at EOT (OR=1.7, P=0.001) and 6 month follow up (OR=1.6, P=0.008) in those with high nicotine <b>dependence</b> (n=526) but not in those with low <b>dependence</b> (n=227).
+DBH	drug	nicotine	24667010	The <strong>DBH</strong> signal observed here may be distinct from a previously reported genome wide significant signal for former <b>smoking</b> status and from the principal haplotype associated with plasma dopamine beta hydroxylase activity.
+DBH	drug	nicotine	24667010	The <strong>DBH</strong> signal observed here may be distinct from a previously reported genome wide significant signal for former <b>smoking</b> status and from the principal haplotype associated with plasma <strong>dopamine beta hydroxylase</strong> activity.
+DBH	drug	amphetamine	24521142	Clinical features of <b>methamphetamine</b> induced paranoia and preliminary genetic association with <strong>DBH</strong> 1021C→T in a Thai treatment cohort.
+DBH	drug	amphetamine	24521142	To explore the clinical features of <b>methamphetamine</b> induced paranoia (MIP) and associations between MIP and a genetic polymorphism in dopamine β hydroxylase (<strong>DBH</strong> 1021C→T).
+DBH	drug	alcohol	24521142	<strong>DBH</strong> effects were confirmed [odds ratio (OR) = 0.7, P = 0.04] after controlling for associated clinical variables (MD severity, OR = 3.4, P < 0.001; antisocial personality disorder, OR = 2.2, P < 0.001; <b>alcohol</b> dependence, OR = 1.4, P = 0.05; and nicotine dependence, OR = 1.4, P = 0.06).
+DBH	drug	nicotine	24521142	<strong>DBH</strong> effects were confirmed [odds ratio (OR) = 0.7, P = 0.04] after controlling for associated clinical variables (MD severity, OR = 3.4, P < 0.001; antisocial personality disorder, OR = 2.2, P < 0.001; alcohol dependence, OR = 1.4, P = 0.05; and <b>nicotine</b> dependence, OR = 1.4, P = 0.06).
+DBH	addiction	dependence	24521142	<strong>DBH</strong> effects were confirmed [odds ratio (OR) = 0.7, P = 0.04] after controlling for associated clinical variables (MD severity, OR = 3.4, P < 0.001; antisocial personality disorder, OR = 2.2, P < 0.001; alcohol <b>dependence</b>, OR = 1.4, P = 0.05; and nicotine <b>dependence</b>, OR = 1.4, P = 0.06).
+DBH	drug	nicotine	24444411	Genetic variants in DRD2, DRD4, ANKK1, DAT1, COMT and <strong>DBH</strong> genes show some promise in informing personalized prescribing of <b>smoking</b> cessation pharmacotherapies.
+DBH	drug	cocaine	24068832	Inhibitors of dopamine β hydroxylase (<strong>DBH</strong>), the enzyme that converts dopamine (DA) to norepinephrine (NE) in noradrenergic cells, have shown promise for the treatment of <b>cocaine</b> abuse disorders.
+DBH	drug	cocaine	24068832	We used the drug discrimination paradigm to determine the impact of <strong>DBH</strong> inhibitors on the interoceptive stimulus properties of <b>cocaine</b>.
+DBH	drug	alcohol	24068832	On test days, subjects were pretreated with the nonselective <strong>DBH</strong> inhibitor <b>disulfiram</b> (0 100.0 mg/kg i.p.)
+DBH	drug	cocaine	24068832	These results indicate that pharmacological inhibition of <strong>DBH</strong> does not produce <b>cocaine</b> like interoceptive stimulus effects alone, but functionally enhances the interoceptive stimulus effects of <b>cocaine</b>, possibly due to facilitated increases in DA released from noradrenergic terminals.
+DBH	drug	cocaine	24068832	These findings suggest that <strong>DBH</strong> inhibitors have low abuse liability and provide support to clinical reports that some subjective effects produced by <b>cocaine</b>, particularly aversive effects, are enhanced after <strong>DBH</strong> inhibition.
+DBH	addiction	aversion	24068832	These findings suggest that <strong>DBH</strong> inhibitors have low abuse liability and provide support to clinical reports that some subjective effects produced by cocaine, particularly <b>aversive</b> effects, are enhanced after <strong>DBH</strong> inhibition.
+DBH	drug	alcohol	23906995	Association of functional <strong>DBH</strong> genetic variants with <b>alcohol</b> dependence risk and related depression and suicide attempt phenotypes: results from a large multicenter association study.
+DBH	addiction	dependence	23906995	Association of functional <strong>DBH</strong> genetic variants with alcohol <b>dependence</b> risk and related depression and suicide attempt phenotypes: results from a large multicenter association study.
+DBH	drug	alcohol	23906995	<strong>DBH</strong>, located on chromosome 9q34.2 has variants with potential functional consequences which may be related to alterations of neurotransmitter function and several psychiatric phenotypes, including <b>alcohol</b> dependence (AD), depression (MD) and suicidal behavior (SA).
+DBH	addiction	dependence	23906995	<strong>DBH</strong>, located on chromosome 9q34.2 has variants with potential functional consequences which may be related to alterations of neurotransmitter function and several psychiatric phenotypes, including alcohol <b>dependence</b> (AD), depression (MD) and suicidal behavior (SA).
+DBH	drug	alcohol	23906995	The aim of this association study in a large multicenter sample of <b>alcohol</b> dependent individuals and controls is to investigate the role of <strong>DBH</strong> SNPs and haplotypes in AD risk and associated phenotypes (AD with MD or SA).
+DBH	drug	alcohol	23906995	This study presents evidence for a potentially functional <strong>DBH</strong> variant influencing the risk for <b>alcohol</b> dependence while other comorbid conditions are not independently influenced by this SNP.
+DBH	addiction	dependence	23906995	This study presents evidence for a potentially functional <strong>DBH</strong> variant influencing the risk for alcohol <b>dependence</b> while other comorbid conditions are not independently influenced by this SNP.
+DBH	drug	alcohol	23857790	Genes SSTR4, ALDH1L2, GAD1, <strong>DBH</strong> and GABRP may participate in the biological process of <b>alcohol</b> dependence.
+DBH	addiction	dependence	23857790	Genes SSTR4, ALDH1L2, GAD1, <strong>DBH</strong> and GABRP may participate in the biological process of alcohol <b>dependence</b>.
+DBH	drug	cocaine	23561307	Nepicastat is a selective dopamine β hydroxylase (<strong>DBH</strong>) inhibitor that suppresses <b>cocaine</b> primed reinstatement of <b>cocaine</b> seeking in rats.
+DBH	addiction	relapse	23561307	Nepicastat is a selective dopamine β hydroxylase (<strong>DBH</strong>) inhibitor that suppresses cocaine primed <b>reinstatement</b> of cocaine <b>seeking</b> in rats.
+DBH	addiction	relapse	23561307	Moreover, the results suggest that <strong>DBH</strong> inhibitors may be a new class of pharmacological agents potentially useful in the prevention of <b>relapse</b> to food <b>seeking</b> in human dieters.
+DBH	drug	opioid	23510745	Positive association between  1021TT genotype of <strong>dopamine beta hydroxylase</strong> gene and progressive behavior of injection <b>heroin</b> users.
+DBH	drug	opioid	23510745	By balancing the ratios of dopamine and norepinephrine, dopamine beta hydroxylase (<strong>DBH</strong>) plays an important role in brain reward circuit that is involved with behavioral effects of <b>heroin</b> addiction.
+DBH	addiction	addiction	23510745	By balancing the ratios of dopamine and norepinephrine, dopamine beta hydroxylase (<strong>DBH</strong>) plays an important role in brain reward circuit that is involved with behavioral effects of heroin <b>addiction</b>.
+DBH	addiction	reward	23510745	By balancing the ratios of dopamine and norepinephrine, dopamine beta hydroxylase (<strong>DBH</strong>) plays an important role in brain <b>reward</b> circuit that is involved with behavioral effects of heroin addiction.
+DBH	drug	opioid	23510745	By balancing the ratios of dopamine and norepinephrine, <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) plays an important role in brain reward circuit that is involved with behavioral effects of <b>heroin</b> addiction.
+DBH	addiction	addiction	23510745	By balancing the ratios of dopamine and norepinephrine, <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) plays an important role in brain reward circuit that is involved with behavioral effects of heroin <b>addiction</b>.
+DBH	addiction	reward	23510745	By balancing the ratios of dopamine and norepinephrine, <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) plays an important role in brain <b>reward</b> circuit that is involved with behavioral effects of heroin addiction.
+DBH	drug	opioid	23510745	In conclusion, our results support  1021TT genotype may be implicated with a more progressive nature of <b>heroin</b> addiction, although <strong>DBH</strong>  1021C/T is unlikely to be involved in the risk of <b>heroin</b> addiction.
+DBH	addiction	addiction	23510745	In conclusion, our results support  1021TT genotype may be implicated with a more progressive nature of heroin <b>addiction</b>, although <strong>DBH</strong>  1021C/T is unlikely to be involved in the risk of heroin <b>addiction</b>.
+DBH	drug	cocaine	23458673	<strong>DBH</strong> gene as predictor of response in a <b>cocaine</b> vaccine clinical trial.
+DBH	drug	cocaine	23458673	We examined a pharmacogenetic association of the dopamine β hydroxylase (<strong>DBH</strong>) gene with a response to an anti <b>cocaine</b> vaccine that was tested in a recent clinical trial.
+DBH	drug	cocaine	23458673	We genotyped 71 subjects for the rs1611115 ( 1021C>T) variant of the <strong>DBH</strong> gene and compared vaccine to placebo subjects on <b>cocaine</b> free urines.
+DBH	drug	cocaine	23458673	Using repeated measures analysis of variance, corrected for population structure, vaccine pharmacotherapy reduced <b>cocaine</b> positive urines significantly based on <strong>DBH</strong> genotype.
+DBH	drug	cocaine	23458673	This study indicates that a patient's <strong>DBH</strong> genotype could be used to identify a subset of individuals for whom vaccine treatment may be an effective pharmacotherapy for <b>cocaine</b> dependence.
+DBH	addiction	dependence	23458673	This study indicates that a patient's <strong>DBH</strong> genotype could be used to identify a subset of individuals for whom vaccine treatment may be an effective pharmacotherapy for cocaine <b>dependence</b>.
+DBH	drug	alcohol	23289939	The <strong>dopamine beta hydroxylase</strong> inhibitor nepicastat has been shown to reproduce <b>disulfiram</b> ability to suppress the reinstatement of cocaine seeking after extinction in rats.
+DBH	drug	cocaine	23289939	The <strong>dopamine beta hydroxylase</strong> inhibitor nepicastat has been shown to reproduce disulfiram ability to suppress the reinstatement of <b>cocaine</b> seeking after extinction in rats.
+DBH	addiction	relapse	23289939	The <strong>dopamine beta hydroxylase</strong> inhibitor nepicastat has been shown to reproduce disulfiram ability to suppress the <b>reinstatement</b> of cocaine <b>seeking</b> after extinction in rats.
+DBH	drug	alcohol	23209785	<b>Disulfiram</b> inhibits dopamine β hydroxylase (<strong>DBH</strong>), the enzyme that converts dopamine (DA) to norepinephrine (NE) in noradrenergic neurons.
+DBH	drug	alcohol	23209785	The goal of this study was to test the effects of chronic genetic or pharmacological <strong>DBH</strong> inhibition on behavioral responses to cocaine using <strong>DBH</strong> knockout (<strong>Dbh</strong>  / ) mice, <b>disulfiram</b>, and the selective <strong>DBH</strong> inhibitor, nepicastat.
+DBH	drug	cocaine	23209785	The goal of this study was to test the effects of chronic genetic or pharmacological <strong>DBH</strong> inhibition on behavioral responses to <b>cocaine</b> using <strong>DBH</strong> knockout (<strong>Dbh</strong>  / ) mice, disulfiram, and the selective <strong>DBH</strong> inhibitor, nepicastat.
+DBH	drug	alcohol	23209785	Locomotor activity was measured in control (<strong>Dbh</strong> +/ ) and <strong>Dbh</strong>  /  mice during a 5 day regimen of saline+saline, <b>disulfiram</b>+saline, nepicastat+saline, saline+cocaine, <b>disulfiram</b>+cocaine, or nepicastat+cocaine.
+DBH	drug	cocaine	23209785	Locomotor activity was measured in control (<strong>Dbh</strong> +/ ) and <strong>Dbh</strong>  /  mice during a 5 day regimen of saline+saline, disulfiram+saline, nepicastat+saline, saline+<b>cocaine</b>, disulfiram+<b>cocaine</b>, or nepicastat+<b>cocaine</b>.
+DBH	drug	cocaine	23209785	Drug naïve <strong>Dbh</strong>  /  mice were hypersensitive to <b>cocaine</b> induced locomotion and resembled <b>cocaine</b> sensitized <strong>Dbh</strong> +/  mice.
+DBH	drug	alcohol	23209785	Cocaine induced stereotypy was profoundly increased in the <b>disulfiram</b>+cocaine, nepicastat+cocaine, and nepicastat+saline groups upon cocaine challenge after withdrawal in <strong>Dbh</strong> +/  mice.
+DBH	drug	cocaine	23209785	<b>Cocaine</b> induced stereotypy was profoundly increased in the disulfiram+<b>cocaine</b>, nepicastat+<b>cocaine</b>, and nepicastat+saline groups upon <b>cocaine</b> challenge after withdrawal in <strong>Dbh</strong> +/  mice.
+DBH	addiction	withdrawal	23209785	Cocaine induced stereotypy was profoundly increased in the disulfiram+cocaine, nepicastat+cocaine, and nepicastat+saline groups upon cocaine challenge after <b>withdrawal</b> in <strong>Dbh</strong> +/  mice.
+DBH	drug	alcohol	23209785	<b>Disulfiram</b> or nepicastat treatment had no effect on behavioral responses to cocaine in <strong>Dbh</strong>  /  mice.
+DBH	drug	cocaine	23209785	Disulfiram or nepicastat treatment had no effect on behavioral responses to <b>cocaine</b> in <strong>Dbh</strong>  /  mice.
+DBH	drug	cocaine	23209785	These results demonstrate that chronic <strong>DBH</strong> inhibition facilitates behavioral responses to <b>cocaine</b>, although different methods of inhibition (genetic vs. non selective inhibitor vs. selective inhibitor) enhance qualitatively different <b>cocaine</b> induced behaviors.
+DBH	drug	alcohol	22906516	We genotyped the <strong>DBH</strong> gene polymorphism,  1021C/T (rs1611115), that reduces DβH enzyme levels and evaluated its role for increasing cocaine free urines with <b>disulfiram</b>.
+DBH	drug	cocaine	22906516	We genotyped the <strong>DBH</strong> gene polymorphism,  1021C/T (rs1611115), that reduces DβH enzyme levels and evaluated its role for increasing <b>cocaine</b> free urines with disulfiram.
+DBH	drug	alcohol	22906516	With repeated measures analysis of variance, corrected for population structure, <b>disulfiram</b> pharmacotherapy reduced cocaine positive urines from 80% to 62% (p = .0001), and this <b>disulfiram</b> efficacy differed by <strong>DBH</strong> genotype group.
+DBH	drug	cocaine	22906516	With repeated measures analysis of variance, corrected for population structure, disulfiram pharmacotherapy reduced <b>cocaine</b> positive urines from 80% to 62% (p = .0001), and this disulfiram efficacy differed by <strong>DBH</strong> genotype group.
+DBH	drug	alcohol	22906516	Patients with the normal DβH level genotype dropped from 84% to 56% on <b>disulfiram</b> (p = .0001), whereas those with the low <strong>DBH</strong> level genotype showed no <b>disulfiram</b> effect.
+DBH	drug	alcohol	22906516	This study indicates that the <strong>DBH</strong> genotype of a patient could be used to identify a subset of individuals for which <b>disulfiram</b> treatment might be an effective pharmacotherapy for cocaine dependence.
+DBH	drug	cocaine	22906516	This study indicates that the <strong>DBH</strong> genotype of a patient could be used to identify a subset of individuals for which disulfiram treatment might be an effective pharmacotherapy for <b>cocaine</b> dependence.
+DBH	addiction	dependence	22906516	This study indicates that the <strong>DBH</strong> genotype of a patient could be used to identify a subset of individuals for which disulfiram treatment might be an effective pharmacotherapy for cocaine <b>dependence</b>.
+DBH	drug	nicotine	22871345	Association of functional dopamine beta hydroxylase (<strong>DBH</strong>) 19 bp insertion/deletion polymorphism with <b>smoking</b> severity in male schizophrenic <b>smokers</b>.
+DBH	drug	nicotine	22871345	Association of functional <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) 19 bp insertion/deletion polymorphism with <b>smoking</b> severity in male schizophrenic <b>smokers</b>.
+DBH	drug	nicotine	22871345	Recent evidence suggests that a dopamine beta hydroxylase (<strong>DBH</strong>) polymorphism may play a role in determining an individual's predisposition to developing <b>nicotine</b> dependence.
+DBH	addiction	dependence	22871345	Recent evidence suggests that a dopamine beta hydroxylase (<strong>DBH</strong>) polymorphism may play a role in determining an individual's predisposition to developing nicotine <b>dependence</b>.
+DBH	drug	nicotine	22871345	Recent evidence suggests that a <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) polymorphism may play a role in determining an individual's predisposition to developing <b>nicotine</b> dependence.
+DBH	addiction	dependence	22871345	Recent evidence suggests that a <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) polymorphism may play a role in determining an individual's predisposition to developing nicotine <b>dependence</b>.
+DBH	drug	nicotine	22871345	In this study, we hypothesized that the functional polymorphism of <strong>DBH</strong> (DβH5' Ins/Del) was associated with <b>smoking</b> in patients with schizophrenia.
+DBH	drug	nicotine	22871345	The results showed no significant differences in <strong>DBH</strong> 5' Ins/Del genotype and allele distributions between the patients and healthy controls or between <b>smokers</b> and nonsmokers in either patients or healthy controls alone.
+DBH	drug	nicotine	22871345	These results suggest that the <strong>DBH</strong> 5' Ins/Del polymorphism may influence <b>smoking</b> severity among schizophrenic <b>smokers</b>.
+DBH	drug	opioid	22841130	One hundred seven <b>methadone</b> maintenance treatment patients, 36 having an ADHD diagnosis, 176 adult patients with ADHD without SUDs, and 500 healthy controls were genotyped for variants in the DRD4 (exon 3 VNTR), DRD5 (upstream VNTR), HTR1B (rs6296), <strong>DBH</strong> (rs2519152), COMT (rs4680; Val158Met), and OPRM1 (rs1799971; 118A>G) genes.
+DBH	drug	nicotine	22513716	Association between <strong>dopamine beta hydroxylase</strong> rs5320 polymorphism and <b>smoking</b> behaviour in elderly Japanese.
+DBH	drug	nicotine	22513716	This study, the first of its kind, was done to investigate the role of <strong>DBH</strong> rs5320 polymorphism in <b>smoking</b> behaviour of elderly Japanese.
+DBH	drug	nicotine	22513716	This was done by collecting blood samples from 2521 subjects with various <b>smoking</b> habits to genotype the <strong>DBH</strong> rs5320 polymorphism.
+DBH	drug	nicotine	22513716	This study shows that <strong>DBH</strong> rs5320 polymorphism influences <b>nicotine</b> dependence.
+DBH	addiction	dependence	22513716	This study shows that <strong>DBH</strong> rs5320 polymorphism influences nicotine <b>dependence</b>.
+DBH	drug	alcohol	22425177	For example, <b>ethanol</b> interacts with dopamine beta hydroxylase (<strong>DBH</strong>), an enzyme that plays an essential role in the only well established endogenous synthetic pathway for NE, whereby dopamine is hydroxylated to form NE.
+DBH	drug	alcohol	22425177	For example, <b>ethanol</b> interacts with <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>), an enzyme that plays an essential role in the only well established endogenous synthetic pathway for NE, whereby dopamine is hydroxylated to form NE.
+DBH	drug	alcohol	22425177	Importantly, the hypothesis is directly testable in rodents by presenting <b>ethanol</b> to <strong>DBH</strong> knockout mice, which are thought to lack NE, and then measuring if NE is synthesized in these animals.
+DBH	drug	cocaine	20801583	Several studies have looked for a link between <b>cocaine</b> addiction and the genes of the dopaminergic system: the genes DRD2, COMT, SLC6A3 (coding for the dopamine transporter DAT) and <strong>DBH</strong> (coding for the dopamine beta hydroxylase) but unfortunately very few well established results.
+DBH	addiction	addiction	20801583	Several studies have looked for a link between cocaine <b>addiction</b> and the genes of the dopaminergic system: the genes DRD2, COMT, SLC6A3 (coding for the dopamine transporter DAT) and <strong>DBH</strong> (coding for the dopamine beta hydroxylase) but unfortunately very few well established results.
+DBH	drug	cocaine	20801583	Several studies have looked for a link between <b>cocaine</b> addiction and the genes of the dopaminergic system: the genes DRD2, COMT, SLC6A3 (coding for the dopamine transporter DAT) and <strong>DBH</strong> (coding for the <strong>dopamine beta hydroxylase</strong>) but unfortunately very few well established results.
+DBH	addiction	addiction	20801583	Several studies have looked for a link between cocaine <b>addiction</b> and the genes of the dopaminergic system: the genes DRD2, COMT, SLC6A3 (coding for the dopamine transporter DAT) and <strong>DBH</strong> (coding for the <strong>dopamine beta hydroxylase</strong>) but unfortunately very few well established results.
+DBH	drug	cocaine	20801583	The gene <strong>DBH</strong> has particularly been linked with the psychotic effects caused by <b>cocaine</b>.
+DBH	drug	cocaine	20801583	Several functional alterations caused by different mutations of the genes involved in dopaminergic transmission (principally 1021C>T of the gene <strong>DBH</strong>, but also Val158Met of the gene COMT, TaqI A of the gene DRD2 and VNTR 9 repeat of the DAT) could result in a <b>cocaine</b> induced psychosis prone phenotype.
+DBH	drug	alcohol	20736996	We hypothesized that <b>disulfiram</b>'s inhibition of dopamine β hydroxylase (<strong>DBH</strong>), the catecholamine biosynthetic enzyme that converts dopamine (DA) to norepinephrine (NE) in noradrenergic neurons, underlies the drug's ability to treat cocaine dependence.
+DBH	drug	cocaine	20736996	We hypothesized that disulfiram's inhibition of dopamine β hydroxylase (<strong>DBH</strong>), the catecholamine biosynthetic enzyme that converts dopamine (DA) to norepinephrine (NE) in noradrenergic neurons, underlies the drug's ability to treat <b>cocaine</b> dependence.
+DBH	addiction	dependence	20736996	We hypothesized that disulfiram's inhibition of dopamine β hydroxylase (<strong>DBH</strong>), the catecholamine biosynthetic enzyme that converts dopamine (DA) to norepinephrine (NE) in noradrenergic neurons, underlies the drug's ability to treat cocaine <b>dependence</b>.
+DBH	drug	alcohol	20736996	We then compared the effects of <b>disulfiram</b> with those of the selective <strong>DBH</strong> inhibitor, nepicastat.
+DBH	addiction	relapse	20736996	Food primed <b>reinstatement</b> of food <b>seeking</b> was not impaired by <strong>DBH</strong> inhibition.
+DBH	drug	alcohol	20736996	Our results suggest that <b>disulfiram</b>'s efficacy in the treatment of cocaine addiction is associated with the inhibition of <strong>DBH</strong> and interference with the ability of environmental stimuli to trigger relapse.
+DBH	drug	cocaine	20736996	Our results suggest that disulfiram's efficacy in the treatment of <b>cocaine</b> addiction is associated with the inhibition of <strong>DBH</strong> and interference with the ability of environmental stimuli to trigger relapse.
+DBH	addiction	addiction	20736996	Our results suggest that disulfiram's efficacy in the treatment of cocaine <b>addiction</b> is associated with the inhibition of <strong>DBH</strong> and interference with the ability of environmental stimuli to trigger relapse.
+DBH	addiction	relapse	20736996	Our results suggest that disulfiram's efficacy in the treatment of cocaine addiction is associated with the inhibition of <strong>DBH</strong> and interference with the ability of environmental stimuli to trigger <b>relapse</b>.
+DBH	drug	cocaine	20505554	Association study between the DAT1, <strong>DBH</strong> and DRD2 genes and <b>cocaine</b> dependence in a Spanish sample.
+DBH	addiction	dependence	20505554	Association study between the DAT1, <strong>DBH</strong> and DRD2 genes and cocaine <b>dependence</b> in a Spanish sample.
+DBH	drug	cocaine	20505554	We genotyped the Int8 and 3'UTR variable number of tandem repeats of the dopamine transporter gene (DAT1/SLC6A3), the TaqIA (rs1800497) and TaqIB (rs1079597) SNP polymorphisms within the dopamine receptor D2 gene and the 19 bp insertion/deletion and c.444G>A (rs1108580) polymorphisms of the dopamine β hydroxylase gene (<strong>DBH</strong>) in a Spanish sample of 169 patients with <b>cocaine</b> addiction and 169 sex matched controls.
+DBH	addiction	addiction	20505554	We genotyped the Int8 and 3'UTR variable number of tandem repeats of the dopamine transporter gene (DAT1/SLC6A3), the TaqIA (rs1800497) and TaqIB (rs1079597) SNP polymorphisms within the dopamine receptor D2 gene and the 19 bp insertion/deletion and c.444G>A (rs1108580) polymorphisms of the dopamine β hydroxylase gene (<strong>DBH</strong>) in a Spanish sample of 169 patients with cocaine <b>addiction</b> and 169 sex matched controls.
+DBH	drug	cannabinoid	20457524	These results strongly support that PhAR <strong>DBH</strong> Me possesses <b>cannabinoid</b> activity without the reinforcement effects.
+DBH	addiction	reward	20457524	These results strongly support that PhAR <strong>DBH</strong> Me possesses cannabinoid activity without the <b>reinforcement</b> effects.
+DBH	drug	nicotine	20350135	We examined genotypes at two dopamine related loci, DRD2/ANKK1 (rs1800497) and <strong>DBH</strong> (rs77905), in 577 heavy <b>smokers</b> participating in a prospective study of <b>smoking</b> cessation in general care in Germany.
+DBH	drug	alcohol	20201810	Although <b>disulfiram</b>'s mechanism of action in <b>alcohol</b> dependence was long thought to be its effects as a psychological deterrent, more recent studies have uncovered potential anti craving effects as well as direct effects of <b>disulfiram</b> on cocaine abuse, highlighting a few of the many potential and unique benefits <b>disulfiram</b> may have through its inhibition of <strong>dopamine beta hydroxylase</strong>.
+DBH	drug	cocaine	20201810	Although disulfiram's mechanism of action in alcohol dependence was long thought to be its effects as a psychological deterrent, more recent studies have uncovered potential anti craving effects as well as direct effects of disulfiram on <b>cocaine</b> abuse, highlighting a few of the many potential and unique benefits disulfiram may have through its inhibition of <strong>dopamine beta hydroxylase</strong>.
+DBH	addiction	dependence	20201810	Although disulfiram's mechanism of action in alcohol <b>dependence</b> was long thought to be its effects as a psychological deterrent, more recent studies have uncovered potential anti craving effects as well as direct effects of disulfiram on cocaine abuse, highlighting a few of the many potential and unique benefits disulfiram may have through its inhibition of <strong>dopamine beta hydroxylase</strong>.
+DBH	addiction	relapse	20201810	Although disulfiram's mechanism of action in alcohol dependence was long thought to be its effects as a psychological deterrent, more recent studies have uncovered potential anti <b>craving</b> effects as well as direct effects of disulfiram on cocaine abuse, highlighting a few of the many potential and unique benefits disulfiram may have through its inhibition of <strong>dopamine beta hydroxylase</strong>.
+DBH	drug	alcohol	20201810	We will also review recent literature on newer potential applications for <b>disulfiram</b> use via its unique action on <strong>dopamine beta hydroxylase</strong>.
+DBH	drug	alcohol	20083479	In addition to its inhibiting acetaldehyde dehydrogenase, <b>disulfiram</b> inhibits <strong>dopamine beta hydroxylase</strong> and may thereby increase dopamine and decrease norepinephrine cerebral concentrations.
+DBH	drug	alcohol	19720750	Here, we synthesize clinical and animal data that point to <strong>dopamine beta hydroxylase</strong> inhibition as a mechanism underlying the efficacy of <b>disulfiram</b> in the treatment of cocaine dependence.
+DBH	drug	cocaine	19720750	Here, we synthesize clinical and animal data that point to <strong>dopamine beta hydroxylase</strong> inhibition as a mechanism underlying the efficacy of disulfiram in the treatment of <b>cocaine</b> dependence.
+DBH	addiction	dependence	19720750	Here, we synthesize clinical and animal data that point to <strong>dopamine beta hydroxylase</strong> inhibition as a mechanism underlying the efficacy of disulfiram in the treatment of cocaine <b>dependence</b>.
+DBH	drug	nicotine	19415821	In this study, we investigated the association and multilocus gene gene interactions of cytochrome P450 2A6 (CYP2A6), dopamine beta hydroxylase (<strong>DBH</strong>), catechol O methyl transferase (COMT), and monoamine oxidase A (MAOA) polymorphisms with <b>smoking</b> behavior in a community based Chinese male population.
+DBH	drug	nicotine	19415821	In this study, we investigated the association and multilocus gene gene interactions of cytochrome P450 2A6 (CYP2A6), <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>), catechol O methyl transferase (COMT), and monoamine oxidase A (MAOA) polymorphisms with <b>smoking</b> behavior in a community based Chinese male population.
+DBH	drug	alcohol	18329701	Effects of <b>disulfiram</b> and <strong>dopamine beta hydroxylase</strong> knockout on cocaine induced seizures.
+DBH	drug	cocaine	18329701	Effects of disulfiram and <strong>dopamine beta hydroxylase</strong> knockout on <b>cocaine</b> induced seizures.
+DBH	drug	alcohol	18329701	The antialcoholism drug <b>disulfiram</b> has shown recent promise as a pharmacotherapy for treating cocaine dependence, probably via inhibition of dopamine beta hydroxylase (<strong>DBH</strong>), the enzyme that catalyzes the conversion of dopamine (DA) to norepinephrine (NE).
+DBH	drug	cocaine	18329701	The antialcoholism drug disulfiram has shown recent promise as a pharmacotherapy for treating <b>cocaine</b> dependence, probably via inhibition of dopamine beta hydroxylase (<strong>DBH</strong>), the enzyme that catalyzes the conversion of dopamine (DA) to norepinephrine (NE).
+DBH	addiction	dependence	18329701	The antialcoholism drug disulfiram has shown recent promise as a pharmacotherapy for treating cocaine <b>dependence</b>, probably via inhibition of dopamine beta hydroxylase (<strong>DBH</strong>), the enzyme that catalyzes the conversion of dopamine (DA) to norepinephrine (NE).
+DBH	drug	alcohol	18329701	The antialcoholism drug <b>disulfiram</b> has shown recent promise as a pharmacotherapy for treating cocaine dependence, probably via inhibition of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>), the enzyme that catalyzes the conversion of dopamine (DA) to norepinephrine (NE).
+DBH	drug	cocaine	18329701	The antialcoholism drug disulfiram has shown recent promise as a pharmacotherapy for treating <b>cocaine</b> dependence, probably via inhibition of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>), the enzyme that catalyzes the conversion of dopamine (DA) to norepinephrine (NE).
+DBH	addiction	dependence	18329701	The antialcoholism drug disulfiram has shown recent promise as a pharmacotherapy for treating cocaine <b>dependence</b>, probably via inhibition of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>), the enzyme that catalyzes the conversion of dopamine (DA) to norepinephrine (NE).
+DBH	drug	alcohol	18329701	We previously showed that <strong>DBH</strong> knockout (<strong>Dbh</strong>  / ) mice, which lack NE, are susceptible to seizures and are hypersensitive to the psychomotor, rewarding, and aversive effects of cocaine, suggesting that <b>disulfiram</b> might exacerbate cocaine induced seizures (CIS) by inhibiting <strong>DBH</strong>.
+DBH	drug	cocaine	18329701	We previously showed that <strong>DBH</strong> knockout (<strong>Dbh</strong>  / ) mice, which lack NE, are susceptible to seizures and are hypersensitive to the psychomotor, rewarding, and aversive effects of <b>cocaine</b>, suggesting that disulfiram might exacerbate <b>cocaine</b> induced seizures (CIS) by inhibiting <strong>DBH</strong>.
+DBH	addiction	aversion	18329701	We previously showed that <strong>DBH</strong> knockout (<strong>Dbh</strong>  / ) mice, which lack NE, are susceptible to seizures and are hypersensitive to the psychomotor, rewarding, and <b>aversive</b> effects of cocaine, suggesting that disulfiram might exacerbate cocaine induced seizures (CIS) by inhibiting <strong>DBH</strong>.
+DBH	drug	alcohol	18329701	To test this, we examined CIS in wild type and <strong>Dbh</strong>  /  mice following administration of <b>disulfiram</b> or the selective <strong>DBH</strong> inhibitor nepicastat.
+DBH	drug	alcohol	18329701	We found that <strong>Dbh</strong> genotype had no effect on CIS probability or frequency, whereas <b>disulfiram</b>, but not nepicastat, increased the probability of having CIS in both wild type and <strong>Dbh</strong>  /  mice.
+DBH	drug	alcohol	18329701	Both <b>disulfiram</b> and nepicastat increased CIS frequency in wild type but not <strong>Dbh</strong>  /  mice.
+DBH	drug	alcohol	18329701	There were no genotype or treatment effects on serum cocaine levels, except for an increase in <b>disulfiram</b> treated <strong>Dbh</strong>  /  mice at the highest dose of cocaine.
+DBH	drug	cocaine	18329701	There were no genotype or treatment effects on serum <b>cocaine</b> levels, except for an increase in disulfiram treated <strong>Dbh</strong>  /  mice at the highest dose of <b>cocaine</b>.
+DBH	drug	alcohol	18329701	These results suggest that <b>disulfiram</b> enhances CIS via two distinct mechanisms: it both increases CIS frequency by inhibiting <strong>DBH</strong> and increases CIS frequency in a <strong>DBH</strong> independent manner.
+DBH	drug	cocaine	18173840	<strong>Dopamine beta hydroxylase</strong> polymorphism and <b>cocaine</b> addiction.
+DBH	addiction	addiction	18173840	<strong>Dopamine beta hydroxylase</strong> polymorphism and cocaine <b>addiction</b>.
+DBH	drug	cocaine	18173840	Dopamine beta hydroxylase (<strong>DbH</strong>) catalyzes the conversion of dopamine to norepinephrine and could, therefore, have an influence on both <b>cocaine</b> action and the basal sensitivity of neurotransmitter systems to <b>cocaine</b>.
+DBH	drug	cocaine	18173840	<strong>Dopamine beta hydroxylase</strong> (<strong>DbH</strong>) catalyzes the conversion of dopamine to norepinephrine and could, therefore, have an influence on both <b>cocaine</b> action and the basal sensitivity of neurotransmitter systems to <b>cocaine</b>.
+DBH	drug	cocaine	18083142	In this study, we evaluated the performance of dopamine beta hydroxylase knockout (<strong>Dbh</strong>  / ) mice, which lack norepinephrine (NE), in the elevated plus maze (EPM) to examine the contribution of noradrenergic signaling to <b>cocaine</b> induced anxiety.
+DBH	drug	cocaine	18083142	In this study, we evaluated the performance of <strong>dopamine beta hydroxylase</strong> knockout (<strong>Dbh</strong>  / ) mice, which lack norepinephrine (NE), in the elevated plus maze (EPM) to examine the contribution of noradrenergic signaling to <b>cocaine</b> induced anxiety.
+DBH	drug	cocaine	18083142	We found that <b>cocaine</b> dose dependently increased anxiety like behavior in control (<strong>Dbh</strong> +/ ) mice, as measured by a decrease in open arm exploration.
+DBH	drug	cocaine	18083142	The <strong>Dbh</strong>  /  mice had normal baseline performance in the EPM but were completely resistant to the anxiogenic effects of <b>cocaine</b>.
+DBH	drug	alcohol	18083142	Cocaine induced anxiety was also attenuated in <strong>Dbh</strong> +/  mice following administration of <b>disulfiram</b>, a dopamine beta hydroxylase (<strong>DBH</strong>) inhibitor.
+DBH	drug	cocaine	18083142	<b>Cocaine</b> induced anxiety was also attenuated in <strong>Dbh</strong> +/  mice following administration of disulfiram, a dopamine beta hydroxylase (<strong>DBH</strong>) inhibitor.
+DBH	drug	alcohol	18083142	Cocaine induced anxiety was also attenuated in <strong>Dbh</strong> +/  mice following administration of <b>disulfiram</b>, a <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) inhibitor.
+DBH	drug	cocaine	18083142	<b>Cocaine</b> induced anxiety was also attenuated in <strong>Dbh</strong> +/  mice following administration of disulfiram, a <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) inhibitor.
+DBH	drug	cocaine	18083142	In experiments using specific adrenergic antagonists, we found that pretreatment with the beta adrenergic receptor antagonist propranolol blocked <b>cocaine</b> induced anxiety like behavior in <strong>Dbh</strong> +/  and wild type C57BL6/J mice, while the alpha(1) antagonist prazosin and the alpha(2) antagonist yohimbine had no effect.
+DBH	drug	nicotine	17372541	Genetic polymorphisms of the dopamine D1, D2, D4 and D5 receptors, dopamine transporter (DAT1) and dopamine B hydroxylase (<strong>DBH</strong>) have been associated at least once with clinical aspects of <b>tobacco</b> use (initiation, dependence and intensity) and temperament traits as novelty seeking, the latter being lower in <b>smokers</b> and thus considered as a vulnerable marker in accordance with the reinforcement effect of <b>nicotine</b>.
+DBH	addiction	dependence	17372541	Genetic polymorphisms of the dopamine D1, D2, D4 and D5 receptors, dopamine transporter (DAT1) and dopamine B hydroxylase (<strong>DBH</strong>) have been associated at least once with clinical aspects of tobacco use (initiation, <b>dependence</b> and intensity) and temperament traits as novelty seeking, the latter being lower in smokers and thus considered as a vulnerable marker in accordance with the reinforcement effect of nicotine.
+DBH	addiction	relapse	17372541	Genetic polymorphisms of the dopamine D1, D2, D4 and D5 receptors, dopamine transporter (DAT1) and dopamine B hydroxylase (<strong>DBH</strong>) have been associated at least once with clinical aspects of tobacco use (initiation, dependence and intensity) and temperament traits as novelty <b>seeking</b>, the latter being lower in smokers and thus considered as a vulnerable marker in accordance with the reinforcement effect of nicotine.
+DBH	addiction	reward	17372541	Genetic polymorphisms of the dopamine D1, D2, D4 and D5 receptors, dopamine transporter (DAT1) and dopamine B hydroxylase (<strong>DBH</strong>) have been associated at least once with clinical aspects of tobacco use (initiation, dependence and intensity) and temperament traits as novelty seeking, the latter being lower in smokers and thus considered as a vulnerable marker in accordance with the <b>reinforcement</b> effect of nicotine.
+DBH	drug	alcohol	17164822	Of particular interest is <b>disulfiram</b>, an inhibitor of the NE biosynthetic enzyme <strong>dopamine beta hydroxylase</strong>, which has demonstrated promising efficacy in the treatment of cocaine dependence in preliminary clinical trials.
+DBH	drug	cocaine	17164822	Of particular interest is disulfiram, an inhibitor of the NE biosynthetic enzyme <strong>dopamine beta hydroxylase</strong>, which has demonstrated promising efficacy in the treatment of <b>cocaine</b> dependence in preliminary clinical trials.
+DBH	addiction	dependence	17164822	Of particular interest is disulfiram, an inhibitor of the NE biosynthetic enzyme <strong>dopamine beta hydroxylase</strong>, which has demonstrated promising efficacy in the treatment of cocaine <b>dependence</b> in preliminary clinical trials.
+DBH	drug	cocaine	17157269	<strong>Dopamine beta hydroxylase</strong> gene (DbetaH)  1021C  >T influences self reported paranoia during <b>cocaine</b> self administration.
+DBH	drug	cocaine	17157269	Variation in the gene for <strong>dopamine beta hydroxylase</strong> (DbetaH) has been reported to associate with <b>cocaine</b> induced paranoia as assessed by retrospective self report.
+DBH	addiction	addiction	16899413	To determine whether noradrenaline (NA) is an essential neurotransmitter for <b>addictive</b> and appetitive behaviors, we measured drug and food seeking in transgenic mice lacking dopamine beta hydroxylase (<strong>Dbh</strong>), the enzyme responsible for synthesizing NA.
+DBH	addiction	relapse	16899413	To determine whether noradrenaline (NA) is an essential neurotransmitter for addictive and appetitive behaviors, we measured drug and food <b>seeking</b> in transgenic mice lacking dopamine beta hydroxylase (<strong>Dbh</strong>), the enzyme responsible for synthesizing NA.
+DBH	addiction	addiction	16899413	To determine whether noradrenaline (NA) is an essential neurotransmitter for <b>addictive</b> and appetitive behaviors, we measured drug and food seeking in transgenic mice lacking <strong>dopamine beta hydroxylase</strong> (<strong>Dbh</strong>), the enzyme responsible for synthesizing NA.
+DBH	addiction	relapse	16899413	To determine whether noradrenaline (NA) is an essential neurotransmitter for addictive and appetitive behaviors, we measured drug and food <b>seeking</b> in transgenic mice lacking <strong>dopamine beta hydroxylase</strong> (<strong>Dbh</strong>), the enzyme responsible for synthesizing NA.
+DBH	drug	cocaine	16899413	Using the conditioned place preference test (CPP), we show that <strong>Dbh</strong>  /  mice do not exhibit rewarding behavior to morphine, <b>cocaine</b>, or the mixed reuptake inhibitor bupropion.
+DBH	drug	opioid	16899413	Using the conditioned place preference test (CPP), we show that <strong>Dbh</strong>  /  mice do not exhibit rewarding behavior to <b>morphine</b>, cocaine, or the mixed reuptake inhibitor bupropion.
+DBH	addiction	reward	16899413	Using the conditioned place preference test (<b>CPP</b>), we show that <strong>Dbh</strong>  /  mice do not exhibit rewarding behavior to morphine, cocaine, or the mixed reuptake inhibitor bupropion.
+DBH	addiction	relapse	16899413	Drug <b>seeking</b> was induced when NA was restored to the central nervous system of <strong>Dbh</strong>  /  mice by administration of l threo 3,4 dihydroxyphenylserine (DOPS) and carbidopa.
+DBH	drug	cocaine	16899413	When a NK1 receptor antagonist was co administered with morphine or <b>cocaine</b>, it produced aversive behavior in <strong>Dbh</strong>  /  mice while it abolished place preference in the controls.
+DBH	drug	opioid	16899413	When a NK1 receptor antagonist was co administered with <b>morphine</b> or cocaine, it produced aversive behavior in <strong>Dbh</strong>  /  mice while it abolished place preference in the controls.
+DBH	addiction	aversion	16899413	When a NK1 receptor antagonist was co administered with morphine or cocaine, it produced <b>aversive</b> behavior in <strong>Dbh</strong>  /  mice while it abolished place preference in the controls.
+DBH	drug	opioid	16484499	In mice lacking dopamine beta hydroxylase (<strong>DBH</strong>), an enzyme critical for NE synthesis, we found that NE was necessary for <b>morphine</b> induced conditioned place preference (CPP; a measure of reward) and locomotion.
+DBH	addiction	reward	16484499	In mice lacking dopamine beta hydroxylase (<strong>DBH</strong>), an enzyme critical for NE synthesis, we found that NE was necessary for morphine induced conditioned place preference (<b>CPP</b>; a measure of <b>reward</b>) and locomotion.
+DBH	drug	opioid	16484499	In mice lacking <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>), an enzyme critical for NE synthesis, we found that NE was necessary for <b>morphine</b> induced conditioned place preference (CPP; a measure of reward) and locomotion.
+DBH	addiction	reward	16484499	In mice lacking <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>), an enzyme critical for NE synthesis, we found that NE was necessary for morphine induced conditioned place preference (<b>CPP</b>; a measure of <b>reward</b>) and locomotion.
+DBH	drug	opioid	16484499	Viral restoration of <strong>DBH</strong> expression in the nucleus tractus solitarius, but not in the locus coeruleus, restored CPP for <b>morphine</b>.
+DBH	addiction	reward	16484499	Viral restoration of <strong>DBH</strong> expression in the nucleus tractus solitarius, but not in the locus coeruleus, restored <b>CPP</b> for morphine.
+DBH	drug	opioid	16484499	<b>Morphine</b> induced locomotion was partially restored by <strong>DBH</strong> expression in either brain region.
+DBH	drug	cocaine	16395294	<strong>Dopamine beta hydroxylase</strong> knockout mice have alterations in dopamine signaling and are hypersensitive to <b>cocaine</b>.
+DBH	drug	amphetamine	16395294	Basal extracellular DA levels were significantly attenuated in the nucleus accumbens (NAc) and caudate putamen (CP), but not prefrontal cortex (PFC), of <strong>Dbh</strong> /  mice, while <b>amphetamine</b> induced DA release was absent in the NAc and attenuated in the CP and PFC.
+DBH	drug	cocaine	16395294	As a behavioral consequence of these neurochemical changes, <strong>Dbh</strong> /  mice were hypersensitive to the psychomotor, rewarding, and aversive effects of <b>cocaine</b>, as measured by locomotor activity and conditioned place preference.
+DBH	addiction	aversion	16395294	As a behavioral consequence of these neurochemical changes, <strong>Dbh</strong> /  mice were hypersensitive to the psychomotor, rewarding, and <b>aversive</b> effects of cocaine, as measured by locomotor activity and conditioned place preference.
+DBH	drug	cocaine	16395294	Antagonists of DA, but not 5 HT, receptors attenuated the locomotor hypersensitivity to <b>cocaine</b> in <strong>Dbh</strong> /  mice.
+DBH	drug	alcohol	16395294	As <strong>DBH</strong> activity in humans is genetically controlled and the <strong>DBH</strong> inhibitor <b>disulfiram</b> has shown promise as a pharmacotherapy for cocaine dependence, these results have implications for the influence of genetic and pharmacological <strong>DBH</strong> inhibition on DA system function and drug addiction.
+DBH	drug	cocaine	16395294	As <strong>DBH</strong> activity in humans is genetically controlled and the <strong>DBH</strong> inhibitor disulfiram has shown promise as a pharmacotherapy for <b>cocaine</b> dependence, these results have implications for the influence of genetic and pharmacological <strong>DBH</strong> inhibition on DA system function and drug addiction.
+DBH	addiction	addiction	16395294	As <strong>DBH</strong> activity in humans is genetically controlled and the <strong>DBH</strong> inhibitor disulfiram has shown promise as a pharmacotherapy for cocaine dependence, these results have implications for the influence of genetic and pharmacological <strong>DBH</strong> inhibition on DA system function and drug <b>addiction</b>.
+DBH	addiction	dependence	16395294	As <strong>DBH</strong> activity in humans is genetically controlled and the <strong>DBH</strong> inhibitor disulfiram has shown promise as a pharmacotherapy for cocaine <b>dependence</b>, these results have implications for the influence of genetic and pharmacological <strong>DBH</strong> inhibition on DA system function and drug addiction.
+DBH	drug	nicotine	16272956	CYP2A6, MAOA, <strong>DBH</strong>, DRD4, and 5HT2A genotypes, <b>smoking</b> behaviour and cotinine levels in 1518 UK adolescents.
+DBH	drug	nicotine	16272956	No significant associations were identified for <strong>DBH</strong>, MAOA, DRD4 and 5HT2A markers, with <b>smoking</b> status or cotinine level at either age.
+DBH	drug	alcohol	16252068	<strong>DBH</strong>*444G/A polymorphism of the dopamine beta hydroxylase gene is associated with <b>alcoholism</b> but not with severe <b>alcohol</b> withdrawal symptoms.
+DBH	addiction	withdrawal	16252068	<strong>DBH</strong>*444G/A polymorphism of the dopamine beta hydroxylase gene is associated with alcoholism but not with severe alcohol <b>withdrawal</b> symptoms.
+DBH	drug	alcohol	16252068	<strong>DBH</strong>*444G/A polymorphism of the <strong>dopamine beta hydroxylase</strong> gene is associated with <b>alcoholism</b> but not with severe <b>alcohol</b> withdrawal symptoms.
+DBH	addiction	withdrawal	16252068	<strong>DBH</strong>*444G/A polymorphism of the <strong>dopamine beta hydroxylase</strong> gene is associated with alcoholism but not with severe alcohol <b>withdrawal</b> symptoms.
+DBH	drug	alcohol	16252068	As the enzyme dopamine beta hydroxylase (DbetaH) converts dopamine to norepinephrine and both transmitters seem to be involved in the pathology of <b>alcoholism</b> and severe <b>alcohol</b> withdrawal symptoms, the gene encoding DbetaH (<strong>DBH</strong>) was applied to explore the genetic background of <b>alcoholism</b> and severe withdrawal symptoms.
+DBH	addiction	withdrawal	16252068	As the enzyme dopamine beta hydroxylase (DbetaH) converts dopamine to norepinephrine and both transmitters seem to be involved in the pathology of alcoholism and severe alcohol <b>withdrawal</b> symptoms, the gene encoding DbetaH (<strong>DBH</strong>) was applied to explore the genetic background of alcoholism and severe <b>withdrawal</b> symptoms.
+DBH	drug	alcohol	16252068	As the enzyme <strong>dopamine beta hydroxylase</strong> (DbetaH) converts dopamine to norepinephrine and both transmitters seem to be involved in the pathology of <b>alcoholism</b> and severe <b>alcohol</b> withdrawal symptoms, the gene encoding DbetaH (<strong>DBH</strong>) was applied to explore the genetic background of <b>alcoholism</b> and severe withdrawal symptoms.
+DBH	addiction	withdrawal	16252068	As the enzyme <strong>dopamine beta hydroxylase</strong> (DbetaH) converts dopamine to norepinephrine and both transmitters seem to be involved in the pathology of alcoholism and severe alcohol <b>withdrawal</b> symptoms, the gene encoding DbetaH (<strong>DBH</strong>) was applied to explore the genetic background of alcoholism and severe <b>withdrawal</b> symptoms.
+DBH	drug	alcohol	16252068	102 healthy control subjects and 208 <b>alcoholics</b>, including 97 patients with a history of mild withdrawal symptoms, 57 with a history of <b>alcohol</b> withdrawal seizure (AWS) and 82 with a history of delirium tremens (DT) were genotyped for the <strong>DBH</strong>*444G/A polymorphism revealing a significantly elevated frequency of genotypes carrying the A allele (p = 0.02; after Bonferroni adjustment for multiple tests) in <b>alcoholics</b> compared to healthy controls.
+DBH	addiction	withdrawal	16252068	102 healthy control subjects and 208 alcoholics, including 97 patients with a history of mild <b>withdrawal</b> symptoms, 57 with a history of alcohol <b>withdrawal</b> seizure (AWS) and 82 with a history of delirium tremens (DT) were genotyped for the <strong>DBH</strong>*444G/A polymorphism revealing a significantly elevated frequency of genotypes carrying the A allele (p = 0.02; after Bonferroni adjustment for multiple tests) in alcoholics compared to healthy controls.
+DBH	drug	amphetamine	15836801	Since we found <b>amphetamine</b> induced fos activated cells closely associated with <strong>dopamine beta hydroxylase</strong> immunoreactive varicosities in the bed nucleus of the stria terminalis (BNST), we investigated the effect of a bilateral micro injection of timolol into this nucleus.
+DBH	drug	opioid	15734726	Other genes of the endogenous <b>opioid</b> and monoaminergic systems, particularly genes encoding <strong>dopamine beta hydroxylase</strong>, and the dopamine, serotonin, and norepinephrine transporters have also been implicated.
+DBH	addiction	relapse	15318029	As well as supporting linkage of HA to D8S549, this method also produces an MALOD of 2.4 (P=0.002) near <strong>DBH</strong> and several positive lod scores for novelty <b>seeking</b>, the largest being MALODs of 3.1 (P=0.0004) near D12S391 and 3.4 (P=0.0003) near D17S1299.
+DBH	drug	alcohol	15233592	<b>Disulfiram</b> and selegiline increase brain dopamine concentrations by inhibition of dopamine catabolising enzymes (<strong>dopamine beta hydroxylase</strong> and monoamine oxidase B, respectively).
+DBH	drug	nicotine	15077009	Polymorphisms in the dopamine D2 receptor (DRD2 C/T and DRD2 A/G) and in dopamine beta hydroxylase (<strong>DBH</strong> A/G) have been implicated in modulation of <b>smoking</b> and other reward seeking behaviours.
+DBH	addiction	relapse	15077009	Polymorphisms in the dopamine D2 receptor (DRD2 C/T and DRD2 A/G) and in dopamine beta hydroxylase (<strong>DBH</strong> A/G) have been implicated in modulation of smoking and other reward <b>seeking</b> behaviours.
+DBH	addiction	reward	15077009	Polymorphisms in the dopamine D2 receptor (DRD2 C/T and DRD2 A/G) and in dopamine beta hydroxylase (<strong>DBH</strong> A/G) have been implicated in modulation of smoking and other <b>reward</b> seeking behaviours.
+DBH	drug	nicotine	15077009	Polymorphisms in the dopamine D2 receptor (DRD2 C/T and DRD2 A/G) and in <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong> A/G) have been implicated in modulation of <b>smoking</b> and other reward seeking behaviours.
+DBH	addiction	relapse	15077009	Polymorphisms in the dopamine D2 receptor (DRD2 C/T and DRD2 A/G) and in <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong> A/G) have been implicated in modulation of smoking and other reward <b>seeking</b> behaviours.
+DBH	addiction	reward	15077009	Polymorphisms in the dopamine D2 receptor (DRD2 C/T and DRD2 A/G) and in <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong> A/G) have been implicated in modulation of smoking and other <b>reward</b> seeking behaviours.
+DBH	drug	nicotine	15077009	In the 755 cases in which DNA was successfully genotyped, we examined associations between the polymorphisms in DRD2 and <strong>DBH</strong>, and <b>smoking</b> cessation.
+DBH	drug	nicotine	15077009	<b>Smokers</b> with both DRD2 CT/TT and <strong>DBH</strong> GA/AA genotypes had an OR of 3.6 (2.0 6.5) compared to 1.4 (1.0 2.1) for others (P = 0.01).
+DBH	drug	nicotine	15077009	Short term effectiveness of the <b>nicotine</b> patch may be related to <strong>dopamine beta hydroxylase</strong> and dopamine D2 receptor genotype.
+DBH	drug	alcohol	14573319	<b>Disulfiram</b> (DS; <b>Antabuse</b>) inhibits <strong>dopamine beta hydroxylase</strong> leading to increased brain dopamine levels and shows treatment efficacy for cocaine addiction.
+DBH	drug	cocaine	14573319	Disulfiram (DS; Antabuse) inhibits <strong>dopamine beta hydroxylase</strong> leading to increased brain dopamine levels and shows treatment efficacy for <b>cocaine</b> addiction.
+DBH	addiction	addiction	14573319	Disulfiram (DS; Antabuse) inhibits <strong>dopamine beta hydroxylase</strong> leading to increased brain dopamine levels and shows treatment efficacy for cocaine <b>addiction</b>.
+DBH	drug	amphetamine	12542666	Single administration of either IL 1 or <b>amphetamine</b> causes three weeks later a selective decrease in relative <strong>DBH</strong> innervation density in those subnuclei of the PVN that contain high numbers of corticotrophin releasing hormone (CRH) producing neurons: the dorsal parvocellular and medial parvocellular PVN.
+DBH	drug	amphetamine	12542666	We conclude that (1) long lasting sensitization induced by single exposure to IL 1 and <b>amphetamine</b> induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative <strong>DBH</strong> innervation density in CRH rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.
+DBH	addiction	sensitization	12542666	We conclude that (1) long lasting <b>sensitization</b> induced by single exposure to IL 1 and amphetamine induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative <strong>DBH</strong> innervation density in CRH rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.
+DBH	drug	alcohol	12488060	A genotype controlled analysis of plasma <strong>dopamine beta hydroxylase</strong> in healthy and <b>alcoholic</b> subjects: evidence for <b>alcohol</b> related differences in noradrenergic function.
+DBH	drug	alcohol	12488060	Our study investigated whether the <strong>DBH</strong> 1021C  >T polymorphism and plasma DbetaH activity were associated with <b>alcoholism</b> or with delirium tremens (DT) during <b>alcohol</b> withdrawal by analyzing 207 German <b>alcoholic</b> and 102 healthy control subjects.
+DBH	addiction	withdrawal	12488060	Our study investigated whether the <strong>DBH</strong> 1021C  >T polymorphism and plasma DbetaH activity were associated with alcoholism or with delirium tremens (DT) during alcohol <b>withdrawal</b> by analyzing 207 German alcoholic and 102 healthy control subjects.
+DBH	drug	alcohol	12488060	The data indicate that the <b>alcoholism</b> related reduction in plasma DbetaH activity is independent of genotype at <strong>DBH</strong> 1021C  >T and replicate the finding that <strong>DBH</strong> 1021C  >T is strongly associated with plasma DbetaH activity in a native Western European population.
+DBH	drug	amphetamine	12370425	Surprisingly, <strong>Dbh</strong> /  animals were hypersensitive to the behavioral effects of <b>amphetamine</b>.
+DBH	drug	amphetamine	12370425	<b>Amphetamine</b> (2 mg/kg) elicited greater locomotor activity in <strong>Dbh</strong> /  mice compared to controls, whereas 5 mg/kg caused stereotypy in <strong>Dbh</strong> /  mice, which is only observed in control mice at higher doses.
+DBH	drug	amphetamine	12370425	Changes in the sensitivity of dopamine (DA) signaling pathways may contribute to the altered <b>amphetamine</b> responses of <strong>Dbh</strong> /  mice because they were relatively insensitive to a D1 agonist and hypersensitive to a D2 agonist.
+DBH	drug	amphetamine	12370425	Daily <b>amphetamine</b> administration resulted in behavioral sensitization in both <strong>Dbh</strong>+/  and <strong>Dbh</strong> /  mice, demonstrating that NE is not required for the development or expression of behavioral sensitization.
+DBH	addiction	sensitization	12370425	Daily amphetamine administration resulted in behavioral <b>sensitization</b> in both <strong>Dbh</strong>+/  and <strong>Dbh</strong> /  mice, demonstrating that NE is not required for the development or expression of behavioral <b>sensitization</b>.
+DBH	addiction	sensitization	12370425	Daily prazosin administration blunted but did not completely block locomotor <b>sensitization</b> in <strong>Dbh</strong>+/  mice, suggesting that alpha1AR signaling contributes to, but is not required for <b>sensitization</b> in <strong>Dbh</strong>+/  control animals.
+DBH	drug	alcohol	11093800	<b>Ethanol</b> treatment elevated dopamine beta hydroxylase (<strong>DBH</strong>, EC 1.14.17.1) mRNA and protein levels and increased releasable norepinephrine in SH SY5Y cultures.
+DBH	drug	alcohol	11093800	<b>Ethanol</b> treatment elevated <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>, EC 1.14.17.1) mRNA and protein levels and increased releasable norepinephrine in SH SY5Y cultures.
+DBH	drug	alcohol	11093800	Acute <b>ethanol</b> also increased <strong>DBH</strong> mRNA levels in mouse adrenal gland, suggesting in vivo functional consequences for <b>ethanol</b> regulation of <strong>DBH</strong>.
+DBH	drug	nicotine	10975602	<b>Smokers</b> with <strong>DBH</strong> 1368 GG genotype smoked fewer cigarettes than those with GA/AA [mean difference  2.9 cigarettes, 95% confidence interval (CI)  5.5,  0.4; P = 0.022].
+DBH	drug	nicotine	10975602	More heavy <b>smokers</b> (> 20 a day) had the <strong>DBH</strong> 1368A allele when compared to light <b>smokers</b> (< 10 a day).
+DBH	drug	nicotine	10975602	The trend for increasing prevalence of the <strong>DBH</strong> A allele in heavy <b>smokers</b> was greater when analysis was restricted to Caucasians (relative risk 3.2, 95% CI 1.3, 8.2, P = 0.004).
+DBH	drug	nicotine	10975602	Variations in <strong>DBH</strong> and MAO predict whether a person is a heavy <b>smoker</b> and how many cigarettes they consume.
+DBH	drug	alcohol	10777779	We took a genetic approach to determine the effect of NE depletion on <b>ethanol</b> mediated behaviors by using dopamine beta hydroxylase knockout (<strong>Dbh</strong>  / ) mice that specifically lack the ability to synthesize NE.
+DBH	drug	alcohol	10777779	We took a genetic approach to determine the effect of NE depletion on <b>ethanol</b> mediated behaviors by using <strong>dopamine beta hydroxylase</strong> knockout (<strong>Dbh</strong>  / ) mice that specifically lack the ability to synthesize NE.
+DBH	drug	alcohol	10777779	<strong>Dbh</strong>  /  males have reduced <b>ethanol</b> preference in a two bottle choice paradigm and show a delay in extinguishing an <b>ethanol</b> conditioned taste aversion, suggesting that they drink less <b>ethanol</b> in part because they find its effects more aversive.
+DBH	addiction	aversion	10777779	<strong>Dbh</strong>  /  males have reduced ethanol preference in a two bottle choice paradigm and show a delay in extinguishing an ethanol conditioned taste <b>aversion</b>, suggesting that they drink less ethanol in part because they find its effects more <b>aversive</b>.
+DBH	drug	alcohol	10777779	Both male and female <strong>Dbh</strong>  /  mice are hypersensitive to the sedative and hypothermic effects of systemic <b>ethanol</b> administration, and the sedation phenotype can be rescued pharmacologically by acute replacement of central NE.
+DBH	drug	alcohol	10723850	<b>Disulfiram</b> inhibits <strong>dopamine beta hydroxylase</strong> resulting in an excess of dopamine and decreased synthesis of norepinephrine.
+DBH	drug	alcohol	10637824	As a correlary approach to substitution, however, aspects of dopamine function can be augmented by <strong>dopamine beta hydroxylase</strong> inhibitors such as <b>disulfiram</b> to increase the aversive properties of stimulants and decrease their abuse.
+DBH	addiction	aversion	10637824	As a correlary approach to substitution, however, aspects of dopamine function can be augmented by <strong>dopamine beta hydroxylase</strong> inhibitors such as disulfiram to increase the <b>aversive</b> properties of stimulants and decrease their abuse.
+DBH	drug	alcohol	7546340	Serum dopamine beta hydroxylase (<strong>DBH</strong>) inhibition has been reported in lead workers treated with CaNa2EDTA and in <b>alcoholic</b> patients repeatedly treated with the <b>alcohol</b> aversive drug <b>Disulfiram</b>.
+DBH	addiction	aversion	7546340	Serum dopamine beta hydroxylase (<strong>DBH</strong>) inhibition has been reported in lead workers treated with CaNa2EDTA and in alcoholic patients repeatedly treated with the alcohol <b>aversive</b> drug Disulfiram.
+DBH	drug	alcohol	7546340	Serum <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) inhibition has been reported in lead workers treated with CaNa2EDTA and in <b>alcoholic</b> patients repeatedly treated with the <b>alcohol</b> aversive drug <b>Disulfiram</b>.
+DBH	addiction	aversion	7546340	Serum <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) inhibition has been reported in lead workers treated with CaNa2EDTA and in alcoholic patients repeatedly treated with the alcohol <b>aversive</b> drug Disulfiram.
+DBH	drug	alcohol	7546340	The effect of CaNa2EDTA and <b>Disulfiram</b> on serum <strong>DBH</strong> has been compared to the effect of dithiocarbamate pesticides in vitro for the possible use of serum <strong>DBH</strong> determination for the biological monitoring of workers exposed to these pesticides.
+DBH	drug	alcohol	8572926	Comparative effects of two dithiocarbamates <b>disulfiram</b> and thiram, on adrenal catecholamine content and on plasma <strong>dopamine beta hydroxylase</strong> activity.
+DBH	drug	alcohol	8572926	Plasma <strong>DBH</strong> activity was significantly reduced 4 h and 24 h after dosing with thiram, but was unchanged after treatment with <b>disulfiram</b>.
+DBH	drug	alcohol	8572926	The determination of plasma <strong>DBH</strong> activity could be a marker to monitor the effect of thiram on catecholamine metabolism in occupationally exposed workers but not that of <b>disulfiram</b> in abstinent <b>alcoholics</b>.
+DBH	drug	alcohol	7785486	Among males, high SSSV scores, high testosterone levels, and low MAO activity contributed to the variance in <b>alcohol</b> use, whereas among females, a significant proportion of the variability in <b>alcohol</b> use was accounted for by high SSSV scores, high <strong>DBH</strong> activity, and younger age.
+DBH	drug	alcohol	2064756	Attenuation of voluntary <b>ethanol</b> consumption by <strong>dopamine beta hydroxylase</strong> inhibition (FLA 57): mediated by changes in aversion, reinforcement or both.
+DBH	addiction	aversion	2064756	Attenuation of voluntary ethanol consumption by <strong>dopamine beta hydroxylase</strong> inhibition (FLA 57): mediated by changes in <b>aversion</b>, reinforcement or both.
+DBH	addiction	reward	2064756	Attenuation of voluntary ethanol consumption by <strong>dopamine beta hydroxylase</strong> inhibition (FLA 57): mediated by changes in aversion, <b>reinforcement</b> or both.
+DBH	drug	alcohol	2064756	The <strong>dopamine beta hydroxylase</strong> inhibitor, FLA 57, was reported by several investigators to reduce voluntary <b>ethanol</b> consumption in rats.
+DBH	drug	alcohol	2815672	Increase in content of II oxycorticosteroids and in activity of <strong>dopamine beta hydroxylase</strong> in blood serum, decrease in concentration of adrenaline in adrenal glands with simultaneous accumulation of the catecholamine in myocardium were observed in rats after intensive alcoholization within 5 days (intragastric administration of <b>ethanol</b> 4 5 g/kg twice daily).
+DBH	drug	opioid	3176874	An alteration of the central noradrenergic activity and the <b>opioid</b> system can be assumed because of increased <strong>dopamine beta hydroxylase</strong> (D beta H) activity and decreased methionine enkephalin (Met Enk) levels in the cerebrospinal fluid (CSF).
+DBH	drug	alcohol	2906541	Dopamine content of blood, activity of adenylate  and guanylate cyclases in platelets and lymphocytes, catechol O methyltransferase in erythrocytes, <strong>dopamine beta hydroxylase</strong> in blood plasma, monoamine oxidase in platelets, cAMP and cGMP content of blood, and the intensity of 3H DA uptake by platelets have been investigated in <b>alcoholic</b> patients at different clinical states.
+DBH	drug	alcohol	3816539	Serum <strong>dopamine beta hydroxylase</strong> activity and <b>alcohol</b> withdrawal symptoms.
+DBH	addiction	withdrawal	3816539	Serum <strong>dopamine beta hydroxylase</strong> activity and alcohol <b>withdrawal</b> symptoms.
+DBH	drug	alcohol	3816539	Fifty male <b>alcoholics</b> had serum dopamine beta hydroxylase (<strong>DBH</strong>) activity, and serum prolactin (PRL) levels measured on the day of withdrawal, and 22 of them also on days 7 and 28 after it.
+DBH	addiction	withdrawal	3816539	Fifty male alcoholics had serum dopamine beta hydroxylase (<strong>DBH</strong>) activity, and serum prolactin (PRL) levels measured on the day of <b>withdrawal</b>, and 22 of them also on days 7 and 28 after it.
+DBH	drug	alcohol	3816539	Fifty male <b>alcoholics</b> had serum <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) activity, and serum prolactin (PRL) levels measured on the day of withdrawal, and 22 of them also on days 7 and 28 after it.
+DBH	addiction	withdrawal	3816539	Fifty male alcoholics had serum <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) activity, and serum prolactin (PRL) levels measured on the day of <b>withdrawal</b>, and 22 of them also on days 7 and 28 after it.
+DBH	drug	alcohol	3816539	Serum <strong>DBH</strong> activity decreased significantly by day 7, however a further fall of it occurred by day 28 only in patients receiving high doses (500 mg) of <b>disulfiram</b>.
+DBH	addiction	withdrawal	3816539	No correlation was found between serum <strong>DBH</strong> activity and the severity of <b>withdrawal</b> symptoms.
+DBH	addiction	withdrawal	2860239	No increase in adrenal <strong>dopamine beta hydroxylase</strong> activity was seen until day 3 of <b>withdrawal</b> and this activity peaked at 5 days to 160% of control values.
+DBH	addiction	relapse	3991764	<strong>Dopamine beta hydroxylase</strong> inhibitors, feeding and locomotor activity: <b>reinstatement</b> of feeding following central norepinephrine.
+DBH	drug	alcohol	6373096	Effect of <b>alcohol</b> withdrawal on blood pressure, plasma renin activity, aldosterone, cortisol and <strong>dopamine beta hydroxylase</strong>.
+DBH	addiction	withdrawal	6373096	Effect of alcohol <b>withdrawal</b> on blood pressure, plasma renin activity, aldosterone, cortisol and <strong>dopamine beta hydroxylase</strong>.
+DBH	drug	alcohol	6373096	Sixty five <b>alcoholic</b> patients admitted for detoxification had blood pressure, withdrawal symptoms, plasma cortisol (PC) and plasma aldosterone (PA) levels, plasma renin activity (PRA), and serum dopamine beta hydroxylase (<strong>DBH</strong>) levels measured on the first and fourth days after admission.
+DBH	addiction	withdrawal	6373096	Sixty five alcoholic patients admitted for detoxification had blood pressure, <b>withdrawal</b> symptoms, plasma cortisol (PC) and plasma aldosterone (PA) levels, plasma renin activity (PRA), and serum dopamine beta hydroxylase (<strong>DBH</strong>) levels measured on the first and fourth days after admission.
+DBH	drug	alcohol	6373096	Sixty five <b>alcoholic</b> patients admitted for detoxification had blood pressure, withdrawal symptoms, plasma cortisol (PC) and plasma aldosterone (PA) levels, plasma renin activity (PRA), and serum <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) levels measured on the first and fourth days after admission.
+DBH	addiction	withdrawal	6373096	Sixty five alcoholic patients admitted for detoxification had blood pressure, <b>withdrawal</b> symptoms, plasma cortisol (PC) and plasma aldosterone (PA) levels, plasma renin activity (PRA), and serum <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) levels measured on the first and fourth days after admission.
+DBH	drug	nicotine	6420400	Secretion of catecholamines, induced by veratridine or <b>nicotine</b>, a cholinergic agonist, was suppressed when NaCl in the medium was replaced by isosmotic sucrose and unexpectedly low levels of <strong>dopamine beta hydroxylase</strong> were observed in some cases.
+DBH	drug	alcohol	6400122	Blood pressure, <b>alcohol</b> withdrawal symptoms and plasma levels of cortisol, aldosterone and renin activity and serum <strong>dopamine beta hydroxylase</strong> concentrations were measured in 65 <b>alcoholics</b> on the first and fourth days after admission for detoxification.
+DBH	addiction	withdrawal	6400122	Blood pressure, alcohol <b>withdrawal</b> symptoms and plasma levels of cortisol, aldosterone and renin activity and serum <strong>dopamine beta hydroxylase</strong> concentrations were measured in 65 alcoholics on the first and fourth days after admission for detoxification.
+DBH	drug	alcohol	6635046	[<strong>Dopamine beta hydroxylase</strong> activity in the <b>alcohol</b> withdrawal syndrome].
+DBH	addiction	withdrawal	6635046	[<strong>Dopamine beta hydroxylase</strong> activity in the alcohol <b>withdrawal</b> syndrome].
+DBH	drug	alcohol	7136724	Effects of <strong>dopamine beta hydroxylase</strong> inhibitors FLA 57 and FLA 63 on <b>ethanol</b> metabolism and aldehyde dehydrogenase activity in rats.
+DBH	drug	alcohol	7136724	In rats pretreated with the dopamine beta hydroxylase (<strong>DBH</strong>) inhibitors FLA 57 and FLA 63 (60 mg/kg, intraperitoneally, for 4 and 18 hrs), no effects on the blood acetaldehyde level after <b>ethanol</b> administration or on the activity of the low Km aldehyde dehydrogenase (ALDH) in the liver were found.
+DBH	drug	alcohol	7136724	In rats pretreated with the <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) inhibitors FLA 57 and FLA 63 (60 mg/kg, intraperitoneally, for 4 and 18 hrs), no effects on the blood acetaldehyde level after <b>ethanol</b> administration or on the activity of the low Km aldehyde dehydrogenase (ALDH) in the liver were found.
+DBH	drug	alcohol	6127425	Continuous <b>ethanol</b> intoxication, however, significantly reduced NE contents and tended to decrease the activity of <strong>dopamine beta hydroxylase</strong> in the hippocampus.
+DBH	addiction	intoxication	6127425	Continuous ethanol <b>intoxication</b>, however, significantly reduced NE contents and tended to decrease the activity of <strong>dopamine beta hydroxylase</strong> in the hippocampus.
+DBH	drug	alcohol	7349621	<strong>Dopamine beta hydroxylase</strong> activity levels in men at high risk for <b>alcoholism</b> and controls.
+DBH	drug	alcohol	7349621	Plasma <strong>DBH</strong> activity levels were determined for 22 nonalcoholic young men with <b>alcoholic</b> close relatives (the FHP or family history positive group) and results compared to family history negative (FHN) controls matched on demography, height/weight ratio, and drinking history.
+DBH	addiction	intoxication	7349621	Base line <strong>DBH</strong> activities correlated significantly with the level of <b>intoxication</b> for the FHN group (r = 0.44, p less than 0.025) with a trend for an inverse correlation with the average drinking history.
+DBH	addiction	intoxication	7349621	FHP men, on the other hand, demonstrated only a nonsignificant association between peak <b>intoxication</b> level and base line <strong>DBH</strong> and a positive correlation (r = 0.37, p less than 0.05) with the average number of drinks/drinking day.
+DBH	drug	alcohol	7349621	These results are not consistent with the probability that a premorbid <strong>DBH</strong> assay could be used as one indicator of propensity towards <b>alcoholism</b>.
+DBH	drug	alcohol	7349621	The differences between FHP and FHN groups on correlations between <strong>DBH</strong> and peak intoxication or usual drinking history raise speculations that the "normal" (FHN) relationship between <b>alcohol</b> intake and plasma <strong>DBH</strong> activity may be impaired in individuals at high risk (FHP) for the future development of <b>alcoholism</b>.
+DBH	addiction	intoxication	7349621	The differences between FHP and FHN groups on correlations between <strong>DBH</strong> and peak <b>intoxication</b> or usual drinking history raise speculations that the "normal" (FHN) relationship between alcohol intake and plasma <strong>DBH</strong> activity may be impaired in individuals at high risk (FHP) for the future development of alcoholism.
+DBH	drug	alcohol	531076	Suppression of oral intake of <b>ethanol</b> by FLA 57 has been reported for rats and was attributed to an inhibition of <strong>dopamine beta hydroxylase</strong>.
+DBH	drug	alcohol	371446	Changes in the metabolism of biogenic amines in <b>alcoholism</b>  especially regarding CSF monoamine metabolites and serum <strong>DBH</strong> activity.
+DBH	drug	alcohol	371446	Concentrations of the major metabolites of biogenic amines in cerebrospinal fluid and activity of serum <strong>dopamine beta hydroxylase</strong> in abstinent <b>alcoholics</b> were measured, suggesting that withdrawal symptoms of <b>alcoholics</b> were based on the abnormality of serotonin and dopamine metabolism in the body.
+DBH	addiction	withdrawal	371446	Concentrations of the major metabolites of biogenic amines in cerebrospinal fluid and activity of serum <strong>dopamine beta hydroxylase</strong> in abstinent alcoholics were measured, suggesting that <b>withdrawal</b> symptoms of alcoholics were based on the abnormality of serotonin and dopamine metabolism in the body.
+DBH	drug	alcohol	697539	Platelet monoamine oxidase and serum <strong>dopamine beta hydroxylase</strong> activity in chronic <b>alcoholics</b>.
+DBH	drug	alcohol	697539	Previous independent reports suggest that low platelet monoamine oxidase (MAO) activity and high serum dopamine beta hydroxylase (<strong>DBH</strong>) activity may be associated with <b>alcoholism</b> or vulnerability toward <b>alcoholism</b>.
+DBH	drug	alcohol	697539	Previous independent reports suggest that low platelet monoamine oxidase (MAO) activity and high serum <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) activity may be associated with <b>alcoholism</b> or vulnerability toward <b>alcoholism</b>.
+DBH	drug	alcohol	697539	We measured both platelet MAO and serum <strong>DBH</strong> activity in <b>alcoholics</b> followed up at periodic intervals for 12 months after hospitalization for acute <b>alcoholism</b>.
+DBH	drug	alcohol	697539	Platelet MAO activity in the <b>alcoholics</b> was significantly lower compared to that of nonpsychiatric controls throughout the 12 month period, whereas serum <strong>DBH</strong> activity in the <b>alcoholics</b> was essentially the same as control values.
+DBH	drug	alcohol	568508	Variations in serum <strong>dopamine beta hydroxylase</strong> in normal subjects and chronic <b>alcoholics</b>.
+DBH	drug	alcohol	568508	<strong>DBH</strong> activity was determined in 20 normal subjects and 6 chronic <b>alcoholics</b> during <b>alcohol</b> ingestion and withdrawal, under controlled and standardized conditions.
+DBH	addiction	withdrawal	568508	<strong>DBH</strong> activity was determined in 20 normal subjects and 6 chronic alcoholics during alcohol ingestion and <b>withdrawal</b>, under controlled and standardized conditions.
+DBH	drug	opioid	666451	Suppression of voluntary ingestion of <b>morphine</b> by inhibition of <strong>dopamine beta hydroxylase</strong>.
+DBH	drug	alcohol	290737	MHPG concentration in CSF, urinary excretion of NA and A as well as activity of serum <strong>DBH</strong> were significantly elevated during <b>alcohol</b> delirium as compared to the recovery period.
+DBH	drug	alcohol	603311	Extinction of <b>ethanol</b> drinking behavior in laboratory rats by inhibition of <strong>dopamine beta hydroxylase</strong>.
+DBH	drug	alcohol	603310	Noradrenergic mediation of the positive reinforcing properties of <b>ethanol</b>: I. Suppression of <b>ethanol</b> consumption in laboratory rats following <strong>dopamine beta hydroxylase</strong> inhibition.
+DBH	addiction	reward	603310	Noradrenergic mediation of the positive <b>reinforcing</b> properties of ethanol: I. Suppression of ethanol consumption in laboratory rats following <strong>dopamine beta hydroxylase</strong> inhibition.
+DBH	drug	alcohol	603310	<b>Ethanol</b> drinking rats were injected with the <strong>dopamine beta hydroxylase</strong> inhibitor FLA 57, prior to free choice presentations of <b>ethanol</b> and water either for 5 alternate days (25 or 40 mg/kg i.p.)
+DBH	drug	alcohol	921518	In eight male patients with <b>alcoholic</b> delirium concentrations of 3 methoxy 4 hydroxyphenylglycol (MHPG) and homovannilic acid (HVA) in CSF, activity of dopamine beta hydroxylase (<strong>DBH</strong>) and urinary excretion of noradrenaline (NA), adrenaline (A), and dopamine (DA) were measured during the delirium and a drug free control period.
+DBH	drug	alcohol	921518	In eight male patients with <b>alcoholic</b> delirium concentrations of 3 methoxy 4 hydroxyphenylglycol (MHPG) and homovannilic acid (HVA) in CSF, activity of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>) and urinary excretion of noradrenaline (NA), adrenaline (A), and dopamine (DA) were measured during the delirium and a drug free control period.
+DBH	addiction	reward	913244	We found that rats will self administer acetaldehyde delivered into the cerebral ventricles, and that this <b>operant</b> behaviour can be attenuated by injections of a <strong>dopamine beta hydroxylase</strong> inhibitor.
+DBH	addiction	reward	1035186	3) FLA63 and U 14,624, <strong>dopamine beta hydroxylase</strong> inhibitors, suppressed the SS in the moderate intensity <b>reinforcement</b>.
+DBH	drug	alcohol	996056	After injections of l DOPA in cats pretreated with RO 4 4602, an inhibitor of peripheral decarboxylase, or <b>disulfiram</b>, a <strong>dopamine beta hydroxylase</strong> inhibitor, the inhibitory action on the reinforcing system was enhanced.
+DBH	addiction	reward	996056	After injections of l DOPA in cats pretreated with RO 4 4602, an inhibitor of peripheral decarboxylase, or disulfiram, a <strong>dopamine beta hydroxylase</strong> inhibitor, the inhibitory action on the <b>reinforcing</b> system was enhanced.
+DBH	addiction	withdrawal	181193	Lithium does not importantly alter patterns of catecholamine excretion, blood pressures, heart rate, serum cyclic adenosine monophosphate (AMP), serum dopamine beta hydroxylase (<strong>DBH</strong>), sleep pattern, or tremor amplitude during <b>withdrawal</b>.
+DBH	addiction	withdrawal	181193	Lithium does not importantly alter patterns of catecholamine excretion, blood pressures, heart rate, serum cyclic adenosine monophosphate (AMP), serum <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>), sleep pattern, or tremor amplitude during <b>withdrawal</b>.
+DBH	drug	alcohol	1241912	Since treatment of schizophrenic patients with <b>disulfiram</b>, an inhibitor of norepinephrine synthesis that acts at the level of the enzyme <strong>dopamine beta hydroxylase</strong>, thereby leading to increased dopamine concentrations, had been found to profoundly exaggerate psychotic symptomatology, amphetamine behavioral syndrome in the cat as it is modified by pretreatment with <b>disulfiram</b>.
+DBH	drug	amphetamine	1241912	Since treatment of schizophrenic patients with disulfiram, an inhibitor of norepinephrine synthesis that acts at the level of the enzyme <strong>dopamine beta hydroxylase</strong>, thereby leading to increased dopamine concentrations, had been found to profoundly exaggerate psychotic symptomatology, <b>amphetamine</b> behavioral syndrome in the cat as it is modified by pretreatment with disulfiram.
+DBH	drug	amphetamine	168592	The role of brain noradrenergic neurons in mediating the reinforcing properties of small intravenous doses of morphine and d <b>amphetamine</b> was investigated by pretreatment of rats with the norepinephrine depleting agents diethyldithiocarbamate and U 14,624, inhibitors of dopamine beta hydroxylase (<strong>DBH</strong>).
+DBH	drug	opioid	168592	The role of brain noradrenergic neurons in mediating the reinforcing properties of small intravenous doses of <b>morphine</b> and d amphetamine was investigated by pretreatment of rats with the norepinephrine depleting agents diethyldithiocarbamate and U 14,624, inhibitors of dopamine beta hydroxylase (<strong>DBH</strong>).
+DBH	addiction	reward	168592	The role of brain noradrenergic neurons in mediating the <b>reinforcing</b> properties of small intravenous doses of morphine and d amphetamine was investigated by pretreatment of rats with the norepinephrine depleting agents diethyldithiocarbamate and U 14,624, inhibitors of dopamine beta hydroxylase (<strong>DBH</strong>).
+DBH	drug	amphetamine	168592	The role of brain noradrenergic neurons in mediating the reinforcing properties of small intravenous doses of morphine and d <b>amphetamine</b> was investigated by pretreatment of rats with the norepinephrine depleting agents diethyldithiocarbamate and U 14,624, inhibitors of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>).
+DBH	drug	opioid	168592	The role of brain noradrenergic neurons in mediating the reinforcing properties of small intravenous doses of <b>morphine</b> and d amphetamine was investigated by pretreatment of rats with the norepinephrine depleting agents diethyldithiocarbamate and U 14,624, inhibitors of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>).
+DBH	addiction	reward	168592	The role of brain noradrenergic neurons in mediating the <b>reinforcing</b> properties of small intravenous doses of morphine and d amphetamine was investigated by pretreatment of rats with the norepinephrine depleting agents diethyldithiocarbamate and U 14,624, inhibitors of <strong>dopamine beta hydroxylase</strong> (<strong>DBH</strong>).
+DBH	addiction	reward	168592	Pretreatment with a <strong>DBH</strong> inhibitor also prevented the development of a secondary (conditioned) reinforcer based on primary <b>reinforcement</b> assosiated with either drug.
+DBH	drug	opioid	4858783	Effect of 1 phenyl 3 (2 thiazolyl) 2 thiourea, a <strong>dopamine beta hydroxylase</strong> inhibitor on <b>morphine</b> analgesia, tolerance and physical dependence.
+DBH	addiction	dependence	4858783	Effect of 1 phenyl 3 (2 thiazolyl) 2 thiourea, a <strong>dopamine beta hydroxylase</strong> inhibitor on morphine analgesia, tolerance and physical <b>dependence</b>.
+SLC6A3	drug	opioid	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (TH), DOPA decarboxylase (DDC), solute carrier family 6 member 3 (<strong>SLC6A3</strong>) and DA beta hydroxylase (DBH), with six important phenotypes of <b>heroin</b> dependence.
+SLC6A3	addiction	dependence	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (TH), DOPA decarboxylase (DDC), solute carrier family 6 member 3 (<strong>SLC6A3</strong>) and DA beta hydroxylase (DBH), with six important phenotypes of heroin <b>dependence</b>.
+SLC6A3	drug	opioid	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (TH), DOPA decarboxylase (DDC), <strong>solute carrier family 6 member 3</strong> (<strong>SLC6A3</strong>) and DA beta hydroxylase (DBH), with six important phenotypes of <b>heroin</b> dependence.
+SLC6A3	addiction	dependence	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (TH), DOPA decarboxylase (DDC), <strong>solute carrier family 6 member 3</strong> (<strong>SLC6A3</strong>) and DA beta hydroxylase (DBH), with six important phenotypes of heroin <b>dependence</b>.
+SLC6A3	drug	nicotine	32371614	The effect of <strong>SLC6A3</strong> variable number of tandem repeats and methylation levels on individual susceptibility to start <b>tobacco</b> <b>smoking</b> and on the ability of <b>smokers</b> to quit <b>smoking</b>.
+SLC6A3	drug	nicotine	32371614	We studied variations of two variable numbers of tandem repeats (VNTRs), 40 and 30 bp in length, in <strong>SLC6A3</strong> gene together with six DNA methylation sites located in a first intron of the gene in relation to several <b>smoking</b> related phenotypes in a study population consisting of 1230 Whites of Russian origin.
+SLC6A3	drug	nicotine	32371614	Both the 5R allele of 30 bp VNTR and the 9R allele of 40 bp VNTR in <strong>SLC6A3</strong> were associated with a reduced risk to <b>tobacco</b> <b>smoking</b> [odds ratio (OR) 0.53, 95% confidence interval (CI) 0.37 0.75; OR 0.62, 95% CI 0.43 0.88].
+SLC6A3	drug	nicotine	32371614	Also, current <b>smokers</b> had more than 2.5 fold likelihood to have increased <strong>SLC6A3</strong> methylation levels than former <b>smokers</b> (OR 2.72, 95% CI 1.63 4.53).
+SLC6A3	drug	nicotine	32371614	The <strong>SLC6A3</strong> 5R of 30 bp and 9R of 40 bp VNTR variants may lead to a reduced risk to start <b>smoking</b> through decreased dopamine availability, and can also affect the success in subsequent <b>smoking</b> cessation attempts.
+SLC6A3	drug	nicotine	32371614	Moreover, the elevated mean methylation values in the first intron of <strong>SLC6A3</strong> may be related to <b>nicotine</b> dependence via a more active dopamine transporter.
+SLC6A3	addiction	dependence	32371614	Moreover, the elevated mean methylation values in the first intron of <strong>SLC6A3</strong> may be related to nicotine <b>dependence</b> via a more active dopamine transporter.
+SLC6A3	drug	alcohol	31087723	Pharmacogenetic role of dopamine transporter (<strong>SLC6A3</strong>) variation on response to <b>disulfiram</b> treatment for cocaine addiction.
+SLC6A3	drug	cocaine	31087723	Pharmacogenetic role of dopamine transporter (<strong>SLC6A3</strong>) variation on response to disulfiram treatment for <b>cocaine</b> addiction.
+SLC6A3	addiction	addiction	31087723	Pharmacogenetic role of dopamine transporter (<strong>SLC6A3</strong>) variation on response to disulfiram treatment for cocaine <b>addiction</b>.
+SLC6A3	drug	alcohol	31087723	Patients with two <strong>SLC6A3</strong> (DAT1) rs28363170 10 repeat alleles who have with genetically high dopamine transporter (DAT) levels may benefit from increased dopamine levels resulting from <b>disulfiram</b> treatment.
+SLC6A3	drug	alcohol	31087723	Patients with two <strong>SLC6A3</strong> (<strong>DAT1</strong>) rs28363170 10 repeat alleles who have with genetically high dopamine transporter (DAT) levels may benefit from increased dopamine levels resulting from <b>disulfiram</b> treatment.
+SLC6A3	drug	alcohol	31087723	We genotyped the <strong>SLC6A3</strong> (DAT1) 40 bp 3' untranslated region variable number tandem repeat variant and evaluated its role in moderating <b>disulfiram</b> efficacy for cocaine dependence.
+SLC6A3	drug	cocaine	31087723	We genotyped the <strong>SLC6A3</strong> (DAT1) 40 bp 3' untranslated region variable number tandem repeat variant and evaluated its role in moderating disulfiram efficacy for <b>cocaine</b> dependence.
+SLC6A3	addiction	dependence	31087723	We genotyped the <strong>SLC6A3</strong> (DAT1) 40 bp 3' untranslated region variable number tandem repeat variant and evaluated its role in moderating disulfiram efficacy for cocaine <b>dependence</b>.
+SLC6A3	drug	alcohol	31087723	We genotyped the <strong>SLC6A3</strong> (<strong>DAT1</strong>) 40 bp 3' untranslated region variable number tandem repeat variant and evaluated its role in moderating <b>disulfiram</b> efficacy for cocaine dependence.
+SLC6A3	drug	cocaine	31087723	We genotyped the <strong>SLC6A3</strong> (<strong>DAT1</strong>) 40 bp 3' untranslated region variable number tandem repeat variant and evaluated its role in moderating disulfiram efficacy for <b>cocaine</b> dependence.
+SLC6A3	addiction	dependence	31087723	We genotyped the <strong>SLC6A3</strong> (<strong>DAT1</strong>) 40 bp 3' untranslated region variable number tandem repeat variant and evaluated its role in moderating disulfiram efficacy for cocaine <b>dependence</b>.
+SLC6A3	drug	alcohol	30472966	Platelet monoamine oxidase (MAO) activity, dopamine transporter gene (<strong>DAT1</strong>) and neuropeptide S receptor 1 (NPSR1) gene polymorphisms have been identified as markers of impulsivity, <b>alcohol</b> use and excessive risk taking.
+SLC6A3	drug	alcohol	30230123	This study analyzed whether variation at a variable number tandem repeat polymorphism in DAT1/<strong>SLC6A3</strong>, the gene encoding the dopamine transporter, moderated the predictive relationships between acute response to <b>alcohol</b> and future AUD symptoms among participants enrolled in the Chicago Social Drinking Project (first two cohorts).
+SLC6A3	drug	alcohol	30230123	This study analyzed whether variation at a variable number tandem repeat polymorphism in <strong>DAT1</strong>/<strong>SLC6A3</strong>, the gene encoding the dopamine transporter, moderated the predictive relationships between acute response to <b>alcohol</b> and future AUD symptoms among participants enrolled in the Chicago Social Drinking Project (first two cohorts).
+SLC6A3	drug	alcohol	30230123	<strong>DAT1</strong> genotype significantly moderated the interactions between follow up time and <b>alcohol</b> liking (P = 0.006) and wanting (P = 0.006) in predicting future AUD symptoms.
+SLC6A3	drug	alcohol	30230123	Exploratory analyses indicated that <strong>DAT1</strong> effects on the relationship between <b>alcohol</b> liking and AUD symptoms appeared stronger for females (n = 79) than males (n = 118) (P = 0.0496).
+SLC6A3	drug	alcohol	30230123	These data suggest that heavy drinking <strong>DAT1</strong> 9 repeat allele carriers who display high <b>alcohol</b> induced reward in young adulthood may be predisposed to persistent AUD symptoms and support combining genotypic and phenotypic information to predict future AUD risk.
+SLC6A3	addiction	reward	30230123	These data suggest that heavy drinking <strong>DAT1</strong> 9 repeat allele carriers who display high alcohol induced <b>reward</b> in young adulthood may be predisposed to persistent AUD symptoms and support combining genotypic and phenotypic information to predict future AUD risk.
+SLC6A3	drug	alcohol	30192917	The current candidate gene and environment interaction (cGxE) study examined whether the effects of an experimentally manipulated psychosocial stressor on self reported drinking urge and implicit attentional bias for <b>alcohol</b> cues differ as a function of a cumulative genetic score of 5 HTTLPR, MAO A, DRD4, <strong>DAT1</strong> and DRD2 genotypes.
+SLC6A3	addiction	reward	29362512	<strong>DAT1</strong> genotype significantly moderated medication effects, such that APZ, relative to placebo, reduced VS activation and bar lab drinking only among carriers of the <strong>DAT1</strong> 9 repeat allele, previously associated with lower DAT expression and greater <b>reward</b> related brain activation.
+SLC6A3	drug	cocaine	29332099	Association between the Intron 8 VNTR Polymorphism of the <strong>DAT1</strong> Gene and Crack <b>Cocaine</b> Addiction.
+SLC6A3	addiction	addiction	29332099	Association between the Intron 8 VNTR Polymorphism of the <strong>DAT1</strong> Gene and Crack Cocaine <b>Addiction</b>.
+SLC6A3	drug	cocaine	29332099	This study aims to compare allele and genotype frequencies of a 30 bp variable number of tandem repeats (VNTR) polymorphism of the <strong>DAT1</strong> gene, located at intron 8, between adult crack <b>cocaine</b> users and nonaddicted individuals.
+SLC6A3	addiction	addiction	29332099	Our results are consistent with the role of <strong>DAT1</strong> in the neurobiology of drug <b>addiction</b>.
+SLC6A3	drug	opioid	29039297	There was no effect of PC:EtOH on mRNA expression of the µ <b>opioid</b> receptor, tyrosine hydroxylase (Th), dopamine receptor type 2 (Drd2) or dopamine active transporter (<strong>Slc6a3</strong>).
+SLC6A3	drug	alcohol	29030974	We hypothesized that methylomic variation in the DAT gene (DAT1/<strong>SLC6A3</strong>) affects DAT expression, thus contributing to differences in brain reward circuitry in individuals with <b>alcohol</b> dependence (ALC).
+SLC6A3	addiction	dependence	29030974	We hypothesized that methylomic variation in the DAT gene (DAT1/<strong>SLC6A3</strong>) affects DAT expression, thus contributing to differences in brain reward circuitry in individuals with alcohol <b>dependence</b> (ALC).
+SLC6A3	addiction	reward	29030974	We hypothesized that methylomic variation in the DAT gene (DAT1/<strong>SLC6A3</strong>) affects DAT expression, thus contributing to differences in brain <b>reward</b> circuitry in individuals with alcohol dependence (ALC).
+SLC6A3	drug	alcohol	29030974	We hypothesized that methylomic variation in the DAT gene (<strong>DAT1</strong>/<strong>SLC6A3</strong>) affects DAT expression, thus contributing to differences in brain reward circuitry in individuals with <b>alcohol</b> dependence (ALC).
+SLC6A3	addiction	dependence	29030974	We hypothesized that methylomic variation in the DAT gene (<strong>DAT1</strong>/<strong>SLC6A3</strong>) affects DAT expression, thus contributing to differences in brain reward circuitry in individuals with alcohol <b>dependence</b> (ALC).
+SLC6A3	addiction	reward	29030974	We hypothesized that methylomic variation in the DAT gene (<strong>DAT1</strong>/<strong>SLC6A3</strong>) affects DAT expression, thus contributing to differences in brain <b>reward</b> circuitry in individuals with alcohol dependence (ALC).
+SLC6A3	addiction	reward	29030974	Employing regression models, we examined effects of <strong>SLC6A3</strong> methylation on nucleus accumbens (NAc) blood oxygen level dependent (BOLD) responses during anticipation of high/low <b>reward</b>/loss.
+SLC6A3	drug	alcohol	28862750	Erratum: Meta Analysis Reveals Significant Association of the 3' UTR VNTR in <strong>SLC6A3</strong> With <b>Alcohol</b> Dependence.
+SLC6A3	addiction	dependence	28862750	Erratum: Meta Analysis Reveals Significant Association of the 3' UTR VNTR in <strong>SLC6A3</strong> With Alcohol <b>Dependence</b>.
+SLC6A3	drug	alcohol	28744152	The objectives of this study were to evaluate the correlation between DRD2, <strong>SLC6A3</strong> (DAT) and COMT genetic polymorphisms and to investigate their effect on the development of adverse drug reactions in patients with <b>alcohol</b> use disorder who received haloperidol.
+SLC6A3	drug	alcohol	28182634	The <strong>SLC6A3</strong> gene possibly affects susceptibility to late onset <b>alcohol</b> dependence but not specific personality traits in a Han Chinese population.
+SLC6A3	addiction	dependence	28182634	The <strong>SLC6A3</strong> gene possibly affects susceptibility to late onset alcohol <b>dependence</b> but not specific personality traits in a Han Chinese population.
+SLC6A3	drug	alcohol	28139629	To explore the genetic influence of a family history of <b>alcohol</b> use disorders and the dopamine transporter <strong>SLC6A3</strong> (DAT1) and dopamine beta hydroxylase (DBH) gene polymorphisms on the risk of severe complications (withdrawal seizures (AWS) and delirium tremens (DT)) during <b>alcohol</b> withdrawal in <b>alcohol</b> dependent men.
+SLC6A3	addiction	withdrawal	28139629	To explore the genetic influence of a family history of alcohol use disorders and the dopamine transporter <strong>SLC6A3</strong> (DAT1) and dopamine beta hydroxylase (DBH) gene polymorphisms on the risk of severe complications (<b>withdrawal</b> seizures (AWS) and delirium tremens (DT)) during alcohol <b>withdrawal</b> in alcohol dependent men.
+SLC6A3	drug	alcohol	28139629	To explore the genetic influence of a family history of <b>alcohol</b> use disorders and the dopamine transporter <strong>SLC6A3</strong> (<strong>DAT1</strong>) and dopamine beta hydroxylase (DBH) gene polymorphisms on the risk of severe complications (withdrawal seizures (AWS) and delirium tremens (DT)) during <b>alcohol</b> withdrawal in <b>alcohol</b> dependent men.
+SLC6A3	addiction	withdrawal	28139629	To explore the genetic influence of a family history of alcohol use disorders and the dopamine transporter <strong>SLC6A3</strong> (<strong>DAT1</strong>) and dopamine beta hydroxylase (DBH) gene polymorphisms on the risk of severe complications (<b>withdrawal</b> seizures (AWS) and delirium tremens (DT)) during alcohol <b>withdrawal</b> in alcohol dependent men.
+SLC6A3	drug	alcohol	28139629	We investigated the effects of 3 previously reported candidate genetic variations: 40 bp variable number tandem repeat (VNTR) polymorphism and C/T exon 15 (rs27072) in the 3' untranslated region (3' UTR) of the <strong>SLC6A3</strong>(DAT1) gene, and  1021 C/T (rs1611115) of DBH gene in 266 <b>alcohol</b> dependent Russian male inpatients in two groups by presence (SC group: AWS, DT, AWS+DT, n=130) or absence (n=136) of severe complications diagnosed by ICD 10 during current <b>alcohol</b> withdrawal.
+SLC6A3	addiction	withdrawal	28139629	We investigated the effects of 3 previously reported candidate genetic variations: 40 bp variable number tandem repeat (VNTR) polymorphism and C/T exon 15 (rs27072) in the 3' untranslated region (3' UTR) of the <strong>SLC6A3</strong>(DAT1) gene, and  1021 C/T (rs1611115) of DBH gene in 266 alcohol dependent Russian male inpatients in two groups by presence (SC group: AWS, DT, AWS+DT, n=130) or absence (n=136) of severe complications diagnosed by ICD 10 during current alcohol <b>withdrawal</b>.
+SLC6A3	drug	alcohol	28139629	We investigated the effects of 3 previously reported candidate genetic variations: 40 bp variable number tandem repeat (VNTR) polymorphism and C/T exon 15 (rs27072) in the 3' untranslated region (3' UTR) of the <strong>SLC6A3</strong>(<strong>DAT1</strong>) gene, and  1021 C/T (rs1611115) of DBH gene in 266 <b>alcohol</b> dependent Russian male inpatients in two groups by presence (SC group: AWS, DT, AWS+DT, n=130) or absence (n=136) of severe complications diagnosed by ICD 10 during current <b>alcohol</b> withdrawal.
+SLC6A3	addiction	withdrawal	28139629	We investigated the effects of 3 previously reported candidate genetic variations: 40 bp variable number tandem repeat (VNTR) polymorphism and C/T exon 15 (rs27072) in the 3' untranslated region (3' UTR) of the <strong>SLC6A3</strong>(<strong>DAT1</strong>) gene, and  1021 C/T (rs1611115) of DBH gene in 266 alcohol dependent Russian male inpatients in two groups by presence (SC group: AWS, DT, AWS+DT, n=130) or absence (n=136) of severe complications diagnosed by ICD 10 during current alcohol <b>withdrawal</b>.
+SLC6A3	drug	opioid	27547496	In this study, we produced DA neurons differentiated using iPSCs derived from <b>opioid</b> dependent and control subjects carrying different 3' VNTR (variable number tandem repeat) polymorphism in the human dopamine transporter (DAT or <strong>SLC6A3</strong>).
+SLC6A3	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of catechol O methyltransferase (COMT), dopamine receptor D2 (DRD2) gene score and <b>smoking</b> cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (ANKK1), dopamine transporter (<strong>SLC6A3</strong>), dopamine receptor D4 (DRD4) gene score and <b>smoking</b> cessation.
+SLC6A3	drug	nicotine	27490263	A significant multiplicative model interaction between <b>nicotine</b> dependence and the <strong>SLC6A3</strong> gene score on <b>smoking</b> cessation was also observed (p = .03).
+SLC6A3	addiction	dependence	27490263	A significant multiplicative model interaction between nicotine <b>dependence</b> and the <strong>SLC6A3</strong> gene score on smoking cessation was also observed (p = .03).
+SLC6A3	drug	nicotine	27490263	There is a significant multiplicative model interaction of <strong>SLC6A3</strong> gene score and <b>nicotine</b> dependence on <b>smoking</b> cessation.
+SLC6A3	addiction	dependence	27490263	There is a significant multiplicative model interaction of <strong>SLC6A3</strong> gene score and nicotine <b>dependence</b> on smoking cessation.
+SLC6A3	drug	nicotine	27287604	Meta analysis update of association between dopamine transporter <strong>SLC6A3</strong> gene polymorphism and <b>smoking</b> cessation.
+SLC6A3	drug	nicotine	27287604	The <strong>SLC6A3</strong> gene is involved in the dopamine pathway, which influences <b>smoking</b> behavior.
+SLC6A3	drug	nicotine	27287604	This study was conducted to present updated results of a meta analysis to evaluate the association between <strong>SLC6A3</strong> polymorphism and <b>smoking</b> cessation.
+SLC6A3	drug	nicotine	27287604	No significant association between <strong>SLC6A3</strong> genotype and <b>smoking</b> cessation was observed for the main analysis (odds ratio = 1.128; 95% confidence interval = 0.981 1.298).
+SLC6A3	drug	nicotine	27287604	In conclusion, the genetic variations in <strong>SLC6A3</strong> are not associated with <b>smoking</b> cessation, which is not consistent with the results of the previous meta analysis.
+SLC6A3	drug	alcohol	27219321	Meta Analysis Reveals Significant Association of the 3' UTR VNTR in <strong>SLC6A3</strong> with <b>Alcohol</b> Dependence.
+SLC6A3	addiction	dependence	27219321	Meta Analysis Reveals Significant Association of the 3' UTR VNTR in <strong>SLC6A3</strong> with Alcohol <b>Dependence</b>.
+SLC6A3	drug	alcohol	27219321	Although many studies have analyzed the association of 3' untranslated region variable number tandem repeat (VNTR) polymorphism in <strong>SLC6A3</strong> with <b>alcohol</b> dependence (AD), the results remain controversial.
+SLC6A3	addiction	dependence	27219321	Although many studies have analyzed the association of 3' untranslated region variable number tandem repeat (VNTR) polymorphism in <strong>SLC6A3</strong> with alcohol <b>dependence</b> (AD), the results remain controversial.
+SLC6A3	addiction	addiction	27064247	Polymorphisms in genes such as <strong>DAT1</strong>, 5HTTLPR, D4DR4, and MAO A have been linked to attention deficit hyperactivity disorder (ADHD) and susceptibility for opiate <b>addiction</b>.
+SLC6A3	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (OPRM1), kappa <b>opioid</b> receptors (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (<strong>SLC6A3</strong>, DAT1) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+SLC6A3	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (OPRM1), kappa <b>opioid</b> receptors (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (<strong>SLC6A3</strong>, <strong>DAT1</strong>) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+SLC6A3	drug	nicotine	26416825	Three hundred sixty four Mexican Mestizo Mexico City residents from 87 families with at least one <b>smoker</b> were assessed for association of 12 gene variants of six candidate genes (CHRNA4, CHRNB2, DRD2, ANKK1, <strong>SLC6A3</strong>, and CYP2A6) with cigarette consumption, age of initiation and <b>smoking</b> duration.
+SLC6A3	drug	opioid	26288297	It was genotyped polymorphisms in the following genes: mu <b>opioid</b> receptor (OPRM1), kappa <b>opioid</b> receptor (OPRK1), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (<strong>DAT1</strong>).
+SLC6A3	drug	alcohol	26146874	Polymorphisms of the DRD2, ANKK1, <strong>DAT1</strong>, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of <b>alcohol</b>, opioid, and cocaine use disorders.
+SLC6A3	drug	cocaine	26146874	Polymorphisms of the DRD2, ANKK1, <strong>DAT1</strong>, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of alcohol, opioid, and <b>cocaine</b> use disorders.
+SLC6A3	drug	opioid	26146874	Polymorphisms of the DRD2, ANKK1, <strong>DAT1</strong>, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of alcohol, <b>opioid</b>, and cocaine use disorders.
+SLC6A3	drug	alcohol	26041607	In this association study of two independent samples, a number of candidate gene variants (5HT2A T102C, 5 HTTLPR, DRD Ins 141Del, <strong>DAT1</strong> VNTR) were related to violent criminal behavior and <b>alcohol</b> related aggressive traits.
+SLC6A3	drug	alcohol	25862379	<strong>DAT1</strong> methylation changes in <b>alcohol</b> dependent individuals vs. controls.
+SLC6A3	drug	cocaine	25850966	Genetic variation of the dopamine transporter (<strong>DAT1</strong>) influences the acute subjective responses to <b>cocaine</b> in volunteers with <b>cocaine</b> use disorders.
+SLC6A3	drug	cocaine	25850966	The aim of this study was to identify gene variants of DAT1 (<strong>SLC6A3</strong>) that modulate subjective responses to acute <b>cocaine</b> exposure.
+SLC6A3	drug	cocaine	25850966	The aim of this study was to identify gene variants of <strong>DAT1</strong> (<strong>SLC6A3</strong>) that modulate subjective responses to acute <b>cocaine</b> exposure.
+SLC6A3	drug	cocaine	25850966	Carriers of the 9 allele of the <strong>DAT1</strong> 3' untranslated region (9,9 and 9,10) exhibited greater responses to <b>cocaine</b> for 'high', 'any drug effect', 'anxious', and 'stimulated' (all P values<0.001) compared with individuals homozygous for the 10 allele.
+SLC6A3	drug	cocaine	25850966	The data presented here show for the first time support for the hypothesis that genetic differences in <strong>DAT1</strong> contribute to the variation in subjective responses to <b>cocaine</b> among participants with <b>cocaine</b> use disorders.
+SLC6A3	drug	amphetamine	25747272	The presynaptic, cocaine  and <b>amphetamine</b> sensitive dopamine (DA) transporter (DAT, <strong>SLC6A3</strong>) controls the intensity and duration of synaptic dopamine signals by rapid clearance of DA back into presynaptic nerve terminals.
+SLC6A3	drug	cocaine	25747272	The presynaptic, <b>cocaine</b>  and amphetamine sensitive dopamine (DA) transporter (DAT, <strong>SLC6A3</strong>) controls the intensity and duration of synaptic dopamine signals by rapid clearance of DA back into presynaptic nerve terminals.
+SLC6A3	drug	alcohol	25684044	Association study of the <strong>SLC6A3</strong> VNTR (DAT) and DRD2/ANKK1 Taq1A polymorphisms with <b>alcohol</b> dependence in a population from northeastern Brazil.
+SLC6A3	addiction	dependence	25684044	Association study of the <strong>SLC6A3</strong> VNTR (DAT) and DRD2/ANKK1 Taq1A polymorphisms with alcohol <b>dependence</b> in a population from northeastern Brazil.
+SLC6A3	addiction	relapse	25683821	Although harm avoidance and novelty <b>seeking</b> scores were significantly higher in patients than in controls, <strong>DAT1</strong> polymorphisms did not influence these scores.
+SLC6A3	drug	nicotine	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (ANKK1), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (<strong>SLC6A3</strong>) and cytochrome P450 2A6 (CYP2A6) genes influence <b>smoking</b> cessation and <b>nicotine</b> dependence in a Japanese population.
+SLC6A3	addiction	dependence	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (ANKK1), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (<strong>SLC6A3</strong>) and cytochrome P450 2A6 (CYP2A6) genes influence smoking cessation and nicotine <b>dependence</b> in a Japanese population.
+SLC6A3	drug	nicotine	25526961	In 96 current and former <b>smokers</b>, genotyping frequencies for the ANKK1/DRD2 TaqIA, <strong>SLC6A3</strong> VNTR, and CYP2A6 polymorphisms were subjected to chi square analysis, and regression analyses were used to determine the association of the genotypes of current <b>smokers</b> with a Heavy <b>Smoking</b> Index, in addition to evaluating the effect of the subjects' <b>smoking</b> history on the association.
+SLC6A3	drug	nicotine	25526961	Genotyping results suggested that <b>nicotine</b> dependence among current <b>smokers</b> homozygous for the <strong>SLC6A3</strong> 10r allele was lower than that of <b>smokers</b> carrying the minor alleles, and that the CYP2A6 polymorphism might mediate this association.
+SLC6A3	addiction	dependence	25526961	Genotyping results suggested that nicotine <b>dependence</b> among current smokers homozygous for the <strong>SLC6A3</strong> 10r allele was lower than that of smokers carrying the minor alleles, and that the CYP2A6 polymorphism might mediate this association.
+SLC6A3	drug	cocaine	25247548	Crack <b>cocaine</b> users show differences in genotype frequencies of the 3' UTR variable number of tandem repeats of the dopamine transporter gene (DAT1/<strong>SLC6A3</strong>).
+SLC6A3	drug	cocaine	25247548	Crack <b>cocaine</b> users show differences in genotype frequencies of the 3' UTR variable number of tandem repeats of the dopamine transporter gene (<strong>DAT1</strong>/<strong>SLC6A3</strong>).
+SLC6A3	addiction	addiction	25247548	Due to the mechanism of action of the dopamine transporter (DAT) in drug <b>addiction</b>, the <strong>DAT1</strong> gene is a potential candidate for molecular studies.
+SLC6A3	drug	alcohol	24946437	[The analysis of the polymorphic variations of the dopamine gen transporter (<strong>DAT1</strong>) and the serotonin transporter (5 HTTLPR) in patients with <b>alcohol</b> dependence syndrome with inclusion of the phenotypic feature of sweet liking preference].
+SLC6A3	addiction	dependence	24946437	[The analysis of the polymorphic variations of the dopamine gen transporter (<strong>DAT1</strong>) and the serotonin transporter (5 HTTLPR) in patients with alcohol <b>dependence</b> syndrome with inclusion of the phenotypic feature of sweet liking preference].
+SLC6A3	drug	opioid	26574964	Blood samples were taken for the determination of serum levels of racemic <b>methadone</b> and its R and S enantiomers, and for typing of candidate alleles of POR, CYP2B6, ABCB1, GRIN1, OPRM1, <strong>SLC6A3</strong>, DßH and ARRB2 genes, all associated with the metabolism, tissue distribution and mechanism of action of <b>methadone</b>.
+SLC6A3	drug	nicotine	24444411	Genetic variants in DRD2, DRD4, ANKK1, <strong>DAT1</strong>, COMT and DBH genes show some promise in informing personalized prescribing of <b>smoking</b> cessation pharmacotherapies.
+SLC6A3	drug	alcohol	24421289	Interactive effects of OPRM1 and <strong>DAT1</strong> genetic variation on subjective responses to <b>alcohol</b>.
+SLC6A3	drug	alcohol	24421289	Recently, the dopamine transporter (DAT1) variable number of tandem repeat (VNTR; <strong>SLC6A3</strong>) has been found to interact with the OPRM1 A118G SNP in predicting neural and behavioral responses to <b>naltrexone</b> and to <b>alcohol</b>.
+SLC6A3	drug	alcohol	24421289	Recently, the dopamine transporter (<strong>DAT1</strong>) variable number of tandem repeat (VNTR; <strong>SLC6A3</strong>) has been found to interact with the OPRM1 A118G SNP in predicting neural and behavioral responses to <b>naltrexone</b> and to <b>alcohol</b>.
+SLC6A3	drug	alcohol	24421289	This exploratory study examines the OPRM1 × <strong>DAT1</strong> interaction on subjective responses to <b>alcohol</b>.
+SLC6A3	drug	alcohol	24421289	Analyses revealed significant <b>Alcohol</b> × OPRM1 × <strong>DAT1</strong> interactions for <b>alcohol</b> induced stimulation, vigor and positive mood as well as significant <b>Alcohol</b> × OPRM1 × <strong>DAT1</strong> × Time interactions for stimulation and positive mood.
+SLC6A3	drug	alcohol	24421289	All <b>Alcohol</b> × OPRM1 × <strong>DAT1</strong> interactions remained significant when analyses were restricted to a subsample of Caucasian participants (n = 34); however, 4 way interactions did not reach statistical significance in this subsample.
+SLC6A3	drug	alcohol	24421289	This study suggests that the contribution of OPRM1 genotype to <b>alcohol</b> induced stimulation, vigor and positive mood is moderated by <strong>DAT1</strong> genotype.
+SLC6A3	drug	opioid	24274990	<strong>DAT1</strong> gene variants such as allele 10, previously reported in association with personality and behavioral problems, would have influenced the effects of BUP induced dopamine release, modulated through mu and kappa <b>opioid</b> receptors, and probably the related reinforcing capacity of the drug.
+SLC6A3	addiction	reward	24274990	<strong>DAT1</strong> gene variants such as allele 10, previously reported in association with personality and behavioral problems, would have influenced the effects of BUP induced dopamine release, modulated through mu and kappa opioid receptors, and probably the related <b>reinforcing</b> capacity of the drug.
+SLC6A3	addiction	reward	24273683	We also genotyped the patient using a <b>reward</b> gene panel including (9 genes 18 alleles): DRD 2,3,4; MOA A; COMT; <strong>DAT1</strong>; 5HTTLLR; OPRM1; and GABRA3.
+SLC6A3	drug	nicotine	23941313	Age, gender, Fagerström Test for <b>Nicotine</b> Dependence, dopamine pathway genotypes (rs1800497 [ANKK1 E713K], rs4680 [COMT V158M], DRD4 exon 3 variable number of tandem repeats polymorphism [DRD4 VNTR], <strong>SLC6A3</strong>,3' VNTR) analyzed both separately and as part of an AGES, time to first lapse and point prevalence abstinence at end of treatment.
+SLC6A3	addiction	dependence	23941313	Age, gender, Fagerström Test for Nicotine <b>Dependence</b>, dopamine pathway genotypes (rs1800497 [ANKK1 E713K], rs4680 [COMT V158M], DRD4 exon 3 variable number of tandem repeats polymorphism [DRD4 VNTR], <strong>SLC6A3</strong>,3' VNTR) analyzed both separately and as part of an AGES, time to first lapse and point prevalence abstinence at end of treatment.
+SLC6A3	drug	opioid	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol O methyl transferase (COMT) and dopamine transporter (<strong>SLC6A3</strong>) genes and <b>heroin</b> dependence in Hungarian patients.
+SLC6A3	addiction	dependence	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol O methyl transferase (COMT) and dopamine transporter (<strong>SLC6A3</strong>) genes and heroin <b>dependence</b> in Hungarian patients.
+SLC6A3	addiction	addiction	23761898	Functional polymorphisms in the dopamine transporter gene (DAT1 or <strong>SLC6A3</strong>) modulate responsiveness to salient stimuli, such that carriers of one 9R allele of DAT1 (compared with homozygote carriers of the 10R allele) show heightened reactivity to drug related reinforcement in <b>addiction</b>.
+SLC6A3	addiction	reward	23761898	Functional polymorphisms in the dopamine transporter gene (DAT1 or <strong>SLC6A3</strong>) modulate responsiveness to salient stimuli, such that carriers of one 9R allele of DAT1 (compared with homozygote carriers of the 10R allele) show heightened reactivity to drug related <b>reinforcement</b> in addiction.
+SLC6A3	addiction	addiction	23761898	Functional polymorphisms in the dopamine transporter gene (<strong>DAT1</strong> or <strong>SLC6A3</strong>) modulate responsiveness to salient stimuli, such that carriers of one 9R allele of <strong>DAT1</strong> (compared with homozygote carriers of the 10R allele) show heightened reactivity to drug related reinforcement in <b>addiction</b>.
+SLC6A3	addiction	reward	23761898	Functional polymorphisms in the dopamine transporter gene (<strong>DAT1</strong> or <strong>SLC6A3</strong>) modulate responsiveness to salient stimuli, such that carriers of one 9R allele of <strong>DAT1</strong> (compared with homozygote carriers of the 10R allele) show heightened reactivity to drug related <b>reinforcement</b> in addiction.
+SLC6A3	drug	cocaine	24892317	The present results indicate that the VNTR  6R polymorphism of the gene <strong>SLC6A3</strong> and the genotype 3435CC in the ABCB1 gene, are both associated with addictive behavior to heroin or <b>cocaine</b>.
+SLC6A3	drug	opioid	24892317	The present results indicate that the VNTR  6R polymorphism of the gene <strong>SLC6A3</strong> and the genotype 3435CC in the ABCB1 gene, are both associated with addictive behavior to <b>heroin</b> or cocaine.
+SLC6A3	addiction	addiction	24892317	The present results indicate that the VNTR  6R polymorphism of the gene <strong>SLC6A3</strong> and the genotype 3435CC in the ABCB1 gene, are both associated with <b>addictive</b> behavior to heroin or cocaine.
+SLC6A3	drug	nicotine	23061530	Here, we explored associations between attentional bias for SCs and neural responses to SCs among 'sated' <b>smokers</b> genotyped for the <strong>SLC6A3</strong> polymorphism.
+SLC6A3	drug	nicotine	23061530	Pseudo continuous arterial spin labeled perfusion functional magnetic resonance imaging images were acquired during SC exposure in 35 <b>smokers</b> genotyped for the <strong>SLC6A3</strong> variable number of tandem repeats polymorphism (n = 16, 9 repeats; n = 19, 10/10 repeats).
+SLC6A3	drug	alcohol	23032071	Interacting effects of <b>naltrexone</b> and OPRM1 and <strong>DAT1</strong> variation on the neural response to <b>alcohol</b> cues.
+SLC6A3	addiction	reward	23032071	Secondarily, variation at a variable number tandem repeat polymorphism in the dopamine transporter gene (DAT1/<strong>SLC6A3</strong>), which has been associated with increased <b>reward</b> related activation in VS, was analyzed as a moderator of medication and A118G effects.
+SLC6A3	addiction	reward	23032071	Secondarily, variation at a variable number tandem repeat polymorphism in the dopamine transporter gene (<strong>DAT1</strong>/<strong>SLC6A3</strong>), which has been associated with increased <b>reward</b> related activation in VS, was analyzed as a moderator of medication and A118G effects.
+SLC6A3	addiction	reward	23032071	Polymorphic variation in OPRM1 and <strong>DAT1</strong> should be considered in future studies of NTX, particularly regarding its effects on <b>reward</b> processing.
+SLC6A3	drug	alcohol	22698582	DRD2/ANKK1 TaqIA and <strong>SLC6A3</strong> VNTR polymorphisms in <b>alcohol</b> dependence: association and gene gene interaction study in a population of Central Italy.
+SLC6A3	addiction	dependence	22698582	DRD2/ANKK1 TaqIA and <strong>SLC6A3</strong> VNTR polymorphisms in alcohol <b>dependence</b>: association and gene gene interaction study in a population of Central Italy.
+SLC6A3	drug	alcohol	22691013	Dopamine transporter (<strong>DAT1</strong>) VNTR polymorphism and <b>alcoholism</b> in two culturally different populations of south India.
+SLC6A3	drug	alcohol	22691013	To assess the role of this gene in <b>alcoholism</b>, we genotyped the VNTR of <strong>DAT1</strong> gene in a sample of 206 subjects from the Kota population (111 <b>alcohol</b> dependence cases and 95 controls) and 142 subjects from Badaga population (81 <b>alcohol</b> dependence cases and 61 controls).
+SLC6A3	addiction	dependence	22691013	To assess the role of this gene in alcoholism, we genotyped the VNTR of <strong>DAT1</strong> gene in a sample of 206 subjects from the Kota population (111 alcohol <b>dependence</b> cases and 95 controls) and 142 subjects from Badaga population (81 alcohol <b>dependence</b> cases and 61 controls).
+SLC6A3	drug	alcohol	22691013	The association of <strong>DAT1</strong> with <b>alcoholism</b> was tested by using the Clump v1.9 program which uses the Monte Carlo method.
+SLC6A3	drug	alcohol	22691013	The <strong>DAT1</strong> VNTR was significantly associated with <b>alcoholism</b> in Badaga population but not in Kota population.
+SLC6A3	drug	alcohol	22551036	<b>Naltrexone</b> modification of drinking effects in a subacute treatment and bar lab paradigm: influence of OPRM1 and dopamine transporter (<strong>SLC6A3</strong>) genes.
+SLC6A3	drug	alcohol	22551036	Two hundred and sixty five nontreatment seeking individuals with <b>alcohol</b> dependence were genotyped a priori for the OPRM1 asn40asp SNP and post hoc for DAT (<strong>SLC6A3</strong>) 9 and 10 VNTRs.
+SLC6A3	addiction	dependence	22551036	Two hundred and sixty five nontreatment seeking individuals with alcohol <b>dependence</b> were genotyped a priori for the OPRM1 asn40asp SNP and post hoc for DAT (<strong>SLC6A3</strong>) 9 and 10 VNTRs.
+SLC6A3	addiction	relapse	22551036	Two hundred and sixty five nontreatment <b>seeking</b> individuals with alcohol dependence were genotyped a priori for the OPRM1 asn40asp SNP and post hoc for DAT (<strong>SLC6A3</strong>) 9 and 10 VNTRs.
+SLC6A3	drug	alcohol	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, DRD2, DRD3, DRD4) and the dopamine transporter gene (<strong>SLC6A3</strong>), which have been implicated in neurobiological studies of craving, as well as alpha synuclein (SNCA), which has been previously found to be associated with craving, were associated with <b>alcohol</b> craving in this sample.
+SLC6A3	addiction	relapse	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, DRD2, DRD3, DRD4) and the dopamine transporter gene (<strong>SLC6A3</strong>), which have been implicated in neurobiological studies of <b>craving</b>, as well as alpha synuclein (SNCA), which has been previously found to be associated with <b>craving</b>, were associated with alcohol <b>craving</b> in this sample.
+SLC6A3	addiction	reward	22342427	Impulsivity has been linked with variation in <b>reward</b> related activation in the ventral striatum (VS), altered dopamine signaling, and functional polymorphisms of DRD2 and <strong>DAT1</strong> genes.
+SLC6A3	drug	cocaine	22070124	Here we measured DNA methylation at promoter CpG sites of the dopamine transporter (<strong>DAT1</strong>) and serotonin transporter (SERT) and neurokinin3 receptor (NK3 R) receptor (TACR3) coding genes in marmoset monkeys after repeated <b>cocaine</b> injections in a conditioned place preference paradigm.
+SLC6A3	drug	nicotine	22028400	Among susceptible youth (N = 246), older age at baseline, living with a <b>smoker</b>, and three different genes (HTR2A, DRD2, <strong>SLC6A3</strong>) predicted experimentation.
+SLC6A3	drug	nicotine	21806388	The purpose of the present work was to examine the association of SNPs in the DOPA decarboxylase (DDC), dopamine receptor D2 (DRD2) and dopamine transporter (<strong>SLC6A3</strong>) genes with <b>smoking</b> cessation in a large retrospective study featuring approximately 900 cessation events.
+SLC6A3	drug	nicotine	21806388	Restricting the analyses to subjects who reported to have regularly smoked > 20 cigarettes per day at some point in their life, we used survival analysis methods to model the time from initiation of regular <b>smoking</b> to cessation (defined as quitting with abstinence lasting until enrollment) and its relation with eight polymorphisms in the aforementioned genes (five in DDC, two in DRD2 and one in <strong>SLC6A3</strong>) in 1446 participants.
+SLC6A3	drug	alcohol	21554332	The association between the <strong>SLC6A3</strong> VNTR 9 repeat allele and <b>alcoholism</b> a meta analysis.
+SLC6A3	drug	alcohol	21554332	Dopamine transporter gene (<strong>SLC6A3</strong>) represents a promising candidate involved in the development of <b>alcoholism</b>.
+SLC6A3	drug	alcohol	21554332	This study aimed to explore the association between the 9 repeat allele (A9) of a 40 bp variable number tandem repeat (VNTR) polymorphism in the 3' un translated region (3' UTR) of the <strong>SLC6A3</strong> gene and <b>alcoholism</b>.
+SLC6A3	drug	alcohol	21554332	The <strong>SLC6A3</strong> VNTR was genotyped by PCR in unrelated Mexican Americans including 337 controls and 365 <b>alcoholics</b>.
+SLC6A3	drug	alcohol	21554332	Meta analyses were performed for population based case control association studies of the <strong>SLC6A3</strong> VNTR polymorphism with <b>alcoholism</b>.
+SLC6A3	drug	alcohol	21554332	No significant difference of the <strong>SLC6A3</strong> VNTR A9 was noted between controls and <b>alcoholics</b> at the genotypic and allelic level when all ethnic populations, only Caucasian populations, or only Asian populations were considered (p > 0.05).
+SLC6A3	drug	alcohol	21554332	Significant associations were observed between <strong>SLC6A3</strong> VNTR A9 and <b>alcoholics</b> with AWS or DT at the genotypic as well as allelic level when all ethnic populations or only Caucasian populations were considered (p < 0.05, OR 1.5 2.1).
+SLC6A3	drug	alcohol	21554332	Meta analyses suggest a possible association between the <strong>SLC6A3</strong> VNTR A9 and <b>alcoholic</b> subgroup with AWS or DT.
+SLC6A3	drug	nicotine	21299752	Previously we demonstrated profound effects of dopamine transporter (DAT) <strong>SLC6A3</strong> genotype on limbic responses to <b>smoking</b> cues (SCs).
+SLC6A3	drug	nicotine	21299752	To test the reliability of the initial findings, we examined perfusion functional magnetic resonance images acquired during SC exposure in a new cohort of <b>smokers</b> (N=26) who were genotyped for the <strong>SLC6A3</strong> polymorphism.
+SLC6A3	drug	alcohol	21078357	Previous genetic association studies have reported a possible role of the dopamine transporter (DAT, gene symbol: <strong>SLC6A3</strong>) gene in the etiology of <b>alcohol</b> dependence, but the results were conflicting with each other.
+SLC6A3	addiction	dependence	21078357	Previous genetic association studies have reported a possible role of the dopamine transporter (DAT, gene symbol: <strong>SLC6A3</strong>) gene in the etiology of alcohol <b>dependence</b>, but the results were conflicting with each other.
+SLC6A3	drug	alcohol	21078357	We conducted a pooled analysis of published population based case control genetic studies investigating associations between polymorphisms in <strong>SLC6A3</strong> and <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	21078357	We conducted a pooled analysis of published population based case control genetic studies investigating associations between polymorphisms in <strong>SLC6A3</strong> and alcohol <b>dependence</b>.
+SLC6A3	drug	alcohol	21078357	Through combining 13 studies with 2483 cases and 1753 controls, the 40 base pair variable number tandem repeat (VNTR) in the 3' un translated region, the well studied polymorphism in <strong>SLC6A3</strong>, did not show any association with <b>alcohol</b> dependence in general or in stratified analyses according to geographic area, ethnicity, gender, and diagnostic criteria.
+SLC6A3	addiction	dependence	21078357	Through combining 13 studies with 2483 cases and 1753 controls, the 40 base pair variable number tandem repeat (VNTR) in the 3' un translated region, the well studied polymorphism in <strong>SLC6A3</strong>, did not show any association with alcohol <b>dependence</b> in general or in stratified analyses according to geographic area, ethnicity, gender, and diagnostic criteria.
+SLC6A3	drug	alcohol	21078357	Due to limited studies focused on polymorphisms in other regions of the <strong>SLC6A3</strong> gene, we cannot rule out the role of the <strong>SLC6A3</strong> gene in the involvement of the genetic risk of <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	21078357	Due to limited studies focused on polymorphisms in other regions of the <strong>SLC6A3</strong> gene, we cannot rule out the role of the <strong>SLC6A3</strong> gene in the involvement of the genetic risk of alcohol <b>dependence</b>.
+SLC6A3	drug	alcohol	21078357	Further clarification of the genetic role of <strong>SLC6A3</strong> in the susceptibility to <b>alcohol</b> dependence should be centered on other potential functional regions of the <strong>SLC6A3</strong> gene.
+SLC6A3	addiction	dependence	21078357	Further clarification of the genetic role of <strong>SLC6A3</strong> in the susceptibility to alcohol <b>dependence</b> should be centered on other potential functional regions of the <strong>SLC6A3</strong> gene.
+SLC6A3	drug	cocaine	20801583	Several studies have looked for a link between <b>cocaine</b> addiction and the genes of the dopaminergic system: the genes DRD2, COMT, <strong>SLC6A3</strong> (coding for the dopamine transporter DAT) and DBH (coding for the dopamine beta hydroxylase) but unfortunately very few well established results.
+SLC6A3	addiction	addiction	20801583	Several studies have looked for a link between cocaine <b>addiction</b> and the genes of the dopaminergic system: the genes DRD2, COMT, <strong>SLC6A3</strong> (coding for the dopamine transporter DAT) and DBH (coding for the dopamine beta hydroxylase) but unfortunately very few well established results.
+SLC6A3	drug	cocaine	20505554	Association study between the <strong>DAT1</strong>, DBH and DRD2 genes and <b>cocaine</b> dependence in a Spanish sample.
+SLC6A3	addiction	dependence	20505554	Association study between the <strong>DAT1</strong>, DBH and DRD2 genes and cocaine <b>dependence</b> in a Spanish sample.
+SLC6A3	drug	cocaine	20505554	We genotyped the Int8 and 3'UTR variable number of tandem repeats of the dopamine transporter gene (DAT1/<strong>SLC6A3</strong>), the TaqIA (rs1800497) and TaqIB (rs1079597) SNP polymorphisms within the dopamine receptor D2 gene and the 19 bp insertion/deletion and c.444G>A (rs1108580) polymorphisms of the dopamine β hydroxylase gene (DBH) in a Spanish sample of 169 patients with <b>cocaine</b> addiction and 169 sex matched controls.
+SLC6A3	addiction	addiction	20505554	We genotyped the Int8 and 3'UTR variable number of tandem repeats of the dopamine transporter gene (DAT1/<strong>SLC6A3</strong>), the TaqIA (rs1800497) and TaqIB (rs1079597) SNP polymorphisms within the dopamine receptor D2 gene and the 19 bp insertion/deletion and c.444G>A (rs1108580) polymorphisms of the dopamine β hydroxylase gene (DBH) in a Spanish sample of 169 patients with cocaine <b>addiction</b> and 169 sex matched controls.
+SLC6A3	drug	cocaine	20505554	We genotyped the Int8 and 3'UTR variable number of tandem repeats of the dopamine transporter gene (<strong>DAT1</strong>/<strong>SLC6A3</strong>), the TaqIA (rs1800497) and TaqIB (rs1079597) SNP polymorphisms within the dopamine receptor D2 gene and the 19 bp insertion/deletion and c.444G>A (rs1108580) polymorphisms of the dopamine β hydroxylase gene (DBH) in a Spanish sample of 169 patients with <b>cocaine</b> addiction and 169 sex matched controls.
+SLC6A3	addiction	addiction	20505554	We genotyped the Int8 and 3'UTR variable number of tandem repeats of the dopamine transporter gene (<strong>DAT1</strong>/<strong>SLC6A3</strong>), the TaqIA (rs1800497) and TaqIB (rs1079597) SNP polymorphisms within the dopamine receptor D2 gene and the 19 bp insertion/deletion and c.444G>A (rs1108580) polymorphisms of the dopamine β hydroxylase gene (DBH) in a Spanish sample of 169 patients with cocaine <b>addiction</b> and 169 sex matched controls.
+SLC6A3	drug	cocaine	20505554	The case control study showed a nominal overrepresentation of the 5R/5R genotype of the Int8 variable number of tandem repeats within <strong>DAT1</strong> in <b>cocaine</b> abusers (P=0.016).
+SLC6A3	drug	opioid	20497233	The aim of this study was to examine whether the dopamine transporter gene (DAT1; <strong>SLC6A3</strong>) is associated with the development of <b>heroin</b> dependence (HD) and whether DAT1 influences personality traits in patients with HD.
+SLC6A3	addiction	dependence	20497233	The aim of this study was to examine whether the dopamine transporter gene (DAT1; <strong>SLC6A3</strong>) is associated with the development of heroin <b>dependence</b> (HD) and whether DAT1 influences personality traits in patients with HD.
+SLC6A3	drug	opioid	20497233	The aim of this study was to examine whether the dopamine transporter gene (<strong>DAT1</strong>; <strong>SLC6A3</strong>) is associated with the development of <b>heroin</b> dependence (HD) and whether <strong>DAT1</strong> influences personality traits in patients with HD.
+SLC6A3	addiction	dependence	20497233	The aim of this study was to examine whether the dopamine transporter gene (<strong>DAT1</strong>; <strong>SLC6A3</strong>) is associated with the development of heroin <b>dependence</b> (HD) and whether <strong>DAT1</strong> influences personality traits in patients with HD.
+SLC6A3	addiction	relapse	20497233	These <strong>DAT1</strong> polymorphisms did not influence novelty <b>seeking</b> and harm avoidance scores in HD patients.
+SLC6A3	drug	cocaine	20170711	Association analysis between polymorphisms in the dopamine D2 receptor (DRD2) and dopamine transporter (<strong>DAT1</strong>) genes with <b>cocaine</b> dependence.
+SLC6A3	addiction	dependence	20170711	Association analysis between polymorphisms in the dopamine D2 receptor (DRD2) and dopamine transporter (<strong>DAT1</strong>) genes with cocaine <b>dependence</b>.
+SLC6A3	drug	cocaine	20170711	<b>Cocaine</b> dependent individuals (n=347) and unaffected controls (n=257) of African descent were genotyped for the polymorphisms in the DRD2 and <strong>DAT1</strong> genes.
+SLC6A3	drug	nicotine	19761593	Influences of polymorphic variants of DRD2 and <strong>SLC6A3</strong> genes, and their combinations on <b>smoking</b> in Polish population.
+SLC6A3	drug	nicotine	19761593	In turn, the 9 repeat allele of dopamine transporter gene (<strong>SLC6A3</strong>) has been associated with a substantial reduction in dopamine transporter, what might result in the higher level of dopamine in the synaptic cleft, and thereby protective role of this allele from <b>smoking</b>.
+SLC6A3	drug	nicotine	19761593	In the present study we investigated whether polymorphic variants of DRD2 and <strong>SLC6A3</strong> genes and their combinations are associated with the <b>smoking</b> habit in the Polish population.
+SLC6A3	drug	nicotine	19761593	Genotyping for TaqIA polymorphism of DRD2 and <strong>SLC6A3</strong> VNTR polymorphism was performed in 150 ever <b>smokers</b> and 158 never <b>smokers</b>.
+SLC6A3	drug	nicotine	19761593	At the used alpha levels no association between DRD2 and <strong>SLC6A3</strong> genotypes and <b>smoking</b> status was found.
+SLC6A3	drug	nicotine	19761593	Carriers of *9 allele of <strong>SLC6A3</strong> had over twice a lower risk to start <b>smoking</b> before the age of 20 years compared to non carriers (sex adjusted OR = 0.44; 95% CI: 0.22 0.89; p = 0.0017), and subjects with A1 /9  genotype combination had a higher risk for staring regular <b>smoking</b> before the age of 20 years in comparison to subjects with A1+/9+ genotype combination (sex adjusted OR = 3.79; 95% CI:1.03 13.90; p = 0.003).
+SLC6A3	drug	nicotine	19761593	Polymorphic variants of DRD2 and <strong>SLC6A3</strong> genes may influence some aspects of the <b>smoking</b> behavior, including age of starting regular <b>smoking</b>, the level of cigarette consumption, and periods of abstinence.
+SLC6A3	drug	alcohol	19740369	Recent evidence suggests that heterogeneity in the age at onset could explain the inconsistent findings of association studies relating the dopamine transporter (<strong>DAT1</strong>) gene with <b>alcohol</b> and nicotine consumption.
+SLC6A3	drug	nicotine	19740369	Recent evidence suggests that heterogeneity in the age at onset could explain the inconsistent findings of association studies relating the dopamine transporter (<strong>DAT1</strong>) gene with alcohol and <b>nicotine</b> consumption.
+SLC6A3	drug	alcohol	19740369	The aim of this study was to examine interactions between two <strong>DAT1</strong> polymorphisms and different initiation ages with regard to <b>alcohol</b> and tobacco consumption levels and dependence.
+SLC6A3	drug	nicotine	19740369	The aim of this study was to examine interactions between two <strong>DAT1</strong> polymorphisms and different initiation ages with regard to alcohol and <b>tobacco</b> consumption levels and dependence.
+SLC6A3	addiction	dependence	19740369	The aim of this study was to examine interactions between two <strong>DAT1</strong> polymorphisms and different initiation ages with regard to alcohol and tobacco consumption levels and <b>dependence</b>.
+SLC6A3	drug	nicotine	19740369	Results suggest that age at onset of intensive consumption moderated the association of the <strong>DAT1</strong> gene with early adult substance use and dependence, revealing a <strong>DAT1</strong> effect only among individuals homozygous for the 10r allele of the 40 bp VNTR who had started daily <b>smoking</b> or being intoxicated early in life.
+SLC6A3	addiction	dependence	19740369	Results suggest that age at onset of intensive consumption moderated the association of the <strong>DAT1</strong> gene with early adult substance use and <b>dependence</b>, revealing a <strong>DAT1</strong> effect only among individuals homozygous for the 10r allele of the 40 bp VNTR who had started daily smoking or being intoxicated early in life.
+SLC6A3	drug	opioid	19664686	Potential association of DRD2 and <strong>DAT1</strong> genetic variation with <b>heroin</b> dependence.
+SLC6A3	addiction	dependence	19664686	Potential association of DRD2 and <strong>DAT1</strong> genetic variation with heroin <b>dependence</b>.
+SLC6A3	drug	amphetamine	19462300	The 10/10 repeat respond poorly to methylphenidate pharmacotherapy and the 9/9 <strong>DAT1</strong> variant show blunted euphoria and physiological response to <b>amphetamine</b>.
+SLC6A3	drug	alcohol	19462300	<b>Disulfiram</b> and methylphenidate pharmacotherapies for cocaine addiction are optimized by considering polymorphisms affecting DbetaH and <strong>DAT1</strong> respectively.
+SLC6A3	drug	cocaine	19462300	Disulfiram and methylphenidate pharmacotherapies for <b>cocaine</b> addiction are optimized by considering polymorphisms affecting DbetaH and <strong>DAT1</strong> respectively.
+SLC6A3	addiction	addiction	19462300	Disulfiram and methylphenidate pharmacotherapies for cocaine <b>addiction</b> are optimized by considering polymorphisms affecting DbetaH and <strong>DAT1</strong> respectively.
+SLC6A3	drug	amphetamine	19462300	Altered subjective effects for <b>amphetamine</b> in <strong>DAT1</strong> VNTR variants suggest a 'protected' phenotype.
+SLC6A3	drug	alcohol	19450132	Polymorphisms in the dopamine transporter gene (<strong>SLC6A3</strong>/DAT1) and <b>alcohol</b> dependence in humans: a systematic review.
+SLC6A3	addiction	dependence	19450132	Polymorphisms in the dopamine transporter gene (<strong>SLC6A3</strong>/DAT1) and alcohol <b>dependence</b> in humans: a systematic review.
+SLC6A3	drug	alcohol	19450132	Polymorphisms in the dopamine transporter gene (<strong>SLC6A3</strong>/<strong>DAT1</strong>) and <b>alcohol</b> dependence in humans: a systematic review.
+SLC6A3	addiction	dependence	19450132	Polymorphisms in the dopamine transporter gene (<strong>SLC6A3</strong>/<strong>DAT1</strong>) and alcohol <b>dependence</b> in humans: a systematic review.
+SLC6A3	drug	alcohol	19450132	The dopamine transporter terminates dopaminergic neurotransmission, making the gene encoding the transporter (<strong>SLC6A3</strong>/DAT1) an attractive candidate in clinical studies on <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	19450132	The dopamine transporter terminates dopaminergic neurotransmission, making the gene encoding the transporter (<strong>SLC6A3</strong>/DAT1) an attractive candidate in clinical studies on alcohol <b>dependence</b>.
+SLC6A3	drug	alcohol	19450132	The dopamine transporter terminates dopaminergic neurotransmission, making the gene encoding the transporter (<strong>SLC6A3</strong>/<strong>DAT1</strong>) an attractive candidate in clinical studies on <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	19450132	The dopamine transporter terminates dopaminergic neurotransmission, making the gene encoding the transporter (<strong>SLC6A3</strong>/<strong>DAT1</strong>) an attractive candidate in clinical studies on alcohol <b>dependence</b>.
+SLC6A3	drug	alcohol	19450132	We conducted a systematic review of 18 studies examining associations between polymorphisms in <strong>DAT1</strong> and <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	19450132	We conducted a systematic review of 18 studies examining associations between polymorphisms in <strong>DAT1</strong> and alcohol <b>dependence</b>.
+SLC6A3	drug	alcohol	19450132	The <strong>DAT1</strong> variable number tandem repeat, the most frequent studied polymorphism in <strong>DAT1</strong>, did not show a direct association with <b>alcohol</b> dependence in general.
+SLC6A3	addiction	dependence	19450132	The <strong>DAT1</strong> variable number tandem repeat, the most frequent studied polymorphism in <strong>DAT1</strong>, did not show a direct association with alcohol <b>dependence</b> in general.
+SLC6A3	drug	alcohol	19450132	Several, but not all, studies found that the <strong>DAT1</strong> variable number tandem repeat (9 repeat allele) was associated with <b>alcohol</b> withdrawal symptoms, such as seizures and delirium tremens.
+SLC6A3	addiction	withdrawal	19450132	Several, but not all, studies found that the <strong>DAT1</strong> variable number tandem repeat (9 repeat allele) was associated with alcohol <b>withdrawal</b> symptoms, such as seizures and delirium tremens.
+SLC6A3	drug	alcohol	19352220	Association between harmful <b>alcohol</b> consumption behavior and dopamine transporter (<strong>DAT1</strong>) gene polymorphisms in a male Finnish population.
+SLC6A3	addiction	reward	19352220	Within this <b>reward</b> system, the DA transporter (<strong>DAT1</strong>) plays a key role in the regulation of dopaminergic neurotransmission through presynaptic DA reuptake.
+SLC6A3	drug	alcohol	19352220	This study investigated whether <strong>DAT1</strong> genetic variation was associated with either <b>alcohol</b> consumption behavior or <b>alcohol</b> dependence in a Finnish cohort.
+SLC6A3	addiction	dependence	19352220	This study investigated whether <strong>DAT1</strong> genetic variation was associated with either alcohol consumption behavior or alcohol <b>dependence</b> in a Finnish cohort.
+SLC6A3	drug	alcohol	19352220	The present findings suggest that <strong>DAT1</strong> genetic variation influences drinking behavior in our Finnish population, where the rs6350 A and rs463379 G alleles provide a protective role against high <b>alcohol</b> consumption and <b>alcohol</b> dependence, respectively.
+SLC6A3	addiction	dependence	19352220	The present findings suggest that <strong>DAT1</strong> genetic variation influences drinking behavior in our Finnish population, where the rs6350 A and rs463379 G alleles provide a protective role against high alcohol consumption and alcohol <b>dependence</b>, respectively.
+SLC6A3	drug	alcohol	19247849	This study explored possible associations between the most frequent <strong>DAT1</strong> polymorphism, namely the A10 VNTR, and personality traits as measured by the Temperament and Character Inventory (TCI) and the NEO Five Factor Inventory (NEO FFI) in <b>alcohol</b> dependent patients (ADP).
+SLC6A3	drug	alcohol	19219710	Two studies reported a significant association of <b>alcohol</b> withdrawal delirium with the dopamine transporter gene (<strong>SLC6A3</strong>) and the dopamine receptor 3 (DRD3).
+SLC6A3	addiction	withdrawal	19219710	Two studies reported a significant association of alcohol <b>withdrawal</b> delirium with the dopamine transporter gene (<strong>SLC6A3</strong>) and the dopamine receptor 3 (DRD3).
+SLC6A3	addiction	reward	19183461	To investigate the contribution of the dopamine transporter to dopaminergic <b>reward</b> related behaviors and anthropometry, we evaluated associations between polymorphisms at the dopamine transporter gene(<strong>SLC6A3</strong>) and body mass index (BMI), among participants in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial.
+SLC6A3	drug	nicotine	19183461	Four polymorphisms (rs6350, rs6413429, rs6347 and the 3' variable number of tandem repeat (3' VNTR) polymorphism) at the <strong>SLC6A3</strong> gene were genotyped in 2,364 participants selected from the screening arm of PLCO randomly within strata of sex, age and <b>smoking</b> history.
+SLC6A3	drug	nicotine	18781857	Several candidate genes within the dopamine pathway (e.g., DRD2 and COMT) have been reported to be associated with the efficacy of bupropion and <b>nicotine</b> replacement therapy, and others (e.g., <strong>SLC6A3</strong> and DRD4) have been reported to be associated with <b>smoking</b> cessation independent of pharmacotherapy.
+SLC6A3	drug	nicotine	18704100	To test this hypothesis, perfusion fMR images were acquired during cue exposure in 19 <b>smokers</b> genotyped for the 40 bp VNTR polymorphism in the <strong>SLC6A3</strong> gene.
+SLC6A3	drug	nicotine	18690118	The increase in <b>smoking</b> amount owing to negative mood was associated with: dopamine D2 receptor (DRD2) C957T (CC>TT or CT), <strong>SLC6A3</strong> (presence of 9 repeat>absence of 9), and among those given a <b>nicotine</b> cigarette, DRD4 (presence of 7 repeat>absence of 7) and DRD2/ANKK1 TaqIA (TT or CT>CC).
+SLC6A3	drug	nicotine	18690118	<strong>SLC6A3</strong>, and DRD2/ANKK1 TaqIA were also associated with <b>smoking</b> reward and <b>smoking</b> latency.
+SLC6A3	addiction	reward	18690118	<strong>SLC6A3</strong>, and DRD2/ANKK1 TaqIA were also associated with smoking <b>reward</b> and smoking latency.
+SLC6A3	drug	opioid	18690117	Very few or no significant associations were seen for the DRD2/ANKK1 TaqIA polymorphism, the serotonin transporter promoter VNTR or 5HTTLPR (SLC6A4), the dopamine transporter 3' VNTR (<strong>SLC6A3</strong>), and the mu <b>opioid</b> receptor A118G single nucleotide polymorphism (mu <b>opioid</b> receptor polymorphism 1).
+SLC6A3	drug	alcohol	18552399	The aim of this study was to investigate the potential association between functional polymorphisms of dopaminergic [dopamine receptor D2 (DRD2), dopamine receptor D3 (DRD3) and dopamine transporter (<strong>SLC6A3</strong>)] and serotonergic [serotonin 2A receptor (HTR2A) and serotonin transporter (SLC6A4)] genes and treatment outcome in <b>alcohol</b> dependent patients.
+SLC6A3	drug	alcohol	18070248	The 3' part of the dopamine transporter gene DAT1/<strong>SLC6A3</strong> is associated with withdrawal seizures in patients with <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	18070248	The 3' part of the dopamine transporter gene DAT1/<strong>SLC6A3</strong> is associated with withdrawal seizures in patients with alcohol <b>dependence</b>.
+SLC6A3	addiction	withdrawal	18070248	The 3' part of the dopamine transporter gene DAT1/<strong>SLC6A3</strong> is associated with <b>withdrawal</b> seizures in patients with alcohol dependence.
+SLC6A3	drug	alcohol	18070248	The 3' part of the dopamine transporter gene <strong>DAT1</strong>/<strong>SLC6A3</strong> is associated with withdrawal seizures in patients with <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	18070248	The 3' part of the dopamine transporter gene <strong>DAT1</strong>/<strong>SLC6A3</strong> is associated with withdrawal seizures in patients with alcohol <b>dependence</b>.
+SLC6A3	addiction	withdrawal	18070248	The 3' part of the dopamine transporter gene <strong>DAT1</strong>/<strong>SLC6A3</strong> is associated with <b>withdrawal</b> seizures in patients with alcohol dependence.
+SLC6A3	drug	alcohol	18070248	Some studies have reported that the A9 allele of the variable nucleotide tandem repeat (VNTR) of the gene which encodes the dopamine transporter (DAT1/<strong>SLC6A3</strong>) is associated with <b>alcoholism</b> withdrawal symptoms such as <b>alcohol</b> withdrawal seizures (WSs), whereas others did not.
+SLC6A3	addiction	withdrawal	18070248	Some studies have reported that the A9 allele of the variable nucleotide tandem repeat (VNTR) of the gene which encodes the dopamine transporter (DAT1/<strong>SLC6A3</strong>) is associated with alcoholism <b>withdrawal</b> symptoms such as alcohol <b>withdrawal</b> seizures (WSs), whereas others did not.
+SLC6A3	drug	alcohol	18070248	Some studies have reported that the A9 allele of the variable nucleotide tandem repeat (VNTR) of the gene which encodes the dopamine transporter (<strong>DAT1</strong>/<strong>SLC6A3</strong>) is associated with <b>alcoholism</b> withdrawal symptoms such as <b>alcohol</b> withdrawal seizures (WSs), whereas others did not.
+SLC6A3	addiction	withdrawal	18070248	Some studies have reported that the A9 allele of the variable nucleotide tandem repeat (VNTR) of the gene which encodes the dopamine transporter (<strong>DAT1</strong>/<strong>SLC6A3</strong>) is associated with alcoholism <b>withdrawal</b> symptoms such as alcohol <b>withdrawal</b> seizures (WSs), whereas others did not.
+SLC6A3	drug	alcohol	18070248	We investigated whether polymorphisms within the <strong>DAT1</strong> gene are associated with WS taking into account some of the confounding factors such as the severity of <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	18070248	We investigated whether polymorphisms within the <strong>DAT1</strong> gene are associated with WS taking into account some of the confounding factors such as the severity of alcohol <b>dependence</b>.
+SLC6A3	drug	alcohol	18070248	To further assess the role of this gene in WS, we genotyped the VNTR and 7 single nucleotide polymorphisms (SNPs) encompassing the <strong>DAT1</strong> gene in a sample of 250 <b>alcohol</b> dependent subjects (175 men and 75 women), of whom 24% exhibited WSs, taking into account the severity of <b>alcohol</b> dependence.
+SLC6A3	addiction	dependence	18070248	To further assess the role of this gene in WS, we genotyped the VNTR and 7 single nucleotide polymorphisms (SNPs) encompassing the <strong>DAT1</strong> gene in a sample of 250 alcohol dependent subjects (175 men and 75 women), of whom 24% exhibited WSs, taking into account the severity of alcohol <b>dependence</b>.
+SLC6A3	drug	alcohol	18070248	The present study adds evidence for a significant role of the 3' part of the <strong>DAT1</strong> gene in WS of <b>alcohol</b> dependent patients, not only because it is in accordance with previous work, but also because of larger statistical power (as relying on a sample over sampled with the studied phenotype), as it gives a more precise analysis of different SNPs within the <strong>DAT1</strong> gene, and as it confirms the association when major potentially confounding factors are taken into account in a logistical regression analysis.
+SLC6A3	drug	nicotine	17654295	<b>Smokers</b> of European ancestry (N = 291), who were randomized to receive bupropion or placebo (12 weeks) plus counseling, were genotyped for the dopamine D2 receptor (DRD2 Taq1A), dopamine transporter (<strong>SLC6A3</strong> 3' VNTR), and cytochrome P450 2B6 (CYP2B6 1459 CT) polymorphisms.
+SLC6A3	drug	nicotine	17508996	This review assessed the evidence of an association between genotypes of the dopamine transporter (DAT1, <strong>SLC6A3</strong>) 3' untranslated region (3'UTR) variable number of tandem repeats (VNTR) and <b>smoking</b> cessation.
+SLC6A3	drug	nicotine	17508996	This review assessed the evidence of an association between genotypes of the dopamine transporter (<strong>DAT1</strong>, <strong>SLC6A3</strong>) 3' untranslated region (3'UTR) variable number of tandem repeats (VNTR) and <b>smoking</b> cessation.
+SLC6A3	drug	nicotine	17508996	These results support the hypothesis that the <strong>DAT1</strong> 3'UTR VNTR polymorphism is associated with <b>smoking</b> cessation.
+SLC6A3	drug	nicotine	17427187	Applying a multifactorial model, we examined the role of genetic variation in the dopamine transporter (<strong>DAT1</strong>) in <b>smoking</b> initiation (SI) and <b>nicotine</b> dependence.
+SLC6A3	addiction	dependence	17427187	Applying a multifactorial model, we examined the role of genetic variation in the dopamine transporter (<strong>DAT1</strong>) in smoking initiation (SI) and nicotine <b>dependence</b>.
+SLC6A3	drug	nicotine	17427187	These findings indicate that in the context of a multifactorial model, haplotypes in the 3' region of <strong>DAT1</strong> influence the propensity of young women to initiate <b>smoking</b> as well as the severity of <b>nicotine</b> dependence once the habit is established.
+SLC6A3	addiction	dependence	17427187	These findings indicate that in the context of a multifactorial model, haplotypes in the 3' region of <strong>DAT1</strong> influence the propensity of young women to initiate smoking as well as the severity of nicotine <b>dependence</b> once the habit is established.
+SLC6A3	drug	nicotine	17427187	A haplotype in the 3' untranslated region of <strong>DAT1</strong> modifies the effect of lifetime traumatic experience on the severity of <b>nicotine</b> dependence.
+SLC6A3	addiction	dependence	17427187	A haplotype in the 3' untranslated region of <strong>DAT1</strong> modifies the effect of lifetime traumatic experience on the severity of nicotine <b>dependence</b>.
+SLC6A3	drug	nicotine	17372541	Genetic polymorphisms of the dopamine D1, D2, D4 and D5 receptors, dopamine transporter (<strong>DAT1</strong>) and dopamine B hydroxylase (DBH) have been associated at least once with clinical aspects of <b>tobacco</b> use (initiation, dependence and intensity) and temperament traits as novelty seeking, the latter being lower in <b>smokers</b> and thus considered as a vulnerable marker in accordance with the reinforcement effect of <b>nicotine</b>.
+SLC6A3	addiction	dependence	17372541	Genetic polymorphisms of the dopamine D1, D2, D4 and D5 receptors, dopamine transporter (<strong>DAT1</strong>) and dopamine B hydroxylase (DBH) have been associated at least once with clinical aspects of tobacco use (initiation, <b>dependence</b> and intensity) and temperament traits as novelty seeking, the latter being lower in smokers and thus considered as a vulnerable marker in accordance with the reinforcement effect of nicotine.
+SLC6A3	addiction	relapse	17372541	Genetic polymorphisms of the dopamine D1, D2, D4 and D5 receptors, dopamine transporter (<strong>DAT1</strong>) and dopamine B hydroxylase (DBH) have been associated at least once with clinical aspects of tobacco use (initiation, dependence and intensity) and temperament traits as novelty <b>seeking</b>, the latter being lower in smokers and thus considered as a vulnerable marker in accordance with the reinforcement effect of nicotine.
+SLC6A3	addiction	reward	17372541	Genetic polymorphisms of the dopamine D1, D2, D4 and D5 receptors, dopamine transporter (<strong>DAT1</strong>) and dopamine B hydroxylase (DBH) have been associated at least once with clinical aspects of tobacco use (initiation, dependence and intensity) and temperament traits as novelty seeking, the latter being lower in smokers and thus considered as a vulnerable marker in accordance with the <b>reinforcement</b> effect of nicotine.
+SLC6A3	drug	nicotine	17264803	To examine the association between polymorphisms in the dopamine transporter gene (<strong>SLC6A3</strong>, DAT1) and treatment outcome in <b>smokers</b> attempting to quit using either <b>nicotine</b> replacement therapy or bupropion.
+SLC6A3	drug	nicotine	17264803	To examine the association between polymorphisms in the dopamine transporter gene (<strong>SLC6A3</strong>, <strong>DAT1</strong>) and treatment outcome in <b>smokers</b> attempting to quit using either <b>nicotine</b> replacement therapy or bupropion.
+SLC6A3	drug	nicotine	17264803	At 1 week after <b>smoking</b> cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30 bp intron 8 VNTR <strong>DAT1</strong> genotypes were associated with the ability to stop <b>smoking</b> (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2 3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0 2.9), controlling for potential confounders.
+SLC6A3	drug	nicotine	17264803	We find evidence, although modest, of a medium sized effect of <strong>DAT1</strong> genotype on the ability to stop <b>smoking</b> early in a <b>smoking</b> cessation attempt.
+SLC6A3	drug	nicotine	17264803	If the effect is real, and is strongest in the very early stages of <b>smoking</b> cessation, this suggests that the primary utility of <strong>DAT1</strong> screening in this field will be in the identification of those most at risk of early relapse after quitting.
+SLC6A3	addiction	relapse	17264803	If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of <strong>DAT1</strong> screening in this field will be in the identification of those most at risk of early <b>relapse</b> after quitting.
+SLC6A3	drug	cocaine	16537431	The dopamine (DA) transporter <strong>DAT1</strong> is a major target bound by <b>cocaine</b> in brain.
+SLC6A3	drug	cocaine	16537431	We examined the influence of functional genetic variants in <strong>DAT1</strong> on <b>cocaine</b> addiction.
+SLC6A3	addiction	addiction	16537431	We examined the influence of functional genetic variants in <strong>DAT1</strong> on cocaine <b>addiction</b>.
+SLC6A3	drug	cocaine	16537431	We demonstrate a robust association between <b>cocaine</b> dependence and a VNTR allele in <strong>SLC6A3</strong>, conferring a small but detectable effect, and we show that this VNTR may be functional.
+SLC6A3	addiction	dependence	16537431	We demonstrate a robust association between cocaine <b>dependence</b> and a VNTR allele in <strong>SLC6A3</strong>, conferring a small but detectable effect, and we show that this VNTR may be functional.
+SLC6A3	drug	cocaine	16537431	This study suggests that <strong>DAT1</strong> gene variation may play a role in <b>cocaine</b> dependence etiology.
+SLC6A3	addiction	dependence	16537431	This study suggests that <strong>DAT1</strong> gene variation may play a role in cocaine <b>dependence</b> etiology.
+SLC6A3	drug	opioid	16526040	The effect of dopamine D2, D5 receptor and transporter (<strong>SLC6A3</strong>) polymorphisms on the cue elicited <b>heroin</b> craving in Chinese.
+SLC6A3	addiction	relapse	16526040	The effect of dopamine D2, D5 receptor and transporter (<strong>SLC6A3</strong>) polymorphisms on the cue elicited heroin <b>craving</b> in Chinese.
+SLC6A3	addiction	relapse	16526040	Furthermore, we did not observed significant association of cue elicited <b>craving</b> with the nine repeat allelic variants in dopamine transporter gene (DAT) <strong>SLC6A3</strong> and with the dinucleotide repeat polymorphism (DRP) 148bp allele in D5 dopamine receptor gene (DRD5).
+SLC6A3	drug	alcohol	16125912	One hundred and eleven male patients with <b>alcohol</b> dependence and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 (ADH2), aldehyde dehydrogenase 2 (ALDH2), serotonin transporter (5 HTT) and dopamine transporter (<strong>DAT1</strong>).
+SLC6A3	addiction	dependence	16125912	One hundred and eleven male patients with alcohol <b>dependence</b> and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of alcohol dehydrogenase 2 (ADH2), aldehyde dehydrogenase 2 (ALDH2), serotonin transporter (5 HTT) and dopamine transporter (<strong>DAT1</strong>).
+SLC6A3	drug	alcohol	16125912	Neither 5 HTTLPR L/S nor <strong>DAT1</strong> G2319A SNP genotypes nor alleles discriminated <b>alcoholic</b> patients from normal controls.
+SLC6A3	drug	opioid	16109590	Polymorphism of a variable number of tandem repeats (VNTR) in the 3' untranslated region of exon 15 of the <strong>SLC6A3</strong> gene, coding for the dopamine transporter (DAT), was analysed to test whether length variation contributes to differences in the individual susceptibility to aggressive   criminal behaviour and liability to <b>heroin</b> dependence.
+SLC6A3	addiction	dependence	16109590	Polymorphism of a variable number of tandem repeats (VNTR) in the 3' untranslated region of exon 15 of the <strong>SLC6A3</strong> gene, coding for the dopamine transporter (DAT), was analysed to test whether length variation contributes to differences in the individual susceptibility to aggressive   criminal behaviour and liability to heroin <b>dependence</b>.
+SLC6A3	drug	alcohol	15996968	It was investigated whether the allele A9 of the dopamine transporter gene (DAT1; <strong>SLC6A3</strong>) is associated with <b>alcoholism</b>, delirium tremens (DT), <b>alcohol</b> withdrawal seizures (AWS), or the daily <b>alcohol</b> intake.
+SLC6A3	addiction	withdrawal	15996968	It was investigated whether the allele A9 of the dopamine transporter gene (DAT1; <strong>SLC6A3</strong>) is associated with alcoholism, delirium tremens (DT), alcohol <b>withdrawal</b> seizures (AWS), or the daily alcohol intake.
+SLC6A3	drug	alcohol	15996968	It was investigated whether the allele A9 of the dopamine transporter gene (<strong>DAT1</strong>; <strong>SLC6A3</strong>) is associated with <b>alcoholism</b>, delirium tremens (DT), <b>alcohol</b> withdrawal seizures (AWS), or the daily <b>alcohol</b> intake.
+SLC6A3	addiction	withdrawal	15996968	It was investigated whether the allele A9 of the dopamine transporter gene (<strong>DAT1</strong>; <strong>SLC6A3</strong>) is associated with alcoholism, delirium tremens (DT), alcohol <b>withdrawal</b> seizures (AWS), or the daily alcohol intake.
+SLC6A3	drug	alcohol	15542698	PCR based assays showed that <b>alcoholism</b> was associated with polymorphisms of the dopamine D2 receptor (DRD2) TaqI B (P = .029) and the GABAA beta2 subunit C1412T (P = .012) genes, but not with the glutamate receptor subunit gene NMDAR2B (366C/G), the serotonin transporter gene (5HTTL PR), the dopamine transporter gene DAT1(<strong>SLC6A3</strong>), the dopamine D2 receptor gene DRD2 TaqI A, or the GABAA alpha1(A15G), alpha6(T1519C), and gamma2(G3145A) subunit genes.
+SLC6A3	drug	alcohol	15542698	PCR based assays showed that <b>alcoholism</b> was associated with polymorphisms of the dopamine D2 receptor (DRD2) TaqI B (P = .029) and the GABAA beta2 subunit C1412T (P = .012) genes, but not with the glutamate receptor subunit gene NMDAR2B (366C/G), the serotonin transporter gene (5HTTL PR), the dopamine transporter gene <strong>DAT1</strong>(<strong>SLC6A3</strong>), the dopamine D2 receptor gene DRD2 TaqI A, or the GABAA alpha1(A15G), alpha6(T1519C), and gamma2(G3145A) subunit genes.
+SLC6A3	drug	nicotine	15381926	Effects of dopamine D2 receptor (DRD2) and transporter (<strong>SLC6A3</strong>) polymorphisms on <b>smoking</b> cue induced cigarette craving among African American <b>smokers</b>.
+SLC6A3	addiction	relapse	15381926	Effects of dopamine D2 receptor (DRD2) and transporter (<strong>SLC6A3</strong>) polymorphisms on smoking cue induced cigarette <b>craving</b> among African American smokers.
+SLC6A3	drug	nicotine	15381926	<b>Smokers</b> carrying either the DRD2 (D2 dopamine receptor gene) TaqI A1 RFLP or the <strong>SLC6A3</strong> (dopamine transporter gene) 9 repeat VNTR polymorphisms had stronger cue induced cravings than noncarriers (Ps <0.05 and 0.01, respectively).
+SLC6A3	addiction	reward	15213032	We assessed the effects of food <b>reinforcement</b> and the interaction of food <b>reinforcement</b> with the dopamine transporter (<strong>SLC6A3</strong>) genotype and the dopamine D(2) receptor (DRD(2)) genotype on energy consumption.
+SLC6A3	addiction	reward	15213032	Subjects high in food <b>reinforcement</b> who lacked an <strong>SLC6A3</strong>*9 allele consumed significantly more calories (>150 kcal; P = 0.015) than did subjects low in food <b>reinforcement</b> or those high in food <b>reinforcement</b> who carried at least one <strong>SLC6A3</strong>*9 allele.
+SLC6A3	addiction	reward	15213032	Food <b>reinforcement</b> has a significant effect on energy intake, and the effect is moderated by the dopamine loci <strong>SLC6A3</strong> and DRD(2).
+SLC6A3	drug	alcohol	15148564	A polymorphism of the DAT gene (<strong>SLC6A3</strong>) was associated with the in vivo transporter availability and with the severity of <b>alcohol</b> withdrawal.
+SLC6A3	addiction	withdrawal	15148564	A polymorphism of the DAT gene (<strong>SLC6A3</strong>) was associated with the in vivo transporter availability and with the severity of alcohol <b>withdrawal</b>.
+SLC6A3	addiction	relapse	14732864	Stress induced cigarette <b>craving</b>: effects of the DRD2 TaqI RFLP and <strong>SLC6A3</strong> VNTR polymorphisms.
+SLC6A3	addiction	relapse	14732864	Significantly stronger stress induced cigarette <b>craving</b> was found for individuals carrying either the DRD2 (D2 dopamine receptor gene) A1, or the <strong>SLC6A3</strong> (dopamine transporter gene) nine repeat allelic variants.
+SLC6A3	drug	nicotine	14685824	Previous studies suggested that a polymorphism in the dopamine transporter gene (<strong>SLC6A3</strong>) is associated with <b>nicotine</b> dependence and age of <b>smoking</b> onset, but the conclusion was controversial.
+SLC6A3	addiction	dependence	14685824	Previous studies suggested that a polymorphism in the dopamine transporter gene (<strong>SLC6A3</strong>) is associated with nicotine <b>dependence</b> and age of smoking onset, but the conclusion was controversial.
+SLC6A3	drug	nicotine	14685824	To detect the association of a G  >A polymorphism (NCBI dbSNP cluster ID: rs27072) in 3' untranslated region of the <strong>SLC6A3</strong> with <b>nicotine</b> dependence and early <b>smoking</b> onset, we recruited 253 sibships including 668 <b>nicotine</b> dependent siblings from a rural district of China.
+SLC6A3	addiction	dependence	14685824	To detect the association of a G  >A polymorphism (NCBI dbSNP cluster ID: rs27072) in 3' untranslated region of the <strong>SLC6A3</strong> with nicotine <b>dependence</b> and early smoking onset, we recruited 253 sibships including 668 nicotine dependent siblings from a rural district of China.
+SLC6A3	drug	nicotine	14685824	Although these findings are preliminary and need validation, the results suggest that a polymorphism in the <strong>SLC6A3</strong> may play important roles in <b>smoking</b> onset, and there may be an interactive effect between the <strong>SLC6A3</strong> and early <b>smoking</b> onset on modulating the susceptibility of <b>nicotine</b> dependence.
+SLC6A3	addiction	dependence	14685824	Although these findings are preliminary and need validation, the results suggest that a polymorphism in the <strong>SLC6A3</strong> may play important roles in smoking onset, and there may be an interactive effect between the <strong>SLC6A3</strong> and early smoking onset on modulating the susceptibility of nicotine <b>dependence</b>.
+SLC6A3	drug	nicotine	14570538	Assessments included the dopamine D2 receptor (DRD2) genotype, dopamine transporter (<strong>SLC6A3</strong>) genotype, demographic factors, and <b>nicotine</b> dependence.
+SLC6A3	addiction	dependence	14570538	Assessments included the dopamine D2 receptor (DRD2) genotype, dopamine transporter (<strong>SLC6A3</strong>) genotype, demographic factors, and nicotine <b>dependence</b>.
+SLC6A3	drug	nicotine	14570538	The results provided evidence for a significant DRD2 * <strong>SLC6A3</strong> interaction effect on prolonged <b>smoking</b> abstinence and time to relapse at EOT, independent of treatment condition.
+SLC6A3	addiction	relapse	14570538	The results provided evidence for a significant DRD2 * <strong>SLC6A3</strong> interaction effect on prolonged smoking abstinence and time to <b>relapse</b> at EOT, independent of treatment condition.
+SLC6A3	drug	amphetamine	12931138	To clarify the latter, we investigated the association between <b>methamphetamine</b> (<b>METH</b>) dependence/psychosis and the hDAT1 gene (<strong>SLC6A3</strong>) encoding the dopamine transporter, which is the primary site of <b>METH</b> activity in the brain.
+SLC6A3	addiction	dependence	12931138	To clarify the latter, we investigated the association between methamphetamine (METH) <b>dependence</b>/psychosis and the hDAT1 gene (<strong>SLC6A3</strong>) encoding the dopamine transporter, which is the primary site of METH activity in the brain.
+SLC6A3	drug	alcohol	12401557	Two new polymorphisms in the 3' untranslated region (3'UTR) of the dopamine transporter (<strong>DAT1</strong>) gene, adjacent to the known variable number of tandem repeats (VNTR) polymorphism, have been investigated in the present population based association study including 351 <b>alcoholics</b> and 336 controls.
+SLC6A3	drug	alcohol	12401557	Our findings provide further evidence that the 3'UTR of the <strong>DAT1</strong> gene affects vulnerability to severe <b>alcohol</b> withdrawal.
+SLC6A3	addiction	withdrawal	12401557	Our findings provide further evidence that the 3'UTR of the <strong>DAT1</strong> gene affects vulnerability to severe alcohol <b>withdrawal</b>.
+SLC6A3	addiction	addiction	12215242	The dopamine transporter (DAT) gene (<strong>SLC6A3</strong>) encodes a protein that regulates synaptic levels of dopamine in the brain and is a candidate gene for <b>addictive</b> behaviors.
+SLC6A3	drug	alcohol	11807408	141C Ins/Del) and variable number of tandem repeat polymorphism at the 3' untranslated region of the dopamine transporter (DAT) gene (<strong>SLC6A3</strong>) with <b>alcoholism</b> in a case control study.
+SLC6A3	drug	alcohol	11244477	DRD4 and <strong>DAT1</strong> as modifying genes in <b>alcoholism</b>: interaction with novelty seeking on level of <b>alcohol</b> consumption.
+SLC6A3	addiction	relapse	11244477	DRD4 and <strong>DAT1</strong> as modifying genes in alcoholism: interaction with novelty <b>seeking</b> on level of alcohol consumption.
+SLC6A3	drug	alcohol	10871694	A polymorphism of the DAT gene (<strong>SLC6A3</strong>) was associated with the in vivo transporter availability in the putamen of abstinent <b>alcoholics</b> and control subjects.
+SLC6A3	drug	alcohol	10649826	In vivo availability of striatal dopamine transporter (DAT) protein has been reported to be reduced among <b>alcoholics</b>, and allelic variation of the DAT gene (<strong>SLC6A3</strong>) has been associated with severity of <b>alcohol</b> withdrawal.
+SLC6A3	addiction	withdrawal	10649826	In vivo availability of striatal dopamine transporter (DAT) protein has been reported to be reduced among alcoholics, and allelic variation of the DAT gene (<strong>SLC6A3</strong>) has been associated with severity of alcohol <b>withdrawal</b>.
+SLC6A3	drug	alcohol	10649826	We examined the VNTR polymorphism of the 3' untranslated region of <strong>SLC6A3</strong> and DAT protein availability in 14 abstinent <b>alcoholics</b> and 11 control subjects.
+SLC6A3	addiction	relapse	10581482	No evidence favoring linkage between D2, D4, or <strong>DAT1</strong> was found for TPQ novelty <b>seeking</b>.
+SLC6A3	drug	cocaine	10581396	The dopamine transporter (DAT; <strong>SLC6A3</strong>) is densely expressed by the dopaminergic midbrain neurons that play central roles in drug reward and is believed to be a primary site of action for <b>cocaine</b> reward.
+SLC6A3	addiction	reward	10581396	The dopamine transporter (DAT; <strong>SLC6A3</strong>) is densely expressed by the dopaminergic midbrain neurons that play central roles in drug <b>reward</b> and is believed to be a primary site of action for cocaine <b>reward</b>.
+SLC6A3	drug	alcohol	10088054	<strong>DAT1</strong> gene polymorphism in <b>alcoholism</b>: a family based association study.
+SLC6A3	drug	alcohol	10088054	The present study tests the hypothesis that the 9 repeat allele of the dopamine transporter gene (DAT1; <strong>SLC6A3</strong>) is more frequent in <b>alcohol</b> dependent probands  and in particular those with severe withdrawal symptoms (seizures and/or delirium)  compared to nonalcoholics.
+SLC6A3	addiction	withdrawal	10088054	The present study tests the hypothesis that the 9 repeat allele of the dopamine transporter gene (DAT1; <strong>SLC6A3</strong>) is more frequent in alcohol dependent probands  and in particular those with severe <b>withdrawal</b> symptoms (seizures and/or delirium)  compared to nonalcoholics.
+SLC6A3	drug	alcohol	10088054	The present study tests the hypothesis that the 9 repeat allele of the dopamine transporter gene (<strong>DAT1</strong>; <strong>SLC6A3</strong>) is more frequent in <b>alcohol</b> dependent probands  and in particular those with severe withdrawal symptoms (seizures and/or delirium)  compared to nonalcoholics.
+SLC6A3	addiction	withdrawal	10088054	The present study tests the hypothesis that the 9 repeat allele of the dopamine transporter gene (<strong>DAT1</strong>; <strong>SLC6A3</strong>) is more frequent in alcohol dependent probands  and in particular those with severe <b>withdrawal</b> symptoms (seizures and/or delirium)  compared to nonalcoholics.
+SLC6A3	drug	alcohol	10088054	By applying a family based association approach, we were not able to detect significant association between allele 9 at DAT1 (<strong>SLC6A3</strong>) and <b>alcoholism</b> as well as between patients with or without severe withdrawal symptoms.
+SLC6A3	addiction	withdrawal	10088054	By applying a family based association approach, we were not able to detect significant association between allele 9 at DAT1 (<strong>SLC6A3</strong>) and alcoholism as well as between patients with or without severe <b>withdrawal</b> symptoms.
+SLC6A3	drug	alcohol	10088054	By applying a family based association approach, we were not able to detect significant association between allele 9 at <strong>DAT1</strong> (<strong>SLC6A3</strong>) and <b>alcoholism</b> as well as between patients with or without severe withdrawal symptoms.
+SLC6A3	addiction	withdrawal	10088054	By applying a family based association approach, we were not able to detect significant association between allele 9 at <strong>DAT1</strong> (<strong>SLC6A3</strong>) and alcoholism as well as between patients with or without severe <b>withdrawal</b> symptoms.
+SLC6A3	drug	nicotine	9925040	(1999) report associations between allele 9 of a dopamine transporter gene polymorphism (<strong>SLC6A3</strong> 9) and lack of <b>smoking</b>, late initiation of <b>smoking</b>, and length of quitting attempts.
+SLC6A3	drug	nicotine	9925040	A significant association between <strong>SLC6A3</strong> 9 and <b>smoking</b> status was confirmed and was due to an effect on cessation rather than initiation.
+SLC6A3	drug	nicotine	9925040	The <strong>SLC6A3</strong> 9 polymorphism was also associated with low scores for novelty seeking, which was the most significant personality correlate of <b>smoking</b> cessation.
+SLC6A3	addiction	relapse	9925040	The <strong>SLC6A3</strong> 9 polymorphism was also associated with low scores for novelty <b>seeking</b>, which was the most significant personality correlate of smoking cessation.
+SLC6A3	addiction	reward	9925040	It is hypothesized that individuals carrying the <strong>SLC6A3</strong> 9 polymorphism have altered dopamine transmission, which reduces their need for novelty and <b>reward</b> by external stimuli, including cigarettes.
+SLC6A3	drug	nicotine	9925041	As a means of investigating the risk of <b>smoking</b> associated with genetic polymorphisms in the dopamine transporter (<strong>SLC6A3</strong>) and the D2 dopamine receptor (DRD2) genes, a case control study of 289 <b>smokers</b> and 233 nonsmoking controls and a case series analysis of <b>smokers</b> were conducted.
+SLC6A3	drug	nicotine	9925041	A significant effect for <strong>SLC6A3</strong> and a significant gene gene interaction were found in a logistic regression model, indicating that individuals with <strong>SLC6A3</strong> 9 genotypes were significantly less likely to be <b>smokers</b>, especially if they also had DRD2 A2 genotypes.
+SLC6A3	drug	nicotine	9925041	<b>Smokers</b> with <strong>SLC6A3</strong> 9 genotypes were also significantly less likely to have started <b>smoking</b> before 16 years of age and had prior <b>smoking</b> histories indicating a longer period of prior <b>smoking</b> cessation.
+SLC6A3	drug	nicotine	9925041	This study provides preliminary evidence that the <strong>SLC6A3</strong> gene may influence <b>smoking</b> initiation and <b>nicotine</b> dependence.
+SLC6A3	addiction	dependence	9925041	This study provides preliminary evidence that the <strong>SLC6A3</strong> gene may influence smoking initiation and nicotine <b>dependence</b>.
+SLC6A3	drug	opioid	9790747	Population studies of polymorphisms at loci of neuropsychiatric interest (tryptophan hydroxylase (TPH), dopamine transporter protein (<strong>SLC6A3</strong>), D3 dopamine receptor (DRD3), apolipoprotein E (APOE), mu <b>opioid</b> receptor (OPRM1), and ciliary neurotrophic factor (CNTF)).
+SLC6A3	drug	opioid	9790747	We determined allele frequencies for polymorphisms at several loci of interest in neuropsychiatry tryptophan hydroxylase (TPH), dopamine transporter protein (<strong>SLC6A3</strong>), D3 dopamine receptor (DRD3), apolipoprotein E (APOE), ciliary neurotrophic factor (CNTF), and the mu <b>opioid</b> receptor (OPRM1) in samples of individuals from populations in several different parts of the world.
+SLC6A3	drug	cocaine	9790747	Associations with psychiatric illness have been proposed for specific polymorphisms at TPH (suicide related behaviors and impulsivity), DRD3 (schizophrenia and bipolar affective disorder), <strong>SLC6A3</strong> (susceptibility to <b>cocaine</b> induced paranoia and attention deficit disorder), CNTF (psychosis), and OPRM1 (substance dependence).
+SLC6A3	addiction	dependence	9790747	Associations with psychiatric illness have been proposed for specific polymorphisms at TPH (suicide related behaviors and impulsivity), DRD3 (schizophrenia and bipolar affective disorder), <strong>SLC6A3</strong> (susceptibility to cocaine induced paranoia and attention deficit disorder), CNTF (psychosis), and OPRM1 (substance <b>dependence</b>).
+SLC6A3	drug	alcohol	9545991	Because of the substantial role of monoaminergic transporters in limiting time and space effects of synaptic neurotransmission, the dopamine transporter gene (DAT1; locus symbol: <strong>SLC6A3</strong>) was studied as a candidate gene possibly related to symptoms of uncomplicated <b>alcohol</b> withdrawal.
+SLC6A3	addiction	withdrawal	9545991	Because of the substantial role of monoaminergic transporters in limiting time and space effects of synaptic neurotransmission, the dopamine transporter gene (DAT1; locus symbol: <strong>SLC6A3</strong>) was studied as a candidate gene possibly related to symptoms of uncomplicated alcohol <b>withdrawal</b>.
+SLC6A3	drug	alcohol	9545991	Because of the substantial role of monoaminergic transporters in limiting time and space effects of synaptic neurotransmission, the dopamine transporter gene (<strong>DAT1</strong>; locus symbol: <strong>SLC6A3</strong>) was studied as a candidate gene possibly related to symptoms of uncomplicated <b>alcohol</b> withdrawal.
+SLC6A3	addiction	withdrawal	9545991	Because of the substantial role of monoaminergic transporters in limiting time and space effects of synaptic neurotransmission, the dopamine transporter gene (<strong>DAT1</strong>; locus symbol: <strong>SLC6A3</strong>) was studied as a candidate gene possibly related to symptoms of uncomplicated alcohol <b>withdrawal</b>.
+SLC6A3	drug	alcohol	9545991	In 48 chronically intoxicated <b>alcoholics</b> (diagnosed according to ICD 10), withdrawal symptoms were examined and the presence of a variable number tandem repeat in the 3' untranslated region of the <strong>DAT1</strong> gene was determined.
+SLC6A3	addiction	withdrawal	9545991	In 48 chronically intoxicated alcoholics (diagnosed according to ICD 10), <b>withdrawal</b> symptoms were examined and the presence of a variable number tandem repeat in the 3' untranslated region of the <strong>DAT1</strong> gene was determined.
+SLC6A3	drug	alcohol	9342195	Therefore, we concluded that the VNTR polymorphism in <strong>DAT1</strong> gene is not associated with <b>alcoholism</b> susceptibility genes in our samples.
+SLC6A3	addiction	addiction	9024952	The role of the dopamine transporter in terminating dopaminergic activity in synaptic neurotransmission suggests that variants of the dopamine transporter gene (<strong>DAT1</strong>) might contribute to individual differences in vulnerability to <b>addictive</b> behavior.
+SLC6A3	drug	alcohol	9024952	Our population based association study investigated whether variants of <strong>DAT1</strong> confer susceptibility to <b>alcohol</b> dependence in 293 <b>alcoholics</b> and clinically more homogeneous subgroups formed by: positive family history, early age at onset, delirium, withdrawal seizures, antisocial tendencies, type 1 and 2 <b>alcoholics</b>.
+SLC6A3	addiction	dependence	9024952	Our population based association study investigated whether variants of <strong>DAT1</strong> confer susceptibility to alcohol <b>dependence</b> in 293 alcoholics and clinically more homogeneous subgroups formed by: positive family history, early age at onset, delirium, withdrawal seizures, antisocial tendencies, type 1 and 2 alcoholics.
+SLC6A3	addiction	withdrawal	9024952	Our population based association study investigated whether variants of <strong>DAT1</strong> confer susceptibility to alcohol dependence in 293 alcoholics and clinically more homogeneous subgroups formed by: positive family history, early age at onset, delirium, <b>withdrawal</b> seizures, antisocial tendencies, type 1 and 2 alcoholics.
+SLC6A3	drug	alcohol	9024952	Analyzing a VNTR polymorphism in the 3' untranslated region of <strong>DAT1</strong>, we found a significantly increased prevalence of the nine repeat allele in 93 <b>alcoholics</b> displaying withdrawal seizures or delirium, compared with 93 ethnically matched nonalcoholic controls (p = 0.003; OR = 2.44; 95% confidence interval: 1.35 4.43).
+SLC6A3	addiction	withdrawal	9024952	Analyzing a VNTR polymorphism in the 3' untranslated region of <strong>DAT1</strong>, we found a significantly increased prevalence of the nine repeat allele in 93 alcoholics displaying <b>withdrawal</b> seizures or delirium, compared with 93 ethnically matched nonalcoholic controls (p = 0.003; OR = 2.44; 95% confidence interval: 1.35 4.43).
+SLC6A3	drug	alcohol	9024952	Our data provide evidence that a major genetic determinant of <strong>DAT1</strong> influences vulnerability to severe <b>alcohol</b> withdrawal symptoms.
+SLC6A3	addiction	withdrawal	9024952	Our data provide evidence that a major genetic determinant of <strong>DAT1</strong> influences vulnerability to severe alcohol <b>withdrawal</b> symptoms.
+CAMK2G	drug	amphetamine	32670029	First it was shown that <strong>CaMKII</strong> neurons in the anterior cingulate area (ACA) were co activated by both <b>Meth</b> and sex.
+CAMK2G	drug	amphetamine	32670029	Next, chemogenetic inactivation of ACA <strong>CaMKII</strong> cells using AAV5 CaMKIIa hM4Di mCherry was shown not to affect <b>Meth</b> induced locomotor activity or sexual behavior.
+CAMK2G	drug	amphetamine	32670029	Subsequently, chemogenetic inactivation of ACA <strong>CaMKII</strong> neurons during <b>Meth</b> self administration followed by sexual behavior was shown to prevent the effects of <b>Meth</b> and sex on enhanced reinstatement of <b>Meth</b> seeking but did not affect enhanced drug seeking during extinction tests.
+CAMK2G	addiction	relapse	32670029	Subsequently, chemogenetic inactivation of ACA <strong>CaMKII</strong> neurons during Meth self administration followed by sexual behavior was shown to prevent the effects of Meth and sex on enhanced <b>reinstatement</b> of Meth <b>seeking</b> but did not affect enhanced drug <b>seeking</b> during extinction tests.
+CAMK2G	drug	amphetamine	32670029	These results indicate that ACA <strong>CaMKII</strong> cell activation during exposure to <b>Meth</b> in a sexual context plays an essential role in the subsequent enhancement of drug seeking during reinstatement tests.
+CAMK2G	addiction	relapse	32670029	These results indicate that ACA <strong>CaMKII</strong> cell activation during exposure to Meth in a sexual context plays an essential role in the subsequent enhancement of drug <b>seeking</b> during <b>reinstatement</b> tests.
+CAMK2G	drug	opioid	32407818	<strong>CaMKII</strong> is activated in <b>opioid</b> induced conditioned place preference, but αCaMKII Thr286 autophosphorylation is not necessary for its establishment.
+CAMK2G	drug	cocaine	32407818	Activation of calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), particularly its α isoform, is known to be important for neuronal processes central for learning and memory and has also been implicated in the maladaptive learning involved in drug addiction.Thr286 autophosphorylation of αCaMKII has been shown to be indispensable for establishment of <b>cocaine</b> induced CPP (Easton et al., 2014).
+CAMK2G	addiction	addiction	32407818	Activation of calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), particularly its α isoform, is known to be important for neuronal processes central for learning and memory and has also been implicated in the maladaptive learning involved in drug <b>addiction</b>.Thr286 autophosphorylation of αCaMKII has been shown to be indispensable for establishment of cocaine induced CPP (Easton et al., 2014).
+CAMK2G	addiction	reward	32407818	Activation of calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), particularly its α isoform, is known to be important for neuronal processes central for learning and memory and has also been implicated in the maladaptive learning involved in drug addiction.Thr286 autophosphorylation of αCaMKII has been shown to be indispensable for establishment of cocaine induced <b>CPP</b> (Easton et al., 2014).
+CAMK2G	drug	opioid	32407818	To study the contribution of <strong>CaMKII</strong> in <b>opioid</b> induced conditioned learning, we examined how establishment of conditioned place preference (CPP) induced by 10 or 30 μmol/kg <b>morphine</b> or its active metabolite <b>morphine</b> 6 glucuronide (M6G) affects the levels and Thr286 autophosphorylation of the α  and β isoforms of <strong>CaMKII</strong>, as well as β actin levels, in dorsal and ventral striatum and in hippocampus of mice.
+CAMK2G	addiction	reward	32407818	To study the contribution of <strong>CaMKII</strong> in opioid induced conditioned learning, we examined how establishment of conditioned place preference (<b>CPP</b>) induced by 10 or 30 μmol/kg morphine or its active metabolite morphine 6 glucuronide (M6G) affects the levels and Thr286 autophosphorylation of the α  and β isoforms of <strong>CaMKII</strong>, as well as β actin levels, in dorsal and ventral striatum and in hippocampus of mice.
+CAMK2G	drug	opioid	32407818	Whereas an acute single administration of <b>morphine</b> or M6G caused increases in <strong>CaMKII</strong> levels and phosphorylation at Thr286 and β actin in striatal areas, CPP induced by these <b>opioids</b> was accompanied primarily by an increase in the protein levels of both <strong>CaMKII</strong> isoforms and β actin in dorsal striatum and hippocampus.
+CAMK2G	addiction	reward	32407818	Whereas an acute single administration of morphine or M6G caused increases in <strong>CaMKII</strong> levels and phosphorylation at Thr286 and β actin in striatal areas, <b>CPP</b> induced by these opioids was accompanied primarily by an increase in the protein levels of both <strong>CaMKII</strong> isoforms and β actin in dorsal striatum and hippocampus.
+CAMK2G	drug	amphetamine	31952958	Furthermore, sensitized behavioral responding to and for <b>amphetamine</b> following exposure to uncertainty is accompanied by increased levels of Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and protein kinase C (PKC) phosphorylation as well as altered protein levels of the transcription factor ∆FosB (increased) and glutamate transporter 1 (GLT1; decreased) in NAcc tissues.
+CAMK2G	addiction	dependence	31912366	However, EAAT3 endocytosis is similar in all regards except its <b>dependence</b> upon <strong>CaMKII</strong> activation.
+CAMK2G	drug	amphetamine	31912366	RhoA activation is dependent on calcium, but not <strong>CaMKII</strong>, explaining a divergence in <b>AMPH</b> mediated endocytosis of DAT and NET from that of EAAT3.
+CAMK2G	drug	alcohol	31835746	Individual Differences in <b>Ethanol</b> Drinking and Seeking Behaviors in Rats Exposed to Chronic Intermittent <b>Ethanol</b> Vapor Exposure is Associated with Altered <strong>CaMKII</strong> Autophosphorylation in the Nucleus Accumbens Shell.
+CAMK2G	addiction	relapse	31835746	Individual Differences in Ethanol Drinking and <b>Seeking</b> Behaviors in Rats Exposed to Chronic Intermittent Ethanol Vapor Exposure is Associated with Altered <strong>CaMKII</strong> Autophosphorylation in the Nucleus Accumbens Shell.
+CAMK2G	drug	alcohol	31835746	Future mechanistic studies should evaluate <strong>CaMKII</strong> autophosphorylation dependent remodeling of glutamatergic synapses in the ventral striatum as a plausible mechanism for the CIE induced enhanced <b>ethanol</b> drinking and seeking behaviors.
+CAMK2G	addiction	relapse	31835746	Future mechanistic studies should evaluate <strong>CaMKII</strong> autophosphorylation dependent remodeling of glutamatergic synapses in the ventral striatum as a plausible mechanism for the CIE induced enhanced ethanol drinking and <b>seeking</b> behaviors.
+CAMK2G	drug	opioid	31639423	The D1R antagonist reduced the withdrawal response in <b>morphine</b> exposed rats and decreased the expression of Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), phosphorylated extracellular signal regulated kinase (p ERK) and cAMP response element binding protein (CREB) in the PAG.
+CAMK2G	addiction	withdrawal	31639423	The D1R antagonist reduced the <b>withdrawal</b> response in morphine exposed rats and decreased the expression of Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), phosphorylated extracellular signal regulated kinase (p ERK) and cAMP response element binding protein (CREB) in the PAG.
+CAMK2G	drug	opioid	31639423	Taken together, the results suggest that D1R antagonist decreased the withdrawal response in <b>morphine</b> exposed rats by downregulating the downstream factors, <strong>CaMKII</strong>, p ERK and CREB.
+CAMK2G	addiction	withdrawal	31639423	Taken together, the results suggest that D1R antagonist decreased the <b>withdrawal</b> response in morphine exposed rats by downregulating the downstream factors, <strong>CaMKII</strong>, p ERK and CREB.
+CAMK2G	drug	psychedelics	31541650	<b>Ketamine</b> reduces remifentanil induced postoperative hyperalgesia mediated by <strong>CaMKII</strong> NMDAR in the primary somatosensory cerebral cortex region in mice.
+CAMK2G	drug	psychedelics	31541650	Before surgery, mice received intrathecal injections of the following drugs: <b>ketamine</b>, NMDA, BayK8644 (<strong>CaMKII</strong> activator), and KN93 (<strong>CaMKII</strong> inhibitor).
+CAMK2G	drug	alcohol	31445991	Adaptation in 5 HT2 receptors <strong>CaMKII</strong> signaling in lateral habenula underlies increased nociceptive sensitivity in <b>ethanol</b> withdrawn rats.
+CAMK2G	drug	alcohol	31445991	Additionally, KN 62, a <strong>CaMKII</strong> inhibitor, attenuated the enhancement of EPSCs and firing induced by acute <b>alcohol</b> and by 5 HT2R agonist.
+CAMK2G	drug	alcohol	31445991	Thus adaptation in 5 HT2R <strong>CaMKII</strong> signaling pathway contributes to the hyper glutamatergic state, the hyperactivity of LHb neurons as well as the higher nociceptive sensitivity in rats withdrawn from chronic <b>alcohol</b> consumption.
+CAMK2G	drug	cocaine	31432769	The expression of TRPV1 and Ca2+/calmodulin mediated kinase II (<strong>CaMKII</strong>) in the NAc were determined after <b>cocaine</b> reinstatement.
+CAMK2G	addiction	relapse	31432769	The expression of TRPV1 and Ca2+/calmodulin mediated kinase II (<strong>CaMKII</strong>) in the NAc were determined after cocaine <b>reinstatement</b>.
+CAMK2G	drug	cocaine	31432769	<b>Cocaine</b> reinstatement was mediated by increased TRPV1 expression in the NAc, which involves <strong>CaMKII</strong>.
+CAMK2G	addiction	relapse	31432769	Cocaine <b>reinstatement</b> was mediated by increased TRPV1 expression in the NAc, which involves <strong>CaMKII</strong>.
+CAMK2G	drug	cocaine	31432769	These findings suggest that activation of TRPV1 mediates the stimulation of D1 like DA receptors and <strong>CaMKII</strong> in the NAc, resulting in the facilitation of <b>cocaine</b> reinstatement behaviors.
+CAMK2G	addiction	relapse	31432769	These findings suggest that activation of TRPV1 mediates the stimulation of D1 like DA receptors and <strong>CaMKII</strong> in the NAc, resulting in the facilitation of cocaine <b>reinstatement</b> behaviors.
+CAMK2G	drug	opioid	31173919	Conversely, the lack of extinction training (sham extinction) upregulated genes associated with kinases (<strong>Camk2g</strong>), neurotrophins (Ngfr), synaptic connectivity factors (Ephb2), glutamate neurotransmission (Grm8) and <b>opioid</b> receptors (μ1, Δ1).
+CAMK2G	drug	nicotine	31129809	When kinase signaling was assessed in the nucleus accumbens and hippocampal CA1 region after repeated <b>nicotine</b> administration, both Ca2+/calmodulin dependent protein kinase (<strong>CaMKII</strong>) and extracellular signal regulated kinase (ERK) were upregulated in WT mice but not in D2RKO mice.
+CAMK2G	drug	opioid	30914248	Furthermore, by microinjecting AAV <strong>CaMKII</strong> or AAV RNAi into LHb, we demonstrated that an overexpression of <strong>CaMKII</strong> could reduce <b>morphine</b> induced CPP scores of rats, while knock down CaMΚII could restore <b>morphine</b> induced CPP scores, which were interfered by FSS.
+CAMK2G	addiction	reward	30914248	Furthermore, by microinjecting AAV <strong>CaMKII</strong> or AAV RNAi into LHb, we demonstrated that an overexpression of <strong>CaMKII</strong> could reduce morphine induced <b>CPP</b> scores of rats, while knock down CaMΚII could restore morphine induced <b>CPP</b> scores, which were interfered by FSS.
+CAMK2G	drug	cocaine	30788886	Here, we reported that D1 receptor  <strong>CaMKII</strong> AMPK FoxO3a signaling pathway was involved in acute <b>cocaine</b> application induced autophagy in the nucleus accumbens (NAc) both in vitro and in vivo.
+CAMK2G	drug	opioid	30428335	The main objective of the study was to evaluate the role of <strong>CaMKII</strong> on the spatial memory of rats which previously were sensitized by <b>morphine</b>.
+CAMK2G	drug	opioid	30428335	The effect of <strong>CaMKII</strong> inhibitor (KN 93) on memory changes was investigated by hippocampal microinjection of KN 93 on the <b>morphine</b> sensitized rats.
+CAMK2G	drug	opioid	30428335	It can be concluded that the effect of <strong>CaMKII</strong> on memory retention in <b>morphine</b> sensitized rats depends on NMDA receptor.
+CAMK2G	drug	nicotine	30326594	Two <strong>CaMKII</strong> sites identified in HEK cells were phosphorylated, and 1 PKA site was dephosphorylated following acute <b>nicotine</b> administration in vivo, whereas phosphorylation of the PKA site was increased back to baseline levels following repeated <b>nicotine</b> exposure.
+CAMK2G	drug	nicotine	30326594	These experiments identified putative <strong>CaMKII</strong> and PKA sites on α4/β2* nAChRs and novel <b>nicotine</b> induced phosphorylation sites in mouse brain that can be explored for their consequences on receptor function.
+CAMK2G	drug	opioid	30292787	TRPV1 modulates <b>morphine</b> self administration via activation of the <strong>CaMKII</strong> CREB pathway in the nucleus accumbens.
+CAMK2G	drug	opioid	30292787	We found that treatment with a selective TRPV1 antagonist, SB366791, significantly decreased the <b>morphine</b> SA induced activation of Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), Akt and the cAMP response element binding protein (CREB) in the nucleus accumbens (NAc).
+CAMK2G	drug	opioid	30292787	Taken together, our findings highlight that TRPV1 plays an important role in <b>morphine</b> addiction, likely via activation of the <strong>CaMKII</strong> CREB pathway in the NAc.
+CAMK2G	addiction	addiction	30292787	Taken together, our findings highlight that TRPV1 plays an important role in morphine <b>addiction</b>, likely via activation of the <strong>CaMKII</strong> CREB pathway in the NAc.
+CAMK2G	drug	opioid	30240785	The expressions of Trx 1, N methyl d aspartate receptor 2B subunit (NR2B), phosphorylated Ca2+/calmodulin dependent protein kinase II (p <strong>CaMKII</strong>), phosphorylated extracellular signaling regulated kinases (p ERK), and phosphorylated cAMP response element binding protein (p CREB) were induced in nucleus accumbens (NAc) and hippocampus by <b>morphine</b> or GGA, whereas these proteins were not changed by <b>morphine</b> in GGA treated mice.
+CAMK2G	drug	opioid	30227624	Sinomenine Protects Against <b>Morphine</b> Dependence through the NMDAR1/<strong>CAMKII</strong>/CREB Pathway: A Possible Role of Astrocyte Derived Exosomes.
+CAMK2G	addiction	dependence	30227624	Sinomenine Protects Against Morphine <b>Dependence</b> through the NMDAR1/<strong>CAMKII</strong>/CREB Pathway: A Possible Role of Astrocyte Derived Exosomes.
+CAMK2G	drug	opioid	30227624	Moreover, sinomenine inhibited the expressions of p NMDAR1/NMDAR1, p <strong>CAMKII</strong>/<strong>CAMKII</strong>, and p CREB/CREB in the hippocampusof <b>morphine</b> dependent mice and SH SY5Y cells.
+CAMK2G	drug	opioid	30227624	Results showed that Sino exo reduced the level of cAMP, intracellular Ca2+, and the expression of p <strong>CAMKII</strong>/<strong>CAMKII</strong> and p CREB/CREB in <b>morphine</b> treated SH SY5Y cells.
+CAMK2G	drug	opioid	30227624	In conclusion, we demonstrated that sinomenine exhibited protective effects against <b>morphine</b> dependencein vivo and in vitro through theNMDAR1/<strong>CAMKII</strong>/CREB pathway.
+CAMK2G	drug	alcohol	30213620	Memantine attenuated <b>alcohol</b> withdrawal induced anxiety like behaviors through down regulating NR1 <strong>CaMKII</strong> ERK signaling pathway.
+CAMK2G	addiction	withdrawal	30213620	Memantine attenuated alcohol <b>withdrawal</b> induced anxiety like behaviors through down regulating NR1 <strong>CaMKII</strong> ERK signaling pathway.
+CAMK2G	drug	alcohol	30213620	We found that the NR1 <strong>CaMKII</strong> ERK signaling pathway was activated after <b>alcohol</b> withdrawal in medial prefrontal cortex (mPFC) and nucleus accumbens shell (NAcSh) but not core (NAcC).
+CAMK2G	addiction	withdrawal	30213620	We found that the NR1 <strong>CaMKII</strong> ERK signaling pathway was activated after alcohol <b>withdrawal</b> in medial prefrontal cortex (mPFC) and nucleus accumbens shell (NAcSh) but not core (NAcC).
+CAMK2G	drug	alcohol	30213620	Moreover, memantine uniformly suppressed the phosphorylation of NR1 <strong>CaMKII</strong> ERK pathway induced by <b>alcohol</b> withdrawal.
+CAMK2G	addiction	withdrawal	30213620	Moreover, memantine uniformly suppressed the phosphorylation of NR1 <strong>CaMKII</strong> ERK pathway induced by alcohol <b>withdrawal</b>.
+CAMK2G	drug	alcohol	30213620	Our results suggest that activation of the NR1 <strong>CaMKII</strong> ERK pathway in the mPFC and NAcSh is an important contributor to the molecular mechanisms underlying <b>alcohol</b> withdrawal induced anxiety behaviors.
+CAMK2G	addiction	withdrawal	30213620	Our results suggest that activation of the NR1 <strong>CaMKII</strong> ERK pathway in the mPFC and NAcSh is an important contributor to the molecular mechanisms underlying alcohol <b>withdrawal</b> induced anxiety behaviors.
+CAMK2G	drug	alcohol	29598867	The authors report for the first time that binge <b>alcohol</b> activates JNK2, which subsequently phosphorylates the <strong>CaMKII</strong> protein, enhancing <strong>CaMKII</strong> driven SR Ca2+ mishandling.
+CAMK2G	addiction	intoxication	29598867	The authors report for the first time that <b>binge</b> alcohol activates JNK2, which subsequently phosphorylates the <strong>CaMKII</strong> protein, enhancing <strong>CaMKII</strong> driven SR Ca2+ mishandling.
+CAMK2G	drug	alcohol	29598867	<strong>CaMKII</strong> inhibition eliminates binge <b>alcohol</b> evoked arrhythmic activities.
+CAMK2G	addiction	intoxication	29598867	<strong>CaMKII</strong> inhibition eliminates <b>binge</b> alcohol evoked arrhythmic activities.
+CAMK2G	drug	alcohol	29598867	Our studies demonstrate that binge <b>alcohol</b> exposure activates JNK2 in atria, which then drives <strong>CaMKII</strong> activation, prompting aberrant Ca2+ waves and, thus, enhanced susceptibility to atrial arrhythmia.
+CAMK2G	addiction	intoxication	29598867	Our studies demonstrate that <b>binge</b> alcohol exposure activates JNK2 in atria, which then drives <strong>CaMKII</strong> activation, prompting aberrant Ca2+ waves and, thus, enhanced susceptibility to atrial arrhythmia.
+CAMK2G	drug	amphetamine	29363584	Reinstatement of <b>methamphetamine</b> seeking enhanced autophosphorylation of <strong>CaMKII</strong>, reduced mossy fiber density, and induced hyperexcitability of GCNs.
+CAMK2G	addiction	relapse	29363584	<b>Reinstatement</b> of methamphetamine <b>seeking</b> enhanced autophosphorylation of <strong>CaMKII</strong>, reduced mossy fiber density, and induced hyperexcitability of GCNs.
+CAMK2G	drug	amphetamine	29363584	Inhibition of neurogenesis during abstinence prevented context driven <b>methamphetamine</b> seeking, and these effects correlated with reduced autophosphorylation of <strong>CaMKII</strong>, increased mossy fiber density, and reduced the excitability of GCNs.
+CAMK2G	addiction	relapse	29363584	Inhibition of neurogenesis during abstinence prevented context driven methamphetamine <b>seeking</b>, and these effects correlated with reduced autophosphorylation of <strong>CaMKII</strong>, increased mossy fiber density, and reduced the excitability of GCNs.
+CAMK2G	drug	alcohol	29100991	Cue induced reinstatement of <b>alcohol</b> seeking behavior is associated with increased <strong>CaMKII</strong> T286 phosphorylation in the reward pathway of mice.
+CAMK2G	addiction	relapse	29100991	Cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior is associated with increased <strong>CaMKII</strong> T286 phosphorylation in the reward pathway of mice.
+CAMK2G	addiction	reward	29100991	Cue induced reinstatement of alcohol seeking behavior is associated with increased <strong>CaMKII</strong> T286 phosphorylation in the <b>reward</b> pathway of mice.
+CAMK2G	addiction	reward	29100991	A variety of plasticity events require activation of calcium calmodulin dependent protein kinase II (<strong>CaMKII</strong>) in components of the <b>reward</b> pathway, such as the nucleus accumbens and amygdala.
+CAMK2G	drug	alcohol	29100991	We sought to determine if cue induced reinstatement of <b>alcohol</b> seeking behavior is associated with changes in the activation state (e.g., phosphorylation) of <strong>CaMKII</strong> T286.
+CAMK2G	addiction	relapse	29100991	We sought to determine if cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior is associated with changes in the activation state (e.g., phosphorylation) of <strong>CaMKII</strong> T286.
+CAMK2G	drug	cocaine	29089442	Finally, conditional knock out of Cav1.2 in dopamine D1 receptor (D1R) expressing cells resulted in attenuation of <b>cocaine</b> CPP extinction and lack of extinction dependent changes in hippocampal PSD <strong>CaMKII</strong> expression and S831 GluA1 phosphorylation.
+CAMK2G	addiction	reward	29089442	Finally, conditional knock out of Cav1.2 in dopamine D1 receptor (D1R) expressing cells resulted in attenuation of cocaine <b>CPP</b> extinction and lack of extinction dependent changes in hippocampal PSD <strong>CaMKII</strong> expression and S831 GluA1 phosphorylation.
+CAMK2G	drug	cocaine	29089442	In summary, we demonstrate an essential role for the hippocampal Cav1.2/<strong>CaMKII</strong>/S831 GluA1 pathway in <b>cocaine</b> CPP extinction, with data supporting contribution of hippocampal D1R expressing cells in this process.
+CAMK2G	addiction	reward	29089442	In summary, we demonstrate an essential role for the hippocampal Cav1.2/<strong>CaMKII</strong>/S831 GluA1 pathway in cocaine <b>CPP</b> extinction, with data supporting contribution of hippocampal D1R expressing cells in this process.
+CAMK2G	drug	alcohol	28865912	Inhibition of AMPA receptor and <strong>CaMKII</strong> activity in the lateral habenula reduces depressive like behavior and <b>alcohol</b> intake in rats.
+CAMK2G	drug	alcohol	28865912	In the current study, we tested the hypothesis that withdrawal from repeated cycles of <b>ethanol</b> drinking triggers an increase in LHb AMPAR and <strong>CaMKII</strong> activity concomitant with depression like symptoms, and their inhibitions bring a reduction in depressive like behaviors and <b>alcohol</b> consumption.
+CAMK2G	addiction	withdrawal	28865912	In the current study, we tested the hypothesis that <b>withdrawal</b> from repeated cycles of ethanol drinking triggers an increase in LHb AMPAR and <strong>CaMKII</strong> activity concomitant with depression like symptoms, and their inhibitions bring a reduction in depressive like behaviors and alcohol consumption.
+CAMK2G	drug	alcohol	28865912	Western blotting revealed a higher level of phosphorylated AMPAR GluA1 subunit at a <strong>CaMKII</strong> locus (GluA1 Ser831) in the LHb of <b>ethanol</b> withdrawn rats than that of age matched naïve counterparts.
+CAMK2G	drug	alcohol	28865912	In <b>ethanol</b> withdrawn rats, pharmacological inhibition of LHb AMPAR activity significantly mitigated the depressive like behavior and <b>ethanol</b> drinking and seeking behaviors, but affected neither sucrose intake nor locomotor activity; and inhibition of LHb <strong>CaMKII</strong> activity, or chemogenetic inhibition of LHb activity produced similar effects.
+CAMK2G	addiction	relapse	28865912	In ethanol withdrawn rats, pharmacological inhibition of LHb AMPAR activity significantly mitigated the depressive like behavior and ethanol drinking and <b>seeking</b> behaviors, but affected neither sucrose intake nor locomotor activity; and inhibition of LHb <strong>CaMKII</strong> activity, or chemogenetic inhibition of LHb activity produced similar effects.
+CAMK2G	drug	alcohol	28865912	These results demonstrate that <strong>CaMKII</strong> AMPAR signaling in the LHb exemplifies a molecular basis for depressive like symptoms during <b>ethanol</b> withdrawal and that inhibition of this signaling pathway may offer a new therapeutic approach to address the comorbidity of <b>alcohol</b> abuse and depression.
+CAMK2G	addiction	withdrawal	28865912	These results demonstrate that <strong>CaMKII</strong> AMPAR signaling in the LHb exemplifies a molecular basis for depressive like symptoms during ethanol <b>withdrawal</b> and that inhibition of this signaling pathway may offer a new therapeutic approach to address the comorbidity of alcohol abuse and depression.
+CAMK2G	drug	cocaine	28860971	A New Insight into the Role of CART in <b>Cocaine</b> Reward: Involvement of <strong>CaMKII</strong> and Inhibitory G Protein Coupled Receptor Signaling.
+CAMK2G	addiction	reward	28860971	A New Insight into the Role of CART in Cocaine <b>Reward</b>: Involvement of <strong>CaMKII</strong> and Inhibitory G Protein Coupled Receptor Signaling.
+CAMK2G	drug	cocaine	28860971	Recent research has demonstrated that Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and inhibitory G protein coupled receptor (GPCR) signaling are involved in the mechanism of the effect of CART on <b>cocaine</b> reward.
+CAMK2G	addiction	reward	28860971	Recent research has demonstrated that Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and inhibitory G protein coupled receptor (GPCR) signaling are involved in the mechanism of the effect of CART on cocaine <b>reward</b>.
+CAMK2G	drug	cocaine	28860971	Hence, we review the role of <strong>CaMKII</strong> and inhibitory GPCR signaling in the effect of CART on <b>cocaine</b> reward and provide a new insight into the mechanism of that effect.
+CAMK2G	addiction	reward	28860971	Hence, we review the role of <strong>CaMKII</strong> and inhibitory GPCR signaling in the effect of CART on cocaine <b>reward</b> and provide a new insight into the mechanism of that effect.
+CAMK2G	drug	cocaine	28860971	Then, we will focus on the role of <strong>CaMKII</strong> and inhibitory GPCR signaling in <b>cocaine</b> reward.
+CAMK2G	addiction	reward	28860971	Then, we will focus on the role of <strong>CaMKII</strong> and inhibitory GPCR signaling in cocaine <b>reward</b>.
+CAMK2G	drug	cocaine	28860971	Furthermore, we will discuss how <strong>CaMKII</strong> and inhibitory GPCR signaling are involved in the mechanistic action of CART in <b>cocaine</b> reward.
+CAMK2G	addiction	reward	28860971	Furthermore, we will discuss how <strong>CaMKII</strong> and inhibitory GPCR signaling are involved in the mechanistic action of CART in cocaine <b>reward</b>.
+CAMK2G	drug	cocaine	28860971	Finally, we will provide our opinions regarding the future directions of research on the role of <strong>CaMKII</strong> and inhibitory GPCR signaling in the effect of CART on <b>cocaine</b> reward.
+CAMK2G	addiction	reward	28860971	Finally, we will provide our opinions regarding the future directions of research on the role of <strong>CaMKII</strong> and inhibitory GPCR signaling in the effect of CART on cocaine <b>reward</b>.
+CAMK2G	drug	opioid	28527717	We also found that lateral habenular administration of KN 62, a specific inhibitor for calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), abolished <b>naloxone</b> precipitated CPA in <b>morphine</b> dependent mice.
+CAMK2G	drug	opioid	28527717	Furthermore, we found chronic <b>morphine</b> treatment induced overexpression of <strong>CaMKII</strong> in the LHb.
+CAMK2G	drug	opioid	28527717	In conclusion, our results suggest that the increased expression of <strong>CaMKII</strong> in the LHb is instrumental for <b>morphine</b> driven aversive behaviors.
+CAMK2G	addiction	aversion	28527717	In conclusion, our results suggest that the increased expression of <strong>CaMKII</strong> in the LHb is instrumental for morphine driven <b>aversive</b> behaviors.
+CAMK2G	drug	opioid	28423675	Overall, the data demonstrate that miR 219 5p plays a crucial role in alleviating <b>morphine</b> tolerance by inhibiting the <strong>CaMKII</strong>/NMDA receptor pathway.
+CAMK2G	drug	amphetamine	28223211	On the other hand, exposure to <b>amphetamine</b> significantly slowed mEPSC decay times and increased levels in the PSD of PKA and <strong>CaMKII</strong> as well as phosphorylation by these kinases of the GluA1 S845 and S831 residues selectively in this cellular compartment.
+CAMK2G	drug	alcohol	27906494	Specifically, we show that enzymes that participate in the regulation of NMDAR function including Fyn kinase as well as signaling cascades downstream of NMDAR including calcium/calmodulin dependent protein kinase II (<strong>CamKII</strong>), the α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid receptor (AMPAR) and the mammalian target of rapamycin complex 1 (mTORC1) play a major role in mechanisms underlying <b>alcohol</b> drinking behaviors.
+CAMK2G	addiction	relapse	27445140	Intra basolateral amygdala inhibition of <strong>CaMKII</strong> promoted memory extinction and disrupted reconsolidation, leading to a reduction in subsequent cue induced <b>reinstatement</b>.
+CAMK2G	addiction	addiction	27445140	Therefore, inhibition of <strong>CaMKII</strong> represents a novel mechanism for memory based <b>addiction</b> treatment that leverages both extinction enhancement and reconsolidation disruption to reduce relapse like behavior.
+CAMK2G	addiction	relapse	27445140	Therefore, inhibition of <strong>CaMKII</strong> represents a novel mechanism for memory based addiction treatment that leverages both extinction enhancement and reconsolidation disruption to reduce <b>relapse</b> like behavior.
+CAMK2G	addiction	addiction	27445140	Additionally, using a rodent model of <b>addiction</b>, we show that <strong>CaMKII</strong> inhibition in the amygdala can reduce relapse like behavior.
+CAMK2G	addiction	relapse	27445140	Additionally, using a rodent model of addiction, we show that <strong>CaMKII</strong> inhibition in the amygdala can reduce <b>relapse</b> like behavior.
+CAMK2G	addiction	addiction	27056740	The effects of these drugs of abuse in different animal models of drug reward, dependence and <b>addiction</b> are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (<strong>CaMKII</strong>), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), cyclin dependent kinase 5 (Cdk5), heat shock proteins (Hsp) and other enzymes and proteins.
+CAMK2G	addiction	dependence	27056740	The effects of these drugs of abuse in different animal models of drug reward, <b>dependence</b> and addiction are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (<strong>CaMKII</strong>), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), cyclin dependent kinase 5 (Cdk5), heat shock proteins (Hsp) and other enzymes and proteins.
+CAMK2G	addiction	reward	27056740	The effects of these drugs of abuse in different animal models of drug <b>reward</b>, dependence and addiction are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (<strong>CaMKII</strong>), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), cyclin dependent kinase 5 (Cdk5), heat shock proteins (Hsp) and other enzymes and proteins.
+CAMK2G	drug	alcohol	26742808	Potentiation of amygdala AMPA receptor activity selectively promotes escalated <b>alcohol</b> self administration in a <strong>CaMKII</strong> dependent manner.
+CAMK2G	drug	alcohol	26742808	Because GluA1 S831 is a Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) substrate, we sought to determine if AMPAR regulation of enhanced <b>alcohol</b> self administration is dependent on <strong>CaMKII</strong> activity.
+CAMK2G	drug	alcohol	26742808	Intra CeA infusion of the cell permeable <strong>CaMKII</strong> peptide inhibitor myristolated autocamtide 2 related inhibitory peptide (m AIP) dose dependently reduced <b>alcohol</b> self administration.
+CAMK2G	drug	alcohol	26742808	A subthreshold dose of m AIP also blocked the aniracetam induced escalation of <b>alcohol</b> self administration, demonstrating that AMPAR mediated potentiation of <b>alcohol</b> reinforcement requires <strong>CaMKII</strong> activity in the amygdala.
+CAMK2G	addiction	addiction	26742808	A subthreshold dose of m AIP also blocked the aniracetam induced <b>escalation</b> of alcohol self administration, demonstrating that AMPAR mediated potentiation of alcohol reinforcement requires <strong>CaMKII</strong> activity in the amygdala.
+CAMK2G	addiction	reward	26742808	A subthreshold dose of m AIP also blocked the aniracetam induced escalation of alcohol self administration, demonstrating that AMPAR mediated potentiation of alcohol <b>reinforcement</b> requires <strong>CaMKII</strong> activity in the amygdala.
+CAMK2G	drug	alcohol	26742808	Enhanced activity of plasticity linked AMPAR <strong>CaMKII</strong> signaling in the amygdala may promote escalated <b>alcohol</b> use via increased positive reinforcement during the initial stages of addiction.
+CAMK2G	addiction	addiction	26742808	Enhanced activity of plasticity linked AMPAR <strong>CaMKII</strong> signaling in the amygdala may promote escalated alcohol use via increased positive reinforcement during the initial stages of <b>addiction</b>.
+CAMK2G	addiction	reward	26742808	Enhanced activity of plasticity linked AMPAR <strong>CaMKII</strong> signaling in the amygdala may promote escalated alcohol use via increased positive <b>reinforcement</b> during the initial stages of addiction.
+CAMK2G	drug	alcohol	26608538	<strong>CaMKII</strong> inhibition in the prefrontal cortex specifically increases the positive reinforcing effects of sweetened <b>alcohol</b> in C57BL/6J mice.
+CAMK2G	addiction	reward	26608538	<strong>CaMKII</strong> inhibition in the prefrontal cortex specifically increases the positive <b>reinforcing</b> effects of sweetened alcohol in C57BL/6J mice.
+CAMK2G	drug	alcohol	26608538	Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) is a multifunctional enzyme that is required for synaptic plasticity and has been proposed to be a primary molecular component of the etiology of <b>alcohol</b> addiction.
+CAMK2G	addiction	addiction	26608538	Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) is a multifunctional enzyme that is required for synaptic plasticity and has been proposed to be a primary molecular component of the etiology of alcohol <b>addiction</b>.
+CAMK2G	drug	alcohol	26608538	Here we sought to remove that regulatory control by site specifically inhibiting <strong>CaMKII</strong> activity in the mPFC, and measured effects on the positive reinforcing effects of sweetened <b>alcohol</b> in C57BL/6J mice.
+CAMK2G	addiction	reward	26608538	Here we sought to remove that regulatory control by site specifically inhibiting <strong>CaMKII</strong> activity in the mPFC, and measured effects on the positive <b>reinforcing</b> effects of sweetened alcohol in C57BL/6J mice.
+CAMK2G	drug	alcohol	26608538	Infusion of the <strong>CAMKII</strong> inhibitor KN 93 (0 10.0 μg) in the mPFC primarily increased <b>alcohol</b>+sucrose reinforced response rate in a dose  and time dependent manner.
+CAMK2G	drug	alcohol	26608538	These results suggest that endogenous <strong>CaMKII</strong> activity in the mPFC exerts inhibitory control over the positive reinforcing effects of <b>alcohol</b>.
+CAMK2G	addiction	reward	26608538	These results suggest that endogenous <strong>CaMKII</strong> activity in the mPFC exerts inhibitory control over the positive <b>reinforcing</b> effects of alcohol.
+CAMK2G	drug	alcohol	26608538	Downregulation of <strong>CaMKII</strong> signaling in the mPFC might contribute to escalated <b>alcohol</b> use.
+CAMK2G	drug	cocaine	26377474	We also found that H4R3me2a is upregulated in NAc after repeated <b>cocaine</b> administration, and that H4R3me2a upregulation in turn controls the expression of Cdk5 and <strong>CaMKII</strong>.
+CAMK2G	drug	cocaine	26377474	Additionally, the suppression of PRMT1 in NAc with lentiviral short hairpin PMRT1 decreases levels of <strong>CaMKII</strong> and Cdk5 in the <b>cocaine</b> treated group, demonstrating that PRMT1 affects the ability of <b>cocaine</b> to induce <strong>CaMKII</strong> and Cdk5 in NAc.
+CAMK2G	drug	cocaine	26377474	This study also showed that H4R3me2a controlled transcriptions of Cdk5 and <strong>CaMKII</strong>, and that PRMT1 negatively affected the ability of <b>cocaine</b> to induce <strong>CaMKII</strong> and Cdk5 in NAc.
+CAMK2G	drug	amphetamine	26366944	Moreover, <b>METH</b> inhibited mitogen activated protein kinase (MAPK) signaling activity and altered expression of the N methyl d aspartate (NMDA) receptor subunits NR2A and NR2B as well as calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>).
+CAMK2G	drug	nicotine	26292186	Several recent studies have indicated the involvement of calcium dependent mechanisms, in particular the abundant calcium activated kinase, calcium/calmodulin dependent kinase II (<strong>CaMKII</strong>), in behaviors associated with <b>nicotine</b> dependence in mice.
+CAMK2G	addiction	dependence	26292186	Several recent studies have indicated the involvement of calcium dependent mechanisms, in particular the abundant calcium activated kinase, calcium/calmodulin dependent kinase II (<strong>CaMKII</strong>), in behaviors associated with nicotine <b>dependence</b> in mice.
+CAMK2G	drug	nicotine	26292186	Behavioral and biochemical studies have shown that <strong>CaMKII</strong> is involved in acute and chronic <b>nicotine</b> behaviors and <b>nicotine</b> withdrawal; however, evidence of a role for <strong>CaMKII</strong> in <b>nicotine</b> reward is lacking.
+CAMK2G	addiction	reward	26292186	Behavioral and biochemical studies have shown that <strong>CaMKII</strong> is involved in acute and chronic nicotine behaviors and nicotine withdrawal; however, evidence of a role for <strong>CaMKII</strong> in nicotine <b>reward</b> is lacking.
+CAMK2G	addiction	withdrawal	26292186	Behavioral and biochemical studies have shown that <strong>CaMKII</strong> is involved in acute and chronic nicotine behaviors and nicotine <b>withdrawal</b>; however, evidence of a role for <strong>CaMKII</strong> in nicotine reward is lacking.
+CAMK2G	drug	nicotine	26292186	Thus, the goal of the current study was to examine the role of <strong>CaMKII</strong> in <b>nicotine</b> reward.
+CAMK2G	addiction	reward	26292186	Thus, the goal of the current study was to examine the role of <strong>CaMKII</strong> in nicotine <b>reward</b>.
+CAMK2G	drug	nicotine	26292186	Using pharmacological and genetic tools, we tested <b>nicotine</b> conditioned place preference (CPP) in C57Bl/6 mice after administration of <strong>CaMKII</strong> antagonists and in α <strong>CaMKII</strong> wild type (+/+) and heterozygote (±) mice.
+CAMK2G	addiction	reward	26292186	Using pharmacological and genetic tools, we tested nicotine conditioned place preference (<b>CPP</b>) in C57Bl/6 mice after administration of <strong>CaMKII</strong> antagonists and in α <strong>CaMKII</strong> wild type (+/+) and heterozygote (±) mice.
+CAMK2G	drug	nicotine	26292186	<strong>CaMKII</strong> antagonists blocked expression of <b>nicotine</b> CPP, and the preference score was significantly reduced in α <strong>CaMKII</strong> ± mice compared with their +/+ counterparts.
+CAMK2G	addiction	reward	26292186	<strong>CaMKII</strong> antagonists blocked expression of nicotine <b>CPP</b>, and the preference score was significantly reduced in α <strong>CaMKII</strong> ± mice compared with their +/+ counterparts.
+CAMK2G	drug	nicotine	26292186	Further, we assessed <strong>CaMKII</strong> activity in the ventral tegmental area (VTA), nucleus accumbens (NAc), prefrontal cortex, and hippocampus after <b>nicotine</b> CPP and found significant increases in <strong>CaMKII</strong> activity in the mouse VTA and NAc that were blocked by <strong>CaMKII</strong> antagonists.
+CAMK2G	addiction	reward	26292186	Further, we assessed <strong>CaMKII</strong> activity in the ventral tegmental area (VTA), nucleus accumbens (NAc), prefrontal cortex, and hippocampus after nicotine <b>CPP</b> and found significant increases in <strong>CaMKII</strong> activity in the mouse VTA and NAc that were blocked by <strong>CaMKII</strong> antagonists.
+CAMK2G	drug	nicotine	26292186	The findings from this study show that <strong>CaMKII</strong> mediates <b>nicotine</b> reward and suggest that increases in <strong>CaMKII</strong> activity in the VTA and NAc are relevant to <b>nicotine</b> reward behaviors.
+CAMK2G	addiction	reward	26292186	The findings from this study show that <strong>CaMKII</strong> mediates nicotine <b>reward</b> and suggest that increases in <strong>CaMKII</strong> activity in the VTA and NAc are relevant to nicotine <b>reward</b> behaviors.
+CAMK2G	drug	amphetamine	25905720	<strong>CaMKII</strong> is also involved in the maintenance of LTP and contributes to maintenance of behavioral sensitization by cocaine or <b>amphetamine</b>.
+CAMK2G	drug	cocaine	25905720	<strong>CaMKII</strong> is also involved in the maintenance of LTP and contributes to maintenance of behavioral sensitization by <b>cocaine</b> or amphetamine.
+CAMK2G	addiction	sensitization	25905720	<strong>CaMKII</strong> is also involved in the maintenance of LTP and contributes to maintenance of behavioral <b>sensitization</b> by cocaine or amphetamine.
+CAMK2G	drug	alcohol	25837445	Differential phosphorylation of NMDAR1 <strong>CaMKII</strong> MAPKs in the rat nucleus accumbens following chronic <b>ethanol</b> exposure.
+CAMK2G	drug	alcohol	25837445	N Methyl d aspartate receptor 1 (NMDAR1), Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and extracellular signal regulated kinases (ERKs) have been demonstrated to contribute to and possibly interact in the molecular mechanism underlying <b>ethanol</b> dependence and relapse.
+CAMK2G	addiction	dependence	25837445	N Methyl d aspartate receptor 1 (NMDAR1), Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and extracellular signal regulated kinases (ERKs) have been demonstrated to contribute to and possibly interact in the molecular mechanism underlying ethanol <b>dependence</b> and relapse.
+CAMK2G	addiction	relapse	25837445	N Methyl d aspartate receptor 1 (NMDAR1), Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and extracellular signal regulated kinases (ERKs) have been demonstrated to contribute to and possibly interact in the molecular mechanism underlying ethanol dependence and <b>relapse</b>.
+CAMK2G	drug	alcohol	25837445	However, little is known regarding the mechanisms underlying the effects of <b>ethanol</b> exposure, withdrawal, and re exposure, particularly with regard to NMDAR1 <strong>CaMKII</strong> ERK signaling in accumbens subregions.
+CAMK2G	addiction	withdrawal	25837445	However, little is known regarding the mechanisms underlying the effects of ethanol exposure, <b>withdrawal</b>, and re exposure, particularly with regard to NMDAR1 <strong>CaMKII</strong> ERK signaling in accumbens subregions.
+CAMK2G	drug	alcohol	25837445	Phosphorylation of NMDAR1, <strong>CaMKII</strong> and ERK was significantly decreased in the AcbSh and AcbC following chronic <b>ethanol</b> exposure.
+CAMK2G	drug	alcohol	25837445	<b>Ethanol</b> withdrawal increased phospho NMDAR1 and phospho <strong>CaMKII</strong> expression in the AcbSh.
+CAMK2G	addiction	withdrawal	25837445	Ethanol <b>withdrawal</b> increased phospho NMDAR1 and phospho <strong>CaMKII</strong> expression in the AcbSh.
+CAMK2G	drug	alcohol	25837445	These results indicated that the activation of NMDAR1 <strong>CaMKII</strong> ERK signaling in the AcbSh but not the AcbC would contribute more to <b>ethanol</b> drinking and chronic <b>ethanol</b> related negative emotional states.
+CAMK2G	drug	amphetamine	25752339	We also found that <b>METH</b> altered the expression of the N methyl d aspartate (NMDA) receptor subunits NR2A (79.6%) and NR2B (126.7%) and Ca(2+) /calmodulin dependent protein kinase II (<strong>CAMKII</strong>) (74.0%).
+CAMK2G	drug	amphetamine	25744457	These findings suggest that BV acupuncture may exert a suppressive effect on <b>METH</b> induced addiction via regulation of signaling cascades of ΔFosB, ERK, and <strong>CaMKII</strong> in PFC and NAc.
+CAMK2G	addiction	addiction	25744457	These findings suggest that BV acupuncture may exert a suppressive effect on METH induced <b>addiction</b> via regulation of signaling cascades of ΔFosB, ERK, and <strong>CaMKII</strong> in PFC and NAc.
+CAMK2G	drug	alcohol	25579851	Accordingly, <b>alcohol</b> drinking increased α amino 3 hydroxy 5 methyl 4 isooxazole receptor (AMPAR) in central amygdala (CeA) and phosphorylation of AMPAR GluA1 subunit at a <strong>CaMKII</strong> locus (GluA1 Ser831) in CeA and lateral amygdala.
+CAMK2G	drug	alcohol	25579851	Mechanistic studies showed that targeted pharmacologic inhibition of amygdala <strong>CaMKII</strong> or AMPAR activity specifically inhibited the positive reinforcing properties of <b>alcohol</b> but not sucrose.
+CAMK2G	addiction	reward	25579851	Mechanistic studies showed that targeted pharmacologic inhibition of amygdala <strong>CaMKII</strong> or AMPAR activity specifically inhibited the positive <b>reinforcing</b> properties of alcohol but not sucrose.
+CAMK2G	drug	opioid	25446355	We found that adolescent and adult control mice significantly differed in the expression of several genes in the absence of <b>oxycodone</b> exposure, including those coding for mitogen activated protein kinase, <strong>calcium/calmodulin dependent protein kinase II gamma</strong> subunit, glutamate receptor, ionotropic AMPA2 and metabotropic 5.
+CAMK2G	drug	nicotine	25430056	Both cFos and phosphorylated cJun (p cJun) were immediately increased in the nucleus, together with an increase of calmodulin kinase (<strong>CaMK</strong>) IV but not CaMKII expression after <b>nicotine</b> exposure.
+CAMK2G	drug	nicotine	25430056	Both cFos and phosphorylated cJun (p cJun) were immediately increased in the nucleus, together with an increase of calmodulin kinase (<strong>CaMK</strong>) IV but not <strong>CaMKII</strong> expression after <b>nicotine</b> exposure.
+CAMK2G	drug	alcohol	25190810	We examine the influence of the β4 subunit on PKA, <strong>CaMKII</strong>, and phosphatase modulation of channel activity, and on molecular tolerance to <b>alcohol</b>.
+CAMK2G	drug	amphetamine	24848513	In immunoblotting analyses, calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) autophosphorylation was significantly increased following <b>METH</b> treatment in the striatum of JP DHE mice.
+CAMK2G	drug	amphetamine	24848513	However, <strong>CaMKII</strong> autophosphorylation did not changed by <b>METH</b> treatment in the striatum of JP DKO mouse.
+CAMK2G	drug	amphetamine	24848513	The lack of increased <strong>CaMKII</strong> activity in JP DKO mice was correlated with the impaired <b>METH</b> induced behavioral sensitization.
+CAMK2G	addiction	sensitization	24848513	The lack of increased <strong>CaMKII</strong> activity in JP DKO mice was correlated with the impaired METH induced behavioral <b>sensitization</b>.
+CAMK2G	drug	amphetamine	24848513	Thus, elevated CaN and aberrant <strong>CaMKII</strong> activities in the striatum of JP DKO mice likely accounts for lack of <b>METH</b> induced behavioral sensitization.
+CAMK2G	addiction	sensitization	24848513	Thus, elevated CaN and aberrant <strong>CaMKII</strong> activities in the striatum of JP DKO mice likely accounts for lack of METH induced behavioral <b>sensitization</b>.
+CAMK2G	drug	opioid	24675163	In the present study, we investigated the effect of <b>morphine</b> sensitization on mRNA expression of α and β isoforms and activity of <strong>CaMKII</strong> in the hippocampus of male rats.
+CAMK2G	addiction	sensitization	24675163	In the present study, we investigated the effect of morphine <b>sensitization</b> on mRNA expression of α and β isoforms and activity of <strong>CaMKII</strong> in the hippocampus of male rats.
+CAMK2G	drug	opioid	24675163	In addition, repeated <b>morphine</b> treatment increased mRNA expression of both α and β isoforms of <strong>CaMKII</strong> in the hippocampus.
+CAMK2G	drug	opioid	24675163	The present study also showed that induction of <b>morphine</b> sensitization significantly increased both Ca2+/calmodulin independent and Ca2+/calmodulin dependent activities of <strong>CaMK</strong> II in the rat hippocampus.
+CAMK2G	addiction	sensitization	24675163	The present study also showed that induction of morphine <b>sensitization</b> significantly increased both Ca2+/calmodulin independent and Ca2+/calmodulin dependent activities of <strong>CaMK</strong> II in the rat hippocampus.
+CAMK2G	drug	opioid	24675163	However, acute administration of <b>morphine</b> (5mg/kg) did not alter either α and β <strong>CaMKII</strong> mRNA expression or <strong>CaMKII</strong> activity in the hippocampus.
+CAMK2G	drug	opioid	24675163	The stimulation effects of <b>morphine</b> sensitization on mRNA expression and activity of <strong>CaMKII</strong> were completely abolished by administration of <b>naloxone</b>, 30min prior to s.c. injections of <b>morphine</b> (20mg/kg/day×3 days).
+CAMK2G	addiction	sensitization	24675163	The stimulation effects of morphine <b>sensitization</b> on mRNA expression and activity of <strong>CaMKII</strong> were completely abolished by administration of naloxone, 30min prior to s.c. injections of morphine (20mg/kg/day×3 days).
+CAMK2G	drug	opioid	24675163	Our data demonstrated that induction of <b>morphine</b> sensitization could effectively modulate the activity and the mRNA expression of <strong>CaMKII</strong> in the hippocampus and this effect of <b>morphine</b> was exerted by the activation of <b>opioid</b> receptors.
+CAMK2G	addiction	sensitization	24675163	Our data demonstrated that induction of morphine <b>sensitization</b> could effectively modulate the activity and the mRNA expression of <strong>CaMKII</strong> in the hippocampus and this effect of morphine was exerted by the activation of opioid receptors.
+CAMK2G	addiction	relapse	24269543	Western blotting results showed that the levels of GLT1, VGLUT2, NR2B, p ERK1/2 and p CREB expressions in the mPFC were increased and <strong>CaMKII</strong> was decreased markedly after the stress priming MAP induced CPP <b>reinstatement</b> test.
+CAMK2G	addiction	reward	24269543	Western blotting results showed that the levels of GLT1, VGLUT2, NR2B, p ERK1/2 and p CREB expressions in the mPFC were increased and <strong>CaMKII</strong> was decreased markedly after the stress priming MAP induced <b>CPP</b> reinstatement test.
+CAMK2G	drug	cocaine	24154664	<strong>CaMKII</strong> activity in the ventral tegmental area gates <b>cocaine</b> induced synaptic plasticity in the nucleus accumbens.
+CAMK2G	addiction	addiction	24154664	Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) is a central regulator of long term synaptic plasticity, learning, and drug <b>addiction</b>.
+CAMK2G	drug	cocaine	24154664	We examined whether blocking <strong>CaMKII</strong> activity in the VTA affected <b>cocaine</b> conditioned place preference (CPP) and <b>cocaine</b> evoked synaptic plasticity in its target brain region, the NAc.
+CAMK2G	addiction	reward	24154664	We examined whether blocking <strong>CaMKII</strong> activity in the VTA affected cocaine conditioned place preference (<b>CPP</b>) and cocaine evoked synaptic plasticity in its target brain region, the NAc.
+CAMK2G	drug	cocaine	24154664	We report that intra VTA microinjections of tatCN21 before <b>cocaine</b> conditioning blocked the acquisition of <b>cocaine</b> CPP, whereas intra VTA microinjections of tatCN21 before saline conditioning did not significantly affect <b>cocaine</b> CPP, suggesting that the <strong>CaMKII</strong> inhibitor blocks <b>cocaine</b> CPP through selective disruption of <b>cocaine</b> cue associated learning.
+CAMK2G	addiction	reward	24154664	We report that intra VTA microinjections of tatCN21 before cocaine conditioning blocked the acquisition of cocaine <b>CPP</b>, whereas intra VTA microinjections of tatCN21 before saline conditioning did not significantly affect cocaine <b>CPP</b>, suggesting that the <strong>CaMKII</strong> inhibitor blocks cocaine <b>CPP</b> through selective disruption of cocaine cue associated learning.
+CAMK2G	drug	cocaine	24154664	These results suggest that <strong>CaMKII</strong> activity in the VTA governs <b>cocaine</b> evoked synaptic plasticity in the NAc during the time window of <b>cocaine</b> conditioning.
+CAMK2G	drug	cocaine	23873418	The present study evaluated the hypothesis that protein kinase A (PKA) and calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) activation in the BLA is necessary for the reconsolidation of context response <b>cocaine</b> memories that promote subsequent drug context induced <b>cocaine</b> seeking behavior.
+CAMK2G	addiction	relapse	23873418	The present study evaluated the hypothesis that protein kinase A (PKA) and calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) activation in the BLA is necessary for the reconsolidation of context response cocaine memories that promote subsequent drug context induced cocaine <b>seeking</b> behavior.
+CAMK2G	drug	cocaine	23873418	PKA, but not <strong>CaMKII</strong>, activation in the BLA is critical for <b>cocaine</b> memory re stabilization processes that facilitate subsequent drug context induced instrumental <b>cocaine</b> seeking behavior.
+CAMK2G	addiction	relapse	23873418	PKA, but not <strong>CaMKII</strong>, activation in the BLA is critical for cocaine memory re stabilization processes that facilitate subsequent drug context induced instrumental cocaine <b>seeking</b> behavior.
+CAMK2G	drug	opioid	23549416	Calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) has been shown to have a critical role in <b>morphine</b> induced hyperalgesia.
+CAMK2G	addiction	sensitization	23549416	These results suggest that a temporary rise in the P <strong>CaMKII</strong> level in the central nervous system may correlate with remifentanil induced pain <b>sensitization</b> in the postoperative period.
+CAMK2G	drug	opioid	25337341	Calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) which is highly expressed in the hippocampus is known to play a pivotal role in reward related memories and <b>morphine</b> dependence.
+CAMK2G	addiction	dependence	25337341	Calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) which is highly expressed in the hippocampus is known to play a pivotal role in reward related memories and morphine <b>dependence</b>.
+CAMK2G	addiction	reward	25337341	Calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) which is highly expressed in the hippocampus is known to play a pivotal role in <b>reward</b> related memories and morphine dependence.
+CAMK2G	drug	opioid	25337341	In the present study, repeated <b>morphine</b> injections once daily for 7 days was done to induce <b>morphine</b> tolerance in male Wistar rats, after which gene expression profile of α isoform of <strong>CaMKII</strong> (CaMKIIα) in the hippocampus was evaluated upon discontinuation of <b>morphine</b> injection over 21 days of <b>morphine</b> withdrawal.
+CAMK2G	addiction	withdrawal	25337341	In the present study, repeated morphine injections once daily for 7 days was done to induce morphine tolerance in male Wistar rats, after which gene expression profile of α isoform of <strong>CaMKII</strong> (CaMKIIα) in the hippocampus was evaluated upon discontinuation of morphine injection over 21 days of morphine <b>withdrawal</b>.
+CAMK2G	drug	cocaine	23467346	Here, we demonstrate that ΔFosB is phosphorylated by CaMKIIα at the protein stabilizing Ser27 and that <strong>CaMKII</strong> is required for the <b>cocaine</b> mediated accumulation of ΔFosB in rat NAc.
+CAMK2G	drug	cocaine	23467346	Furthermore, induction of dendritic spines on NAc MSNs and increased behavioral responsiveness to <b>cocaine</b> after NAc overexpression of ΔFosB are both <strong>CaMKII</strong> dependent.
+CAMK2G	drug	cocaine	23467346	Importantly, we demonstrate for the first time induction of ΔFosB and <strong>CaMKII</strong> in the NAc of human <b>cocaine</b> addicts, suggesting possible targets for future therapeutic intervention.
+CAMK2G	drug	cocaine	23467346	These data establish that ΔFosB and <strong>CaMKII</strong> engage in a cell type  and brain region specific positive feedforward loop as a key mechanism for regulating the reward circuitry of the brain in response to chronic <b>cocaine</b>.
+CAMK2G	addiction	reward	23467346	These data establish that ΔFosB and <strong>CaMKII</strong> engage in a cell type  and brain region specific positive feedforward loop as a key mechanism for regulating the <b>reward</b> circuitry of the brain in response to chronic cocaine.
+CAMK2G	drug	cocaine	23352852	Acute <b>cocaine</b> increases phosphorylation of <strong>CaMKII</strong> and GluA1 in the dorsolateral striatum of drug naïve rats, but not <b>cocaine</b> experienced rats.
+CAMK2G	drug	cocaine	23352852	Transport of GluA1 containing AMPA glutamate receptors to synapses in the nucleus accumbens, a process that involves phosphorylation of key serine residues by <strong>CaMKII</strong>, is associated with the reinstatement of <b>cocaine</b> seeking behavior.
+CAMK2G	addiction	relapse	23352852	Transport of GluA1 containing AMPA glutamate receptors to synapses in the nucleus accumbens, a process that involves phosphorylation of key serine residues by <strong>CaMKII</strong>, is associated with the <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+CAMK2G	drug	cocaine	23352852	However, the potential role of <strong>CaMKII</strong> mediated phosphorylation of GluA1 subunits in the dorsolateral (DL) striatum during <b>cocaine</b> reinstatement has not been examined.
+CAMK2G	addiction	relapse	23352852	However, the potential role of <strong>CaMKII</strong> mediated phosphorylation of GluA1 subunits in the dorsolateral (DL) striatum during cocaine <b>reinstatement</b> has not been examined.
+CAMK2G	drug	cocaine	23352852	These results indicate that acute exposure to <b>cocaine</b> in drug naïve rats increased <strong>CaMKII</strong> mediated phosphorylation of GluA1 containing AMPA receptors in the DL striatum, an effect that was not observed during <b>cocaine</b> priming induced reinstatement of drug seeking.
+CAMK2G	addiction	relapse	23352852	These results indicate that acute exposure to cocaine in drug naïve rats increased <strong>CaMKII</strong> mediated phosphorylation of GluA1 containing AMPA receptors in the DL striatum, an effect that was not observed during cocaine priming induced <b>reinstatement</b> of drug <b>seeking</b>.
+CAMK2G	drug	cocaine	23352852	It is possible; therefore, that increased phosphorylation of <strong>CaMKII</strong> and GluA1 following acute <b>cocaine</b> is a compensatory mechanism in the DL striatum.
+CAMK2G	drug	amphetamine	23345217	Persistent reversal of enhanced <b>amphetamine</b> intake by transient <strong>CaMKII</strong> inhibition.
+CAMK2G	drug	amphetamine	23345217	<b>Amphetamine</b> exposure transiently increases Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) α expression in the nucleus accumbens (NAcc) shell and this persistently increases local GluA1 S831 phosphorylation and enhances behavioral responding to the drug.
+CAMK2G	drug	amphetamine	23345217	Here we assessed whether transiently interfering with <strong>CaMKII</strong> signaling using a dominant negative CaMKIIα mutant delivered to the NAcc shell with herpes simplex viral vectors could reverse these long lasting biochemical and behavioral effects observed following exposure to <b>amphetamine</b>.
+CAMK2G	drug	amphetamine	23345217	Remarkably, this transient inhibition of <strong>CaMKII</strong> activity produced a long lasting reversal of the increased GluA1 S831 phosphorylation levels in NAcc shell and persistently blocked the enhanced locomotor response to and self administration of <b>amphetamine</b> normally observed in rats previously exposed to the drug.
+CAMK2G	addiction	addiction	23345217	Together, these results indicate that even transient interference with <strong>CaMKII</strong> signaling may confer long lasting benefits in drug sensitized individuals and point to <strong>CaMKII</strong> and its downstream pathways as attractive therapeutic targets for the treatment of stimulant <b>addiction</b>.
+CAMK2G	addiction	dependence	23313759	The proteins calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and synapsin I are essential for neurotransmitter release and were shown to be involved in drug <b>dependence</b>.
+CAMK2G	drug	nicotine	23313759	In the current study, using pharmacological techniques, we sought to (a) complement previously published behavioral findings from our lab indicating a role for calcium dependent signaling in <b>nicotine</b> dependence and (b) expand on previously published acute biochemical and pharmacological findings indicating the relevance of calcium dependent mechanisms in acute <b>nicotine</b> responses by evaluating the function of <strong>CaMKII</strong> and synapsin I after chronic <b>nicotine</b> and withdrawal in the nucleus accumbens, a brain region implicated in drug dependence.
+CAMK2G	addiction	dependence	23313759	In the current study, using pharmacological techniques, we sought to (a) complement previously published behavioral findings from our lab indicating a role for calcium dependent signaling in nicotine <b>dependence</b> and (b) expand on previously published acute biochemical and pharmacological findings indicating the relevance of calcium dependent mechanisms in acute nicotine responses by evaluating the function of <strong>CaMKII</strong> and synapsin I after chronic nicotine and withdrawal in the nucleus accumbens, a brain region implicated in drug <b>dependence</b>.
+CAMK2G	addiction	withdrawal	23313759	In the current study, using pharmacological techniques, we sought to (a) complement previously published behavioral findings from our lab indicating a role for calcium dependent signaling in nicotine dependence and (b) expand on previously published acute biochemical and pharmacological findings indicating the relevance of calcium dependent mechanisms in acute nicotine responses by evaluating the function of <strong>CaMKII</strong> and synapsin I after chronic nicotine and <b>withdrawal</b> in the nucleus accumbens, a brain region implicated in drug dependence.
+CAMK2G	drug	nicotine	23313759	Results show that phosphorylated and total <strong>CaMKII</strong> and synapsin I protein levels were significantly increased in the nucleus accumbens after chronic <b>nicotine</b> infusion, and reduced after treatment with DHβE, but not MLA.
+CAMK2G	drug	nicotine	23313759	A spontaneous <b>nicotine</b> withdrawal assessment also revealed significant reductions in phosphorylated <strong>CaMKII</strong> and synapsin I levels 24h after cessation of <b>nicotine</b> treatment.
+CAMK2G	addiction	withdrawal	23313759	A spontaneous nicotine <b>withdrawal</b> assessment also revealed significant reductions in phosphorylated <strong>CaMKII</strong> and synapsin I levels 24h after cessation of nicotine treatment.
+CAMK2G	drug	opioid	23244430	The present review further details the potential role of second messengers like calcium (Ca2+) / calmodulin dependent protein kinase (<strong>CaMKII</strong>), nitric oxide synthase, cytokines, arachidonic acid metabolites, corticotropin releasing factor, fos and src kinases in causing <b>opioid</b> withdrawal syndrome.
+CAMK2G	addiction	withdrawal	23244430	The present review further details the potential role of second messengers like calcium (Ca2+) / calmodulin dependent protein kinase (<strong>CaMKII</strong>), nitric oxide synthase, cytokines, arachidonic acid metabolites, corticotropin releasing factor, fos and src kinases in causing opioid <b>withdrawal</b> syndrome.
+CAMK2G	addiction	dependence	22960015	Extracellular signal regulated kinases (ERKs) and Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) have been shown to contribute to the molecular mechanism underlying drug <b>dependence</b> and relapse, and there may be an interaction between the activation of ERKs and <strong>CaMKII</strong>.
+CAMK2G	addiction	relapse	22960015	Extracellular signal regulated kinases (ERKs) and Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) have been shown to contribute to the molecular mechanism underlying drug dependence and <b>relapse</b>, and there may be an interaction between the activation of ERKs and <strong>CaMKII</strong>.
+CAMK2G	drug	alcohol	22960015	However, little is known regarding the mechanisms underlying the effects of <b>alcohol</b> exposure, withdrawal, and relapse, particularly with regard to the interaction between <strong>CaMKII</strong> and ERK1/2 signaling in hippocampal subregions.
+CAMK2G	addiction	relapse	22960015	However, little is known regarding the mechanisms underlying the effects of alcohol exposure, withdrawal, and <b>relapse</b>, particularly with regard to the interaction between <strong>CaMKII</strong> and ERK1/2 signaling in hippocampal subregions.
+CAMK2G	addiction	withdrawal	22960015	However, little is known regarding the mechanisms underlying the effects of alcohol exposure, <b>withdrawal</b>, and relapse, particularly with regard to the interaction between <strong>CaMKII</strong> and ERK1/2 signaling in hippocampal subregions.
+CAMK2G	drug	alcohol	22960015	The activation of <strong>CaMKII</strong> (Thr286) correlated with the effects of <b>alcohol</b> on phospho ERK1/2.
+CAMK2G	drug	alcohol	22960015	Our results indicate that region specific activation <strong>CaMKII</strong> ERK1/2 signaling in the hippocampal CA1 and DG may play an important role in <b>alcohol</b> dependence.
+CAMK2G	addiction	dependence	22960015	Our results indicate that region specific activation <strong>CaMKII</strong> ERK1/2 signaling in the hippocampal CA1 and DG may play an important role in alcohol <b>dependence</b>.
+CAMK2G	drug	opioid	22920535	Pharmacological studies have identified a number of signaling proteins involved in <b>morphine</b> induced tolerance, including the N methyl D aspartate acid glutamate receptor (NMDAR), nitric oxide synthase (NOS), protein kinase C (PKC), protein kinase A (PKA), calcium (Ca²⁺)/calmodulin (CaM) dependent kinase II (<strong>CaMKII</strong>), delta <b>opioid</b> receptor (DOR) and the regulators of G protein signaling (RGS) proteins.
+CAMK2G	addiction	addiction	22884929	Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) is an important molecule involved in the mechanisms of learning and memory, suggesting its roles in drug <b>addiction</b>.
+CAMK2G	drug	opioid	22884929	In this study, we detected the changes of <strong>CaMKII</strong> protein levels in the nucleus accumbens (NAc), a key nucleus involved in drug reward, during the reinstatement of <b>morphine</b> seeking behavior with animal model of <b>morphine</b> self administration in rats.
+CAMK2G	addiction	relapse	22884929	In this study, we detected the changes of <strong>CaMKII</strong> protein levels in the nucleus accumbens (NAc), a key nucleus involved in drug reward, during the <b>reinstatement</b> of morphine <b>seeking</b> behavior with animal model of morphine self administration in rats.
+CAMK2G	addiction	reward	22884929	In this study, we detected the changes of <strong>CaMKII</strong> protein levels in the nucleus accumbens (NAc), a key nucleus involved in drug <b>reward</b>, during the reinstatement of morphine seeking behavior with animal model of morphine self administration in rats.
+CAMK2G	addiction	relapse	22884929	Moreover, considering that the NAc is also involved in the natural reward related learning and memory, we detected the changes of <strong>CaMKII</strong> protein levels in the NAc during the <b>reinstatement</b> of natural reward <b>seeking</b> with animal model of saccharin self administration as a control.
+CAMK2G	addiction	reward	22884929	Moreover, considering that the NAc is also involved in the natural <b>reward</b> related learning and memory, we detected the changes of <strong>CaMKII</strong> protein levels in the NAc during the reinstatement of natural <b>reward</b> seeking with animal model of saccharin self administration as a control.
+CAMK2G	drug	opioid	22884929	These results suggest that increased phosphorylation of <strong>CaMKII</strong> (Thr286) in the NAc shell is involved in the relapse to <b>opioids</b> seeking and the mechanisms underlying the reinstatement of <b>morphine</b> seeking are different from those involved in the reinstatement of natural reward seeking.
+CAMK2G	addiction	relapse	22884929	These results suggest that increased phosphorylation of <strong>CaMKII</strong> (Thr286) in the NAc shell is involved in the <b>relapse</b> to opioids <b>seeking</b> and the mechanisms underlying the <b>reinstatement</b> of morphine <b>seeking</b> are different from those involved in the <b>reinstatement</b> of natural reward <b>seeking</b>.
+CAMK2G	addiction	reward	22884929	These results suggest that increased phosphorylation of <strong>CaMKII</strong> (Thr286) in the NAc shell is involved in the relapse to opioids seeking and the mechanisms underlying the reinstatement of morphine seeking are different from those involved in the reinstatement of natural <b>reward</b> seeking.
+CAMK2G	addiction	withdrawal	22830051	After 2 days of <b>withdrawal</b>, Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) phosphorylates GluA1 subunits at Ser(831), increasing channel conductance.
+CAMK2G	addiction	withdrawal	22830051	To distinguish these possibilities, the current studies used postembedding immunogold electron microscopy to investigate alterations in <strong>CaMKII</strong> signaling at CA1 stratum radiatum synapses after 2 days of FZP <b>withdrawal</b>.
+CAMK2G	drug	benzodiazepine	22830051	The removal of <strong>CaMKII</strong> GluN2B complexes from the PSD during drug withdrawal may serve as a homeostatic mechanism to limit AMPAR mediated CA1 neuron hyperexcitability and <b>benzodiazepine</b> withdrawal anxiety.
+CAMK2G	addiction	withdrawal	22830051	The removal of <strong>CaMKII</strong> GluN2B complexes from the PSD during drug <b>withdrawal</b> may serve as a homeostatic mechanism to limit AMPAR mediated CA1 neuron hyperexcitability and benzodiazepine <b>withdrawal</b> anxiety.
+CAMK2G	drug	opioid	22579819	Inhibition of <strong>CaMKII</strong> activity in the nucleus accumbens shell blocks the reinstatement of <b>morphine</b> seeking behavior in rats.
+CAMK2G	addiction	relapse	22579819	Inhibition of <strong>CaMKII</strong> activity in the nucleus accumbens shell blocks the <b>reinstatement</b> of morphine <b>seeking</b> behavior in rats.
+CAMK2G	addiction	addiction	22579819	The Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) may be a core component in the common molecular pathways for drug <b>addiction</b>.
+CAMK2G	addiction	addiction	22579819	Moreover, studies using animal models of drug <b>addiction</b> have demonstrated that changing <strong>CaMKII</strong> activity or expression influences animals' responses to the drugs of abuse.
+CAMK2G	drug	opioid	22579819	Here, we explored the roles of <strong>CaMKII</strong> in the nucleus accumbens (NAc) shell in the extinction and reinstatement of <b>morphine</b> seeking behavior.
+CAMK2G	addiction	relapse	22579819	Here, we explored the roles of <strong>CaMKII</strong> in the nucleus accumbens (NAc) shell in the extinction and <b>reinstatement</b> of morphine <b>seeking</b> behavior.
+CAMK2G	drug	opioid	22579819	Selective <strong>CaMKII</strong> inhibitor myristoylated autocamtide 2 inhibitory peptide (myr AIP) was injected into the NAc shell of rats after the acquisition of <b>morphine</b> self administration (SA) or before the reinstatement test.
+CAMK2G	addiction	relapse	22579819	Selective <strong>CaMKII</strong> inhibitor myristoylated autocamtide 2 inhibitory peptide (myr AIP) was injected into the NAc shell of rats after the acquisition of morphine self administration (SA) or before the <b>reinstatement</b> test.
+CAMK2G	drug	opioid	22579819	Our results strongly indicate that <strong>CaMKII</strong> activity in the NAc shell is essential to the relapse to <b>morphine</b> seeking.
+CAMK2G	addiction	relapse	22579819	Our results strongly indicate that <strong>CaMKII</strong> activity in the NAc shell is essential to the <b>relapse</b> to morphine <b>seeking</b>.
+CAMK2G	addiction	addiction	22573680	While behavior in rodent <b>addiction</b> models is linked with <strong>CaMKII</strong> activity in the nucleus accumbens (NAc) shell, the key cellular adaptations that forge this link are unclear.
+CAMK2G	drug	cocaine	22573680	This study identifies <strong>CaMKII</strong> regulation of IA in NAc shell neurons as a novel cellular contributor to the sensitization of <b>cocaine</b> reward.
+CAMK2G	addiction	reward	22573680	This study identifies <strong>CaMKII</strong> regulation of IA in NAc shell neurons as a novel cellular contributor to the sensitization of cocaine <b>reward</b>.
+CAMK2G	addiction	sensitization	22573680	This study identifies <strong>CaMKII</strong> regulation of IA in NAc shell neurons as a novel cellular contributor to the <b>sensitization</b> of cocaine reward.
+CAMK2G	drug	opioid	22571262	Long term <b>methadone</b> treatment reduces phosphorylation of <strong>CaMKII</strong> in rat brain.
+CAMK2G	drug	opioid	22004981	Examining the effect of the <strong>CaMKII</strong> inhibitor administration in the locus coeruleus on the <b>naloxone</b> precipitated <b>morphine</b> withdrawal signs in rats.
+CAMK2G	addiction	withdrawal	22004981	Examining the effect of the <strong>CaMKII</strong> inhibitor administration in the locus coeruleus on the naloxone precipitated morphine <b>withdrawal</b> signs in rats.
+CAMK2G	drug	cocaine	21940447	Intra NAc pharmacological manipulations indicate that the Ca(v)1.2 activated CaM kinase II (<strong>CaMKII</strong>) mediates <b>cocaine</b> induced increase in S831 P GluA1 and that both Ca(v)1.2 activated <strong>CaMKII</strong> and extracellular signal regulated kinase 2 (ERK2) mediate the increase in GluA1 cell surface levels specific to the sensitized response.
+CAMK2G	drug	opioid	21436292	Previous studies from our laboratory and others have implicated a critical role of Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) in <b>opioid</b> tolerance and dependence.
+CAMK2G	addiction	dependence	21436292	Previous studies from our laboratory and others have implicated a critical role of Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) in opioid tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	21436292	We discovered in a preliminary study that haloperidol, a butyrophenone antipsychotic drug, inhibited <strong>CaMKII</strong>, which led us to hypothesize that haloperidol can attenuate <b>opioid</b> tolerance and dependence by inhibiting <strong>CaMKII</strong>.
+CAMK2G	addiction	dependence	21436292	We discovered in a preliminary study that haloperidol, a butyrophenone antipsychotic drug, inhibited <strong>CaMKII</strong>, which led us to hypothesize that haloperidol can attenuate opioid tolerance and <b>dependence</b> by inhibiting <strong>CaMKII</strong>.
+CAMK2G	drug	opioid	21436292	Taken together, these data suggest that haloperidol attenuates <b>opioid</b> tolerance and dependence by suppressing <strong>CaMKII</strong> activity.
+CAMK2G	addiction	dependence	21436292	Taken together, these data suggest that haloperidol attenuates opioid tolerance and <b>dependence</b> by suppressing <strong>CaMKII</strong> activity.
+CAMK2G	addiction	withdrawal	21276808	The maintenance of CP AMPARs in NAc synapses during <b>withdrawal</b> is accompanied by activation of <strong>CaMKII</strong> and ERK2 but not CaMKI.
+CAMK2G	drug	benzodiazepine	20445501	The contribution of calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) to enhanced glutamatergic synaptic strength during withdrawal from 1 week oral <b>flurazepam</b> (FZP) administration was further examined in hippocampal slices.
+CAMK2G	addiction	withdrawal	20445501	The contribution of calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) to enhanced glutamatergic synaptic strength during <b>withdrawal</b> from 1 week oral flurazepam (FZP) administration was further examined in hippocampal slices.
+CAMK2G	drug	benzodiazepine	20445501	Synaptic insertion and subsequent <strong>CaMKII</strong> alpha mediated Ser(831) phosphorylation of GluA1 homomers contribute to <b>benzodiazepine</b> withdrawal induced AMPAR potentiation and may represent an important hippocampal pathway mediating both drug induced and activity dependent plasticity.
+CAMK2G	addiction	withdrawal	20445501	Synaptic insertion and subsequent <strong>CaMKII</strong> alpha mediated Ser(831) phosphorylation of GluA1 homomers contribute to benzodiazepine <b>withdrawal</b> induced AMPAR potentiation and may represent an important hippocampal pathway mediating both drug induced and activity dependent plasticity.
+CAMK2G	addiction	sensitization	20345911	Calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) activity is necessary for the long lasting expression of locomotor <b>sensitization</b> and enhanced drug taking observed in rats previously exposed to psychostimulants.
+CAMK2G	addiction	sensitization	20089902	Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) is known to contribute to the expression of psychostimulant <b>sensitization</b> by regulating dopamine (DA) overflow from DA neuron terminals in the nucleus accumbens (NAcc).
+CAMK2G	drug	opioid	19630721	Pharmacological studies have consistently identified a number of signalling proteins relevant to <b>morphine</b> induced tolerance, including the delta <b>opioid</b> receptor (DOR), protein kinase C (PKC), protein kinase A (PKA), calcium/calmodulin dependent kinase II (<strong>CaMKII</strong>), nitric oxide synthase (NOS), N methyl D aspartate acid glutamate receptors (NMDAR), and regulators of G signalling (RGS) proteins.
+CAMK2G	drug	opioid	19630721	The active <strong>CaMKII</strong> promotes the sequestering of <b>morphine</b> activated Gbetagamma dimers by phosducin like proteins (PhLP) and of Galpha subunits by RGS proteins and tolerance to <b>opioids</b> like <b>morphine</b> develops.
+CAMK2G	drug	nicotine	19619563	In general, D2 mice were less sensitive than B6 mice to the acute effects of <b>nicotine</b>, but were more sensitive to blockade of <b>nicotine</b> induced antinociceptive responses by a calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) inhibitor.
+CAMK2G	drug	nicotine	19435931	We first show that administration of <b>nicotine</b> increases <strong>CaMKII</strong> activity in the ventral tegmental area (VTA), nucleus accumbens (NAc), and amygdala.
+CAMK2G	drug	nicotine	19435931	In contrast, alpha7 nAChR KO mice show <b>nicotine</b> induced increases in <strong>CaMKII</strong> activity and pCREB, similar to their wild type littermates.
+CAMK2G	drug	nicotine	19435931	Moreover, we show that when animals are pretreated with the <strong>CaMKII</strong> inhibitors 4 [(2S) 2 [(5 isoquinolinylsulfonyl) methylamino] 3 oxo 3 (4 phenyl 1 piperazinyl)propyl]phenyl isoquinolinesulfonic acid ester (KN 62) and N [2 [[[3 (4 chlorophenyl) 2 propenyl]methylamino]methyl]phenyl] N (2 hydroxyethyl) 4 methoxybenzenesulphonamide (KN 93), <b>nicotine</b> induced increase in the kinase activity and pCREB was attenuated in the VTA and NAc, whereas pretreatment with (2 [N (4 methoxybenzenesulfonyl)]amino N (4 chlorocinnamyl) N methylbenzylamine, phosphate) (KN 92), the inactive analog, did not alter the <b>nicotine</b> induced increase in pCREB.
+CAMK2G	drug	nicotine	19435931	Taken together, these data suggest that the <b>nicotine</b> induced increase in <strong>CaMKII</strong> activity may correlate with the <b>nicotine</b> induced increase in pSynapsin I and pCREB in the VTA and NAc via beta2 subunit containing nAChRs.
+CAMK2G	drug	nicotine	19336664	Studies suggest a role for calcium dependent mechanisms, such as L type calcium channels and calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), in the effects of <b>nicotine</b> dependence; however, the role of these mechanisms in <b>nicotine</b> mediated behaviors is unclear.
+CAMK2G	addiction	dependence	19336664	Studies suggest a role for calcium dependent mechanisms, such as L type calcium channels and calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>), in the effects of nicotine <b>dependence</b>; however, the role of these mechanisms in nicotine mediated behaviors is unclear.
+CAMK2G	drug	nicotine	19336664	Thus, the goal of this study was to elucidate the role of L type calcium channels and <strong>CaMKII</strong> in <b>nicotine</b> withdrawal behaviors.
+CAMK2G	addiction	withdrawal	19336664	Thus, the goal of this study was to elucidate the role of L type calcium channels and <strong>CaMKII</strong> in nicotine <b>withdrawal</b> behaviors.
+CAMK2G	drug	nicotine	19336664	Although our data do provide evidence of a role for <strong>CaMKII</strong> in <b>nicotine</b> withdrawal behaviors, our pharmacological and genetic assessments yielded different results concerning the specific role of the kinase.
+CAMK2G	addiction	withdrawal	19336664	Although our data do provide evidence of a role for <strong>CaMKII</strong> in nicotine <b>withdrawal</b> behaviors, our pharmacological and genetic assessments yielded different results concerning the specific role of the kinase.
+CAMK2G	drug	nicotine	19336664	Pharmacological data suggest that <strong>CaMKII</strong> is involved in somatic signs and affective <b>nicotine</b> withdrawal, and activity level is decreased after <b>nicotine</b> withdrawal, whereas the genetic assessments yielded results suggesting that <strong>CaMKII</strong> is involved only in the anxiety related response, yet the kinase activity may be increased after <b>nicotine</b> withdrawal; thus, future studies are necessary to clarify the precise behavioral specifics of the relevance of <strong>CaMKII</strong> in <b>nicotine</b> withdrawal behaviors.
+CAMK2G	addiction	withdrawal	19336664	Pharmacological data suggest that <strong>CaMKII</strong> is involved in somatic signs and affective nicotine <b>withdrawal</b>, and activity level is decreased after nicotine <b>withdrawal</b>, whereas the genetic assessments yielded results suggesting that <strong>CaMKII</strong> is involved only in the anxiety related response, yet the kinase activity may be increased after nicotine <b>withdrawal</b>; thus, future studies are necessary to clarify the precise behavioral specifics of the relevance of <strong>CaMKII</strong> in nicotine <b>withdrawal</b> behaviors.
+CAMK2G	drug	nicotine	19336664	Overall, our data show that L type calcium channels and <strong>CaMKII</strong> are relevant in <b>nicotine</b> withdrawal and differentially mediate <b>nicotine</b> withdrawal behaviors.
+CAMK2G	addiction	withdrawal	19336664	Overall, our data show that L type calcium channels and <strong>CaMKII</strong> are relevant in nicotine <b>withdrawal</b> and differentially mediate nicotine <b>withdrawal</b> behaviors.
+CAMK2G	addiction	addiction	19217370	Hooked on the D3 receptor: <strong>CaMKII</strong>'s new <b>addiction</b>.
+CAMK2G	addiction	relapse	19217370	<strong>CaMKII</strong> relieves the D3R mediated inhibition on sensitized behavior to foster drug <b>seeking</b> behavior.
+CAMK2G	drug	amphetamine	18929625	Our earlier reports showed that <b>AMPH</b> CPP results in the enhancement of hippocampal <strong>CaMKII</strong> activity and it can be impaired by NMDA antagonist (AP5).
+CAMK2G	addiction	reward	18929625	Our earlier reports showed that AMPH <b>CPP</b> results in the enhancement of hippocampal <strong>CaMKII</strong> activity and it can be impaired by NMDA antagonist (AP5).
+CAMK2G	drug	amphetamine	18929625	In this study <b>AMPH</b> CPP did not alter the NAc <strong>CaMKII</strong> activity, although <b>AMPH</b> CPP was impaired by a blockade of D1 receptors (SCH23390) during conditioning.
+CAMK2G	addiction	reward	18929625	In this study AMPH <b>CPP</b> did not alter the NAc <strong>CaMKII</strong> activity, although AMPH <b>CPP</b> was impaired by a blockade of D1 receptors (SCH23390) during conditioning.
+CAMK2G	drug	amphetamine	18694805	Inhibition of <strong>CaMKII</strong> in the nucleus accumbens shell decreases enhanced <b>amphetamine</b> intake in sensitized rats.
+CAMK2G	drug	amphetamine	18694805	Inhibiting <strong>CaMKII</strong> in this site reduced the enhanced drug intake observed in <b>AMPH</b> exposed rats to levels no longer significantly different from those of saline exposed rats.
+CAMK2G	drug	amphetamine	18694805	Thus, in a manner similar to what has been reported for sensitized locomotion and NAcc DA overflow, these results suggest that inhibiting <strong>CaMKII</strong> in the NAcc shell attenuates the enhanced motivation to obtain a drug reinforcer that is normally displayed in <b>AMPH</b> exposed rats.
+CAMK2G	drug	cocaine	18278040	<strong>CaMKII</strong>: a biochemical bridge linking accumbens dopamine and glutamate systems in <b>cocaine</b> seeking.
+CAMK2G	addiction	relapse	18278040	<strong>CaMKII</strong>: a biochemical bridge linking accumbens dopamine and glutamate systems in cocaine <b>seeking</b>.
+CAMK2G	drug	cocaine	18278040	Here we have tested whether <b>cocaine</b> reinstatement in rats depends on interactions between accumbal dopamine and glutamate systems that are mediated by Ca(2+)/calmodulin mediated kinase II (<strong>CaMKII</strong>).
+CAMK2G	addiction	relapse	18278040	Here we have tested whether cocaine <b>reinstatement</b> in rats depends on interactions between accumbal dopamine and glutamate systems that are mediated by Ca(2+)/calmodulin mediated kinase II (<strong>CaMKII</strong>).
+CAMK2G	drug	cocaine	18278040	We show that stimulation of D1 like dopamine receptors in the nucleus accumbens shell reinstates <b>cocaine</b> seeking by activating L type Ca(2+) channels and <strong>CaMKII</strong>.
+CAMK2G	addiction	relapse	18278040	We show that stimulation of D1 like dopamine receptors in the nucleus accumbens shell reinstates cocaine <b>seeking</b> by activating L type Ca(2+) channels and <strong>CaMKII</strong>.
+CAMK2G	drug	cocaine	18278040	<b>Cocaine</b> reinstatement is associated with D1 like dopamine receptor dependent increases in accumbens shell <strong>CaMKII</strong> phosphorylated on Thr286 and glutamate receptor 1 (GluR1) phosphorylated on Ser831 (a known <strong>CaMKII</strong> phosphorylation site), in addition to increases in cell surface expression of GluR1 containing AMPA receptors in the shell.
+CAMK2G	addiction	relapse	18278040	Cocaine <b>reinstatement</b> is associated with D1 like dopamine receptor dependent increases in accumbens shell <strong>CaMKII</strong> phosphorylated on Thr286 and glutamate receptor 1 (GluR1) phosphorylated on Ser831 (a known <strong>CaMKII</strong> phosphorylation site), in addition to increases in cell surface expression of GluR1 containing AMPA receptors in the shell.
+CAMK2G	drug	cocaine	18278040	Thus, <strong>CaMKII</strong> may be an essential link between accumbens shell dopamine and glutamate systems involved in the neuronal plasticity underlying <b>cocaine</b> craving and relapse.
+CAMK2G	addiction	relapse	18278040	Thus, <strong>CaMKII</strong> may be an essential link between accumbens shell dopamine and glutamate systems involved in the neuronal plasticity underlying cocaine <b>craving</b> and <b>relapse</b>.
+CAMK2G	addiction	reward	18032670	Additionally, these <strong>CaMKII</strong> Cre Cdk5 cKO mice show enhanced <b>incentive</b> motivation for food as assessed by instrumental responding on a progressive ratio schedule of <b>reinforcement</b>.
+CAMK2G	drug	amphetamine	17762518	This study investigates the roles of hippocampal N methyl D aspartate (NMDA) glutamate receptors and <strong>CaMKII</strong> (calcium/calmodulin dependent protein kinase II) in <b>amphetamine</b> produced conditioned place preference (<b>AMPH</b> CPP) in rats.
+CAMK2G	addiction	reward	17762518	This study investigates the roles of hippocampal N methyl D aspartate (NMDA) glutamate receptors and <strong>CaMKII</strong> (calcium/calmodulin dependent protein kinase II) in amphetamine produced conditioned place preference (AMPH <b>CPP</b>) in rats.
+CAMK2G	drug	amphetamine	17762518	An earlier report showed that <b>AMPH</b> CPP resulted in the enhancement of hippocampal <strong>CaMKII</strong> activity.
+CAMK2G	addiction	reward	17762518	An earlier report showed that AMPH <b>CPP</b> resulted in the enhancement of hippocampal <strong>CaMKII</strong> activity.
+CAMK2G	drug	amphetamine	17762518	In this study, <b>AMPH</b> CPP significantly increased hippocampal GluR1 receptors, though <b>AMPH</b> CPP was impaired by either blockade of NMDA receptors (AP5) or inhibition of <strong>CaMKII</strong> (KN 93) during conditioning.
+CAMK2G	addiction	reward	17762518	In this study, AMPH <b>CPP</b> significantly increased hippocampal GluR1 receptors, though AMPH <b>CPP</b> was impaired by either blockade of NMDA receptors (AP5) or inhibition of <strong>CaMKII</strong> (KN 93) during conditioning.
+CAMK2G	drug	amphetamine	17762518	These results, taken together, indicate that NMDA receptor activation and <strong>CaMKII</strong> activity are essential for the <b>AMPH</b> CPP.
+CAMK2G	addiction	reward	17762518	These results, taken together, indicate that NMDA receptor activation and <strong>CaMKII</strong> activity are essential for the AMPH <b>CPP</b>.
+CAMK2G	drug	amphetamine	17762518	<b>AMPH</b> CPP reexposure is similar to the memory reconsolidation process, being disrupted by either a blockade of the NMDA receptor or an inhibition of <strong>CaMKII</strong>.
+CAMK2G	addiction	reward	17762518	AMPH <b>CPP</b> reexposure is similar to the memory reconsolidation process, being disrupted by either a blockade of the NMDA receptor or an inhibition of <strong>CaMKII</strong>.
+CAMK2G	drug	cocaine	17609678	D Serine could participate on these effects, and the objective was to discern the role of VTA D serine after a sensitizing regimen of <b>cocaine</b> (10 mg/kg daily), and to discern consequent expression changes in <strong>CaMKII</strong> and its activated form.
+CAMK2G	addiction	sensitization	17609678	For this purpose, D serine, sodium benzoate (inhibitor of D amino acid oxidase, the degradating enzyme of D serine), and 7 chlorokynurenate (inhibitor of the glycine site of NMDA receptors) were injected into the VTA (in either the induction or expression phase of <b>sensitization</b>), and activation state of <strong>CaMKII</strong> was assessed through blotting.
+CAMK2G	drug	cocaine	17609678	<strong>CaMKII</strong> within the VTA was found to participate in D serine's effects because this kinase, that is activated after repeated <b>cocaine</b>, was further activated after co treatment with D serine or sodium benzoate.
+CAMK2G	drug	amphetamine	17603807	Recent studies have shown that the elevation in calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) may play an important role in <b>amphetamine</b> induced dopamine release, as well as in the increase of dopamine D2 receptor high affinitystates in psychosis.
+CAMK2G	drug	amphetamine	17603807	Because <b>amphetamine</b> sensitization is a widely used animal model of psychosis or schizophrenia, we investigated whether <b>amphetamine</b> sensitization results in an overall increase in the alpha and beta subunits of <strong>CaMKII</strong>.
+CAMK2G	addiction	sensitization	17603807	Because amphetamine <b>sensitization</b> is a widely used animal model of psychosis or schizophrenia, we investigated whether amphetamine <b>sensitization</b> results in an overall increase in the alpha and beta subunits of <strong>CaMKII</strong>.
+CAMK2G	drug	amphetamine	17603807	To answer this question, we measured <strong>CaMKII</strong> alpha and beta subunit mRNA expression using Real Time Quantitative PCR in <b>amphetamine</b> sensitized rat striata, compared to saline treated controls.
+CAMK2G	drug	amphetamine	17603807	Because the levels of both CaMKIIbeta and CaMKIIalpha play a role in neuronal function and synapse formation, the present finding of an elevated level of <strong>CaMKII</strong> beta and alpha subunit mRNA in the <b>amphetamine</b> sensitized model of psychosis points to the possibility of dysregulated levels of <strong>CaMKII</strong> subunits in human psychosis.
+CAMK2G	drug	opioid	17306231	Neurogranin has been suggested to serve as a common regulator synchronizing the activities of PKC and <strong>CaMKII</strong> in acute <b>opioid</b> tolerance.
+CAMK2G	drug	opioid	17306231	Antisense pretreated mice showed decreased neurogranin expression, lack of <b>morphine</b> induced phosphorylation of neurogranin and activation of <strong>CaMKII</strong> and CREB, and absence of <b>naloxone</b> induced withdrawal jumping.
+CAMK2G	addiction	withdrawal	17306231	Antisense pretreated mice showed decreased neurogranin expression, lack of morphine induced phosphorylation of neurogranin and activation of <strong>CaMKII</strong> and CREB, and absence of naloxone induced <b>withdrawal</b> jumping.
+CAMK2G	drug	opioid	17306231	Taken together, these data suggest that neurogranin plays an essential role in acute <b>opioid</b> dependence, possibly by affecting the <strong>CaMKII</strong> and CREB signaling pathway.
+CAMK2G	addiction	dependence	17306231	Taken together, these data suggest that neurogranin plays an essential role in acute opioid <b>dependence</b>, possibly by affecting the <strong>CaMKII</strong> and CREB signaling pathway.
+CAMK2G	drug	cocaine	17160679	Estrogen modulated frontal cortical <strong>CaMKII</strong> activity and behavioral supersensitization induced by prolonged <b>cocaine</b> treatment in female rats.
+CAMK2G	drug	cocaine	17160679	The study was designed to characterize the role of FCX calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) activity in the behavioral supersensitization observed in female rats after prolonged <b>cocaine</b> exposure.
+CAMK2G	drug	cocaine	17160679	FCX <strong>CaMKII</strong> activity was significantly altered by <b>cocaine</b> in females, and this effect was related to estrogen's presence; <b>cocaine</b> induced changes in striatal <strong>CaMKII</strong> activity were, however, less estrogen sensitive.
+CAMK2G	drug	cocaine	17160679	Furthermore, estrogen modulated FCX <strong>CaMKII</strong> activity in <b>cocaine</b> supersensitized rats was dependent on D(1) dopamine receptor activation.
+CAMK2G	drug	cocaine	17160679	Estrogen modulated D(1) dopamine receptor activity mediates the effects of prolonged <b>cocaine</b> exposure on FCX <strong>CaMKII</strong>, and this, in turn, may contribute to the development of behavioral supersensitivity to repeated <b>cocaine</b> treatment in intact female rats.
+CAMK2G	drug	opioid	16824682	Activation of Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and protein kinase C (PKC) are hallmarks of <b>opioid</b> tolerance and dependence.
+CAMK2G	addiction	dependence	16824682	Activation of Ca2+/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) and protein kinase C (PKC) are hallmarks of opioid tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	16824682	The effect appeared to correlate with the changes in the activities of PKC and <strong>CaMKII</strong>, and with the development of <b>opioid</b> tolerance and dependence.
+CAMK2G	addiction	dependence	16824682	The effect appeared to correlate with the changes in the activities of PKC and <strong>CaMKII</strong>, and with the development of opioid tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	16824682	Neurogranin may, therefore, provide a potential mechanism interacting with both <strong>CaMKII</strong> and PKC in <b>opioid</b> tolerance and dependence.
+CAMK2G	addiction	dependence	16824682	Neurogranin may, therefore, provide a potential mechanism interacting with both <strong>CaMKII</strong> and PKC in opioid tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	16505162	Previous studies have suggested that Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) can modulate <b>opioid</b> tolerance and dependence via its action on learning and memory.
+CAMK2G	addiction	dependence	16505162	Previous studies have suggested that Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) can modulate opioid tolerance and <b>dependence</b> via its action on learning and memory.
+CAMK2G	drug	opioid	16505162	In this study, we examined whether <strong>CaMKII</strong> could directly regulate <b>opioid</b> tolerance and dependence.
+CAMK2G	addiction	dependence	16505162	In this study, we examined whether <strong>CaMKII</strong> could directly regulate opioid tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	16505162	<strong>CaMKII</strong> activity was increased after the treatment with <b>morphine</b> (100 mg/kg s.c. or 75 mg s.c. of <b>morphine</b>/pellet/mouse); the effect exhibited a temporal correction with the development of <b>opioid</b> tolerance and dependence.
+CAMK2G	addiction	dependence	16505162	<strong>CaMKII</strong> activity was increased after the treatment with morphine (100 mg/kg s.c. or 75 mg s.c. of morphine/pellet/mouse); the effect exhibited a temporal correction with the development of opioid tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	16505162	In mice treated with <b>morphine</b> (100 mg/kg s.c.), <b>morphine</b> tolerance and dependence developed in 2 to 6 h. An acute supraspinal administration of KN93 [2 [N (2 hydroxyethyl)] N (4 methoxybenzenesulfonyl)]amino N (4 chlorocinnamyl) N methylbenzylamine)], a <strong>CaMKII</strong> inhibitor, was able to dose dependently reverse the already established antinociceptive tolerance to <b>morphine</b> (p < 0.001 for 15 30 nmol; not significant for 5 nmol).
+CAMK2G	addiction	dependence	16505162	In mice treated with morphine (100 mg/kg s.c.), morphine tolerance and <b>dependence</b> developed in 2 to 6 h. An acute supraspinal administration of KN93 [2 [N (2 hydroxyethyl)] N (4 methoxybenzenesulfonyl)]amino N (4 chlorocinnamyl) N methylbenzylamine)], a <strong>CaMKII</strong> inhibitor, was able to dose dependently reverse the already established antinociceptive tolerance to morphine (p < 0.001 for 15 30 nmol; not significant for 5 nmol).
+CAMK2G	drug	opioid	16505162	The effect of acute <strong>CaMKII</strong> inhibition was not limited to the particular experimental model, because KN93 also acutely reversed the established <b>opioid</b> tolerance and dependence in mice treated with <b>morphine</b> (75 mg/pellet/mouse s.c.) for 6 days.
+CAMK2G	addiction	dependence	16505162	The effect of acute <strong>CaMKII</strong> inhibition was not limited to the particular experimental model, because KN93 also acutely reversed the established opioid tolerance and <b>dependence</b> in mice treated with morphine (75 mg/pellet/mouse s.c.) for 6 days.
+CAMK2G	drug	opioid	16505162	Taken together, these data strongly support the hypothesis that <strong>CaMKII</strong> can act as a key and direct factor in promoting <b>opioid</b> tolerance and dependence.
+CAMK2G	addiction	dependence	16505162	Taken together, these data strongly support the hypothesis that <strong>CaMKII</strong> can act as a key and direct factor in promoting opioid tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	16380209	Calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) has been shown to play an important role in the generation and maintenance of <b>opioid</b> tolerance.
+CAMK2G	drug	opioid	16380209	<b>Morphine</b> induced a significant up regulation of supraspinal and spinal <strong>CaMKII</strong> activity in tolerant mice, which was abolished after the pretreatment or acute treatment with trifluoperazine.
+CAMK2G	drug	opioid	16380209	These data suggested that trifluoperazine was capable of suppressing <b>opioid</b> tolerance, possibly by the mechanism of inhibiting <strong>CaMKII</strong>.
+CAMK2G	drug	alcohol	16341213	In addition, the activity of Ca(2+)/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) in the cell controlled channel activity and <b>alcohol</b> modulation.
+CAMK2G	drug	alcohol	16341213	Incremental <strong>CaMKII</strong> mediated phosphorylation of Thr107 in the BK tetramer progressively increased channel activity and gradually switched the channel <b>alcohol</b> responses from robust activation to inhibition.
+CAMK2G	drug	alcohol	16341213	Thus, <strong>CaMKII</strong> phosphorylation of slo Thr107 works as a 'molecular dimmer switch' that could mediate tolerance to <b>alcohol</b>, a form of neuronal plasticity.
+CAMK2G	drug	opioid	16158186	Acute administration of <b>morphine</b> and DAMGO stimulated ERK activity and this stimulation required activation of Ca(2+)/calmodulindependent kinase II (<strong>CaMKII</strong>) and protein kinase C (PKC).
+CAMK2G	drug	opioid	16158186	The principal finding of these studies is demonstration that the activation of <strong>CaMKII</strong> and PKC is required for ERK stimulation following acute <b>opioid</b> treatment while in a chronic <b>morphine</b> treatment and withdrawal, the up regulation of PKC and <strong>CaMKII</strong> pathways seems to be engaged in the ERK inhibition.
+CAMK2G	addiction	withdrawal	16158186	The principal finding of these studies is demonstration that the activation of <strong>CaMKII</strong> and PKC is required for ERK stimulation following acute opioid treatment while in a chronic morphine treatment and <b>withdrawal</b>, the up regulation of PKC and <strong>CaMKII</strong> pathways seems to be engaged in the ERK inhibition.
+CAMK2G	drug	opioid	15464026	The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (NR2A) protein, phosphorylated Ca(2+)/calmodulin kinase II (p <strong>CaMKII</strong>) protein, c fos mRNA, c Fos protein, are observed in the specific brain areas of mice and/or rats showing signs of <b>naloxone</b> precipitated withdrawal.
+CAMK2G	addiction	withdrawal	15464026	The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (NR2A) protein, phosphorylated Ca(2+)/calmodulin kinase II (p <strong>CaMKII</strong>) protein, c fos mRNA, c Fos protein, are observed in the specific brain areas of mice and/or rats showing signs of naloxone precipitated <b>withdrawal</b>.
+CAMK2G	drug	opioid	15464026	The activation of <strong>CaMKII</strong> and increased expression of c Fos protein in the brain of animals with <b>naloxone</b> precipitated withdrawal syndrome are prevented by NMDA receptor antagonists, whereas the increased levels of extracellular glutamate are not prevented by them.
+CAMK2G	addiction	withdrawal	15464026	The activation of <strong>CaMKII</strong> and increased expression of c Fos protein in the brain of animals with naloxone precipitated <b>withdrawal</b> syndrome are prevented by NMDA receptor antagonists, whereas the increased levels of extracellular glutamate are not prevented by them.
+CAMK2G	drug	opioid	15196794	Interestingly, repeated co administration of dizocilpine and <b>morphine</b> prevented the withdrawal induced phosphorylation of Ca2+/calmodulin kinase II (p <strong>CaMK</strong> II) in the cortex, but not in the thalamus.
+CAMK2G	addiction	withdrawal	15196794	Interestingly, repeated co administration of dizocilpine and morphine prevented the <b>withdrawal</b> induced phosphorylation of Ca2+/calmodulin kinase II (p <strong>CaMK</strong> II) in the cortex, but not in the thalamus.
+CAMK2G	drug	opioid	15196794	Acute dizocilpine treatment prior to the <b>naloxone</b> challenge and repeated treatment with dizocilpine alone had no effect on analgesia, withdrawal manifestations, p <strong>CaMK</strong> II levels or c Fos protein levels.
+CAMK2G	addiction	withdrawal	15196794	Acute dizocilpine treatment prior to the naloxone challenge and repeated treatment with dizocilpine alone had no effect on analgesia, <b>withdrawal</b> manifestations, p <strong>CaMK</strong> II levels or c Fos protein levels.
+CAMK2G	drug	opioid	12580100	To observe the change of Ca2+/calmodulin dependent protein kinase II (<strong>CaMK</strong> II) signal pathway in <b>opioid</b> dependent NG108 15 cells.
+CAMK2G	drug	opioid	12580100	When <b>naloxone</b> was added to NG108 15 cells which were long term treated by DPDPE, calmodulin and <strong>CaMK</strong> II activity increased, indicating that <b>naloxone</b> withdrawal can increase Ca2+/<strong>CaMK</strong> II pathway activity.
+CAMK2G	addiction	withdrawal	12580100	When naloxone was added to NG108 15 cells which were long term treated by DPDPE, calmodulin and <strong>CaMK</strong> II activity increased, indicating that naloxone <b>withdrawal</b> can increase Ca2+/<strong>CaMK</strong> II pathway activity.
+CAMK2G	drug	opioid	12580100	The results indicate that Ca2+/<strong>CaMK</strong> II pathway was involved in the mechanisms of <b>opioids</b> dependence when DPDPE was long term administered to NG108 15 cells.
+CAMK2G	addiction	dependence	12580100	The results indicate that Ca2+/<strong>CaMK</strong> II pathway was involved in the mechanisms of opioids <b>dependence</b> when DPDPE was long term administered to NG108 15 cells.
+CAMK2G	drug	opioid	11750924	Neuroadaptive changes in signal transduction following prolonged <b>opioid</b> exposure are mediated by protein kinase systems, such as protein kinase C (PKC), cyclic AMP dependent protein kinase (PKA), Ca2+/camodulin dependent protein kinase II (<strong>CaMKII</strong>), G protein coupled receptor kinases (GRKs) and mitogen activated protein kinases (MAPKs).
+CAMK2G	drug	opioid	11146127	We have recently identified the serine residues, Ser(261) and Ser(266), within the third intracellular loop as two consensus calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) sites required for agonist induced phosphorylation and desensitization of the mu <b>opioid</b> receptor in HEK 293 cells.
+CAMK2G	drug	opioid	11146127	Since the specific pattern of mu <b>opioid</b> receptor regulation in vivo is thought to depend on the cell  and tissue specific complement of protein kinases, we examined the spatial relation between MOR1 and <strong>CaMKII</strong> in rat brain using specific antibodies.
+CAMK2G	drug	opioid	11146127	In naive or saline treated animals the mu <b>opioid</b> receptor was almost exclusively confined to the plasma membrane, while <strong>CaMKII</strong> was localized to vesicle like structures throughout the cytoplasm.
+CAMK2G	drug	opioid	11146127	After subcutaneous administration of the mu <b>opioid</b> receptor agonist, etorphine, a large proportion of the mu <b>opioid</b> receptor proteins redistributed from the plasma membrane into the cytosol where it was frequently co localized with <strong>CaMKII</strong>.
+CAMK2G	drug	opioid	11146127	Together, we identify <strong>CaMKII</strong> as a potential protein kinase, which by virtue of its colocalization with MOR1 may be in a position to phosphorylate the mu <b>opioid</b> receptor and may thus contribute to the development of tolerance to <b>opioid</b> analgesics.
+CAMK2G	drug	opioid	10984639	Based on the recent finding that calcium/calmodulin protein kinase II (<strong>CaMKII</strong>) is essential in learning and memory processes, the present study was performed to examine whether inhibition of hippocampal and amygdala <strong>CaMKII</strong> prevents the dependence and relapse to <b>morphine</b>.
+CAMK2G	addiction	dependence	10984639	Based on the recent finding that calcium/calmodulin protein kinase II (<strong>CaMKII</strong>) is essential in learning and memory processes, the present study was performed to examine whether inhibition of hippocampal and amygdala <strong>CaMKII</strong> prevents the <b>dependence</b> and relapse to morphine.
+CAMK2G	addiction	relapse	10984639	Based on the recent finding that calcium/calmodulin protein kinase II (<strong>CaMKII</strong>) is essential in learning and memory processes, the present study was performed to examine whether inhibition of hippocampal and amygdala <strong>CaMKII</strong> prevents the dependence and <b>relapse</b> to morphine.
+CAMK2G	drug	opioid	10984639	The results showed that inhibition of <strong>CaMKII</strong> by microinjection of specific inhibitors KN 62 into hippocampus decreased the <b>morphine</b> withdrawal syndromes induced by opiate antagonist <b>naloxone</b>.
+CAMK2G	addiction	withdrawal	10984639	The results showed that inhibition of <strong>CaMKII</strong> by microinjection of specific inhibitors KN 62 into hippocampus decreased the morphine <b>withdrawal</b> syndromes induced by opiate antagonist naloxone.
+CAMK2G	drug	opioid	10984639	However, inhibition of <strong>CaMKII</strong> in amygdala, but not in hippocampus, could attenuate the maintenance of <b>morphine</b> CPP.
+CAMK2G	addiction	reward	10984639	However, inhibition of <strong>CaMKII</strong> in amygdala, but not in hippocampus, could attenuate the maintenance of morphine <b>CPP</b>.
+CAMK2G	drug	opioid	10984639	These results suggest that hippocampal <strong>CaMKII</strong> is critically involved in the development of <b>morphine</b> physical and psychological dependence, and amygdala <strong>CaMKII</strong> is some different from hippocampal <strong>CaMKII</strong> in regulating the dependence and relapse to opiates.
+CAMK2G	addiction	dependence	10984639	These results suggest that hippocampal <strong>CaMKII</strong> is critically involved in the development of morphine physical and psychological <b>dependence</b>, and amygdala <strong>CaMKII</strong> is some different from hippocampal <strong>CaMKII</strong> in regulating the <b>dependence</b> and relapse to opiates.
+CAMK2G	addiction	relapse	10984639	These results suggest that hippocampal <strong>CaMKII</strong> is critically involved in the development of morphine physical and psychological dependence, and amygdala <strong>CaMKII</strong> is some different from hippocampal <strong>CaMKII</strong> in regulating the dependence and <b>relapse</b> to opiates.
+CAMK2G	drug	opioid	10385682	Based on the recent findings that calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) is essential in learning and memory processes, and <b>morphine</b> treatment increases <strong>CaMKII</strong> activity in hippocampus, the present study was undertaken to examine whether inhibition of hippocampal <strong>CaMKII</strong> prevents <b>morphine</b> tolerance and dependence.
+CAMK2G	addiction	dependence	10385682	Based on the recent findings that calcium/calmodulin dependent protein kinase II (<strong>CaMKII</strong>) is essential in learning and memory processes, and morphine treatment increases <strong>CaMKII</strong> activity in hippocampus, the present study was undertaken to examine whether inhibition of hippocampal <strong>CaMKII</strong> prevents morphine tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	10385682	Here, we report that inhibition of <strong>CaMKII</strong> by intrahippocampal dentate gyrus administration of the specific inhibitors KN 62 and KN 93 to rats significantly attenuated the tolerance to the analgesic effect of <b>morphine</b> and the abstinence syndrome precipitated by opiate antagonist <b>naloxone</b>.
+CAMK2G	drug	opioid	10385682	In contrast, both KN 04 and KN 92, the inactive structural analogs of KN 62 and KN 93, failed to attenuate <b>morphine</b> tolerance and dependence, indicating that the observed effects of KN 62 and KN 93 are mediated through inhibition of <strong>CaMKII</strong>.
+CAMK2G	addiction	dependence	10385682	In contrast, both KN 04 and KN 92, the inactive structural analogs of KN 62 and KN 93, failed to attenuate morphine tolerance and <b>dependence</b>, indicating that the observed effects of KN 62 and KN 93 are mediated through inhibition of <strong>CaMKII</strong>.
+CAMK2G	drug	opioid	10385682	Furthermore, administration of <strong>CaMKII</strong> antisense oligonucleotide into rat hippocampal dentate gyrus, which decreased the expression of <strong>CaMKII</strong> specifically, also attenuated <b>morphine</b> tolerance and dependence, while the corresponding sense oligonucleotide of <strong>CaMKII</strong> did not exhibit such inhibitory effect.
+CAMK2G	addiction	dependence	10385682	Furthermore, administration of <strong>CaMKII</strong> antisense oligonucleotide into rat hippocampal dentate gyrus, which decreased the expression of <strong>CaMKII</strong> specifically, also attenuated morphine tolerance and <b>dependence</b>, while the corresponding sense oligonucleotide of <strong>CaMKII</strong> did not exhibit such inhibitory effect.
+CAMK2G	drug	opioid	10385682	These results suggest that hippocampal <strong>CaMKII</strong> is critically involved in the development of <b>morphine</b> tolerance and dependence, and inhibition of this kinase may have some therapeutic benefit in the treatment of opiate tolerance and dependence.
+CAMK2G	addiction	dependence	10385682	These results suggest that hippocampal <strong>CaMKII</strong> is critically involved in the development of morphine tolerance and <b>dependence</b>, and inhibition of this kinase may have some therapeutic benefit in the treatment of opiate tolerance and <b>dependence</b>.
+CAMK2G	drug	opioid	10051541	Calcium/calmodulin dependent protein kinase II (<strong>CaMK</strong> II) has been shown to be involved in the regulation of <b>opioid</b> receptor signaling.
+CAMK2G	drug	opioid	10051541	The present study showed that acute <b>morphine</b> treatment significantly increased both Ca2+/calmodulin independent and Ca2+/calmodulin dependent activities of <strong>CaMK</strong> II in the rat hippocampus, with little alteration in the protein level of either alpha or beta isoform of <strong>CaMK</strong> II.
+CAMK2G	drug	opioid	10051541	However, chronic <b>morphine</b> treatment, by which rats were observed to develop apparent tolerance to <b>morphine</b>, significantly down regulated both Ca2+/calmodulin independent and Ca2+/calmodulin dependent activities of <strong>CaMK</strong> II and differentially regulated the expression of alpha and beta isoforms of <strong>CaMK</strong> II at protein and mRNA levels.
+CAMK2G	drug	opioid	10051541	Application of <b>naloxone</b> or discontinuation of <b>morphine</b> treatment after chronic <b>morphine</b> administration, which induced the withdrawal syndrome of <b>morphine</b>, resulted in the overshoot of <strong>CaMK</strong> II (at both protein and mRNA levels) and its kinase activity.
+CAMK2G	addiction	withdrawal	10051541	Application of naloxone or discontinuation of morphine treatment after chronic morphine administration, which induced the <b>withdrawal</b> syndrome of morphine, resulted in the overshoot of <strong>CaMK</strong> II (at both protein and mRNA levels) and its kinase activity.
+CAMK2G	drug	opioid	10051541	The effects of both acute and chronic <b>morphine</b> treatments on <strong>CaMK</strong> II could be completely abolished by the concomitant application of <b>naloxone</b>, indicating that the effects of <b>morphine</b> were achieved through activation of <b>opioid</b> receptors.
+CAMK2G	drug	opioid	10051541	Our data demonstrated that both acute and chronic <b>morphine</b> treatments could effectively modulate the activity and the expression of <strong>CaMK</strong> II in the hippocampus.
+MAOA	addiction	addiction	32454163	The use of the areca nut increases both brain serotonin and noradrenaline levels, whereas arecoline, a potentially <b>addictive</b> areca nut component, has monoamine oxidase A (<strong>MAO A</strong>) inhibitor like properties.
+MAOA	addiction	addiction	32454163	The use of the areca nut increases both brain serotonin and noradrenaline levels, whereas arecoline, a potentially <b>addictive</b> areca nut component, has <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) inhibitor like properties.
+MAOA	drug	nicotine	32241179	Highlight article: Genetic interaction between two VNTRs in the <strong>MAOA</strong> gene is associated with the <b>nicotine</b> dependence.
+MAOA	addiction	dependence	32241179	Highlight article: Genetic interaction between two VNTRs in the <strong>MAOA</strong> gene is associated with the nicotine <b>dependence</b>.
+MAOA	drug	nicotine	32241179	The present study combined the analysis of two transcriptional regulators, uVNTR and dVNTR, in the <strong>MAOA</strong> gene that is an enzyme responsible for the monoamine degradation and identified genetic interaction between these VNTRs in association with the <b>nicotine</b> dependence.
+MAOA	addiction	dependence	32241179	The present study combined the analysis of two transcriptional regulators, uVNTR and dVNTR, in the <strong>MAOA</strong> gene that is an enzyme responsible for the monoamine degradation and identified genetic interaction between these VNTRs in association with the nicotine <b>dependence</b>.
+MAOA	drug	nicotine	31768332	The results showed that the heated <b>tobacco</b> product <b>Tobacco</b> Heating System (THS) 2.2 and the MESH 1.1 e cigarette possessed no MAO inhibitory activity while 3R4F significantly inhibits the levels of MAO activity (3R4F <strong>MAO A</strong> and B; > 2 μM <b>nicotine</b>).
+MAOA	drug	nicotine	31768332	Snus products have similar inhibition profiles as 3R4F but for larger <b>nicotine</b> concentrations (snus <strong>MAO A</strong>; ∼68 fold, snus MAO B; ∼23 fold higher compared to 3R4F).
+MAOA	addiction	withdrawal	30774343	During early cigarette <b>withdrawal</b> there is an elevation in the levels of monoamine oxidase A (<strong>MAO A</strong>), which removes monoamines excessively and induces oxidative stress and is implicated in creating sad mood.
+MAOA	addiction	withdrawal	30774343	During early cigarette <b>withdrawal</b> there is an elevation in the levels of <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>), which removes monoamines excessively and induces oxidative stress and is implicated in creating sad mood.
+MAOA	drug	nicotine	30456877	Interactions between <strong>monoamine oxidase A</strong> rs1137070 and <b>smoking</b> on brain structure and function in male <b>smokers</b>.
+MAOA	drug	nicotine	30456877	The monoamine oxidase A (<strong>MAOA</strong>) enzyme metabolizes monoamine neurotransmitters such as dopamine, serotonin and norepinephrine, and its genetic polymorphism (rs1137070) influences its activity level and is associated with <b>smoking</b> behaviors.
+MAOA	drug	nicotine	30456877	The <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) enzyme metabolizes monoamine neurotransmitters such as dopamine, serotonin and norepinephrine, and its genetic polymorphism (rs1137070) influences its activity level and is associated with <b>smoking</b> behaviors.
+MAOA	drug	nicotine	30456877	These findings suggest that <strong>MAOA</strong> rs1137070 contributes to the susceptibility to <b>nicotine</b> dependence through its influence on brain circuits involved in reward and attention, and interacts with <b>smoking</b> in the progression.
+MAOA	addiction	dependence	30456877	These findings suggest that <strong>MAOA</strong> rs1137070 contributes to the susceptibility to nicotine <b>dependence</b> through its influence on brain circuits involved in reward and attention, and interacts with smoking in the progression.
+MAOA	addiction	reward	30456877	These findings suggest that <strong>MAOA</strong> rs1137070 contributes to the susceptibility to nicotine dependence through its influence on brain circuits involved in <b>reward</b> and attention, and interacts with smoking in the progression.
+MAOA	drug	alcohol	30414913	Early life stress and voluntary <b>alcohol</b> consumption in relation to <strong>Maoa</strong> methylation in male rats.
+MAOA	drug	alcohol	30414913	Monoamine oxidase A (<strong>Maoa</strong>) encodes the enzyme that metabolizes monoaminergic neurotransmitters crucial for the stress response, <b>alcohol</b> reward, and reinforcement.
+MAOA	addiction	reward	30414913	Monoamine oxidase A (<strong>Maoa</strong>) encodes the enzyme that metabolizes monoaminergic neurotransmitters crucial for the stress response, alcohol <b>reward</b>, and <b>reinforcement</b>.
+MAOA	drug	alcohol	30414913	<strong>Monoamine oxidase A</strong> (<strong>Maoa</strong>) encodes the enzyme that metabolizes monoaminergic neurotransmitters crucial for the stress response, <b>alcohol</b> reward, and reinforcement.
+MAOA	addiction	reward	30414913	<strong>Monoamine oxidase A</strong> (<strong>Maoa</strong>) encodes the enzyme that metabolizes monoaminergic neurotransmitters crucial for the stress response, alcohol <b>reward</b>, and <b>reinforcement</b>.
+MAOA	drug	alcohol	30414913	Previously, we reported lower <strong>Maoa</strong> expression in the nucleus accumbens and dorsal striatum of male rats exposed to ELS during the first three postnatal weeks, and to voluntary <b>alcohol</b> consumption in adulthood, compared with controls.
+MAOA	drug	alcohol	30414913	The present study continued to investigate the effect of ELS and <b>alcohol</b> consumption on <strong>Maoa</strong> methylation, and its relation to <strong>Maoa</strong> expression in these animals.
+MAOA	drug	alcohol	30414913	CpG specific methylation correlated with <strong>Maoa</strong> expression, corticosterone levels, and <b>alcohol</b> consumption in a brain region specific manner.
+MAOA	drug	alcohol	30414913	CpG specific methylation in the <strong>Maoa</strong> promoter was a potential moderator of the interaction of ELS with <b>alcohol</b> consumption on <strong>Maoa</strong> expression in the NAc.
+MAOA	drug	alcohol	30414913	In conclusion, CpG specific <strong>Maoa</strong> methylation in the promoter and intron 1 may associate with ELS, <b>alcohol</b> consumption, and <strong>Maoa</strong> expression in reward related brain regions.
+MAOA	addiction	reward	30414913	In conclusion, CpG specific <strong>Maoa</strong> methylation in the promoter and intron 1 may associate with ELS, alcohol consumption, and <strong>Maoa</strong> expression in <b>reward</b> related brain regions.
+MAOA	drug	alcohol	30192917	The current candidate gene and environment interaction (cGxE) study examined whether the effects of an experimentally manipulated psychosocial stressor on self reported drinking urge and implicit attentional bias for <b>alcohol</b> cues differ as a function of a cumulative genetic score of 5 HTTLPR, <strong>MAO A</strong>, DRD4, DAT1 and DRD2 genotypes.
+MAOA	drug	amphetamine	30091820	In addition, we measured expression levels of dopamine and dopamine related genes (<strong>monoamine oxidase A</strong>, DA receptor 1, DA receptor 2, DA active transporter, tyrosine hydroxylase and cAMP response element binding protein 1) in the striatum of the mice after repeated <b>METH</b> treatments, using qRT PCR.
+MAOA	drug	alcohol	29600412	We investigated whether methylation in a region spanning the <strong>MAOA</strong> first exon and part of the first intron was associated with PA and/or SA, <strong>MAOA</strong> genotype, <b>alcohol</b> dependence, drug dependence, depression disorders, anxiety disorders, and conduct disorder.
+MAOA	addiction	dependence	29600412	We investigated whether methylation in a region spanning the <strong>MAOA</strong> first exon and part of the first intron was associated with PA and/or SA, <strong>MAOA</strong> genotype, alcohol <b>dependence</b>, drug <b>dependence</b>, depression disorders, anxiety disorders, and conduct disorder.
+MAOA	drug	alcohol	29600412	SA, not PA, was associated with hypermethylation of the <strong>MAOA</strong> first exon relative to no abuse, and the association was robust to adjustment for psychoactive medication, <b>alcohol</b> and drug dependence, and current substance use.
+MAOA	addiction	dependence	29600412	SA, not PA, was associated with hypermethylation of the <strong>MAOA</strong> first exon relative to no abuse, and the association was robust to adjustment for psychoactive medication, alcohol and drug <b>dependence</b>, and current substance use.
+MAOA	drug	alcohol	29549852	Elevated <strong>monoamine oxidase A</strong> activity and protein levels in rodent brain during acute withdrawal after chronic intermittent <b>ethanol</b> vapor exposure.
+MAOA	addiction	withdrawal	29549852	Elevated <strong>monoamine oxidase A</strong> activity and protein levels in rodent brain during acute <b>withdrawal</b> after chronic intermittent ethanol vapor exposure.
+MAOA	drug	alcohol	29549852	Elevations in <strong>MAO A</strong> level, especially in the prefrontal and anterior cingulate cortex (PFC and ACC), are associated with low mood states, including the dysphoria of early <b>alcohol</b> withdrawal in humans.
+MAOA	addiction	withdrawal	29549852	Elevations in <strong>MAO A</strong> level, especially in the prefrontal and anterior cingulate cortex (PFC and ACC), are associated with low mood states, including the dysphoria of early alcohol <b>withdrawal</b> in humans.
+MAOA	drug	alcohol	29549852	The aim of the present study was to determine whether chronic <b>alcohol</b> vapor exposure causes an upregulation of <strong>MAO A</strong> activity or level in the PFC and ACC of rodents during acute withdrawal.
+MAOA	addiction	withdrawal	29549852	The aim of the present study was to determine whether chronic alcohol vapor exposure causes an upregulation of <strong>MAO A</strong> activity or level in the PFC and ACC of rodents during acute <b>withdrawal</b>.
+MAOA	drug	alcohol	29549852	<strong>MAO A</strong> activity and protein levels were measured immediately after exposure, acute withdrawal (24 h), protracted withdrawal (4 day), and protracted abstinence (3 weeks) (n = 16/group; 8 <b>alcohol</b> exposed, 8 control).
+MAOA	addiction	withdrawal	29549852	<strong>MAO A</strong> activity and protein levels were measured immediately after exposure, acute <b>withdrawal</b> (24 h), protracted <b>withdrawal</b> (4 day), and protracted abstinence (3 weeks) (n = 16/group; 8 alcohol exposed, 8 control).
+MAOA	drug	alcohol	29549852	Chronic <b>ethanol</b> vapor exposure significantly elevated <strong>MAO A</strong> activity and protein levels in the PFC and ACC at 24 h withdrawal (multivariate analysis of variance (MANOVA), activity: F2,13 = 3.82, p = .05, protein: F2,13 = 5.13, p = .02).
+MAOA	addiction	withdrawal	29549852	Chronic ethanol vapor exposure significantly elevated <strong>MAO A</strong> activity and protein levels in the PFC and ACC at 24 h <b>withdrawal</b> (multivariate analysis of variance (MANOVA), activity: F2,13 = 3.82, p = .05, protein: F2,13 = 5.13, p = .02).
+MAOA	drug	alcohol	29549852	The results of this study suggest a causal relationship between acute <b>alcohol</b> withdrawal and elevated <strong>MAO A</strong> levels and activity, clarifying the observation of greater <strong>MAO A</strong> binding in human <b>alcohol</b> withdrawal.
+MAOA	addiction	withdrawal	29549852	The results of this study suggest a causal relationship between acute alcohol <b>withdrawal</b> and elevated <strong>MAO A</strong> levels and activity, clarifying the observation of greater <strong>MAO A</strong> binding in human alcohol <b>withdrawal</b>.
+MAOA	drug	alcohol	29549852	This has important implications for developing methods of targeting <strong>MAO A</strong> and/or sequelae of its dysregulation in <b>alcohol</b> dependence.
+MAOA	addiction	dependence	29549852	This has important implications for developing methods of targeting <strong>MAO A</strong> and/or sequelae of its dysregulation in alcohol <b>dependence</b>.
+MAOA	drug	nicotine	28858992	We studied the 1460 C/T variation and the variable number tandem repeat polymorphism in the <strong>MAOA</strong> gene and A/G variation in intron 13 in the MAOB gene together with four DNA methylation sites in both of these genes in relation to several <b>smoking</b> related phenotypes in a study population of 1230 Whites of Russian origin.
+MAOA	drug	nicotine	28858992	The genotypes studied were found to be associated with <b>smoking</b> status in women; the MAOB G variant allele was more prevalent in female <b>smokers</b> than nonsmokers [odds ratio (OR): 2.16, 95% confidence interval (CI): 1.08 4.33], whereas a reverse relation was observed for the <strong>MAOA</strong> 1460 T variant allele (OR: 0.44, 95% CI: 0.21 0.91) and variable number tandem repeat low activity alleles (OR: 0.49, 95% CI: 0.24 0.98).
+MAOA	drug	nicotine	28858992	Moreover, the mean methylation values of the CpG sites studied in the <strong>MAOA</strong> gene were related to <b>smoking</b> behavior in women.
+MAOA	drug	nicotine	28742414	In the phase of active/chronic <b>smoking</b>, depressive symptoms are characterized as comorbidity related to an enhancement of dopamine release, and <b>smokers</b> have decreased Monoamine oxidase A (<strong>MAO A</strong>).
+MAOA	drug	nicotine	28742414	In the phase of active/chronic <b>smoking</b>, depressive symptoms are characterized as comorbidity related to an enhancement of dopamine release, and <b>smokers</b> have decreased <strong>Monoamine oxidase A</strong> (<strong>MAO A</strong>).
+MAOA	drug	nicotine	28742414	In the withdrawal phase, depressive symptoms are related to the withdrawal syndrome and increased <strong>MAO A</strong>. Stimuli fMRI studies show that there is a negative correlation between level of depressive symptoms and reactivity to negative stimuli in recent abstinent <b>smokers</b>.
+MAOA	addiction	withdrawal	28742414	In the <b>withdrawal</b> phase, depressive symptoms are related to the <b>withdrawal</b> syndrome and increased <strong>MAO A</strong>. Stimuli fMRI studies show that there is a negative correlation between level of depressive symptoms and reactivity to negative stimuli in recent abstinent smokers.
+MAOA	drug	amphetamine	28400844	In addition, both dopamine and tyrosine hydroxylase (TH) levels decreased but monoamine oxidase A (<strong>MAO A</strong>) levels increased in the NAc of the <b>METH</b> treated mice receiving EA compared with those not receiving EA.
+MAOA	drug	amphetamine	28400844	In addition, both dopamine and tyrosine hydroxylase (TH) levels decreased but <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) levels increased in the NAc of the <b>METH</b> treated mice receiving EA compared with those not receiving EA.
+MAOA	drug	amphetamine	28400844	EA may be a useful nonpharmacological approach for treating <b>METH</b> induced behavioral changes, probably because it reduces the <b>METH</b> induced TH expression and dopamine levels and raises <strong>MAO A</strong> expression in the NAc.
+MAOA	drug	opioid	28345608	<strong>MAOA</strong> rs1137070 and <b>heroin</b> addiction interactively alter gray matter volume of the salience network.
+MAOA	addiction	addiction	28345608	<strong>MAOA</strong> rs1137070 and heroin <b>addiction</b> interactively alter gray matter volume of the salience network.
+MAOA	drug	alcohol	28345608	The rs1137070 polymorphism of monoamine oxidase A (<strong>MAOA</strong>) is associated with <b>alcoholism</b> and smoking behavior.
+MAOA	drug	nicotine	28345608	The rs1137070 polymorphism of monoamine oxidase A (<strong>MAOA</strong>) is associated with alcoholism and <b>smoking</b> behavior.
+MAOA	drug	alcohol	28345608	The rs1137070 polymorphism of <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) is associated with <b>alcoholism</b> and smoking behavior.
+MAOA	drug	nicotine	28345608	The rs1137070 polymorphism of <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) is associated with alcoholism and <b>smoking</b> behavior.
+MAOA	drug	opioid	28345608	These findings suggest that the low activity related C allele of <strong>MAOA</strong> rs1137070 is associated with an increase in the sensitivity to <b>heroin</b> addiction and the damaging effects of <b>heroin</b> abuse on cognition and the salience network.
+MAOA	addiction	addiction	28345608	These findings suggest that the low activity related C allele of <strong>MAOA</strong> rs1137070 is associated with an increase in the sensitivity to heroin <b>addiction</b> and the damaging effects of heroin abuse on cognition and the salience network.
+MAOA	drug	nicotine	28057462	Our aim was to test the contribution of the harman and norharman in <b>tobacco</b> smoke to <strong>MAO A</strong> inhibition from <b>tobacco</b> smoke preparations, as part of a re examination of harman and norharman as the cause of the inhibition of <strong>MAO A</strong> inhibition in the brain.
+MAOA	drug	nicotine	28057462	At a <b>nicotine</b> concentration of 0.6μM (a "physiological" concentration in blood) the total <strong>monoamine oxidase A</strong> inhibitory activity measured in these samples was sufficient to inhibit the enzyme by approximately 10%.
+MAOA	drug	nicotine	28057462	These results show that harman and norharman provide only a moderate contribution to the total <strong>monoamine oxidase A</strong> inhibitory activity of <b>tobacco</b> smoke, perhaps under 10%.
+MAOA	drug	alcohol	27333729	There are only a few studies of <b>alcohol</b> addiction researching the connections of the MAO coding gene polymorphism and <b>alcoholism</b>; however, these studies are primarily related to the variable number of tandem repeats (VTNR) polymorphism in the regulatory gene region for <strong>MAO A</strong>, considered to influence the transcription activity/functionality of the enzyme.
+MAOA	addiction	addiction	27333729	There are only a few studies of alcohol <b>addiction</b> researching the connections of the MAO coding gene polymorphism and alcoholism; however, these studies are primarily related to the variable number of tandem repeats (VTNR) polymorphism in the regulatory gene region for <strong>MAO A</strong>, considered to influence the transcription activity/functionality of the enzyme.
+MAOA	drug	psychedelics	27230395	The mechanisms responsible for the anti addictive properties of <b>ayahuasca</b> and its alkaloids are not clarified, apparently involving both peripheral <strong>MAO A</strong> inhibition by the β carbolines and central agonism of DMT at 5 HT2A receptors expressed in brain regions related to the regulation of mood and emotions.
+MAOA	addiction	addiction	27230395	The mechanisms responsible for the anti <b>addictive</b> properties of ayahuasca and its alkaloids are not clarified, apparently involving both peripheral <strong>MAO A</strong> inhibition by the β carbolines and central agonism of DMT at 5 HT2A receptors expressed in brain regions related to the regulation of mood and emotions.
+MAOA	addiction	addiction	27064247	Polymorphisms in genes such as DAT1, 5HTTLPR, D4DR4, and <strong>MAO A</strong> have been linked to attention deficit hyperactivity disorder (ADHD) and susceptibility for opiate <b>addiction</b>.
+MAOA	drug	nicotine	26955970	The results show that (1) tranylcypromine (TCP), a known MAO inhibitor, increases sensitivity to the primary reinforcing effects of <b>nicotine</b>, shifting the dose response curve for <b>nicotine</b> to the left, (2) inhibition of <strong>MAO A</strong>, but not MAO B, increases low dose <b>nicotine</b> self administration, (3) partial <strong>MAO A</strong> inhibition, to the degree observed in chronic cigarette <b>smokers</b>, also increases low dose <b>nicotine</b> self administration, and (4) TCP decreases the threshold <b>nicotine</b> dose required for reinforcement enhancement.
+MAOA	addiction	reward	26955970	The results show that (1) tranylcypromine (TCP), a known MAO inhibitor, increases sensitivity to the primary <b>reinforcing</b> effects of nicotine, shifting the dose response curve for nicotine to the left, (2) inhibition of <strong>MAO A</strong>, but not MAO B, increases low dose nicotine self administration, (3) partial <strong>MAO A</strong> inhibition, to the degree observed in chronic cigarette smokers, also increases low dose nicotine self administration, and (4) TCP decreases the threshold nicotine dose required for <b>reinforcement</b> enhancement.
+MAOA	drug	nicotine	26955970	The results of the present experiments suggest cigarette smoke constituents that inhibit <strong>MAO A</strong>, in the range seen in chronic <b>smokers</b>, are likely to increase the primary reinforcing and reinforcement enhancing effects of low doses of <b>nicotine</b>.
+MAOA	addiction	reward	26955970	The results of the present experiments suggest cigarette smoke constituents that inhibit <strong>MAO A</strong>, in the range seen in chronic smokers, are likely to increase the primary <b>reinforcing</b> and <b>reinforcement</b> enhancing effects of low doses of nicotine.
+MAOA	drug	nicotine	26955970	If the FDA reduces the <b>nicotine</b> content of cigarettes, then variability in constituents that inhibit <strong>MAO A</strong> could impact <b>smoking</b>.
+MAOA	drug	alcohol	26645625	Effect of voluntary <b>alcohol</b> consumption on <strong>Maoa</strong> expression in the mesocorticolimbic brain of adult male rats previously exposed to prolonged maternal separation.
+MAOA	drug	alcohol	26645625	Discordant associations between monoamine oxidase A (<strong>MAOA</strong>) genotype and high <b>alcohol</b> drinking have been reported in human and non human primates.
+MAOA	drug	alcohol	26645625	Discordant associations between <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) genotype and high <b>alcohol</b> drinking have been reported in human and non human primates.
+MAOA	drug	alcohol	26645625	The present study investigated whether early life stress and subsequent adult episodic <b>alcohol</b> consumption affect <strong>Maoa</strong> expression in stress  and reward related brain regions in the rat.
+MAOA	addiction	reward	26645625	The present study investigated whether early life stress and subsequent adult episodic alcohol consumption affect <strong>Maoa</strong> expression in stress  and <b>reward</b> related brain regions in the rat.
+MAOA	drug	alcohol	26645625	After <b>alcohol</b> consumption, lower blood corticosterone and <strong>Maoa</strong> expression in the NAc and DS were found in rats exposed to early life stress compared with control rats.
+MAOA	drug	alcohol	26645625	<b>Alcohol</b> intake before death correlated negatively with <strong>Maoa</strong> expression in DS in high <b>alcohol</b> drinking rats exposed to early life stress.
+MAOA	drug	alcohol	26645625	<strong>Maoa</strong> expression is sensitive to adulthood voluntary <b>alcohol</b> consumption in the presence of early life stress in outbred rats.
+MAOA	drug	alcohol	26645625	These findings add knowledge of the molecular basis of the previously reported associations between early life stress, <strong>MAOA</strong> and susceptibility to <b>alcohol</b> misuse.
+MAOA	drug	nicotine	26508396	The identified data show a clear association between <b>smoking</b> and lower density of <strong>MAO A</strong> and MAO B binding sites in the brains of <b>smokers</b> and strong evidence that MAO is inhibited by a substance or substances in, or derived from, <b>tobacco</b> smoke.
+MAOA	drug	alcohol	26447226	Conversely, some alleles of the 12 SNPs from the DRD2 locus and the 5 from the <strong>MAOA</strong> locus showed significant associations with excessive <b>alcohol</b> consumption.
+MAOA	drug	alcohol	26447226	DRD2 rs1800497 and rs877138 were significantly associated in men, whereas DRD2 rs17601612 and rs4936271 and <strong>MAOA</strong> rs5906898 were associated with excessive <b>alcohol</b> consumption in women.
+MAOA	drug	opioid	26298506	Association between variable number of tandem repeats (VNTR) polymorphism in the promoter region of monoamine oxidase A (<strong>MAOA</strong>) gene and susceptibility to <b>heroin</b> dependence.
+MAOA	addiction	dependence	26298506	Association between variable number of tandem repeats (VNTR) polymorphism in the promoter region of monoamine oxidase A (<strong>MAOA</strong>) gene and susceptibility to heroin <b>dependence</b>.
+MAOA	drug	opioid	26298506	Association between variable number of tandem repeats (VNTR) polymorphism in the promoter region of <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) gene and susceptibility to <b>heroin</b> dependence.
+MAOA	addiction	dependence	26298506	Association between variable number of tandem repeats (VNTR) polymorphism in the promoter region of <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) gene and susceptibility to heroin <b>dependence</b>.
+MAOA	drug	alcohol	26148813	<strong>MAOA</strong> expression predicts vulnerability for <b>alcohol</b> use.
+MAOA	drug	alcohol	26148813	The role of the monoamines dopamine (DA) and serotonin (5HT) and the monoamine metabolizing enzyme monoamine oxidase A (<strong>MAOA</strong>) have been repeatedly implicated in studies of <b>alcohol</b> use and dependence.
+MAOA	addiction	dependence	26148813	The role of the monoamines dopamine (DA) and serotonin (5HT) and the monoamine metabolizing enzyme monoamine oxidase A (<strong>MAOA</strong>) have been repeatedly implicated in studies of alcohol use and <b>dependence</b>.
+MAOA	drug	alcohol	26148813	The role of the monoamines dopamine (DA) and serotonin (5HT) and the monoamine metabolizing enzyme <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) have been repeatedly implicated in studies of <b>alcohol</b> use and dependence.
+MAOA	addiction	dependence	26148813	The role of the monoamines dopamine (DA) and serotonin (5HT) and the monoamine metabolizing enzyme <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) have been repeatedly implicated in studies of alcohol use and <b>dependence</b>.
+MAOA	drug	alcohol	26148813	Genetic investigations of <strong>MAOA</strong> have yielded conflicting associations between a common polymorphism (<strong>MAOA</strong> LPR) and risk for <b>alcohol</b> abuse.
+MAOA	drug	alcohol	26148813	The present study provides direct comparison of tissue specific <strong>MAOA</strong> expression and the level of <b>alcohol</b> consumption.
+MAOA	drug	alcohol	26148813	We analyzed rhesus macaque <strong>MAOA</strong> (rhMAOA) expression in blood from males before and after 12 months of <b>alcohol</b> self administration.
+MAOA	drug	alcohol	26148813	These results provide novel evidence that blood <strong>MAOA</strong> expression predicts <b>alcohol</b> consumption and that heavy <b>alcohol</b> use is linked to low <strong>MAOA</strong> expression in both the blood and NAc core.
+MAOA	drug	alcohol	26148813	Together, the findings suggest a mechanistic link between dampened <strong>MAOA</strong> expression, elevated DA and <b>alcohol</b> abuse.
+MAOA	drug	nicotine	26015071	Effects of Interaction Between Dopamine D2 Receptor and <strong>Monoamine Oxidase A</strong> Genes on <b>Smoking</b> Status in Young Men.
+MAOA	drug	nicotine	26015071	Although the effect of gene gene interaction on <b>nicotine</b> dopamine metabolism for <b>smoking</b> behavior has been reported, polymorphisms of dopamine D2 receptor (DRD2) and monoamine oxidase A (<strong>MAOA</strong>) have not been simultaneously examined among <b>smokers</b>.
+MAOA	drug	nicotine	26015071	Although the effect of gene gene interaction on <b>nicotine</b> dopamine metabolism for <b>smoking</b> behavior has been reported, polymorphisms of dopamine D2 receptor (DRD2) and <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) have not been simultaneously examined among <b>smokers</b>.
+MAOA	drug	nicotine	26015071	In this study, 481 young Taiwanese men completed a self report questionnaire on <b>smoking</b> status, and data were obtained on polymorphisms of DRD2 rs1800497, DRD2 rs1079597, <strong>MAOA</strong> rs309850, and <strong>MAOA</strong> rs1137070, urinary <b>nicotine</b>, and urinary cotinine.
+MAOA	drug	nicotine	26015071	Among <b>smokers</b> with DRD2 rs1079597 GG//<strong>MAOA</strong> rs309850 3 repeat, the OR of heavier <b>smoking</b> was 2.67 times higher (95% confidence interval [CI]: [1.08, 6.59], p = .031) and the score on the Fagerstrom test for <b>nicotine</b> dependence was higher (4.26 vs. 2.83) than in those with DRD2 rs1079597 AA//<strong>MAOA</strong> rs309850 3 repeat.
+MAOA	addiction	dependence	26015071	Among smokers with DRD2 rs1079597 GG//<strong>MAOA</strong> rs309850 3 repeat, the OR of heavier smoking was 2.67 times higher (95% confidence interval [CI]: [1.08, 6.59], p = .031) and the score on the Fagerstrom test for nicotine <b>dependence</b> was higher (4.26 vs. 2.83) than in those with DRD2 rs1079597 AA//<strong>MAOA</strong> rs309850 3 repeat.
+MAOA	drug	nicotine	26015071	These findings suggest that the interaction of DRD2 rs1079597 and <strong>MAOA</strong> rs309850 3 repeat affects <b>smoking</b> intensity in young Taiwanese men.
+MAOA	drug	nicotine	25857233	The human cytochrome P450 2A6 (CYP2A6) and monoamine oxidases (<strong>MAO A</strong> and MAO B), catalyzing <b>nicotine</b> and dopamine metabolisms, respectively, are two therapeutic targets of <b>nicotine</b> dependence.
+MAOA	addiction	dependence	25857233	The human cytochrome P450 2A6 (CYP2A6) and monoamine oxidases (<strong>MAO A</strong> and MAO B), catalyzing nicotine and dopamine metabolisms, respectively, are two therapeutic targets of nicotine <b>dependence</b>.
+MAOA	drug	alcohol	25809512	Monoamine oxidase a promoter variable number of tandem repeats (<strong>MAOA</strong> uVNTR) in <b>alcoholics</b> according to Lesch typology.
+MAOA	drug	alcohol	25809512	<strong>Monoamine oxidase a</strong> promoter variable number of tandem repeats (<strong>MAOA</strong> uVNTR) in <b>alcoholics</b> according to Lesch typology.
+MAOA	drug	alcohol	25809512	The aim of this study was to examine the association between the <strong>MAOA</strong> uVNTR gene polymorphism in a homogeneous subgroups of patients with <b>alcohol</b> dependence categorized according to Lesch's typology.
+MAOA	addiction	dependence	25809512	The aim of this study was to examine the association between the <strong>MAOA</strong> uVNTR gene polymorphism in a homogeneous subgroups of patients with alcohol <b>dependence</b> categorized according to Lesch's typology.
+MAOA	drug	alcohol	25809512	We found no association between <b>alcohol</b> dependence and <strong>MAOA</strong> gene polymorphism.
+MAOA	addiction	dependence	25809512	We found no association between alcohol <b>dependence</b> and <strong>MAOA</strong> gene polymorphism.
+MAOA	drug	alcohol	25660313	Meta analysis of six genes (BDNF, DRD1, DRD3, DRD4, GRIN2B and <strong>MAOA</strong>) involved in neuroplasticity and the risk for <b>alcohol</b> dependence.
+MAOA	addiction	dependence	25660313	Meta analysis of six genes (BDNF, DRD1, DRD3, DRD4, GRIN2B and <strong>MAOA</strong>) involved in neuroplasticity and the risk for alcohol <b>dependence</b>.
+MAOA	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, <strong>MAOA</strong>, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+MAOA	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, <strong>MAOA</strong>, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+MAOA	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, <strong>MAOA</strong>, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+MAOA	drug	nicotine	25466703	In this study, we investigated the effects of both <b>nicotine</b> (6 mg gum) and pharmacologically induced <strong>MAO A</strong> inhibition via moclobemide (75 mg) on P50 event related potential indexed sensory gating in a sample of 24 healthy non <b>smoking</b> males.
+MAOA	drug	nicotine	25466703	Ratio score (rP50) measured gating revealed significant improvement in auditory stimulus suppression after combined <b>nicotine</b> and <strong>MAO A</strong> inhibition compared to placebo and to the <b>nicotine</b> alone condition.
+MAOA	drug	nicotine	25466703	This <b>nicotine</b> + <strong>MAO A</strong> inhibition induced efficient gating was consistent regardless of participants' baseline (placebo) gating efficiency, despite the observation that <b>nicotine</b> in the absence of <strong>MAO A</strong> inhibition exhibited a detrimental effect on gating in participants with high baseline suppression ratios.
+MAOA	drug	cocaine	24837582	Using an imaging genetics approach, the current study tested in 62 <b>cocaine</b> abusers and 57 healthy controls the separate and combined effects of variations in the serotonin transporter (5 HTTLPR) and monoamine oxidase A (<strong>MAOA</strong>) genes on processing of aversive information.
+MAOA	addiction	aversion	24837582	Using an imaging genetics approach, the current study tested in 62 cocaine abusers and 57 healthy controls the separate and combined effects of variations in the serotonin transporter (5 HTTLPR) and monoamine oxidase A (<strong>MAOA</strong>) genes on processing of <b>aversive</b> information.
+MAOA	drug	cocaine	24837582	Using an imaging genetics approach, the current study tested in 62 <b>cocaine</b> abusers and 57 healthy controls the separate and combined effects of variations in the serotonin transporter (5 HTTLPR) and <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) genes on processing of aversive information.
+MAOA	addiction	aversion	24837582	Using an imaging genetics approach, the current study tested in 62 cocaine abusers and 57 healthy controls the separate and combined effects of variations in the serotonin transporter (5 HTTLPR) and <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) genes on processing of <b>aversive</b> information.
+MAOA	drug	nicotine	24513971	CSE significantly reduced <strong>MAO A</strong> and MAO B activities in vitro, whereas <b>nicotine</b> did not.
+MAOA	drug	opioid	24368617	Genetic polymorphisms in the coding or promoter regions of the Mu <b>Opioid</b> Receptor (OPRM1), Corticotropin Releasing Hormone (CRH), Monoamine Oxidase A (<strong>MAOA</strong>), Dopamine D4 Receptor (DRD4), and Serotonin Transporter (SLC6A4) genes have been shown to be functionally similar in humans and rhesus macaques and have been demonstrated to contribute to individual differences in aggression.
+MAOA	drug	opioid	24368617	Genetic polymorphisms in the coding or promoter regions of the Mu <b>Opioid</b> Receptor (OPRM1), Corticotropin Releasing Hormone (CRH), <strong>Monoamine Oxidase A</strong> (<strong>MAOA</strong>), Dopamine D4 Receptor (DRD4), and Serotonin Transporter (SLC6A4) genes have been shown to be functionally similar in humans and rhesus macaques and have been demonstrated to contribute to individual differences in aggression.
+MAOA	drug	opioid	24355137	The association of 5 HTR2A 1438A/G, COMTVal158Met, <strong>MAOA</strong> LPR, DATVNTR and 5 HTTVNTR gene polymorphisms and borderline personality disorder in female <b>heroin</b> dependent Chinese subjects.
+MAOA	drug	opioid	24355137	To explore the association between the 5 HTR2A 1438A/G, COMTVal158Met, <strong>MAOA</strong> LPR, DATVNTR and 5 HTTVNTR polymorphisms with co morbid borderline personality disorder (BPD) in female <b>heroin</b> dependent patients.
+MAOA	drug	opioid	24355137	In a case control study, we compared the polymorphic distributions of 5 HTR2A 1438A/G, COMTVal158Met, <strong>MAOA</strong> LPR, DATVNTR and 5 HTTVNTR in 296 female <b>heroin</b> dependent patients (including 61 patients with BPD and 235 without BPD) and 101 normal females by genotypes, alleles, and interaction between genes.
+MAOA	drug	opioid	24355137	Female <b>heroin</b> dependent subjects with BPD have lower frequency of the high activity allele (L: 4 repeats (4R)) of <strong>MAOA</strong> LPR than those female <b>heroin</b> dependent subjects without BPD, and have higher 5 HTTVNTR 10R/10R genotype frequency than normal female controls, with adjusted P value<0.05 (after adjusted for multiple testing by 1000 fold permutation tests) respectively.
+MAOA	drug	opioid	24355137	By MDR (Multifactor Dimensionality Reduction) analyses, the interactive effects between <strong>MAOA</strong> LPR and 5 HTTVNTR, and among <strong>MAOA</strong> LPR, 5 HTTVNTR and rs6311 were close to the significance level (P=0.05) in predicting the risk of co morbidity of BPD and <b>heroin</b> dependence relative to normal female controls, with 1000 fold permutation testing P value<0.06 however >0.05 respectively.
+MAOA	addiction	dependence	24355137	By MDR (Multifactor Dimensionality Reduction) analyses, the interactive effects between <strong>MAOA</strong> LPR and 5 HTTVNTR, and among <strong>MAOA</strong> LPR, 5 HTTVNTR and rs6311 were close to the significance level (P=0.05) in predicting the risk of co morbidity of BPD and heroin <b>dependence</b> relative to normal female controls, with 1000 fold permutation testing P value<0.06 however >0.05 respectively.
+MAOA	drug	opioid	24355137	5 HTTVNTR and <strong>MAOA</strong> LPR may have independent predictive effects on co morbid BPD in female <b>heroin</b> dependent patients; the gene gene interactions between <strong>MAOA</strong> LPR and 5 HTTVNTR, and among <strong>MAOA</strong> LPR, 5 HTTVNTR and rs6311 might also be involved in the etiology of this co morbidity.
+MAOA	drug	alcohol	24269057	Greater <strong>monoamine oxidase a</strong> binding in <b>alcohol</b> dependence.
+MAOA	addiction	dependence	24269057	Greater <strong>monoamine oxidase a</strong> binding in alcohol <b>dependence</b>.
+MAOA	drug	alcohol	24269057	We hypothesized that <strong>MAO A</strong> VT, an index of <strong>MAO A</strong> level, is elevated in the prefrontal cortex (PFC) during AD, because markers of greater oxidative stress and apoptosis are reported in the brain in AD and a microarray analysis reported greater <strong>MAO A</strong> messenger RNA in the PFC of rodents exposed to <b>alcohol</b> vapor.
+MAOA	drug	alcohol	24252443	The <strong>MAO A</strong> inhibitor clorgyline reduces <b>ethanol</b> induced locomotion and its volitional intake in mice.
+MAOA	drug	opioid	24220688	Monoamine oxidase A (<strong>Maoa</strong>) and neuropeptide Y receptor 5 mRNA levels were lower in adolescent mice than in adult mice without <b>oxycodone</b> exposure.
+MAOA	drug	opioid	24220688	<strong>Monoamine oxidase A</strong> (<strong>Maoa</strong>) and neuropeptide Y receptor 5 mRNA levels were lower in adolescent mice than in adult mice without <b>oxycodone</b> exposure.
+MAOA	drug	opioid	24220688	<b>Oxycodone</b> self administration increased <strong>Maoa</strong> mRNA levels compared to controls in both age groups.
+MAOA	drug	opioid	24220688	There was a positive correlation of the amount of <b>oxycodone</b> self administered in the last session or across 14 sessions with <strong>Maoa</strong> mRNA levels.
+MAOA	drug	nicotine	23988853	The results suggest that inhibition of <strong>MAO A</strong> may contribute to the intensity of withdrawal syndrome in <b>smoking</b> cessation.
+MAOA	addiction	withdrawal	23988853	The results suggest that inhibition of <strong>MAO A</strong> may contribute to the intensity of <b>withdrawal</b> syndrome in smoking cessation.
+MAOA	drug	cocaine	23755928	A <strong>MAOA</strong> gene*<b>cocaine</b> severity interaction on impulsivity and neuropsychological measures of orbitofrontal dysfunction: preliminary results.
+MAOA	drug	cocaine	23755928	Based on previous evidence of a <strong>MAOA</strong> gene*<b>cocaine</b> use interaction on orbitofrontal cortex volume attrition, we tested whether the <strong>MAOA</strong> low activity variant and <b>cocaine</b> use severity are interactively associated with impulsivity and behavioral indices of orbitofrontal dysfunction: emotion recognition and decision making.
+MAOA	drug	cocaine	23755928	72 <b>cocaine</b> dependent individuals and 52 non drug using controls (including healthy individuals and problem gamblers) were genotyped for the <strong>MAOA</strong> gene and tested using the UPPS P Impulsive Behavior Scale, the Iowa Gambling Task and the Ekman's Facial Emotions Recognition Test.
+MAOA	drug	cocaine	23755928	To test the main hypothesis, we conducted hierarchical multiple regression analyses including three sets of predictors: (1) age, (2) <strong>MAOA</strong> genotype and severity of <b>cocaine</b> use, and (3) the interaction between <strong>MAOA</strong> genotype and severity of <b>cocaine</b> use.
+MAOA	drug	cocaine	23755928	We computed the statistical significance of the prediction change yielded by each consecutive set, with 'a priori' interest in the <strong>MAOA</strong>*<b>cocaine</b> severity interaction.
+MAOA	drug	cocaine	23755928	We found significant effects of the <strong>MAOA</strong> gene*<b>cocaine</b> use severity interaction on the emotion recognition scores and the UPPS P's dimensions of Positive Urgency and Sensation Seeking: Low activity carriers with higher <b>cocaine</b> exposure had poorer emotion recognition and higher Positive Urgency and Sensation Seeking.
+MAOA	addiction	relapse	23755928	We found significant effects of the <strong>MAOA</strong> gene*cocaine use severity interaction on the emotion recognition scores and the UPPS P's dimensions of Positive Urgency and Sensation <b>Seeking</b>: Low activity carriers with higher cocaine exposure had poorer emotion recognition and higher Positive Urgency and Sensation <b>Seeking</b>.
+MAOA	drug	cocaine	23755928	<b>Cocaine</b> users carrying the <strong>MAOA</strong> low activity show a greater impact of <b>cocaine</b> use on impulsivity and behavioral measures of orbitofrontal cortex dysfunction.
+MAOA	addiction	reward	23544600	Polymorphisms in the monoamine oxidase A (<strong>MAOA</strong> LPR) and serotonin receptor 2A genes (rs6314) moderated the effect of food <b>reinforcement</b> on BMI, accounting for an additional 5 10% variance and revealed a potential role of the single nucleotide polymorphism, rs6314, in the serotonin 2A receptor as a differential susceptibility factor for obesity.
+MAOA	addiction	reward	23544600	Polymorphisms in the <strong>monoamine oxidase A</strong> (<strong>MAOA</strong> LPR) and serotonin receptor 2A genes (rs6314) moderated the effect of food <b>reinforcement</b> on BMI, accounting for an additional 5 10% variance and revealed a potential role of the single nucleotide polymorphism, rs6314, in the serotonin 2A receptor as a differential susceptibility factor for obesity.
+MAOA	addiction	reward	23544600	The interaction with <strong>MAOA</strong> LPR better fits the diathesis stress model, with the 3.5R/4R allele conferring protection for individuals low in food <b>reinforcement</b>.
+MAOA	drug	cocaine	23499958	The inhibition of both <strong>MAO A</strong> and MAO B by clorgyline and pargyline, respectively, enhanced the effects of <b>cocaine</b> on DARPP 32 phosphorylation.
+MAOA	drug	cocaine	23499958	The acute effect of resveratrol on <b>cocaine</b> induced DARPP 32 phosphorylation was occluded with inhibition of <strong>MAO A</strong> and MAO B.
+MAOA	drug	cocaine	23499958	Thus, this study provides pharmacological evidence that acute resveratrol enhances <b>cocaine</b> induced dopamine neurotransmission and behavioral responses, presumably via mechanisms involving the inhibition of dopamine catabolism by <strong>MAO A</strong> and MAO B. Resveratrol may be useful to treat dysregulated dopamine neurotransmission, but it may enhance the risk of developing drug addiction.
+MAOA	addiction	addiction	23499958	Thus, this study provides pharmacological evidence that acute resveratrol enhances cocaine induced dopamine neurotransmission and behavioral responses, presumably via mechanisms involving the inhibition of dopamine catabolism by <strong>MAO A</strong> and MAO B. Resveratrol may be useful to treat dysregulated dopamine neurotransmission, but it may enhance the risk of developing drug <b>addiction</b>.
+MAOA	addiction	dependence	23377636	Other candidate genes associated with substance <b>dependence</b> phenotypes in Native Americans include OPRM1, CRN1, COMT, GABRA2, <strong>MAOA</strong>, and HTR3 B.
+MAOA	addiction	addiction	23197705	Monoamine oxidase A (<strong>MAO A</strong>), a key brain enzyme which metabolizes monoamines, is implicated in the pathophysiology of stress related illnesses, including major depressive disorder, <b>addiction</b>, and violent behavior.
+MAOA	addiction	addiction	23197705	<strong>Monoamine oxidase A</strong> (<strong>MAO A</strong>), a key brain enzyme which metabolizes monoamines, is implicated in the pathophysiology of stress related illnesses, including major depressive disorder, <b>addiction</b>, and violent behavior.
+MAOA	drug	nicotine	23197705	Twelve healthy, non <b>smoking</b> participants aged 18 50 underwent [(11)C]harmine positron emission tomography to measure brain <strong>MAO A</strong> V(T) on two different days: One under acute psychosocial stress (via Trier Social Stress and Montreal Imaging Stress Tasks) and one under a non stress condition.
+MAOA	drug	alcohol	22640768	It is not surprising that the genes discovered so far act in a variety of ways: via altered metabolism of drug (the <b>alcohol</b> and nicotine metabolic gene variants), via altered function of a drug receptor (the nicotinic receptor, which may alter affinity for nicotine but as discussed may also alter circuitry of reward), and via general mechanisms of addiction (genes such as <strong>monoamine oxidase A</strong> and the serotonin transporter that modulate stress response, emotion, and behavioral control).
+MAOA	drug	nicotine	22640768	It is not surprising that the genes discovered so far act in a variety of ways: via altered metabolism of drug (the alcohol and <b>nicotine</b> metabolic gene variants), via altered function of a drug receptor (the nicotinic receptor, which may alter affinity for <b>nicotine</b> but as discussed may also alter circuitry of reward), and via general mechanisms of addiction (genes such as <strong>monoamine oxidase A</strong> and the serotonin transporter that modulate stress response, emotion, and behavioral control).
+MAOA	addiction	addiction	22640768	It is not surprising that the genes discovered so far act in a variety of ways: via altered metabolism of drug (the alcohol and nicotine metabolic gene variants), via altered function of a drug receptor (the nicotinic receptor, which may alter affinity for nicotine but as discussed may also alter circuitry of reward), and via general mechanisms of <b>addiction</b> (genes such as <strong>monoamine oxidase A</strong> and the serotonin transporter that modulate stress response, emotion, and behavioral control).
+MAOA	addiction	reward	22640768	It is not surprising that the genes discovered so far act in a variety of ways: via altered metabolism of drug (the alcohol and nicotine metabolic gene variants), via altered function of a drug receptor (the nicotinic receptor, which may alter affinity for nicotine but as discussed may also alter circuitry of <b>reward</b>), and via general mechanisms of addiction (genes such as <strong>monoamine oxidase A</strong> and the serotonin transporter that modulate stress response, emotion, and behavioral control).
+MAOA	drug	nicotine	22610759	A latent modeling approach to genotype phenotype relationships: maternal problem behavior clusters, prenatal <b>smoking</b>, and <strong>MAOA</strong> genotype.
+MAOA	addiction	addiction	22239616	Changes in <strong>MAO A</strong> levels are associated with depression, trait aggression, and <b>addiction</b>.
+MAOA	drug	opioid	22239616	The probes were designed to include <strong>MAOA</strong> specific PNA dodecamers, separated by an N terminal spacer to a μ <b>opioid</b> receptor targeting peptide (DAMGO), with a spacer and a fluorophore on the C terminus.
+MAOA	drug	opioid	22138326	The association of 5 HTR2A 1438A/G, COMTVal158Met, <strong>MAOA</strong> LPR, DATVNTR and 5 HTTVNTR gene polymorphisms and antisocial personality disorder in male <b>heroin</b> dependent Chinese subjects.
+MAOA	drug	opioid	22138326	To explore the association between the 5 HTR2A 1438A/G, COMTVal158Met, <strong>MAOA</strong> LPR, DATVNTR and 5 HTTVNTR polymorphisms with comorbidity of antisocial personality disorder in male <b>heroin</b> dependent patients.
+MAOA	drug	opioid	22138326	In case control study, we compared the polymorphic distributions of 5 HTR2A 1438A/G, COMTVal158Met, <strong>MAOA</strong> LPR, DATVNTR and 5 HTTVNTR in 588 male <b>heroin</b> dependent patients (including 311 patients with antisocial personality disorder and 277 patients without antisocial personality disorder) and 194 normal males by genotypes, alleles, and interaction between genes.
+MAOA	drug	nicotine	21810646	<strong>Monoamine oxidase A</strong> binding in the prefrontal and anterior cingulate cortices during acute withdrawal from heavy cigarette <b>smoking</b>.
+MAOA	addiction	withdrawal	21810646	<strong>Monoamine oxidase A</strong> binding in the prefrontal and anterior cingulate cortices during acute <b>withdrawal</b> from heavy cigarette smoking.
+MAOA	addiction	withdrawal	21810646	Substances in cigarette smoke, such as harman, inhibit <strong>MAO A</strong>, and cigarette <b>withdrawal</b> is associated with depressed mood.
+MAOA	addiction	withdrawal	21810646	It is unknown whether <strong>MAO A</strong> binding increases during early cigarette <b>withdrawal</b>.
+MAOA	drug	nicotine	21810646	To measure prefrontal and anterior cingulate cortex <strong>MAO A</strong> binding during acute cigarette withdrawal and to assess the relationship with <b>smoking</b> severity, plasma levels of harman, and severity of depression.
+MAOA	addiction	withdrawal	21810646	To measure prefrontal and anterior cingulate cortex <strong>MAO A</strong> binding during acute cigarette <b>withdrawal</b> and to assess the relationship with smoking severity, plasma levels of harman, and severity of depression.
+MAOA	drug	nicotine	21810646	In heavy <b>smoking</b> individuals, prefrontal and anterior cingulate cortex <strong>MAO A</strong> V(T) was greater during withdrawal (23.7% and 33.3%, respectively; repeated measures multivariate analysis of variance, F(1,22) = 25.58, P < .001).
+MAOA	addiction	withdrawal	21810646	In heavy smoking individuals, prefrontal and anterior cingulate cortex <strong>MAO A</strong> V(T) was greater during <b>withdrawal</b> (23.7% and 33.3%, respectively; repeated measures multivariate analysis of variance, F(1,22) = 25.58, P < .001).
+MAOA	drug	nicotine	21810646	During withdrawal from heavy <b>smoking</b>, prefrontal and anterior cingulate cortex <strong>MAO A</strong> V(T) was greater than in healthy controls (25.0% and 25.6%, respectively; multivariate analysis of variance, F(2,33) = 6.72, P = .004).
+MAOA	addiction	withdrawal	21810646	During <b>withdrawal</b> from heavy smoking, prefrontal and anterior cingulate cortex <strong>MAO A</strong> V(T) was greater than in healthy controls (25.0% and 25.6%, respectively; multivariate analysis of variance, F(2,33) = 6.72, P = .004).
+MAOA	drug	nicotine	21810646	The difference in <strong>MAO A</strong> V(T) in the prefrontal cortex and anterior cingulate cortex between withdrawal and active, heavy <b>smoking</b> covaried with change in plasma harman levels in the prefrontal cortex and anterior cingulate cortex (multivariate analysis of covariance, F(1,10) = 9.97, P = .01).
+MAOA	addiction	withdrawal	21810646	The difference in <strong>MAO A</strong> V(T) in the prefrontal cortex and anterior cingulate cortex between <b>withdrawal</b> and active, heavy smoking covaried with change in plasma harman levels in the prefrontal cortex and anterior cingulate cortex (multivariate analysis of covariance, F(1,10) = 9.97, P = .01).
+MAOA	drug	nicotine	21810646	The change in <strong>MAO A</strong> V(T) between withdrawal and active, heavy <b>smoking</b> also covaried with severity of depression (multivariate analysis of covariance, F(1,10) = 11.91, P = .006).
+MAOA	addiction	withdrawal	21810646	The change in <strong>MAO A</strong> V(T) between <b>withdrawal</b> and active, heavy smoking also covaried with severity of depression (multivariate analysis of covariance, F(1,10) = 11.91, P = .006).
+MAOA	drug	nicotine	21810646	The increase in prefrontal and anterior cingulate cortex <strong>MAO A</strong> binding and associated reduction in plasma harman level represent a novel, additional explanation for depressed mood during withdrawal from heavy cigarette <b>smoking</b>.
+MAOA	addiction	withdrawal	21810646	The increase in prefrontal and anterior cingulate cortex <strong>MAO A</strong> binding and associated reduction in plasma harman level represent a novel, additional explanation for depressed mood during <b>withdrawal</b> from heavy cigarette smoking.
+MAOA	drug	nicotine	21810646	This finding resolves a longstanding paradox regarding the association of cigarette <b>smoking</b> with depression and suicide and argues for additional clinical trials on the effects of <strong>MAO A</strong> inhibitors on quitting heavy cigarette <b>smoking</b>.
+MAOA	drug	opioid	21706389	Genes at which variation moderates these phenotypes include those encoding monoamine oxidase A (<strong>MAOA</strong> LPR), the serotonin transporter (HTTLPR), corticotropin releasing hormone (CRH 248C/T and  2232 C/G), Neuropeptide Y (NPY 1002 T/G), and the μ <b>opioid</b> receptor (OPRM1 C77G).
+MAOA	drug	opioid	21706389	Genes at which variation moderates these phenotypes include those encoding <strong>monoamine oxidase A</strong> (<strong>MAOA</strong> LPR), the serotonin transporter (HTTLPR), corticotropin releasing hormone (CRH 248C/T and  2232 C/G), Neuropeptide Y (NPY 1002 T/G), and the μ <b>opioid</b> receptor (OPRM1 C77G).
+MAOA	drug	nicotine	21696345	It has been suggested that the addictive effects of <b>smoking</b> may be due, in part, to the inhibition of the pair of monoamine oxidase enzymes responsible for a significant fraction of monoamine metabolism, Monoamine Oxidase A and B (<strong>MAO A</strong> and MAO B).
+MAOA	addiction	addiction	21696345	It has been suggested that the <b>addictive</b> effects of smoking may be due, in part, to the inhibition of the pair of monoamine oxidase enzymes responsible for a significant fraction of monoamine metabolism, Monoamine Oxidase A and B (<strong>MAO A</strong> and MAO B).
+MAOA	drug	nicotine	21696345	It has been suggested that the addictive effects of <b>smoking</b> may be due, in part, to the inhibition of the pair of monoamine oxidase enzymes responsible for a significant fraction of monoamine metabolism, <strong>Monoamine Oxidase A</strong> and B (<strong>MAO A</strong> and MAO B).
+MAOA	addiction	addiction	21696345	It has been suggested that the <b>addictive</b> effects of smoking may be due, in part, to the inhibition of the pair of monoamine oxidase enzymes responsible for a significant fraction of monoamine metabolism, <strong>Monoamine Oxidase A</strong> and B (<strong>MAO A</strong> and MAO B).
+MAOA	drug	nicotine	21636610	When <b>tobacco</b> extracts were diluted to contain a physiologically relevant <b>nicotine</b> concentration of 0.2 μM, all samples tested inhibited <strong>MAO A</strong> and MAO B by between 4% and 12% in a standard assay.
+MAOA	drug	cocaine	21383264	To examine variations in gray matter volume (GMV) as a function of lifetime drug use and the genotype of the monoamine oxidase A gene, <strong>MAOA</strong>, in men with <b>cocaine</b> use disorders (CUD) and healthy male controls.
+MAOA	drug	cocaine	21383264	To examine variations in gray matter volume (GMV) as a function of lifetime drug use and the genotype of the <strong>monoamine oxidase A</strong> gene, <strong>MAOA</strong>, in men with <b>cocaine</b> use disorders (CUD) and healthy male controls.
+MAOA	drug	alcohol	21383264	The impact of cocaine addiction on GMV, tested by (1) comparing the CUD group with controls, (2) testing diagnosis × <strong>MAOA</strong> interactions, and (3) correlating GMV with lifetime cocaine, <b>alcohol</b>, and cigarette smoking, and testing their unique contribution to GMV beyond other factors.
+MAOA	drug	cocaine	21383264	The impact of <b>cocaine</b> addiction on GMV, tested by (1) comparing the CUD group with controls, (2) testing diagnosis × <strong>MAOA</strong> interactions, and (3) correlating GMV with lifetime <b>cocaine</b>, alcohol, and cigarette smoking, and testing their unique contribution to GMV beyond other factors.
+MAOA	drug	nicotine	21383264	The impact of cocaine addiction on GMV, tested by (1) comparing the CUD group with controls, (2) testing diagnosis × <strong>MAOA</strong> interactions, and (3) correlating GMV with lifetime cocaine, alcohol, and cigarette <b>smoking</b>, and testing their unique contribution to GMV beyond other factors.
+MAOA	addiction	addiction	21383264	The impact of cocaine <b>addiction</b> on GMV, tested by (1) comparing the CUD group with controls, (2) testing diagnosis × <strong>MAOA</strong> interactions, and (3) correlating GMV with lifetime cocaine, alcohol, and cigarette smoking, and testing their unique contribution to GMV beyond other factors.
+MAOA	drug	cocaine	21383264	(2) The orbitofrontal cortex reductions were uniquely driven by CUD with low  <strong>MAOA</strong> genotype and by lifetime <b>cocaine</b> use.
+MAOA	drug	cocaine	21383264	Long term <b>cocaine</b> users with the low repeat <strong>MAOA</strong> allele have enhanced sensitivity to gray matter loss, specifically in the orbitofrontal cortex, indicating that this genotype may exacerbate the deleterious effects of <b>cocaine</b> in the brain.
+MAOA	addiction	addiction	21118356	<strong>MAO A</strong> and COMT have a minor role in <b>addiction</b> like behaviour that is further complicated by a sexual dimorphism.
+MAOA	drug	alcohol	20477771	<strong>MAOA</strong> interacts with the ALDH2 gene in anxiety depression <b>alcohol</b> dependence.
+MAOA	addiction	dependence	20477771	<strong>MAOA</strong> interacts with the ALDH2 gene in anxiety depression alcohol <b>dependence</b>.
+MAOA	drug	nicotine	20447558	Since <strong>MAO A</strong> is an enzyme involved in the metabolism of neurotransmitters, fluctuations in <strong>MAO A</strong> functionality are associated with psychiatric and neurological disorders as well as with <b>tobacco</b> addiction and behaviour.
+MAOA	addiction	addiction	20447558	Since <strong>MAO A</strong> is an enzyme involved in the metabolism of neurotransmitters, fluctuations in <strong>MAO A</strong> functionality are associated with psychiatric and neurological disorders as well as with tobacco <b>addiction</b> and behaviour.
+MAOA	drug	opioid	20218801	Association of VNTR polymorphisms in the <strong>MAOA</strong> promoter and DRD4 exon 3 with <b>heroin</b> dependence in male Chinese addicts.
+MAOA	addiction	dependence	20218801	Association of VNTR polymorphisms in the <strong>MAOA</strong> promoter and DRD4 exon 3 with heroin <b>dependence</b> in male Chinese addicts.
+MAOA	drug	opioid	20218801	To explore the involvement of variable number tandem repeat (VNTR) polymorphisms in the monoamine oxidase A (<strong>MAOA</strong>) promoter and exon 3 of the dopamine D4 receptor (DRD4) gene in <b>heroin</b> addiction modulate the vulnerability of individuals to <b>heroin</b> addiction.
+MAOA	addiction	addiction	20218801	To explore the involvement of variable number tandem repeat (VNTR) polymorphisms in the monoamine oxidase A (<strong>MAOA</strong>) promoter and exon 3 of the dopamine D4 receptor (DRD4) gene in heroin <b>addiction</b> modulate the vulnerability of individuals to heroin <b>addiction</b>.
+MAOA	drug	opioid	20218801	To explore the involvement of variable number tandem repeat (VNTR) polymorphisms in the <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) promoter and exon 3 of the dopamine D4 receptor (DRD4) gene in <b>heroin</b> addiction modulate the vulnerability of individuals to <b>heroin</b> addiction.
+MAOA	addiction	addiction	20218801	To explore the involvement of variable number tandem repeat (VNTR) polymorphisms in the <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) promoter and exon 3 of the dopamine D4 receptor (DRD4) gene in heroin <b>addiction</b> modulate the vulnerability of individuals to heroin <b>addiction</b>.
+MAOA	drug	opioid	20218801	The long repeat allelic variants (>4 repeats) and 2 repeat allele of the DRD4 exon 3 VNTR polymorphism might be risk alleles for individual vulnerability to <b>heroin</b> addiction in Chinese men, but the <strong>MAOA</strong> promoter VNTR polymorphism does not mean that the partial dominant inherited mode might involved in the genetics of <b>heroin</b> dependence.
+MAOA	addiction	addiction	20218801	The long repeat allelic variants (>4 repeats) and 2 repeat allele of the DRD4 exon 3 VNTR polymorphism might be risk alleles for individual vulnerability to heroin <b>addiction</b> in Chinese men, but the <strong>MAOA</strong> promoter VNTR polymorphism does not mean that the partial dominant inherited mode might involved in the genetics of heroin dependence.
+MAOA	addiction	dependence	20218801	The long repeat allelic variants (>4 repeats) and 2 repeat allele of the DRD4 exon 3 VNTR polymorphism might be risk alleles for individual vulnerability to heroin addiction in Chinese men, but the <strong>MAOA</strong> promoter VNTR polymorphism does not mean that the partial dominant inherited mode might involved in the genetics of heroin <b>dependence</b>.
+MAOA	drug	nicotine	20026027	The effects of harmane (2mg/kg) and norharmane (2mg/kg), were compared to those of <b>nicotine</b> (11microg/kg), of cotinine (0.5mg/kg), of the <strong>monoamine oxidase A</strong> inhibitor befloxatone (0.12mg/kg), and of the monoamine oxidase B inhibitor selegiline (0.5mg/kg).
+MAOA	drug	amphetamine	19958817	The effect of treating rats with clorgyline, an irreversible monoamine oxidase A (<strong>MAO A</strong>) inhibitor, on <b>methamphetamine</b> (<b>METH</b>) induced conditioned place preference (CPP) was investigated.
+MAOA	addiction	reward	19958817	The effect of treating rats with clorgyline, an irreversible monoamine oxidase A (<strong>MAO A</strong>) inhibitor, on methamphetamine (METH) induced conditioned place preference (<b>CPP</b>) was investigated.
+MAOA	drug	amphetamine	19958817	The effect of treating rats with clorgyline, an irreversible <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) inhibitor, on <b>methamphetamine</b> (<b>METH</b>) induced conditioned place preference (CPP) was investigated.
+MAOA	addiction	reward	19958817	The effect of treating rats with clorgyline, an irreversible <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) inhibitor, on methamphetamine (METH) induced conditioned place preference (<b>CPP</b>) was investigated.
+MAOA	drug	nicotine	19777560	The effect of <b>smoking</b> on <strong>MAOA</strong> promoter methylation in DNA prepared from lymphoblasts and whole blood.
+MAOA	drug	nicotine	19777560	Prior work using lymphoblast DNA prepared from 192 subjects from the Iowa Adoption Studies (IAS) demonstrated that decreased <strong>MAOA</strong> promoter methylation was associated with lifetime symptom count for <b>nicotine</b> dependence (ND) and provided suggestive evidence that the amount of methylation is genotype dependent.
+MAOA	addiction	dependence	19777560	Prior work using lymphoblast DNA prepared from 192 subjects from the Iowa Adoption Studies (IAS) demonstrated that decreased <strong>MAOA</strong> promoter methylation was associated with lifetime symptom count for nicotine <b>dependence</b> (ND) and provided suggestive evidence that the amount of methylation is genotype dependent.
+MAOA	drug	nicotine	19777560	We conclude that <b>smoking</b> reliably decreases <strong>MAOA</strong> methylation, but exact characterization of effects on level of methylation depend on genotype, <b>smoking</b> history, current <b>smoking</b> status, gender, and region of the promoter associated CpG Island examined.
+MAOA	drug	nicotine	19415821	Gene gene interactions of CYP2A6 and <strong>MAOA</strong> polymorphisms on <b>smoking</b> behavior in Chinese male population.
+MAOA	drug	nicotine	19415821	In this study, we investigated the association and multilocus gene gene interactions of cytochrome P450 2A6 (CYP2A6), dopamine beta hydroxylase (DBH), catechol O methyl transferase (COMT), and monoamine oxidase A (<strong>MAOA</strong>) polymorphisms with <b>smoking</b> behavior in a community based Chinese male population.
+MAOA	drug	nicotine	19415821	In this study, we investigated the association and multilocus gene gene interactions of cytochrome P450 2A6 (CYP2A6), dopamine beta hydroxylase (DBH), catechol O methyl transferase (COMT), and <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) polymorphisms with <b>smoking</b> behavior in a community based Chinese male population.
+MAOA	drug	nicotine	19415821	Moreover, the best model involved a gene gene interaction between <strong>MAOA</strong> and CYP2A6 was characterized by the multifactor dimensionality reduction method (64.11% accuracy, P<0.001), and indicated that carriers of the combined 1460 T/O genotype for <strong>MAOA</strong> EcoRV and CYP2A6*1/CYP2A6*1 genotypes were at higher risk of <b>smoking</b> (OR=15.4, 95% CI=4.5 52.5).
+MAOA	drug	nicotine	19415821	These findings suggested a substantial influence of CYP2A6 polymorphism as well as the interaction with <strong>MAOA</strong> resulting in risk modulation on <b>smoking</b> behavior in Chinese male population.
+MAOA	drug	alcohol	19302089	<strong>MAOA</strong> uVNTR polymorphism may modify the protective effect of ALDH2 gene against <b>alcohol</b> dependence in antisocial personality disorder.
+MAOA	addiction	dependence	19302089	<strong>MAOA</strong> uVNTR polymorphism may modify the protective effect of ALDH2 gene against alcohol <b>dependence</b> in antisocial personality disorder.
+MAOA	drug	alcohol	19302089	Antisocial <b>alcoholism</b> is related to dopamine and serotonin which are catalyzed by monoamine oxidase A (<strong>MAOA</strong>) and acetaldehyde dehydrogenase 2 (ALDH2).
+MAOA	drug	alcohol	19302089	Antisocial <b>alcoholism</b> is related to dopamine and serotonin which are catalyzed by <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) and acetaldehyde dehydrogenase 2 (ALDH2).
+MAOA	drug	alcohol	19302089	The objective of this study is to determine whether the interaction between the <strong>MAOA</strong> and the ALDH2 genes is associated with subjects with antisocial personality disorder (ASPD) having <b>alcoholism</b>.
+MAOA	drug	alcohol	19302089	However, the protective effects of the ALDH2*2 allele against <b>alcoholism</b> might disappear in subjects with ASPD and carrying <strong>MAOA</strong> uVNTR 4 repeat allele in the Han Chinese male population.
+MAOA	drug	nicotine	19247474	Besides CHRNA3 and CHRNA5, <strong>MAOA</strong> was associated with CPDBI (gene level p<5.4x10( 5)), our analysis provides independent replication of the association between the chr15q25.1 region and <b>smoking</b> intensity and data for multiple other loci associated with <b>smoking</b> behavior that merit further follow up.
+MAOA	drug	nicotine	19142115	Cerebral <strong>monoamine oxidase A</strong> inhibition in <b>tobacco</b> <b>smokers</b> confirmed with PET and [11C]befloxatone.
+MAOA	drug	nicotine	19142115	We investigated cerebral <strong>MAO A</strong> availability in 7 <b>tobacco</b> dependent subjects and 6 healthy nonsmokers, using positron emission tomography (PET) and the <strong>MAO A</strong> selective radioligand [C]befloxatone.
+MAOA	drug	nicotine	19142115	Our findings confirm a widespread inhibition of cerebral <strong>MAO A</strong> in <b>smokers</b>.
+MAOA	drug	alcohol	19120058	Effects of <strong>MAOA</strong> genotype, <b>alcohol</b> consumption, and aging on violent behavior.
+MAOA	drug	alcohol	19120058	However, how <strong>MAOA</strong> LPR modulates the effects of other factors such as <b>alcohol</b> consumption related to antisocial behavior is not completely understood.
+MAOA	drug	alcohol	19120058	This study examines the conjunct effect of <strong>MAOA</strong> LPR, <b>alcohol</b> consumption, and aging on the risk for violent behavior.
+MAOA	drug	alcohol	19120058	The risk for committing new acts of violence increased by 2.3% for each kilogram of increase in yearly mean <b>alcohol</b> consumption (p = 0.004) and decreased by 7.3% for every year among offenders carrying the high activity <strong>MAOA</strong> genotype.
+MAOA	drug	alcohol	19120058	In contrast, <b>alcohol</b> consumption and aging failed to affect violent behavior in the low activity <strong>MAOA</strong> genotyped offenders.
+MAOA	drug	alcohol	19120058	Finnish high activity <strong>MAOA</strong> genotyped risk <b>alcoholics</b> exhibiting antisocial behavior, high <b>alcohol</b> consumption, and abnormal <b>alcohol</b> related impulsive and uncontrolled violence might represent an etiologically distinct <b>alcohol</b> dependence subtype.
+MAOA	addiction	dependence	19120058	Finnish high activity <strong>MAOA</strong> genotyped risk alcoholics exhibiting antisocial behavior, high alcohol consumption, and abnormal alcohol related impulsive and uncontrolled violence might represent an etiologically distinct alcohol <b>dependence</b> subtype.
+MAOA	drug	psychedelics	19076925	Although these toxic effects were shown to be prevented by monoamine oxidase B inhibition, the role of monoamine oxidase A (<strong>MAO A</strong>) in <b>MDMA</b> mediated mitochondrial damage remains to be evaluated.
+MAOA	drug	psychedelics	19076925	Although these toxic effects were shown to be prevented by monoamine oxidase B inhibition, the role of <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) in <b>MDMA</b> mediated mitochondrial damage remains to be evaluated.
+MAOA	drug	psychedelics	19076925	Thus, the aim of the present study was to clarify the potential interference of a specific inhibition of <strong>MAO A</strong> by clorgyline, on the deleterious effects produced by a binge administration of a neurotoxic dose of <b>MDMA</b> (10 mg <b>MDMA</b>/kg of body weight, intraperitoneally, every 2 hours in a total of four administrations) to an adolescent rat model.
+MAOA	addiction	intoxication	19076925	Thus, the aim of the present study was to clarify the potential interference of a specific inhibition of <strong>MAO A</strong> by clorgyline, on the deleterious effects produced by a <b>binge</b> administration of a neurotoxic dose of MDMA (10 mg MDMA/kg of body weight, intraperitoneally, every 2 hours in a total of four administrations) to an adolescent rat model.
+MAOA	drug	psychedelics	19076925	Considering that hyperthermia has been shown to contribute to the neurotoxic effects of <b>MDMA</b>, another objective of the present study was to evaluate the body temperature changes mediated by <b>MDMA</b> with a <strong>MAO A</strong> selective inhibition by clorgyline.
+MAOA	drug	psychedelics	19076925	The obtained results demonstrated that the administration of a neurotoxic binge dose of <b>MDMA</b> to an adolescent rat model previously treated with the specific <strong>MAO A</strong> inhibitor, clorgyline, resulted in synergistic effects on serotonin  (5 HT) mediated behaviour and body temperature, provoking high mortality.
+MAOA	addiction	intoxication	19076925	The obtained results demonstrated that the administration of a neurotoxic <b>binge</b> dose of MDMA to an adolescent rat model previously treated with the specific <strong>MAO A</strong> inhibitor, clorgyline, resulted in synergistic effects on serotonin  (5 HT) mediated behaviour and body temperature, provoking high mortality.
+MAOA	drug	psychedelics	19076925	Inhibition of <strong>MAO A</strong> by clorgyline administration had no protective effect on <b>MDMA</b> induced alterations on brain mitochondria (increased lipid peroxidation, protein carbonylation and decrease in the expression of the respiratory chain subunits NDII and COXI), although it aggravated <b>MDMA</b> induced decrease in the expression of COXI.
+MAOA	drug	psychedelics	19076925	These results reinforce the notion that the concomitant use of <strong>MAO A</strong> inhibitors and <b>MDMA</b> is counter indicated because of the resulting severe synergic toxicity.
+MAOA	drug	alcohol	18827956	Serotonin transporter (5 HTTLPR) and monoamine oxidase (<strong>MAOA</strong>) promoter polymorphisms in women with severe <b>alcoholism</b>.
+MAOA	drug	alcohol	18827956	Genotyping of two functional polymorphisms in the promoter region of the serotonin transporter and monoamine oxidase A, respectively, (5 HTT LPR and <strong>MAOA</strong> VNTR), was performed in a group of women with severe <b>alcohol</b> addiction.
+MAOA	addiction	addiction	18827956	Genotyping of two functional polymorphisms in the promoter region of the serotonin transporter and monoamine oxidase A, respectively, (5 HTT LPR and <strong>MAOA</strong> VNTR), was performed in a group of women with severe alcohol <b>addiction</b>.
+MAOA	drug	alcohol	18827956	Genotyping of two functional polymorphisms in the promoter region of the serotonin transporter and <strong>monoamine oxidase A</strong>, respectively, (5 HTT LPR and <strong>MAOA</strong> VNTR), was performed in a group of women with severe <b>alcohol</b> addiction.
+MAOA	addiction	addiction	18827956	Genotyping of two functional polymorphisms in the promoter region of the serotonin transporter and <strong>monoamine oxidase A</strong>, respectively, (5 HTT LPR and <strong>MAOA</strong> VNTR), was performed in a group of women with severe alcohol <b>addiction</b>.
+MAOA	drug	alcohol	18827956	However, within the group of <b>alcoholics</b>, when the patients with known co morbid psychiatric disorders were excluded, aggressive anti social behaviour was significantly linked to the presence of the high activity <strong>MAOA</strong> allele.
+MAOA	drug	alcohol	18827956	The pattern of associations between genotypes of 5 HTT LPR and <strong>MAOA</strong> VNTR in women with severe <b>alcoholism</b> differs from most corresponding studies on males.
+MAOA	drug	alcohol	18560630	Desoxypeganine (DOP) is a natural alkaloid that has been characterized as a cholinesterase inhibitor and a selective inhibitor of <strong>monoamine oxidase A</strong>. DOP has been investigated for its potential utility in the pharmacological treatment of <b>alcohol</b> abuse and as a smoking cessation aid.
+MAOA	drug	nicotine	18560630	Desoxypeganine (DOP) is a natural alkaloid that has been characterized as a cholinesterase inhibitor and a selective inhibitor of <strong>monoamine oxidase A</strong>. DOP has been investigated for its potential utility in the pharmacological treatment of alcohol abuse and as a <b>smoking</b> cessation aid.
+MAOA	drug	alcohol	18454435	<strong>MAOA</strong> methylation is associated with nicotine and <b>alcohol</b> dependence in women.
+MAOA	drug	nicotine	18454435	<strong>MAOA</strong> methylation is associated with <b>nicotine</b> and alcohol dependence in women.
+MAOA	addiction	dependence	18454435	<strong>MAOA</strong> methylation is associated with nicotine and alcohol <b>dependence</b> in women.
+MAOA	drug	amphetamine	18411704	As to risks of rapid onset of <b>methamphetamine</b> psychosis, worse prognosis or complication of spontaneous relapse, the dopamine D2 receptors, dopamine transporter, <strong>monoamine oxidase A</strong>, catechol O methyltransferese, SOD2, NQO2, PICK1 gene were identified.
+MAOA	addiction	relapse	18411704	As to risks of rapid onset of methamphetamine psychosis, worse prognosis or complication of spontaneous <b>relapse</b>, the dopamine D2 receptors, dopamine transporter, <strong>monoamine oxidase A</strong>, catechol O methyltransferese, SOD2, NQO2, PICK1 gene were identified.
+MAOA	drug	alcohol	18405071	A case group of males with type 2 <b>alcoholism</b> (N=59) and a control group of healthy males (N=282), both of Croatian origin, were analyzed for the frequency distribution of polymorphisms in 5HT transporter (5HTT VNTR2, 5HTT LPR), monoamine oxidase A (<strong>MAOA</strong> uVNTR) and B (MAOB A/G) and tryptophan hydroxylase 1 (TPH1 A218C) and 2 (TPH2 G 703T) genes.
+MAOA	drug	alcohol	18405071	A case group of males with type 2 <b>alcoholism</b> (N=59) and a control group of healthy males (N=282), both of Croatian origin, were analyzed for the frequency distribution of polymorphisms in 5HT transporter (5HTT VNTR2, 5HTT LPR), <strong>monoamine oxidase A</strong> (<strong>MAOA</strong> uVNTR) and B (MAOB A/G) and tryptophan hydroxylase 1 (TPH1 A218C) and 2 (TPH2 G 703T) genes.
+MAOA	drug	nicotine	17912044	This study examined the effects of three MAOIs (phenelzine, clorgyline and pargyline) with varying selectivity for <strong>MAOA</strong> and MAOB in the <b>nicotine</b> drug discrimination procedure in rats.
+MAOA	drug	nicotine	17912044	Although the selective <strong>MAOA</strong> inhibitor clorgyline (3 56 mg/kg) and the selective MAOB inhibitor pargyline (3 56 mg/kg) did not elicit any <b>nicotine</b> appropriate responding, partial substitution was obtained with the nonselective MAO inhibitor phenelzine (1 17 mg/kg).
+MAOA	drug	nicotine	17912044	These findings indicate that concomitant inhibition of <strong>MAOA</strong> and MAOB can enhance the discriminative stimulus effect of <b>nicotine</b> in rats.
+MAOA	drug	alcohol	17476365	<strong>Monoamine oxidase A</strong> polymorphisms might modify the association between the dopamine D2 receptor gene and <b>alcohol</b> dependence.
+MAOA	addiction	dependence	17476365	<strong>Monoamine oxidase A</strong> polymorphisms might modify the association between the dopamine D2 receptor gene and alcohol <b>dependence</b>.
+MAOA	drug	alcohol	17476365	Therefore, the present study investigates whether the association between the dopamine D2 receptor (DRD2) gene and <b>alcoholism</b> is affected by different polymorphisms of the MAO type A (<strong>MAOA</strong>) gene.
+MAOA	drug	alcohol	17347351	For example, it has been shown that childhood maltreatment interacts with a monoamine oxidase A (<strong>MAOA</strong>) gene variant to predict antisocial behavior that is often associated with <b>alcoholism</b>, and an interaction between early life stress and a serotonin transporter promoter variant predicts <b>alcohol</b> abuse in nonhuman primates and depression in humans.
+MAOA	drug	alcohol	17347351	For example, it has been shown that childhood maltreatment interacts with a <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) gene variant to predict antisocial behavior that is often associated with <b>alcoholism</b>, and an interaction between early life stress and a serotonin transporter promoter variant predicts <b>alcohol</b> abuse in nonhuman primates and depression in humans.
+MAOA	drug	nicotine	17229101	<strong>Monoamine oxidase A</strong> rather than monoamine oxidase B inhibition increases <b>nicotine</b> reinforcement in rats.
+MAOA	addiction	reward	17229101	<strong>Monoamine oxidase A</strong> rather than monoamine oxidase B inhibition increases nicotine <b>reinforcement</b> in rats.
+MAOA	drug	nicotine	17229101	It has been shown that <b>tobacco</b> smoke contains monoamine oxidase (MAO) A and B inhibitors and decreases <strong>MAO A</strong> and MAO B activity in <b>smokers</b>.
+MAOA	drug	nicotine	17229101	Here, we investigated the effects of clorgyline hydrochloride (irreversible <strong>MAO A</strong> inhibitor; 2 mg/kg/day), selegiline (irreversible MAO B inhibitor; 4 mg/kg) and the beta carboline norharmane hydrochloride (reversible MAO B inhibitor; 5 mg/kg/day) treatments on <b>nicotine</b> self administration (30 microg/kg/infusion, free base) in rats.
+MAOA	drug	nicotine	17229101	Taken together, these results indicate that <strong>MAO A</strong> inhibition interacts with <b>nicotine</b> to enhance its rewarding effects in rats and suggest that other compounds present in <b>tobacco</b>, such as beta carboline, may also play an important role in sustaining <b>smoking</b> behavior in humans.
+MAOA	drug	amphetamine	17157368	After rats acquired a stable pattern of morphine self administration under a progressive ratio schedule, chronic treatment was initiated with vehicle, L <b>methamphetamine</b>, clorgyline (a selective inhibitor of <strong>MAO A</strong>), or rasagiline (a selective inhibitor of MAO B); with both MAO inhibitors administered at a dose selective for one MAO isoform and a higher dose that inhibited both isoforms.
+MAOA	drug	opioid	17157368	After rats acquired a stable pattern of <b>morphine</b> self administration under a progressive ratio schedule, chronic treatment was initiated with vehicle, L methamphetamine, clorgyline (a selective inhibitor of <strong>MAO A</strong>), or rasagiline (a selective inhibitor of MAO B); with both MAO inhibitors administered at a dose selective for one MAO isoform and a higher dose that inhibited both isoforms.
+MAOA	drug	alcohol	17106424	Allele distribution of a <strong>monoamine oxidase A</strong> gene promoter polymorphism in German <b>alcoholics</b> and in subgroups with severe forms of <b>alcohol</b> withdrawal and its influence on plasma homovanillic acid.
+MAOA	addiction	withdrawal	17106424	Allele distribution of a <strong>monoamine oxidase A</strong> gene promoter polymorphism in German alcoholics and in subgroups with severe forms of alcohol <b>withdrawal</b> and its influence on plasma homovanillic acid.
+MAOA	drug	benzodiazepine	17092192	For people who do not respond to serotonin reuptake inhibitors, treatment options include benzodiazepines (<b>clonazepam</b>, <b>alprazolam</b>, and bromazepam), alpha2delta calcium channel blockers (gabapentin and pregabalin), reversible inhibitors of <strong>monoamine oxidase A</strong> (moclobemide, although agents in this class are not available in the United States), antiepileptics (levetiracetam), and atypical antipsychotics (olanzapine).
+MAOA	drug	nicotine	16893910	<strong>Monoamine oxidase A</strong> knockout mice exhibit impaired <b>nicotine</b> preference but normal responses to novel stimuli.
+MAOA	drug	nicotine	16893910	We examined the impact of constitutive monoamine oxidase A (<strong>MAOA</strong>) deficiency in mice on <b>nicotine</b> reward and responses to novel stimuli.
+MAOA	addiction	reward	16893910	We examined the impact of constitutive monoamine oxidase A (<strong>MAOA</strong>) deficiency in mice on nicotine <b>reward</b> and responses to novel stimuli.
+MAOA	drug	nicotine	16893910	We examined the impact of constitutive <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) deficiency in mice on <b>nicotine</b> reward and responses to novel stimuli.
+MAOA	addiction	reward	16893910	We examined the impact of constitutive <strong>monoamine oxidase A</strong> (<strong>MAOA</strong>) deficiency in mice on nicotine <b>reward</b> and responses to novel stimuli.
+MAOA	drug	nicotine	16893910	Age matched, male <strong>Maoa</strong> knockout (KO) mice and wild type (WT) littermates were tested for <b>nicotine</b> induced conditioned place preference (CPP); voluntary oral <b>nicotine</b> preference/intake; spontaneous locomotor activity in a novel, inescapable open field; and novelty place preference.
+MAOA	addiction	reward	16893910	Age matched, male <strong>Maoa</strong> knockout (KO) mice and wild type (WT) littermates were tested for nicotine induced conditioned place preference (<b>CPP</b>); voluntary oral nicotine preference/intake; spontaneous locomotor activity in a novel, inescapable open field; and novelty place preference.
+MAOA	drug	nicotine	16893910	<b>Nicotine</b> preference in WT mice was reduced in <strong>Maoa</strong> KO mice in the CPP and oral preference/intake tests.
+MAOA	addiction	reward	16893910	Nicotine preference in WT mice was reduced in <strong>Maoa</strong> KO mice in the <b>CPP</b> and oral preference/intake tests.
+MAOA	drug	nicotine	16893910	The observed phenotypes suggest that a constitutive deficiency of <strong>MAOA</strong> reduces the rewarding effects of <b>nicotine</b> without altering behavioral responses to novel stimuli in mice.
+MAOA	drug	nicotine	16893910	Constitutive <strong>MAOA</strong> activity levels are likely to contribute to the vulnerability or resiliency to <b>nicotine</b> addiction by altering the rewarding effects of <b>nicotine</b>.
+MAOA	addiction	addiction	16893910	Constitutive <strong>MAOA</strong> activity levels are likely to contribute to the vulnerability or resiliency to nicotine <b>addiction</b> by altering the rewarding effects of nicotine.
+MAOA	drug	alcohol	16763378	A functional polymorphism in the promoter region of the <strong>monoamine oxidase A</strong> gene is associated with the cigarette smoking quantity in <b>alcohol</b> dependent heavy smokers.
+MAOA	drug	nicotine	16763378	A functional polymorphism in the promoter region of the <strong>monoamine oxidase A</strong> gene is associated with the cigarette <b>smoking</b> quantity in alcohol dependent heavy <b>smokers</b>.
+MAOA	drug	alcohol	16763378	In a logistic regression model (dichotomized), smoking quantity was significantly predicted by <strong>MAO A</strong> genotype while no other variable (age, height, body weight, frequency of smoking, quantity and frequency of <b>alcohol</b> consumption) met the significance level.
+MAOA	drug	nicotine	16763378	In a logistic regression model (dichotomized), <b>smoking</b> quantity was significantly predicted by <strong>MAO A</strong> genotype while no other variable (age, height, body weight, frequency of <b>smoking</b>, quantity and frequency of alcohol consumption) met the significance level.
+MAOA	drug	nicotine	16763378	Since <b>tobacco</b> smoke is a potent inhibitor of <strong>MAO A</strong>, this result could be regarded as a genotype related dosage effect.
+MAOA	drug	alcohol	16763378	Taken together, in <b>alcohol</b> dependent heavily smoking men there is evidence for a <strong>MAO A</strong> gene associated effect on the quantity that is smoked as reflected by the daily number of cigarettes consumed.
+MAOA	drug	nicotine	16763378	Taken together, in alcohol dependent heavily <b>smoking</b> men there is evidence for a <strong>MAO A</strong> gene associated effect on the quantity that is smoked as reflected by the daily number of cigarettes consumed.
+MAOA	drug	alcohol	16526025	<strong>MAOA</strong> uVNTR polymorphism in a Brazilian sample: further support for the association with impulsive behaviors and <b>alcohol</b> dependence.
+MAOA	addiction	dependence	16526025	<strong>MAOA</strong> uVNTR polymorphism in a Brazilian sample: further support for the association with impulsive behaviors and alcohol <b>dependence</b>.
+MAOA	drug	alcohol	16526025	The objective of the present study is to replicate in a different culture the associations between the <strong>MAOA</strong> uVNTR with <b>alcoholism</b> and other phenotypes.
+MAOA	addiction	dependence	16526025	Our results confirmed previous reports showing an association of the low activity 3 repeat allele of <strong>MAOA</strong> uVNTR polymorphism with substance <b>dependence</b> and impulsive/antisocial behaviors.
+MAOA	drug	nicotine	16395299	Among 15 individual or combined MAOIs, including harmane, norharmane, moclobemide, selegiline, pargyline, clorgyline, tranylcypromine and phenelzine, only irreversible inhibitors of both <strong>MAO A</strong> and  B (tranylcypromine, phenelzine, and clorgyline+selegiline) allowed a locomotor response to <b>nicotine</b>.
+MAOA	drug	amphetamine	21901055	Of the MAO inhibitors, the propargylamine derivative clorgyline, an irreversible <strong>MAO A</strong> inhibitor, effectively blocks <b>METH</b> induced hyperlocomotion and behavioral sensitization in rodents.
+MAOA	addiction	sensitization	21901055	Of the MAO inhibitors, the propargylamine derivative clorgyline, an irreversible <strong>MAO A</strong> inhibitor, effectively blocks METH induced hyperlocomotion and behavioral <b>sensitization</b> in rodents.
+MAOA	drug	nicotine	16272956	CYP2A6, <strong>MAOA</strong>, DBH, DRD4, and 5HT2A genotypes, <b>smoking</b> behaviour and cotinine levels in 1518 UK adolescents.
+MAOA	drug	nicotine	16272956	No significant associations were identified for DBH, <strong>MAOA</strong>, DRD4 and 5HT2A markers, with <b>smoking</b> status or cotinine level at either age.
+MAOA	drug	nicotine	16207390	We investigated the association between <strong>MAOA</strong> polymorphisms (a VNTR polymorphism and an EcoRV polymorphism) and <b>smoking</b> status.
+MAOA	drug	nicotine	16207390	Multiple logistic regression models were used to analyse the association of <strong>MAOA</strong> gene polymorphisms with <b>smoking</b> status.
+MAOA	drug	nicotine	16207390	Moreover, <strong>MAOA</strong> gene haplotypes were associated significantly with <b>nicotine</b> dependence in every group.
+MAOA	addiction	dependence	16207390	Moreover, <strong>MAOA</strong> gene haplotypes were associated significantly with nicotine <b>dependence</b> in every group.
+MAOA	drug	nicotine	16207390	In conclusion, there is an important association between <strong>MAOA</strong> polymorphisms and <b>smoking</b> status, suggesting a possible role of <strong>MAOA</strong> gene variants in <b>nicotine</b> dependence.
+MAOA	addiction	dependence	16207390	In conclusion, there is an important association between <strong>MAOA</strong> polymorphisms and smoking status, suggesting a possible role of <strong>MAOA</strong> gene variants in nicotine <b>dependence</b>.
+MAOA	drug	nicotine	16177026	It is known that levels of the enzymes monoamine oxidase A (<strong>MAO A</strong>) and MAO B are reduced in the platelets and brains of <b>smokers</b> and that substances, other than <b>nicotine</b>, present in <b>tobacco</b> smoke have MAO inhibitory activities.
+MAOA	drug	nicotine	16177026	It is known that levels of the enzymes <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) and MAO B are reduced in the platelets and brains of <b>smokers</b> and that substances, other than <b>nicotine</b>, present in <b>tobacco</b> smoke have MAO inhibitory activities.
+MAOA	drug	opioid	16061219	High affinity binding of beta carbolines to imidazoline I2B receptors and <strong>MAO A</strong> in rat tissues: norharman blocks the effect of <b>morphine</b> withdrawal on DOPA/noradrenaline synthesis in the brain.
+MAOA	addiction	withdrawal	16061219	High affinity binding of beta carbolines to imidazoline I2B receptors and <strong>MAO A</strong> in rat tissues: norharman blocks the effect of morphine <b>withdrawal</b> on DOPA/noradrenaline synthesis in the brain.
+MAOA	addiction	intoxication	15635592	Young Caucasian women carrying higher expression <strong>MAOA</strong> VNTR alleles homozygous for the short allelic variant of the 5HTTLPR demonstrated the highest rate of <b>binge</b> drinking by self report, odds ratio (genotype odds: population odds) and 95% confidence intervals, 3.11 (1.14 18.10).
+MAOA	addiction	intoxication	15635592	Individuals carrying higher expression <strong>MAOA</strong> VNTR alleles carrying at least one long 5HTTLPR allelic variant had the lowest risk of <b>binge</b> drinking 0.46 (0.28 0.71).
+MAOA	drug	alcohol	15251892	Sequence variation within serotonin system genes, for example, a repeat polymorphism in the transcriptional control region of the monoamine oxidase gene (<strong>MAOA</strong> LPR), increases the propensity for adolescent males to consume <b>alcohol</b>.
+MAOA	drug	opioid	15088154	Analysis of monoamine oxidase A (<strong>MAO A</strong>) promoter polymorphism in male <b>heroin</b> dependent subjects: behavioural and personality correlates.
+MAOA	drug	opioid	15088154	Analysis of <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) promoter polymorphism in male <b>heroin</b> dependent subjects: behavioural and personality correlates.
+MAOA	drug	opioid	15088154	The promoter of the monoamine oxidase A (<strong>MAO A</strong>) gene was analysed to test whether length variation of the repeat polymorphism contributes to variation in individual vulnerability to aggressive criminal behaviour, and liability to <b>heroin</b> dependence.
+MAOA	addiction	dependence	15088154	The promoter of the monoamine oxidase A (<strong>MAO A</strong>) gene was analysed to test whether length variation of the repeat polymorphism contributes to variation in individual vulnerability to aggressive criminal behaviour, and liability to heroin <b>dependence</b>.
+MAOA	drug	opioid	15088154	The promoter of the <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) gene was analysed to test whether length variation of the repeat polymorphism contributes to variation in individual vulnerability to aggressive criminal behaviour, and liability to <b>heroin</b> dependence.
+MAOA	addiction	dependence	15088154	The promoter of the <strong>monoamine oxidase A</strong> (<strong>MAO A</strong>) gene was analysed to test whether length variation of the repeat polymorphism contributes to variation in individual vulnerability to aggressive criminal behaviour, and liability to heroin <b>dependence</b>.
+MAOA	drug	opioid	15088154	The repeat number of the <strong>MAO A</strong> polymorphism was assessed in 199 male subjects of Italian descent, a sample comprising 95 healthy subjects and 104 <b>heroin</b> dependent subjects including 52 addicted individuals with violent behaviour and antisocial personality disorder.
+MAOA	drug	opioid	15088154	No significant difference was evidenced in the frequencies of the <strong>MAO A</strong> alleles between <b>heroin</b> dependent subjects in general and control subjects.
+MAOA	drug	opioid	15088154	Our findings suggest that the low activity 3 repeat allele of the <strong>MAO A</strong> promoter polymorphism confers increased susceptibility to antisocial violent behavior and aggressiveness, rather than drug dependence per se, in <b>heroin</b> dependent males.
+MAOA	addiction	dependence	15088154	Our findings suggest that the low activity 3 repeat allele of the <strong>MAO A</strong> promoter polymorphism confers increased susceptibility to antisocial violent behavior and aggressiveness, rather than drug <b>dependence</b> per se, in heroin dependent males.
+MAOA	drug	alcohol	12824808	Neither antisocial personality disorder nor antisocial <b>alcoholism</b> is associated with the <strong>MAO A</strong> gene in Han Chinese males.
+MAOA	drug	alcohol	12824808	Recent studies on the genetics of <b>alcoholism</b> have suggested an association between antisocial <b>alcoholism</b> and the <strong>MAO A</strong> gene.
+MAOA	drug	alcohol	12824808	Consequently, the finding of an association between the <strong>MAO A</strong> gene and <b>alcoholism</b> or antisocial personality disorder seems tenuous.
+MAOA	drug	alcohol	12824808	Therefore, association studies of <b>alcoholism</b> or antisocial personality disorder in Chinese may be more reliable if pure antisocial <b>alcoholics</b>, pure antisocial personality disorders, and normal controls as <strong>MAO A</strong> gene are examined.
+MAOA	drug	alcohol	12824808	In this study, the associations among antisocial <b>alcoholism</b>, antisocial personality disorder, and the uVNTR and EcoRV polymorphisms of the <strong>MAO A</strong> gene, both individually and as a haplotype, were investigated among male adults recruited from jails in Taipei.
+MAOA	drug	alcohol	12824808	Thus, neither antisocial <b>alcoholism</b> nor antisocial personality disorder was associated with the genetic variants of <strong>MAO A</strong> gene.
+MAOA	drug	cocaine	12557270	Inasmuch as increases in NAc DA are associated with the reinforcing effects of <b>cocaine</b>, these results obtained in rodents suggest that <strong>MAO A</strong> and  B inhibition may not be a suitable strategy to antagonize <b>cocaine</b>'s reinforcing effects during <b>cocaine</b> detoxification.
+MAOA	addiction	reward	12557270	Inasmuch as increases in NAc DA are associated with the <b>reinforcing</b> effects of cocaine, these results obtained in rodents suggest that <strong>MAO A</strong> and  B inhibition may not be a suitable strategy to antagonize cocaine's <b>reinforcing</b> effects during cocaine detoxification.
+MAOA	drug	alcohol	12218658	Antisocial <b>alcoholism</b> symptom severity was higher with <strong>monoamine oxidase A</strong> C homozygotes or hemizygotes, indicating that low monoamine oxidase activity may be important.
+MAOA	drug	psychedelics	11877331	2 BFI; its cogeners BU216, BU224, BU226 and LSL60101; the reversible <strong>MAO A</strong> inhibitors moclobemide and RO41 1049; the beta carbolines harmane, norharmane and harmaline which also reversibly inhibit <strong>MAO A</strong>, and the anti addictive substance <b>ibogaine</b> exhibited potent, dose dependent substitution for 2 BFI.
+MAOA	addiction	addiction	11877331	2 BFI; its cogeners BU216, BU224, BU226 and LSL60101; the reversible <strong>MAO A</strong> inhibitors moclobemide and RO41 1049; the beta carbolines harmane, norharmane and harmaline which also reversibly inhibit <strong>MAO A</strong>, and the anti <b>addictive</b> substance ibogaine exhibited potent, dose dependent substitution for 2 BFI.
+MAOA	drug	nicotine	11694206	Previous studies have found that constituents in <b>tobacco</b> inhibit both forms of the enzyme monoamine oxidase (<strong>MAO A</strong> and MAO B).
+MAOA	drug	amphetamine	11471875	Chemically, 4 MTA is an <b>amphetamine</b> derivative and is a potent, non neurotoxic serotonin releasing agent and reversible inhibitor of rat <strong>monoamine oxidase A</strong>.
+MAOA	drug	nicotine	11343627	<b>Smokers</b> have 30 40 % lower MAOB and 20 30 % lower <strong>MAOA</strong> activity than non <b>smokers</b>.
+MAOA	drug	cocaine	11245920	Inhibition of <strong>MAO A</strong> fails to alter <b>cocaine</b> induced increases in extracellular dopamine and norepinephrine in rat nucleus accumbens.
+MAOA	drug	cocaine	11245920	In the present study, we tested the hypothesis that inhibition of catecholamine metabolism with the <strong>MAO A</strong> inhibitor, clorgyline, might enhance <b>cocaine</b> induced increases in extracellular dopamine and norepinephrine in rat nucleus accumbens.
+MAOA	drug	nicotine	10975602	<b>Smokers</b> with <strong>MAO A</strong> 1460 TT/TO smoked more cigarettes than those with CC/CT/CO (2.9, 95% CI 0.6, 5.1, P = 0.013).
+MAOA	drug	nicotine	10975602	Conversely, heavy <b>smokers</b> were less likely to have the <strong>MAO A</strong> 1460C allele (relative risk 0.3, 95% CI 0.1, 0.7, P = 0.012).
+MAOA	drug	alcohol	10943908	Different allele distribution of a regulatory <strong>MAOA</strong> gene promoter polymorphism in antisocial and anxious depressive <b>alcoholics</b>.
+MAOA	drug	alcohol	10943908	The present study tested whether a novel functional polymorphism in the promotor region of the X chromosomal monoamine oxidase A gene (<strong>MAOA</strong>) was related to antisocial and anxious depressive traits in <b>alcoholics</b>.
+MAOA	drug	alcohol	10943908	The present study tested whether a novel functional polymorphism in the promotor region of the X chromosomal <strong>monoamine oxidase A</strong> gene (<strong>MAOA</strong>) was related to antisocial and anxious depressive traits in <b>alcoholics</b>.
+MAOA	drug	alcohol	10943908	Due to the X chromosomal localization of the <strong>MAOA</strong> gene, psychobiological traits were compared separately for both genders of 298 male and 66 female <b>alcoholics</b>.
+MAOA	drug	alcohol	10943908	Taken together, these findings suggest that the 3 repeat allele of the <strong>MAOA</strong> polymorphism contributes modestly to the dimension of overand underreactive behaviors as possible antecedents of <b>alcoholism</b>.
+MAOA	drug	alcohol	10548268	The reversible <strong>MAO A</strong> inhibitor, befloxatone (0.3 3 mg/kg), and the irreversible <strong>MAO A</strong> inhibitor, clorgyline (10 30 mg/kg), also reduced <b>ethanol</b> self administration.
+MAOA	drug	alcohol	10359483	Association of a regulatory polymorphism in the promoter region of the <strong>monoamine oxidase A</strong> gene with antisocial <b>alcoholism</b>.
+MAOA	drug	alcohol	10359483	We analyzed a novel functional 30 bp repeat polymorphism in the promoter region of the X chromosomal monoamine oxidase A gene (<strong>MAOA</strong>) to test whether length variation of the repeat polymorphism contributes to variation in the individual vulnerability to antisocial behavior and liability to <b>alcohol</b> dependence.
+MAOA	addiction	dependence	10359483	We analyzed a novel functional 30 bp repeat polymorphism in the promoter region of the X chromosomal monoamine oxidase A gene (<strong>MAOA</strong>) to test whether length variation of the repeat polymorphism contributes to variation in the individual vulnerability to antisocial behavior and liability to alcohol <b>dependence</b>.
+MAOA	drug	alcohol	10359483	We analyzed a novel functional 30 bp repeat polymorphism in the promoter region of the X chromosomal <strong>monoamine oxidase A</strong> gene (<strong>MAOA</strong>) to test whether length variation of the repeat polymorphism contributes to variation in the individual vulnerability to antisocial behavior and liability to <b>alcohol</b> dependence.
+MAOA	addiction	dependence	10359483	We analyzed a novel functional 30 bp repeat polymorphism in the promoter region of the X chromosomal <strong>monoamine oxidase A</strong> gene (<strong>MAOA</strong>) to test whether length variation of the repeat polymorphism contributes to variation in the individual vulnerability to antisocial behavior and liability to alcohol <b>dependence</b>.
+MAOA	drug	alcohol	10359483	The repeat number (3 5) of the <strong>MAOA</strong> polymorphism was assessed in 488 male subjects of German descent, a sample comprising 185 psychiatrically screened control subjects and 303 <b>alcohol</b> dependent subjects including 59 <b>alcoholics</b> with antisocial personality disorder.
+MAOA	drug	alcohol	10359483	Our findings suggest that the low activity 3 repeat allele of the <strong>MAOA</strong> promoter polymorphism confers increased susceptibility to antisocial behavior rather than <b>alcohol</b> dependence per se in <b>alcohol</b> dependent males.
+MAOA	addiction	dependence	10359483	Our findings suggest that the low activity 3 repeat allele of the <strong>MAOA</strong> promoter polymorphism confers increased susceptibility to antisocial behavior rather than alcohol <b>dependence</b> per se in alcohol dependent males.
+MAOA	drug	alcohol	9444785	Therefore we used the histochemical approach for examination of the effect of chronic <b>alcohol</b> consumption on <strong>MAO A</strong> and B activities in definite brain structures: various types of aminergic neurons, glial cells and blood capillaries.
+MAOA	drug	alcohol	9444785	Despite the significant differences in the degree and direction of the changes in the activity of the MAO forms in rats with different <b>alcohol</b> craving, the calculated share of <strong>MAO A</strong> in the total MAO activity was regularly increased in all structures studied both in EP and WP animals; the share of MAO B activity accordingly decreased.
+MAOA	addiction	relapse	9444785	Despite the significant differences in the degree and direction of the changes in the activity of the MAO forms in rats with different alcohol <b>craving</b>, the calculated share of <strong>MAO A</strong> in the total MAO activity was regularly increased in all structures studied both in EP and WP animals; the share of MAO B activity accordingly decreased.
+MAOA	drug	nicotine	9179504	Effects of past history of major depression on <b>smoking</b> characteristics, <strong>monoamine oxidase A</strong> and  B activities and withdrawal symptoms in dependent <b>smokers</b>.
+MAOA	addiction	withdrawal	9179504	Effects of past history of major depression on smoking characteristics, <strong>monoamine oxidase A</strong> and  B activities and <b>withdrawal</b> symptoms in dependent smokers.
+MAOA	drug	nicotine	9179504	We have shown in a previous study that lifetime prevalence of major depression is higher in dependent <b>smokers</b> and they have lower <strong>monoamine oxidase A</strong> and  B activities than non <b>smokers</b>.
+MAOA	drug	nicotine	9179504	Adjusted for gender and body mass index dependent <b>smokers</b> with or without past history of depression had similar <strong>MAO A</strong> and MAO B activities but <b>smokers</b> with past history of major depression had significantly lower resting plasma norepinephrine levels.
+MAOA	drug	benzodiazepine	9352586	Tricyclic antidepressants (amitriptyline, desipramine), atypical agents (mianserin), selective serotonin reuptake inhibitors (paroxetine, sertraline, fluvoxamine), reversible inhibitors of <strong>monoamine oxidase A</strong> (moclobemide), as well as putative antidepressants such as 5 hydroxytryptamine1A agonists (zalospirone, ipsapirone), noncompetitive N methyl D aspartate antagonists (MK 801) and triazolobenzodiazepines (<b>alprazolam</b>, <b>adinazolam</b>), have demonstrated antidepressant like activity in this model.
+MAOA	drug	alcohol	8780428	Association of <strong>monoamine oxidase A</strong> alleles with <b>alcoholism</b> among male Chinese in Taiwan.
+MAOA	drug	alcohol	8780428	Restriction fragment length polymorphisms (RFLP) and dinucleotide repeat polymorphisms (DNRP) were used to determine <strong>MAOA</strong> and MAOB alleles in male <b>alcoholic</b> patients and nonalcoholic comparison subjects among Han Chinese and four aboriginal groups.
+MAOA	drug	alcohol	8780428	Significant associations of <b>alcohol</b> dependence with <strong>MAOA</strong> alleles (RFLP and DNRP) were found among the Han Chinese, but not among the aboriginal groups.
+MAOA	addiction	dependence	8780428	Significant associations of alcohol <b>dependence</b> with <strong>MAOA</strong> alleles (RFLP and DNRP) were found among the Han Chinese, but not among the aboriginal groups.
+MAOA	drug	alcohol	8780428	Genetic heterogeneity may underlie <b>alcoholism</b> among different ethnic groups in Taiwan, and <strong>MAOA</strong> mutations may play a role in susceptibility to <b>alcoholism</b> among Han Chinese.
+MAOA	addiction	withdrawal	8584234	Rat brain <strong>monoamine oxidase A</strong> and B inhibitory (tribulin) activity during drug <b>withdrawal</b> anxiety.
+MAOA	drug	alcohol	8584234	Morphine, <b>ethanol</b>, lorazepam and nicotine withdrawal was associated with significant anxiety and corresponding increase in brain tribulin activity, particularly its <strong>MAO A</strong> inhibitory component.
+MAOA	drug	benzodiazepine	8584234	Morphine, ethanol, <b>lorazepam</b> and nicotine withdrawal was associated with significant anxiety and corresponding increase in brain tribulin activity, particularly its <strong>MAO A</strong> inhibitory component.
+MAOA	drug	nicotine	8584234	Morphine, ethanol, lorazepam and <b>nicotine</b> withdrawal was associated with significant anxiety and corresponding increase in brain tribulin activity, particularly its <strong>MAO A</strong> inhibitory component.
+MAOA	drug	opioid	8584234	<b>Morphine</b>, ethanol, lorazepam and nicotine withdrawal was associated with significant anxiety and corresponding increase in brain tribulin activity, particularly its <strong>MAO A</strong> inhibitory component.
+MAOA	addiction	withdrawal	8584234	Morphine, ethanol, lorazepam and nicotine <b>withdrawal</b> was associated with significant anxiety and corresponding increase in brain tribulin activity, particularly its <strong>MAO A</strong> inhibitory component.
+MAOA	drug	nicotine	7586937	A reversible <strong>monoamine oxidase A</strong> inhibitor (moclobemide) facilitates <b>smoking</b> cessation and abstinence in heavy, dependent <b>smokers</b>.
+MAOA	addiction	withdrawal	7586937	Secondary outcome measures were <b>withdrawal</b> symptoms, Montgomery Asberg Depression Rating Scale, Hamilton anxiety rating scores, platelet MAO B activity, and plasma dihydroxyphenylglycol as a measure of <strong>MAO A</strong> activity.
+MAOA	drug	alcohol	7969881	Changes in the brain content of DA and qualitative and quantitative changes in MAO (an increase and solubilization of <strong>MAO A</strong> and B activity in the liver) were identified in the offspring of <b>alcoholic</b> rats.
+MAOA	drug	amphetamine	8473997	l Deprenyl produced clear generalization to the d <b>amphetamine</b> stimulus only at very high doses of 17.0 to 30.0 mg/kg, doses about 10 fold higher than those that have a selective action on MAO B vs. <strong>MAO A</strong> and which start to have marked rate decreasing actions on food reinforced responding.
+MAOA	addiction	intoxication	24925295	It is found that in rats predisposed to catalepsy the threshold of audiogenic seizures is elevated; the activity of tryptophan hydroxylase in striatum is higher in rats predisposed to catalepsy genetically and due to a chronic methylphenidate <b>intoxication</b> as compared to control animals; noradrenaline content and noradrenaline/dopamine ratio is lower in the diencephalon of rats predisposed to catalepsy than in controls; cataleptic rats have a higher content of homovanillic acid in N.accumbens , and a higher frequency of inversion of hemispheric asymmetry as estimated by levels of dopamine and dioxyphenylacetic acid in N.accumbens and caudate nucleus, than normal rats; MAO B/<strong>MAO A</strong> ratio is higher in the brain stem of cataleptic than normal rats.
+MAOA	addiction	reward	3011984	the serotonin releasing compounds p chloroamphetamine (PCA) and fenfluramine, the <strong>MAO A</strong> inhibitors and serotonin releasing agents amiflamine and alpha ethyltryptamine and the serotonin agonists 5 methoxy N, N dimethyltryptamine (5 MeODMT), 8 hydroxy 2 (di n propylamino) tetraline (8 OH DPAT), m chlorophenyl piperazine (m <b>CPP</b>) and 5 methoxy 3 (1,2,3,6 tetrahydropyridin 4 yl)1H indole (RU 24969), did not leave their home cages when the grid covers were removed in contrast to normal rats who almost immediately left the cages.
+MAOA	drug	benzodiazepine	6121956	Biochemical studies have revealed beta carbolines' several actions, including inhibition of <strong>MAO A</strong>, competitive inhibition of 5 HT uptake, general inhibition of Na+ dependent transports, binding to <b>benzodiazepine</b> and opiate receptors and probable action on dopamine receptors, which may all participate to a variable degree in the actions of different beta carbolines.
+MAOA	drug	benzodiazepine	6121956	It has been suggested that some beta carbolines act as the physiological ligands (agonists) of the <b>benzodiazepine</b> receptors, but the physiological beta carbolines so far known seem to have other effects, such as the inhibition of <strong>MAO A</strong> or 5 HT uptake in low concentrations.
+SLC1A2	drug	alcohol	32099993	In this study, we investigated the effects of cocaine exposure and ampicillin/sulbactam (AMP/SUL), a β lactam antibiotic known to upregulate <strong>GLT 1</strong> and xCT, on relapse like <b>ethanol</b> intake and the expression of astrocytic glutamate transporters in mesocorticolimbic brain regions.
+SLC1A2	drug	cocaine	32099993	In this study, we investigated the effects of <b>cocaine</b> exposure and ampicillin/sulbactam (AMP/SUL), a β lactam antibiotic known to upregulate <strong>GLT 1</strong> and xCT, on relapse like ethanol intake and the expression of astrocytic glutamate transporters in mesocorticolimbic brain regions.
+SLC1A2	addiction	relapse	32099993	In this study, we investigated the effects of cocaine exposure and ampicillin/sulbactam (AMP/SUL), a β lactam antibiotic known to upregulate <strong>GLT 1</strong> and xCT, on <b>relapse</b> like ethanol intake and the expression of astrocytic glutamate transporters in mesocorticolimbic brain regions.
+SLC1A2	drug	alcohol	32099993	Cocaine exposure induced an <b>alcohol</b> deprivation effect (ADE), which was associated in part by a decrease in the expression of <strong>GLT 1</strong> and xCT in the nucleus accumbens (NAc) core.
+SLC1A2	drug	cocaine	32099993	<b>Cocaine</b> exposure induced an alcohol deprivation effect (ADE), which was associated in part by a decrease in the expression of <strong>GLT 1</strong> and xCT in the nucleus accumbens (NAc) core.
+SLC1A2	drug	alcohol	32099993	reduced <b>ethanol</b> intake during 4 days of <b>ethanol</b> re exposure and upregulated <strong>GLT 1</strong> and xCT expression in the NAc core, NAc shell and dorsomedial prefrontal cortex (dmPFC).
+SLC1A2	drug	cocaine	31998080	Astroglial mechanisms for maintaining extracellular glutamate homeostasis through cysteine/glutamate exchanger (xCT) and glutamate transporter <strong>GLT1</strong> are dysregulated following <b>cocaine</b> exposure and contribute to altered glutamatergic synaptic plasticity.
+SLC1A2	drug	amphetamine	31952958	Furthermore, sensitized behavioral responding to and for <b>amphetamine</b> following exposure to uncertainty is accompanied by increased levels of Ca2+/calmodulin dependent protein kinase II (CaMKII) and protein kinase C (PKC) phosphorylation as well as altered protein levels of the transcription factor ∆FosB (increased) and glutamate transporter 1 (<strong>GLT1</strong>; decreased) in NAcc tissues.
+SLC1A2	addiction	relapse	31952958	Increased ∆FosB and decreased <strong>GLT1</strong> levels are observed following psychostimulant exposure, are associated with increased drug taking and <b>seeking</b>, and are known to modulate AMPA receptors and extracellular glutamate levels respectively.
+SLC1A2	drug	alcohol	31733014	<b>Alcohol</b> intake either on the chronic phase or following deprivation and re access led to a 50% reduction of cortical glutamate transporter <strong>GLT 1</strong> levels, while aspirin administration fully returned <strong>GLT 1</strong> to normal levels.
+SLC1A2	addiction	relapse	31733014	N acetylcysteine administration did not alter <strong>GLT 1</strong> levels, while N acetylcysteine may activate the cystine/glutamate transport xCT, presynaptically inhibiting <b>relapse</b>.
+SLC1A2	addiction	addiction	31630007	<strong>GLT 1</strong> expression and glutamate uptake can be affected by <b>addictive</b> drugs and can be used as a target in <b>addiction</b> pharmacotherapy.
+SLC1A2	drug	opioid	31630007	In the present study, in <b>morphine</b> dependent rats, the effect of minocycline on expression of <strong>GLT 1</strong> in nucleus accumbens was investigated by immunohistochemistry.
+SLC1A2	addiction	addiction	31630007	In line with other studies, our findings showed that restoring <strong>GLT 1</strong> expression with minocycline might be considered as a potential target for correcting pre clinical and clinical manifestations of drug <b>addiction</b>.
+SLC1A2	drug	nicotine	31330570	<b>Nicotine</b> self administration is associated with decreased expression of the glial glutamate transporter (<strong>GLT 1</strong>) and the cystine glutamate exchange protein xCT within the nucleus accumbens core (NAcore).
+SLC1A2	drug	nicotine	31330570	Here, we confirm that extinction of <b>nicotine</b> seeking behavior is associated with impaired NAcore <strong>GLT 1</strong> function and expression and demonstrates that reinstatement of <b>nicotine</b> seeking rapidly enhances membrane fraction <strong>GLT 1</strong> expression.
+SLC1A2	addiction	relapse	31330570	Here, we confirm that extinction of nicotine <b>seeking</b> behavior is associated with impaired NAcore <strong>GLT 1</strong> function and expression and demonstrates that <b>reinstatement</b> of nicotine <b>seeking</b> rapidly enhances membrane fraction <strong>GLT 1</strong> expression.
+SLC1A2	drug	nicotine	31330570	In separate experiments, rats received NAC and an antisense vivo morpholino to selectively suppress <strong>GLT 1</strong> expression in the NAcore during extinction and were subsequently tested for cue induced reinstatement of <b>nicotine</b> seeking.
+SLC1A2	addiction	relapse	31330570	In separate experiments, rats received NAC and an antisense vivo morpholino to selectively suppress <strong>GLT 1</strong> expression in the NAcore during extinction and were subsequently tested for cue induced <b>reinstatement</b> of nicotine <b>seeking</b>.
+SLC1A2	drug	nicotine	31330570	NAC treatment rescued NAcore <strong>GLT 1</strong> expression and attenuated cue induced <b>nicotine</b> seeking, which was blocked by <strong>GLT 1</strong> antisense.
+SLC1A2	addiction	relapse	31330570	NAC treatment rescued NAcore <strong>GLT 1</strong> expression and attenuated cue induced nicotine <b>seeking</b>, which was blocked by <strong>GLT 1</strong> antisense.
+SLC1A2	drug	nicotine	31330570	Viral manipulation of the NF κB pathway, which is downstream of TNFα, revealed that cue induced <b>nicotine</b> seeking is regulated by NF κB pathway signaling in the NAcore independent of <strong>GLT 1</strong> expression.
+SLC1A2	addiction	relapse	31330570	Viral manipulation of the NF κB pathway, which is downstream of TNFα, revealed that cue induced nicotine <b>seeking</b> is regulated by NF κB pathway signaling in the NAcore independent of <strong>GLT 1</strong> expression.
+SLC1A2	drug	alcohol	31286996	Knockdown of the glutamate transporter <strong>GLT 1</strong> by the intracerebral administration of an antisense oligonucleotide fully abolished the inhibitory effect of the secretome on <b>ethanol</b> and nicotine intake.
+SLC1A2	drug	nicotine	31286996	Knockdown of the glutamate transporter <strong>GLT 1</strong> by the intracerebral administration of an antisense oligonucleotide fully abolished the inhibitory effect of the secretome on ethanol and <b>nicotine</b> intake.
+SLC1A2	drug	alcohol	31286996	The non invasive intranasal administration of secretome generated by human adipose tissue derived activated mesenchymal stem cells markedly inhibits <b>alcohol</b> and nicotine self administration, an effect mediated by the glutamate <strong>GLT 1</strong> transporter.
+SLC1A2	drug	nicotine	31286996	The non invasive intranasal administration of secretome generated by human adipose tissue derived activated mesenchymal stem cells markedly inhibits alcohol and <b>nicotine</b> self administration, an effect mediated by the glutamate <strong>GLT 1</strong> transporter.
+SLC1A2	drug	cocaine	31266052	After extinction training, we assessed surface expression of the glutamate transporter <strong>GLT 1</strong> and glutamate efflux in the nucleus accumbens (NA) core during the reinstatement of <b>cocaine</b> seeking.
+SLC1A2	addiction	relapse	31266052	After extinction training, we assessed surface expression of the glutamate transporter <strong>GLT 1</strong> and glutamate efflux in the nucleus accumbens (NA) core during the <b>reinstatement</b> of cocaine <b>seeking</b>.
+SLC1A2	drug	alcohol	31266052	However, we noted significant changes in glutamate homeostasis in the NA core of cocaine + <b>alcohol</b> rats relative to rats consuming cocaine alone, such as increased surface <strong>GLT 1</strong> expression and a lack of increase in glutamate efflux during reinstatement of cocaine seeking.
+SLC1A2	drug	cocaine	31266052	However, we noted significant changes in glutamate homeostasis in the NA core of <b>cocaine</b> + alcohol rats relative to rats consuming <b>cocaine</b> alone, such as increased surface <strong>GLT 1</strong> expression and a lack of increase in glutamate efflux during reinstatement of <b>cocaine</b> seeking.
+SLC1A2	addiction	relapse	31266052	However, we noted significant changes in glutamate homeostasis in the NA core of cocaine + alcohol rats relative to rats consuming cocaine alone, such as increased surface <strong>GLT 1</strong> expression and a lack of increase in glutamate efflux during <b>reinstatement</b> of cocaine <b>seeking</b>.
+SLC1A2	drug	cocaine	31100299	We also analyzed the ability of the β lactam antibiotic, ceftriaxone, to attenuate the persistence of CPP after a <b>cocaine</b> free period in animals showing vulnerability to <b>cocaine</b> rewarding effects, and furthermore we determined <strong>GLT 1</strong>, xCT, NF κB and Nrf2 protein expression.
+SLC1A2	addiction	reward	31100299	We also analyzed the ability of the β lactam antibiotic, ceftriaxone, to attenuate the persistence of <b>CPP</b> after a cocaine free period in animals showing vulnerability to cocaine rewarding effects, and furthermore we determined <strong>GLT 1</strong>, xCT, NF κB and Nrf2 protein expression.
+SLC1A2	drug	cocaine	31100299	Moreover, repeated administrations of ceftriaxone during <b>cocaine</b> free perios attenuated CPP persistence and normalized <strong>GLT 1</strong> level in the NAc.
+SLC1A2	addiction	reward	31100299	Moreover, repeated administrations of ceftriaxone during cocaine free perios attenuated <b>CPP</b> persistence and normalized <strong>GLT 1</strong> level in the NAc.
+SLC1A2	drug	cocaine	31100299	Future experiments may resolve the question concerning whether modulation exclusively of the <strong>GLT 1</strong> expression in the HIP may attenuate <b>cocaine</b> induced place preference or relapse.
+SLC1A2	addiction	relapse	31100299	Future experiments may resolve the question concerning whether modulation exclusively of the <strong>GLT 1</strong> expression in the HIP may attenuate cocaine induced place preference or <b>relapse</b>.
+SLC1A2	drug	cannabinoid	30978452	We demonstrated that riluzole significantly inhibited HU210 induced glutamate release through increased expression of glial glutamate transporter 1 (<strong>GLT 1</strong>) in cultured astrocytes, and an infusion of riluzole into the bilateral VTA in rats prevented the potent <b>cannabinoid</b> HU210 facilitated LTD induction in 2 month old animals, which was blocked by bath application of dihydrokainate (DHK), a selective <strong>GLT 1</strong> inhibitor.
+SLC1A2	drug	amphetamine	30926546	We hypothesized that, like cocaine, this glutamate 'overflow' during <b>methamphetamine</b> seeking arises via decreased expression of the astroglial glutamate transporter <strong>GLT 1</strong>, and withdrawal of perisynaptic astroglial processes (PAPs) from synapses.
+SLC1A2	drug	cocaine	30926546	We hypothesized that, like <b>cocaine</b>, this glutamate 'overflow' during methamphetamine seeking arises via decreased expression of the astroglial glutamate transporter <strong>GLT 1</strong>, and withdrawal of perisynaptic astroglial processes (PAPs) from synapses.
+SLC1A2	addiction	relapse	30926546	We hypothesized that, like cocaine, this glutamate 'overflow' during methamphetamine <b>seeking</b> arises via decreased expression of the astroglial glutamate transporter <strong>GLT 1</strong>, and withdrawal of perisynaptic astroglial processes (PAPs) from synapses.
+SLC1A2	addiction	withdrawal	30926546	We hypothesized that, like cocaine, this glutamate 'overflow' during methamphetamine seeking arises via decreased expression of the astroglial glutamate transporter <strong>GLT 1</strong>, and <b>withdrawal</b> of perisynaptic astroglial processes (PAPs) from synapses.
+SLC1A2	drug	amphetamine	30926546	As expected, <b>methamphetamine</b> self administration and extinction decreased the level of contact made by PAPs in the NAcore, yet did not impact glutamate uptake, <strong>GLT 1</strong> expression, or the general structural characteristics of astrocytes.
+SLC1A2	drug	amphetamine	30926546	Interestingly, systemic administration of N acetylcysteine (NAC), a drug that both upregulates <strong>GLT 1</strong> and promotes glial glutamate release, reduced cued <b>methamphetamine</b> seeking.
+SLC1A2	addiction	relapse	30926546	Interestingly, systemic administration of N acetylcysteine (NAC), a drug that both upregulates <strong>GLT 1</strong> and promotes glial glutamate release, reduced cued methamphetamine <b>seeking</b>.
+SLC1A2	drug	alcohol	30820030	The therapeutic effect of mesenchymal stem cells is mediated by increased levels of the brain <strong>GLT 1</strong> glutamate transporter, indicating that glutamate signaling is pivotal for <b>alcohol</b> relapse.
+SLC1A2	addiction	relapse	30820030	The therapeutic effect of mesenchymal stem cells is mediated by increased levels of the brain <strong>GLT 1</strong> glutamate transporter, indicating that glutamate signaling is pivotal for alcohol <b>relapse</b>.
+SLC1A2	drug	alcohol	30716289	Cocaine, <b>ethanol</b>, and methamphetamine reduce the expression of cystine glutamate antiporter (xCT) and primary glial glutamate transporter 1 (<strong>GLT1</strong>) leading to increased extrasynaptic glutamate.
+SLC1A2	drug	amphetamine	30716289	Cocaine, ethanol, and <b>methamphetamine</b> reduce the expression of cystine glutamate antiporter (xCT) and primary glial glutamate transporter 1 (<strong>GLT1</strong>) leading to increased extrasynaptic glutamate.
+SLC1A2	drug	cocaine	30716289	<b>Cocaine</b>, ethanol, and methamphetamine reduce the expression of cystine glutamate antiporter (xCT) and primary glial glutamate transporter 1 (<strong>GLT1</strong>) leading to increased extrasynaptic glutamate.
+SLC1A2	drug	alcohol	30716289	Ceftriaxone (CTX) restores xCT and <strong>GLT1</strong> expression and effectively suppresses cocaine and <b>ethanol</b> reinstatement, however, the effects of CTX on amphetamine (AMP) reinstatement are not determined.
+SLC1A2	drug	amphetamine	30716289	Ceftriaxone (CTX) restores xCT and <strong>GLT1</strong> expression and effectively suppresses cocaine and ethanol reinstatement, however, the effects of CTX on <b>amphetamine</b> (AMP) reinstatement are not determined.
+SLC1A2	drug	cocaine	30716289	Ceftriaxone (CTX) restores xCT and <strong>GLT1</strong> expression and effectively suppresses <b>cocaine</b> and ethanol reinstatement, however, the effects of CTX on amphetamine (AMP) reinstatement are not determined.
+SLC1A2	addiction	relapse	30716289	Ceftriaxone (CTX) restores xCT and <strong>GLT1</strong> expression and effectively suppresses cocaine and ethanol <b>reinstatement</b>, however, the effects of CTX on amphetamine (AMP) <b>reinstatement</b> are not determined.
+SLC1A2	addiction	relapse	30716289	We hypothesized that EC rearing would reduce <b>reinstatement</b> by altering <strong>GLT1</strong> or xCT expression in the NAc and medial prefrontal cortex (mPFC).
+SLC1A2	drug	cocaine	30714803	Research using the <b>cocaine</b> self administration and reinstatement animal model of relapse finds that the beta lactam antibiotic, ceftriaxone, attenuates <b>cocaine</b> primed reinstatement of <b>cocaine</b> seeking and upregulates two proteins that regulate glutamate release and reuptake (xCT and <strong>GLT 1</strong>, respectively) in the nucleus accumbens core (NAc).
+SLC1A2	addiction	relapse	30714803	Research using the cocaine self administration and <b>reinstatement</b> animal model of <b>relapse</b> finds that the beta lactam antibiotic, ceftriaxone, attenuates cocaine primed <b>reinstatement</b> of cocaine <b>seeking</b> and upregulates two proteins that regulate glutamate release and reuptake (xCT and <strong>GLT 1</strong>, respectively) in the nucleus accumbens core (NAc).
+SLC1A2	addiction	relapse	30714803	We tested three compounds with beta lactam rings for their ability to attenuate cue primed <b>reinstatement</b> and increase <strong>GLT 1</strong> and xCT expression in the NAc and prefrontal cortex (PFC).
+SLC1A2	drug	cocaine	30714803	Furthermore, the upregulation of both <strong>GLT 1</strong> and xCT in the NAc may be needed to attenuate <b>cocaine</b> seeking.
+SLC1A2	addiction	relapse	30714803	Furthermore, the upregulation of both <strong>GLT 1</strong> and xCT in the NAc may be needed to attenuate cocaine <b>seeking</b>.
+SLC1A2	addiction	relapse	30471010	Ample evidence showed that β lactam antibiotics are effective in upregulating <strong>GLT 1</strong> and xCT expression, thus improving glutamate homeostasis and attenuating <b>relapse</b> to drugs of abuse.
+SLC1A2	drug	alcohol	30471010	Chronic exposure to <b>ethanol</b> decreased the expression of <strong>GLT 1</strong> and xCT in the NAc shell, but not in the NAc core or dmPFC.
+SLC1A2	drug	alcohol	30471010	CA treatment blocked the reinstatement of METH seeking, decreased <b>ethanol</b> intake, and restored the expression of <strong>GLT 1</strong> and xCT in the NAc shell.
+SLC1A2	drug	amphetamine	30471010	CA treatment blocked the reinstatement of <b>METH</b> seeking, decreased ethanol intake, and restored the expression of <strong>GLT 1</strong> and xCT in the NAc shell.
+SLC1A2	addiction	relapse	30471010	CA treatment blocked the <b>reinstatement</b> of METH <b>seeking</b>, decreased ethanol intake, and restored the expression of <strong>GLT 1</strong> and xCT in the NAc shell.
+SLC1A2	drug	cannabinoid	30257184	In this study, we investigated the effects of Ampicillin/Sulbactam, β lactam compounds known to upregulate <strong>GLT 1</strong> and xCT, on <b>cannabinoid</b> seeking behavior using CP.
+SLC1A2	addiction	relapse	30257184	In this study, we investigated the effects of Ampicillin/Sulbactam, β lactam compounds known to upregulate <strong>GLT 1</strong> and xCT, on cannabinoid <b>seeking</b> behavior using CP.
+SLC1A2	addiction	relapse	30257184	Importantly, Ampicillin/Sulbactam treatment during the extinction phase attenuated CP induced <b>reinstatement</b> and restored the expression of <strong>GLT 1</strong> and xCT in mesocorticolimbic brain regions.
+SLC1A2	drug	cannabinoid	30257184	These findings suggest that β lactams may play a potential therapeutic role in attenuating dependence to <b>cannabinoids</b>, in part, through upregulation of <strong>GLT 1</strong> and xCT.
+SLC1A2	addiction	dependence	30257184	These findings suggest that β lactams may play a potential therapeutic role in attenuating <b>dependence</b> to cannabinoids, in part, through upregulation of <strong>GLT 1</strong> and xCT.
+SLC1A2	drug	alcohol	30239077	(2) Intranasally administered exosomes were found in the brain within 24 hours; (3) fully reversed both <b>alcohol</b> induced hippocampal oxidative stress, evidenced by a lower ratio of oxidized to reduced glutathione, and neuroinflammation, shown by a reduced astrocyte activation and microglial density; and (4) increased glutamate transporter <strong>GLT1</strong> expression in nucleus accumbens, counteracting the inhibition of glutamate transporter activity, reportedly depressed under oxidative stress conditions.
+SLC1A2	drug	cocaine	30144237	In <b>cocaine</b> naïve animals, SERT removal led to reduced baseline Hb mRNA levels of critical determinants of glutamate transmission, such as <strong>SLC1A2</strong>, the main glutamate transporter and N methyl D aspartate (Grin1, Grin2A and Grin2B) as well as α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (Gria1 and Gria2) receptor subunits, with no changes in the scaffolding protein Dlg4.
+SLC1A2	drug	cocaine	30144237	In response to ShA and LgA <b>cocaine</b> intake, <strong>SLC1A2</strong> and Grin1 mRNA levels decreased in SERT+/+ rats to levels equal of those of SERT /  rats.
+SLC1A2	addiction	relapse	29604365	), known to upregulate <strong>GLT 1</strong> and xCT, on <b>reinstatement</b> to HYD (5 mg/kg, i.p.)
+SLC1A2	drug	alcohol	29567966	The MSC spheroid administration fully normalized <b>alcohol</b> induced neuroinflammation, as shown by a reduced astrocyte activation, and markedly increased the levels of the astrocyte Na glutamate (<strong>GLT 1</strong>) transporter.
+SLC1A2	drug	cocaine	29567092	Ceftriaxone restores <b>cocaine</b> induced deficits in both system xc  and <strong>GLT 1</strong> expression and function in the nucleus accumbens core (NAc).
+SLC1A2	drug	cocaine	29567092	We recently demonstrated that restoration of <strong>GLT 1</strong> expression in the NAc is necessary for ceftriaxone to attenuate reinstatement of <b>cocaine</b> seeking.
+SLC1A2	addiction	relapse	29567092	We recently demonstrated that restoration of <strong>GLT 1</strong> expression in the NAc is necessary for ceftriaxone to attenuate <b>reinstatement</b> of cocaine <b>seeking</b>.
+SLC1A2	drug	cocaine	29567092	These results indicate that upregulation of NAc <strong>GLT 1</strong> transporters alone is not sufficient to prevent the reinstatement of <b>cocaine</b> seeking and implicate additional mechanisms in regulating glutamate efflux.
+SLC1A2	addiction	relapse	29567092	These results indicate that upregulation of NAc <strong>GLT 1</strong> transporters alone is not sufficient to prevent the <b>reinstatement</b> of cocaine <b>seeking</b> and implicate additional mechanisms in regulating glutamate efflux.
+SLC1A2	drug	cocaine	29380665	To evaluate the role of glutamate on BDNF independent changes, we investigated the expression of the transporter <strong>GLT 1</strong> and the activation of the NMDA receptor subunit GluN2B, which were both increased in the PL cortex while reduced in the IL cortex.Conclusions: Our results show that adolescent <b>cocaine</b> exposure modulates BDNF system early after treatment in the mesocorticolimbic pathway, identifying a complex but specific set of changes that could provide clues for treatment.
+SLC1A2	drug	cocaine	29197981	In male rats, ceftriaxone attenuates the reinstatement of <b>cocaine</b> seeking while increasing glutamate transporter 1 (<strong>GLT 1</strong>) and xCT expression in the nucleus accumbens core (NAc).
+SLC1A2	addiction	relapse	29197981	In male rats, ceftriaxone attenuates the <b>reinstatement</b> of cocaine <b>seeking</b> while increasing glutamate transporter 1 (<strong>GLT 1</strong>) and xCT expression in the nucleus accumbens core (NAc).
+SLC1A2	drug	alcohol	29128307	The relationship between <strong>GLT 1</strong> maladaptation, LHb activity, and abnormal behaviors related to <b>alcohol</b> withdrawal, however, remains unknown.
+SLC1A2	addiction	withdrawal	29128307	The relationship between <strong>GLT 1</strong> maladaptation, LHb activity, and abnormal behaviors related to alcohol <b>withdrawal</b>, however, remains unknown.
+SLC1A2	drug	alcohol	29128307	Here we show that dihydrokainic acid (DHK), a <strong>GLT 1</strong> blocker, potentiated glutamatergic transmission to LHb neurons in slices from <b>ethanol</b> naïve rats; this potentiation, though, was not observed in slices from rats withdrawn from repeated in vivo <b>ethanol</b> administration, suggesting reduced <strong>GLT 1</strong> function.
+SLC1A2	drug	alcohol	29128307	These findings highlight the significant role of LHb astrocytic <strong>GLT 1</strong> in the hyperactivity of LHb neurons, and in depressive  and anxiety like behaviors during <b>ethanol</b> withdrawal.
+SLC1A2	addiction	withdrawal	29128307	These findings highlight the significant role of LHb astrocytic <strong>GLT 1</strong> in the hyperactivity of LHb neurons, and in depressive  and anxiety like behaviors during ethanol <b>withdrawal</b>.
+SLC1A2	drug	alcohol	29128307	Thus, <strong>GLT 1</strong> in the LHb could serve as a therapeutic target for psychiatric disorders comorbid with <b>ethanol</b> withdrawal.
+SLC1A2	addiction	withdrawal	29128307	Thus, <strong>GLT 1</strong> in the LHb could serve as a therapeutic target for psychiatric disorders comorbid with ethanol <b>withdrawal</b>.
+SLC1A2	drug	cocaine	28990593	Riluzole Impairs <b>Cocaine</b> Reinstatement and Restores Adaptations in Intrinsic Excitability and <strong>GLT 1</strong> Expression.
+SLC1A2	addiction	relapse	28990593	Riluzole Impairs Cocaine <b>Reinstatement</b> and Restores Adaptations in Intrinsic Excitability and <strong>GLT 1</strong> Expression.
+SLC1A2	drug	cocaine	28990593	Riluzole also reversed the <b>cocaine</b> induced suppression of the high affinity glutamate transporter 1 (<strong>EAAT2</strong>/GLT 1) in the nucleus accumbens (NAc).
+SLC1A2	drug	cocaine	28990593	Riluzole also reversed the <b>cocaine</b> induced suppression of the high affinity glutamate transporter 1 (<strong>EAAT2</strong>/<strong>GLT 1</strong>) in the nucleus accumbens (NAc).
+SLC1A2	drug	cocaine	28990593	<strong>GLT 1</strong> is responsible for the majority of glutamate uptake in the brain, and has been previously reported to be downregulated by <b>cocaine</b>.
+SLC1A2	drug	cocaine	28919080	Regulation of glutamate transporter 1 (<strong>GLT 1</strong>) gene expression by <b>cocaine</b> self administration and withdrawal.
+SLC1A2	addiction	withdrawal	28919080	Regulation of glutamate transporter 1 (<strong>GLT 1</strong>) gene expression by cocaine self administration and <b>withdrawal</b>.
+SLC1A2	drug	cocaine	28919080	The decrease in <strong>GLT 1</strong> protein expression following <b>cocaine</b> self administration is dependent on both the amount of <b>cocaine</b> self administered and the length of withdrawal, with longer access to <b>cocaine</b> and longer withdrawal periods leading to greater decreases in <strong>GLT 1</strong> protein.
+SLC1A2	addiction	withdrawal	28919080	The decrease in <strong>GLT 1</strong> protein expression following cocaine self administration is dependent on both the amount of cocaine self administered and the length of <b>withdrawal</b>, with longer access to cocaine and longer <b>withdrawal</b> periods leading to greater decreases in <strong>GLT 1</strong> protein.
+SLC1A2	drug	cocaine	28919080	However, the mechanism(s) by which <b>cocaine</b> downregulates <strong>GLT 1</strong> protein remains unknown.
+SLC1A2	drug	cocaine	28919080	We used qRT PCR to examine gene expression of <strong>GLT 1</strong> splice isoforms (GLT 1A, GLT 1B) in the NAc, prelimbic cortex (PL) and basolateral amygdala (BLA) of rats, following two widely used models of <b>cocaine</b> self administration: short access (ShA) self administration, and the long access (LgA) self administration/incubation model.
+SLC1A2	drug	cocaine	28919080	While downregulation of <strong>GLT 1</strong> protein is observed following ShA <b>cocaine</b> self administration and extinction, this model did not lead to a change in GLT 1A or GLT 1B gene expression in any brain region examined.
+SLC1A2	drug	cocaine	28919080	In addition, LgA <b>cocaine</b> self administration and withdrawal induced hypermethylation of the <strong>GLT 1</strong> gene in the NAc.
+SLC1A2	addiction	withdrawal	28919080	In addition, LgA cocaine self administration and <b>withdrawal</b> induced hypermethylation of the <strong>GLT 1</strong> gene in the NAc.
+SLC1A2	drug	cocaine	28919080	These results indicate that a decrease in NAc <strong>GLT 1</strong> mRNA is only observed after extended access to <b>cocaine</b> combined with protracted abstinence, and that epigenetic mechanisms likely contribute to this effect.
+SLC1A2	drug	alcohol	28826758	Studies from our laboratory showed that upregulation of glutamate transporter 1 (<strong>GLT 1</strong>) and cystine glutamate exchanger (xCT) expression with ceftriaxone, β lactam antibiotic, in the brain was associated with attenuation of <b>ethanol</b> consumption.
+SLC1A2	drug	alcohol	28826758	In this study, we tested clavulanic acid, which is another β lactam compound with negligible antimicrobial activity, on <b>ethanol</b> consumption and expression of <strong>GLT 1</strong>, xCT and glutamate aspartate transporter (GLAST) in male <b>alcohol</b> preferring (P) rats.
+SLC1A2	drug	alcohol	28826758	These findings revealed that clavulanic acid at 20 40 fold lower dose than ceftriaxone can attenuate <b>ethanol</b> consumption, in part through upregulation of <strong>GLT 1</strong> and xCT expression in the nucleus accumbens.
+SLC1A2	addiction	addiction	28785205	Differential <strong>SLC1A2</strong> Promoter Methylation in Bipolar Disorder With or Without <b>Addiction</b>.
+SLC1A2	addiction	addiction	28785205	This study thus focused on epigenetic DNA methylation regulation of <strong>SLC1A2</strong>, encoding for EAAT2, in BD with variable environmental influences of <b>addiction</b>.
+SLC1A2	addiction	addiction	28785205	This study thus focused on epigenetic DNA methylation regulation of <strong>SLC1A2</strong>, encoding for <strong>EAAT2</strong>, in BD with variable environmental influences of <b>addiction</b>.
+SLC1A2	addiction	addiction	28785205	In comparison to controls, the <strong>SLC1A2</strong> promoter region was hypermethylated in BD without <b>addiction</b> but was hypomethylated in BD with <b>addiction</b>.
+SLC1A2	addiction	addiction	28785205	These results suggest that individual point methylation within the <strong>SLC1A2</strong> promoter region may be modified by exogenous <b>addiction</b> and may have a potential for developing clinically valuable epigenetic biomarkers for BD diagnosis and monitoring.
+SLC1A2	addiction	relapse	28726801	Inducing glutamate spillover by blocking astroglial glutamate transporters (<strong>GLT 1</strong>) had no effect on reinstated sucrose <b>seeking</b>.
+SLC1A2	drug	alcohol	28687200	Ceftriaxone (Cef) increases expression and function of both transporters following extinction from cocaine self administration and here we sought to determine if Cef would similarly decrease <b>alcohol</b> consumption while increasing xCT and <strong>GLT 1</strong> in the NA core.
+SLC1A2	drug	cocaine	28687200	Ceftriaxone (Cef) increases expression and function of both transporters following extinction from <b>cocaine</b> self administration and here we sought to determine if Cef would similarly decrease alcohol consumption while increasing xCT and <strong>GLT 1</strong> in the NA core.
+SLC1A2	drug	alcohol	28687200	Furthermore, a history of <b>alcohol</b> consumption did not alter xCT and <strong>GLT 1</strong> expression relative to <b>alcohol</b> naïve controls.
+SLC1A2	drug	alcohol	28687200	These results indicate that while Cef reduces <b>alcohol</b> consumption in outbred rats, its ability to do so is not associated with an increase in <strong>GLT 1</strong> expression.
+SLC1A2	drug	cocaine	28624317	Studies have reported that chronic exposure to <b>cocaine</b> induces downregulation of glutamate transporter 1 (<strong>GLT 1</strong>) and cystine/glutamate exchanger (xCT) in the central reward brain regions.
+SLC1A2	addiction	reward	28624317	Studies have reported that chronic exposure to cocaine induces downregulation of glutamate transporter 1 (<strong>GLT 1</strong>) and cystine/glutamate exchanger (xCT) in the central <b>reward</b> brain regions.
+SLC1A2	drug	cocaine	28624317	Ceftriaxone, a β lactam antibiotic, restored <strong>GLT 1</strong> expression and consequently reduced cue induced reinstatement of <b>cocaine</b> seeking behavior.
+SLC1A2	addiction	relapse	28624317	Ceftriaxone, a β lactam antibiotic, restored <strong>GLT 1</strong> expression and consequently reduced cue induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+SLC1A2	drug	cocaine	28624317	Moreover, <strong>GLT 1</strong> and xCT were downregulated in the NAc core and shell, but not in the dmPFC, following <b>cocaine</b> primed reinstatement.
+SLC1A2	addiction	relapse	28624317	Moreover, <strong>GLT 1</strong> and xCT were downregulated in the NAc core and shell, but not in the dmPFC, following cocaine primed <b>reinstatement</b>.
+SLC1A2	drug	cocaine	28495973	Contrasting the Role of xCT and <strong>GLT 1</strong> Upregulation in the Ability of Ceftriaxone to Attenuate the Cue Induced Reinstatement of <b>Cocaine</b> Seeking and Normalize AMPA Receptor Subunit Expression.
+SLC1A2	addiction	relapse	28495973	Contrasting the Role of xCT and <strong>GLT 1</strong> Upregulation in the Ability of Ceftriaxone to Attenuate the Cue Induced <b>Reinstatement</b> of Cocaine <b>Seeking</b> and Normalize AMPA Receptor Subunit Expression.
+SLC1A2	drug	cocaine	28495973	Long term treatment with ceftriaxone attenuates the reinstatement of <b>cocaine</b> seeking while increasing the function of the glutamate transporter 1 (<strong>GLT 1</strong>) and system xC  (Sxc) in the nucleus accumbens core (NAc).
+SLC1A2	addiction	relapse	28495973	Long term treatment with ceftriaxone attenuates the <b>reinstatement</b> of cocaine <b>seeking</b> while increasing the function of the glutamate transporter 1 (<strong>GLT 1</strong>) and system xC  (Sxc) in the nucleus accumbens core (NAc).
+SLC1A2	drug	cocaine	28495973	Here we used antisense to decrease the expression of <strong>GLT 1</strong> and xCT (a catalytic subunit of Sxc) to determine the relative importance of both proteins in mediating the ability of ceftriaxone to prevent cue induced reinstatement of <b>cocaine</b> seeking and normalize glutamatergic proteins in the NAc of rats.
+SLC1A2	addiction	relapse	28495973	Here we used antisense to decrease the expression of <strong>GLT 1</strong> and xCT (a catalytic subunit of Sxc) to determine the relative importance of both proteins in mediating the ability of ceftriaxone to prevent cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and normalize glutamatergic proteins in the NAc of rats.
+SLC1A2	addiction	relapse	28495973	Intra NAc xCT knockdown prevented ceftriaxone from attenuating <b>reinstatement</b> and from upregulating <strong>GLT 1</strong> and resulted in increased surface expression of AMPA receptor subunits GluA1 and GluA2.
+SLC1A2	addiction	relapse	28495973	Intra NAc <strong>GLT 1</strong> knockdown also prevented ceftriaxone from attenuating <b>reinstatement</b> and from upregulating xCT expression, without affecting GluA1 and GluA2 expression.
+SLC1A2	drug	cocaine	28495973	In the absence of <b>cocaine</b> or ceftriaxone treatment, xCT knockdown in the NAc increased the expression of both GluA1 and GluA2 without affecting <strong>GLT 1</strong> expression while <strong>GLT 1</strong> knockdown had no effect.
+SLC1A2	drug	cocaine	28495973	While upregulation of both xCT and <strong>GLT 1</strong> are essential to the ability of ceftriaxone to attenuate cue induced reinstatement of <b>cocaine</b> seeking, each protein uniquely affects the expression of other glutamate receptor and transporter proteins.
+SLC1A2	addiction	relapse	28495973	While upregulation of both xCT and <strong>GLT 1</strong> are essential to the ability of ceftriaxone to attenuate cue induced <b>reinstatement</b> of cocaine <b>seeking</b>, each protein uniquely affects the expression of other glutamate receptor and transporter proteins.
+SLC1A2	drug	cocaine	28442364	<b>Cocaine</b> exposure has been shown to induce a dysregulation in glutamate homeostasis and a decrease in the expression of <strong>GLT 1</strong> and xCT in the nucleus accumbens (NAc).
+SLC1A2	drug	alcohol	28442364	Co exposure of cocaine and <b>ethanol</b> decreased the relative mRNA expression and the expression of <strong>GLT 1</strong> in the NAc but not in the medial prefrontal cortex (mPFC).
+SLC1A2	drug	cocaine	28442364	Co exposure of <b>cocaine</b> and ethanol decreased the relative mRNA expression and the expression of <strong>GLT 1</strong> in the NAc but not in the medial prefrontal cortex (mPFC).
+SLC1A2	drug	nicotine	28347687	In the present study, for the first time, we investigated the effect of chronic exposure to electronic (e) cigarette vapor containing <b>nicotine</b>, for one hour daily for six months, on <strong>GLT 1</strong>, xCT, and GLAST expression in frontal cortex (FC), striatum (STR), and hippocampus (HIP) in outbred female CD1 mice.
+SLC1A2	drug	opioid	28341892	Evidence suggests that AQP4 is associated with glutamate transporter 1 (<strong>GLT 1</strong>) for glutamate clearance and contributes to <b>morphine</b> dependence.
+SLC1A2	addiction	dependence	28341892	Evidence suggests that AQP4 is associated with glutamate transporter 1 (<strong>GLT 1</strong>) for glutamate clearance and contributes to morphine <b>dependence</b>.
+SLC1A2	drug	opioid	28341892	In this study, we focused on whether AQP4 could form macromolecular complex with <strong>GLT 1</strong> and mu <b>opioid</b> receptor (MOR) and participates in <b>morphine</b> dependence.
+SLC1A2	addiction	dependence	28341892	In this study, we focused on whether AQP4 could form macromolecular complex with <strong>GLT 1</strong> and mu opioid receptor (MOR) and participates in morphine <b>dependence</b>.
+SLC1A2	drug	opioid	28341892	These findings may help to reveal the mechanism that AQP4, <strong>GLT 1</strong>, and MOR form protein complex and participate in <b>morphine</b> dependence, and deeply understand the reason that AQP4 deficiency maintains extracellular glutamate homeostasis and attenuates <b>morphine</b> dependence, moreover emphasizes the function of astrocyte in <b>morphine</b> dependence.
+SLC1A2	addiction	dependence	28341892	These findings may help to reveal the mechanism that AQP4, <strong>GLT 1</strong>, and MOR form protein complex and participate in morphine <b>dependence</b>, and deeply understand the reason that AQP4 deficiency maintains extracellular glutamate homeostasis and attenuates morphine <b>dependence</b>, moreover emphasizes the function of astrocyte in morphine <b>dependence</b>.
+SLC1A2	drug	alcohol	28242339	<b>Alcohol</b> consumption induced downregulation of glutamate transporter 1 (<strong>GLT 1</strong>) as reported in previous studies from our laboratory.
+SLC1A2	drug	cocaine	28213190	NAC reverses the disruption of glutamate homeostasis caused by long term <b>cocaine</b> use restoring function of the cystine glutamate exchanger in glial cells and reversing the downregulated <strong>GLT 1</strong> receptor.
+SLC1A2	drug	alcohol	27993695	Parenteral treatment with ceftriaxone, β lactam antibiotic, has been reported to attenuate <b>ethanol</b> consumption and reinstatement to cocaine seeking behavior, in part, by restoring the expression of <strong>GLT 1</strong> and xCT in mesocorticolimbic brain regions in rats.
+SLC1A2	drug	cocaine	27993695	Parenteral treatment with ceftriaxone, β lactam antibiotic, has been reported to attenuate ethanol consumption and reinstatement to <b>cocaine</b> seeking behavior, in part, by restoring the expression of <strong>GLT 1</strong> and xCT in mesocorticolimbic brain regions in rats.
+SLC1A2	addiction	relapse	27993695	Parenteral treatment with ceftriaxone, β lactam antibiotic, has been reported to attenuate ethanol consumption and <b>reinstatement</b> to cocaine <b>seeking</b> behavior, in part, by restoring the expression of <strong>GLT 1</strong> and xCT in mesocorticolimbic brain regions in rats.
+SLC1A2	drug	alcohol	27993695	Therefore, we examined the effects of orally administered Augmentin on <b>ethanol</b> intake as well as <strong>GLT 1</strong>, xCT and GLAST expression in male <b>alcohol</b> preferring (P) rats.
+SLC1A2	drug	alcohol	27993695	Importantly, the attenuation in <b>ethanol</b> consumption was associated with a significant upregulation of <strong>GLT 1</strong> and xCT expression in nucleus accumbens (NAc) and prefrontal cortex (PFC).
+SLC1A2	drug	cocaine	27685834	Previous studies have established a role for <strong>EAAT2</strong> mediated re uptake on reinstatement of <b>cocaine</b> seeking following extended withdrawal and extinction training.
+SLC1A2	addiction	relapse	27685834	Previous studies have established a role for <strong>EAAT2</strong> mediated re uptake on <b>reinstatement</b> of cocaine <b>seeking</b> following extended withdrawal and extinction training.
+SLC1A2	addiction	withdrawal	27685834	Previous studies have established a role for <strong>EAAT2</strong> mediated re uptake on reinstatement of cocaine seeking following extended <b>withdrawal</b> and extinction training.
+SLC1A2	drug	opioid	27461080	By expression of a dominant negative TNF peptide via lentiviral vector injection in rat PAG to sequester soluble TNF (solTNF), we demonstrate that solTNF mediates <b>morphine</b> tolerance induced by TLR4 signaling, stimulates neuroinflammation (increased IL 1β and TLR4 mRNA), and disrupts glutamate reuptake (decreased <strong>GLT 1</strong> and GLAST mRNA).
+SLC1A2	drug	alcohol	27207718	The increase in basal glutamate was not associated with changes in the surface expression of <strong>GLT 1</strong>, however, a decrease in slope of the no net flux dialysis function was observed following <b>ethanol</b> consumption, indicating a potential decrease in glutamate reuptake.
+SLC1A2	drug	alcohol	27199635	Importantly, we recently reported that amoxicillin and Augmentin (amoxicillin/clavulanate) upreglulated <strong>GLT 1</strong> expression in nucleus accumbens (NAc) and prefrontal cortex (PFC) as well as reduced <b>ethanol</b> consumption in male P rats.
+SLC1A2	drug	alcohol	27199635	In this study, we examined the effects of amoxicillin and Augmentin on <strong>GLT 1</strong> isoforms (GLT 1a and GLT 1b), xCT, and glutamate/aspartate transporter (GLAST) expression in NAc and PFC as well as <b>ethanol</b> intake in male P rats.
+SLC1A2	drug	alcohol	27199635	These findings demonstrated that Augmentin and amoxicillin have the potential to upregulate <strong>GLT 1</strong> isoforms and xCT expression, and consequently attenuate <b>ethanol</b> dependence.
+SLC1A2	addiction	dependence	27199635	These findings demonstrated that Augmentin and amoxicillin have the potential to upregulate <strong>GLT 1</strong> isoforms and xCT expression, and consequently attenuate ethanol <b>dependence</b>.
+SLC1A2	drug	alcohol	27060486	Effects of ceftriaxone on <b>ethanol</b>, nicotine or sucrose intake by <b>alcohol</b> preferring (P) rats and its association with <strong>GLT 1</strong> expression.
+SLC1A2	drug	nicotine	27060486	Effects of ceftriaxone on ethanol, <b>nicotine</b> or sucrose intake by alcohol preferring (P) rats and its association with <strong>GLT 1</strong> expression.
+SLC1A2	drug	alcohol	27060486	We have shown that administration of ceftriaxone (CEF), a β lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (<strong>GLT 1</strong>) expression in mesocorticolimbic regions of male and female <b>alcohol</b> preferring (P) rats.
+SLC1A2	drug	cocaine	27060486	The present results along with previous reports of CEF's efficacy in reducing <b>cocaine</b> self administration in rats suggest that modulation of <strong>GLT 1</strong> expression and/or activity is an important pharmacological target for treating polysubstance abuse and dependence.
+SLC1A2	addiction	dependence	27060486	The present results along with previous reports of CEF's efficacy in reducing cocaine self administration in rats suggest that modulation of <strong>GLT 1</strong> expression and/or activity is an important pharmacological target for treating polysubstance abuse and <b>dependence</b>.
+SLC1A2	drug	alcohol	26821293	We found that binge <b>ethanol</b> withdrawal escalated post withdrawal <b>ethanol</b> intake, which was associated with downregulation of <strong>GLT 1</strong> expression in both mPFC and NAc.
+SLC1A2	addiction	intoxication	26821293	We found that <b>binge</b> ethanol withdrawal escalated post withdrawal ethanol intake, which was associated with downregulation of <strong>GLT 1</strong> expression in both mPFC and NAc.
+SLC1A2	addiction	withdrawal	26821293	We found that binge ethanol <b>withdrawal</b> escalated post <b>withdrawal</b> ethanol intake, which was associated with downregulation of <strong>GLT 1</strong> expression in both mPFC and NAc.
+SLC1A2	drug	alcohol	26790351	Previously, we have reported that cefazolin and cefoperazone treatments attenuated <b>ethanol</b> consumption, at least in part, through upregulation of <strong>GLT 1</strong> expression in male <b>alcohol</b> preferring (P) rats.
+SLC1A2	drug	alcohol	26790351	We found that cefazolin and cefoperazone treatments decreased <b>ethanol</b> intake and upregulated both <strong>GLT 1</strong> isoforms, GLT 1a and GLT 1b, in nucleus accumbens (NAc) and prefrontal cortex (PFC) compared to saline treated group.
+SLC1A2	addiction	relapse	26706696	We have demonstrated that the mechanism of action by which ceftriaxone attenuates <b>reinstatement</b> involves increased NAc <strong>GLT 1</strong> expression and a reduction in NAc glutamate efflux during <b>reinstatement</b>.
+SLC1A2	addiction	relapse	26706696	Here we investigated the effects of ceftriaxone (100 and 200 mg/kg) on context primed <b>relapse</b> following abstinence without extinction training and examined the effects of ceftriaxone on GluA1, GluA2 and <strong>GLT 1</strong> expression.
+SLC1A2	addiction	relapse	26706696	While <b>relapse</b> was accompanied by an increase in NAc glutamate, ceftriaxone (200 mg/kg) was unable to significantly reduce NAc glutamate efflux during <b>relapse</b> despite its ability to upregulate <strong>GLT 1</strong>.
+SLC1A2	drug	alcohol	26589642	We and others have shown increased extracellular glutamate concentration, which was associated with down regulation of the major glutamate transporter, glutamate transporter 1 (<strong>GLT 1</strong>), in brain reward regions of animals exposed to drug abuse, including nicotine and <b>ethanol</b>.
+SLC1A2	drug	nicotine	26589642	We and others have shown increased extracellular glutamate concentration, which was associated with down regulation of the major glutamate transporter, glutamate transporter 1 (<strong>GLT 1</strong>), in brain reward regions of animals exposed to drug abuse, including <b>nicotine</b> and ethanol.
+SLC1A2	addiction	reward	26589642	We and others have shown increased extracellular glutamate concentration, which was associated with down regulation of the major glutamate transporter, glutamate transporter 1 (<strong>GLT 1</strong>), in brain <b>reward</b> regions of animals exposed to drug abuse, including nicotine and ethanol.
+SLC1A2	addiction	dependence	26589642	Importantly, studies from our laboratory and others showed that upregulation of <strong>GLT 1</strong> expression in the mesocorticolimbic brain regions may have potential therapeutic effects in drug <b>dependence</b>.
+SLC1A2	drug	nicotine	26589642	In this review article, we discussed the effect of antagonizing presynaptic nAChRs in glutamate release, the upregulatory effect in <strong>GLT 1</strong> expression and the role of glutamate receptors antagonists in the treatment of <b>nicotine</b> dependence.
+SLC1A2	addiction	dependence	26589642	In this review article, we discussed the effect of antagonizing presynaptic nAChRs in glutamate release, the upregulatory effect in <strong>GLT 1</strong> expression and the role of glutamate receptors antagonists in the treatment of nicotine <b>dependence</b>.
+SLC1A2	drug	alcohol	26569416	Expressions of glutamate transporters, namely the excitatory amino acid transporter 2 (<strong>EAAT2</strong>) and EAAT3, in white blood cells were measured with the real time polymerase chain reaction (RT PCR) method in early (first day) and late (28(th) day) withdrawal in <b>alcoholic</b> patients and once in the controls.
+SLC1A2	addiction	withdrawal	26569416	Expressions of glutamate transporters, namely the excitatory amino acid transporter 2 (<strong>EAAT2</strong>) and EAAT3, in white blood cells were measured with the real time polymerase chain reaction (RT PCR) method in early (first day) and late (28(th) day) <b>withdrawal</b> in alcoholic patients and once in the controls.
+SLC1A2	addiction	withdrawal	26569416	<strong>EAAT2</strong> and EAAT3 expressions in the patients during both early and late <b>withdrawal</b> were higher than those of the controls.
+SLC1A2	drug	alcohol	26569416	The study revealed an upregulation of glutamate transporters <strong>EAAT2</strong> and EAAT3 during early and late withdrawal in patients with <b>alcohol</b> withdrawal.
+SLC1A2	addiction	withdrawal	26569416	The study revealed an upregulation of glutamate transporters <strong>EAAT2</strong> and EAAT3 during early and late <b>withdrawal</b> in patients with alcohol <b>withdrawal</b>.
+SLC1A2	drug	cocaine	26543027	Clavulanic acid enhances glutamate transporter subtype I (<strong>GLT 1</strong>) expression and decreases reinforcing efficacy of <b>cocaine</b> in mice.
+SLC1A2	addiction	reward	26543027	Clavulanic acid enhances glutamate transporter subtype I (<strong>GLT 1</strong>) expression and decreases <b>reinforcing</b> efficacy of cocaine in mice.
+SLC1A2	drug	cocaine	26543027	The β lactam antibiotic ceftriaxone (CTX) reduces <b>cocaine</b> reinforcement and relapse in preclinical assays through a mechanism involving activation of glutamate transporter subtype 1 (<strong>GLT 1</strong>).
+SLC1A2	addiction	relapse	26543027	The β lactam antibiotic ceftriaxone (CTX) reduces cocaine reinforcement and <b>relapse</b> in preclinical assays through a mechanism involving activation of glutamate transporter subtype 1 (<strong>GLT 1</strong>).
+SLC1A2	addiction	reward	26543027	The β lactam antibiotic ceftriaxone (CTX) reduces cocaine <b>reinforcement</b> and relapse in preclinical assays through a mechanism involving activation of glutamate transporter subtype 1 (<strong>GLT 1</strong>).
+SLC1A2	drug	cocaine	26543027	Here, we tested the hypothesis that CA (1, 10 mg/kg ip) would enhance <strong>GLT 1</strong> expression and decrease <b>cocaine</b> self administration (SA) in mice, but at lower doses than CTX.
+SLC1A2	drug	psychedelics	26442907	Previous data indicate that <b>ketamine</b> causes a reduction in the number of Excitatory Amino Acid Transporter Type 2 (<strong>EAAT2</strong>) containing astrocytes.
+SLC1A2	drug	psychedelics	26442907	As <strong>EAAT2</strong> is a principal mechanism of glutamate clearance from the synapse, the current study tests the hypothesis that ceftriaxone may reverse functional consequences of <b>ketamine</b> exposure.
+SLC1A2	drug	alcohol	26168897	Amoxicillin and amoxicillin/clavulanate reduce <b>ethanol</b> intake and increase <strong>GLT 1</strong> expression as well as AKT phosphorylation in mesocorticolimbic regions.
+SLC1A2	drug	alcohol	26168897	Studies have shown that administration of the β lactam antibiotic ceftriaxone (CEF) attenuates <b>ethanol</b> consumption and cocaine seeking behavior as well as prevents <b>ethanol</b> induced downregulation of glutamate transporter 1 (<strong>GLT 1</strong>) expression in central reward brain regions.
+SLC1A2	drug	cocaine	26168897	Studies have shown that administration of the β lactam antibiotic ceftriaxone (CEF) attenuates ethanol consumption and <b>cocaine</b> seeking behavior as well as prevents ethanol induced downregulation of glutamate transporter 1 (<strong>GLT 1</strong>) expression in central reward brain regions.
+SLC1A2	addiction	relapse	26168897	Studies have shown that administration of the β lactam antibiotic ceftriaxone (CEF) attenuates ethanol consumption and cocaine <b>seeking</b> behavior as well as prevents ethanol induced downregulation of glutamate transporter 1 (<strong>GLT 1</strong>) expression in central reward brain regions.
+SLC1A2	addiction	reward	26168897	Studies have shown that administration of the β lactam antibiotic ceftriaxone (CEF) attenuates ethanol consumption and cocaine seeking behavior as well as prevents ethanol induced downregulation of glutamate transporter 1 (<strong>GLT 1</strong>) expression in central <b>reward</b> brain regions.
+SLC1A2	drug	alcohol	26168897	Therefore, the present study examined the effects of two other β lactam antibiotics, amoxicillin (AMOX) and amoxicillin/clavulanate (Augmentin, AUG), on <b>ethanol</b> drinking, as well as <strong>GLT 1</strong> and phosphorylated AKT (pAKT) levels in the nucleus accumbens (Acb) and medial prefrontal cortex (mPFC) of <b>alcohol</b> preferring (P) rats.
+SLC1A2	drug	alcohol	26168897	Both compounds significantly decreased <b>ethanol</b> intake and significantly increased <strong>GLT 1</strong> expression in the Acb.
+SLC1A2	drug	alcohol	26168897	Results for changes in pAKT levels matched those for <strong>GLT 1</strong>, indicating that β lactam antibiotic induced reductions in <b>ethanol</b> intake are negatively associated with increases in <strong>GLT 1</strong> and pAKT levels within two critical brains regions mediating drug reward and reinforcement.
+SLC1A2	addiction	reward	26168897	Results for changes in pAKT levels matched those for <strong>GLT 1</strong>, indicating that β lactam antibiotic induced reductions in ethanol intake are negatively associated with increases in <strong>GLT 1</strong> and pAKT levels within two critical brains regions mediating drug <b>reward</b> and <b>reinforcement</b>.
+SLC1A2	drug	alcohol	26168897	These findings add to a growing literature that pharmacological increases in <strong>GLT 1</strong> expression are associated with decreases in <b>ethanol</b> intake and suggest that one mechanism mediating this effect may be increased phosphorylation of AKT.
+SLC1A2	drug	alcohol	26168897	Thus, <strong>GLT 1</strong> and pAKT may serve as molecular targets for the treatment of <b>alcohol</b> and drug abuse/dependence.
+SLC1A2	addiction	dependence	26168897	Thus, <strong>GLT 1</strong> and pAKT may serve as molecular targets for the treatment of alcohol and drug abuse/<b>dependence</b>.
+SLC1A2	drug	alcohol	26071905	Several studies from our laboratory demonstrated that attenuation of <b>ethanol</b> intkae was associated in part with upregulation of xCT and <strong>GLT 1</strong> expression suggesting the important role of these transporters in the treatment of <b>ethanol</b> dependence.
+SLC1A2	addiction	dependence	26071905	Several studies from our laboratory demonstrated that attenuation of ethanol intkae was associated in part with upregulation of xCT and <strong>GLT 1</strong> expression suggesting the important role of these transporters in the treatment of ethanol <b>dependence</b>.
+SLC1A2	drug	alcohol	26071905	We found recently that β lactam antibiotic, ampicillin, upregulated <strong>GLT 1</strong> expression in the prefrontal cortex (PFC) and nucleus accumbens (NAc) and consequently reduced <b>ethanol</b> intake in <b>alcohol</b> preferring (P) rats.
+SLC1A2	drug	alcohol	26071905	Our findings provide significant role of ampicillin on upregulating xCT and <strong>GLT 1</strong> isoforms expression, might be suggested as possible targets for the attenuation of <b>ethanol</b> consumption.
+SLC1A2	addiction	addiction	26022265	The purpose of this review is to highlight the effects of <b>addictive</b> drug use on <strong>GLT 1</strong> and glutamate uptake, and using <strong>GLT 1</strong> as a target in <b>addiction</b> pharmacotherapy.
+SLC1A2	drug	alcohol	26022265	Cocaine, opioids, <b>ethanol</b>, nicotine, amphetamines, and cannabinoids each affect <strong>GLT 1</strong> expression and glutamate uptake, and restoring <strong>GLT 1</strong> expression with N acetylcysteine or ceftriaxone shows promise in correcting pre clinical and clinical manifestations of drug addiction.
+SLC1A2	drug	cannabinoid	26022265	Cocaine, opioids, ethanol, nicotine, amphetamines, and <b>cannabinoids</b> each affect <strong>GLT 1</strong> expression and glutamate uptake, and restoring <strong>GLT 1</strong> expression with N acetylcysteine or ceftriaxone shows promise in correcting pre clinical and clinical manifestations of drug addiction.
+SLC1A2	drug	cocaine	26022265	<b>Cocaine</b>, opioids, ethanol, nicotine, amphetamines, and cannabinoids each affect <strong>GLT 1</strong> expression and glutamate uptake, and restoring <strong>GLT 1</strong> expression with N acetylcysteine or ceftriaxone shows promise in correcting pre clinical and clinical manifestations of drug addiction.
+SLC1A2	drug	nicotine	26022265	Cocaine, opioids, ethanol, <b>nicotine</b>, amphetamines, and cannabinoids each affect <strong>GLT 1</strong> expression and glutamate uptake, and restoring <strong>GLT 1</strong> expression with N acetylcysteine or ceftriaxone shows promise in correcting pre clinical and clinical manifestations of drug addiction.
+SLC1A2	drug	opioid	26022265	Cocaine, <b>opioids</b>, ethanol, nicotine, amphetamines, and cannabinoids each affect <strong>GLT 1</strong> expression and glutamate uptake, and restoring <strong>GLT 1</strong> expression with N acetylcysteine or ceftriaxone shows promise in correcting pre clinical and clinical manifestations of drug addiction.
+SLC1A2	addiction	addiction	26022265	Cocaine, opioids, ethanol, nicotine, amphetamines, and cannabinoids each affect <strong>GLT 1</strong> expression and glutamate uptake, and restoring <strong>GLT 1</strong> expression with N acetylcysteine or ceftriaxone shows promise in correcting pre clinical and clinical manifestations of drug <b>addiction</b>.
+SLC1A2	drug	alcohol	26002627	Ceftriaxone attenuates <b>ethanol</b> drinking and restores extracellular glutamate concentration through normalization of <strong>GLT 1</strong> in nucleus accumbens of male <b>alcohol</b> preferring rats.
+SLC1A2	drug	alcohol	26002627	We have previously reported that chronic <b>ethanol</b> drinking downregulated glutamate transporter 1 (<strong>GLT 1</strong>) in nucleus accumbens (NAc) in male P rats in a manner that was reversed by ceftriaxone treatment.
+SLC1A2	drug	alcohol	26002627	In addition, <strong>GLT 1</strong> protein was decreased in <b>ethanol</b> exposed animals and ceftriaxone treatment reversed this deficit.
+SLC1A2	drug	alcohol	26002627	Our present study demonstrates that ceftriaxone treatment prevents <b>ethanol</b> drinking in part through normalization of extracellular glutamate concentrations in NAc of male P rats via <strong>GLT 1</strong>.
+SLC1A2	drug	alcohol	25954150	Regarding glutamatergic homeostasis, ceftriaxone, MS 153, and GPI 1046, which upregulate glutamate transporter 1 (<strong>GLT1</strong>) expression in mesocorticolimbic brain regions, reduce <b>alcohol</b> intake in genetic animal models of <b>alcoholism</b>.
+SLC1A2	drug	alcohol	25813713	Effects of ampicillin, cefazolin and cefoperazone treatments on <strong>GLT 1</strong> expressions in the mesocorticolimbic system and <b>ethanol</b> intake in <b>alcohol</b> preferring rats.
+SLC1A2	drug	alcohol	25813713	Chronic <b>ethanol</b> consumption is known to downregulate expression of the major glutamate transporter 1 (<strong>GLT 1</strong>), which increases extracellular glutamate concentrations in subregions of the mesocorticolimbic reward pathway.
+SLC1A2	addiction	reward	25813713	Chronic ethanol consumption is known to downregulate expression of the major glutamate transporter 1 (<strong>GLT 1</strong>), which increases extracellular glutamate concentrations in subregions of the mesocorticolimbic <b>reward</b> pathway.
+SLC1A2	addiction	addiction	25813713	While β lactam antibiotics were initially identified as potent upregulators of <strong>GLT 1</strong> expression, only ceftriaxone has been extensively studied in various drug <b>addiction</b> models.
+SLC1A2	drug	opioid	25787747	We investigated the effect of chronic treatment with ceftriaxone (CFT), an excitatory amino acid transporter (<strong>EAAT2</strong>) enhancer, and acute administration of topiramate (TPM), a glutamate release inhibitor, on <b>morphine</b> withdrawal syndrome and withdrawal induced glutamate receptor (GluR) desensitization in LC neurons from <b>morphine</b> dependent rats.
+SLC1A2	addiction	withdrawal	25787747	We investigated the effect of chronic treatment with ceftriaxone (CFT), an excitatory amino acid transporter (<strong>EAAT2</strong>) enhancer, and acute administration of topiramate (TPM), a glutamate release inhibitor, on morphine <b>withdrawal</b> syndrome and <b>withdrawal</b> induced glutamate receptor (GluR) desensitization in LC neurons from morphine dependent rats.
+SLC1A2	addiction	withdrawal	25787747	Acute treatment with the specific <strong>EAAT2</strong> inhibitor dihydrokainic acid (DHK) prevented the effect of CFT on <b>withdrawal</b> syndrome and GluR desensitization.
+SLC1A2	addiction	withdrawal	25787747	Our results suggest that a reduction of synaptic concentrations of glutamate by enhancing <strong>EAAT2</strong> mediated uptake or inhibiting glutamate release alleviates the behavioral response and the cellular changes in the LC during opiate <b>withdrawal</b>.
+SLC1A2	drug	alcohol	25619881	Effects of ceftriaxone on <strong>GLT1</strong> isoforms, xCT and associated signaling pathways in P rats exposed to <b>ethanol</b>.
+SLC1A2	drug	alcohol	25619881	We focus in this study to determine the effects of ceftriaxone, β lactam antibiotic, on glial proteins such as <strong>GLT1</strong> isoforms, xCT, glutamate aspartate transporter (GLAST), and several associated signaling pathways as well as <b>ethanol</b> intake in P rats.
+SLC1A2	drug	alcohol	25619881	The reduction in <b>ethanol</b> intake was associated with significantly enhanced expression of <strong>GLT1</strong>, GLT1a, GLT1b, and xCT in the nucleus accumbens (NAc) and prefrontal cortex (PFC) of 5 day ceftriaxone treated P rats.
+SLC1A2	drug	alcohol	25601490	We recently showed that glutamate transporter 1 (<strong>GLT 1</strong>) is downregulated following chronic exposure to <b>ethanol</b> for 5 weeks in <b>alcohol</b> preferring (P) rats and that upregulation of the <strong>GLT 1</strong> levels in nucleus accumbens and prefrontal cortex results, in part, in attenuating <b>ethanol</b> consumption.
+SLC1A2	drug	alcohol	25601490	This study examines the effect of a synthetic compound, (R) ( ) 5 methyl 1 nicotinoyl 2 pyrazoline (MS 153), on <b>ethanol</b> drinking and expressions of <strong>GLT 1</strong> and xCT in the amygdala and the hippocampus of P rats.
+SLC1A2	drug	alcohol	25601490	It was revealed that <strong>GLT 1</strong> and xCT expressions were downregulated in both the amygdala and the hippocampus of <b>ethanol</b> vehicle treated rats (<b>ethanol</b> vehicle group) compared with water control animals.
+SLC1A2	drug	alcohol	25400560	Effects of MS 153 on chronic <b>ethanol</b> consumption and <strong>GLT1</strong> modulation of glutamate levels in male <b>alcohol</b> preferring rats.
+SLC1A2	drug	alcohol	25400560	We have recently shown that upregulation of glutamate transporter 1 (<strong>GLT1</strong>) in the brain is associated in part with reduction in <b>ethanol</b> intake in <b>alcohol</b> preferring (P) male rats.
+SLC1A2	drug	alcohol	25400560	In this study, we investigated the effects of a synthetic compound, (R) ( ) 5 methyl 1 nicotinoyl 2 pyrazoline (MS 153), known to activate <strong>GLT1</strong> on <b>ethanol</b> consumption as well as <strong>GLT1</strong> expression and certain signaling pathways in P rats.
+SLC1A2	drug	alcohol	25400560	These findings reveal MS 153 as a <strong>GLT1</strong> modulator that may have potential as a therapeutic drug for the treatment of <b>alcohol</b> dependence.
+SLC1A2	addiction	dependence	25400560	These findings reveal MS 153 as a <strong>GLT1</strong> modulator that may have potential as a therapeutic drug for the treatment of alcohol <b>dependence</b>.
+SLC1A2	drug	alcohol	25236726	Studies using mice lacking the equilibrative nucleoside transporter 1 have illuminated how adenosine functions through neuroglial interactions involving glutamate uptake transporter GLT 1 [referred to as excitatory amino acid transporter 2 (<strong>EAAT2</strong>) in human] and possibly water channel aquaporin 4 to regulate <b>ethanol</b> sensitivity, reward related motivational processes, and <b>alcohol</b> intake.
+SLC1A2	addiction	reward	25236726	Studies using mice lacking the equilibrative nucleoside transporter 1 have illuminated how adenosine functions through neuroglial interactions involving glutamate uptake transporter GLT 1 [referred to as excitatory amino acid transporter 2 (<strong>EAAT2</strong>) in human] and possibly water channel aquaporin 4 to regulate ethanol sensitivity, <b>reward</b> related motivational processes, and alcohol intake.
+SLC1A2	drug	alcohol	25236726	Studies using mice lacking the equilibrative nucleoside transporter 1 have illuminated how adenosine functions through neuroglial interactions involving glutamate uptake transporter <strong>GLT 1</strong> [referred to as excitatory amino acid transporter 2 (<strong>EAAT2</strong>) in human] and possibly water channel aquaporin 4 to regulate <b>ethanol</b> sensitivity, reward related motivational processes, and <b>alcohol</b> intake.
+SLC1A2	addiction	reward	25236726	Studies using mice lacking the equilibrative nucleoside transporter 1 have illuminated how adenosine functions through neuroglial interactions involving glutamate uptake transporter <strong>GLT 1</strong> [referred to as excitatory amino acid transporter 2 (<strong>EAAT2</strong>) in human] and possibly water channel aquaporin 4 to regulate ethanol sensitivity, <b>reward</b> related motivational processes, and alcohol intake.
+SLC1A2	drug	opioid	24741055	Through multiple functional assays of glutamate uptake and analyzing NMDA receptor mediated currents, we show that <b>heroin</b> self administration produced long lasting downregulation of glutamate uptake and surface expression of the transporter <strong>GLT 1</strong>.
+SLC1A2	drug	opioid	24741055	Ceftriaxone induced inhibition of reinstated <b>heroin</b> seeking was blocked by morpholino antisense targeting <strong>GLT 1</strong> synthesis.
+SLC1A2	addiction	relapse	24741055	Ceftriaxone induced inhibition of reinstated heroin <b>seeking</b> was blocked by morpholino antisense targeting <strong>GLT 1</strong> synthesis.
+SLC1A2	drug	alcohol	24687412	Effects of ceftriaxone on <b>ethanol</b> intake: a possible role for xCT and <strong>GLT 1</strong> isoforms modulation of glutamate levels in P rats.
+SLC1A2	drug	alcohol	24687412	We have recently demonstrated that ceftriaxone treatment induced upregulation of <strong>GLT1</strong> levels and attenuated <b>ethanol</b> intake; however, less is known about the involvement of xCT on <b>ethanol</b> intake.
+SLC1A2	drug	alcohol	24687412	In this study, we investigated the effects of ceftriaxone on the levels of xCT in both continuous and relapse like <b>ethanol</b> drinking, as well as <strong>GLT 1</strong> isoforms, and glutamate aspartate transporter (GLAST) in relapse like <b>ethanol</b> intake.
+SLC1A2	addiction	relapse	24687412	In this study, we investigated the effects of ceftriaxone on the levels of xCT in both continuous and <b>relapse</b> like ethanol drinking, as well as <strong>GLT 1</strong> isoforms, and glutamate aspartate transporter (GLAST) in <b>relapse</b> like ethanol intake.
+SLC1A2	drug	alcohol	24687412	These findings suggest that xCT and <strong>GLT 1</strong> isoforms might be target proteins for the treatment of <b>alcohol</b> dependence.
+SLC1A2	addiction	dependence	24687412	These findings suggest that xCT and <strong>GLT 1</strong> isoforms might be target proteins for the treatment of alcohol <b>dependence</b>.
+SLC1A2	drug	alcohol	24655029	We investigated the role of astrocytic glutamate uptake in <b>ethanol</b> (EtOH) binge drinking in mice, using the "drinking in the dark" (DID) paradigm by blocking the astrocytic glutamate transporter (<strong>GLT 1</strong>) with intracerebroventricular (ICV) administration of dihydrokainic acid (DHK).
+SLC1A2	addiction	intoxication	24655029	We investigated the role of astrocytic glutamate uptake in ethanol (EtOH) <b>binge</b> drinking in mice, using the "drinking in the dark" (DID) paradigm by blocking the astrocytic glutamate transporter (<strong>GLT 1</strong>) with intracerebroventricular (ICV) administration of dihydrokainic acid (DHK).
+SLC1A2	drug	cocaine	24612076	Glutamate transporter <strong>GLT 1</strong> mediates N acetylcysteine inhibition of <b>cocaine</b> reinstatement.
+SLC1A2	addiction	relapse	24612076	Glutamate transporter <strong>GLT 1</strong> mediates N acetylcysteine inhibition of cocaine <b>reinstatement</b>.
+SLC1A2	drug	cocaine	24612076	<b>Cocaine</b> self administration in rats reduces both cystine glutamate exchange and glutamate transport via <strong>GLT 1</strong> in the nucleus accumbens, and NAC treatment normalizes these two glial processes critical for maintaining glutamate homeostasis.
+SLC1A2	drug	cocaine	24612076	To determine whether the restoration of <strong>GLT 1</strong> and/or cystine glutamate exchange is required for NAC to inhibit cue induced reinstatement of <b>cocaine</b> seeking, we utilized the rat self administration/extinction/reinstatement model of <b>cocaine</b> relapse.
+SLC1A2	addiction	relapse	24612076	To determine whether the restoration of <strong>GLT 1</strong> and/or cystine glutamate exchange is required for NAC to inhibit cue induced <b>reinstatement</b> of cocaine <b>seeking</b>, we utilized the rat self administration/extinction/<b>reinstatement</b> model of cocaine <b>relapse</b>.
+SLC1A2	drug	cocaine	24612076	In contrast, suppressing NAC induced restoration of <strong>GLT 1</strong> not only prevented NAC from inhibiting reinstatement, but augmented the capacity of cues to reinstate <b>cocaine</b> seeking.
+SLC1A2	addiction	relapse	24612076	In contrast, suppressing NAC induced restoration of <strong>GLT 1</strong> not only prevented NAC from inhibiting <b>reinstatement</b>, but augmented the capacity of cues to reinstate cocaine <b>seeking</b>.
+SLC1A2	addiction	relapse	24612076	We hypothesized that the increased <b>reinstatement</b> after inhibiting NAC induction of <strong>GLT 1</strong> resulted from increased extracellular glutamate, and show that augmented <b>reinstatement</b> is prevented by blocking mGluR5.
+SLC1A2	drug	cocaine	24612076	Restoring <strong>GLT 1</strong>, not cystine glutamate exchange, is a key mechanism whereby daily NAC reduces cue induced <b>cocaine</b> reinstatement.
+SLC1A2	addiction	relapse	24612076	Restoring <strong>GLT 1</strong>, not cystine glutamate exchange, is a key mechanism whereby daily NAC reduces cue induced cocaine <b>reinstatement</b>.
+SLC1A2	drug	alcohol	24535561	Effects of ceftriaxone on chronic <b>ethanol</b> consumption: a potential role for xCT and <strong>GLT1</strong> modulation of glutamate levels in male P rats.
+SLC1A2	drug	alcohol	24535561	We have previously shown that ceftriaxone, a β lactam antibiotic known to upregulate glutamate transporter 1 (<strong>GLT1</strong>), reduced <b>ethanol</b> intake after 5 weeks of free choice <b>ethanol</b> drinking paradigm in male <b>alcohol</b> preferring (P) rats.
+SLC1A2	addiction	reward	24535561	These might be due in part through the upregulation of both xCT and <strong>GLT1</strong> levels in brain <b>reward</b> regions.
+SLC1A2	drug	alcohol	24452391	Attenuation of <b>ethanol</b> withdrawal by ceftriaxone induced upregulation of glutamate transporter <strong>EAAT2</strong>.
+SLC1A2	addiction	withdrawal	24452391	Attenuation of ethanol <b>withdrawal</b> by ceftriaxone induced upregulation of glutamate transporter <strong>EAAT2</strong>.
+SLC1A2	drug	alcohol	24452391	Using a rat model of <b>ethanol</b> withdrawal, we tested whether ceftriaxone, a β lactam antibiotic known to increase the expression and activity of glutamate uptake transporter <strong>EAAT2</strong>, reduces the occurrence or severity of <b>ethanol</b> withdrawal manifestations.
+SLC1A2	addiction	withdrawal	24452391	Using a rat model of ethanol <b>withdrawal</b>, we tested whether ceftriaxone, a β lactam antibiotic known to increase the expression and activity of glutamate uptake transporter <strong>EAAT2</strong>, reduces the occurrence or severity of ethanol <b>withdrawal</b> manifestations.
+SLC1A2	drug	alcohol	24452391	Finally, ceftriaxone treatment was associated with lasting upregulation of <b>ethanol</b> withdrawal induced downregulation of <strong>EAAT2</strong> in the striatum.
+SLC1A2	addiction	withdrawal	24452391	Finally, ceftriaxone treatment was associated with lasting upregulation of ethanol <b>withdrawal</b> induced downregulation of <strong>EAAT2</strong> in the striatum.
+SLC1A2	drug	alcohol	24409344	The role of <strong>GLT1</strong> has been tested in <b>alcohol</b> and other drugs of abuse models with dysfunction in glutamate transmission.
+SLC1A2	drug	alcohol	24409344	We recently reported that treatment of <b>alcohol</b> preferring rats with compounds ceftriaxone and GPI 1046, known to upregulate <strong>GLT1</strong> levels, showed reduction in <b>alcohol</b> intake and attenuation of relapse like <b>ethanol</b> drinking behaviour.
+SLC1A2	addiction	relapse	24409344	We recently reported that treatment of alcohol preferring rats with compounds ceftriaxone and GPI 1046, known to upregulate <strong>GLT1</strong> levels, showed reduction in alcohol intake and attenuation of <b>relapse</b> like ethanol drinking behaviour.
+SLC1A2	drug	cocaine	24409344	Furthermore, we demonstrated that upregulation of <strong>GLT1</strong> was associated with attenuation of cue induced <b>cocaine</b> relapse.
+SLC1A2	addiction	relapse	24409344	Furthermore, we demonstrated that upregulation of <strong>GLT1</strong> was associated with attenuation of cue induced cocaine <b>relapse</b>.
+SLC1A2	drug	alcohol	24409344	Together, we suggest that <strong>GLT1</strong> is considered as a potential therapeutic target for the treatment of drug dependence, including <b>alcohol</b>.
+SLC1A2	addiction	dependence	24409344	Together, we suggest that <strong>GLT1</strong> is considered as a potential therapeutic target for the treatment of drug <b>dependence</b>, including alcohol.
+SLC1A2	drug	alcohol	24409344	The aim of this critical review was to discuss the potential therapeutic role of <strong>GLT1</strong> for the treatment of <b>alcohol</b> dependence.
+SLC1A2	addiction	dependence	24409344	The aim of this critical review was to discuss the potential therapeutic role of <strong>GLT1</strong> for the treatment of alcohol <b>dependence</b>.
+SLC1A2	addiction	relapse	24269543	Western blotting results showed that the levels of <strong>GLT1</strong>, VGLUT2, NR2B, p ERK1/2 and p CREB expressions in the mPFC were increased and CaMKII was decreased markedly after the stress priming MAP induced CPP <b>reinstatement</b> test.
+SLC1A2	addiction	reward	24269543	Western blotting results showed that the levels of <strong>GLT1</strong>, VGLUT2, NR2B, p ERK1/2 and p CREB expressions in the mPFC were increased and CaMKII was decreased markedly after the stress priming MAP induced <b>CPP</b> reinstatement test.
+SLC1A2	drug	cocaine	23985782	Chronic administration of the methylxanthine propentofylline impairs reinstatement to <b>cocaine</b> by a <strong>GLT 1</strong> dependent mechanism.
+SLC1A2	addiction	relapse	23985782	Chronic administration of the methylxanthine propentofylline impairs <b>reinstatement</b> to cocaine by a <strong>GLT 1</strong> dependent mechanism.
+SLC1A2	addiction	relapse	23985782	In particular, compounds that increase expression of the astroglial glutamate transporter <strong>GLT 1</strong> (N acetylcysteine and ceftriaxone) can decrease measures of drug <b>seeking</b>.
+SLC1A2	addiction	relapse	23985782	However, it is unknown whether the compounds that influence broad measures of glial physiology can influence behavioral measures of drug <b>relapse</b>, nor is it clear whether the upregulated <strong>GLT 1</strong> is functionally important for suppressing of drug <b>seeking</b>.
+SLC1A2	addiction	relapse	23985782	We next determined whether the effect of systemic PPF on <b>reinstatement</b> depended upon its ability to restore expression of <strong>GLT 1</strong> in the nucleus accumbens.
+SLC1A2	drug	cocaine	23985782	PPF restored the <b>cocaine</b> induced decrease in <strong>GLT 1</strong> in the accumbens core; then, using an antisense strategy against glutamate transporter <strong>GLT 1</strong>, we found that restored transporter expression was necessary for PPF to inhibit cue primed <b>cocaine</b> seeking.
+SLC1A2	addiction	relapse	23985782	PPF restored the cocaine induced decrease in <strong>GLT 1</strong> in the accumbens core; then, using an antisense strategy against glutamate transporter <strong>GLT 1</strong>, we found that restored transporter expression was necessary for PPF to inhibit cue primed cocaine <b>seeking</b>.
+SLC1A2	drug	opioid	23793269	We used fluorescence activated cell sorting of neurons (Thy1+), astrocytes (<strong>GLT1</strong>+), and microglia (CD11b+) from the NAcc for the analysis of cell type specific gene expression following <b>morphine</b> or saline treatment.
+SLC1A2	drug	cocaine	23719800	Role of the major glutamate transporter <strong>GLT1</strong> in nucleus accumbens core versus shell in cue induced <b>cocaine</b> seeking behavior.
+SLC1A2	addiction	relapse	23719800	Role of the major glutamate transporter <strong>GLT1</strong> in nucleus accumbens core versus shell in cue induced cocaine <b>seeking</b> behavior.
+SLC1A2	drug	cocaine	23719800	Decreased expression of glutamate type I transporter (<strong>GLT1</strong>), which is responsible for >90% of glutamate clearance, occurs in the core of rats withdrawn from <b>cocaine</b> self administration, while treatment with ceftriaxone, a β lactam antibiotic previously shown to increase <strong>GLT1</strong> expression and function in rodents, upregulates <strong>GLT1</strong> and attenuates cue induced <b>cocaine</b> reinstatement.
+SLC1A2	addiction	relapse	23719800	Decreased expression of glutamate type I transporter (<strong>GLT1</strong>), which is responsible for >90% of glutamate clearance, occurs in the core of rats withdrawn from cocaine self administration, while treatment with ceftriaxone, a β lactam antibiotic previously shown to increase <strong>GLT1</strong> expression and function in rodents, upregulates <strong>GLT1</strong> and attenuates cue induced cocaine <b>reinstatement</b>.
+SLC1A2	drug	cocaine	23719800	Here, we tested the effects of increasing <strong>GLT1</strong> expression on cue induced <b>cocaine</b> seeking in rats exposed to either limited (2 h/d) or extended (6 h/d) <b>cocaine</b> access followed by short (2 d) or long (45 d) withdrawal periods.
+SLC1A2	addiction	relapse	23719800	Here, we tested the effects of increasing <strong>GLT1</strong> expression on cue induced cocaine <b>seeking</b> in rats exposed to either limited (2 h/d) or extended (6 h/d) cocaine access followed by short (2 d) or long (45 d) withdrawal periods.
+SLC1A2	addiction	withdrawal	23719800	Here, we tested the effects of increasing <strong>GLT1</strong> expression on cue induced cocaine seeking in rats exposed to either limited (2 h/d) or extended (6 h/d) cocaine access followed by short (2 d) or long (45 d) <b>withdrawal</b> periods.
+SLC1A2	drug	cocaine	23719800	upregulated core <strong>GLT1</strong> expression and attenuated cue induced <b>cocaine</b> seeking behavior only in rats exposed to long withdrawal periods, with a greater effect in the extended access condition.
+SLC1A2	addiction	relapse	23719800	upregulated core <strong>GLT1</strong> expression and attenuated cue induced cocaine <b>seeking</b> behavior only in rats exposed to long withdrawal periods, with a greater effect in the extended access condition.
+SLC1A2	addiction	withdrawal	23719800	upregulated core <strong>GLT1</strong> expression and attenuated cue induced cocaine seeking behavior only in rats exposed to long <b>withdrawal</b> periods, with a greater effect in the extended access condition.
+SLC1A2	drug	cocaine	23719800	Pearson's correlation revealed <strong>GLT1</strong> expression in core to be inversely correlated with cue induced <b>cocaine</b> seeking behavior.
+SLC1A2	addiction	relapse	23719800	Pearson's correlation revealed <strong>GLT1</strong> expression in core to be inversely correlated with cue induced cocaine <b>seeking</b> behavior.
+SLC1A2	drug	cocaine	23719800	Rats withdrawn from <b>cocaine</b> self administration were treated with the same dose of ceftriaxone followed by intracore or intrashell infusions of one of two <strong>GLT1</strong> blockers, dihydrokainic acid (500 μM) or DL threo β benzyloxyaspartate (250 μM), or saline.
+SLC1A2	drug	cocaine	23719800	Our results reveal that the ceftriaxone mediated attenuation of cue induced <b>cocaine</b> reinstatement is reversed by <strong>GLT1</strong> blockade in core, but not shell, and further implicate core <strong>GLT1</strong> as a potential therapeutic target for <b>cocaine</b> relapse.
+SLC1A2	addiction	relapse	23719800	Our results reveal that the ceftriaxone mediated attenuation of cue induced cocaine <b>reinstatement</b> is reversed by <strong>GLT1</strong> blockade in core, but not shell, and further implicate core <strong>GLT1</strong> as a potential therapeutic target for cocaine <b>relapse</b>.
+SLC1A2	drug	alcohol	23537837	We recently reported that the administration of ceftriaxone (CEF), a β lactam antibiotic known to upregulate glutamate transporter 1 (<strong>GLT1</strong>) levels/activity, decreased the maintenance of EtOH intake in adult male <b>alcohol</b> preferring (P) rats.
+SLC1A2	drug	alcohol	23537837	These findings provide further support for <strong>GLT1</strong> associated mechanisms in high <b>alcohol</b> consuming behavior, and hold promise for the development of effective treatments targeting <b>alcohol</b> abuse and dependence.
+SLC1A2	addiction	dependence	23537837	These findings provide further support for <strong>GLT1</strong> associated mechanisms in high alcohol consuming behavior, and hold promise for the development of effective treatments targeting alcohol abuse and <b>dependence</b>.
+SLC1A2	drug	alcohol	23518814	Moreover, CEF mediated attenuation in relapse to <b>ethanol</b> drinking behavior was associated with upregulation of <strong>GLT1</strong> level in prefrontal cortex and nucleus accumbens core.
+SLC1A2	addiction	relapse	23518814	Moreover, CEF mediated attenuation in <b>relapse</b> to ethanol drinking behavior was associated with upregulation of <strong>GLT1</strong> level in prefrontal cortex and nucleus accumbens core.
+SLC1A2	drug	nicotine	23503685	Chronic <b>nicotine</b> administration in rats decreases the expression of the glutamate transporter 1 (<strong>GLT 1</strong>) and cysteine glutamate exchanger (system xC ) in the nucleus accumbens.
+SLC1A2	drug	nicotine	23503685	We hypothesized that ceftriaxone, a <strong>GLT 1</strong> and system xC  activator, would decrease murine behavioral aspects of <b>nicotine</b> dependence.
+SLC1A2	addiction	dependence	23503685	We hypothesized that ceftriaxone, a <strong>GLT 1</strong> and system xC  activator, would decrease murine behavioral aspects of nicotine <b>dependence</b>.
+SLC1A2	drug	cannabinoid	23253111	Reduction of dependence to <b>cannabinoids</b> by <strong>GLT 1</strong> activating property of the beta lactam antibiotic.
+SLC1A2	addiction	dependence	23253111	Reduction of <b>dependence</b> to cannabinoids by <strong>GLT 1</strong> activating property of the beta lactam antibiotic.
+SLC1A2	drug	cannabinoid	23253111	All together, it can be hypothesized that beta lactam antibiotics may reduce the development of dependence to <b>cannabinoids</b> through activating <strong>GLT 1</strong>.
+SLC1A2	addiction	dependence	23253111	All together, it can be hypothesized that beta lactam antibiotics may reduce the development of <b>dependence</b> to cannabinoids through activating <strong>GLT 1</strong>.
+SLC1A2	addiction	addiction	23054634	Specifically, NMDAR antagonists such as MK 801, and an inducer of the expression of glutamate transporter subtype 1 (<strong>GLT 1</strong>) (ceftriaxone) are known to inhibit <b>addictive</b> behavior.
+SLC1A2	addiction	reward	23054634	The combined action of a low dose of an NMDAR antagonist (MK 801) and <strong>GLT 1</strong> activation by ceftriaxone effectively changed different phases of <b>CPP</b> behavior.
+SLC1A2	drug	opioid	23051665	According to the recent evidence that AQP4 might form a functional complex with glutamate transporter 1 (<strong>GLT 1</strong>), this study focused on whether AQP4 participates in the modulation of <strong>GLT 1</strong> and glutamate homeostasis in <b>morphine</b> dependent mice.
+SLC1A2	drug	opioid	23051665	We found that AQP4 knockout prevented the down regulations of <strong>GLT 1</strong> expression and glutamate clearance when mice were repeatedly treated with <b>morphine</b>.
+SLC1A2	drug	opioid	23051665	Further study revealed that inhibition of <strong>GLT 1</strong> by dihydrokainic acid (DHK) initiated <b>morphine</b> dependence in AQP4 knockout mice.
+SLC1A2	addiction	dependence	23051665	Further study revealed that inhibition of <strong>GLT 1</strong> by dihydrokainic acid (DHK) initiated morphine <b>dependence</b> in AQP4 knockout mice.
+SLC1A2	drug	opioid	23051665	AQP4 deficiency suppresses the down regulation of <strong>GLT 1</strong>, and the disruption of glutamate homeostasis caused by repeated exposure to <b>morphine</b>, pointing to a strategy for maintaining glutamate homeostasis and thereby treating addiction through the modulation of AQP4 function and expression.
+SLC1A2	addiction	addiction	23051665	AQP4 deficiency suppresses the down regulation of <strong>GLT 1</strong>, and the disruption of glutamate homeostasis caused by repeated exposure to morphine, pointing to a strategy for maintaining glutamate homeostasis and thereby treating <b>addiction</b> through the modulation of AQP4 function and expression.
+SLC1A2	drug	cocaine	22956831	We have previously shown that chronic treatment with the antibiotic ceftriaxone restores xCT and <strong>GLT 1</strong> expression following <b>cocaine</b> self administration and attenuates both cue  and <b>cocaine</b> primed reinstatement.
+SLC1A2	addiction	relapse	22956831	We have previously shown that chronic treatment with the antibiotic ceftriaxone restores xCT and <strong>GLT 1</strong> expression following cocaine self administration and attenuates both cue  and cocaine primed <b>reinstatement</b>.
+SLC1A2	drug	cocaine	22956831	Here we used a (3)H glutamate uptake assay and microdialysis to test the hypothesis that ceftriaxone restores the function of both <strong>GLT 1</strong> and xCT (glutamate reuptake and export, respectively) in the NA core following <b>cocaine</b> self administration.
+SLC1A2	drug	nicotine	22719919	By genotyping with the Sequenom MassARRAY iPLEX platform and subsequent statistical analysis using Plink software, we show that two of the SNPs studied, in the <strong>SLC1A2</strong> (rs1083658) and ACTN1 (rs2268983) genes, were associated with <b>smoking</b> behavior in our study population.
+SLC1A2	addiction	dependence	22680643	Similar to neurodegenerative disease models, in which there is dysfunction of the glutamatergic excitatory system, the role of <strong>GLT1</strong> has been tested in drug <b>dependence</b> models that show dysfunction of glutamate transmission.
+SLC1A2	drug	cocaine	22680643	We and others have recently found that ceftriaxone, an FDA approved drug known to elevate <strong>GLT1</strong> expression, attenuates cue induced <b>cocaine</b> relapse.
+SLC1A2	addiction	relapse	22680643	We and others have recently found that ceftriaxone, an FDA approved drug known to elevate <strong>GLT1</strong> expression, attenuates cue induced cocaine <b>relapse</b>.
+SLC1A2	drug	alcohol	22680643	This review provides information about the potential therapeutic role of <strong>GLT1</strong> for the treatment of <b>alcohol</b> abuse and dependence.
+SLC1A2	addiction	dependence	22680643	This review provides information about the potential therapeutic role of <strong>GLT1</strong> for the treatment of alcohol abuse and <b>dependence</b>.
+SLC1A2	drug	cocaine	22433294	Consistent with this view, glutamate type 1 transporter (<strong>GLT1</strong>), the transporter responsible for >90% of glutamate uptake, is downregulated in NAc after several days of withdrawal in rats previously trained to self administer <b>cocaine</b> under limited access conditions (1 2 h/d).
+SLC1A2	addiction	withdrawal	22433294	Consistent with this view, glutamate type 1 transporter (<strong>GLT1</strong>), the transporter responsible for >90% of glutamate uptake, is downregulated in NAc after several days of <b>withdrawal</b> in rats previously trained to self administer cocaine under limited access conditions (1 2 h/d).
+SLC1A2	drug	cocaine	22433294	Here, we determined the combined effects of manipulating <b>cocaine</b> access and withdrawal on <strong>GLT1</strong> expression in NAc core and shell.
+SLC1A2	addiction	withdrawal	22433294	Here, we determined the combined effects of manipulating cocaine access and <b>withdrawal</b> on <strong>GLT1</strong> expression in NAc core and shell.
+SLC1A2	drug	cocaine	22433294	We found that although <b>cocaine</b> withdrawal decreases <strong>GLT1</strong> expression in both core and shell, only in core is <strong>GLT1</strong> downregulation sensitive to both access and withdrawal.
+SLC1A2	addiction	withdrawal	22433294	We found that although cocaine <b>withdrawal</b> decreases <strong>GLT1</strong> expression in both core and shell, only in core is <strong>GLT1</strong> downregulation sensitive to both access and <b>withdrawal</b>.
+SLC1A2	addiction	withdrawal	22433294	In fact, after long <b>withdrawal</b>, <strong>GLT1</strong> in core is downregulated more than in shell in either the limited or extended access condition.
+SLC1A2	drug	opioid	21865493	In contrast, ultra low dose (15 ng) <b>naloxone</b> enhanced the antinociceptive effect of <b>morphine</b> (10 μg), with an increase in the paw withdrawal threshold to thermal stimulus (from 19% to 35%) and to tactile stimulus (from 33% to 55%) compared with <b>morphine</b> treatment alone, and this was associated with restoration of GLAST and <strong>GLT 1</strong> expression to control levels (102% and 114%, respectively) in the astrocytes of laminae I and II in the spinal cord dorsal horn ipsilateral to the PST hindlimb and a decrease in EAA levels in the CSF dialysate (glutamate: 10.0 μM; aspartate: 1.1 μM).
+SLC1A2	addiction	withdrawal	21865493	In contrast, ultra low dose (15 ng) naloxone enhanced the antinociceptive effect of morphine (10 μg), with an increase in the paw <b>withdrawal</b> threshold to thermal stimulus (from 19% to 35%) and to tactile stimulus (from 33% to 55%) compared with morphine treatment alone, and this was associated with restoration of GLAST and <strong>GLT 1</strong> expression to control levels (102% and 114%, respectively) in the astrocytes of laminae I and II in the spinal cord dorsal horn ipsilateral to the PST hindlimb and a decrease in EAA levels in the CSF dialysate (glutamate: 10.0 μM; aspartate: 1.1 μM).
+SLC1A2	drug	opioid	21865493	Ultra low dose <b>naloxone</b> enhanced the antinociceptive effect of <b>morphine</b> in PST rats, possibly by restoration of GLAST and <strong>GLT 1</strong> expression in astrocytes, which inhibited the accumulation of EAAs in the synapses, resulting in a neuroprotective effect.
+SLC1A2	drug	cocaine	21824497	It has previously been shown that <strong>GLT 1</strong> expression is decreased in the nucleus accumbens following <b>cocaine</b> self administration and extinction training; ceftriaxone given in the days immediately prior to reinstatement testing attenuates both cue  and <b>cocaine</b> primed reinstatement.
+SLC1A2	addiction	relapse	21824497	It has previously been shown that <strong>GLT 1</strong> expression is decreased in the nucleus accumbens following cocaine self administration and extinction training; ceftriaxone given in the days immediately prior to <b>reinstatement</b> testing attenuates both cue  and cocaine primed <b>reinstatement</b>.
+SLC1A2	addiction	relapse	21824497	This attenuation in <b>reinstatement</b> was accompanied by a restoration of <strong>GLT 1</strong> expression in the nucleus accumbens.
+SLC1A2	drug	cannabinoid	21536061	Role of <strong>GLT 1</strong> transporter activation in prevention of <b>cannabinoid</b> tolerance by the β lactam antibiotic, ceftriaxone, in mice.
+SLC1A2	drug	cannabinoid	21536061	Our results suggest that repeated treatment with ceftriaxone prevents the development of tolerance to the analgesic and hypothermic effects of <b>cannabinoids</b>, and <strong>GLT 1</strong> activation appears to play a key role in this preventive effect of beta lactam antibiotics.
+SLC1A2	drug	amphetamine	21524862	Glutamate transporter subtype 1 (<strong>GLT 1</strong>) activator ceftriaxone attenuates <b>amphetamine</b> induced hyperactivity and behavioral sensitization in rats.
+SLC1A2	addiction	sensitization	21524862	Glutamate transporter subtype 1 (<strong>GLT 1</strong>) activator ceftriaxone attenuates amphetamine induced hyperactivity and behavioral <b>sensitization</b> in rats.
+SLC1A2	drug	amphetamine	21524862	The β lactam antibiotic and glutamate transporter subtype 1 (<strong>GLT 1</strong>) activator ceftriaxone prevents relapse to cocaine seeking and inhibits morphine induced physical dependence and tolerance in rats, but its efficacy against <b>amphetamine</b> induced behaviors is unknown.
+SLC1A2	drug	cocaine	21524862	The β lactam antibiotic and glutamate transporter subtype 1 (<strong>GLT 1</strong>) activator ceftriaxone prevents relapse to <b>cocaine</b> seeking and inhibits morphine induced physical dependence and tolerance in rats, but its efficacy against amphetamine induced behaviors is unknown.
+SLC1A2	drug	opioid	21524862	The β lactam antibiotic and glutamate transporter subtype 1 (<strong>GLT 1</strong>) activator ceftriaxone prevents relapse to cocaine seeking and inhibits <b>morphine</b> induced physical dependence and tolerance in rats, but its efficacy against amphetamine induced behaviors is unknown.
+SLC1A2	addiction	dependence	21524862	The β lactam antibiotic and glutamate transporter subtype 1 (<strong>GLT 1</strong>) activator ceftriaxone prevents relapse to cocaine seeking and inhibits morphine induced physical <b>dependence</b> and tolerance in rats, but its efficacy against amphetamine induced behaviors is unknown.
+SLC1A2	addiction	relapse	21524862	The β lactam antibiotic and glutamate transporter subtype 1 (<strong>GLT 1</strong>) activator ceftriaxone prevents <b>relapse</b> to cocaine <b>seeking</b> and inhibits morphine induced physical dependence and tolerance in rats, but its efficacy against amphetamine induced behaviors is unknown.
+SLC1A2	drug	alcohol	21422004	We hypothesized that because glutamate transporter 1 (<strong>GLT1</strong>) is responsible for the removal of most extracellular glutamate, up regulation or activation of <strong>GLT1</strong> would attenuate <b>ethanol</b> consumption.
+SLC1A2	drug	alcohol	21422004	These results indicate that CEF effectively reduces <b>ethanol</b> intake, possibly through activation of <strong>GLT1</strong>, and may be a potential therapeutic drug for <b>alcohol</b> addiction treatment.
+SLC1A2	addiction	addiction	21422004	These results indicate that CEF effectively reduces ethanol intake, possibly through activation of <strong>GLT1</strong>, and may be a potential therapeutic drug for alcohol <b>addiction</b> treatment.
+SLC1A2	drug	alcohol	20374202	ENT1 regulates <b>ethanol</b> sensitive <strong>EAAT2</strong> expression and function in astrocytes.
+SLC1A2	drug	alcohol	20374202	We also examined the effect of 0 to 200 mM <b>ethanol</b> doses for 0 to 24 hours of <b>ethanol</b> exposure on <strong>EAAT2</strong> expression and glutamate uptake activity.
+SLC1A2	drug	alcohol	20374202	We further examined the effect of ENT1 knockdown by a specific siRNA on <b>ethanol</b> induced <strong>EAAT2</strong> expression.
+SLC1A2	drug	alcohol	20374202	Interestingly, 100 or 200 mM <b>ethanol</b> exposure increased <strong>EAAT2</strong> mRNA expression as well as glutamate uptake activity.
+SLC1A2	drug	alcohol	20374202	Moreover, we found that ENT1 knockdown inhibited the <b>ethanol</b> induced <strong>EAAT2</strong> up regulation.
+SLC1A2	drug	alcohol	20374202	Our results suggest that ENT1 regulates glutamate uptake activity by altering <strong>EAAT2</strong> expression and function, which might be implicated in <b>ethanol</b> intoxication and preference.
+SLC1A2	addiction	intoxication	20374202	Our results suggest that ENT1 regulates glutamate uptake activity by altering <strong>EAAT2</strong> expression and function, which might be implicated in ethanol <b>intoxication</b> and preference.
+SLC1A2	drug	alcohol	20153402	The decreased expression of GLAST, <strong>GLT 1</strong> and GluR2 in the <b>alcoholic</b> patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug seeking and chronic relapse.
+SLC1A2	addiction	relapse	20153402	The decreased expression of GLAST, <strong>GLT 1</strong> and GluR2 in the alcoholic patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug <b>seeking</b> and chronic <b>relapse</b>.
+SLC1A2	drug	opioid	19806886	In order to investigate the role of spinal glutamate transporter 1 (<strong>GLT 1</strong>) in the neuropathic pain and <b>morphine</b> tolerance, rat chronic constriction injury (CCI) of sciatic nerve was performed, and the mechanical allodynia was evaluated by mechanical withdrawal threshold (MWT), the expression of <strong>GLT 1</strong> was measured by real time PCR and Western blotting analysis.
+SLC1A2	addiction	withdrawal	19806886	In order to investigate the role of spinal glutamate transporter 1 (<strong>GLT 1</strong>) in the neuropathic pain and morphine tolerance, rat chronic constriction injury (CCI) of sciatic nerve was performed, and the mechanical allodynia was evaluated by mechanical <b>withdrawal</b> threshold (MWT), the expression of <strong>GLT 1</strong> was measured by real time PCR and Western blotting analysis.
+SLC1A2	drug	opioid	19806886	Administration of <b>morphine</b> alone could develop tolerance rapidly in initial two days, and then had no significant difference with CCI group, the expression of <strong>GLT 1</strong> was down regulated.
+SLC1A2	drug	opioid	19806886	Co administration of ceftriaxone sodium with <b>morphine</b> attenuated <b>morphine</b> tolerance and up regulated <strong>GLT 1</strong> expression, and the MWT remained at high level after 6 days.
+SLC1A2	drug	opioid	19806886	In conclusion, change of spinal <strong>GLT 1</strong> expression and function has close correlation with the development of neuropathic pain and <b>morphine</b> tolerance.
+SLC1A2	drug	cocaine	19717140	We hypothesized that <b>cocaine</b> self administration reduces <strong>GLT 1</strong> and that <strong>GLT 1</strong> upregulation inhibits <b>cocaine</b> seeking.
+SLC1A2	addiction	relapse	19717140	We hypothesized that cocaine self administration reduces <strong>GLT 1</strong> and that <strong>GLT 1</strong> upregulation inhibits cocaine <b>seeking</b>.
+SLC1A2	drug	cocaine	19717140	We measured [(3)H] glutamate uptake and protein expression of <strong>GLT 1</strong> and xCT, the catalytic subunit of the cystine glutamate exchanger, following <b>cocaine</b> self administration and 3 weeks of extinction training.
+SLC1A2	drug	cocaine	19717140	<b>Cocaine</b> self administration reduced glutamate uptake and the expression of both <strong>GLT 1</strong> and xCT.
+SLC1A2	drug	cocaine	19717140	Ceftriaxone restored <strong>GLT 1</strong> and xCT levels and prevented cue  and <b>cocaine</b> induced reinstatement of drug seeking.
+SLC1A2	addiction	relapse	19717140	Ceftriaxone restored <strong>GLT 1</strong> and xCT levels and prevented cue  and cocaine induced <b>reinstatement</b> of drug <b>seeking</b>.
+SLC1A2	drug	cocaine	19625514	Upregulation of <strong>GLT1</strong> attenuates cue induced reinstatement of <b>cocaine</b> seeking behavior in rats.
+SLC1A2	addiction	relapse	19625514	Upregulation of <strong>GLT1</strong> attenuates cue induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior in rats.
+SLC1A2	drug	cocaine	19625514	Because <strong>GLT1</strong> is responsible for the uptake of >or=90% of extracellular glutamate, we tested the hypothesis that increased <strong>GLT1</strong> expression attenuates <b>cocaine</b> relapse.
+SLC1A2	addiction	relapse	19625514	Because <strong>GLT1</strong> is responsible for the uptake of >or=90% of extracellular glutamate, we tested the hypothesis that increased <strong>GLT1</strong> expression attenuates cocaine <b>relapse</b>.
+SLC1A2	drug	cocaine	19625514	Immunoblotting confirmed that the ceftriaxone induced blockade of <b>cocaine</b> relapse was associated with an increase in <strong>GLT1</strong> expression in both PFC and NAcc.
+SLC1A2	addiction	relapse	19625514	Immunoblotting confirmed that the ceftriaxone induced blockade of cocaine <b>relapse</b> was associated with an increase in <strong>GLT1</strong> expression in both PFC and NAcc.
+SLC1A2	drug	cocaine	19625514	Our results suggest that glutamate plays a key role in cue induced relapse to <b>cocaine</b> seeking behavior, implicating <strong>GLT1</strong> as a potential therapeutic target for <b>cocaine</b> addiction.
+SLC1A2	addiction	addiction	19625514	Our results suggest that glutamate plays a key role in cue induced relapse to cocaine seeking behavior, implicating <strong>GLT1</strong> as a potential therapeutic target for cocaine <b>addiction</b>.
+SLC1A2	addiction	relapse	19625514	Our results suggest that glutamate plays a key role in cue induced <b>relapse</b> to cocaine <b>seeking</b> behavior, implicating <strong>GLT1</strong> as a potential therapeutic target for cocaine addiction.
+SLC1A2	drug	nicotine	19103434	Somatic signs of withdrawal were measured and immunoblotting was performed 12 hours after the last <b>nicotine</b> exposure to determine if the catalytic subunit of the cystine glutamate exchanger, xCT, or the glial glutamate transporter, <strong>GLT 1</strong>, were altered in the ventral tegmental area (VTA), nucleus accumbens, prefrontal cortex, or amygdala.
+SLC1A2	addiction	withdrawal	19103434	Somatic signs of <b>withdrawal</b> were measured and immunoblotting was performed 12 hours after the last nicotine exposure to determine if the catalytic subunit of the cystine glutamate exchanger, xCT, or the glial glutamate transporter, <strong>GLT 1</strong>, were altered in the ventral tegmental area (VTA), nucleus accumbens, prefrontal cortex, or amygdala.
+SLC1A2	drug	nicotine	19103434	Rats receiving <b>nicotine</b> via self administration or minipumps displayed somatic signs of withdrawal, but only <b>nicotine</b> self administering rats showed decreased xCT expression in the nucleus accumbens and VTA and decreased <strong>GLT 1</strong> expression in the nucleus accumbens.
+SLC1A2	addiction	withdrawal	19103434	Rats receiving nicotine via self administration or minipumps displayed somatic signs of <b>withdrawal</b>, but only nicotine self administering rats showed decreased xCT expression in the nucleus accumbens and VTA and decreased <strong>GLT 1</strong> expression in the nucleus accumbens.
+SLC1A2	drug	opioid	18973795	(4) Repeated <b>morphine</b> administration down regulated cerebral glutamate transporter 1 (<strong>GLT 1</strong>) expression in wild type mice.
+SLC1A2	drug	opioid	18973795	The suppression of down regulation of cerebral <strong>GLT1</strong> expression might mediate the attenuation of AQP4 deficiency to <b>morphine</b> tolerance and dependence.
+SLC1A2	addiction	dependence	18973795	The suppression of down regulation of cerebral <strong>GLT1</strong> expression might mediate the attenuation of AQP4 deficiency to morphine tolerance and <b>dependence</b>.
+SLC1A2	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, <strong>EAAT2</strong> 1, <strong>EAAT2</strong> 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+SLC1A2	drug	opioid	18342307	<strong>GLT 1</strong> has been implicated in diverse neurological disorders and in <b>opioid</b> dependence and withdrawal.
+SLC1A2	addiction	dependence	18342307	<strong>GLT 1</strong> has been implicated in diverse neurological disorders and in opioid <b>dependence</b> and withdrawal.
+SLC1A2	addiction	withdrawal	18342307	<strong>GLT 1</strong> has been implicated in diverse neurological disorders and in opioid dependence and <b>withdrawal</b>.
+SLC1A2	drug	amphetamine	16324108	Gene transfer of <strong>GLT 1</strong>, a glutamate transporter, into the nucleus accumbens shell attenuates <b>methamphetamine</b>  and morphine induced conditioned place preference in rats.
+SLC1A2	drug	opioid	16324108	Gene transfer of <strong>GLT 1</strong>, a glutamate transporter, into the nucleus accumbens shell attenuates methamphetamine  and <b>morphine</b> induced conditioned place preference in rats.
+SLC1A2	drug	amphetamine	16324108	In the present study, we examined the effects of gene transfer of a glial glutamate transporter, <strong>GLT 1</strong>, into the NAc shell by recombinant adenoviruses on <b>methamphetamine</b>  and morphine induced conditioned place preference in rats.
+SLC1A2	drug	opioid	16324108	In the present study, we examined the effects of gene transfer of a glial glutamate transporter, <strong>GLT 1</strong>, into the NAc shell by recombinant adenoviruses on methamphetamine  and <b>morphine</b> induced conditioned place preference in rats.
+SLC1A2	drug	amphetamine	16324108	Intra NAc shell overexpression of <strong>GLT 1</strong> before the conditioning significantly attenuated the conditioned place preference induced by <b>methamphetamine</b> or morphine, when compared with control.
+SLC1A2	drug	opioid	16324108	Intra NAc shell overexpression of <strong>GLT 1</strong> before the conditioning significantly attenuated the conditioned place preference induced by methamphetamine or <b>morphine</b>, when compared with control.
+SLC1A2	drug	amphetamine	16324108	These results suggest that <strong>GLT 1</strong> within the NAc shell plays an inhibitory role in the conditioned rewarding effects of <b>methamphetamine</b> and morphine but not the physical dependence on morphine.
+SLC1A2	drug	opioid	16324108	These results suggest that <strong>GLT 1</strong> within the NAc shell plays an inhibitory role in the conditioned rewarding effects of methamphetamine and <b>morphine</b> but not the physical dependence on <b>morphine</b>.
+SLC1A2	addiction	dependence	16324108	These results suggest that <strong>GLT 1</strong> within the NAc shell plays an inhibitory role in the conditioned rewarding effects of methamphetamine and morphine but not the physical <b>dependence</b> on morphine.
+SLC1A2	drug	alcohol	15770106	The <b>ethanol</b> induced deficit in glutamate uptake was not associated with decreased total tissue levels of the transporters GLAST or <strong>GLT1</strong>.
+SLC1A2	drug	opioid	15542740	Here we show that a glial glutamate transporter <strong>GLT 1</strong> could be involved in physical and psychological <b>morphine</b> dependence.
+SLC1A2	addiction	dependence	15542740	Here we show that a glial glutamate transporter <strong>GLT 1</strong> could be involved in physical and psychological morphine <b>dependence</b>.
+SLC1A2	drug	opioid	15542740	By Northern blot analysis, the expression of glial glutamate transporter <strong>GLT 1</strong>, but not GLAST, mRNA was decreased in the striatum/nucleus accumbens (NAc) and thalamus of <b>morphine</b> dependent rats.
+SLC1A2	drug	opioid	15542740	Furthermore, gene transfer techniques using recombinant adenoviruses revealed that <strong>GLT 1</strong> in the locus coeruleus and NAc shell plays inhibitory roles in physical and psychological <b>morphine</b> dependence, respectively.
+SLC1A2	addiction	dependence	15542740	Furthermore, gene transfer techniques using recombinant adenoviruses revealed that <strong>GLT 1</strong> in the locus coeruleus and NAc shell plays inhibitory roles in physical and psychological morphine <b>dependence</b>, respectively.
+SLC1A2	drug	opioid	15542740	These findings may provide evidence that a glial glutamate transporter <strong>GLT 1</strong> could be a new target for preventing physical and psychological <b>morphine</b> dependence.
+SLC1A2	addiction	dependence	15542740	These findings may provide evidence that a glial glutamate transporter <strong>GLT 1</strong> could be a new target for preventing physical and psychological morphine <b>dependence</b>.
+SLC1A2	drug	alcohol	15542698	The glial glutamate transporter gene <strong>EAAT2</strong> polymorphism G603A was associated with <b>alcoholic</b> cirrhosis (P = .048).
+SLC1A2	drug	alcohol	15542698	The genotype for the most active <b>alcohol</b> dehydrogenase enzyme ADH1C was associated with a lower risk of <b>alcoholism</b> (P = .026) and was less prevalent in <b>alcoholics</b> with DRD2TaqIA2/A2 (P = .047), GABAA beta2 1412C/C (P = .01), or <strong>EAAT2</strong> 603G/A (P = .022) genotypes.
+SLC1A2	drug	alcohol	15542698	Combined DRD2TaqI A or B with GABAA beta2 or <strong>EAAT2</strong> G603A genotypes may have a concerted influence in the predisposition to <b>alcoholism</b>.
+SLC1A2	drug	alcohol	15345266	DRD2A, DRD2B, GABB2, <strong>EAAT2</strong>, and 5HTT genotypes did not divide <b>alcoholic</b> cases and controls on N methyl d aspartate (NMDA) receptor parameters.
+SLC1A2	drug	amphetamine	15044042	The ability of repeated D <b>amphetamine</b> (2 mg/kg) treatment to induce behavioral sensitization in rats and alter glial fibrillary acidic protein (GFAP), dopamine transporter (DAT) and glutamate transporter 1 (<strong>GLT 1</strong>) immunoreactivities was assessed after a 10 day drug abstinence period.
+SLC1A2	addiction	sensitization	15044042	The ability of repeated D amphetamine (2 mg/kg) treatment to induce behavioral <b>sensitization</b> in rats and alter glial fibrillary acidic protein (GFAP), dopamine transporter (DAT) and glutamate transporter 1 (<strong>GLT 1</strong>) immunoreactivities was assessed after a 10 day drug abstinence period.
+SLC1A2	drug	opioid	14750980	Effect of gene transfer of <strong>GLT 1</strong>, a glutamate transporter, into the locus coeruleus by recombinant adenoviruses on <b>morphine</b> physical dependence in rats.
+SLC1A2	addiction	dependence	14750980	Effect of gene transfer of <strong>GLT 1</strong>, a glutamate transporter, into the locus coeruleus by recombinant adenoviruses on morphine physical <b>dependence</b> in rats.
+SLC1A2	drug	opioid	14750980	We previously reported changes in the mRNA expression of a glial glutamate transporter <strong>GLT 1</strong> in some brain regions of <b>morphine</b> dependent and <b>naloxone</b> precipitated withdrawal rats, and inhibition of <b>morphine</b> physical dependence by a glutamate transporter activator in mice.
+SLC1A2	addiction	dependence	14750980	We previously reported changes in the mRNA expression of a glial glutamate transporter <strong>GLT 1</strong> in some brain regions of morphine dependent and naloxone precipitated withdrawal rats, and inhibition of morphine physical <b>dependence</b> by a glutamate transporter activator in mice.
+SLC1A2	addiction	withdrawal	14750980	We previously reported changes in the mRNA expression of a glial glutamate transporter <strong>GLT 1</strong> in some brain regions of morphine dependent and naloxone precipitated <b>withdrawal</b> rats, and inhibition of morphine physical dependence by a glutamate transporter activator in mice.
+SLC1A2	drug	opioid	14750980	These findings support the possibility that glutamate transporters such as <strong>GLT 1</strong> are involved in <b>morphine</b> dependence.
+SLC1A2	addiction	dependence	14750980	These findings support the possibility that glutamate transporters such as <strong>GLT 1</strong> are involved in morphine <b>dependence</b>.
+SLC1A2	drug	opioid	14750980	In this study, we examined the effects of gene transfer of <strong>GLT 1</strong> into the locus coeruleus (LC) by recombinant adenoviruses on <b>morphine</b> physical dependence in rats.
+SLC1A2	addiction	dependence	14750980	In this study, we examined the effects of gene transfer of <strong>GLT 1</strong> into the locus coeruleus (LC) by recombinant adenoviruses on morphine physical <b>dependence</b> in rats.
+SLC1A2	drug	opioid	14750980	Local overexpression of <strong>GLT 1</strong> within the bilateral LC by the recombinant adenoviruses before implantation of the <b>morphine</b> pellet significantly inhibited various somatic signs of <b>naloxone</b> precipitated <b>morphine</b> withdrawal, compared with the control.
+SLC1A2	addiction	withdrawal	14750980	Local overexpression of <strong>GLT 1</strong> within the bilateral LC by the recombinant adenoviruses before implantation of the morphine pellet significantly inhibited various somatic signs of naloxone precipitated morphine <b>withdrawal</b>, compared with the control.
+SLC1A2	drug	opioid	14750980	These results suggest that <strong>GLT 1</strong> within the LC plays an inhibitory role in <b>morphine</b> physical dependence.
+SLC1A2	addiction	dependence	14750980	These results suggest that <strong>GLT 1</strong> within the LC plays an inhibitory role in morphine physical <b>dependence</b>.
+SLC1A2	drug	opioid	12805317	<b>Morphine</b> withdrawal increases glutamate uptake and surface expression of glutamate transporter <strong>GLT1</strong> at hippocampal synapses.
+SLC1A2	addiction	withdrawal	12805317	Morphine <b>withdrawal</b> increases glutamate uptake and surface expression of glutamate transporter <strong>GLT1</strong> at hippocampal synapses.
+SLC1A2	drug	opioid	12805317	Moreover, the increase in glutamate uptake was reproduced in cultured neurons during <b>morphine</b> withdrawal, and the increase of uptake in neurons could be blocked by dihydrokainate, a specific inhibitor of <strong>GLT1</strong>.
+SLC1A2	addiction	withdrawal	12805317	Moreover, the increase in glutamate uptake was reproduced in cultured neurons during morphine <b>withdrawal</b>, and the increase of uptake in neurons could be blocked by dihydrokainate, a specific inhibitor of <strong>GLT1</strong>.
+SLC1A2	drug	opioid	12805317	Cell surface biotinylation and immunoblot analysis showed that <b>morphine</b> withdrawal produced an increase in <strong>GLT1</strong> expression rather than EAAC1 (excitatory amino acids carrier 1), a neuronal subtype, at the cultured neuronal cell surface, whereas no significant change was observed in that of cultured astrocytes.
+SLC1A2	addiction	withdrawal	12805317	Cell surface biotinylation and immunoblot analysis showed that morphine <b>withdrawal</b> produced an increase in <strong>GLT1</strong> expression rather than EAAC1 (excitatory amino acids carrier 1), a neuronal subtype, at the cultured neuronal cell surface, whereas no significant change was observed in that of cultured astrocytes.
+SLC1A2	drug	opioid	12805317	These results suggest that <strong>GLT1</strong> in hippocampal neurons can be induced to translocate to the nerve terminals and express on the cell surface during <b>morphine</b> withdrawal.
+SLC1A2	addiction	withdrawal	12805317	These results suggest that <strong>GLT1</strong> in hippocampal neurons can be induced to translocate to the nerve terminals and express on the cell surface during morphine <b>withdrawal</b>.
+SLC1A2	drug	opioid	12805317	The translocation of <strong>GLT1</strong> at synapses during <b>morphine</b> withdrawal provides a neuronal mechanism for modulation of excitatory neurotransmission during opiate abuse.
+SLC1A2	addiction	withdrawal	12805317	The translocation of <strong>GLT1</strong> at synapses during morphine <b>withdrawal</b> provides a neuronal mechanism for modulation of excitatory neurotransmission during opiate abuse.
+SLC1A2	drug	opioid	11558151	By northern blot analysis, the expression of <strong>GLT 1</strong> mRNA was found to decrease significantly in the striatum and thalamus of <b>morphine</b> dependent rats, and to increase significantly in the striatum 2 hr after the <b>naloxone</b> precipitated withdrawal.
+SLC1A2	addiction	withdrawal	11558151	By northern blot analysis, the expression of <strong>GLT 1</strong> mRNA was found to decrease significantly in the striatum and thalamus of morphine dependent rats, and to increase significantly in the striatum 2 hr after the naloxone precipitated <b>withdrawal</b>.
+SLC1A2	drug	opioid	11558151	In vivo microdialysis experiments revealed that the extracellular glutamate levels was elevated in the striatum and nucleus accumbens, in which the changes of <strong>GLT 1</strong> mRNA level were observed, during <b>naloxone</b> precipitated <b>morphine</b> withdrawal.
+SLC1A2	addiction	withdrawal	11558151	In vivo microdialysis experiments revealed that the extracellular glutamate levels was elevated in the striatum and nucleus accumbens, in which the changes of <strong>GLT 1</strong> mRNA level were observed, during naloxone precipitated morphine <b>withdrawal</b>.
+SLC1A2	drug	opioid	11558151	In cultured astrocytes, the expression of <strong>GLT 1</strong> mRNA was regulated by agents activating the cAMP pathway, as well as beta adrenergic agonist and dopamine, but not <b>morphine</b>.
+SLC1A2	drug	opioid	11558151	These results suggest that the changes of <strong>GLT 1</strong> expression, which alter the glutamate uptake and affect the glutamatergic transmission efficiency, play a role in the development of <b>morphine</b> dependence and the expression of <b>morphine</b> withdrawal.
+SLC1A2	addiction	dependence	11558151	These results suggest that the changes of <strong>GLT 1</strong> expression, which alter the glutamate uptake and affect the glutamatergic transmission efficiency, play a role in the development of morphine <b>dependence</b> and the expression of morphine withdrawal.
+SLC1A2	addiction	withdrawal	11558151	These results suggest that the changes of <strong>GLT 1</strong> expression, which alter the glutamate uptake and affect the glutamatergic transmission efficiency, play a role in the development of morphine dependence and the expression of morphine <b>withdrawal</b>.
+SLC1A2	drug	opioid	11423104	The expression of mRNAs for the glial glutamate transporters, <strong>GLT 1</strong> and GLAST, in the rat brain accompanied with <b>morphine</b> dependence and <b>naloxone</b> precipitated withdrawal was investigated by Northern blot analysis.
+SLC1A2	addiction	dependence	11423104	The expression of mRNAs for the glial glutamate transporters, <strong>GLT 1</strong> and GLAST, in the rat brain accompanied with morphine <b>dependence</b> and naloxone precipitated withdrawal was investigated by Northern blot analysis.
+SLC1A2	addiction	withdrawal	11423104	The expression of mRNAs for the glial glutamate transporters, <strong>GLT 1</strong> and GLAST, in the rat brain accompanied with morphine dependence and naloxone precipitated <b>withdrawal</b> was investigated by Northern blot analysis.
+SLC1A2	drug	opioid	11423104	The expression of <strong>GLT 1</strong> mRNA was significantly decreased in the striatum and thalamus of <b>morphine</b> dependent rats, and significantly increased in the striatum 2 h after the <b>naloxone</b> precipitated withdrawal, compared with that of naive rats.
+SLC1A2	addiction	withdrawal	11423104	The expression of <strong>GLT 1</strong> mRNA was significantly decreased in the striatum and thalamus of morphine dependent rats, and significantly increased in the striatum 2 h after the naloxone precipitated <b>withdrawal</b>, compared with that of naive rats.
+SLC1A2	drug	opioid	11423104	These results suggest the involvement of <strong>GLT 1</strong> in the development of <b>morphine</b> dependence and the expression of <b>morphine</b> withdrawal.
+SLC1A2	addiction	dependence	11423104	These results suggest the involvement of <strong>GLT 1</strong> in the development of morphine <b>dependence</b> and the expression of morphine withdrawal.
+SLC1A2	addiction	withdrawal	11423104	These results suggest the involvement of <strong>GLT 1</strong> in the development of morphine dependence and the expression of morphine <b>withdrawal</b>.
+SLC1A2	drug	amphetamine	11406296	<b>Amphetamine</b> administration does not alter protein levels of the <strong>GLT 1</strong> and EAAC1 glutamate transporter subtypes in rat midbrain, nucleus accumbens, striatum, or prefrontal cortex.
+SLC1A2	drug	amphetamine	11406296	The goal of this study was to determine whether repeated <b>amphetamine</b> administration influences the expression of two glutamate transporter subtypes, <strong>GLT 1</strong> and EAAC1.
+SLC1A2	drug	amphetamine	11406296	We found no significant change in levels of <strong>GLT 1</strong> or EAAC1 in response to either acute or chronic <b>amphetamine</b> treatment.
+SLC1A2	drug	alcohol	11204345	Genetic variation of the glutamate transporter <strong>EAAT2</strong> gene and vulnerability to <b>alcohol</b> dependence.
+SLC1A2	addiction	dependence	11204345	Genetic variation of the glutamate transporter <strong>EAAT2</strong> gene and vulnerability to alcohol <b>dependence</b>.
+SLC1A2	drug	alcohol	11204345	The present association study tested the candidate gene hypothesis that variation of the gene encoding the astroglial glutamate transporter <strong>EAAT2</strong> confers vulnerability to <b>alcohol</b> dependence.
+SLC1A2	addiction	dependence	11204345	The present association study tested the candidate gene hypothesis that variation of the gene encoding the astroglial glutamate transporter <strong>EAAT2</strong> confers vulnerability to alcohol <b>dependence</b>.
+SLC1A2	drug	alcohol	11204345	Genotypes of a silent G603A nucleotide exchange in exon 5 of the <strong>EAAT2</strong> gene were assessed in 565 subjects of German descent, comprising 342 <b>alcohol</b> dependent subjects and 223 control subjects.
+SLC1A2	drug	alcohol	11204345	These two consistent lines of evidence suggest that genetic variation of the <strong>EAAT2</strong> gene confers vulnerability to risk taking behavior in <b>alcoholics</b>.
+SLC1A2	drug	alcohol	9416769	In addition, the <b>ethanol</b> induced increase in Vmax for glutamate was reversed by the protein kinase C inhibitors, calphostin C and bisindolylmaleimide, and was not associated with an increase in the expression of either of the major glutamate transporter proteins, <strong>GLT 1</strong> or GLAST.
+SLC1A2	drug	amphetamine	9201764	We have examined the immunoreactivities of a glutamate (Glu) transporter, <strong>GLT 1</strong>, in rat brains treated with a single or repeated intermittent administration of <b>methamphetamine</b> (MAP).
+SLC1A2	drug	alcohol	7698742	In an interspecific backcross analysis <strong>Eaat2</strong> maps to the central region of mouse chromosome 2, where it is located near quantitative trait loci that modulate neuroexcitability and seizure frequency in mouse models of <b>alcohol</b> withdrawal and epilepsy.
+SLC1A2	addiction	withdrawal	7698742	In an interspecific backcross analysis <strong>Eaat2</strong> maps to the central region of mouse chromosome 2, where it is located near quantitative trait loci that modulate neuroexcitability and seizure frequency in mouse models of alcohol <b>withdrawal</b> and epilepsy.
+GRIN2B	drug	alcohol	32720424	Recently, we demonstrated that two <b>ethanol</b> binge like episodes in young adult rats selectively blocked NMDA LTD in hippocampal slices, increased NMDA receptor sensitivity to a <strong>GluN2B</strong> subunit antagonist, and induced cognitive deficits.
+GRIN2B	addiction	intoxication	32720424	Recently, we demonstrated that two ethanol <b>binge</b> like episodes in young adult rats selectively blocked NMDA LTD in hippocampal slices, increased NMDA receptor sensitivity to a <strong>GluN2B</strong> subunit antagonist, and induced cognitive deficits.
+GRIN2B	drug	alcohol	32720424	In the absence of <b>ethanol</b>, hsf2 /  mice show a selective loss of LTD in the hippocampus, which is associated with an increased sensitivity of NMDA field excitatory postsynaptic potentials (fEPSPs) to a <strong>GluN2B</strong> antagonist, compared with wild type (WT) mice.
+GRIN2B	drug	alcohol	32720424	After 1 month of chronic <b>ethanol</b> consumption in a two bottle choice paradigm, WT mice showed an increase in hippocampal synaptic transmission, an enhanced sensitivity to <strong>GluN2B</strong> antagonist, and a blockade of LTD.
+GRIN2B	drug	amphetamine	32203791	Then we detected and found that <b>METH</b> increased the expression of N methyl d asparate (NMDA) receptor subunit 2B (<strong>NR2B</strong>) and the level of glutamate (Glu) in the ventral tegmental area (VTA) and nucleus accumbens (NAc), while Trx 1 overexpression suppressed the increases.
+GRIN2B	drug	opioid	32032749	Western blotting and qRT PCR revealed no differences in NR2A subunit expression among <b>heroin</b> exposure, <b>heroin</b> withdrawal, and control group rats; in contrast, expression of <strong>NR2B</strong> was significantly higher in the <b>heroin</b> exposure group, whereas expression levels of NR2C and NR2D were significantly higher in the <b>heroin</b> withdrawal group relative to the controls.
+GRIN2B	addiction	withdrawal	32032749	Western blotting and qRT PCR revealed no differences in NR2A subunit expression among heroin exposure, heroin <b>withdrawal</b>, and control group rats; in contrast, expression of <strong>NR2B</strong> was significantly higher in the heroin exposure group, whereas expression levels of NR2C and NR2D were significantly higher in the heroin <b>withdrawal</b> group relative to the controls.
+GRIN2B	drug	amphetamine	31981057	Ifenprodil Attenuates <b>Methamphetamine</b> Induced Behavioral Sensitization Through the <strong>GluN2B</strong> PP2A AKT Cascade in the Dorsal Striatum of Mice.
+GRIN2B	addiction	sensitization	31981057	Ifenprodil Attenuates Methamphetamine Induced Behavioral <b>Sensitization</b> Through the <strong>GluN2B</strong> PP2A AKT Cascade in the Dorsal Striatum of Mice.
+GRIN2B	drug	amphetamine	31981057	The results showed that <b>METH</b> increased the level of p <strong>GluN2B</strong> (Ser 1303) and PP2A/B in the DS and ifenprodil blocked this increase.
+GRIN2B	drug	amphetamine	31981057	Taken together, these results indicated that the <strong>GluN2B</strong> PP2A AKT cascade was involved in <b>METH</b> induced behavioral sensitization.
+GRIN2B	addiction	sensitization	31981057	Taken together, these results indicated that the <strong>GluN2B</strong> PP2A AKT cascade was involved in METH induced behavioral <b>sensitization</b>.
+GRIN2B	drug	alcohol	31820733	We further show that inhibition of <strong>GluN2B</strong> in the OFC attenuates <b>alcohol</b> dependent mTORC1 activation, <b>alcohol</b> seeking and habitual responding for <b>alcohol</b>.
+GRIN2B	addiction	relapse	31820733	We further show that inhibition of <strong>GluN2B</strong> in the OFC attenuates alcohol dependent mTORC1 activation, alcohol <b>seeking</b> and habitual responding for alcohol.
+GRIN2B	drug	alcohol	31820733	Together, these data suggest that the <strong>GluN2B</strong>/mTORC1 axis in the OFC drives <b>alcohol</b> seeking and habit.
+GRIN2B	addiction	relapse	31820733	Together, these data suggest that the <strong>GluN2B</strong>/mTORC1 axis in the OFC drives alcohol <b>seeking</b> and habit.
+GRIN2B	drug	psychedelics	31706797	After a molecular analysis of <b>ketamine</b> modulation of <strong>GluN2B</strong>, GluA1 and mGluR5 receptors levels in nucleus accumbens, hippocampus and amygdala, two behavioural models were used to investigate <b>ketamine</b> effects: i) context induced renewal of sucrose seeking, and ii) sucrose memory reconsolidation.
+GRIN2B	addiction	relapse	31706797	After a molecular analysis of ketamine modulation of <strong>GluN2B</strong>, GluA1 and mGluR5 receptors levels in nucleus accumbens, hippocampus and amygdala, two behavioural models were used to investigate ketamine effects: i) context induced renewal of sucrose <b>seeking</b>, and ii) sucrose memory reconsolidation.
+GRIN2B	drug	psychedelics	31706797	At the molecular level, <b>ketamine</b> i) decreased <strong>GluN2B</strong>, GluA1 and mGluR5 receptors in hippocampus, ii) decreased GluA1 and mGluR5 but increased <strong>GluN2B</strong> in nucleus accumbens and iii) increased <strong>GluN2B</strong> and mGluR5 in amygdala.
+GRIN2B	drug	alcohol	31636539	In adult mice, chronic <b>ethanol</b> induces long term changes in <strong>GluN2B</strong> containing NMDA receptors (NMDARs) of the BNST.
+GRIN2B	drug	psychedelics	31541650	In this study, we examined the possible effects of <b>ketamine</b> on calcium/calmodulin dependent protein kinase II α (CaMKIIα) and N methyl d aspartate receptor (NMDAR) subunit <strong>NR2B</strong> in a mouse model of remifentanil induced postoperative hyperalgesia (RIPH) in the primary somatosensory cerebral cortex (SI) region.
+GRIN2B	drug	cocaine	31361029	Administration of the GluN2A  and <strong>GluN2B</strong> NMDA receptor antagonists, NVP AAM077 and ifenprodil, respectively, immediately following recall abrogated an established <b>cocaine</b> place preference, while preventing the activation of GSK3β in the amygdala, nucleus accumbens, and hippocampus during <b>cocaine</b> memory reactivation.
+GRIN2B	drug	opioid	31220544	Furthermore, spinal inhibition of SGK1 suppressed <b>morphine</b> induced phosphorylation of nuclear factor kappa B (NF κB) p65 and upregulation of NMDAR NR1 and <strong>NR2B</strong> expression in the spinal dorsal horn.
+GRIN2B	drug	opioid	31220544	In addition, <b>morphine</b> induced upregulation of <strong>NR2B</strong>, but not NR1, was significantly abolished by intrathecal pretreatment with PDTC, a specific NF κB activation inhibitor.
+GRIN2B	drug	opioid	31220544	Finally, spinal delivery of SGK1 small interfering RNA exhibited similar inhibitory effects on <b>morphine</b> induced tolerance, phosphorylation of NF κB p65, as well as upregulation of NR1 and <strong>NR2B</strong> expression.
+GRIN2B	addiction	aversion	31087376	In our experiments, adolescent and adult Sprague Dawley rats were tested for <b>CTA</b> following challenge with one of the following pharmacological agents: glutamatergic AMPA1 receptor antagonist NBQX, glutamatergic N methyl d aspartate <strong>NR2B</strong> receptor antagonist ifenprodil, and extrasynaptic GABAA receptor agonist THIP to determine whether these induced age specific <b>aversive</b> sensitivities like those seen with EtOH.
+GRIN2B	addiction	aversion	31087376	Thus, only antagonism of <strong>NR2B</strong> receptors in male rats mimicked age specific sensitivities to the <b>aversive</b> effects of EtOH.
+GRIN2B	addiction	intoxication	31056842	Memory and plasticity impairment after <b>binge</b> drinking in adolescent rat hippocampus: GluN2A/<strong>GluN2B</strong> NMDA receptor subunits imbalance through HDAC2.
+GRIN2B	addiction	intoxication	31056842	Previously, we reported that two <b>binge</b> like exposures to EtOH (3 g/kg, ip, 9 h apart) in adolescent rats abolished long term synaptic depression (LTD) in hippocampus slices, induced learning deficits, and increased N methyl d aspartate (NMDA) receptor signaling through its <strong>GluN2B</strong> subunit after 48 hours.
+GRIN2B	addiction	intoxication	31056842	In conclusion, the memory impairing effects of two <b>binge</b> like EtOH exposure involve NMDA receptor dependent LTD deficits due to a GluN2A/<strong>GluN2B</strong> imbalance resulting from changes in <strong>GluN2B</strong> expression induced by HDAC2.
+GRIN2B	drug	cocaine	31056833	From the nucleus to the cytosol, HMGB1 binds to glutamate receptor subunits (GluA2/<strong>GluN2B</strong>) on the membrane, which regulates <b>cocaine</b> induced synaptic adaptation and the formation of <b>cocaine</b> related memory.
+GRIN2B	drug	alcohol	30903572	Correlation between the epigenetic modification of histone H3K9 acetylation of <strong>NR2B</strong> gene promoter in rat hippocampus and <b>ethanol</b> withdrawal syndrome.
+GRIN2B	addiction	withdrawal	30903572	Correlation between the epigenetic modification of histone H3K9 acetylation of <strong>NR2B</strong> gene promoter in rat hippocampus and ethanol <b>withdrawal</b> syndrome.
+GRIN2B	drug	alcohol	30903572	Our results suggest that chronic <b>ethanol</b> exposure may result in epigenetic modification of histone H3K9 acetylation in <strong>NR2B</strong> gene promoter in rat hippocampus, and the expression levels of <strong>NR2B</strong> were found to be positively correlated with <b>ethanol</b> withdrawal syndrome.
+GRIN2B	addiction	withdrawal	30903572	Our results suggest that chronic ethanol exposure may result in epigenetic modification of histone H3K9 acetylation in <strong>NR2B</strong> gene promoter in rat hippocampus, and the expression levels of <strong>NR2B</strong> were found to be positively correlated with ethanol <b>withdrawal</b> syndrome.
+GRIN2B	addiction	withdrawal	30733663	We then analyzed the expression levels of presynaptic (vGlut1, vGlut2, CB1 receptor, synaptophysin) and postsynaptic (PSD95, GluN1, GluN2A, <strong>GluN2B</strong>, GluA1, GluA2, mGluR1 and mGluR5) proteins after 7 days EtOH incubation or after EtOH <b>withdrawal</b>.
+GRIN2B	drug	amphetamine	30693312	We propose that <b>METH</b> SA selectively upregulates <strong>GluN2B</strong> lacking NMDA receptors (NMDAR) in the PFC of female rats.
+GRIN2B	drug	alcohol	30536923	We show that systemic administration of AZD0530 prevents <b>alcohol</b> induced Fyn activation and <strong>GluN2B</strong> phosphorylation in the DMS of mice.
+GRIN2B	drug	cocaine	30315226	Finally, loss of GluD1 increased the <strong>GluN2B</strong> subunit contribution to NMDA receptor currents in MSNs and a partial agonist of <strong>GluN2B</strong> containing NMDA receptors normalized the higher active cofilin and <b>cocaine</b> preference in GluD1 KO mice.
+GRIN2B	drug	opioid	30240785	The expressions of Trx 1, N methyl d aspartate receptor 2B subunit (<strong>NR2B</strong>), phosphorylated Ca2+/calmodulin dependent protein kinase II (p CaMKII), phosphorylated extracellular signaling regulated kinases (p ERK), and phosphorylated cAMP response element binding protein (p CREB) were induced in nucleus accumbens (NAc) and hippocampus by <b>morphine</b> or GGA, whereas these proteins were not changed by <b>morphine</b> in GGA treated mice.
+GRIN2B	drug	opioid	30240785	Our results indicate that GGA may prevent the reinstatement of <b>morphine</b> CPP through strengthening the expression of Trx 1 and regulating <strong>NR2B</strong>/ERK pathway.
+GRIN2B	addiction	relapse	30240785	Our results indicate that GGA may prevent the <b>reinstatement</b> of morphine CPP through strengthening the expression of Trx 1 and regulating <strong>NR2B</strong>/ERK pathway.
+GRIN2B	addiction	reward	30240785	Our results indicate that GGA may prevent the reinstatement of morphine <b>CPP</b> through strengthening the expression of Trx 1 and regulating <strong>NR2B</strong>/ERK pathway.
+GRIN2B	drug	cocaine	30144237	In <b>cocaine</b> naïve animals, SERT removal led to reduced baseline Hb mRNA levels of critical determinants of glutamate transmission, such as SLC1A2, the main glutamate transporter and N methyl D aspartate (Grin1, Grin2A and <strong>Grin2B</strong>) as well as α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (Gria1 and Gria2) receptor subunits, with no changes in the scaffolding protein Dlg4.
+GRIN2B	drug	opioid	30024967	Intrathecal injection of <b>tramadol</b> suppressed synaptic NMDAR expression mainly by changing the synaptic phosphorylation state of <strong>NR2B</strong> subunit at Tyr1472.
+GRIN2B	drug	cocaine	29982266	Genetic loss of <strong>GluN2B</strong> in D1 expressing cell types enhances long term <b>cocaine</b> reward and potentiation of thalamo accumbens synapses.
+GRIN2B	addiction	reward	29982266	Genetic loss of <strong>GluN2B</strong> in D1 expressing cell types enhances long term cocaine <b>reward</b> and potentiation of thalamo accumbens synapses.
+GRIN2B	drug	cocaine	29982266	Transient upregulation of <strong>GluN2B</strong> containing NMDA receptors (R) in the nucleus accumbens (NAc) is proposed as an intermediate to long term AMPAR plasticity associated with persistent <b>cocaine</b> related behaviors.
+GRIN2B	drug	cocaine	29982266	However, cell type  and input specific contributions of <strong>GluN2B</strong> underlying lasting actions of <b>cocaine</b> remain to be elucidated.
+GRIN2B	drug	cocaine	29982266	We utilized <strong>GluN2B</strong> cell type specific knockouts and optogenetics to deconstruct the role of <strong>GluN2B</strong> in <b>cocaine</b> induced NAc synaptic and behavioral plasticity.
+GRIN2B	addiction	reward	29982266	While <b>reward</b> learning was unaffected, loss of <strong>GluN2B</strong> in D1 dopamine receptor expressing cells (D1) led to prolonged retention of <b>reward</b> memory.
+GRIN2B	drug	cocaine	29982266	In D1 <strong>GluN2B</strong> /  mice, the potentiation of mThal D1(+) NAc AMPAR function persisted following withdrawal, corresponding with continued expression of <b>cocaine</b> reward behavior.
+GRIN2B	addiction	reward	29982266	In D1 <strong>GluN2B</strong> /  mice, the potentiation of mThal D1(+) NAc AMPAR function persisted following withdrawal, corresponding with continued expression of cocaine <b>reward</b> behavior.
+GRIN2B	addiction	withdrawal	29982266	In D1 <strong>GluN2B</strong> /  mice, the potentiation of mThal D1(+) NAc AMPAR function persisted following <b>withdrawal</b>, corresponding with continued expression of cocaine reward behavior.
+GRIN2B	addiction	reward	29982266	These data suggest NAc <strong>GluN2B</strong> containing NMDARs serve a feedback role and may weaken <b>reward</b> related memories.
+GRIN2B	drug	amphetamine	29981334	We also examined the expression of N methyl D asparate (NMDA) receptor 2B subunit (<strong>GluN2b</strong>), the levels of phosphorylated extracellular signal regulated kinase (p ERK) and phosphorylated cAMP response element binding protein (p CREB) in the NAc by western blot analysis, and found that the <strong>GluN2b</strong> expression, p ERK and p CREB levels were increased in the NAc in response to low dose <b>METH</b> in AAV shRNA mTrx 1 mice, but were not changed in control and AAV vehicle mice.
+GRIN2B	drug	amphetamine	29981334	These data indicate that the increased <strong>GluN2b</strong> expression, and p ERK and p CREB levels in the NAc of AAV shRNA mTrx 1 mice may be responsible for the <b>METH</b> primed reinstatement.
+GRIN2B	addiction	relapse	29981334	These data indicate that the increased <strong>GluN2b</strong> expression, and p ERK and p CREB levels in the NAc of AAV shRNA mTrx 1 mice may be responsible for the METH primed <b>reinstatement</b>.
+GRIN2B	addiction	addiction	29766293	Data obtained using Western blotting technique showed a significant increase in the level of GluN1 and <strong>GluN2B</strong>, but not in GluN2A subunits in all the three regions (mPFC, lPFC, and OFC) of men whom suffered from <b>addiction</b> as compared to the appropriate controls.
+GRIN2B	addiction	addiction	29766293	These findings showed a novel role for GluN1, <strong>GluN2B</strong> subunits, rather than the GluN2A subunit of NMDARs, in the pathophysiology of <b>addiction</b> and suggested their role in the drug induced plasticity of NMDARs.
+GRIN2B	drug	alcohol	29704590	Protective influences of N acetylcysteine against <b>alcohol</b> abstinence induced depression by regulating biochemical and GRIN2A, <strong>GRIN2B</strong> gene expression of NMDA receptor signaling pathway in rats.
+GRIN2B	drug	alcohol	29704590	The increased expression levels of GRIN2A and <strong>GRIN2B</strong> following <b>ethanol</b> abstinence were reversed with a higher dose of NAC (100 mg/kg) treatment.
+GRIN2B	drug	alcohol	29704590	In conclusion, the results of the study reveal that NAC has remarkable protective effects in the <b>alcohol</b> abstinence induced depression by modulating <b>alcohol</b> markers, serotonin levels and GRIN2A, <strong>GRIN2B</strong> gene expression of NMDAR signaling pathway in rats.
+GRIN2B	drug	cocaine	29626166	After short term withdrawal from <b>cocaine</b> self administration, despite no actual change in the AMPA receptor mediated excitatory synaptic strength, <strong>GluN2B</strong> NMDA receptors, the SMHC sensors of synaptic strength, are upregulated.
+GRIN2B	addiction	withdrawal	29626166	After short term <b>withdrawal</b> from cocaine self administration, despite no actual change in the AMPA receptor mediated excitatory synaptic strength, <strong>GluN2B</strong> NMDA receptors, the SMHC sensors of synaptic strength, are upregulated.
+GRIN2B	drug	cocaine	29380665	To evaluate the role of glutamate on BDNF independent changes, we investigated the expression of the transporter GLT 1 and the activation of the NMDA receptor subunit <strong>GluN2B</strong>, which were both increased in the PL cortex while reduced in the IL cortex.Conclusions: Our results show that adolescent <b>cocaine</b> exposure modulates BDNF system early after treatment in the mesocorticolimbic pathway, identifying a complex but specific set of changes that could provide clues for treatment.
+GRIN2B	addiction	reward	29305627	Antagonism at the <strong>NR2B</strong> subunit of NMDA receptors induces increased connectivity of the prefrontal and subcortical regions regulating <b>reward</b> behavior.
+GRIN2B	drug	psychedelics	29305627	Evidence indicates that <b>ketamine</b>'s rapid antidepressant efficacy likely results from its antagonism of <strong>NR2B</strong> subunit containing NMDA receptors (NMDAR).
+GRIN2B	drug	psychedelics	29305627	Since <b>ketamine</b> equally blocks NR2A  and <strong>NR2B</strong> containing NMDAR, and has affinity to other receptors, <strong>NR2B</strong> selective drugs might have improved therapeutic efficiency and side effect profile.
+GRIN2B	drug	psychedelics	29305627	We aimed to compare the effects of (S) <b>ketamine</b> and two different types of <strong>NR2B</strong> selective antagonists on functional brain networks in rats, in order to find common circuits, where their effects intersect, and that might explain their antidepressant action.
+GRIN2B	drug	psychedelics	29305627	The effects common to <b>ketamine</b> and <strong>NR2B</strong> selective compounds were localized to the same brain regions as those reported in depression, but in the opposite direction.
+GRIN2B	addiction	reward	29305627	The upregulation of the <b>reward</b> circuitry might partially underlie the antidepressant and anti anhedonic effects of the antagonists and could potentially serve as a translational imaging phenotype for testing putative antidepressants, especially those targeting the <strong>NR2B</strong> receptor subtype.
+GRIN2B	drug	cocaine	29196318	Despite blocking tissue GluA1 increases in <b>cocaine</b> self administering animals, the HSV dnGluN1 treatment resulted in increased membrane levels of GluA1 and <strong>GluN2B</strong>, along with markedly higher locomotor responses to intra VTA infusions of AMPA, suggesting a paradoxical increase in VTA AMPA receptor responsiveness.
+GRIN2B	addiction	withdrawal	29139560	This increase persisted during EtOH <b>withdrawal</b>, along with an increase in <strong>NR2B</strong> Y1472 phosphorylation, mature brain derived neurotrophic factor, and phosphorylated TrkB.
+GRIN2B	drug	opioid	29116553	Evidence suggests that the dopamine receptor rate limiting enzyme, tyrosine hydroxylase (TH), and the glutamate receptor, N methyl D aspartate receptor 2B (<strong>NR2B</strong>), contribute to <b>morphine</b> dependence.
+GRIN2B	addiction	dependence	29116553	Evidence suggests that the dopamine receptor rate limiting enzyme, tyrosine hydroxylase (TH), and the glutamate receptor, N methyl D aspartate receptor 2B (<strong>NR2B</strong>), contribute to morphine <b>dependence</b>.
+GRIN2B	drug	opioid	29116553	Conditioned place preference (CPP) mouse model was established using <b>morphine</b> (9 mg/kg, s.c.), and their expression levels of TH and <strong>NR2B</strong> were observed by immunohistochemistry.
+GRIN2B	addiction	reward	29116553	Conditioned place preference (<b>CPP</b>) mouse model was established using morphine (9 mg/kg, s.c.), and their expression levels of TH and <strong>NR2B</strong> were observed by immunohistochemistry.
+GRIN2B	drug	opioid	29116553	Results showed that high sinomenine dose (80 mg/kg) effectively attenuated the behavior of CPP mice and reversed increased expression levels of TH and <strong>NR2B</strong> induced by <b>morphine</b>.
+GRIN2B	addiction	reward	29116553	Results showed that high sinomenine dose (80 mg/kg) effectively attenuated the behavior of <b>CPP</b> mice and reversed increased expression levels of TH and <strong>NR2B</strong> induced by morphine.
+GRIN2B	drug	opioid	29116553	In summary, these data indicate that sinomenine can inhibit <b>morphine</b> dependence by increasing the expression levels of TH, <strong>NR2B</strong>, and MOR in the mouse brain; however, DOR may not contribute to this effect.
+GRIN2B	addiction	dependence	29116553	In summary, these data indicate that sinomenine can inhibit morphine <b>dependence</b> by increasing the expression levels of TH, <strong>NR2B</strong>, and MOR in the mouse brain; however, DOR may not contribute to this effect.
+GRIN2B	drug	alcohol	29030082	We additionally examined the effects of ADX 47273 on the expression of the NMDA receptors subunit, <strong>GluN2B</strong>, in the hippocampus and prefrontal cortex, on the 13th day of <b>ethanol</b> withdrawal.
+GRIN2B	addiction	withdrawal	29030082	We additionally examined the effects of ADX 47273 on the expression of the NMDA receptors subunit, <strong>GluN2B</strong>, in the hippocampus and prefrontal cortex, on the 13th day of ethanol <b>withdrawal</b>.
+GRIN2B	drug	alcohol	29030082	The 13th day of <b>ethanol</b> abstinence decreased the expression of the <strong>GluN2B</strong> subunit in the selected brain regions, but ADX 47273 administration increased it.
+GRIN2B	drug	cocaine	28973019	<b>Cocaine</b> self administration increased the A/N ratio and <strong>GluN2B</strong> NMDARs in WT MSNs and, although the A/N ratio also increased in KO MSNs, this was accompanied by fewer <strong>GluN2B</strong> NMDARs and an appearance of calcium permeable AMPARs.
+GRIN2B	addiction	reward	28973019	Finally, to examine the consequences of reduced basal <strong>GluN2B</strong> NMDARs in <b>reward</b> processing seen in KO mice, we chronically infused ifenprodil, a <strong>GluN2B</strong> antagonist, into the NAc shell of WT mice.
+GRIN2B	drug	psychedelics	28948570	Since <strong>GluN2B</strong>, via inhibition of ERK, regulates the membrane expression of GluA1, we measured ERK2 phosphorylation in the crude synaptosomal fraction of these brain regions, which was significantly reduced suggesting that <b>ketamine</b> induced phosphorylation of αCaMKII promotes <strong>GluN2B</strong> (S1303) phosphorylation that, in turn, inhibits ERK 2 signaling, an effect that results in reduced membrane expression and phosphorylation of GluA1.
+GRIN2B	drug	psychedelics	28948570	Taken together, our findings point to αCaMKII autophosphorylation as a critical signature of <b>ketamine</b> self administration providing an intracellular mechanism to explain the different effects caused by αCaMKII autophosphorylation on the post synaptic <strong>GluN2B</strong>  and GluA1 mediated functions.
+GRIN2B	drug	nicotine	28900078	The relationship of HTR4 (rs3995090), HTR2A (rs6313), GRIK5 (rs8099939), <strong>GRIN2B</strong> (rs2268132), and CHRNB4 (rs1948) gene polymorphisms and COPD, as well as the contribution of these polymorphisms to the variations in quantitative characteristics that describe respiratory function, <b>smoking</b> behavior, and <b>nicotine</b> dependence was assessed in an ethnically homogeneous Tatar population.
+GRIN2B	addiction	dependence	28900078	The relationship of HTR4 (rs3995090), HTR2A (rs6313), GRIK5 (rs8099939), <strong>GRIN2B</strong> (rs2268132), and CHRNB4 (rs1948) gene polymorphisms and COPD, as well as the contribution of these polymorphisms to the variations in quantitative characteristics that describe respiratory function, smoking behavior, and nicotine <b>dependence</b> was assessed in an ethnically homogeneous Tatar population.
+GRIN2B	drug	nicotine	28900078	Importantly, the HTR2A (rs6313), <strong>GRIN2B</strong> (rs2268132), and GRIK5 (rs8099939) polymorphisms were only associated with COPD in <b>smokers</b>.
+GRIN2B	drug	nicotine	28900078	The TT genotype of <strong>GRIN2B</strong> (rs2268132) was associated with COPD in subjects with high <b>nicotine</b> dependence according to the Fagerstrõm test (P = 0.002, OR = 2.98).
+GRIN2B	addiction	dependence	28900078	The TT genotype of <strong>GRIN2B</strong> (rs2268132) was associated with COPD in subjects with high nicotine <b>dependence</b> according to the Fagerstrõm test (P = 0.002, OR = 2.98).
+GRIN2B	drug	nicotine	28900078	The CC genotype of HTR2A (rs6313) and the TT genotype of <strong>GRIN2B</strong> (rs2268132) were associated with higher levels of <b>nicotine</b> dependence according to the Fagerstrõm test (P = 0.0011 and P = 0.037).
+GRIN2B	addiction	dependence	28900078	The CC genotype of HTR2A (rs6313) and the TT genotype of <strong>GRIN2B</strong> (rs2268132) were associated with higher levels of nicotine <b>dependence</b> according to the Fagerstrõm test (P = 0.0011 and P = 0.037).
+GRIN2B	drug	opioid	28884870	Phosphorylated SNAP25 in the CA1 regulates <b>morphine</b> associated contextual memory retrieval via increasing <strong>GluN2B</strong> NMDAR surface localization.
+GRIN2B	drug	opioid	28884870	Although our previous studies have demonstrated both protein kinase C (PKC) and <strong>GluN2B</strong> containing N methyl d aspartate receptor (<strong>GluN2B</strong> NMDAR) play crucial roles in <b>morphine</b> associated learning and memory, the relationship between them remains unexplored.
+GRIN2B	drug	opioid	28884870	In this study, we validated the enhanced PKC and membrane <strong>GluN2B</strong> protein expression in the hippocampal CA1 after <b>morphine</b> conditioned place preference (CPP) expression in rats.
+GRIN2B	addiction	reward	28884870	In this study, we validated the enhanced PKC and membrane <strong>GluN2B</strong> protein expression in the hippocampal CA1 after morphine conditioned place preference (<b>CPP</b>) expression in rats.
+GRIN2B	drug	opioid	28884870	Blocking the pSer187 SNAP25 by intra CA1 injection of an interfering peptide impaired <b>morphine</b> CPP expression and accompanied by the reduced ratio of <strong>GluN2B</strong> membrane/total in the CA1.
+GRIN2B	addiction	reward	28884870	Blocking the pSer187 SNAP25 by intra CA1 injection of an interfering peptide impaired morphine <b>CPP</b> expression and accompanied by the reduced ratio of <strong>GluN2B</strong> membrane/total in the CA1.
+GRIN2B	addiction	addiction	28884870	Therefore, our results reveal that enhanced pSer187 SNAP25 by PKC recruits <strong>GluN2B</strong> NMDAR to the membrane surface in the hippocampal CA1 and mediates context induced <b>addiction</b> memory retrieval.
+GRIN2B	drug	alcohol	28838956	<b>Ethanol</b> enhances <strong>GluN2B</strong> containing NMDAR function and phosphorylation (Tyr 1472) of the <strong>GluN2B</strong> NMDAR subunit in the dorsal medial striatum (DMS) through a protein kinase A (PKA) dependent pathway.
+GRIN2B	drug	alcohol	28838956	Our hypothesis is that loss of AC1 activity will prevent <b>ethanol</b> induced locomotor sensitization and associated DMS <strong>GluN2B</strong> NMDAR adaptations.
+GRIN2B	addiction	sensitization	28838956	Our hypothesis is that loss of AC1 activity will prevent ethanol induced locomotor <b>sensitization</b> and associated DMS <strong>GluN2B</strong> NMDAR adaptations.
+GRIN2B	drug	alcohol	28838956	We evaluated AC1's contribution to <b>ethanol</b> evoked locomotor responses and DMS <strong>GluN2B</strong> NMDAR phosphorylation and function using AC1 knockout (AC1KO) mice.
+GRIN2B	drug	alcohol	28838956	Repeated exposure to <b>ethanol</b> in the sensitization procedure significantly increased pTyr 1472 <strong>GluN2B</strong> levels and <strong>GluN2B</strong> containing NMDAR transmission in the DMS of WT mice.
+GRIN2B	addiction	sensitization	28838956	Repeated exposure to ethanol in the <b>sensitization</b> procedure significantly increased pTyr 1472 <strong>GluN2B</strong> levels and <strong>GluN2B</strong> containing NMDAR transmission in the DMS of WT mice.
+GRIN2B	drug	alcohol	28838956	Together, these data support a critical and specific role for AC1 in striatal signaling that mediates <b>ethanol</b> induced behavioral sensitization, and identify <strong>GluN2B</strong> containing NMDARs as an important AC1 target.
+GRIN2B	addiction	sensitization	28838956	Together, these data support a critical and specific role for AC1 in striatal signaling that mediates ethanol induced behavioral <b>sensitization</b>, and identify <strong>GluN2B</strong> containing NMDARs as an important AC1 target.
+GRIN2B	drug	cocaine	28585567	Role of Src Family Kinases in BDNF Mediated Suppression of <b>Cocaine</b> Seeking and Prevention of <b>Cocaine</b> Induced ERK, GluN2A, and <strong>GluN2B</strong> Dephosphorylation in the Prelimbic Cortex.
+GRIN2B	addiction	relapse	28585567	Role of Src Family Kinases in BDNF Mediated Suppression of Cocaine <b>Seeking</b> and Prevention of Cocaine Induced ERK, GluN2A, and <strong>GluN2B</strong> Dephosphorylation in the Prelimbic Cortex.
+GRIN2B	drug	cocaine	28585567	As previously reported, infusion of BDNF into the PrL cortex blocked <b>cocaine</b> SA induced dephosphorylation of ERK, GluN2A, and <strong>GluN2B</strong> containing receptors.
+GRIN2B	drug	alcohol	28558131	To analyze the relationship between <strong>GRIN2B</strong> and suicide attempts, the selected rs2268115 polymorphism was genotyped in a sample of 345 <b>alcohol</b> dependent individuals stratified by the history of suicide attempts.
+GRIN2B	drug	alcohol	28558131	The major contribution of the present study is a novel finding of the possible association between <strong>GRIN2B</strong> rs2268115 polymorphism and suicide attempts in <b>alcohol</b> dependent individuals.
+GRIN2B	drug	cocaine	28535798	Pretreatment of Kal7KO mice with a low dose of ifenprodil, a selective <strong>GluN2B</strong> antagonist, eliminated their enhanced locomotor response to <b>cocaine</b>, revealing an important role for <strong>GluN2B</strong> in this behavior.
+GRIN2B	drug	cocaine	28535798	The <b>cocaine</b> sensitive neuronal pathways which are most sensitive to altered Kalirin function may be the pathways most dependent on <strong>GluN2B</strong> and Drd2.
+GRIN2B	drug	nicotine	28462940	Chronic <b>Nicotine</b> Alters Corticostriatal Plasticity in the Striatopallidal Pathway Mediated By <strong>NR2B</strong> Containing Silent Synapses.
+GRIN2B	drug	opioid	28380057	Chronic <b>morphine</b> also increased glutamatergic plasticity and the proportion of <strong>Grin2B</strong> NMDARs in striatal projection neurons.
+GRIN2B	drug	opioid	28206989	IL 4 mediated by HSV vector suppresses <b>morphine</b> withdrawal response and decreases TNFα, <strong>NR2B</strong>, and pC/EBPβ in the periaqueductal gray in rats.
+GRIN2B	addiction	withdrawal	28206989	IL 4 mediated by HSV vector suppresses morphine <b>withdrawal</b> response and decreases TNFα, <strong>NR2B</strong>, and pC/EBPβ in the periaqueductal gray in rats.
+GRIN2B	drug	alcohol	28109345	Reduced <b>ethanol</b> drinking following selective cortical interneuron deletion of the <strong>GluN2B</strong> NMDA receptors subunit.
+GRIN2B	drug	alcohol	28109345	The current study examined the role of <strong>GluN2B</strong> containing NMDARs expressed on cortical principal neurons and cortical interneurons in mouse <b>ethanol</b> drinking.
+GRIN2B	drug	alcohol	28109345	Consumption of escalating concentrations of <b>ethanol</b> was measured in mice with <strong>GluN2B</strong> gene deletion in either cortical principal neurons (GluN2BCxNULL) or interneurons (GluN2BInterNULL), using a two bottle choice paradigm.
+GRIN2B	drug	alcohol	28109345	These findings provide novel evidence for a contribution of interneuronal <strong>GluN2B</strong> containing NMDARs in the regulation of <b>ethanol</b> drinking.
+GRIN2B	addiction	sensitization	28107590	Early SCS caused partial reversal of mechanical hypersensitivity with corresponding changes in the biomarker of central <b>sensitization</b>, [phospho Tyr1472 ] <strong>GluN2B</strong>.
+GRIN2B	drug	opioid	28106041	Furthermore, DREADD mediated specific inactivation of the EC dDG pathway or disconnection of the pathway with local postsynaptic <strong>GluN2B</strong> ERK1/2 signaling both decreased context induced reinstatement of <b>heroin</b> seeking.
+GRIN2B	addiction	relapse	28106041	Furthermore, DREADD mediated specific inactivation of the EC dDG pathway or disconnection of the pathway with local postsynaptic <strong>GluN2B</strong> ERK1/2 signaling both decreased context induced <b>reinstatement</b> of heroin <b>seeking</b>.
+GRIN2B	drug	opioid	28106041	Our results indicate that the EC dDG pathway mediates context induced reinstatement of <b>heroin</b> seeking, via the activation of postsynaptic <strong>GluN2B</strong> ERK1/2 signaling in the dDG.
+GRIN2B	addiction	relapse	28106041	Our results indicate that the EC dDG pathway mediates context induced <b>reinstatement</b> of heroin <b>seeking</b>, via the activation of postsynaptic <strong>GluN2B</strong> ERK1/2 signaling in the dDG.
+GRIN2B	addiction	reward	27881347	The protein expressions of TH, <strong>NR2B</strong> and GLUR2 in the brain of zebrafish with <b>CPP</b> were detected with Western blotting.
+GRIN2B	drug	amphetamine	27881347	Compared with the control group, zebrafish in <b>methamphetamine</b> group showed significant variations in the staying time and swimming distance in the drug box after conditioning (P<0.05) with obvious alterations of <strong>NR2B</strong>, TH and GLUR2 expressions in the brain (P<0.05).
+GRIN2B	drug	amphetamine	27881347	Treatment of <b>methamphetamine</b> dependent zebrafish with high dose rhynchophylline significantly reduced the variations in the staying time and swimming distance in the drug box (P<0.05) and in the expressions of <strong>NR2B</strong>, TH and GLUR2 in the brain (P<0.05).
+GRIN2B	drug	amphetamine	27881347	Rhynchophylline can inhibit <b>methamphetamine</b> dependence in zebrafish, the mechanism of which may involve the expressions of TH, <strong>NR2B</strong> and GLUR2 proteins in the brain.
+GRIN2B	addiction	dependence	27881347	Rhynchophylline can inhibit methamphetamine <b>dependence</b> in zebrafish, the mechanism of which may involve the expressions of TH, <strong>NR2B</strong> and GLUR2 proteins in the brain.
+GRIN2B	drug	cocaine	27871669	Additionally, the <strong>NR2B</strong> selective N methyl D aspartate receptor antagonists ifenprodil and CP 101,606 blocked <b>cocaine</b> induced habits; this was dependent on Abl family signaling in the oPFC.
+GRIN2B	drug	psychedelics	27642050	Following behavioral training, rats received treatments of the NMDA receptor ligands MK 801 (uncompetitive antagonist; 0, 0.003, 0.01, or 0.03mg/kg), <b>ketamine</b> (uncompetitive antagonist; 0, 1.0, 5.0, or 10.0mg/kg), and ifenprodil (<strong>NR2B</strong> selective non competitive antagonist; 0, 1.0, 3.0, or 10.0mg/kg).
+GRIN2B	addiction	reward	27267684	During a first testing phase, adult male rats implanted with bilateral ventral midbrain cannulae were injected every second day for three days with D [Tyr11]neurotensin (1.5 nmol/side), the preferred NMDA GluN2A/B antagonist, <b>CPP</b> (40 or 120 pmol/side), the selective <strong>GluN2B</strong> antagonist, Ro04 5595 (200 or 1200 pmol/side), <b>CPP</b> (40 or 120 pmol/side) + D [Tyr11]neurotensin (1.5 nmol/side) or Ro04 5595 (200 or 1200 pmol/side) + D [Tyr11]neurotensin (1.5 nmol/side) and locomotor activity was measured immediately after the injection.
+GRIN2B	drug	amphetamine	27267684	These results support the hypothesis that neurotensin is stimulating glutamate neurotransmission to initiate neural changes that sub serve <b>amphetamine</b> sensitization and that glutamate is acting on NMDA receptors that are mostly likely composed of GluN2A, but not <strong>GluN2B</strong>, subunits.
+GRIN2B	addiction	sensitization	27267684	These results support the hypothesis that neurotensin is stimulating glutamate neurotransmission to initiate neural changes that sub serve amphetamine <b>sensitization</b> and that glutamate is acting on NMDA receptors that are mostly likely composed of GluN2A, but not <strong>GluN2B</strong>, subunits.
+GRIN2B	drug	cocaine	27765467	In the present study, infusion of the GluN2A containing NMDA receptor antagonist, TCN 201, or the <strong>GluN2B</strong> containing NMDA receptor antagonist, Ro 25 6981, into the prelimbic cortex of rats blocked the suppressive effect of BDNF on <b>cocaine</b> seeking.
+GRIN2B	addiction	relapse	27765467	In the present study, infusion of the GluN2A containing NMDA receptor antagonist, TCN 201, or the <strong>GluN2B</strong> containing NMDA receptor antagonist, Ro 25 6981, into the prelimbic cortex of rats blocked the suppressive effect of BDNF on cocaine <b>seeking</b>.
+GRIN2B	drug	cocaine	27765467	During early withdrawal from <b>cocaine</b> self administration, tyrosine phosphorylation of ERK, GluN2A, and <strong>GluN2B</strong> in the prelimbic cortex was reduced and this reduction of phospho proteins was prevented by intra prelimbic BDNF infusion.
+GRIN2B	addiction	withdrawal	27765467	During early <b>withdrawal</b> from cocaine self administration, tyrosine phosphorylation of ERK, GluN2A, and <strong>GluN2B</strong> in the prelimbic cortex was reduced and this reduction of phospho proteins was prevented by intra prelimbic BDNF infusion.
+GRIN2B	drug	cocaine	27765467	These data demonstrate that BDNF mediated activation of GluN2A  and <strong>GluN2B</strong> containing NMDA receptors underlies ERK activation in the prelimbic cortex during early withdrawal, preventing subsequent relapse to <b>cocaine</b> seeking.
+GRIN2B	addiction	relapse	27765467	These data demonstrate that BDNF mediated activation of GluN2A  and <strong>GluN2B</strong> containing NMDA receptors underlies ERK activation in the prelimbic cortex during early withdrawal, preventing subsequent <b>relapse</b> to cocaine <b>seeking</b>.
+GRIN2B	addiction	withdrawal	27765467	These data demonstrate that BDNF mediated activation of GluN2A  and <strong>GluN2B</strong> containing NMDA receptors underlies ERK activation in the prelimbic cortex during early <b>withdrawal</b>, preventing subsequent relapse to cocaine seeking.
+GRIN2B	drug	alcohol	27706932	This review will address recent and past findings suggesting that NMDAR activity promotes drug  and <b>alcohol</b> related behaviors, with a particular focus on <strong>GluN2B</strong> subunits as possible central regulators of many addictive behaviors, as well as newer studies examining the importance of non canonical NMDAR subunits and endogenous NMDAR cofactors.
+GRIN2B	addiction	addiction	27706932	This review will address recent and past findings suggesting that NMDAR activity promotes drug  and alcohol related behaviors, with a particular focus on <strong>GluN2B</strong> subunits as possible central regulators of many <b>addictive</b> behaviors, as well as newer studies examining the importance of non canonical NMDAR subunits and endogenous NMDAR cofactors.
+GRIN2B	drug	amphetamine	27703043	After the second dose of <b>amphetamine</b>, the LR rats exhibited more c Fos and <strong>GluN2B</strong> activation in layers II and III of the M1/M2 motor cortex area and prefrontal cortex (PRE, PRL, IL) and also presented with more <strong>GluN2B</strong> activation in the basal amygdala.
+GRIN2B	drug	amphetamine	27544406	However, the function of <strong>GluN2B</strong> containing NMDARs and their potential downstream cascade(s) in the acquisition and expression of behavioral sensitization to <b>methamphetamine</b> (<b>METH</b>) have not been explored.
+GRIN2B	addiction	sensitization	27544406	However, the function of <strong>GluN2B</strong> containing NMDARs and their potential downstream cascade(s) in the acquisition and expression of behavioral <b>sensitization</b> to methamphetamine (METH) have not been explored.
+GRIN2B	drug	amphetamine	27544406	In this study, 2.5, 5, and 10mg/kg ifenprodil, the specific inhibitor of <strong>GluN2B</strong>, was used to explore the function of these receptors in distinct phases of behavioral sensitization to <b>METH</b> in mice.
+GRIN2B	addiction	sensitization	27544406	In this study, 2.5, 5, and 10mg/kg ifenprodil, the specific inhibitor of <strong>GluN2B</strong>, was used to explore the function of these receptors in distinct phases of behavioral <b>sensitization</b> to METH in mice.
+GRIN2B	drug	amphetamine	27544406	In conclusion, <strong>GluN2B</strong> containing NMDARs contribute to both the acquisition and expression of behavioral sensitization to <b>METH</b> in mice.
+GRIN2B	addiction	sensitization	27544406	In conclusion, <strong>GluN2B</strong> containing NMDARs contribute to both the acquisition and expression of behavioral <b>sensitization</b> to METH in mice.
+GRIN2B	addiction	reward	27531839	We found that destabilization of MeAM <b>CPP</b> after the application of ANI was blocked by the N methyl d aspartate receptor (NMDAR) antagonist MK 801 and the <strong>NR2B</strong> antagonist ifenprodil (IFN) but not by the NR2A antagonist NVP AAM077 (NVP).
+GRIN2B	drug	alcohol	27498914	Genetic variation within <strong>GRIN2B</strong> in adolescents with <b>alcohol</b> use disorder may be associated with larger left posterior cingulate cortex volume.
+GRIN2B	drug	cocaine	27478879	<b>Cocaine</b> Self Administration Elevates <strong>GluN2B</strong> within dmPFC Mediating Heightened Cue Elicited Operant Responding.
+GRIN2B	addiction	reward	27478879	Cocaine Self Administration Elevates <strong>GluN2B</strong> within dmPFC Mediating Heightened Cue Elicited <b>Operant</b> Responding.
+GRIN2B	drug	cocaine	27478879	<b>Cocaine</b> seeking rats exhibited elevated <strong>GluN2B</strong> expression within the dorsomedial aspect of the PFC (dmPFC); this effect was apparent at both 3 and 30 days withdrawal and occurred in <b>cocaine</b> experienced rats, regardless of experiencing an extinction test or not.
+GRIN2B	addiction	relapse	27478879	Cocaine <b>seeking</b> rats exhibited elevated <strong>GluN2B</strong> expression within the dorsomedial aspect of the PFC (dmPFC); this effect was apparent at both 3 and 30 days withdrawal and occurred in cocaine experienced rats, regardless of experiencing an extinction test or not.
+GRIN2B	addiction	withdrawal	27478879	Cocaine seeking rats exhibited elevated <strong>GluN2B</strong> expression within the dorsomedial aspect of the PFC (dmPFC); this effect was apparent at both 3 and 30 days <b>withdrawal</b> and occurred in cocaine experienced rats, regardless of experiencing an extinction test or not.
+GRIN2B	drug	cocaine	27478879	Thus, elevated dmPFC <strong>GluN2B</strong> expression appears to reflect a pharmacodynamic response to excessive <b>cocaine</b> intake that is independent of the duration of drug withdrawal or re exposure to drug taking context.
+GRIN2B	addiction	withdrawal	27478879	Thus, elevated dmPFC <strong>GluN2B</strong> expression appears to reflect a pharmacodynamic response to excessive cocaine intake that is independent of the duration of drug <b>withdrawal</b> or re exposure to drug taking context.
+GRIN2B	addiction	relapse	27478879	The functional relevance of elevated dmPFC <strong>GluN2B</strong> expression for drug <b>seeking</b> was assessed by the local infusion of the prototypical <strong>GluN2B</strong> selective antagonist ifenprodil (1.0 µg/side).
+GRIN2B	addiction	reward	27478879	Thus, the effects of an intra dmPFC ifenprodil infusion upon cue reactivity are reinforcer specific, arguing in favor of targeting <strong>GluN2B</strong> containing NMDA receptors as a pharmacological strategy for reducing behavioral reactivity to drug associated cues with the potential benefit of heightening the <b>reinforcing</b> properties of cues associated with non drug primary rewards.
+GRIN2B	drug	opioid	27457480	Antisense oligodeoxynucleotides of NMDA receptor subunits NR1, NR2A, <strong>NR2B</strong> significantly enhanced the inhibition of paeoniflorin on excitatory amino acid and high dose <b>morphine</b> induced nociception.
+GRIN2B	drug	opioid	27457480	Results of this study indicate that paeoniflorin induced inhibition of excitatory amino acid agonist  and high dose <b>morphine</b> induced nociceptive behaviors might be due to modulation of NMDA receptors, specifically the <strong>NR2B</strong> subunit.
+GRIN2B	drug	amphetamine	27339870	However, the role of <strong>GluN2B</strong> containing receptors and their downstream signaling pathway(s) in behavioral sensitization induced by <b>methamphetamine</b> (<b>METH</b>) have not been investigated yet.
+GRIN2B	addiction	sensitization	27339870	However, the role of <strong>GluN2B</strong> containing receptors and their downstream signaling pathway(s) in behavioral <b>sensitization</b> induced by methamphetamine (METH) have not been investigated yet.
+GRIN2B	drug	amphetamine	27339870	In this study, we used different doses of ifenprodil (2.5, 5, 10 mg/kg), a selective antagonist of the <strong>GluN2B</strong> subunit, to investigate the role of <strong>GluN2B</strong> containing NMDARs in <b>METH</b> induced behavioral sensitization.
+GRIN2B	addiction	sensitization	27339870	In this study, we used different doses of ifenprodil (2.5, 5, 10 mg/kg), a selective antagonist of the <strong>GluN2B</strong> subunit, to investigate the role of <strong>GluN2B</strong> containing NMDARs in METH induced behavioral <b>sensitization</b>.
+GRIN2B	drug	amphetamine	27339870	Moreover, <strong>GluN2B</strong> containing NMDARs and their downstream Ras ERK ∆FosB signaling pathway in the CPu might be involved in <b>METH</b> induced behavioral sensitization.
+GRIN2B	addiction	sensitization	27339870	Moreover, <strong>GluN2B</strong> containing NMDARs and their downstream Ras ERK ∆FosB signaling pathway in the CPu might be involved in METH induced behavioral <b>sensitization</b>.
+GRIN2B	drug	opioid	27217103	Over expression of the <strong>GluN2B</strong> subunit in the forebrain facilitates the acquisition of <b>morphine</b> related positive and aversive memory in rats.
+GRIN2B	addiction	aversion	27217103	Over expression of the <strong>GluN2B</strong> subunit in the forebrain facilitates the acquisition of morphine related positive and <b>aversive</b> memory in rats.
+GRIN2B	drug	opioid	27217103	Selective blockage of <strong>GluN2B</strong> containing NMDA receptors (<strong>GluN2B</strong> NMDARs) has been shown to impair <b>morphine</b> induced conditioned place preference (CPP) without affecting natural reward induced CPP.
+GRIN2B	addiction	reward	27217103	Selective blockage of <strong>GluN2B</strong> containing NMDA receptors (<strong>GluN2B</strong> NMDARs) has been shown to impair morphine induced conditioned place preference (<b>CPP</b>) without affecting natural <b>reward</b> induced <b>CPP</b>.
+GRIN2B	drug	opioid	27217103	In the present study, <strong>GluN2B</strong> transgenic rats with over expressed <strong>GluN2B</strong> subunits in the forebrain were used to assess the susceptibility to CPP induced by <b>morphine</b> and natural rewards as well as to <b>naloxone</b> induced conditioned place aversion (CPA).
+GRIN2B	addiction	aversion	27217103	In the present study, <strong>GluN2B</strong> transgenic rats with over expressed <strong>GluN2B</strong> subunits in the forebrain were used to assess the susceptibility to CPP induced by morphine and natural rewards as well as to naloxone induced conditioned place <b>aversion</b> (CPA).
+GRIN2B	addiction	reward	27217103	In the present study, <strong>GluN2B</strong> transgenic rats with over expressed <strong>GluN2B</strong> subunits in the forebrain were used to assess the susceptibility to <b>CPP</b> induced by morphine and natural rewards as well as to naloxone induced conditioned place aversion (CPA).
+GRIN2B	drug	opioid	27217103	The results showed that <strong>GluN2B</strong> transgenic rats exhibited a relatively higher susceptibility to <b>morphine</b> induced CPP and <b>naloxone</b> induced CPA than their wild type littermates did, while they retained the similar sensitivity as wild type rats to CPP induced by natural reinforcers (food and sucrose).
+GRIN2B	addiction	reward	27217103	The results showed that <strong>GluN2B</strong> transgenic rats exhibited a relatively higher susceptibility to morphine induced <b>CPP</b> and naloxone induced CPA than their wild type littermates did, while they retained the similar sensitivity as wild type rats to <b>CPP</b> induced by natural reinforcers (food and sucrose).
+GRIN2B	drug	opioid	27161447	We also found that expression of the hippocampal <strong>NR2B</strong> subunit, rather than the NR1 subunit, of N methyl D aspartate receptors (NMDARs) was down regulated after chronic <b>morphine</b> treatment, and agmatine inhibited this reduction.
+GRIN2B	drug	amphetamine	27009763	Inhibiting effects of rhynchophylline on zebrafish <b>methamphetamine</b> dependence are associated with amelioration of neurotransmitters content and down regulation of TH and <strong>NR2B</strong> expression.
+GRIN2B	addiction	dependence	27009763	Inhibiting effects of rhynchophylline on zebrafish methamphetamine <b>dependence</b> are associated with amelioration of neurotransmitters content and down regulation of TH and <strong>NR2B</strong> expression.
+GRIN2B	drug	amphetamine	27009763	Others and we have reported that rhynchophylline reverses <b>amphetamine</b> induced conditioned place preference (CPP) effect which may be partly mediated by amelioration of central neurotransmitters and N methyl d aspartate receptor 2B (<strong>NR2B</strong>) levels in the rat brains.
+GRIN2B	addiction	reward	27009763	Others and we have reported that rhynchophylline reverses amphetamine induced conditioned place preference (<b>CPP</b>) effect which may be partly mediated by amelioration of central neurotransmitters and N methyl d aspartate receptor 2B (<strong>NR2B</strong>) levels in the rat brains.
+GRIN2B	drug	amphetamine	27009763	Results revealed that rhynchophylline (100mg/kg) significantly inhibited the acquisition of <b>METH</b> induced CPP, reduced the content of dopamine and glutamate and down regulated the expression of TH and <strong>NR2B</strong> in the CPP zebrafish brains.
+GRIN2B	addiction	reward	27009763	Results revealed that rhynchophylline (100mg/kg) significantly inhibited the acquisition of METH induced <b>CPP</b>, reduced the content of dopamine and glutamate and down regulated the expression of TH and <strong>NR2B</strong> in the <b>CPP</b> zebrafish brains.
+GRIN2B	drug	amphetamine	27009763	Taken together, these data indicate that the inhibition of the formation of <b>METH</b> dependence by rhynchophylline in zebrafish is associated with amelioration of the neurotransmitters dopamine and glutamate content and down regulation of TH and <strong>NR2B</strong> expression.
+GRIN2B	addiction	dependence	27009763	Taken together, these data indicate that the inhibition of the formation of METH <b>dependence</b> by rhynchophylline in zebrafish is associated with amelioration of the neurotransmitters dopamine and glutamate content and down regulation of TH and <strong>NR2B</strong> expression.
+GRIN2B	drug	cocaine	26861675	The ERK CREB Fos pathway and the NMDA receptor <strong>NR2B</strong> subunits in the NAc were involved in the <b>cocaine</b> induced behavioral sensitization.
+GRIN2B	addiction	sensitization	26861675	The ERK CREB Fos pathway and the NMDA receptor <strong>NR2B</strong> subunits in the NAc were involved in the cocaine induced behavioral <b>sensitization</b>.
+GRIN2B	drug	alcohol	26771436	Association of N Methyl D Aspartate receptor 2B Subunit (<strong>GRIN2B</strong>) polymorphism with earlier age at onset of withdrawal symptoms in Indian <b>alcohol</b> dependent subjects.
+GRIN2B	addiction	withdrawal	26771436	Association of N Methyl D Aspartate receptor 2B Subunit (<strong>GRIN2B</strong>) polymorphism with earlier age at onset of <b>withdrawal</b> symptoms in Indian alcohol dependent subjects.
+GRIN2B	drug	alcohol	26771436	The associations of <strong>GRIN2B</strong> polymorphism (rs1806201) with <b>alcohol</b> withdrawal and related clinical parameters in <b>alcohol</b> dependent subjects were investigated.
+GRIN2B	addiction	withdrawal	26771436	The associations of <strong>GRIN2B</strong> polymorphism (rs1806201) with alcohol <b>withdrawal</b> and related clinical parameters in alcohol dependent subjects were investigated.
+GRIN2B	drug	alcohol	26771436	The SNP rs1806201 in <strong>GRIN2B</strong> may play an important role in genetic susceptibility to earlier age of withdrawal in <b>alcohol</b> dependent patients.
+GRIN2B	addiction	withdrawal	26771436	The SNP rs1806201 in <strong>GRIN2B</strong> may play an important role in genetic susceptibility to earlier age of <b>withdrawal</b> in alcohol dependent patients.
+GRIN2B	drug	opioid	26692025	Re exposure to <b>morphine</b> associated context facilitated long term potentiation in the vSUB NAc glutamatergic pathway via <strong>GluN2B</strong> containing receptor activation.
+GRIN2B	drug	opioid	26692025	Here, we found that the long term potentiation (LTP) in the vSUB NAc pathway was facilitated and the <strong>GluN2B</strong> subunit protein level was elevated in synaptoneurosomes of the NAc shell, but not in the core, following <b>morphine</b> induced conditioned place preference (CPP) expression in rats.
+GRIN2B	addiction	reward	26692025	Here, we found that the long term potentiation (LTP) in the vSUB NAc pathway was facilitated and the <strong>GluN2B</strong> subunit protein level was elevated in synaptoneurosomes of the NAc shell, but not in the core, following morphine induced conditioned place preference (<b>CPP</b>) expression in rats.
+GRIN2B	drug	opioid	26692025	The <strong>GluN2B</strong> NMDARs may be regarded as a potential target for erasing <b>morphine</b> related memory.
+GRIN2B	drug	opioid	26596557	2) The involvement of the NO pathway in <b>morphine</b> CPP requires <strong>NR2B</strong> containing NMDA receptors (<strong>NR2B</strong> NMDARs).
+GRIN2B	addiction	reward	26596557	2) The involvement of the NO pathway in morphine <b>CPP</b> requires <strong>NR2B</strong> containing NMDA receptors (<strong>NR2B</strong> NMDARs).
+GRIN2B	drug	opioid	26596557	<strong>NR2B</strong> NMDAR expression was elevated in the CA1 following <b>morphine</b> CPP expression, and intra CA1 injection of the <strong>NR2B</strong> NMDAR antagonist Ro25 6981 not only blocked <b>morphine</b> CPP expression but also inhibited the up regulation of nNOS, sGC and PKG.
+GRIN2B	addiction	reward	26596557	<strong>NR2B</strong> NMDAR expression was elevated in the CA1 following morphine <b>CPP</b> expression, and intra CA1 injection of the <strong>NR2B</strong> NMDAR antagonist Ro25 6981 not only blocked morphine <b>CPP</b> expression but also inhibited the up regulation of nNOS, sGC and PKG.
+GRIN2B	drug	opioid	26596557	Collectively, the results of our study demonstrated that the activation of the <strong>NR2B</strong> NMDAR/NO/sGC/PKG signaling pathway is necessary for the retrieval of <b>morphine</b> associated reward memory.
+GRIN2B	addiction	reward	26596557	Collectively, the results of our study demonstrated that the activation of the <strong>NR2B</strong> NMDAR/NO/sGC/PKG signaling pathway is necessary for the retrieval of morphine associated <b>reward</b> memory.
+GRIN2B	drug	alcohol	26549202	Chronic intermittent <b>alcohol</b> disrupts the <strong>GluN2B</strong> associated proteome and specifically regulates group I mGlu receptor dependent long term depression.
+GRIN2B	drug	alcohol	26549202	Recent work suggests that chronic <b>alcohol</b> treatment preferentially modulates both the expression and subcellular localization of NMDARs containing the <strong>GluN2B</strong> subunit.
+GRIN2B	drug	alcohol	26549202	We employed a discovery based proteomic approach in subcellular fractions of hippocampal tissue from chronic intermittent <b>alcohol</b> (CIE) exposed C57Bl/6J mice to gain insight into <b>alcohol</b> induced changes in <strong>GluN2B</strong> signaling complexes.
+GRIN2B	drug	amphetamine	26366944	Moreover, <b>METH</b> inhibited mitogen activated protein kinase (MAPK) signaling activity and altered expression of the N methyl d aspartate (NMDA) receptor subunits NR2A and <strong>NR2B</strong> as well as calcium/calmodulin dependent protein kinase II (CaMKII).
+GRIN2B	drug	alcohol	26266540	In the present study, we used human embryonic stem cell (hESC) derived cortical neurons as in vitro cellular models to investigate <b>alcohol</b> induced expression changes of genes involved in <b>alcohol</b> metabolism (ALDH2), anti apoptosis (BCL2 and CCND2), neurotransmission (NMDA receptor subunit genes: GRIN1, GRIN2A, <strong>GRIN2B</strong>, and GRIN2D), calcium channel activity (ITPR2), or transcriptional repression (JARID2).
+GRIN2B	drug	alcohol	26266540	After a 7 day <b>ethanol</b> (50 mM) exposure followed by a 24 hour <b>ethanol</b> withdrawal treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93 fold, P = 0.003; GRIN2A: 1.40 fold, P = 0.003; <strong>GRIN2B</strong>: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; BCL2: 1.34 fold, P = 0.031), and the results of GRIN1, GRIN2A, and <strong>GRIN2B</strong> survived multiple comparison correction.
+GRIN2B	addiction	withdrawal	26266540	After a 7 day ethanol (50 mM) exposure followed by a 24 hour ethanol <b>withdrawal</b> treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93 fold, P = 0.003; GRIN2A: 1.40 fold, P = 0.003; <strong>GRIN2B</strong>: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; BCL2: 1.34 fold, P = 0.031), and the results of GRIN1, GRIN2A, and <strong>GRIN2B</strong> survived multiple comparison correction.
+GRIN2B	drug	alcohol	26254123	Two Binges of <b>Ethanol</b> a Day Keep the Memory Away in Adolescent Rats: Key Role for <strong>GLUN2B</strong> Subunit.
+GRIN2B	drug	alcohol	25916683	Regardless of prior <b>alcohol</b> injection (2 g/kg), UCMS mice exhibited elevated NAC shell levels of mGlu1α, <strong>GluN2b</strong> and Homer2, as well as lower phospholipase Cβ within this subregion.
+GRIN2B	drug	amphetamine	25865928	Recognition of novelty depends upon intact perirhinal (pRh) cortex function, which is compromised by <b>meth</b> induced downregulation of <strong>GluN2B</strong> containing N methyl D aspartate (NMDA) receptors.
+GRIN2B	drug	amphetamine	25865928	We hypothesized that <b>meth</b> induced downregulation of <strong>GluN2B</strong> receptors would compromise pRh LTD, leading to loss of NOR memory.
+GRIN2B	drug	amphetamine	25865928	Furthermore, blockade of <strong>GluN2B</strong> containing NMDA receptors with Ro 25 6981 prevented DCS restoration of pRh LTD in <b>meth</b> subjects.
+GRIN2B	drug	alcohol	25800798	On the other hand <b>ethanol</b> significantly decreased NR2A and <strong>NR2B</strong> mRNAs expression, and increase GABAA mRNA expression.
+GRIN2B	drug	alcohol	25755642	Homer2 deletion alters dendritic spine morphology but not <b>alcohol</b> associated adaptations in <strong>GluN2B</strong> containing N methyl D aspartate receptors in the nucleus accumbens.
+GRIN2B	drug	alcohol	25755642	Western blot analysis of tissue samples from the NAc enriched for PSD proteins revealed a main effect of <b>ethanol</b> treatment on the expression of <strong>GluN2B</strong>, but there was no effect of genotype or treatment on the expression other glutamate receptor subunits or PSD95.
+GRIN2B	drug	amphetamine	25752339	We also found that <b>METH</b> altered the expression of the N methyl d aspartate (NMDA) receptor subunits NR2A (79.6%) and <strong>NR2B</strong> (126.7%) and Ca(2+) /calmodulin dependent protein kinase II (CAMKII) (74.0%).
+GRIN2B	drug	alcohol	25660313	Meta analysis of six genes (BDNF, DRD1, DRD3, DRD4, <strong>GRIN2B</strong> and MAOA) involved in neuroplasticity and the risk for <b>alcohol</b> dependence.
+GRIN2B	addiction	dependence	25660313	Meta analysis of six genes (BDNF, DRD1, DRD3, DRD4, <strong>GRIN2B</strong> and MAOA) involved in neuroplasticity and the risk for alcohol <b>dependence</b>.
+GRIN2B	drug	alcohol	25616726	The glutamate N methyl d aspartate (NMDA) receptor <strong>NR2B</strong> subunits are sensitive to <b>ethanol</b> and are found in brain areas related to <b>ethanol</b> addiction, dependence, development of <b>alcohol</b> tolerance, and <b>alcohol</b> withdrawal syndrome.
+GRIN2B	addiction	addiction	25616726	The glutamate N methyl d aspartate (NMDA) receptor <strong>NR2B</strong> subunits are sensitive to ethanol and are found in brain areas related to ethanol <b>addiction</b>, dependence, development of alcohol tolerance, and alcohol withdrawal syndrome.
+GRIN2B	addiction	dependence	25616726	The glutamate N methyl d aspartate (NMDA) receptor <strong>NR2B</strong> subunits are sensitive to ethanol and are found in brain areas related to ethanol addiction, <b>dependence</b>, development of alcohol tolerance, and alcohol withdrawal syndrome.
+GRIN2B	addiction	withdrawal	25616726	The glutamate N methyl d aspartate (NMDA) receptor <strong>NR2B</strong> subunits are sensitive to ethanol and are found in brain areas related to ethanol addiction, dependence, development of alcohol tolerance, and alcohol <b>withdrawal</b> syndrome.
+GRIN2B	drug	opioid	25616726	<strong>NR2B</strong> containing NMDA receptors in the NAC are involved in both non <b>opioid</b> and <b>opioid</b> receptor mediated reward.
+GRIN2B	addiction	reward	25616726	<strong>NR2B</strong> containing NMDA receptors in the NAC are involved in both non opioid and opioid receptor mediated <b>reward</b>.
+GRIN2B	drug	alcohol	25616726	Our aim was to evaluate the putative [(3)H]ifenprodil binding alterations of <strong>NR2B</strong> receptors in limbic, hippocampal, and cortical brain areas of type 1 <b>alcoholics</b> (n=8), type 2 <b>alcoholics</b> (n=8), and control subjects (n=10) by postmortem whole hemisphere autoradiography.
+GRIN2B	drug	alcohol	25616726	Although preliminary and from relatively small diagnostic groups, these results suggest pathological alterations in the <strong>NR2B</strong> mediated reward system of type 2 <b>alcoholics</b>.
+GRIN2B	addiction	reward	25616726	Although preliminary and from relatively small diagnostic groups, these results suggest pathological alterations in the <strong>NR2B</strong> mediated <b>reward</b> system of type 2 alcoholics.
+GRIN2B	drug	cocaine	25539508	An overall decrease was observed in the mRNA expression of the glutamate synthesizing gene kidney type glutaminase (KGA), the metabotropic glutamate receptors (mGluR3 and GluR), and subunits of NMDA ionotropic receptors (NR1, NR2A, <strong>NR2B</strong> and NR2C) after acute <b>cocaine</b> administration, while mice repeatedly exposed to <b>cocaine</b> only displayed an increase in NR2C.
+GRIN2B	drug	amphetamine	25463524	Conversely, <b>methamphetamine</b> produced hypophosphorylation of N methyl d aspartate (NMDA) receptor subunit 2B (<strong>GluN2B</strong>) at Tyr 1472 in the ventral hippocampus, indicating reduced receptor activation.
+GRIN2B	drug	cocaine	25408547	The present study focused on metabotropic glutamatergic receptors type 5 (mGluR(5)) and N methyl D aspartate receptor subunits (NMDAR: GluN1, GluN2A, <strong>GluN2B</strong>) proteins during <b>cocaine</b> self administration and after 10 day of extinction training in rats.
+GRIN2B	drug	cocaine	25408547	Extinction training in animals with a history of <b>cocaine</b> self administration resulted in an elevation of the hippocampal GluN2A/<strong>GluN2B</strong> subunits and accumbal mGluR(5), and in a 50 % decrease of mGluR(5) protein expression in the dorsal striatum.
+GRIN2B	addiction	reward	25360085	The NMDA evoked ([(3)H]D Asp) overflow was partially antagonized by the NMDAR antagonists MK801, D AP5, 5,7 DCKA and R( )<b>CPP</b> and unaffected by the <strong>GluN2B</strong> NMDAR antagonists Ro256981 and ifenprodil.
+GRIN2B	addiction	withdrawal	25268928	Within the first few hours of <b>withdrawal</b>, there is a marked decrease in tyrosine phosphorylation of critical intracellular and membrane bound proteins in the dmPFC that include ERK/MAP kinase and the NMDA receptor subunits, GluN1 and <strong>GluN2B</strong>.
+GRIN2B	drug	alcohol	25262781	<strong>GRIN2B</strong> (encoding GluN2B), was up regulated in both <b>alcoholics</b> and cocaine addicts (FDR corrected P = 0.008).
+GRIN2B	drug	cocaine	25262781	<strong>GRIN2B</strong> (encoding GluN2B), was up regulated in both alcoholics and <b>cocaine</b> addicts (FDR corrected P = 0.008).
+GRIN2B	drug	alcohol	25262781	<strong>GRIN2B</strong> (encoding <strong>GluN2B</strong>), was up regulated in both <b>alcoholics</b> and cocaine addicts (FDR corrected P = 0.008).
+GRIN2B	drug	cocaine	25262781	<strong>GRIN2B</strong> (encoding <strong>GluN2B</strong>), was up regulated in both alcoholics and <b>cocaine</b> addicts (FDR corrected P = 0.008).
+GRIN2B	addiction	addiction	25262781	The NMDA <strong>GluN2B</strong> receptor subunit might be implicated in a common pathway to <b>addiction</b>, possibly in conjunction with the GABAB1 receptor subunit.
+GRIN2B	drug	amphetamine	25193707	Effect of rhynchophylline on conditioned place preference on expression of <strong>NR2B</strong> in <b>methamphetamine</b> dependent mice.
+GRIN2B	drug	amphetamine	25193707	Place preference mice models were established by <b>methamphetamine</b>; the expression of <strong>NR2B</strong> was observed by immunohistochemistry technique and Western blot.
+GRIN2B	drug	amphetamine	25193707	<b>Methamphetamine</b> (4mg/kg) induced place preference mice model was successfully established; ketamine (15mg/kg), rhynchophylline (40mg/kg) and rhynchophylline (80mg/kg) can eliminate place preference; Immunohistochemistry showed that the number of <strong>NR2B</strong> positive neurons in hippocampus was increased in the <b>methamphetamine</b> model group, whereas less <strong>NR2B</strong> positive neurons were found in the ketamine group, low and high dosage rhynchophylline group.
+GRIN2B	drug	psychedelics	25193707	Methamphetamine (4mg/kg) induced place preference mice model was successfully established; <b>ketamine</b> (15mg/kg), rhynchophylline (40mg/kg) and rhynchophylline (80mg/kg) can eliminate place preference; Immunohistochemistry showed that the number of <strong>NR2B</strong> positive neurons in hippocampus was increased in the methamphetamine model group, whereas less <strong>NR2B</strong> positive neurons were found in the <b>ketamine</b> group, low and high dosage rhynchophylline group.
+GRIN2B	drug	psychedelics	25193707	Western blot showed that the expression of <strong>NR2B</strong> protein was significantly increased in the model group, whereas less expression was found in the <b>ketamine</b> group, low and high dosage rhynchophylline group.
+GRIN2B	drug	amphetamine	25193707	<strong>NR2B</strong> plays an important role in the formation of <b>methamphetamine</b> induced place preference in mice.
+GRIN2B	drug	amphetamine	25193707	Rhynchophylline reversed the expression of <strong>NR2B</strong> in the hippocampus demonstrates the potential effect of mediates <b>methamphetamine</b> induced rewarding effect.
+GRIN2B	drug	cocaine	25035084	<strong>GluN2B</strong> containing NMDA receptors blockade rescues bidirectional synaptic plasticity in the bed nucleus of the stria terminalis of <b>cocaine</b> self administering rats.
+GRIN2B	drug	cocaine	25035084	<b>Cocaine</b> self administering rats exhibited impairment in NMDA dependent long term depression (LTD) that could be rescued by <strong>GluN2B</strong> containing NMDA receptor blockade.
+GRIN2B	drug	cocaine	25035084	Sucrose self administering rats demonstrated no impairment in NMDA dependent LTD. During the maintenance period of self administration, in vivo (daily intraperitoneally for 5 days) pharmacologic blockade of <strong>GluN2B</strong> containing NMDA receptors did not reduce lever pressing for <b>cocaine</b>.
+GRIN2B	drug	cocaine	25035084	However, in vivo <strong>GluN2B</strong> blockade did normalize A:N ratios in <b>cocaine</b> self administrating rats, and dissociated the magnitude of ovBNST A:N ratios from drug seeking behavior after protracted withdrawal.
+GRIN2B	addiction	relapse	25035084	However, in vivo <strong>GluN2B</strong> blockade did normalize A:N ratios in cocaine self administrating rats, and dissociated the magnitude of ovBNST A:N ratios from drug <b>seeking</b> behavior after protracted withdrawal.
+GRIN2B	addiction	withdrawal	25035084	However, in vivo <strong>GluN2B</strong> blockade did normalize A:N ratios in cocaine self administrating rats, and dissociated the magnitude of ovBNST A:N ratios from drug seeking behavior after protracted <b>withdrawal</b>.
+GRIN2B	drug	cocaine	24847958	However, both GluN2A and <strong>GluN2B</strong> subunit expression in the nucleus accumbens increased following <b>cocaine</b> self administration, and this increased expression was relatively resistant to modulation by extinction.
+GRIN2B	drug	cocaine	24832868	In addition, repeated <b>cocaine</b> altered NMDA receptor subunit expression in the ventral hippocampus, reducing the NR2A : <strong>NR2B</strong> subunit ratio.
+GRIN2B	drug	cocaine	24832868	This was associated with reduced ventral hippocampal NR2A:<strong>NR2B</strong> subunit ratio, suggesting that repeated exposure to <b>cocaine</b> produces changes in hippocampal NMDA receptor composition that lead to enhanced ventral hippocampus nucleus accumbens communication.
+GRIN2B	drug	opioid	24797707	Dopamine D3 receptor regulated <strong>NR2B</strong> subunits of N methyl d aspartate receptors in the nucleus accumbens involves in <b>morphine</b> induced locomotor activity.
+GRIN2B	drug	opioid	24797707	Hyperlocomotion and behavioral locomotor sensitization were significantly suppressed when ifenprodil (5 mg/kg), a selective <strong>NR2B</strong> subunit containing N methyl d aspartate (NMDA) receptor antagonist, or nafadotride (25 μg/kg), a dopamine D3 receptor (D3R) preferring antagonist, was coadministered with <b>morphine</b>.
+GRIN2B	addiction	sensitization	24797707	Hyperlocomotion and behavioral locomotor <b>sensitization</b> were significantly suppressed when ifenprodil (5 mg/kg), a selective <strong>NR2B</strong> subunit containing N methyl d aspartate (NMDA) receptor antagonist, or nafadotride (25 μg/kg), a dopamine D3 receptor (D3R) preferring antagonist, was coadministered with morphine.
+GRIN2B	drug	opioid	24797707	Western blot analysis showed that <b>morphine</b> behavioral sensitization induced a region specific increase in phosphorylation of <strong>NR2B</strong> (pNR2B) and total levels of <strong>NR2B</strong> (<strong>NR2B</strong>) expression in the NAc.
+GRIN2B	addiction	sensitization	24797707	Western blot analysis showed that morphine behavioral <b>sensitization</b> induced a region specific increase in phosphorylation of <strong>NR2B</strong> (pNR2B) and total levels of <strong>NR2B</strong> (<strong>NR2B</strong>) expression in the NAc.
+GRIN2B	drug	opioid	24797707	Systemically administered nafadotride attenuated behavioral locomotor sensitization induced by <b>morphine</b> and significantly reversed the overexpression of pNR2B and <strong>NR2B</strong> subunit containing NMDA receptor in the NAc.
+GRIN2B	addiction	sensitization	24797707	Systemically administered nafadotride attenuated behavioral locomotor <b>sensitization</b> induced by morphine and significantly reversed the overexpression of pNR2B and <strong>NR2B</strong> subunit containing NMDA receptor in the NAc.
+GRIN2B	drug	opioid	24797707	These findings suggest that D3Rs are involved in <b>morphine</b> induced behavioral locomotor sensitization in mice by regulating the <strong>NR2B</strong> subunits of NMDA receptors in the NAc.
+GRIN2B	addiction	sensitization	24797707	These findings suggest that D3Rs are involved in morphine induced behavioral locomotor <b>sensitization</b> in mice by regulating the <strong>NR2B</strong> subunits of NMDA receptors in the NAc.
+GRIN2B	drug	cocaine	24760865	Infralimbic BDNF/TrkB enhancement of <strong>GluN2B</strong> currents facilitates extinction of a <b>cocaine</b> conditioned place preference.
+GRIN2B	addiction	reward	24760865	Blockade of infralimbic TrkB receptors or <strong>GluN2B</strong> containing NMDARs disrupted consolidation of extinction of the <b>CPP</b>.
+GRIN2B	drug	cocaine	24760865	The 7,8DHF induced enhancement of extinction was prevented by infralimbic infusions of a <strong>GluN2B</strong> specific receptor antagonist, demonstrating that TrkB receptor activation enhances extinction of <b>cocaine</b> CPP via <strong>GluN2B</strong> containing NMDARs.
+GRIN2B	addiction	reward	24760865	The 7,8DHF induced enhancement of extinction was prevented by infralimbic infusions of a <strong>GluN2B</strong> specific receptor antagonist, demonstrating that TrkB receptor activation enhances extinction of cocaine <b>CPP</b> via <strong>GluN2B</strong> containing NMDARs.
+GRIN2B	drug	alcohol	24588427	Previously, we found that <b>ethanol</b> activates Fyn in the dorsomedial striatum (DMS) leading to <strong>GluN2B</strong> phosphorylation, which, in turn, underlies the development of <b>ethanol</b> intake (J.
+GRIN2B	drug	alcohol	24588427	Here, we tested the hypothesis that inhibition of STEP61 by <b>ethanol</b> is upstream of Fyn/<strong>GluN2B</strong>.
+GRIN2B	drug	alcohol	24588427	Specific knockdown of STEP61 in the DMS of mice enhanced <b>ethanol</b> mediated Fyn activation and <strong>GluN2B</strong> phosphorylation, and increased <b>ethanol</b> intake without altering the level of water, saccharine, quinine consumption or spontaneous locomotor activity.
+GRIN2B	drug	alcohol	24588427	Together, our data suggest that blockade of STEP61 activity in response to <b>ethanol</b> is sufficient for the activation of the Fyn/<strong>GluN2B</strong> pathway in the DMS.
+GRIN2B	drug	alcohol	24588427	Being upstream of Fyn and <strong>GluN2B</strong>, inactive STEP61 in the DMS primes the induction of <b>ethanol</b> intake.
+GRIN2B	drug	alcohol	24588427	We show that <b>ethanol</b> mediated inhibition of STEP61 in the DMS leads to Fyn activation and <strong>GluN2B</strong> phosphorylation.
+GRIN2B	drug	alcohol	24588427	The inhibition of STEP61 activity contributes to the activation of Fyn in response to <b>ethanol</b>, which, in turn, phosphorylates <strong>GluN2B</strong>.
+GRIN2B	drug	nicotine	24549882	The magnesium lacks of effect after nicotinic treatment suggests that there is no change in expression of <strong>NR2B</strong> subunit of NMDA receptors, then, the effect of <b>nicotine</b> treatment on amplitude of NMDA currents may be due to an increase in the quantity of receptors or to a change in the unitary conductance, rather than a change in the expression of the subunits that constitute it.
+GRIN2B	drug	opioid	24403152	Here we report that <b>morphine</b> CPP is associated with increased basal synaptic transmission, impaired hippocampal long term potentiation (LTP), and increased synaptic expression of the NR1 and <strong>NR2b</strong> NMDAR subunits.
+GRIN2B	addiction	reward	24403152	Here we report that morphine <b>CPP</b> is associated with increased basal synaptic transmission, impaired hippocampal long term potentiation (LTP), and increased synaptic expression of the NR1 and <strong>NR2b</strong> NMDAR subunits.
+GRIN2B	drug	opioid	24403152	Changes in synaptic plasticity, synaptic NR1 and <strong>NR2b</strong> expression, and <b>morphine</b> CPP were absent when <b>morphine</b> was not paired with a specific context.
+GRIN2B	addiction	reward	24403152	Changes in synaptic plasticity, synaptic NR1 and <strong>NR2b</strong> expression, and morphine <b>CPP</b> were absent when morphine was not paired with a specific context.
+GRIN2B	drug	opioid	24403152	Furthermore, hippocampal LTP was impaired and synaptic <strong>NR2b</strong> expression was increased after extinction of <b>morphine</b> CPP, indicating that these alterations in plasticity may be involved in the mechanisms underlying the learning of drug environment associations.
+GRIN2B	addiction	reward	24403152	Furthermore, hippocampal LTP was impaired and synaptic <strong>NR2b</strong> expression was increased after extinction of morphine <b>CPP</b>, indicating that these alterations in plasticity may be involved in the mechanisms underlying the learning of drug environment associations.
+GRIN2B	drug	opioid	24403152	Finally, we found that reinstatement of <b>morphine</b> CPP was prevented by the selective blockade of the <strong>NR2b</strong> subunit in the hippocampus.
+GRIN2B	addiction	relapse	24403152	Finally, we found that <b>reinstatement</b> of morphine CPP was prevented by the selective blockade of the <strong>NR2b</strong> subunit in the hippocampus.
+GRIN2B	addiction	reward	24403152	Finally, we found that reinstatement of morphine <b>CPP</b> was prevented by the selective blockade of the <strong>NR2b</strong> subunit in the hippocampus.
+GRIN2B	addiction	reward	24373903	The NMDA evoked [(3)H]dopamine outflow was blocked by MK801 (1 μM) and inhibited by the selective <strong>GluN2B</strong> selective antagonists ifenprodil (1 μM) and RO 25 6981 (1 μM), but not by the GluN2A preferring antagonists <b>CPP</b> 19755 (1 μM) and ZnCl2 (1 nM).
+GRIN2B	drug	nicotine	24373903	Notably, <b>nicotine</b> pretreatment significantly decreased the density of biotin tagged <strong>GluN2B</strong> proteins in NAc synaptosomes.
+GRIN2B	addiction	sensitization	24361916	In addition, genes encoding molecules that are important in central <b>sensitization</b> such as glutamate transporters and N methyl d aspartate receptor 2B (<strong>NMDAR2B</strong>), and neuro immune related genes such as neuronal nitric oxide synthase (nNOS1), chemokine CX3CL1 (a mediator for microglial activation), toll like receptor 2 (TLR2), and leptin were differentially modulated by MDA7.
+GRIN2B	addiction	sensitization	24315834	We examined NR1, NR2A, and <strong>NR2B</strong> expression throughout the brain during the development phase of EtOH <b>sensitization</b>, as well as after a 14 day withdrawal period.
+GRIN2B	addiction	withdrawal	24315834	We examined NR1, NR2A, and <strong>NR2B</strong> expression throughout the brain during the development phase of EtOH sensitization, as well as after a 14 day <b>withdrawal</b> period.
+GRIN2B	addiction	relapse	24269543	Western blotting results showed that the levels of GLT1, VGLUT2, <strong>NR2B</strong>, p ERK1/2 and p CREB expressions in the mPFC were increased and CaMKII was decreased markedly after the stress priming MAP induced CPP <b>reinstatement</b> test.
+GRIN2B	addiction	reward	24269543	Western blotting results showed that the levels of GLT1, VGLUT2, <strong>NR2B</strong>, p ERK1/2 and p CREB expressions in the mPFC were increased and CaMKII was decreased markedly after the stress priming MAP induced <b>CPP</b> reinstatement test.
+GRIN2B	drug	cocaine	24183704	Combining ex vivo patch clamp recordings, mouse genetics, and subcellular Ca(2+) imaging, we observe that <b>cocaine</b> drives the insertion of NMDARs that are quasi Ca(2+) impermeable and contain GluN3A and <strong>GluN2B</strong> subunits.
+GRIN2B	drug	amphetamine	24120858	<strong>GluN2B</strong> receptor subtype was decreased in the perirhinal cortex, yet remained unaffected in the prefrontal cortex and hippocampus of <b>meth</b> rats.
+GRIN2B	drug	alcohol	24005290	<b>Ethanol</b> mediated Fyn activation in the DMS leads to the phosphorylation of the <strong>GluN2B</strong> subunit of the NMDA receptor, to the enhancement of the channel's activity, and to the development and/or maintenance of <b>ethanol</b> drinking behaviors (Wang et al., 2007, 2010).
+GRIN2B	drug	alcohol	24005290	Here we tested the hypothesis that PTPα in the DMS is part of the Fyn/<strong>GluN2B</strong> pathway and is thus a major contributor to the neuroadaptations underlying excessive <b>ethanol</b> intake behaviors.
+GRIN2B	drug	alcohol	24005290	Furthermore, downregulation of PTPα in the DMS of mice significantly reduces <b>ethanol</b> mediated Fyn activation, <strong>GluN2B</strong> phosphorylation, and <b>ethanol</b> withdrawal induced long term facilitation of NMDAR activity without altering the intrinsic features of DMS neurons.
+GRIN2B	addiction	withdrawal	24005290	Furthermore, downregulation of PTPα in the DMS of mice significantly reduces ethanol mediated Fyn activation, <strong>GluN2B</strong> phosphorylation, and ethanol <b>withdrawal</b> induced long term facilitation of NMDAR activity without altering the intrinsic features of DMS neurons.
+GRIN2B	drug	alcohol	23966068	A 30 day history of binge <b>alcohol</b> drinking (for example, 4 5 g kg( 1) per 2 h( 1)) elevated CeA levels of mGluR1, <strong>GluN2B</strong>, Homer2a/b and phospholipase C (PLC) β3, without significantly altering protein expression within the adjacent basolateral amygdala.
+GRIN2B	addiction	intoxication	23966068	A 30 day history of <b>binge</b> alcohol drinking (for example, 4 5 g kg( 1) per 2 h( 1)) elevated CeA levels of mGluR1, <strong>GluN2B</strong>, Homer2a/b and phospholipase C (PLC) β3, without significantly altering protein expression within the adjacent basolateral amygdala.
+GRIN2B	drug	cocaine	23894151	Additionally, transcripts encoding the <strong>NR2B</strong> subunit of the NMDA receptor increased in Wt mice that self administered <b>cocaine</b> but were unchanged in similarly experienced Kal7(KO) mice.
+GRIN2B	drug	alcohol	23889203	Long term <b>ethanol</b> and corticosterone co exposure sensitize the hippocampal ca1 region pyramidal cells to insult during <b>ethanol</b> withdrawal in an NMDA <strong>GluN2B</strong> subunit dependent manner.
+GRIN2B	addiction	withdrawal	23889203	Long term ethanol and corticosterone co exposure sensitize the hippocampal ca1 region pyramidal cells to insult during ethanol <b>withdrawal</b> in an NMDA <strong>GluN2B</strong> subunit dependent manner.
+GRIN2B	drug	cocaine	23872878	<b>Cocaine</b> seeking behavior (non reinforced active lever pressing) was then assessed in the previously <b>cocaine</b> paired and extinction contexts after AP5 (N methyl D aspartate glutamate (NMDA) receptor (NMDAR) antagonist; 0.25 or 2.5 μg/0.5 μl/hemisphere), PP2 (Src family kinase inhibitor; 6.25 or 62.5 ng/0.5 μl/hemisphere), Ro25 6981 (<strong>NR2B</strong> subunit containing NMDAR antagonist; 0.2 or 2 μg/0.5 μl/hemisphere), or vehicle administration into the DH.
+GRIN2B	addiction	relapse	23872878	Cocaine <b>seeking</b> behavior (non reinforced active lever pressing) was then assessed in the previously cocaine paired and extinction contexts after AP5 (N methyl D aspartate glutamate (NMDA) receptor (NMDAR) antagonist; 0.25 or 2.5 μg/0.5 μl/hemisphere), PP2 (Src family kinase inhibitor; 6.25 or 62.5 ng/0.5 μl/hemisphere), Ro25 6981 (<strong>NR2B</strong> subunit containing NMDAR antagonist; 0.2 or 2 μg/0.5 μl/hemisphere), or vehicle administration into the DH.
+GRIN2B	drug	cocaine	23872878	<b>Cocaine</b> seeking behavior during the first 20 min of the test session in the <b>cocaine</b> paired context was associated with an increase in <strong>NR2B</strong> subunit activation, and intra DH PP2 pretreatment disrupted this relationship.
+GRIN2B	addiction	relapse	23872878	Cocaine <b>seeking</b> behavior during the first 20 min of the test session in the cocaine paired context was associated with an increase in <strong>NR2B</strong> subunit activation, and intra DH PP2 pretreatment disrupted this relationship.
+GRIN2B	drug	cocaine	23872878	Together, these findings suggest that Src family kinase activation, NMDAR stimulation, and likely Src family kinase mediated <strong>NR2B</strong> subunit containing NMDAR activation in the DH are necessary for incentive motivational and/or memory processes that promote contextual <b>cocaine</b> seeking behavior.
+GRIN2B	addiction	relapse	23872878	Together, these findings suggest that Src family kinase activation, NMDAR stimulation, and likely Src family kinase mediated <strong>NR2B</strong> subunit containing NMDAR activation in the DH are necessary for incentive motivational and/or memory processes that promote contextual cocaine <b>seeking</b> behavior.
+GRIN2B	addiction	reward	23872878	Together, these findings suggest that Src family kinase activation, NMDAR stimulation, and likely Src family kinase mediated <strong>NR2B</strong> subunit containing NMDAR activation in the DH are necessary for <b>incentive</b> motivational and/or memory processes that promote contextual cocaine seeking behavior.
+GRIN2B	drug	opioid	23855403	Deep resequencing of 17 glutamate system genes identifies rare variants in DISC1 and <strong>GRIN2B</strong> affecting risk of <b>opioid</b> dependence.
+GRIN2B	addiction	dependence	23855403	Deep resequencing of 17 glutamate system genes identifies rare variants in DISC1 and <strong>GRIN2B</strong> affecting risk of opioid <b>dependence</b>.
+GRIN2B	drug	nicotine	23671067	In support of this hypothesis, we found that pharmacological inhibition of GluN2A with 3 Chloro 4 fluoro N [4 [[2 (phenylcarbonyl)hydrazino]carbonyl]benzyl]benzenesulfonamide (TCN 201) or <strong>GluN2B</strong> with ifenprodil abolished reinstated <b>nicotine</b> seeking.
+GRIN2B	addiction	relapse	23671067	In support of this hypothesis, we found that pharmacological inhibition of GluN2A with 3 Chloro 4 fluoro N [4 [[2 (phenylcarbonyl)hydrazino]carbonyl]benzyl]benzenesulfonamide (TCN 201) or <strong>GluN2B</strong> with ifenprodil abolished reinstated nicotine <b>seeking</b>.
+GRIN2B	drug	nicotine	23671067	These results indicate that up regulated GluN2A, <strong>GluN2B</strong>, and rapid synaptic potentiation in the accumbens contribute to cue induced relapse to <b>nicotine</b> use.
+GRIN2B	addiction	relapse	23671067	These results indicate that up regulated GluN2A, <strong>GluN2B</strong>, and rapid synaptic potentiation in the accumbens contribute to cue induced <b>relapse</b> to nicotine use.
+GRIN2B	drug	cocaine	23624776	GluN1, <strong>GluN2B</strong>, and phospho <strong>GluN2B</strong> Tyr1472 in the dmPFC were decreased after ShA and LgA <b>cocaine</b>.
+GRIN2B	drug	psychedelics	23439125	Computational models predicted dependence on NMDA receptor (NMDAR) <strong>NR2B</strong> stimulation, and Delay cell persistent firing was abolished by local <strong>NR2B</strong> NMDAR blockade or by systemic <b>ketamine</b> administration.
+GRIN2B	addiction	dependence	23439125	Computational models predicted <b>dependence</b> on NMDA receptor (NMDAR) <strong>NR2B</strong> stimulation, and Delay cell persistent firing was abolished by local <strong>NR2B</strong> NMDAR blockade or by systemic ketamine administration.
+GRIN2B	drug	opioid	23373221	Compared with the physiological saline treatment group, C. yanhusuo (2, 1 g x kg( 1)) and L THP (3.76 and 1.88 mg x kg( 1)) groups showed a notably shorter retention period of rats in white boxes (<b>morphine</b> accompanied boxes) (P < 0.05 or P < 0.01) and remarkably lower glutamic acid content in VTA, NAc and PFC and <strong>NR2B</strong> expression.
+GRIN2B	drug	opioid	23373221	Both C. yanhusuo and L THP can substantially inhibit the effect of <b>morphine</b> CPP, reduce the increasing glutamic acid content in VTA NAc PFC neuroanatomical circuit and down regulated <strong>NR2B</strong> expression, which may be one of mechanisms on reducing the effect of <b>morphine</b> CPP.
+GRIN2B	addiction	reward	23373221	Both C. yanhusuo and L THP can substantially inhibit the effect of morphine <b>CPP</b>, reduce the increasing glutamic acid content in VTA NAc PFC neuroanatomical circuit and down regulated <strong>NR2B</strong> expression, which may be one of mechanisms on reducing the effect of morphine <b>CPP</b>.
+GRIN2B	addiction	reward	23373221	C. yanhusuo preparations containing L THP (1 x) showed 24 fold effect of L THP monomer of single application in terms of the behaviouristics of inhibitory effect on <b>CPP</b> as well as the similarity in terms of transmitter glutamic acid of in VTA NAc PFC neuroanatomical circuit and pharmacological mechanism of <strong>NR2B</strong>.
+GRIN2B	drug	alcohol	23357553	Dephosphorylation of <strong>GluN2B</strong> C terminal tyrosine residues does not contribute to acute <b>ethanol</b> inhibition of recombinant NMDA receptors.
+GRIN2B	drug	alcohol	23357553	Recent findings in the literature suggest that <b>ethanol</b>, via facilitation of tyrosine phosphatase activity, may dephosphorylate key tyrosine residues in the C terminus of <strong>GluN2B</strong> subunits resulting in diminished channel function.
+GRIN2B	drug	alcohol	23357553	These findings suggest that dephosphorylation of C terminal tyrosine residues does not account for <b>ethanol</b> inhibition of <strong>GluN2B</strong> receptors.
+GRIN2B	addiction	dependence	23352746	Our studies show that the downregulation of N methyl d aspartate (NMDA) receptor subunit <strong>GluN2B</strong> expression in the nucleus accumbens, amygdala, medial prefrontal cortex, and hippocampal CA1 area by rhynchophylline is beneficial for the treatment of psychological <b>dependence</b> on amphetamines.
+GRIN2B	drug	psychedelics	23303054	Both GLYX 13 and <b>ketamine</b> persistently (24 h) enhanced the induction of long term potentiation of synaptic transmission and the magnitude of NMDAR <strong>NR2B</strong> conductance at rat Schaffer collateral CA1 synapses in vitro.
+GRIN2B	drug	psychedelics	23303054	Cell surface biotinylation studies showed that both GLYX 13 and <b>ketamine</b> led to increases in both <strong>NR2B</strong> and GluR1 protein levels, as measured by Western analysis, whereas no changes were seen in mRNA expression (microarray and qRT PCR).
+GRIN2B	drug	psychedelics	23303054	These results suggest that GLYX 13 produces an antidepressant like effect without the side effects seen with <b>ketamine</b> at least in part by directly modulating <strong>NR2B</strong> containing NMDARs in the MPFC.
+GRIN2B	drug	opioid	23242725	Furthermore, exogenous H2S can decrease the high level of p NR1 and can increase the low levels of p NR2A and p <strong>NR2B</strong> caused by <b>heroin</b>.
+GRIN2B	drug	alcohol	23100433	We found previously that acute ex vivo as well as repeated cycles of in vivo <b>ethanol</b> exposure and withdrawal, including excessive voluntary consumption of <b>ethanol</b>, produces a long lasting increase in the activity of <strong>NR2B</strong> containing NMDA receptors (<strong>NR2B</strong> NMDARs) in the dorsomedial striatum (DMS) of rats (Wang et al., 2010a).
+GRIN2B	addiction	withdrawal	23100433	We found previously that acute ex vivo as well as repeated cycles of in vivo ethanol exposure and <b>withdrawal</b>, including excessive voluntary consumption of ethanol, produces a long lasting increase in the activity of <strong>NR2B</strong> containing NMDA receptors (<strong>NR2B</strong> NMDARs) in the dorsomedial striatum (DMS) of rats (Wang et al., 2010a).
+GRIN2B	drug	alcohol	23100433	We found that ex vivo acute exposure of striatal slices to, and withdrawal from, <b>ethanol</b> facilitates the induction of LTP in DMS neurons, which is abolished by the inhibition of <strong>NR2B</strong> NMDARs.
+GRIN2B	addiction	withdrawal	23100433	We found that ex vivo acute exposure of striatal slices to, and <b>withdrawal</b> from, ethanol facilitates the induction of LTP in DMS neurons, which is abolished by the inhibition of <strong>NR2B</strong> NMDARs.
+GRIN2B	drug	alcohol	23100433	We also report that repeated systemic administration of <b>ethanol</b> causes an <strong>NR2B</strong> NMDAR dependent facilitation of LTP in the DMS.
+GRIN2B	drug	benzodiazepine	22830051	The removal of CaMKII <strong>GluN2B</strong> complexes from the PSD during drug withdrawal may serve as a homeostatic mechanism to limit AMPAR mediated CA1 neuron hyperexcitability and <b>benzodiazepine</b> withdrawal anxiety.
+GRIN2B	addiction	withdrawal	22830051	The removal of CaMKII <strong>GluN2B</strong> complexes from the PSD during drug <b>withdrawal</b> may serve as a homeostatic mechanism to limit AMPAR mediated CA1 neuron hyperexcitability and benzodiazepine <b>withdrawal</b> anxiety.
+GRIN2B	drug	nicotine	22819974	Repeated treatment with <b>nicotine</b> induces phosphorylation of NMDA receptor <strong>NR2B</strong> subunit in the brain regions involved in behavioral sensitization.
+GRIN2B	addiction	sensitization	22819974	Repeated treatment with nicotine induces phosphorylation of NMDA receptor <strong>NR2B</strong> subunit in the brain regions involved in behavioral <b>sensitization</b>.
+GRIN2B	drug	nicotine	22819974	In the present study, we investigated the levels of <strong>NR2B</strong> phosphorylation at Tyr1472 and Ser1303 in the nucleus accumbens, striatum, frontal cortex, and hippocampus of rats that exhibit behavioral sensitization to <b>nicotine</b>.
+GRIN2B	addiction	sensitization	22819974	In the present study, we investigated the levels of <strong>NR2B</strong> phosphorylation at Tyr1472 and Ser1303 in the nucleus accumbens, striatum, frontal cortex, and hippocampus of rats that exhibit behavioral <b>sensitization</b> to nicotine.
+GRIN2B	drug	nicotine	22819974	Repeated treatment of rats with <b>nicotine</b> (0.6mg/kg, s.c., for 7 days) produced locomotor sensitization accompanied by increased <strong>NR2B</strong> phosphorylation at Tyr1472 in the nucleus accumbens and striatum, brain regions involved in behavioral sensitization.
+GRIN2B	addiction	sensitization	22819974	Repeated treatment of rats with nicotine (0.6mg/kg, s.c., for 7 days) produced locomotor <b>sensitization</b> accompanied by increased <strong>NR2B</strong> phosphorylation at Tyr1472 in the nucleus accumbens and striatum, brain regions involved in behavioral <b>sensitization</b>.
+GRIN2B	drug	nicotine	22819974	In contrast, no changes in <strong>NR2B</strong> phosphorylation were observed after a single treatment with <b>nicotine</b> in these brain regions.
+GRIN2B	drug	nicotine	22819974	In addition, no changes in <strong>NR2B</strong> phosphorylation at Ser1303 were observed after repeated treatment with <b>nicotine</b> in any examined brain regions.
+GRIN2B	drug	nicotine	22819974	These results suggest that repeated treatment with <b>nicotine</b> induces <strong>NR2B</strong> phosphorylation at Tyr1472 in the nucleus accumbens and striatum, which might contribute to the development of synaptic and behavioral plasticity in response to <b>nicotine</b>.
+GRIN2B	drug	opioid	22776695	Essential role of <strong>NR2B</strong> containing NMDA receptor ERK pathway in nucleus accumbens shell in <b>morphine</b> associated contextual memory.
+GRIN2B	addiction	reward	22776695	Selective inhibition of <strong>NR2B</strong> containing NMDA receptor in the NAc shell by ifenprodil prevented <b>CPP</b> expression and down regulated local ERK1/2 phosphorylation.
+GRIN2B	drug	opioid	22776695	These findings collectively suggest that recall of <b>morphine</b> associated contextual memory depends specifically upon ERK1/2 activation in the NAc shell and that ERK1/2 phosphorylation is regulated by the upstream <strong>NR2B</strong> containing NMDA receptor.
+GRIN2B	addiction	withdrawal	22666364	Unexpectedly, this increase in NR1 and <strong>NR2B</strong> was no longer observed after 1 week of <b>withdrawal</b> in spite of a persistent increase in synaptic NMDA currents.
+GRIN2B	drug	cocaine	22655064	Our results revealed differences only in the dSTR, where we found that after acute <b>cocaine</b>, <strong>GluN2B</strong>(Tyr 1472) phosphorylation was significantly greater in LCRs, compared to HCRs and controls.
+GRIN2B	drug	opioid	22621711	Gentiopicroside attenuates <b>morphine</b> rewarding effect through downregulation of <strong>GluN2B</strong> receptors in nucleus accumbens.
+GRIN2B	drug	opioid	22621711	Gent significantly reversed overexpression of <strong>GluN2B</strong> containing NMDA receptors and dopamine D2 receptors in NAc during the first week of <b>morphine</b> withdrawal.
+GRIN2B	addiction	withdrawal	22621711	Gent significantly reversed overexpression of <strong>GluN2B</strong> containing NMDA receptors and dopamine D2 receptors in NAc during the first week of morphine <b>withdrawal</b>.
+GRIN2B	drug	opioid	22621711	Our study provides strong evidence that Gent inhibits <b>morphine</b> dependence through downregulation of <strong>GluN2B</strong> containing NMDA receptors in the NAc.
+GRIN2B	addiction	dependence	22621711	Our study provides strong evidence that Gent inhibits morphine <b>dependence</b> through downregulation of <strong>GluN2B</strong> containing NMDA receptors in the NAc.
+GRIN2B	drug	nicotine	22521583	We then investigated by Western blot analysis the effects of <b>nicotine</b> on hippocampal estrogen receptor beta (ER β), <strong>NR2B</strong> and pCREB.
+GRIN2B	drug	nicotine	22521583	Western blot analysis revealed that <b>nicotine</b> decreased protein levels of ER β, <strong>NR2B</strong>, and pCREB.
+GRIN2B	drug	alcohol	22493886	[Effect of butylphthalide on levels of glutamate and expression of <strong>NR2B</strong> in the hippocampus of rats with <b>alcohol</b> addiction].
+GRIN2B	addiction	addiction	22493886	[Effect of butylphthalide on levels of glutamate and expression of <strong>NR2B</strong> in the hippocampus of rats with alcohol <b>addiction</b>].
+GRIN2B	drug	alcohol	22486492	Finally, we examined changes in mRNA expression of the NMDA receptor subunit genes GRIN1, GRIN2A, <strong>GRIN2B</strong>, and GRIN2D after 7 days of <b>alcohol</b> exposure and after 24 hour withdrawal from chronic <b>alcohol</b> exposure.
+GRIN2B	addiction	withdrawal	22486492	Finally, we examined changes in mRNA expression of the NMDA receptor subunit genes GRIN1, GRIN2A, <strong>GRIN2B</strong>, and GRIN2D after 7 days of alcohol exposure and after 24 hour <b>withdrawal</b> from chronic alcohol exposure.
+GRIN2B	drug	alcohol	22432643	Limited access <b>alcohol</b> drinking under DID procedures up regulated NAC shell Homer2 levels, concomitant with increases in mGluR5 and <strong>NR2B</strong>.
+GRIN2B	drug	alcohol	22219357	<strong>GluN2B</strong> subunit deletion reveals key role in acute and chronic <b>ethanol</b> sensitivity of glutamate synapses in bed nucleus of the stria terminalis.
+GRIN2B	drug	alcohol	22219357	Thus, we use a conditional <strong>GluN2B</strong> KO mouse line to assess both basal and <b>ethanol</b> dependent function of this subunit at glutamate synapses in the BNST.
+GRIN2B	drug	alcohol	22219357	Deletion of <strong>GluN2B</strong> eliminated LTP, as well as actions of <b>ethanol</b> on NMDAR function.
+GRIN2B	drug	alcohol	22219357	These findings demonstrate that <strong>GluN2B</strong> is a key point of regulation for <b>ethanol</b>'s actions and suggest a unique role of extrasynaptic <strong>GluN2B</strong> containing receptors in facilitating LTP.
+GRIN2B	drug	opioid	22084102	Accordingly, blocking <strong>NR2B</strong> before reinstating <b>heroin</b> seeking prevented the induction of LTP like changes in spine remodeling and synaptic strength, and inhibited <b>heroin</b> relapse.
+GRIN2B	addiction	relapse	22084102	Accordingly, blocking <strong>NR2B</strong> before reinstating heroin <b>seeking</b> prevented the induction of LTP like changes in spine remodeling and synaptic strength, and inhibited heroin <b>relapse</b>.
+GRIN2B	drug	opioid	22084102	These data show that LTP like neuroplasticity in prefrontal accumbens synapses is initiated by <strong>NR2B</strong> stimulation and strongly contributes to <b>heroin</b> relapse.
+GRIN2B	addiction	relapse	22084102	These data show that LTP like neuroplasticity in prefrontal accumbens synapses is initiated by <strong>NR2B</strong> stimulation and strongly contributes to heroin <b>relapse</b>.
+GRIN2B	drug	opioid	22084102	Moreover, the data reveal <strong>NR2B</strong> containing NMDA receptors as a previously unexplored therapeutic target for treating <b>heroin</b> addiction.
+GRIN2B	addiction	addiction	22084102	Moreover, the data reveal <strong>NR2B</strong> containing NMDA receptors as a previously unexplored therapeutic target for treating heroin <b>addiction</b>.
+GRIN2B	drug	alcohol	22037411	Behavioral deficits and cellular damage following developmental <b>ethanol</b> exposure in rats are attenuated by CP 101,606, an NMDAR antagonist with unique <strong>NR2B</strong> specificity.
+GRIN2B	addiction	withdrawal	22037411	Previous studies suggest that both neuronal cell death and some of the behavioral deficits can be reduced by NMDAR antagonism during <b>withdrawal</b>, including antagonism of a subpopulation of receptors containing <strong>NR2B</strong> subunits.
+GRIN2B	drug	alcohol	22037411	Our findings show that CP 101,606, a drug that blocks the <strong>NR2B</strong>/2B receptor, can reduce some of the damaging effects of "3rd trimester" <b>alcohol</b> exposure in our rodent model.
+GRIN2B	drug	alcohol	21985328	The NMDA receptor is a major target of <b>ethanol</b> in the brain, and accumulating evidence suggests that Fyn mediates the effects of <b>ethanol</b> by regulating the phosphorylation of <strong>GluN2B</strong> NMDA receptor subunits.
+GRIN2B	drug	alcohol	21985328	Furthermore, Fyn has been shown to regulate <b>alcohol</b> withdrawal and acute tolerance to <b>ethanol</b> through a <strong>GluN2B</strong> dependent mechanism.
+GRIN2B	addiction	withdrawal	21985328	Furthermore, Fyn has been shown to regulate alcohol <b>withdrawal</b> and acute tolerance to ethanol through a <strong>GluN2B</strong> dependent mechanism.
+GRIN2B	drug	alcohol	21945132	This provides evidence of the effects of altered levels of NR1 expression on <b>ethanol</b> withdrawal and consumption, and suggests that concomitant changes in the levels of <strong>NR2B</strong> may contribute to that effect.
+GRIN2B	addiction	withdrawal	21945132	This provides evidence of the effects of altered levels of NR1 expression on ethanol <b>withdrawal</b> and consumption, and suggests that concomitant changes in the levels of <strong>NR2B</strong> may contribute to that effect.
+GRIN2B	drug	alcohol	21886913	<b>Ethanol</b> withdrawal increased N methyl D aspartate (NMDA) evoked neuronal death, probably by altering the ratio between GluN2A and <strong>GluN2B</strong> NMDA receptor subunits.
+GRIN2B	addiction	withdrawal	21886913	Ethanol <b>withdrawal</b> increased N methyl D aspartate (NMDA) evoked neuronal death, probably by altering the ratio between GluN2A and <strong>GluN2B</strong> NMDA receptor subunits.
+GRIN2B	drug	opioid	21861871	Western blot and RT PCR analysis showed that the levels of protein and mRNA of NMDA receptor NR1 and <strong>NR2B</strong> subunits were significantly higher in the lumbar spinal cords of rats (p14) exposed to prenatal <b>morphine</b>; the co administration of DM could reverse the effect of <b>morphine</b> on NR1 and attenuate the effect on <strong>NR2B</strong>.
+GRIN2B	drug	alcohol	21814037	Histone H3K9 modifications are a local chromatin event involved in <b>ethanol</b> induced neuroadaptation of the <strong>NR2B</strong> gene.
+GRIN2B	drug	alcohol	21814037	Expression of the NMDA receptor 2B (<strong>NR2B</strong>) gene is upregulated following chronic intermittent <b>ethanol</b> (CIE) treatment and withdrawal, which underlies behavioral alterations in addiction.
+GRIN2B	addiction	addiction	21814037	Expression of the NMDA receptor 2B (<strong>NR2B</strong>) gene is upregulated following chronic intermittent ethanol (CIE) treatment and withdrawal, which underlies behavioral alterations in <b>addiction</b>.
+GRIN2B	addiction	withdrawal	21814037	Expression of the NMDA receptor 2B (<strong>NR2B</strong>) gene is upregulated following chronic intermittent ethanol (CIE) treatment and <b>withdrawal</b>, which underlies behavioral alterations in addiction.
+GRIN2B	drug	alcohol	21814037	To investigate the involvement of histone acetylation in the effect of <b>ethanol</b> on the <strong>NR2B</strong> gene, we examined the influence of CIE on histone acetylation in the 5' regulatory region of <strong>NR2B</strong> using a qChIP assay.
+GRIN2B	drug	alcohol	21814037	Taken together, the findings suggest a mechanism where the changes in H3K9 modifications in the local chromatin of the <strong>NR2B</strong> gene underlie <b>alcohol</b> induced neuroadaptation.
+GRIN2B	drug	cocaine	21632938	Using a combination of viral vector mediated genetic manipulations, biochemistry, and electrophysiology in a locomotor sensitization paradigm with repeated, daily, noncontingent <b>cocaine</b> (15 mg/kg) injections, we show that dominant negative cAMP element binding protein (CREB) prevents <b>cocaine</b> induced generation of silent synapses of young (30 d old) rats, whereas constitutively active CREB is sufficient to increase the number of <strong>NR2B</strong> containing NMDA receptors (NMDARs) at synapses and to generate silent synapses.
+GRIN2B	addiction	sensitization	21632938	Using a combination of viral vector mediated genetic manipulations, biochemistry, and electrophysiology in a locomotor <b>sensitization</b> paradigm with repeated, daily, noncontingent cocaine (15 mg/kg) injections, we show that dominant negative cAMP element binding protein (CREB) prevents cocaine induced generation of silent synapses of young (30 d old) rats, whereas constitutively active CREB is sufficient to increase the number of <strong>NR2B</strong> containing NMDA receptors (NMDARs) at synapses and to generate silent synapses.
+GRIN2B	drug	cocaine	21632938	Blockade of <strong>NR2B</strong> containing NMDARs by administration of the <strong>NR2B</strong> selective antagonist Ro256981 directly into the NAc, under conditions that inhibit <b>cocaine</b> induced silent synapses, prevents the development of <b>cocaine</b> elicited locomotor sensitization.
+GRIN2B	addiction	sensitization	21632938	Blockade of <strong>NR2B</strong> containing NMDARs by administration of the <strong>NR2B</strong> selective antagonist Ro256981 directly into the NAc, under conditions that inhibit cocaine induced silent synapses, prevents the development of cocaine elicited locomotor <b>sensitization</b>.
+GRIN2B	drug	cocaine	21632938	Our data are consistent with a cellular cascade whereby <b>cocaine</b> induced activation of CREB promotes CREB dependent transcription of <strong>NR2B</strong> and synaptic incorporation of <strong>NR2B</strong> containing NMDARs, which generates new silent synapses within the NAc.
+GRIN2B	drug	alcohol	21615425	Ex vivo or in vivo <b>ethanol</b> exposure and withdrawal causes a long lasting increase in <strong>NR2B</strong> subunit containing NMDA receptor activity in the DMS, contributing to <b>ethanol</b> drinking.
+GRIN2B	addiction	withdrawal	21615425	Ex vivo or in vivo ethanol exposure and <b>withdrawal</b> causes a long lasting increase in <strong>NR2B</strong> subunit containing NMDA receptor activity in the DMS, contributing to ethanol drinking.
+GRIN2B	drug	alcohol	21615425	Analyses of neuronal activation associated with <b>alcohol</b> withdrawal and site directed lesions in mice implicate the rostroventral caudate putamen, a ventrolateral segment of the DMS, in genetically determined differences in risk for <b>alcohol</b> withdrawal involved in physical association of the multi PDZ domain protein, MPDZ, with 5 HT(2C) receptors and/or <strong>NR2B</strong>.
+GRIN2B	addiction	withdrawal	21615425	Analyses of neuronal activation associated with alcohol <b>withdrawal</b> and site directed lesions in mice implicate the rostroventral caudate putamen, a ventrolateral segment of the DMS, in genetically determined differences in risk for alcohol <b>withdrawal</b> involved in physical association of the multi PDZ domain protein, MPDZ, with 5 HT(2C) receptors and/or <strong>NR2B</strong>.
+GRIN2B	drug	psychedelics	21606828	<b>Ketamine</b>, its active metabolite norketamine, and the <strong>NR2B</strong> selective antagonist traxoprodil (CP 101,606) were tested in rat models of acute antinociception (paw withdrawal response to heat) and chronic neuropathic pain (spared nerve injury).
+GRIN2B	addiction	withdrawal	21606828	Ketamine, its active metabolite norketamine, and the <strong>NR2B</strong> selective antagonist traxoprodil (CP 101,606) were tested in rat models of acute antinociception (paw <b>withdrawal</b> response to heat) and chronic neuropathic pain (spared nerve injury).
+GRIN2B	drug	opioid	21601998	<strong>NR2B</strong> subunit of NMDA receptor at nucleus accumbens is involved in <b>morphine</b> rewarding effect by siRNA study.
+GRIN2B	drug	opioid	21601998	In this study, we further investigate the role of the <strong>NR2B</strong> subunit of NMDA receptors at NAc or VTA in <b>morphine</b> rewarding effects and behavioral sensitization.
+GRIN2B	addiction	sensitization	21601998	In this study, we further investigate the role of the <strong>NR2B</strong> subunit of NMDA receptors at NAc or VTA in morphine rewarding effects and behavioral <b>sensitization</b>.
+GRIN2B	drug	opioid	21601998	Results showed that <b>morphine</b> induced rewarding behavior but not behavioral sensitization was abolished when the <strong>NR2B</strong> subunit of NMDA receptors at the NAc were significantly decreased.
+GRIN2B	addiction	sensitization	21601998	Results showed that morphine induced rewarding behavior but not behavioral <b>sensitization</b> was abolished when the <strong>NR2B</strong> subunit of NMDA receptors at the NAc were significantly decreased.
+GRIN2B	drug	opioid	21601998	These findings suggest that the <strong>NR2B</strong> subunit of NMDA receptors at the NAc is involved in <b>morphine</b> induced rewarding effect and may not be through directly interacting with dopamine neurons.
+GRIN2B	drug	cannabinoid	21519057	In the present study, we also tested the <b>cannabinoid</b> effect on the expression of <strong>NR2B</strong>.
+GRIN2B	drug	cannabinoid	21519057	These data indicated that intrathecal administration of <b>cannabinoid</b> receptor agonists might relieve cancer pain, probably by reducing <strong>NR2B</strong> dependent activity in the spinal cord.
+GRIN2B	drug	alcohol	21352242	Effect of the selective NMDA <strong>NR2B</strong> antagonist, ifenprodil, on acute tolerance to <b>ethanol</b> induced motor impairment in adolescent and adult rats.
+GRIN2B	drug	alcohol	21352242	This study explored the role of NMDA <strong>NR2B</strong> receptors in the development of acute tolerance to <b>ethanol</b> induced motor impairment in male adolescent [postnatal day (P)28 30] and adult (P68 70) Sprague Dawley rats.
+GRIN2B	drug	benzodiazepine	21277878	Importantly, the reduced inhibition also operated to enhance NMDARs functions after peripheral inflammation, because spinal injection of <b>diazepam</b> to rescue the inhibition in inflamed mice greatly depressed PKA phosphorylation of NR1 S897, reduced the synaptic concentration of NR1/<strong>NR2B</strong> and meanwhile, alleviated the inflammatory pain.
+GRIN2B	drug	cocaine	21232547	Furthermore, because <b>cocaine</b> generated silent synapses are enriched in NMDARs containing the <strong>NR2B</strong> subunit, the enhanced <strong>NR2B</strong> signaling may set up a selective recruitment of certain types of AMPARs.
+GRIN2B	drug	opioid	21152977	In the present study, the role of N methyl D aspartate (NMDA) receptors, particularly those containing <strong>NR2B</strong> subunits, in <b>morphine</b> induced conditioned place preference (CPP) and Morris water maze (MWM) learning and memory task was investigated.
+GRIN2B	addiction	reward	21152977	In the present study, the role of N methyl D aspartate (NMDA) receptors, particularly those containing <strong>NR2B</strong> subunits, in morphine induced conditioned place preference (<b>CPP</b>) and Morris water maze (MWM) learning and memory task was investigated.
+GRIN2B	drug	opioid	21152977	We found that ifenprodil, an antagonist highly selective for <strong>NR2B</strong> containing NMDA receptors, dose dependently blocked the development, maintenance and reinstatement of <b>morphine</b> induced CPP, without evident impairment of the acquisition and retrieval of spatial memory in the MWM task.
+GRIN2B	addiction	relapse	21152977	We found that ifenprodil, an antagonist highly selective for <strong>NR2B</strong> containing NMDA receptors, dose dependently blocked the development, maintenance and <b>reinstatement</b> of morphine induced CPP, without evident impairment of the acquisition and retrieval of spatial memory in the MWM task.
+GRIN2B	addiction	reward	21152977	We found that ifenprodil, an antagonist highly selective for <strong>NR2B</strong> containing NMDA receptors, dose dependently blocked the development, maintenance and reinstatement of morphine induced <b>CPP</b>, without evident impairment of the acquisition and retrieval of spatial memory in the MWM task.
+GRIN2B	drug	opioid	21152977	These results clearly demonstrate that <strong>NR2B</strong> containing NMDA receptors are actively involved in addiction memory induced by <b>morphine</b> conditioning, but not in the acquisition and retrieval of spatial learning and memory.
+GRIN2B	addiction	addiction	21152977	These results clearly demonstrate that <strong>NR2B</strong> containing NMDA receptors are actively involved in <b>addiction</b> memory induced by morphine conditioning, but not in the acquisition and retrieval of spatial learning and memory.
+GRIN2B	addiction	addiction	21152977	In conclusion, <strong>NR2B</strong> containing NMDA receptors can be considered potential targets for the treatment of opiate <b>addiction</b>.
+GRIN2B	drug	cocaine	21055728	Cyclic adenosine monophosphate independent tyrosine phosphorylation of <strong>NR2B</strong> mediates <b>cocaine</b> induced extracellular signal regulated kinase activation.
+GRIN2B	drug	cocaine	21055728	We also demonstrate that the D1R/Src family kinases/<strong>NR2B</strong> pathway is responsible for ERK activation by <b>cocaine</b> in vivo.
+GRIN2B	drug	cocaine	21055728	Our results show that potentiation of <strong>NR2B</strong> containing NMDAR by D1R is necessary and sufficient to trigger <b>cocaine</b> induced ERK activation.
+GRIN2B	drug	alcohol	20947635	These observations demonstrate that 1) accumbal synaptic depression is mediated by <strong>NR2B</strong> receptors, 2) accumbal synaptic depression is highly sensitive to both acute and chronic <b>ethanol</b> exposure, and 3) alterations in this synaptic process may constitute a neural adaptation that contributes to the induction and/or expression of <b>ethanol</b> dependence.
+GRIN2B	addiction	dependence	20947635	These observations demonstrate that 1) accumbal synaptic depression is mediated by <strong>NR2B</strong> receptors, 2) accumbal synaptic depression is highly sensitive to both acute and chronic ethanol exposure, and 3) alterations in this synaptic process may constitute a neural adaptation that contributes to the induction and/or expression of ethanol <b>dependence</b>.
+GRIN2B	drug	benzodiazepine	20935233	Down regulation of synaptic <strong>GluN2B</strong> subunit containing N methyl D aspartate receptors: a physiological brake on CA1 neuron α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid hyperexcitability during <b>benzodiazepine</b> withdrawal.
+GRIN2B	addiction	withdrawal	20935233	Down regulation of synaptic <strong>GluN2B</strong> subunit containing N methyl D aspartate receptors: a physiological brake on CA1 neuron α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid hyperexcitability during benzodiazepine <b>withdrawal</b>.
+GRIN2B	drug	benzodiazepine	20935233	Collectively, these findings suggest that a reduction of <strong>GluN2B</strong> containing NMDAR may serve as a homeostatic feedback mechanism to modulate glutamatergic synaptic strength during FZP withdrawal to alleviate <b>benzodiazepine</b> withdrawal symptoms.
+GRIN2B	addiction	withdrawal	20935233	Collectively, these findings suggest that a reduction of <strong>GluN2B</strong> containing NMDAR may serve as a homeostatic feedback mechanism to modulate glutamatergic synaptic strength during FZP <b>withdrawal</b> to alleviate benzodiazepine <b>withdrawal</b> symptoms.
+GRIN2B	drug	opioid	20869946	It is concluded that <b>morphine</b> does not affect the neurosteroid modulatory effect on ifenprodil binding in the rat hippocampus or hypothalamus but does significantly affect both the expression of the <strong>NR2B</strong> subunit and the 3α5βS modulatory effect on ifenprodil binding in the frontal cortex.
+GRIN2B	drug	opioid	20869946	It is suggested that the observed effect of long term <b>morphine</b> on the properties of <strong>NR2B</strong> in the frontal cortex may be associated with the mechanism underlying the development of opiate dependence.
+GRIN2B	addiction	dependence	20869946	It is suggested that the observed effect of long term morphine on the properties of <strong>NR2B</strong> in the frontal cortex may be associated with the mechanism underlying the development of opiate <b>dependence</b>.
+GRIN2B	drug	benzodiazepine	20853509	Immunogold electron microscopic evidence of differential regulation of GluN1, GluN2A, and <strong>GluN2B</strong>, NMDA type glutamate receptor subunits in rat hippocampal CA1 synapses during <b>benzodiazepine</b> withdrawal.
+GRIN2B	addiction	withdrawal	20853509	Immunogold electron microscopic evidence of differential regulation of GluN1, GluN2A, and <strong>GluN2B</strong>, NMDA type glutamate receptor subunits in rat hippocampal CA1 synapses during benzodiazepine <b>withdrawal</b>.
+GRIN2B	drug	benzodiazepine	20853509	Therefore, in this study ultrastructural evidence for possible reductions in NMDAR GluN1, GluN2A, and <strong>GluN2B</strong> subunits was sought at CA1 stratum radiatum synapses in proximal dendrites using postembedding immunogold labeling of tissues from rats withdrawn for 2 days from 1 week daily oral administration of the <b>benzodiazepine</b>, <b>flurazepam</b> (FZP).
+GRIN2B	addiction	withdrawal	20853509	Similar decreases were observed for <strong>GluN2B</strong> subunits; however, the relative lateral distribution of <strong>GluN2B</strong> immunolabeling within the postsynaptic density did not change after BZ <b>withdrawal</b>.
+GRIN2B	addiction	withdrawal	20853509	The data therefore provide direct evidence for reduced synaptic GluN1/<strong>GluN2B</strong> receptors and preservation of GluN1/GluN2A receptors in the CA1 stratum radiatum region during BZ <b>withdrawal</b>.
+GRIN2B	drug	alcohol	20831600	This resistance occurred without an increase in the NMDAR subunit expression but was associated with decreases in the levels of phospho Y 1472 <strong>NR2B</strong>, increases in the levels of STEP33, increases in phospho p38 mitogen activated protein kinase (pp38 MAPK), and acquisition of tolerance to the sedative effects of <b>ethanol</b>.
+GRIN2B	drug	alcohol	20668202	Long lasting adaptations of the <strong>NR2B</strong> containing NMDA receptors in the dorsomedial striatum play a crucial role in <b>alcohol</b> consumption and relapse.
+GRIN2B	addiction	relapse	20668202	Long lasting adaptations of the <strong>NR2B</strong> containing NMDA receptors in the dorsomedial striatum play a crucial role in alcohol consumption and <b>relapse</b>.
+GRIN2B	drug	alcohol	20668202	We previously observed that ex vivo acute exposure of the dorsal striatum to, and withdrawal from, <b>alcohol</b> induces long term facilitation (LTF) of the activity of <strong>NR2B</strong> containing NMDA receptors (<strong>NR2B</strong> NMDARs) in a mechanism that requires the Src family protein tyrosine kinase (PTK), Fyn (Wang et al., 2007).
+GRIN2B	addiction	withdrawal	20668202	We previously observed that ex vivo acute exposure of the dorsal striatum to, and <b>withdrawal</b> from, alcohol induces long term facilitation (LTF) of the activity of <strong>NR2B</strong> containing NMDA receptors (<strong>NR2B</strong> NMDARs) in a mechanism that requires the Src family protein tyrosine kinase (PTK), Fyn (Wang et al., 2007).
+GRIN2B	drug	alcohol	20668202	We found that <b>alcohol</b> mediated induction of LTF of <strong>NR2B</strong> NMDAR activity is centered in the DMS.
+GRIN2B	drug	alcohol	20668202	We observed that repeated daily administration of <b>alcohol</b> results in a long lasting increase in the activity of the <strong>NR2B</strong> NMDARs in the DMS.
+GRIN2B	drug	alcohol	20668202	Finally, we show that inhibition of <strong>NR2B</strong> NMDARs or Src family PTKs in the DMS, but not in the DLS, significantly decreases operant self administration of <b>alcohol</b> and reduces <b>alcohol</b> priming induced reinstatement of <b>alcohol</b> seeking.
+GRIN2B	addiction	relapse	20668202	Finally, we show that inhibition of <strong>NR2B</strong> NMDARs or Src family PTKs in the DMS, but not in the DLS, significantly decreases operant self administration of alcohol and reduces alcohol priming induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+GRIN2B	addiction	reward	20668202	Finally, we show that inhibition of <strong>NR2B</strong> NMDARs or Src family PTKs in the DMS, but not in the DLS, significantly decreases <b>operant</b> self administration of alcohol and reduces alcohol priming induced reinstatement of alcohol seeking.
+GRIN2B	drug	alcohol	20668202	Our results suggest that the upregulation of <strong>NR2B</strong> NMDAR activity within the DMS by <b>alcohol</b> contributes to the maladaptive synaptic changes that lead to excessive <b>alcohol</b> intake and relapse.
+GRIN2B	addiction	relapse	20668202	Our results suggest that the upregulation of <strong>NR2B</strong> NMDAR activity within the DMS by alcohol contributes to the maladaptive synaptic changes that lead to excessive alcohol intake and <b>relapse</b>.
+GRIN2B	drug	amphetamine	20649838	<b>Amphetamine</b> regulates <strong>NR2B</strong> expression in Go2α knockout mice and thereby sustains behavioral sensitization.
+GRIN2B	addiction	sensitization	20649838	Amphetamine regulates <strong>NR2B</strong> expression in Go2α knockout mice and thereby sustains behavioral <b>sensitization</b>.
+GRIN2B	drug	amphetamine	20649838	In this line, repeated <b>amphetamine</b> injections led to a twofold increase in the amount of the NMDA receptor subunit <strong>NR2B</strong> in Go2α /  mice resulting in an enhanced inhibition of the indirect DA pathway.
+GRIN2B	drug	alcohol	20603193	After 2 weeks of <b>ethanol</b> vapor exposure N methyl d aspartate receptor NR1 subunit (NR1), N methyl d aspartate receptor NR2A subunit (NR2A), and N methyl d aspartate receptor <strong>NR2B</strong> subunit (<strong>NR2B</strong>) subunit expression was found to be increased in hippocampus of the adults.
+GRIN2B	drug	alcohol	20603193	In contrast, 2 weeks of <b>ethanol</b> exposure resulted in no significant changes in NR1 and <strong>NR2B</strong> subunits and a reduction NR2A subunit expression in hippocampus in adolescents.
+GRIN2B	drug	alcohol	20603193	In frontal cortex, 2 weeks of chronic <b>ethanol</b> exposure produced decreases in NR1 subunit expression in both adults and adolescents but also produced decreases in NR2A and <strong>NR2B</strong> subunit expression in adults that returned or exceeded control levels by 2 weeks following withdrawal from <b>ethanol</b> vapor.
+GRIN2B	addiction	withdrawal	20603193	In frontal cortex, 2 weeks of chronic ethanol exposure produced decreases in NR1 subunit expression in both adults and adolescents but also produced decreases in NR2A and <strong>NR2B</strong> subunit expression in adults that returned or exceeded control levels by 2 weeks following <b>withdrawal</b> from ethanol vapor.
+GRIN2B	drug	opioid	20519536	<b>Morphine</b> exposure and withdrawal increase phosphorylation of NR1 and <strong>NR2B</strong> receptors, ERK1/2, calmodulin dependent kinase II, and cAMP response element binding proteins; and such phosphorylation is suppressed by either spinal inhibition or targeted mutation of MMP 9.
+GRIN2B	addiction	withdrawal	20519536	Morphine exposure and <b>withdrawal</b> increase phosphorylation of NR1 and <strong>NR2B</strong> receptors, ERK1/2, calmodulin dependent kinase II, and cAMP response element binding proteins; and such phosphorylation is suppressed by either spinal inhibition or targeted mutation of MMP 9.
+GRIN2B	drug	opioid	20519536	Further, spinal administration of exogenous MMP 9 induces <b>morphine</b> withdrawal like behavioral signs and mechanical allodynia, activates NR1 and NR2 receptors, and downregulates integrin beta1, while a function neutralizing antibody against integrin beta1 suppresses MMP 9 induced phosphorylation of NR1 and <strong>NR2B</strong>.
+GRIN2B	addiction	withdrawal	20519536	Further, spinal administration of exogenous MMP 9 induces morphine <b>withdrawal</b> like behavioral signs and mechanical allodynia, activates NR1 and NR2 receptors, and downregulates integrin beta1, while a function neutralizing antibody against integrin beta1 suppresses MMP 9 induced phosphorylation of NR1 and <strong>NR2B</strong>.
+GRIN2B	drug	opioid	20519536	Thus, we hypothesize that spinal MMP 9 may contribute to the development of <b>morphine</b> dependence primarily through neuronal activation and interaction with NR1 and <strong>NR2B</strong> receptors via integrin beta1 and NO pathways.
+GRIN2B	addiction	dependence	20519536	Thus, we hypothesize that spinal MMP 9 may contribute to the development of morphine <b>dependence</b> primarily through neuronal activation and interaction with NR1 and <strong>NR2B</strong> receptors via integrin beta1 and NO pathways.
+GRIN2B	drug	amphetamine	20422365	Rhynchophylline down regulates <strong>NR2B</strong> expression in cortex and hippocampal CA1 area of <b>amphetamine</b> induced conditioned place preference rat.
+GRIN2B	addiction	reward	20422365	N methyl D aspartate receptor 2B subunit (<strong>NR2B</strong>) has an important role in the development of conditioned place preference (<b>CPP</b>) and psychostimulant abuse.
+GRIN2B	drug	amphetamine	20422365	<b>Amphetamine</b> CPP rats showed a significantly increased <strong>NR2B</strong> mRNA and protein expression in medial prefrontal cortex and hippocampal CA1 areas as compared to the control group.
+GRIN2B	addiction	reward	20422365	Amphetamine <b>CPP</b> rats showed a significantly increased <strong>NR2B</strong> mRNA and protein expression in medial prefrontal cortex and hippocampal CA1 areas as compared to the control group.
+GRIN2B	drug	amphetamine	20422365	Rhynchophylline reversed <strong>NR2B</strong> mRNA and protein levels induced by <b>amphetamine</b> but rhynchophylline by itself had no effect on <strong>NR2B</strong> expression in control rats.
+GRIN2B	drug	amphetamine	20422365	These results indicate that rhynchophylline inhibits the expression of <b>amphetamine</b> induced rewarding effect, and this action might be related to down regulation of <strong>NR2B</strong> expression in medial prefrontal cortex and hippocampal CA1 area.
+GRIN2B	drug	alcohol	20098704	We recently reported that NMDA receptor 2B (<strong>NR2B</strong>) gene expression was persistently up regulated following chronic intermittent <b>ethanol</b> (CIE) treatment.
+GRIN2B	addiction	withdrawal	20098704	Analysis of individual CpG methylation sites within the <strong>NR2B</strong> 5'regulatory area revealed three regions with clusters of site specific CpG demethylation following CIE treatment and <b>withdrawal</b>.
+GRIN2B	drug	alcohol	20098704	These results suggest an important role of DNA demethylation in mediating CIE induced <strong>NR2B</strong> gene up regulation, thus implicating a novel molecular site of <b>alcohol</b> action.
+GRIN2B	drug	alcohol	20008487	After chronic <b>ethanol</b> exposure, there was a significant increase in the clustering of NR1 and <strong>NR2B</strong> subunits and their colocalization with the synaptic proteins synaptophysin and postsynaptic density protein 95, respectively.
+GRIN2B	drug	alcohol	20008487	Receptor removal from the synapse during <b>ethanol</b> withdrawal was associated with changes in the phosphorylation state of <strong>NR2B</strong> Ser1480, controlled by the protein kinase CK2.
+GRIN2B	addiction	withdrawal	20008487	Receptor removal from the synapse during ethanol <b>withdrawal</b> was associated with changes in the phosphorylation state of <strong>NR2B</strong> Ser1480, controlled by the protein kinase CK2.
+GRIN2B	drug	cocaine	19607791	Furthermore, this <b>cocaine</b> induced generation of silent synapses is mediated by membrane insertions of new, <strong>NR2B</strong> containing N methyl D aspartic acid receptors (NMDARs).
+GRIN2B	drug	cocaine	19524640	We found that inhibition of NR2A containing NMDARs by NVP AAM077, or <strong>NR2B</strong> containing receptors by ifenprodil, blocked <b>cocaine</b> induced increase in the AMPAR/NMDAR currents ratio, a measure of long term potentiation (LTP) in vivo, in VTA neurons 24h following a single <b>cocaine</b> injection.
+GRIN2B	drug	cocaine	19474322	Here, we show that repeated noncontingent <b>cocaine</b> injections increased NAc NMDAR subunits, NR1, NR2A, and <strong>NR2B</strong> 21 d, but not 1 d, after withdrawal from <b>cocaine</b>.
+GRIN2B	addiction	withdrawal	19474322	Here, we show that repeated noncontingent cocaine injections increased NAc NMDAR subunits, NR1, NR2A, and <strong>NR2B</strong> 21 d, but not 1 d, after <b>withdrawal</b> from cocaine.
+GRIN2B	drug	cocaine	19474322	Furthermore, the increase in GluR1 and ERK activity was blocked after inhibition of <strong>NR2B</strong> containing NMDAR during the development of <b>cocaine</b> psychomotor sensitization or when the MEK (mitogen activated protein/ERK kinase) inhibitor was microinjected into the NAc 21 d after withdrawal from <b>cocaine</b>.
+GRIN2B	addiction	sensitization	19474322	Furthermore, the increase in GluR1 and ERK activity was blocked after inhibition of <strong>NR2B</strong> containing NMDAR during the development of cocaine psychomotor <b>sensitization</b> or when the MEK (mitogen activated protein/ERK kinase) inhibitor was microinjected into the NAc 21 d after withdrawal from cocaine.
+GRIN2B	addiction	withdrawal	19474322	Furthermore, the increase in GluR1 and ERK activity was blocked after inhibition of <strong>NR2B</strong> containing NMDAR during the development of cocaine psychomotor sensitization or when the MEK (mitogen activated protein/ERK kinase) inhibitor was microinjected into the NAc 21 d after <b>withdrawal</b> from cocaine.
+GRIN2B	drug	psychedelics	19421743	Three distinct patterns of antagonist effect were evident from the VI assays used: a uniform decrease in responding produced by (S) (+) <b>ketamine</b>, memantine and NVP AAM077, a uniform increase in responding caused by the <strong>NR2B</strong> subunit preferring antagonists Ro 25 6981 and CP 101 606, and variable bidirectional effects of PCP, SDZ 220,581 and MK 801.
+GRIN2B	drug	alcohol	19350219	N methyl D aspartate 2b receptor subtype (<strong>NR2B</strong>) promoter methylation in patients during <b>alcohol</b> withdrawal.
+GRIN2B	addiction	withdrawal	19350219	N methyl D aspartate 2b receptor subtype (<strong>NR2B</strong>) promoter methylation in patients during alcohol <b>withdrawal</b>.
+GRIN2B	drug	alcohol	19350219	NMDA receptors and especially the <strong>NR2B</strong> receptor subtype play a crucial role during chronic <b>ethanol</b> consumption and <b>alcohol</b> withdrawal.
+GRIN2B	addiction	withdrawal	19350219	NMDA receptors and especially the <strong>NR2B</strong> receptor subtype play a crucial role during chronic ethanol consumption and alcohol <b>withdrawal</b>.
+GRIN2B	drug	alcohol	19350219	Therefore, the <strong>NR2B</strong> receptor subtype expression in peripheral blood cells of 32 male patients suffering from <b>alcohol</b> dependency were assessed through quantitative RT PCR and to explore regulating epigenetic mechanisms, a methylation analysis was conducted using bisulfite sequencing of a fragment of the <strong>NR2B</strong> promoter region.
+GRIN2B	addiction	withdrawal	19350219	The expression of the <strong>NR2B</strong> receptor increased significantly during the first 24 h of <b>withdrawal</b> treatment (day 1; t = 4.1, P = 0.001), and also on and day 3 (t = 2.4; P = 0.029).
+GRIN2B	drug	alcohol	19350219	The severity of <b>alcohol</b> drinking pattern, measured by lifetime drinking and daily <b>ethanol</b> intake, was negatively correlated with the methylation of a defined cluster of five CPG sites within the <strong>NR2B</strong> promoter (lifetime drinking: Spearman's rho =  0.55; P = 0.013; daily <b>ethanol</b> intake: rho =  0.46; P = 0.043).
+GRIN2B	drug	amphetamine	19349975	We examined the turnover and trafficking of NMDA receptors and found that chronic exposure to the psychostimulant <b>amphetamine</b> (<b>AMPH</b>) induced selective downregulation of NMDA receptor <strong>NR2B</strong> subunits in the confined surface membrane pool of rat striatal neurons at synaptic sites.
+GRIN2B	drug	amphetamine	19349975	Behaviorally, genetic disruption of <strong>NR2B</strong> induced and restoration of <strong>NR2B</strong> loss prevented behavioral sensitization to <b>AMPH</b>.
+GRIN2B	addiction	sensitization	19349975	Behaviorally, genetic disruption of <strong>NR2B</strong> induced and restoration of <strong>NR2B</strong> loss prevented behavioral <b>sensitization</b> to AMPH.
+GRIN2B	drug	amphetamine	19349975	Our data identify <strong>NR2B</strong> as an important regulator in the remodeling of excitatory synapses and persistent psychomotor plasticity in response to <b>AMPH</b>.
+GRIN2B	drug	cocaine	19306440	In contrast, extended access to <b>cocaine</b> resulted in distinct and long lasting alterations of protein expression within the mPFC that included: increased levels of Homer1b/c at 1 day, <strong>NR2b</strong> at 14 days, and NR2a at 60 days, of withdrawal.
+GRIN2B	addiction	withdrawal	19306440	In contrast, extended access to cocaine resulted in distinct and long lasting alterations of protein expression within the mPFC that included: increased levels of Homer1b/c at 1 day, <strong>NR2b</strong> at 14 days, and NR2a at 60 days, of <b>withdrawal</b>.
+GRIN2B	drug	alcohol	19077056	Repeated <b>ethanol</b> administration also down regulates the expression of DRD2 and <strong>NMDAR2B</strong> phosphorylation in prefrontal cortex of adolescent animals, but not of adult rats.
+GRIN2B	drug	cocaine	19046409	Here we show that application of <b>cocaine</b> both in slices and in vivo induced an increase in tyrosine phosphorylation of the NR2A, but not the <strong>NR2B</strong> subunit of the NMDAR in juvenile rats.
+GRIN2B	drug	cocaine	19046409	<b>Cocaine</b> induced an increase in the activity of both Fyn and Src kinases, and the Src protein tyrosine kinase (Src PTKs) inhibitor, 4 amino 5 (4 chlorophenyl) 7 (t butyl)pyrazolo[3,4 d]pyrimidine (PP2), abolished both <b>cocaine</b> induced increase in tyrosine phosphorylation of the NR2A subunit and the increase in the expression of NR1, NR2A, and <strong>NR2B</strong> in the VTA.
+GRIN2B	drug	opioid	18851757	Distinct expression of synaptic NR2A and <strong>NR2B</strong> in the central nervous system and impaired <b>morphine</b> tolerance and physical dependence in mice deficient in postsynaptic density 93 protein.
+GRIN2B	addiction	dependence	18851757	Distinct expression of synaptic NR2A and <strong>NR2B</strong> in the central nervous system and impaired morphine tolerance and physical <b>dependence</b> in mice deficient in postsynaptic density 93 protein.
+GRIN2B	drug	opioid	18851757	These findings indicate that impaired NMDAR dependent neuronal plasticity following repeated <b>morphine</b> injection in PSD 93 knockout mice is attributed to PSD 93 deletion induced alterations of synaptic NR2A and <strong>NR2B</strong> expression in dorsal horn and forebrain cortex neurons.
+GRIN2B	drug	alcohol	18849153	Fyn tyrosine kinase is a member of the Scr family that phosphorylates the NR2A and <strong>NR2B</strong> subunits of the NMDA receptors reducing the inhibitory effects of <b>ethanol</b> and therefore may regulate the individual sensitivity to <b>ethanol</b>.
+GRIN2B	drug	opioid	18803856	Cingulate NMDA <strong>NR2B</strong> receptors contribute to <b>morphine</b> induced analgesic tolerance.
+GRIN2B	drug	opioid	18803856	In this study, Ro 256981, an antagonist of the NMDA receptor subunit <strong>NR2B</strong>, was used to reduce the expression of analgesic tolerance to <b>morphine</b>.
+GRIN2B	drug	opioid	18803856	Since NMDA <strong>NR2B</strong> receptors in the anterior cingulate cortex (ACC) play roles in the establishment of LTP and fear memory, we explored their role in changes that occur in this region after chronic <b>morphine</b>.
+GRIN2B	drug	opioid	18803856	Both systemic and intra ACC inhibition of <strong>NR2B</strong> in <b>morphine</b> tolerant animals inhibited the expression of analgesic tolerance.
+GRIN2B	drug	opioid	18803856	This study suggests that selective inhibition of NMDA <strong>NR2B</strong> receptors may prove useful in combating the development of analgesic tolerance to <b>morphine</b> and proposes a novel role for the ACC in <b>opioid</b> tolerance and <b>morphine</b> induced changes in synaptic plasticity.
+GRIN2B	drug	opioid	18772347	Chronic <b>morphine</b> exposure and withdrawal significantly increased phosphorylation of N methyl D aspartate receptor subunit <strong>NR2B</strong> as well as the activated forms of extracellular signal regulated kinase and the cAMP response element binding protein in SC.
+GRIN2B	addiction	withdrawal	18772347	Chronic morphine exposure and <b>withdrawal</b> significantly increased phosphorylation of N methyl D aspartate receptor subunit <strong>NR2B</strong> as well as the activated forms of extracellular signal regulated kinase and the cAMP response element binding protein in SC.
+GRIN2B	drug	opioid	18772347	These findings indicate that EphB receptor signaling, probably by interacting with <strong>NR2B</strong> in SC, contributes to the development of <b>opioid</b> physical dependence and withdrawal effects.
+GRIN2B	addiction	dependence	18772347	These findings indicate that EphB receptor signaling, probably by interacting with <strong>NR2B</strong> in SC, contributes to the development of opioid physical <b>dependence</b> and withdrawal effects.
+GRIN2B	addiction	withdrawal	18772347	These findings indicate that EphB receptor signaling, probably by interacting with <strong>NR2B</strong> in SC, contributes to the development of opioid physical dependence and <b>withdrawal</b> effects.
+GRIN2B	drug	alcohol	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and <strong>NR2B</strong>; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with <b>alcohol</b> dependence using multivariate statistical analysis.
+GRIN2B	addiction	dependence	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and <strong>NR2B</strong>; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with alcohol <b>dependence</b> using multivariate statistical analysis.
+GRIN2B	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and <strong>NR2B</strong>), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRIN2B	drug	alcohol	18369402	Especially, the expression of the <strong>NR2B</strong> and certain splice variant forms of the NR1 subunits were increased in primary neuronal cultures treated intermittently with <b>ethanol</b>.
+GRIN2B	drug	alcohol	18369402	In accordance with these changes, the inhibitory potential of <strong>NR2B</strong> subunit selective NMDAR antagonists is also increased, demonstrating excellent potency against <b>alcohol</b> withdrawal induced in vitro cytotoxicity.
+GRIN2B	addiction	withdrawal	18369402	In accordance with these changes, the inhibitory potential of <strong>NR2B</strong> subunit selective NMDAR antagonists is also increased, demonstrating excellent potency against alcohol <b>withdrawal</b> induced in vitro cytotoxicity.
+GRIN2B	drug	alcohol	18369402	Although in vivo data are few with these compounds, according to the effectiveness of the classic NMDAR antagonists in attenuation, not only the physical symptoms, but also some affective and motivational components of <b>alcohol</b> withdrawal, novel <strong>NR2B</strong> subunit selective NMDAR antagonists may offer a preferable alternative in the pharmacotherapy of <b>alcohol</b> dependence.
+GRIN2B	addiction	dependence	18369402	Although in vivo data are few with these compounds, according to the effectiveness of the classic NMDAR antagonists in attenuation, not only the physical symptoms, but also some affective and motivational components of alcohol withdrawal, novel <strong>NR2B</strong> subunit selective NMDAR antagonists may offer a preferable alternative in the pharmacotherapy of alcohol <b>dependence</b>.
+GRIN2B	addiction	withdrawal	18369402	Although in vivo data are few with these compounds, according to the effectiveness of the classic NMDAR antagonists in attenuation, not only the physical symptoms, but also some affective and motivational components of alcohol <b>withdrawal</b>, novel <strong>NR2B</strong> subunit selective NMDAR antagonists may offer a preferable alternative in the pharmacotherapy of alcohol dependence.
+GRIN2B	drug	alcohol	18358639	The relative mRNA expression of exon 5 inclusion/exclusion variants of the NR1 subunit, and the relative expression of NR2A, <strong>NR2B</strong> and NR2C subunits was examined in rats subjected to long term free choice, <b>alcohol</b> self administration with repeated <b>alcohol</b> deprivation phases.
+GRIN2B	drug	alcohol	17982573	These observations led us to propose a molecular model for <b>ethanol</b> induced plasticity at excitatory synapses in which increases in <strong>NR2B</strong> containing NMDA receptors and PSD 95 at the PSD provide an expanded scaffolding platform for the recruitment and activation of signaling molecules that regulate spine actin dynamics, protein translation, and synaptic plasticity.
+GRIN2B	drug	cocaine	17950706	In both species, withdrawal from repeated <b>cocaine</b> administration down regulated Homer1b/c and Homer2a/b within the shell, but not the core, of the nucleus accumbens (NAC), and the reduced Homer levels were accompanied by decreases in mGluR1a, NR2a and <strong>NR2b</strong>.
+GRIN2B	addiction	withdrawal	17950706	In both species, <b>withdrawal</b> from repeated cocaine administration down regulated Homer1b/c and Homer2a/b within the shell, but not the core, of the nucleus accumbens (NAC), and the reduced Homer levels were accompanied by decreases in mGluR1a, NR2a and <strong>NR2b</strong>.
+GRIN2B	drug	cocaine	17950706	In the PFC, repeated <b>cocaine</b> up regulated Homer2a/b, mGluR1 and <strong>NR2b</strong> expression, without affecting Homer1b/c levels.
+GRIN2B	drug	amphetamine	17651730	Western blot analysis of the caudate after <b>methamphetamine</b> revealed little change in Alpha Amino 3 Hydroxy 5 Methyl 4 Isoxazole Propionic Acid (AMPA) GluR1 or N Methyl d Aspartate (NMDA) <strong>NR2B</strong> subunits, or their phosphorylation state.
+GRIN2B	drug	amphetamine	17651730	<b>Methamphetamine</b> also increased levels of PFC <strong>NR2B</strong> subunit, but these increases were not attenuated by deprenyl.
+GRIN2B	drug	alcohol	17625498	<b>Alcohol</b> inhibits <strong>NR2B</strong> containing NMDA receptors in the ventral bed nucleus of the stria terminalis.
+GRIN2B	drug	alcohol	17625498	While genetic removal of NR2A did not alter the magnitude of <b>ethanol</b> inhibition, pharmacological blockade of <strong>NR2B</strong> rendered synaptically activated NMDARs insensitive to <b>ethanol</b> inhibition.
+GRIN2B	drug	opioid	17447466	Role of tyrosine kinase dependent phosphorylation of <strong>NR2B</strong> subunit containing NMDA receptor in <b>morphine</b> reward.
+GRIN2B	addiction	reward	17447466	Role of tyrosine kinase dependent phosphorylation of <strong>NR2B</strong> subunit containing NMDA receptor in morphine <b>reward</b>.
+GRIN2B	drug	opioid	17447466	We previously demonstrated that the <b>morphine</b> induced rewarding effect was dramatically suppressed by cotreatment with an <strong>NR2B</strong> subunit containing N methyl D aspartate (NMDA) receptor antagonist ifenprodil.
+GRIN2B	drug	opioid	17447466	Therefore we propose here that the <strong>NR2B</strong> subunit containing NMDA receptor may be involved in the rewarding effect of <b>morphine</b>.
+GRIN2B	drug	opioid	17447466	The following review provides our recent findings regarding the role of tyrosine kinase dependent phosphorylation of the <strong>NR2B</strong> subunit containing NMDA receptor in the development of psychological dependence on <b>morphine</b>.
+GRIN2B	addiction	dependence	17447466	The following review provides our recent findings regarding the role of tyrosine kinase dependent phosphorylation of the <strong>NR2B</strong> subunit containing NMDA receptor in the development of psychological <b>dependence</b> on morphine.
+GRIN2B	drug	cocaine	17393777	The results suggest that <strong>NR2B</strong> containing NMDA receptor mediated mechanisms modulate the discriminative stimulus effects of <b>cocaine</b> in rhesus monkeys.
+GRIN2B	drug	alcohol	17392475	<b>Ethanol</b> induces long term facilitation of <strong>NR2B</strong> NMDA receptor activity in the dorsal striatum: implications for <b>alcohol</b> drinking behavior.
+GRIN2B	drug	alcohol	17392475	We found that, in the dorsal striatum, <b>alcohol</b> (<b>ethanol</b>) exposure produced an increase in the phosphorylation of the <strong>NR2B</strong> subunit of the NMDAR, and a corresponding increase in the activity of Fyn kinase, which phosphorylates <strong>NR2B</strong>.
+GRIN2B	drug	alcohol	17392475	We further observed an <b>ethanol</b> mediated long term facilitation (LTF) of the activity of <strong>NR2B</strong> containing NMDARs (<strong>NR2B</strong> NMDARs) in the dorsal striatum.
+GRIN2B	drug	alcohol	17392475	Finally, dorsal but not ventral striatum infusion of a Fyn or <strong>NR2B</strong> NMDAR inhibitor reduced rat operant self administration of <b>ethanol</b>.
+GRIN2B	addiction	reward	17392475	Finally, dorsal but not ventral striatum infusion of a Fyn or <strong>NR2B</strong> NMDAR inhibitor reduced rat <b>operant</b> self administration of ethanol.
+GRIN2B	drug	alcohol	17392475	Our results suggest that the Fyn mediated phosphorylation and LTF of <strong>NR2B</strong> NMDAR activity in the dorsal striatum after exposure to <b>ethanol</b> may underlie aberrant plasticity that contributes to mechanisms underlying <b>alcohol</b> drinking behavior.
+GRIN2B	drug	alcohol	17229098	These observations support a model in which chronic <b>ethanol</b> exposure induces homeostatic increases of <strong>NR2B</strong> containing NMDA receptors and PSD 95 to the postsynaptic density.
+GRIN2B	drug	alcohol	17156796	Changes in function of NMDA receptor <strong>NR2B</strong> subunit in spinal cord of rats with neuropathy following chronic <b>ethanol</b> consumption.
+GRIN2B	drug	alcohol	17156796	Under these conditions, mRNA and protein levels of NR1, NR2A and <strong>NR2B</strong> subunits did not change in the spinal cord of chronic <b>ethanol</b> fed rats.
+GRIN2B	drug	alcohol	17156796	Interestingly, phosphorylated Ser 1303 <strong>NR2B</strong> (p Ser1303 <strong>NR2B</strong>) subunit was significantly increased in the spinal cord of chronic <b>ethanol</b> fed rats, whereas p Tyr1472 <strong>NR2B</strong> was not affected in the superficial spinal dorsal horn of <b>ethanol</b> fed rats.
+GRIN2B	drug	alcohol	17156796	These findings suggest that spinal p Ser1303 <strong>NR2B</strong> plays a significant role in the development of the <b>ethanol</b> dependent neuropathic pain like state in rats.
+GRIN2B	drug	opioid	17014848	<strong>NR2B</strong> containing NMDA receptor is required for <b>morphine</b> but not stress induced reinstatement.
+GRIN2B	addiction	relapse	17014848	<strong>NR2B</strong> containing NMDA receptor is required for morphine but not stress induced <b>reinstatement</b>.
+GRIN2B	drug	opioid	17014848	These results indicate that the <strong>NR2B</strong> containing NMDA receptors in the NAc and the dorsal hippocampus play a significant role in mediating the reinstatement of rewarding responses to <b>morphine</b>.
+GRIN2B	addiction	relapse	17014848	These results indicate that the <strong>NR2B</strong> containing NMDA receptors in the NAc and the dorsal hippocampus play a significant role in mediating the <b>reinstatement</b> of rewarding responses to morphine.
+GRIN2B	drug	cocaine	16914681	Accordingly, NMDAR mediated EPSC decay time kinetics were significantly slower after <b>cocaine</b>, suggesting an increased number of <strong>NR2B</strong> containing NMDARs.
+GRIN2B	drug	cocaine	16914681	Together, our data suggest that acute <b>cocaine</b> increases NMDAR function in the VTA via activation of the cAMP/PKA pathway mediated by a DA D5 like receptor, leading to the insertion of <strong>NR2B</strong> containing NMDARs in the membrane.
+GRIN2B	drug	opioid	16859831	Our results demonstrate that <strong>NR2B</strong> selective conantokins, viz., con G, con G[S(16)Y] and con G[gamma(7)K], are potent inhibitors of <b>naloxone</b> induced jumping at low doses (2 15 nmol/kg) compared with con T, con R[1 17], and small molecule antagonists of the NMDAR, including the <strong>NR2B</strong> selective agent, ifenprodil.
+GRIN2B	addiction	dependence	16859831	We conclude that the <strong>NR2B</strong> selective conantokins may find utility as neuropharmacological tools for probing NMDAR related mechanisms of opiate <b>dependence</b>.
+GRIN2B	addiction	withdrawal	16839855	CIE treatment caused a relatively higher increase in <strong>NR2B</strong> protein, and this was the only sustained increase after long term <b>withdrawal</b>.
+GRIN2B	drug	cocaine	16794574	Reversal of <b>cocaine</b> induced behavioral sensitization and associated phosphorylation of the <strong>NR2B</strong> and GluR1 subunits of the NMDA and AMPA receptors.
+GRIN2B	addiction	sensitization	16794574	Reversal of cocaine induced behavioral <b>sensitization</b> and associated phosphorylation of the <strong>NR2B</strong> and GluR1 subunits of the NMDA and AMPA receptors.
+GRIN2B	addiction	sensitization	16794574	<b>Sensitization</b> was associated with increased <strong>NR2B</strong> expression in the accumbens (NAc) shell and decreased Tyr1472 phosphorylation in the NAc core, as well as increased Ser845 phosphorylation of the GluR1 subunit in prefrontal cortex, NAc core, and shell.
+GRIN2B	drug	opioid	16631172	The role of <strong>NR2B</strong> containing NMDA receptor in place preference conditioned with <b>morphine</b> and natural reinforcers in rats.
+GRIN2B	drug	opioid	16631172	Experimental results showed that (1) an augmented expression of <strong>NR2B</strong> subunit was revealed by Western blotting in the nucleus accumbens (NAc) and the hippocampus in rats with CPP induced by <b>morphine</b>, but not by natural rewards such as food, novel environment and social interaction.
+GRIN2B	addiction	reward	16631172	Experimental results showed that (1) an augmented expression of <strong>NR2B</strong> subunit was revealed by Western blotting in the nucleus accumbens (NAc) and the hippocampus in rats with <b>CPP</b> induced by morphine, but not by natural rewards such as food, novel environment and social interaction.
+GRIN2B	drug	opioid	16631172	(2) Ifenprodil, an antagonist highly selective for <strong>NR2B</strong> subunit of the NMDA receptor, produced a dose dependent reduction in CPP induced by <b>morphine</b> and novel environment, but not that by food consumption and social interaction.
+GRIN2B	addiction	reward	16631172	(2) Ifenprodil, an antagonist highly selective for <strong>NR2B</strong> subunit of the NMDA receptor, produced a dose dependent reduction in <b>CPP</b> induced by morphine and novel environment, but not that by food consumption and social interaction.
+GRIN2B	drug	opioid	16631172	Taking together, these findings suggested that <strong>NR2B</strong> containing NMDA receptor may be more involved with <b>morphine</b> reward rather than natural rewards, and that antagonism of <strong>NR2B</strong> may have a potential for the treatment of <b>morphine</b> abuse.
+GRIN2B	addiction	reward	16631172	Taking together, these findings suggested that <strong>NR2B</strong> containing NMDA receptor may be more involved with morphine <b>reward</b> rather than natural rewards, and that antagonism of <strong>NR2B</strong> may have a potential for the treatment of morphine abuse.
+GRIN2B	addiction	withdrawal	16616767	Importantly, the opiate <b>withdrawal</b> induced increase in GluR2/3 was dependent on the activation of glucocorticoid receptors and NMDA receptors, as it was prevented by the glucocorticoid receptor antagonist RU38486, or intrahippocampal injection of the NMDA receptor antagonist AP 5 or the antagonist to <strong>NR2B</strong> containing NMDA receptors, Ro25 6981.
+GRIN2B	drug	psychedelics	16474203	Phencyclidine, MK 801, and <b>ketamine</b>, non competitive NMDA receptor antagonists, generalized to the discriminative stimulus effects of U 50,488H, but not those of TRK 820, whereas (+/ ) 3 (2 carbaxypiperazine 4 yl) propyl 1 phosphonic acid (CPP), a competitive NMDA receptor antagonist, and ifenprodil, an NR1/<strong>NR2B</strong> NMDA receptor antagonist, did not, suggesting that non competitive NMDA receptor antagonists possess U 50,488H like discriminative stimulus effects in rats.
+GRIN2B	addiction	reward	16474203	Phencyclidine, MK 801, and ketamine, non competitive NMDA receptor antagonists, generalized to the discriminative stimulus effects of U 50,488H, but not those of TRK 820, whereas (+/ ) 3 (2 carbaxypiperazine 4 yl) propyl 1 phosphonic acid (<b>CPP</b>), a competitive NMDA receptor antagonist, and ifenprodil, an NR1/<strong>NR2B</strong> NMDA receptor antagonist, did not, suggesting that non competitive NMDA receptor antagonists possess U 50,488H like discriminative stimulus effects in rats.
+GRIN2B	drug	opioid	16453311	In this study we examined the effects of chronic <b>morphine</b> administration on gene and protein expression of three major NMDA receptors subunits (NR1, NR2A, and <strong>NR2B</strong>) in NAcc and CeA.
+GRIN2B	drug	opioid	16453311	However, at the protein level, immunoblotting revealed that chronic <b>morphine</b> significantly increased levels of NR1 and <strong>NR2B</strong> subunits.
+GRIN2B	drug	alcohol	16396741	Chronic <b>ethanol</b> exposure did not affect protein levels of the NR1 and <strong>NR2B</strong> subunits.
+GRIN2B	drug	alcohol	16179537	The increase in NMDA receptor number in response to chronic <b>ethanol</b> exposure both in vivo and in vitro is accompanied by an increase in NMDAR1 and <strong>NMDAR2B</strong> polypeptide levels.
+GRIN2B	drug	opioid	16117034	It is shown that NMDA receptor antagonists and specific diets able to negatively modulate <strong>NR2B</strong> subunit containing NMDA receptors prevented abnormal pain hypersensitivity, partially reversed chronic pain and restored the <b>opioid</b> effectiveness on <b>opioid</b> resistant pain models.
+GRIN2B	addiction	withdrawal	16052244	At 1 week <b>withdrawal</b>, mRNA levels for NR1 and <strong>NR2B</strong> subunits were significantly decreased.
+GRIN2B	drug	alcohol	16009711	Here we show that exposure of hippocampal neurons to <b>ethanol</b> increases the internalization of the NR2A but not <strong>NR2B</strong> subunit of the NMDAR via the endocytic pathway.
+GRIN2B	drug	alcohol	16009711	Importantly, <b>ethanol</b> treatment alters functional subunit composition from NR2A/<strong>NR2B</strong>  to mainly <strong>NR2B</strong> containing NMDARs.
+GRIN2B	drug	alcohol	16009352	The <b>ethanol</b> sensitive NMDA receptor subunits NR1, NR2A and <strong>NR2B</strong> were quantified by Western immunoblot analysis.
+GRIN2B	drug	alcohol	16009352	Exposure to <b>ethanol</b> (50 mM) caused an increase in the levels of NR1 (137 +/  11% of untreated control, P = 0.009), NR2A (128 +/  14%, P = 0.022) and <strong>NR2B</strong> (136 +/  19%, P = 0.012).
+GRIN2B	drug	alcohol	16009352	Coincubation with memantine (10 microM) completely blocked the <b>ethanol</b> induced up regulation of NR1 (102 +/  4%), NR2A (95 +/  7%) and <strong>NR2B</strong> (105 +/  13%).
+GRIN2B	drug	cocaine	15953359	In the basolateral amygdala, GluR1 but not GluR2 levels were increased on days 1 and 30, NR2A levels were increased on day 1, and <strong>NR2B</strong> levels were decreased on day 30 of withdrawal from <b>cocaine</b>.
+GRIN2B	addiction	withdrawal	15953359	In the basolateral amygdala, GluR1 but not GluR2 levels were increased on days 1 and 30, NR2A levels were increased on day 1, and <strong>NR2B</strong> levels were decreased on day 30 of <b>withdrawal</b> from cocaine.
+GRIN2B	drug	cocaine	15953359	In the central amygdala, GluR2 but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or <strong>NR2B</strong> levels were not altered after withdrawal from <b>cocaine</b>.
+GRIN2B	addiction	withdrawal	15953359	In the central amygdala, GluR2 but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and NR2A or <strong>NR2B</strong> levels were not altered after <b>withdrawal</b> from cocaine.
+GRIN2B	addiction	withdrawal	15919065	Western blot analysis of NMDA receptor subunit expression showed that, at 7 days of <b>withdrawal</b>, the level of protein for NR2A and <strong>NR2B</strong> subunits was elevated in the CA1 region of hippocampal slices from CIE treated animals compared with slices from age matched controls.
+GRIN2B	drug	alcohol	15829254	In a comprehensive fashion, we studied dose response curves, employing the following selective pharmacological agents: the NMDAR competitive antagonist CGP37849, the glycine binding site antagonist L 701.324, the <strong>NR2B</strong> subunit selective antagonist ifenprodil, which acts at the polyamine binding site, the NMDAR channel blocker neramexane, and <b>ethanol</b>, which acts as a functional antagonist at the NMDAR.
+GRIN2B	drug	alcohol	15812607	NMDA receptor 2B (<strong>NR2B</strong>) is a subunit that confers a high sensitivity to <b>ethanol</b> induced inhibition.
+GRIN2B	drug	alcohol	15812607	Previously we had reported a lack of association between the single nucleotide polymorphism (SNP) rs1806201 in the NR2B gene (<strong>GRIN2B</strong>) and <b>alcoholism</b>.
+GRIN2B	drug	alcohol	15812607	Previously we had reported a lack of association between the single nucleotide polymorphism (SNP) rs1806201 in the <strong>NR2B</strong> gene (<strong>GRIN2B</strong>) and <b>alcoholism</b>.
+GRIN2B	drug	alcohol	15812607	One aim of the present study was to test whether the association between the <strong>GRIN2B</strong> polymorphism rs1806201 and early onset <b>alcoholism</b> can be replicated in a larger sample.
+GRIN2B	drug	alcohol	15812607	Moreover, we hypothesized that another genetic variation within <strong>GRIN2B</strong> (rs1806191) may have an effect in the etiology of <b>alcoholism</b> or withdrawal related traits.
+GRIN2B	addiction	withdrawal	15812607	Moreover, we hypothesized that another genetic variation within <strong>GRIN2B</strong> (rs1806191) may have an effect in the etiology of alcoholism or <b>withdrawal</b> related traits.
+GRIN2B	drug	psychedelics	15764736	The magnitude of reversal was greater than other negative modulators of the NMDA receptor studied, such as uncompetitive channel blockers (e.g., memantine, dizocilpine, and <b>ketamine</b>), a <strong>NR2B</strong> selective antagonist (e.g., ifenprodil), and other glutamate antagonists [e.g., selfotel, 3 (2 carboxypiperazin 4 yl)propyl 1 phosphonic acid (CPP), D,L (E) 2 amino 4 propyl 5 phosphono 3 pentenoic acid (CGP 39653)], up to doses that suppressed operant rates of responding.
+GRIN2B	addiction	reward	15764736	The magnitude of reversal was greater than other negative modulators of the NMDA receptor studied, such as uncompetitive channel blockers (e.g., memantine, dizocilpine, and ketamine), a <strong>NR2B</strong> selective antagonist (e.g., ifenprodil), and other glutamate antagonists [e.g., selfotel, 3 (2 carboxypiperazin 4 yl)propyl 1 phosphonic acid (<b>CPP</b>), D,L (E) 2 amino 4 propyl 5 phosphono 3 pentenoic acid (CGP 39653)], up to doses that suppressed <b>operant</b> rates of responding.
+GRIN2B	drug	alcohol	15630096	<b>Ethanol</b> withdrawal seizures are controlled by tissue plasminogen activator via modulation of <strong>NR2B</strong> containing NMDA receptors.
+GRIN2B	addiction	withdrawal	15630096	Ethanol <b>withdrawal</b> seizures are controlled by tissue plasminogen activator via modulation of <strong>NR2B</strong> containing NMDA receptors.
+GRIN2B	drug	alcohol	15630096	tPA interacts with <strong>NR2B</strong> containing NMDA receptors and is required for up regulation of the <strong>NR2B</strong> subunit in response to <b>ethanol</b>.
+GRIN2B	drug	alcohol	15630096	These results indicate that tPA mediates the development of physical dependence on <b>ethanol</b> by regulating <strong>NR2B</strong> containing NMDA receptors.
+GRIN2B	addiction	dependence	15630096	These results indicate that tPA mediates the development of physical <b>dependence</b> on ethanol by regulating <strong>NR2B</strong> containing NMDA receptors.
+GRIN2B	drug	alcohol	15542698	PCR based assays showed that <b>alcoholism</b> was associated with polymorphisms of the dopamine D2 receptor (DRD2) TaqI B (P = .029) and the GABAA beta2 subunit C1412T (P = .012) genes, but not with the glutamate receptor subunit gene <strong>NMDAR2B</strong> (366C/G), the serotonin transporter gene (5HTTL PR), the dopamine transporter gene DAT1(SLC6A3), the dopamine D2 receptor gene DRD2 TaqI A, or the GABAA alpha1(A15G), alpha6(T1519C), and gamma2(G3145A) subunit genes.
+GRIN2B	drug	alcohol	15356198	Similar effects were observed with <strong>NR2B</strong> clustering after chronic <b>ethanol</b> exposure.
+GRIN2B	drug	alcohol	15301608	Pretreatment with channel blockers MK 801 and ketamine, NMDA <strong>NR2B</strong> receptor subunit antagonists ifenprodil and CP 101,606, and the glycine(B) partial agonist (+) HA 966 did not alter acquisition of <b>ethanol</b> induced conditioned place preference (CPP) in mice.
+GRIN2B	drug	psychedelics	15301608	Pretreatment with channel blockers MK 801 and <b>ketamine</b>, NMDA <strong>NR2B</strong> receptor subunit antagonists ifenprodil and CP 101,606, and the glycine(B) partial agonist (+) HA 966 did not alter acquisition of ethanol induced conditioned place preference (CPP) in mice.
+GRIN2B	addiction	reward	15301608	Pretreatment with channel blockers MK 801 and ketamine, NMDA <strong>NR2B</strong> receptor subunit antagonists ifenprodil and CP 101,606, and the glycine(B) partial agonist (+) HA 966 did not alter acquisition of ethanol induced conditioned place preference (<b>CPP</b>) in mice.
+GRIN2B	drug	opioid	15263066	Taken together with our recent molecular studies, our data are consistent with a shift away from NMDA receptor subunit (NR) <strong>NR2B</strong> and 2C function toward increased NR2A subunit expression or function after chronic <b>morphine</b>, a process that could alter excitability and integrative properties and may represent a neuroadaptation of NAcc medium spiny neurons underlying <b>morphine</b> dependence.
+GRIN2B	addiction	dependence	15263066	Taken together with our recent molecular studies, our data are consistent with a shift away from NMDA receptor subunit (NR) <strong>NR2B</strong> and 2C function toward increased NR2A subunit expression or function after chronic morphine, a process that could alter excitability and integrative properties and may represent a neuroadaptation of NAcc medium spiny neurons underlying morphine <b>dependence</b>.
+GRIN2B	drug	nicotine	15256539	The <strong>NR2B</strong> selective N methyl D aspartate receptor antagonist Ro 25 6981 [(+/ ) (R*,S*) alpha (4 hydroxyphenyl) beta methyl 4 (phenylmethyl) 1 piperidine propanol] potentiates the effect of <b>nicotine</b> on locomotor activity and dopamine release in the nucleus accumbens.
+GRIN2B	drug	nicotine	15256539	In the present study, we investigated the effect of the <strong>NR2B</strong> selective NMDA receptor antagonist Ro 25 6981 [(+/ ) (R*,S*) alpha (4 hydroxyphenyl) beta methyl 4 (phenylmethyl) 1 piperidine propanol] on <b>nicotine</b> stimulated LMA and <b>nicotine</b> induced DA release in the nucleus accumbens (NAcc) in rats.
+GRIN2B	drug	nicotine	15256539	The data suggest that, compared with other subunits of the NMDA receptor, the <strong>NR2B</strong> subunit might play a different role in the reinforcing effects of <b>nicotine</b>.
+GRIN2B	addiction	reward	15256539	The data suggest that, compared with other subunits of the NMDA receptor, the <strong>NR2B</strong> subunit might play a different role in the <b>reinforcing</b> effects of nicotine.
+GRIN2B	drug	alcohol	15180478	The <strong>NR2B</strong> subtype of NMDA receptor: a potential target for the treatment of <b>alcohol</b> dependence.
+GRIN2B	addiction	dependence	15180478	The <strong>NR2B</strong> subtype of NMDA receptor: a potential target for the treatment of alcohol <b>dependence</b>.
+GRIN2B	drug	alcohol	15180478	Our results showed that especially the <strong>NR2B</strong> subunit expression is increased in cultured hippocampal and cortical neurones after 3 days of intermittent <b>ethanol</b> treatment.
+GRIN2B	drug	alcohol	15180478	According to the high calcium permeability, the increased agonist sensitivity and the relatively slow closing kinetics of NMDA ion channels composed of <strong>NR2B</strong> subunits, the above mentioned changes may underlie the enhanced NMDA receptor activation observed after long term <b>ethanol</b> exposure.
+GRIN2B	drug	alcohol	15180478	Accordingly, we have tested <strong>NR2B</strong> subunit selective NMDA receptor antagonists in primary cultures of rat cortical neurones pre treated with <b>ethanol</b> intermittently for 3 days and found that these compounds potently inhibited the neurotoxic effect of <b>ethanol</b> withdrawal.
+GRIN2B	addiction	withdrawal	15180478	Accordingly, we have tested <strong>NR2B</strong> subunit selective NMDA receptor antagonists in primary cultures of rat cortical neurones pre treated with ethanol intermittently for 3 days and found that these compounds potently inhibited the neurotoxic effect of ethanol <b>withdrawal</b>.
+GRIN2B	drug	alcohol	15180478	Hypothesising the involvement of enhanced <strong>NR2B</strong> subunit expression in development of <b>alcohol</b> dependence and withdrawal symptoms and considering the tolerable side effect profile of the <strong>NR2B</strong> subunit selective NMDA receptor antagonists, the <strong>NR2B</strong> type of NMDA receptor subunit may serve as a possible drug target in pharmacological interventions for <b>alcoholism</b>.
+GRIN2B	addiction	dependence	15180478	Hypothesising the involvement of enhanced <strong>NR2B</strong> subunit expression in development of alcohol <b>dependence</b> and withdrawal symptoms and considering the tolerable side effect profile of the <strong>NR2B</strong> subunit selective NMDA receptor antagonists, the <strong>NR2B</strong> type of NMDA receptor subunit may serve as a possible drug target in pharmacological interventions for alcoholism.
+GRIN2B	addiction	withdrawal	15180478	Hypothesising the involvement of enhanced <strong>NR2B</strong> subunit expression in development of alcohol dependence and <b>withdrawal</b> symptoms and considering the tolerable side effect profile of the <strong>NR2B</strong> subunit selective NMDA receptor antagonists, the <strong>NR2B</strong> type of NMDA receptor subunit may serve as a possible drug target in pharmacological interventions for alcoholism.
+GRIN2B	drug	alcohol	15180478	The aim of this review is to give an update on the role of altered structure and function of NMDA receptors after <b>ethanol</b> exposure and to summarise the recent data about the activity of <strong>NR2B</strong> subunit selective NMDA receptor antagonists in model systems related to <b>alcoholism</b>.
+GRIN2B	drug	opioid	15157688	In contrast, the polyamine (<strong>NR2B</strong>) site antagonist, Ro 25 6981, attenuated <b>morphine</b> analgesia at all doses.
+GRIN2B	drug	opioid	15157688	Strikingly, the non competitive antagonists produced no modulation of <b>morphine</b> analgesia whatsoever in female mice, whereas no sex differences were observed using competitive or <strong>NR2B</strong> antagonists.
+GRIN2B	addiction	withdrawal	15057640	Recently emerged <strong>NR2B</strong> SSNAs (CP 101606 (Pfizer Inc), Co 101244 (Pfizer Inc/Purdue Neuroscience Corp/Senju Pharmaceutical Co Ltd), CI 1041 (Purdue Neuroscience Corp/Pfizer Inc) and indole 2 carboxamide derivatives) have demonstrated excellent in vitro potency against <b>withdrawal</b> induced cytotoxicity.
+GRIN2B	drug	alcohol	15057640	Although in vivo data are few, according to their in vitro efficacy and good tolerability, novel NMDA antagonists, especially the <strong>NR2B</strong> selective antagonists, may offer a preferable alternative to the presently available pharmacotherapies for treating <b>alcoholism</b>.
+GRIN2B	drug	alcohol	14973247	Ifenprodil also occluded the <b>ethanol</b> effect, suggesting that <strong>NR2B</strong> subunit containing receptors may be involved.
+GRIN2B	drug	alcohol	14684447	Preliminary studies with microdialysis and real time PCR analysis support this idea: local <b>ethanol</b> administration in vivo had no effect on glutamate release, but chronic <b>ethanol</b> nearly tripled the expression of <strong>NR2B</strong> subunits (the most <b>ethanol</b> sensitive) in CeA.
+GRIN2B	drug	alcohol	14634488	Fyn kinase and <strong>NR2B</strong> containing NMDA receptors regulate acute <b>ethanol</b> sensitivity but not <b>ethanol</b> intake or conditioned reward.
+GRIN2B	addiction	reward	14634488	Fyn kinase and <strong>NR2B</strong> containing NMDA receptors regulate acute ethanol sensitivity but not ethanol intake or conditioned <b>reward</b>.
+GRIN2B	drug	alcohol	14634488	Recently, we found that the compartmentalization of Fyn to the <strong>NR2B</strong> subunit of the NMDA receptor (NMDAR) in the hippocampus regulates Fyn phosphorylation of <strong>NR2B</strong> in response to <b>ethanol</b>, which mediates the acute tolerance of NMDAR to <b>ethanol</b> inhibition in hippocampal slices.
+GRIN2B	drug	alcohol	14634488	In this study we determined, first, whether acute tolerance to <b>ethanol</b> inhibition is mediated via <strong>NR2B</strong> containing NMDARs in vivo and, second, whether the increase in acute sensitivity to <b>ethanol</b> in the Fyn /  mice influences <b>ethanol</b> consumption or <b>ethanol</b>'s conditioned rewarding effects.
+GRIN2B	drug	alcohol	14634488	We found that systemic injection of the <strong>NR2B</strong> containing NMDAR selective antagonist, ifenprodil, abolished the differences between Fyn+/+ and Fyn /  mice in sensitivity to the acute sedative effects of <b>ethanol</b>.
+GRIN2B	drug	alcohol	14634488	Our results suggest that the interaction between Fyn and <strong>NR2B</strong> mediates the acute sedative effects of <b>ethanol</b>, and that alteration in acute <b>ethanol</b> sensitivity does not necessarily correlate with levels of <b>ethanol</b> consumption or the rewarding properties of <b>ethanol</b>.
+GRIN2B	drug	alcohol	14634487	Polypeptide levels of mGluR5s and the NR1 and <strong>NR2B</strong> subunits of NMDARs were also determined via Western blot analyses after 10 days of <b>ethanol</b> exposure.
+GRIN2B	drug	alcohol	14634487	The polypeptide levels of mGluR5s and NR1 and <strong>NR2B</strong> subunits of NMDARs were all increased after <b>ethanol</b> exposure; however, the increase in mGluR5s did not achieve statistical significance.
+GRIN2B	drug	alcohol	14573320	Genotyping of the <strong>NMDAR2B</strong> polymorphism revealed a significantly reduced T allele in Cloninger type 2 <b>alcoholics</b> and in patients reporting an early onset compared with control subjects.
+GRIN2B	drug	alcohol	14534353	These findings suggest that <strong>NR2B</strong> containing receptors may be specifically enhanced and suggest that processes dependent upon calcium influx through amygdala NMDA receptors may potentially be enhanced by chronic <b>ethanol</b> ingestion.
+GRIN2B	drug	alcohol	14534353	Most GAD , presumed projection neurons expressed both NR2A and <strong>NR2B</strong> mRNAs, and this profile did not change during chronic <b>ethanol</b> exposure.
+GRIN2B	drug	alcohol	12963084	<strong>NR2B</strong> subunit selective NMDA antagonists inhibit neurotoxic effect of <b>alcohol</b> withdrawal in primary cultures of rat cortical neurones.
+GRIN2B	addiction	withdrawal	12963084	<strong>NR2B</strong> subunit selective NMDA antagonists inhibit neurotoxic effect of alcohol <b>withdrawal</b> in primary cultures of rat cortical neurones.
+GRIN2B	drug	alcohol	12963084	N Methyl D aspartate (NMDA) receptor mediated glutamatergic neurotransmission is thought to play a central role in the development of <b>alcohol</b> dependence and this alteration is supposed to be due to a differential up regulation of the <strong>NR2B</strong> type of subunits.
+GRIN2B	addiction	dependence	12963084	N Methyl D aspartate (NMDA) receptor mediated glutamatergic neurotransmission is thought to play a central role in the development of alcohol <b>dependence</b> and this alteration is supposed to be due to a differential up regulation of the <strong>NR2B</strong> type of subunits.
+GRIN2B	drug	alcohol	12963084	In this work, we examined the effect of some known (CP 101,606; CI 1041 and Co 101,244) and novel indole 2 carboxamide derivative <strong>NR2B</strong> subunit selective NMDA receptor antagonists (SSNAs) (RG 13579 and RG 1103) on the neurotoxic effect of withdrawal in <b>ethanol</b> pre treated cultures of rat cortical neurones.
+GRIN2B	addiction	withdrawal	12963084	In this work, we examined the effect of some known (CP 101,606; CI 1041 and Co 101,244) and novel indole 2 carboxamide derivative <strong>NR2B</strong> subunit selective NMDA receptor antagonists (SSNAs) (RG 13579 and RG 1103) on the neurotoxic effect of <b>withdrawal</b> in ethanol pre treated cultures of rat cortical neurones.
+GRIN2B	drug	alcohol	12963084	Here, we demonstrate that <strong>NR2B</strong> SSNAs given in the course of the withdrawal potently reduced the LDH release in <b>ethanol</b> pre treated cultures.
+GRIN2B	addiction	withdrawal	12963084	Here, we demonstrate that <strong>NR2B</strong> SSNAs given in the course of the <b>withdrawal</b> potently reduced the LDH release in ethanol pre treated cultures.
+GRIN2B	drug	alcohol	12963084	According to these observations, <strong>NR2B</strong> SSNAs are potent inhibitors of <b>ethanol</b> withdrawal induced neurotoxicity and considering that these agents have acceptable side effect profiles, they could be promising therapeutic candidates in the pharmacotherapy for physical signs of acute <b>alcohol</b> withdrawal and associated neuronal damage.
+GRIN2B	addiction	withdrawal	12963084	According to these observations, <strong>NR2B</strong> SSNAs are potent inhibitors of ethanol <b>withdrawal</b> induced neurotoxicity and considering that these agents have acceptable side effect profiles, they could be promising therapeutic candidates in the pharmacotherapy for physical signs of acute alcohol <b>withdrawal</b> and associated neuronal damage.
+GRIN2B	drug	alcohol	12736333	During acute exposure to <b>ethanol</b>, RACK1 is dissociated from the complex, thereby facilitating Fyn mediated phosphorylation of <strong>NR2B</strong>, which enhances channel activity, counteracting the inhibitory actions of <b>ethanol</b>.
+GRIN2B	drug	cocaine	12457264	Repeated administration of <b>cocaine</b> alters the expression of the NMDA receptor subunits, NR1 and <strong>NR2B</strong> in a region  and withdrawal time dependent manner.
+GRIN2B	addiction	withdrawal	12457264	Repeated administration of cocaine alters the expression of the NMDA receptor subunits, NR1 and <strong>NR2B</strong> in a region  and <b>withdrawal</b> time dependent manner.
+GRIN2B	drug	alcohol	12441166	Indeed, we provided evidence for increased expression of the <strong>NR2B</strong> and the C1 and C2' cassette containing splice variant forms of the NR1 subunit proteins in <b>ethanol</b> pre treated cultures in further experiments using a flow cytometry based immunocytochemical method.
+GRIN2B	drug	alcohol	12399115	This apparent lack of <b>alcohol</b> withdrawal induced behavioural effects was associated with increased Fyn activity and tyrosine phosphorylation of several proteins including the NMDA receptor subunit <strong>NR2B</strong> in the different mutant lines.
+GRIN2B	addiction	withdrawal	12399115	This apparent lack of alcohol <b>withdrawal</b> induced behavioural effects was associated with increased Fyn activity and tyrosine phosphorylation of several proteins including the NMDA receptor subunit <strong>NR2B</strong> in the different mutant lines.
+GRIN2B	drug	alcohol	12399115	<strong>NR2B</strong> phosphorylation itself remained unaffected by the chronic <b>alcohol</b> ingestion and subsequent withdrawal, but challenge with an <strong>NR2B</strong> antagonist, ifenprodil, restored a normal behavioural response in <b>alcohol</b> withdrawn fyn mutants.
+GRIN2B	addiction	withdrawal	12399115	<strong>NR2B</strong> phosphorylation itself remained unaffected by the chronic alcohol ingestion and subsequent <b>withdrawal</b>, but challenge with an <strong>NR2B</strong> antagonist, ifenprodil, restored a normal behavioural response in alcohol withdrawn fyn mutants.
+GRIN2B	drug	alcohol	12399115	Together, these results suggest that Fyn can modulate <b>alcohol</b> consumption and prevent behavioural changes during <b>alcohol</b> withdrawal, possibly via phosphorylation of <strong>NR2B</strong>.
+GRIN2B	addiction	withdrawal	12399115	Together, these results suggest that Fyn can modulate alcohol consumption and prevent behavioural changes during alcohol <b>withdrawal</b>, possibly via phosphorylation of <strong>NR2B</strong>.
+GRIN2B	drug	cocaine	12325043	These findings suggest that the disruption of NR1, <strong>NR2B</strong>, and NR2C subunits in the discrete brain regions occurs under the <b>cocaine</b> related behavioral abnormalities and would be closely implicated in the initiation and expression of behavioral sensitization induced by repeated <b>cocaine</b> administration.
+GRIN2B	addiction	sensitization	12325043	These findings suggest that the disruption of NR1, <strong>NR2B</strong>, and NR2C subunits in the discrete brain regions occurs under the cocaine related behavioral abnormalities and would be closely implicated in the initiation and expression of behavioral <b>sensitization</b> induced by repeated cocaine administration.
+GRIN2B	drug	cocaine	11801363	Moreover, we observed that rats sensitized to <b>cocaine</b> presented a significant increase in the levels of GLUR1, NR1 and <strong>NR2B</strong>, in the nucleus accumbens, and of <strong>NR2B</strong> in the hippocampus compared to control animals.
+GRIN2B	drug	alcohol	11696675	Unexpectedly, we found that expression of NR1 (including the expression of NR1 subunits containing the N1, C1, and C2 inserts), NR2A, <strong>NR2B</strong>, NR2C, GluR1, GluR2/3, GluR5, GluR6/7, and KA2 subunits was not altered in hippocampal homogenates from <b>ethanol</b> exposed rats.
+GRIN2B	drug	alcohol	11530236	<b>Ethanol</b> inhibition of the CA1 <strong>NR2B</strong> mediated component was five to seven times lower in NR2A(DeltaC/DeltaC) than in C57Bl/6.
+GRIN2B	drug	alcohol	11530236	The altered sensitivities to <b>ethanol</b> of both NR2A  and <strong>NR2B</strong> mediated responses in the CA1 of NR2A(DeltaC/DeltaC) imply that NR2A  and <strong>NR2B</strong> subunit containing NMDA receptors may be linked by a common target of <b>ethanol</b>.
+GRIN2B	drug	alcohol	11369029	In HEK 293 cells, <b>acamprosate</b> showed almost no effect on NR1 1a/NR2A or NR1 1a/<strong>NR2B</strong> recombinants (IC(50)s not calculated).
+GRIN2B	drug	opioid	11233291	treatment with a specific antibody against the carboxyl terminal region of the <strong>NR2B</strong> subunit abolishes the <b>morphine</b> induced place preference, whereas antibodies against the NR1 and NR2A subunits do not affect the rewarding effect of <b>morphine</b>, indicating that the blockade of the <strong>NR2B</strong> subunit suppresses the development of the <b>morphine</b> induced rewarding effect.
+GRIN2B	drug	opioid	11233291	Under these conditions, the <strong>NR2B</strong> subunit protein is up regulated in the limbic forebrain of <b>morphine</b> conditioned mice.
+GRIN2B	drug	opioid	11233291	These findings suggest that the NMDA receptor, especially <strong>NR2B</strong> subunit, is an important modulator of the development and/or expression of psychological dependence on <b>morphine</b>.
+GRIN2B	addiction	dependence	11233291	These findings suggest that the NMDA receptor, especially <strong>NR2B</strong> subunit, is an important modulator of the development and/or expression of psychological <b>dependence</b> on morphine.
+GRIN2B	addiction	withdrawal	11152389	<strong>NR2B</strong> subunit mRNA was decreased in the cerebral cortex, caudate putamen, thalamus, CA3 of hippocampus in butorphanol <b>withdrawal</b> rats.
+GRIN2B	drug	alcohol	11141032	However, both <b>ethanol</b> and the NMDAR <strong>NR2B</strong> receptor antagonist ifenprodil inhibited the late component of hippocampal NMDAR fEPSPs to a greater extent in ISS, than in ILS, mice.
+GRIN2B	drug	alcohol	11137280	LDH release induced by <b>alcohol</b> withdrawal was significantly reduced by re addition of <b>ethanol</b>, as well as by administration of non competitive (MK 801) or <strong>NR2B</strong> selective (threo ifenprodil) N methyl D aspartate (NMDA) receptor antagonists.
+GRIN2B	addiction	withdrawal	11137280	LDH release induced by alcohol <b>withdrawal</b> was significantly reduced by re addition of ethanol, as well as by administration of non competitive (MK 801) or <strong>NR2B</strong> selective (threo ifenprodil) N methyl D aspartate (NMDA) receptor antagonists.
+GRIN2B	drug	cocaine	11032893	The present study characterized the effects of withdrawal from <b>cocaine</b> on the expression of NMDA receptor subunits (NR1, <strong>NR2B</strong>) and neuronal nitric oxide synthase.
+GRIN2B	addiction	withdrawal	11032893	The present study characterized the effects of <b>withdrawal</b> from cocaine on the expression of NMDA receptor subunits (NR1, <strong>NR2B</strong>) and neuronal nitric oxide synthase.
+GRIN2B	drug	cocaine	11032893	Administration of <b>cocaine</b> followed by 24 h, 72 h, or 14 days of withdrawal resulted in alterations of NR1 and <strong>NR2B</strong> subunits and neuronal nitric oxide synthase expression as measured by immunohistochemical labeling of rat brain sections.
+GRIN2B	addiction	withdrawal	11032893	Administration of cocaine followed by 24 h, 72 h, or 14 days of <b>withdrawal</b> resulted in alterations of NR1 and <strong>NR2B</strong> subunits and neuronal nitric oxide synthase expression as measured by immunohistochemical labeling of rat brain sections.
+GRIN2B	addiction	withdrawal	11032893	Structure specific and <b>withdrawal</b> time dependent alterations in <strong>NR2B</strong> expression were also found.
+GRIN2B	drug	cocaine	11032893	After 24 h of withdrawal, <b>cocaine</b> induced decreases in <strong>NR2B</strong> expression were observed in the nucleus accumbens shell, whereas increases in <strong>NR2B</strong> expression were found in medial cortical areas.
+GRIN2B	addiction	withdrawal	11032893	After 24 h of <b>withdrawal</b>, cocaine induced decreases in <strong>NR2B</strong> expression were observed in the nucleus accumbens shell, whereas increases in <strong>NR2B</strong> expression were found in medial cortical areas.
+GRIN2B	drug	cocaine	11032893	Two weeks of withdrawal from <b>cocaine</b> caused an approximately 50% increase in <strong>NR2B</strong> subunit expression in regions of the cortex, neostriatum, and nucleus accumbens.
+GRIN2B	addiction	withdrawal	11032893	Two weeks of <b>withdrawal</b> from cocaine caused an approximately 50% increase in <strong>NR2B</strong> subunit expression in regions of the cortex, neostriatum, and nucleus accumbens.
+GRIN2B	drug	alcohol	10924926	Implications of the <strong>NR2B</strong> subunit containing NMDA receptor localized in mouse limbic forebrain in <b>ethanol</b> dependence.
+GRIN2B	addiction	dependence	10924926	Implications of the <strong>NR2B</strong> subunit containing NMDA receptor localized in mouse limbic forebrain in ethanol <b>dependence</b>.
+GRIN2B	drug	alcohol	10924926	The present study was designed to further investigate the direct involvement of the <strong>NR2B</strong> containing NMDA receptor in <b>ethanol</b> dependence.
+GRIN2B	addiction	dependence	10924926	The present study was designed to further investigate the direct involvement of the <strong>NR2B</strong> containing NMDA receptor in ethanol <b>dependence</b>.
+GRIN2B	drug	alcohol	10924926	Treatment with a selective <strong>NR2B</strong> containing NMDA receptor antagonist, ifenprodil, significantly suppressed the expression of <b>ethanol</b> withdrawal signs.
+GRIN2B	addiction	withdrawal	10924926	Treatment with a selective <strong>NR2B</strong> containing NMDA receptor antagonist, ifenprodil, significantly suppressed the expression of ethanol <b>withdrawal</b> signs.
+GRIN2B	drug	alcohol	10924926	The protein level of <strong>NR2B</strong> subunits in the limbic forebrain, but not the cerebral cortex, during chronic <b>ethanol</b> treatment was markedly increased with respect to the levels in control mice.
+GRIN2B	drug	alcohol	10924926	The significant up regulation of <strong>NR2B</strong> subunits lasted for at least 9 h after the discontinuation of <b>ethanol</b> and returned to the basal level by 48 h after the withdrawal.
+GRIN2B	addiction	withdrawal	10924926	The significant up regulation of <strong>NR2B</strong> subunits lasted for at least 9 h after the discontinuation of ethanol and returned to the basal level by 48 h after the <b>withdrawal</b>.
+GRIN2B	drug	alcohol	10924926	These findings suggest that the up regulation of <strong>NR2B</strong> subunits during chronic <b>ethanol</b> exposure may be implicated in the initial development of physical dependence on <b>ethanol</b>.
+GRIN2B	addiction	dependence	10924926	These findings suggest that the up regulation of <strong>NR2B</strong> subunits during chronic ethanol exposure may be implicated in the initial development of physical <b>dependence</b> on ethanol.
+GRIN2B	drug	alcohol	10405999	The NR1/NR2A and NR1/<strong>NR2B</strong> combinations are preferentially sensitive to <b>ethanol</b> inhibition.
+GRIN2B	drug	alcohol	10225371	NR2A subunit levels were significantly increased only in hippocampus from <b>ethanol</b> dependent male rats, whereas <strong>NR2B</strong> subunit levels significantly increased in cerebral cortex of both female and male rats.
+GRIN2B	addiction	withdrawal	10082858	<strong>NR2B</strong> mRNA expression was elevated during exposure, but returned to control levels 18 h after <b>withdrawal</b>.
+GRIN2B	drug	opioid	9988122	Using in situ hybridization techniques, the effects of chronic <b>morphine</b> treatment on the expression of mRNAs encoding the NMDA receptor subunits NRI, NR2A, and <strong>NR2B</strong> were investigated.
+GRIN2B	drug	opioid	9988122	The expression of NR2A and <strong>NR2B</strong> subunit mRNAs did not change after <b>morphine</b> treatment in any brain region.
+GRIN2B	drug	alcohol	9765326	In situ hybridization studies suggest that expression of <strong>NR2B</strong> subunit mRNA may be enhanced in explants after chronic <b>ethanol</b> exposure.
+GRIN2B	drug	alcohol	9756034	Recent research has focused on the N methyl D aspartate receptor system as a major site of <b>ethanol</b> action in the brain and specifically on compensatory changes in the expression of the polyamine sensitive <strong>NR2B</strong> subunit.
+GRIN2B	drug	alcohol	9685652	We investigated the effect of chronic <b>ethanol</b> administration and its withdrawal on the polypeptide levels of NMDA receptor subunits such as NR1, NR2A, and <strong>NR2B</strong> in the rat cerebral cortex and hippocampus using Western blot analysis technique.
+GRIN2B	addiction	withdrawal	9685652	We investigated the effect of chronic ethanol administration and its <b>withdrawal</b> on the polypeptide levels of NMDA receptor subunits such as NR1, NR2A, and <strong>NR2B</strong> in the rat cerebral cortex and hippocampus using Western blot analysis technique.
+GRIN2B	drug	alcohol	9685652	Our results indicate that chronic <b>ethanol</b> treatment upregulates NMDA receptor subunits NR1, NR2A, and <strong>NR2B</strong> (approximately 35%).
+GRIN2B	drug	alcohol	9670216	The sensitivity of NMDA receptors to <b>ethanol</b> block is proposed to involve the <strong>NMDAR2B</strong> subunit in certain brain regions, but this subunit does not appear to be the sole determinant of this interaction.
+GRIN2B	drug	alcohol	9670216	Tolerance to <b>ethanol</b> results in enhanced EAA neurotransmission and NMDA receptor upregulation, which appears to involve selective increases in <strong>NMDAR2B</strong> subunit levels and other molecular changes in specific brain loci.
+GRIN2B	drug	benzodiazepine	9543260	The protein levels of the NR1 and <strong>NR2B</strong>, but not NR2A, subunits were significantly increased in <b>diazepam</b> withdrawn rats compared to those in control rats.
+GRIN2B	drug	benzodiazepine	9543260	Therefore, an increase in the NR1 and <strong>NR2B</strong> subunit proteins may be responsible for both the previously observed upregulation of [3H]dizocilpine binding in the cerebral cortex and the appearance of <b>diazepam</b> withdrawal signs.
+GRIN2B	addiction	withdrawal	9543260	Therefore, an increase in the NR1 and <strong>NR2B</strong> subunit proteins may be responsible for both the previously observed upregulation of [3H]dizocilpine binding in the cerebral cortex and the appearance of diazepam <b>withdrawal</b> signs.
+GRIN2B	drug	alcohol	9145911	Immunoblot analysis of expression of NR1, NR2A, and <strong>NR2B</strong> receptor subunits showed no difference between control and chronic <b>ethanol</b> treated cultures.
+GRIN2B	drug	alcohol	8912402	Furthermore, since there is evidence that eliprodil produces its pharmacological actions through a specific inhibition of NMDAR1 and/or <strong>NMDAR2B</strong> subunits, these data may indicate that certain NMDA receptor subunits may be of particular importance for the mediation of seizure activity following the discontinuation of chronic <b>ethanol</b> exposure.
+CYP2E1	drug	alcohol	32724497	These results indicate that MANF has potential protection on <b>alcohol</b> induced liver injury, and the underlying mechanisms may be associated with meliorating the overactivated ER stress triggered by inflammation and oxidative stress via inhibiting and reducing NO/NF κB and <strong>CYP2E1</strong>/ROS, respectively.
+CYP2E1	drug	alcohol	31024054	Plasma exosomes exacerbate <b>alcohol</b>  and acetaminophen induced toxicity via <strong>CYP2E1</strong> pathway.
+CYP2E1	drug	alcohol	31024054	Cellular <strong>CYP2E1</strong> is well known to mediate <b>alcohol</b>  (ALC) and acetaminophen  (APAP) induced toxicity in hepatic and extra hepatic cells.
+CYP2E1	addiction	intoxication	31024054	Our results showed that ALC exposure caused a significant induction of the plasma exosomal <strong>CYP2E1</strong> level in a <b>binge</b> drinking murine model.
+CYP2E1	drug	alcohol	30931596	The P450 <strong>CYP2E1</strong> *5 c2, an inducible microsomal oxidase, upregulated by <b>ethanol</b> and by formation of acetaldehyde and reactive oxygen species, increases liver toxicity.
+CYP2E1	drug	alcohol	30603740	Induction of the cytochrome P450 2E1 (<strong>CYP2E1</strong>) enzyme by chronic and excessive <b>alcohol</b> intake is known to play a role in the pathogenesis of ALD.
+CYP2E1	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 <strong>CYP2E1</strong> cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+CYP2E1	drug	alcohol	30574039	Three metabolic pathways of <b>ethanol</b> were describe in human   <b>alcohol</b> dehydrogenase (ADH), microsomal <b>ethanol</b> oxidizing system (MEOS, <strong>CYP2E1</strong>) and catalase.
+CYP2E1	drug	alcohol	30237578	The <b>ethanol</b> induced expression of cytochrome P450 2E1 (<strong>CYP2E1</strong>), pro inflammatory proteins, cytokines, chemokines and reactive oxygen species (ROS) levels were also reduced in the livers of AXT administrated group.
+CYP2E1	drug	alcohol	30071471	Binge <b>alcohol</b> exposure induced leaky gut with significantly elevated plasma endotoxin and inflammatory fatty liver by increasing the levels of oxidative and nitrative stress marker proteins such as <b>ethanol</b> inducible <strong>CYP2E1</strong>, inducible nitric oxide synthase, and nitrated proteins in the small intestine and liver.
+CYP2E1	addiction	intoxication	30071471	<b>Binge</b> alcohol exposure induced leaky gut with significantly elevated plasma endotoxin and inflammatory fatty liver by increasing the levels of oxidative and nitrative stress marker proteins such as ethanol inducible <strong>CYP2E1</strong>, inducible nitric oxide synthase, and nitrated proteins in the small intestine and liver.
+CYP2E1	drug	alcohol	29588096	No association of <strong>CYP2E1</strong> genetic polymorphisms with <b>alcohol</b> dependence in Han Taiwanese population.
+CYP2E1	addiction	dependence	29588096	No association of <strong>CYP2E1</strong> genetic polymorphisms with alcohol <b>dependence</b> in Han Taiwanese population.
+CYP2E1	drug	alcohol	29588096	Cytochrome P450 2E1 (<strong>CYP2E1</strong>) gene is one of the candidate genes for <b>alcohol</b> dependence (AD).
+CYP2E1	addiction	dependence	29588096	Cytochrome P450 2E1 (<strong>CYP2E1</strong>) gene is one of the candidate genes for alcohol <b>dependence</b> (AD).
+CYP2E1	drug	alcohol	29458168	The levels of intestinal <strong>CYP2E1</strong>, iNOS, nitrated proteins and apoptosis related marker proteins were significantly elevated in binge <b>alcohol</b> exposed rodents.
+CYP2E1	addiction	intoxication	29458168	The levels of intestinal <strong>CYP2E1</strong>, iNOS, nitrated proteins and apoptosis related marker proteins were significantly elevated in <b>binge</b> alcohol exposed rodents.
+CYP2E1	drug	alcohol	29458168	Consistently, the levels of TJ proteins (claudin 1, claudin 4, occludin and zonula occludens 1), AJ proteins (β catenin and E cadherin) and desmosome plakoglobin were very low in binge <b>alcohol</b> exposed rats, wild type mice, and autopsied human ileums but not in <strong>Cyp2e1</strong> null mice.
+CYP2E1	addiction	intoxication	29458168	Consistently, the levels of TJ proteins (claudin 1, claudin 4, occludin and zonula occludens 1), AJ proteins (β catenin and E cadherin) and desmosome plakoglobin were very low in <b>binge</b> alcohol exposed rats, wild type mice, and autopsied human ileums but not in <strong>Cyp2e1</strong> null mice.
+CYP2E1	drug	alcohol	29458168	Additionally, pretreatment with specific inhibitors of <strong>CYP2E1</strong> and iNOS prevented disorganization and/or degradation of TJ proteins in <b>alcohol</b> exposed T84 colonic cells.
+CYP2E1	drug	alcohol	29458168	These results demonstrated for the first time the critical roles of <strong>CYP2E1</strong>, apoptosis of enterocytes, and nitration followed by ubiquitin dependent proteolytic degradation of the junctional complex proteins, in promoting binge <b>alcohol</b> induced gut leakiness and endotoxemia, contributing to inflammatory liver disease.
+CYP2E1	addiction	intoxication	29458168	These results demonstrated for the first time the critical roles of <strong>CYP2E1</strong>, apoptosis of enterocytes, and nitration followed by ubiquitin dependent proteolytic degradation of the junctional complex proteins, in promoting <b>binge</b> alcohol induced gut leakiness and endotoxemia, contributing to inflammatory liver disease.
+CYP2E1	addiction	intoxication	29431616	In both genotypes, <b>binge</b> EtOH induced triglyceride accumulation was associated with inhibition of fatty acid β oxidation and upregulation of Srebp 1c  regulated lipogenic genes and hepatic <strong>CYP2E1</strong> protein.
+CYP2E1	drug	alcohol	29404485	This study investigated the role of <b>ethanol</b> inducible cytochrome P450 2E1 (<strong>CYP2E1</strong>) in enhancing <strong>CYP2E1</strong> and other P450 proteins in extracellular vesicles (EVs) from <b>alcohol</b> exposed rodents and human patients with <b>alcoholism</b> and their effects on oxidative hepatocyte injury.
+CYP2E1	drug	alcohol	29404485	Female Fischer rats and wild type or <strong>Cyp2e1</strong> null mice were exposed to three oral doses of binge <b>ethanol</b> or dextrose control at 12 hour intervals.
+CYP2E1	addiction	intoxication	29404485	Female Fischer rats and wild type or <strong>Cyp2e1</strong> null mice were exposed to three oral doses of <b>binge</b> ethanol or dextrose control at 12 hour intervals.
+CYP2E1	drug	alcohol	29404485	The number of EVs and the amounts of EV <strong>CYP2E1</strong>, CYP2A, CYP1A1/2, and CYP4B proteins were markedly elevated in both patients with <b>alcoholism</b> and <b>alcohol</b> exposed rats and mice.
+CYP2E1	drug	alcohol	29404485	The increased number of EVs and EV <strong>CYP2E1</strong> and other P450 isoforms in <b>alcohol</b> exposed wild types were significantly reduced in the corresponding <strong>Cyp2e1</strong> null mice.
+CYP2E1	drug	alcohol	29404485	Elevated EV <strong>CYP2E1</strong> detected after withdrawal from <b>alcohol</b> or exposure to the <strong>CYP2E1</strong> inducer pyrazole can be a potential biomarker for liver injury.
+CYP2E1	addiction	withdrawal	29404485	Elevated EV <strong>CYP2E1</strong> detected after <b>withdrawal</b> from alcohol or exposure to the <strong>CYP2E1</strong> inducer pyrazole can be a potential biomarker for liver injury.
+CYP2E1	addiction	intoxication	29036399	Analysis of liver enzymes revealed a robust induction of <strong>CYP2E1</strong> in C57 and cHAP mice maintained on EtOH DW+<b>Binge</b> or LDE+<b>Binge</b>.
+CYP2E1	drug	alcohol	28951767	Baicalin Ameliorates Liver Injury Induced by Chronic plus Binge <b>Ethanol</b> Feeding by Modulating Oxidative Stress and Inflammation via <strong>CYP2E1</strong> and NRF2 in Mice.
+CYP2E1	addiction	intoxication	28951767	Baicalin Ameliorates Liver Injury Induced by Chronic plus <b>Binge</b> Ethanol Feeding by Modulating Oxidative Stress and Inflammation via <strong>CYP2E1</strong> and NRF2 in Mice.
+CYP2E1	drug	alcohol	28951767	Baicalin inhibited <b>ethanol</b> induced expression of reactive oxygen species (ROS) generating enzymes NOX2, p67phox, xanthine oxidase, and iNOS in addition to <strong>CYP2E1</strong> activities.
+CYP2E1	drug	alcohol	28924552	WZ administration also inhibited <strong>CYP2E1</strong> expression induced by <b>alcohol</b>, and elevated the level of GSH and the activity of SOD in the liver.
+CYP2E1	drug	alcohol	28103636	We measured a number of markers associated with early  and later stage liver disruption, including liver steatosis, measures of liver cytochrome P4502E1 (<strong>CYP2E1</strong>) and <b>alcohol</b> dehydrogenase (ADH), <b>alcohol</b> metabolism, expression of cytokine mRNA, accumulation of 4 hydroxynonenal (4 HNE) as an indicator of oxidative stress, and alanine transaminase/aspartate transaminase as a measure of hepatocyte injury.
+CYP2E1	drug	alcohol	28103636	In addition, <b>alcohol</b> exposure can increase rates of <b>alcohol</b> metabolism through <strong>CYP2E1</strong> and ADH, which can potentially increase oxidative stress and liver dysfunction.
+CYP2E1	drug	alcohol	28103636	Intermittent, excessive <b>alcohol</b> intake increased liver <strong>CYP2E1</strong> mRNA, protein, and activity, as well as ADH mRNA and activity.
+CYP2E1	drug	alcohol	28032633	PPT enhanced catalase, DPN reduced ALDH2, while G1 had no effect on the activity of either enzyme, and none of the agonists influenced <b>alcohol</b> dehydrogenase or <strong>CYP2E1</strong> activities in the myocardium.
+CYP2E1	drug	alcohol	27627966	Hepatic <strong>CYP2E1</strong> was elevated in <b>alcohol</b> treated Tlr4 wild type mice but not in Tlr4 mutant mice.
+CYP2E1	drug	alcohol	27538709	Chronic plus binge <b>ethanol</b> exposure increased the expression of ADH1 and <strong>CYP2E1</strong>.
+CYP2E1	addiction	intoxication	27538709	Chronic plus <b>binge</b> ethanol exposure increased the expression of ADH1 and <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	27375174	Indices of liver injury (alanine and aspartate aminotransferases [ALT and AST]; cytochrome p450 2E1 [<strong>CYP2E1</strong>]; <b>alcohol</b> dehydrogenase [ADH]; Oil Red O and triglyceride content; lipid peroxidation; inflammatory cytokine expression; and macrophage infiltration), and lung inflammatory cell count, proinflammatory cytokine expression, and lipid peroxidation were measured.
+CYP2E1	drug	alcohol	26848198	Characterization of polymorphisms of genes ADH2, ADH3, ALDH2 and <strong>CYP2E1</strong> and relationship to the <b>alcoholism</b> in a Colombian population.
+CYP2E1	drug	alcohol	26848198	Identify and characterize polymorphisms of genes ADH2, ADH3, ALDH2 and <strong>CYP2E1</strong> in a Colombian population residing in the city of Bogotá and determine its possible relationship to the <b>alcoholism</b>.
+CYP2E1	drug	alcohol	26848198	ADH2, ADH3, ALDH2, and <strong>CYP2E1</strong> genotypes a population of 148 individuals with non problematic <b>alcohol</b> and 65 individuals with <b>alcoholism</b> were determined with TaqMan probes and PCR RFLP.
+CYP2E1	drug	alcohol	26848198	In women, the relative frequency for c1 allele in <strong>CYP2E1</strong> was lower in controls than <b>alcoholics</b>.
+CYP2E1	drug	alcohol	26848198	Since substance dependence requires interaction of multiple genes, the combination of genotypes ADH2 * 2, <strong>CYP2E1</strong> * 1 combined with genotype homozygous ALDH2 * 1 found in this study could be leading to the population to a potential risk to <b>alcoholism</b>.
+CYP2E1	addiction	dependence	26848198	Since substance <b>dependence</b> requires interaction of multiple genes, the combination of genotypes ADH2 * 2, <strong>CYP2E1</strong> * 1 combined with genotype homozygous ALDH2 * 1 found in this study could be leading to the population to a potential risk to alcoholism.
+CYP2E1	drug	alcohol	26848198	Se determinaron los genotipos ADH2, ADH3, ALDH2 y <strong>CYP2E1</strong> a una población de 148 individuos con un consumo no problemático de <b>alcohol</b> y 65 individuos con alcoholismo.
+CYP2E1	drug	alcohol	26802685	In higher blood concentrations or in <b>alcoholism</b>, cytochrome's P 450 coenzyme <strong>CYP2E1</strong> also plays an important role in this process.
+CYP2E1	drug	alcohol	26642652	No effect of <b>acamprosate</b> on 4 nitrophenol hydroxylase, a marker of <strong>CYP2E1</strong> activity, was observed.
+CYP2E1	drug	alcohol	26610587	Chronic followed by binge <b>ethanol</b> exacerbated fat accumulation, necrosis, decrease in hepatic SAM and SAM:SAH ratio, increase in adenosine levels, and elevated <strong>CYP2E1</strong> levels.
+CYP2E1	addiction	intoxication	26610587	Chronic followed by <b>binge</b> ethanol exacerbated fat accumulation, necrosis, decrease in hepatic SAM and SAM:SAH ratio, increase in adenosine levels, and elevated <strong>CYP2E1</strong> levels.
+CYP2E1	drug	alcohol	25872594	Expression of <strong>CYP2E1</strong> and CYP2U1 proteins in amygdala and prefrontal cortex: influence of <b>alcoholism</b> and smoking.
+CYP2E1	drug	nicotine	25872594	Expression of <strong>CYP2E1</strong> and CYP2U1 proteins in amygdala and prefrontal cortex: influence of alcoholism and <b>smoking</b>.
+CYP2E1	drug	alcohol	25872594	Of the P450s studied, <strong>CYP2E1</strong> and CYP2U1 were expressed in all samples analyzed (n = 26 and 22 for <strong>CYP2E1</strong> and CYP2U1, respectively), and elevated in <b>alcoholics</b>.
+CYP2E1	drug	alcohol	25514903	Genetic variability in <strong>CYP2E1</strong> and catalase gene among currently and formerly <b>alcohol</b> dependent male subjects.
+CYP2E1	drug	alcohol	25514903	Our findings suggest that the CAT c. 262C>T genetic polymorphism influences the susceptibility to <b>alcohol</b> dependence and severity of <b>alcohol</b> dependence, while <strong>CYP2E1</strong> c. 1053C>T polymorphism influences the expression of obsessive compulsive and anxiety symptoms.
+CYP2E1	addiction	addiction	25514903	Our findings suggest that the CAT c. 262C>T genetic polymorphism influences the susceptibility to alcohol dependence and severity of alcohol dependence, while <strong>CYP2E1</strong> c. 1053C>T polymorphism influences the expression of obsessive <b>compulsive</b> and anxiety symptoms.
+CYP2E1	addiction	dependence	25514903	Our findings suggest that the CAT c. 262C>T genetic polymorphism influences the susceptibility to alcohol <b>dependence</b> and severity of alcohol <b>dependence</b>, while <strong>CYP2E1</strong> c. 1053C>T polymorphism influences the expression of obsessive compulsive and anxiety symptoms.
+CYP2E1	drug	alcohol	25427919	The primary enzymes involved in <b>ethanol</b> metabolism include <b>alcohol</b> dehydrogenase (ADH), cytochrome P450 isoform 2E1, (<strong>CYP2E1</strong>), catalase (CAT), and aldehyde dehydrogenases (ALDH).
+CYP2E1	drug	alcohol	25236742	Binge <b>alcohol</b> promotes hypoxic liver injury through a <strong>CYP2E1</strong> HIF 1α dependent apoptosis pathway in mice and humans.
+CYP2E1	addiction	intoxication	25236742	<b>Binge</b> alcohol promotes hypoxic liver injury through a <strong>CYP2E1</strong> HIF 1α dependent apoptosis pathway in mice and humans.
+CYP2E1	drug	alcohol	25236742	Binge <b>alcohol</b> promoted acute liver injury in mice with elevated levels of <b>ethanol</b> inducible cytochrome P450 2E1 (<strong>CYP2E1</strong>) and hypoxia, both of which were colocalized in the centrilobular areas.
+CYP2E1	addiction	intoxication	25236742	<b>Binge</b> alcohol promoted acute liver injury in mice with elevated levels of ethanol inducible cytochrome P450 2E1 (<strong>CYP2E1</strong>) and hypoxia, both of which were colocalized in the centrilobular areas.
+CYP2E1	drug	alcohol	25236742	We observed positive correlations among elevated BAC, <strong>CYP2E1</strong>, and HIF 1α in mice and humans exposed to binge <b>alcohol</b>.
+CYP2E1	addiction	intoxication	25236742	We observed positive correlations among elevated BAC, <strong>CYP2E1</strong>, and HIF 1α in mice and humans exposed to <b>binge</b> alcohol.
+CYP2E1	drug	alcohol	25236742	Binge <b>alcohol</b> promoted protein nitration and apoptosis with significant correlations observed between inducible nitric oxide synthase and BAC, <strong>CYP2E1</strong>, or HIF 1α in human specimens.
+CYP2E1	addiction	intoxication	25236742	<b>Binge</b> alcohol promoted protein nitration and apoptosis with significant correlations observed between inducible nitric oxide synthase and BAC, <strong>CYP2E1</strong>, or HIF 1α in human specimens.
+CYP2E1	drug	alcohol	25236742	Binge <b>alcohol</b> induced HIF 1α activation and subsequent protein nitration or apoptosis seen in wild type were significantly alleviated in the corresponding <strong>Cyp2e1</strong> null mice, whereas pretreatment with an HIF 1α inhibitor, PX 478, prevented HIF 1α elevation with a trend of decreased levels of 3 nitrotyrosine and apoptosis, supporting the roles of <strong>CYP2E1</strong> and HIF 1α in binge <b>alcohol</b> mediated protein nitration and hepatotoxicity.
+CYP2E1	addiction	intoxication	25236742	<b>Binge</b> alcohol induced HIF 1α activation and subsequent protein nitration or apoptosis seen in wild type were significantly alleviated in the corresponding <strong>Cyp2e1</strong> null mice, whereas pretreatment with an HIF 1α inhibitor, PX 478, prevented HIF 1α elevation with a trend of decreased levels of 3 nitrotyrosine and apoptosis, supporting the roles of <strong>CYP2E1</strong> and HIF 1α in <b>binge</b> alcohol mediated protein nitration and hepatotoxicity.
+CYP2E1	drug	alcohol	25236742	Thus binge <b>alcohol</b> promotes acute liver injury in mice and humans at least partly through a <strong>CYP2E1</strong> HIF 1α dependent apoptosis pathway.
+CYP2E1	addiction	intoxication	25236742	Thus <b>binge</b> alcohol promotes acute liver injury in mice and humans at least partly through a <strong>CYP2E1</strong> HIF 1α dependent apoptosis pathway.
+CYP2E1	drug	alcohol	25180626	Staining for <strong>CYP2E1</strong> and 4 NHE demonstrated marked increases in the hepatic tissue of all the groups of OLETF rats treated with <b>ethanol</b> compared with OLET rats.
+CYP2E1	drug	alcohol	25162931	Cytochrome P4502E1 (<strong>CYP2E1</strong>) has been demonstrated to play crucial roles in chronic <b>ethanol</b> induced fatty liver, while its role in acute <b>ethanol</b> induced fatty liver remains unclear.
+CYP2E1	drug	alcohol	25162931	The current study was designed to evaluate the effects of chlormethiazole (CMZ), a specific inhibitor of <strong>CYP2E1</strong>, on acute <b>ethanol</b> induced fatty liver, and to explore the mechanisms.
+CYP2E1	drug	alcohol	25162931	Collectively, the results of the current study demonstrated that CMZ could effectively attenuate acute <b>ethanol</b> induced fatty liver possibly by suppressing oxidative stress and adiponectin decline, and activating autophagy, which suggest that <strong>CYP2E1</strong> might also play important roles in acute <b>ethanol</b> induced fatty liver.
+CYP2E1	drug	alcohol	24618581	Depolarization was linked to <b>ethanol</b> metabolism, since deficiency of <b>alcohol</b> dehydrogenase and cytochrome P450 2E1 (<strong>CYP2E1</strong>), the major <b>ethanol</b> metabolizing enzymes, decreased mitochondrial depolarization by ∼ 70% and ∼ 20%, respectively.
+CYP2E1	drug	alcohol	24481563	The data indicate an increased susceptibility of fatty liver to <b>ethanol</b> and suggest that the synergistic effect of diet and <b>ethanol</b> on lipid dysmetabolism might be mediated, at least in part, by PPARs and cytochromes CYP4A1 and <strong>CYP2E1</strong>.
+CYP2E1	drug	cannabinoid	24398069	<b>Cannabidiol</b> per se can increase autophagy both in <strong>CYP2E1</strong> expressing HepG2 cells and in mouse liver.
+CYP2E1	drug	alcohol	24064383	<strong>CYP2E1</strong> potentiates binge <b>alcohol</b> induced gut leakiness, steatohepatitis, and apoptosis.
+CYP2E1	addiction	intoxication	24064383	<strong>CYP2E1</strong> potentiates <b>binge</b> alcohol induced gut leakiness, steatohepatitis, and apoptosis.
+CYP2E1	drug	alcohol	24064383	<b>Ethanol</b> inducible cytochrome P450 2E1 (<strong>CYP2E1</strong>) contributes to increased oxidative stress and steatosis in chronic <b>alcohol</b> exposure models.
+CYP2E1	drug	alcohol	24064383	This study was aimed at investigating the role of <strong>CYP2E1</strong> in binge <b>alcohol</b> induced gut leakiness and the mechanisms of steatohepatitis.
+CYP2E1	addiction	intoxication	24064383	This study was aimed at investigating the role of <strong>CYP2E1</strong> in <b>binge</b> alcohol induced gut leakiness and the mechanisms of steatohepatitis.
+CYP2E1	drug	alcohol	24064383	Female wild type (WT) and <strong>Cyp2e1</strong> null mice were treated with three doses of binge <b>ethanol</b> (WT EtOH or <strong>Cyp2e1</strong> null EtOH) (6g/kg oral gavage at 12 h intervals) or dextrose (negative control).
+CYP2E1	addiction	intoxication	24064383	Female wild type (WT) and <strong>Cyp2e1</strong> null mice were treated with three doses of <b>binge</b> ethanol (WT EtOH or <strong>Cyp2e1</strong> null EtOH) (6g/kg oral gavage at 12 h intervals) or dextrose (negative control).
+CYP2E1	drug	alcohol	24064383	These data indicate that both intestinal and hepatic <strong>CYP2E1</strong> induced by binge <b>alcohol</b> seems critical in binge <b>alcohol</b> mediated increased nitroxidative stress, gut leakage, and endotoxemia; altered fat metabolism; and inflammation contributing to hepatic apoptosis and steatohepatitis.
+CYP2E1	addiction	intoxication	24064383	These data indicate that both intestinal and hepatic <strong>CYP2E1</strong> induced by <b>binge</b> alcohol seems critical in <b>binge</b> alcohol mediated increased nitroxidative stress, gut leakage, and endotoxemia; altered fat metabolism; and inflammation contributing to hepatic apoptosis and steatohepatitis.
+CYP2E1	drug	alcohol	24060752	Sulforaphane induces Nrf2 and protects against <strong>CYP2E1</strong> dependent binge <b>alcohol</b> induced liver steatosis.
+CYP2E1	addiction	intoxication	24060752	Sulforaphane induces Nrf2 and protects against <strong>CYP2E1</strong> dependent <b>binge</b> alcohol induced liver steatosis.
+CYP2E1	drug	alcohol	24060752	<strong>CYP2E1</strong> generated ROS contributes to the <b>ethanol</b> induced oxidant stress and inhibition of <strong>CYP2E1</strong> activity decreases <b>ethanol</b> induced fatty liver.
+CYP2E1	drug	alcohol	24060752	The current study was designed to evaluate the ability of sulforaphane, an activator of Nrf2, to blunt <strong>CYP2E1</strong> dependent, <b>ethanol</b> induced steatosis in vivo and in vitro.
+CYP2E1	drug	alcohol	24060752	Similar results were found in vitro as addition of sulforaphane to HepG2 E47 cells, which express <strong>CYP2E1</strong>, elevated Nrf2 levels and decreased the accumulation of lipid in cells cultured with <b>ethanol</b>.
+CYP2E1	drug	alcohol	23639433	<b>Ethanol</b> self administration and nicotine treatment induce brain levels of CYP2B6 and <strong>CYP2E1</strong> in African green monkeys.
+CYP2E1	drug	nicotine	23639433	Ethanol self administration and <b>nicotine</b> treatment induce brain levels of CYP2B6 and <strong>CYP2E1</strong> in African green monkeys.
+CYP2E1	drug	alcohol	23639433	Human smokers and <b>alcoholics</b> have elevated levels of CYP2B6 and <strong>CYP2E1</strong> in certain brain regions, which may contribute to altered drug efficacy, neurotoxicity and metabolic tolerance.
+CYP2E1	drug	nicotine	23639433	Human <b>smokers</b> and alcoholics have elevated levels of CYP2B6 and <strong>CYP2E1</strong> in certain brain regions, which may contribute to altered drug efficacy, neurotoxicity and metabolic tolerance.
+CYP2E1	drug	alcohol	23639433	The objective of this study was to determine the effects of <b>ethanol</b> self administration and nicotine treatment, alone and in combination, on brain CYP2B6 and <strong>CYP2E1</strong> levels in monkeys.
+CYP2E1	drug	nicotine	23639433	The objective of this study was to determine the effects of ethanol self administration and <b>nicotine</b> treatment, alone and in combination, on brain CYP2B6 and <strong>CYP2E1</strong> levels in monkeys.
+CYP2E1	drug	alcohol	23639433	Immunocytochemistry revealed induction of both CYP2B6 and <strong>CYP2E1</strong> protein in certain brain regions and cells within monkey brain as a result of <b>ethanol</b> self administration, nicotine treatment and combined exposure to both drugs.
+CYP2E1	drug	nicotine	23639433	Immunocytochemistry revealed induction of both CYP2B6 and <strong>CYP2E1</strong> protein in certain brain regions and cells within monkey brain as a result of ethanol self administration, <b>nicotine</b> treatment and combined exposure to both drugs.
+CYP2E1	drug	alcohol	23639433	Immunoblotting analyses demonstrated CYP2B6 induction by <b>ethanol</b> in the caudate, putamen and cerebellum (1.5 3.2 fold, P < 0.05), and <strong>CYP2E1</strong> induction by nicotine in the frontal cortex and putamen (1.6 2.0 fold, P < 0.05).
+CYP2E1	drug	nicotine	23639433	Immunoblotting analyses demonstrated CYP2B6 induction by ethanol in the caudate, putamen and cerebellum (1.5 3.2 fold, P < 0.05), and <strong>CYP2E1</strong> induction by <b>nicotine</b> in the frontal cortex and putamen (1.6 2.0 fold, P < 0.05).
+CYP2E1	drug	alcohol	23639433	Combined <b>ethanol</b> and nicotine exposure induced CYP2B6 in the caudate, putamen, thalamus and cerebellum (1.4 2.4 fold, P < 0.05), and <strong>CYP2E1</strong> in the frontal cortex and putamen (1.5 1.8, P < 0.05).
+CYP2E1	drug	nicotine	23639433	Combined ethanol and <b>nicotine</b> exposure induced CYP2B6 in the caudate, putamen, thalamus and cerebellum (1.4 2.4 fold, P < 0.05), and <strong>CYP2E1</strong> in the frontal cortex and putamen (1.5 1.8, P < 0.05).
+CYP2E1	drug	alcohol	23639433	CYP2B6 and <strong>CYP2E1</strong> mRNA levels were unaffected by <b>ethanol</b> or nicotine exposure.
+CYP2E1	drug	nicotine	23639433	CYP2B6 and <strong>CYP2E1</strong> mRNA levels were unaffected by ethanol or <b>nicotine</b> exposure.
+CYP2E1	drug	alcohol	23639433	In summary, <b>ethanol</b> and nicotine can induce CYP2B6 and <strong>CYP2E1</strong> protein in the primate brain, which could potentially result in altered sensitivity to centrally acting drugs and toxins.
+CYP2E1	drug	nicotine	23639433	In summary, ethanol and <b>nicotine</b> can induce CYP2B6 and <strong>CYP2E1</strong> protein in the primate brain, which could potentially result in altered sensitivity to centrally acting drugs and toxins.
+CYP2E1	drug	alcohol	23421770	Sprague Dawley rats were fed a liquid <b>ethanol</b> diet, control diet or <b>ethanol</b> diet supplemented with <strong>CYP2E1</strong> inhibitor, chlormethiazole (CMZ), for 4 weeks.
+CYP2E1	drug	alcohol	23421770	In vitro, isolated Kupffer cells from control rats were exposed to <b>ethanol</b> with different CMZ concentration; <strong>CYP2E1</strong> expression and reactive oxygen species (ROS) generation were compared.
+CYP2E1	drug	alcohol	23421770	The identified CMZ concentration was further utilized to evaluate the role of <strong>CYP2E1</strong> on the sensitization of <b>ethanol</b> induced Kupffer cell to LPS.
+CYP2E1	addiction	sensitization	23421770	The identified CMZ concentration was further utilized to evaluate the role of <strong>CYP2E1</strong> on the <b>sensitization</b> of ethanol induced Kupffer cell to LPS.
+CYP2E1	drug	alcohol	23421770	<b>Ethanol</b> feeding increased hepatic <strong>CYP2E1</strong> level, nuclear accumulation of NF κB p65 and TNF α expression in rats.
+CYP2E1	drug	alcohol	23421770	In cultured Kupffer cells, increased <strong>CYP2E1</strong> content and ROS production by in vitro <b>ethanol</b> induction were dose dependently inhibited by CMZ.
+CYP2E1	drug	alcohol	23421770	In cultured Kupffer cell, using CMZ as inhibitor, <b>ethanol</b> induced <strong>CYP2E1</strong> overexpression was proved to contribute to the sensitization of Kupffer cells to LPS stimuli, with amplification of ROS production and activation of NF κB, resulting in increased TNF α production.
+CYP2E1	addiction	sensitization	23421770	In cultured Kupffer cell, using CMZ as inhibitor, ethanol induced <strong>CYP2E1</strong> overexpression was proved to contribute to the <b>sensitization</b> of Kupffer cells to LPS stimuli, with amplification of ROS production and activation of NF κB, resulting in increased TNF α production.
+CYP2E1	drug	alcohol	23400924	The role of <strong>CYP2E1</strong> in <b>alcohol</b> metabolism and sensitivity in the central nervous system.
+CYP2E1	drug	alcohol	23400924	Catalase and cytochrome P450 2E1 (<strong>CYP2E1</strong>) represent the major enzymes in the CNS that catalyze <b>ethanol</b> oxidation.
+CYP2E1	drug	alcohol	23400924	This chapter focuses on the discussion of <strong>CYP2E1</strong> in <b>ethanol</b> metabolism in the CNS, covering topics including how it is regulated, where it is expressed and how it influences sensitivity to <b>ethanol</b> in the brain.
+CYP2E1	drug	alcohol	23363738	An existing inhibitor of <strong>CYP2E1</strong> is the drug <b>disulfiram</b>.
+CYP2E1	drug	alcohol	23363738	<b>Disulfiram</b> inhibits <strong>CYP2E1</strong> at conventional therapeutic dosages and increases blood acetone levels in humans and animals.
+CYP2E1	drug	alcohol	23352848	However, sodium azide, a catalase inhibitor, and allyl sulfide, an inhibitor of cytochrome P450 2E1 (<strong>CYP2E1</strong>), failed to overcome LTP inhibition by 60mM <b>ethanol</b>.
+CYP2E1	drug	alcohol	23118795	In addition; levels of <b>alcohol</b> dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), the activities of cytochrome P450 2E1 (<strong>CYP2E1</strong>), selected antioxidative enzymes, and the contents of malonaldehyde (MDA) were measured.
+CYP2E1	drug	alcohol	22819980	The goal of the current study was to evaluate whether <strong>CYP2E1</strong> plays a role in binge <b>ethanol</b> induced steatosis and if autophagy impacts <strong>CYP2E1</strong> mediated hepatotoxicity, oxidative stress and fatty liver formation produced by <b>ethanol</b>.
+CYP2E1	addiction	intoxication	22819980	The goal of the current study was to evaluate whether <strong>CYP2E1</strong> plays a role in <b>binge</b> ethanol induced steatosis and if autophagy impacts <strong>CYP2E1</strong> mediated hepatotoxicity, oxidative stress and fatty liver formation produced by ethanol.
+CYP2E1	drug	alcohol	22819980	Wild type (WT), <strong>CYP2E1</strong> knockin (KI) and <strong>CYP2E1</strong> knockout (KO) mice were gavaged with 3g/kg body wt <b>ethanol</b> twice a day for four days.
+CYP2E1	drug	alcohol	22819980	Inhibition of macroautophagy by administration of 3 methyladenine enhanced the binge <b>ethanol</b> hepatotoxicity, steatosis and oxidant stress in <strong>CYP2E1</strong> KI, but not <strong>CYP2E1</strong> KO mice.
+CYP2E1	addiction	intoxication	22819980	Inhibition of macroautophagy by administration of 3 methyladenine enhanced the <b>binge</b> ethanol hepatotoxicity, steatosis and oxidant stress in <strong>CYP2E1</strong> KI, but not <strong>CYP2E1</strong> KO mice.
+CYP2E1	drug	alcohol	22819980	Treatment of HepG2 E47 cells which express <strong>CYP2E1</strong> with 100mM <b>ethanol</b> for 8 days increased fat accumulation and oxidant stress but decreased autophagy.
+CYP2E1	drug	alcohol	22819980	<b>Ethanol</b> had no effect on these reactions in HepG2 C34 cells which do not express <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	22819980	The antioxidant N acetylcysteine, and <strong>CYP2E1</strong> inhibitor chlormethiazole blunted these effects of <b>ethanol</b>.
+CYP2E1	drug	alcohol	22819980	These results indicate that <strong>CYP2E1</strong> plays an important role in binge <b>ethanol</b> induced fatty liver.
+CYP2E1	addiction	intoxication	22819980	These results indicate that <strong>CYP2E1</strong> plays an important role in <b>binge</b> ethanol induced fatty liver.
+CYP2E1	drug	alcohol	22819980	Inhibition of autophagy promotes binge <b>ethanol</b> induced hepatotoxicity, steatosis and oxidant stress via <strong>CYP2E1</strong>.
+CYP2E1	addiction	intoxication	22819980	Inhibition of autophagy promotes <b>binge</b> ethanol induced hepatotoxicity, steatosis and oxidant stress via <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	22749809	Recent studies showed that chronic <b>ethanol</b> induced fatty liver was, at least in part, <strong>CYP2E1</strong> dependent.
+CYP2E1	drug	alcohol	22749809	The mechanism of acute <b>alcohol</b> induced steatosis and whether <strong>CYP2E1</strong> plays any role are still unclear.
+CYP2E1	drug	alcohol	22749809	We used <strong>CYP2E1</strong> knockout (KO) mice, a JNK inhibitor, and JNK1 or JNK2 knockout mice to test the role of <strong>CYP2E1</strong>, JNK, and the individual role of JNK1 and JNK2 in acute <b>alcohol</b> induced steatosis.
+CYP2E1	drug	alcohol	22749809	In wild type (WT) mice, acute <b>alcohol</b> activates <strong>CYP2E1</strong> and increases oxidative stress, which reciprocally increases activation of the JNK signaling pathway.
+CYP2E1	drug	alcohol	22749809	Acute <b>alcohol</b> induced fatty liver and oxidative stress were blunted in <strong>CYP2E1</strong> KO mice and by the JNK inhibitor in WT mice.
+CYP2E1	drug	alcohol	22749809	The antioxidant N acetylcysteine decreased the acute <b>alcohol</b> induced oxidative stress, the activation of JNK, and the steatosis but not the activation of <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	22749809	The results show that acute <b>alcohol</b> elevation of <strong>CYP2E1</strong>, oxidative stress, and activation of JNK interact to lower autophagy and increase lipogenic SREBP resulting in fatty liver.
+CYP2E1	drug	alcohol	22577853	Nine hundred fifty single nucleotide polymorphisms (SNPs) spanning 14 genes (ACN9, ACSS1, ACSS2, ALDH1A1, CAT, <strong>CYP2E1</strong>, GOT1, GOT2, MDH1, MDH2, SLC25A10, SLC25A11, SLC25A12, SLC25A13) were genotyped in 352 young adults who participated in an <b>alcohol</b> challenge study.
+CYP2E1	drug	alcohol	22577853	However, based on the breath <b>alcohol</b> data, variation in the promoter of <strong>CYP2E1</strong> may play a role in preabsorptive or early hepatic <b>alcohol</b> metabolism, but more samples are required to validate this finding.
+CYP2E1	drug	alcohol	22552773	<b>Ethanol</b> induction of CYP2A5: role of <strong>CYP2E1</strong> ROS Nrf2 pathway.
+CYP2E1	drug	alcohol	22552773	Chronic <b>ethanol</b> consumption was previously shown to induce CYP2A5 in mice, and this induction of CYP2A5 by <b>ethanol</b> was <strong>CYP2E1</strong> dependent.
+CYP2E1	drug	alcohol	22552773	In this study, the mechanisms of <strong>CYP2E1</strong> dependent <b>ethanol</b> induction of CYP2A5 were investigated.
+CYP2E1	drug	alcohol	22552773	<strong>CYP2E1</strong> was induced by chronic <b>ethanol</b> consumption to the same degree in wild type (WT) mice and CYP2A5 knockout (Cyp2a5 ( / )) mice, suggesting that unlike the <strong>CYP2E1</strong> dependent <b>ethanol</b> induction of CYP2A5, <b>ethanol</b> induction of <strong>CYP2E1</strong> is not CYP2A5 dependent.
+CYP2E1	drug	alcohol	22552773	Microsomal <b>ethanol</b> oxidation was about 25% lower in Cyp2a5 ( / ) mice compared with that in WT mice, suggesting that CYP2A5 can oxidize <b>ethanol</b> although to a lesser extent than <strong>CYP2E1</strong> does.
+CYP2E1	drug	alcohol	22552773	CYP2A5 was induced by short term <b>ethanol</b> consumption in human <strong>CYP2E1</strong> transgenic knockin (<strong>Cyp2e1</strong> ( / ) KI) mice but not in <strong>CYP2E1</strong> knockout (<strong>Cyp2e1</strong> ( / )) mice.
+CYP2E1	drug	alcohol	22552773	The redox sensitive transcription factor nuclear factor erythroid 2 related factor 2 (Nrf2) was also induced by acute <b>ethanol</b> in <strong>Cyp2e1</strong> ( / ) KI mice but not in <strong>Cyp2e1</strong> ( / ) mice.
+CYP2E1	drug	alcohol	22552773	<b>Ethanol</b> induction of CYP2A5 in Nrf2 knockout (Nrf2 ( / )) mice was lower compared with that in WT mice, whereas <strong>CYP2E1</strong> induction by <b>ethanol</b> was comparable in WT and Nrf2 ( / ) mice.
+CYP2E1	drug	alcohol	22552773	Antioxidants (N acetyl cysteine and vitamin C), which blocked oxidative stress induced by chronic <b>ethanol</b> in WT mice and acute <b>ethanol</b> in <strong>Cyp2e1</strong> ( / ) KI mice, also blunted the induction of CYP2A5 and Nrf2 by <b>ethanol</b> but not the induction of <strong>CYP2E1</strong> by <b>ethanol</b>.
+CYP2E1	drug	alcohol	22552773	These results suggest that oxidative stress induced by <b>ethanol</b> via induction of <strong>CYP2E1</strong> upregulates Nrf2 activity, which in turn regulates <b>ethanol</b> induction of CYP2A5.
+CYP2E1	drug	alcohol	22545783	The significant changes in proteome profile in chronic <b>ethanol</b> binge were accompanied by a marked increase in liver injury as evidenced by enhanced steatosis, necrosis, increased 4 hydroxynonenal labeled proteins, <strong>CYP2E1</strong> expression, and decreased histone H2AX phosphorylation.
+CYP2E1	addiction	intoxication	22545783	The significant changes in proteome profile in chronic ethanol <b>binge</b> were accompanied by a marked increase in liver injury as evidenced by enhanced steatosis, necrosis, increased 4 hydroxynonenal labeled proteins, <strong>CYP2E1</strong> expression, and decreased histone H2AX phosphorylation.
+CYP2E1	drug	alcohol	22331481	Three SNPs in genes in the <b>alcohol</b> metabolism pathway were genotyped: <b>alcohol</b> dehydrogenase 2, <b>alcohol</b> dehydrogenase 3, and <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	21929725	This review will focus on one particular CYP, <strong>CYP2E1</strong>, which represents a significant source of reactive oxygen species and is involved in the metabolism of small molecule substrates including <b>ethanol</b>, drugs and carcinogens.
+CYP2E1	drug	alcohol	21929725	Since hepatic <strong>CYP2E1</strong> expression is increased in different physiopathological situations such as type 2 diabetes, obesity and <b>ethanol</b> intoxication, the presence of significant levels of this CYP within the mitochondria could have major deleterious effects.
+CYP2E1	addiction	intoxication	21929725	Since hepatic <strong>CYP2E1</strong> expression is increased in different physiopathological situations such as type 2 diabetes, obesity and ethanol <b>intoxication</b>, the presence of significant levels of this CYP within the mitochondria could have major deleterious effects.
+CYP2E1	drug	alcohol	21868470	Independent and combined effects of <b>ethanol</b> self administration and nicotine treatment on hepatic <strong>CYP2E1</strong> in African green monkeys.
+CYP2E1	drug	nicotine	21868470	Independent and combined effects of ethanol self administration and <b>nicotine</b> treatment on hepatic <strong>CYP2E1</strong> in African green monkeys.
+CYP2E1	drug	alcohol	21868470	This study investigated the induction of hepatic <strong>CYP2E1</strong> by <b>ethanol</b> and nicotine, alone and in combination, in a nonhuman primate model.
+CYP2E1	drug	nicotine	21868470	This study investigated the induction of hepatic <strong>CYP2E1</strong> by ethanol and <b>nicotine</b>, alone and in combination, in a nonhuman primate model.
+CYP2E1	drug	alcohol	21868470	Chlorzoxazone (CZN) was used as a probe drug to phenotype in vivo <strong>CYP2E1</strong> activity before and after chronic <b>ethanol</b> and/or nicotine exposure.
+CYP2E1	drug	nicotine	21868470	Chlorzoxazone (CZN) was used as a probe drug to phenotype in vivo <strong>CYP2E1</strong> activity before and after chronic ethanol and/or <b>nicotine</b> exposure.
+CYP2E1	drug	alcohol	21868470	<b>Ethanol</b> and nicotine increased <strong>CYP2E1</strong> protein levels and in vitro CZN metabolism, with combined exposure to both drugs resulting in the greatest increase.
+CYP2E1	drug	nicotine	21868470	Ethanol and <b>nicotine</b> increased <strong>CYP2E1</strong> protein levels and in vitro CZN metabolism, with combined exposure to both drugs resulting in the greatest increase.
+CYP2E1	drug	alcohol	21868470	Chronic exposure to <b>ethanol</b> and nicotine induced hepatic <strong>CYP2E1</strong> activity and protein levels, particularly when both drugs were used in combination and when <b>ethanol</b> intake was high.
+CYP2E1	drug	nicotine	21868470	Chronic exposure to ethanol and <b>nicotine</b> induced hepatic <strong>CYP2E1</strong> activity and protein levels, particularly when both drugs were used in combination and when ethanol intake was high.
+CYP2E1	drug	alcohol	21868470	These results have important implications for public health, given the association between elevated <strong>CYP2E1</strong> and disease, and the large proportion of individuals who are exposed to <b>ethanol</b> and nicotine, often in combination.
+CYP2E1	drug	nicotine	21868470	These results have important implications for public health, given the association between elevated <strong>CYP2E1</strong> and disease, and the large proportion of individuals who are exposed to ethanol and <b>nicotine</b>, often in combination.
+CYP2E1	drug	alcohol	21813270	These results suggest that soy protein may improve <b>alcohol</b> induced lipid accumulation, oxidative stress and inflammation by decreasing proinflammatory cytokines and <strong>CYP2E1</strong> protein expression and by increasing PPARα and CYP4A protein expressions and fecal lipid excretion, thereby producing beneficial effects on ALD during <b>ethanol</b> withdrawal.
+CYP2E1	addiction	withdrawal	21813270	These results suggest that soy protein may improve alcohol induced lipid accumulation, oxidative stress and inflammation by decreasing proinflammatory cytokines and <strong>CYP2E1</strong> protein expression and by increasing PPARα and CYP4A protein expressions and fecal lipid excretion, thereby producing beneficial effects on ALD during ethanol <b>withdrawal</b>.
+CYP2E1	drug	alcohol	21284674	Exposing 4 dpf zebrafish larvae to 2% <b>ethanol</b> (EtOH) for 32 hours achieves ∼80 mM intracellular EtOH and upregulation of hepatic <strong>cyp2e1</strong>, sod, and bip, indicating that EtOH is metabolized and provokes oxidative stress.
+CYP2E1	drug	alcohol	20958327	The inhibitor of cytochrome P450 2E1 (<strong>CYP2E1</strong>) had no effect on <b>ethanol</b> induced DNA damage, and <strong>CYP2E1</strong> mRNA expression was not affected by <b>ethanol</b>.
+CYP2E1	drug	alcohol	20828554	The <b>ethanol</b> elimination rate is regulated by <b>alcohol</b> metabolizing enzymes, primarily <b>alcohol</b> dehydrogenase (ADH1), acetaldehyde dehydrogenase (ALDH), and cytochrome P450 (<strong>CYP2E1</strong>).
+CYP2E1	drug	alcohol	20598484	The most well known metabolic pathways from <b>ethanol</b> to acetaldehyde include <b>alcohol</b> dehydrogenase (ADH) and the microsomal <b>ethanol</b> oxidizing system that involves cytochrome P450 2E1 (<strong>CYP2E1</strong>).
+CYP2E1	drug	alcohol	20598484	The genetic variation of ADH1B, ALDH2, and <strong>CYP2E1</strong> is different among racial populations and cause difference in elimination rates of <b>alcohol</b>.
+CYP2E1	drug	alcohol	20598484	This study may be useful in epidemiological studies of the influence of ADH1B, ALDH2, <strong>CYP2E1</strong>*6, and <strong>CYP2E1</strong>*7B polymorphisms on diseases, including several types of cancer related to <b>alcohol</b> consumption and <b>alcohol</b> dependence.
+CYP2E1	addiction	dependence	20598484	This study may be useful in epidemiological studies of the influence of ADH1B, ALDH2, <strong>CYP2E1</strong>*6, and <strong>CYP2E1</strong>*7B polymorphisms on diseases, including several types of cancer related to alcohol consumption and alcohol <b>dependence</b>.
+CYP2E1	drug	alcohol	20401433	The purpose of this study was to investigate the differences, if present, in the allele and genotype frequency of <b>alcohol</b> dehydrogenase 1B (ADH1B), ADH1C and the microsomal <b>ethanol</b> oxidizing system (MEOS/<strong>CYP2E1</strong>) between <b>alcohol</b> dependent individuals and controls and also to determine if these genotypes cause a difference in the age at which the patients become <b>alcohol</b> dependent.
+CYP2E1	drug	alcohol	20401433	The allele and genotype frequencies of ADH1B, ADH1C, and <strong>CYP2E1</strong> were determined in 204 <b>alcohol</b> dependent men and 172 healthy volunteers who do not drink <b>alcohol</b> (control group).
+CYP2E1	drug	alcohol	20401433	The persons with ADH1C*1/*1 and <strong>CYP2E1</strong>*c1/*c2 genotypes became <b>alcohol</b> dependent at a considerably younger age than the subjects with ADH1C*1/*2, ADH1C*2/*2 and <strong>CYP2E1</strong>*c1/*c1 genotypes (28.08, 25.67 years vs 36.0, 45.05, 34.45 years, respectively).
+CYP2E1	drug	alcohol	20401433	However, subjects with ADH1C*1/*1 and <strong>CYP2E1</strong>*c1/*c2 genotypes become <b>alcohol</b> dependent at a considerably younger age than the subjects with ADH1C*1/*2, ADH1C*2/*2 and <strong>CYP2E1</strong>*c1/*c1 genotypes.
+CYP2E1	drug	alcohol	20304569	In <b>alcoholics</b> during detoxification, because activity of microsomal enzyme (<strong>CYP2E1</strong>) is boosted, the <b>ethanol</b> elimination rate might be 25 35 mg/100mL/h.
+CYP2E1	drug	alcohol	19177030	<b>Ethanol</b> intake and <b>ethanol</b> induced locomotion and locomotor sensitization in <strong>Cyp2e1</strong> knockout mice.
+CYP2E1	addiction	sensitization	19177030	Ethanol intake and ethanol induced locomotion and locomotor <b>sensitization</b> in <strong>Cyp2e1</strong> knockout mice.
+CYP2E1	drug	alcohol	19079654	<b>Ethanol</b>, alone and in high concentrations, was found to greatly affect cell function as shown by decreased cellular ATP levels, increased LDH release, and a downregulated expression of <strong>CYP2E1</strong> gene.
+CYP2E1	addiction	addiction	19004845	Published data and data obtained from the drug's manufacturer implies that the dose <b>escalation</b> after 48 hours is to compensate for fomepizole induced increased body clearance resulting from autoinduction of the cytochrome P450 (CYP) drug metabolizing enzyme <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	18804449	Use of <strong>CYP2E1</strong> knockout mice demonstrated that <b>ethanol</b> induced acetylation was not dependent solely on <strong>CYP2E1</strong> expression.
+CYP2E1	drug	alcohol	18326880	Distribution and differential induction of <strong>CYP2E1</strong> by <b>ethanol</b> and acetone in the mesocorticolimbic system of rat.
+CYP2E1	drug	alcohol	18326880	The expression of cytochrome P4502E1 (<strong>CYP2E1</strong>) in the brain has been demonstrated in several regions, nevertheless there is a lack of specific studies on the constitutive expression and induction at the mesocorticolimbic system, the most relevant brain pathway in the context of drug addiction and <b>alcoholism</b>.
+CYP2E1	addiction	addiction	18326880	The expression of cytochrome P4502E1 (<strong>CYP2E1</strong>) in the brain has been demonstrated in several regions, nevertheless there is a lack of specific studies on the constitutive expression and induction at the mesocorticolimbic system, the most relevant brain pathway in the context of drug <b>addiction</b> and alcoholism.
+CYP2E1	drug	alcohol	18326880	(i) <strong>CYP2E1</strong> was expressed in PFC, Nac, and VTA, with the order of magnitude of the levels being VTA approximately PFC > Nac, and approximately 3 13% of it was encountered in liver; (ii) acetone treatment significantly increased <strong>CYP2E1</strong> expression in Nac, up to 212% of the control levels, whereas not significant changes were observed in VTA and PFC; (iii) chronic <b>ethanol</b> treatment only resulted in a significant induction of enzyme levels in VTA (124%).
+CYP2E1	drug	alcohol	18267108	Betaine supplied in drinking water for 2 weeks attenuated the induction of <b>alcoholic</b> liver injury and <strong>Cyp2e1</strong> significantly.
+CYP2E1	drug	alcohol	17978975	Section 1 focuses on the <b>alcohol</b> and acetaldehyde dehydrogenases, while section 2 focuses on <strong>CYP2E1</strong> and its possible role in <b>alcohol</b> and tobacco dependence.
+CYP2E1	drug	nicotine	17978975	Section 1 focuses on the alcohol and acetaldehyde dehydrogenases, while section 2 focuses on <strong>CYP2E1</strong> and its possible role in alcohol and <b>tobacco</b> dependence.
+CYP2E1	addiction	dependence	17978975	Section 1 focuses on the alcohol and acetaldehyde dehydrogenases, while section 2 focuses on <strong>CYP2E1</strong> and its possible role in alcohol and tobacco <b>dependence</b>.
+CYP2E1	drug	alcohol	17718403	The primary enzymes involved are aldehyde dehydrogenase (ALDH), <b>alcohol</b> dehydrogenase (ADH), cytochrome P450 (<strong>CYP2E1</strong>), and catalase.
+CYP2E1	drug	alcohol	17590863	The presence in rat mammary tissue of low activities of additional enzymes able to generate acetaldehyde was established (<b>alcohol</b> dehydrogenase: 0.97+/ 0.84 mU mg( 1) protein; <strong>CYP2E1</strong>: 1.30+/ 0.12 x 10( 2) pmol 4 nitrocatechol min( 1) mg( 1) protein) and a low activity of aldehyde dehydrogenase was observed in the cytosolic, mitochondrial and microsomal fractions (0.02+/ 0.04; 0.35+/ 0.09 and 0.72+/ 0.19 mU mg( 1) protein, respectively).
+CYP2E1	drug	alcohol	17392391	Role of CYP3A and <strong>CYP2E1</strong> in <b>alcohol</b> mediated increases in acetaminophen hepatotoxicity: comparison of wild type and <strong>Cyp2e1</strong>( / ) mice.
+CYP2E1	drug	alcohol	17392391	<strong>CYP2E1</strong> is widely accepted as the sole form of cytochrome P450 responsible for <b>alcohol</b> mediated increases in acetaminophen (APAP) hepatotoxicity.
+CYP2E1	drug	alcohol	17392391	However, we previously found that <b>alcohol</b> [<b>ethanol</b> and isopentanol (EIP)] causes increases in APAP hepatotoxicity in <strong>Cyp2e1</strong>( / ) mice, indicating that <strong>CYP2E1</strong> is not essential.
+CYP2E1	drug	alcohol	17392391	At the time of APAP administration, which followed an 11 h withdrawal from the alcohols, <b>alcohol</b> induced levels of CYP3A were sustained in both mouse lines, whereas <strong>CYP2E1</strong> was decreased to constitutive levels in wild type mice.
+CYP2E1	addiction	withdrawal	17392391	At the time of APAP administration, which followed an 11 h <b>withdrawal</b> from the alcohols, alcohol induced levels of CYP3A were sustained in both mouse lines, whereas <strong>CYP2E1</strong> was decreased to constitutive levels in wild type mice.
+CYP2E1	drug	alcohol	17392391	In conclusion, these findings suggest that both CYP3A and <strong>CYP2E1</strong> contribute to APAP hepatotoxicity in <b>alcohol</b> treated mice.
+CYP2E1	drug	alcohol	17058263	Binge or chronic <b>alcohol</b> exposure significantly elevated nitric oxide, inducible nitric oxide synthase, and <b>ethanol</b> inducible <strong>CYP2E1</strong>.
+CYP2E1	addiction	intoxication	17058263	<b>Binge</b> or chronic alcohol exposure significantly elevated nitric oxide, inducible nitric oxide synthase, and ethanol inducible <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	16923312	Furthermore, hydroxyethyl free radicals (HER) are also generated during <b>ethanol</b> metabolism by <strong>CYP2E1</strong>.
+CYP2E1	addiction	sensitization	16549397	In order to evaluate the biochemical and toxicological actions of <strong>CYP2E1</strong> and its <b>sensitization</b> of hepatotoxin induced injury, an adenovirus which can mediate overexpression of <strong>CYP2E1</strong> was constructed.
+CYP2E1	drug	alcohol	16337880	<strong>CYP2E1</strong> plays an important role in toxicity of many chemicals and <b>ethanol</b> and produces oxidant stress.
+CYP2E1	addiction	withdrawal	16337880	Serum <b>withdrawal</b> induced E47 cell death could be rescued by antioxidants, the mitochondrial permeability transition inhibitor cyclosporine A, z DEVD fmk, and a <strong>CYP2E1</strong> inhibitor 4 methylpyrazole.
+CYP2E1	addiction	withdrawal	16337880	We propose that the mechanism of this serum <b>withdrawal</b> plus <strong>CYP2E1</strong> toxicity involves increased production of intracellular ROS, lipid peroxidation, and decline of GSH levels, which results in mitochondrial membrane damage and loss of membrane potential, followed by apoptosis.
+CYP2E1	drug	alcohol	16337880	Potentiation of serum deprivation induced cell death by <strong>CYP2E1</strong> may contribute to the sensitivity of the liver to <b>alcohol</b> induced ischemia and growth factor deprivation.
+CYP2E1	drug	alcohol	16337197	In this study, we asked whether <b>ethanol</b>, a known inducer of microsomal <strong>CYP2E1</strong>, could also increase <strong>CYP2E1</strong> within mitochondria.
+CYP2E1	drug	alcohol	16337197	Our findings indicated that <b>ethanol</b> increased microsomal and mitochondrial <strong>CYP2E1</strong> in cultured rat hepatocytes and in the liver of lean mice.
+CYP2E1	drug	alcohol	16337197	In contrast, in leptin deficient obese mice, <b>ethanol</b> administration did not increase mitochondrial <strong>CYP2E1</strong>, nor it depleted mitochondrial glutathione, suggesting that leptin deficiency hampers mitochondrial targeting of <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	16337197	Thus, <b>ethanol</b> intoxication increases <strong>CYP2E1</strong> not only in the endoplasmic reticulum but also in mitochondria, thus favouring oxidative stress in these compartments.
+CYP2E1	addiction	intoxication	16337197	Thus, ethanol <b>intoxication</b> increases <strong>CYP2E1</strong> not only in the endoplasmic reticulum but also in mitochondria, thus favouring oxidative stress in these compartments.
+CYP2E1	drug	alcohol	16317704	<b>Alcohol</b> administration to ob/ob mice did not increase oxidative stress despite increased <strong>CYP2E1</strong>, but increased plasma TNF alpha, further increased Hsp70, and profoundly decreased p65 nuclear factor kappaB (NF kappaB) protein and DNA binding activity in nuclear extracts.
+CYP2E1	drug	alcohol	16311924	Inter individual genetic polymorphisms of the <strong>CYP2E1</strong> gene are associated with different cancer diseases as well as <b>alcohol</b> and nicotine dependence.
+CYP2E1	drug	nicotine	16311924	Inter individual genetic polymorphisms of the <strong>CYP2E1</strong> gene are associated with different cancer diseases as well as alcohol and <b>nicotine</b> dependence.
+CYP2E1	addiction	dependence	16311924	Inter individual genetic polymorphisms of the <strong>CYP2E1</strong> gene are associated with different cancer diseases as well as alcohol and nicotine <b>dependence</b>.
+CYP2E1	drug	alcohol	15982967	After 4 weeks of <b>ethanol</b> intoxication, although cytochrome <strong>CYP2E1</strong> was increased, liver lipid peroxidation remained unchanged when protein carbonyls augmented selectively for high molecular weight with a decrease of the proteasome activities in <b>ethanol</b> rats.
+CYP2E1	addiction	intoxication	15982967	After 4 weeks of ethanol <b>intoxication</b>, although cytochrome <strong>CYP2E1</strong> was increased, liver lipid peroxidation remained unchanged when protein carbonyls augmented selectively for high molecular weight with a decrease of the proteasome activities in ethanol rats.
+CYP2E1	drug	alcohol	15961886	Because cytochrome P4502E1 (<strong>CYP2E1</strong>) is upregulated in Kupffer cells after <b>ethanol</b>, we hypothesized that this effect primes Kupffer cells, sensitizing them to increase TNF alpha production in response to LPS.
+CYP2E1	addiction	sensitization	15961886	Oxidant generation after <strong>CYP2E1</strong> overexpression appears to be central to macrophage priming and their <b>sensitization</b> to LPS.
+CYP2E1	drug	alcohol	15961886	Accordingly, <strong>CYP2E1</strong> priming could explain the sensitization of Kupffer cells to LPS activation by <b>ethanol</b>, a critical early step in <b>alcoholic</b> liver disease.
+CYP2E1	addiction	sensitization	15961886	Accordingly, <strong>CYP2E1</strong> priming could explain the <b>sensitization</b> of Kupffer cells to LPS activation by ethanol, a critical early step in alcoholic liver disease.
+CYP2E1	drug	alcohol	15066702	Mexican Americans have a low frequency of the protective alleles ADH1B(*)2 and ALDH2(*)2 and a relatively high frequency of <strong>CYP2E1</strong> c2, which is associated with early onset <b>alcoholism</b>.
+CYP2E1	drug	alcohol	14695664	Hepatitis C virus (HCV) and HCV core protein are hypothesized to induce hepatic oxidative stress and exacerbate injury caused by other toxins such as <b>ethanol</b> that induce the cytochrome P450 enzyme, <strong>CYP2E1</strong>.
+CYP2E1	addiction	sensitization	14695664	These studies show simultaneous expression of HCV core protein and <strong>CYP2E1</strong> increases parameters indicative of oxidative stress as well as <b>sensitization</b> to cell injury induced by GSH depletion.
+CYP2E1	drug	alcohol	12777962	<strong>CYP2E1</strong>*1D regulatory polymorphism: association with <b>alcohol</b> and nicotine dependence.
+CYP2E1	drug	nicotine	12777962	<strong>CYP2E1</strong>*1D regulatory polymorphism: association with alcohol and <b>nicotine</b> dependence.
+CYP2E1	addiction	dependence	12777962	<strong>CYP2E1</strong>*1D regulatory polymorphism: association with alcohol and nicotine <b>dependence</b>.
+CYP2E1	drug	alcohol	12777962	<strong>CYP2E1</strong> bioactivates environmental protoxins and metabolizes <b>alcohol</b>.
+CYP2E1	drug	alcohol	12777962	<strong>CYP2E1</strong> is induced by <b>alcohol</b> and cigarette smoking and may contribute to metabolic tolerance in <b>alcoholics</b>.
+CYP2E1	drug	nicotine	12777962	<strong>CYP2E1</strong> is induced by alcohol and cigarette <b>smoking</b> and may contribute to metabolic tolerance in alcoholics.
+CYP2E1	drug	alcohol	12777962	Further, the Canadian Native Indian, South east Asian Canadian and Caucasian Canadian groups were stratified by <b>alcohol</b> and nicotine dependence (as measured by DSM IV criteria) to examine the potential association of <strong>CYP2E1</strong>*1D with drug dependence.
+CYP2E1	drug	nicotine	12777962	Further, the Canadian Native Indian, South east Asian Canadian and Caucasian Canadian groups were stratified by alcohol and <b>nicotine</b> dependence (as measured by DSM IV criteria) to examine the potential association of <strong>CYP2E1</strong>*1D with drug dependence.
+CYP2E1	addiction	dependence	12777962	Further, the Canadian Native Indian, South east Asian Canadian and Caucasian Canadian groups were stratified by alcohol and nicotine <b>dependence</b> (as measured by DSM IV criteria) to examine the potential association of <strong>CYP2E1</strong>*1D with drug <b>dependence</b>.
+CYP2E1	drug	alcohol	12777962	Although the power of the association study was low among some subgroups, the <strong>CYP2E1</strong>*1D genotype (subjects with at least one variant allele) was associated with <b>alcohol</b> as well as nicotine dependence.
+CYP2E1	drug	nicotine	12777962	Although the power of the association study was low among some subgroups, the <strong>CYP2E1</strong>*1D genotype (subjects with at least one variant allele) was associated with alcohol as well as <b>nicotine</b> dependence.
+CYP2E1	addiction	dependence	12777962	Although the power of the association study was low among some subgroups, the <strong>CYP2E1</strong>*1D genotype (subjects with at least one variant allele) was associated with alcohol as well as nicotine <b>dependence</b>.
+CYP2E1	drug	alcohol	12777962	Specifically, Canadian Native Indians dependent on nicotine alone or <b>alcohol</b> alone exhibited significantly greater <strong>CYP2E1</strong>*1D frequencies compared to non drug dependent controls, while the variant frequency among Southeast Asians dependent on nicotine was greater than their non drug dependent counterparts.
+CYP2E1	drug	nicotine	12777962	Specifically, Canadian Native Indians dependent on <b>nicotine</b> alone or alcohol alone exhibited significantly greater <strong>CYP2E1</strong>*1D frequencies compared to non drug dependent controls, while the variant frequency among Southeast Asians dependent on <b>nicotine</b> was greater than their non drug dependent counterparts.
+CYP2E1	drug	alcohol	12777962	The association of <strong>CYP2E1</strong>*1D with <b>alcohol</b> and nicotine dependence suggests that <strong>CYP2E1</strong> may contribute to the development of these dependencies.
+CYP2E1	drug	nicotine	12777962	The association of <strong>CYP2E1</strong>*1D with alcohol and <b>nicotine</b> dependence suggests that <strong>CYP2E1</strong> may contribute to the development of these dependencies.
+CYP2E1	addiction	dependence	12777962	The association of <strong>CYP2E1</strong>*1D with alcohol and nicotine <b>dependence</b> suggests that <strong>CYP2E1</strong> may contribute to the development of these dependencies.
+CYP2E1	drug	alcohol	12710951	The ADH3*2 and <strong>CYP2E1</strong> c2 alleles increase the risk of <b>alcoholism</b> in Mexican American men.
+CYP2E1	drug	alcohol	12710951	To identify the association between the polymorphisms of genes encoding <b>alcohol</b> metabolizing enzymes and <b>alcoholism</b>, the <b>alcohol</b> dehydrogenase 2 (ADH2), <b>alcohol</b> dehydrogenase 3 (ADH3), aldehyde dehydrogenase 2 (ALDH2), and cytochrome P450 2E1 (<strong>CYP2E1</strong>) genes were studied in 101 male Mexican American <b>alcoholics</b>.
+CYP2E1	drug	alcohol	12710951	Association was also found between the <strong>CYP2E1</strong> RsaI c2 allele and <b>alcohol</b> dependence; the percentage of subjects who carry the RsaI c2 allele was significantly higher in <b>alcoholics</b> (34.7%) than in nonalcoholics (22.1%).
+CYP2E1	addiction	dependence	12710951	Association was also found between the <strong>CYP2E1</strong> RsaI c2 allele and alcohol <b>dependence</b>; the percentage of subjects who carry the RsaI c2 allele was significantly higher in alcoholics (34.7%) than in nonalcoholics (22.1%).
+CYP2E1	drug	alcohol	12710951	The subjects whose <b>alcohol</b> drinking onset age is younger than 25 have much higher <strong>CYP2E1</strong> c2 allele frequency than those whose <b>alcohol</b> drinking onset age is older than 25 (22.1% vs 15.7%).
+CYP2E1	drug	alcohol	12710951	Among 101 <b>alcoholics</b>, only 18 subjects carry neither ADH3*2 nor <strong>CYP2E1</strong> c2 alleles.
+CYP2E1	drug	alcohol	12710951	For those subjects who have an ADH*1/*1 background, a strong association is found between <strong>CYP2E1</strong> RsaI/DraI genotype and <b>alcoholism</b>; the <strong>CYP2E1</strong> RsaI c2 and DraI C allele frequencies are much higher in <b>alcoholics</b> than in nonalcoholics (26.4% vs 9.6% for c2 and 27.8% vs 13.5% for C allele).
+CYP2E1	drug	alcohol	12710951	Taken together, ADH3*2 and <strong>CYP2E1</strong> c2/C alleles might independently contribute to the development of <b>alcoholism</b> in Mexican American men.
+CYP2E1	drug	alcohol	12707490	<strong>CYP2E1</strong> and clinical features in <b>alcoholics</b>.
+CYP2E1	drug	alcohol	12707490	Persons who are either hetereozygous or mutant homozygous for <strong>CYP2E1</strong> (C1/C2 or C2/C2) can drink much more <b>alcohol</b> than persons who are normal homozygous for <strong>CYP2E1</strong> (C1/C1) among those whose aldehyde dehydrogenase 2 genotype is heterozygous.
+CYP2E1	drug	alcohol	12707490	We have shown that the genotypes of <strong>CYP2E1</strong> are associated with clinical features of <b>alcoholics</b>.
+CYP2E1	drug	alcohol	12433812	Chronic <b>ethanol</b> consumption potentiates acetaminophen (APAP) hepatotoxicity through enhanced NAPQI formation via <strong>CYP2E1</strong> induction and selective depletion of mitochondrial glutathione.
+CYP2E1	drug	alcohol	12433812	The highest <b>ethanol</b> containing diet (36% energy as <b>ethanol</b>) was replaced by control diet for 2, 5, 12, and 17 h. Maximal <strong>CYP2E1</strong> induction was caused by 36% energy as <b>ethanol</b> diet (2.2 fold, p < 0.05 versus control).
+CYP2E1	drug	alcohol	12433812	In conclusion, high dose <b>ethanol</b> potentiated APAP hepatotoxicity via <strong>CYP2E1</strong> induction and selective mitochondrial GSH depletion.
+CYP2E1	drug	alcohol	11812920	The liver expresses many cytochrome P450 isoforms, including <b>ethanol</b> induced <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	11812920	<strong>CYP2E1</strong> generates ROS, activates many toxicologically important substrates, and may be the central pathway by which <b>ethanol</b> causes oxidative stress.
+CYP2E1	drug	alcohol	11804663	Chronic <b>ethanol</b> consumption results in the induction of hepatic cytochrome P4502E1 (<strong>CYP2E1</strong>) in man, which is believed to play an important role in the pathogenesis of <b>alcoholic</b> liver disease.
+CYP2E1	drug	alcohol	11804663	However, the amount and duration of <b>alcohol</b> intake associated with <strong>CYP2E1</strong> induction is not known but limited information is available on the disappearance of <strong>CYP2E1</strong> following <b>alcohol</b> withdrawal.
+CYP2E1	addiction	withdrawal	11804663	However, the amount and duration of alcohol intake associated with <strong>CYP2E1</strong> induction is not known but limited information is available on the disappearance of <strong>CYP2E1</strong> following alcohol <b>withdrawal</b>.
+CYP2E1	drug	alcohol	11804663	<strong>CYP2E1</strong> induction was monitored by using the chlorzoxazone test before and every week following the start of <b>alcohol</b> ingestion.
+CYP2E1	drug	alcohol	11804663	In addition, <strong>CYP2E1</strong> was also determined in five <b>alcoholics</b> 1, 3, 8 and 15 days following <b>ethanol</b> withdrawal and in five patients with non <b>alcoholic</b> liver disease.
+CYP2E1	addiction	withdrawal	11804663	In addition, <strong>CYP2E1</strong> was also determined in five alcoholics 1, 3, 8 and 15 days following ethanol <b>withdrawal</b> and in five patients with non alcoholic liver disease.
+CYP2E1	drug	alcohol	11804663	A significant <strong>CYP2E1</strong> induction occurred 1 week following the ingestion of 40 g <b>ethanol</b> per day and increased further after 4 weeks.
+CYP2E1	drug	alcohol	11804663	The disappearance of <strong>CYP2E1</strong> was found to be significant 3 days following <b>ethanol</b> withdrawal and further decreased up to day 8.
+CYP2E1	addiction	withdrawal	11804663	The disappearance of <strong>CYP2E1</strong> was found to be significant 3 days following ethanol <b>withdrawal</b> and further decreased up to day 8.
+CYP2E1	drug	alcohol	11804663	Thereafter, no significant change occurred and <strong>CYP2E1</strong> activities were comparable with those in patients with non <b>alcoholic</b> liver disease.
+CYP2E1	drug	alcohol	11804663	These data show a significant and quick induction of <strong>CYP2E1</strong> activity, already at moderate <b>alcohol</b> consumption, which may be of importance in the pathogenesis of <b>alcoholic</b> liver disease, of <b>ethanol</b>, drug and vitamin A interactions and in <b>alcohol</b> associated carcinogenesis.
+CYP2E1	drug	alcohol	11762131	Cytochrome P450 2E1 (<strong>CYP2E1</strong>) is the key enzyme of the microsomal pathway of <b>ethanol</b> oxidation.
+CYP2E1	drug	alcohol	11762131	Therefore, heavy consumption of <b>alcohol</b>, which results in <strong>CYP2E1</strong> induction, increases individual susceptibility to the toxic or carcinogenic effects of these xenobiotics.
+CYP2E1	drug	alcohol	11755313	<b>Ethanol</b> withdrawal induced <strong>CYP2E1</strong> degradation in vivo, blocked by proteasomal inhibitor PS 341.
+CYP2E1	addiction	withdrawal	11755313	Ethanol <b>withdrawal</b> induced <strong>CYP2E1</strong> degradation in vivo, blocked by proteasomal inhibitor PS 341.
+CYP2E1	drug	alcohol	11755313	Previously, only in vitro evidence showed that <strong>CYP2E1</strong> induced by <b>ethanol</b> is degraded by the proteasome.
+CYP2E1	drug	alcohol	11755313	<b>Ethanol</b> treatment induced a 3 fold increase in <strong>CYP2E1</strong> levels determined by Western blot.
+CYP2E1	drug	alcohol	11755313	When <b>ethanol</b> was withdrawn, <strong>CYP2E1</strong> decreased to control levels.
+CYP2E1	drug	alcohol	11755313	In <b>ethanol</b> withdrawn rats injected with PS 341, <strong>CYP2E1</strong> remained at the induced level.
+CYP2E1	drug	alcohol	11755313	These results show, for the first time, that the proteasome is responsible for <b>ethanol</b> induced <strong>CYP2E1</strong> degradation in vivo.
+CYP2E1	drug	alcohol	11398342	The cytochrome P450 2E1 (<strong>CYP2E1</strong>) gene, which is mapped to chromosome 10q24.3 qter contributes also the conversion of <b>ethanol</b> to acetaldehyde.
+CYP2E1	drug	alcohol	11391053	The presentations were (1) Mutations in the exons, exon intron junctions, and promoter regions of human <strong>CYP2E1</strong> gene and <b>alcoholism</b>, by Fumio Nomura; (2) Genetic variability in <b>alcohol</b> metabolism and drinking habits in Japanese, by Shoji Harada; (3) Genetic studies of <b>alcohol</b> dependence using <b>alcoholics</b> with inactive ALDH2, by Susumu Higuchi; and (4) <b>Alcohol</b> consumption, apolipoprotein polymorphisms, and cardiovascular disorders, by Dharam P. Agarwal.
+CYP2E1	addiction	dependence	11391053	The presentations were (1) Mutations in the exons, exon intron junctions, and promoter regions of human <strong>CYP2E1</strong> gene and alcoholism, by Fumio Nomura; (2) Genetic variability in alcohol metabolism and drinking habits in Japanese, by Shoji Harada; (3) Genetic studies of alcohol <b>dependence</b> using alcoholics with inactive ALDH2, by Susumu Higuchi; and (4) Alcohol consumption, apolipoprotein polymorphisms, and cardiovascular disorders, by Dharam P. Agarwal.
+CYP2E1	drug	alcohol	11236836	We evaluated the role of three polymorphic genes related to <b>alcohol</b> metabolism (<strong>CYP2E1</strong>) and, possibly, dependence (DRD2 and SLC6A4 promoter) in a series of 60 <b>alcoholics</b> admitted to a specialized referral center in Florence, Italy.
+CYP2E1	addiction	dependence	11236836	We evaluated the role of three polymorphic genes related to alcohol metabolism (<strong>CYP2E1</strong>) and, possibly, <b>dependence</b> (DRD2 and SLC6A4 promoter) in a series of 60 alcoholics admitted to a specialized referral center in Florence, Italy.
+CYP2E1	drug	alcohol	11236836	No difference was found in the frequency of the <strong>CYP2E1</strong> Rsal c2 allele (2.5% among <b>alcoholics</b> and 4.7% among controls) and the DraI C allele (6.7% and 10.1%).
+CYP2E1	drug	alcohol	11173972	The intragastric <b>alcohol</b> infusion rat model (IAIRM) of <b>alcoholic</b> liver disease (ALD) has been utilized in various laboratories to study various aspects of ALD pathogenesis including oxidative stress, cytokine upregulation, hypoxic damage, apoptosis, ubiquitin proteasome pathway and <strong>CYP2E1</strong> induction.
+CYP2E1	drug	alcohol	10964266	Since treatment of experimental <b>alcoholic</b> liver disease with <strong>CYP2E1</strong> inhibitors had an ameliorating effect on liver injury in the rat, chlormethiazole was used to see if it had a similar effect.
+CYP2E1	drug	alcohol	10964266	The <strong>CYP2E1</strong> apoprotein levels, which were increased by <b>ethanol</b> feeding, were also increased when chlormethiazole was fed with <b>ethanol</b>.
+CYP2E1	drug	alcohol	10964266	Chlormethiazole inhibited the increase in the <b>ethanol</b> induced <strong>CYP2E1</strong> activity in vivo, as measured by chlorzoxazone 6 hydroxylation, but did not affect the level of <strong>CYP2E1</strong> apoprotein.
+CYP2E1	drug	alcohol	10759684	In animals, chronic <b>ethanol</b> causes induction of hepatic microsomal enzymes and increases paracetamol hepatotoxicity as expected (<b>ethanol</b> primarily induces <strong>CYP2E1</strong> and this isoform is important in the oxidative metabolism of paracetamol).
+CYP2E1	drug	alcohol	10759684	However, in man, chronic <b>alcohol</b> ingestion causes only modest (about twofold) and short lived induction of <strong>CYP2E1</strong>, and there is no corresponding increase (as claimed) in the toxic metabolic activation of paracetamol.
+CYP2E1	drug	alcohol	10759684	The paracetamol <b>ethanol</b> interaction is not specific for any one isoform of cytochrome P450, and it seems that isoenzymes other than <strong>CYP2E1</strong> are primarily responsible for the oxidative metabolism of paracetamol in man.
+CYP2E1	drug	alcohol	10456581	Two days following <b>alcohol</b> withdrawal, the apparent activity of the <b>alcohol</b> inducible form of cytochrome P450 (<strong>CYP2E1</strong>) was unchanged although total cytochrome P450 content was increased.
+CYP2E1	addiction	withdrawal	10456581	Two days following alcohol <b>withdrawal</b>, the apparent activity of the alcohol inducible form of cytochrome P450 (<strong>CYP2E1</strong>) was unchanged although total cytochrome P450 content was increased.
+CYP2E1	drug	alcohol	10333489	Relationship between cytochrome P450 catalytic cycling and stability: fast degradation of <b>ethanol</b> inducible cytochrome P450 2E1 (<strong>CYP2E1</strong>) in hepatoma cells is abolished by inactivation of its electron donor NADPH cytochrome P450 reductase.
+CYP2E1	drug	alcohol	10333489	<b>Ethanol</b> inducible cytochrome P450 2E1 (<strong>CYP2E1</strong>) involved in the metabolism of gluconeogenetic precursors and some cytotoxins is distinguished from other cytochrome P450 enzymes by its rapid turnover (in vivo half life of 4 7 h), with ligands to the haem iron, both substrates and inhibitors, stabilizing the protein.
+CYP2E1	addiction	withdrawal	10333489	Fao hepatoma cells, where <strong>CYP2E1</strong> showed a half life of 4 h upon serum <b>withdrawal</b>, were treated for 1 h with 0.3 microM diphenylene iodonium (DPI), a suicide inhibitor of flavoenzymes, which resulted in approximately 90% inhibition of the microsomal NADPH cytochrome P450 reductase and <strong>CYP2E1</strong> dependent chlorzoxazone hydroxylase activities.
+CYP2E1	drug	alcohol	9813460	Relationship between <b>alcoholism</b> and <strong>CYP2E1</strong> C/D polymorphism.
+CYP2E1	drug	alcohol	9813460	The genotypes of the <strong>CYP2E1</strong> loci of 35 <b>alcoholic</b> and 130 nonalcoholic (healthy controls) Japanese were investigated to determine the relationship between <strong>CYP2E1</strong> (C/D) polymorphism and susceptibility to <b>alcohol</b> dependence.
+CYP2E1	addiction	dependence	9813460	The genotypes of the <strong>CYP2E1</strong> loci of 35 alcoholic and 130 nonalcoholic (healthy controls) Japanese were investigated to determine the relationship between <strong>CYP2E1</strong> (C/D) polymorphism and susceptibility to alcohol <b>dependence</b>.
+CYP2E1	drug	alcohol	9813460	= 1, chi2 = 11.0, p < 0.001) difference in the <strong>CYP2E1</strong> C gene frequency between <b>alcohol</b> dependents (0.41) and controls (0.28), suggesting that the C gene of <strong>CYP2E1</strong> may be related to the risk of developing <b>alcoholism</b> in Japanese, whereas the frequency of the D gene was higher among controls than <b>alcoholics</b>.
+CYP2E1	drug	alcohol	9731720	The RsaI polymorphism of <strong>CYP2E1</strong> and susceptibility to <b>alcoholic</b> liver disease in Caucasians: effect on age of presentation and dependence on <b>alcohol</b> dehydrogenase genotype.
+CYP2E1	addiction	dependence	9731720	The RsaI polymorphism of <strong>CYP2E1</strong> and susceptibility to alcoholic liver disease in Caucasians: effect on age of presentation and <b>dependence</b> on alcohol dehydrogenase genotype.
+CYP2E1	drug	alcohol	9731720	Caucasians are polymorphic at only two of these gene loci  cytochrome P450 2E1 (<strong>CYP2E1</strong>) and <b>alcohol</b> dehydrogenase 3 (ADH3).
+CYP2E1	drug	alcohol	9731720	We examined the frequency of the RsaI polymorphism of <strong>CYP2E1</strong> and ADH3 genotype in 264 patients with <b>alcoholic</b> liver disease and 121 local control individuals.
+CYP2E1	drug	alcohol	9731720	This study demonstrates that, although rare in Caucasians, possession of the mutant c2 allele of <strong>CYP2E1</strong> increases the risk of <b>alcoholic</b> liver disease at a given level of cumulative <b>alcohol</b> consumption.
+CYP2E1	drug	alcohol	9731720	This risk appears to be particularly manifest in individuals carrying the ADH3*2 allele, presumably reflecting increased metabolism of <b>ethanol</b> by <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	9695719	Inhibition of <strong>CYP2E1</strong> by chlormethiazole as measured by chlorzoxazone pharmacokinetics in patients with <b>alcoholism</b> and in healthy volunteers.
+CYP2E1	drug	alcohol	9695719	It is known that <strong>CYP2E1</strong> is involved in the activation of many low molecular weight toxins and carcinogens and may be involved in the development of <b>alcohol</b> induced liver disease.
+CYP2E1	drug	alcohol	9695719	The pharmacokinetics of a single oral dose of 250 mg chlorzoxazone, a marker of the activity of <strong>CYP2E1</strong>, were measured in five healthy drug free volunteers and in 16 patients with <b>alcoholism</b> receiving 1.2 gm or 2.4 gm chlormethiazole per day for 1, 2, or 3 days.
+CYP2E1	drug	alcohol	9695719	The patients were starting an <b>alcohol</b> withdrawal program and were supposed to have an induced <strong>CYP2E1</strong> activity.
+CYP2E1	addiction	withdrawal	9695719	The patients were starting an alcohol <b>withdrawal</b> program and were supposed to have an induced <strong>CYP2E1</strong> activity.
+CYP2E1	drug	alcohol	26734919	It was also reported that polymorphism of ALDH2 and/or <strong>CYP2E1</strong> may be associated with the susceptibility to <b>alcohol</b> induced liver injury.
+CYP2E1	drug	alcohol	26734919	Concerning blood <b>ethanol</b> elimination kinetics, it was reported that the c2 gene of <strong>CYP2E1</strong> and the ALDH2*1 gene may have greater effects on <b>ethanol</b> and acetaldehyde elimination than the other genotypes, when the blood <b>ethanol</b> level is below 20 m M.
+CYP2E1	drug	alcohol	9633991	<b>Alcohol</b> mediated increases in acetaminophen hepatotoxicity: role of <strong>CYP2E</strong> and CYP3A.
+CYP2E1	drug	alcohol	9633991	This commentary focuses on the roles of CYP3A and <strong>CYP2E</strong> in <b>alcohol</b> mediated increases in acetaminophen hepatotoxicity.
+CYP2E1	drug	alcohol	9633991	However, CYP3A, which is also induced by <b>alcohol</b>, has been shown to have a greater affinity for acetaminophen than <strong>CYP2E</strong>.
+CYP2E1	drug	alcohol	9633991	Previous experiments implicating <strong>CYP2E</strong> in <b>alcohol</b> mediated increases in acetaminophen hepatotoxicity have used inhibitors of this form of P450 that are now proving to be non specific.
+CYP2E1	drug	alcohol	9633991	<strong>CYP2E</strong> may not have a major role due to the rapid loss of induced levels in the absence of continued exposure to <b>ethanol</b>.
+CYP2E1	drug	alcohol	9483936	[Relationship between <b>alcoholism</b> and <strong>CYP2E1</strong> genotypes].
+CYP2E1	drug	alcohol	9483936	The genotype of the <strong>CYP2E1</strong> loci in 36 <b>alcoholic</b> and 42 non <b>alcoholic</b> (healthy) Japanese were investigated to examine the relationship between the polymorphisms of <strong>CYP2E1</strong> (C/D) and the susceptibility to <b>alcohol</b> dependence.
+CYP2E1	addiction	dependence	9483936	The genotype of the <strong>CYP2E1</strong> loci in 36 alcoholic and 42 non alcoholic (healthy) Japanese were investigated to examine the relationship between the polymorphisms of <strong>CYP2E1</strong> (C/D) and the susceptibility to alcohol <b>dependence</b>.
+CYP2E1	drug	alcohol	9483936	There was a significant (df = 1, chi 2 = 4.39, p < 0.05) difference in <strong>CYP2E1</strong> CD (heterozygote) genotype frequency between <b>alcohol</b> dependents (56%) and controls (33%), suggesting that the CD (heterozygote) genotype of <strong>CYP2E1</strong> may have something to the risk of developing <b>alcoholism</b> in Japanese, whereas DD (homozygote) genotype was high among controls.
+CYP2E1	drug	alcohol	9390106	<b>Ethanol</b> is a well known inducer of <strong>CYP2E1</strong>; whether or not it is an inducer of other cytochromes has not been investigated systematically.
+CYP2E1	addiction	withdrawal	9249006	In the Fao hepatoma cell line, <strong>CYP2E1</strong> was found to be fairly stable (half life of 26 h), but serum <b>withdrawal</b> resulted in its rapid disappearance from the microsomal fraction (half life of about 7 h) as evaluated using cycloheximide chase.
+CYP2E1	drug	alcohol	9249006	The effect of serum withdrawal was specific for <strong>CYP2E1</strong> since (a) no concomitant fast degradation of CYP2B1 and NADPH cytochrome P 450 reductase was observed and (b) the <strong>CYP2E1</strong> ligands <b>ethanol</b> and imidazole prevented the fast degradation of the enzyme.
+CYP2E1	addiction	withdrawal	9249006	The effect of serum <b>withdrawal</b> was specific for <strong>CYP2E1</strong> since (a) no concomitant fast degradation of CYP2B1 and NADPH cytochrome P 450 reductase was observed and (b) the <strong>CYP2E1</strong> ligands ethanol and imidazole prevented the fast degradation of the enzyme.
+CYP2E1	drug	alcohol	9144448	<strong>CYP2E</strong> is considered the only form of cytochrome P450 responsible for <b>ethanol</b> mediated increases in acetaminophen hepatotoxicity.
+CYP2E1	drug	alcohol	9144448	In rats, <strong>CYP2E</strong> has been shown to decrease to control levels after this time period of withdrawal from <b>ethanol</b>.
+CYP2E1	addiction	withdrawal	9144448	In rats, <strong>CYP2E</strong> has been shown to decrease to control levels after this time period of <b>withdrawal</b> from ethanol.
+CYP2E1	drug	alcohol	9144448	We have previously shown in cultured human and rat hepatocytes, and in intact rats, that <b>ethanol</b> induces CYP3A in addition to <strong>CYP2E</strong>.
+CYP2E1	drug	alcohol	9144448	To determine if there might be a role for CYP3A in <b>ethanol</b> mediated APAP hepatotoxicity in addition to the recognized role for <strong>CYP2E</strong>, we investigated the effect of triacetyloleandomycin (TAO) on acetaminophen hepatotoxicity in <b>ethanol</b> pretreated rats, as well as the effect of 11 hr withdrawal from <b>ethanol</b> on hepatic levels of CYP3A and <strong>CYP2E</strong>.
+CYP2E1	addiction	withdrawal	9144448	To determine if there might be a role for CYP3A in ethanol mediated APAP hepatotoxicity in addition to the recognized role for <strong>CYP2E</strong>, we investigated the effect of triacetyloleandomycin (TAO) on acetaminophen hepatotoxicity in ethanol pretreated rats, as well as the effect of 11 hr <b>withdrawal</b> from ethanol on hepatic levels of CYP3A and <strong>CYP2E</strong>.
+CYP2E1	drug	alcohol	9144448	This 11 hr withdrawal from <b>ethanol</b> resulted in a decrease in hepatic levels of <b>ethanol</b> induced <strong>CYP2E</strong>; however, considerable induction was still evident.
+CYP2E1	addiction	withdrawal	9144448	This 11 hr <b>withdrawal</b> from ethanol resulted in a decrease in hepatic levels of ethanol induced <strong>CYP2E</strong>; however, considerable induction was still evident.
+CYP2E1	drug	alcohol	8948088	We have studied the hepatic microsomal metabolism of <b>ethanol</b> (MEOS), <strong>CYP2E1</strong> expression and catalytic activity, and the response to phenobarbital (PB) induction or CCl4 challenge in rats of either sex genetically selected for their preference (P) or aversion (NP) for <b>ethanol</b>.
+CYP2E1	addiction	aversion	8948088	We have studied the hepatic microsomal metabolism of ethanol (MEOS), <strong>CYP2E1</strong> expression and catalytic activity, and the response to phenobarbital (PB) induction or CCl4 challenge in rats of either sex genetically selected for their preference (P) or <b>aversion</b> (NP) for ethanol.
+CYP2E1	drug	alcohol	8948088	These results indicate that, in females only, the behavioural trait of <b>ethanol</b> preference is apparently associated not only with higher constitutive levels of <strong>CYP2E1</strong> and rate of microsomal metabolism of <b>ethanol</b> but also with altered susceptibility to PB induction.
+CYP2E1	drug	alcohol	8812268	Metabolism of 1,2 difluoroethane by cytochrome P450 (most likely <strong>CYP2E1</strong>) is suspected because pretreatment of rats or mice with SKF 525F, <b>disulfiram</b>, or dimethyl sulfoxide prevented or delayed the toxicity observed in rats not pretreated.
+CYP2E1	drug	alcohol	8597391	Although little is known about the mechanism of CAC neurotoxicity, the hippocampal endangerment model which relies heavily on the cellular weakening, site specific effect of continuous or chronic, intermittent (withdrawal, binge drinking) elevation of GCs, even less is known about the mechanism of neurotoxicity of activating the <b>ethanol</b> inducible <strong>CYP2E1</strong> system.
+CYP2E1	addiction	intoxication	8597391	Although little is known about the mechanism of CAC neurotoxicity, the hippocampal endangerment model which relies heavily on the cellular weakening, site specific effect of continuous or chronic, intermittent (withdrawal, <b>binge</b> drinking) elevation of GCs, even less is known about the mechanism of neurotoxicity of activating the ethanol inducible <strong>CYP2E1</strong> system.
+CYP2E1	addiction	withdrawal	8597391	Although little is known about the mechanism of CAC neurotoxicity, the hippocampal endangerment model which relies heavily on the cellular weakening, site specific effect of continuous or chronic, intermittent (<b>withdrawal</b>, binge drinking) elevation of GCs, even less is known about the mechanism of neurotoxicity of activating the ethanol inducible <strong>CYP2E1</strong> system.
+CYP2E1	drug	alcohol	8531136	This increase was completely prevented by 4 methylpyrazole and <b>ethanol</b> indicating its dependence on <strong>CYP2E1</strong>.
+CYP2E1	addiction	dependence	8531136	This increase was completely prevented by 4 methylpyrazole and ethanol indicating its <b>dependence</b> on <strong>CYP2E1</strong>.
+CYP2E1	drug	alcohol	7573775	<strong>CYP2E1</strong> and ALDH2 genotypes and <b>alcohol</b> dependence in Japanese.
+CYP2E1	addiction	dependence	7573775	<strong>CYP2E1</strong> and ALDH2 genotypes and alcohol <b>dependence</b> in Japanese.
+CYP2E1	drug	alcohol	7573775	The genotypes of the <strong>CYP2E1</strong> and ALDH2 loci of <b>alcoholic</b> (<b>alcohol</b> dependence) and nonalcoholic (healthy) Japanese were investigated to examine the relationship between the polymorphism of <strong>CYP2E1</strong> (C1/C2) and ALDH2 (ALDH2*1/ALDH2*2), and the susceptibility to <b>alcoholism</b>.
+CYP2E1	addiction	dependence	7573775	The genotypes of the <strong>CYP2E1</strong> and ALDH2 loci of alcoholic (alcohol <b>dependence</b>) and nonalcoholic (healthy) Japanese were investigated to examine the relationship between the polymorphism of <strong>CYP2E1</strong> (C1/C2) and ALDH2 (ALDH2*1/ALDH2*2), and the susceptibility to alcoholism.
+CYP2E1	drug	alcohol	7573775	There was no significant difference in C2 gene frequency between <b>alcoholics</b> (0.19) and nonalcoholics (controls) (0.20), whereas there was a significant difference in ALDH2 allele frequency, suggesting that, in Japanese, the C2 genotype of <strong>CYP2E1</strong> may have nothing to do with the risk of developing <b>alcohol</b> dependence.
+CYP2E1	addiction	dependence	7573775	There was no significant difference in C2 gene frequency between alcoholics (0.19) and nonalcoholics (controls) (0.20), whereas there was a significant difference in ALDH2 allele frequency, suggesting that, in Japanese, the C2 genotype of <strong>CYP2E1</strong> may have nothing to do with the risk of developing alcohol <b>dependence</b>.
+CYP2E1	drug	alcohol	7786308	Rapid changes in cytochrome P4502E1 (<strong>CYP2E1</strong>) activity and other P450 isozymes following <b>ethanol</b> withdrawal in rats.
+CYP2E1	addiction	withdrawal	7786308	Rapid changes in cytochrome P4502E1 (<strong>CYP2E1</strong>) activity and other P450 isozymes following ethanol <b>withdrawal</b> in rats.
+CYP2E1	drug	alcohol	7786308	Microsomes were prepared, and <b>ethanol</b> inducible cytochrome P4502E1 (<strong>CYP2E1</strong>) activity was measured using the enzyme markers N nitrosodimethylamine demethylase (NDMAd), p nitrophenol hydroxylase (PNPH) and aniline hydroxylase (AH).
+CYP2E1	addiction	withdrawal	7786308	The prolonged induction of AH activity following ETOH <b>withdrawal</b> indicates that it is not a specific marker of <strong>CYP2E1</strong> catalyzed reactions.
+CYP2E1	drug	alcohol	7545990	In this study, microsomal cytochrome P 450 2E1 (<strong>CYP2E1</strong>) contents and activities were tested in liver, kidney and lung from Wistar rats after the following treatments (1) oral administration of a 10% <b>ethanol</b> solution for 4 weeks; (2) pair fed controls; (3) oral administration of a 5% acetone solution for 1 week; (4) inhalation of <b>ethanol</b> vapour for 4 weeks.
+CYP2E1	drug	alcohol	7545990	Inhalation was clearly the most efficient way of inducing <strong>CYP2E1</strong>, probably due to the continuous and high <b>alcohol</b> exposure.
+CYP2E1	addiction	intoxication	7545990	The <strong>CYP2E1</strong> activities decreased to control values in the three tissues tested, within 24 h after cessation of <b>intoxication</b>.
+CYP2E1	drug	alcohol	7625570	To evaluate cytochrome P4502E1 (<strong>CYP2E1</strong>) induction in <b>alcoholics</b>, the ratio of the concentrations of 6 hydroxychlorzoxazone (6 OH CHZ) and chlorzoxazone (CHZ) was measured in blood 2 hr after CHZ ingestion using a HPLC method.
+CYP2E1	addiction	withdrawal	7625570	This ratio decreased rapidly during <b>withdrawal</b> as attested by the short half life of <strong>CYP2E1</strong>, which was found to be 2.5 days.
+CYP2E1	drug	alcohol	7802633	Induction of <strong>CYP2E1</strong> in liver, kidney, brain and intestine during chronic <b>ethanol</b> administration and withdrawal: evidence that <strong>CYP2E1</strong> possesses a rapid phase half life of 6 hours or less.
+CYP2E1	addiction	withdrawal	7802633	Induction of <strong>CYP2E1</strong> in liver, kidney, brain and intestine during chronic ethanol administration and <b>withdrawal</b>: evidence that <strong>CYP2E1</strong> possesses a rapid phase half life of 6 hours or less.
+CYP2E1	drug	alcohol	7802633	Controversy exists as to whether the induction of <strong>CYP2E1</strong> by <b>ethanol</b> occurs via increased protein synthesis or protein stabilization.
+CYP2E1	drug	alcohol	7802633	To address these issues in vivo, we chronically administered <b>ethanol</b> to rats and determined levels of immunoreactive <strong>CYP2E1</strong> in liver, kidney, brain and upper gastro intestinal tract (GI).
+CYP2E1	drug	alcohol	7802633	Our data shows that chronic <b>ethanol</b> administration induces hepatic (5 6 fold over pair fed controls) and extra hepatic <strong>CYP2E1</strong>, an effect which is strikingly absent 12 hours after <b>ethanol</b> withdrawal.
+CYP2E1	addiction	withdrawal	7802633	Our data shows that chronic ethanol administration induces hepatic (5 6 fold over pair fed controls) and extra hepatic <strong>CYP2E1</strong>, an effect which is strikingly absent 12 hours after ethanol <b>withdrawal</b>.
+CYP2E1	drug	alcohol	7802633	No changes in <strong>CYP2E1</strong> mRNA were observed at any time, suggesting these changes are mainly post translational at a blood <b>ethanol</b> concentration of 0.15% w/v.
+CYP2E1	drug	alcohol	7802633	Our experimental data indicates that <strong>CYP2E1</strong> possesses a half life of 6 hours or less in the liver and is rapidly degraded following the removal of <b>ethanol</b>.
+CYP2E1	drug	alcohol	8014872	<b>Ethanol</b> inducible cytochrome P450 (CYP) 2E1 (<strong>CYP2E1</strong>) is responsible for the metabolism of many xenobiotics which exert toxic effects in humans.
+CYP2E1	drug	alcohol	8014872	In the present investigation we have evaluated the effects of a drug used for treatment of <b>ethanol</b> withdrawal states, chloromethiazole (CMZ), on <strong>CYP2E1</strong> expression in rat liver.
+CYP2E1	addiction	withdrawal	8014872	In the present investigation we have evaluated the effects of a drug used for treatment of ethanol <b>withdrawal</b> states, chloromethiazole (CMZ), on <strong>CYP2E1</strong> expression in rat liver.
+CYP2E1	drug	alcohol	8014872	Rats treated with <b>ethanol</b> in a total enteral nutrition model had higher <strong>CYP2E1</strong> dependent hepatic microsomal activities of p nitrophenol hydroxylase and carbon tetrachloride induced lipid peroxidation than controls, and simultaneous CMZ treatment abolished the <b>ethanol</b> dependent induction.
+NTRK2	addiction	intoxication	32458406	Our findings show that <b>binge</b> KET impaired memory, increased pro BDNF and <strong>TrkB</strong> levels in the hippocampus, and increased lipid peroxidation (LP) in the kidney and hippocampus, while SbChro KET impaired memory, increased pro BDNF, and decreased both BDNF and <strong>TrkB</strong> levels in the hippocampus, and increased LP in the kidney, liver, and hippocampus.
+NTRK2	addiction	intoxication	32458406	Our findings show that <b>binge</b> KET impaired memory, increased pro BDNF and <strong><strong>TrkB</strong></strong> levels in the hippocampus, and increased lipid peroxidation (LP) in the kidney and hippocampus, while SbChro KET impaired memory, increased pro BDNF, and decreased both BDNF and <strong><strong>TrkB</strong></strong> levels in the hippocampus, and increased LP in the kidney, liver, and hippocampus.
+NTRK2	drug	amphetamine	32388619	Binge <b>METH</b> (40 mg/kg, i.p., over 1 day) dramatically altered striatal and hippocampal dopamine, DOPAC, 5 HT, 5 HIAA, BDNF, and <strong>TrkB</strong> 75 days after drug exposure.
+NTRK2	addiction	intoxication	32388619	<b>Binge</b> METH (40 mg/kg, i.p., over 1 day) dramatically altered striatal and hippocampal dopamine, DOPAC, 5 HT, 5 HIAA, BDNF, and <strong>TrkB</strong> 75 days after drug exposure.
+NTRK2	drug	amphetamine	32388619	Binge <b>METH</b> (40 mg/kg, i.p., over 1 day) dramatically altered striatal and hippocampal dopamine, DOPAC, 5 HT, 5 HIAA, BDNF, and <strong><strong>TrkB</strong></strong> 75 days after drug exposure.
+NTRK2	addiction	intoxication	32388619	<b>Binge</b> METH (40 mg/kg, i.p., over 1 day) dramatically altered striatal and hippocampal dopamine, DOPAC, 5 HT, 5 HIAA, BDNF, and <strong><strong>TrkB</strong></strong> 75 days after drug exposure.
+NTRK2	addiction	relapse	32369970	These results suggest that stimulation of the <strong>TrkB</strong> receptor may contribute to reward <b>craving</b> and <b>relapse</b> in AUD, particularly in females.
+NTRK2	addiction	reward	32369970	These results suggest that stimulation of the <strong>TrkB</strong> receptor may contribute to <b>reward</b> craving and relapse in AUD, particularly in females.
+NTRK2	addiction	relapse	32369970	These results suggest that stimulation of the <strong><strong>TrkB</strong></strong> receptor may contribute to reward <b>craving</b> and <b>relapse</b> in AUD, particularly in females.
+NTRK2	addiction	reward	32369970	These results suggest that stimulation of the <strong><strong>TrkB</strong></strong> receptor may contribute to <b>reward</b> craving and relapse in AUD, particularly in females.
+NTRK2	drug	amphetamine	31693929	Time and region dependent manner of increased brain derived neurotrophic factor and <strong>TrkB</strong> in rat brain after binge like <b>methamphetamine</b> exposure.
+NTRK2	addiction	intoxication	31693929	Time and region dependent manner of increased brain derived neurotrophic factor and <strong>TrkB</strong> in rat brain after <b>binge</b> like methamphetamine exposure.
+NTRK2	drug	amphetamine	31693929	Time and region dependent manner of increased brain derived neurotrophic factor and <strong><strong>TrkB</strong></strong> in rat brain after binge like <b>methamphetamine</b> exposure.
+NTRK2	addiction	intoxication	31693929	Time and region dependent manner of increased brain derived neurotrophic factor and <strong><strong>TrkB</strong></strong> in rat brain after <b>binge</b> like methamphetamine exposure.
+NTRK2	addiction	intoxication	31693929	This study investigated the effect of <b>binge</b> like MA dosing (4 x 4 mg/kg, s.c., 2 h (h) apart) at a range of different time points (from 2 h to 7 days after treatment) on brain derived neurotrophic factor (BDNF) levels and its receptors, <strong>TrkB</strong> and p75NTR.
+NTRK2	addiction	intoxication	31693929	This study investigated the effect of <b>binge</b> like MA dosing (4 x 4 mg/kg, s.c., 2 h (h) apart) at a range of different time points (from 2 h to 7 days after treatment) on brain derived neurotrophic factor (BDNF) levels and its receptors, <strong><strong>TrkB</strong></strong> and p75NTR.
+NTRK2	addiction	intoxication	31693929	In the striatum, BDNF expression was increased at 12 and 24 h after <b>binge</b> like MA treatment and had returned to normal at 36 h. Increased expression of the <strong>TrkB</strong> receptor was observed in the frontal cortex at 2, 24 and 48 h after MA treatment and in the striatum at 24 and 48 h after the MA regimen.
+NTRK2	addiction	intoxication	31693929	In the striatum, BDNF expression was increased at 12 and 24 h after <b>binge</b> like MA treatment and had returned to normal at 36 h. Increased expression of the <strong><strong>TrkB</strong></strong> receptor was observed in the frontal cortex at 2, 24 and 48 h after MA treatment and in the striatum at 24 and 48 h after the MA regimen.
+NTRK2	addiction	intoxication	31693929	These findings show that the <b>binge</b> like regimen of MA affects expression of BDNF and its receptors, particularly the <strong>TrkB</strong> receptor, in a time and region dependent manner, and highlights the importance of the frontal cortex and the striatum in the response following MA <b>binge</b> like dosing.
+NTRK2	addiction	intoxication	31693929	These findings show that the <b>binge</b> like regimen of MA affects expression of BDNF and its receptors, particularly the <strong><strong>TrkB</strong></strong> receptor, in a time and region dependent manner, and highlights the importance of the frontal cortex and the striatum in the response following MA <b>binge</b> like dosing.
+NTRK2	drug	opioid	31689445	Besides, (m CF3 PhSe)2 downregulated the proBDNF/p 75NTR/JNK pro apoptotic pathway without affecting the mBDNF/<strong>TrkB</strong>/ERK/CREB pro survival signaling in the hippocampus of <b>morphine</b> withdrawn mice.
+NTRK2	drug	opioid	31689445	Besides, (m CF3 PhSe)2 downregulated the proBDNF/p 75NTR/JNK pro apoptotic pathway without affecting the mBDNF/<strong><strong>TrkB</strong></strong>/ERK/CREB pro survival signaling in the hippocampus of <b>morphine</b> withdrawn mice.
+NTRK2	drug	alcohol	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (<strong>TrkB</strong>), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate <b>alcohol</b> drinking and other behaviors related to <b>alcohol</b> addiction.
+NTRK2	addiction	addiction	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (<strong>TrkB</strong>), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate alcohol drinking and other behaviors related to alcohol <b>addiction</b>.
+NTRK2	drug	alcohol	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (<strong><strong>TrkB</strong></strong>), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate <b>alcohol</b> drinking and other behaviors related to <b>alcohol</b> addiction.
+NTRK2	addiction	addiction	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (<strong><strong>TrkB</strong></strong>), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate alcohol drinking and other behaviors related to alcohol <b>addiction</b>.
+NTRK2	drug	alcohol	31617071	This review will examine the preclinical evidence describing <strong>TrkB</strong>, RET, ALK, FGFR, and EGFR modulation of <b>alcohol</b> drinking and other behaviors relevant to <b>alcohol</b> abuse.
+NTRK2	drug	alcohol	31617071	This review will examine the preclinical evidence describing <strong><strong>TrkB</strong></strong>, RET, ALK, FGFR, and EGFR modulation of <b>alcohol</b> drinking and other behaviors relevant to <b>alcohol</b> abuse.
+NTRK2	drug	cocaine	31606593	Interestingly, <b>cocaine</b> exposed serotonin transporter knockout rats showed increased BDNF levels, with no signs of phospho <strong>TrkB</strong> receptor coupling to phospho Akt and phospho ERK1.
+NTRK2	drug	cocaine	31606593	Interestingly, <b>cocaine</b> exposed serotonin transporter knockout rats showed increased BDNF levels, with no signs of phospho <strong><strong>TrkB</strong></strong> receptor coupling to phospho Akt and phospho ERK1.
+NTRK2	drug	cocaine	31417375	Infralimbic Estradiol Enhances Neuronal Excitability and Facilitates Extinction of <b>Cocaine</b> Seeking in Female Rats via a BDNF/<strong>TrkB</strong> Mechanism.
+NTRK2	addiction	relapse	31417375	Infralimbic Estradiol Enhances Neuronal Excitability and Facilitates Extinction of Cocaine <b>Seeking</b> in Female Rats via a BDNF/<strong>TrkB</strong> Mechanism.
+NTRK2	drug	cocaine	31417375	Infralimbic Estradiol Enhances Neuronal Excitability and Facilitates Extinction of <b>Cocaine</b> Seeking in Female Rats via a BDNF/<strong><strong>TrkB</strong></strong> Mechanism.
+NTRK2	addiction	relapse	31417375	Infralimbic Estradiol Enhances Neuronal Excitability and Facilitates Extinction of Cocaine <b>Seeking</b> in Female Rats via a BDNF/<strong><strong>TrkB</strong></strong> Mechanism.
+NTRK2	drug	cocaine	31417375	Moreover, blockade of <strong>TrkB</strong> signaling impaired E2 facilitated extinction of <b>cocaine</b> seeking in OVX female rats.
+NTRK2	addiction	relapse	31417375	Moreover, blockade of <strong>TrkB</strong> signaling impaired E2 facilitated extinction of cocaine <b>seeking</b> in OVX female rats.
+NTRK2	drug	cocaine	31417375	Moreover, blockade of <strong><strong>TrkB</strong></strong> signaling impaired E2 facilitated extinction of <b>cocaine</b> seeking in OVX female rats.
+NTRK2	addiction	relapse	31417375	Moreover, blockade of <strong><strong>TrkB</strong></strong> signaling impaired E2 facilitated extinction of cocaine <b>seeking</b> in OVX female rats.
+NTRK2	drug	cocaine	31417375	Thus, E2 enhances IL mPFC neuronal excitability in a <strong>TrkB</strong> dependent manner to support extinction of <b>cocaine</b> seeking.
+NTRK2	addiction	relapse	31417375	Thus, E2 enhances IL mPFC neuronal excitability in a <strong>TrkB</strong> dependent manner to support extinction of cocaine <b>seeking</b>.
+NTRK2	drug	cocaine	31417375	Thus, E2 enhances IL mPFC neuronal excitability in a <strong><strong>TrkB</strong></strong> dependent manner to support extinction of <b>cocaine</b> seeking.
+NTRK2	addiction	relapse	31417375	Thus, E2 enhances IL mPFC neuronal excitability in a <strong><strong>TrkB</strong></strong> dependent manner to support extinction of cocaine <b>seeking</b>.
+NTRK2	drug	cocaine	31417375	Our findings suggest that pharmacological enhancement of E2 or BDNF/<strong>TrkB</strong> signaling during extinction based therapies would improve therapeutic outcome in <b>cocaine</b> addicted women.
+NTRK2	drug	cocaine	31417375	Our findings suggest that pharmacological enhancement of E2 or BDNF/<strong><strong>TrkB</strong></strong> signaling during extinction based therapies would improve therapeutic outcome in <b>cocaine</b> addicted women.
+NTRK2	drug	nicotine	31316930	Expressions of brain derived neurotrophic factor and tyrosine kinase B (<strong>TrkB</strong>) were decreased in the <b>nicotine</b> withdrawal rats, in contrast, treadmill running increased brain derived neurotrophic factor and <strong>TrkB</strong> expressions.
+NTRK2	addiction	withdrawal	31316930	Expressions of brain derived neurotrophic factor and tyrosine kinase B (<strong>TrkB</strong>) were decreased in the nicotine <b>withdrawal</b> rats, in contrast, treadmill running increased brain derived neurotrophic factor and <strong>TrkB</strong> expressions.
+NTRK2	drug	nicotine	31316930	Expressions of brain derived neurotrophic factor and tyrosine kinase B (<strong><strong>TrkB</strong></strong>) were decreased in the <b>nicotine</b> withdrawal rats, in contrast, treadmill running increased brain derived neurotrophic factor and <strong><strong>TrkB</strong></strong> expressions.
+NTRK2	addiction	withdrawal	31316930	Expressions of brain derived neurotrophic factor and tyrosine kinase B (<strong><strong>TrkB</strong></strong>) were decreased in the nicotine <b>withdrawal</b> rats, in contrast, treadmill running increased brain derived neurotrophic factor and <strong><strong>TrkB</strong></strong> expressions.
+NTRK2	drug	cocaine	31218603	We found that acute pharmacological stimulation of the tyrosine/tropomyosin receptor kinase B (<strong>trkB</strong>) via 7,8 dihydroxyflavone (7,8 DHF) or 3,4 methylenedioxymethamphetamine (MDMA) blocked <b>cocaine</b> induced habit biases by strengthening memory for action outcome associations.
+NTRK2	drug	psychedelics	31218603	We found that acute pharmacological stimulation of the tyrosine/tropomyosin receptor kinase B (<strong>trkB</strong>) via 7,8 dihydroxyflavone (7,8 DHF) or 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>) blocked cocaine induced habit biases by strengthening memory for action outcome associations.
+NTRK2	drug	cocaine	31218603	We found that acute pharmacological stimulation of the tyrosine/tropomyosin receptor kinase B (<strong><strong>trkB</strong></strong>) via 7,8 dihydroxyflavone (7,8 DHF) or 3,4 methylenedioxymethamphetamine (MDMA) blocked <b>cocaine</b> induced habit biases by strengthening memory for action outcome associations.
+NTRK2	drug	psychedelics	31218603	We found that acute pharmacological stimulation of the tyrosine/tropomyosin receptor kinase B (<strong><strong>trkB</strong></strong>) via 7,8 dihydroxyflavone (7,8 DHF) or 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>) blocked cocaine induced habit biases by strengthening memory for action outcome associations.
+NTRK2	drug	psychedelics	31218603	We believe that <b>MDMA</b> acts by stimulating neurotrophin/<strong>trkB</strong> systems in the orbitofrontal cortex (OFC), a region involved in prospectively evaluating the consequences of one's action, because 1) <b>MDMA</b> also increased brain derived neurotrophic factor (BDNF) in the OFC, 2) <b>MDMA</b> corrected habit biases due to Bdnf loss in the OFC, and 3) overexpression of a truncated isoform of <strong>trkB</strong> occluded the memory enhancing effects of <b>MDMA</b>.
+NTRK2	drug	psychedelics	31218603	We believe that <b>MDMA</b> acts by stimulating neurotrophin/<strong><strong>trkB</strong></strong> systems in the orbitofrontal cortex (OFC), a region involved in prospectively evaluating the consequences of one's action, because 1) <b>MDMA</b> also increased brain derived neurotrophic factor (BDNF) in the OFC, 2) <b>MDMA</b> corrected habit biases due to Bdnf loss in the OFC, and 3) overexpression of a truncated isoform of <strong><strong>trkB</strong></strong> occluded the memory enhancing effects of <b>MDMA</b>.
+NTRK2	drug	cocaine	31218603	Thus, selecting actions based on their consequences requires BDNF <strong>trkB</strong> in the OFC, the stimulation of which may improve goal attainment in both drug naïve and <b>cocaine</b> exposed individuals.
+NTRK2	drug	cocaine	31218603	Thus, selecting actions based on their consequences requires BDNF <strong><strong>trkB</strong></strong> in the OFC, the stimulation of which may improve goal attainment in both drug naïve and <b>cocaine</b> exposed individuals.
+NTRK2	drug	alcohol	31156431	The BDNF signaling mechanism is complex and depends on two receptor systems, <strong>TrkB</strong> and p75NTR, which appear to have opposite effects on <b>alcohol</b> seeking behavior in animal models.
+NTRK2	addiction	relapse	31156431	The BDNF signaling mechanism is complex and depends on two receptor systems, <strong>TrkB</strong> and p75NTR, which appear to have opposite effects on alcohol <b>seeking</b> behavior in animal models.
+NTRK2	drug	alcohol	31156431	The BDNF signaling mechanism is complex and depends on two receptor systems, <strong><strong>TrkB</strong></strong> and p75NTR, which appear to have opposite effects on <b>alcohol</b> seeking behavior in animal models.
+NTRK2	addiction	relapse	31156431	The BDNF signaling mechanism is complex and depends on two receptor systems, <strong><strong>TrkB</strong></strong> and p75NTR, which appear to have opposite effects on alcohol <b>seeking</b> behavior in animal models.
+NTRK2	drug	alcohol	31068789	Interestingly, OEA alone or combined with THC also decreased the mRNA levels of neurotrophic factors (Bdnf, Ntf3) and the NT3 receptor TrkC, but increased the BDNF receptor <strong>TrkB</strong> in the hippocampus of <b>ethanol</b> exposed rats.
+NTRK2	drug	cannabinoid	31068789	Interestingly, OEA alone or combined with <b>THC</b> also decreased the mRNA levels of neurotrophic factors (Bdnf, Ntf3) and the NT3 receptor TrkC, but increased the BDNF receptor <strong>TrkB</strong> in the hippocampus of ethanol exposed rats.
+NTRK2	drug	alcohol	31068789	Interestingly, OEA alone or combined with THC also decreased the mRNA levels of neurotrophic factors (Bdnf, Ntf3) and the NT3 receptor TrkC, but increased the BDNF receptor <strong><strong>TrkB</strong></strong> in the hippocampus of <b>ethanol</b> exposed rats.
+NTRK2	drug	cannabinoid	31068789	Interestingly, OEA alone or combined with <b>THC</b> also decreased the mRNA levels of neurotrophic factors (Bdnf, Ntf3) and the NT3 receptor TrkC, but increased the BDNF receptor <strong><strong>TrkB</strong></strong> in the hippocampus of ethanol exposed rats.
+NTRK2	drug	amphetamine	30877026	mBDNF, proBDNF, <strong>TrkB</strong>, MMP 9, MMP 9 activity, and M/P were significantly correlated with the MoCA score in the <b>METH</b> abstainers.
+NTRK2	drug	amphetamine	30877026	mBDNF, proBDNF, <strong><strong>TrkB</strong></strong>, MMP 9, MMP 9 activity, and M/P were significantly correlated with the MoCA score in the <b>METH</b> abstainers.
+NTRK2	drug	amphetamine	30877026	The combination of mBDNF, <strong>TrkB</strong>, MMP 9, and MMP 9 activity demonstrated excellent diagnostic potential for cognitive impairment of <b>METH</b> abusers during early withdrawal (AUC = 0.978).
+NTRK2	addiction	withdrawal	30877026	The combination of mBDNF, <strong>TrkB</strong>, MMP 9, and MMP 9 activity demonstrated excellent diagnostic potential for cognitive impairment of METH abusers during early <b>withdrawal</b> (AUC = 0.978).
+NTRK2	drug	amphetamine	30877026	The combination of mBDNF, <strong><strong>TrkB</strong></strong>, MMP 9, and MMP 9 activity demonstrated excellent diagnostic potential for cognitive impairment of <b>METH</b> abusers during early withdrawal (AUC = 0.978).
+NTRK2	addiction	withdrawal	30877026	The combination of mBDNF, <strong><strong>TrkB</strong></strong>, MMP 9, and MMP 9 activity demonstrated excellent diagnostic potential for cognitive impairment of METH abusers during early <b>withdrawal</b> (AUC = 0.978).
+NTRK2	drug	alcohol	30758322	<strong>TrkB</strong> dependent disinhibition of the nucleus accumbens is enhanced by <b>ethanol</b>.
+NTRK2	drug	alcohol	30758322	<strong><strong>TrkB</strong></strong> dependent disinhibition of the nucleus accumbens is enhanced by <b>ethanol</b>.
+NTRK2	drug	alcohol	30758322	This long term depression is postsynaptically expressed, tropomyosin kinase B (<strong>TrkB</strong>) receptor mediated, and augmented in the presence of <b>ethanol</b>.
+NTRK2	drug	alcohol	30758322	This long term depression is postsynaptically expressed, tropomyosin kinase B (<strong><strong>TrkB</strong></strong>) receptor mediated, and augmented in the presence of <b>ethanol</b>.
+NTRK2	drug	alcohol	30758322	Our findings support the emerging view that <strong>TrkB</strong> signaling regulates inhibitory synaptic plasticity and suggest this mechanism in the nucleus accumbens as a target for <b>ethanol</b> modulation of reward.
+NTRK2	addiction	reward	30758322	Our findings support the emerging view that <strong>TrkB</strong> signaling regulates inhibitory synaptic plasticity and suggest this mechanism in the nucleus accumbens as a target for ethanol modulation of <b>reward</b>.
+NTRK2	drug	alcohol	30758322	Our findings support the emerging view that <strong><strong>TrkB</strong></strong> signaling regulates inhibitory synaptic plasticity and suggest this mechanism in the nucleus accumbens as a target for <b>ethanol</b> modulation of reward.
+NTRK2	addiction	reward	30758322	Our findings support the emerging view that <strong><strong>TrkB</strong></strong> signaling regulates inhibitory synaptic plasticity and suggest this mechanism in the nucleus accumbens as a target for ethanol modulation of <b>reward</b>.
+NTRK2	drug	cocaine	30738029	7,8 Dihydroxyflavone blocks the development of behavioral sensitization to MDPV, but not to <b>cocaine</b>: Differential role of the BDNF <strong>TrkB</strong> pathway.
+NTRK2	addiction	sensitization	30738029	7,8 Dihydroxyflavone blocks the development of behavioral <b>sensitization</b> to MDPV, but not to cocaine: Differential role of the BDNF <strong>TrkB</strong> pathway.
+NTRK2	drug	cocaine	30738029	7,8 Dihydroxyflavone blocks the development of behavioral sensitization to MDPV, but not to <b>cocaine</b>: Differential role of the BDNF <strong><strong>TrkB</strong></strong> pathway.
+NTRK2	addiction	sensitization	30738029	7,8 Dihydroxyflavone blocks the development of behavioral <b>sensitization</b> to MDPV, but not to cocaine: Differential role of the BDNF <strong><strong>TrkB</strong></strong> pathway.
+NTRK2	drug	cocaine	30738029	In this study we aimed to investigate the bidirectional cross sensitization between MDPV and <b>cocaine</b>, as well as to evaluate the role of the BDNF <strong>TrkB</strong> signaling pathway in the development of locomotor sensitization to both drugs.
+NTRK2	addiction	sensitization	30738029	In this study we aimed to investigate the bidirectional cross <b>sensitization</b> between MDPV and cocaine, as well as to evaluate the role of the BDNF <strong>TrkB</strong> signaling pathway in the development of locomotor <b>sensitization</b> to both drugs.
+NTRK2	drug	cocaine	30738029	In this study we aimed to investigate the bidirectional cross sensitization between MDPV and <b>cocaine</b>, as well as to evaluate the role of the BDNF <strong><strong>TrkB</strong></strong> signaling pathway in the development of locomotor sensitization to both drugs.
+NTRK2	addiction	sensitization	30738029	In this study we aimed to investigate the bidirectional cross <b>sensitization</b> between MDPV and cocaine, as well as to evaluate the role of the BDNF <strong><strong>TrkB</strong></strong> signaling pathway in the development of locomotor <b>sensitization</b> to both drugs.
+NTRK2	drug	cocaine	30738029	Interestingly, such decline was involved in the development of locomotor sensitization, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a <strong>TrkB</strong> agonist, blocked the development of sensitization to MDPV but not to <b>cocaine</b>, for which no changes in the BDNF <strong>TrkB</strong> signaling pathway were observed at early withdrawal.
+NTRK2	addiction	sensitization	30738029	Interestingly, such decline was involved in the development of locomotor <b>sensitization</b>, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a <strong>TrkB</strong> agonist, blocked the development of <b>sensitization</b> to MDPV but not to cocaine, for which no changes in the BDNF <strong>TrkB</strong> signaling pathway were observed at early withdrawal.
+NTRK2	addiction	withdrawal	30738029	Interestingly, such decline was involved in the development of locomotor sensitization, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a <strong>TrkB</strong> agonist, blocked the development of sensitization to MDPV but not to cocaine, for which no changes in the BDNF <strong>TrkB</strong> signaling pathway were observed at early <b>withdrawal</b>.
+NTRK2	drug	cocaine	30738029	Interestingly, such decline was involved in the development of locomotor sensitization, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a <strong><strong>TrkB</strong></strong> agonist, blocked the development of sensitization to MDPV but not to <b>cocaine</b>, for which no changes in the BDNF <strong><strong>TrkB</strong></strong> signaling pathway were observed at early withdrawal.
+NTRK2	addiction	sensitization	30738029	Interestingly, such decline was involved in the development of locomotor <b>sensitization</b>, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a <strong><strong>TrkB</strong></strong> agonist, blocked the development of <b>sensitization</b> to MDPV but not to cocaine, for which no changes in the BDNF <strong><strong>TrkB</strong></strong> signaling pathway were observed at early withdrawal.
+NTRK2	addiction	withdrawal	30738029	Interestingly, such decline was involved in the development of locomotor sensitization, thus the pretreatment with 7,8 dihydroxyflavone (10 mg/kg), a <strong><strong>TrkB</strong></strong> agonist, blocked the development of sensitization to MDPV but not to cocaine, for which no changes in the BDNF <strong><strong>TrkB</strong></strong> signaling pathway were observed at early <b>withdrawal</b>.
+NTRK2	addiction	sensitization	30738029	Our findings suggest that decreased BDNF <strong>TrkB</strong> signaling has an important role in the behavioral <b>sensitization</b> to MDPV, pointing <strong>TrkB</strong> modulation as a target to prevent MDPV <b>sensitization</b>.
+NTRK2	addiction	sensitization	30738029	Our findings suggest that decreased BDNF <strong><strong>TrkB</strong></strong> signaling has an important role in the behavioral <b>sensitization</b> to MDPV, pointing <strong><strong>TrkB</strong></strong> modulation as a target to prevent MDPV <b>sensitization</b>.
+NTRK2	drug	amphetamine	30544074	Additional experiments showed that expression of brain derived neurotrophic factor (BDNF), phosphorylated tropomyosin receptor kinase B (p <strong>TrkB</strong>), phosphorylated extracellular signal related kinase 1/2 (p ERK1/2) and phosphorylated cAMP response element binding protein (p CREB) were decreased in the hippocampus and prefrontal cortex of mice in <b>METH</b> group and the level of mitogen activated protein kinase phosphatase 1 (MKP 1) was increased.
+NTRK2	drug	amphetamine	30544074	Additional experiments showed that expression of brain derived neurotrophic factor (BDNF), phosphorylated tropomyosin receptor kinase B (p <strong><strong>TrkB</strong></strong>), phosphorylated extracellular signal related kinase 1/2 (p ERK1/2) and phosphorylated cAMP response element binding protein (p CREB) were decreased in the hippocampus and prefrontal cortex of mice in <b>METH</b> group and the level of mitogen activated protein kinase phosphatase 1 (MKP 1) was increased.
+NTRK2	drug	alcohol	30457048	In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and <b>alcohol</b> dependence, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand receptor systems, voltage gated calcium channels (VGCCs) and brain derived neurotrophic factor (BDNF) tyrosine kinase B (<strong>TrkB</strong>).
+NTRK2	addiction	dependence	30457048	In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and alcohol <b>dependence</b>, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand receptor systems, voltage gated calcium channels (VGCCs) and brain derived neurotrophic factor (BDNF) tyrosine kinase B (<strong>TrkB</strong>).
+NTRK2	drug	alcohol	30457048	In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and <b>alcohol</b> dependence, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand receptor systems, voltage gated calcium channels (VGCCs) and brain derived neurotrophic factor (BDNF) tyrosine kinase B (<strong><strong>TrkB</strong></strong>).
+NTRK2	addiction	dependence	30457048	In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and alcohol <b>dependence</b>, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand receptor systems, voltage gated calcium channels (VGCCs) and brain derived neurotrophic factor (BDNF) tyrosine kinase B (<strong><strong>TrkB</strong></strong>).
+NTRK2	drug	opioid	30222083	(1) The PAG is involved in the learning and memory changes of the addicted rats; (2) the activation of DA D1 receptor will increase the GAD67, reduce the damage to peripheral neurons, and improve the learning and memory of the addicted rats; and (3) D1 receptor agonists further reduced <strong>TrkB</strong> expression in <b>morphine</b> addicted rats, whereas <strong>TrkB</strong> levels deviated from changes in rat behavior.
+NTRK2	drug	opioid	30222083	(1) The PAG is involved in the learning and memory changes of the addicted rats; (2) the activation of DA D1 receptor will increase the GAD67, reduce the damage to peripheral neurons, and improve the learning and memory of the addicted rats; and (3) D1 receptor agonists further reduced <strong><strong>TrkB</strong></strong> expression in <b>morphine</b> addicted rats, whereas <strong><strong>TrkB</strong></strong> levels deviated from changes in rat behavior.
+NTRK2	addiction	relapse	29890020	Blocking <strong>TrkB</strong> or inactivating BDNF in NAcore potentiated active lever pressing, showing that endogenous BDNF tone was present and supplying inhibitory tone on cue induced <b>reinstatement</b>.
+NTRK2	addiction	relapse	29890020	Blocking <strong><strong>TrkB</strong></strong> or inactivating BDNF in NAcore potentiated active lever pressing, showing that endogenous BDNF tone was present and supplying inhibitory tone on cue induced <b>reinstatement</b>.
+NTRK2	drug	cocaine	29890020	BDNF decreased <b>cocaine</b> seeking through <strong>TrkB</strong> receptor binding, but had no effect on inactive lever pressing, spontaneous or <b>cocaine</b> induced locomotion, or on reinstated sucrose seeking.
+NTRK2	addiction	relapse	29890020	BDNF decreased cocaine <b>seeking</b> through <strong>TrkB</strong> receptor binding, but had no effect on inactive lever pressing, spontaneous or cocaine induced locomotion, or on reinstated sucrose <b>seeking</b>.
+NTRK2	drug	cocaine	29890020	BDNF decreased <b>cocaine</b> seeking through <strong><strong>TrkB</strong></strong> receptor binding, but had no effect on inactive lever pressing, spontaneous or <b>cocaine</b> induced locomotion, or on reinstated sucrose seeking.
+NTRK2	addiction	relapse	29890020	BDNF decreased cocaine <b>seeking</b> through <strong><strong>TrkB</strong></strong> receptor binding, but had no effect on inactive lever pressing, spontaneous or cocaine induced locomotion, or on reinstated sucrose <b>seeking</b>.
+NTRK2	drug	cocaine	29890020	Together, these data show that endogenous BDNF acts on <strong>TrKB</strong> to provide inhibitory tone on reinstated <b>cocaine</b> seeking, and this effect was recapitulated by exogenous BDNF.
+NTRK2	addiction	relapse	29890020	Together, these data show that endogenous BDNF acts on <strong>TrKB</strong> to provide inhibitory tone on reinstated cocaine <b>seeking</b>, and this effect was recapitulated by exogenous BDNF.
+NTRK2	drug	cocaine	29890020	Together, these data show that endogenous BDNF acts on <strong><strong>TrKB</strong></strong> to provide inhibitory tone on reinstated <b>cocaine</b> seeking, and this effect was recapitulated by exogenous BDNF.
+NTRK2	addiction	relapse	29890020	Together, these data show that endogenous BDNF acts on <strong><strong>TrKB</strong></strong> to provide inhibitory tone on reinstated cocaine <b>seeking</b>, and this effect was recapitulated by exogenous BDNF.
+NTRK2	drug	alcohol	29520063	We found that the protein levels of proBDNF and p75NTR were increased, but not the sortilin protein level; while the <strong>TrkB</strong> protein level was decreased in the <b>alcohol</b> dependence patients compared with healthy controls.
+NTRK2	addiction	dependence	29520063	We found that the protein levels of proBDNF and p75NTR were increased, but not the sortilin protein level; while the <strong>TrkB</strong> protein level was decreased in the alcohol <b>dependence</b> patients compared with healthy controls.
+NTRK2	drug	alcohol	29520063	We found that the protein levels of proBDNF and p75NTR were increased, but not the sortilin protein level; while the <strong><strong>TrkB</strong></strong> protein level was decreased in the <b>alcohol</b> dependence patients compared with healthy controls.
+NTRK2	addiction	dependence	29520063	We found that the protein levels of proBDNF and p75NTR were increased, but not the sortilin protein level; while the <strong><strong>TrkB</strong></strong> protein level was decreased in the alcohol <b>dependence</b> patients compared with healthy controls.
+NTRK2	drug	alcohol	29520063	The ELISA results of mBDNF and <strong>TrkB</strong> were declined in the <b>alcohol</b> dependence group.
+NTRK2	addiction	dependence	29520063	The ELISA results of mBDNF and <strong>TrkB</strong> were declined in the alcohol <b>dependence</b> group.
+NTRK2	drug	alcohol	29520063	The ELISA results of mBDNF and <strong><strong>TrkB</strong></strong> were declined in the <b>alcohol</b> dependence group.
+NTRK2	addiction	dependence	29520063	The ELISA results of mBDNF and <strong><strong>TrkB</strong></strong> were declined in the alcohol <b>dependence</b> group.
+NTRK2	drug	alcohol	29520063	The levels of mBDNF and <strong>TrkB</strong> were negatively correlated with the average amount of daily <b>ethanol</b> consumption, and the levels of proBDNF, p75NTR and sortilin were positively correlated with the average amount of <b>ethanol</b> consumption per day.
+NTRK2	drug	alcohol	29520063	The levels of mBDNF and <strong><strong>TrkB</strong></strong> were negatively correlated with the average amount of daily <b>ethanol</b> consumption, and the levels of proBDNF, p75NTR and sortilin were positively correlated with the average amount of <b>ethanol</b> consumption per day.
+NTRK2	drug	alcohol	29520063	The balance between the proBDNF/p75NTR and mBDNF/<strong>TrkB</strong> signalling pathways appeared dysregulated in <b>alcohol</b> dependence.
+NTRK2	addiction	dependence	29520063	The balance between the proBDNF/p75NTR and mBDNF/<strong>TrkB</strong> signalling pathways appeared dysregulated in alcohol <b>dependence</b>.
+NTRK2	drug	alcohol	29520063	The balance between the proBDNF/p75NTR and mBDNF/<strong><strong>TrkB</strong></strong> signalling pathways appeared dysregulated in <b>alcohol</b> dependence.
+NTRK2	addiction	dependence	29520063	The balance between the proBDNF/p75NTR and mBDNF/<strong><strong>TrkB</strong></strong> signalling pathways appeared dysregulated in alcohol <b>dependence</b>.
+NTRK2	drug	opioid	29294331	This study examined the effects of systemic administration of the <strong>TrkB</strong> receptor antagonist (ANA 12) on the severity of physical and psychological dependence and <b>morphine</b> induced locomotor sensitization, the ventral tegmental area (VTA) nucleus accumbens (NAc) BDNF levels in <b>morphine</b> dependent and withdrawn rats.
+NTRK2	addiction	dependence	29294331	This study examined the effects of systemic administration of the <strong>TrkB</strong> receptor antagonist (ANA 12) on the severity of physical and psychological <b>dependence</b> and morphine induced locomotor sensitization, the ventral tegmental area (VTA) nucleus accumbens (NAc) BDNF levels in morphine dependent and withdrawn rats.
+NTRK2	addiction	sensitization	29294331	This study examined the effects of systemic administration of the <strong>TrkB</strong> receptor antagonist (ANA 12) on the severity of physical and psychological dependence and morphine induced locomotor <b>sensitization</b>, the ventral tegmental area (VTA) nucleus accumbens (NAc) BDNF levels in morphine dependent and withdrawn rats.
+NTRK2	drug	opioid	29294331	This study examined the effects of systemic administration of the <strong><strong>TrkB</strong></strong> receptor antagonist (ANA 12) on the severity of physical and psychological dependence and <b>morphine</b> induced locomotor sensitization, the ventral tegmental area (VTA) nucleus accumbens (NAc) BDNF levels in <b>morphine</b> dependent and withdrawn rats.
+NTRK2	addiction	dependence	29294331	This study examined the effects of systemic administration of the <strong><strong>TrkB</strong></strong> receptor antagonist (ANA 12) on the severity of physical and psychological <b>dependence</b> and morphine induced locomotor sensitization, the ventral tegmental area (VTA) nucleus accumbens (NAc) BDNF levels in morphine dependent and withdrawn rats.
+NTRK2	addiction	sensitization	29294331	This study examined the effects of systemic administration of the <strong><strong>TrkB</strong></strong> receptor antagonist (ANA 12) on the severity of physical and psychological dependence and morphine induced locomotor <b>sensitization</b>, the ventral tegmental area (VTA) nucleus accumbens (NAc) BDNF levels in morphine dependent and withdrawn rats.
+NTRK2	drug	alcohol	29139560	The Mammalian Circadian Clock Exhibits Chronic <b>Ethanol</b> Tolerance and Withdrawal Induced Glutamate Hypersensitivity, Accompanied by Changes in Glutamate and <strong>TrkB</strong> Receptor Proteins.
+NTRK2	addiction	withdrawal	29139560	The Mammalian Circadian Clock Exhibits Chronic Ethanol Tolerance and <b>Withdrawal</b> Induced Glutamate Hypersensitivity, Accompanied by Changes in Glutamate and <strong>TrkB</strong> Receptor Proteins.
+NTRK2	drug	alcohol	29139560	The Mammalian Circadian Clock Exhibits Chronic <b>Ethanol</b> Tolerance and Withdrawal Induced Glutamate Hypersensitivity, Accompanied by Changes in Glutamate and <strong><strong>TrkB</strong></strong> Receptor Proteins.
+NTRK2	addiction	withdrawal	29139560	The Mammalian Circadian Clock Exhibits Chronic Ethanol Tolerance and <b>Withdrawal</b> Induced Glutamate Hypersensitivity, Accompanied by Changes in Glutamate and <strong><strong>TrkB</strong></strong> Receptor Proteins.
+NTRK2	addiction	withdrawal	29139560	This increase persisted during EtOH <b>withdrawal</b>, along with an increase in NR2B Y1472 phosphorylation, mature brain derived neurotrophic factor, and phosphorylated <strong>TrkB</strong>.
+NTRK2	addiction	withdrawal	29139560	This increase persisted during EtOH <b>withdrawal</b>, along with an increase in NR2B Y1472 phosphorylation, mature brain derived neurotrophic factor, and phosphorylated <strong><strong>TrkB</strong></strong>.
+NTRK2	drug	opioid	28811779	Effect of exercise and <b>morphine</b> on psychological and physical dependencies, BDNF and <strong>TrkB</strong> gene expression in rat's hippocampus.
+NTRK2	drug	opioid	28811779	Effect of exercise and <b>morphine</b> on psychological and physical dependencies, BDNF and <strong><strong>TrkB</strong></strong> gene expression in rat's hippocampus.
+NTRK2	drug	opioid	28811779	Correlation between exercise level, <b>morphine</b> injection, concurrent <b>morphine</b> administration and exercise with <b>morphine</b> CPP, BDNF and <strong>TrkB</strong> genes was determined.
+NTRK2	addiction	reward	28811779	Correlation between exercise level, morphine injection, concurrent morphine administration and exercise with morphine <b>CPP</b>, BDNF and <strong>TrkB</strong> genes was determined.
+NTRK2	drug	opioid	28811779	Correlation between exercise level, <b>morphine</b> injection, concurrent <b>morphine</b> administration and exercise with <b>morphine</b> CPP, BDNF and <strong><strong>TrkB</strong></strong> genes was determined.
+NTRK2	addiction	reward	28811779	Correlation between exercise level, morphine injection, concurrent morphine administration and exercise with morphine <b>CPP</b>, BDNF and <strong><strong>TrkB</strong></strong> genes was determined.
+NTRK2	drug	opioid	28811779	A significant (P<0.001) correlation between exercise level, <b>morphine</b> injection, concurrent <b>morphine</b> administration and exercise with <b>morphine</b> CPP and BDNFand <strong>TrKB</strong> gene expressions was found.
+NTRK2	addiction	reward	28811779	A significant (P<0.001) correlation between exercise level, morphine injection, concurrent morphine administration and exercise with morphine <b>CPP</b> and BDNFand <strong>TrKB</strong> gene expressions was found.
+NTRK2	drug	opioid	28811779	A significant (P<0.001) correlation between exercise level, <b>morphine</b> injection, concurrent <b>morphine</b> administration and exercise with <b>morphine</b> CPP and BDNFand <strong><strong>TrKB</strong></strong> gene expressions was found.
+NTRK2	addiction	reward	28811779	A significant (P<0.001) correlation between exercise level, morphine injection, concurrent morphine administration and exercise with morphine <b>CPP</b> and BDNFand <strong><strong>TrKB</strong></strong> gene expressions was found.
+NTRK2	addiction	reward	28811779	Voluntary exercise in different levels potentiates the brain rewarding system, <b>CPP</b> scale, and hippocampal BDNF and <strong>TrKB</strong> expressions.
+NTRK2	addiction	reward	28811779	Voluntary exercise in different levels potentiates the brain rewarding system, <b>CPP</b> scale, and hippocampal BDNF and <strong><strong>TrKB</strong></strong> expressions.
+NTRK2	drug	cocaine	28808012	BDNF <strong>TrkB</strong> controls <b>cocaine</b> induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors.
+NTRK2	addiction	addiction	28808012	BDNF <strong>TrkB</strong> controls cocaine induced dendritic spines in rodent nucleus accumbens dissociated from increases in <b>addictive</b> behaviors.
+NTRK2	drug	cocaine	28808012	BDNF <strong><strong>TrkB</strong></strong> controls <b>cocaine</b> induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors.
+NTRK2	addiction	addiction	28808012	BDNF <strong><strong>TrkB</strong></strong> controls cocaine induced dendritic spines in rodent nucleus accumbens dissociated from increases in <b>addictive</b> behaviors.
+NTRK2	drug	cocaine	28808012	Here we show that brain derived neurotrophic factor (BDNF) signaling through tyrosine kinase B (<strong>TrkB</strong>) receptors in NACsh neurons is necessary for <b>cocaine</b> induced dendritic spine formation by using either localized <strong>TrkB</strong> knockout or viral mediated expression of a dominant negative, kinase dead <strong>TrkB</strong> mutant.
+NTRK2	drug	cocaine	28808012	Here we show that brain derived neurotrophic factor (BDNF) signaling through tyrosine kinase B (<strong><strong>TrkB</strong></strong>) receptors in NACsh neurons is necessary for <b>cocaine</b> induced dendritic spine formation by using either localized <strong><strong>TrkB</strong></strong> knockout or viral mediated expression of a dominant negative, kinase dead <strong><strong>TrkB</strong></strong> mutant.
+NTRK2	drug	cocaine	28808012	Interestingly, augmenting wild type <strong>TrkB</strong> expression after chronic <b>cocaine</b> self administration reverses the sustained increase in dendritic spine density, an effect mediated by <strong>TrkB</strong> signaling pathways that converge on extracellular regulated kinase.
+NTRK2	drug	cocaine	28808012	Interestingly, augmenting wild type <strong><strong>TrkB</strong></strong> expression after chronic <b>cocaine</b> self administration reverses the sustained increase in dendritic spine density, an effect mediated by <strong><strong>TrkB</strong></strong> signaling pathways that converge on extracellular regulated kinase.
+NTRK2	drug	cocaine	28808012	Loss of <strong>TrkB</strong> function after <b>cocaine</b> self administration, however, leaves spine density intact but markedly enhances the motivation for <b>cocaine</b>, an effect mediated by specific loss of <strong>TrkB</strong> signaling through phospholipase Cgamma1 (PLCγ1).
+NTRK2	drug	cocaine	28808012	Loss of <strong><strong>TrkB</strong></strong> function after <b>cocaine</b> self administration, however, leaves spine density intact but markedly enhances the motivation for <b>cocaine</b>, an effect mediated by specific loss of <strong><strong>TrkB</strong></strong> signaling through phospholipase Cgamma1 (PLCγ1).
+NTRK2	drug	cocaine	28808012	Together, these findings indicate that BDNF <strong>TrkB</strong> signaling both mediates and reverses <b>cocaine</b> induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in addictive behavior.
+NTRK2	addiction	addiction	28808012	Together, these findings indicate that BDNF <strong>TrkB</strong> signaling both mediates and reverses cocaine induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in <b>addictive</b> behavior.
+NTRK2	drug	cocaine	28808012	Together, these findings indicate that BDNF <strong><strong>TrkB</strong></strong> signaling both mediates and reverses <b>cocaine</b> induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in addictive behavior.
+NTRK2	addiction	addiction	28808012	Together, these findings indicate that BDNF <strong><strong>TrkB</strong></strong> signaling both mediates and reverses cocaine induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in <b>addictive</b> behavior.
+NTRK2	drug	psychedelics	28670835	administered at time zero, for: (1) chronic NMDA receptor inhibition with subcutaneously implanted 7 day delivery osmotic pumps loaded with <b>ketamine</b>; (2) <strong>TrkB</strong> receptor inhibition with intraperitoneal (i.p.)
+NTRK2	drug	psychedelics	28670835	administered at time zero, for: (1) chronic NMDA receptor inhibition with subcutaneously implanted 7 day delivery osmotic pumps loaded with <b>ketamine</b>; (2) <strong><strong>TrkB</strong></strong> receptor inhibition with intraperitoneal (i.p.)
+NTRK2	addiction	relapse	28585567	Inhibiting BDNF's receptor, <strong>TrkB</strong>, ERK/MAP kinase activation, or NMDA receptors blocks this attenuating effect, indicating that the interaction between glutamate mediated synaptic activity and <strong>TrkB</strong> signaling is imperative to BDNF's suppressive effect on drug <b>seeking</b>.
+NTRK2	addiction	relapse	28585567	Inhibiting BDNF's receptor, <strong><strong>TrkB</strong></strong>, ERK/MAP kinase activation, or NMDA receptors blocks this attenuating effect, indicating that the interaction between glutamate mediated synaptic activity and <strong><strong>TrkB</strong></strong> signaling is imperative to BDNF's suppressive effect on drug <b>seeking</b>.
+NTRK2	drug	cocaine	28466092	Repeated social defeat and the rewarding effects of <b>cocaine</b> in adult and adolescent mice: dopamine transcription factors, proBDNF signaling pathways, and the <strong>TrkB</strong> receptor in the mesolimbic system.
+NTRK2	drug	cocaine	28466092	Repeated social defeat and the rewarding effects of <b>cocaine</b> in adult and adolescent mice: dopamine transcription factors, proBDNF signaling pathways, and the <strong><strong>TrkB</strong></strong> receptor in the mesolimbic system.
+NTRK2	drug	cocaine	28466092	The aim of the present study was to compare the long term effects of RSD on the conditioned rewarding effects of <b>cocaine</b> and levels of the transcription factors Pitx3 and Nurr1 in the ventral tegmental area (VTA), the dopamine transporter (DAT), the D2 dopamine receptor (D2DR) and precursor of brain derived neurotrophic factor (proBDNF) signaling pathways, and the tropomyosin related kinase B (<strong>TrkB</strong>) receptor in the nucleus accumbens (NAc) in adult and adolescent mice.
+NTRK2	drug	cocaine	28466092	The aim of the present study was to compare the long term effects of RSD on the conditioned rewarding effects of <b>cocaine</b> and levels of the transcription factors Pitx3 and Nurr1 in the ventral tegmental area (VTA), the dopamine transporter (DAT), the D2 dopamine receptor (D2DR) and precursor of brain derived neurotrophic factor (proBDNF) signaling pathways, and the tropomyosin related kinase B (<strong><strong>TrkB</strong></strong>) receptor in the nucleus accumbens (NAc) in adult and adolescent mice.
+NTRK2	drug	cocaine	28466092	Our findings suggest that dopaminergic pathways and proBDNF signaling and <strong>TrkB</strong> receptors play different roles in social defeat stressed mice exposed to <b>cocaine</b>.
+NTRK2	drug	cocaine	28466092	Our findings suggest that dopaminergic pathways and proBDNF signaling and <strong><strong>TrkB</strong></strong> receptors play different roles in social defeat stressed mice exposed to <b>cocaine</b>.
+NTRK2	drug	alcohol	28032807	Reverse transcription PCR (RT PCR) was performed to measure mRNA levels for BDNF, <strong>TrkB</strong>, P75NTR, and sortilin in the prefrontal cortex, hippocampus, and dorsal striatum of Kunming mice after chronic <b>alcohol</b> exposure.
+NTRK2	drug	alcohol	28032807	Reverse transcription PCR (RT PCR) was performed to measure mRNA levels for BDNF, <strong><strong>TrkB</strong></strong>, P75NTR, and sortilin in the prefrontal cortex, hippocampus, and dorsal striatum of Kunming mice after chronic <b>alcohol</b> exposure.
+NTRK2	drug	alcohol	28032807	In Kunming mice, chronic <b>alcohol</b> exposure up regulated BDNF and <strong>TrkB</strong> mRNA levels in the prefrontal cortex, but decreased sortilin and P75 mRNA levels in the dorsal striatum.
+NTRK2	drug	alcohol	28032807	In Kunming mice, chronic <b>alcohol</b> exposure up regulated BDNF and <strong><strong>TrkB</strong></strong> mRNA levels in the prefrontal cortex, but decreased sortilin and P75 mRNA levels in the dorsal striatum.
+NTRK2	drug	cocaine	27765467	Intra prelimbic infusion of BDNF decreases <b>cocaine</b> seeking in a <strong>TrkB</strong> ERK MAP kinase dependent manner.
+NTRK2	addiction	relapse	27765467	Intra prelimbic infusion of BDNF decreases cocaine <b>seeking</b> in a <strong>TrkB</strong> ERK MAP kinase dependent manner.
+NTRK2	drug	cocaine	27765467	Intra prelimbic infusion of BDNF decreases <b>cocaine</b> seeking in a <strong><strong>TrkB</strong></strong> ERK MAP kinase dependent manner.
+NTRK2	addiction	relapse	27765467	Intra prelimbic infusion of BDNF decreases cocaine <b>seeking</b> in a <strong><strong>TrkB</strong></strong> ERK MAP kinase dependent manner.
+NTRK2	drug	cocaine	27735948	Transactivation of <strong>TrkB</strong> by Sigma 1 receptor mediates <b>cocaine</b> induced changes in dendritic spine density and morphology in hippocampal and cortical neurons.
+NTRK2	drug	cocaine	27735948	Transactivation of <strong><strong>TrkB</strong></strong> by Sigma 1 receptor mediates <b>cocaine</b> induced changes in dendritic spine density and morphology in hippocampal and cortical neurons.
+NTRK2	drug	cocaine	27735948	Intriguingly, in hippocampal neurons <b>cocaine</b> mediated effects on spine density and morphology involved sigma 1 receptor (Sig 1 R) and its downstream <strong>TrkB</strong> signaling, which were not the case in cortical neurons.
+NTRK2	drug	cocaine	27735948	Intriguingly, in hippocampal neurons <b>cocaine</b> mediated effects on spine density and morphology involved sigma 1 receptor (Sig 1 R) and its downstream <strong><strong>TrkB</strong></strong> signaling, which were not the case in cortical neurons.
+NTRK2	drug	cocaine	27735948	Furthermore, pharmacological inhibition of Sig 1 R prevented <b>cocaine</b> induced <strong>TrkB</strong> activation in hippocampal neurons.
+NTRK2	drug	cocaine	27735948	Furthermore, pharmacological inhibition of Sig 1 R prevented <b>cocaine</b> induced <strong><strong>TrkB</strong></strong> activation in hippocampal neurons.
+NTRK2	drug	alcohol	27683907	For example, activation of the BDNF receptor tropomyosin receptor kinase B (<strong>TrkB</strong>) in the DLS reduces intake in rats that consume moderate amounts of <b>alcohol</b>.
+NTRK2	drug	alcohol	27683907	For example, activation of the BDNF receptor tropomyosin receptor kinase B (<strong><strong>TrkB</strong></strong>) in the DLS reduces intake in rats that consume moderate amounts of <b>alcohol</b>.
+NTRK2	drug	alcohol	27683907	We report that intermittent access to 20% <b>alcohol</b> in a two bottle choice paradigm that models excessive <b>alcohol</b> drinking produces a mobilization of DLS p75 neurotrophin receptor (p75NTR), whose activities oppose those of the Trk receptors, including <strong>TrkB</strong>.
+NTRK2	drug	alcohol	27683907	We report that intermittent access to 20% <b>alcohol</b> in a two bottle choice paradigm that models excessive <b>alcohol</b> drinking produces a mobilization of DLS p75 neurotrophin receptor (p75NTR), whose activities oppose those of the Trk receptors, including <strong><strong>TrkB</strong></strong>.
+NTRK2	drug	alcohol	27683907	We previously showed that brain derived neurotrophic factor and its receptor, <strong>TrkB</strong>, in the dorsolateral striatum (DLS), are part of an endogenous system that keeps <b>alcohol</b> drinking in moderation.
+NTRK2	drug	alcohol	27683907	We previously showed that brain derived neurotrophic factor and its receptor, <strong><strong>TrkB</strong></strong>, in the dorsolateral striatum (DLS), are part of an endogenous system that keeps <b>alcohol</b> drinking in moderation.
+NTRK2	drug	cocaine	27576164	Re exposure to the <b>cocaine</b> associated context in adulthood energized responding in 'stable responders', which could then be reduced by the GABAB agonist baclofen and the putative tyrosine receptor kinase B (<strong>trkB</strong>) agonist, 7,8 dihydroxyflavone.
+NTRK2	drug	cocaine	27576164	Re exposure to the <b>cocaine</b> associated context in adulthood energized responding in 'stable responders', which could then be reduced by the GABAB agonist baclofen and the putative tyrosine receptor kinase B (<strong><strong>trkB</strong></strong>) agonist, 7,8 dihydroxyflavone.
+NTRK2	drug	cocaine	27488635	Systemic Delivery of a Brain Penetrant <strong>TrkB</strong> Antagonist Reduces <b>Cocaine</b> Self Administration and Normalizes <strong>TrkB</strong> Signaling in the Nucleus Accumbens and Prefrontal Cortex.
+NTRK2	drug	cocaine	27488635	Systemic Delivery of a Brain Penetrant <strong><strong>TrkB</strong></strong> Antagonist Reduces <b>Cocaine</b> Self Administration and Normalizes <strong><strong>TrkB</strong></strong> Signaling in the Nucleus Accumbens and Prefrontal Cortex.
+NTRK2	drug	cocaine	27488635	BDNF signaling through <strong>TrkB</strong> receptors differentially modulates <b>cocaine</b> self administration, depending on the brain regions involved.
+NTRK2	drug	cocaine	27488635	BDNF signaling through <strong><strong>TrkB</strong></strong> receptors differentially modulates <b>cocaine</b> self administration, depending on the brain regions involved.
+NTRK2	drug	cocaine	27488635	In the present study, we determined how brain wide inhibition of <strong>TrkB</strong> signaling affects <b>cocaine</b> intake, the motivation for the drug, and reinstatement of drug taking after extinction.
+NTRK2	addiction	relapse	27488635	In the present study, we determined how brain wide inhibition of <strong>TrkB</strong> signaling affects cocaine intake, the motivation for the drug, and <b>reinstatement</b> of drug taking after extinction.
+NTRK2	drug	cocaine	27488635	In the present study, we determined how brain wide inhibition of <strong><strong>TrkB</strong></strong> signaling affects <b>cocaine</b> intake, the motivation for the drug, and reinstatement of drug taking after extinction.
+NTRK2	addiction	relapse	27488635	In the present study, we determined how brain wide inhibition of <strong><strong>TrkB</strong></strong> signaling affects cocaine intake, the motivation for the drug, and <b>reinstatement</b> of drug taking after extinction.
+NTRK2	drug	cocaine	27488635	<b>Cocaine</b> self administration increased <strong>TrkB</strong> signaling and activated the downstream Akt pathway in the nucleus accumbens, and had opposite effects in the prefrontal cortex.
+NTRK2	drug	cocaine	27488635	<b>Cocaine</b> self administration increased <strong><strong>TrkB</strong></strong> signaling and activated the downstream Akt pathway in the nucleus accumbens, and had opposite effects in the prefrontal cortex.
+NTRK2	drug	cocaine	27488635	<b>Cocaine</b> self administration also increased <strong>TrkB</strong> signaling in the ventral tegmental area, where the dopaminergic projections originate, but pretreatment with tat cyclotraxin B did not alter this effect.
+NTRK2	drug	cocaine	27488635	<b>Cocaine</b> self administration also increased <strong><strong>TrkB</strong></strong> signaling in the ventral tegmental area, where the dopaminergic projections originate, but pretreatment with tat cyclotraxin B did not alter this effect.
+NTRK2	drug	cocaine	27488635	Altogether, our data show that systemic administration of a brain penetrant <strong>TrkB</strong> antagonist leads to brain region specific effects and may be a potential pharmacological strategy for the treatment of <b>cocaine</b> addiction.
+NTRK2	addiction	addiction	27488635	Altogether, our data show that systemic administration of a brain penetrant <strong>TrkB</strong> antagonist leads to brain region specific effects and may be a potential pharmacological strategy for the treatment of cocaine <b>addiction</b>.
+NTRK2	drug	cocaine	27488635	Altogether, our data show that systemic administration of a brain penetrant <strong><strong>TrkB</strong></strong> antagonist leads to brain region specific effects and may be a potential pharmacological strategy for the treatment of <b>cocaine</b> addiction.
+NTRK2	addiction	addiction	27488635	Altogether, our data show that systemic administration of a brain penetrant <strong><strong>TrkB</strong></strong> antagonist leads to brain region specific effects and may be a potential pharmacological strategy for the treatment of cocaine <b>addiction</b>.
+NTRK2	drug	cocaine	27488635	Brain derived neurotrophic factor (BDNF) signaling through <strong>TrkB</strong> receptors plays a well established role in <b>cocaine</b> reinforcement.
+NTRK2	addiction	reward	27488635	Brain derived neurotrophic factor (BDNF) signaling through <strong>TrkB</strong> receptors plays a well established role in cocaine <b>reinforcement</b>.
+NTRK2	drug	cocaine	27488635	Brain derived neurotrophic factor (BDNF) signaling through <strong><strong>TrkB</strong></strong> receptors plays a well established role in <b>cocaine</b> reinforcement.
+NTRK2	addiction	reward	27488635	Brain derived neurotrophic factor (BDNF) signaling through <strong><strong>TrkB</strong></strong> receptors plays a well established role in cocaine <b>reinforcement</b>.
+NTRK2	drug	cocaine	27488635	However, local manipulation of BDNF signaling yields divergent effects, depending on the brain region, thereby questioning the viability of systemic <strong>TrkB</strong> targeting for the treatment of <b>cocaine</b> use disorders.
+NTRK2	drug	cocaine	27488635	However, local manipulation of BDNF signaling yields divergent effects, depending on the brain region, thereby questioning the viability of systemic <strong><strong>TrkB</strong></strong> targeting for the treatment of <b>cocaine</b> use disorders.
+NTRK2	drug	cocaine	27488635	Our study provides first time evidence that systemic administration of a brain penetrant <strong>TrkB</strong> antagonist (tat cyclotraxin B) reduces several behavioral measures of <b>cocaine</b> dependence, without altering motor performance or reinforcement by a sweet palatable solution.
+NTRK2	addiction	dependence	27488635	Our study provides first time evidence that systemic administration of a brain penetrant <strong>TrkB</strong> antagonist (tat cyclotraxin B) reduces several behavioral measures of cocaine <b>dependence</b>, without altering motor performance or reinforcement by a sweet palatable solution.
+NTRK2	addiction	reward	27488635	Our study provides first time evidence that systemic administration of a brain penetrant <strong>TrkB</strong> antagonist (tat cyclotraxin B) reduces several behavioral measures of cocaine dependence, without altering motor performance or <b>reinforcement</b> by a sweet palatable solution.
+NTRK2	drug	cocaine	27488635	Our study provides first time evidence that systemic administration of a brain penetrant <strong><strong>TrkB</strong></strong> antagonist (tat cyclotraxin B) reduces several behavioral measures of <b>cocaine</b> dependence, without altering motor performance or reinforcement by a sweet palatable solution.
+NTRK2	addiction	dependence	27488635	Our study provides first time evidence that systemic administration of a brain penetrant <strong><strong>TrkB</strong></strong> antagonist (tat cyclotraxin B) reduces several behavioral measures of cocaine <b>dependence</b>, without altering motor performance or reinforcement by a sweet palatable solution.
+NTRK2	addiction	reward	27488635	Our study provides first time evidence that systemic administration of a brain penetrant <strong><strong>TrkB</strong></strong> antagonist (tat cyclotraxin B) reduces several behavioral measures of cocaine dependence, without altering motor performance or <b>reinforcement</b> by a sweet palatable solution.
+NTRK2	drug	cocaine	27488635	In addition, although <b>cocaine</b> self administration produced opposite effects on <strong>TrkB</strong> signaling in the nucleus accumbens and prefrontal cortex, tat cyclotraxin B administration normalized these <b>cocaine</b> induced changes in both brain regions.
+NTRK2	drug	cocaine	27488635	In addition, although <b>cocaine</b> self administration produced opposite effects on <strong><strong>TrkB</strong></strong> signaling in the nucleus accumbens and prefrontal cortex, tat cyclotraxin B administration normalized these <b>cocaine</b> induced changes in both brain regions.
+NTRK2	drug	opioid	27094549	Treatments blocking the epigenetically mediated up regulation of these genes or administration of <strong>TrkB</strong> or κ <b>opioid</b> receptor antagonists may improve the clinical utility of <b>opioids</b>, particularly after surgery.
+NTRK2	drug	opioid	27094549	Treatments blocking the epigenetically mediated up regulation of these genes or administration of <strong><strong>TrkB</strong></strong> or κ <b>opioid</b> receptor antagonists may improve the clinical utility of <b>opioids</b>, particularly after surgery.
+NTRK2	addiction	reward	26960698	However, treatment with a BDNF tropomyosin receptor kinase B (<strong>TrkB</strong>) receptor antagonist, K252a (5 μg/kg), did not affect rottlerin's suppressing effect on COC induced <b>CPP</b> and treatment with 7,8 dihydroxyflavone (10 mg/kg x 6, 7,8 DHF), a selective <strong>TrkB</strong> agonist, prior to each conditioning trial did not affect COC induced <b>CPP</b>.
+NTRK2	addiction	reward	26960698	However, treatment with a BDNF tropomyosin receptor kinase B (<strong><strong>TrkB</strong></strong>) receptor antagonist, K252a (5 μg/kg), did not affect rottlerin's suppressing effect on COC induced <b>CPP</b> and treatment with 7,8 dihydroxyflavone (10 mg/kg x 6, 7,8 DHF), a selective <strong><strong>TrkB</strong></strong> agonist, prior to each conditioning trial did not affect COC induced <b>CPP</b>.
+NTRK2	drug	alcohol	26659122	<b>Alcohol</b> dependence induced regulation of the proliferation and survival of adult brain progenitors is associated with altered BDNF <strong>TrkB</strong> signaling.
+NTRK2	addiction	dependence	26659122	Alcohol <b>dependence</b> induced regulation of the proliferation and survival of adult brain progenitors is associated with altered BDNF <strong>TrkB</strong> signaling.
+NTRK2	drug	alcohol	26659122	<b>Alcohol</b> dependence induced regulation of the proliferation and survival of adult brain progenitors is associated with altered BDNF <strong><strong>TrkB</strong></strong> signaling.
+NTRK2	addiction	dependence	26659122	Alcohol <b>dependence</b> induced regulation of the proliferation and survival of adult brain progenitors is associated with altered BDNF <strong><strong>TrkB</strong></strong> signaling.
+NTRK2	drug	opioid	26567727	In some rats, BDNF receptor antagonist K252a (8.5 ng per side) or BDNF scavenger <strong>TrkB</strong> FC (0.65 μg per side) was bilaterally microinjected into amygdala before <b>naloxone</b> injection.
+NTRK2	drug	opioid	26567727	In some rats, BDNF receptor antagonist K252a (8.5 ng per side) or BDNF scavenger <strong><strong>TrkB</strong></strong> FC (0.65 μg per side) was bilaterally microinjected into amygdala before <b>naloxone</b> injection.
+NTRK2	drug	cocaine	26538265	The Results showed that <b>cocaine</b> sensitization was associated with increased BDNF, ILK activity, phospho Akt Ser(473), p75(NTR), and <strong>TrkB</strong> protein levels in the mPFC and NAc core.
+NTRK2	addiction	sensitization	26538265	The Results showed that cocaine <b>sensitization</b> was associated with increased BDNF, ILK activity, phospho Akt Ser(473), p75(NTR), and <strong>TrkB</strong> protein levels in the mPFC and NAc core.
+NTRK2	drug	cocaine	26538265	The Results showed that <b>cocaine</b> sensitization was associated with increased BDNF, ILK activity, phospho Akt Ser(473), p75(NTR), and <strong><strong>TrkB</strong></strong> protein levels in the mPFC and NAc core.
+NTRK2	addiction	sensitization	26538265	The Results showed that cocaine <b>sensitization</b> was associated with increased BDNF, ILK activity, phospho Akt Ser(473), p75(NTR), and <strong><strong>TrkB</strong></strong> protein levels in the mPFC and NAc core.
+NTRK2	drug	amphetamine	26506052	BDNF <strong>TrkB</strong> signaling in the nucleus accumbens shell of mice has key role in <b>methamphetamine</b> withdrawal symptoms.
+NTRK2	addiction	withdrawal	26506052	BDNF <strong>TrkB</strong> signaling in the nucleus accumbens shell of mice has key role in methamphetamine <b>withdrawal</b> symptoms.
+NTRK2	drug	amphetamine	26506052	BDNF <strong><strong>TrkB</strong></strong> signaling in the nucleus accumbens shell of mice has key role in <b>methamphetamine</b> withdrawal symptoms.
+NTRK2	addiction	withdrawal	26506052	BDNF <strong><strong>TrkB</strong></strong> signaling in the nucleus accumbens shell of mice has key role in methamphetamine <b>withdrawal</b> symptoms.
+NTRK2	drug	amphetamine	26506052	In this study, we examined the role of BDNF <strong>TrkB</strong> signaling in different brain regions of male mice with <b>METH</b> withdrawal symptoms.
+NTRK2	addiction	withdrawal	26506052	In this study, we examined the role of BDNF <strong>TrkB</strong> signaling in different brain regions of male mice with METH <b>withdrawal</b> symptoms.
+NTRK2	drug	amphetamine	26506052	In this study, we examined the role of BDNF <strong><strong>TrkB</strong></strong> signaling in different brain regions of male mice with <b>METH</b> withdrawal symptoms.
+NTRK2	addiction	withdrawal	26506052	In this study, we examined the role of BDNF <strong><strong>TrkB</strong></strong> signaling in different brain regions of male mice with METH <b>withdrawal</b> symptoms.
+NTRK2	drug	amphetamine	26506052	<b>METH</b> induced depression like behavior, behavioral sensitization and dendritic changes in the NAc shell were improved by subsequent subchronic administration of <strong>TrkB</strong> antagonist ANA 12 (0.5 mg kg( 1) per day for 14 days), but not <strong>TrkB</strong> agonist 7,8 dihydroxyflavone (10 mg kg( 1) per day for 14 days).
+NTRK2	addiction	sensitization	26506052	METH induced depression like behavior, behavioral <b>sensitization</b> and dendritic changes in the NAc shell were improved by subsequent subchronic administration of <strong>TrkB</strong> antagonist ANA 12 (0.5 mg kg( 1) per day for 14 days), but not <strong>TrkB</strong> agonist 7,8 dihydroxyflavone (10 mg kg( 1) per day for 14 days).
+NTRK2	drug	amphetamine	26506052	<b>METH</b> induced depression like behavior, behavioral sensitization and dendritic changes in the NAc shell were improved by subsequent subchronic administration of <strong><strong>TrkB</strong></strong> antagonist ANA 12 (0.5 mg kg( 1) per day for 14 days), but not <strong><strong>TrkB</strong></strong> agonist 7,8 dihydroxyflavone (10 mg kg( 1) per day for 14 days).
+NTRK2	addiction	sensitization	26506052	METH induced depression like behavior, behavioral <b>sensitization</b> and dendritic changes in the NAc shell were improved by subsequent subchronic administration of <strong><strong>TrkB</strong></strong> antagonist ANA 12 (0.5 mg kg( 1) per day for 14 days), but not <strong><strong>TrkB</strong></strong> agonist 7,8 dihydroxyflavone (10 mg kg( 1) per day for 14 days).
+NTRK2	drug	amphetamine	26506052	These findings suggest that increased BDNF <strong>TrkB</strong> signaling in the NAc shell has an important role in the behavioral abnormalities after withdrawal from repeated <b>METH</b> administration, and that <strong>TrkB</strong> antagonists are potential therapeutic drugs for withdrawal symptoms in <b>METH</b> abusers.
+NTRK2	addiction	withdrawal	26506052	These findings suggest that increased BDNF <strong>TrkB</strong> signaling in the NAc shell has an important role in the behavioral abnormalities after <b>withdrawal</b> from repeated METH administration, and that <strong>TrkB</strong> antagonists are potential therapeutic drugs for <b>withdrawal</b> symptoms in METH abusers.
+NTRK2	drug	amphetamine	26506052	These findings suggest that increased BDNF <strong><strong>TrkB</strong></strong> signaling in the NAc shell has an important role in the behavioral abnormalities after withdrawal from repeated <b>METH</b> administration, and that <strong><strong>TrkB</strong></strong> antagonists are potential therapeutic drugs for withdrawal symptoms in <b>METH</b> abusers.
+NTRK2	addiction	withdrawal	26506052	These findings suggest that increased BDNF <strong><strong>TrkB</strong></strong> signaling in the NAc shell has an important role in the behavioral abnormalities after <b>withdrawal</b> from repeated METH administration, and that <strong><strong>TrkB</strong></strong> antagonists are potential therapeutic drugs for <b>withdrawal</b> symptoms in METH abusers.
+NTRK2	drug	opioid	26346883	Expression of BDNF and <strong>TrkB</strong> Phosphorylation in the Rat Frontal Cortex During <b>Morphine</b> Withdrawal are NO Dependent.
+NTRK2	addiction	withdrawal	26346883	Expression of BDNF and <strong>TrkB</strong> Phosphorylation in the Rat Frontal Cortex During Morphine <b>Withdrawal</b> are NO Dependent.
+NTRK2	drug	opioid	26346883	Expression of BDNF and <strong><strong>TrkB</strong></strong> Phosphorylation in the Rat Frontal Cortex During <b>Morphine</b> Withdrawal are NO Dependent.
+NTRK2	addiction	withdrawal	26346883	Expression of BDNF and <strong><strong>TrkB</strong></strong> Phosphorylation in the Rat Frontal Cortex During Morphine <b>Withdrawal</b> are NO Dependent.
+NTRK2	drug	opioid	26346883	<b>Morphine</b> withdrawal was accompanied by upregulation of BDNF, IGF1, and their receptors <strong>TrkB</strong> and IGF1R, respectively, on the mRNA level in the frontal cortex, and only BDNF in hippocampus and midbrain.
+NTRK2	addiction	withdrawal	26346883	Morphine <b>withdrawal</b> was accompanied by upregulation of BDNF, IGF1, and their receptors <strong>TrkB</strong> and IGF1R, respectively, on the mRNA level in the frontal cortex, and only BDNF in hippocampus and midbrain.
+NTRK2	drug	opioid	26346883	<b>Morphine</b> withdrawal was accompanied by upregulation of BDNF, IGF1, and their receptors <strong><strong>TrkB</strong></strong> and IGF1R, respectively, on the mRNA level in the frontal cortex, and only BDNF in hippocampus and midbrain.
+NTRK2	addiction	withdrawal	26346883	Morphine <b>withdrawal</b> was accompanied by upregulation of BDNF, IGF1, and their receptors <strong><strong>TrkB</strong></strong> and IGF1R, respectively, on the mRNA level in the frontal cortex, and only BDNF in hippocampus and midbrain.
+NTRK2	drug	opioid	26346883	While <b>morphine</b> abstinence did not affect <strong>TrkB</strong> protein levels as well as its phosphorylation status, inhibition of NO synthesis decreased levels of phosphorylated <strong>TrkB</strong> after withdrawal.
+NTRK2	addiction	withdrawal	26346883	While morphine abstinence did not affect <strong>TrkB</strong> protein levels as well as its phosphorylation status, inhibition of NO synthesis decreased levels of phosphorylated <strong>TrkB</strong> after <b>withdrawal</b>.
+NTRK2	drug	opioid	26346883	While <b>morphine</b> abstinence did not affect <strong><strong>TrkB</strong></strong> protein levels as well as its phosphorylation status, inhibition of NO synthesis decreased levels of phosphorylated <strong><strong>TrkB</strong></strong> after withdrawal.
+NTRK2	addiction	withdrawal	26346883	While morphine abstinence did not affect <strong><strong>TrkB</strong></strong> protein levels as well as its phosphorylation status, inhibition of NO synthesis decreased levels of phosphorylated <strong><strong>TrkB</strong></strong> after <b>withdrawal</b>.
+NTRK2	addiction	dependence	26346883	Thus, NO signaling during induction of <b>dependence</b> may be involved in the mechanisms of BDNF expression and processing at abstinence, thereby affecting signaling through <strong>TrkB</strong> in the frontal cortex.
+NTRK2	addiction	dependence	26346883	Thus, NO signaling during induction of <b>dependence</b> may be involved in the mechanisms of BDNF expression and processing at abstinence, thereby affecting signaling through <strong><strong>TrkB</strong></strong> in the frontal cortex.
+NTRK2	drug	amphetamine	26019338	Incubation of <b>methamphetamine</b> craving is associated with selective increases in expression of Bdnf and <strong>trkb</strong>, glutamate receptors, and epigenetic enzymes in cue activated fos expressing dorsal striatal neurons.
+NTRK2	addiction	relapse	26019338	Incubation of methamphetamine <b>craving</b> is associated with selective increases in expression of Bdnf and <strong>trkb</strong>, glutamate receptors, and epigenetic enzymes in cue activated fos expressing dorsal striatal neurons.
+NTRK2	drug	amphetamine	26019338	Incubation of <b>methamphetamine</b> craving is associated with selective increases in expression of Bdnf and <strong><strong>trkb</strong></strong>, glutamate receptors, and epigenetic enzymes in cue activated fos expressing dorsal striatal neurons.
+NTRK2	addiction	relapse	26019338	Incubation of methamphetamine <b>craving</b> is associated with selective increases in expression of Bdnf and <strong><strong>trkb</strong></strong>, glutamate receptors, and epigenetic enzymes in cue activated fos expressing dorsal striatal neurons.
+NTRK2	drug	amphetamine	25463524	Expression of brain derived neurotrophic factor (BDNF; a regulator of LTP and neurogenesis), and its receptor tropomyosin related kinase B (<strong>TrkB</strong>) were studied in the dorsal and ventral hippocampal tissue lysates in rats that intravenously self administered <b>methamphetamine</b> in a limited access (1h/day) or extended access (6h/day) paradigm for 17days post baseline sessions.
+NTRK2	drug	amphetamine	25463524	Expression of brain derived neurotrophic factor (BDNF; a regulator of LTP and neurogenesis), and its receptor tropomyosin related kinase B (<strong><strong>TrkB</strong></strong>) were studied in the dorsal and ventral hippocampal tissue lysates in rats that intravenously self administered <b>methamphetamine</b> in a limited access (1h/day) or extended access (6h/day) paradigm for 17days post baseline sessions.
+NTRK2	drug	amphetamine	25463524	<b>Methamphetamine</b> induced enhancements in BDNF expression were not associated with <strong>TrkB</strong> receptor activation as indicated by phospho (p) <strong>TrkB</strong> 706 levels.
+NTRK2	drug	amphetamine	25463524	<b>Methamphetamine</b> induced enhancements in BDNF expression were not associated with <strong><strong>TrkB</strong></strong> receptor activation as indicated by phospho (p) <strong><strong>TrkB</strong></strong> 706 levels.
+NTRK2	drug	nicotine	25450229	Rare variants in NRXN1, CHRNA9, CHRNA2, <strong>NTRK2</strong>, GABBR2, GRIN3A, DNM1, NRXN2, NRXN3 and ARRB2 were significantly associated with <b>smoking</b> status in the MSTCC AA sample, with weighted sum statistic (WSS) P values ranging from 2.42 × 10( 3) to 1.31 × 10( 4) after 10(6) phenotype rearrangements.
+NTRK2	drug	opioid	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for GluR1 AMPA receptor (AMPAR), phosphorylated ERK2 (pERK2), CREB (pCREB), <strong>TrKB</strong> (pTrkB) were performed in brain areas relevant for sensitization from KO and WT and/or <b>naloxone</b>  and vehicle pre treated animals.
+NTRK2	addiction	sensitization	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for GluR1 AMPA receptor (AMPAR), phosphorylated ERK2 (pERK2), CREB (pCREB), <strong>TrKB</strong> (pTrkB) were performed in brain areas relevant for <b>sensitization</b> from KO and WT and/or naloxone  and vehicle pre treated animals.
+NTRK2	drug	opioid	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for GluR1 AMPA receptor (AMPAR), phosphorylated ERK2 (pERK2), CREB (pCREB), <strong><strong>TrKB</strong></strong> (pTrkB) were performed in brain areas relevant for sensitization from KO and WT and/or <b>naloxone</b>  and vehicle pre treated animals.
+NTRK2	addiction	sensitization	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for GluR1 AMPA receptor (AMPAR), phosphorylated ERK2 (pERK2), CREB (pCREB), <strong><strong>TrKB</strong></strong> (pTrkB) were performed in brain areas relevant for <b>sensitization</b> from KO and WT and/or naloxone  and vehicle pre treated animals.
+NTRK2	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, <strong>Ntrk2</strong>, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+NTRK2	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, <strong>Ntrk2</strong>, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+NTRK2	drug	opioid	24853771	In the present study, we show that GABAergic activity is selectively modulated in D1 type MSNs of the NAc by signaling of brain derived neurotrophic factor (BDNF) and its receptor, tyrosine receptor kinase B (<strong>TrkB</strong>), and that such adaptations control rewarding responses to <b>morphine</b>.
+NTRK2	drug	opioid	24853771	In the present study, we show that GABAergic activity is selectively modulated in D1 type MSNs of the NAc by signaling of brain derived neurotrophic factor (BDNF) and its receptor, tyrosine receptor kinase B (<strong><strong>TrkB</strong></strong>), and that such adaptations control rewarding responses to <b>morphine</b>.
+NTRK2	drug	opioid	24853771	Optical activation of D1 type MSNs, or the knockout of <strong>TrkB</strong> from D1 type MSNs (D1 <strong>TrkB</strong> KO), enhances <b>morphine</b> reward, effects not seen for D2 type MSNs.
+NTRK2	addiction	reward	24853771	Optical activation of D1 type MSNs, or the knockout of <strong>TrkB</strong> from D1 type MSNs (D1 <strong>TrkB</strong> KO), enhances morphine <b>reward</b>, effects not seen for D2 type MSNs.
+NTRK2	drug	opioid	24853771	Optical activation of D1 type MSNs, or the knockout of <strong><strong>TrkB</strong></strong> from D1 type MSNs (D1 <strong><strong>TrkB</strong></strong> KO), enhances <b>morphine</b> reward, effects not seen for D2 type MSNs.
+NTRK2	addiction	reward	24853771	Optical activation of D1 type MSNs, or the knockout of <strong><strong>TrkB</strong></strong> from D1 type MSNs (D1 <strong><strong>TrkB</strong></strong> KO), enhances morphine <b>reward</b>, effects not seen for D2 type MSNs.
+NTRK2	drug	opioid	24853771	Furthermore, we found that GABAAR antagonism in the NAc enhances <b>morphine</b> reward and that <b>morphine</b> exposure decreases <strong>TrkB</strong> expression as well as GABAergic activity in D1 type MSNs.
+NTRK2	addiction	reward	24853771	Furthermore, we found that GABAAR antagonism in the NAc enhances morphine <b>reward</b> and that morphine exposure decreases <strong>TrkB</strong> expression as well as GABAergic activity in D1 type MSNs.
+NTRK2	drug	opioid	24853771	Furthermore, we found that GABAAR antagonism in the NAc enhances <b>morphine</b> reward and that <b>morphine</b> exposure decreases <strong><strong>TrkB</strong></strong> expression as well as GABAergic activity in D1 type MSNs.
+NTRK2	addiction	reward	24853771	Furthermore, we found that GABAAR antagonism in the NAc enhances morphine <b>reward</b> and that morphine exposure decreases <strong><strong>TrkB</strong></strong> expression as well as GABAergic activity in D1 type MSNs.
+NTRK2	drug	opioid	24853771	Together, these data provide evidence for the enhancement of <b>morphine</b> reward through reduction of inhibitory GABAAR responses, an adaptation mediated by <b>morphine</b> induced reduction of BDNF <strong>TrkB</strong> signaling in D1 type MSNs.
+NTRK2	addiction	reward	24853771	Together, these data provide evidence for the enhancement of morphine <b>reward</b> through reduction of inhibitory GABAAR responses, an adaptation mediated by morphine induced reduction of BDNF <strong>TrkB</strong> signaling in D1 type MSNs.
+NTRK2	drug	opioid	24853771	Together, these data provide evidence for the enhancement of <b>morphine</b> reward through reduction of inhibitory GABAAR responses, an adaptation mediated by <b>morphine</b> induced reduction of BDNF <strong><strong>TrkB</strong></strong> signaling in D1 type MSNs.
+NTRK2	addiction	reward	24853771	Together, these data provide evidence for the enhancement of morphine <b>reward</b> through reduction of inhibitory GABAAR responses, an adaptation mediated by morphine induced reduction of BDNF <strong><strong>TrkB</strong></strong> signaling in D1 type MSNs.
+NTRK2	drug	cocaine	24760865	Infralimbic BDNF/<strong>TrkB</strong> enhancement of GluN2B currents facilitates extinction of a <b>cocaine</b> conditioned place preference.
+NTRK2	drug	cocaine	24760865	Infralimbic BDNF/<strong><strong>TrkB</strong></strong> enhancement of GluN2B currents facilitates extinction of a <b>cocaine</b> conditioned place preference.
+NTRK2	addiction	reward	24760865	Blockade of infralimbic <strong>TrkB</strong> receptors or GluN2B containing NMDARs disrupted consolidation of extinction of the <b>CPP</b>.
+NTRK2	addiction	reward	24760865	Blockade of infralimbic <strong><strong>TrkB</strong></strong> receptors or GluN2B containing NMDARs disrupted consolidation of extinction of the <b>CPP</b>.
+NTRK2	drug	cocaine	24760865	The 7,8DHF induced enhancement of extinction was prevented by infralimbic infusions of a GluN2B specific receptor antagonist, demonstrating that <strong>TrkB</strong> receptor activation enhances extinction of <b>cocaine</b> CPP via GluN2B containing NMDARs.
+NTRK2	addiction	reward	24760865	The 7,8DHF induced enhancement of extinction was prevented by infralimbic infusions of a GluN2B specific receptor antagonist, demonstrating that <strong>TrkB</strong> receptor activation enhances extinction of cocaine <b>CPP</b> via GluN2B containing NMDARs.
+NTRK2	drug	cocaine	24760865	The 7,8DHF induced enhancement of extinction was prevented by infralimbic infusions of a GluN2B specific receptor antagonist, demonstrating that <strong><strong>TrkB</strong></strong> receptor activation enhances extinction of <b>cocaine</b> CPP via GluN2B containing NMDARs.
+NTRK2	addiction	reward	24760865	The 7,8DHF induced enhancement of extinction was prevented by infralimbic infusions of a GluN2B specific receptor antagonist, demonstrating that <strong><strong>TrkB</strong></strong> receptor activation enhances extinction of cocaine <b>CPP</b> via GluN2B containing NMDARs.
+NTRK2	drug	cocaine	24752656	We also investigated the effects of <b>cocaine</b> delivery speed on corticostriatal expression of brain derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (<strong>TrkB</strong>) mRNA.
+NTRK2	drug	cocaine	24752656	We also investigated the effects of <b>cocaine</b> delivery speed on corticostriatal expression of brain derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (<strong><strong>TrkB</strong></strong>) mRNA.
+NTRK2	drug	cocaine	24752656	In parallel, only rats self administering rapid <b>cocaine</b> injections had altered BDNF and <strong>TrkB</strong> mRNA levels in corticostriatal regions.
+NTRK2	drug	cocaine	24752656	In parallel, only rats self administering rapid <b>cocaine</b> injections had altered BDNF and <strong><strong>TrkB</strong></strong> mRNA levels in corticostriatal regions.
+NTRK2	drug	alcohol	24584330	Indeed, blockade of the BDNF pathway by the <strong>TrkB</strong> selective antagonist ANA 12 reversed chronic stable <b>ethanol</b> intake and strongly decreased the striatal expression of D3R.
+NTRK2	drug	alcohol	24584330	Indeed, blockade of the BDNF pathway by the <strong><strong>TrkB</strong></strong> selective antagonist ANA 12 reversed chronic stable <b>ethanol</b> intake and strongly decreased the striatal expression of D3R.
+NTRK2	addiction	aversion	24523535	BDNF deletion or <strong>TrkB</strong> impairment in amygdala inhibits both appetitive and <b>aversive</b> learning.
+NTRK2	addiction	aversion	24523535	BDNF deletion or <strong><strong>TrkB</strong></strong> impairment in amygdala inhibits both appetitive and <b>aversive</b> learning.
+NTRK2	addiction	aversion	24523535	Although the necessity of amygdala bdnf expression and <strong>TrkB</strong> activation for associative learning within <b>aversive</b> contexts has been explored, it is unclear to what extent this interaction is involved in appetitive learning.
+NTRK2	addiction	aversion	24523535	Although the necessity of amygdala bdnf expression and <strong><strong>TrkB</strong></strong> activation for associative learning within <b>aversive</b> contexts has been explored, it is unclear to what extent this interaction is involved in appetitive learning.
+NTRK2	addiction	aversion	24523535	Together, these data suggest that BDNF <strong>TrkB</strong> signaling is critical for amygdala dependent learning of both appetitive and <b>aversive</b> emotional memories.
+NTRK2	addiction	aversion	24523535	Together, these data suggest that BDNF <strong><strong>TrkB</strong></strong> signaling is critical for amygdala dependent learning of both appetitive and <b>aversive</b> emotional memories.
+NTRK2	addiction	addiction	24369067	The striatal BDNF/<strong>TrkB</strong> system is thereby implicated in many physiologic and pathophysiologic processes, the latter including mood disorders, <b>addiction</b>, and Huntington's disease.
+NTRK2	addiction	addiction	24369067	The striatal BDNF/<strong><strong>TrkB</strong></strong> system is thereby implicated in many physiologic and pathophysiologic processes, the latter including mood disorders, <b>addiction</b>, and Huntington's disease.
+NTRK2	drug	amphetamine	24354924	In this study, we examined the necessity for BDNF <strong>TrkB</strong> signaling in the NAc shell during social defeat stress induced cross sensitization to <b>amphetamine</b>.
+NTRK2	addiction	sensitization	24354924	In this study, we examined the necessity for BDNF <strong>TrkB</strong> signaling in the NAc shell during social defeat stress induced cross <b>sensitization</b> to amphetamine.
+NTRK2	drug	amphetamine	24354924	In this study, we examined the necessity for BDNF <strong><strong>TrkB</strong></strong> signaling in the NAc shell during social defeat stress induced cross sensitization to <b>amphetamine</b>.
+NTRK2	addiction	sensitization	24354924	In this study, we examined the necessity for BDNF <strong><strong>TrkB</strong></strong> signaling in the NAc shell during social defeat stress induced cross <b>sensitization</b> to amphetamine.
+NTRK2	addiction	sensitization	24354924	In contrast, NAc <strong>TrkB</strong> knockdown prevented social defeat stress induced cross <b>sensitization</b>.
+NTRK2	addiction	sensitization	24354924	In contrast, NAc <strong><strong>TrkB</strong></strong> knockdown prevented social defeat stress induced cross <b>sensitization</b>.
+NTRK2	addiction	sensitization	24354924	These findings indicated that BDNF <strong>TrkB</strong> signaling in the NAc shell was required for social defeat stress induced cross <b>sensitization</b>.
+NTRK2	addiction	sensitization	24354924	These findings indicated that BDNF <strong><strong>TrkB</strong></strong> signaling in the NAc shell was required for social defeat stress induced cross <b>sensitization</b>.
+NTRK2	addiction	sensitization	24354924	NAc <strong>TrkB</strong> BDNF signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc ΔFosB accumulation that could trigger cross <b>sensitization</b> after social defeat stress.
+NTRK2	addiction	sensitization	24354924	NAc <strong><strong>TrkB</strong></strong> BDNF signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc ΔFosB accumulation that could trigger cross <b>sensitization</b> after social defeat stress.
+NTRK2	drug	cannabinoid	24219803	Western blot was employed to measure BDNF receptor (<strong>TrkB</strong>) and <b>cannabinoid</b> receptor CB1.
+NTRK2	drug	cannabinoid	24219803	Western blot was employed to measure BDNF receptor (<strong><strong>TrkB</strong></strong>) and <b>cannabinoid</b> receptor CB1.
+NTRK2	drug	alcohol	24076087	But the most important finding in our study is that augmenting BDNF actions through the use of tyrosine kinase B (<strong>TrkB</strong>, a BDNF receptor) agonist restored neurogenesis and abolished the <b>alcohol</b> induced anhedonia and despair behaviors seen during the withdrawal/abstinence period.
+NTRK2	addiction	withdrawal	24076087	But the most important finding in our study is that augmenting BDNF actions through the use of tyrosine kinase B (<strong>TrkB</strong>, a BDNF receptor) agonist restored neurogenesis and abolished the alcohol induced anhedonia and despair behaviors seen during the <b>withdrawal</b>/abstinence period.
+NTRK2	drug	alcohol	24076087	But the most important finding in our study is that augmenting BDNF actions through the use of tyrosine kinase B (<strong><strong>TrkB</strong></strong>, a BDNF receptor) agonist restored neurogenesis and abolished the <b>alcohol</b> induced anhedonia and despair behaviors seen during the withdrawal/abstinence period.
+NTRK2	addiction	withdrawal	24076087	But the most important finding in our study is that augmenting BDNF actions through the use of tyrosine kinase B (<strong><strong>TrkB</strong></strong>, a BDNF receptor) agonist restored neurogenesis and abolished the alcohol induced anhedonia and despair behaviors seen during the <b>withdrawal</b>/abstinence period.
+NTRK2	drug	alcohol	24061482	Our primary interest is the examination of how regions that receive BF cholinergic projections are influenced by short term <b>ethanol</b> exposure through alterations in the mRNA levels of neurotrophic factors [nerve growth factor/TrkA, brain derived neurotrophic factor/<strong>TrkB</strong>, and glial derived neurotrophic factor (GDNF)/GDNF family receptor α1].
+NTRK2	drug	alcohol	24061482	Our primary interest is the examination of how regions that receive BF cholinergic projections are influenced by short term <b>ethanol</b> exposure through alterations in the mRNA levels of neurotrophic factors [nerve growth factor/TrkA, brain derived neurotrophic factor/<strong><strong>TrkB</strong></strong>, and glial derived neurotrophic factor (GDNF)/GDNF family receptor α1].
+NTRK2	drug	nicotine	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, CHRNB2, BDNF, and <strong>NTRK2</strong> associated with <b>nicotine</b> dependence in the Study of Addiction: Genetics and Environment sample, suggesting the biological role of these genes in <b>nicotine</b> dependence development.
+NTRK2	addiction	addiction	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, CHRNB2, BDNF, and <strong>NTRK2</strong> associated with nicotine dependence in the Study of <b>Addiction</b>: Genetics and Environment sample, suggesting the biological role of these genes in nicotine dependence development.
+NTRK2	addiction	dependence	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, CHRNB2, BDNF, and <strong>NTRK2</strong> associated with nicotine <b>dependence</b> in the Study of Addiction: Genetics and Environment sample, suggesting the biological role of these genes in nicotine <b>dependence</b> development.
+NTRK2	drug	opioid	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (<strong>TrkB</strong>), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ <b>opioid</b> receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of <b>morphine</b> exposure, withdrawal and post withdrawal stress.
+NTRK2	addiction	withdrawal	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (<strong>TrkB</strong>), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ opioid receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of morphine exposure, <b>withdrawal</b> and post <b>withdrawal</b> stress.
+NTRK2	drug	opioid	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (<strong><strong>TrkB</strong></strong>), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ <b>opioid</b> receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of <b>morphine</b> exposure, withdrawal and post withdrawal stress.
+NTRK2	addiction	withdrawal	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (<strong><strong>TrkB</strong></strong>), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ opioid receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (TPH2) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of morphine exposure, <b>withdrawal</b> and post <b>withdrawal</b> stress.
+NTRK2	drug	opioid	24055683	Expression levels of BDNF, <strong>TrkB</strong> and CRF R1 mRNA were decreased during both <b>morphine</b> exposure and following 7days of withdrawal.
+NTRK2	addiction	withdrawal	24055683	Expression levels of BDNF, <strong>TrkB</strong> and CRF R1 mRNA were decreased during both morphine exposure and following 7days of <b>withdrawal</b>.
+NTRK2	drug	opioid	24055683	Expression levels of BDNF, <strong><strong>TrkB</strong></strong> and CRF R1 mRNA were decreased during both <b>morphine</b> exposure and following 7days of withdrawal.
+NTRK2	addiction	withdrawal	24055683	Expression levels of BDNF, <strong><strong>TrkB</strong></strong> and CRF R1 mRNA were decreased during both morphine exposure and following 7days of <b>withdrawal</b>.
+NTRK2	drug	amphetamine	23934209	7,8 Dihydroxyflavone, a <strong>TrkB</strong> agonist, attenuates behavioral abnormalities and neurotoxicity in mice after administration of <b>methamphetamine</b>.
+NTRK2	drug	amphetamine	23934209	7,8 Dihydroxyflavone, a <strong><strong>TrkB</strong></strong> agonist, attenuates behavioral abnormalities and neurotoxicity in mice after administration of <b>methamphetamine</b>.
+NTRK2	drug	amphetamine	23934209	Several lines of evidence suggest a role for brain derived neurotrophic factor (BDNF) and its specific receptor, tropomyosin related kinase (<strong>TrkB</strong>), in <b>METH</b> induced behavioral abnormalities.
+NTRK2	drug	amphetamine	23934209	Several lines of evidence suggest a role for brain derived neurotrophic factor (BDNF) and its specific receptor, tropomyosin related kinase (<strong><strong>TrkB</strong></strong>), in <b>METH</b> induced behavioral abnormalities.
+NTRK2	drug	amphetamine	23934209	In this study, we examined whether 7,8 dihydroxyflavone (7,8 DHF), a novel potent <strong>TrkB</strong> agonist, could attenuate behavioral abnormalities and dopaminergic neurotoxicity in mice after administration of <b>METH</b>.
+NTRK2	drug	amphetamine	23934209	In this study, we examined whether 7,8 dihydroxyflavone (7,8 DHF), a novel potent <strong><strong>TrkB</strong></strong> agonist, could attenuate behavioral abnormalities and dopaminergic neurotoxicity in mice after administration of <b>METH</b>.
+NTRK2	drug	amphetamine	23934209	Pretreatment with 7,8 DHF (3.0, 10, or 30 mg/kg), but not the inactive <strong>TrkB</strong> compound, 5,7 dihydroxyflavone (5,7 DHF) (30 mg/kg), attenuated hyperlocomotion in mice after a single administration of <b>METH</b> (3.0 mg/kg), in a dose dependent manner.
+NTRK2	drug	amphetamine	23934209	Pretreatment with 7,8 DHF (3.0, 10, or 30 mg/kg), but not the inactive <strong><strong>TrkB</strong></strong> compound, 5,7 dihydroxyflavone (5,7 DHF) (30 mg/kg), attenuated hyperlocomotion in mice after a single administration of <b>METH</b> (3.0 mg/kg), in a dose dependent manner.
+NTRK2	drug	amphetamine	23934209	Treatment with ANA 12 (0.5 mg/kg), a potent <strong>TrkB</strong> antagonist, blocked the protective effects of 7,8 DHF on the <b>METH</b> induced reduction of DAT in the striatum.
+NTRK2	drug	amphetamine	23934209	Treatment with ANA 12 (0.5 mg/kg), a potent <strong><strong>TrkB</strong></strong> antagonist, blocked the protective effects of 7,8 DHF on the <b>METH</b> induced reduction of DAT in the striatum.
+NTRK2	drug	amphetamine	23934209	It is likely, therefore, that <strong>TrkB</strong> agonists such as 7,8 DHF may prove to be potential therapeutic drugs for several symptoms associated with <b>METH</b> abuse in humans.
+NTRK2	drug	amphetamine	23934209	It is likely, therefore, that <strong><strong>TrkB</strong></strong> agonists such as 7,8 DHF may prove to be potential therapeutic drugs for several symptoms associated with <b>METH</b> abuse in humans.
+NTRK2	drug	amphetamine	23726845	<b>METH</b> also caused changes in ΔFosB, BDNF and <strong>TrkB</strong> protein levels, with increases after 2 and 24h, but decreases after 1month of drug abstinence.
+NTRK2	drug	amphetamine	23726845	<b>METH</b> also caused changes in ΔFosB, BDNF and <strong><strong>TrkB</strong></strong> protein levels, with increases after 2 and 24h, but decreases after 1month of drug abstinence.
+NTRK2	drug	opioid	23651024	Out of the 110 variants analyzed, 12 SNPs (in BDNF, <strong>NTRK2</strong>, OPRM1, DRD2 and ANKK1) were associated with <b>methadone</b> dose (nominal p < 0.05).
+NTRK2	drug	opioid	23333681	The dynorphin (DYN), μ <b>opioid</b> receptor (mu <b>opioid</b>), neuropeptide Y (NPY), brain derived neurotrophic factor (BDNF), tropomyosin related tyrosine kinase B receptor (<strong>TrkB</strong>) and corticotropin releasing factor receptor type 1 (CRF R1) gene expression were measured by the reverse transcription polymerase chain reaction (RT PCR).
+NTRK2	drug	opioid	23333681	The dynorphin (DYN), μ <b>opioid</b> receptor (mu <b>opioid</b>), neuropeptide Y (NPY), brain derived neurotrophic factor (BDNF), tropomyosin related tyrosine kinase B receptor (<strong><strong>TrkB</strong></strong>) and corticotropin releasing factor receptor type 1 (CRF R1) gene expression were measured by the reverse transcription polymerase chain reaction (RT PCR).
+NTRK2	drug	cocaine	23325250	Attenuating BDNF <strong>TrkB</strong> signaling in shell did not affect <b>cocaine</b> seeking on WD1 or WD45 but significantly decreased <b>cocaine</b> seeking on WD90.
+NTRK2	addiction	relapse	23325250	Attenuating BDNF <strong>TrkB</strong> signaling in shell did not affect cocaine <b>seeking</b> on WD1 or WD45 but significantly decreased cocaine <b>seeking</b> on WD90.
+NTRK2	drug	cocaine	23325250	Attenuating BDNF <strong><strong>TrkB</strong></strong> signaling in shell did not affect <b>cocaine</b> seeking on WD1 or WD45 but significantly decreased <b>cocaine</b> seeking on WD90.
+NTRK2	addiction	relapse	23325250	Attenuating BDNF <strong><strong>TrkB</strong></strong> signaling in shell did not affect cocaine <b>seeking</b> on WD1 or WD45 but significantly decreased cocaine <b>seeking</b> on WD90.
+NTRK2	drug	alcohol	23291223	Susceptibility to <b>ethanol</b> sensitization is differentially associated with changes in pCREB, <strong>trkB</strong> and BDNF mRNA expression in the mouse brain.
+NTRK2	addiction	sensitization	23291223	Susceptibility to ethanol <b>sensitization</b> is differentially associated with changes in pCREB, <strong>trkB</strong> and BDNF mRNA expression in the mouse brain.
+NTRK2	drug	alcohol	23291223	Susceptibility to <b>ethanol</b> sensitization is differentially associated with changes in pCREB, <strong><strong>trkB</strong></strong> and BDNF mRNA expression in the mouse brain.
+NTRK2	addiction	sensitization	23291223	Susceptibility to ethanol <b>sensitization</b> is differentially associated with changes in pCREB, <strong><strong>trkB</strong></strong> and BDNF mRNA expression in the mouse brain.
+NTRK2	drug	alcohol	23291223	The goal of the present study was to examine whether variability in the sensitization response to <b>ethanol</b> (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely BDNF and its receptor <strong>trkB</strong>, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after withdrawal from chronic, intermittent EtOH exposure.
+NTRK2	addiction	sensitization	23291223	The goal of the present study was to examine whether variability in the <b>sensitization</b> response to ethanol (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely BDNF and its receptor <strong>trkB</strong>, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after withdrawal from chronic, intermittent EtOH exposure.
+NTRK2	addiction	withdrawal	23291223	The goal of the present study was to examine whether variability in the sensitization response to ethanol (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely BDNF and its receptor <strong>trkB</strong>, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after <b>withdrawal</b> from chronic, intermittent EtOH exposure.
+NTRK2	drug	alcohol	23291223	The goal of the present study was to examine whether variability in the sensitization response to <b>ethanol</b> (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely BDNF and its receptor <strong><strong>trkB</strong></strong>, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after withdrawal from chronic, intermittent EtOH exposure.
+NTRK2	addiction	sensitization	23291223	The goal of the present study was to examine whether variability in the <b>sensitization</b> response to ethanol (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely BDNF and its receptor <strong><strong>trkB</strong></strong>, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after withdrawal from chronic, intermittent EtOH exposure.
+NTRK2	addiction	withdrawal	23291223	The goal of the present study was to examine whether variability in the sensitization response to ethanol (EtOH) is differentially associated with regional brain changes in specific molecular markers associated with neuroplasticity, namely BDNF and its receptor <strong><strong>trkB</strong></strong>, and levels of phosphorylated cyclic AMP regulated element binding protein (pCREB), 14 days after <b>withdrawal</b> from chronic, intermittent EtOH exposure.
+NTRK2	addiction	sensitization	23291223	The observed decrease in BDNF and <strong>trkB</strong> mRNA in the Non sensitized group suggests the possibility that EtOH may have neurotoxic effects in a subpopulation of mice, which might in turn prevent the development of behavioural <b>sensitization</b>.
+NTRK2	addiction	sensitization	23291223	The observed decrease in BDNF and <strong><strong>trkB</strong></strong> mRNA in the Non sensitized group suggests the possibility that EtOH may have neurotoxic effects in a subpopulation of mice, which might in turn prevent the development of behavioural <b>sensitization</b>.
+NTRK2	addiction	sensitization	23291223	The lack of a difference in BDNF and <strong>trkB</strong> mRNA expression between Sensitized and SAL mice suggests that EtOH <b>sensitization</b> may be mediated by mechanisms different from those mediating <b>sensitization</b> to other psychostimulants.
+NTRK2	addiction	sensitization	23291223	The lack of a difference in BDNF and <strong><strong>trkB</strong></strong> mRNA expression between Sensitized and SAL mice suggests that EtOH <b>sensitization</b> may be mediated by mechanisms different from those mediating <b>sensitization</b> to other psychostimulants.
+NTRK2	drug	opioid	23277131	Two primary gene candidates were supported by the linkage association, gene expression profiling, and network analysis: neurotrophic tyrosine kinase receptor, type 2 (<strong>NTRK2</strong>), and the <b>opioid</b> receptor, κ1 (OPRK1).
+NTRK2	addiction	aversion	23250006	Prelimbic BDNF and <strong>TrkB</strong> signaling regulates consolidation of both appetitive and <b>aversive</b> emotional learning.
+NTRK2	addiction	aversion	23250006	Prelimbic BDNF and <strong><strong>TrkB</strong></strong> signaling regulates consolidation of both appetitive and <b>aversive</b> emotional learning.
+NTRK2	drug	cocaine	23250006	The site specific <strong>TrkB</strong> antagonism and viral mediated bdnf deletion within the PL resulted in deficits in both <b>cocaine</b> dependent associative learning and fear expression.
+NTRK2	drug	cocaine	23250006	The site specific <strong><strong>TrkB</strong></strong> antagonism and viral mediated bdnf deletion within the PL resulted in deficits in both <b>cocaine</b> dependent associative learning and fear expression.
+NTRK2	addiction	aversion	23250006	Deficiencies were rescued by the novel <strong>TrkB</strong> agonist 7,8 dihydroxyflavone, indicating that PL BDNF expression and downstream signaling through the <strong>TrkB</strong> receptor are required for memory formation in both appetitive and <b>aversive</b> domains.
+NTRK2	addiction	aversion	23250006	Deficiencies were rescued by the novel <strong><strong>TrkB</strong></strong> agonist 7,8 dihydroxyflavone, indicating that PL BDNF expression and downstream signaling through the <strong><strong>TrkB</strong></strong> receptor are required for memory formation in both appetitive and <b>aversive</b> domains.
+NTRK2	drug	cocaine	23242310	Administration of a BDNF receptor antagonist (the <strong>TrkB</strong> receptor antagonist ANA 12) reversed the diminished <b>cocaine</b> self administration in male <b>cocaine</b> sired rats.
+NTRK2	drug	cocaine	23242310	Administration of a BDNF receptor antagonist (the <strong><strong>TrkB</strong></strong> receptor antagonist ANA 12) reversed the diminished <b>cocaine</b> self administration in male <b>cocaine</b> sired rats.
+NTRK2	drug	cocaine	22832183	Intra ventricular infusion with K252a, a mixed TrkA and <strong>TrkB</strong> antagonist, did not affect the protective effects of companions on local NGF, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and <b>cocaine</b> induced CPP.
+NTRK2	addiction	reward	22832183	Intra ventricular infusion with K252a, a mixed TrkA and <strong>TrkB</strong> antagonist, did not affect the protective effects of companions on local NGF, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and cocaine induced <b>CPP</b>.
+NTRK2	drug	cocaine	22832183	Intra ventricular infusion with K252a, a mixed TrkA and <strong><strong>TrkB</strong></strong> antagonist, did not affect the protective effects of companions on local NGF, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and <b>cocaine</b> induced CPP.
+NTRK2	addiction	reward	22832183	Intra ventricular infusion with K252a, a mixed TrkA and <strong><strong>TrkB</strong></strong> antagonist, did not affect the protective effects of companions on local NGF, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and cocaine induced <b>CPP</b>.
+NTRK2	drug	opioid	22790874	Association of time dependent changes in mu <b>opioid</b> receptor mRNA, but not BDNF, <strong>TrkB</strong>, or MeCP2 mRNA and protein expression in the rat nucleus accumbens with incubation of <b>heroin</b> craving.
+NTRK2	addiction	relapse	22790874	Association of time dependent changes in mu opioid receptor mRNA, but not BDNF, <strong>TrkB</strong>, or MeCP2 mRNA and protein expression in the rat nucleus accumbens with incubation of heroin <b>craving</b>.
+NTRK2	drug	opioid	22790874	Association of time dependent changes in mu <b>opioid</b> receptor mRNA, but not BDNF, <strong><strong>TrkB</strong></strong>, or MeCP2 mRNA and protein expression in the rat nucleus accumbens with incubation of <b>heroin</b> craving.
+NTRK2	addiction	relapse	22790874	Association of time dependent changes in mu opioid receptor mRNA, but not BDNF, <strong><strong>TrkB</strong></strong>, or MeCP2 mRNA and protein expression in the rat nucleus accumbens with incubation of heroin <b>craving</b>.
+NTRK2	drug	opioid	22790874	We trained rats to self administer <b>heroin</b> or saline for 9 10 days and then dissected the NAc, DS, and mPFC at different abstinence days and measured mRNA and protein levels of BDNF, <strong>TrkB</strong>, and MeCP2, as well as MOR mRNA (Oprm1).
+NTRK2	drug	opioid	22790874	We trained rats to self administer <b>heroin</b> or saline for 9 10 days and then dissected the NAc, DS, and mPFC at different abstinence days and measured mRNA and protein levels of BDNF, <strong><strong>TrkB</strong></strong>, and MeCP2, as well as MOR mRNA (Oprm1).
+NTRK2	drug	opioid	21872672	This study demonstrates that voluntary exercise ameliorates, via a <strong>TrkB</strong> mediated mechanism, the cognitive deficits that are induced by chronic <b>morphine</b>.
+NTRK2	drug	opioid	21872672	This study demonstrates that voluntary exercise ameliorates, via a <strong><strong>TrkB</strong></strong> mediated mechanism, the cognitive deficits that are induced by chronic <b>morphine</b>.
+NTRK2	drug	cocaine	21867882	This resilience was mediated, in part, through repression of BDNF <strong>TrkB</strong> CREB signaling, which was induced after repeated <b>cocaine</b> or stress.
+NTRK2	drug	cocaine	21867882	This resilience was mediated, in part, through repression of BDNF <strong><strong>TrkB</strong></strong> CREB signaling, which was induced after repeated <b>cocaine</b> or stress.
+NTRK2	addiction	intoxication	21453757	This experiment examined the effects of a MA <b>binge</b> dosing regimen (10 mg/kg x 4 at 2 h intervals, s.c.) in Sprague Dawley rats on BDNF, tropomyosin receptor kinase B (<strong>TrkB</strong>), and tyrosine hydroxylase (TH) mRNA expression, and plasma corticosterone.
+NTRK2	addiction	intoxication	21453757	This experiment examined the effects of a MA <b>binge</b> dosing regimen (10 mg/kg x 4 at 2 h intervals, s.c.) in Sprague Dawley rats on BDNF, tropomyosin receptor kinase B (<strong><strong>TrkB</strong></strong>), and tyrosine hydroxylase (TH) mRNA expression, and plasma corticosterone.
+NTRK2	drug	opioid	21277174	Both sensitized locomotion in <b>morphine</b> paired rats and enhanced Drd3 mRNA were suppressed by intra NAc infusion of anti tyrosine kinase receptor B (<strong>TrkB</strong>) IgG.
+NTRK2	drug	opioid	21277174	Both sensitized locomotion in <b>morphine</b> paired rats and enhanced Drd3 mRNA were suppressed by intra NAc infusion of anti tyrosine kinase receptor B (<strong><strong>TrkB</strong></strong>) IgG.
+NTRK2	drug	opioid	21277174	Altogether, these results suggest that BDNF/<strong>TrkB</strong> signaling and activation of Drd3 in the NAc are required for the expression of <b>morphine</b> induced context specific locomotor sensitization.
+NTRK2	addiction	sensitization	21277174	Altogether, these results suggest that BDNF/<strong>TrkB</strong> signaling and activation of Drd3 in the NAc are required for the expression of morphine induced context specific locomotor <b>sensitization</b>.
+NTRK2	drug	opioid	21277174	Altogether, these results suggest that BDNF/<strong><strong>TrkB</strong></strong> signaling and activation of Drd3 in the NAc are required for the expression of <b>morphine</b> induced context specific locomotor sensitization.
+NTRK2	addiction	sensitization	21277174	Altogether, these results suggest that BDNF/<strong><strong>TrkB</strong></strong> signaling and activation of Drd3 in the NAc are required for the expression of morphine induced context specific locomotor <b>sensitization</b>.
+NTRK2	drug	cocaine	21248106	This study elucidates a mechanism whereby BDNF/<strong>TrkB</strong> (tropomyosin receptor kinase B) activates ERK regulated CREB phosphorylation in the dmPFC to counteract the neuroadaptations induced by <b>cocaine</b> SA and subsequent relapse to <b>cocaine</b> seeking.
+NTRK2	addiction	relapse	21248106	This study elucidates a mechanism whereby BDNF/<strong>TrkB</strong> (tropomyosin receptor kinase B) activates ERK regulated CREB phosphorylation in the dmPFC to counteract the neuroadaptations induced by cocaine SA and subsequent <b>relapse</b> to cocaine <b>seeking</b>.
+NTRK2	drug	cocaine	21248106	This study elucidates a mechanism whereby BDNF/<strong><strong>TrkB</strong></strong> (tropomyosin receptor kinase B) activates ERK regulated CREB phosphorylation in the dmPFC to counteract the neuroadaptations induced by <b>cocaine</b> SA and subsequent relapse to <b>cocaine</b> seeking.
+NTRK2	addiction	relapse	21248106	This study elucidates a mechanism whereby BDNF/<strong><strong>TrkB</strong></strong> (tropomyosin receptor kinase B) activates ERK regulated CREB phosphorylation in the dmPFC to counteract the neuroadaptations induced by cocaine SA and subsequent <b>relapse</b> to cocaine <b>seeking</b>.
+NTRK2	drug	cocaine	20947769	We show that deletion of <strong>TrkB</strong>, the brain derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppositely affects <b>cocaine</b> reward.
+NTRK2	addiction	reward	20947769	We show that deletion of <strong>TrkB</strong>, the brain derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppositely affects cocaine <b>reward</b>.
+NTRK2	drug	cocaine	20947769	We show that deletion of <strong><strong>TrkB</strong></strong>, the brain derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppositely affects <b>cocaine</b> reward.
+NTRK2	addiction	reward	20947769	We show that deletion of <strong><strong>TrkB</strong></strong>, the brain derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppositely affects cocaine <b>reward</b>.
+NTRK2	drug	cocaine	20947769	Because loss of <strong>TrkB</strong> in D2+ neurons increases their neuronal excitability, we next used optogenetic tools to control selectively the firing rate of D1+ and D2+ nucleus accumbens neurons and studied consequent effects on <b>cocaine</b> reward.
+NTRK2	addiction	reward	20947769	Because loss of <strong>TrkB</strong> in D2+ neurons increases their neuronal excitability, we next used optogenetic tools to control selectively the firing rate of D1+ and D2+ nucleus accumbens neurons and studied consequent effects on cocaine <b>reward</b>.
+NTRK2	drug	cocaine	20947769	Because loss of <strong><strong>TrkB</strong></strong> in D2+ neurons increases their neuronal excitability, we next used optogenetic tools to control selectively the firing rate of D1+ and D2+ nucleus accumbens neurons and studied consequent effects on <b>cocaine</b> reward.
+NTRK2	addiction	reward	20947769	Because loss of <strong><strong>TrkB</strong></strong> in D2+ neurons increases their neuronal excitability, we next used optogenetic tools to control selectively the firing rate of D1+ and D2+ nucleus accumbens neurons and studied consequent effects on cocaine <b>reward</b>.
+NTRK2	drug	cocaine	20947769	Activation of D2+ neurons, mimicking the loss of <strong>TrkB</strong>, suppresses <b>cocaine</b> reward, with opposite effects induced by activation of D1+ neurons.
+NTRK2	addiction	reward	20947769	Activation of D2+ neurons, mimicking the loss of <strong>TrkB</strong>, suppresses cocaine <b>reward</b>, with opposite effects induced by activation of D1+ neurons.
+NTRK2	drug	cocaine	20947769	Activation of D2+ neurons, mimicking the loss of <strong><strong>TrkB</strong></strong>, suppresses <b>cocaine</b> reward, with opposite effects induced by activation of D1+ neurons.
+NTRK2	addiction	reward	20947769	Activation of D2+ neurons, mimicking the loss of <strong><strong>TrkB</strong></strong>, suppresses cocaine <b>reward</b>, with opposite effects induced by activation of D1+ neurons.
+NTRK2	drug	cocaine	20826313	Downregulating <strong>TrkB</strong> expression bilaterally in the mPFC reduced the locomotor hypersensitivity to <b>cocaine</b> 8 days after <b>cocaine</b> withdrawal.
+NTRK2	addiction	withdrawal	20826313	Downregulating <strong>TrkB</strong> expression bilaterally in the mPFC reduced the locomotor hypersensitivity to cocaine 8 days after cocaine <b>withdrawal</b>.
+NTRK2	drug	cocaine	20826313	Downregulating <strong><strong>TrkB</strong></strong> expression bilaterally in the mPFC reduced the locomotor hypersensitivity to <b>cocaine</b> 8 days after <b>cocaine</b> withdrawal.
+NTRK2	addiction	withdrawal	20826313	Downregulating <strong><strong>TrkB</strong></strong> expression bilaterally in the mPFC reduced the locomotor hypersensitivity to cocaine 8 days after cocaine <b>withdrawal</b>.
+NTRK2	drug	cocaine	20176040	<strong>TrkB</strong> signaling is required for behavioral sensitization and conditioned place preference induced by a single injection of <b>cocaine</b>.
+NTRK2	addiction	sensitization	20176040	<strong>TrkB</strong> signaling is required for behavioral <b>sensitization</b> and conditioned place preference induced by a single injection of cocaine.
+NTRK2	drug	cocaine	20176040	<strong><strong>TrkB</strong></strong> signaling is required for behavioral sensitization and conditioned place preference induced by a single injection of <b>cocaine</b>.
+NTRK2	addiction	sensitization	20176040	<strong><strong>TrkB</strong></strong> signaling is required for behavioral <b>sensitization</b> and conditioned place preference induced by a single injection of cocaine.
+NTRK2	drug	cocaine	20176040	However, it is unclear whether BDNF signaling through the <strong>TrkB</strong> receptor can mediate these behavioral responses when animals are given a single <b>cocaine</b> exposure.
+NTRK2	drug	cocaine	20176040	However, it is unclear whether BDNF signaling through the <strong><strong>TrkB</strong></strong> receptor can mediate these behavioral responses when animals are given a single <b>cocaine</b> exposure.
+NTRK2	drug	cocaine	20176040	We found that a single exposure to <b>cocaine</b> was sufficient to increase p <strong>TrkB</strong> within the NAc 9 12h after administration.
+NTRK2	drug	cocaine	20176040	We found that a single exposure to <b>cocaine</b> was sufficient to increase p <strong><strong>TrkB</strong></strong> within the NAc 9 12h after administration.
+NTRK2	drug	cocaine	20176040	Expression of the dnTrkB transgene not only prevented the acute <b>cocaine</b> induced increase in p <strong>TrkB</strong>, but it also prevented behavioral sensitization and CPP following a single <b>cocaine</b> injection.
+NTRK2	addiction	reward	20176040	Expression of the dnTrkB transgene not only prevented the acute cocaine induced increase in p <strong>TrkB</strong>, but it also prevented behavioral sensitization and <b>CPP</b> following a single cocaine injection.
+NTRK2	addiction	sensitization	20176040	Expression of the dnTrkB transgene not only prevented the acute cocaine induced increase in p <strong>TrkB</strong>, but it also prevented behavioral <b>sensitization</b> and CPP following a single cocaine injection.
+NTRK2	drug	cocaine	20176040	Expression of the dnTrkB transgene not only prevented the acute <b>cocaine</b> induced increase in p <strong><strong>TrkB</strong></strong>, but it also prevented behavioral sensitization and CPP following a single <b>cocaine</b> injection.
+NTRK2	addiction	reward	20176040	Expression of the dnTrkB transgene not only prevented the acute cocaine induced increase in p <strong><strong>TrkB</strong></strong>, but it also prevented behavioral sensitization and <b>CPP</b> following a single cocaine injection.
+NTRK2	addiction	sensitization	20176040	Expression of the dnTrkB transgene not only prevented the acute cocaine induced increase in p <strong><strong>TrkB</strong></strong>, but it also prevented behavioral <b>sensitization</b> and CPP following a single cocaine injection.
+NTRK2	drug	cocaine	20176040	These findings demonstrate that <strong>TrkB</strong> activation is required both for behavioral sensitization and CPP to a single <b>cocaine</b> exposure.
+NTRK2	addiction	reward	20176040	These findings demonstrate that <strong>TrkB</strong> activation is required both for behavioral sensitization and <b>CPP</b> to a single cocaine exposure.
+NTRK2	addiction	sensitization	20176040	These findings demonstrate that <strong>TrkB</strong> activation is required both for behavioral <b>sensitization</b> and CPP to a single cocaine exposure.
+NTRK2	drug	cocaine	20176040	These findings demonstrate that <strong><strong>TrkB</strong></strong> activation is required both for behavioral sensitization and CPP to a single <b>cocaine</b> exposure.
+NTRK2	addiction	reward	20176040	These findings demonstrate that <strong><strong>TrkB</strong></strong> activation is required both for behavioral sensitization and <b>CPP</b> to a single cocaine exposure.
+NTRK2	addiction	sensitization	20176040	These findings demonstrate that <strong><strong>TrkB</strong></strong> activation is required both for behavioral <b>sensitization</b> and CPP to a single cocaine exposure.
+NTRK2	drug	cocaine	20176040	The fact that enhanced <strong>TrkB</strong> activation is induced within 9h of a single injection of <b>cocaine</b> suggests that inhibition of <strong>TrkB</strong> signaling commencing hours after <b>cocaine</b> exposure may prevent at least the initial antecedents to the sensitizing and reinforcing effects of this psychostimulant.
+NTRK2	addiction	reward	20176040	The fact that enhanced <strong>TrkB</strong> activation is induced within 9h of a single injection of cocaine suggests that inhibition of <strong>TrkB</strong> signaling commencing hours after cocaine exposure may prevent at least the initial antecedents to the sensitizing and <b>reinforcing</b> effects of this psychostimulant.
+NTRK2	drug	cocaine	20176040	The fact that enhanced <strong><strong>TrkB</strong></strong> activation is induced within 9h of a single injection of <b>cocaine</b> suggests that inhibition of <strong><strong>TrkB</strong></strong> signaling commencing hours after <b>cocaine</b> exposure may prevent at least the initial antecedents to the sensitizing and reinforcing effects of this psychostimulant.
+NTRK2	addiction	reward	20176040	The fact that enhanced <strong><strong>TrkB</strong></strong> activation is induced within 9h of a single injection of cocaine suggests that inhibition of <strong><strong>TrkB</strong></strong> signaling commencing hours after cocaine exposure may prevent at least the initial antecedents to the sensitizing and <b>reinforcing</b> effects of this psychostimulant.
+NTRK2	drug	cocaine	19843976	Intracerebroventricular injection of the neurotrophin <strong>TrkB</strong> receptor inhibitor, K252a, blocked <b>cocaine</b> induced USV behavior but not locomotor activity.
+NTRK2	drug	cocaine	19843976	Intracerebroventricular injection of the neurotrophin <strong><strong>TrkB</strong></strong> receptor inhibitor, K252a, blocked <b>cocaine</b> induced USV behavior but not locomotor activity.
+NTRK2	drug	cocaine	18990365	To further investigate BDNF signaling in the mesolimbic dopamine system, we analyzed tropomyosin related kinase B (<strong>TrkB</strong>) messenger RNA (mRNA) and protein changes in the NAc and ventral tegmental area (VTA) in rats following 3 weeks of <b>cocaine</b> self administration.
+NTRK2	drug	cocaine	18990365	To further investigate BDNF signaling in the mesolimbic dopamine system, we analyzed tropomyosin related kinase B (<strong><strong>TrkB</strong></strong>) messenger RNA (mRNA) and protein changes in the NAc and ventral tegmental area (VTA) in rats following 3 weeks of <b>cocaine</b> self administration.
+NTRK2	drug	cocaine	18990365	To study the role of BDNF <strong>TrkB</strong> activity in the VTA and NAc in <b>cocaine</b> reward, we used localized viral mediated Cre recombinase expression in floxed BDNF and floxed <strong>TrkB</strong> mice to knockdown BDNF or <strong>TrkB</strong> in the VTA and NAc in <b>cocaine</b> place conditioning tests and <strong>TrkB</strong> in the NAc in <b>cocaine</b> self administration tests.
+NTRK2	addiction	reward	18990365	To study the role of BDNF <strong>TrkB</strong> activity in the VTA and NAc in cocaine <b>reward</b>, we used localized viral mediated Cre recombinase expression in floxed BDNF and floxed <strong>TrkB</strong> mice to knockdown BDNF or <strong>TrkB</strong> in the VTA and NAc in cocaine place conditioning tests and <strong>TrkB</strong> in the NAc in cocaine self administration tests.
+NTRK2	drug	cocaine	18990365	To study the role of BDNF <strong><strong>TrkB</strong></strong> activity in the VTA and NAc in <b>cocaine</b> reward, we used localized viral mediated Cre recombinase expression in floxed BDNF and floxed <strong><strong>TrkB</strong></strong> mice to knockdown BDNF or <strong><strong>TrkB</strong></strong> in the VTA and NAc in <b>cocaine</b> place conditioning tests and <strong><strong>TrkB</strong></strong> in the NAc in <b>cocaine</b> self administration tests.
+NTRK2	addiction	reward	18990365	To study the role of BDNF <strong><strong>TrkB</strong></strong> activity in the VTA and NAc in cocaine <b>reward</b>, we used localized viral mediated Cre recombinase expression in floxed BDNF and floxed <strong><strong>TrkB</strong></strong> mice to knockdown BDNF or <strong><strong>TrkB</strong></strong> in the VTA and NAc in cocaine place conditioning tests and <strong><strong>TrkB</strong></strong> in the NAc in cocaine self administration tests.
+NTRK2	drug	cocaine	18990365	We found that 3 weeks of active <b>cocaine</b> self administration significantly increased <strong>TrkB</strong> protein levels in the NAc shell, while yoked (passive) <b>cocaine</b> exposure produced a similar increase in the VTA.
+NTRK2	drug	cocaine	18990365	We found that 3 weeks of active <b>cocaine</b> self administration significantly increased <strong><strong>TrkB</strong></strong> protein levels in the NAc shell, while yoked (passive) <b>cocaine</b> exposure produced a similar increase in the VTA.
+NTRK2	drug	cocaine	18990365	Localized BDNF knockdown in either region reduced <b>cocaine</b> reward in place conditioning, whereas only <strong>TrkB</strong> knockdown in the NAc reduced <b>cocaine</b> reward.
+NTRK2	addiction	reward	18990365	Localized BDNF knockdown in either region reduced cocaine <b>reward</b> in place conditioning, whereas only <strong>TrkB</strong> knockdown in the NAc reduced cocaine <b>reward</b>.
+NTRK2	drug	cocaine	18990365	Localized BDNF knockdown in either region reduced <b>cocaine</b> reward in place conditioning, whereas only <strong><strong>TrkB</strong></strong> knockdown in the NAc reduced <b>cocaine</b> reward.
+NTRK2	addiction	reward	18990365	Localized BDNF knockdown in either region reduced cocaine <b>reward</b> in place conditioning, whereas only <strong><strong>TrkB</strong></strong> knockdown in the NAc reduced cocaine <b>reward</b>.
+NTRK2	drug	cocaine	18990365	In mice self administering <b>cocaine</b>, <strong>TrkB</strong> knockdown in the NAc produced a downward shift in the <b>cocaine</b> self administration dose response curve but had no effect on the acquisition of <b>cocaine</b> or sucrose self administration.
+NTRK2	drug	cocaine	18990365	In mice self administering <b>cocaine</b>, <strong><strong>TrkB</strong></strong> knockdown in the NAc produced a downward shift in the <b>cocaine</b> self administration dose response curve but had no effect on the acquisition of <b>cocaine</b> or sucrose self administration.
+NTRK2	drug	cocaine	18990365	Together, these data suggest that BDNF synthesized in either VTA or NAc neurons is important for maintaining sensitivity to <b>cocaine</b> reward but only BDNF activation of <strong>TrkB</strong> receptors in the NAc mediates this effect.
+NTRK2	addiction	reward	18990365	Together, these data suggest that BDNF synthesized in either VTA or NAc neurons is important for maintaining sensitivity to cocaine <b>reward</b> but only BDNF activation of <strong>TrkB</strong> receptors in the NAc mediates this effect.
+NTRK2	drug	cocaine	18990365	Together, these data suggest that BDNF synthesized in either VTA or NAc neurons is important for maintaining sensitivity to <b>cocaine</b> reward but only BDNF activation of <strong><strong>TrkB</strong></strong> receptors in the NAc mediates this effect.
+NTRK2	addiction	reward	18990365	Together, these data suggest that BDNF synthesized in either VTA or NAc neurons is important for maintaining sensitivity to cocaine <b>reward</b> but only BDNF activation of <strong><strong>TrkB</strong></strong> receptors in the NAc mediates this effect.
+NTRK2	drug	cocaine	18990365	In addition, up regulation of NAc <strong>TrkB</strong> with chronic <b>cocaine</b> use could promote the transition to more addicted biological states.
+NTRK2	drug	cocaine	18990365	In addition, up regulation of NAc <strong><strong>TrkB</strong></strong> with chronic <b>cocaine</b> use could promote the transition to more addicted biological states.
+NTRK2	drug	cocaine	18551281	Role of accumbens BDNF and <strong>TrkB</strong> in <b>cocaine</b> induced psychomotor sensitization, conditioned place preference, and reinstatement in rats.
+NTRK2	addiction	relapse	18551281	Role of accumbens BDNF and <strong>TrkB</strong> in cocaine induced psychomotor sensitization, conditioned place preference, and <b>reinstatement</b> in rats.
+NTRK2	addiction	sensitization	18551281	Role of accumbens BDNF and <strong>TrkB</strong> in cocaine induced psychomotor <b>sensitization</b>, conditioned place preference, and reinstatement in rats.
+NTRK2	drug	cocaine	18551281	Role of accumbens BDNF and <strong><strong>TrkB</strong></strong> in <b>cocaine</b> induced psychomotor sensitization, conditioned place preference, and reinstatement in rats.
+NTRK2	addiction	relapse	18551281	Role of accumbens BDNF and <strong><strong>TrkB</strong></strong> in cocaine induced psychomotor sensitization, conditioned place preference, and <b>reinstatement</b> in rats.
+NTRK2	addiction	sensitization	18551281	Role of accumbens BDNF and <strong><strong>TrkB</strong></strong> in cocaine induced psychomotor <b>sensitization</b>, conditioned place preference, and reinstatement in rats.
+NTRK2	drug	cocaine	18551281	The goal of this study is to explore the role of BDNF and <strong>TrkB</strong> in the rat nucleus accumbens (NAc) in <b>cocaine</b> induced psychomotor sensitization and in conditioned place preference acquisition, expression, and reinstatement.
+NTRK2	addiction	relapse	18551281	The goal of this study is to explore the role of BDNF and <strong>TrkB</strong> in the rat nucleus accumbens (NAc) in cocaine induced psychomotor sensitization and in conditioned place preference acquisition, expression, and <b>reinstatement</b>.
+NTRK2	addiction	sensitization	18551281	The goal of this study is to explore the role of BDNF and <strong>TrkB</strong> in the rat nucleus accumbens (NAc) in cocaine induced psychomotor <b>sensitization</b> and in conditioned place preference acquisition, expression, and reinstatement.
+NTRK2	drug	cocaine	18551281	The goal of this study is to explore the role of BDNF and <strong><strong>TrkB</strong></strong> in the rat nucleus accumbens (NAc) in <b>cocaine</b> induced psychomotor sensitization and in conditioned place preference acquisition, expression, and reinstatement.
+NTRK2	addiction	relapse	18551281	The goal of this study is to explore the role of BDNF and <strong><strong>TrkB</strong></strong> in the rat nucleus accumbens (NAc) in cocaine induced psychomotor sensitization and in conditioned place preference acquisition, expression, and <b>reinstatement</b>.
+NTRK2	addiction	sensitization	18551281	The goal of this study is to explore the role of BDNF and <strong><strong>TrkB</strong></strong> in the rat nucleus accumbens (NAc) in cocaine induced psychomotor <b>sensitization</b> and in conditioned place preference acquisition, expression, and reinstatement.
+NTRK2	addiction	sensitization	18551281	BDNF and/or its receptor <strong>TrkB</strong> in the NAc enhance drug induced locomotor activity and induce <b>sensitization</b> in rats.
+NTRK2	addiction	sensitization	18551281	BDNF and/or its receptor <strong><strong>TrkB</strong></strong> in the NAc enhance drug induced locomotor activity and induce <b>sensitization</b> in rats.
+NTRK2	drug	cocaine	18551281	Furthermore, LV BDNF  and LV <strong>TrkB</strong> treated rats display enhanced <b>cocaine</b> induced CPP, delayed CPP extinction upon repeated measurements, and increased CPP reinstatement.
+NTRK2	addiction	relapse	18551281	Furthermore, LV BDNF  and LV <strong>TrkB</strong> treated rats display enhanced cocaine induced CPP, delayed CPP extinction upon repeated measurements, and increased CPP <b>reinstatement</b>.
+NTRK2	addiction	reward	18551281	Furthermore, LV BDNF  and LV <strong>TrkB</strong> treated rats display enhanced cocaine induced <b>CPP</b>, delayed <b>CPP</b> extinction upon repeated measurements, and increased <b>CPP</b> reinstatement.
+NTRK2	drug	cocaine	18551281	Furthermore, LV BDNF  and LV <strong><strong>TrkB</strong></strong> treated rats display enhanced <b>cocaine</b> induced CPP, delayed CPP extinction upon repeated measurements, and increased CPP reinstatement.
+NTRK2	addiction	relapse	18551281	Furthermore, LV BDNF  and LV <strong><strong>TrkB</strong></strong> treated rats display enhanced cocaine induced CPP, delayed CPP extinction upon repeated measurements, and increased CPP <b>reinstatement</b>.
+NTRK2	addiction	reward	18551281	Furthermore, LV BDNF  and LV <strong><strong>TrkB</strong></strong> treated rats display enhanced cocaine induced <b>CPP</b>, delayed <b>CPP</b> extinction upon repeated measurements, and increased <b>CPP</b> reinstatement.
+NTRK2	addiction	reward	18551281	We show that BDNF and <strong>TrkB</strong> induced <b>CPP</b> takes place during the learning period (conditioning), whereas extinction leads to the loss of <b>CPP</b>.
+NTRK2	addiction	reward	18551281	We show that BDNF and <strong><strong>TrkB</strong></strong> induced <b>CPP</b> takes place during the learning period (conditioning), whereas extinction leads to the loss of <b>CPP</b>.
+NTRK2	drug	cocaine	18551281	Extinction is delayed when rats are injected LV BDNF or LV <strong>TrkB</strong>, and in turn, priming injections of 2 mg/kg of <b>cocaine</b> reinstates it.
+NTRK2	drug	cocaine	18551281	Extinction is delayed when rats are injected LV BDNF or LV <strong><strong>TrkB</strong></strong>, and in turn, priming injections of 2 mg/kg of <b>cocaine</b> reinstates it.
+NTRK2	drug	cocaine	18551281	These results demonstrate the crucial function of BDNF through its receptor <strong>TrkB</strong> in the enhancement of locomotor activity, sensitization, conditioned place preference, CPP reinstatement, and rewarding effects of <b>cocaine</b> in the mesolimbic dopaminergic pathway.
+NTRK2	addiction	relapse	18551281	These results demonstrate the crucial function of BDNF through its receptor <strong>TrkB</strong> in the enhancement of locomotor activity, sensitization, conditioned place preference, CPP <b>reinstatement</b>, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+NTRK2	addiction	reward	18551281	These results demonstrate the crucial function of BDNF through its receptor <strong>TrkB</strong> in the enhancement of locomotor activity, sensitization, conditioned place preference, <b>CPP</b> reinstatement, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+NTRK2	addiction	sensitization	18551281	These results demonstrate the crucial function of BDNF through its receptor <strong>TrkB</strong> in the enhancement of locomotor activity, <b>sensitization</b>, conditioned place preference, CPP reinstatement, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+NTRK2	drug	cocaine	18551281	These results demonstrate the crucial function of BDNF through its receptor <strong><strong>TrkB</strong></strong> in the enhancement of locomotor activity, sensitization, conditioned place preference, CPP reinstatement, and rewarding effects of <b>cocaine</b> in the mesolimbic dopaminergic pathway.
+NTRK2	addiction	relapse	18551281	These results demonstrate the crucial function of BDNF through its receptor <strong><strong>TrkB</strong></strong> in the enhancement of locomotor activity, sensitization, conditioned place preference, CPP <b>reinstatement</b>, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+NTRK2	addiction	reward	18551281	These results demonstrate the crucial function of BDNF through its receptor <strong><strong>TrkB</strong></strong> in the enhancement of locomotor activity, sensitization, conditioned place preference, <b>CPP</b> reinstatement, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+NTRK2	addiction	sensitization	18551281	These results demonstrate the crucial function of BDNF through its receptor <strong><strong>TrkB</strong></strong> in the enhancement of locomotor activity, <b>sensitization</b>, conditioned place preference, CPP reinstatement, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.
+NTRK2	drug	nicotine	18534558	Gene gene interactions among CHRNA4, CHRNB2, BDNF, and <strong>NTRK2</strong> in <b>nicotine</b> dependence.
+NTRK2	addiction	dependence	18534558	Gene gene interactions among CHRNA4, CHRNB2, BDNF, and <strong>NTRK2</strong> in nicotine <b>dependence</b>.
+NTRK2	drug	nicotine	18534558	To determine if gene gene interactions exist among the four genes, we genotyped six single nucleotide polymorphisms (SNPs) for CHRNA4 and BDNF, nine SNPs for <strong>NTRK2</strong>, and four SNPs for CHRNB2 in a case control sample containing 275 unrelated <b>smokers</b> with a Fagerström Test for <b>Nicotine</b> Dependence score of 4.0 or more and 348 unrelated nonsmokers.
+NTRK2	addiction	dependence	18534558	To determine if gene gene interactions exist among the four genes, we genotyped six single nucleotide polymorphisms (SNPs) for CHRNA4 and BDNF, nine SNPs for <strong>NTRK2</strong>, and four SNPs for CHRNB2 in a case control sample containing 275 unrelated smokers with a Fagerström Test for Nicotine <b>Dependence</b> score of 4.0 or more and 348 unrelated nonsmokers.
+NTRK2	drug	alcohol	18394710	Polymorphisms in the genes coding for BDNF and its receptor <strong>TrkB</strong> are linked to affective, substance abuse and appetitive disorders and therefore may play a role in the development of <b>alcoholism</b>.
+NTRK2	drug	alcohol	18394710	Polymorphisms in the genes coding for BDNF and its receptor <strong><strong>TrkB</strong></strong> are linked to affective, substance abuse and appetitive disorders and therefore may play a role in the development of <b>alcoholism</b>.
+NTRK2	drug	alcohol	18394710	This review summarizes historical and pre clinical data on BDNF and <strong>TrkB</strong> as it relates to <b>ethanol</b> toxicity and addiction.
+NTRK2	addiction	addiction	18394710	This review summarizes historical and pre clinical data on BDNF and <strong>TrkB</strong> as it relates to ethanol toxicity and <b>addiction</b>.
+NTRK2	drug	alcohol	18394710	This review summarizes historical and pre clinical data on BDNF and <strong><strong>TrkB</strong></strong> as it relates to <b>ethanol</b> toxicity and addiction.
+NTRK2	addiction	addiction	18394710	This review summarizes historical and pre clinical data on BDNF and <strong><strong>TrkB</strong></strong> as it relates to ethanol toxicity and <b>addiction</b>.
+NTRK2	drug	alcohol	18322102	Here, we report that the anxiolytic effects of acute <b>ethanol</b> were associated with increased brain derived neurotrophic factor (BDNF) and tyrosine kinase B (<strong>trkB</strong>) expression, increased phosphorylation of extracellular signal regulated kinases 1/2 (Erk1/2), Elk 1, and cAMP responsive element binding protein (CREB), increased Arc expression, and increased dendritic spine density (DSD) in both the central amygdala (CeA) and medial amygdala (MeA) but not in the basolateral amygdala (BLA) of rats.
+NTRK2	drug	alcohol	18322102	Here, we report that the anxiolytic effects of acute <b>ethanol</b> were associated with increased brain derived neurotrophic factor (BDNF) and tyrosine kinase B (<strong><strong>trkB</strong></strong>) expression, increased phosphorylation of extracellular signal regulated kinases 1/2 (Erk1/2), Elk 1, and cAMP responsive element binding protein (CREB), increased Arc expression, and increased dendritic spine density (DSD) in both the central amygdala (CeA) and medial amygdala (MeA) but not in the basolateral amygdala (BLA) of rats.
+NTRK2	drug	alcohol	18322102	Conversely, the anxiogenic effects of withdrawal after long term <b>ethanol</b> exposure were associated with decreased BDNF and <strong>trkB</strong> expression, decreased phosphorylation of Erk1/2, Elk 1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+NTRK2	addiction	withdrawal	18322102	Conversely, the anxiogenic effects of <b>withdrawal</b> after long term ethanol exposure were associated with decreased BDNF and <strong>trkB</strong> expression, decreased phosphorylation of Erk1/2, Elk 1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+NTRK2	drug	alcohol	18322102	Conversely, the anxiogenic effects of withdrawal after long term <b>ethanol</b> exposure were associated with decreased BDNF and <strong><strong>trkB</strong></strong> expression, decreased phosphorylation of Erk1/2, Elk 1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+NTRK2	addiction	withdrawal	18322102	Conversely, the anxiogenic effects of <b>withdrawal</b> after long term ethanol exposure were associated with decreased BDNF and <strong><strong>trkB</strong></strong> expression, decreased phosphorylation of Erk1/2, Elk 1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats.
+NTRK2	drug	cocaine	18234897	Because components of the neurotrophin system including brain derived neurotrophic factor and <strong>TrkB</strong> are developmentally regulated, their role in the age specific effects of <b>cocaine</b> was determined using the Trk receptor antagonist K252a.
+NTRK2	drug	cocaine	18234897	Because components of the neurotrophin system including brain derived neurotrophic factor and <strong><strong>TrkB</strong></strong> are developmentally regulated, their role in the age specific effects of <b>cocaine</b> was determined using the Trk receptor antagonist K252a.
+NTRK2	drug	alcohol	18077569	Also, recent human genetic studies have supported a role of BDNF signaling in addictive behaviors by allele , genotype , and haplotype based association of the <strong>TrkB</strong> gene, which encodes the cognate receptor for BDNF, with <b>alcohol</b> dependence.
+NTRK2	addiction	addiction	18077569	Also, recent human genetic studies have supported a role of BDNF signaling in <b>addictive</b> behaviors by allele , genotype , and haplotype based association of the <strong>TrkB</strong> gene, which encodes the cognate receptor for BDNF, with alcohol dependence.
+NTRK2	addiction	dependence	18077569	Also, recent human genetic studies have supported a role of BDNF signaling in addictive behaviors by allele , genotype , and haplotype based association of the <strong>TrkB</strong> gene, which encodes the cognate receptor for BDNF, with alcohol <b>dependence</b>.
+NTRK2	drug	alcohol	18077569	Also, recent human genetic studies have supported a role of BDNF signaling in addictive behaviors by allele , genotype , and haplotype based association of the <strong><strong>TrkB</strong></strong> gene, which encodes the cognate receptor for BDNF, with <b>alcohol</b> dependence.
+NTRK2	addiction	addiction	18077569	Also, recent human genetic studies have supported a role of BDNF signaling in <b>addictive</b> behaviors by allele , genotype , and haplotype based association of the <strong><strong>TrkB</strong></strong> gene, which encodes the cognate receptor for BDNF, with alcohol dependence.
+NTRK2	addiction	dependence	18077569	Also, recent human genetic studies have supported a role of BDNF signaling in addictive behaviors by allele , genotype , and haplotype based association of the <strong><strong>TrkB</strong></strong> gene, which encodes the cognate receptor for BDNF, with alcohol <b>dependence</b>.
+NTRK2	drug	cocaine	17618281	We found that 4 h of intravenous <b>cocaine</b> self administration in rats induced a transient increase in brain derived neurotrophic factor (BDNF) and activation of <strong>TrkB</strong> mediated signaling in the nucleus accumbens (NAc).
+NTRK2	drug	cocaine	17618281	We found that 4 h of intravenous <b>cocaine</b> self administration in rats induced a transient increase in brain derived neurotrophic factor (BDNF) and activation of <strong><strong>TrkB</strong></strong> mediated signaling in the nucleus accumbens (NAc).
+NTRK2	drug	nicotine	17503330	We applied our proposed method to a genetics study of four genes that were reported to be associated with <b>nicotine</b> dependence and found significant joint action between CHRNB4 and <strong>NTRK2</strong>.
+NTRK2	addiction	dependence	17503330	We applied our proposed method to a genetics study of four genes that were reported to be associated with nicotine <b>dependence</b> and found significant joint action between CHRNB4 and <strong>NTRK2</strong>.
+NTRK2	drug	alcohol	17200667	To identify sequence variants in genes that may have roles in neuronal responses to <b>alcohol</b>, we resequenced the 5' region of tyrosine kinase B neurotrophin receptor gene (<strong>NTRK2</strong>) and determined linkage disequilibrium (LD) values, haplotype structure, and performed association analyses using 43 single nucleotide polymorphisms (SNPs) covering the entire <strong>NTRK2</strong> region in a Finnish Caucasian sample of 229 <b>alcohol</b> dependent subjects with antisocial personality disorder (ASPD) and 287 healthy controls.
+NTRK2	drug	alcohol	17200667	Individually, three SNPs were associated with <b>alcohol</b> dependence and <b>alcohol</b> abuse (AD) (P value from 0.0019 to 0.0059, significance level was set at P<or=0.01 corrected for multiple testing), whereas a common 18 locus haplotype within the largest LD block of <strong>NTRK2</strong>, a 119 kb region containing the 5' flanking region and exons 1 15, was marginally overrepresented in control subjects compared to AD individuals (global P=0.057).
+NTRK2	addiction	dependence	17200667	Individually, three SNPs were associated with alcohol <b>dependence</b> and alcohol abuse (AD) (P value from 0.0019 to 0.0059, significance level was set at P<or=0.01 corrected for multiple testing), whereas a common 18 locus haplotype within the largest LD block of <strong>NTRK2</strong>, a 119 kb region containing the 5' flanking region and exons 1 15, was marginally overrepresented in control subjects compared to AD individuals (global P=0.057).
+NTRK2	addiction	addiction	17200667	Taken together, these results support a role for the <strong>NTRK2</strong> gene in <b>addiction</b> in a Caucasian population with AD and a subtype of ASPD.
+NTRK2	drug	amphetamine	17065446	We found a significant elevation of <strong>TrkB</strong> like immunoreactivity specifically in CA3/dentate gyrus (DG) subregions of the hippocampus after <b>AMPH</b> (0.3 mg/kg) induced CPP, but not in the delayed paired (control) <b>AMPH</b> condition.
+NTRK2	addiction	reward	17065446	We found a significant elevation of <strong>TrkB</strong> like immunoreactivity specifically in CA3/dentate gyrus (DG) subregions of the hippocampus after AMPH (0.3 mg/kg) induced <b>CPP</b>, but not in the delayed paired (control) AMPH condition.
+NTRK2	drug	amphetamine	17065446	We found a significant elevation of <strong><strong>TrkB</strong></strong> like immunoreactivity specifically in CA3/dentate gyrus (DG) subregions of the hippocampus after <b>AMPH</b> (0.3 mg/kg) induced CPP, but not in the delayed paired (control) <b>AMPH</b> condition.
+NTRK2	addiction	reward	17065446	We found a significant elevation of <strong><strong>TrkB</strong></strong> like immunoreactivity specifically in CA3/dentate gyrus (DG) subregions of the hippocampus after AMPH (0.3 mg/kg) induced <b>CPP</b>, but not in the delayed paired (control) AMPH condition.
+NTRK2	drug	amphetamine	17065446	A higher <b>AMPH</b> dose (1.0 mg/kg) induced both CPP and CMS and elevated <strong>TrkB</strong> in the CA3/DG as well as in the nucleus accumbens shell.
+NTRK2	addiction	reward	17065446	A higher AMPH dose (1.0 mg/kg) induced both <b>CPP</b> and CMS and elevated <strong>TrkB</strong> in the CA3/DG as well as in the nucleus accumbens shell.
+NTRK2	drug	amphetamine	17065446	A higher <b>AMPH</b> dose (1.0 mg/kg) induced both CPP and CMS and elevated <strong><strong>TrkB</strong></strong> in the CA3/DG as well as in the nucleus accumbens shell.
+NTRK2	addiction	reward	17065446	A higher AMPH dose (1.0 mg/kg) induced both <b>CPP</b> and CMS and elevated <strong><strong>TrkB</strong></strong> in the CA3/DG as well as in the nucleus accumbens shell.
+NTRK2	drug	amphetamine	17065446	These findings reveal that CPP and CMS are induced by different doses of <b>AMPH</b> and are associated with <strong>TrkB</strong> changes in particular brain regions.
+NTRK2	addiction	reward	17065446	These findings reveal that <b>CPP</b> and CMS are induced by different doses of AMPH and are associated with <strong>TrkB</strong> changes in particular brain regions.
+NTRK2	drug	amphetamine	17065446	These findings reveal that CPP and CMS are induced by different doses of <b>AMPH</b> and are associated with <strong><strong>TrkB</strong></strong> changes in particular brain regions.
+NTRK2	addiction	reward	17065446	These findings reveal that <b>CPP</b> and CMS are induced by different doses of AMPH and are associated with <strong><strong>TrkB</strong></strong> changes in particular brain regions.
+NTRK2	drug	nicotine	16794563	Regulation by <b>nicotine</b> of Gpr51 and <strong>Ntrk2</strong> expression in various rat brain regions.
+NTRK2	drug	nicotine	16794563	Our previous genetic studies demonstrated that variants of the gamma Aminobutyric acid B receptor subunit 2 (GPR51) and neurotrophic tyrosine kinase receptor type 2 (<strong>NTRK2</strong>) genes are significantly associated with <b>nicotine</b> dependence (ND) in <b>smokers</b>.
+NTRK2	addiction	dependence	16794563	Our previous genetic studies demonstrated that variants of the gamma Aminobutyric acid B receptor subunit 2 (GPR51) and neurotrophic tyrosine kinase receptor type 2 (<strong>NTRK2</strong>) genes are significantly associated with nicotine <b>dependence</b> (ND) in smokers.
+NTRK2	drug	nicotine	16794563	In this study, we investigated the regulatory effect of <b>nicotine</b> on the expression of Gpr51 and <strong>Ntrk2</strong> in seven rat brain regions during the administration of <b>nicotine</b> in a daily dose of 3.15 mg/kg for 7 days.
+NTRK2	drug	nicotine	16794563	Similarly, the mRNA level of <strong>Ntrk2</strong> was enhanced by <b>nicotine</b> in the striatum (86%) and PFC (38%), but decreased in the NA ( 46%) and ventral tegmental area (VTA;  49%).
+NTRK2	drug	nicotine	16794563	In summary, our results demonstrate that the expression of Gpr51 and <strong>Ntrk2</strong> is significantly regulated by <b>nicotine</b> at both the mRNA and protein levels in various brain regions, which provides further evidence that these two genes are involved in the etiology of ND, as reported in our previous genetic association studies in humans.
+NTRK2	drug	nicotine	16713586	Association of specific haplotypes of neurotrophic tyrosine kinase receptor 2 gene (<strong>NTRK2</strong>) with vulnerability to <b>nicotine</b> dependence in African Americans and European Americans.
+NTRK2	addiction	dependence	16713586	Association of specific haplotypes of neurotrophic tyrosine kinase receptor 2 gene (<strong>NTRK2</strong>) with vulnerability to nicotine <b>dependence</b> in African Americans and European Americans.
+NTRK2	drug	nicotine	16713586	The gene encoding neurotrophic tyrosine kinase receptor 2 (<strong>NTRK2</strong>) has been localized to a region on chromosome 9q22 q23 that showed a "suggestive" linkage to <b>nicotine</b> dependence (ND) in our previous linkage analyses.
+NTRK2	addiction	dependence	16713586	The gene encoding neurotrophic tyrosine kinase receptor 2 (<strong>NTRK2</strong>) has been localized to a region on chromosome 9q22 q23 that showed a "suggestive" linkage to nicotine <b>dependence</b> (ND) in our previous linkage analyses.
+NTRK2	drug	cocaine	16633344	We found that after withdrawal from repeated <b>cocaine</b> exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous brain derived neurotrophic factor tyrosine kinase B (BDNF <strong>TrkB</strong>) signaling.
+NTRK2	addiction	withdrawal	16633344	We found that after <b>withdrawal</b> from repeated cocaine exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous brain derived neurotrophic factor tyrosine kinase B (BDNF <strong>TrkB</strong>) signaling.
+NTRK2	drug	cocaine	16633344	We found that after withdrawal from repeated <b>cocaine</b> exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous brain derived neurotrophic factor tyrosine kinase B (BDNF <strong><strong>TrkB</strong></strong>) signaling.
+NTRK2	addiction	withdrawal	16633344	We found that after <b>withdrawal</b> from repeated cocaine exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous brain derived neurotrophic factor tyrosine kinase B (BDNF <strong><strong>TrkB</strong></strong>) signaling.
+NTRK2	drug	cocaine	16423334	Alterations in BDNF and <strong>trkB</strong> mRNAs following acute or sensitizing <b>cocaine</b> treatments and withdrawal.
+NTRK2	addiction	withdrawal	16423334	Alterations in BDNF and <strong>trkB</strong> mRNAs following acute or sensitizing cocaine treatments and <b>withdrawal</b>.
+NTRK2	drug	cocaine	16423334	Alterations in BDNF and <strong><strong>trkB</strong></strong> mRNAs following acute or sensitizing <b>cocaine</b> treatments and withdrawal.
+NTRK2	addiction	withdrawal	16423334	Alterations in BDNF and <strong><strong>trkB</strong></strong> mRNAs following acute or sensitizing cocaine treatments and <b>withdrawal</b>.
+NTRK2	drug	cocaine	16423334	In the present study, we used in situ hybridization to examine the influence of acute or repeated <b>cocaine</b> administrations and withdrawal from repeated <b>cocaine</b> treatment on the level of brain derived neurotrophic factor (BDNF) and its receptor <strong>trkB</strong> mRNAs in rat brain.
+NTRK2	addiction	withdrawal	16423334	In the present study, we used in situ hybridization to examine the influence of acute or repeated cocaine administrations and <b>withdrawal</b> from repeated cocaine treatment on the level of brain derived neurotrophic factor (BDNF) and its receptor <strong>trkB</strong> mRNAs in rat brain.
+NTRK2	drug	cocaine	16423334	In the present study, we used in situ hybridization to examine the influence of acute or repeated <b>cocaine</b> administrations and withdrawal from repeated <b>cocaine</b> treatment on the level of brain derived neurotrophic factor (BDNF) and its receptor <strong><strong>trkB</strong></strong> mRNAs in rat brain.
+NTRK2	addiction	withdrawal	16423334	In the present study, we used in situ hybridization to examine the influence of acute or repeated cocaine administrations and <b>withdrawal</b> from repeated cocaine treatment on the level of brain derived neurotrophic factor (BDNF) and its receptor <strong><strong>trkB</strong></strong> mRNAs in rat brain.
+NTRK2	drug	cocaine	16423334	<b>Cocaine</b> treatments induced a brain region specific decrease in the levels of <strong>trkB</strong> mRNA.
+NTRK2	drug	cocaine	16423334	<b>Cocaine</b> treatments induced a brain region specific decrease in the levels of <strong><strong>trkB</strong></strong> mRNA.
+NTRK2	drug	alcohol	15246696	Alterations of cerebellar mRNA specific for BDNF, p75NTR, and <strong>TrkB</strong> receptor isoforms occur within hours of <b>ethanol</b> administration to 4 day old rat pups.
+NTRK2	drug	alcohol	15246696	Alterations of cerebellar mRNA specific for BDNF, p75NTR, and <strong><strong>TrkB</strong></strong> receptor isoforms occur within hours of <b>ethanol</b> administration to 4 day old rat pups.
+NTRK2	drug	alcohol	15246696	<b>Ethanol</b> exposure during this vulnerable window induces rapid apoptotic Purkinje cell death that is hypothesized to result from <b>ethanol</b> inhibition in brain derived nerve growth factor (BDNF) <strong>TrkB</strong> neurotrophic signaling that results in loss of apoptotic suppression.
+NTRK2	drug	alcohol	15246696	<b>Ethanol</b> exposure during this vulnerable window induces rapid apoptotic Purkinje cell death that is hypothesized to result from <b>ethanol</b> inhibition in brain derived nerve growth factor (BDNF) <strong><strong>TrkB</strong></strong> neurotrophic signaling that results in loss of apoptotic suppression.
+NTRK2	drug	alcohol	15246696	In this study, the effect that different concentrations of <b>ethanol</b> (1.5, 3.0, 4.5 and 6.0 g/kg) have on steady state mRNA expression of BDNF and different <strong>TrkB</strong> receptor isoforms in the cerebellum on PN4 was determined at 1, 4, 6, and 8 h after treatment.
+NTRK2	drug	alcohol	15246696	In this study, the effect that different concentrations of <b>ethanol</b> (1.5, 3.0, 4.5 and 6.0 g/kg) have on steady state mRNA expression of BDNF and different <strong><strong>TrkB</strong></strong> receptor isoforms in the cerebellum on PN4 was determined at 1, 4, 6, and 8 h after treatment.
+NTRK2	drug	alcohol	15246696	Significant decreases in mRNA specific for BDNF and <strong>TrkB</strong> isoforms were detected within 1 h after <b>ethanol</b> administration.
+NTRK2	drug	alcohol	15246696	Significant decreases in mRNA specific for BDNF and <strong><strong>TrkB</strong></strong> isoforms were detected within 1 h after <b>ethanol</b> administration.
+NTRK2	drug	alcohol	15246696	These results support the hypothesis that <b>ethanol</b> induces a disruption of BDNF <strong>TrkB</strong> signaling that results in loss of apoptotic suppression in vulnerable Purkinje cells by growth factor withdrawal.
+NTRK2	addiction	withdrawal	15246696	These results support the hypothesis that ethanol induces a disruption of BDNF <strong>TrkB</strong> signaling that results in loss of apoptotic suppression in vulnerable Purkinje cells by growth factor <b>withdrawal</b>.
+NTRK2	drug	alcohol	15246696	These results support the hypothesis that <b>ethanol</b> induces a disruption of BDNF <strong><strong>TrkB</strong></strong> signaling that results in loss of apoptotic suppression in vulnerable Purkinje cells by growth factor withdrawal.
+NTRK2	addiction	withdrawal	15246696	These results support the hypothesis that ethanol induces a disruption of BDNF <strong><strong>TrkB</strong></strong> signaling that results in loss of apoptotic suppression in vulnerable Purkinje cells by growth factor <b>withdrawal</b>.
+NTRK2	drug	cocaine	12358776	However, there was an increase in <strong>TrkB</strong> protein in the nucleus accumbens core of <b>cocaine</b> treated rats without a corresponding alteration in mRNA.
+NTRK2	drug	cocaine	12358776	However, there was an increase in <strong><strong>TrkB</strong></strong> protein in the nucleus accumbens core of <b>cocaine</b> treated rats without a corresponding alteration in mRNA.
+NTRK2	drug	alcohol	11743997	To test the hypothesis that <b>ethanol</b> alters neurotrophin signaling leading to Purkinje neuronal death, the immunohistochemical expression of <strong>TrkB</strong> and TrkC receptors on Purkinje cells of rat pups following a moderate dose of <b>ethanol</b> was determined at various times surrounding the period of postnatal <b>ethanol</b> vulnerability.
+NTRK2	drug	alcohol	11743997	To test the hypothesis that <b>ethanol</b> alters neurotrophin signaling leading to Purkinje neuronal death, the immunohistochemical expression of <strong><strong>TrkB</strong></strong> and TrkC receptors on Purkinje cells of rat pups following a moderate dose of <b>ethanol</b> was determined at various times surrounding the period of postnatal <b>ethanol</b> vulnerability.
+NTRK2	drug	alcohol	11743997	<b>Ethanol</b> selectively decreased Purkinje cell expression of <strong>TrkB</strong> and TrkC receptors following exposures within the vulnerable period (PN4 6).
+NTRK2	drug	alcohol	11743997	<b>Ethanol</b> selectively decreased Purkinje cell expression of <strong><strong>TrkB</strong></strong> and TrkC receptors following exposures within the vulnerable period (PN4 6).
+NTRK2	drug	alcohol	11532337	Early postnatal <b>ethanol</b> exposure selectively decreases BDNF and truncated <strong>TrkB</strong> T2 receptor mRNA expression in the rat cerebellum.
+NTRK2	drug	alcohol	11532337	Early postnatal <b>ethanol</b> exposure selectively decreases BDNF and truncated <strong><strong>TrkB</strong></strong> T2 receptor mRNA expression in the rat cerebellum.
+NTRK2	drug	alcohol	11532337	We hypothesize that disruption of <strong>TrkB</strong> and/or TrkC mediated neurotrophin communication is, in part, responsible for the <b>ethanol</b> induced loss of Purkinje cells during development.
+NTRK2	drug	alcohol	11532337	We hypothesize that disruption of <strong><strong>TrkB</strong></strong> and/or TrkC mediated neurotrophin communication is, in part, responsible for the <b>ethanol</b> induced loss of Purkinje cells during development.
+NTRK2	drug	alcohol	11532337	The current study was undertaken to define the impact of <b>ethanol</b> exposure at the onset of <b>ethanol</b> vulnerability on the relative concentrations of mRNA encoding the neurotrophic factor receptors <strong>TrkB</strong> and TrkC.
+NTRK2	drug	alcohol	11532337	The current study was undertaken to define the impact of <b>ethanol</b> exposure at the onset of <b>ethanol</b> vulnerability on the relative concentrations of mRNA encoding the neurotrophic factor receptors <strong><strong>TrkB</strong></strong> and TrkC.
+NTRK2	addiction	addiction	9852605	The neurotrophins brain derived neurotrophic factor (BDNF) and neurotrophin 3 (NT 3) and their receptors <strong>trkB</strong> and trkC, respectively, are expressed in the locus coeruleus (LC) and ventral tegmental area (VTA), brain regions known to be involved in opiate <b>addiction</b>.
+NTRK2	addiction	addiction	9852605	The neurotrophins brain derived neurotrophic factor (BDNF) and neurotrophin 3 (NT 3) and their receptors <strong><strong>trkB</strong></strong> and trkC, respectively, are expressed in the locus coeruleus (LC) and ventral tegmental area (VTA), brain regions known to be involved in opiate <b>addiction</b>.
+NTRK2	drug	opioid	9852605	In this study, BDNF, NT 3, <strong>trkB</strong>, and trkC mRNAs were analyzed in these regions after chronic <b>morphine</b> treatment and during antagonist precipitated withdrawal.
+NTRK2	addiction	withdrawal	9852605	In this study, BDNF, NT 3, <strong>trkB</strong>, and trkC mRNAs were analyzed in these regions after chronic morphine treatment and during antagonist precipitated <b>withdrawal</b>.
+NTRK2	drug	opioid	9852605	In this study, BDNF, NT 3, <strong><strong>trkB</strong></strong>, and trkC mRNAs were analyzed in these regions after chronic <b>morphine</b> treatment and during antagonist precipitated withdrawal.
+NTRK2	addiction	withdrawal	9852605	In this study, BDNF, NT 3, <strong><strong>trkB</strong></strong>, and trkC mRNAs were analyzed in these regions after chronic morphine treatment and during antagonist precipitated <b>withdrawal</b>.
+NTRK2	drug	opioid	9852605	Levels of <strong>trkB</strong> and trkC mRNAs, which were unchanged by chronic <b>morphine</b> treatment, were elevated in LC at 2 and 6 hr of withdrawal.
+NTRK2	addiction	withdrawal	9852605	Levels of <strong>trkB</strong> and trkC mRNAs, which were unchanged by chronic morphine treatment, were elevated in LC at 2 and 6 hr of <b>withdrawal</b>.
+NTRK2	drug	opioid	9852605	Levels of <strong><strong>trkB</strong></strong> and trkC mRNAs, which were unchanged by chronic <b>morphine</b> treatment, were elevated in LC at 2 and 6 hr of withdrawal.
+NTRK2	addiction	withdrawal	9852605	Levels of <strong><strong>trkB</strong></strong> and trkC mRNAs, which were unchanged by chronic morphine treatment, were elevated in LC at 2 and 6 hr of <b>withdrawal</b>.
+NTRK2	addiction	withdrawal	9852605	In contrast to the substantial alterations observed in LC, there was no regulation of the neurotrophins or trk mRNAs within the VTA during chronic opiate treatment or <b>withdrawal</b>, with the exception of an increase in <strong>trkB</strong> mRNA at 6 hr of <b>withdrawal</b>.
+NTRK2	addiction	withdrawal	9852605	In contrast to the substantial alterations observed in LC, there was no regulation of the neurotrophins or trk mRNAs within the VTA during chronic opiate treatment or <b>withdrawal</b>, with the exception of an increase in <strong><strong>trkB</strong></strong> mRNA at 6 hr of <b>withdrawal</b>.
+EGR1	drug	opioid	32388931	We also demonstrated that cells expressing mu <b>opioid</b> receptors (MOR, gene name Oprm1) in the MPOA displayed increased <strong>Egr1</strong> expression when adolescent rats were engaged in social play using double immunofluorescence labeling of MOR and <strong>Egr1</strong>.
+EGR1	drug	amphetamine	31669508	Finally, dopamine denervated rats displayed a less marked increase in <strong>Zif 268</strong> positive neurons in the NAc shell after <b>amphetamine</b> challenge, compared with sham operated rats.
+EGR1	drug	cocaine	31653935	Consistent with this in vivo observation, we found that lack of Rhes in mice caused a greater increase in striatal <b>cocaine</b> dependent D1R/cAMP/PKA signaling, along with considerable enhancement of Arc, <strong>zif268</strong>, and Homer1 mRNA expression.
+EGR1	drug	amphetamine	31605697	Association of medial corticostriatal regions with <b>amphetamine</b> induced emission of 50 kHz vocalizations as studied by <strong>Zif 268</strong> expression in the rat brain.
+EGR1	addiction	sensitization	31605697	The present study sought to address this by performing a minimal <b>sensitization</b> protocol, utilizing only two injections, to investigate expression of the inducible transcription factor <strong>Zif 268</strong> (Zif) among brain regions thought to be associated with 50 kHz USV emission.
+EGR1	drug	cocaine	31043484	Further motif recognition analysis of the ChIP seq data showed that <b>cocaine</b> associated differential H3.3 accumulation correlated with the presence of several transcription factor binding motifs, including RBPJ1, <strong>EGR1</strong>, and SOX4, suggesting that these are potentially important regulators of molecular cascades associated with <b>cocaine</b> induced neuronal plasticity.
+EGR1	addiction	aversion	30550948	qPCR was employed to detect the expression of brain derived neurotrophic factor (Bdnf) and the immediate early genes (IEG) <strong>early growth response 1</strong> (Egr 1) and activity regulated cytoskeletal associated protein (Arc) mRNAs in the VTA and mPFC at different time points of the conditioned place <b>aversion</b> (CPA) paradigm: after the conditioning phase and after the test phase.
+EGR1	drug	alcohol	30483137	MTEP reduced <strong>Egr1</strong> expression within the AcbSh, irrespective of <b>alcohol</b> drinking history or age of drinking onset.
+EGR1	drug	opioid	29964093	<strong>EGR1</strong> and EGR2 were suppressed in mesolimbic regions with <b>heroin</b> taking and environmental enrichment.
+EGR1	drug	opioid	29964093	Site specific methylation analysis of <strong>EGR1</strong> and EGR2 promoter regions using bisulfite amplicon sequencing (BSAS) revealed hypo methylation in the EGR2 promoter region and <strong>EGR1</strong> intragenic CpG sites with <b>heroin</b> taking and environmental enrichment that was associated with decreased mRNA expression.
+EGR1	drug	alcohol	29306704	At transcriptional level, <b>ethanol</b> reduced the upregulation of a subset of IEGs encoding for transcription factors such as Atf3, c Fos, FosB, <strong>Egr1</strong>, Egr3 and Npas4 but did not affect the upregulation of others (e.g.
+EGR1	drug	alcohol	29306704	Notably, the majority of genes were sensitive to <b>ethanol</b> only when administered before TBI and not afterwards (the exceptions being c Fos, <strong>Egr1</strong> and Dusp5).
+EGR1	addiction	reward	29093669	Gene expression analysis after <b>CPP</b> test revealed specific up regulation in the CAF COC group of Drd1a, cFos, and FosB in the NAc, and cFos, <strong>Egr1</strong>, and Npas4 in the mPFC.
+EGR1	addiction	aversion	27728875	Interestingly, we observed that GCs were only increased in sham dependent rodents during <b>aversive</b> withdrawal memory consolidation, and that GR expression correlated with phosphorylated cAMP response element binding (pCREB) protein, <strong>early growth response 1</strong> (Egr 1) and activity regulated cytoskeletal associated (Arc) mRNA induction in this experimental group.
+EGR1	addiction	withdrawal	27728875	Interestingly, we observed that GCs were only increased in sham dependent rodents during aversive <b>withdrawal</b> memory consolidation, and that GR expression correlated with phosphorylated cAMP response element binding (pCREB) protein, <strong>early growth response 1</strong> (Egr 1) and activity regulated cytoskeletal associated (Arc) mRNA induction in this experimental group.
+EGR1	drug	psychedelics	27343386	In a second part, we found an effective disruption of contextual fear reconsolidation by the N methyl d aspartate receptor antagonist <b>ketamine</b>, associated with a down regulation of early growth response 1 (<strong>Egr1</strong>) in the hippocampal CA1 area, and up regulation of brain derived neurotrophic factor (Bdnf) mRNA levels in the prelimbic and infralimbic cortices.
+EGR1	drug	psychedelics	27343386	In a second part, we found an effective disruption of contextual fear reconsolidation by the N methyl d aspartate receptor antagonist <b>ketamine</b>, associated with a down regulation of <strong>early growth response 1</strong> (<strong>Egr1</strong>) in the hippocampal CA1 area, and up regulation of brain derived neurotrophic factor (Bdnf) mRNA levels in the prelimbic and infralimbic cortices.
+EGR1	drug	cocaine	27265728	Three weeks after repeated tDCS, we investigated the induction of a gene expression marker (<strong>Zif268</strong>) by <b>cocaine</b> (25 mg/kg) in 26 cortical and 23 striatal regions using in situ hybridization histochemistry.
+EGR1	drug	cocaine	27265728	tDCS pretreatment increased basal expression and attenuated <b>cocaine</b> (25 mg/kg) induced expression of <strong>Zif268</strong> in specific corticostriatal circuits.
+EGR1	drug	cocaine	26674058	We aimed to clarify the regulatory role of the NAc in the <b>cocaine</b> memory reconsolidation process, by examining the effect of applying different pharmacological interventions to the NAc on <strong>Zif 268</strong> and Fos B expression in the entire reward circuit after <b>cocaine</b> memory reactivation.
+EGR1	addiction	reward	26674058	We aimed to clarify the regulatory role of the NAc in the cocaine memory reconsolidation process, by examining the effect of applying different pharmacological interventions to the NAc on <strong>Zif 268</strong> and Fos B expression in the entire <b>reward</b> circuit after cocaine memory reactivation.
+EGR1	drug	cocaine	26674058	Through the <b>cocaine</b> induced conditioned place preference (CPP) model, immunohistochemical and immunofluorescence staining for <strong>Zif 268</strong> and Fos B were used to explore the functional activated brain nuclei after <b>cocaine</b> memory reactivation.
+EGR1	addiction	reward	26674058	Through the cocaine induced conditioned place preference (<b>CPP</b>) model, immunohistochemical and immunofluorescence staining for <strong>Zif 268</strong> and Fos B were used to explore the functional activated brain nuclei after cocaine memory reactivation.
+EGR1	addiction	addiction	26674058	Further, bilateral NAc shell infusion of MK 801 and SCH 23390, but not raclopride or propranolol, prior to <b>addictive</b> memory reconsolidation, decreased <strong>Zif 268</strong> and Fos B expression in the entire reward circuit, except for the amygdala, and effectively disturbed subsequent CPP related behavior.
+EGR1	addiction	reward	26674058	Further, bilateral NAc shell infusion of MK 801 and SCH 23390, but not raclopride or propranolol, prior to addictive memory reconsolidation, decreased <strong>Zif 268</strong> and Fos B expression in the entire <b>reward</b> circuit, except for the amygdala, and effectively disturbed subsequent <b>CPP</b> related behavior.
+EGR1	drug	cocaine	26674058	In summary, N methyl d aspartate (NMDA) and dopamine D1 receptors, but not dopamine D2 or β adrenergic receptors, within the NAc shell, may regulate <strong>Zif 268</strong> and Fos B expression in most brain nuclei of the reward circuit after <b>cocaine</b> memory reactivation.
+EGR1	addiction	reward	26674058	In summary, N methyl d aspartate (NMDA) and dopamine D1 receptors, but not dopamine D2 or β adrenergic receptors, within the NAc shell, may regulate <strong>Zif 268</strong> and Fos B expression in most brain nuclei of the <b>reward</b> circuit after cocaine memory reactivation.
+EGR1	drug	cocaine	26221832	As the therapeutically most promising finding, only four 15 min episodes of dyadic social interaction were able to inhibit both the subsequent reacquisition/re expression of preference for <b>cocaine</b> and the neural activation associated with this behavior, that is, an increase in the expression of the immediate early gene Early Growth Response protein 1 (<strong>EGR1</strong>, Zif268) in the nucleus accumbens, basolateral and central amygdala, and the ventral tegmental area.
+EGR1	drug	cocaine	26221832	As the therapeutically most promising finding, only four 15 min episodes of dyadic social interaction were able to inhibit both the subsequent reacquisition/re expression of preference for <b>cocaine</b> and the neural activation associated with this behavior, that is, an increase in the expression of the immediate early gene Early Growth Response protein 1 (<strong>EGR1</strong>, <strong>Zif268</strong>) in the nucleus accumbens, basolateral and central amygdala, and the ventral tegmental area.
+EGR1	drug	cocaine	26221832	The time spent in the <b>cocaine</b> associated conditioning compartment was correlated with the density of <strong>EGR1</strong> activated neurons not only in the medial core (AcbCm) and medial shell (AcbShm) of the nucleus accumbens, but was observed in all regions medial to the anterior commissure ('accumbens corridor'), including (from medial to lateral), the vertical limb of the diagonal band and the medial septum (VDB+MS), the major island of Calleja and the intermediate nucleus of the lateral septum (ICjM+LSI), the AcbShm, and the AcbCm.
+EGR1	addiction	intoxication	26048424	The hyper emotionality exhibited by <b>binge</b> drinking mice was apparent at both withdrawal time points and correlated with higher <strong>Egr1</strong>+ cell counts in the CEA and BNST, compared to controls.
+EGR1	addiction	withdrawal	26048424	The hyper emotionality exhibited by binge drinking mice was apparent at both <b>withdrawal</b> time points and correlated with higher <strong>Egr1</strong>+ cell counts in the CEA and BNST, compared to controls.
+EGR1	drug	amphetamine	25991653	These effects were associated with lower levels of <strong>Zif 268</strong> after <b>amphetamine</b> challenge and spontaneous alternation deficits.
+EGR1	drug	alcohol	25727639	Using markers of neuronal activation c Fos, <strong>EGR1</strong>, and phophorylated extracellar signal regulated kinase (pERK1/2), adult responses to a moderate and binge drinking <b>ethanol</b> challenge, e.g., 2 or 4 g/kg, were determined.
+EGR1	addiction	intoxication	25727639	Using markers of neuronal activation c Fos, <strong>EGR1</strong>, and phophorylated extracellar signal regulated kinase (pERK1/2), adult responses to a moderate and <b>binge</b> drinking ethanol challenge, e.g., 2 or 4 g/kg, were determined.
+EGR1	drug	cocaine	25592253	Both <b>cocaine</b> and social interaction place preference conditioning lead to increased neuronal expression of the immediate early gene <strong>EGR1</strong> in the nucleus accumbens, a central region of the reward pathway, suggesting that both drug and natural rewards may be processed in similar brain regions.
+EGR1	addiction	reward	25592253	Both cocaine and social interaction place preference conditioning lead to increased neuronal expression of the immediate early gene <strong>EGR1</strong> in the nucleus accumbens, a central region of the <b>reward</b> pathway, suggesting that both drug and natural rewards may be processed in similar brain regions.
+EGR1	drug	cocaine	25566008	The increased <b>cocaine</b> CPP was associated with an increased expression of the immediate early genes (IEGs) c Fos and Early Growth Related Protein 1 (<strong>EGR1</strong>) in the accumbens corridor, i.e., a region stretching from the anterior commissure to the interhemispheric border and comprising the medial nucleus accumbens core and shell, the major island of Calleja and intermediate part of the lateral septum, as well as the vertical limb of the diagonal band and medial septum.
+EGR1	addiction	reward	25566008	The increased cocaine <b>CPP</b> was associated with an increased expression of the immediate early genes (IEGs) c Fos and Early Growth Related Protein 1 (<strong>EGR1</strong>) in the accumbens corridor, i.e., a region stretching from the anterior commissure to the interhemispheric border and comprising the medial nucleus accumbens core and shell, the major island of Calleja and intermediate part of the lateral septum, as well as the vertical limb of the diagonal band and medial septum.
+EGR1	drug	cocaine	25566008	The <b>cocaine</b> CPP induced <strong>EGR1</strong> expression was only observed in D1  and D2 medium spiny neurons, whereas other types of neurons or glial cells were not involved.
+EGR1	addiction	reward	25566008	The cocaine <b>CPP</b> induced <strong>EGR1</strong> expression was only observed in D1  and D2 medium spiny neurons, whereas other types of neurons or glial cells were not involved.
+EGR1	drug	cocaine	25566008	With respect to the activation by contingent vs. non contingent <b>cocaine</b> <strong>EGR1</strong> seemed to be a more sensitive marker than c Fos.
+EGR1	drug	cocaine	25530939	Thus, we measured the effects of a 6 day repeated treatment with methylphenidate (5 mg/kg), fluoxetine (5 mg/kg) or their combination on the inducibility (by <b>cocaine</b>) of neuroplasticity related IEGs (<strong>Zif268</strong>, Homer1a) in the striatum, by in situ hybridization histochemistry.
+EGR1	drug	cocaine	25332000	This study was designed to reveal neuronal c Fos, <strong>Zif268</strong> expression pattern in 10 brain regions following <b>cocaine</b> context associated reward memory retrieval in mice, combining animal behavioral study and immunofluorescence method.
+EGR1	addiction	reward	25332000	This study was designed to reveal neuronal c Fos, <strong>Zif268</strong> expression pattern in 10 brain regions following cocaine context associated <b>reward</b> memory retrieval in mice, combining animal behavioral study and immunofluorescence method.
+EGR1	drug	cocaine	25332000	The results showed that: Neuronal c Fos, <strong>Zif268</strong> protein expression levels in nucleus accumbens (NAc) core both were elevated in <b>Cocaine</b> retrieval group compared with those in Saline retrieval (Control) group during <b>cocaine</b> context associated reward memory retrieval.
+EGR1	addiction	reward	25332000	The results showed that: Neuronal c Fos, <strong>Zif268</strong> protein expression levels in nucleus accumbens (NAc) core both were elevated in Cocaine retrieval group compared with those in Saline retrieval (Control) group during cocaine context associated <b>reward</b> memory retrieval.
+EGR1	drug	cocaine	25332000	<strong>Zif268</strong> protein expression level in basolateral amygdala (BLA) was also elevated in <b>Cocaine</b> retrieval group compared with that in control mice.
+EGR1	drug	cocaine	25309368	Contrary to our expectations, we found that all regions of the accumbens corridor showed increased expression of the early growth response protein 1 (<strong>EGR1</strong>, Zif268) in rats 2 h after reacquisition of CPP for <b>cocaine</b> after a history of <b>cocaine</b> CPP acquisition and extinction.
+EGR1	addiction	reward	25309368	Contrary to our expectations, we found that all regions of the accumbens corridor showed increased expression of the early growth response protein 1 (<strong>EGR1</strong>, Zif268) in rats 2 h after reacquisition of <b>CPP</b> for cocaine after a history of cocaine <b>CPP</b> acquisition and extinction.
+EGR1	drug	cocaine	25309368	Contrary to our expectations, we found that all regions of the accumbens corridor showed increased expression of the early growth response protein 1 (<strong>EGR1</strong>, <strong>Zif268</strong>) in rats 2 h after reacquisition of CPP for <b>cocaine</b> after a history of <b>cocaine</b> CPP acquisition and extinction.
+EGR1	addiction	reward	25309368	Contrary to our expectations, we found that all regions of the accumbens corridor showed increased expression of the early growth response protein 1 (<strong>EGR1</strong>, <strong>Zif268</strong>) in rats 2 h after reacquisition of <b>CPP</b> for cocaine after a history of cocaine <b>CPP</b> acquisition and extinction.
+EGR1	addiction	reward	25309368	Cholinergic interneurons or GABAergic interneurons positive for parvalbumin, neuropeptide Y or calretinin were not involved in these <b>CPP</b> related <strong>EGR1</strong> changes.
+EGR1	drug	opioid	25290009	To better dissect the time course of <b>opioid</b> produced IEG induction, we used in situ hybridization to examine the expression of the IEGs c fos, <strong>zif268</strong> and arc in the mouse forebrain at several time points after acute <b>morphine</b> injection.
+EGR1	drug	cocaine	24452697	MPH + FLX, or <b>cocaine</b> exposure in juvenile mice increased mRNA expression of ERK2 and its downstream targets (CREB, cFos, and <strong>Zif268</strong>), and increased protein phosphorylation of ERK2 and CREB 2 months after drug exposure.
+EGR1	addiction	relapse	24069163	After extinction training and <b>reinstatement</b> testing, where both cues were presented in separate sessions, rats were sacrificed and processed for cellular analysis of temporal activity by fluorescent in situ hybridization (CatFISH) for activity regulated cytoskeleton associated protein (Arc) mRNA and for radioactive in situ hybridization for Arc and <strong>zif268</strong> mRNAs.
+EGR1	addiction	relapse	24069163	We have shown that while rats reinstate drug <b>seeking</b> in response to temporally discrete presentations of distinct drug associated cues, such <b>reinstatement</b> is not associated with increased transcriptional activation of Arc or <strong>zif268</strong> mRNAs, suggesting that expression of these genes may not be necessary for cue induced <b>reinstatement</b> of drug <b>seeking</b> behavior.
+EGR1	drug	cannabinoid	23873727	This study investigated brain and spinal cord expression of genes implicated in pain  and fear related plasticity (<strong>Zif268</strong> and Sgk1), following expression of formalin evoked nociception, contextual fear or <b>endocannabinoid</b> mediated FCA.
+EGR1	drug	cannabinoid	23873727	The present findings suggest that <strong>Zif268</strong> in the DHSC is an important molecular correlate of <b>endocannabinoid</b> mediated FCA, and that fear related expression of <strong>Zif268</strong> in the RVM is influenced by the presence of nociceptive tone.
+EGR1	drug	cocaine	23763573	We measured, by in situ hybridization histochemistry, the effects of a 5 day repeated treatment with methylphenidate (5 mg/kg), fluoxetine (5 mg/kg) or a combination on the inducibility (by <b>cocaine</b>) of neuroplasticity related genes (<strong>Zif268</strong>, Homer1a) in the striatum.
+EGR1	drug	cocaine	23632436	<b>Cocaine</b> modulation of frontostriatal expression of <strong>Zif268</strong>, D2, and 5 HT2c receptors in high and low impulsive rats.
+EGR1	drug	cocaine	23632436	We used in situ hybridization to map brain expression of two major genes implicated in impulsivity, encoding the dopamine D2 receptor (DA D2R) and the 5 HT2c receptor (5 HT2cR), and an immediate early gene associated with neuronal plasticity, <strong>zif268</strong>, in groups of rats selected for HI and low impulsivity (LI) on a 5 choice serial reaction time task (5 CSRTT) immediately after 5 CSRTT training, and following 10 or 50 days of <b>cocaine</b> self administration.
+EGR1	drug	cocaine	23632436	<b>Cocaine</b> exposure decreased striatal D2R mRNA in both HI and LI rats, decreased 5 HT2cR mRNA differentially in striatal and prefrontal areas between HI and LI rats, and selectively decreased <strong>zif268</strong> mRNA in the orbitofrontal and infralimbic cortices of HI animals.
+EGR1	drug	opioid	23238466	Among them, a cluster of 8 genes, including 6 inducible transcription factors (c fos, fra 2, junB, zif268 (<strong>egr1</strong>), egr2, NGFI B) and 2 effector IEG (arc and mkp1) seemed to be regulated in concert in response to <b>morphine</b>.
+EGR1	drug	opioid	23238466	Among them, a cluster of 8 genes, including 6 inducible transcription factors (c fos, fra 2, junB, <strong>zif268</strong> (<strong>egr1</strong>), egr2, NGFI B) and 2 effector IEG (arc and mkp1) seemed to be regulated in concert in response to <b>morphine</b>.
+EGR1	drug	cocaine	23201361	Antagonizing 5 HT₂A receptors with M100907 and stimulating 5 HT₂C receptors with Ro60 0175 blocks <b>cocaine</b> induced locomotion and <strong>zif268</strong> mRNA expression in Sprague Dawley rats.
+EGR1	drug	cocaine	23201361	To investigate the possible brain regions involved in the interactions between 5 HT(2A) or 5 HT(2C) receptor ligands and <b>cocaine</b> induced behaviour, we examined the effects of M100907 or Ro60 0175 on <b>cocaine</b> induced locomotion and mRNA expression of the immediate early gene <strong>zif268</strong>.
+EGR1	drug	cocaine	23201361	<b>Cocaine</b> increased locomotor activity and <strong>zif268</strong> mRNA expression consistently in the nucleus accumbens core, the orbitofrontal cortex and the caudate.
+EGR1	drug	cocaine	23201361	M100907 attenuated <b>cocaine</b> induced locomotion and <strong>zif268</strong> mRNA expression in these brain regions in a defined subset of rats but failed to alter any effects of <b>cocaine</b> in another defined subset of rats.
+EGR1	drug	cocaine	23201361	Ro60 0175 blocked <b>cocaine</b> induced locomotion and <strong>zif268</strong> mRNA expression in similar brain regions.
+EGR1	drug	amphetamine	22534623	24 days) of <b>amphetamine</b> conditioned place preference (CPP) and a decreased expression in the insula of <strong>zif268</strong>, a crucial protein in memory reconsolidation, when anisomycin (ANI) was microinjected into the RAIC immediately after the reactivation of the conditioned <b>amphetamine</b>/context memory.
+EGR1	addiction	reward	22534623	24 days) of amphetamine conditioned place preference (<b>CPP</b>) and a decreased expression in the insula of <strong>zif268</strong>, a crucial protein in memory reconsolidation, when anisomycin (ANI) was microinjected into the RAIC immediately after the reactivation of the conditioned amphetamine/context memory.
+EGR1	addiction	relapse	22403532	These protective effects of social interaction were paralleled by a reduced activation, as assessed by <strong>Zif268</strong> expression, in brain areas known to play pivotal roles in drug <b>seeking</b> behavior.
+EGR1	drug	alcohol	22141421	<strong>Early growth response 1</strong> contributes to steatosis development after acute <b>ethanol</b> administration.
+EGR1	drug	alcohol	22141421	Previous work demonstrated that the transcription factor, <strong>early growth response 1</strong> (Egr 1), participates in the development of steatosis (fatty liver) after chronic <b>ethanol</b> (EtOH) administration.
+EGR1	drug	cocaine	22056598	Juvenile and adult rats differ in <b>cocaine</b> reward and expression of <strong>zif268</strong> in the forebrain.
+EGR1	addiction	reward	22056598	Juvenile and adult rats differ in cocaine <b>reward</b> and expression of <strong>zif268</strong> in the forebrain.
+EGR1	drug	cocaine	22056598	The aim of this study was to first compare behavioral responses to novelty and <b>cocaine</b> between juvenile and adult rats and then compare levels of the immediate early gene <strong>zif268</strong> activation in several forebrain areas via in situ hybridization.
+EGR1	drug	cocaine	22056598	A developmental effect for increased <strong>zif268</strong> mRNA was also observed in the striatum and nucleus accumbens, but there was no interaction with the <b>cocaine</b> dose.
+EGR1	drug	cocaine	21976515	Consequently, TDE altered <b>cocaine</b> induced regulation of genes bearing SRE site(s) in their promoters, including c fos, <strong>zif268</strong>, ΔFosB, and arc/arg3.1 (activity regulated cytoskeleton associated protein).
+EGR1	drug	cocaine	21318636	Regulation of the immediate early genes arc and <strong>zif268</strong> in a mouse operant model of <b>cocaine</b> seeking reinstatement.
+EGR1	addiction	relapse	21318636	Regulation of the immediate early genes arc and <strong>zif268</strong> in a mouse operant model of cocaine <b>seeking</b> <b>reinstatement</b>.
+EGR1	addiction	reward	21318636	Regulation of the immediate early genes arc and <strong>zif268</strong> in a mouse <b>operant</b> model of cocaine seeking reinstatement.
+EGR1	drug	cocaine	21318636	The aim of the present study was to assess regional brain activation, as measured by induction of the immediate early genes (IEG) arc and <strong>zif268</strong>, during priming  or cue elicited reinstatement of <b>cocaine</b> seeking using this new mouse model and the in situ hybridization technique.
+EGR1	addiction	relapse	21318636	The aim of the present study was to assess regional brain activation, as measured by induction of the immediate early genes (IEG) arc and <strong>zif268</strong>, during priming  or cue elicited <b>reinstatement</b> of cocaine <b>seeking</b> using this new mouse model and the in situ hybridization technique.
+EGR1	drug	cocaine	21309948	Reversal of <b>cocaine</b> conditioned place preference and mesocorticolimbic <strong>Zif268</strong> expression by social interaction in rats.
+EGR1	drug	cocaine	21309948	Social interaction also reversed <b>cocaine</b> CPP induced expression of the immediate early gene <strong>zif268</strong> in the nucleus accumbens shell, the central and basolateral amygdala and the ventral tegmental area.
+EGR1	addiction	reward	21309948	Social interaction also reversed cocaine <b>CPP</b> induced expression of the immediate early gene <strong>zif268</strong> in the nucleus accumbens shell, the central and basolateral amygdala and the ventral tegmental area.
+EGR1	drug	amphetamine	21229349	Acute injection of <b>METH</b> increased c fos, fosB, fra2, junB, <strong>Egr1</strong> 3, Nr4a1 (Nur77), and Nr4a3 (Nor 1) mRNA levels in the striatum of saline pretreated rats.
+EGR1	addiction	relapse	20802017	The effects of <strong>zif268</strong> knockdown were measured in two complementary paradigms widely used to assess the impact of drug paired CSs upon drug <b>seeking</b>: the acquisition of a new instrumental response with conditioned reinforcement and conditioned place preference.
+EGR1	addiction	reward	20802017	The effects of <strong>zif268</strong> knockdown were measured in two complementary paradigms widely used to assess the impact of drug paired CSs upon drug seeking: the acquisition of a new instrumental response with conditioned <b>reinforcement</b> and conditioned place preference.
+EGR1	drug	cocaine	20802017	The results show that both intranucleus accumbens core and intrabasolateral amygdala <strong>zif268</strong> ASO infusions at memory reactivation impaired the reconsolidation of the memory underlying a <b>cocaine</b> conditioned place preference.
+EGR1	drug	cocaine	20802017	However, knockdown of <strong>zif268</strong> in the nucleus accumbens at memory reactivation had no effect on the memory underlying the conditioned reinforcing properties of the <b>cocaine</b> paired CS measured subsequently, and this is in contrast to the marked impairment observed previously following intrabasolateral amygdala <strong>zif268</strong> ASO infusions.
+EGR1	addiction	reward	20802017	However, knockdown of <strong>zif268</strong> in the nucleus accumbens at memory reactivation had no effect on the memory underlying the conditioned <b>reinforcing</b> properties of the cocaine paired CS measured subsequently, and this is in contrast to the marked impairment observed previously following intrabasolateral amygdala <strong>zif268</strong> ASO infusions.
+EGR1	drug	cocaine	20704593	Our results show that SSRIs potentiate methylphenidate induced expression of the transcription factor genes <strong>zif268</strong> and c fos in the striatum, rendering these molecular changes more <b>cocaine</b> like.
+EGR1	addiction	sensitization	20675054	Evidence of central <b>sensitization</b> in cervical spinal cord segments that receive sensory projections from the forelimbs was provided by immunohistochemistry for <strong>Zif268</strong>, a functional marker of neuroplasticity.
+EGR1	drug	cocaine	20654701	In this study, the expression patterns of <strong>zif268</strong> and activity regulated cytoskeleton associated gene (arc) were investigated in the basolateral amygdala (BLA) and dorsal hippocampal (dHPC) subregions during context induced drug seeking following 22 h or 15 d abstinence from <b>cocaine</b> self administration.
+EGR1	addiction	relapse	20654701	In this study, the expression patterns of <strong>zif268</strong> and activity regulated cytoskeleton associated gene (arc) were investigated in the basolateral amygdala (BLA) and dorsal hippocampal (dHPC) subregions during context induced drug <b>seeking</b> following 22 h or 15 d abstinence from cocaine self administration.
+EGR1	drug	cocaine	20654701	In contrast, <strong>zif268</strong> mRNA in the BLA was greater in <b>cocaine</b> treated rats returned to the chamber with levers extended vs. levers retracted only after 15 d of abstinence.
+EGR1	drug	cocaine	20654701	In the dentate gyrus (DG) following 22 h of abstinence, <strong>zif268</strong> mRNA was greater in rats returned to the chamber where levers were absent regardless of drug treatment whereas arc mRNA was increased in CA1 (cell bodies and dendrites) and CA3 only in <b>cocaine</b> treated groups.
+EGR1	drug	cocaine	20654701	These data suggest that the temporal dynamics of arc and <strong>zif268</strong> gene expression in the BLA and dHPC encode different key elements of drug context induced <b>cocaine</b> seeking.
+EGR1	addiction	relapse	20654701	These data suggest that the temporal dynamics of arc and <strong>zif268</strong> gene expression in the BLA and dHPC encode different key elements of drug context induced cocaine <b>seeking</b>.
+EGR1	drug	cocaine	20554270	Within the nucleus accumbens, impaired cellular responses to <b>cocaine</b> are conspicuous; a pronounced deficit in <b>cocaine</b> elicited extracellular dopamine release, expression of the key IEGs c Fos and <strong>Zif268</strong>, and phosphorylation of extracellular signal regulated kinases 1/2 in mutants were observed.
+EGR1	drug	amphetamine	20020108	In experiment 2, we aimed to replicate and enhance the effects observed in experiment 1, and we also examined the effects of methylphenidate self administration during adolescence on adult <b>amphetamine</b> induced <strong>zif268</strong> messenger ribonucleic acid (mRNA) expression.
+EGR1	drug	amphetamine	20020108	Adolescent methylphenidate self administration also enhanced <b>amphetamine</b> induced <strong>zif268</strong> mRNA expression in the nucleus accumbens.
+EGR1	drug	cocaine	19419424	Long lasting dysregulation of gene expression in corticostriatal circuits after repeated <b>cocaine</b> treatment in adult rats: effects on <strong>zif 268</strong> and homer 1a.
+EGR1	drug	cocaine	19419424	We employed gene markers (<strong>zif 268</strong> and homer 1a) that offer a high anatomical resolution to map <b>cocaine</b> induced changes in 22 cortical areas and 23 functionally related striatal sectors, in order to determine the corticostriatal circuits altered by repeated <b>cocaine</b> exposure (25 mg/kg, 5 days).
+EGR1	drug	cocaine	19419424	Repeated <b>cocaine</b> treatment increased basal expression of <strong>zif 268</strong> predominantly in sensorimotor areas of the cortex.
+EGR1	drug	cocaine	19419424	In the insular cortex, the <b>cocaine</b> challenge produced a decrease in <strong>zif 268</strong> expression after the 21 day, but not 1 day, withdrawal period.
+EGR1	addiction	withdrawal	19419424	In the insular cortex, the cocaine challenge produced a decrease in <strong>zif 268</strong> expression after the 21 day, but not 1 day, <b>withdrawal</b> period.
+EGR1	drug	cocaine	19419424	Repeated <b>cocaine</b> resulted in blunted inducibility of both <strong>zif 268</strong> and homer 1a, changes that were still very robust 3 weeks later.
+EGR1	drug	cocaine	19245875	The purpose of the present study was to correlate <b>cocaine</b> induced locomotor activity with neuronal activation in subregions of the striatum and cortex by acute <b>cocaine</b> in young adolescent (postnatal (PN) 28) and adult (PN 65) male rats by measuring the induction of the plasticity associated immediate early genes (IEGs) c fos and <strong>zif268</strong> using in situ hybridization.
+EGR1	drug	cocaine	19245875	Low dose <b>cocaine</b> induced more locomotor activity and striatal c fos expression in adolescents than adults whereas high dose <b>cocaine</b> induced more locomotor activity, striatal c fos, and striatal <strong>zif268</strong> expression in adults.
+EGR1	drug	cocaine	19144966	This elevation of <b>cocaine</b> seeking was correlated with an increase in the expression of the reconsolidation associated gene <strong>zif268</strong>.
+EGR1	addiction	relapse	19144966	This elevation of cocaine <b>seeking</b> was correlated with an increase in the expression of the reconsolidation associated gene <strong>zif268</strong>.
+EGR1	drug	cocaine	19005643	We have recently found that the behavioral effects of <b>cocaine</b> as well as its ability to increase expression of <strong>zif 268</strong> are reduced in mice reared in enriched environments (EE).
+EGR1	drug	opioid	19005643	We assessed the influence of EE on the ability of <b>heroin</b> to (1) induce conditioned place preferences, (2) induce behavioral sensitization, (3) increase dopamine levels in the nucleus accumbens (NAc), and (4) increase expression of the immediate early gene <strong>zif 268</strong> in the striatum.
+EGR1	addiction	sensitization	19005643	We assessed the influence of EE on the ability of heroin to (1) induce conditioned place preferences, (2) induce behavioral <b>sensitization</b>, (3) increase dopamine levels in the nucleus accumbens (NAc), and (4) increase expression of the immediate early gene <strong>zif 268</strong> in the striatum.
+EGR1	drug	opioid	19005643	<b>Heroin</b> induced similar increases in dopamine levels and in the expression of <strong>zif 268</strong> in the NAc of EE and SE mice.
+EGR1	drug	cocaine	18463628	On the other hand, they were associated with reduced <b>cocaine</b> induced expression of the immediate early gene <strong>zif 268</strong> in the nucleus accumbens (shell and core) of EE mice.
+EGR1	drug	alcohol	18427989	Effects of <b>naltrexone</b> and <b>acamprosate</b> on <b>alcohol</b> induced <strong>NGFI A</strong> expression in mouse brain.
+EGR1	drug	alcohol	18427989	In search for the substrate of <b>naltrexone</b> and <b>acamprosate</b> action on <b>alcohol</b> craving, we investigated the effects of <b>ethanol</b> alone and combined with <b>naltrexone</b> or <b>acamprosate</b> on expression of nerve growth factor inducible clone A (<strong>NGFI A</strong>; zif268).
+EGR1	addiction	relapse	18427989	In search for the substrate of naltrexone and acamprosate action on alcohol <b>craving</b>, we investigated the effects of ethanol alone and combined with naltrexone or acamprosate on expression of nerve growth factor inducible clone A (<strong>NGFI A</strong>; zif268).
+EGR1	drug	alcohol	18427989	In search for the substrate of <b>naltrexone</b> and <b>acamprosate</b> action on <b>alcohol</b> craving, we investigated the effects of <b>ethanol</b> alone and combined with <b>naltrexone</b> or <b>acamprosate</b> on expression of nerve growth factor inducible clone A (<strong>NGFI A</strong>; <strong>zif268</strong>).
+EGR1	addiction	relapse	18427989	In search for the substrate of naltrexone and acamprosate action on alcohol <b>craving</b>, we investigated the effects of ethanol alone and combined with naltrexone or acamprosate on expression of nerve growth factor inducible clone A (<strong>NGFI A</strong>; <strong>zif268</strong>).
+EGR1	drug	alcohol	18427989	Both <b>ethanol</b> and <b>naltrexone</b> alone induced <strong>NGFI A</strong> in the central amygdala, but not in several other areas; these effects were additive.
+EGR1	drug	alcohol	18427989	However, <b>acamprosate</b> alone or in combination with <b>ethanol</b> had no effect on <strong>NGFI A</strong> mRNA, while nor BNI induced <strong>NGFI A</strong> mRNA in the basolateral amygdala.
+EGR1	drug	amphetamine	18093743	Regional adaptations in PSD 95, <strong>NGFI A</strong> and secretogranin gene transcripts related to vulnerability to behavioral sensitization to <b>amphetamine</b> in the Roman rat strains.
+EGR1	addiction	sensitization	18093743	Regional adaptations in PSD 95, <strong>NGFI A</strong> and secretogranin gene transcripts related to vulnerability to behavioral <b>sensitization</b> to amphetamine in the Roman rat strains.
+EGR1	drug	amphetamine	18093743	The expression patterns of nerve growth factor inducible clone A (<strong>NGFI A</strong>), secretogranin, post synaptic density protein of 95 Kd (PSD 95), prodynorphin and proenkephalin mRNA were also analyzed using in situ hybridization, after the challenge with <b>amphetamine</b>.
+EGR1	drug	amphetamine	18093743	On the other hand, high induction of <strong>NGFI A</strong> mRNA in the central amygdala was observed in RLA I rats when they experienced <b>amphetamine</b> for the first time in the challenge.
+EGR1	addiction	withdrawal	17151272	However, infusion of <strong>Zif268</strong> antisense oligodeoxynucleotide into the BLA before reactivation of the CS <b>withdrawal</b> association abolished this conditioned suppression in a reactivation dependent manner.
+EGR1	addiction	withdrawal	17151272	We also report that reconsolidation of CS <b>withdrawal</b> memories upregulates <strong>Zif268</strong> protein in the basolateral but not central nucleus of the amygdala and that <strong>Zif268</strong> knockdown occurs selectively in the BLA.
+EGR1	drug	amphetamine	17049170	Neurotoxic <b>AMPH</b> pretreatment resulted in significantly diminished <b>AMPH</b> challenge induced mRNA increases of activity regulated cytoskeletal protein (ARC), nerve growth factor inducible protein A (<strong>NGFI A</strong>), and nerve growth factor inducible protein B (NGFI B) in the parietal cortex while neither saline pretreatment nor non neurotoxic <b>AMPH</b> pretreatment did.
+EGR1	drug	amphetamine	17049170	In the striatum, there were no differences between saline, neurotoxic <b>AMPH</b>, and non neurotoxic <b>AMPH</b> pretreatments on ARC, <strong>NGFI A</strong> or NGFI B expression elicited by the <b>AMPH</b> challenge.
+EGR1	drug	amphetamine	16771831	Potentiation of <b>amphetamine</b> mediated responses in caffeine sensitized rats involves modifications in A2A receptors and <strong>zif 268</strong> mRNAs in striatal neurons.
+EGR1	drug	amphetamine	16771831	Results showed that the sensitized motor response to caffeine was associated with a decrease of adenosine A(2A) receptor and <strong>zif 268</strong> mRNA levels in the striatum and nucleus accumbens, whereas cross sensitization to <b>amphetamine</b> was linked to a more pronounced increase of <strong>zif 268</strong> mRNA levels in the striatum, but not in the nucleus accumbens.
+EGR1	addiction	sensitization	16771831	Results showed that the sensitized motor response to caffeine was associated with a decrease of adenosine A(2A) receptor and <strong>zif 268</strong> mRNA levels in the striatum and nucleus accumbens, whereas cross <b>sensitization</b> to amphetamine was linked to a more pronounced increase of <strong>zif 268</strong> mRNA levels in the striatum, but not in the nucleus accumbens.
+EGR1	drug	amphetamine	16771831	Single cell analysis showed that <strong>zif 268</strong> mRNA modifications occurred in Enk(+) striatopallidal neurons after acute or subchronic treatment with caffeine and in Enk( ) striatonigral neurons after acute <b>amphetamine</b> administration.
+EGR1	drug	cocaine	16738229	Here we show that blockade of drug memory reconsolidation, through infusion of <strong>Zif268</strong> antisense oligodeoxynucleotides into the basolateral amygdala shortly before reexposure to a <b>cocaine</b> associated stimulus but not simply to the training context, severely impaired subsequently cue maintained <b>cocaine</b> seeking under a second order schedule of reinforcement and abolished cue induced reinstatement of and relapse to <b>cocaine</b> seeking.
+EGR1	addiction	relapse	16738229	Here we show that blockade of drug memory reconsolidation, through infusion of <strong>Zif268</strong> antisense oligodeoxynucleotides into the basolateral amygdala shortly before reexposure to a cocaine associated stimulus but not simply to the training context, severely impaired subsequently cue maintained cocaine <b>seeking</b> under a second order schedule of reinforcement and abolished cue induced <b>reinstatement</b> of and <b>relapse</b> to cocaine <b>seeking</b>.
+EGR1	addiction	reward	16738229	Here we show that blockade of drug memory reconsolidation, through infusion of <strong>Zif268</strong> antisense oligodeoxynucleotides into the basolateral amygdala shortly before reexposure to a cocaine associated stimulus but not simply to the training context, severely impaired subsequently cue maintained cocaine seeking under a second order schedule of <b>reinforcement</b> and abolished cue induced reinstatement of and relapse to cocaine seeking.
+EGR1	drug	cocaine	16672671	Plasticity associated gene <strong>Krox24</strong>/Zif268 is required for long lasting behavioral effects of <b>cocaine</b>.
+EGR1	drug	cocaine	16672671	Plasticity associated gene <strong>Krox24</strong>/<strong>Zif268</strong> is required for long lasting behavioral effects of <b>cocaine</b>.
+EGR1	drug	cocaine	16672671	We examined the role of <strong>Zif268</strong>, an immediate early gene induced by drugs of abuse under the control of ERK, in behavioral responses to <b>cocaine</b> using knock in mutant mice in which <strong>Zif268</strong> was replaced by LacZ.
+EGR1	drug	cocaine	16672671	In contrast, locomotor sensitization to single or repeated <b>cocaine</b> injections was dramatically diminished in both heterozygous and homozygous <strong>Zif268</strong> mutant mice.
+EGR1	addiction	sensitization	16672671	In contrast, locomotor <b>sensitization</b> to single or repeated cocaine injections was dramatically diminished in both heterozygous and homozygous <strong>Zif268</strong> mutant mice.
+EGR1	drug	cocaine	16672671	Conditioned place preference in response to <b>cocaine</b> was prevented in <strong>Zif268</strong> deficient mice.
+EGR1	drug	cocaine	16672671	Our results provide direct genetic evidence for the requirement of <strong>Zif268</strong> for long lasting association of environmental context with specific behavioral responses after short exposures to <b>cocaine</b>.
+EGR1	drug	alcohol	16470400	Eight hours after <b>ethanol</b> withdrawal, anxiety like behaviour was tested in the elevated plus maze, blood corticosterone levels were measured, and expression level of markers of neuronal activity and plasticity, c fos and <strong>zif268</strong>, was assessed.
+EGR1	addiction	withdrawal	16470400	Eight hours after ethanol <b>withdrawal</b>, anxiety like behaviour was tested in the elevated plus maze, blood corticosterone levels were measured, and expression level of markers of neuronal activity and plasticity, c fos and <strong>zif268</strong>, was assessed.
+EGR1	drug	alcohol	16410364	gAcrp also normalized LPS stimulated DNA binding activity of <strong>early growth response 1</strong> with greater sensitivity in Kupffer cells from rats fed chronic <b>ethanol</b>.
+EGR1	drug	cocaine	16339038	In MSK1 knock out (KO) mice CREB and H3 phosphorylation in response to <b>cocaine</b> (10 mg/kg) were blocked, and induction of c Fos and dynorphin was prevented, whereas the induction of Egr 1 (<strong>early growth response 1</strong>)/zif268/Krox24 was unaltered.
+EGR1	drug	cocaine	16339038	In MSK1 knock out (KO) mice CREB and H3 phosphorylation in response to <b>cocaine</b> (10 mg/kg) were blocked, and induction of c Fos and dynorphin was prevented, whereas the induction of Egr 1 (<strong>early growth response 1</strong>)/zif268/<strong>Krox24</strong> was unaltered.
+EGR1	drug	cocaine	16339038	In MSK1 knock out (KO) mice CREB and H3 phosphorylation in response to <b>cocaine</b> (10 mg/kg) were blocked, and induction of c Fos and dynorphin was prevented, whereas the induction of Egr 1 (<strong>early growth response 1</strong>)/<strong>zif268</strong>/<strong>Krox24</strong> was unaltered.
+EGR1	drug	opioid	16262673	After more than 3 weeks of abstinence during extinction training, cue exposure robustly reinstated <b>heroin</b> and sucrose seeking, but induced distinct and even opposing changes in the expression of the neuronal activation marker <strong>zif268</strong> in the prelimbic cortex and striatal complex, respectively.
+EGR1	addiction	relapse	16262673	After more than 3 weeks of abstinence during extinction training, cue exposure robustly reinstated heroin and sucrose <b>seeking</b>, but induced distinct and even opposing changes in the expression of the neuronal activation marker <strong>zif268</strong> in the prelimbic cortex and striatal complex, respectively.
+EGR1	drug	opioid	16262673	Because in the prelimbic area <strong>zif268</strong> expression was enhanced during cue induced <b>heroin</b> seeking but unaffected during sucrose seeking, a pharmacological intervention was aimed at this prefrontal region.
+EGR1	addiction	relapse	16262673	Because in the prelimbic area <strong>zif268</strong> expression was enhanced during cue induced heroin <b>seeking</b> but unaffected during sucrose <b>seeking</b>, a pharmacological intervention was aimed at this prefrontal region.
+EGR1	drug	cocaine	16157275	Here, we show that infusion of <strong>Zif268</strong> antisense oligodeoxynucleotides into the basolateral amygdala, prior to the reactivation of a well learned memory for a conditioned stimulus (CS) <b>cocaine</b> association, abolishes the acquired conditioned reinforcing properties of the drug associated stimulus and thus its impact on the learning of a new <b>cocaine</b> seeking response.
+EGR1	addiction	relapse	16157275	Here, we show that infusion of <strong>Zif268</strong> antisense oligodeoxynucleotides into the basolateral amygdala, prior to the reactivation of a well learned memory for a conditioned stimulus (CS) cocaine association, abolishes the acquired conditioned reinforcing properties of the drug associated stimulus and thus its impact on the learning of a new cocaine <b>seeking</b> response.
+EGR1	addiction	reward	16157275	Here, we show that infusion of <strong>Zif268</strong> antisense oligodeoxynucleotides into the basolateral amygdala, prior to the reactivation of a well learned memory for a conditioned stimulus (CS) cocaine association, abolishes the acquired conditioned <b>reinforcing</b> properties of the drug associated stimulus and thus its impact on the learning of a new cocaine seeking response.
+EGR1	drug	cocaine	16115217	The patterns of <b>cocaine</b> induced c Fos, JunB and <strong>Zif268</strong> protein expression were investigated, using an immunohistochemical approach, within distinct nuclei of the amygdala, either in the presence or absence of a selective inhibitor of the ERK pathway, SL327.
+EGR1	drug	cocaine	16115217	In particular, whereas c Fos and JunB expressions were augmented following chronic <b>cocaine</b> treatment, as compared with acute treatment, <strong>Zif268</strong> expression was decreased by this chronic treatment.
+EGR1	drug	cocaine	16115217	Additionally, chronic blocking of ERK activation affected <b>cocaine</b> induced c Fos and JunB but not <strong>Zif268</strong> expression.
+EGR1	drug	nicotine	15785859	We previously reported that <b>nicotine</b> withdrawal up regulates transcription of some immediately early genes (IEGs), c fos (Ichino et al., 1999) and <strong>egr1</strong>, nur77 (Ichino et al., 2002) in cultures of pheochromocytoma PC12 cells, which are of neuronal lineage.
+EGR1	addiction	withdrawal	15785859	We previously reported that nicotine <b>withdrawal</b> up regulates transcription of some immediately early genes (IEGs), c fos (Ichino et al., 1999) and <strong>egr1</strong>, nur77 (Ichino et al., 2002) in cultures of pheochromocytoma PC12 cells, which are of neuronal lineage.
+EGR1	drug	cocaine	15496936	Brief social defeat stress: long lasting effects on <b>cocaine</b> taking during a binge and <strong>zif268</strong> mRNA expression in the amygdala and prefrontal cortex.
+EGR1	addiction	intoxication	15496936	Brief social defeat stress: long lasting effects on cocaine taking during a <b>binge</b> and <strong>zif268</strong> mRNA expression in the amygdala and prefrontal cortex.
+EGR1	drug	cocaine	15496936	The objectives of the current study were to examine the enduring consequences of brief episodes of social defeat stress on <b>cocaine</b> bingeing (during 24 h of continuous access) and on the emergence of neural adaptations as revealed by <strong>zif268</strong> immediate early gene expression.
+EGR1	drug	cocaine	15496936	After 2 months, <b>cocaine</b> binges or <strong>zif268</strong> mRNA gene expression were studied after confirming behavioral cross sensitization to stimulant challenge.
+EGR1	addiction	sensitization	15496936	After 2 months, cocaine binges or <strong>zif268</strong> mRNA gene expression were studied after confirming behavioral cross <b>sensitization</b> to stimulant challenge.
+EGR1	drug	amphetamine	15496936	Persistent stress induced levels of <strong>zif268</strong> in the central and medial amygdala were attenuated by an injection of <b>amphetamine</b> (1.0 mg/kg).
+EGR1	drug	cocaine	12752796	Induction of the learning and plasticity associated gene <strong>Zif268</strong> following exposure to a discrete <b>cocaine</b> associated stimulus.
+EGR1	drug	cocaine	12752796	We investigated whether the expression of the plasticity associated gene, <strong>zif268</strong>, was associated with memories retrieved by exposure to a discrete stimulus that had been associated with <b>cocaine</b>, either self administered or administered noncontingently.
+EGR1	drug	cocaine	12752796	In the absence of drug, passive presentation of a <b>cocaine</b> associated light stimulus induced changes in the expression of <strong>zif268</strong> measured by in situ hybridization within a limbic cortical ventral striatal circuit that was not only regionally selective but related to whether the rats had originally received response contingent or noncontingent stimulus drug pairings.
+EGR1	drug	cocaine	12752796	In rats that had self administered drug, the <b>cocaine</b> conditioned stimulus (CS) increased <strong>zif268</strong> expression in neurons of the ventral tegmental area, nucleus accumbens core and shell, and basal nucleus of the amygdala but not hippocampus, prelimbic area of the medial prefrontal cortex or amygdala central nucleus.
+EGR1	drug	cocaine	12752796	The same CS that had been associated with <b>cocaine</b> administered noncontingently additionally increased <strong>zif268</strong> mRNA levels in area Cg1 of the anterior cingulate cortex, ventral and lateral regions of the orbitofrontal cortex and lateral nucleus of the amygdala.
+EGR1	drug	cocaine	12752796	<strong>Zif268</strong> induction was related to the predictive relationship between the stimulus and <b>cocaine</b> as no changes were seen in <b>cocaine</b> experienced rats that had received unpaired light and drug presentations during training.
+EGR1	addiction	relapse	12752796	<strong>Zif268</strong> may participate in the molecular mechanisms underlying the reconsolidation or re encoding of Pavlovian stimulus drug associations across a distributed limbic cortical ventral striatal neural network and that may contribute to the basis of the enduring drug <b>seeking</b> behaviour produced by environmental cues.
+EGR1	drug	cannabinoid	12657697	In vivo <b>THC</b> induced the expression of immediate early genes products (c Fos protein, <strong>Zif268</strong>, and BDNF mRNAs), and this induction was prevented by an inhibitor of MEK.
+EGR1	drug	amphetamine	12638131	Using these criteria, the mRNA for three immediate early genes (IEGs), coding for activity regulated cytoskeletal associated protein (Arc), nerve growth factor induced protein A (<strong>NGFI A</strong>; early growth response protein 1) and nerve growth factor induced protein B (NGFI B), were upregulated 1 and 3 h after <b>amphetamine</b> as previously described.
+EGR1	drug	amphetamine	12112395	Similarly, in the second experiment it was found that the D1R dependent induction by <b>AMPH</b> of Fos, FosB, and JunB, but not <strong>NGFI A</strong>, in the NAc was enhanced in rats exposed 1 week earlier to repeated VTA <b>AMPH</b>.
+EGR1	drug	cannabinoid	11388413	Effects of <b>cannabinoids</b> in <strong>Krox 24</strong> targeted mice.
+EGR1	drug	cannabinoid	11388413	<strong>Krox 24</strong> is an immediate early gene encoding a zinc finger transcription factor implicated in several adaptive responses, and its induction by <b>cannabinoids</b> has been reported.
+EGR1	drug	cannabinoid	11388413	We used mice targeted in the <strong>Krox 24</strong> gene to specifically dissect the role of this protein in the acute and chronic central actions of <b>cannabinoids</b>.
+EGR1	drug	cannabinoid	11388413	We show that <strong>Krox 24</strong> is not involved in the acute analgesic effects of delta9 <b>THC</b> and in the SR precipitated delta9 <b>THC</b> withdrawal syndrome.
+EGR1	addiction	withdrawal	11388413	We show that <strong>Krox 24</strong> is not involved in the acute analgesic effects of delta9 THC and in the SR precipitated delta9 THC <b>withdrawal</b> syndrome.
+EGR1	drug	cocaine	11098116	Reduction of <strong>zif268</strong> messenger RNA expression during prolonged withdrawal following "binge" <b>cocaine</b> self administration in rats.
+EGR1	addiction	intoxication	11098116	Reduction of <strong>zif268</strong> messenger RNA expression during prolonged withdrawal following "<b>binge</b>" cocaine self administration in rats.
+EGR1	addiction	withdrawal	11098116	Reduction of <strong>zif268</strong> messenger RNA expression during prolonged <b>withdrawal</b> following "binge" cocaine self administration in rats.
+EGR1	drug	cocaine	11098116	The neuronal correlates of these behavioral and neurochemical effects of a <b>cocaine</b> binge were assessed using in situ hybridization histochemistry to detect changes in <strong>zif268</strong> messenger RNA expression.
+EGR1	addiction	intoxication	11098116	The neuronal correlates of these behavioral and neurochemical effects of a cocaine <b>binge</b> were assessed using in situ hybridization histochemistry to detect changes in <strong>zif268</strong> messenger RNA expression.
+EGR1	drug	cocaine	11098116	The level of <strong>zif268</strong> messenger RNA was lower upon termination of <b>cocaine</b> self administration than in both yoked treatment groups in the ventral tegmental area and hippocampus.
+EGR1	drug	cocaine	11098116	In contrast, <strong>zif268</strong> messenger RNA expression increased in the periaqueductal gray matter one day after termination of passive <b>cocaine</b> treatment, coincident with enhanced expression of ultrasonic vocalizations.
+EGR1	drug	cocaine	11098116	<strong>Zif268</strong> messenger RNA expression decreased over time in the nucleus accumbens core and infralimbic cortex, with reduced expression observed in the nucleus accumbens core, caudatoputamen, hippocampus and amygdala 14 days after termination of <b>cocaine</b> self administration.
+EGR1	drug	cocaine	11098116	The results suggest that withdrawal following a <b>cocaine</b> self administration binge produces a long lasting reduction of constitutive <strong>zif268</strong> messenger RNA expression in mesocorticolimbic brain regions related to the nucleus accumbens.
+EGR1	addiction	intoxication	11098116	The results suggest that withdrawal following a cocaine self administration <b>binge</b> produces a long lasting reduction of constitutive <strong>zif268</strong> messenger RNA expression in mesocorticolimbic brain regions related to the nucleus accumbens.
+EGR1	addiction	withdrawal	11098116	The results suggest that <b>withdrawal</b> following a cocaine self administration binge produces a long lasting reduction of constitutive <strong>zif268</strong> messenger RNA expression in mesocorticolimbic brain regions related to the nucleus accumbens.
+EGR1	drug	cocaine	10986339	The suppressive effects of pentobarbital were not specific to c Fos, such that pentobarbital also suppressed expression of ITFs FosB and <strong>Egr1</strong> in the striatum of <b>cocaine</b> treated rats.
+EGR1	drug	cocaine	10971643	A low dose of <b>cocaine</b>, by itself essentially ineffective, produced an increase in c fos and <strong>NGFI A</strong> mRNA in the cerebral cortex in mice that had been drinking caffeine.
+EGR1	drug	cocaine	10971643	<b>Cocaine</b> and caffeine also synergistically increased <strong>NGFI A</strong> expression in caudate putamen.
+EGR1	drug	cocaine	10683479	C57BL/6J, DBA/2J, and 129/OlaHsd mice were compared as to their propensity to self administer <b>cocaine</b>, the ability of <b>cocaine</b> injection to prevent extinction of nose poking in the absence of <b>cocaine</b> infusion, and <b>cocaine</b>'s effect on <strong>NGFI A</strong> and secretogranin II mRNA.
+EGR1	drug	cocaine	10683479	A single <b>cocaine</b> injection (2 mg kg( )(1)) increased <strong>NGFI A</strong> mRNA and decreased secretogranin II mRNA in the caudate putamen in C57 mice.
+EGR1	drug	amphetamine	10683413	Differential regional <strong>zif268</strong> messenger RNA expression in an escalating dose/binge model of <b>amphetamine</b> induced psychosis.
+EGR1	addiction	intoxication	10683413	Differential regional <strong>zif268</strong> messenger RNA expression in an escalating dose/<b>binge</b> model of amphetamine induced psychosis.
+EGR1	drug	amphetamine	10683413	Acute <b>amphetamine</b> resulted in a significant elevation of <strong>zif268</strong> messenger RNA in both the nucleus accumbens and dorsal striatum.
+EGR1	drug	amphetamine	10683413	Agranular insular cortex and medial olfactory tubercle <strong>zif268</strong> messenger RNA expression was also markedly increased after acute <b>amphetamine</b> treatment but, unlike the nucleus accumbens and dorsal striatum, this increase was not significantly attenuated by either single daily injection or multiple binge treatment.
+EGR1	addiction	intoxication	10683413	Agranular insular cortex and medial olfactory tubercle <strong>zif268</strong> messenger RNA expression was also markedly increased after acute amphetamine treatment but, unlike the nucleus accumbens and dorsal striatum, this increase was not significantly attenuated by either single daily injection or multiple <b>binge</b> treatment.
+EGR1	addiction	intoxication	10683413	<strong>Zif268</strong> messenger RNA expression in the lateral nucleus of the amygdala also remained elevated above baseline after <b>binge</b> treatment.
+EGR1	drug	cocaine	10564376	Expression of c fos, <strong>NGFI A</strong> and secretogranin II mRNA in brain regions during initiation of <b>cocaine</b> self administration in mice.
+EGR1	drug	cocaine	10564376	Intravenous <b>cocaine</b> self administration in mice was studied to find correlates of the acquisition of <b>cocaine</b> oriented operant behaviour in the expression of nerve growth factor induced clone A (<strong>NGFI A</strong>), c fos and secretogranin II mRNAs.
+EGR1	addiction	reward	10564376	Intravenous cocaine self administration in mice was studied to find correlates of the acquisition of cocaine oriented <b>operant</b> behaviour in the expression of nerve growth factor induced clone A (<strong>NGFI A</strong>), c fos and secretogranin II mRNAs.
+EGR1	drug	cocaine	10564376	Non contingent <b>cocaine</b> infusions increased <strong>NGFI A</strong> mRNA expression in the core of nucleus accumbens, medial caudate putamen and frontal cortex, whereas self administration eliminated these effects.
+EGR1	drug	alcohol	10443996	In this study, immunohistochemical expression analysis of immediate early genes c fos, fosB, and <strong>zif268</strong> was performed in brain of C57BL/6J mice after voluntary <b>alcohol</b> consumption.
+EGR1	drug	alcohol	10443996	Consumption of the <b>ethanol</b>/sucrose solution also significantly reduced FosB expression in the basolateral amygdala and lateral hypothalamus, and <strong>Zif268</strong> expression in the CA1 region of the hippocampus of stressed animals.
+EGR1	drug	cocaine	9387892	Interestingly, the repression of 8G226 immediately after <b>cocaine</b> treatment is in direct contrast to the <b>cocaine</b> dependent increase in expression documented for <strong>NGFI A</strong>, another zinc finger protein which also functions as a transcriptional regulator.
+EGR1	addiction	sensitization	9403355	During the "central <b>sensitization</b>" phenomenon, noxious stimuli lead to expression of IEGs (c fos, c jun, <strong>krox 24</strong>); their proteic products have been postulated to convert short term stimulations into long lasting responses in dorsal horn neurons.
+EGR1	drug	alcohol	8749800	The present study examined fetal <b>alcohol</b> effects (FAE) on the induction of the immediate early genes (IEGs) c fos, jun B, c jun, and <strong>zif268</strong> mRNAs in the prefrontal cortex, hippocampus, and other brain regions after testing in an alternation task.
+EGR1	drug	amphetamine	7784961	This study illustrates how a 2 week, twice daily 7.5 mg/kg d <b>amphetamine</b> or saline regimen alters rat brain regional expression of transcription factor genes, including c fos, fos B, jun B, c jun, and <strong>zif 268</strong>, and seeks potential correlations between those changes and alterations in neurotransmitter levels and behavioral novelty responses.
+EGR1	drug	cocaine	7854036	Previous studies have demonstrated that the IEGs <strong>NGFI A</strong> (zif268) and c fos are each rapidly induced in the caudate putamen (CP) by treatment with the indirect dopamine agonist <b>cocaine</b>.
+EGR1	drug	cocaine	7854036	Previous studies have demonstrated that the IEGs <strong>NGFI A</strong> (<strong>zif268</strong>) and c fos are each rapidly induced in the caudate putamen (CP) by treatment with the indirect dopamine agonist <b>cocaine</b>.
+EGR1	drug	cocaine	7854036	Levels of <strong>NGFI A</strong> and c fos were measured in the CP of rats by Northern blot analysis, which confirmed that <b>cocaine</b> induced increases of <strong>NGFI A</strong> and c fos mRNA lasts for several hours after drug administration.
+EGR1	drug	cocaine	7854036	Immediately following this induction, however, there is a prolonged period during which a marked reduction in the relative amount of mRNA for both <strong>NGFI A</strong> and c fos is observed in <b>cocaine</b> treated animals when compared to matched, vehicle treated controls.
+EGR1	drug	cocaine	1631058	We therefore examined changes in the mRNA levels for the IEGs c fos, c jun, fosB, junB, and <strong>zif268</strong> in the NAc of rats treated acutely and chronically with <b>cocaine</b>.
+CHRNA3	drug	nicotine	32184221	Human genome wide association studies have linked polymorphisms in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, coding for the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, to <b>nicotine</b> addiction.
+CHRNA3	addiction	addiction	32184221	Human genome wide association studies have linked polymorphisms in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, coding for the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, to nicotine <b>addiction</b>.
+CHRNA3	drug	nicotine	32184221	These data indicate that β4 is a critical modulator of reward related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster and <b>nicotine</b> addiction.
+CHRNA3	addiction	addiction	32184221	These data indicate that β4 is a critical modulator of reward related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster and nicotine <b>addiction</b>.
+CHRNA3	addiction	reward	32184221	These data indicate that β4 is a critical modulator of <b>reward</b> related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster and nicotine addiction.
+CHRNA3	drug	nicotine	31402126	Gene polymorphisms of <strong>CHRNA3</strong> (rs578776) and CHRNA4 (rs1044396 and rs2229959) were associated with the success of <b>smoking</b> cessation after the diagnosis of lung cancer, which should be considered in the management of <b>smoking</b> cessation after patients are diagnosed with lung cancer.
+CHRNA3	drug	nicotine	31061854	This article contains data on the allele and genotype frequency for single nucleotide polymorphisms (SNPs) in candidate genes CHRNA5 (rs16969968, rs17408276, rs680244) <strong>CHRNA3</strong> (rs6495307, rs12914385) NRXN1 (rs10865246, rs1882296, rs985919) and HTR2A (rs6311, rs6313) previously evaluated as genetic risk variants for cigarette <b>smoking</b> at an early age and relapse to <b>smoking</b> cessation treatment Pérez Rubio et al., 2018.
+CHRNA3	addiction	relapse	31061854	This article contains data on the allele and genotype frequency for single nucleotide polymorphisms (SNPs) in candidate genes CHRNA5 (rs16969968, rs17408276, rs680244) <strong>CHRNA3</strong> (rs6495307, rs12914385) NRXN1 (rs10865246, rs1882296, rs985919) and HTR2A (rs6311, rs6313) previously evaluated as genetic risk variants for cigarette smoking at an early age and <b>relapse</b> to smoking cessation treatment Pérez Rubio et al., 2018.
+CHRNA3	drug	nicotine	30453884	Searching for variants with evidence of regulatory functions, we have reported interactions between CHRNA5 and <strong>CHRNA3</strong> enhancer variants (tagged by rs880395 and rs1948, respectively) and rs16969968, forming 3 SNP haplotypes and diplotypes that may more accurately reflect the cluster's combined effects on <b>nicotine</b> dependence (Barrie et al., Hum Mutat 38:112 9, 2017).
+CHRNA3	addiction	dependence	30453884	Searching for variants with evidence of regulatory functions, we have reported interactions between CHRNA5 and <strong>CHRNA3</strong> enhancer variants (tagged by rs880395 and rs1948, respectively) and rs16969968, forming 3 SNP haplotypes and diplotypes that may more accurately reflect the cluster's combined effects on nicotine <b>dependence</b> (Barrie et al., Hum Mutat 38:112 9, 2017).
+CHRNA3	drug	nicotine	30453884	These results indicate rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of <strong>CHRNA3</strong> and CHRNA5, modulates the effect of rs16969968 on <b>nicotine</b> dependence risk.
+CHRNA3	addiction	dependence	30453884	These results indicate rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of <strong>CHRNA3</strong> and CHRNA5, modulates the effect of rs16969968 on nicotine <b>dependence</b> risk.
+CHRNA3	drug	nicotine	29993116	<strong>CHRNA3</strong> rs1051730 and CHRNA5 rs16969968 polymorphisms are associated with heavy <b>smoking</b>, lung cancer, and chronic obstructive pulmonary disease in a mexican population.
+CHRNA3	drug	nicotine	29993116	Polymorphisms in <strong>CHRNA3</strong>, CHRNA5, and CHRNB4 receptors play a critical role in <b>nicotine</b> dependence, lung cancer (LC) risk, and chronic obstructive pulmonary disease (COPD).
+CHRNA3	addiction	dependence	29993116	Polymorphisms in <strong>CHRNA3</strong>, CHRNA5, and CHRNB4 receptors play a critical role in nicotine <b>dependence</b>, lung cancer (LC) risk, and chronic obstructive pulmonary disease (COPD).
+CHRNA3	drug	nicotine	29993116	This study characterized the <strong>CHRNA3</strong> rs1051730 and CHRNA5 rs16969968 polymorphisms in a Mexican population and its association with <b>nicotine</b> dependence, LC, and COPD.
+CHRNA3	addiction	dependence	29993116	This study characterized the <strong>CHRNA3</strong> rs1051730 and CHRNA5 rs16969968 polymorphisms in a Mexican population and its association with nicotine <b>dependence</b>, LC, and COPD.
+CHRNA3	drug	nicotine	29993116	The <b>smokers</b> were stratified in heavy <b>smokers</b> and moderate/light <b>smokers</b>, and we found in A alleles an OR = 2.86 (P = 0.01) to <strong>CHRNA3</strong> rs1051730 and OR = 3.12 (P = 0.03) to CHRNA5 rs16969968.
+CHRNA3	drug	nicotine	29993116	<strong>CHRNA3</strong>/5 polymorphisms are associated with <b>nicotine</b> dependence, LC, and COPD in Mexicans.
+CHRNA3	addiction	dependence	29993116	<strong>CHRNA3</strong>/5 polymorphisms are associated with nicotine <b>dependence</b>, LC, and COPD in Mexicans.
+CHRNA3	drug	nicotine	29758381	However, our results confirmed the role of the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster of nicotinic acetylcholine receptor subunit genes in <b>tobacco</b> use.
+CHRNA3	drug	nicotine	29666375	Association and cis mQTL analysis of variants in <strong>CHRNA3</strong> A5, CHRNA7, CHRNB2, and CHRNB4 in relation to <b>nicotine</b> dependence in a Chinese Han population.
+CHRNA3	addiction	dependence	29666375	Association and cis mQTL analysis of variants in <strong>CHRNA3</strong> A5, CHRNA7, CHRNB2, and CHRNB4 in relation to nicotine <b>dependence</b> in a Chinese Han population.
+CHRNA3	drug	nicotine	29666375	Our results indicated that the SNPs rs1948 and rs7178270 in CHRNB4 and rs3743075 in <strong>CHRNA3</strong> were significantly associated with the Fagerström Test for <b>Nicotine</b> Dependence (FTND) score (p = 6.6 × 10 5; p = 2.0 × 10 4, and p = 7.0 × 10 4, respectively).
+CHRNA3	addiction	dependence	29666375	Our results indicated that the SNPs rs1948 and rs7178270 in CHRNB4 and rs3743075 in <strong>CHRNA3</strong> were significantly associated with the Fagerström Test for Nicotine <b>Dependence</b> (FTND) score (p = 6.6 × 10 5; p = 2.0 × 10 4, and p = 7.0 × 10 4, respectively).
+CHRNA3	drug	nicotine	29621993	In the context of personalized medicine, the aims of this study were to evaluate whether cholinergic receptor nicotinic alpha 2 (CHRNA2), cholinergic receptor nicotinic alpha 3 (<strong>CHRNA3</strong>), cholinergic receptor nicotinic alpha 5 (CHRNA5) and cholinergic receptor nicotinic beta 3 (CHRNB3) polymorphisms were associated with <b>nicotine</b> dependence severity, and to investigate possible pharmacogenetics markers of <b>smoking</b> cessation treatment.
+CHRNA3	addiction	dependence	29621993	In the context of personalized medicine, the aims of this study were to evaluate whether cholinergic receptor nicotinic alpha 2 (CHRNA2), cholinergic receptor nicotinic alpha 3 (<strong>CHRNA3</strong>), cholinergic receptor nicotinic alpha 5 (CHRNA5) and cholinergic receptor nicotinic beta 3 (CHRNB3) polymorphisms were associated with nicotine <b>dependence</b> severity, and to investigate possible pharmacogenetics markers of smoking cessation treatment.
+CHRNA3	drug	nicotine	29172281	SNP rs16969968 as a Strong Predictor of <b>Nicotine</b> Dependence and Lung Cancer Risk in a North Indian Population Background: The 15q24 25 loci contain genes (CHRNA5 and <strong>CHRNA3</strong>) encoding nicotinic acetylcholine receptor subunits.
+CHRNA3	addiction	dependence	29172281	SNP rs16969968 as a Strong Predictor of Nicotine <b>Dependence</b> and Lung Cancer Risk in a North Indian Population Background: The 15q24 25 loci contain genes (CHRNA5 and <strong>CHRNA3</strong>) encoding nicotinic acetylcholine receptor subunits.
+CHRNA3	drug	nicotine	29172281	We here determined for the first time the association of genetic variants rs16969968 and rs3743074 in CHRNA5 and <strong>CHRNA3</strong>, respectively, on <b>nicotine</b> dependence and lung cancer risk in a North Indian population by a case control approach.
+CHRNA3	addiction	dependence	29172281	We here determined for the first time the association of genetic variants rs16969968 and rs3743074 in CHRNA5 and <strong>CHRNA3</strong>, respectively, on nicotine <b>dependence</b> and lung cancer risk in a North Indian population by a case control approach.
+CHRNA3	drug	nicotine	28972577	In this largest ever GWAS meta analysis for <b>nicotine</b> dependence and the largest ever cross ancestry GWAS meta analysis for any <b>smoking</b> phenotype, we reconfirmed the well known CHRNA5 <strong>CHRNA3</strong> CHRNB4 genes and further yielded a novel association in the DNA methyltransferase gene DNMT3B.
+CHRNA3	addiction	dependence	28972577	In this largest ever GWAS meta analysis for nicotine <b>dependence</b> and the largest ever cross ancestry GWAS meta analysis for any smoking phenotype, we reconfirmed the well known CHRNA5 <strong>CHRNA3</strong> CHRNB4 genes and further yielded a novel association in the DNA methyltransferase gene DNMT3B.
+CHRNA3	addiction	dependence	28368157	Suggestive associations were consistent with previous findings from studies of substance use and <b>dependence</b>, including variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster with cigarettes smoked per day.
+CHRNA3	drug	nicotine	27871728	Genome wide association studies (GWASs) have identified associations between the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster and <b>smoking</b> heaviness and <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	27871728	Genome wide association studies (GWASs) have identified associations between the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster and smoking heaviness and nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	27871728	GWASs of <b>smoking</b> related health outcomes have also identified this signal in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster.
+CHRNA3	drug	nicotine	27302872	Polymorphisms in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster (Chr15q25) have been robustly associated with <b>nicotine</b> dependence, including genome wide studies, as well as with cognitive and neuropsychological measures.
+CHRNA3	addiction	dependence	27302872	Polymorphisms in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster (Chr15q25) have been robustly associated with nicotine <b>dependence</b>, including genome wide studies, as well as with cognitive and neuropsychological measures.
+CHRNA3	drug	nicotine	27302872	Here, we evaluated the effect of polymorphisms in CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster and their interaction with <b>tobacco</b> <b>smoking</b> status on cognition in patients with Attention Deficit/Hyperactivity Disorder (ADHD).
+CHRNA3	drug	nicotine	27127891	Association Between <strong>CHRNA3</strong> and CHRNA5 <b>Nicotine</b> Receptor Subunit Gene Variants and <b>Nicotine</b> Dependence in an Isolated Populationof Kashubians in Poland.
+CHRNA3	addiction	dependence	27127891	Association Between <strong>CHRNA3</strong> and CHRNA5 Nicotine Receptor Subunit Gene Variants and Nicotine <b>Dependence</b> in an Isolated Populationof Kashubians in Poland.
+CHRNA3	drug	nicotine	26997181	The associations between CHRNA5 <strong>CHRNA3</strong> CHRNB4 variants and cigarettes per day (CPD), the Fagerström Test for <b>Nicotine</b> Dependence (FTND), and craving were analyzed in data from 662 lifetime <b>smokers</b> from an Israeli adult Jewish household sample.
+CHRNA3	addiction	dependence	26997181	The associations between CHRNA5 <strong>CHRNA3</strong> CHRNB4 variants and cigarettes per day (CPD), the Fagerström Test for Nicotine <b>Dependence</b> (FTND), and craving were analyzed in data from 662 lifetime smokers from an Israeli adult Jewish household sample.
+CHRNA3	addiction	relapse	26997181	The associations between CHRNA5 <strong>CHRNA3</strong> CHRNB4 variants and cigarettes per day (CPD), the Fagerström Test for Nicotine Dependence (FTND), and <b>craving</b> were analyzed in data from 662 lifetime smokers from an Israeli adult Jewish household sample.
+CHRNA3	addiction	relapse	26997181	At <strong>CHRNA3</strong>, allele G of rs3743078 was associated with increased <b>craving</b>, CPD, and FTND scores: Participants with one or two copies of the G allele had, on average, higher scores on the <b>craving</b> scale (p = .0025), more cigarettes smoked (p = .0057), and higher scores on the FTND (p =.0024).
+CHRNA3	drug	nicotine	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 addiction genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to <b>smoking</b> behavior and <b>nicotine</b> metabolism: CHRNA5 <strong>CHRNA3</strong> CHRNB4 and CYP2A6 CYP2B6.
+CHRNA3	addiction	addiction	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 <b>addiction</b> genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to smoking behavior and nicotine metabolism: CHRNA5 <strong>CHRNA3</strong> CHRNB4 and CYP2A6 CYP2B6.
+CHRNA3	drug	nicotine	26751916	CHRNA5/<strong>CHRNA3</strong> Locus Associates with Increased Mortality among <b>Smokers</b>.
+CHRNA3	drug	nicotine	26751916	Polymorphisms in the nicotinic acetylcholine receptor gene (CHRNA5/<strong>CHRNA3</strong> locus) have been associated with several <b>smoking</b> related traits such as <b>nicotine</b> dependence, cigarette consumption, <b>smoking</b> cessation, lung cancer, and COPD.
+CHRNA3	addiction	dependence	26751916	Polymorphisms in the nicotinic acetylcholine receptor gene (CHRNA5/<strong>CHRNA3</strong> locus) have been associated with several smoking related traits such as nicotine <b>dependence</b>, cigarette consumption, smoking cessation, lung cancer, and COPD.
+CHRNA3	drug	nicotine	26751916	CHRNA5/<strong>CHRNA3</strong> locus tagged by rs1051730, which has been previously associated with several <b>smoking</b> related diseases was now shown to be associated also with increased all cause mortality among long term <b>smokers</b> with or without clinical COPD further emphasizing the clinical importance of the finding.
+CHRNA3	drug	nicotine	25958762	This approach allowed the identification of the first susceptibility gene in addiction (<b>tobacco</b>), with genes CHRNA5, <strong>CHRNA3</strong> and CHRNB4 encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for <b>tobacco</b> dependence.
+CHRNA3	addiction	addiction	25958762	This approach allowed the identification of the first susceptibility gene in <b>addiction</b> (tobacco), with genes CHRNA5, <strong>CHRNA3</strong> and CHRNB4 encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for tobacco dependence.
+CHRNA3	addiction	dependence	25958762	This approach allowed the identification of the first susceptibility gene in addiction (tobacco), with genes CHRNA5, <strong>CHRNA3</strong> and CHRNB4 encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for tobacco <b>dependence</b>.
+CHRNA3	drug	nicotine	25948103	Genome wide association studies have implicated the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster in risk for heavy <b>smoking</b> and several <b>smoking</b> related disorders.
+CHRNA3	drug	nicotine	25948103	These findings support differential aversive response to <b>nicotine</b> as one likely mechanism for the association of CHRNA5 <strong>CHRNA3</strong> CHRNB4 with heavy <b>smoking</b>.
+CHRNA3	addiction	aversion	25948103	These findings support differential <b>aversive</b> response to nicotine as one likely mechanism for the association of CHRNA5 <strong>CHRNA3</strong> CHRNB4 with heavy smoking.
+CHRNA3	drug	nicotine	25632390	In this study we tested the association of <b>smoking</b> initiation, age at onset of daily <b>smoking</b>, and heaviness of <b>smoking</b> with five single nucleotide polymorphisms (SNPs) within the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster.
+CHRNA3	drug	nicotine	25632390	This study provides strong evidence for the role of the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster in heaviness of <b>nicotine</b> addiction.
+CHRNA3	addiction	addiction	25632390	This study provides strong evidence for the role of the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster in heaviness of nicotine <b>addiction</b>.
+CHRNA3	drug	alcohol	25603899	SNPs in the <b>alcohol</b> metabolizing genes, in the cholinergic gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4, and in the DRD2 and ANNK1 genes, are, to date, the most replicated and significant gene variants associated with <b>alcohol</b>  and nicotine related phenotypes.
+CHRNA3	drug	nicotine	25603899	SNPs in the alcohol metabolizing genes, in the cholinergic gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4, and in the DRD2 and ANNK1 genes, are, to date, the most replicated and significant gene variants associated with alcohol  and <b>nicotine</b> related phenotypes.
+CHRNA3	drug	nicotine	25555482	No GWS associations were observed at the chromosome 15 nicotinic receptor gene cluster (CHRNA5 <strong>CHRNA3</strong> CHRNB4) previously associated with <b>nicotine</b> dependence and <b>smoking</b> quantity traits.
+CHRNA3	addiction	dependence	25555482	No GWS associations were observed at the chromosome 15 nicotinic receptor gene cluster (CHRNA5 <strong>CHRNA3</strong> CHRNB4) previously associated with nicotine <b>dependence</b> and smoking quantity traits.
+CHRNA3	drug	nicotine	25233467	Our findings suggest that <b>nicotine</b> dependence plays an important role between genetic variants in the CHRNA5/A3/B4 region, especially <strong>CHRNA3</strong>, and lung adenocarcinoma.
+CHRNA3	addiction	dependence	25233467	Our findings suggest that nicotine <b>dependence</b> plays an important role between genetic variants in the CHRNA5/A3/B4 region, especially <strong>CHRNA3</strong>, and lung adenocarcinoma.
+CHRNA3	drug	nicotine	25214750	Genomics and personalized medicine: CHRNA5 <strong>CHRNA3</strong> CHRNB4 and <b>smoking</b> cessation treatment.
+CHRNA3	drug	nicotine	25214750	We review the significance of variants in the nicotinic receptor gene cluster (CHRNA5 <strong>CHRNA3</strong> CHRNB4) in the prediction of <b>smoking</b> quantity, <b>smoking</b> cessation, and response to cessation medication in multiple studies of <b>smoking</b> cessation.
+CHRNA3	drug	nicotine	25214750	The genetic variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 region that predict <b>nicotine</b> dependence also predict a later age of <b>smoking</b> cessation in a community based sample.
+CHRNA3	addiction	dependence	25214750	The genetic variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 region that predict nicotine <b>dependence</b> also predict a later age of smoking cessation in a community based sample.
+CHRNA3	drug	nicotine	25139936	A <b>nicotine</b> dependence associated and lung cancer variant, <strong>CHRNA3</strong> rs578776 [OR, 1.16; 95% confidence interval (CI), 1.05 1.26; P = 0.004], and two breast cancer variants, EMBP1 rs11249433 and TOX3 rs3803662 (OR, 1.16; 95% CI, 1.04 1.28; P = 0.005 and OR, 1.13; 95% CI, 1.03 1.23; P = 0.006), were significantly associated with risk of IMPC.
+CHRNA3	addiction	dependence	25139936	A nicotine <b>dependence</b> associated and lung cancer variant, <strong>CHRNA3</strong> rs578776 [OR, 1.16; 95% confidence interval (CI), 1.05 1.26; P = 0.004], and two breast cancer variants, EMBP1 rs11249433 and TOX3 rs3803662 (OR, 1.16; 95% CI, 1.04 1.28; P = 0.005 and OR, 1.13; 95% CI, 1.03 1.23; P = 0.006), were significantly associated with risk of IMPC.
+CHRNA3	drug	nicotine	25072098	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 locus is associated with self reported <b>smoking</b> behavior and also harbors the strongest genetic associations with chronic obstructive pulmonary disease (COPD) and lung cancer.
+CHRNA3	drug	nicotine	25072098	Because the associations with lung disease remain after adjustment for self reported <b>smoking</b> behaviors, it has been asserted that CHRNA5 <strong>CHRNA3</strong> CHRNB4 variants increase COPD and lung cancer susceptibility independently of their effects on <b>smoking</b>.
+CHRNA3	drug	nicotine	25072098	Variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 locus, including rs16969968, a nonsynonymous variant in CHRNA5, are genomewide association study significantly associated with CO (β = 2.66; 95% confidence interval [CI], 1.74 3.58; P = 1.65 × 10( 8)), and this association remains strong after adjusting for <b>smoking</b> behavior (β = 2.18; 95% CI, 1.32 3.04; P = 7.47 × 10( 7)).
+CHRNA3	drug	nicotine	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, <strong>CHRNA3</strong>, CHRNB4, CHRNA6 and CHRNB3 genes and found that rare missense variants at conserved residues in CHRNB4 are associated with reduced risk of <b>nicotine</b> dependence among African Americans.
+CHRNA3	addiction	dependence	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, <strong>CHRNA3</strong>, CHRNB4, CHRNA6 and CHRNB3 genes and found that rare missense variants at conserved residues in CHRNB4 are associated with reduced risk of nicotine <b>dependence</b> among African Americans.
+CHRNA3	drug	opioid	24750073	In addition, two human datasets revealed a protective role for variants in the <strong>CHRNA3</strong> gene, which codes for the α3 nACh receptor subunit, in <b>opioid</b> dependence and withdrawal.
+CHRNA3	addiction	dependence	24750073	In addition, two human datasets revealed a protective role for variants in the <strong>CHRNA3</strong> gene, which codes for the α3 nACh receptor subunit, in opioid <b>dependence</b> and withdrawal.
+CHRNA3	addiction	withdrawal	24750073	In addition, two human datasets revealed a protective role for variants in the <strong>CHRNA3</strong> gene, which codes for the α3 nACh receptor subunit, in opioid dependence and <b>withdrawal</b>.
+CHRNA3	drug	alcohol	24505444	We investigated six variants known to influence nicotine addiction or <b>alcohol</b> metabolism, including rs16969968 (CHRNA5), rs578776 (<strong>CHRNA3</strong>), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+CHRNA3	drug	nicotine	24505444	We investigated six variants known to influence <b>nicotine</b> addiction or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (<strong>CHRNA3</strong>), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+CHRNA3	addiction	addiction	24505444	We investigated six variants known to influence nicotine <b>addiction</b> or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (<strong>CHRNA3</strong>), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (ADH7), and rs4767364 (ALDH2).
+CHRNA3	drug	nicotine	24478678	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, encoding the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, has been linked to <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	24478678	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, encoding the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, has been linked to nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	24337855	However, no association between the <b>smoking</b> habit and the <strong>CHRNA3</strong> rs1051730 polymorphism was observed in this study.
+CHRNA3	drug	nicotine	24186853	Distinct loci in the CHRNA5/<strong>CHRNA3</strong>/CHRNB4 gene cluster are associated with onset of regular <b>smoking</b>.
+CHRNA3	drug	nicotine	24186853	Neuronal nicotinic acetylcholine receptor (nAChR) genes (CHRNA5/<strong>CHRNA3</strong>/CHRNB4) have been reproducibly associated with <b>nicotine</b> dependence, <b>smoking</b> behaviors, and lung cancer risk.
+CHRNA3	addiction	dependence	24186853	Neuronal nicotinic acetylcholine receptor (nAChR) genes (CHRNA5/<strong>CHRNA3</strong>/CHRNB4) have been reproducibly associated with nicotine <b>dependence</b>, smoking behaviors, and lung cancer risk.
+CHRNA3	drug	nicotine	24163739	Large scale, multi cohort GWAS of mainly Caucasian, <b>smoking</b>, populations have identified strong associations for lung cancer mapped to chromosomal regions 15q [nicotinic acetylcholine receptor (nAChR) subunits: <strong>CHRNA3</strong>, CHRNA5], 5p (TERT CLPTM1L locus) and 6p (BAT3 MSH5).
+CHRNA3	drug	nicotine	24163739	GWAS of <b>smoking</b> behaviour have identified risk loci for <b>smoking</b> quantity at 15q (similar genes to lung cancer susceptibility: <strong>CHRNA3</strong>, CHRNA5) and 19q (CYP2A6).
+CHRNA3	drug	nicotine	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster associated with heavy <b>smoking</b> and higher relapse risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster associated with heavy smoking and higher relapse risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of nicotine <b>dependence</b>.
+CHRNA3	addiction	relapse	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster associated with heavy smoking and higher <b>relapse</b> risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of nicotine dependence.
+CHRNA3	drug	nicotine	24065931	The <strong>CHRNA3</strong> rs578776 Variant is Associated with an Intrinsic Reward Sensitivity Deficit in <b>Smokers</b>.
+CHRNA3	addiction	reward	24065931	The <strong>CHRNA3</strong> rs578776 Variant is Associated with an Intrinsic <b>Reward</b> Sensitivity Deficit in Smokers.
+CHRNA3	drug	nicotine	24065931	We examined genetic polymorphisms within the CHRNA5 A3 B4 gene cluster (<strong>CHRNA3</strong> rs578776, CHRNA5 rs16969968, LOC123688 rs8034191, and <strong>CHRNA3</strong> rs1051730), the ANKK1 gene (rs1800497), and the D2 dopamine receptor gene (DRD2 rs1079597, DRD2 rs1799732) from 104 <b>smokers</b> of European ancestry in a <b>smoking</b> cessation trial.
+CHRNA3	drug	nicotine	24065931	The <strong>CHRNA3</strong> rs578776 polymorphism did not differ on questionnaires of <b>nicotine</b> dependence, depressed mood, or trait affective disposition and did not predict abstinence at 6 months after the quit date.
+CHRNA3	addiction	dependence	24065931	The <strong>CHRNA3</strong> rs578776 polymorphism did not differ on questionnaires of nicotine <b>dependence</b>, depressed mood, or trait affective disposition and did not predict abstinence at 6 months after the quit date.
+CHRNA3	drug	nicotine	24062692	Recently, variants in the nAChR genes <strong>CHRNA3</strong>, CHRNA5, and CHRNB4 have been implicated in <b>nicotine</b> dependence and lung cancer susceptibility.
+CHRNA3	addiction	dependence	24062692	Recently, variants in the nAChR genes <strong>CHRNA3</strong>, CHRNA5, and CHRNB4 have been implicated in nicotine <b>dependence</b> and lung cancer susceptibility.
+CHRNA3	drug	alcohol	24057674	Rare missense variants in CHRNB3 and <strong>CHRNA3</strong> are associated with risk of <b>alcohol</b> and cocaine dependence.
+CHRNA3	drug	cocaine	24057674	Rare missense variants in CHRNB3 and <strong>CHRNA3</strong> are associated with risk of alcohol and <b>cocaine</b> dependence.
+CHRNA3	addiction	dependence	24057674	Rare missense variants in CHRNB3 and <strong>CHRNA3</strong> are associated with risk of alcohol and cocaine <b>dependence</b>.
+CHRNA3	drug	alcohol	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically <b>alcohol</b> and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, <strong>CHRNA3</strong>, CHRNB4, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of <b>Alcoholism</b> (COGA).
+CHRNA3	drug	cocaine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically alcohol and <b>cocaine</b> dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, <strong>CHRNA3</strong>, CHRNB4, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA3	drug	nicotine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than <b>nicotine</b> dependence, specifically alcohol and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, <strong>CHRNA3</strong>, CHRNB4, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA3	addiction	dependence	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine <b>dependence</b>, specifically alcohol and cocaine <b>dependence</b>, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, <strong>CHRNA3</strong>, CHRNB4, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA3	drug	cocaine	24057674	For African Americans, we find decreased <b>cocaine</b> dependence symptoms among carriers of missense variants in <strong>CHRNA3</strong> (FamSKAT P = 0.005).
+CHRNA3	addiction	dependence	24057674	For African Americans, we find decreased cocaine <b>dependence</b> symptoms among carriers of missense variants in <strong>CHRNA3</strong> (FamSKAT P = 0.005).
+CHRNA3	drug	alcohol	24057674	These are the first results to implicate rare variants in CHRNB3 or <strong>CHRNA3</strong> in risk for <b>alcohol</b> dependence or cocaine dependence.
+CHRNA3	drug	cocaine	24057674	These are the first results to implicate rare variants in CHRNB3 or <strong>CHRNA3</strong> in risk for alcohol dependence or <b>cocaine</b> dependence.
+CHRNA3	addiction	dependence	24057674	These are the first results to implicate rare variants in CHRNB3 or <strong>CHRNA3</strong> in risk for alcohol <b>dependence</b> or cocaine <b>dependence</b>.
+CHRNA3	drug	nicotine	24055497	Second, genetic variation that modifies noxious responses to <b>nicotine</b> and thereby influences vulnerability to <b>tobacco</b> dependence, in particular variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 nicotinic acetylcholine receptor (nAChR) subunit gene cluster, will be discussed.
+CHRNA3	addiction	dependence	24055497	Second, genetic variation that modifies noxious responses to nicotine and thereby influences vulnerability to tobacco <b>dependence</b>, in particular variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 nicotinic acetylcholine receptor (nAChR) subunit gene cluster, will be discussed.
+CHRNA3	drug	alcohol	23875064	Scrutiny of the CHRNA5 <strong>CHRNA3</strong> CHRNB4 smoking behavior locus reveals a novel association with <b>alcohol</b> use in a Finnish population based study.
+CHRNA3	drug	nicotine	23875064	Scrutiny of the CHRNA5 <strong>CHRNA3</strong> CHRNB4 <b>smoking</b> behavior locus reveals a novel association with alcohol use in a Finnish population based study.
+CHRNA3	drug	nicotine	23875064	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster on chromosome 15q25.1 encoding the cholinergic nicotinic receptor subunits is robustly associated with <b>smoking</b> behavior and <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	23875064	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster on chromosome 15q25.1 encoding the cholinergic nicotinic receptor subunits is robustly associated with smoking behavior and nicotine <b>dependence</b>.
+CHRNA3	drug	alcohol	23872218	<strong>CHRNA3</strong>/B4 intergenic single nucleotide polymorphisms (SNPs) rs1948 and rs8023462 have been associated with early initiation of <b>alcohol</b> and tobacco use, and rs6495309 has been associated with nicotine dependence and risk for lung cancer.
+CHRNA3	drug	nicotine	23872218	<strong>CHRNA3</strong>/B4 intergenic single nucleotide polymorphisms (SNPs) rs1948 and rs8023462 have been associated with early initiation of alcohol and <b>tobacco</b> use, and rs6495309 has been associated with <b>nicotine</b> dependence and risk for lung cancer.
+CHRNA3	addiction	dependence	23872218	<strong>CHRNA3</strong>/B4 intergenic single nucleotide polymorphisms (SNPs) rs1948 and rs8023462 have been associated with early initiation of alcohol and tobacco use, and rs6495309 has been associated with nicotine <b>dependence</b> and risk for lung cancer.
+CHRNA3	drug	nicotine	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non <b>smoking</b> adolescents, we aimed to elucidate the impact of genome wide significant <b>smoking</b> associated variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster on reward related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to addiction.
+CHRNA3	addiction	addiction	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non smoking adolescents, we aimed to elucidate the impact of genome wide significant smoking associated variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster on reward related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to <b>addiction</b>.
+CHRNA3	addiction	reward	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non smoking adolescents, we aimed to elucidate the impact of genome wide significant smoking associated variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster on <b>reward</b> related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to addiction.
+CHRNA3	drug	nicotine	23604333	The effect of <b>nicotine</b> on sensorimotor gating is modulated by a <strong>CHRNA3</strong> polymorphism.
+CHRNA3	drug	nicotine	23604333	Moreover, the TT genotype of the nicotinic acetylcholine receptor (nAChR) α3 subunit (<strong>CHRNA3</strong>) rs1051730 polymorphism has previously been associated with diminished PPI and <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	23604333	Moreover, the TT genotype of the nicotinic acetylcholine receptor (nAChR) α3 subunit (<strong>CHRNA3</strong>) rs1051730 polymorphism has previously been associated with diminished PPI and nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	23604333	We tested whether this <strong>CHRNA3</strong> polymorphism also modulates the <b>nicotine</b> induced enhancement of PPI.
+CHRNA3	drug	nicotine	23604333	We assessed the effect of <b>nicotine</b> on PPI, startle reactivity, and habituation in 52 healthy nonsmoking volunteers genotyped for <strong>CHRNA3</strong> rs1051730 in a double blind, placebo controlled, counterbalanced, within subjects design.
+CHRNA3	drug	nicotine	23143843	Indeed, genetic variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to <b>tobacco</b> dependence and <b>smoking</b> associated diseases including lung cancer.
+CHRNA3	addiction	dependence	23143843	Indeed, genetic variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to tobacco <b>dependence</b> and smoking associated diseases including lung cancer.
+CHRNA3	drug	nicotine	23061658	Genome wide association (GWA) studies both in lung cancer and COPD highlighted the same variants (SNPs) on chromosome 15q25 marking the gene cluster <strong>CHRNA3</strong> CHRNB4 CHRNA5 for these <b>smoking</b> related diseases, showing a stimulating connection between this common genetic region and <b>smoking</b> behavior and <b>smoking</b> related illnesses.
+CHRNA3	drug	nicotine	23061658	Moreover variants on the gene cluster <strong>CHRNA3</strong> CHRNB4 CHRNA5 are associated with <b>nicotine</b> addiction antismoking therapy and antismoking therapy side effects.
+CHRNA3	addiction	addiction	23061658	Moreover variants on the gene cluster <strong>CHRNA3</strong> CHRNB4 CHRNA5 are associated with nicotine <b>addiction</b> antismoking therapy and antismoking therapy side effects.
+CHRNA3	drug	nicotine	23029550	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster on 15q25 has consistently been associated with <b>smoking</b> quantity, <b>nicotine</b> dependence and lung cancer.
+CHRNA3	addiction	dependence	23029550	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster on 15q25 has consistently been associated with smoking quantity, nicotine <b>dependence</b> and lung cancer.
+CHRNA3	drug	nicotine	22884254	Several genetic variants within the nicotinic cholinergic receptor gene cluster, CHRNA5 <strong>CHRNA3</strong> CHRNB4 have been reported to be associated with <b>nicotine</b> dependence (ND), and this association has been validated in multiple studies.
+CHRNA3	addiction	dependence	22884254	Several genetic variants within the nicotinic cholinergic receptor gene cluster, CHRNA5 <strong>CHRNA3</strong> CHRNB4 have been reported to be associated with nicotine <b>dependence</b> (ND), and this association has been validated in multiple studies.
+CHRNA3	drug	nicotine	22648373	Interplay of genetic risk factors (CHRNA5 <strong>CHRNA3</strong> CHRNB4) and cessation treatments in <b>smoking</b> cessation success.
+CHRNA3	drug	nicotine	22648373	This study tested whether variants in the nicotinic receptor gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4 predict age at <b>smoking</b> cessation and relapse after an attempt to quit <b>smoking</b>.
+CHRNA3	addiction	relapse	22648373	This study tested whether variants in the nicotinic receptor gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4 predict age at smoking cessation and <b>relapse</b> after an attempt to quit smoking.
+CHRNA3	drug	nicotine	22648373	In a community based, crosssectional study (N=5,216) and a randomized comparative effectiveness <b>smoking</b> cessation trial (N=1,073), the authors used Cox proportional hazard models and logistic regression to model the relationships of <b>smoking</b> cessation (self reported quit age in the community study and point prevalence abstinence at the end of treatment in the clinical trial) to three common haplotypes in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 region defined by rs16969968 and rs680244.
+CHRNA3	drug	nicotine	22648373	The genetic variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 region that predict <b>nicotine</b> dependence also predicted a later age at <b>smoking</b> cessation in the community sample.
+CHRNA3	addiction	dependence	22648373	The genetic variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 region that predict nicotine <b>dependence</b> also predicted a later age at smoking cessation in the community sample.
+CHRNA3	drug	nicotine	22544838	From men to mice: CHRNA5/<strong>CHRNA3</strong>, <b>smoking</b> behavior and disease.
+CHRNA3	drug	nicotine	22441734	<strong>CHRNA3</strong> genotype, <b>nicotine</b> dependence, lung function and disease in the general population.
+CHRNA3	addiction	dependence	22441734	<strong>CHRNA3</strong> genotype, nicotine <b>dependence</b>, lung function and disease in the general population.
+CHRNA3	drug	nicotine	22441734	The <strong>CHRNA3</strong> rs1051730 polymorphism has been associated to chronic obstructive pulmonary disease (COPD), lung cancer and <b>nicotine</b> dependence in case control studies with high <b>smoking</b> exposure; however, its influence on lung function and COPD severity in the general population is largely unknown.
+CHRNA3	addiction	dependence	22441734	The <strong>CHRNA3</strong> rs1051730 polymorphism has been associated to chronic obstructive pulmonary disease (COPD), lung cancer and nicotine <b>dependence</b> in case control studies with high smoking exposure; however, its influence on lung function and COPD severity in the general population is largely unknown.
+CHRNA3	drug	nicotine	22441734	In ever <b>smokers</b>, the <strong>CHRNA3</strong> rs1051730 genotype associated with reduced lung function and increased COPD severity.
+CHRNA3	drug	alcohol	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster) with <b>alcohol</b> dependence, nicotine dependence and smoking related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNA3	drug	nicotine	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster) with alcohol dependence, <b>nicotine</b> dependence and <b>smoking</b> related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNA3	addiction	dependence	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster) with alcohol <b>dependence</b>, nicotine <b>dependence</b> and smoking related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNA3	drug	alcohol	22438940	To further examine the impact of these genes on the development of substance use disorders, we tested whether variants within and flanking the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster affect the transition to daily smoking (individuals who smoked cigarettes 4 or more days per week) in a cross sectional sample of adolescents and young adults from the COGA (Collaborative Study of the Genetics of <b>Alcoholism</b>) families.
+CHRNA3	drug	nicotine	22438940	To further examine the impact of these genes on the development of substance use disorders, we tested whether variants within and flanking the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster affect the transition to daily <b>smoking</b> (individuals who smoked cigarettes 4 or more days per week) in a cross sectional sample of adolescents and young adults from the COGA (Collaborative Study of the Genetics of Alcoholism) families.
+CHRNA3	drug	nicotine	22241830	Analysis of detailed phenotype profiles reveals CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster association with several <b>nicotine</b> dependence traits.
+CHRNA3	addiction	dependence	22241830	Analysis of detailed phenotype profiles reveals CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster association with several nicotine <b>dependence</b> traits.
+CHRNA3	drug	nicotine	22241830	In this study, we included all 15 tagging single nucleotide polymorphisms (SNPs) within the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster and tested associations with 30 <b>smoking</b> related phenotypes.
+CHRNA3	drug	nicotine	22223462	One CHRNA5 (rs16969968) and two <strong>CHRNA3</strong> (rs1051703, rs6495308) SNPs were examined for their ability to predict <b>smokers</b> who "ever" reported ND based on three phenotypic classifications: (1) 25+ CPD, (2) TTF < 10 min, and (3) HSI ≥ 4.
+CHRNA3	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), <strong>CHRNA3</strong> 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CHRNA3	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), <strong>CHRNA3</strong> 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CHRNA3	drug	nicotine	22042774	Genome wide association studies have identified common variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 and CHRNA6 CHRNB3 gene clusters that contribute to <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	22042774	Genome wide association studies have identified common variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 and CHRNA6 CHRNB3 gene clusters that contribute to nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, <strong>CHRNA3</strong>, CHRNB4, CHRNA6 and CHRNB3 genes in African American and European American <b>nicotine</b> dependent <b>smokers</b> and <b>smokers</b> without symptoms of dependence.
+CHRNA3	addiction	dependence	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, <strong>CHRNA3</strong>, CHRNB4, CHRNA6 and CHRNB3 genes in African American and European American nicotine dependent smokers and smokers without symptoms of <b>dependence</b>.
+CHRNA3	drug	nicotine	22042774	The minor allele of each polymorphism increased cellular response to <b>nicotine</b> (T375I P = 0.01, T91I P = 0.02, R37H P = 0.003), but the largest effect on in vitro receptor activity was seen in the presence of both CHRNB4 T91I and <strong>CHRNA3</strong> R37H (P = 2 × 10( 6)).
+CHRNA3	drug	nicotine	22042234	Genetic variation in the CHRNA5/<strong>CHRNA3</strong>/CHRNB4 gene cluster has been associated with early substance experimentation, <b>nicotine</b> dependence, and other drug behaviors.
+CHRNA3	addiction	dependence	22042234	Genetic variation in the CHRNA5/<strong>CHRNA3</strong>/CHRNB4 gene cluster has been associated with early substance experimentation, nicotine <b>dependence</b>, and other drug behaviors.
+CHRNA3	drug	nicotine	22017462	An interaction between <b>tobacco</b> smoke exposure and a <strong>CHRNA3</strong>/5 polymorphism was found for BHR in children, but <strong>CHRNA3</strong>/5 was not associated with asthma or lung function.
+CHRNA3	drug	nicotine	21858091	Genome wide association studies implicate variations in CHRNA5 and <strong>CHRNA3</strong> as being associated with <b>nicotine</b> addiction (NA).
+CHRNA3	addiction	addiction	21858091	Genome wide association studies implicate variations in CHRNA5 and <strong>CHRNA3</strong> as being associated with nicotine <b>addiction</b> (NA).
+CHRNA3	drug	nicotine	21810735	Single nucleotide polymorphisms in CHRNA5 rs16969968, <strong>CHRNA3</strong> rs578776, and LOC123688 rs8034191 are associated with heaviness of <b>smoking</b> in women in Northeastern Ontario, Canada.
+CHRNA3	drug	nicotine	21810735	Women with the variant AA genotype of <strong>CHRNA3</strong> rs578775 were at significantly decreased risk of heavy <b>smoking</b>, with an age adjusted OR of 0.3 (95% CI: 0.12 0.90).
+CHRNA3	drug	nicotine	21778810	A genome wide association (GWA) study has recently demonstrated that <strong>CHRNA3</strong>/5 in 15q25 was associated with COPD compared with control <b>smokers</b>.
+CHRNA3	drug	nicotine	21778810	It was of interest that the <strong>CHRNA3</strong>/5 locus was associated with <b>nicotine</b> dependence and lung cancer as well.
+CHRNA3	addiction	dependence	21778810	It was of interest that the <strong>CHRNA3</strong>/5 locus was associated with nicotine <b>dependence</b> and lung cancer as well.
+CHRNA3	drug	nicotine	21748402	A twin association study of <b>nicotine</b> dependence with markers in the <strong>CHRNA3</strong> and CHRNA5 genes.
+CHRNA3	addiction	dependence	21748402	A twin association study of nicotine <b>dependence</b> with markers in the <strong>CHRNA3</strong> and CHRNA5 genes.
+CHRNA3	drug	nicotine	21747048	Relationship between CYP2A6 and CHRNA5 <strong>CHRNA3</strong> CHRNB4 variation and <b>smoking</b> behaviors and lung cancer risk.
+CHRNA3	drug	nicotine	21747048	Genetic variations in the CYP2A6 <b>nicotine</b> metabolic gene and the CHRNA5 <strong>CHRNA3</strong> CHRNB4 (CHRNA5 A3 B4) nicotinic gene cluster have been independently associated with lung cancer.
+CHRNA3	drug	nicotine	21740894	Consistent with this possibility, human genome wide association studies have shown that genetic variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster located in chromosome region 15q25, which encode the α5, α3 and β4 nAChR subunits, respectively, increases vulnerability to <b>tobacco</b> addiction and <b>smoking</b> related diseases.
+CHRNA3	addiction	addiction	21740894	Consistent with this possibility, human genome wide association studies have shown that genetic variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster located in chromosome region 15q25, which encode the α5, α3 and β4 nAChR subunits, respectively, increases vulnerability to tobacco <b>addiction</b> and smoking related diseases.
+CHRNA3	drug	nicotine	21690317	<strong>CHRNA3</strong> rs1051730 genotype and short term <b>smoking</b> cessation.
+CHRNA3	drug	nicotine	21555077	<b>Nicotine</b> dependence is linked to single nucleotide polymorphisms in the CHRNB4 <strong>CHRNA3</strong> CHRNA5 gene cluster encoding the α3β4α5 nicotinic acetylcholine receptor (nAChR).
+CHRNA3	addiction	dependence	21555077	Nicotine <b>dependence</b> is linked to single nucleotide polymorphisms in the CHRNB4 <strong>CHRNA3</strong> CHRNA5 gene cluster encoding the α3β4α5 nicotinic acetylcholine receptor (nAChR).
+CHRNA3	drug	nicotine	21511889	Variant within the promoter region of the <strong>CHRNA3</strong> gene associated with FTN dependence is not related to self reported willingness to quit <b>smoking</b>.
+CHRNA3	addiction	dependence	21511889	Variant within the promoter region of the <strong>CHRNA3</strong> gene associated with FTN <b>dependence</b> is not related to self reported willingness to quit smoking.
+CHRNA3	drug	nicotine	21511889	Common variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene region is robustly associated with <b>smoking</b> quantity.
+CHRNA3	drug	nicotine	21511889	Conversely, the association between one of the most significant single nucleotide polymorphisms (SNPs; rs1051730 within the <strong>CHRNA3</strong> gene) with perceived difficulty or willingness to quit <b>smoking</b> among current <b>smokers</b> is unknown.
+CHRNA3	drug	nicotine	21498873	As the physiological effects of <b>nicotine</b> are mediated by nicotinic acetylcholine receptors (nAChRs), we aimed at examining whether single nucleotide polymorphisms (SNPs) residing in nAChR subunit (CHRN) genes, other than <strong>CHRNA3</strong>/CHRNA5/CHRNB4 gene cluster previously showing association in our sample, are associated with <b>smoking</b> quantity or serum cotinine levels.
+CHRNA3	drug	nicotine	21385908	Association of the <b>nicotine</b> metabolite ratio and CHRNA5/<strong>CHRNA3</strong> polymorphisms with <b>smoking</b> rate among treatment seeking <b>smokers</b>.
+CHRNA3	addiction	relapse	21385908	Association of the nicotine metabolite ratio and CHRNA5/<strong>CHRNA3</strong> polymorphisms with smoking rate among treatment <b>seeking</b> smokers.
+CHRNA3	drug	nicotine	21268243	We focused on eight SNPs in the 15q24 region, which contains the genes for the nicotinic cholinergic receptor subunits CHRNA5, <strong>CHRNA3</strong>, and CHRNB4, and has previously been implicated in <b>nicotine</b> addiction and <b>smoking</b> cessation.
+CHRNA3	addiction	addiction	21268243	We focused on eight SNPs in the 15q24 region, which contains the genes for the nicotinic cholinergic receptor subunits CHRNA5, <strong>CHRNA3</strong>, and CHRNB4, and has previously been implicated in nicotine <b>addiction</b> and smoking cessation.
+CHRNA3	drug	nicotine	21268243	Analyses of baseline <b>smoking</b> quantity (SQ) identified an association between SQ and both the functional CHRNA5 SNP rs16969968 (D398N) and the <strong>CHRNA3</strong> SNP rs1051730 (Y215Y) in a combined cohort containing MT1 and MT2.
+CHRNA3	addiction	relapse	21268243	Pharmacogenetic analysis showed a significant association between rs8192475 (R37H) in <strong>CHRNA3</strong> and both higher <b>craving</b> after quitting and increased withdrawal symptoms over time in MT2.
+CHRNA3	addiction	withdrawal	21268243	Pharmacogenetic analysis showed a significant association between rs8192475 (R37H) in <strong>CHRNA3</strong> and both higher craving after quitting and increased <b>withdrawal</b> symptoms over time in MT2.
+CHRNA3	drug	nicotine	21232152	Genotypes for two SNPs in the <strong>CHRNA3</strong>/5 region (rs8034191, rs1051730) previously associated with <b>nicotine</b> dependence and COPD were analyzed for association to COPD and <b>nicotine</b> dependence phenotypes.
+CHRNA3	addiction	dependence	21232152	Genotypes for two SNPs in the <strong>CHRNA3</strong>/5 region (rs8034191, rs1051730) previously associated with nicotine <b>dependence</b> and COPD were analyzed for association to COPD and nicotine <b>dependence</b> phenotypes.
+CHRNA3	drug	nicotine	21232152	Both <strong>CHRNA3</strong>/5 SNPs were associated with FTND in current <b>smokers</b>.
+CHRNA3	drug	nicotine	21232152	An association of genetic variants in <strong>CHRNA3</strong>/5 with severity of emphysema was only found in former <b>smokers</b>, but not in current <b>smokers</b>.
+CHRNA3	drug	nicotine	21228559	An exploratory study on the <strong>CHRNA3</strong> CHRNA5 CHRNB4 cluster, <b>smoking</b>, and Parkinson's disease.
+CHRNA3	drug	nicotine	21228559	Recent genome wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the <strong>CHRNA3</strong> CHRNA5 CHRNB4 cluster on chromosome 15.q25 to <b>smoking</b> behaviors and <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	21228559	Recent genome wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the <strong>CHRNA3</strong> CHRNA5 CHRNB4 cluster on chromosome 15.q25 to smoking behaviors and nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	21228559	Four SNPs in linkage disequilibrium from the <strong>CHRNA3</strong> CHRNA5 CHRNB4 cluster were associated with <b>smoking</b> duration (OR >1.3, p < 0.05).
+CHRNA3	drug	nicotine	21191315	On the basis of known associations with <b>nicotine</b> dependence, we genotyped eight single nucleotide polymorphisms (SNPs) on chromosome 8 (three bins) in the regions of CHRNB3 and CHRNA6, and six SNPs on chromosome 15 (three bins) in the regions of CHRNA5 and <strong>CHRNA3</strong>.
+CHRNA3	addiction	dependence	21191315	On the basis of known associations with nicotine <b>dependence</b>, we genotyped eight single nucleotide polymorphisms (SNPs) on chromosome 8 (three bins) in the regions of CHRNB3 and CHRNA6, and six SNPs on chromosome 15 (three bins) in the regions of CHRNA5 and <strong>CHRNA3</strong>.
+CHRNA3	drug	nicotine	21168125	TTC12 ANKK1 DRD2 and CHRNA5 <strong>CHRNA3</strong> CHRNB4 influence different pathways leading to <b>smoking</b> behavior from adolescence to mid adulthood.
+CHRNA3	drug	nicotine	21168125	CHRNA5 <strong>CHRNA3</strong> CHRNB4 and TTC12 ANKK1 DRD2 gene clusters influence <b>smoking</b> behavior.
+CHRNA3	drug	nicotine	21168125	<strong>CHRNA3</strong> rs1051730[A] was more common among heavy/regular <b>smokers</b> than nonsmokers with similar effect sizes at age 14 years (odds ratio [95% CI]: 1.27 [1.06 1.52]) and 31 years (1.28 [1.13 1.44]).
+CHRNA3	drug	nicotine	21168125	In adolescence, carriers of three four risk alleles at either <strong>CHRNA3</strong> rs1051730 or TTC12 rs10502172 had almost threefold odds of <b>smoking</b> regularly than subjects with no risk alleles.
+CHRNA3	drug	nicotine	21168125	Effect of <strong>CHRNA3</strong> rs1051730 on <b>smoking</b> in adulthood was direct.
+CHRNA3	drug	nicotine	21168125	In contrast, CHRNA5 <strong>CHRNA3</strong> CHRNB4 is involved in the transition toward heavy <b>smoking</b> in mid adulthood and in <b>smoking</b> persistence.
+CHRNA3	drug	alcohol	21048701	Recent human genetic association studies have implicated the gene cluster <strong>CHRNA3</strong> CHRNA5 CHRNB4 encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop nicotine and <b>alcohol</b> dependence; however, their role in <b>ethanol</b> mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNA3	drug	nicotine	21048701	Recent human genetic association studies have implicated the gene cluster <strong>CHRNA3</strong> CHRNA5 CHRNB4 encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop <b>nicotine</b> and alcohol dependence; however, their role in ethanol mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNA3	addiction	dependence	21048701	Recent human genetic association studies have implicated the gene cluster <strong>CHRNA3</strong> CHRNA5 CHRNB4 encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop nicotine and alcohol <b>dependence</b>; however, their role in ethanol mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNA3	drug	alcohol	21048701	Together, these data provide further support for the human genetic association studies, implicating <strong>CHRNA3</strong> and CHRNB4 genes in <b>ethanol</b> mediated behaviors.
+CHRNA3	drug	nicotine	21045689	Recent genome wide association studies have associated single nucleotide polymorphisms spanning the nAChR encoding genes cluster <strong>CHRNA3</strong>/A5/B4 with both <b>nicotine</b> dependence and lung cancer incidence and susceptibility.
+CHRNA3	addiction	dependence	21045689	Recent genome wide association studies have associated single nucleotide polymorphisms spanning the nAChR encoding genes cluster <strong>CHRNA3</strong>/A5/B4 with both nicotine <b>dependence</b> and lung cancer incidence and susceptibility.
+CHRNA3	drug	nicotine	20886544	Risk gene variants for <b>nicotine</b> dependence in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster are associated with cognitive performance.
+CHRNA3	addiction	dependence	20886544	Risk gene variants for nicotine <b>dependence</b> in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster are associated with cognitive performance.
+CHRNA3	drug	nicotine	20886544	Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4 with <b>nicotine</b> dependence (ND).
+CHRNA3	addiction	dependence	20886544	Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4 with nicotine <b>dependence</b> (ND).
+CHRNA3	drug	nicotine	20871796	BACKGROUND: Several studies have found replicable associations between <b>nicotine</b> dependence and specific variants in the nicotinic receptor genes CHRNA5(rs16969968) and <strong>CHRNA3</strong>(rs3743078).
+CHRNA3	addiction	dependence	20871796	BACKGROUND: Several studies have found replicable associations between nicotine <b>dependence</b> and specific variants in the nicotinic receptor genes CHRNA5(rs16969968) and <strong>CHRNA3</strong>(rs3743078).
+CHRNA3	drug	nicotine	20840187	Here we test the hypothesis that the nicotinic receptor genes CHRNA5 (rs16969968), <strong>CHRNA3</strong> (rs578776), CHRNB3 (rs13277254) and CHRND (rs12466358) modify the risk for <b>nicotine</b> dependence associated with peer <b>smoking</b>.
+CHRNA3	addiction	dependence	20840187	Here we test the hypothesis that the nicotinic receptor genes CHRNA5 (rs16969968), <strong>CHRNA3</strong> (rs578776), CHRNB3 (rs13277254) and CHRND (rs12466358) modify the risk for nicotine <b>dependence</b> associated with peer smoking.
+CHRNA3	drug	nicotine	20808433	Multiple genome wide and targeted association studies reveal a significant association of variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 (CHRNA5/A3/B4) gene cluster on chromosome 15 with <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	20808433	Multiple genome wide and targeted association studies reveal a significant association of variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 (CHRNA5/A3/B4) gene cluster on chromosome 15 with nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	20725741	A variant in the 3' untranslated region of <strong>CHRNA3</strong> (rs660652[G]) was significantly associated with 1.7 fold higher odds of lifetime <b>smoking</b> (p < 0.0092), 1.1 unit higher NDS (p < 0.0007), 0.7 more pack years of cigarette <b>smoking</b> (p < 0.0038), and 0.8 more lifetime attempts to quit (p < 0.0084).
+CHRNA3	drug	nicotine	20712524	This study evaluates the relationship of six polymorphisms found in the <strong>CHRNA3</strong>, DRD2 and COMT genes with <b>nicotine</b> dependence, the ability to quit <b>smoking</b> and the occurrence of withdrawal symptoms after short term use of <b>nicotine</b> patch in hospitalized patients.
+CHRNA3	addiction	dependence	20712524	This study evaluates the relationship of six polymorphisms found in the <strong>CHRNA3</strong>, DRD2 and COMT genes with nicotine <b>dependence</b>, the ability to quit smoking and the occurrence of withdrawal symptoms after short term use of nicotine patch in hospitalized patients.
+CHRNA3	addiction	withdrawal	20712524	This study evaluates the relationship of six polymorphisms found in the <strong>CHRNA3</strong>, DRD2 and COMT genes with nicotine dependence, the ability to quit smoking and the occurrence of <b>withdrawal</b> symptoms after short term use of nicotine patch in hospitalized patients.
+CHRNA3	drug	nicotine	20712524	Using a cutoff point for the FTND score, the <strong>CHRNA3</strong> Tyr215Tyr (rs1051730) polymorphism was also associated with <b>nicotine</b> dependence (p = 0.037 and p = 0.074 after correction for multiple testing).
+CHRNA3	addiction	dependence	20712524	Using a cutoff point for the FTND score, the <strong>CHRNA3</strong> Tyr215Tyr (rs1051730) polymorphism was also associated with nicotine <b>dependence</b> (p = 0.037 and p = 0.074 after correction for multiple testing).
+CHRNA3	drug	nicotine	20712524	This study confirms the reported association of the <strong>CHRNA3</strong> locus with <b>nicotine</b> dependence and shows the involvement of two independent DRD2 polymorphisms in <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	20712524	This study confirms the reported association of the <strong>CHRNA3</strong> locus with nicotine <b>dependence</b> and shows the involvement of two independent DRD2 polymorphisms in nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	20700436	Recently, genetic association findings for <b>nicotine</b> dependence, <b>smoking</b> behavior, and <b>smoking</b> related diseases converged to implicate the chromosome 15q25.1 region, which includes the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cholinergic nicotinic receptor subunit genes.
+CHRNA3	addiction	dependence	20700436	Recently, genetic association findings for nicotine <b>dependence</b>, smoking behavior, and smoking related diseases converged to implicate the chromosome 15q25.1 region, which includes the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cholinergic nicotinic receptor subunit genes.
+CHRNA3	drug	nicotine	20631687	Variation in the nicotinic acetylcholine receptor gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4 and its interaction with recent <b>tobacco</b> use influence cognitive flexibility.
+CHRNA3	drug	nicotine	20631687	Variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster have been associated with <b>nicotine</b> dependence (ND) and ND related traits.
+CHRNA3	addiction	dependence	20631687	Variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster have been associated with nicotine <b>dependence</b> (ND) and ND related traits.
+CHRNA3	drug	nicotine	20631687	These findings suggest that variation in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster influences cognitive flexibility differentially in AAs and EAs and that current <b>smoking</b> moderates this effect.
+CHRNA3	drug	nicotine	20584212	Several independent studies show that the chromosome 15q25.1 region, which contains the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, harbors variants strongly associated with <b>nicotine</b> dependence, other <b>smoking</b> behaviors, lung cancer and chronic obstructive pulmonary disease.
+CHRNA3	addiction	dependence	20584212	Several independent studies show that the chromosome 15q25.1 region, which contains the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, harbors variants strongly associated with nicotine <b>dependence</b>, other smoking behaviors, lung cancer and chronic obstructive pulmonary disease.
+CHRNA3	drug	alcohol	20496163	This report explores the association between six nAChR subunit genes (<strong>Chrna3</strong>, Chrna4, Chrnb4, Chrnb2, Chrna5, and Chrna7) with <b>alcohol</b> preference (AP) using co segregation of AP with nAChR subunit genotypes in a F(2) population produced from reciprocal crosses of <b>alcohol</b> preferring C57BL/6J (B6) and <b>alcohol</b> avoiding DBA/2J (D2) strains of mice.
+CHRNA3	drug	nicotine	20393456	Recent human genetic studies also imply that <b>tobacco</b> dependence is affected by polymorphisms in the alpha3/alpha5 subunits of the nAChR (<strong>CHRNA3</strong>/CHRNA5) gene cluster.
+CHRNA3	addiction	dependence	20393456	Recent human genetic studies also imply that tobacco <b>dependence</b> is affected by polymorphisms in the alpha3/alpha5 subunits of the nAChR (<strong>CHRNA3</strong>/CHRNA5) gene cluster.
+CHRNA3	drug	nicotine	19859904	Association and interaction analysis of variants in CHRNA5/<strong>CHRNA3</strong>/CHRNB4 gene cluster with <b>nicotine</b> dependence in African and European Americans.
+CHRNA3	addiction	dependence	19859904	Association and interaction analysis of variants in CHRNA5/<strong>CHRNA3</strong>/CHRNB4 gene cluster with nicotine <b>dependence</b> in African and European Americans.
+CHRNA3	drug	nicotine	19859904	Several previous genome wide and targeted association studies revealed that variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 (CHRNA5/A3/B4) gene cluster on chromosome 15 that encode the alpha5, alpha3, and beta4 subunits of the nicotinic acetylcholine receptors (nAChRs) are associated with <b>nicotine</b> dependence (ND) in European Americans (EAs) or others of European origin.
+CHRNA3	addiction	dependence	19859904	Several previous genome wide and targeted association studies revealed that variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 (CHRNA5/A3/B4) gene cluster on chromosome 15 that encode the alpha5, alpha3, and beta4 subunits of the nicotinic acetylcholine receptors (nAChRs) are associated with nicotine <b>dependence</b> (ND) in European Americans (EAs) or others of European origin.
+CHRNA3	drug	nicotine	19706762	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 nicotinic receptor subunit gene cluster affects risk for <b>nicotine</b> dependence in African Americans and in European Americans.
+CHRNA3	addiction	dependence	19706762	The CHRNA5 <strong>CHRNA3</strong> CHRNB4 nicotinic receptor subunit gene cluster affects risk for nicotine <b>dependence</b> in African Americans and in European Americans.
+CHRNA3	drug	nicotine	19706762	Genetic association studies have shown the importance of variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cholinergic nicotinic receptor subunit gene cluster on chromosome 15q24 25.1 for the risk of <b>nicotine</b> dependence, <b>smoking</b>, and lung cancer in populations of European descent.
+CHRNA3	addiction	dependence	19706762	Genetic association studies have shown the importance of variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cholinergic nicotinic receptor subunit gene cluster on chromosome 15q24 25.1 for the risk of nicotine <b>dependence</b>, smoking, and lung cancer in populations of European descent.
+CHRNA3	drug	nicotine	19706762	The <strong>CHRNA3</strong> SNP rs578776, which has a low correlation with rs16969968, is associated with <b>nicotine</b> dependence in European Americans but not in African Americans.
+CHRNA3	addiction	dependence	19706762	The <strong>CHRNA3</strong> SNP rs578776, which has a low correlation with rs16969968, is associated with nicotine <b>dependence</b> in European Americans but not in African Americans.
+CHRNA3	drug	nicotine	19698703	20 tag SNPs in five <b>nicotine</b> receptor subunit genes (<strong>CHRNA3</strong>, 4, and 6; CHRNB2 and 3) were genotyped and analysed for single marker and haplotype associations.
+CHRNA3	drug	nicotine	19696770	Role of genetic variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster in <b>nicotine</b> dependence risk: importance of gene environment interplay.
+CHRNA3	addiction	dependence	19696770	Role of genetic variants in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 cluster in nicotine <b>dependence</b> risk: importance of gene environment interplay.
+CHRNA3	drug	nicotine	19641473	These findings suggest that SNPs in the <strong>CHRNA3</strong> and CHRNA5 region contribute to lung cancer risk, and while variant alleles are less frequent in African Americans, risk in this group may be greater than in whites and less likely to reflect an indirect effect on lung cancer risk through <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	19641473	These findings suggest that SNPs in the <strong>CHRNA3</strong> and CHRNA5 region contribute to lung cancer risk, and while variant alleles are less frequent in African Americans, risk in this group may be greater than in whites and less likely to reflect an indirect effect on lung cancer risk through nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	19628476	A cluster of three nicotinic acetylcholine receptor genes on chromosome 15 (CHRNA5/<strong>CHRNA3</strong>/CHRNB4) has been shown to be associated with <b>nicotine</b> dependence and <b>smoking</b> quantity.
+CHRNA3	addiction	dependence	19628476	A cluster of three nicotinic acetylcholine receptor genes on chromosome 15 (CHRNA5/<strong>CHRNA3</strong>/CHRNB4) has been shown to be associated with nicotine <b>dependence</b> and smoking quantity.
+CHRNA3	drug	nicotine	19628476	Variation at CHRNA5/<strong>CHRNA3</strong>/CHRNB4 cluster influences <b>nicotine</b> level, measured as cotinine, more strongly than <b>smoking</b> quantity, measured by CPD, and appears thus to be involved in regulation of <b>nicotine</b> levels among <b>smokers</b>.
+CHRNA3	drug	nicotine	19443489	<b>Nicotine</b> dependence risk and lung cancer risk are associated with variants in a region of chromosome 15 encompassing genes encoding the nicotinic receptor subunits CHRNA5, <strong>CHRNA3</strong> and CHRNB4.
+CHRNA3	addiction	dependence	19443489	Nicotine <b>dependence</b> risk and lung cancer risk are associated with variants in a region of chromosome 15 encompassing genes encoding the nicotinic receptor subunits CHRNA5, <strong>CHRNA3</strong> and CHRNB4.
+CHRNA3	drug	nicotine	19429911	A common genetic variant in the 15q24 nicotinic acetylcholine receptor gene cluster (CHRNA5 <strong>CHRNA3</strong> CHRNB4) is associated with a reduced ability of women to quit <b>smoking</b> in pregnancy.
+CHRNA3	drug	nicotine	19429911	A recent genome wide association study demonstrated an association between a common polymorphism (rs1051730) in the nicotinic acetylcholine receptor gene cluster (CHRNA5 <strong>CHRNA3</strong> CHRNB4) and both <b>smoking</b> quantity and <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	19429911	A recent genome wide association study demonstrated an association between a common polymorphism (rs1051730) in the nicotinic acetylcholine receptor gene cluster (CHRNA5 <strong>CHRNA3</strong> CHRNB4) and both smoking quantity and nicotine <b>dependence</b>.
+CHRNA3	drug	nicotine	19247474	In the chr15q25.1 region spanning the nicotinic receptors <strong>CHRNA3</strong> and CHRNA5, we identified multiple SNPs associated with CPD (p<10( 3)), including rs1051730, which has been associated with <b>nicotine</b> dependence, <b>smoking</b> intensity and lung cancer risk.
+CHRNA3	addiction	dependence	19247474	In the chr15q25.1 region spanning the nicotinic receptors <strong>CHRNA3</strong> and CHRNA5, we identified multiple SNPs associated with CPD (p<10( 3)), including rs1051730, which has been associated with nicotine <b>dependence</b>, smoking intensity and lung cancer risk.
+CHRNA3	drug	nicotine	19247474	Besides <strong>CHRNA3</strong> and CHRNA5, MAOA was associated with CPDBI (gene level p<5.4x10( 5)), our analysis provides independent replication of the association between the chr15q25.1 region and <b>smoking</b> intensity and data for multiple other loci associated with <b>smoking</b> behavior that merit further follow up.
+CHRNA3	drug	nicotine	19064933	Genetic association studies indicate that a genetic locus, which includes the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, plays a role in <b>nicotine</b> consumption and dependence.
+CHRNA3	addiction	dependence	19064933	Genetic association studies indicate that a genetic locus, which includes the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster, plays a role in nicotine consumption and <b>dependence</b>.
+CHRNA3	drug	nicotine	19029397	Compared with the most common allele, two separate groups of single nucleotide polymorphisms (SNP) in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster were associated with heavy <b>smoking</b> with a very high statistical significance.
+CHRNA3	drug	nicotine	19029397	Our findings identify two loci in the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster that predict <b>smoking</b> behavior and provide strong evidence for the involvement of the alpha5 nicotinic receptor in heavy <b>smoking</b>.
+CHRNA3	drug	nicotine	19010884	A locus at 15q24/15q25.1, which includes the nicotinic acetylcholine receptor A subunits 3 and 5 (<strong>CHRNA3</strong> and CHRNA5) genes, has recently been associated with lung cancer risk, self reported number of cigarettes smoked per day, and a <b>nicotine</b> dependence scale.
+CHRNA3	addiction	dependence	19010884	A locus at 15q24/15q25.1, which includes the nicotinic acetylcholine receptor A subunits 3 and 5 (<strong>CHRNA3</strong> and CHRNA5) genes, has recently been associated with lung cancer risk, self reported number of cigarettes smoked per day, and a nicotine <b>dependence</b> scale.
+CHRNA3	drug	nicotine	19010884	We used urinary biomarkers to test whether two linked lung cancer risk variants in <strong>CHRNA3</strong> (rs1051730) and CHRNA5 (rs16969968) are associated with intensity of <b>smoking</b> and exposure to a <b>tobacco</b> specific carcinogenic nitrosamine per cigarette dose.
+CHRNA3	drug	nicotine	19010884	Thus, <b>smokers</b> who carry the <strong>CHRNA3</strong> and CHRNA5 variants are expected to be at increased risk for lung cancer compared with <b>smokers</b> who do not carry these alleles even if they smoked the same number of cigarettes.
+CHRNA3	drug	cocaine	18759969	We applied this method to correlated SNPs in the cholinergic nicotinic receptor gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4, in a case control study of <b>cocaine</b> dependence composed of 504 European American and 583 African American samples.
+CHRNA3	addiction	dependence	18759969	We applied this method to correlated SNPs in the cholinergic nicotinic receptor gene cluster CHRNA5 <strong>CHRNA3</strong> CHRNB4, in a case control study of cocaine <b>dependence</b> composed of 504 European American and 583 African American samples.
+CHRNA3	drug	nicotine	18519524	The purpose of this study was to replicate these findings in an independent data set and more thoroughly investigate the role of genetic variation in the cluster of physically linked nicotinic receptors, CHRNA5 <strong>CHRNA3</strong> CHRNB4, and the risk of <b>smoking</b>.
+CHRNA3	drug	nicotine	18414406	Recently a candidate gene study in <b>nicotine</b> dependent cases and nondependent <b>smoking</b> controls reported strong associations between a missense mutation (rs16969968) in exon 5 of the CHRNA5 gene and a variant in the 3' UTR of the <strong>CHRNA3</strong> gene and <b>nicotine</b> dependence.
+CHRNA3	addiction	dependence	18414406	Recently a candidate gene study in nicotine dependent cases and nondependent smoking controls reported strong associations between a missense mutation (rs16969968) in exon 5 of the CHRNA5 gene and a variant in the 3' UTR of the <strong>CHRNA3</strong> gene and nicotine <b>dependence</b>.
+CHRNA3	drug	alcohol	18414406	In this study we performed a comprehensive association analysis of the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster in the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) families to investigate the role of genetic variants in risk for <b>alcohol</b> dependence.
+CHRNA3	addiction	dependence	18414406	In this study we performed a comprehensive association analysis of the CHRNA5 <strong>CHRNA3</strong> CHRNB4 gene cluster in the Collaborative Study on the Genetics of Alcoholism (COGA) families to investigate the role of genetic variants in risk for alcohol <b>dependence</b>.
+CHRNA3	drug	alcohol	18414406	Using the family based association test, we observed that a different group of polymorphisms, spanning CHRNA5 <strong>CHRNA3</strong>, demonstrate association with <b>alcohol</b> dependence defined by Diagnostic and Statistical Manual of Mental Disorders, 4th edn (DSM IV) criteria.
+CHRNA3	addiction	dependence	18414406	Using the family based association test, we observed that a different group of polymorphisms, spanning CHRNA5 <strong>CHRNA3</strong>, demonstrate association with alcohol <b>dependence</b> defined by Diagnostic and Statistical Manual of Mental Disorders, 4th edn (DSM IV) criteria.
+MTOR	addiction	dependence	32656088	Taken together these results highlight the increased <b>dependence</b> of advanced PCa on the <strong>mTOR</strong> pathway, supporting the development of a targeted approach for advanced, bone metastatic PCa.
+MTOR	drug	alcohol	32333810	Chronic Binge <b>Alcohol</b> Exposure During Pregnancy Alters <strong>mTOR</strong> System in Rat Fetal Hippocampus.
+MTOR	addiction	intoxication	32333810	Chronic <b>Binge</b> Alcohol Exposure During Pregnancy Alters <strong>mTOR</strong> System in Rat Fetal Hippocampus.
+MTOR	drug	alcohol	32333810	Based on our previous quantitative mass spectrometry proteomic studies, we hypothesized that gestational chronic binge <b>alcohol</b> exposure alters <strong>mTOR</strong> signaling and downstream pathways in the fetal hippocampus.
+MTOR	addiction	intoxication	32333810	Based on our previous quantitative mass spectrometry proteomic studies, we hypothesized that gestational chronic <b>binge</b> alcohol exposure alters <strong>mTOR</strong> signaling and downstream pathways in the fetal hippocampus.
+MTOR	drug	alcohol	32333810	The phosphorylation level of <strong>mTOR</strong> (P <strong>mTOR</strong>) in the fetal hippocampus was decreased in the <b>Alcohol</b> group compared with controls.
+MTOR	drug	amphetamine	32120831	Lupenone Protects Neuroblastoma SH SY5y Cells Against <b>Methamphetamine</b> Induced Apoptotic Cell Death via PI3K/Akt/<strong>mTOR</strong> Signaling Pathway.
+MTOR	drug	nicotine	32111983	Since FGF19 could be induced by <b>smoking</b> or endoplasmic reticulum stress, to tackle the more malignant FGF19 overproducing LSQ, we reported for the first time that inhibiting <strong>mTOR</strong> pathway by using AZD2014 was effective and feasible.
+MTOR	addiction	sensitization	31785230	Inhibitors against PI3K, AKT and mammalian target of rapamycin (<strong>mTOR</strong>) have remarkable effects on tumor cell proliferation and radiotherapy <b>sensitization</b> in cell cultures and mouse models.
+MTOR	drug	opioid	31756370	Several mechanisms are involved in the tolerance to analgesic <b>opioids</b>, including desensitization or internalization of the <b>opioid</b> receptor, elevation of cAMP levels, microglial activation and neuroinflammation, elevation of spinal <strong>mTOR</strong> activity and change in the expression of some proteins involved in tolerance, such as nNOS.
+MTOR	drug	opioid	31756370	Activation of the AMPK pathway inhibits <strong>mTOR</strong> and p38 MAPK ameliorating neuroinflammation and tolerance induced by <b>morphine</b>.
+MTOR	drug	opioid	31747048	Moreover, <b>morphine</b> treatment significantly increased Beclin 1 expression and decreased the p <strong>mTOR</strong>/<strong>mTOR</strong> and SQSTM1/p62 levels, whereas knockdown of RACK1 prevented <b>morphine</b> induced autophagy in vitro.
+MTOR	drug	opioid	31747048	Furthermore, we found that in the mouse hippocampus, knockdown of RACK1 also markedly suppressed <b>morphine</b> induced autophagy (decreased LC3 II/LC3 I ratio and increased p <strong>mTOR</strong>/<strong>mTOR</strong> ratio).
+MTOR	drug	alcohol	31733664	Results also showed that <b>alcohol</b> use was associated with a general reduction in Akt/<strong>mTOR</strong> signaling via several phosphoproteins (IR, IRS1, IGF1R, PTEN, ERK, <strong>mTOR</strong>, p70S6K, RPS6) in multiple brain regions including hippocampus and entorhinal cortex.
+MTOR	drug	alcohol	31733664	Dysregulation of Akt/<strong>mTOR</strong> phosphoproteins suggests <b>alcohol</b> may target this pathway in AD progression.
+MTOR	drug	alcohol	31733185	To determine the role of adipose autophagy and mechanistic target of rapamycin (<strong>mTOR</strong>) in <b>alcohol</b> induced adipose and liver pathogenesis, we generated adipocyte specific Atg5 knockout (KO), adipocyte specific <strong>mTOR</strong> KO, adipocyte specific Raptor KO, and adipocyte specific tuberous sclerosis complex 1 KO mice by crossing floxed mice with Adipoq Cre.
+MTOR	drug	alcohol	31733185	Chronic plus binge <b>alcohol</b> induced adipose atrophy with increased autophagy and decreased Akt/<strong>mTOR</strong> signaling in epididymal adipose tissue in wild type mice.
+MTOR	addiction	intoxication	31733185	Chronic plus <b>binge</b> alcohol induced adipose atrophy with increased autophagy and decreased Akt/<strong>mTOR</strong> signaling in epididymal adipose tissue in wild type mice.
+MTOR	drug	alcohol	31733185	Adipocyte specific Raptor KO mice experienced exacerbated <b>alcohol</b> induced steatosis, but neither adipocyte specific <strong>mTOR</strong> nor adipocyte specific tuberous sclerosis complex 1 KO mice exhibited similar detrimental effects.
+MTOR	drug	alcohol	31329447	We identified significant protein expression changes in the mechanistic target of rapamycin (<strong>mTOR</strong>) canonical pathway between control and <b>ethanol</b> induced impulsive mice.
+MTOR	drug	alcohol	31167126	<b>Ethanol</b> challenge upregulated autophagy (p < 0.001), promoted AMPK phosphorylation and Sirt1 levels (p < 0.003) while suppressing <strong>mTOR</strong> phosphorylation and Skp2 levels (p < 0.02).
+MTOR	drug	alcohol	31167126	Taken together, our data revealed that CD74 ablation counteracts acute <b>ethanol</b> challenge induced myocardial dysfunction, inflammation and apoptosis possibly through an AMPK <strong>mTOR</strong> Skp2 mediated regulation of autophagy.
+MTOR	drug	psychedelics	31128500	Augmentation effect of <b>ketamine</b> by guanosine in the novelty suppressed feeding test is dependent on <strong>mTOR</strong> signaling pathway.
+MTOR	drug	psychedelics	31128500	Our results suggest that augmentation response of <b>ketamine</b> by guanosine in the NSF test probably involves the activation of <strong>mTOR</strong> signaling, since the treatment with rapamycin (0.2 nmol/site, i.c.v., a selective <strong>mTOR</strong> inhibitor) completely abolished this effect.
+MTOR	addiction	reward	31128500	This augmentation strategy also increased <strong>mTOR</strong> phosphorylation (Ser2448) in the hippocampus, <b>reinforcing</b> the role of <strong>mTOR</strong> in this augmentation response.
+MTOR	drug	psychedelics	31128500	Overall, results provide evidence that guanosine is able to augment the effect of <b>ketamine</b> in the NSF test via <strong>mTOR</strong> activation, a finding that might have therapeutic implications for the management of depression/anxiety.
+MTOR	addiction	addiction	30887859	The <strong>mTOR</strong> signaling pathway regulates protein synthesis processes that have recently been linked to the development of drug <b>addiction</b>.
+MTOR	drug	opioid	30887859	To assess the effects of <b>morphine</b> self administration and its subsequent extinction on the expression of several genes that act in this pathway, and on the levels of specific phosphoproteins (Akt, Gsk3α/β, <strong>mTOR</strong>, PDK1 and p70 S6 kinase) in the amygdala, nucleus accumbens, and the prefrontal cortex.
+MTOR	drug	amphetamine	30574066	Autophagy Induction by HIV Tat and <b>Methamphetamine</b> in Primary Midbrain Neuronal Cells of Tree Shrews via the <strong>mTOR</strong> Signaling and ATG5/ATG7 Pathway.
+MTOR	drug	amphetamine	30574066	In addition, it was found that <strong>mTOR</strong> inhibition via pharmacological intervention could trigger autophagy and promote <b>METH</b> and HIV Tat induced autophagy.
+MTOR	drug	opioid	30547365	Co intraperitoneal injection of rapamycin also attenuated the <b>morphine</b> induced increases in the levels of phosphorylated <strong>mTOR</strong> and its downstream target phosphorylated 4E BP1 in the spinal cord dorsal horn.
+MTOR	drug	opioid	30547365	Systemic <strong>mTOR</strong> inhibitors could serve as promising medications for use as adjuvants with <b>opioids</b> in clinical chronic pain management.
+MTOR	drug	amphetamine	30261225	HIV 1 Tat and <b>methamphetamine</b> co induced oxidative cellular injury is mitigated by N acetylcysteine amide (NACA) through rectifying <strong>mTOR</strong> signaling.
+MTOR	drug	amphetamine	30261225	Collectively, our study shows that NACA protects against <b>Meth</b> and/or Tat induced cellular injury in vitro and in the rat striatum in vivo by attenuating oxidative stress, apoptosis and autophagy, at least in part, via modulation of <strong>mTOR</strong> signaling.
+MTOR	drug	opioid	30179451	What emerged from these studies is the discovery that certain deleterious actions mediated by the κ <b>opioid</b> receptors appear due to specific activation of <strong>mTOR</strong> pathways.
+MTOR	drug	opioid	30146703	Several studies have shown that mammalian target of rapamycin (<strong>mTOR</strong>) plays a crucial role in the development of <b>opioid</b> tolerance.
+MTOR	drug	opioid	30146703	<strong>mTOR</strong> activation suppresses <b>opioid</b> induced antinociception, and its activity has also been increased during <b>opioid</b> tolerance.
+MTOR	drug	alcohol	30130465	In large part, these <b>alcohol</b> induced changes are mediated by a decrease in protein synthesis that in turn is governed by impaired activity of a protein kinase, the mechanistic target of rapamycin (<strong>mTOR</strong>).
+MTOR	drug	alcohol	30130465	Herein, we summarize recent advances in understanding <strong>mTOR</strong> signal transduction, similarities and differences between the effects of <b>alcohol</b> on this central metabolic controller in skeletal muscle and in the heart, and the effects of acute versus chronic <b>alcohol</b> intake.
+MTOR	drug	alcohol	30114398	The current study sought to determine whether binge <b>ethanol</b> exposure induces ER stress in adult mouse brain and the role <strong>mTOR</strong> signaling during this process.
+MTOR	addiction	intoxication	30114398	The current study sought to determine whether <b>binge</b> ethanol exposure induces ER stress in adult mouse brain and the role <strong>mTOR</strong> signaling during this process.
+MTOR	drug	alcohol	30114398	Binge <b>ethanol</b> exposure caused neurodegeneration and neuroinflammation after 5 days of exposure, and a concomitant increase of ER stress and inhibition of <strong>mTOR</strong>.
+MTOR	addiction	intoxication	30114398	<b>Binge</b> ethanol exposure caused neurodegeneration and neuroinflammation after 5 days of exposure, and a concomitant increase of ER stress and inhibition of <strong>mTOR</strong>.
+MTOR	drug	alcohol	30114398	These results suggested that <strong>mTOR</strong> signaling is upstream of ER stress and may thereby mediate <b>ethanol</b> induced ER stress.
+MTOR	drug	opioid	30082888	Phosphoproteomic approach for agonist specific signaling in mouse brains: <strong>mTOR</strong> pathway is involved in κ <b>opioid</b> aversion.
+MTOR	addiction	aversion	30082888	Phosphoproteomic approach for agonist specific signaling in mouse brains: <strong>mTOR</strong> pathway is involved in κ opioid <b>aversion</b>.
+MTOR	addiction	aversion	30082888	Inhibition of the <strong>mTOR</strong> pathway by rapamycin abolished U50,488H induced <b>aversion</b>, without affecting analgesic, anti scratch, and sedative effects and motor incoordination.
+MTOR	addiction	aversion	30082888	The results indicate that the <strong>mTOR</strong> pathway is involved in KOR agonist induced <b>aversion</b>.
+MTOR	addiction	aversion	30082888	Furthermore, this is one of the first two reports that the <strong>mTOR</strong> pathway mediates <b>aversion</b> caused by KOR activation.
+MTOR	addiction	addiction	30061532	This review addresses the role of <strong>mTOR</strong> dependent autophagy dysfunction in a variety of neuropsychiatric disorders, to focus mainly on psychiatric syndromes including schizophrenia and drug <b>addiction</b>.
+MTOR	drug	amphetamine	30061532	For this reason, in the present review, a special emphasis is placed on the role of <strong>mTOR</strong> on <b>methamphetamine</b> induced brain alterations.
+MTOR	addiction	dependence	30044707	Instead, the 2 signals exhibited dynamic alterations in opposite directions, which could be explained by the <b>dependence</b> of MTORC1 (<strong>MTOR</strong> complex 1) activation on TFEB supported lysosome function and the feedback suppression of TFEB by MTORC1.
+MTOR	addiction	aversion	29930108	Thus, we discovered enrichment of the mechanistic target of rapamycin (<strong>mTOR</strong>) pathway by U 50,488H, an agonist causing <b>aversion</b>, which is a typical KOR mediated side effect.
+MTOR	addiction	aversion	29930108	Consequently, <strong>mTOR</strong> inhibition during KOR activation abolished <b>aversion</b> while preserving beneficial antinociceptive and anticonvulsant effects.
+MTOR	drug	alcohol	29864452	With wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with <b>ethanol</b> (3.0 g/kg) for 2 weeks, we show that binge like <b>ethanol</b> exposure in adolescence impairs autophagy machinery by increasing autophagy inhibitor <strong>mTOR</strong> by lowering LC3 II levels and accumulating p62.
+MTOR	addiction	intoxication	29864452	With wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with ethanol (3.0 g/kg) for 2 weeks, we show that <b>binge</b> like ethanol exposure in adolescence impairs autophagy machinery by increasing autophagy inhibitor <strong>mTOR</strong> by lowering LC3 II levels and accumulating p62.
+MTOR	drug	alcohol	29864452	Inhibition of <strong>mTOR</strong>, by rapamycin, restores the levels of excitatory scaffolding synaptic proteins (PSD 95 or SHANK3), p62, and partly reestablishes the LC3 II levels in the prefrontal cortices of <b>ethanol</b> treated WT mice.
+MTOR	drug	alcohol	29782848	Mice were placed on diets of regular <b>ethanol</b> feeding plus an acute binge to induce liver damage (<b>ethanol</b> diet); some mice also were given injections of torin 1, an inhibitor of the kinase activity of the mechanistic target of rapamycin (<strong>mTOR</strong>).
+MTOR	addiction	intoxication	29782848	Mice were placed on diets of regular ethanol feeding plus an acute <b>binge</b> to induce liver damage (ethanol diet); some mice also were given injections of torin 1, an inhibitor of the kinase activity of the mechanistic target of rapamycin (<strong>mTOR</strong>).
+MTOR	drug	alcohol	29782848	Hepatocytes from mice on the <b>ethanol</b> diet had increased translocation of <strong>mTOR</strong> into lysosomes, resulting in increased <strong>mTOR</strong> activation.
+MTOR	drug	alcohol	29782848	Strategies to block <strong>mTOR</strong> activity or increase levels of TFEB might be developed to protect the liver from <b>ethanol</b> induced damage.
+MTOR	drug	amphetamine	29574227	<strong>mTOR</strong> signaling in the nucleus accumbens mediates behavioral sensitization to <b>methamphetamine</b>.
+MTOR	addiction	sensitization	29574227	<strong>mTOR</strong> signaling in the nucleus accumbens mediates behavioral <b>sensitization</b> to methamphetamine.
+MTOR	drug	amphetamine	29574227	The mammalian target of the rapamycin (<strong>mTOR</strong>) signaling pathway, a key regulator of synaptic neuroplasticity, in the ventral striatum of <b>methamphetamine</b> (<b>METH</b>)  sensitized mice was investigated to determine if a link exists with the development of <b>METH</b> sensitization.
+MTOR	addiction	sensitization	29574227	The mammalian target of the rapamycin (<strong>mTOR</strong>) signaling pathway, a key regulator of synaptic neuroplasticity, in the ventral striatum of methamphetamine (METH)  sensitized mice was investigated to determine if a link exists with the development of METH <b>sensitization</b>.
+MTOR	drug	amphetamine	29574227	Behaviorally, <b>METH</b> sensitized mice possessed increased levels of phosphorylated <strong>mTOR</strong>/S2448 and its down stream regulator p70S6K and pS6 in the ventral striatum.
+MTOR	drug	amphetamine	29574227	Systemic treatment with rapamycin, a specific <strong>mTOR</strong> inhibitor, coincident with a daily <b>METH</b> injection suppressed the induction of <b>METH</b> sensitization and reduced the number of dendritic spines in the shell and core of the nucleus accumbens.
+MTOR	addiction	sensitization	29574227	Systemic treatment with rapamycin, a specific <strong>mTOR</strong> inhibitor, coincident with a daily METH injection suppressed the induction of METH <b>sensitization</b> and reduced the number of dendritic spines in the shell and core of the nucleus accumbens.
+MTOR	drug	amphetamine	29574227	The infusion of lentivirus expressing <strong>mTOR</strong> shRNA into the shell region of the nucleus accumbens inhibited the induction of behavioral sensitization to <b>METH</b>, which was comparable to the effect of rapamycin.
+MTOR	addiction	sensitization	29574227	The infusion of lentivirus expressing <strong>mTOR</strong> shRNA into the shell region of the nucleus accumbens inhibited the induction of behavioral <b>sensitization</b> to METH, which was comparable to the effect of rapamycin.
+MTOR	drug	alcohol	29457836	DEP domain containing <strong>mTOR</strong> interacting protein suppresses lipogenesis and ameliorates hepatic steatosis and acute on chronic liver injury in <b>alcoholic</b> liver disease.
+MTOR	drug	alcohol	29457836	Chronic plus binge <b>ethanol</b> feeding led to hyperactivation of mTORC1, as evidenced by increased phosphorylation of <strong>mTOR</strong> and its downstream kinase S6 kinase 1 (S6K1) in hepatocytes.
+MTOR	addiction	intoxication	29457836	Chronic plus <b>binge</b> ethanol feeding led to hyperactivation of mTORC1, as evidenced by increased phosphorylation of <strong>mTOR</strong> and its downstream kinase S6 kinase 1 (S6K1) in hepatocytes.
+MTOR	drug	alcohol	29457836	Aberrant activation of mTORC1 was likely attributed to the defects of the DEP domain containing <strong>mTOR</strong> interacting protein (DEPTOR) and the nicotinamide adenine dinucleotide dependent deacetylase sirtuin 1 (SIRT1) in the liver of chronic plus binge <b>ethanol</b> fed mice and in the liver of patients with ALD.
+MTOR	addiction	intoxication	29457836	Aberrant activation of mTORC1 was likely attributed to the defects of the DEP domain containing <strong>mTOR</strong> interacting protein (DEPTOR) and the nicotinamide adenine dinucleotide dependent deacetylase sirtuin 1 (SIRT1) in the liver of chronic plus <b>binge</b> ethanol fed mice and in the liver of patients with ALD.
+MTOR	drug	alcohol	29408587	Ingenuity analysis identified proteins involved in protein homeostasis, oxidative stress, mitochondrial dysfunction, and <strong>mTOR</strong> as major pathways in the cortex and hippocampus significantly (P < .05) affected by <b>alcohol</b>.
+MTOR	drug	psychedelics	29276735	Dr. Eric Wohleb and Dr. Ron Duman provided new data associating decreased mammalian target of rapamycin (<strong>mTOR</strong>) signaling and neurobiological changes in the synapses in response to chronic unpredictable stress, and highlighted the potential for the novel antidepressant <b>ketamine</b> to rescue synaptic and behavioral effects.
+MTOR	drug	amphetamine	29063964	Although THC can accelerate the onset of schizophrenia, CBD displays antipsychotic properties, can prevent the acquisition of emotionally irrelevant memories, and reverses <b>amphetamine</b> induced neuronal sensitization through selective phosphorylation of the mechanistic target of rapamycin (<strong>mTOR</strong>) molecular signaling pathway.
+MTOR	drug	cannabinoid	29063964	Although <b>THC</b> can accelerate the onset of schizophrenia, CBD displays antipsychotic properties, can prevent the acquisition of emotionally irrelevant memories, and reverses amphetamine induced neuronal sensitization through selective phosphorylation of the mechanistic target of rapamycin (<strong>mTOR</strong>) molecular signaling pathway.
+MTOR	addiction	sensitization	29063964	Although THC can accelerate the onset of schizophrenia, CBD displays antipsychotic properties, can prevent the acquisition of emotionally irrelevant memories, and reverses amphetamine induced neuronal <b>sensitization</b> through selective phosphorylation of the mechanistic target of rapamycin (<strong>mTOR</strong>) molecular signaling pathway.
+MTOR	drug	cocaine	29039413	VTA <strong>mTOR</strong> Signaling Regulates Dopamine Dynamics, <b>Cocaine</b> Induced Synaptic Alterations, and Reward.
+MTOR	addiction	reward	29039413	VTA <strong>mTOR</strong> Signaling Regulates Dopamine Dynamics, Cocaine Induced Synaptic Alterations, and <b>Reward</b>.
+MTOR	drug	cocaine	29039413	The <strong>mTOR</strong> inhibitor rapamycin has been shown to attenuate the behavioral effects of drugs of abuse, including <b>cocaine</b>.
+MTOR	drug	cocaine	29039413	Using viral vectors to selectively delete <strong>mTOR</strong> in the ventral tegmental area (VTA) in adult male mTORloxP/loxP mice, we investigated the role of <strong>mTOR</strong> in regulating neuronal morphology, basal synaptic transmission, dopamine dynamics, and <b>cocaine</b> induced synaptic plasticity and rewarding effects.
+MTOR	drug	cocaine	29039413	Furthermore, <strong>mTOR</strong> deletion attenuated conditioned place preference to <b>cocaine</b> and <b>cocaine</b> induced potentiation of excitation and reduction of GABAergic inhibition in VTA dopamine neurons.
+MTOR	drug	cocaine	29039413	In addition, VTA <strong>mTOR</strong> signaling regulates <b>cocaine</b> cue associative learning and <b>cocaine</b> induced synaptic plasticity in VTA dopamine neurons.
+MTOR	drug	alcohol	28674727	Novel therapeutic targets for correcting <b>alcohol</b> induced osteopenia are also reviewed, such as modulation of proinflammatory cytokines and Wnt and <strong>mTOR</strong> signaling and the application of new drugs.
+MTOR	drug	alcohol	28466267	A single subcutaneous injection of <b>ethanol</b> induced oxidative stress triggered phospho c jun N terminal kinase (p JNK) and phospho mammalian target of rapamycin (p <strong>mTOR</strong>) accompanied by neuroinflammation and widespread neurodegeneration.
+MTOR	drug	cocaine	27899881	New functional pathways were also identified for <b>cocaine</b> modulation (e.g., Rho GTPase signaling) and environmental enrichment (e.g., signaling of EIF2, <strong>mTOR</strong>, ephrin).
+MTOR	drug	opioid	27773571	Deletion of NF1 in striatal neurons prevents the <b>opioid</b> receptor induced activation of Ras and eliminates its coupling to Akt <strong>mTOR</strong> signaling pathway.
+MTOR	drug	psychedelics	27738380	DM exhibited a <b>ketamine</b> like rapid acting antidepressant effect, thought to be mediated by <strong>mTOR</strong> activation (related to NMDA PCP site antagonism, sigma 1 and beta adrenergic receptor stimulation) and 5HTT inhibition, resulting in AMPA receptor trafficking, and dendritogenesis, spinogenesis, synaptogenesis, and increased neuronal survival (related to NMDA antagonism and sigma 1 and <strong>mTOR</strong> signaling).
+MTOR	drug	cocaine	27282818	<strong>mTOR</strong> signalling in the nucleus accumbens shell is critical for augmented effect of TFF3 on behavioural response to <b>cocaine</b>.
+MTOR	drug	cocaine	27282818	TFF3 significantly augmented the increment of the dopamine concentration in the NAc and the activity of the <strong>mTOR</strong> signalling pathway induced by acute <b>cocaine</b> exposure (10 mg/kg, i.p.)
+MTOR	drug	cocaine	27282818	Furthermore, the findings indicated that <strong>mTOR</strong> signalling pathway in the NAc shell is important for TFF3 induced enhancement on the <b>cocaine</b> induced behavioral changes.
+MTOR	drug	amphetamine	27147666	Cannabidiol Counteracts <b>Amphetamine</b> Induced Neuronal and Behavioral Sensitization of the Mesolimbic Dopamine Pathway through a Novel <strong>mTOR</strong>/p70S6 Kinase Signaling Pathway.
+MTOR	drug	cannabinoid	27147666	<b>Cannabidiol</b> Counteracts Amphetamine Induced Neuronal and Behavioral Sensitization of the Mesolimbic Dopamine Pathway through a Novel <strong>mTOR</strong>/p70S6 Kinase Signaling Pathway.
+MTOR	addiction	sensitization	27147666	Cannabidiol Counteracts Amphetamine Induced Neuronal and Behavioral <b>Sensitization</b> of the Mesolimbic Dopamine Pathway through a Novel <strong>mTOR</strong>/p70S6 Kinase Signaling Pathway.
+MTOR	addiction	sensitization	27147666	Specifically, we report that CBD can attenuate both behavioral and dopaminergic neuronal correlates of mesolimbic dopaminergic <b>sensitization</b>, via a direct interaction with <strong>mTOR</strong>/p70S6 kinase signaling within the mesolimbic pathway.
+MTOR	addiction	addiction	27056740	The effects of these drugs of abuse in different animal models of drug reward, dependence and <b>addiction</b> are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (<strong>mTOR</strong>), cyclin dependent kinase 5 (Cdk5), heat shock proteins (Hsp) and other enzymes and proteins.
+MTOR	addiction	dependence	27056740	The effects of these drugs of abuse in different animal models of drug reward, <b>dependence</b> and addiction are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (<strong>mTOR</strong>), cyclin dependent kinase 5 (Cdk5), heat shock proteins (Hsp) and other enzymes and proteins.
+MTOR	addiction	reward	27056740	The effects of these drugs of abuse in different animal models of drug <b>reward</b>, dependence and addiction are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (<strong>mTOR</strong>), cyclin dependent kinase 5 (Cdk5), heat shock proteins (Hsp) and other enzymes and proteins.
+MTOR	drug	alcohol	26773198	Binge <b>alcohol</b> intake decreased mGlu5 levels in females, whereas it decreased indices of phosphoinositide 3 kinase (PI3K), mammalian target of rapamycin (<strong>mTOR</strong>), 4E binding protein 1, and p70 ribosomal protein S6 kinase in males.
+MTOR	addiction	intoxication	26773198	<b>Binge</b> alcohol intake decreased mGlu5 levels in females, whereas it decreased indices of phosphoinositide 3 kinase (PI3K), mammalian target of rapamycin (<strong>mTOR</strong>), 4E binding protein 1, and p70 ribosomal protein S6 kinase in males.
+MTOR	addiction	intoxication	26773198	The functional implication of these differences was investigated in a separate study by inhibiting <strong>mTOR</strong> in the NAC (via infusions of rapamycin) before <b>binge</b> drinking sessions.
+MTOR	drug	alcohol	26773198	Altogether these results highlight that <strong>mTOR</strong> signaling in the NAC was necessary to maintain binge <b>alcohol</b> consumption only in male mice and that binge drinking recruits sexually divergent signaling cascades downstream of PI3K and presumably, Group 1 mGlus.
+MTOR	addiction	intoxication	26773198	Altogether these results highlight that <strong>mTOR</strong> signaling in the NAC was necessary to maintain <b>binge</b> alcohol consumption only in male mice and that <b>binge</b> drinking recruits sexually divergent signaling cascades downstream of PI3K and presumably, Group 1 mGlus.
+MTOR	drug	opioid	26566757	The current study was to examine the underlying mechanisms responsible for the role of mammalian target of rapamycin (<strong>mTOR</strong>) in regulating bone cancer evoked pain and the tolerance of systemic <b>morphine</b>.
+MTOR	addiction	sensitization	26566757	Our data for the first time revealed specific signaling pathways leading to bone cancer pain, including the activation of <strong>mTOR</strong> and PI3K and downstream PKCɛ/PKA, and resultant <b>sensitization</b> of MOR.
+MTOR	drug	cocaine	26314207	Essential role of D1R in the regulation of <strong>mTOR</strong> complex1 signaling induced by <b>cocaine</b>.
+MTOR	drug	cocaine	26314207	The mammalian target of rapamycin (<strong>mTOR</strong>) is a serine/threonine kinase that is involved in neuronal adaptions that underlie <b>cocaine</b> induced sensitization and reward.
+MTOR	addiction	reward	26314207	The mammalian target of rapamycin (<strong>mTOR</strong>) is a serine/threonine kinase that is involved in neuronal adaptions that underlie cocaine induced sensitization and <b>reward</b>.
+MTOR	addiction	sensitization	26314207	The mammalian target of rapamycin (<strong>mTOR</strong>) is a serine/threonine kinase that is involved in neuronal adaptions that underlie cocaine induced <b>sensitization</b> and reward.
+MTOR	drug	cocaine	26314207	Specifically, <b>cocaine</b> treatment increased the phosphorylation on residues Thr2446 and Ser2481 but not on Ser2448 in the nucleus accumbens (NAc) and that this increase in phosphorylated <strong>mTOR</strong> levels was also apparent when complexed with its binding partner Raptor.
+MTOR	drug	cocaine	26314207	Lastly deletion of <strong>mTOR</strong> or Raptor in D1R expressing neurons reduced <b>cocaine</b> induced locomotor activity.
+MTOR	drug	cannabinoid	26283212	<b>Cannabidiol</b>, a <b>Cannabis</b> sativa constituent, inhibits cocaine induced seizures in mice: Possible role of the <strong>mTOR</strong> pathway and reduction in glutamate release.
+MTOR	drug	cocaine	26283212	Cannabidiol, a Cannabis sativa constituent, inhibits <b>cocaine</b> induced seizures in mice: Possible role of the <strong>mTOR</strong> pathway and reduction in glutamate release.
+MTOR	drug	cannabinoid	26283212	Finally, the protective effect of this <b>cannabinoid</b> against cocaine induced seizure was reversed by rapamycin (1 and 5mg/kg), an inhibitor of the mammalian target of rapamycin (<strong>mTOR</strong>) intracellular pathway.
+MTOR	drug	cocaine	26283212	Finally, the protective effect of this cannabinoid against <b>cocaine</b> induced seizure was reversed by rapamycin (1 and 5mg/kg), an inhibitor of the mammalian target of rapamycin (<strong>mTOR</strong>) intracellular pathway.
+MTOR	drug	amphetamine	26271595	Lithium protects against <b>methamphetamine</b> induced neurotoxicity in PC12 cells via Akt/GSK3β/<strong>mTOR</strong> pathway.
+MTOR	addiction	sensitization	26271595	Moreover, GSK3β and <strong>mTOR</strong> are implicated in the locomotor <b>sensitization</b> induced by psychostimulants and <strong>mTOR</strong> plays a critical role in MA induced toxicity.
+MTOR	drug	alcohol	26101849	Importantly, the association between several genetic variants within the mGluR eEF2 AMPAR pathway and <b>alcohol</b> use behavior (i.e., consumption and <b>alcohol</b> related problems) replicated in the Grady Trauma Project (GTP), an independent sample of adults living in Atlanta, Georgia (n = 1034; 95% African American), including individual variants in GRM1, GRM5, EEF2, <strong>MTOR</strong>, GRIA1, GRIA4 and HOMER2 (P < 0.05).
+MTOR	drug	opioid	26096047	Modulation of <strong>mTOR</strong> Activity by μ <b>Opioid</b> Receptor is Dependent upon the Association of Receptor and FK506 Binding Protein 12.
+MTOR	drug	opioid	26096047	Mechanistic/mammalian target of rapamycin (<strong>mTOR</strong>) activation by μ <b>opioid</b> receptor (OPRM1) participates in antinociceptive tolerance, hyperalgesia, and physical dependence.
+MTOR	addiction	dependence	26096047	Mechanistic/mammalian target of rapamycin (<strong>mTOR</strong>) activation by μ opioid receptor (OPRM1) participates in antinociceptive tolerance, hyperalgesia, and physical <b>dependence</b>.
+MTOR	drug	opioid	26096047	OPRM1 activation by <b>morphine</b> induced time dependent <strong>mTOR</strong> activation.
+MTOR	drug	opioid	26096047	However, <b>morphine</b> induced <strong>mTOR</strong> activation was totally blocked at all time points in cells expressing FKBP12 association deficient mutant receptor.
+MTOR	drug	opioid	26096047	FKBP12 knockdown also blocked <b>morphine</b> induced <strong>mTOR</strong> activation.
+MTOR	drug	opioid	26096047	Further analysis demonstrated that <b>morphine</b> treatment enhanced the association of receptor with phosphorylated <strong>mTOR</strong>, whereas decreased association was observed after FKBP12 knockdown, <strong>mTOR</strong> inhibition or in cells expressing FKBP12 association deficient mutant.
+MTOR	drug	alcohol	25759394	This inhibitory effect of <b>alcohol</b> is mediated, at least in part, by a reduction in <strong>mTOR</strong> kinase activity via a mechanism that remains poorly defined but likely involves altered protein protein interactions within <strong>mTOR</strong> complex 1.
+MTOR	drug	alcohol	25759394	Furthermore, <b>alcohol</b> can exacerbate the decrement in <strong>mTOR</strong> and/or muscle protein synthesis present in other catabolic states.
+MTOR	drug	alcohol	25623400	<b>Alcohol</b> intoxication following muscle contraction in mice decreases muscle protein synthesis but not <strong>mTOR</strong> signal transduction.
+MTOR	addiction	intoxication	25623400	Alcohol <b>intoxication</b> following muscle contraction in mice decreases muscle protein synthesis but not <strong>mTOR</strong> signal transduction.
+MTOR	drug	alcohol	25623400	<b>Alcohol</b> (<b>ethanol</b> [EtOH]) intoxication antagonizes stimulation of muscle protein synthesis and mammalian target of rapamycin (<strong>mTOR</strong>) signaling.
+MTOR	addiction	intoxication	25623400	Alcohol (ethanol [EtOH]) <b>intoxication</b> antagonizes stimulation of muscle protein synthesis and mammalian target of rapamycin (<strong>mTOR</strong>) signaling.
+MTOR	drug	alcohol	25257868	<b>Alcohol</b> impairs skeletal muscle protein synthesis and <strong>mTOR</strong> signaling in a time dependent manner following electrically stimulated muscle contraction.
+MTOR	drug	alcohol	25257868	<b>Alcohol</b> (EtOH) decreases protein synthesis and mammalian target of rapamycin (<strong>mTOR</strong>) mediated signaling and blunts the anabolic response to growth factors in skeletal muscle.
+MTOR	addiction	intoxication	25257868	The purpose of the current investigation was to determine whether acute EtOH <b>intoxication</b> antagonizes the contraction induced increase in protein synthesis and <strong>mTOR</strong> signaling in skeletal muscle.
+MTOR	addiction	intoxication	25257868	The stimulation induced increase in the phosphorylation of S6K1 Thr(421)/Ser(424) (20 52%), S6K1 Thr(389) (45 57%), and its substrate rpS6 Ser(240/244) (37 72%) was blunted by EtOH at 30 min, 4 h, and 12 h. Phosphorylation of 4E BP1 Ser(65) was also attenuated by EtOH (61%) at 4 h. Conversely, phosphorylation of extracellular signal regulated kinase Thr(202)/Tyr(204) was increased by stimulation in Control and EtOH mice at 30 min but only in Control at 4 h. Our data indicate that acute EtOH <b>intoxication</b> suppresses muscle protein synthesis for at least 12 h and greatly impairs contraction induced changes in synthesis and <strong>mTOR</strong> signaling.
+MTOR	drug	cocaine	24595501	Reactivation of <b>cocaine</b> reward memory engages the Akt/GSK3/<strong>mTOR</strong> signaling pathway and can be disrupted by GSK3 inhibition.
+MTOR	addiction	reward	24595501	Reactivation of cocaine <b>reward</b> memory engages the Akt/GSK3/<strong>mTOR</strong> signaling pathway and can be disrupted by GSK3 inhibition.
+MTOR	drug	psychedelics	24520403	Also similarly to <b>ketamine</b>, Radix Polygalae appeared to acutely decrease phosphorylation of GluR1 serine 845 in the hippocampus while leaving the phosphorylation of hippocampal <strong>mTOR</strong> serine 2448 unchanged.
+MTOR	addiction	relapse	24103337	These findings suggest that rapamycin could erase the acquired drug CPP in rats, and that <strong>mTOR</strong> activity plays an important role in drug reconsolidation and is required for drug <b>relapse</b>.
+MTOR	addiction	reward	24103337	These findings suggest that rapamycin could erase the acquired drug <b>CPP</b> in rats, and that <strong>mTOR</strong> activity plays an important role in drug reconsolidation and is required for drug relapse.
+MTOR	drug	nicotine	23850638	Serum hs CRP, complement factors (C3 and C4) and <strong>FRAP</strong> levels were significantly higher in the opium <b>smokers</b> (8.93 ± 1.93; 138.47 ± 13.39; 68.79 ± 7.02 and 972.75 ± 11.55, respectively) relative to the control group (0.72 ± 0.09; 93.36 ± 8.73; 33.08 ± 7.39 and 761.95 ± 18.61, respectively).
+MTOR	drug	alcohol	23747720	Cancer cells treated with the plant derived perillyl <b>alcohol</b> (POH) or the mechanistic target of rapamycin (<strong>mTOR</strong>) inhibitor rapamycin dephosphorylate eIF4E binding protein (4E BP1) and attenuate cap dependent translation.
+MTOR	drug	cannabinoid	23727505	This study evaluated the status of <b>cannabinoid</b> (CB) CB1 and CB2 receptors, the endocytic cycle of CB1 receptors, G protein coupled receptor regulatory kinases (GRK), and associated signaling (mammalian target of rapamicin (<strong>mTOR</strong>) and 70kDa ribosomal protein S6 kinase (p70S6K)) in brain cortices of drug abusers and cocaine  and <b>cannabinoid</b> treated rodents.
+MTOR	drug	cocaine	23727505	This study evaluated the status of cannabinoid (CB) CB1 and CB2 receptors, the endocytic cycle of CB1 receptors, G protein coupled receptor regulatory kinases (GRK), and associated signaling (mammalian target of rapamicin (<strong>mTOR</strong>) and 70kDa ribosomal protein S6 kinase (p70S6K)) in brain cortices of drug abusers and <b>cocaine</b>  and cannabinoid treated rodents.
+MTOR	drug	cannabinoid	23727505	<b>Rimonabant</b> and AM281 also behaved as inverse agonists on the activation of <strong>mTOR</strong> and its target p70S6K.
+MTOR	drug	cocaine	23727505	Chronic <b>cocaine</b> in mice was associated with tolerance to the acute activation of <strong>mTOR</strong> and p70S6K.
+MTOR	drug	cocaine	23727505	In long term <b>cocaine</b> addicts, <strong>mTOR</strong> and p70S6K activations were not altered when compared with controls, indicating that CB1 receptor signaling was dampened.
+MTOR	drug	cocaine	23727505	The dysregulation of CB1 receptor, GRK2/3/5, and <strong>mTOR</strong>/p70S6K signaling by <b>cocaine</b> may contribute to alterations of neuroplasticity and/or neurotoxicity in brains of <b>cocaine</b> addicts.
+MTOR	drug	alcohol	23466691	<strong>mTOR</strong> activation is required for the anti <b>alcohol</b> effect of ketamine, but not memantine, in <b>alcohol</b> preferring rats.
+MTOR	drug	psychedelics	23466691	<strong>mTOR</strong> activation is required for the anti alcohol effect of <b>ketamine</b>, but not memantine, in alcohol preferring rats.
+MTOR	drug	alcohol	23466691	Finally, <b>ethanol</b> self administration was assessed in rats administered with either memantine or ketamine but pretreated with the <strong>mTOR</strong> inhibitor rapamycin (2.5mg/kg).
+MTOR	drug	psychedelics	23466691	Finally, ethanol self administration was assessed in rats administered with either memantine or <b>ketamine</b> but pretreated with the <strong>mTOR</strong> inhibitor rapamycin (2.5mg/kg).
+MTOR	drug	psychedelics	23466691	The <strong>mTOR</strong> inhibitor rapamycin blocked the effects of <b>ketamine</b>, but not those of memantine.
+MTOR	drug	psychedelics	23466691	The effects of <b>ketamine</b>, but not memantine, are mediated by <strong>mTOR</strong>.
+MTOR	addiction	relapse	23400686	In multivariate analysis, node positive status, subglottic transglottic location, surgery other than total laryngectomy and <strong>mTOR</strong>/CCND1 mRNA interaction with a hazard ratio of 2.16 (p value for interaction: 0.0010) were independent predictors of <b>relapse</b>, while node positive status and subglottic transglottic location were associated with higher risk for death.
+MTOR	drug	alcohol	22819980	Autophagy was impaired in <b>ethanol</b> treated KI mice compared to KO mice as reflected by a decline in the LC3 II/LC3 I ratio and lower total LC 3 and Beclin 1 levels coupled to increases in P62, pAKT/AKT and <strong>mTOR</strong>.
+MTOR	drug	alcohol	22451512	<b>Ethanol</b> dampened and stimulated, respectively, the phosphorylation of <strong>mTOR</strong> and Raptor, the effects of which were abolished by AMPK deficiency.
+MTOR	drug	opioid	22196333	Role for <strong>mTOR</strong> signaling and neuronal activity in <b>morphine</b> induced adaptations in ventral tegmental area dopamine neurons.
+MTOR	drug	opioid	21392180	Previous studies implicate <strong>mTOR</strong> in regulating stimulant induced sensitization and antidepressive like behavior in rodents, as well as drug craving in abstinent <b>heroin</b> addicts.
+MTOR	addiction	relapse	21392180	Previous studies implicate <strong>mTOR</strong> in regulating stimulant induced sensitization and antidepressive like behavior in rodents, as well as drug <b>craving</b> in abstinent heroin addicts.
+MTOR	addiction	sensitization	21392180	Previous studies implicate <strong>mTOR</strong> in regulating stimulant induced <b>sensitization</b> and antidepressive like behavior in rodents, as well as drug craving in abstinent heroin addicts.
+MTOR	drug	cocaine	21392180	To determine if signaling downstream of <strong>mTOR</strong> is affected by repeated <b>cocaine</b> administration in reward associated brain regions, and if inhibition of <strong>mTOR</strong> alters <b>cocaine</b> induced behavioral plasticity, C57BL/6J mice received four intraperitoneal (i.p.)
+MTOR	addiction	reward	21392180	To determine if signaling downstream of <strong>mTOR</strong> is affected by repeated cocaine administration in <b>reward</b> associated brain regions, and if inhibition of <strong>mTOR</strong> alters cocaine induced behavioral plasticity, C57BL/6J mice received four intraperitoneal (i.p.)
+MTOR	drug	cocaine	21392180	injections of 15 mg/kg <b>cocaine</b> and levels of phosphorylated P70S6 kinase and ribosomal S6 protein two translational regulators directly downstream of <strong>mTOR</strong> were analyzed by immunoblotting across several brain regions.
+MTOR	drug	cocaine	21392180	<b>Cocaine</b> place preference and locomotor sensitization were elicited by four pairings of <b>cocaine</b> with a distinct environment and the effects of <strong>mTOR</strong> inhibition were assessed by pre treating the mice with 10 mg/kg rapamycin, 1 hour prior to: (1) each saline/<b>cocaine</b> conditioning session; (2) a post conditioning test; or (3) a test for locomotor sensitization conducted at 3 weeks withdrawal.
+MTOR	addiction	sensitization	21392180	Cocaine place preference and locomotor <b>sensitization</b> were elicited by four pairings of cocaine with a distinct environment and the effects of <strong>mTOR</strong> inhibition were assessed by pre treating the mice with 10 mg/kg rapamycin, 1 hour prior to: (1) each saline/cocaine conditioning session; (2) a post conditioning test; or (3) a test for locomotor <b>sensitization</b> conducted at 3 weeks withdrawal.
+MTOR	addiction	withdrawal	21392180	Cocaine place preference and locomotor sensitization were elicited by four pairings of cocaine with a distinct environment and the effects of <strong>mTOR</strong> inhibition were assessed by pre treating the mice with 10 mg/kg rapamycin, 1 hour prior to: (1) each saline/cocaine conditioning session; (2) a post conditioning test; or (3) a test for locomotor sensitization conducted at 3 weeks <b>withdrawal</b>.
+MTOR	drug	cocaine	21392180	These findings suggest a role for <strong>mTOR</strong> activity, and perhaps translational control, in the expression of <b>cocaine</b> induced place preference and locomotor sensitization.
+MTOR	addiction	sensitization	21392180	These findings suggest a role for <strong>mTOR</strong> activity, and perhaps translational control, in the expression of cocaine induced place preference and locomotor <b>sensitization</b>.
+MTOR	drug	cocaine	20977929	In the present study, we found that <b>cocaine</b> exposure stimulates <strong>mTOR</strong> activity in rat brain.
+MTOR	drug	cocaine	20977929	Furthermore, inhibition of <strong>mTOR</strong> by rapamycin blocked the induction as well as the expression of <b>cocaine</b> induced locomotor sensitization in rats.
+MTOR	addiction	sensitization	20977929	Furthermore, inhibition of <strong>mTOR</strong> by rapamycin blocked the induction as well as the expression of cocaine induced locomotor <b>sensitization</b> in rats.
+MTOR	drug	cocaine	20977929	These data elucidate a novel mechanism by which the <strong>mTOR</strong> pathway mediates <b>cocaine</b> induced behavioral changes and could suggest a new interventional strategy for drug abuse.
+MTOR	addiction	addiction	20861369	The mammalian target of rapamycin (<strong>mTOR</strong>), a serine/threonine protein kinase that regulates cell growth and survival by controlling translation in response to nutrients and growth factors, has been demonstrated to be involved in neuronal adaptations that underlie drug <b>addiction</b> and learning and memory.
+MTOR	drug	cocaine	20861369	We investigated the potential role of the <strong>mTOR</strong> signaling pathway in relapse to <b>cocaine</b> seeking by using the cue induced reinstatement model in self administering rats.
+MTOR	addiction	relapse	20861369	We investigated the potential role of the <strong>mTOR</strong> signaling pathway in <b>relapse</b> to cocaine <b>seeking</b> by using the cue induced <b>reinstatement</b> model in self administering rats.
+MTOR	drug	cocaine	20861369	We found that exposure to a <b>cocaine</b> related cue induced reinstatement to <b>cocaine</b> seeking and increased phosphorylation of p70s6 kinase (p70s6k) and ribosomal protein s6 (rps6), measures of <strong>mTOR</strong> activity, in the nucleus accumbens (NAc) core but not shell.
+MTOR	addiction	relapse	20861369	We found that exposure to a cocaine related cue induced <b>reinstatement</b> to cocaine <b>seeking</b> and increased phosphorylation of p70s6 kinase (p70s6k) and ribosomal protein s6 (rps6), measures of <strong>mTOR</strong> activity, in the nucleus accumbens (NAc) core but not shell.
+MTOR	drug	cocaine	20861369	These findings indicate that cue induced reinstatement of <b>cocaine</b> seeking is mediated by activation of the <strong>mTOR</strong> signaling pathway in the NAc core.
+MTOR	addiction	relapse	20861369	These findings indicate that cue induced <b>reinstatement</b> of cocaine <b>seeking</b> is mediated by activation of the <strong>mTOR</strong> signaling pathway in the NAc core.
+MTOR	drug	nicotine	20851953	The antiproliferative effects of curcumin were associated with inhibition of the AKT/<strong>MTOR</strong> pathway in presence and absence of <b>nicotine</b>, which also induced this pathway.
+MTOR	drug	nicotine	20851953	This is the first study to demonstrate that curcumin inhibits the adverse effects of <b>nicotine</b> by blocking <b>nicotine</b> induced activation of the AKT/<strong>MTOR</strong> pathway in HNSCC, which retards cell migration.
+MTOR	drug	opioid	20826199	Here, we tested the role of PI3K/Akt <strong>mTOR</strong> p70S6K signaling pathway in <b>morphine</b> induced CPP in the hippocampus.
+MTOR	addiction	reward	20826199	Here, we tested the role of PI3K/Akt <strong>mTOR</strong> p70S6K signaling pathway in morphine induced <b>CPP</b> in the hippocampus.
+MTOR	drug	opioid	20826199	Likewise, levels of phosphorylated <strong>mTOR</strong> and p70S6K were significantly enhanced in the CA3 following <b>morphine</b> CPP.
+MTOR	addiction	reward	20826199	Likewise, levels of phosphorylated <strong>mTOR</strong> and p70S6K were significantly enhanced in the CA3 following morphine <b>CPP</b>.
+MTOR	addiction	reward	20826199	More importantly, microinjection of PI3K inhibitor (LY294002) or <strong>mTOR</strong> inhibitor (Rapamycin) into the CA3 prevented the acquisition of <b>CPP</b> and inhibited the activation of PI3K Akt signaling pathway.
+MTOR	drug	alcohol	20237068	Acute <b>alcohol</b> intoxication decreases skeletal muscle protein synthesis by impairing mammalian target of rapamycin (<strong>mTOR</strong>).
+MTOR	addiction	intoxication	20237068	Acute alcohol <b>intoxication</b> decreases skeletal muscle protein synthesis by impairing mammalian target of rapamycin (<strong>mTOR</strong>).
+MTOR	drug	alcohol	20237068	<b>Alcohol</b> decreased protein synthesis in WT mice, a change associated with less 4EBP1 phosphorylation, eIF4E eIF4G binding, and raptor 4EBP1 binding, but greater <strong>mTOR</strong> raptor complex formation.
+MTOR	drug	alcohol	19154606	<b>Alcohol</b> induced decrease in muscle protein synthesis associated with increased binding of <strong>mTOR</strong> and raptor: Comparable effects in young and mature rats.
+MTOR	drug	alcohol	19154606	Acute <b>alcohol</b> (EtOH) intoxication decreases muscle protein synthesis via inhibition of <strong>mTOR</strong> dependent translation initiation.
+MTOR	addiction	intoxication	19154606	Acute alcohol (EtOH) <b>intoxication</b> decreases muscle protein synthesis via inhibition of <strong>mTOR</strong> dependent translation initiation.
+MTOR	drug	alcohol	18336631	The mechanism by which acute <b>alcohol</b> (EtOH) intoxication decreases basal muscle protein synthesis via inhibition of the Ser/Thr kinase mammalian target of rapamycin (<strong>mTOR</strong>) is poorly defined.
+MTOR	addiction	intoxication	18336631	The mechanism by which acute alcohol (EtOH) <b>intoxication</b> decreases basal muscle protein synthesis via inhibition of the Ser/Thr kinase mammalian target of rapamycin (<strong>mTOR</strong>) is poorly defined.
+MTOR	drug	alcohol	15608593	Furthermore, the mRNA expression of heat shock proteins, myristoylated alanine rich protein kinase C substrate, phosphatase and tensin homolog deleted on chromosome 10, and FK506 binding protein rapamycin associated protein (FKBP) (<strong>mTOR</strong>) was also decreased in <b>ethanol</b> treated cortical neurons.
+MTOR	drug	alcohol	15608593	Our results indicate that chronic <b>ethanol</b> treatment of cortical neurons resulted in decreased mRNA expression of genes involving the ubiquitin proteasome pathway and ribosomal proteins together with <strong>mTOR</strong> expression leading to disruption of protein degradation mechanism and impairment of protein synthesis machinery.
+MTOR	drug	nicotine	15473763	The fluorescence recovery after photobleaching (<strong>FRAP</strong>) method and the fluorescence correlation spectroscopy (FCS) have been applied on suspensions of highly charged colloidal spheres with a small content of rod shaped <b>tobacco</b> mosaic virus (TMV) particles.
+MTOR	addiction	dependence	15473763	Thus a comparison of the results that were obtained by FCS and <strong>FRAP</strong>, in combination with Brownian Dynamics simulations, gives insight into the time <b>dependence</b> of the self diffusion coefficient of an interacting colloidal system.
+MTOR	drug	alcohol	15388509	Acute <b>alcohol</b> intoxication enhances myocardial eIF4G phosphorylation despite reducing <strong>mTOR</strong> signaling.
+MTOR	addiction	intoxication	15388509	Acute alcohol <b>intoxication</b> enhances myocardial eIF4G phosphorylation despite reducing <strong>mTOR</strong> signaling.
+MTOR	drug	alcohol	15388509	The purpose of the present set of experiments was to determine whether acute <b>alcohol</b> intoxication alters the phosphorylation state of eukaryotic initiation factor (eIF) 4G, eIF4G.eIF4E complex formation, and the mammalian target of rapamycin (<strong>mTOR</strong>) signaling pathway in the heart.
+MTOR	addiction	intoxication	15388509	The purpose of the present set of experiments was to determine whether acute alcohol <b>intoxication</b> alters the phosphorylation state of eukaryotic initiation factor (eIF) 4G, eIF4G.eIF4E complex formation, and the mammalian target of rapamycin (<strong>mTOR</strong>) signaling pathway in the heart.
+MTOR	drug	alcohol	15388509	Phosphorylation of 4E BP1 and S6 kinase 1 (Thr(389)), downstream targets of <strong>mTOR</strong>, were also reduced after acute <b>alcohol</b> administration.
+MTOR	drug	alcohol	15388509	These data suggest that acute <b>alcohol</b> induced impairments in myocardial mRNA translation initiation result, in part, from marked decreases in eIF4G.eIF4E complex formation, which appear to be independent of changes in phosphorylation of eIF4G but dependent on <strong>mTOR</strong>.
+MTOR	drug	alcohol	12944322	<b>Alcohol</b> impairs leucine mediated phosphorylation of 4E BP1, S6K1, eIF4G, and <strong>mTOR</strong> in skeletal muscle.
+MTOR	drug	alcohol	12944322	Hence, <b>ethanol</b> produces a leucine resistance in skeletal muscle, as evidenced by the impaired phosphorylation of 4E BP1, eIF4G, S6K1, and <strong>mTOR</strong>, that is independent of elevations in endogenous glucocorticoids.
+POMC	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous opioid peptide precursors including proopiomelanocortin (<strong>Pomc</strong>), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+POMC	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous <b>opioid</b> peptide precursors including proopiomelanocortin (<strong>Pomc</strong>), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+POMC	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous opioid peptide precursors including <strong>proopiomelanocortin</strong> (<strong>Pomc</strong>), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+POMC	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous <b>opioid</b> peptide precursors including <strong>proopiomelanocortin</strong> (<strong>Pomc</strong>), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+POMC	drug	cocaine	32730947	In the CPu, <b>cocaine</b> self administration significantly increased the mRNA levels of Penk and Pdyn and abolished the mRNA levels of <strong>Pomc</strong>.
+POMC	drug	cocaine	32730947	In the PFC, <b>cocaine</b> self administration only increased Pdyn mRNA levels without changing the mRNA levels of <strong>Pomc</strong> and Penk.
+POMC	drug	opioid	32487735	Since then, ~20 peptides with <b>opioid</b> receptor activity have been discovered, all of which are generated from three precursors (proenkephalin, prodynorphin, and <strong>proopiomelanocortin</strong>) by sequential proteolytic processing by prohormone convertases and carboxypeptidase E. Each of these peptides bind to all three of the <b>opioid</b> receptor types (mu, delta, kappa), albeit with differing affinities.
+POMC	drug	opioid	32393639	It is generally thought that the three types of <b>opioid</b> receptors (μ, δ, κ) are activated by endogenous peptides derived from three different precursors: <strong>Proopiomelanocortin</strong>, proenkephalin, and prodynorphin.
+POMC	drug	opioid	32387350	The dopamine  and <b>opioid</b> related gene expression in central reward system and <strong>POMC</strong> expression in hypothalamus was elevated in these adult offspring.
+POMC	addiction	reward	32387350	The dopamine  and opioid related gene expression in central <b>reward</b> system and <strong>POMC</strong> expression in hypothalamus was elevated in these adult offspring.
+POMC	drug	alcohol	32353460	Likewise, genes associated with HPA axis activity were not significantly changed by <b>ethanol</b> drinking [i.e., corticotrophin releasing hormone (Crh), adrenocorticotrophic hormone (Acth), and proopiomelanocortin (<strong>Pomc</strong>)] in these brain regions.
+POMC	drug	alcohol	32353460	Likewise, genes associated with HPA axis activity were not significantly changed by <b>ethanol</b> drinking [i.e., corticotrophin releasing hormone (Crh), adrenocorticotrophic hormone (Acth), and <strong>proopiomelanocortin</strong> (<strong>Pomc</strong>)] in these brain regions.
+POMC	drug	alcohol	32304714	<b>Ethanol</b> has concentration dependent effects on hypothalamic <strong>POMC</strong> neuronal excitability.
+POMC	addiction	reward	32304714	One particular component of this system consists of pro opiomelanocortin (<strong>POMC</strong>)  producing neurons in the arcuate nucleus (ArcN) of the hypothalamus, which project to <b>reward</b> related brain areas.
+POMC	drug	alcohol	32304714	To identify the physiological effects of <b>ethanol</b> on ArcN <strong>POMC</strong> neurons, we utilized whole cell patch clamp recordings and bath application of <b>ethanol</b> (5 40 mM) to identify alterations in spontaneous baseline activity, rheobase, spiking characteristics, or intrinsic neuronal properties.
+POMC	drug	alcohol	32304714	Interestingly, we found that basal firing rates of ArcN <strong>POMC</strong> neurons may predict physiological responding to <b>ethanol</b>.
+POMC	drug	alcohol	32304714	These results suggest that <b>ethanol</b> has concentration dependent modulatory effects on ArcN <strong>POMC</strong> neuronal activity, which may be relevant to treatments for <b>alcohol</b> use disorders that target endogenous opioid systems.
+POMC	drug	opioid	32304714	These results suggest that ethanol has concentration dependent modulatory effects on ArcN <strong>POMC</strong> neuronal activity, which may be relevant to treatments for alcohol use disorders that target endogenous <b>opioid</b> systems.
+POMC	drug	opioid	31940647	In particular, adrenocorticotropic hormone (ACTH) and cortisol secretion, as well as satiety regulating <strong>proopiomelanocortin</strong> peptides α melanocyte stimulating hormone (MSH) and β endorphin (END) in a cohort of <b>opioid</b> dependent patients in diamorphine maintenance treatment concerning the clinical severity of their childhood trauma.
+POMC	addiction	reward	31474426	Saliva underwent transcriptomic analysis for 4 select genes involved in homeostatic and <b>hedonic</b> feeding regulation (neuropeptide Y2 receptor [NPY2R], proopiomelanocortin [<strong>POMC</strong>], leptin receptor [LEPR], dopamine type 2 receptor [DRD2]).
+POMC	addiction	reward	31474426	Saliva underwent transcriptomic analysis for 4 select genes involved in homeostatic and <b>hedonic</b> feeding regulation (neuropeptide Y2 receptor [NPY2R], <strong>proopiomelanocortin</strong> [<strong>POMC</strong>], leptin receptor [LEPR], dopamine type 2 receptor [DRD2]).
+POMC	drug	alcohol	31339663	Nuclear transcriptional changes in hypothalamus of <strong>Pomc</strong> enhancer knockout mice after excessive <b>alcohol</b> drinking.
+POMC	drug	alcohol	31339663	Persistent alterations of proopiomelanocortin (<strong>Pomc</strong>) and mu opioid receptor (Oprm1) activity and stress responses after <b>alcohol</b> are critically involved in vulnerability to <b>alcohol</b> dependency.
+POMC	drug	opioid	31339663	Persistent alterations of proopiomelanocortin (<strong>Pomc</strong>) and mu <b>opioid</b> receptor (Oprm1) activity and stress responses after alcohol are critically involved in vulnerability to alcohol dependency.
+POMC	drug	alcohol	31339663	Persistent alterations of <strong>proopiomelanocortin</strong> (<strong>Pomc</strong>) and mu opioid receptor (Oprm1) activity and stress responses after <b>alcohol</b> are critically involved in vulnerability to <b>alcohol</b> dependency.
+POMC	drug	opioid	31339663	Persistent alterations of <strong>proopiomelanocortin</strong> (<strong>Pomc</strong>) and mu <b>opioid</b> receptor (Oprm1) activity and stress responses after alcohol are critically involved in vulnerability to alcohol dependency.
+POMC	drug	alcohol	31339663	Mice with genome wide deletion of neuronal <strong>Pomc</strong> enhancer1 (nPE1 / ), had hypothalamic specific partial reductions of beta endorphin and displayed lower <b>alcohol</b> consumption, compared to wildtype littermates (nPE1+/+).
+POMC	drug	alcohol	31339663	nPE1 /  had lower basal <strong>Pomc</strong> and Pdyn (prodynorphin) levels compared to nPE1+/+ , coupled with increased basal Oprm1 and Oprk1 (kappa opioid receptor) levels, and low <b>alcohol</b> drinking increased <strong>Pomc</strong> and Pdyn to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and Oprk1.
+POMC	drug	opioid	31339663	nPE1 /  had lower basal <strong>Pomc</strong> and Pdyn (prodynorphin) levels compared to nPE1+/+ , coupled with increased basal Oprm1 and Oprk1 (kappa <b>opioid</b> receptor) levels, and low alcohol drinking increased <strong>Pomc</strong> and Pdyn to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and Oprk1.
+POMC	drug	alcohol	31339663	In nPE1+/+ , excessive <b>alcohol</b> intake increased <strong>Pomc</strong> and Oprm1, with no effect on Pdyn or Oprk1.
+POMC	drug	alcohol	31329297	We have recently shown that binge or heavy levels of <b>alcohol</b> drinking increase deoxyribonucleic acid (DNA) methylation and reduce gene expression of proopiomelanocortin (<strong>POMC</strong>) and period 2 (PER2) in adult human subjects (Gangisetty et al., <b>Alcohol</b> Clin Exp Res, 43, 2019, 212).
+POMC	addiction	intoxication	31329297	We have recently shown that <b>binge</b> or heavy levels of alcohol drinking increase deoxyribonucleic acid (DNA) methylation and reduce gene expression of proopiomelanocortin (<strong>POMC</strong>) and period 2 (PER2) in adult human subjects (Gangisetty et al., Alcohol Clin Exp Res, 43, 2019, 212).
+POMC	drug	alcohol	31329297	We have recently shown that binge or heavy levels of <b>alcohol</b> drinking increase deoxyribonucleic acid (DNA) methylation and reduce gene expression of <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and period 2 (PER2) in adult human subjects (Gangisetty et al., <b>Alcohol</b> Clin Exp Res, 43, 2019, 212).
+POMC	addiction	intoxication	31329297	We have recently shown that <b>binge</b> or heavy levels of alcohol drinking increase deoxyribonucleic acid (DNA) methylation and reduce gene expression of <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and period 2 (PER2) in adult human subjects (Gangisetty et al., Alcohol Clin Exp Res, 43, 2019, 212).
+POMC	drug	alcohol	31329297	We conducted a series of studies to determine DNA methylation changes in stress regulatory genes proopiomelanocortin (<strong>POMC</strong>) and period 2 (PER2) using biological samples from 3 separate cohorts of patients: (i) pregnant women who consumed moderate to high levels of <b>alcohol</b> or low/unexposed controls, (ii) children with PAE and non <b>alcohol</b> exposed controls, and (iii) children with PAE treated with or without choline.
+POMC	drug	alcohol	31329297	We conducted a series of studies to determine DNA methylation changes in stress regulatory genes <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and period 2 (PER2) using biological samples from 3 separate cohorts of patients: (i) pregnant women who consumed moderate to high levels of <b>alcohol</b> or low/unexposed controls, (ii) children with PAE and non <b>alcohol</b> exposed controls, and (iii) children with PAE treated with or without choline.
+POMC	drug	alcohol	31329297	We found pregnant women who consumed moderate to high levels of <b>alcohol</b> and gave birth to PAE children had higher DNA methylation of <strong>POMC</strong> and PER2.
+POMC	drug	nicotine	31329297	The differences in the gene methylation of PER2 and <strong>POMC</strong> between PAE and controls did not differ by maternal <b>smoking</b> status.
+POMC	drug	alcohol	31117084	<b>Alcohol</b> Withdrawal and <strong>Proopiomelanocortin</strong> Neuropeptides in an Animal Model of <b>Alcohol</b> Dependence.
+POMC	addiction	dependence	31117084	Alcohol Withdrawal and <strong>Proopiomelanocortin</strong> Neuropeptides in an Animal Model of Alcohol <b>Dependence</b>.
+POMC	addiction	withdrawal	31117084	Alcohol <b>Withdrawal</b> and <strong>Proopiomelanocortin</strong> Neuropeptides in an Animal Model of Alcohol Dependence.
+POMC	drug	alcohol	31117084	Many studies suppose the hypothalamic pituitary adrenal axis, especially the proopiomelanocortin (<strong>POMC</strong>) derived neuropeptides, to mediate craving during withdrawal in <b>alcohol</b> dependence.
+POMC	addiction	dependence	31117084	Many studies suppose the hypothalamic pituitary adrenal axis, especially the proopiomelanocortin (<strong>POMC</strong>) derived neuropeptides, to mediate craving during withdrawal in alcohol <b>dependence</b>.
+POMC	addiction	relapse	31117084	Many studies suppose the hypothalamic pituitary adrenal axis, especially the proopiomelanocortin (<strong>POMC</strong>) derived neuropeptides, to mediate <b>craving</b> during withdrawal in alcohol dependence.
+POMC	addiction	withdrawal	31117084	Many studies suppose the hypothalamic pituitary adrenal axis, especially the proopiomelanocortin (<strong>POMC</strong>) derived neuropeptides, to mediate craving during <b>withdrawal</b> in alcohol dependence.
+POMC	drug	alcohol	31117084	Many studies suppose the hypothalamic pituitary adrenal axis, especially the <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) derived neuropeptides, to mediate craving during withdrawal in <b>alcohol</b> dependence.
+POMC	addiction	dependence	31117084	Many studies suppose the hypothalamic pituitary adrenal axis, especially the <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) derived neuropeptides, to mediate craving during withdrawal in alcohol <b>dependence</b>.
+POMC	addiction	relapse	31117084	Many studies suppose the hypothalamic pituitary adrenal axis, especially the <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) derived neuropeptides, to mediate <b>craving</b> during withdrawal in alcohol dependence.
+POMC	addiction	withdrawal	31117084	Many studies suppose the hypothalamic pituitary adrenal axis, especially the <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) derived neuropeptides, to mediate craving during <b>withdrawal</b> in alcohol dependence.
+POMC	drug	alcohol	31117084	Evidence is available that the two <strong>POMC</strong> proteins, α melanocyte stimulating hormone (α MSH) and β endorphin (β END) are altered by <b>alcohol</b> consumption and influence <b>alcohol</b> consumption, respectively.
+POMC	drug	amphetamine	30929417	Lorcaserin stimulates proopiomelanocortin (<strong>POMC</strong>)/cocaine  and <b>amphetamine</b> regulated transcript (CART) neurons and inhibits neuropeptide Y (NPY)/agouti related peptide (AgRP) neurons, which results in the activation of melanocortin 3/4 receptors.
+POMC	drug	cocaine	30929417	Lorcaserin stimulates proopiomelanocortin (<strong>POMC</strong>)/<b>cocaine</b>  and amphetamine regulated transcript (CART) neurons and inhibits neuropeptide Y (NPY)/agouti related peptide (AgRP) neurons, which results in the activation of melanocortin 3/4 receptors.
+POMC	drug	amphetamine	30929417	Lorcaserin stimulates <strong>proopiomelanocortin</strong> (<strong>POMC</strong>)/cocaine  and <b>amphetamine</b> regulated transcript (CART) neurons and inhibits neuropeptide Y (NPY)/agouti related peptide (AgRP) neurons, which results in the activation of melanocortin 3/4 receptors.
+POMC	drug	cocaine	30929417	Lorcaserin stimulates <strong>proopiomelanocortin</strong> (<strong>POMC</strong>)/<b>cocaine</b>  and amphetamine regulated transcript (CART) neurons and inhibits neuropeptide Y (NPY)/agouti related peptide (AgRP) neurons, which results in the activation of melanocortin 3/4 receptors.
+POMC	drug	alcohol	30929417	<b>Naltrexone</b>/bupropion stimulates <strong>POMC</strong> neurons through bupropion; this stimulation is augmented by blocking the autoinhibitory mechanism of <strong>POMC</strong> with <b>naltrexone</b>.
+POMC	addiction	reward	30929417	The hypophagic effect of liraglutide is mediated through the direct activation of <strong>POMC</strong>/CART neurons and the indirect suppression of NPY/AgRP neurons through γ aminobutyric acid dependent signaling, with adjunctive suppression of the mesolimbic dopamine <b>reward</b> system.
+POMC	drug	alcohol	30908671	Neuronal <strong>proopiomelanocortin</strong> enhancer (nPE) knockout mice with brain specific deficiency of beta endorphin (endogenous ligand of MOP r) were used as a genetic control for the <b>naltrexone</b> effects.
+POMC	drug	alcohol	30597578	Hypermethylation of <strong>Proopiomelanocortin</strong> and Period 2 Genes in Blood Are Associated with Greater Subjective and Behavioral Motivation for <b>Alcohol</b> in Humans.
+POMC	drug	alcohol	30597578	Methylation specific polymerase chain reaction (PCR) assays were used to measure changes in gene methylation of period 2 (PER2) and proopiomelanocortin (<strong>POMC</strong>) genes in peripheral blood samples collected from nonsmoking moderate, nonbinging, binge, and heavy social drinkers who participated in a 3 day behavioral <b>alcohol</b> motivation experiment of imagery exposure to either stress, neutral, or <b>alcohol</b> related cues, 1 per day, presented on consecutive days in counterbalanced order.
+POMC	addiction	intoxication	30597578	Methylation specific polymerase chain reaction (PCR) assays were used to measure changes in gene methylation of period 2 (PER2) and proopiomelanocortin (<strong>POMC</strong>) genes in peripheral blood samples collected from nonsmoking moderate, nonbinging, <b>binge</b>, and heavy social drinkers who participated in a 3 day behavioral alcohol motivation experiment of imagery exposure to either stress, neutral, or alcohol related cues, 1 per day, presented on consecutive days in counterbalanced order.
+POMC	drug	alcohol	30597578	Methylation specific polymerase chain reaction (PCR) assays were used to measure changes in gene methylation of period 2 (PER2) and <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) genes in peripheral blood samples collected from nonsmoking moderate, nonbinging, binge, and heavy social drinkers who participated in a 3 day behavioral <b>alcohol</b> motivation experiment of imagery exposure to either stress, neutral, or <b>alcohol</b> related cues, 1 per day, presented on consecutive days in counterbalanced order.
+POMC	addiction	intoxication	30597578	Methylation specific polymerase chain reaction (PCR) assays were used to measure changes in gene methylation of period 2 (PER2) and <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) genes in peripheral blood samples collected from nonsmoking moderate, nonbinging, <b>binge</b>, and heavy social drinkers who participated in a 3 day behavioral alcohol motivation experiment of imagery exposure to either stress, neutral, or alcohol related cues, 1 per day, presented on consecutive days in counterbalanced order.
+POMC	addiction	intoxication	30597578	In the sample of moderate, <b>binge</b>, and heavy drinkers, we found increased methylation of the PER2 and <strong>POMC</strong> DNA, reduced expression of these genes in the blood samples of the <b>binge</b> and heavy drinkers relative to the moderate, nonbinge drinkers.
+POMC	drug	alcohol	30597578	Increased PER2 and <strong>POMC</strong> DNA methylation was also significantly predictive of both increased levels of subjective <b>alcohol</b> craving immediately following imagery (p < 0.0001), and with presentation of the <b>alcohol</b> (2 beers) (p < 0.0001) prior to the ATT, as well as with <b>alcohol</b> amount consumed during the ATT (p < 0.003).
+POMC	addiction	relapse	30597578	Increased PER2 and <strong>POMC</strong> DNA methylation was also significantly predictive of both increased levels of subjective alcohol <b>craving</b> immediately following imagery (p < 0.0001), and with presentation of the alcohol (2 beers) (p < 0.0001) prior to the ATT, as well as with alcohol amount consumed during the ATT (p < 0.003).
+POMC	drug	alcohol	30597578	These data establish significant association between binge or heavy levels of <b>alcohol</b> drinking and elevated levels of methylation and reduced levels of expression of <strong>POMC</strong> and PER2 genes.
+POMC	addiction	intoxication	30597578	These data establish significant association between <b>binge</b> or heavy levels of alcohol drinking and elevated levels of methylation and reduced levels of expression of <strong>POMC</strong> and PER2 genes.
+POMC	drug	alcohol	30597578	Furthermore, elevated methylation of <strong>POMC</strong> and PER2 genes is associated with greater subjective and behavioral motivation for <b>alcohol</b>.
+POMC	drug	cocaine	30506236	Levels of <strong>POMC</strong> in the arcuate nucleus were elevated in Mor F1 males compared to Sal F1 males, a main effect driven primarily by <strong>POMC</strong> levels in the acute <b>cocaine</b> condition.
+POMC	drug	amphetamine	30396596	Finally, rats were sacrificed and agouti related peptide (AgRP), neuropeptide Y (NPY), pro opiomelanocortin (<strong>POMC</strong>) and cocaine  and <b>amphetamine</b> regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+POMC	drug	cocaine	30396596	Finally, rats were sacrificed and agouti related peptide (AgRP), neuropeptide Y (NPY), pro opiomelanocortin (<strong>POMC</strong>) and <b>cocaine</b>  and amphetamine regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+POMC	drug	opioid	30171993	<b>Opioid</b> related genes, including OPRM1, OPRD1, OPRK1, and <strong>POMC</strong>, are obvious candidates for HD.
+POMC	addiction	aversion	29911992	Furthermore, activation of arcuate nucleus <strong>proopiomelanocortin</strong> neurons projecting to the ventral striatum increased the activity of striatal neurons in an MC4R dependent manner and elicited <b>aversion</b>.
+POMC	drug	nicotine	29871818	Epigenetic alterations of the <strong>POMC</strong> promoter in <b>tobacco</b> dependence.
+POMC	addiction	dependence	29871818	Epigenetic alterations of the <strong>POMC</strong> promoter in tobacco <b>dependence</b>.
+POMC	drug	nicotine	29871818	<b>Smoking</b> interferes with HPA axis by activating proopiomelanocortin (<strong>POMC</strong>) neurons and thus stimulating the expression of <strong>POMC</strong>.
+POMC	drug	nicotine	29871818	<b>Smoking</b> interferes with HPA axis by activating <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) neurons and thus stimulating the expression of <strong>POMC</strong>.
+POMC	drug	alcohol	29871818	In <b>alcohol</b> dependence, <strong>POMC</strong> promoter methylation is associated with craving.
+POMC	addiction	dependence	29871818	In alcohol <b>dependence</b>, <strong>POMC</strong> promoter methylation is associated with craving.
+POMC	addiction	relapse	29871818	In alcohol dependence, <strong>POMC</strong> promoter methylation is associated with <b>craving</b>.
+POMC	drug	nicotine	29871818	Here, we describe evidence of altered <strong>POMC</strong> promoter methylation in <b>smoking</b>.
+POMC	drug	nicotine	29871818	To determine how <b>tobacco</b> dependence and its withdrawal affect <strong>POMC</strong> promoter specific DNA methylation, we assessed blood samples of 36 <b>tobacco</b> dependent individuals at day 1, 7 and 14 of withdrawal compared to 41 healthy controls using direct bisulfite sequencing.
+POMC	addiction	dependence	29871818	To determine how tobacco <b>dependence</b> and its withdrawal affect <strong>POMC</strong> promoter specific DNA methylation, we assessed blood samples of 36 tobacco dependent individuals at day 1, 7 and 14 of withdrawal compared to 41 healthy controls using direct bisulfite sequencing.
+POMC	addiction	withdrawal	29871818	To determine how tobacco dependence and its <b>withdrawal</b> affect <strong>POMC</strong> promoter specific DNA methylation, we assessed blood samples of 36 tobacco dependent individuals at day 1, 7 and 14 of <b>withdrawal</b> compared to 41 healthy controls using direct bisulfite sequencing.
+POMC	drug	nicotine	29871818	We found that <strong>POMC</strong> promoter methylation is significantly higher in <b>smokers</b> than in non <b>smokers</b>.
+POMC	drug	nicotine	29871818	Alternatively, <b>smoking</b> may activate <strong>POMC</strong> neurons and its protein expression.
+POMC	drug	nicotine	29871818	In either way, altered <strong>POMC</strong> methylation in <b>smokers</b> seems to indicate an adaptation of stress signaling, thereby potentially serving as a marker for stress related functions that support the addiction.
+POMC	addiction	addiction	29871818	In either way, altered <strong>POMC</strong> methylation in smokers seems to indicate an adaptation of stress signaling, thereby potentially serving as a marker for stress related functions that support the <b>addiction</b>.
+POMC	drug	opioid	29510398	Injection of DAM blunted stress hormone levels and the <strong>POMC</strong> promoter methylation of <b>heroin</b> dependent patients.
+POMC	drug	amphetamine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [proopiomelanocortin (<strong>POMC</strong>), cocaine  and <b>amphetamine</b> related transcript (CART), neuropeptide Y (NPY), and agouti related peptide (AgRP)].
+POMC	drug	cocaine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [proopiomelanocortin (<strong>POMC</strong>), <b>cocaine</b>  and amphetamine related transcript (CART), neuropeptide Y (NPY), and agouti related peptide (AgRP)].
+POMC	drug	amphetamine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [<strong>proopiomelanocortin</strong> (<strong>POMC</strong>), cocaine  and <b>amphetamine</b> related transcript (CART), neuropeptide Y (NPY), and agouti related peptide (AgRP)].
+POMC	drug	cocaine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [<strong>proopiomelanocortin</strong> (<strong>POMC</strong>), <b>cocaine</b>  and amphetamine related transcript (CART), neuropeptide Y (NPY), and agouti related peptide (AgRP)].
+POMC	drug	alcohol	28511993	Furthermore, rats exposed to early life stress had high inherent <strong>Pomc</strong> expression in the amygdala but low expression after <b>ethanol</b> intake.
+POMC	drug	amphetamine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, <strong>POMC</strong>, AgRP, cocaine  and <b>amphetamine</b> related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+POMC	drug	cocaine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, <strong>POMC</strong>, AgRP, <b>cocaine</b>  and amphetamine related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+POMC	addiction	reward	27890744	Pro opiomelanocortin (<strong>POMC</strong>) derived peptides and their receptors have been shown to play important roles in natural and drug induced <b>reward</b> and <b>reinforcement</b>.
+POMC	addiction	reward	27890744	<b>Reward</b> process may involve the regulation of <strong>POMC</strong> gene expression and the gene expression of <strong>POMC</strong> derived peptide receptors.
+POMC	drug	nicotine	27890744	The present study investigated the alterations observed in the transcript levels of <strong>POMC</strong>, melanocortin 3 (MC3R), melanocortin 4 (MC4R) and mu opioid receptors (MOR) in the hypothalamus and mesocorticolimbic system during <b>nicotine</b> exposure.
+POMC	drug	opioid	27890744	The present study investigated the alterations observed in the transcript levels of <strong>POMC</strong>, melanocortin 3 (MC3R), melanocortin 4 (MC4R) and mu <b>opioid</b> receptors (MOR) in the hypothalamus and mesocorticolimbic system during nicotine exposure.
+POMC	drug	nicotine	27890744	Our results showed that treatment with 0.6mg/kg/day <b>nicotine</b> upregulated <strong>POMC</strong> mRNA in the hypothalamus and MC4R mRNA in the mPFC.
+POMC	drug	alcohol	27870313	Hypothalamic specific <strong>proopiomelanocortin</strong> deficiency reduces <b>alcohol</b> drinking in male and female mice.
+POMC	drug	alcohol	27870313	This study investigated whether hypothalamic proopiomelanocortin (<strong>POMC</strong>) neurons (producing beta endorphin and melanocortins) play a role in <b>alcohol</b> drinking behaviors.
+POMC	drug	alcohol	27870313	This study investigated whether hypothalamic <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) neurons (producing beta endorphin and melanocortins) play a role in <b>alcohol</b> drinking behaviors.
+POMC	drug	alcohol	27870313	Both male and female mice with targeted deletion of two neuronal <strong>Pomc</strong> enhancers nPE1 and nPE2 (nPE / ), resulting in hypothalamic specific <strong>POMC</strong> deficiency, were studied in short access (4 h/day) drinking in the dark (DID, <b>alcohol</b> in one bottle, intermittent access (IA, 24 h cycles of <b>alcohol</b> access every other day, <b>alcohol</b> vs. water in a two bottle choice) and <b>alcohol</b> deprivation effect (ADE) models.
+POMC	drug	alcohol	27870313	Our results suggest that neuronal <strong>POMC</strong> is involved in modulation of <b>alcohol</b> 'binge' drinking, escalation and 'relapse', probably via hypothalamic mediated mechanisms, with sex differences.
+POMC	addiction	addiction	27870313	Our results suggest that neuronal <strong>POMC</strong> is involved in modulation of alcohol 'binge' drinking, <b>escalation</b> and 'relapse', probably via hypothalamic mediated mechanisms, with sex differences.
+POMC	addiction	intoxication	27870313	Our results suggest that neuronal <strong>POMC</strong> is involved in modulation of alcohol '<b>binge</b>' drinking, escalation and 'relapse', probably via hypothalamic mediated mechanisms, with sex differences.
+POMC	addiction	relapse	27870313	Our results suggest that neuronal <strong>POMC</strong> is involved in modulation of alcohol 'binge' drinking, escalation and '<b>relapse</b>', probably via hypothalamic mediated mechanisms, with sex differences.
+POMC	drug	opioid	27078155	We attempt to define the temporal window of <b>morphine</b>'s inhibition effect on adult neurogenesis by using the <strong>POMC</strong> EGFP mouse model, in which newborn granular cells (GCs) can be visualized between days 3 28 post mitotic.
+POMC	drug	opioid	27078155	The <strong>POMC</strong> EGFP mice were trained under the 3 chambers conditioned place preference (CPP) paradigm with either saline or <b>morphine</b>.
+POMC	addiction	reward	27078155	The <strong>POMC</strong> EGFP mice were trained under the 3 chambers conditioned place preference (<b>CPP</b>) paradigm with either saline or morphine.
+POMC	drug	cannabinoid	27071101	Orexin A represses satiety inducing <strong>POMC</strong> neurons and contributes to obesity via stimulation of <b>endocannabinoid</b> signaling.
+POMC	drug	cannabinoid	27071101	<strong>POMC</strong> neurons receive orexin A (OX A) expressing inputs and express both OX A receptor type 1 (OX 1R) and <b>cannabinoid</b> receptor type 1 (CB1R) on the plasma membrane.
+POMC	drug	alcohol	27063791	Candidate genes for mediating the behavioral interaction between <b>ethanol</b> consumption and wheel running include multiple potassium channel genes, Oprm1, Prkcg, Stxbp1, Crhr1, Gabra3, Slc6a13, Stx1b, <strong>Pomc</strong>, Rassf5 and Camta2.
+POMC	drug	opioid	27038750	This group had higher <strong>POMC</strong> in the arcuate nucleus (ARC), higher tyrosine hydroxylase (TH) in the VTA, higher dopa decarboxylase (DDc), higher D2R and μu <b>opioid</b> receptor in the NAc.
+POMC	addiction	reward	27038750	Thus, neonatal BRO injection, depending on the time of treatment, leads to different long term dysfunctions in the dopaminergic <b>reward</b> system, food intake behavior and anxiety levels, findings that could be partially due to PRL and <strong>POMC</strong> changes.
+POMC	drug	opioid	26806779	In this review, we will discuss the dysregulation of several stress responsive systems in opiate addiction: vasopressin and its receptor system, endogenous <b>opioid</b> systems (including <strong>proopiomelanocortin</strong>/mu <b>opioid</b> receptor and dynorphin/kappa <b>opioid</b> receptor), orexin and its receptor system, and the hypothalamic pituitary adrenal axis.
+POMC	addiction	addiction	26806779	In this review, we will discuss the dysregulation of several stress responsive systems in opiate <b>addiction</b>: vasopressin and its receptor system, endogenous opioid systems (including <strong>proopiomelanocortin</strong>/mu opioid receptor and dynorphin/kappa opioid receptor), orexin and its receptor system, and the hypothalamic pituitary adrenal axis.
+POMC	drug	cocaine	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (<strong>Pomc</strong>, Penk, Pdyn) and cognate receptors (Oprm, Oprk and Oprd) in reward related brain regions, after exposure to either <b>cocaine</b> self administration or yoked saline, in the aforementioned translational paradigm.
+POMC	drug	opioid	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous <b>opioid</b> peptides (<strong>Pomc</strong>, Penk, Pdyn) and cognate receptors (Oprm, Oprk and Oprd) in reward related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+POMC	addiction	reward	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (<strong>Pomc</strong>, Penk, Pdyn) and cognate receptors (Oprm, Oprk and Oprd) in <b>reward</b> related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+POMC	drug	opioid	26535894	The expression of proopiomelanocortin <strong>Pomc</strong> encoding β endorphin and Oprm1 encoding the mu <b>opioid</b> receptor were upregulated peripherally after incision; moreover, Oprm1 expression was further increased under DNMT inhibitor treatment.
+POMC	drug	opioid	26535894	The expression of <strong>proopiomelanocortin</strong> <strong>Pomc</strong> encoding β endorphin and Oprm1 encoding the mu <b>opioid</b> receptor were upregulated peripherally after incision; moreover, Oprm1 expression was further increased under DNMT inhibitor treatment.
+POMC	drug	opioid	26108334	Proopiomelanocortin (<strong>POMC</strong>) derived melanocortin (MC) and <b>opioid</b> peptides are produced in the same neurons in the brain, and recent preclinical evidence shows that MC receptor (MCR) agonists reduce excessive EtOH drinking in animal models.
+POMC	drug	opioid	26108334	<strong>Proopiomelanocortin</strong> (<strong>POMC</strong>) derived melanocortin (MC) and <b>opioid</b> peptides are produced in the same neurons in the brain, and recent preclinical evidence shows that MC receptor (MCR) agonists reduce excessive EtOH drinking in animal models.
+POMC	drug	opioid	26019998	Additionally, the molecular mechanisms of lappaconitine's analgesic effects may be related to affect the expression levels of endogenous <b>opioid</b> system genes (<strong>POMC</strong>, PENK and MOR), as well as apoptosis related genes (Xiap, Smac, Bim, NF κB and p53).
+POMC	drug	opioid	25854026	The mRNA expressions of µ <b>opioid</b> receptor (MOR), κ <b>opioid</b> receptor (KOR), δ <b>opioid</b> receptor (DOR), proopiomelanocortin (<strong>POMC</strong>) and prodynorphin (PDYN) in dorsal root ganglion (DRG) and lumbar spinal cord dorsal horn (SCDH) of L4 L6 of the affected side were detected by PCR method.
+POMC	drug	opioid	25854026	The mRNA expressions of µ <b>opioid</b> receptor (MOR), κ <b>opioid</b> receptor (KOR), δ <b>opioid</b> receptor (DOR), <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and prodynorphin (PDYN) in dorsal root ganglion (DRG) and lumbar spinal cord dorsal horn (SCDH) of L4 L6 of the affected side were detected by PCR method.
+POMC	drug	cocaine	25595971	Persistent increases in rat hypothalamic <strong>POMC</strong> gene expression following chronic withdrawal from chronic "binge" pattern escalating dose, but not steady dose, <b>cocaine</b>.
+POMC	addiction	intoxication	25595971	Persistent increases in rat hypothalamic <strong>POMC</strong> gene expression following chronic withdrawal from chronic "<b>binge</b>" pattern escalating dose, but not steady dose, cocaine.
+POMC	addiction	withdrawal	25595971	Persistent increases in rat hypothalamic <strong>POMC</strong> gene expression following chronic <b>withdrawal</b> from chronic "binge" pattern escalating dose, but not steady dose, cocaine.
+POMC	drug	cocaine	25595971	Recent research suggests an involvement of pro opiomelanocortin (<strong>POMC</strong>) gene products (e.g., beta endorphin) in modulating <b>cocaine</b> induced reward and addiction like behaviors in rodents.
+POMC	addiction	addiction	25595971	Recent research suggests an involvement of pro opiomelanocortin (<strong>POMC</strong>) gene products (e.g., beta endorphin) in modulating cocaine induced reward and <b>addiction</b> like behaviors in rodents.
+POMC	addiction	reward	25595971	Recent research suggests an involvement of pro opiomelanocortin (<strong>POMC</strong>) gene products (e.g., beta endorphin) in modulating cocaine induced <b>reward</b> and addiction like behaviors in rodents.
+POMC	drug	cocaine	25595971	In this study, we investigated whether chronic "binge" <b>cocaine</b> and its withdrawal altered <strong>POMC</strong> gene expression in the brain of rats.
+POMC	addiction	intoxication	25595971	In this study, we investigated whether chronic "<b>binge</b>" cocaine and its withdrawal altered <strong>POMC</strong> gene expression in the brain of rats.
+POMC	addiction	withdrawal	25595971	In this study, we investigated whether chronic "binge" cocaine and its <b>withdrawal</b> altered <strong>POMC</strong> gene expression in the brain of rats.
+POMC	drug	cocaine	25595971	Although there was no <strong>POMC</strong> mRNA alteration after chronic steady dose <b>cocaine</b>, a significant decrease in <strong>POMC</strong> mRNA levels in the hypothalamus was found after chronic escalating dose <b>cocaine</b>.
+POMC	addiction	intoxication	25595971	In contrast, after acute (1 day) withdrawal from chronic "<b>binge</b>" escalating dose regimen, but not steady dose regimen, there were increased hypothalamic <strong>POMC</strong> mRNA levels that persisted into 14days of protracted withdrawal.
+POMC	addiction	withdrawal	25595971	In contrast, after acute (1 day) <b>withdrawal</b> from chronic "binge" escalating dose regimen, but not steady dose regimen, there were increased hypothalamic <strong>POMC</strong> mRNA levels that persisted into 14days of protracted <b>withdrawal</b>.
+POMC	drug	cocaine	25595971	To study the role of the endogenous opioid systems in the <b>cocaine</b> withdrawal effects, we administered a single naloxone injection (1mg/kg) that caused elevated <strong>POMC</strong> mRNA levels observed 24h later in <b>cocaine</b> naïve rats, but it did not lead to further increases in <b>cocaine</b> withdrawn rats.
+POMC	drug	opioid	25595971	To study the role of the endogenous <b>opioid</b> systems in the cocaine withdrawal effects, we administered a single <b>naloxone</b> injection (1mg/kg) that caused elevated <strong>POMC</strong> mRNA levels observed 24h later in cocaine naïve rats, but it did not lead to further increases in cocaine withdrawn rats.
+POMC	addiction	withdrawal	25595971	To study the role of the endogenous opioid systems in the cocaine <b>withdrawal</b> effects, we administered a single naloxone injection (1mg/kg) that caused elevated <strong>POMC</strong> mRNA levels observed 24h later in cocaine naïve rats, but it did not lead to further increases in cocaine withdrawn rats.
+POMC	drug	cocaine	25595971	Our results suggest that during withdrawal from chronic "binge" escalating dose <b>cocaine</b>: (1) there was a persistent increase in hypothalamic <strong>POMC</strong> gene expression; and (2) hyposensitivity of the <strong>POMC</strong> gene expression to naloxone indicates altered opioidergic tone at or above the hypothalamic level.
+POMC	drug	opioid	25595971	Our results suggest that during withdrawal from chronic "binge" escalating dose cocaine: (1) there was a persistent increase in hypothalamic <strong>POMC</strong> gene expression; and (2) hyposensitivity of the <strong>POMC</strong> gene expression to <b>naloxone</b> indicates altered opioidergic tone at or above the hypothalamic level.
+POMC	addiction	intoxication	25595971	Our results suggest that during withdrawal from chronic "<b>binge</b>" escalating dose cocaine: (1) there was a persistent increase in hypothalamic <strong>POMC</strong> gene expression; and (2) hyposensitivity of the <strong>POMC</strong> gene expression to naloxone indicates altered opioidergic tone at or above the hypothalamic level.
+POMC	addiction	withdrawal	25595971	Our results suggest that during <b>withdrawal</b> from chronic "binge" escalating dose cocaine: (1) there was a persistent increase in hypothalamic <strong>POMC</strong> gene expression; and (2) hyposensitivity of the <strong>POMC</strong> gene expression to naloxone indicates altered opioidergic tone at or above the hypothalamic level.
+POMC	drug	opioid	25446223	Individual differences in gene expression of vasopressin, D2 receptor, <strong>POMC</strong> and orexin: vulnerability to relapse to <b>heroin</b> seeking in rats.
+POMC	addiction	relapse	25446223	Individual differences in gene expression of vasopressin, D2 receptor, <strong>POMC</strong> and orexin: vulnerability to <b>relapse</b> to heroin <b>seeking</b> in rats.
+POMC	drug	opioid	25446223	In this study, we tested whether individual differences in the FS induced <b>heroin</b> seeking were associated with alterations of AVP and V1b, as well as other stress responsive systems, including pro opiomelanocortin (<strong>POMC</strong>), orexin, plasma ACTH and corticosterone, as well as dopamine D2 receptor (D2) and plasma prolactin.
+POMC	addiction	relapse	25446223	In this study, we tested whether individual differences in the FS induced heroin <b>seeking</b> were associated with alterations of AVP and V1b, as well as other stress responsive systems, including pro opiomelanocortin (<strong>POMC</strong>), orexin, plasma ACTH and corticosterone, as well as dopamine D2 receptor (D2) and plasma prolactin.
+POMC	drug	opioid	25446223	However, <b>heroin</b> priming resulted in similar reinstatement in both groups and produced similarly low <strong>POMC</strong> and high orexin mRNA levels in hypothalamus.
+POMC	addiction	relapse	25446223	However, heroin priming resulted in similar <b>reinstatement</b> in both groups and produced similarly low <strong>POMC</strong> and high orexin mRNA levels in hypothalamus.
+POMC	drug	opioid	25446223	Our results indicate that: 1) enhanced amygdalar AVP and reduced striatal D2 expression may be related to individual vulnerability to stress induced reinstatement of <b>heroin</b>  seeking; and 2) <b>heroin</b> abstinence associated alterations of hypothalamic orexin and <strong>POMC</strong> expression may be involved in drug priming induced <b>heroin</b> seeking.
+POMC	addiction	relapse	25446223	Our results indicate that: 1) enhanced amygdalar AVP and reduced striatal D2 expression may be related to individual vulnerability to stress induced <b>reinstatement</b> of heroin  <b>seeking</b>; and 2) heroin abstinence associated alterations of hypothalamic orexin and <strong>POMC</strong> expression may be involved in drug priming induced heroin <b>seeking</b>.
+POMC	addiction	reward	24936193	Centrally, the α7nAChR modulates activity of hypothalamic neurons involved in food intake regulation, including <strong>proopiomelanocortin</strong> and neuropeptide Y. α7nAChRs also modulate glutamatergic and dopaminergic systems controlling <b>reward</b> processes that affect food intake.
+POMC	drug	alcohol	24929109	Addictions to specific drugs such as <b>alcohol</b>, psychostimulants and opiates (e.g., heroin) have some common direct or downstream effects on several brain stress responsive systems, including vasopressin and its receptor system (Section II), <strong>POMC</strong> and mu opioid receptor system (Section III) and dynorphin and kappa opioid receptor systems (Section IV).
+POMC	drug	opioid	24929109	Addictions to specific drugs such as alcohol, psychostimulants and opiates (e.g., <b>heroin</b>) have some common direct or downstream effects on several brain stress responsive systems, including vasopressin and its receptor system (Section II), <strong>POMC</strong> and mu <b>opioid</b> receptor system (Section III) and dynorphin and kappa <b>opioid</b> receptor systems (Section IV).
+POMC	drug	alcohol	24501814	Moreover, studies on the CNS receptor gene expression showed that the extract of kudzu possibly acts through opioid system and exhibits antagonist activity by influencing the opioid receptors mi, delta and the expression of endogenous opioid precursors (<strong>proopiomelanocortin</strong>) similarly as <b>naltrexone</b>.
+POMC	drug	opioid	24501814	Moreover, studies on the CNS receptor gene expression showed that the extract of kudzu possibly acts through <b>opioid</b> system and exhibits antagonist activity by influencing the <b>opioid</b> receptors mi, delta and the expression of endogenous <b>opioid</b> precursors (<strong>proopiomelanocortin</strong>) similarly as naltrexone.
+POMC	drug	alcohol	24271034	CAGn repeat of the androgen receptor is linked to <strong>proopiomelanocortin</strong> promoter methylation relevance for craving of male <b>alcohol</b> dependent patients?
+POMC	addiction	relapse	24271034	CAGn repeat of the androgen receptor is linked to <strong>proopiomelanocortin</strong> promoter methylation relevance for <b>craving</b> of male alcohol dependent patients?
+POMC	drug	alcohol	24271034	Previous findings of the Franconian <b>Alcoholism</b> Research Studies showed that both the CAGn of the androgen receptor (AR) and the promoter methylation of the hypothalamic peptide proopiomelanocortin (<strong>POMC</strong>) were associated with craving of male <b>alcohol</b> dependent patients.
+POMC	addiction	relapse	24271034	Previous findings of the Franconian Alcoholism Research Studies showed that both the CAGn of the androgen receptor (AR) and the promoter methylation of the hypothalamic peptide proopiomelanocortin (<strong>POMC</strong>) were associated with <b>craving</b> of male alcohol dependent patients.
+POMC	drug	alcohol	24271034	Previous findings of the Franconian <b>Alcoholism</b> Research Studies showed that both the CAGn of the androgen receptor (AR) and the promoter methylation of the hypothalamic peptide <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) were associated with craving of male <b>alcohol</b> dependent patients.
+POMC	addiction	relapse	24271034	Previous findings of the Franconian Alcoholism Research Studies showed that both the CAGn of the androgen receptor (AR) and the promoter methylation of the hypothalamic peptide <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) were associated with <b>craving</b> of male alcohol dependent patients.
+POMC	drug	alcohol	24271034	Based on the strong interactions between the hypothalamic pituitary gonadal (HPG) and the hypothalamic pituitary adrenal axis (HPA), this study investigated the relationships between the CAGn repeat of the AR, <strong>POMC</strong> promoter methylation and craving of male <b>alcohol</b> dependent patients.
+POMC	addiction	relapse	24271034	Based on the strong interactions between the hypothalamic pituitary gonadal (HPG) and the hypothalamic pituitary adrenal axis (HPA), this study investigated the relationships between the CAGn repeat of the AR, <strong>POMC</strong> promoter methylation and <b>craving</b> of male alcohol dependent patients.
+POMC	addiction	relapse	24271034	Altogether, the <strong>POMC</strong> promoter methylation accounted for 33 % of the relationship between CAGn AR polymorphism and <b>craving</b>.
+POMC	drug	alcohol	24271034	This work shows that the AR and the <strong>POMC</strong> gene might functionally interact with each other and subsequently mediate craving in <b>alcohol</b> dependent patients.
+POMC	addiction	relapse	24271034	This work shows that the AR and the <strong>POMC</strong> gene might functionally interact with each other and subsequently mediate <b>craving</b> in alcohol dependent patients.
+POMC	drug	opioid	24035914	This neuromodulator system is composed of three receptors, mu, delta and kappa, interacting with a family of <b>opioid</b> peptides derived from <strong>POMC</strong> (β endorphin), preproenkephalin (pEnk) and preprodynorphin (pDyn) precursors.
+POMC	drug	alcohol	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (OPRK1) opioid receptors and precursors of their ligands   proopiomelanocortin (<strong>POMC</strong>), coding for beta endorphin and prodynorphin (PDYN) coding for dynorphins, were analyzed in a case control study that included 354 male <b>alcohol</b> dependent and 357 male control subjects from Croatian population.
+POMC	drug	opioid	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (OPRK1) <b>opioid</b> receptors and precursors of their ligands   proopiomelanocortin (<strong>POMC</strong>), coding for beta endorphin and prodynorphin (PDYN) coding for dynorphins, were analyzed in a case control study that included 354 male alcohol dependent and 357 male control subjects from Croatian population.
+POMC	drug	alcohol	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (OPRK1) opioid receptors and precursors of their ligands   <strong>proopiomelanocortin</strong> (<strong>POMC</strong>), coding for beta endorphin and prodynorphin (PDYN) coding for dynorphins, were analyzed in a case control study that included 354 male <b>alcohol</b> dependent and 357 male control subjects from Croatian population.
+POMC	drug	opioid	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (OPRK1) <b>opioid</b> receptors and precursors of their ligands   <strong>proopiomelanocortin</strong> (<strong>POMC</strong>), coding for beta endorphin and prodynorphin (PDYN) coding for dynorphins, were analyzed in a case control study that included 354 male alcohol dependent and 357 male control subjects from Croatian population.
+POMC	drug	alcohol	24035285	Thus, the data obtained suggest no association of the selected polymorphisms of the genes OPRM1/<strong>POMC</strong> and OPRK1/PDYN with <b>alcoholism</b> in Croatian population.
+POMC	drug	opioid	23891651	<b>Morphine</b> treatment selectively regulates expression of rat pituitary <strong>POMC</strong> and the prohormone convertases PC1/3 and PC2.
+POMC	drug	alcohol	23891651	In order to test the hypothesis that exogenous opioids regulate the endogenous opioid system and the enzymes responsible for their biosynthesis, we studied the effect of short term morphine or <b>naltrexone</b> treatment on pituitary PC1/3 and PC2 as well as on the level of pro opiomelanocortin (<strong>POMC</strong>), the precursor gene for the biosynthesis of the endogenous opioid peptide, β endorphin.
+POMC	drug	opioid	23891651	In order to test the hypothesis that exogenous <b>opioids</b> regulate the endogenous <b>opioid</b> system and the enzymes responsible for their biosynthesis, we studied the effect of short term <b>morphine</b> or naltrexone treatment on pituitary PC1/3 and PC2 as well as on the level of pro opiomelanocortin (<strong>POMC</strong>), the precursor gene for the biosynthesis of the endogenous <b>opioid</b> peptide, β endorphin.
+POMC	drug	opioid	23805290	Chronic <b>morphine</b> exposure or pair feeding did not significantly affect hypothalamic expression of selected stress  and metabolic related neuropeptides   corticotropin releasing hormone (CRH), urocortin 2 (UCN2) and proopiomelanocortin (<strong>POMC</strong>) compared to placebo implanted and pair fed animals.
+POMC	drug	opioid	23805290	Chronic <b>morphine</b> exposure or pair feeding did not significantly affect hypothalamic expression of selected stress  and metabolic related neuropeptides   corticotropin releasing hormone (CRH), urocortin 2 (UCN2) and <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) compared to placebo implanted and pair fed animals.
+POMC	drug	alcohol	23792540	There is experimental evidence that chronic <b>ethanol</b> exposure reduces α MSH expression in the limbic and hypothalamic brain regions and alters central pro opiomelanocortin (<strong>POMC</strong>) mRNA activity in adult rats.
+POMC	addiction	withdrawal	23771528	In the anterior pituitary, pro opiomelanocortin (<strong>POMC</strong>) mRNA levels were increased during acute <b>withdrawal</b> and retuned to control levels after chronic <b>withdrawal</b>.
+POMC	addiction	withdrawal	23771528	In the medial hypothalamus, however, the <strong>POMC</strong> mRNA levels were decreased during acute <b>withdrawal</b>, and increased after chronic <b>withdrawal</b>.
+POMC	drug	opioid	23346966	Finally, we assessed the expression of the genes proopiomelanocortin (<strong>POMC</strong>), pro dynorphin (PDyn) and pro enkephalin (PEnk), coding for the <b>opioids</b> peptides in the NAcc and the mPFC in both groups.
+POMC	drug	opioid	23346966	Finally, we assessed the expression of the genes <strong>proopiomelanocortin</strong> (<strong>POMC</strong>), pro dynorphin (PDyn) and pro enkephalin (PEnk), coding for the <b>opioids</b> peptides in the NAcc and the mPFC in both groups.
+POMC	drug	opioid	23337531	Proopiomelanocortin (<strong>POMC</strong>) expression and conditioned place aversion during protracted withdrawal from chronic intermittent escalating dose <b>heroin</b> in <strong>POMC</strong> EGFP promoter transgenic mice.
+POMC	addiction	aversion	23337531	Proopiomelanocortin (<strong>POMC</strong>) expression and conditioned place <b>aversion</b> during protracted withdrawal from chronic intermittent escalating dose heroin in <strong>POMC</strong> EGFP promoter transgenic mice.
+POMC	addiction	withdrawal	23337531	Proopiomelanocortin (<strong>POMC</strong>) expression and conditioned place aversion during protracted <b>withdrawal</b> from chronic intermittent escalating dose heroin in <strong>POMC</strong> EGFP promoter transgenic mice.
+POMC	drug	opioid	23337531	<strong>Proopiomelanocortin</strong> (<strong>POMC</strong>) expression and conditioned place aversion during protracted withdrawal from chronic intermittent escalating dose <b>heroin</b> in <strong>POMC</strong> EGFP promoter transgenic mice.
+POMC	addiction	aversion	23337531	<strong>Proopiomelanocortin</strong> (<strong>POMC</strong>) expression and conditioned place <b>aversion</b> during protracted withdrawal from chronic intermittent escalating dose heroin in <strong>POMC</strong> EGFP promoter transgenic mice.
+POMC	addiction	withdrawal	23337531	<strong>Proopiomelanocortin</strong> (<strong>POMC</strong>) expression and conditioned place aversion during protracted <b>withdrawal</b> from chronic intermittent escalating dose heroin in <strong>POMC</strong> EGFP promoter transgenic mice.
+POMC	drug	opioid	23337531	Here, we investigate changes in proopiomelanocortin (<strong>POMC</strong>) expression at three time points across an extended period of <b>heroin</b> withdrawal in a clinically relevant rodent model of addiction using conditioned place aversion (CPA) in <strong>POMC</strong> EGFP (<strong>POMC</strong> enhanced green fluorescent protein) bacterial artificial chromosome (BAC) transgenic mice.
+POMC	addiction	addiction	23337531	Here, we investigate changes in proopiomelanocortin (<strong>POMC</strong>) expression at three time points across an extended period of heroin withdrawal in a clinically relevant rodent model of <b>addiction</b> using conditioned place aversion (CPA) in <strong>POMC</strong> EGFP (<strong>POMC</strong> enhanced green fluorescent protein) bacterial artificial chromosome (BAC) transgenic mice.
+POMC	addiction	aversion	23337531	Here, we investigate changes in proopiomelanocortin (<strong>POMC</strong>) expression at three time points across an extended period of heroin withdrawal in a clinically relevant rodent model of addiction using conditioned place <b>aversion</b> (CPA) in <strong>POMC</strong> EGFP (<strong>POMC</strong> enhanced green fluorescent protein) bacterial artificial chromosome (BAC) transgenic mice.
+POMC	addiction	withdrawal	23337531	Here, we investigate changes in proopiomelanocortin (<strong>POMC</strong>) expression at three time points across an extended period of heroin <b>withdrawal</b> in a clinically relevant rodent model of addiction using conditioned place aversion (CPA) in <strong>POMC</strong> EGFP (<strong>POMC</strong> enhanced green fluorescent protein) bacterial artificial chromosome (BAC) transgenic mice.
+POMC	drug	opioid	23337531	Here, we investigate changes in <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) expression at three time points across an extended period of <b>heroin</b> withdrawal in a clinically relevant rodent model of addiction using conditioned place aversion (CPA) in <strong>POMC</strong> EGFP (<strong>POMC</strong> enhanced green fluorescent protein) bacterial artificial chromosome (BAC) transgenic mice.
+POMC	addiction	addiction	23337531	Here, we investigate changes in <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) expression at three time points across an extended period of heroin withdrawal in a clinically relevant rodent model of <b>addiction</b> using conditioned place aversion (CPA) in <strong>POMC</strong> EGFP (<strong>POMC</strong> enhanced green fluorescent protein) bacterial artificial chromosome (BAC) transgenic mice.
+POMC	addiction	aversion	23337531	Here, we investigate changes in <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) expression at three time points across an extended period of heroin withdrawal in a clinically relevant rodent model of addiction using conditioned place <b>aversion</b> (CPA) in <strong>POMC</strong> EGFP (<strong>POMC</strong> enhanced green fluorescent protein) bacterial artificial chromosome (BAC) transgenic mice.
+POMC	addiction	withdrawal	23337531	Here, we investigate changes in <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) expression at three time points across an extended period of heroin <b>withdrawal</b> in a clinically relevant rodent model of addiction using conditioned place aversion (CPA) in <strong>POMC</strong> EGFP (<strong>POMC</strong> enhanced green fluorescent protein) bacterial artificial chromosome (BAC) transgenic mice.
+POMC	drug	opioid	23337531	After 12 h withdrawal, <b>heroin</b> treated mice showed lower signal intensity of <strong>POMC</strong> EGFP positive cells in the ARC, higher levels of <strong>POMC</strong> mRNA in the amygdala but lower levels in the hippocampus than saline controls.
+POMC	addiction	withdrawal	23337531	After 12 h <b>withdrawal</b>, heroin treated mice showed lower signal intensity of <strong>POMC</strong> EGFP positive cells in the ARC, higher levels of <strong>POMC</strong> mRNA in the amygdala but lower levels in the hippocampus than saline controls.
+POMC	drug	opioid	23337531	After 7 d withdrawal, <b>heroin</b> treated mice showed fewer <strong>POMC</strong> EGFP positive cells in the MeA and lower <strong>POMC</strong> mRNA in the amygdala than saline controls.
+POMC	addiction	withdrawal	23337531	After 7 d <b>withdrawal</b>, heroin treated mice showed fewer <strong>POMC</strong> EGFP positive cells in the MeA and lower <strong>POMC</strong> mRNA in the amygdala than saline controls.
+POMC	drug	opioid	23337531	After extended (14days) withdrawal, <b>heroin</b> treated mice showed more <strong>POMC</strong> EGFP positive cells in BMA and DG, increased intensity of <strong>POMC</strong> EGFP signal in DG, and higher <strong>POMC</strong> mRNA levels in the hippocampus compared to controls.
+POMC	addiction	withdrawal	23337531	After extended (14days) <b>withdrawal</b>, heroin treated mice showed more <strong>POMC</strong> EGFP positive cells in BMA and DG, increased intensity of <strong>POMC</strong> EGFP signal in DG, and higher <strong>POMC</strong> mRNA levels in the hippocampus compared to controls.
+POMC	drug	opioid	23337531	Our results show dynamic changes in <strong>POMC</strong> in hypothalamic and extra hypothalamic regions that may contribute to the negative affective/emotional state of <b>heroin</b> withdrawal shown by CPA from acute to extended periods of <b>heroin</b> withdrawal.
+POMC	addiction	withdrawal	23337531	Our results show dynamic changes in <strong>POMC</strong> in hypothalamic and extra hypothalamic regions that may contribute to the negative affective/emotional state of heroin <b>withdrawal</b> shown by CPA from acute to extended periods of heroin <b>withdrawal</b>.
+POMC	drug	cocaine	23069669	Recent research suggests an involvement of pro opiomelanocortin (<strong>POMC</strong>) gene products in modulating <b>cocaine</b> reward and addiction like behaviors in rodents.
+POMC	addiction	addiction	23069669	Recent research suggests an involvement of pro opiomelanocortin (<strong>POMC</strong>) gene products in modulating cocaine reward and <b>addiction</b> like behaviors in rodents.
+POMC	addiction	reward	23069669	Recent research suggests an involvement of pro opiomelanocortin (<strong>POMC</strong>) gene products in modulating cocaine <b>reward</b> and addiction like behaviors in rodents.
+POMC	drug	cocaine	23069669	In this study, we investigated whether <b>cocaine</b> induced conditioned place preference (CPP) alters <strong>POMC</strong> gene expression in the brain or pituitary of rats.
+POMC	addiction	reward	23069669	In this study, we investigated whether cocaine induced conditioned place preference (<b>CPP</b>) alters <strong>POMC</strong> gene expression in the brain or pituitary of rats.
+POMC	drug	cocaine	23069669	<b>Cocaine</b> place conditioning at 10 and 30 mg/kg doses increased <strong>POMC</strong> mRNA levels in a dose dependent manner in the hypothalamus, with no effect in the amygdala.
+POMC	drug	cocaine	23069669	<b>Cocaine</b> CPP had no effect on <strong>POMC</strong> mRNA levels in the anterior pituitary or on plasma ACTH or corticosterone levels.
+POMC	addiction	reward	23069669	Cocaine <b>CPP</b> had no effect on <strong>POMC</strong> mRNA levels in the anterior pituitary or on plasma ACTH or corticosterone levels.
+POMC	drug	cocaine	23069669	In rats that received <b>cocaine</b> at 30 mg/kg without conditioning, there was no such effect on hypothalamic <strong>POMC</strong> mRNA levels.
+POMC	drug	cocaine	23069669	Alteration of <strong>POMC</strong> gene expression in the hypothalamus is region specific after <b>cocaine</b> place conditioning, and dose dependent.
+POMC	drug	cocaine	23069669	The increased <strong>POMC</strong> gene expression in the hypothalamus suggests that it is involved in the reward/learning process of <b>cocaine</b> induced conditioning.
+POMC	addiction	reward	23069669	The increased <strong>POMC</strong> gene expression in the hypothalamus suggests that it is involved in the <b>reward</b>/learning process of cocaine induced conditioning.
+POMC	addiction	dependence	23028917	Identification of <strong>POMC</strong> exonic variants associated with substance <b>dependence</b> and body mass index.
+POMC	addiction	dependence	23028917	Risk of substance <b>dependence</b> (SD) and obesity has been linked to the function of melanocortin peptides encoded by the proopiomelanocortin gene (<strong>POMC</strong>).
+POMC	addiction	dependence	23028917	Risk of substance <b>dependence</b> (SD) and obesity has been linked to the function of melanocortin peptides encoded by the <strong>proopiomelanocortin</strong> gene (<strong>POMC</strong>).
+POMC	addiction	sensitization	22952458	In order to study the role of β Endorphin in the development of locomotor <b>sensitization</b> to repeated EtOH exposure, we tested transgenic mice that vary in their capacity to synthesize this peptide as a result of constitutive modification of the <strong>Pomc</strong> gene.
+POMC	drug	nicotine	22483037	These studies investigated the effect of acute, 1mg/kg, sc, and chronic, daily injection of 1mg/kg, sc, for 14 days, administration of free base <b>nicotine</b> on brain β endorphin and its precursor proopiomelanocortin (<strong>POMC</strong>).
+POMC	drug	nicotine	22483037	These studies investigated the effect of acute, 1mg/kg, sc, and chronic, daily injection of 1mg/kg, sc, for 14 days, administration of free base <b>nicotine</b> on brain β endorphin and its precursor <strong>proopiomelanocortin</strong> (<strong>POMC</strong>).
+POMC	drug	nicotine	22483037	<strong>POMC</strong> mRNA in hypothalamus and prefrontal cortex was unchanged following acute <b>nicotine</b>, but it decreased moderately with chronic treatment.
+POMC	addiction	reward	22442070	Hypothalamic proopiomelanocortin (<strong>POMC</strong>) neurons and their peptide products mediate important aspects of energy balance, analgesia, and <b>reward</b>.
+POMC	addiction	reward	22442070	Hypothalamic <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) neurons and their peptide products mediate important aspects of energy balance, analgesia, and <b>reward</b>.
+POMC	drug	opioid	22442070	To determine whether the release of GABA and glutamate from <strong>POMC</strong> terminals can be readily modulated, <b>opioid</b> and GABA(B) receptor agonists were applied.
+POMC	drug	opioid	22442070	Agonists for μ  and κ , but not δ <b>opioid</b> receptors inhibited transmitter release from <strong>POMC</strong> neurons, as did the GABA(B) receptor agonist baclofen.
+POMC	drug	opioid	22442070	This regulation indicates that <b>opioids</b> and GABA released from <strong>POMC</strong> neurons may act at presynaptic receptors on <strong>POMC</strong> terminals in an autoregulatory manner to limit continued transmission.
+POMC	drug	alcohol	22014186	Given the important role of the proopiomelanocortin (<strong>POMc</strong>) derived opioid peptide beta endorphin, an endogenous mu  and delta opioid receptor agonist, in some of the behavioral effects of <b>ethanol</b>, we hypothesized that beta endorphin would also be involved in <b>ethanol</b> conditioning.
+POMC	drug	opioid	22014186	Given the important role of the proopiomelanocortin (<strong>POMc</strong>) derived <b>opioid</b> peptide beta endorphin, an endogenous mu  and delta <b>opioid</b> receptor agonist, in some of the behavioral effects of ethanol, we hypothesized that beta endorphin would also be involved in ethanol conditioning.
+POMC	drug	alcohol	22014186	Given the important role of the <strong>proopiomelanocortin</strong> (<strong>POMc</strong>) derived opioid peptide beta endorphin, an endogenous mu  and delta opioid receptor agonist, in some of the behavioral effects of <b>ethanol</b>, we hypothesized that beta endorphin would also be involved in <b>ethanol</b> conditioning.
+POMC	drug	opioid	22014186	Given the important role of the <strong>proopiomelanocortin</strong> (<strong>POMc</strong>) derived <b>opioid</b> peptide beta endorphin, an endogenous mu  and delta <b>opioid</b> receptor agonist, in some of the behavioral effects of ethanol, we hypothesized that beta endorphin would also be involved in ethanol conditioning.
+POMC	drug	cocaine	21677651	Here, we examined the gene expression alterations of AVP in the hypothalamus, and V1b receptor and pro opiomelanocortin (<strong>POMC</strong>) in the anterior pituitary, as well as HPA hormonal changes, in Fischer rats after chronic <b>cocaine</b> and withdrawal, using two different chronic (14 day) 'binge' pattern administration regimens: steady dose <b>cocaine</b> (SDC, 45 mg/kg/day) and escalating dose <b>cocaine</b> (EDC, 45 up to 90 mg/kg/day).
+POMC	addiction	intoxication	21677651	Here, we examined the gene expression alterations of AVP in the hypothalamus, and V1b receptor and pro opiomelanocortin (<strong>POMC</strong>) in the anterior pituitary, as well as HPA hormonal changes, in Fischer rats after chronic cocaine and withdrawal, using two different chronic (14 day) '<b>binge</b>' pattern administration regimens: steady dose cocaine (SDC, 45 mg/kg/day) and escalating dose cocaine (EDC, 45 up to 90 mg/kg/day).
+POMC	addiction	withdrawal	21677651	Here, we examined the gene expression alterations of AVP in the hypothalamus, and V1b receptor and pro opiomelanocortin (<strong>POMC</strong>) in the anterior pituitary, as well as HPA hormonal changes, in Fischer rats after chronic cocaine and <b>withdrawal</b>, using two different chronic (14 day) 'binge' pattern administration regimens: steady dose cocaine (SDC, 45 mg/kg/day) and escalating dose cocaine (EDC, 45 up to 90 mg/kg/day).
+POMC	drug	nicotine	21653710	<b>Nicotine</b> excites hypothalamic arcuate anorexigenic <strong>proopiomelanocortin</strong> neurons and orexigenic neuropeptide Y neurons: similarities and differences.
+POMC	drug	nicotine	21653710	Here we address the hypothesis that if weight reducing actions of <b>nicotine</b> are mediated by anorexigenic proopiomelanocortin (<strong>POMC</strong>) neurons of the hypothalamic arcuate nucleus, <b>nicotine</b> should excite these cells.
+POMC	drug	nicotine	21653710	Here we address the hypothesis that if weight reducing actions of <b>nicotine</b> are mediated by anorexigenic <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) neurons of the hypothalamic arcuate nucleus, <b>nicotine</b> should excite these cells.
+POMC	drug	nicotine	21653710	<b>Nicotine</b> at concentrations similar to those found in <b>smokers</b>, 100 1,000 nM, excited <strong>POMC</strong> cells by mechanisms based on increased spike frequency, depolarization of membrane potential, and opening of ion channels.
+POMC	drug	nicotine	21653710	<b>Nicotine</b> exerted similar actions on <strong>POMC</strong> and NPY cells, with a slightly greater depolarizing action on <strong>POMC</strong> cells.
+POMC	drug	nicotine	21653710	We found no differences in the relative desensitization to <b>nicotine</b> between <strong>POMC</strong> and NPY neurons.
+POMC	drug	nicotine	21653710	<b>Nicotine</b> inhibited excitatory synaptic activity recorded in NPY, but not <strong>POMC</strong>, cells.
+POMC	drug	nicotine	21653710	<b>Nicotine</b> also excited hypocretin/orexin neurons that enhance cognitive arousal, but the responses were smaller than in NPY or <strong>POMC</strong> cells.
+POMC	drug	nicotine	21653710	Together, these results indicate that <b>nicotine</b> has a number of similar actions, but also a few different actions, on <strong>POMC</strong> and NPY neurons that could contribute to the weight loss associated with <b>smoking</b>.
+POMC	drug	opioid	20651230	Moreover, Tat expression widely disrupted the endogenous <b>opioid</b> system, altering mu and kappa, but not delta, <b>opioid</b> receptor and <strong>proopiomelanocortin</strong>, proenkephalin, and prodynorphin transcript levels in cortex, hippocampus, and striatum.
+POMC	drug	alcohol	20191296	DNA methylation of the <strong>POMC</strong> gene promoter is associated with craving in <b>alcohol</b> dependence.
+POMC	addiction	dependence	20191296	DNA methylation of the <strong>POMC</strong> gene promoter is associated with craving in alcohol <b>dependence</b>.
+POMC	addiction	relapse	20191296	DNA methylation of the <strong>POMC</strong> gene promoter is associated with <b>craving</b> in alcohol dependence.
+POMC	drug	alcohol	20191296	We analysed the DNA methylation of the 5' promoter of the <strong>POMC</strong> gene that is embedded in a CpG island using bisulfite sequencing in 145 <b>alcohol</b> dependent patients and 37 healthy controls taken from the Franconian <b>Alcoholism</b> Research Studies.
+POMC	drug	alcohol	19860799	<b>Ethanol</b> intake significantly decreased <strong>proopiomelanocortin</strong> expression in the arcuate nucleus (38.31%) and micro opioid DAMGO stimulated [(35)S] GTPgamma binding in the caudate putamen (40%), nucleus accumbens core (AccC) (32.87%), and shell (AccS) (34.21%).
+POMC	drug	opioid	19860799	Ethanol intake significantly decreased <strong>proopiomelanocortin</strong> expression in the arcuate nucleus (38.31%) and micro <b>opioid</b> DAMGO stimulated [(35)S] GTPgamma binding in the caudate putamen (40%), nucleus accumbens core (AccC) (32.87%), and shell (AccS) (34.21%).
+POMC	drug	opioid	19804558	In an initial step, reverse transcription polymerase chain reaction (RT PCR) provided the first evidence that transcripts of three different <b>opioid</b> receptors (MOR, DOR, KOR), as well as the neuropeptide Y 5 receptor (NPY5R), leptin receptor (LEPR) and proopiomelanocortin (<strong>POMC</strong>), are expressed in both the porcine amygdala and hypothalamus.
+POMC	drug	opioid	19804558	In an initial step, reverse transcription polymerase chain reaction (RT PCR) provided the first evidence that transcripts of three different <b>opioid</b> receptors (MOR, DOR, KOR), as well as the neuropeptide Y 5 receptor (NPY5R), leptin receptor (LEPR) and <strong>proopiomelanocortin</strong> (<strong>POMC</strong>), are expressed in both the porcine amygdala and hypothalamus.
+POMC	drug	opioid	19789384	The <b>opioid</b> system consists of three receptors, mu, delta, and kappa, which are activated by endogenous <b>opioid</b> peptides processed from three protein precursors, <strong>proopiomelanocortin</strong>, proenkephalin, and prodynorphin.
+POMC	drug	opioid	19723567	We studied the effects of supraspinally administered <b>morphine</b> on the expression of the hypothalamic pro opiomelanocortin (<strong>POMC</strong>) gene and beta endorphin.
+POMC	drug	opioid	19723567	A single <b>morphine</b> administration significantly increased the hypothalamic <strong>POMC</strong> gene and beta endorphin expression at 2h after application in dose dependent fashion; however, repeated <b>morphine</b> administration had no effect on the hypothalamic <strong>POMC</strong> gene and beta endorphin expression.
+POMC	drug	opioid	19723567	Meanwhile, <b>naloxone</b> as well as muscimol and baclofen significantly attenuated the increases of the <strong>POMC</strong> gene expression induced by a single <b>morphine</b> administration.
+POMC	drug	opioid	19723567	These results imply that the hypothalamic <strong>POMC</strong> gene and beta endorphin expression may play an important role in the development of an acute physical dependency of <b>morphine</b>.
+POMC	drug	opioid	19723567	In that, GABAergic neurotransmission appear to be involved in the regulation of the hypothalamic <strong>POMC</strong> gene expression induced by supraspinal <b>morphine</b> administration.
+POMC	drug	psychedelics	19523041	Moreover, the consequences of acute and chronic <b>MDMA</b> administration on pro enkephalin (Penk) and pro opiomelanocortin (<strong>Pomc</strong>) gene expression were assessed by real time quantitative polymerase chain reaction (QPCR).
+POMC	drug	psychedelics	19523041	Penk gene expression was not modulated by acute <b>MDMA</b>, but a decrease of <strong>Pomc</strong> gene expression was observed, which was not antagonized by NTI.
+POMC	drug	psychedelics	19523041	Following chronic <b>MDMA</b> treatment, only the level of <strong>Pomc</strong> was modulated.
+POMC	drug	opioid	19481570	Besides actions of peptides from all three classical <b>opioid</b> precursors (proenkephalin, prodynorphin, <strong>proopiomelanocortin</strong>) on the three classical <b>opioid</b> receptors (delta, mu and kappa), dynorphins were also shown to exert non <b>opioid</b> effects mainly through direct effects on NMDA receptors.
+POMC	drug	alcohol	19389193	<strong>Proopiomelanocortin</strong> peptides are not essential for development of <b>ethanol</b> induced behavioral sensitization.
+POMC	addiction	sensitization	19389193	<strong>Proopiomelanocortin</strong> peptides are not essential for development of ethanol induced behavioral <b>sensitization</b>.
+POMC	drug	alcohol	19389193	Proopiomelanocortin (<strong>POMC</strong>) derived peptides including beta endorphin and alpha melanocyte stimulating hormone have been implicated in development of behavioral sensitization and the reinforcing effects of <b>alcohol</b> and other drugs of abuse.
+POMC	addiction	reward	19389193	Proopiomelanocortin (<strong>POMC</strong>) derived peptides including beta endorphin and alpha melanocyte stimulating hormone have been implicated in development of behavioral sensitization and the <b>reinforcing</b> effects of alcohol and other drugs of abuse.
+POMC	addiction	sensitization	19389193	Proopiomelanocortin (<strong>POMC</strong>) derived peptides including beta endorphin and alpha melanocyte stimulating hormone have been implicated in development of behavioral <b>sensitization</b> and the reinforcing effects of alcohol and other drugs of abuse.
+POMC	drug	alcohol	19389193	<strong>Proopiomelanocortin</strong> (<strong>POMC</strong>) derived peptides including beta endorphin and alpha melanocyte stimulating hormone have been implicated in development of behavioral sensitization and the reinforcing effects of <b>alcohol</b> and other drugs of abuse.
+POMC	addiction	reward	19389193	<strong>Proopiomelanocortin</strong> (<strong>POMC</strong>) derived peptides including beta endorphin and alpha melanocyte stimulating hormone have been implicated in development of behavioral sensitization and the <b>reinforcing</b> effects of alcohol and other drugs of abuse.
+POMC	addiction	sensitization	19389193	<strong>Proopiomelanocortin</strong> (<strong>POMC</strong>) derived peptides including beta endorphin and alpha melanocyte stimulating hormone have been implicated in development of behavioral <b>sensitization</b> and the reinforcing effects of alcohol and other drugs of abuse.
+POMC	drug	alcohol	19389193	This study used a genetically engineered mouse strain that is deficient for neural <strong>POMC</strong> to directly determine if any <strong>POMC</strong> peptides are necessary for the development of <b>ethanol</b> induced locomotor sensitization.
+POMC	addiction	sensitization	19389193	This study used a genetically engineered mouse strain that is deficient for neural <strong>POMC</strong> to directly determine if any <strong>POMC</strong> peptides are necessary for the development of ethanol induced locomotor <b>sensitization</b>.
+POMC	drug	alcohol	19389193	Adult female mice deficient for <strong>POMC</strong> in neurons only (<strong>Pomc</strong>( / )Tg/Tg, KO) and wildtype (<strong>Pomc</strong>(+/+)Tg/Tg, WT) littermates were injected once daily with either saline or <b>ethanol</b> (i.p.)
+POMC	drug	alcohol	19389193	Central <strong>POMC</strong> peptides are not required for either the acute locomotor stimulatory effect of <b>ethanol</b> or the development of <b>ethanol</b> induced locomotor sensitization.
+POMC	addiction	sensitization	19389193	Central <strong>POMC</strong> peptides are not required for either the acute locomotor stimulatory effect of ethanol or the development of ethanol induced locomotor <b>sensitization</b>.
+POMC	addiction	dependence	19217079	We tested whether <strong>POMC</strong> genetic variation affects risk for substance <b>dependence</b>.
+POMC	addiction	dependence	19217079	Given these replicated results, we conclude that variation in <strong>POMC</strong> confers vulnerability to multiple forms of substance <b>dependence</b>.
+POMC	drug	opioid	19155191	<strong>proopiomelanocortin</strong>, mu <b>opioid</b> receptor, dynorphin, and kappa <b>opioid</b> receptor), brain stress responsive systems (e.g.
+POMC	drug	alcohol	18589403	Interestingly, we found a two marker haplotype in the <strong>POMC</strong> gene that was associated with <b>alcohol</b> dependence in females in both cohorts.
+POMC	addiction	dependence	18589403	Interestingly, we found a two marker haplotype in the <strong>POMC</strong> gene that was associated with alcohol <b>dependence</b> in females in both cohorts.
+POMC	drug	alcohol	18162070	Because <b>ethanol</b> decreases <strong>POMC</strong> mRNA levels, we determined if exposure to an <b>ethanol</b> containing diet (ED) would significantly reduce central immunoreactivity of the MC peptide alpha MSH in rats.
+POMC	drug	alcohol	18034691	The brain pro opiomelanocortin (<strong>POMC</strong>) system which has important mediating roles in <b>alcohol</b> intake also has important functions in prolactin regulation and energy homeostasis.
+POMC	drug	alcohol	18034691	Consequently, the <strong>POMC</strong> system may have a role in integrating regulation of <b>alcohol</b> effects and these seemingly disparate regulatory systems.
+POMC	drug	opioid	17934066	We observed a significant decrease in the expression of <b>opioid</b> peptide precursors (<strong>proopiomelanocortin</strong>, proenkephalin, and prodynorphin) and of the kappa <b>opioid</b> receptor after 48 and 72 h of EtOH exposure (10 and 40 mM).
+POMC	drug	alcohol	17503481	We analyzed 18 OPRM1 SNPs, 18 OPRD1 SNPs, 7 PENK SNPs, and 7 <strong>POMC</strong> SNPs in a sample of 1923 European Americans from 219 multiplex <b>alcohol</b> dependent families.
+POMC	drug	opioid	17503481	Secondary analyses employing the narrower phenotype of <b>opioid</b> dependence (83 affected individuals) demonstrated association with SNPs in PENK and <strong>POMC</strong>, but not in OPRM1 or OPRD1.
+POMC	addiction	dependence	17503481	Secondary analyses employing the narrower phenotype of opioid <b>dependence</b> (83 affected individuals) demonstrated association with SNPs in PENK and <strong>POMC</strong>, but not in OPRM1 or OPRD1.
+POMC	drug	opioid	17503481	Haplotype analyses provided further support for the association of PENK and <strong>POMC</strong> with <b>opioid</b> dependence.
+POMC	addiction	dependence	17503481	Haplotype analyses provided further support for the association of PENK and <strong>POMC</strong> with opioid <b>dependence</b>.
+POMC	drug	alcohol	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, OPRD1, PENK and <strong>POMC</strong> are associated with <b>alcohol</b> dependence or general illicit drug dependence, but variations in PENK and <strong>POMC</strong> appear to be associated with the narrower phenotype of opioid dependence in these families.
+POMC	drug	opioid	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, OPRD1, PENK and <strong>POMC</strong> are associated with alcohol dependence or general illicit drug dependence, but variations in PENK and <strong>POMC</strong> appear to be associated with the narrower phenotype of <b>opioid</b> dependence in these families.
+POMC	addiction	dependence	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, OPRD1, PENK and <strong>POMC</strong> are associated with alcohol <b>dependence</b> or general illicit drug <b>dependence</b>, but variations in PENK and <strong>POMC</strong> appear to be associated with the narrower phenotype of opioid <b>dependence</b> in these families.
+POMC	drug	opioid	17467916	Mutant mice selectively lacking all forms of the beta endorphin peptides derived from the proopiomelanocortin (<strong>Pomc</strong>) gene did not show increased MOR P2 IR, decreased <b>morphine</b> antinociception, or reduced <b>morphine</b> CPP following pSNL.
+POMC	addiction	reward	17467916	Mutant mice selectively lacking all forms of the beta endorphin peptides derived from the proopiomelanocortin (<strong>Pomc</strong>) gene did not show increased MOR P2 IR, decreased morphine antinociception, or reduced morphine <b>CPP</b> following pSNL.
+POMC	drug	opioid	17467916	Mutant mice selectively lacking all forms of the beta endorphin peptides derived from the <strong>proopiomelanocortin</strong> (<strong>Pomc</strong>) gene did not show increased MOR P2 IR, decreased <b>morphine</b> antinociception, or reduced <b>morphine</b> CPP following pSNL.
+POMC	addiction	reward	17467916	Mutant mice selectively lacking all forms of the beta endorphin peptides derived from the <strong>proopiomelanocortin</strong> (<strong>Pomc</strong>) gene did not show increased MOR P2 IR, decreased morphine antinociception, or reduced morphine <b>CPP</b> following pSNL.
+POMC	drug	alcohol	17347308	We also found that immediately after <b>ethanol</b> treatments there was a significant reduction in the expression of <strong>proopiomelanocortin</strong> and adenylyl cyclases mRNA and an increased expression of several TGF beta1 linked apoptotic genes in beta EP neurons isolated by laser captured microdissection from arcuate nuclei of young rats.
+POMC	drug	opioid	17065397	In this study, we investigated the effects of acute <b>morphine</b> administration, chronic intermittent escalating dose <b>morphine</b> administration and spontaneous withdrawal from chronic <b>morphine</b> on mRNA levels of mu <b>opioid</b> receptor (MOP r), and the <b>opioid</b> peptides pro opiomelanocortin (<strong>POMC</strong>) and preprodynorphin (ppDyn) in several key brain regions of the rat, associated with drug reward and motivated behaviors: lateral hypothalamus (lat.hyp), nucleus accumbens (NAc) core, amygdala, and caudate putamen (CPu).
+POMC	addiction	reward	17065397	In this study, we investigated the effects of acute morphine administration, chronic intermittent escalating dose morphine administration and spontaneous withdrawal from chronic morphine on mRNA levels of mu opioid receptor (MOP r), and the opioid peptides pro opiomelanocortin (<strong>POMC</strong>) and preprodynorphin (ppDyn) in several key brain regions of the rat, associated with drug <b>reward</b> and motivated behaviors: lateral hypothalamus (lat.hyp), nucleus accumbens (NAc) core, amygdala, and caudate putamen (CPu).
+POMC	addiction	withdrawal	17065397	In this study, we investigated the effects of acute morphine administration, chronic intermittent escalating dose morphine administration and spontaneous <b>withdrawal</b> from chronic morphine on mRNA levels of mu opioid receptor (MOP r), and the opioid peptides pro opiomelanocortin (<strong>POMC</strong>) and preprodynorphin (ppDyn) in several key brain regions of the rat, associated with drug reward and motivated behaviors: lateral hypothalamus (lat.hyp), nucleus accumbens (NAc) core, amygdala, and caudate putamen (CPu).
+POMC	drug	opioid	17065397	Activation of the stress responsive hypothalamic pituitary adrenal axis by 12 h withdrawal from chronic <b>morphine</b> was confirmed; both <strong>POMC</strong> mRNA levels in the anterior pituitary and plasma adrenocorticotropic hormone levels were significantly elevated.
+POMC	addiction	withdrawal	17065397	Activation of the stress responsive hypothalamic pituitary adrenal axis by 12 h <b>withdrawal</b> from chronic morphine was confirmed; both <strong>POMC</strong> mRNA levels in the anterior pituitary and plasma adrenocorticotropic hormone levels were significantly elevated.
+POMC	drug	cocaine	16237390	To explore neuropharmacological interactions between methadone maintenance and <b>cocaine</b> conditioning, we quantitatively measured mRNA levels of mu opioid receptor (MOR) and <strong>proopiomelanocortin</strong> genes 10 days after methadone maintenance.
+POMC	drug	opioid	16237390	To explore neuropharmacological interactions between <b>methadone</b> maintenance and cocaine conditioning, we quantitatively measured mRNA levels of mu <b>opioid</b> receptor (MOR) and <strong>proopiomelanocortin</strong> genes 10 days after <b>methadone</b> maintenance.
+POMC	drug	cocaine	16039786	The present studies were undertaken to determine whether: (1) 14 day (chronic) "binge" pattern <b>cocaine</b> administration (45 mg/kg/day) or its withdrawal for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters arginine vasopressin mRNA levels in amygdala or hypothalamus; (2) the opioid receptor antagonist naloxone (1mg/kg) alters arginine vasopressin mRNA or hypothalamic pituitary adrenal hormonal responses in acute <b>cocaine</b> withdrawal; and (3) there are associated changes of mu opioid receptor or <strong>proopiomelanocortin</strong> mRNA levels.
+POMC	drug	opioid	16039786	The present studies were undertaken to determine whether: (1) 14 day (chronic) "binge" pattern cocaine administration (45 mg/kg/day) or its withdrawal for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters arginine vasopressin mRNA levels in amygdala or hypothalamus; (2) the <b>opioid</b> receptor antagonist <b>naloxone</b> (1mg/kg) alters arginine vasopressin mRNA or hypothalamic pituitary adrenal hormonal responses in acute cocaine withdrawal; and (3) there are associated changes of mu <b>opioid</b> receptor or <strong>proopiomelanocortin</strong> mRNA levels.
+POMC	addiction	intoxication	16039786	The present studies were undertaken to determine whether: (1) 14 day (chronic) "<b>binge</b>" pattern cocaine administration (45 mg/kg/day) or its withdrawal for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters arginine vasopressin mRNA levels in amygdala or hypothalamus; (2) the opioid receptor antagonist naloxone (1mg/kg) alters arginine vasopressin mRNA or hypothalamic pituitary adrenal hormonal responses in acute cocaine withdrawal; and (3) there are associated changes of mu opioid receptor or <strong>proopiomelanocortin</strong> mRNA levels.
+POMC	addiction	withdrawal	16039786	The present studies were undertaken to determine whether: (1) 14 day (chronic) "binge" pattern cocaine administration (45 mg/kg/day) or its <b>withdrawal</b> for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters arginine vasopressin mRNA levels in amygdala or hypothalamus; (2) the opioid receptor antagonist naloxone (1mg/kg) alters arginine vasopressin mRNA or hypothalamic pituitary adrenal hormonal responses in acute cocaine <b>withdrawal</b>; and (3) there are associated changes of mu opioid receptor or <strong>proopiomelanocortin</strong> mRNA levels.
+POMC	drug	cocaine	16039786	In hypothalamus, neither chronic <b>cocaine</b> nor acute withdrawal altered arginine vasopressin, <strong>proopiomelanocortin</strong> or mu opioid receptor mRNA levels.
+POMC	drug	opioid	16039786	In hypothalamus, neither chronic cocaine nor acute withdrawal altered arginine vasopressin, <strong>proopiomelanocortin</strong> or mu <b>opioid</b> receptor mRNA levels.
+POMC	addiction	withdrawal	16039786	In hypothalamus, neither chronic cocaine nor acute <b>withdrawal</b> altered arginine vasopressin, <strong>proopiomelanocortin</strong> or mu opioid receptor mRNA levels.
+POMC	drug	cannabinoid	15901756	Collectively, these data reveal that guinea pig ARC neurons, including <strong>proopiomelanocortin</strong> neurons, express a prominent I(A) that is positively modulated by <b>cannabinoids</b> in a sex specific way by altering the voltage dependence of its inactivation.
+POMC	addiction	dependence	15901756	Collectively, these data reveal that guinea pig ARC neurons, including <strong>proopiomelanocortin</strong> neurons, express a prominent I(A) that is positively modulated by cannabinoids in a sex specific way by altering the voltage <b>dependence</b> of its inactivation.
+POMC	drug	alcohol	15834231	Vasoactive intestinal peptide and corticotropin releasing hormone increase beta endorphin release and <strong>proopiomelanocortin</strong> messenger RNA levels in primary cultures of hypothalamic cells: effects of acute and chronic <b>ethanol</b> treatment.
+POMC	drug	cocaine	15519677	Effects of selective D1  or D2 like dopamine receptor antagonists with acute "binge" pattern <b>cocaine</b> on corticotropin releasing hormone and <strong>proopiomelanocortin</strong> mRNA levels in the hypothalamus.
+POMC	addiction	intoxication	15519677	Effects of selective D1  or D2 like dopamine receptor antagonists with acute "<b>binge</b>" pattern cocaine on corticotropin releasing hormone and <strong>proopiomelanocortin</strong> mRNA levels in the hypothalamus.
+POMC	drug	cocaine	15519677	In the anterior pituitary, acute "binge" <b>cocaine</b> or its combinations with either DA antagonist did not alter CRH R1 receptor or <strong>POMC</strong> mRNA levels.
+POMC	addiction	intoxication	15519677	In the anterior pituitary, acute "<b>binge</b>" cocaine or its combinations with either DA antagonist did not alter CRH R1 receptor or <strong>POMC</strong> mRNA levels.
+POMC	drug	cocaine	15519677	The second aim of our study was to investigate the roles that D1R or D2R could play in regulation of <strong>POMC</strong> mRNA levels in the hypothalamus in response to acute "binge" <b>cocaine</b>.
+POMC	addiction	intoxication	15519677	The second aim of our study was to investigate the roles that D1R or D2R could play in regulation of <strong>POMC</strong> mRNA levels in the hypothalamus in response to acute "<b>binge</b>" cocaine.
+POMC	drug	cocaine	15519677	The <strong>POMC</strong> mRNA increases induced by the D2R blockade were attenuated by acute "binge" <b>cocaine</b>.
+POMC	addiction	intoxication	15519677	The <strong>POMC</strong> mRNA increases induced by the D2R blockade were attenuated by acute "<b>binge</b>" cocaine.
+POMC	drug	cocaine	15519677	Neither the D2R blockade nor acute "binge" <b>cocaine</b> altered <strong>POMC</strong> mRNA levels in the amygdala, anterior pituitary or neurointermediate lobe of the pituitary.
+POMC	addiction	intoxication	15519677	Neither the D2R blockade nor acute "<b>binge</b>" cocaine altered <strong>POMC</strong> mRNA levels in the amygdala, anterior pituitary or neurointermediate lobe of the pituitary.
+POMC	drug	cocaine	15519677	In contrast to the D2R, the D1R blockade by SCH23390, acute "binge" <b>cocaine</b> or their combination had no effect on hypothalamic <strong>POMC</strong> mRNA levels.
+POMC	addiction	intoxication	15519677	In contrast to the D2R, the D1R blockade by SCH23390, acute "<b>binge</b>" cocaine or their combination had no effect on hypothalamic <strong>POMC</strong> mRNA levels.
+POMC	drug	cocaine	15519677	These results support a specific role for D2R in acute <b>cocaine</b>'s effects on hypothalamic <strong>POMC</strong> gene expression.
+POMC	drug	alcohol	14709806	We previously demonstrated that chronic daily <b>ethanol</b> consumption and daily withdrawal by male rats in a modified <b>ethanol</b> liquid diet paradigm produced (a) chronically increased adrenal glucocorticoid activity; (b) decreased plasma testosterone; (c) decreased forebrain <strong>proopiomelanocortin</strong> gene expression; and (d) corresponding alterations in plasma leptin levels all of which are consistent with reported changes during <b>alcohol</b> abuse and <b>alcoholism</b>.
+POMC	addiction	withdrawal	14709806	We previously demonstrated that chronic daily ethanol consumption and daily <b>withdrawal</b> by male rats in a modified ethanol liquid diet paradigm produced (a) chronically increased adrenal glucocorticoid activity; (b) decreased plasma testosterone; (c) decreased forebrain <strong>proopiomelanocortin</strong> gene expression; and (d) corresponding alterations in plasma leptin levels all of which are consistent with reported changes during alcohol abuse and alcoholism.
+POMC	drug	opioid	14568335	The relationships between the CRF, which enhances the proopiomelanocortin (<strong>POMC</strong>) biosynthesis, and <strong>POMC</strong> derived peptides (<b>opioids</b> and melanocortins) might be a new target for rational treatment of <b>morphine</b> tolerance.
+POMC	drug	opioid	14568335	The relationships between the CRF, which enhances the <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) biosynthesis, and <strong>POMC</strong> derived peptides (<b>opioids</b> and melanocortins) might be a new target for rational treatment of <b>morphine</b> tolerance.
+POMC	drug	opioid	12851316	Because the <b>opioid</b> peptide beta endorphin is co synthesized and released with melanocortins from proopiomelanocortin (<strong>POMC</strong>) neuronal terminals, we examined the physiological role of beta endorphin in feeding and energy homeostasis using a strain of mutant mice with a selective deficiency of beta endorphin.
+POMC	drug	opioid	12851316	Because the <b>opioid</b> peptide beta endorphin is co synthesized and released with melanocortins from <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) neuronal terminals, we examined the physiological role of beta endorphin in feeding and energy homeostasis using a strain of mutant mice with a selective deficiency of beta endorphin.
+POMC	drug	cannabinoid	12641731	Spontaneous <b>cannabinoid</b> withdrawal produced time related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (TH) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (PENK) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (<strong>POMC</strong>) gene expression in the arcuate nucleus of the hypothalamus.
+POMC	addiction	withdrawal	12641731	Spontaneous cannabinoid <b>withdrawal</b> produced time related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (TH) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (PENK) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (<strong>POMC</strong>) gene expression in the arcuate nucleus of the hypothalamus.
+POMC	drug	cocaine	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of <strong>proopiomelanocortin</strong> and corticotropin releasing hormone receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic 'binge' <b>cocaine</b> and withdrawal.
+POMC	addiction	intoxication	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of <strong>proopiomelanocortin</strong> and corticotropin releasing hormone receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic '<b>binge</b>' cocaine and withdrawal.
+POMC	addiction	withdrawal	12576179	Alterations in hypothalamic pituitary adrenal axis activity and in levels of <strong>proopiomelanocortin</strong> and corticotropin releasing hormone receptor 1 mRNAs in the pituitary and hypothalamus of the rat during chronic 'binge' cocaine and <b>withdrawal</b>.
+POMC	drug	cocaine	12576179	In the anterior pituitary, levels of both proopiomelanocortin (<strong>POMC</strong>) and CRH receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic 'binge' <b>cocaine</b> and were at control levels on the 4th day of withdrawal.
+POMC	addiction	intoxication	12576179	In the anterior pituitary, levels of both proopiomelanocortin (<strong>POMC</strong>) and CRH receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic '<b>binge</b>' cocaine and were at control levels on the 4th day of withdrawal.
+POMC	addiction	withdrawal	12576179	In the anterior pituitary, levels of both proopiomelanocortin (<strong>POMC</strong>) and CRH receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic 'binge' cocaine and were at control levels on the 4th day of <b>withdrawal</b>.
+POMC	drug	cocaine	12576179	In the anterior pituitary, levels of both <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and CRH receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic 'binge' <b>cocaine</b> and were at control levels on the 4th day of withdrawal.
+POMC	addiction	intoxication	12576179	In the anterior pituitary, levels of both <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and CRH receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic '<b>binge</b>' cocaine and were at control levels on the 4th day of withdrawal.
+POMC	addiction	withdrawal	12576179	In the anterior pituitary, levels of both <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and CRH receptor 1 (R1) mRNAs were significantly higher than saline controls on the 14th day of chronic 'binge' cocaine and were at control levels on the 4th day of <b>withdrawal</b>.
+POMC	drug	cocaine	12576179	In the neurointermediate lobe of the pituitary, a sustained reduction in <strong>POMC</strong> mRNA levels was observed on the 3rd, 7th and 14th day of chronic 'binge' <b>cocaine</b>, but <strong>POMC</strong> mRNA was at control levels by the 4th day of withdrawal.
+POMC	addiction	intoxication	12576179	In the neurointermediate lobe of the pituitary, a sustained reduction in <strong>POMC</strong> mRNA levels was observed on the 3rd, 7th and 14th day of chronic '<b>binge</b>' cocaine, but <strong>POMC</strong> mRNA was at control levels by the 4th day of withdrawal.
+POMC	addiction	withdrawal	12576179	In the neurointermediate lobe of the pituitary, a sustained reduction in <strong>POMC</strong> mRNA levels was observed on the 3rd, 7th and 14th day of chronic 'binge' cocaine, but <strong>POMC</strong> mRNA was at control levels by the 4th day of <b>withdrawal</b>.
+POMC	drug	cocaine	12576179	In the hypothalamus, <strong>POMC</strong> mRNA levels showed a transient decrease on the 1st day of 'binge' <b>cocaine</b> with no change during chronic 'binge' <b>cocaine</b> or its withdrawal.
+POMC	addiction	intoxication	12576179	In the hypothalamus, <strong>POMC</strong> mRNA levels showed a transient decrease on the 1st day of '<b>binge</b>' cocaine with no change during chronic '<b>binge</b>' cocaine or its withdrawal.
+POMC	addiction	withdrawal	12576179	In the hypothalamus, <strong>POMC</strong> mRNA levels showed a transient decrease on the 1st day of 'binge' cocaine with no change during chronic 'binge' cocaine or its <b>withdrawal</b>.
+POMC	drug	cocaine	12576179	In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by <b>cocaine</b> withdrawal may be, at least in part, due to the increased <strong>POMC</strong> and/or CRH R1 gene expression observed in the anterior pituitary after chronic 'binge' <b>cocaine</b>.
+POMC	addiction	intoxication	12576179	In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine withdrawal may be, at least in part, due to the increased <strong>POMC</strong> and/or CRH R1 gene expression observed in the anterior pituitary after chronic '<b>binge</b>' cocaine.
+POMC	addiction	withdrawal	12576179	In addition to being associated with CRH input from the hypothalamus, the activation of the HPA axis by cocaine <b>withdrawal</b> may be, at least in part, due to the increased <strong>POMC</strong> and/or CRH R1 gene expression observed in the anterior pituitary after chronic 'binge' cocaine.
+POMC	drug	cocaine	12125043	Effects of acute "binge" <b>cocaine</b> on preprodynorphin, preproenkephalin, <strong>proopiomelanocortin</strong>, and corticotropin releasing hormone receptor mRNA levels in the striatum and hypothalamic pituitary adrenal axis of mu opioid receptor knockout mice.
+POMC	drug	opioid	12125043	Effects of acute "binge" cocaine on preprodynorphin, preproenkephalin, <strong>proopiomelanocortin</strong>, and corticotropin releasing hormone receptor mRNA levels in the striatum and hypothalamic pituitary adrenal axis of mu <b>opioid</b> receptor knockout mice.
+POMC	addiction	intoxication	12125043	Effects of acute "<b>binge</b>" cocaine on preprodynorphin, preproenkephalin, <strong>proopiomelanocortin</strong>, and corticotropin releasing hormone receptor mRNA levels in the striatum and hypothalamic pituitary adrenal axis of mu opioid receptor knockout mice.
+POMC	drug	cocaine	12125043	Hypothalamic CRH(1) receptor and <strong>POMC</strong> mRNAs were expressed at similar levels in untreated and in <b>cocaine</b> treated mice of each genotype.
+POMC	drug	opioid	12101431	The phase 2 response in animals treated with formalin and <b>naloxone</b> did not differ significantly from the control, implying that the analgesic effects of <strong>POMC</strong> cDNA particle injection in phase 2 of the formalin test are reversed by <b>naloxone</b>.
+POMC	drug	opioid	12015197	The endogenous <b>opioid</b> system consists of three <b>opioid</b> peptide precursor genes encoding enkephalins (preproenkephalin, Penk), dynorphins (preprodynorphin, Pdyn) and beta endorphin (betaend), proopiomelanocortin (<strong>POMC</strong>) and three receptor genes encoding mu opiod receptor (MOR), delta opiod receptor (DOR) and kappa opiod receptor (KOR).
+POMC	drug	opioid	12015197	The endogenous <b>opioid</b> system consists of three <b>opioid</b> peptide precursor genes encoding enkephalins (preproenkephalin, Penk), dynorphins (preprodynorphin, Pdyn) and beta endorphin (betaend), <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and three receptor genes encoding mu opiod receptor (MOR), delta opiod receptor (DOR) and kappa opiod receptor (KOR).
+POMC	drug	alcohol	11981131	Although forebrain pro opiomelanocortin (<strong>POMC</strong>) producing neurons seem to mediate or modulate many responses to <b>ethanol</b> consumption, changes in activity of this opiomelanocortinergic system in response to chronic <b>ethanol</b> consumption, withdrawal, and subsequent abstinence remain unresolved.
+POMC	addiction	withdrawal	11981131	Although forebrain pro opiomelanocortin (<strong>POMC</strong>) producing neurons seem to mediate or modulate many responses to ethanol consumption, changes in activity of this opiomelanocortinergic system in response to chronic ethanol consumption, <b>withdrawal</b>, and subsequent abstinence remain unresolved.
+POMC	drug	alcohol	11981131	We investigated the effects of chronic daily <b>ethanol</b> consumption, withdrawal, and subsequent abstinence on adult male Sprague Dawley rat forebrain opiomelanocortinergic activity as reflected by changes in hypothalamic <strong>POMC</strong> messenger RNA (mRNA) content by using a well characterized liquid diet model that we have previously demonstrated to accurately simulate not only daily oral <b>ethanol</b> consumption quantity and pattern, but also both neuroendocrine and behavioral changes characteristic of actively drinking and subsequently abstinent <b>alcoholics</b>.
+POMC	addiction	withdrawal	11981131	We investigated the effects of chronic daily ethanol consumption, <b>withdrawal</b>, and subsequent abstinence on adult male Sprague Dawley rat forebrain opiomelanocortinergic activity as reflected by changes in hypothalamic <strong>POMC</strong> messenger RNA (mRNA) content by using a well characterized liquid diet model that we have previously demonstrated to accurately simulate not only daily oral ethanol consumption quantity and pattern, but also both neuroendocrine and behavioral changes characteristic of actively drinking and subsequently abstinent alcoholics.
+POMC	drug	alcohol	11981131	After 7 weeks of daily <b>ethanol</b> consumption at night and withdrawal during the day, evening mediobasal hypothalamus <strong>POMC</strong> mRNA concentrations were suppressed versus both ad libitum fed and pair fed controls.
+POMC	addiction	withdrawal	11981131	After 7 weeks of daily ethanol consumption at night and <b>withdrawal</b> during the day, evening mediobasal hypothalamus <strong>POMC</strong> mRNA concentrations were suppressed versus both ad libitum fed and pair fed controls.
+POMC	drug	alcohol	11981131	Three weeks after gradual removal of <b>ethanol</b> from the diet, mediobasal hypothalamus <strong>POMC</strong> mRNA concentrations were increased relative to ad libitum fed and pair fed controls.
+POMC	drug	alcohol	11981131	Because each of these hormones has been demonstrated to modify forebrain <strong>POMC</strong> gene expression under some conditions, the overall changes in forebrain opiomelanocortinergic regulation in response to chronic daily <b>ethanol</b>/withdrawal and subsequent abstinence probably reflect, at least in part, regulation by multiple endocrine mechanisms, together with responses to stress, development of tolerance during chronic daily <b>ethanol</b> consumption, and rebound of function after termination of this consumption.
+POMC	addiction	withdrawal	11981131	Because each of these hormones has been demonstrated to modify forebrain <strong>POMC</strong> gene expression under some conditions, the overall changes in forebrain opiomelanocortinergic regulation in response to chronic daily ethanol/<b>withdrawal</b> and subsequent abstinence probably reflect, at least in part, regulation by multiple endocrine mechanisms, together with responses to stress, development of tolerance during chronic daily ethanol consumption, and rebound of function after termination of this consumption.
+POMC	drug	alcohol	11981131	Overall, the demonstrated changes in forebrain <strong>POMC</strong> gene expression are consistent with significant roles for forebrain opiomelanocortinergic regulation in mediating <b>alcohol</b> dependence, propensity to relapse, and the <b>alcohol</b> deprivation effect.
+POMC	addiction	dependence	11981131	Overall, the demonstrated changes in forebrain <strong>POMC</strong> gene expression are consistent with significant roles for forebrain opiomelanocortinergic regulation in mediating alcohol <b>dependence</b>, propensity to relapse, and the alcohol deprivation effect.
+POMC	addiction	relapse	11981131	Overall, the demonstrated changes in forebrain <strong>POMC</strong> gene expression are consistent with significant roles for forebrain opiomelanocortinergic regulation in mediating alcohol dependence, propensity to <b>relapse</b>, and the alcohol deprivation effect.
+POMC	drug	opioid	11858765	This study was aimed to evaluate the effects of <b>morphine</b> on hypothalamo pituitary adrenocortical (HPA) axis, namely proopiomelanocortin (<strong>POMC</strong>) mRNA and plasma corticosterone, in relation to its influence on glutamate receptor gene expression in central and peripheral sites related to HPA axis regulation.
+POMC	drug	opioid	11858765	This study was aimed to evaluate the effects of <b>morphine</b> on hypothalamo pituitary adrenocortical (HPA) axis, namely <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) mRNA and plasma corticosterone, in relation to its influence on glutamate receptor gene expression in central and peripheral sites related to HPA axis regulation.
+POMC	drug	opioid	11858765	Present data obtained in females allow to suggest that <b>morphine</b> exerts some of its effects on HPA axis by <strong>POMC</strong> unrelated mechanisms seemingly in a gender specific manner.
+POMC	drug	opioid	11744066	The <b>opioid</b> peptide <strong>proopiomelanocortin</strong> proved extraordinarily rich in mutations that often lead to severe phenotypical consequences.
+POMC	drug	alcohol	11141043	In an initial experiment in which <b>ethanol</b> (5%, w/v) was incrementally introduced to liquid diet over a 1 week period followed by 4 weeks of chronic <b>ethanol</b> consumption, not only <b>ethanol</b> treated rats but also pair fed control rats exhibited decreased (p < 0.05 vs. ad libitum fed controls) anterior pituitary pro opiomelanocortin (<strong>POMC</strong>) mRNA concentrations and associated decreases in plasma corticosterone and adrenocorticotropin (ACTH) levels for at least 3 weeks after gradual withdrawal of <b>ethanol</b> from the diet.
+POMC	addiction	withdrawal	11141043	In an initial experiment in which ethanol (5%, w/v) was incrementally introduced to liquid diet over a 1 week period followed by 4 weeks of chronic ethanol consumption, not only ethanol treated rats but also pair fed control rats exhibited decreased (p < 0.05 vs. ad libitum fed controls) anterior pituitary pro opiomelanocortin (<strong>POMC</strong>) mRNA concentrations and associated decreases in plasma corticosterone and adrenocorticotropin (ACTH) levels for at least 3 weeks after gradual <b>withdrawal</b> of ethanol from the diet.
+POMC	drug	alcohol	11141043	Three weeks after gradual withdrawal of <b>ethanol</b> from the diet, anterior pituitary <strong>POMC</strong> mRNA concentrations were suppressed (p < 0.05) and thymus and spleen weights were increased (p < 0.05) versus both pair fed and ad libitum fed controls, accompanied by trends for decreased basal plasma corticosterone and adrenal weights.
+POMC	addiction	withdrawal	11141043	Three weeks after gradual <b>withdrawal</b> of ethanol from the diet, anterior pituitary <strong>POMC</strong> mRNA concentrations were suppressed (p < 0.05) and thymus and spleen weights were increased (p < 0.05) versus both pair fed and ad libitum fed controls, accompanied by trends for decreased basal plasma corticosterone and adrenal weights.
+POMC	drug	alcohol	11045867	Reduced hypothalamic <strong>POMC</strong> and anterior pituitary CRF1 receptor mRNA levels after acute, but not chronic, daily "binge" intragastric <b>alcohol</b> administration.
+POMC	addiction	intoxication	11045867	Reduced hypothalamic <strong>POMC</strong> and anterior pituitary CRF1 receptor mRNA levels after acute, but not chronic, daily "<b>binge</b>" intragastric alcohol administration.
+POMC	drug	alcohol	11045867	Endogenous corticotropin releasing factor (CRF), its pituitary CRF1 receptor, and proopiomelanocortin (<strong>POMC</strong>) may be involved in the hypothalamic pituitary adrenal (HPA) responses to <b>alcohol</b>.
+POMC	drug	alcohol	11045867	Endogenous corticotropin releasing factor (CRF), its pituitary CRF1 receptor, and <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) may be involved in the hypothalamic pituitary adrenal (HPA) responses to <b>alcohol</b>.
+POMC	drug	alcohol	11045867	The levels of CRF, CRF1 receptor, and <strong>POMC</strong> mRNAs in the hypothalamic pituitary axis were measured after acute (1 day) or chronic (14 days) binge pattern <b>alcohol</b> administration.
+POMC	addiction	intoxication	11045867	The levels of CRF, CRF1 receptor, and <strong>POMC</strong> mRNAs in the hypothalamic pituitary axis were measured after acute (1 day) or chronic (14 days) <b>binge</b> pattern alcohol administration.
+POMC	drug	alcohol	11045867	<strong>POMC</strong> mRNA levels in the anterior pituitary were not altered by either acute or chronic <b>alcohol</b> administration.
+POMC	drug	alcohol	11045867	In the hypothalamus, <strong>POMC</strong> mRNA levels were decreased significantly after acute but not chronic binge <b>alcohol</b> administration.
+POMC	addiction	intoxication	11045867	In the hypothalamus, <strong>POMC</strong> mRNA levels were decreased significantly after acute but not chronic <b>binge</b> alcohol administration.
+POMC	drug	alcohol	11045867	These results suggest that (1) rats exposed to chronic binge <b>alcohol</b> develop tolerance in HPA activity, as shown by no elevation of ACTH and an attenuated corticosterone response to chronic <b>alcohol</b> after initial dramatic elevations by acute <b>alcohol</b> administration; (2) a concurrent acute decrease in CRF1 receptor mRNA levels in the anterior pituitary is associated with increased HPA activity, and (3) alterations of <strong>POMC</strong> gene expression in the hypothalamic region may have implications for a molecular understanding of the neuroendocrine response to <b>alcohol</b>.
+POMC	addiction	intoxication	11045867	These results suggest that (1) rats exposed to chronic <b>binge</b> alcohol develop tolerance in HPA activity, as shown by no elevation of ACTH and an attenuated corticosterone response to chronic alcohol after initial dramatic elevations by acute alcohol administration; (2) a concurrent acute decrease in CRF1 receptor mRNA levels in the anterior pituitary is associated with increased HPA activity, and (3) alterations of <strong>POMC</strong> gene expression in the hypothalamic region may have implications for a molecular understanding of the neuroendocrine response to alcohol.
+POMC	addiction	addiction	10821116	In situ hybridization was used to compare the content of <strong>proopiomelanocortin</strong>, proenkephalin and prodynorphin mRNA in distinct brain regions known to be involved in the reinforcing properties of <b>addictive</b> drugs, between rats from each line.
+POMC	addiction	reward	10821116	In situ hybridization was used to compare the content of <strong>proopiomelanocortin</strong>, proenkephalin and prodynorphin mRNA in distinct brain regions known to be involved in the <b>reinforcing</b> properties of addictive drugs, between rats from each line.
+POMC	drug	cannabinoid	10219981	Repeated administration of delta9 <b>tetrahydrocannabinol</b> produces a differential time related responsiveness on proenkephalin, <strong>proopiomelanocortin</strong> and corticotropin releasing factor gene expression in the hypothalamus and pituitary gland of the rat.
+POMC	drug	cannabinoid	10201639	The purpose of the present study was to explore the molecular mechanisms by which the <b>cannabinoid</b> system may interact with the hypothalamic pituitary adrenal axis and the <strong>proopiomelanocortin</strong> opioid system.
+POMC	drug	opioid	10201639	The purpose of the present study was to explore the molecular mechanisms by which the cannabinoid system may interact with the hypothalamic pituitary adrenal axis and the <strong>proopiomelanocortin</strong> <b>opioid</b> system.
+POMC	drug	cannabinoid	10201639	These results revealed that chronic <b>cannabinoid</b> administration enhances corticotropin releasing factor and <strong>proopiomelanocortin</strong> gene expression in the hypothalamus and anterior pituitary, a process that may be considered as part of a molecular integrative response to the stress associated to <b>cannabinoid</b> drug abuse.
+POMC	drug	nicotine	9695129	Effects of chronic <b>nicotine</b> treatment and withdrawal on hypothalamic <strong>proopiomelanocortin</strong> gene expression and neuroendocrine regulation.
+POMC	addiction	withdrawal	9695129	Effects of chronic nicotine treatment and <b>withdrawal</b> on hypothalamic <strong>proopiomelanocortin</strong> gene expression and neuroendocrine regulation.
+POMC	drug	nicotine	9695129	Since we have proposed that interactions between mediobasohypothalamic (MBH) dopaminergic and beta endorphinergic mechanisms have a key role in neuroendocrine integration, we investigated the effects of chronic <b>nicotine</b> treatment and withdrawal on: (1) MBH concentrations of proopiomelanocortin (<strong>POMC</strong>, precursor for beta endorphin biosynthesis) mRNA; (2) MBH concentrations of tyrosine hydroxylase (TH, rate limiting enzyme in catecholamine biosynthesis) mRNA; (3) corresponding serum prolacin, corticosterone, luteinizing hormone (LH), and testosterone concentrations.
+POMC	addiction	withdrawal	9695129	Since we have proposed that interactions between mediobasohypothalamic (MBH) dopaminergic and beta endorphinergic mechanisms have a key role in neuroendocrine integration, we investigated the effects of chronic nicotine treatment and <b>withdrawal</b> on: (1) MBH concentrations of proopiomelanocortin (<strong>POMC</strong>, precursor for beta endorphin biosynthesis) mRNA; (2) MBH concentrations of tyrosine hydroxylase (TH, rate limiting enzyme in catecholamine biosynthesis) mRNA; (3) corresponding serum prolacin, corticosterone, luteinizing hormone (LH), and testosterone concentrations.
+POMC	drug	nicotine	9695129	Since we have proposed that interactions between mediobasohypothalamic (MBH) dopaminergic and beta endorphinergic mechanisms have a key role in neuroendocrine integration, we investigated the effects of chronic <b>nicotine</b> treatment and withdrawal on: (1) MBH concentrations of <strong>proopiomelanocortin</strong> (<strong>POMC</strong>, precursor for beta endorphin biosynthesis) mRNA; (2) MBH concentrations of tyrosine hydroxylase (TH, rate limiting enzyme in catecholamine biosynthesis) mRNA; (3) corresponding serum prolacin, corticosterone, luteinizing hormone (LH), and testosterone concentrations.
+POMC	addiction	withdrawal	9695129	Since we have proposed that interactions between mediobasohypothalamic (MBH) dopaminergic and beta endorphinergic mechanisms have a key role in neuroendocrine integration, we investigated the effects of chronic nicotine treatment and <b>withdrawal</b> on: (1) MBH concentrations of <strong>proopiomelanocortin</strong> (<strong>POMC</strong>, precursor for beta endorphin biosynthesis) mRNA; (2) MBH concentrations of tyrosine hydroxylase (TH, rate limiting enzyme in catecholamine biosynthesis) mRNA; (3) corresponding serum prolacin, corticosterone, luteinizing hormone (LH), and testosterone concentrations.
+POMC	drug	nicotine	9695129	Chronic daily <b>nicotine</b> administration induced significant changes in serum corticosterone, serum prolactin, MBH TH mRNA, and MBH <strong>POMC</strong> mRNA concentrations that tended to persist through day 3 of withdrawal; serum prolactin and MBH <strong>POMC</strong> mRNA concentrations were suppressed whereas serum corticosterone and MBH TH mRNA concentrations were stimulated.
+POMC	addiction	withdrawal	9695129	Chronic daily nicotine administration induced significant changes in serum corticosterone, serum prolactin, MBH TH mRNA, and MBH <strong>POMC</strong> mRNA concentrations that tended to persist through day 3 of <b>withdrawal</b>; serum prolactin and MBH <strong>POMC</strong> mRNA concentrations were suppressed whereas serum corticosterone and MBH TH mRNA concentrations were stimulated.
+POMC	drug	nicotine	9695129	None of the parameters were significantly different from control levels following 7 or more days of withdrawal from <b>nicotine</b>, except for a significant decrease of MBH <strong>POMC</strong> mRNA concentrations on day 21.
+POMC	addiction	withdrawal	9695129	None of the parameters were significantly different from control levels following 7 or more days of <b>withdrawal</b> from nicotine, except for a significant decrease of MBH <strong>POMC</strong> mRNA concentrations on day 21.
+POMC	drug	nicotine	9695129	These results suggest that chronic <b>nicotine</b> inhibited <strong>POMC</strong> gene expression and thus, probably, biosynthesis of beta endorphin and other opiomelanocortins.
+POMC	drug	alcohol	9665316	The effect of an acute <b>ethanol</b> exposure on the rat brain <strong>POMC</strong> opiopeptide system.
+POMC	drug	alcohol	9512064	In a second study, pituitary beta endorphin gene expression (proopiomelanocortin or <strong>POMC</strong> messenger ribonucleic acid mRNA) was compared in another pair of rat lines selectively bred for high or low <b>alcohol</b> intake (<b>alcohol</b> preferring or P and <b>alcohol</b> nonpreferring or NP lines).
+POMC	drug	alcohol	9512064	In a second study, pituitary beta endorphin gene expression (<strong>proopiomelanocortin</strong> or <strong>POMC</strong> messenger ribonucleic acid mRNA) was compared in another pair of rat lines selectively bred for high or low <b>alcohol</b> intake (<b>alcohol</b> preferring or P and <b>alcohol</b> nonpreferring or NP lines).
+POMC	drug	alcohol	9512064	A repeated <b>alcohol</b> challenge (1.0 g/kg b.wt./day, IP for 4 days) produced a greater increase in <strong>POMC</strong> mRNA in the anterior and neurointermediate lobes of the pituitary of P rats compared with NP rats.
+POMC	drug	opioid	8883945	Effect of <b>morphine</b> on <strong>proopiomelanocortin</strong> gene expression and peptide levels in the hypothalamus.
+POMC	drug	opioid	8883945	We have therefore examined <strong>POMC</strong> gene expression and peptide levels in the MBH of castrated rats after 10 days of treatment with subcutaneous <b>morphine</b> or placebo pellets and after pellet removal.
+POMC	drug	opioid	8883945	In castrated male rats, the mean <strong>POMC</strong> mRNA concentration in the MBH was 1.67 +/  0.11 pg/microgram RNA in the control animals and decreased to 1.17 +/  0.11 pg/microgram RNA in the <b>morphine</b> treated animals (P < 0.01).
+POMC	drug	opioid	8883945	Similarly in castrated, estradiol replaced female rats, the mean <strong>POMC</strong> mRNA level in the MBH was 1.36 +/  0.19 pg/microgram RNA and decreased to 0.82 +/  0.08 pg/microgram RNA after <b>morphine</b> treatment (P < 0.05).
+POMC	drug	opioid	8883945	When castrated male rats were similarly <b>morphine</b> pelleted and killed either on day 10 or 2 days later after pellet removal, the mean <strong>POMC</strong> mRNA level again fell from 1.83 +/  0.21 in the controls to 1.28 +/  0.20 pg/microgram RNA after 10 days of <b>morphine</b>; 2 days after pellet removal levels remained suppressed at 0.80 +/  0.08 pg/microgram RNA (P < 0.01).
+POMC	drug	opioid	8883945	We conclude that <b>morphine</b> suppresses <strong>POMC</strong> gene expression in the hypothalamus of chronically treated male and female rats.
+POMC	drug	alcohol	7969792	In situ hybridization and specific radioimmunoassays were used to study the influence of <b>ethanol</b> on proopiomelanocortin (<strong>POMC</strong>) and prodynorphin (PDYN) biosynthesis in the rat pituitary.
+POMC	drug	alcohol	7969792	In situ hybridization and specific radioimmunoassays were used to study the influence of <b>ethanol</b> on <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) and prodynorphin (PDYN) biosynthesis in the rat pituitary.
+POMC	drug	alcohol	7969792	Repeated intragastric <b>ethanol</b> administration (starting with a total daily dose of 5 g/kg every 2nd day, until a dose of 10 g/kg was attained on the 10th day and that dose was maintained by the 19th day) resulted in a reduction in the <strong>POMC</strong> mRNA level (about 20%) in the intermediate lobe of the pituitary (3 h after the last dose), whereas the level of beta endorphin in the neurointermediate lobe was attenuated (by about 32%) only during the withdrawal (48 h after the last dose).
+POMC	addiction	withdrawal	7969792	Repeated intragastric ethanol administration (starting with a total daily dose of 5 g/kg every 2nd day, until a dose of 10 g/kg was attained on the 10th day and that dose was maintained by the 19th day) resulted in a reduction in the <strong>POMC</strong> mRNA level (about 20%) in the intermediate lobe of the pituitary (3 h after the last dose), whereas the level of beta endorphin in the neurointermediate lobe was attenuated (by about 32%) only during the <b>withdrawal</b> (48 h after the last dose).
+POMC	drug	alcohol	7969792	On the other hand, acute <b>ethanol</b> had no effect on the <strong>POMC</strong> and PDYN mRNA levels, nor did it affect the alpha neoendorphin concentration in the pituitary.
+POMC	drug	alcohol	1471770	<strong>Proopiomelanocortin</strong> messenger RNA is decreased in the mediobasal hypothalamus of rats made dependent on <b>ethanol</b>.
+POMC	drug	alcohol	1471770	It is thought that certain actions of <b>ethanol</b> involve an interaction with endogenous opioids, including <strong>proopiomelanocortin</strong> derived peptides such as beta endorphin.
+POMC	drug	opioid	1471770	It is thought that certain actions of ethanol involve an interaction with endogenous <b>opioids</b>, including <strong>proopiomelanocortin</strong> derived peptides such as beta endorphin.
+POMC	drug	alcohol	1471770	To examine this possibility, we used a sensitive and specific assay for <strong>proopiomelanocortin</strong> mRNA to obtain an estimate of the activity of the endorphinergic system in the mediobasal hypothalamus and the pituitary of rats exposed for 10 days in an inhalation chamber to either <b>ethanol</b> or water.
+POMC	drug	alcohol	1471770	While <b>ethanol</b> treatment did not affect <strong>proopiomelanocortin</strong> mRNA levels in the pituitary, the level in hypothalamus was significantly lower in the <b>ethanol</b> treated animals than in controls.
+POMC	drug	opioid	1346939	Clinical studies show that chronic use of <b>methadone</b> allows normalization of release and peripheral levels of one of the classes of endogenous <b>opioids</b>, beta endorphin, and the related peptides derived from <strong>POMC</strong> released and processed from the anterior pituitary in humans.
+POMC	addiction	relapse	2598523	Finally, N <strong>POMC</strong> levels did not decrease significantly after successful treatment of lung cancer (by surgery or chemotherapy) but were markedly higher after <b>relapse</b>.
+POMC	addiction	relapse	2598523	These results suggest that N <strong>POMC</strong>, despite the fact that it cannot be used to discriminate lung cancer patients from controls, is a biomarker which may predict <b>relapse</b> in patients successfully treated by chemotherapy for their pulmonary neoplasm.
+POMC	drug	opioid	2534967	Down regulation of <strong>proopiomelanocortin</strong> synthesis and beta endorphin utilization in hypothalamus of <b>morphine</b> tolerant rats.
+POMC	drug	opioid	2534967	Hypothalamic proopiomelanocortin (<strong>POMC</strong>) mRNA, <strong>POMC</strong>, and corticotropin like intermediate lobe peptide content were decreased by 50% in <b>morphine</b> dependent rats.
+POMC	drug	opioid	2534967	Hypothalamic <strong>proopiomelanocortin</strong> (<strong>POMC</strong>) mRNA, <strong>POMC</strong>, and corticotropin like intermediate lobe peptide content were decreased by 50% in <b>morphine</b> dependent rats.
+POMC	drug	alcohol	2534967	A single injection of <b>naltrexone</b> (2 mg/kg) 1 hour before decapitation did not reverse the decrease in <strong>POMC</strong> mRNA and <strong>POMC</strong> content elicited by morphine.
+POMC	drug	opioid	2534967	A single injection of naltrexone (2 mg/kg) 1 hour before decapitation did not reverse the decrease in <strong>POMC</strong> mRNA and <strong>POMC</strong> content elicited by <b>morphine</b>.
+POMC	addiction	withdrawal	2534967	However, a slower, spontaneous <b>withdrawal</b> caused by removal of the pellets did reverse (after two days) the down regulation of the hypothalamic <strong>POMC</strong> system.
+POMC	drug	opioid	3267021	Neither acute nor chronic <b>morphine</b> administration altered either (a) hypothalamic parvocellular or magnocellular CRF mRNA, or (b) anterior pituitary or pars intermedia <strong>POMC</strong> mRNA.
+POMC	drug	opioid	3267021	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal resulted in a marked increase in parvocellular (but not magnocellular) CRF mRNA within 4 h and levels remained elevated through 24 h. There was no change in arcuate nucleus or pars intermedia <strong>POMC</strong> mRNA, but in the anterior pituitary there was a delayed increase, significant at 24 h. 5.
+POMC	addiction	withdrawal	3267021	Naloxone precipitated morphine <b>withdrawal</b> resulted in a marked increase in parvocellular (but not magnocellular) CRF mRNA within 4 h and levels remained elevated through 24 h. There was no change in arcuate nucleus or pars intermedia <strong>POMC</strong> mRNA, but in the anterior pituitary there was a delayed increase, significant at 24 h. 5.
+POMC	drug	opioid	2969250	"Reinforcing" effects are ascribed to endogenous <b>opioids</b>, particularly to the pro opiomelanocortin (<strong>POMC</strong>) derived beta endorphin 1 31, the most potent opiate active substance.
+POMC	addiction	reward	2969250	"<b>Reinforcing</b>" effects are ascribed to endogenous opioids, particularly to the pro opiomelanocortin (<strong>POMC</strong>) derived beta endorphin 1 31, the most potent opiate active substance.
+POMC	drug	alcohol	2969250	<b>Alcohol</b> induces variations in the genetic processing of the precursor <strong>POMC</strong> and of beta endorphin at different levels.
+POMC	drug	alcohol	2969250	Chronic <b>alcohol</b> intake significantly reduces <strong>POMC</strong> mRNA in the lobes of the pituitary.
+POMC	drug	alcohol	2969250	Clinical studies show a disproportion of <strong>POMC</strong> cleavage products in the CSF of chronic <b>alcoholics</b> (reduced beta endorphin versus increased ACTH contents), together with remarkable indications for baseline differences in beta endorphin levels.
+POMC	drug	alcohol	2969250	Errors within the genetic sequence of <strong>POMC</strong> are suggested to underlie <b>alcohol</b> seeking behavior.
+POMC	addiction	relapse	2969250	Errors within the genetic sequence of <strong>POMC</strong> are suggested to underlie alcohol <b>seeking</b> behavior.
+POMC	drug	alcohol	2963739	Effects of <b>ethanol</b> treatment and withdrawal on biosynthesis and processing of <strong>proopiomelanocortin</strong> by the rat neurointermediate lobe.
+POMC	addiction	withdrawal	2963739	Effects of ethanol treatment and <b>withdrawal</b> on biosynthesis and processing of <strong>proopiomelanocortin</strong> by the rat neurointermediate lobe.
+POMC	drug	alcohol	2963739	The in vitro incorporation of [3H]phenylalanine into <strong>POMC</strong>, beta lipotropin and beta EP was found to be higher in the <b>ethanol</b> treated animals than in the controls on days 0, 1, and 3 after <b>ethanol</b> withdrawal, with no significant difference on days 8 and 15 after <b>ethanol</b> withdrawal.
+POMC	addiction	withdrawal	2963739	The in vitro incorporation of [3H]phenylalanine into <strong>POMC</strong>, beta lipotropin and beta EP was found to be higher in the ethanol treated animals than in the controls on days 0, 1, and 3 after ethanol <b>withdrawal</b>, with no significant difference on days 8 and 15 after ethanol <b>withdrawal</b>.
+POMC	drug	alcohol	2963739	Furthermore, in both the <b>ethanol</b> treated animals and their pair fed controls the rate of incorporation of [3H]phenylalanine into total proteins, <strong>POMC</strong>, beta lipotropin, and beta EP was significantly higher on days 8 and 15 after <b>ethanol</b> withdrawal than on the day of <b>ethanol</b> withdrawal (day 0), suggesting the implication of a nutritional factor.
+POMC	addiction	withdrawal	2963739	Furthermore, in both the ethanol treated animals and their pair fed controls the rate of incorporation of [3H]phenylalanine into total proteins, <strong>POMC</strong>, beta lipotropin, and beta EP was significantly higher on days 8 and 15 after ethanol <b>withdrawal</b> than on the day of ethanol <b>withdrawal</b> (day 0), suggesting the implication of a nutritional factor.
+POMC	addiction	addiction	2463689	Although the exact mechanisms are unknown, prenatal <strong>POMC</strong> disregulation, <b>addiction</b> to endogenous opiates and elevated pain threshold have been proposed to account for this behavior.
+GFAP	drug	cannabinoid	32057593	In the mPFC and hippocampus, EtOH rats had significantly higher mRNA expression of <b>endocannabinoid</b> signaling (mPFC: Ppara, Dagla, Daglb and Napepld; and hippocampus: Cnr2, Dagla and Mgll) and neuroinflammation associated genes (mPFC: <strong>Gfap</strong>; and hippocampus: Aif1) than in controls.
+GFAP	drug	amphetamine	32044305	Retinal cell death and astrocyte activation by <b>METH</b> treatment were confirmed by TUNEL assay and <strong>glial fibrillary acidic protein</strong> expression, respectively.
+GFAP	drug	cocaine	31998080	In parallel, <b>cocaine</b> self administration alone specifically and differentially affects activation of glial cells by decreasing <strong>GFAP</strong> expression in astrocytes but increasing Iba1 expression in microglia.
+GFAP	drug	cocaine	31559425	Five immunohistochemical markers (CD3, zonula occludens 1 [ZO 1], intracellular adhesion molecule 1 [ICAM 1], vascular cell adhesion molecule [VCAM 1], and glial fibrillary acidic protein [<strong>GFAP</strong>]) were assessed on postmortem brain samples collected from drug abusers who died from acute intoxication of <b>cocaine</b>, heroin, or a combination of both, compared with controls.
+GFAP	drug	opioid	31559425	Five immunohistochemical markers (CD3, zonula occludens 1 [ZO 1], intracellular adhesion molecule 1 [ICAM 1], vascular cell adhesion molecule [VCAM 1], and glial fibrillary acidic protein [<strong>GFAP</strong>]) were assessed on postmortem brain samples collected from drug abusers who died from acute intoxication of cocaine, <b>heroin</b>, or a combination of both, compared with controls.
+GFAP	addiction	intoxication	31559425	Five immunohistochemical markers (CD3, zonula occludens 1 [ZO 1], intracellular adhesion molecule 1 [ICAM 1], vascular cell adhesion molecule [VCAM 1], and glial fibrillary acidic protein [<strong>GFAP</strong>]) were assessed on postmortem brain samples collected from drug abusers who died from acute <b>intoxication</b> of cocaine, heroin, or a combination of both, compared with controls.
+GFAP	drug	cocaine	31559425	Five immunohistochemical markers (CD3, zonula occludens 1 [ZO 1], intracellular adhesion molecule 1 [ICAM 1], vascular cell adhesion molecule [VCAM 1], and <strong>glial fibrillary acidic protein</strong> [<strong>GFAP</strong>]) were assessed on postmortem brain samples collected from drug abusers who died from acute intoxication of <b>cocaine</b>, heroin, or a combination of both, compared with controls.
+GFAP	drug	opioid	31559425	Five immunohistochemical markers (CD3, zonula occludens 1 [ZO 1], intracellular adhesion molecule 1 [ICAM 1], vascular cell adhesion molecule [VCAM 1], and <strong>glial fibrillary acidic protein</strong> [<strong>GFAP</strong>]) were assessed on postmortem brain samples collected from drug abusers who died from acute intoxication of cocaine, <b>heroin</b>, or a combination of both, compared with controls.
+GFAP	addiction	intoxication	31559425	Five immunohistochemical markers (CD3, zonula occludens 1 [ZO 1], intracellular adhesion molecule 1 [ICAM 1], vascular cell adhesion molecule [VCAM 1], and <strong>glial fibrillary acidic protein</strong> [<strong>GFAP</strong>]) were assessed on postmortem brain samples collected from drug abusers who died from acute <b>intoxication</b> of cocaine, heroin, or a combination of both, compared with controls.
+GFAP	drug	opioid	31349928	Cessation of <b>morphine</b> on day 11th results in withdrawal symptoms and BBB breakdown to proteins in the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus, brain stem and spinal cord along with activation of glial fibrillary acidic protein (<strong>GFAP</strong>) and HSP immunoreactivity.
+GFAP	addiction	withdrawal	31349928	Cessation of morphine on day 11th results in <b>withdrawal</b> symptoms and BBB breakdown to proteins in the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus, brain stem and spinal cord along with activation of glial fibrillary acidic protein (<strong>GFAP</strong>) and HSP immunoreactivity.
+GFAP	drug	opioid	31349928	Cessation of <b>morphine</b> on day 11th results in withdrawal symptoms and BBB breakdown to proteins in the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus, brain stem and spinal cord along with activation of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) and HSP immunoreactivity.
+GFAP	addiction	withdrawal	31349928	Cessation of morphine on day 11th results in <b>withdrawal</b> symptoms and BBB breakdown to proteins in the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus, brain stem and spinal cord along with activation of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) and HSP immunoreactivity.
+GFAP	addiction	withdrawal	31349928	Ondansetron treatment significantly reduced <b>withdrawal</b> symptoms on the day 13th in a dose dependent manner and attenuated BBB breakdown, edema formation, <strong>GFAP</strong> and HSP expression and neuronal injuries.
+GFAP	drug	nicotine	31330570	Extinction and cue induced reinstatement of <b>nicotine</b> seeking was also associated with increased tumor necrosis factor alpha (TNFα) and decreased glial fibrillary acidic protein (<strong>GFAP</strong>) expression in the NAcore.
+GFAP	addiction	relapse	31330570	Extinction and cue induced <b>reinstatement</b> of nicotine <b>seeking</b> was also associated with increased tumor necrosis factor alpha (TNFα) and decreased glial fibrillary acidic protein (<strong>GFAP</strong>) expression in the NAcore.
+GFAP	drug	nicotine	31330570	Extinction and cue induced reinstatement of <b>nicotine</b> seeking was also associated with increased tumor necrosis factor alpha (TNFα) and decreased <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) expression in the NAcore.
+GFAP	addiction	relapse	31330570	Extinction and cue induced <b>reinstatement</b> of nicotine <b>seeking</b> was also associated with increased tumor necrosis factor alpha (TNFα) and decreased <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) expression in the NAcore.
+GFAP	drug	opioid	31321003	The injection of chronic <b>morphine</b> increased the levels of proteins involved in neuroinflammation (p38 MAPK and <strong>GFAP</strong>) in NAcc.
+GFAP	drug	alcohol	31096703	Moreover, curcumin regulated the expression of the glial cell markers in <b>ethanol</b> treated mice brains, as analyzed by the relative expression TLR4 (Toll like Receptor 4), RAGE (Receptor for Advanced Glycations End products), <strong>GFAP</strong> (Glial fibrillary acidic protein), and Iba 1 (Ionized calcium binding adaptor molecule 1), through Western blot and confocal microscopic analysis.
+GFAP	drug	alcohol	31096703	Moreover, curcumin regulated the expression of the glial cell markers in <b>ethanol</b> treated mice brains, as analyzed by the relative expression TLR4 (Toll like Receptor 4), RAGE (Receptor for Advanced Glycations End products), <strong>GFAP</strong> (<strong>Glial fibrillary acidic protein</strong>), and Iba 1 (Ionized calcium binding adaptor molecule 1), through Western blot and confocal microscopic analysis.
+GFAP	drug	amphetamine	30714656	In this respect, we investigated genome wide mRNA expression using high throughput RNA seq technology and confirmatory quantitative real time PCR, accompanied by stereological analysis of cerebellar layers along with identification of reactive astrogliosis by <strong>glial fibrillary acidic protein</strong> and behavioral assessment following <b>METH</b> exposure.
+GFAP	drug	alcohol	30625475	Moreover, astrocyte activation occurred following <b>ethanol</b> exposure as <strong>GFAP</strong> immunoreactivity was increased over 120% in mice that experienced 3 cycles of <b>ethanol</b> binges.
+GFAP	drug	amphetamine	30456731	Seven days after <b>METH</b> injection, the brains were removed for biochemical assessments, glial fibrillary acidic protein (<strong>GFAP</strong>), and caspase 3 immunohistochemistry staining.
+GFAP	drug	amphetamine	30456731	Seven days after <b>METH</b> injection, the brains were removed for biochemical assessments, <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), and caspase 3 immunohistochemistry staining.
+GFAP	drug	amphetamine	30456731	Moreover, H2S could significantly decrease caspase 3 and <strong>GFAP</strong> positive cells in the CA1 region of the hippocampus (P < 0.01) compared to the <b>METH</b> group.
+GFAP	drug	alcohol	30273595	Adult male and female <strong>GFAP</strong> TK transgenic rats experienced six weeks of chronic intermittent <b>ethanol</b> vapor inhalation (CIE).
+GFAP	drug	amphetamine	30259275	Seven days after <b>METH</b> injection, the rats' brains were removed for biochemical assessment using the ELISA technique, and immunohistochemistry staining was used for caspase 3 and glial fibrillary acidic protein (<strong>GFAP</strong>) detection.
+GFAP	drug	amphetamine	30259275	Seven days after <b>METH</b> injection, the rats' brains were removed for biochemical assessment using the ELISA technique, and immunohistochemistry staining was used for caspase 3 and <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) detection.
+GFAP	drug	nicotine	30035805	Marked increases in hippocampal oxidative stress (GSSG/GSH) and neuroinflammation (astrocyte reactivity, <strong>GFAP</strong>) were observed after both chronic EtOH and chronic <b>nicotine</b> treatment.
+GFAP	drug	opioid	29782623	We hypothesized that increased immunohistochemical labeling of an astrocytic marker, glial fibrillary acidic protein (<strong>GFAP</strong>) in the VTA following chronic administration of <b>morphine</b> will not differ with age.
+GFAP	drug	opioid	29782623	We hypothesized that increased immunohistochemical labeling of an astrocytic marker, <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) in the VTA following chronic administration of <b>morphine</b> will not differ with age.
+GFAP	drug	opioid	29782623	We report an increase in both (1) <strong>GFAP</strong> labeling intensity, as well as (2) the percent area occupied by astrocytes that are immunoreactive for <strong>GFAP</strong> following chronic <b>morphine</b> when compared to saline treatment in the VTA only for the adults (n=6/group) but not infant rats at PD7 (n=5/group).
+GFAP	addiction	withdrawal	29752970	The reduced BDNF level observed shortly after BEI recovered upon <b>withdrawal</b>, whereas increased <strong>GFAP</strong> immunoreactivity was persistent up to 14 days post administration in adulthood.
+GFAP	drug	cocaine	29567092	Rats self administered <b>cocaine</b> for two weeks and received injections of either AAV <strong>GFAP</strong> GLT 1a or AAV <strong>GFAP</strong> eGFP in the NAc following the last day of self administration.
+GFAP	drug	cocaine	29567092	Rats that received AAV <strong>GFAP</strong> GLT 1a reinstated cue primed <b>cocaine</b> seeking in a similar manner as rats that received the control AAV <strong>GFAP</strong> eGFP.
+GFAP	addiction	relapse	29567092	Rats that received AAV <strong>GFAP</strong> GLT 1a reinstated cue primed cocaine <b>seeking</b> in a similar manner as rats that received the control AAV <strong>GFAP</strong> eGFP.
+GFAP	addiction	sensitization	29557083	Significant alterations were observed in mRNA expression of orexin, dopamine, and adenosine receptors and in the expression of <strong>GFAP</strong> and Iba 1, showing a broad range of interactions in the mesolimbic system among orexin, dopamine, adenosine, and glial cells during behavioral <b>sensitization</b>.
+GFAP	drug	psychedelics	29512789	Tetrahydropalmatine also suppressed iNOS protein expression, weakened caspase‑3 and caspase‑9 activation, inhibited nuclear factor‑κB, <strong>glial fibrillary acidic protein</strong>, cytochrome c and phospholipase C‑γ1 protein expression, and induced glial cell‑derived neurotrophic factor protein expression in <b>ketamine</b>‑induced mice.
+GFAP	drug	alcohol	29396480	Chronic exposure to 1.5 g/kg <b>ethanol</b> increased <strong>GFAP</strong> expression and induced mislocation of the astrocyte specific water channel aquaporin 4 (AQP4), but decreased the levels of several cytokines.
+GFAP	drug	alcohol	29396480	Low doses of chronic <b>ethanol</b> intake were associated with a significant decrease in <strong>GFAP</strong> expression, with little change in the cytokine profile compared with the saline group.
+GFAP	drug	amphetamine	29363584	Male <strong>GFAP</strong> TK rats were trained to self administer <b>methamphetamine</b> or sucrose and were administered the antiviral drug valganciclovir (Valcyte) to produce apoptosis of actively dividing <strong>GFAP</strong> type 1 stem like cells to inhibit neurogenesis during abstinence.
+GFAP	drug	opioid	29146238	Using a transgenic murine model that expresses HIV 1 Tat protein in a <strong>GFAP</strong> regulated, doxycycline inducible manner, we assessed <b>morphine</b> tolerance, dependence, and reward.
+GFAP	addiction	dependence	29146238	Using a transgenic murine model that expresses HIV 1 Tat protein in a <strong>GFAP</strong> regulated, doxycycline inducible manner, we assessed morphine tolerance, <b>dependence</b>, and reward.
+GFAP	addiction	reward	29146238	Using a transgenic murine model that expresses HIV 1 Tat protein in a <strong>GFAP</strong> regulated, doxycycline inducible manner, we assessed morphine tolerance, dependence, and <b>reward</b>.
+GFAP	drug	opioid	28659367	Measuring <strong>GFAP</strong> could possibly aid in the diagnosis of <b>heroin</b> induced myelopathy.
+GFAP	addiction	withdrawal	28654797	Changes in brain gene expression levels of induced nitric oxide synthase (iNOS), astroglia marker, glial fibrillary acidic protein (<strong>GFAP</strong>), ionized calcium binding protein (Iba1) a microglia activation marker, a pro inflammatory mediator and tumor necrosis alpha (TNF α) were measured after <b>withdrawal</b> by real time polymerase chain reaction (RT PCR).
+GFAP	addiction	withdrawal	28654797	Changes in brain gene expression levels of induced nitric oxide synthase (iNOS), astroglia marker, <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), ionized calcium binding protein (Iba1) a microglia activation marker, a pro inflammatory mediator and tumor necrosis alpha (TNF α) were measured after <b>withdrawal</b> by real time polymerase chain reaction (RT PCR).
+GFAP	drug	opioid	28654797	Administration of <b>naloxone</b> was associated with the increased expression of TNF α, <strong>GFAP</strong>, Iba1 and iNOS in the brain samples of <b>morphine</b> dependent mice, while the nine days treatment with both 5 and 10mg/kg simvastatin reduced such changes.
+GFAP	addiction	withdrawal	28062186	We attempted to verify <b>withdrawal</b> regulation of induced nitric oxide synthase (iNOS), astroglia marker, glial fibrillary acidic protein (<strong>GFAP</strong>), ionized calcium binding protein (Iba1), a microglia activation marker, a pro inflammatory mediator, tumor necrosis alpha (TNF α) and immune receptor, toll like receptor 4 (TLR 4) genes by real time polymerase chain reaction (RT PCR).
+GFAP	addiction	withdrawal	28062186	We attempted to verify <b>withdrawal</b> regulation of induced nitric oxide synthase (iNOS), astroglia marker, <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), ionized calcium binding protein (Iba1), a microglia activation marker, a pro inflammatory mediator, tumor necrosis alpha (TNF α) and immune receptor, toll like receptor 4 (TLR 4) genes by real time polymerase chain reaction (RT PCR).
+GFAP	drug	opioid	28062186	Brain expression levels of TNF α, <strong>GFAP</strong>, Iba1 and iNOS increased in <b>morphine</b> withdrawn animals which were attenuated by nine days treatment with atorvastatin.
+GFAP	drug	amphetamine	27931227	Naïve C57black6 mice that experience acute exposure to <b>amphetamine</b> (4 mg/kg, by injection intraperitoneally) show expression of both total and phosphorylated (S259) HDAC5 antigens in <strong>GFAP</strong>+ and <strong>GFAP</strong>  cells, but the appearance of these cells was attenuated in the chronic paradigm.
+GFAP	drug	amphetamine	27931227	Moreover, SPION miD2861 identified enhanced HDAC5 expression in the lateral septum and the striatum after <b>amphetamine</b>, where we found neurprogenitor cells coexpressing NeuN and <strong>GFAP</strong>.
+GFAP	drug	opioid	27875800	Immunohistochemistry (IHC) experiments on striatal brain slices were performed to assess the expression of glial markers (Iba1, <strong>GFAP</strong> and CD68) during 14days after <b>morphine</b> discontinuation.
+GFAP	drug	amphetamine	27642078	<b>Amphetamine</b> caused an enhanced loss of striatal dopaminergic terminals, together with a highly significant aggravation of <b>amphetamine</b> induced increase in the number of <strong>GFAP</strong> positive astrocytes, in the striatum of PTN Tg mice compared to WT mice.
+GFAP	drug	alcohol	27537918	Previous literature indicates that acute binge like <b>ethanol</b> exposure in postnatal day 7 (P7) mice induces apoptotic neurodegeneration, transient activation of microglia resulting in phagocytosis of degenerating neurons, and a prolonged increase in <strong>glial fibrillary acidic protein</strong> positive astrocytes.
+GFAP	addiction	intoxication	27537918	Previous literature indicates that acute <b>binge</b> like ethanol exposure in postnatal day 7 (P7) mice induces apoptotic neurodegeneration, transient activation of microglia resulting in phagocytosis of degenerating neurons, and a prolonged increase in <strong>glial fibrillary acidic protein</strong> positive astrocytes.
+GFAP	drug	amphetamine	27098516	Using logistic regression models, we analyzed associations of <b>Meth</b> with cerebral gliosis (immunohistochemistry for ionized calcium binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (<strong>GFAP</strong>) in frontal, temporo parietal, and putamen internal capsule regions), synaptodendritic loss (confocal microscopy for synaptophysin (SYP) and microtubule associated protein 2 (MAP2) in frontal cortex), β amyloid plaque deposition (immunohistochemistry in frontal and temporo parietal cortex and putamen), and arteriolosclerosis (histopathology in forebrain white matter).
+GFAP	drug	amphetamine	27098516	Using logistic regression models, we analyzed associations of <b>Meth</b> with cerebral gliosis (immunohistochemistry for ionized calcium binding adapter molecule 1 (Iba1) and <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) in frontal, temporo parietal, and putamen internal capsule regions), synaptodendritic loss (confocal microscopy for synaptophysin (SYP) and microtubule associated protein 2 (MAP2) in frontal cortex), β amyloid plaque deposition (immunohistochemistry in frontal and temporo parietal cortex and putamen), and arteriolosclerosis (histopathology in forebrain white matter).
+GFAP	drug	amphetamine	27098516	There was no significant association of <b>Meth</b> with <strong>GFAP</strong> gliosis, SYP or MAP2 loss, β amyloid plaque deposition, or arteriolosclerosis.
+GFAP	addiction	reward	27026056	Significant increases in both astrocytic, <strong>glial fibrillary acidic protein</strong>, and microglial, ionization basic acid 1, markers were observed in the NAc at the end of <b>CPP</b> testing.
+GFAP	drug	cocaine	26946381	<b>Cocaine</b> Self Administration and Extinction Leads to Reduced <strong>Glial Fibrillary Acidic Protein</strong> Expression and Morphometric Features of Astrocytes in the Nucleus Accumbens Core.
+GFAP	drug	cocaine	26946381	We investigated the effects of extinction from daily <b>cocaine</b> self administration on astrocyte characteristics including glial fibrillary acidic protein (<strong>GFAP</strong>) expression, surface area, volume, and colocalization with a synaptic marker.
+GFAP	drug	cocaine	26946381	We investigated the effects of extinction from daily <b>cocaine</b> self administration on astrocyte characteristics including <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) expression, surface area, volume, and colocalization with a synaptic marker.
+GFAP	drug	cocaine	26946381	<b>Cocaine</b> or saline self administration and extinction were paired with <strong>GFAP</strong> Westerns, immunohistochemistry, and fluorescent imaging of NAc core astrocytes (30 saline administering and 36 <b>cocaine</b> administering male Sprague Dawley rats were employed).
+GFAP	drug	cocaine	26946381	<strong>GFAP</strong> expression was significantly reduced in the NAc core following <b>cocaine</b> self administration and extinction.
+GFAP	drug	opioid	28462096	The repeated administration of <b>morphine</b> increased Iba 1 and <strong>GFAP</strong> immune reactivities in the spinal cord; however, these activations were inhibited by the preadministration of YKS.
+GFAP	drug	opioid	26478469	The aim of the present study was to investigate the molecular effects of perinatal exposure to lead (Pb) on protein and mRNA expression of purine receptors: P2X4, P2X7, adenosine receptor A1; and astrocytes (<strong>GFAP</strong> mRNA expression) and on microglia activation (Iba1 mRNA expression) in several structures of the mesolimbic system (striatum, hippocampus, prefrontal cortex) in rats expressing tolerance to the antinociceptive effect of <b>morphine</b>.
+GFAP	drug	amphetamine	26427884	Similarly, <b>METH</b> increased striatal <strong>glial fibrillary acidic protein</strong>, indicating neurotoxicity.
+GFAP	drug	amphetamine	26366944	The results showed that <b>METH</b> caused a decrease in neuronal phenotypes as determined by the expressions of nestin, doublecortin (DCX) and beta III tubulin while causing an increase in glial fibrillary acidic protein (<strong>GFAP</strong>) expression.
+GFAP	drug	amphetamine	26366944	The results showed that <b>METH</b> caused a decrease in neuronal phenotypes as determined by the expressions of nestin, doublecortin (DCX) and beta III tubulin while causing an increase in <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) expression.
+GFAP	drug	alcohol	26088166	Male astrocyte responses were consistent with astrocyte deactivation with reduced <strong>GFAP</strong> expression during <b>ethanol</b> exposure.
+GFAP	drug	psychedelics	26068050	The data, together with the observed lack of <strong>GFAP</strong> activation, support the view that chronic <b>MDMA</b> effects, regardless of the rat developmental age, extends beyond neurotransmitter systems to impair other hippocampal structural cell markers.
+GFAP	drug	alcohol	25833026	Differential response of <strong>glial fibrillary acidic protein</strong> positive astrocytes in the rat prefrontal cortex following <b>ethanol</b> self administration.
+GFAP	drug	alcohol	25760047	GT tg transgenic mice, where Tat protein is conditionally expressed in brain by a doxycycline dependent <strong>GFAP</strong> linked promoter, were used to test the effects of Tat on <b>ethanol</b> conditioned place preference (CPP).
+GFAP	addiction	reward	25760047	GT tg transgenic mice, where Tat protein is conditionally expressed in brain by a doxycycline dependent <strong>GFAP</strong> linked promoter, were used to test the effects of Tat on ethanol conditioned place preference (<b>CPP</b>).
+GFAP	drug	amphetamine	25746685	VMAT2 HI mice were also spared from the inflammatory response that follows <b>METH</b> treatment, showing an increase in astroglial markers that was approximately one third of that of wildtype animals (117% vs 36% increase in <strong>GFAP</strong>, wildtype vs VMAT2 HI).
+GFAP	drug	amphetamine	25645392	In contrast, 24 h after the binge <b>METH</b> treatment prior <b>METH</b> self administration: 1) attenuated deficits in DA content, DAT function and vesicular monoamine transporter 2 function; and 2) prevented increases in <strong>glial fibrillary acidic protein</strong> and DAT complex immunoreactivity.
+GFAP	addiction	intoxication	25645392	In contrast, 24 h after the <b>binge</b> METH treatment prior METH self administration: 1) attenuated deficits in DA content, DAT function and vesicular monoamine transporter 2 function; and 2) prevented increases in <strong>glial fibrillary acidic protein</strong> and DAT complex immunoreactivity.
+GFAP	drug	nicotine	25637801	<b>Nicotine</b> also promoted elevations in the expression of glial fibrillary acidic protein (<strong>GFAP</strong>), a biomarker of activated astrocytes, and the microglia biomarker ionized calcium binding adapter molecule 1 (Iba1).
+GFAP	drug	nicotine	25637801	<b>Nicotine</b> also promoted elevations in the expression of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), a biomarker of activated astrocytes, and the microglia biomarker ionized calcium binding adapter molecule 1 (Iba1).
+GFAP	drug	amphetamine	25261212	Exposure to hot ambient temperature exacerbated <b>METH</b> toxicity evidenced by striatal reductions in TH and DAT and increased <strong>GFAP</strong> immmunoreactivity.
+GFAP	drug	amphetamine	25261212	At both ambient temperatures tested modafinil did induce increments in <strong>GFAP</strong>, but the magnitude was significantly lower than the one induced by <b>METH</b>.
+GFAP	drug	opioid	25108770	We observed that single <b>morphine</b> injection and chronic <b>morphine</b> increased <strong>glial fibrillary acidic protein</strong> expression in the ventral tegmental area (VTA).
+GFAP	drug	alcohol	24786333	S100B protein was increased in the cerebrospinal fluid (CSF) in the group treated with <b>alcohol</b>, and alterations in <strong>GFAP</strong> expression were also shown.
+GFAP	drug	amphetamine	24704312	Since gliosis is typically associated with brain damage and is observed in animal models of <b>methamphetamine</b> exposure, we measured protein levels (intact protein and fragments, if any) of markers of microgliosis (glucose transporter 5, human leukocyte antigens HLA DRα [TAL.1B5] and HLA DR/DQ/DPβ [CR3/43]) and astrogliosis (<strong>glial fibrillary acidic protein</strong>, vimentin, and heat shock protein 27) in homogenates of autopsied brain of chronic <b>methamphetamine</b> users (n=20) and matched controls (n=23).
+GFAP	drug	cocaine	24409127	Additionally, we measured cell apoptosis (as monitored by the expression of cleaved caspase 3) and glial activation [by analyzing the expression of glial fibrillary acidic protein (<strong>GFAP</strong>) and Iba 1] in the striatum and hippocampus during acute and repeated (4 days) <b>cocaine</b> administration (20 mg/kg).
+GFAP	drug	cocaine	24409127	Additionally, we measured cell apoptosis (as monitored by the expression of cleaved caspase 3) and glial activation [by analyzing the expression of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) and Iba 1] in the striatum and hippocampus during acute and repeated (4 days) <b>cocaine</b> administration (20 mg/kg).
+GFAP	drug	cannabinoid	24409127	Both acute and repeated cocaine exposure increased the number of cleaved caspase 3 , <strong>GFAP</strong>  and Iba1 ir cells in the hippocampus, and this effect was counteracted by AM630 or <b>Rimonabant</b>, which increased the number of BrdU , <strong>GFAP</strong> , and Iba1 ir cells in the hippocampus.
+GFAP	drug	cocaine	24409127	Both acute and repeated <b>cocaine</b> exposure increased the number of cleaved caspase 3 , <strong>GFAP</strong>  and Iba1 ir cells in the hippocampus, and this effect was counteracted by AM630 or Rimonabant, which increased the number of BrdU , <strong>GFAP</strong> , and Iba1 ir cells in the hippocampus.
+GFAP	drug	opioid	23707980	Chronic <b>morphine</b> induces tPA expression in glial fibrillary acidic protein (<strong>GFAP</strong>) expressing spinal cord astrocytes.
+GFAP	drug	opioid	23707980	Chronic <b>morphine</b> induces tPA expression in <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) expressing spinal cord astrocytes.
+GFAP	drug	opioid	23707980	Chronic <b>morphine</b> also increases IL 1β expression in <strong>GFAP</strong> expressing astrocytes, which is abolished in tPA deficient mice.
+GFAP	drug	opioid	23396227	At this time point, ( ) <b>naloxone</b>, but not (+) <b>naloxone</b>, increased <strong>GFAP</strong> in satellite glial cells; conversely, both <b>naloxone</b> steroisomers similarly increased <strong>GFAP</strong> in the spinal cord.
+GFAP	drug	opioid	23213573	We also examined extinction responding patterns following <b>heroin</b> self administration in glial fibrillary acidic protein thymidine kinase (<strong>GFAP</strong> tk) transgenic mice, which have been previously demonstrated to show reduced formation of immature and mature neurons in the DG following treatment with ganciclovir (GCV).
+GFAP	drug	opioid	23213573	We also examined extinction responding patterns following <b>heroin</b> self administration in <strong>glial fibrillary acidic protein</strong> thymidine kinase (<strong>GFAP</strong> tk) transgenic mice, which have been previously demonstrated to show reduced formation of immature and mature neurons in the DG following treatment with ganciclovir (GCV).
+GFAP	drug	amphetamine	23178526	Astrocytosis, a process in which astrocytes undergo proliferation and enhancement of glial fibrillary acidic protein (<strong>GFAP</strong>) expression, has been suggested to play important roles in the maintenance of dependence to <b>amphetamine</b> and its derivatives.
+GFAP	addiction	dependence	23178526	Astrocytosis, a process in which astrocytes undergo proliferation and enhancement of glial fibrillary acidic protein (<strong>GFAP</strong>) expression, has been suggested to play important roles in the maintenance of <b>dependence</b> to amphetamine and its derivatives.
+GFAP	drug	amphetamine	23178526	Astrocytosis, a process in which astrocytes undergo proliferation and enhancement of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) expression, has been suggested to play important roles in the maintenance of dependence to <b>amphetamine</b> and its derivatives.
+GFAP	addiction	dependence	23178526	Astrocytosis, a process in which astrocytes undergo proliferation and enhancement of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) expression, has been suggested to play important roles in the maintenance of <b>dependence</b> to amphetamine and its derivatives.
+GFAP	drug	cannabinoid	22737214	The <b>cannabinoid</b> 1 receptor antagonist O 2050 reduced preferences for HFDs after 3, 7, or 14 days of HFD consumption and reduced expression of <strong>GFAP</strong> after 14 days of HFD consumption.
+GFAP	drug	opioid	22362187	In the present study, by combining the techniques of in situ hybridization of MOR mRNA with immunohistochemistry of glial fibrillary acidic protein (<strong>GFAP</strong>; an astrocyte marker) and Iba1 (a microglial marker), we examined expression and distribution of <strong>GFAP</strong>, Iba1, and MOR mRNA in the spinal cord of rats under chronic <b>morphine</b> tolerance conditions.
+GFAP	drug	opioid	22362187	In the present study, by combining the techniques of in situ hybridization of MOR mRNA with immunohistochemistry of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>; an astrocyte marker) and Iba1 (a microglial marker), we examined expression and distribution of <strong>GFAP</strong>, Iba1, and MOR mRNA in the spinal cord of rats under chronic <b>morphine</b> tolerance conditions.
+GFAP	drug	opioid	22362187	Intrathecal injections of <b>morphine</b> twice daily for 7 days reduced <b>morphine</b> analgesic effect and increased both <strong>GFAP</strong> and Iba1 immunostaining densities in the spinal cord.
+GFAP	drug	opioid	22050217	Immunohistochemistry and Western blot with <strong>GFAP</strong> revealed that melatonin significantly decreased <b>morphine</b> induced over expression of <strong>GFAP</strong> in spinal cord (p < .05).
+GFAP	addiction	withdrawal	22037228	Bilateral paw pressure threshold and paw <b>withdrawal</b> latencies were measured, and the extent of glial activation was dertermined by measuring macrophage antigen complex 1 (Mac 1) and glial fibrillary acidic protein (<strong>GFAP</strong>).
+GFAP	addiction	withdrawal	22037228	Bilateral paw pressure threshold and paw <b>withdrawal</b> latencies were measured, and the extent of glial activation was dertermined by measuring macrophage antigen complex 1 (Mac 1) and <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>).
+GFAP	drug	amphetamine	22034657	It is noteworthy that <b>METH</b> self administration mitigated the persistent deficits in dopaminergic neuronal function, as well as the increases in <strong>glial fibrillary acidic protein</strong> immunoreactivity, caused by a subsequent binge <b>METH</b> exposure.
+GFAP	addiction	intoxication	22034657	It is noteworthy that METH self administration mitigated the persistent deficits in dopaminergic neuronal function, as well as the increases in <strong>glial fibrillary acidic protein</strong> immunoreactivity, caused by a subsequent <b>binge</b> METH exposure.
+GFAP	drug	amphetamine	21855565	Further systematic analysis of Ki 67 cells with <strong>GFAP</strong>, Sox2, and DCX revealed that LgA <b>methamphetamine</b> induced inhibition of hippocampal neurogenesis was attributable to impairment in the development of neuronal progenitors from preneuronal progenitors to immature neurons.
+GFAP	drug	amphetamine	21704677	However, we detected a significant increase of glial fibrillary acidic protein (<strong>GFAP</strong>) positive cells in the striatum of <b>amphetamine</b> treated MK /  mice compared to MK+/+ mice, suggesting an enhanced <b>amphetamine</b> induced astrocytosis in absence of endogenous MK.
+GFAP	drug	amphetamine	21704677	However, we detected a significant increase of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) positive cells in the striatum of <b>amphetamine</b> treated MK /  mice compared to MK+/+ mice, suggesting an enhanced <b>amphetamine</b> induced astrocytosis in absence of endogenous MK.
+GFAP	drug	opioid	21392541	Mitosis activated protein kinase1 (MAPK1) was increased in the stages of extinction and reinstatement of <b>morphine</b> induced CPP, while glial fibrillary acidic protein (<strong>GFAP</strong>) was decreased in the stage of extinction.
+GFAP	addiction	relapse	21392541	Mitosis activated protein kinase1 (MAPK1) was increased in the stages of extinction and <b>reinstatement</b> of morphine induced CPP, while glial fibrillary acidic protein (<strong>GFAP</strong>) was decreased in the stage of extinction.
+GFAP	addiction	reward	21392541	Mitosis activated protein kinase1 (MAPK1) was increased in the stages of extinction and reinstatement of morphine induced <b>CPP</b>, while glial fibrillary acidic protein (<strong>GFAP</strong>) was decreased in the stage of extinction.
+GFAP	drug	opioid	21392541	Mitosis activated protein kinase1 (MAPK1) was increased in the stages of extinction and reinstatement of <b>morphine</b> induced CPP, while <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) was decreased in the stage of extinction.
+GFAP	addiction	relapse	21392541	Mitosis activated protein kinase1 (MAPK1) was increased in the stages of extinction and <b>reinstatement</b> of morphine induced CPP, while <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) was decreased in the stage of extinction.
+GFAP	addiction	reward	21392541	Mitosis activated protein kinase1 (MAPK1) was increased in the stages of extinction and reinstatement of morphine induced <b>CPP</b>, while <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) was decreased in the stage of extinction.
+GFAP	drug	opioid	21068718	Here we report that chronic <b>morphine</b> withdrawal induced upregulation of glial fibrillary acidic protein (<strong>GFAP</strong>), tumor necrosis factor alpha (TNFα) and phosphorylation of ERK1/2 (pERK1/2) in the caudal ventrolateral PAG (vlPAG).
+GFAP	addiction	withdrawal	21068718	Here we report that chronic morphine <b>withdrawal</b> induced upregulation of glial fibrillary acidic protein (<strong>GFAP</strong>), tumor necrosis factor alpha (TNFα) and phosphorylation of ERK1/2 (pERK1/2) in the caudal ventrolateral PAG (vlPAG).
+GFAP	drug	opioid	21068718	Here we report that chronic <b>morphine</b> withdrawal induced upregulation of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), tumor necrosis factor alpha (TNFα) and phosphorylation of ERK1/2 (pERK1/2) in the caudal ventrolateral PAG (vlPAG).
+GFAP	addiction	withdrawal	21068718	Here we report that chronic morphine <b>withdrawal</b> induced upregulation of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), tumor necrosis factor alpha (TNFα) and phosphorylation of ERK1/2 (pERK1/2) in the caudal ventrolateral PAG (vlPAG).
+GFAP	drug	opioid	21068718	Microinjection of HSV vector expressing sTNFR into the PAG before the start of <b>morphine</b> treatment significantly reduced the <b>naloxone</b> precipitated withdrawal behavioral response and downregulated the expression of <strong>GFAP</strong> and TNFα in astrocytes of the PAG.
+GFAP	addiction	withdrawal	21068718	Microinjection of HSV vector expressing sTNFR into the PAG before the start of morphine treatment significantly reduced the naloxone precipitated <b>withdrawal</b> behavioral response and downregulated the expression of <strong>GFAP</strong> and TNFα in astrocytes of the PAG.
+GFAP	drug	amphetamine	20192945	In immunohystochemistry studies, we found that <b>amphetamine</b> (10 mg/kg, four times, every 2 hours) causes a significant increase of <strong>glial fibrillary acidic protein</strong> positive cells in the striatum of <b>amphetamine</b> treated PTN  /  mice compared with WT mice 4 days after last administration of the drug, suggesting an enhanced <b>amphetamine</b> induced astrocytosis in the absence of endogenous PTN.
+GFAP	drug	cannabinoid	20168044	The <b>cannabinoid</b> CB(1) receptor antagonist O 2050 reduced the preference for HFD and expression of <strong>GFAP</strong> in the hypothalamus.
+GFAP	drug	amphetamine	20098750	Importantly, <b>meth</b> self administration was associated with significant dose dependent increases in <strong>glial fibrillary acidic protein</strong> in both striatum and cortex, with these changes being of greater magnitude in the striatum.
+GFAP	drug	amphetamine	19598248	In WT mice, mEH like immunoreactivity was expressed in astrocytes labeled by <strong>GFAP</strong> or S100B after <b>METH</b> treatment.
+GFAP	drug	cocaine	19203409	Further studies through immunohistochemistry and immunoblot analysis showed that AQP4 knockout sustained the levels of <strong>glial fibrillary acidic protein</strong> in the hippocampus, and suppressed the enhancement of extracellular signal regulated kinase phosphorylation induced by repeated <b>cocaine</b> administration.
+GFAP	drug	cocaine	18504425	Increased levels of proteins in the <b>cocaine</b> exposed monkeys include <strong>glial fibrillary acidic protein</strong>, syntaxin binding protein 3, protein kinase C isoform, adenylate kinase isoenzyme 5 and mitochondrial related proteins, whereas decreased levels of proteins included beta soluble N ethylmaleimide sensitive factor attachment protein and neural and non neural enolase.
+GFAP	addiction	withdrawal	18486243	This was not accompanied by enhanced neurotoxicity or reactive gliosis as demonstrated by the immunohistological analysis using the apoptotic marker activated Caspase 3 and <strong>GFAP</strong> (glial fibrillary acidic protein; a marker for astrocytes) following both short  and long term <b>withdrawal</b> periods.
+GFAP	addiction	withdrawal	18486243	This was not accompanied by enhanced neurotoxicity or reactive gliosis as demonstrated by the immunohistological analysis using the apoptotic marker activated Caspase 3 and <strong>GFAP</strong> (<strong>glial fibrillary acidic protein</strong>; a marker for astrocytes) following both short  and long term <b>withdrawal</b> periods.
+GFAP	drug	amphetamine	17767502	<b>METH</b> treated animals also showed strong immunoreactivity for glial fibrillary acidic protein (<strong>GFAP</strong>), possibly suggesting acute abnormality or damage of astrocytes.
+GFAP	drug	amphetamine	17767502	<b>METH</b> treated animals also showed strong immunoreactivity for <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), possibly suggesting acute abnormality or damage of astrocytes.
+GFAP	drug	amphetamine	17767502	<b>METH</b> induced changes in brain water, albumin and <strong>GFAP</strong> correlated linearly with NAcc temperature (r = 0.93, 0.98 and 0.98, respectively), suggesting a key role of brain hyperthermia in BBB permeability, development of brain edema and subsequent functional and structural neural abnormalities.
+GFAP	drug	opioid	17123717	Yohimbine prevents <b>morphine</b> induced changes of <strong>glial fibrillary acidic protein</strong> in brainstem and alpha2 adrenoceptor gene expression in hippocampus.
+GFAP	drug	opioid	17123717	In the present study we have checked the effects of yohimbine on <b>morphine</b> induced alterations of the expression of key proteins (glial fibrillary acidic protein, <strong>GFAP</strong>) and genes (alpha(2) adrenoceptors) in rat brain areas known to be relevant in <b>opioid</b> dependence, addiction and individual vulnerability to drug abuse.
+GFAP	addiction	addiction	17123717	In the present study we have checked the effects of yohimbine on morphine induced alterations of the expression of key proteins (glial fibrillary acidic protein, <strong>GFAP</strong>) and genes (alpha(2) adrenoceptors) in rat brain areas known to be relevant in opioid dependence, <b>addiction</b> and individual vulnerability to drug abuse.
+GFAP	addiction	dependence	17123717	In the present study we have checked the effects of yohimbine on morphine induced alterations of the expression of key proteins (glial fibrillary acidic protein, <strong>GFAP</strong>) and genes (alpha(2) adrenoceptors) in rat brain areas known to be relevant in opioid <b>dependence</b>, addiction and individual vulnerability to drug abuse.
+GFAP	drug	opioid	17123717	In the present study we have checked the effects of yohimbine on <b>morphine</b> induced alterations of the expression of key proteins (<strong>glial fibrillary acidic protein</strong>, <strong>GFAP</strong>) and genes (alpha(2) adrenoceptors) in rat brain areas known to be relevant in <b>opioid</b> dependence, addiction and individual vulnerability to drug abuse.
+GFAP	addiction	addiction	17123717	In the present study we have checked the effects of yohimbine on morphine induced alterations of the expression of key proteins (<strong>glial fibrillary acidic protein</strong>, <strong>GFAP</strong>) and genes (alpha(2) adrenoceptors) in rat brain areas known to be relevant in opioid dependence, <b>addiction</b> and individual vulnerability to drug abuse.
+GFAP	addiction	dependence	17123717	In the present study we have checked the effects of yohimbine on morphine induced alterations of the expression of key proteins (<strong>glial fibrillary acidic protein</strong>, <strong>GFAP</strong>) and genes (alpha(2) adrenoceptors) in rat brain areas known to be relevant in opioid <b>dependence</b>, addiction and individual vulnerability to drug abuse.
+GFAP	drug	opioid	17123717	<b>Morphine</b> administration increased <strong>GFAP</strong> expression both in LC and NST as it was previously reported in other brain areas.
+GFAP	drug	opioid	17123717	Yohimbine was found to efficiently prevent <b>morphine</b> induced <strong>GFAP</strong> upregulation.
+GFAP	drug	amphetamine	16760923	Administration of <b>METH</b> (5 mg/kg x 3) to Swiss Webster mice decreased striatal tyrosine hydroxylase (TH) immunoreactive neurons and significantly increased glial fibrillary acidic protein (<strong>GFAP</strong>) expression, confirming the neurotoxic potential of <b>METH</b> in mice.
+GFAP	drug	amphetamine	16760923	Administration of <b>METH</b> (5 mg/kg x 3) to Swiss Webster mice decreased striatal tyrosine hydroxylase (TH) immunoreactive neurons and significantly increased <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) expression, confirming the neurotoxic potential of <b>METH</b> in mice.
+GFAP	addiction	sensitization	16631293	Glial fibrillary acidic protein (<strong>GFAP</strong>) up regulation is considered a marker of astrogliosis, and it has been associated to behavioral <b>sensitization</b>.
+GFAP	addiction	sensitization	16631293	<strong>Glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) up regulation is considered a marker of astrogliosis, and it has been associated to behavioral <b>sensitization</b>.
+GFAP	drug	amphetamine	16631293	We aimed to investigate the behavioral effects of acute and chronic <b>AMPH</b> on rat locomotion and assess <strong>GFAP</strong> levels in rat cortex and hippocampus.
+GFAP	drug	amphetamine	16631293	Chronic, but not acute, administration of <b>AMPH</b> increased <strong>GFAP</strong> levels in rat hippocampus.
+GFAP	drug	alcohol	16484281	However, it is unclear if withdrawal from free choice <b>ethanol</b> drinking causes changes in the numbers of astrocytes expressing GS or the cytoskeletal protein of astrocytes glial fibrillary acidic protein (<strong>GFAP</strong>).
+GFAP	addiction	withdrawal	16484281	However, it is unclear if <b>withdrawal</b> from free choice ethanol drinking causes changes in the numbers of astrocytes expressing GS or the cytoskeletal protein of astrocytes glial fibrillary acidic protein (<strong>GFAP</strong>).
+GFAP	drug	alcohol	16484281	However, it is unclear if withdrawal from free choice <b>ethanol</b> drinking causes changes in the numbers of astrocytes expressing GS or the cytoskeletal protein of astrocytes <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>).
+GFAP	addiction	withdrawal	16484281	However, it is unclear if <b>withdrawal</b> from free choice ethanol drinking causes changes in the numbers of astrocytes expressing GS or the cytoskeletal protein of astrocytes <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>).
+GFAP	drug	alcohol	16484281	<b>Ethanol</b> withdrawal significantly increased the packing density of GS  and <strong>GFAP</strong> IR astrocytes in the PLC of P rats as compared with P rats with continuous access to <b>ethanol</b>.
+GFAP	addiction	withdrawal	16484281	Ethanol <b>withdrawal</b> significantly increased the packing density of GS  and <strong>GFAP</strong> IR astrocytes in the PLC of P rats as compared with P rats with continuous access to ethanol.
+GFAP	drug	alcohol	16484281	The present results suggest the involvement of astrocytes in the regulation of the glutamatergic activation associated with withdrawal from free choice <b>ethanol</b> consumption and point to differential adaptations of GS and <strong>GFAP</strong> to prolonged <b>alcohol</b> drinking in the PLC of P rats.
+GFAP	addiction	withdrawal	16484281	The present results suggest the involvement of astrocytes in the regulation of the glutamatergic activation associated with <b>withdrawal</b> from free choice ethanol consumption and point to differential adaptations of GS and <strong>GFAP</strong> to prolonged alcohol drinking in the PLC of P rats.
+GFAP	drug	alcohol	15897721	Lower packing density of <strong>glial fibrillary acidic protein</strong> immunoreactive astrocytes in the prelimbic cortex of <b>alcohol</b> naive and <b>alcohol</b> drinking <b>alcohol</b> preferring rats as compared with <b>alcohol</b> nonpreferring and Wistar rats.
+GFAP	drug	alcohol	15897721	The packing density of <strong>GFAP</strong> IR astrocytes was significantly lower in both <b>alcohol</b> naive and <b>alcohol</b> exposed P rats than in NP rats or Wistar rats.
+GFAP	drug	alcohol	15897721	The area fraction of <strong>GFAP</strong> immunoreactivity was significantly lower in the <b>alcohol</b> exposed P rats than in NP rats, Wistar rats, and <b>alcohol</b> naive P rats.
+GFAP	drug	alcohol	15897721	These results suggest that low density of <strong>GFAP</strong> IR astrocytes in the PLC of P rats predates the exposure to <b>alcohol</b> and might be a factor contributing to the increased risk for <b>alcohol</b> dependence.
+GFAP	addiction	dependence	15897721	These results suggest that low density of <strong>GFAP</strong> IR astrocytes in the PLC of P rats predates the exposure to alcohol and might be a factor contributing to the increased risk for alcohol <b>dependence</b>.
+GFAP	drug	alcohol	15897721	In addition, prolonged free choice <b>alcohol</b> drinking may reduce the extent of <strong>GFAP</strong> IR processes in the PLC of P rats.
+GFAP	drug	amphetamine	15542715	Exposure to <b>METH</b> induces long term deficits in dopamine transporter (DAT) and tyrosine hydroxylase (TH) levels as well as induction of glial fibrillary acidic protein (<strong>GFAP</strong>) in the caudate putamen (CPu) and the nucleus accumbens (NAc).
+GFAP	drug	amphetamine	15542715	Exposure to <b>METH</b> induces long term deficits in dopamine transporter (DAT) and tyrosine hydroxylase (TH) levels as well as induction of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>) in the caudate putamen (CPu) and the nucleus accumbens (NAc).
+GFAP	drug	amphetamine	15542715	Moreover, pretreatment with WIN 51,708 also prevented the reduction of TH levels induced by <b>METH</b> as well as the induction of <strong>GFAP</strong> in astrocytes.
+GFAP	drug	amphetamine	15044042	Repeated <b>amphetamine</b> treatment causes a persistent elevation of <strong>glial fibrillary acidic protein</strong> in the caudate putamen.
+GFAP	drug	amphetamine	15044042	The ability of repeated D <b>amphetamine</b> (2 mg/kg) treatment to induce behavioral sensitization in rats and alter glial fibrillary acidic protein (<strong>GFAP</strong>), dopamine transporter (DAT) and glutamate transporter 1 (GLT 1) immunoreactivities was assessed after a 10 day drug abstinence period.
+GFAP	addiction	sensitization	15044042	The ability of repeated D amphetamine (2 mg/kg) treatment to induce behavioral <b>sensitization</b> in rats and alter glial fibrillary acidic protein (<strong>GFAP</strong>), dopamine transporter (DAT) and glutamate transporter 1 (GLT 1) immunoreactivities was assessed after a 10 day drug abstinence period.
+GFAP	drug	amphetamine	15044042	The ability of repeated D <b>amphetamine</b> (2 mg/kg) treatment to induce behavioral sensitization in rats and alter <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), dopamine transporter (DAT) and glutamate transporter 1 (GLT 1) immunoreactivities was assessed after a 10 day drug abstinence period.
+GFAP	addiction	sensitization	15044042	The ability of repeated D amphetamine (2 mg/kg) treatment to induce behavioral <b>sensitization</b> in rats and alter <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), dopamine transporter (DAT) and glutamate transporter 1 (GLT 1) immunoreactivities was assessed after a 10 day drug abstinence period.
+GFAP	drug	amphetamine	15044042	Results showed that a sensitizing regimen of <b>amphetamine</b> caused a persistent increase in the number of <strong>GFAP</strong> positive cells in the dorsal and ventral caudate putamen.
+GFAP	drug	amphetamine	15044042	Although the elevated <strong>GFAP</strong> expression may be due to a mild neurotoxicity, it is also possible that <b>amphetamine</b> induced increases in <strong>GFAP</strong> reflect adaptive changes that may be associated with processes underlying behavioral sensitization.
+GFAP	addiction	sensitization	15044042	Although the elevated <strong>GFAP</strong> expression may be due to a mild neurotoxicity, it is also possible that amphetamine induced increases in <strong>GFAP</strong> reflect adaptive changes that may be associated with processes underlying behavioral <b>sensitization</b>.
+GFAP	addiction	withdrawal	12670315	Following the 3 week <b>withdrawal</b> period, immunoblotting revealed increased <strong>GFAP</strong> expression in the prefrontal cortex (PFC) and in the shell and core compartments of the nucleus accumbens (NAshell and NAcore).
+GFAP	drug	cocaine	12670315	Upregulation of <strong>GFAP</strong> did not occur in the striatum or in any brain region tested following shorter withdrawal times from repeated <b>cocaine</b> (24 h or 1 week) or following 2 h withdrawal from an acute <b>cocaine</b> injection (30 mg/kg i.p.).
+GFAP	addiction	withdrawal	12670315	Upregulation of <strong>GFAP</strong> did not occur in the striatum or in any brain region tested following shorter <b>withdrawal</b> times from repeated cocaine (24 h or 1 week) or following 2 h <b>withdrawal</b> from an acute cocaine injection (30 mg/kg i.p.).
+GFAP	drug	cocaine	12670315	However, <strong>GFAP</strong> expression increased following a 3 week withdrawal from a single <b>cocaine</b> injection selectively in the NAshell.
+GFAP	addiction	withdrawal	12670315	However, <strong>GFAP</strong> expression increased following a 3 week <b>withdrawal</b> from a single cocaine injection selectively in the NAshell.
+GFAP	drug	alcohol	12480169	Colocalization of taurine and <strong>glial fibrillary acidic protein</strong> immunoreactivity in mouse hippocampus induced by short term <b>ethanol</b> exposure.
+GFAP	drug	alcohol	12480169	<b>Ethanol</b> administration resulted in a significant increase in the accumulation of taurine and <strong>GFAP</strong> immunoreactivity (IR) in the stratum lacunosum moleculare (sl m) of the hippocampus.
+GFAP	drug	cannabinoid	12457068	Reduced <strong>glial fibrillary acidic protein</strong> and glutamine synthetase expression in astrocytes and Bergmann glial cells in the rat cerebellum caused by delta(9) <b>tetrahydrocannabinol</b> administration during development.
+GFAP	drug	cannabinoid	12457068	To determine whether <b>THC</b> during development directly modifies astroglial growth, this study investigated the effects of <b>THC</b> on astroglial morphological changes and on the expression of specific astroglial markers (glial fibrillary acidic protein: <strong>GFAP</strong> and glutamine synthetase: GS).
+GFAP	drug	cannabinoid	12457068	To determine whether <b>THC</b> during development directly modifies astroglial growth, this study investigated the effects of <b>THC</b> on astroglial morphological changes and on the expression of specific astroglial markers (<strong>glial fibrillary acidic protein</strong>: <strong>GFAP</strong> and glutamine synthetase: GS).
+GFAP	drug	cannabinoid	12457068	The effect of <b>cannabinoids</b> on the development of cerebellar astroglial cells (astrocytes and Bergmann glial cells) is to reduce protein synthesis, since both <strong>GFAP</strong> and GS decreased in astroglial cells, not only during <b>THC</b> exposure but also in adult ages.
+GFAP	drug	cannabinoid	12457068	Our data suggest that pre  and perinatal <b>THC</b> exposure directly interferes with astroglial maturation by disrupting normal cytoskeletal formation, as indicated by the irregular disposition of <strong>GFAP</strong> and the lower <strong>GFAP</strong> expression observed at all the ages studied.
+GFAP	drug	alcohol	11011006	Short term <b>ethanol</b> exposure alters calbindin D28k and <strong>glial fibrillary acidic protein</strong> immunoreactivity in hippocampus of mice.
+GFAP	drug	alcohol	11011006	In agreement with the discrepancy percentage of neuronal cell loss and increase of reactive astrocytes detected by calbindin and <strong>GFAP</strong> IR using image quantitative analysis, the regional differences in the vulnerability to the neurotoxic effects following short term <b>ethanol</b> exposure were found: CA3>CA2>CA1>DG.
+GFAP	drug	alcohol	11011006	These findings also illustrate the importance of correlation between calbindin and <strong>GFAP</strong> IR when determining the morphological alteration of neuron and astroglial following short term <b>ethanol</b> treatment.
+GFAP	drug	opioid	10900081	The immunodensities of <strong>GFAP</strong> (the specific glial cytoskeletol protein), alpha internexin (a neuronal filament related to NF L) and synaptophysin (a synapse specific protein) were found unchanged, suggesting a lack of gross changes in glial reaction, other intermediate filaments of the neuronal cytoskeletol, and synaptic density in the prefrontal cortex of <b>opioid</b> addicts.
+GFAP	drug	alcohol	10564744	The results revealed that short term <b>ethanol</b> exposure led to strong expression of <strong>GFAP</strong> immunoreactivity (<strong>GFAP</strong> IR) in the dorsomedial part of the SCN.
+GFAP	drug	alcohol	9309310	In coronal frozen sections through parietal cortex labeled immunohistochemically for <strong>glial fibrillary acidic protein</strong>, the pups exposed to <b>alcohol</b> by intubation had a significantly greater density of <strong>glial fibrillary acidic protein</strong> positive astrocytes per unit volume, compared with littermate controls intubated with a maltose dextrin formula; <b>alcohol</b> also induced fibrillary hypertrophy of the labeled astrocytes.
+GFAP	drug	alcohol	8654528	The combined effects of acute <b>alcoholic</b> intoxication and moderate traumatic brain injury (TBI) on zif/268, glial fibrillary acidic protein (<strong>GFAP</strong>), and preproenkephalin (PPE) mRNA expression were examined.
+GFAP	addiction	intoxication	8654528	The combined effects of acute alcoholic <b>intoxication</b> and moderate traumatic brain injury (TBI) on zif/268, glial fibrillary acidic protein (<strong>GFAP</strong>), and preproenkephalin (PPE) mRNA expression were examined.
+GFAP	drug	alcohol	8654528	The combined effects of acute <b>alcoholic</b> intoxication and moderate traumatic brain injury (TBI) on zif/268, <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), and preproenkephalin (PPE) mRNA expression were examined.
+GFAP	addiction	intoxication	8654528	The combined effects of acute alcoholic <b>intoxication</b> and moderate traumatic brain injury (TBI) on zif/268, <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>), and preproenkephalin (PPE) mRNA expression were examined.
+GFAP	drug	alcohol	8654528	However, <b>alcohol</b> inhibited the temporal induction of <strong>GFAP</strong> mRNA in the FTCTX and P/A triggered by TBI at 6 and 24 h. These results suggest that although acute <b>alcohol</b> intoxication prior to TBI does not influence gene expression patterns immediately after injury, it may minimize the transcriptional activation of astrocytes particularly in more distant brain regions that were influenced by the impact in nonintoxicated rats.
+GFAP	addiction	intoxication	8654528	However, alcohol inhibited the temporal induction of <strong>GFAP</strong> mRNA in the FTCTX and P/A triggered by TBI at 6 and 24 h. These results suggest that although acute alcohol <b>intoxication</b> prior to TBI does not influence gene expression patterns immediately after injury, it may minimize the transcriptional activation of astrocytes particularly in more distant brain regions that were influenced by the impact in nonintoxicated rats.
+GFAP	drug	alcohol	8869159	Indeed, as seen for chronic morphine and cocaine treatments, we show here that chronic <b>ethanol</b> treatment increased levels of tyrosine hydroxylase and <strong>glial fibrillary acidic protein</strong> immunoreactivity, and decreases levels of neurofilament protein immunoreactivity, in the VTA.
+GFAP	drug	cocaine	8869159	Indeed, as seen for chronic morphine and <b>cocaine</b> treatments, we show here that chronic ethanol treatment increased levels of tyrosine hydroxylase and <strong>glial fibrillary acidic protein</strong> immunoreactivity, and decreases levels of neurofilament protein immunoreactivity, in the VTA.
+GFAP	drug	opioid	8869159	Indeed, as seen for chronic <b>morphine</b> and cocaine treatments, we show here that chronic ethanol treatment increased levels of tyrosine hydroxylase and <strong>glial fibrillary acidic protein</strong> immunoreactivity, and decreases levels of neurofilament protein immunoreactivity, in the VTA.
+GFAP	drug	opioid	8545003	Chronic <b>morphine</b> treatment also increases levels of <strong>glial fibrillary acidic protein</strong> in this brain region.
+GFAP	drug	opioid	8545003	In addition, neurotrophin 4 prevented the <b>morphine</b> induced increase in <strong>glial fibrillary acidic protein</strong>.
+GFAP	drug	opioid	8545003	Nerve growth factor alone had no effect on tyrosine hydroxylase or <strong>glial fibrillary acidic protein</strong> levels and did not affect <b>morphine</b>'s ability to induce these proteins.
+GFAP	drug	opioid	8228992	<strong>Glial fibrillary acidic protein</strong> and the mesolimbic dopamine system: regulation by chronic <b>morphine</b> and Lewis Fischer strain differences in the rat ventral tegmental area.
+GFAP	drug	opioid	8228992	In this study we demonstrate that a 51 kDa phosphoprotein, previously identified as <b>morphine</b> regulated and showing different basal levels among rat strains, is glial fibrillary acidic protein (<strong>GFAP</strong>).
+GFAP	drug	opioid	8228992	In this study we demonstrate that a 51 kDa phosphoprotein, previously identified as <b>morphine</b> regulated and showing different basal levels among rat strains, is <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>).
+GFAP	drug	opioid	8228992	Chronic <b>morphine</b> increased levels of <strong>GFAP</strong> immunoreactivity by > 70% in the ventral tegmental area (VTA) of outbred Sprague Dawley rats.
+GFAP	drug	alcohol	8228992	This increase in <strong>GFAP</strong> content was not observed in rats that were treated concomitantly with morphine and <b>naltrexone</b>, an opiate receptor antagonist, and did not occur in response to a single acute injection with morphine.
+GFAP	drug	opioid	8228992	This increase in <strong>GFAP</strong> content was not observed in rats that were treated concomitantly with <b>morphine</b> and naltrexone, an opiate receptor antagonist, and did not occur in response to a single acute injection with <b>morphine</b>.
+GFAP	drug	opioid	8228992	No alterations in <strong>GFAP</strong> levels were observed in response to chronic <b>morphine</b> in several other regions of the CNS studied, including the substantia nigra, locus coeruleus, cerebral cortex, and spinal cord.
+GFAP	drug	opioid	8228992	There were also inherent differences in levels of <strong>GFAP</strong> immunoreactivity in the VTA of drug naive Fischer 344 and Lewis rats, two inbred rat strains that differ in their relative preference for <b>morphine</b> and other drugs of abuse.
+GFAP	addiction	addiction	8228992	Because the mesolimbic dopamine system is thought to play a critical role in mediating the reinforcing properties of opiates and other drugs of abuse, it is possible that the opiate induction of <strong>GFAP</strong> and inherent Lewis versus Fischer strain differences in <strong>GFAP</strong> levels in the VTA may be related to the reinforcing and/or <b>addictive</b> properties of opiates mediated by this brain region, as well as to genetic differences in drug preference.
+GFAP	addiction	reward	8228992	Because the mesolimbic dopamine system is thought to play a critical role in mediating the <b>reinforcing</b> properties of opiates and other drugs of abuse, it is possible that the opiate induction of <strong>GFAP</strong> and inherent Lewis versus Fischer strain differences in <strong>GFAP</strong> levels in the VTA may be related to the <b>reinforcing</b> and/or addictive properties of opiates mediated by this brain region, as well as to genetic differences in drug preference.
+GFAP	drug	alcohol	8453767	The astrocyte response to central nervous system injury induced by neonatal <b>alcohol</b> exposure was evaluated using radioimmunoassay and immunocytochemistry of glial fibrillary acidic protein (<strong>GFAP</strong>).
+GFAP	drug	alcohol	8453767	The astrocyte response to central nervous system injury induced by neonatal <b>alcohol</b> exposure was evaluated using radioimmunoassay and immunocytochemistry of <strong>glial fibrillary acidic protein</strong> (<strong>GFAP</strong>).
+GFAP	drug	alcohol	8453767	On postnatal day 10, <strong>GFAP</strong> concentration increased as a function of BAC, and the 10.2% <b>alcohol</b> treatment significantly and dramatically increased <strong>GFAP</strong> in the cortex (325% of SC).
+GFAP	drug	alcohol	8453767	In addition, a generalized increase in <strong>GFAP</strong> immunoreactivity was present in the deep layers of the cortex in all <b>alcohol</b> groups, marked by astrocytic fibrillary hypertrophy and increased density.
+CYP2D6	drug	opioid	31206401	<b>Methadone</b> is metabolized by several cytochrome P450 isoenzymes; primarily CYP3A4, CYP2B6, and <strong>CYP2D6</strong> before renal and fecal elimination.
+CYP2D6	drug	opioid	31005596	<b>Tramadol</b> labeling indicates cytochrome P450 (CYP) isozyme 2D6 ultrarapid metabolizer can produce dangerous (+) M1 levels, and <strong>CYP2D6</strong> poor metabolizers insufficient (+) M1 for analgesia.
+CYP2D6	drug	opioid	30907440	Relevance of CYP2B6 and <strong>CYP2D6</strong> genotypes to <b>methadone</b> pharmacokinetics and response in the OPAL study.
+CYP2D6	drug	opioid	30907440	Our study aimed to evaluate the impacts of the cytochrome P450 (CYP) 2B6 G516T and <strong>CYP2D6</strong> genetic polymorphisms on pharmacokinetic and clinical parameters in patients receiving <b>methadone</b> maintenance treatment.
+CYP2D6	drug	opioid	30907440	The <strong>CYP2D6</strong> phenotypes did not seem to be relevant with regard to <b>methadone</b> levels.
+CYP2D6	drug	opioid	30907440	On multivariate analysis, neither the CYP2B6 genotype nor the <strong>CYP2D6</strong> phenotype explained the (R) <b>methadone</b> concentration/dose values (P = .92; P = .86); the (S) <b>methadone</b> concentration/dose values (P = .052; P = .95 [although there was a difference between the TT group and GT and GG groups {P = .019}]); or opiate cessation (P = .12; P = .90).
+CYP2D6	drug	amphetamine	30783122	We uncovered that Theophylline's metabolism and elimination could be retarded due to competition and/or blockage of the <strong>CYP2D6</strong> enzyme by <b>Amphetamine</b>; We also found that the synergies between these two metabolites cause Captagon's psychoactive effects to act faster and far more potently than those of <b>Amphetamine</b> alone.
+CYP2D6	drug	nicotine	30734152	Correlation between PK and <strong>CYP2D6</strong> inhibitor use, <b>smoking</b> status, and PGx were examined by regression analysis.
+CYP2D6	drug	nicotine	30734152	<b>Smoking</b> status (p = 0.07) and the CYP2C19 phenotype (p = 0.07), but not the <strong>CYP2D6</strong> genotype (p = 0.61), showed marginally significant effects on TOR activity.
+CYP2D6	drug	opioid	30508992	Fundamental Considerations for Genetically Guided Pain Management with <b>Opioids</b> Based on <strong>CYP2D6</strong> and OPRM1 Polymorphisms.
+CYP2D6	drug	opioid	30508992	Clinically actionable polymorphisms in <strong>CYP2D6</strong> (cytochrome p450 2D6) and OPRM1 (mu 1 <b>opioid</b> receptor), the most important gene coding, respectively, for a metabolizing enzyme and receptor for <b>opioids</b> are reviewed, and functional effects described.
+CYP2D6	drug	opioid	30508992	Patients at high risk with dysfunctional <strong>CYP2D6</strong> or OPRM1 account for ~14% of the population and are best managed with non <b>opioids</b>.
+CYP2D6	drug	opioid	30508992	Patients at low risk with functional <strong>CYP2D6</strong> and OPRM1 account for ~38% of the population and should be availed to <b>opioid</b> therapy.
+CYP2D6	drug	opioid	30508992	Pain management, <b>opioids</b>, <strong>CYP2D6</strong>, OPRM1, clinical decision support, pharmacokinetics, pharmacodynamics, pharmacogenetics, combinatorial genotypes.
+CYP2D6	drug	opioid	30248201	Such PK differences among individuals are known not only for <b>codeine</b> and <b>tramadol</b> through pharmacogenetic variants of <strong>CYP2D6</strong> but also for non <strong>CYP2D6</strong> substrate <b>opioids</b> including <b>oxycodone</b>, indicating difficulties of eliminating PK uncertainty by simply replacing an <b>opioid</b> with another.
+CYP2D6	drug	opioid	30205091	<b>Methadone</b> undergoes N demethylation by multiple cytochrome P450 (CYP) enzymes including CYP3A4, CYP2B6, CYP2C19, <strong>CYP2D6</strong>, CYP2C9, and CYP2C8.
+CYP2D6	drug	opioid	30205091	In vivo, polymorphism effects on <b>methadone</b> systemic exposure have been noted for CYP2B6, CYP3A4, and <strong>CYP2D6</strong>.
+CYP2D6	drug	alcohol	29988737	Effects of <strong>CYP2D6</strong> genetic polymorphisms on the efficacy and safety of fluvoxamine in patients with depressive disorder and comorbid <b>alcohol</b> use disorder.
+CYP2D6	drug	alcohol	29988737	The primary objective of our study was to investigate the effects of <strong>CYP2D6</strong> genetic polymorphisms on the efficacy and safety of fluvoxamine in patients with depressive disorder and comorbid <b>alcohol</b> use disorder, in order to develop the algorithms of optimization of fluvoxamine therapy for reducing the risk of dose dependent undesirable side effects and pharmacoresistance.
+CYP2D6	drug	alcohol	29988737	This study demonstrated the lower efficacy and safety of fluvoxamine in patients with depressive disorder and comorbid <b>alcohol</b> use disorders with GA genotype in <strong>CYP2D6</strong> 1846G>A polymorphic marker.
+CYP2D6	drug	opioid	29963937	Interaction between <strong>CYP2D6</strong> inhibitor antidepressants and <b>codeine</b>: is this relevant?
+CYP2D6	drug	opioid	29963937	Expert opinion: The literature review highlighted that antidepressants with moderate to strong inhibition of <strong>CYP2D6</strong> should be avoided in patients receiving <b>codeine</b>.
+CYP2D6	drug	opioid	29963937	However, 0.44% of the 12,296 sampled patients received concomitant <b>codeine</b> and <strong>CYP2D6</strong> inhibitor between January 2015 and June 2015.
+CYP2D6	drug	opioid	29524157	Moreover, the ratios of ODMT/<b>tramadol</b>, NDMT/<b>tramadol</b> and NODMT/NDMT were well correlated with the <strong>CYP2D6</strong> genotypes.
+CYP2D6	drug	opioid	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, <strong>CYP2D6</strong>, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+CYP2D6	addiction	dependence	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, <strong>CYP2D6</strong>, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+CYP2D6	drug	amphetamine	29258368	D <b>amphetamine</b> is then further metabolized by <strong>CYP2D6</strong>.
+CYP2D6	drug	psychedelics	28917081	<b>MDMA</b> exerted greater inhibitory effects on cytochrome P450 3A4 (CYP3A4) than on cytochrome P450 2D6 (<strong>CYP2D6</strong>).
+CYP2D6	drug	psychedelics	28917081	However, <b>MDMA</b> was introduced as <strong>CYP2D6</strong> inhibitor; in this study, <b>MDMA</b> inhibited CYP3A4 isoenzymes as well.
+CYP2D6	drug	nicotine	28837793	Inducing rat brain <strong>CYP2D</strong> with <b>nicotine</b> increases the rate of codeine tolerance; predicting the rate of tolerance from acute analgesic response.
+CYP2D6	drug	opioid	28837793	Inducing rat brain <strong>CYP2D</strong> with nicotine increases the rate of <b>codeine</b> tolerance; predicting the rate of tolerance from acute analgesic response.
+CYP2D6	drug	opioid	28837793	Brain <strong>CYP2D</strong> metabolizes <b>codeine</b> to <b>morphine</b>, a bioactivation step required for <b>codeine</b> analgesia.
+CYP2D6	drug	nicotine	28837793	Higher brain, but not liver, <strong>CYP2D</strong> is found in <b>smokers</b> and <b>nicotine</b> induces rat brain, but not liver, <strong>CYP2D</strong> expression and activity.
+CYP2D6	drug	nicotine	28837793	<b>Nicotine</b> induction of rat brain <strong>CYP2D</strong> increases acute codeine conversion to morphine, and analgesia, however the role of brain <strong>CYP2D</strong> on the effects of repeated codeine exposure and tolerance is unknown.
+CYP2D6	drug	opioid	28837793	Nicotine induction of rat brain <strong>CYP2D</strong> increases acute <b>codeine</b> conversion to <b>morphine</b>, and analgesia, however the role of brain <strong>CYP2D</strong> on the effects of repeated <b>codeine</b> exposure and tolerance is unknown.
+CYP2D6	drug	nicotine	28837793	Rats were pretreated with <b>nicotine</b> (brain <strong>CYP2D</strong> inducer; 1mg/kg subcutaneously) or vehicle (saline; 1ml/kg subcutaneously).
+CYP2D6	drug	nicotine	28837793	Inducing brain <strong>CYP2D</strong> with <b>nicotine</b> did not alter acute morphine analgesia (1.03 fold; p>0.8), or the rate of morphine tolerance (8.1%/day versus 7.6%; p>0.9).
+CYP2D6	drug	opioid	28837793	Inducing brain <strong>CYP2D</strong> with nicotine did not alter acute <b>morphine</b> analgesia (1.03 fold; p>0.8), or the rate of <b>morphine</b> tolerance (8.1%/day versus 7.6%; p>0.9).
+CYP2D6	drug	alcohol	28787271	Genotyping and phenotyping of <strong>CYP2D6</strong> and CYP3A isoenzymes in patients with <b>alcohol</b> use disorder: correlation with haloperidol plasma concentration.
+CYP2D6	drug	alcohol	28787271	The primary objective of this study was to investigate the effects of <strong>CYP2D6</strong> and CYP3A5 genetic polymorphisms on haloperidol equilibrium concentration in patients with <b>alcohol</b> use disorder.
+CYP2D6	drug	alcohol	28787271	The study demonstrates that <strong>CYP2D6</strong> genetic polymorphism (1846G>A) can affect haloperidol concentration levels in patients with <b>alcohol</b> use disorder.
+CYP2D6	drug	opioid	27861439	It is a prodrug that is metabolized by cytochrome P450 (CYP) enzymes <strong>CYP2D6</strong> and CYP3A4 to its more potent <b>opioid</b> analgesic metabolites, particularly the O demethylation product M1.
+CYP2D6	addiction	relapse	27738380	Upon full <b>relapse</b> in DSM 5 MDD while taking 600 mg/day of the strong <strong>CYP2D6</strong> inhibitor bupropion XL, a 300 mg oral loading dose of DM was given, followed by 60 mg po bid after an additional dose finding period, without side effects.
+CYP2D6	drug	psychedelics	27734823	After oral application, 80% of <b>ibogaine</b> is subjected to the Odemethylation into noribogaine; main catalyzing enzyme is cytochrome <strong>CYP2D6</strong>.
+CYP2D6	drug	alcohol	27695358	The correlation between <strong>CYP2D6</strong> isoenzyme activity and haloperidol efficacy and safety profile in patients with <b>alcohol</b> addiction during the exacerbation of the addiction.
+CYP2D6	addiction	addiction	27695358	The correlation between <strong>CYP2D6</strong> isoenzyme activity and haloperidol efficacy and safety profile in patients with alcohol <b>addiction</b> during the exacerbation of the <b>addiction</b>.
+CYP2D6	drug	alcohol	27695358	The aim of this study was to evaluate the correlation between the activity of <strong>CYP2D6</strong> and the efficacy and safety of haloperidol in patients with diagnosed <b>alcohol</b> abuse.
+CYP2D6	drug	alcohol	27695358	This study demonstrated the correlations between the activity of <strong>CYP2D6</strong> isozyme and the efficacy and safety of haloperidol in patients with <b>alcohol</b> addiction.
+CYP2D6	addiction	addiction	27695358	This study demonstrated the correlations between the activity of <strong>CYP2D6</strong> isozyme and the efficacy and safety of haloperidol in patients with alcohol <b>addiction</b>.
+CYP2D6	addiction	dependence	27618912	The metabolite specific interactions in the current studies seem at variance with earlier reports of the <b>dependence</b> of PQ on <strong>CYP2D6</strong> metabolism, and enhanced PQ anti malarial activity/reduced toxicity in the presence of CQ/QN.
+CYP2D6	drug	psychedelics	27400739	The major CYP enzymes involved in the metabolism of 25I <b>NBOMe</b> and 25INBOH were identified as CYP3A4 and <strong>CYP2D6</strong>, respectively.
+CYP2D6	drug	alcohol	27376791	Although several environmental and socio demographic/diagnostic variables such as <b>alcohol</b>/drug abuse, and medication non compliance accounted for a significant proportion of the ability to predict RD prevalence and frequency, the pharmacogenetics of CYP, particularly <strong>CYP2D6</strong>, may help to identify BD patients at risk for ADRs and TFs.
+CYP2D6	drug	opioid	27061230	To examine whether certain genotypes were associated with this, we examined the frequencies of 29 SNPs located in candidate genes related to <b>opioid</b> pharmacology: ABCB1, OPRM1, UGT2B7, CYP3A5, CYP2B6, CYP2C19, <strong>CYP2D6</strong>, COMT, KCNJ6 and SCN9A in 274 deceased patients with OA (DOA), 309 living patients with OA (LOA) and in 394 healthy volunteers (HV).
+CYP2D6	drug	opioid	27042732	The potency of <b>codeine</b> and <b>tramadol</b> is strongly influenced by the cytochrome P450 isoenzyme <strong>CYP2D6</strong> genotype, which varies widely from one person to another.
+CYP2D6	drug	opioid	27042732	The potency of <b>morphine</b> and that of <b>buprenorphine</b>, an <b>opioid</b> receptor agonist antagonist, appears to be independent of <strong>CYP2D6</strong> activity.
+CYP2D6	drug	opioid	26986973	There was also a large variability in calculated ratios of <b>morphine</b> to <b>codeine</b>, C6G to <b>codeine</b> and norcodeine to <b>codeine</b> in all matrices, and <strong>CYP2D6</strong> genotype was not a reliable predictor of these ratios.
+CYP2D6	drug	psychedelics	26807959	PHARMACOKINETICS AND PHARMACODYNAMICS: <b>Ibogaine</b> is metabolized mainly by <strong>CYP2D6</strong> to the primary metabolite noribogaine (10 hydroxyibogamine).
+CYP2D6	drug	psychedelics	26807959	TOXICITY FROM DRUG DRUG INTERACTION: Polymorphism in the <strong>CYP2D6</strong> enzyme can influence blood concentrations of both <b>ibogaine</b> and its primary metabolite, which may have implications when a patient is taking other medication that is subject to significant <strong>CYP2D6</strong> metabolism.
+CYP2D6	drug	opioid	26591180	<b>Codeine</b> is one of the centrally acting narcotic <b>opioids</b> approved for use as an antitussive, a prodrug that is bioactivated by <strong>CYP2D6</strong> into <b>morphine</b> in the liver.
+CYP2D6	drug	opioid	26479786	In contrast to <b>codeine</b> and <b>tramadol</b>, DHC analgesia seem to be irrespective of <strong>CYP2D6</strong> activity due to parent compound analgesic effects, multiple metabolic pathways and limited role of dihydromorphine in DHC analgesia.
+CYP2D6	drug	nicotine	26287939	Effect of genotype and methylation of <strong>CYP2D6</strong> on <b>smoking</b> behaviour.
+CYP2D6	drug	nicotine	26287939	We studied eight functional gene variants of one of the most important drug metabolizing enzymes, <strong>CYP2D6</strong>, in relation to <b>smoking</b> behaviour in our well characterized study population consisting of 1230 Whites of Russian origin.
+CYP2D6	drug	nicotine	26287939	In addition, potential associations between methylation levels in a CpG island in the <strong>CYP2D6</strong> gene and sex, age, different <b>smoking</b> related phenotypes and <strong>CYP2D6</strong> genotypes were studied.
+CYP2D6	addiction	dependence	26287939	The <strong>CYP2D6</strong> methylation pattern also showed high genotype <b>dependence</b>; compared with the extensive metabolizer genotype, the poor metabolizer genotype occurred notably more frequently with higher methylation status (odds ratio 5.05, 95% confidence interval 2.14 11.90).
+CYP2D6	drug	nicotine	26287939	We also found associations between the <strong>CYP2D6</strong> genotype and <b>smoking</b> habits; the poor metabolizer genotype tended to decrease the risk of becoming a heavy <b>smoker</b> compared with the extensive metabolizers, whereas the ultrarapid metabolism related genotypes tended to increase the risk.
+CYP2D6	drug	opioid	25998998	<strong>CYP2D6</strong> genetic polymorphisms and their relevance for poisoning due to amfetamines, <b>opioid</b> analgesics and antidepressants.
+CYP2D6	drug	opioid	25998998	This review will focus specifically on <strong>CYP2D6</strong> genetic polymorphisms and their relevance for poisoning due to amfetamines, <b>opioid</b> analgesics and antidepressants in humans.
+CYP2D6	addiction	intoxication	25998998	PubMed (up to August 2013) was searched with the following selection criteria: '<strong>CYP2D6</strong> AND (toxicology OR poisoning OR <b>intoxication</b> OR overdose)'.
+CYP2D6	drug	opioid	25998998	Of the 454 citations retrieved, only 46 papers dealt with the impact of <strong>CYP2D6</strong> polymorphisms on poisoning due to amfetamines, <b>opioid</b> analgesics and antidepressants.
+CYP2D6	drug	psychedelics	25998998	While some in vitro studies suggest that <strong>CYP2D6</strong> mediated metabolites of 3,4 methylenedioxymethamfetamine (<b>MDMA</b>) are substantially more cytotoxic compared with unchanged <b>MDMA</b>, it is not yet confirmed in human cases of <b>MDMA</b> intoxication that extensive/ultra rapid <strong>CYP2D6</strong> metabolisers could be at higher risk.
+CYP2D6	addiction	intoxication	25998998	While some in vitro studies suggest that <strong>CYP2D6</strong> mediated metabolites of 3,4 methylenedioxymethamfetamine (MDMA) are substantially more cytotoxic compared with unchanged MDMA, it is not yet confirmed in human cases of MDMA <b>intoxication</b> that extensive/ultra rapid <strong>CYP2D6</strong> metabolisers could be at higher risk.
+CYP2D6	drug	opioid	25998998	<strong>CYP2D6</strong> ultra rapid metabolisers are more likely to experience the adverse effects of <b>codeine</b> and <b>tramadol</b>.
+CYP2D6	drug	opioid	25998998	<b>Opioid</b> analgesics that do not rely on <strong>CYP2D6</strong> for therapeutic activity, such as <b>morphine</b> and <b>hydromorphone</b>, may therefore be a better alternative to <b>codeine</b> and <b>tramadol</b>, with the limitation that these drugs have their own set of adverse reactions.
+CYP2D6	drug	opioid	25998998	Either poor or extensive/ultra rapid <strong>CYP2D6</strong> metabolisers may be exposed to toxic effects of amfetamines, <b>opioid</b> analgesics and antidepressants.
+CYP2D6	drug	opioid	25825958	Impact of <strong>CYP2D6</strong> Polymorphisms on Postoperative <b>Fentanyl</b> Analgesia in Gastric Cancer Patients.
+CYP2D6	drug	opioid	25825958	This study investigated the influence of human cytochrome P450 2D6 (<strong>CYP2D6</strong>) gene polymorphism in gastric cancer (GC) patients to understand the pharmacogenomic basis for patient response to postoperative <b>fentanyl</b> analgesia.
+CYP2D6	drug	opioid	25825958	<strong>CYP2D6</strong> polymorphism influenced patient response to postoperative <b>fentanyl</b> analgesia in GC patients.
+CYP2D6	drug	opioid	25670515	For <b>opioids</b> requiring <strong>CYP2D6</strong> O demethylation to active metabolites, poor metabolizers have reduced metabolite formation and minimal pain reduction.
+CYP2D6	drug	benzodiazepine	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) methadone), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the <b>midazolam</b> test, R,S methadone trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, ABCB1, CYP2B6, CYP3A5, CYP2C19 and <strong>CYP2D6</strong> genes.
+CYP2D6	drug	opioid	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) <b>methadone</b>), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the midazolam test, R,S <b>methadone</b> trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, ABCB1, CYP2B6, CYP3A5, CYP2C19 and <strong>CYP2D6</strong> genes.
+CYP2D6	drug	opioid	25104495	Additionally, there are reports of severe or fatal toxicity due to <strong>CYP2D6</strong> ultrarapid hepatic metabolism of <b>codeine</b> to <b>morphine</b> among some ethnic groups, especially those from Eastern Africa.
+CYP2D6	drug	opioid	25104495	Overdose and death following the institution of <b>codeine</b> therapy are not more commonly observed among immigrants from world regions with a high prevalence of ultrarapid <strong>CYP2D6</strong> status relative to those born in Canada.
+CYP2D6	drug	alcohol	24611668	<b>Ethanol</b> self administration and nicotine treatment increase brain levels of <strong>CYP2D</strong> in African green monkeys.
+CYP2D6	drug	nicotine	24611668	Ethanol self administration and <b>nicotine</b> treatment increase brain levels of <strong>CYP2D</strong> in African green monkeys.
+CYP2D6	drug	alcohol	24611668	<b>Alcohol</b> consumers and smokers have higher levels of <strong>CYP2D6</strong> in brain, but not liver, suggesting <b>ethanol</b> and/or nicotine may induce human brain <strong>CYP2D6</strong>.
+CYP2D6	drug	nicotine	24611668	Alcohol consumers and <b>smokers</b> have higher levels of <strong>CYP2D6</strong> in brain, but not liver, suggesting ethanol and/or <b>nicotine</b> may induce human brain <strong>CYP2D6</strong>.
+CYP2D6	drug	alcohol	24611668	We investigated the independent and combined effects of chronic <b>ethanol</b> self administration and nicotine treatment on <strong>CYP2D</strong> expression in African green monkeys.
+CYP2D6	drug	nicotine	24611668	We investigated the independent and combined effects of chronic ethanol self administration and <b>nicotine</b> treatment on <strong>CYP2D</strong> expression in African green monkeys.
+CYP2D6	drug	alcohol	24611668	Both nicotine and <b>ethanol</b> dose dependently increased <strong>CYP2D</strong> in brain; brain mRNA was unaffected, and neither drug altered hepatic <strong>CYP2D</strong> protein or mRNA.
+CYP2D6	drug	nicotine	24611668	Both <b>nicotine</b> and ethanol dose dependently increased <strong>CYP2D</strong> in brain; brain mRNA was unaffected, and neither drug altered hepatic <strong>CYP2D</strong> protein or mRNA.
+CYP2D6	drug	alcohol	24611668	The combination of <b>ethanol</b> and nicotine increased brain <strong>CYP2D</strong> protein levels to a greater extent than either drug alone (1.2 2.2 fold, P < 0.05 among the eight brain regions assessed).
+CYP2D6	drug	nicotine	24611668	The combination of ethanol and <b>nicotine</b> increased brain <strong>CYP2D</strong> protein levels to a greater extent than either drug alone (1.2 2.2 fold, P < 0.05 among the eight brain regions assessed).
+CYP2D6	drug	alcohol	24611668	<b>Ethanol</b> and nicotine increase brain <strong>CYP2D</strong> protein levels in monkeys, in a region and treatment specific manner, suggesting that CNS drug responses, neurodegeneration and personality may be affected among people who consume <b>alcohol</b> and/or nicotine.
+CYP2D6	drug	nicotine	24611668	Ethanol and <b>nicotine</b> increase brain <strong>CYP2D</strong> protein levels in monkeys, in a region and treatment specific manner, suggesting that CNS drug responses, neurodegeneration and personality may be affected among people who consume alcohol and/or <b>nicotine</b>.
+CYP2D6	drug	opioid	24495562	The <strong>CYP2D6</strong> gene determines <b>oxycodone</b>'s phenotype specific addictive potential: implications for addiction prevention and treatment.
+CYP2D6	addiction	addiction	24495562	The <strong>CYP2D6</strong> gene determines oxycodone's phenotype specific <b>addictive</b> potential: implications for <b>addiction</b> prevention and treatment.
+CYP2D6	drug	opioid	24495562	We hypothesize that a patient's <strong>CYP2D6</strong> phenotype determines <b>oxycodone</b>'s addictive potential, in part, via genotype specific regulation of its clearance; although, other possible modulators of <b>oxycodone</b>'s addiction potential exist.
+CYP2D6	addiction	addiction	24495562	We hypothesize that a patient's <strong>CYP2D6</strong> phenotype determines oxycodone's <b>addictive</b> potential, in part, via genotype specific regulation of its clearance; although, other possible modulators of oxycodone's <b>addiction</b> potential exist.
+CYP2D6	drug	opioid	24495562	Using <strong>CYP2D6</strong> phenotype specific <b>oxycodone</b> pharmacokinetic parameter values derived from published data, our hypothesis predicted that the canonical order of <b>oxycodone</b>'s addictive potential was UM>EM>IM>PM, with corresponding LAP values of 0.24, 0.21, 0.17, and 0.15 respectively.
+CYP2D6	addiction	addiction	24495562	Using <strong>CYP2D6</strong> phenotype specific oxycodone pharmacokinetic parameter values derived from published data, our hypothesis predicted that the canonical order of oxycodone's <b>addictive</b> potential was UM>EM>IM>PM, with corresponding LAP values of 0.24, 0.21, 0.17, and 0.15 respectively.
+CYP2D6	addiction	dependence	24167729	We performed a review of the efficacy of pharmacogenomic markers and their abilities to predict adverse events, <b>dependence</b>, and associated economic costs, focusing on two genes: OPRM1 and <strong>CYP2D6</strong>.
+CYP2D6	drug	opioid	24122908	TRV130 pharmacokinetics were modestly affected by <strong>CYP2D6</strong> phenotype: clearance was reduced by 53% in <strong>CYP2D6</strong> poor metabolizers.TRV130 caused dose  and exposure related pupil constriction, confirming central compartment µ <b>opioid</b> receptor engagement.
+CYP2D6	drug	opioid	23739600	Genetic variation in <strong>CYP2D6</strong> is related to efficacy of <b>methadone</b> treatment for opiate dependence.
+CYP2D6	addiction	dependence	23739600	Genetic variation in <strong>CYP2D6</strong> is related to efficacy of methadone treatment for opiate <b>dependence</b>.
+CYP2D6	drug	opioid	23527673	Pharmacogenomics is of growing relevance to the pain field, for example cytochrome P450 2D6 (<strong>CYP2D6</strong>) polymorphisms with resulting variation in degree of <strong>CYP2D6</strong> expression may affect <b>codeine</b> analgesia.
+CYP2D6	drug	psychedelics	23030234	Polymorphisms in <strong>CYP2D6</strong>, resulting in poor metabolism status, as well as co exposure of <b>MDMA</b> with specific substances (e.g.
+CYP2D6	drug	amphetamine	22503241	To minimize estimation errors in such cases, we also analyzed genotype of <strong>CYP2D6</strong>, which influenced <b>methamphetamine</b> metabolism.
+CYP2D6	drug	opioid	22406651	Suspected <b>opioid</b> overdose case resolved by <strong>CYP2D6</strong> genotyping.
+CYP2D6	addiction	intoxication	22406651	A 14 year old female with suspected narcotic overdose had <strong>CYP2D6</strong> genotyping performed to verify opiate <b>intoxication</b>.
+CYP2D6	drug	opioid	22352453	Pharmacogenomics of <b>codeine</b>, <b>morphine</b>, and <b>morphine</b> 6 glucuronide: model based analysis of the influence of <strong>CYP2D6</strong> activity, UGT2B7 activity, renal impairment, and CYP3A4 inhibition.
+CYP2D6	drug	opioid	22352453	By means of a generic modeling approach integrating prior physiologic knowledge, we systematically investigated the complex dependence of <b>opioid</b> exposure on cytochrome P450 2D6 and 3A4 (<strong>CYP2D6</strong> and CYP3A4), and uridine diphosphate glucuronosyltransferase 2B7 (UGT2B7) activity, as well as renal function, by means of a virtual clinical trial.
+CYP2D6	addiction	dependence	22352453	By means of a generic modeling approach integrating prior physiologic knowledge, we systematically investigated the complex <b>dependence</b> of opioid exposure on cytochrome P450 2D6 and 3A4 (<strong>CYP2D6</strong> and CYP3A4), and uridine diphosphate glucuronosyltransferase 2B7 (UGT2B7) activity, as well as renal function, by means of a virtual clinical trial.
+CYP2D6	drug	opioid	22352453	First, the known dominant role of <strong>CYP2D6</strong> activity for <b>morphine</b> exposure was reproduced.
+CYP2D6	drug	opioid	21790905	<b>Methadone</b> metabolism is attributed primarily to cytochrome P450 enzymes CYP3A4, CYP2B6 and <strong>CYP2D6</strong>.
+CYP2D6	drug	opioid	21691803	Near fatal <b>tramadol</b> cardiotoxicity in a <strong>CYP2D6</strong> ultrarapid metabolizer.
+CYP2D6	drug	opioid	21691803	The marketed <b>tramadol</b> is a racemic mixture containing 50% (+)<b>tramadol</b> and 50% ( )<b>tramadol</b> and is mainly metabolized to O desmethyltramadol (M1) by the cytochrome P450 <strong>CYP2D6</strong>.
+CYP2D6	drug	opioid	21691803	Genotyping of <strong>CYP2D6</strong> revealed the patient to be heterozygous for a duplicated wild type allele, predictive of a <strong>CYP2D6</strong> ultrarapid metabolizer (UM) phenotype, confirmed by calculation of the <b>tramadol</b>/M1 (MR1) metabolic ratio at all time points.
+CYP2D6	drug	opioid	21691803	In patients with excessive morphinomimetic effects, levels of <b>tramadol</b> and its main metabolite M1could be measured, ideally combined with <strong>CYP2D6</strong> genotyping, to identify individuals at risk of <b>tramadol</b> related cardiotoxicity.
+CYP2D6	drug	opioid	21589866	Patients were clinically assessed and blood samples were obtained to determine plasma concentrations of (R,S) , (R) and (S) <b>methadone</b> and to study allelic variants of genes encoding CYP3A5, <strong>CYP2D6</strong>, CYP2B6, CYP2C9, CYP2C19, and P glycoprotein.
+CYP2D6	drug	opioid	21589866	Only <strong>CYP2D6</strong> metabolizing phenotype differences were found in outcome status, <b>methadone</b> dose requirements, and plasma concentrations, being higher in the ultrarapid metabolizers.
+CYP2D6	drug	opioid	21241245	Genetic transmission of cytochrome P450 2D6 (<strong>CYP2D6</strong>) ultrarapid metabolism: implications for breastfeeding women taking <b>codeine</b>.
+CYP2D6	drug	opioid	21241245	The safety of <b>codeine</b> during breastfeeding is related in part to the extent of the active <b>morphine</b> metabolite catalyzed from <b>codeine</b> via the cytochrome P450 2D6 (<strong>CYP2D6</strong>) enzyme.
+CYP2D6	drug	opioid	21241245	In mothers who have greater than two functional copies of the <strong>CYP2D6</strong> gene (<strong>CYP2D6</strong> ultrarapid metabolism phenotype; UM) a substantially higher proportion of <b>morphine</b> is produced.
+CYP2D6	drug	opioid	21241245	To address the immediate issue of <strong>CYP2D6</strong> UM inheritance in family members of a breastfed infant who succumbed to fatal <b>opioid</b> intoxication and whose <b>codeine</b> prescribed mother was a <strong>CYP2D6</strong> UM, we constructed a pedigree.
+CYP2D6	addiction	intoxication	21241245	To address the immediate issue of <strong>CYP2D6</strong> UM inheritance in family members of a breastfed infant who succumbed to fatal opioid <b>intoxication</b> and whose codeine prescribed mother was a <strong>CYP2D6</strong> UM, we constructed a pedigree.
+CYP2D6	drug	opioid	21209234	The aim of this study was to evaluate the plasma dispositions of <b>oxycodone</b> and its demethylates and dose escalation based on genetic polymorphisms of <strong>CYP2D6</strong>, CYP3A5, ABCB1, and OPRM1 in cancer patients receiving <b>oxycodone</b>.
+CYP2D6	addiction	addiction	21209234	The aim of this study was to evaluate the plasma dispositions of oxycodone and its demethylates and dose <b>escalation</b> based on genetic polymorphisms of <strong>CYP2D6</strong>, CYP3A5, ABCB1, and OPRM1 in cancer patients receiving oxycodone.
+CYP2D6	drug	opioid	21209234	Oxymorphone C(12) and its ratio to <b>oxycodone</b> C(12) were significantly higher in <strong>CYP2D6</strong> extensive metabolizers than in intermediate metabolizers but did not affect dose escalation.
+CYP2D6	addiction	addiction	21209234	Oxymorphone C(12) and its ratio to oxycodone C(12) were significantly higher in <strong>CYP2D6</strong> extensive metabolizers than in intermediate metabolizers but did not affect dose <b>escalation</b>.
+CYP2D6	addiction	intoxication	20942780	In addition, the pharmacokinetic and pharmacodynamic drug drug interactions between harmaline and 5 MeO DMT, potential involvement of <strong>CYP2D6</strong> pharmacogenetics, and risks of 5 MeO DMT <b>intoxication</b> are discussed.
+CYP2D6	drug	amphetamine	20727252	One source of differential vulnerability could come from genotypic variability in metabolic clearance of <b>meth</b>, dependent on the activity of cytochrome P450 2D6 (<strong>CYP2D6</strong>).
+CYP2D6	drug	amphetamine	20727252	We compared neuropsychological performance in 52 individuals with a history of <b>meth</b> dependence according with their <strong>CYP2D6</strong> phenotype.
+CYP2D6	addiction	dependence	20727252	We compared neuropsychological performance in 52 individuals with a history of meth <b>dependence</b> according with their <strong>CYP2D6</strong> phenotype.
+CYP2D6	drug	opioid	20540693	The impact of <strong>CYP2D6</strong> activity on DHC analgesia was discussed and a proposal of calculation equianalgesic doses of DHC to other <b>opioids</b> was put forward.
+CYP2D6	drug	opioid	20394193	It was shown that molecular genetic studies at postmortem <b>morphine</b> concentrations of up to 0.5 mg/l as a rule identify mutant alleles (<strong>CYP2D6</strong>*3*4; CYP2C19*2*3).
+CYP2D6	drug	opioid	20394193	Mutant alleles <strong>CYP2D6</strong>* and CYP2C19* are most frequently detected at postmortem blood <b>morphine</b> levels ranging from 1 to 4 mg/I.
+CYP2D6	drug	opioid	20394193	The remaining subjects lacking mutations in <strong>CYP2D6</strong> and CYP2C19 genes are considered to be ordinary metabolizers dying at toxic concentrations of <b>morphine</b> in their blood (from 1 to 4 mg/I); such cases need no genetic studies to be carried out to identify <strong>CYP2D6</strong> and CYP2C19 polymorphism.
+CYP2D6	drug	opioid	20119466	<strong>CYP2D6</strong> related prodrug activation of <b>codeine</b> to <b>morphine</b>), alter pharmacodynamic mechanisms (e.g.
+CYP2D6	drug	opioid	19902987	Genetically caused inactivity of <strong>CYP2D6</strong> renders <b>codeine</b> ineffective owing to lack of <b>morphine</b> formation, decreases the efficacy of <b>tramadol</b> owing to reduced formation of the active O desmethyl <b>tramadol</b> and reduces the clearance of <b>methadone</b>.
+CYP2D6	addiction	relapse	19902987	Tamoxifen treated cancer patients carrying <strong>CYP2D6</strong>*4, *5, *10, or *41 associated with significantly decreased formation of antiestrogenic metabolites had significantly more recurrences of breast cancer and shorter <b>relapse</b> free periods.
+CYP2D6	drug	opioid	19615406	Other polymorphisms alter pharmacokinetic mechanisms controlling the local availability of active analgesic molecules at their effector sites (e.g., decreased <strong>CYP2D6</strong> related prodrug activation of <b>codeine</b> to <b>morphine</b>).
+CYP2D6	drug	amphetamine	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, <strong>CYP2D6</strong>, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with <b>METH</b> psychosis.
+CYP2D6	addiction	dependence	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, <strong>CYP2D6</strong>, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.
+CYP2D6	drug	opioid	19133059	Contribution of the activities of CYP3A, <strong>CYP2D6</strong>, CYP1A2 and other potential covariates to the disposition of <b>methadone</b> in patients undergoing <b>methadone</b> maintenance treatment.
+CYP2D6	drug	benzodiazepine	19133059	<strong>CYP2D6</strong> activity [3 h plasma metabolic ratio of dextromethorphan (DEX) to dextrorphan (DOR)] was determined in 44 patients (29 male; 24 55 years), CYP1A2 activity (salivary caffeine elimination half life) in 44 patients (21 male; 24 55 years) and CYP3A activity (oral clearance of <b>midazolam</b>) in 49 patients (33 male; 23 55 years).
+CYP2D6	drug	opioid	19133059	Neither <strong>CYP2D6</strong> nor CYP1A2 activity was related to <b>methadone</b> disposition.
+CYP2D6	drug	opioid	19059064	The value of <strong>CYP2D6</strong> and OPRM1 pharmacogenetic testing for <b>opioid</b> therapy.
+CYP2D6	drug	opioid	19059064	This article focuses on <b>opioid</b> use for pain management, their risks of toxicity and addiction, adverse reactions, undertreatment for fear of addiction, and integration of novel diagnostics, such as the pharmacogenetic biomarkers <strong>CYP2D6</strong> and OPRM1 as holding promise for assessing a patient's risk of adverse events or likelihood of efficacy.
+CYP2D6	addiction	addiction	19059064	This article focuses on opioid use for pain management, their risks of toxicity and <b>addiction</b>, adverse reactions, undertreatment for fear of <b>addiction</b>, and integration of novel diagnostics, such as the pharmacogenetic biomarkers <strong>CYP2D6</strong> and OPRM1 as holding promise for assessing a patient's risk of adverse events or likelihood of efficacy.
+CYP2D6	drug	opioid	18971888	<strong>CYP2D6</strong>: a key enzyme in <b>morphine</b> synthesis in animals.
+CYP2D6	drug	opioid	18971888	Among the many enzymes involved in this process, <strong>CYP2D6</strong> is of particular importance because of its role in multiple steps of <b>morphine</b> precursor metabolism, as well as its distribution in a variety of tissues, such as neuronal and immune.
+CYP2D6	drug	opioid	18713907	Respiratory depression with <b>tramadol</b> in a patient with renal impairment and <strong>CYP2D6</strong> gene duplication.
+CYP2D6	drug	opioid	18713907	Analysis of the patient's genotype revealed a <strong>CYP2D6</strong> gene duplication resulting in ultra rapid metabolism of <b>tramadol</b> to its active metabolite (+)O desmethyltramadol.
+CYP2D6	drug	opioid	18713907	This genetic <strong>CYP2D6</strong> variant is particularly common in specific ethnic populations and should be a future diagnostic target whenever administration of <b>tramadol</b> or <b>codeine</b> is anticipated, as both drugs are subject to a comparable <strong>CYP2D6</strong> dependent metabolism.
+CYP2D6	drug	opioid	18584566	Caucasians with various forms of the <strong>CYP2D6</strong> enzyme results in a 'poor metabolizer' phenotype and appear to be protected from developing <b>opioid</b> dependence.
+CYP2D6	addiction	dependence	18584566	Caucasians with various forms of the <strong>CYP2D6</strong> enzyme results in a 'poor metabolizer' phenotype and appear to be protected from developing opioid <b>dependence</b>.
+CYP2D6	drug	opioid	18584566	These patients can do well using <b>buprenorphine</b> because it is not significantly metabolized by <strong>CYP2D6</strong>.
+CYP2D6	addiction	intoxication	18359183	Life threatening dextromethorphan <b>intoxication</b> associated with interaction with amitriptyline in a poor <strong>CYP2D6</strong> metabolizer: a single case re exposure study.
+CYP2D6	drug	opioid	18328640	Since quinidine (QND) affects <strong>CYP2D6</strong> mediated metabolism and P glycoprotein governed transport, we sought to determine whether co treatment with QND would affect brain levels of DXM and DXT as well as the effect of these compounds on <b>opioid</b> withdrawal syndrome in mice.
+CYP2D6	addiction	withdrawal	18328640	Since quinidine (QND) affects <strong>CYP2D6</strong> mediated metabolism and P glycoprotein governed transport, we sought to determine whether co treatment with QND would affect brain levels of DXM and DXT as well as the effect of these compounds on opioid <b>withdrawal</b> syndrome in mice.
+CYP2D6	drug	amphetamine	18280655	Reduced <strong>CYP2D6</strong> activity is a negative risk factor for <b>methamphetamine</b> dependence.
+CYP2D6	addiction	dependence	18280655	Reduced <strong>CYP2D6</strong> activity is a negative risk factor for methamphetamine <b>dependence</b>.
+CYP2D6	drug	amphetamine	18280655	Because <b>methamphetamine</b> (<b>METH</b>) is metabolized by <strong>CYP2D6</strong> at the first step of hydroxylation and demethylation, it is possible that functional variants of <strong>CYP2D6</strong> alter susceptibility to <b>methamphetamine</b> induced dependence.
+CYP2D6	addiction	dependence	18280655	Because methamphetamine (METH) is metabolized by <strong>CYP2D6</strong> at the first step of hydroxylation and demethylation, it is possible that functional variants of <strong>CYP2D6</strong> alter susceptibility to methamphetamine induced <b>dependence</b>.
+CYP2D6	drug	amphetamine	18280655	We genotyped <strong>CYP2D6</strong>*1, *4, *5, *10, and *14 for 202 patients with <b>METH</b> dependence and 337 controls in a Japanese population and found a significant association of the <strong>CYP2D6</strong> gene with <b>METH</b> dependence (p=0.0299).
+CYP2D6	addiction	dependence	18280655	We genotyped <strong>CYP2D6</strong>*1, *4, *5, *10, and *14 for 202 patients with METH <b>dependence</b> and 337 controls in a Japanese population and found a significant association of the <strong>CYP2D6</strong> gene with METH <b>dependence</b> (p=0.0299).
+CYP2D6	drug	amphetamine	18280655	There was no poor metabolizer among our Japanese subjects, and intermediate metabolizers of <strong>CYP2D6</strong> were significantly fewer in <b>methamphetamine</b> dependent subjects than in controls (p=0.0212), with an odds ratio of 0.62 (95% confidence interval: 0.51 0.76).
+CYP2D6	drug	amphetamine	18280655	The present study demonstrated that reduced <strong>CYP2D6</strong> activity was a negative risk factor for <b>methamphetamine</b> dependence.
+CYP2D6	addiction	dependence	18280655	The present study demonstrated that reduced <strong>CYP2D6</strong> activity was a negative risk factor for methamphetamine <b>dependence</b>.
+CYP2D6	drug	amphetamine	17389081	Determination of <b>amphetamine</b>, <b>methamphetamine</b>, and hydroxyamphetamine derivatives in urine by gas chromatography mass spectrometry and its relation to <strong>CYP2D6</strong> phenotype of drug users.
+CYP2D6	drug	amphetamine	17389081	<b>Amphetamine</b>, a <strong>CYP2D6</strong> substrate, is widely used by truck drivers, and the extent to which different people metabolize the drug has only been determined in an isolated or reduced number of samples.
+CYP2D6	drug	amphetamine	17389081	The main improvements are the use of liquid liquid extraction, the trapping of the amphetamines as their hydrochloride salt, as a solution to the volatility of these analytes, and its application to assess the <strong>CYP2D6</strong> metabolic phenotype of <b>amphetamine</b> users, which is innovative.
+CYP2D6	drug	nicotine	17372541	Some variants of the cytochrome P450 seem to be more frequent among dependent <b>smokers</b> than controls or ever <b>smokers</b> (CYP2A6) and heavier <b>smokers</b> (<strong>CYP2D6</strong>).
+CYP2D6	drug	opioid	17339873	The polymorphic <strong>CYP2D6</strong> regulates the O demethylation of <b>codeine</b> and other weak <b>opioids</b> to more potent metabolites with poor metabolizers having reduced antinociception in some cases.
+CYP2D6	drug	psychedelics	16714321	Implications of mechanism based inhibition of <strong>CYP2D6</strong> for the pharmacokinetics and toxicity of <b>MDMA</b>.
+CYP2D6	drug	psychedelics	16714321	The aim of this study was to model the in vivo kinetic consequences of mechanism based inhibition (MBI) of <strong>CYP2D6</strong> by 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>, <b>ecstasy</b>).
+CYP2D6	drug	psychedelics	16714321	A model with physiologically based components of drug metabolism was developed, taking account of change in the hepatic content of active <strong>CYP2D6</strong> due to MBI by <b>MDMA</b>.
+CYP2D6	drug	psychedelics	16714321	The analysis suggested that a typical recreational <b>MDMA</b> dose could inactivate most hepatic <strong>CYP2D6</strong> within an hour, and the return to a basal level of <strong>CYP2D6</strong> could take at least 10 days.
+CYP2D6	drug	psychedelics	16714321	Thus, the genetic polymorphism of <strong>CYP2D6</strong> and coadministration of <strong>CYP2D6</strong> inhibitors may have less impact on <b>MDMA</b> pharmacokinetics and the risk of acute toxicity than previously thought.
+CYP2D6	drug	psychedelics	16714321	This is consistent with clinical observations that indicate no obvious link between inherited <strong>CYP2D6</strong> deficiency and acute <b>MDMA</b> intoxication.
+CYP2D6	addiction	intoxication	16714321	This is consistent with clinical observations that indicate no obvious link between inherited <strong>CYP2D6</strong> deficiency and acute MDMA <b>intoxication</b>.
+CYP2D6	drug	amphetamine	16250257	It is metabolized in the organism with a reaction that is catalyzed by cytochrome P450, mainly by the <strong>CYP2D</strong> and CYP3A subfamily, 4 hydroxyamphetamine and <b>amphetamine</b> being dominant metabolites.
+CYP2D6	drug	opioid	15625333	<b>Codeine</b> intoxication associated with ultrarapid <strong>CYP2D6</strong> metabolism.
+CYP2D6	addiction	intoxication	15625333	Codeine <b>intoxication</b> associated with ultrarapid <strong>CYP2D6</strong> metabolism.
+CYP2D6	drug	opioid	15625333	<b>Codeine</b> is bioactivated by <strong>CYP2D6</strong> into <b>morphine</b>, which then undergoes further glucuronidation.
+CYP2D6	drug	opioid	15625333	<strong>CYP2D6</strong> genotyping showed that the patient had three or more functional alleles, a finding consistent with ultrarapid metabolism of <b>codeine</b>.
+CYP2D6	drug	opioid	15501692	<strong>CYP2D6</strong> and probably CYP1A2 are also involved in <b>methadone</b> metabolism.
+CYP2D6	drug	psychedelics	14673568	<b>MDMA</b> metabolism is regulated by the levels of <strong>CYP2D6</strong> and COMT (both exhibit some genetic polymorphism), and range of activity of these enzymes may account for some inter individual differences in terms of toxic responses to the drug.
+CYP2D6	drug	opioid	14624403	A rapid and simple <strong>CYP2D6</strong> genotyping assay  case study with the analgetic <b>tramadol</b>.
+CYP2D6	drug	opioid	14624403	We therefore developed a robust assay that detects common <strong>CYP2D6</strong> alleles within 60 minutes of blood withdrawal and links carriers of the variant <strong>CYP2D6</strong>*3 and *4 alleles to the pharmacokinetics of <b>tramadol</b>.
+CYP2D6	addiction	withdrawal	14624403	We therefore developed a robust assay that detects common <strong>CYP2D6</strong> alleles within 60 minutes of blood <b>withdrawal</b> and links carriers of the variant <strong>CYP2D6</strong>*3 and *4 alleles to the pharmacokinetics of tramadol.
+CYP2D6	addiction	withdrawal	14624403	This new genotyping assay employs fluorescence resonance energy transfer (FRET) analysis, which permits parallel identification of the <strong>CYP2D6</strong>*3 and <strong>CYP2D6</strong>*4 alleles within 60 minutes of blood <b>withdrawal</b>.
+CYP2D6	drug	opioid	14624403	We determined the genotypes of 100 healthy unrelated individuals and studied the pharmacokinetics of <b>tramadol</b> in 24 <strong>CYP2D6</strong> genotyped healthy subjects.
+CYP2D6	drug	opioid	14624403	We observed a statistically significant correlation between plasma <b>tramadol</b> AUC and production of the O desmethyl metabolite in <strong>CYP2D6</strong> genotyped healthy volunteers.
+CYP2D6	drug	opioid	12560936	Unlike <b>morphine</b>, <b>oxycodone</b> is metabolized by the cytochrome isoenzyme <strong>CYP2D6</strong>, which is severely impaired by liver dysfunction.
+CYP2D6	drug	opioid	12405865	Inhibitors of CYP3A4, such as fluconazole, and of <strong>CYP2D6</strong>, such as paroxetine, increase <b>methadone</b> blood concentrations.
+CYP2D6	drug	opioid	12006904	<b>Codeine</b> is O demethylated by cytochrome P450 2D6 (<strong>CYP2D6</strong>) to form the more potent drug <b>morphine</b>, accounting for much of <b>codeine</b>'s analgesic and dependence producing properties.
+CYP2D6	addiction	dependence	12006904	Codeine is O demethylated by cytochrome P450 2D6 (<strong>CYP2D6</strong>) to form the more potent drug morphine, accounting for much of codeine's analgesic and <b>dependence</b> producing properties.
+CYP2D6	drug	opioid	12006904	Because <b>morphine</b> production can be decreased by inhibition of <strong>CYP2D6</strong>, the authors hypothesized that <strong>CYP2D6</strong> inhibition could be used to treat <b>codeine</b> dependence.
+CYP2D6	addiction	dependence	12006904	Because morphine production can be decreased by inhibition of <strong>CYP2D6</strong>, the authors hypothesized that <strong>CYP2D6</strong> inhibition could be used to treat codeine <b>dependence</b>.
+CYP2D6	drug	opioid	12006904	In this small sample, <strong>CYP2D6</strong> inhibitors did not appear to have a useful role in the treatment of <b>codeine</b> dependence.
+CYP2D6	addiction	dependence	12006904	In this small sample, <strong>CYP2D6</strong> inhibitors did not appear to have a useful role in the treatment of codeine <b>dependence</b>.
+CYP2D6	drug	opioid	11825096	Lack of <b>morphine</b> formation from <b>codeine</b> as a result of <strong>CYP2D6</strong> inhibition by quinidine results in an almost complete loss of the analgesic effects of <b>codeine</b>.
+CYP2D6	drug	amphetamine	11505218	The <strong>CYP2D6</strong> substrates amitriptyline, and (+) and ( ) <b>methamphetamine</b> (MAMP) are both p hydroxylated and N demethylated (NDM).
+CYP2D6	drug	psychedelics	11505218	It was apparent that (+) and ( ) MAMP NDM and <b>MDMA</b> demethylenation were most significantly different in <strong>CYP2D6</strong>.10.
+CYP2D6	drug	psychedelics	11505218	Using DEX as the substrate, the ratios of Ki(*10)/Ki(*1) for inhibitors were: budipine (1.3), sparteine (1.6), debrisoquine (8.1), fluoxetine (16), norfluoxetine (30), paroxetine (14), <b>MDMA</b> (21) and MMDA 2 (7.1), indicating that <strong>CYP2D6</strong>.10 shows drug specific altered susceptibility to inhibition.
+CYP2D6	addiction	dependence	11505218	Taken together, these data suggest that <strong>CYP2D6</strong>*10/*10 individuals may be expected to require different drug doses; and show altered susceptibility to toxicity, interaction risk and, in the case of the amphetamines, drug <b>dependence</b> and toxicity compared to <strong>CYP2D6</strong>*1/*1 individuals.
+CYP2D6	drug	psychedelics	11085338	The majority of <b>ibogaine</b> biotransformation proceeds via <strong>CYP2D6</strong>, including the O demethylation of <b>ibogaine</b> to 12 hydroxyibogamine (noribogaine).
+CYP2D6	drug	benzodiazepine	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes <strong>CYP2D6</strong> (codeine, amphetamines, dextromethorphan), CYP2A6 (nicotine) and CYP2C19 (<b>flunitrazepam</b>).
+CYP2D6	drug	nicotine	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes <strong>CYP2D6</strong> (codeine, amphetamines, dextromethorphan), CYP2A6 (<b>nicotine</b>) and CYP2C19 (flunitrazepam).
+CYP2D6	drug	opioid	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes <strong>CYP2D6</strong> (<b>codeine</b>, amphetamines, dextromethorphan), CYP2A6 (nicotine) and CYP2C19 (flunitrazepam).
+CYP2D6	drug	opioid	10911933	In addition, we inhibited <strong>CYP2D6</strong> and decreased individuals' risk of dependence experimentally (<b>codeine</b>, dextromethorphan) and treated <b>codeine</b> dependence.
+CYP2D6	addiction	dependence	10911933	In addition, we inhibited <strong>CYP2D6</strong> and decreased individuals' risk of <b>dependence</b> experimentally (codeine, dextromethorphan) and treated codeine <b>dependence</b>.
+CYP2D6	drug	nicotine	10911933	In epidemiologic studies <strong>CYP2D6</strong> and CYP2A6 null mutations protect individuals from becoming codeine and <b>tobacco</b> dependent, respectively.
+CYP2D6	drug	opioid	10911933	In epidemiologic studies <strong>CYP2D6</strong> and CYP2A6 null mutations protect individuals from becoming <b>codeine</b> and tobacco dependent, respectively.
+CYP2D6	drug	opioid	10653207	<b>Codeine</b> is a substrate of <strong>CYP2D6</strong>, a genetically polymorphic P450 enzyme, and is metabolized to the more potent drug <b>morphine</b>.
+CYP2D6	drug	opioid	10653207	<strong>CYP2D6</strong> activity can be inhibited by fluoxetine, and the inhibition of <b>morphine</b> formation may help individuals reduce their use of <b>codeine</b>.
+CYP2D6	drug	psychedelics	9698290	In this report, evidence is presented that the O demethylation of <b>ibogaine</b> observed in human hepatic microsomes is catalyzed primarily by the polymorphically expressed cytochrome P 4502D6 (<strong>CYP2D6</strong>).
+CYP2D6	drug	psychedelics	9698290	In hepatic microsomes from a panel of human donors, the low KMapp <b>ibogaine</b> O demethylase activity correlated with <strong>CYP2D6</strong> catalyzed bufuralol 1' hydroxylase activity but not with other P450 isoform specific activities.
+CYP2D6	drug	psychedelics	9698290	Quinidine, a <strong>CYP2D6</strong> specific inhibitor, inhibited <b>ibogaine</b> O demethylase (IC50 = 0.2 microM), whereas other P450 isoform specific inhibitors did not inhibit this activity.
+CYP2D6	drug	psychedelics	9698290	Thus, it is concluded that <b>ibogaine</b> O demethylase is catalyzed by <strong>CYP2D6</strong> and that this isoform is the predominant enzyme of <b>ibogaine</b> O demethylation in humans.
+CYP2D6	addiction	dependence	9352573	Genetically deficient <strong>CYP2D6</strong> metabolism provides protection against oral opiate <b>dependence</b>.
+CYP2D6	drug	opioid	9352573	<b>codeine</b>, <b>oxycodone</b>, and <b>hydrocodone</b>) are metabolized by cytochrome <strong>CYP2D6</strong> to metabolites of increased activity (e.g.
+CYP2D6	addiction	dependence	9352573	We tested whether the failure to activate oral opiates was a protection factor in opiate <b>dependence</b> by genotyping (<strong>CYP2D6</strong>*3 and <strong>CYP2D6</strong>*4 defective mutant alleles) caucasians who met or didn't meet DSM criteria for oral opiate <b>dependence</b>.
+CYP2D6	addiction	dependence	9352573	This under representation of poor metabolizers (Fisher's exact test, p < or = 0.05) in people dependent on oral opiates suggests that the <strong>CYP2D6</strong> defective genotype is a pharmacogenetic protection factor for oral opiate <b>dependence</b> (estimated odds ratio > 7).
+CYP2D6	drug	amphetamine	9311621	Oxidation of <b>methamphetamine</b> and methylenedioxymethamphetamine by <strong>CYP2D6</strong>.
+CYP2D6	drug	psychedelics	9311621	Oxidation of methamphetamine and <b>methylenedioxymethamphetamine</b> by <strong>CYP2D6</strong>.
+CYP2D6	drug	psychedelics	9311621	The results of studies with human liver microsomes including those from a genetically poor metabolizer with respect to <strong>CYP2D6</strong>, showing correlation between MeAmp and metoprolol hydroxylation and <b>MDMA</b> demethylenation, were consistent with a major involvement of <strong>CYP2D6</strong> in the aromatic 4 hydroxylation of MeAmp.
+CYP2D6	drug	psychedelics	9311621	In contrast to MeAmp, <b>MDMA</b> was not N demethylated by <strong>CYP2D6</strong>.
+CYP2D6	addiction	addiction	9311621	Since <strong>CYP2D6</strong> participates in the major steps of MeAmp metabolism, pharmacokinetic interactions are likely with other drug substrates proposed for the treatment of MeAmp <b>addiction</b>.
+CYP2D6	drug	amphetamine	9833017	In rats, <b>amphetamine</b> (AMP) conversion to 4 OH AMP is metabolized by CYP2D1, the rat equivalent of the human enzyme <strong>CYP2D6</strong>.
+CYP2D6	drug	opioid	9067326	Humans that lack cytochrome P450 2D6 (<strong>CYP2D6</strong>) activity may have an altered risk of drug dependence or abuse because this enzyme is important in the metabolism of some drugs of abuse, including <b>hydrocodone</b>.
+CYP2D6	addiction	dependence	9067326	Humans that lack cytochrome P450 2D6 (<strong>CYP2D6</strong>) activity may have an altered risk of drug <b>dependence</b> or abuse because this enzyme is important in the metabolism of some drugs of abuse, including hydrocodone.
+CYP2D6	drug	opioid	9067326	In rats, <b>hydrocodone</b> conversion to <b>hydromorphone</b> is catalyzed by CYP2D1, the rat homolog of the human <strong>CYP2D6</strong>.
+CYP2D6	drug	opioid	9067326	Because inhibition of CYP2D1 in this rat strain is proposed to be a useful animal counterpart for studying the impact of <strong>CYP2D6</strong> polymorphism in humans, these data suggest that differences in <strong>CYP2D6</strong> phenotype will have limited influence on the drug response to <b>hydrocodone</b> after nonoral administration.
+CYP2D6	drug	opioid	9190321	The rate of production of this M1 derivative (O demethyl <b>tramadol</b>), is influenced by a polymorphic isoenzyme of the debrisoquine type, cytochrome P450 2D6 (<strong>CYP2D6</strong>).
+CYP2D6	drug	opioid	9118585	<b>Codeine</b> is O demethylated to its active metabolite <b>morphine</b> by the genetically polymorphic <strong>CYP2D6</strong> isozyme.
+CYP2D6	drug	opioid	9118585	Conversely, those with a very rapid <strong>CYP2D6</strong> catalytic activity may have an increased potential for <b>codeine</b> abuse and dependence.
+CYP2D6	addiction	dependence	9118585	Conversely, those with a very rapid <strong>CYP2D6</strong> catalytic activity may have an increased potential for codeine abuse and <b>dependence</b>.
+CYP2D6	drug	opioid	8845855	Lack of influence of <b>codeine</b> on experimental pain in PM as well as in EM treated with the <strong>CYP2D6</strong> blocker quinidine, who are both practically unable to convert <b>codeine</b> to <b>morphine</b>, has supported an old hypothesis that <b>codeine</b> acts through metabolically formed <b>morphine</b>.
+CYP2D6	drug	opioid	8845855	Such a local <b>morphine</b> formation from <b>codeine</b>, which supposedly is also catalysed by <strong>CYP2D6</strong>, could explain why the hypoalgesic effect of <b>codeine</b> stems from <b>morphine</b> despite relatively low plasma levels of <b>morphine</b> after standard hypoalgesic doses of <b>codeine</b>.
+CYP2D6	drug	opioid	8845855	Dependence of <b>codeine</b> hypoalgesia on <b>morphine</b> formation via <strong>CYP2D6</strong> makes this effect liable to interaction with drugs that are inhibitors of <strong>CYP2D6</strong>.
+CYP2D6	addiction	dependence	8845855	<b>Dependence</b> of codeine hypoalgesia on morphine formation via <strong>CYP2D6</strong> makes this effect liable to interaction with drugs that are inhibitors of <strong>CYP2D6</strong>.
+CYP2D6	drug	opioid	8845855	Less potent inhibitors, such as tricyclic antidepressants, will probably also reduce the pain relieving effect of <b>codeine</b>, since <b>codeine</b> has a low affinity for <strong>CYP2D6</strong>.
+CYP2D6	drug	opioid	8845855	Biosynthesis of <b>morphine</b> in humans may also include steps catalyse by <strong>CYP2D6</strong>.
+NEUROTENSIN	drug	alcohol	32623746	Heightened Exploratory Behavior Following Chronic Excessive <b>Ethanol</b> Drinking: Mediation by <strong>Neurotensin</strong> Receptor Type 2 in the Anterior Paraventricular Thalamus.
+NEUROTENSIN	drug	alcohol	32623746	We recently demonstrated, in rats, that <strong>neurotensin</strong> (NTS) in the paraventricular thalamus (PVT) regulates excessive <b>ethanol</b> drinking.
+NEUROTENSIN	addiction	addiction	32470395	Small molecule <strong>neurotensin</strong> receptor 1 (NTSR1) agonists have been pursued for more than 40 years as potential therapeutics for psychiatric disorders, including drug <b>addiction</b>.
+NEUROTENSIN	addiction	reward	32057800	<strong>Neurotensin</strong> in <b>reward</b> processes.
+NEUROTENSIN	addiction	reward	32057800	This review provides a general survey of the role of <strong>neurotensin</strong> with a focus on modalities that we believe to be particularly relevant to the study of <b>reward</b>.
+NEUROTENSIN	drug	alcohol	31744862	Manipulations of Central Amygdala <strong>Neurotensin</strong> Neurons Alter the Consumption of <b>Ethanol</b> and Sweet Fluids in Mice.
+NEUROTENSIN	drug	alcohol	31744862	Here we show that <strong>neurotensin</strong> neurons in the central nucleus of the amygdala of male mice are activated by in vivo <b>ethanol</b> consumption and that genetic ablation of these neurons decreases <b>ethanol</b> consumption and preference in non <b>ethanol</b> dependent animals.
+NEUROTENSIN	addiction	aversion	31744862	We found that the most robust projection of the central amygdala <strong>neurotensin</strong> neurons was to the parabrachial nucleus, a brain region known to be important in feeding behaviors, conditioned taste <b>aversion</b>, and alarm.
+NEUROTENSIN	drug	alcohol	31744862	Here we show that ablation of a population of <strong>neurotensin</strong> expressing neurons in the central amygdala decreases intake of and preference for <b>ethanol</b> in non dependent animals, whereas the projection of these neurons to the parabrachial nucleus promotes consumption of <b>ethanol</b> as well as other palatable fluids.
+NEUROTENSIN	drug	amphetamine	31742874	<strong>Neurotensin</strong> receptor 1 deletion decreases <b>methamphetamine</b> self administration and the associated reduction in dopamine cell firing.
+NEUROTENSIN	drug	amphetamine	31742874	We previously reported that a non selective pharmacological blockade of <strong>neurotensin</strong> receptors in the ventral tegmental area (VTA) decreases <b>methamphetamine</b> (<b>METH</b>) self administration in mice.
+NEUROTENSIN	drug	amphetamine	31742874	Here, we explored the consequences of genetic deletion of <strong>neurotensin</strong> receptor 1 (NtsR1) on <b>METH</b> self administration and VTA dopamine neuron firing activity.
+NEUROTENSIN	drug	cannabinoid	30342013	They include peptides targeting Ca2+, Na+ and K+ voltage gated ion channels, the neuronal nicotinic receptors (nAChR), transient receptor potential channels (TRP), and different non opioid G protein coupled receptors (GPCRs), like the calcitonin gen related peptide (CGRP), <b>cannabinoid</b>, bradykinin and <strong>neurotensin</strong> receptors, among others.
+NEUROTENSIN	drug	opioid	30342013	They include peptides targeting Ca2+, Na+ and K+ voltage gated ion channels, the neuronal nicotinic receptors (nAChR), transient receptor potential channels (TRP), and different non <b>opioid</b> G protein coupled receptors (GPCRs), like the calcitonin gen related peptide (CGRP), cannabinoid, bradykinin and <strong>neurotensin</strong> receptors, among others.
+NEUROTENSIN	drug	amphetamine	29272412	Antagonism of <strong>Neurotensin</strong> Receptors in the Ventral Tegmental Area Decreases <b>Methamphetamine</b> Self Administration and <b>Methamphetamine</b> Seeking in Mice.
+NEUROTENSIN	addiction	relapse	29272412	Antagonism of <strong>Neurotensin</strong> Receptors in the Ventral Tegmental Area Decreases Methamphetamine Self Administration and Methamphetamine <b>Seeking</b> in Mice.
+NEUROTENSIN	drug	amphetamine	29272412	<b>Methamphetamine</b> self administration increases <strong>neurotensin</strong> levels in the ventral tegmental area, but the consequences for self administration behavior have not been described.
+NEUROTENSIN	drug	amphetamine	29272412	Here we test the hypothesis that antagonizing <strong>neurotensin</strong> receptors in the ventral tegmental area attenuates the acquisition of <b>methamphetamine</b> self administration and <b>methamphetamine</b> intake.
+NEUROTENSIN	drug	amphetamine	29272412	Mice receiving microinfusions of the <strong>neurotensin</strong> NTS1/NTS2 receptor antagonist SR142948A in the ventral tegmental area (10 ng/side) prior to the first 5 days of <b>methamphetamine</b> self administration required more sessions to reach acquisition criteria.
+NEUROTENSIN	drug	amphetamine	29272412	Mice receiving microinfusions of the <strong>neurotensin</strong> <strong>NTS1</strong>/NTS2 receptor antagonist SR142948A in the ventral tegmental area (10 ng/side) prior to the first 5 days of <b>methamphetamine</b> self administration required more sessions to reach acquisition criteria.
+NEUROTENSIN	drug	amphetamine	29272412	Our results suggest that <strong>neurotensin</strong> input in the ventral tegmental area during initial <b>methamphetamine</b> exposure contributes to the acquisition of <b>methamphetamine</b> self administration and modulates later intake and <b>methamphetamine</b> seeking behavior in mice.
+NEUROTENSIN	addiction	relapse	29272412	Our results suggest that <strong>neurotensin</strong> input in the ventral tegmental area during initial methamphetamine exposure contributes to the acquisition of methamphetamine self administration and modulates later intake and methamphetamine <b>seeking</b> behavior in mice.
+NEUROTENSIN	drug	amphetamine	29272412	Furthermore, our results highlight the role of endogenous <strong>neurotensin</strong> in the ventral tegmental area in the reinforcing efficacy of <b>methamphetamine</b>, independent of its psychomotor effects.
+NEUROTENSIN	addiction	reward	29272412	Furthermore, our results highlight the role of endogenous <strong>neurotensin</strong> in the ventral tegmental area in the <b>reinforcing</b> efficacy of methamphetamine, independent of its psychomotor effects.
+NEUROTENSIN	drug	cannabinoid	29120924	Recent studies provide evidence for peptide YY3 36, glucagon like peptide 1, ghrelin, <strong>neurotensin</strong> and <b>oleoylethanolamide</b> as mediators of postoperative eating behaviour changes.
+NEUROTENSIN	drug	amphetamine	28729827	It is also home to a heterogeneous population of neurons that express and co express multiple neuropeptides including hypocretin (Hcrt), melanin concentrating hormone (MCH), cocaine  and <b>amphetamine</b> regulated transcript (CART) and <strong>neurotensin</strong> (NT).
+NEUROTENSIN	drug	cocaine	28729827	It is also home to a heterogeneous population of neurons that express and co express multiple neuropeptides including hypocretin (Hcrt), melanin concentrating hormone (MCH), <b>cocaine</b>  and amphetamine regulated transcript (CART) and <strong>neurotensin</strong> (NT).
+NEUROTENSIN	drug	amphetamine	28686721	Systemic PD149163, a <strong>neurotensin</strong> receptor 1 agonist, decreases <b>methamphetamine</b> self administration in DBA/2J mice without causing excessive sedation.
+NEUROTENSIN	drug	amphetamine	28686721	<b>METH</b> activates the central dopaminergic "reward" circuitry, and with repeated use increases levels of the neuromodulatory peptide <strong>neurotensin</strong> in the nucleus accumbens and ventral tegmental area.
+NEUROTENSIN	addiction	reward	28686721	METH activates the central dopaminergic "<b>reward</b>" circuitry, and with repeated use increases levels of the neuromodulatory peptide <strong>neurotensin</strong> in the nucleus accumbens and ventral tegmental area.
+NEUROTENSIN	drug	amphetamine	28686721	Previous studies in rats suggest that <strong>neurotensin</strong> agonism decreases <b>METH</b> self administration, but these studies did not examine the effect of <strong>neurotensin</strong> agonism on the pattern of self administration or open field locomotion.
+NEUROTENSIN	drug	amphetamine	28686721	In our studies, we established intravenous <b>METH</b> self administration in male, DBA/2J mice (fixed ratio 3, 2 hr sessions) and examined the effect of pretreatment with the <strong>NTS1</strong> receptor agonist PD149163 on <b>METH</b> self administration behavior.
+NEUROTENSIN	drug	amphetamine	28686721	These results suggest that a systemically delivered <strong>NTS1</strong> receptor agonist decreases <b>METH</b> self administration in mice.
+NEUROTENSIN	drug	amphetamine	28522313	We hypothesized that increasing <strong>neurotensin</strong> activity in the NAc attenuates the expression of antipsychotic induced dopamine supersensitivity, which is indicated by a potentiated psychomotor response to <b>amphetamine</b>.
+NEUROTENSIN	drug	amphetamine	28522313	Three to 5 days later, we injected <strong>neurotensin</strong> into the NAc and measured <b>amphetamine</b> induced locomotion.
+NEUROTENSIN	drug	amphetamine	28522313	Compared to intra NAc saline, intra NAc <strong>neurotensin</strong> suppressed <b>amphetamine</b> induced locomotion in CONT HAL rats, but not in INT HAL or control rats.
+NEUROTENSIN	drug	amphetamine	28130052	Pharmacological activation of the <strong>neurotensin</strong> receptor 1 abrogates the <b>methamphetamine</b> induced striatal apoptosis in the mouse brain.
+NEUROTENSIN	drug	amphetamine	28130052	In this study, we investigated the role of the neuropeptide <strong>neurotensin</strong> on the <b>METH</b> induced apoptosis of some striatal neurons in mice.
+NEUROTENSIN	drug	amphetamine	28130052	An agonist of the <strong>neurotensin</strong> receptor 1 (PD149163, ip at various doses) attenuated the <b>METH</b> induced striatal neuron apoptosis.
+NEUROTENSIN	drug	amphetamine	28130052	Utilizing quantitative real time PCR, we showed that <b>METH</b> also up regulated <strong>neurotensin</strong> gene expression with 96% increase in preproneurotensin mRNA levels in the striatum as compared to the control.
+NEUROTENSIN	drug	amphetamine	28130052	To investigate the role of <strong>neurotensin</strong> without affecting core body temperature, we performed stereotactic injection of PD149163 into the striatum and observed that this compound maintained attenuated the <b>METH</b> induced apoptosis in the striatum, while leaving core body temperature unaffected.
+NEUROTENSIN	drug	amphetamine	28130052	These data indicate that the neuropeptide <strong>neurotensin</strong> modulates the striatal neuronal apoptosis induced by <b>METH</b> through diverse mechanisms that need to be investigated.
+NEUROTENSIN	drug	amphetamine	28130052	Furthermore, due to its neuroprotective properties, <strong>neurotensin</strong> receptor agonists show potential as drug candidates for the treatment of <b>METH</b> abuse and some neurological disorders.
+NEUROTENSIN	drug	nicotine	28028605	Blockade of hypocretin 1 and nociceptin receptors and stimulation of galanin and <strong>neurotensin</strong> receptors diminishes the rewarding effects of <b>nicotine</b>.
+NEUROTENSIN	drug	amphetamine	27267684	Repeated ventral midbrain <strong>neurotensin</strong> injections sensitize to <b>amphetamine</b> induced locomotion and ERK activation: A role for NMDA receptors.
+NEUROTENSIN	drug	amphetamine	27267684	In view of the recent evidence that <strong>neurotensin</strong> modulates ventral midbrain glutamate neurotransmission, we tested the hypothesis that <strong>neurotensin</strong> is acting upstream to glutamate to initiate sensitization to the behavioral and neurochemical effects of <b>amphetamine</b>.
+NEUROTENSIN	addiction	sensitization	27267684	In view of the recent evidence that <strong>neurotensin</strong> modulates ventral midbrain glutamate neurotransmission, we tested the hypothesis that <strong>neurotensin</strong> is acting upstream to glutamate to initiate <b>sensitization</b> to the behavioral and neurochemical effects of amphetamine.
+NEUROTENSIN	addiction	reward	27267684	During a first testing phase, adult male rats implanted with bilateral ventral midbrain cannulae were injected every second day for three days with D [Tyr11]<strong>neurotensin</strong> (1.5 nmol/side), the preferred NMDA GluN2A/B antagonist, <b>CPP</b> (40 or 120 pmol/side), the selective GluN2B antagonist, Ro04 5595 (200 or 1200 pmol/side), <b>CPP</b> (40 or 120 pmol/side) + D [Tyr11]<strong>neurotensin</strong> (1.5 nmol/side) or Ro04 5595 (200 or 1200 pmol/side) + D [Tyr11]<strong>neurotensin</strong> (1.5 nmol/side) and locomotor activity was measured immediately after the injection.
+NEUROTENSIN	drug	amphetamine	27267684	Results show that <b>amphetamine</b> induced significantly stronger locomotor activity and pERK1/2 expression in the nucleus accumbens shell and infralimbic cortex in <strong>neurotensin</strong> pre exposed animals than in controls (vehicle pre exposed).
+NEUROTENSIN	addiction	reward	27267684	These sensitization effects initiated by <strong>neurotensin</strong> were prevented by <b>CPP</b>, but not Ro04 5595.
+NEUROTENSIN	addiction	sensitization	27267684	These <b>sensitization</b> effects initiated by <strong>neurotensin</strong> were prevented by CPP, but not Ro04 5595.
+NEUROTENSIN	drug	amphetamine	27267684	These results support the hypothesis that <strong>neurotensin</strong> is stimulating glutamate neurotransmission to initiate neural changes that sub serve <b>amphetamine</b> sensitization and that glutamate is acting on NMDA receptors that are mostly likely composed of GluN2A, but not GluN2B, subunits.
+NEUROTENSIN	addiction	sensitization	27267684	These results support the hypothesis that <strong>neurotensin</strong> is stimulating glutamate neurotransmission to initiate neural changes that sub serve amphetamine <b>sensitization</b> and that glutamate is acting on NMDA receptors that are mostly likely composed of GluN2A, but not GluN2B, subunits.
+NEUROTENSIN	drug	opioid	27523794	Heterodimerization of the kappa <b>opioid</b> receptor and <strong>neurotensin</strong> receptor 1 contributes to a novel β arrestin 2 biased pathway.
+NEUROTENSIN	drug	opioid	27509866	The objective of the study was to investigate the possibility of modulation of skin inflammation by topical treatment with a novel compound: an <b>opioid</b> <strong>neurotensin</strong> hybrid peptide PK20 encompassing endomorphin 2 analog and modified fragment of <strong>neurotensin</strong> (8 13).
+NEUROTENSIN	drug	amphetamine	27119457	ML314: A Biased <strong>Neurotensin</strong> Receptor Ligand for <b>Methamphetamine</b> Abuse.
+NEUROTENSIN	drug	amphetamine	27119457	<strong>Neurotensin</strong> receptor NTR1 and dopamine receptor distributions coincide in brain areas regulating <b>methamphetamine</b> associated reward, and <strong>neurotensin</strong> peptides produce behaviors opposing psychostimulants.
+NEUROTENSIN	addiction	reward	27119457	<strong>Neurotensin</strong> receptor NTR1 and dopamine receptor distributions coincide in brain areas regulating methamphetamine associated <b>reward</b>, and <strong>neurotensin</strong> peptides produce behaviors opposing psychostimulants.
+NEUROTENSIN	drug	nicotine	27074301	Sex differences in <strong>neurotensin</strong> and substance P following <b>nicotine</b> self administration in rats.
+NEUROTENSIN	drug	nicotine	27074301	Investigator administered <b>nicotine</b> alters <strong>neurotensin</strong> and substance P levels in Sprague Dawley rats.
+NEUROTENSIN	drug	nicotine	27074301	We sought to extend this observation by determining the responses of <strong>neurotensin</strong> and substance P systems (assessed using radioimmunoassay) in male and female rats following <b>nicotine</b> self administration (SA).
+NEUROTENSIN	drug	nicotine	27074301	<b>Nicotine</b> SA increased tissue levels of <strong>neurotensin</strong> in the males in the anterior and posterior caudate, globus pallidus, frontal cortex, nucleus accumbens core and shell, and ventral tegmental area.
+NEUROTENSIN	drug	nicotine	27074301	<b>Nicotine</b> SA also increased tissue levels of <strong>neurotensin</strong> in the females in the anterior caudate, globus pallidus, nucleus accumbens core and shell, but not in the posterior caudate, frontal cortex, or ventral tegmental area.
+NEUROTENSIN	drug	cannabinoid	26976581	Although morphine analgesia is independent of these 6TM mu receptor isoforms, we now show that the selective loss of the 6TM variants in a knockout model eliminates the analgesic actions of delta and kappa opioids and of α2 adrenergic compounds, but not <b>cannabinoid</b>, <strong>neurotensin</strong>, or muscarinic drugs.
+NEUROTENSIN	drug	opioid	26976581	Although <b>morphine</b> analgesia is independent of these 6TM mu receptor isoforms, we now show that the selective loss of the 6TM variants in a knockout model eliminates the analgesic actions of delta and kappa <b>opioids</b> and of α2 adrenergic compounds, but not cannabinoid, <strong>neurotensin</strong>, or muscarinic drugs.
+NEUROTENSIN	drug	cocaine	26901162	A <strong>neurotensin</strong> analog blocks <b>cocaine</b> conditioned place preference and reinstatement.
+NEUROTENSIN	addiction	relapse	26901162	A <strong>neurotensin</strong> analog blocks cocaine conditioned place preference and <b>reinstatement</b>.
+NEUROTENSIN	drug	cocaine	26901162	We studied the effects of the nonselective NT receptor agonist NT69L, which has equal affinity for the two major NT receptors, <strong>NTS1</strong> and NTS2, on the expression of <b>cocaine</b> conditioned place preference (<b>cocaine</b> CPP) and reinstatement after extinction.
+NEUROTENSIN	addiction	relapse	26901162	We studied the effects of the nonselective NT receptor agonist NT69L, which has equal affinity for the two major NT receptors, <strong>NTS1</strong> and NTS2, on the expression of cocaine conditioned place preference (cocaine CPP) and <b>reinstatement</b> after extinction.
+NEUROTENSIN	addiction	reward	26901162	We studied the effects of the nonselective NT receptor agonist NT69L, which has equal affinity for the two major NT receptors, <strong>NTS1</strong> and NTS2, on the expression of cocaine conditioned place preference (cocaine <b>CPP</b>) and reinstatement after extinction.
+NEUROTENSIN	drug	cannabinoid	26650254	Serotonin [5 hydroxytryptamine (5 HT)], dopamine (DA), <b>endocannabinoids</b>, and endogenous opiates are the main neurotransmitter systems involved in the rewarding effects of MDMA in rodents, but other neurotransmitters such as glutamate, acetylcholine, adenosine, and <strong>neurotensin</strong> are also involved.
+NEUROTENSIN	drug	psychedelics	26650254	Serotonin [5 hydroxytryptamine (5 HT)], dopamine (DA), endocannabinoids, and endogenous opiates are the main neurotransmitter systems involved in the rewarding effects of <b>MDMA</b> in rodents, but other neurotransmitters such as glutamate, acetylcholine, adenosine, and <strong>neurotensin</strong> are also involved.
+NEUROTENSIN	drug	alcohol	26384852	SNP rs3915568 in NTSR1, which encodes <strong>neurotensin</strong> receptor, and SNP rs1389752 in MPDZ, which encodes the multiple PDZ domain protein, were previously associated with heroin addiction or <b>alcohol</b> addiction, respectively.
+NEUROTENSIN	drug	opioid	26384852	SNP rs3915568 in NTSR1, which encodes <strong>neurotensin</strong> receptor, and SNP rs1389752 in MPDZ, which encodes the multiple PDZ domain protein, were previously associated with <b>heroin</b> addiction or alcohol addiction, respectively.
+NEUROTENSIN	addiction	addiction	26384852	SNP rs3915568 in NTSR1, which encodes <strong>neurotensin</strong> receptor, and SNP rs1389752 in MPDZ, which encodes the multiple PDZ domain protein, were previously associated with heroin <b>addiction</b> or alcohol <b>addiction</b>, respectively.
+NEUROTENSIN	drug	amphetamine	25963809	Effect of low doses of <b>methamphetamine</b> on rat limbic related <strong>neurotensin</strong> systems.
+NEUROTENSIN	drug	amphetamine	25963809	Administration of <b>methamphetamine</b> (<b>METH</b>) alters limbic related (LR) <strong>neurotensin</strong> (NT) systems.
+NEUROTENSIN	drug	cocaine	25379267	<strong>Neurotensin</strong> agonist attenuates nicotine potentiation to <b>cocaine</b> sensitization.
+NEUROTENSIN	drug	nicotine	25379267	<strong>Neurotensin</strong> agonist attenuates <b>nicotine</b> potentiation to cocaine sensitization.
+NEUROTENSIN	addiction	sensitization	25379267	<strong>Neurotensin</strong> agonist attenuates nicotine potentiation to cocaine <b>sensitization</b>.
+NEUROTENSIN	addiction	reward	25379267	<strong>Neurotensin</strong> (NT) is a 13 amino acid neuropeptide that modulates dopamine, acetylcholine, glutamate, and GABA neurotransmission in brain <b>reward</b> pathways.
+NEUROTENSIN	drug	cocaine	25379267	The effect of the <strong>neurotensin</strong> agonist on <b>cocaine</b> sensitization in the nicotine treated group indicated a possible therapeutic effect for <b>cocaine</b> addiction, even in the presence of enhanced behavioral sensitization induced by nicotine.
+NEUROTENSIN	drug	nicotine	25379267	The effect of the <strong>neurotensin</strong> agonist on cocaine sensitization in the <b>nicotine</b> treated group indicated a possible therapeutic effect for cocaine addiction, even in the presence of enhanced behavioral sensitization induced by <b>nicotine</b>.
+NEUROTENSIN	addiction	addiction	25379267	The effect of the <strong>neurotensin</strong> agonist on cocaine sensitization in the nicotine treated group indicated a possible therapeutic effect for cocaine <b>addiction</b>, even in the presence of enhanced behavioral sensitization induced by nicotine.
+NEUROTENSIN	addiction	sensitization	25379267	The effect of the <strong>neurotensin</strong> agonist on cocaine <b>sensitization</b> in the nicotine treated group indicated a possible therapeutic effect for cocaine addiction, even in the presence of enhanced behavioral <b>sensitization</b> induced by nicotine.
+NEUROTENSIN	drug	amphetamine	24969625	Role of context in <strong>neurotensin</strong> induced sensitization to the locomotor stimulant effect of <b>amphetamine</b>.
+NEUROTENSIN	addiction	sensitization	24969625	Role of context in <strong>neurotensin</strong> induced <b>sensitization</b> to the locomotor stimulant effect of amphetamine.
+NEUROTENSIN	drug	amphetamine	24969625	Previous studies have shown that repeated central injections of <strong>neurotensin</strong>, or its active analog, D Tyr([11])<strong>neurotensin</strong>, sensitize to the locomotor stimulant effect of <b>amphetamine</b>.
+NEUROTENSIN	drug	amphetamine	24969625	The present study was thus aimed at determining whether the induction of <b>amphetamine</b> sensitization by <strong>neurotensin</strong> is modulated by the context in which <strong>neurotensin</strong> is administered.
+NEUROTENSIN	addiction	sensitization	24969625	The present study was thus aimed at determining whether the induction of amphetamine <b>sensitization</b> by <strong>neurotensin</strong> is modulated by the context in which <strong>neurotensin</strong> is administered.
+NEUROTENSIN	drug	amphetamine	24969625	This context dependency was not found however for <b>amphetamine</b> induced non ambulatory and vertical activity suggesting that <strong>neurotensin</strong> can induce both a context dependent and context independent sensitization.
+NEUROTENSIN	addiction	sensitization	24969625	This context dependency was not found however for amphetamine induced non ambulatory and vertical activity suggesting that <strong>neurotensin</strong> can induce both a context dependent and context independent <b>sensitization</b>.
+NEUROTENSIN	drug	amphetamine	24522333	Responses of the rat basal ganglia <strong>neurotensin</strong> systems to low doses of <b>methamphetamine</b>.
+NEUROTENSIN	drug	opioid	24400381	[<strong>Neurotensin</strong> NT (8  13) dipeptide analog dilept increases the pain threshold and decreases the severity of <b>morphine</b> withdrawal syndrome in rats].
+NEUROTENSIN	addiction	withdrawal	24400381	[<strong>Neurotensin</strong> NT (8  13) dipeptide analog dilept increases the pain threshold and decreases the severity of morphine <b>withdrawal</b> syndrome in rats].
+NEUROTENSIN	drug	opioid	24400381	The pain threshold effects of a <strong>neurotensin</strong> NT (8   13) dipeptide analog (dilept), <b>morphine</b>, and their combination have been studied using the tail flick test in rats.
+NEUROTENSIN	addiction	relapse	24332089	A scaffold hop program <b>seeking</b> full agonists of the <strong>neurotensin</strong> 1 (NTR1) receptor identified the probe molecule ML301 (1) and associated analogs, including its naphthyl analog (14) which exhibited similar properties.
+NEUROTENSIN	drug	alcohol	23743782	Association between <strong>neurotensin</strong> receptor 1 gene polymorphisms and <b>alcohol</b> dependence in a male Han Chinese population.
+NEUROTENSIN	addiction	dependence	23743782	Association between <strong>neurotensin</strong> receptor 1 gene polymorphisms and alcohol <b>dependence</b> in a male Han Chinese population.
+NEUROTENSIN	drug	amphetamine	23685547	Response of <strong>neurotensin</strong> basal ganglia systems during extinction of <b>methamphetamine</b> self administration in rat.
+NEUROTENSIN	drug	amphetamine	23685547	Thus, we investigated the response of central nervous system <strong>neurotensin</strong> (NT) systems to <b>METH</b> self administration (SA) and their interaction with basal ganglia dopamine (DA) pathways.
+NEUROTENSIN	drug	cannabinoid	23448481	substance P, <strong>neurotensin</strong>, cholecystokinin, <b>cannabinoids</b>, melanocortin ligands, etc.).
+NEUROTENSIN	drug	amphetamine	22245499	Response of limbic <strong>neurotensin</strong> systems to <b>methamphetamine</b> self administration.
+NEUROTENSIN	drug	amphetamine	22245499	Thus, we and others have studied the <b>METH</b> induced responses of <strong>neurotensin</strong> (NT) systems.
+NEUROTENSIN	drug	cocaine	21720755	Effects of <strong>neurotensin</strong> gene knockout in mice on the behavioral effects of <b>cocaine</b>.
+NEUROTENSIN	drug	opioid	21134256	PK20, a new <b>opioid</b> <strong>neurotensin</strong> hybrid peptide that exhibits central and peripheral antinociceptive effects.
+NEUROTENSIN	drug	opioid	21134256	<strong>Neurotensin</strong> induced antinociception is not mediated through the <b>opioid</b> system.
+NEUROTENSIN	drug	opioid	21134256	Therefore, hybridizing <strong>neurotensin</strong> with <b>opioid</b> elements may result in a potent synergistic antinociceptor.
+NEUROTENSIN	drug	opioid	21134256	Using the known structure activity relationships of <strong>neurotensin</strong> we have synthesized a new chimeric <b>opioid</b> <strong>neurotensin</strong> compound PK20 which is characterized by a very strong antinociceptive potency.
+NEUROTENSIN	drug	opioid	21134256	The <b>opioid</b> <strong>neurotensin</strong> hybrid analogue PK20, in which <b>opioid</b> and <strong>neurotensin</strong> pharmacophores overlap partially, expresses high antinociceptive tail flick effects after central as well as peripheral applications.
+NEUROTENSIN	drug	amphetamine	21131268	Effect of <b>methamphetamine</b> self administration on <strong>neurotensin</strong> systems of the basal ganglia.
+NEUROTENSIN	drug	amphetamine	21131268	For this reason, we and others have examined the <b>METH</b> induced responses of <strong>neurotensin</strong> (NT) systems in the basal ganglia.
+NEUROTENSIN	drug	nicotine	21047685	A <strong>neurotensin</strong> analog, NT69L, attenuates intravenous <b>nicotine</b> self administration in rats.
+NEUROTENSIN	drug	nicotine	21047685	NT69L is a <strong>neurotensin</strong> analog that blocks <b>nicotine</b> induced locomotor activity and has sustained efficacy in a rat model of <b>nicotine</b> induced sensitization when administered peripherally.
+NEUROTENSIN	addiction	sensitization	21047685	NT69L is a <strong>neurotensin</strong> analog that blocks nicotine induced locomotor activity and has sustained efficacy in a rat model of nicotine induced <b>sensitization</b> when administered peripherally.
+NEUROTENSIN	drug	alcohol	21039631	Increased <b>ethanol</b> consumption and preference in mice lacking <strong>neurotensin</strong> receptor type 2.
+NEUROTENSIN	drug	alcohol	21039631	Although NT and <strong>neurotensin</strong> receptors type 1 (NTS1) are implicated in some of the behavioral effects of <b>ethanol</b>, the functional roles of <strong>neurotensin</strong> receptors type 2 (NTS2) in <b>ethanol</b> intoxication and consumption remain unknown.
+NEUROTENSIN	addiction	intoxication	21039631	Although NT and <strong>neurotensin</strong> receptors type 1 (NTS1) are implicated in some of the behavioral effects of ethanol, the functional roles of <strong>neurotensin</strong> receptors type 2 (NTS2) in ethanol <b>intoxication</b> and consumption remain unknown.
+NEUROTENSIN	drug	alcohol	21039631	Although NT and <strong>neurotensin</strong> receptors type 1 (<strong>NTS1</strong>) are implicated in some of the behavioral effects of <b>ethanol</b>, the functional roles of <strong>neurotensin</strong> receptors type 2 (NTS2) in <b>ethanol</b> intoxication and consumption remain unknown.
+NEUROTENSIN	addiction	intoxication	21039631	Although NT and <strong>neurotensin</strong> receptors type 1 (<strong>NTS1</strong>) are implicated in some of the behavioral effects of ethanol, the functional roles of <strong>neurotensin</strong> receptors type 2 (NTS2) in ethanol <b>intoxication</b> and consumption remain unknown.
+NEUROTENSIN	drug	alcohol	20974215	Recent study shows that NT69L, an analog of <strong>neurotensin</strong> (NT) (8 13), reduces <b>ethanol</b> consumption and preference in mice through modulation of <strong>neurotensin</strong> receptor subtype one.
+NEUROTENSIN	drug	alcohol	20122953	<strong>Neurotensin</strong> receptor type 1 regulates <b>ethanol</b> intoxication and consumption in mice.
+NEUROTENSIN	addiction	intoxication	20122953	<strong>Neurotensin</strong> receptor type 1 regulates ethanol <b>intoxication</b> and consumption in mice.
+NEUROTENSIN	drug	alcohol	20122953	In this study, we found that <strong>NTS1</strong> null mice displayed decreased sensitivity to the ataxic effect of <b>ethanol</b> on the rotarod and increased <b>ethanol</b> consumption when given a free choice between <b>ethanol</b> and tap water containing bottles.
+NEUROTENSIN	drug	alcohol	20122953	Interestingly, the administration of NT69L, a brain permeable NT analog, increased <b>ethanol</b> sensitivity in wild type littermates but had no such effect in <strong>NTS1</strong> null mice, suggesting that <strong>NTS1</strong> contributes to NT mediated <b>ethanol</b> intoxication.
+NEUROTENSIN	addiction	intoxication	20122953	Interestingly, the administration of NT69L, a brain permeable NT analog, increased ethanol sensitivity in wild type littermates but had no such effect in <strong>NTS1</strong> null mice, suggesting that <strong>NTS1</strong> contributes to NT mediated ethanol <b>intoxication</b>.
+NEUROTENSIN	drug	alcohol	20122953	Furthermore, the daily treatment of NT69L, for 4 consecutive days, significantly reduced <b>alcohol</b> preference and consumption in wild type littermates but had no such effects in <strong>NTS1</strong> null mice in a two bottle drinking experiment.
+NEUROTENSIN	drug	opioid	19580660	Central <strong>neurotensin</strong> (NT) administration results in a <b>naloxone</b> insensitive antinociceptive response in animal models of acute and persistent pain.
+NEUROTENSIN	drug	cocaine	19442653	<strong>Neurotensin</strong> (NT) is a neuropeptide involved in <b>cocaine</b> reward, and in learning and memory processes related to drug use within the mesolimbic dopamine (DA) system.
+NEUROTENSIN	addiction	reward	19442653	<strong>Neurotensin</strong> (NT) is a neuropeptide involved in cocaine <b>reward</b>, and in learning and memory processes related to drug use within the mesolimbic dopamine (DA) system.
+NEUROTENSIN	drug	amphetamine	18991855	Differential response of <strong>neurotensin</strong> to <b>methamphetamine</b> self administration.
+NEUROTENSIN	drug	opioid	18706409	Evidence for a role of endogenous <strong>neurotensin</strong> in the development of sensitization to the locomotor stimulant effect of <b>morphine</b>.
+NEUROTENSIN	addiction	sensitization	18706409	Evidence for a role of endogenous <strong>neurotensin</strong> in the development of <b>sensitization</b> to the locomotor stimulant effect of morphine.
+NEUROTENSIN	drug	opioid	18706409	This experiment was aimed at exploring the role of endogenous <strong>neurotensin</strong> in the development of sensitization to the locomotor stimulant effect of <b>morphine</b>.
+NEUROTENSIN	addiction	sensitization	18706409	This experiment was aimed at exploring the role of endogenous <strong>neurotensin</strong> in the development of <b>sensitization</b> to the locomotor stimulant effect of morphine.
+NEUROTENSIN	drug	opioid	18706409	The present results suggest that endogenous <strong>neurotensin</strong> contributes to the acute locomotor stimulant effect of <b>morphine</b> and to the induction of its sensitization.
+NEUROTENSIN	addiction	sensitization	18706409	The present results suggest that endogenous <strong>neurotensin</strong> contributes to the acute locomotor stimulant effect of morphine and to the induction of its <b>sensitization</b>.
+NEUROTENSIN	drug	nicotine	18687313	Effect of a novel <strong>neurotensin</strong> analog, NT69L, on <b>nicotine</b> induced alterations in monoamine levels in rat brain.
+NEUROTENSIN	addiction	addiction	18687313	NT69L, is a novel <strong>neurotensin</strong> (8 13) analog that participates in the modulation of the dopaminergic pathways implicated in <b>addiction</b> to psychostimulants.
+NEUROTENSIN	drug	nicotine	18687313	These data further support a role for NT69L or other <strong>neurotensin</strong> receptor agonists to treat <b>nicotine</b> addiction.
+NEUROTENSIN	addiction	addiction	18687313	These data further support a role for NT69L or other <strong>neurotensin</strong> receptor agonists to treat nicotine <b>addiction</b>.
+NEUROTENSIN	drug	cocaine	18538358	In this autopsied brain study, our major objective was to establish by radioimmunoassay whether levels of dynorphin and other neuropeptides (e.g., metenkephalin, <strong>neurotensin</strong> and substance P) are increased in the dopamine rich caudate, putamen, and nucleus accumbens of human chronic <b>cocaine</b> users (n=12) vs. matched control subjects (n=17) as predicted by animal findings.
+NEUROTENSIN	drug	psychedelics	18410947	Effects of the selective <strong>neurotensin</strong> antagonist SR 142948A on 3,4 <b>methylenedioxymethamphetamine</b> induced behaviours in mice.
+NEUROTENSIN	drug	psychedelics	18410947	<strong>Neurotensin</strong> is one of the genes previously found up regulated in mice striatum after acute injection of <b>MDMA</b> (9 mg/kg).
+NEUROTENSIN	drug	psychedelics	18410947	In order to examine the pharmacological significance of this effect, the involvement of the neurotensinergic system in <b>MDMA</b> induced behaviors was explored in mice using the <strong>neurotensin</strong> receptor antagonist SR142948A (1mg/kg).
+NEUROTENSIN	drug	psychedelics	18410947	We also studied the effects of acute and repeated exposure to <b>MDMA</b> on the mRNA level of <strong>neurotensin</strong> in mice striatum.
+NEUROTENSIN	drug	psychedelics	18410947	Kinetic analysis of the regulation 1, 2, 6 and 12h after acute injection of <b>MDMA</b> showed that the drug transiently up regulates <strong>neurotensin</strong> mRNA in this structure.
+NEUROTENSIN	drug	psychedelics	18410947	Repeated exposure to <b>MDMA</b> following the same injection pattern used in the CPP paradigm revealed an increase in mRNA level of <strong>neurotensin</strong> in mice striatum.
+NEUROTENSIN	addiction	reward	18410947	Repeated exposure to MDMA following the same injection pattern used in the <b>CPP</b> paradigm revealed an increase in mRNA level of <strong>neurotensin</strong> in mice striatum.
+NEUROTENSIN	drug	psychedelics	18410947	These results indicate that endogenous <strong>neurotensin</strong> plays a role in both the acute locomotor activity and the expression of CPP induced by <b>MDMA</b>.
+NEUROTENSIN	addiction	reward	18410947	These results indicate that endogenous <strong>neurotensin</strong> plays a role in both the acute locomotor activity and the expression of <b>CPP</b> induced by MDMA.
+NEUROTENSIN	drug	cocaine	18252810	<strong>Neurotensin</strong> in the ventral pallidum increases extracellular gamma aminobutyric acid and differentially affects cue  and <b>cocaine</b> primed reinstatement.
+NEUROTENSIN	addiction	relapse	18252810	<strong>Neurotensin</strong> in the ventral pallidum increases extracellular gamma aminobutyric acid and differentially affects cue  and cocaine primed <b>reinstatement</b>.
+NEUROTENSIN	drug	cocaine	18252810	Therefore, the present study determined whether <strong>neurotensin</strong> increases GABA release in the VP, antagonizes <b>cocaine</b> induced decreases in GABA, and prevents reinstatement of <b>cocaine</b> seeking.
+NEUROTENSIN	addiction	relapse	18252810	Therefore, the present study determined whether <strong>neurotensin</strong> increases GABA release in the VP, antagonizes cocaine induced decreases in GABA, and prevents <b>reinstatement</b> of cocaine <b>seeking</b>.
+NEUROTENSIN	drug	cocaine	18252810	In vivo microdialysis revealed that the <strong>neurotensin</strong> agonist <strong>neurotensin</strong> peptide fragment 8 13 [NT(8 13)] increased GABA in the VP in a <strong>neurotensin</strong> receptor and tetrodotoxin dependent manner and blocked the <b>cocaine</b> induced decrease in GABA.
+NEUROTENSIN	drug	cocaine	18252810	The <strong>neurotensin</strong> antagonist SR142948 (2 [[[5 (2,6 dimethoxyphenyl) 1 [4 [[[3 (dimethylamino)propyl]methylamino]carbonyl] 2 (1 methylethyl)phenyl] 1H  pyrazol 3 yl]carbonyl]amino] tricyclo [3.3.1.13,7]decane 2 carboxylic acid) had no effect on any behavioral measure when infused in the VP at the dose tested but attenuated <b>cocaine</b> primed reinstatement when administered systemically.
+NEUROTENSIN	addiction	relapse	18252810	The <strong>neurotensin</strong> antagonist SR142948 (2 [[[5 (2,6 dimethoxyphenyl) 1 [4 [[[3 (dimethylamino)propyl]methylamino]carbonyl] 2 (1 methylethyl)phenyl] 1H  pyrazol 3 yl]carbonyl]amino] tricyclo [3.3.1.13,7]decane 2 carboxylic acid) had no effect on any behavioral measure when infused in the VP at the dose tested but attenuated cocaine primed <b>reinstatement</b> when administered systemically.
+NEUROTENSIN	drug	cocaine	18252810	Three conclusions can be drawn from these data: 1) <strong>neurotensin</strong> promotes GABA release in the VP and correspondingly inhibits cue induced reinstatement, 2) <strong>neurotensin</strong> and <b>cocaine</b> interact in a manner that countermands the <strong>neurotensin</strong> induced increase in GABA and promotes reinstatement, and 3) endogenous release of <strong>neurotensin</strong> in the VP is not necessary for reinstatement.
+NEUROTENSIN	addiction	relapse	18252810	Three conclusions can be drawn from these data: 1) <strong>neurotensin</strong> promotes GABA release in the VP and correspondingly inhibits cue induced <b>reinstatement</b>, 2) <strong>neurotensin</strong> and cocaine interact in a manner that countermands the <strong>neurotensin</strong> induced increase in GABA and promotes <b>reinstatement</b>, and 3) endogenous release of <strong>neurotensin</strong> in the VP is not necessary for <b>reinstatement</b>.
+NEUROTENSIN	drug	nicotine	17689525	Nicotinic and dopamine D2 receptors mediate <b>nicotine</b> induced changes in ventral tegmental area <strong>neurotensin</strong> system.
+NEUROTENSIN	drug	nicotine	17689525	Because <strong>neurotensin</strong> has been linked with both mesolimbic and mesocortical dopamine function, we examined the impact of <b>nicotine</b> treatment on central nervous <strong>neurotensin</strong> systems by measuring changes in <strong>neurotensin</strong> tissue content because it has been shown that such changes reflect alterations in release and activity of this peptide system.
+NEUROTENSIN	drug	nicotine	17689525	The <b>nicotine</b> treatment significantly decreased <strong>neurotensin</strong> like immunoreactivity content in the ventral tegmental area, as well as related regions such as prefrontal cortex, substantia nigra, and anterior striatal region 12 18 h after drug treatment, but not the nucleus accumbens.
+NEUROTENSIN	drug	nicotine	17689525	The <b>nicotine</b> mediated decrease in the <strong>neurotensin</strong> like immunoreactivity of the ventral tegmental area was selectively blocked by a specific dopamine D(2), but not a dopamine D(1), receptor antagonist, while mecamylamine attenuated at the low (3.0 mg/kg) and completely blocked at high (6.0 mg/kg) dose this <b>nicotine</b> effect.
+NEUROTENSIN	drug	nicotine	17689525	These findings with previous studies, suggest that <b>nicotine</b> mediated dopamine release activates D(2) receptors which in turn increases <strong>neurotensin</strong> release, turnover and acutely reduces tissue levels in the ventral tegmental area and other limbic and basal ganglia structures.
+NEUROTENSIN	drug	cocaine	17356568	<strong>Neurotensin</strong> receptor antagonist administered during <b>cocaine</b> withdrawal decreases locomotor sensitization and conditioned place preference.
+NEUROTENSIN	addiction	sensitization	17356568	<strong>Neurotensin</strong> receptor antagonist administered during cocaine withdrawal decreases locomotor <b>sensitization</b> and conditioned place preference.
+NEUROTENSIN	addiction	withdrawal	17356568	<strong>Neurotensin</strong> receptor antagonist administered during cocaine <b>withdrawal</b> decreases locomotor sensitization and conditioned place preference.
+NEUROTENSIN	drug	amphetamine	17276509	Blockade of <strong>neurotensin</strong> receptors during <b>amphetamine</b> discontinuation indicates individual variability.
+NEUROTENSIN	drug	amphetamine	17276509	The effects of repeated treatment with the <strong>neurotensin</strong> antagonist SR48692 after <b>amphetamine</b> discontinuation were investigated in mice previously classified as high responders (HRs) or low responders (LRs) to novelty.
+NEUROTENSIN	drug	amphetamine	17276509	These data suggest that <strong>neurotensin</strong> plays a role in individual variability to <b>amphetamine</b> induced sensitization.
+NEUROTENSIN	addiction	sensitization	17276509	These data suggest that <strong>neurotensin</strong> plays a role in individual variability to amphetamine induced <b>sensitization</b>.
+NEUROTENSIN	addiction	reward	17113052	The <strong>neurotensin</strong> receptor agonist NT69L suppresses sucrose reinforced <b>operant</b> behavior in the rat.
+NEUROTENSIN	addiction	sensitization	16882012	Intra VTA <strong>neurotensin</strong> activates dopaminergic neurons and plays an important role in the development of behavioural <b>sensitization</b> to psychostimulant drugs and possibly in schizophrenia.
+NEUROTENSIN	drug	amphetamine	16882012	Using gold coupled wheatgerm agglutinin as retrograde tracer in combination with nonisotopic in situ hybridization for <strong>neurotensin</strong> mRNA or <strong>neurotensin</strong> antibodies after colchicine treatment, the present study was undertaken to demonstrate the neurotensinergic neurons projecting to the VTA and determine whether (and in which subpopulations) <strong>neurotensin</strong> expression is regulated in VTA projecting neurons after administrations of the psychostimulant drug <b>methamphetamine</b> or the antipsychotic haloperidol.
+NEUROTENSIN	drug	amphetamine	16882012	The up regulation of <strong>neurotensin</strong> expression selectively in VTA projecting neurons in the accumbens shell following <b>methamphetamine</b> administration may be an important factor in the development of behavioural sensitization.
+NEUROTENSIN	addiction	sensitization	16882012	The up regulation of <strong>neurotensin</strong> expression selectively in VTA projecting neurons in the accumbens shell following methamphetamine administration may be an important factor in the development of behavioural <b>sensitization</b>.
+NEUROTENSIN	drug	cocaine	16574078	<strong>Neurotensin</strong> receptor activation sensitizes to the locomotor stimulant effect of <b>cocaine</b>: a role for NMDA receptors.
+NEUROTENSIN	drug	cocaine	16574078	This study was aimed at determining whether repeated activation of <strong>neurotensin</strong> receptors sensitizes to <b>cocaine</b> induced locomotor activity and whether this effect can be prevented by blockade of N methyl d aspartate receptors.
+NEUROTENSIN	addiction	reward	16574078	Independent groups of male rats were injected on four occasions, every other day (training phase), with vehicle or one of two doses (4 and 8 mg/kg) of the NMDA antagonist <b>CPP</b> [(+/ ) 3 (2 carboxypiperazine 4 yl) propanephosphonic)] followed by an intracerebroventricular injection of 18 nmol/10 microl of d Tyr[(11)]<strong>neurotensin</strong>, or its vehicle.
+NEUROTENSIN	addiction	reward	16574078	Results show that during the training phase d Tyr[(11)]<strong>neurotensin</strong> produced an initial suppression of all locomotor responses followed by an augmentation of ambulatory and non ambulatory activity compared to controls, effects that were only slightly altered by <b>CPP</b>.
+NEUROTENSIN	drug	cocaine	16574078	<b>Cocaine</b> produced higher ambulatory and non ambulatory activity in animals pre exposed to <strong>neurotensin</strong> than in the vehicle pre exposed animals, a sensitization effect that was not prevented by CPP at 1 week post training but that was blocked at 3 weeks at the high dose.
+NEUROTENSIN	addiction	reward	16574078	Cocaine produced higher ambulatory and non ambulatory activity in animals pre exposed to <strong>neurotensin</strong> than in the vehicle pre exposed animals, a sensitization effect that was not prevented by <b>CPP</b> at 1 week post training but that was blocked at 3 weeks at the high dose.
+NEUROTENSIN	addiction	sensitization	16574078	Cocaine produced higher ambulatory and non ambulatory activity in animals pre exposed to <strong>neurotensin</strong> than in the vehicle pre exposed animals, a <b>sensitization</b> effect that was not prevented by CPP at 1 week post training but that was blocked at 3 weeks at the high dose.
+NEUROTENSIN	drug	cocaine	16574078	When given alone, the low dose of CPP produced an effect very similar to that of <strong>neurotensin</strong> on <b>cocaine</b> sensitization.
+NEUROTENSIN	addiction	reward	16574078	When given alone, the low dose of <b>CPP</b> produced an effect very similar to that of <strong>neurotensin</strong> on cocaine sensitization.
+NEUROTENSIN	addiction	sensitization	16574078	When given alone, the low dose of CPP produced an effect very similar to that of <strong>neurotensin</strong> on cocaine <b>sensitization</b>.
+NEUROTENSIN	addiction	sensitization	16574078	These results further confirm that <strong>neurotensin</strong> plays a role in <b>sensitization</b> to psychostimulant drugs and suggests that NMDA receptors are involved in the long term effect of exposure to <strong>neurotensin</strong>.
+NEUROTENSIN	drug	nicotine	16122577	Neurobiologic basis of <b>nicotine</b> addiction and psychostimulant abuse: a role for <strong>neurotensin</strong>?
+NEUROTENSIN	addiction	addiction	16122577	Neurobiologic basis of nicotine <b>addiction</b> and psychostimulant abuse: a role for <strong>neurotensin</strong>?
+NEUROTENSIN	addiction	addiction	16122577	<strong>Neurotensin</strong> has been postulated to be an endogenous neuroleptic, and the performance of <strong>neurotensin</strong> analogues in animal models of <b>addiction</b> makes such compounds intriguing candidates for treatment of <b>addiction</b> in high risk psychiatric populations.
+NEUROTENSIN	drug	cocaine	16010538	Activation of central <strong>neurotensin</strong> receptors reinstates <b>cocaine</b> seeking in the rat: modulation by a D1/D5, but not D2/D3, receptor antagonist.
+NEUROTENSIN	addiction	relapse	16010538	Activation of central <strong>neurotensin</strong> receptors reinstates cocaine <b>seeking</b> in the rat: modulation by a D1/D5, but not D2/D3, receptor antagonist.
+NEUROTENSIN	addiction	reward	15680187	Antinociceptive, hypothermic, hypotensive, and <b>reinforcing</b> effects of a novel <strong>neurotensin</strong> receptor agonist, NT69L, in rhesus monkeys.
+NEUROTENSIN	addiction	reward	15680187	NT has been implicated in the actions of antipsychotic drugs and psychostimulants, and animal studies suggest that <strong>neurotensin</strong> directly injected into brain has <b>reinforcing</b> effects.
+NEUROTENSIN	drug	amphetamine	15680187	Previously, we showed that one of our brain penetrating analogs of <strong>neurotensin</strong>, NT69L (N methyl L Arg, L Lys, L Pro, L neo Trp, L tert Leu, L Leu), has many pharmacological effects in rats including antinociception, hypothermia, and blockade of the hyperactivity caused by psychostimulants (cocaine, D <b>amphetamine</b>, and nicotine).
+NEUROTENSIN	drug	cocaine	15680187	Previously, we showed that one of our brain penetrating analogs of <strong>neurotensin</strong>, NT69L (N methyl L Arg, L Lys, L Pro, L neo Trp, L tert Leu, L Leu), has many pharmacological effects in rats including antinociception, hypothermia, and blockade of the hyperactivity caused by psychostimulants (<b>cocaine</b>, D amphetamine, and nicotine).
+NEUROTENSIN	drug	nicotine	15680187	Previously, we showed that one of our brain penetrating analogs of <strong>neurotensin</strong>, NT69L (N methyl L Arg, L Lys, L Pro, L neo Trp, L tert Leu, L Leu), has many pharmacological effects in rats including antinociception, hypothermia, and blockade of the hyperactivity caused by psychostimulants (cocaine, D amphetamine, and <b>nicotine</b>).
+NEUROTENSIN	drug	amphetamine	15637639	Endogenous <strong>neurotensin</strong> in the ventral tegmental area contributes to <b>amphetamine</b> behavioral sensitization.
+NEUROTENSIN	addiction	sensitization	15637639	Endogenous <strong>neurotensin</strong> in the ventral tegmental area contributes to amphetamine behavioral <b>sensitization</b>.
+NEUROTENSIN	drug	amphetamine	15637639	Studies showing psychostimulant like effects of exogenous <strong>neurotensin</strong> (NT) infused into the ventral tegmental area (VTA) prompted us to examine the role in the VTA of the endogenous NT in behavioral sensitization to <b>amphetamine</b>.
+NEUROTENSIN	addiction	sensitization	15637639	Studies showing psychostimulant like effects of exogenous <strong>neurotensin</strong> (NT) infused into the ventral tegmental area (VTA) prompted us to examine the role in the VTA of the endogenous NT in behavioral <b>sensitization</b> to amphetamine.
+NEUROTENSIN	drug	amphetamine	14751589	Excitotoxic lesions of the prefrontal cortex attenuate the potentiation of <b>amphetamine</b> induced locomotion by repeated <strong>neurotensin</strong> receptor activation.
+NEUROTENSIN	drug	amphetamine	14751589	This study was aimed at determining the role of prefrontal cortex neurons in the development of the potentiation of <b>amphetamine</b> induced locomotor activity by repeated central injections of D Tyr[11]<strong>neurotensin</strong>.
+NEUROTENSIN	drug	amphetamine	14751589	However, sham rats pre exposed to the high dose of D Tyr[11]<strong>neurotensin</strong> showed stronger non ambulatory and vertical movements than saline pre exposed rats when tested with <b>amphetamine</b>; this sensitization effect was not observed in lesioned rats.
+NEUROTENSIN	addiction	sensitization	14751589	However, sham rats pre exposed to the high dose of D Tyr[11]<strong>neurotensin</strong> showed stronger non ambulatory and vertical movements than saline pre exposed rats when tested with amphetamine; this <b>sensitization</b> effect was not observed in lesioned rats.
+NEUROTENSIN	drug	amphetamine	14751589	The present results show that prefrontal cortex neurons are part of the neural circuitry involved in the development of <b>amphetamine</b> sensitization by repeated activation of central <strong>neurotensin</strong> receptors.
+NEUROTENSIN	addiction	sensitization	14751589	The present results show that prefrontal cortex neurons are part of the neural circuitry involved in the development of amphetamine <b>sensitization</b> by repeated activation of central <strong>neurotensin</strong> receptors.
+NEUROTENSIN	drug	nicotine	12850594	Novel <strong>neurotensin</strong> analog blocks the initiation and expression of <b>nicotine</b> induced locomotor sensitization.
+NEUROTENSIN	addiction	sensitization	12850594	Novel <strong>neurotensin</strong> analog blocks the initiation and expression of nicotine induced locomotor <b>sensitization</b>.
+NEUROTENSIN	drug	nicotine	12850594	<strong>Neurotensin</strong> is a tridecapeptide that participates in regulation of dopaminergic pathways implicated in <b>nicotine</b> addiction.
+NEUROTENSIN	addiction	addiction	12850594	<strong>Neurotensin</strong> is a tridecapeptide that participates in regulation of dopaminergic pathways implicated in nicotine <b>addiction</b>.
+NEUROTENSIN	drug	nicotine	12850594	Previously, we showed that one of our brain penetrating <strong>neurotensin</strong> analogs, NT69L, blocks <b>nicotine</b> induced locomotor sensitization.
+NEUROTENSIN	addiction	sensitization	12850594	Previously, we showed that one of our brain penetrating <strong>neurotensin</strong> analogs, NT69L, blocks nicotine induced locomotor <b>sensitization</b>.
+NEUROTENSIN	drug	nicotine	12498914	Blockade of <b>nicotine</b> induced locomotor sensitization by a novel <strong>neurotensin</strong> analog in rats.
+NEUROTENSIN	addiction	sensitization	12498914	Blockade of nicotine induced locomotor <b>sensitization</b> by a novel <strong>neurotensin</strong> analog in rats.
+NEUROTENSIN	drug	amphetamine	12498914	Previously we showed that one of our brain penetrating <strong>neurotensin</strong> analogs, NT69L (N met L Arg, L Lys, L Pro, L neo Trp, L tert Leu, L Leu), blocks cocaine  and D <b>amphetamine</b> induced hyperactivity in rats.
+NEUROTENSIN	drug	cocaine	12498914	Previously we showed that one of our brain penetrating <strong>neurotensin</strong> analogs, NT69L (N met L Arg, L Lys, L Pro, L neo Trp, L tert Leu, L Leu), blocks <b>cocaine</b>  and D amphetamine induced hyperactivity in rats.
+NEUROTENSIN	drug	nicotine	12498914	The present study is the first report, to our knowledge, of a possible role for <strong>neurotensin</strong> in the development of <b>nicotine</b> dependence, and suggests that <strong>neurotensin</strong> analogs such as NT69L may be explored as treatment for <b>nicotine</b> and other psychostimulant abuse.
+NEUROTENSIN	addiction	dependence	12498914	The present study is the first report, to our knowledge, of a possible role for <strong>neurotensin</strong> in the development of nicotine <b>dependence</b>, and suggests that <strong>neurotensin</strong> analogs such as NT69L may be explored as treatment for nicotine and other psychostimulant abuse.
+NEUROTENSIN	drug	amphetamine	11779043	The <strong>neurotensin</strong> receptor antagonist, SR48692, attenuates the expression of <b>amphetamine</b> induced behavioural sensitisation in mice.
+NEUROTENSIN	drug	amphetamine	11779043	The effects of acute administration of the <strong>neurotensin</strong> receptor antagonist, SR48692 (2 [[1 (7 chloroquinolin 4 yl) 5 (2,6 dimethoxyphenyl) 1H pyrazol 3 carbonyl]amino]adamantane 2 carboxylic acid), on <b>amphetamine</b> induced behavioural sensitisation were studied with the locomotor activity of mice in an open field as an experimental parameter.
+NEUROTENSIN	drug	amphetamine	11751033	Chronic blockade of <strong>neurotensin</strong> receptors strongly reduces sensitized, but not acute, behavioral response to D <b>amphetamine</b>.
+NEUROTENSIN	drug	amphetamine	11751033	This study investigated the effect of a chronic blockade of <strong>neurotensin</strong> (NT) receptors on the sensitized behavioral response to <b>amphetamine</b> using a nonpeptide NT receptor antagonist, SR 48692.
+NEUROTENSIN	drug	amphetamine	11440814	Despite the administration of haloperidol and D <b>amphetamine</b> to elicit and enhance <strong>neurotensin</strong>/neuromedin N messenger RNA expression in striatum, including the nucleus accumbens and olfactory tubercle, no double labeled neurons were observed there.
+NEUROTENSIN	drug	psychedelics	11407274	In addition, although it has not been mentioned much in the literature, <b>MDMA</b> disturbs dopaminergic function either directly, or through the peptidergic systems (<strong>neurotensin</strong>, substance P, dynorphines).
+NEUROTENSIN	drug	amphetamine	11182247	Differential effects of cocaine and <b>methamphetamine</b> on <strong>neurotensin</strong>/neuromedin N and preprotachykinin messenger RNA expression in unique regions of the striatum.
+NEUROTENSIN	drug	cocaine	11182247	Differential effects of <b>cocaine</b> and methamphetamine on <strong>neurotensin</strong>/neuromedin N and preprotachykinin messenger RNA expression in unique regions of the striatum.
+NEUROTENSIN	drug	amphetamine	11182247	This study employed in situ hybridization to directly compare the effects of cocaine and <b>methamphetamine</b> on <strong>neurotensin</strong>/neuromedin N and preprotachykinin messenger RNAs in distinct striatal regions.
+NEUROTENSIN	drug	cocaine	11182247	This study employed in situ hybridization to directly compare the effects of <b>cocaine</b> and methamphetamine on <strong>neurotensin</strong>/neuromedin N and preprotachykinin messenger RNAs in distinct striatal regions.
+NEUROTENSIN	drug	amphetamine	11182247	The pattern of changes in <strong>neurotensin</strong>/neuromedin N messenger RNA caused by <b>methamphetamine</b> and cocaine after 3h was even more distinct.
+NEUROTENSIN	drug	cocaine	11182247	The pattern of changes in <strong>neurotensin</strong>/neuromedin N messenger RNA caused by methamphetamine and <b>cocaine</b> after 3h was even more distinct.
+NEUROTENSIN	drug	amphetamine	11182247	Cocaine produced significant increases in <strong>neurotensin</strong>/neuromedin N messenger RNA in all regions of the rostral striatum, whereas <b>methamphetamine</b> had no effect in these areas.
+NEUROTENSIN	drug	cocaine	11182247	<b>Cocaine</b> produced significant increases in <strong>neurotensin</strong>/neuromedin N messenger RNA in all regions of the rostral striatum, whereas methamphetamine had no effect in these areas.
+NEUROTENSIN	drug	amphetamine	11182247	Furthermore, in more caudal sections, cocaine predominantly affected <strong>neurotensin</strong>/neuromedin N expression in dorsal aspects of the striatum, whereas <b>methamphetamine</b> significantly increased <strong>neurotensin</strong>/neuromedin N messenger RNA in all regions.
+NEUROTENSIN	drug	cocaine	11182247	Furthermore, in more caudal sections, <b>cocaine</b> predominantly affected <strong>neurotensin</strong>/neuromedin N expression in dorsal aspects of the striatum, whereas methamphetamine significantly increased <strong>neurotensin</strong>/neuromedin N messenger RNA in all regions.
+NEUROTENSIN	drug	amphetamine	11182247	The only significant effect was an increase in <strong>neurotensin</strong>/neuromedin N messenger RNA in the core region 3h after <b>methamphetamine</b> administration.
+NEUROTENSIN	drug	amphetamine	11182247	These results indicate that <b>methamphetamine</b> and cocaine increase preprotachykinin and <strong>neurotensin</strong>/neuromedin N messenger RNAs in distinct regions of the striatum.
+NEUROTENSIN	drug	cocaine	11182247	These results indicate that methamphetamine and <b>cocaine</b> increase preprotachykinin and <strong>neurotensin</strong>/neuromedin N messenger RNAs in distinct regions of the striatum.
+NEUROTENSIN	drug	cannabinoid	11103879	Drugs that do not have affinity for dopamine receptors but act through <strong>neurotensin</strong>, sigma or <b>cannabinoid</b> CB1 receptors or glutamatergic mechanisms are currently being evaluated.
+NEUROTENSIN	drug	alcohol	10888062	<strong>Neurotensin</strong> receptors in the neurons of the ventral tegmental area facilitate dopamine release, making the <strong>neurotensin</strong> gene an excellent candidate gene for <b>alcohol</b> dependence and for other behaviors that involve reinforcement.
+NEUROTENSIN	addiction	dependence	10888062	<strong>Neurotensin</strong> receptors in the neurons of the ventral tegmental area facilitate dopamine release, making the <strong>neurotensin</strong> gene an excellent candidate gene for alcohol <b>dependence</b> and for other behaviors that involve reinforcement.
+NEUROTENSIN	addiction	reward	10888062	<strong>Neurotensin</strong> receptors in the neurons of the ventral tegmental area facilitate dopamine release, making the <strong>neurotensin</strong> gene an excellent candidate gene for alcohol dependence and for other behaviors that involve <b>reinforcement</b>.
+NEUROTENSIN	drug	amphetamine	10884569	Evidence for a role of endogenous <strong>neurotensin</strong> in the initiation of <b>amphetamine</b> sensitization.
+NEUROTENSIN	addiction	sensitization	10884569	Evidence for a role of endogenous <strong>neurotensin</strong> in the initiation of amphetamine <b>sensitization</b>.
+NEUROTENSIN	drug	amphetamine	10884569	This study was aimed at testing the hypothesis that endogenous <strong>neurotensin</strong> plays a role in the initiation of sensitization to the locomotor activating effect of <b>amphetamine</b>.
+NEUROTENSIN	addiction	sensitization	10884569	This study was aimed at testing the hypothesis that endogenous <strong>neurotensin</strong> plays a role in the initiation of <b>sensitization</b> to the locomotor activating effect of amphetamine.
+NEUROTENSIN	drug	amphetamine	10884569	During an initial training phase, different groups of male rats were injected on four occasions (every second day: Days 1, 3, 5 and 7) with one of three doses (40, 80 or 160 microg/kg, ip) of the <strong>neurotensin</strong> antagonist, SR 48692, or its vehicle, followed 30 min later by <b>amphetamine</b> (1.5 mg/kg, ip), or saline.
+NEUROTENSIN	drug	amphetamine	10884569	The present results demonstrate that activation of <strong>neurotensin</strong> receptors by endogenous <strong>neurotensin</strong> is required for the initiation of <b>amphetamine</b> sensitization.
+NEUROTENSIN	addiction	sensitization	10884569	The present results demonstrate that activation of <strong>neurotensin</strong> receptors by endogenous <strong>neurotensin</strong> is required for the initiation of amphetamine <b>sensitization</b>.
+NEUROTENSIN	drug	psychedelics	10564747	Because <b>ibogaine</b> influences the activity of <strong>neurotensin</strong> systems, a dopamine linked neuropeptide, the present study investigated if <b>ibogaine</b> also influences dynorphin (DYN) pathways.
+NEUROTENSIN	drug	psychedelics	10564747	Unlike <strong>neurotensin</strong> responses, <b>ibogaine</b> alone did not alter DYN levels in the striatum, substantia nigra or nucleus accumbens.
+NEUROTENSIN	drug	opioid	10375678	Dual immunofluorescence labelling showed that PKCgamma was not randomly distributed amongst non GABAergic neurons, since it was present in 76% of cells with <strong>neurotensin</strong> and 45% of those with somatostatin, but only 5% of those with the mu <b>opioid</b> receptor (MOR 1).
+NEUROTENSIN	addiction	reward	10372570	Activation of the VTA dopamine (DA) system may produce <b>reinforcing</b> effects in general because (a) <strong>neurotensin</strong> is self administered into the VTA, and injection of <strong>neurotensin</strong> into the VTA produces <b>CPP</b> and enhances DA release in the nucleus accumbens (NAC), and (b) GABA(A) antagonists are self administered into the anterior VTA and injections of GABA(A) antagonists into the anterior VTA enhance DA release in the NAC.
+NEUROTENSIN	drug	cocaine	9914442	Differential responses by <strong>neurotensin</strong> systems in extrapyramidal and limbic structures to ibogaine and <b>cocaine</b>.
+NEUROTENSIN	drug	psychedelics	9914442	Differential responses by <strong>neurotensin</strong> systems in extrapyramidal and limbic structures to <b>ibogaine</b> and cocaine.
+NEUROTENSIN	drug	amphetamine	9914442	Since previous studies demonstrated differential effects of psychotomimetic drugs (cocaine and <b>methamphetamine</b>) on neuropeptides such as <strong>neurotensin</strong> (NT), the present study was designed to determine: (1) the effects of ibogaine on striatal, nigral, cortical, and accumbens <strong>neurotensin</strong> like immunoreactivity (NTLI); (2) the effects of selective dopamine antagonists on ibogaine induced changes in NT concentrations in these brain areas; and (3) the effects of ibogaine pretreatment on cocaine induced changes in striatal, nigral, cortical and accumbens NTLI content.
+NEUROTENSIN	drug	cocaine	9914442	Since previous studies demonstrated differential effects of psychotomimetic drugs (<b>cocaine</b> and methamphetamine) on neuropeptides such as <strong>neurotensin</strong> (NT), the present study was designed to determine: (1) the effects of ibogaine on striatal, nigral, cortical, and accumbens <strong>neurotensin</strong> like immunoreactivity (NTLI); (2) the effects of selective dopamine antagonists on ibogaine induced changes in NT concentrations in these brain areas; and (3) the effects of ibogaine pretreatment on <b>cocaine</b> induced changes in striatal, nigral, cortical and accumbens NTLI content.
+NEUROTENSIN	drug	psychedelics	9914442	Since previous studies demonstrated differential effects of psychotomimetic drugs (cocaine and methamphetamine) on neuropeptides such as <strong>neurotensin</strong> (NT), the present study was designed to determine: (1) the effects of <b>ibogaine</b> on striatal, nigral, cortical, and accumbens <strong>neurotensin</strong> like immunoreactivity (NTLI); (2) the effects of selective dopamine antagonists on <b>ibogaine</b> induced changes in NT concentrations in these brain areas; and (3) the effects of <b>ibogaine</b> pretreatment on cocaine induced changes in striatal, nigral, cortical and accumbens NTLI content.
+NEUROTENSIN	addiction	sensitization	9795122	In addition to the behavioral <b>sensitization</b>, Amp pretreated rats showed a reduction in the ability of the acute Amp challenge to induce c fos mRNA in the medial prefrontal cortex and <strong>neurotensin</strong>/neuromedin N (NT/N) mRNA in the nucleus accumbens shell.
+NEUROTENSIN	addiction	sensitization	9795122	In addition to the behavioral <b>sensitization</b>, Amp pretreated rats showed a reduction in the ability of the acute Amp challenge to induce c fos mRNA in the medial prefrontal cortex and <strong>neurotensin</strong>/neuromedin N (<strong>NT/N</strong>) mRNA in the nucleus accumbens shell.
+NEUROTENSIN	addiction	sensitization	9795122	At doses that blocked the initiation of behavioral <b>sensitization</b> to Amp, clozapine fully and haloperidol partially restored the capacity of acute Amp to induce c fos and <strong>NT/N</strong> gene expression.
+NEUROTENSIN	addiction	sensitization	9655895	Accompanying behavioral <b>sensitization</b> were two postsynaptic neuroadaptive responses: reduction in the ability of Amp to induce c fos gene expression in the infralimbic/ventral prelimbic cortex and <strong>NT/N</strong> mRNA in the accumbal shell.
+NEUROTENSIN	drug	amphetamine	9218694	Repeated activation of <strong>neurotensin</strong> receptors sensitizes to the stimulant effect of <b>amphetamine</b>.
+NEUROTENSIN	drug	cocaine	9073175	Chronic <b>cocaine</b> increases <strong>neurotensin</strong> gene expression in the shell of the nucleus accumbens and in discrete regions of the striatum.
+NEUROTENSIN	drug	cocaine	9073175	The effects of chronic <b>cocaine</b> administration on <strong>neurotensin</strong> (NT) mRNA expression were investigated in the rat brain using in situ hybridization.
+NEUROTENSIN	drug	alcohol	8724449	<strong>Neurotensin</strong> attenuates the reduction in <b>alcohol</b> drinking produced by angiotensin II.
+NEUROTENSIN	drug	alcohol	8724449	<strong>Neurotensin</strong> enhances some of the behavioral effects of <b>alcohol</b> including motor impairment, narcosis, hypothermia and also interacts with some of the physiological actions of angiotensin (ANG) II including aldosterone release and increased blood pressure.
+NEUROTENSIN	drug	alcohol	8724449	The present study is the first to examine the interaction between <strong>neurotensin</strong> and angiotensin in the behavioral context of oral <b>alcohol</b> self administration.
+NEUROTENSIN	drug	alcohol	8724449	<strong>Neurotensin</strong> alone did not affect <b>alcohol</b> intake at any of the doses tested but did attenuate, in a dose dependent fashion, the reduction in <b>alcohol</b> intake produced by ANG II.
+NEUROTENSIN	drug	alcohol	8724449	These results demonstrate <strong>neurotensin</strong>'s ability to alter the behavioral effect of ANG II on <b>alcohol</b> intake.
+NEUROTENSIN	drug	alcohol	8741146	Effects of <b>ethanol</b> administration on brain <strong>neurotensin</strong> like immunoreactivity in rats.
+NEUROTENSIN	drug	alcohol	8741146	The effects of acute and chronic <b>ethanol</b> administration on <strong>neurotensin</strong> like immunoreactivity (NTLI) were investigated in discrete regions of the rat brain.
+NEUROTENSIN	drug	amphetamine	7758407	The participants in this symposium discussed evidence that (i) the initiation of stimulant induced behavioral sensitization involves NMDA receptor stimulation in the ventral tegmental area (VTA), (ii) competitive and non competitive NMDA antagonists block the dopaminergic neurotoxic actions of <b>methamphetamine</b>, and (iii) NMDA receptor antagonists block cocaine and <b>methamphetamine</b> induced increases in striatal <strong>neurotensin</strong> and dynorphin expression.
+NEUROTENSIN	drug	cocaine	7758407	The participants in this symposium discussed evidence that (i) the initiation of stimulant induced behavioral sensitization involves NMDA receptor stimulation in the ventral tegmental area (VTA), (ii) competitive and non competitive NMDA antagonists block the dopaminergic neurotoxic actions of methamphetamine, and (iii) NMDA receptor antagonists block <b>cocaine</b> and methamphetamine induced increases in striatal <strong>neurotensin</strong> and dynorphin expression.
+NEUROTENSIN	addiction	sensitization	7758407	The participants in this symposium discussed evidence that (i) the initiation of stimulant induced behavioral <b>sensitization</b> involves NMDA receptor stimulation in the ventral tegmental area (VTA), (ii) competitive and non competitive NMDA antagonists block the dopaminergic neurotoxic actions of methamphetamine, and (iii) NMDA receptor antagonists block cocaine and methamphetamine induced increases in striatal <strong>neurotensin</strong> and dynorphin expression.
+NEUROTENSIN	drug	cocaine	7865101	Preexposure to, but not cotreatment with, the <strong>neurotensin</strong> antagonist SR 48692 delays the development of <b>cocaine</b> sensitization.
+NEUROTENSIN	addiction	sensitization	7865101	Preexposure to, but not cotreatment with, the <strong>neurotensin</strong> antagonist SR 48692 delays the development of cocaine <b>sensitization</b>.
+NEUROTENSIN	drug	cocaine	7865101	This study examined the role of <strong>neurotensin</strong> (NT) in the development of <b>cocaine</b> sensitization using the novel nonpeptide NT antagonist SR 48692.
+NEUROTENSIN	addiction	sensitization	7865101	This study examined the role of <strong>neurotensin</strong> (NT) in the development of cocaine <b>sensitization</b> using the novel nonpeptide NT antagonist SR 48692.
+NEUROTENSIN	addiction	sensitization	7846201	The behavioral <b>sensitization</b> produced by daily <strong>neurotensin</strong> microinjection into the ventral tegmental area was also prevented by the coadministration of H8.
+NEUROTENSIN	drug	cocaine	8242350	<strong>Neurotensin</strong> injected into the nucleus accumbens blocks the psychostimulant effects of <b>cocaine</b> but does not attenuate <b>cocaine</b> self administration in the rat.
+NEUROTENSIN	drug	cocaine	8242350	In the present study, the hypothesis that <strong>neurotensin</strong> injected into the nucleus accumbens might modulate the psychostimulant and reinforcing actions of <b>cocaine</b> was tested.
+NEUROTENSIN	addiction	reward	8242350	In the present study, the hypothesis that <strong>neurotensin</strong> injected into the nucleus accumbens might modulate the psychostimulant and <b>reinforcing</b> actions of cocaine was tested.
+NEUROTENSIN	drug	cocaine	8242350	No significant effects were found with any of the doses of <strong>neurotensin</strong> tested on the self administration of <b>cocaine</b>.
+NEUROTENSIN	drug	cocaine	8242350	However, in experiment 2, <strong>neurotensin</strong> at doses of 4.2 and 16.7 micrograms injected into the nucleus accumbens significantly reduced the locomotor activation induced by an acute injection of <b>cocaine</b> (15 mg/kg i.p.)
+NEUROTENSIN	drug	cocaine	8242350	Thus, <strong>neurotensin</strong> in the nucleus accumbens appears to specifically modulate the acute locomotor activating properties of <b>cocaine</b> but not <b>cocaine</b> self administration.
+NEUROTENSIN	drug	cocaine	8507352	Chronic continuous or intermittent infusion of <b>cocaine</b> differentially alter the concentration of <strong>neurotensin</strong> like immunoreactivity in specific rat brain regions.
+NEUROTENSIN	drug	alcohol	8100076	Chronic <b>ethanol</b> administration downregulates <strong>neurotensin</strong> receptors in long  and short sleep mice.
+NEUROTENSIN	drug	alcohol	8100076	<strong>Neurotensin</strong> (NT) has been shown to differentially alter many of the physiologic responses to <b>ethanol</b> administration in long sleep (LS) and short sleep (SS) mice, which were selectively bred for differences in hypnotic sensitivity to <b>ethanol</b>.
+NEUROTENSIN	drug	alcohol	8100076	The finding that both acute and chronic <b>ethanol</b> significantly downregulate the <strong>neurotensin</strong> receptor systems further supports the hypothesis that <b>ethanol</b>'s actions may be mediated in part by neurotensinergic systems.
+NEUROTENSIN	addiction	reward	1319909	Facilitation of brain stimulation <b>reward</b> by mesencephalic injections of <strong>neurotensin</strong> (1 13).
+NEUROTENSIN	addiction	reward	1319909	The effects on brain stimulation <b>reward</b> of <strong>neurotensin</strong> (1 13) microinjected at different concentrations (2.5, 5, 10 and 20 micrograms/0.5 microliters) into the ventral mesencephalic region containing mesocorticolimbic dopamine neurons were tested in 12 male rats.
+NEUROTENSIN	addiction	reward	1319909	<strong>Neurotensin</strong> lowered the stimulation frequency required to sustain threshold levels of responding for brain stimulation <b>reward</b>, suggesting that this neuropeptide is involved in modulating the activity of dopamine neurons that mediate behaviors motivated by positive reinforces.
+NEUROTENSIN	addiction	reward	1319909	The magnitude of the facilitatory effect of <strong>neurotensin</strong> on brain stimulation <b>reward</b> was dependent on the concentration injected and to a significant extent also on whether the peptide was administered in an ascending or a descending order of concentration.
+NEUROTENSIN	drug	opioid	1319909	Subsequent injection of <b>morphine</b> (2.5 5 micrograms/0.5 microliter) into the same site produced a weaker facilitation of brain stimulation reward than expected, suggesting that local damage after multiple central injections or prior injections of <strong>neurotensin</strong> itself reduced the responsiveness of dopamine neurons to opiates.
+NEUROTENSIN	addiction	reward	1319909	Subsequent injection of morphine (2.5 5 micrograms/0.5 microliter) into the same site produced a weaker facilitation of brain stimulation <b>reward</b> than expected, suggesting that local damage after multiple central injections or prior injections of <strong>neurotensin</strong> itself reduced the responsiveness of dopamine neurons to opiates.
+NEUROTENSIN	addiction	reward	1319909	Taken together, the results are consistent with data indicating that activation of <strong>neurotensin</strong> receptors in the ventral mesencephalon stimulates dopamine cell firing and axonal dopamine release in limbic terminal fields and suggest that endogenous <strong>neurotensin</strong> is involved in the control of behavior motivated by positive <b>reinforcement</b>.
+NEUROTENSIN	drug	opioid	1726061	Distribution of excitatory and inhibitory amino acid, sigma, monoamine, catecholamine, acetylcholine, <b>opioid</b>, <strong>neurotensin</strong>, substance P, adenosine and neuropeptide Y receptors in human motor and somatosensory cortex.
+NEUROTENSIN	drug	benzodiazepine	1726061	Autoradiography was used to visualise N methyl D aspartate, phencyclidine, strychnine insensitive glycine, alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid, kainic acid, <b>benzodiazepine</b>, gamma aminobutyric acid type A, sigma, serotonergic, dopaminergic, alpha 2 adrenergic, beta adrenergic, muscarinic cholinergic, nicotinic, opioid, <strong>neurotensin</strong>, substance P, adenosine A1 and neuropeptide Y receptors in the human primary motor (Brodmann's area 4) and somatosensory cortex (Brodmann's areas 3, 2 and 1).
+NEUROTENSIN	drug	opioid	1726061	Autoradiography was used to visualise N methyl D aspartate, phencyclidine, strychnine insensitive glycine, alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid, kainic acid, benzodiazepine, gamma aminobutyric acid type A, sigma, serotonergic, dopaminergic, alpha 2 adrenergic, beta adrenergic, muscarinic cholinergic, nicotinic, <b>opioid</b>, <strong>neurotensin</strong>, substance P, adenosine A1 and neuropeptide Y receptors in the human primary motor (Brodmann's area 4) and somatosensory cortex (Brodmann's areas 3, 2 and 1).
+NEUROTENSIN	drug	cocaine	1821482	Chronic <b>cocaine</b> administration and withdrawal of <b>cocaine</b> modify <strong>neurotensin</strong> binding in rat brain.
+NEUROTENSIN	addiction	withdrawal	1821482	Chronic cocaine administration and <b>withdrawal</b> of cocaine modify <strong>neurotensin</strong> binding in rat brain.
+NEUROTENSIN	drug	cocaine	1821482	<strong>Neurotensin</strong> (NT) is a peptide colocalized with dopamine (DA) within some mesocorticolimbic DA neurons that are affected by <b>cocaine</b>.
+NEUROTENSIN	drug	opioid	1709289	In the present experiments, substance P (SP), <strong>neurotensin</strong> (NT), d ala metenkephalin (DALA) and <b>morphine</b> sulfate (MS) were injected bilaterally into the VTA and their effects on conditioned reinforcement were assessed.
+NEUROTENSIN	addiction	reward	1709289	In the present experiments, substance P (SP), <strong>neurotensin</strong> (NT), d ala metenkephalin (DALA) and morphine sulfate (MS) were injected bilaterally into the VTA and their effects on conditioned <b>reinforcement</b> were assessed.
+NEUROTENSIN	drug	cocaine	1652092	Chronic <b>cocaine</b> administration and withdrawal from <b>cocaine</b> modify central <strong>neurotensin</strong> receptors in rats.
+NEUROTENSIN	addiction	withdrawal	1652092	Chronic cocaine administration and <b>withdrawal</b> from cocaine modify central <strong>neurotensin</strong> receptors in rats.
+NEUROTENSIN	addiction	reward	2471221	<strong>Neurotensin</strong>, substance P, neurokinin alpha, and enkephalin: injection into ventral tegmental area in the rat produces differential effects on <b>operant</b> responding.
+NEUROTENSIN	drug	amphetamine	2906429	Qualitative generalization to the vehicle occurred after injecting 10, 20 and 200 micrograms/kg unsulfated CCK 8, 10, 20 and 200 micrograms/kg CCK 4, 5 micrograms/kg CCK 8 and 1 microgram/kg caerulein, <strong>neurotensin</strong> or bombesin and 200 micrograms/kg apomorphine or 320 micrograms/kg <b>amphetamine</b>.
+NEUROTENSIN	addiction	dependence	2887481	Calcium <b>dependence</b> of <strong>neurotensin</strong> stimulation of circular colonic muscle of the rabbit.
+NEUROTENSIN	drug	opioid	2887481	<strong>Neurotensin</strong> stimulation of both proximal and distal colon was unaffected by tetrodotoxin, phentolamine, propranolol, <b>naloxone</b>, or atropine.
+NEUROTENSIN	drug	alcohol	2950866	Calcium influence on <strong>neurotensin</strong> and beta endorphin enhancement of <b>ethanol</b> sensitivity in selectively bred mouse lines.
+NEUROTENSIN	drug	alcohol	2950866	Intracerebroventricular (icv) administration of <strong>neurotensin</strong> produced a dose dependent increase in <b>ethanol</b> sensitivity as measured by blood <b>ethanol</b> concentration at loss of righting reflex in SS/Ibg (SS) but not in LS/Ibg (LS) mice.
+NEUROTENSIN	drug	alcohol	2950866	Concurrent icv administration of calcium and <strong>neurotensin</strong> resulted in an additional enhancement of sensitivity to <b>ethanol</b> over that seen with either substance alone in both mouse lines.
+NEUROTENSIN	drug	alcohol	2950866	These results suggest a specific interaction of calcium and <strong>neurotensin</strong> may be involved in the mechanism through which <b>ethanol</b> elicits intoxication.
+NEUROTENSIN	addiction	intoxication	2950866	These results suggest a specific interaction of calcium and <strong>neurotensin</strong> may be involved in the mechanism through which ethanol elicits <b>intoxication</b>.
+NEUROTENSIN	drug	alcohol	3010391	A number of peptides, including cholecystokinin (CCK), <strong>neurotensin</strong>, and bombesin, have been shown to interact with the CNS actions of <b>alcohol</b> and may play a role in <b>alcohol</b> withdrawal.
+NEUROTENSIN	addiction	withdrawal	3010391	A number of peptides, including cholecystokinin (CCK), <strong>neurotensin</strong>, and bombesin, have been shown to interact with the CNS actions of alcohol and may play a role in alcohol <b>withdrawal</b>.
+NEUROTENSIN	drug	nicotine	2412241	None of the other neuropeptides measure, substance P, <strong>neurotensin</strong>, or [met5] enkephalin was altered by <b>nicotine</b> treatment.
+NEUROTENSIN	addiction	reward	2417253	Studies employing conditioned <b>operant</b> behavior of squirrel monkeys, rabbits and pigeons have demonstrated that the neuroactive peptides thyrotropin releasing hormone (TRH), substance P (SP) and <strong>neurotensin</strong> (NT) produce marked behavioral effects under a wide range of procedures.
+NEUROTENSIN	drug	alcohol	6820242	Effects of <strong>neurotensin</strong> on the actions of barbiturates and <b>ethanol</b>.
+NEUROTENSIN	drug	alcohol	6267562	<b>Ethanol</b> (3.5 g/kg, IP) given simultaneously with <strong>neurotensin</strong> (30 micrograms, IC), bombesin (30 micrograms, IC) or beta endorphin (20 micrograms, IC) caused a greater impairment of the reflex than <b>ethanol</b> alone.
+NEUROTENSIN	drug	alcohol	6267562	TRH (10 100 micrograms, IC, or 1 40 mg/kg, IV) and <strong>neurotensin</strong> (10 100 micrograms, IC) had no effect on these <b>ethanol</b> withdrawal signs.
+NEUROTENSIN	addiction	withdrawal	6267562	TRH (10 100 micrograms, IC, or 1 40 mg/kg, IV) and <strong>neurotensin</strong> (10 100 micrograms, IC) had no effect on these ethanol <b>withdrawal</b> signs.
+NEUROTENSIN	drug	alcohol	6267562	Because TRH, <strong>neurotensin</strong>, bombesin and beta endorphin do not alter all actions of <b>ethanol</b> in the same way, an interaction of <b>ethanol</b> with many functionally independent neuronal circuits is suggested.
+CYP3A4	drug	benzodiazepine	32354497	To clarify the cause of cardiogenic shock, we performed whole exome sequencing and screened relative single nucleotide variants of 2 cytochrome P450 (CYP) isoforms, <strong>CYP3A4</strong> and CYP3A5, which play a dominant role in the metabolic elimination of <b>midazolam</b>.
+CYP3A4	drug	alcohol	32336193	<strong>CYP3A</strong> subfamily activity affects the equilibrium concentration of Phenazepam® in patients with anxiety disorders and comorbid <b>alcohol</b> use disorder.
+CYP3A4	drug	opioid	32302325	Although <strong>CYP3A4</strong> was conventionally considered the principal <b>methadone</b> metabolizing enzyme, more recent data have identified CYP2B6 as the principal enzyme.
+CYP3A4	drug	opioid	31929398	The AUC ratios of norbuprenorphine and norbuprenorphine glucuronide to <b>buprenorphine</b>, a measure of <strong>CYP3A</strong> mediated N demethylation, were 1.89, 1.84, and 1.33 during the 1 and 2, 3 trimesters, and postpartum, respectively.
+CYP3A4	drug	opioid	31676110	We conducted a retrospective cohort study of 113 patients undergoing <b>buprenorphine</b> based OUD management in Northeast Washington D.C. to determine if clinical pharmacogenomics testing for <strong>CYP3A4</strong> and CYP3A5 would impact treatment outcomes.
+CYP3A4	drug	cocaine	31257858	Sequentially, we looked into the detail of (1) the addiction to <b>cocaine</b> and fentanyl by binding to the dopamine transporter and the μ opioid receptor (DAT and μOR, respectively), (2) the potential drug drug interaction of <b>cocaine</b> and fentanyl via p glycoprotein (P gp) efflux, (3) the metabolism of <b>cocaine</b> and fentanyl in <strong>CYP3A4</strong>, and (4) the physiologically based pharmacokinetic (PBPK) model for two drugs and their drug drug interaction at the absorption, distribution, metabolism, and excretion (ADME) level.
+CYP3A4	drug	opioid	31257858	Sequentially, we looked into the detail of (1) the addiction to cocaine and <b>fentanyl</b> by binding to the dopamine transporter and the μ <b>opioid</b> receptor (DAT and μOR, respectively), (2) the potential drug drug interaction of cocaine and <b>fentanyl</b> via p glycoprotein (P gp) efflux, (3) the metabolism of cocaine and <b>fentanyl</b> in <strong>CYP3A4</strong>, and (4) the physiologically based pharmacokinetic (PBPK) model for two drugs and their drug drug interaction at the absorption, distribution, metabolism, and excretion (ADME) level.
+CYP3A4	addiction	addiction	31257858	Sequentially, we looked into the detail of (1) the <b>addiction</b> to cocaine and fentanyl by binding to the dopamine transporter and the μ opioid receptor (DAT and μOR, respectively), (2) the potential drug drug interaction of cocaine and fentanyl via p glycoprotein (P gp) efflux, (3) the metabolism of cocaine and fentanyl in <strong>CYP3A4</strong>, and (4) the physiologically based pharmacokinetic (PBPK) model for two drugs and their drug drug interaction at the absorption, distribution, metabolism, and excretion (ADME) level.
+CYP3A4	drug	opioid	31206401	<b>Methadone</b> is metabolized by several cytochrome P450 isoenzymes; primarily <strong>CYP3A4</strong>, CYP2B6, and CYP2D6 before renal and fecal elimination.
+CYP3A4	drug	opioid	31206401	Various studies demonstrate that through <strong>CYP3A4</strong> inhibition, grapefruit juice increases serum levels of <b>opioids</b>, such as <b>methadone</b>, though no clinically significant effects have been reported.
+CYP3A4	addiction	addiction	30916851	Dosing of major <strong>CYP3A</strong> substrate drugs needs to be reduced in palliative patients with haematological diseases, otherwise <b>escalation</b> of debilitating symptoms due to drug interactions might occur.
+CYP3A4	drug	benzodiazepine	30520338	<b>Clonazepam</b> undergoes nitroreduction to 7 amino <b>clonazepam</b> via <strong>CYP3A4</strong>/5, followed by acetylation to 7 acetamido <b>clonazepam</b> via NAT2 enzyme.
+CYP3A4	drug	opioid	30205091	<b>Methadone</b> undergoes N demethylation by multiple cytochrome P450 (CYP) enzymes including <strong>CYP3A4</strong>, CYP2B6, CYP2C19, CYP2D6, CYP2C9, and CYP2C8.
+CYP3A4	drug	opioid	30205091	In vivo, polymorphism effects on <b>methadone</b> systemic exposure have been noted for CYP2B6, <strong>CYP3A4</strong>, and CYP2D6.
+CYP3A4	drug	benzodiazepine	29375004	Metabolism of four <strong>CYP3A4</strong> probes (testosterone, <b>midazolam</b>, verapamil and atorvastatin) and three CYP2C9 probes (tolbutamide, diclofenac and S warfarin) in human liver microsomes (HLM) and cDNA expressed recombinant CYP450 (Rec CYP450) systems were characterized and RAFCL value was estimated as ratio of probe intrinsic clearance in HLM to that in Rec CYP450.
+CYP3A4	drug	alcohol	29343979	The primary aim of this study was to estimate the relationship between CYP3A5 gene polymorphism, activity of the <strong>CYP3A</strong> isoenzyme, and the risk of development of adverse drug reactions by haloperidol in patients with <b>alcohol</b> abuse.
+CYP3A4	drug	opioid	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, <strong>CYP3A4</strong>) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+CYP3A4	addiction	dependence	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP2D6, <strong>CYP3A4</strong>) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+CYP3A4	drug	benzodiazepine	28958437	Given that <b>clobazam</b> is primarily demethylated to N CLB by cytochrome P450 (CYP) enzyme, <strong>CYP3A4</strong>, the mean plasma time concentration profile of <b>clobazam</b> was unchanged with the exclusion of CYP2C19 poor metabolizers.
+CYP3A4	drug	psychedelics	28917081	<b>MDMA</b> exerted greater inhibitory effects on cytochrome P450 3A4 (<strong>CYP3A4</strong>) than on cytochrome P450 2D6 (CYP2D6).
+CYP3A4	drug	psychedelics	28917081	However, <b>MDMA</b> was introduced as CYP2D6 inhibitor; in this study, <b>MDMA</b> inhibited <strong>CYP3A4</strong> isoenzymes as well.
+CYP3A4	drug	alcohol	28787271	Genotyping and phenotyping of CYP2D6 and <strong>CYP3A</strong> isoenzymes in patients with <b>alcohol</b> use disorder: correlation with haloperidol plasma concentration.
+CYP3A4	drug	opioid	28263461	Initial in vitro studies identified <strong>CYP3A4</strong> as metabolizing <b>methadone</b>.
+CYP3A4	drug	opioid	28263461	Subsequently, by extrapolation, <strong>CYP3A4</strong> was long assumed to be responsible for clinical <b>methadone</b> disposition.
+CYP3A4	drug	opioid	28263461	It has now been unequivocally established that CYP2B6, not <strong>CYP3A4</strong>, is the principal determinant of <b>methadone</b> metabolism, clearance, elimination, and plasma concentrations in humans.
+CYP3A4	addiction	dependence	28238899	In the present study, therefore, the possibility of buffer condition <b>dependence</b> of the fraction metabolized by CYP2C8 (fm2C8) for repaglinide, a dual substrate of CYP2C8 and <strong>CYP3A4</strong>, was estimated using human liver microsomes under various buffer conditions.
+CYP3A4	drug	benzodiazepine	28238899	Montelukast and ketoconazole showed a potent and concentration dependent inhibition of CYP2C8 mediated paclitaxel 6α hydroxylation and <strong>CYP3A4</strong> mediated <b>triazolam</b> α hydroxylation, respectively, without dependence on the buffer condition.
+CYP3A4	addiction	dependence	28238899	Montelukast and ketoconazole showed a potent and concentration dependent inhibition of CYP2C8 mediated paclitaxel 6α hydroxylation and <strong>CYP3A4</strong> mediated triazolam α hydroxylation, respectively, without <b>dependence</b> on the buffer condition.
+CYP3A4	drug	opioid	27861439	It is a prodrug that is metabolized by cytochrome P450 (CYP) enzymes CYP2D6 and <strong>CYP3A4</strong> to its more potent <b>opioid</b> analgesic metabolites, particularly the O demethylation product M1.
+CYP3A4	drug	alcohol	27695358	In our previous investigation, we found a medium correlation between the efficacy and safety of haloperidol and the activity of <strong>CYP3A4</strong> in patients with <b>alcohol</b> abuse.
+CYP3A4	drug	benzodiazepine	27639091	Optimization of <b>Clonazepam</b> Therapy Adjusted to Patient's <strong>CYP3A</strong> Status and NAT2 Genotype.
+CYP3A4	drug	benzodiazepine	27639091	Since the prominent role in <b>clonazepam</b> nitro reduction and acetylation of 7 amino <b>clonazepam</b> is assigned to CYP3A and N acetyl transferase 2 enzymes, respectively, the association between the patients' CYP3A status (CYP3A5 genotype, <strong>CYP3A4</strong> expression) or N acetyl transferase 2 acetylator phenotype and <b>clonazepam</b> metabolism (plasma concentrations of <b>clonazepam</b> and 7 amino <b>clonazepam</b>) was evaluated in 98 psychiatric patients suffering from schizophrenia or bipolar disorders.
+CYP3A4	drug	benzodiazepine	27639091	Since the prominent role in <b>clonazepam</b> nitro reduction and acetylation of 7 amino <b>clonazepam</b> is assigned to <strong>CYP3A</strong> and N acetyl transferase 2 enzymes, respectively, the association between the patients' <strong>CYP3A</strong> status (CYP3A5 genotype, <strong>CYP3A4</strong> expression) or N acetyl transferase 2 acetylator phenotype and <b>clonazepam</b> metabolism (plasma concentrations of <b>clonazepam</b> and 7 amino <b>clonazepam</b>) was evaluated in 98 psychiatric patients suffering from schizophrenia or bipolar disorders.
+CYP3A4	drug	benzodiazepine	27639091	The patients' <strong>CYP3A4</strong> expression was found to be the major determinant of <b>clonazepam</b> plasma concentrations normalized by the dose and bodyweight (1263.5±482.9 and 558.5±202.4ng/mL per mg/kg bodyweight in low and normal expressers, respectively, P<.0001).
+CYP3A4	drug	benzodiazepine	27639091	Consequently, the dose requirement for the therapeutic concentration of <b>clonazepam</b> was substantially lower in low <strong>CYP3A4</strong> expresser patients than in normal expressers (0.029±0.011 vs 0.058±0.024mg/kg bodyweight, P<.0001).
+CYP3A4	drug	benzodiazepine	27639091	Furthermore, significantly higher (about 2 fold) plasma concentration ratio of 7 amino <b>clonazepam</b> and <b>clonazepam</b> was observed in the patients displaying normal <strong>CYP3A4</strong> expression and slower N acetylation than all the others.
+CYP3A4	drug	benzodiazepine	27639091	Prospective assaying of <strong>CYP3A4</strong> expression and N acetyl transferase 2 acetylator phenotype can better identify the patients with higher risk of adverse reactions and can facilitate the improvement of personalized <b>clonazepam</b> therapy and withdrawal regimen.
+CYP3A4	addiction	withdrawal	27639091	Prospective assaying of <strong>CYP3A4</strong> expression and N acetyl transferase 2 acetylator phenotype can better identify the patients with higher risk of adverse reactions and can facilitate the improvement of personalized clonazepam therapy and <b>withdrawal</b> regimen.
+CYP3A4	drug	psychedelics	27400739	The major CYP enzymes involved in the metabolism of 25I <b>NBOMe</b> and 25INBOH were identified as <strong>CYP3A4</strong> and CYP2D6, respectively.
+CYP3A4	drug	psychedelics	27400739	Users of 25I <b>NBOMe</b> may be subject to drug drug interactions (DDI) if 25I <b>NBOMe</b> is taken with a strong <strong>CYP3A4</strong> inhibitor.
+CYP3A4	drug	opioid	27286724	(S) <b>methadone</b> clearance was influenced by cytochrome P450 (CYP) 2B6 activity, ABCB1 3435C>T, and α 1 acid glycoprotein level, while (R) <b>methadone</b> clearance was influenced by CYP2B6 activity, POR*28, and <strong>CYP3A4</strong>*22.
+CYP3A4	drug	alcohol	30085479	EFFECT OF CARBAMAZEPINE ON THE ACTIVITY OF <strong>CYP3A4</strong> ISOENZYME IN PATIENTS WITH <b>ALCOHOL</b> ADDICTION.
+CYP3A4	addiction	addiction	30085479	EFFECT OF CARBAMAZEPINE ON THE ACTIVITY OF <strong>CYP3A4</strong> ISOENZYME IN PATIENTS WITH ALCOHOL <b>ADDICTION</b>.
+CYP3A4	drug	alcohol	30085479	The purpose of the study was to evaluate the effect of carbamazepine on the <strong>CYP3A4</strong> activity in patients with <b>alcohol</b> addiction.
+CYP3A4	addiction	addiction	30085479	The purpose of the study was to evaluate the effect of carbamazepine on the <strong>CYP3A4</strong> activity in patients with alcohol <b>addiction</b>.
+CYP3A4	addiction	dependence	30085479	The results were used to construct a plot and derive an equation of logarithmic regression reflecting the <b>dependence</b> of <strong>CYP3A4</strong> activity on the dose of carbamazepine: y = (5.5   9.1) x 10⁻⁵   ΔΔx².
+CYP3A4	drug	alcohol	30085479	These data demonstrate a statistically significant effect of carbamazepine on the activity of <strong>CYP3A4</strong> isoenzyme in patients with <b>alcohol</b> addiction treated by haloperidol.
+CYP3A4	addiction	addiction	30085479	These data demonstrate a statistically significant effect of carbamazepine on the activity of <strong>CYP3A4</strong> isoenzyme in patients with alcohol <b>addiction</b> treated by haloperidol.
+CYP3A4	drug	alcohol	26639694	<strong>CYP3A4</strong> activity and haloperidol effects in <b>alcohol</b> addicts.
+CYP3A4	drug	alcohol	26639694	To estimate the correlation between <strong>CYP3A4</strong> isoenzyme activity and the efficacy and safety of haloperidol in patients with <b>alcohol</b> abuse during the exacerbation of the addiction.
+CYP3A4	addiction	addiction	26639694	To estimate the correlation between <strong>CYP3A4</strong> isoenzyme activity and the efficacy and safety of haloperidol in patients with alcohol abuse during the exacerbation of the <b>addiction</b>.
+CYP3A4	addiction	addiction	26639694	Data analysis demonstrated a correlation between the activity of isoenzyme <strong>CYP3A4</strong> and the scores of pathological <b>addiction</b> (r1 =  0,36), HARS (r2 =  0,45), UKU Side Effect Rating Scale (r3 =  0.15) in the entire group (p < 0.05).
+CYP3A4	drug	alcohol	26639694	The results demonstrate the correlation between <strong>CYP3A4</strong> activities and the efficacy and safety of haloperidol in <b>alcohol</b> abusers during the exacerbation of the addiction.
+CYP3A4	addiction	addiction	26639694	The results demonstrate the correlation between <strong>CYP3A4</strong> activities and the efficacy and safety of haloperidol in alcohol abusers during the exacerbation of the <b>addiction</b>.
+CYP3A4	drug	opioid	26312962	Concurrent administration of <b>oxycodone</b> and phenytoin may cause, through induction of <strong>CYP3A4</strong> enzymes, decreased analgesic effects of <b>oxycodone</b>.
+CYP3A4	drug	benzodiazepine	26290405	Effect of buffer conditions on CYP2C8 mediated paclitaxel 6α hydroxylation and <strong>CYP3A4</strong> mediated <b>triazolam</b> α  and 4 hydroxylation by human liver microsomes.
+CYP3A4	drug	benzodiazepine	26290405	The present study investigated the effect of buffer components (phosphate or Tris HCl) and their concentration (10 200 mM) on the CYP2C8 and <strong>CYP3A4</strong> activities of HLM, using paclitaxel and <b>triazolam</b>, respectively, as marker substrates.
+CYP3A4	drug	cannabinoid	26002511	<strong>CYP3A4</strong> Mediates Oxidative Metabolism of the Synthetic <b>Cannabinoid</b> AKB 48.
+CYP3A4	drug	opioid	25556837	A modest correlation was observed between liver/intestinal <strong>CYP3A4</strong> activity and <b>methadone</b> dose at steady state (Spearman rank correlation coefficient [rs ] = 0.21, P = 0.06) but not with highest dose ever used (rs = 0.15, P = 0.18) or dose normalized R,S <b>methadone</b> trough concentrations (rs =  0.05, P = 0.64).
+CYP3A4	drug	opioid	25556837	Concomitant <strong>CYP3A4</strong> inhibitors only affected the relationship between <b>methadone</b> dose and R,S <b>methadone</b> trough concentration.
+CYP3A4	drug	opioid	25556837	<b>Methadone</b> maintenance dose was predicted by sociodemographic and clinical variables rather than genetic polymorphisms or liver/intestinal <strong>CYP3A4</strong> activity in stable patients.
+CYP3A4	drug	benzodiazepine	25470746	In addition, the effect of doravirine (120 mg for 14 days) on single dose pharmacokinetics of the <strong>CYP3A</strong> substrate <b>midazolam</b> was evaluated (10 subjects).
+CYP3A4	drug	opioid	25278738	We found that the SNPs on CYP2B6 were associated with plasma S <b>methadone</b> concentration; SNPs on <strong>CYP3A4</strong> were associated with withdrawal symptoms and side effects; and SNPs on CYP2C19 were associated with <b>methadone</b> dose.
+CYP3A4	addiction	withdrawal	25278738	We found that the SNPs on CYP2B6 were associated with plasma S methadone concentration; SNPs on <strong>CYP3A4</strong> were associated with <b>withdrawal</b> symptoms and side effects; and SNPs on CYP2C19 were associated with methadone dose.
+CYP3A4	drug	opioid	25176283	<b>Fentanyl</b> is N dealkylated by <strong>CYP3A4</strong> into the inactive norfentanyl.
+CYP3A4	drug	benzodiazepine	24003250	Heterotropic activation of the <b>midazolam</b> hydroxylase activity of <strong>CYP3A</strong> by a positive allosteric modulator of mGlu5: in vitro to in vivo translation and potential impact on clinically relevant drug drug interactions.
+CYP3A4	drug	benzodiazepine	24003250	The prototypical compound from this series, 5 (4 fluorobenzyl) 2 ((3 fluorophenoxy)methyl) 4,5,6,7 tetrahydropyrazolo[1,5 a]pyrazine (VU0448187), was found to activate <strong>CYP3A4</strong> to >100% of its baseline intrinsic <b>midazolam</b> (MDZ) hydroxylase activity in vitro; activation was CYP3A substrate specific and mGlu(5) PAM dependent.
+CYP3A4	drug	benzodiazepine	24003250	The prototypical compound from this series, 5 (4 fluorobenzyl) 2 ((3 fluorophenoxy)methyl) 4,5,6,7 tetrahydropyrazolo[1,5 a]pyrazine (VU0448187), was found to activate <strong>CYP3A4</strong> to >100% of its baseline intrinsic <b>midazolam</b> (MDZ) hydroxylase activity in vitro; activation was <strong>CYP3A</strong> substrate specific and mGlu(5) PAM dependent.
+CYP3A4	addiction	dependence	24003250	Additional studies revealed the concentration <b>dependence</b> of <strong>CYP3A</strong> activation by VU0448187 in multispecies hepatic and intestinal microsomes and hepatocytes, as well as a diminished effect observed in the presence of ketoconazole.
+CYP3A4	drug	benzodiazepine	23230035	Due to the potential for serious or potentially life threatening adverse events, boceprevir use is contraindicated in patients receiving any of a wide range of drugs whose clearance is highly dependent on cytochrome P 450 (CYP) isoenzymes 3A4/5 (e.g., cisapride, lovastatin, <b>midazolam</b>, sildenafil); boceprevir is also contraindicated for patients receiving potent <strong>CYP3A4</strong>/5 inducers such as carbamazepine, phenytoin, and rifampin, whose concurrent use can diminish boceprevir's virologic activity.
+CYP3A4	drug	opioid	22926601	Multiple regression analysis revealed that 33% of the overall variation in unbound (R) <b>methadone</b> EC50 was explained by 3 variables, namely <strong>CYP3A</strong> activity (9%), age (16%), and sex (8%).
+CYP3A4	drug	opioid	22926601	Finally, it was established that <strong>CYP3A</strong> activity, years of dependent use, sex, and age are major determinants of <b>methadone</b> EC50 with respect to TMDS.
+CYP3A4	drug	opioid	22926004	Study goals were to (1) characterize changes in <b>methadone</b> dose across childbearing, (2) determine enantiomer specific <b>methadone</b> withdrawal kinetics from steady state during late pregnancy, (3) assess enantiomer specific changes in <b>methadone</b> level/dose (L/D) ratios across childbearing, and (4) explore relationships between CYP2B6, CYP2C19, and <strong>CYP3A4</strong> single nucleotide polymorphisms and maternal dose, plasma concentration, and L/D.
+CYP3A4	addiction	withdrawal	22926004	Study goals were to (1) characterize changes in methadone dose across childbearing, (2) determine enantiomer specific methadone <b>withdrawal</b> kinetics from steady state during late pregnancy, (3) assess enantiomer specific changes in methadone level/dose (L/D) ratios across childbearing, and (4) explore relationships between CYP2B6, CYP2C19, and <strong>CYP3A4</strong> single nucleotide polymorphisms and maternal dose, plasma concentration, and L/D.
+CYP3A4	drug	opioid	22685215	Initial in vitro data suggested that <strong>CYP3A4</strong> is the major isoform responsible for the in vivo clearance of <b>methadone</b> in humans.
+CYP3A4	drug	opioid	22682979	As <b>methadone</b> is metabolized by <strong>CYP3A4</strong> and lersivirine is a weak <strong>CYP3A4</strong> inducer, it is possible that lersivirine may decrease <b>methadone</b> concentrations.
+CYP3A4	drug	opioid	22511698	<b>Methadone</b> is primarily metabolized by N demethylation to an inactive metabolite 2 ethylidene 1,5 dimethyl 3,3 diphenylpyrrolidene (EDDP) by <strong>CYP3A4</strong> and CYP2B6.
+CYP3A4	drug	opioid	22352453	Pharmacogenomics of <b>codeine</b>, <b>morphine</b>, and <b>morphine</b> 6 glucuronide: model based analysis of the influence of CYP2D6 activity, UGT2B7 activity, renal impairment, and <strong>CYP3A4</strong> inhibition.
+CYP3A4	drug	opioid	22352453	By means of a generic modeling approach integrating prior physiologic knowledge, we systematically investigated the complex dependence of <b>opioid</b> exposure on cytochrome P450 2D6 and 3A4 (CYP2D6 and <strong>CYP3A4</strong>), and uridine diphosphate glucuronosyltransferase 2B7 (UGT2B7) activity, as well as renal function, by means of a virtual clinical trial.
+CYP3A4	addiction	dependence	22352453	By means of a generic modeling approach integrating prior physiologic knowledge, we systematically investigated the complex <b>dependence</b> of opioid exposure on cytochrome P450 2D6 and 3A4 (CYP2D6 and <strong>CYP3A4</strong>), and uridine diphosphate glucuronosyltransferase 2B7 (UGT2B7) activity, as well as renal function, by means of a virtual clinical trial.
+CYP3A4	drug	opioid	22352453	Second, the model demonstrated that mild and moderate renal impairment and co administration of <strong>CYP3A4</strong> inhibitors have only minor influences on <b>opioid</b> exposure.
+CYP3A4	drug	opioid	21902501	Genetic polymorphisms in <strong>CYP3A4</strong> are associated with withdrawal symptoms and adverse reactions in <b>methadone</b> maintenance patients.
+CYP3A4	addiction	withdrawal	21902501	Genetic polymorphisms in <strong>CYP3A4</strong> are associated with <b>withdrawal</b> symptoms and adverse reactions in methadone maintenance patients.
+CYP3A4	drug	opioid	21902501	The isozyme <strong>CYP3A4</strong> of the CYP system is one of the metabolic enzymes, as well as CYP2B6, responsible for the metabolism of <b>methadone</b>.
+CYP3A4	drug	opioid	21902501	The aim of the present study is to evaluate the potential use of genetic polymorphisms in <strong>CYP3A4</strong> as biomarkers for the prediction of <b>methadone</b> treatment responses.
+CYP3A4	drug	opioid	21902501	These results suggested that genetic variants in the <strong>CYP3A4</strong> gene may be useful indicators for the severity of side effects and withdrawal symptoms for <b>methadone</b> treatment.
+CYP3A4	addiction	withdrawal	21902501	These results suggested that genetic variants in the <strong>CYP3A4</strong> gene may be useful indicators for the severity of side effects and <b>withdrawal</b> symptoms for methadone treatment.
+CYP3A4	drug	opioid	21790905	<b>Methadone</b> metabolism is attributed primarily to cytochrome P450 enzymes <strong>CYP3A4</strong>, CYP2B6 and CYP2D6.
+CYP3A4	drug	benzodiazepine	21058916	In contrast, the absolute ranges of CL(int) for the low clearance <strong>CYP3A4</strong> substrate <b>alprazolam</b> were similar between the systems, indicating independence of hepatocyte bias from enzyme.
+CYP3A4	drug	opioid	20829393	In HepG2 cells, <b>buprenorphine</b> significantly increased human PXR mediated CYP2B6 and <strong>CYP3A4</strong> reporter activities.
+CYP3A4	drug	opioid	20829393	Real time reverse transcription polymerase chain reaction analysis revealed that <b>buprenorphine</b> strongly induced <strong>CYP3A4</strong> expression in both PXR  and CAR transfected HepG2 cells.
+CYP3A4	drug	opioid	20829393	However, treatment with the same concentrations of <b>buprenorphine</b> in HPHs resulted in literally no induction of <strong>CYP3A4</strong> or CYP2B6 expression.
+CYP3A4	drug	opioid	20829393	Further studies indicated that <b>buprenorphine</b> could neither translocate human CAR to the nucleus nor activate CYP2B6/<strong>CYP3A4</strong> reporter activities in transfected HPHs.
+CYP3A4	drug	benzodiazepine	20233841	By using the <strong>CYP3A4</strong> specific substrates luciferin 6' benzyl ether, testosterone, and <b>midazolam</b>, we could confirm that the increased <strong>CYP3A4</strong> gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the <strong>CYP3A4</strong> selective inhibitor ketoconazole.
+CYP3A4	drug	benzodiazepine	20043009	The pharmacokinetics of GS 9350 and its efficacy in increasing systemic exposure of the probe <strong>CYP3A</strong> substrate <b>midazolam</b> were examined in a study involving single  and multiple dose escalations of GS 9350 from 50 to 400 mg.
+CYP3A4	addiction	withdrawal	19924124	We aimed to assess the effect of coadministration and <b>withdrawal</b> of a potent cytochrome P450 3A (<strong>CYP3A</strong>) inhibitor (ritonavir) and a potent <strong>CYP3A</strong> inducer (St John's wort) on <strong>CYP3A</strong> enzyme activity in an open, fixed sequence study design.
+CYP3A4	addiction	withdrawal	19924124	Induction may be unmasked after the <b>withdrawal</b> of a combination of a potent <strong>CYP3A</strong> inhibitor and a potent <strong>CYP3A</strong> inducer, leading to substantial drops in drug exposure of <strong>CYP3A</strong> substrates.
+CYP3A4	drug	benzodiazepine	19889885	A pharmacokinetic model developed for this study, which described the time course of concentrations of both FK1706 and <b>midazolam</b> and incorporated <strong>CYP3A4</strong>/5 inactivation in the liver and intestine, successfully predicted the change in the pharmacokinetics of <b>midazolam</b> using in vitro k(inact) and K(I) values (1.66  to 2.81 fold increases in AUC predicted) and estimated the in vivo inactivation rate to be 0.00404 to 0.0318 h( 1) x ml/ng.
+CYP3A4	drug	benzodiazepine	19884365	A cytochrome P450 3A (<strong>CYP3A</strong>) substudy with <b>midazolam</b> was conducted with the 25 mg dose.
+CYP3A4	drug	benzodiazepine	19884365	The half life was approximately 15 h. S/GSK1349572 had no impact on <b>midazolam</b> exposure, indicating that it does not modulate <strong>CYP3A</strong> activity.
+CYP3A4	drug	opioid	19133059	Contribution of the activities of <strong>CYP3A</strong>, CYP2D6, CYP1A2 and other potential covariates to the disposition of <b>methadone</b> in patients undergoing <b>methadone</b> maintenance treatment.
+CYP3A4	drug	benzodiazepine	19133059	CYP2D6 activity [3 h plasma metabolic ratio of dextromethorphan (DEX) to dextrorphan (DOR)] was determined in 44 patients (29 male; 24 55 years), CYP1A2 activity (salivary caffeine elimination half life) in 44 patients (21 male; 24 55 years) and <strong>CYP3A</strong> activity (oral clearance of <b>midazolam</b>) in 49 patients (33 male; 23 55 years).
+CYP3A4	drug	opioid	19133059	Between 61 and 68% of the overall variation in total plasma trough concentrations of (RS) , (R)  and (S) <b>methadone</b> was explained by <b>methadone</b> dose, duration of addiction before starting MMT, <strong>CYP3A</strong> activity and illicit <b>morphine</b> use.
+CYP3A4	addiction	addiction	19133059	Between 61 and 68% of the overall variation in total plasma trough concentrations of (RS) , (R)  and (S) methadone was explained by methadone dose, duration of <b>addiction</b> before starting MMT, <strong>CYP3A</strong> activity and illicit morphine use.
+CYP3A4	drug	opioid	19133059	<strong>CYP3A</strong> activity explained 22, 16, 15 and 23% of the variation in unbound (R) , unbound (S) , total (RS)  and total (S) <b>methadone</b> clearances, respectively.
+CYP3A4	drug	opioid	19133059	<strong>CYP3A</strong> activity has a modest influence on <b>methadone</b> disposition.
+CYP3A4	drug	opioid	17480178	Recent studies suggest that QT prolongation with <b>methadone</b> is context dependent: occurrence is more frequent with high doses of <b>methadone</b>, concomitant administration of <strong>CYP3A4</strong> inhibitors, hypokalemia, hepatic failure, administration of other QT prolonging drugs and pre existing heart disease.
+CYP3A4	drug	alcohol	17392391	Role of <strong>CYP3A</strong> and CYP2E1 in <b>alcohol</b> mediated increases in acetaminophen hepatotoxicity: comparison of wild type and Cyp2e1( / ) mice.
+CYP3A4	drug	alcohol	17392391	At the time of APAP administration, which followed an 11 h withdrawal from the alcohols, <b>alcohol</b> induced levels of <strong>CYP3A</strong> were sustained in both mouse lines, whereas CYP2E1 was decreased to constitutive levels in wild type mice.
+CYP3A4	addiction	withdrawal	17392391	At the time of APAP administration, which followed an 11 h <b>withdrawal</b> from the alcohols, alcohol induced levels of <strong>CYP3A</strong> were sustained in both mouse lines, whereas CYP2E1 was decreased to constitutive levels in wild type mice.
+CYP3A4	drug	alcohol	17392391	In conclusion, these findings suggest that both <strong>CYP3A</strong> and CYP2E1 contribute to APAP hepatotoxicity in <b>alcohol</b> treated mice.
+CYP3A4	addiction	dependence	17284003	Cytochrome P450 3A4 (<strong>CYP3A4</strong>) is a key enzyme responsible for the metabolism of 50% of all orally administered drugs which exhibit an intriguing kinetic behavior typified by a sigmoidal <b>dependence</b> of the reaction velocity on the substrate concentration.
+CYP3A4	drug	benzodiazepine	17284003	<b>Diazepam</b> is such a drug that undergoes metabolism by <strong>CYP3A4</strong> with sigmoidal dependence.
+CYP3A4	addiction	dependence	17284003	Diazepam is such a drug that undergoes metabolism by <strong>CYP3A4</strong> with sigmoidal <b>dependence</b>.
+CYP3A4	drug	opioid	17084876	Thus, our aim was to study the consequences of <strong>CYP3A</strong> induction on <b>buprenorphine</b> associated effects on resting ventilation in rats.
+CYP3A4	drug	opioid	17084876	In dexamethasone pretreated rats, there was no significant alteration in the respiratory parameters, despite <strong>CYP3A</strong> induction and significant increase of the ratio of plasma norbuprenorphine to <b>buprenorphine</b> concentrations.
+CYP3A4	drug	opioid	17084876	Our results suggest a limited role of drug mediated <strong>CYP3A</strong> induction in the occurrence of <b>buprenorphine</b> attributed respiratory depression in addicts.
+CYP3A4	drug	opioid	16634729	Possible causes, such as the inhibition of <strong>CYP3A4</strong> induced by cyclosporine causing elevations of serum <b>fentanyl</b>, are discussed.
+CYP3A4	drug	opioid	16507617	QT interval increases were observed with <b>buprenorphine</b>/<b>naloxone</b> in combination with either delavirdine or ritonavir, which inhibit <strong>CYP3A4</strong>.
+CYP3A4	drug	amphetamine	16250257	It is metabolized in the organism with a reaction that is catalyzed by cytochrome P450, mainly by the CYP2D and <strong>CYP3A</strong> subfamily, 4 hydroxyamphetamine and <b>amphetamine</b> being dominant metabolites.
+CYP3A4	drug	opioid	16184033	To determine if atazanavir, a once daily protease inhibitor and moderate inhibitor of P450 <strong>CYP3A4</strong>, exhibited pharmacokinetic interactions with (R) <b>methadone</b>.
+CYP3A4	drug	alcohol	16126318	<b>Ethanol</b> has been reported to be either an inducer or an inhibitor of <strong>CYP3A</strong> expression.
+CYP3A4	drug	opioid	15966752	<b>Buprenorphine</b> dosage does not need to be significantly adjusted in patients with renal impairment; however, since <strong>CYP3A</strong> activity may be decreased in patients with severe chronic liver disease, it is possible that the metabolism of <b>buprenorphine</b> will be altered in these patients.
+CYP3A4	drug	opioid	15966752	Although there is limited evidence in the literature to date, drugs that are known to inhibit or induce <strong>CYP3A4</strong> have the potential to diminish or enhance <b>buprenorphine</b> N dealkylation.
+CYP3A4	drug	opioid	15509185	The O demethylation of <b>tramadol</b> to M1, the main analgesic effective metabolite, is catalysed by cytochrome P450 (CYP) 2D6, whereas N demethylation to M2 is catalysed by CYP2B6 and <strong>CYP3A4</strong>.
+CYP3A4	drug	opioid	15501692	<b>Methadone</b> is mostly metabolised in the liver; the main step consists in the N demethylation by <strong>CYP3A4</strong> to EDDP (2 ethylidene 1,5 dimethyl 3,3 diphenylpyrrolidine), an inactive metabolite.
+CYP3A4	drug	opioid	15501692	The activity of <strong>CYP3A4</strong> varies considerably among individuals, and such variability is the responsible for the large differences in <b>methadone</b> bioavailability.
+CYP3A4	drug	opioid	15501692	In particular, antiretrovirals, which are <strong>CYP3A4</strong> inducers, can decrease the levels of <b>methadone</b>, so causing withdrawal symptoms.
+CYP3A4	addiction	withdrawal	15501692	In particular, antiretrovirals, which are <strong>CYP3A4</strong> inducers, can decrease the levels of methadone, so causing <b>withdrawal</b> symptoms.
+CYP3A4	drug	opioid	15501692	<b>Buprenorphine</b>, too, is metabolised by <strong>CYP3A4</strong>, and may undergo the same interactions as <b>methadone</b>.
+CYP3A4	drug	opioid	15371986	However, the role of <strong>CYP3A4</strong> in human <b>methadone</b> disposition in vivo is unclear.
+CYP3A4	drug	opioid	15371986	This investigation tested the hypothesis that <strong>CYP3A</strong> induction (or inhibition) would increase (or decrease) <b>methadone</b> metabolism and clearance in humans.
+CYP3A4	drug	benzodiazepine	15371986	They received intravenous (IV) <b>midazolam</b> (to assess <strong>CYP3A4</strong> activity) and then simultaneous oral deuterium labeled and IV unlabeled methadone after pretreatment with rifampin (INN, rifampicin) (hepatic/intestinal CYP3A induction), troleandomycin (hepatic/intestinal CYP3A inhibition), grapefruit juice (selective intestinal CYP3A inhibition), or nothing.
+CYP3A4	drug	opioid	15371986	They received intravenous (IV) midazolam (to assess <strong>CYP3A4</strong> activity) and then simultaneous oral deuterium labeled and IV unlabeled <b>methadone</b> after pretreatment with rifampin (INN, rifampicin) (hepatic/intestinal CYP3A induction), troleandomycin (hepatic/intestinal CYP3A inhibition), grapefruit juice (selective intestinal CYP3A inhibition), or nothing.
+CYP3A4	drug	benzodiazepine	15371986	They received intravenous (IV) <b>midazolam</b> (to assess <strong>CYP3A4</strong> activity) and then simultaneous oral deuterium labeled and IV unlabeled methadone after pretreatment with rifampin (INN, rifampicin) (hepatic/intestinal <strong>CYP3A</strong> induction), troleandomycin (hepatic/intestinal <strong>CYP3A</strong> inhibition), grapefruit juice (selective intestinal <strong>CYP3A</strong> inhibition), or nothing.
+CYP3A4	drug	opioid	15371986	They received intravenous (IV) midazolam (to assess <strong>CYP3A4</strong> activity) and then simultaneous oral deuterium labeled and IV unlabeled <b>methadone</b> after pretreatment with rifampin (INN, rifampicin) (hepatic/intestinal <strong>CYP3A</strong> induction), troleandomycin (hepatic/intestinal <strong>CYP3A</strong> inhibition), grapefruit juice (selective intestinal <strong>CYP3A</strong> inhibition), or nothing.
+CYP3A4	drug	opioid	15371986	There was no correlation between <b>methadone</b> clearance and hepatic <strong>CYP3A4</strong> activity.
+CYP3A4	drug	opioid	15371986	In vitro experiments showed a predominant role for both <strong>CYP3A4</strong> and CYP2B6 in liver microsomal <b>methadone</b> N  demethylation.
+CYP3A4	drug	opioid	15371986	Intestinal and hepatic <strong>CYP3A</strong> activity only slightly affects human <b>methadone</b> N  demethylation but has no significant effect on <b>methadone</b> concentrations, clearance, or clinical effects.
+CYP3A4	drug	opioid	15371986	Interindividual variability and drug interactions affecting intestinal transporter and hepatic <strong>CYP3A</strong> and CYP2B6 activity may alter <b>methadone</b> disposition.
+CYP3A4	drug	nicotine	15364541	<b>Nicotine</b>, the psychoactive and addictive chemical in cigarettes, and a known inducer of brain CYP2B6, was an efficacious activator of PXR and inducer of <strong>CYP3A4</strong> transcription.
+CYP3A4	addiction	addiction	15364541	Nicotine, the psychoactive and <b>addictive</b> chemical in cigarettes, and a known inducer of brain CYP2B6, was an efficacious activator of PXR and inducer of <strong>CYP3A4</strong> transcription.
+CYP3A4	drug	benzodiazepine	14586385	We analyzed whether <strong>CYP3A4</strong> messenger ribonucleic acid (mRNA) concentrations in leukocytes reflect CYP3A activity in the liver measured by <b>alprazolam</b> as an in vivo probe drug.
+CYP3A4	drug	benzodiazepine	14586385	We analyzed whether <strong>CYP3A4</strong> messenger ribonucleic acid (mRNA) concentrations in leukocytes reflect <strong>CYP3A</strong> activity in the liver measured by <b>alprazolam</b> as an in vivo probe drug.
+CYP3A4	drug	benzodiazepine	14586385	However, mRNA concentrations before and during rifampin induction were largely overlapping, and there was a poor correlation between mRNA concentrations and <b>alprazolam</b> 10 hour trough concentrations reflecting <strong>CYP3A4</strong> activity (r =  0.4, P <.001).
+CYP3A4	drug	benzodiazepine	12751920	While <b>triazolam</b> and <b>midazolam</b> are biotransformed almost entirely via <strong>CYP3A4</strong>, the newer hypnosedatives are biotransformed by several CYP isozymes in addition to <strong>CYP3A4</strong>, resulting in <strong>CYP3A4</strong> inhibitors and inducers having a lesser effect on their biotransformation.
+CYP3A4	drug	opioid	12621385	Systemic clearance of the <b>opioid</b> alfentanil after intravenous administration is an excellent in vivo probe for hepatic cytochrome P4503A (<strong>CYP3A</strong>) activity and drug interactions.
+CYP3A4	drug	opioid	12405865	Rifampicin (rifampin), phenobarbital, phenytoin, carbamazepine, nevirapine, and efavirenz decrease <b>methadone</b> blood concentrations, probably by induction of <strong>CYP3A4</strong> activity, which can result in severe withdrawal symptoms.
+CYP3A4	addiction	withdrawal	12405865	Rifampicin (rifampin), phenobarbital, phenytoin, carbamazepine, nevirapine, and efavirenz decrease methadone blood concentrations, probably by induction of <strong>CYP3A4</strong> activity, which can result in severe <b>withdrawal</b> symptoms.
+CYP3A4	drug	opioid	12405865	Inhibitors of <strong>CYP3A4</strong>, such as fluconazole, and of CYP2D6, such as paroxetine, increase <b>methadone</b> blood concentrations.
+CYP3A4	drug	opioid	11504799	Metabolism of <b>methadone</b> and levo alpha acetylmethadol (LAAM) by human intestinal cytochrome P450 3A4 (<strong>CYP3A4</strong>): potential contribution of intestinal metabolism to presystemic clearance and bioactivation.
+CYP3A4	drug	opioid	11504799	<b>Methadone</b> and LAAM are metabolized by <strong>CYP3A4</strong> in human liver.
+CYP3A4	drug	opioid	11504799	Since they are administered orally, and <strong>CYP3A4</strong> is expressed in human intestine, we tested the hypotheses that human intestine can metabolize <b>methadone</b> and LAAM, and evaluated the participation of <strong>CYP3A4</strong>.
+CYP3A4	drug	opioid	11504799	<b>Methadone</b> N demethylation by <strong>CYP3A4</strong> showed biphasic Eadie Hofstee plots without evidence of positive cooperativity; K(m) values were 10 and 1100 microM for EDDP and 20 and 1000 microM for EMDP formation.
+CYP3A4	drug	opioid	11504799	We conclude that <b>methadone</b>, LAAM, and nor LAAM are metabolized by human intestinal microsomes; <strong>CYP3A4</strong> is the predominant cytochrome P450 isoform; <strong>CYP3A4</strong> catalyzed <b>methadone</b>, LAAM, and nor LAAM metabolism is characterized by noncooperative, multisite kinetics; and intestinal metabolism may contribute to presystemic <b>methadone</b> inactivation and LAAM bioactivation.
+CYP3A4	drug	benzodiazepine	11259570	LAAM and nor LAAM metabolism was inhibited by the <strong>CYP3A4</strong> selective inhibitors troleandomycin, erythromycin, ketoconazole, and <b>midazolam</b>.
+CYP3A4	drug	opioid	11069437	Steady state pharmacokinetics of unbound <b>methadone</b> are stereoselective, and there is large interindividual variability consistent with <strong>CYP3A4</strong> mediated metabolism to the major metabolite EDDP; the variability did not obscure a significant dose plasma concentration relationship.
+CYP3A4	drug	benzodiazepine	10935688	The findings are consistent with the complete dependence of <b>triazolam</b> clearance on <strong>CYP3A</strong> activity, compared with the partial dependence of zolpidem clearance on <strong>CYP3A</strong>.
+CYP3A4	addiction	dependence	10935688	The findings are consistent with the complete <b>dependence</b> of triazolam clearance on <strong>CYP3A</strong> activity, compared with the partial <b>dependence</b> of zolpidem clearance on <strong>CYP3A</strong>.
+CYP3A4	drug	benzodiazepine	10773013	The complete dependence of <b>triazolam</b> clearance on <strong>CYP3A</strong> activity, as opposed to the mixed CYP participation in zolpidem clearance, may explain the differing sex effects on clearance of the two compounds.
+CYP3A4	addiction	dependence	10773013	The complete <b>dependence</b> of triazolam clearance on <strong>CYP3A</strong> activity, as opposed to the mixed CYP participation in zolpidem clearance, may explain the differing sex effects on clearance of the two compounds.
+CYP3A4	drug	benzodiazepine	10770452	In vitro data show the inhibition of <b>alprazolam</b> metabolism by sertraline via <strong>CYP3A4</strong>; therefore, using a randomized, double blind, placebo controlled design, the authors conducted this study to assess the potential for similar in vivo inhibition in humans.
+CYP3A4	drug	opioid	10641980	Because ritonavir can induce <strong>CYP3A</strong>, it can decrease <b>methadone</b> plasma levels.
+CYP3A4	drug	opioid	10383559	A time dependent increase in the clearance of <b>methadone</b> is consistent with auto induction of <strong>CYP3A4</strong>, the enzyme responsible for much of the metabolism of the drug.
+CYP3A4	drug	alcohol	9633991	<b>Alcohol</b> mediated increases in acetaminophen hepatotoxicity: role of CYP2E and <strong>CYP3A</strong>.
+CYP3A4	drug	alcohol	9633991	This commentary focuses on the roles of <strong>CYP3A</strong> and CYP2E in <b>alcohol</b> mediated increases in acetaminophen hepatotoxicity.
+CYP3A4	drug	alcohol	9633991	However, <strong>CYP3A</strong>, which is also induced by <b>alcohol</b>, has been shown to have a greater affinity for acetaminophen than CYP2E.
+CYP3A4	drug	alcohol	9633991	In rats treated with <b>ethanol</b> or the combination of <b>ethanol</b> and isopentanol, the major higher chain <b>alcohol</b> in <b>alcoholic</b> beverages, TAO protects animals from increases in acetaminophen hepatotoxicity, suggesting a major role of <strong>CYP3A</strong>.
+CYP3A4	drug	alcohol	9144448	Role of <strong>CYP3A</strong> in <b>ethanol</b> mediated increases in acetaminophen hepatotoxicity.
+CYP3A4	drug	alcohol	9144448	We have previously shown in cultured human and rat hepatocytes, and in intact rats, that <b>ethanol</b> induces <strong>CYP3A</strong> in addition to CYP2E.
+CYP3A4	drug	alcohol	9144448	To determine if there might be a role for <strong>CYP3A</strong> in <b>ethanol</b> mediated APAP hepatotoxicity in addition to the recognized role for CYP2E, we investigated the effect of triacetyloleandomycin (TAO) on acetaminophen hepatotoxicity in <b>ethanol</b> pretreated rats, as well as the effect of 11 hr withdrawal from <b>ethanol</b> on hepatic levels of <strong>CYP3A</strong> and CYP2E.
+CYP3A4	addiction	withdrawal	9144448	To determine if there might be a role for <strong>CYP3A</strong> in ethanol mediated APAP hepatotoxicity in addition to the recognized role for CYP2E, we investigated the effect of triacetyloleandomycin (TAO) on acetaminophen hepatotoxicity in ethanol pretreated rats, as well as the effect of 11 hr <b>withdrawal</b> from ethanol on hepatic levels of <strong>CYP3A</strong> and CYP2E.
+CYP3A4	drug	alcohol	9144448	In <b>ethanol</b> pretreated rats, exposure to APAP in the absence of TAO was associated with a 75% decrease in <strong>CYP3A</strong>, compared to animals exposed to APAP in the presence of TAO.
+CYP3A4	drug	alcohol	9144448	Our findings suggest that <strong>CYP3A</strong> has a major role in <b>ethanol</b> mediated increases in acetaminophen hepatotoxicity.
+CORT	drug	opioid	32407964	The consequences of exciting or destroying the prelimbic cortex (PrL) or the basolateral amygdala (BLA) remain unclear, including the effects on <b>morphine</b> induced conditioned taste aversion (CTA) in the conditioning and extinction phases, plasma corticosterone (<strong>CORT</strong>) levels, and c Fos/p ERK expressions in the subareas of the medial prefrontal cortex (i.e., PrL, infralimbic cortex [IL], cingulate cortex 1 [Cg1]), basolateral amygdala (BLA), central amygdala (CeA), hippocampus (i.e., CA1, CA2, CA3, and dentate gyrus [DG]), nucleus accumbens (NAc), lateral hypothalamus (LH), and piriform cortex (PC).
+CORT	addiction	aversion	32407964	The consequences of exciting or destroying the prelimbic cortex (PrL) or the basolateral amygdala (BLA) remain unclear, including the effects on morphine induced conditioned taste <b>aversion</b> (<b>CTA</b>) in the conditioning and extinction phases, plasma corticosterone (<strong>CORT</strong>) levels, and c Fos/p ERK expressions in the subareas of the medial prefrontal cortex (i.e., PrL, infralimbic cortex [IL], cingulate cortex 1 [Cg1]), basolateral amygdala (BLA), central amygdala (CeA), hippocampus (i.e., CA1, CA2, CA3, and dentate gyrus [DG]), nucleus accumbens (NAc), lateral hypothalamus (LH), and piriform cortex (PC).
+CORT	drug	opioid	32407964	During conditioning, excitation of the PrL glutamate neurons via NMDA injections disrupted <b>morphine</b> induced CTA and decreased plasma <strong>CORT</strong> levels; moreover, c Fos and p ERK expression was hyperactive in the PrL and IL but hypoactive in the Cg1 and BLA.
+CORT	addiction	aversion	32407964	During conditioning, excitation of the PrL glutamate neurons via NMDA injections disrupted morphine induced <b>CTA</b> and decreased plasma <strong>CORT</strong> levels; moreover, c Fos and p ERK expression was hyperactive in the PrL and IL but hypoactive in the Cg1 and BLA.
+CORT	drug	opioid	32407964	In conditioning, excitation of the BLA glutamate neurons via NMDA injections facilitated <b>morphine</b> induced CTA and increased plasma <strong>CORT</strong> levels.
+CORT	addiction	aversion	32407964	In conditioning, excitation of the BLA glutamate neurons via NMDA injections facilitated morphine induced <b>CTA</b> and increased plasma <strong>CORT</strong> levels.
+CORT	drug	opioid	32407964	During extinction, lesion of the PrL glutamate neurons via NMDA injections impaired <b>morphine</b> induced CTA extinction and enhanced plasma <strong>CORT</strong> levels.
+CORT	addiction	aversion	32407964	During extinction, lesion of the PrL glutamate neurons via NMDA injections impaired morphine induced <b>CTA</b> extinction and enhanced plasma <strong>CORT</strong> levels.
+CORT	drug	opioid	32407964	In extinction, excitation of the PrL glutamatergic neurons via NMDA injections facilitated <b>morphine</b> induced CTA extinction and did not affect plasma <strong>CORT</strong> levels; moreover, the expression of c Fos and p ERK was hypoactive in the Cg1, PrL, and IL but hyperactive in the BLA.
+CORT	addiction	aversion	32407964	In extinction, excitation of the PrL glutamatergic neurons via NMDA injections facilitated morphine induced <b>CTA</b> extinction and did not affect plasma <strong>CORT</strong> levels; moreover, the expression of c Fos and p ERK was hypoactive in the Cg1, PrL, and IL but hyperactive in the BLA.
+CORT	addiction	sensitization	31506004	CB1 receptor antagonism disrupted the expression of <strong>CORT</strong> response habituation and some of the c fos mRNA reduction associated with it and facilitated novel stressor <b>sensitization</b> in doses that did not potentiate acute responses to these stressors.
+CORT	drug	cocaine	31103524	This study measured differences in cognitive behavior performance on the object recognition test (ORT) and social recognition test (SRT) and serum levels of corticosterone (<strong>CORT</strong>) between C57BL/6J and BALB/cJ mice after 14 day chronic exposure to either <b>cocaine</b> (5 mg/kg) or morphine (3 mg/kg) at a dosage of 10 ml/kg/day.
+CORT	drug	opioid	31103524	This study measured differences in cognitive behavior performance on the object recognition test (ORT) and social recognition test (SRT) and serum levels of corticosterone (<strong>CORT</strong>) between C57BL/6J and BALB/cJ mice after 14 day chronic exposure to either cocaine (5 mg/kg) or <b>morphine</b> (3 mg/kg) at a dosage of 10 ml/kg/day.
+CORT	drug	cocaine	31103524	In conclusion, changes in object and social learning recognition indicate that C57BL/6J mice are more sensitive than BALB/cJ mice to chronic drug exposure, especially to <b>cocaine</b>; concomitant changes in serum <strong>CORT</strong> may mediate these effects.
+CORT	drug	nicotine	31099135	Stress and <b>nicotine</b> during adolescence resulted in higher expression of hippocampal glucocorticoid receptors and corticotropin releasing factor receptors and blunted restraint induced <strong>CORT</strong> release in adulthood.
+CORT	drug	alcohol	30946835	After the housing/running procedure, we tested anxiety like behavior using the elevated plus maze and stress responsivity by measuring corticosterone (<strong>CORT</strong>) levels before and after a swim stressor; then, rats were allowed intermittent access to <b>ethanol</b> in two bottle choice design for four weeks.
+CORT	drug	opioid	30898663	WBDs increased glucocorticoid receptor immunoreactivity in the pre frontal cortex, increasing corticosterone (<strong>CORT</strong>) and adrenocorticotrophic hormone (ACTH) per se and after <b>morphine</b> reinstatement.
+CORT	addiction	relapse	30898663	WBDs increased glucocorticoid receptor immunoreactivity in the pre frontal cortex, increasing corticosterone (<strong>CORT</strong>) and adrenocorticotrophic hormone (ACTH) per se and after morphine <b>reinstatement</b>.
+CORT	addiction	addiction	30450375	Experiment 1 examined adaptation in the corticosterone (<strong>CORT</strong>) response at key points in the 11 day procedure, and found that the <b>escalation</b> in stressors disrupted habituation to restraint, whereas the <strong>CORT</strong> response to daily forced swim exposure increased across days.
+CORT	addiction	addiction	30326391	Delays in pubertal timing and decreases in <strong>CORT</strong> levels were correlated, however, with increased novelty seeking in adult males   a phenotype associated with increased <b>addiction</b> vulnerability.
+CORT	addiction	relapse	30326391	Delays in pubertal timing and decreases in <strong>CORT</strong> levels were correlated, however, with increased novelty <b>seeking</b> in adult males   a phenotype associated with increased addiction vulnerability.
+CORT	drug	alcohol	30322021	Adolescent corticosterone (<strong>CORT</strong>) exposure increased <b>alcohol</b>, but not sucrose, self administration, and enhanced stress induced reinstatement with yohimbine in adulthood.
+CORT	addiction	relapse	30322021	Adolescent corticosterone (<strong>CORT</strong>) exposure increased alcohol, but not sucrose, self administration, and enhanced stress induced <b>reinstatement</b> with yohimbine in adulthood.
+CORT	drug	alcohol	30322021	Phosphoproteomic analysis indicated that the amygdala phosphoproteome was significantly altered by adolescent <strong>CORT</strong> exposure, generating a list of potential novel mechanisms involved in the risk of <b>alcohol</b> drinking.
+CORT	addiction	intoxication	29966824	Plasma <strong>CORT</strong> levels were increased significantly in both <b>binge</b> and control animals after PS.
+CORT	addiction	intoxication	29966824	<strong>CORT</strong> levels at 24 h withdrawal from daily 10E intake were highest in the groups with elevated 10E licks (i.e., <b>binge</b> males and control females).
+CORT	addiction	withdrawal	29966824	<strong>CORT</strong> levels at 24 h <b>withdrawal</b> from daily 10E intake were highest in the groups with elevated 10E licks (i.e., binge males and control females).
+CORT	drug	alcohol	29572015	Differences in <b>alcohol</b> intake, blood <b>alcohol</b> level, and plasma <strong>CORT</strong> levels did not explain results.
+CORT	drug	opioid	29486222	Because the <b>opioid</b> system and HPA axis are sexually dimorphic, we examined NTX's effect on adrenocorticotropic hormone (ACTH) and corticosterone (<strong>CORT</strong>) levels.
+CORT	drug	alcohol	29486222	However, NTX increased <strong>CORT</strong> levels for longer durations in <b>alcohol</b> drinking males relative to <b>alcohol</b> drinking females in diestrus.
+CORT	drug	cannabinoid	29413435	<b>Cannabis</b> smokers reporting at least one trauma exposure had higher <strong>CORT</strong> and anxiety overall compared to those reporting no trauma.
+CORT	drug	nicotine	29413435	Cannabis <b>smokers</b> reporting at least one trauma exposure had higher <strong>CORT</strong> and anxiety overall compared to those reporting no trauma.
+CORT	drug	alcohol	29115641	Positive correlations between <b>alcohol</b> preference and ACTH and <strong>CORT</strong> levels were also observed.
+CORT	drug	cocaine	29061385	Regardless of rearing condition, rats exposed to modSPS had greater corticosterone (<strong>CORT</strong>) release and reduced <b>cocaine</b> self administration during initial acquisition compared to non stressed controls.
+CORT	drug	alcohol	28647675	Here, we investigated effects of repeated <b>ethanol</b> intoxication withdrawal cycles (using chronic intermittent <b>ethanol</b> vapor inhalation; CIE) and abstinence from CIE on peak and nadir plasma corticosterone (<strong>CORT</strong>) levels.
+CORT	addiction	intoxication	28647675	Here, we investigated effects of repeated ethanol <b>intoxication</b> withdrawal cycles (using chronic intermittent ethanol vapor inhalation; CIE) and abstinence from CIE on peak and nadir plasma corticosterone (<strong>CORT</strong>) levels.
+CORT	addiction	withdrawal	28647675	Here, we investigated effects of repeated ethanol intoxication <b>withdrawal</b> cycles (using chronic intermittent ethanol vapor inhalation; CIE) and abstinence from CIE on peak and nadir plasma corticosterone (<strong>CORT</strong>) levels.
+CORT	drug	alcohol	28647675	Further, voluntary <b>ethanol</b> drinking in CIE (CIE ED) and CIE naïve (ED) rats, and effects of CIE ED and ED on peak <strong>CORT</strong> levels and mPFC GR were investigated during acute withdrawal (8h) and protracted abstinence (28d).
+CORT	addiction	withdrawal	28647675	Further, voluntary ethanol drinking in CIE (CIE ED) and CIE naïve (ED) rats, and effects of CIE ED and ED on peak <strong>CORT</strong> levels and mPFC GR were investigated during acute <b>withdrawal</b> (8h) and protracted abstinence (28d).
+CORT	addiction	withdrawal	28647675	Collectively, the data demonstrate that acute <b>withdrawal</b> from CIE produces robust alterations in GR signaling, <strong>CORT</strong> and negative affect symptoms which could facilitate excessive drinking.
+CORT	drug	cocaine	28550455	Then, we tested acute systemic LY2444296 in reducing anxiety  and depression like behaviors, as well as releasing the stress hormone corticosterone (<strong>CORT</strong>), observed after chronic extended access (18 h/day for 14 days) <b>cocaine</b> self administration.
+CORT	addiction	aversion	28550455	LY2444296 blocked U69,593 induced place <b>aversion</b> and  reduced motor activity as well as U69,593 induced release of serum <strong>CORT</strong>, confirming its major site of action, without exerting an effect per se.
+CORT	drug	cocaine	28550455	Acute systemic administration of LY2444296 reduced anxiety like and depressive like behaviors, as well as <strong>CORT</strong> release, in rats tested after chronic extended access <b>cocaine</b> self administration, but not in <b>cocaine</b> naïve rats.
+CORT	drug	alcohol	28522965	In all experiments, blood samples were collected for later assessment of corticosterone (<strong>CORT</strong>), blood <b>ethanol</b> concentrations (BECs), and the cellular fraction of blood was analyzed for cytokine gene expression.
+CORT	drug	alcohol	27527158	(1) Fkbp5 KO and wild type (WT) EtOH consumption was tested using a two bottle choice paradigm; (2) The EtOH elimination rate was measured after intraperitoneal (IP) injection of 2.0 g/kg EtOH; (3) Blood <b>alcohol</b> concentration (BAC) was measured after 3 h limited access of <b>alcohol</b>; (4) Brain region expression of Fkbp5 was identified using LacZ staining; (5) Baseline corticosterone (<strong>CORT</strong>) was assessed.
+CORT	addiction	relapse	27316790	Antalarmin, a selective CRF1 receptor antagonist, Metyrapone, a corticosterone (<strong>CORT</strong>) synthesis inhibitor and <strong>CORT</strong> were evaluated for their effects on the <b>reinstatement</b> test in a cue induced <b>relapse</b> model.
+CORT	drug	cocaine	27001454	Finally, the presence of companions decreased the magnitude of the CPP could not seem to be accounted for by <b>cocaine</b> stimulated corticosterone (<strong>CORT</strong>) release.
+CORT	addiction	reward	27001454	Finally, the presence of companions decreased the magnitude of the <b>CPP</b> could not seem to be accounted for by cocaine stimulated corticosterone (<strong>CORT</strong>) release.
+CORT	drug	alcohol	26537217	Previous research has shown that hyperactivation in ventral medial prefrontal cortex (VmPFC) and rostral anterior cingulate cortex (rACC) and high cortisol to corticotrophin ratio (<strong>cort</strong>:ACTH ratio) during neutral relaxed states predict relapse in <b>alcohol</b> dependent (AD) patients.
+CORT	addiction	relapse	26537217	Previous research has shown that hyperactivation in ventral medial prefrontal cortex (VmPFC) and rostral anterior cingulate cortex (rACC) and high cortisol to corticotrophin ratio (<strong>cort</strong>:ACTH ratio) during neutral relaxed states predict <b>relapse</b> in alcohol dependent (AD) patients.
+CORT	drug	alcohol	26537217	Neutral relaxed state <strong>cort</strong>:ACTH ratio was significantly associated with VmPFC hyperreactivity to neutral relaxing cues, and also with hypoactivation in response to <b>alcohol</b> and stress cues in AD patients.
+CORT	addiction	relapse	26537217	Basal heart rate, neutral <strong>cort</strong>:ACTH ratio and neutral VmPFC hyperreactivty were each associated with risk of <b>relapse</b>.
+CORT	addiction	relapse	26537217	However, abnormal VmPFC activation and elevated <strong>cort</strong>:ACTH ratio overlap in predicting risk for <b>relapse</b>, and dysfunctional VmPFC response was the sole significant predictor of odds of <b>relapse</b> in a joint model of <b>relapse</b> risk.
+CORT	drug	alcohol	26537217	These findings suggest that the <strong>cort</strong>:ACTH ratio may serve as a peripheral marker of VmPFC brain dysfunction, while aberrant VmPFC responses need further evaluation as a potential biomarker of <b>alcohol</b> relapse risk in clinical outcome studies.
+CORT	addiction	relapse	26537217	These findings suggest that the <strong>cort</strong>:ACTH ratio may serve as a peripheral marker of VmPFC brain dysfunction, while aberrant VmPFC responses need further evaluation as a potential biomarker of alcohol <b>relapse</b> risk in clinical outcome studies.
+CORT	drug	cocaine	26309224	We have previously shown that DHEA attenuates <b>cocaine</b> seeking behaviour, and also that DHEA decreases corticosterone (<strong>CORT</strong>) levels in plasma and the prefrontal cortex.
+CORT	addiction	relapse	26309224	We have previously shown that DHEA attenuates cocaine <b>seeking</b> behaviour, and also that DHEA decreases corticosterone (<strong>CORT</strong>) levels in plasma and the prefrontal cortex.
+CORT	drug	cocaine	26309224	Previous studies have found that rats demonstrate <b>cocaine</b> seeking behaviour only when the level of <strong>CORT</strong> reaches a minimum threshold.
+CORT	addiction	relapse	26309224	Previous studies have found that rats demonstrate cocaine <b>seeking</b> behaviour only when the level of <strong>CORT</strong> reaches a minimum threshold.
+CORT	drug	cocaine	26309224	In the present study, we investigated whether the attenuating effect of DHEA on <b>cocaine</b> seeking is a result of it reducing <strong>CORT</strong> levels rather than a result of any unique neurosteroid properties.
+CORT	addiction	relapse	26309224	In the present study, we investigated whether the attenuating effect of DHEA on cocaine <b>seeking</b> is a result of it reducing <strong>CORT</strong> levels rather than a result of any unique neurosteroid properties.
+CORT	drug	cocaine	26309224	We found that both DHEA treated and DHEA + <strong>CORT</strong> treated groups showed a significantly lower number of active lever presses compared to controls throughout training and extinction sessions, as well as at <b>cocaine</b> primed reinstatement.
+CORT	addiction	relapse	26309224	We found that both DHEA treated and DHEA + <strong>CORT</strong> treated groups showed a significantly lower number of active lever presses compared to controls throughout training and extinction sessions, as well as at cocaine primed <b>reinstatement</b>.
+CORT	drug	cocaine	26309224	These findings indicate that DHEA attenuates <b>cocaine</b> seeking behaviour independently of fluctuations in <strong>CORT</strong> levels.
+CORT	addiction	relapse	26309224	These findings indicate that DHEA attenuates cocaine <b>seeking</b> behaviour independently of fluctuations in <strong>CORT</strong> levels.
+CORT	drug	alcohol	25709101	Males also showed elevated <strong>CORT</strong> levels following an acute <b>alcohol</b> injection of 2.0 g/kg, while females displayed blunted ACTH levels.
+CORT	drug	cocaine	25655510	Rats raised in these housing conditions were tested for their <b>cocaine</b> responding after pretreatment with the GR antagonist, RU486, or the GR agonist, corticosterone (<strong>CORT</strong>).
+CORT	drug	cocaine	25655510	IC rats were unaffected by RU486 pretreatment, but earned significantly more <b>cocaine</b> than EC rats after pretreatment with <strong>CORT</strong> (10mg/kg).
+CORT	drug	cocaine	25613133	Didehydro <strong>cortistatin</strong> A inhibits HIV 1 Tat mediated neuroinflammation and prevents potentiation of <b>cocaine</b> reward in Tat transgenic mice.
+CORT	addiction	reward	25613133	Didehydro <strong>cortistatin</strong> A inhibits HIV 1 Tat mediated neuroinflammation and prevents potentiation of cocaine <b>reward</b> in Tat transgenic mice.
+CORT	addiction	intoxication	25601008	Given that glucocorticoids can function as anti inflammatories, are known to increase with EtOH exposure, and influence neurotoxicity, we hypothesized that males and females may exhibit an altered corticosterone (<strong>CORT</strong>) response following chronic <b>intoxication</b>.
+CORT	addiction	withdrawal	25601008	Analysis of serum <strong>CORT</strong> levels revealed the expected increase during <b>withdrawal</b> with no difference between males and females, while control males but not females exhibited higher <strong>CORT</strong> concentrations than naive animals.
+CORT	drug	alcohol	25441946	RIA showed significantly increased plasma levels of <strong>CORT</strong> and ACTH in the <b>ethanol</b> withdrawn rats compared with the saline treated rats, which were inhibited significantly by the acupuncture at the acupoint ST36 but not at the non acupoint.
+CORT	addiction	reward	25086310	In addition, we examined for comparison another <b>reinforcing</b> substance, sucrose, and also took measurements of stress related behaviors and circulating corticosterone (<strong>CORT</strong>) and triglycerides (TG), to determine if they contribute to these substances' behavioral and physiological effects.
+CORT	drug	alcohol	25086310	Adult Sprague Dawley rats were gavaged three times daily over 5 days with 3.5 mL of water, Intralipid (20% v/v), <b>ethanol</b> (12% v/v), nicotine (0.01% w/v) or sucrose (22% w/v) (approximately 7 kcal/dose), and tail vein blood was collected for measurements of circulating <strong>CORT</strong> and TG.
+CORT	drug	nicotine	25086310	Adult Sprague Dawley rats were gavaged three times daily over 5 days with 3.5 mL of water, Intralipid (20% v/v), ethanol (12% v/v), <b>nicotine</b> (0.01% w/v) or sucrose (22% w/v) (approximately 7 kcal/dose), and tail vein blood was collected for measurements of circulating <strong>CORT</strong> and TG.
+CORT	drug	alcohol	25086310	While having little effect on stress related behaviors or <strong>CORT</strong> levels, fat, <b>ethanol</b>, and nicotine all increased circulating levels of TG.
+CORT	drug	nicotine	25086310	While having little effect on stress related behaviors or <strong>CORT</strong> levels, fat, ethanol, and <b>nicotine</b> all increased circulating levels of TG.
+CORT	addiction	relapse	24874934	Behaviour in unknown environment was examined in open field test (Laboras), active drug <b>seeking</b> behaviour in conditioned place preference test (CPP), spatial memory in the Morris water maze (MWM), and levels of corticosterone (<strong>CORT</strong>) were analyzed by enzyme immunoassay (EIA).
+CORT	addiction	reward	24874934	Behaviour in unknown environment was examined in open field test (Laboras), active drug seeking behaviour in conditioned place preference test (<b>CPP</b>), spatial memory in the Morris water maze (MWM), and levels of corticosterone (<strong>CORT</strong>) were analyzed by enzyme immunoassay (EIA).
+CORT	drug	alcohol	23994181	LMS increases <b>ethanol</b> induced locomotor response and self administration, possibly due to changes in <strong>CORT</strong> release and/or monoamine concentrations.
+CORT	drug	alcohol	23994181	This study examined the effects of LMS in association with chronic <b>ethanol</b> treatment on plasma <strong>CORT</strong> and brain monoamine concentrations in male and female Swiss mice, which were kept undisturbed (animal facility rearing   AFR) or separated from their mothers for 3h/day, from 2 to 14 days of age (LMS).
+CORT	drug	alcohol	23994181	Locomotor activity, plasma <strong>CORT</strong> levels and monoamines in the frontal cortex, striatum and hippocampus of AFR and LMS mice were evaluated in non treated, acute and chronic <b>ethanol</b> treated animals.
+CORT	drug	alcohol	23994181	Moreover, chronic <b>ethanol</b> treatment resulted in higher <strong>CORT</strong> concentrations in LMS than in AFR males.
+CORT	drug	alcohol	23994181	Overall, these results indicate that LMS mice were more susceptible to the effects of chronic <b>ethanol</b> administration on <strong>CORT</strong> and brain monoamine concentrations, and that these effects were sex dependent.
+CORT	drug	alcohol	23827168	Following 2 weeks of experience with each schedule, blood samples were collected at the conclusion of the last 60 min session to evaluate <strong>CORT</strong> and the blood <b>ethanol</b> concentration (BEC) achieved.
+CORT	addiction	aversion	23827168	In contrast, <strong>CORT</strong> levels rose monotonically with incremental increases in the FT interval regardless of the strain examined or fluid type offered, indicating that glucocorticoid release likely reflects the <b>aversive</b> aspects of increasing intervals between reinforcement rather than engagement in adjunctive behavior.
+CORT	addiction	reward	23827168	In contrast, <strong>CORT</strong> levels rose monotonically with incremental increases in the FT interval regardless of the strain examined or fluid type offered, indicating that glucocorticoid release likely reflects the aversive aspects of increasing intervals between <b>reinforcement</b> rather than engagement in adjunctive behavior.
+CORT	drug	amphetamine	23727174	Enriched environments decreased the response to <b>AMPH</b> and stress induced <strong>CORT</strong> regardless of trait but selectively decreased pTrkB and increased D2 mRNA levels in high anxiety animals.
+CORT	drug	alcohol	23643750	To model a period of heightened elevations in <strong>CORT</strong>, the present work assessed the effects of chronic exposure to the stress hormone <strong>CORT</strong> on <b>alcohol</b> self administration.
+CORT	addiction	reward	23643750	Following stable baseline <b>operant</b> self administration, rats received <strong>CORT</strong> in the drinking water for 7 days.
+CORT	drug	alcohol	23643750	A transient increase in <b>alcohol</b> self administration was observed on the first self administration session following <strong>CORT</strong> exposure, and behavior returned to control levels by the second session.
+CORT	drug	alcohol	23643750	Control experiments determined that this increase in <b>alcohol</b> self administration was specific to <b>alcohol</b>, unrelated to general motor activation, and functionally dissociated from decreased <strong>CORT</strong> levels at the time of testing.
+CORT	drug	alcohol	23643750	Given that maladaptive drinking patterns, such as escalated <b>alcohol</b> drinking following stressful episodes, have the potential to put an individual at risk for future drinking disorders, utilization of this model will be important for examination of neuroadaptations that occur as a consequence of <strong>CORT</strong> exposure in order to better understand escalated drinking following stressful episodes in nondependent individuals.
+CORT	drug	cocaine	23212389	Furthermore, 20 mg/kg nor BNI reduced both the locomotor response to <b>cocaine</b> on Test 2 and the effect of <b>cocaine</b> and food restriction on <strong>CORT</strong> plasma levels.
+CORT	addiction	intoxication	22500955	Using a rat model of <b>binge</b> like <b>intoxication</b>, we tested whether elevated corticosterone (<strong>Cort</strong>) levels contribute to the neurotoxic consequences of EtOH exposure.
+CORT	drug	alcohol	22500955	Basal <strong>Cort</strong> replacement concentrations in EtOH treated Adx animals did not exacerbate <b>alcohol</b> induced neurodegeneration in the hippocampal dentate gyrus (DG) or the entorhinal cortex (EC) as observed by amino cupric silver staining.
+CORT	drug	alcohol	22384198	Our results showed that acute and repeated binge pattern <b>alcohol</b> treatment increased plasma ACTH and <strong>CORT</strong> levels in both E(2)  and Ch treated groups, however habituation to repeated binge pattern <b>alcohol</b> exposure was evident only in E(2) treated animals.
+CORT	addiction	intoxication	22384198	Our results showed that acute and repeated <b>binge</b> pattern alcohol treatment increased plasma ACTH and <strong>CORT</strong> levels in both E(2)  and Ch treated groups, however habituation to repeated <b>binge</b> pattern alcohol exposure was evident only in E(2) treated animals.
+CORT	addiction	sensitization	22333290	Because CRF/CRF₁ initiate EtOH induced activation of the hypothalamic pituitary adrenal axis, we investigated <strong>CORT</strong> effects on EtOH <b>sensitization</b>.
+CORT	addiction	sensitization	22333290	The <strong>CORT</strong> synthesis inhibitor metyrapone prevented the acquisition, but not the expression, of EtOH <b>sensitization</b>.
+CORT	addiction	sensitization	22333290	Exogenous <strong>CORT</strong> administration sensitized the locomotor response to a subsequent EtOH challenge; we observed, however, that the exogenous <strong>CORT</strong> levels necessary to induce <b>sensitization</b> to EtOH were significantly higher than those produced by EtOH treatment.
+CORT	addiction	sensitization	22333290	Therefore, participation of <strong>CORT</strong> seems to be necessary, but not sufficient, to explain the role of CRF/CRF₁ in the acquisition of <b>sensitization</b> to EtOH.
+CORT	drug	cocaine	22309318	Oxytocin and corticosterone (<strong>CORT</strong>) interact to mediate hormonal stress responses and can be altered by <b>cocaine</b> use.
+CORT	drug	alcohol	22051944	The 0.5g/kg <b>ethanol</b> dose did not affect plasma corticosterone (<strong>CORT</strong>) measured 5h after maternal separation or 20min after <b>ethanol</b> injection.
+CORT	drug	alcohol	22016195	Given that interoceptive/subjective drug cues are a fundamental factor in drug taking behavior, we sought to determine the effects of exposure to repeated elevations in the glucocorticoid corticosterone (<strong>CORT</strong>) on the interoceptive effects of <b>alcohol</b> in rats using drug discrimination techniques.
+CORT	drug	alcohol	22016195	Male Long Evans rats trained to discriminate <b>alcohol</b> (1 g/kg, IG) vs. water were exposed to <strong>CORT</strong> (300 μg/ml) in the home cage drinking water for 7 days.
+CORT	drug	alcohol	22016195	The interoceptive effects of experimenter  and self administered <b>alcohol</b> were blunted following <strong>CORT</strong>.
+CORT	addiction	relapse	21863233	Levels of <b>reinstatement</b> and plasma corticosterone (<strong>CORT</strong>) were determined each week for four consecutive weeks.
+CORT	drug	alcohol	21863233	Plasma <strong>CORT</strong> levels in response to injection of both vehicle and yohimbine were significantly higher in the <b>ethanol</b> trained animals compared to sucrose controls.
+CORT	addiction	sensitization	21792578	It has been shown in some studies that the rise in corticosterone (<strong>CORT</strong>) concentration is indispensable for both the induction and the expression of behavioral <b>sensitization</b>.
+CORT	drug	amphetamine	21792578	Therefore, it might be suspected that behavioral hyposensitivity to <b>amphetamine</b> (<b>AMPH</b>) is somehow related to a reduced <strong>CORT</strong> response to the psychostimulant subsequent to the chlorphenvinphos (CVP) intoxication.
+CORT	addiction	intoxication	21792578	Therefore, it might be suspected that behavioral hyposensitivity to amphetamine (AMPH) is somehow related to a reduced <strong>CORT</strong> response to the psychostimulant subsequent to the chlorphenvinphos (CVP) <b>intoxication</b>.
+CORT	drug	amphetamine	21792578	2) Three weeks after the CVP exposure, the <strong>CORT</strong> response to <b>AMPH</b> was significantly increased.
+CORT	drug	alcohol	21533237	Our previous studies showed that binge pattern <b>ethanol</b> (EtOH) treatment during pubertal development negatively dysregulated the responsiveness of the hypothalamo pituitary adrenal (HPA) axis, as manifested by alterations in corticotrophin releasing hormone (CRH), arginine vasopressin (AVP), and corticosterone (<strong>CORT</strong>) during this time period.
+CORT	addiction	intoxication	21533237	Our previous studies showed that <b>binge</b> pattern ethanol (EtOH) treatment during pubertal development negatively dysregulated the responsiveness of the hypothalamo pituitary adrenal (HPA) axis, as manifested by alterations in corticotrophin releasing hormone (CRH), arginine vasopressin (AVP), and corticosterone (<strong>CORT</strong>) during this time period.
+CORT	drug	nicotine	21396990	Hypothalamic pituitary adrenal (HPA) responses to single dose <b>nicotine</b> (NIC) are sexually diergic: Female rats have higher adrenocorticotropic hormone (ACTH) and corticosterone (<strong>CORT</strong>) responses than do males.
+CORT	drug	alcohol	21309957	Pre treatment with SoRI 9409 decreased yohimbine stress induced reinstatement of <b>ethanol</b> seeking but did not affect yohimbine induced increases in plasma <strong>CORT</strong> levels.
+CORT	addiction	relapse	21309957	Pre treatment with SoRI 9409 decreased yohimbine stress induced <b>reinstatement</b> of ethanol <b>seeking</b> but did not affect yohimbine induced increases in plasma <strong>CORT</strong> levels.
+CORT	drug	amphetamine	20713076	We examined the habituation of exploratory movement, <b>amphetamine</b> (<b>AMPH</b>) induced motor activity, as well as changes in serum corticosterone (<strong>CORT</strong>) and glucose levels.
+CORT	drug	psychedelics	20634423	Although chronic unpredictable stress (CUS) enhances the acute hyperthermic and long term monoamine depleting effects of the psychostimulant +3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>), the roles of hyperthermia and corticosterone (<strong>CORT</strong>) in mediating the stress induced enhancement of <b>MDMA</b> induced serotonin (5 HT) and dopamine (DA) depletions are unknown.
+CORT	drug	psychedelics	20634423	Prior exposure to CUS augmented <b>MDMA</b> induced hyperthermia and plasma <strong>CORT</strong> secretion and the long term depletions in 5 HT content in striatum, hippocampus, and frontal cortex and DA content in striatum.
+CORT	drug	psychedelics	20634423	A reduced ambient temperature of 21°C attenuated the hyperthermia, <strong>CORT</strong> secretion, and 5 HT decreases after <b>MDMA</b> in nonstressed rats.
+CORT	drug	psychedelics	20634423	The lower ambient temperature also prevented the augmented hyperthermia, <strong>CORT</strong> secretion, and enhanced 5 HT and DA depletions after <b>MDMA</b> in chronically stressed rats to levels exhibited by nonstressed, <b>MDMA</b> treated rats.
+CORT	drug	psychedelics	20634423	To investigate the role of <strong>CORT</strong> on monoamine depletions in response to <b>MDMA</b>, stressed and nonstressed rats were treated with the <strong>CORT</strong> synthesis inhibitor metyrapone during exposure to <b>MDMA</b>.
+CORT	drug	psychedelics	20634423	This study suggests that enhanced <strong>CORT</strong> is a consequence of enhanced hyperthermia and the CUS induced enhancements of <b>MDMA</b> induced monoamine depletions may be mediated by hyperthermia but not <strong>CORT</strong>.
+CORT	drug	alcohol	19952347	Our results showed that <b>ethanol</b> increased plasma corticosterone (<strong>CORT</strong>) levels in both sexes, yet binge treated animals had significantly lower <strong>CORT</strong> levels than animals exposed to a single dose, suggesting that the hypothalamo pituitary adrenal (HPA) axis habituated to the repeated stressful stimuli of <b>ethanol</b>.
+CORT	addiction	intoxication	19952347	Our results showed that ethanol increased plasma corticosterone (<strong>CORT</strong>) levels in both sexes, yet <b>binge</b> treated animals had significantly lower <strong>CORT</strong> levels than animals exposed to a single dose, suggesting that the hypothalamo pituitary adrenal (HPA) axis habituated to the repeated stressful stimuli of ethanol.
+CORT	drug	amphetamine	19879056	Therefore the objective of these studies was to determine if 10 days of chronic unpredictable stress modulates corticosterone (<strong>CORT</strong>) responses to <b>methamphetamine</b> and furthermore how chronic stress may modulate <b>methamphetamine</b> induced increases in hyperthermia and <strong>CORT</strong>.
+CORT	drug	amphetamine	19879056	As chronic stress potentiates hyperthermic responses to serotonin 2 (5 HT2) stimulation and 5 HT2 receptors are important in mediating both hyperthermic and <strong>CORT</strong> responses, we also investigated if 5 HT2 antagonism would block hyperthermia and <strong>CORT</strong> secretion by the serial exposure to stress and <b>methamphetamine</b> (stress/<b>methamphetamine</b>).
+CORT	drug	amphetamine	19879056	The results of these studies illustrate that stress potentiates <b>methamphetamine</b> induced increases in body temperature and <strong>CORT</strong> secretion and that these increases are blocked by the 5 HT2 antagonist ketanserin.
+CORT	drug	opioid	19179436	This study addressed the role of <b>morphine</b> withdrawal induced corticosterone (<strong>CORT</strong>) release in regulation of tyrosine hydroxylase (TH), the rate limiting enzyme of catecholamine biosynthesis in adrenalectomized (ADX) rats supplemented with low <strong>CORT</strong> pellet (ADX plus <strong>CORT</strong>).
+CORT	addiction	withdrawal	19179436	This study addressed the role of morphine <b>withdrawal</b> induced corticosterone (<strong>CORT</strong>) release in regulation of tyrosine hydroxylase (TH), the rate limiting enzyme of catecholamine biosynthesis in adrenalectomized (ADX) rats supplemented with low <strong>CORT</strong> pellet (ADX plus <strong>CORT</strong>).
+CORT	drug	opioid	19179436	However, this induction of TH expression is not detected in ADX plus <strong>CORT</strong> rats that are unable to mount <strong>CORT</strong> secretory response to <b>morphine</b> withdrawal.
+CORT	addiction	withdrawal	19179436	However, this induction of TH expression is not detected in ADX plus <strong>CORT</strong> rats that are unable to mount <strong>CORT</strong> secretory response to morphine <b>withdrawal</b>.
+CORT	drug	opioid	19179436	Total TH protein levels were elevated in the NTS A(2) from sham operated rats during <b>morphine</b> dependence and withdrawal, whereas we did not find any alteration in ADX plus <strong>CORT</strong> animals.
+CORT	addiction	dependence	19179436	Total TH protein levels were elevated in the NTS A(2) from sham operated rats during morphine <b>dependence</b> and withdrawal, whereas we did not find any alteration in ADX plus <strong>CORT</strong> animals.
+CORT	addiction	withdrawal	19179436	Total TH protein levels were elevated in the NTS A(2) from sham operated rats during morphine dependence and <b>withdrawal</b>, whereas we did not find any alteration in ADX plus <strong>CORT</strong> animals.
+CORT	drug	opioid	19179436	However, induction of <b>morphine</b> withdrawal to ADX plus <strong>CORT</strong> animals did not alter the phosphorylation (activation) of TH in NTS A(2) and decreased TH activity in the PVN.
+CORT	addiction	withdrawal	19179436	However, induction of morphine <b>withdrawal</b> to ADX plus <strong>CORT</strong> animals did not alter the phosphorylation (activation) of TH in NTS A(2) and decreased TH activity in the PVN.
+CORT	drug	alcohol	18945222	Blood <b>alcohol</b> content (BAC) and corticosterone (<strong>CORT</strong>) content were analyzed in a separate series of intact and GDX males and females with and without ADX in response to the EtOH challenge.
+CORT	drug	amphetamine	18614766	Body weight (BW), blood pressure (BP), fluid intake, salt preference, response to <b>amphetamine</b>, open field behavior, plasma adrenocorticotropin hormone (ACTH), plasma corticosterone (<strong>Cort</strong>), and adrenal gland weight were measured.
+CORT	drug	alcohol	18279498	The objectives of this paper are to examine the prolactin (PRL) and <strong>CORT</strong> response to dl fenfluramine in a large cohort of males with <b>alcohol</b> dependence who had been abstinent for 3 weeks, and to compare this with an age matched control group.
+CORT	addiction	dependence	18279498	The objectives of this paper are to examine the prolactin (PRL) and <strong>CORT</strong> response to dl fenfluramine in a large cohort of males with alcohol <b>dependence</b> who had been abstinent for 3 weeks, and to compare this with an age matched control group.
+CORT	drug	alcohol	18279498	<strong>CORT</strong> response was significantly lower in abstinent <b>alcoholics</b> than in controls (F = 10.0, d.f.
+CORT	drug	alcohol	18279498	The reduced <strong>CORT</strong> response in abstinent <b>alcoholics</b> further supports evidence of hypofunction of the adrenocortical system in this group.
+CORT	drug	alcohol	18218724	Mood, craving for <b>alcohol</b>, and salivary cortisol levels (<strong>CORT</strong>) were measured before and after tryptophan and after stress induction.
+CORT	addiction	relapse	18218724	Mood, <b>craving</b> for alcohol, and salivary cortisol levels (<strong>CORT</strong>) were measured before and after tryptophan and after stress induction.
+CORT	drug	alcohol	18218724	Stress increased <strong>CORT</strong>, HR, negative mood, and craving for <b>alcohol</b>.
+CORT	addiction	relapse	18218724	Stress increased <strong>CORT</strong>, HR, negative mood, and <b>craving</b> for alcohol.
+CORT	drug	alcohol	18218724	Among heavy drinkers HiHs report higher craving for <b>alcohol</b> and show greater reactivity to stress as measured by <strong>CORT</strong> and negative mood.
+CORT	addiction	relapse	18218724	Among heavy drinkers HiHs report higher <b>craving</b> for alcohol and show greater reactivity to stress as measured by <strong>CORT</strong> and negative mood.
+CORT	drug	cocaine	17689506	<b>Cocaine</b> self administering rats displayed reduced basal plasma corticosterone (<strong>CORT</strong>) levels but showed an augmented restraint induced percent increase response from baseline compared to saline self administering controls when measured 24 days after SA testing.
+CORT	drug	cocaine	17689506	This augmented <strong>CORT</strong> response may have been attributable to impaired glucocorticoid receptor (GR) mediated feedback regulation of HPA function, since <b>cocaine</b> self administering rats were also less susceptible to dexamethasone (0.01 mg/kg, i.p.)
+CORT	addiction	sensitization	17675171	In males, LMS and BMS increased the <strong>CORT</strong> response to EtOH but did not modify behavioural <b>sensitization</b>.
+CORT	addiction	sensitization	17675171	Therefore, we postulate that LMS female mice exhibited a faster development of behavioural <b>sensitization</b>, but <strong>CORT</strong> levels were not involved with this effect.
+CORT	drug	opioid	17654090	The purpose of this study was to determine the <b>morphine</b> induced place preference in rats pre exposed to footshock stress and corticosterone (<strong>CORT</strong>).
+CORT	drug	opioid	17654090	The results showed that chronic footshock or <strong>CORT</strong> exposure but not acute footshock or <strong>CORT</strong> exposure similarly potentiated the conditioned place preference to <b>morphine</b>.
+CORT	drug	opioid	17654090	The findings suggest that the increase of dopamine levels in NAc induced by <strong>CORT</strong> might be the medium between stress and <b>morphine</b>.
+CORT	drug	alcohol	17561882	To investigate the role of the Avpr1b in the HPA axis response to acute stress, we measured ACTH and corticosterone (<strong>CORT</strong>) plasma levels in Avpr1b knockout (KO) mice and wild type controls in response to bacterial lipopolysaccharide (LPS) challenge and <b>ethanol</b> (EtOH) administration.
+CORT	addiction	addiction	17534378	A surgical adrenalectomy and corticosterone replacement (ADX/C) regimen that eliminated SA induced increases in corticosterone (<strong>CORT</strong>) while maintaining the diurnal pattern of secretion failed to alter SA or reinstatement in ShA rats but slowed <b>escalation</b> and attenuated later reinstatement in LgA rats when applied before but not after chronic LgA SA testing.
+CORT	addiction	relapse	17534378	A surgical adrenalectomy and corticosterone replacement (ADX/C) regimen that eliminated SA induced increases in corticosterone (<strong>CORT</strong>) while maintaining the diurnal pattern of secretion failed to alter SA or <b>reinstatement</b> in ShA rats but slowed escalation and attenuated later <b>reinstatement</b> in LgA rats when applied before but not after chronic LgA SA testing.
+CORT	drug	cocaine	17534378	The inability of daily <strong>CORT</strong> administration before daily ShA SA, at a dose that reproduced the response during LgA SA, to mimic the effects of LgA SA suggests that elevated glucocorticoids during SA may play a permissive role in <b>cocaine</b> induced neuroplasticity that contributes to addiction.
+CORT	addiction	addiction	17534378	The inability of daily <strong>CORT</strong> administration before daily ShA SA, at a dose that reproduced the response during LgA SA, to mimic the effects of LgA SA suggests that elevated glucocorticoids during SA may play a permissive role in cocaine induced neuroplasticity that contributes to <b>addiction</b>.
+CORT	drug	amphetamine	17460357	<b>METH</b> increases plasma corticosterone (<strong>CORT</strong>) in both strains.
+CORT	drug	amphetamine	17460357	However, the intensity of increment of <strong>CORT</strong> by repeated <b>METH</b> was lower in LE rats than that in WIS rats.
+CORT	drug	amphetamine	17460357	Repeated <b>METH</b> treatment decreased the expression of <b>METH</b> transposable and <strong>CORT</strong> sensitive transporter, organic cation transporter 3 (OCT3), in the brain of WIS rats.
+CORT	drug	amphetamine	17460357	Taken together, these results suggest that the lack of establishment of BS in LE rats might have been caused by the unchanged brain penetration of <b>METH</b> after repeated <b>METH</b> administration, and that the differential <strong>CORT</strong> response to <b>METH</b> is an important strain difference.
+CORT	drug	cocaine	17293045	Basal <strong>CORT</strong> was also unaffected by prior <b>cocaine</b> administration, but the <strong>CORT</strong> response measured immediately after restraint was significantly augmented in <b>cocaine</b> withdrawn rats.
+CORT	drug	amphetamine	17244944	Plasma <strong>CORT</strong> level, highly elevated by <b>AMPH</b> (+337 Delta %), was attenuated nearly by 50% under beta adrenergic blockade.
+CORT	drug	amphetamine	17129610	During the experimental task, ACTH and <strong>CORT</strong> increased significantly less in <b>METH</b> patients than in BUP patients and CONT.
+CORT	addiction	intoxication	16707557	To further delineate the mechanism of impaired intestinal barrier function, the present study examined the role of corticosterone (<strong>CORT</strong>) and interleukin (IL) 18, as <strong>CORT</strong> and IL 18 are elevated following a combined insult of EtOH <b>intoxication</b> and burn injury.
+CORT	addiction	intoxication	16707557	These findings suggest that a combined insult of EtOH and burn injury results in increased <strong>CORT</strong> levels, which in turn up regulates intestinal IL 18 levels and thereby causes altered intestinal barrier function following a combined insult of EtOH <b>intoxication</b> and burn injury.
+CORT	addiction	addiction	16641943	Surgical adrenalectomy along with diurnal corticosterone (<strong>CORT</strong>) replacement prevented EFS induced <b>escalation</b> without altering SA in the absence of EFS, indicating that increases in circulating glucocorticoids were necessary for the escalating effects of EFS.
+CORT	drug	cocaine	16641943	failed to reproduce the effects of repeated daily EFS on SA, but restored the escalating effects of EFS in adrenalectomized rats with <strong>CORT</strong> replacement, suggesting that an elevation of glucocorticoids was necessary but alone was not sufficient for the escalation of <b>cocaine</b> SA by EFS.
+CORT	addiction	addiction	16641943	failed to reproduce the effects of repeated daily EFS on SA, but restored the escalating effects of EFS in adrenalectomized rats with <strong>CORT</strong> replacement, suggesting that an elevation of glucocorticoids was necessary but alone was not sufficient for the <b>escalation</b> of cocaine SA by EFS.
+CORT	drug	opioid	16584846	We have previously shown that the <strong>CORT</strong> response to <b>morphine</b>, but not to a previous uncontrollable stressor, is necessary for the stress induced potentiation of <b>morphine</b>'s rewarding effects.
+CORT	drug	opioid	16584846	Here, we test (1) the necessity of <strong>CORT</strong> during inescapable stress (IS) and/or <b>morphine</b> for IS potentiation of <b>morphine</b> induced NAcs DA and (2) the sufficiency of enhanced <strong>CORT</strong>, in the absence of prior IS, to potentiate <b>morphine</b> induced NAcs DA as well as <b>morphine</b> conditioned place preference (CPP) in male Sprague Dawley rats.
+CORT	addiction	reward	16584846	Here, we test (1) the necessity of <strong>CORT</strong> during inescapable stress (IS) and/or morphine for IS potentiation of morphine induced NAcs DA and (2) the sufficiency of enhanced <strong>CORT</strong>, in the absence of prior IS, to potentiate morphine induced NAcs DA as well as morphine conditioned place preference (<b>CPP</b>) in male Sprague Dawley rats.
+CORT	drug	opioid	16584846	In the first experiment, we administered the <strong>CORT</strong> synthesis inhibitors metyrapone and aminoglutethimide (100mg/kg each, sc) to suppress the <strong>CORT</strong> response to either IS (100 1 mA tailshocks) or subsequent <b>morphine</b> (3 mg/kg, sc) treatment.
+CORT	drug	opioid	16584846	In the next experiments, <strong>CORT</strong> (1 mg/kg, sc) was injected 20 or 30 min before <b>morphine</b> during either microdialysis or CPP testing, respectively, in non stressed rats.
+CORT	addiction	reward	16584846	In the next experiments, <strong>CORT</strong> (1 mg/kg, sc) was injected 20 or 30 min before morphine during either microdialysis or <b>CPP</b> testing, respectively, in non stressed rats.
+CORT	drug	opioid	16584846	We found that IS potentiated subsequent <b>morphine</b> induced NAcs DA and this was completely blocked by <strong>CORT</strong> suppression before <b>morphine</b>, but not before IS.
+CORT	drug	opioid	16584846	However, elevated levels of <strong>CORT</strong> concurrent with <b>morphine</b>, but in the absence of a stressor, failed to potentiate NAcs DA or CPP.
+CORT	addiction	reward	16584846	However, elevated levels of <strong>CORT</strong> concurrent with morphine, but in the absence of a stressor, failed to potentiate NAcs DA or <b>CPP</b>.
+CORT	drug	opioid	16584846	These results suggest that the <strong>CORT</strong> response to <b>morphine</b> is necessary, but not sufficient in the absence of prior IS, for sensitized NAcs DA and CPP responding to <b>morphine</b>, and provide further evidence that <strong>CORT</strong> is involved in the expression, but not the induction, of this sensitization.
+CORT	addiction	reward	16584846	These results suggest that the <strong>CORT</strong> response to morphine is necessary, but not sufficient in the absence of prior IS, for sensitized NAcs DA and <b>CPP</b> responding to morphine, and provide further evidence that <strong>CORT</strong> is involved in the expression, but not the induction, of this sensitization.
+CORT	addiction	sensitization	16584846	These results suggest that the <strong>CORT</strong> response to morphine is necessary, but not sufficient in the absence of prior IS, for sensitized NAcs DA and CPP responding to morphine, and provide further evidence that <strong>CORT</strong> is involved in the expression, but not the induction, of this <b>sensitization</b>.
+CORT	drug	amphetamine	16563358	The aim of the present study was to investigate stress and <b>AMPH</b>  induced release of adrenocorticotropic hormone (ACTH) and corticosterone (<strong>CORT</strong>) during withdrawal from an escalating dosage schedule of <b>AMPH</b> known to produce depression like effects in rats.
+CORT	addiction	withdrawal	16563358	The aim of the present study was to investigate stress and AMPH  induced release of adrenocorticotropic hormone (ACTH) and corticosterone (<strong>CORT</strong>) during <b>withdrawal</b> from an escalating dosage schedule of AMPH known to produce depression like effects in rats.
+CORT	drug	amphetamine	16563358	We found no effect of <b>AMPH</b> withdrawal in the Porsolt swim test and on the ACTH or <strong>CORT</strong> response following restraint stress.
+CORT	addiction	withdrawal	16563358	We found no effect of AMPH <b>withdrawal</b> in the Porsolt swim test and on the ACTH or <strong>CORT</strong> response following restraint stress.
+CORT	drug	amphetamine	16563358	<b>AMPH</b> withdrawn animals expressed behavioral sensitization in terms of locomotion and reduced ACTH and <strong>CORT</strong> plasma levels following a 1 mg/kg <b>AMPH</b> challenge in comparison to the controls.
+CORT	addiction	sensitization	16563358	AMPH withdrawn animals expressed behavioral <b>sensitization</b> in terms of locomotion and reduced ACTH and <strong>CORT</strong> plasma levels following a 1 mg/kg AMPH challenge in comparison to the controls.
+CORT	drug	opioid	15821955	First, the <strong>CORT</strong> response to 3.0 mg/kg <b>morphine</b> was measured in male Sprague Dawley rats 24 h following exposure to IS.
+CORT	drug	opioid	15821955	Finally, we used the temporary <strong>CORT</strong> synthesis inhibitors metyrapone and aminoglutethimide to determine the necessity of <strong>CORT</strong> rises during either IS or <b>morphine</b> administration on the potentiated CPP response.
+CORT	addiction	reward	15821955	Finally, we used the temporary <strong>CORT</strong> synthesis inhibitors metyrapone and aminoglutethimide to determine the necessity of <strong>CORT</strong> rises during either IS or morphine administration on the potentiated <b>CPP</b> response.
+CORT	drug	opioid	15821955	Prior IS significantly potentiated the <strong>CORT</strong> response to <b>morphine</b>.
+CORT	drug	opioid	15821955	However, <strong>CORT</strong> inhibition during IS had no effect on the IS potentiation of <b>morphine</b> CPP, whereas inhibition during <b>morphine</b> administration completely blocked this potentiation.
+CORT	addiction	reward	15821955	However, <strong>CORT</strong> inhibition during IS had no effect on the IS potentiation of morphine <b>CPP</b>, whereas inhibition during morphine administration completely blocked this potentiation.
+CORT	drug	opioid	15821955	The results indicate that the <strong>CORT</strong> response to <b>morphine</b> is enhanced in rats that were previously exposed to an uncontrollable stressor, and that this response to the drug, not the stressor, is necessary for the stress enhanced potentiation of <b>morphine</b> CPP.
+CORT	addiction	reward	15821955	The results indicate that the <strong>CORT</strong> response to morphine is enhanced in rats that were previously exposed to an uncontrollable stressor, and that this response to the drug, not the stressor, is necessary for the stress enhanced potentiation of morphine <b>CPP</b>.
+CORT	addiction	intoxication	15718389	In this study, we examined whether corticosterone (<strong>Cort</strong>) plays any role in suppressing MLN T cell function and bacterial accumulation after EtOH <b>intoxication</b> and burn injury.
+CORT	addiction	intoxication	15718389	Two days after injury, a significant increase in blood <strong>Cort</strong> levels and suppression of MLN T cell proliferation and IL 2 production was observed in rats receiving combined insult of EtOH <b>intoxication</b> and burn injury compared with rats receiving EtOH <b>intoxication</b> or burn injury alone.
+CORT	addiction	intoxication	15718389	These findings suggest that EtOH <b>intoxication</b> before burn injury augments <strong>Cort</strong> release, which suppresses MLN T cell function by inhibiting p38 and ERK1/2 activation and promotes bacterial accumulation in MLN after EtOH and burn injury.
+CORT	drug	alcohol	15369760	Specifically, <b>alcohol</b> acts as a crucial regulator of the hypothalamic pituitary adrenal (HPA) axis, thereby modulating the release of hormones, particularly adrenocorticotropic hormone (ACTH) and corticosterone (<strong>CORT</strong>).
+CORT	drug	opioid	14687867	During the experimentally induced aggressiveness, plasma adrenocorticotropic hormone (ACTH) and cortisol (<strong>CORT</strong>) concentrations increased less significantly, and norepinephrine (NE) and epinephrine (EPI) levels, together with heart rate (HR), increased more significantly in abstinent <b>heroin</b> dependent subjects than in healthy subjects.
+CORT	drug	opioid	14687867	PSAP aggressive responses positively correlated with catecholamine changes, BDHI "direct" and "irritability" scores, MMPI "psychopathic deviate" scores in <b>heroin</b> dependent subjects and controls, and with <strong>CORT</strong> responses only in healthy subjects.
+CORT	drug	alcohol	12920386	Withdrawal symptoms, mood changes, cardiovascular indexes (heart rate, blood pressure), norepinephrine (NE), epinephrine (EPI), adrenocorticotropic hormone (ACTH) and cortisol (<strong>CORT</strong>) were evaluated during naloxone <b>naltrexone</b> administration on the second day of detoxification treatment.
+CORT	drug	opioid	12920386	Withdrawal symptoms, mood changes, cardiovascular indexes (heart rate, blood pressure), norepinephrine (NE), epinephrine (EPI), adrenocorticotropic hormone (ACTH) and cortisol (<strong>CORT</strong>) were evaluated during <b>naloxone</b> naltrexone administration on the second day of detoxification treatment.
+CORT	addiction	withdrawal	12920386	<b>Withdrawal</b> symptoms, mood changes, cardiovascular indexes (heart rate, blood pressure), norepinephrine (NE), epinephrine (EPI), adrenocorticotropic hormone (ACTH) and cortisol (<strong>CORT</strong>) were evaluated during naloxone naltrexone administration on the second day of detoxification treatment.
+CORT	drug	opioid	12920386	Slight and transient withdrawal symptoms and mood changes were demonstrated on the second day in the whole sample of patients, in association with a significant, but moderate, elevation of heart rate, blood pressure, NE (two fold), EPI (five fold), ACTH (two fold) and <strong>CORT</strong> (two fold) plasma levels, in response to <b>opioid</b> receptor antagonist administration.
+CORT	addiction	withdrawal	12920386	Slight and transient <b>withdrawal</b> symptoms and mood changes were demonstrated on the second day in the whole sample of patients, in association with a significant, but moderate, elevation of heart rate, blood pressure, NE (two fold), EPI (five fold), ACTH (two fold) and <strong>CORT</strong> (two fold) plasma levels, in response to opioid receptor antagonist administration.
+CORT	drug	cocaine	12892653	The purpose of the present study was to investigate the effects of 14 days of ShA or LgA, high dose <b>cocaine</b> SA on plasma corticosterone (<strong>CORT</strong>), prolactin (PRL), and related mRNAs.
+CORT	drug	cocaine	12892653	Acutely, <b>cocaine</b> SA increased plasma <strong>CORT</strong> and reduced plasma PRL levels.
+CORT	drug	cocaine	12892653	SA training produced circadian increases in <strong>CORT</strong> that appeared to occur in anticipation of <b>cocaine</b> availability.
+CORT	drug	cocaine	12892653	With repeated LgA, high dose SA, the daily <strong>CORT</strong> area under the curve (AUC) progressively decreased, apparently due to tolerance to <b>cocaine</b>'s effects on <strong>CORT</strong> and a reduction in basal <strong>CORT</strong> levels.
+CORT	drug	amphetamine	12576877	ESC and INT <b>AMPH</b> withdrawal had no effect on any of these tests or on stress responsiveness as measured by increased plasma levels of corticosterone (<strong>CORT</strong>) and adrenocorticotropin following the swim test, although basal <strong>CORT</strong> levels were higher in <b>AMPH</b> withdrawn animals compared to controls.
+CORT	addiction	withdrawal	12576877	ESC and INT AMPH <b>withdrawal</b> had no effect on any of these tests or on stress responsiveness as measured by increased plasma levels of corticosterone (<strong>CORT</strong>) and adrenocorticotropin following the swim test, although basal <strong>CORT</strong> levels were higher in AMPH withdrawn animals compared to controls.
+CORT	addiction	sensitization	11850143	The main purpose the present study was, therefore, to determine the effects of psychostimulant cross <b>sensitization</b> on the stress induced release of adrenocorticotropic hormone (ACTH) and corticosterone (<strong>CORT</strong>).
+CORT	drug	amphetamine	11850143	Prior d <b>amphetamine</b> had no effect upon levels of <strong>CORT</strong> and ACTH in the non stressed animals.
+CORT	drug	amphetamine	11850143	A second experiment confirmed behavioral sensitization to the current schedule of d <b>amphetamine</b> injections, and demonstrated neuroendocrine sensitization of ACTH and <strong>CORT</strong> to a subsequent drug challenge.
+CORT	addiction	sensitization	11850143	A second experiment confirmed behavioral <b>sensitization</b> to the current schedule of d amphetamine injections, and demonstrated neuroendocrine <b>sensitization</b> of ACTH and <strong>CORT</strong> to a subsequent drug challenge.
+CORT	drug	amphetamine	11850143	The augmented release of <strong>CORT</strong> and ACTH observed in d <b>amphetamine</b> treated rats might have important implications for human disorders in which processes resembling neurochemical sensitization have been hypothesized to play an etiological role.
+CORT	addiction	sensitization	11850143	The augmented release of <strong>CORT</strong> and ACTH observed in d amphetamine treated rats might have important implications for human disorders in which processes resembling neurochemical <b>sensitization</b> have been hypothesized to play an etiological role.
+CORT	addiction	withdrawal	11797058	Regional brain CRF like immunoreactivity (CRF LI), plasma ACTH LI and <strong>CORT</strong> LI levels were determined from 1 day to 6 weeks post <b>withdrawal</b>.
+CORT	drug	alcohol	11797058	<b>Ethanol</b> withdrawn rats also initially had reduced hippocampal, frontal cortical and hypothalamic CRF LI levels and time dependent reductions in basal <strong>CORT</strong> levels.
+CORT	drug	cocaine	11797058	<b>Cocaine</b> withdrawn rats showed time dependent elevations in frontal cortical CRF LI and basal <strong>CORT</strong> levels.
+CORT	drug	alcohol	11797058	Protracted withdrawal from <b>ethanol</b> or cocaine is associated with altered limbic CRF LI and circulating <strong>CORT</strong> levels beyond the detoxification stage.
+CORT	drug	cocaine	11797058	Protracted withdrawal from ethanol or <b>cocaine</b> is associated with altered limbic CRF LI and circulating <strong>CORT</strong> levels beyond the detoxification stage.
+CORT	addiction	withdrawal	11797058	Protracted <b>withdrawal</b> from ethanol or cocaine is associated with altered limbic CRF LI and circulating <strong>CORT</strong> levels beyond the detoxification stage.
+CORT	drug	cocaine	11512040	Novelty induced (but not <b>cocaine</b> induced) locomotor activity, pre SA plasma <strong>CORT</strong>, and pre SA food reinforced lever pressing predicted SA, but only at the lowest <b>cocaine</b> dose tested.
+CORT	drug	cocaine	10898093	Effects of adrenalectomy (ADX) and corticosterone (<strong>CORT</strong>) on the development and expression of sensitization to the locomotor effect of <b>cocaine</b> (COC) were studied in rats.
+CORT	addiction	sensitization	10898093	Effects of adrenalectomy (ADX) and corticosterone (<strong>CORT</strong>) on the development and expression of <b>sensitization</b> to the locomotor effect of cocaine (COC) were studied in rats.
+CORT	addiction	sensitization	10898093	Pretreatment with <strong>CORT</strong>, 10 mg/kg, but not 5 mg/kg, before each of the 5 daily COC injections facilitated the development of COC <b>sensitization</b>, tested after a 5 day withdrawal.
+CORT	addiction	withdrawal	10898093	Pretreatment with <strong>CORT</strong>, 10 mg/kg, but not 5 mg/kg, before each of the 5 daily COC injections facilitated the development of COC sensitization, tested after a 5 day <b>withdrawal</b>.
+CORT	addiction	sensitization	10898093	When pretreated with <strong>CORT</strong> alone (10 mg/kg), the challenge dose of COC administered on day 10 induced cross <b>sensitization</b> to <strong>CORT</strong>.
+CORT	addiction	sensitization	10898093	<strong>CORT</strong> (10 mg/kg) injected acutely before COC on day 10, potentiated the expression of COC <b>sensitization</b>.
+CORT	addiction	sensitization	10898093	Our results indicate that <strong>CORT</strong> facilitates the development and expression of COC <b>sensitization</b>, while ADX blocks the initiation of the behavioral phenomenon only.
+CORT	addiction	sensitization	10898093	Moreover, there takes place cross <b>sensitization</b> between <strong>CORT</strong> and COC, which indicates a close relationship between the drug related mechanism and behavioral <b>sensitization</b>.
+CORT	drug	cocaine	10871318	<b>cocaine</b> self administration under "naturalistic" conditions on plasma corticosterone (<strong>CORT</strong>) and prolactin (PRL) were investigated in male Sprague Dawley rats.
+CORT	drug	cocaine	10871318	After the determination of plasma <strong>CORT</strong> and PRL levels under basal conditions before access to <b>cocaine</b> for self administration, rats were allowed to self administer <b>cocaine</b> (0.25, 0.5, 1.0, or 2.0 mg/kg/infusion i.v.)
+CORT	drug	cocaine	10871318	The effects of <b>cocaine</b> on plasma <strong>CORT</strong> were intake dependent, as demonstrated by significant positive correlations between postsession plasma <strong>CORT</strong> and total <b>cocaine</b> intake within the preceding sessions.
+CORT	drug	psychedelics	10664829	Prolactin (PRL) and cortisol (<strong>CORT</strong>) responses to the serotonergic agonist d fenfluramine (D fen), clinical psychobehavioral changes, and psychometric measures were evaluated 3 weeks and then 12 months after <b>MDMA</b> discontinuation.
+CORT	drug	psychedelics	10664829	<b>MDMA</b> users showed significantly reduced PRL and <strong>CORT</strong> responses in comparison with control subjects at 3 weeks (respectively, p < .001; p < .005).
+CORT	drug	psychedelics	10664829	In contrast, <strong>CORT</strong> responses in <b>MDMA</b> users were restored after 12 months of abstinence, with significantly higher responses to D fen, in comparison with 3 week responses (p < .05).
+CORT	drug	psychedelics	10664829	<strong>CORT</strong> restored responses to D fen at 12 months, and the correlation of neuroendocrine changes with <b>MDMA</b> exposure suggest that the neuroendocrine impairment may be due to a partially reversible neurotoxic action of <b>MDMA</b> on the human brain.
+CORT	drug	amphetamine	10654663	<b>AMPH</b> exerted a paradoxical effect on <strong>CORT</strong> secretion only in maternally deprived subjects while affecting behaviour mainly in deprived female subjects, which showed a generalised shift to the left in the dose response curve to this drug.
+CORT	drug	alcohol	10642377	<b>Ethanol</b> did not increase circulating epinephrine, norepinephrine, or cortisol concentration (<strong>Cort</strong>) above Ex elevations.
+CORT	drug	alcohol	10642377	It is concluded that, although this blood <b>ethanol</b> concentration is insufficient to acutely increase <strong>Cort</strong> above that caused by Ex alone, it appears that <b>ethanol</b> may have a prolonged effect beyond the Ex response.
+CORT	drug	opioid	10475168	Since these modulatory effects of stress on the locomotor effects of <b>morphine</b> might be mediated via the release of endogenous corticosteroids we also tested the influence of repeated intermittent and chronic administration of corticosterone (<strong>CORT</strong>) and the synthetic corticosteroid dexamethasone (DEX) on the locomotor response to <b>morphine</b>.
+CORT	drug	opioid	10475168	Further, stress induced <strong>CORT</strong> release seems to be involved in stress induced behavioural sensitization to <b>morphine</b>.
+CORT	addiction	sensitization	10475168	Further, stress induced <strong>CORT</strong> release seems to be involved in stress induced behavioural <b>sensitization</b> to morphine.
+CORT	drug	alcohol	10069560	We tested the hypothesis that prenatal <b>ethanol</b> exposure would result in increased plasma corticosterone (<strong>CORT</strong>) and adrenocorticotropin (ACTH) responses and increased peptide [corticotropin releasing factor and vasopressin] mRNA levels in the paraventricular nucleus (PVN) of the hypothalamus compared to that in control animals.
+CORT	addiction	sensitization	10069560	<b>Sensitization</b> of the <strong>CORT</strong> response to acute stress was observed in males but not females across all prenatal treatment groups.
+CORT	drug	cocaine	9822801	In order to test this hypothesis, the effects of long term (3 and 6 weeks) 'binge' pattern <b>cocaine</b> administration (3x15 mg/kg <b>cocaine</b>, i.p., daily, during the early phase of the light cycle) on body weight, adrenal gland weight, basal and stress induced activity of the corticosterone (<strong>CORT</strong>) and basal plasma testosterone (T) levels were measured.
+CORT	addiction	intoxication	9822801	In order to test this hypothesis, the effects of long term (3 and 6 weeks) '<b>binge</b>' pattern cocaine administration (3x15 mg/kg cocaine, i.p., daily, during the early phase of the light cycle) on body weight, adrenal gland weight, basal and stress induced activity of the corticosterone (<strong>CORT</strong>) and basal plasma testosterone (T) levels were measured.
+CORT	drug	cocaine	9822801	Both 3 and 6 weeks 'binge' <b>cocaine</b> administration decreased body weight gain, increased the weight of adrenal glands and increased basal <strong>CORT</strong> levels.
+CORT	addiction	intoxication	9822801	Both 3 and 6 weeks '<b>binge</b>' cocaine administration decreased body weight gain, increased the weight of adrenal glands and increased basal <strong>CORT</strong> levels.
+CORT	drug	cocaine	9822801	Neither chronic saline nor <b>cocaine</b> administration altered stress induced <strong>CORT</strong> secretion.
+CORT	drug	cocaine	9822801	<strong>CORT</strong> levels 60 min following the restraint stress (recovery) were significantly lower than pre stress basal levels after 3 and 6 weeks of <b>cocaine</b>, but not saline, administration.
+CORT	drug	cocaine	9554945	Elevated blood concentrations of corticosterone (<strong>CORT</strong>), an adrenal steroid associated with stress responses, is one of the endocrine correlates of <b>cocaine</b> treatment.
+CORT	drug	cocaine	9554945	), on the test day, prior to exposure to <b>cocaine</b> associated contextual cues, attenuated the subsequent conditioned increase in blood <strong>CORT</strong> concentrations.
+CORT	drug	cocaine	9554945	Because the hypothalamic pituitary adrenal (HPA) axis has been implicated in modulating the actions of <b>cocaine</b>, it is plausible that such conditioned increases in <strong>CORT</strong> release by <b>cocaine</b> associated cues may further predispose an organism to the reinforcing effects of the drug or enhance the susceptibility to drug taking behavior.
+CORT	addiction	reward	9554945	Because the hypothalamic pituitary adrenal (HPA) axis has been implicated in modulating the actions of cocaine, it is plausible that such conditioned increases in <strong>CORT</strong> release by cocaine associated cues may further predispose an organism to the <b>reinforcing</b> effects of the drug or enhance the susceptibility to drug taking behavior.
+CORT	addiction	sensitization	9537679	To determine if a similar phenomenon occurred with stress induced <b>sensitization</b>, male Sprague Dawley rats were given a sham ADX, ADX surgery, or ADX plus s.c. implanted corticosterone (<strong>CORT</strong>) pellets (<strong>CORT</strong> 12.5% pellets or <strong>CORT</strong> 50% pellets).
+CORT	drug	cocaine	9537679	Animals given ADX surgery or ADX and <strong>CORT</strong> 12.5% pellets did not demonstrate sensitization to repeated stress, while <strong>CORT</strong> 50% pellets in ADX rats restored the sensitized horizontal response to <b>cocaine</b> challenge at late withdrawal.
+CORT	addiction	sensitization	9537679	Animals given ADX surgery or ADX and <strong>CORT</strong> 12.5% pellets did not demonstrate <b>sensitization</b> to repeated stress, while <strong>CORT</strong> 50% pellets in ADX rats restored the sensitized horizontal response to cocaine challenge at late withdrawal.
+CORT	addiction	withdrawal	9537679	Animals given ADX surgery or ADX and <strong>CORT</strong> 12.5% pellets did not demonstrate sensitization to repeated stress, while <strong>CORT</strong> 50% pellets in ADX rats restored the sensitized horizontal response to cocaine challenge at late <b>withdrawal</b>.
+CORT	drug	cocaine	9537679	In contrast, stress pretreated rats which were given <strong>CORT</strong> 50% pellets during the 2 week withdrawal period after the stress showed a marked decrease in horizontal activity in response to <b>cocaine</b> challenge at late withdrawal.
+CORT	addiction	withdrawal	9537679	In contrast, stress pretreated rats which were given <strong>CORT</strong> 50% pellets during the 2 week <b>withdrawal</b> period after the stress showed a marked decrease in horizontal activity in response to cocaine challenge at late <b>withdrawal</b>.
+CORT	drug	cocaine	9537679	Together with our previous study on the role of <strong>CORT</strong> in <b>cocaine</b> induced sensitization, the results indicate that <strong>CORT</strong> is not the common factor mediating the long term sensitization to <b>cocaine</b> and stress.
+CORT	addiction	sensitization	9537679	Together with our previous study on the role of <strong>CORT</strong> in cocaine induced <b>sensitization</b>, the results indicate that <strong>CORT</strong> is not the common factor mediating the long term <b>sensitization</b> to cocaine and stress.
+CORT	drug	cocaine	9406871	<strong>CORT</strong> levels were higher in <b>cocaine</b> versus saline treated animals (P < 0.01).
+CORT	drug	nicotine	7870994	Other investigators have suggested that tolerance to multiple <b>nicotine</b> injections in mice may be due, in part, to elevated plasma corticosterone (<strong>CORT</strong>) levels, since repeated <b>nicotine</b> injections are associated with elevated <strong>CORT</strong>, chronically elevated <strong>CORT</strong> reduces <b>nicotine</b> responsiveness and adrenalectomy disrupts <b>nicotine</b> tolerance.
+CORT	drug	nicotine	7870994	Three experiments tested the feasibility of this hypothesis, as a mechanism for conditioned <b>nicotine</b> tolerance in rats, by determining whether acute administration of <strong>CORT</strong> or manipulations that increase adrenocortical activity reduce <b>nicotine</b> responsiveness.
+CORT	drug	nicotine	7870994	In experiment 1, male rats were injected IP with <strong>CORT</strong> (1 mg/kg), vehicle (ETOH + distilled water) or no injection 10 min before <b>nicotine</b> (0.75 mg/kg, SC) and tested for <b>nicotine</b> induced analgesia every other day for 10 days.
+CORT	drug	nicotine	7870994	A significant reduction in withdrawal latencies was obtained for <strong>CORT</strong> pretreated rats compared to animals given only <b>nicotine</b>.
+CORT	addiction	withdrawal	7870994	A significant reduction in <b>withdrawal</b> latencies was obtained for <strong>CORT</strong> pretreated rats compared to animals given only nicotine.
+CORT	drug	nicotine	7870994	Results also suggest that a conditioned release of endogenous <strong>CORT</strong> was triggered by stimuli associated with <b>nicotine</b> delivery.
+CORT	drug	nicotine	7870994	These data are consistent with the hypothesis that a conditioned release of <strong>CORT</strong> could contribute to the development of tolerance to some of <b>nicotine</b>'s effects.
+EGFR	drug	opioid	32111605	<strong>EGFR</strong> signaling causes <b>morphine</b> tolerance and mechanical sensitization in rats.
+EGFR	addiction	sensitization	32111605	<strong>EGFR</strong> signaling causes morphine tolerance and mechanical <b>sensitization</b> in rats.
+EGFR	drug	opioid	32111605	It has been shown that the platelet derived growth factor receptor beta (PDGFR ↓), an RTK that has been shown to interact with the <strong>EGFR</strong>, mediates <b>opioid</b> tolerance but does not induce analgesia.
+EGFR	drug	opioid	32111605	Therefore, we sought to determine whether <strong>EGFR</strong> signaling was involved in <b>opioid</b> tolerance and if <strong>EGFR</strong> and PDGFR signaling could induce pain in rats.We found that gefitinib, an <strong>EGFR</strong> antagonist, eliminated <b>morphine</b> tolerance.
+EGFR	addiction	sensitization	32111605	<strong>EGFR</strong> and PDGFR ↓ signaling interacted to produce this <b>sensitization</b>.
+EGFR	drug	opioid	32111605	<strong>EGFR</strong> was widely expressed in primary sensory afferent cell bodies, demonstrating a neuroanatomical substrate for our findings.Taken together, our results suggest a direct mechanistic link between <b>opioid</b> tolerance and mechanical sensitization.
+EGFR	addiction	sensitization	32111605	<strong>EGFR</strong> was widely expressed in primary sensory afferent cell bodies, demonstrating a neuroanatomical substrate for our findings.Taken together, our results suggest a direct mechanistic link between opioid tolerance and mechanical <b>sensitization</b>.
+EGFR	drug	opioid	32111605	<strong>EGFR</strong> antagonism could eventually play an important clinical role in the treatment of <b>opioid</b> tolerance and neuropathic pain that is refractory to <b>opioid</b> treatment.SIGNIFICANCE STATEMENT <b>Opioid</b> tolerance and associated reduced effectiveness of <b>opioids</b> against neuropathic pain are two major clinical problems that are prime contributors to the <b>opioid</b> epidemic.
+EGFR	drug	opioid	32111605	Here we show that <strong>EGFR</strong> antagonism not only blocks <b>morphine</b> tolerance but also restores the effectiveness of <b>opioids</b> against neuropathic pain.
+EGFR	drug	opioid	32111605	<strong>EGFR</strong> antagonism could eventually play an important role in the treatment of <b>opioid</b> tolerance and severe neuropathic pain that requires ever increasing doses of <b>opioids</b>.
+EGFR	drug	alcohol	31883696	There was a significant interaction between <b>alcohol</b> consumption and <strong>eGFR</strong> for CKD progression.
+EGFR	addiction	intoxication	31883696	The slopes of <strong>eGFR</strong> decline were steeper in <b>binge</b> drinkers among patients with <strong>eGFR</strong> less than 60 mL/min/1.73 m2.
+EGFR	drug	nicotine	31710020	The clinicopathological data included age, gender, <b>smoking</b> history, tumor staging, lymph node staging, surgical methods, subtypes, thyroid transcription factor 1 (TTF 1) expression, <strong>EGFR</strong> gene mutation and follow up records were investigated.
+EGFR	drug	alcohol	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (<strong>EGFR</strong>)) modulate <b>alcohol</b> drinking and other behaviors related to <b>alcohol</b> addiction.
+EGFR	addiction	addiction	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (<strong>EGFR</strong>)) modulate alcohol drinking and other behaviors related to alcohol <b>addiction</b>.
+EGFR	drug	alcohol	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>)) modulate <b>alcohol</b> drinking and other behaviors related to <b>alcohol</b> addiction.
+EGFR	addiction	addiction	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>)) modulate alcohol drinking and other behaviors related to alcohol <b>addiction</b>.
+EGFR	drug	alcohol	31617071	This review will examine the preclinical evidence describing TrkB, RET, ALK, FGFR, and <strong>EGFR</strong> modulation of <b>alcohol</b> drinking and other behaviors relevant to <b>alcohol</b> abuse.
+EGFR	drug	nicotine	31393548	Forty eight patients (55%) were never <b>smokers</b>, 45 patients (51%) were of Eastern Cooperative Oncology Group performance status 1, and 59 patients (67%) had <strong>EGFR</strong> exon 19 deletion.
+EGFR	addiction	relapse	31230189	The renal end point (doubling of serum creatinine or ESRD) occurred in 8% of the patients; however, <strong>eGFR</strong> in patients with <b>relapse</b> was similar to that of non recurrent at the diagnoses, but it decreased over time more in the relapsing than in non relapsing patients (p group = 0.20; p time = 0.001; p time × group interactions = 0.04).
+EGFR	drug	nicotine	31125062	In certain subgroups, PFS was positively associated with PD L1 expression (KRAS, <strong>EGFR</strong>) and with <b>smoking</b> status (BRAF, HER2).
+EGFR	drug	nicotine	30598264	We demonstrated the correlation between <b>nicotine</b> and epidermal growth factor receptor (<strong>EGFR</strong>) signaling.
+EGFR	drug	nicotine	30598264	We demonstrated the correlation between <b>nicotine</b> and <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>) signaling.
+EGFR	drug	nicotine	30598264	<b>Nicotine</b> treatment induced HSC 2 cell proliferation and migration and the phosphorylation of <strong>EGFR</strong>.
+EGFR	drug	nicotine	30598264	Furthermore, <b>nicotine</b> treatment activated the <strong>EGFR</strong> downstream effectors phosphatidylinositol 3 kinase/AKT and p44/42 mitogen activated protein kinases (ERK), which, in turn, promoted cell proliferation.
+EGFR	addiction	addiction	30449623	Cetuximab, an <strong>epidermal growth factor receptor</strong> inhibitor, has been proposed for treatment de <b>escalation</b> in this setting to reduce the toxicity of standard cisplatin treatment, but no randomised evidence exists for the efficacy of this strategy.
+EGFR	drug	nicotine	30431077	To the best of our knowledge, the present study is the first to demonstrate the role of <b>nicotine</b> in metastasis and anti‑<strong>EGFR</strong>‑therapy resistance of HNSCC.
+EGFR	drug	nicotine	30431077	The present findings demonstrated that <b>nicotine</b> increased proliferation, migration, invasion, p‑<strong>EGFR</strong> nuclear translocation and protein kinase B (Akt) phosphorylation in HNSCC cells.
+EGFR	drug	nicotine	30431077	Finally, an in vivo experiment revealed that <b>nicotine</b> increased lymph node metastasis of xenografted tumors, whereas an nAChR inhibitor suppressed lymph node metastasis and p‑<strong>EGFR</strong> nuclear localization of xenografted tumors.
+EGFR	drug	nicotine	30431077	Taken together, these results demonstrated that <b>nicotine</b> induced nuclear accumulation of p‑<strong>EGFR</strong>, and activation of Akt signaling.
+EGFR	addiction	relapse	30230541	During follow up, one female patient with <strong>EGFR</strong> exon 19 deletion and NF1 Q1815X comutation showed poor response to <strong>EGFR</strong> TKIs (Gefitinib and Osimertinib) after disease <b>relapse</b>.
+EGFR	addiction	aversion	30038519	No significant difference was found between <b>CTA</b> expression and <strong>epidermal growth factor receptor</strong> mutant status.
+EGFR	drug	alcohol	29774782	The Neuroprotective Effect of <b>Ethanol</b> Intoxication in Traumatic Brain Injury Is Associated with the Suppression of <strong>ErbB</strong> Signaling in Parvalbumin Positive Interneurons.
+EGFR	addiction	intoxication	29774782	The Neuroprotective Effect of Ethanol <b>Intoxication</b> in Traumatic Brain Injury Is Associated with the Suppression of <strong>ErbB</strong> Signaling in Parvalbumin Positive Interneurons.
+EGFR	drug	alcohol	29774782	Administration of selective <strong>ErbB</strong> inhibitors was able to recapitulate, to a significant extent, the neuroprotective effects of <b>ethanol</b> both in sensorimotor performance and structural integrity.
+EGFR	addiction	addiction	29570930	Cigarette smoke enhances oncogene <b>addiction</b> to c MET and desensitizes <strong>EGFR</strong> expressing non small cell lung cancer to <strong>EGFR</strong> TKIs.
+EGFR	drug	nicotine	29570930	Cigarette <b>smoking</b> is one of the leading risks for lung cancer and is associated with the insensitivity of non small cell lung cancer (NSCLC) to epidermal growth factor receptor (<strong>EGFR</strong>) tyrosine kinase inhibitors (TKIs).
+EGFR	drug	nicotine	29570930	Cigarette <b>smoking</b> is one of the leading risks for lung cancer and is associated with the insensitivity of non small cell lung cancer (NSCLC) to <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>) tyrosine kinase inhibitors (TKIs).
+EGFR	drug	nicotine	29570930	In this study, our data showed that chronic exposure to cigarette smoke extract (CSE) or <b>tobacco</b> smoke derived carcinogen benzo[α]pyrene, B[α]P, but not <b>nicotine</b> derived nitrosamine ketone (NNK), reduced the sensitivity of wild type <strong>EGFR</strong> expressing NSCLC cells to <strong>EGFR</strong> TKIs.
+EGFR	drug	nicotine	29471517	The gender, tumour differentiation, <strong>epidermal growth factor receptor</strong> mutation, <b>smoking</b> habits, lymphovascular space invasion, tumour size, maximum standard uptake value and carcinoembryonic antigen levels were significantly different in the 2 groups.
+EGFR	drug	opioid	29216892	<b>Opioid</b> agonist therapy has been widely used to reduce harms among individuals with <b>opioid</b> use disorder but its effectiveness has not been evaluated in the Middle East North African (<strong>MENA</strong>) region.
+EGFR	drug	opioid	29216892	Results support expanding the access to <b>opioid</b> agonist therapy in other <strong>MENA</strong> countries to treat substance dependence and reduce harms among individuals with <b>opioid</b> use disorder.
+EGFR	addiction	dependence	29216892	Results support expanding the access to opioid agonist therapy in other <strong>MENA</strong> countries to treat substance <b>dependence</b> and reduce harms among individuals with opioid use disorder.
+EGFR	drug	nicotine	29186353	<strong>EGFR</strong> mutations were found predominantly in never <b>smokers</b>; KRAS in current/former <b>smokers</b>.
+EGFR	drug	nicotine	28974261	Why are mutation rates in epidermal growth factor receptor (<strong>EGFR</strong>) and erb b2 receptor tyrosine kinase 2 (ERBB2) higher in lung cancer from never <b>smokers</b> than that from <b>smokers</b>?
+EGFR	drug	nicotine	28974261	Why are mutation rates in <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>) and erb b2 receptor tyrosine kinase 2 (ERBB2) higher in lung cancer from never <b>smokers</b> than that from <b>smokers</b>?
+EGFR	addiction	reward	28284947	Behavioral characterization of blocking the <strong>ErbB</strong> signaling during adolescent and adulthood in <b>reward</b> liking (preference) and <b>reward</b> related learning.
+EGFR	drug	alcohol	28284947	In the current study, we extend our findings and explore whether inhibition of the <strong>ErbB</strong> pathway during adolescence or adulthood also affects <b>alcohol</b> preference (hedonic "liking"), avoidance learning, and motivational reward "wanting".
+EGFR	addiction	reward	28284947	In the current study, we extend our findings and explore whether inhibition of the <strong>ErbB</strong> pathway during adolescence or adulthood also affects alcohol preference (<b>hedonic</b> "liking"), avoidance learning, and motivational <b>reward</b> "wanting".
+EGFR	drug	alcohol	28284947	We demonstrated that chronic administration of the pan <strong>ErbB</strong> kinase inhibitor JNJ28871063 (JNJ) to adolescent mice, but not to adult mice, reduced <b>alcohol</b> preference compared with the saline injected group, without affecting avoidance learning as measured by increasing concentrations of quinine in the bitter avoidance test.
+EGFR	addiction	reward	28284947	These data support our initial findings that interruption of the <strong>ErbB</strong> pathway during adolescence emerges in a reduced <b>hedonic</b> capacity that persists into adulthood, without disturbing avoidance and <b>reward</b> learning.
+EGFR	addiction	reward	28284947	In addition, this paper provides a further behavioral role of the <strong>ErbB</strong> signaling pathway in the <b>reward</b> system, and suggests a different time period for the involvement of the pathway in the "liking" and the "wanting" components of the system.
+EGFR	drug	nicotine	27843633	<b>Smoking</b> habits, histological subtype, and <strong>epidermal growth factor receptor</strong> mutation status were not associated with PD L1 expression score.
+EGFR	drug	alcohol	26700849	For example, we demonstrate that MEK inhibitors amplify the viability effect of the clinically used anti <b>alcoholism</b> drug <b>disulfiram</b> and show that the <strong>EGFR</strong> inhibitor tyrphostin AG555 has off target activity on the proteasome.
+EGFR	drug	amphetamine	26322025	Similarly, compared to only infected mice, epidermal growth factor receptor (<strong>EGFR</strong>) in <b>METH</b> exposed LCMV infected mice were up regulated.
+EGFR	drug	amphetamine	26322025	Similarly, compared to only infected mice, <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>) in <b>METH</b> exposed LCMV infected mice were up regulated.
+EGFR	drug	nicotine	26246248	"Impact of <b>Smoking</b> Cessation Treatment" on Lung Function and Response Rate in <strong>EGFR</strong> Mutated Patients: A Short Term Cohort Study.
+EGFR	drug	nicotine	26246248	A group of ten current <b>smokers</b> affected by NSCLC with <strong>EGFR</strong> activating mutation and concurrent mild COPD undergoing anti <strong>EGFR</strong> treatment without <b>smoking</b> cessation was used to compare clinical and functional data.
+EGFR	drug	nicotine	26246248	The combination of anti <strong>EGFR</strong> treatment and concurrent therapy for <b>smoking</b> cessation seems to be more effective than erlotinib alone in improving lung function and clinical response in advanced NSCLC patients with <strong>EGFR</strong> mutations.
+EGFR	drug	nicotine	26026961	Here, we hypothesized that nickel accumulation in lung tissues could contribute to <strong>EGFR</strong> mutations in never <b>smokers</b> with lung cancer.
+EGFR	drug	nicotine	25456362	In this open label, multicentre, phase 2 trial, we enrolled treatment naive patients with advanced lung cancer who had clinical (never <b>smokers</b> [<100 cigarettes per lifetime] or former light <b>smokers</b> [<10 pack years per lifetime] and ≥15 years since last cigarette) or molecular (<strong>EGFR</strong> mutation, regardless of <b>smoking</b> status) characteristics associated with response to <strong>EGFR</strong> inhibitors.
+EGFR	drug	nicotine	25442336	In addition to the well known characteristics of patients carrying <strong>EGFR</strong> mutations (female, adenocarcinoma, and never/light <b>smoker</b>), the proportion of cases with smaller primary lesions (T1/2) was found to be higher in patients with <strong>EGFR</strong> mutations than in those with wild type <strong>EGFR</strong>.
+EGFR	addiction	relapse	25442336	Patients with <strong>EGFR</strong> mutations showed similar response rate, <b>relapse</b> free survival, and 2 year <b>relapse</b> free rates as compared to patients with wild type <strong>EGFR</strong>.
+EGFR	addiction	relapse	25442336	Local relapses as the site of initial <b>relapse</b> occurred significantly less frequently in patients with <strong>EGFR</strong> mutation (4% vs 21%; P=.045).
+EGFR	drug	nicotine	25152623	<b>Smoking</b>, a solid predominant pattern, and a mucinous component were independently associated with fewer <strong>EGFR</strong> mutations.
+EGFR	drug	alcohol	24923262	Compared with abstinence, the odds ratio for a decrease in estimated glomerular filtration rate (<strong>eGFR</strong>) was 0.14 (95% CI: 0.01 0.91) among heavy drinkers, and 0.42 (95% CI: 0.17 0.98) among binge drinkers and the association between the amount of mean daily <b>alcohol</b> intake, binge drinking status and a likelihood of reduced <strong>eGFR</strong> value showed significant trends (p = 0.041 and p = 0.038, respectively), after adjusting for age, smoking status, amount of physical activity, morbid hypertension, diabetes, dyslipidaemia, anaemia and body mass index.
+EGFR	drug	nicotine	24923262	Compared with abstinence, the odds ratio for a decrease in estimated glomerular filtration rate (<strong>eGFR</strong>) was 0.14 (95% CI: 0.01 0.91) among heavy drinkers, and 0.42 (95% CI: 0.17 0.98) among binge drinkers and the association between the amount of mean daily alcohol intake, binge drinking status and a likelihood of reduced <strong>eGFR</strong> value showed significant trends (p = 0.041 and p = 0.038, respectively), after adjusting for age, <b>smoking</b> status, amount of physical activity, morbid hypertension, diabetes, dyslipidaemia, anaemia and body mass index.
+EGFR	addiction	intoxication	24923262	Compared with abstinence, the odds ratio for a decrease in estimated glomerular filtration rate (<strong>eGFR</strong>) was 0.14 (95% CI: 0.01 0.91) among heavy drinkers, and 0.42 (95% CI: 0.17 0.98) among <b>binge</b> drinkers and the association between the amount of mean daily alcohol intake, <b>binge</b> drinking status and a likelihood of reduced <strong>eGFR</strong> value showed significant trends (p = 0.041 and p = 0.038, respectively), after adjusting for age, smoking status, amount of physical activity, morbid hypertension, diabetes, dyslipidaemia, anaemia and body mass index.
+EGFR	drug	alcohol	24923262	<b>Alcohol</b> consumption was inversely associated with a reduction in <strong>eGFR</strong> in Korean men.
+EGFR	drug	alcohol	24710718	We hypothesized that Cav 1 could attenuate <b>ethanol</b> mediated nitrosative stress and liver damage through regulating epidermal growth factor receptor/signal transducer and activator of transcription 3/inducible nitric oxide synthase (<strong>EGFR</strong>/STAT3/iNOS) signaling cascades.
+EGFR	drug	alcohol	24710718	We hypothesized that Cav 1 could attenuate <b>ethanol</b> mediated nitrosative stress and liver damage through regulating <strong>epidermal growth factor receptor</strong>/signal transducer and activator of transcription 3/inducible nitric oxide synthase (<strong>EGFR</strong>/STAT3/iNOS) signaling cascades.
+EGFR	drug	alcohol	24710718	Furthermore, the results revealed that the <b>ethanol</b> mediated Cav 1 increase was in an extracellular signal regulated kinase dependent manner, and Cav 1 protected hepatocytes from <b>ethanol</b> mediated apoptosis by inhibiting iNOS activity and regulating <strong>EGFR</strong>  and STAT3 signaling cascades.
+EGFR	drug	alcohol	24710718	Cav 1 could be a cellular defense protein against <b>alcoholic</b> hepatic injury through inhibiting reactive nitrogen species and regulating <strong>EGFR</strong>/STAT3/iNOS signaling cascades.
+EGFR	drug	opioid	24304333	In prior studies, we discovered that the mechanism of TSP1 regulation by μ <b>opioids</b> in astrocytes involves crosstalk between three different classes of receptors, μ <b>opioid</b> receptor, <strong>EGFR</strong> and TGFβR.
+EGFR	drug	opioid	24304333	Moreover, TGFβ1 stimulated TSP1 expression via <strong>EGFR</strong> and ERK/MAPK activation, indicating that <strong>EGFR</strong> is a signaling hub for <b>opioid</b> and TGFβ1 actions.
+EGFR	addiction	relapse	23775406	ANCCA expression was evaluated by immunohistochemistry in 143 surgically resected lung adenocarcinomas and was correlated with clinicopathologic and molecular variables including adenocarcinoma histologic subtypes, tumor, node, metastasis status, <b>relapse</b> free survival, overall survival, <strong>EGFR</strong> mutations, KRAS mutations, HER2 mutations and ALK fusions.
+EGFR	drug	alcohol	23400686	In 289 patients with T3 4 (77.8%), node negative (84.1%) tumors of the larynx, high <strong>EGFR</strong> and CCND1 mRNA correlated with no or ex smoking, (p = 0.003 and p = 0.029, respectively), while low Akt3 mRNA correlated with <b>alcohol</b> abuse, N0 stage, total laryngectomy, and absence of neck dissection.
+EGFR	drug	nicotine	23400686	In 289 patients with T3 4 (77.8%), node negative (84.1%) tumors of the larynx, high <strong>EGFR</strong> and CCND1 mRNA correlated with no or ex <b>smoking</b>, (p = 0.003 and p = 0.029, respectively), while low Akt3 mRNA correlated with alcohol abuse, N0 stage, total laryngectomy, and absence of neck dissection.
+EGFR	drug	nicotine	23150706	Patients with lung adenocarcinomas with RET fusion gene had more poorly differentiated tumors (63.6%; P = .029 for RET v ALK, P = .007 for RET v <strong>EGFR</strong>), with a tendency to be younger (≤ 60 years; 72.7%) and never <b>smokers</b> (81.8%) and to have solid subtype (63.6%) and a smaller tumor (≤ 3 cm) with N2 disease (54.4%).
+EGFR	drug	opioid	23142605	<strong>EGFR</strong> dependent subcellular communication was responsible for <b>morphine</b> mediated AC superactivation.
+EGFR	drug	opioid	23142605	In the present study, we demonstrated that chronic <b>morphine</b> treatment sensitized <strong>EGFR</strong> signaling by augmenting <strong>EGFR</strong> phosphorylation and translocation into ER, which was essential for CRT MOR tethering within the lipid rafts and AC5 superactivation.
+EGFR	drug	opioid	23142605	Taken together, our data raised the possibility that an adaptive change in MOR and <strong>EGFR</strong> signal systems might establish CRT related subcellular communication, the signaling network within brain synaptic zone was proposed to implicate in <b>morphine</b> tolerance and dependence.
+EGFR	addiction	dependence	23142605	Taken together, our data raised the possibility that an adaptive change in MOR and <strong>EGFR</strong> signal systems might establish CRT related subcellular communication, the signaling network within brain synaptic zone was proposed to implicate in morphine tolerance and <b>dependence</b>.
+EGFR	drug	nicotine	22464348	<strong>EGFR</strong> mutations are more frequent in never <b>smokers</b>, as are EML4 ALK fusions.
+EGFR	drug	nicotine	22247002	Matted nodes were a poor prognostic factor independent of T classification, HPV, <strong>EGFR</strong>, and <b>smoking</b> status.
+EGFR	drug	nicotine	22085699	In this study, we demonstrated a novel signaling mechanism by which <b>nicotine</b> exposure activated Src to sensitize epidermal growth factor receptor (<strong>EGFR</strong>) mediated pathways for breast cancer cell growth promotion.
+EGFR	drug	nicotine	22085699	In this study, we demonstrated a novel signaling mechanism by which <b>nicotine</b> exposure activated Src to sensitize <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>) mediated pathways for breast cancer cell growth promotion.
+EGFR	drug	nicotine	22085699	After the ligation of nAChR with <b>nicotine</b>, <strong>EGFR</strong> was shown to be activated and then internalized in both MCF10A and MDA MB 231 breast cancer cells.
+EGFR	drug	nicotine	22085699	We further demonstrated that through Src, the ligation of <b>nicotine</b> with nAChR stimulated the <strong>EGFR</strong>/ERK1/2 pathway for the activation of E2F1 and further cell progression.
+EGFR	drug	nicotine	22085699	Our study reveals the existence of a potential, regulatory network governed by the interaction of <b>nicotine</b> and nAChR that integrates the conventional, mitogenic Src and <strong>EGFR</strong> signals for breast cancer development.
+EGFR	addiction	dependence	21673064	FGFR and epidermal growth factor receptor (<strong>EGFR</strong>) <b>dependence</b> was defined by sensitivity to multiple inhibitors selective for FGFRs or <strong>EGFR</strong>.
+EGFR	addiction	dependence	21673064	FGFR and <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>) <b>dependence</b> was defined by sensitivity to multiple inhibitors selective for FGFRs or <strong>EGFR</strong>.
+EGFR	drug	nicotine	21655907	In addition, most adenocarcinomas in never <b>smokers</b> harbor one of the proto oncogene aberrations that occur in a mutually exclusive manner (<strong>EGFR</strong> mutation, KRAS mutation, HER2 mutations, or ALK translocation).
+EGFR	addiction	relapse	21247966	<strong>EGFR</strong> gene copy number gain is related to high tumor SUV and frequent <b>relapse</b> after adjuvant chemotherapy in resected lung adenocarcinoma.
+EGFR	drug	nicotine	21247966	<strong>EGFR</strong> copy number change did not correlate with age, gender or <b>smoking</b> history.
+EGFR	addiction	relapse	21247966	<strong>EGFR</strong> copy number gain is associated with aggressive tumor biology and is a poor prognostic factor for tumor <b>relapse</b> in resected lung adenocarcinoma patients receiving adjuvant chemotherapy of paclitaxel and carboplatin.
+EGFR	drug	nicotine	21178720	The nine selected studies covered a broad range of topics including possible hormonal role in the development of lung adenocarcinoma, lung cancer in never <b>smokers</b>, stereotactic radiotherapy for early stage lung cancer, prognostic role of pleural lavage cytology, neoadjuvant chemotherapy for operable lung cancer, maintenance erlotinib, use of erlotinib after gefitinib, comparison of the two <strong>epidermal growth factor receptor</strong> tyrosine kinase inhibitors, and risk of central nervous system relapse in patients treated with <strong>epidermal growth factor receptor</strong> tyrosine kinase inhibitors.
+EGFR	addiction	relapse	21178720	The nine selected studies covered a broad range of topics including possible hormonal role in the development of lung adenocarcinoma, lung cancer in never smokers, stereotactic radiotherapy for early stage lung cancer, prognostic role of pleural lavage cytology, neoadjuvant chemotherapy for operable lung cancer, maintenance erlotinib, use of erlotinib after gefitinib, comparison of the two <strong>epidermal growth factor receptor</strong> tyrosine kinase inhibitors, and risk of central nervous system <b>relapse</b> in patients treated with <strong>epidermal growth factor receptor</strong> tyrosine kinase inhibitors.
+EGFR	drug	nicotine	20404520	Interestingly, treatment with these small molecule, reversible <strong>EGFR</strong> TKIs leads to more positive response rates in patients with adenocarcinoma, in females, Asians, and patients with no history of <b>smoking</b>.
+EGFR	addiction	relapse	19609951	We summarized the result of the <strong>EGFR</strong> mutation analysis for 1,176 patients performed at the time of diagnosis or <b>relapse</b>.
+EGFR	drug	nicotine	19609951	The <strong>EGFR</strong> mutation was significantly associated with adenocarcinoma (p = 0.006) and light <b>smoking</b> (p < 0.0001), but not gender.
+EGFR	drug	alcohol	19490888	(2009) now implicate a new Ste20 family kinase (Happyhour) and the <strong>EGFR</strong>/ERK signaling pathway it antagonizes in <b>alcohol</b> intoxication in flies.
+EGFR	addiction	intoxication	19490888	(2009) now implicate a new Ste20 family kinase (Happyhour) and the <strong>EGFR</strong>/ERK signaling pathway it antagonizes in alcohol <b>intoxication</b> in flies.
+EGFR	drug	alcohol	19307230	<b>Alcohol</b> intake of >or=30 g/day was associated with an increased risk of albuminuria after adjustment for age, sex and baseline kidney function (OR = 1.59, 95% CI 1.07 2.36), but a reduced risk of <strong>eGFR</strong> <60 mL/min/1.73 m(2) (OR = 0.59, 95% CI 0.37 0.95), compared with consumption of <10 g/day.
+EGFR	addiction	relapse	20731908	[Analysis of Treatment Response and Chest CT Characteristics for Patients treated by <strong>EGFR</strong> TKI in <b>Relapse</b> Advanced Lung Adenocarcinoma.].
+EGFR	drug	nicotine	20731908	For previously treated recurrent non small cell lung cancer, many studies have proven that inhibitors of the tyrosine kinase of epidermal growth factor receptor (<strong>EGFR</strong> TKI),such as gefitinib and erlotinib can increase survival, especially in non <b>smoker</b> adenocarcinoma.
+EGFR	drug	nicotine	20731908	For previously treated recurrent non small cell lung cancer, many studies have proven that inhibitors of the tyrosine kinase of <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong> TKI),such as gefitinib and erlotinib can increase survival, especially in non <b>smoker</b> adenocarcinoma.
+EGFR	drug	nicotine	18262213	Recurrent exposure to <b>nicotine</b> differentiates human bronchial epithelial cells via <strong>epidermal growth factor receptor</strong> activation.
+EGFR	drug	nicotine	18262213	We also demonstrate that <b>nicotine</b> treatment induced NF kB translocation to the nucleus, phosphorylation of the epidermal growth factor receptor (<strong>EGFR</strong>), and accumulation of heparin binding EGF in the extracellular medium.
+EGFR	drug	nicotine	18262213	We also demonstrate that <b>nicotine</b> treatment induced NF kB translocation to the nucleus, phosphorylation of the <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>), and accumulation of heparin binding EGF in the extracellular medium.
+EGFR	drug	nicotine	18262213	Moreover, addition of AG1478, an inhibitor of <strong>EGFR</strong> tyrosine phosphorylation, or cetuximab, a monoclonal antibody that precludes ligand binding to the same receptor, prevented cell differentiation by <b>nicotine</b>.
+EGFR	drug	nicotine	17932690	<b>Smoking</b> status (never <b>smoker</b> vs. <b>smoker</b>, P=0.0032), and pathological subtypes (adenocarcinoma vs. non adenocarcinoma, P=0.0011), but not <strong>EGFR</strong> amplification (P=0.1278), were correlated with survival of lung cancers.
+EGFR	drug	nicotine	17649787	The initial positive effect of combination chemotherapy with erlotinib as the first line of treatment correlates with several positive predictors including the type of carcinoma, non <b>smoking</b> status, occurrence of rash and the presence of exon 19 <strong>EGFR</strong> gene mutation.
+EGFR	addiction	relapse	17649787	Later, during the <b>relapse</b>, the same mutation was still present and, in addition, a T790M mutation in exon 20 of <strong>EGFR</strong> was found.
+EGFR	drug	nicotine	17315157	The <b>tobacco</b> carcinogen <b>nicotine</b> derived nitrosamine 4 (N methyl N nitrosamino) 1 (3 pyridyl) 1 butanone (NNK) stimulates the proliferation of human PAC cells and small airway epithelial cells through beta 1 adrenorecptor mediated transactivation of the epidermal growth factor receptor (<strong>EGFR</strong>).
+EGFR	drug	nicotine	17315157	The <b>tobacco</b> carcinogen <b>nicotine</b> derived nitrosamine 4 (N methyl N nitrosamino) 1 (3 pyridyl) 1 butanone (NNK) stimulates the proliferation of human PAC cells and small airway epithelial cells through beta 1 adrenorecptor mediated transactivation of the <strong>epidermal growth factor receptor</strong> (<strong>EGFR</strong>).
+EGFR	drug	nicotine	16503085	Epidermal growth factor receptor (<strong>EGFR</strong>) gene mutations are frequently detected in lung cancer, especially in adenocarcinoma, in females, and non <b>smoking</b> patients.
+EGFR	drug	nicotine	16503085	<strong>Epidermal growth factor receptor</strong> (<strong>EGFR</strong>) gene mutations are frequently detected in lung cancer, especially in adenocarcinoma, in females, and non <b>smoking</b> patients.
+EGFR	addiction	addiction	15464447	Mutations and <b>addiction</b> to <strong>EGFR</strong>: the Achilles 'heal' of lung cancers?
+EGFR	addiction	relapse	14566828	Clinical value of p53, c <strong>erbB</strong> 2, CEA and CA125 regarding <b>relapse</b>, metastasis and death in resectable non small cell lung cancer.
+EGFR	addiction	relapse	7793243	Data reported here suggest that <strong>EGFR</strong> expression probably plays a role not only by regulating the growth of laryngeal cancer, but also by identifying a sub set of laryngeal cancer patients at a higher degree of <b>relapse</b> risk and with an unfavorable prognosis.
+EGFR	addiction	relapse	7915830	Age at diagnosis, number of recurrences, analysis as well as time to <b>relapse</b> or metastases were similar in c <strong>erbB</strong> 2 positive and  negative malignant tumours.
+PTGS2	drug	nicotine	32479813	This idea is supported by dose dependent attenuation of <b>nicotine</b> preference by the selective <strong>COX 2</strong> inhibitors valdecoxib and LM 4131.
+PTGS2	drug	alcohol	31845992	Similarly, no changes on the expression of ERK1/2, SAPK/JNK, COX 1 or <strong>COX 2</strong> were found in the LV during <b>ethanol</b> withdrawal.
+PTGS2	addiction	withdrawal	31845992	Similarly, no changes on the expression of ERK1/2, SAPK/JNK, COX 1 or <strong>COX 2</strong> were found in the LV during ethanol <b>withdrawal</b>.
+PTGS2	drug	amphetamine	31775383	Additionally, Ingenuity® Pathway Analysis along with details of RNA expression changes revealed cyclo oxygenase 2 (<strong>COX2</strong>) driven prostaglandin (PG) E2 synthesis, glutamine uptake, and the Nuclear factor erythroid2 related factor 2 (NRF2) canonical pathway in microglia were associated with the binge administration regimen of <b>METH</b>.
+PTGS2	addiction	intoxication	31775383	Additionally, Ingenuity® Pathway Analysis along with details of RNA expression changes revealed cyclo oxygenase 2 (<strong>COX2</strong>) driven prostaglandin (PG) E2 synthesis, glutamine uptake, and the Nuclear factor erythroid2 related factor 2 (NRF2) canonical pathway in microglia were associated with the <b>binge</b> administration regimen of METH.
+PTGS2	addiction	relapse	31570459	<strong>COX2</strong> expression was correlated with poor <b>relapse</b> free survival in patients overall, and in p16 positive patients.
+PTGS2	drug	nicotine	31570459	<b>Smoking</b> was positively associated with <strong>COX2</strong> expression.
+PTGS2	drug	opioid	31294469	Nonsteroidal anti inflammatory drugs (NSAIDs), selective <strong>COX 2</strong> inhibitors and <b>opioid</b> drugs can temporarily reduce osteoporotic pain but have relevant side effects, such as addiction, tolerability and safety.
+PTGS2	addiction	addiction	31294469	Nonsteroidal anti inflammatory drugs (NSAIDs), selective <strong>COX 2</strong> inhibitors and opioid drugs can temporarily reduce osteoporotic pain but have relevant side effects, such as <b>addiction</b>, tolerability and safety.
+PTGS2	drug	alcohol	31228610	Neurotoxicity to dopamine neurons after the serial exposure to <b>alcohol</b> and methamphetamine: Protection by <strong>COX 2</strong> antagonism.
+PTGS2	drug	amphetamine	31228610	Neurotoxicity to dopamine neurons after the serial exposure to alcohol and <b>methamphetamine</b>: Protection by <strong>COX 2</strong> antagonism.
+PTGS2	drug	amphetamine	31228610	Intervention with a selective <strong>COX 2</strong> inhibitor during EtOH drinking prevented the changes in microglia, and attenuated the increase in cleaved caspase 3, and decreases in TH and DAT after <b>Meth</b> administration.
+PTGS2	drug	cannabinoid	30796025	In addition to arachidonic acid, <strong>COX 2</strong> oxidizes the <b>endocannabinoid</b> 2 arachidonoylglycerol (2 AG) to produce prostaglandin E2 (PGE2) glycerol (PGE2 G); PGE2 G is known to produce hyperalgesia.
+PTGS2	drug	alcohol	30710549	Our studies show that the vascular hypocontractility induced by <b>ethanol</b> withdrawal is independent of the endothelium and it is mediated by PGI2 derived from <strong>COX 2</strong>.
+PTGS2	addiction	withdrawal	30710549	Our studies show that the vascular hypocontractility induced by ethanol <b>withdrawal</b> is independent of the endothelium and it is mediated by PGI2 derived from <strong>COX 2</strong>.
+PTGS2	drug	cannabinoid	30618769	In addition to the well characterized hydrolytic pathways, cyclooxygenase 2 (<strong>COX 2</strong>) mediated oxygenation is thought to be an alternative route for <b>endocannabinoid</b> metabolism and therefore provides a new avenue for drug intervention.
+PTGS2	drug	opioid	30388619	Astrocyte EV Induced lincRNA <strong>Cox2</strong> Regulates Microglial Phagocytosis: Implications for <b>Morphine</b> Mediated Neurodegeneration.
+PTGS2	drug	opioid	30388619	Herein, we show that EVs derived from astrocytes exposed to <b>morphine</b> can be taken up by microglial endosomes, leading, in turn, to activation of Toll like receptor 7 (TLR7) with a subsequent upregulation of lincRNA <strong>Cox2</strong> expression, ultimately resulting in impaired microglial phagocytosis.
+PTGS2	drug	opioid	30388619	Additionally, we also showed that intranasal delivery of EVs containing lincRNA <strong>Cox2</strong> siRNA (small interfering RNA) was able to restore microglial phagocytic activity in mice administered <b>morphine</b>.
+PTGS2	drug	amphetamine	30002494	Exposure to CUS prior to unrestricted <b>Meth</b> self administration had no effect on <b>Meth</b> intake in rats; however, the pro inflammatory mediator cyclooxygenase 2 (<strong>COX 2</strong>) and the breakdown of cell matrix adhesion protein β dystroglycan in isolated cerebral cortical capillaries were increased after 3 days of abstinence and persisted for 7 days.
+PTGS2	drug	amphetamine	30002494	The decrease in occludin was blocked by the <strong>COX 2</strong> specific inhibitor nimesulide treatment during abstinence from <b>Meth</b>.
+PTGS2	drug	amphetamine	30002494	The changes in <strong>COX 2</strong>, β dystroglycan, and occludin were only evident following the serial exposure to stress and <b>Meth</b> but not after either one alone.
+PTGS2	drug	amphetamine	30002494	Furthermore, <strong>COX 2</strong> inhibition may be a viable pharmacological intervention to block vascular changes after <b>Meth</b> exposure.
+PTGS2	drug	opioid	29992509	Chronic pain after osteoporotic fractures requires a multifaceted approach, which includes a large spectrum of drugs (antiosteoporosis treatment, acetaminophen, NSAIDs, selective <strong>COX 2</strong> inhibitors, weak and strong <b>opioids</b>) and non pharmacological treatment.
+PTGS2	drug	amphetamine	29944913	In the present study, we observed that the toxic high dose of <b>METH</b> treated neuroblastoma SH SY5Y cells significantly decreased cell viability but increased apoptotic cell death, the active cleaved form of calcineurin, the nuclear translocation of NFAT, and <strong>COX 2</strong> levels.
+PTGS2	drug	amphetamine	29944913	These findings might emphasize the role of calpastatin against <b>METH</b> induced toxicity by a mechanism related to calpain dependent CaN NFAT activation induced <strong>COX 2</strong> expression.
+PTGS2	drug	opioid	29619540	Chronic pain after osteoporotic fractures requires a multifaceted approach, which includes a large spectrum of drugs (antiosteoporosis treatment, acetaminophen, NSAIDs, selective <strong>COX 2</strong> inhibitors, weak and strong <b>opioids</b>) and non pharmacological treatment.
+PTGS2	drug	opioid	29576123	Accumulated evidence suggests that spinal cyclooxygenase 2 (<strong>COX 2</strong>) and prostaglandin E2 (PGE2) may be implicated in the development of <b>opioid</b> induced hyperalgesia.
+PTGS2	drug	opioid	29576123	This behavioural change was paralleled with an increase in spinal <strong>COX 2</strong> mRNA and PGE2 after <b>fentanyl</b> administration.
+PTGS2	drug	psychedelics	29404791	Regional analgesia and agents such as <b>ketamine</b>, gabapentinoids, and <strong>COX 2</strong> inhibitors have also been found to decrease the risks of developing chronic pain to varying degrees.
+PTGS2	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (Cnr1, Cnr2, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, <strong>Ptgs2</strong>, and Alox12), and TRPV1 sensitizing kinases (Mapk3, Mapk14, Prkcg, and Prkaca).
+PTGS2	drug	amphetamine	28856500	Cyclooxygenase inhibition by ketoprofen during EtOH drinking blocked the increases in LPS and <strong>COX 2</strong> and the enhanced decreases in dopamine and serotonin produced by <b>Meth</b>.
+PTGS2	drug	alcohol	28408342	These data were supported by functional evidence since chronic <b>alcohol</b> consumption produced no changes in the expression of TNF α or <strong>COX 2</strong>.
+PTGS2	addiction	sensitization	28126501	The prevention of this hyperalgesia by diclofenac (1 10μg), the inhibitors of COX 1 SC 560 (0.1 1μg) or <strong>COX 2</strong> celecoxib (1 5μg), the TRPV1 antagonist capsazepine (0.03 0.3μg) or the TRPA1 antagonist HC030031 (10 50μg) demonstrates the involvement of prostaglandin synthesis and TRP <b>sensitization</b> in CCL5 evoked hyperalgesia.
+PTGS2	drug	cannabinoid	27470501	In 7 days pregnant wild type, but not <b>cannabinoid</b> receptor type 1 knockout (CB1 KO) mice, LPS increased <strong>COX 2</strong> expression and prostaglandin F2α (PGF2α) production in the uterus leading to lower expression of prolactin receptor in the ovary and a marked regression of corpora lutea (CL), suggesting that the eCS mediates the deleterious effects of LPS on reproductive events.
+PTGS2	addiction	withdrawal	27470501	Treatment of 7 day pregnant WT mice with LPS induced a P4 <b>withdrawal</b> (p < 0.05), increased in uterine <strong>COX 2</strong> mRNA and protein expression (p < 0.05) as well as an increase in uterine PGF2α production (p < 0.05).
+PTGS2	drug	opioid	27547561	We assess the perception of risk and the perception of ADR associated with <strong>COX2</strong> Inbitors, paracetamol, NSAIDs, and <b>morphine</b> in medical students and residents of northeast of Mexico.
+PTGS2	drug	alcohol	26857094	OEA reduced the levels of interleukin 1beta (IL 1β), the monocyte chemoattractant protein 1 (MCP 1), and the enzymes cyclooxygenase 2 (<strong>COX 2</strong>) and inducible nitric oxide synthase (iNOS) in <b>ethanol</b> binged animals.
+PTGS2	drug	opioid	26803746	Multimodal analgesia that includes prophylactic administration of selective cyclooxygenase 2 (<strong>COX 2</strong>) inhibitors can improve postoperative pain and reduce <b>opioid</b> analgesic consumption after total knee arthroplasty (TKA).
+PTGS2	drug	cannabinoid	25712641	The results of this study seemed to indicate that the interaction between <b>cannabinoid</b>, <strong>COX 2</strong> and NOS(s) systems might exist.
+PTGS2	drug	alcohol	25486089	Using wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with <b>ethanol</b> (3.0g/kg) for 2weeks, we show that binge like <b>ethanol</b> treatment activates TLR4 signaling pathways (MAPK, NFκB) leading to the up regulation of cytokines and pro inflammatory mediators (<strong>COX 2</strong>, iNOS, HMGB1), impairing synaptic and myelin protein levels and causing ultrastructural alterations.
+PTGS2	addiction	intoxication	25486089	Using wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with ethanol (3.0g/kg) for 2weeks, we show that <b>binge</b> like ethanol treatment activates TLR4 signaling pathways (MAPK, NFκB) leading to the up regulation of cytokines and pro inflammatory mediators (<strong>COX 2</strong>, iNOS, HMGB1), impairing synaptic and myelin protein levels and causing ultrastructural alterations.
+PTGS2	drug	opioid	25241065	In support, MOR dependent Protein Kinase A (PKA) opposed TLR4 signaling, as PKA inhibition (H 89) also unmasked ( ) <b>morphine</b> induced TNFα and <strong>COX2</strong> mRNA upregulation.
+PTGS2	drug	opioid	24284847	cyclo oxygenase 2 (<strong>COX 2</strong>) nonsteroidal anti inflammatory drugs (NSAIDs), <b>tramadol</b>, and <b>opioids</b> were commonly used.
+PTGS2	drug	cannabinoid	24008428	We evaluated the pharmacology of spinal selective <b>cannabinoid</b> (CB) receptor agonists and a cyclooxygenase 2 (<strong>COX 2</strong>) inhibitor on bone tumor pain.
+PTGS2	addiction	withdrawal	24008428	Intrathecal CB1 (ACEA) and CB2 receptor (AM 1241) agonists and a <strong>COX 2</strong> inhibitor (DuP 697) dose dependently increased the <b>withdrawal</b> threshold.
+PTGS2	drug	opioid	23243929	Equally dangerous can be an abuse of <b>tramadol</b>, <b>codeine</b> and <strong>COX 2</strong> inhibitors.
+PTGS2	drug	opioid	22845665	Induction of P glycoprotein and Bcrp at the rat blood brain barrier following a subchronic <b>morphine</b> treatment is mediated through NMDA/<strong>COX 2</strong> activation.
+PTGS2	drug	alcohol	22749946	Chronic self administration of <b>ethanol</b> reduced the expression of the C fos gene 4  to 12 fold and increased expression of the <strong>COX 2</strong> (up to 4 fold) and Homer1a genes in the rat prefrontal cortex.
+PTGS2	drug	cannabinoid	22363560	It was suggested that <b>endocannabinoids</b> are metabolized by cyclooxygenase (COX) 2 in the spinal cord of rats with kaolin/λ carrageenan induced knee inflammation, and that this mechanism contributes to the analgesic effects of <strong>COX 2</strong> inhibitors in this experimental model.
+PTGS2	drug	cannabinoid	22363560	We report the development of a specific method for the identification of <b>endocannabinoid</b> <strong>COX 2</strong> metabolites, its application to measure the levels of these compounds in tissues, and the finding of prostamide F(2α) (PMF(2α)) in mice with knee inflammation.
+PTGS2	drug	cannabinoid	22363560	Whereas the levels of spinal <b>endocannabinoids</b> were not significantly altered by kaolin/λ carrageenan induced knee inflammation, those of the <strong>COX 2</strong> metabolite of AEA, PMF(2α), were strongly elevated.
+PTGS2	drug	nicotine	21210228	Furthermore, <strong>COX 2</strong> signal was induced by <b>nicotine</b> treatment and is involved in <b>nicotine</b> enhanced fibronectin expression.
+PTGS2	drug	opioid	20967889	In this article, the phase 1 and 2 metabolisms of seven of the most important classes of drugs monitored in horseracing are reviewed, including: anabolic androgenic steroids (AAS), β₂  agonists, stimulants, sedatives/tranquilizers, local anesthetics, non steroidal anti inflammatory analgesics (NSAIDS)/cyclooxygenase 2 (<strong>COX 2</strong>) inhibitors, and <b>opioid</b> analgesics.
+PTGS2	drug	opioid	20346263	To determine which class of non <b>opioid</b> analgesics   paracetamol (acetaminophen), NSAIDs or <strong>COX 2</strong> inhibitors   is the most effective at reducing <b>morphine</b> consumption and associated adverse effects when used as part of multimodal analgesia following major surgery.
+PTGS2	drug	opioid	20346263	Randomised controlled trials comparing paracetamol, NSAIDs or <strong>COX 2</strong> inhibitors to each other or placebo, in adults receiving patient controlled analgesia (PCA) with <b>morphine</b> following major surgery, were included.
+PTGS2	drug	opioid	20346263	When paracetamol, NSAIDs or <strong>COX 2</strong> inhibitors were added to PCA <b>morphine</b>, there was a statistically significant reduction in <b>morphine</b> consumption: paracetamol (MD  6.34 mg; 95% CrI  9.02 to  3.65); NSAIDs (MD  10.18; 95% CrI  11.65 to  8.72); and <strong>COX 2</strong> inhibitors (MD  10.92; 95% CrI  12.77 to  9.08).
+PTGS2	drug	opioid	20346263	24 hour <b>morphine</b> consumption decreased by 6.3 mg to 10.9 mg, compared to placebo, when paracetamol, NSAID or <strong>COX 2</strong> inhibitors were added to PCA <b>morphine</b> following surgery.
+PTGS2	drug	cannabinoid	19879047	Recently, however, <strong>COX 2</strong> was shown to be also involved in the metabolism of <b>endocannabinoids</b>.
+PTGS2	drug	cannabinoid	19879047	The reversal of spinal hyperexcitability by <strong>COX 2</strong> inhibitors was prevented or partially reversed by AM 251, an antagonist at the <b>cannabinoid</b> 1 receptor.
+PTGS2	drug	cannabinoid	19879047	We conclude that inhibition of spinal <strong>COX 2</strong> not only reduces PG production but also <b>endocannabinoid</b> breakdown and provide evidence that reversal of inflammation evoked spinal hyperexcitability by <strong>COX 2</strong> inhibitors is more related to endocannabinoidergic mechanisms than to inhibition of spinal PG synthesis.
+PTGS2	drug	nicotine	18805435	Treatment of cells with alpha bungarotoxin (alpha BTX, alpha7nAChR antagonist) or propranolol (beta adrenergic receptor antagonist) blocked NNK induced <strong>COX 2</strong>/PGE(2) and cell proliferation, while <b>nicotine</b> mediated cell growth and <strong>COX 2</strong>/PGE(2) induction can only be suppressed by propranolol, but not alpha BTX.
+PTGS2	drug	nicotine	18805435	Moreover, in contrast to the dependence of growth promoting effect of <b>nicotine</b> on Erk activation, inhibitor of p38 mitogen activated protein kinase (MAPK) repressed NNK induced <strong>COX 2</strong> upregulation and resulted in suppression of cell growth.
+PTGS2	addiction	dependence	18805435	Moreover, in contrast to the <b>dependence</b> of growth promoting effect of nicotine on Erk activation, inhibitor of p38 mitogen activated protein kinase (MAPK) repressed NNK induced <strong>COX 2</strong> upregulation and resulted in suppression of cell growth.
+PTGS2	drug	nicotine	18805435	In addition, <b>nicotine</b> and NNK mediated <strong>COX 2</strong> induction via different receptors to modulate several G1/S transition regulatory proteins and promote gastric cancer cell growth.
+PTGS2	drug	nicotine	18805435	Selective <strong>COX 2</strong> inhibitor (SC 236) caused G1 arrest and abrogated <b>nicotine</b>/NNK induced cell proliferation.
+PTGS2	drug	opioid	17642469	Some of them are: DREAM which constitututively suppresses transcription of mRNA for <b>opioid</b> peptides, oncostatin M, <strong>COX 2</strong> inhibitors, cFOS protein, tachykinins, gamma butyric acid agonist, L type Ca++ channels.
+PTGS2	drug	opioid	17315406	With the withdrawal of <strong>COX 2</strong> inhibitors, <b>opioids</b> are an obvious alternative choice for pain.
+PTGS2	addiction	withdrawal	17315406	With the <b>withdrawal</b> of <strong>COX 2</strong> inhibitors, opioids are an obvious alternative choice for pain.
+PTGS2	drug	alcohol	17284196	Because we have demonstrated that chronic <b>ethanol</b> treatment induces inflammatory processes in the brain, we investigate whether intermittent <b>ethanol</b> intoxication enhances cyclooxygenase 2 (<strong>COX 2</strong>) and inducible nitric oxide synthase (iNOS) in adolescent rats, and whether these mediators induce brain damage and cause permanent cognitive dysfunctions.
+PTGS2	addiction	intoxication	17284196	Because we have demonstrated that chronic ethanol treatment induces inflammatory processes in the brain, we investigate whether intermittent ethanol <b>intoxication</b> enhances cyclooxygenase 2 (<strong>COX 2</strong>) and inducible nitric oxide synthase (iNOS) in adolescent rats, and whether these mediators induce brain damage and cause permanent cognitive dysfunctions.
+PTGS2	drug	alcohol	17284196	Levels of <strong>COX 2</strong>, iNOS and cell death were assessed in the neocortex, hippocampus and cerebellum 24 h after the final <b>ethanol</b> administration.
+PTGS2	drug	alcohol	17284196	Our results show that intermittent <b>ethanol</b> intoxication upregulates <strong>COX 2</strong> and iNOS levels, and increases cell death in the neocortex, hippocampus and cerebellum.
+PTGS2	addiction	intoxication	17284196	Our results show that intermittent ethanol <b>intoxication</b> upregulates <strong>COX 2</strong> and iNOS levels, and increases cell death in the neocortex, hippocampus and cerebellum.
+PTGS2	drug	alcohol	17284196	Administration of indomethacin, a <strong>COX 2</strong> inhibitor, abolishes the induction of <strong>COX 2</strong> and iNOS expression and cell death, preventing <b>ethanol</b> induced behavioural deficits.
+PTGS2	drug	alcohol	17127267	Recent findings indicate that low concentrations of <b>ethanol</b> (10 mM) promote inflammatory processes in brain and in glial cells by up regulating cytokines and inflammatory mediators (iNOS, NO, <strong>COX 2</strong>), and by activating signaling pathways (IKK, MAPKs) and transcriptional factors (NF kappaB, AP 1) implicated in inflammatory injury.
+PTGS2	drug	alcohol	17067360	Binge <b>ethanol</b> treatment also caused microglia activation, increased NF kappaB DNA binding and <strong>COX2</strong> expression.
+PTGS2	addiction	intoxication	17067360	<b>Binge</b> ethanol treatment also caused microglia activation, increased NF kappaB DNA binding and <strong>COX2</strong> expression.
+PTGS2	addiction	intoxication	17067360	Butylated hydroxytoluene reduced <b>binge</b> induced NF kappaB DNA binding and <strong>COX2</strong> expression.
+PTGS2	drug	opioid	17049975	In this study, we have evaluated the effects of indomethacin (a non selective COX inhibitor) and celecoxib (a selective <strong>COX 2</strong> inhibitor) on the acquisition of <b>morphine</b> induced conditioned place preference (CPP) in male Swiss mice.
+PTGS2	addiction	reward	17049975	In this study, we have evaluated the effects of indomethacin (a non selective COX inhibitor) and celecoxib (a selective <strong>COX 2</strong> inhibitor) on the acquisition of morphine induced conditioned place preference (<b>CPP</b>) in male Swiss mice.
+PTGS2	drug	opioid	16741783	These guidelines, formulated in response to recent developments concerning <strong>COX 2</strong> inhibitors and other NSAIDs, focus on paracetamol as the baseline drug for chronic pain management; when greater analgesia is desired, the addition of weak <b>opioids</b> is recommended based on a preferable GI and cardiovascular profile, compared with non steroidal anti inflammatory drugs.
+PTGS2	drug	alcohol	16318954	Protective effect of cyclooxygenase 2 (<strong>COX 2</strong>) inhibitors but not non selective cyclooxygenase (COX) inhibitors on <b>ethanol</b> withdrawal induced behavioural changes.
+PTGS2	addiction	withdrawal	16318954	Protective effect of cyclooxygenase 2 (<strong>COX 2</strong>) inhibitors but not non selective cyclooxygenase (COX) inhibitors on ethanol <b>withdrawal</b> induced behavioural changes.
+PTGS2	drug	alcohol	16318954	In the present study we examined the effect of nimesulide (a preferential <strong>COX 2</strong> inhibitor), rofecoxib (a highly selective <strong>COX 2</strong> inhibitor) or naproxen (a non selective COX inhibitor displaying high affinity towards the COX 1 isoenzyme) on <b>alcohol</b> induced withdrawal symptoms.
+PTGS2	addiction	withdrawal	16318954	In the present study we examined the effect of nimesulide (a preferential <strong>COX 2</strong> inhibitor), rofecoxib (a highly selective <strong>COX 2</strong> inhibitor) or naproxen (a non selective COX inhibitor displaying high affinity towards the COX 1 isoenzyme) on alcohol induced <b>withdrawal</b> symptoms.
+PTGS2	drug	alcohol	16318954	The results of the present study suggest strongly the possible role of cyclooxygenases, particularly <strong>COX 2</strong> inhibitors, on <b>ethanol</b> induced withdrawal symptoms and the potential use of <strong>COX 2</strong> inhibitors in their prevention and treatment.
+PTGS2	addiction	withdrawal	16318954	The results of the present study suggest strongly the possible role of cyclooxygenases, particularly <strong>COX 2</strong> inhibitors, on ethanol induced <b>withdrawal</b> symptoms and the potential use of <strong>COX 2</strong> inhibitors in their prevention and treatment.
+PTGS2	drug	cannabinoid	16259716	Hopefully, recent adverse publicity about <strong>COX 2</strong> inhibitory drugs might stimulate serious re assessment of some traditional anti inflammatory therapies with low APT activity for the management of both acute pain (non addictive <b>cannabinoids</b>, celery seed, etc.)
+PTGS2	addiction	addiction	16259716	Hopefully, recent adverse publicity about <strong>COX 2</strong> inhibitory drugs might stimulate serious re assessment of some traditional anti inflammatory therapies with low APT activity for the management of both acute pain (non <b>addictive</b> cannabinoids, celery seed, etc.)
+PTGS2	drug	opioid	16034581	Non <b>opioid</b> drugs, especially <strong>COX 2</strong> inhibitors are extensively evaluated.
+PTGS2	addiction	sensitization	15985101	Terminating migraine with allodynia and ongoing central <b>sensitization</b> using parenteral administration of COX1/<strong>COX2</strong> inhibitors.
+PTGS2	addiction	sensitization	15985101	To determine whether delayed infusion of COX1/<strong>COX2</strong> inhibitors (ketorolac, indomethacin) will stop migraine in allodynic patients, and suppress ongoing <b>sensitization</b> in central trigeminovascular neurons in the rat.
+PTGS2	addiction	sensitization	15985101	The induction of <b>sensitization</b> (using topical application of inflammatory soup on the dura) and its suppression by COX1/<strong>COX2</strong> inhibitors were assessed by monitoring changes in spontaneous activity and responses to mechanical and thermal stimuli.
+PTGS2	addiction	sensitization	15985101	In the rat, infusion of COX1/<strong>COX2</strong> inhibitors blocked <b>sensitization</b> in meningeal nociceptors and suppressed ongoing <b>sensitization</b> in spinal trigeminovascular neurons.
+PTGS2	addiction	sensitization	15985101	The termination of migraine with ongoing allodynia using COX1/<strong>COX2</strong> inhibitors is achieved through the suppression of central <b>sensitization</b>.
+PTGS2	addiction	relapse	15985101	Although parenteral administration of COX1/<strong>COX2</strong> inhibitors is impractical as routine migraine therapy, it should be the rescue therapy of choice for patients <b>seeking</b> emergency care for migraine.
+PTGS2	addiction	relapse	14763357	HISTORY BEFORE ANTI <strong>COX 2</strong>: The past history of ulcer increases the risk of <b>relapse</b> by 14 to 17 with non steroidal anti inflammatory drugs intake compared to patients without previous ulcer.
+PTGS2	drug	alcohol	14648704	Both nonselective and selective <strong>COX 2</strong> inhibitors suppressed IFN gamma + LPS induced NO production, which was largely restored by exogenous PGE(2) or EP(4) receptor agonist PGE(1) <b>alcohol</b>.
+PTGS2	drug	nicotine	12941074	Currently, there is limited information on the regulation of <strong>COX 2</strong> expression in <b>smoking</b> associated periodontal disease.
+PTGS2	drug	nicotine	12941074	The aim of the present study was to investigate the effects of <b>nicotine</b> on the expression of cyclooxygenase 2 (<strong>COX 2</strong>) mRNA gene and protein in cultured human gingival fibroblasts (HGFs).
+PTGS2	drug	nicotine	12941074	Furthermore, to elucidate whether induction of <strong>COX 2</strong> may be associated with <b>nicotine</b>  induced cytotoxicity, NS 398 (a selective <strong>COX 2</strong> inhibitor), was added to test its protective effect.
+PTGS2	drug	nicotine	12941074	The exposure of quiescent human HGFs to <b>nicotine</b> resulted in the induction of <strong>COX 2</strong> mRNA expression.
+PTGS2	drug	nicotine	12941074	The levels of the <strong>COX 2</strong> mRNAs increased about 1.5 and 2.5 fold after exposure to 2.5 and 15 mm <b>nicotine</b> for 2 h (P < 0.05), respectively.
+PTGS2	drug	nicotine	12941074	Moreover, the peak of <strong>COX 2</strong> mRNA levels induced by <b>nicotine</b> was 10 mm at 2 h incubation period.
+PTGS2	drug	nicotine	12941074	Investigations of the time dependence of <strong>COX 2</strong> mRNA expression in <b>nicotine</b> treated HGFs revealed a rapid accumulation of the transcript, a signal first detectable at 30 min and diminished to control level after 8 h. In addition, 10 mm <b>nicotine</b> also induced <strong>COX 2</strong> protein expression in HGFs.
+PTGS2	addiction	dependence	12941074	Investigations of the time <b>dependence</b> of <strong>COX 2</strong> mRNA expression in nicotine treated HGFs revealed a rapid accumulation of the transcript, a signal first detectable at 30 min and diminished to control level after 8 h. In addition, 10 mm nicotine also induced <strong>COX 2</strong> protein expression in HGFs.
+PTGS2	drug	nicotine	12941074	The kinetics of this response showed that <strong>COX 2</strong> was detectable at 4 h and diminished nearly to control level after 24 h. NS 398 at non cytotoxic dose is not able to prevent <b>nicotine</b> induced cytotoxicity.
+PTGS2	drug	nicotine	12941074	Taken together, the activation of <strong>COX 2</strong> expression by <b>nicotine</b> suggests a potential role for <b>nicotine</b> in the pathogenesis of <b>smoking</b> associated periodontal disease.
+PTGS2	drug	nicotine	12941074	In addition, <b>nicotine</b> induced cytotoxicity is not directly via the induction of <strong>COX 2</strong> expression.
+PTGS2	drug	psychedelics	12522725	It consists of the simultaneous administration of low dose <b>ketamine</b>, co administration of an alpha 2 agonist, and the administration of a selective <strong>COX 2</strong> inhibitor (refecoxib, parecoxib) respectively.
+PTGS2	drug	opioid	12086297	For this reason, <strong>COX 2</strong> selective inhibitors (coxibs) are attractive <b>opioid</b> sparing analgesic options in the perioperative setting.
+PTGS2	drug	opioid	12086297	Clinical studies show that <strong>COX 2</strong> selective inhibitors are effective for the treatment of preoperative and postoperative pain and reduce postsurgical requirements for <b>opioids</b>.
+PTGS2	addiction	sensitization	12086297	This evidence supports a role for <strong>COX 2</strong> derived prostaglandins as key mediators of nociceptive pain and peripheral <b>sensitization</b> (hyperalgesia).
+PTGS2	drug	alcohol	11994208	<b>Ethanol</b> and LPS modulate NF kappaB activation, inducible NO synthase and <strong>COX 2</strong> gene expression in rat liver cells in vivo.
+PTGS2	drug	alcohol	11994208	<b>Ethanol</b> and LPS are immunomodulators, whose actions are associated with the activation of the transcription factor, NF kappaB, that mediates the expression of a number of rapid response genes involved in the whole body inflammatory response to injury, including transcriptional regulation of iNOS and <strong>COX 2</strong>.
+PTGS2	drug	alcohol	11994208	We investigated modulation by acute <b>ethanol</b> (EtOH) intoxication, LPS and LPS tolerance of NF kappaB activation in hepatocytes, Kupffer cells and sinusoidal endothelial cells (SEC), concurrent regulation of iNOS and <strong>COX 2</strong> gene expression and the influence of gender on these mechanisms.
+PTGS2	addiction	intoxication	11994208	We investigated modulation by acute ethanol (EtOH) <b>intoxication</b>, LPS and LPS tolerance of NF kappaB activation in hepatocytes, Kupffer cells and sinusoidal endothelial cells (SEC), concurrent regulation of iNOS and <strong>COX 2</strong> gene expression and the influence of gender on these mechanisms.
+PTGS2	drug	opioid	11976266	Acute intrathecal pre treatment with a CGRP receptor antagonist, CGRP(8   37) (4, 8 microg), a substance P receptor antagonist, SR 140333 (1.4, 2.8 microg), a cyclo oxygenase (COX) inhibitor, ketorolac (30, 45 microg), and <strong>COX 2</strong> selective inhibitors, DuP 697 (10, 30 microg) and nimesulide (30 microg), 30 min before <b>naloxone</b> challenge, partially attenuated the symptoms of <b>morphine</b> withdrawal.
+PTGS2	addiction	withdrawal	11976266	Acute intrathecal pre treatment with a CGRP receptor antagonist, CGRP(8   37) (4, 8 microg), a substance P receptor antagonist, SR 140333 (1.4, 2.8 microg), a cyclo oxygenase (COX) inhibitor, ketorolac (30, 45 microg), and <strong>COX 2</strong> selective inhibitors, DuP 697 (10, 30 microg) and nimesulide (30 microg), 30 min before naloxone challenge, partially attenuated the symptoms of morphine <b>withdrawal</b>.
+PTGS2	drug	opioid	11932069	While acute treatment with <b>morphine</b> has some analgesic effect on hind limb sparing the selective <strong>COX 2</strong> inhibitor, celebrex, has no influence on the pain related behavioural changes in this model.
+PTGS2	drug	opioid	10422661	Synergistic antiallodynic effects of spinal <b>morphine</b> with ketorolac and selective COX1  and <strong>COX2</strong> inhibitors in nerve injured rats.
+PTGS2	drug	opioid	10422661	These findings suggest that spinal prostanoids produced via both COX1 and <strong>COX2</strong> pathways may play a role in neuropathic pain states and suggest the clinical utility of <b>opioid</b> plus COX inhibitor combination therapy.
+PTGS2	drug	alcohol	10235299	<b>Ethanol</b> intoxication and the hyperexcitability of <b>ethanol</b> withdrawal may be influenced by inducible proteins, thus we investigated <strong>COX 2</strong> in the rat brain during acute and chronic <b>ethanol</b> treatment, <b>ethanol</b> withdrawal, and after peripheral administration of excitatory amino acids.
+PTGS2	addiction	intoxication	10235299	Ethanol <b>intoxication</b> and the hyperexcitability of ethanol withdrawal may be influenced by inducible proteins, thus we investigated <strong>COX 2</strong> in the rat brain during acute and chronic ethanol treatment, ethanol withdrawal, and after peripheral administration of excitatory amino acids.
+PTGS2	addiction	withdrawal	10235299	Ethanol intoxication and the hyperexcitability of ethanol <b>withdrawal</b> may be influenced by inducible proteins, thus we investigated <strong>COX 2</strong> in the rat brain during acute and chronic ethanol treatment, ethanol <b>withdrawal</b>, and after peripheral administration of excitatory amino acids.
+PTGS2	drug	alcohol	10235299	Chronic <b>ethanol</b> treatment (4 days intragastric) robustly induced <strong>COX 2</strong> in limbic cortex, isocortex, and amygdala.
+PTGS2	drug	alcohol	10235299	During <b>ethanol</b> withdrawal, <strong>COX 2</strong> expression increased further in some regions, peaking in most areas 16 hr after the last dose of <b>ethanol</b>.
+PTGS2	addiction	withdrawal	10235299	During ethanol <b>withdrawal</b>, <strong>COX 2</strong> expression increased further in some regions, peaking in most areas 16 hr after the last dose of ethanol.
+PTGS2	drug	alcohol	10235299	These results indicate that <strong>COX 2</strong> immunoreactivity is: 1) increased in the brain during acute <b>ethanol</b> exposure that increases further during chronic treatment; 2) sensitive to excitatory amino acid receptor stimulation; and 3) dramatically increased during <b>ethanol</b> withdrawal.
+PTGS2	addiction	withdrawal	10235299	These results indicate that <strong>COX 2</strong> immunoreactivity is: 1) increased in the brain during acute ethanol exposure that increases further during chronic treatment; 2) sensitive to excitatory amino acid receptor stimulation; and 3) dramatically increased during ethanol <b>withdrawal</b>.
+PTGS2	drug	alcohol	10235299	These studies suggest that <strong>COX 2</strong> induction may be involved in the acute and chronic effects of <b>ethanol</b>.
+NOS1	drug	opioid	32113678	Uncoupling <strong>nNOS</strong> PSD 95 in mPFC inhibits <b>morphine</b> priming induced reinstatement after extinction training.
+NOS1	addiction	relapse	32113678	Uncoupling <strong>nNOS</strong> PSD 95 in mPFC inhibits morphine priming induced <b>reinstatement</b> after extinction training.
+NOS1	drug	opioid	32113678	Uncoupling <strong><strong>nNOS</strong></strong> PSD 95 in mPFC inhibits <b>morphine</b> priming induced reinstatement after extinction training.
+NOS1	addiction	relapse	32113678	Uncoupling <strong><strong>nNOS</strong></strong> PSD 95 in mPFC inhibits morphine priming induced <b>reinstatement</b> after extinction training.
+NOS1	drug	opioid	32113678	Using <b>morphine</b> conditioned place preference (CPP) model, we show that association of neuronal nitric oxide synthase (<strong>nNOS</strong>) with postsynaptic density 95 (PSD 95) plays a significant role in <b>morphine</b> priming induced reinstatement.
+NOS1	addiction	relapse	32113678	Using morphine conditioned place preference (CPP) model, we show that association of neuronal nitric oxide synthase (<strong>nNOS</strong>) with postsynaptic density 95 (PSD 95) plays a significant role in morphine priming induced <b>reinstatement</b>.
+NOS1	addiction	reward	32113678	Using morphine conditioned place preference (<b>CPP</b>) model, we show that association of neuronal nitric oxide synthase (<strong>nNOS</strong>) with postsynaptic density 95 (PSD 95) plays a significant role in morphine priming induced reinstatement.
+NOS1	drug	opioid	32113678	Using <b>morphine</b> conditioned place preference (CPP) model, we show that association of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) with postsynaptic density 95 (PSD 95) plays a significant role in <b>morphine</b> priming induced reinstatement.
+NOS1	addiction	relapse	32113678	Using morphine conditioned place preference (CPP) model, we show that association of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) with postsynaptic density 95 (PSD 95) plays a significant role in morphine priming induced <b>reinstatement</b>.
+NOS1	addiction	reward	32113678	Using morphine conditioned place preference (<b>CPP</b>) model, we show that association of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) with postsynaptic density 95 (PSD 95) plays a significant role in morphine priming induced reinstatement.
+NOS1	drug	opioid	32113678	The <strong>nNOS</strong> PSD 95 coupling and c Fos expression in the medial prefrontal cortex (mPFC) was significantly increased after extinction of <b>morphine</b> CPP.
+NOS1	addiction	reward	32113678	The <strong>nNOS</strong> PSD 95 coupling and c Fos expression in the medial prefrontal cortex (mPFC) was significantly increased after extinction of morphine <b>CPP</b>.
+NOS1	drug	opioid	32113678	The <strong><strong>nNOS</strong></strong> PSD 95 coupling and c Fos expression in the medial prefrontal cortex (mPFC) was significantly increased after extinction of <b>morphine</b> CPP.
+NOS1	addiction	reward	32113678	The <strong><strong>nNOS</strong></strong> PSD 95 coupling and c Fos expression in the medial prefrontal cortex (mPFC) was significantly increased after extinction of morphine <b>CPP</b>.
+NOS1	drug	opioid	32113678	Dissociation of <strong>nNOS</strong> PSD 95 in the mPFC by ZL006 inhibited the reinstatement of <b>morphine</b> CPP induced by a priming dose of <b>morphine</b>.
+NOS1	addiction	relapse	32113678	Dissociation of <strong>nNOS</strong> PSD 95 in the mPFC by ZL006 inhibited the <b>reinstatement</b> of morphine CPP induced by a priming dose of morphine.
+NOS1	addiction	reward	32113678	Dissociation of <strong>nNOS</strong> PSD 95 in the mPFC by ZL006 inhibited the reinstatement of morphine <b>CPP</b> induced by a priming dose of morphine.
+NOS1	drug	opioid	32113678	Dissociation of <strong><strong>nNOS</strong></strong> PSD 95 in the mPFC by ZL006 inhibited the reinstatement of <b>morphine</b> CPP induced by a priming dose of <b>morphine</b>.
+NOS1	addiction	relapse	32113678	Dissociation of <strong><strong>nNOS</strong></strong> PSD 95 in the mPFC by ZL006 inhibited the <b>reinstatement</b> of morphine CPP induced by a priming dose of morphine.
+NOS1	addiction	reward	32113678	Dissociation of <strong><strong>nNOS</strong></strong> PSD 95 in the mPFC by ZL006 inhibited the reinstatement of morphine <b>CPP</b> induced by a priming dose of morphine.
+NOS1	drug	opioid	32113678	Uncoupling <strong>nNOS</strong> PSD 95 reversed the <b>morphine</b> induced CREB dysfunction.
+NOS1	drug	opioid	32113678	Uncoupling <strong><strong>nNOS</strong></strong> PSD 95 reversed the <b>morphine</b> induced CREB dysfunction.
+NOS1	drug	opioid	32113678	Moreover, effects of ZL006 on the reinstatement of <b>morphine</b> CPP and CREB activation depended on <strong>nNOS</strong> PSD 95 target.
+NOS1	addiction	relapse	32113678	Moreover, effects of ZL006 on the <b>reinstatement</b> of morphine CPP and CREB activation depended on <strong>nNOS</strong> PSD 95 target.
+NOS1	addiction	reward	32113678	Moreover, effects of ZL006 on the reinstatement of morphine <b>CPP</b> and CREB activation depended on <strong>nNOS</strong> PSD 95 target.
+NOS1	drug	opioid	32113678	Moreover, effects of ZL006 on the reinstatement of <b>morphine</b> CPP and CREB activation depended on <strong><strong>nNOS</strong></strong> PSD 95 target.
+NOS1	addiction	relapse	32113678	Moreover, effects of ZL006 on the <b>reinstatement</b> of morphine CPP and CREB activation depended on <strong><strong>nNOS</strong></strong> PSD 95 target.
+NOS1	addiction	reward	32113678	Moreover, effects of ZL006 on the reinstatement of morphine <b>CPP</b> and CREB activation depended on <strong><strong>nNOS</strong></strong> PSD 95 target.
+NOS1	drug	opioid	32113678	Together, our findings suggest that <strong>nNOS</strong> PSD 95 in the mPFC contributes to reinstatement of <b>morphine</b> CPP, possibly through CREB dysfunction, offering a potential target to prevent relapse of drug abuse.
+NOS1	addiction	relapse	32113678	Together, our findings suggest that <strong>nNOS</strong> PSD 95 in the mPFC contributes to <b>reinstatement</b> of morphine CPP, possibly through CREB dysfunction, offering a potential target to prevent <b>relapse</b> of drug abuse.
+NOS1	addiction	reward	32113678	Together, our findings suggest that <strong>nNOS</strong> PSD 95 in the mPFC contributes to reinstatement of morphine <b>CPP</b>, possibly through CREB dysfunction, offering a potential target to prevent relapse of drug abuse.
+NOS1	drug	opioid	32113678	Together, our findings suggest that <strong><strong>nNOS</strong></strong> PSD 95 in the mPFC contributes to reinstatement of <b>morphine</b> CPP, possibly through CREB dysfunction, offering a potential target to prevent relapse of drug abuse.
+NOS1	addiction	relapse	32113678	Together, our findings suggest that <strong><strong>nNOS</strong></strong> PSD 95 in the mPFC contributes to <b>reinstatement</b> of morphine CPP, possibly through CREB dysfunction, offering a potential target to prevent <b>relapse</b> of drug abuse.
+NOS1	addiction	reward	32113678	Together, our findings suggest that <strong><strong>nNOS</strong></strong> PSD 95 in the mPFC contributes to reinstatement of morphine <b>CPP</b>, possibly through CREB dysfunction, offering a potential target to prevent relapse of drug abuse.
+NOS1	drug	opioid	31756370	Several mechanisms are involved in the tolerance to analgesic <b>opioids</b>, including desensitization or internalization of the <b>opioid</b> receptor, elevation of cAMP levels, microglial activation and neuroinflammation, elevation of spinal mTOR activity and change in the expression of some proteins involved in tolerance, such as <strong>nNOS</strong>.
+NOS1	drug	opioid	31756370	Several mechanisms are involved in the tolerance to analgesic <b>opioids</b>, including desensitization or internalization of the <b>opioid</b> receptor, elevation of cAMP levels, microglial activation and neuroinflammation, elevation of spinal mTOR activity and change in the expression of some proteins involved in tolerance, such as <strong><strong>nNOS</strong></strong>.
+NOS1	drug	alcohol	31487373	[Effects of <strong>Nitric Oxide Synthase 1</strong> Exon 1f VNTR Gene Polymorphism on the Clinical Symptoms of <b>Alcohol</b> Dependence,Impulsivity and Comorbid Attention Deficit Hyperactivity Disorder].
+NOS1	addiction	dependence	31487373	[Effects of <strong>Nitric Oxide Synthase 1</strong> Exon 1f VNTR Gene Polymorphism on the Clinical Symptoms of Alcohol <b>Dependence</b>,Impulsivity and Comorbid Attention Deficit Hyperactivity Disorder].
+NOS1	drug	alcohol	31487373	We planned to compare individuals with <b>alcohol</b> dependence (AD) and healthy controls on the frequency of <strong>NOS1</strong> exon 1f VNTR gene polymorphism and to investigate the effects of this polymorphism on the clinical symptoms of <b>alcohol</b> dependence, impulsiveness and comorbid attention deficit hyperactivity disorder (ADHD) symptoms.
+NOS1	addiction	dependence	31487373	We planned to compare individuals with alcohol <b>dependence</b> (AD) and healthy controls on the frequency of <strong>NOS1</strong> exon 1f VNTR gene polymorphism and to investigate the effects of this polymorphism on the clinical symptoms of alcohol <b>dependence</b>, impulsiveness and comorbid attention deficit hyperactivity disorder (ADHD) symptoms.
+NOS1	drug	amphetamine	31288386	Additionally, the proportion of GAL expressing cell bodies simultaneously immunoreactive to vasoactive intestinal peptide (VIP), neuronal nitric oxide synthase (<strong>nNOS</strong>) and cocaine  and <b>amphetamine</b>  regulated transcript peptide (CART) also increased.
+NOS1	drug	cocaine	31288386	Additionally, the proportion of GAL expressing cell bodies simultaneously immunoreactive to vasoactive intestinal peptide (VIP), neuronal nitric oxide synthase (<strong>nNOS</strong>) and <b>cocaine</b>  and amphetamine  regulated transcript peptide (CART) also increased.
+NOS1	drug	amphetamine	31288386	Additionally, the proportion of GAL expressing cell bodies simultaneously immunoreactive to vasoactive intestinal peptide (VIP), neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) and cocaine  and <b>amphetamine</b>  regulated transcript peptide (CART) also increased.
+NOS1	drug	cocaine	31288386	Additionally, the proportion of GAL expressing cell bodies simultaneously immunoreactive to vasoactive intestinal peptide (VIP), neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) and <b>cocaine</b>  and amphetamine  regulated transcript peptide (CART) also increased.
+NOS1	addiction	intoxication	31288386	The results suggest neurotrophic or/and neuroprotective properties of GAL and possible co operation of GAL with VIP, <strong>nNOS</strong>, CART in the recovery processes in the stomach enteric nervous system (ENS) neurons following acrylamide <b>intoxication</b>.
+NOS1	addiction	intoxication	31288386	The results suggest neurotrophic or/and neuroprotective properties of GAL and possible co operation of GAL with VIP, <strong><strong>nNOS</strong></strong>, CART in the recovery processes in the stomach enteric nervous system (ENS) neurons following acrylamide <b>intoxication</b>.
+NOS1	drug	cocaine	29992335	To understand the cellular mechanisms involved in regulating MOR expression, this study explored whether neuronal nitric oxide synthase (<strong>nNOS</strong>) modulates the neurochemical and behavioral effects of acute and repeated <b>cocaine</b> administration.
+NOS1	drug	cocaine	29992335	To understand the cellular mechanisms involved in regulating MOR expression, this study explored whether neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) modulates the neurochemical and behavioral effects of acute and repeated <b>cocaine</b> administration.
+NOS1	addiction	reward	29992335	conditioning sessions, and levels of MOR and <strong>nNOS</strong> mRNA and protein in the NAc were measured following <b>CPP</b> test.
+NOS1	addiction	reward	29992335	conditioning sessions, and levels of MOR and <strong><strong>nNOS</strong></strong> mRNA and protein in the NAc were measured following <b>CPP</b> test.
+NOS1	drug	cocaine	29992335	Acute <b>cocaine</b> administration significantly enhanced <strong>nNOS</strong> and MOR mRNA and protein expression in the NAc, and this increase in MOR expression was blocked by 7 NI.
+NOS1	drug	cocaine	29992335	Acute <b>cocaine</b> administration significantly enhanced <strong><strong>nNOS</strong></strong> and MOR mRNA and protein expression in the NAc, and this increase in MOR expression was blocked by 7 NI.
+NOS1	drug	cocaine	29992335	These findings suggest that <strong>nNOS</strong> modulates MOR expression following acute <b>cocaine</b> administration, and that <b>cocaine</b> CPP and associated upregulation of MOR expression involve both <strong>nNOS</strong> dependent and independent mechanisms.
+NOS1	addiction	reward	29992335	These findings suggest that <strong>nNOS</strong> modulates MOR expression following acute cocaine administration, and that cocaine <b>CPP</b> and associated upregulation of MOR expression involve both <strong>nNOS</strong> dependent and independent mechanisms.
+NOS1	drug	cocaine	29992335	These findings suggest that <strong><strong>nNOS</strong></strong> modulates MOR expression following acute <b>cocaine</b> administration, and that <b>cocaine</b> CPP and associated upregulation of MOR expression involve both <strong><strong>nNOS</strong></strong> dependent and independent mechanisms.
+NOS1	addiction	reward	29992335	These findings suggest that <strong><strong>nNOS</strong></strong> modulates MOR expression following acute cocaine administration, and that cocaine <b>CPP</b> and associated upregulation of MOR expression involve both <strong><strong>nNOS</strong></strong> dependent and independent mechanisms.
+NOS1	drug	alcohol	29525685	A neuronal nitric oxide synthase (<strong>nNOS</strong>) inhibitor, 7 nitroindazole (7NI), was administered along with <b>ethanol</b> and CUS to test its effects on behavioral sensitization.
+NOS1	addiction	sensitization	29525685	A neuronal nitric oxide synthase (<strong>nNOS</strong>) inhibitor, 7 nitroindazole (7NI), was administered along with ethanol and CUS to test its effects on behavioral <b>sensitization</b>.
+NOS1	drug	alcohol	29525685	A neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitor, 7 nitroindazole (7NI), was administered along with <b>ethanol</b> and CUS to test its effects on behavioral sensitization.
+NOS1	addiction	sensitization	29525685	A neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitor, 7 nitroindazole (7NI), was administered along with ethanol and CUS to test its effects on behavioral <b>sensitization</b>.
+NOS1	drug	alcohol	29525685	<strong>nNOS</strong> inhibition by 7NI reduced both <b>ethanol</b> sensitization and cross sensitization.
+NOS1	addiction	sensitization	29525685	<strong>nNOS</strong> inhibition by 7NI reduced both ethanol <b>sensitization</b> and cross <b>sensitization</b>.
+NOS1	drug	alcohol	29525685	<strong><strong>nNOS</strong></strong> inhibition by 7NI reduced both <b>ethanol</b> sensitization and cross sensitization.
+NOS1	addiction	sensitization	29525685	<strong><strong>nNOS</strong></strong> inhibition by 7NI reduced both ethanol <b>sensitization</b> and cross <b>sensitization</b>.
+NOS1	drug	nicotine	29158387	Chronic <b>nicotine</b> treatment altered the translational profile of more than 1,000 genes in α5  Amigo1 neurons, including neuronal nitric oxide synthase (<strong>Nos1</strong>) and somatostatin (Sst).
+NOS1	drug	nicotine	29158387	This loss of <b>nicotine</b> reward was mimicked by shRNA mediated knockdown of <strong>Nos1</strong> in the IPN.
+NOS1	addiction	reward	29158387	This loss of nicotine <b>reward</b> was mimicked by shRNA mediated knockdown of <strong>Nos1</strong> in the IPN.
+NOS1	drug	cocaine	28893594	Intra mPFC injection of the non selective NO synthase (NOS) inhibitor L NAME or the neuronal NOS (<strong>nNOS</strong>) selective inhibitor L NPA during the conditioning phase disrupted <b>cocaine</b> CPP.
+NOS1	addiction	reward	28893594	Intra mPFC injection of the non selective NO synthase (NOS) inhibitor L NAME or the neuronal NOS (<strong>nNOS</strong>) selective inhibitor L NPA during the conditioning phase disrupted cocaine <b>CPP</b>.
+NOS1	drug	cocaine	28893594	Intra mPFC injection of the non selective NO synthase (NOS) inhibitor L NAME or the neuronal NOS (<strong><strong>nNOS</strong></strong>) selective inhibitor L NPA during the conditioning phase disrupted <b>cocaine</b> CPP.
+NOS1	addiction	reward	28893594	Intra mPFC injection of the non selective NO synthase (NOS) inhibitor L NAME or the neuronal NOS (<strong><strong>nNOS</strong></strong>) selective inhibitor L NPA during the conditioning phase disrupted cocaine <b>CPP</b>.
+NOS1	addiction	relapse	28726801	Reinstated drug <b>seeking</b> in animal models of <b>relapse</b> relies on glutamate spillover from cortical terminals synapsing in the nucleus accumbens core (NAcore) to stimulate metabotropic glutamate receptor5 (mGluR5) on neuronal nitric oxide synthase (<strong>nNOS</strong>) interneurons.
+NOS1	addiction	relapse	28726801	Reinstated drug <b>seeking</b> in animal models of <b>relapse</b> relies on glutamate spillover from cortical terminals synapsing in the nucleus accumbens core (NAcore) to stimulate metabotropic glutamate receptor5 (mGluR5) on neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) interneurons.
+NOS1	drug	cocaine	28726801	In <b>cocaine</b> trained rodents mGluR5 stimulation reinstates drug seeking by activating <strong>nNOS</strong>, but activating mGluR5 did not promote reinstated sucrose seeking, nor was potentiated reinstatement after mGluR2/3 blockade reduced by blocking <strong>nNOS</strong>.
+NOS1	addiction	relapse	28726801	In cocaine trained rodents mGluR5 stimulation reinstates drug <b>seeking</b> by activating <strong>nNOS</strong>, but activating mGluR5 did not promote reinstated sucrose <b>seeking</b>, nor was potentiated <b>reinstatement</b> after mGluR2/3 blockade reduced by blocking <strong>nNOS</strong>.
+NOS1	drug	cocaine	28726801	In <b>cocaine</b> trained rodents mGluR5 stimulation reinstates drug seeking by activating <strong><strong>nNOS</strong></strong>, but activating mGluR5 did not promote reinstated sucrose seeking, nor was potentiated reinstatement after mGluR2/3 blockade reduced by blocking <strong><strong>nNOS</strong></strong>.
+NOS1	addiction	relapse	28726801	In cocaine trained rodents mGluR5 stimulation reinstates drug <b>seeking</b> by activating <strong><strong>nNOS</strong></strong>, but activating mGluR5 did not promote reinstated sucrose <b>seeking</b>, nor was potentiated <b>reinstatement</b> after mGluR2/3 blockade reduced by blocking <strong><strong>nNOS</strong></strong>.
+NOS1	addiction	relapse	28726801	However, chemogenetic activation of <strong>nNOS</strong> interneurons in the NAcore reinstated sucrose <b>seeking</b>.
+NOS1	addiction	relapse	28726801	However, chemogenetic activation of <strong><strong>nNOS</strong></strong> interneurons in the NAcore reinstated sucrose <b>seeking</b>.
+NOS1	addiction	relapse	28726801	These data indicate that dysregulated presynaptic mGluR2/3 signaling is a possible site of shared signaling in drug <b>seeking</b> and potentiated reinstated sucrose <b>seeking</b>, but that downregulated glutamate transport and subsequent activation of <strong>nNOS</strong> by synaptic glutamate spillover is not shared.
+NOS1	addiction	relapse	28726801	These data indicate that dysregulated presynaptic mGluR2/3 signaling is a possible site of shared signaling in drug <b>seeking</b> and potentiated reinstated sucrose <b>seeking</b>, but that downregulated glutamate transport and subsequent activation of <strong><strong>nNOS</strong></strong> by synaptic glutamate spillover is not shared.
+NOS1	drug	cocaine	28123012	Accumbens <strong>nNOS</strong> Interneurons Regulate <b>Cocaine</b> Relapse.
+NOS1	addiction	relapse	28123012	Accumbens <strong>nNOS</strong> Interneurons Regulate Cocaine <b>Relapse</b>.
+NOS1	drug	cocaine	28123012	Accumbens <strong><strong>nNOS</strong></strong> Interneurons Regulate <b>Cocaine</b> Relapse.
+NOS1	addiction	relapse	28123012	Accumbens <strong><strong>nNOS</strong></strong> Interneurons Regulate Cocaine <b>Relapse</b>.
+NOS1	addiction	relapse	28123012	Using a transgene strategy to express and stimulate designer receptors that mimicked mGluR5 signaling through Gq in <strong>nNOS</strong> interneurons, we recapitulated cue induced <b>reinstatement</b> in the absence of cues.
+NOS1	addiction	relapse	28123012	Using a transgene strategy to express and stimulate designer receptors that mimicked mGluR5 signaling through Gq in <strong><strong>nNOS</strong></strong> interneurons, we recapitulated cue induced <b>reinstatement</b> in the absence of cues.
+NOS1	addiction	relapse	28123012	Conversely, using a transgenic caspase strategy, the intensity of cue induced <b>reinstatement</b> was correlated with the extent of selective elimination of <strong>nNOS</strong> interneurons.
+NOS1	addiction	relapse	28123012	Conversely, using a transgenic caspase strategy, the intensity of cue induced <b>reinstatement</b> was correlated with the extent of selective elimination of <strong><strong>nNOS</strong></strong> interneurons.
+NOS1	addiction	relapse	28123012	The induction of t SP during cued <b>reinstatement</b> depends on activating matrix metalloproteinases (MMPs) and selective chemogenetic stimulation of <strong>nNOS</strong> interneurons recapitulated MMP activation and t SP induction (increase in AMPA currents in MSNs).
+NOS1	addiction	relapse	28123012	The induction of t SP during cued <b>reinstatement</b> depends on activating matrix metalloproteinases (MMPs) and selective chemogenetic stimulation of <strong><strong>nNOS</strong></strong> interneurons recapitulated MMP activation and t SP induction (increase in AMPA currents in MSNs).
+NOS1	drug	cocaine	28123012	These data demonstrate critical involvement of a sparse population of <strong>nNOS</strong> expressing interneurons in cue induced <b>cocaine</b> seeking, revealing a bottleneck in brain processing of drug associated cues where therapeutic interventions could be effective in treating drug addiction.
+NOS1	addiction	addiction	28123012	These data demonstrate critical involvement of a sparse population of <strong>nNOS</strong> expressing interneurons in cue induced cocaine seeking, revealing a bottleneck in brain processing of drug associated cues where therapeutic interventions could be effective in treating drug <b>addiction</b>.
+NOS1	addiction	relapse	28123012	These data demonstrate critical involvement of a sparse population of <strong>nNOS</strong> expressing interneurons in cue induced cocaine <b>seeking</b>, revealing a bottleneck in brain processing of drug associated cues where therapeutic interventions could be effective in treating drug addiction.
+NOS1	drug	cocaine	28123012	These data demonstrate critical involvement of a sparse population of <strong><strong>nNOS</strong></strong> expressing interneurons in cue induced <b>cocaine</b> seeking, revealing a bottleneck in brain processing of drug associated cues where therapeutic interventions could be effective in treating drug addiction.
+NOS1	addiction	addiction	28123012	These data demonstrate critical involvement of a sparse population of <strong><strong>nNOS</strong></strong> expressing interneurons in cue induced cocaine seeking, revealing a bottleneck in brain processing of drug associated cues where therapeutic interventions could be effective in treating drug <b>addiction</b>.
+NOS1	addiction	relapse	28123012	These data demonstrate critical involvement of a sparse population of <strong><strong>nNOS</strong></strong> expressing interneurons in cue induced cocaine <b>seeking</b>, revealing a bottleneck in brain processing of drug associated cues where therapeutic interventions could be effective in treating drug addiction.
+NOS1	addiction	aversion	27591981	Independent groups of male Wistar rats submitted to the contextual fear conditioning received bilateral intra hippocampal injections (500 nL/side) of the following drugs or vehicle before re exposure to the <b>aversive</b> context: AM251 (CB1 antagonist; 0.1, 0.3 and 1nmol); AP7 (NMDA antagonist; 1nmol)+AM251 (0.3nmol); NPLA (0.01nmol; <strong>nNOS</strong> inhibitor)+AM251 (0.3nmol); Bicuculline (1.3pmol; GABAA antagonist)+AM251 (0.1 and 1nmol).
+NOS1	addiction	aversion	27591981	Independent groups of male Wistar rats submitted to the contextual fear conditioning received bilateral intra hippocampal injections (500 nL/side) of the following drugs or vehicle before re exposure to the <b>aversive</b> context: AM251 (CB1 antagonist; 0.1, 0.3 and 1nmol); AP7 (NMDA antagonist; 1nmol)+AM251 (0.3nmol); NPLA (0.01nmol; <strong><strong>nNOS</strong></strong> inhibitor)+AM251 (0.3nmol); Bicuculline (1.3pmol; GABAA antagonist)+AM251 (0.1 and 1nmol).
+NOS1	drug	opioid	26596557	Specifically, the <strong>nNOS</strong>, sGC and PKG protein levels in the CA1 were increased after the expression of <b>morphine</b> conditioned place preference (CPP).
+NOS1	addiction	reward	26596557	Specifically, the <strong>nNOS</strong>, sGC and PKG protein levels in the CA1 were increased after the expression of morphine conditioned place preference (<b>CPP</b>).
+NOS1	drug	opioid	26596557	Specifically, the <strong><strong>nNOS</strong></strong>, sGC and PKG protein levels in the CA1 were increased after the expression of <b>morphine</b> conditioned place preference (CPP).
+NOS1	addiction	reward	26596557	Specifically, the <strong><strong>nNOS</strong></strong>, sGC and PKG protein levels in the CA1 were increased after the expression of morphine conditioned place preference (<b>CPP</b>).
+NOS1	drug	opioid	26596557	NR2B NMDAR expression was elevated in the CA1 following <b>morphine</b> CPP expression, and intra CA1 injection of the NR2B NMDAR antagonist Ro25 6981 not only blocked <b>morphine</b> CPP expression but also inhibited the up regulation of <strong>nNOS</strong>, sGC and PKG.
+NOS1	addiction	reward	26596557	NR2B NMDAR expression was elevated in the CA1 following morphine <b>CPP</b> expression, and intra CA1 injection of the NR2B NMDAR antagonist Ro25 6981 not only blocked morphine <b>CPP</b> expression but also inhibited the up regulation of <strong>nNOS</strong>, sGC and PKG.
+NOS1	drug	opioid	26596557	NR2B NMDAR expression was elevated in the CA1 following <b>morphine</b> CPP expression, and intra CA1 injection of the NR2B NMDAR antagonist Ro25 6981 not only blocked <b>morphine</b> CPP expression but also inhibited the up regulation of <strong><strong>nNOS</strong></strong>, sGC and PKG.
+NOS1	addiction	reward	26596557	NR2B NMDAR expression was elevated in the CA1 following morphine <b>CPP</b> expression, and intra CA1 injection of the NR2B NMDAR antagonist Ro25 6981 not only blocked morphine <b>CPP</b> expression but also inhibited the up regulation of <strong><strong>nNOS</strong></strong>, sGC and PKG.
+NOS1	drug	opioid	26596557	<b>Morphine</b> CPP expression enhanced the pAkt(Ser473) level, which has been corroborated to regulate <strong>nNOS</strong> activity, and this effect was reversed by intra CA1 injection of Ro25 6981.
+NOS1	addiction	reward	26596557	Morphine <b>CPP</b> expression enhanced the pAkt(Ser473) level, which has been corroborated to regulate <strong>nNOS</strong> activity, and this effect was reversed by intra CA1 injection of Ro25 6981.
+NOS1	drug	opioid	26596557	<b>Morphine</b> CPP expression enhanced the pAkt(Ser473) level, which has been corroborated to regulate <strong><strong>nNOS</strong></strong> activity, and this effect was reversed by intra CA1 injection of Ro25 6981.
+NOS1	addiction	reward	26596557	Morphine <b>CPP</b> expression enhanced the pAkt(Ser473) level, which has been corroborated to regulate <strong><strong>nNOS</strong></strong> activity, and this effect was reversed by intra CA1 injection of Ro25 6981.
+NOS1	drug	cocaine	26576217	The aim of the current study was to investigate the effects of 7 nitroindazole (7 NI), a selective inhibitor of neuronal nitric oxide synthase (<strong>nNOS</strong>), on <b>cocaine</b> withdrawal and neurotoxicity in male Wistar rats.
+NOS1	addiction	withdrawal	26576217	The aim of the current study was to investigate the effects of 7 nitroindazole (7 NI), a selective inhibitor of neuronal nitric oxide synthase (<strong>nNOS</strong>), on cocaine <b>withdrawal</b> and neurotoxicity in male Wistar rats.
+NOS1	drug	cocaine	26576217	The aim of the current study was to investigate the effects of 7 nitroindazole (7 NI), a selective inhibitor of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>), on <b>cocaine</b> withdrawal and neurotoxicity in male Wistar rats.
+NOS1	addiction	withdrawal	26576217	The aim of the current study was to investigate the effects of 7 nitroindazole (7 NI), a selective inhibitor of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>), on cocaine <b>withdrawal</b> and neurotoxicity in male Wistar rats.
+NOS1	drug	cocaine	26576217	<b>Cocaine</b> repeated treatment resulted in development of physical dependence, judged by withdrawal symptoms (decreased locomotion, increased salivation and breathing rate), accompanied by an increased <strong>nNOS</strong> activity and oxidative stress.
+NOS1	addiction	dependence	26576217	Cocaine repeated treatment resulted in development of physical <b>dependence</b>, judged by withdrawal symptoms (decreased locomotion, increased salivation and breathing rate), accompanied by an increased <strong>nNOS</strong> activity and oxidative stress.
+NOS1	addiction	withdrawal	26576217	Cocaine repeated treatment resulted in development of physical dependence, judged by <b>withdrawal</b> symptoms (decreased locomotion, increased salivation and breathing rate), accompanied by an increased <strong>nNOS</strong> activity and oxidative stress.
+NOS1	drug	cocaine	26576217	<b>Cocaine</b> repeated treatment resulted in development of physical dependence, judged by withdrawal symptoms (decreased locomotion, increased salivation and breathing rate), accompanied by an increased <strong><strong>nNOS</strong></strong> activity and oxidative stress.
+NOS1	addiction	dependence	26576217	Cocaine repeated treatment resulted in development of physical <b>dependence</b>, judged by withdrawal symptoms (decreased locomotion, increased salivation and breathing rate), accompanied by an increased <strong><strong>nNOS</strong></strong> activity and oxidative stress.
+NOS1	addiction	withdrawal	26576217	Cocaine repeated treatment resulted in development of physical dependence, judged by <b>withdrawal</b> symptoms (decreased locomotion, increased salivation and breathing rate), accompanied by an increased <strong><strong>nNOS</strong></strong> activity and oxidative stress.
+NOS1	drug	cocaine	26576217	7 NI administered along with <b>cocaine</b> not only attenuated the withdrawal, due to its <strong>nNOS</strong> inhibition, but also reversed both the GSH levels and antioxidant enzyme activities near control levels.
+NOS1	addiction	withdrawal	26576217	7 NI administered along with cocaine not only attenuated the <b>withdrawal</b>, due to its <strong>nNOS</strong> inhibition, but also reversed both the GSH levels and antioxidant enzyme activities near control levels.
+NOS1	drug	cocaine	26576217	7 NI administered along with <b>cocaine</b> not only attenuated the withdrawal, due to its <strong><strong>nNOS</strong></strong> inhibition, but also reversed both the GSH levels and antioxidant enzyme activities near control levels.
+NOS1	addiction	withdrawal	26576217	7 NI administered along with cocaine not only attenuated the <b>withdrawal</b>, due to its <strong><strong>nNOS</strong></strong> inhibition, but also reversed both the GSH levels and antioxidant enzyme activities near control levels.
+NOS1	drug	psychedelics	26520463	The effect of acute <b>ketamine</b> on <strong>nNOS</strong> activities was estimated with nicotinamide adenine dinucleotide hydrogen phosphate diaphorase (NADPH d) histochemistry.
+NOS1	drug	psychedelics	26520463	The effect of acute <b>ketamine</b> on <strong><strong>nNOS</strong></strong> activities was estimated with nicotinamide adenine dinucleotide hydrogen phosphate diaphorase (NADPH d) histochemistry.
+NOS1	drug	psychedelics	26520463	These results suggest that <b>ketamine</b> induced locomotor sensitization and <strong>nNOS</strong> activation in the frontal cortex striatum neuronal circuit are positively correlated and that the NMDAR GluN2D subunit plays an important role in the acquisition and maintenance of <b>ketamine</b> induced behavioral sensitization.
+NOS1	addiction	sensitization	26520463	These results suggest that ketamine induced locomotor <b>sensitization</b> and <strong>nNOS</strong> activation in the frontal cortex striatum neuronal circuit are positively correlated and that the NMDAR GluN2D subunit plays an important role in the acquisition and maintenance of ketamine induced behavioral <b>sensitization</b>.
+NOS1	drug	psychedelics	26520463	These results suggest that <b>ketamine</b> induced locomotor sensitization and <strong><strong>nNOS</strong></strong> activation in the frontal cortex striatum neuronal circuit are positively correlated and that the NMDAR GluN2D subunit plays an important role in the acquisition and maintenance of <b>ketamine</b> induced behavioral sensitization.
+NOS1	addiction	sensitization	26520463	These results suggest that ketamine induced locomotor <b>sensitization</b> and <strong><strong>nNOS</strong></strong> activation in the frontal cortex striatum neuronal circuit are positively correlated and that the NMDAR GluN2D subunit plays an important role in the acquisition and maintenance of ketamine induced behavioral <b>sensitization</b>.
+NOS1	drug	nicotine	26235957	Striatal <strong>NOS1</strong> has dimorphic expression and activity under stress and <b>nicotine</b> sensitization.
+NOS1	addiction	sensitization	26235957	Striatal <strong>NOS1</strong> has dimorphic expression and activity under stress and nicotine <b>sensitization</b>.
+NOS1	drug	nicotine	26235957	To determine the specific role of this enzyme, we analyzed both NOS expression and NO synthesis in the striatum of wild type and <strong>NOS1</strong> knocked out (KO) mice of both sexes in situations of <b>nicotine</b> sensitization and stress.
+NOS1	addiction	sensitization	26235957	To determine the specific role of this enzyme, we analyzed both NOS expression and NO synthesis in the striatum of wild type and <strong>NOS1</strong> knocked out (KO) mice of both sexes in situations of nicotine <b>sensitization</b> and stress.
+NOS1	addiction	dependence	26096126	Further, our studies established the <b>dependence</b> of the central CB1R mediated pressor response on neuronal nitric oxide synthase (<strong>nNOS</strong>) and extracellular signal regulated kinase1/2 (ERK1/2) phosphorylation in the RVLM.
+NOS1	addiction	dependence	26096126	Further, our studies established the <b>dependence</b> of the central CB1R mediated pressor response on neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) and extracellular signal regulated kinase1/2 (ERK1/2) phosphorylation in the RVLM.
+NOS1	drug	psychedelics	24308186	To observe the effects of electroacupuncture(EA) stimulation of "Zusanli"(ST 36) and "Sanyinjiao"(SP 6) at different time points of a day on the expression of c fos and neuronal nitric oxide synthase (<strong>nNOS</strong>) in the medial prefrontal cortex (mPFC) in rats with <b>ketamine</b> addiction.
+NOS1	addiction	addiction	24308186	To observe the effects of electroacupuncture(EA) stimulation of "Zusanli"(ST 36) and "Sanyinjiao"(SP 6) at different time points of a day on the expression of c fos and neuronal nitric oxide synthase (<strong>nNOS</strong>) in the medial prefrontal cortex (mPFC) in rats with ketamine <b>addiction</b>.
+NOS1	drug	psychedelics	24308186	To observe the effects of electroacupuncture(EA) stimulation of "Zusanli"(ST 36) and "Sanyinjiao"(SP 6) at different time points of a day on the expression of c fos and neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) in the medial prefrontal cortex (mPFC) in rats with <b>ketamine</b> addiction.
+NOS1	addiction	addiction	24308186	To observe the effects of electroacupuncture(EA) stimulation of "Zusanli"(ST 36) and "Sanyinjiao"(SP 6) at different time points of a day on the expression of c fos and neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) in the medial prefrontal cortex (mPFC) in rats with ketamine <b>addiction</b>.
+NOS1	drug	psychedelics	24308186	EA of ST 36 and SP 6 at 11 : 00 and 17 : 00 can decrease the expression o fc fos and <strong>nNOS</strong> in the mPFC in <b>ketamine</b> addiction rats, which may contribute to its effects in improving the rats' behavior activity.
+NOS1	addiction	addiction	24308186	EA of ST 36 and SP 6 at 11 : 00 and 17 : 00 can decrease the expression o fc fos and <strong>nNOS</strong> in the mPFC in ketamine <b>addiction</b> rats, which may contribute to its effects in improving the rats' behavior activity.
+NOS1	drug	psychedelics	24308186	EA of ST 36 and SP 6 at 11 : 00 and 17 : 00 can decrease the expression o fc fos and <strong><strong>nNOS</strong></strong> in the mPFC in <b>ketamine</b> addiction rats, which may contribute to its effects in improving the rats' behavior activity.
+NOS1	addiction	addiction	24308186	EA of ST 36 and SP 6 at 11 : 00 and 17 : 00 can decrease the expression o fc fos and <strong><strong>nNOS</strong></strong> in the mPFC in ketamine <b>addiction</b> rats, which may contribute to its effects in improving the rats' behavior activity.
+NOS1	drug	cocaine	23579428	Involvement of <strong>nNOS</strong>/NO/sGC/cGMP signaling pathway in <b>cocaine</b> sensitization and in the associated hippocampal alterations: does phosphodiesterase 5 inhibition help to drug vulnerability?
+NOS1	addiction	sensitization	23579428	Involvement of <strong>nNOS</strong>/NO/sGC/cGMP signaling pathway in cocaine <b>sensitization</b> and in the associated hippocampal alterations: does phosphodiesterase 5 inhibition help to drug vulnerability?
+NOS1	drug	cocaine	23579428	Involvement of <strong><strong>nNOS</strong></strong>/NO/sGC/cGMP signaling pathway in <b>cocaine</b> sensitization and in the associated hippocampal alterations: does phosphodiesterase 5 inhibition help to drug vulnerability?
+NOS1	addiction	sensitization	23579428	Involvement of <strong><strong>nNOS</strong></strong>/NO/sGC/cGMP signaling pathway in cocaine <b>sensitization</b> and in the associated hippocampal alterations: does phosphodiesterase 5 inhibition help to drug vulnerability?
+NOS1	drug	cocaine	23579428	Nitric oxide could be involved in the acquisition and maintenance of behavioral <b>cocaine</b> effects, probably by activation of neuronal nitric oxide synthase (<strong>nNOS</strong>)/NO/soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP) signaling pathway, since inhibition of the <strong>nNOS</strong> enzyme attenuates development of sensitization in rats.
+NOS1	addiction	sensitization	23579428	Nitric oxide could be involved in the acquisition and maintenance of behavioral cocaine effects, probably by activation of neuronal nitric oxide synthase (<strong>nNOS</strong>)/NO/soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP) signaling pathway, since inhibition of the <strong>nNOS</strong> enzyme attenuates development of <b>sensitization</b> in rats.
+NOS1	drug	cocaine	23579428	Nitric oxide could be involved in the acquisition and maintenance of behavioral <b>cocaine</b> effects, probably by activation of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>)/NO/soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP) signaling pathway, since inhibition of the <strong><strong>nNOS</strong></strong> enzyme attenuates development of sensitization in rats.
+NOS1	addiction	sensitization	23579428	Nitric oxide could be involved in the acquisition and maintenance of behavioral cocaine effects, probably by activation of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>)/NO/soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP) signaling pathway, since inhibition of the <strong><strong>nNOS</strong></strong> enzyme attenuates development of <b>sensitization</b> in rats.
+NOS1	drug	cocaine	23579428	The objective of this study is to determine whether the pharmacological manipulation of <strong>nNOS</strong>/NO/sGC/cGMP signaling pathway altered changes induced by repeated <b>cocaine</b> exposure.
+NOS1	drug	cocaine	23579428	The objective of this study is to determine whether the pharmacological manipulation of <strong><strong>nNOS</strong></strong>/NO/sGC/cGMP signaling pathway altered changes induced by repeated <b>cocaine</b> exposure.
+NOS1	drug	cocaine	23579428	The present investigation showed a relationship between behavioral <b>cocaine</b> sensitization, reduced threshold to generate long term potentiation (LTP) in hippocampal dentate gyrus, and increased <strong>nNOS</strong> activity in this structure.
+NOS1	addiction	sensitization	23579428	The present investigation showed a relationship between behavioral cocaine <b>sensitization</b>, reduced threshold to generate long term potentiation (LTP) in hippocampal dentate gyrus, and increased <strong>nNOS</strong> activity in this structure.
+NOS1	drug	cocaine	23579428	The present investigation showed a relationship between behavioral <b>cocaine</b> sensitization, reduced threshold to generate long term potentiation (LTP) in hippocampal dentate gyrus, and increased <strong><strong>nNOS</strong></strong> activity in this structure.
+NOS1	addiction	sensitization	23579428	The present investigation showed a relationship between behavioral cocaine <b>sensitization</b>, reduced threshold to generate long term potentiation (LTP) in hippocampal dentate gyrus, and increased <strong><strong>nNOS</strong></strong> activity in this structure.
+NOS1	drug	cocaine	23579428	We demonstrate a key role of the <strong>nNOS</strong> activity and NO/sGC/cGMP signaling pathway in the development of <b>cocaine</b> sensitization and in the associated enhancement of hippocampal synaptic transmission.
+NOS1	addiction	sensitization	23579428	We demonstrate a key role of the <strong>nNOS</strong> activity and NO/sGC/cGMP signaling pathway in the development of cocaine <b>sensitization</b> and in the associated enhancement of hippocampal synaptic transmission.
+NOS1	drug	cocaine	23579428	We demonstrate a key role of the <strong><strong>nNOS</strong></strong> activity and NO/sGC/cGMP signaling pathway in the development of <b>cocaine</b> sensitization and in the associated enhancement of hippocampal synaptic transmission.
+NOS1	addiction	sensitization	23579428	We demonstrate a key role of the <strong><strong>nNOS</strong></strong> activity and NO/sGC/cGMP signaling pathway in the development of cocaine <b>sensitization</b> and in the associated enhancement of hippocampal synaptic transmission.
+NOS1	drug	nicotine	23305719	The aim of this study was to determine how chronic <b>nicotine</b> withdrawal influences neuronal nitric oxide (NO) synthase (<strong>nNOS</strong>) and galanin immunoreactivity in the DRN and LC of adult rats.
+NOS1	addiction	withdrawal	23305719	The aim of this study was to determine how chronic nicotine <b>withdrawal</b> influences neuronal nitric oxide (NO) synthase (<strong>nNOS</strong>) and galanin immunoreactivity in the DRN and LC of adult rats.
+NOS1	drug	nicotine	23305719	The aim of this study was to determine how chronic <b>nicotine</b> withdrawal influences neuronal nitric oxide (NO) synthase (<strong><strong>nNOS</strong></strong>) and galanin immunoreactivity in the DRN and LC of adult rats.
+NOS1	addiction	withdrawal	23305719	The aim of this study was to determine how chronic nicotine <b>withdrawal</b> influences neuronal nitric oxide (NO) synthase (<strong><strong>nNOS</strong></strong>) and galanin immunoreactivity in the DRN and LC of adult rats.
+NOS1	drug	nicotine	23305719	Compared with saline, <b>nicotine</b> increased nicotinamide adenine dinucleotide phosphate diaphorase profiles within distinct DRN subregions and also enhanced intensity in <strong>nNOS</strong> and galanin cell bodies in the rostral DRN as well as galanin in the LC.
+NOS1	drug	nicotine	23305719	Compared with saline, <b>nicotine</b> increased nicotinamide adenine dinucleotide phosphate diaphorase profiles within distinct DRN subregions and also enhanced intensity in <strong><strong>nNOS</strong></strong> and galanin cell bodies in the rostral DRN as well as galanin in the LC.
+NOS1	drug	nicotine	23305719	<b>Nicotine</b> induced <strong>nNOS</strong>/galanin staining of somata was abundant in the rostral ventromedial DRN.
+NOS1	drug	nicotine	23305719	<b>Nicotine</b> induced <strong><strong>nNOS</strong></strong>/galanin staining of somata was abundant in the rostral ventromedial DRN.
+NOS1	drug	opioid	22860427	[The different roles of the spinal protein <strong>nNOS</strong> and iNOS in <b>morphine</b> <b>naloxone</b> precipitated withdrawal response].
+NOS1	addiction	withdrawal	22860427	[The different roles of the spinal protein <strong>nNOS</strong> and iNOS in morphine naloxone precipitated <b>withdrawal</b> response].
+NOS1	drug	opioid	22860427	[The different roles of the spinal protein <strong><strong>nNOS</strong></strong> and iNOS in <b>morphine</b> <b>naloxone</b> precipitated withdrawal response].
+NOS1	addiction	withdrawal	22860427	[The different roles of the spinal protein <strong><strong>nNOS</strong></strong> and iNOS in morphine naloxone precipitated <b>withdrawal</b> response].
+NOS1	drug	opioid	22860427	To explore the effects of intrathecal injection of neuronal nitric oxide synthase (<strong>nNOS</strong>) inhibitors 7 Nitroindazole (7 Ni) and inducible nitric oxide synthase(iNOS) inhibitors aminoguanidine (AG) on the behavioral changes of <b>morphine</b> induced dependent and withdrawal rats; the expression of Fos, <strong>nNOS</strong> and iNOS in spinal cord.
+NOS1	addiction	withdrawal	22860427	To explore the effects of intrathecal injection of neuronal nitric oxide synthase (<strong>nNOS</strong>) inhibitors 7 Nitroindazole (7 Ni) and inducible nitric oxide synthase(iNOS) inhibitors aminoguanidine (AG) on the behavioral changes of morphine induced dependent and <b>withdrawal</b> rats; the expression of Fos, <strong>nNOS</strong> and iNOS in spinal cord.
+NOS1	drug	opioid	22860427	To explore the effects of intrathecal injection of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitors 7 Nitroindazole (7 Ni) and inducible nitric oxide synthase(iNOS) inhibitors aminoguanidine (AG) on the behavioral changes of <b>morphine</b> induced dependent and withdrawal rats; the expression of Fos, <strong><strong>nNOS</strong></strong> and iNOS in spinal cord.
+NOS1	addiction	withdrawal	22860427	To explore the effects of intrathecal injection of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitors 7 Nitroindazole (7 Ni) and inducible nitric oxide synthase(iNOS) inhibitors aminoguanidine (AG) on the behavioral changes of morphine induced dependent and <b>withdrawal</b> rats; the expression of Fos, <strong><strong>nNOS</strong></strong> and iNOS in spinal cord.
+NOS1	drug	opioid	22860427	7 Ni, an <strong>nNOS</strong> inhibitor or iNOS inhibitors AG were intrathecally injected 30 min before the administration of <b>naloxone</b> respectively.
+NOS1	drug	opioid	22860427	7 Ni, an <strong><strong>nNOS</strong></strong> inhibitor or iNOS inhibitors AG were intrathecally injected 30 min before the administration of <b>naloxone</b> respectively.
+NOS1	drug	opioid	22860427	One hour after <b>naloxone</b> precipitated withdrawal, Fos protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of <strong>nNOS</strong> and iNOS in the rat spinal cord.
+NOS1	addiction	withdrawal	22860427	One hour after naloxone precipitated <b>withdrawal</b>, Fos protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of <strong>nNOS</strong> and iNOS in the rat spinal cord.
+NOS1	drug	opioid	22860427	One hour after <b>naloxone</b> precipitated withdrawal, Fos protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of <strong><strong>nNOS</strong></strong> and iNOS in the rat spinal cord.
+NOS1	addiction	withdrawal	22860427	One hour after naloxone precipitated <b>withdrawal</b>, Fos protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of <strong><strong>nNOS</strong></strong> and iNOS in the rat spinal cord.
+NOS1	drug	opioid	22860427	Intrathecal administration of <strong>nNOS</strong> inhibitor 7 Ni and iNOS inhibitors AG decreased the scores of <b>morphine</b> withdrawal, attenuated <b>morphine</b> withdrawal induced allodynia and also inhibited the increase of Fos protein expression in the spinal cord of <b>morphine</b> withdrawal rats.
+NOS1	addiction	withdrawal	22860427	Intrathecal administration of <strong>nNOS</strong> inhibitor 7 Ni and iNOS inhibitors AG decreased the scores of morphine <b>withdrawal</b>, attenuated morphine <b>withdrawal</b> induced allodynia and also inhibited the increase of Fos protein expression in the spinal cord of morphine <b>withdrawal</b> rats.
+NOS1	drug	opioid	22860427	Intrathecal administration of <strong><strong>nNOS</strong></strong> inhibitor 7 Ni and iNOS inhibitors AG decreased the scores of <b>morphine</b> withdrawal, attenuated <b>morphine</b> withdrawal induced allodynia and also inhibited the increase of Fos protein expression in the spinal cord of <b>morphine</b> withdrawal rats.
+NOS1	addiction	withdrawal	22860427	Intrathecal administration of <strong><strong>nNOS</strong></strong> inhibitor 7 Ni and iNOS inhibitors AG decreased the scores of morphine <b>withdrawal</b>, attenuated morphine <b>withdrawal</b> induced allodynia and also inhibited the increase of Fos protein expression in the spinal cord of morphine <b>withdrawal</b> rats.
+NOS1	addiction	withdrawal	22860427	<strong>nNOS</strong> and iNOS positive neurons in dorsal horn in <strong>nNOS</strong> group and iNOS group were significantly lower than that in <b>withdrawal</b> group.
+NOS1	addiction	withdrawal	22860427	<strong><strong>nNOS</strong></strong> and iNOS positive neurons in dorsal horn in <strong><strong>nNOS</strong></strong> group and iNOS group were significantly lower than that in <b>withdrawal</b> group.
+NOS1	addiction	withdrawal	22860427	Compared with <b>withdrawal</b> group, level of <strong>nNOS</strong> and iNOS protein in spinal cord in <strong>nNOS</strong> group and iNOS group were significantly lower.
+NOS1	addiction	withdrawal	22860427	Compared with <b>withdrawal</b> group, level of <strong><strong>nNOS</strong></strong> and iNOS protein in spinal cord in <strong><strong>nNOS</strong></strong> group and iNOS group were significantly lower.
+NOS1	drug	opioid	22860427	It is suggested that <strong>nNOS</strong> and iNOS in the spinal cord may contribute to <b>naloxone</b> precipitated withdrawal in rats and may play different roles in the above mentioned effect.
+NOS1	addiction	withdrawal	22860427	It is suggested that <strong>nNOS</strong> and iNOS in the spinal cord may contribute to naloxone precipitated <b>withdrawal</b> in rats and may play different roles in the above mentioned effect.
+NOS1	drug	opioid	22860427	It is suggested that <strong><strong>nNOS</strong></strong> and iNOS in the spinal cord may contribute to <b>naloxone</b> precipitated withdrawal in rats and may play different roles in the above mentioned effect.
+NOS1	addiction	withdrawal	22860427	It is suggested that <strong><strong>nNOS</strong></strong> and iNOS in the spinal cord may contribute to naloxone precipitated <b>withdrawal</b> in rats and may play different roles in the above mentioned effect.
+NOS1	drug	opioid	22820534	Intra CA1 injection of the neuronal NO synthase (<strong>nNOS</strong>) inhibitor 7 NI, the sGC inhibitor ODQ or the PKG inhibitor Rp 8 Br PET cGMPS had no effect on the acquisition of CPP by 4mg/kg <b>morphine</b>.
+NOS1	addiction	reward	22820534	Intra CA1 injection of the neuronal NO synthase (<strong>nNOS</strong>) inhibitor 7 NI, the sGC inhibitor ODQ or the PKG inhibitor Rp 8 Br PET cGMPS had no effect on the acquisition of <b>CPP</b> by 4mg/kg morphine.
+NOS1	drug	opioid	22820534	Intra CA1 injection of the neuronal NO synthase (<strong><strong>nNOS</strong></strong>) inhibitor 7 NI, the sGC inhibitor ODQ or the PKG inhibitor Rp 8 Br PET cGMPS had no effect on the acquisition of CPP by 4mg/kg <b>morphine</b>.
+NOS1	addiction	reward	22820534	Intra CA1 injection of the neuronal NO synthase (<strong><strong>nNOS</strong></strong>) inhibitor 7 NI, the sGC inhibitor ODQ or the PKG inhibitor Rp 8 Br PET cGMPS had no effect on the acquisition of <b>CPP</b> by 4mg/kg morphine.
+NOS1	drug	alcohol	22343344	The focus of this work is aimed to determine local changes in the <strong>nNOS</strong> like immunoreactive (<strong>nNOS</strong> LIR) cell populations of the SGL after chronic <b>ethanol</b> exposure in young adult and mature adult rats.
+NOS1	drug	alcohol	22343344	The focus of this work is aimed to determine local changes in the <strong><strong>nNOS</strong></strong> like immunoreactive (<strong><strong>nNOS</strong></strong> LIR) cell populations of the SGL after chronic <b>ethanol</b> exposure in young adult and mature adult rats.
+NOS1	addiction	withdrawal	22097732	Global <b>withdrawal</b> score, Touch evoked agitation scores (TEA score), immunohistochemical and Western blot technique were undertaken to evaluate behavioral changes and expression of FOS, <strong>nNOS</strong> and iNOS in spinal cord respectively.
+NOS1	addiction	withdrawal	22097732	Global <b>withdrawal</b> score, Touch evoked agitation scores (TEA score), immunohistochemical and Western blot technique were undertaken to evaluate behavioral changes and expression of FOS, <strong><strong>nNOS</strong></strong> and iNOS in spinal cord respectively.
+NOS1	addiction	withdrawal	22097732	Also <strong>nNOS</strong> and iNOS positive neurons in dorsal horn of U0126 group were 180 +/  32, 10.8 +/  2.8 respectively, which were significantly lower than that of <b>withdrawal</b> group (239 +/  45, 16.8 +/  5.1, P < 0.05).
+NOS1	addiction	withdrawal	22097732	Also <strong><strong>nNOS</strong></strong> and iNOS positive neurons in dorsal horn of U0126 group were 180 +/  32, 10.8 +/  2.8 respectively, which were significantly lower than that of <b>withdrawal</b> group (239 +/  45, 16.8 +/  5.1, P < 0.05).
+NOS1	addiction	withdrawal	22097732	Compared with <b>withdrawal</b> group, levels of <strong>nNOS</strong> and iNOS protein in spinal cord of U0126 group were significantly lower.
+NOS1	addiction	withdrawal	22097732	Compared with <b>withdrawal</b> group, levels of <strong><strong>nNOS</strong></strong> and iNOS protein in spinal cord of U0126 group were significantly lower.
+NOS1	drug	amphetamine	21886582	Genetic Association Analysis of <strong>NOS1</strong> and <b>Methamphetamine</b> Induced Psychosis Among Japanese.
+NOS1	drug	amphetamine	21886582	Because the symptomatology of <b>methamphetamine</b> (<b>METH</b>) use disorder patients with psychosis is similar to that of patients with schizophrenia, <strong>NOS1</strong> is a good candidate gene for <b>METH</b> induced psychosis.
+NOS1	drug	amphetamine	21886582	Therefore, we conducted a case control association study between <strong>NOS1</strong> and <b>METH</b> induced psychosis with Japanese subjects (183 with <b>METH</b> induced psychosis patients and 519 controls).
+NOS1	drug	amphetamine	21886582	No significant association was found between <strong>NOS1</strong> and <b>METH</b> induced psychosis in the allele/genotype wise or haplotype wise analyses.
+NOS1	drug	amphetamine	21886582	In conclusion, we suggest that <strong>NOS1</strong> might not contribute to the risk of <b>METH</b> induced psychosis in the Japanese population.
+NOS1	drug	cocaine	21705300	Urinary <b>cocaine</b> concentration was determined using the GC/MS method.<b>Cocaine</b> administration increased brain <strong>nNOS</strong> activity by 55 % (p<0.05) in respect to control, which indicates the development of tolerance and dependence.
+NOS1	addiction	dependence	21705300	Urinary cocaine concentration was determined using the GC/MS method.Cocaine administration increased brain <strong>nNOS</strong> activity by 55 % (p<0.05) in respect to control, which indicates the development of tolerance and <b>dependence</b>.
+NOS1	drug	cocaine	21705300	Urinary <b>cocaine</b> concentration was determined using the GC/MS method.<b>Cocaine</b> administration increased brain <strong><strong>nNOS</strong></strong> activity by 55 % (p<0.05) in respect to control, which indicates the development of tolerance and dependence.
+NOS1	addiction	dependence	21705300	Urinary cocaine concentration was determined using the GC/MS method.Cocaine administration increased brain <strong><strong>nNOS</strong></strong> activity by 55 % (p<0.05) in respect to control, which indicates the development of tolerance and <b>dependence</b>.
+NOS1	drug	cocaine	21705300	In the combination group, nifedipine decreased the <strong>nNOS</strong> activity in respect to the <b>cocaine</b> only group.In the liver, <b>cocaine</b> significantly decreased and nifedipine significantly increased cytochrome P450, ethylmorphine N demethylase, and anilinehydroxylase in respect to control.
+NOS1	drug	cocaine	21705300	In the combination group, nifedipine decreased the <strong><strong>nNOS</strong></strong> activity in respect to the <b>cocaine</b> only group.In the liver, <b>cocaine</b> significantly decreased and nifedipine significantly increased cytochrome P450, ethylmorphine N demethylase, and anilinehydroxylase in respect to control.
+NOS1	drug	cocaine	21125397	In this study, we attempted to determine whether inhibition of neuronal nitric oxide synthase (<strong>nNOS</strong>) altered the changes induced by repeated <b>cocaine</b> exposure and withdrawal.
+NOS1	addiction	withdrawal	21125397	In this study, we attempted to determine whether inhibition of neuronal nitric oxide synthase (<strong>nNOS</strong>) altered the changes induced by repeated cocaine exposure and <b>withdrawal</b>.
+NOS1	drug	cocaine	21125397	In this study, we attempted to determine whether inhibition of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) altered the changes induced by repeated <b>cocaine</b> exposure and withdrawal.
+NOS1	addiction	withdrawal	21125397	In this study, we attempted to determine whether inhibition of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) altered the changes induced by repeated cocaine exposure and <b>withdrawal</b>.
+NOS1	drug	cocaine	21125397	), or <b>cocaine</b> and the <strong>nNOS</strong> inhibitor 7 NI (50 mg/kg, i.p.)
+NOS1	drug	cocaine	21125397	), or <b>cocaine</b> and the <strong><strong>nNOS</strong></strong> inhibitor 7 NI (50 mg/kg, i.p.)
+NOS1	drug	cocaine	21125397	We found that <strong>nNOS</strong> inhibition prevented <b>cocaine</b> sensitization and the increased membrane excitability of pyramidal cells, evidenced by an increased number of evoked spikes and reductions in inward rectification observed after short term withdrawal from <b>cocaine</b>.
+NOS1	addiction	sensitization	21125397	We found that <strong>nNOS</strong> inhibition prevented cocaine <b>sensitization</b> and the increased membrane excitability of pyramidal cells, evidenced by an increased number of evoked spikes and reductions in inward rectification observed after short term withdrawal from cocaine.
+NOS1	addiction	withdrawal	21125397	We found that <strong>nNOS</strong> inhibition prevented cocaine sensitization and the increased membrane excitability of pyramidal cells, evidenced by an increased number of evoked spikes and reductions in inward rectification observed after short term <b>withdrawal</b> from cocaine.
+NOS1	drug	cocaine	21125397	We found that <strong><strong>nNOS</strong></strong> inhibition prevented <b>cocaine</b> sensitization and the increased membrane excitability of pyramidal cells, evidenced by an increased number of evoked spikes and reductions in inward rectification observed after short term withdrawal from <b>cocaine</b>.
+NOS1	addiction	sensitization	21125397	We found that <strong><strong>nNOS</strong></strong> inhibition prevented cocaine <b>sensitization</b> and the increased membrane excitability of pyramidal cells, evidenced by an increased number of evoked spikes and reductions in inward rectification observed after short term withdrawal from cocaine.
+NOS1	addiction	withdrawal	21125397	We found that <strong><strong>nNOS</strong></strong> inhibition prevented cocaine sensitization and the increased membrane excitability of pyramidal cells, evidenced by an increased number of evoked spikes and reductions in inward rectification observed after short term <b>withdrawal</b> from cocaine.
+NOS1	drug	opioid	20519536	<b>Morphine</b> withdrawal induced MMP 9 activity is also reduced by an <strong>nNOS</strong> inhibitor.
+NOS1	addiction	withdrawal	20519536	Morphine <b>withdrawal</b> induced MMP 9 activity is also reduced by an <strong>nNOS</strong> inhibitor.
+NOS1	drug	opioid	20519536	<b>Morphine</b> withdrawal induced MMP 9 activity is also reduced by an <strong><strong>nNOS</strong></strong> inhibitor.
+NOS1	addiction	withdrawal	20519536	Morphine <b>withdrawal</b> induced MMP 9 activity is also reduced by an <strong><strong>nNOS</strong></strong> inhibitor.
+NOS1	drug	cocaine	20477932	Therefore NFkappaB activity, oxidative stress, neuronal nitric oxide synthase (<strong>nNOS</strong>) activity, spatial learning and memory as well as the effect of topiramate, a previously proposed therapy for <b>cocaine</b> addiction, were evaluated in an experimental model of <b>cocaine</b> administration in rats.
+NOS1	addiction	addiction	20477932	Therefore NFkappaB activity, oxidative stress, neuronal nitric oxide synthase (<strong>nNOS</strong>) activity, spatial learning and memory as well as the effect of topiramate, a previously proposed therapy for cocaine <b>addiction</b>, were evaluated in an experimental model of cocaine administration in rats.
+NOS1	drug	cocaine	20477932	Therefore NFkappaB activity, oxidative stress, neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) activity, spatial learning and memory as well as the effect of topiramate, a previously proposed therapy for <b>cocaine</b> addiction, were evaluated in an experimental model of <b>cocaine</b> administration in rats.
+NOS1	addiction	addiction	20477932	Therefore NFkappaB activity, oxidative stress, neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) activity, spatial learning and memory as well as the effect of topiramate, a previously proposed therapy for cocaine <b>addiction</b>, were evaluated in an experimental model of cocaine administration in rats.
+NOS1	drug	cocaine	20477932	NFkappaB activity was decreased in the frontal cortex of <b>cocaine</b> treated rats, as well as GSH concentration and glutathione peroxidase activity in the hippocampus, whereas <strong>nNOS</strong> activity in the hippocampus was increased.
+NOS1	drug	cocaine	20477932	NFkappaB activity was decreased in the frontal cortex of <b>cocaine</b> treated rats, as well as GSH concentration and glutathione peroxidase activity in the hippocampus, whereas <strong><strong>nNOS</strong></strong> activity in the hippocampus was increased.
+NOS1	addiction	relapse	20186396	fast decision making and excitement <b>seeking</b> behaviour) were higher in subjects with the <strong>NOS1</strong> ex1f VNTR short/short genotype if they belonged to the platelet MAO medium activity (interquartile) range.
+NOS1	drug	cocaine	19775503	Discrimination between <b>cocaine</b> associated context and cue in a modified conditioned place preference paradigm: role of the <strong>nNOS</strong> gene in cue conditioning.
+NOS1	drug	cocaine	19775503	Discrimination between <b>cocaine</b> associated context and cue in a modified conditioned place preference paradigm: role of the <strong><strong>nNOS</strong></strong> gene in cue conditioning.
+NOS1	drug	cocaine	19775503	Wild type (WT) and <strong>nNOS</strong> knockout (KO) mice were trained by <b>cocaine</b> (20 mg/kg) in a discrete context paired with a light cue (a compound context cue stimulus).
+NOS1	drug	cocaine	19775503	Wild type (WT) and <strong><strong>nNOS</strong></strong> knockout (KO) mice were trained by <b>cocaine</b> (20 mg/kg) in a discrete context paired with a light cue (a compound context cue stimulus).
+NOS1	drug	cocaine	19775503	<strong>nNOS</strong> KO mice acquired approach behaviour for the <b>cocaine</b> associated context but not cue.
+NOS1	drug	cocaine	19775503	<strong><strong>nNOS</strong></strong> KO mice acquired approach behaviour for the <b>cocaine</b> associated context but not cue.
+NOS1	drug	cocaine	19429176	The neuronal nitric oxide synthase (<strong>nNOS</strong>) gene contributes to the regulation of tyrosine hydroxylase (TH) by <b>cocaine</b>.
+NOS1	drug	cocaine	19429176	The neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene contributes to the regulation of tyrosine hydroxylase (TH) by <b>cocaine</b>.
+NOS1	drug	cocaine	19429176	Anderson, Y. Itzhak, Differential role of the <strong>nNOS</strong> gene in the development of behavioral sensitization to <b>cocaine</b> in adolescent and adult B6;129S mice, Psychopharmacology (Berl) 200 (2008) 509 519].
+NOS1	addiction	sensitization	19429176	Anderson, Y. Itzhak, Differential role of the <strong>nNOS</strong> gene in the development of behavioral <b>sensitization</b> to cocaine in adolescent and adult B6;129S mice, Psychopharmacology (Berl) 200 (2008) 509 519].
+NOS1	drug	cocaine	19429176	Anderson, Y. Itzhak, Differential role of the <strong><strong>nNOS</strong></strong> gene in the development of behavioral sensitization to <b>cocaine</b> in adolescent and adult B6;129S mice, Psychopharmacology (Berl) 200 (2008) 509 519].
+NOS1	addiction	sensitization	19429176	Anderson, Y. Itzhak, Differential role of the <strong><strong>nNOS</strong></strong> gene in the development of behavioral <b>sensitization</b> to cocaine in adolescent and adult B6;129S mice, Psychopharmacology (Berl) 200 (2008) 509 519].
+NOS1	drug	cocaine	19429176	Given the requirement of dopamine (DA) transmission in <b>cocaine</b> induced behavioral sensitization and the interactions between NO and DA systems, the present study investigated the role of the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene and the effect of <b>cocaine</b> on the expression of tyrosine hydroxylase (TH) immunoreactive ( ir) neurons.
+NOS1	addiction	sensitization	19429176	Given the requirement of dopamine (DA) transmission in cocaine induced behavioral <b>sensitization</b> and the interactions between NO and DA systems, the present study investigated the role of the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene and the effect of cocaine on the expression of tyrosine hydroxylase (TH) immunoreactive ( ir) neurons.
+NOS1	drug	cocaine	19429176	Given the requirement of dopamine (DA) transmission in <b>cocaine</b> induced behavioral sensitization and the interactions between NO and DA systems, the present study investigated the role of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene and the effect of <b>cocaine</b> on the expression of tyrosine hydroxylase (TH) immunoreactive ( ir) neurons.
+NOS1	addiction	sensitization	19429176	Given the requirement of dopamine (DA) transmission in cocaine induced behavioral <b>sensitization</b> and the interactions between NO and DA systems, the present study investigated the role of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene and the effect of cocaine on the expression of tyrosine hydroxylase (TH) immunoreactive ( ir) neurons.
+NOS1	drug	cocaine	19429176	Adult (postnatal day 80) wild type (WT) and <strong>nNOS</strong> knockout (KO) mice received saline or a sensitizing regimen of <b>cocaine</b> (20mg/kg) for 5 days.
+NOS1	drug	cocaine	19429176	Adult (postnatal day 80) wild type (WT) and <strong><strong>nNOS</strong></strong> knockout (KO) mice received saline or a sensitizing regimen of <b>cocaine</b> (20mg/kg) for 5 days.
+NOS1	drug	cocaine	19429176	We report that (a) <strong>nNOS</strong> KO mice express lower levels of TH ir neurons in the VTA compared to WT counterparts, (b) <b>cocaine</b> administration to WT mice significantly increased striatal TH expression, and (c) the same <b>cocaine</b> administration to <strong>nNOS</strong> KO mice significantly decreased striatal TH expression.
+NOS1	drug	cocaine	19429176	We report that (a) <strong><strong>nNOS</strong></strong> KO mice express lower levels of TH ir neurons in the VTA compared to WT counterparts, (b) <b>cocaine</b> administration to WT mice significantly increased striatal TH expression, and (c) the same <b>cocaine</b> administration to <strong><strong>nNOS</strong></strong> KO mice significantly decreased striatal TH expression.
+NOS1	drug	alcohol	19362797	Role of the <strong>nNOS</strong> gene in <b>ethanol</b> induced conditioned place preference in mice.
+NOS1	drug	alcohol	19362797	Role of the <strong><strong>nNOS</strong></strong> gene in <b>ethanol</b> induced conditioned place preference in mice.
+NOS1	drug	alcohol	19362797	Nitric oxide (NO) produced by neuronal nitric oxide synthase (<strong>nNOS</strong>) has a role in synaptic plasticity, and evidence suggests its role in a range of effects produced by <b>alcohol</b> in the central nervous system.
+NOS1	drug	alcohol	19362797	Nitric oxide (NO) produced by neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) has a role in synaptic plasticity, and evidence suggests its role in a range of effects produced by <b>alcohol</b> in the central nervous system.
+NOS1	drug	alcohol	19362797	The aim of the current study was to investigate the role of the <strong>nNOS</strong> gene in the development of <b>ethanol</b> induced conditioned place preference (CPP) in mice.
+NOS1	addiction	reward	19362797	The aim of the current study was to investigate the role of the <strong>nNOS</strong> gene in the development of ethanol induced conditioned place preference (<b>CPP</b>) in mice.
+NOS1	drug	alcohol	19362797	The aim of the current study was to investigate the role of the <strong><strong>nNOS</strong></strong> gene in the development of <b>ethanol</b> induced conditioned place preference (CPP) in mice.
+NOS1	addiction	reward	19362797	The aim of the current study was to investigate the role of the <strong><strong>nNOS</strong></strong> gene in the development of ethanol induced conditioned place preference (<b>CPP</b>) in mice.
+NOS1	drug	alcohol	19362797	Adult male and female wild type (WT) and <strong>nNOS</strong> knockout (KO) mice on a mixed B6;129S genetic background were trained by a morning saline session and afternoon <b>ethanol</b> (1, 2, and 3 g/kg; intraperitoneally) session for 4 days.
+NOS1	drug	alcohol	19362797	Adult male and female wild type (WT) and <strong><strong>nNOS</strong></strong> knockout (KO) mice on a mixed B6;129S genetic background were trained by a morning saline session and afternoon <b>ethanol</b> (1, 2, and 3 g/kg; intraperitoneally) session for 4 days.
+NOS1	drug	alcohol	19362797	Results show that WT males and females developed robust CPP, whereas <strong>nNOS</strong> KO mice did not (with the exception of female <strong>nNOS</strong> KO mice conditioned by 2 g/kg <b>ethanol</b>).
+NOS1	addiction	reward	19362797	Results show that WT males and females developed robust <b>CPP</b>, whereas <strong>nNOS</strong> KO mice did not (with the exception of female <strong>nNOS</strong> KO mice conditioned by 2 g/kg ethanol).
+NOS1	drug	alcohol	19362797	Results show that WT males and females developed robust CPP, whereas <strong><strong>nNOS</strong></strong> KO mice did not (with the exception of female <strong><strong>nNOS</strong></strong> KO mice conditioned by 2 g/kg <b>ethanol</b>).
+NOS1	addiction	reward	19362797	Results show that WT males and females developed robust <b>CPP</b>, whereas <strong><strong>nNOS</strong></strong> KO mice did not (with the exception of female <strong><strong>nNOS</strong></strong> KO mice conditioned by 2 g/kg ethanol).
+NOS1	drug	alcohol	19362797	To investigate if the absence of the <strong>nNOS</strong> gene causes specific impairment in processing the motivational effect of <b>ethanol</b> or an overall impairment in associative learning, WT and <strong>nNOS</strong> KO mice were trained by LiCl (150 mg/kg) which causes conditioned place aversion (CPA).
+NOS1	addiction	aversion	19362797	To investigate if the absence of the <strong>nNOS</strong> gene causes specific impairment in processing the motivational effect of ethanol or an overall impairment in associative learning, WT and <strong>nNOS</strong> KO mice were trained by LiCl (150 mg/kg) which causes conditioned place <b>aversion</b> (CPA).
+NOS1	drug	alcohol	19362797	To investigate if the absence of the <strong><strong>nNOS</strong></strong> gene causes specific impairment in processing the motivational effect of <b>ethanol</b> or an overall impairment in associative learning, WT and <strong><strong>nNOS</strong></strong> KO mice were trained by LiCl (150 mg/kg) which causes conditioned place aversion (CPA).
+NOS1	addiction	aversion	19362797	To investigate if the absence of the <strong><strong>nNOS</strong></strong> gene causes specific impairment in processing the motivational effect of ethanol or an overall impairment in associative learning, WT and <strong><strong>nNOS</strong></strong> KO mice were trained by LiCl (150 mg/kg) which causes conditioned place <b>aversion</b> (CPA).
+NOS1	drug	alcohol	19362797	The findings that the absence of the <strong>nNOS</strong> gene impaired <b>ethanol</b> induced CPP but not LiCl induced CPA suggest that NO signaling has a specific role in processing the motivational effect of <b>ethanol</b>.
+NOS1	addiction	reward	19362797	The findings that the absence of the <strong>nNOS</strong> gene impaired ethanol induced <b>CPP</b> but not LiCl induced CPA suggest that NO signaling has a specific role in processing the motivational effect of ethanol.
+NOS1	drug	alcohol	19362797	The findings that the absence of the <strong><strong>nNOS</strong></strong> gene impaired <b>ethanol</b> induced CPP but not LiCl induced CPA suggest that NO signaling has a specific role in processing the motivational effect of <b>ethanol</b>.
+NOS1	addiction	reward	19362797	The findings that the absence of the <strong><strong>nNOS</strong></strong> gene impaired ethanol induced <b>CPP</b> but not LiCl induced CPA suggest that NO signaling has a specific role in processing the motivational effect of ethanol.
+NOS1	drug	alcohol	19362797	Hence, inhibition of <strong>nNOS</strong> may attenuate the development of maladaptive behaviors associated with <b>alcohol</b> exposure.
+NOS1	drug	alcohol	19362797	Hence, inhibition of <strong><strong>nNOS</strong></strong> may attenuate the development of maladaptive behaviors associated with <b>alcohol</b> exposure.
+NOS1	drug	cocaine	19114050	Development and persistence of long lasting behavioral sensitization to <b>cocaine</b> in female mice: role of the <strong>nNOS</strong> gene.
+NOS1	addiction	sensitization	19114050	Development and persistence of long lasting behavioral <b>sensitization</b> to cocaine in female mice: role of the <strong>nNOS</strong> gene.
+NOS1	drug	cocaine	19114050	Development and persistence of long lasting behavioral sensitization to <b>cocaine</b> in female mice: role of the <strong><strong>nNOS</strong></strong> gene.
+NOS1	addiction	sensitization	19114050	Development and persistence of long lasting behavioral <b>sensitization</b> to cocaine in female mice: role of the <strong><strong>nNOS</strong></strong> gene.
+NOS1	drug	cocaine	19114050	Our recent studies have shown that the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene is required for the development and persistence of psychomotor sensitization to <b>cocaine</b> in adult but not adolescent male mice (Balda, M.A., Anderson, K.L., Itzhak, Y., 2008.
+NOS1	addiction	sensitization	19114050	Our recent studies have shown that the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene is required for the development and persistence of psychomotor <b>sensitization</b> to cocaine in adult but not adolescent male mice (Balda, M.A., Anderson, K.L., Itzhak, Y., 2008.
+NOS1	drug	cocaine	19114050	Our recent studies have shown that the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene is required for the development and persistence of psychomotor sensitization to <b>cocaine</b> in adult but not adolescent male mice (Balda, M.A., Anderson, K.L., Itzhak, Y., 2008.
+NOS1	addiction	sensitization	19114050	Our recent studies have shown that the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene is required for the development and persistence of psychomotor <b>sensitization</b> to cocaine in adult but not adolescent male mice (Balda, M.A., Anderson, K.L., Itzhak, Y., 2008.
+NOS1	drug	cocaine	19114050	Differential role of the <strong>nNOS</strong> gene in the development of behavioral sensitization to <b>cocaine</b> in adolescent and adult B6;129S mice.
+NOS1	addiction	sensitization	19114050	Differential role of the <strong>nNOS</strong> gene in the development of behavioral <b>sensitization</b> to cocaine in adolescent and adult B6;129S mice.
+NOS1	drug	cocaine	19114050	Differential role of the <strong><strong>nNOS</strong></strong> gene in the development of behavioral sensitization to <b>cocaine</b> in adolescent and adult B6;129S mice.
+NOS1	addiction	sensitization	19114050	Differential role of the <strong><strong>nNOS</strong></strong> gene in the development of behavioral <b>sensitization</b> to cocaine in adolescent and adult B6;129S mice.
+NOS1	drug	cocaine	19114050	The aim of the present study was to investigate the contribution of the <strong>nNOS</strong> gene to <b>cocaine</b> induced behavioral sensitization in adolescent and adult female mice.
+NOS1	addiction	sensitization	19114050	The aim of the present study was to investigate the contribution of the <strong>nNOS</strong> gene to cocaine induced behavioral <b>sensitization</b> in adolescent and adult female mice.
+NOS1	drug	cocaine	19114050	The aim of the present study was to investigate the contribution of the <strong><strong>nNOS</strong></strong> gene to <b>cocaine</b> induced behavioral sensitization in adolescent and adult female mice.
+NOS1	addiction	sensitization	19114050	The aim of the present study was to investigate the contribution of the <strong><strong>nNOS</strong></strong> gene to cocaine induced behavioral <b>sensitization</b> in adolescent and adult female mice.
+NOS1	drug	cocaine	19114050	Adolescent and adult wild type (WT) and <strong>nNOS</strong> knockout (KO) mice received saline or <b>cocaine</b> (20 mg/kg) for 5 days and then were challenged with <b>cocaine</b> (20 mg/kg) after a drug free period of either 10, 30, or 90 days.
+NOS1	drug	cocaine	19114050	Adolescent and adult wild type (WT) and <strong><strong>nNOS</strong></strong> knockout (KO) mice received saline or <b>cocaine</b> (20 mg/kg) for 5 days and then were challenged with <b>cocaine</b> (20 mg/kg) after a drug free period of either 10, 30, or 90 days.
+NOS1	addiction	sensitization	19114050	An effect of genotype was observed in the initiation of <b>sensitization</b>, e.g., delayed onset in the absence of the <strong>nNOS</strong> gene.
+NOS1	addiction	sensitization	19114050	An effect of genotype was observed in the initiation of <b>sensitization</b>, e.g., delayed onset in the absence of the <strong><strong>nNOS</strong></strong> gene.
+NOS1	drug	cocaine	19114050	The present study suggests that long term expression of <b>cocaine</b> induced behavioral sensitization in females (adolescent and adult) is <strong>nNOS</strong> independent, unlike our previous findings in adult males.
+NOS1	addiction	sensitization	19114050	The present study suggests that long term expression of cocaine induced behavioral <b>sensitization</b> in females (adolescent and adult) is <strong>nNOS</strong> independent, unlike our previous findings in adult males.
+NOS1	drug	cocaine	19114050	The present study suggests that long term expression of <b>cocaine</b> induced behavioral sensitization in females (adolescent and adult) is <strong><strong>nNOS</strong></strong> independent, unlike our previous findings in adult males.
+NOS1	addiction	sensitization	19114050	The present study suggests that long term expression of cocaine induced behavioral <b>sensitization</b> in females (adolescent and adult) is <strong><strong>nNOS</strong></strong> independent, unlike our previous findings in adult males.
+NOS1	drug	opioid	19041302	Peripheral antinociceptive effects of mu  and delta <b>opioid</b> receptor agonists in NOS2 and <strong>NOS1</strong> knockout mice during chronic inflammatory pain.
+NOS1	drug	opioid	19041302	The aim of this study is to investigate the involvement of nitric oxide synthesized by the inducible (NOS2) or neuronal (<strong>NOS1</strong>) nitric oxide synthases in the local antinociceptive effects produced by micro  and delta <b>opioid</b> receptor agonists during chronic inflammatory pain.
+NOS1	drug	opioid	19041302	Moreover, the local administration of <b>morphine</b> or DPDPE also failed to reverse the decrease of ipsilateral paw withdrawal latency induced by complete Freund's adjuvant in <strong>NOS1</strong> knockout mice throughout 10 days of peripheral inflammation.
+NOS1	addiction	withdrawal	19041302	Moreover, the local administration of morphine or DPDPE also failed to reverse the decrease of ipsilateral paw <b>withdrawal</b> latency induced by complete Freund's adjuvant in <strong>NOS1</strong> knockout mice throughout 10 days of peripheral inflammation.
+NOS1	drug	opioid	19041302	These results indicate the different roles played by nitric oxide synthesized by NOS2 or <strong>NOS1</strong> in the maintenance of mechanical allodynia and thermal hyperalgesia induced by chronic inflammatory pain as well as, in the antinociceptive effects produced by micro  and delta <b>opioid</b> receptor agonists during peripheral inflammatory pain.
+NOS1	drug	cocaine	18991881	In the present study the effects of the NMDA receptor antagonist, MK 801, and the <strong>nNOS</strong> inhibitor 7 nitroindazole (7 NI) on memory reconsolidation of <b>cocaine</b> induced CPP in mice were investigated.
+NOS1	addiction	reward	18991881	In the present study the effects of the NMDA receptor antagonist, MK 801, and the <strong>nNOS</strong> inhibitor 7 nitroindazole (7 NI) on memory reconsolidation of cocaine induced <b>CPP</b> in mice were investigated.
+NOS1	drug	cocaine	18991881	In the present study the effects of the NMDA receptor antagonist, MK 801, and the <strong><strong>nNOS</strong></strong> inhibitor 7 nitroindazole (7 NI) on memory reconsolidation of <b>cocaine</b> induced CPP in mice were investigated.
+NOS1	addiction	reward	18991881	In the present study the effects of the NMDA receptor antagonist, MK 801, and the <strong><strong>nNOS</strong></strong> inhibitor 7 nitroindazole (7 NI) on memory reconsolidation of cocaine induced <b>CPP</b> in mice were investigated.
+NOS1	drug	cocaine	18991881	Male <strong>nNOS</strong> knockout (KO) mice acquired short lived <b>cocaine</b> CPP compared to wild type (WT) mice.
+NOS1	addiction	reward	18991881	Male <strong>nNOS</strong> knockout (KO) mice acquired short lived cocaine <b>CPP</b> compared to wild type (WT) mice.
+NOS1	drug	cocaine	18991881	Male <strong><strong>nNOS</strong></strong> knockout (KO) mice acquired short lived <b>cocaine</b> CPP compared to wild type (WT) mice.
+NOS1	addiction	reward	18991881	Male <strong><strong>nNOS</strong></strong> knockout (KO) mice acquired short lived cocaine <b>CPP</b> compared to wild type (WT) mice.
+NOS1	addiction	reward	18991881	A single acute administration of the NO donor molsidomine to <strong>nNOS</strong> KO mice immediately after retrieval of <b>CPP</b> prolonged the expression of place preference compared to controls that received saline, suggesting partial strengthening of memory reconsolidation.
+NOS1	addiction	reward	18991881	A single acute administration of the NO donor molsidomine to <strong><strong>nNOS</strong></strong> KO mice immediately after retrieval of <b>CPP</b> prolonged the expression of place preference compared to controls that received saline, suggesting partial strengthening of memory reconsolidation.
+NOS1	drug	alcohol	18652592	<b>Ethanol</b> induced behavioral sensitization in adolescent and adult mice: role of the <strong>nNOS</strong> gene.
+NOS1	addiction	sensitization	18652592	Ethanol induced behavioral <b>sensitization</b> in adolescent and adult mice: role of the <strong>nNOS</strong> gene.
+NOS1	drug	alcohol	18652592	<b>Ethanol</b> induced behavioral sensitization in adolescent and adult mice: role of the <strong><strong>nNOS</strong></strong> gene.
+NOS1	addiction	sensitization	18652592	Ethanol induced behavioral <b>sensitization</b> in adolescent and adult mice: role of the <strong><strong>nNOS</strong></strong> gene.
+NOS1	drug	alcohol	18652592	The current study investigated the role of the <strong>nNOS</strong> gene in the development of behavioral sensitization to <b>ethanol</b> in adolescent and adult mice.
+NOS1	addiction	sensitization	18652592	The current study investigated the role of the <strong>nNOS</strong> gene in the development of behavioral <b>sensitization</b> to ethanol in adolescent and adult mice.
+NOS1	drug	alcohol	18652592	The current study investigated the role of the <strong><strong>nNOS</strong></strong> gene in the development of behavioral sensitization to <b>ethanol</b> in adolescent and adult mice.
+NOS1	addiction	sensitization	18652592	The current study investigated the role of the <strong><strong>nNOS</strong></strong> gene in the development of behavioral <b>sensitization</b> to ethanol in adolescent and adult mice.
+NOS1	drug	alcohol	18652592	Adolescent and adult wild type (WT; B6;129SF2) and nNOS knockout (KO; B6;129S4 <strong>Nos1</strong>) mice of both sexes received saline or <b>ethanol</b> (1.5 g/kg; intraperitoneally) for 5 consecutive days, and locomotor activity was recorded daily.
+NOS1	drug	alcohol	18652592	Adolescent and adult wild type (WT; B6;129SF2) and <strong>nNOS</strong> knockout (KO; B6;129S4 <strong>Nos1</strong>) mice of both sexes received saline or <b>ethanol</b> (1.5 g/kg; intraperitoneally) for 5 consecutive days, and locomotor activity was recorded daily.
+NOS1	drug	alcohol	18652592	Adolescent and adult wild type (WT; B6;129SF2) and <strong><strong>nNOS</strong></strong> knockout (KO; B6;129S4 <strong>Nos1</strong>) mice of both sexes received saline or <b>ethanol</b> (1.5 g/kg; intraperitoneally) for 5 consecutive days, and locomotor activity was recorded daily.
+NOS1	drug	alcohol	18652592	Adolescent WT but not <strong>nNOS</strong> KO mice developed a long lasting sensitized response to <b>ethanol</b> as well as context dependent hyperlocomotion (in response to saline) from adolescence through adulthood; sex dependent differences were not observed.
+NOS1	drug	alcohol	18652592	Adolescent WT but not <strong><strong>nNOS</strong></strong> KO mice developed a long lasting sensitized response to <b>ethanol</b> as well as context dependent hyperlocomotion (in response to saline) from adolescence through adulthood; sex dependent differences were not observed.
+NOS1	addiction	sensitization	18652592	Adult <strong>nNOS</strong> KO males (like their adolescent counterparts) did not develop behavioral <b>sensitization</b>; no significant differences between adult <strong>nNOS</strong> KO and WT females were observed.
+NOS1	addiction	sensitization	18652592	Adult <strong><strong>nNOS</strong></strong> KO males (like their adolescent counterparts) did not develop behavioral <b>sensitization</b>; no significant differences between adult <strong><strong>nNOS</strong></strong> KO and WT females were observed.
+NOS1	drug	alcohol	18652592	(1) The <strong>nNOS</strong> gene is required for the development of behavioral sensitization to <b>ethanol</b> in adolescent male and female mice.
+NOS1	addiction	sensitization	18652592	(1) The <strong>nNOS</strong> gene is required for the development of behavioral <b>sensitization</b> to ethanol in adolescent male and female mice.
+NOS1	drug	alcohol	18652592	(1) The <strong><strong>nNOS</strong></strong> gene is required for the development of behavioral sensitization to <b>ethanol</b> in adolescent male and female mice.
+NOS1	addiction	sensitization	18652592	(1) The <strong><strong>nNOS</strong></strong> gene is required for the development of behavioral <b>sensitization</b> to ethanol in adolescent male and female mice.
+NOS1	drug	alcohol	18652592	(4) <b>Ethanol</b> induced behavioral sensitization in adulthood is <strong>nNOS</strong> dependent in males but not in females.
+NOS1	addiction	sensitization	18652592	(4) Ethanol induced behavioral <b>sensitization</b> in adulthood is <strong>nNOS</strong> dependent in males but not in females.
+NOS1	drug	alcohol	18652592	(4) <b>Ethanol</b> induced behavioral sensitization in adulthood is <strong><strong>nNOS</strong></strong> dependent in males but not in females.
+NOS1	addiction	sensitization	18652592	(4) Ethanol induced behavioral <b>sensitization</b> in adulthood is <strong><strong>nNOS</strong></strong> dependent in males but not in females.
+NOS1	drug	alcohol	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; MGLUR5; <strong>NNOS</strong>; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with <b>alcohol</b> dependence using multivariate statistical analysis.
+NOS1	addiction	dependence	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; MGLUR5; <strong>NNOS</strong>; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with alcohol <b>dependence</b> using multivariate statistical analysis.
+NOS1	drug	alcohol	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; MGLUR5; <strong><strong>NNOS</strong></strong>; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with <b>alcohol</b> dependence using multivariate statistical analysis.
+NOS1	addiction	dependence	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; MGLUR5; <strong><strong>NNOS</strong></strong>; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with alcohol <b>dependence</b> using multivariate statistical analysis.
+NOS1	drug	cocaine	18592222	Differential role of the <strong>nNOS</strong> gene in the development of behavioral sensitization to <b>cocaine</b> in adolescent and adult B6;129S mice.
+NOS1	addiction	sensitization	18592222	Differential role of the <strong>nNOS</strong> gene in the development of behavioral <b>sensitization</b> to cocaine in adolescent and adult B6;129S mice.
+NOS1	drug	cocaine	18592222	Differential role of the <strong><strong>nNOS</strong></strong> gene in the development of behavioral sensitization to <b>cocaine</b> in adolescent and adult B6;129S mice.
+NOS1	addiction	sensitization	18592222	Differential role of the <strong><strong>nNOS</strong></strong> gene in the development of behavioral <b>sensitization</b> to cocaine in adolescent and adult B6;129S mice.
+NOS1	addiction	sensitization	18592222	Previous studies have suggested the involvement of neuronal nitric oxide synthase (<strong>nNOS</strong>) in the development of <b>sensitization</b> to psychostimulants.
+NOS1	addiction	sensitization	18592222	Previous studies have suggested the involvement of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) in the development of <b>sensitization</b> to psychostimulants.
+NOS1	drug	cocaine	18592222	The objectives were to investigate (a) the short  and long term consequences of adolescent and adult <b>cocaine</b> exposure on behavioral sensitization and (b) the role of the <strong>nNOS</strong> gene in behavioral sensitization in adolescent and adult mice.
+NOS1	addiction	sensitization	18592222	The objectives were to investigate (a) the short  and long term consequences of adolescent and adult cocaine exposure on behavioral <b>sensitization</b> and (b) the role of the <strong>nNOS</strong> gene in behavioral <b>sensitization</b> in adolescent and adult mice.
+NOS1	drug	cocaine	18592222	The objectives were to investigate (a) the short  and long term consequences of adolescent and adult <b>cocaine</b> exposure on behavioral sensitization and (b) the role of the <strong><strong>nNOS</strong></strong> gene in behavioral sensitization in adolescent and adult mice.
+NOS1	addiction	sensitization	18592222	The objectives were to investigate (a) the short  and long term consequences of adolescent and adult cocaine exposure on behavioral <b>sensitization</b> and (b) the role of the <strong><strong>nNOS</strong></strong> gene in behavioral <b>sensitization</b> in adolescent and adult mice.
+NOS1	drug	cocaine	18592222	Adolescent and adult wild type (WT) and <strong>nNOS</strong> knockout (KO) mice received saline or <b>cocaine</b> (20 mg/kg) for 5 days and then were challenged with <b>cocaine</b> (20 mg/kg) after a drug free period of 10 or 30 days.
+NOS1	drug	cocaine	18592222	Adolescent and adult wild type (WT) and <strong><strong>nNOS</strong></strong> knockout (KO) mice received saline or <b>cocaine</b> (20 mg/kg) for 5 days and then were challenged with <b>cocaine</b> (20 mg/kg) after a drug free period of 10 or 30 days.
+NOS1	drug	cocaine	18592222	<strong>nNOS</strong> immunoreactive (ir) neurons in the dorsal and ventral striatum were quantified 24 h after repeated administration of <b>cocaine</b> to adolescent and adult WT mice.
+NOS1	drug	cocaine	18592222	<strong><strong>nNOS</strong></strong> immunoreactive (ir) neurons in the dorsal and ventral striatum were quantified 24 h after repeated administration of <b>cocaine</b> to adolescent and adult WT mice.
+NOS1	drug	cocaine	18592222	Repeated administration of <b>cocaine</b> to either WT or <strong>nNOS</strong> KO mice during adolescence resulted in locomotor sensitization, which persisted into adulthood.
+NOS1	addiction	sensitization	18592222	Repeated administration of cocaine to either WT or <strong>nNOS</strong> KO mice during adolescence resulted in locomotor <b>sensitization</b>, which persisted into adulthood.
+NOS1	drug	cocaine	18592222	Repeated administration of <b>cocaine</b> to either WT or <strong><strong>nNOS</strong></strong> KO mice during adolescence resulted in locomotor sensitization, which persisted into adulthood.
+NOS1	addiction	sensitization	18592222	Repeated administration of cocaine to either WT or <strong><strong>nNOS</strong></strong> KO mice during adolescence resulted in locomotor <b>sensitization</b>, which persisted into adulthood.
+NOS1	drug	cocaine	18592222	Repeated <b>cocaine</b> administration resulted in a 96% increase in the expression of <strong>nNOS</strong> ir neurons in the dorsal striatum of adult but not adolescent WT mice.
+NOS1	drug	cocaine	18592222	Repeated <b>cocaine</b> administration resulted in a 96% increase in the expression of <strong><strong>nNOS</strong></strong> ir neurons in the dorsal striatum of adult but not adolescent WT mice.
+NOS1	drug	cocaine	18592222	The <strong>nNOS</strong> gene is essential for the induction of behavioral sensitization to <b>cocaine</b> in adulthood but not in adolescence.
+NOS1	addiction	sensitization	18592222	The <strong>nNOS</strong> gene is essential for the induction of behavioral <b>sensitization</b> to cocaine in adulthood but not in adolescence.
+NOS1	drug	cocaine	18592222	The <strong><strong>nNOS</strong></strong> gene is essential for the induction of behavioral sensitization to <b>cocaine</b> in adulthood but not in adolescence.
+NOS1	addiction	sensitization	18592222	The <strong><strong>nNOS</strong></strong> gene is essential for the induction of behavioral <b>sensitization</b> to cocaine in adulthood but not in adolescence.
+NOS1	addiction	sensitization	18592222	The increased expression of <strong>nNOS</strong> ir neurons in the dorsal striatum may underlie the induction of behavioral <b>sensitization</b> in adulthood.
+NOS1	addiction	sensitization	18592222	The increased expression of <strong><strong>nNOS</strong></strong> ir neurons in the dorsal striatum may underlie the induction of behavioral <b>sensitization</b> in adulthood.
+NOS1	addiction	withdrawal	18512210	However, it is not fully understood whether or not <strong>nNOS</strong> containing neurons in the various brain regions play an important role in butorphanol <b>withdrawal</b>.
+NOS1	addiction	withdrawal	18512210	However, it is not fully understood whether or not <strong><strong>nNOS</strong></strong> containing neurons in the various brain regions play an important role in butorphanol <b>withdrawal</b>.
+NOS1	addiction	withdrawal	18512210	Therefore, this study was conducted to determine whether the selective <strong>nNOS</strong> inhibitor, 7 NI, modifies the development of butorphanol <b>withdrawal</b> and changes of <strong>nNOS</strong> expressions in different brain regions in physically butorphanol dependent rats.
+NOS1	addiction	withdrawal	18512210	Therefore, this study was conducted to determine whether the selective <strong><strong>nNOS</strong></strong> inhibitor, 7 NI, modifies the development of butorphanol <b>withdrawal</b> and changes of <strong><strong>nNOS</strong></strong> expressions in different brain regions in physically butorphanol dependent rats.
+NOS1	addiction	dependence	18512210	Therefore, 7 NI decreased in butorphanol induced physical <b>dependence</b> and <strong>nNOS</strong> expression.
+NOS1	addiction	dependence	18512210	Therefore, 7 NI decreased in butorphanol induced physical <b>dependence</b> and <strong><strong>nNOS</strong></strong> expression.
+NOS1	drug	opioid	18512210	Taken together, these findings suggest that the <strong>nNOS</strong> system is involved in the development of butorphanol induced physical dependence, and 7 NI has potential clinical application as a candidate for the treatment of <b>opioid</b> withdrawal syndrome.
+NOS1	addiction	dependence	18512210	Taken together, these findings suggest that the <strong>nNOS</strong> system is involved in the development of butorphanol induced physical <b>dependence</b>, and 7 NI has potential clinical application as a candidate for the treatment of opioid withdrawal syndrome.
+NOS1	addiction	withdrawal	18512210	Taken together, these findings suggest that the <strong>nNOS</strong> system is involved in the development of butorphanol induced physical dependence, and 7 NI has potential clinical application as a candidate for the treatment of opioid <b>withdrawal</b> syndrome.
+NOS1	drug	opioid	18512210	Taken together, these findings suggest that the <strong><strong>nNOS</strong></strong> system is involved in the development of butorphanol induced physical dependence, and 7 NI has potential clinical application as a candidate for the treatment of <b>opioid</b> withdrawal syndrome.
+NOS1	addiction	dependence	18512210	Taken together, these findings suggest that the <strong><strong>nNOS</strong></strong> system is involved in the development of butorphanol induced physical <b>dependence</b>, and 7 NI has potential clinical application as a candidate for the treatment of opioid withdrawal syndrome.
+NOS1	addiction	withdrawal	18512210	Taken together, these findings suggest that the <strong><strong>nNOS</strong></strong> system is involved in the development of butorphanol induced physical dependence, and 7 NI has potential clinical application as a candidate for the treatment of opioid <b>withdrawal</b> syndrome.
+NOS1	drug	opioid	17989510	These results suggest that <strong>nNOS</strong> and phospholipase A2, which might increase free radicals, play an important role in the expression of <b>morphine</b> induced withdrawal syndrome.
+NOS1	addiction	withdrawal	17989510	These results suggest that <strong>nNOS</strong> and phospholipase A2, which might increase free radicals, play an important role in the expression of morphine induced <b>withdrawal</b> syndrome.
+NOS1	drug	opioid	17989510	These results suggest that <strong><strong>nNOS</strong></strong> and phospholipase A2, which might increase free radicals, play an important role in the expression of <b>morphine</b> induced withdrawal syndrome.
+NOS1	addiction	withdrawal	17989510	These results suggest that <strong><strong>nNOS</strong></strong> and phospholipase A2, which might increase free radicals, play an important role in the expression of morphine induced <b>withdrawal</b> syndrome.
+NOS1	drug	cocaine	17853433	In the present study the role of NO in reconsolidation of LTM of <b>cocaine</b> associate context was investigated in wild type (WT) and neuronal nitric oxide synthase (<strong>nNOS</strong>) deficient mice (knockout; KO).
+NOS1	drug	cocaine	17853433	In the present study the role of NO in reconsolidation of LTM of <b>cocaine</b> associate context was investigated in wild type (WT) and neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) deficient mice (knockout; KO).
+NOS1	drug	cocaine	17853433	LTM of <b>cocaine</b> associated context was established in both WT and <strong>nNOS</strong> KO mice by conditioned place preference learning.
+NOS1	drug	cocaine	17853433	LTM of <b>cocaine</b> associated context was established in both WT and <strong><strong>nNOS</strong></strong> KO mice by conditioned place preference learning.
+NOS1	drug	cocaine	17853433	Results suggest that in the absence of <strong>nNOS</strong> activity, particularly during the reconsolidation phase, LTM of <b>cocaine</b> associated context is extinguished.
+NOS1	drug	cocaine	17853433	Results suggest that in the absence of <strong><strong>nNOS</strong></strong> activity, particularly during the reconsolidation phase, LTM of <b>cocaine</b> associated context is extinguished.
+NOS1	drug	opioid	21162268	[The effect of sinomenine on <strong>nNOS</strong> activity of brain tissues in <b>morphine</b> dependent and withdrawal mice].
+NOS1	addiction	withdrawal	21162268	[The effect of sinomenine on <strong>nNOS</strong> activity of brain tissues in morphine dependent and <b>withdrawal</b> mice].
+NOS1	drug	opioid	21162268	[The effect of sinomenine on <strong><strong>nNOS</strong></strong> activity of brain tissues in <b>morphine</b> dependent and withdrawal mice].
+NOS1	addiction	withdrawal	21162268	[The effect of sinomenine on <strong><strong>nNOS</strong></strong> activity of brain tissues in morphine dependent and <b>withdrawal</b> mice].
+NOS1	drug	opioid	21162265	To investigate the effect of CSF contacting neurons (CSF CNs) lesion in rat dorsal raphe nucleus (DRN) on the scores of <b>morphine</b> withdrawal symptoms precipitated by <b>naloxone</b> and the <strong>nNOS</strong> expression in dorsal horn of spinal cord, and study the relationship between the distal CSF CNs in rat brain parenchyma and the development of <b>morphine</b> dependence and withdrawal.
+NOS1	addiction	dependence	21162265	To investigate the effect of CSF contacting neurons (CSF CNs) lesion in rat dorsal raphe nucleus (DRN) on the scores of morphine withdrawal symptoms precipitated by naloxone and the <strong>nNOS</strong> expression in dorsal horn of spinal cord, and study the relationship between the distal CSF CNs in rat brain parenchyma and the development of morphine <b>dependence</b> and withdrawal.
+NOS1	addiction	withdrawal	21162265	To investigate the effect of CSF contacting neurons (CSF CNs) lesion in rat dorsal raphe nucleus (DRN) on the scores of morphine <b>withdrawal</b> symptoms precipitated by naloxone and the <strong>nNOS</strong> expression in dorsal horn of spinal cord, and study the relationship between the distal CSF CNs in rat brain parenchyma and the development of morphine dependence and <b>withdrawal</b>.
+NOS1	drug	opioid	21162265	To investigate the effect of CSF contacting neurons (CSF CNs) lesion in rat dorsal raphe nucleus (DRN) on the scores of <b>morphine</b> withdrawal symptoms precipitated by <b>naloxone</b> and the <strong><strong>nNOS</strong></strong> expression in dorsal horn of spinal cord, and study the relationship between the distal CSF CNs in rat brain parenchyma and the development of <b>morphine</b> dependence and withdrawal.
+NOS1	addiction	dependence	21162265	To investigate the effect of CSF contacting neurons (CSF CNs) lesion in rat dorsal raphe nucleus (DRN) on the scores of morphine withdrawal symptoms precipitated by naloxone and the <strong><strong>nNOS</strong></strong> expression in dorsal horn of spinal cord, and study the relationship between the distal CSF CNs in rat brain parenchyma and the development of morphine <b>dependence</b> and withdrawal.
+NOS1	addiction	withdrawal	21162265	To investigate the effect of CSF contacting neurons (CSF CNs) lesion in rat dorsal raphe nucleus (DRN) on the scores of morphine <b>withdrawal</b> symptoms precipitated by naloxone and the <strong><strong>nNOS</strong></strong> expression in dorsal horn of spinal cord, and study the relationship between the distal CSF CNs in rat brain parenchyma and the development of morphine dependence and <b>withdrawal</b>.
+NOS1	addiction	dependence	21162265	After the lesion, the <strong>nNOS</strong> expression and the quantity of the <strong>nNOS</strong> positive neurons in dorsal horn of spinal cord decreased significantly compared to that of withdrawal group without lesion (P < 0.05), but it also increased significantly compared to that of normal group and <b>dependence</b> group (P < 0.01).
+NOS1	addiction	withdrawal	21162265	After the lesion, the <strong>nNOS</strong> expression and the quantity of the <strong>nNOS</strong> positive neurons in dorsal horn of spinal cord decreased significantly compared to that of <b>withdrawal</b> group without lesion (P < 0.05), but it also increased significantly compared to that of normal group and dependence group (P < 0.01).
+NOS1	addiction	dependence	21162265	After the lesion, the <strong><strong>nNOS</strong></strong> expression and the quantity of the <strong><strong>nNOS</strong></strong> positive neurons in dorsal horn of spinal cord decreased significantly compared to that of withdrawal group without lesion (P < 0.05), but it also increased significantly compared to that of normal group and <b>dependence</b> group (P < 0.01).
+NOS1	addiction	withdrawal	21162265	After the lesion, the <strong><strong>nNOS</strong></strong> expression and the quantity of the <strong><strong>nNOS</strong></strong> positive neurons in dorsal horn of spinal cord decreased significantly compared to that of <b>withdrawal</b> group without lesion (P < 0.05), but it also increased significantly compared to that of normal group and dependence group (P < 0.01).
+NOS1	drug	opioid	21162265	The lesion of distal CSF contacting neurons attenuated the scores of <b>morphine</b> withdrawal symptoms precipitated by <b>naloxone</b> and the <strong>nNOS</strong> expression in dorsal horn of spinal cord.
+NOS1	addiction	withdrawal	21162265	The lesion of distal CSF contacting neurons attenuated the scores of morphine <b>withdrawal</b> symptoms precipitated by naloxone and the <strong>nNOS</strong> expression in dorsal horn of spinal cord.
+NOS1	drug	opioid	21162265	The lesion of distal CSF contacting neurons attenuated the scores of <b>morphine</b> withdrawal symptoms precipitated by <b>naloxone</b> and the <strong><strong>nNOS</strong></strong> expression in dorsal horn of spinal cord.
+NOS1	addiction	withdrawal	21162265	The lesion of distal CSF contacting neurons attenuated the scores of morphine <b>withdrawal</b> symptoms precipitated by naloxone and the <strong><strong>nNOS</strong></strong> expression in dorsal horn of spinal cord.
+NOS1	drug	opioid	17625935	Selective blockade of <strong>nNOS</strong> by 7 NI attenuated <b>morphine</b> withdrawal in opiate dependent rats, suggesting <strong>nNOS</strong> as a viable target for development of pharmacotherapies.
+NOS1	addiction	withdrawal	17625935	Selective blockade of <strong>nNOS</strong> by 7 NI attenuated morphine <b>withdrawal</b> in opiate dependent rats, suggesting <strong>nNOS</strong> as a viable target for development of pharmacotherapies.
+NOS1	drug	opioid	17625935	Selective blockade of <strong><strong>nNOS</strong></strong> by 7 NI attenuated <b>morphine</b> withdrawal in opiate dependent rats, suggesting <strong><strong>nNOS</strong></strong> as a viable target for development of pharmacotherapies.
+NOS1	addiction	withdrawal	17625935	Selective blockade of <strong><strong>nNOS</strong></strong> by 7 NI attenuated morphine <b>withdrawal</b> in opiate dependent rats, suggesting <strong><strong>nNOS</strong></strong> as a viable target for development of pharmacotherapies.
+NOS1	drug	opioid	17625935	We hypothesize that, by inhibiting <strong>nNOS</strong> and reducing NO levels, ADMA may decrease mu opiate receptor constitutive activity, resulting in alteration of the analgesic dose response curve of <b>morphine</b>.
+NOS1	drug	opioid	17625935	We hypothesize that, by inhibiting <strong><strong>nNOS</strong></strong> and reducing NO levels, ADMA may decrease mu opiate receptor constitutive activity, resulting in alteration of the analgesic dose response curve of <b>morphine</b>.
+NOS1	drug	opioid	17579782	[Effects of sinomenine on NO/<strong>nNOS</strong> system in cerebellum and spinal cord of <b>morphine</b> dependent and withdrawal mice].
+NOS1	addiction	withdrawal	17579782	[Effects of sinomenine on NO/<strong>nNOS</strong> system in cerebellum and spinal cord of morphine dependent and <b>withdrawal</b> mice].
+NOS1	drug	opioid	17579782	[Effects of sinomenine on NO/<strong><strong>nNOS</strong></strong> system in cerebellum and spinal cord of <b>morphine</b> dependent and withdrawal mice].
+NOS1	addiction	withdrawal	17579782	[Effects of sinomenine on NO/<strong><strong>nNOS</strong></strong> system in cerebellum and spinal cord of morphine dependent and <b>withdrawal</b> mice].
+NOS1	drug	opioid	17579782	To explore the effect of sinomenine on the nitric oxide (NO)/neural nitric oxide synthase (<strong>nNOS</strong>) system in the cerebellum and spinal cord of <b>morphine</b> dependent and <b>morphine</b> withdrawal Kunming mice, mice were subjected to injection of <b>morphine</b> with an increasing dose for 5 d, and then were treated with sinomenine (40 mg/kg, i.p.)
+NOS1	addiction	withdrawal	17579782	To explore the effect of sinomenine on the nitric oxide (NO)/neural nitric oxide synthase (<strong>nNOS</strong>) system in the cerebellum and spinal cord of morphine dependent and morphine <b>withdrawal</b> Kunming mice, mice were subjected to injection of morphine with an increasing dose for 5 d, and then were treated with sinomenine (40 mg/kg, i.p.)
+NOS1	drug	opioid	17579782	To explore the effect of sinomenine on the nitric oxide (NO)/neural nitric oxide synthase (<strong><strong>nNOS</strong></strong>) system in the cerebellum and spinal cord of <b>morphine</b> dependent and <b>morphine</b> withdrawal Kunming mice, mice were subjected to injection of <b>morphine</b> with an increasing dose for 5 d, and then were treated with sinomenine (40 mg/kg, i.p.)
+NOS1	addiction	withdrawal	17579782	To explore the effect of sinomenine on the nitric oxide (NO)/neural nitric oxide synthase (<strong><strong>nNOS</strong></strong>) system in the cerebellum and spinal cord of morphine dependent and morphine <b>withdrawal</b> Kunming mice, mice were subjected to injection of morphine with an increasing dose for 5 d, and then were treated with sinomenine (40 mg/kg, i.p.)
+NOS1	drug	opioid	17579782	(2) Sinomenine also reduced the increases in <strong>nNOS</strong> mRNA expression and <strong>nNOS</strong> activity resulting from <b>morphine</b> dependence, and simultaneously attenuated the high level of NO in both tissues following <b>morphine</b> withdrawal.
+NOS1	addiction	dependence	17579782	(2) Sinomenine also reduced the increases in <strong>nNOS</strong> mRNA expression and <strong>nNOS</strong> activity resulting from morphine <b>dependence</b>, and simultaneously attenuated the high level of NO in both tissues following morphine withdrawal.
+NOS1	addiction	withdrawal	17579782	(2) Sinomenine also reduced the increases in <strong>nNOS</strong> mRNA expression and <strong>nNOS</strong> activity resulting from morphine dependence, and simultaneously attenuated the high level of NO in both tissues following morphine <b>withdrawal</b>.
+NOS1	drug	opioid	17579782	(2) Sinomenine also reduced the increases in <strong><strong>nNOS</strong></strong> mRNA expression and <strong><strong>nNOS</strong></strong> activity resulting from <b>morphine</b> dependence, and simultaneously attenuated the high level of NO in both tissues following <b>morphine</b> withdrawal.
+NOS1	addiction	dependence	17579782	(2) Sinomenine also reduced the increases in <strong><strong>nNOS</strong></strong> mRNA expression and <strong><strong>nNOS</strong></strong> activity resulting from morphine <b>dependence</b>, and simultaneously attenuated the high level of NO in both tissues following morphine withdrawal.
+NOS1	addiction	withdrawal	17579782	(2) Sinomenine also reduced the increases in <strong><strong>nNOS</strong></strong> mRNA expression and <strong><strong>nNOS</strong></strong> activity resulting from morphine dependence, and simultaneously attenuated the high level of NO in both tissues following morphine <b>withdrawal</b>.
+NOS1	drug	opioid	17579782	The results obtained indicate that sinomenine may attenuate <b>morphine</b> addiction and significantly alleviate <b>morphine</b> withdrawal symptoms, and the mechanism may be associated with the effect of sinomenine on the NO/<strong>nNOS</strong> system in the cerebellum and spinal cord.
+NOS1	addiction	addiction	17579782	The results obtained indicate that sinomenine may attenuate morphine <b>addiction</b> and significantly alleviate morphine withdrawal symptoms, and the mechanism may be associated with the effect of sinomenine on the NO/<strong>nNOS</strong> system in the cerebellum and spinal cord.
+NOS1	addiction	withdrawal	17579782	The results obtained indicate that sinomenine may attenuate morphine addiction and significantly alleviate morphine <b>withdrawal</b> symptoms, and the mechanism may be associated with the effect of sinomenine on the NO/<strong>nNOS</strong> system in the cerebellum and spinal cord.
+NOS1	drug	opioid	17579782	The results obtained indicate that sinomenine may attenuate <b>morphine</b> addiction and significantly alleviate <b>morphine</b> withdrawal symptoms, and the mechanism may be associated with the effect of sinomenine on the NO/<strong><strong>nNOS</strong></strong> system in the cerebellum and spinal cord.
+NOS1	addiction	addiction	17579782	The results obtained indicate that sinomenine may attenuate morphine <b>addiction</b> and significantly alleviate morphine withdrawal symptoms, and the mechanism may be associated with the effect of sinomenine on the NO/<strong><strong>nNOS</strong></strong> system in the cerebellum and spinal cord.
+NOS1	addiction	withdrawal	17579782	The results obtained indicate that sinomenine may attenuate morphine addiction and significantly alleviate morphine <b>withdrawal</b> symptoms, and the mechanism may be associated with the effect of sinomenine on the NO/<strong><strong>nNOS</strong></strong> system in the cerebellum and spinal cord.
+NOS1	drug	psychedelics	17521446	Intrathecal administration of CPP and <b>ketamine</b> reduced <strong>nNOS</strong> expression in monoarthritic rats but increased the expression of iNOS and eNOS.
+NOS1	addiction	reward	17521446	Intrathecal administration of <b>CPP</b> and ketamine reduced <strong>nNOS</strong> expression in monoarthritic rats but increased the expression of iNOS and eNOS.
+NOS1	drug	psychedelics	17521446	Intrathecal administration of CPP and <b>ketamine</b> reduced <strong><strong>nNOS</strong></strong> expression in monoarthritic rats but increased the expression of iNOS and eNOS.
+NOS1	addiction	reward	17521446	Intrathecal administration of <b>CPP</b> and ketamine reduced <strong><strong>nNOS</strong></strong> expression in monoarthritic rats but increased the expression of iNOS and eNOS.
+NOS1	drug	opioid	16712881	pretreatment with either the non selective nitric oxide synthase (NOS) inhibitor N(G) nitro L arginine methyl ester (L NAME), neuronal NOS (<strong>nNOS</strong>) inhibitor 7 nitro indazole (7 NI), or the inducible NOS (iNOS) inhibitor aminoguanidine (AG), could reduce <b>morphine</b> withdrawal induced increase of phospho ERK1/2 (pERK1/2) expression in the rat spinal cord.
+NOS1	addiction	withdrawal	16712881	pretreatment with either the non selective nitric oxide synthase (NOS) inhibitor N(G) nitro L arginine methyl ester (L NAME), neuronal NOS (<strong>nNOS</strong>) inhibitor 7 nitro indazole (7 NI), or the inducible NOS (iNOS) inhibitor aminoguanidine (AG), could reduce morphine <b>withdrawal</b> induced increase of phospho ERK1/2 (pERK1/2) expression in the rat spinal cord.
+NOS1	drug	opioid	16712881	pretreatment with either the non selective nitric oxide synthase (NOS) inhibitor N(G) nitro L arginine methyl ester (L NAME), neuronal NOS (<strong><strong>nNOS</strong></strong>) inhibitor 7 nitro indazole (7 NI), or the inducible NOS (iNOS) inhibitor aminoguanidine (AG), could reduce <b>morphine</b> withdrawal induced increase of phospho ERK1/2 (pERK1/2) expression in the rat spinal cord.
+NOS1	addiction	withdrawal	16712881	pretreatment with either the non selective nitric oxide synthase (NOS) inhibitor N(G) nitro L arginine methyl ester (L NAME), neuronal NOS (<strong><strong>nNOS</strong></strong>) inhibitor 7 nitro indazole (7 NI), or the inducible NOS (iNOS) inhibitor aminoguanidine (AG), could reduce morphine <b>withdrawal</b> induced increase of phospho ERK1/2 (pERK1/2) expression in the rat spinal cord.
+NOS1	drug	opioid	16712881	On the other hand, attenuation of the spinal ERK phosphorylation by the MAPK kinase (MEK) inhibitor U0126 also could inhibit the increase of <strong>nNOS</strong> and iNOS expression in the spinal cord of <b>morphine</b> withdrawal rats.
+NOS1	addiction	withdrawal	16712881	On the other hand, attenuation of the spinal ERK phosphorylation by the MAPK kinase (MEK) inhibitor U0126 also could inhibit the increase of <strong>nNOS</strong> and iNOS expression in the spinal cord of morphine <b>withdrawal</b> rats.
+NOS1	drug	opioid	16712881	On the other hand, attenuation of the spinal ERK phosphorylation by the MAPK kinase (MEK) inhibitor U0126 also could inhibit the increase of <strong><strong>nNOS</strong></strong> and iNOS expression in the spinal cord of <b>morphine</b> withdrawal rats.
+NOS1	addiction	withdrawal	16712881	On the other hand, attenuation of the spinal ERK phosphorylation by the MAPK kinase (MEK) inhibitor U0126 also could inhibit the increase of <strong><strong>nNOS</strong></strong> and iNOS expression in the spinal cord of morphine <b>withdrawal</b> rats.
+NOS1	drug	cocaine	16698049	Adolescent and adult responsiveness to the incentive value of <b>cocaine</b> reward in mice: role of neuronal nitric oxide synthase (<strong>nNOS</strong>) gene.
+NOS1	addiction	reward	16698049	Adolescent and adult responsiveness to the <b>incentive</b> value of cocaine <b>reward</b> in mice: role of neuronal nitric oxide synthase (<strong>nNOS</strong>) gene.
+NOS1	drug	cocaine	16698049	Adolescent and adult responsiveness to the incentive value of <b>cocaine</b> reward in mice: role of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene.
+NOS1	addiction	reward	16698049	Adolescent and adult responsiveness to the <b>incentive</b> value of cocaine <b>reward</b> in mice: role of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene.
+NOS1	drug	cocaine	16698049	The aims of the present study were to investigate: a) the acquisition, expression, maintenance and reinstatement of <b>cocaine</b> CPP from periadolescence (PD24 45) through adulthood (PD70); b) potential sexual dimorphism in adolescence and adulthood in response to <b>cocaine</b> induced CPP; and c) the role of the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene in long term neural plasticity underlying responsiveness to <b>cocaine</b> and <b>cocaine</b> associated cues.
+NOS1	addiction	relapse	16698049	The aims of the present study were to investigate: a) the acquisition, expression, maintenance and <b>reinstatement</b> of cocaine CPP from periadolescence (PD24 45) through adulthood (PD70); b) potential sexual dimorphism in adolescence and adulthood in response to cocaine induced CPP; and c) the role of the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene in long term neural plasticity underlying responsiveness to cocaine and cocaine associated cues.
+NOS1	addiction	reward	16698049	The aims of the present study were to investigate: a) the acquisition, expression, maintenance and reinstatement of cocaine <b>CPP</b> from periadolescence (PD24 45) through adulthood (PD70); b) potential sexual dimorphism in adolescence and adulthood in response to cocaine induced <b>CPP</b>; and c) the role of the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene in long term neural plasticity underlying responsiveness to cocaine and cocaine associated cues.
+NOS1	drug	cocaine	16698049	The aims of the present study were to investigate: a) the acquisition, expression, maintenance and reinstatement of <b>cocaine</b> CPP from periadolescence (PD24 45) through adulthood (PD70); b) potential sexual dimorphism in adolescence and adulthood in response to <b>cocaine</b> induced CPP; and c) the role of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene in long term neural plasticity underlying responsiveness to <b>cocaine</b> and <b>cocaine</b> associated cues.
+NOS1	addiction	relapse	16698049	The aims of the present study were to investigate: a) the acquisition, expression, maintenance and <b>reinstatement</b> of cocaine CPP from periadolescence (PD24 45) through adulthood (PD70); b) potential sexual dimorphism in adolescence and adulthood in response to cocaine induced CPP; and c) the role of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene in long term neural plasticity underlying responsiveness to cocaine and cocaine associated cues.
+NOS1	addiction	reward	16698049	The aims of the present study were to investigate: a) the acquisition, expression, maintenance and reinstatement of cocaine <b>CPP</b> from periadolescence (PD24 45) through adulthood (PD70); b) potential sexual dimorphism in adolescence and adulthood in response to cocaine induced <b>CPP</b>; and c) the role of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene in long term neural plasticity underlying responsiveness to cocaine and cocaine associated cues.
+NOS1	drug	cocaine	16698049	In contrast, <b>cocaine</b> CPP acquired between PD26 and PD31 in adolescent <strong>nNOS</strong> knockout (KO) mice, was neither maintained nor reinstated by <b>cocaine</b>.
+NOS1	addiction	reward	16698049	In contrast, cocaine <b>CPP</b> acquired between PD26 and PD31 in adolescent <strong>nNOS</strong> knockout (KO) mice, was neither maintained nor reinstated by cocaine.
+NOS1	drug	cocaine	16698049	In contrast, <b>cocaine</b> CPP acquired between PD26 and PD31 in adolescent <strong><strong>nNOS</strong></strong> knockout (KO) mice, was neither maintained nor reinstated by <b>cocaine</b>.
+NOS1	addiction	reward	16698049	In contrast, cocaine <b>CPP</b> acquired between PD26 and PD31 in adolescent <strong><strong>nNOS</strong></strong> knockout (KO) mice, was neither maintained nor reinstated by cocaine.
+NOS1	drug	cocaine	16698049	Results suggest that the <strong>nNOS</strong> gene is essential during adolescence of both sexes for the development of long term neural plasticity underlying responsiveness to the incentive value of <b>cocaine</b> reward.
+NOS1	addiction	reward	16698049	Results suggest that the <strong>nNOS</strong> gene is essential during adolescence of both sexes for the development of long term neural plasticity underlying responsiveness to the <b>incentive</b> value of cocaine <b>reward</b>.
+NOS1	drug	cocaine	16698049	Results suggest that the <strong><strong>nNOS</strong></strong> gene is essential during adolescence of both sexes for the development of long term neural plasticity underlying responsiveness to the incentive value of <b>cocaine</b> reward.
+NOS1	addiction	reward	16698049	Results suggest that the <strong><strong>nNOS</strong></strong> gene is essential during adolescence of both sexes for the development of long term neural plasticity underlying responsiveness to the <b>incentive</b> value of cocaine <b>reward</b>.
+NOS1	drug	cocaine	16698049	Sexual dimorphism in response to <b>cocaine</b> CPP emerges in adulthood; <strong>nNOS</strong> contribution to long term plasticity is therefore sexually dimorphic and age dependent in female but not in male subjects.
+NOS1	addiction	reward	16698049	Sexual dimorphism in response to cocaine <b>CPP</b> emerges in adulthood; <strong>nNOS</strong> contribution to long term plasticity is therefore sexually dimorphic and age dependent in female but not in male subjects.
+NOS1	drug	cocaine	16698049	Sexual dimorphism in response to <b>cocaine</b> CPP emerges in adulthood; <strong><strong>nNOS</strong></strong> contribution to long term plasticity is therefore sexually dimorphic and age dependent in female but not in male subjects.
+NOS1	addiction	reward	16698049	Sexual dimorphism in response to cocaine <b>CPP</b> emerges in adulthood; <strong><strong>nNOS</strong></strong> contribution to long term plasticity is therefore sexually dimorphic and age dependent in female but not in male subjects.
+NOS1	drug	opioid	16598705	Here we studied the effects of prenatal <b>morphine</b> exposure on postsynaptic density protein 95 (PSD 95), an important cytoskeletal specialization involved in the anchoring of the NMDAR and neuronal nitric oxide synthase (<strong>nNOS</strong>), of the hippocampal CA1 subregion from young offspring at postnatal day 14 (P14).
+NOS1	drug	opioid	16598705	Here we studied the effects of prenatal <b>morphine</b> exposure on postsynaptic density protein 95 (PSD 95), an important cytoskeletal specialization involved in the anchoring of the NMDAR and neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>), of the hippocampal CA1 subregion from young offspring at postnatal day 14 (P14).
+NOS1	drug	opioid	16598705	In addition, prenatal <b>morphine</b> exposure reduced not only the expression of <strong>nNOS</strong> and the phosphorylation of cAMP responsive element binding protein at serine 133 (CREB(Serine 133)), but also the magnitude of long term depression (LTD) at P14.
+NOS1	drug	opioid	16598705	In addition, prenatal <b>morphine</b> exposure reduced not only the expression of <strong><strong>nNOS</strong></strong> and the phosphorylation of cAMP responsive element binding protein at serine 133 (CREB(Serine 133)), but also the magnitude of long term depression (LTD) at P14.
+NOS1	drug	opioid	16598705	Collectively, the study demonstrates that maternal exposure to <b>morphine</b> decreases the magnitude of PSD 95, <strong>nNOS</strong>, the phosphorylation of CREB(Serine 133), and LTD expression in hippocampal CA1 subregion of young offspring (e.g., P14).
+NOS1	drug	opioid	16598705	Collectively, the study demonstrates that maternal exposure to <b>morphine</b> decreases the magnitude of PSD 95, <strong><strong>nNOS</strong></strong>, the phosphorylation of CREB(Serine 133), and LTD expression in hippocampal CA1 subregion of young offspring (e.g., P14).
+NOS1	drug	cocaine	16300892	Differential effects of morphine  and <b>cocaine</b> induced <strong>nNOS</strong> immunoreactivity in the dentate gyrus of hippocampus of mice lacking mu opioid receptors.
+NOS1	drug	opioid	16300892	Differential effects of <b>morphine</b>  and cocaine induced <strong>nNOS</strong> immunoreactivity in the dentate gyrus of hippocampus of mice lacking mu <b>opioid</b> receptors.
+NOS1	drug	cocaine	16300892	Differential effects of morphine  and <b>cocaine</b> induced <strong><strong>nNOS</strong></strong> immunoreactivity in the dentate gyrus of hippocampus of mice lacking mu opioid receptors.
+NOS1	drug	opioid	16300892	Differential effects of <b>morphine</b>  and cocaine induced <strong><strong>nNOS</strong></strong> immunoreactivity in the dentate gyrus of hippocampus of mice lacking mu <b>opioid</b> receptors.
+NOS1	drug	cocaine	16300892	This study investigated the expression of <strong>nNOS</strong> after repeated morphine or <b>cocaine</b> administration in order to determine if <strong>nNOS</strong> (neuronal nitric oxide synthase) is involved in the morphine  or <b>cocaine</b> induced behavioral sensitization in mu opioid receptor knockout (MOR( / )) mice.
+NOS1	drug	opioid	16300892	This study investigated the expression of <strong>nNOS</strong> after repeated <b>morphine</b> or cocaine administration in order to determine if <strong>nNOS</strong> (neuronal nitric oxide synthase) is involved in the <b>morphine</b>  or cocaine induced behavioral sensitization in mu <b>opioid</b> receptor knockout (MOR( / )) mice.
+NOS1	addiction	sensitization	16300892	This study investigated the expression of <strong>nNOS</strong> after repeated morphine or cocaine administration in order to determine if <strong>nNOS</strong> (neuronal nitric oxide synthase) is involved in the morphine  or cocaine induced behavioral <b>sensitization</b> in mu opioid receptor knockout (MOR( / )) mice.
+NOS1	drug	cocaine	16300892	This study investigated the expression of <strong><strong>nNOS</strong></strong> after repeated morphine or <b>cocaine</b> administration in order to determine if <strong><strong>nNOS</strong></strong> (neuronal nitric oxide synthase) is involved in the morphine  or <b>cocaine</b> induced behavioral sensitization in mu opioid receptor knockout (MOR( / )) mice.
+NOS1	drug	opioid	16300892	This study investigated the expression of <strong><strong>nNOS</strong></strong> after repeated <b>morphine</b> or cocaine administration in order to determine if <strong><strong>nNOS</strong></strong> (neuronal nitric oxide synthase) is involved in the <b>morphine</b>  or cocaine induced behavioral sensitization in mu <b>opioid</b> receptor knockout (MOR( / )) mice.
+NOS1	addiction	sensitization	16300892	This study investigated the expression of <strong><strong>nNOS</strong></strong> after repeated morphine or cocaine administration in order to determine if <strong><strong>nNOS</strong></strong> (neuronal nitric oxide synthase) is involved in the morphine  or cocaine induced behavioral <b>sensitization</b> in mu opioid receptor knockout (MOR( / )) mice.
+NOS1	drug	cocaine	16300892	Higher numbers of <strong>nNOS</strong> positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild type (MOR(+/+)) mice repeatedly treated with either morphine or <b>cocaine</b> than in the saline treated MOR(+/+) mice (morphine, +122%; <b>cocaine</b>, +82%).
+NOS1	drug	opioid	16300892	Higher numbers of <strong>nNOS</strong> positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild type (MOR(+/+)) mice repeatedly treated with either <b>morphine</b> or cocaine than in the saline treated MOR(+/+) mice (<b>morphine</b>, +122%; cocaine, +82%).
+NOS1	drug	cocaine	16300892	Higher numbers of <strong><strong>nNOS</strong></strong> positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild type (MOR(+/+)) mice repeatedly treated with either morphine or <b>cocaine</b> than in the saline treated MOR(+/+) mice (morphine, +122%; <b>cocaine</b>, +82%).
+NOS1	drug	opioid	16300892	Higher numbers of <strong><strong>nNOS</strong></strong> positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild type (MOR(+/+)) mice repeatedly treated with either <b>morphine</b> or cocaine than in the saline treated MOR(+/+) mice (<b>morphine</b>, +122%; cocaine, +82%).
+NOS1	drug	cocaine	16300892	Moreover, the MOR( / ) mice also showed significantly higher morphine  or <b>cocaine</b> induced <strong>nNOS</strong> expression levels in the DG than in the saline treated MOR(+/+) mice (morphine, +234%; <b>cocaine</b>, +54%).
+NOS1	drug	opioid	16300892	Moreover, the MOR( / ) mice also showed significantly higher <b>morphine</b>  or cocaine induced <strong>nNOS</strong> expression levels in the DG than in the saline treated MOR(+/+) mice (<b>morphine</b>, +234%; cocaine, +54%).
+NOS1	drug	cocaine	16300892	Moreover, the MOR( / ) mice also showed significantly higher morphine  or <b>cocaine</b> induced <strong><strong>nNOS</strong></strong> expression levels in the DG than in the saline treated MOR(+/+) mice (morphine, +234%; <b>cocaine</b>, +54%).
+NOS1	drug	opioid	16300892	Moreover, the MOR( / ) mice also showed significantly higher <b>morphine</b>  or cocaine induced <strong><strong>nNOS</strong></strong> expression levels in the DG than in the saline treated MOR(+/+) mice (<b>morphine</b>, +234%; cocaine, +54%).
+NOS1	drug	cocaine	16300892	The MOR( / ) mice showed a significantly higher morphine induced <strong>nNOS</strong> expression level (+103%) or a lower <b>cocaine</b> induced <strong>nNOS</strong> expression level (+38%) in the DG than in the morphine  or <b>cocaine</b> treated MOR(+/+) mice.
+NOS1	drug	opioid	16300892	The MOR( / ) mice showed a significantly higher <b>morphine</b> induced <strong>nNOS</strong> expression level (+103%) or a lower cocaine induced <strong>nNOS</strong> expression level (+38%) in the DG than in the <b>morphine</b>  or cocaine treated MOR(+/+) mice.
+NOS1	drug	cocaine	16300892	The MOR( / ) mice showed a significantly higher morphine induced <strong><strong>nNOS</strong></strong> expression level (+103%) or a lower <b>cocaine</b> induced <strong><strong>nNOS</strong></strong> expression level (+38%) in the DG than in the morphine  or <b>cocaine</b> treated MOR(+/+) mice.
+NOS1	drug	opioid	16300892	The MOR( / ) mice showed a significantly higher <b>morphine</b> induced <strong><strong>nNOS</strong></strong> expression level (+103%) or a lower cocaine induced <strong><strong>nNOS</strong></strong> expression level (+38%) in the DG than in the <b>morphine</b>  or cocaine treated MOR(+/+) mice.
+NOS1	drug	cocaine	16300892	These results suggest that morphine and <b>cocaine</b> sensitization is differentially regulated by the mu opioid receptors in MOR( / ) mice via the <strong>nNOS</strong> systems in the DG.
+NOS1	drug	opioid	16300892	These results suggest that <b>morphine</b> and cocaine sensitization is differentially regulated by the mu <b>opioid</b> receptors in MOR( / ) mice via the <strong>nNOS</strong> systems in the DG.
+NOS1	addiction	sensitization	16300892	These results suggest that morphine and cocaine <b>sensitization</b> is differentially regulated by the mu opioid receptors in MOR( / ) mice via the <strong>nNOS</strong> systems in the DG.
+NOS1	drug	cocaine	16300892	These results suggest that morphine and <b>cocaine</b> sensitization is differentially regulated by the mu opioid receptors in MOR( / ) mice via the <strong><strong>nNOS</strong></strong> systems in the DG.
+NOS1	drug	opioid	16300892	These results suggest that <b>morphine</b> and cocaine sensitization is differentially regulated by the mu <b>opioid</b> receptors in MOR( / ) mice via the <strong><strong>nNOS</strong></strong> systems in the DG.
+NOS1	addiction	sensitization	16300892	These results suggest that morphine and cocaine <b>sensitization</b> is differentially regulated by the mu opioid receptors in MOR( / ) mice via the <strong><strong>nNOS</strong></strong> systems in the DG.
+NOS1	addiction	reward	16154200	Results from our laboratory indicate that dopamine dependent psychomotor, <b>reinforcing</b>, and neurotoxic effects of amphetamines are diminished by pharmacological blockade of <strong>nNOS</strong> or deletion of the <strong>nNOS</strong> gene.
+NOS1	addiction	reward	16154200	Results from our laboratory indicate that dopamine dependent psychomotor, <b>reinforcing</b>, and neurotoxic effects of amphetamines are diminished by pharmacological blockade of <strong><strong>nNOS</strong></strong> or deletion of the <strong><strong>nNOS</strong></strong> gene.
+NOS1	drug	opioid	15950775	Evidence of involvement of the <strong>nNOS</strong> and the kappa <b>opioid</b> receptor in the same intracellular network of the rat periaqueductal gray that controls <b>morphine</b> tolerance and dependence.
+NOS1	addiction	dependence	15950775	Evidence of involvement of the <strong>nNOS</strong> and the kappa opioid receptor in the same intracellular network of the rat periaqueductal gray that controls morphine tolerance and <b>dependence</b>.
+NOS1	drug	opioid	15950775	Evidence of involvement of the <strong><strong>nNOS</strong></strong> and the kappa <b>opioid</b> receptor in the same intracellular network of the rat periaqueductal gray that controls <b>morphine</b> tolerance and dependence.
+NOS1	addiction	dependence	15950775	Evidence of involvement of the <strong><strong>nNOS</strong></strong> and the kappa opioid receptor in the same intracellular network of the rat periaqueductal gray that controls morphine tolerance and <b>dependence</b>.
+NOS1	drug	opioid	15950775	Our results point to an involvement of KOR and <strong>nNOS</strong> in the same intracellular network that controls the development of <b>morphine</b> tolerance and dependence.
+NOS1	addiction	dependence	15950775	Our results point to an involvement of KOR and <strong>nNOS</strong> in the same intracellular network that controls the development of morphine tolerance and <b>dependence</b>.
+NOS1	drug	opioid	15950775	Our results point to an involvement of KOR and <strong><strong>nNOS</strong></strong> in the same intracellular network that controls the development of <b>morphine</b> tolerance and dependence.
+NOS1	addiction	dependence	15950775	Our results point to an involvement of KOR and <strong><strong>nNOS</strong></strong> in the same intracellular network that controls the development of morphine tolerance and <b>dependence</b>.
+NOS1	drug	nicotine	15854753	Reduced <strong>nNOS</strong> expression induced by repeated <b>nicotine</b> treatment in mu opioid receptor knockout mice.
+NOS1	drug	opioid	15854753	Reduced <strong>nNOS</strong> expression induced by repeated nicotine treatment in mu <b>opioid</b> receptor knockout mice.
+NOS1	drug	nicotine	15854753	Reduced <strong><strong>nNOS</strong></strong> expression induced by repeated <b>nicotine</b> treatment in mu opioid receptor knockout mice.
+NOS1	drug	opioid	15854753	Reduced <strong><strong>nNOS</strong></strong> expression induced by repeated nicotine treatment in mu <b>opioid</b> receptor knockout mice.
+NOS1	drug	nicotine	15854753	To determine whether neuronal nitric oxide synthase (<strong>nNOS</strong>) is involved in <b>nicotine</b> induced behavioral sensitization in mu opioid receptor knockout mice we adopted an immunohistochemical approach.
+NOS1	drug	opioid	15854753	To determine whether neuronal nitric oxide synthase (<strong>nNOS</strong>) is involved in nicotine induced behavioral sensitization in mu <b>opioid</b> receptor knockout mice we adopted an immunohistochemical approach.
+NOS1	addiction	sensitization	15854753	To determine whether neuronal nitric oxide synthase (<strong>nNOS</strong>) is involved in nicotine induced behavioral <b>sensitization</b> in mu opioid receptor knockout mice we adopted an immunohistochemical approach.
+NOS1	drug	nicotine	15854753	To determine whether neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) is involved in <b>nicotine</b> induced behavioral sensitization in mu opioid receptor knockout mice we adopted an immunohistochemical approach.
+NOS1	drug	opioid	15854753	To determine whether neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) is involved in nicotine induced behavioral sensitization in mu <b>opioid</b> receptor knockout mice we adopted an immunohistochemical approach.
+NOS1	addiction	sensitization	15854753	To determine whether neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) is involved in nicotine induced behavioral <b>sensitization</b> in mu opioid receptor knockout mice we adopted an immunohistochemical approach.
+NOS1	drug	nicotine	15854753	Higher numbers of <strong>nNOS</strong> positive cells were observed in the striatum of wild type mice repeatedly treated with <b>nicotine</b> than in saline treated wild type mice.
+NOS1	drug	nicotine	15854753	Higher numbers of <strong><strong>nNOS</strong></strong> positive cells were observed in the striatum of wild type mice repeatedly treated with <b>nicotine</b> than in saline treated wild type mice.
+NOS1	drug	nicotine	15854753	However, mu opioid receptor knockout mice showed significantly lower <b>nicotine</b> induced <strong>nNOS</strong> expression in the striatum versus wild type mice.
+NOS1	drug	opioid	15854753	However, mu <b>opioid</b> receptor knockout mice showed significantly lower nicotine induced <strong>nNOS</strong> expression in the striatum versus wild type mice.
+NOS1	drug	nicotine	15854753	However, mu opioid receptor knockout mice showed significantly lower <b>nicotine</b> induced <strong><strong>nNOS</strong></strong> expression in the striatum versus wild type mice.
+NOS1	drug	opioid	15854753	However, mu <b>opioid</b> receptor knockout mice showed significantly lower nicotine induced <strong><strong>nNOS</strong></strong> expression in the striatum versus wild type mice.
+NOS1	drug	nicotine	15854753	These findings demonstrate that the absence of mu opioid receptors can cause a significant reduction in the expression of <strong>nNOS</strong> in the striatum, as induced by repeated <b>nicotine</b> treatment.
+NOS1	drug	opioid	15854753	These findings demonstrate that the absence of mu <b>opioid</b> receptors can cause a significant reduction in the expression of <strong>nNOS</strong> in the striatum, as induced by repeated nicotine treatment.
+NOS1	drug	nicotine	15854753	These findings demonstrate that the absence of mu opioid receptors can cause a significant reduction in the expression of <strong><strong>nNOS</strong></strong> in the striatum, as induced by repeated <b>nicotine</b> treatment.
+NOS1	drug	opioid	15854753	These findings demonstrate that the absence of mu <b>opioid</b> receptors can cause a significant reduction in the expression of <strong><strong>nNOS</strong></strong> in the striatum, as induced by repeated nicotine treatment.
+NOS1	drug	benzodiazepine	15740792	Both inducible NOS (iNOS) and neuronal NOS (<strong>nNOS</strong>) protein levels in the spinal cord were significantly increased after injection of formalin, which could be inhibited by pretreatment with <b>midazolam</b>.
+NOS1	drug	benzodiazepine	15740792	Both inducible NOS (iNOS) and neuronal NOS (<strong><strong>nNOS</strong></strong>) protein levels in the spinal cord were significantly increased after injection of formalin, which could be inhibited by pretreatment with <b>midazolam</b>.
+NOS1	drug	opioid	15605124	Nifedipine treatment decreased the brain <strong>nNOS</strong> activity, induced by multiple administration of <b>morphine</b>.
+NOS1	drug	opioid	15605124	Nifedipine treatment decreased the brain <strong><strong>nNOS</strong></strong> activity, induced by multiple administration of <b>morphine</b>.
+NOS1	drug	amphetamine	15542708	Differential response of <strong>nNOS</strong> knockout mice to MDMA ("ecstasy")  and <b>methamphetamine</b> induced psychomotor sensitization and neurotoxicity.
+NOS1	drug	psychedelics	15542708	Differential response of <strong>nNOS</strong> knockout mice to <b>MDMA</b> ("<b>ecstasy</b>")  and methamphetamine induced psychomotor sensitization and neurotoxicity.
+NOS1	addiction	sensitization	15542708	Differential response of <strong>nNOS</strong> knockout mice to MDMA ("ecstasy")  and methamphetamine induced psychomotor <b>sensitization</b> and neurotoxicity.
+NOS1	drug	amphetamine	15542708	Differential response of <strong><strong>nNOS</strong></strong> knockout mice to MDMA ("ecstasy")  and <b>methamphetamine</b> induced psychomotor sensitization and neurotoxicity.
+NOS1	drug	psychedelics	15542708	Differential response of <strong><strong>nNOS</strong></strong> knockout mice to <b>MDMA</b> ("<b>ecstasy</b>")  and methamphetamine induced psychomotor sensitization and neurotoxicity.
+NOS1	addiction	sensitization	15542708	Differential response of <strong><strong>nNOS</strong></strong> knockout mice to MDMA ("ecstasy")  and methamphetamine induced psychomotor <b>sensitization</b> and neurotoxicity.
+NOS1	drug	amphetamine	15542708	It has been shown that mice deficient in neuronal nitric oxide synthase (<strong>nNOS</strong>) gene are resistant to cocaine induced psychomotor sensitization and <b>methamphetamine</b> (<b>METH</b>) induced dopaminergic neurotoxicity.
+NOS1	drug	cocaine	15542708	It has been shown that mice deficient in neuronal nitric oxide synthase (<strong>nNOS</strong>) gene are resistant to <b>cocaine</b> induced psychomotor sensitization and methamphetamine (METH) induced dopaminergic neurotoxicity.
+NOS1	addiction	sensitization	15542708	It has been shown that mice deficient in neuronal nitric oxide synthase (<strong>nNOS</strong>) gene are resistant to cocaine induced psychomotor <b>sensitization</b> and methamphetamine (METH) induced dopaminergic neurotoxicity.
+NOS1	drug	amphetamine	15542708	It has been shown that mice deficient in neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene are resistant to cocaine induced psychomotor sensitization and <b>methamphetamine</b> (<b>METH</b>) induced dopaminergic neurotoxicity.
+NOS1	drug	cocaine	15542708	It has been shown that mice deficient in neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene are resistant to <b>cocaine</b> induced psychomotor sensitization and methamphetamine (METH) induced dopaminergic neurotoxicity.
+NOS1	addiction	sensitization	15542708	It has been shown that mice deficient in neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene are resistant to cocaine induced psychomotor <b>sensitization</b> and methamphetamine (METH) induced dopaminergic neurotoxicity.
+NOS1	drug	amphetamine	15542708	The response of <strong>nNOS</strong> knockout (KO) and wild type (WT) mice to the psychomotor stimulating and neurotoxic effects of 3,4 methylenedioxymethamphetamine (MDMA; "Ecstasy") and <b>METH</b> were investigated.
+NOS1	drug	psychedelics	15542708	The response of <strong>nNOS</strong> knockout (KO) and wild type (WT) mice to the psychomotor stimulating and neurotoxic effects of 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>; "<b>Ecstasy</b>") and METH were investigated.
+NOS1	drug	amphetamine	15542708	The response of <strong><strong>nNOS</strong></strong> knockout (KO) and wild type (WT) mice to the psychomotor stimulating and neurotoxic effects of 3,4 methylenedioxymethamphetamine (MDMA; "Ecstasy") and <b>METH</b> were investigated.
+NOS1	drug	psychedelics	15542708	The response of <strong><strong>nNOS</strong></strong> knockout (KO) and wild type (WT) mice to the psychomotor stimulating and neurotoxic effects of 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>; "<b>Ecstasy</b>") and METH were investigated.
+NOS1	drug	amphetamine	15542708	Repeated administration of MDMA for 5 days resulted in psychomotor sensitization in both WT and <strong>nNOS</strong> KO mice, while repeated administration of <b>METH</b> caused psychomotor sensitization in WT but not in KO mice.
+NOS1	drug	psychedelics	15542708	Repeated administration of <b>MDMA</b> for 5 days resulted in psychomotor sensitization in both WT and <strong>nNOS</strong> KO mice, while repeated administration of METH caused psychomotor sensitization in WT but not in KO mice.
+NOS1	addiction	sensitization	15542708	Repeated administration of MDMA for 5 days resulted in psychomotor <b>sensitization</b> in both WT and <strong>nNOS</strong> KO mice, while repeated administration of METH caused psychomotor <b>sensitization</b> in WT but not in KO mice.
+NOS1	drug	amphetamine	15542708	Repeated administration of MDMA for 5 days resulted in psychomotor sensitization in both WT and <strong><strong>nNOS</strong></strong> KO mice, while repeated administration of <b>METH</b> caused psychomotor sensitization in WT but not in KO mice.
+NOS1	drug	psychedelics	15542708	Repeated administration of <b>MDMA</b> for 5 days resulted in psychomotor sensitization in both WT and <strong><strong>nNOS</strong></strong> KO mice, while repeated administration of METH caused psychomotor sensitization in WT but not in KO mice.
+NOS1	addiction	sensitization	15542708	Repeated administration of MDMA for 5 days resulted in psychomotor <b>sensitization</b> in both WT and <strong><strong>nNOS</strong></strong> KO mice, while repeated administration of METH caused psychomotor <b>sensitization</b> in WT but not in KO mice.
+NOS1	drug	amphetamine	15542708	Sensitization to both MDMA and <b>METH</b> was persistent for 40 days in WT mice, but not in <strong>nNOS</strong> KO mice.
+NOS1	drug	psychedelics	15542708	Sensitization to both <b>MDMA</b> and METH was persistent for 40 days in WT mice, but not in <strong>nNOS</strong> KO mice.
+NOS1	addiction	sensitization	15542708	<b>Sensitization</b> to both MDMA and METH was persistent for 40 days in WT mice, but not in <strong>nNOS</strong> KO mice.
+NOS1	drug	amphetamine	15542708	Sensitization to both MDMA and <b>METH</b> was persistent for 40 days in WT mice, but not in <strong><strong>nNOS</strong></strong> KO mice.
+NOS1	drug	psychedelics	15542708	Sensitization to both <b>MDMA</b> and METH was persistent for 40 days in WT mice, but not in <strong><strong>nNOS</strong></strong> KO mice.
+NOS1	addiction	sensitization	15542708	<b>Sensitization</b> to both MDMA and METH was persistent for 40 days in WT mice, but not in <strong><strong>nNOS</strong></strong> KO mice.
+NOS1	drug	psychedelics	15542708	For the neurochemical studies, a high dose of <b>MDMA</b> caused marked depletion of 5 HT in several brain regions of both WT and KO mice, suggesting that the absence of the <strong>nNOS</strong> gene did not afford protection against <b>MDMA</b> induced depletion of 5 HT.
+NOS1	drug	psychedelics	15542708	For the neurochemical studies, a high dose of <b>MDMA</b> caused marked depletion of 5 HT in several brain regions of both WT and KO mice, suggesting that the absence of the <strong><strong>nNOS</strong></strong> gene did not afford protection against <b>MDMA</b> induced depletion of 5 HT.
+NOS1	drug	amphetamine	15542708	The differential response of <strong>nNOS</strong> KO mice to the behavioral and neurotoxic effects of MDMA and <b>METH</b> suggests that the <strong>nNOS</strong> gene is required for the expression and persistence of DA mediated effects of <b>METH</b> and MDMA, while 5 HT mediated effects of MDMA (induction of sensitization and 5 HT depletion) are not dependent on <strong>nNOS</strong>.
+NOS1	drug	psychedelics	15542708	The differential response of <strong>nNOS</strong> KO mice to the behavioral and neurotoxic effects of <b>MDMA</b> and METH suggests that the <strong>nNOS</strong> gene is required for the expression and persistence of DA mediated effects of METH and <b>MDMA</b>, while 5 HT mediated effects of <b>MDMA</b> (induction of sensitization and 5 HT depletion) are not dependent on <strong>nNOS</strong>.
+NOS1	addiction	sensitization	15542708	The differential response of <strong>nNOS</strong> KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the <strong>nNOS</strong> gene is required for the expression and persistence of DA mediated effects of METH and MDMA, while 5 HT mediated effects of MDMA (induction of <b>sensitization</b> and 5 HT depletion) are not dependent on <strong>nNOS</strong>.
+NOS1	drug	amphetamine	15542708	The differential response of <strong><strong>nNOS</strong></strong> KO mice to the behavioral and neurotoxic effects of MDMA and <b>METH</b> suggests that the <strong><strong>nNOS</strong></strong> gene is required for the expression and persistence of DA mediated effects of <b>METH</b> and MDMA, while 5 HT mediated effects of MDMA (induction of sensitization and 5 HT depletion) are not dependent on <strong><strong>nNOS</strong></strong>.
+NOS1	drug	psychedelics	15542708	The differential response of <strong><strong>nNOS</strong></strong> KO mice to the behavioral and neurotoxic effects of <b>MDMA</b> and METH suggests that the <strong><strong>nNOS</strong></strong> gene is required for the expression and persistence of DA mediated effects of METH and <b>MDMA</b>, while 5 HT mediated effects of <b>MDMA</b> (induction of sensitization and 5 HT depletion) are not dependent on <strong><strong>nNOS</strong></strong>.
+NOS1	addiction	sensitization	15542708	The differential response of <strong><strong>nNOS</strong></strong> KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the <strong><strong>nNOS</strong></strong> gene is required for the expression and persistence of DA mediated effects of METH and MDMA, while 5 HT mediated effects of MDMA (induction of <b>sensitization</b> and 5 HT depletion) are not dependent on <strong><strong>nNOS</strong></strong>.
+NOS1	drug	opioid	15033281	The effects of 7 nitroindazole (7 NI), a neural nitric oxide synthase (<strong>nNOS</strong>) inhibitor, on spontaneous locomotor activity, <b>morphine</b> induced hyperactivity, acquisition of place conditioning and <b>morphine</b> induced conditioned place preference (CPP) were evaluated in male mice.
+NOS1	addiction	reward	15033281	The effects of 7 nitroindazole (7 NI), a neural nitric oxide synthase (<strong>nNOS</strong>) inhibitor, on spontaneous locomotor activity, morphine induced hyperactivity, acquisition of place conditioning and morphine induced conditioned place preference (<b>CPP</b>) were evaluated in male mice.
+NOS1	drug	opioid	15033281	The effects of 7 nitroindazole (7 NI), a neural nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitor, on spontaneous locomotor activity, <b>morphine</b> induced hyperactivity, acquisition of place conditioning and <b>morphine</b> induced conditioned place preference (CPP) were evaluated in male mice.
+NOS1	addiction	reward	15033281	The effects of 7 nitroindazole (7 NI), a neural nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitor, on spontaneous locomotor activity, morphine induced hyperactivity, acquisition of place conditioning and morphine induced conditioned place preference (<b>CPP</b>) were evaluated in male mice.
+NOS1	drug	opioid	14698461	Agmatine reduces only peripheral related behavioral signs, not the central signs, of <b>morphine</b> withdrawal in <strong>nNOS</strong> deficient transgenic mice.
+NOS1	addiction	withdrawal	14698461	Agmatine reduces only peripheral related behavioral signs, not the central signs, of morphine <b>withdrawal</b> in <strong>nNOS</strong> deficient transgenic mice.
+NOS1	drug	opioid	14698461	Agmatine reduces only peripheral related behavioral signs, not the central signs, of <b>morphine</b> withdrawal in <strong><strong>nNOS</strong></strong> deficient transgenic mice.
+NOS1	addiction	withdrawal	14698461	Agmatine reduces only peripheral related behavioral signs, not the central signs, of morphine <b>withdrawal</b> in <strong><strong>nNOS</strong></strong> deficient transgenic mice.
+NOS1	drug	amphetamine	14559429	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, <b>methamphetamine</b>, and methylphenidate (indirect dopamine agonists) are blocked by co administration of the neuronal nitric oxide synthase (<strong>nNOS</strong>) inhibitor 7 nitroindazole (7 NI).
+NOS1	drug	cocaine	14559429	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to <b>cocaine</b>, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co administration of the neuronal nitric oxide synthase (<strong>nNOS</strong>) inhibitor 7 nitroindazole (7 NI).
+NOS1	addiction	sensitization	14559429	We have previously shown that the induction, expression, and maintenance of psychomotor <b>sensitization</b> to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co administration of the neuronal nitric oxide synthase (<strong>nNOS</strong>) inhibitor 7 nitroindazole (7 NI).
+NOS1	drug	amphetamine	14559429	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to cocaine, <b>methamphetamine</b>, and methylphenidate (indirect dopamine agonists) are blocked by co administration of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitor 7 nitroindazole (7 NI).
+NOS1	drug	cocaine	14559429	We have previously shown that the induction, expression, and maintenance of psychomotor sensitization to <b>cocaine</b>, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co administration of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitor 7 nitroindazole (7 NI).
+NOS1	addiction	sensitization	14559429	We have previously shown that the induction, expression, and maintenance of psychomotor <b>sensitization</b> to cocaine, methamphetamine, and methylphenidate (indirect dopamine agonists) are blocked by co administration of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) inhibitor 7 nitroindazole (7 NI).
+NOS1	drug	psychedelics	14559429	These findings, coupled with our previous studies, suggest the following: (a) The induction and expression of psychomotor sensitization to <b>MDMA</b> and PCA are independent of <strong>nNOS</strong> activity and involve primarily serotonergic transmission.
+NOS1	addiction	sensitization	14559429	These findings, coupled with our previous studies, suggest the following: (a) The induction and expression of psychomotor <b>sensitization</b> to MDMA and PCA are independent of <strong>nNOS</strong> activity and involve primarily serotonergic transmission.
+NOS1	drug	psychedelics	14559429	These findings, coupled with our previous studies, suggest the following: (a) The induction and expression of psychomotor sensitization to <b>MDMA</b> and PCA are independent of <strong><strong>nNOS</strong></strong> activity and involve primarily serotonergic transmission.
+NOS1	addiction	sensitization	14559429	These findings, coupled with our previous studies, suggest the following: (a) The induction and expression of psychomotor <b>sensitization</b> to MDMA and PCA are independent of <strong><strong>nNOS</strong></strong> activity and involve primarily serotonergic transmission.
+NOS1	addiction	sensitization	14559429	(b) The maintenance of psychomotor <b>sensitization</b> is dependent on intact <strong>nNOS</strong> activity and involves primarily dopaminergic transmission.
+NOS1	addiction	sensitization	14559429	(b) The maintenance of psychomotor <b>sensitization</b> is dependent on intact <strong><strong>nNOS</strong></strong> activity and involves primarily dopaminergic transmission.
+NOS1	drug	opioid	12905572	[Study on the changes of <strong>ncNOS</strong> in chronic <b>heroin</b> dependence and spontaneous withdrawal in rats].
+NOS1	addiction	dependence	12905572	[Study on the changes of <strong>ncNOS</strong> in chronic heroin <b>dependence</b> and spontaneous withdrawal in rats].
+NOS1	addiction	withdrawal	12905572	[Study on the changes of <strong>ncNOS</strong> in chronic heroin dependence and spontaneous <b>withdrawal</b> in rats].
+NOS1	drug	opioid	12905572	To study the changes and actions of neuronal constructive nitric oxide synthase(<strong>ncNOS</strong>) in <b>heroin</b> drug abuse.
+NOS1	drug	opioid	12905572	The expression of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA in neurons of cerebral cortex, periaqueductal gray matter and the ventral tegmental area was observed by immunohistochemistry, in situ hybridization and image analysis technique after <b>heroin</b> dependence and spontaneous withdrawal in rats.
+NOS1	addiction	dependence	12905572	The expression of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA in neurons of cerebral cortex, periaqueductal gray matter and the ventral tegmental area was observed by immunohistochemistry, in situ hybridization and image analysis technique after heroin <b>dependence</b> and spontaneous withdrawal in rats.
+NOS1	addiction	withdrawal	12905572	The expression of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA in neurons of cerebral cortex, periaqueductal gray matter and the ventral tegmental area was observed by immunohistochemistry, in situ hybridization and image analysis technique after heroin dependence and spontaneous <b>withdrawal</b> in rats.
+NOS1	drug	opioid	12905572	The quantity of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA rised clearly and the number of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA positive cells increased greatly in <b>heroin</b> dependence and withdrawal.
+NOS1	addiction	dependence	12905572	The quantity of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA rised clearly and the number of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA positive cells increased greatly in heroin <b>dependence</b> and withdrawal.
+NOS1	addiction	withdrawal	12905572	The quantity of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA rised clearly and the number of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA positive cells increased greatly in heroin dependence and <b>withdrawal</b>.
+NOS1	addiction	dependence	12905572	The changes of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA in spontaneous withdrawal were more clear than ones of <b>dependence</b>.
+NOS1	addiction	withdrawal	12905572	The changes of <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA in spontaneous <b>withdrawal</b> were more clear than ones of dependence.
+NOS1	drug	opioid	12905572	<b>Heroin</b> dependence and withdrawal led to alterations in <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA expression in important regions implicated in the physical tolerance and dependence.
+NOS1	addiction	dependence	12905572	Heroin <b>dependence</b> and withdrawal led to alterations in <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA expression in important regions implicated in the physical tolerance and <b>dependence</b>.
+NOS1	addiction	withdrawal	12905572	Heroin dependence and <b>withdrawal</b> led to alterations in <strong>ncNOS</strong> and <strong>ncNOS</strong> mRNA expression in important regions implicated in the physical tolerance and dependence.
+NOS1	drug	opioid	12905572	The <strong>ncNOS</strong> plays an important role in <b>heroin</b> dependence and withdrawal.
+NOS1	addiction	dependence	12905572	The <strong>ncNOS</strong> plays an important role in heroin <b>dependence</b> and withdrawal.
+NOS1	addiction	withdrawal	12905572	The <strong>ncNOS</strong> plays an important role in heroin dependence and <b>withdrawal</b>.
+NOS1	drug	opioid	12905572	The <strong>ncNOS</strong> immunohistochemical changes observed in the present study might be useful for the forensic pathological diagnosis of <b>heroin</b> drug abuse.
+NOS1	drug	alcohol	12581836	Chronic <b>ethanol</b> exposure differentially regulates <strong>NOS1</strong> mRNA levels depending on rat brain area.
+NOS1	drug	alcohol	12581836	Several works have suggested a potential role for nitric oxide in <b>alcohol</b> seeking behavior and we have recently shown that the specific blockade of the expression of the neuronal nitric oxide synthase (<strong>NOS1</strong>) decreases rat <b>ethanol</b> intake.
+NOS1	addiction	relapse	12581836	Several works have suggested a potential role for nitric oxide in alcohol <b>seeking</b> behavior and we have recently shown that the specific blockade of the expression of the neuronal nitric oxide synthase (<strong>NOS1</strong>) decreases rat ethanol intake.
+NOS1	drug	alcohol	12581836	In the present study, we examine the effects of chronic administration of <b>ethanol</b> on the <strong>NOS1</strong> mRNA levels measured with the competitive reverse transcriptase polymerase chain reaction technique.
+NOS1	drug	alcohol	12581836	Chronic administration of <b>ethanol</b> differentially regulated <strong>NOS1</strong> mRNA levels depending on rat brain area.
+NOS1	drug	alcohol	12581836	Chronic <b>ethanol</b> exposure had no effect on the <strong>NOS1</strong> mRNA levels in frontal cortex, but decreased the <strong>NOS1</strong> mRNA levels in hippocampus (P<0.01, 39% decrease) and induced a strong increase in striatum (P<0.01, 92% increase).
+NOS1	drug	alcohol	12581836	These data further support that <strong>NOS1</strong> is regulated by chronic exposure to <b>ethanol</b> and that these effects are related to modifications of mRNA levels.
+NOS1	drug	opioid	12147190	M2 muscarinic receptor of spinal cord mediated increase of <strong>nNOS</strong> expression in locus coeruleus during <b>morphine</b> withdrawal.
+NOS1	addiction	withdrawal	12147190	M2 muscarinic receptor of spinal cord mediated increase of <strong>nNOS</strong> expression in locus coeruleus during morphine <b>withdrawal</b>.
+NOS1	drug	opioid	12147190	M2 muscarinic receptor of spinal cord mediated increase of <strong><strong>nNOS</strong></strong> expression in locus coeruleus during <b>morphine</b> withdrawal.
+NOS1	addiction	withdrawal	12147190	M2 muscarinic receptor of spinal cord mediated increase of <strong><strong>nNOS</strong></strong> expression in locus coeruleus during morphine <b>withdrawal</b>.
+NOS1	drug	opioid	12147190	To investigate the effects of different muscarinic receptor (M) subtypes in the spinal cord on the scores of <b>naloxone</b> precipitated <b>morphine</b> withdrawal symptoms and the changes of <strong>nNOS</strong> expression in locus coeruleus (LC).
+NOS1	addiction	withdrawal	12147190	To investigate the effects of different muscarinic receptor (M) subtypes in the spinal cord on the scores of naloxone precipitated morphine <b>withdrawal</b> symptoms and the changes of <strong>nNOS</strong> expression in locus coeruleus (LC).
+NOS1	drug	opioid	12147190	To investigate the effects of different muscarinic receptor (M) subtypes in the spinal cord on the scores of <b>naloxone</b> precipitated <b>morphine</b> withdrawal symptoms and the changes of <strong><strong>nNOS</strong></strong> expression in locus coeruleus (LC).
+NOS1	addiction	withdrawal	12147190	To investigate the effects of different muscarinic receptor (M) subtypes in the spinal cord on the scores of naloxone precipitated morphine <b>withdrawal</b> symptoms and the changes of <strong><strong>nNOS</strong></strong> expression in locus coeruleus (LC).
+NOS1	drug	opioid	12147190	The expression of <strong>nNOS</strong> positive neurons in the LC increased in <b>morphine</b> dependent rats and increased to a greater extent during <b>morphine</b> withdrawal.
+NOS1	addiction	withdrawal	12147190	The expression of <strong>nNOS</strong> positive neurons in the LC increased in morphine dependent rats and increased to a greater extent during morphine <b>withdrawal</b>.
+NOS1	drug	opioid	12147190	The expression of <strong><strong>nNOS</strong></strong> positive neurons in the LC increased in <b>morphine</b> dependent rats and increased to a greater extent during <b>morphine</b> withdrawal.
+NOS1	addiction	withdrawal	12147190	The expression of <strong><strong>nNOS</strong></strong> positive neurons in the LC increased in morphine dependent rats and increased to a greater extent during morphine <b>withdrawal</b>.
+NOS1	drug	opioid	12147190	Intrathecal injection of M2 AS inhibited the increase of <strong>nNOS</strong> expression in LC during <b>morphine</b> withdrawal, but there was no effect in case of M1 AS.
+NOS1	addiction	withdrawal	12147190	Intrathecal injection of M2 AS inhibited the increase of <strong>nNOS</strong> expression in LC during morphine <b>withdrawal</b>, but there was no effect in case of M1 AS.
+NOS1	drug	opioid	12147190	Intrathecal injection of M2 AS inhibited the increase of <strong><strong>nNOS</strong></strong> expression in LC during <b>morphine</b> withdrawal, but there was no effect in case of M1 AS.
+NOS1	addiction	withdrawal	12147190	Intrathecal injection of M2 AS inhibited the increase of <strong><strong>nNOS</strong></strong> expression in LC during morphine <b>withdrawal</b>, but there was no effect in case of M1 AS.
+NOS1	drug	opioid	12147190	M2 muscarinic receptor of spinal cord mediated the increase of <strong>nNOS</strong> expression in LC during <b>morphine</b> withdrawal.
+NOS1	addiction	withdrawal	12147190	M2 muscarinic receptor of spinal cord mediated the increase of <strong>nNOS</strong> expression in LC during morphine <b>withdrawal</b>.
+NOS1	drug	opioid	12147190	M2 muscarinic receptor of spinal cord mediated the increase of <strong><strong>nNOS</strong></strong> expression in LC during <b>morphine</b> withdrawal.
+NOS1	addiction	withdrawal	12147190	M2 muscarinic receptor of spinal cord mediated the increase of <strong><strong>nNOS</strong></strong> expression in LC during morphine <b>withdrawal</b>.
+NOS1	drug	opioid	12065191	Increased neuronal nitric oxide synthase (<strong>nNOS</strong>) expression is reported to exist in <b>morphine</b> tolerant animals.
+NOS1	drug	opioid	12065191	Increased neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) expression is reported to exist in <b>morphine</b> tolerant animals.
+NOS1	drug	amphetamine	11821029	The present study investigated the role of nitric oxide (NO) in the rewarding effects of D <b>methamphetamine</b> using 7 nitroindazole, a potent inhibitor of neuronal nitric oxide synthase (<strong>nNOS</strong>), as determined by the conditioned place preference paradigm.
+NOS1	drug	amphetamine	11821029	The present study investigated the role of nitric oxide (NO) in the rewarding effects of D <b>methamphetamine</b> using 7 nitroindazole, a potent inhibitor of neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>), as determined by the conditioned place preference paradigm.
+NOS1	drug	amphetamine	11821029	These findings indicate that nitric oxide (NO) is involved in the rewarding properties of <b>methamphetamine</b> and suggest that selective <strong>nNOS</strong> inhibitors maybe useful in the management of <b>methamphetamine</b> abuse.
+NOS1	drug	amphetamine	11821029	These findings indicate that nitric oxide (NO) is involved in the rewarding properties of <b>methamphetamine</b> and suggest that selective <strong><strong>nNOS</strong></strong> inhibitors maybe useful in the management of <b>methamphetamine</b> abuse.
+NOS1	drug	opioid	11747755	Intrathecal injection of <strong>nNOS</strong> antisense oligonucleotides (<strong>nNOS</strong> AS) inhibited the increase of Fos protein and NMDA(1A)R mRNA expression in the rat spinal cord during <b>morphine</b> withdrawal and decreased the scores of <b>morphine</b> withdrawal symptoms.
+NOS1	addiction	withdrawal	11747755	Intrathecal injection of <strong>nNOS</strong> antisense oligonucleotides (<strong>nNOS</strong> AS) inhibited the increase of Fos protein and NMDA(1A)R mRNA expression in the rat spinal cord during morphine <b>withdrawal</b> and decreased the scores of morphine <b>withdrawal</b> symptoms.
+NOS1	drug	opioid	11747755	Intrathecal injection of <strong><strong>nNOS</strong></strong> antisense oligonucleotides (<strong><strong>nNOS</strong></strong> AS) inhibited the increase of Fos protein and NMDA(1A)R mRNA expression in the rat spinal cord during <b>morphine</b> withdrawal and decreased the scores of <b>morphine</b> withdrawal symptoms.
+NOS1	addiction	withdrawal	11747755	Intrathecal injection of <strong><strong>nNOS</strong></strong> antisense oligonucleotides (<strong><strong>nNOS</strong></strong> AS) inhibited the increase of Fos protein and NMDA(1A)R mRNA expression in the rat spinal cord during morphine <b>withdrawal</b> and decreased the scores of morphine <b>withdrawal</b> symptoms.
+NOS1	drug	opioid	11354804	Intrathecal injection of L NA, <strong>nNOS</strong> antisense oligonucleotides significantly inhibited the expression of Fos LI in the spinal cord and decreased the scores for <b>morphine</b> withdrawal symptoms in <b>morphine</b> withdrawal rats, but not in <strong>nNOS</strong> S group.
+NOS1	addiction	withdrawal	11354804	Intrathecal injection of L NA, <strong>nNOS</strong> antisense oligonucleotides significantly inhibited the expression of Fos LI in the spinal cord and decreased the scores for morphine <b>withdrawal</b> symptoms in morphine <b>withdrawal</b> rats, but not in <strong>nNOS</strong> S group.
+NOS1	drug	opioid	11354804	Intrathecal injection of L NA, <strong><strong>nNOS</strong></strong> antisense oligonucleotides significantly inhibited the expression of Fos LI in the spinal cord and decreased the scores for <b>morphine</b> withdrawal symptoms in <b>morphine</b> withdrawal rats, but not in <strong><strong>nNOS</strong></strong> S group.
+NOS1	addiction	withdrawal	11354804	Intrathecal injection of L NA, <strong><strong>nNOS</strong></strong> antisense oligonucleotides significantly inhibited the expression of Fos LI in the spinal cord and decreased the scores for morphine <b>withdrawal</b> symptoms in morphine <b>withdrawal</b> rats, but not in <strong><strong>nNOS</strong></strong> S group.
+NOS1	drug	opioid	11354793	Intrathecal injection of <strong>nNOS</strong> AS ONs significantly inhibited the increased expression of NMDA1AR mRNA in the spinal cord and brainstem of <b>morphine</b> withdrawal rats.
+NOS1	addiction	withdrawal	11354793	Intrathecal injection of <strong>nNOS</strong> AS ONs significantly inhibited the increased expression of NMDA1AR mRNA in the spinal cord and brainstem of morphine <b>withdrawal</b> rats.
+NOS1	drug	opioid	11354793	Intrathecal injection of <strong><strong>nNOS</strong></strong> AS ONs significantly inhibited the increased expression of NMDA1AR mRNA in the spinal cord and brainstem of <b>morphine</b> withdrawal rats.
+NOS1	addiction	withdrawal	11354793	Intrathecal injection of <strong><strong>nNOS</strong></strong> AS ONs significantly inhibited the increased expression of NMDA1AR mRNA in the spinal cord and brainstem of morphine <b>withdrawal</b> rats.
+NOS1	drug	alcohol	11164095	Intracerebroventricular injection of antisense oligos to <strong>nNOS</strong> decreases rat <b>ethanol</b> intake.
+NOS1	drug	alcohol	11164095	Intracerebroventricular injection of antisense oligos to <strong><strong>nNOS</strong></strong> decreases rat <b>ethanol</b> intake.
+NOS1	drug	alcohol	11164095	We used an antisense oligodeoxynucleotide directed against <strong>nNOS</strong> in <b>ethanol</b> dependent male Wistar rats to examine the specific contribution of <strong>nNOS</strong> in the control of <b>ethanol</b> intake.
+NOS1	drug	alcohol	11164095	We used an antisense oligodeoxynucleotide directed against <strong><strong>nNOS</strong></strong> in <b>ethanol</b> dependent male Wistar rats to examine the specific contribution of <strong><strong>nNOS</strong></strong> in the control of <b>ethanol</b> intake.
+NOS1	drug	alcohol	11164095	All these results suggest that <strong>nNOS</strong> is involved in the regulation of <b>alcohol</b> dependence.
+NOS1	addiction	dependence	11164095	All these results suggest that <strong>nNOS</strong> is involved in the regulation of alcohol <b>dependence</b>.
+NOS1	drug	alcohol	11164095	All these results suggest that <strong><strong>nNOS</strong></strong> is involved in the regulation of <b>alcohol</b> dependence.
+NOS1	addiction	dependence	11164095	All these results suggest that <strong><strong>nNOS</strong></strong> is involved in the regulation of alcohol <b>dependence</b>.
+NOS1	drug	alcohol	11139418	In the <b>alcoholic</b> brain, <strong>nNOS</strong> protein expression was increased in the following regions: frontal cortex (85%), the cingulate gyrus (294%), the nucleus accumbens (54%), the entorhinal cortex (85%) and the thalamus (51%).
+NOS1	drug	alcohol	11139418	In the <b>alcoholic</b> brain, <strong><strong>nNOS</strong></strong> protein expression was increased in the following regions: frontal cortex (85%), the cingulate gyrus (294%), the nucleus accumbens (54%), the entorhinal cortex (85%) and the thalamus (51%).
+NOS1	addiction	reward	11139418	Interestingly, <strong>nNOS</strong> protein content was increased in the frontal cortex and the nucleus accumbens, brain regions which are suggested to be involved in the dopaminergic mesolimbic <b>reward</b> system.
+NOS1	addiction	reward	11139418	Interestingly, <strong><strong>nNOS</strong></strong> protein content was increased in the frontal cortex and the nucleus accumbens, brain regions which are suggested to be involved in the dopaminergic mesolimbic <b>reward</b> system.
+NOS1	drug	amphetamine	11085313	The involvement of the neuronal and inducible nitric oxide synthase (<strong>nNOS</strong> and iNOS, respectively) in <b>methamphetamine</b> (<b>METH</b>) induced dopaminergic neurotoxicity and behavioral sensitization was investigated.
+NOS1	addiction	sensitization	11085313	The involvement of the neuronal and inducible nitric oxide synthase (<strong>nNOS</strong> and iNOS, respectively) in methamphetamine (METH) induced dopaminergic neurotoxicity and behavioral <b>sensitization</b> was investigated.
+NOS1	drug	amphetamine	11085313	The involvement of the neuronal and inducible nitric oxide synthase (<strong><strong>nNOS</strong></strong> and iNOS, respectively) in <b>methamphetamine</b> (<b>METH</b>) induced dopaminergic neurotoxicity and behavioral sensitization was investigated.
+NOS1	addiction	sensitization	11085313	The involvement of the neuronal and inducible nitric oxide synthase (<strong><strong>nNOS</strong></strong> and iNOS, respectively) in methamphetamine (METH) induced dopaminergic neurotoxicity and behavioral <b>sensitization</b> was investigated.
+NOS1	drug	amphetamine	11085313	To determine <b>METH</b> induced neurotoxicity, mice deficient in the <strong>nNOS</strong> and iNOS genes, <strong>nNOS</strong>( / ) and iNOS( / ) mice, and wild type controls received either saline or <b>METH</b> (5 mg/kg x 3).
+NOS1	drug	amphetamine	11085313	To determine <b>METH</b> induced neurotoxicity, mice deficient in the <strong><strong>nNOS</strong></strong> and iNOS genes, <strong><strong>nNOS</strong></strong>( / ) and iNOS( / ) mice, and wild type controls received either saline or <b>METH</b> (5 mg/kg x 3).
+NOS1	drug	amphetamine	11085313	Administration of <b>METH</b> to <strong>nNOS</strong>( / ) mice had no significant effect on the level of striatal dopamine, 3,4 dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), or dopamine transporter (DAT) binding sites.
+NOS1	drug	amphetamine	11085313	Administration of <b>METH</b> to <strong><strong>nNOS</strong></strong>( / ) mice had no significant effect on the level of striatal dopamine, 3,4 dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), or dopamine transporter (DAT) binding sites.
+NOS1	drug	amphetamine	11085313	The intensity of <b>METH</b> induced locomotion in <strong>nNOS</strong>( / ) mice on day 1 and 4 was similar, suggesting that locomotor sensitization did not develop.
+NOS1	addiction	sensitization	11085313	The intensity of METH induced locomotion in <strong>nNOS</strong>( / ) mice on day 1 and 4 was similar, suggesting that locomotor <b>sensitization</b> did not develop.
+NOS1	drug	amphetamine	11085313	The intensity of <b>METH</b> induced locomotion in <strong><strong>nNOS</strong></strong>( / ) mice on day 1 and 4 was similar, suggesting that locomotor sensitization did not develop.
+NOS1	addiction	sensitization	11085313	The intensity of METH induced locomotion in <strong><strong>nNOS</strong></strong>( / ) mice on day 1 and 4 was similar, suggesting that locomotor <b>sensitization</b> did not develop.
+NOS1	drug	amphetamine	11085313	The present findings indicate that <strong>nNOS</strong>( / ) mice are more resistant to <b>METH</b> induced neurotoxicity and behavioral sensitization than iNOS( / ) mice.
+NOS1	addiction	sensitization	11085313	The present findings indicate that <strong>nNOS</strong>( / ) mice are more resistant to METH induced neurotoxicity and behavioral <b>sensitization</b> than iNOS( / ) mice.
+NOS1	drug	amphetamine	11085313	The present findings indicate that <strong><strong>nNOS</strong></strong>( / ) mice are more resistant to <b>METH</b> induced neurotoxicity and behavioral sensitization than iNOS( / ) mice.
+NOS1	addiction	sensitization	11085313	The present findings indicate that <strong><strong>nNOS</strong></strong>( / ) mice are more resistant to METH induced neurotoxicity and behavioral <b>sensitization</b> than iNOS( / ) mice.
+NOS1	drug	amphetamine	11085313	These results suggest a major role for <strong>nNOS</strong> rather than iNOS in the effects of <b>METH</b>.
+NOS1	drug	amphetamine	11085313	These results suggest a major role for <strong><strong>nNOS</strong></strong> rather than iNOS in the effects of <b>METH</b>.
+NOS1	drug	amphetamine	20575850	In the present study, we examined the role of the neuronal nitric oxide synthase (<strong>nNOS</strong>), susceptibility of <strong>nNOS</strong> knockout (KO) mice and sensitization to psychostimulants after neurotoxic doses of <b>METH</b>.
+NOS1	addiction	sensitization	20575850	In the present study, we examined the role of the neuronal nitric oxide synthase (<strong>nNOS</strong>), susceptibility of <strong>nNOS</strong> knockout (KO) mice and <b>sensitization</b> to psychostimulants after neurotoxic doses of METH.
+NOS1	drug	amphetamine	20575850	In the present study, we examined the role of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>), susceptibility of <strong><strong>nNOS</strong></strong> knockout (KO) mice and sensitization to psychostimulants after neurotoxic doses of <b>METH</b>.
+NOS1	addiction	sensitization	20575850	In the present study, we examined the role of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>), susceptibility of <strong><strong>nNOS</strong></strong> knockout (KO) mice and <b>sensitization</b> to psychostimulants after neurotoxic doses of METH.
+NOS1	drug	amphetamine	20575850	In follow up experiments <strong>nNOS</strong> KO mice along with appropriate control (C57BL/6N, SV129 and B6JSV129) mice were treated with <b>METH</b> (5 mg/kg,ip, q 3h x 3) and were sacrificed 72 h after dosing.
+NOS1	drug	amphetamine	20575850	In follow up experiments <strong><strong>nNOS</strong></strong> KO mice along with appropriate control (C57BL/6N, SV129 and B6JSV129) mice were treated with <b>METH</b> (5 mg/kg,ip, q 3h x 3) and were sacrificed 72 h after dosing.
+NOS1	drug	amphetamine	20575850	This schedule of <b>METH</b> administrations resulted in only 10 20% decrease in tissue content of DA and no apparent change in the number of DAT binding sites in <strong>nNOS</strong> KO mice.
+NOS1	drug	amphetamine	20575850	This schedule of <b>METH</b> administrations resulted in only 10 20% decrease in tissue content of DA and no apparent change in the number of DAT binding sites in <strong><strong>nNOS</strong></strong> KO mice.
+NOS1	drug	amphetamine	20575850	However, the <strong>nNOS</strong> KO mice show no sensitization in response to <b>METH</b> after single or multiple injections of <b>METH</b>.
+NOS1	addiction	sensitization	20575850	However, the <strong>nNOS</strong> KO mice show no <b>sensitization</b> in response to METH after single or multiple injections of METH.
+NOS1	drug	amphetamine	20575850	However, the <strong><strong>nNOS</strong></strong> KO mice show no sensitization in response to <b>METH</b> after single or multiple injections of <b>METH</b>.
+NOS1	addiction	sensitization	20575850	However, the <strong><strong>nNOS</strong></strong> KO mice show no <b>sensitization</b> in response to METH after single or multiple injections of METH.
+NOS1	drug	amphetamine	20575850	Therefore, these studies strongly suggest the role of peroxynitrite, <strong>nNOS</strong> and DA system in <b>METH</b> induced neurotoxicity and behavioral sensitization.
+NOS1	addiction	sensitization	20575850	Therefore, these studies strongly suggest the role of peroxynitrite, <strong>nNOS</strong> and DA system in METH induced neurotoxicity and behavioral <b>sensitization</b>.
+NOS1	drug	amphetamine	20575850	Therefore, these studies strongly suggest the role of peroxynitrite, <strong><strong>nNOS</strong></strong> and DA system in <b>METH</b> induced neurotoxicity and behavioral sensitization.
+NOS1	addiction	sensitization	20575850	Therefore, these studies strongly suggest the role of peroxynitrite, <strong><strong>nNOS</strong></strong> and DA system in METH induced neurotoxicity and behavioral <b>sensitization</b>.
+NOS1	drug	cocaine	10790861	We have shown previously that the neuronal nitric oxide synthase (<strong>nNOS</strong>) is involved in the rewarding effect of <b>cocaine</b> as determined by the conditioned place preference (CPP) paradigm.
+NOS1	addiction	reward	10790861	We have shown previously that the neuronal nitric oxide synthase (<strong>nNOS</strong>) is involved in the rewarding effect of cocaine as determined by the conditioned place preference (<b>CPP</b>) paradigm.
+NOS1	drug	cocaine	10790861	We have shown previously that the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) is involved in the rewarding effect of <b>cocaine</b> as determined by the conditioned place preference (CPP) paradigm.
+NOS1	addiction	reward	10790861	We have shown previously that the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) is involved in the rewarding effect of cocaine as determined by the conditioned place preference (<b>CPP</b>) paradigm.
+NOS1	drug	nicotine	10790861	In the present study we investigated the effect of the <strong>nNOS</strong> inhibitor 7 nitroindazole (7 NI) on <b>nicotine</b> induced CPP and LiCl induced conditioned place aversion (CPA) in Swiss Webster mice.
+NOS1	addiction	aversion	10790861	In the present study we investigated the effect of the <strong>nNOS</strong> inhibitor 7 nitroindazole (7 NI) on nicotine induced CPP and LiCl induced conditioned place <b>aversion</b> (CPA) in Swiss Webster mice.
+NOS1	addiction	reward	10790861	In the present study we investigated the effect of the <strong>nNOS</strong> inhibitor 7 nitroindazole (7 NI) on nicotine induced <b>CPP</b> and LiCl induced conditioned place aversion (CPA) in Swiss Webster mice.
+NOS1	drug	nicotine	10790861	In the present study we investigated the effect of the <strong><strong>nNOS</strong></strong> inhibitor 7 nitroindazole (7 NI) on <b>nicotine</b> induced CPP and LiCl induced conditioned place aversion (CPA) in Swiss Webster mice.
+NOS1	addiction	aversion	10790861	In the present study we investigated the effect of the <strong><strong>nNOS</strong></strong> inhibitor 7 nitroindazole (7 NI) on nicotine induced CPP and LiCl induced conditioned place <b>aversion</b> (CPA) in Swiss Webster mice.
+NOS1	addiction	reward	10790861	In the present study we investigated the effect of the <strong><strong>nNOS</strong></strong> inhibitor 7 nitroindazole (7 NI) on nicotine induced <b>CPP</b> and LiCl induced conditioned place aversion (CPA) in Swiss Webster mice.
+NOS1	drug	cocaine	10708693	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (<strong>nNOS</strong>) prevents the development of sensitization to the locomotor stimulating effect of <b>cocaine</b> and <b>cocaine</b> induced conditioned place preference (CPP).
+NOS1	addiction	reward	10708693	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (<strong>nNOS</strong>) prevents the development of sensitization to the locomotor stimulating effect of cocaine and cocaine induced conditioned place preference (<b>CPP</b>).
+NOS1	addiction	sensitization	10708693	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (<strong>nNOS</strong>) prevents the development of <b>sensitization</b> to the locomotor stimulating effect of cocaine and cocaine induced conditioned place preference (CPP).
+NOS1	drug	cocaine	10708693	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) prevents the development of sensitization to the locomotor stimulating effect of <b>cocaine</b> and <b>cocaine</b> induced conditioned place preference (CPP).
+NOS1	addiction	reward	10708693	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) prevents the development of sensitization to the locomotor stimulating effect of cocaine and cocaine induced conditioned place preference (<b>CPP</b>).
+NOS1	addiction	sensitization	10708693	Our previous studies indicated that inhibition or ablation of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) prevents the development of <b>sensitization</b> to the locomotor stimulating effect of cocaine and cocaine induced conditioned place preference (CPP).
+NOS1	drug	alcohol	10708693	The present study was undertaken to investigate the effect of the <strong>nNOS</strong> inhibitor, 7 nitroindazole (7 NI), on <b>ethanol</b> induced locomotor sensitization and CPP in DBA/2J mice.
+NOS1	addiction	reward	10708693	The present study was undertaken to investigate the effect of the <strong>nNOS</strong> inhibitor, 7 nitroindazole (7 NI), on ethanol induced locomotor sensitization and <b>CPP</b> in DBA/2J mice.
+NOS1	addiction	sensitization	10708693	The present study was undertaken to investigate the effect of the <strong>nNOS</strong> inhibitor, 7 nitroindazole (7 NI), on ethanol induced locomotor <b>sensitization</b> and CPP in DBA/2J mice.
+NOS1	drug	alcohol	10708693	The present study was undertaken to investigate the effect of the <strong><strong>nNOS</strong></strong> inhibitor, 7 nitroindazole (7 NI), on <b>ethanol</b> induced locomotor sensitization and CPP in DBA/2J mice.
+NOS1	addiction	reward	10708693	The present study was undertaken to investigate the effect of the <strong><strong>nNOS</strong></strong> inhibitor, 7 nitroindazole (7 NI), on ethanol induced locomotor sensitization and <b>CPP</b> in DBA/2J mice.
+NOS1	addiction	sensitization	10708693	The present study was undertaken to investigate the effect of the <strong><strong>nNOS</strong></strong> inhibitor, 7 nitroindazole (7 NI), on ethanol induced locomotor <b>sensitization</b> and CPP in DBA/2J mice.
+NOS1	drug	alcohol	10708693	Taken together, results of the present study indicate that blockade of <strong>nNOS</strong> by 7 NI attenuated <b>ethanol</b> induced behavioral sensitization and completely blocked the rewarding effect of <b>ethanol</b>.
+NOS1	addiction	sensitization	10708693	Taken together, results of the present study indicate that blockade of <strong>nNOS</strong> by 7 NI attenuated ethanol induced behavioral <b>sensitization</b> and completely blocked the rewarding effect of ethanol.
+NOS1	drug	alcohol	10708693	Taken together, results of the present study indicate that blockade of <strong><strong>nNOS</strong></strong> by 7 NI attenuated <b>ethanol</b> induced behavioral sensitization and completely blocked the rewarding effect of <b>ethanol</b>.
+NOS1	addiction	sensitization	10708693	Taken together, results of the present study indicate that blockade of <strong><strong>nNOS</strong></strong> by 7 NI attenuated ethanol induced behavioral <b>sensitization</b> and completely blocked the rewarding effect of ethanol.
+NOS1	drug	alcohol	10708693	These findings support the role of NO in <b>ethanol</b> actions and further suggest that the <strong>nNOS</strong> system is relevant to the rewarding effects of various drugs of abuse.
+NOS1	drug	alcohol	10708693	These findings support the role of NO in <b>ethanol</b> actions and further suggest that the <strong><strong>nNOS</strong></strong> system is relevant to the rewarding effects of various drugs of abuse.
+NOS1	drug	opioid	10663419	The present study was undertaken to determine the effect of chronic <b>morphine</b> treatment and abstinence on the expression of neuronal NO synthase (neuronal NOS, <strong>nNOS</strong>) in several brain regions of mice.
+NOS1	drug	opioid	10663419	The present study was undertaken to determine the effect of chronic <b>morphine</b> treatment and abstinence on the expression of neuronal NO synthase (neuronal NOS, <strong><strong>nNOS</strong></strong>) in several brain regions of mice.
+NOS1	drug	opioid	10663419	Fifteen minutes after the <b>naloxone</b> injection, brains were removed and <strong>nNOS</strong> expression was studied by using immunohistochemical methods.
+NOS1	drug	opioid	10663419	Fifteen minutes after the <b>naloxone</b> injection, brains were removed and <strong><strong>nNOS</strong></strong> expression was studied by using immunohistochemical methods.
+NOS1	drug	opioid	10663419	<b>Morphine</b> dependence produced an increase in the number of <strong>nNOS</strong> positive cells in the main and accessory olfactory bulb, olfactory nuclei, cerebellum, locus coeruleus, medulla oblongata (nucleus of the solitary tract and prepositus hypoglossal nucleus), and a decrease in <strong>nNOS</strong> immunoreactivity in hypothalamus.
+NOS1	addiction	dependence	10663419	Morphine <b>dependence</b> produced an increase in the number of <strong>nNOS</strong> positive cells in the main and accessory olfactory bulb, olfactory nuclei, cerebellum, locus coeruleus, medulla oblongata (nucleus of the solitary tract and prepositus hypoglossal nucleus), and a decrease in <strong>nNOS</strong> immunoreactivity in hypothalamus.
+NOS1	drug	opioid	10663419	<b>Morphine</b> dependence produced an increase in the number of <strong><strong>nNOS</strong></strong> positive cells in the main and accessory olfactory bulb, olfactory nuclei, cerebellum, locus coeruleus, medulla oblongata (nucleus of the solitary tract and prepositus hypoglossal nucleus), and a decrease in <strong><strong>nNOS</strong></strong> immunoreactivity in hypothalamus.
+NOS1	addiction	dependence	10663419	Morphine <b>dependence</b> produced an increase in the number of <strong><strong>nNOS</strong></strong> positive cells in the main and accessory olfactory bulb, olfactory nuclei, cerebellum, locus coeruleus, medulla oblongata (nucleus of the solitary tract and prepositus hypoglossal nucleus), and a decrease in <strong><strong>nNOS</strong></strong> immunoreactivity in hypothalamus.
+NOS1	drug	opioid	10663419	The administration of <b>naloxone</b> to <b>morphine</b> dependent mice to induce abstinence increased <strong>nNOS</strong> immunoreactivity in the hypothalamus and locus coeruleus.
+NOS1	drug	opioid	10663419	The administration of <b>naloxone</b> to <b>morphine</b> dependent mice to induce abstinence increased <strong><strong>nNOS</strong></strong> immunoreactivity in the hypothalamus and locus coeruleus.
+NOS1	drug	opioid	10663419	These results indicate that the chronic treatment with <b>morphine</b> leads to alterations in <strong>nNOS</strong> expression in important regions implicated in the physical tolerance and dependence to opiates and suggest the use of specific inhibitors of this isoform in these conditions.
+NOS1	addiction	dependence	10663419	These results indicate that the chronic treatment with morphine leads to alterations in <strong>nNOS</strong> expression in important regions implicated in the physical tolerance and <b>dependence</b> to opiates and suggest the use of specific inhibitors of this isoform in these conditions.
+NOS1	drug	opioid	10663419	These results indicate that the chronic treatment with <b>morphine</b> leads to alterations in <strong><strong>nNOS</strong></strong> expression in important regions implicated in the physical tolerance and dependence to opiates and suggest the use of specific inhibitors of this isoform in these conditions.
+NOS1	addiction	dependence	10663419	These results indicate that the chronic treatment with morphine leads to alterations in <strong><strong>nNOS</strong></strong> expression in important regions implicated in the physical tolerance and <b>dependence</b> to opiates and suggest the use of specific inhibitors of this isoform in these conditions.
+NOS1	drug	amphetamine	10529724	Since evidence supported the involvement of the neuronal nitric oxide synthase (<strong>nNOS</strong>) isoform in the dopaminergic neurotoxicity, the present study was undertaken to investigate whether the inducible nitric oxide synthase (iNOS) isoform is also associated with <b>METH</b>  and MPTP induced neurotoxicity.
+NOS1	drug	amphetamine	10529724	Since evidence supported the involvement of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) isoform in the dopaminergic neurotoxicity, the present study was undertaken to investigate whether the inducible nitric oxide synthase (iNOS) isoform is also associated with <b>METH</b>  and MPTP induced neurotoxicity.
+NOS1	drug	amphetamine	10529724	Moreover, in contrast to <strong>nNOS</strong> deficiency, iNOS deficiency did not affect <b>METH</b> induced behavioral sensitization.
+NOS1	addiction	sensitization	10529724	Moreover, in contrast to <strong>nNOS</strong> deficiency, iNOS deficiency did not affect METH induced behavioral <b>sensitization</b>.
+NOS1	drug	amphetamine	10529724	Moreover, in contrast to <strong><strong>nNOS</strong></strong> deficiency, iNOS deficiency did not affect <b>METH</b> induced behavioral sensitization.
+NOS1	addiction	sensitization	10529724	Moreover, in contrast to <strong><strong>nNOS</strong></strong> deficiency, iNOS deficiency did not affect METH induced behavioral <b>sensitization</b>.
+NOS1	addiction	dependence	10516186	The specific reasons why the pial arteriolar CO(2) reactivity gains a K(+) channel and epoxygenase <b>dependence</b> only under conditions of <strong>nNOS</strong> inhibition and cGMP restoration remain to be identified.
+NOS1	addiction	dependence	10516186	The specific reasons why the pial arteriolar CO(2) reactivity gains a K(+) channel and epoxygenase <b>dependence</b> only under conditions of <strong><strong>nNOS</strong></strong> inhibition and cGMP restoration remain to be identified.
+NOS1	drug	alcohol	10328522	To test for a possible role of nitric oxide (NO) in the neurotoxicity of <b>ethanol</b>, we studied the effects of <b>ethanol</b> on the neuronal NO synthase (<strong>nNOS</strong>) both in vitro and in vivo.
+NOS1	drug	alcohol	10328522	To test for a possible role of nitric oxide (NO) in the neurotoxicity of <b>ethanol</b>, we studied the effects of <b>ethanol</b> on the neuronal NO synthase (<strong><strong>nNOS</strong></strong>) both in vitro and in vivo.
+NOS1	drug	alcohol	10328522	These results indicate that <strong>nNOS</strong> is resistant to <b>ethanol</b> at clinically relevant concentrations and that <b>ethanol</b> affects the NO operated system in the brain through a pathway other than that of <strong>nNOS</strong>.
+NOS1	drug	alcohol	10328522	These results indicate that <strong><strong>nNOS</strong></strong> is resistant to <b>ethanol</b> at clinically relevant concentrations and that <b>ethanol</b> affects the NO operated system in the brain through a pathway other than that of <strong><strong>nNOS</strong></strong>.
+NOS1	drug	cocaine	9877018	The present study was undertaken to investigate whether mice lacking the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene are protected from <b>cocaine</b> induced behavioral sensitization.
+NOS1	addiction	sensitization	9877018	The present study was undertaken to investigate whether mice lacking the neuronal nitric oxide synthase (<strong>nNOS</strong>) gene are protected from cocaine induced behavioral <b>sensitization</b>.
+NOS1	drug	cocaine	9877018	The present study was undertaken to investigate whether mice lacking the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene are protected from <b>cocaine</b> induced behavioral sensitization.
+NOS1	addiction	sensitization	9877018	The present study was undertaken to investigate whether mice lacking the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) gene are protected from cocaine induced behavioral <b>sensitization</b>.
+NOS1	drug	cocaine	9877018	Male homozygote <strong>nNOS</strong>( / ) mice were sensitive to the acute effect of <b>cocaine</b> (15 mg/kg) on day 1; however, they developed neither a sensitized response to <b>cocaine</b> (on day 5 and 15) nor a conditioned locomotion.
+NOS1	drug	cocaine	9877018	Male homozygote <strong><strong>nNOS</strong></strong>( / ) mice were sensitive to the acute effect of <b>cocaine</b> (15 mg/kg) on day 1; however, they developed neither a sensitized response to <b>cocaine</b> (on day 5 and 15) nor a conditioned locomotion.
+NOS1	drug	cocaine	9877018	Female homozygote <strong>nNOS</strong>( / ) mice neither were responsive to 15 mg/kg <b>cocaine</b> on day 1,5 and 15, nor did they develop a conditioned locomotion.
+NOS1	drug	cocaine	9877018	Female homozygote <strong><strong>nNOS</strong></strong>( / ) mice neither were responsive to 15 mg/kg <b>cocaine</b> on day 1,5 and 15, nor did they develop a conditioned locomotion.
+NOS1	drug	cocaine	9877018	In contrast, the same <b>cocaine</b> regimen delivered to male and female heterozygote <strong>nNOS</strong>(+/ ) mice, and wild type mice (B6 J/sv129, C57BL/6 and sv129) resulted in sensitization to <b>cocaine</b> induced locomotor activity and context dependent locomotion.
+NOS1	addiction	sensitization	9877018	In contrast, the same cocaine regimen delivered to male and female heterozygote <strong>nNOS</strong>(+/ ) mice, and wild type mice (B6 J/sv129, C57BL/6 and sv129) resulted in <b>sensitization</b> to cocaine induced locomotor activity and context dependent locomotion.
+NOS1	drug	cocaine	9877018	In contrast, the same <b>cocaine</b> regimen delivered to male and female heterozygote <strong><strong>nNOS</strong></strong>(+/ ) mice, and wild type mice (B6 J/sv129, C57BL/6 and sv129) resulted in sensitization to <b>cocaine</b> induced locomotor activity and context dependent locomotion.
+NOS1	addiction	sensitization	9877018	In contrast, the same cocaine regimen delivered to male and female heterozygote <strong><strong>nNOS</strong></strong>(+/ ) mice, and wild type mice (B6 J/sv129, C57BL/6 and sv129) resulted in <b>sensitization</b> to cocaine induced locomotor activity and context dependent locomotion.
+NOS1	drug	cocaine	9877018	Taken together, our results suggest that the resistance of homozygote <strong>nNOS</strong>( / ) mice to <b>cocaine</b> induced behavioral sensitization is primarily due to the deletion of the <strong>nNOS</strong> gene.
+NOS1	addiction	sensitization	9877018	Taken together, our results suggest that the resistance of homozygote <strong>nNOS</strong>( / ) mice to cocaine induced behavioral <b>sensitization</b> is primarily due to the deletion of the <strong>nNOS</strong> gene.
+NOS1	drug	cocaine	9877018	Taken together, our results suggest that the resistance of homozygote <strong><strong>nNOS</strong></strong>( / ) mice to <b>cocaine</b> induced behavioral sensitization is primarily due to the deletion of the <strong><strong>nNOS</strong></strong> gene.
+NOS1	addiction	sensitization	9877018	Taken together, our results suggest that the resistance of homozygote <strong><strong>nNOS</strong></strong>( / ) mice to cocaine induced behavioral <b>sensitization</b> is primarily due to the deletion of the <strong><strong>nNOS</strong></strong> gene.
+NOS1	addiction	sensitization	9721919	Previous studies suggested the involvement of the neuronal nitric oxide synthase (<strong>nNOS</strong>) in the development of <b>sensitization</b> to psychostimulants.
+NOS1	addiction	sensitization	9721919	Previous studies suggested the involvement of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) in the development of <b>sensitization</b> to psychostimulants.
+NOS1	drug	cocaine	9721919	In the present study we investigated the role of <strong>nNOS</strong> in the rewarding properties of <b>cocaine</b>.
+NOS1	drug	cocaine	9721919	In the present study we investigated the role of <strong><strong>nNOS</strong></strong> in the rewarding properties of <b>cocaine</b>.
+NOS1	drug	cocaine	9721919	Pretreatment with the <strong>nNOS</strong> inhibitor, 7 nitroindazole (7 NI; 25 mg/kg), completely blocked <b>cocaine</b> induced CPP.
+NOS1	addiction	reward	9721919	Pretreatment with the <strong>nNOS</strong> inhibitor, 7 nitroindazole (7 NI; 25 mg/kg), completely blocked cocaine induced <b>CPP</b>.
+NOS1	drug	cocaine	9721919	Pretreatment with the <strong><strong>nNOS</strong></strong> inhibitor, 7 nitroindazole (7 NI; 25 mg/kg), completely blocked <b>cocaine</b> induced CPP.
+NOS1	addiction	reward	9721919	Pretreatment with the <strong><strong>nNOS</strong></strong> inhibitor, 7 nitroindazole (7 NI; 25 mg/kg), completely blocked cocaine induced <b>CPP</b>.
+NOS1	drug	cocaine	9721919	Mice deficient for the <strong>nNOS</strong> gene (homozygote <strong>nNOS</strong>( / ) mice) were resistant to <b>cocaine</b> induced CPP, while wild type <strong>nNOS</strong>(+/+) mice developed a marked CPP following <b>cocaine</b> administration.
+NOS1	addiction	reward	9721919	Mice deficient for the <strong>nNOS</strong> gene (homozygote <strong>nNOS</strong>( / ) mice) were resistant to cocaine induced <b>CPP</b>, while wild type <strong>nNOS</strong>(+/+) mice developed a marked <b>CPP</b> following cocaine administration.
+NOS1	drug	cocaine	9721919	Mice deficient for the <strong><strong>nNOS</strong></strong> gene (homozygote <strong><strong>nNOS</strong></strong>( / ) mice) were resistant to <b>cocaine</b> induced CPP, while wild type <strong><strong>nNOS</strong></strong>(+/+) mice developed a marked CPP following <b>cocaine</b> administration.
+NOS1	addiction	reward	9721919	Mice deficient for the <strong><strong>nNOS</strong></strong> gene (homozygote <strong><strong>nNOS</strong></strong>( / ) mice) were resistant to cocaine induced <b>CPP</b>, while wild type <strong><strong>nNOS</strong></strong>(+/+) mice developed a marked <b>CPP</b> following cocaine administration.
+NOS1	drug	cocaine	9721919	Both, the pharmacological and genetic manipulations of <strong>nNOS</strong> suggest that nitric oxide (NO) is involved in the rewarding properties of <b>cocaine</b>.
+NOS1	drug	cocaine	9721919	Both, the pharmacological and genetic manipulations of <strong><strong>nNOS</strong></strong> suggest that nitric oxide (NO) is involved in the rewarding properties of <b>cocaine</b>.
+NOS1	drug	amphetamine	9495865	We have recently reported that blockade of the neuronal nitric oxide synthase (<strong>nNOS</strong>) isoform by 7 nitroindazole provides protection against <b>METH</b> induced neurotoxicity in Swiss Webster mice.
+NOS1	drug	amphetamine	9495865	We have recently reported that blockade of the neuronal nitric oxide synthase (<strong><strong>nNOS</strong></strong>) isoform by 7 nitroindazole provides protection against <b>METH</b> induced neurotoxicity in Swiss Webster mice.
+NOS1	drug	amphetamine	9495865	The present study was undertaken to investigate the effect of a neurotoxic dose of <b>METH</b> on mutant mice lacking the <strong>nNOS</strong> gene [<strong>nNOS</strong>( / )] and wild type controls.
+NOS1	drug	amphetamine	9495865	The present study was undertaken to investigate the effect of a neurotoxic dose of <b>METH</b> on mutant mice lacking the <strong><strong>nNOS</strong></strong> gene [<strong><strong>nNOS</strong></strong>( / )] and wild type controls.
+NOS1	drug	amphetamine	9495865	Homozygote <strong>nNOS</strong>( / ), heterozygote <strong>nNOS</strong>(+/ ) and wild type animals were administered either saline or <b>METH</b> (5 mg/kg x 3).
+NOS1	drug	amphetamine	9495865	Homozygote <strong><strong>nNOS</strong></strong>( / ), heterozygote <strong><strong>nNOS</strong></strong>(+/ ) and wild type animals were administered either saline or <b>METH</b> (5 mg/kg x 3).
+NOS1	drug	amphetamine	9495865	This regimen of <b>METH</b> given to <strong>nNOS</strong>( / ) mice affected neither the tissue content of dopamine and its metabolites nor the number of DAT binding sites.
+NOS1	drug	amphetamine	9495865	This regimen of <b>METH</b> given to <strong><strong>nNOS</strong></strong>( / ) mice affected neither the tissue content of dopamine and its metabolites nor the number of DAT binding sites.
+NOS1	drug	amphetamine	9495865	<b>METH</b> induced hyperthermia was observed in all animal strains examined except the <strong>nNOS</strong>( / ) mice.
+NOS1	drug	amphetamine	9495865	<b>METH</b> induced hyperthermia was observed in all animal strains examined except the <strong><strong>nNOS</strong></strong>( / ) mice.
+NOS1	drug	amphetamine	9495865	A low dose of <b>METH</b> (1.0 mg/kg) administered to naive animals (<strong>nNOS</strong>( / ) and wild type) resulted in a similar intensity of locomotor stimulation.
+NOS1	drug	amphetamine	9495865	A low dose of <b>METH</b> (1.0 mg/kg) administered to naive animals (<strong><strong>nNOS</strong></strong>( / ) and wild type) resulted in a similar intensity of locomotor stimulation.
+NOS1	drug	amphetamine	9495865	However, 68 to 72 h after exposure to the high dose <b>METH</b> regimen, a marked sensitized responses to a challenge <b>METH</b> injection was observed in the wild type mice but not in the <strong>nNOS</strong>( / ) mice.
+NOS1	drug	amphetamine	9495865	However, 68 to 72 h after exposure to the high dose <b>METH</b> regimen, a marked sensitized responses to a challenge <b>METH</b> injection was observed in the wild type mice but not in the <strong><strong>nNOS</strong></strong>( / ) mice.
+NOS1	drug	amphetamine	9495865	Taken together, these results indicate that <strong>nNOS</strong>( / ) mice are protected against <b>METH</b> induced dopaminergic neurotoxicity and locomotor sensitization.
+NOS1	addiction	sensitization	9495865	Taken together, these results indicate that <strong>nNOS</strong>( / ) mice are protected against METH induced dopaminergic neurotoxicity and locomotor <b>sensitization</b>.
+NOS1	drug	amphetamine	9495865	Taken together, these results indicate that <strong><strong>nNOS</strong></strong>( / ) mice are protected against <b>METH</b> induced dopaminergic neurotoxicity and locomotor sensitization.
+NOS1	addiction	sensitization	9495865	Taken together, these results indicate that <strong><strong>nNOS</strong></strong>( / ) mice are protected against METH induced dopaminergic neurotoxicity and locomotor <b>sensitization</b>.
+NOS1	drug	amphetamine	9495865	It also appears that a partial deficit of dopaminergic transmission in wild type animals does not prevent the development of sensitization to <b>METH</b>, whereas a deficit in <strong>nNOS</strong> may attenuate this process.
+NOS1	addiction	sensitization	9495865	It also appears that a partial deficit of dopaminergic transmission in wild type animals does not prevent the development of <b>sensitization</b> to METH, whereas a deficit in <strong>nNOS</strong> may attenuate this process.
+NOS1	drug	amphetamine	9495865	It also appears that a partial deficit of dopaminergic transmission in wild type animals does not prevent the development of sensitization to <b>METH</b>, whereas a deficit in <strong><strong>nNOS</strong></strong> may attenuate this process.
+NOS1	addiction	sensitization	9495865	It also appears that a partial deficit of dopaminergic transmission in wild type animals does not prevent the development of <b>sensitization</b> to METH, whereas a deficit in <strong><strong>nNOS</strong></strong> may attenuate this process.
+BCL2	drug	amphetamine	32203791	We further examined ER stress related proteins and mitochondrial apoptosis pathway in the VTA and NAc, and found that <b>METH</b> increased the expressions of glucose regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and Bax, as same time decreased the expressions of procaspase12, <strong>Bcl 2</strong>, and procaspase3, while Trx 1 overexpression blocked these changes.
+BCL2	drug	amphetamine	32120831	Moreover, diminished expression of anti apoptotic proteins, including <strong>Bcl 2</strong>, Caspase3, Caspase7, and Caspase8 in <b>METH</b> exposed SH SY5y cells, was significantly recovered by treatment with lupenone.
+BCL2	drug	opioid	31680075	<b>Methadone</b> hydrochloride induced apoptosis in HL 60 cells involved upregulation of Bid and caspase 8 expression and downregulation of <strong>Bcl 2</strong>, p21 and survivin expression.
+BCL2	drug	amphetamine	31396089	Ad libitum HRW consumption also had an inhibitory effect on the <b>METH</b> induced increase in the expression of Bax/<strong>Bcl 2</strong>, cleaved caspase 3, glucose related protein 78 (GRP 78), CCAAT/enhancer binding protein homologous protein (CHOP), and p NF kB p65 expression and elevation of interleukin (IL) 6 and tumor necrosis factor (TNF) α levels in the hippocampus.
+BCL2	drug	alcohol	31171771	We recently showed that <b>ethanol</b> exposure can lead to pre mRNA missplicing of Mcl 1, a pro survival member of the <strong>Bcl 2</strong> family, by downregulating the expression levels of serine/arginine rich splicing factor 1 (SRSF1).
+BCL2	drug	amphetamine	30629943	<b>Methamphetamine</b> also increased <strong>Bcl 2</strong> protein levels in CPu of all the cohorts.
+BCL2	addiction	intoxication	29431616	Also, PXR dependent was the <b>binge</b> EtOH induced inhibition of hepatic Akr1b8 mRNA, and protein levels of aldehyde dehydrogenase (ALDH) 1A1 and anti apoptotic <strong>Bcl 2</strong>, but increased pro apoptotic Bax protein expression, leading to increases in residual EtOH concentration and the cellular oxidative stress marker, malondialdehyde.
+BCL2	drug	alcohol	28369910	Acute <b>ethanol</b> exposure induced autophagy mediated cardiac injury via activation of the ROS JNK <strong>Bcl 2</strong> pathway.
+BCL2	drug	alcohol	28369910	In addition, we found that <b>ethanol</b> induced autophagy and cardiac injury largely via the sequential triggering of reactive oxygen species (ROS) accumulation, activation of c Jun NH2 terminal kinase (JNK), phosphorylation of <strong>Bcl 2</strong>, and dissociation of the Beclin 1/<strong>Bcl 2</strong> complex.
+BCL2	drug	alcohol	28369910	In conclusion, our findings suggest that acute <b>ethanol</b> exposure induced autophagy mediated heart toxicity and injury mainly through the ROS JNK <strong>Bcl 2</strong> signaling pathway.
+BCL2	drug	alcohol	28095363	Furthermore, <b>alcohol</b> induced significant reduction were observed in reduced form of glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and CREB, BDNF and <strong>Bcl 2</strong> levels.
+BCL2	drug	alcohol	27628528	Moreover, bilateral microinjections of <b>ethanol</b> did not change the expression of either pro apoptotic (caspase 3 and Bax) or anti apoptotic (<strong>Bcl 2</strong>) proteins, suggesting that the dose was safe and validating the method used in the current study.
+BCL2	drug	opioid	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, Bax, <strong>Bcl 2</strong> and Caspase 3, of prefrontal cortex neurons in <b>morphine</b> relapse rats, an effective, successful <b>morphine</b> relapse rat model using the conditioned place preference (CPP) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+BCL2	addiction	relapse	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, Bax, <strong>Bcl 2</strong> and Caspase 3, of prefrontal cortex neurons in morphine <b>relapse</b> rats, an effective, successful morphine <b>relapse</b> rat model using the conditioned place preference (CPP) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+BCL2	addiction	reward	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, Bax, <strong>Bcl 2</strong> and Caspase 3, of prefrontal cortex neurons in morphine relapse rats, an effective, successful morphine relapse rat model using the conditioned place preference (<b>CPP</b>) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+BCL2	drug	opioid	27544013	The results showed that the expression of <strong>Bcl 2</strong> was very weak and those of Bax and Caspase 3 were hardly seen in group normal saline; the expressions of Bax and Caspase 3 were strong and that of <strong>Bcl 2</strong> was weak in group <b>morphine</b> and compared to group normal saline, there were significant differences (P<0.05); the expressions of Bax, Caspase 3 and the ratios of Bax/<strong>Bcl 2</strong> have a gradually decreased trend in the sequence of group 0.01μg, group 0.1μg and group 1.0μg, but the expression of <strong>Bcl 2</strong> has an opposite trend in the same sequence, and compared to group <b>morphine</b>, there were significant differences (P<0.05) excluding group 0.01μg.
+BCL2	drug	opioid	27544013	So we draw a conclusion that CCK 8 (0.1 and 1.0μg, i.c.v) could protect neurons of prefrontal cortex through up regulating the expression of <strong>Bcl 2</strong>, down regulating those of Bax and Caspase 3 and reducing Bax/<strong>Bcl 2</strong> ratio in the model of <b>morphine</b> relapse rats.
+BCL2	addiction	relapse	27544013	So we draw a conclusion that CCK 8 (0.1 and 1.0μg, i.c.v) could protect neurons of prefrontal cortex through up regulating the expression of <strong>Bcl 2</strong>, down regulating those of Bax and Caspase 3 and reducing Bax/<strong>Bcl 2</strong> ratio in the model of morphine <b>relapse</b> rats.
+BCL2	drug	nicotine	26909550	This effect correlated with the induction of <strong>Bcl 2</strong>, Bax, Survivin and Caspase 3 by <b>nicotine</b> in gastric cell lines.
+BCL2	drug	alcohol	26266540	In the present study, we used human embryonic stem cell (hESC) derived cortical neurons as in vitro cellular models to investigate <b>alcohol</b> induced expression changes of genes involved in <b>alcohol</b> metabolism (ALDH2), anti apoptosis (<strong>BCL2</strong> and CCND2), neurotransmission (NMDA receptor subunit genes: GRIN1, GRIN2A, GRIN2B, and GRIN2D), calcium channel activity (ITPR2), or transcriptional repression (JARID2).
+BCL2	drug	alcohol	26266540	In the present study, we used human embryonic stem cell (hESC) derived cortical neurons as in vitro cellular models to investigate <b>alcohol</b> induced expression changes of genes involved in <b>alcohol</b> metabolism (ALDH2), anti apoptosis (<strong><strong>BCL2</strong></strong> and CCND2), neurotransmission (NMDA receptor subunit genes: GRIN1, GRIN2A, GRIN2B, and GRIN2D), calcium channel activity (ITPR2), or transcriptional repression (JARID2).
+BCL2	drug	alcohol	26266540	After a 7 day <b>ethanol</b> (50 mM) exposure followed by a 24 hour <b>ethanol</b> withdrawal treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93 fold, P = 0.003; GRIN2A: 1.40 fold, P = 0.003; GRIN2B: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; <strong>BCL2</strong>: 1.34 fold, P = 0.031), and the results of GRIN1, GRIN2A, and GRIN2B survived multiple comparison correction.
+BCL2	addiction	withdrawal	26266540	After a 7 day ethanol (50 mM) exposure followed by a 24 hour ethanol <b>withdrawal</b> treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93 fold, P = 0.003; GRIN2A: 1.40 fold, P = 0.003; GRIN2B: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; <strong>BCL2</strong>: 1.34 fold, P = 0.031), and the results of GRIN1, GRIN2A, and GRIN2B survived multiple comparison correction.
+BCL2	drug	alcohol	26266540	After a 7 day <b>ethanol</b> (50 mM) exposure followed by a 24 hour <b>ethanol</b> withdrawal treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93 fold, P = 0.003; GRIN2A: 1.40 fold, P = 0.003; GRIN2B: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; <strong><strong>BCL2</strong></strong>: 1.34 fold, P = 0.031), and the results of GRIN1, GRIN2A, and GRIN2B survived multiple comparison correction.
+BCL2	addiction	withdrawal	26266540	After a 7 day ethanol (50 mM) exposure followed by a 24 hour ethanol <b>withdrawal</b> treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93 fold, P = 0.003; GRIN2A: 1.40 fold, P = 0.003; GRIN2B: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; <strong><strong>BCL2</strong></strong>: 1.34 fold, P = 0.031), and the results of GRIN1, GRIN2A, and GRIN2B survived multiple comparison correction.
+BCL2	drug	opioid	25850855	In addition, <b>morphine</b> upregulated LPS induced Beclin1 level, but downregulated <strong>Bcl 2</strong> level.
+BCL2	drug	psychedelics	25748203	In addition, <b>ketamine</b> induced the expression of Bax, cytochrome c and capase 3, but inhibited the expression of NF κB and <strong>bcl 2</strong>.
+BCL2	drug	opioid	25712644	The results showed that <b>morphine</b> significantly increased lipid peroxidation, mitochondrial GSH level, concentration of Bax; caspase 3 and caspase 9 activities while decreasing <strong>Bcl 2</strong> concentration.
+BCL2	drug	alcohol	25623404	Apoptotic cell death and temporal expression of apoptotic proteins <strong>Bcl 2</strong> and Bax in the hippocampus, following binge <b>ethanol</b> in the neonatal rat model.
+BCL2	addiction	intoxication	25623404	Apoptotic cell death and temporal expression of apoptotic proteins <strong>Bcl 2</strong> and Bax in the hippocampus, following <b>binge</b> ethanol in the neonatal rat model.
+BCL2	addiction	intoxication	25623404	Western blot analysis determined expression of pro apoptotic Bax and anti apoptotic <strong>Bcl 2</strong>, 12, 24, and 48 hours after <b>binge</b> EtOH exposure on PN6.
+BCL2	addiction	intoxication	25623404	<b>Binge</b> EtOH exposure on PN6 resulted in a significant increase in expression of <strong>Bcl 2</strong> and the <strong>Bcl 2</strong>:Bax ratio in the CA1/DG region at 24 hours after EtOH exposure on PN6.
+BCL2	addiction	intoxication	25623404	This finding may be explained in part by changes in the <strong>Bcl 2</strong>:Bax ratio after a single <b>binge</b> EtOH exposure.
+BCL2	drug	amphetamine	25463524	In addition, <b>methamphetamine</b> enhanced expression of anti apoptotic protein <strong>Bcl 2</strong> and reduced pro apoptotic protein Bax levels in the ventral hippocampus, suggesting a mechanism for reducing cell death.
+BCL2	drug	amphetamine	25463524	These data reveal that alterations in <strong>Bcl 2</strong> and Bax levels by <b>methamphetamine</b> were not associated with enhanced Akt expression.
+BCL2	drug	opioid	24959978	In this study, we investigated the effects of <b>morphine</b> induced conditioned place preference (CPP) in the presence and absence of stress on the changes of apoptotic factors (Bax/<strong>Bcl 2</strong> ratio, caspase 3 activation and PARP degradation) in the MCL system.
+BCL2	addiction	reward	24959978	In this study, we investigated the effects of morphine induced conditioned place preference (<b>CPP</b>) in the presence and absence of stress on the changes of apoptotic factors (Bax/<strong>Bcl 2</strong> ratio, caspase 3 activation and PARP degradation) in the MCL system.
+BCL2	drug	opioid	24959978	In the <b>morphine</b> treated animals, AS and SS increased apoptotic factors remarkably (except for the Bax/<strong>Bcl 2</strong> ratio after AS and SS in the Str and caspase 3 activation after AS in the NAc) and also decreased conditioning scores.
+BCL2	drug	opioid	24906198	We found that chronic exposure to <b>morphine</b> impaired spatial and aversive memory and remarkably suppressed the expression of <strong>Bcl 2</strong>, but Bax expression remained constant.
+BCL2	addiction	aversion	24906198	We found that chronic exposure to morphine impaired spatial and <b>aversive</b> memory and remarkably suppressed the expression of <strong>Bcl 2</strong>, but Bax expression remained constant.
+BCL2	drug	opioid	24906198	Both voluntary and treadmill exercise alleviated memory impairment, increased the expression of <strong>Bcl 2</strong> protein, and only the later suppressed the expression of Bax protein in <b>morphine</b> dependent animals.
+BCL2	drug	opioid	24281942	In the HPC, <b>morphine</b> significantly increased the ratio of Bax/<strong>Bcl 2</strong>, caspases 3, and PARP by the lowest dose (0.5 mg/kg), but, in the VTA, a considerable increase was seen in the dose of 5 mg/kg; promotion of apoptotic factors in the HPC and VTA insinuates that <b>morphine</b> can affect the molecular mechanisms that interfere with apoptosis through different receptors.
+BCL2	drug	opioid	24096212	In the NAc, <b>morphine</b> significantly increased the Bax/<strong>Bcl 2</strong> ratio, caspase3 and PARP in the lowest dose (0.5mg/kg) but in the PFC considerable increase was seen in dose of 5mg/kg.
+BCL2	drug	alcohol	23981442	Twenty four of the differentially regulated genes were previously identified by genome wide association studies of <b>alcohol</b> use disorders; this raises the potential interest of genes not normally associated with <b>alcoholism</b>, such as suppression of tumorigenicity 18 (ST18), <strong>BCL2</strong> associated athanogene 3 (BAG3), and von Willebrand factor (VWF).
+BCL2	drug	alcohol	23981442	Twenty four of the differentially regulated genes were previously identified by genome wide association studies of <b>alcohol</b> use disorders; this raises the potential interest of genes not normally associated with <b>alcoholism</b>, such as suppression of tumorigenicity 18 (ST18), <strong><strong>BCL2</strong></strong> associated athanogene 3 (BAG3), and von Willebrand factor (VWF).
+BCL2	drug	opioid	23936592	This study aimed to investigate neuronal apoptosis and expression of apoptosis related proteins (Fas, Caspase 3 and <strong>Bcl 2</strong>) in the brain of rates with <b>morphine</b> addiction.
+BCL2	addiction	addiction	23936592	This study aimed to investigate neuronal apoptosis and expression of apoptosis related proteins (Fas, Caspase 3 and <strong>Bcl 2</strong>) in the brain of rates with morphine <b>addiction</b>.
+BCL2	addiction	addiction	23936592	When compared with the control group, the proportion of apoptotic neurons increased significantly in the <b>addiction</b> group and the abstinence group (P<0.01), accompanied by significantly increased expressions of Fas and Caspase 3 (P<0.01) and markedly decreased <strong>Bcl 2</strong> expression (P<0.01) in the hippocampuse.
+BCL2	drug	opioid	23936592	Long term use of <b>morphine</b> can induce neuronal apoptosis in the brain by increasing the expressions of pro apoptotic Fas and Caspase 3 and decreasing the anti apoptotic <strong>Bcl 2</strong> expression, which might be one of mechanisms underlying the opiate induced neuronal damage.
+BCL2	drug	alcohol	23735546	Influence of acute <b>ethanol</b> intoxication on neuronal apoptosis and <strong>Bcl 2</strong> protein expression after severe traumatic brain injury in rats.
+BCL2	addiction	intoxication	23735546	Influence of acute ethanol <b>intoxication</b> on neuronal apoptosis and <strong>Bcl 2</strong> protein expression after severe traumatic brain injury in rats.
+BCL2	drug	psychedelics	23508639	There was a significant increase in Bax protein expression in the <b>MDMA</b>+SCH group and a significant decrease in <strong>Bcl 2</strong> protein expression in the <b>MDMA</b>+SCH group (p<0.05).
+BCL2	drug	psychedelics	23508639	A2A receptors have a role in the apoptotic effects of <b>MDMA</b> via the Bax and <strong>Bcl 2</strong> pathways.
+BCL2	addiction	reward	27385959	In this study, the effects of acute and subchronic stress on the changes in apoptotic factors (Bax/<strong>Bcl 2</strong> ratio, caspase 3 activation and PARP degradation) in the HYP and HIP during conditioned place preference (<b>CPP</b>) paradigm were evaluated.
+BCL2	drug	opioid	27385959	On the other hand, in the HIP, Bax/<strong>Bcl 2</strong> ratio in saline treated animals increased significantly during AS and SS, while in <b>morphine</b> treated animals this ratio did not have any significant alteration during AS and was decreased during SS compared with <b>morphine</b> control group.
+BCL2	drug	amphetamine	23056363	We also evaluated the striatal expression of the pro apoptotic BAX and anti apoptotic <strong>Bcl 2</strong> proteins, which are known to mediate <b>methamphetamine</b> induced apoptotic effects.
+BCL2	drug	amphetamine	23056363	Modafinil also counteracted the decrease in tyrosine hydroxylase and dopamine transporter levels and prevented <b>methamphetamine</b> induced increases in the pro apoptotic BAX and decreases in the anti apoptotic <strong>Bcl 2</strong> protein expression.
+BCL2	addiction	reward	23041599	Measures to reduce the ongoing apoptosis of osteocytes require <b>reinforcing</b> the effects of members of the <strong>Bcl 2</strong> family (<strong>Bcl 2</strong> itself and Mcl 1), the Wnt/catenin pathways (using an available sclerostin antibody) and HSPs (by application of local heat using US, deep wave diathermy or infrared), as well as administration of bisphosphonates and nitrates.
+BCL2	drug	opioid	22210043	Protein expression of cleaved caspase 3 and Bax decreased, whereas <strong>Bcl 2</strong> protein levels in hippocampus increased with exogenous H(2)S. Exogenous H(2)S alleviated <b>heroin</b> induced rat hippocampal damage through antioxidant and antiapoptosis effects.
+BCL2	drug	amphetamine	22174933	Importantly, <b>METH</b> caused decreases in the mitochondrial anti apoptotic protein, <strong>Bcl 2</strong>, but increases in the pro apoptotic proteins, Bax, Bad and cytochrome c, in a SCH23390 sensitive fashion.
+BCL2	drug	opioid	21560342	[The expression of <strong>Bcl 2</strong> and Bax in the <b>morphine</b> dependence on male rat germ cell].
+BCL2	addiction	dependence	21560342	[The expression of <strong>Bcl 2</strong> and Bax in the morphine <b>dependence</b> on male rat germ cell].
+BCL2	drug	opioid	21559519	<b>Morphine</b> caused a dramatic decrease in <strong>Bcl 2</strong> level but increase in Bax level in wild type microglia, but not in TLR9 deficient microglia.
+BCL2	drug	opioid	21483469	Enhanced toxicity by Tat and <b>morphine</b> was accompanied by increased numbers of TUNEL positive apoptotic neurons, elevated caspase 3 levels and decreased ratio of anti  and pro apoptotic proteins, <strong>Bcl2</strong>/Bax.
+BCL2	drug	opioid	21483469	Enhanced toxicity by Tat and <b>morphine</b> was accompanied by increased numbers of TUNEL positive apoptotic neurons, elevated caspase 3 levels and decreased ratio of anti  and pro apoptotic proteins, <strong><strong>Bcl2</strong></strong>/Bax.
+BCL2	drug	nicotine	20727180	While low concentrations of <b>nicotine</b> induced activation of NF κB, Akt, <strong>Bcl2</strong>, MAPKs, AP1 and IAPs in H1299, it failed to induce NF κB in A549, and compared to H1299, almost 100 times higher concentration of <b>nicotine</b> was required to induce all other survival signals in A549.
+BCL2	drug	nicotine	20727180	While low concentrations of <b>nicotine</b> induced activation of NF κB, Akt, <strong><strong>Bcl2</strong></strong>, MAPKs, AP1 and IAPs in H1299, it failed to induce NF κB in A549, and compared to H1299, almost 100 times higher concentration of <b>nicotine</b> was required to induce all other survival signals in A549.
+BCL2	drug	opioid	20190558	<b>Morphine</b> increases Beclin 1 expression and reduces the interaction between Beclin 1 and <strong>Bcl 2</strong>, thus releasing Beclin 1 for its pro autophagic activity.
+BCL2	drug	opioid	20190558	<strong>Bcl 2</strong> overexpression inhibits <b>morphine</b> induced autophagy, whereas knockdown of Beclin 1 or knockout of ATG5 prevents <b>morphine</b> induced autophagy.
+BCL2	drug	alcohol	20090911	Myocardium from <b>ethanol</b> treated mice displayed enhanced Bax, Caspase 3 and decreased <strong>Bcl 2</strong> expression, the effect of which with the exception of Caspase 3 was augmented by ADH.
+BCL2	drug	nicotine	19911375	Interestingly, a week after the exposure to <b>nicotine</b> or <b>nicotine</b> plus NNK, <strong>Bcl 2</strong> expression was augmented, accompanied with the increased resistance to cisplatin induced apoptosis.
+BCL2	drug	cocaine	19879923	This study was conducted to determine how repeated exposure to <b>cocaine</b> phosphorylates B cell leukemia/lymphoma 2 (<strong>Bcl2</strong>), which may be responsible for the regulation of behavioral alterations in the rat dorsal striatum.
+BCL2	drug	cocaine	19879923	This study was conducted to determine how repeated exposure to <b>cocaine</b> phosphorylates B cell leukemia/lymphoma 2 (<strong><strong>Bcl2</strong></strong>), which may be responsible for the regulation of behavioral alterations in the rat dorsal striatum.
+BCL2	drug	cocaine	19879923	The results revealed that repeated systemic injections of <b>cocaine</b> (20 mg/kg) once a day for 7 consecutive days increased the phosphorylation of <strong>Bcl2</strong> at serine 70 (<strong>Bcl2</strong> S70).
+BCL2	drug	cocaine	19879923	The results revealed that repeated systemic injections of <b>cocaine</b> (20 mg/kg) once a day for 7 consecutive days increased the phosphorylation of <strong><strong>Bcl2</strong></strong> at serine 70 (<strong><strong>Bcl2</strong></strong> S70).
+BCL2	drug	cocaine	19879923	In addition, elevation of behavioral locomotor activity after repeated exposure to <b>cocaine</b> was partially reduced by the inhibition of <strong>Bcl2</strong>.
+BCL2	drug	cocaine	19879923	In addition, elevation of behavioral locomotor activity after repeated exposure to <b>cocaine</b> was partially reduced by the inhibition of <strong><strong>Bcl2</strong></strong>.
+BCL2	drug	cocaine	19879923	These data suggest that stimulation of dopamine D1 receptors, group I mGluRs, and NMDA receptors following repeated <b>cocaine</b> administration is necessary for the induction of <strong>Bcl2</strong> S70 phosphorylation, which contributes to the expression of behavioral sensitization.
+BCL2	addiction	sensitization	19879923	These data suggest that stimulation of dopamine D1 receptors, group I mGluRs, and NMDA receptors following repeated cocaine administration is necessary for the induction of <strong>Bcl2</strong> S70 phosphorylation, which contributes to the expression of behavioral <b>sensitization</b>.
+BCL2	drug	cocaine	19879923	These data suggest that stimulation of dopamine D1 receptors, group I mGluRs, and NMDA receptors following repeated <b>cocaine</b> administration is necessary for the induction of <strong><strong>Bcl2</strong></strong> S70 phosphorylation, which contributes to the expression of behavioral sensitization.
+BCL2	addiction	sensitization	19879923	These data suggest that stimulation of dopamine D1 receptors, group I mGluRs, and NMDA receptors following repeated cocaine administration is necessary for the induction of <strong><strong>Bcl2</strong></strong> S70 phosphorylation, which contributes to the expression of behavioral <b>sensitization</b>.
+BCL2	drug	psychedelics	19579000	<b>Ketamine</b> withdrawal has no effect on the expression of VEGF, MMP2, or <strong>BCL 2</strong>.
+BCL2	addiction	withdrawal	19579000	Ketamine <b>withdrawal</b> has no effect on the expression of VEGF, MMP2, or <strong>BCL 2</strong>.
+BCL2	drug	psychedelics	19579000	The findings indicate a promoting effect of risperidone and haloperidol on survival of young neurons in the hippocampus by enhancing the expression of the anti apoptotic protein <strong>BCL 2</strong> and by activation of VEGF/MMP2, whereby an interference with <b>ketamine</b> and thus a priority role of the NMDA system was not evident.
+BCL2	drug	opioid	18928115	EA at "Zusanli" (ST 36) can inhibit <b>morphine</b> induced downregulation of <strong>Bcl 2</strong> and upregulation of Fas and FasL expression, which may contribute to its effect in resisting thymus apoptosis in <b>morphine</b> withdrawal rats.
+BCL2	addiction	withdrawal	18928115	EA at "Zusanli" (ST 36) can inhibit morphine induced downregulation of <strong>Bcl 2</strong> and upregulation of Fas and FasL expression, which may contribute to its effect in resisting thymus apoptosis in morphine <b>withdrawal</b> rats.
+BCL2	drug	nicotine	18705409	Statistically significant associations between high Ki67 and poorly differentiated tumors (P = 0.016) and a <b>smoking</b> history (P = 0.053); p53 positivity and high Ki67 (P = 0.002); HER 2 positivity and adenocarcinoma subtype (P = 0.015) and presence of lymph node involvement (P = 0.006); and <strong>Bcl 2</strong> positivity and squamous cell carcinoma subtype (P = 0.058) were observed.
+BCL2	drug	opioid	17384938	This study analyzes the effects of prolonged administration of <b>methadone</b> and withdrawal on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and caspase 8) and the mitochondrial (<strong>Bcl 2</strong>, Bcl x(L), Bad, and Bax) apoptotic pathways.
+BCL2	addiction	withdrawal	17384938	This study analyzes the effects of prolonged administration of methadone and <b>withdrawal</b> on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and caspase 8) and the mitochondrial (<strong>Bcl 2</strong>, Bcl x(L), Bad, and Bax) apoptotic pathways.
+BCL2	drug	opioid	17250679	Nonetheless, in street <b>heroin</b> treated cortical neurons, cytochrome c was released, accompanied by a decrease in mitochondrial potential and <strong>Bcl 2</strong>/Bax.
+BCL2	drug	amphetamine	17161385	Finally, the <b>METH</b> injection was associated with increased expression of the proapoptotic proteins, Bax and Bid, but with decreased expression of the antideath protein, <strong>Bcl2</strong>.
+BCL2	drug	amphetamine	17161385	Finally, the <b>METH</b> injection was associated with increased expression of the proapoptotic proteins, Bax and Bid, but with decreased expression of the antideath protein, <strong><strong>Bcl2</strong></strong>.
+BCL2	drug	alcohol	17008791	In vitro induction of apoptosis in U937 cells by perillyl <b>alcohol</b> with sensitization by pentoxifylline: increased <strong>BCL 2</strong> and BAX protein expression.
+BCL2	addiction	sensitization	17008791	In vitro induction of apoptosis in U937 cells by perillyl alcohol with <b>sensitization</b> by pentoxifylline: increased <strong>BCL 2</strong> and BAX protein expression.
+BCL2	drug	nicotine	15785859	Expression levels of Rab2, a G protein, and Bag 1, a <strong>Bcl 2</strong> binding protein are controlled by withdrawal of <b>nicotine</b> from cultured pheochromocytoma PC12 cells.
+BCL2	addiction	withdrawal	15785859	Expression levels of Rab2, a G protein, and Bag 1, a <strong>Bcl 2</strong> binding protein are controlled by <b>withdrawal</b> of nicotine from cultured pheochromocytoma PC12 cells.
+BCL2	drug	nicotine	15785859	Considering the neuroprotective effect of <b>nicotine</b>, we also examined the level of Bag 1 protein, which is a binding protein for <strong>Bcl 2</strong>, an anti apoptotic factor, and found a slight increase in the gene expression of Bag 1 following <b>nicotine</b> withdrawal.
+BCL2	addiction	withdrawal	15785859	Considering the neuroprotective effect of nicotine, we also examined the level of Bag 1 protein, which is a binding protein for <strong>Bcl 2</strong>, an anti apoptotic factor, and found a slight increase in the gene expression of Bag 1 following nicotine <b>withdrawal</b>.
+BCL2	drug	cannabinoid	15545023	Finally, <b>cannabinoids</b> might also be involved in the apoptotic death that occurs during brain development, possibly by influencing the expression of <strong>Bcl 2</strong>/Bax system.
+BCL2	drug	alcohol	12876071	Acute and chronic effects of <b>alcohol</b> exposure on skeletal muscle c myc, p53, and <strong>Bcl 2</strong> mRNA expression.
+BCL2	drug	alcohol	12876071	We hypothesized that 1) increases in c myc mRNA levels also occur in muscle exposed chronically to <b>alcohol</b>, 2) muscle of female rats is more sensitive than that from male rats, 3) raising acetaldehyde will also increase c myc, 4) prior starvation will cause further increases in c myc mRNA expression in response to <b>ethanol</b>, and 5) other genes involved in apoptosis (i.e., p53 and <strong>Bcl 2</strong>) would also be affected by <b>alcohol</b>.
+BCL2	drug	alcohol	12876071	The results showed that 1) in male rats fed <b>ethanol</b> chronically, there were no increases in c myc mRNA; 2) increases, however, occurred in c myc mRNA in muscle from female rats fed <b>ethanol</b> chronically; 3) raising endogenous acetaldehyde with cyanamide increased c myc mRNA in acute studies; 4) starvation per se increased c myc mRNA levels and at 1 day potentiated the acute effects of <b>ethanol</b>, indicative of a sensitization response; 5) the only effect seen with p53 mRNA levels was a decrease in muscle of rats starved for 1 day compared with fed rats, and there was no statistically significant effect on <strong>Bcl 2</strong> mRNA in any of the experimental conditions.
+BCL2	addiction	sensitization	12876071	The results showed that 1) in male rats fed ethanol chronically, there were no increases in c myc mRNA; 2) increases, however, occurred in c myc mRNA in muscle from female rats fed ethanol chronically; 3) raising endogenous acetaldehyde with cyanamide increased c myc mRNA in acute studies; 4) starvation per se increased c myc mRNA levels and at 1 day potentiated the acute effects of ethanol, indicative of a <b>sensitization</b> response; 5) the only effect seen with p53 mRNA levels was a decrease in muscle of rats starved for 1 day compared with fed rats, and there was no statistically significant effect on <strong>Bcl 2</strong> mRNA in any of the experimental conditions.
+BCL2	drug	benzodiazepine	12730627	Reversal of <strong>Bcl 2</strong> mediated resistance of the EW36 human B cell lymphoma cell line to arsenite  and pesticide induced apoptosis by PK11195, a ligand of the mitochondrial <b>benzodiazepine</b> receptor.
+BCL2	drug	alcohol	12603597	<b>Ethanol</b> decreased Jurkat cell expression of <strong>Bcl 2</strong>, whereas <b>ethanol</b> increased Jurkat cell expression of Bax.
+BCL2	addiction	intoxication	12603597	In in vivo studies, after <b>binge</b> drinking, T cell expression of <strong>Bcl 2</strong> also decreased.
+BCL2	drug	alcohol	12043192	Changes of <strong>bcl 2</strong> and bax mRNA expressions in the <b>ethanol</b> treated mouse brain.
+BCL2	drug	alcohol	12043192	To characterize the biochemical mechanism of cell death induced by <b>ethanol</b> intoxication, we examined expression of mRNAs of <strong>bcl 2</strong> and bax genes in the brain, which are related to apoptosis, by using the reverse transcription polymerase chain reaction method (RT PCR).
+BCL2	addiction	intoxication	12043192	To characterize the biochemical mechanism of cell death induced by ethanol <b>intoxication</b>, we examined expression of mRNAs of <strong>bcl 2</strong> and bax genes in the brain, which are related to apoptosis, by using the reverse transcription polymerase chain reaction method (RT PCR).
+BCL2	drug	alcohol	12043192	According to <b>ethanol</b> administrations, the expression of <strong>bcl 2</strong> mRNA in the cerebral cortex decreased after 1 day and be recovered after 3 days.
+BCL2	drug	alcohol	12043192	We found that <strong>bcl 2</strong> or bax mRNA expressions in the brain were changed after short term <b>ethanol</b> exposure.
+BCL2	drug	alcohol	12043192	These results suggest that <strong>bcl 2</strong> or bax may have functional significance about <b>ethanol</b> intoxication.
+BCL2	addiction	intoxication	12043192	These results suggest that <strong>bcl 2</strong> or bax may have functional significance about ethanol <b>intoxication</b>.
+BCL2	drug	opioid	10693926	Finally, <b>opioids</b> prevented the elevation of the <strong>Bcl 2</strong> and Bak proteins following serum deprivation to the levels attained by serum supplementation.
+BCL2	drug	opioid	10534122	<b>Morphine</b> treated Jurkat cells also showed a decreased expression of <strong>bcl 2</strong> and an enhanced expression of bax.
+BCL2	drug	opioid	10355747	Exposure of 'variant' small cell lung carcinoma (SCLC) and non SCLC cells, which secrete low concentrations (< 0.01 pmol/mg protein) of bombesin, to nanomolar concentrations of <b>methadone</b> resulted in increased levels of mitogen activated protein (MAP) kinase phosphatases and inactivation of MAP kinase, suppression of the <strong>bcl 2</strong> protein, and induction of apoptosis.
+BCL2	drug	nicotine	9600337	The present study provides evidence that <b>nicotine</b> (a) activates the mitogen activated protein (MAP) kinase signalling pathway in lung cancer cells, specifically extracellular signal regulated kinase (ERK2), resulting in increased expression of the <strong>bcl 2</strong> protein and inhibition of apoptosis in these cells; and (b) blocks the inhibition of protein kinase C (PKC) and ERK2 activity in lung cancer cells by anti cancer agents, such as therapeutic opioid drugs, and thus can adversely affect cancer therapy.
+BCL2	drug	opioid	9600337	The present study provides evidence that nicotine (a) activates the mitogen activated protein (MAP) kinase signalling pathway in lung cancer cells, specifically extracellular signal regulated kinase (ERK2), resulting in increased expression of the <strong>bcl 2</strong> protein and inhibition of apoptosis in these cells; and (b) blocks the inhibition of protein kinase C (PKC) and ERK2 activity in lung cancer cells by anti cancer agents, such as therapeutic <b>opioid</b> drugs, and thus can adversely affect cancer therapy.
+IGBP1	addiction	dependence	26440539	We identified genome wide significant association in the <strong>alpha 4</strong> nicotinic receptor subunit (CHRNA4) gene on chromosome 20q13: lowest P=8.0 × 10( 9) across all the samples for rs2273500 C (frequency=0.15; odds ratio=1.12 and 95% confidence interval=1.08 1.17 for severe vs mild <b>dependence</b>).
+IGBP1	drug	nicotine	26451072	Gamma aminobutyric acid B receptor 2 (GABBR2), dopa decarboxylase (DDC), and cholinergic receptor nicotinic <strong>alpha 4</strong> (CHRNA4) are three examples of genes that have previously shown strong associations with <b>nicotine</b> dependence.
+IGBP1	addiction	dependence	26451072	Gamma aminobutyric acid B receptor 2 (GABBR2), dopa decarboxylase (DDC), and cholinergic receptor nicotinic <strong>alpha 4</strong> (CHRNA4) are three examples of genes that have previously shown strong associations with nicotine <b>dependence</b>.
+IGBP1	drug	nicotine	21740768	Association of nicotinic acetylcholine receptor subunit <strong>alpha 4</strong> polymorphisms with <b>smoking</b> behaviors in Chinese male <b>smokers</b>.
+IGBP1	drug	nicotine	21683344	Rare nonsynonymous variants in <strong>alpha 4</strong> nicotinic acetylcholine receptor gene protect against <b>nicotine</b> dependence.
+IGBP1	addiction	dependence	21683344	Rare nonsynonymous variants in <strong>alpha 4</strong> nicotinic acetylcholine receptor gene protect against nicotine <b>dependence</b>.
+IGBP1	drug	nicotine	21683344	Several studies report association of <strong>alpha 4</strong> nicotinic acetylcholine receptors (encoded by CHRNA4) with <b>nicotine</b> dependence (ND).
+IGBP1	addiction	dependence	21683344	Several studies report association of <strong>alpha 4</strong> nicotinic acetylcholine receptors (encoded by CHRNA4) with nicotine <b>dependence</b> (ND).
+IGBP1	drug	nicotine	21267362	Studies suggest that the <strong>alpha 4</strong> beta 2 <b>nicotine</b> acetylcholine receptor subtype is the main receptor that mediates <b>nicotine</b> dependence.
+IGBP1	addiction	dependence	21267362	Studies suggest that the <strong>alpha 4</strong> beta 2 nicotine acetylcholine receptor subtype is the main receptor that mediates nicotine <b>dependence</b>.
+IGBP1	drug	nicotine	20829327	Varenicline, a partial <strong>alpha 4</strong> beta 2 nicotinic receptor agonist, could be a solution to help former <b>smokers</b> to stop long term use of <b>nicotine</b> gums or lozenges.
+IGBP1	drug	nicotine	20114055	Structural differences determine the relative selectivity of nicotinic compounds for native <strong>alpha 4</strong> beta 2* , alpha 6 beta 2* , alpha 3 beta 4*  and alpha 7 <b>nicotine</b> acetylcholine receptors.
+IGBP1	drug	nicotine	20114055	Among known subtypes of receptors, <strong>alpha 4</strong> beta 2* and alpha 6 beta 2* nAChR have the highest affinity for <b>nicotine</b> (where * indicates possibility of other subunits).
+IGBP1	drug	nicotine	19693267	Analysis of the genotyping data identified two single nucleotide polymorphisms (SNPs) in the gene encoding the <strong>alpha 4</strong> <b>nicotine</b> receptor (CHRNA4, rs4603829 and rs4522666) that are significantly associated with harm avoidance, a risk attitude measurement drawn from the psychology literature.
+IGBP1	drug	nicotine	19482438	Association of genes coding for the <strong>alpha 4</strong>, alpha 5, beta 2 and beta 3 subunits of nicotinic receptors with cigarette <b>smoking</b> and <b>nicotine</b> dependence.
+IGBP1	addiction	dependence	19482438	Association of genes coding for the <strong>alpha 4</strong>, alpha 5, beta 2 and beta 3 subunits of nicotinic receptors with cigarette smoking and nicotine <b>dependence</b>.
+IGBP1	drug	nicotine	19482438	We assessed whether <b>smoking</b> behavior was associated with nine polymorphisms in genes coding for the nicotinic receptor subunits <strong>alpha 4</strong> (rs1044394, rs1044396, rs2236196 and rs2273504), alpha 5 (rs16969968), beta 2 (rs2072661 and rs4845378) and beta 3 (rs4953 and rs6474413).We conducted an Internet survey and collected saliva by mail for DNA and cotinine analyses, in Switzerland in 2003.
+IGBP1	drug	nicotine	19290018	Association of nicotinic acetylcholine receptor subunit <strong>alpha 4</strong> polymorphisms with <b>nicotine</b> dependence in 5500 Germans.
+IGBP1	addiction	dependence	19290018	Association of nicotinic acetylcholine receptor subunit <strong>alpha 4</strong> polymorphisms with nicotine <b>dependence</b> in 5500 Germans.
+IGBP1	drug	nicotine	19290018	Polymorphisms in the CHRNA4 gene coding the nicotinic acetylcholine receptor subunit <strong>alpha 4</strong> have recently been suggested to play a role in the determination of <b>smoking</b> related phenotypes.
+IGBP1	drug	nicotine	18798299	The objective of this study was to evaluate the efficacy of varenicline, a novel partial agonist at <strong>alpha 4</strong> beta 2 and full agonist at alpha 7 nicotinic acetylcholine receptor (nAChR) subtypes, in blocking the locomotor effects of acute or repeated treatments with <b>nicotine</b> (0.4 mg/kg, s.c.) in rats.
+IGBP1	drug	nicotine	18797314	Regional differential effects of chronic <b>nicotine</b> on brain <strong>alpha 4</strong> containing and alpha 6 containing receptors.
+IGBP1	drug	nicotine	17712039	<b>Nicotine</b> responses in hypersensitive and knockout <strong>alpha 4</strong> mice account for tolerance to both hypothermia and locomotor suppression in wild type mice.
+IGBP1	drug	nicotine	17712039	Nicotinic receptors containing the <strong>alpha 4</strong> subunit (<strong>alpha 4</strong>* nAChRs) have high sensitivity and are widely expressed in the central nervous system, yet their contributions to behavioral tolerance, a hallmark of <b>nicotine</b> dependence, are unclear.
+IGBP1	addiction	dependence	17712039	Nicotinic receptors containing the <strong>alpha 4</strong> subunit (<strong>alpha 4</strong>* nAChRs) have high sensitivity and are widely expressed in the central nervous system, yet their contributions to behavioral tolerance, a hallmark of nicotine <b>dependence</b>, are unclear.
+IGBP1	drug	nicotine	17712039	To evaluate the contribution of <strong>alpha 4</strong>* and non <strong>alpha 4</strong> nAChRs in the development of tolerance to hypothermia and locomotor suppression, <strong>alpha 4</strong> knockout (KO), hypersensitive Leu9'Ala <strong>alpha 4</strong> knock in, and wild type (WT) mice received daily <b>nicotine</b> injections, and their behaviors were compared.
+IGBP1	drug	nicotine	17712039	In addition, daily selective activation of <strong>alpha 4</strong>* nAChRs elicited locomotor activation in Leu9'Ala mice, but <b>nicotine</b> suppressed activity in <strong>alpha 4</strong> KO mice and this did not change with daily drug exposure.
+IGBP1	drug	nicotine	17670967	Chronic <b>nicotine</b> cell specifically upregulates functional <strong>alpha 4</strong>* nicotinic receptors: basis for both tolerance in midbrain and enhanced long term potentiation in perforant path.
+IGBP1	drug	nicotine	17584502	These results indicate that beta2 containing nAChRs, such as the <strong>alpha 4</strong> beta 2 receptor, mediate <b>nicotine</b> withdrawal deficits in contextual fear conditioning.
+IGBP1	addiction	withdrawal	17584502	These results indicate that beta2 containing nAChRs, such as the <strong>alpha 4</strong> beta 2 receptor, mediate nicotine <b>withdrawal</b> deficits in contextual fear conditioning.
+IGBP1	drug	nicotine	16894067	Cigarette <b>smoking</b> saturates brain <strong>alpha 4</strong> beta 2 nicotinic acetylcholine receptors.
+IGBP1	drug	nicotine	16894067	To determine the effect of cigarette <b>smoking</b> on <strong>alpha 4</strong> beta 2* nAChR occupancy in <b>tobacco</b> dependent <b>smokers</b>.
+IGBP1	drug	nicotine	16894067	Main Outcome Measure Dose dependent effect of <b>smoking</b> on occupancy of <strong>alpha 4</strong> beta 2* nAChRs, as measured with 2 FA and PET in nAChR rich brain regions.
+IGBP1	drug	nicotine	16894067	<b>Smoking</b> 0.13 (1 to 2 puffs) of a cigarette resulted in 50% occupancy of <strong>alpha 4</strong> beta 2* nAChRs for 3.1 hours after <b>smoking</b>.
+IGBP1	drug	nicotine	16894067	A venous plasma <b>nicotine</b> concentration of 0.87 ng/mL (roughly 1/25th of the level achieved in typical daily <b>smokers</b>) was associated with 50% occupancy of <strong>alpha 4</strong> beta 2* nAChRs.
+IGBP1	drug	nicotine	16894067	Cigarette <b>smoking</b> in amounts used by typical daily <b>smokers</b> leads to nearly complete occupancy of <strong>alpha 4</strong> beta 2* nAChRs, indicating that <b>tobacco</b> dependent <b>smokers</b> maintain <strong>alpha 4</strong> beta 2* nAChR saturation throughout the day.
+IGBP1	drug	nicotine	16894067	Because prolonged binding of <b>nicotine</b> to <strong>alpha 4</strong> beta 2* nAChRs is associated with desensitization of these receptors, the extent of receptor occupancy found herein suggests that <b>smoking</b> may lead to withdrawal alleviation by maintaining nAChRs in the desensitized state.
+IGBP1	addiction	withdrawal	16894067	Because prolonged binding of nicotine to <strong>alpha 4</strong> beta 2* nAChRs is associated with desensitization of these receptors, the extent of receptor occupancy found herein suggests that smoking may lead to <b>withdrawal</b> alleviation by maintaining nAChRs in the desensitized state.
+IGBP1	drug	nicotine	16622038	Differential regulation of mesolimbic alpha 3/alpha 6 beta 2 and <strong>alpha 4</strong> beta 2 nicotinic acetylcholine receptor sites and function after long term oral <b>nicotine</b> to monkeys.
+IGBP1	drug	nicotine	15741168	Exocytic trafficking is required for <b>nicotine</b> induced up regulation of <strong>alpha 4</strong> beta 2 nicotinic acetylcholine receptors.
+IGBP1	drug	nicotine	15154117	A common haplotype of the <b>nicotine</b> acetylcholine receptor <strong>alpha 4</strong> subunit gene is associated with vulnerability to <b>nicotine</b> addiction in men.
+IGBP1	addiction	addiction	15154117	A common haplotype of the nicotine acetylcholine receptor <strong>alpha 4</strong> subunit gene is associated with vulnerability to nicotine <b>addiction</b> in men.
+IGBP1	drug	alcohol	14625373	<b>Ethanol</b> enhances <strong>alpha 4</strong> beta 3 delta and alpha 6 beta 3 delta gamma aminobutyric acid type A receptors at low concentrations known to affect humans.
+IGBP1	drug	nicotine	12061141	Thus, it is suggested that alpha 7 nAChR is involved in the attention deficit of schizophrenic patients and that <strong>alpha 4</strong> beta 2 nAChR is related to <b>nicotine</b> dependence or the withdrawal symptoms.
+IGBP1	addiction	dependence	12061141	Thus, it is suggested that alpha 7 nAChR is involved in the attention deficit of schizophrenic patients and that <strong>alpha 4</strong> beta 2 nAChR is related to nicotine <b>dependence</b> or the withdrawal symptoms.
+IGBP1	addiction	withdrawal	12061141	Thus, it is suggested that alpha 7 nAChR is involved in the attention deficit of schizophrenic patients and that <strong>alpha 4</strong> beta 2 nAChR is related to nicotine dependence or the <b>withdrawal</b> symptoms.
+IGBP1	drug	benzodiazepine	11960630	Hormone withdrawal also produced increases in the <strong>alpha 4</strong> containing GABAR, an effect correlated with insensitivity of the GABAR to modulation by the <b>benzodiazepine</b> class of tranquilizers, as would normally occur under control conditions.
+IGBP1	addiction	withdrawal	11960630	Hormone <b>withdrawal</b> also produced increases in the <strong>alpha 4</strong> containing GABAR, an effect correlated with insensitivity of the GABAR to modulation by the benzodiazepine class of tranquilizers, as would normally occur under control conditions.
+IGBP1	drug	psychedelics	11906717	Both <b>ibogaine</b> and 18 methoxycoronaridine were antagonists at alpha 3 beta 4 nicotinic receptors and both agents were more potent at this site than at <strong>alpha 4</strong> beta 2 nicotinic receptors or at NMDA or 5 HT(3) receptors; 18 methoxycoronaridine was more selective in this regard than <b>ibogaine</b>.
+IGBP1	drug	nicotine	11854451	There were no changes in the levels of <strong>alpha 4</strong>, alpha 5, alpha 6, alpha 7, beta 2, and beta 4 mRNA, or in [(125)I]epibatidine and [(3)H]<b>nicotine</b> binding between +/T and +/+ mice.
+IGBP1	drug	alcohol	9689472	The effects of <b>ethanol</b> dependence on additional GABAA receptor subunit peptide levels (<strong>alpha 4</strong>, beta 2/3 and gamma 2) were similar, but not identical, between female and male rat cortex.
+IGBP1	addiction	dependence	9689472	The effects of ethanol <b>dependence</b> on additional GABAA receptor subunit peptide levels (<strong>alpha 4</strong>, beta 2/3 and gamma 2) were similar, but not identical, between female and male rat cortex.
+IGBP1	drug	alcohol	9422812	In general, the alpha 3 beta 2, <strong>alpha 4</strong> 1 beta 2 and <strong>alpha 4</strong> 1 beta 4 subunit combinations were less sensitive to low concentrations of <b>ethanol</b>, but respectively showed potentiations of up to 178%, 226% and 154% at high EtOH concentrations.
+IGBP1	drug	benzodiazepine	8913357	Pharmacological modulation of the <b>diazepam</b> insensitive recombinant gamma aminobutyric acidA receptors <strong>alpha 4</strong> beta 2 gamma 2 and alpha 6 beta 2 gamma 2.
+IGBP1	drug	benzodiazepine	8913357	We characterized modulation of the gamma aminobutyric acid (GABA) evoked responses of the <b>diazepam</b> insensitive <strong>alpha 4</strong> beta 2 gamma2 and alpha 6 beta 2 gamma 2 recombinant GABAA receptors.
+IGBP1	addiction	dependence	8913357	The partial agonist bretazenil potentiated the responses of both receptors with similar dose <b>dependence</b> but with a higher maximal enhancement at the <strong>alpha 4</strong> beta 2 gamma 2 receptor.
+IGBP1	addiction	dependence	8913357	The imidazobenzodiazepine inverse agonist Ro 15 4513, which is known to bind with high affinity to the alpha 6 beta 2 gamma 2 receptor, potentiated the GABA responses of the <strong>alpha 4</strong> beta 2 gamma 2 and alpha 6 beta 2 gamma 2 receptor subtypes with similar dose <b>dependence</b> over the concentration range of 0.1 10 microM.
+IGBP1	drug	benzodiazepine	8913357	Thus, although the <strong>alpha 4</strong> beta 2 gamma 2 receptors are insensitive to <b>benzodiazepine</b> binding site full agonists, such as <b>diazepam</b>, they can be modulated by certain ligands acting as partial and inverse agonists at <b>diazepam</b> sensitive receptors and thereby contribute to the respective pharmacological profiles.
+IGBP1	drug	alcohol	8768698	Levels for the alpha 1 and <strong>alpha 4</strong> subunit showed only slight alteration during withdrawal whereas we had previously observed a significant decrease in alpha 1 and a significant increase in <strong>alpha 4</strong> mRNA levels in <b>ethanol</b> dependent (not withdrawing) animals.
+IGBP1	addiction	withdrawal	8768698	Levels for the alpha 1 and <strong>alpha 4</strong> subunit showed only slight alteration during <b>withdrawal</b> whereas we had previously observed a significant decrease in alpha 1 and a significant increase in <strong>alpha 4</strong> mRNA levels in ethanol dependent (not withdrawing) animals.
+IGBP1	drug	benzodiazepine	9014161	The levels of <strong>alpha 4</strong>  and alpha , beta 1  and gamma 3 subunit mRNAs were significantly increased after 7 days of <b>diazepam</b> treatment, and this effect was maintained at 14 days.
+IGBP1	drug	alcohol	7476917	We find that chronic <b>ethanol</b> consumption elicits a significant increase in <strong>alpha 4</strong> subunit mRNA levels that is equal, in absolute amount, to a decrease in alpha 1 subunit mRNA levels.
+IGBP1	drug	nicotine	7935334	Acetylcholine receptors of the same (<strong>alpha 4</strong>)2(beta 2)3 subunit composition as the predominant subtype of brain nicotinic receptors with high affinity for <b>nicotine</b> have been expressed in Xenopus oocytes and in a permanently transfected fibroblast cell line.
+IGBP1	drug	nicotine	7935334	Chronic exposure of these cells to <b>nicotine</b> or another agonist is shown to result in an increase in receptor amount, indicating that <b>nicotine</b> induced up regulation reflects properties of the <strong>alpha 4</strong> beta 2 receptor protein, rather than being an adaptive response unique to the neurons in which these receptors are normally expressed.
+IGBP1	drug	nicotine	8192688	Although multiple subtypes of <b>nicotine</b> receptor are expressed in the brain, attention has focused on a prevalent subtype (containing <strong>alpha 4</strong> and beta 2 subunits) which is believed to represent the prime target for '<b>smoking</b> doses' of <b>nicotine</b>.
+IGBP1	addiction	addiction	1378342	<strong>Alpha 4</strong> 2 beta 2 and other nicotinic acetylcholine receptor subtypes as targets of psychoactive and <b>addictive</b> drugs.
+CCL2	drug	cocaine	32278944	Further validation experiments showed that <b>cocaine</b> self administered mice had significantly increased mRNA expression of <strong>ccl2</strong> and IL1β in the striatum but not the mPFc compared to saline controls.
+CCL2	drug	cocaine	32278944	Consistently, we found elevated protein levels of Iba1, <strong>CCL2</strong>, TLR4 and mature IL1β in the striatum, not in the mPFc of <b>cocaine</b> receiving mice.
+CCL2	drug	alcohol	31838202	Pre treatment of mice with P Esbp prior to <b>alcohol</b> binge attenuated <b>alcohol</b> induced serum transaminase (ALT, AST) elevation, reduced pro inflammatory cytokines (TNFα and IL 1ẞ) and chemokines (MIP 2/CXCL2 and MCP 1/<strong>CCL2</strong>) in National Institute on <b>Alcohol</b> Abuse and <b>Alcoholism</b> (NIAAA) model.
+CCL2	addiction	intoxication	31838202	Pre treatment of mice with P Esbp prior to alcohol <b>binge</b> attenuated alcohol induced serum transaminase (ALT, AST) elevation, reduced pro inflammatory cytokines (TNFα and IL 1ẞ) and chemokines (MIP 2/CXCL2 and MCP 1/<strong>CCL2</strong>) in National Institute on Alcohol Abuse and Alcoholism (NIAAA) model.
+CCL2	drug	alcohol	31838202	Pre treatment of mice with P Esbp prior to <b>alcohol</b> binge attenuated <b>alcohol</b> induced serum transaminase (ALT, AST) elevation, reduced pro inflammatory cytokines (TNFα and IL 1ẞ) and chemokines (MIP 2/CXCL2 and <strong>MCP 1</strong>/<strong>CCL2</strong>) in National Institute on <b>Alcohol</b> Abuse and <b>Alcoholism</b> (NIAAA) model.
+CCL2	addiction	intoxication	31838202	Pre treatment of mice with P Esbp prior to alcohol <b>binge</b> attenuated alcohol induced serum transaminase (ALT, AST) elevation, reduced pro inflammatory cytokines (TNFα and IL 1ẞ) and chemokines (MIP 2/CXCL2 and <strong>MCP 1</strong>/<strong>CCL2</strong>) in National Institute on Alcohol Abuse and Alcoholism (NIAAA) model.
+CCL2	drug	alcohol	31398460	We hypothesized that chronic <b>alcohol</b> consumption impairs memory and increases the inflammatory cytokines TNFα, IL6, <strong>MCP1</strong>, and IL1β in the hippocampus and prefrontal cortex regions in the brain.
+CCL2	addiction	intoxication	31030249	GABAAR α2 activated neuroimmune signal controls <b>binge</b> drinking and impulsivity through regulation of the <strong>CCL2</strong>/CX3CL1 balance.
+CCL2	addiction	intoxication	31030249	Focus is on the effect of TLR4 signal activation on the balance between pro  and anti inflammatory chemokines [chemokine (C C motif) ligand 2 (<strong>CCL2</strong>)/chemokine (C X3 C motif) ligand 1 (CX3CL1)] and its effect on <b>binge</b> drinking.
+CCL2	drug	psychedelics	30582133	Supplementation of HFD with iboga extract at <b>ibogaine</b> doses of 0.83 (low) and 2.07 (high) mg/kg/day did not improve these HFD induced metabolic effects except for a reduction of plasma <strong>MCP 1</strong> in the low dose group, indicative of an anti inflammatory effect.
+CCL2	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements <strong>MCP 1</strong> monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+CCL2	drug	alcohol	30368255	<b>Alcohol</b> feeding significantly increased the expression of proinflammatory cytokines such as Tnfα, <strong>Mcp1</strong>, Hmgb1, Il 17, and Il 23 in the brain and intestine.
+CCL2	drug	opioid	30079432	Participants having higher levels of plasma <strong>MCP 1</strong> reported higher SOWS, most notably after the <b>buprenorphine</b> taper ended.
+CCL2	drug	opioid	30079432	High correlations between <strong>MCP 1</strong> and <b>opioid</b> withdrawal symptoms support a role of proinflammatory processes in <b>opioid</b> withdrawal.
+CCL2	addiction	withdrawal	30079432	High correlations between <strong>MCP 1</strong> and opioid <b>withdrawal</b> symptoms support a role of proinflammatory processes in opioid <b>withdrawal</b>.
+CCL2	drug	opioid	29791013	Frontline Science: <b>Buprenorphine</b> decreases <strong>CCL2</strong> mediated migration of CD14+ CD16+ monocytes.
+CCL2	drug	opioid	29791013	The effects of <b>buprenorphine</b> on <strong>CCL2</strong> mediated CD14+ CD16+ monocytes transmigration across the BBB, a critical mechanism that promotes neuroinflammation and HAND, have not been characterized.
+CCL2	drug	opioid	29791013	We showed for the first time that <b>buprenorphine</b> decreases several steps of <strong>CCL2</strong> mediated human mature monocyte transmigration.
+CCL2	addiction	withdrawal	29572015	When a single injection of minocycline was given during extended <b>withdrawal</b>, it decreased <strong>CCL2</strong> mRNA levels, but did not reverse the elevation of <strong>CCL2</strong> protein.
+CCL2	drug	cannabinoid	29540562	Complementary genetic and pharmacologic approaches revealed that the antiallodynic effects of each drug require both <b>cannabinoid</b> receptors, CB1 and CB2 MJN110 reduced paclitaxel mediated increased expression of monocyte chemoattractant protein 1 (MCP 1, <strong>CCL2</strong>) and phospho p38 MAPK in dorsal root ganglia as well as MCP 1 in spinal dorsal horn.
+CCL2	drug	cannabinoid	29540562	Complementary genetic and pharmacologic approaches revealed that the antiallodynic effects of each drug require both <b>cannabinoid</b> receptors, CB1 and CB2 MJN110 reduced paclitaxel mediated increased expression of monocyte chemoattractant protein 1 (<strong>MCP 1</strong>, <strong>CCL2</strong>) and phospho p38 MAPK in dorsal root ganglia as well as <strong>MCP 1</strong> in spinal dorsal horn.
+CCL2	drug	alcohol	29499275	Altered hippocampal synaptic function in transgenic mice with increased astrocyte expression of <strong>CCL2</strong> after withdrawal from chronic <b>alcohol</b>.
+CCL2	addiction	withdrawal	29499275	Altered hippocampal synaptic function in transgenic mice with increased astrocyte expression of <strong>CCL2</strong> after <b>withdrawal</b> from chronic alcohol.
+CCL2	drug	alcohol	29499275	CNS actions of the chemokine <strong>CCL2</strong> are thought to play a role in a variety of conditions that can have detrimental consequences to CNS function, including <b>alcohol</b> use disorders.
+CCL2	drug	alcohol	29499275	We used transgenic mice that express elevated levels of <strong>CCL2</strong> in the CNS (<strong>CCL2</strong> tg) and their non transgenic (non tg) littermate control mice to investigate long term consequences of <strong>CCL2</strong>/<b>alcohol</b>/withdrawal interactions on hippocampal synaptic function, including excitatory synaptic transmission, somatic excitability, and synaptic plasticity.
+CCL2	addiction	withdrawal	29499275	We used transgenic mice that express elevated levels of <strong>CCL2</strong> in the CNS (<strong>CCL2</strong> tg) and their non transgenic (non tg) littermate control mice to investigate long term consequences of <strong>CCL2</strong>/alcohol/<b>withdrawal</b> interactions on hippocampal synaptic function, including excitatory synaptic transmission, somatic excitability, and synaptic plasticity.
+CCL2	drug	alcohol	29499275	Both <b>alcohol</b> exposure/withdrawal paradigms resulted in <strong>CCL2</strong> dependent interactions that altered the effects of <b>alcohol</b> on synaptic function.
+CCL2	addiction	withdrawal	29499275	Both alcohol exposure/<b>withdrawal</b> paradigms resulted in <strong>CCL2</strong> dependent interactions that altered the effects of alcohol on synaptic function.
+CCL2	addiction	withdrawal	29499275	The 2BC drinking/<b>withdrawal</b> treatment had no apparent long term consequences on synaptic responses and long term potentiation (LTP) in hippocampal slices from non tg mice, whereas synaptic transmission was reduced but LTP was enhanced in hippocampal slices from <strong>CCL2</strong> tg mice.
+CCL2	addiction	withdrawal	29499275	In contrast, the CIE/2BC/<b>withdrawal</b> treatment enhanced synaptic transmission but reduced LTP in the non tg hippocampus, whereas there were no apparent long term consequences to synaptic transmission and LTP in hippocampus from <strong>CCL2</strong> tg mice, although somatic excitability was enhanced.
+CCL2	drug	alcohol	29499275	These results support the idea that <b>alcohol</b> induced <strong>CCL2</strong> production can modulate the effects of <b>alcohol</b> exposure/withdrawal on synaptic function and indicate that <strong>CCL2</strong>/<b>alcohol</b> interactions can vary depending on the <b>alcohol</b> exposure/withdrawal protocol used.
+CCL2	addiction	withdrawal	29499275	These results support the idea that alcohol induced <strong>CCL2</strong> production can modulate the effects of alcohol exposure/<b>withdrawal</b> on synaptic function and indicate that <strong>CCL2</strong>/alcohol interactions can vary depending on the alcohol exposure/<b>withdrawal</b> protocol used.
+CCL2	drug	amphetamine	29174638	Upregulation of CCL7 and <strong>CCL2</strong> in reward system mediated through dopamine D1 receptor signaling underlies <b>methamphetamine</b> induced place preference in mice.
+CCL2	addiction	reward	29174638	Upregulation of CCL7 and <strong>CCL2</strong> in <b>reward</b> system mediated through dopamine D1 receptor signaling underlies methamphetamine induced place preference in mice.
+CCL2	drug	amphetamine	29174638	We previously showed that the CC chemokine ligand 2 (<strong>CCL2</strong>) CC chemokine receptor 2 (CCR2) system is responsible for conditioned place preference (CPP) by <b>methamphetamine</b> (<b>Meth</b>).
+CCL2	addiction	reward	29174638	We previously showed that the CC chemokine ligand 2 (<strong>CCL2</strong>) CC chemokine receptor 2 (CCR2) system is responsible for conditioned place preference (<b>CPP</b>) by methamphetamine (Meth).
+CCL2	drug	amphetamine	29174638	Consistent with these results, the <b>Meth</b> induced upregulation of CCL7 and <strong>CCL2</strong> were attenuated by SCH 23390, and a single administration of SKF 81297 upregulated mRNA expression levels of CCL7 and <strong>CCL2</strong> in the PFC.
+CCL2	drug	amphetamine	29174638	Furthermore, <b>Meth</b> induced CPP was prevented by INCB 3284, a selective antagonist of CCR2, a receptor that binds both CCL7 and <strong>CCL2</strong>.
+CCL2	addiction	reward	29174638	Furthermore, Meth induced <b>CPP</b> was prevented by INCB 3284, a selective antagonist of CCR2, a receptor that binds both CCL7 and <strong>CCL2</strong>.
+CCL2	drug	amphetamine	29174638	Collectively, we identified two CC chemokines (i.e., CCL7 and <strong>CCL2</strong>) as key regulatory factors in <b>Meth</b> induced reward.
+CCL2	addiction	reward	29174638	Collectively, we identified two CC chemokines (i.e., CCL7 and <strong>CCL2</strong>) as key regulatory factors in Meth induced <b>reward</b>.
+CCL2	drug	opioid	29146238	Protein array analyses revealed only minor changes to cytokine profiles when <b>morphine</b> was administered acutely or repeatedly; however, 24 h post <b>morphine</b> administration, the expression of several cytokines was greatly increased, including endogenous CCR5 chemokine ligands (CCL3, CCL4, and CCL5), as well as <strong>CCL2</strong>.
+CCL2	drug	alcohol	29112774	Neuroactive Steroid (3α,5α)3 hydroxypregnan 20 one (3α,5α THP) and Pro inflammatory Cytokine <strong>MCP 1</strong> Levels in Hippocampus CA1 are Correlated with Voluntary <b>Ethanol</b> Consumption in Cynomolgus Monkey.
+CCL2	drug	alcohol	28951767	Baicalin attenuated <b>ethanol</b> induced proinflammatory molecules such as TNF α, IL 1β, MIP 2, and <strong>MCP 1</strong> and reversed redox sensitive transcription factor NF κB activation.
+CCL2	drug	alcohol	28935932	CBD significantly attenuated the <b>alcohol</b> feeding induced serum transaminase elevations, hepatic inflammation (mRNA expressions of TNFα, <strong>MCP1</strong>, IL1β, MIP2 and E Selectin, and neutrophil accumulation), oxidative/nitrative stress (lipid peroxidation, 3 nitrotyrosine formation, and expression of reactive oxygen species generating enzyme NOX2).
+CCL2	drug	alcohol	28669319	Our aim is to describe changes in serum concentration for the pro inflammatory factors TNF α, IFN γ, IL 1β, IL 8, IL 6, IL 10, IL 12 and <strong>MCP 1</strong>, for the satiety factor leptin and for factors associated with neuronal changes, neuron specific enolase (NSE) and glial activation S100 beta protein (S100 β), and explore their association with abstinence in <b>alcohol</b> dependent subjects after withdrawal.
+CCL2	addiction	withdrawal	28669319	Our aim is to describe changes in serum concentration for the pro inflammatory factors TNF α, IFN γ, IL 1β, IL 8, IL 6, IL 10, IL 12 and <strong>MCP 1</strong>, for the satiety factor leptin and for factors associated with neuronal changes, neuron specific enolase (NSE) and glial activation S100 beta protein (S100 β), and explore their association with abstinence in alcohol dependent subjects after <b>withdrawal</b>.
+CCL2	drug	alcohol	28669319	The levels of TNF α, IL 1β, IL 8, IL 6, IL 12, <strong>MCP 1</strong>, and leptin decreased after withdrawal and remained low until M6, regardless of <b>alcohol</b> consumption.
+CCL2	addiction	withdrawal	28669319	The levels of TNF α, IL 1β, IL 8, IL 6, IL 12, <strong>MCP 1</strong>, and leptin decreased after <b>withdrawal</b> and remained low until M6, regardless of alcohol consumption.
+CCL2	drug	alcohol	28431906	Transgenic mice with increased astrocyte expression of <strong>CCL2</strong> show altered behavioral effects of <b>alcohol</b>.
+CCL2	drug	alcohol	28431906	Recently, studies have also shown that both acute and chronic <b>alcohol</b> consumption can produce activation of CNS glial cells and the production of neuroimmune factors, particularly the chemokine ligand 2 (<strong>CCL2</strong>).
+CCL2	drug	alcohol	28431906	The consequences of <b>alcohol</b> induced increases in <strong>CCL2</strong> levels in the CNS have yet to be fully elucidated.
+CCL2	drug	alcohol	28431906	Our studies focus on the hypothesis that increased levels of <strong>CCL2</strong> in the CNS produce neuroadaptive changes that modify the actions of <b>alcohol</b> on the CNS.
+CCL2	drug	alcohol	28431906	Comparisons between <b>alcohol</b> naïve, non dependent, and <b>alcohol</b> dependent <strong>CCL2</strong> transgenic and non transgenic mice show that elevated levels of <strong>CCL2</strong> in the CNS interact with <b>alcohol</b> in tests for <b>alcohol</b> drinking, spatial learning, and associative learning.
+CCL2	drug	alcohol	28427424	Acute <b>ethanol</b> withdrawal dose dependently increased neuroimmune gene (e.g., TNFα, <strong>Ccl2</strong>, IL 1ra, IL 4) expression beginning at high doses.
+CCL2	addiction	withdrawal	28427424	Acute ethanol <b>withdrawal</b> dose dependently increased neuroimmune gene (e.g., TNFα, <strong>Ccl2</strong>, IL 1ra, IL 4) expression beginning at high doses.
+CCL2	drug	alcohol	28427424	BV2 cells showed biphasic changes in pro inflammatory (e.g., TNFα, <strong>Ccl2</strong>) gene expression following <b>ethanol</b> treatment in vitro.
+CCL2	drug	alcohol	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, <strong>Ccl2</strong>) gene expression and enhanced anti inflammatory (e.g., IL 1ra, IL 4) gene expression during acute binge <b>ethanol</b> withdrawal.
+CCL2	addiction	intoxication	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, <strong>Ccl2</strong>) gene expression and enhanced anti inflammatory (e.g., IL 1ra, IL 4) gene expression during acute <b>binge</b> ethanol withdrawal.
+CCL2	addiction	withdrawal	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, <strong>Ccl2</strong>) gene expression and enhanced anti inflammatory (e.g., IL 1ra, IL 4) gene expression during acute binge ethanol <b>withdrawal</b>.
+CCL2	drug	alcohol	28398003	Midkine in the mouse ventral tegmental area limits <b>ethanol</b> intake and <strong>Ccl2</strong> gene expression.
+CCL2	drug	alcohol	28398003	These results demonstrate that MDK functions in the VTA to limit <b>ethanol</b> consumption and levels of <strong>CCL2</strong>, a chemokine known to increase <b>ethanol</b> consumption.
+CCL2	drug	opioid	28352316	However, the role of spinal <strong>MCP 1</strong> in the development of <b>morphine</b> tolerance in patients with cancer induced bone pain remains unclear.
+CCL2	drug	opioid	28352316	The aim of the present study was to investigate the role of spinal <strong>MCP 1</strong> in <b>morphine</b> tolerance in bone cancer pain rats (MTBP rats).
+CCL2	addiction	withdrawal	28352316	In addition, anti <strong>MCP 1</strong> antibodies were intrathecally injected to rats in various groups in order to investigate the association of <strong>MCP 1</strong> with mechanical and heat hyperalgesia using the paw <b>withdrawal</b> threshold (PWT) and thermal <b>withdrawal</b> latency (TWL) tests, respectively.
+CCL2	drug	opioid	28352316	In conclusion, <strong>MCP 1</strong>/CCR2 signaling may serve a crucial role in <b>morphine</b> tolerance development in rats suffering from cancer induced bone pain.
+CCL2	drug	alcohol	28350851	Expression of liver mRNA tumor necrosis factor alpha (Tnfα), C X C motif chemokine ligand 1 (Cxcl1) and circulating protein monocyte chemoattractant protein 1 (<strong>MCP 1</strong>) were also reduced in antibiotic treated <b>alcohol</b> fed mice.
+CCL2	drug	opioid	28178176	In response to LPS, there was a significant increase in the expression of the pro inflammatory cytokine/chemokine genes interleukin 1 beta (Il 1β), interleukin 6 (Il 6), C C motif chemokine ligand 2 (<strong>Ccl2</strong>), C C motif chemokine ligand 7 (Ccl7), C X C motif chemokine ligand 1 (Cxcl1), and C X C motif chemokine ligand 3 (Cxcl3) and a significant decrease in the anti inflammatory NLRP12 gene in both <b>morphine</b> tolerant and placebo control rats compared to saline treated rats, although the changes were greater in the placebo control animals.
+CCL2	drug	opioid	28178176	In response to LPS, there was a significant increase in the expression of the pro inflammatory cytokine/chemokine genes interleukin 1 beta (Il 1β), interleukin 6 (Il 6), <strong>C C motif chemokine ligand 2</strong> (<strong>Ccl2</strong>), C C motif chemokine ligand 7 (Ccl7), C X C motif chemokine ligand 1 (Cxcl1), and C X C motif chemokine ligand 3 (Cxcl3) and a significant decrease in the anti inflammatory NLRP12 gene in both <b>morphine</b> tolerant and placebo control rats compared to saline treated rats, although the changes were greater in the placebo control animals.
+CCL2	drug	alcohol	28131626	In the present study, we subjected adult male and female rats to different regimens of <b>alcohol</b> vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for tumor necrosis factor alpha (TNFα), interleukin 6 (IL 6), and chemokine (C C motif) ligand 2 (<strong>CCL2</strong>) in reward related brain regions.
+CCL2	addiction	reward	28131626	In the present study, we subjected adult male and female rats to different regimens of alcohol vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for tumor necrosis factor alpha (TNFα), interleukin 6 (IL 6), and chemokine (C C motif) ligand 2 (<strong>CCL2</strong>) in <b>reward</b> related brain regions.
+CCL2	drug	alcohol	28131626	Interestingly, chronic <b>alcohol</b> exposure also robustly increased <strong>CCL2</strong> mRNA expression in the BLA and VTA in males but not females.
+CCL2	drug	alcohol	28090151	The impact of sustained elevated levels of <strong>MCP 1</strong> even after the clearance of blood <b>alcohol</b> content deserves attention.
+CCL2	drug	alcohol	27711160	Chronic binge <b>alcohol</b> induces adipose tissue inflammation in vivo in female mice, which is illustrated by increased expression of TNFα, IL 6, and <strong>CCL2</strong>, compared to only IL 6 induction in male adipose tissue.
+CCL2	addiction	intoxication	27711160	Chronic <b>binge</b> alcohol induces adipose tissue inflammation in vivo in female mice, which is illustrated by increased expression of TNFα, IL 6, and <strong>CCL2</strong>, compared to only IL 6 induction in male adipose tissue.
+CCL2	drug	alcohol	27699959	The results showed that <b>alcohol</b> intoxication increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (<strong>MCP 1</strong>) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+CCL2	addiction	intoxication	27699959	The results showed that alcohol <b>intoxication</b> increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (<strong>MCP 1</strong>) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+CCL2	drug	alcohol	27699959	In wild type female adolescent mice, intermittent <b>ethanol</b> treatment increased the levels of several cytokines (IL 17A and IL 1β) and chemokines (<strong>MCP 1</strong>, MIP 1α and fractalkine) in PFC and in serum (IL 17A, <strong>MCP 1</strong> and MIP 1α), but significant differences in the fractalkine levels in PFC were observed only in male mice.
+CCL2	drug	alcohol	27665607	Age related differences in anxiety like behavior and amygdalar <strong>CCL2</strong> responsiveness to stress following <b>alcohol</b> withdrawal in male Wistar rats.
+CCL2	addiction	withdrawal	27665607	Age related differences in anxiety like behavior and amygdalar <strong>CCL2</strong> responsiveness to stress following alcohol <b>withdrawal</b> in male Wistar rats.
+CCL2	drug	alcohol	27665607	The relation of anxiety like behavior to amygdalar <strong>CCL2</strong> responses following stress after withdrawal from chronic intermittent <b>alcohol</b> (CIA) was investigated in adolescent and adult rats.
+CCL2	addiction	withdrawal	27665607	The relation of anxiety like behavior to amygdalar <strong>CCL2</strong> responses following stress after <b>withdrawal</b> from chronic intermittent alcohol (CIA) was investigated in adolescent and adult rats.
+CCL2	drug	alcohol	27527870	<b>Ethanol</b> caused pancreatic inflammation which was indicated by the induction of TNF alpha, IL 1beta, IL 6, <strong>MCP 1</strong> and CCR2, and the increase of CD68 positive macrophages in the pancreas.
+CCL2	drug	alcohol	27043532	Inflammatory cytokines (interferon γ induced protein 10 (IP 10); monocyte chemoattractant protein 1 (<strong>MCP1</strong>); regulated on activation, normal T cell expressed and secreted (RANTES)) were significantly elevated in <b>alcoholism</b> compared to controls while bone marrow derived hematopoietic cytokines and chemokines (granulocyte colony stimulating factor (GCSF); soluble CD40 ligand (sCD40L); growth related oncogene (GRO)) were significantly reduced.
+CCL2	drug	amphetamine	26946780	Therefore, we examined the role of CC chemokine ligand 2 (<strong>CCL2</strong>), a proinflammatory chemokine, in the development of psychic dependence on <b>methamphetamine</b>.
+CCL2	addiction	dependence	26946780	Therefore, we examined the role of CC chemokine ligand 2 (<strong>CCL2</strong>), a proinflammatory chemokine, in the development of psychic <b>dependence</b> on methamphetamine.
+CCL2	drug	amphetamine	26946780	In mice treated with <b>methamphetamine</b>, <strong>CCL2</strong> mRNA was significantly increased in prefrontal cortex and nucleus accumbens.
+CCL2	drug	amphetamine	26946780	The increment of pTH Ser40 levels in the VTA by <b>methamphetamine</b> was attenuated by RS504393, a selective CC chemokine receptor 2 (CCR2) antagonist, indicating that the increased <strong>CCL2</strong> activates the brain reward system via CCR2 activation.
+CCL2	addiction	reward	26946780	The increment of pTH Ser40 levels in the VTA by methamphetamine was attenuated by RS504393, a selective CC chemokine receptor 2 (CCR2) antagonist, indicating that the increased <strong>CCL2</strong> activates the brain <b>reward</b> system via CCR2 activation.
+CCL2	drug	amphetamine	26946780	These results suggest that the activation of the brain reward system via <strong>CCL2</strong> CCR2 pathway plays an important role in the development of psychic dependence on <b>methamphetamine</b>.
+CCL2	addiction	dependence	26946780	These results suggest that the activation of the brain reward system via <strong>CCL2</strong> CCR2 pathway plays an important role in the development of psychic <b>dependence</b> on methamphetamine.
+CCL2	addiction	reward	26946780	These results suggest that the activation of the brain <b>reward</b> system via <strong>CCL2</strong> CCR2 pathway plays an important role in the development of psychic dependence on methamphetamine.
+CCL2	drug	alcohol	26857094	OEA reduced the levels of interleukin 1beta (IL 1β), the monocyte chemoattractant protein 1 (<strong>MCP 1</strong>), and the enzymes cyclooxygenase 2 (COX 2) and inducible nitric oxide synthase (iNOS) in <b>ethanol</b> binged animals.
+CCL2	drug	alcohol	26683974	Among the evidence implicating neuroimmune signaling in <b>alcohol</b> use disorders are increased levels of the chemokine monocyte chemoattractant protein 1 (<strong>MCP 1</strong>) in the brains of human <b>alcoholics</b> and animal models of <b>alcohol</b> abuse.
+CCL2	drug	alcohol	26683974	However, it is not known whether neuroimmune signaling can directly increase <b>ethanol</b> (EtOH) consumption, and whether <strong>MCP 1</strong> is involved in that mechanism.
+CCL2	addiction	reward	26683974	Our hypothesis was that increasing <strong>MCP 1</strong> signaling by directly infusing it into the brain would increase <b>operant</b> EtOH self administration.
+CCL2	addiction	reward	26683974	We implanted osmotic minipumps to chronically infuse either one of several doses of <strong>MCP 1</strong> or vehicle into the cerebral ventricles (intracerebroventricular) of Long Evans rats and then tested them in the <b>operant</b> self administration of a sweetened EtOH solution for 8 weeks.
+CCL2	addiction	withdrawal	26683974	<strong>MCP 1</strong> did not influence the acquisition of self administration (measured across the first 5 days), the motivation to consume EtOH (time to lever press or progressive ratio), <b>withdrawal</b> induced anxiety, or the consumption of sucrose alone.
+CCL2	drug	alcohol	26683974	Continued research into this mechanism, particularly using models of <b>alcohol</b> dependence, will help determine whether targeting <strong>MCP 1</strong> signaling has therapeutic potential in the treatment of <b>alcohol</b> use disorders.
+CCL2	addiction	dependence	26683974	Continued research into this mechanism, particularly using models of alcohol <b>dependence</b>, will help determine whether targeting <strong>MCP 1</strong> signaling has therapeutic potential in the treatment of alcohol use disorders.
+CCL2	drug	alcohol	26556523	Withdrawal from Chronic <b>Alcohol</b> Induces a Unique <strong>CCL2</strong> mRNA Increase in Adolescent But Not Adult Brain  Relationship to Blood <b>Alcohol</b> Levels and Seizures.
+CCL2	addiction	withdrawal	26556523	<b>Withdrawal</b> from Chronic Alcohol Induces a Unique <strong>CCL2</strong> mRNA Increase in Adolescent But Not Adult Brain  Relationship to Blood Alcohol Levels and Seizures.
+CCL2	drug	alcohol	26556523	Further, a greater increase in <strong>CCL2</strong> mRNA was observed in the cortex of adolescents at 7% CAD, which correlated with higher blood <b>alcohol</b> levels (BALs).
+CCL2	addiction	withdrawal	26556523	Relative to other cytokine mRNAs, <strong>CCL2</strong> exhibits a unique response profile during <b>withdrawal</b> from CAD.
+CCL2	drug	alcohol	26365610	Building on evidence that <b>ethanol</b> stimulates neuroimmune factors such as the chemokine <strong>CCL2</strong> that in adult rats is shown to colocalize with the orexigenic peptide, melanin concentrating hormone (MCH) in the lateral hypothalamus (LH), the present study sought to investigate the possibility that <strong>CCL2</strong> or its receptor CCR2 in LH is stimulated by prenatal <b>ethanol</b> exposure, perhaps specifically within MCH neurons.
+CCL2	drug	alcohol	26365610	Whereas <strong>CCL2</strong>(+) cells at this age were low in density and unaffected by <b>ethanol</b>, CCR2(+) cells were dense in LH and increased by prenatal <b>ethanol</b>, with a large percentage (83 87%) identified as neurons and found to colocalize MCH.
+CCL2	drug	alcohol	26151816	<b>Alcohol</b> consumption affects the immune phenotype of CD8 cells since binge drinking pattern was found to be associated with high CD69 and low TLR4, CXCR4 and CCR2 expression, which suggest recent activation, decreased sensitivity to LPS and lower migration capacity in response to chemokines SDF 1 and <strong>MCP 1</strong>.
+CCL2	addiction	intoxication	26151816	Alcohol consumption affects the immune phenotype of CD8 cells since <b>binge</b> drinking pattern was found to be associated with high CD69 and low TLR4, CXCR4 and CCR2 expression, which suggest recent activation, decreased sensitivity to LPS and lower migration capacity in response to chemokines SDF 1 and <strong>MCP 1</strong>.
+CCL2	drug	cocaine	25762940	The results showed that the concentrations of chemokine (C C motif) ligand 2/monocyte chemotactic protein 1 (<strong>CCL2</strong>/MCP 1) and chemokine (C X C motif) ligand 12/stromal cell derived factor 1 (CXCL12/SDF 1) were only affected by history of <b>cocaine</b> addiction.
+CCL2	addiction	addiction	25762940	The results showed that the concentrations of chemokine (C C motif) ligand 2/monocyte chemotactic protein 1 (<strong>CCL2</strong>/MCP 1) and chemokine (C X C motif) ligand 12/stromal cell derived factor 1 (CXCL12/SDF 1) were only affected by history of cocaine <b>addiction</b>.
+CCL2	drug	cocaine	25762940	The results showed that the concentrations of chemokine (C C motif) ligand 2/monocyte chemotactic protein 1 (<strong>CCL2</strong>/<strong>MCP 1</strong>) and chemokine (C X C motif) ligand 12/stromal cell derived factor 1 (CXCL12/SDF 1) were only affected by history of <b>cocaine</b> addiction.
+CCL2	addiction	addiction	25762940	The results showed that the concentrations of chemokine (C C motif) ligand 2/monocyte chemotactic protein 1 (<strong>CCL2</strong>/<strong>MCP 1</strong>) and chemokine (C X C motif) ligand 12/stromal cell derived factor 1 (CXCL12/SDF 1) were only affected by history of cocaine <b>addiction</b>.
+CCL2	drug	opioid	25716997	<b>Buprenorphine</b> decreases the <strong>CCL2</strong> mediated chemotactic response of monocytes.
+CCL2	drug	opioid	25716997	<b>Buprenorphine</b> decreases the formation of membrane projections in response to <strong>CCL2</strong>.
+CCL2	drug	opioid	25716997	It also decreases <strong>CCL2</strong> induced chemotaxis and mediates a delay in reinsertion of the <strong>CCL2</strong> receptor, CCR2, into the cell membrane after <strong>CCL2</strong> mediated receptor internalization, suggesting a mechanism of action of <b>buprenorphine</b>.
+CCL2	drug	opioid	25716997	We show that <b>buprenorphine</b> decreases these phosphorylations in <strong>CCL2</strong> treated monocytes.
+CCL2	drug	opioid	25716997	Using DAMGO, CTAP, and Nor BNI, we demonstrate that the effect of <b>buprenorphine</b> on <strong>CCL2</strong> signaling is <b>opioid</b> receptor mediated.
+CCL2	drug	opioid	25716997	To identify additional potential mechanisms by which <b>buprenorphine</b> inhibits <strong>CCL2</strong> induced monocyte migration, we performed proteomic analyses to characterize additional proteins in monocytes whose phosphorylation after <strong>CCL2</strong> treatment was inhibited by <b>buprenorphine</b>.
+CCL2	drug	opioid	25716997	We propose that <b>buprenorphine</b> limits <strong>CCL2</strong> mediated monocyte transmigration into the CNS, thereby reducing neuroinflammation characteristic of HAND.
+CCL2	drug	alcohol	25567426	CRF amplified neuronal TLR4/<strong>MCP 1</strong> signaling regulates <b>alcohol</b> self administration.
+CCL2	drug	alcohol	25567426	We report that <b>alcohol</b> preferring P rats have innately elevated levels of Toll like receptor 4 (TLR4) and monocyte chemotactic protein 1 (<strong>MCP 1</strong>) that colocalize in neurons from the central nucleus of the amygdala (CeA) and ventral tegmental area (VTA).
+CCL2	addiction	intoxication	25567426	Infusion of amplicons for TLR4 or <strong>MCP 1</strong> siRNA into the CeA or VTA from the P rats inhibited target gene expression and blunted <b>binge</b> drinking.
+CCL2	drug	alcohol	25567426	A similarly delivered amplicon for scrambled siRNA did not inhibit TLR4 or <strong>MCP 1</strong> expression nor reduce binge drinking, identifying a neuronal TLR4/<strong>MCP 1</strong> signal that regulates the initiation of voluntary <b>alcohol</b> self administration.
+CCL2	addiction	intoxication	25567426	A similarly delivered amplicon for scrambled siRNA did not inhibit TLR4 or <strong>MCP 1</strong> expression nor reduce <b>binge</b> drinking, identifying a neuronal TLR4/<strong>MCP 1</strong> signal that regulates the initiation of voluntary alcohol self administration.
+CCL2	drug	alcohol	24772072	<strong>CCL2</strong> <b>ethanol</b> interactions and hippocampal synaptic protein expression in a transgenic mouse model.
+CCL2	drug	alcohol	24772072	Recent data show that <b>ethanol</b> induces glial cells of the brain to produce elevated levels of neuroimmune factors including <strong>CCL2</strong>, a key innate immune chemokine.
+CCL2	drug	alcohol	24772072	Depending on the conditions of <b>ethanol</b> exposure, the upregulated levels of <strong>CCL2</strong> can be transient or persistent and outlast the period of <b>ethanol</b> exposure.
+CCL2	drug	alcohol	24772072	Importantly, results indicate that the upregulated levels of <strong>CCL2</strong> may lead to <strong>CCL2</strong> <b>ethanol</b> interactions that mediate or regulate the effects of <b>ethanol</b> on the brain.
+CCL2	drug	alcohol	24772072	To investigate this possibility, we are studying effects of chronic <b>ethanol</b> on hippocampal synaptic function in a transgenic mouse model that expresses elevated levels of <strong>CCL2</strong> in the brain through enhanced glial expression, a situation know to occur in <b>alcoholics</b>.
+CCL2	drug	alcohol	24772072	Both <strong>CCL2</strong> and <b>ethanol</b> have been reported to alter synaptic function in the hippocampus.
+CCL2	drug	alcohol	24772072	In the current study, we determined if interactions are evident between <strong>CCL2</strong> and <b>ethanol</b> at the level of hippocampal synaptic proteins.
+CCL2	drug	alcohol	24772072	Results show modest effects of both <b>ethanol</b> exposure paradigms on the level of synaptic proteins in the hippocampus of <strong>CCL2</strong> transgenic mice compared with their non transgenic littermate controls, consistent with <b>ethanol</b> <strong>CCL2</strong> interactions.
+CCL2	drug	alcohol	24772072	No evidence of toxic effects of <strong>CCL2</strong> or <strong>CCL2</strong> <b>ethanol</b> interactions was observed.
+CCL2	drug	alcohol	24772072	Taken together, these results support the idea that <b>ethanol</b> induced astrocyte production of <strong>CCL2</strong> can result in neuroadaptive changes that interact with the actions of <b>ethanol</b>.
+CCL2	drug	alcohol	24766056	In patients with mild ALD, 1 week of <b>alcohol</b> withdrawal was sufficient to decrease expression level of total macrophage markers in the adipose tissue, to orient adipose tissue macrophages (ATM) towards an anti inflammatory M2 phenotype and to decrease the mRNA expression of cytokines/chemokines (IL18, <strong>CCL2</strong>, osteopontin, semaphorin 7A).
+CCL2	addiction	withdrawal	24766056	In patients with mild ALD, 1 week of alcohol <b>withdrawal</b> was sufficient to decrease expression level of total macrophage markers in the adipose tissue, to orient adipose tissue macrophages (ATM) towards an anti inflammatory M2 phenotype and to decrease the mRNA expression of cytokines/chemokines (IL18, <strong>CCL2</strong>, osteopontin, semaphorin 7A).
+CCL2	drug	amphetamine	24748435	Because neuroinflammation underlies several neurological disorders, we investigated whether CC chemokine ligand 2 (<strong>CCL2</strong>) participates in the <b>methamphetamine</b> dependence using mice.
+CCL2	addiction	dependence	24748435	Because neuroinflammation underlies several neurological disorders, we investigated whether CC chemokine ligand 2 (<strong>CCL2</strong>) participates in the methamphetamine <b>dependence</b> using mice.
+CCL2	drug	amphetamine	24748435	Upregulation of <strong>CCL2</strong> but not CC chemokine receptor 2 (CCR2), a dominant receptor for <strong>CCL2</strong>, mRNA in both the prefrontal cortex (PFC) and nucleus accumbens (NAC) was observed after <b>methamphetamine</b> (3 mg/kg, s.c.) administration.
+CCL2	drug	amphetamine	24748435	Taken together, we demonstrate that activation of dopamine neurons, which enhances reward system activity, via the <strong>CCL2</strong> CCR2 axis plays a crucial role in psychic dependence on <b>methamphetamine</b>.
+CCL2	addiction	dependence	24748435	Taken together, we demonstrate that activation of dopamine neurons, which enhances reward system activity, via the <strong>CCL2</strong> CCR2 axis plays a crucial role in psychic <b>dependence</b> on methamphetamine.
+CCL2	addiction	reward	24748435	Taken together, we demonstrate that activation of dopamine neurons, which enhances <b>reward</b> system activity, via the <strong>CCL2</strong> CCR2 axis plays a crucial role in psychic dependence on methamphetamine.
+CCL2	drug	alcohol	22709825	<b>Ethanol</b> pretreatment potentiated poly I:C induced brain TNFα (345%), IL 1β (331%), IL 6 (255%), and <strong>MCP 1</strong>(190%).
+CCL2	drug	alcohol	22626265	For qRT PCR studies, we measured the expression of TNF α, NOS 2, <strong>Ccl2</strong> (MCP 1), MHC II invariant chain CD74, and the TNF receptor Tnfrsf1a in CeA and DVC samples from adult male rats exposed to a liquid <b>alcohol</b> diet for thirty five days and in similarly treated animals at four hours and forty eight hours following <b>alcohol</b> withdrawal.
+CCL2	addiction	withdrawal	22626265	For qRT PCR studies, we measured the expression of TNF α, NOS 2, <strong>Ccl2</strong> (MCP 1), MHC II invariant chain CD74, and the TNF receptor Tnfrsf1a in CeA and DVC samples from adult male rats exposed to a liquid alcohol diet for thirty five days and in similarly treated animals at four hours and forty eight hours following alcohol <b>withdrawal</b>.
+CCL2	drug	alcohol	22626265	For qRT PCR studies, we measured the expression of TNF α, NOS 2, <strong>Ccl2</strong> (<strong>MCP 1</strong>), MHC II invariant chain CD74, and the TNF receptor Tnfrsf1a in CeA and DVC samples from adult male rats exposed to a liquid <b>alcohol</b> diet for thirty five days and in similarly treated animals at four hours and forty eight hours following <b>alcohol</b> withdrawal.
+CCL2	addiction	withdrawal	22626265	For qRT PCR studies, we measured the expression of TNF α, NOS 2, <strong>Ccl2</strong> (<strong>MCP 1</strong>), MHC II invariant chain CD74, and the TNF receptor Tnfrsf1a in CeA and DVC samples from adult male rats exposed to a liquid alcohol diet for thirty five days and in similarly treated animals at four hours and forty eight hours following alcohol <b>withdrawal</b>.
+CCL2	drug	alcohol	22626265	Following a chronic <b>alcohol</b> exposure, withdrawal resulted in a statistically significant increase in the expression of mRNAs specific for innate immune markers <strong>Ccl2</strong>, TNF α, NOS 2, Tnfrsf1a, and CD74.
+CCL2	addiction	withdrawal	22626265	Following a chronic alcohol exposure, <b>withdrawal</b> resulted in a statistically significant increase in the expression of mRNAs specific for innate immune markers <strong>Ccl2</strong>, TNF α, NOS 2, Tnfrsf1a, and CD74.
+CCL2	drug	alcohol	22626265	This study demonstrates the rapid induction of <strong>Ccl2</strong>, TNF α, NOS 2, Tnfrsf1a and CD74 expression during <b>alcohol</b> withdrawal in both the CeA and DVC.
+CCL2	addiction	withdrawal	22626265	This study demonstrates the rapid induction of <strong>Ccl2</strong>, TNF α, NOS 2, Tnfrsf1a and CD74 expression during alcohol <b>withdrawal</b> in both the CeA and DVC.
+CCL2	drug	alcohol	22140596	In this study, we used a PCR array containing 46 primer pairs of selected genes to compare mRNA expression in the spleen, an immune system organ, of adolescent rats following binge drinking of <b>alcohol</b> solutions containing either 20% or 52% <b>ethanol</b> (v/v, 4.8 g/kg daily dosage), or water (control) for 3 d. We found that, expression of IL 1β, IL 6, <strong>CCL2</strong>, and GABA(A) receptor α2 subunit in the spleen were decreased, and mGluR5 and 5 HT3A receptor expression were increased after administration of an <b>ethanol</b> solution containing 52% <b>ethanol</b>, but not one with 20% <b>ethanol</b>.
+CCL2	addiction	intoxication	22140596	In this study, we used a PCR array containing 46 primer pairs of selected genes to compare mRNA expression in the spleen, an immune system organ, of adolescent rats following <b>binge</b> drinking of alcohol solutions containing either 20% or 52% ethanol (v/v, 4.8 g/kg daily dosage), or water (control) for 3 d. We found that, expression of IL 1β, IL 6, <strong>CCL2</strong>, and GABA(A) receptor α2 subunit in the spleen were decreased, and mGluR5 and 5 HT3A receptor expression were increased after administration of an ethanol solution containing 52% ethanol, but not one with 20% ethanol.
+CCL2	drug	cocaine	21601240	We determined circulating endothelial cells (CECs) and plasma levels of stromal cell derived factor 1 (SDF 1), monocyte chemotactic protein 1(<strong>MCP 1</strong>), soluble intracellular adhesion molecule (sICAM), high sensitivity C reactive protein (hsCRP) and endothelin 1(ET 1), in DSM IV <b>cocaine</b> addicts at baseline and after one month of <b>cocaine</b> abstinence.
+CCL2	addiction	intoxication	21593683	Furthermore, a significant increase in IL 6 and <strong>MCP 1</strong> was observed in circulation after EtOH <b>intoxication</b> and burn injury compared with either EtOH <b>intoxication</b> or burn injury alone; no other cytokines were detected in circulation.
+CCL2	drug	cannabinoid	21463073	Chronic Δ⁹ <b>THC</b> also significantly reduced CB 1 and CB 2 receptor levels in the hippocampus, attenuated the expression of a proinflammatory cytokine (<strong>MCP 1</strong>), and did not increase viral load in plasma, cerebrospinal fluid, or brain tissue compared to vehicle treated subjects with SIV.
+CCL2	drug	cocaine	21424761	As previous studies suggested that the chemokine <strong>CCL2</strong> enhanced striatal dopamine release and as its cognate CCR2 receptor was located in brain structures implicated in <b>cocaine</b> reward, we tested the hypothesis that CCR2/<strong>CCL2</strong> could be involved in <b>cocaine</b> induced behavioral response.
+CCL2	addiction	reward	21424761	As previous studies suggested that the chemokine <strong>CCL2</strong> enhanced striatal dopamine release and as its cognate CCR2 receptor was located in brain structures implicated in cocaine <b>reward</b>, we tested the hypothesis that CCR2/<strong>CCL2</strong> could be involved in cocaine induced behavioral response.
+CCL2	drug	alcohol	21402143	Human post mortem <b>alcoholic</b> brain has increased NF κB and NF κB target gene message, increased microglial markers and chemokine <strong>MCP1</strong>.
+CCL2	addiction	withdrawal	21377524	To test for a possible interaction between cytokines and CRF, a CRF1 receptor antagonist (SSR125543) administered prior to the repeated administration of TNFα or MCP 1/<strong>CCL2</strong> reduced the magnitude of the <b>withdrawal</b> induced anxiety.
+CCL2	addiction	withdrawal	21377524	To test for a possible interaction between cytokines and CRF, a CRF1 receptor antagonist (SSR125543) administered prior to the repeated administration of TNFα or <strong>MCP 1</strong>/<strong>CCL2</strong> reduced the magnitude of the <b>withdrawal</b> induced anxiety.
+CCL2	drug	alcohol	20201932	<b>Ethanol</b> induces proinflammatory cytokines TNFalpha, <strong>MCP 1</strong>, and IL 1beta, proinflammatory proteases TACE, and tissue plasminogen activator (tPA) as well as inducible nitric oxide synthase.
+CCL2	drug	opioid	18815890	CCL5/RANTES gene deletion attenuates <b>opioid</b> induced increases in glial <strong>CCL2</strong>/MCP 1 immunoreactivity and activation in HIV 1 Tat exposed mice.
+CCL2	drug	opioid	18815890	CCL5/RANTES gene deletion attenuates <b>opioid</b> induced increases in glial <strong>CCL2</strong>/<strong>MCP 1</strong> immunoreactivity and activation in HIV 1 Tat exposed mice.
+CCL2	drug	opioid	18815890	In CCL5( / ) mice, the reductions in Tat +/  <b>morphine</b> induced gliosis coincided with significant declines in the proportion of <strong>CCL2</strong>/MCP 1 immunoreactive astrocytes and macrophages/microglia compared to wild type counterparts.
+CCL2	drug	opioid	18815890	In CCL5( / ) mice, the reductions in Tat +/  <b>morphine</b> induced gliosis coincided with significant declines in the proportion of <strong>CCL2</strong>/<strong>MCP 1</strong> immunoreactive astrocytes and macrophages/microglia compared to wild type counterparts.
+CCL2	drug	opioid	18815890	In knockout mice, neither Tat alone nor in combination with <b>morphine</b> increased the proportion of <strong>CCL2</strong> immunoreactive astrocytes above percentages seen in vehicle injected controls.
+CCL2	drug	opioid	18815890	Macrophages/microglia differed showing modest, albeit significant, increases in the proportion of <strong>CCL2</strong> positive cells with combined Tat and <b>morphine</b> exposure, suggesting that CCL5 preferentially affects <strong>CCL2</strong> expression by astroglia.
+CCL2	drug	alcohol	17551540	administrations of the cytokines IL 1 beta, <strong>CCL2</strong> (MCP 1) or TNFalpha (cytokine/withdrawal protocol) before exposure and withdrawal from a 5 day cycle of chronic <b>ethanol</b> diet.
+CCL2	addiction	withdrawal	17551540	administrations of the cytokines IL 1 beta, <strong>CCL2</strong> (MCP 1) or TNFalpha (cytokine/<b>withdrawal</b> protocol) before exposure and <b>withdrawal</b> from a 5 day cycle of chronic ethanol diet.
+CCL2	drug	alcohol	17551540	administrations of the cytokines IL 1 beta, <strong>CCL2</strong> (<strong>MCP 1</strong>) or TNFalpha (cytokine/withdrawal protocol) before exposure and withdrawal from a 5 day cycle of chronic <b>ethanol</b> diet.
+CCL2	addiction	withdrawal	17551540	administrations of the cytokines IL 1 beta, <strong>CCL2</strong> (<strong>MCP 1</strong>) or TNFalpha (cytokine/<b>withdrawal</b> protocol) before exposure and <b>withdrawal</b> from a 5 day cycle of chronic ethanol diet.
+CCL2	drug	opioid	16831471	To assess the role of <strong>CCL2</strong>/MCP 1 in opiate drug abuse and HIV 1 comorbidity, the effects of systemic <b>morphine</b> and intrastriatal HIV 1 Tat on macrophage/microglial and astroglial activation were assessed in wild type and CCR2 null mice.
+CCL2	drug	opioid	16831471	To assess the role of <strong>CCL2</strong>/<strong>MCP 1</strong> in opiate drug abuse and HIV 1 comorbidity, the effects of systemic <b>morphine</b> and intrastriatal HIV 1 Tat on macrophage/microglial and astroglial activation were assessed in wild type and CCR2 null mice.
+CCL2	drug	opioid	16831471	Tat and/or <b>morphine</b> additively increased the proportion of <strong>CCL2</strong> immunoreactive astroglia.
+CCL2	drug	nicotine	16332510	In the present study, the combined effects of <b>nicotine</b> and bacterial LPS on the expression of IL 6, IL 8, GRO alpha and <strong>MCP 1</strong> in cell lines of human coronary artery endothelial cells (HCAEC) and pulmonary monocytes (THP 1) were examined by quantitative real time PCR and ELISA.
+CCL2	drug	alcohol	16105698	To test the hypothesis that chemokines exhibit previously undiscovered pleiotropic effects important for the behavioral actions of <b>ethanol</b>, we studied mutant mice with deletion of the Ccr2, Ccr5, <strong>Ccl2</strong> or Ccl3 genes.
+CCL2	drug	alcohol	16105698	Deletion of Ccr2, <strong>Ccl2</strong> (females) or Ccl3 in mice resulted in lower preference for <b>alcohol</b> and consumption of lower amounts of <b>alcohol</b> in a two bottle choice test as compared with wild type mice.
+CCL2	addiction	aversion	16105698	induced stronger conditioned taste <b>aversion</b> in Ccr2, <strong>Ccl2</strong> or Ccl3 null mutant mice than in controls.
+CCL2	drug	alcohol	16105698	Ccr2 and Ccr5 null mutant mice did not differ from wild type mice in <b>ethanol</b> induced loss of righting reflex (LORR), but mice lacking <strong>Ccl2</strong> or Ccl3 showed longer LORR than wild type mice.
+CCL2	drug	alcohol	16105698	Genetic mapping of chromosome 11 for the <strong>Ccl2</strong> and Ccl3 genes (46.5 and 47.6 cM, respectively) revealed that an <b>alcohol</b> induced LORR QTL region was contained within the introgressed region derived from 129/SvJ, which may cause some behavioral phenotypes observed in the null mice.
+CCL2	drug	alcohol	12821046	Serum keratinocyte chemoattractant (KC) and monocyte chemoattractant protein 1 (<strong>MCP 1</strong>) levels were significantly increased in the GAL+<b>ethanol</b> group.
+CCL2	drug	alcohol	12821046	In GAL+<b>ethanol</b> treated mice, IL 10 treatment reduced ALT release, KC and <strong>MCP 1</strong> serum and hepatic mRNA levels, and improved liver inflammation.
+CCL2	drug	alcohol	12045006	Serum ALT, endotoxin, MIP 1alpha, <strong>MCP 1</strong> and RANTES, (but not CINC and MIP 2) were also increased in the <b>ethanol</b> fed rats than in the pair fed group.
+CCL2	drug	alcohol	12045006	Isolated Kupffer cells from <b>ethanol</b> fed rats were primed for enhanced MIP 1alpha, <strong>MCP 1</strong>, and RANTES production in vitro, while the endothelial cells were primed for enhanced MIP 1alpha release only.
+CCL2	drug	alcohol	11388697	Results show that in vivo <b>ethanol</b> was associated with downregulation of MIP 1alpha and <strong>MCP 1</strong> mRNA expression and protein release in primary cultures of Kupffer cells.
+CCL2	addiction	relapse	11293664	The mRNA for cytokines IL 1beta, IL 6, IL 10 and the chemokines CINC, MIP 1alpha, <strong>MCP 1</strong> were significantly (P < 0.05) elevated and persisted for 2 weeks, decreased in 6 weeks and increased again during <b>relapse</b>.
+CCL2	drug	alcohol	10719799	This work tests the hypotheses that Kupffer cells are a major source of CC chemokines (MIP 1alpha, <strong>MCP 1</strong>, RANTES) during acute endotoxemia and that acute <b>ethanol</b> intoxication modulates Escherichia coli lipopolysaccharide (LPS, 1 mg/Kg, i.v.)
+CCL2	addiction	intoxication	10719799	This work tests the hypotheses that Kupffer cells are a major source of CC chemokines (MIP 1alpha, <strong>MCP 1</strong>, RANTES) during acute endotoxemia and that acute ethanol <b>intoxication</b> modulates Escherichia coli lipopolysaccharide (LPS, 1 mg/Kg, i.v.)
+CCL2	drug	alcohol	10719799	CC chemokine release and mRNA expression in hepatic sinusoidal endothelial cells were not significantly altered by <b>ethanol</b>, except for <strong>MCP 1</strong> release.
+CCL2	drug	opioid	8856246	Since <b>morphine</b> activates MC to produce superoxide and DMTU attenuated the effect of superoxide on MC, the effect of <b>morphine</b> on the migration of macrophages may be mediated through superoxide induced generation of <strong>MCP 1</strong>.
+GRM1	drug	alcohol	32482639	We also demonstrated that enhancement of <b>ethanol</b> excitation requires the activity of the metabotropic glutamate receptor, <strong>mGluR1</strong>, which is known to couple with ERα at the plasma membrane.
+GRM1	drug	alcohol	32482639	17β Estradiol mediated enhancement of <b>ethanol</b> induced excitation required the metabotropic glutamate receptor <strong>mGluR1</strong>.
+GRM1	drug	alcohol	31518024	Transplantation of fecal microbiota from patients with <b>alcoholism</b> induces anxiety/depression behaviors and decreases brain <strong>mGluR1</strong>/PKC ε levels in mouse.
+GRM1	drug	alcohol	31518024	Compared to mice transplanted with fecal microbiota from healthy male adults, the mice accepting fecal microbiota from patients with <b>alcoholism</b> showed (a) anxiety like and depression like behaviors, (b) decreased social interaction behaviors, (c) spontaneous <b>alcohol</b> preference, and (d) decreased brain derived neurotrophic factor (BDNF), alpha 1 subunit of GABA type A receptor (α1GABAA R) in mPFC and decreased metabotropic glutamate receptors 1 (<strong>mGluR1</strong>), protein kinase C (PKC) ε in NAc.
+GRM1	drug	cocaine	31146278	Additionally, for <b>cocaine</b>, we previously observed a withdrawal dependent decrease in <strong>mGlu1</strong> surface expression that precedes and enables CP AMPAR accumulation and incubation of craving, reflecting weakening of <strong>mGlu1</strong> dependent mechanisms that normally limit synaptic CP AMPAR levels in the NAc core.
+GRM1	addiction	relapse	31146278	Additionally, for cocaine, we previously observed a withdrawal dependent decrease in <strong>mGlu1</strong> surface expression that precedes and enables CP AMPAR accumulation and incubation of <b>craving</b>, reflecting weakening of <strong>mGlu1</strong> dependent mechanisms that normally limit synaptic CP AMPAR levels in the NAc core.
+GRM1	addiction	withdrawal	31146278	Additionally, for cocaine, we previously observed a <b>withdrawal</b> dependent decrease in <strong>mGlu1</strong> surface expression that precedes and enables CP AMPAR accumulation and incubation of craving, reflecting weakening of <strong>mGlu1</strong> dependent mechanisms that normally limit synaptic CP AMPAR levels in the NAc core.
+GRM1	drug	amphetamine	31146278	Here, we observed no change in surface or total <strong>mGlu1</strong> protein or its coupling to Homer scaffolding proteins after <b>methamphetamine</b> withdrawal, nor did elevation of <strong>mGlu1</strong> tone through repeated injections of an <strong>mGlu1</strong> positive allosteric modulator delay incubation of craving.
+GRM1	addiction	relapse	31146278	Here, we observed no change in surface or total <strong>mGlu1</strong> protein or its coupling to Homer scaffolding proteins after methamphetamine withdrawal, nor did elevation of <strong>mGlu1</strong> tone through repeated injections of an <strong>mGlu1</strong> positive allosteric modulator delay incubation of <b>craving</b>.
+GRM1	addiction	withdrawal	31146278	Here, we observed no change in surface or total <strong>mGlu1</strong> protein or its coupling to Homer scaffolding proteins after methamphetamine <b>withdrawal</b>, nor did elevation of <strong>mGlu1</strong> tone through repeated injections of an <strong>mGlu1</strong> positive allosteric modulator delay incubation of craving.
+GRM1	drug	amphetamine	31146278	These findings suggest a common role for increased GluA1 translation, but not decreased <strong>mGlu1</strong> function, in the incubation of <b>methamphetamine</b> and cocaine craving.
+GRM1	drug	cocaine	31146278	These findings suggest a common role for increased GluA1 translation, but not decreased <strong>mGlu1</strong> function, in the incubation of methamphetamine and <b>cocaine</b> craving.
+GRM1	addiction	relapse	31146278	These findings suggest a common role for increased GluA1 translation, but not decreased <strong>mGlu1</strong> function, in the incubation of methamphetamine and cocaine <b>craving</b>.
+GRM1	drug	alcohol	30991250	The function of group I metabotropic glutamate receptors <strong>mGluR1</strong> and mGluR5 is involved in the hyperglutamatergic state caused by chronic <b>alcohol</b>.
+GRM1	drug	alcohol	30991250	Increased [³H]quisqualic acid binding might suggest a beneficial impact of <strong>mGluR1</strong>/5 modulators in the treatment of <b>alcoholism</b>.
+GRM1	addiction	withdrawal	30733663	We then analyzed the expression levels of presynaptic (vGlut1, vGlut2, CB1 receptor, synaptophysin) and postsynaptic (PSD95, GluN1, GluN2A, GluN2B, GluA1, GluA2, <strong>mGluR1</strong> and mGluR5) proteins after 7 days EtOH incubation or after EtOH <b>withdrawal</b>.
+GRM1	drug	amphetamine	30599269	<b>Amphetamine</b> induced Conditioned Place Preference and Changes in <strong>mGlu1</strong>/5 Receptor Expression and Signaling in the Rat Medial Prefrontal Cortex.
+GRM1	drug	amphetamine	30599269	We thus in this study investigated changes in <strong>mGlu1</strong>/5 receptor expression and function in the rat mPFC in response to conditioned place preference (CPP) induced by <b>amphetamine</b>.
+GRM1	addiction	reward	30599269	We thus in this study investigated changes in <strong>mGlu1</strong>/5 receptor expression and function in the rat mPFC in response to conditioned place preference (<b>CPP</b>) induced by amphetamine.
+GRM1	drug	amphetamine	30599269	In mPFC neurons, the <strong>mGlu1</strong>/5 agonist stimulated phosphoinositide signaling pathway was upregulated in its efficacy following <b>amphetamine</b> conditioning.
+GRM1	drug	amphetamine	30599269	The <strong>mGlu1</strong>/5 agonist stimulated Src kinase phosphorylation was also augmented in rats treated with <b>amphetamine</b>.
+GRM1	drug	amphetamine	30599269	These results demonstrate the sensitivity of mPFC <strong>mGlu1</strong>/5 receptors to <b>amphetamine</b> induced CPP.
+GRM1	addiction	reward	30599269	These results demonstrate the sensitivity of mPFC <strong>mGlu1</strong>/5 receptors to amphetamine induced <b>CPP</b>.
+GRM1	drug	amphetamine	30599269	<b>Amphetamine</b> conditioning results in the upregulation of <strong>mGlu1</strong>/5 receptor expression at subcellular and/or subsynaptic levels and <strong>mGlu1</strong>/5 mediated postreceptor signaling in mPFC neurons.
+GRM1	drug	cocaine	30459590	Emergence of Endocytosis Dependent <strong>mGlu1</strong> LTD at Nucleus Accumbens Synapses After Withdrawal From <b>Cocaine</b> Self Administration.
+GRM1	addiction	withdrawal	30459590	Emergence of Endocytosis Dependent <strong>mGlu1</strong> LTD at Nucleus Accumbens Synapses After <b>Withdrawal</b> From Cocaine Self Administration.
+GRM1	addiction	relapse	30459590	Rats evaluated after >1 month of withdrawal (when incubation of <b>craving</b> is robust) display alterations in excitatory synapses onto medium spiny neurons (MSNs) of the nucleus accumbens (NAc), including elevated levels of Ca2+ permeable AMPA receptors (CP AMPAR) and a transition from group I metabotropic glutamate receptor (mGluR) mGlu5  to <strong>mGlu1</strong> mediated synaptic depression.
+GRM1	addiction	withdrawal	30459590	Rats evaluated after >1 month of <b>withdrawal</b> (when incubation of craving is robust) display alterations in excitatory synapses onto medium spiny neurons (MSNs) of the nucleus accumbens (NAc), including elevated levels of Ca2+ permeable AMPA receptors (CP AMPAR) and a transition from group I metabotropic glutamate receptor (mGluR) mGlu5  to <strong>mGlu1</strong> mediated synaptic depression.
+GRM1	drug	cocaine	30459590	It is important to further characterize the emergent form of <strong>mGlu1</strong> mediated synaptic depression because it has been demonstrated that <strong>mGlu1</strong> stimulation, by normalizing CP AMPAR transmission, reduces cue induced <b>cocaine</b> craving.
+GRM1	addiction	relapse	30459590	It is important to further characterize the emergent form of <strong>mGlu1</strong> mediated synaptic depression because it has been demonstrated that <strong>mGlu1</strong> stimulation, by normalizing CP AMPAR transmission, reduces cue induced cocaine <b>craving</b>.
+GRM1	drug	cocaine	30459590	Bath application of the nonselective group I mGluR agonist dihydroxyphenylglycine (DHPG) produced a transient mGlu5 mediated synaptic depression in saline controls, whereas a persistent <strong>mGlu1</strong> mediated synaptic depression emerged in <b>cocaine</b> rats.
+GRM1	drug	amphetamine	30459590	Collectively, these results reveal similarities but also differences from <strong>mGlu1</strong> LTD observed in other brain regions, and further our understanding of a form of plasticity that may be targeted to reduce cue induced craving for cocaine and <b>methamphetamine</b>.
+GRM1	drug	cocaine	30459590	Collectively, these results reveal similarities but also differences from <strong>mGlu1</strong> LTD observed in other brain regions, and further our understanding of a form of plasticity that may be targeted to reduce cue induced craving for <b>cocaine</b> and methamphetamine.
+GRM1	addiction	relapse	30459590	Collectively, these results reveal similarities but also differences from <strong>mGlu1</strong> LTD observed in other brain regions, and further our understanding of a form of plasticity that may be targeted to reduce cue induced <b>craving</b> for cocaine and methamphetamine.
+GRM1	drug	cocaine	30222904	Consistent with this, we previously showed in nucleus accumbens (NAc) medium spiny neurons (MSNs) that reduced <strong>mGlu1</strong> tone enables and <strong>mGlu1</strong> positive allosteric modulation reverses the elevation of CP AMPAR levels in the NAc that underlies enhanced <b>cocaine</b> craving in the "incubation of craving" rat model of addiction.
+GRM1	addiction	addiction	30222904	Consistent with this, we previously showed in nucleus accumbens (NAc) medium spiny neurons (MSNs) that reduced <strong>mGlu1</strong> tone enables and <strong>mGlu1</strong> positive allosteric modulation reverses the elevation of CP AMPAR levels in the NAc that underlies enhanced cocaine craving in the "incubation of craving" rat model of <b>addiction</b>.
+GRM1	addiction	relapse	30222904	Consistent with this, we previously showed in nucleus accumbens (NAc) medium spiny neurons (MSNs) that reduced <strong>mGlu1</strong> tone enables and <strong>mGlu1</strong> positive allosteric modulation reverses the elevation of CP AMPAR levels in the NAc that underlies enhanced cocaine <b>craving</b> in the "incubation of <b>craving</b>" rat model of addiction.
+GRM1	drug	cocaine	30222904	To better understand <strong>mGlu1</strong>/CP AMPAR interactions, we used a NAc/prefrontal cortex co culture system in which NAc MSNs express high CP AMPAR levels, providing an in vitro model for NAc MSNs after the incubation of <b>cocaine</b> craving.
+GRM1	addiction	relapse	30222904	To better understand <strong>mGlu1</strong>/CP AMPAR interactions, we used a NAc/prefrontal cortex co culture system in which NAc MSNs express high CP AMPAR levels, providing an in vitro model for NAc MSNs after the incubation of cocaine <b>craving</b>.
+GRM1	drug	cocaine	29622268	We compared basal overall translation and its regulation by metabotropic glutamate receptor 1 (<strong>mGlu1</strong>), mGlu5, and N methyl D aspartate receptors (NMDARs) in drug naïve, saline control, and <b>cocaine</b> rats, and we compared GluA1 and GluA2 translation by immunoprecipitating puromycin labeled proteins.
+GRM1	drug	cocaine	29152855	We discuss how stimulation of <strong>mGlu1</strong>/5 receptors increases the activational state of both canonical and noncanonical intracellular signaling pathways and present a theoretical molecular model in which the activation of several kinase effectors, including protein kinase C, extracellular signal regulated kinase and phosphoinositide 3 kinase (PI3K) might lead to receptor desensitization to account for persistent <b>cocaine</b> craving during protracted withdrawal.
+GRM1	addiction	relapse	29152855	We discuss how stimulation of <strong>mGlu1</strong>/5 receptors increases the activational state of both canonical and noncanonical intracellular signaling pathways and present a theoretical molecular model in which the activation of several kinase effectors, including protein kinase C, extracellular signal regulated kinase and phosphoinositide 3 kinase (PI3K) might lead to receptor desensitization to account for persistent cocaine <b>craving</b> during protracted withdrawal.
+GRM1	addiction	withdrawal	29152855	We discuss how stimulation of <strong>mGlu1</strong>/5 receptors increases the activational state of both canonical and noncanonical intracellular signaling pathways and present a theoretical molecular model in which the activation of several kinase effectors, including protein kinase C, extracellular signal regulated kinase and phosphoinositide 3 kinase (PI3K) might lead to receptor desensitization to account for persistent cocaine craving during protracted <b>withdrawal</b>.
+GRM1	drug	cocaine	28624317	However, <b>cocaine</b> exposure increased the expression of <strong>mGluR1</strong> in the NAc core, but not in the NAc shell or dmPFC.
+GRM1	drug	cocaine	28624317	These findings demonstrated that glial glutamate transporters and <strong>mGluR1</strong> in the mesocorticolimbic area could be potential therapeutic targets for the attenuation of reinstatement to <b>cocaine</b> seeking behavior.
+GRM1	addiction	relapse	28624317	These findings demonstrated that glial glutamate transporters and <strong>mGluR1</strong> in the mesocorticolimbic area could be potential therapeutic targets for the attenuation of <b>reinstatement</b> to cocaine <b>seeking</b> behavior.
+GRM1	drug	alcohol	28242339	Among the glutamate receptors involved in <b>alcohol</b> drinking behavior are the metabotropic receptors such as <strong>mGluR1</strong>/5, mGluR2/3, and mGluR7, as well as the ionotropic receptors, NMDA and AMPA.
+GRM1	drug	cocaine	27264310	Through metabotropic glutamate receptor 1 (<strong>mGluR1</strong>) mediated synaptic depression, <strong>mGluR1</strong> positive allosteric modulators remove CP AMPARs from these synapses and thereby reduce <b>cocaine</b> craving.
+GRM1	addiction	relapse	27264310	Through metabotropic glutamate receptor 1 (<strong>mGluR1</strong>) mediated synaptic depression, <strong>mGluR1</strong> positive allosteric modulators remove CP AMPARs from these synapses and thereby reduce cocaine <b>craving</b>.
+GRM1	addiction	relapse	27264310	After withdrawal periods ranging from 1 to >40 days, rats underwent one of the following procedures: 1) whole cell patch clamp recordings to characterize AMPAR transmission, 2) intra NAc core injection of the CP AMPAR antagonist 1 naphthyl acetyl spermine followed by a <b>seeking</b> test, or 3) systemic administration of a <strong>mGluR1</strong> positive allosteric modulator followed by a <b>seeking</b> test.
+GRM1	addiction	withdrawal	27264310	After <b>withdrawal</b> periods ranging from 1 to >40 days, rats underwent one of the following procedures: 1) whole cell patch clamp recordings to characterize AMPAR transmission, 2) intra NAc core injection of the CP AMPAR antagonist 1 naphthyl acetyl spermine followed by a seeking test, or 3) systemic administration of a <strong>mGluR1</strong> positive allosteric modulator followed by a seeking test.
+GRM1	addiction	relapse	27264310	Expression of incubated <b>craving</b> was decreased by intra NAc core 1 naphthyl acetyl spermine injection or systemic <strong>mGluR1</strong> positive allosteric modulator administration.
+GRM1	drug	amphetamine	27264310	However, a common <strong>mGluR1</strong> based therapeutic strategy may be helpful for recovering cocaine and <b>methamphetamine</b> addicts.
+GRM1	drug	cocaine	27264310	However, a common <strong>mGluR1</strong> based therapeutic strategy may be helpful for recovering <b>cocaine</b> and methamphetamine addicts.
+GRM1	drug	alcohol	26773198	Expression of genes encoding <strong>mGlu1</strong>, mGlu5, the NR2A subunit of the NMDA receptor, and Homer2 were all decreased by binge <b>alcohol</b> consumption in males, while females were relatively resistant (only phosphoinositide dependent protein kinase 1 was decreased).
+GRM1	addiction	intoxication	26773198	Expression of genes encoding <strong>mGlu1</strong>, mGlu5, the NR2A subunit of the NMDA receptor, and Homer2 were all decreased by <b>binge</b> alcohol consumption in males, while females were relatively resistant (only phosphoinositide dependent protein kinase 1 was decreased).
+GRM1	drug	amphetamine	26496011	We detected six downregulated genes in the frontal cortex and the hippocampus of chronic <b>METH</b> treated mice, including five IEGs (Arc, Egr2, Fos, Klf10, and Nr4a1) and one neuronal receptor gene (<strong>Grm1</strong>), compared with normal saline treated group, but only four genes (Arc, Egr2, Fos, and Nr4a1) were confirmed to be different.
+GRM1	drug	alcohol	26442908	Group 1 mGlu family proteins (i.e., mGlu) consist of <strong>mGlu1</strong> and mGlu5 and their activity may influence voluntary <b>ethanol</b> intake.
+GRM1	addiction	withdrawal	26442908	Rat hippocampal explants were exposed to CIE with or without the addition of <strong>mGlu1</strong> antagonist (7 hydroxyimino)cyclopropa[b]chromen 1a carboxylate ethyl ester (CPCCOEt; 0.5, 1, and 3μM) or mGlu5 antagonist (E) 2 methyl 6 styryl pyridine (SIB 1893; 20, 100, and 200μM) to assess sparing of <b>withdrawal</b> induced cytotoxicity.
+GRM1	drug	cannabinoid	26171253	Activation of <strong>mGluR1</strong> caused depression of synaptic transmission via retrograde <b>endocannabinoid</b> signalling but had no significant effect at ectopic sites.
+GRM1	drug	alcohol	26101849	Importantly, the association between several genetic variants within the mGluR eEF2 AMPAR pathway and <b>alcohol</b> use behavior (i.e., consumption and <b>alcohol</b> related problems) replicated in the Grady Trauma Project (GTP), an independent sample of adults living in Atlanta, Georgia (n = 1034; 95% African American), including individual variants in <strong>GRM1</strong>, GRM5, EEF2, MTOR, GRIA1, GRIA4 and HOMER2 (P < 0.05).
+GRM1	drug	alcohol	26101849	Gene based analyses conducted in the GTP indicated that <strong>GRM1</strong> (empirical P < 0.05) and EEF2 (empirical P < 0.01) withstood multiple test corrections and predicted increased <b>alcohol</b> consumption and related problems.
+GRM1	drug	amphetamine	25871318	We also provide evidence of altered mRNA expression of (1) voltage gated calcium channels P/Q type Cacna1a (Cav 2.1), N type Cacna1b (Cav 2.2), T type Cav 3.1 Cacna1g, Cav 3.2 Cacna1h, Cav 3.3 Cacna1i and the auxiliary subunit Cacna2d1 (α2δ1); (2) hyperpolarization activated cyclic nucleotide gated channels Hcn1 and Hcn2; and (3) glutamate receptors subunits AMPA type Gria1, NMDA type Grin1 and metabotropic <strong>Grm1</strong> in the mouse mPFC after repeated <b>METH</b> treatment.
+GRM1	drug	cocaine	25829143	<b>Cocaine</b> Decreases Metabotropic Glutamate Receptor <strong>mGluR1</strong> Currents in Dopamine Neurons by Activating mGluR5.
+GRM1	drug	cocaine	25829143	A single injection of <b>cocaine</b> decreased the current activated by <strong>mGluR1</strong> in dopamine neurons, and it had no effect on the size of the mGluR5 mediated current.
+GRM1	drug	cocaine	25829143	When the injection of <b>cocaine</b> was preceded by treatment of the animals with a blocker of mGluR5 receptors (MPEP), <b>cocaine</b> no longer decreased the <strong>mGluR1</strong> current.
+GRM1	drug	cocaine	25829143	Thus, the activation of mGluR5 was required for the <b>cocaine</b> mediated suppression of <strong>mGluR1</strong> mediated currents in dopamine neurons.
+GRM1	drug	cocaine	25829143	The results support the hypothesis that mGluR5 coordinates a reduction in <strong>mGluR1</strong> functional activity after <b>cocaine</b> treatment.
+GRM1	addiction	withdrawal	24553949	Rats evaluated after ∼1 month of <b>withdrawal</b> from such regimens ("incubated rats") exhibit changes in medium spiny neurons (MSNs) of the nucleus accumbens (NAc) that include accumulation of Ca(2+) permeable AMPA receptors (CP AMPARs) and a switch in group I metabotropic glutamate receptor (mGluR) mediated suppression of synaptic transmission from mGluR5 dependent to <strong>mGluR1</strong> dependent.
+GRM1	drug	cocaine	24506432	The present study sought to determine the role of accumbens core <strong>mGluR1</strong>, mGluR5 and protein kinase C (PKC) in <b>cocaine</b> priming induced reinstatement of drug seeking.
+GRM1	addiction	relapse	24506432	The present study sought to determine the role of accumbens core <strong>mGluR1</strong>, mGluR5 and protein kinase C (PKC) in cocaine priming induced <b>reinstatement</b> of drug <b>seeking</b>.
+GRM1	drug	cocaine	24506432	Here, we show that intra accumbens core administration of the <strong>mGluR1</strong>/5 agonist DHPG (250 μM) promoted <b>cocaine</b> seeking in rats.
+GRM1	addiction	relapse	24506432	Here, we show that intra accumbens core administration of the <strong>mGluR1</strong>/5 agonist DHPG (250 μM) promoted cocaine <b>seeking</b> in rats.
+GRM1	drug	cocaine	24506432	Consistent with these results, administration of an <strong>mGluR1</strong> (50.0 μM YM 298198) or mGluR5 (9.0 μM MPEP) antagonist directly into the accumbens core prior to a priming injection of <b>cocaine</b> (10 mg/kg) attenuated the reinstatement of drug seeking.
+GRM1	addiction	relapse	24506432	Consistent with these results, administration of an <strong>mGluR1</strong> (50.0 μM YM 298198) or mGluR5 (9.0 μM MPEP) antagonist directly into the accumbens core prior to a priming injection of cocaine (10 mg/kg) attenuated the <b>reinstatement</b> of drug <b>seeking</b>.
+GRM1	addiction	relapse	24506432	There were no effects of pharmacological inhibition of <strong>mGluR1</strong>, mGluR5 or PKC in the accumbens core on sucrose <b>seeking</b>.
+GRM1	drug	cocaine	24506432	Together, these findings indicate that <strong>mGluR1</strong> and mGluR5 activation in the accumbens core promotes <b>cocaine</b> seeking and that these effects are reinforcer specific.
+GRM1	addiction	relapse	24506432	Together, these findings indicate that <strong>mGluR1</strong> and mGluR5 activation in the accumbens core promotes cocaine <b>seeking</b> and that these effects are reinforcer specific.
+GRM1	drug	cocaine	24506432	Furthermore, stimulation of <strong>mGluR1</strong> and mGluR5 in the accumbens core may regulate <b>cocaine</b> seeking, in part, through activation of PKCγ.
+GRM1	addiction	relapse	24506432	Furthermore, stimulation of <strong>mGluR1</strong> and mGluR5 in the accumbens core may regulate cocaine <b>seeking</b>, in part, through activation of PKCγ.
+GRM1	drug	cocaine	24478360	Incubation of <b>cocaine</b> seeking following brief <b>cocaine</b> experience in mice is enhanced by <strong>mGluR1</strong> blockade.
+GRM1	addiction	relapse	24478360	Incubation of cocaine <b>seeking</b> following brief cocaine experience in mice is enhanced by <strong>mGluR1</strong> blockade.
+GRM1	drug	cocaine	24478360	Because of the pivotal role of <strong>mGluR1</strong> in the control of <b>cocaine</b> induced plasticity, we investigated the role of <strong>mGluR1</strong> in the formation of drug cue mediated <b>cocaine</b> seeking.
+GRM1	addiction	relapse	24478360	Because of the pivotal role of <strong>mGluR1</strong> in the control of cocaine induced plasticity, we investigated the role of <strong>mGluR1</strong> in the formation of drug cue mediated cocaine <b>seeking</b>.
+GRM1	drug	cocaine	24478360	After prolonged withdrawal, mice in which an <strong>mGluR1</strong> antagonist was administered following <b>cocaine</b> self administration displayed increased <b>cocaine</b> seeking compared to vehicle treated mice.
+GRM1	addiction	relapse	24478360	After prolonged withdrawal, mice in which an <strong>mGluR1</strong> antagonist was administered following cocaine self administration displayed increased cocaine <b>seeking</b> compared to vehicle treated mice.
+GRM1	addiction	withdrawal	24478360	After prolonged <b>withdrawal</b>, mice in which an <strong>mGluR1</strong> antagonist was administered following cocaine self administration displayed increased cocaine seeking compared to vehicle treated mice.
+GRM1	drug	cocaine	24478360	These results suggest that limited <b>cocaine</b> experience is sufficient to induce neurobiological changes that enable an initially neutral cue to acquire motivational value that increases over time, an effect that likely involves glutamate signaling through <strong>mGluR1</strong>.
+GRM1	drug	alcohol	24467847	<strong>mGluR1</strong> within the nucleus accumbens regulates <b>alcohol</b> intake in mice under limited access conditions.
+GRM1	drug	alcohol	24467847	Idiopathic or <b>alcohol</b> induced increases in the expression and function of the Group1 metabotropic glutamate receptor subtype 1 (<strong>mGluR1</strong>) within the extended amygdala are theorized to contribute to an individual's propensity to consume excessive amounts of <b>alcohol</b>.
+GRM1	drug	alcohol	24467847	In the past, the detailed study of the functional relevance of <strong>mGluR1</strong> for <b>alcoholism</b> related behaviors in animal models was hampered by the poor solubility and non specific side effects of available inhibitors; however, the advent of the highly potent and soluble <strong>mGluR1</strong> negative allosteric modulator JNJ 16259685 [(3,4 Dihydro 2H pyrano[2,3 b]quinolin 7 yl) (cis 4 methoxycyclohexyl) methanone] has instigated a re examination of the role for this mGluR subtype in mediating the behavioral effects of <b>alcohol</b>.
+GRM1	drug	alcohol	24467847	These data provide novel evidence in support of a critical role for <strong>mGluR1</strong> PLC signaling, scaffolded by Homer2, within the NAC shell, in maintaining <b>alcohol</b> consumption under limited access procedures.
+GRM1	drug	cocaine	24270186	Synaptic depression via <strong>mGluR1</strong> positive allosteric modulation suppresses cue induced <b>cocaine</b> craving.
+GRM1	addiction	relapse	24270186	Synaptic depression via <strong>mGluR1</strong> positive allosteric modulation suppresses cue induced cocaine <b>craving</b>.
+GRM1	addiction	withdrawal	24270186	Thus, restoring <strong>mGluR1</strong> transmission by administering repeated injections of an <strong>mGluR1</strong> positive allosteric modulator (PAM) prevented CP AMPAR accumulation and incubation, whereas blocking <strong>mGluR1</strong> transmission at even earlier <b>withdrawal</b> times accelerated CP AMPAR accumulation.
+GRM1	addiction	relapse	24270186	In studies conducted after prolonged withdrawal, when CP AMPAR levels and cue induced <b>craving</b> are high, we found that systemic administration of an <strong>mGluR1</strong> PAM attenuated the expression of incubated <b>craving</b> by reducing CP AMPAR transmission in the NAc to control levels.
+GRM1	addiction	withdrawal	24270186	In studies conducted after prolonged <b>withdrawal</b>, when CP AMPAR levels and cue induced craving are high, we found that systemic administration of an <strong>mGluR1</strong> PAM attenuated the expression of incubated craving by reducing CP AMPAR transmission in the NAc to control levels.
+GRM1	drug	cocaine	23986250	Here, we show that intra accumbens shell administration of an mGluR5 (9.0 μm MPEP), but not <strong>mGluR1</strong> (50.0 μm YM 298198), antagonist before a priming injection of <b>cocaine</b> (10 mg/kg) attenuated the reinstatement of drug seeking in rats.
+GRM1	addiction	relapse	23986250	Here, we show that intra accumbens shell administration of an mGluR5 (9.0 μm MPEP), but not <strong>mGluR1</strong> (50.0 μm YM 298198), antagonist before a priming injection of cocaine (10 mg/kg) attenuated the <b>reinstatement</b> of drug <b>seeking</b> in rats.
+GRM1	drug	cocaine	23986250	Consistent with these results, intra shell microinjection of the <strong>mGluR1</strong>/5 agonist DHPG (250 μm) promoted <b>cocaine</b> seeking.
+GRM1	addiction	relapse	23986250	Consistent with these results, intra shell microinjection of the <strong>mGluR1</strong>/5 agonist DHPG (250 μm) promoted cocaine <b>seeking</b>.
+GRM1	drug	alcohol	23966068	A 30 day history of binge <b>alcohol</b> drinking (for example, 4 5 g kg( 1) per 2 h( 1)) elevated CeA levels of <strong>mGluR1</strong>, GluN2B, Homer2a/b and phospholipase C (PLC) β3, without significantly altering protein expression within the adjacent basolateral amygdala.
+GRM1	addiction	intoxication	23966068	A 30 day history of <b>binge</b> alcohol drinking (for example, 4 5 g kg( 1) per 2 h( 1)) elevated CeA levels of <strong>mGluR1</strong>, GluN2B, Homer2a/b and phospholipase C (PLC) β3, without significantly altering protein expression within the adjacent basolateral amygdala.
+GRM1	addiction	intoxication	23966068	An intra CeA infusion of <strong>mGluR1</strong>, mGluR5 and PLC inhibitors all dose dependently reduced <b>binge</b> intake, without influencing sucrose drinking.
+GRM1	addiction	intoxication	23966068	The effects of co infusing <strong>mGluR1</strong> and PLC inhibitors were additive, whereas those of coinhibiting mGluR5 and PLC were not, indicating that the efficacy of <strong>mGluR1</strong> blockade to lower <b>binge</b> intake involves a pathway independent of PLC activation.
+GRM1	addiction	intoxication	23966068	The efficacy of <strong>mGluR1</strong>, mGluR5 and PLC inhibitors to reduce <b>binge</b> intake depended upon intact Homer2 expression as revealed through neuropharmacological studies of Homer2 null mutant mice.
+GRM1	drug	alcohol	23747173	There was also a large negative correlation between anandamide concentration and <strong>mGlu1</strong>/5 receptor density in the hippocampi of Cloninger type 1 <b>alcoholics</b> (R =  0.88, p = 0.002), which was not seen in Cloninger type 2 <b>alcoholics</b> or in controls.
+GRM1	addiction	withdrawal	23727437	First, <strong>mGluR1</strong> has been shown to negatively regulate CP AMPAR levels in NAc synapses, and it is possible that a <b>withdrawal</b> dependent decrease in this effect may help explain CP AMPAR accumulation during incubation.
+GRM1	drug	cocaine	23385114	Using metabotropic glutamate receptors to modulate <b>cocaine</b>'s synaptic and behavioral effects: <strong>mGluR1</strong> finds a niche.
+GRM1	drug	cocaine	23385114	Therefore, activation of <strong>mGluR1</strong> with positive allosteric modulators (PAM) may reduce cue induced relapse in abstinent <b>cocaine</b> addicts.
+GRM1	addiction	relapse	23385114	Therefore, activation of <strong>mGluR1</strong> with positive allosteric modulators (PAM) may reduce cue induced <b>relapse</b> in abstinent cocaine addicts.
+GRM1	drug	cocaine	23348064	Metabotropic glutamate receptor I (<strong>mGluR1</strong>) antagonism impairs <b>cocaine</b> induced conditioned place preference via inhibition of protein synthesis.
+GRM1	drug	cocaine	23348064	Antagonism of group I metabotropic glutamate receptors (<strong>mGluR1</strong> and mGluR5) reduces behavioral effects of drugs of abuse, including <b>cocaine</b>.
+GRM1	drug	cocaine	23348064	We also show that <b>cocaine</b> conditioning activated translation machinery in the VTA via an <strong>mGluR1</strong> dependent mechanism.
+GRM1	drug	cocaine	23348064	Furthermore, intra VTA microinjections of <strong>mGluR1</strong> antagonist JNJ16259685 and protein synthesis inhibitor cycloheximide significantly attenuated or blocked the acquisition of <b>cocaine</b> induced conditioned place preference (CPP) and activation of translation elongation factors.
+GRM1	addiction	reward	23348064	Furthermore, intra VTA microinjections of <strong>mGluR1</strong> antagonist JNJ16259685 and protein synthesis inhibitor cycloheximide significantly attenuated or blocked the acquisition of cocaine induced conditioned place preference (<b>CPP</b>) and activation of translation elongation factors.
+GRM1	drug	cocaine	23348064	Taken together, these results suggest that <strong>mGluR1</strong> antagonism inhibits de novo protein synthesis; this effect may block the formation of <b>cocaine</b> cue associations and thus provide a mechanism for the reduction in CPP to <b>cocaine</b>.
+GRM1	addiction	reward	23348064	Taken together, these results suggest that <strong>mGluR1</strong> antagonism inhibits de novo protein synthesis; this effect may block the formation of cocaine cue associations and thus provide a mechanism for the reduction in <b>CPP</b> to cocaine.
+GRM1	drug	cocaine	23303930	These behavioral phenomena were associated with a time dependent reduction in <strong>mGluR1</strong>/5 expression within ventromedial PFC (vmPFC) of <b>cocaine</b> experienced animals exposed to extinction testing but not in untested ones.
+GRM1	drug	cocaine	23303930	Interestingly, pharmacological manipulations of vmPFC <strong>mGluR1</strong>/5 produced no immediate effects on cue induced <b>cocaine</b> seeking behavior but produced residual effects on a subsequent test for <b>cocaine</b> seeking.
+GRM1	addiction	relapse	23303930	Interestingly, pharmacological manipulations of vmPFC <strong>mGluR1</strong>/5 produced no immediate effects on cue induced cocaine <b>seeking</b> behavior but produced residual effects on a subsequent test for cocaine <b>seeking</b>.
+GRM1	drug	cocaine	23303930	At 3 d withdrawal, <b>cocaine</b> experienced rats infused intra vmPFC with <strong>mGluR1</strong>/5 antagonists, either before or after an initial test for <b>cocaine</b> seeking, persisted in their <b>cocaine</b> seeking akin to <b>cocaine</b> experienced rats in protracted withdrawal.
+GRM1	addiction	relapse	23303930	At 3 d withdrawal, cocaine experienced rats infused intra vmPFC with <strong>mGluR1</strong>/5 antagonists, either before or after an initial test for cocaine <b>seeking</b>, persisted in their cocaine <b>seeking</b> akin to cocaine experienced rats in protracted withdrawal.
+GRM1	addiction	withdrawal	23303930	At 3 d <b>withdrawal</b>, cocaine experienced rats infused intra vmPFC with <strong>mGluR1</strong>/5 antagonists, either before or after an initial test for cocaine seeking, persisted in their cocaine seeking akin to cocaine experienced rats in protracted <b>withdrawal</b>.
+GRM1	drug	cocaine	23303930	Conversely, <b>cocaine</b> experienced rats infused with an <strong>mGluR1</strong>/5 agonist before the initial test for <b>cocaine</b> seeking at 30 d withdrawal exhibited a facilitation of extinction learning.
+GRM1	addiction	relapse	23303930	Conversely, cocaine experienced rats infused with an <strong>mGluR1</strong>/5 agonist before the initial test for cocaine <b>seeking</b> at 30 d withdrawal exhibited a facilitation of extinction learning.
+GRM1	addiction	withdrawal	23303930	Conversely, cocaine experienced rats infused with an <strong>mGluR1</strong>/5 agonist before the initial test for cocaine seeking at 30 d <b>withdrawal</b> exhibited a facilitation of extinction learning.
+GRM1	drug	alcohol	23149043	<strong>mGluR1</strong>/5 receptor densities in the brains of <b>alcoholic</b> subjects: a whole hemisphere autoradiography study.
+GRM1	drug	alcohol	23149043	Type 5 metabotropic glutamate receptor (mGlur5) is abundant in brain regions known to be involved in drug reinforcement, yet very little has been published on <strong>mGluR1</strong>/5 expression in <b>alcoholics</b>.
+GRM1	addiction	reward	23149043	Type 5 metabotropic glutamate receptor (mGlur5) is abundant in brain regions known to be involved in drug <b>reinforcement</b>, yet very little has been published on <strong>mGluR1</strong>/5 expression in alcoholics.
+GRM1	drug	alcohol	23149043	We evaluated the densities of <strong>mGluR1</strong>/5 binding in the hippocampus and striatum of post mortem human brains by using [(3)H]Quisqualic acid as a radioligand in whole hemispheric autoradiography of Cloninger type 1 (n=9) and 2 (n=8) <b>alcoholics</b> and healthy controls (n=10).
+GRM1	drug	alcohol	23149043	We observed a 30 40% higher <strong>mGluR1</strong>/5 binding density in the CA2 area of hippocampus in type 1 <b>alcoholics</b> when compared with either type 2 <b>alcoholics</b> or healthy subjects.
+GRM1	drug	alcohol	23149043	Although preliminary, and from a relatively small number of subjects from these diagnostic groups, these results suggest that the <strong>mGluR1</strong>/5 receptors may be increased in type 1 <b>alcoholics</b> in certain brain areas.
+GRM1	drug	cocaine	22815535	Within the group I family of metabotropic glutamate receptors (mGluRs), substantial evidence points to a role for mGluR5 mechanisms in <b>cocaine</b>'s abuse related behavioral effects, but less is understood about the contribution of <strong>mGluR1</strong>, which also belongs to the group I mGluR family.
+GRM1	drug	amphetamine	22815535	The selective <strong>mGluR1</strong> antagonist JNJ16259685 [(3,4 dihydro 2H pyrano [2,3 b]quinolin 7 yl) (cis 4 methoxycyclohexyl) methanone] was used to investigate the role of <strong>mGluR1</strong> in the behavioral effects of cocaine and <b>methamphetamine</b>.
+GRM1	drug	cocaine	22815535	The selective <strong>mGluR1</strong> antagonist JNJ16259685 [(3,4 dihydro 2H pyrano [2,3 b]quinolin 7 yl) (cis 4 methoxycyclohexyl) methanone] was used to investigate the role of <strong>mGluR1</strong> in the behavioral effects of <b>cocaine</b> and methamphetamine.
+GRM1	drug	cocaine	22754497	Loss of <strong>mGluR1</strong> tone during <b>cocaine</b> withdrawal may contribute to CP AMPAR accumulation in the NAc.
+GRM1	addiction	withdrawal	22754497	Loss of <strong>mGluR1</strong> tone during cocaine <b>withdrawal</b> may contribute to CP AMPAR accumulation in the NAc.
+GRM1	drug	cocaine	22754497	Thus, results in both brain regions point to the possibility of using positive modulators of <strong>mGluR1</strong> as treatments for <b>cocaine</b> addiction.
+GRM1	addiction	addiction	22754497	Thus, results in both brain regions point to the possibility of using positive modulators of <strong>mGluR1</strong> as treatments for cocaine <b>addiction</b>.
+GRM1	drug	amphetamine	22732517	We hypothesized that the maintenance of <b>Meth</b> induced CPP would also require activated mGluR, and that the role of <strong>mGluR1</strong> vs. mGluR5 group I subtypes may differ.
+GRM1	addiction	reward	22732517	We hypothesized that the maintenance of Meth induced <b>CPP</b> would also require activated mGluR, and that the role of <strong>mGluR1</strong> vs. mGluR5 group I subtypes may differ.
+GRM1	drug	cocaine	21994370	Interestingly, the effect of DHPG in the <b>cocaine</b> group was mediated by <strong>mGluR1</strong> whereas its effect in the saline group was mediated by mGluR5.
+GRM1	drug	cocaine	21994370	Furthermore, they suggest that activation of <strong>mGluR1</strong> may represent a potential strategy for reducing cue induced <b>cocaine</b> craving in abstinent <b>cocaine</b> addicts.
+GRM1	addiction	relapse	21994370	Furthermore, they suggest that activation of <strong>mGluR1</strong> may represent a potential strategy for reducing cue induced cocaine <b>craving</b> in abstinent cocaine addicts.
+GRM1	drug	opioid	21971021	The present study examined the effects of the <strong>mGluR1</strong> antagonist JNJ16259685 (JNJ) and the mGluR5 antagonist 2 methyl 6 phenylethynylpyridine (MPEP) alone and in combination with <b>morphine</b> in two acute pain models (hotplate, warm water tail withdrawal), and a persistent, inflammatory pain model (capsaicin).
+GRM1	addiction	withdrawal	21971021	The present study examined the effects of the <strong>mGluR1</strong> antagonist JNJ16259685 (JNJ) and the mGluR5 antagonist 2 methyl 6 phenylethynylpyridine (MPEP) alone and in combination with morphine in two acute pain models (hotplate, warm water tail <b>withdrawal</b>), and a persistent, inflammatory pain model (capsaicin).
+GRM1	drug	opioid	21971021	The present findings suggest that the effects produced by <strong>mGluR1</strong> and mGluR5 antagonists alone and in combination with <b>morphine</b> can be differentiated in models of both acute and persistent pain.
+GRM1	drug	alcohol	21946112	The objective of the present study was to evaluate the effects of a selective mGlu5 receptors antagonist  MTEP, and <strong>mGlu1</strong> receptors antagonist  EMQMCM, on two processes relevant to <b>alcohol</b> addiction: the expression of <b>ethanol</b> induced conditioned place preference (CPP) paradigm, and <b>ethanol</b> withdrawal audiogenic seizures in rats.
+GRM1	addiction	addiction	21946112	The objective of the present study was to evaluate the effects of a selective mGlu5 receptors antagonist  MTEP, and <strong>mGlu1</strong> receptors antagonist  EMQMCM, on two processes relevant to alcohol <b>addiction</b>: the expression of ethanol induced conditioned place preference (CPP) paradigm, and ethanol withdrawal audiogenic seizures in rats.
+GRM1	addiction	reward	21946112	The objective of the present study was to evaluate the effects of a selective mGlu5 receptors antagonist  MTEP, and <strong>mGlu1</strong> receptors antagonist  EMQMCM, on two processes relevant to alcohol addiction: the expression of ethanol induced conditioned place preference (<b>CPP</b>) paradigm, and ethanol withdrawal audiogenic seizures in rats.
+GRM1	addiction	withdrawal	21946112	The objective of the present study was to evaluate the effects of a selective mGlu5 receptors antagonist  MTEP, and <strong>mGlu1</strong> receptors antagonist  EMQMCM, on two processes relevant to alcohol addiction: the expression of ethanol induced conditioned place preference (CPP) paradigm, and ethanol <b>withdrawal</b> audiogenic seizures in rats.
+GRM1	drug	alcohol	21946112	Our study shows the importance of mGlu5 and <strong>mGlu1</strong> receptors for the expression of <b>ethanol</b> induced CPP and withdrawal seizures, although mGlu5 receptors antagonist (MTEP) was more potent than the antagonist of <strong>mGlu1</strong> receptors (EMQMCM).
+GRM1	addiction	reward	21946112	Our study shows the importance of mGlu5 and <strong>mGlu1</strong> receptors for the expression of ethanol induced <b>CPP</b> and withdrawal seizures, although mGlu5 receptors antagonist (MTEP) was more potent than the antagonist of <strong>mGlu1</strong> receptors (EMQMCM).
+GRM1	addiction	withdrawal	21946112	Our study shows the importance of mGlu5 and <strong>mGlu1</strong> receptors for the expression of ethanol induced CPP and <b>withdrawal</b> seizures, although mGlu5 receptors antagonist (MTEP) was more potent than the antagonist of <strong>mGlu1</strong> receptors (EMQMCM).
+GRM1	drug	cocaine	21749491	<strong>mGluR1</strong>, but not mGluR5, agonist induced long term potentiation (<strong>mGluR1</strong> LTP) in the BLA CeLc pathway was reduced in rats withdrawal from <b>cocaine</b> for 2 and 14 days, and exhibited an altered concentration response to picrotoxin.
+GRM1	addiction	withdrawal	21749491	<strong>mGluR1</strong>, but not mGluR5, agonist induced long term potentiation (<strong>mGluR1</strong> LTP) in the BLA CeLc pathway was reduced in rats <b>withdrawal</b> from cocaine for 2 and 14 days, and exhibited an altered concentration response to picrotoxin.
+GRM1	drug	cannabinoid	21749491	Blocking <b>cannabinoid</b> receptor 1 (CB(1)) reduced <strong>mGluR1</strong> LTP in the saline treated but not cocaine withdrawn group.
+GRM1	drug	cocaine	21749491	Blocking cannabinoid receptor 1 (CB(1)) reduced <strong>mGluR1</strong> LTP in the saline treated but not <b>cocaine</b> withdrawn group.
+GRM1	drug	cannabinoid	21749491	Additionally, increasing <b>endocannabinoid</b> (eCB) levels abolished <strong>mGluR1</strong> LTP in the saline but not cocaine withdrawn group.
+GRM1	drug	cocaine	21749491	Additionally, increasing endocannabinoid (eCB) levels abolished <strong>mGluR1</strong> LTP in the saline but not <b>cocaine</b> withdrawn group.
+GRM1	drug	cocaine	21749491	However, CB(1) and CB(2) protein levels were increased in the amygdala of <b>cocaine</b> withdrawn rats while <strong>mGluR1</strong> and mGluR5 remained unchanged.
+GRM1	drug	cocaine	21749491	These data suggested that the mechanisms underlying the diminished <strong>mGluR1</strong> LTP in <b>cocaine</b> withdrawn rats involve an altered GABAergic synaptic inhibition mediated by modulation of downstream eCB signaling.
+GRM1	drug	cocaine	21521425	The present study evaluated the contribution of metabotropic glutamate receptor subtype 1 (<strong>mGluR1</strong>) and α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA)/kainate receptor populations to drug context induced reinstatement of <b>cocaine</b> seeking behavior.
+GRM1	addiction	relapse	21521425	The present study evaluated the contribution of metabotropic glutamate receptor subtype 1 (<strong>mGluR1</strong>) and α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (AMPA)/kainate receptor populations to drug context induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+GRM1	drug	cocaine	21521425	<b>Cocaine</b> seeking behavior (non reinforced active lever pressing) was then assessed in the previously <b>cocaine</b> paired and extinction contexts after JNJ16259685 (<strong>mGluR1</strong> antagonist: 0.0, 0.6, or 30 pg/0.3 µl/hemisphere) or CNQX (AMPA/kainate receptor antagonist: 0.0, 0.03, or 0.3 µg/0.3 µl /hemisphere) administration into the NAC core, medial or lateral NAC shell, or the ventral caudate putamen (vCPu, anatomical control).
+GRM1	addiction	relapse	21521425	Cocaine <b>seeking</b> behavior (non reinforced active lever pressing) was then assessed in the previously cocaine paired and extinction contexts after JNJ16259685 (<strong>mGluR1</strong> antagonist: 0.0, 0.6, or 30 pg/0.3 µl/hemisphere) or CNQX (AMPA/kainate receptor antagonist: 0.0, 0.03, or 0.3 µg/0.3 µl /hemisphere) administration into the NAC core, medial or lateral NAC shell, or the ventral caudate putamen (vCPu, anatomical control).
+GRM1	drug	cocaine	21521425	Thus, glutamate mediated changes in drug context induced motivation for <b>cocaine</b> involve distinct neuropharmacological mechanisms within the core and shell subregions of the NAC, with the stimulation of <strong>mGlu1</strong> and AMPA/kainate receptors in the NAC core and the stimulation of AMPA/kainate, but not <strong>mGlu1</strong>, receptors in the NAC shell being necessary for this phenomenon.
+GRM1	drug	alcohol	21376087	After <b>ethanol</b> withdrawal, hippocampal levels of <strong>mGlu1</strong> receptors were higher in unstressed rats, but lower in PRS rats, whereas NPY and CRH levels were similar in the two groups of rats.
+GRM1	addiction	withdrawal	21376087	After ethanol <b>withdrawal</b>, hippocampal levels of <strong>mGlu1</strong> receptors were higher in unstressed rats, but lower in PRS rats, whereas NPY and CRH levels were similar in the two groups of rats.
+GRM1	drug	alcohol	20807241	Regardless of prior <b>alcohol</b> experience, C57BL/6J mice exhibited higher accumbens levels of <strong>mGluR1</strong>/5, Homer2a/b, NR2a and activated kinases vs. DBA2/J mice, whereas an <b>alcohol</b> induced rise in dorsal striatum <strong>mGluR1</strong>/5 expression was observed only in C57BL/6J mice.
+GRM1	drug	amphetamine	20649838	Furthermore, <b>amphetamine</b> but not cocaine treatment maintained the ratio between the glutamate receptor <strong>mGluR1</strong>/5 interacting proteins Homer and Homer1a in the knockouts thereby sustaining the direct pathway.
+GRM1	drug	cocaine	20649838	Furthermore, amphetamine but not <b>cocaine</b> treatment maintained the ratio between the glutamate receptor <strong>mGluR1</strong>/5 interacting proteins Homer and Homer1a in the knockouts thereby sustaining the direct pathway.
+GRM1	drug	alcohol	20477778	<b>Ethanol</b> acutely modulates <strong>mGluR1</strong> dependent long term depression in cerebellum.
+GRM1	drug	cocaine	19936864	The aim of the present study was to test, whether group I metabotropic glutamate receptors (mGluRs) antagonists (<strong>mGluR1</strong> and mGluR5) differentially regulate toxic versus behavioral effects of <b>cocaine</b>, both phenomena relevant to the psychopathology of <b>cocaine</b> addiction in humans.
+GRM1	addiction	addiction	19936864	The aim of the present study was to test, whether group I metabotropic glutamate receptors (mGluRs) antagonists (<strong>mGluR1</strong> and mGluR5) differentially regulate toxic versus behavioral effects of cocaine, both phenomena relevant to the psychopathology of cocaine <b>addiction</b> in humans.
+GRM1	drug	cocaine	19936864	In the present study, we assessed the impact of <strong>mGluR1</strong> antagonist EMQMCM and mGluR5 antagonist MTEP on the <b>cocaine</b> induced lethality and the expression of sensitization to hyperlocomotor effect of <b>cocaine</b> in mice.
+GRM1	addiction	sensitization	19936864	In the present study, we assessed the impact of <strong>mGluR1</strong> antagonist EMQMCM and mGluR5 antagonist MTEP on the cocaine induced lethality and the expression of <b>sensitization</b> to hyperlocomotor effect of cocaine in mice.
+GRM1	drug	cocaine	19936864	Our results suggest that stimulation of <strong>mGluR1</strong> and mGluR5 is involved in lethal effect of <b>cocaine</b> overdose and <b>cocaine</b> seeking behavior evaluated in behavioral sensitization test.
+GRM1	addiction	relapse	19936864	Our results suggest that stimulation of <strong>mGluR1</strong> and mGluR5 is involved in lethal effect of cocaine overdose and cocaine <b>seeking</b> behavior evaluated in behavioral sensitization test.
+GRM1	addiction	sensitization	19936864	Our results suggest that stimulation of <strong>mGluR1</strong> and mGluR5 is involved in lethal effect of cocaine overdose and cocaine seeking behavior evaluated in behavioral <b>sensitization</b> test.
+GRM1	drug	cocaine	19936864	However, the participation of <strong>mGluR1</strong> in these <b>cocaine</b> effects seems to be dominant.
+GRM1	drug	cocaine	19936864	Therefore, antagonists showing preferences towards <strong>mGluR1</strong> might be useful in therapy of <b>cocaine</b> toxicity and abuse.
+GRM1	drug	cocaine	19847405	Effects of <strong>mGluR1</strong> antagonism in the dorsal hippocampus on drug context induced reinstatement of <b>cocaine</b> seeking behavior in rats.
+GRM1	addiction	relapse	19847405	Effects of <strong>mGluR1</strong> antagonism in the dorsal hippocampus on drug context induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior in rats.
+GRM1	drug	cocaine	19847405	Given the known significance of group I metabotropic glutamate receptors (mGluRs), including the <strong>mGluR1</strong> subtype, in drug induced behaviors, the present study was designed to evaluate the contribution of mGluR1s in the DH to drug context induced reinstatement of extinguished <b>cocaine</b> seeking behavior.
+GRM1	addiction	relapse	19847405	Given the known significance of group I metabotropic glutamate receptors (mGluRs), including the <strong>mGluR1</strong> subtype, in drug induced behaviors, the present study was designed to evaluate the contribution of mGluR1s in the DH to drug context induced <b>reinstatement</b> of extinguished cocaine <b>seeking</b> behavior.
+GRM1	addiction	addiction	19847405	These findings indicate that the <strong>mGluR1</strong> is an interesting target from an <b>addiction</b> treatment perspective.
+GRM1	drug	alcohol	19641121	We found that systemic antagonism of metabotropic glutamate subtype 5 (mGlu5) receptors [10 mg/kg 2 methyl 6 (phenylethynyl)pyridine (MPEP) and 3 mg/kg 3 ((2 methyl 1,3 thiazol 4 yl)ethynyl)pyridine], but not <strong>mGlu1</strong> receptors ([0.3 3 mg/kg JNJ16259685) (3,4 dihydro 2H pyrano[2,3]beta quinolin 7 yl)(cis 4 methoxycyclohexyl) methanone)], inhibited the discriminative stimulus effects of <b>alcohol</b>.
+GRM1	drug	cocaine	19597494	We combined ex vivo electrophysiology in acute brain slices with behavioral assays modeling drug relapse in mice and found that the duration of the <b>cocaine</b> evoked synaptic plasticity in the VTA is gated by <strong>mGluR1</strong>.
+GRM1	addiction	relapse	19597494	We combined ex vivo electrophysiology in acute brain slices with behavioral assays modeling drug <b>relapse</b> in mice and found that the duration of the cocaine evoked synaptic plasticity in the VTA is gated by <strong>mGluR1</strong>.
+GRM1	addiction	addiction	19597494	Impaired <strong>mGluR1</strong> function in vulnerable individuals could represent a first step in the recruitment of the neuronal network that underlies drug <b>addiction</b>.
+GRM1	drug	cocaine	19128205	Similarly, the <strong>mGluR1</strong>/5 antagonists, 2 methyl 6 (phenylethynyl)pyridine and 3 [2 methyl 4 thiazolyl)ethynyl]pyridine, have shown to be effective in preclinical models of <b>cocaine</b> addiction.
+GRM1	addiction	addiction	19128205	Similarly, the <strong>mGluR1</strong>/5 antagonists, 2 methyl 6 (phenylethynyl)pyridine and 3 [2 methyl 4 thiazolyl)ethynyl]pyridine, have shown to be effective in preclinical models of cocaine <b>addiction</b>.
+GRM1	drug	alcohol	18838071	Antagonists of group I mGlu receptors, such as MTEP ([(2 methyl 1,3 thiazol 4 yl) ethynyl] pyridine, mGlu5 receptor) or EMQMCM (3 ethyl 2 methyl quinolin 6 yl (4 methoxy cyclohexyl) methanone methanesulfonate, <strong>mGlu1</strong> receptor), caused similar effects to <b>acamprosate</b>.
+GRM1	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (<strong>mGluR1</strong>, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRM1	drug	alcohol	18164577	Effects of <strong>mGlu1</strong> receptor blockade on <b>ethanol</b> self administration in inbred <b>alcohol</b> preferring rats.
+GRM1	drug	alcohol	18164577	The purpose of this work was to examine the role of <strong>mGlu1</strong> receptor antagonism in the maintenance of <b>ethanol</b> self administration and the self administration of an alternate nondrug reward, sucrose.
+GRM1	addiction	reward	18164577	The purpose of this work was to examine the role of <strong>mGlu1</strong> receptor antagonism in the maintenance of ethanol self administration and the self administration of an alternate nondrug <b>reward</b>, sucrose.
+GRM1	drug	alcohol	18164577	Male <b>alcohol</b> preferring inbred rats were trained to self administer <b>ethanol</b> (15% vol/vol) versus water on a concurrent schedule of reinforcement, and the effect of the <strong>mGlu1</strong> receptor antagonist JNJ16259685 (0.1 1.0mg/kg intraperitoneal [IP]) was evaluated on self administration.
+GRM1	addiction	reward	18164577	Male alcohol preferring inbred rats were trained to self administer ethanol (15% vol/vol) versus water on a concurrent schedule of <b>reinforcement</b>, and the effect of the <strong>mGlu1</strong> receptor antagonist JNJ16259685 (0.1 1.0mg/kg intraperitoneal [IP]) was evaluated on self administration.
+GRM1	drug	alcohol	18164577	Interestingly, <b>ethanol</b> self administration was more sensitive to <strong>mGlu1</strong> receptor antagonism than sucrose self administration as lower JNJ16259685 doses reduced <b>ethanol</b> reinforced responding and motor behavior.
+GRM1	drug	alcohol	18164577	Together, these results suggest that <strong>mGlu1</strong> receptors do not play a specific role in modulating <b>ethanol</b> self administration or the self administration of an alternate nondrug reward (i.e., sucrose).
+GRM1	addiction	reward	18164577	Together, these results suggest that <strong>mGlu1</strong> receptors do not play a specific role in modulating ethanol self administration or the self administration of an alternate nondrug <b>reward</b> (i.e., sucrose).
+GRM1	drug	alcohol	18162077	Emerging evidence indicates that Group I metabotropic glutamate receptors (<strong>mGluR1</strong> and mGluR5) differentially regulates <b>ethanol</b> self administration in several rodent behavioral models.
+GRM1	drug	alcohol	18162077	The <strong>mGluR1</strong> antagonist, 3,4 dihydro 2H pyrano[2,3]b quinolin 7 yl (cis 4 methoxycyclohexyl) methanone (JNJ 16259685; 0 to 1 mg/kg) and the mGluR5 antagonist, 6 methyl 2 (phenylethynyl) pyridine (MPEP; 0 to 10 mg/kg) dose dependently reduced <b>ethanol</b> break point.
+GRM1	drug	alcohol	18162077	Thus, the reduction in <b>ethanol</b> break point by <strong>mGluR1</strong> antagonism was probably a result of a motor impairment.
+GRM1	drug	cocaine	17950706	In the PFC, repeated <b>cocaine</b> up regulated Homer2a/b, <strong>mGluR1</strong> and NR2b expression, without affecting Homer1b/c levels.
+GRM1	drug	amphetamine	17499349	We examined whether a dopamine D1 agonist can reverse behavioral sensitization once established by repeated <b>amphetamine</b> (AMP) administrations and determined the mRNA expression levels of the D1 and D2 receptors, metabotropic glutamate receptor 1 (<strong>mGluR1</strong>), and activity regulated cytoskeleton associated protein (arc) in rats.
+GRM1	addiction	sensitization	17499349	We examined whether a dopamine D1 agonist can reverse behavioral <b>sensitization</b> once established by repeated amphetamine (AMP) administrations and determined the mRNA expression levels of the D1 and D2 receptors, metabotropic glutamate receptor 1 (<strong>mGluR1</strong>), and activity regulated cytoskeleton associated protein (arc) in rats.
+GRM1	drug	opioid	17222405	Comparison of the effects of <strong>mGluR1</strong> and mGluR5 antagonists on the expression of behavioral sensitization to the locomotor effect of <b>morphine</b> and the <b>morphine</b> withdrawal jumping in mice.
+GRM1	addiction	sensitization	17222405	Comparison of the effects of <strong>mGluR1</strong> and mGluR5 antagonists on the expression of behavioral <b>sensitization</b> to the locomotor effect of morphine and the morphine withdrawal jumping in mice.
+GRM1	addiction	withdrawal	17222405	Comparison of the effects of <strong>mGluR1</strong> and mGluR5 antagonists on the expression of behavioral sensitization to the locomotor effect of morphine and the morphine <b>withdrawal</b> jumping in mice.
+GRM1	drug	opioid	17222405	The aim of the present study was to compare the influence of group I metabotropic glutamate receptor (mGluR) antagonists (<strong>mGluR1</strong> and mGluR5) on the expression of sensitization to the locomotor effect of <b>morphine</b>.
+GRM1	addiction	sensitization	17222405	The aim of the present study was to compare the influence of group I metabotropic glutamate receptor (mGluR) antagonists (<strong>mGluR1</strong> and mGluR5) on the expression of <b>sensitization</b> to the locomotor effect of morphine.
+GRM1	drug	opioid	17222405	The results suggest that both subtypes of the group I mGluRs (<strong>mGluR1</strong> and mGluR5) take part in the expression of <b>morphine</b> sensitization processes but <strong>mGluR1</strong> is not involved in the expression of <b>morphine</b> withdrawal jumps in mice.
+GRM1	addiction	sensitization	17222405	The results suggest that both subtypes of the group I mGluRs (<strong>mGluR1</strong> and mGluR5) take part in the expression of morphine <b>sensitization</b> processes but <strong>mGluR1</strong> is not involved in the expression of morphine withdrawal jumps in mice.
+GRM1	addiction	withdrawal	17222405	The results suggest that both subtypes of the group I mGluRs (<strong>mGluR1</strong> and mGluR5) take part in the expression of morphine sensitization processes but <strong>mGluR1</strong> is not involved in the expression of morphine <b>withdrawal</b> jumps in mice.
+GRM1	drug	nicotine	16963088	<strong>mGlu1</strong> receptor blockade attenuates cue  and <b>nicotine</b> induced reinstatement of extinguished <b>nicotine</b> self administration behavior in rats.
+GRM1	addiction	relapse	16963088	<strong>mGlu1</strong> receptor blockade attenuates cue  and nicotine induced <b>reinstatement</b> of extinguished nicotine self administration behavior in rats.
+GRM1	drug	nicotine	16963088	Pretreatment with the <strong>mGlu1</strong> receptor antagonist EMQMCM (JNJ16567083, (3 ethyl 2 methyl quinolin 6 yl) (4 methoxy cyclohexyl) methanone methanesulfonate) significantly inhibited cue induced reinstatement of <b>nicotine</b> seeking behavior (5 and 10, but not 2.5 mg/kg).
+GRM1	addiction	relapse	16963088	Pretreatment with the <strong>mGlu1</strong> receptor antagonist EMQMCM (JNJ16567083, (3 ethyl 2 methyl quinolin 6 yl) (4 methoxy cyclohexyl) methanone methanesulfonate) significantly inhibited cue induced <b>reinstatement</b> of nicotine <b>seeking</b> behavior (5 and 10, but not 2.5 mg/kg).
+GRM1	drug	nicotine	16963088	Taken together with the previous reports, the present findings further suggest that blockade of <strong>mGlu1</strong> receptors may be beneficial for preventing relapse to <b>tobacco</b> <b>smoking</b> in <b>nicotine</b> dependent individuals.
+GRM1	addiction	relapse	16963088	Taken together with the previous reports, the present findings further suggest that blockade of <strong>mGlu1</strong> receptors may be beneficial for preventing <b>relapse</b> to tobacco smoking in nicotine dependent individuals.
+GRM1	drug	cocaine	16896963	These findings indicate that the expression of behavioral sensitization to <b>cocaine</b> induced stimulation of locomotor activity may be modulated by group I mGluR antagonists (<strong>mGluR1</strong> rather than mGluR5), but these effects occur at the dose levels that attenuate vertical activity.
+GRM1	addiction	sensitization	16896963	These findings indicate that the expression of behavioral <b>sensitization</b> to cocaine induced stimulation of locomotor activity may be modulated by group I mGluR antagonists (<strong>mGluR1</strong> rather than mGluR5), but these effects occur at the dose levels that attenuate vertical activity.
+GRM1	drug	opioid	16793067	The aims of the present study were to assess: (i) the role of <strong>mGlu1</strong> and mGlu5 receptors in inflammatory pain using selective antagonist EMQMCM, 1.25 5 mg/kg, as the <strong>mGlu1</strong> receptor antagonist, and MPEP or MTEP, 2.5 10 mg/kg, as mGlu5 receptor antagonist; (ii) the possible interaction between <strong>mGlu1</strong> and mGlu5 receptor antagonists and <b>morphine</b>; and (iii) whether tolerance develops to the analgesic effects of these antagonists after prolonged treatment.
+GRM1	drug	opioid	16793067	In the present study, the suppressive effect on formalin induced pain behaviour was much stronger when <strong>mGlu1</strong> and mGlu5 receptor antagonists were co injected compared to administration of a single antagonist, but this effect was not seen when mGlu receptor antagonist was co administered with <b>morphine</b>.
+GRM1	drug	cannabinoid	16723539	In <b>THC</b> tolerant mice, an increase of the basal release probability was found at PF PC synapses, in parallel with a facilitation of slow <strong>mGluR1</strong> (metabotropic glutamate receptor type 1) mediated excitatory postsynaptic currents and a reduced sensitivity to the inhibitory effects of the CB1R agonist CP55,940 [( ) cis 3 [2 hydroxy 4 (1,1 dimethylheptyl)phenyl] trans 4 (3 hydroxypropyl)cyclohexanol].
+GRM1	drug	cannabinoid	16554472	First, a combined activation of group I mGluRs (<strong>mGluR1</strong> and mGluR5) induces a transient depression that is <b>cannabinoid</b> 1 receptor dependent.
+GRM1	drug	cannabinoid	16301180	<b>Endocannabinoid</b> release and LTD induction both depend upon activation of the metabotropic glutamate receptor <strong>mGluR1</strong>, require postsynaptic calcium increases, are synapse specific, and have a similar dependence on the associative activation of PF and climbing fiber synapses.
+GRM1	addiction	dependence	16301180	Endocannabinoid release and LTD induction both depend upon activation of the metabotropic glutamate receptor <strong>mGluR1</strong>, require postsynaptic calcium increases, are synapse specific, and have a similar <b>dependence</b> on the associative activation of PF and climbing fiber synapses.
+GRM1	drug	alcohol	16292590	Effects of <strong>mGluR1</strong>, mGluR2/3, and mGluR5 antagonists were then tested on parameters of <b>ethanol</b> self administration behavior.
+GRM1	drug	alcohol	15717208	After the establishment of operant <b>ethanol</b> self administration, subjects were treated with various metabotropic glutamate receptor (mGluR) subtype antagonists immediately prior to experimental sessions: the mGluR5 antagonist MPEP (1, 3, and 10 mg/kg); the mGluR2  3 antagonist LY 341495 (1, 3, and 10 mg/kg); and the <strong>mGluR1</strong> antagonist CPCCOEt (1, 3, and 10 mg/kg).
+GRM1	addiction	reward	15717208	After the establishment of <b>operant</b> ethanol self administration, subjects were treated with various metabotropic glutamate receptor (mGluR) subtype antagonists immediately prior to experimental sessions: the mGluR5 antagonist MPEP (1, 3, and 10 mg/kg); the mGluR2  3 antagonist LY 341495 (1, 3, and 10 mg/kg); and the <strong>mGluR1</strong> antagonist CPCCOEt (1, 3, and 10 mg/kg).
+GRM1	drug	alcohol	15365315	In the CA3 region, the mRNA expression of <strong>mGlu1</strong>, mGlu5, and mGlu7 receptors showed substantial decreases after <b>ethanol</b> exposure.
+GRM1	drug	opioid	15183518	In the core, neuronal apoptotic inhibitory protein (NAIP), GABA A alpha1 subunit, GRIN2C, GRIA1, <strong>mGluR1</strong>, D4 dopamine receptor and PSD 95 were upregulated by <b>morphine</b> administration whereas bax, bcl x, cox 1 and MAP2 were decreased.
+GRM1	drug	opioid	15178357	Effects of <strong>mGlu1</strong> and mGlu5 metabotropic glutamate antagonists to reverse <b>morphine</b> tolerance in mice.
+GRM1	drug	amphetamine	11418936	Differentially altered <strong>mGluR1</strong> and mGluR5 mRNA expression in rat caudate nucleus and nucleus accumbens in the development and expression of behavioral sensitization to repeated <b>amphetamine</b> administration.
+GRM1	addiction	sensitization	11418936	Differentially altered <strong>mGluR1</strong> and mGluR5 mRNA expression in rat caudate nucleus and nucleus accumbens in the development and expression of behavioral <b>sensitization</b> to repeated amphetamine administration.
+GRM1	drug	amphetamine	11418936	Three hours after acute administration of <b>AMPH</b> to naive rats, <strong>mGluR1</strong> and mGluR5 mRNA expression in the dorsal (caudatoputamen) and ventral (nucleus accumbens) striatum showed no change as compared to acute saline injection.
+GRM1	drug	amphetamine	11418936	In rats that developed behavioral sensitization to repeated <b>AMPH</b>, <strong>mGluR1</strong> levels in the dorsal and ventral striatum were increased by 53% and 43%, respectively, 3 h after the final <b>AMPH</b> treatment.
+GRM1	addiction	sensitization	11418936	In rats that developed behavioral <b>sensitization</b> to repeated AMPH, <strong>mGluR1</strong> levels in the dorsal and ventral striatum were increased by 53% and 43%, respectively, 3 h after the final AMPH treatment.
+GRIN1	drug	cocaine	32751823	We found an up regulation of the accumbal levels of <strong>GluN1</strong> and GluN2A following <b>cocaine</b> self administration that was paralleled by an increase of Munc13 and RIM1 levels.
+GRIN1	drug	cocaine	32751823	At the same time, we also demonstrated that different conditions of <b>cocaine</b> abstinence abolished changes in NMDA receptor subunits (except for higher <strong>GluN1</strong> levels after <b>cocaine</b> abstinence with extinction training), while an increase in the Munc13 concentration was shown in rats housed in an enriched environment.
+GRIN1	addiction	reward	32593543	Then, using small interfering RNAs (siRNAs), we tested the effect of tVTA downregulation of the <strong>GluN1</strong> subunit of the NMDA receptor on <b>reward</b> and locomotor activity.
+GRIN1	addiction	reward	32593543	On the other hand, a reduction in <strong>GluN1</strong> subunits used a marked decrease in <b>operant</b> responding for <b>ICSS</b>, but failed to alter <b>ICSS</b> <b>reward</b> and the <b>reward</b> enhancing effect of PPPA.
+GRIN1	drug	cocaine	32522229	Here, we assess the role of homeostatic mechanisms in the neurobiology of <b>cocaine</b> addiction by providing a brief overview of the parallels between <b>cocaine</b> induced synaptic potentiation and long term synaptic adaptations, focusing on the regulation of GluA1  and <strong>GluN1</strong>  containing receptors.
+GRIN1	addiction	addiction	32522229	Here, we assess the role of homeostatic mechanisms in the neurobiology of cocaine <b>addiction</b> by providing a brief overview of the parallels between cocaine induced synaptic potentiation and long term synaptic adaptations, focusing on the regulation of GluA1  and <strong>GluN1</strong>  containing receptors.
+GRIN1	drug	alcohol	32415404	Western blot analysis indicated that <strong>GluN1</strong> expression in the hippocampus of <b>alcohol</b> drinking group was lower than that in the control group, while the expression of <strong>GluN1</strong> was increased in MMP 9 overexpressing mice.
+GRIN1	drug	alcohol	32062779	We aimed to investigate whether <b>ethanol</b> (EtOH) and acetaldehyde (AcH) can affect glutamate and its receptors <strong>GluN1</strong> and GluA1 in the hippocampus of Aldh2 knockout (Aldh2 KO) and C57BL/6N (wild type (WT)) mice.
+GRIN1	addiction	intoxication	32062779	Together, these in vivo and ex vivo data suggest that EtOH and AcH decrease extracellular glutamate in the hippocampus of mice with a concomitant decrease in <strong>GluN1</strong> and GluA1 subunits, but these effects require relatively high concentrations and may, therefore, explain the consequences of EtOH <b>intoxication</b>.
+GRIN1	drug	alcohol	31978422	Results showed that the mRNA levels of GluN2A but not <strong>GluN1</strong> in NAc are higher after <b>ethanol</b> CPP.
+GRIN1	addiction	reward	31978422	Results showed that the mRNA levels of GluN2A but not <strong>GluN1</strong> in NAc are higher after ethanol <b>CPP</b>.
+GRIN1	drug	cocaine	31161451	Exercise initiated during early, but not late abstinence, reduced <b>cocaine</b> seeking; this effect was strongly associated with dmPFC Grm5 expression (gene encoding mGlu5), and modestly associated with dmPFC <strong>Grin1</strong> and Bdnf IV expression.
+GRIN1	addiction	relapse	31161451	Exercise initiated during early, but not late abstinence, reduced cocaine <b>seeking</b>; this effect was strongly associated with dmPFC Grm5 expression (gene encoding mGlu5), and modestly associated with dmPFC <strong>Grin1</strong> and Bdnf IV expression.
+GRIN1	addiction	withdrawal	30733663	We then analyzed the expression levels of presynaptic (vGlut1, vGlut2, CB1 receptor, synaptophysin) and postsynaptic (PSD95, <strong>GluN1</strong>, GluN2A, GluN2B, GluA1, GluA2, mGluR1 and mGluR5) proteins after 7 days EtOH incubation or after EtOH <b>withdrawal</b>.
+GRIN1	drug	alcohol	30371539	Green tea polyphenols ameliorate <b>ethanol</b> induced spatial learning and memory impairments by enhancing hippocampus <strong>NMDAR1</strong> expression and CREB activity in rats.
+GRIN1	drug	alcohol	30371539	Moreover, 8 week <b>ethanol</b> gavage decreased the density of pyramidal layer neurons, expression of <strong>NMDAR1</strong>, and CREB phosphorylation in the hippocampus region.
+GRIN1	drug	alcohol	30371539	The current findings indicated that GTP intervention can improve <b>ethanol</b> induced spatial learning and memory impairments in rats after <b>ethanol</b> withdrawal, which is related to the upregulated density of pyramidal layer neurons, expression of <strong>NMDAR1</strong>, and CREB phosphorylation in the hippocampus region.
+GRIN1	addiction	withdrawal	30371539	The current findings indicated that GTP intervention can improve ethanol induced spatial learning and memory impairments in rats after ethanol <b>withdrawal</b>, which is related to the upregulated density of pyramidal layer neurons, expression of <strong>NMDAR1</strong>, and CREB phosphorylation in the hippocampus region.
+GRIN1	drug	opioid	30227624	Sinomenine Protects Against <b>Morphine</b> Dependence through the <strong>NMDAR1</strong>/CAMKII/CREB Pathway: A Possible Role of Astrocyte Derived Exosomes.
+GRIN1	addiction	dependence	30227624	Sinomenine Protects Against Morphine <b>Dependence</b> through the <strong>NMDAR1</strong>/CAMKII/CREB Pathway: A Possible Role of Astrocyte Derived Exosomes.
+GRIN1	drug	opioid	30227624	Moreover, sinomenine inhibited the expressions of p <strong>NMDAR1</strong>/<strong>NMDAR1</strong>, p CAMKII/CAMKII, and p CREB/CREB in the hippocampusof <b>morphine</b> dependent mice and SH SY5Y cells.
+GRIN1	drug	cocaine	30144237	In <b>cocaine</b> naïve animals, SERT removal led to reduced baseline Hb mRNA levels of critical determinants of glutamate transmission, such as SLC1A2, the main glutamate transporter and N methyl D aspartate (<strong>Grin1</strong>, Grin2A and Grin2B) as well as α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (Gria1 and Gria2) receptor subunits, with no changes in the scaffolding protein Dlg4.
+GRIN1	drug	cocaine	30144237	In response to ShA and LgA <b>cocaine</b> intake, SLC1A2 and <strong>Grin1</strong> mRNA levels decreased in SERT+/+ rats to levels equal of those of SERT /  rats.
+GRIN1	drug	amphetamine	30056065	In this study, we measured the effects of single dose injections of modafinil and <b>METH</b> on the protein levels of acetylated histone H3 (H3ac) and H4ac, deacetylases HDAC1 and HDAC2, and of the NMDA subunit <strong>GluN1</strong> in the medial PFC (mPFC) of mice euthanized 1 h after drug administration.
+GRIN1	drug	amphetamine	30056065	Acute modafinil and <b>METH</b> injections caused similar effects on total histone acetylation, increasing H3ac and decreasing H4ac, and they also increased HDAC1, HDAC2 and <strong>GluN1</strong> protein levels in the mouse mPFC.
+GRIN1	drug	amphetamine	30056065	Analysis of histone 3/4 enrichment at specific promoters revealed: i) distinct effects of the drugs on histone 3 acetylation, with modafinil increasing H3ac at Drd1 and Adra1b promoters, but <b>METH</b> increasing H3ac at Adra1a; ii) distinct effects on histone 4 acetylation enrichment, with modafinil increasing H4ac at the Drd2 promoter and decreasing it at Hrh1, but <b>METH</b> increasing H4ac at Drd1; iii) comparable effects of both psychostimulants, increasing H3ac at Drd2, Hcrtr1, and Hrh1 promoters, decreasing H3ac at Hrh3, increasing H4ac at Hcrtr1, and decreasing H4ac at Hcrtr2, Hrh3, and <strong>Grin1</strong> promoters.
+GRIN1	drug	amphetamine	30056065	Interestingly, only <b>METH</b> altered mRNA levels of genes with altered histone acetylation status, inducing increased expression of Drd1a, Adra1a, Hcrtr1, and Hrh1, and decreasing <strong>Grin1</strong>.
+GRIN1	addiction	addiction	29766293	Data obtained using Western blotting technique showed a significant increase in the level of <strong>GluN1</strong> and GluN2B, but not in GluN2A subunits in all the three regions (mPFC, lPFC, and OFC) of men whom suffered from <b>addiction</b> as compared to the appropriate controls.
+GRIN1	addiction	addiction	29766293	These findings showed a novel role for <strong>GluN1</strong>, GluN2B subunits, rather than the GluN2A subunit of NMDARs, in the pathophysiology of <b>addiction</b> and suggested their role in the drug induced plasticity of NMDARs.
+GRIN1	drug	amphetamine	29247759	<b>METH</b> treated mice also showed i) decreased levels of total H3ac and H4ac, and increased levels of 5 mC, ii) decreased H3ac enrichment at promoters of Drd2, Hcrtr1/2, Hrh1 and <strong>Grin1</strong>, and increased H4ac enrichment at Drd1, Hrh1 and <strong>Grin1</strong>, iii) increased mRNA of Drd1a, <strong>Grin1</strong> and Gria1.
+GRIN1	addiction	addiction	29234834	One day after the final self administration session, the rats were euthanized and the dmPFC was removed for quantification of mRNA expression of critical glutamatergic signaling genes, Homer2, <strong>Grin1</strong>, and Dlg4, as these genes and brain region have been previously implicated in <b>addiction</b>, learning, and memory.
+GRIN1	drug	cocaine	29234834	Lastly, Homer2, <strong>Grin1</strong>, and Dlg4 mRNA were impacted by both duration and mode of <b>cocaine</b> exposure.
+GRIN1	drug	cocaine	29196318	In this study, we used viral mediated expression of a dominant negative <strong>GluN1</strong> subunit (HSV dnGluN1) in VTA neurons to study the effect of transient NMDAR inactivation on the GluA1 increases induced by chronic <b>cocaine</b> self administration in male rats.
+GRIN1	drug	psychedelics	28877967	<b>Ketamine</b> binding decreases occupancy of desensitized states of the <strong>GluN1</strong>/2B NMDAR subtype.
+GRIN1	addiction	reward	27012890	To examine how striatal NMDAR function modulates <b>reward</b> related behaviors, we generated D1  and A2A specific genetic deletions of the obligatory <strong>GluN1</strong> subunit.
+GRIN1	drug	cocaine	27012890	Interestingly, we observed no differences in any <strong>GluN1</strong> /  genotype in reward learning as assessed by acquisition or extinction of <b>cocaine</b> conditioned place preference (CPP).
+GRIN1	addiction	reward	27012890	Interestingly, we observed no differences in any <strong>GluN1</strong> /  genotype in <b>reward</b> learning as assessed by acquisition or extinction of cocaine conditioned place preference (<b>CPP</b>).
+GRIN1	drug	cocaine	26811312	In contrast, locomotor sensitization to <b>cocaine</b> produced an up regulation of several glutamate receptor related genes and, specifically, an increased protein expression of the <strong>GluN1</strong> receptor subunit.
+GRIN1	addiction	sensitization	26811312	In contrast, locomotor <b>sensitization</b> to cocaine produced an up regulation of several glutamate receptor related genes and, specifically, an increased protein expression of the <strong>GluN1</strong> receptor subunit.
+GRIN1	drug	cannabinoid	26811312	Overall, these findings suggest that repeated cocaine administration resulting in locomotor sensitization induces a down regulation of the <b>endocannabinoid</b> signaling that could contribute to the specifically increased <strong>GluN1</strong> expression observed in the hippocampus of cocaine sensitized mice.
+GRIN1	drug	cocaine	26811312	Overall, these findings suggest that repeated <b>cocaine</b> administration resulting in locomotor sensitization induces a down regulation of the endocannabinoid signaling that could contribute to the specifically increased <strong>GluN1</strong> expression observed in the hippocampus of <b>cocaine</b> sensitized mice.
+GRIN1	addiction	sensitization	26811312	Overall, these findings suggest that repeated cocaine administration resulting in locomotor <b>sensitization</b> induces a down regulation of the endocannabinoid signaling that could contribute to the specifically increased <strong>GluN1</strong> expression observed in the hippocampus of cocaine sensitized mice.
+GRIN1	addiction	relapse	26687341	Ex vivo reverse transcription polymerase chain reaction analysis of brain tissue found reduced sensitivity to punished EtOH <b>seeking</b> after CIE exposure was accompanied by a significant increase in gene expression of the <strong>GluN1</strong> and GluN2A subunits of the N methyl d aspartate receptor, specifically in the medial orbitofrontal cortex.
+GRIN1	drug	amphetamine	26640076	Importantly, saline treated and <b>AMPH</b> treated mice lacking TAAR1 demonstrated significant alterations in the total levels and phosphorylation of the critical subunit of NMDA glutamate receptors, <strong>GluN1</strong>, in the striatum, suggesting a role of TAAR1 in the modulation of frontostriatal glutamate transmission; this effect could underlie the observed alterations in conditioning processes.
+GRIN1	drug	alcohol	26609150	Here we evaluated the contribution of mesolimbic NMDARs and AMPARs in mediating <b>alcohol</b> seeking responses induced by environmental stimuli and relapse behavior using four inducible mutant mouse lines lacking the glutamate receptor genes <strong>Grin1</strong> or Gria1 in either DA transporter (DAT) or D1R expressing neurons.
+GRIN1	addiction	relapse	26609150	Here we evaluated the contribution of mesolimbic NMDARs and AMPARs in mediating alcohol <b>seeking</b> responses induced by environmental stimuli and <b>relapse</b> behavior using four inducible mutant mouse lines lacking the glutamate receptor genes <strong>Grin1</strong> or Gria1 in either DA transporter (DAT) or D1R expressing neurons.
+GRIN1	drug	alcohol	26609150	We then show that <strong>GluN1</strong> and GluA1 receptor subunits within these neuronal subpopulations mediate the <b>alcohol</b> deprivation effect, while having no impact on context  plus cue induced reinstatement of <b>alcohol</b> seeking behavior.
+GRIN1	addiction	relapse	26609150	We then show that <strong>GluN1</strong> and GluA1 receptor subunits within these neuronal subpopulations mediate the alcohol deprivation effect, while having no impact on context  plus cue induced <b>reinstatement</b> of alcohol <b>seeking</b> behavior.
+GRIN1	drug	alcohol	26289945	The aim of the current study was to determine genotype effects of four single nucleotide polymorphisms (SNPs) in the genes of the N Methyl d aspartate receptor (<strong>GRIN1</strong>, GRIN2A, GRIN2C) and kainate receptor (GRIK1), which have been previously associated with <b>alcoholism</b>, on behavior, neural cue reactivity and drinking outcome.
+GRIN1	drug	alcohol	26266540	In the present study, we used human embryonic stem cell (hESC) derived cortical neurons as in vitro cellular models to investigate <b>alcohol</b> induced expression changes of genes involved in <b>alcohol</b> metabolism (ALDH2), anti apoptosis (BCL2 and CCND2), neurotransmission (NMDA receptor subunit genes: <strong>GRIN1</strong>, GRIN2A, GRIN2B, and GRIN2D), calcium channel activity (ITPR2), or transcriptional repression (JARID2).
+GRIN1	drug	alcohol	26266540	After a 7 day <b>ethanol</b> (50 mM) exposure followed by a 24 hour <b>ethanol</b> withdrawal treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (<strong>GRIN1</strong>: 1.93 fold, P = 0.003; GRIN2A: 1.40 fold, P = 0.003; GRIN2B: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; BCL2: 1.34 fold, P = 0.031), and the results of <strong>GRIN1</strong>, GRIN2A, and GRIN2B survived multiple comparison correction.
+GRIN1	addiction	withdrawal	26266540	After a 7 day ethanol (50 mM) exposure followed by a 24 hour ethanol <b>withdrawal</b> treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (<strong>GRIN1</strong>: 1.93 fold, P = 0.003; GRIN2A: 1.40 fold, P = 0.003; GRIN2B: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; BCL2: 1.34 fold, P = 0.031), and the results of <strong>GRIN1</strong>, GRIN2A, and GRIN2B survived multiple comparison correction.
+GRIN1	drug	amphetamine	25871318	We also provide evidence of altered mRNA expression of (1) voltage gated calcium channels P/Q type Cacna1a (Cav 2.1), N type Cacna1b (Cav 2.2), T type Cav 3.1 Cacna1g, Cav 3.2 Cacna1h, Cav 3.3 Cacna1i and the auxiliary subunit Cacna2d1 (α2δ1); (2) hyperpolarization activated cyclic nucleotide gated channels Hcn1 and Hcn2; and (3) glutamate receptors subunits AMPA type Gria1, NMDA type <strong>Grin1</strong> and metabotropic Grm1 in the mouse mPFC after repeated <b>METH</b> treatment.
+GRIN1	drug	alcohol	25837445	Differential phosphorylation of <strong>NMDAR1</strong> CaMKII MAPKs in the rat nucleus accumbens following chronic <b>ethanol</b> exposure.
+GRIN1	drug	alcohol	25837445	N Methyl d aspartate receptor 1 (<strong>NMDAR1</strong>), Ca(2+)/calmodulin dependent protein kinase II (CaMKII) and extracellular signal regulated kinases (ERKs) have been demonstrated to contribute to and possibly interact in the molecular mechanism underlying <b>ethanol</b> dependence and relapse.
+GRIN1	addiction	dependence	25837445	N Methyl d aspartate receptor 1 (<strong>NMDAR1</strong>), Ca(2+)/calmodulin dependent protein kinase II (CaMKII) and extracellular signal regulated kinases (ERKs) have been demonstrated to contribute to and possibly interact in the molecular mechanism underlying ethanol <b>dependence</b> and relapse.
+GRIN1	addiction	relapse	25837445	N Methyl d aspartate receptor 1 (<strong>NMDAR1</strong>), Ca(2+)/calmodulin dependent protein kinase II (CaMKII) and extracellular signal regulated kinases (ERKs) have been demonstrated to contribute to and possibly interact in the molecular mechanism underlying ethanol dependence and <b>relapse</b>.
+GRIN1	drug	alcohol	25837445	However, little is known regarding the mechanisms underlying the effects of <b>ethanol</b> exposure, withdrawal, and re exposure, particularly with regard to <strong>NMDAR1</strong> CaMKII ERK signaling in accumbens subregions.
+GRIN1	addiction	withdrawal	25837445	However, little is known regarding the mechanisms underlying the effects of ethanol exposure, <b>withdrawal</b>, and re exposure, particularly with regard to <strong>NMDAR1</strong> CaMKII ERK signaling in accumbens subregions.
+GRIN1	drug	alcohol	25837445	Phosphorylation of <strong>NMDAR1</strong>, CaMKII and ERK was significantly decreased in the AcbSh and AcbC following chronic <b>ethanol</b> exposure.
+GRIN1	drug	alcohol	25837445	<b>Ethanol</b> withdrawal increased phospho <strong>NMDAR1</strong> and phospho CaMKII expression in the AcbSh.
+GRIN1	addiction	withdrawal	25837445	Ethanol <b>withdrawal</b> increased phospho <strong>NMDAR1</strong> and phospho CaMKII expression in the AcbSh.
+GRIN1	drug	alcohol	25837445	These results indicated that the activation of <strong>NMDAR1</strong> CaMKII ERK signaling in the AcbSh but not the AcbC would contribute more to <b>ethanol</b> drinking and chronic <b>ethanol</b> related negative emotional states.
+GRIN1	drug	cocaine	25408547	The present study focused on metabotropic glutamatergic receptors type 5 (mGluR(5)) and N methyl D aspartate receptor subunits (NMDAR: <strong>GluN1</strong>, GluN2A, GluN2B) proteins during <b>cocaine</b> self administration and after 10 day of extinction training in rats.
+GRIN1	drug	cocaine	25408547	Our results revealed that <b>cocaine</b> self administration selectively increased <strong>GluN1</strong> and GluN2A subunit in the rat hippocampus and dorsal striatum, respectively, while mGluR(5) protein expression was similarly increased in the dorsal striatum of both experimental groups.
+GRIN1	drug	cocaine	25408547	Withdrawal from both contingent and non contingent <b>cocaine</b> delivery induced parallel increases in prefrontal cortical GluN2A protein expression, hippocampal mGluR(5), and <strong>GluN1</strong> protein expression as well as in accumbal <strong>GluN1</strong> subunit expression, while the mGluR(5) expression was reduced in the prefrontal cortex.
+GRIN1	addiction	withdrawal	25408547	<b>Withdrawal</b> from both contingent and non contingent cocaine delivery induced parallel increases in prefrontal cortical GluN2A protein expression, hippocampal mGluR(5), and <strong>GluN1</strong> protein expression as well as in accumbal <strong>GluN1</strong> subunit expression, while the mGluR(5) expression was reduced in the prefrontal cortex.
+GRIN1	addiction	withdrawal	25268928	Within the first few hours of <b>withdrawal</b>, there is a marked decrease in tyrosine phosphorylation of critical intracellular and membrane bound proteins in the dmPFC that include ERK/MAP kinase and the NMDA receptor subunits, <strong>GluN1</strong> and GluN2B.
+GRIN1	drug	psychedelics	25245072	Recent animal studies have shown that repeated <b>ketamine</b> administration significantly increases NMDA receptor subunit gene expression, in particular subunit 1 (NR1 or <strong>GluN1</strong>) levels.
+GRIN1	drug	cocaine	25070539	D1R/<strong>GluN1</strong> complexes in the striatum integrate dopamine and glutamate signalling to control synaptic plasticity and <b>cocaine</b> induced responses.
+GRIN1	addiction	addiction	25070539	Our findings uncover D1R/<strong>GluN1</strong> complexes as a major substrate for the dopamine glutamate interaction in MSN that is usurped by <b>addictive</b> drugs to elicit persistent behavioural alterations.
+GRIN1	drug	opioid	26574964	Blood samples were taken for the determination of serum levels of racemic <b>methadone</b> and its R and S enantiomers, and for typing of candidate alleles of POR, CYP2B6, ABCB1, <strong>GRIN1</strong>, OPRM1, SLC6A3, DßH and ARRB2 genes, all associated with the metabolism, tissue distribution and mechanism of action of <b>methadone</b>.
+GRIN1	drug	alcohol	24523671	Out of the 16 glutamate receptor subunits, mRNAs encoding two AMPA [2 amino 3 (3 hydroxy 5 methyl isoxazol 4 yl)propanoic acid] receptor subunits GluA2 and GluA3; three kainate receptor subunits GluK2, GluK3 and GluK5 and five NMDA (N methyl D aspartate) receptor subunits <strong>GluN1</strong>, GluN2A, GluN2C, GluN2D, and GluN3A were significantly increased in the HP DG region in <b>alcoholics</b>.
+GRIN1	drug	alcohol	24244696	In this study, we determined how expression of a mutant <strong>GluN1</strong> subunit (F639A) that reduces <b>ethanol</b> inhibition of NMDARs affects <b>ethanol</b> induced behaviors in mice.
+GRIN1	drug	amphetamine	24239129	Chronic <b>METH</b> decreased transcript and protein expression of GluA1 and GluA2 alpha amino 3 hydroxy 5 methyl 4 isoxazole propionic acid receptor (AMPAR) and <strong>GluN1</strong> N methyl D aspartate receptor subunits.
+GRIN1	drug	amphetamine	24239129	Chromatin immunoprecipitation polymerase chain reaction revealed that <b>METH</b> decreased enrichment of acetylated histone H4 on GluA1, GluA2, and <strong>GluN1</strong> promoters.
+GRIN1	drug	opioid	24223972	Sub acute <b>morphine</b> administration resulted in a decrease of <strong>NMDAR1</strong> and Arrb2 whereas during longer <b>opioid</b> treatment the expression <strong>NMDAR1</strong> and Arrb2 mRNA increased again to baseline values.
+GRIN1	drug	psychedelics	24223972	Coadministration of s <b>ketamine</b> or clonidine resulted in a reversal of the mechanical hyperalgesia and inhibited the normalization of <strong>NMDAR1</strong> mRNA expression but had no effect on the expression of Arrb2 mRNA.
+GRIN1	drug	cocaine	24102978	Conversely, in <b>cocaine</b> treated animals, stress dynamically altered the glutamatergic synapse by: (1) enhancing the presynaptic vesicular mediators of glutamate release; (2) reducing the transporters responsible for glutamate clearance; (3) increasing the postsynaptic responsiveness of the N methyl D aspartate subunit <strong>GluN1</strong>; and (4) causing hyperresponsive spines as evidenced by increased activation of the postsynaptic cdc42 Pak pathway.
+GRIN1	drug	amphetamine	23880023	Genetic variation of <strong>GRIN1</strong> confers vulnerability to <b>methamphetamine</b> dependent psychosis in a Thai population.
+GRIN1	addiction	dependence	23880023	Variations of <strong>GRIN1</strong> have been identified as a risk factor for schizophrenia and drug <b>dependence</b>, supporting hypotheses of glutamatergic dysfunction in these disorders.
+GRIN1	drug	amphetamine	23880023	<b>Methamphetamine</b> (<b>METH</b>) is a psychostimulant drug which can induce psychotic symptoms reminiscent of those found in schizophrenia; thus <strong>GRIN1</strong> is a candidate gene for vulnerability to <b>METH</b> dependence or <b>METH</b> dependent psychosis.
+GRIN1	addiction	dependence	23880023	Methamphetamine (METH) is a psychostimulant drug which can induce psychotic symptoms reminiscent of those found in schizophrenia; thus <strong>GRIN1</strong> is a candidate gene for vulnerability to METH <b>dependence</b> or METH dependent psychosis.
+GRIN1	drug	amphetamine	23880023	The present study examined two polymorphisms of <strong>GRIN1</strong>, rs11146020 (G1001C) and rs1126442 (G2108A), in 100 male Thai <b>METH</b> dependent patients and 103 healthy controls using PCR RFLP techniques.
+GRIN1	drug	amphetamine	23880023	The present findings indicate that the rs1126442 of <strong>GRIN1</strong> contributes to the genetic vulnerability to psychosis in <b>METH</b> dependent subjects in the Thai population.
+GRIN1	drug	cocaine	23624776	<strong>GluN1</strong>, GluN2B, and phospho GluN2B Tyr1472 in the dmPFC were decreased after ShA and LgA <b>cocaine</b>.
+GRIN1	drug	alcohol	23372792	Differential phosphorylation of <strong>GluN1</strong> MAPKs in rat brain reward circuits following long term <b>alcohol</b> exposure.
+GRIN1	addiction	reward	23372792	Differential phosphorylation of <strong>GluN1</strong> MAPKs in rat brain <b>reward</b> circuits following long term alcohol exposure.
+GRIN1	drug	alcohol	23372792	The effects of long term <b>alcohol</b> consumption on the mitogen activated protein kinases (MAPKs) pathway and N methyl D aspartate type glutamate receptor 1 (<strong>GluN1</strong>) subunits in the mesocorticolimbic system remain unclear.
+GRIN1	drug	alcohol	23372792	Those results suggest that the long term <b>alcohol</b> consumption can inhibits <strong>GluN1</strong> and ERK phosphorylation, but not JNK or p38 in the mesocorticolimbic system, and these changes may be relevant to <b>alcohol</b> dependence.
+GRIN1	addiction	dependence	23372792	Those results suggest that the long term alcohol consumption can inhibits <strong>GluN1</strong> and ERK phosphorylation, but not JNK or p38 in the mesocorticolimbic system, and these changes may be relevant to alcohol <b>dependence</b>.
+GRIN1	drug	alcohol	23372792	To differentiate <b>alcohol</b> induced changes in ERK and <strong>GluN1</strong> between acute and chronic <b>alcohol</b> exposure, we have determined levels of phospho ERK, phospho <strong>GluN1</strong> and total levels of <strong>GluN1</strong> after acute <b>alcohol</b> exposure.
+GRIN1	drug	alcohol	23372792	Our data show that 30 min following a 2.5 g/kg dose of <b>alcohol</b> (administered intragastrically), levels of phospho ERK are decreased while those of phospho <strong>GluN1</strong> are elevated with no change in total <strong>GluN1</strong> levels.
+GRIN1	drug	alcohol	23372792	At 24 h following the single <b>alcohol</b> dose, levels of phospho ERK are elevated in several brain regions while there are no differences between controls and <b>alcohol</b> treated animals in phospho <strong>GluN1</strong> or total <strong>GluN1</strong>.
+GRIN1	drug	alcohol	23372792	Those results suggest that <b>alcohol</b> may differentially regulate <strong>GluN1</strong> function and ERK activation depending on <b>alcohol</b> dose and exposure time in the central nervous system.
+GRIN1	drug	psychedelics	23352746	Individual and combined effects of rhynchophylline and <b>ketamine</b> on proliferation, <strong>NMDAR1</strong> and GluA2/3 protein expression in PC12 cells.
+GRIN1	drug	psychedelics	23352746	The individual and combined effects of rhynchophylline and <b>ketamine</b> on proliferation and <strong>GluN1</strong> and GluA2/3 protein expression in PC12 cells were investigated.
+GRIN1	drug	psychedelics	23352746	<strong>GluN1</strong> protein expression was downregulated by rhynchophylline (1 mmol/L), while treatment with <b>ketamine</b>, either alone or with rhynchophylline, had no effect.
+GRIN1	drug	psychedelics	23352746	These findings demonstrate that rhynchophylline suppresses GluA2/3 expression in <b>ketamine</b> induced PC12 cells and downregulates <strong>GluN1</strong> expression.
+GRIN1	drug	psychedelics	23352746	<b>Ketamine</b>'s lack of effect on <strong>GluN1</strong> expression offers a partial explanation for <b>ketamine</b> addiction and the anti addictive properties of rhynchophylline.
+GRIN1	addiction	addiction	23352746	Ketamine's lack of effect on <strong>GluN1</strong> expression offers a partial explanation for ketamine <b>addiction</b> and the anti <b>addictive</b> properties of rhynchophylline.
+GRIN1	drug	opioid	23031399	Additionally, SP dependent upregulation of prodynorphin, <strong>NMDA1</strong> and NK1 receptor expression in spinal cord was seen after <b>morphine</b> treatment and incision.
+GRIN1	drug	alcohol	22486492	Finally, we examined changes in mRNA expression of the NMDA receptor subunit genes <strong>GRIN1</strong>, GRIN2A, GRIN2B, and GRIN2D after 7 days of <b>alcohol</b> exposure and after 24 hour withdrawal from chronic <b>alcohol</b> exposure.
+GRIN1	addiction	withdrawal	22486492	Finally, we examined changes in mRNA expression of the NMDA receptor subunit genes <strong>GRIN1</strong>, GRIN2A, GRIN2B, and GRIN2D after 7 days of alcohol exposure and after 24 hour <b>withdrawal</b> from chronic alcohol exposure.
+GRIN1	drug	alcohol	22486492	After 7 days of chronic <b>alcohol</b> exposure, there were significant increases in mRNA expression of <strong>GRIN1</strong>, GRIN2A, and GRIN2D in cultures derived from <b>alcoholic</b> subjects but not in cultures derived from nonalcoholics.
+GRIN1	drug	cocaine	22349092	Similarly, alterations in the glutamatergic <strong>GluN1</strong> or GluA1 channels have been implicated in triggering sensitization to other addictive drugs such as <b>cocaine</b>, amphetamines and opiates.
+GRIN1	addiction	addiction	22349092	Similarly, alterations in the glutamatergic <strong>GluN1</strong> or GluA1 channels have been implicated in triggering sensitization to other <b>addictive</b> drugs such as cocaine, amphetamines and opiates.
+GRIN1	addiction	sensitization	22349092	Similarly, alterations in the glutamatergic <strong>GluN1</strong> or GluA1 channels have been implicated in triggering <b>sensitization</b> to other addictive drugs such as cocaine, amphetamines and opiates.
+GRIN1	addiction	withdrawal	21855055	In ventral tegmental area, Extinction training reversed the decreased postsynaptic density <strong>NMDAR1</strong> protein in the Home and Box <b>withdrawal</b> groups.
+GRIN1	drug	benzodiazepine	20853509	Immunogold electron microscopic evidence of differential regulation of <strong>GluN1</strong>, GluN2A, and GluN2B, NMDA type glutamate receptor subunits in rat hippocampal CA1 synapses during <b>benzodiazepine</b> withdrawal.
+GRIN1	addiction	withdrawal	20853509	Immunogold electron microscopic evidence of differential regulation of <strong>GluN1</strong>, GluN2A, and GluN2B, NMDA type glutamate receptor subunits in rat hippocampal CA1 synapses during benzodiazepine <b>withdrawal</b>.
+GRIN1	drug	benzodiazepine	20853509	Therefore, in this study ultrastructural evidence for possible reductions in NMDAR <strong>GluN1</strong>, GluN2A, and GluN2B subunits was sought at CA1 stratum radiatum synapses in proximal dendrites using postembedding immunogold labeling of tissues from rats withdrawn for 2 days from 1 week daily oral administration of the <b>benzodiazepine</b>, <b>flurazepam</b> (FZP).
+GRIN1	addiction	withdrawal	20853509	The data therefore provide direct evidence for reduced synaptic <strong>GluN1</strong>/GluN2B receptors and preservation of <strong>GluN1</strong>/GluN2A receptors in the CA1 stratum radiatum region during BZ <b>withdrawal</b>.
+GRIN1	drug	opioid	20543469	NMDA receptor 1 (<strong>NMDA1</strong>) and nitric oxide synthase (NOS) were measured on Day 7 after the <b>morphine</b> injection.
+GRIN1	drug	alcohol	20043891	The effects of chronic <b>ethanol</b> self administration on glutamate receptor ionotropic NMDA (GRIN), as well as <strong>GRIN1</strong> splice variant mRNA expression was studied in the orbitofrontal cortex (OFC; Area 13), dorsolateral prefrontal cortex (DLPFC; Area 46) and anterior cingulate cortex (ACC; Area 24) of male cynomolgus monkeys.
+GRIN1	drug	opioid	19819303	Biochemical traits related to <b>morphine</b>'s sensitizing effects were altered by intra VTA anti FGF 1 because <b>morphine</b> induced upregulation of both tyrosine hydroxylase (TH) and N methyl d aspartate glutamate receptor 1 (<strong>NMDAR1</strong>) in the VTA was blocked after anti FGF 1.
+GRIN1	drug	amphetamine	19478962	Therefore, the aim of the present study was to examine the effects of <b>METH</b> administration on the expression of glutamate N methyl D aspartate receptor subunit 1 (<strong>NMDAR1</strong>) in frontal cortex, striatum, and hippocampal formation after acute and subacute exposure to <b>METH</b> by western blotting.
+GRIN1	drug	cocaine	19368820	The effects of extinction following <b>cocaine</b> self administration on the expression and synaptosomal distribution of GluR1 and <strong>NMDAR1</strong> glutamate receptor subunits in the NA shell and core and the dorsolateral striatum were examined.
+GRIN1	drug	cocaine	19368820	These data suggest that extinguished <b>cocaine</b> seeking is associated with changes in GluR1 and <strong>NMDAR1</strong> expression and subcellular distribution that are region specific and consist of both a reversal of <b>cocaine</b> induced adaptations and emergent extinction related alterations that include receptor subunit redistribution and may involve alterations in scaffolding proteins.
+GRIN1	addiction	relapse	19368820	These data suggest that extinguished cocaine <b>seeking</b> is associated with changes in GluR1 and <strong>NMDAR1</strong> expression and subcellular distribution that are region specific and consist of both a reversal of cocaine induced adaptations and emergent extinction related alterations that include receptor subunit redistribution and may involve alterations in scaffolding proteins.
+GRIN1	drug	alcohol	16179537	An old story with a new twist: do <strong>NMDAR1</strong> mRNA binding proteins regulate expression of the <strong>NMDAR1</strong> receptor in the presence of <b>alcohol</b>?
+GRIN1	drug	alcohol	16179537	The increase in NMDA receptor number in response to chronic <b>ethanol</b> exposure both in vivo and in vitro is accompanied by an increase in <strong>NMDAR1</strong> and NMDAR2B polypeptide levels.
+GRIN1	drug	alcohol	16179537	At the molecular level, chronic <b>ethanol</b> exposure of fetal cortical neurons selectively increases expression of <strong>NMDAR1</strong> splice variants lacking exon 5 and exon 22.
+GRIN1	drug	alcohol	16179537	Chronic <b>ethanol</b> exposure of fetal cortical neurons also increases <strong>NMDAR1</strong> mRNA half life in these neurons.
+GRIN1	drug	alcohol	15635650	<strong>GRIN1</strong> locus may modify the susceptibility to seizures during <b>alcohol</b> withdrawal.
+GRIN1	addiction	withdrawal	15635650	<strong>GRIN1</strong> locus may modify the susceptibility to seizures during alcohol <b>withdrawal</b>.
+GRIN1	drug	alcohol	15635650	The expression and alternative splicing of the obligatory NR1 subunit is altered by <b>alcohol</b> exposure, emphasizing the involvement of the NR1 subunit, which is coded by the <strong>GRIN1</strong> gene, in <b>alcohol</b> mediated effects.
+GRIN1	drug	alcohol	15635650	We performed an association study in patients with <b>alcohol</b> dependence with the <strong>GRIN1</strong> locus.
+GRIN1	addiction	dependence	15635650	We performed an association study in patients with alcohol <b>dependence</b> with the <strong>GRIN1</strong> locus.
+GRIN1	drug	alcohol	15635650	These findings support the hypothesis that the <strong>GRIN1</strong> locus may modify the susceptibility to seizures during <b>alcohol</b> withdrawal.
+GRIN1	addiction	withdrawal	15635650	These findings support the hypothesis that the <strong>GRIN1</strong> locus may modify the susceptibility to seizures during alcohol <b>withdrawal</b>.
+GRIN1	drug	cocaine	14636974	Acute or chronic morphine and <b>cocaine</b> administration increased <strong>NMDAR1</strong> mRNA level in the central and basolateral nuclei of the amygdala; morphine did so 3 h after the last dose and 48 h after withdrawal, <b>cocaine</b> 3 h after acute and last chronic dose.
+GRIN1	drug	opioid	14636974	Acute or chronic <b>morphine</b> and cocaine administration increased <strong>NMDAR1</strong> mRNA level in the central and basolateral nuclei of the amygdala; <b>morphine</b> did so 3 h after the last dose and 48 h after withdrawal, cocaine 3 h after acute and last chronic dose.
+GRIN1	addiction	withdrawal	14636974	Acute or chronic morphine and cocaine administration increased <strong>NMDAR1</strong> mRNA level in the central and basolateral nuclei of the amygdala; morphine did so 3 h after the last dose and 48 h after <b>withdrawal</b>, cocaine 3 h after acute and last chronic dose.
+GRIN1	drug	cocaine	14636974	Morphine did not change the <strong>NMDAR1</strong> mRNA level in the hippocampal formation, but chronic <b>cocaine</b> did decrease it in the dentate gyrus only.
+GRIN1	drug	opioid	14636974	<b>Morphine</b> did not change the <strong>NMDAR1</strong> mRNA level in the hippocampal formation, but chronic cocaine did decrease it in the dentate gyrus only.
+GRIN1	drug	cocaine	14636974	Our study suggests a possible link between the expression of <strong>NMDAR1</strong> and changes in limbic system neuronal activity and behaviour after administration of morphine and <b>cocaine</b>.
+GRIN1	drug	opioid	14636974	Our study suggests a possible link between the expression of <strong>NMDAR1</strong> and changes in limbic system neuronal activity and behaviour after administration of <b>morphine</b> and cocaine.
+GRIN1	drug	cocaine	14636974	In summary, the present study demonstrated that morphine and <b>cocaine</b> influenced the expression of <strong>NMDAR1</strong> in the structure of the limbic system which could be involved in dependence phenomena.
+GRIN1	drug	opioid	14636974	In summary, the present study demonstrated that <b>morphine</b> and cocaine influenced the expression of <strong>NMDAR1</strong> in the structure of the limbic system which could be involved in dependence phenomena.
+GRIN1	addiction	dependence	14636974	In summary, the present study demonstrated that morphine and cocaine influenced the expression of <strong>NMDAR1</strong> in the structure of the limbic system which could be involved in <b>dependence</b> phenomena.
+GRIN1	drug	alcohol	14573320	The genotype frequencies of the <strong>NMDAR1</strong> polymorphism differed significantly between control and <b>alcoholic</b> subjects.
+GRIN1	drug	cocaine	12787079	In the accumbens of <b>cocaine</b> trained rats, GluR1 and <strong>NMDAR1</strong> levels were increased on days 1 and 90, while GluR2 levels were increased on days 1 and 30, but not day 90; PKA activity levels were increased on days 1 and 30, but not day 90, while AC activity, TH and cdk5 levels were unaltered.
+GRIN1	drug	cocaine	12787079	In the VTA of <b>cocaine</b> trained rats, <strong>NMDAR1</strong> levels were increased for up to 90 days, while GluR2 levels were increased only on day 1; TH and Cdk5 levels were increased only on day 1, while PKA and AC activity levels were unaltered.
+GRIN1	drug	cocaine	12716423	Array analysis revealed significant up regulation of numerous transcripts in the VTA, but not in the l SN, of <b>cocaine</b> overdose victims including <strong>NMDAR1</strong>, GluR2, GluR5 and KA2 receptor mRNA (p < 0.05).
+GRIN1	drug	cocaine	12716423	Correspondingly, western blot analysis revealed VTA selective up regulation of CREB (p < 0.01), <strong>NMDAR1</strong> (p < 0.01), GluR2 (p < 0.05), GluR5 (p < 0.01) and KA2 (p < 0.05) protein levels of <b>cocaine</b> overdose victims.
+GRIN1	drug	alcohol	12586454	The aim of this study was to evaluate the influence of the glycine binding site of the NMDA receptor on the behavioral effects of <b>alcohol</b> by investigating mice with an 80% reduced affinity of the NMDA R1 subunit for glycine (<strong>Grin1</strong>(D481N)).
+GRIN1	drug	alcohol	12586454	In contrast to wild type mice, <b>alcohol</b> associated anxiolysis and motor impairment was attenuated in <strong>Grin1</strong>(D481N) mice during intoxication.
+GRIN1	addiction	intoxication	12586454	In contrast to wild type mice, alcohol associated anxiolysis and motor impairment was attenuated in <strong>Grin1</strong>(D481N) mice during <b>intoxication</b>.
+GRIN1	drug	alcohol	12586454	Free choice <b>alcohol</b> intake did not differ between wild type and <strong>Grin1</strong>(D481N) mice.
+GRIN1	drug	cocaine	12105087	Neuroadaptive changes in <strong>NMDAR1</strong> gene expression after extinction of <b>cocaine</b> self administration.
+GRIN1	drug	cocaine	12105087	The aim of the present work was to study the time course effects in levels of mRNA encoding N methyl d aspartate receptor subunit 1 (<strong>NMDAR1</strong>) after long term <b>cocaine</b> self administration (1 mg/kg/ injection) and its extinction using a yoked box procedure.
+GRIN1	drug	cocaine	12105087	<strong>NMDAR1</strong> content was measured by quantitative in situ hybridization histochemistry in prefrontal cortex, caudate putamen, nucleus accumbens, olfactory tubercle, and piriform cortex immediately after cessation of the last session of <b>cocaine</b> self administration (Day 0) and 1, 5, and 10 days after the extinction period.
+GRIN1	drug	cocaine	12105087	The results show that long term <b>cocaine</b> self administration and its extinction alter <strong>NMDAR1</strong> gene expression in these forebrain regions, and that the changes depend upon the brain region examined and the type of <b>cocaine</b> administration (contingent, noncontingent, and saline).
+GRIN1	drug	cocaine	12105087	Compared to saline and noncontingent <b>cocaine</b> administration, contingent <b>cocaine</b> produced an up regulation in <strong>NMDAR1</strong> gene expression on Day 0 in all the brain regions analyzed.
+GRIN1	drug	cocaine	12105087	<strong>NMDAR1</strong> levels of contingent animals decreased progressively in the absence of <b>cocaine</b>, and the decrement persisted 10 days after the extinction of <b>cocaine</b> self administration behavior in all the forebrain areas, with the exception of olfactory tubercle.
+GRIN1	drug	cocaine	12105087	In contrast, noncontingent <b>cocaine</b> administration did not produce any change in <strong>NMDAR1</strong> gene expression on Day 0, and extinction resulted in an increase of <strong>NMDAR1</strong> mRNA content on Days 1 and 5 and returned to control (saline) values on Day 10.
+GRIN1	drug	cocaine	12105087	These results suggest that an interaction between environmental stimuli and the pharmacological action of <b>cocaine</b> during drug self administration and its extinction may represent an important factor in the regulation of <b>cocaine</b> effects on <strong>NMDAR1</strong> gene expression.
+GRIN1	drug	opioid	11858765	Single dose of <b>morphine</b> was followed by a decrease in gene expression of glutamate receptor subunit <strong>NMDAR1</strong> in the adrenal gland.
+GRIN1	drug	amphetamine	10510180	Withdrawal from repeated <b>amphetamine</b> administration reduces <strong>NMDAR1</strong> expression in the rat substantia nigra, nucleus accumbens and medial prefrontal cortex.
+GRIN1	addiction	withdrawal	10510180	<b>Withdrawal</b> from repeated amphetamine administration reduces <strong>NMDAR1</strong> expression in the rat substantia nigra, nucleus accumbens and medial prefrontal cortex.
+GRIN1	drug	amphetamine	10510180	This study determined whether expression of the <strong>NMDAR1</strong> subunit of the NMDA receptor is altered by repeated <b>amphetamine</b> administration.
+GRIN1	drug	amphetamine	10510180	We quantified <strong>NMDAR1</strong> mRNA (using in situ hybridization with 35S labelled oligonucleotide probes) and immunolabelling (using immunocytochemistry with 35S labelled secondary antibodies) in rat ventral midbrain, nucleus accumbens and prefrontal cortex after 3 or 14 days of withdrawal from five daily injections of saline or <b>amphetamine</b> sulphate (5 mg/kg/day).
+GRIN1	addiction	withdrawal	10510180	We quantified <strong>NMDAR1</strong> mRNA (using in situ hybridization with 35S labelled oligonucleotide probes) and immunolabelling (using immunocytochemistry with 35S labelled secondary antibodies) in rat ventral midbrain, nucleus accumbens and prefrontal cortex after 3 or 14 days of <b>withdrawal</b> from five daily injections of saline or amphetamine sulphate (5 mg/kg/day).
+GRIN1	addiction	withdrawal	10510180	No changes in <strong>NMDAR1</strong> expression were observed after 3 days of <b>withdrawal</b>, whereas significant decreases were observed in all regions after 14 days.
+GRIN1	drug	cocaine	10349849	GluR1, GluR2/3, and <strong>NMDAR1</strong> subunits of glutamate receptors were quantified from immunoblots in these brain nuclei in rats at 24 h and 3 weeks after discontinuing 1 week of daily <b>cocaine</b> injections.
+GRIN1	addiction	withdrawal	10349849	Conversely, sensitized animals showed a significant increase in <strong>NMDAR1</strong> and GluR1 levels in the ventral tegmental area at 1 day but not at 3 weeks of <b>withdrawal</b>.
+GRIN1	drug	alcohol	8912402	Furthermore, since there is evidence that eliprodil produces its pharmacological actions through a specific inhibition of <strong>NMDAR1</strong> and/or NMDAR2B subunits, these data may indicate that certain NMDA receptor subunits may be of particular importance for the mediation of seizure activity following the discontinuation of chronic <b>ethanol</b> exposure.
+GRIN1	drug	cocaine	8613793	By immunoblotting procedures using subunit specific antibodies, we found that repeated, but not acute, <b>cocaine</b> treatment increased the levels of immunoreactivity of GluR1 (an AMPA receptor subunit) and <strong>NMDAR1</strong> (an NMDA receptor subunit) in the ventral tegmental area (VTA), a nucleus containing mesolimbic DA neurons.
+GRIN1	drug	cocaine	8613793	Unlike <b>cocaine</b>, morphine, and stress, repeated treatment with other psychotropic drugs (haloperidol, raclopride, sertraline, and desipramine) that lack reinforcing or sensitizing properties did not regulate GluR1 or <strong>NMDAR1</strong> subunit levels in the VTA.
+GRIN1	drug	opioid	8613793	Unlike cocaine, <b>morphine</b>, and stress, repeated treatment with other psychotropic drugs (haloperidol, raclopride, sertraline, and desipramine) that lack reinforcing or sensitizing properties did not regulate GluR1 or <strong>NMDAR1</strong> subunit levels in the VTA.
+GRIN1	addiction	reward	8613793	Unlike cocaine, morphine, and stress, repeated treatment with other psychotropic drugs (haloperidol, raclopride, sertraline, and desipramine) that lack <b>reinforcing</b> or sensitizing properties did not regulate GluR1 or <strong>NMDAR1</strong> subunit levels in the VTA.
+GRIN1	drug	alcohol	8869159	It was found that long term, but not short term, <b>ethanol</b> exposure increased levels of immunoreactivity of the <strong>NMDAR1</strong> subunit, an obligatory component of NMDA glutamate receptors, and of the GluR1 subunit, a component of many AMPA glutamate receptors; but at the same time, long term <b>ethanol</b> exposure decreased immunoreactivity levels of the alpha 1 subunit of the GABAA receptor complex.
+GRIN1	drug	alcohol	8133290	Chronic ingestion of <b>ethanol</b> up regulates <strong>NMDAR1</strong> receptor subunit immunoreactivity in rat hippocampus.
+GRIN1	drug	alcohol	8133290	We examined the effects of chronic <b>ethanol</b> exposure on the levels of N methyl D aspartate receptor subunit 1 (<strong>NMDAR1</strong>) protein, an essential component of N methyl D aspartate glutamate receptors, in rat brain.
+GRIN1	drug	alcohol	8133290	By immunoblotting procedures using a specific antibody for the <strong>NMDAR1</strong> subunit, we found that <b>ethanol</b> dramatically up regulated (by 65%) <strong>NMDAR1</strong> immunoreactivity in the hippocampus but not in the nucleus accumbens, cerebral cortex, or striatum.
+GRIN1	drug	alcohol	8133290	Increased <strong>NMDAR1</strong> subunit levels in the hippocampus after chronic <b>ethanol</b> exposure may represent an important neurochemical substrate for some of the features associated with <b>ethanol</b> dependence and withdrawal.
+GRIN1	addiction	dependence	8133290	Increased <strong>NMDAR1</strong> subunit levels in the hippocampus after chronic ethanol exposure may represent an important neurochemical substrate for some of the features associated with ethanol <b>dependence</b> and withdrawal.
+GRIN1	addiction	withdrawal	8133290	Increased <strong>NMDAR1</strong> subunit levels in the hippocampus after chronic ethanol exposure may represent an important neurochemical substrate for some of the features associated with ethanol dependence and <b>withdrawal</b>.
+GRIN1	drug	alcohol	8974321	In addition, we examined the levels of <strong>NMDAR1</strong> receptor subunit mRNAs since chronic <b>ethanol</b> administration results in increased levels of [3H]MK 801 recognition sites on NMDA receptors.
+GRIN1	drug	alcohol	8974321	<strong>NMDAR1</strong> receptor subunit mRNAs were not altered following chronic <b>ethanol</b> exposure in rat cortex or hippocampus.
+GABRA2	drug	alcohol	30984232	Genetic variation at the <strong>GABRA2</strong> locus has been implicated in epilepsy, affective and psychiatric disorders, <b>alcoholism</b> and drug abuse.
+GABRA2	drug	alcohol	30984232	These results suggest that naturally occurring variation in <strong>GABRA2</strong> levels between B6J and other substrains or inbred strains may also explain strain differences in anxiety like or <b>alcohol</b> and drug response traits related to striatal function.
+GABRA2	drug	cocaine	30724801	One potential mechanism in humans is suggested by findings that ELS interacts with polymorphisms of the <strong>GABRA2</strong> gene, encoding α2 subunits of GABAA receptors, to increase the risk for both post traumatic stress disorder and vulnerability to <b>cocaine</b> addiction.
+GABRA2	addiction	addiction	30724801	One potential mechanism in humans is suggested by findings that ELS interacts with polymorphisms of the <strong>GABRA2</strong> gene, encoding α2 subunits of GABAA receptors, to increase the risk for both post traumatic stress disorder and vulnerability to cocaine <b>addiction</b>.
+GABRA2	drug	alcohol	30555510	Sex and β Endorphin Influence the Effects of <b>Ethanol</b> on Limbic <strong>Gabra2</strong> Expression in a Mouse Binge Drinking Model.
+GABRA2	addiction	intoxication	30555510	Sex and β Endorphin Influence the Effects of Ethanol on Limbic <strong>Gabra2</strong> Expression in a Mouse <b>Binge</b> Drinking Model.
+GABRA2	drug	alcohol	30555510	Among its many effects, <b>alcohol</b> consumption reduces anxiety via the inhibitory neurotransmitter GABA, most likely acting upon receptors containing the α 2 subunit (<strong>Gabra2</strong>).
+GABRA2	addiction	intoxication	30555510	Because βE works via GABA signaling to reduce anxiety, we sought to determine whether sexually dimorphic <b>binge</b> drinking behavior in βE deficient mice is coupled with differences in CNS <strong>Gabra2</strong> expression.
+GABRA2	addiction	intoxication	30555510	Following a <b>binge</b> test on day 4, limbic tissue was collected and frozen for subsequent qRT PCR analysis of <strong>Gabra2</strong> mRNA expression.
+GABRA2	drug	alcohol	30555510	Genotype alone had no effect on <b>alcohol</b> consumption or drug induced increase in <strong>Gabra2</strong> expression.
+GABRA2	addiction	intoxication	30555510	In contrast, βE expression had bi directional effects in females: in wildtypes, <strong>Gabra2</strong> mRNA was reduced by <b>binge</b> EtOH consumption, while EtOH increased expression in βE  /  females to levels commensurate with drug naïve βE +/+ females.
+GABRA2	drug	cocaine	30138693	The genetic association of <strong>Gabra2</strong> haplotypes with <b>cocaine</b> addiction appears to be evident primarily in individuals who had experienced childhood trauma.
+GABRA2	addiction	addiction	30138693	The genetic association of <strong>Gabra2</strong> haplotypes with cocaine <b>addiction</b> appears to be evident primarily in individuals who had experienced childhood trauma.
+GABRA2	drug	cocaine	30138693	Given this association of childhood trauma, <b>cocaine</b> abuse and the <strong>Gabra2</strong> haplotypes, we have explored in a mouse model of early life adversity (ELA) whether such events influence the behavioral effects of <b>cocaine</b> and if, as suggested by the human studies, α2 GABAARs in the nucleus accumbens (NAc) are involved in these perturbed behaviors.
+GABRA2	drug	opioid	30061709	<strong>GABRA2</strong> rs279858 linked variants are associated with disrupted structural connectome of reward circuits in <b>heroin</b> abusers.
+GABRA2	addiction	reward	30061709	<strong>GABRA2</strong> rs279858 linked variants are associated with disrupted structural connectome of <b>reward</b> circuits in heroin abusers.
+GABRA2	drug	opioid	30061709	<strong>GABRA2</strong> rs279858 linked variants might be a key genetic modulator for <b>heroin</b> vulnerability by affecting the connections of reward network and cognition.
+GABRA2	addiction	reward	30061709	<strong>GABRA2</strong> rs279858 linked variants might be a key genetic modulator for heroin vulnerability by affecting the connections of <b>reward</b> network and cognition.
+GABRA2	drug	alcohol	29528673	<strong>GABRA2</strong>, <b>alcohol</b>, and illicit drug use: An event level model of genetic risk for polysubstance use.
+GABRA2	drug	alcohol	29528673	<strong>GABRA2</strong>, the gene encoding the α2 subunit of the GABAA receptor, potentially plays a role in the etiology of problematic drinking, as <strong>GABRA2</strong> genotype has been associated with subjective response to <b>alcohol</b> and other <b>alcohol</b> related reward processes.
+GABRA2	addiction	reward	29528673	<strong>GABRA2</strong>, the gene encoding the α2 subunit of the GABAA receptor, potentially plays a role in the etiology of problematic drinking, as <strong>GABRA2</strong> genotype has been associated with subjective response to alcohol and other alcohol related <b>reward</b> processes.
+GABRA2	drug	alcohol	29528673	The <strong>GABRA2</strong> gene has also been associated with illicit drug use, but the extent to which associations with drug use are independent of associations with <b>alcohol</b> use remains unclear, partly because most previous research has used a cross sectional design that cannot discriminate comorbidity at the between person level and co occurrence within persons.
+GABRA2	addiction	intoxication	29528673	Moreover, the effect of <strong>GABRA2</strong> variation on drug use was moderated by an individual's degree of <b>intoxication</b>.
+GABRA2	drug	alcohol	29528673	These findings are consistent with recent genetic and neuroscience research, and they suggest <strong>GABRA2</strong> variation influences drug seeking behavior through both <b>alcohol</b> related and <b>alcohol</b> independent pathways.
+GABRA2	addiction	relapse	29528673	These findings are consistent with recent genetic and neuroscience research, and they suggest <strong>GABRA2</strong> variation influences drug <b>seeking</b> behavior through both alcohol related and alcohol independent pathways.
+GABRA2	drug	alcohol	27717041	Effects of <strong>Gabra2</strong> Point Mutations on <b>Alcohol</b> Intake: Increased Binge Like and Blunted Chronic Drinking by Mice.
+GABRA2	addiction	intoxication	27717041	Effects of <strong>Gabra2</strong> Point Mutations on Alcohol Intake: Increased <b>Binge</b> Like and Blunted Chronic Drinking by Mice.
+GABRA2	drug	alcohol	27717041	<b>Alcohol</b> use disorders are associated with single nucleotide polymorphisms in <strong>GABRA2</strong>, the gene encoding the GABAA receptor α2 subunit in humans.
+GABRA2	drug	alcohol	27117237	<b>Alcohol</b> Induced Stimulation Mediates the Effect of a <strong>GABRA2</strong> SNP on <b>Alcohol</b> Self Administrated among <b>Alcohol</b> Dependent Individuals.
+GABRA2	drug	alcohol	27117237	A single nucleotide polymorphism (SNP) in <strong>GABRA2</strong> (rs279858) may moderate subjective response (SR) to <b>alcohol</b>.
+GABRA2	drug	alcohol	26902358	Acute exposure to <b>ethanol</b> elevated expression of genes Gabrb1 (by 1.7 times), Gabra1 (by 3.8 times), and Gabra4 (by 6.5 times), although it diminished expression of <strong>Gabra2</strong> gene by 1.4 times.
+GABRA2	addiction	addiction	26635556	Motivational Effects of Methylphenidate are Associated with <strong>GABRA2</strong> Variants Conferring <b>Addiction</b> Risk.
+GABRA2	addiction	addiction	26635556	Variations in the <strong>GABRA2</strong> gene, encoding α2 subunits of GABAA receptors, have been associated with risk for <b>addiction</b> to several drugs, but the mechanisms by which variations in non coding regions of <strong>GABRA2</strong> increase risk for addictions are not understood.
+GABRA2	drug	cocaine	26635556	Healthy human volunteers carrying either <b>cocaine</b> addiction "risk" or "protective" <strong>GABRA2</strong> single nucleotide polymorphism (SNPs) were tested for their subjective responses to methylphenidate, and methylphenidate's ability to facilitate conditioned reinforcement (CRf) for visual stimuli (CS+) associated with monetary reward.
+GABRA2	addiction	addiction	26635556	Healthy human volunteers carrying either cocaine <b>addiction</b> "risk" or "protective" <strong>GABRA2</strong> single nucleotide polymorphism (SNPs) were tested for their subjective responses to methylphenidate, and methylphenidate's ability to facilitate conditioned reinforcement (CRf) for visual stimuli (CS+) associated with monetary reward.
+GABRA2	addiction	reward	26635556	Healthy human volunteers carrying either cocaine addiction "risk" or "protective" <strong>GABRA2</strong> single nucleotide polymorphism (SNPs) were tested for their subjective responses to methylphenidate, and methylphenidate's ability to facilitate conditioned <b>reinforcement</b> (CRf) for visual stimuli (CS+) associated with monetary <b>reward</b>.
+GABRA2	drug	alcohol	26250693	<strong>GABRA2</strong> <b>Alcohol</b> Dependence Risk Allele is Associated with Reduced Expression of Chromosome 4p12 GABAA Subunit Genes in Human Neural Cultures.
+GABRA2	addiction	dependence	26250693	<strong>GABRA2</strong> Alcohol <b>Dependence</b> Risk Allele is Associated with Reduced Expression of Chromosome 4p12 GABAA Subunit Genes in Human Neural Cultures.
+GABRA2	drug	alcohol	26250693	Genetic variation in a region of chromosome 4p12 that includes the GABAA subunit gene <strong>GABRA2</strong> has been reproducibly associated with <b>alcohol</b> dependence (AD).
+GABRA2	addiction	dependence	26250693	Genetic variation in a region of chromosome 4p12 that includes the GABAA subunit gene <strong>GABRA2</strong> has been reproducibly associated with alcohol <b>dependence</b> (AD).
+GABRA2	drug	alcohol	26116794	Association of GABAA receptor α2 subunit gene (<strong>GABRA2</strong>) with <b>alcohol</b> dependence related aggressive behavior.
+GABRA2	addiction	dependence	26116794	Association of GABAA receptor α2 subunit gene (<strong>GABRA2</strong>) with alcohol <b>dependence</b> related aggressive behavior.
+GABRA2	drug	alcohol	26116794	Recent studies have demonstrated that polymorphisms of the gene encoding the GABAA receptor α2 subunit (<strong>GABRA2</strong>) are associated with <b>alcohol</b> dependence in different populations of European ancestry.
+GABRA2	addiction	dependence	26116794	Recent studies have demonstrated that polymorphisms of the gene encoding the GABAA receptor α2 subunit (<strong>GABRA2</strong>) are associated with alcohol <b>dependence</b> in different populations of European ancestry.
+GABRA2	drug	alcohol	26116794	As aggression often occurs in the context of <b>alcohol</b> dependence, the aim of this study was to examine the allelic and haplotypic association of <strong>GABRA2</strong> gene with <b>alcohol</b> dependence and related aggressive behavior in subjects of Eastern European (Croatian) origin.
+GABRA2	addiction	dependence	26116794	As aggression often occurs in the context of alcohol <b>dependence</b>, the aim of this study was to examine the allelic and haplotypic association of <strong>GABRA2</strong> gene with alcohol <b>dependence</b> and related aggressive behavior in subjects of Eastern European (Croatian) origin.
+GABRA2	drug	alcohol	26116794	Genotyping of the 3 single nucleotide polymorphisms (SNPs) across the <strong>GABRA2</strong> gene (rs567926, rs279858 and rs9291283) was performed in patients with <b>alcohol</b> dependence (N=654) and healthy control subjects (N=574).
+GABRA2	addiction	dependence	26116794	Genotyping of the 3 single nucleotide polymorphisms (SNPs) across the <strong>GABRA2</strong> gene (rs567926, rs279858 and rs9291283) was performed in patients with alcohol <b>dependence</b> (N=654) and healthy control subjects (N=574).
+GABRA2	drug	alcohol	26116794	These findings support the involvement of <strong>GABRA2</strong> gene in <b>alcohol</b> dependence related aggressive behavior.
+GABRA2	addiction	dependence	26116794	These findings support the involvement of <strong>GABRA2</strong> gene in alcohol <b>dependence</b> related aggressive behavior.
+GABRA2	drug	alcohol	26087834	Adaptation of Subjective Responses to <b>Alcohol</b> is Affected by an Interaction of <strong>GABRA2</strong> Genotype and Recent Drinking.
+GABRA2	drug	alcohol	26087834	This study assessed the effect of variation in the GABAA receptor genes GABRG1 and <strong>GABRA2</strong> and recent drinking history on the acute adaptation of subjective responses to <b>alcohol</b>.
+GABRA2	drug	alcohol	26087834	Analysis of covariance tested whether <strong>GABRA2</strong> and GABRG1 single nucleotide polymorphism (SNP) genotypes, gender, placebo session, family history of <b>alcoholism</b>, recent drinking history, and the genotype × recent drinking history interaction significantly predicted the adaptive response.
+GABRA2	drug	alcohol	26087834	Recent drinking history (p = 0.01), and recent drinking history × genotype interaction (p = 0.01) were significantly associated with acute adaptation of the subjective responses to <b>alcohol</b> for the <strong>GABRA2</strong> SNP rs279858.
+GABRA2	drug	alcohol	26087834	We postulate that the <strong>GABRA2</strong> effect on <b>alcohol</b> dependence may, in part, be due to its effect on subjective responses to <b>alcohol</b>.
+GABRA2	addiction	dependence	26087834	We postulate that the <strong>GABRA2</strong> effect on alcohol <b>dependence</b> may, in part, be due to its effect on subjective responses to alcohol.
+GABRA2	drug	alcohol	25804982	The current study tested whether two important forms of disinhibition in adolescence, impulsivity and sensation seeking, mediated the effects of <strong>GABRA2</strong> on hyperactive inattentive symptoms, conduct problems, and <b>alcohol</b> problems.
+GABRA2	addiction	relapse	25804982	The current study tested whether two important forms of disinhibition in adolescence, impulsivity and sensation <b>seeking</b>, mediated the effects of <strong>GABRA2</strong> on hyperactive inattentive symptoms, conduct problems, and alcohol problems.
+GABRA2	drug	alcohol	25804982	Impulsivity mediated the effect of <strong>GABRA2</strong> on <b>alcohol</b> problems, hyperactive inattentive symptoms, and conduct problems, whereas sensation seeking mediated the effect of <strong>GABRA2</strong> on <b>alcohol</b> problems (AA/AG genotypes conferred risk).
+GABRA2	addiction	relapse	25804982	Impulsivity mediated the effect of <strong>GABRA2</strong> on alcohol problems, hyperactive inattentive symptoms, and conduct problems, whereas sensation <b>seeking</b> mediated the effect of <strong>GABRA2</strong> on alcohol problems (AA/AG genotypes conferred risk).
+GABRA2	drug	alcohol	25804982	<strong>GABRA2</strong> directly predicted adolescent <b>alcohol</b> problems, but the GG genotype conferred risk.
+GABRA2	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, <strong>GABRA2</strong>, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+GABRA2	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, <strong>GABRA2</strong>, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+GABRA2	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, <strong>GABRA2</strong>, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+GABRA2	drug	alcohol	25399692	More recent studies in family based samples have implicated <strong>GABRA2</strong>, nicotinic receptor genes such as CHRNB3, and a number of other specific single genes as associated with <b>alcohol</b> use disorders.
+GABRA2	drug	alcohol	25307596	A number of other genes important in AUD have been identified and replicated, including <strong>GABRA2</strong> and <b>alcohol</b> dehydrogenases 1B and 4.
+GABRA2	drug	alcohol	24975023	Effect of <strong>GABRA2</strong> genotype on development of incentive motivation circuitry in a sample enriched for <b>alcoholism</b> risk.
+GABRA2	addiction	reward	24975023	Effect of <strong>GABRA2</strong> genotype on development of <b>incentive</b> motivation circuitry in a sample enriched for alcoholism risk.
+GABRA2	drug	alcohol	24975023	Variants in <strong>GABRA2</strong> have been associated with adult <b>alcohol</b> dependence as well as phenotypic precursors, including impulsiveness and externalizing behaviors.
+GABRA2	addiction	dependence	24975023	Variants in <strong>GABRA2</strong> have been associated with adult alcohol <b>dependence</b> as well as phenotypic precursors, including impulsiveness and externalizing behaviors.
+GABRA2	addiction	reward	24975023	We investigated the impact of <strong>GABRA2</strong> on the developmental trajectory of nucleus accumbens (NAcc) activation during anticipation of monetary <b>reward</b> from childhood to young adulthood.
+GABRA2	drug	alcohol	24975023	This work demonstrates an impact of <strong>GABRA2</strong> genotype on incentive motivation neurocircuitry in adolescence, with implications for vulnerability to <b>alcoholism</b>.
+GABRA2	addiction	reward	24975023	This work demonstrates an impact of <strong>GABRA2</strong> genotype on <b>incentive</b> motivation neurocircuitry in adolescence, with implications for vulnerability to alcoholism.
+GABRA2	drug	alcohol	24692236	Linkage studies of <b>alcoholism</b> have implicated several chromosome regions, leading to the successful identification of susceptibility genes, including ADH4 and <strong>GABRA2</strong> on chromosome 4.
+GABRA2	drug	alcohol	24687270	Examination of genetic variation in <strong>GABRA2</strong> with conduct disorder and <b>alcohol</b> abuse and dependence in a longitudinal study.
+GABRA2	addiction	dependence	24687270	Examination of genetic variation in <strong>GABRA2</strong> with conduct disorder and alcohol abuse and <b>dependence</b> in a longitudinal study.
+GABRA2	drug	alcohol	24687270	Previous studies have shown associations between single nucleotide polymorphisms (SNPs) in gamma aminobutyric acid receptor alpha 2 (<strong>GABRA2</strong>) and adolescent conduct disorder (CD) and <b>alcohol</b> dependence in adulthood, but not adolescent <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	24687270	Previous studies have shown associations between single nucleotide polymorphisms (SNPs) in gamma aminobutyric acid receptor alpha 2 (<strong>GABRA2</strong>) and adolescent conduct disorder (CD) and alcohol <b>dependence</b> in adulthood, but not adolescent alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	24687270	Although the analysis provided nominal support for an association with rs9291283 and AAD in adulthood and CD in adolescence, the current study failed to replicate previous associations between two well replicated <strong>GABRA2</strong> SNPs and CD and <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	24687270	Although the analysis provided nominal support for an association with rs9291283 and AAD in adulthood and CD in adolescence, the current study failed to replicate previous associations between two well replicated <strong>GABRA2</strong> SNPs and CD and alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	24557088	We used linear mixed models to examine the effects of dutasteride and <b>alcohol</b> on BAES and SS responses and the interaction of dutasteride with the <strong>GABRA2</strong> <b>alcohol</b> dependence associated polymorphism rs279858.
+GABRA2	addiction	dependence	24557088	We used linear mixed models to examine the effects of dutasteride and alcohol on BAES and SS responses and the interaction of dutasteride with the <strong>GABRA2</strong> alcohol <b>dependence</b> associated polymorphism rs279858.
+GABRA2	drug	alcohol	24166645	A <strong>GABRA2</strong> variant is associated with increased stimulation and 'high' following <b>alcohol</b> administration.
+GABRA2	drug	alcohol	24166645	We sought to replicate and extend previous findings of a moderating effect of single nucleotide polymorphisms (SNPs) in <strong>GABRA2</strong> (which encodes the GABAA α 2 subunit) on the subjective effects of <b>alcohol</b> by examining SNPs in this and the adjacent GABRG1 gene on chromosome 4.
+GABRA2	drug	alcohol	24136292	Association of gamma aminobutyric acid A receptor α2 gene (<strong>GABRA2</strong>) with <b>alcohol</b> use disorder.
+GABRA2	drug	alcohol	24136292	To reconcile the conflicting associations with substance dependence traits, we performed a meta analysis of variants in the GABAA receptor genes (GABRB2, GABRA6, GABRA1, and GABRG2 on chromosome 5q and <strong>GABRA2</strong> on chromosome 4p12) using genotype data from 4739 cases of <b>alcohol</b>, opioid, or methamphetamine dependence and 4924 controls.
+GABRA2	drug	amphetamine	24136292	To reconcile the conflicting associations with substance dependence traits, we performed a meta analysis of variants in the GABAA receptor genes (GABRB2, GABRA6, GABRA1, and GABRG2 on chromosome 5q and <strong>GABRA2</strong> on chromosome 4p12) using genotype data from 4739 cases of alcohol, opioid, or <b>methamphetamine</b> dependence and 4924 controls.
+GABRA2	drug	opioid	24136292	To reconcile the conflicting associations with substance dependence traits, we performed a meta analysis of variants in the GABAA receptor genes (GABRB2, GABRA6, GABRA1, and GABRG2 on chromosome 5q and <strong>GABRA2</strong> on chromosome 4p12) using genotype data from 4739 cases of alcohol, <b>opioid</b>, or methamphetamine dependence and 4924 controls.
+GABRA2	addiction	dependence	24136292	To reconcile the conflicting associations with substance <b>dependence</b> traits, we performed a meta analysis of variants in the GABAA receptor genes (GABRB2, GABRA6, GABRA1, and GABRG2 on chromosome 5q and <strong>GABRA2</strong> on chromosome 4p12) using genotype data from 4739 cases of alcohol, opioid, or methamphetamine <b>dependence</b> and 4924 controls.
+GABRA2	drug	alcohol	24136292	Using a Bonferroni corrected threshold of 0.007, we found strong associations between <strong>GABRA2</strong> and AD (P=9 × 10( 6) and odds ratio (OR) 95% confidence interval (CI)=1.27 (1.15, 1.4) for rs567926, P=4 × 10( 5) and OR=1.21 (1.1, 1.32) for rs279858), and between GABRG2 and both dependence on <b>alcohol</b> and dependence on heroin (P=0.0005 and OR=1.22 (1.09, 1.37) for rs211014).
+GABRA2	drug	opioid	24136292	Using a Bonferroni corrected threshold of 0.007, we found strong associations between <strong>GABRA2</strong> and AD (P=9 × 10( 6) and odds ratio (OR) 95% confidence interval (CI)=1.27 (1.15, 1.4) for rs567926, P=4 × 10( 5) and OR=1.21 (1.1, 1.32) for rs279858), and between GABRG2 and both dependence on alcohol and dependence on <b>heroin</b> (P=0.0005 and OR=1.22 (1.09, 1.37) for rs211014).
+GABRA2	addiction	dependence	24136292	Using a Bonferroni corrected threshold of 0.007, we found strong associations between <strong>GABRA2</strong> and AD (P=9 × 10( 6) and odds ratio (OR) 95% confidence interval (CI)=1.27 (1.15, 1.4) for rs567926, P=4 × 10( 5) and OR=1.21 (1.1, 1.32) for rs279858), and between GABRG2 and both <b>dependence</b> on alcohol and <b>dependence</b> on heroin (P=0.0005 and OR=1.22 (1.09, 1.37) for rs211014).
+GABRA2	drug	alcohol	23974430	Gender specific gene environment interaction in <b>alcohol</b> dependence: the impact of daily life events and <strong>GABRA2</strong>.
+GABRA2	addiction	dependence	23974430	Gender specific gene environment interaction in alcohol <b>dependence</b>: the impact of daily life events and <strong>GABRA2</strong>.
+GABRA2	drug	alcohol	23974430	The current study examined the influence of gender, negative and positive daily life events, and <strong>GABRA2</strong> genotype (SNP rs279871) on <b>alcohol</b> dependence, testing two  and three way interactions between these variables using multi level regression models fit to data from 2,281 White participants in the Collaborative Study on the Genetics of <b>Alcoholism</b>.
+GABRA2	addiction	dependence	23974430	The current study examined the influence of gender, negative and positive daily life events, and <strong>GABRA2</strong> genotype (SNP rs279871) on alcohol <b>dependence</b>, testing two  and three way interactions between these variables using multi level regression models fit to data from 2,281 White participants in the Collaborative Study on the Genetics of Alcoholism.
+GABRA2	drug	alcohol	23712313	Studies continue to reveal other genes in which variants affect the risk of <b>alcoholism</b> or related traits, including <strong>GABRA2</strong>, CHRM2, KCNJ6 and AUTS2.
+GABRA2	drug	alcohol	23692184	Genetic influences on <b>alcohol</b> use across stages of development: <strong>GABRA2</strong> and longitudinal trajectories of drunkenness from adolescence to young adulthood.
+GABRA2	drug	alcohol	23692184	In this study, we test for genetic effects of <strong>GABRA2</strong>, a gene previously associated with <b>alcohol</b> dependence, on trajectories of drunkenness from age 14 to 25.
+GABRA2	addiction	dependence	23692184	In this study, we test for genetic effects of <strong>GABRA2</strong>, a gene previously associated with alcohol <b>dependence</b>, on trajectories of drunkenness from age 14 to 25.
+GABRA2	drug	alcohol	23566244	Impulsiveness mediates the association between <strong>GABRA2</strong> SNPs and lifetime <b>alcohol</b> problems.
+GABRA2	drug	alcohol	23566244	Genetic variants in <strong>GABRA2</strong> have previously been shown to be associated with <b>alcohol</b> measures, electroencephalography (EEG) β waves and impulsiveness related traits.
+GABRA2	drug	alcohol	23566244	Our results suggest that <strong>GABRA2</strong> variation in the region between introns 3 and 4 is associated with impulsiveness and this effect partially influences the development of <b>alcohol</b> problems, but a direct effect of <strong>GABRA2</strong> on problem drinking remains.
+GABRA2	drug	alcohol	23561058	Our results suggest that the pathway by which <strong>GABRA2</strong> initially confers risk for eventual <b>alcohol</b> problems begins with a predisposition to sensation seeking early in adolescence.
+GABRA2	addiction	relapse	23561058	Our results suggest that the pathway by which <strong>GABRA2</strong> initially confers risk for eventual alcohol problems begins with a predisposition to sensation <b>seeking</b> early in adolescence.
+GABRA2	addiction	dependence	23377636	Other candidate genes associated with substance <b>dependence</b> phenotypes in Native Americans include OPRM1, CRN1, COMT, <strong>GABRA2</strong>, MAOA, and HTR3 B.
+GABRA2	drug	alcohol	23134043	In addition, a gene encoding one of the receptors for the neurotransmitter γ aminobutyric acid (GABA) known as <strong>GABRA2</strong> seems to have a role in the development of <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	23134043	In addition, a gene encoding one of the receptors for the neurotransmitter γ aminobutyric acid (GABA) known as <strong>GABRA2</strong> seems to have a role in the development of alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	23115637	Deletion of the <strong>gabra2</strong> gene results in hypersensitivity to the acute effects of <b>ethanol</b> but does not alter <b>ethanol</b> self administration.
+GABRA2	drug	alcohol	23115637	Human genetic studies have suggested that polymorphisms of the <strong>GABRA2</strong> gene encoding the GABA(A) α2 subunit are associated with <b>ethanol</b> dependence.
+GABRA2	addiction	dependence	23115637	Human genetic studies have suggested that polymorphisms of the <strong>GABRA2</strong> gene encoding the GABA(A) α2 subunit are associated with ethanol <b>dependence</b>.
+GABRA2	drug	alcohol	23115637	To ensure the acute effects are not due to the <strong>gabra2</strong> deletion affecting pharmacokinetics, blood <b>ethanol</b> concentrations were measured at 20 minute intervals after acute administration (2 g/kg i.p.
+GABRA2	drug	alcohol	22921455	Moreover, polymorphisms in the <strong>GABRA2</strong> gene encoding the GABA(A) receptor α2 subunit have been found to be linked to chronic <b>alcohol</b> dependence and to polydrug abuse.
+GABRA2	addiction	dependence	22921455	Moreover, polymorphisms in the <strong>GABRA2</strong> gene encoding the GABA(A) receptor α2 subunit have been found to be linked to chronic alcohol <b>dependence</b> and to polydrug abuse.
+GABRA2	drug	cocaine	22882391	Among single nucleotide polymorphism markers in 13 candidate genes examined for association with <b>cocaine</b> cue reactivity, two were statistically significant: <strong>GABRA2</strong> (coding for GABA A receptor alpha 2 subunit; rs11503014, nominal p= .001) and OPRM1 (coding for mu opioid receptor; rs2236256, nominal p= .03).
+GABRA2	drug	opioid	22882391	Among single nucleotide polymorphism markers in 13 candidate genes examined for association with cocaine cue reactivity, two were statistically significant: <strong>GABRA2</strong> (coding for GABA A receptor alpha 2 subunit; rs11503014, nominal p= .001) and OPRM1 (coding for mu <b>opioid</b> receptor; rs2236256, nominal p= .03).
+GABRA2	drug	cocaine	22882391	These pilot results suggest that <b>cocaine</b> craving shows variability among <b>cocaine</b> dependent subjects, and that <strong>GABRA2</strong> and OPRM1 polymorphisms have differential influences on <b>cocaine</b> cue reactivity, warranting studies in future research.
+GABRA2	addiction	relapse	22882391	These pilot results suggest that cocaine <b>craving</b> shows variability among cocaine dependent subjects, and that <strong>GABRA2</strong> and OPRM1 polymorphisms have differential influences on cocaine cue reactivity, warranting studies in future research.
+GABRA2	addiction	dependence	22882390	It was also positively correlated, in women, with a <strong>GABRA2</strong> variant previously implicated as a risk factor for substance <b>dependence</b> and an objective electroencephalographic feature previously associated with <strong>GABRA2</strong> and relapse risk.
+GABRA2	addiction	relapse	22882390	It was also positively correlated, in women, with a <strong>GABRA2</strong> variant previously implicated as a risk factor for substance dependence and an objective electroencephalographic feature previously associated with <strong>GABRA2</strong> and <b>relapse</b> risk.
+GABRA2	addiction	dependence	22882390	The second analysis confirmed that the correlation between BMI and the substance <b>dependence</b> associated <strong>GABRA2</strong> genotype was reliable and sex specific.
+GABRA2	drug	alcohol	22817768	We developed a human progressive ratio (PR) paradigm using the computer assisted self infusion of <b>ethanol</b> (CASE) system that overcomes such variability and conducted a pilot study to assess its utility for detecting an interaction of subjects' <strong>GABRA2</strong> or GABRG1 genotype and pretreatment with 1 mg of lorazepam (LZ) vs. placebo on their willingness to work for <b>alcohol</b> rewards.
+GABRA2	drug	benzodiazepine	22817768	We developed a human progressive ratio (PR) paradigm using the computer assisted self infusion of ethanol (CASE) system that overcomes such variability and conducted a pilot study to assess its utility for detecting an interaction of subjects' <strong>GABRA2</strong> or GABRG1 genotype and pretreatment with 1 mg of <b>lorazepam</b> (LZ) vs. placebo on their willingness to work for alcohol rewards.
+GABRA2	drug	alcohol	22662011	We have evaluated the linkage disequilibrium patterns and haplotype frequencies of GABRG1 and <strong>GABRA2</strong> genes in 133 <b>alcoholics</b> divided according to Lesch's typology and in 145 matched controls.
+GABRA2	drug	alcohol	22501025	<strong>GABRA2</strong> markers moderate the subjective effects of <b>alcohol</b>.
+GABRA2	drug	alcohol	22501025	Variation in the GABA(A) α2 receptor subunit gene (<strong>GABRA2</strong>) has been associated with <b>alcohol</b> dependence (AD).
+GABRA2	addiction	dependence	22501025	Variation in the GABA(A) α2 receptor subunit gene (<strong>GABRA2</strong>) has been associated with alcohol <b>dependence</b> (AD).
+GABRA2	drug	alcohol	22501025	Therefore, we examined whether individual differences in SRs, which reflect sensitivity to the effects of <b>alcohol</b>, are associated with variation in <strong>GABRA2</strong>.
+GABRA2	drug	alcohol	22501025	We genotyped single nucleotide polymorphisms (SNPs) across the chromosome 4 region spanning <strong>GABRA2</strong> and analyzed the effect of genotype and haplotypes on subjective responses to <b>alcohol</b>.
+GABRA2	drug	alcohol	22501025	Our findings provide further evidence that variation within <strong>GABRA2</strong> is associated with attenuated negative responses to <b>alcohol</b>, a known risk factor for vulnerability to <b>alcohol</b> use disorders.
+GABRA2	drug	alcohol	22253714	There were also expression changes specific to cocaine addicts (GAD1, GAD2), <b>alcoholics</b> (<strong>GABRA2</strong>) and P rats (ABAT, GABRG3).
+GABRA2	drug	cocaine	22253714	There were also expression changes specific to <b>cocaine</b> addicts (GAD1, GAD2), alcoholics (<strong>GABRA2</strong>) and P rats (ABAT, GABRG3).
+GABRA2	addiction	relapse	22129841	<strong>GABRA2</strong> and KIBRA genotypes predict early <b>relapse</b> to substance use.
+GABRA2	drug	alcohol	22129841	The analysis used logistic and Cox regression methods to evaluate the contributions of age; sex; number of intake <b>alcohol</b>, drug use, and depression symptoms; and either <strong>GABRA2</strong>, CHRM2, ANKK1, BDNF, or KIBRA SNP genotypes to outcome.
+GABRA2	addiction	relapse	22129841	<strong>GABRA2</strong> and KIBRA genotypes, as well as the number of intake drug abuse problems and a younger age, were associated with an increased risk of <b>relapse</b>.
+GABRA2	drug	alcohol	22047728	Cerebellum volume in high risk offspring from multiplex <b>alcohol</b> dependence families: association with allelic variation in <strong>GABRA2</strong> and BDNF.
+GABRA2	addiction	dependence	22047728	Cerebellum volume in high risk offspring from multiplex alcohol <b>dependence</b> families: association with allelic variation in <strong>GABRA2</strong> and BDNF.
+GABRA2	drug	alcohol	21919924	GABRG1 and <strong>GABRA2</strong> variation associated with <b>alcohol</b> dependence in African Americans.
+GABRA2	addiction	dependence	21919924	GABRG1 and <strong>GABRA2</strong> variation associated with alcohol <b>dependence</b> in African Americans.
+GABRA2	drug	alcohol	21919924	Association of <b>alcohol</b> dependence (AD) with markers located at the 3' region of <strong>GABRA2</strong> has been replicated in several studies, but recent studies suggested the possibility that the signal may be attributable to the adjacent gene, GABRG1, located 90 kb distant in the 3' direction.
+GABRA2	addiction	dependence	21919924	Association of alcohol <b>dependence</b> (AD) with markers located at the 3' region of <strong>GABRA2</strong> has been replicated in several studies, but recent studies suggested the possibility that the signal may be attributable to the adjacent gene, GABRG1, located 90 kb distant in the 3' direction.
+GABRA2	drug	alcohol	21683760	Genetic association study of <strong>GABRA2</strong> single nucleotide polymorphisms and electroencephalography in <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	21683760	Genetic association study of <strong>GABRA2</strong> single nucleotide polymorphisms and electroencephalography in alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	21683760	The role of the GABA receptor alpha 2 gene (<strong>GABRA2</strong>) in human <b>alcohol</b> dependence was determined in a genetic and electrophysiological study.
+GABRA2	addiction	dependence	21683760	The role of the GABA receptor alpha 2 gene (<strong>GABRA2</strong>) in human alcohol <b>dependence</b> was determined in a genetic and electrophysiological study.
+GABRA2	drug	alcohol	21683760	Genotyping for seven <strong>GABRA2</strong> single nucleotide polymorphisms (SNPs), identified from the literature as positively associated with <b>alcohol</b> dependence, was performed with success rates of 90% or greater.
+GABRA2	addiction	dependence	21683760	Genotyping for seven <strong>GABRA2</strong> single nucleotide polymorphisms (SNPs), identified from the literature as positively associated with alcohol <b>dependence</b>, was performed with success rates of 90% or greater.
+GABRA2	drug	alcohol	21683760	This allelic association study provides no evidence for an association between <strong>GABRA2</strong> polymorphisms and <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	21683760	This allelic association study provides no evidence for an association between <strong>GABRA2</strong> polymorphisms and alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	21683760	This dissociation of effect may reflect the fact that the EEG is a more direct marker of phenotypic <strong>GABRA2</strong> expression than the more heterogeneous <b>alcohol</b> dependence phenotype.
+GABRA2	addiction	dependence	21683760	This dissociation of effect may reflect the fact that the EEG is a more direct marker of phenotypic <strong>GABRA2</strong> expression than the more heterogeneous alcohol <b>dependence</b> phenotype.
+GABRA2	drug	alcohol	21483437	Impulsiveness and insula activation during reward anticipation are associated with genetic variants in <strong>GABRA2</strong> in a family sample enriched for <b>alcoholism</b>.
+GABRA2	addiction	reward	21483437	Impulsiveness and insula activation during <b>reward</b> anticipation are associated with genetic variants in <strong>GABRA2</strong> in a family sample enriched for alcoholism.
+GABRA2	drug	alcohol	21483437	One of very few confirmed genetic association findings differentiating <b>alcoholics</b> from non <b>alcoholics</b> is with variants in the inhibitory γ amino butyric acid α2 receptor subunit (<strong>GABRA2</strong>) gene.
+GABRA2	drug	alcohol	21483437	Here we report the association of two of these <strong>GABRA2</strong> variants with measures of <b>alcohol</b> symptoms, impulsivity and with insula cortex activation during anticipation of reward or loss using functional magnetic resonance imaging (fMRI).
+GABRA2	addiction	reward	21483437	Here we report the association of two of these <strong>GABRA2</strong> variants with measures of alcohol symptoms, impulsivity and with insula cortex activation during anticipation of <b>reward</b> or loss using functional magnetic resonance imaging (fMRI).
+GABRA2	addiction	reward	21483437	A subset of offspring from these families (n=44, 20 females), genotyped for <strong>GABRA2</strong>, participated in an fMRI study using a monetary <b>incentive</b> delay task.
+GABRA2	drug	alcohol	21118274	Role of <strong>GABRA2</strong> in moderating subjective responses to <b>alcohol</b>.
+GABRA2	drug	alcohol	21118274	Recent genetic studies suggest an association between <b>alcohol</b> dependence and genetic variation in the γ aminobutyric acid A (GABA(A)) receptor α2 subunit gene (<strong>GABRA2</strong>).
+GABRA2	addiction	dependence	21118274	Recent genetic studies suggest an association between alcohol <b>dependence</b> and genetic variation in the γ aminobutyric acid A (GABA(A)) receptor α2 subunit gene (<strong>GABRA2</strong>).
+GABRA2	drug	alcohol	21118274	Based on a haplotypic association of <b>alcohol</b> dependence with <strong>GABRA2</strong>, we investigated whether <strong>GABRA2</strong> alleles are associated with the subjective responses to clamped <b>alcohol</b> concentration.
+GABRA2	addiction	dependence	21118274	Based on a haplotypic association of alcohol <b>dependence</b> with <strong>GABRA2</strong>, we investigated whether <strong>GABRA2</strong> alleles are associated with the subjective responses to clamped alcohol concentration.
+GABRA2	drug	alcohol	21118274	Among these 7 SNPs, 3 SNPs (rs279869, rs279858, and rs279837) located in the middle of the <strong>GABRA2</strong> gene showed significant associations with subjective effects of <b>alcohol</b>.
+GABRA2	drug	alcohol	21118274	These findings confirm and extend the observation that the <strong>GABRA2</strong> alleles affect the subjective responses to <b>alcohol</b>, and suggest that the genetic variations in <strong>GABRA2</strong> might play a role in the risk of <b>alcohol</b> use disorders by moderating the subjective effects of <b>alcohol</b>.
+GABRA2	drug	alcohol	20876231	Interestingly, though, a chromosomal cluster of four GABA(A) R subunit genes, including α2 (<strong>Gabra2</strong>), was associated with human <b>alcoholism</b> (Am J Hum Genet 74:705 714, 2004; Pharmacol Biochem Behav 90:95 104, 2008; J Psychiatr Res 42:184 191, 2008).
+GABRA2	drug	alcohol	20698837	A polymorphism in <strong>GABRA2</strong> is associated with the medial frontal response to <b>alcohol</b> cues in an fMRI study.
+GABRA2	drug	alcohol	20698837	Significant evidence has accumulated to suggest an association between single nucleotide polymorphisms (SNPs) in the <strong>GABRA2</strong> gene and <b>alcoholism</b>.
+GABRA2	drug	alcohol	20698837	In this study, we stratified subjects who had participated in an fMRI study of <b>alcohol</b> cue responses according to their genotype at a SNP in <strong>GABRA2</strong> (rs279871) shown to be associated with <b>alcohol</b> dependence (Edenberg et al., 2004).
+GABRA2	addiction	dependence	20698837	In this study, we stratified subjects who had participated in an fMRI study of alcohol cue responses according to their genotype at a SNP in <strong>GABRA2</strong> (rs279871) shown to be associated with alcohol <b>dependence</b> (Edenberg et al., 2004).
+GABRA2	drug	alcohol	20698837	These are the first data to suggest that <strong>GABRA2</strong> genotype could affect the brain's responses to cues associated with <b>alcohol</b>.
+GABRA2	drug	opioid	20482509	We consider four neurotransmitter systems: opioidergic, dopaminergic, GABAergic, and glutamatergic and focus on one receptor protein in each: OPRM1 (the &#micro; <b>opioid</b> receptor gene), DRD4 (the D(4) dopamine receptor gene), <strong>GABRA2</strong> (GABA(A) receptor alpha 2 subunit gene), and GRIK1 (the kainite receptor GluR5 subunit gene).
+GABRA2	drug	alcohol	20482509	Promising findings include the observations that a polymorphism in <strong>GABRA2</strong> predicts the response to specific psychotherapies; a polymorphism in DRD4 predicts the effects of the antipsychotic olanzapine on craving for <b>alcohol</b> and drinking behavior; and a polymorphism in GRIKI predicts adverse events resulting from treatment with the anticonvulsant topiramate.
+GABRA2	addiction	relapse	20482509	Promising findings include the observations that a polymorphism in <strong>GABRA2</strong> predicts the response to specific psychotherapies; a polymorphism in DRD4 predicts the effects of the antipsychotic olanzapine on <b>craving</b> for alcohol and drinking behavior; and a polymorphism in GRIKI predicts adverse events resulting from treatment with the anticonvulsant topiramate.
+GABRA2	drug	alcohol	20225194	First, we tested whether a single nucleotide polymorphism within <strong>GABRA2</strong> gene, which encodes a subunit of the GABA(A) receptor, and that has been associated with AD, influences 'extreme' <b>alcohol</b> intake and second, the efficacy of three psychotherapies for <b>alcoholism</b> in treating extreme drinking behavior.
+GABRA2	drug	cocaine	20133874	Consistent with a role of these receptors in addiction, we found specific markers and haplotypes of the <strong>GABRA2</strong> gene to be associated with human <b>cocaine</b> addiction.
+GABRA2	addiction	addiction	20133874	Consistent with a role of these receptors in <b>addiction</b>, we found specific markers and haplotypes of the <strong>GABRA2</strong> gene to be associated with human cocaine <b>addiction</b>.
+GABRA2	drug	alcohol	20102561	<strong>GABRA2</strong> and <b>alcohol</b> use disorders: no evidence of an association in an Italian case control study.
+GABRA2	drug	alcohol	20102561	The proposed association between the 3' half of the gene encoding the alpha 2 subunit of GABA receptor (3' <strong>GABRA2</strong>) and <b>alcohol</b> use disorders (AUDs) has received several independent confirmations.
+GABRA2	drug	alcohol	20102561	In this study, 10 single nucleotide polymorphisms (SNPs) of the 3' <strong>GABRA2</strong> gene, previously reported to be implicated in <b>alcohol</b> dependence, were used to evaluate the linkage between selected SNPs and AUDs in an Italian sample and to compare findings with those of previous studies.
+GABRA2	addiction	dependence	20102561	In this study, 10 single nucleotide polymorphisms (SNPs) of the 3' <strong>GABRA2</strong> gene, previously reported to be implicated in alcohol <b>dependence</b>, were used to evaluate the linkage between selected SNPs and AUDs in an Italian sample and to compare findings with those of previous studies.
+GABRA2	drug	alcohol	20102561	No evidence of an association was found at the allele, genotype, haplotype, or diplotype levels between the 3' <strong>GABRA2</strong> polymorphisms investigated and <b>alcoholism</b> in 149 Italian <b>alcoholics</b> (98 <b>alcohol</b> dependents and 51 <b>alcohol</b> abusers) and 278 controls.
+GABRA2	drug	alcohol	19833324	The influence of <strong>GABRA2</strong>, childhood trauma, and their interaction on <b>alcohol</b>, heroin, and cocaine dependence.
+GABRA2	drug	cocaine	19833324	The influence of <strong>GABRA2</strong>, childhood trauma, and their interaction on alcohol, heroin, and <b>cocaine</b> dependence.
+GABRA2	drug	opioid	19833324	The influence of <strong>GABRA2</strong>, childhood trauma, and their interaction on alcohol, <b>heroin</b>, and cocaine dependence.
+GABRA2	addiction	dependence	19833324	The influence of <strong>GABRA2</strong>, childhood trauma, and their interaction on alcohol, heroin, and cocaine <b>dependence</b>.
+GABRA2	addiction	addiction	19833324	The <strong>GABRA2</strong> gene has been implicated in <b>addiction</b>.
+GABRA2	addiction	addiction	19833324	We hypothesized that childhood trauma, <strong>GABRA2</strong> variation, and their interaction would influence <b>addiction</b> vulnerability.
+GABRA2	addiction	dependence	19833324	Our results suggest that at least in African American men, childhood trauma, <strong>GABRA2</strong> variation, and their interaction play a role in risk resilience for substance <b>dependence</b>.
+GABRA2	drug	alcohol	19783384	Test of association between <strong>GABRA2</strong> (SNP rs279871) and adolescent conduct/<b>alcohol</b> use disorders utilizing a sample of clinic referred youth with serious substance and conduct problems, controls and available first degree relatives.
+GABRA2	drug	alcohol	19783384	Recent findings have linked the <strong>GABRA2</strong> gene with antisocial personality disorder and <b>alcohol</b> dependence (AD) in adults and conduct disorder (CD), but not AD symptoms, in children and adolescents.
+GABRA2	addiction	dependence	19783384	Recent findings have linked the <strong>GABRA2</strong> gene with antisocial personality disorder and alcohol <b>dependence</b> (AD) in adults and conduct disorder (CD), but not AD symptoms, in children and adolescents.
+GABRA2	drug	alcohol	19672139	Role of <strong>GABRA2</strong> on risk for <b>alcohol</b>, nicotine, and cannabis dependence in the Iowa Adoption Studies.
+GABRA2	drug	cannabinoid	19672139	Role of <strong>GABRA2</strong> on risk for alcohol, nicotine, and <b>cannabis</b> dependence in the Iowa Adoption Studies.
+GABRA2	drug	nicotine	19672139	Role of <strong>GABRA2</strong> on risk for alcohol, <b>nicotine</b>, and cannabis dependence in the Iowa Adoption Studies.
+GABRA2	addiction	dependence	19672139	Role of <strong>GABRA2</strong> on risk for alcohol, nicotine, and cannabis <b>dependence</b> in the Iowa Adoption Studies.
+GABRA2	drug	alcohol	19672139	A number of studies have shown that genetic variation at <strong>GABRA2</strong> alters vulnerability to <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	19672139	A number of studies have shown that genetic variation at <strong>GABRA2</strong> alters vulnerability to alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	19672139	Therefore, we genotyped 516 individuals from the Iowa Adoption Studies, a large longitudinal case and control adoption study of substance use, at 39 single nucleotide polymorphisms encompassing the <strong>GABRA2</strong> locus and analyzed them with respect to their lifetime history of three common forms of substance use dependence [<b>alcohol</b> dependence (AD), nicotine dependence (ND), and cannabis dependence (CD)] in the Iowa Adoption Studies and relevant exposure variables.
+GABRA2	drug	cannabinoid	19672139	Therefore, we genotyped 516 individuals from the Iowa Adoption Studies, a large longitudinal case and control adoption study of substance use, at 39 single nucleotide polymorphisms encompassing the <strong>GABRA2</strong> locus and analyzed them with respect to their lifetime history of three common forms of substance use dependence [alcohol dependence (AD), nicotine dependence (ND), and <b>cannabis</b> dependence (CD)] in the Iowa Adoption Studies and relevant exposure variables.
+GABRA2	drug	nicotine	19672139	Therefore, we genotyped 516 individuals from the Iowa Adoption Studies, a large longitudinal case and control adoption study of substance use, at 39 single nucleotide polymorphisms encompassing the <strong>GABRA2</strong> locus and analyzed them with respect to their lifetime history of three common forms of substance use dependence [alcohol dependence (AD), <b>nicotine</b> dependence (ND), and cannabis dependence (CD)] in the Iowa Adoption Studies and relevant exposure variables.
+GABRA2	addiction	dependence	19672139	Therefore, we genotyped 516 individuals from the Iowa Adoption Studies, a large longitudinal case and control adoption study of substance use, at 39 single nucleotide polymorphisms encompassing the <strong>GABRA2</strong> locus and analyzed them with respect to their lifetime history of three common forms of substance use <b>dependence</b> [alcohol <b>dependence</b> (AD), nicotine <b>dependence</b> (ND), and cannabis <b>dependence</b> (CD)] in the Iowa Adoption Studies and relevant exposure variables.
+GABRA2	drug	alcohol	19536785	The genes encoding several GABA A receptor subunits, including <strong>GABRA2</strong>, have been associated with <b>alcoholism</b>, suggesting that variations in gaba signaling contribute to risk.
+GABRA2	drug	alcohol	19487630	We describe analyses aimed at characterizing the pathway of risk associated with <strong>GABRA2</strong>, a gene previously associated with adult <b>alcohol</b> dependence, in a community sample of children followed longitudinally from childhood through young adulthood.
+GABRA2	addiction	dependence	19487630	We describe analyses aimed at characterizing the pathway of risk associated with <strong>GABRA2</strong>, a gene previously associated with adult alcohol <b>dependence</b>, in a community sample of children followed longitudinally from childhood through young adulthood.
+GABRA2	drug	alcohol	19487630	The <strong>GABRA2</strong> gene was associated with class membership, with subjects who showed persistent elevated trajectories of externalizing behavior more likely to carry the genotype previously associated with increased risk of adult <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	19487630	The <strong>GABRA2</strong> gene was associated with class membership, with subjects who showed persistent elevated trajectories of externalizing behavior more likely to carry the genotype previously associated with increased risk of adult alcohol <b>dependence</b>.
+GABRA2	drug	nicotine	19207358	A previous association analysis identified polymorphisms in gamma aminobutyric acid receptor A, subunit 4 (GABRA4) and <strong>GABRA2</strong> to be associated with <b>nicotine</b> dependence, as assessed by a score of 4 or more on the Fagerström Test for <b>Nicotine</b> Dependence (FTND).
+GABRA2	addiction	dependence	19207358	A previous association analysis identified polymorphisms in gamma aminobutyric acid receptor A, subunit 4 (GABRA4) and <strong>GABRA2</strong> to be associated with nicotine <b>dependence</b>, as assessed by a score of 4 or more on the Fagerström Test for Nicotine <b>Dependence</b> (FTND).
+GABRA2	drug	nicotine	19207358	In 1049 cases (FTND of 4 or more) and 872 controls (<b>smokers</b> with FTND of 0) from the United States and Australia, we examine the association between 23 GABRA4 and 39 <strong>GABRA2</strong> recently genotyped single nucleotide polymorphisms (SNPs) and <b>nicotine</b> dependence using logistic regression based association analyses using the genomic analysis package PLINK.
+GABRA2	addiction	dependence	19207358	In 1049 cases (FTND of 4 or more) and 872 controls (smokers with FTND of 0) from the United States and Australia, we examine the association between 23 GABRA4 and 39 <strong>GABRA2</strong> recently genotyped single nucleotide polymorphisms (SNPs) and nicotine <b>dependence</b> using logistic regression based association analyses using the genomic analysis package PLINK.
+GABRA2	drug	nicotine	19207358	Two and 18 additional SNPs in GABRA4 and <strong>GABRA2</strong>, respectively, were associated with <b>nicotine</b> dependence.
+GABRA2	addiction	dependence	19207358	Two and 18 additional SNPs in GABRA4 and <strong>GABRA2</strong>, respectively, were associated with nicotine <b>dependence</b>.
+GABRA2	drug	nicotine	19207358	Our findings demonstrate consistently the role of GABRA4 and <strong>GABRA2</strong> in <b>nicotine</b> dependence.
+GABRA2	addiction	dependence	19207358	Our findings demonstrate consistently the role of GABRA4 and <strong>GABRA2</strong> in nicotine <b>dependence</b>.
+GABRA2	drug	alcohol	18818659	GABRG1 and <strong>GABRA2</strong> as independent predictors for <b>alcoholism</b> in two populations.
+GABRA2	drug	alcohol	18818659	Variation in one chromosome 4 gene, <strong>GABRA2</strong>, has been robustly associated with <b>alcohol</b> use disorders (AUD) although no functional locus has been identified.
+GABRA2	drug	alcohol	18818659	We genotyped 24 SNPs across GABRG1 and <strong>GABRA2</strong> in two population isolates: 547 Finnish Caucasian men (266 <b>alcoholics</b>) and 311 community derived Plains Indian men and women (181 <b>alcoholics</b>).
+GABRA2	drug	alcohol	18818659	In both the Plains Indians and the Caucasians: (1) the GABRG1 haplotype block(s) did not extend to <strong>GABRA2</strong>; (2) GABRG1 haplotypes and SNPs were significantly associated with AUD; (3) there was no association between <strong>GABRA2</strong> haplotypes and AUD; (4) there were several common (>or=0.05) haplotypes that spanned GABRG1 and <strong>GABRA2</strong> (341 kb), three of which were present in both populations: one of these ancestral haplotypes was associated with AUD, the other two were more common in non <b>alcoholics</b>; this association was determined by GABRG1; (5) in the Finns, three less common (<0.05) extended haplotypes showed an association with AUD that was determined by <strong>GABRA2</strong>.
+GABRA2	drug	alcohol	18818659	Our results suggest that there are likely to be independent, complex contributions from both GABRG1 and <strong>GABRA2</strong> to <b>alcoholism</b> vulnerability.
+GABRA2	drug	alcohol	18781239	These results demonstrated that <strong>GABRA2</strong>  originally associated with a diagnosis of <b>alcohol</b> dependence in adults  also predicted the onset of symptoms among subjects in their 20s, confirmed specific hypotheses about three other predictors in the fi nal model, and suggested the utility of incorporating biological and nonbiological predictors to optimally predict young adult <b>alcohol</b> problems.
+GABRA2	addiction	dependence	18781239	These results demonstrated that <strong>GABRA2</strong>  originally associated with a diagnosis of alcohol <b>dependence</b> in adults  also predicted the onset of symptoms among subjects in their 20s, confirmed specific hypotheses about three other predictors in the fi nal model, and suggested the utility of incorporating biological and nonbiological predictors to optimally predict young adult alcohol problems.
+GABRA2	drug	alcohol	18727688	The role of <strong>GABRA2</strong> in <b>alcohol</b> dependence, smoking, and illicit drug use in an Australian population sample.
+GABRA2	drug	nicotine	18727688	The role of <strong>GABRA2</strong> in alcohol dependence, <b>smoking</b>, and illicit drug use in an Australian population sample.
+GABRA2	addiction	dependence	18727688	The role of <strong>GABRA2</strong> in alcohol <b>dependence</b>, smoking, and illicit drug use in an Australian population sample.
+GABRA2	drug	alcohol	18727688	Multiple studies have shown that genetic variation in the alpha 2 subunit of the gamma aminobutyric acid type A (GABA(A)) receptor (<strong>GABRA2</strong>) is associated with risk for <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	18727688	Multiple studies have shown that genetic variation in the alpha 2 subunit of the gamma aminobutyric acid type A (GABA(A)) receptor (<strong>GABRA2</strong>) is associated with risk for alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	18727688	Recent reports have suggested that <strong>GABRA2</strong> may exert its influence on dependence through factors such as sensitivity to <b>alcohol</b>'s intoxicating effects and that <strong>GABRA2</strong> may also contribute to a common underlying genetic vulnerability to both <b>alcohol</b> and drug dependence.
+GABRA2	addiction	dependence	18727688	Recent reports have suggested that <strong>GABRA2</strong> may exert its influence on <b>dependence</b> through factors such as sensitivity to alcohol's intoxicating effects and that <strong>GABRA2</strong> may also contribute to a common underlying genetic vulnerability to both alcohol and drug <b>dependence</b>.
+GABRA2	drug	alcohol	18727688	The present study tested for association between <strong>GABRA2</strong> and <b>alcohol</b> dependence, smoking, and illicit drug use within the Australian population.
+GABRA2	drug	nicotine	18727688	The present study tested for association between <strong>GABRA2</strong> and alcohol dependence, <b>smoking</b>, and illicit drug use within the Australian population.
+GABRA2	addiction	dependence	18727688	The present study tested for association between <strong>GABRA2</strong> and alcohol <b>dependence</b>, smoking, and illicit drug use within the Australian population.
+GABRA2	drug	alcohol	18727688	We observed evidence of association (p < 0.05) between multiple <strong>GABRA2</strong> SNPs and quantitative measures of <b>alcohol</b> dependence, including symptom scores and principal component factor scores from the 9 criteria for DSM IV <b>alcohol</b> dependence, in the opposite direction to that previously reported.
+GABRA2	addiction	dependence	18727688	We observed evidence of association (p < 0.05) between multiple <strong>GABRA2</strong> SNPs and quantitative measures of alcohol <b>dependence</b>, including symptom scores and principal component factor scores from the 9 criteria for DSM IV alcohol <b>dependence</b>, in the opposite direction to that previously reported.
+GABRA2	drug	alcohol	18727688	In contrast, <strong>GABRA2</strong> was not associated overall with dichotomous measure of <b>alcohol</b> dependence nor with smoking, cannabis, or illicit drug use.
+GABRA2	drug	cannabinoid	18727688	In contrast, <strong>GABRA2</strong> was not associated overall with dichotomous measure of alcohol dependence nor with smoking, <b>cannabis</b>, or illicit drug use.
+GABRA2	drug	nicotine	18727688	In contrast, <strong>GABRA2</strong> was not associated overall with dichotomous measure of alcohol dependence nor with <b>smoking</b>, cannabis, or illicit drug use.
+GABRA2	addiction	dependence	18727688	In contrast, <strong>GABRA2</strong> was not associated overall with dichotomous measure of alcohol <b>dependence</b> nor with smoking, cannabis, or illicit drug use.
+GABRA2	drug	alcohol	18727688	The <strong>GABRA2</strong> allelic associations found in clinical case control studies have detectable but minor effects on DSM defined <b>alcohol</b> dependence in the general community.
+GABRA2	addiction	dependence	18727688	The <strong>GABRA2</strong> allelic associations found in clinical case control studies have detectable but minor effects on DSM defined alcohol <b>dependence</b> in the general community.
+GABRA2	drug	cannabinoid	18519829	Genes such as ELTD1 on chromosome 1, in addition to genes on chromosomes 4 (eg, <strong>GABRA2</strong>) and 6 (eg, CNR1), may be associated with the genetic risk for <b>cannabis</b> use disorders.
+GABRA2	drug	alcohol	18482426	Compelling evidence suggests that <strong>GABRA2</strong> is associated with <b>alcohol</b> and drug dependence.
+GABRA2	addiction	dependence	18482426	Compelling evidence suggests that <strong>GABRA2</strong> is associated with alcohol and drug <b>dependence</b>.
+GABRA2	drug	nicotine	18482426	We found evidence for association between four SNPs in GABRA4, two SNPs in <strong>GABRA2</strong> and one SNP in GABRE with <b>nicotine</b> dependence.
+GABRA2	addiction	dependence	18482426	We found evidence for association between four SNPs in GABRA4, two SNPs in <strong>GABRA2</strong> and one SNP in GABRE with nicotine <b>dependence</b>.
+GABRA2	drug	alcohol	18482426	These included a synonymous polymorphism in <strong>GABRA2</strong> (rs279858), lying in a highly conserved region, which has been shown previously to be associated with <b>alcohol</b> and drug dependence.
+GABRA2	addiction	dependence	18482426	These included a synonymous polymorphism in <strong>GABRA2</strong> (rs279858), lying in a highly conserved region, which has been shown previously to be associated with alcohol and drug <b>dependence</b>.
+GABRA2	drug	nicotine	18482426	Significant haplotypes associated with <b>nicotine</b> dependence were found for <strong>GABRA2</strong>.
+GABRA2	addiction	dependence	18482426	Significant haplotypes associated with nicotine <b>dependence</b> were found for <strong>GABRA2</strong>.
+GABRA2	drug	alcohol	18440057	Several recent studies have provided strong evidence that one of these genes, <strong>GABRA2</strong>, is implicated in <b>alcoholism</b> in humans.
+GABRA2	drug	alcohol	18361719	Effects of <strong>GABRA2</strong> variation on physiological, psychomotor and subjective responses in the <b>alcohol</b> challenge twin study.
+GABRA2	drug	alcohol	18361719	Multiple reports have identified variation in the <strong>GABRA2</strong> gene as contributing to the genetic susceptibility to <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	18361719	Multiple reports have identified variation in the <strong>GABRA2</strong> gene as contributing to the genetic susceptibility to alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	18361719	We have therefore tested whether <strong>GABRA2</strong> variation is associated with variation in the subjective and objective effects of a standard dose of <b>alcohol</b> in humans.
+GABRA2	drug	alcohol	18361719	Data on responses to <b>alcohol</b> from the <b>Alcohol</b> Challenge Twin Study (Martin et al., 1985) have been tested against allelic and haplotype information obtained by typing 41 single nucleotide polymorphisms in or close to the <strong>GABRA2</strong> gene.
+GABRA2	drug	alcohol	19569404	Analyses of a later wave of the Collaborative Study on the Genetics of <b>Alcoholism</b> reveal a complex interplay of the <strong>GABRA2</strong> gene with social structural factors to produce cases meeting DSM/ICD diagnoses.
+GABRA2	drug	alcohol	18005236	In fact, recent studies have shown an association between the gene for the alpha2 subunit of the GABA(A) receptor (<strong>GABRA2</strong>) and <b>alcoholism</b>.
+GABRA2	drug	alcohol	18005236	In the present study, we examined the functional relevance of the <strong>GABRA2</strong> gene in <b>alcohol</b> dependence by assessing brain <strong>GABRA2</strong> mRNA and GABA(A)alpha2 subunit protein levels in post mortem prefrontal cortical tissue collected from control and <b>alcohol</b> dependent individuals.
+GABRA2	addiction	dependence	18005236	In the present study, we examined the functional relevance of the <strong>GABRA2</strong> gene in alcohol <b>dependence</b> by assessing brain <strong>GABRA2</strong> mRNA and GABA(A)alpha2 subunit protein levels in post mortem prefrontal cortical tissue collected from control and alcohol dependent individuals.
+GABRA2	drug	alcohol	18005236	In addition, using an endophenotype approach, we tested whether the <strong>GABRA2</strong> gene moderates sensitivity to the acute effects of <b>alcohol</b> in two independent samples from distinct human <b>alcohol</b> challenge studies.
+GABRA2	drug	alcohol	18005236	<strong>GABRA2</strong> single nucleotide polymorphisms (rs573400, rs279871 and rs279858) were significantly associated with sensitivity to the acute effects of <b>alcohol</b>.
+GABRA2	drug	alcohol	18005236	Specifically, there was a significant main effect of <strong>GABRA2</strong> x breath <b>alcohol</b> concentration on several measures of subjective responses to <b>alcohol</b>, including the hedonic value of <b>alcohol</b>.
+GABRA2	addiction	reward	18005236	Specifically, there was a significant main effect of <strong>GABRA2</strong> x breath alcohol concentration on several measures of subjective responses to alcohol, including the <b>hedonic</b> value of alcohol.
+GABRA2	drug	alcohol	18005236	In summary, these results extend previous findings and provide new insights into the putative biobehavioral mechanisms that may moderate the association between the <strong>GABRA2</strong> gene, sensitivity to the acute effects of <b>alcohol</b> and ultimately <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	18005236	In summary, these results extend previous findings and provide new insights into the putative biobehavioral mechanisms that may moderate the association between the <strong>GABRA2</strong> gene, sensitivity to the acute effects of alcohol and ultimately alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	17982586	We found significant linkage and association between brain oscillations and genes involved with inhibitory neural networks (e.g., <strong>GABRA2</strong>, CHRM2), including frontal networks that are deficient in individuals with <b>alcohol</b> dependence, impulsivity, and related disinhibitory disorders.
+GABRA2	addiction	dependence	17982586	We found significant linkage and association between brain oscillations and genes involved with inhibitory neural networks (e.g., <strong>GABRA2</strong>, CHRM2), including frontal networks that are deficient in individuals with alcohol <b>dependence</b>, impulsivity, and related disinhibitory disorders.
+GABRA2	drug	alcohol	17982586	We reported significant linkage and linkage disequilibrium for the beta frequency of the EEG and <strong>GABRA2</strong>, a GABAA receptor gene on chromosome 4, which we found is also associated with diagnosis of <b>alcohol</b> dependence and related disorders.
+GABRA2	addiction	dependence	17982586	We reported significant linkage and linkage disequilibrium for the beta frequency of the EEG and <strong>GABRA2</strong>, a GABAA receptor gene on chromosome 4, which we found is also associated with diagnosis of alcohol <b>dependence</b> and related disorders.
+GABRA2	drug	alcohol	17976953	The <strong>GABRA2</strong> locus has been found to be associated with <b>alcohol</b> dependence in several studies, but no functional variant that can account for this association has been identified.
+GABRA2	addiction	dependence	17976953	The <strong>GABRA2</strong> locus has been found to be associated with alcohol <b>dependence</b> in several studies, but no functional variant that can account for this association has been identified.
+GABRA2	drug	alcohol	17949392	Previous studies demonstrated, and replicated, an association between single nucleotide polymorphisms (SNPs) within the <strong>GABRA2</strong> gene and risk for <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	17949392	Previous studies demonstrated, and replicated, an association between single nucleotide polymorphisms (SNPs) within the <strong>GABRA2</strong> gene and risk for alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	17949392	The present study examines the association of a <strong>GABRA2</strong> SNP with another definition of <b>alcohol</b> involvement and with the effects of psychosocial treatment.
+GABRA2	drug	alcohol	17690794	The role of the <strong>GABRA2</strong> polymorphism in multiplex <b>alcohol</b> dependence families with minimal comorbidity: within family association and linkage analyses.
+GABRA2	addiction	dependence	17690794	The role of the <strong>GABRA2</strong> polymorphism in multiplex alcohol <b>dependence</b> families with minimal comorbidity: within family association and linkage analyses.
+GABRA2	drug	alcohol	17690794	Analyses of multiplex families found a particular gene, <strong>GABRA2</strong>, to be highly associated with <b>alcohol</b> dependence, using within family association tests and other methods.
+GABRA2	addiction	dependence	17690794	Analyses of multiplex families found a particular gene, <strong>GABRA2</strong>, to be highly associated with alcohol <b>dependence</b>, using within family association tests and other methods.
+GABRA2	drug	alcohol	17690794	Linkage and association of <strong>GABRA2</strong> and <b>alcohol</b> dependence were evaluated using SIBPAL (a nonparametric linkage package) and both the Pedigree Disequilibrium Test and the Family Based Association Test, respectively.
+GABRA2	addiction	dependence	17690794	Linkage and association of <strong>GABRA2</strong> and alcohol <b>dependence</b> were evaluated using SIBPAL (a nonparametric linkage package) and both the Pedigree Disequilibrium Test and the Family Based Association Test, respectively.
+GABRA2	drug	alcohol	17690794	We find no evidence of a relationship between <strong>GABRA2</strong> and <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	17690794	We find no evidence of a relationship between <strong>GABRA2</strong> and alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	17507911	Markers in the 5' region of GABRG1 associate to <b>alcohol</b> dependence and are in linkage disequilibrium with markers in the adjacent <strong>GABRA2</strong> gene.
+GABRA2	addiction	dependence	17507911	Markers in the 5' region of GABRG1 associate to alcohol <b>dependence</b> and are in linkage disequilibrium with markers in the adjacent <strong>GABRA2</strong> gene.
+GABRA2	drug	alcohol	17507911	Following an initial report, there have been multiple replications of an association of <b>alcohol</b> dependence (AD) to markers within a haplotype block that includes the 3' half of the gene encoding the GABA(A) alpha 2 subunit (<strong>GABRA2</strong>), on chromosome 4p.
+GABRA2	addiction	dependence	17507911	Following an initial report, there have been multiple replications of an association of alcohol <b>dependence</b> (AD) to markers within a haplotype block that includes the 3' half of the gene encoding the GABA(A) alpha 2 subunit (<strong>GABRA2</strong>), on chromosome 4p.
+GABRA2	drug	alcohol	17207817	GABA A2 receptor subunit gene (<strong>GABRA2</strong>) polymorphisms and risk for <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	17207817	GABA A2 receptor subunit gene (<strong>GABRA2</strong>) polymorphisms and risk for alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	17207817	Recent studies have suggested that genetic variants of the GABA A receptor alpha2 subunit gene (<strong>GABRA2</strong>) are associated with <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	17207817	Recent studies have suggested that genetic variants of the GABA A receptor alpha2 subunit gene (<strong>GABRA2</strong>) are associated with alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	17207817	The aim of this study is to confirm and extend the role of <strong>GABRA2</strong> haplotypes in the liability to <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	17207817	The aim of this study is to confirm and extend the role of <strong>GABRA2</strong> haplotypes in the liability to alcohol <b>dependence</b>.
+GABRA2	addiction	addiction	16894595	These results delineate the haplotypes and patterns of linkage disequilibrium in this region, focus attention of the <strong>GABRA2</strong> gene and identify modest associations between <strong>GABRA2</strong> genotypes and <b>addiction</b> phenotypes.
+GABRA2	addiction	addiction	16894595	These results are consistent with modest roles for <strong>GABRA2</strong> variants in <b>addiction</b> vulnerabilities.
+GABRA2	drug	alcohol	16622805	Association of <strong>GABRA2</strong> with drug dependence in the collaborative study of the genetics of <b>alcoholism</b> sample.
+GABRA2	addiction	dependence	16622805	Association of <strong>GABRA2</strong> with drug <b>dependence</b> in the collaborative study of the genetics of alcoholism sample.
+GABRA2	drug	cannabinoid	16622805	Results suggested association between <b>marijuana</b> dependence and illicit drug dependence with SNPs in the <strong>GABRA2</strong> gene.
+GABRA2	addiction	dependence	16622805	Results suggested association between marijuana <b>dependence</b> and illicit drug <b>dependence</b> with SNPs in the <strong>GABRA2</strong> gene.
+GABRA2	drug	alcohol	16612210	(d) Examination of family based samples has identified several genes including <strong>GABRA2</strong> and CHRM2 thought to be associated with <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	16612210	(d) Examination of family based samples has identified several genes including <strong>GABRA2</strong> and CHRM2 thought to be associated with alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	16562401	Marital status, <b>alcohol</b> dependence, and <strong>GABRA2</strong>: evidence for gene environment correlation and interaction.
+GABRA2	addiction	dependence	16562401	Marital status, alcohol <b>dependence</b>, and <strong>GABRA2</strong>: evidence for gene environment correlation and interaction.
+GABRA2	drug	alcohol	16562401	The gene <strong>GABRA2</strong> has been associated with the risk for <b>alcohol</b> dependence in independent samples.
+GABRA2	addiction	dependence	16562401	The gene <strong>GABRA2</strong> has been associated with the risk for alcohol <b>dependence</b> in independent samples.
+GABRA2	drug	alcohol	16562401	A series of analyses was performed to evaluate the relationship between the following: (1) <strong>GABRA2</strong> and <b>alcohol</b> dependence, (2) marital status and <b>alcohol</b> dependence, (3) <strong>GABRA2</strong> and marital status, and (4) interactions between <strong>GABRA2</strong> and marital status on the development of <b>alcohol</b> dependence in the high risk COGA sample.
+GABRA2	addiction	dependence	16562401	A series of analyses was performed to evaluate the relationship between the following: (1) <strong>GABRA2</strong> and alcohol <b>dependence</b>, (2) marital status and alcohol <b>dependence</b>, (3) <strong>GABRA2</strong> and marital status, and (4) interactions between <strong>GABRA2</strong> and marital status on the development of alcohol <b>dependence</b> in the high risk COGA sample.
+GABRA2	drug	alcohol	16562401	Both <strong>GABRA2</strong> and marital status contributed independently to the development of <b>alcohol</b> dependence in the COGA sample.
+GABRA2	addiction	dependence	16562401	Both <strong>GABRA2</strong> and marital status contributed independently to the development of alcohol <b>dependence</b> in the COGA sample.
+GABRA2	drug	alcohol	16562401	These analyses provide evidence of both gene environment correlation and gene environment interaction associated with <strong>GABRA2</strong>, marital status, and <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	16562401	These analyses provide evidence of both gene environment correlation and gene environment interaction associated with <strong>GABRA2</strong>, marital status, and alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	16557364	The role of <strong>GABRA2</strong> in risk for conduct disorder and <b>alcohol</b> and drug dependence across developmental stages.
+GABRA2	addiction	dependence	16557364	The role of <strong>GABRA2</strong> in risk for conduct disorder and alcohol and drug <b>dependence</b> across developmental stages.
+GABRA2	drug	alcohol	16557364	We use findings from the behavior genetics literature about how genetic factors (latently) influence <b>alcohol</b> dependence and related disorders to develop and test hypotheses about the risk associated with a specific gene, <strong>GABRA2</strong>, across different developmental stages.
+GABRA2	addiction	dependence	16557364	We use findings from the behavior genetics literature about how genetic factors (latently) influence alcohol <b>dependence</b> and related disorders to develop and test hypotheses about the risk associated with a specific gene, <strong>GABRA2</strong>, across different developmental stages.
+GABRA2	drug	alcohol	16557364	In a sample of children and adolescents ascertained as part of the COGA project, we find that <strong>GABRA2</strong> is significantly associated with childhood conduct disorder symptoms, but not with childhood <b>alcohol</b> dependence symptoms.
+GABRA2	addiction	dependence	16557364	In a sample of children and adolescents ascertained as part of the COGA project, we find that <strong>GABRA2</strong> is significantly associated with childhood conduct disorder symptoms, but not with childhood alcohol <b>dependence</b> symptoms.
+GABRA2	drug	alcohol	16557364	A consistent elevation in risk for <b>alcohol</b> dependence associated with <strong>GABRA2</strong> is not evident until the mid 20s and then remains throughout adulthood.
+GABRA2	addiction	dependence	16557364	A consistent elevation in risk for alcohol <b>dependence</b> associated with <strong>GABRA2</strong> is not evident until the mid 20s and then remains throughout adulthood.
+GABRA2	addiction	dependence	16557364	<strong>GABRA2</strong> is also associated with other drug <b>dependence</b> in our sample, both in adolescence and adulthood.
+GABRA2	drug	alcohol	16395124	Confirmation of association of the <strong>GABRA2</strong> gene with <b>alcohol</b> dependence by subtype specific analysis.
+GABRA2	addiction	dependence	16395124	Confirmation of association of the <strong>GABRA2</strong> gene with alcohol <b>dependence</b> by subtype specific analysis.
+GABRA2	drug	alcohol	16395124	Three recent studies revealed a haplotypic association of <b>alcohol</b> dependence with the gene encoding the alpha2 subunit of the gamma aminobutyric acid type A (GABAA) receptor (<strong>GABRA2</strong>).
+GABRA2	addiction	dependence	16395124	Three recent studies revealed a haplotypic association of alcohol <b>dependence</b> with the gene encoding the alpha2 subunit of the gamma aminobutyric acid type A (GABAA) receptor (<strong>GABRA2</strong>).
+GABRA2	drug	alcohol	16395124	The present study examined whether variation of the <strong>GABRA2</strong> gene confers susceptibility to different subtypes of <b>alcohol</b> dependence in the German population.
+GABRA2	addiction	dependence	16395124	The present study examined whether variation of the <strong>GABRA2</strong> gene confers susceptibility to different subtypes of alcohol <b>dependence</b> in the German population.
+GABRA2	drug	alcohol	16395124	A total of 257 German <b>alcohol</b> dependent patients and 88 healthy population controls were genotyped for six single nucleotide polymorphisms covering the middle part and the 3' end of <strong>GABRA2</strong>.
+GABRA2	drug	alcohol	16395124	The overall <b>alcohol</b> dependent patients vs. control group comparison confirmed positive allelic association for five of six single nucleotide polymorphisms mapping from intron 3 to the 3' end of <strong>GABRA2</strong> (P=0.01 0.02).
+GABRA2	drug	alcohol	16395124	Although our study was limited by the number of cases being larger than the number of controls, the results confirm <strong>GABRA2</strong> as a susceptibility gene for <b>alcohol</b> dependence in the German population.
+GABRA2	addiction	dependence	16395124	Although our study was limited by the number of cases being larger than the number of controls, the results confirm <strong>GABRA2</strong> as a susceptibility gene for alcohol <b>dependence</b> in the German population.
+GABRA2	drug	alcohol	16341909	In this paper we summarize published results from linkage and association analyses of two chromosomal regions in which the use of endophenotypes has successfully led to the identification of genes associated with <b>alcohol</b> dependence [<strong>GABRA2</strong> (Edenberg et al., (2004).
+GABRA2	addiction	dependence	16341909	In this paper we summarize published results from linkage and association analyses of two chromosomal regions in which the use of endophenotypes has successfully led to the identification of genes associated with alcohol <b>dependence</b> [<strong>GABRA2</strong> (Edenberg et al., (2004).
+GABRA2	drug	alcohol	15950776	Non coding variations in <strong>GABRA2</strong>, the gene encoding the alpha2 subunit, are associated with the risk for <b>alcoholism</b>, suggesting that regulatory differences are important.
+GABRA2	drug	alcohol	15834213	Two recent large genetic studies in the US population have reported association between genetic variation in gamma amino butyric acid alpha2 receptor subtype (<strong>GABRA2</strong>) and risk for <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	15834213	Two recent large genetic studies in the US population have reported association between genetic variation in gamma amino butyric acid alpha2 receptor subtype (<strong>GABRA2</strong>) and risk for alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	15834213	The goal of this study was to test whether <strong>GABRA2</strong> is associated with <b>alcohol</b> dependence in a sample of Russian <b>alcohol</b> dependent men.
+GABRA2	addiction	dependence	15834213	The goal of this study was to test whether <strong>GABRA2</strong> is associated with alcohol <b>dependence</b> in a sample of Russian alcohol dependent men.
+GABRA2	drug	alcohol	15834213	A total of 113 Russian <b>alcohol</b> dependent men and 100 male population control subjects were recruited in St. Petersburg and genotyped for seven <strong>GABRA2</strong> single nucleotide polymorphisms (SNPs) using real time PCR (TaqMan).
+GABRA2	drug	alcohol	15834213	Six SNPs were located in a <strong>GABRA2</strong> haplotype block previously associated with <b>alcohol</b> dependence (AD) in the US population.
+GABRA2	addiction	dependence	15834213	Six SNPs were located in a <strong>GABRA2</strong> haplotype block previously associated with alcohol <b>dependence</b> (AD) in the US population.
+GABRA2	drug	alcohol	15702134	<strong>GABRA2</strong> alleles moderate the subjective effects of <b>alcohol</b>, which are attenuated by finasteride.
+GABRA2	drug	alcohol	15702134	Based on a haplotypic association of <b>alcohol</b> dependence with the gene encoding the GABA(A) receptor alpha 2 subunit (<strong>GABRA2</strong>), we examined whether <strong>GABRA2</strong> alleles are associated with the subjective response to <b>alcohol</b>.
+GABRA2	addiction	dependence	15702134	Based on a haplotypic association of alcohol <b>dependence</b> with the gene encoding the GABA(A) receptor alpha 2 subunit (<strong>GABRA2</strong>), we examined whether <strong>GABRA2</strong> alleles are associated with the subjective response to alcohol.
+GABRA2	drug	alcohol	15702134	These findings provide preliminary evidence that the risk of <b>alcoholism</b> associated with <strong>GABRA2</strong> alleles may be related to differences in the subjective response to <b>alcohol</b>.
+GABRA2	drug	alcohol	15274050	Allelic and haplotypic association of <strong>GABRA2</strong> with <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	15274050	Allelic and haplotypic association of <strong>GABRA2</strong> with alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	15274050	A recent effort to fine map that region showed a haplotypic association of <b>alcohol</b> dependence to the gene encoding the GABAA receptor alpha 2 subunit (<strong>GABRA2</strong>).
+GABRA2	addiction	dependence	15274050	A recent effort to fine map that region showed a haplotypic association of alcohol <b>dependence</b> to the gene encoding the GABAA receptor alpha 2 subunit (<strong>GABRA2</strong>).
+GABRA2	drug	alcohol	15274050	There was evidence of association to <b>alcohol</b> dependence for seven adjacent markers spanning 98,000 bp in the middle and 3' portion of the <strong>GABRA2</strong> gene (range of P values = 0.008 0.03).
+GABRA2	addiction	dependence	15274050	There was evidence of association to alcohol <b>dependence</b> for seven adjacent markers spanning 98,000 bp in the middle and 3' portion of the <strong>GABRA2</strong> gene (range of P values = 0.008 0.03).
+GABRA2	drug	alcohol	15274050	These findings replicate and extend recently reported findings, which together underscore the potential contribution of polymorphic variation at the <strong>GABRA2</strong> locus to the risk for <b>alcohol</b> dependence.
+GABRA2	addiction	dependence	15274050	These findings replicate and extend recently reported findings, which together underscore the potential contribution of polymorphic variation at the <strong>GABRA2</strong> locus to the risk for alcohol <b>dependence</b>.
+GABRA2	drug	alcohol	15024690	Variations in <strong>GABRA2</strong>, encoding the alpha 2 subunit of the GABA(A) receptor, are associated with <b>alcohol</b> dependence and with brain oscillations.
+GABRA2	addiction	dependence	15024690	Variations in <strong>GABRA2</strong>, encoding the alpha 2 subunit of the GABA(A) receptor, are associated with alcohol <b>dependence</b> and with brain oscillations.
+GABRA2	drug	alcohol	15024690	Thirty one SNPs in <strong>GABRA2</strong>, but only 1 of the 20 SNPs in the flanking genes, showed significant association with <b>alcoholism</b>.
+GABRA2	drug	alcohol	15024690	The region of strongest association with <b>alcohol</b> dependence extended from intron 3 past the 3' end of <strong>GABRA2</strong>; all 43 of the consecutive three SNP haplotypes in this region of <strong>GABRA2</strong> were highly significant.
+GABRA2	addiction	dependence	15024690	The region of strongest association with alcohol <b>dependence</b> extended from intron 3 past the 3' end of <strong>GABRA2</strong>; all 43 of the consecutive three SNP haplotypes in this region of <strong>GABRA2</strong> were highly significant.
+GABRA2	drug	alcohol	15024690	The very strong association of <strong>GABRA2</strong> with both <b>alcohol</b> dependence and the beta frequency of the electroencephalogram, combined with biological evidence for a role of this gene in both phenotypes, suggest that <strong>GABRA2</strong> might influence susceptibility to <b>alcohol</b> dependence by modulating the level of neural excitation.
+GABRA2	addiction	dependence	15024690	The very strong association of <strong>GABRA2</strong> with both alcohol <b>dependence</b> and the beta frequency of the electroencephalogram, combined with biological evidence for a role of this gene in both phenotypes, suggest that <strong>GABRA2</strong> might influence susceptibility to alcohol <b>dependence</b> by modulating the level of neural excitation.
+CXCR1	drug	amphetamine	32416183	Partial MHC/neuroantigen peptide constructs attenuate <b>methamphetamine</b> seeking and brain chemokine (<strong>C C</strong> motif) ligand 2 levels in rats.
+CXCR1	addiction	relapse	32416183	Partial MHC/neuroantigen peptide constructs attenuate methamphetamine <b>seeking</b> and brain chemokine (<strong>C C</strong> motif) ligand 2 levels in rats.
+CXCR1	addiction	addiction	31773399	Besides, the <strong>C C</strong> haplotype decreases risk of <b>addiction</b>, BP II and MDD.
+CXCR1	addiction	intoxication	31030249	Focus is on the effect of TLR4 signal activation on the balance between pro  and anti inflammatory chemokines [chemokine (<strong>C C</strong> motif) ligand 2 (CCL2)/chemokine (C X3 C motif) ligand 1 (CX3CL1)] and its effect on <b>binge</b> drinking.
+CXCR1	drug	alcohol	29274031	After <b>alcohol</b> exposure, <strong>C C</strong> motif chemokine ligand 4 (CCL4) was significantly increased in female AE pups on PD5 and PD8.
+CXCR1	drug	opioid	29146238	These effects may involve the <strong>C C</strong> chemokine receptor type 5 (CCR5); however, the behavioral contribution of CCR5 on Tat/<b>opioid</b> interactions is not known.
+CXCR1	drug	opioid	28178176	In response to LPS, there was a significant increase in the expression of the pro inflammatory cytokine/chemokine genes interleukin 1 beta (Il 1β), interleukin 6 (Il 6), <strong>C C</strong> motif chemokine ligand 2 (Ccl2), <strong>C C</strong> motif chemokine ligand 7 (Ccl7), C X C motif chemokine ligand 1 (Cxcl1), and C X C motif chemokine ligand 3 (Cxcl3) and a significant decrease in the anti inflammatory NLRP12 gene in both <b>morphine</b> tolerant and placebo control rats compared to saline treated rats, although the changes were greater in the placebo control animals.
+CXCR1	drug	alcohol	28131626	In the present study, we subjected adult male and female rats to different regimens of <b>alcohol</b> vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for tumor necrosis factor alpha (TNFα), interleukin 6 (IL 6), and chemokine (<strong>C C</strong> motif) ligand 2 (CCL2) in reward related brain regions.
+CXCR1	addiction	reward	28131626	In the present study, we subjected adult male and female rats to different regimens of alcohol vapor exposure (acute, subchronic, or chronic) and measured relative mRNA expression for tumor necrosis factor alpha (TNFα), interleukin 6 (IL 6), and chemokine (<strong>C C</strong> motif) ligand 2 (CCL2) in <b>reward</b> related brain regions.
+CXCR1	drug	amphetamine	27967329	The presence of the rs769404 rs701492 (GAD1) <strong>C C</strong> haplotype was associated with <b>METH</b> psychosis.
+CXCR1	drug	alcohol	27747329	For <b>ethanol</b>, the DFT and DFT + vdW results are in contrast, namely, DFT yields a perpendicular orientation of the <strong>C C</strong> bond with respect to the surface, while we obtained a parallel orientation of the <strong>C C</strong> bond using DFT + vdW, which maximizes the adsorption energies.
+CXCR1	drug	nicotine	27429644	The density functional theory calculations conducted using B3LYP correlation function established that the scission of the phenyl <strong>C C</strong> bond in <b>nicotine</b> and β nicotyrine, and C N phenyl bond in 3,5 dimethyl 1 phenylpyrazole were respectively 87.40, 118.24 and 121.38 kcal/mol.
+CXCR1	drug	nicotine	27429644	Clearly, the value of the bond dissociation energy was found to be dependent on the π π interactions which plays a primary role in stabilizing the phenyl <strong>C C</strong> in <b>nicotine</b> and β nicotyrine and the phenyl C N linkages in 3,5 dimethyl 1 phenylpyrazole.
+CXCR1	drug	alcohol	27046089	The infrared active (IR) vibrational mode of <b>ethanol</b> (EtOH) associated with the asymmetrical stretching of the <strong>C C</strong> O bond in pico liter volumes of EtOH water binary mixtures is calorimetrically measured using photothermal microfluidic cantilever deflection spectroscopy (PMCDS).
+CXCR1	drug	amphetamine	25764907	Haplotype analysis of rs16917204 rs16917234 rs2030324 revealed that a major <strong>C C</strong> T haplotype was significantly associated a lower odds of <b>methamphetamine</b> abuse, even after Bonferroni correction.
+CXCR1	drug	cocaine	25762940	The results showed that the concentrations of chemokine (<strong>C C</strong> motif) ligand 2/monocyte chemotactic protein 1 (CCL2/MCP 1) and chemokine (C X C motif) ligand 12/stromal cell derived factor 1 (CXCL12/SDF 1) were only affected by history of <b>cocaine</b> addiction.
+CXCR1	addiction	addiction	25762940	The results showed that the concentrations of chemokine (<strong>C C</strong> motif) ligand 2/monocyte chemotactic protein 1 (CCL2/MCP 1) and chemokine (C X C motif) ligand 12/stromal cell derived factor 1 (CXCL12/SDF 1) were only affected by history of cocaine <b>addiction</b>.
+CXCR1	drug	cocaine	25658879	On the other hand, chemokine <strong>C C</strong> motif ligand 2 and jun proto oncogene expression were unaffected in <b>cocaine</b> abusing subjects dying of gunshot wounds, in contrast to the differential expression previously reported in <b>cocaine</b> related fatalities.
+CXCR1	drug	alcohol	25446642	Effect of repeated <b>alcohol</b> exposure during the third trimester equivalent on messenger RNA levels for interleukin 1β, chemokine (<strong>C C</strong> motif) ligand 2, and interleukin 10 in the developing rat brain after injection of lipopolysaccharide.
+CXCR1	drug	cocaine	24854157	Tumor necrosis factor alpha, chemokine (<strong>C C</strong> motif) ligand 2/monocyte chemotactic protein 1 and chemokine (C X C motif) ligand 12 (CXCL12)/stromal cell derived factor 1 (SDF 1) were decreased in <b>cocaine</b> users, although all cytokines were identified as predictors of a lifetime pathological use of <b>cocaine</b>.
+CXCR1	drug	alcohol	24571103	However, the direct catalytic conversion of synthetic gas to <b>ethanol</b> remains challenging, and no commercial process exists as of today although the research has been ongoing for the past 90 years, since such the process suffers from low yield and poor selectivity due to slow kinetics of the initial <strong>C C</strong> bond formation and fast chain growth of the C2 intermediates.
+CXCR1	drug	alcohol	23701841	<b>Ethanol</b> selectively increased mRNA levels of the chemokine (<strong>C C</strong> motif) ligand 2/monocyte chemotactic protein 1 in the hippocampus and cerebellum, but not in the cortex of aged mice relative to control animals.
+CXCR1	drug	opioid	22564729	Significantly more <strong>C C</strong> <strong>C C</strong> A haplotypes (p=0.0053 after Bonferroni correction) and significantly fewer T C A C A haplotypes (p=0.0003 after Bonferroni correction) were found in <b>heroin</b> dependent subjects.
+CXCR1	drug	opioid	21931991	It is concluded that APD and RS 102895 attenuate <b>morphine</b> withdrawal signs possibly by a NF κB and <strong>C C</strong> chemokine receptor 2 activation pathway linked mechanisms potentially in an interdependent manner.
+CXCR1	addiction	withdrawal	21931991	It is concluded that APD and RS 102895 attenuate morphine <b>withdrawal</b> signs possibly by a NF κB and <strong>C C</strong> chemokine receptor 2 activation pathway linked mechanisms potentially in an interdependent manner.
+CXCR1	drug	cocaine	21487658	This study of 47 treatment seeking <b>cocaine</b> addicts analyzes intertemporal choices of two commodities (equated amounts of <b>cocaine</b> and money), specifically between <b>cocaine</b> now vs. <b>cocaine</b> later (<strong>C C</strong>), money now vs. money later (M M), <b>cocaine</b> now vs. money later (C M), and money now vs. <b>cocaine</b> later (M C).
+CXCR1	addiction	relapse	21487658	This study of 47 treatment <b>seeking</b> cocaine addicts analyzes intertemporal choices of two commodities (equated amounts of cocaine and money), specifically between cocaine now vs. cocaine later (<strong>C C</strong>), money now vs. money later (M M), cocaine now vs. money later (C M), and money now vs. cocaine later (M C).
+CXCR1	drug	cocaine	21487658	<b>Cocaine</b> addicts discounted significantly more in the <strong>C C</strong> condition than in M M (P = 0.032), consistent with previous reports.
+IL2	drug	alcohol	29976100	Objective <b>Alcohol</b> is a hypnotic that modifies immune function, specifically the cytokines interferon gamma (IFN γ) and interleukin 2 (<strong>IL 2</strong>).
+IL2	drug	alcohol	29976100	Objective <b>Alcohol</b> is a hypnotic that modifies immune function, specifically the cytokines interferon gamma (IFN γ) and <strong>interleukin 2</strong> (<strong>IL 2</strong>).
+IL2	drug	alcohol	29976100	We evaluated the association between unscheduled napping and acute <b>alcohol</b> induced augmentation of IFN γ and <strong>IL 2</strong> expression.
+IL2	addiction	intoxication	29976100	The ex vivo IFN γ and <strong>IL 2</strong> levels significantly increased at all time points after <b>binge</b> consumption in the nappers, but not in the non nappers.
+IL2	drug	alcohol	29976100	Conclusion Augmented IFN γ and <strong>IL 2</strong> levels are associated with unscheduled napping after binge <b>alcohol</b> consumption.
+IL2	addiction	intoxication	29976100	Conclusion Augmented IFN γ and <strong>IL 2</strong> levels are associated with unscheduled napping after <b>binge</b> alcohol consumption.
+IL2	drug	alcohol	28951527	<b>Ethanol</b> Stimulates Locomotion via a Gαs Signaling Pathway in <strong>IL2</strong> Neurons in Caenorhabditis elegans.
+IL2	drug	alcohol	28951527	We identify that the requirement for HSF 1 in this phenotype was <strong>IL2</strong> neuron specific and required the downstream expression of the α crystallin ortholog HSP 16.48 Using a combination of pharmacology, optogenetics, and phenotypic analyses we determine that <b>ethanol</b> activates a Gαs cAMP protein kinase A signaling pathway in <strong>IL2</strong> neurons to stimulate nematode locomotion.
+IL2	drug	opioid	28870114	In contrast to <b>morphine</b>, EA stimulation of BCP rats increased splenic concanavalin A (Con A) induced T cell proliferation and plasma <strong>IL 2</strong> content, as well as increased the percentages of splenic CD3+CD4+ and CD3+CD8+ T cell subsets.
+IL2	addiction	withdrawal	28468077	Before and after the 14(th) day of <b>withdrawal</b>, levels of immunoglobulin (IgM, IgA, IgG), T cell subsets (CD(3)(+), CD(4)(+), CD(8)(+), CD(4)(+)/CD(8)(+)) and cytokines (<strong>IL 2</strong>, IFN γ, IL 4, IFN γ/IL 4) were detected.
+IL2	drug	opioid	28468077	Results: Compared with healthy people, immunity function before withdrawal among the <b>opioid</b> abusers showed higher levels of IgM, <strong>IL 2</strong>, IFN γ, IL 4 and lower level of CD(3)(+)T, as (1.67±0.87) g/L, (14.44±13.50)%, (20.23±15.10)%, (1.97±1.59)%, (47.01±13.62)%, respectively, with difference statistically significant (P<0.05).
+IL2	addiction	withdrawal	28468077	Results: Compared with healthy people, immunity function before <b>withdrawal</b> among the opioid abusers showed higher levels of IgM, <strong>IL 2</strong>, IFN γ, IL 4 and lower level of CD(3)(+)T, as (1.67±0.87) g/L, (14.44±13.50)%, (20.23±15.10)%, (1.97±1.59)%, (47.01±13.62)%, respectively, with difference statistically significant (P<0.05).
+IL2	addiction	relapse	28126360	In a longitudinal design we measured plasma levels of the pro inflammatory interleukin 6 (IL 6), the soluble alpha (Tac) subunit of the <strong>interleukin 2</strong> receptor (sIL 2r), and the circulating soluble form of the intercellular adhesion molecule one (sICAM 1), in 79 help <b>seeking</b> UHR individuals (13 25years of age).
+IL2	drug	alcohol	27699959	The results showed that <b>alcohol</b> intoxication increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, <strong>IL 2</strong>, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+IL2	addiction	intoxication	27699959	The results showed that alcohol <b>intoxication</b> increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, <strong>IL 2</strong>, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+IL2	addiction	intoxication	27455577	It was established in experiments on noninbred albino rats that the acute <b>intoxication</b> with methanol (1.0 LD50) decreased cellular and humoral immune responses, Th2 lymphocyte activity (to a greater extent as compared to the function of Th1 cells), reduced the blood concentration of immunoregulatory (IFN g, <strong>IL 2</strong>, IL 4) and proinflammatory (TNF, IL 1b, IL 6) cytokines on the average by 36.5% (p < 0.05), and did not affect the content of anti inflammatory cytokines (IL 10, IL 13).
+IL2	drug	alcohol	27455577	Methanol antidote 4 methylpyrazole (non competitive inhibitor of <b>alcohol</b> dehydrogenase) administered upon acute intoxication with methanol at a dose of 1.0 DL50 partially reduces the intoxication induced suppression of humoral and cellular immune response, activity of T helper cells, and production of IL 4 and restores blood levels of TNF, IL 1b, IFN γ, IL 4, <strong>IL 2</strong>, IL 6 to the control values.
+IL2	addiction	intoxication	27455577	Methanol antidote 4 methylpyrazole (non competitive inhibitor of alcohol dehydrogenase) administered upon acute <b>intoxication</b> with methanol at a dose of 1.0 DL50 partially reduces the <b>intoxication</b> induced suppression of humoral and cellular immune response, activity of T helper cells, and production of IL 4 and restores blood levels of TNF, IL 1b, IFN γ, IL 4, <strong>IL 2</strong>, IL 6 to the control values.
+IL2	drug	amphetamine	26322025	An essential cytokine for T lymphocyte homeostasis, Interleukin 2 (<strong>IL 2</strong>) in serum was prominently reduced in <b>METH</b> exposed infected mice.
+IL2	drug	amphetamine	26322025	An essential cytokine for T lymphocyte homeostasis, <strong>Interleukin 2</strong> (<strong>IL 2</strong>) in serum was prominently reduced in <b>METH</b> exposed infected mice.
+IL2	drug	amphetamine	26322025	In addition, the serum pro inflammatory (TNF, IL12 p70, IL1β, IL 6, and KC GRO) and Th2 (<strong>IL 2</strong>, IL 10, and IL 4) cytokine profiles were also altered in the presence of <b>METH</b>.
+IL2	drug	amphetamine	26302754	We also show by TAAR1 knockdown that the down regulation of <strong>IL 2</strong> in T cells by <b>methamphetamine</b>, which we reported earlier, is indeed regulated by TAAR1.
+IL2	drug	amphetamine	26302754	In summary, the ability of <b>methamphetamine</b> to activate trace TAAR1 in vitro and to regulate important T cell functions, such as cAMP activation and <strong>IL 2</strong> production; the expression of TAAR1 in T lymphocytes in peripheral lymphoid organs, such as lymph nodes; and our in vitro HIV 1 infection model in PBMCs suggests that TAAR1 may play an important role in <b>methamphetamine</b>  mediated immune modulatory responses.
+IL2	addiction	sensitization	24389455	TH1 cytokines (<strong>IL 2</strong>, IFN γ) and TH2 cytokines (IL 4, IL 5) releases from lymph node cell culture were also investigated as contact <b>sensitization</b> endpoints.
+IL2	drug	amphetamine	23460798	Treatment with RTL551 also attenuated the <b>methamphetamine</b> induced increases in hypothalamic interleukin 2 (<strong>IL 2</strong>) levels.
+IL2	drug	amphetamine	23460798	Treatment with RTL551 also attenuated the <b>methamphetamine</b> induced increases in hypothalamic <strong>interleukin 2</strong> (<strong>IL 2</strong>) levels.
+IL2	drug	alcohol	22803049	Experiments of outbred albino rats showed that chronic <b>ethanol</b> intoxication (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1 cells, increased blood corticosterone concentration, reduced T lymphocyte acetylcholinesterase activity, blood concentrations of IFN γ, <strong>IL 2</strong>, IL 4, IL 10, and increased IL 6 level.
+IL2	addiction	intoxication	22803049	Experiments of outbred albino rats showed that chronic ethanol <b>intoxication</b> (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1 cells, increased blood corticosterone concentration, reduced T lymphocyte acetylcholinesterase activity, blood concentrations of IFN γ, <strong>IL 2</strong>, IL 4, IL 10, and increased IL 6 level.
+IL2	drug	alcohol	22634720	We have shown previously that acute <b>alcohol</b>/<b>ethanol</b> (EtOH) intoxication combined with burn injury suppresses mesenteric lymph node (MLN) T cell interleukin 2 (<strong>IL 2</strong>) and interferon γ (IFN γ) production.
+IL2	addiction	intoxication	22634720	We have shown previously that acute alcohol/ethanol (EtOH) <b>intoxication</b> combined with burn injury suppresses mesenteric lymph node (MLN) T cell interleukin 2 (<strong>IL 2</strong>) and interferon γ (IFN γ) production.
+IL2	drug	alcohol	22634720	We have shown previously that acute <b>alcohol</b>/<b>ethanol</b> (EtOH) intoxication combined with burn injury suppresses mesenteric lymph node (MLN) T cell <strong>interleukin 2</strong> (<strong>IL 2</strong>) and interferon γ (IFN γ) production.
+IL2	addiction	intoxication	22634720	We have shown previously that acute alcohol/ethanol (EtOH) <b>intoxication</b> combined with burn injury suppresses mesenteric lymph node (MLN) T cell <strong>interleukin 2</strong> (<strong>IL 2</strong>) and interferon γ (IFN γ) production.
+IL2	drug	opioid	21747891	We found that chronic <b>morphine</b> induced decrease of splenic T lymphocyte proliferation and <strong>IL 2</strong> production can be significantly raised by 2 Hz EA, and the fluctuation of CD4(+)/CD8(+) ratio was also run to the baseline level by the EA.
+IL2	drug	alcohol	21508281	Binge <b>alcohol</b> treatment prior to injury significantly suppressed the increase in serum levels of interleukin (IL) 6, white blood cells, <strong>IL 2</strong>, IL 10, and C reactive protein after the fracture.
+IL2	addiction	intoxication	21508281	<b>Binge</b> alcohol treatment prior to injury significantly suppressed the increase in serum levels of interleukin (IL) 6, white blood cells, <strong>IL 2</strong>, IL 10, and C reactive protein after the fracture.
+IL2	drug	alcohol	21508281	However, <b>alcohol</b> treated animals were found to have increased pulmonary levels of IL 6, IL 1β, <strong>IL 2</strong>, and macrophage inflammatory protein 1α following bilateral femoral fracture.
+IL2	drug	alcohol	21254593	It was established in experiments on noninbred rats that their <b>ethanol</b> intoxication (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, <strong>IL 2</strong>, IL 4, IL 10, increases the concentration of IL 6, suppresses the immune responses, and reduces the interrelation IFNgamma/IL 4 in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes.
+IL2	addiction	intoxication	21254593	It was established in experiments on noninbred rats that their ethanol <b>intoxication</b> (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, <strong>IL 2</strong>, IL 4, IL 10, increases the concentration of IL 6, suppresses the immune responses, and reduces the interrelation IFNgamma/IL 4 in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes.
+IL2	drug	alcohol	19710466	ERK and not p38 pathway is required for IL 12 restoration of T cell <strong>IL 2</strong> and IFN gamma in a rodent model of <b>alcohol</b> intoxication and burn injury.
+IL2	addiction	intoxication	19710466	ERK and not p38 pathway is required for IL 12 restoration of T cell <strong>IL 2</strong> and IFN gamma in a rodent model of alcohol <b>intoxication</b> and burn injury.
+IL2	drug	alcohol	19710466	Previous studies from our laboratory have shown that acute <b>alcohol</b>/<b>ethanol</b> (EtOH) intoxication combined with burn injury suppresses T cell <strong>IL 2</strong> and IFN gamma production by inhibiting p38 and ERK activation.
+IL2	addiction	intoxication	19710466	Previous studies from our laboratory have shown that acute alcohol/ethanol (EtOH) <b>intoxication</b> combined with burn injury suppresses T cell <strong>IL 2</strong> and IFN gamma production by inhibiting p38 and ERK activation.
+IL2	addiction	intoxication	18684924	Furthermore, we show in a model of acute IPA <b>intoxication</b> that animals became immunosuppressed as judged by their reduced ability to release <strong>IL 2</strong> and IFN gamma in the serum in response to staphylococcal enterotoxin B.
+IL2	drug	opioid	18502094	injection of 1mg/kg of naltroxone 48 h after implantation of 75 mg <b>morphine</b> pellets) did not alter blood to brain transport of IL 1alpha or TNF alpha, both the chronic <b>morphine</b> treatment and withdrawal from <b>morphine</b> groups had increased blood to brain transport of <strong>IL 2</strong>.
+IL2	addiction	withdrawal	18502094	injection of 1mg/kg of naltroxone 48 h after implantation of 75 mg morphine pellets) did not alter blood to brain transport of IL 1alpha or TNF alpha, both the chronic morphine treatment and <b>withdrawal</b> from morphine groups had increased blood to brain transport of <strong>IL 2</strong>.
+IL2	drug	opioid	18502094	Whereas IL 1alpha, <strong>IL 2</strong>, and TNF alpha are all proinflammatory cytokines, <b>morphine</b> exposure has individualized effects on their blood to brain transport.
+IL2	drug	opioid	18294814	An altered Th1/Th2 balance, characterized by reduced IL 4, IFN gamma and TNF alpha but normal <strong>IL 2</strong> levels, was present in untreated <b>heroin</b> addicted subjects, while the Th1/Th2 balance was well conserved in the <b>methadone</b> and <b>buprenorphine</b> groups.
+IL2	drug	opioid	17974159	The in vitro presence of <b>naloxone</b> induced further inhibition of the PHA proliferative response and <strong>IL 2</strong> production.
+IL2	drug	amphetamine	16720325	Drug abuse may alter the change from the (CD4+)CD45RA+ to the (CD4+)CD45RA  phenotype selectively, which recovers in HIV 1+ <b>methamphetamine</b> abusers during treatment from baseline to 4 weeks, as manifested by improved <strong>IL 2</strong> production in vitro.
+IL2	drug	opioid	15729143	Suppression of <b>morphine</b> withdrawal syndrome by <strong>interleukin 2</strong> and its gene.
+IL2	addiction	withdrawal	15729143	Suppression of morphine <b>withdrawal</b> syndrome by <strong>interleukin 2</strong> and its gene.
+IL2	drug	opioid	15729143	The <b>naloxone</b> precipitated withdrawal syndrome in mice and rats after intrathecal injection of recombinant human <strong>interleukin 2</strong> protein (rIL 2) or its gene was studied.
+IL2	addiction	withdrawal	15729143	The naloxone precipitated <b>withdrawal</b> syndrome in mice and rats after intrathecal injection of recombinant human <strong>interleukin 2</strong> protein (rIL 2) or its gene was studied.
+IL2	drug	opioid	15729143	Furthermore, pcDNA3 <strong>IL 2</strong> (8 microg DNA) had a similar effect as 1x10 IU rIL 2 protein on inhibition of <b>morphine</b> withdrawal syndrome in mice, and the expression of rIL 2 protein in spinal cord could be detected for 6 days.
+IL2	addiction	withdrawal	15729143	Furthermore, pcDNA3 <strong>IL 2</strong> (8 microg DNA) had a similar effect as 1x10 IU rIL 2 protein on inhibition of morphine <b>withdrawal</b> syndrome in mice, and the expression of rIL 2 protein in spinal cord could be detected for 6 days.
+IL2	addiction	intoxication	15718389	Two days after injury, a significant increase in blood Cort levels and suppression of MLN T cell proliferation and <strong>IL 2</strong> production was observed in rats receiving combined insult of EtOH <b>intoxication</b> and burn injury compared with rats receiving EtOH <b>intoxication</b> or burn injury alone.
+IL2	drug	opioid	15055740	Similarly, production of <strong>IL 2</strong>, IL 10 and IFNgamma was higher in the group of <b>heroin</b> addicts than in healthy controls.
+IL2	drug	opioid	14741432	We had previously shown that chronic <b>morphine</b> treatment in vivo and in vitro decreases <strong>IL 2</strong> and IFNgamma (Th1) protein levels and increases IL 4 and IL 5 (Th2) protein levels in a time dependent manner.
+IL2	drug	opioid	14741432	In addition in this paper, we show that chronic <b>morphine</b> treatment resulted in a decrease in IFNgamma and <strong>IL 2</strong> mRNA and an increase in IL 4 and IL 5 mRNA accumulation in murine splenocytes.
+IL2	drug	cannabinoid	12668119	<b>Cannabinol</b> (CBN) or Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>; 50 mg/kg, ip), administered daily for 3 consecutive days before sensitization and then before challenge, significantly attenuated the elevation of <strong>IL 2</strong>, IL 4, IL 5, and IL 13 steady state mRNA expression elicited by Ova challenge in the lungs.
+IL2	addiction	sensitization	12668119	Cannabinol (CBN) or Delta(9) tetrahydrocannabinol (Delta(9) THC; 50 mg/kg, ip), administered daily for 3 consecutive days before <b>sensitization</b> and then before challenge, significantly attenuated the elevation of <strong>IL 2</strong>, IL 4, IL 5, and IL 13 steady state mRNA expression elicited by Ova challenge in the lungs.
+IL2	drug	alcohol	12488491	The enriched T cells of chronic <b>ethanol</b> mice secreted more IFN gamma and IL 4 than controls and equivalent <strong>IL 2</strong> at early times after stimulation (6 24 h).
+IL2	drug	opioid	12421473	<strong>Interleukin 2</strong> induced antinociception in <b>morphine</b> insensitive rats.
+IL2	drug	opioid	12421473	To investigate <strong>interleukin 2</strong> induced antinociception in <b>morphine</b> insensitive rats.
+IL2	drug	opioid	12421473	PWL was also markedly increased by <strong>IL 2</strong> in 45 d post complete Freund's adjuvant (CFA) treated rats, which have been proven <b>morphine</b> insensitive.
+IL2	drug	opioid	12421473	<strong>IL 2</strong> induced antinociception was partially blocked by <b>naloxone</b> (1 mg/kg, ip) in normal rats but remained unchanged in CFA group.
+IL2	drug	opioid	12421473	<strong>IL 2</strong> induced antinociception is partially mediated by mu <b>opioid</b> receptors.
+IL2	drug	opioid	12421473	Therapeutic applications of <strong>IL 2</strong> may also be expanded to relieve <b>morphine</b> insensitive pain.
+IL2	drug	opioid	12044458	The antinociceptive effect of pcDNA3 <strong>IL 2</strong> could be blocked by <b>naloxone</b>, showing some relationship of the antinociceptive effect produced by <strong>IL 2</strong> gene to the <b>opioid</b> receptors.
+IL2	drug	alcohol	11728854	Carbohydrate deficient transferrin, monoamine oxidase B, soluble <strong>interleukin 2</strong> receptor and cholesterol have been proposed as markers of suicidal risk in <b>alcohol</b> dependent patients, although nonspecific and with low predictive value.
+IL2	addiction	withdrawal	11021983	Inhibition of nociceptive <b>withdrawal</b> reflex by microinjection of <strong>interleukin 2</strong> into rat locus coeruleus.
+IL2	drug	opioid	11021983	The results clearly show that <strong>IL 2</strong> receptors present in LC mediate descending inhibition of the spinal nociception, which may couple with the activation of <b>opioid</b> receptors on LC neurons.
+IL2	drug	opioid	10936512	In this study, it was shown that injection of an equianalgesic dose of <b>buprenorphine</b> (related to <b>morphine</b>) into the ventral caudal PAG did not alter splenic NK cell, T cell, and macrophage functions, whereas <b>morphine</b> significantly (p<0.001) suppressed splenic NK cell cytotoxic activity (14 50% reduction), splenic and thymic T cell proliferation to concanavalin A (Con A, 43 76% reduction), antiTCR (T cell receptor) (85% reduction) and <strong>IL 2</strong> (36 48% reduction), and macrophage functions including nitric oxide (36 41% reduction) and TNF alpha production (26%), and phagocytosis of Candida albicans (39%).
+IL2	drug	alcohol	10798594	This study compared NK activity, interleukin (IL) 2 stimulated NK activity, and concanavalin A stimulated peripheral blood mononuclear cell production of Th1 (IL 12 and <strong>IL 2</strong>), Th2 (IL 10), and proinflammatory (IL 6) cytokines in 31 hospitalized chronic <b>alcoholic</b> patients and 31 age matched controls who were stratified on the basis of ethnicity.
+IL2	drug	alcohol	10798594	NK cell responses were significantly different across the four groups, and African American <b>alcoholics</b> showed the lowest levels of NK activity (F = 9.5;p < 0.001) and <strong>IL 2</strong> stimulated NK activity (F = 2.9; p < 0.05).
+IL2	drug	opioid	26735445	drug use on CD4 lymphocyte count and serum levels of beta2  microglobulin (beta2 m) and soluble <strong>interleukin 2</strong> receptor (sIL 2R) were prospectively investigated in 41 HIV positive drug users enrolled in a <b>methadone</b> treatment programme.
+IL2	drug	cannabinoid	8807671	The production of the cytokine <strong>interleukin 2</strong> by T helper cells was markedly suppressed in both tolerant and abstinent mice, whereas the production of interleukin 4 was significantly suppressed only in <b>THC</b> abstinent mice.
+IL2	drug	alcohol	7496798	Morphine tolerance and abstinence were associated with suppression of <strong>IL 2</strong> production, which was completely blocked by <b>naltrexone</b>.
+IL2	drug	opioid	7496798	<b>Morphine</b> tolerance and abstinence were associated with suppression of <strong>IL 2</strong> production, which was completely blocked by naltrexone.
+IL2	drug	opioid	7713351	Production of <strong>IL 2</strong> was suppressed by 0.1 100 microM of <b>heroin</b>, whereas exposure to <b>methadone</b> appeared to result in a generalized modulation, with suppression of <strong>IL 2</strong> at most concentrations.
+IL2	drug	opioid	8032870	<b>Morphine</b> tolerance was associated with suppressed B cell proliferation following in vitro stimulation, as well as interleukin 2 (<strong>IL 2</strong>) and interleukin 4 production by T cells.
+IL2	drug	opioid	8032870	<b>Morphine</b> tolerance was associated with suppressed B cell proliferation following in vitro stimulation, as well as <strong>interleukin 2</strong> (<strong>IL 2</strong>) and interleukin 4 production by T cells.
+IL2	drug	opioid	8032870	NK cell activity was significantly reduced in <b>morphine</b> tolerant, but not in <b>morphine</b> abstinent, mice following a 24 h incubation in the presence or absence of <strong>IL 2</strong>.
+IL2	drug	opioid	7880626	Acute <b>morphine</b> intoxication during high dose recombinant <strong>interleukin 2</strong> treatment for metastatic renal cell cancer.
+IL2	addiction	intoxication	7880626	Acute morphine <b>intoxication</b> during high dose recombinant <strong>interleukin 2</strong> treatment for metastatic renal cell cancer.
+IL2	drug	opioid	7684680	To assess the degree of immune system activation associated with addiction or hepatotropic viruses infection, we examined 60 HIV negative <b>heroin</b> addicts for the presence of hepatitis B virus (HBV) infection markers, hepatitis C virus antibodies (anti HCV), various auto antibodies, and serum levels of soluble <strong>interleukin 2</strong> receptors (sIL 2R).
+IL2	addiction	addiction	7684680	To assess the degree of immune system activation associated with <b>addiction</b> or hepatotropic viruses infection, we examined 60 HIV negative heroin addicts for the presence of hepatitis B virus (HBV) infection markers, hepatitis C virus antibodies (anti HCV), various auto antibodies, and serum levels of soluble <strong>interleukin 2</strong> receptors (sIL 2R).
+IL2	drug	amphetamine	2819708	The antitumor efficacy, as well as the toxicity, of polyethylene glycol interleukin 2 (PEG <strong>IL 2</strong>) was compared to that of rhIL 2 in three transplantable syngeneic murine tumor models, <b>Meth</b> A fibrosarcoma, B16 melanoma, and Pan 02 pancreatic carcinoma.
+IL2	drug	amphetamine	2819708	The antitumor efficacy, as well as the toxicity, of polyethylene glycol <strong>interleukin 2</strong> (PEG <strong>IL 2</strong>) was compared to that of rhIL 2 in three transplantable syngeneic murine tumor models, <b>Meth</b> A fibrosarcoma, B16 melanoma, and Pan 02 pancreatic carcinoma.
+IL2	drug	amphetamine	2819708	This efficacy of PEG <strong>IL 2</strong> was dose dependent and was greatest on a Q7D x 2 schedule in <b>Meth</b> A and B16.
+IL2	drug	alcohol	2679202	This defect is not caused by the direct effects of <b>ethanol</b> on the cells and probably is not caused by an inability of the cells from <b>ethanol</b> treated animals to produce the lymphocyte growth factor <strong>interleukin 2</strong>.
+IL2	addiction	dependence	2783463	Sequence <b>dependence</b> of administration of human recombinant tumor necrosis factor and <strong>interleukin 2</strong> in murine tumor therapy.
+DRD1	drug	alcohol	32032698	Our results revealed four distinct <b>ethanol</b> preference phenotypes (Light, Heavy, Negative Reinforcement, and Inflexible), each showing different transcriptional regulation patterns of the <strong>drd1</strong>, drd2, grin1a, gria2a, and gabbr1b receptors.
+DRD1	addiction	reward	32032698	Our results revealed four distinct ethanol preference phenotypes (Light, Heavy, Negative <b>Reinforcement</b>, and Inflexible), each showing different transcriptional regulation patterns of the <strong>drd1</strong>, drd2, grin1a, gria2a, and gabbr1b receptors.
+DRD1	drug	psychedelics	31749223	Pretreatment with SCH23390 (SCH), Haloperidol (HAL), and ketanserin (KS), antagonists of dopamine D1 (<strong>DRD1</strong>), dopamine D2 (DRD2), and serotonin 2A (5 HT2A receptor) receptors, respectively, was utilized during a CPP test to investigate the involvement of the dopaminergic and serotonergic systems in 25B <b>NBOMe</b> mediated effects.
+DRD1	addiction	reward	31749223	Pretreatment with SCH23390 (SCH), Haloperidol (HAL), and ketanserin (KS), antagonists of dopamine D1 (<strong>DRD1</strong>), dopamine D2 (DRD2), and serotonin 2A (5 HT2A receptor) receptors, respectively, was utilized during a <b>CPP</b> test to investigate the involvement of the dopaminergic and serotonergic systems in 25B NBOMe mediated effects.
+DRD1	drug	psychedelics	31749223	Moreover, 25B <b>NBOMe</b> altered the <strong>DRD1</strong> , DRD2 , and dopamine transporter expression and increased dopamine levels.
+DRD1	addiction	aversion	31462765	The classical view on the field postulates that NAc <strong>dopamine receptor D1</strong> expressing medium spiny neurons (D1 MSNs) convey reward signals, while dopamine receptor D2 expressing MSNs (D2 MSNs) encode <b>aversion</b>.
+DRD1	addiction	reward	31462765	The classical view on the field postulates that NAc <strong>dopamine receptor D1</strong> expressing medium spiny neurons (D1 MSNs) convey <b>reward</b> signals, while dopamine receptor D2 expressing MSNs (D2 MSNs) encode aversion.
+DRD1	addiction	relapse	31422417	Next, we determined the effect of pharmacological inactivation of NAc core and shell by either GABAA and GABAB agonists (muscimol + baclofen, 50 + 50 ng/side), <strong>Drd1</strong> Drd2 antagonist (flupenthixol, 10 µg/side), or the selective <strong>Drd1</strong> or Drd2 antagonists (SCH39166, 1.0 µg/side or raclopride, 1.0 µg/side) during the <b>relapse</b> tests.
+DRD1	drug	amphetamine	31422417	Incubated <b>methamphetamine</b> seeking after voluntary abstinence was associated with a selective increase of Fos expression in the NAc core, but not shell, and Fos was colabeled with both <strong>Drd1</strong>  and Drd2 MSNs.
+DRD1	addiction	relapse	31422417	Incubated methamphetamine <b>seeking</b> after voluntary abstinence was associated with a selective increase of Fos expression in the NAc core, but not shell, and Fos was colabeled with both <strong>Drd1</strong>  and Drd2 MSNs.
+DRD1	drug	amphetamine	31422417	Together, our results suggest that dopamine transmission through <strong>Drd1</strong> and Drd2 in NAc core is critical to the incubation of <b>methamphetamine</b> craving after voluntary abstinence.
+DRD1	addiction	relapse	31422417	Together, our results suggest that dopamine transmission through <strong>Drd1</strong> and Drd2 in NAc core is critical to the incubation of methamphetamine <b>craving</b> after voluntary abstinence.
+DRD1	drug	opioid	31192519	<b>Heroin</b> delay discounting and impulsivity: Modulation by <strong>DRD1</strong> genetic variation.
+DRD1	addiction	addiction	31192519	Dopamine D1 receptors (encoded by <strong>DRD1</strong>) are implicated in drug <b>addiction</b> and high risk behaviors.
+DRD1	drug	opioid	31192519	<strong>DRD1</strong> variants have been linked with increased DD (in healthy volunteers) and <b>opioid</b> abuse.
+DRD1	drug	opioid	31192519	Substance use, DD, and genotype data (<strong>DRD1</strong> rs686 and rs5326, DRD3 rs6280, COMT rs4680) were obtained from 106 current <b>heroin</b> users.
+DRD1	drug	opioid	31192519	<strong>DRD1</strong> rs686 (A/A, n = 25; G/A, n = 56; G/G, n = 25) was linearly related to the difference in <b>heroin</b> DD (area under the curve; AUC) between the <b>heroin</b> satiation and withdrawal conditions; specifically, G/G homozygotes had a significantly smaller (satiation minus withdrawal) AUC difference score had higher drug use impulsivity questionnaire scores, relative to A/A homozygotes, with G/A intermediate.
+DRD1	addiction	withdrawal	31192519	<strong>DRD1</strong> rs686 (A/A, n = 25; G/A, n = 56; G/G, n = 25) was linearly related to the difference in heroin DD (area under the curve; AUC) between the heroin satiation and <b>withdrawal</b> conditions; specifically, G/G homozygotes had a significantly smaller (satiation minus <b>withdrawal</b>) AUC difference score had higher drug use impulsivity questionnaire scores, relative to A/A homozygotes, with G/A intermediate.
+DRD1	drug	opioid	31192519	<strong>DRD1</strong> rs686 modulated the difference in <b>heroin</b> DD score between pharmacological states and was associated with drug use impulsivity.
+DRD1	drug	opioid	31192519	These data support a role of <strong>DRD1</strong> in <b>opioid</b> DD and impulsive behaviors.
+DRD1	drug	cocaine	30952156	Dopamine receptor D1 (<strong>DRD1</strong>) expression was also significantly reduced in the orbitofrontal cortex of high <b>cocaine</b> escalating rats.
+DRD1	drug	cocaine	30952156	<strong>Dopamine receptor D1</strong> (<strong>DRD1</strong>) expression was also significantly reduced in the orbitofrontal cortex of high <b>cocaine</b> escalating rats.
+DRD1	drug	alcohol	30516420	The result obtained with this model point out that the relation among high fat diet consumption and <b>alcohol</b> intake appears to depend on the presence or absence of the diet when <b>alcohol</b> intake is evaluated, and that an imbalance in the mesocorticolimbic dopaminergic pathway, observed by the transcriptional regulation of the dopamine receptors (<strong>Drd1</strong>/Drd2) and GABAB receptors subunit (Gabbr1/Gabbr2), can be driving the <b>alcohol</b> intake.
+DRD1	drug	opioid	30268777	The mRNA and protein level of <strong>DRD1</strong> increased in the VTA, NAC and amygdala of <b>opioid</b> abusers.
+DRD1	drug	cocaine	30210305	When investigating if the reduced level of glutamate co release from DA neurons caused a detectable post synaptic effect on MSNs, patch clamp analysis identified an enhanced baseline AMPA/NMDA ratio in DA receptor subtype 1 (<strong>DRD1</strong>) expressing accumbal MSNs which occluded the effect of <b>cocaine</b> on synaptic transmission.
+DRD1	drug	amphetamine	30056065	Whole cell patch clamp in transgenic BAC <strong>Drd1a</strong> tdTomato mice showed that <b>METH</b>, but not modafinil, induced paired pulse facilitation of EPSCs, suggesting reduced presynaptic probability of glutamate release onto layer V pyramidal neurons.
+DRD1	drug	amphetamine	30056065	Analysis of histone 3/4 enrichment at specific promoters revealed: i) distinct effects of the drugs on histone 3 acetylation, with modafinil increasing H3ac at <strong>Drd1</strong> and Adra1b promoters, but <b>METH</b> increasing H3ac at Adra1a; ii) distinct effects on histone 4 acetylation enrichment, with modafinil increasing H4ac at the Drd2 promoter and decreasing it at Hrh1, but <b>METH</b> increasing H4ac at <strong>Drd1</strong>; iii) comparable effects of both psychostimulants, increasing H3ac at Drd2, Hcrtr1, and Hrh1 promoters, decreasing H3ac at Hrh3, increasing H4ac at Hcrtr1, and decreasing H4ac at Hcrtr2, Hrh3, and Grin1 promoters.
+DRD1	drug	amphetamine	30056065	Interestingly, only <b>METH</b> altered mRNA levels of genes with altered histone acetylation status, inducing increased expression of <strong>Drd1a</strong>, Adra1a, Hcrtr1, and Hrh1, and decreasing Grin1.
+DRD1	addiction	reward	29909784	The results demonstrated a regional specificity with which the functional polymorphism rs686 of the D1 dopamine receptor (<strong>DRD1</strong>) gene and Taq1A of the ANKK1 gene influenced medial and lateral OFC activation during <b>reward</b> anticipation, respectively.
+DRD1	drug	alcohol	29909784	Importantly, our path model revealed a significant indirect relationship between the rs686 of the <strong>DRD1</strong> gene and early onset of <b>alcohol</b> misuse through a medial OFC × VS interaction.
+DRD1	addiction	relapse	29656870	Here, we show that contextual control over <b>relapse</b> and abstinence is embedded within distinct output circuits of dopamine 1 receptor (<strong>Drd1</strong>) expressing AcbSh neurons.
+DRD1	drug	alcohol	29656870	We report anatomical and functional segregation of <strong>Drd1</strong> AcbSh output pathways during context induced reinstatement and extinction of <b>alcohol</b> seeking.
+DRD1	addiction	relapse	29656870	We report anatomical and functional segregation of <strong>Drd1</strong> AcbSh output pathways during context induced <b>reinstatement</b> and extinction of alcohol <b>seeking</b>.
+DRD1	drug	alcohol	29568676	Furthermore, voluntary <b>ethanol</b> consumption attenuated stress response and modified expression of reward system genes: enhancing <strong>Drd1</strong> and Drd2, and reducing Gabbr2 in the striatum.
+DRD1	addiction	reward	29568676	Furthermore, voluntary ethanol consumption attenuated stress response and modified expression of <b>reward</b> system genes: enhancing <strong>Drd1</strong> and Drd2, and reducing Gabbr2 in the striatum.
+DRD1	drug	alcohol	29383684	A downregulation of <strong>DRD1</strong> but not DRD2 expression was seen in <b>alcoholics</b>.
+DRD1	drug	alcohol	29383684	Dysregulation of DYN/KOR system and dopamine signaling through both alterations in co expression patterns of opioid genes and decreased <strong>DRD1</strong> gene expression may contribute to imbalance in the activity of D1  and D2 containing pathways which may lead to the negative affective state in human <b>alcoholics</b>.
+DRD1	drug	opioid	29383684	Dysregulation of DYN/KOR system and dopamine signaling through both alterations in co expression patterns of <b>opioid</b> genes and decreased <strong>DRD1</strong> gene expression may contribute to imbalance in the activity of D1  and D2 containing pathways which may lead to the negative affective state in human alcoholics.
+DRD1	drug	amphetamine	29247759	<b>METH</b> treated mice also showed i) decreased levels of total H3ac and H4ac, and increased levels of 5 mC, ii) decreased H3ac enrichment at promoters of Drd2, Hcrtr1/2, Hrh1 and Grin1, and increased H4ac enrichment at <strong>Drd1</strong>, Hrh1 and Grin1, iii) increased mRNA of Drd1a, Grin1 and Gria1.
+DRD1	drug	amphetamine	29247759	<b>METH</b> treated mice also showed i) decreased levels of total H3ac and H4ac, and increased levels of 5 mC, ii) decreased H3ac enrichment at promoters of Drd2, Hcrtr1/2, Hrh1 and Grin1, and increased H4ac enrichment at <strong>Drd1</strong>, Hrh1 and Grin1, iii) increased mRNA of <strong>Drd1a</strong>, Grin1 and Gria1.
+DRD1	addiction	reward	29093669	Gene expression analysis after <b>CPP</b> test revealed specific up regulation in the CAF COC group of <strong>Drd1a</strong>, cFos, and FosB in the NAc, and cFos, Egr1, and Npas4 in the mPFC.
+DRD1	drug	cocaine	28535798	Selective knockout of Kalirin in dopamine transporter expressing neurons produced a transient enhancement of <b>cocaine</b> induced locomotion, while knockout of Kalirin in <strong>Drd1a</strong>  or Drd2 dopamine receptor expressing neurons was without effect.
+DRD1	drug	alcohol	28524260	Interestingly, the glycine evoked currents in dissociated <strong>DRD1</strong> positive MSNs were potentiated by <b>ethanol</b>.
+DRD1	drug	alcohol	28524260	Also, the potentiation of the GlyR mediated tonic current by <b>ethanol</b> suggests that they modulate the excitability of <strong>DRD1</strong> positive MSNs in nAc.
+DRD1	drug	amphetamine	28123032	Between tests, the rats underwent voluntary abstinence (using a discrete choice procedure between <b>methamphetamine</b> and food; 20 trials/d) for 19 d. We used in situ hybridization to measure the colabeling of the activity marker Fos with <strong>Drd1</strong> and Drd2 in DMS and DLS after the tests.
+DRD1	drug	amphetamine	28123032	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both <strong>Drd1</strong> and Drd2 DMS injections of SCH39166 or raclopride selectively decreased <b>methamphetamine</b> seeking after 21 abstinence days.
+DRD1	addiction	relapse	28123032	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both <strong>Drd1</strong> and Drd2 DMS injections of SCH39166 or raclopride selectively decreased methamphetamine <b>seeking</b> after 21 abstinence days.
+DRD1	drug	cocaine	27939396	In addition, the PGC 1α promoter has binding sites for early growth response 3 (Egr3), which plays a dynamic role in <b>cocaine</b> action in nucleus accumbens (NAc) medium spiny neuron (MSN) subtypes, those enriched in <strong>dopamine receptor D1</strong> (D1 MSN) versus D2 (D2 MSN).
+DRD1	drug	nicotine	27428758	<b>Nicotine</b> intake is correlated negatively with Chrnb2, Chrna7 and positively with <strong>Drd1</strong> expression.
+DRD1	drug	alcohol	26609150	Using various inducible and site specific transgenic mouse models and pharmacological validation experiments, we show that critical subunits of NMDARs and AMPARs expressed either in dopamine neurons or in <strong>dopamine receptor D1</strong> containing neurons play an important role in the <b>alcohol</b> deprivation effect (the increase in <b>alcohol</b> intake after a period of abstinence) while having no impact on context  plus cue induced reinstatement of <b>alcohol</b> seeking responses.
+DRD1	addiction	relapse	26609150	Using various inducible and site specific transgenic mouse models and pharmacological validation experiments, we show that critical subunits of NMDARs and AMPARs expressed either in dopamine neurons or in <strong>dopamine receptor D1</strong> containing neurons play an important role in the alcohol deprivation effect (the increase in alcohol intake after a period of abstinence) while having no impact on context  plus cue induced <b>reinstatement</b> of alcohol <b>seeking</b> responses.
+DRD1	drug	cocaine	26059306	In particular, p11 in the ChAT+ cells or <strong>DRD1</strong>+ MSN of the NAc, controls depressive like behavior or <b>cocaine</b> reward, respectively.
+DRD1	addiction	reward	26059306	In particular, p11 in the ChAT+ cells or <strong>DRD1</strong>+ MSN of the NAc, controls depressive like behavior or cocaine <b>reward</b>, respectively.
+DRD1	drug	opioid	25966176	Single nucleotide polymorphisms in <strong>dopamine receptor D1</strong> are associated with <b>heroin</b> dependence but not impulsive behavior.
+DRD1	addiction	dependence	25966176	Single nucleotide polymorphisms in <strong>dopamine receptor D1</strong> are associated with heroin <b>dependence</b> but not impulsive behavior.
+DRD1	drug	opioid	25966176	In this study, we examined whether dopamine receptor D1 (<strong>DRD1</strong>) is associated with <b>heroin</b> dependence and the impulsive behavior in patients with <b>heroin</b> dependence.
+DRD1	addiction	dependence	25966176	In this study, we examined whether dopamine receptor D1 (<strong>DRD1</strong>) is associated with heroin <b>dependence</b> and the impulsive behavior in patients with heroin <b>dependence</b>.
+DRD1	drug	opioid	25966176	In this study, we examined whether <strong>dopamine receptor D1</strong> (<strong>DRD1</strong>) is associated with <b>heroin</b> dependence and the impulsive behavior in patients with <b>heroin</b> dependence.
+DRD1	addiction	dependence	25966176	In this study, we examined whether <strong>dopamine receptor D1</strong> (<strong>DRD1</strong>) is associated with heroin <b>dependence</b> and the impulsive behavior in patients with heroin <b>dependence</b>.
+DRD1	drug	opioid	25966176	We examined the potential association between <b>heroin</b> dependence and 8 single nucleotide polymorphisms (rs686, rs4867798, rs1799914, rs4532, rs5326, rs265981, rs10078714, rs10078866) of <strong>DRD1</strong>, and the associations between single single nucleotide polymorphism, haplotypes, and impulsive behavior.
+DRD1	addiction	dependence	25966176	We examined the potential association between heroin <b>dependence</b> and 8 single nucleotide polymorphisms (rs686, rs4867798, rs1799914, rs4532, rs5326, rs265981, rs10078714, rs10078866) of <strong>DRD1</strong>, and the associations between single single nucleotide polymorphism, haplotypes, and impulsive behavior.
+DRD1	drug	opioid	25966176	These findings indicate that <strong>DRD1</strong> gene polymorphisms are related to <b>heroin</b> dependence in a Chinese Han population and may be informative for future genetic or biological studies on <b>heroin</b> dependence.
+DRD1	addiction	dependence	25966176	These findings indicate that <strong>DRD1</strong> gene polymorphisms are related to heroin <b>dependence</b> in a Chinese Han population and may be informative for future genetic or biological studies on heroin <b>dependence</b>.
+DRD1	drug	nicotine	25907750	In adolescent and adult male rats, we examined (1) alterations occurring in dopamine receptor related mRNAs (<strong>DRD1</strong>, DRD2, DRD3 and D3nf) at two time points during a sensitizing regimen of <b>nicotine</b> and (2) whether DRD3 antagonism either during the initial treatment (induction) or at a later challenge exposure (expression) is able to block <b>nicotine</b> sensitization.
+DRD1	addiction	sensitization	25907750	In adolescent and adult male rats, we examined (1) alterations occurring in dopamine receptor related mRNAs (<strong>DRD1</strong>, DRD2, DRD3 and D3nf) at two time points during a sensitizing regimen of nicotine and (2) whether DRD3 antagonism either during the initial treatment (induction) or at a later challenge exposure (expression) is able to block nicotine <b>sensitization</b>.
+DRD1	drug	nicotine	25907750	Adolescents and adults showed opposite <strong>DRD1</strong> mRNA responses to <b>nicotine</b> treatment, while no age  and <b>nicotine</b> related changes in DRD2 mRNA were observed.
+DRD1	drug	nicotine	25907750	These data reveal important age dependent regulation of <strong>DRD1</strong>  and DRD3 related mRNAs during the course of <b>nicotine</b> exposure.
+DRD1	drug	cocaine	25900179	Using preadolescent <strong>drd1a</strong> EGFP mice and a binge <b>cocaine</b> treatment protocol we demonstrate that the D1 receptor is post transcriptionally regulated in the caudate putamen of <b>cocaine</b> sensitized animal.
+DRD1	addiction	intoxication	25900179	Using preadolescent <strong>drd1a</strong> EGFP mice and a <b>binge</b> cocaine treatment protocol we demonstrate that the D1 receptor is post transcriptionally regulated in the caudate putamen of cocaine sensitized animal.
+DRD1	addiction	withdrawal	25762751	During <b>withdrawal</b>, intact females displayed an increase in anxiety like behavior in both tests and CRF, UCN, and <strong>Drd1</strong> gene expression.
+DRD1	drug	opioid	25729949	<strong>Dopamine receptor D1</strong> but not D3 essential for <b>morphine</b> induced conditioned responses.
+DRD1	drug	opioid	25729949	The <strong>dopamine receptor D1</strong> but not the D3 is also critical for <b>morphine</b> induced BDNF expression in the NAc and PFC.
+DRD1	drug	alcohol	25660313	Meta analysis of six genes (BDNF, <strong>DRD1</strong>, DRD3, DRD4, GRIN2B and MAOA) involved in neuroplasticity and the risk for <b>alcohol</b> dependence.
+DRD1	addiction	dependence	25660313	Meta analysis of six genes (BDNF, <strong>DRD1</strong>, DRD3, DRD4, GRIN2B and MAOA) involved in neuroplasticity and the risk for alcohol <b>dependence</b>.
+DRD1	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, <strong>Drd1a</strong>, Gria1, and Pdyn.
+DRD1	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, <strong>Drd1a</strong>, Gria1, and Pdyn.
+DRD1	drug	cocaine	25319571	Confirming our previous results, <b>cocaine</b> withdrawal selectively impaired DHPG LTD in NAc shell <strong>Drd1</strong> expressing direct and Drd2 expressing indirect pathway MSNs.
+DRD1	addiction	withdrawal	25319571	Confirming our previous results, cocaine <b>withdrawal</b> selectively impaired DHPG LTD in NAc shell <strong>Drd1</strong> expressing direct and Drd2 expressing indirect pathway MSNs.
+DRD1	drug	alcohol	25003712	In this study, we used whole cell ex vivo slice electrophysiology in <strong>Drd1</strong> eGFP mice to investigate cell type specific alterations in NAc synaptic plasticity following <b>ethanol</b> exposure.
+DRD1	drug	cocaine	24966820	To test the cell specificity of this hypothesis we examined the effects of a dominant negative CREB protein variant expressed in <strong>dopamine receptor D1</strong> (D1R) neurons on <b>cocaine</b> induced behaviors.
+DRD1	drug	nicotine	24927283	The aims of this study were to analyze associations of dopamine receptor genes (<strong>DRD1</strong> 5) with Major Depressive Disorder (MDD) and <b>nicotine</b> dependence (ND), and to investigate whether ND moderates genetic influences on MDD.
+DRD1	addiction	dependence	24927283	The aims of this study were to analyze associations of dopamine receptor genes (<strong>DRD1</strong> 5) with Major Depressive Disorder (MDD) and nicotine <b>dependence</b> (ND), and to investigate whether ND moderates genetic influences on MDD.
+DRD1	drug	opioid	24561386	Using optogenetics we demonstrate that activation of Channelrhodopsin2 in Rgs9 2 expressing neurons, or in D1 dopamine receptor (<strong>Drd1</strong>) enriched medium spiny neurons, accelerates the development of <b>morphine</b> tolerance, whereas activation of D2 dopamine receptor (Drd2) enriched neurons does not significantly affect the development of tolerance.
+DRD1	drug	cocaine	24527678	Topiramate and <b>cocaine</b> co administration caused an up regulation of dopamine (<strong>Drd1</strong>, Th) and opioid (Oprm1) receptor genes.
+DRD1	drug	opioid	24527678	Topiramate and cocaine co administration caused an up regulation of dopamine (<strong>Drd1</strong>, Th) and <b>opioid</b> (Oprm1) receptor genes.
+DRD1	drug	opioid	24269875	L stepholidine, a natural <strong>dopamine receptor D1</strong> agonist and D2 antagonist, inhibits <b>heroin</b> induced reinstatement.
+DRD1	addiction	relapse	24269875	L stepholidine, a natural <strong>dopamine receptor D1</strong> agonist and D2 antagonist, inhibits heroin induced <b>reinstatement</b>.
+DRD1	drug	alcohol	24135011	Statistically significant associations of polymorphisms in <strong>DRD1</strong> and DRD4 with <b>alcoholism</b> were found.
+DRD1	drug	cocaine	24095672	Preadolescent <strong>drd1</strong> EGFP mice exhibit <b>cocaine</b> induced behavioral sensitization.
+DRD1	addiction	sensitization	24095672	Preadolescent <strong>drd1</strong> EGFP mice exhibit cocaine induced behavioral <b>sensitization</b>.
+DRD1	drug	cocaine	24095672	Here we studied <b>cocaine</b> induced locomotor sensitization in preadolescent <strong>drd1</strong> EGFP reporter mice.
+DRD1	addiction	sensitization	24095672	Here we studied cocaine induced locomotor <b>sensitization</b> in preadolescent <strong>drd1</strong> EGFP reporter mice.
+DRD1	drug	cocaine	24095672	We administered 15mg/kg <b>cocaine</b> three times daily at 1h intervals for seven consecutive days beginning on postnatal day 23 to <strong>drd1</strong> EGFP reporter mice and the commonly used C57BL/6 mice.
+DRD1	drug	cocaine	24095672	Under this regimen, preadolescent mice of both strains exhibited <b>cocaine</b> induced locomotor sensitization; however, by day 7 the <b>cocaine</b> induced locomotor activity in the <strong>drd1</strong> EGFP mice was maintained for a longer duration compared to the C57BL/6 mice.
+DRD1	addiction	sensitization	24095672	Under this regimen, preadolescent mice of both strains exhibited cocaine induced locomotor <b>sensitization</b>; however, by day 7 the cocaine induced locomotor activity in the <strong>drd1</strong> EGFP mice was maintained for a longer duration compared to the C57BL/6 mice.
+DRD1	drug	cocaine	24095672	The <b>cocaine</b> induced locomotor sensitization was not retained when the <strong>drd1</strong> EGFP mice were maintained <b>cocaine</b> free for two weeks suggesting that in preadolescent <strong>drd1</strong> EGFP mice the <b>cocaine</b> induced changes do not persist.
+DRD1	addiction	sensitization	24095672	The cocaine induced locomotor <b>sensitization</b> was not retained when the <strong>drd1</strong> EGFP mice were maintained cocaine free for two weeks suggesting that in preadolescent <strong>drd1</strong> EGFP mice the cocaine induced changes do not persist.
+DRD1	addiction	dependence	24078558	<strong>DRD1</strong> and DRD2 have been linked to substance <b>dependence</b>; whether they predict HIV associated neurocognitive disorder (HAND) is unclear.
+DRD1	drug	cocaine	24078558	We observed that both <strong>DRD1</strong> and DRD2 polymorphisms were associated with opiate and <b>cocaine</b> dependence (P < 0.05) in Caucasian subjects, but not African American individuals.
+DRD1	addiction	dependence	24078558	We observed that both <strong>DRD1</strong> and DRD2 polymorphisms were associated with opiate and cocaine <b>dependence</b> (P < 0.05) in Caucasian subjects, but not African American individuals.
+DRD1	drug	cocaine	24001687	In an effort to identify <b>cocaine</b> induced alterations in D1 r  versus D2 r expressing cells during the initial stages of addiction, we examined cells that expressed D1 rs in <strong>Drd1</strong> eGFP mice, or D2 rs in Drd2 eGFP mice, after an acute, 1 day binge pattern of <b>cocaine</b> administration.
+DRD1	addiction	addiction	24001687	In an effort to identify cocaine induced alterations in D1 r  versus D2 r expressing cells during the initial stages of <b>addiction</b>, we examined cells that expressed D1 rs in <strong>Drd1</strong> eGFP mice, or D2 rs in Drd2 eGFP mice, after an acute, 1 day binge pattern of cocaine administration.
+DRD1	addiction	intoxication	24001687	In an effort to identify cocaine induced alterations in D1 r  versus D2 r expressing cells during the initial stages of addiction, we examined cells that expressed D1 rs in <strong>Drd1</strong> eGFP mice, or D2 rs in Drd2 eGFP mice, after an acute, 1 day <b>binge</b> pattern of cocaine administration.
+DRD1	drug	cocaine	24001687	Compared to saline controls, <strong>Drd1</strong> eGFP mice that received <b>cocaine</b> had a higher count of D1 r labeled cells in the dorsolateral (DL) striatum, at the 30 min and 24 h time points.
+DRD1	drug	opioid	23976958	Dopamine D1 receptor (<strong>DRD1</strong>) modulates <b>opioid</b> reinforcement, reward, and <b>opioid</b> induced neuroadaptation.
+DRD1	addiction	reward	23976958	Dopamine D1 receptor (<strong>DRD1</strong>) modulates opioid <b>reinforcement</b>, <b>reward</b>, and opioid induced neuroadaptation.
+DRD1	drug	opioid	23976958	We propose that <strong>DRD1</strong> polymorphism affects susceptibility to <b>opioid</b> dependence (OD), the efficiency of transition to OD, and <b>opioid</b> induced pleasure response.
+DRD1	addiction	dependence	23976958	We propose that <strong>DRD1</strong> polymorphism affects susceptibility to opioid <b>dependence</b> (OD), the efficiency of transition to OD, and opioid induced pleasure response.
+DRD1	drug	opioid	23976958	We analyzed potential association between seven <strong>DRD1</strong> polymorphisms with the following traits: duration of transition from the first use to dependence (DTFUD), subjective pleasure responses to <b>opioid</b> on first use and post dependence use, and OD risk in 425 Chinese with OD and 514 healthy controls.
+DRD1	addiction	dependence	23976958	We analyzed potential association between seven <strong>DRD1</strong> polymorphisms with the following traits: duration of transition from the first use to <b>dependence</b> (DTFUD), subjective pleasure responses to opioid on first use and post <b>dependence</b> use, and OD risk in 425 Chinese with OD and 514 healthy controls.
+DRD1	drug	opioid	23976958	In conclusion, <strong>DRD1</strong> rs686 minor allele decreases the OD risk by prolonging the transition to dependence and attenuating <b>opioid</b> induced pleasure in Chinese.
+DRD1	addiction	dependence	23976958	In conclusion, <strong>DRD1</strong> rs686 minor allele decreases the OD risk by prolonging the transition to <b>dependence</b> and attenuating opioid induced pleasure in Chinese.
+DRD1	drug	alcohol	23873704	Moreover, overexpression of miR 382 significantly attenuated <b>alcohol</b> induced up regulation of <strong>DRD1</strong> and DeltaFosB, decreased voluntary intake of and preference for <b>alcohol</b> and inhibited the <strong>DRD1</strong> induced action potential responses.
+DRD1	drug	cocaine	23864683	Here, we report a D1 like dopamine receptor (<strong>DRD1</strong>) mediated long term potentiation of GABAA IPSCs (D1 LTPGABA) in the oval bed nucleus of the stria terminalis that was positively correlated with motivation to self administer <b>cocaine</b> in rats.
+DRD1	drug	cocaine	23864683	Likewise, in vivo intra oval bed nucleus of the stria terminalis <strong>DRD1</strong> pharmacological blockade reduced lever pressing for <b>cocaine</b> more effectively in rats showing enhanced motivation toward <b>cocaine</b>.
+DRD1	drug	opioid	23661099	The <strong>dopamine receptor D1</strong> gene is associated with the length of interval between first <b>heroin</b> use and onset of dependence in Chinese Han <b>heroin</b> addicts.
+DRD1	addiction	dependence	23661099	The <strong>dopamine receptor D1</strong> gene is associated with the length of interval between first heroin use and onset of <b>dependence</b> in Chinese Han heroin addicts.
+DRD1	addiction	dependence	23661099	Previous researches showed that the dopamine receptor D1 (<strong>DRD1</strong>) may play a critical role in drug <b>dependence</b>.
+DRD1	addiction	dependence	23661099	Previous researches showed that the <strong>dopamine receptor D1</strong> (<strong>DRD1</strong>) may play a critical role in drug <b>dependence</b>.
+DRD1	drug	opioid	23661099	This research aimed to determine whether <strong>DRD1</strong> played a role in development of <b>heroin</b> dependence in Chinese <b>heroin</b> dependent patients.
+DRD1	addiction	dependence	23661099	This research aimed to determine whether <strong>DRD1</strong> played a role in development of heroin <b>dependence</b> in Chinese heroin dependent patients.
+DRD1	drug	opioid	23661099	The results found that the frequencies of <strong>DRD1</strong> SNP genotypes or haplotypes were not different between <b>heroin</b> dependent patients and controls.
+DRD1	drug	opioid	23661099	The results indicated that <strong>DRD1</strong> gene polymorphism may not play an important role in the susceptibility of <b>heroin</b> dependence in the Chinese Han population, but it may be associated with the rapidity of <b>heroin</b> dependence development from first drug use.
+DRD1	addiction	dependence	23661099	The results indicated that <strong>DRD1</strong> gene polymorphism may not play an important role in the susceptibility of heroin <b>dependence</b> in the Chinese Han population, but it may be associated with the rapidity of heroin <b>dependence</b> development from first drug use.
+DRD1	drug	amphetamine	23626822	<b>Methamphetamine</b> and <strong>dopamine receptor D1</strong> regulate entrainment of murine circadian oscillators.
+DRD1	addiction	reward	23447334	Dopaine D1 receptor (<strong>DRD1</strong>) mRNAs and receptors are localized in <b>reward</b> related brain regions, which receive cholinergic input.
+DRD1	drug	nicotine	23447334	<strong>DRD1</strong> mRNA expression was significantly higher in the PFC of the <b>nicotine</b> treated group compared with controls; similar trends were observed in the VTA and STR.
+DRD1	drug	nicotine	23447334	Our results suggest that intermittent subcutaneous <b>nicotine</b> administration increases the expression of <strong>DRD1</strong> mRNA in the PFC of rats, and this increase may be due to changes in histone H4 acetylation of the 2kb promoter of the <strong>DRD1</strong> gene.
+DRD1	drug	cocaine	23285158	These embryos were exposed to <b>cocaine</b> hydrochloride (HCl) at 5 hours post fertilization (hpf) and were then collected at 8, 16, 24, 48 and 72 hpf to study the expression of dopamine receptors, <strong>drd1</strong>, drd2a, drd2b and drd3, by quantitative real time PCR (qPCR) and in situ hybridization (ISH, only at 24 hpf).
+DRD1	drug	nicotine	22495174	<strong>DRD1</strong> associations with <b>smoking</b> abstinence across slow and normal <b>nicotine</b> metabolizers.
+DRD1	drug	nicotine	22495174	Our findings support the role of <strong>DRD1</strong> in <b>nicotine</b> dependence, and identify genetic and <b>nicotine</b> metabolism profiles that may interact to impact <b>nicotine</b> dependence.
+DRD1	addiction	dependence	22495174	Our findings support the role of <strong>DRD1</strong> in nicotine <b>dependence</b>, and identify genetic and nicotine metabolism profiles that may interact to impact nicotine <b>dependence</b>.
+DRD1	drug	alcohol	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (<strong>DRD1</strong>, DRD2, DRD3, DRD4) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of craving, as well as alpha synuclein (SNCA), which has been previously found to be associated with craving, were associated with <b>alcohol</b> craving in this sample.
+DRD1	addiction	relapse	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (<strong>DRD1</strong>, DRD2, DRD3, DRD4) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of <b>craving</b>, as well as alpha synuclein (SNCA), which has been previously found to be associated with <b>craving</b>, were associated with alcohol <b>craving</b> in this sample.
+DRD1	drug	opioid	21807019	<b>Heroin</b> had dose related effects on <strong>Drd1a</strong> mRNA in the hypothalamus and on Drd2 mRNA in the caudate putamen.
+DRD1	addiction	addiction	21642609	In the current study, we have identified, for the first time, that propofol is able to induce the <b>addictive</b> signaling molecule DeltaFosB in NAc via <strong>dopamine receptor D1</strong>.
+DRD1	drug	nicotine	20456319	Association of polymorphisms in the BDNF, <strong>DRD1</strong> and DRD3 genes with <b>tobacco</b> <b>smoking</b> in schizophrenia.
+DRD1	drug	nicotine	20456319	Emerging evidence indicates that the <strong>DRD1</strong> BDNF DRD3 cluster plays an important role in <b>nicotine</b> addiction.
+DRD1	addiction	addiction	20456319	Emerging evidence indicates that the <strong>DRD1</strong> BDNF DRD3 cluster plays an important role in nicotine <b>addiction</b>.
+DRD1	drug	nicotine	20456319	Both <strong>DRD1</strong> markers tested (rs4532 and rs686) and the DRD3 marker (rs1025398) showed association with quantity of <b>tobacco</b> smoked (p = 0.01, 0.005 and 0.002, respectively).
+DRD1	drug	nicotine	20456319	Our findings are preliminary; however, they support the involvement of the <strong>DRD1</strong>, BDNF and DRD3 genes in <b>smoking</b> behaviour.
+DRD1	drug	alcohol	19563515	<strong>DRD1</strong> 5'UTR variation, sex and early infant stress influence <b>ethanol</b> consumption in rhesus macaques.
+DRD1	drug	alcohol	19563515	We tested whether variation in <strong>DRD1</strong> influences <b>alcohol</b> consumption in rhesus macaques and whether its influence is mediated by sex and early rearing experience.
+DRD1	drug	alcohol	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (<strong>DRD1</strong>), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as <b>alcohol</b> dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and diazepam binding inhibitor (DBI).
+DRD1	drug	benzodiazepine	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (<strong>DRD1</strong>), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as alcohol dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and <b>diazepam</b> binding inhibitor (DBI).
+DRD1	addiction	addiction	19179847	Here, we will review the information collected implicating the receptors of the D1 family (<strong>DRD1</strong> and DRD5) and of the D2 family (DRD2, DRD3 and DRD4) in drug <b>addiction</b>.
+DRD1	drug	nicotine	19135651	Previously, we reported that dopamine D1 receptor gene (<strong>DRD1</strong>) is associated with <b>nicotine</b> dependence (ND) and demonstrated that two alleles (A and G) of polymorphism rs686 in the 3' untranslated region (3'UTR) of <strong>DRD1</strong> are expressed differentially.
+DRD1	addiction	dependence	19135651	Previously, we reported that dopamine D1 receptor gene (<strong>DRD1</strong>) is associated with nicotine <b>dependence</b> (ND) and demonstrated that two alleles (A and G) of polymorphism rs686 in the 3' untranslated region (3'UTR) of <strong>DRD1</strong> are expressed differentially.
+DRD1	drug	alcohol	18341651	A haplotype of the <strong>DRD1</strong> gene is associated with <b>alcohol</b> dependence.
+DRD1	addiction	dependence	18341651	A haplotype of the <strong>DRD1</strong> gene is associated with alcohol <b>dependence</b>.
+DRD1	drug	cocaine	18341651	Indeed, <strong>DRD1</strong> antagonists may reduce <b>cocaine</b> seeking behavior and the acquisition of <b>cocaine</b> cue associations.
+DRD1	addiction	relapse	18341651	Indeed, <strong>DRD1</strong> antagonists may reduce cocaine <b>seeking</b> behavior and the acquisition of cocaine cue associations.
+DRD1	drug	alcohol	18341651	The D1.1/r4532 marker of the <strong>DRD1</strong> gene has been associated with a large set of phenotypes including addictive behaviors, but none with <b>alcohol</b> dependence per se.
+DRD1	addiction	addiction	18341651	The D1.1/r4532 marker of the <strong>DRD1</strong> gene has been associated with a large set of phenotypes including <b>addictive</b> behaviors, but none with alcohol dependence per se.
+DRD1	addiction	dependence	18341651	The D1.1/r4532 marker of the <strong>DRD1</strong> gene has been associated with a large set of phenotypes including addictive behaviors, but none with alcohol <b>dependence</b> per se.
+DRD1	drug	alcohol	18341651	We analyzed a population of 134 patients with <b>alcohol</b> dependence, also assessing more homogeneous (severe) phenotypes, comparing this sample with a healthy control population, assessing two SNPs within the <strong>DRD1</strong> gene in order to depict the role of <strong>DRD1</strong> polymorphisms and haplotypes.
+DRD1	addiction	dependence	18341651	We analyzed a population of 134 patients with alcohol <b>dependence</b>, also assessing more homogeneous (severe) phenotypes, comparing this sample with a healthy control population, assessing two SNPs within the <strong>DRD1</strong> gene in order to depict the role of <strong>DRD1</strong> polymorphisms and haplotypes.
+DRD1	drug	alcohol	18341651	The T allele of the rs686 polymorphism within <strong>DRD1</strong> gene was significantly more frequent in patients with <b>alcohol</b> dependence (p = 0.0008), with a larger excess for patients with severe dependence (p = 6 x 10( 6)), and even more for patients with severe complications such as withdrawal seizures (p = 7 x 10( 7)).
+DRD1	addiction	dependence	18341651	The T allele of the rs686 polymorphism within <strong>DRD1</strong> gene was significantly more frequent in patients with alcohol <b>dependence</b> (p = 0.0008), with a larger excess for patients with severe <b>dependence</b> (p = 6 x 10( 6)), and even more for patients with severe complications such as withdrawal seizures (p = 7 x 10( 7)).
+DRD1	addiction	withdrawal	18341651	The T allele of the rs686 polymorphism within <strong>DRD1</strong> gene was significantly more frequent in patients with alcohol dependence (p = 0.0008), with a larger excess for patients with severe dependence (p = 6 x 10( 6)), and even more for patients with severe complications such as <b>withdrawal</b> seizures (p = 7 x 10( 7)).
+DRD1	drug	alcohol	18341651	A specific haplotype rs686*T rs4532*G within the <strong>DRD1</strong> gene was significantly more precisely associated with <b>alcohol</b> dependence in our sample (p = 5 x 10( 6)).
+DRD1	addiction	dependence	18341651	A specific haplotype rs686*T rs4532*G within the <strong>DRD1</strong> gene was significantly more precisely associated with alcohol <b>dependence</b> in our sample (p = 5 x 10( 6)).
+DRD1	drug	alcohol	18341651	Even though chance finding cannot be ruled out, convergent evidence is given that the <strong>DRD1</strong> gene is a susceptibility gene in <b>alcohol</b> dependence, regarding the fact that relying on more homogeneous phenotypes (i.e., more severe patients) and more informative genetic markers (i.e., haplotypes) reinforce the initial association.
+DRD1	addiction	dependence	18341651	Even though chance finding cannot be ruled out, convergent evidence is given that the <strong>DRD1</strong> gene is a susceptibility gene in alcohol <b>dependence</b>, regarding the fact that relying on more homogeneous phenotypes (i.e., more severe patients) and more informative genetic markers (i.e., haplotypes) reinforce the initial association.
+DRD1	drug	nicotine	18092181	Significant association of <strong>DRD1</strong> with <b>nicotine</b> dependence.
+DRD1	addiction	dependence	18092181	Significant association of <strong>DRD1</strong> with nicotine <b>dependence</b>.
+DRD1	drug	nicotine	18092181	In this study, we examined five single nucleotide polymorphisms (SNPs) within or near the dopamine D(1) receptor gene (<strong>DRD1</strong>) for their association with ND, which was assessed by <b>smoking</b> quantity (SQ), the Heaviness of <b>Smoking</b> Index (HSI), and the Fagerström Test for ND (FTND).
+DRD1	drug	alcohol	17466946	5' UTR polymorphism of dopamine receptor D1 (<strong>DRD1</strong>) associated with severity and temperament of <b>alcoholism</b>.
+DRD1	drug	alcohol	17466946	5' UTR polymorphism of <strong>dopamine receptor D1</strong> (<strong>DRD1</strong>) associated with severity and temperament of <b>alcoholism</b>.
+DRD1	drug	alcohol	17466946	To examine the genetic effects of the Dopamine Receptor D1 (DRD) gene family (<strong>DRD1</strong> DRD5) in the Korean population, 11 polymorphisms in the DRD gene family were genotyped and analyzed in 535 <b>alcohol</b> dependent subjects and 273 population controls.
+DRD1	drug	alcohol	17466946	To examine the genetic effects of the <strong>Dopamine Receptor D1</strong> (DRD) gene family (<strong>DRD1</strong> DRD5) in the Korean population, 11 polymorphisms in the DRD gene family were genotyped and analyzed in 535 <b>alcohol</b> dependent subjects and 273 population controls.
+DRD1	drug	alcohol	17466946	Although none of the polymorphisms of <strong>DRD1</strong> 5 genes were found to be associated with the risk of <b>alcoholism</b>, one 5' UTR polymorphism in the <strong>DRD1</strong> (<strong>DRD1</strong> 48A>G) gene was significantly associated with severity of <b>alcohol</b> related problem, as measured by the <b>Alcohol</b> Use Disorders Identification Test (AUDIT) in a gene dose dependent manner, i.e., 24.37 (+/ 8.19) among patients with  48A/A genotype, 22.37 (+/ 9.49) among those with  48A/G genotype, and 17.38 (+/ 8.28) among those with  48G/G genotype (P=0.002).
+DRD1	drug	alcohol	17466946	The genetic effects of <strong>DRD1</strong> 48A>G were further analyzed with other phenotypes among <b>alcohol</b> dependent subjects.
+DRD1	addiction	relapse	17466946	Interestingly, the <strong>DRD1</strong> 48A>A genotype was also found to be associated with novelty <b>seeking</b> (NC), harm avoidance (HA), and persistence (P) (P =0.01, 0.02, and 0.003, respectively).
+DRD1	drug	amphetamine	17063155	We explored the biochemical and behavioral responses to cocaine and D <b>amphetamine</b> (D <b>amph</b>) in mice with heterozygous mutations of genes encoding D1R and Galphaolf (<strong>Drd1a</strong>+/  and Gnal+/ ), which express decreased levels of the corresponding proteins in the striatum.
+DRD1	drug	cocaine	17063155	We explored the biochemical and behavioral responses to <b>cocaine</b> and D amphetamine (D amph) in mice with heterozygous mutations of genes encoding D1R and Galphaolf (<strong>Drd1a</strong>+/  and Gnal+/ ), which express decreased levels of the corresponding proteins in the striatum.
+DRD1	drug	amphetamine	17063155	Dopamine stimulated cAMP production in vitro and phosphorylation of AMPA receptor GluR1 subunit in response to D <b>amph</b> in vivo were decreased in Gnal+/ , but not <strong>Drd1a</strong>+/  mice.
+DRD1	drug	amphetamine	17063155	Acute locomotor responses to D1 agonist SKF81259, D <b>amph</b> and cocaine were altered in Gnal+/  mice, and not in <strong>Drd1a</strong>+/  mice.
+DRD1	drug	cocaine	17063155	Acute locomotor responses to D1 agonist SKF81259, D amph and <b>cocaine</b> were altered in Gnal+/  mice, and not in <strong>Drd1a</strong>+/  mice.
+DRD1	drug	amphetamine	16916582	Also, the expression of <strong>Drd1</strong> gene in the striatum and Drd2 gene in the mesolimbic structures of wild type mice were up regulated under the influence of <b>amphetamine</b>.
+DRD1	drug	amphetamine	16916582	The lack of development of up regulation of <strong>Drd1</strong> and Drd2 genes after repeated treatment with <b>amphetamine</b> probably explains the reduced place conditioning in CCK(2) receptor deficient mice.
+DRD1	drug	cocaine	16492766	After 28 days of <b>cocaine</b> treatment and 2 days of withdrawal, spine density increased in both <strong>Drd1</strong> EGFP  and Drd2 EGFP positive neurons.
+DRD1	addiction	withdrawal	16492766	After 28 days of cocaine treatment and 2 days of <b>withdrawal</b>, spine density increased in both <strong>Drd1</strong> EGFP  and Drd2 EGFP positive neurons.
+DRD1	addiction	withdrawal	16492766	However, the increase in spine density was maintained only in <strong>Drd1</strong> EGFP positive neurons 30 days after drug <b>withdrawal</b>.
+DRD1	addiction	withdrawal	16492766	Notably, increased DeltaFosB expression also was observed in <strong>Drd1</strong> EGFP  and Drd2 EGFP positive neurons after 2 days of drug <b>withdrawal</b> but only in <strong>Drd1</strong> EGFP positive neurons after 30 days of drug <b>withdrawal</b>.
+DRD1	drug	alcohol	12966314	Association between <strong>dopamine receptor D1</strong> gene DdeI polymorphism and sensation seeking in <b>alcohol</b> dependent men.
+DRD1	addiction	relapse	12966314	Association between <strong>dopamine receptor D1</strong> gene DdeI polymorphism and sensation <b>seeking</b> in alcohol dependent men.
+DRD1	drug	alcohol	12966314	We investigated whether the <strong>DRD1</strong> DdeI polymorphism could be associated with the sensation seeking level among a sample of 72 <b>alcohol</b> dependent male and female patients.
+DRD1	addiction	relapse	12966314	We investigated whether the <strong>DRD1</strong> DdeI polymorphism could be associated with the sensation <b>seeking</b> level among a sample of 72 alcohol dependent male and female patients.
+DRD1	addiction	relapse	12966314	Analyses of variance were performed to test for an effect between the <strong>DRD1</strong> DdeI genotypes and sensation <b>seeking</b> scores according to the 40 item Zuckerman scale.
+DRD1	drug	alcohol	12966314	That is the first report of a male limited association between the <strong>DRD1</strong> gene polymorphism and sensation seeking score in <b>alcohol</b> dependent subjects.
+DRD1	addiction	relapse	12966314	That is the first report of a male limited association between the <strong>DRD1</strong> gene polymorphism and sensation <b>seeking</b> score in alcohol dependent subjects.
+DRD1	drug	cocaine	12687634	Acute "binge" <b>cocaine</b> also increased mRNA levels for glutamate receptor GluR2, <strong>dopamine receptor D1</strong>, and a number of phosphatases.
+DRD1	addiction	intoxication	12687634	Acute "<b>binge</b>" cocaine also increased mRNA levels for glutamate receptor GluR2, <strong>dopamine receptor D1</strong>, and a number of phosphatases.
+DRD1	drug	alcohol	11347517	More than 80% of <b>alcoholics</b> smoke cigarettes in the U.S.A. Other genetic methods such as linkage analysis, allele sharing methods, association studies and analysis of inbred, transgenic and gene knockout rodents, have partially agreed in showing that the 5HT 1B serotonin receptor and the <strong>DRD1</strong>, DRD2 and DRD4 dopamine receptors, as well as the dopamine transporter DAT, play an important role in behaviors related to <b>alcoholism</b> and substance abuse.
+DRD1	drug	alcohol	9603612	The present study discovered no <strong>DRD1</strong> coding region mutations in any of the Tourette's syndrome or <b>alcohol</b> dependent patients.
+DRD1	drug	alcohol	9603612	The non polymorphic structure of the <strong>DRD1</strong> gene among the Tourette's syndrome, Tourette's syndrome comorbid with AD HD and OCD and the <b>alcohol</b> dependent populations screened by SSCP suggests that coding region mutations of the <strong>DRD1</strong> gene are unlikely to contribute to the inheritance of these disorders.
+DRD1	drug	nicotine	9154217	To test the hypothesis that the <strong>DRD1</strong> gene might play a role in addictive behaviors we examined the alleles of the Dde I polymorphism in three independent groups of subjects with varying types of compulsive, addictive behaviors Tourette syndrome probands, <b>smokers</b> and pathological gamblers.
+DRD1	addiction	addiction	9154217	To test the hypothesis that the <strong>DRD1</strong> gene might play a role in <b>addictive</b> behaviors we examined the alleles of the Dde I polymorphism in three independent groups of subjects with varying types of <b>compulsive</b>, <b>addictive</b> behaviors Tourette syndrome probands, smokers and pathological gamblers.
+DRD1	addiction	addiction	9154217	In all three groups there was a significant in the frequency of homozygosity for the <strong>DRD1</strong> Dde I 1 or 2 alleles in subjects with <b>addictive</b> behaviors.
+DRD1	drug	nicotine	9154217	In the TS group and <b>smokers</b> there was a significant additive effect of the <strong>DRD1</strong> and DRD2 genes.
+DRD1	addiction	addiction	9154217	These results support a role for genetic variants of the <strong>DRD1</strong> gene in some <b>addictive</b> behaviors, and an interaction of genetic variants at the <strong>DRD1</strong> and DRD2 genes.
+DRD1	drug	cocaine	1365665	The effects of the <strong>dopamine receptor D1</strong> partial agonist, SKF 38393, on behavior maintained by <b>cocaine</b> was assessed in squirrel monkeys (Saimiri sciureus).
+PCDHA4	drug	cannabinoid	32433545	<b>Cannabinoid</b> receptor <strong>CNR1</strong> expression and DNA methylation in human prefrontal cortex, hippocampus and caudate in brain development and schizophrenia.
+PCDHA4	drug	cannabinoid	32433545	The type 1 <b>cannabinoid</b> receptor (CB1), encoded by the <strong>CNR1</strong> gene, is a key component of the <b>endocannabinoid</b> system.
+PCDHA4	drug	alcohol	32433545	THC or <b>ethanol</b> are each significantly associated with dysregulated expression of <strong>CNR1</strong> in the PFC of patients with affective disorder, and the expression of <strong>CNR1</strong> is significantly upregulated in the PFC of schizophrenia patients who completed suicide.
+PCDHA4	drug	cannabinoid	32433545	<b>THC</b> or ethanol are each significantly associated with dysregulated expression of <strong>CNR1</strong> in the PFC of patients with affective disorder, and the expression of <strong>CNR1</strong> is significantly upregulated in the PFC of schizophrenia patients who completed suicide.
+PCDHA4	drug	cannabinoid	32414087	<b>Cannabis</b> Constituents and Acetylcholinesterase Interaction: Molecular Docking, In Vitro Studies and Association with <strong>CNR1</strong> rs806368 and ACHE rs17228602.
+PCDHA4	drug	cannabinoid	32414087	Further, genetic predisposition to <b>cannabis</b> addiction was investigated by association analysis of <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) single nucleotide polymorphism (SNP) rs806368 and ACHE rs17228602 using restriction fragment length polymorphism (RFLP) method.
+PCDHA4	addiction	addiction	32414087	Further, genetic predisposition to cannabis <b>addiction</b> was investigated by association analysis of cannabinoid receptor 1 (<strong>CNR1</strong>) single nucleotide polymorphism (SNP) rs806368 and ACHE rs17228602 using restriction fragment length polymorphism (RFLP) method.
+PCDHA4	drug	cannabinoid	31445429	The combination of comparative genomics and CRISPR/CAS9 disruption used in our study to determine the functional effects of genetic and epigenetic changes on the activity of tissue specific regulatory elements at the <strong>CNR1</strong> locus represent an important first step in gaining a mechanistic understanding of <b>cannabinoid</b> regulatory pharmacogenetics.
+PCDHA4	drug	cannabinoid	31184938	<strong>CNR1</strong> and FAAH variation and affective states induced by <b>marijuana</b> smoking.
+PCDHA4	drug	nicotine	31184938	<strong>CNR1</strong> and FAAH variation and affective states induced by marijuana <b>smoking</b>.
+PCDHA4	drug	cannabinoid	31184938	Background: Polymorphisms in <b>cannabinoid</b> receptor type 1 (encoded by <strong>CNR1</strong>) and fatty acid amide hydrolase (encoded by FAAH) have been associated with <b>cannabis</b> dependence, but it remains unknown whether variation within these genes influences <b>cannabis</b>' acute effects on affect.
+PCDHA4	addiction	dependence	31184938	Background: Polymorphisms in cannabinoid receptor type 1 (encoded by <strong>CNR1</strong>) and fatty acid amide hydrolase (encoded by FAAH) have been associated with cannabis <b>dependence</b>, but it remains unknown whether variation within these genes influences cannabis' acute effects on affect.
+PCDHA4	drug	cannabinoid	31184938	Objective: Conduct a secondary data analysis study to determine whether previously observed acute effects of <b>tetrahydrocannabinol</b> (<b>THC</b>) on mood was dependent upon variation in <strong>CNR1</strong> and FAAH.
+PCDHA4	drug	cannabinoid	31184938	Results: <b>THC</b> increased levels of POMS Tension Anxiety and Confusion Bewilderment over and above the effects of variation in <strong>CNR1</strong> and FAAH.
+PCDHA4	drug	cannabinoid	31013550	Single nucleotide polymorphisms (SNPs) in the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>; rs1049353 and rs806378) and fatty acid amide hydrolase (FAAH) gene (rs324420) have been implicated in CUD.
+PCDHA4	drug	cannabinoid	31013550	Results indicated that <strong>CNR1</strong> rs1049353 GG carriers showed increased state satiety after <b>THC</b>/<b>THC</b> + CBD administration in comparison with placebo and reduced the salience of appetitive cues after <b>THC</b> in comparison with CBD administration; A carriers did not vary on either of these measures indicative of a vulnerability to CUD.
+PCDHA4	drug	cannabinoid	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>), because it is related to addictive behavior and reward processing.
+PCDHA4	addiction	addiction	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the cannabinoid receptor 1 (<strong>CNR1</strong>), because it is related to <b>addictive</b> behavior and reward processing.
+PCDHA4	addiction	reward	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the cannabinoid receptor 1 (<strong>CNR1</strong>), because it is related to addictive behavior and <b>reward</b> processing.
+PCDHA4	drug	opioid	30063884	By means of real time polymerase chain reaction (PCR), we also analysed relative gene expression of tyrosine hydroxylase (TH) in the ventral tegmental area (VTA), and of mu <b>opioid</b> receptor (OPRM1), <strong>CNR1</strong> and CNR2 in the nucleus accumbens (NAcc).
+PCDHA4	drug	cannabinoid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the opioid μ receptor (Oprm1), <b>cannabinoid</b> CB1 receptor (<strong>Cnr1</strong>) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+PCDHA4	drug	opioid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the <b>opioid</b> μ receptor (Oprm1), cannabinoid CB1 receptor (<strong>Cnr1</strong>) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+PCDHA4	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (<strong>Cnr1</strong>, Cnr2, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and TRPV1 sensitizing kinases (Mapk3, Mapk14, Prkcg, and Prkaca).
+PCDHA4	drug	cannabinoid	28930056	Developmentally Specific Associations Between <strong>CNR1</strong> Genotype and <b>Cannabis</b> Use Across Emerging Adulthood.
+PCDHA4	drug	cannabinoid	28930056	Previous studies have found preliminary evidence for associations between common single nucleotide polymorphisms (SNPs) in the <b>cannabinoid</b> receptor gene <strong>CNR1</strong> and <b>cannabis</b> use and dependence.
+PCDHA4	addiction	dependence	28930056	Previous studies have found preliminary evidence for associations between common single nucleotide polymorphisms (SNPs) in the cannabinoid receptor gene <strong>CNR1</strong> and cannabis use and <b>dependence</b>.
+PCDHA4	drug	cannabinoid	28930056	The present study examined a set of eight independent SNPs in or near <strong>CNR1</strong> in relation to <b>cannabis</b> use measured longitudinally across emerging adulthood.
+PCDHA4	drug	cannabinoid	28930056	Using latent growth curve modeling of 10 waves of longitudinal data spanning mean ages 18.4 23.8 years in a sample of non Hispanic White individuals (n = 334), we tested if genotype at each <strong>CNR1</strong> SNP was associated with both level and growth of <b>cannabis</b> use over time.
+PCDHA4	drug	cannabinoid	27453054	<b>Cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during nicotine withdrawal.
+PCDHA4	drug	nicotine	27453054	Cannabinoid receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during <b>nicotine</b> withdrawal.
+PCDHA4	addiction	withdrawal	27453054	Cannabinoid receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during nicotine <b>withdrawal</b>.
+PCDHA4	drug	cannabinoid	27453054	Variation on the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) has been related to nicotine dependence, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+PCDHA4	drug	nicotine	27453054	Variation on the cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been related to <b>nicotine</b> dependence, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+PCDHA4	addiction	dependence	27453054	Variation on the cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been related to nicotine <b>dependence</b>, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+PCDHA4	drug	nicotine	27453054	We targeted <strong>CNR1</strong> variants as moderators of a validated neural marker of <b>nicotine</b> withdrawal related cognitive disruption.
+PCDHA4	addiction	withdrawal	27453054	We targeted <strong>CNR1</strong> variants as moderators of a validated neural marker of nicotine <b>withdrawal</b> related cognitive disruption.
+PCDHA4	drug	cannabinoid	27394933	Five genes known to play a role in the <b>endocannabinoid</b> system and CUDs were examined in a community sample of young adult Mexican Americans (MAs): <strong>CNR1</strong>, MGLL, FAAH, DAGLA, and DAGLB.
+PCDHA4	drug	cannabinoid	26833047	An Information Theoretical Study of the Epistasis Between the <strong>CNR1</strong> 1359 G/A Polymorphism and the Taq1A and Taq1B DRD2 Polymorphisms: Assessing the Susceptibility to <b>Cannabis</b> Addiction in a Turkish Population.
+PCDHA4	addiction	addiction	26833047	An Information Theoretical Study of the Epistasis Between the <strong>CNR1</strong> 1359 G/A Polymorphism and the Taq1A and Taq1B DRD2 Polymorphisms: Assessing the Susceptibility to Cannabis <b>Addiction</b> in a Turkish Population.
+PCDHA4	drug	cannabinoid	26833047	In this study, we discuss the interaction between the 1359 G/A polymorphism of the <strong>CNR1</strong> gene and the DRD2 gene polymorphisms and the net effect of any possible epistasis on the <b>cannabis</b> addiction phenotype in a Turkish population.
+PCDHA4	addiction	addiction	26833047	In this study, we discuss the interaction between the 1359 G/A polymorphism of the <strong>CNR1</strong> gene and the DRD2 gene polymorphisms and the net effect of any possible epistasis on the cannabis <b>addiction</b> phenotype in a Turkish population.
+PCDHA4	drug	cannabinoid	26833047	We hypothesize that overlapping expressions of CB1 and D2R is the cause of CB1 D2R interactions in cases of substance abuse and the different polymorphisms of <strong>CNR1</strong> and DRD2 genes may have decisive roles in the nature of these interactions in terms of promoting or alleviating the <b>cannabis</b> addiction risk factor of the individual.
+PCDHA4	addiction	addiction	26833047	We hypothesize that overlapping expressions of CB1 and D2R is the cause of CB1 D2R interactions in cases of substance abuse and the different polymorphisms of <strong>CNR1</strong> and DRD2 genes may have decisive roles in the nature of these interactions in terms of promoting or alleviating the cannabis <b>addiction</b> risk factor of the individual.
+PCDHA4	drug	cannabinoid	26756393	The association between young adult patterns of <b>cannabis</b> use or <b>cannabis</b> abuse/dependence was tested with genetic variation in the <b>cannabinoid</b> gene, <strong>CNR1</strong>, the ANKK1 DRD2 gene, and childhood developmental trajectories of P300.
+PCDHA4	addiction	dependence	26756393	The association between young adult patterns of cannabis use or cannabis abuse/<b>dependence</b> was tested with genetic variation in the cannabinoid gene, <strong>CNR1</strong>, the ANKK1 DRD2 gene, and childhood developmental trajectories of P300.
+PCDHA4	drug	cannabinoid	26756393	Although <strong>CNR1</strong> variation overall was not significantly associated with these patterns, among individuals with <b>cannabis</b> abuse/dependence the presence of one or both copies of the rs806368 A > G minor allele conferred a 5.4 fold increase (P = 0.003) in the likelihood that they would be in the frequent and persistent use group rather than the declining use group.
+PCDHA4	addiction	dependence	26756393	Although <strong>CNR1</strong> variation overall was not significantly associated with these patterns, among individuals with cannabis abuse/<b>dependence</b> the presence of one or both copies of the rs806368 A > G minor allele conferred a 5.4 fold increase (P = 0.003) in the likelihood that they would be in the frequent and persistent use group rather than the declining use group.
+PCDHA4	drug	cannabinoid	26684509	Sex dependence of anxiety like behavior in <b>cannabinoid</b> receptor 1 (<strong>Cnr1</strong>) knockout mice.
+PCDHA4	addiction	dependence	26684509	Sex <b>dependence</b> of anxiety like behavior in cannabinoid receptor 1 (<strong>Cnr1</strong>) knockout mice.
+PCDHA4	drug	cannabinoid	26684509	We observe greater anxiety like behavior in male mice with global knockout of the <b>cannabinoid</b> 1 receptor (<strong>Cnr1</strong>) compared to male, wild type controls as measured by percent open arm entries on an elevated plus maze test.
+PCDHA4	drug	cannabinoid	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism: MGLL, FAAH; binding: <strong>CNR1</strong>; SNPs N = 65) and childhood sexual abuse (CSA) predict <b>cannabis</b> dependence symptoms.
+PCDHA4	addiction	dependence	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism: MGLL, FAAH; binding: <strong>CNR1</strong>; SNPs N = 65) and childhood sexual abuse (CSA) predict cannabis <b>dependence</b> symptoms.
+PCDHA4	drug	cannabinoid	26342856	Reduced avoidance behaviour was associated with lower telencepahalic gene expression levels of <b>cannabinoid</b> receptor 1 (<strong>cnr1</strong>) and higher gene expression levels of corticotropin releasing factor (crf).
+PCDHA4	drug	cannabinoid	26331953	Given the preclinical and clinical evidence regarding the associations between <b>cannabinoid</b> systems and both opiate dependence and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the <b>cannabinoid</b> receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable methadone treatment.
+PCDHA4	drug	opioid	26331953	Given the preclinical and clinical evidence regarding the associations between cannabinoid systems and both opiate dependence and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the cannabinoid receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable <b>methadone</b> treatment.
+PCDHA4	addiction	dependence	26331953	Given the preclinical and clinical evidence regarding the associations between cannabinoid systems and both opiate <b>dependence</b> and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the cannabinoid receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable methadone treatment.
+PCDHA4	drug	cannabinoid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ opioid receptor (OPRD1), <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+PCDHA4	drug	opioid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ <b>opioid</b> receptor (OPRD1), cannabinoid receptor 1 (<strong>CNR1</strong>), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+PCDHA4	drug	cannabinoid	25258300	The <b>cannabinoid</b> receptor subtype 1 gene <strong>CNR1</strong> is not only associated with phenotypes such as cognitive performance, addiction and anxiety, but is also known to be crucially involved in responses to acute and chronic psychological and cellular stress conditions.
+PCDHA4	addiction	addiction	25258300	The cannabinoid receptor subtype 1 gene <strong>CNR1</strong> is not only associated with phenotypes such as cognitive performance, <b>addiction</b> and anxiety, but is also known to be crucially involved in responses to acute and chronic psychological and cellular stress conditions.
+PCDHA4	drug	opioid	25252306	[Association study of <strong>CNR1</strong>, GAD1 and BDNF polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan].
+PCDHA4	addiction	dependence	25252306	[Association study of <strong>CNR1</strong>, GAD1 and BDNF polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan].
+PCDHA4	drug	cannabinoid	25252306	In order to analyze the association of <strong>CNR1</strong>(<b>Cannabinoid</b> receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+PCDHA4	drug	opioid	25252306	In order to analyze the association of <strong>CNR1</strong>(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+PCDHA4	addiction	dependence	25252306	In order to analyze the association of <strong>CNR1</strong>(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+PCDHA4	drug	opioid	25252306	A case control study was performed with 8 SNPs from <strong>CNR1</strong>, GAD1, and BDNF genes in 165 <b>heroin</b> dependent males and 170 healthy males of the Dai population.
+PCDHA4	drug	opioid	25252306	Furthermore, polymorphisms in <strong>CNR1</strong> (rs1049353), GAD1 (rs1978340 and rs11542313), and BDNF (rs6265 and rs13306221) were associated with <b>heroin</b> dependence in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be <b>heroin</b> dependent.
+PCDHA4	addiction	dependence	25252306	Furthermore, polymorphisms in <strong>CNR1</strong> (rs1049353), GAD1 (rs1978340 and rs11542313), and BDNF (rs6265 and rs13306221) were associated with heroin <b>dependence</b> in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be heroin dependent.
+PCDHA4	drug	cannabinoid	24980155	Research investigating the impact of genetic variants in the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) and of early rearing conditions has demonstrated that both factors contribute to the prediction of impulsivity related phenotypes.
+PCDHA4	drug	cannabinoid	24607771	F344 rats displayed higher levels of <b>cannabinoid</b> receptor binding in the lateral globus pallidus and weaker <strong>CNR1</strong> gene expression in the prefrontal cortex (PFc) than LEW rats.
+PCDHA4	drug	alcohol	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with <b>alcohol</b>, tobacco and/or cannabis consumption in young individuals (n = 91).
+PCDHA4	drug	cannabinoid	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, tobacco and/or <b>cannabis</b> consumption in young individuals (n = 91).
+PCDHA4	drug	nicotine	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, <b>tobacco</b> and/or cannabis consumption in young individuals (n = 91).
+PCDHA4	drug	cannabinoid	24152087	One of the single nucleotide polymorphisms (SNP) of the <strong>CNR1</strong> gene, which codes for <b>cannabinoid</b> receptor 1 (CB1R), is the rs2180619, located in a regulatory region of this gene (6q14 q15).
+PCDHA4	drug	alcohol	24060590	Therefore, we studied the expression of <strong>CNR1</strong> and CNR2, and the novel cannabinoid G protein coupled receptor (GPCR) 55 (GPR55) in human monocyte derived dendritic cells (MDDCs) from <b>alcohol</b> users.
+PCDHA4	drug	cannabinoid	24060590	Therefore, we studied the expression of <strong>CNR1</strong> and CNR2, and the novel <b>cannabinoid</b> G protein coupled receptor (GPCR) 55 (GPR55) in human monocyte derived dendritic cells (MDDCs) from alcohol users.
+PCDHA4	addiction	aversion	23227007	The influence of CB1 receptors on the <b>aversion</b> driven spatial learning in the Morris water maze test is strongly age dependent: mice with genetic deletion of CB1 receptors (<strong>Cnr1</strong>( / )) show superior learning when young but inferior learning when old compared to age matched wild type mice.
+PCDHA4	drug	cannabinoid	23190435	Participants with at least one copy of the minor allele for SNPs in synaptosomal associated protein 25 gene (SNAP25; rs363035 OR = 0.53; P = 0.005) and <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>; rs6454672 OR = 0.62; P = 0.022) have decreased likelihood of meeting PA recommendations.
+PCDHA4	drug	cannabinoid	22850347	MAPK14 and <strong>CNR1</strong> gene variant interactions: effects on brain volume deficits in schizophrenia patients with <b>marijuana</b> misuse.
+PCDHA4	drug	cannabinoid	22850347	We previously reported that <b>marijuana</b> misuse in conjunction with specific <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) genetic variants (rs12720071 G allele carriers) contributed to white matter (WM) brain volume deficits in schizophrenia patients.
+PCDHA4	drug	cannabinoid	22850347	In this study, we assessed the influence of another <b>cannabinoid</b> related gene, mitogen activated protein kinase 14 (MAPK14), and potential MAPK14 <strong>CNR1</strong> gene gene interactions in conferring brain volume abnormalities among schizophrenia patients with <b>marijuana</b> abuse/dependence.
+PCDHA4	addiction	dependence	22850347	In this study, we assessed the influence of another cannabinoid related gene, mitogen activated protein kinase 14 (MAPK14), and potential MAPK14 <strong>CNR1</strong> gene gene interactions in conferring brain volume abnormalities among schizophrenia patients with marijuana abuse/<b>dependence</b>.
+PCDHA4	drug	cannabinoid	22850347	There were significant main effects of the MAPK14 <strong>CNR1</strong> diplotype and diplotype × <b>marijuana</b> interaction on WM brain volumes, with both genetic variants having additive contributions to WM volume deficits only in patients with <b>marijuana</b> misuse.
+PCDHA4	drug	cannabinoid	22850347	Given that <strong>CNR1</strong> induced apoptosis is preceded by increased MAPK phosphorylation, our study suggests that potential MAPK14 <strong>CNR1</strong> gene gene interactions may mediate brain morphometric features in schizophrenia patients with heavy <b>marijuana</b> use.
+PCDHA4	drug	cannabinoid	22669173	Associations between <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) variation and hippocampus and amygdala volumes in heavy <b>cannabis</b> users.
+PCDHA4	drug	cannabinoid	22669173	A single nucleotide polymorphism in the <b>cannabis</b> receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced withdrawal, cue elicited craving, and parahippocampal activation to <b>cannabis</b> cues.
+PCDHA4	addiction	relapse	22669173	A single nucleotide polymorphism in the cannabis receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced withdrawal, cue elicited <b>craving</b>, and parahippocampal activation to cannabis cues.
+PCDHA4	addiction	withdrawal	22669173	A single nucleotide polymorphism in the cannabis receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced <b>withdrawal</b>, cue elicited craving, and parahippocampal activation to cannabis cues.
+PCDHA4	drug	cannabinoid	22669173	These data replicate previous findings of reduced hippocampal and amygdalar volume among heavy <b>cannabis</b> users, and suggest that <strong>CNR1</strong> rs2023239 variation may predispose smaller hippocampal volume after heavy <b>cannabis</b> use.
+PCDHA4	drug	cannabinoid	22362764	Allele specific differences in activity of a novel <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene intronic enhancer in hypothalamus, dorsal root ganglia, and hippocampus.
+PCDHA4	drug	cannabinoid	22362764	Polymorphisms within intron 2 of the <strong>CNR1</strong> gene, which encodes <b>cannabinoid</b> receptor 1 (CB(1)), have been associated with addiction, obesity, and brain volume deficits.
+PCDHA4	addiction	addiction	22362764	Polymorphisms within intron 2 of the <strong>CNR1</strong> gene, which encodes cannabinoid receptor 1 (CB(1)), have been associated with <b>addiction</b>, obesity, and brain volume deficits.
+PCDHA4	drug	cannabinoid	22085192	Given the potential role of <b>endocannabinoid</b> system in AD, polymorphisms within <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) have been potentially associated with susceptibility to this disease.
+PCDHA4	drug	alcohol	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with dependence to <b>alcohol</b> and other substances and emphasizes the relevance of endocannabinoid system in AD.
+PCDHA4	drug	cannabinoid	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with dependence to alcohol and other substances and emphasizes the relevance of <b>endocannabinoid</b> system in AD.
+PCDHA4	addiction	dependence	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with <b>dependence</b> to alcohol and other substances and emphasizes the relevance of endocannabinoid system in AD.
+PCDHA4	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], <strong>CNR1</strong> 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+PCDHA4	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], <strong>CNR1</strong> 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+PCDHA4	drug	cannabinoid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (OPRM1) or <b>cannabinoid</b> receptors (<strong>CNR1</strong>).
+PCDHA4	drug	nicotine	22046326	Overall, our results suggest that genetic variants potentially involved in <b>nicotine</b> metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with <b>smoking</b> related phenotypes, as opposed to genetic variants influencing the brain effects of <b>nicotine</b>, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (OPRM1) or cannabinoid receptors (<strong>CNR1</strong>).
+PCDHA4	drug	opioid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), <b>opioid</b> (OPRM1) or cannabinoid receptors (<strong>CNR1</strong>).
+PCDHA4	drug	cannabinoid	21937688	The <b>cannabinoid</b> receptor (<strong>CNR1</strong>) and the fatty acid amide hydrolase (FAAH) genes are located on chromosomes 6 and 1 in the 6q15 and 1p33 cytogenetic bands, respectively.
+PCDHA4	addiction	addiction	21937688	However, many works have repeatedly associated polymorphisms in the <strong>CNR1</strong> and FAAH genes with drug related behaviours; this suggests that these genes should be examined in further genetic studies focusing on drug <b>addiction</b> and other psychiatric disorders.
+PCDHA4	drug	amphetamine	21886587	Association Study of Two Cannabinoid Receptor Genes, <strong>CNR1</strong> and CNR2, with <b>Methamphetamine</b> Dependence.
+PCDHA4	drug	cannabinoid	21886587	Association Study of Two <b>Cannabinoid</b> Receptor Genes, <strong>CNR1</strong> and CNR2, with Methamphetamine Dependence.
+PCDHA4	addiction	dependence	21886587	Association Study of Two Cannabinoid Receptor Genes, <strong>CNR1</strong> and CNR2, with Methamphetamine <b>Dependence</b>.
+PCDHA4	drug	amphetamine	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode cannabinoid receptors CB1 and CB2, with <b>methamphetamine</b> dependence, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+PCDHA4	drug	cannabinoid	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode <b>cannabinoid</b> receptors CB1 and CB2, with methamphetamine dependence, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+PCDHA4	addiction	dependence	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode cannabinoid receptors CB1 and CB2, with methamphetamine <b>dependence</b>, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+PCDHA4	drug	amphetamine	21886587	Rs806379 of the <strong>CNR1</strong> gene showed a significant association with the phenotype of latency of psychosis after the first consumption of <b>methamphetamine</b>.
+PCDHA4	drug	amphetamine	21886587	The present study suggests a possibility that genetic variants of the <strong>CNR1</strong> gene may produce a liability to the complication of psychotic state after abuse of <b>methamphetamine</b>; however, our findings need to be confirmed by future replications.
+PCDHA4	drug	cannabinoid	21808284	rs806365 in <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) had a significant male specific gene treatment interaction at 6 month follow up (adjusted P = 3.9 × 10( 5)); within males using nasal spray, rs806365 was associated with a decrease in odds of abstinence (OR = 0.04; 95% CI: 0.01 0.2).
+PCDHA4	drug	nicotine	21808284	While the role of <strong>CNR1</strong> in substance abuse has been well studied, we report EPB41 for the first time in the <b>nicotine</b> literature.
+PCDHA4	drug	cocaine	21790903	Further evidence for association of polymorphisms in the <strong>CNR1</strong> gene with <b>cocaine</b> addiction: confirmation in an independent sample and meta analysis.
+PCDHA4	addiction	addiction	21790903	Further evidence for association of polymorphisms in the <strong>CNR1</strong> gene with cocaine <b>addiction</b>: confirmation in an independent sample and meta analysis.
+PCDHA4	drug	cannabinoid	21790903	The <b>cannabinoid</b> receptor 1 protein regulates both the <b>endocannabinoid</b> and dopaminergic neurobiological systems, and polymorphisms in the <b>cannabinoid</b> receptor gene, <strong>CNR1</strong>, have been associated previously with substance dependence.
+PCDHA4	addiction	dependence	21790903	The cannabinoid receptor 1 protein regulates both the endocannabinoid and dopaminergic neurobiological systems, and polymorphisms in the cannabinoid receptor gene, <strong>CNR1</strong>, have been associated previously with substance <b>dependence</b>.
+PCDHA4	drug	cocaine	21790903	<b>Cocaine</b> addicted individuals (n=860) and unaffected controls (n=334) of African descent were genotyped for two single nucleotide polymorphisms (SNPs) in <strong>CNR1</strong> (rs6454674, rs806368).
+PCDHA4	drug	cocaine	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance dependence or are specific to <b>cocaine</b> addiction.
+PCDHA4	addiction	addiction	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance dependence or are specific to cocaine <b>addiction</b>.
+PCDHA4	addiction	dependence	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance <b>dependence</b> or are specific to cocaine addiction.
+PCDHA4	drug	cocaine	21785434	We found that systemic, intranasal or intra accumbens local administration of JWH133, a selective CB(2) receptor agonist, dose dependently inhibited intravenous <b>cocaine</b> self administration, <b>cocaine</b> enhanced locomotion, and <b>cocaine</b> enhanced accumbens extracellular dopamine in wild type and CB(1) receptor knockout (CB(1)( / ), also known as <strong>Cnr1</strong>( / )) mice, but not in CB(2)( / ) (Cnr2( / )) mice.
+PCDHA4	drug	cannabinoid	21714860	Variation in the human <b>cannabinoid</b> receptor <strong>CNR1</strong> gene modulates gaze duration for happy faces.
+PCDHA4	drug	cannabinoid	21714860	In this study, we tested whether variations in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene are associated with gaze duration towards happy faces.
+PCDHA4	drug	cannabinoid	21714860	This gene was selected because <strong>CNR1</strong> is a key component of the <b>endocannabinoid</b> system, which is involved in processing reward, and in our previous functional magnetic resonance imaging (fMRI) study, we found that variations in <strong>CNR1</strong> modulate the striatal response to happy (but not disgust) faces.
+PCDHA4	addiction	reward	21714860	This gene was selected because <strong>CNR1</strong> is a key component of the endocannabinoid system, which is involved in processing <b>reward</b>, and in our previous functional magnetic resonance imaging (fMRI) study, we found that variations in <strong>CNR1</strong> modulate the striatal response to happy (but not disgust) faces.
+PCDHA4	addiction	reward	21714860	These results suggest that <strong>CNR1</strong> variations modulate the striatal function that underlies the perception of signals of social <b>reward</b>, such as happy faces.
+PCDHA4	drug	cannabinoid	21513772	Association between a <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism and <b>cannabinoid</b> induced alterations of the auditory event related P300 potential.
+PCDHA4	drug	cannabinoid	21513772	Recently, an (AAT)n triplet repeat polymorphism within the <b>cannabinoid</b> receptor gene <strong>CNR1</strong> has been found to be associated with both schizophrenia and substance dependence, and to modulate the P300 potential.
+PCDHA4	addiction	dependence	21513772	Recently, an (AAT)n triplet repeat polymorphism within the cannabinoid receptor gene <strong>CNR1</strong> has been found to be associated with both schizophrenia and substance <b>dependence</b>, and to modulate the P300 potential.
+PCDHA4	drug	cannabinoid	21513772	Moreover, it appears that variations within <strong>CNR1</strong> may differentially alter the sensitivity to the acute effects of <b>cannabinoids</b> on P300 generation in healthy subjects.
+PCDHA4	drug	cannabinoid	21497918	We summarize <b>endocannabinoid</b> signaling in pathways related to anxiety and depression, identify the serotonergic system as the most likely candidate to mediate the side effects of CB₁ receptor antagonists, and propose that poloymorphisms in <strong>CNR1</strong>, SLC6A4 and certain CYP 450 enzymes could help to identify individuals who may benefit from treatment with CB₁ receptor antagonist without psychiatric side effects.
+PCDHA4	drug	cannabinoid	21420833	<b>Cannabinoid</b> receptor 1 (CB1/<strong>CNR1</strong>) is the principal brain receptor mediating <b>marijuana</b> effects.
+PCDHA4	drug	cannabinoid	21420833	No study to date has systematically investigated the impact of <strong>CNR1</strong> on quantitative phenotypic features in schizophrenia and inter relationships with <b>marijuana</b> misuse.
+PCDHA4	drug	alcohol	21420833	Effects of <strong>CNR1</strong> tSNPs and marijuana abuse/dependence on brain volumes and neurocognition were assessed using ANCOVA, including co morbid <b>alcohol</b>/non marijuana illicit drug misuse as covariates.
+PCDHA4	drug	cannabinoid	21420833	Effects of <strong>CNR1</strong> tSNPs and <b>marijuana</b> abuse/dependence on brain volumes and neurocognition were assessed using ANCOVA, including co morbid alcohol/non <b>marijuana</b> illicit drug misuse as covariates.
+PCDHA4	addiction	dependence	21420833	Effects of <strong>CNR1</strong> tSNPs and marijuana abuse/<b>dependence</b> on brain volumes and neurocognition were assessed using ANCOVA, including co morbid alcohol/non marijuana illicit drug misuse as covariates.
+PCDHA4	drug	cannabinoid	21420833	Our findings suggest that heavy <b>cannabis</b> use in the context of specific <strong>CNR1</strong> genotypes may contribute to greater WM volume deficits and cognitive impairment, which could in turn increase schizophrenia risk.
+PCDHA4	drug	cannabinoid	21341382	In M. mulatta, the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) mRNA was expressed in the all tissues; in contrast, the <b>cannabinoid</b> receptor 2 (CNR2) mRNA was only present in the spleen.
+PCDHA4	drug	alcohol	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in <b>ethanol</b>'s reinforcing and addictive properties prompted us to study the levels and distribution of CB1R after chronic <b>ethanol</b> intake, in the presence and absence of DRD2.
+PCDHA4	drug	cannabinoid	20958329	The anatomical proximity of the <b>cannabinoid</b> type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and addictive properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+PCDHA4	addiction	addiction	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and <b>addictive</b> properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+PCDHA4	addiction	reward	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's <b>reinforcing</b> and addictive properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+PCDHA4	addiction	addiction	20192949	<strong>CNR1</strong> gene polymorphisms in <b>addictive</b> disorders: a systematic review and a meta analysis.
+PCDHA4	drug	cannabinoid	20192949	The aim of the present work was to systematically review all association studies of <b>cannabis</b> receptor 1 (<strong>CNR1</strong>) polymorphisms with dependence syndrome and to perform a meta analysis.
+PCDHA4	addiction	dependence	20192949	The aim of the present work was to systematically review all association studies of cannabis receptor 1 (<strong>CNR1</strong>) polymorphisms with <b>dependence</b> syndrome and to perform a meta analysis.
+PCDHA4	addiction	dependence	20192949	In line with the polygenic model, our meta analysis supports a minor implication for <strong>CNR1</strong> AAT polymorphism in illicit substance <b>dependence</b> vulnerability.
+PCDHA4	drug	cannabinoid	20010914	Association of polymorphisms of the <b>cannabinoid</b> receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with heroin addiction: impact of long repeats of <strong>CNR1</strong>.
+PCDHA4	drug	opioid	20010914	Association of polymorphisms of the cannabinoid receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with <b>heroin</b> addiction: impact of long repeats of <strong>CNR1</strong>.
+PCDHA4	addiction	addiction	20010914	Association of polymorphisms of the cannabinoid receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with heroin <b>addiction</b>: impact of long repeats of <strong>CNR1</strong>.
+PCDHA4	drug	cannabinoid	20010914	Alterations in expression of a <b>cannabinoid</b> receptor (<strong>CNR1</strong>, CB1), and of fatty acid amide hydrolase (FAAH) that degrades endogenous ligands of CB1, may contribute to the development of addiction.
+PCDHA4	addiction	addiction	20010914	Alterations in expression of a cannabinoid receptor (<strong>CNR1</strong>, CB1), and of fatty acid amide hydrolase (FAAH) that degrades endogenous ligands of CB1, may contribute to the development of <b>addiction</b>.
+PCDHA4	drug	opioid	20010914	The 385C>A in the FAAH gene and six polymorphisms of <strong>CNR1</strong> were genotyped in former <b>heroin</b> addicts and control subjects (247 Caucasians, 161 Hispanics, 179 African Americans and 19 Asians).
+PCDHA4	drug	cannabinoid	20010552	Individual and additive effects of the <strong>CNR1</strong> and FAAH genes on brain response to <b>marijuana</b> cues.
+PCDHA4	drug	cannabinoid	20010552	As previous work has highlighted the significance of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with respect to <b>cannabis</b> dependence (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+PCDHA4	addiction	dependence	20010552	As previous work has highlighted the significance of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with respect to cannabis <b>dependence</b> (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+PCDHA4	drug	cannabinoid	20010552	Between group comparisons showed that carriers of the <strong>CNR1</strong> rs2023239 G allele had significantly greater activity in reward related areas of the brain, such as the orbitofrontal cortex (OFC), inferior frontal gyrus (IFG), and anterior cingulate gyrus (ACG), during exposure to <b>marijuana</b> cues, as compared with those with the A/A genotype for this SNP.
+PCDHA4	addiction	reward	20010552	Between group comparisons showed that carriers of the <strong>CNR1</strong> rs2023239 G allele had significantly greater activity in <b>reward</b> related areas of the brain, such as the orbitofrontal cortex (OFC), inferior frontal gyrus (IFG), and anterior cingulate gyrus (ACG), during exposure to marijuana cues, as compared with those with the A/A genotype for this SNP.
+PCDHA4	drug	cannabinoid	20010552	These findings are in accord with earlier reported associations between <strong>CNR1</strong> and FAAH and CD intermediate phenotypes, and suggest that the underlying mechanism of these genetic effects may be enhanced neural response in reward areas of the brain in carriers of the <strong>CNR1</strong> G allele and FAAH C/C genotype in response to <b>marijuana</b> cues.
+PCDHA4	addiction	reward	20010552	These findings are in accord with earlier reported associations between <strong>CNR1</strong> and FAAH and CD intermediate phenotypes, and suggest that the underlying mechanism of these genetic effects may be enhanced neural response in <b>reward</b> areas of the brain in carriers of the <strong>CNR1</strong> G allele and FAAH C/C genotype in response to marijuana cues.
+PCDHA4	drug	cannabinoid	19886064	The implication of <strong>CNR1</strong> gene's polymorphisms in the modulation of <b>endocannabinoid</b> system effects.
+PCDHA4	drug	cannabinoid	19886064	It is composed of <b>cannabinoid</b> receptors CB1 and CB2, and their genes (<strong>CNR1</strong> and CNR2), their endogenous ligands and the enzymes which mediate endogenous ligands' biosynthesis and degradation.
+PCDHA4	drug	cannabinoid	19443135	The association between <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) and <b>cannabis</b> dependence symptoms in adolescents and young adults.
+PCDHA4	addiction	dependence	19443135	The association between cannabinoid receptor 1 gene (<strong>CNR1</strong>) and cannabis <b>dependence</b> symptoms in adolescents and young adults.
+PCDHA4	drug	cannabinoid	19443135	This study examined the genetic association between variation in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene and <b>cannabis</b> dependence symptoms.
+PCDHA4	addiction	dependence	19443135	This study examined the genetic association between variation in the cannabinoid receptor 1 (<strong>CNR1</strong>) gene and cannabis <b>dependence</b> symptoms.
+PCDHA4	drug	cannabinoid	19443135	Additional family based studies are needed to clarify the role of the <strong>CNR1</strong> gene, and its various SNPs, in the development of <b>cannabis</b> use disorders.
+PCDHA4	drug	cannabinoid	19335651	Gene association studies are presented for (a) genes posited to have specific influences on <b>cannabis</b> use disorders: <strong>CNR1</strong>, CB2, FAAH, MGLL, TRPV1 and GPR55 and (b) genes from various neurotransmitter systems that are likely to exert a non specific influence on risk of <b>cannabis</b> use disorders, e.g.
+PCDHA4	drug	cocaine	19052543	Interaction between two independent <strong>CNR1</strong> variants increases risk for <b>cocaine</b> dependence in European Americans: a replication study in family based sample and population based sample.
+PCDHA4	addiction	dependence	19052543	Interaction between two independent <strong>CNR1</strong> variants increases risk for cocaine <b>dependence</b> in European Americans: a replication study in family based sample and population based sample.
+PCDHA4	drug	cannabinoid	19052543	We recently reported that, in a European American (EA) sample, the interaction between two <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug dependence (DD), including cocaine dependence (CD).
+PCDHA4	drug	cocaine	19052543	We recently reported that, in a European American (EA) sample, the interaction between two cannabinoid receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug dependence (DD), including <b>cocaine</b> dependence (CD).
+PCDHA4	addiction	dependence	19052543	We recently reported that, in a European American (EA) sample, the interaction between two cannabinoid receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug <b>dependence</b> (DD), including cocaine <b>dependence</b> (CD).
+PCDHA4	drug	cannabinoid	19016476	Evidence for association between polymorphisms in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene and <b>cannabis</b> dependence.
+PCDHA4	addiction	dependence	19016476	Evidence for association between polymorphisms in the cannabinoid receptor 1 (<strong>CNR1</strong>) gene and cannabis <b>dependence</b>.
+PCDHA4	drug	cannabinoid	19016476	The <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) on chromosome 6q14 15 is an excellent candidate gene for <b>cannabis</b> dependence due to the important role of the G protein coupled receptor encoded by this gene in the rewarding effects of Delta9 <b>tetrahydrocannabinol</b>.
+PCDHA4	addiction	dependence	19016476	The cannabinoid receptor 1 gene (<strong>CNR1</strong>) on chromosome 6q14 15 is an excellent candidate gene for cannabis <b>dependence</b> due to the important role of the G protein coupled receptor encoded by this gene in the rewarding effects of Delta9 tetrahydrocannabinol.
+PCDHA4	drug	cannabinoid	19016476	We investigate the association between 9 SNPs spanning <strong>CNR1</strong> and <b>cannabis</b> dependence in 1,923 individuals.
+PCDHA4	addiction	dependence	19016476	We investigate the association between 9 SNPs spanning <strong>CNR1</strong> and cannabis <b>dependence</b> in 1,923 individuals.
+PCDHA4	drug	alcohol	18977415	These <b>alcohol</b> related behaviors are linked to differential changes in <strong>CNR1</strong> and NR1 subunit mRNA transcripts.
+PCDHA4	drug	cannabinoid	18977415	In conclusion, pharmacological inactivation of the glycine binding site of NMDA receptors may control <b>cannabinoid</b> induced relapse like drinking, which is associated with altered expression of <strong>CNR1</strong> and NR1 gene expression as observed after WIN treatment.
+PCDHA4	addiction	relapse	18977415	In conclusion, pharmacological inactivation of the glycine binding site of NMDA receptors may control cannabinoid induced <b>relapse</b> like drinking, which is associated with altered expression of <strong>CNR1</strong> and NR1 gene expression as observed after WIN treatment.
+PCDHA4	drug	cannabinoid	18705688	<b>Marijuana</b> withdrawal and craving: influence of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+PCDHA4	addiction	relapse	18705688	Marijuana withdrawal and <b>craving</b>: influence of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+PCDHA4	addiction	withdrawal	18705688	Marijuana <b>withdrawal</b> and craving: influence of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+PCDHA4	drug	cannabinoid	18705688	To examine whether withdrawal after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the <b>endocannabinoid</b> system, <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+PCDHA4	addiction	relapse	18705688	To examine whether withdrawal after abstinence and cue elicited <b>craving</b> were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+PCDHA4	addiction	withdrawal	18705688	To examine whether <b>withdrawal</b> after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+PCDHA4	drug	cannabinoid	18705688	Two single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> (rs2023239) and FAAH (rs324420) genes, associated previously with substance abuse and functional changes in <b>cannabinoid</b> regulation, were examined in a sample of daily <b>marijuana</b> smokers.
+PCDHA4	drug	nicotine	18705688	Two single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> (rs2023239) and FAAH (rs324420) genes, associated previously with substance abuse and functional changes in cannabinoid regulation, were examined in a sample of daily marijuana <b>smokers</b>.
+PCDHA4	addiction	relapse	18705688	The <strong>CNR1</strong> SNP displayed a significant abstinence x genotype interaction on withdrawal, as well as a main effect on overall levels of <b>craving</b>, while the FAAH SNP displayed a significant abstinence x genotype interaction on <b>craving</b>.
+PCDHA4	addiction	withdrawal	18705688	The <strong>CNR1</strong> SNP displayed a significant abstinence x genotype interaction on <b>withdrawal</b>, as well as a main effect on overall levels of craving, while the FAAH SNP displayed a significant abstinence x genotype interaction on craving.
+PCDHA4	drug	alcohol	18606956	The incentive salience of <b>alcohol</b>: translating the effects of genetic variant in <strong>CNR1</strong>.
+PCDHA4	addiction	reward	18606956	The <b>incentive</b> salience of alcohol: translating the effects of genetic variant in <strong>CNR1</strong>.
+PCDHA4	drug	alcohol	18606956	The gene that codes for cannabinoid receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of <b>alcohol</b> dependence.
+PCDHA4	drug	cannabinoid	18606956	The gene that codes for <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of alcohol dependence.
+PCDHA4	addiction	dependence	18606956	The gene that codes for cannabinoid receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of alcohol <b>dependence</b>.
+PCDHA4	drug	alcohol	18606956	To achieve a better understanding of the role of the <strong>CNR1</strong> gene in the etiology and treatment of <b>alcohol</b> dependence.
+PCDHA4	addiction	dependence	18606956	To achieve a better understanding of the role of the <strong>CNR1</strong> gene in the etiology and treatment of alcohol <b>dependence</b>.
+PCDHA4	drug	cannabinoid	18606954	The <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene is 1 of the 2 receptors expressed in the brain.
+PCDHA4	drug	nicotine	18606954	To test the hypothesis that the <strong>CNR1</strong> gene is associated with <b>nicotine</b> dependence.
+PCDHA4	addiction	dependence	18606954	To test the hypothesis that the <strong>CNR1</strong> gene is associated with nicotine <b>dependence</b>.
+PCDHA4	drug	nicotine	18606954	Variants and haplotypes in the <strong>CNR1</strong> gene may alter the risk for <b>nicotine</b> dependence, and the associations are likely sex specific.
+PCDHA4	addiction	dependence	18606954	Variants and haplotypes in the <strong>CNR1</strong> gene may alter the risk for nicotine <b>dependence</b>, and the associations are likely sex specific.
+PCDHA4	drug	cannabinoid	18579347	<b>Cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene: impact on antidepressant treatment response and emotion processing in major depression.
+PCDHA4	drug	cannabinoid	18579347	Therefore, the impact of <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) variants rs1049353 and rs12720071 on antidepressant treatment response was evaluated in 256 Caucasian patients with Major Depression.
+PCDHA4	addiction	reward	18579347	This analysis provides preliminary support for a role of <strong>CNR1</strong> gene variation in depression and anxiety, potentially mediated by subcortical hypo responsiveness to social <b>reward</b> stimuli.
+PCDHA4	drug	cannabinoid	18519829	For DSM IV <b>cannabis</b> dependence, a modest LOD score on chromosome 6 (1.42) near <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) was identified.
+PCDHA4	addiction	dependence	18519829	For DSM IV cannabis <b>dependence</b>, a modest LOD score on chromosome 6 (1.42) near cannabinoid receptor 1 (<strong>CNR1</strong>) was identified.
+PCDHA4	drug	cannabinoid	18519829	Genes such as ELTD1 on chromosome 1, in addition to genes on chromosomes 4 (eg, GABRA2) and 6 (eg, <strong>CNR1</strong>), may be associated with the genetic risk for <b>cannabis</b> use disorders.
+PCDHA4	drug	cannabinoid	17945506	Human studies show that <b>marijuana</b> dependence is frequently associated with cocaine dependence, and that the <b>cannabinoid</b> receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine addiction.
+PCDHA4	drug	cocaine	17945506	Human studies show that marijuana dependence is frequently associated with <b>cocaine</b> dependence, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to <b>cocaine</b> addiction.
+PCDHA4	addiction	addiction	17945506	Human studies show that marijuana dependence is frequently associated with cocaine dependence, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine <b>addiction</b>.
+PCDHA4	addiction	dependence	17945506	Human studies show that marijuana <b>dependence</b> is frequently associated with cocaine <b>dependence</b>, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine addiction.
+PCDHA4	drug	alcohol	17509535	<strong>CNR1</strong> variation modulates risk for drug and <b>alcohol</b> dependence.
+PCDHA4	addiction	dependence	17509535	<strong>CNR1</strong> variation modulates risk for drug and alcohol <b>dependence</b>.
+PCDHA4	drug	cannabinoid	17509535	Human <b>cannabinoid</b> receptor 1 (CB1), which is encoded by the <strong>CNR1</strong> gene, may play a role in the development of substance dependence (SD).
+PCDHA4	addiction	dependence	17509535	Human cannabinoid receptor 1 (CB1), which is encoded by the <strong>CNR1</strong> gene, may play a role in the development of substance <b>dependence</b> (SD).
+PCDHA4	drug	alcohol	17508995	Polymorphisms of the dopamine D4 receptor gene (DRD4 VNTR) and cannabinoid CB1 receptor gene (<strong>CNR1</strong>) are not strongly related to cue reactivity after <b>alcohol</b> exposure.
+PCDHA4	drug	cannabinoid	17508995	Polymorphisms of the dopamine D4 receptor gene (DRD4 VNTR) and <b>cannabinoid</b> CB1 receptor gene (<strong>CNR1</strong>) are not strongly related to cue reactivity after alcohol exposure.
+PCDHA4	drug	alcohol	17508995	Polymorphisms in the D4 dopamine receptor gene (DRD4) and the CB1 cannabinoid receptor gene (<strong>CNR1</strong>) have been associated with a differential response to <b>alcohol</b> after consumption.
+PCDHA4	drug	cannabinoid	17508995	Polymorphisms in the D4 dopamine receptor gene (DRD4) and the CB1 <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) have been associated with a differential response to alcohol after consumption.
+PCDHA4	drug	alcohol	17508995	As weekly <b>alcohol</b> consumption increased, the <strong>CNR1</strong> C allele group tended to report more craving for <b>alcohol</b> during the <b>alcohol</b> exposure than the T allele group.
+PCDHA4	addiction	relapse	17508995	As weekly alcohol consumption increased, the <strong>CNR1</strong> C allele group tended to report more <b>craving</b> for alcohol during the alcohol exposure than the T allele group.
+PCDHA4	drug	alcohol	17508995	The DRD4 and <strong>CNR1</strong> polymorphisms do not appear to strongly moderate cue reactivity after <b>alcohol</b> cue exposure, in male heavy drinkers.
+PCDHA4	drug	cannabinoid	17401783	[<b>Endocannabinoid</b> system and <strong>CNR1</strong> gene polymorphisms in schizophrenia and addictive disorders].
+PCDHA4	addiction	addiction	17401783	[Endocannabinoid system and <strong>CNR1</strong> gene polymorphisms in schizophrenia and <b>addictive</b> disorders].
+PCDHA4	drug	cannabinoid	16917946	<b>Cannabis</b> is a major substance of abuse, and the gene encoding for the central <b>cannabinoid</b> receptor (<strong>CNR1</strong>) is a logical candidate gene for vulnerability toward developing symptoms of <b>cannabis</b> dependence.
+PCDHA4	addiction	dependence	16917946	Cannabis is a major substance of abuse, and the gene encoding for the central cannabinoid receptor (<strong>CNR1</strong>) is a logical candidate gene for vulnerability toward developing symptoms of cannabis <b>dependence</b>.
+PCDHA4	drug	cannabinoid	16917946	We studied four single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> gene for association with having one or more symptoms of <b>cannabis</b> dependence in 541 adolescent subjects who had all tried <b>cannabis</b> five or more times.
+PCDHA4	addiction	dependence	16917946	We studied four single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> gene for association with having one or more symptoms of cannabis <b>dependence</b> in 541 adolescent subjects who had all tried cannabis five or more times.
+PCDHA4	drug	cannabinoid	16917946	Univariate (single marker) association tests demonstrated that SNP rs806380, located in intron 2 of the <strong>CNR1</strong> gene, was significantly associated with developing one or more <b>cannabis</b> dependence symptoms, with the G allele having a protective effect (P < 0.02).
+PCDHA4	addiction	dependence	16917946	Univariate (single marker) association tests demonstrated that SNP rs806380, located in intron 2 of the <strong>CNR1</strong> gene, was significantly associated with developing one or more cannabis <b>dependence</b> symptoms, with the G allele having a protective effect (P < 0.02).
+PCDHA4	drug	cannabinoid	16917946	Our findings provide evidence suggesting that a common <strong>CNR1</strong> haplotype is associated with developing fewer <b>cannabis</b> dependence symptoms among adolescents who have experimented with <b>cannabis</b>.
+PCDHA4	addiction	dependence	16917946	Our findings provide evidence suggesting that a common <strong>CNR1</strong> haplotype is associated with developing fewer cannabis <b>dependence</b> symptoms among adolescents who have experimented with cannabis.
+PCDHA4	drug	cannabinoid	16788767	(AAT)n repeat in the <b>cannabinoid</b> receptor gene, <strong>CNR1</strong>: association with schizophrenia in a Spanish population.
+PCDHA4	drug	cannabinoid	16788767	The <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) has been associated with addictive disorders and schizophrenia in different studies.
+PCDHA4	addiction	addiction	16788767	The cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been associated with <b>addictive</b> disorders and schizophrenia in different studies.
+PCDHA4	addiction	dependence	16741937	Association study of the <strong>CNR1</strong> gene exon 3 alternative promoter region polymorphisms and substance <b>dependence</b>.
+PCDHA4	drug	cannabinoid	16741937	An alternative promoter producing a novel 5' untranslated region of <b>cannabinoid</b> receptor mRNA has recently been described in <strong>CNR1</strong>, the gene encoding the <b>cannabinoid</b> receptor protein.
+PCDHA4	drug	alcohol	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., <b>alcohol</b>, cocaine, and opioids), as well as with polysubstance dependence.
+PCDHA4	drug	cocaine	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., alcohol, <b>cocaine</b>, and opioids), as well as with polysubstance dependence.
+PCDHA4	drug	opioid	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., alcohol, cocaine, and <b>opioids</b>), as well as with polysubstance dependence.
+PCDHA4	addiction	dependence	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance <b>dependence</b> diagnoses (i.e., alcohol, cocaine, and opioids), as well as with polysubstance <b>dependence</b>.
+PCDHA4	drug	cannabinoid	16623851	Variations in the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene modulate striatal responses to happy faces.
+PCDHA4	drug	cannabinoid	16623851	The <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) is the best characterized molecule of the <b>endocannabinoid</b> system, involved in processing rewards.
+PCDHA4	addiction	reward	16623851	This suggests a role for the variations of the <strong>CNR1</strong> gene in underlying social <b>reward</b> responsivity.
+PCDHA4	drug	cannabinoid	16314880	(AAT)n repeat in the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>): association with cocaine addiction in an African Caribbean population.
+PCDHA4	drug	cocaine	16314880	(AAT)n repeat in the cannabinoid receptor gene (<strong>CNR1</strong>): association with <b>cocaine</b> addiction in an African Caribbean population.
+PCDHA4	addiction	addiction	16314880	(AAT)n repeat in the cannabinoid receptor gene (<strong>CNR1</strong>): association with cocaine <b>addiction</b> in an African Caribbean population.
+PCDHA4	drug	cannabinoid	16314880	We examined the (AAT)n triplet repeat polymorphism nearby the <strong>CNR1</strong> gene, which encodes human <b>cannabinoid</b> (CB1) receptor, in a male Afro Caribbean population.
+PCDHA4	drug	cocaine	16314880	Our results support that the (AAT)n polymorphism nearby the <strong>CNR1</strong> gene could be associated with predisposition to <b>cocaine</b> dependency.
+PCDHA4	addiction	addiction	15289816	A number of lines of evidence make the gene that encodes the G protein coupled CB1/<strong>Cnr1</strong> receptor a strong candidate to harbor variants that might contribute to individual differences in human <b>addiction</b> vulnerability.
+PCDHA4	drug	cannabinoid	15289816	The CB1/<strong>Cnr1</strong> receptor is the major brain site at which <b>cannabinoid</b> <b>marijuana</b> constituents are psychoactive as well as the principal brain receptor for endogenous anandamide ligands.
+PCDHA4	addiction	addiction	15289816	CB1/ <strong>Cnr1</strong> genomic variation thus appears to play roles in human <b>addiction</b> vulnerability.
+PCDHA4	drug	alcohol	14714115	The aim of this study is to test the potential influence of a bi allelic cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe <b>alcohol</b> withdrawal syndromes.
+PCDHA4	drug	cannabinoid	14714115	The aim of this study is to test the potential influence of a bi allelic <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe alcohol withdrawal syndromes.
+PCDHA4	addiction	withdrawal	14714115	The aim of this study is to test the potential influence of a bi allelic cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe alcohol <b>withdrawal</b> syndromes.
+PCDHA4	drug	alcohol	14714115	After correcting for multiple testing, no association of the A  or G allele of <strong>CNR1</strong> polymorphism with a history of <b>alcohol</b> withdrawal induced seizures was detected.
+PCDHA4	addiction	withdrawal	14714115	After correcting for multiple testing, no association of the A  or G allele of <strong>CNR1</strong> polymorphism with a history of alcohol <b>withdrawal</b> induced seizures was detected.
+PCDHA4	drug	alcohol	12657705	Furthermore, foot shock stress had no affect on <b>alcohol</b> preference in <strong>Cnr1</strong> /  mice, although it induced a dramatic increase in <strong>Cnr1</strong>+/+ animals.
+PCDHA4	drug	alcohol	11841893	Association of a CB1 cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism with severe <b>alcohol</b> dependence.
+PCDHA4	drug	cannabinoid	11841893	Association of a CB1 <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism with severe alcohol dependence.
+PCDHA4	addiction	dependence	11841893	Association of a CB1 cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism with severe alcohol <b>dependence</b>.
+PCDHA4	drug	alcohol	11841893	Due to the involvement of the endogenous cannabinoid system in brain reward mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human cannabinoid receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian <b>alcoholics</b> and 136 most likely non <b>alcoholic</b> controls.
+PCDHA4	drug	cannabinoid	11841893	Due to the involvement of the endogenous <b>cannabinoid</b> system in brain reward mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian alcoholics and 136 most likely non alcoholic controls.
+PCDHA4	addiction	reward	11841893	Due to the involvement of the endogenous cannabinoid system in brain <b>reward</b> mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human cannabinoid receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian alcoholics and 136 most likely non alcoholic controls.
+PCDHA4	drug	alcohol	11841893	This finding suggests that the homozygous genotype <strong>CNR1</strong> 1359A/A confers vulnerability to <b>alcohol</b> withdrawal delirium.
+PCDHA4	addiction	withdrawal	11841893	This finding suggests that the homozygous genotype <strong>CNR1</strong> 1359A/A confers vulnerability to alcohol <b>withdrawal</b> delirium.
+PCDHA4	drug	cannabinoid	11526463	Association study of <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) alleles and drug dependence.
+PCDHA4	addiction	dependence	11526463	Association study of cannabinoid receptor gene (<strong>CNR1</strong>) alleles and drug <b>dependence</b>.
+PCDHA4	drug	cannabinoid	11341859	The <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) is not affected in German i.v.
+PCDHA4	drug	cannabinoid	11341859	The aim of the study was to investigate a possible contribution of the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) to the development of i.v.
+PCDHA4	drug	cannabinoid	10441206	A frequent polymorphism in the coding exon of the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene.
+PCDHA4	drug	cannabinoid	10441206	The cloning of the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene facilitates molecular genetic studies in disorders like Gilles de la Tourette syndrome (GTS), obsessive compulsive disorder (OCD), Parkinsons disease, Alzheimers disease or other neuro psychiatric or neurological diseases, which may be predisposed or influenced by mutations or variants in the <strong>CNR1</strong> gene.
+PCDHA4	addiction	addiction	10441206	The cloning of the human cannabinoid receptor (<strong>CNR1</strong>) gene facilitates molecular genetic studies in disorders like Gilles de la Tourette syndrome (GTS), obsessive <b>compulsive</b> disorder (OCD), Parkinsons disease, Alzheimers disease or other neuro psychiatric or neurological diseases, which may be predisposed or influenced by mutations or variants in the <strong>CNR1</strong> gene.
+PCDHA4	drug	cannabinoid	9106243	Association between the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) and the P300 event related potential.
+PCDHA4	drug	cannabinoid	9106243	In our prior study we observed a significant association between homozygosity for the > or = alleles of a microsatellite polymorphism of <b>cannabinoid</b> receptor genes (<strong>CNR1</strong>) and drug dependence.
+PCDHA4	addiction	dependence	9106243	In our prior study we observed a significant association between homozygosity for the > or = alleles of a microsatellite polymorphism of cannabinoid receptor genes (<strong>CNR1</strong>) and drug <b>dependence</b>.
+PCDHA4	drug	alcohol	9106243	Since marijuana intoxication has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 <b>alcohol</b> and drug addicts, by MANOVA.
+PCDHA4	drug	cannabinoid	9106243	Since <b>marijuana</b> intoxication has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 alcohol and drug addicts, by MANOVA.
+PCDHA4	addiction	intoxication	9106243	Since marijuana <b>intoxication</b> has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 alcohol and drug addicts, by MANOVA.
+PCDHA4	drug	cannabinoid	9106242	<b>Cannabinoid</b> receptor gene (<strong>CNR1</strong>): association with i.v.
+PCDHA4	drug	cannabinoid	9106242	A microsatellite polymorphism (AAT)n at the <b>cannabinoid</b> CB1 (brain) receptor gene (<strong>CNR1</strong>) consists of 9 alleles.
+PCDHA4	drug	alcohol	9106242	Since the cannabinoid system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to <b>alcohol</b> or drug dependence.
+PCDHA4	drug	cannabinoid	9106242	Since the <b>cannabinoid</b> system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug dependence.
+PCDHA4	addiction	dependence	9106242	Since the cannabinoid system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug <b>dependence</b>.
+PCDHA4	addiction	reward	9106242	Since the cannabinoid system is part of the <b>reward</b> pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug dependence.
+CNR1	drug	cannabinoid	32433545	<b>Cannabinoid</b> receptor <strong>CNR1</strong> expression and DNA methylation in human prefrontal cortex, hippocampus and caudate in brain development and schizophrenia.
+CNR1	drug	cannabinoid	32433545	The type 1 <b>cannabinoid</b> receptor (CB1), encoded by the <strong>CNR1</strong> gene, is a key component of the <b>endocannabinoid</b> system.
+CNR1	drug	alcohol	32433545	THC or <b>ethanol</b> are each significantly associated with dysregulated expression of <strong>CNR1</strong> in the PFC of patients with affective disorder, and the expression of <strong>CNR1</strong> is significantly upregulated in the PFC of schizophrenia patients who completed suicide.
+CNR1	drug	cannabinoid	32433545	<b>THC</b> or ethanol are each significantly associated with dysregulated expression of <strong>CNR1</strong> in the PFC of patients with affective disorder, and the expression of <strong>CNR1</strong> is significantly upregulated in the PFC of schizophrenia patients who completed suicide.
+CNR1	drug	cannabinoid	32414087	<b>Cannabis</b> Constituents and Acetylcholinesterase Interaction: Molecular Docking, In Vitro Studies and Association with <strong>CNR1</strong> rs806368 and ACHE rs17228602.
+CNR1	drug	cannabinoid	32414087	Further, genetic predisposition to <b>cannabis</b> addiction was investigated by association analysis of <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) single nucleotide polymorphism (SNP) rs806368 and ACHE rs17228602 using restriction fragment length polymorphism (RFLP) method.
+CNR1	addiction	addiction	32414087	Further, genetic predisposition to cannabis <b>addiction</b> was investigated by association analysis of cannabinoid receptor 1 (<strong>CNR1</strong>) single nucleotide polymorphism (SNP) rs806368 and ACHE rs17228602 using restriction fragment length polymorphism (RFLP) method.
+CNR1	drug	cannabinoid	31445429	The combination of comparative genomics and CRISPR/CAS9 disruption used in our study to determine the functional effects of genetic and epigenetic changes on the activity of tissue specific regulatory elements at the <strong>CNR1</strong> locus represent an important first step in gaining a mechanistic understanding of <b>cannabinoid</b> regulatory pharmacogenetics.
+CNR1	drug	cannabinoid	31184938	<strong>CNR1</strong> and FAAH variation and affective states induced by <b>marijuana</b> smoking.
+CNR1	drug	nicotine	31184938	<strong>CNR1</strong> and FAAH variation and affective states induced by marijuana <b>smoking</b>.
+CNR1	drug	cannabinoid	31184938	Background: Polymorphisms in <b>cannabinoid</b> receptor type 1 (encoded by <strong>CNR1</strong>) and fatty acid amide hydrolase (encoded by FAAH) have been associated with <b>cannabis</b> dependence, but it remains unknown whether variation within these genes influences <b>cannabis</b>' acute effects on affect.
+CNR1	addiction	dependence	31184938	Background: Polymorphisms in cannabinoid receptor type 1 (encoded by <strong>CNR1</strong>) and fatty acid amide hydrolase (encoded by FAAH) have been associated with cannabis <b>dependence</b>, but it remains unknown whether variation within these genes influences cannabis' acute effects on affect.
+CNR1	drug	cannabinoid	31184938	Objective: Conduct a secondary data analysis study to determine whether previously observed acute effects of <b>tetrahydrocannabinol</b> (<b>THC</b>) on mood was dependent upon variation in <strong>CNR1</strong> and FAAH.
+CNR1	drug	cannabinoid	31184938	Results: <b>THC</b> increased levels of POMS Tension Anxiety and Confusion Bewilderment over and above the effects of variation in <strong>CNR1</strong> and FAAH.
+CNR1	drug	cannabinoid	31013550	Single nucleotide polymorphisms (SNPs) in the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>; rs1049353 and rs806378) and fatty acid amide hydrolase (FAAH) gene (rs324420) have been implicated in CUD.
+CNR1	drug	cannabinoid	31013550	Results indicated that <strong>CNR1</strong> rs1049353 GG carriers showed increased state satiety after <b>THC</b>/<b>THC</b> + CBD administration in comparison with placebo and reduced the salience of appetitive cues after <b>THC</b> in comparison with CBD administration; A carriers did not vary on either of these measures indicative of a vulnerability to CUD.
+CNR1	drug	cannabinoid	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>), because it is related to addictive behavior and reward processing.
+CNR1	addiction	addiction	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the cannabinoid receptor 1 (<strong>CNR1</strong>), because it is related to <b>addictive</b> behavior and reward processing.
+CNR1	addiction	reward	30546300	To investigate this issue, we focused on rs1049353, a single nucleotide polymorphism of the cannabinoid receptor 1 (<strong>CNR1</strong>), because it is related to addictive behavior and <b>reward</b> processing.
+CNR1	drug	opioid	30063884	By means of real time polymerase chain reaction (PCR), we also analysed relative gene expression of tyrosine hydroxylase (TH) in the ventral tegmental area (VTA), and of mu <b>opioid</b> receptor (OPRM1), <strong>CNR1</strong> and CNR2 in the nucleus accumbens (NAcc).
+CNR1	drug	cannabinoid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the opioid μ receptor (Oprm1), <b>cannabinoid</b> CB1 receptor (<strong>Cnr1</strong>) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+CNR1	drug	opioid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the <b>opioid</b> μ receptor (Oprm1), cannabinoid CB1 receptor (<strong>Cnr1</strong>) and CB2 receptor (Cnr2) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+CNR1	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (<strong>Cnr1</strong>, Cnr2, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and TRPV1 sensitizing kinases (Mapk3, Mapk14, Prkcg, and Prkaca).
+CNR1	drug	cannabinoid	28930056	Developmentally Specific Associations Between <strong>CNR1</strong> Genotype and <b>Cannabis</b> Use Across Emerging Adulthood.
+CNR1	drug	cannabinoid	28930056	Previous studies have found preliminary evidence for associations between common single nucleotide polymorphisms (SNPs) in the <b>cannabinoid</b> receptor gene <strong>CNR1</strong> and <b>cannabis</b> use and dependence.
+CNR1	addiction	dependence	28930056	Previous studies have found preliminary evidence for associations between common single nucleotide polymorphisms (SNPs) in the cannabinoid receptor gene <strong>CNR1</strong> and cannabis use and <b>dependence</b>.
+CNR1	drug	cannabinoid	28930056	The present study examined a set of eight independent SNPs in or near <strong>CNR1</strong> in relation to <b>cannabis</b> use measured longitudinally across emerging adulthood.
+CNR1	drug	cannabinoid	28930056	Using latent growth curve modeling of 10 waves of longitudinal data spanning mean ages 18.4 23.8 years in a sample of non Hispanic White individuals (n = 334), we tested if genotype at each <strong>CNR1</strong> SNP was associated with both level and growth of <b>cannabis</b> use over time.
+CNR1	drug	cannabinoid	27453054	<b>Cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during nicotine withdrawal.
+CNR1	drug	nicotine	27453054	Cannabinoid receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during <b>nicotine</b> withdrawal.
+CNR1	addiction	withdrawal	27453054	Cannabinoid receptor 1 (<strong>CNR1</strong>) gene variant moderates neural index of cognitive disruption during nicotine <b>withdrawal</b>.
+CNR1	drug	cannabinoid	27453054	Variation on the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) has been related to nicotine dependence, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	drug	nicotine	27453054	Variation on the cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been related to <b>nicotine</b> dependence, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	addiction	dependence	27453054	Variation on the cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been related to nicotine <b>dependence</b>, and <strong>CNR1</strong> antagonists may increase attention and memory functioning.
+CNR1	drug	nicotine	27453054	We targeted <strong>CNR1</strong> variants as moderators of a validated neural marker of <b>nicotine</b> withdrawal related cognitive disruption.
+CNR1	addiction	withdrawal	27453054	We targeted <strong>CNR1</strong> variants as moderators of a validated neural marker of nicotine <b>withdrawal</b> related cognitive disruption.
+CNR1	drug	cannabinoid	27394933	Five genes known to play a role in the <b>endocannabinoid</b> system and CUDs were examined in a community sample of young adult Mexican Americans (MAs): <strong>CNR1</strong>, MGLL, FAAH, DAGLA, and DAGLB.
+CNR1	drug	cannabinoid	26833047	An Information Theoretical Study of the Epistasis Between the <strong>CNR1</strong> 1359 G/A Polymorphism and the Taq1A and Taq1B DRD2 Polymorphisms: Assessing the Susceptibility to <b>Cannabis</b> Addiction in a Turkish Population.
+CNR1	addiction	addiction	26833047	An Information Theoretical Study of the Epistasis Between the <strong>CNR1</strong> 1359 G/A Polymorphism and the Taq1A and Taq1B DRD2 Polymorphisms: Assessing the Susceptibility to Cannabis <b>Addiction</b> in a Turkish Population.
+CNR1	drug	cannabinoid	26833047	In this study, we discuss the interaction between the 1359 G/A polymorphism of the <strong>CNR1</strong> gene and the DRD2 gene polymorphisms and the net effect of any possible epistasis on the <b>cannabis</b> addiction phenotype in a Turkish population.
+CNR1	addiction	addiction	26833047	In this study, we discuss the interaction between the 1359 G/A polymorphism of the <strong>CNR1</strong> gene and the DRD2 gene polymorphisms and the net effect of any possible epistasis on the cannabis <b>addiction</b> phenotype in a Turkish population.
+CNR1	drug	cannabinoid	26833047	We hypothesize that overlapping expressions of CB1 and D2R is the cause of CB1 D2R interactions in cases of substance abuse and the different polymorphisms of <strong>CNR1</strong> and DRD2 genes may have decisive roles in the nature of these interactions in terms of promoting or alleviating the <b>cannabis</b> addiction risk factor of the individual.
+CNR1	addiction	addiction	26833047	We hypothesize that overlapping expressions of CB1 and D2R is the cause of CB1 D2R interactions in cases of substance abuse and the different polymorphisms of <strong>CNR1</strong> and DRD2 genes may have decisive roles in the nature of these interactions in terms of promoting or alleviating the cannabis <b>addiction</b> risk factor of the individual.
+CNR1	drug	cannabinoid	26756393	The association between young adult patterns of <b>cannabis</b> use or <b>cannabis</b> abuse/dependence was tested with genetic variation in the <b>cannabinoid</b> gene, <strong>CNR1</strong>, the ANKK1 DRD2 gene, and childhood developmental trajectories of P300.
+CNR1	addiction	dependence	26756393	The association between young adult patterns of cannabis use or cannabis abuse/<b>dependence</b> was tested with genetic variation in the cannabinoid gene, <strong>CNR1</strong>, the ANKK1 DRD2 gene, and childhood developmental trajectories of P300.
+CNR1	drug	cannabinoid	26756393	Although <strong>CNR1</strong> variation overall was not significantly associated with these patterns, among individuals with <b>cannabis</b> abuse/dependence the presence of one or both copies of the rs806368 A > G minor allele conferred a 5.4 fold increase (P = 0.003) in the likelihood that they would be in the frequent and persistent use group rather than the declining use group.
+CNR1	addiction	dependence	26756393	Although <strong>CNR1</strong> variation overall was not significantly associated with these patterns, among individuals with cannabis abuse/<b>dependence</b> the presence of one or both copies of the rs806368 A > G minor allele conferred a 5.4 fold increase (P = 0.003) in the likelihood that they would be in the frequent and persistent use group rather than the declining use group.
+CNR1	drug	cannabinoid	26684509	Sex dependence of anxiety like behavior in <b>cannabinoid</b> receptor 1 (<strong>Cnr1</strong>) knockout mice.
+CNR1	addiction	dependence	26684509	Sex <b>dependence</b> of anxiety like behavior in cannabinoid receptor 1 (<strong>Cnr1</strong>) knockout mice.
+CNR1	drug	cannabinoid	26684509	We observe greater anxiety like behavior in male mice with global knockout of the <b>cannabinoid</b> 1 receptor (<strong>Cnr1</strong>) compared to male, wild type controls as measured by percent open arm entries on an elevated plus maze test.
+CNR1	drug	cannabinoid	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism: MGLL, FAAH; binding: <strong>CNR1</strong>; SNPs N = 65) and childhood sexual abuse (CSA) predict <b>cannabis</b> dependence symptoms.
+CNR1	addiction	dependence	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism: MGLL, FAAH; binding: <strong>CNR1</strong>; SNPs N = 65) and childhood sexual abuse (CSA) predict cannabis <b>dependence</b> symptoms.
+CNR1	drug	cannabinoid	26342856	Reduced avoidance behaviour was associated with lower telencepahalic gene expression levels of <b>cannabinoid</b> receptor 1 (<strong>cnr1</strong>) and higher gene expression levels of corticotropin releasing factor (crf).
+CNR1	drug	cannabinoid	26331953	Given the preclinical and clinical evidence regarding the associations between <b>cannabinoid</b> systems and both opiate dependence and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the <b>cannabinoid</b> receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable methadone treatment.
+CNR1	drug	opioid	26331953	Given the preclinical and clinical evidence regarding the associations between cannabinoid systems and both opiate dependence and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the cannabinoid receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable <b>methadone</b> treatment.
+CNR1	addiction	dependence	26331953	Given the preclinical and clinical evidence regarding the associations between cannabinoid systems and both opiate <b>dependence</b> and psychiatric disorders, we chose to address whether one single nucleotide polymorphism (SNP) of the cannabinoid receptor type 1 gene (<strong>CNR1</strong>) named rs2023239 would be associated with lifetime MDD and SB in a population of opiate dependent outpatients remitted under stable methadone treatment.
+CNR1	drug	cannabinoid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ opioid receptor (OPRD1), <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+CNR1	drug	opioid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ <b>opioid</b> receptor (OPRD1), cannabinoid receptor 1 (<strong>CNR1</strong>), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+CNR1	drug	cannabinoid	25258300	The <b>cannabinoid</b> receptor subtype 1 gene <strong>CNR1</strong> is not only associated with phenotypes such as cognitive performance, addiction and anxiety, but is also known to be crucially involved in responses to acute and chronic psychological and cellular stress conditions.
+CNR1	addiction	addiction	25258300	The cannabinoid receptor subtype 1 gene <strong>CNR1</strong> is not only associated with phenotypes such as cognitive performance, <b>addiction</b> and anxiety, but is also known to be crucially involved in responses to acute and chronic psychological and cellular stress conditions.
+CNR1	drug	opioid	25252306	[Association study of <strong>CNR1</strong>, GAD1 and BDNF polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan].
+CNR1	addiction	dependence	25252306	[Association study of <strong>CNR1</strong>, GAD1 and BDNF polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan].
+CNR1	drug	cannabinoid	25252306	In order to analyze the association of <strong>CNR1</strong>(<b>Cannabinoid</b> receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	drug	opioid	25252306	In order to analyze the association of <strong>CNR1</strong>(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	addiction	dependence	25252306	In order to analyze the association of <strong>CNR1</strong>(Cannabinoid receptor 1), GAD1(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+CNR1	drug	opioid	25252306	A case control study was performed with 8 SNPs from <strong>CNR1</strong>, GAD1, and BDNF genes in 165 <b>heroin</b> dependent males and 170 healthy males of the Dai population.
+CNR1	drug	opioid	25252306	Furthermore, polymorphisms in <strong>CNR1</strong> (rs1049353), GAD1 (rs1978340 and rs11542313), and BDNF (rs6265 and rs13306221) were associated with <b>heroin</b> dependence in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be <b>heroin</b> dependent.
+CNR1	addiction	dependence	25252306	Furthermore, polymorphisms in <strong>CNR1</strong> (rs1049353), GAD1 (rs1978340 and rs11542313), and BDNF (rs6265 and rs13306221) were associated with heroin <b>dependence</b> in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be heroin dependent.
+CNR1	drug	cannabinoid	24980155	Research investigating the impact of genetic variants in the <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) and of early rearing conditions has demonstrated that both factors contribute to the prediction of impulsivity related phenotypes.
+CNR1	drug	cannabinoid	24607771	F344 rats displayed higher levels of <b>cannabinoid</b> receptor binding in the lateral globus pallidus and weaker <strong>CNR1</strong> gene expression in the prefrontal cortex (PFc) than LEW rats.
+CNR1	drug	alcohol	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with <b>alcohol</b>, tobacco and/or cannabis consumption in young individuals (n = 91).
+CNR1	drug	cannabinoid	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, tobacco and/or <b>cannabis</b> consumption in young individuals (n = 91).
+CNR1	drug	nicotine	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the <strong>CNR1</strong> (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), ANKK1 (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, <b>tobacco</b> and/or cannabis consumption in young individuals (n = 91).
+CNR1	drug	cannabinoid	24152087	One of the single nucleotide polymorphisms (SNP) of the <strong>CNR1</strong> gene, which codes for <b>cannabinoid</b> receptor 1 (CB1R), is the rs2180619, located in a regulatory region of this gene (6q14 q15).
+CNR1	drug	alcohol	24060590	Therefore, we studied the expression of <strong>CNR1</strong> and CNR2, and the novel cannabinoid G protein coupled receptor (GPCR) 55 (GPR55) in human monocyte derived dendritic cells (MDDCs) from <b>alcohol</b> users.
+CNR1	drug	cannabinoid	24060590	Therefore, we studied the expression of <strong>CNR1</strong> and CNR2, and the novel <b>cannabinoid</b> G protein coupled receptor (GPCR) 55 (GPR55) in human monocyte derived dendritic cells (MDDCs) from alcohol users.
+CNR1	addiction	aversion	23227007	The influence of CB1 receptors on the <b>aversion</b> driven spatial learning in the Morris water maze test is strongly age dependent: mice with genetic deletion of CB1 receptors (<strong>Cnr1</strong>( / )) show superior learning when young but inferior learning when old compared to age matched wild type mice.
+CNR1	drug	cannabinoid	23190435	Participants with at least one copy of the minor allele for SNPs in synaptosomal associated protein 25 gene (SNAP25; rs363035 OR = 0.53; P = 0.005) and <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>; rs6454672 OR = 0.62; P = 0.022) have decreased likelihood of meeting PA recommendations.
+CNR1	drug	cannabinoid	22850347	MAPK14 and <strong>CNR1</strong> gene variant interactions: effects on brain volume deficits in schizophrenia patients with <b>marijuana</b> misuse.
+CNR1	drug	cannabinoid	22850347	We previously reported that <b>marijuana</b> misuse in conjunction with specific <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) genetic variants (rs12720071 G allele carriers) contributed to white matter (WM) brain volume deficits in schizophrenia patients.
+CNR1	drug	cannabinoid	22850347	In this study, we assessed the influence of another <b>cannabinoid</b> related gene, mitogen activated protein kinase 14 (MAPK14), and potential MAPK14 <strong>CNR1</strong> gene gene interactions in conferring brain volume abnormalities among schizophrenia patients with <b>marijuana</b> abuse/dependence.
+CNR1	addiction	dependence	22850347	In this study, we assessed the influence of another cannabinoid related gene, mitogen activated protein kinase 14 (MAPK14), and potential MAPK14 <strong>CNR1</strong> gene gene interactions in conferring brain volume abnormalities among schizophrenia patients with marijuana abuse/<b>dependence</b>.
+CNR1	drug	cannabinoid	22850347	There were significant main effects of the MAPK14 <strong>CNR1</strong> diplotype and diplotype × <b>marijuana</b> interaction on WM brain volumes, with both genetic variants having additive contributions to WM volume deficits only in patients with <b>marijuana</b> misuse.
+CNR1	drug	cannabinoid	22850347	Given that <strong>CNR1</strong> induced apoptosis is preceded by increased MAPK phosphorylation, our study suggests that potential MAPK14 <strong>CNR1</strong> gene gene interactions may mediate brain morphometric features in schizophrenia patients with heavy <b>marijuana</b> use.
+CNR1	drug	cannabinoid	22669173	Associations between <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) variation and hippocampus and amygdala volumes in heavy <b>cannabis</b> users.
+CNR1	drug	cannabinoid	22669173	A single nucleotide polymorphism in the <b>cannabis</b> receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced withdrawal, cue elicited craving, and parahippocampal activation to <b>cannabis</b> cues.
+CNR1	addiction	relapse	22669173	A single nucleotide polymorphism in the cannabis receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced withdrawal, cue elicited <b>craving</b>, and parahippocampal activation to cannabis cues.
+CNR1	addiction	withdrawal	22669173	A single nucleotide polymorphism in the cannabis receptor 1 gene (<strong>CNR1</strong>), rs2023239, has been associated with CD diagnosis and intermediate phenotypes, including abstinence induced <b>withdrawal</b>, cue elicited craving, and parahippocampal activation to cannabis cues.
+CNR1	drug	cannabinoid	22669173	These data replicate previous findings of reduced hippocampal and amygdalar volume among heavy <b>cannabis</b> users, and suggest that <strong>CNR1</strong> rs2023239 variation may predispose smaller hippocampal volume after heavy <b>cannabis</b> use.
+CNR1	drug	cannabinoid	22362764	Allele specific differences in activity of a novel <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene intronic enhancer in hypothalamus, dorsal root ganglia, and hippocampus.
+CNR1	drug	cannabinoid	22362764	Polymorphisms within intron 2 of the <strong>CNR1</strong> gene, which encodes <b>cannabinoid</b> receptor 1 (CB(1)), have been associated with addiction, obesity, and brain volume deficits.
+CNR1	addiction	addiction	22362764	Polymorphisms within intron 2 of the <strong>CNR1</strong> gene, which encodes cannabinoid receptor 1 (CB(1)), have been associated with <b>addiction</b>, obesity, and brain volume deficits.
+CNR1	drug	cannabinoid	22085192	Given the potential role of <b>endocannabinoid</b> system in AD, polymorphisms within <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) have been potentially associated with susceptibility to this disease.
+CNR1	drug	alcohol	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with dependence to <b>alcohol</b> and other substances and emphasizes the relevance of endocannabinoid system in AD.
+CNR1	drug	cannabinoid	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with dependence to alcohol and other substances and emphasizes the relevance of <b>endocannabinoid</b> system in AD.
+CNR1	addiction	dependence	22085192	Our findings support previously reported associations of <strong>CNR1</strong> with <b>dependence</b> to alcohol and other substances and emphasizes the relevance of endocannabinoid system in AD.
+CNR1	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], <strong>CNR1</strong> 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CNR1	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], <strong>CNR1</strong> 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CNR1	drug	cannabinoid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (OPRM1) or <b>cannabinoid</b> receptors (<strong>CNR1</strong>).
+CNR1	drug	nicotine	22046326	Overall, our results suggest that genetic variants potentially involved in <b>nicotine</b> metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with <b>smoking</b> related phenotypes, as opposed to genetic variants influencing the brain effects of <b>nicotine</b>, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), opioid (OPRM1) or cannabinoid receptors (<strong>CNR1</strong>).
+CNR1	drug	opioid	22046326	Overall, our results suggest that genetic variants potentially involved in nicotine metabolization (mainly, CYP2A6 polymorphisms) are those showing the strongest association with smoking related phenotypes, as opposed to genetic variants influencing the brain effects of nicotine, e.g., through nicotinic acetylcholine (CHRNA5), serotoninergic (HTR2A), <b>opioid</b> (OPRM1) or cannabinoid receptors (<strong>CNR1</strong>).
+CNR1	drug	cannabinoid	21937688	The <b>cannabinoid</b> receptor (<strong>CNR1</strong>) and the fatty acid amide hydrolase (FAAH) genes are located on chromosomes 6 and 1 in the 6q15 and 1p33 cytogenetic bands, respectively.
+CNR1	addiction	addiction	21937688	However, many works have repeatedly associated polymorphisms in the <strong>CNR1</strong> and FAAH genes with drug related behaviours; this suggests that these genes should be examined in further genetic studies focusing on drug <b>addiction</b> and other psychiatric disorders.
+CNR1	drug	amphetamine	21886587	Association Study of Two Cannabinoid Receptor Genes, <strong>CNR1</strong> and CNR2, with <b>Methamphetamine</b> Dependence.
+CNR1	drug	cannabinoid	21886587	Association Study of Two <b>Cannabinoid</b> Receptor Genes, <strong>CNR1</strong> and CNR2, with Methamphetamine Dependence.
+CNR1	addiction	dependence	21886587	Association Study of Two Cannabinoid Receptor Genes, <strong>CNR1</strong> and CNR2, with Methamphetamine <b>Dependence</b>.
+CNR1	drug	amphetamine	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode cannabinoid receptors CB1 and CB2, with <b>methamphetamine</b> dependence, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+CNR1	drug	cannabinoid	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode <b>cannabinoid</b> receptors CB1 and CB2, with methamphetamine dependence, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+CNR1	addiction	dependence	21886587	To examine the possible association of the <strong>CNR1</strong> and CNR2 genes, which encode cannabinoid receptors CB1 and CB2, with methamphetamine <b>dependence</b>, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the <strong>CNR1</strong> gene and a nonsynonymous SNP, Q63R, in the CNR2 gene.
+CNR1	drug	amphetamine	21886587	Rs806379 of the <strong>CNR1</strong> gene showed a significant association with the phenotype of latency of psychosis after the first consumption of <b>methamphetamine</b>.
+CNR1	drug	amphetamine	21886587	The present study suggests a possibility that genetic variants of the <strong>CNR1</strong> gene may produce a liability to the complication of psychotic state after abuse of <b>methamphetamine</b>; however, our findings need to be confirmed by future replications.
+CNR1	drug	cannabinoid	21808284	rs806365 in <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) had a significant male specific gene treatment interaction at 6 month follow up (adjusted P = 3.9 × 10( 5)); within males using nasal spray, rs806365 was associated with a decrease in odds of abstinence (OR = 0.04; 95% CI: 0.01 0.2).
+CNR1	drug	nicotine	21808284	While the role of <strong>CNR1</strong> in substance abuse has been well studied, we report EPB41 for the first time in the <b>nicotine</b> literature.
+CNR1	drug	cocaine	21790903	Further evidence for association of polymorphisms in the <strong>CNR1</strong> gene with <b>cocaine</b> addiction: confirmation in an independent sample and meta analysis.
+CNR1	addiction	addiction	21790903	Further evidence for association of polymorphisms in the <strong>CNR1</strong> gene with cocaine <b>addiction</b>: confirmation in an independent sample and meta analysis.
+CNR1	drug	cannabinoid	21790903	The <b>cannabinoid</b> receptor 1 protein regulates both the <b>endocannabinoid</b> and dopaminergic neurobiological systems, and polymorphisms in the <b>cannabinoid</b> receptor gene, <strong>CNR1</strong>, have been associated previously with substance dependence.
+CNR1	addiction	dependence	21790903	The cannabinoid receptor 1 protein regulates both the endocannabinoid and dopaminergic neurobiological systems, and polymorphisms in the cannabinoid receptor gene, <strong>CNR1</strong>, have been associated previously with substance <b>dependence</b>.
+CNR1	drug	cocaine	21790903	<b>Cocaine</b> addicted individuals (n=860) and unaffected controls (n=334) of African descent were genotyped for two single nucleotide polymorphisms (SNPs) in <strong>CNR1</strong> (rs6454674, rs806368).
+CNR1	drug	cocaine	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance dependence or are specific to <b>cocaine</b> addiction.
+CNR1	addiction	addiction	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance dependence or are specific to cocaine <b>addiction</b>.
+CNR1	addiction	dependence	21790903	However, because there is considerable co morbidity of CD with other drugs of abuse, additional studies are necessary to determine whether polymorphisms in <strong>CNR1</strong> induce a general susceptibility to substance <b>dependence</b> or are specific to cocaine addiction.
+CNR1	drug	cocaine	21785434	We found that systemic, intranasal or intra accumbens local administration of JWH133, a selective CB(2) receptor agonist, dose dependently inhibited intravenous <b>cocaine</b> self administration, <b>cocaine</b> enhanced locomotion, and <b>cocaine</b> enhanced accumbens extracellular dopamine in wild type and CB(1) receptor knockout (CB(1)( / ), also known as <strong>Cnr1</strong>( / )) mice, but not in CB(2)( / ) (Cnr2( / )) mice.
+CNR1	drug	cannabinoid	21714860	Variation in the human <b>cannabinoid</b> receptor <strong>CNR1</strong> gene modulates gaze duration for happy faces.
+CNR1	drug	cannabinoid	21714860	In this study, we tested whether variations in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene are associated with gaze duration towards happy faces.
+CNR1	drug	cannabinoid	21714860	This gene was selected because <strong>CNR1</strong> is a key component of the <b>endocannabinoid</b> system, which is involved in processing reward, and in our previous functional magnetic resonance imaging (fMRI) study, we found that variations in <strong>CNR1</strong> modulate the striatal response to happy (but not disgust) faces.
+CNR1	addiction	reward	21714860	This gene was selected because <strong>CNR1</strong> is a key component of the endocannabinoid system, which is involved in processing <b>reward</b>, and in our previous functional magnetic resonance imaging (fMRI) study, we found that variations in <strong>CNR1</strong> modulate the striatal response to happy (but not disgust) faces.
+CNR1	addiction	reward	21714860	These results suggest that <strong>CNR1</strong> variations modulate the striatal function that underlies the perception of signals of social <b>reward</b>, such as happy faces.
+CNR1	drug	cannabinoid	21513772	Association between a <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism and <b>cannabinoid</b> induced alterations of the auditory event related P300 potential.
+CNR1	drug	cannabinoid	21513772	Recently, an (AAT)n triplet repeat polymorphism within the <b>cannabinoid</b> receptor gene <strong>CNR1</strong> has been found to be associated with both schizophrenia and substance dependence, and to modulate the P300 potential.
+CNR1	addiction	dependence	21513772	Recently, an (AAT)n triplet repeat polymorphism within the cannabinoid receptor gene <strong>CNR1</strong> has been found to be associated with both schizophrenia and substance <b>dependence</b>, and to modulate the P300 potential.
+CNR1	drug	cannabinoid	21513772	Moreover, it appears that variations within <strong>CNR1</strong> may differentially alter the sensitivity to the acute effects of <b>cannabinoids</b> on P300 generation in healthy subjects.
+CNR1	drug	cannabinoid	21497918	We summarize <b>endocannabinoid</b> signaling in pathways related to anxiety and depression, identify the serotonergic system as the most likely candidate to mediate the side effects of CB₁ receptor antagonists, and propose that poloymorphisms in <strong>CNR1</strong>, SLC6A4 and certain CYP 450 enzymes could help to identify individuals who may benefit from treatment with CB₁ receptor antagonist without psychiatric side effects.
+CNR1	drug	cannabinoid	21420833	<b>Cannabinoid</b> receptor 1 (CB1/<strong>CNR1</strong>) is the principal brain receptor mediating <b>marijuana</b> effects.
+CNR1	drug	cannabinoid	21420833	No study to date has systematically investigated the impact of <strong>CNR1</strong> on quantitative phenotypic features in schizophrenia and inter relationships with <b>marijuana</b> misuse.
+CNR1	drug	alcohol	21420833	Effects of <strong>CNR1</strong> tSNPs and marijuana abuse/dependence on brain volumes and neurocognition were assessed using ANCOVA, including co morbid <b>alcohol</b>/non marijuana illicit drug misuse as covariates.
+CNR1	drug	cannabinoid	21420833	Effects of <strong>CNR1</strong> tSNPs and <b>marijuana</b> abuse/dependence on brain volumes and neurocognition were assessed using ANCOVA, including co morbid alcohol/non <b>marijuana</b> illicit drug misuse as covariates.
+CNR1	addiction	dependence	21420833	Effects of <strong>CNR1</strong> tSNPs and marijuana abuse/<b>dependence</b> on brain volumes and neurocognition were assessed using ANCOVA, including co morbid alcohol/non marijuana illicit drug misuse as covariates.
+CNR1	drug	cannabinoid	21420833	Our findings suggest that heavy <b>cannabis</b> use in the context of specific <strong>CNR1</strong> genotypes may contribute to greater WM volume deficits and cognitive impairment, which could in turn increase schizophrenia risk.
+CNR1	drug	cannabinoid	21341382	In M. mulatta, the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) mRNA was expressed in the all tissues; in contrast, the <b>cannabinoid</b> receptor 2 (CNR2) mRNA was only present in the spleen.
+CNR1	drug	alcohol	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in <b>ethanol</b>'s reinforcing and addictive properties prompted us to study the levels and distribution of CB1R after chronic <b>ethanol</b> intake, in the presence and absence of DRD2.
+CNR1	drug	cannabinoid	20958329	The anatomical proximity of the <b>cannabinoid</b> type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and addictive properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	addiction	addiction	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's reinforcing and <b>addictive</b> properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	addiction	reward	20958329	The anatomical proximity of the cannabinoid type 1 (<strong>CNR1</strong>/CB1R) and the dopamine D2 receptors (DRD2), their ability to form CB1R DRD2 heteromers, their opposing roles in locomotion, and their involvement in ethanol's <b>reinforcing</b> and addictive properties prompted us to study the levels and distribution of CB1R after chronic ethanol intake, in the presence and absence of DRD2.
+CNR1	addiction	addiction	20192949	<strong>CNR1</strong> gene polymorphisms in <b>addictive</b> disorders: a systematic review and a meta analysis.
+CNR1	drug	cannabinoid	20192949	The aim of the present work was to systematically review all association studies of <b>cannabis</b> receptor 1 (<strong>CNR1</strong>) polymorphisms with dependence syndrome and to perform a meta analysis.
+CNR1	addiction	dependence	20192949	The aim of the present work was to systematically review all association studies of cannabis receptor 1 (<strong>CNR1</strong>) polymorphisms with <b>dependence</b> syndrome and to perform a meta analysis.
+CNR1	addiction	dependence	20192949	In line with the polygenic model, our meta analysis supports a minor implication for <strong>CNR1</strong> AAT polymorphism in illicit substance <b>dependence</b> vulnerability.
+CNR1	drug	cannabinoid	20010914	Association of polymorphisms of the <b>cannabinoid</b> receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with heroin addiction: impact of long repeats of <strong>CNR1</strong>.
+CNR1	drug	opioid	20010914	Association of polymorphisms of the cannabinoid receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with <b>heroin</b> addiction: impact of long repeats of <strong>CNR1</strong>.
+CNR1	addiction	addiction	20010914	Association of polymorphisms of the cannabinoid receptor (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with heroin <b>addiction</b>: impact of long repeats of <strong>CNR1</strong>.
+CNR1	drug	cannabinoid	20010914	Alterations in expression of a <b>cannabinoid</b> receptor (<strong>CNR1</strong>, CB1), and of fatty acid amide hydrolase (FAAH) that degrades endogenous ligands of CB1, may contribute to the development of addiction.
+CNR1	addiction	addiction	20010914	Alterations in expression of a cannabinoid receptor (<strong>CNR1</strong>, CB1), and of fatty acid amide hydrolase (FAAH) that degrades endogenous ligands of CB1, may contribute to the development of <b>addiction</b>.
+CNR1	drug	opioid	20010914	The 385C>A in the FAAH gene and six polymorphisms of <strong>CNR1</strong> were genotyped in former <b>heroin</b> addicts and control subjects (247 Caucasians, 161 Hispanics, 179 African Americans and 19 Asians).
+CNR1	drug	cannabinoid	20010552	Individual and additive effects of the <strong>CNR1</strong> and FAAH genes on brain response to <b>marijuana</b> cues.
+CNR1	drug	cannabinoid	20010552	As previous work has highlighted the significance of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with respect to <b>cannabis</b> dependence (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+CNR1	addiction	dependence	20010552	As previous work has highlighted the significance of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes with respect to cannabis <b>dependence</b> (CD), this study sought to characterize the neural mechanisms that underlie these genetic effects.
+CNR1	drug	cannabinoid	20010552	Between group comparisons showed that carriers of the <strong>CNR1</strong> rs2023239 G allele had significantly greater activity in reward related areas of the brain, such as the orbitofrontal cortex (OFC), inferior frontal gyrus (IFG), and anterior cingulate gyrus (ACG), during exposure to <b>marijuana</b> cues, as compared with those with the A/A genotype for this SNP.
+CNR1	addiction	reward	20010552	Between group comparisons showed that carriers of the <strong>CNR1</strong> rs2023239 G allele had significantly greater activity in <b>reward</b> related areas of the brain, such as the orbitofrontal cortex (OFC), inferior frontal gyrus (IFG), and anterior cingulate gyrus (ACG), during exposure to marijuana cues, as compared with those with the A/A genotype for this SNP.
+CNR1	drug	cannabinoid	20010552	These findings are in accord with earlier reported associations between <strong>CNR1</strong> and FAAH and CD intermediate phenotypes, and suggest that the underlying mechanism of these genetic effects may be enhanced neural response in reward areas of the brain in carriers of the <strong>CNR1</strong> G allele and FAAH C/C genotype in response to <b>marijuana</b> cues.
+CNR1	addiction	reward	20010552	These findings are in accord with earlier reported associations between <strong>CNR1</strong> and FAAH and CD intermediate phenotypes, and suggest that the underlying mechanism of these genetic effects may be enhanced neural response in <b>reward</b> areas of the brain in carriers of the <strong>CNR1</strong> G allele and FAAH C/C genotype in response to marijuana cues.
+CNR1	drug	cannabinoid	19886064	The implication of <strong>CNR1</strong> gene's polymorphisms in the modulation of <b>endocannabinoid</b> system effects.
+CNR1	drug	cannabinoid	19886064	It is composed of <b>cannabinoid</b> receptors CB1 and CB2, and their genes (<strong>CNR1</strong> and CNR2), their endogenous ligands and the enzymes which mediate endogenous ligands' biosynthesis and degradation.
+CNR1	drug	cannabinoid	19443135	The association between <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) and <b>cannabis</b> dependence symptoms in adolescents and young adults.
+CNR1	addiction	dependence	19443135	The association between cannabinoid receptor 1 gene (<strong>CNR1</strong>) and cannabis <b>dependence</b> symptoms in adolescents and young adults.
+CNR1	drug	cannabinoid	19443135	This study examined the genetic association between variation in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene and <b>cannabis</b> dependence symptoms.
+CNR1	addiction	dependence	19443135	This study examined the genetic association between variation in the cannabinoid receptor 1 (<strong>CNR1</strong>) gene and cannabis <b>dependence</b> symptoms.
+CNR1	drug	cannabinoid	19443135	Additional family based studies are needed to clarify the role of the <strong>CNR1</strong> gene, and its various SNPs, in the development of <b>cannabis</b> use disorders.
+CNR1	drug	cannabinoid	19335651	Gene association studies are presented for (a) genes posited to have specific influences on <b>cannabis</b> use disorders: <strong>CNR1</strong>, CB2, FAAH, MGLL, TRPV1 and GPR55 and (b) genes from various neurotransmitter systems that are likely to exert a non specific influence on risk of <b>cannabis</b> use disorders, e.g.
+CNR1	drug	cocaine	19052543	Interaction between two independent <strong>CNR1</strong> variants increases risk for <b>cocaine</b> dependence in European Americans: a replication study in family based sample and population based sample.
+CNR1	addiction	dependence	19052543	Interaction between two independent <strong>CNR1</strong> variants increases risk for cocaine <b>dependence</b> in European Americans: a replication study in family based sample and population based sample.
+CNR1	drug	cannabinoid	19052543	We recently reported that, in a European American (EA) sample, the interaction between two <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug dependence (DD), including cocaine dependence (CD).
+CNR1	drug	cocaine	19052543	We recently reported that, in a European American (EA) sample, the interaction between two cannabinoid receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug dependence (DD), including <b>cocaine</b> dependence (CD).
+CNR1	addiction	dependence	19052543	We recently reported that, in a European American (EA) sample, the interaction between two cannabinoid receptor 1 gene (<strong>CNR1</strong>) variants significantly increased risk for drug <b>dependence</b> (DD), including cocaine <b>dependence</b> (CD).
+CNR1	drug	cannabinoid	19016476	Evidence for association between polymorphisms in the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene and <b>cannabis</b> dependence.
+CNR1	addiction	dependence	19016476	Evidence for association between polymorphisms in the cannabinoid receptor 1 (<strong>CNR1</strong>) gene and cannabis <b>dependence</b>.
+CNR1	drug	cannabinoid	19016476	The <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) on chromosome 6q14 15 is an excellent candidate gene for <b>cannabis</b> dependence due to the important role of the G protein coupled receptor encoded by this gene in the rewarding effects of Delta9 <b>tetrahydrocannabinol</b>.
+CNR1	addiction	dependence	19016476	The cannabinoid receptor 1 gene (<strong>CNR1</strong>) on chromosome 6q14 15 is an excellent candidate gene for cannabis <b>dependence</b> due to the important role of the G protein coupled receptor encoded by this gene in the rewarding effects of Delta9 tetrahydrocannabinol.
+CNR1	drug	cannabinoid	19016476	We investigate the association between 9 SNPs spanning <strong>CNR1</strong> and <b>cannabis</b> dependence in 1,923 individuals.
+CNR1	addiction	dependence	19016476	We investigate the association between 9 SNPs spanning <strong>CNR1</strong> and cannabis <b>dependence</b> in 1,923 individuals.
+CNR1	drug	alcohol	18977415	These <b>alcohol</b> related behaviors are linked to differential changes in <strong>CNR1</strong> and NR1 subunit mRNA transcripts.
+CNR1	drug	cannabinoid	18977415	In conclusion, pharmacological inactivation of the glycine binding site of NMDA receptors may control <b>cannabinoid</b> induced relapse like drinking, which is associated with altered expression of <strong>CNR1</strong> and NR1 gene expression as observed after WIN treatment.
+CNR1	addiction	relapse	18977415	In conclusion, pharmacological inactivation of the glycine binding site of NMDA receptors may control cannabinoid induced <b>relapse</b> like drinking, which is associated with altered expression of <strong>CNR1</strong> and NR1 gene expression as observed after WIN treatment.
+CNR1	drug	cannabinoid	18705688	<b>Marijuana</b> withdrawal and craving: influence of the <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	addiction	relapse	18705688	Marijuana withdrawal and <b>craving</b>: influence of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	addiction	withdrawal	18705688	Marijuana <b>withdrawal</b> and craving: influence of the cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH) genes.
+CNR1	drug	cannabinoid	18705688	To examine whether withdrawal after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the <b>endocannabinoid</b> system, <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	addiction	relapse	18705688	To examine whether withdrawal after abstinence and cue elicited <b>craving</b> were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	addiction	withdrawal	18705688	To examine whether <b>withdrawal</b> after abstinence and cue elicited craving were associated with polymorphisms within two genes involved in regulating the endocannabinoid system, cannabinoid receptor 1 (<strong>CNR1</strong>) and fatty acid amide hydrolase (FAAH).
+CNR1	drug	cannabinoid	18705688	Two single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> (rs2023239) and FAAH (rs324420) genes, associated previously with substance abuse and functional changes in <b>cannabinoid</b> regulation, were examined in a sample of daily <b>marijuana</b> smokers.
+CNR1	drug	nicotine	18705688	Two single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> (rs2023239) and FAAH (rs324420) genes, associated previously with substance abuse and functional changes in cannabinoid regulation, were examined in a sample of daily marijuana <b>smokers</b>.
+CNR1	addiction	relapse	18705688	The <strong>CNR1</strong> SNP displayed a significant abstinence x genotype interaction on withdrawal, as well as a main effect on overall levels of <b>craving</b>, while the FAAH SNP displayed a significant abstinence x genotype interaction on <b>craving</b>.
+CNR1	addiction	withdrawal	18705688	The <strong>CNR1</strong> SNP displayed a significant abstinence x genotype interaction on <b>withdrawal</b>, as well as a main effect on overall levels of craving, while the FAAH SNP displayed a significant abstinence x genotype interaction on craving.
+CNR1	drug	alcohol	18606956	The incentive salience of <b>alcohol</b>: translating the effects of genetic variant in <strong>CNR1</strong>.
+CNR1	addiction	reward	18606956	The <b>incentive</b> salience of alcohol: translating the effects of genetic variant in <strong>CNR1</strong>.
+CNR1	drug	alcohol	18606956	The gene that codes for cannabinoid receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of <b>alcohol</b> dependence.
+CNR1	drug	cannabinoid	18606956	The gene that codes for <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of alcohol dependence.
+CNR1	addiction	dependence	18606956	The gene that codes for cannabinoid receptor 1 (<strong>CNR1</strong>) represents an important target for investigations designed to elucidate individual differences in the etiology of alcohol <b>dependence</b>.
+CNR1	drug	alcohol	18606956	To achieve a better understanding of the role of the <strong>CNR1</strong> gene in the etiology and treatment of <b>alcohol</b> dependence.
+CNR1	addiction	dependence	18606956	To achieve a better understanding of the role of the <strong>CNR1</strong> gene in the etiology and treatment of alcohol <b>dependence</b>.
+CNR1	drug	cannabinoid	18606954	The <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene is 1 of the 2 receptors expressed in the brain.
+CNR1	drug	nicotine	18606954	To test the hypothesis that the <strong>CNR1</strong> gene is associated with <b>nicotine</b> dependence.
+CNR1	addiction	dependence	18606954	To test the hypothesis that the <strong>CNR1</strong> gene is associated with nicotine <b>dependence</b>.
+CNR1	drug	nicotine	18606954	Variants and haplotypes in the <strong>CNR1</strong> gene may alter the risk for <b>nicotine</b> dependence, and the associations are likely sex specific.
+CNR1	addiction	dependence	18606954	Variants and haplotypes in the <strong>CNR1</strong> gene may alter the risk for nicotine <b>dependence</b>, and the associations are likely sex specific.
+CNR1	drug	cannabinoid	18579347	<b>Cannabinoid</b> receptor 1 (<strong>CNR1</strong>) gene: impact on antidepressant treatment response and emotion processing in major depression.
+CNR1	drug	cannabinoid	18579347	Therefore, the impact of <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) variants rs1049353 and rs12720071 on antidepressant treatment response was evaluated in 256 Caucasian patients with Major Depression.
+CNR1	addiction	reward	18579347	This analysis provides preliminary support for a role of <strong>CNR1</strong> gene variation in depression and anxiety, potentially mediated by subcortical hypo responsiveness to social <b>reward</b> stimuli.
+CNR1	drug	cannabinoid	18519829	For DSM IV <b>cannabis</b> dependence, a modest LOD score on chromosome 6 (1.42) near <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) was identified.
+CNR1	addiction	dependence	18519829	For DSM IV cannabis <b>dependence</b>, a modest LOD score on chromosome 6 (1.42) near cannabinoid receptor 1 (<strong>CNR1</strong>) was identified.
+CNR1	drug	cannabinoid	18519829	Genes such as ELTD1 on chromosome 1, in addition to genes on chromosomes 4 (eg, GABRA2) and 6 (eg, <strong>CNR1</strong>), may be associated with the genetic risk for <b>cannabis</b> use disorders.
+CNR1	drug	cannabinoid	17945506	Human studies show that <b>marijuana</b> dependence is frequently associated with cocaine dependence, and that the <b>cannabinoid</b> receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine addiction.
+CNR1	drug	cocaine	17945506	Human studies show that marijuana dependence is frequently associated with <b>cocaine</b> dependence, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to <b>cocaine</b> addiction.
+CNR1	addiction	addiction	17945506	Human studies show that marijuana dependence is frequently associated with cocaine dependence, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine <b>addiction</b>.
+CNR1	addiction	dependence	17945506	Human studies show that marijuana <b>dependence</b> is frequently associated with cocaine <b>dependence</b>, and that the cannabinoid receptor <strong>CNR1</strong> gene polymorphism might be related to cocaine addiction.
+CNR1	drug	alcohol	17509535	<strong>CNR1</strong> variation modulates risk for drug and <b>alcohol</b> dependence.
+CNR1	addiction	dependence	17509535	<strong>CNR1</strong> variation modulates risk for drug and alcohol <b>dependence</b>.
+CNR1	drug	cannabinoid	17509535	Human <b>cannabinoid</b> receptor 1 (CB1), which is encoded by the <strong>CNR1</strong> gene, may play a role in the development of substance dependence (SD).
+CNR1	addiction	dependence	17509535	Human cannabinoid receptor 1 (CB1), which is encoded by the <strong>CNR1</strong> gene, may play a role in the development of substance <b>dependence</b> (SD).
+CNR1	drug	alcohol	17508995	Polymorphisms of the dopamine D4 receptor gene (DRD4 VNTR) and cannabinoid CB1 receptor gene (<strong>CNR1</strong>) are not strongly related to cue reactivity after <b>alcohol</b> exposure.
+CNR1	drug	cannabinoid	17508995	Polymorphisms of the dopamine D4 receptor gene (DRD4 VNTR) and <b>cannabinoid</b> CB1 receptor gene (<strong>CNR1</strong>) are not strongly related to cue reactivity after alcohol exposure.
+CNR1	drug	alcohol	17508995	Polymorphisms in the D4 dopamine receptor gene (DRD4) and the CB1 cannabinoid receptor gene (<strong>CNR1</strong>) have been associated with a differential response to <b>alcohol</b> after consumption.
+CNR1	drug	cannabinoid	17508995	Polymorphisms in the D4 dopamine receptor gene (DRD4) and the CB1 <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) have been associated with a differential response to alcohol after consumption.
+CNR1	drug	alcohol	17508995	As weekly <b>alcohol</b> consumption increased, the <strong>CNR1</strong> C allele group tended to report more craving for <b>alcohol</b> during the <b>alcohol</b> exposure than the T allele group.
+CNR1	addiction	relapse	17508995	As weekly alcohol consumption increased, the <strong>CNR1</strong> C allele group tended to report more <b>craving</b> for alcohol during the alcohol exposure than the T allele group.
+CNR1	drug	alcohol	17508995	The DRD4 and <strong>CNR1</strong> polymorphisms do not appear to strongly moderate cue reactivity after <b>alcohol</b> cue exposure, in male heavy drinkers.
+CNR1	drug	cannabinoid	17401783	[<b>Endocannabinoid</b> system and <strong>CNR1</strong> gene polymorphisms in schizophrenia and addictive disorders].
+CNR1	addiction	addiction	17401783	[Endocannabinoid system and <strong>CNR1</strong> gene polymorphisms in schizophrenia and <b>addictive</b> disorders].
+CNR1	drug	cannabinoid	16917946	<b>Cannabis</b> is a major substance of abuse, and the gene encoding for the central <b>cannabinoid</b> receptor (<strong>CNR1</strong>) is a logical candidate gene for vulnerability toward developing symptoms of <b>cannabis</b> dependence.
+CNR1	addiction	dependence	16917946	Cannabis is a major substance of abuse, and the gene encoding for the central cannabinoid receptor (<strong>CNR1</strong>) is a logical candidate gene for vulnerability toward developing symptoms of cannabis <b>dependence</b>.
+CNR1	drug	cannabinoid	16917946	We studied four single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> gene for association with having one or more symptoms of <b>cannabis</b> dependence in 541 adolescent subjects who had all tried <b>cannabis</b> five or more times.
+CNR1	addiction	dependence	16917946	We studied four single nucleotide polymorphisms (SNPs) in the <strong>CNR1</strong> gene for association with having one or more symptoms of cannabis <b>dependence</b> in 541 adolescent subjects who had all tried cannabis five or more times.
+CNR1	drug	cannabinoid	16917946	Univariate (single marker) association tests demonstrated that SNP rs806380, located in intron 2 of the <strong>CNR1</strong> gene, was significantly associated with developing one or more <b>cannabis</b> dependence symptoms, with the G allele having a protective effect (P < 0.02).
+CNR1	addiction	dependence	16917946	Univariate (single marker) association tests demonstrated that SNP rs806380, located in intron 2 of the <strong>CNR1</strong> gene, was significantly associated with developing one or more cannabis <b>dependence</b> symptoms, with the G allele having a protective effect (P < 0.02).
+CNR1	drug	cannabinoid	16917946	Our findings provide evidence suggesting that a common <strong>CNR1</strong> haplotype is associated with developing fewer <b>cannabis</b> dependence symptoms among adolescents who have experimented with <b>cannabis</b>.
+CNR1	addiction	dependence	16917946	Our findings provide evidence suggesting that a common <strong>CNR1</strong> haplotype is associated with developing fewer cannabis <b>dependence</b> symptoms among adolescents who have experimented with cannabis.
+CNR1	drug	cannabinoid	16788767	(AAT)n repeat in the <b>cannabinoid</b> receptor gene, <strong>CNR1</strong>: association with schizophrenia in a Spanish population.
+CNR1	drug	cannabinoid	16788767	The <b>cannabinoid</b> receptor 1 gene (<strong>CNR1</strong>) has been associated with addictive disorders and schizophrenia in different studies.
+CNR1	addiction	addiction	16788767	The cannabinoid receptor 1 gene (<strong>CNR1</strong>) has been associated with <b>addictive</b> disorders and schizophrenia in different studies.
+CNR1	addiction	dependence	16741937	Association study of the <strong>CNR1</strong> gene exon 3 alternative promoter region polymorphisms and substance <b>dependence</b>.
+CNR1	drug	cannabinoid	16741937	An alternative promoter producing a novel 5' untranslated region of <b>cannabinoid</b> receptor mRNA has recently been described in <strong>CNR1</strong>, the gene encoding the <b>cannabinoid</b> receptor protein.
+CNR1	drug	alcohol	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., <b>alcohol</b>, cocaine, and opioids), as well as with polysubstance dependence.
+CNR1	drug	cocaine	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., alcohol, <b>cocaine</b>, and opioids), as well as with polysubstance dependence.
+CNR1	drug	opioid	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance dependence diagnoses (i.e., alcohol, cocaine, and <b>opioids</b>), as well as with polysubstance dependence.
+CNR1	addiction	dependence	16741937	We examined the association of 4 SNPs (rs6928499, rs806379, rs1535255, rs2023239) in the distal region of intron 2 of <strong>CNR1</strong> both with individual substance <b>dependence</b> diagnoses (i.e., alcohol, cocaine, and opioids), as well as with polysubstance <b>dependence</b>.
+CNR1	drug	cannabinoid	16623851	Variations in the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene modulate striatal responses to happy faces.
+CNR1	drug	cannabinoid	16623851	The <b>cannabinoid</b> receptor 1 (<strong>CNR1</strong>) is the best characterized molecule of the <b>endocannabinoid</b> system, involved in processing rewards.
+CNR1	addiction	reward	16623851	This suggests a role for the variations of the <strong>CNR1</strong> gene in underlying social <b>reward</b> responsivity.
+CNR1	drug	cannabinoid	16314880	(AAT)n repeat in the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>): association with cocaine addiction in an African Caribbean population.
+CNR1	drug	cocaine	16314880	(AAT)n repeat in the cannabinoid receptor gene (<strong>CNR1</strong>): association with <b>cocaine</b> addiction in an African Caribbean population.
+CNR1	addiction	addiction	16314880	(AAT)n repeat in the cannabinoid receptor gene (<strong>CNR1</strong>): association with cocaine <b>addiction</b> in an African Caribbean population.
+CNR1	drug	cannabinoid	16314880	We examined the (AAT)n triplet repeat polymorphism nearby the <strong>CNR1</strong> gene, which encodes human <b>cannabinoid</b> (CB1) receptor, in a male Afro Caribbean population.
+CNR1	drug	cocaine	16314880	Our results support that the (AAT)n polymorphism nearby the <strong>CNR1</strong> gene could be associated with predisposition to <b>cocaine</b> dependency.
+CNR1	addiction	addiction	15289816	A number of lines of evidence make the gene that encodes the G protein coupled CB1/<strong>Cnr1</strong> receptor a strong candidate to harbor variants that might contribute to individual differences in human <b>addiction</b> vulnerability.
+CNR1	drug	cannabinoid	15289816	The CB1/<strong>Cnr1</strong> receptor is the major brain site at which <b>cannabinoid</b> <b>marijuana</b> constituents are psychoactive as well as the principal brain receptor for endogenous anandamide ligands.
+CNR1	addiction	addiction	15289816	CB1/ <strong>Cnr1</strong> genomic variation thus appears to play roles in human <b>addiction</b> vulnerability.
+CNR1	drug	alcohol	14714115	The aim of this study is to test the potential influence of a bi allelic cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe <b>alcohol</b> withdrawal syndromes.
+CNR1	drug	cannabinoid	14714115	The aim of this study is to test the potential influence of a bi allelic <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe alcohol withdrawal syndromes.
+CNR1	addiction	withdrawal	14714115	The aim of this study is to test the potential influence of a bi allelic cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism (G1359A) on severe alcohol <b>withdrawal</b> syndromes.
+CNR1	drug	alcohol	14714115	After correcting for multiple testing, no association of the A  or G allele of <strong>CNR1</strong> polymorphism with a history of <b>alcohol</b> withdrawal induced seizures was detected.
+CNR1	addiction	withdrawal	14714115	After correcting for multiple testing, no association of the A  or G allele of <strong>CNR1</strong> polymorphism with a history of alcohol <b>withdrawal</b> induced seizures was detected.
+CNR1	drug	alcohol	12657705	Furthermore, foot shock stress had no affect on <b>alcohol</b> preference in <strong>Cnr1</strong> /  mice, although it induced a dramatic increase in <strong>Cnr1</strong>+/+ animals.
+CNR1	drug	alcohol	11841893	Association of a CB1 cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism with severe <b>alcohol</b> dependence.
+CNR1	drug	cannabinoid	11841893	Association of a CB1 <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) polymorphism with severe alcohol dependence.
+CNR1	addiction	dependence	11841893	Association of a CB1 cannabinoid receptor gene (<strong>CNR1</strong>) polymorphism with severe alcohol <b>dependence</b>.
+CNR1	drug	alcohol	11841893	Due to the involvement of the endogenous cannabinoid system in brain reward mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human cannabinoid receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian <b>alcoholics</b> and 136 most likely non <b>alcoholic</b> controls.
+CNR1	drug	cannabinoid	11841893	Due to the involvement of the endogenous <b>cannabinoid</b> system in brain reward mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian alcoholics and 136 most likely non alcoholic controls.
+CNR1	addiction	reward	11841893	Due to the involvement of the endogenous cannabinoid system in brain <b>reward</b> mechanisms a silent polymorphism (1359G/A; Thr453Thr) in the single coding exon of the CB1 human cannabinoid receptor gene (<strong>CNR1</strong>) was analysed in 121 severely affected Caucasian alcoholics and 136 most likely non alcoholic controls.
+CNR1	drug	alcohol	11841893	This finding suggests that the homozygous genotype <strong>CNR1</strong> 1359A/A confers vulnerability to <b>alcohol</b> withdrawal delirium.
+CNR1	addiction	withdrawal	11841893	This finding suggests that the homozygous genotype <strong>CNR1</strong> 1359A/A confers vulnerability to alcohol <b>withdrawal</b> delirium.
+CNR1	drug	cannabinoid	11526463	Association study of <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) alleles and drug dependence.
+CNR1	addiction	dependence	11526463	Association study of cannabinoid receptor gene (<strong>CNR1</strong>) alleles and drug <b>dependence</b>.
+CNR1	drug	cannabinoid	11341859	The <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) is not affected in German i.v.
+CNR1	drug	cannabinoid	11341859	The aim of the study was to investigate a possible contribution of the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) to the development of i.v.
+CNR1	drug	cannabinoid	10441206	A frequent polymorphism in the coding exon of the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene.
+CNR1	drug	cannabinoid	10441206	The cloning of the human <b>cannabinoid</b> receptor (<strong>CNR1</strong>) gene facilitates molecular genetic studies in disorders like Gilles de la Tourette syndrome (GTS), obsessive compulsive disorder (OCD), Parkinsons disease, Alzheimers disease or other neuro psychiatric or neurological diseases, which may be predisposed or influenced by mutations or variants in the <strong>CNR1</strong> gene.
+CNR1	addiction	addiction	10441206	The cloning of the human cannabinoid receptor (<strong>CNR1</strong>) gene facilitates molecular genetic studies in disorders like Gilles de la Tourette syndrome (GTS), obsessive <b>compulsive</b> disorder (OCD), Parkinsons disease, Alzheimers disease or other neuro psychiatric or neurological diseases, which may be predisposed or influenced by mutations or variants in the <strong>CNR1</strong> gene.
+CNR1	drug	cannabinoid	9106243	Association between the <b>cannabinoid</b> receptor gene (<strong>CNR1</strong>) and the P300 event related potential.
+CNR1	drug	cannabinoid	9106243	In our prior study we observed a significant association between homozygosity for the > or = alleles of a microsatellite polymorphism of <b>cannabinoid</b> receptor genes (<strong>CNR1</strong>) and drug dependence.
+CNR1	addiction	dependence	9106243	In our prior study we observed a significant association between homozygosity for the > or = alleles of a microsatellite polymorphism of cannabinoid receptor genes (<strong>CNR1</strong>) and drug <b>dependence</b>.
+CNR1	drug	alcohol	9106243	Since marijuana intoxication has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 <b>alcohol</b> and drug addicts, by MANOVA.
+CNR1	drug	cannabinoid	9106243	Since <b>marijuana</b> intoxication has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 alcohol and drug addicts, by MANOVA.
+CNR1	addiction	intoxication	9106243	Since marijuana <b>intoxication</b> has a potent blocking effect on short term memory we examined the association between the <strong>CNR1</strong> alleles and the P300 wave amplitude at three electrodes in 35 alcohol and drug addicts, by MANOVA.
+CNR1	drug	cannabinoid	9106242	<b>Cannabinoid</b> receptor gene (<strong>CNR1</strong>): association with i.v.
+CNR1	drug	cannabinoid	9106242	A microsatellite polymorphism (AAT)n at the <b>cannabinoid</b> CB1 (brain) receptor gene (<strong>CNR1</strong>) consists of 9 alleles.
+CNR1	drug	alcohol	9106242	Since the cannabinoid system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to <b>alcohol</b> or drug dependence.
+CNR1	drug	cannabinoid	9106242	Since the <b>cannabinoid</b> system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug dependence.
+CNR1	addiction	dependence	9106242	Since the cannabinoid system is part of the reward pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug <b>dependence</b>.
+CNR1	addiction	reward	9106242	Since the cannabinoid system is part of the <b>reward</b> pathway we examined the hypothesis that genetic variants of the <strong>CNR1</strong> gene might be associated with susceptibility to alcohol or drug dependence.
+BAX	drug	amphetamine	32203791	We further examined ER stress related proteins and mitochondrial apoptosis pathway in the VTA and NAc, and found that <b>METH</b> increased the expressions of glucose regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and <strong>Bax</strong>, as same time decreased the expressions of procaspase12, Bcl 2, and procaspase3, while Trx 1 overexpression blocked these changes.
+BAX	drug	amphetamine	32035215	Results further showed that luteolin pretreatment significantly repressed the <b>METH</b> induced increases of PI3K, Akt, p Akt, p53, <strong>Bax</strong>, caspase 3, normalized the ratio of p Akt/Akt, and autophagy related proteins (Beclin1, Atg5 and LC3 II) expression.
+BAX	drug	amphetamine	31396089	Ad libitum HRW consumption also had an inhibitory effect on the <b>METH</b> induced increase in the expression of <strong>Bax</strong>/Bcl 2, cleaved caspase 3, glucose related protein 78 (GRP 78), CCAAT/enhancer binding protein homologous protein (CHOP), and p NF kB p65 expression and elevation of interleukin (IL) 6 and tumor necrosis factor (TNF) α levels in the hippocampus.
+BAX	drug	alcohol	31105269	<b>Alcohol</b> increased IL 17A production and pro apoptotic signaling evidenced by <strong>Bax</strong>, Bim, caspase 3, and caspase 8 increases via endoplasmic reticulum (ER) stress indicated by C/EBP homologous protein (CHOP) upregulation; this was prevented by the ER stress inhibitor, 4 PBA, in isolated crypts in vitro and in vivo.
+BAX	addiction	intoxication	29431616	Also, PXR dependent was the <b>binge</b> EtOH induced inhibition of hepatic Akr1b8 mRNA, and protein levels of aldehyde dehydrogenase (ALDH) 1A1 and anti apoptotic Bcl 2, but increased pro apoptotic <strong>Bax</strong> protein expression, leading to increases in residual EtOH concentration and the cellular oxidative stress marker, malondialdehyde.
+BAX	drug	alcohol	29404485	Furthermore, cell death rates were elevated when primary hepatocytes or human hepatoma cells were exposed to EVs from <b>alcohol</b> exposed rodents and patients with <b>alcoholism</b>, demonstrating that EVs from <b>alcohol</b> exposed rats and patients with <b>alcoholism</b> are functional and can promote cell death by activating the apoptosis signaling pathway, including phospho c Jun N terminal kinase, proapoptotic <strong>Bax</strong>, and activated caspase 3.
+BAX	addiction	intoxication	28342134	Whereas in vivo MA <b>binge</b> exposure reduced locomotor activity in wild type (WT) mice, this was significantly attenuated in DAT p53KO mice and associated with significant differences in the levels of the p53 target genes <strong>BAX</strong> and p21 between WT and DAT p53KO.
+BAX	drug	alcohol	28095363	Also, <b>alcohol</b> administration augmented lipid peroxidation, mitochondrial oxidized glutathione (GSSG), interleukin 1 beta (IL 1β), tumor necrosis factor alpha (TNF α) and <strong>Bax</strong> levels in isolated hippocampal tissues.
+BAX	drug	alcohol	27628528	Moreover, bilateral microinjections of <b>ethanol</b> did not change the expression of either pro apoptotic (caspase 3 and <strong>Bax</strong>) or anti apoptotic (Bcl 2) proteins, suggesting that the dose was safe and validating the method used in the current study.
+BAX	drug	alcohol	27565756	Immunoblot analysis showed decreased Mre11, Rad51, Rad50, and Ku86 as well as increased <strong>Bax</strong> and p21 in samples from <b>ethanol</b> treated rats.
+BAX	drug	opioid	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, <strong>Bax</strong>, Bcl 2 and Caspase 3, of prefrontal cortex neurons in <b>morphine</b> relapse rats, an effective, successful <b>morphine</b> relapse rat model using the conditioned place preference (CPP) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+BAX	addiction	relapse	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, <strong>Bax</strong>, Bcl 2 and Caspase 3, of prefrontal cortex neurons in morphine <b>relapse</b> rats, an effective, successful morphine <b>relapse</b> rat model using the conditioned place preference (CPP) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+BAX	addiction	reward	27544013	In order to elucidate the influences of CCK 8 on expressions of apoptosis related genes, <strong>Bax</strong>, Bcl 2 and Caspase 3, of prefrontal cortex neurons in morphine relapse rats, an effective, successful morphine relapse rat model using the conditioned place preference (<b>CPP</b>) under CCK 8 (0.01, 0.1 and 1.0μg, i.c.v) intervention was established.
+BAX	drug	opioid	27544013	The results showed that the expression of Bcl 2 was very weak and those of <strong>Bax</strong> and Caspase 3 were hardly seen in group normal saline; the expressions of <strong>Bax</strong> and Caspase 3 were strong and that of Bcl 2 was weak in group <b>morphine</b> and compared to group normal saline, there were significant differences (P<0.05); the expressions of <strong>Bax</strong>, Caspase 3 and the ratios of <strong>Bax</strong>/Bcl 2 have a gradually decreased trend in the sequence of group 0.01μg, group 0.1μg and group 1.0μg, but the expression of Bcl 2 has an opposite trend in the same sequence, and compared to group <b>morphine</b>, there were significant differences (P<0.05) excluding group 0.01μg.
+BAX	drug	opioid	27544013	So we draw a conclusion that CCK 8 (0.1 and 1.0μg, i.c.v) could protect neurons of prefrontal cortex through up regulating the expression of Bcl 2, down regulating those of <strong>Bax</strong> and Caspase 3 and reducing <strong>Bax</strong>/Bcl 2 ratio in the model of <b>morphine</b> relapse rats.
+BAX	addiction	relapse	27544013	So we draw a conclusion that CCK 8 (0.1 and 1.0μg, i.c.v) could protect neurons of prefrontal cortex through up regulating the expression of Bcl 2, down regulating those of <strong>Bax</strong> and Caspase 3 and reducing <strong>Bax</strong>/Bcl 2 ratio in the model of morphine <b>relapse</b> rats.
+BAX	drug	nicotine	26909550	This effect correlated with the induction of Bcl 2, <strong>Bax</strong>, Survivin and Caspase 3 by <b>nicotine</b> in gastric cell lines.
+BAX	drug	cocaine	26790673	Levels of MDA and TNFα in PFC, and levels of MDA, SOD, GSH, IL 6, IL 1β, TNFα, caspase 3 and <strong>BAX</strong> in HP, but not SIRT1 expression in both regions were significantly changed during <b>cocaine</b> withdrawal period.
+BAX	addiction	withdrawal	26790673	Levels of MDA and TNFα in PFC, and levels of MDA, SOD, GSH, IL 6, IL 1β, TNFα, caspase 3 and <strong>BAX</strong> in HP, but not SIRT1 expression in both regions were significantly changed during cocaine <b>withdrawal</b> period.
+BAX	drug	cocaine	26560700	Importantly, caffeine <b>cocaine</b> combination potentiated the <b>cocaine</b> induced germ cell loss, and induced pro apoptotic <strong>BAX</strong> protein expression and diminished adenosine receptor A1 mRNA levels.
+BAX	drug	opioid	26339395	The overall objective of this study was to investigate neuronal apoptosis and expression of apoptosis related proteins (c jun, cytc and <strong>Bax</strong>) in the cerebellum of rates with <b>heroin</b> addiction.
+BAX	addiction	addiction	26339395	The overall objective of this study was to investigate neuronal apoptosis and expression of apoptosis related proteins (c jun, cytc and <strong>Bax</strong>) in the cerebellum of rates with heroin <b>addiction</b>.
+BAX	drug	opioid	26339395	Compared with the control group, the proportion of apoptotic neurons increased significantly in the <b>heroin</b> addiction groups (10 d, 20 d, 30 d, 40 d) (P < 0.05), also accompanied by markedly increased expressions of c jun, cytc and <strong>Bax</strong> (P < 0.05) depending on doses of <b>heroin</b> in the cerebellum.
+BAX	addiction	addiction	26339395	Compared with the control group, the proportion of apoptotic neurons increased significantly in the heroin <b>addiction</b> groups (10 d, 20 d, 30 d, 40 d) (P < 0.05), also accompanied by markedly increased expressions of c jun, cytc and <strong>Bax</strong> (P < 0.05) depending on doses of heroin in the cerebellum.
+BAX	drug	opioid	26339395	Long term use of <b>heroin</b> may induce neuronal apoptosis in the cerebellum by raising the expressions of pro apoptotic c jun, cytc and <strong>Bax</strong>, which might be one of mechanisms underlying the <b>heroin</b> induced cerebellum neuronal damage.
+BAX	drug	amphetamine	26176977	Melatonin attenuates the mitochondrial translocation of mitochondrial fission proteins and <strong>Bax</strong>, cytosolic calcium overload and cell death in <b>methamphetamine</b> induced toxicity in neuroblastoma SH SY5Y cells.
+BAX	drug	amphetamine	26176977	The results of the present study demonstrated that <b>METH</b> significantly decreases cell viability and increases the levels of mitochondrial fission (Fis1 and Drp1) proteins and pro apoptotic protein, <strong>Bax</strong> in isolated mitochondria.
+BAX	drug	amphetamine	26176977	Melatonin reversed the toxic effects of <b>METH</b> by restoring cell viability and inhibiting the increase in mitochondrial Fis1 levels and the mitochondrial translocation of Drp1 and <strong>Bax</strong>.
+BAX	drug	psychedelics	26068050	In fact, chronic <b>MDMA</b> inhibited proteins of the apoptotic pathway (i.e., pro apoptotic FADD, <strong>Bax</strong> and cytochrome c) leading to an inhibition of cell death markers (i.e., p JNK1/2, cleavage of PARP 1) and suggesting regulatory mechanisms in response to the neurochemical changes caused by the drug.
+BAX	drug	psychedelics	25937004	24h following washout of the specific drug, a significant elevation of the pro apoptotic marker <strong>BAX</strong>, as well as activated Caspase 3 positive neurons, could be detected in cultures exposed to 100μM MK801 and 25μM S(+) <b>ketamine</b>.
+BAX	drug	alcohol	25881894	In the <b>ethanol</b> treated cerebellar granule neurons we find an increased expression of genes related to apoptosis (Mapk8 and <strong>Bax</strong>), but also of genes previously described as neuroprotective (Dhcr24 and Bdnf), which might suggest an actively maintained viability.
+BAX	drug	opioid	25846801	Various regimens of <b>morphine</b> reduced TWI, cortisol levels, <strong>Bax</strong> activity, caspase 3, caspase 9, TNF α, and IL 1β and lipid peroxidation.
+BAX	drug	psychedelics	25748203	In addition, <b>ketamine</b> induced the expression of <strong>Bax</strong>, cytochrome c and capase 3, but inhibited the expression of NF κB and bcl 2.
+BAX	drug	opioid	25712644	The results showed that <b>morphine</b> significantly increased lipid peroxidation, mitochondrial GSH level, concentration of <strong>Bax</strong>; caspase 3 and caspase 9 activities while decreasing Bcl 2 concentration.
+BAX	drug	alcohol	25623404	Apoptotic cell death and temporal expression of apoptotic proteins Bcl 2 and <strong>Bax</strong> in the hippocampus, following binge <b>ethanol</b> in the neonatal rat model.
+BAX	addiction	intoxication	25623404	Apoptotic cell death and temporal expression of apoptotic proteins Bcl 2 and <strong>Bax</strong> in the hippocampus, following <b>binge</b> ethanol in the neonatal rat model.
+BAX	addiction	intoxication	25623404	Western blot analysis determined expression of pro apoptotic <strong>Bax</strong> and anti apoptotic Bcl 2, 12, 24, and 48 hours after <b>binge</b> EtOH exposure on PN6.
+BAX	addiction	intoxication	25623404	<b>Binge</b> EtOH exposure on PN6 resulted in a significant increase in expression of Bcl 2 and the Bcl 2:<strong>Bax</strong> ratio in the CA1/DG region at 24 hours after EtOH exposure on PN6.
+BAX	addiction	intoxication	25623404	This finding may be explained in part by changes in the Bcl 2:<strong>Bax</strong> ratio after a single <b>binge</b> EtOH exposure.
+BAX	drug	opioid	25597171	Group II also exhibited a significantly reduced epididymal perm count (P < 0.05) and remarkably upregulated expressions of <strong>Bax</strong> and Caspase 3 in comparison with group I. <b>Morphine</b> might increase testicular cell apoptosis and reduce sperm concentration by upregulating the expressions of <strong>Bax</strong> and Caspase 3 in the rat model of <b>morphine</b> tolerance.
+BAX	drug	amphetamine	25463524	In addition, <b>methamphetamine</b> enhanced expression of anti apoptotic protein Bcl 2 and reduced pro apoptotic protein <strong>Bax</strong> levels in the ventral hippocampus, suggesting a mechanism for reducing cell death.
+BAX	drug	amphetamine	25463524	These data reveal that alterations in Bcl 2 and <strong>Bax</strong> levels by <b>methamphetamine</b> were not associated with enhanced Akt expression.
+BAX	drug	opioid	24959978	In this study, we investigated the effects of <b>morphine</b> induced conditioned place preference (CPP) in the presence and absence of stress on the changes of apoptotic factors (<strong>Bax</strong>/Bcl 2 ratio, caspase 3 activation and PARP degradation) in the MCL system.
+BAX	addiction	reward	24959978	In this study, we investigated the effects of morphine induced conditioned place preference (<b>CPP</b>) in the presence and absence of stress on the changes of apoptotic factors (<strong>Bax</strong>/Bcl 2 ratio, caspase 3 activation and PARP degradation) in the MCL system.
+BAX	drug	opioid	24959978	In the <b>morphine</b> treated animals, AS and SS increased apoptotic factors remarkably (except for the <strong>Bax</strong>/Bcl 2 ratio after AS and SS in the Str and caspase 3 activation after AS in the NAc) and also decreased conditioning scores.
+BAX	drug	opioid	24906198	We found that chronic exposure to <b>morphine</b> impaired spatial and aversive memory and remarkably suppressed the expression of Bcl 2, but <strong>Bax</strong> expression remained constant.
+BAX	addiction	aversion	24906198	We found that chronic exposure to morphine impaired spatial and <b>aversive</b> memory and remarkably suppressed the expression of Bcl 2, but <strong>Bax</strong> expression remained constant.
+BAX	drug	opioid	24906198	Both voluntary and treadmill exercise alleviated memory impairment, increased the expression of Bcl 2 protein, and only the later suppressed the expression of <strong>Bax</strong> protein in <b>morphine</b> dependent animals.
+BAX	drug	opioid	24281942	In the HPC, <b>morphine</b> significantly increased the ratio of <strong>Bax</strong>/Bcl 2, caspases 3, and PARP by the lowest dose (0.5 mg/kg), but, in the VTA, a considerable increase was seen in the dose of 5 mg/kg; promotion of apoptotic factors in the HPC and VTA insinuates that <b>morphine</b> can affect the molecular mechanisms that interfere with apoptosis through different receptors.
+BAX	drug	opioid	24096212	In the NAc, <b>morphine</b> significantly increased the <strong>Bax</strong>/Bcl 2 ratio, caspase3 and PARP in the lowest dose (0.5mg/kg) but in the PFC considerable increase was seen in dose of 5mg/kg.
+BAX	drug	amphetamine	23975636	<b>METH</b> activates the upregulation of the <strong>Bax</strong>, cytochrome c, cleavage caspase 9 and 3 proteins, and downregulation of Bcl XL protein in cascade.
+BAX	drug	psychedelics	23508639	There was a significant increase in <strong>Bax</strong> protein expression in the <b>MDMA</b>+SCH group and a significant decrease in Bcl 2 protein expression in the <b>MDMA</b>+SCH group (p<0.05).
+BAX	drug	psychedelics	23508639	A2A receptors have a role in the apoptotic effects of <b>MDMA</b> via the <strong>Bax</strong> and Bcl 2 pathways.
+BAX	drug	opioid	23319379	<strong>Bax</strong> and cleaved caspase 3 were positive only in the <b>heroin</b> subjects.
+BAX	addiction	reward	27385959	In this study, the effects of acute and subchronic stress on the changes in apoptotic factors (<strong>Bax</strong>/Bcl 2 ratio, caspase 3 activation and PARP degradation) in the HYP and HIP during conditioned place preference (<b>CPP</b>) paradigm were evaluated.
+BAX	drug	opioid	27385959	On the other hand, in the HIP, <strong>Bax</strong>/Bcl 2 ratio in saline treated animals increased significantly during AS and SS, while in <b>morphine</b> treated animals this ratio did not have any significant alteration during AS and was decreased during SS compared with <b>morphine</b> control group.
+BAX	drug	opioid	23262244	Upregulated Bim translocated to mitochondria and <strong>Bax</strong> was activated under <b>heroin</b> treatment.
+BAX	drug	amphetamine	23056363	We also evaluated the striatal expression of the pro apoptotic <strong>BAX</strong> and anti apoptotic Bcl 2 proteins, which are known to mediate <b>methamphetamine</b> induced apoptotic effects.
+BAX	drug	amphetamine	23056363	Modafinil also counteracted the decrease in tyrosine hydroxylase and dopamine transporter levels and prevented <b>methamphetamine</b> induced increases in the pro apoptotic <strong>BAX</strong> and decreases in the anti apoptotic Bcl 2 protein expression.
+BAX	drug	opioid	22210043	Protein expression of cleaved caspase 3 and <strong>Bax</strong> decreased, whereas Bcl 2 protein levels in hippocampus increased with exogenous H(2)S. Exogenous H(2)S alleviated <b>heroin</b> induced rat hippocampal damage through antioxidant and antiapoptosis effects.
+BAX	drug	amphetamine	22174933	Importantly, <b>METH</b> caused decreases in the mitochondrial anti apoptotic protein, Bcl 2, but increases in the pro apoptotic proteins, <strong>Bax</strong>, Bad and cytochrome c, in a SCH23390 sensitive fashion.
+BAX	drug	alcohol	21803053	After 4h, a single dose of <b>ethanol</b> induced upregulation of <strong>Bax</strong>, release of mitochondrial cytochrome c into the cytosol, activation of caspase 3 and cleavage of poly (ADP ribose) polymerase (PARP 1), all of which promote apoptosis.
+BAX	drug	opioid	21560342	[The expression of Bcl 2 and <strong>Bax</strong> in the <b>morphine</b> dependence on male rat germ cell].
+BAX	addiction	dependence	21560342	[The expression of Bcl 2 and <strong>Bax</strong> in the morphine <b>dependence</b> on male rat germ cell].
+BAX	drug	opioid	21559519	<b>Morphine</b> caused a dramatic decrease in Bcl 2 level but increase in <strong>Bax</strong> level in wild type microglia, but not in TLR9 deficient microglia.
+BAX	drug	opioid	21483469	Enhanced toxicity by Tat and <b>morphine</b> was accompanied by increased numbers of TUNEL positive apoptotic neurons, elevated caspase 3 levels and decreased ratio of anti  and pro apoptotic proteins, Bcl2/<strong>Bax</strong>.
+BAX	drug	cocaine	20948987	In microglia, <b>cocaine</b> up regulated the immunoregulatory and pro apoptotic genes IL 1β and <strong>BAX</strong>.
+BAX	drug	alcohol	20090911	Myocardium from <b>ethanol</b> treated mice displayed enhanced <strong>Bax</strong>, Caspase 3 and decreased Bcl 2 expression, the effect of which with the exception of Caspase 3 was augmented by ADH.
+BAX	drug	opioid	18849879	<b>Morphine</b> downregulates proapoptotic factor <strong>Bax</strong> levels in cultured human neurons.
+BAX	drug	amphetamine	17669262	Gene expression profiling of rewarding effect in <b>methamphetamine</b> treated <strong>Bax</strong> deficient mouse.
+BAX	drug	amphetamine	17669262	According to a previous study, <strong>Bax</strong> was involved in neurotoxicity by <b>methamphetamine</b>, but the function of <strong>Bax</strong> in rewarding effect has not yet been elucidated.
+BAX	drug	amphetamine	17669262	In the present study, we treated chronic <b>methamphetamine</b> exposure in a <strong>Bax</strong> deficient mouse model and examined behavioral change using a conditioned place preference (CPP) test.
+BAX	addiction	reward	17669262	In the present study, we treated chronic methamphetamine exposure in a <strong>Bax</strong> deficient mouse model and examined behavioral change using a conditioned place preference (<b>CPP</b>) test.
+BAX	addiction	reward	17669262	The <b>CPP</b> score in <strong>Bax</strong> knockout mice was decreased compared to that of wild type mice.
+BAX	drug	amphetamine	17669262	Expression of the Tgfbr2 gene was decreased by <b>methamphetamine</b> in <strong>Bax</strong> knockout mice, and the gene was overexpressed in <strong>Bax</strong> wild type mice.
+BAX	drug	opioid	17384938	This study analyzes the effects of prolonged administration of <b>methadone</b> and withdrawal on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and caspase 8) and the mitochondrial (Bcl 2, Bcl x(L), Bad, and <strong>Bax</strong>) apoptotic pathways.
+BAX	addiction	withdrawal	17384938	This study analyzes the effects of prolonged administration of methadone and <b>withdrawal</b> on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and caspase 8) and the mitochondrial (Bcl 2, Bcl x(L), Bad, and <strong>Bax</strong>) apoptotic pathways.
+BAX	drug	opioid	17250679	Nonetheless, in street <b>heroin</b> treated cortical neurons, cytochrome c was released, accompanied by a decrease in mitochondrial potential and Bcl 2/<strong>Bax</strong>.
+BAX	drug	amphetamine	17161385	Finally, the <b>METH</b> injection was associated with increased expression of the proapoptotic proteins, <strong>Bax</strong> and Bid, but with decreased expression of the antideath protein, Bcl2.
+BAX	drug	alcohol	17008791	In vitro induction of apoptosis in U937 cells by perillyl <b>alcohol</b> with sensitization by pentoxifylline: increased BCL 2 and <strong>BAX</strong> protein expression.
+BAX	addiction	sensitization	17008791	In vitro induction of apoptosis in U937 cells by perillyl alcohol with <b>sensitization</b> by pentoxifylline: increased BCL 2 and <strong>BAX</strong> protein expression.
+BAX	drug	cannabinoid	15545023	Finally, <b>cannabinoids</b> might also be involved in the apoptotic death that occurs during brain development, possibly by influencing the expression of Bcl 2/<strong>Bax</strong> system.
+BAX	drug	opioid	15183518	In the core, neuronal apoptotic inhibitory protein (NAIP), GABA A alpha1 subunit, GRIN2C, GRIA1, mGluR1, D4 dopamine receptor and PSD 95 were upregulated by <b>morphine</b> administration whereas <strong>bax</strong>, bcl x, cox 1 and MAP2 were decreased.
+BAX	drug	alcohol	14502238	<b>Ethanol</b> induced neuronal apoptosis in vivo requires <strong>BAX</strong> in the developing mouse brain.
+BAX	drug	alcohol	14502238	We also found that <b>ethanol</b> triggers robust caspase 3 activation and apoptotic neurodegeneration in C57BL/6 wildtype mice, but induces neither phenomenon in homozygous <strong>Bax</strong> deficient mice.
+BAX	drug	alcohol	14502238	Therefore, it appears that <b>ethanol</b> induced neuroapoptosis is an intrinsic pathway mediated phenomenon involving <strong>Bax</strong> induced disruption of mitochondrial membranes and cytochrome c release as early events leading to caspase 3 activation.
+BAX	drug	alcohol	12603597	<b>Ethanol</b> decreased Jurkat cell expression of Bcl 2, whereas <b>ethanol</b> increased Jurkat cell expression of <strong>Bax</strong>.
+BAX	drug	alcohol	12043192	Changes of bcl 2 and <strong>bax</strong> mRNA expressions in the <b>ethanol</b> treated mouse brain.
+BAX	drug	alcohol	12043192	To characterize the biochemical mechanism of cell death induced by <b>ethanol</b> intoxication, we examined expression of mRNAs of bcl 2 and <strong>bax</strong> genes in the brain, which are related to apoptosis, by using the reverse transcription polymerase chain reaction method (RT PCR).
+BAX	addiction	intoxication	12043192	To characterize the biochemical mechanism of cell death induced by ethanol <b>intoxication</b>, we examined expression of mRNAs of bcl 2 and <strong>bax</strong> genes in the brain, which are related to apoptosis, by using the reverse transcription polymerase chain reaction method (RT PCR).
+BAX	drug	alcohol	12043192	We found that bcl 2 or <strong>bax</strong> mRNA expressions in the brain were changed after short term <b>ethanol</b> exposure.
+BAX	drug	alcohol	12043192	These results suggest that bcl 2 or <strong>bax</strong> may have functional significance about <b>ethanol</b> intoxication.
+BAX	addiction	intoxication	12043192	These results suggest that bcl 2 or <strong>bax</strong> may have functional significance about ethanol <b>intoxication</b>.
+BAX	addiction	withdrawal	10602513	Regardless of the steady state of the <strong>Bax</strong> protein, we found that in both K562 and K562 Tat cells, this protein is located in the nucleus, but after serum <b>withdrawal</b> its localization was mainly in the cytoplasm.
+BAX	drug	opioid	10534122	<b>Morphine</b> treated Jurkat cells also showed a decreased expression of bcl 2 and an enhanced expression of <strong>bax</strong>.
+BAX	drug	opioid	9469450	<b>Morphine</b> promoted the synthesis of <strong>Bax</strong> and p53 proteins by Mphi.
+BAX	drug	opioid	9469450	The effector phase of <b>morphine</b> induced apoptosis appears to proceed through the accumulation of <strong>Bax</strong> and activation of ICE 1.
+PPARA	drug	alcohol	32553670	The selective <strong>PPAR</strong> delta agonist seladelpar reduces <b>ethanol</b> induced liver disease by restoring gut barrier function and bile acid homeostasis in mice.
+PPARA	drug	alcohol	32553670	Here, we evaluated the effect of the selective <strong>PPAR</strong> delta agonist seladelpar (MBX 8025) on gut barrier function and bile acid metabolism in a mouse model of <b>ethanol</b> induced liver disease.
+PPARA	drug	cannabinoid	32057593	In the mPFC and hippocampus, EtOH rats had significantly higher mRNA expression of <b>endocannabinoid</b> signaling (mPFC: <strong>Ppara</strong>, Dagla, Daglb and Napepld; and hippocampus: Cnr2, Dagla and Mgll) and neuroinflammation associated genes (mPFC: Gfap; and hippocampus: Aif1) than in controls.
+PPARA	drug	cannabinoid	31868943	A systematic review of the effects of <b>oleoylethanolamide</b>, a high affinity endogenous ligand of <strong>PPAR</strong> α, on the management and prevention of obesity.
+PPARA	drug	cannabinoid	31868943	<b>Oleoylethanolamide</b> (OEA), a high affinity endogenous ligand of nuclear receptor <strong>peroxisome proliferator activated receptor alpha</strong> (PPAR α), plays important physiological and metabolic actions.
+PPARA	drug	cannabinoid	31868943	<b>Oleoylethanolamide</b> (OEA), a high affinity endogenous ligand of nuclear receptor <strong>peroxisome proliferator activated receptor alpha</strong> (<strong>PPAR</strong> α), plays important physiological and metabolic actions.
+PPARA	drug	cannabinoid	31868943	The evidence reviewed here indicates that OEA, an <b>endocannabinoid</b> like compound, leads to satiation or meal termination through <strong>PPAR</strong> α activation and fatty acid translocase (FAT)/CD36.
+PPARA	drug	opioid	31712968	A recently discovered fatty acid amide, N oleoylglycine (OlGly), which has been suggested to act as a fatty acid amide hydrolase (FAAH) inhibitor and as a <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonist, was previously shown to interfere with a <b>naloxone</b> precipitated MWD induced CPA in rats.
+PPARA	drug	cannabinoid	30993360	Oleoyl glycine (OlGly), a recently discovered fatty acid amide that is structurally similar to N  <b>acylethanolamines</b>, which include the <b>endocannabinoid</b>, anandamide (AEA), as well as endogenous <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonists <b>oleoylethanolamide</b> (OEA) and <b>palmitoylethanolamide</b> (PEA), has been shown to interfere with nicotine reward and dependence in mice.
+PPARA	drug	nicotine	30993360	Oleoyl glycine (OlGly), a recently discovered fatty acid amide that is structurally similar to N  acylethanolamines, which include the endocannabinoid, anandamide (AEA), as well as endogenous <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonists oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), has been shown to interfere with <b>nicotine</b> reward and dependence in mice.
+PPARA	addiction	dependence	30993360	Oleoyl glycine (OlGly), a recently discovered fatty acid amide that is structurally similar to N  acylethanolamines, which include the endocannabinoid, anandamide (AEA), as well as endogenous <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonists oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), has been shown to interfere with nicotine reward and <b>dependence</b> in mice.
+PPARA	addiction	reward	30993360	Oleoyl glycine (OlGly), a recently discovered fatty acid amide that is structurally similar to N  acylethanolamines, which include the endocannabinoid, anandamide (AEA), as well as endogenous <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonists oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), has been shown to interfere with nicotine <b>reward</b> and dependence in mice.
+PPARA	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B <strong>PPAR</strong> peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+PPARA	drug	nicotine	30439418	Activation of <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) by synthetic or endogenous agonists was shown to suppress <b>nicotine</b> induced activation of mesolimbic dopamine system, one of the major neurobiological substrates of <b>nicotine</b> dependence, and <b>nicotine</b> seeking behavior in rats and monkeys.
+PPARA	addiction	dependence	30439418	Activation of <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) by synthetic or endogenous agonists was shown to suppress nicotine induced activation of mesolimbic dopamine system, one of the major neurobiological substrates of nicotine <b>dependence</b>, and nicotine seeking behavior in rats and monkeys.
+PPARA	addiction	relapse	30439418	Activation of <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) by synthetic or endogenous agonists was shown to suppress nicotine induced activation of mesolimbic dopamine system, one of the major neurobiological substrates of nicotine dependence, and nicotine <b>seeking</b> behavior in rats and monkeys.
+PPARA	drug	cannabinoid	30391203	PEA targets not only the <strong>peroxisome proliferator activated receptor alpha</strong> (PPAR α), but also the <b>endocannabinoid</b> system, binding the G protein coupled receptor 55, a non CB1/CB2 <b>cannabinoid</b> receptor, and also the CB1/CB2 receptors, although with a weak affinity.
+PPARA	drug	cannabinoid	30391203	PEA targets not only the <strong>peroxisome proliferator activated receptor alpha</strong> (<strong>PPAR</strong> α), but also the <b>endocannabinoid</b> system, binding the G protein coupled receptor 55, a non CB1/CB2 <b>cannabinoid</b> receptor, and also the CB1/CB2 receptors, although with a weak affinity.
+PPARA	drug	nicotine	30260990	Testing the <strong>PPAR</strong> hypothesis of <b>tobacco</b> use disorder in humans: A randomized trial of the impact of gemfibrozil (a partial PPARα agonist) in <b>smokers</b>.
+PPARA	drug	nicotine	30260990	Although preclinical studies with <strong>PPAR</strong> α agonists showed promising results, this preliminary study did not demonstrate positive effect of gemfibrozil on <b>tobacco</b> use and cessation indices.
+PPARA	drug	cannabinoid	30238023	Based on quality of evidence to date, promising first tier neurochemical receptor targets include: noradrenergic (α1 and β antagonist, α2 agonist), kappa opioid antagonist, nociceptin antagonist, orexin 1 antagonist, and <b>endocannabinoid</b> modulation (e.g., <b>cannabidiol</b>, FAAH inhibition); second tier candidates may include corticotropin releasing factor 1 antagonists, serotonergic agents (e.g., 5 HT reuptake inhibitors, 5 HT3 antagonists), glutamatergic agents (e.g., mGluR2/3 agonist/positive allosteric modulator, mGluR5 antagonist/negative allosteric modulator), GABA promoters (e.g., pregabalin, tiagabine), vasopressin 1b antagonist, NK 1 antagonist, and <strong>PPAR</strong> γ agonist (e.g., pioglitazone).
+PPARA	drug	opioid	30238023	Based on quality of evidence to date, promising first tier neurochemical receptor targets include: noradrenergic (α1 and β antagonist, α2 agonist), kappa <b>opioid</b> antagonist, nociceptin antagonist, orexin 1 antagonist, and endocannabinoid modulation (e.g., cannabidiol, FAAH inhibition); second tier candidates may include corticotropin releasing factor 1 antagonists, serotonergic agents (e.g., 5 HT reuptake inhibitors, 5 HT3 antagonists), glutamatergic agents (e.g., mGluR2/3 agonist/positive allosteric modulator, mGluR5 antagonist/negative allosteric modulator), GABA promoters (e.g., pregabalin, tiagabine), vasopressin 1b antagonist, NK 1 antagonist, and <strong>PPAR</strong> γ agonist (e.g., pioglitazone).
+PPARA	drug	alcohol	30195735	Among them, drugs interacting with acylethanolamide receptors including cannabinoid CB1 receptor antagonists/inverse agonists, <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonists or peroxisome proliferator activated receptor gamma (PPARγ) agonists have demonstrated utility in the reduction of <b>alcohol</b> intake in animal models.
+PPARA	drug	cannabinoid	30195735	Among them, drugs interacting with acylethanolamide receptors including <b>cannabinoid</b> CB1 receptor antagonists/inverse agonists, <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonists or peroxisome proliferator activated receptor gamma (PPARγ) agonists have demonstrated utility in the reduction of alcohol intake in animal models.
+PPARA	drug	alcohol	29996215	目的： 研究抗氧化剂N 乙酰 L 半胱氨酸（N acetyl L cysteine，NAC）对小鼠酒精性脂肪肝（<b>alcoholic</b> fatty liver，AFL）的保护作用。 方法： SPF级雄性C57BL/6小鼠随机分为对照组、模型组及NAC干预组，每组10只。模型组及NAC干预组小鼠连续灌胃给予3次6 g/kg乙醇口服诱导急性AFL，对照组小鼠给予等体积等能量的麦芽糖糊精溶液。NAC在每次乙醇染毒前1 h腹腔注射给予100 mg/kg。末次乙醇染毒后6 h，处死小鼠取肝脏和附睾脂肪组织；病理学检查肝脏脂肪蓄积情况，生化试剂盒测定肝脏甘油三酯（triglyceride，TG）含量；Western blot测定相关蛋白的表达。 结果： 与对照组小鼠比较，模型组小鼠肝脏明显增大，肝重及肝脏系数明显增加，差异有统计学意义（P<0.05）。与模型组比较，NAC干预组小鼠肝脏系数和肝组织TG含量明显降低，差异有统计学意义（P<0.05）。病理学检查结果显示，模型组小鼠肝脏切片中有大量橙红色的脂滴，而NAC干预组小鼠肝脏切片中脂肪滴明显减少。与模型组比较，NAC干预组小鼠肝脏中过氧化物酶体增殖物活化受体α（<strong>PPAR</strong> α）、乙酰辅酶A氧化酶（ACOX）略有减少，固醇调节元件结合蛋白 1c（SREBP 1c）、脂肪酸合成酶（FAS）的蛋白含量无明显改变。附睾脂肪中激素敏感性脂肪酶（HSL）总蛋白在3组小鼠之间未见明显差异。NAC干预组小鼠脂肪组织中p HSL(ser563)和p HSL(ser660)的蛋白含量较模型组小鼠明显降低，差异有统计学意义（P<0.05）。 结论： 预先给予NAC可以明显减轻急性乙醇染毒导致的小鼠肝脏中TG的蓄积，其作用可能与抑制外周脂肪动员有关。.
+PPARA	drug	nicotine	29567093	Our respective in vitro and in vivo observations that OlGly activated <strong>peroxisome proliferator activated receptor alpha</strong> (PPAR α) and the PPAR α antagonist GW6471 prevented the OlGly induced reduction of <b>nicotine</b> CPP in mice suggests that this lipid acts as a functional PPAR α agonist to attenuate <b>nicotine</b> reward.
+PPARA	addiction	reward	29567093	Our respective in vitro and in vivo observations that OlGly activated <strong>peroxisome proliferator activated receptor alpha</strong> (PPAR α) and the PPAR α antagonist GW6471 prevented the OlGly induced reduction of nicotine <b>CPP</b> in mice suggests that this lipid acts as a functional PPAR α agonist to attenuate nicotine <b>reward</b>.
+PPARA	drug	nicotine	29567093	Our respective in vitro and in vivo observations that OlGly activated <strong>peroxisome proliferator activated receptor alpha</strong> (<strong>PPAR</strong> α) and the <strong>PPAR</strong> α antagonist GW6471 prevented the OlGly induced reduction of <b>nicotine</b> CPP in mice suggests that this lipid acts as a functional <strong>PPAR</strong> α agonist to attenuate <b>nicotine</b> reward.
+PPARA	addiction	reward	29567093	Our respective in vitro and in vivo observations that OlGly activated <strong>peroxisome proliferator activated receptor alpha</strong> (<strong>PPAR</strong> α) and the <strong>PPAR</strong> α antagonist GW6471 prevented the OlGly induced reduction of nicotine <b>CPP</b> in mice suggests that this lipid acts as a functional <strong>PPAR</strong> α agonist to attenuate nicotine <b>reward</b>.
+PPARA	drug	alcohol	29179698	Our results showed that while the FF diet clearly induced non <b>alcoholic</b> steatohepatitis and metabolic syndrome, NAFLD also attenuates APAP induced ALI by inducing anti inflammatory molecules such as <strong>PPAR</strong> γ.
+PPARA	addiction	addiction	29020601	Possibly through their actions upon glia, peroxisome proliferator activated receptor agonists (<strong>PPAR</strong>) have been shown to alter the abuse potential of <b>addictive</b> drugs in several preclinical models.
+PPARA	drug	nicotine	29020601	The current study extends this research into the human laboratory as the first clinical study into the effects of the <strong>PPAR</strong> gamma agonist, pioglitazone, on the abuse potential of <b>nicotine</b>.
+PPARA	addiction	intoxication	28882574	However, neither GdCl3 nor etanercept could affect <b>binge</b> drinking induced decrease of <strong>PPAR</strong> α, ACOX, FAS, ACC and SCD protein levels, or increase of the LC3 II/LC3 I ratio and p62 protein level.
+PPARA	drug	alcohol	28769774	Fenofibrate is a <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonist, which induces the proliferation of peroxisomes in the liver, leading to increases in catalase levels that result in acetaldehyde accumulation at aversive levels in the blood when animals consume <b>ethanol</b>.
+PPARA	addiction	aversion	28769774	Fenofibrate is a <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) agonist, which induces the proliferation of peroxisomes in the liver, leading to increases in catalase levels that result in acetaldehyde accumulation at <b>aversive</b> levels in the blood when animals consume ethanol.
+PPARA	drug	cocaine	28498501	<strong>PPAR</strong> gamma agonist pioglitazone modifies craving intensity and brain white matter integrity in patients with primary <b>cocaine</b> use disorder: a double blind randomized controlled pilot trial.
+PPARA	addiction	relapse	28498501	<strong>PPAR</strong> gamma agonist pioglitazone modifies <b>craving</b> intensity and brain white matter integrity in patients with primary cocaine use disorder: a double blind randomized controlled pilot trial.
+PPARA	drug	cocaine	28498501	Pioglitazone (PIO), a potent agonist of <strong>PPAR</strong> gamma, is a promising candidate treatment for <b>cocaine</b> use disorder (CUD).
+PPARA	drug	alcohol	28088358	The <strong>peroxisome proliferator activated receptor alpha</strong> agonist fenofibrate attenuates <b>alcohol</b> self administration in rats.
+PPARA	drug	cannabinoid	27720681	<b>Palmitoylethanolamide</b> (PEA), an endogenous anti inflammatory molecule, acts by down modulating MCs following activation of the <b>cannabinoid</b> CB2 receptor and peroxisome proliferator activated receptor α (<strong>PPAR</strong> α).
+PPARA	drug	opioid	27255640	We have previously demonstrated that peripheral administration of 15d PGJ2 in the Temporomandibular joint (TMJ) of rats can prevent nociceptor sensitization, mediated by peroxisome proliferator activated receptor γ (<strong>PPAR</strong> γ), and κ  and δ  <b>opioid</b> receptors.
+PPARA	addiction	sensitization	27255640	We have previously demonstrated that peripheral administration of 15d PGJ2 in the Temporomandibular joint (TMJ) of rats can prevent nociceptor <b>sensitization</b>, mediated by peroxisome proliferator activated receptor γ (<strong>PPAR</strong> γ), and κ  and δ  opioid receptors.
+PPARA	drug	opioid	27255640	However, the mechanism that underlies the signaling of <strong>PPAR</strong> γ (upon activation by 15d PGJ2) to induce antinociception, and how the <b>opioid</b> receptors are activated via 15d PGJ2 are not fully understood.
+PPARA	drug	opioid	27255640	Once activated by 15d PGJ2, <strong>PPAR</strong> γ induces the release of β endorphin and dynorphin, which activates κ  and δ <b>opioid</b> receptors in primary sensory neurons to induce the antinociceptive effect.
+PPARA	drug	nicotine	26864774	FAAH inhibition has been recently identified as having a critical involvement in behaviors related to <b>nicotine</b> addiction and has been shown to reduce the effect of <b>nicotine</b> on the mesolimbic dopaminergic system via CB1R and <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα).
+PPARA	addiction	addiction	26864774	FAAH inhibition has been recently identified as having a critical involvement in behaviors related to nicotine <b>addiction</b> and has been shown to reduce the effect of nicotine on the mesolimbic dopaminergic system via CB1R and <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα).
+PPARA	drug	alcohol	26857685	Several peroxisome proliferator activated receptor (<strong>PPAR</strong>) agonists reduce voluntary <b>alcohol</b> consumption in rodent models, and evidence suggests that PPARα and γ subunits play an important role in this effect.
+PPARA	drug	alcohol	26857541	In the accompanying article, we showed that activation of <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) signaling by fenofibrate and tesaglitazar decreases <b>ethanol</b> (EtOH) consumption in mice.
+PPARA	drug	alcohol	26857541	These studies indicate the complexity of EtOH dependent and EtOH independent behaviors that are altered by <strong>PPAR</strong> agonists and provide evidence for novel behavioral actions of these drugs that may contribute to <strong>PPAR</strong> mediated effects on <b>alcohol</b> drinking.
+PPARA	drug	cannabinoid	26590655	Next, we investigated the potential targets involved in the effects of Δ(9) <b>THC</b> BDS by selectively blocking CB(1) or <strong>PPAR</strong> γ receptors, and we found a complete reversion of neurological benefits and the reduction in cell aggregates only with <b>rimonabant</b>, a selective CB(1) receptor antagonist.
+PPARA	drug	alcohol	26037332	Here we show that <b>alcohol</b> administration causes the release of OEA in rodents, which in turn reduces <b>alcohol</b> consumption by engaging <strong>peroxisome proliferator activated receptor alpha</strong> (PPAR α).
+PPARA	drug	alcohol	26037332	Here we show that <b>alcohol</b> administration causes the release of OEA in rodents, which in turn reduces <b>alcohol</b> consumption by engaging <strong>peroxisome proliferator activated receptor alpha</strong> (<strong>PPAR</strong> α).
+PPARA	drug	alcohol	26037332	This effect appears to rely on peripheral signaling mechanisms as <b>alcohol</b> self administration is unaltered by intracerebral <strong>PPAR</strong> α agonist administration, and the lesion of sensory afferent fibers (by capsaicin) abrogates the effect of systemically administered OEA on <b>alcohol</b> intake.
+PPARA	drug	nicotine	25895948	Primate and rodent models show that <strong>peroxisome proliferator activated receptor alpha</strong> (PPAR α) ligands, including fibrate medications, reduce <b>nicotine</b> reinforcement, reward, and related effects.
+PPARA	addiction	reward	25895948	Primate and rodent models show that <strong>peroxisome proliferator activated receptor alpha</strong> (PPAR α) ligands, including fibrate medications, reduce nicotine <b>reinforcement</b>, <b>reward</b>, and related effects.
+PPARA	drug	nicotine	25895948	Primate and rodent models show that <strong>peroxisome proliferator activated receptor alpha</strong> (<strong>PPAR</strong> α) ligands, including fibrate medications, reduce <b>nicotine</b> reinforcement, reward, and related effects.
+PPARA	addiction	reward	25895948	Primate and rodent models show that <strong>peroxisome proliferator activated receptor alpha</strong> (<strong>PPAR</strong> α) ligands, including fibrate medications, reduce nicotine <b>reinforcement</b>, <b>reward</b>, and related effects.
+PPARA	drug	cannabinoid	25754762	Both FAAH inhibitors: (1) blocked FAAH activity in brain and liver, increasing levels of endogenous ligands for <b>cannabinoid</b> and α type peroxisome proliferator activated (<strong>PPAR</strong> α) receptors; (2) shifted nicotine self administration dose response functions in a manner consistent with reduced nicotine reward; (3) blocked reinstatement of nicotine seeking induced by reexposure to either nicotine priming or nicotine associated cues; and (4) had no effect on cocaine or food self administration.
+PPARA	drug	cocaine	25754762	Both FAAH inhibitors: (1) blocked FAAH activity in brain and liver, increasing levels of endogenous ligands for cannabinoid and α type peroxisome proliferator activated (<strong>PPAR</strong> α) receptors; (2) shifted nicotine self administration dose response functions in a manner consistent with reduced nicotine reward; (3) blocked reinstatement of nicotine seeking induced by reexposure to either nicotine priming or nicotine associated cues; and (4) had no effect on <b>cocaine</b> or food self administration.
+PPARA	drug	nicotine	25754762	Both FAAH inhibitors: (1) blocked FAAH activity in brain and liver, increasing levels of endogenous ligands for cannabinoid and α type peroxisome proliferator activated (<strong>PPAR</strong> α) receptors; (2) shifted <b>nicotine</b> self administration dose response functions in a manner consistent with reduced <b>nicotine</b> reward; (3) blocked reinstatement of <b>nicotine</b> seeking induced by reexposure to either <b>nicotine</b> priming or <b>nicotine</b> associated cues; and (4) had no effect on cocaine or food self administration.
+PPARA	addiction	relapse	25754762	Both FAAH inhibitors: (1) blocked FAAH activity in brain and liver, increasing levels of endogenous ligands for cannabinoid and α type peroxisome proliferator activated (<strong>PPAR</strong> α) receptors; (2) shifted nicotine self administration dose response functions in a manner consistent with reduced nicotine reward; (3) blocked <b>reinstatement</b> of nicotine <b>seeking</b> induced by reexposure to either nicotine priming or nicotine associated cues; and (4) had no effect on cocaine or food self administration.
+PPARA	addiction	reward	25754762	Both FAAH inhibitors: (1) blocked FAAH activity in brain and liver, increasing levels of endogenous ligands for cannabinoid and α type peroxisome proliferator activated (<strong>PPAR</strong> α) receptors; (2) shifted nicotine self administration dose response functions in a manner consistent with reduced nicotine <b>reward</b>; (3) blocked reinstatement of nicotine seeking induced by reexposure to either nicotine priming or nicotine associated cues; and (4) had no effect on cocaine or food self administration.
+PPARA	drug	nicotine	25754762	The effects of FAAH inhibition on <b>nicotine</b> self administration and <b>nicotine</b> priming induced reinstatement were reversed by the <strong>PPAR</strong> α antagonist, MK886.
+PPARA	addiction	relapse	25754762	The effects of FAAH inhibition on nicotine self administration and nicotine priming induced <b>reinstatement</b> were reversed by the <strong>PPAR</strong> α antagonist, MK886.
+PPARA	drug	cannabinoid	25754762	URB694 self administration was blocked by pretreatment with an antagonist for either <strong>PPAR</strong> α (MK886) or <b>cannabinoid</b> CB1 receptors (<b>rimonabant</b>).
+PPARA	drug	alcohol	25516156	Peroxisome proliferator activated receptor (<strong>PPAR</strong>) agonists reduce voluntary <b>ethanol</b> (EtOH) consumption in rat models and are promising therapeutics in the treatment for drug addictions.
+PPARA	drug	alcohol	25516156	We studied the effects of different classes of <strong>PPAR</strong> agonists on chronic EtOH intake and preference in mice with a genetic predisposition for high <b>alcohol</b> consumption and then examined human genomewide association data for polymorphisms in <strong>PPAR</strong> genes in <b>alcohol</b> dependent subjects.
+PPARA	drug	alcohol	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different PPAR genes (<strong>PPARA</strong>, PPARD, PPARG, and PPARGC1A) with 2 phenotypes: DSM IV <b>alcohol</b> dependence (AD) and the DSM IV criterion of withdrawal.
+PPARA	addiction	dependence	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of Alcoholism (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different PPAR genes (<strong>PPARA</strong>, PPARD, PPARG, and PPARGC1A) with 2 phenotypes: DSM IV alcohol <b>dependence</b> (AD) and the DSM IV criterion of withdrawal.
+PPARA	addiction	withdrawal	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of Alcoholism (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different PPAR genes (<strong>PPARA</strong>, PPARD, PPARG, and PPARGC1A) with 2 phenotypes: DSM IV alcohol dependence (AD) and the DSM IV criterion of <b>withdrawal</b>.
+PPARA	drug	alcohol	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different <strong>PPAR</strong> genes (<strong>PPARA</strong>, PPARD, PPARG, and PPARGC1A) with 2 phenotypes: DSM IV <b>alcohol</b> dependence (AD) and the DSM IV criterion of withdrawal.
+PPARA	addiction	dependence	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of Alcoholism (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different <strong>PPAR</strong> genes (<strong>PPARA</strong>, PPARD, PPARG, and PPARGC1A) with 2 phenotypes: DSM IV alcohol <b>dependence</b> (AD) and the DSM IV criterion of withdrawal.
+PPARA	addiction	withdrawal	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of Alcoholism (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different <strong>PPAR</strong> genes (<strong>PPARA</strong>, PPARD, PPARG, and PPARGC1A) with 2 phenotypes: DSM IV alcohol dependence (AD) and the DSM IV criterion of <b>withdrawal</b>.
+PPARA	drug	alcohol	25516156	The GWAS from COGA supported an association of SNPs in <strong>PPARA</strong> and PPARG with <b>alcohol</b> withdrawal and PPARGC1A with AD but found no association for PPARD with either phenotype.
+PPARA	addiction	withdrawal	25516156	The GWAS from COGA supported an association of SNPs in <strong>PPARA</strong> and PPARG with alcohol <b>withdrawal</b> and PPARGC1A with AD but found no association for PPARD with either phenotype.
+PPARA	drug	alcohol	25288222	Recently, <strong>PPAR</strong> γ activation has emerged as a potential treatment for <b>alcoholism</b>.
+PPARA	drug	alcohol	25288222	Hence, naringin, a bioflavonoid isolated from citrus fruits and recently identified as a natural ligand of <strong>PPAR</strong> γ, has begun to be evaluated for treatment of <b>alcoholism</b>.
+PPARA	drug	alcohol	25288222	Taken together, the present findings are the first to implicate naringin and <strong>PPAR</strong> γ receptors in the behavioral and reward related effects of <b>ethanol</b> and raise the question of whether specific drugs that target <strong>PPAR</strong> γ receptors could potentially reduce excessive <b>ethanol</b> consumption and preference.
+PPARA	addiction	reward	25288222	Taken together, the present findings are the first to implicate naringin and <strong>PPAR</strong> γ receptors in the behavioral and <b>reward</b> related effects of ethanol and raise the question of whether specific drugs that target <strong>PPAR</strong> γ receptors could potentially reduce excessive ethanol consumption and preference.
+PPARA	drug	alcohol	25162931	However, acute <b>ethanol</b> induced increase of peroxisome proliferator activated receptor α (<strong>PPAR</strong> α) protein level was suppressed by CMZ, while the protein levels of sterol regulatory element binding protein 1c (SREBP 1) and diacylglycerol acyltransferase 2 (DGAT2) were not significantly affected by <b>ethanol</b> or CMZ.
+PPARA	drug	alcohol	25036611	<strong>PPAR</strong> agonists regulate brain gene expression: relationship to their effects on <b>ethanol</b> consumption.
+PPARA	addiction	addiction	25036611	Although prescribed for dyslipidemia and type II diabetes, <strong>PPAR</strong> agonists also possess anti <b>addictive</b> characteristics.
+PPARA	drug	alcohol	25036611	<strong>PPAR</strong> agonists decrease <b>ethanol</b> consumption and reduce withdrawal severity and susceptibility to stress induced relapse in rodents.
+PPARA	addiction	relapse	25036611	<strong>PPAR</strong> agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress induced <b>relapse</b> in rodents.
+PPARA	addiction	withdrawal	25036611	<strong>PPAR</strong> agonists decrease ethanol consumption and reduce <b>withdrawal</b> severity and susceptibility to stress induced relapse in rodents.
+PPARA	drug	alcohol	25036611	We tested three <strong>PPAR</strong> agonists in a continuous access two bottle choice (2BC) drinking paradigm and found that tesaglitazar (PPARα/γ; 1.5 mg/kg) and fenofibrate (PPARα; 150 mg/kg) decreased <b>ethanol</b> consumption in male C57BL/6J mice while bezafibrate (PPARα/γ/β; 75 mg/kg) did not.
+PPARA	drug	alcohol	25036611	Our results reveal gene targets through which <strong>PPAR</strong> agonists can affect <b>alcohol</b> consumption behavior.
+PPARA	drug	opioid	24899385	The purpose of the present study is to investigate the effects of pioglitazone, a peroxisome proliferator activated receptors gamma (<strong>PPAR</strong> γ) agonist, on the <b>morphine</b> induced tolerance and dependence.
+PPARA	addiction	dependence	24899385	The purpose of the present study is to investigate the effects of pioglitazone, a peroxisome proliferator activated receptors gamma (<strong>PPAR</strong> γ) agonist, on the morphine induced tolerance and <b>dependence</b>.
+PPARA	drug	opioid	24504689	The purpose of the present study was to investigate the effects of the acute administration of pioglitazone, a selective agonist of peroxisome proliferator activated receptors gamma (<strong>PPAR</strong> γ), on the <b>morphine</b> withdrawal syndrome in the rat.
+PPARA	addiction	withdrawal	24504689	The purpose of the present study was to investigate the effects of the acute administration of pioglitazone, a selective agonist of peroxisome proliferator activated receptors gamma (<strong>PPAR</strong> γ), on the morphine <b>withdrawal</b> syndrome in the rat.
+PPARA	drug	opioid	24504689	It seems that pioglitazone suppresses <b>morphine</b> withdrawal syndrome through <strong>PPAR</strong> γ independent mechanisms.
+PPARA	addiction	withdrawal	24504689	It seems that pioglitazone suppresses morphine <b>withdrawal</b> syndrome through <strong>PPAR</strong> γ independent mechanisms.
+PPARA	drug	cannabinoid	23813098	These actions may be mediated by PEA acting through "receptor pleiotropism," i.e., both direct and indirect interactions of PEA with different receptor targets, e.g., <b>cannabinoid</b> CB2 and <strong>peroxisome proliferator activated receptor alpha</strong>.
+PPARA	drug	cannabinoid	23794089	Dual role of <strong>PPAR</strong> γ in induction and expression of behavioral sensitization to <b>cannabinoid</b> receptor agonist WIN55,212 2.
+PPARA	addiction	sensitization	23794089	Dual role of <strong>PPAR</strong> γ in induction and expression of behavioral <b>sensitization</b> to cannabinoid receptor agonist WIN55,212 2.
+PPARA	drug	cannabinoid	23794089	<b>Cannabinoids</b> like WIN55,212 2 act as potential activators of <strong>PPAR</strong> γ and affects the inflammatory status of the CNS.
+PPARA	addiction	addiction	23333350	Inhibition of FAAH and activation of <strong>PPAR</strong>: new approaches to the treatment of cognitive dysfunction and drug <b>addiction</b>.
+PPARA	drug	cannabinoid	23333350	Inhibitors of fatty acid amide hydrolase (FAAH) prevent the breakdown of endogenous ligands for <b>cannabinoid</b> receptors and peroxisome proliferator activated receptors (<strong>PPAR</strong>), prolonging and enhancing the effects of these ligands when they are naturally released.
+PPARA	addiction	addiction	23333350	This review considers recent research on the effects of FAAH inhibitors and <strong>PPAR</strong> activators in animal models of <b>addiction</b> and cognition (specifically learning and memory).
+PPARA	drug	cannabinoid	23333350	These studies show that FAAH inhibitors can produce potentially therapeutic effects, some through <b>cannabinoid</b> receptors and some through <strong>PPAR</strong>.
+PPARA	drug	cannabinoid	23163925	<b>Oleoylethanolamide</b> (OEA) is an acylethanolamide that acts as an agonist of nuclear <strong>peroxisome proliferator activated receptor alpha</strong> (PPARα) to exert their biological functions, which include the regulation of appetite and metabolism.
+PPARA	drug	nicotine	22799258	We apply this approach to two datasets: one from a hepatotoxicity study in rats using a <strong>PPAR</strong> pathway, and the other from a study of the effects of <b>smoking</b> on the epithelial transcriptome, using a global transcription factor network.
+PPARA	drug	cannabinoid	22705310	AEA and these other substrates activate non <b>cannabinoid</b> receptor systems, including TRPV1 and <strong>PPAR</strong> α receptors.
+PPARA	drug	cannabinoid	21631400	The present review discusses these therapeutic targets including noradrenaline and 5 HT reuptake inhibitors; sodium, calcium and potassium channels; inhibitory and excitatory neurotransmitters; neuropeptides including bradykinin, tachykinin, cholecystokinin, neuropeptide Y, vasoactive intestinal peptide, and CGRP; pro inflammatory cytokines; MAP kinases; <strong>PPAR</strong> γ; Na(+)/Ca(2+) exchanger; nitric oxide; purinergic receptors; neuronal nicotinic receptors; cation dependent chloride transporters; oxidative stress; matrix metalloproteinase and plasminogen activators; growth factors; transient receptor potential (TRP) channels; <b>endocannabinoids</b>; histamine receptors; dopamine; sigma receptors, beta adrenergic receptors, endothelins, and D amino acid oxidase.
+PPARA	drug	nicotine	21557729	Since recent evidence indicates that <strong>PPAR</strong> α can modulate <b>nicotine</b> reward, it is unclear whether AEA plays a role in the effects of URB597 on <b>nicotine</b> reward.
+PPARA	addiction	reward	21557729	Since recent evidence indicates that <strong>PPAR</strong> α can modulate nicotine <b>reward</b>, it is unclear whether AEA plays a role in the effects of URB597 on nicotine <b>reward</b>.
+PPARA	drug	cannabinoid	20801430	Inhibition of FAAH increases levels of several endogenous substances in the brain, including the <b>endocannabinoid</b> anandamide and the noncannabinoid fatty acid ethanolamides <b>oleoylethanolamide</b> (OEA) and <b>palmitoylethanolamide</b>, which are ligands for alpha type peroxisome proliferator activated nuclear receptors (<strong>PPAR</strong> α).
+PPARA	drug	nicotine	20801430	Here, we evaluated whether directly acting <strong>PPAR</strong> α agonists can modulate reward related effects of <b>nicotine</b>.
+PPARA	addiction	reward	20801430	Here, we evaluated whether directly acting <strong>PPAR</strong> α agonists can modulate <b>reward</b> related effects of nicotine.
+PPARA	drug	cannabinoid	20801430	We combined behavioral, neurochemical, and electrophysiological approaches to evaluate effects of the <strong>PPAR</strong> α agonists [[4 Chloro 6 [(2,3 dimethylphenyl)amino] 2 pyrimidinyl]thio]acetic acid (WY14643) and methyl <b>oleoylethanolamide</b> (methOEA; a long lasting form of OEA) on 1) nicotine self administration in rats and squirrel monkeys; 2) reinstatement of nicotine seeking behavior in rats and monkeys; 3) nicotine discrimination in rats; 4) nicotine induced electrophysiological activity of ventral tegmental area dopamine neurons in anesthetized rats; and 5) nicotine induced elevation of dopamine levels in the nucleus accumbens shell of freely moving rats.
+PPARA	drug	nicotine	20801430	We combined behavioral, neurochemical, and electrophysiological approaches to evaluate effects of the <strong>PPAR</strong> α agonists [[4 Chloro 6 [(2,3 dimethylphenyl)amino] 2 pyrimidinyl]thio]acetic acid (WY14643) and methyl oleoylethanolamide (methOEA; a long lasting form of OEA) on 1) <b>nicotine</b> self administration in rats and squirrel monkeys; 2) reinstatement of <b>nicotine</b> seeking behavior in rats and monkeys; 3) <b>nicotine</b> discrimination in rats; 4) <b>nicotine</b> induced electrophysiological activity of ventral tegmental area dopamine neurons in anesthetized rats; and 5) <b>nicotine</b> induced elevation of dopamine levels in the nucleus accumbens shell of freely moving rats.
+PPARA	addiction	relapse	20801430	We combined behavioral, neurochemical, and electrophysiological approaches to evaluate effects of the <strong>PPAR</strong> α agonists [[4 Chloro 6 [(2,3 dimethylphenyl)amino] 2 pyrimidinyl]thio]acetic acid (WY14643) and methyl oleoylethanolamide (methOEA; a long lasting form of OEA) on 1) nicotine self administration in rats and squirrel monkeys; 2) <b>reinstatement</b> of nicotine <b>seeking</b> behavior in rats and monkeys; 3) nicotine discrimination in rats; 4) nicotine induced electrophysiological activity of ventral tegmental area dopamine neurons in anesthetized rats; and 5) nicotine induced elevation of dopamine levels in the nucleus accumbens shell of freely moving rats.
+PPARA	drug	cocaine	20801430	The <strong>PPAR</strong> α agonists dose dependently decreased nicotine self administration and nicotine induced reinstatement in rats and monkeys but did not alter food  or <b>cocaine</b> reinforced operant behavior or the interoceptive effects of nicotine.
+PPARA	drug	nicotine	20801430	The <strong>PPAR</strong> α agonists dose dependently decreased <b>nicotine</b> self administration and <b>nicotine</b> induced reinstatement in rats and monkeys but did not alter food  or cocaine reinforced operant behavior or the interoceptive effects of <b>nicotine</b>.
+PPARA	addiction	relapse	20801430	The <strong>PPAR</strong> α agonists dose dependently decreased nicotine self administration and nicotine induced <b>reinstatement</b> in rats and monkeys but did not alter food  or cocaine reinforced operant behavior or the interoceptive effects of nicotine.
+PPARA	addiction	reward	20801430	The <strong>PPAR</strong> α agonists dose dependently decreased nicotine self administration and nicotine induced reinstatement in rats and monkeys but did not alter food  or cocaine reinforced <b>operant</b> behavior or the interoceptive effects of nicotine.
+PPARA	drug	nicotine	20801430	The <strong>PPAR</strong> α agonists also dose dependently decreased <b>nicotine</b> induced excitation of dopamine neurons in the ventral tegmental area and <b>nicotine</b> induced elevations of dopamine levels in the nucleus accumbens shell of rats.
+PPARA	drug	nicotine	20801430	The ability of WY14643 and methOEA to counteract the behavioral, electrophysiological, and neurochemical effects of <b>nicotine</b> was reversed by the <strong>PPAR</strong> α antagonist 1 [(4 Chlorophenyl)methyl] 3 [(1,1 dimethylethyl)thio] a,a dimethyl 5 (1 methylethyl) 1H Indole 2 propanoic acid (MK886).
+PPARA	drug	alcohol	20661551	In a rat model of early <b>alcohol</b> exposure (i.e., in utero and during lactation), we studied the effect of the lipid lowering peroxisome proliferator activated receptor (<strong>PPAR</strong>) alpha activator fenofibrate on psychobehavioral impairments.
+PPARA	drug	alcohol	20661551	Our results with fenofibrate suggest that the pharmacological modulation of nuclear receptors such as <strong>PPAR</strong> alpha may constitute a new therapeutic approach to managing the psychobehavioral disorders associated with early <b>alcohol</b> exposure.
+PPARA	drug	alcohol	20585647	<b>Ethanol</b> exposure led to glucose intolerance, elevated plasma insulin, compromised cardiac contractile and intracellular Ca(2+) properties, downregulated protein phosphatase PP2A subunit and <strong>PPAR</strong> gamma, as well as phosphorylation of AMPK, ACC and LKB1, all of which except plasma insulin were overtly accentuated by ADH transgene.
+PPARA	drug	nicotine	20570248	Among these, endogenous ligands to the nuclear receptor transcription factor peroxisome proliferator activated receptors type alpha (<strong>PPARalpha</strong>) have been recently found to suppress <b>nicotine</b> induced responses of dopamine neurons.
+PPARA	drug	nicotine	20570248	Additionally, <strong>PPARalpha</strong> activation in vivo reduces both the number of spontaneously active dopamine neurons and <b>nicotine</b> induced increased locomotion.
+PPARA	drug	nicotine	20570248	Thus, <strong>PPARalpha</strong> ligands might prove beneficial in treating disorders in which dopamine dysfunction plays a prominent role, such as schizophrenia and <b>nicotine</b> addiction.
+PPARA	addiction	addiction	20570248	Thus, <strong>PPARalpha</strong> ligands might prove beneficial in treating disorders in which dopamine dysfunction plays a prominent role, such as schizophrenia and nicotine <b>addiction</b>.
+PPARA	drug	cocaine	20477753	Effects of fatty acid amide hydrolase inhibition on neuronal responses to nicotine, <b>cocaine</b> and morphine in the nucleus accumbens shell and ventral tegmental area: involvement of <strong>PPAR</strong> alpha nuclear receptors.
+PPARA	drug	nicotine	20477753	Effects of fatty acid amide hydrolase inhibition on neuronal responses to <b>nicotine</b>, cocaine and morphine in the nucleus accumbens shell and ventral tegmental area: involvement of <strong>PPAR</strong> alpha nuclear receptors.
+PPARA	drug	opioid	20477753	Effects of fatty acid amide hydrolase inhibition on neuronal responses to nicotine, cocaine and <b>morphine</b> in the nucleus accumbens shell and ventral tegmental area: involvement of <strong>PPAR</strong> alpha nuclear receptors.
+PPARA	drug	cocaine	19698765	The absence of a functional <strong>peroxisome proliferator activated receptor alpha</strong> gene in mice enhances motor sensitizing effects of morphine, but not <b>cocaine</b>.
+PPARA	drug	opioid	19698765	The absence of a functional <strong>peroxisome proliferator activated receptor alpha</strong> gene in mice enhances motor sensitizing effects of <b>morphine</b>, but not cocaine.
+PPARA	drug	cocaine	19698765	The objectives were to examine the involvement of nuclear <strong>PPAR</strong> alpha in motor sensitization to morphine and <b>cocaine</b>, by using null mice (<strong>PPAR</strong> alpha  / mice), or the injection of a selective <strong>PPAR</strong> alpha agonist, [[4 chloro 6 [(2,3 dimethylphenyl)amino] 2 pyrimidinyl] thio]acetic acid (WY14643), in morphine treated mice.
+PPARA	drug	opioid	19698765	The objectives were to examine the involvement of nuclear <strong>PPAR</strong> alpha in motor sensitization to <b>morphine</b> and cocaine, by using null mice (<strong>PPAR</strong> alpha  / mice), or the injection of a selective <strong>PPAR</strong> alpha agonist, [[4 chloro 6 [(2,3 dimethylphenyl)amino] 2 pyrimidinyl] thio]acetic acid (WY14643), in <b>morphine</b> treated mice.
+PPARA	addiction	sensitization	19698765	The objectives were to examine the involvement of nuclear <strong>PPAR</strong> alpha in motor <b>sensitization</b> to morphine and cocaine, by using null mice (<strong>PPAR</strong> alpha  / mice), or the injection of a selective <strong>PPAR</strong> alpha agonist, [[4 chloro 6 [(2,3 dimethylphenyl)amino] 2 pyrimidinyl] thio]acetic acid (WY14643), in morphine treated mice.
+PPARA	drug	cocaine	19698765	The findings indicate that <strong>PPAR</strong> alpha plays an inhibitory role in the expression (not induction) of motor sensitization to morphine, but it is devoid of effects on sensitization to <b>cocaine</b>, suggesting that this nuclear receptor participates in motor activating effects of opiates but not psychostimulants.
+PPARA	drug	opioid	19698765	The findings indicate that <strong>PPAR</strong> alpha plays an inhibitory role in the expression (not induction) of motor sensitization to <b>morphine</b>, but it is devoid of effects on sensitization to cocaine, suggesting that this nuclear receptor participates in motor activating effects of opiates but not psychostimulants.
+PPARA	addiction	sensitization	19698765	The findings indicate that <strong>PPAR</strong> alpha plays an inhibitory role in the expression (not induction) of motor <b>sensitization</b> to morphine, but it is devoid of effects on <b>sensitization</b> to cocaine, suggesting that this nuclear receptor participates in motor activating effects of opiates but not psychostimulants.
+PPARA	drug	cocaine	19698765	Furthermore, brain <strong>PPAR</strong> alpha expression is upregulated after the highest dose of repeated morphine, but not chronic <b>cocaine</b>, suggesting that this receptor could play a homeostatic role.
+PPARA	drug	opioid	19698765	Furthermore, brain <strong>PPAR</strong> alpha expression is upregulated after the highest dose of repeated <b>morphine</b>, but not chronic cocaine, suggesting that this receptor could play a homeostatic role.
+PPARA	drug	opioid	19698765	In accordance, systemic WY14643 was able to block sensitization to <b>morphine</b>, confirming that <strong>PPAR</strong> alpha plays a homeostatic role opposing <b>morphine</b> induced motor sensitization, likely through a reduction of inflammation associated changes.
+PPARA	addiction	sensitization	19698765	In accordance, systemic WY14643 was able to block <b>sensitization</b> to morphine, confirming that <strong>PPAR</strong> alpha plays a homeostatic role opposing morphine induced motor <b>sensitization</b>, likely through a reduction of inflammation associated changes.
+PPARA	drug	alcohol	19673747	Increasing evidence supports a role for the nuclear factor (NF) kappaB, the NF kappaB inhibitor alpha (NFKBIA), and the peroxisome proliferator activated receptor (<strong>PPAR</strong>) gamma in the pathogenesis of <b>alcoholic</b> liver disease, raising the possibility that common polymorphisms in genes encoding these molecules may confer susceptibility to ALC.
+PPARA	drug	nicotine	19091987	They blocked the effects of <b>nicotine</b> by activation of the <strong>peroxisome proliferator activated receptor alpha</strong> (PPAR alpha), a nuclear receptor transcription factor involved in several aspects of lipid metabolism and energy balance.
+PPARA	drug	nicotine	19091987	They blocked the effects of <b>nicotine</b> by activation of the <strong>peroxisome proliferator activated receptor alpha</strong> (<strong>PPAR</strong> alpha), a nuclear receptor transcription factor involved in several aspects of lipid metabolism and energy balance.
+PPARA	drug	nicotine	19091987	These data indicate for the first time that the anorexic lipids OEA and PEA possess neuromodulatory properties as endogenous ligands of <strong>PPAR</strong> alpha in the brain and provide a potential new target for the treatment of <b>nicotine</b> addiction.
+PPARA	addiction	addiction	19091987	These data indicate for the first time that the anorexic lipids OEA and PEA possess neuromodulatory properties as endogenous ligands of <strong>PPAR</strong> alpha in the brain and provide a potential new target for the treatment of nicotine <b>addiction</b>.
+PPARA	drug	cannabinoid	19015836	Since anandamide is a ligand for not only <b>cannabinoid</b> receptors but also transient receptor potential vanilloid 1 (TRPV1) receptors, and as recently suggested, peroxisome proliferator activated nuclear receptor alpha (<strong>PPARalpha</strong>), we also determined whether anandamide's effects in this task were mediated by each of these receptors.
+PPARA	drug	cannabinoid	19015836	These effects were blocked by the TRPV1 antagonist capsazepine, but not by the <b>cannabinoid</b> receptor antagonist <b>rimonabant</b> or the <strong>PPARalpha</strong> antagonist MK886.
+PPARA	drug	cannabinoid	18724387	The <b>cannabinoid</b> receptor type 1 (CB(1)) antagonist AM251 (N (piperidin 1 yl) 5 (4 iodophenyl) 1 (2,4 dichlorophenyl) 4 methyl 1H pyrazole 3 carboxamide) and the peroxisome proliferator activated receptor (<strong>PPAR</strong>) alpha antagonist GW6471 ([(2S) 2 [[(1Z) 1 methyl 3 oxo 3 [4 (trifluoromethyl)phenyl] 1 propenyl]amino] 3 [4 [2 (5 methyl 2 phenyl 4 oxa zolyl)ethoxy]phenyl]propyl] carbamic acid ethyl ester) were used to investigate the roles of these receptors in mediating the effects of URB597.
+PPARA	addiction	sensitization	18724387	These data support the contention that URB597 exerts its antinociceptive effects by indirect inhibition of <b>sensitization</b> of neuronal responses at least partly through <strong>PPAR</strong> alpha activation due to enhanced EC levels.
+PPARA	drug	amphetamine	17019405	We examined the involvement of PPARgamma, one of the isotypes of <strong>PPAR</strong>, in development of behavioral sensitization to the stimulant effect of <b>methamphetamine</b> (<b>METH</b>) (1 mg/kg, subcutaneously) in mice.
+PPARA	addiction	sensitization	17019405	We examined the involvement of PPARgamma, one of the isotypes of <strong>PPAR</strong>, in development of behavioral <b>sensitization</b> to the stimulant effect of methamphetamine (METH) (1 mg/kg, subcutaneously) in mice.
+PPARA	drug	cannabinoid	15879057	<b>Oleoylethanolamide</b> (OEA), a lipid synthesized in the intestine, reduces food intake and stimulates lipolysis through <strong>peroxisome proliferator activated receptor alpha</strong>.
+PPARA	addiction	sensitization	15318101	Peroxisome proliferator activated receptor gamma (<strong>PPAR</strong> gamma), which is a ligand dependent transcriptional factor, forms a heterodimer with retinoid X receptor (RXR) and controls many genes that are relevant to the regulation of lipid metabolism and insulin <b>sensitization</b>.
+PPARA	drug	alcohol	15318101	In this study, we investigated the effects of pioglitazone, a ligand for <strong>PPAR</strong> gamma, on acute liver injury induced by <b>ethanol</b> and LPS.
+PPARA	drug	alcohol	15318101	<strong>PPAR</strong> gamma mRNA levels were suppressed by <b>ethanol</b> and LPS but recaptured by pioglitazone.
+PPARA	drug	alcohol	12805475	This study was intended to determine whether pioglitazone, a <strong>PPAR</strong> gamma agonist, could prevent <b>alcohol</b> induced liver injury.
+PPARA	drug	alcohol	11840500	Mutation analysis of the retinoid X receptor beta, nuclear related receptor 1, and <strong>peroxisome proliferator activated receptor alpha</strong> genes in schizophrenia and <b>alcohol</b> dependence: possible haplotype association of nuclear related receptor 1 gene to <b>alcohol</b> dependence.
+PPARA	addiction	dependence	11840500	Mutation analysis of the retinoid X receptor beta, nuclear related receptor 1, and <strong>peroxisome proliferator activated receptor alpha</strong> genes in schizophrenia and alcohol <b>dependence</b>: possible haplotype association of nuclear related receptor 1 gene to alcohol <b>dependence</b>.
+PPARA	drug	alcohol	11840500	We examined 48 Japanese patients with schizophrenia and 32 patients with <b>alcohol</b> dependence to detect mutations in the retinoid X receptor beta gene (RXRB) on chromosome 6p21.3, the NURR1 gene (NR4A2) on chromosome 2q22 q23, and the PPAR alpha gene (<strong>PPARA</strong>) on chromosome 22q12.2 13.1.
+PPARA	addiction	dependence	11840500	We examined 48 Japanese patients with schizophrenia and 32 patients with alcohol <b>dependence</b> to detect mutations in the retinoid X receptor beta gene (RXRB) on chromosome 6p21.3, the NURR1 gene (NR4A2) on chromosome 2q22 q23, and the PPAR alpha gene (<strong>PPARA</strong>) on chromosome 22q12.2 13.1.
+PPARA	drug	alcohol	11840500	We examined 48 Japanese patients with schizophrenia and 32 patients with <b>alcohol</b> dependence to detect mutations in the retinoid X receptor beta gene (RXRB) on chromosome 6p21.3, the NURR1 gene (NR4A2) on chromosome 2q22 q23, and the <strong>PPAR</strong> alpha gene (<strong>PPARA</strong>) on chromosome 22q12.2 13.1.
+PPARA	addiction	dependence	11840500	We examined 48 Japanese patients with schizophrenia and 32 patients with alcohol <b>dependence</b> to detect mutations in the retinoid X receptor beta gene (RXRB) on chromosome 6p21.3, the NURR1 gene (NR4A2) on chromosome 2q22 q23, and the <strong>PPAR</strong> alpha gene (<strong>PPARA</strong>) on chromosome 22q12.2 13.1.
+IL4	drug	alcohol	31510019	<b>Ethanol</b> Induction of Innate Immune Signals Across BV2 Microglia and SH SY5Y Neuroblastoma Involves Induction of <strong>IL 4</strong> and IL 13.
+IL4	drug	alcohol	31510019	In contrast, co culture resulted in <b>ethanol</b> upregulation of cytokines <strong>IL 4</strong> and IL 13 in BV2 and corresponding receptors, that is, <strong>IL 4</strong> and IL 13 receptors, in SH SY5Y, suggesting induction of a novel signaling pathway.
+IL4	addiction	intoxication	30625475	<b>Binge</b> like consumption resulted in a 67% decrease in IL 10 immunoreactivity but had no effect on <strong>IL 4</strong> or IL 6 compared with the water drinking control group.
+IL4	drug	nicotine	30218019	<b>Nicotine</b> and <strong>IL 4</strong> levels were predictors of higher pain threshold.
+IL4	drug	alcohol	30090529	Chronic high dosage fish oil exacerbates gut liver axis injury in <b>alcoholic</b> steatohepatitis in mice: the roles of endotoxin and <strong>IL 4</strong> in Kupffer cell polarization imbalance.
+IL4	drug	alcohol	30090529	Overall, our results showed that a chronic high dosage of fish oil exacerbated gut liver axis injury in <b>alcoholic</b> liver disease in mice, and endotoxin/<strong>IL 4</strong> induced Kupffer cell polarization imbalance might play an important role in that process.
+IL4	drug	alcohol	29733875	We measured the acute concentrations and dynamics of lipoxins LxA4 and LxB4 and the interleukins <strong>IL 4</strong>, IL 5, IL 9, IL 10, and IL 13 in the serum of patients treated with methyl <b>alcohol</b> poisoning and the follow up concentrations in survivors two years after discharge from the hospital.
+IL4	drug	opioid	29615715	Blocking <strong>interleukin 4</strong> enhances efficacy of vaccines for treatment of <b>opioid</b> abuse and prevention of <b>opioid</b> overdose.
+IL4	drug	opioid	29615715	Blockage of <strong>IL 4</strong> signaling increased vaccine efficacy in blocking <b>oxycodone</b> distribution to the brain and protection against <b>opioid</b> induced behavior and toxicity in mice.
+IL4	addiction	withdrawal	28468077	Before and after the 14(th) day of <b>withdrawal</b>, levels of immunoglobulin (IgM, IgA, IgG), T cell subsets (CD(3)(+), CD(4)(+), CD(8)(+), CD(4)(+)/CD(8)(+)) and cytokines (IL 2, IFN γ, <strong>IL 4</strong>, IFN γ/<strong>IL 4</strong>) were detected.
+IL4	drug	opioid	28468077	Results: Compared with healthy people, immunity function before withdrawal among the <b>opioid</b> abusers showed higher levels of IgM, IL 2, IFN γ, <strong>IL 4</strong> and lower level of CD(3)(+)T, as (1.67±0.87) g/L, (14.44±13.50)%, (20.23±15.10)%, (1.97±1.59)%, (47.01±13.62)%, respectively, with difference statistically significant (P<0.05).
+IL4	addiction	withdrawal	28468077	Results: Compared with healthy people, immunity function before <b>withdrawal</b> among the opioid abusers showed higher levels of IgM, IL 2, IFN γ, <strong>IL 4</strong> and lower level of CD(3)(+)T, as (1.67±0.87) g/L, (14.44±13.50)%, (20.23±15.10)%, (1.97±1.59)%, (47.01±13.62)%, respectively, with difference statistically significant (P<0.05).
+IL4	addiction	withdrawal	28468077	At the 14(th) day of <b>withdrawal</b> in placebo group, levels of <strong>IL 4</strong> returned to normal while IFN γ/<strong>IL 4</strong> ratio increased by 3.43 times (P<0.05).
+IL4	drug	opioid	28468077	Level of <strong>IL 4</strong> abnormally rose up by 0.54 times in Jitai tablet plus <b>buprenorphine</b> group, while IFN γ/<strong>IL 4</strong> ratio been switched back at the 14(th) day of withdrawal.
+IL4	addiction	withdrawal	28468077	Level of <strong>IL 4</strong> abnormally rose up by 0.54 times in Jitai tablet plus buprenorphine group, while IFN γ/<strong>IL 4</strong> ratio been switched back at the 14(th) day of <b>withdrawal</b>.
+IL4	drug	alcohol	28427424	Acute <b>ethanol</b> withdrawal dose dependently increased neuroimmune gene (e.g., TNFα, Ccl2, IL 1ra, <strong>IL 4</strong>) expression beginning at high doses.
+IL4	addiction	withdrawal	28427424	Acute ethanol <b>withdrawal</b> dose dependently increased neuroimmune gene (e.g., TNFα, Ccl2, IL 1ra, <strong>IL 4</strong>) expression beginning at high doses.
+IL4	drug	alcohol	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, Ccl2) gene expression and enhanced anti inflammatory (e.g., IL 1ra, <strong>IL 4</strong>) gene expression during acute binge <b>ethanol</b> withdrawal.
+IL4	addiction	intoxication	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, Ccl2) gene expression and enhanced anti inflammatory (e.g., IL 1ra, <strong>IL 4</strong>) gene expression during acute <b>binge</b> ethanol withdrawal.
+IL4	addiction	withdrawal	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, Ccl2) gene expression and enhanced anti inflammatory (e.g., IL 1ra, <strong>IL 4</strong>) gene expression during acute binge ethanol <b>withdrawal</b>.
+IL4	drug	opioid	28206989	<strong>IL 4</strong> mediated by HSV vector suppresses <b>morphine</b> withdrawal response and decreases TNFα, NR2B, and pC/EBPβ in the periaqueductal gray in rats.
+IL4	addiction	withdrawal	28206989	<strong>IL 4</strong> mediated by HSV vector suppresses morphine <b>withdrawal</b> response and decreases TNFα, NR2B, and pC/EBPβ in the periaqueductal gray in rats.
+IL4	drug	opioid	28206989	Here, we used recombinant herpes simplex virus vector S4IL4 that encode mouse <strong>il4</strong> gene to evaluate the therapeutic potential of IL 4 in <b>naloxone</b> precipitation <b>morphine</b> withdrawal (MW).
+IL4	addiction	withdrawal	28206989	Here, we used recombinant herpes simplex virus vector S4IL4 that encode mouse <strong>il4</strong> gene to evaluate the therapeutic potential of IL 4 in naloxone precipitation morphine <b>withdrawal</b> (MW).
+IL4	drug	opioid	28206989	Here, we used recombinant herpes simplex virus vector S4IL4 that encode mouse <strong>il4</strong> gene to evaluate the therapeutic potential of <strong>IL 4</strong> in <b>naloxone</b> precipitation <b>morphine</b> withdrawal (MW).
+IL4	addiction	withdrawal	28206989	Here, we used recombinant herpes simplex virus vector S4IL4 that encode mouse <strong>il4</strong> gene to evaluate the therapeutic potential of <strong>IL 4</strong> in naloxone precipitation morphine <b>withdrawal</b> (MW).
+IL4	drug	alcohol	27699959	The results showed that <b>alcohol</b> intoxication increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, <strong>IL 4</strong>, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+IL4	addiction	intoxication	27699959	The results showed that alcohol <b>intoxication</b> increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, <strong>IL 4</strong>, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+IL4	drug	alcohol	27640210	The current study furthers this research by determining the impact of excessive <b>ethanol</b> consumption on interleukin 10 (IL 10) and interleukin 4 (<strong>IL 4</strong>) activity in a model of non dependent binge consumption called the "drinking in the dark" (DID) paradigm.
+IL4	addiction	intoxication	27640210	The current study furthers this research by determining the impact of excessive ethanol consumption on interleukin 10 (IL 10) and interleukin 4 (<strong>IL 4</strong>) activity in a model of non dependent <b>binge</b> consumption called the "drinking in the dark" (DID) paradigm.
+IL4	drug	alcohol	27640210	The current study furthers this research by determining the impact of excessive <b>ethanol</b> consumption on interleukin 10 (IL 10) and <strong>interleukin 4</strong> (<strong>IL 4</strong>) activity in a model of non dependent binge consumption called the "drinking in the dark" (DID) paradigm.
+IL4	addiction	intoxication	27640210	The current study furthers this research by determining the impact of excessive ethanol consumption on interleukin 10 (IL 10) and <strong>interleukin 4</strong> (<strong>IL 4</strong>) activity in a model of non dependent <b>binge</b> consumption called the "drinking in the dark" (DID) paradigm.
+IL4	drug	alcohol	27640210	Immunohistochemistry analyses determined that <b>ethanol</b> decreased IL 10 by 50 % in the basolateral amygdala (BLA) but had no effect on <strong>IL 4</strong>.
+IL4	addiction	intoxication	27455577	It was established in experiments on noninbred albino rats that the acute <b>intoxication</b> with methanol (1.0 LD50) decreased cellular and humoral immune responses, Th2 lymphocyte activity (to a greater extent as compared to the function of Th1 cells), reduced the blood concentration of immunoregulatory (IFN g, IL 2, <strong>IL 4</strong>) and proinflammatory (TNF, IL 1b, IL 6) cytokines on the average by 36.5% (p < 0.05), and did not affect the content of anti inflammatory cytokines (IL 10, IL 13).
+IL4	drug	alcohol	27455577	Methanol antidote 4 methylpyrazole (non competitive inhibitor of <b>alcohol</b> dehydrogenase) administered upon acute intoxication with methanol at a dose of 1.0 DL50 partially reduces the intoxication induced suppression of humoral and cellular immune response, activity of T helper cells, and production of <strong>IL 4</strong> and restores blood levels of TNF, IL 1b, IFN γ, <strong>IL 4</strong>, IL 2, IL 6 to the control values.
+IL4	addiction	intoxication	27455577	Methanol antidote 4 methylpyrazole (non competitive inhibitor of alcohol dehydrogenase) administered upon acute <b>intoxication</b> with methanol at a dose of 1.0 DL50 partially reduces the <b>intoxication</b> induced suppression of humoral and cellular immune response, activity of T helper cells, and production of <strong>IL 4</strong> and restores blood levels of TNF, IL 1b, IFN γ, <strong>IL 4</strong>, IL 2, IL 6 to the control values.
+IL4	drug	amphetamine	26322025	In addition, the serum pro inflammatory (TNF, IL12 p70, IL1β, IL 6, and KC GRO) and Th2 (IL 2, IL 10, and <strong>IL 4</strong>) cytokine profiles were also altered in the presence of <b>METH</b>.
+IL4	drug	alcohol	25661730	Importantly, several cytokines and chemokines (e.g., MIP 2, MIP 1, <strong>IL 4</strong>, IL 6 and osteopontin) involved in neutrophil infiltration were upregulated in hepatic NKT cells isolated from chronic plus binge <b>ethanol</b> fed mice compared to pair fed mice.
+IL4	addiction	intoxication	25661730	Importantly, several cytokines and chemokines (e.g., MIP 2, MIP 1, <strong>IL 4</strong>, IL 6 and osteopontin) involved in neutrophil infiltration were upregulated in hepatic NKT cells isolated from chronic plus <b>binge</b> ethanol fed mice compared to pair fed mice.
+IL4	addiction	sensitization	25524712	Prior studies have shown that exposure to lead is associated with atopic <b>sensitization</b> and modulation of several cytokines (eg, interleukin [IL] 12, IL 10, interferon [IFN] γ, and <strong>IL 4</strong> production) and with T cell dysregulation and bias toward T helper 2 (Th2) activity.
+IL4	addiction	sensitization	24389455	TH1 cytokines (IL 2, IFN γ) and TH2 cytokines (<strong>IL 4</strong>, IL 5) releases from lymph node cell culture were also investigated as contact <b>sensitization</b> endpoints.
+IL4	addiction	relapse	24050582	Mizadj, clinically EDSS and <b>relapse</b> rate as well as immunological factors (<strong>IL 4</strong>, IFN γ and IL 17) were assessed at baseline and after 6 months.
+IL4	drug	amphetamine	23026442	Elevated levels of <strong>IL 4</strong>, but decreased levels of IL 10 were also found in samples of lung explants after <b>AMPH</b> treatment.
+IL4	drug	amphetamine	23026442	Our data strongly indicate that <b>AMPH</b> positively modulates allergic lung inflammation via the increase of ICAM 1, PECAM 1, Mac 1 and <strong>IL 4</strong>.
+IL4	drug	alcohol	22803049	Experiments of outbred albino rats showed that chronic <b>ethanol</b> intoxication (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1 cells, increased blood corticosterone concentration, reduced T lymphocyte acetylcholinesterase activity, blood concentrations of IFN γ, IL 2, <strong>IL 4</strong>, IL 10, and increased IL 6 level.
+IL4	addiction	intoxication	22803049	Experiments of outbred albino rats showed that chronic ethanol <b>intoxication</b> (20 days, summary dose 5 LD(50)) inhibited immune reactions mainly mediated by Th1 cells, increased blood corticosterone concentration, reduced T lymphocyte acetylcholinesterase activity, blood concentrations of IFN γ, IL 2, <strong>IL 4</strong>, IL 10, and increased IL 6 level.
+IL4	drug	alcohol	22003193	Pulmonary exposure to 2% furfuryl <b>alcohol</b> resulted in enhanced airway hyperreactivity, eosinophilic infiltration into the lungs, and enhanced cytokine production (<strong>IL 4</strong>, IL 5, and interferon γ) by ex vivo stimulated lung associated draining lymphoid cells.
+IL4	drug	alcohol	21421450	<b>Alcoholics</b> admitted for programmed withdrawal showed higher IL 6, IFN γ, IL 10, <strong>Il 4</strong> and ICAM 1 serum levels than healthy controls.
+IL4	addiction	withdrawal	21421450	Alcoholics admitted for programmed <b>withdrawal</b> showed higher IL 6, IFN γ, IL 10, <strong>Il 4</strong> and ICAM 1 serum levels than healthy controls.
+IL4	drug	alcohol	21254593	It was established in experiments on noninbred rats that their <b>ethanol</b> intoxication (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, IL 2, <strong>IL 4</strong>, IL 10, increases the concentration of IL 6, suppresses the immune responses, and reduces the interrelation IFNgamma/<strong>IL 4</strong> in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes.
+IL4	addiction	intoxication	21254593	It was established in experiments on noninbred rats that their ethanol <b>intoxication</b> (13 days; total dose, 2.6 LD50) significantly reduces the concentration of blood cytokines IFNgamma, IL 2, <strong>IL 4</strong>, IL 10, increases the concentration of IL 6, suppresses the immune responses, and reduces the interrelation IFNgamma/<strong>IL 4</strong> in comparison to the control, which testifies to the greater damage of Th1 cells in comparison to Th2 lymphocytes.
+IL4	drug	opioid	20440572	Here, we demonstrate that a single <b>morphine</b> injection (10 mg/kg) reduces basal MHC II protein expression on circulating B lymphocytes by 33%, while also impairing the ability of B lymphocytes to increase MHC II upon <strong>interleukin 4</strong> induction.
+IL4	addiction	sensitization	19672097	Ovalbumin <b>sensitization</b> and challenge caused rhinitis pathology including inflammatory cell infiltration, <strong>IL 4</strong>, and protein leakage in the nasal lavage fluid (NLF) and presence of inflammatory cells in nasal epithelium.
+IL4	drug	alcohol	19485975	Monocytes were cultured with human <strong>IL 4</strong> (10 ng/ml) and GM CSF (50 ng/ml) in the absence and presence of <b>alcohol</b> (50 mM).
+IL4	drug	alcohol	19185507	Common polymorphisms in interleukin genes (<strong>IL4</strong>, IL6, IL8 and IL12) are not associated with <b>alcoholic</b> liver disease or <b>alcoholism</b> in Spanish men.
+IL4	drug	amphetamine	18706494	Concordantly, splenocytes of mice administered with diazepam and/or <b>methamphetamine</b> produced less <strong>IL 4</strong> and IFN gamma upon ex vivo re stimulation with OVA, as compared to the vehicle treated control.
+IL4	drug	benzodiazepine	18706494	Concordantly, splenocytes of mice administered with <b>diazepam</b> and/or methamphetamine produced less <strong>IL 4</strong> and IFN gamma upon ex vivo re stimulation with OVA, as compared to the vehicle treated control.
+IL4	drug	nicotine	18410779	Environmental <b>tobacco</b> smoke and <strong>interleukin 4</strong> polymorphism (C 589T) gene: environment interaction increases risk of wheezing in African American infants.
+IL4	drug	nicotine	18410779	To determine whether infants exposed to environmental <b>tobacco</b> smoke (ETS) having the interleukin 4 (<strong>IL 4</strong>) or interleukin 13 (IL 13) gene polymorphisms were at increased risk of wheezing.
+IL4	drug	nicotine	18410779	To determine whether infants exposed to environmental <b>tobacco</b> smoke (ETS) having the <strong>interleukin 4</strong> (<strong>IL 4</strong>) or interleukin 13 (IL 13) gene polymorphisms were at increased risk of wheezing.
+IL4	drug	opioid	18294814	An altered Th1/Th2 balance, characterized by reduced <strong>IL 4</strong>, IFN gamma and TNF alpha but normal IL 2 levels, was present in untreated <b>heroin</b> addicted subjects, while the Th1/Th2 balance was well conserved in the <b>methadone</b> and <b>buprenorphine</b> groups.
+IL4	drug	opioid	17974159	Moreover, <strong>IL 4</strong> production was suppressed in Hw, but not in HBw groups and the in vitro presence of <b>naloxone</b> did not affect the level of <strong>IL 4</strong> in both groups.
+IL4	drug	opioid	16081842	It was determined that 24 h <b>morphine</b> withdrawal resulted in a decrease in IFN gamma, the Th1 signature cytokine, whereas the Th2 cytokine, <strong>IL 4</strong>, was increased.
+IL4	addiction	withdrawal	16081842	It was determined that 24 h morphine <b>withdrawal</b> resulted in a decrease in IFN gamma, the Th1 signature cytokine, whereas the Th2 cytokine, <strong>IL 4</strong>, was increased.
+IL4	drug	nicotine	15495789	Epidemiological data showed that total IgE and <strong>IL 4</strong> levels in cigarette <b>smokers</b> were elevated, comparable to those in the asthmatics.
+IL4	drug	nicotine	15495789	In contrast, significant levels of <strong>IL 4</strong>, IL 12, and IFN gamma were observed in antigen challenged cultures from <b>nicotine</b> treated mice.
+IL4	drug	alcohol	15289211	In 36 <b>alcoholics</b> without liver disease, at the point of commencing withdrawal from <b>alcohol</b>, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, IL1RA, <strong>IL4</strong>, IL6, IL8, IL10 and IL12).
+IL4	addiction	withdrawal	15289211	In 36 alcoholics without liver disease, at the point of commencing <b>withdrawal</b> from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, IL1RA, <strong>IL4</strong>, IL6, IL8, IL10 and IL12).
+IL4	addiction	sensitization	15007352	These findings not only suggested that variants in the <strong>IL4</strong>, IL13, and IL4RA genes play an important role in controlling specific IgE response but also strengthened our understanding of gene gene and gene environment interaction on the development of specific <b>sensitization</b> in this study population.
+IL4	drug	opioid	14741432	We had previously shown that chronic <b>morphine</b> treatment in vivo and in vitro decreases IL 2 and IFNgamma (Th1) protein levels and increases <strong>IL 4</strong> and IL 5 (Th2) protein levels in a time dependent manner.
+IL4	drug	opioid	14741432	In addition in this paper, we show that chronic <b>morphine</b> treatment resulted in a decrease in IFNgamma and IL 2 mRNA and an increase in <strong>IL 4</strong> and IL 5 mRNA accumulation in murine splenocytes.
+IL4	drug	opioid	14741432	Furthermore, chronic <b>morphine</b> treatment inhibited IFNgamma promoter activity and increased <strong>IL 4</strong> promoter activity in respective promoter transfected primary T cells.
+IL4	drug	nicotine	12907840	We provided a self administered questionnaire to evaluate sleep habits, <b>smoking</b> and medical disorders to 578 men without any toxic exposure (20 64 years old), and measured natural killer (NK) cell activity in 324 men and production of interferon gamma (IFN gamma) and interleukin 4 (<strong>IL 4</strong>) after stimulation with phytohemagglutinin in 254 men.
+IL4	drug	nicotine	12907840	We provided a self administered questionnaire to evaluate sleep habits, <b>smoking</b> and medical disorders to 578 men without any toxic exposure (20 64 years old), and measured natural killer (NK) cell activity in 324 men and production of interferon gamma (IFN gamma) and <strong>interleukin 4</strong> (<strong>IL 4</strong>) after stimulation with phytohemagglutinin in 254 men.
+IL4	drug	cannabinoid	12668119	T cells are sensitive to modulation by <b>cannabinoids</b> as evidenced by their ability to inhibit expression of cytokines, including interleukin (IL) 2 and <strong>IL 4</strong>.
+IL4	drug	cannabinoid	12668119	<b>Cannabinol</b> (CBN) or Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>; 50 mg/kg, ip), administered daily for 3 consecutive days before sensitization and then before challenge, significantly attenuated the elevation of IL 2, <strong>IL 4</strong>, IL 5, and IL 13 steady state mRNA expression elicited by Ova challenge in the lungs.
+IL4	addiction	sensitization	12668119	Cannabinol (CBN) or Delta(9) tetrahydrocannabinol (Delta(9) THC; 50 mg/kg, ip), administered daily for 3 consecutive days before <b>sensitization</b> and then before challenge, significantly attenuated the elevation of IL 2, <strong>IL 4</strong>, IL 5, and IL 13 steady state mRNA expression elicited by Ova challenge in the lungs.
+IL4	drug	alcohol	12488491	The enriched T cells of chronic <b>ethanol</b> mice secreted more IFN gamma and <strong>IL 4</strong> than controls and equivalent IL 2 at early times after stimulation (6 24 h).
+IL4	drug	alcohol	11505051	The ratio of <strong>IL 4</strong> to interferon gamma production by phytohemagglutinin stimulated PBMCs (as an approach to Th2/Th1 balance) was significantly lower in <b>alcoholics</b> than in healthy controls, both in the atopic and in the nonatopic group.
+IL4	addiction	withdrawal	10470972	After a <b>withdrawal</b> period of > or =1 yr, ALC patients did not show significant changes in the cytoplasmic expression of Th 1 associated cytokines compared with the control group; in contrast, these patients showed a marked increase on the proportion of CD4+ and CD8strong+ T cells expressing <strong>IL 4</strong>, a Th 2 associated cytokine (p<0.01).
+IL4	drug	cannabinoid	8807671	The production of the cytokine interleukin 2 by T helper cells was markedly suppressed in both tolerant and abstinent mice, whereas the production of <strong>interleukin 4</strong> was significantly suppressed only in <b>THC</b> abstinent mice.
+IL4	addiction	withdrawal	9815906	Patients were treated at levels of up to 300 microgram/m2/injection of <strong>IL 4</strong> before the study was closed due to <b>withdrawal</b> of the drug by the manufacturer.
+IL4	addiction	withdrawal	9815906	Because of the <strong>IL 4</strong> <b>withdrawal</b>, the maximum tolerated dose for this combination of drugs given by the route and schedule used here was not determined and will require additional testing.
+IL4	drug	opioid	8032870	<b>Morphine</b> tolerance was associated with suppressed B cell proliferation following in vitro stimulation, as well as interleukin 2 (IL 2) and <strong>interleukin 4</strong> production by T cells.
+ANKK1	drug	opioid	32588604	Significant association of DRD2 and <strong>ANKK1</strong> genes with rural <b>heroin</b> dependence and relapse in men.
+ANKK1	addiction	dependence	32588604	Significant association of DRD2 and <strong>ANKK1</strong> genes with rural heroin <b>dependence</b> and relapse in men.
+ANKK1	addiction	relapse	32588604	Significant association of DRD2 and <strong>ANKK1</strong> genes with rural heroin dependence and <b>relapse</b> in men.
+ANKK1	addiction	addiction	32260442	<strong>Ankyrin Repeat and Kinase Domain Containing 1</strong> Gene, and <b>Addiction</b> Vulnerability.
+ANKK1	drug	alcohol	32260442	In antisocial <b>alcoholism</b>, epistasis between <strong>ANKK1</strong> TaqIA and DRD2 C957T SNVs has been described.
+ANKK1	drug	alcohol	32260442	This clinical finding has been supported by the study of <strong>ANKK1</strong> expression in peripheral blood mononuclear cells of <b>alcoholic</b> patients and controls.
+ANKK1	addiction	addiction	32260442	Together, these findings of the <strong>ANKK1</strong> gene and its protein suggest that the TaqIA SNV is a marker of brain differences, both in structure and in dopaminergic function, that increase individual risk to <b>addiction</b> development.
+ANKK1	drug	nicotine	31867628	Genetic and Epigenetic Analysis Revealing Variants in the NCAM1 TTC12 <strong>ANKK1</strong> DRD2 Cluster Associated Significantly With <b>Nicotine</b> Dependence in Chinese Han <b>Smokers</b>.
+ANKK1	addiction	dependence	31867628	Genetic and Epigenetic Analysis Revealing Variants in the NCAM1 TTC12 <strong>ANKK1</strong> DRD2 Cluster Associated Significantly With Nicotine <b>Dependence</b> in Chinese Han Smokers.
+ANKK1	drug	nicotine	31867628	Further, we identified four significant <b>smoking</b> associated DMRs, three of which are located in the DRD2/<strong>ANKK1</strong> region (p = .0012 .00005).
+ANKK1	drug	nicotine	31867628	We found the majority of <b>smoking</b> related DMRs are located in the <strong>ANKK1</strong>/DRD2 region, indicating a likely causative relation between non synonymous SNPs and DMRs.
+ANKK1	drug	nicotine	31867628	This study shows that there exist significant association of variants and haplotypes in <strong>ANKK1</strong>/DRD2 region with ND in Chinese male <b>smokers</b>.
+ANKK1	drug	nicotine	30104163	A neurobiological pathway to <b>smoking</b> in adolescence: TTC12 <strong>ANKK1</strong> DRD2 variants and reward response.
+ANKK1	addiction	reward	30104163	A neurobiological pathway to smoking in adolescence: TTC12 <strong>ANKK1</strong> DRD2 variants and <b>reward</b> response.
+ANKK1	drug	nicotine	30104163	The TTC12 <strong>ANKK1</strong> DRD2 gene cluster has been implicated in adult <b>smoking</b>.
+ANKK1	drug	nicotine	30104163	Here, we investigated the contribution of individual genes in the TTC12 <strong>ANKK1</strong> DRD2 cluster in <b>smoking</b> and their association with <b>smoking</b> associated reward processing in adolescence.
+ANKK1	addiction	reward	30104163	Here, we investigated the contribution of individual genes in the TTC12 <strong>ANKK1</strong> DRD2 cluster in smoking and their association with smoking associated <b>reward</b> processing in adolescence.
+ANKK1	drug	nicotine	30104163	A meta analysis of TTC12 <strong>ANKK1</strong> DRD2 variants and self reported <b>smoking</b> behaviours was performed in four European adolescent cohorts (N = 14,084).
+ANKK1	drug	nicotine	30104163	These data suggest a role for the TTC12 <strong>ANKK1</strong> DRD2 gene cluster in adolescent <b>smoking</b> behaviours, provide evidence for the involvement of DRD2 in the early stages of addiction and support the notion that genetically driven inter individual differences in dopaminergic transmission mediate reward sensitivity and risk to <b>smoking</b>.
+ANKK1	addiction	addiction	30104163	These data suggest a role for the TTC12 <strong>ANKK1</strong> DRD2 gene cluster in adolescent smoking behaviours, provide evidence for the involvement of DRD2 in the early stages of <b>addiction</b> and support the notion that genetically driven inter individual differences in dopaminergic transmission mediate reward sensitivity and risk to smoking.
+ANKK1	addiction	reward	30104163	These data suggest a role for the TTC12 <strong>ANKK1</strong> DRD2 gene cluster in adolescent smoking behaviours, provide evidence for the involvement of DRD2 in the early stages of addiction and support the notion that genetically driven inter individual differences in dopaminergic transmission mediate <b>reward</b> sensitivity and risk to smoking.
+ANKK1	addiction	reward	29909784	The results demonstrated a regional specificity with which the functional polymorphism rs686 of the D1 dopamine receptor (DRD1) gene and Taq1A of the <strong>ANKK1</strong> gene influenced medial and lateral OFC activation during <b>reward</b> anticipation, respectively.
+ANKK1	drug	amphetamine	29702335	DRD2/<strong>ANKK1</strong> gene polymorphisms in forensic autopsies of <b>methamphetamine</b> intoxication fatalities.
+ANKK1	addiction	intoxication	29702335	DRD2/<strong>ANKK1</strong> gene polymorphisms in forensic autopsies of methamphetamine <b>intoxication</b> fatalities.
+ANKK1	addiction	addiction	29702335	Dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/<strong>ANKK1</strong>) gene polymorphisms have been associated with responses to psychotropic drugs and <b>addiction</b>.
+ANKK1	addiction	addiction	29702335	Dopamine D2 receptor/<strong>ankyrin repeat and kinase domain containing 1</strong> (DRD2/<strong>ANKK1</strong>) gene polymorphisms have been associated with responses to psychotropic drugs and <b>addiction</b>.
+ANKK1	drug	amphetamine	29702335	We analyzed two DRD2/<strong>ANKK1</strong> polymorphisms, Taq1A and  141C Ins/Del, in 37 fatal <b>methamphetamine</b> (MA) intoxication cases and 235 control cases in which MA and psychotropic drugs were not detected.
+ANKK1	addiction	intoxication	29702335	We analyzed two DRD2/<strong>ANKK1</strong> polymorphisms, Taq1A and  141C Ins/Del, in 37 fatal methamphetamine (MA) <b>intoxication</b> cases and 235 control cases in which MA and psychotropic drugs were not detected.
+ANKK1	addiction	intoxication	29702335	No significant associations were observed between  141C Ins/Del polymorphisms and MA <b>intoxication</b> cases or between DRD2/<strong>ANKK1</strong> polymorphisms and CSF dopamine concentrations.
+ANKK1	addiction	intoxication	29702335	Our findings suggest that the DRD2/<strong>ANKK1</strong> Taq1A polymorphism is associated with susceptibility to fatal MA <b>intoxication</b>.
+ANKK1	drug	opioid	29550268	A 35.8 kilobases haplotype spanning <strong>ANKK1</strong> and DRD2 is associated with <b>heroin</b> dependence in Han Chinese males.
+ANKK1	addiction	dependence	29550268	A 35.8 kilobases haplotype spanning <strong>ANKK1</strong> and DRD2 is associated with heroin <b>dependence</b> in Han Chinese males.
+ANKK1	drug	opioid	29550268	Ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) and dopamine receptor D2 (DRD2) gene polymorphisms have long been considered to contribute to susceptibility to <b>heroin</b> dependence.
+ANKK1	addiction	dependence	29550268	Ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) and dopamine receptor D2 (DRD2) gene polymorphisms have long been considered to contribute to susceptibility to heroin <b>dependence</b>.
+ANKK1	drug	opioid	29550268	<strong>Ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) and dopamine receptor D2 (DRD2) gene polymorphisms have long been considered to contribute to susceptibility to <b>heroin</b> dependence.
+ANKK1	addiction	dependence	29550268	<strong>Ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) and dopamine receptor D2 (DRD2) gene polymorphisms have long been considered to contribute to susceptibility to heroin <b>dependence</b>.
+ANKK1	drug	opioid	29550268	Despite their adjacent locations, few studies have elucidated the role of the potential interaction between <strong>ANKK1</strong> and DRD2 in <b>heroin</b> dependence.
+ANKK1	addiction	dependence	29550268	Despite their adjacent locations, few studies have elucidated the role of the potential interaction between <strong>ANKK1</strong> and DRD2 in heroin <b>dependence</b>.
+ANKK1	drug	opioid	29550268	According to our results, polymorphisms of four unreported loci were associated with <b>heroin</b> dependence, among which rs11214598 of <strong>ANKK1</strong> were still significant after multiple testing.
+ANKK1	addiction	dependence	29550268	According to our results, polymorphisms of four unreported loci were associated with heroin <b>dependence</b>, among which rs11214598 of <strong>ANKK1</strong> were still significant after multiple testing.
+ANKK1	drug	opioid	29550268	Notably, a 35.8 kilobases (kb) haplotype spanning <strong>ANKK1</strong> and DRD2 was found to be a strong protective factor for <b>heroin</b> dependence.
+ANKK1	addiction	dependence	29550268	Notably, a 35.8 kilobases (kb) haplotype spanning <strong>ANKK1</strong> and DRD2 was found to be a strong protective factor for heroin <b>dependence</b>.
+ANKK1	drug	alcohol	29275025	Genes of the brain pathway of motivation and reward, including DRD2 and <strong>ANKK1</strong>, are associated with <b>alcohol</b> dependence.
+ANKK1	addiction	dependence	29275025	Genes of the brain pathway of motivation and reward, including DRD2 and <strong>ANKK1</strong>, are associated with alcohol <b>dependence</b>.
+ANKK1	addiction	reward	29275025	Genes of the brain pathway of motivation and <b>reward</b>, including DRD2 and <strong>ANKK1</strong>, are associated with alcohol dependence.
+ANKK1	drug	opioid	28854834	DRD2 and <strong>ANKK1</strong> genes associate with late onset <b>heroin</b> dependence in men.
+ANKK1	addiction	dependence	28854834	DRD2 and <strong>ANKK1</strong> genes associate with late onset heroin <b>dependence</b> in men.
+ANKK1	drug	alcohol	28574012	Association of ankyrin repeats & kinase domain containing 1 (<strong>ANKK1</strong>) gene polymorphism with co morbid <b>alcohol</b> & nicotine dependence: A pilot study from a tertiary care treatment centre in north India.
+ANKK1	drug	nicotine	28574012	Association of ankyrin repeats & kinase domain containing 1 (<strong>ANKK1</strong>) gene polymorphism with co morbid alcohol & <b>nicotine</b> dependence: A pilot study from a tertiary care treatment centre in north India.
+ANKK1	addiction	dependence	28574012	Association of ankyrin repeats & kinase domain containing 1 (<strong>ANKK1</strong>) gene polymorphism with co morbid alcohol & nicotine <b>dependence</b>: A pilot study from a tertiary care treatment centre in north India.
+ANKK1	drug	alcohol	28574012	This study was undertaken to investigate the possible association of <b>alcohol</b> and tobacco use variables with <strong>ANKK1</strong> polymorphism in co morbid <b>alcohol</b>  and nicotine dependent treatment seekers visiting a tertiary care centre in north India.
+ANKK1	drug	nicotine	28574012	This study was undertaken to investigate the possible association of alcohol and <b>tobacco</b> use variables with <strong>ANKK1</strong> polymorphism in co morbid alcohol  and <b>nicotine</b> dependent treatment seekers visiting a tertiary care centre in north India.
+ANKK1	drug	alcohol	28574012	The socio demographic data, along with <b>alcohol</b> and tobacco use profile, was recorded and <strong>ANKK1</strong> profiling was carried out.
+ANKK1	drug	nicotine	28574012	The socio demographic data, along with alcohol and <b>tobacco</b> use profile, was recorded and <strong>ANKK1</strong> profiling was carried out.
+ANKK1	drug	alcohol	28574012	The study provides an indication for the association of <strong>ANKK1</strong> polymorphism in the form of higher substance consumption among <b>alcohol</b> dependent smokers, who are A1 carriers and thus may require higher attention of the treatment provider.
+ANKK1	drug	nicotine	28574012	The study provides an indication for the association of <strong>ANKK1</strong> polymorphism in the form of higher substance consumption among alcohol dependent <b>smokers</b>, who are A1 carriers and thus may require higher attention of the treatment provider.
+ANKK1	drug	nicotine	27611310	CHRNA4 and <strong>ANKK1</strong> Polymorphisms Influence <b>Smoking</b> Induced Nicotinic Acetylcholine Receptor Upregulation.
+ANKK1	drug	nicotine	27611310	The CHRNA4 SNP rs2236196 and <strong>ANKK1</strong> SNP rs4938015 were associated with significantly higher cerebellar and cortical β2* nAChR availability in <b>smokers</b> versus nonsmokers for specific genotypes.
+ANKK1	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of catechol O methyltransferase (COMT), dopamine receptor D2 (DRD2) gene score and <b>smoking</b> cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>), dopamine transporter (SLC6A3), dopamine receptor D4 (DRD4) gene score and <b>smoking</b> cessation.
+ANKK1	drug	nicotine	27490263	After adjusting for age, occupation, education, marital status, self rating anxiety score, and disease status, we observed significant negative associations of catechol O methyltransferase (COMT), dopamine receptor D2 (DRD2) gene score and <b>smoking</b> cessation, as well as significant positive associations between <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>), dopamine transporter (SLC6A3), dopamine receptor D4 (DRD4) gene score and <b>smoking</b> cessation.
+ANKK1	drug	alcohol	27399274	This study investigated the effect of the dopamine related polymorphism in the DRD2/<strong>ANKK1</strong> gene (rs1800497) and a serotonin related polymorphism in the HTR2A gene (rs6313) on associations between impulsivity, cognition, and <b>alcohol</b> misuse in 120 emerging adults (18 21years).
+ANKK1	drug	alcohol	27180960	Case control study of <strong>ANKK1</strong> Taq 1A polymorphism in patients with <b>alcohol</b> dependence classified according to Lesch's typology.
+ANKK1	addiction	dependence	27180960	Case control study of <strong>ANKK1</strong> Taq 1A polymorphism in patients with alcohol <b>dependence</b> classified according to Lesch's typology.
+ANKK1	drug	alcohol	27180960	The aim of this study was to examine the association between the Taq 1A polymorphism of the <strong>ANKK1</strong> gene in homogeneous subgroups of patients with <b>alcohol</b> dependence syndrome divided according to Lesch's typology.
+ANKK1	addiction	dependence	27180960	The aim of this study was to examine the association between the Taq 1A polymorphism of the <strong>ANKK1</strong> gene in homogeneous subgroups of patients with alcohol <b>dependence</b> syndrome divided according to Lesch's typology.
+ANKK1	drug	alcohol	27180960	We found no association between <b>alcohol</b> dependence and <strong>ANKK1</strong> Taq 1A polymorphism.
+ANKK1	addiction	dependence	27180960	We found no association between alcohol <b>dependence</b> and <strong>ANKK1</strong> Taq 1A polymorphism.
+ANKK1	drug	alcohol	27180911	However, genetic variations in <strong>ANKK1</strong> (rs1800497) and HOMER1 (rs7713917) play an equal role in predicting <b>alcohol</b> drinking two years later and are most important in predicting the increase in <b>alcohol</b> consumption.
+ANKK1	drug	alcohol	27045283	Corrigendum to "DRD2/<strong>ANKK1</strong> TaqI A genotype moderates the relationship between alexithymia and the relative value of <b>alcohol</b> among male college binge drinkers" [Pharmacol.
+ANKK1	addiction	intoxication	27045283	Corrigendum to "DRD2/<strong>ANKK1</strong> TaqI A genotype moderates the relationship between alexithymia and the relative value of alcohol among male college <b>binge</b> drinkers" [Pharmacol.
+ANKK1	drug	cannabinoid	26756393	The association between young adult patterns of <b>cannabis</b> use or <b>cannabis</b> abuse/dependence was tested with genetic variation in the <b>cannabinoid</b> gene, CNR1, the <strong>ANKK1</strong> DRD2 gene, and childhood developmental trajectories of P300.
+ANKK1	addiction	dependence	26756393	The association between young adult patterns of cannabis use or cannabis abuse/<b>dependence</b> was tested with genetic variation in the cannabinoid gene, CNR1, the <strong>ANKK1</strong> DRD2 gene, and childhood developmental trajectories of P300.
+ANKK1	drug	nicotine	26416825	Three hundred sixty four Mexican Mestizo Mexico City residents from 87 families with at least one <b>smoker</b> were assessed for association of 12 gene variants of six candidate genes (CHRNA4, CHRNB2, DRD2, <strong>ANKK1</strong>, SLC6A3, and CYP2A6) with cigarette consumption, age of initiation and <b>smoking</b> duration.
+ANKK1	drug	nicotine	26220612	The aim of this study is to examine associations between delay discounting and two a priori loci, rs4680 in COMT and rs1800497 in <strong>ANKK1</strong>, and three exploratory haplotypes proximal to rs1800497 in a sample of daily <b>smokers</b>.
+ANKK1	drug	nicotine	26153084	Thus, the aim of the present study was to evaluate whether the CYP2B6 and <strong>ANKK1</strong> polymorphisms are associated with the response to <b>smoking</b> cessation therapies in patients from a <b>smoking</b> cessation assistance program.
+ANKK1	drug	alcohol	26146874	Polymorphisms of the DRD2, <strong>ANKK1</strong>, DAT1, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of <b>alcohol</b>, opioid, and cocaine use disorders.
+ANKK1	drug	cocaine	26146874	Polymorphisms of the DRD2, <strong>ANKK1</strong>, DAT1, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of alcohol, opioid, and <b>cocaine</b> use disorders.
+ANKK1	drug	opioid	26146874	Polymorphisms of the DRD2, <strong>ANKK1</strong>, DAT1, DBH, and DRD4 genes have been found to moderate the effects of pharmacotherapy of alcohol, <b>opioid</b>, and cocaine use disorders.
+ANKK1	drug	opioid	26138154	Association between the traditional Chinese medicine pathological factors of <b>opioid</b> addiction and DRD2/<strong>ANKK1</strong> TaqIA polymorphisms.
+ANKK1	addiction	addiction	26138154	Association between the traditional Chinese medicine pathological factors of opioid <b>addiction</b> and DRD2/<strong>ANKK1</strong> TaqIA polymorphisms.
+ANKK1	drug	opioid	26138154	We aimed to explore the possible mechanism of how <strong>ANKK1</strong> TaqIA (A1/A2) [rs1800497(T/C)] affects the relapse of <b>opioid</b> addiction on the perspective of Chinese traditional medicine.
+ANKK1	addiction	addiction	26138154	We aimed to explore the possible mechanism of how <strong>ANKK1</strong> TaqIA (A1/A2) [rs1800497(T/C)] affects the relapse of opioid <b>addiction</b> on the perspective of Chinese traditional medicine.
+ANKK1	addiction	relapse	26138154	We aimed to explore the possible mechanism of how <strong>ANKK1</strong> TaqIA (A1/A2) [rs1800497(T/C)] affects the <b>relapse</b> of opioid addiction on the perspective of Chinese traditional medicine.
+ANKK1	drug	opioid	26138154	The <strong>ANKK1</strong> TaqIA (A1/A2) [rs1800497(T/C)] of the dopamine D2 receptor (DRD2) polymorphisms were genotyped in a case control sample consisting of 347 <b>opioid</b> addicts and 155 healthy controls with RT PCR and the TCM pathological factors were collected by means of Syndrome Elements Differentiation in the case control sample.
+ANKK1	drug	opioid	26138154	DRD2/<strong>ANKK1</strong> TaqIA Polymorphisms has no relation with <b>opioid</b> addiction relapse; but for those who were diagnosed with phlegm syndrome, DRD2/<strong>ANKK1</strong> TaqIA Polymorphisms affect the replapse of apioid addiction (P < 0.05).
+ANKK1	addiction	addiction	26138154	DRD2/<strong>ANKK1</strong> TaqIA Polymorphisms has no relation with opioid <b>addiction</b> relapse; but for those who were diagnosed with phlegm syndrome, DRD2/<strong>ANKK1</strong> TaqIA Polymorphisms affect the replapse of apioid <b>addiction</b> (P < 0.05).
+ANKK1	addiction	relapse	26138154	DRD2/<strong>ANKK1</strong> TaqIA Polymorphisms has no relation with opioid addiction <b>relapse</b>; but for those who were diagnosed with phlegm syndrome, DRD2/<strong>ANKK1</strong> TaqIA Polymorphisms affect the replapse of apioid addiction (P < 0.05).
+ANKK1	drug	opioid	26138154	DRD2/<strong>ANKK1</strong> TaqIA is associated with <b>opioid</b> addict and it is obvious in <b>opioid</b> addicts who suffer from the phlegm syndrome.
+ANKK1	addiction	addiction	25958762	Finally, DRD2 and <strong>ANKK1</strong> genes, involved in the dopaminergic pathway, and which were initially associated with AD, are now considered to be involved in a broader phenotype (<b>addiction</b> to psychoactive substances) including opiates.
+ANKK1	drug	alcohol	25684044	Association study of the SLC6A3 VNTR (DAT) and DRD2/<strong>ANKK1</strong> Taq1A polymorphisms with <b>alcohol</b> dependence in a population from northeastern Brazil.
+ANKK1	addiction	dependence	25684044	Association study of the SLC6A3 VNTR (DAT) and DRD2/<strong>ANKK1</strong> Taq1A polymorphisms with alcohol <b>dependence</b> in a population from northeastern Brazil.
+ANKK1	drug	nicotine	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (<strong>ANKK1</strong>), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (SLC6A3) and cytochrome P450 2A6 (CYP2A6) genes influence <b>smoking</b> cessation and <b>nicotine</b> dependence in a Japanese population.
+ANKK1	addiction	dependence	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (<strong>ANKK1</strong>), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (SLC6A3) and cytochrome P450 2A6 (CYP2A6) genes influence smoking cessation and nicotine <b>dependence</b> in a Japanese population.
+ANKK1	drug	nicotine	25526961	This study investigated whether polymorphisms of the <strong>ankyrin repeat and kinase domain containing 1</strong> gene (<strong>ANKK1</strong>), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (SLC6A3) and cytochrome P450 2A6 (CYP2A6) genes influence <b>smoking</b> cessation and <b>nicotine</b> dependence in a Japanese population.
+ANKK1	addiction	dependence	25526961	This study investigated whether polymorphisms of the <strong>ankyrin repeat and kinase domain containing 1</strong> gene (<strong>ANKK1</strong>), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (SLC6A3) and cytochrome P450 2A6 (CYP2A6) genes influence smoking cessation and nicotine <b>dependence</b> in a Japanese population.
+ANKK1	drug	nicotine	25526961	In 96 current and former <b>smokers</b>, genotyping frequencies for the <strong>ANKK1</strong>/DRD2 TaqIA, SLC6A3 VNTR, and CYP2A6 polymorphisms were subjected to chi square analysis, and regression analyses were used to determine the association of the genotypes of current <b>smokers</b> with a Heavy <b>Smoking</b> Index, in addition to evaluating the effect of the subjects' <b>smoking</b> history on the association.
+ANKK1	addiction	dependence	25500252	Association between DRD2/<strong>ANKK1</strong> TaqIA polymorphism and common illicit drug <b>dependence</b>: evidence from a meta analysis.
+ANKK1	drug	cannabinoid	25500252	Growing evidence indicated conflicting results about the dopamine receptor D2 (DRD2)/kinase domain containing 1 gene (<strong>ANKK1</strong>) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug dependence risk including stimulants, opioid and <b>marijuana</b>.
+ANKK1	drug	opioid	25500252	Growing evidence indicated conflicting results about the dopamine receptor D2 (DRD2)/kinase domain containing 1 gene (<strong>ANKK1</strong>) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug dependence risk including stimulants, <b>opioid</b> and marijuana.
+ANKK1	addiction	dependence	25500252	Growing evidence indicated conflicting results about the dopamine receptor D2 (DRD2)/kinase domain containing 1 gene (<strong>ANKK1</strong>) TaqIA single nucleotide polymorphism (rs1800497) and common illicit drug <b>dependence</b> risk including stimulants, opioid and marijuana.
+ANKK1	drug	opioid	25500252	We found the DRD2/<strong>ANKK1</strong> TaqIA polymorphism was significantly associated with increased risk of <b>opioid</b> dependence under homozygote, dominant, and recessive genetic model, respectively (homozygote: OR=1.546, 95%CI=1.279 1.87; dominant: OR=1.265, 95%CI=1.055 1.516; recessive: OR=1.409, 95%CI=1.182 1.680).
+ANKK1	addiction	dependence	25500252	We found the DRD2/<strong>ANKK1</strong> TaqIA polymorphism was significantly associated with increased risk of opioid <b>dependence</b> under homozygote, dominant, and recessive genetic model, respectively (homozygote: OR=1.546, 95%CI=1.279 1.87; dominant: OR=1.265, 95%CI=1.055 1.516; recessive: OR=1.409, 95%CI=1.182 1.680).
+ANKK1	drug	cannabinoid	25500252	The current meta analysis suggested that DRD2/<strong>ANKK1</strong> TaqIA polymorphism might be associated with opioid dependence risk, but not associated with stimulants or <b>marijuana</b> dependence.
+ANKK1	drug	opioid	25500252	The current meta analysis suggested that DRD2/<strong>ANKK1</strong> TaqIA polymorphism might be associated with <b>opioid</b> dependence risk, but not associated with stimulants or marijuana dependence.
+ANKK1	addiction	dependence	25500252	The current meta analysis suggested that DRD2/<strong>ANKK1</strong> TaqIA polymorphism might be associated with opioid <b>dependence</b> risk, but not associated with stimulants or marijuana <b>dependence</b>.
+ANKK1	drug	nicotine	25450229	We also observed a significant excess of rare nonsynonymous variants exclusive to EA <b>smokers</b> in NRXN1, CHRNA9, TAS2R38, GRIN3A, DBH, <strong>ANKK1</strong>/DRD2, NRXN3 and CDH13 with WSS P values between 3.5 × 10( 5) and 1 × 10( 6).
+ANKK1	drug	alcohol	25415204	Suicidal behavior and haplotypes of the dopamine receptor gene (DRD2) and <strong>ANKK1</strong> gene polymorphisms in patients with <b>alcohol</b> dependence  preliminary report.
+ANKK1	addiction	dependence	25415204	Suicidal behavior and haplotypes of the dopamine receptor gene (DRD2) and <strong>ANKK1</strong> gene polymorphisms in patients with alcohol <b>dependence</b>  preliminary report.
+ANKK1	drug	alcohol	25415204	In our study,  we have analyzed selected SNPs polymorphisms in the DRD2 and <strong>ANKK1</strong> genes in patients with <b>alcohol</b> dependence syndrome (169 Caucasian subjects) including a subgroup of individuals (n = 61) who have experienced at least one suicide attempt.
+ANKK1	addiction	dependence	25415204	In our study,  we have analyzed selected SNPs polymorphisms in the DRD2 and <strong>ANKK1</strong> genes in patients with alcohol <b>dependence</b> syndrome (169 Caucasian subjects) including a subgroup of individuals (n = 61) who have experienced at least one suicide attempt.
+ANKK1	drug	nicotine	25273375	NCAM1 TTC12 <strong>ANKK1</strong> DRD2 variants and <b>smoking</b> motives as intermediate phenotypes for <b>nicotine</b> dependence.
+ANKK1	addiction	dependence	25273375	NCAM1 TTC12 <strong>ANKK1</strong> DRD2 variants and smoking motives as intermediate phenotypes for nicotine <b>dependence</b>.
+ANKK1	drug	nicotine	25273375	Based on prior evidence of the role of genetic variation in the NCAM1 TTC12 <strong>ANKK1</strong> DRD2 region on chromosome 11q23 in <b>smoking</b> behavior, associations among 12 region loci with <b>nicotine</b> dependence and PDM phenotypes were examined using haplotype and individual loci approaches.
+ANKK1	addiction	dependence	25273375	Based on prior evidence of the role of genetic variation in the NCAM1 TTC12 <strong>ANKK1</strong> DRD2 region on chromosome 11q23 in smoking behavior, associations among 12 region loci with nicotine <b>dependence</b> and PDM phenotypes were examined using haplotype and individual loci approaches.
+ANKK1	drug	nicotine	25273375	NCAM1 TTC12 <strong>ANKK1</strong> DRD2 region loci and haplotypes were significantly associated with the motive of Automaticity and, further, Automaticity significantly mediated associations among NCAM1 TTC12 <strong>ANKK1</strong> DRD2 cluster variants and <b>nicotine</b> dependence.
+ANKK1	addiction	dependence	25273375	NCAM1 TTC12 <strong>ANKK1</strong> DRD2 region loci and haplotypes were significantly associated with the motive of Automaticity and, further, Automaticity significantly mediated associations among NCAM1 TTC12 <strong>ANKK1</strong> DRD2 cluster variants and nicotine <b>dependence</b>.
+ANKK1	drug	nicotine	25273375	Further, NCAM1 TTC12 <strong>ANKK1</strong> DRD2 variants may increase the likelihood that a person will become dependent via a highly automatic <b>smoking</b> ritual that can be elicited with little awareness.
+ANKK1	drug	alcohol	25139281	Considering new evidence supporting the association of DRD2 and its adjacent gene ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) with various addictions, in this paper, we provide an updated view of the involvement of variants in DRD2 and <strong>ANKK1</strong> in the etiology of nicotine dependence (ND) and <b>alcohol</b> dependence (AD) based on linkage, association, and molecular studies.
+ANKK1	drug	nicotine	25139281	Considering new evidence supporting the association of DRD2 and its adjacent gene ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) with various addictions, in this paper, we provide an updated view of the involvement of variants in DRD2 and <strong>ANKK1</strong> in the etiology of <b>nicotine</b> dependence (ND) and alcohol dependence (AD) based on linkage, association, and molecular studies.
+ANKK1	addiction	dependence	25139281	Considering new evidence supporting the association of DRD2 and its adjacent gene ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) with various addictions, in this paper, we provide an updated view of the involvement of variants in DRD2 and <strong>ANKK1</strong> in the etiology of nicotine <b>dependence</b> (ND) and alcohol <b>dependence</b> (AD) based on linkage, association, and molecular studies.
+ANKK1	drug	alcohol	25139281	Considering new evidence supporting the association of DRD2 and its adjacent gene <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) with various addictions, in this paper, we provide an updated view of the involvement of variants in DRD2 and <strong>ANKK1</strong> in the etiology of nicotine dependence (ND) and <b>alcohol</b> dependence (AD) based on linkage, association, and molecular studies.
+ANKK1	drug	nicotine	25139281	Considering new evidence supporting the association of DRD2 and its adjacent gene <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) with various addictions, in this paper, we provide an updated view of the involvement of variants in DRD2 and <strong>ANKK1</strong> in the etiology of <b>nicotine</b> dependence (ND) and alcohol dependence (AD) based on linkage, association, and molecular studies.
+ANKK1	addiction	dependence	25139281	Considering new evidence supporting the association of DRD2 and its adjacent gene <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) with various addictions, in this paper, we provide an updated view of the involvement of variants in DRD2 and <strong>ANKK1</strong> in the etiology of nicotine <b>dependence</b> (ND) and alcohol <b>dependence</b> (AD) based on linkage, association, and molecular studies.
+ANKK1	drug	alcohol	24629326	Impulsivity related cognition in <b>alcohol</b> dependence: Is it moderated by DRD2/<strong>ANKK1</strong> gene status and executive dysfunction?
+ANKK1	addiction	dependence	24629326	Impulsivity related cognition in alcohol <b>dependence</b>: Is it moderated by DRD2/<strong>ANKK1</strong> gene status and executive dysfunction?
+ANKK1	drug	alcohol	24629326	These results suggest that, in <b>alcohol</b> dependence, perceived impaired control is a cognitive mediator of impulsivity related constructs that may be unaffected by DRD2/<strong>ANKK1</strong> and neurocognitive processes underlying the retrieval of verbal information.
+ANKK1	addiction	dependence	24629326	These results suggest that, in alcohol <b>dependence</b>, perceived impaired control is a cognitive mediator of impulsivity related constructs that may be unaffected by DRD2/<strong>ANKK1</strong> and neurocognitive processes underlying the retrieval of verbal information.
+ANKK1	drug	cocaine	24528631	A variant in <strong>ANKK1</strong> modulates acute subjective effects of <b>cocaine</b>: a preliminary study.
+ANKK1	drug	cocaine	24528631	This study aimed to evaluate whether functional variants in the ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) gene and/or the dopamine receptor D2 (DRD2) gene modulate the subjective effects (reward or non reward response to a stimulus) produced by <b>cocaine</b> administration.
+ANKK1	addiction	reward	24528631	This study aimed to evaluate whether functional variants in the ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) gene and/or the dopamine receptor D2 (DRD2) gene modulate the subjective effects (<b>reward</b> or non <b>reward</b> response to a stimulus) produced by cocaine administration.
+ANKK1	drug	cocaine	24528631	This study aimed to evaluate whether functional variants in the <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) gene and/or the dopamine receptor D2 (DRD2) gene modulate the subjective effects (reward or non reward response to a stimulus) produced by <b>cocaine</b> administration.
+ANKK1	addiction	reward	24528631	This study aimed to evaluate whether functional variants in the <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) gene and/or the dopamine receptor D2 (DRD2) gene modulate the subjective effects (<b>reward</b> or non <b>reward</b> response to a stimulus) produced by cocaine administration.
+ANKK1	drug	cocaine	24528631	The influence of polymorphisms in the <strong>ANKK1</strong> and DRD2 genes on subjective experience of <b>cocaine</b> in the laboratory was tested.
+ANKK1	drug	cocaine	24528631	A participant's <strong>ANKK1</strong> genotype may identify individuals who are likely to experience greater positive subjective effects following <b>cocaine</b> exposure, including greater 'high' and 'like', and these individuals may have increased vulnerability to continue using <b>cocaine</b> or they may be at greater risk to relapse during periods of abstinence.
+ANKK1	addiction	relapse	24528631	A participant's <strong>ANKK1</strong> genotype may identify individuals who are likely to experience greater positive subjective effects following cocaine exposure, including greater 'high' and 'like', and these individuals may have increased vulnerability to continue using cocaine or they may be at greater risk to <b>relapse</b> during periods of abstinence.
+ANKK1	drug	nicotine	24444411	Genetic variants in DRD2, DRD4, <strong>ANKK1</strong>, DAT1, COMT and DBH genes show some promise in informing personalized prescribing of <b>smoking</b> cessation pharmacotherapies.
+ANKK1	drug	alcohol	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), <strong>ANKK1</strong> (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with <b>alcohol</b>, tobacco and/or cannabis consumption in young individuals (n = 91).
+ANKK1	drug	cannabinoid	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), <strong>ANKK1</strong> (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, tobacco and/or <b>cannabis</b> consumption in young individuals (n = 91).
+ANKK1	drug	nicotine	24407958	Here, we made a preliminary screening among ten Single Nucleotide Polymorphisms (SNP) of the CNR1 (rs806368, rs1049353, rs6454674, rs7766029), FAAH (rs324420, rs12075550), DRD2 (rs6277), <strong>ANKK1</strong> (rs1800497), COMT (rs4680), and OPRM1 (rs1799971) genes to identify that SNPs that were more directly associated with alcohol, <b>tobacco</b> and/or cannabis consumption in young individuals (n = 91).
+ANKK1	drug	nicotine	24065931	We examined genetic polymorphisms within the CHRNA5 A3 B4 gene cluster (CHRNA3 rs578776, CHRNA5 rs16969968, LOC123688 rs8034191, and CHRNA3 rs1051730), the <strong>ANKK1</strong> gene (rs1800497), and the D2 dopamine receptor gene (DRD2 rs1079597, DRD2 rs1799732) from 104 <b>smokers</b> of European ancestry in a <b>smoking</b> cessation trial.
+ANKK1	drug	nicotine	23941313	Age, gender, Fagerström Test for <b>Nicotine</b> Dependence, dopamine pathway genotypes (rs1800497 [<strong>ANKK1</strong> E713K], rs4680 [COMT V158M], DRD4 exon 3 variable number of tandem repeats polymorphism [DRD4 VNTR], SLC6A3,3' VNTR) analyzed both separately and as part of an AGES, time to first lapse and point prevalence abstinence at end of treatment.
+ANKK1	addiction	dependence	23941313	Age, gender, Fagerström Test for Nicotine <b>Dependence</b>, dopamine pathway genotypes (rs1800497 [<strong>ANKK1</strong> E713K], rs4680 [COMT V158M], DRD4 exon 3 variable number of tandem repeats polymorphism [DRD4 VNTR], SLC6A3,3' VNTR) analyzed both separately and as part of an AGES, time to first lapse and point prevalence abstinence at end of treatment.
+ANKK1	drug	opioid	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), <strong>ANKK1</strong> (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol O methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and <b>heroin</b> dependence in Hungarian patients.
+ANKK1	addiction	dependence	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), <strong>ANKK1</strong> (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol O methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and heroin <b>dependence</b> in Hungarian patients.
+ANKK1	drug	opioid	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), <strong>ANKK1</strong> (<strong>ankyrin repeat and kinase domain containing 1</strong>), dopamine D4 receptor (DRD4), catechol O methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and <b>heroin</b> dependence in Hungarian patients.
+ANKK1	addiction	dependence	23840506	To study the potential association between allelic variants of dopamine D2 receptor (DRD2), <strong>ANKK1</strong> (<strong>ankyrin repeat and kinase domain containing 1</strong>), dopamine D4 receptor (DRD4), catechol O methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and heroin <b>dependence</b> in Hungarian patients.
+ANKK1	drug	opioid	23840506	303 <b>heroin</b> dependent subjects and 555 healthy controls were genotyped for 7 single nucleotide polymorphisms (SNPs) rs4680 of the COMT gene; rs1079597 and rs1800498 of the DRD2 gene; rs1800497 of the <strong>ANKK1</strong> gene; rs1800955, rs936462 and rs747302 of the DRD4 gene.
+ANKK1	drug	nicotine	23691092	Associations of prenatal <b>nicotine</b> exposure and the dopamine related genes <strong>ANKK1</strong> and DRD2 to verbal language.
+ANKK1	drug	nicotine	23691092	Our results show that <b>smoking</b> during pregnancy increases the risk for LI and poor performance on language tasks and that <strong>ANKK1</strong>/DRD2 contributes to language performance.
+ANKK1	drug	nicotine	23691092	Our association of <strong>ANKK1</strong>/DRD2 further implicates the role of <b>nicotine</b> related pathways and dopamine signaling in language processing, particularly in comprehension and phonological memory.
+ANKK1	drug	opioid	23651024	Out of the 110 variants analyzed, 12 SNPs (in BDNF, NTRK2, OPRM1, DRD2 and <strong>ANKK1</strong>) were associated with <b>methadone</b> dose (nominal p < 0.05).
+ANKK1	drug	alcohol	23635803	<strong>ANKK1</strong> and DRD2 pharmacogenetics of <b>disulfiram</b> treatment for cocaine abuse.
+ANKK1	drug	cocaine	23635803	<strong>ANKK1</strong> and DRD2 pharmacogenetics of disulfiram treatment for <b>cocaine</b> abuse.
+ANKK1	drug	alcohol	23635803	Since dopamine deficiency has been found with cocaine addiction, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) and/or the dopamine receptor D2 (DRD2) genes interact with response to treatment with <b>disulfiram</b>.
+ANKK1	drug	cocaine	23635803	Since dopamine deficiency has been found with <b>cocaine</b> addiction, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) and/or the dopamine receptor D2 (DRD2) genes interact with response to treatment with disulfiram.
+ANKK1	addiction	addiction	23635803	Since dopamine deficiency has been found with cocaine <b>addiction</b>, our objective was to examine whether functional variants in the ankyrin repeat and kinase domain containing 1 (<strong>ANKK1</strong>) and/or the dopamine receptor D2 (DRD2) genes interact with response to treatment with disulfiram.
+ANKK1	drug	alcohol	23635803	Since dopamine deficiency has been found with cocaine addiction, our objective was to examine whether functional variants in the <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) and/or the dopamine receptor D2 (DRD2) genes interact with response to treatment with <b>disulfiram</b>.
+ANKK1	drug	cocaine	23635803	Since dopamine deficiency has been found with <b>cocaine</b> addiction, our objective was to examine whether functional variants in the <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) and/or the dopamine receptor D2 (DRD2) genes interact with response to treatment with disulfiram.
+ANKK1	addiction	addiction	23635803	Since dopamine deficiency has been found with cocaine <b>addiction</b>, our objective was to examine whether functional variants in the <strong>ankyrin repeat and kinase domain containing 1</strong> (<strong>ANKK1</strong>) and/or the dopamine receptor D2 (DRD2) genes interact with response to treatment with disulfiram.
+ANKK1	drug	alcohol	23635803	They were genotyped for <strong>ANKK1</strong> (rs1800497) and DRD2 (rs2283265) polymorphisms, and the data were evaluated for an association between a cocaine free state, as assessed by cocaine free urine samples, and <b>disulfiram</b> treatment.
+ANKK1	drug	cocaine	23635803	They were genotyped for <strong>ANKK1</strong> (rs1800497) and DRD2 (rs2283265) polymorphisms, and the data were evaluated for an association between a <b>cocaine</b> free state, as assessed by <b>cocaine</b> free urine samples, and disulfiram treatment.
+ANKK1	drug	alcohol	23635803	Patients with CT or TT <strong>ANKK1</strong> genotypes dropped from 80 to 52% cocaine positive urines on <b>disulfiram</b> (N=13; P≤0.0001), whereas those on placebo (N=20) showed no treatment effect.
+ANKK1	drug	cocaine	23635803	Patients with CT or TT <strong>ANKK1</strong> genotypes dropped from 80 to 52% <b>cocaine</b> positive urines on disulfiram (N=13; P≤0.0001), whereas those on placebo (N=20) showed no treatment effect.
+ANKK1	drug	alcohol	23635803	Patients carrying the CC <strong>ANKK1</strong> genotype showed no effect on treatment with <b>disulfiram</b> (N=18) or placebo (N=17).
+ANKK1	drug	alcohol	23635803	A patient's genotype for <strong>ANKK1</strong>, DRD2, or both, may be used to identify individuals for whom <b>disulfiram</b> may be an effective pharmacotherapy for cocaine dependence.
+ANKK1	drug	cocaine	23635803	A patient's genotype for <strong>ANKK1</strong>, DRD2, or both, may be used to identify individuals for whom disulfiram may be an effective pharmacotherapy for <b>cocaine</b> dependence.
+ANKK1	addiction	dependence	23635803	A patient's genotype for <strong>ANKK1</strong>, DRD2, or both, may be used to identify individuals for whom disulfiram may be an effective pharmacotherapy for cocaine <b>dependence</b>.
+ANKK1	drug	alcohol	23558112	The association of DRD2  141C and <strong>ANKK1</strong> TaqIA polymorphisms with <b>alcohol</b> dependence in Korean population classified by the Lesch typology.
+ANKK1	addiction	dependence	23558112	The association of DRD2  141C and <strong>ANKK1</strong> TaqIA polymorphisms with alcohol <b>dependence</b> in Korean population classified by the Lesch typology.
+ANKK1	drug	alcohol	23558112	Therefore, we investigated the association of three single nucleotide polymorphisms (SNPs) in DRD2 and ankyrin repeat and kinase domain containing one (<strong>ANKK1</strong>) genes with <b>alcohol</b> dependence in Korean subjects, who were classified by the criteria of the Lesch typology.
+ANKK1	addiction	dependence	23558112	Therefore, we investigated the association of three single nucleotide polymorphisms (SNPs) in DRD2 and ankyrin repeat and kinase domain containing one (<strong>ANKK1</strong>) genes with alcohol <b>dependence</b> in Korean subjects, who were classified by the criteria of the Lesch typology.
+ANKK1	drug	alcohol	23558112	The DRD2  141C (Insertion (Ins)/Deletion (Del)), exon8 (A/G) and the <strong>ANKK1</strong> TaqIA (A1/A2) polymorphisms were genotyped in a case control sample consisting of 245 <b>alcohol</b> dependent (AD) patients and 110 healthy controls.
+ANKK1	drug	alcohol	23443985	DRD2 and <strong>ANKK1</strong> gene polymorphisms and <b>alcohol</b> dependence: a case control study among a Mendelian population of East Asian ancestry.
+ANKK1	addiction	dependence	23443985	DRD2 and <strong>ANKK1</strong> gene polymorphisms and alcohol <b>dependence</b>: a case control study among a Mendelian population of East Asian ancestry.
+ANKK1	drug	opioid	23303482	<strong>ANKK1</strong>, TTC12, and NCAM1 polymorphisms and <b>heroin</b> dependence: importance of considering drug exposure.
+ANKK1	addiction	dependence	23303482	<strong>ANKK1</strong>, TTC12, and NCAM1 polymorphisms and heroin <b>dependence</b>: importance of considering drug exposure.
+ANKK1	drug	opioid	23303482	To examine association of 1430 candidate gene single nucleotide polymorphisms (SNPs) with <b>heroin</b> dependence, reporting here only the 71 SNPs in the chromosome 11 gene cluster (NCAM1, TTC12, <strong>ANKK1</strong>, DRD2) that include the strongest observed associations.
+ANKK1	addiction	dependence	23303482	To examine association of 1430 candidate gene single nucleotide polymorphisms (SNPs) with heroin <b>dependence</b>, reporting here only the 71 SNPs in the chromosome 11 gene cluster (NCAM1, TTC12, <strong>ANKK1</strong>, DRD2) that include the strongest observed associations.
+ANKK1	drug	alcohol	23238469	Influence of DRD2 and <strong>ANKK1</strong> polymorphisms on the manifestation of withdrawal syndrome symptoms in <b>alcohol</b> addiction.
+ANKK1	addiction	addiction	23238469	Influence of DRD2 and <strong>ANKK1</strong> polymorphisms on the manifestation of withdrawal syndrome symptoms in alcohol <b>addiction</b>.
+ANKK1	addiction	withdrawal	23238469	Influence of DRD2 and <strong>ANKK1</strong> polymorphisms on the manifestation of <b>withdrawal</b> syndrome symptoms in alcohol addiction.
+ANKK1	addiction	withdrawal	23238469	We investigated the relationship between <b>withdrawal</b> syndrome symptoms and dopamine receptor 2 DRD2 gene polymorphisms 141 C I/D (rs1799732) exon 8 G/A (rs6276) and <strong>ANKK1</strong> (Ankyrin Repeat and Kinase Domain Containing 1) gene polymorphism Taq1A (rs1800497).
+ANKK1	addiction	withdrawal	23238469	We investigated the relationship between <b>withdrawal</b> syndrome symptoms and dopamine receptor 2 DRD2 gene polymorphisms 141 C I/D (rs1799732) exon 8 G/A (rs6276) and <strong>ANKK1</strong> (<strong>Ankyrin Repeat and Kinase Domain Containing 1</strong>) gene polymorphism Taq1A (rs1800497).
+ANKK1	drug	alcohol	23203481	A large scale meta analysis of the association between the <strong>ANKK1</strong>/DRD2 Taq1A polymorphism and <b>alcohol</b> dependence.
+ANKK1	addiction	dependence	23203481	A large scale meta analysis of the association between the <strong>ANKK1</strong>/DRD2 Taq1A polymorphism and alcohol <b>dependence</b>.
+ANKK1	drug	nicotine	23153044	A prospective study of the effects of the DRD2/<strong>ANKK1</strong> TaqIA polymorphism and impulsivity on <b>smoking</b> initiation.
+ANKK1	drug	nicotine	23153044	This study tested whether DRD2/<strong>ANKK1</strong> TaqIA genotype predicted <b>smoking</b> initiation and subsequent use, and effects were mediated by sensation seeking and negative urgency.
+ANKK1	addiction	relapse	23153044	This study tested whether DRD2/<strong>ANKK1</strong> TaqIA genotype predicted smoking initiation and subsequent use, and effects were mediated by sensation <b>seeking</b> and negative urgency.
+ANKK1	drug	alcohol	22970887	The association between DRD2/<strong>ANKK1</strong> and genetically informed measures of <b>alcohol</b> use and problems.
+ANKK1	drug	alcohol	22970887	After correction for multiple testing across SNPs and phenotypes, of the 31 SNPs genotyped across DRD2/<strong>ANKK1</strong>, one SNP (rs10891549) showed significant association with the general <b>alcohol</b> consumption and problems factor score (P = 0.004), and four SNPs (rs10891549, rs1554929, rs6275, rs6279), representing two independent signals after accounting for linkage disequilibrium, showed significant association with the <b>alcohol</b> problems genetic factor score (P = 0.005, P = 0.005, P = 0.003, P = 0.003).
+ANKK1	drug	alcohol	22970887	In this study, we provide additional positive evidence for the association between DRD2/<strong>ANKK1</strong> and <b>alcohol</b> outcomes, including frequency of drinking and drinking problems.
+ANKK1	drug	nicotine	22949583	Trial participants (n = 36) were genotyped for <strong>ANKK1</strong> rs1800497 and were randomized to receive genetic feedback (GF) plus standard behavioral counseling (BC) for <b>smoking</b> cessation or BC without GF.
+ANKK1	drug	alcohol	22728571	DRD2/<strong>ANKK1</strong> TaqI A genotype moderates the relationship between alexithymia and the relative value of <b>alcohol</b> among male college binge drinkers.
+ANKK1	addiction	intoxication	22728571	DRD2/<strong>ANKK1</strong> TaqI A genotype moderates the relationship between alexithymia and the relative value of alcohol among male college <b>binge</b> drinkers.
+ANKK1	drug	alcohol	22728571	The present study hypothesized that DRD2/<strong>ANKK1</strong> TaqI A (rs1800497) genotype would moderate the relationship between alexithymia and an <b>alcohol</b> purchase task (APT) among male college binge drinkers.
+ANKK1	addiction	intoxication	22728571	The present study hypothesized that DRD2/<strong>ANKK1</strong> TaqI A (rs1800497) genotype would moderate the relationship between alexithymia and an alcohol purchase task (APT) among male college <b>binge</b> drinkers.
+ANKK1	drug	alcohol	22698582	DRD2/<strong>ANKK1</strong> TaqIA and SLC6A3 VNTR polymorphisms in <b>alcohol</b> dependence: association and gene gene interaction study in a population of Central Italy.
+ANKK1	addiction	dependence	22698582	DRD2/<strong>ANKK1</strong> TaqIA and SLC6A3 VNTR polymorphisms in alcohol <b>dependence</b>: association and gene gene interaction study in a population of Central Italy.
+ANKK1	drug	alcohol	22509987	The COMT Val158Met and DRD2/<strong>ANKK1</strong> Taq1A genotypes have been suggested to affect both stress sensitivity and the risk for <b>alcohol</b> dependence.
+ANKK1	addiction	dependence	22509987	The COMT Val158Met and DRD2/<strong>ANKK1</strong> Taq1A genotypes have been suggested to affect both stress sensitivity and the risk for alcohol <b>dependence</b>.
+ANKK1	drug	alcohol	22509987	This study tested the hypothesis that genetic variation in COMT Val158Met and DRD2/<strong>ANKK1</strong> Taq1A interacts with childhood adverse experiences to predict <b>alcohol</b> dependence.
+ANKK1	addiction	dependence	22509987	This study tested the hypothesis that genetic variation in COMT Val158Met and DRD2/<strong>ANKK1</strong> Taq1A interacts with childhood adverse experiences to predict alcohol <b>dependence</b>.
+ANKK1	drug	alcohol	22509987	Male abstinent <b>alcohol</b> dependent patients (n = 110) and age matched healthy male controls (n = 99) were genotyped for the COMT Val158Met and the DRD2/<strong>ANKK1</strong> Taq1A genotypes.
+ANKK1	drug	alcohol	22509987	The DRD2/<strong>ANKK1</strong> Taq1A genotype was not related to <b>alcohol</b> dependence, nor did it interact with childhood adversity in predicting <b>alcohol</b> dependence.
+ANKK1	addiction	dependence	22509987	The DRD2/<strong>ANKK1</strong> Taq1A genotype was not related to alcohol <b>dependence</b>, nor did it interact with childhood adversity in predicting alcohol <b>dependence</b>.
+ANKK1	drug	nicotine	22382052	A DRD2 and <strong>ANKK1</strong> haplotype is associated with <b>nicotine</b> dependence.
+ANKK1	addiction	dependence	22382052	A DRD2 and <strong>ANKK1</strong> haplotype is associated with nicotine <b>dependence</b>.
+ANKK1	drug	nicotine	22382052	To test the importance of the dopamine D2 receptor (DRD2) region in <b>nicotine</b> dependence, 150 <b>smokers</b> and 228 controls were genotyped for the DRD2 C957T,  141delC and <strong>ANKK1</strong> TaqIA polymorphisms (rs6277, rs1799732 and rs1800497, respectively).
+ANKK1	addiction	dependence	22382052	To test the importance of the dopamine D2 receptor (DRD2) region in nicotine <b>dependence</b>, 150 smokers and 228 controls were genotyped for the DRD2 C957T,  141delC and <strong>ANKK1</strong> TaqIA polymorphisms (rs6277, rs1799732 and rs1800497, respectively).
+ANKK1	drug	nicotine	22382052	Our findings suggest that the DRD2 C957T polymorphism and the <strong>ANKK1</strong> TaqIA polymorphism are key contributors to the genetic susceptibility to <b>nicotine</b> dependence.
+ANKK1	addiction	dependence	22382052	Our findings suggest that the DRD2 C957T polymorphism and the <strong>ANKK1</strong> TaqIA polymorphism are key contributors to the genetic susceptibility to nicotine <b>dependence</b>.
+ANKK1	drug	alcohol	22232963	The aim of this study was to assess the relation between the <b>alcohol</b> dependence syndrome (ADS) and the polymorphism of the selected genes (GRIK3, 5HTT, <strong>ANKK1</strong>, ADH4).
+ANKK1	addiction	dependence	22232963	The aim of this study was to assess the relation between the alcohol <b>dependence</b> syndrome (ADS) and the polymorphism of the selected genes (GRIK3, 5HTT, <strong>ANKK1</strong>, ADH4).
+ANKK1	drug	alcohol	22129841	The analysis used logistic and Cox regression methods to evaluate the contributions of age; sex; number of intake <b>alcohol</b>, drug use, and depression symptoms; and either GABRA2, CHRM2, <strong>ANKK1</strong>, BDNF, or KIBRA SNP genotypes to outcome.
+ANKK1	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 <strong>ANKK1</strong> 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+ANKK1	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], CYP2B6*4 (785A>G), CYP2B6*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 <strong>ANKK1</strong> 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+ANKK1	drug	nicotine	22046326	Compared with carriers of variant alleles, the odds ratio (OR) for being a non <b>smoker</b> in individuals with the wild type genotype of CYP2A6*12 and DRD2 <strong>ANKK1</strong> 2137G>A (Taq1A) polymorphisms was 3.60 (95%CI: 1.75, 7.44) and 2.63 (95%CI: 1.41, 4.89) respectively.
+ANKK1	drug	nicotine	22046326	We found a significant genotype effect (all P≤0.017) for the following <b>smoking</b> related phenotypes: (i) cigarettes smoked per day and CYP2A13*3; (ii) pack years smoked and CYP2A6*2, CYP2A6*1×2, CYP2A13*7, CYP2B6*4 and DRD2 <strong>ANKK1</strong> 2137G>A (Taq1A); (iii) <b>nicotine</b> dependence (assessed with the Fagestrom test) and CYP2A6*9.
+ANKK1	addiction	dependence	22046326	We found a significant genotype effect (all P≤0.017) for the following smoking related phenotypes: (i) cigarettes smoked per day and CYP2A13*3; (ii) pack years smoked and CYP2A6*2, CYP2A6*1×2, CYP2A13*7, CYP2B6*4 and DRD2 <strong>ANKK1</strong> 2137G>A (Taq1A); (iii) nicotine <b>dependence</b> (assessed with the Fagestrom test) and CYP2A6*9.
+ANKK1	drug	cannabinoid	21997315	<strong>ANKK1</strong>/DRD2 locus variants are associated with <b>rimonabant</b> efficacy in aiding smoking cessation: pilot data.
+ANKK1	drug	nicotine	21997315	<strong>ANKK1</strong>/DRD2 locus variants are associated with rimonabant efficacy in aiding <b>smoking</b> cessation: pilot data.
+ANKK1	drug	nicotine	21936764	The role of <strong>ANKK1</strong> and TTC12 genes on drinking behaviour in <b>tobacco</b> dependent subjects.
+ANKK1	drug	alcohol	21936764	Our aim was to investigate whether drinking behaviour in the past 12 months and smoking relapse due to <b>alcohol</b> use in TD subjects was associated with polymorphisms flanking the TTC12/<strong>ANKK1</strong>/DRD2 region since associations have been found between these genes and AUD and TD as separate disorders.
+ANKK1	drug	nicotine	21936764	Our aim was to investigate whether drinking behaviour in the past 12 months and <b>smoking</b> relapse due to alcohol use in TD subjects was associated with polymorphisms flanking the TTC12/<strong>ANKK1</strong>/DRD2 region since associations have been found between these genes and AUD and TD as separate disorders.
+ANKK1	addiction	relapse	21936764	Our aim was to investigate whether drinking behaviour in the past 12 months and smoking <b>relapse</b> due to alcohol use in TD subjects was associated with polymorphisms flanking the TTC12/<strong>ANKK1</strong>/DRD2 region since associations have been found between these genes and AUD and TD as separate disorders.
+ANKK1	drug	nicotine	21936764	Associations were found between <strong>ANKK1</strong> haplotype rs4938015C_rs11604671A and age of onset of daily <b>smoking</b>, as well as with hazardous drinking.
+ANKK1	addiction	addiction	21723677	Determining the influences of genes involved in metabolizing dopamine and encoding dopamine receptors, such as the aldehyde dehydrogenase 2 (ALDH2) and dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/<strong>ANKK1</strong>) genes, is critical for understanding <b>addictive</b> behavior.
+ANKK1	addiction	addiction	21723677	Determining the influences of genes involved in metabolizing dopamine and encoding dopamine receptors, such as the aldehyde dehydrogenase 2 (ALDH2) and dopamine D2 receptor/<strong>ankyrin repeat and kinase domain containing 1</strong> (DRD2/<strong>ANKK1</strong>) genes, is critical for understanding <b>addictive</b> behavior.
+ANKK1	drug	opioid	21723677	Therefore, we investigated the association between the ALDH2 and DRD2/<strong>ANKK1</strong> Taq IA polymorphisms and <b>heroin</b> dependence.
+ANKK1	addiction	dependence	21723677	Therefore, we investigated the association between the ALDH2 and DRD2/<strong>ANKK1</strong> Taq IA polymorphisms and heroin <b>dependence</b>.
+ANKK1	drug	nicotine	21540761	Association between DRD2/<strong>ANKK1</strong> Taq1A genotypes, depression and <b>smoking</b> cessation with <b>nicotine</b> replacement therapy.
+ANKK1	drug	nicotine	21540761	Variant genotypes of the Taq1A (DRD2/<strong>ANKK1</strong>, 32806T, rs1800497) polymorphism have been associated with failure to stop <b>smoking</b> in some studies, but not others.
+ANKK1	drug	alcohol	21403585	Lack of allelic association between markers at the DRD2 and <strong>ANKK1</strong> gene loci with the <b>alcohol</b> dependence syndrome and criminal activity.
+ANKK1	addiction	dependence	21403585	Lack of allelic association between markers at the DRD2 and <strong>ANKK1</strong> gene loci with the alcohol <b>dependence</b> syndrome and criminal activity.
+ANKK1	drug	nicotine	21244814	Waterpipe <b>Smoking</b> And The DRD2/<strong>ANKK1</strong> Genotype.
+ANKK1	drug	nicotine	21244814	A polymorphism (TaqI) in the 3' untranslated region of the dopamine receptor gene (DRD2), later localized to the neighboring <strong>ANKK1</strong> gene, has been previously linked to cigarette <b>smoking</b>.
+ANKK1	drug	nicotine	21168125	TTC12 <strong>ANKK1</strong> DRD2 and CHRNA5 CHRNA3 CHRNB4 influence different pathways leading to <b>smoking</b> behavior from adolescence to mid adulthood.
+ANKK1	drug	nicotine	21168125	CHRNA5 CHRNA3 CHRNB4 and TTC12 <strong>ANKK1</strong> DRD2 gene clusters influence <b>smoking</b> behavior.
+ANKK1	drug	nicotine	21168125	TTC12 <strong>ANKK1</strong> DRD2s seemed to influence <b>smoking</b> behavior mainly in adolescence, and its effect is partially mediated by personality characteristics promoting drug seeking behavior.
+ANKK1	addiction	relapse	21168125	TTC12 <strong>ANKK1</strong> DRD2s seemed to influence smoking behavior mainly in adolescence, and its effect is partially mediated by personality characteristics promoting drug <b>seeking</b> behavior.
+ANKK1	drug	alcohol	21070510	Interaction between ALDH2*1*1 and DRD2/<strong>ANKK1</strong> TaqI A1A1 genes may be associated with antisocial personality disorder not co morbid with <b>alcoholism</b>.
+ANKK1	drug	alcohol	20554694	Earlier findings on the associations of DRD2 and NPY with <b>alcohol</b> dependence were supported: DRD2/<strong>ANKK1</strong> Taq1A(1) increased (P = 0.04) and NPY Pro7 decreased (P = 0.01) the risk of <b>alcohol</b> dependence.
+ANKK1	addiction	dependence	20554694	Earlier findings on the associations of DRD2 and NPY with alcohol <b>dependence</b> were supported: DRD2/<strong>ANKK1</strong> Taq1A(1) increased (P = 0.04) and NPY Pro7 decreased (P = 0.01) the risk of alcohol <b>dependence</b>.
+ANKK1	drug	nicotine	20350135	We examined genotypes at two dopamine related loci, DRD2/<strong>ANKK1</strong> (rs1800497) and DBH (rs77905), in 577 heavy <b>smokers</b> participating in a prospective study of <b>smoking</b> cessation in general care in Germany.
+ANKK1	drug	nicotine	20350135	<b>Smoking</b> status after 1 year was significantly associated with DRD2/<strong>ANKK1</strong>, odds of abstinence being 4.4 fold (95% CI: 1.5 12.9) increased in TT  versus CC homozygous subjects (p = 0.008).
+ANKK1	drug	nicotine	20133381	Sex differences in TTC12/<strong>ANKK1</strong> haplotype associations with daily <b>tobacco</b> <b>smoking</b> in Black and White Americans.
+ANKK1	drug	alcohol	19914044	The A1 allele of the <strong>ANKK1</strong> TaqIa polymorphism is associated with lower dopaminergic tone and greater risk for <b>alcoholism</b>, but the mechanisms are unclear.
+ANKK1	addiction	addiction	19900188	Polymorphisms of DRD2 and <strong>ANKK1</strong> have been associated with psychiatric syndromes where there is believed to be an underlying learning process deficit such as <b>addiction</b>, post traumatic stress disorder and psychopathy.
+ANKK1	drug	alcohol	19900188	We investigated the effects of the DRD2 C957T and <strong>ANKK1</strong> TaqIA single nucleotide polymorphism (SNP), which have been associated with psychopathic traits in <b>alcoholic</b> patients, on fear conditioning and aversive priming in healthy volunteers.
+ANKK1	addiction	aversion	19900188	We investigated the effects of the DRD2 C957T and <strong>ANKK1</strong> TaqIA single nucleotide polymorphism (SNP), which have been associated with psychopathic traits in alcoholic patients, on fear conditioning and <b>aversive</b> priming in healthy volunteers.
+ANKK1	addiction	aversion	19900188	We found that the DRD2 C957T SNP, but not the <strong>ANKK1</strong> TaqIA SNP, was associated with both differential conditioning of the skin conductance response and the <b>aversive</b> priming effect.
+ANKK1	drug	alcohol	19796663	Influence of DRD2 and <strong>ANKK1</strong> genotypes on apomorphine induced growth hormone (GH) response in <b>alcohol</b> dependent patients.
+ANKK1	drug	alcohol	19796663	Apomorphine challenge tests measuring GH responses on 5 time points were performed on day 1 of <b>alcohol</b> detoxification in 43 patients with <b>alcohol</b> dependence; patients were genotyped for 11 polymorphisms including DRD2, <strong>ANKK1</strong>, NCAM1 and TTC12.
+ANKK1	addiction	dependence	19796663	Apomorphine challenge tests measuring GH responses on 5 time points were performed on day 1 of alcohol detoxification in 43 patients with alcohol <b>dependence</b>; patients were genotyped for 11 polymorphisms including DRD2, <strong>ANKK1</strong>, NCAM1 and TTC12.
+ANKK1	drug	alcohol	19796663	This has been the first study showing significant associations between apomorphine induced GH response and SNPs in DRD2 and <strong>ANKK1</strong> in <b>alcohol</b> dependent patients.
+ANKK1	drug	opioid	19373123	Here, we comprehensively analyzed the DRD2 gene locus, and in addition, the <strong>ANKK1</strong> rs1800497C>T single nucleotide polymorphism (SNP), formerly known as 'dopamine D2 receptor Taq1A C>T polymorphism', for associations with the risk of opiate addiction and the <b>methadone</b> dosage requirements.
+ANKK1	addiction	addiction	19373123	Here, we comprehensively analyzed the DRD2 gene locus, and in addition, the <strong>ANKK1</strong> rs1800497C>T single nucleotide polymorphism (SNP), formerly known as 'dopamine D2 receptor Taq1A C>T polymorphism', for associations with the risk of opiate <b>addiction</b> and the methadone dosage requirements.
+ANKK1	drug	opioid	19373123	Allelic frequencies of DRD2/<strong>ANKK1</strong> polymorphisms were compared between 85 <b>methadone</b> substituted Caucasian patients and a random sample of 99 healthy Caucasian controls.
+ANKK1	drug	opioid	19373123	Within patients, the average and maximum daily <b>methadone</b> dose during the first year of treatment and the time when that maximum dose was reached were analyzed for an association with DRD2/<strong>ANKK1</strong> genetics.
+ANKK1	drug	opioid	19373123	On the basis of an analysis spanning the whole gene locus, from the DRD2 promoter to the <strong>ANKK1</strong> rs1800497C>T polymorphism, DRD2 genetic polymorphisms modulate both the risk of opiate addiction, leading to the necessity of <b>methadone</b> substitution therapy, and the course of this therapy in terms of dosage requirements.
+ANKK1	addiction	addiction	19373123	On the basis of an analysis spanning the whole gene locus, from the DRD2 promoter to the <strong>ANKK1</strong> rs1800497C>T polymorphism, DRD2 genetic polymorphisms modulate both the risk of opiate <b>addiction</b>, leading to the necessity of methadone substitution therapy, and the course of this therapy in terms of dosage requirements.
+ANKK1	drug	alcohol	18828801	Haplotypic variants in DRD2, <strong>ANKK1</strong>, TTC12, and NCAM1 are associated with comorbid <b>alcohol</b> and drug dependence.
+ANKK1	addiction	dependence	18828801	Haplotypic variants in DRD2, <strong>ANKK1</strong>, TTC12, and NCAM1 are associated with comorbid alcohol and drug <b>dependence</b>.
+ANKK1	drug	nicotine	18690118	The increase in <b>smoking</b> amount owing to negative mood was associated with: dopamine D2 receptor (DRD2) C957T (CC>TT or CT), SLC6A3 (presence of 9 repeat>absence of 9), and among those given a <b>nicotine</b> cigarette, DRD4 (presence of 7 repeat>absence of 7) and DRD2/<strong>ANKK1</strong> TaqIA (TT or CT>CC).
+ANKK1	drug	nicotine	18690118	SLC6A3, and DRD2/<strong>ANKK1</strong> TaqIA were also associated with <b>smoking</b> reward and <b>smoking</b> latency.
+ANKK1	addiction	reward	18690118	SLC6A3, and DRD2/<strong>ANKK1</strong> TaqIA were also associated with smoking <b>reward</b> and smoking latency.
+ANKK1	drug	opioid	18690117	Very few or no significant associations were seen for the DRD2/<strong>ANKK1</strong> TaqIA polymorphism, the serotonin transporter promoter VNTR or 5HTTLPR (SLC6A4), the dopamine transporter 3' VNTR (SLC6A3), and the mu <b>opioid</b> receptor A118G single nucleotide polymorphism (mu <b>opioid</b> receptor polymorphism 1).
+ANKK1	drug	nicotine	18354387	Significant association of <strong>ANKK1</strong> and detection of a functional polymorphism with <b>nicotine</b> dependence in an African American sample.
+ANKK1	addiction	dependence	18354387	Significant association of <strong>ANKK1</strong> and detection of a functional polymorphism with nicotine <b>dependence</b> in an African American sample.
+ANKK1	drug	nicotine	18354387	We examined 16 single nucleotide polymorphisms (SNPs) at DRD2 and 7 SNPs at <strong>ANKK1</strong> in our Mid South <b>Tobacco</b> Family cohort, which consisted of 2037 participants representing two distinct American populations.
+ANKK1	drug	nicotine	18354387	We conclude that <strong>ANKK1</strong> is associated with ND and polymorphism rs2734849 in <strong>ANKK1</strong> represents a functional causative variant for ND in African American <b>smokers</b>.
+ANKK1	drug	nicotine	18058350	DRD2/<strong>ANKK1</strong> TaqI polymorphism and <b>smoking</b> behavior of Egyptian male cigarette <b>smokers</b>.
+ANKK1	drug	alcohol	17948892	The association between DRD2/<strong>ANKK1</strong>, 5 HTTLPR gene, and specific personality trait on antisocial <b>alcoholism</b> among Han Chinese in Taiwan.
+ANKK1	drug	alcohol	17850642	Family based association analyses of <b>alcohol</b> dependence phenotypes across DRD2 and neighboring gene <strong>ANKK1</strong>.
+ANKK1	addiction	dependence	17850642	Family based association analyses of alcohol <b>dependence</b> phenotypes across DRD2 and neighboring gene <strong>ANKK1</strong>.
+ANKK1	drug	alcohol	17850642	To more carefully characterize evidence for association across this region, we genotyped 26 single nucleotide polymorphisms (SNPs) spanning DRD2 and <strong>ANKK1</strong> in a sample of 219 Caucasian families (n = 1,923) from the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA), making this the most extensive analysis to date of association between this region and <b>alcohol</b> dependence.
+ANKK1	addiction	dependence	17850642	To more carefully characterize evidence for association across this region, we genotyped 26 single nucleotide polymorphisms (SNPs) spanning DRD2 and <strong>ANKK1</strong> in a sample of 219 Caucasian families (n = 1,923) from the Collaborative Study on the Genetics of Alcoholism (COGA), making this the most extensive analysis to date of association between this region and alcohol <b>dependence</b>.
+ANKK1	drug	alcohol	17850642	The association in <strong>ANKK1</strong> is strongest among the subsets of <b>alcoholics</b> with medical complications and with antisocial personality disorder.
+ANKK1	drug	alcohol	17850642	More extensive genotyping across DRD2 and <strong>ANKK1</strong> suggests that the association with <b>alcohol</b> dependence observed in this region may be due to genetic variants in the <strong>ANKK1</strong> gene.
+ANKK1	addiction	dependence	17850642	More extensive genotyping across DRD2 and <strong>ANKK1</strong> suggests that the association with alcohol <b>dependence</b> observed in this region may be due to genetic variants in the <strong>ANKK1</strong> gene.
+ANKK1	addiction	addiction	17850642	<strong>ANKK1</strong> is involved in signal transduction pathways and is a plausible biological candidate for involvement in <b>addictive</b> disorders.
+ANKK1	drug	alcohol	17761687	Association of haplotypic variants in DRD2, <strong>ANKK1</strong>, TTC12 and NCAM1 to <b>alcohol</b> dependence in independent case control and family samples.
+ANKK1	addiction	dependence	17761687	Association of haplotypic variants in DRD2, <strong>ANKK1</strong>, TTC12 and NCAM1 to alcohol <b>dependence</b> in independent case control and family samples.
+ANKK1	drug	nicotine	17085484	Haplotype spanning TTC12 and <strong>ANKK1</strong>, flanked by the DRD2 and NCAM1 loci, is strongly associated to <b>nicotine</b> dependence in two distinct American populations.
+ANKK1	addiction	dependence	17085484	Haplotype spanning TTC12 and <strong>ANKK1</strong>, flanked by the DRD2 and NCAM1 loci, is strongly associated to nicotine <b>dependence</b> in two distinct American populations.
+ANKK1	addiction	dependence	17085484	DRD2 and NCAM1 are functional candidate genes for substance <b>dependence</b>; the TTC12 and <strong>ANKK1</strong> loci are not well characterized.
+ANKK1	addiction	addiction	15146457	If this is the case, then changes in <strong>ANKK1</strong> activity may provide an alternative explanation for previously described associations between the DRD2 Taq1A RFLP and neuropsychiatric disorders such as <b>addiction</b>.
+WARS1	drug	opioid	31711720	Opium <strong>Wars</strong> to the <b>Opioid</b> Epidemic: The Same Narcotics Cause Addiction and Kill.
+WARS1	addiction	addiction	31711720	Opium <strong>Wars</strong> to the Opioid Epidemic: The Same Narcotics Cause <b>Addiction</b> and Kill.
+WARS1	drug	nicotine	30498062	E cigarettes: Tar <strong>Wars</strong>: The (<b>Tobacco</b>) Empire Strikes Back.
+WARS1	drug	alcohol	28214434	Compared to the general population, veterans of the <strong>wars</strong> in Afghanistan and Iraq (OEF/OIF) are more likely to engage in hazardous <b>alcohol</b> use and meet criteria for mental health disorders including Posttraumatic Stress Disorder (PTSD) and Major Depressive Disorder.
+WARS1	drug	nicotine	27659441	Cigarette <b>Smoking</b> Status and Receipt of an Opioid Prescription Among Veterans of Recent <strong>Wars</strong>.
+WARS1	drug	opioid	27659441	Cigarette Smoking Status and Receipt of an <b>Opioid</b> Prescription Among Veterans of Recent <strong>Wars</strong>.
+WARS1	drug	alcohol	27036408	Young adult veterans from the <strong>wars</strong> in Iraq and Afghanistan represent a population at risk for heavy and problematic <b>alcohol</b> use.
+WARS1	drug	opioid	26068436	In Asia, the use of <b>opioids</b> is sensitive because of the Opium <strong>Wars</strong> in the 19th century and for this reason, the focus of controlled substances policies has been on the prevention of diversion and dependence.
+WARS1	addiction	dependence	26068436	In Asia, the use of opioids is sensitive because of the Opium <strong>Wars</strong> in the 19th century and for this reason, the focus of controlled substances policies has been on the prevention of diversion and <b>dependence</b>.
+WARS1	drug	alcohol	24773573	The purpose of this study was to test the efficacy of 2 brief interventions for <b>alcohol</b> misuse in a sample of combat veterans of the <strong>wars</strong> in Iraq and Afghanistan.
+WARS1	addiction	relapse	23129288	In a convenience sample of 157 U.S. service members from the Afghanistan and Iraq <strong>wars</strong> <b>seeking</b> health care services at a Veterans Administration (VA) hospital, this study examined (a) the impact of attachment characteristics on several key mental health symptoms in this new generation of veterans, (b) the relative frequencies of prominent attachment styles in the sample, and (c) how these higher order orientations related to study outcomes.
+WARS1	drug	alcohol	22522738	The present study evaluated the impact of combat and interpersonal trauma exposure in a sample of 115 U.S. women veterans from Gulf War I and the Iraq and Afghanistan <strong>wars</strong> on 3 postdeployment trauma related mental health outcomes: posttraumatic stress disorder symptoms (PSS), depressive symptom severity (DSS), and <b>alcohol</b> misuse.
+WARS1	drug	alcohol	22253714	GABRG2, encoding the <strong>gamma2</strong> subunit required for postsynaptic clustering of GABAA receptors together with GPHN, encoding the associated scaffolding protein gephryin, were both down regulated in <b>alcoholics</b> and cocaine addicts but were both up regulated in P rats.
+WARS1	drug	cocaine	22253714	GABRG2, encoding the <strong>gamma2</strong> subunit required for postsynaptic clustering of GABAA receptors together with GPHN, encoding the associated scaffolding protein gephryin, were both down regulated in alcoholics and <b>cocaine</b> addicts but were both up regulated in P rats.
+WARS1	drug	alcohol	22089316	The <strong>wars</strong> in Iraq and Afghanistan are associated with high rates of post traumatic stress disorder (PTSD) and comorbid <b>alcohol</b> use disorders.
+WARS1	drug	benzodiazepine	20219525	To determine if the observed changes in gene expression produced functional changes in the locomotor responses to drugs known to either preferentially or generally activate GABA(A) receptors normally possessing the significantly altered subunits, separate cohorts of animals were challenged with one of several low doses of zolpidem (alpha1 selective), etomidate (beta2/3 selective), or <b>flurazepam</b> (<strong>gamma2</strong> directed) and assessed for locomotor alterations.
+WARS1	drug	alcohol	19133912	Litigation and <b>alcohol</b> policy: lessons from the US Tobacco <strong>Wars</strong>.
+WARS1	drug	nicotine	19133912	Litigation and alcohol policy: lessons from the US <b>Tobacco</b> <strong>Wars</strong>.
+WARS1	drug	alcohol	19135472	Gamma1  and <strong>gamma2</strong> melanocyte stimulating hormones induce central anxiogenic effects and potentiate <b>ethanol</b> withdrawal responses in the elevated plus maze test in mice.
+WARS1	addiction	withdrawal	19135472	Gamma1  and <strong>gamma2</strong> melanocyte stimulating hormones induce central anxiogenic effects and potentiate ethanol <b>withdrawal</b> responses in the elevated plus maze test in mice.
+WARS1	drug	alcohol	19135472	This study provides the first demonstration of an anxiogenic effect of gamma1  and <strong>gamma2</strong> MSH, their synergistic/additive effect on <b>ethanol</b> withdrawal induced anxiety behaviour, and an antagonism of peptides involved in the anxiolytic action of <b>ethanol</b>.
+WARS1	addiction	withdrawal	19135472	This study provides the first demonstration of an anxiogenic effect of gamma1  and <strong>gamma2</strong> MSH, their synergistic/additive effect on ethanol <b>withdrawal</b> induced anxiety behaviour, and an antagonism of peptides involved in the anxiolytic action of ethanol.
+WARS1	drug	alcohol	19012816	Hazardous <b>alcohol</b> use and receipt of risk reduction counseling among U.S. veterans of the <strong>wars</strong> in Iraq and Afghanistan.
+WARS1	drug	alcohol	18698065	High rates of <b>alcohol</b> misuse after deployment have been reported among personnel returning from past conflicts, yet investigations of <b>alcohol</b> misuse after return from the current <strong>wars</strong> in Iraq and Afghanistan are lacking.
+WARS1	addiction	intoxication	17989301	A cross linking assay and Western blot analysis of microdissected CA1 area of hippocampal slices obtained 1 h after EtOH <b>intoxication</b> (5 g/kg, gavage), revealed decreases in the cell surface fraction of alpha4 and delta, but not alpha1, alpha5, or <strong>gamma2</strong> GABA(A)R subunits, without changes in their total content.
+WARS1	drug	alcohol	17428292	beta1 and <strong>gamma2</strong> expression was significantly reduced in samples from <b>ethanol</b> exposed amygdala.
+WARS1	drug	alcohol	16927170	Tyrosine kinase phosphorylation of GABA(A) receptor alpha1, beta2 and <strong>gamma2</strong> subunits following chronic intermittent <b>ethanol</b> (CIE) exposure of cultured cortical neurons of mice.
+WARS1	drug	benzodiazepine	16876255	Classical benzodiazepines bind non selectively to GABA(A) receptors containing a <strong>gamma2</strong> subunit, whereas non <b>benzodiazepine</b> hypnotics bind with higher relative affinity to alpha1 containing receptors.
+WARS1	addiction	withdrawal	16839855	Most of the changes returned to control levels after <b>withdrawal</b>, except for the <strong>gamma2</strong> subunit protein, which was lower than controls.
+WARS1	addiction	withdrawal	16436183	We report that the DBA/2J mouse strain, which exhibits severe <b>withdrawal</b> from sedative hypnotic drugs, encodes a unique GABA(A) receptor <strong>gamma2</strong> subunit variant compared with other standard inbred strains including the genetically similar DBA/1J strain.
+WARS1	addiction	dependence	16436183	Our results, together with recent knockout studies, point to the GABA(A) receptor <strong>gamma2</strong> subunit gene (Gabrg2) as a promising candidate gene to underlie phenotypic differences in sedative hypnotic physiological <b>dependence</b> and associated withdrawal episodes.
+WARS1	addiction	withdrawal	16436183	Our results, together with recent knockout studies, point to the GABA(A) receptor <strong>gamma2</strong> subunit gene (Gabrg2) as a promising candidate gene to underlie phenotypic differences in sedative hypnotic physiological dependence and associated <b>withdrawal</b> episodes.
+WARS1	drug	alcohol	15630072	The GABA(A) gene cluster on chromosome 5q34 is of particular interest in the genetics of <b>alcohol</b> dependence because of the <strong>gamma2</strong> subunit requirement for <b>ethanol</b>'s modulatory action on GABA(A) receptors, previous linkage findings in mice and humans implicating both GABRA6 and GABRG2, and reported associations of GABRA6, GABRB2, and GABRG2 alleles with <b>alcohol</b> dependence.
+WARS1	addiction	dependence	15630072	The GABA(A) gene cluster on chromosome 5q34 is of particular interest in the genetics of alcohol <b>dependence</b> because of the <strong>gamma2</strong> subunit requirement for ethanol's modulatory action on GABA(A) receptors, previous linkage findings in mice and humans implicating both GABRA6 and GABRG2, and reported associations of GABRA6, GABRB2, and GABRG2 alleles with alcohol <b>dependence</b>.
+WARS1	drug	alcohol	15596326	The causes of the increase in STDs are many, but we believe that alterations in family structures, drug and <b>alcohol</b> addiction, <strong>wars</strong> and mobilization of armies and movement of populations, in addition to change in sexual behaviors and lax morality are the main ones.
+WARS1	addiction	addiction	15596326	The causes of the increase in STDs are many, but we believe that alterations in family structures, drug and alcohol <b>addiction</b>, <strong>wars</strong> and mobilization of armies and movement of populations, in addition to change in sexual behaviors and lax morality are the main ones.
+WARS1	drug	alcohol	15542698	PCR based assays showed that <b>alcoholism</b> was associated with polymorphisms of the dopamine D2 receptor (DRD2) TaqI B (P = .029) and the GABAA beta2 subunit C1412T (P = .012) genes, but not with the glutamate receptor subunit gene NMDAR2B (366C/G), the serotonin transporter gene (5HTTL PR), the dopamine transporter gene DAT1(SLC6A3), the dopamine D2 receptor gene DRD2 TaqI A, or the GABAA alpha1(A15G), alpha6(T1519C), and <strong>gamma2</strong>(G3145A) subunit genes.
+WARS1	drug	alcohol	14751585	The role of the alpha6 subunit gene cluster in the <b>ethanol</b> non preferring phenotype was here investigated by measuring the levels of alpha1, alpha6 and <strong>gamma2</strong> peptide in the cerebellum of normal (RR) and mutated (QQ) sNP rats after 2 weeks of chronic <b>ethanol</b> administration.
+WARS1	drug	alcohol	14751585	Interestingly, chronic <b>ethanol</b> administration decreased alpha1 peptide levels in the cerebellum of both rat lines to a similar extent (30.99%+/ 6.74 and 27.12%+/ 9.83 in RR and QQ rats, respectively), while <strong>gamma2</strong> peptide levels remained unchanged.
+WARS1	drug	benzodiazepine	14572465	Deletion of the <strong>gamma2</strong> subunit in the third postnatal week resulted in loss of <b>benzodiazepine</b> binding sites and parallel loss of punctate immunoreactivity for postsynaptic GABA(A) receptors and gephyrin.
+WARS1	addiction	reward	14572465	Thus, the <strong>gamma2</strong> subunit contributes to postsynaptic localization of GABA(A) receptors and gephyrin by a mechanism that is <b>operant</b> in mature neurons and not limited to immature neurons, most likely through interaction with proteins involved in trafficking of synaptic GABA(A) receptors.
+WARS1	drug	cocaine	12966149	Five GABA A receptor subunit mRNAs (alpha4, alpha6, beta2, <strong>gamma2</strong>, and delta) were down regulated at both 1 and 20 days of <b>cocaine</b> self administration.
+WARS1	drug	alcohol	12591165	Molecular characterization of new polymorphisms at the beta2, alpha1, <strong>gamma2</strong> GABA(A) receptor subunit genes associated to a rat nonpreferring <b>ethanol</b> phenotype.
+WARS1	drug	alcohol	12591165	Recent preclinical and clinical studies have indicated a possible involvement of the genes encoding for the GABA(A) receptor subunits alpha6, beta2, alpha1 and <strong>gamma2</strong> in the genetic susceptibility to <b>alcohol</b> abuse.
+WARS1	drug	alcohol	12591165	In the present study the molecular composition of other GABA(A) subunits (beta2, alpha1 and <strong>gamma2</strong>) were analyzed in order to further investigate the involvement of the GABA(A) receptors in the genetic predisposition to voluntary <b>alcohol</b> intake.
+WARS1	drug	alcohol	12591165	These results sustain the synteny for these clusters between the rodent and human genomes, and suggest that mutated GABA(A) beta2, alpha6, alpha1 and <strong>gamma2</strong> subunit genes might contribute to the expression of an <b>ethanol</b> nonpreferring phenotype in a rat line that voluntarily avoids <b>alcoholic</b> solutions.
+WARS1	drug	benzodiazepine	12488536	Immunoblotting revealed decrease in alpha1 and delta expression and increase in <strong>gamma2</strong> and alpha4 subunits in hippocampus of CIE rats, confirmed by an increase in <b>diazepam</b> insensitive binding for ethyl 8 azido 5,6 dihydro 5 methyl 6 oxo 4H imidazo(1,5 alpha)(1,4)<b>benzodiazepine</b> 3 carboxylate (Ro15 4513).
+WARS1	drug	amphetamine	11642656	Then the authors determined the <b>methamphetamine</b> concentration in rat brain striatum by gas chromatography mass spectrometry (GC MS) The results showed that the concentration of <b>methamphetamine</b> <strong>wars</strong> significantly higher in the rats 24 hours, and also 7 days after withdrawal of citalopram administration, compared to the control rats.
+WARS1	addiction	withdrawal	11642656	Then the authors determined the methamphetamine concentration in rat brain striatum by gas chromatography mass spectrometry (GC MS) The results showed that the concentration of methamphetamine <strong>wars</strong> significantly higher in the rats 24 hours, and also 7 days after <b>withdrawal</b> of citalopram administration, compared to the control rats.
+WARS1	drug	alcohol	11410716	However, the significant decrease in <strong>gamma2</strong> subunit L/S splice variant ratio in the hippocampus implies changes in GABAA receptor function, possibly involving protein phosphorylation by protein kinase C. Altered receptor trafficking and turnover associated with synaptic plasticity may contribute to the observed reduced inhibition in the hippocampus and other signs of <b>alcohol</b> dependence produced by CIE.
+WARS1	addiction	dependence	11410716	However, the significant decrease in <strong>gamma2</strong> subunit L/S splice variant ratio in the hippocampus implies changes in GABAA receptor function, possibly involving protein phosphorylation by protein kinase C. Altered receptor trafficking and turnover associated with synaptic plasticity may contribute to the observed reduced inhibition in the hippocampus and other signs of alcohol <b>dependence</b> produced by CIE.
+WARS1	drug	alcohol	11391054	The presentations were (1) Protein kinase Cepsilon regulated sensitivity of gamma aminobutyric acid type A (GABAA) receptors to allosteric agonists, by Robert O. Messing, A. M. Sanchez Perez, C. W. Hodge, T. McMahon, D. Wang, K. K. Mehmert, S. P. Kelley, A. Haywood, and M. F. Olive; (2) Genetic and functional analysis of a GABAA receptor <strong>gamma2</strong> subunit variant: A candidate for quantitative trait loci involved in <b>alcohol</b> sensitivity and withdrawal, by Kari J. Buck and Heather M. Hood; (3) Tryptophan scanning mutagenesis in GABAA receptor subunits: Channel gating and <b>alcohol</b> actions, by Susumu Ueno; and (4) Can a single binding site account for actions of alcohols on GABAA and glycine receptors?
+WARS1	addiction	withdrawal	11391054	The presentations were (1) Protein kinase Cepsilon regulated sensitivity of gamma aminobutyric acid type A (GABAA) receptors to allosteric agonists, by Robert O. Messing, A. M. Sanchez Perez, C. W. Hodge, T. McMahon, D. Wang, K. K. Mehmert, S. P. Kelley, A. Haywood, and M. F. Olive; (2) Genetic and functional analysis of a GABAA receptor <strong>gamma2</strong> subunit variant: A candidate for quantitative trait loci involved in alcohol sensitivity and <b>withdrawal</b>, by Kari J. Buck and Heather M. Hood; (3) Tryptophan scanning mutagenesis in GABAA receptor subunits: Channel gating and alcohol actions, by Susumu Ueno; and (4) Can a single binding site account for actions of alcohols on GABAA and glycine receptors?
+WARS1	drug	nicotine	11285101	This article examines the use of the Tar <strong>Wars</strong> curriculum with the public health problem of preteen <b>smoking</b> and outlines interventions with a middle school population by community health student nurses from a state university.
+WARS1	drug	cocaine	11018794	There was a significant decrease in the level of alpha 1, alpha 6, beta 2, beta 3, and <strong>gamma 2</strong> subunits mRNA, with no alteration of [(35)S]TBPS binding in any regions in the brain of rats at 1 h following a single injection of <b>cocaine</b>.
+WARS1	drug	alcohol	11003197	Allelic variation in the GABA A receptor <strong>gamma2</strong> subunit is associated with genetic susceptibility to <b>ethanol</b> induced motor incoordination and hypothermia, conditioned taste aversion, and withdrawal in BXD/Ty recombinant inbred mice.
+WARS1	addiction	aversion	11003197	Allelic variation in the GABA A receptor <strong>gamma2</strong> subunit is associated with genetic susceptibility to ethanol induced motor incoordination and hypothermia, conditioned taste <b>aversion</b>, and withdrawal in BXD/Ty recombinant inbred mice.
+WARS1	addiction	withdrawal	11003197	Allelic variation in the GABA A receptor <strong>gamma2</strong> subunit is associated with genetic susceptibility to ethanol induced motor incoordination and hypothermia, conditioned taste aversion, and <b>withdrawal</b> in BXD/Ty recombinant inbred mice.
+WARS1	drug	alcohol	10947837	We conclude that acute functional tolerance to <b>ethanol</b> is very sensitive to the amount of GABAA receptor <strong>gamma2</strong> subunit available (regardless of whether it is gamma2L or gamma2S) but overexpression of neither subunit isoform alters other behavioural and biochemical phenotypes.
+WARS1	drug	alcohol	10889533	In this study, three RFLPs at the GABA(A)beta2, GABAAalpha6, GABA(A)alpha1 and two at the GABA(A)<strong>gamma2</strong> receptor subunit genes, were examined for association with <b>alcohol</b> dependence in 189 subjects meeting DSM III R criteria for this disorder and 152 unrelated controls from a Japanese population.
+WARS1	addiction	dependence	10889533	In this study, three RFLPs at the GABA(A)beta2, GABAAalpha6, GABA(A)alpha1 and two at the GABA(A)<strong>gamma2</strong> receptor subunit genes, were examined for association with alcohol <b>dependence</b> in 189 subjects meeting DSM III R criteria for this disorder and 152 unrelated controls from a Japanese population.
+WARS1	drug	alcohol	10889533	However, the NciI RFLP at the GABA(A)<strong>gamma2</strong> receptor subunit gene was associated with <b>alcohol</b> dependence comorbid with antisocial personality disorder (P = 0.021).
+WARS1	addiction	dependence	10889533	However, the NciI RFLP at the GABA(A)<strong>gamma2</strong> receptor subunit gene was associated with alcohol <b>dependence</b> comorbid with antisocial personality disorder (P = 0.021).
+WARS1	drug	alcohol	10889533	This supports a recent finding reporting an association between the GABA(A)<strong>gamma2</strong> receptor subunit gene and <b>alcohol</b> dependence with criminal record in a Finnish population.
+WARS1	addiction	dependence	10889533	This supports a recent finding reporting an association between the GABA(A)<strong>gamma2</strong> receptor subunit gene and alcohol <b>dependence</b> with criminal record in a Finnish population.
+WARS1	drug	alcohol	10871693	Role of the GABA(A)beta2, GABA(A)alpha6, GABA(A)alpha1 and GABA(A)<strong>gamma2</strong> receptor subunit genes cluster in drug responses and the development of <b>alcohol</b> dependence.
+WARS1	addiction	dependence	10871693	Role of the GABA(A)beta2, GABA(A)alpha6, GABA(A)alpha1 and GABA(A)<strong>gamma2</strong> receptor subunit genes cluster in drug responses and the development of alcohol <b>dependence</b>.
+WARS1	drug	alcohol	10871693	GABA(A) subunit mRNA expression in cell models has suggested that the long form of the <strong>gamma2</strong> subunit is essential for <b>ethanol</b> enhanced potentiation of GABA(A) receptors, by phosphorylation of a serine contained within the extra eight amino acids.
+WARS1	drug	alcohol	10871693	Several animal studies have demonstrated that alterations in drug and <b>alcohol</b> responses may be caused by amino acid differences at the GABA(A)alpha6 and GABA(A)<strong>gamma2</strong> subunits.
+WARS1	drug	alcohol	10871693	Several loci related to <b>alcohol</b> withdrawal on mouse chromosome 11 which corresponds to the region containing four GABA(A) subunit (beta2, alpha6, alpha1 and <strong>gamma2</strong>) genes on human chromosome 5q33 34, were also identified.
+WARS1	addiction	withdrawal	10871693	Several loci related to alcohol <b>withdrawal</b> on mouse chromosome 11 which corresponds to the region containing four GABA(A) subunit (beta2, alpha6, alpha1 and <strong>gamma2</strong>) genes on human chromosome 5q33 34, were also identified.
+WARS1	drug	benzodiazepine	10871693	Gene knockout studies of the role of GABA(A)alpha6 and GABA(A)<strong>gamma2</strong> subunit genes in mice have demonstrated an essential role in the modulation of other GABA(A) subunit expression and the efficacy of <b>benzodiazepine</b> binding.
+WARS1	drug	alcohol	10871693	Human genetic association studies have suggested that the GABA(A)beta2, alpha6, alpha1 and <strong>gamma2</strong> subunit genes have a role in the development of <b>alcohol</b> dependence, although their contributions may vary between ethnic group and phenotype.
+WARS1	addiction	dependence	10871693	Human genetic association studies have suggested that the GABA(A)beta2, alpha6, alpha1 and <strong>gamma2</strong> subunit genes have a role in the development of alcohol <b>dependence</b>, although their contributions may vary between ethnic group and phenotype.
+WARS1	drug	alcohol	10871693	In summary, in vitro cell, animal and human genetic association studies have suggested that the GABA(A)beta2, alpha6, alpha1 and <strong>gamma2</strong> subunit genes have an important role in <b>alcohol</b> related phenotypes (300 words).
+WARS1	drug	benzodiazepine	10336082	Temporal and regional regulation of alpha1, beta2 and beta3, but not alpha2, alpha4, alpha5, alpha6, beta1 or <strong>gamma2</strong> GABA(A) receptor subunit messenger RNAs following one week oral <b>flurazepam</b> administration.
+WARS1	drug	benzodiazepine	10336082	The effect of prolonged <b>benzodiazepine</b> administration on GABA(A) receptor subunit (alpha1 6, beta1 3, <strong>gamma2</strong>) messenger RNAs was investigated in the rat hippocampus and cortex, among other brain areas.
+WARS1	drug	benzodiazepine	10336082	There was a trend toward an increased level of alpha5, beta3 and <strong>gamma2</strong> subunit messenger RNAs in CA1, CA3 and dentate gyrus cells, which was significant for the beta3 and <strong>gamma2</strong> subunit messenger RNAs in the frontal cortex seven days after ending <b>flurazepam</b> treatment.
+WARS1	drug	alcohol	10218866	Normal electrophysiological and behavioral responses to <b>ethanol</b> in mice lacking the long splice variant of the <strong>gamma2</strong> subunit of the gamma aminobutyrate type A receptor.
+WARS1	drug	alcohol	10218866	The long splice variant of the <strong>gamma2</strong> subunit (gamma2L) has been postulated to be essential in mediating the modulatory actions of <b>ethanol</b> at the GABA(A) R. In order to evaluate this hypothesis, gene targeting was used to delete the 24bp exon which distinguishes gamma2L from the short splice variant (gamma2S).
+WARS1	drug	alcohol	10195814	Association analysis of sequence variants of GABA(A) alpha6, beta2, and <strong>gamma2</strong> gene cluster and <b>alcohol</b> dependence.
+WARS1	addiction	dependence	10195814	Association analysis of sequence variants of GABA(A) alpha6, beta2, and <strong>gamma2</strong> gene cluster and alcohol <b>dependence</b>.
+WARS1	drug	alcohol	10195814	Quantitative trait analyses in mice suggest a vulnerability locus for physiological <b>alcohol</b> withdrawal severity on a chromosomal segment that harbors the genes encoding the alpha1, alpha6, beta2, and <strong>gamma2</strong> subunits of the gamma aminobutyric acid type A receptor (GABR).
+WARS1	addiction	withdrawal	10195814	Quantitative trait analyses in mice suggest a vulnerability locus for physiological alcohol <b>withdrawal</b> severity on a chromosomal segment that harbors the genes encoding the alpha1, alpha6, beta2, and <strong>gamma2</strong> subunits of the gamma aminobutyric acid type A receptor (GABR).
+WARS1	drug	alcohol	10195814	We tested whether genetic variation at the human GABA(A) alpha6, beta2, and <strong>gamma2</strong> gene cluster on chromosome 5q33 confers vulnerability to <b>alcohol</b> dependence.
+WARS1	addiction	dependence	10195814	We tested whether genetic variation at the human GABA(A) alpha6, beta2, and <strong>gamma2</strong> gene cluster on chromosome 5q33 confers vulnerability to alcohol <b>dependence</b>.
+WARS1	drug	benzodiazepine	10082878	Changes in the mRNA encoding alpha1, alpha2, beta2 and <strong>gamma2</strong> subunits of the GABAA receptor associated with the anxiolytic effects of <b>alprazolam</b> were measured in 20 brain regions using in situ hybridization techniques.
+WARS1	addiction	addiction	10082878	<b>Punishment</b> increased beta2 mRNA levels in ventroposterior thalamic nucleus and <strong>gamma2</strong> mRNA levels in the CA2 area of the hippocampus.
+WARS1	drug	alcohol	9880662	Genetic association of a GABA(A) receptor <strong>gamma2</strong> subunit variant with severity of acute physiological dependence on <b>alcohol</b>.
+WARS1	addiction	dependence	9880662	Genetic association of a GABA(A) receptor <strong>gamma2</strong> subunit variant with severity of acute physiological <b>dependence</b> on alcohol.
+WARS1	drug	alcohol	9880662	Analysis using BXD strain means for acute <b>alcohol</b> withdrawal severity suggests that the <strong>gamma2</strong> subunit polymorphism is genetically correlated with <b>alcohol</b> withdrawal severity.
+WARS1	addiction	withdrawal	9880662	Analysis using BXD strain means for acute alcohol <b>withdrawal</b> severity suggests that the <strong>gamma2</strong> subunit polymorphism is genetically correlated with alcohol <b>withdrawal</b> severity.
+WARS1	drug	alcohol	9689472	The effects of <b>ethanol</b> dependence on additional GABAA receptor subunit peptide levels (alpha 4, beta 2/3 and <strong>gamma 2</strong>) were similar, but not identical, between female and male rat cortex.
+WARS1	addiction	dependence	9689472	The effects of ethanol <b>dependence</b> on additional GABAA receptor subunit peptide levels (alpha 4, beta 2/3 and <strong>gamma 2</strong>) were similar, but not identical, between female and male rat cortex.
+WARS1	drug	alcohol	9670216	The molecular basis for the selectivity of the action of <b>ethanol</b> on GaBAA receptors has been proposed to involve a combination of benzodiazepine subtype, beta 2 subunit, and a splice variant of the <strong>gamma 2</strong> subunit, but substantial controversy on this issue currently remains.
+WARS1	drug	benzodiazepine	9670216	The molecular basis for the selectivity of the action of ethanol on GaBAA receptors has been proposed to involve a combination of <b>benzodiazepine</b> subtype, beta 2 subunit, and a splice variant of the <strong>gamma 2</strong> subunit, but substantial controversy on this issue currently remains.
+WARS1	drug	alcohol	9602154	Search for mutations near the alternatively spliced 8 amino acid exon in the GABAA receptor <strong>gamma 2</strong> subunit gene and lack of allelic association with <b>alcoholism</b> among four aboriginal groups and Han Chinese in Taiwan.
+WARS1	drug	alcohol	9602154	The alternatively spliced 8 amino acid exon for the GABAA receptor <strong>gamma2</strong> subunit gene (GABRC2) has been postulated to mediate behavioral actions of <b>alcohol</b>.
+WARS1	drug	benzodiazepine	9586850	While GABA enhancement of <b>benzodiazepine</b> binding was reduced in the nucleus accumbens after repeated <b>diazepam</b> treatment, there was little evidence to support adaptive changes in GABA(A) receptors or GABA(A) subunit gene expression (<strong>gamma2</strong>, alpha1, or alpha4) as underlying the functional changes in the identified circuits.
+WARS1	drug	cannabinoid	9515986	The major results are that most Americans rely on the mass media for information about the scope of the drug abuse problem; Americans do not think that the <strong>Wars</strong> on Drugs have succeeded, but they do not want to quit on these efforts; weak support exists for increasing funding for drug treatment; support for preventive education has increased during the 1990s; criminal justice responses remain very popular; for many, illicit drug use is a moral rather than a public health issue; the public supports allowing physicians to prescribe <b>marijuana</b> for severe illness, but opposes the general legalization of <b>marijuana</b> and other illicit drugs; and needle exchange programs are supported by a bare majority, but only when they are told that the American Medical Association supports these programs.
+WARS1	drug	benzodiazepine	8913357	Pharmacological modulation of the <b>diazepam</b> insensitive recombinant gamma aminobutyric acidA receptors alpha 4 beta 2 <strong>gamma 2</strong> and alpha 6 beta 2 <strong>gamma 2</strong>.
+WARS1	drug	benzodiazepine	8913357	We characterized modulation of the gamma aminobutyric acid (GABA) evoked responses of the <b>diazepam</b> insensitive alpha 4 beta 2 gamma2 and alpha 6 beta 2 <strong>gamma 2</strong> recombinant GABAA receptors.
+WARS1	drug	benzodiazepine	8913357	We characterized modulation of the gamma aminobutyric acid (GABA) evoked responses of the <b>diazepam</b> insensitive alpha 4 beta 2 <strong>gamma2</strong> and alpha 6 beta 2 <strong>gamma 2</strong> recombinant GABAA receptors.
+WARS1	addiction	dependence	8913357	The partial agonist bretazenil potentiated the responses of both receptors with similar dose <b>dependence</b> but with a higher maximal enhancement at the alpha 4 beta 2 <strong>gamma 2</strong> receptor.
+WARS1	addiction	dependence	8913357	The imidazobenzodiazepine inverse agonist Ro 15 4513, which is known to bind with high affinity to the alpha 6 beta 2 <strong>gamma 2</strong> receptor, potentiated the GABA responses of the alpha 4 beta 2 <strong>gamma 2</strong> and alpha 6 beta 2 <strong>gamma 2</strong> receptor subtypes with similar dose <b>dependence</b> over the concentration range of 0.1 10 microM.
+WARS1	drug	benzodiazepine	8913357	Thus, although the alpha 4 beta 2 <strong>gamma 2</strong> receptors are insensitive to <b>benzodiazepine</b> binding site full agonists, such as <b>diazepam</b>, they can be modulated by certain ligands acting as partial and inverse agonists at <b>diazepam</b> sensitive receptors and thereby contribute to the respective pharmacological profiles.
+WARS1	drug	benzodiazepine	8786565	By using the baculovirus expression system, we report decreases in allosteric coupling at individual gamma aminobutyric acid (GABA)(A) receptor subtypes (alpha 1, beta 2 and <strong>gamma 2</strong>, alpha 2, beta 3 and <strong>gamma 2</strong> and alpha 5, beta 3 and <strong>gamma 2</strong>) after chronic <b>benzodiazepine</b> exposure that replicate coupling changes measured in rat cortical membranes after in vivo <b>benzodiazepine</b> exposure.
+WARS1	addiction	withdrawal	8787126	This was in contrast to alpha 1  and <strong>gamma 2</strong> subunit mRNA, which in tolerant animals are unchanged, but for which <b>withdrawal</b> triggers a surge in levels.
+WARS1	drug	benzodiazepine	9014161	<strong>Gamma 2</strong> Subunit mRNA was significantly decreased after 14 days of either <b>diazepam</b> or abecarnil exposure.
+WARS1	drug	benzodiazepine	7931299	Short and long form <strong>gamma 2</strong> subunits of the GABAA/<b>benzodiazepine</b> receptors.
+WARS1	drug	benzodiazepine	7931299	Three novel antisera to the <strong>gamma 2</strong> subunit of the gamma aminobutyric acidA (GABAA) receptor/<b>benzodiazepine</b> receptor (GABAAR/BZDR) complex have been made.
+WARS1	drug	alcohol	8080592	Two recent findings warrant further molecular biological studies on the interaction between <b>ethanol</b> and the GABAA receptor, and the extension of the studies to human <b>alcoholics</b>: first, the effects of <b>ethanol</b> on the GABAA receptor are dependent on a specific <strong>gamma 2</strong> subunit with an additional phosphorylation site; second, genetically enhanced sensitivity to the motor impairing effect of moderate <b>ethanol</b> doses has a likely biological basis in a single nucleotide mutation in a cerebellum specific GABAA receptor subunit.
+WARS1	drug	alcohol	8974321	Chronic <b>ethanol</b> administration increased [3H]zolpidem binding with no effect on levels of GABAA receptor beta 2 and <strong>gamma 2</strong> subunit mRNAs.
+WARS1	drug	benzodiazepine	8388991	Comparison of interactions of [3H]muscimol, t butylbicyclophosphoro[35S]thionate, and [3H]<b>flunitrazepam</b> with cloned gamma aminobutyric acidA receptors of the alpha 1 beta 2 and alpha 1 beta 2 <strong>gamma 2</strong> subtypes.
+WARS1	drug	benzodiazepine	8388991	The number of <b>benzodiazepine</b> binding sites increased as the level of the <strong>gamma 2</strong> virion was raised and reached that of GABA high affinity sites at a <strong>gamma 2</strong> to alpha 1 beta 2 ratio of 0.5 or more.
+WARS1	drug	benzodiazepine	8388991	In all preparations, the dissociation constants for <b>flunitrazepam</b>, muscimol, and TBPS were fairly constant, and the maximal number of binding sites for TBPS appeared to be equal to that for muscimol, with no dependence on the <strong>gamma 2</strong> virion levels.
+WARS1	addiction	dependence	8388991	In all preparations, the dissociation constants for flunitrazepam, muscimol, and TBPS were fairly constant, and the maximal number of binding sites for TBPS appeared to be equal to that for muscimol, with no <b>dependence</b> on the <strong>gamma 2</strong> virion levels.
+WARS1	drug	opioid	2506600	Infusion of <strong>gamma 2</strong> MSH produce a conditioned taste aversion in <b>morphine</b> dependent rats.
+WARS1	addiction	aversion	2506600	Infusion of <strong>gamma 2</strong> MSH produce a conditioned taste <b>aversion</b> in morphine dependent rats.
+WARS1	drug	opioid	2506600	However, in rats made dependent by SC implantation of a <b>morphine</b> pellet 4 days earlier 15 micrograms <strong>gamma 2</strong> MSH/infusion produced a taste aversion that was comparable to that produced by infusion of a low dose of the competitive <b>opioid</b> receptor antagonist <b>naloxone</b> (0.32 micrograms).
+WARS1	addiction	aversion	2506600	However, in rats made dependent by SC implantation of a morphine pellet 4 days earlier 15 micrograms <strong>gamma 2</strong> MSH/infusion produced a taste <b>aversion</b> that was comparable to that produced by infusion of a low dose of the competitive opioid receptor antagonist naloxone (0.32 micrograms).
+WARS1	drug	opioid	2506600	The findings confirm with a conditioning procedure and with opiate dependent animals the <b>naloxone</b> like effects of <strong>gamma 2</strong> MSH.
+WARS1	addiction	addiction	2875491	Other pituitary hormones, like ACTH, <strong>gamma 2</strong> MSH and prolactin have also been implicated in brain reward and drug <b>addiction</b>.
+WARS1	addiction	reward	2875491	Other pituitary hormones, like ACTH, <strong>gamma 2</strong> MSH and prolactin have also been implicated in brain <b>reward</b> and drug addiction.
+WARS1	drug	opioid	6316060	Concerning the ACTH/MSH related peptides, a decreasing effect of <b>heroin</b> intake was found following treatment with (D Phe7) ACTH 4 10, with a high dose of the ACTH 4 9 analog Org 2766 and with <strong>gamma 2</strong> MSH, while ACTH 1 24, ACTH 4 10 and a low dose of Org 2766 did not significantly influence self injecting behavior.
+EGF	drug	opioid	32111605	In addition, repeated epidermal growth factor (<strong>EGF</strong>) administration rendered animals unresponsive to subsequent analgesic doses of <b>morphine</b>, a phenomenon we call 'pre tolerance'.
+EGF	drug	opioid	32111605	In addition, repeated <strong>epidermal growth factor</strong> (<strong>EGF</strong>) administration rendered animals unresponsive to subsequent analgesic doses of <b>morphine</b>, a phenomenon we call 'pre tolerance'.
+EGF	drug	opioid	32111605	Rather, it reversed insensitivity to <b>morphine</b> analgesia ('pre tolerance') caused by the release of <strong>EGF</strong> by injured nerves.
+EGF	drug	opioid	32111605	Chronic <strong>EGF</strong> or PDGF administration induces mechanical sensitization, a prominent component of neuropathic pain, and renders animals 'pre tolerant' to subsequent analgesic doses of <b>morphine</b>.
+EGF	addiction	sensitization	32111605	Chronic <strong>EGF</strong> or PDGF administration induces mechanical <b>sensitization</b>, a prominent component of neuropathic pain, and renders animals 'pre tolerant' to subsequent analgesic doses of morphine.
+EGF	drug	alcohol	31747882	Recombinant human milk fat globule <strong>EGF</strong> factor VIII (rhMFG E8) as a therapy for sepsis after acute exposure to <b>alcohol</b>.
+EGF	drug	alcohol	31747882	<b>Alcohol</b> and sepsis inhibit the expression of milk fat globule <strong>epidermal growth factor</strong> factor VIII (MFG E8), a glycoprotein essential for optimal efferocytosis, resulting in the release of proinflammatory molecules and increased sepsis severity.
+EGF	drug	alcohol	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and <strong>epidermal growth factor</strong> receptor (EGFR)) modulate <b>alcohol</b> drinking and other behaviors related to <b>alcohol</b> addiction.
+EGF	addiction	addiction	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), RET proto oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and <strong>epidermal growth factor</strong> receptor (EGFR)) modulate alcohol drinking and other behaviors related to alcohol <b>addiction</b>.
+EGF	drug	nicotine	30598264	We demonstrated the correlation between <b>nicotine</b> and <strong>epidermal growth factor</strong> receptor (EGFR) signaling.
+EGF	drug	nicotine	30598264	Overall, our study suggests that <b>nicotine</b> promotes cell growth and migration through epidermal growth factor (<strong>EGF</strong>) signaling and plays an important role in oral cancer progression.
+EGF	drug	nicotine	30598264	Overall, our study suggests that <b>nicotine</b> promotes cell growth and migration through <strong>epidermal growth factor</strong> (<strong>EGF</strong>) signaling and plays an important role in oral cancer progression.
+EGF	addiction	addiction	30449623	Cetuximab, an <strong>epidermal growth factor</strong> receptor inhibitor, has been proposed for treatment de <b>escalation</b> in this setting to reduce the toxicity of standard cisplatin treatment, but no randomised evidence exists for the efficacy of this strategy.
+EGF	addiction	aversion	30038519	No significant difference was found between <b>CTA</b> expression and <strong>epidermal growth factor</strong> receptor mutant status.
+EGF	drug	nicotine	29570930	Cigarette <b>smoking</b> is one of the leading risks for lung cancer and is associated with the insensitivity of non small cell lung cancer (NSCLC) to <strong>epidermal growth factor</strong> receptor (EGFR) tyrosine kinase inhibitors (TKIs).
+EGF	drug	nicotine	29471517	The gender, tumour differentiation, <strong>epidermal growth factor</strong> receptor mutation, <b>smoking</b> habits, lymphovascular space invasion, tumour size, maximum standard uptake value and carcinoembryonic antigen levels were significantly different in the 2 groups.
+EGF	drug	nicotine	28974261	Why are mutation rates in <strong>epidermal growth factor</strong> receptor (EGFR) and erb b2 receptor tyrosine kinase 2 (ERBB2) higher in lung cancer from never <b>smokers</b> than that from <b>smokers</b>?
+EGF	drug	nicotine	27843633	<b>Smoking</b> habits, histological subtype, and <strong>epidermal growth factor</strong> receptor mutation status were not associated with PD L1 expression score.
+EGF	drug	amphetamine	26322025	Similarly, compared to only infected mice, <strong>epidermal growth factor</strong> receptor (EGFR) in <b>METH</b> exposed LCMV infected mice were up regulated.
+EGF	drug	alcohol	24710718	We hypothesized that Cav 1 could attenuate <b>ethanol</b> mediated nitrosative stress and liver damage through regulating <strong>epidermal growth factor</strong> receptor/signal transducer and activator of transcription 3/inducible nitric oxide synthase (EGFR/STAT3/iNOS) signaling cascades.
+EGF	drug	nicotine	23999525	NRG3 is a neural enriched member of the <strong>epidermal growth factor</strong> family, and a specific ligand for the receptor tyrosine kinase ErbB4, which is also upregulated following <b>nicotine</b> treatment and WD.
+EGF	drug	nicotine	22085699	In this study, we demonstrated a novel signaling mechanism by which <b>nicotine</b> exposure activated Src to sensitize <strong>epidermal growth factor</strong> receptor (EGFR) mediated pathways for breast cancer cell growth promotion.
+EGF	addiction	dependence	21673064	FGFR and <strong>epidermal growth factor</strong> receptor (EGFR) <b>dependence</b> was defined by sensitivity to multiple inhibitors selective for FGFRs or EGFR.
+EGF	drug	alcohol	21223309	Validation of specific genes by Sequenom analysis demonstrated that <b>alcohol</b> exposure prevented methylation of specific genes associated with neural development [cut like 2 (cutl2), insulin like growth factor 1 (Igf1), <strong>epidermal growth factor</strong> containing fibulin like extracellular matrix protein 1 (Efemp1), and SRY box containing gene 7 (Sox 7)]; eye development, lens intrinsic membrane protein 2 (Lim 2); the epigenetic mark Smarca2 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2); and developmental disorder [DiGeorge syndrome critical region gene 2 (Dgcr2)].
+EGF	drug	nicotine	21178720	The nine selected studies covered a broad range of topics including possible hormonal role in the development of lung adenocarcinoma, lung cancer in never <b>smokers</b>, stereotactic radiotherapy for early stage lung cancer, prognostic role of pleural lavage cytology, neoadjuvant chemotherapy for operable lung cancer, maintenance erlotinib, use of erlotinib after gefitinib, comparison of the two <strong>epidermal growth factor</strong> receptor tyrosine kinase inhibitors, and risk of central nervous system relapse in patients treated with <strong>epidermal growth factor</strong> receptor tyrosine kinase inhibitors.
+EGF	addiction	relapse	21178720	The nine selected studies covered a broad range of topics including possible hormonal role in the development of lung adenocarcinoma, lung cancer in never smokers, stereotactic radiotherapy for early stage lung cancer, prognostic role of pleural lavage cytology, neoadjuvant chemotherapy for operable lung cancer, maintenance erlotinib, use of erlotinib after gefitinib, comparison of the two <strong>epidermal growth factor</strong> receptor tyrosine kinase inhibitors, and risk of central nervous system <b>relapse</b> in patients treated with <strong>epidermal growth factor</strong> receptor tyrosine kinase inhibitors.
+EGF	drug	alcohol	20586751	Milk fat globule <strong>EGF</strong> factor 8 attenuates sepsis induced apoptosis and organ injury in <b>alcohol</b> intoxicated rats.
+EGF	drug	alcohol	20332099	Assessment of possible replication in 847 cases of European descent from a large independent sample, the Collaborative Study of the Genetics of <b>Alcoholism</b>, yielded replication for DKK2 but not <strong>EGF</strong>.
+EGF	drug	nicotine	20731908	For previously treated recurrent non small cell lung cancer, many studies have proven that inhibitors of the tyrosine kinase of <strong>epidermal growth factor</strong> receptor (EGFR TKI),such as gefitinib and erlotinib can increase survival, especially in non <b>smoker</b> adenocarcinoma.
+EGF	drug	nicotine	18262213	Recurrent exposure to <b>nicotine</b> differentiates human bronchial epithelial cells via <strong>epidermal growth factor</strong> receptor activation.
+EGF	drug	nicotine	18262213	We also demonstrate that <b>nicotine</b> treatment induced NF kB translocation to the nucleus, phosphorylation of the epidermal growth factor receptor (EGFR), and accumulation of heparin binding <strong>EGF</strong> in the extracellular medium.
+EGF	drug	nicotine	18262213	We also demonstrate that <b>nicotine</b> treatment induced NF kB translocation to the nucleus, phosphorylation of the <strong>epidermal growth factor</strong> receptor (EGFR), and accumulation of heparin binding <strong>EGF</strong> in the extracellular medium.
+EGF	drug	nicotine	17315157	The <b>tobacco</b> carcinogen <b>nicotine</b> derived nitrosamine 4 (N methyl N nitrosamino) 1 (3 pyridyl) 1 butanone (NNK) stimulates the proliferation of human PAC cells and small airway epithelial cells through beta 1 adrenorecptor mediated transactivation of the <strong>epidermal growth factor</strong> receptor (EGFR).
+EGF	drug	nicotine	16503085	<strong>Epidermal growth factor</strong> receptor (EGFR) gene mutations are frequently detected in lung cancer, especially in adenocarcinoma, in females, and non <b>smoking</b> patients.
+EGF	drug	amphetamine	15542770	Conditioned place preference and locomotor sensitization after repeated administration of cocaine or <b>methamphetamine</b> in rats treated with <strong>epidermal growth factor</strong> during the neonatal period.
+EGF	drug	cocaine	15542770	Conditioned place preference and locomotor sensitization after repeated administration of <b>cocaine</b> or methamphetamine in rats treated with <strong>epidermal growth factor</strong> during the neonatal period.
+EGF	addiction	sensitization	15542770	Conditioned place preference and locomotor <b>sensitization</b> after repeated administration of cocaine or methamphetamine in rats treated with <strong>epidermal growth factor</strong> during the neonatal period.
+EGF	drug	amphetamine	15542770	At the adult stage, <strong>EGF</strong> treated rats were challenged with cocaine (15 mg/kg) or <b>methamphetamine</b> (1 mg/kg), and conditioned place preference and locomotor activity were examined.
+EGF	drug	cocaine	15542770	At the adult stage, <strong>EGF</strong> treated rats were challenged with <b>cocaine</b> (15 mg/kg) or methamphetamine (1 mg/kg), and conditioned place preference and locomotor activity were examined.
+EGF	drug	amphetamine	15542770	The rats that received <strong>EGF</strong> during the neonatal period had significantly higher conditioned place preference for where cocaine or <b>methamphetamine</b> was administered than controls.
+EGF	drug	cocaine	15542770	The rats that received <strong>EGF</strong> during the neonatal period had significantly higher conditioned place preference for where <b>cocaine</b> or methamphetamine was administered than controls.
+EGF	drug	amphetamine	15542770	The neonatal <strong>EGF</strong> treatment enhanced behavioral response to <b>methamphetamine</b> and behavioral sensitization to cocaine at the adult stage.
+EGF	drug	cocaine	15542770	The neonatal <strong>EGF</strong> treatment enhanced behavioral response to methamphetamine and behavioral sensitization to <b>cocaine</b> at the adult stage.
+EGF	addiction	sensitization	15542770	The neonatal <strong>EGF</strong> treatment enhanced behavioral response to methamphetamine and behavioral <b>sensitization</b> to cocaine at the adult stage.
+EGF	drug	cocaine	15542770	Drug naive controls gradually increased locomotor responses to <b>cocaine</b> during their daily injections, whereas <strong>EGF</strong> treated rats exhibited a larger increase in <b>cocaine</b> responses.
+EGF	addiction	addiction	15542770	Our findings indicate a potential link between <strong>EGF</strong> receptor activation and drug <b>addiction</b>.
+EGF	drug	alcohol	12068256	<strong>Epidermal growth factor</strong> protects the liver against <b>alcohol</b> induced injury and sensitization to bacterial lipopolysaccharide.
+EGF	addiction	sensitization	12068256	<strong>Epidermal growth factor</strong> protects the liver against alcohol induced injury and <b>sensitization</b> to bacterial lipopolysaccharide.
+EGF	drug	alcohol	12068256	This study investigated (1) the hepatic protective effect of an anti inflammatory cytokine, epidermal growth factor (<strong>EGF</strong>), against deleterious effects of <b>alcohol</b> and sensitization to bacterial lipopolysaccharide (LPS), and (2) the possible mechanisms that underlie such protection.
+EGF	addiction	sensitization	12068256	This study investigated (1) the hepatic protective effect of an anti inflammatory cytokine, epidermal growth factor (<strong>EGF</strong>), against deleterious effects of alcohol and <b>sensitization</b> to bacterial lipopolysaccharide (LPS), and (2) the possible mechanisms that underlie such protection.
+EGF	drug	alcohol	12068256	This study investigated (1) the hepatic protective effect of an anti inflammatory cytokine, <strong>epidermal growth factor</strong> (<strong>EGF</strong>), against deleterious effects of <b>alcohol</b> and sensitization to bacterial lipopolysaccharide (LPS), and (2) the possible mechanisms that underlie such protection.
+EGF	addiction	sensitization	12068256	This study investigated (1) the hepatic protective effect of an anti inflammatory cytokine, <strong>epidermal growth factor</strong> (<strong>EGF</strong>), against deleterious effects of alcohol and <b>sensitization</b> to bacterial lipopolysaccharide (LPS), and (2) the possible mechanisms that underlie such protection.
+EGF	drug	alcohol	12068256	<strong>EGF</strong> protects the liver against both <b>alcohol</b> induced liver damage and liver sensitization to bacterial LPS through down regulation of apoptosis.
+EGF	addiction	sensitization	12068256	<strong>EGF</strong> protects the liver against both alcohol induced liver damage and liver <b>sensitization</b> to bacterial LPS through down regulation of apoptosis.
+EGF	drug	opioid	11602657	These data suggest that a TK, but most likely not an Src/<strong>EGF</strong> receptor TK, is important in cardioprotection via <b>opioid</b> receptor stimulation and that the pathway for TK activation is downstream from or parallel to PKC activation in the in situ rat heart since genistein could not affect PKC translocation of selective isoforms induced by TAN 67 and assessed by immunohistochemistry.
+EGF	drug	nicotine	11195134	The general detrimental effects of cigarette <b>smoking</b> in the gastric mucosa include reduction of circulating <strong>epidermal growth factor</strong>, increase in tissue free radical production and the presence of free radicals in smoke, together with reduction of mucosal constitutive nitric oxide synthase activity.
+EGF	drug	nicotine	10471051	No significantly elevated or decreased serum values for p53 protein, <strong>EGF</strong> R, or anti p53 antibodies as a function of histological tumour type, age, or degree and type of exposure (asbestos, <b>smoking</b>, ionizing radiation) could be found.
+EGF	drug	opioid	9729296	Opposing actions of the <strong>EGF</strong> family and <b>opioids</b>: heparin binding epidermal growth factor (HB <strong>EGF</strong>) protects mouse cerebellar neuroblasts against the antiproliferative effect of <b>morphine</b>.
+EGF	drug	opioid	9729296	Opposing actions of the <strong>EGF</strong> family and <b>opioids</b>: heparin binding <strong>epidermal growth factor</strong> (HB <strong>EGF</strong>) protects mouse cerebellar neuroblasts against the antiproliferative effect of <b>morphine</b>.
+EGF	drug	opioid	9729296	We examined whether, heparin binding epidermal growth factor like growth factor (HB <strong>EGF</strong>), a recently described member of the epidermal growth factor (<strong>EGF</strong>) family, might compete with an inhibitory <b>opioid</b> signal.
+EGF	drug	opioid	9729296	We examined whether, heparin binding <strong>epidermal growth factor</strong> like growth factor (HB <strong>EGF</strong>), a recently described member of the <strong>epidermal growth factor</strong> (<strong>EGF</strong>) family, might compete with an inhibitory <b>opioid</b> signal.
+EGF	drug	opioid	9729296	The results confirmed our ongoing studies that <b>morphine</b> inhibited neuroblast proliferation, while HB <strong>EGF</strong> enhanced cell replication.
+EGF	drug	opioid	9729296	HB <strong>EGF</strong> not only counteracted the antiproliferative <b>morphine</b> signal, but invariably enhanced DNA synthesis irrespective of <b>morphine</b> treatment.
+EGF	drug	opioid	9729296	Our findings suggest that regional and temporal differences in the availability of endogenous HB <strong>EGF</strong> may serve to limit the response of EGL neuroblasts to <b>opioids</b>, and HB <strong>EGF</strong> may be neuroprotective in opiate drug abuse.
+EGF	drug	opioid	9729296	If similar responses occur in vivo, then the <strong>EGF</strong> family and the <b>opioid</b> system may represent distinct and contrasting components of an extracellular signaling system serving to coordinate EGL neurogenesis.
+EGF	addiction	withdrawal	21556542	Serum deprivation and direct steroid <b>withdrawal</b> during the culture triggered cell death by apoptosis, an event which could be overcome by <strong>EGF</strong> stimulation, particularly for the well differentiated PNT2 cells.
+EGF	drug	nicotine	8322024	An analysis of <b>nicotine</b>, acid secretion, gastrin, catecholamines, <strong>epidermal growth factor</strong>, prostaglandin E2, and bile acids.
+EGF	drug	nicotine	8322024	<strong>Epidermal growth factor</strong> concentrations were decreased in gastric juice after MSF during non <b>smoking</b> (p = 0.01) but not during <b>smoking</b>.
+EGF	drug	alcohol	2677050	Arrest of <strong>epidermal growth factor</strong> dependent growth in fetal hepatocytes after <b>ethanol</b> exposure.
+EGF	drug	alcohol	2677050	Exposure of the fetal rat hepatocyte to <b>ethanol</b> in vitro blocks epidermal growth factor (<strong>EGF</strong>) dependent cell replication.
+EGF	drug	alcohol	2677050	Exposure of the fetal rat hepatocyte to <b>ethanol</b> in vitro blocks <strong>epidermal growth factor</strong> (<strong>EGF</strong>) dependent cell replication.
+EGF	drug	alcohol	2677050	To define possible mechanisms for this growth arrest, we determined the effects of <b>ethanol</b> on <strong>EGF</strong> binding and <strong>EGF</strong> receptor (<strong>EGF</strong> R) levels.
+EGF	drug	alcohol	2677050	During a 24 h exposure to <b>ethanol</b> (1.7 mg/ml, 31 mM), cell replication was completely blocked while <strong>EGF</strong> binding per cell doubled.
+EGF	drug	alcohol	2677050	Significantly increased <strong>EGF</strong> binding was seen after 6 h of <b>ethanol</b> exposure, and both growth arrest and enhanced <strong>EGF</strong> binding were reversed within 12 h of <b>ethanol</b> withdrawal.
+EGF	addiction	withdrawal	2677050	Significantly increased <strong>EGF</strong> binding was seen after 6 h of ethanol exposure, and both growth arrest and enhanced <strong>EGF</strong> binding were reversed within 12 h of ethanol <b>withdrawal</b>.
+EGF	drug	alcohol	2677050	Total RNA, beta actin mRNA, and <strong>EGF</strong> R mRNA were increased 50 70% in <b>ethanol</b> exposed cells.
+EGF	drug	alcohol	2677050	However, direct measurements of <strong>EGF</strong> R synthesis rates by [35S]methionine incorporation revealed no differences between control and <b>ethanol</b> exposed cells.
+EGF	drug	alcohol	2677050	Internalization of <strong>EGF</strong> R was significantly altered by <b>ethanol</b> exposure.
+EGF	drug	alcohol	2677050	A 2 h incubation resulted in the internalization of 57% of the ligand in control cells, while only 31% of bound <strong>EGF</strong> was internalized in the <b>ethanol</b> exposed cells.
+EGF	drug	alcohol	3557310	Fetal liver cells were grown in custom Williams' E medium (without L arginine and with L ornithine) and exposed to <strong>epidermal growth factor</strong> (0, 1, 2 or 5 ng per ml) and <b>ethanol</b> (1.7 +/  0.1 or 3.9 +/  0.2 mg per ml).
+CHRNB4	drug	nicotine	32184221	Human genome wide association studies have linked polymorphisms in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, coding for the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, to <b>nicotine</b> addiction.
+CHRNB4	addiction	addiction	32184221	Human genome wide association studies have linked polymorphisms in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, coding for the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, to nicotine <b>addiction</b>.
+CHRNB4	drug	nicotine	32184221	These data indicate that β4 is a critical modulator of reward related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster and <b>nicotine</b> addiction.
+CHRNB4	addiction	addiction	32184221	These data indicate that β4 is a critical modulator of reward related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster and nicotine <b>addiction</b>.
+CHRNB4	addiction	reward	32184221	These data indicate that β4 is a critical modulator of <b>reward</b> related behaviors.SIGNIFICANCE STATEMENT Human genetic studies have provided strong evidence for a relationship between variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster and nicotine addiction.
+CHRNB4	drug	nicotine	30453884	These results indicate rs4887074 is associated with <strong>CHRNB4</strong> expression, and along with two regulatory variants of CHRNA3 and CHRNA5, modulates the effect of rs16969968 on <b>nicotine</b> dependence risk.
+CHRNB4	addiction	dependence	30453884	These results indicate rs4887074 is associated with <strong>CHRNB4</strong> expression, and along with two regulatory variants of CHRNA3 and CHRNA5, modulates the effect of rs16969968 on nicotine <b>dependence</b> risk.
+CHRNB4	drug	nicotine	29993116	Polymorphisms in CHRNA3, CHRNA5, and <strong>CHRNB4</strong> receptors play a critical role in <b>nicotine</b> dependence, lung cancer (LC) risk, and chronic obstructive pulmonary disease (COPD).
+CHRNB4	addiction	dependence	29993116	Polymorphisms in CHRNA3, CHRNA5, and <strong>CHRNB4</strong> receptors play a critical role in nicotine <b>dependence</b>, lung cancer (LC) risk, and chronic obstructive pulmonary disease (COPD).
+CHRNB4	drug	nicotine	29758381	However, our results confirmed the role of the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster of nicotinic acetylcholine receptor subunit genes in <b>tobacco</b> use.
+CHRNB4	drug	nicotine	29666375	Association and cis mQTL analysis of variants in CHRNA3 A5, CHRNA7, CHRNB2, and <strong>CHRNB4</strong> in relation to <b>nicotine</b> dependence in a Chinese Han population.
+CHRNB4	addiction	dependence	29666375	Association and cis mQTL analysis of variants in CHRNA3 A5, CHRNA7, CHRNB2, and <strong>CHRNB4</strong> in relation to nicotine <b>dependence</b> in a Chinese Han population.
+CHRNB4	drug	nicotine	29666375	Our results indicated that the SNPs rs1948 and rs7178270 in <strong>CHRNB4</strong> and rs3743075 in CHRNA3 were significantly associated with the Fagerström Test for <b>Nicotine</b> Dependence (FTND) score (p = 6.6 × 10 5; p = 2.0 × 10 4, and p = 7.0 × 10 4, respectively).
+CHRNB4	addiction	dependence	29666375	Our results indicated that the SNPs rs1948 and rs7178270 in <strong>CHRNB4</strong> and rs3743075 in CHRNA3 were significantly associated with the Fagerström Test for Nicotine <b>Dependence</b> (FTND) score (p = 6.6 × 10 5; p = 2.0 × 10 4, and p = 7.0 × 10 4, respectively).
+CHRNB4	drug	nicotine	28972577	In this largest ever GWAS meta analysis for <b>nicotine</b> dependence and the largest ever cross ancestry GWAS meta analysis for any <b>smoking</b> phenotype, we reconfirmed the well known CHRNA5 CHRNA3 <strong>CHRNB4</strong> genes and further yielded a novel association in the DNA methyltransferase gene DNMT3B.
+CHRNB4	addiction	dependence	28972577	In this largest ever GWAS meta analysis for nicotine <b>dependence</b> and the largest ever cross ancestry GWAS meta analysis for any smoking phenotype, we reconfirmed the well known CHRNA5 CHRNA3 <strong>CHRNB4</strong> genes and further yielded a novel association in the DNA methyltransferase gene DNMT3B.
+CHRNB4	drug	nicotine	28900078	The relationship of HTR4 (rs3995090), HTR2A (rs6313), GRIK5 (rs8099939), GRIN2B (rs2268132), and <strong>CHRNB4</strong> (rs1948) gene polymorphisms and COPD, as well as the contribution of these polymorphisms to the variations in quantitative characteristics that describe respiratory function, <b>smoking</b> behavior, and <b>nicotine</b> dependence was assessed in an ethnically homogeneous Tatar population.
+CHRNB4	addiction	dependence	28900078	The relationship of HTR4 (rs3995090), HTR2A (rs6313), GRIK5 (rs8099939), GRIN2B (rs2268132), and <strong>CHRNB4</strong> (rs1948) gene polymorphisms and COPD, as well as the contribution of these polymorphisms to the variations in quantitative characteristics that describe respiratory function, smoking behavior, and nicotine <b>dependence</b> was assessed in an ethnically homogeneous Tatar population.
+CHRNB4	addiction	dependence	28368157	Suggestive associations were consistent with previous findings from studies of substance use and <b>dependence</b>, including variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster with cigarettes smoked per day.
+CHRNB4	drug	nicotine	27871728	Genome wide association studies (GWASs) have identified associations between the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster and <b>smoking</b> heaviness and <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	27871728	Genome wide association studies (GWASs) have identified associations between the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster and smoking heaviness and nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	27871728	GWASs of <b>smoking</b> related health outcomes have also identified this signal in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster.
+CHRNB4	drug	nicotine	27302872	Polymorphisms in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster (Chr15q25) have been robustly associated with <b>nicotine</b> dependence, including genome wide studies, as well as with cognitive and neuropsychological measures.
+CHRNB4	addiction	dependence	27302872	Polymorphisms in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster (Chr15q25) have been robustly associated with nicotine <b>dependence</b>, including genome wide studies, as well as with cognitive and neuropsychological measures.
+CHRNB4	drug	nicotine	27302872	Here, we evaluated the effect of polymorphisms in CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster and their interaction with <b>tobacco</b> <b>smoking</b> status on cognition in patients with Attention Deficit/Hyperactivity Disorder (ADHD).
+CHRNB4	drug	nicotine	26997181	The associations between CHRNA5 CHRNA3 <strong>CHRNB4</strong> variants and cigarettes per day (CPD), the Fagerström Test for <b>Nicotine</b> Dependence (FTND), and craving were analyzed in data from 662 lifetime <b>smokers</b> from an Israeli adult Jewish household sample.
+CHRNB4	addiction	dependence	26997181	The associations between CHRNA5 CHRNA3 <strong>CHRNB4</strong> variants and cigarettes per day (CPD), the Fagerström Test for Nicotine <b>Dependence</b> (FTND), and craving were analyzed in data from 662 lifetime smokers from an Israeli adult Jewish household sample.
+CHRNB4	addiction	relapse	26997181	The associations between CHRNA5 CHRNA3 <strong>CHRNB4</strong> variants and cigarettes per day (CPD), the Fagerström Test for Nicotine Dependence (FTND), and <b>craving</b> were analyzed in data from 662 lifetime smokers from an Israeli adult Jewish household sample.
+CHRNB4	drug	nicotine	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 addiction genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to <b>smoking</b> behavior and <b>nicotine</b> metabolism: CHRNA5 CHRNA3 <strong>CHRNB4</strong> and CYP2A6 CYP2B6.
+CHRNB4	addiction	addiction	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 <b>addiction</b> genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to smoking behavior and nicotine metabolism: CHRNA5 CHRNA3 <strong>CHRNB4</strong> and CYP2A6 CYP2B6.
+CHRNB4	drug	nicotine	26220977	Of the eight cis meQTL SNPs, only the intronic <strong>CHRNB4</strong> SNP rs11636753 was associated with CHRNA5 methylation independently of the known SNP effects in prefrontal cortex, and it was the most significantly associated SNP with <b>nicotine</b> dependence across five independent cohorts (total N = 7858 European ancestry and 3238 AA participants): P = 6.7 × 10( 4), odds ratio (OR) [95% confidence interval (CI)] = 1.11 (1.05 1.18).
+CHRNB4	addiction	dependence	26220977	Of the eight cis meQTL SNPs, only the intronic <strong>CHRNB4</strong> SNP rs11636753 was associated with CHRNA5 methylation independently of the known SNP effects in prefrontal cortex, and it was the most significantly associated SNP with nicotine <b>dependence</b> across five independent cohorts (total N = 7858 European ancestry and 3238 AA participants): P = 6.7 × 10( 4), odds ratio (OR) [95% confidence interval (CI)] = 1.11 (1.05 1.18).
+CHRNB4	drug	nicotine	25958762	This approach allowed the identification of the first susceptibility gene in addiction (<b>tobacco</b>), with genes CHRNA5, CHRNA3 and <strong>CHRNB4</strong> encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for <b>tobacco</b> dependence.
+CHRNB4	addiction	addiction	25958762	This approach allowed the identification of the first susceptibility gene in <b>addiction</b> (tobacco), with genes CHRNA5, CHRNA3 and <strong>CHRNB4</strong> encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for tobacco dependence.
+CHRNB4	addiction	dependence	25958762	This approach allowed the identification of the first susceptibility gene in addiction (tobacco), with genes CHRNA5, CHRNA3 and <strong>CHRNB4</strong> encoding the α5, α3 and b4 subunits involved in the formation of nicotinic receptors, explaining 14% of the attributable risk for tobacco <b>dependence</b>.
+CHRNB4	drug	nicotine	25948103	Genome wide association studies have implicated the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster in risk for heavy <b>smoking</b> and several <b>smoking</b> related disorders.
+CHRNB4	drug	nicotine	25948103	These findings support differential aversive response to <b>nicotine</b> as one likely mechanism for the association of CHRNA5 CHRNA3 <strong>CHRNB4</strong> with heavy <b>smoking</b>.
+CHRNB4	addiction	aversion	25948103	These findings support differential <b>aversive</b> response to nicotine as one likely mechanism for the association of CHRNA5 CHRNA3 <strong>CHRNB4</strong> with heavy smoking.
+CHRNB4	drug	nicotine	25632390	In this study we tested the association of <b>smoking</b> initiation, age at onset of daily <b>smoking</b>, and heaviness of <b>smoking</b> with five single nucleotide polymorphisms (SNPs) within the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster.
+CHRNB4	drug	nicotine	25632390	This study provides strong evidence for the role of the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster in heaviness of <b>nicotine</b> addiction.
+CHRNB4	addiction	addiction	25632390	This study provides strong evidence for the role of the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster in heaviness of nicotine <b>addiction</b>.
+CHRNB4	drug	alcohol	25603899	SNPs in the <b>alcohol</b> metabolizing genes, in the cholinergic gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong>, and in the DRD2 and ANNK1 genes, are, to date, the most replicated and significant gene variants associated with <b>alcohol</b>  and nicotine related phenotypes.
+CHRNB4	drug	nicotine	25603899	SNPs in the alcohol metabolizing genes, in the cholinergic gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong>, and in the DRD2 and ANNK1 genes, are, to date, the most replicated and significant gene variants associated with alcohol  and <b>nicotine</b> related phenotypes.
+CHRNB4	addiction	relapse	25572450	The <strong>CHRNB4</strong> promoter SNP rs3813567 was associated with both point prevalence abstinence and post quit <b>craving</b>.
+CHRNB4	drug	nicotine	25555482	No GWS associations were observed at the chromosome 15 nicotinic receptor gene cluster (CHRNA5 CHRNA3 <strong>CHRNB4</strong>) previously associated with <b>nicotine</b> dependence and <b>smoking</b> quantity traits.
+CHRNB4	addiction	dependence	25555482	No GWS associations were observed at the chromosome 15 nicotinic receptor gene cluster (CHRNA5 CHRNA3 <strong>CHRNB4</strong>) previously associated with nicotine <b>dependence</b> and smoking quantity traits.
+CHRNB4	drug	nicotine	25214750	Genomics and personalized medicine: CHRNA5 CHRNA3 <strong>CHRNB4</strong> and <b>smoking</b> cessation treatment.
+CHRNB4	drug	nicotine	25214750	We review the significance of variants in the nicotinic receptor gene cluster (CHRNA5 CHRNA3 <strong>CHRNB4</strong>) in the prediction of <b>smoking</b> quantity, <b>smoking</b> cessation, and response to cessation medication in multiple studies of <b>smoking</b> cessation.
+CHRNB4	drug	nicotine	25214750	The genetic variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> region that predict <b>nicotine</b> dependence also predict a later age of <b>smoking</b> cessation in a community based sample.
+CHRNB4	addiction	dependence	25214750	The genetic variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> region that predict nicotine <b>dependence</b> also predict a later age of smoking cessation in a community based sample.
+CHRNB4	drug	nicotine	25072098	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> locus is associated with self reported <b>smoking</b> behavior and also harbors the strongest genetic associations with chronic obstructive pulmonary disease (COPD) and lung cancer.
+CHRNB4	drug	nicotine	25072098	Because the associations with lung disease remain after adjustment for self reported <b>smoking</b> behaviors, it has been asserted that CHRNA5 CHRNA3 <strong>CHRNB4</strong> variants increase COPD and lung cancer susceptibility independently of their effects on <b>smoking</b>.
+CHRNB4	drug	nicotine	25072098	Variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> locus, including rs16969968, a nonsynonymous variant in CHRNA5, are genomewide association study significantly associated with CO (β = 2.66; 95% confidence interval [CI], 1.74 3.58; P = 1.65 × 10( 8)), and this association remains strong after adjusting for <b>smoking</b> behavior (β = 2.18; 95% CI, 1.32 3.04; P = 7.47 × 10( 7)).
+CHRNB4	drug	nicotine	24804708	Functional characterization improves associations between rare non synonymous variants in <strong>CHRNB4</strong> and <b>smoking</b> behavior.
+CHRNB4	drug	nicotine	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, <strong>CHRNB4</strong>, CHRNA6 and CHRNB3 genes and found that rare missense variants at conserved residues in <strong>CHRNB4</strong> are associated with reduced risk of <b>nicotine</b> dependence among African Americans.
+CHRNB4	addiction	dependence	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, <strong>CHRNB4</strong>, CHRNA6 and CHRNB3 genes and found that rare missense variants at conserved residues in <strong>CHRNB4</strong> are associated with reduced risk of nicotine <b>dependence</b> among African Americans.
+CHRNB4	drug	nicotine	24478678	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, encoding the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, has been linked to <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	24478678	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, encoding the α5, α3, and β4 nicotinic acetylcholine receptor (nAChR) subunits, has been linked to nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	24478678	Given that β4 is rate limiting for receptor activity and that single nucleotide polymorphisms (SNPs) in <strong>CHRNB4</strong> have been linked to altered risk of <b>nicotine</b> dependence in humans, we were interested in determining the contribution of allelic variants of β4 to <b>nicotine</b> receptor activity in the MHb.
+CHRNB4	addiction	dependence	24478678	Given that β4 is rate limiting for receptor activity and that single nucleotide polymorphisms (SNPs) in <strong>CHRNB4</strong> have been linked to altered risk of nicotine <b>dependence</b> in humans, we were interested in determining the contribution of allelic variants of β4 to nicotine receptor activity in the MHb.
+CHRNB4	drug	nicotine	24478678	Mice injected with the β4 containing virus showed pronounced aversion to <b>nicotine</b> as previously observed in transgenic Tabac mice overexpressing <strong>Chrnb4</strong> at endogenous sites including the MHb.
+CHRNB4	addiction	aversion	24478678	Mice injected with the β4 containing virus showed pronounced <b>aversion</b> to nicotine as previously observed in transgenic Tabac mice overexpressing <strong>Chrnb4</strong> at endogenous sites including the MHb.
+CHRNB4	drug	nicotine	24478678	Altogether, these data confirm the critical role of habenular β4 in <b>nicotine</b> consumption, and identify specific SNPs in <strong>CHRNB4</strong> that modify <b>nicotine</b> elicited currents and alter <b>nicotine</b> consumption in mice.
+CHRNB4	drug	nicotine	24186853	Distinct loci in the CHRNA5/CHRNA3/<strong>CHRNB4</strong> gene cluster are associated with onset of regular <b>smoking</b>.
+CHRNB4	drug	nicotine	24186853	Neuronal nicotinic acetylcholine receptor (nAChR) genes (CHRNA5/CHRNA3/<strong>CHRNB4</strong>) have been reproducibly associated with <b>nicotine</b> dependence, <b>smoking</b> behaviors, and lung cancer risk.
+CHRNB4	addiction	dependence	24186853	Neuronal nicotinic acetylcholine receptor (nAChR) genes (CHRNA5/CHRNA3/<strong>CHRNB4</strong>) have been reproducibly associated with nicotine <b>dependence</b>, smoking behaviors, and lung cancer risk.
+CHRNB4	drug	nicotine	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster associated with heavy <b>smoking</b> and higher relapse risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster associated with heavy smoking and higher relapse risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of nicotine <b>dependence</b>.
+CHRNB4	addiction	relapse	24082085	The discovery of genetic variants in the cholinergic receptor nicotinic CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster associated with heavy smoking and higher <b>relapse</b> risk has led to the identification of the midbrain habenula interpeduncular axis as a critical relay circuit in the control of nicotine dependence.
+CHRNB4	drug	nicotine	24062692	Recently, variants in the nAChR genes CHRNA3, CHRNA5, and <strong>CHRNB4</strong> have been implicated in <b>nicotine</b> dependence and lung cancer susceptibility.
+CHRNB4	addiction	dependence	24062692	Recently, variants in the nAChR genes CHRNA3, CHRNA5, and <strong>CHRNB4</strong> have been implicated in nicotine <b>dependence</b> and lung cancer susceptibility.
+CHRNB4	drug	alcohol	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically <b>alcohol</b> and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, <strong>CHRNB4</strong>, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of <b>Alcoholism</b> (COGA).
+CHRNB4	drug	cocaine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically alcohol and <b>cocaine</b> dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, <strong>CHRNB4</strong>, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNB4	drug	nicotine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than <b>nicotine</b> dependence, specifically alcohol and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, <strong>CHRNB4</strong>, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNB4	addiction	dependence	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine <b>dependence</b>, specifically alcohol and cocaine <b>dependence</b>, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, <strong>CHRNB4</strong>, CHRNA6 and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNB4	drug	nicotine	24055497	Second, genetic variation that modifies noxious responses to <b>nicotine</b> and thereby influences vulnerability to <b>tobacco</b> dependence, in particular variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> nicotinic acetylcholine receptor (nAChR) subunit gene cluster, will be discussed.
+CHRNB4	addiction	dependence	24055497	Second, genetic variation that modifies noxious responses to nicotine and thereby influences vulnerability to tobacco <b>dependence</b>, in particular variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> nicotinic acetylcholine receptor (nAChR) subunit gene cluster, will be discussed.
+CHRNB4	drug	alcohol	23875064	Scrutiny of the CHRNA5 CHRNA3 <strong>CHRNB4</strong> smoking behavior locus reveals a novel association with <b>alcohol</b> use in a Finnish population based study.
+CHRNB4	drug	nicotine	23875064	Scrutiny of the CHRNA5 CHRNA3 <strong>CHRNB4</strong> <b>smoking</b> behavior locus reveals a novel association with alcohol use in a Finnish population based study.
+CHRNB4	drug	nicotine	23875064	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster on chromosome 15q25.1 encoding the cholinergic nicotinic receptor subunits is robustly associated with <b>smoking</b> behavior and <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	23875064	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster on chromosome 15q25.1 encoding the cholinergic nicotinic receptor subunits is robustly associated with smoking behavior and nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	23872218	Much work has been done to describe the rat <strong>Chrnb4</strong>/a3 intergenic region, but few studies have examined the human intergenic region effects on expression; therefore, these studies greatly aid human genetic research as it relates to observed <b>nicotine</b> phenotypes, lung cancer risk and potential underlying genetic mechanisms.
+CHRNB4	drug	alcohol	23691088	Specifically, rs1948, a single nucleotide polymorphism (SNP) located in the <strong>CHRNB4</strong> 3' untranslated region (UTR), has been associated to early age of initiation for both <b>alcohol</b> and tobacco use.
+CHRNB4	drug	nicotine	23691088	Specifically, rs1948, a single nucleotide polymorphism (SNP) located in the <strong>CHRNB4</strong> 3' untranslated region (UTR), has been associated to early age of initiation for both alcohol and <b>tobacco</b> use.
+CHRNB4	drug	nicotine	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non <b>smoking</b> adolescents, we aimed to elucidate the impact of genome wide significant <b>smoking</b> associated variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster on reward related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to addiction.
+CHRNB4	addiction	addiction	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non smoking adolescents, we aimed to elucidate the impact of genome wide significant smoking associated variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster on reward related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to <b>addiction</b>.
+CHRNB4	addiction	reward	23689675	Applying an imaging genetics approach in two cohorts (N=487; N=478) of healthy non smoking adolescents, we aimed to elucidate the impact of genome wide significant smoking associated variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster on <b>reward</b> related neural responses in central regions such as the striatum, orbitofrontal and anterior cingulate cortex (ACC), and personality traits related to addiction.
+CHRNB4	drug	nicotine	23458267	Recently, rare variants (MAF < 0.05) in <strong>CHRNB4</strong> have been reported to be associated with a decreased risk of developing <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	23458267	Recently, rare variants (MAF < 0.05) in <strong>CHRNB4</strong> have been reported to be associated with a decreased risk of developing nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	23143843	Indeed, genetic variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to <b>tobacco</b> dependence and <b>smoking</b> associated diseases including lung cancer.
+CHRNB4	addiction	dependence	23143843	Indeed, genetic variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, encoding the α5, α3, and β4 nAChR subunits, respectively, has been shown to increase vulnerability to tobacco <b>dependence</b> and smoking associated diseases including lung cancer.
+CHRNB4	drug	nicotine	23061658	Genome wide association (GWA) studies both in lung cancer and COPD highlighted the same variants (SNPs) on chromosome 15q25 marking the gene cluster CHRNA3 <strong>CHRNB4</strong> CHRNA5 for these <b>smoking</b> related diseases, showing a stimulating connection between this common genetic region and <b>smoking</b> behavior and <b>smoking</b> related illnesses.
+CHRNB4	drug	nicotine	23061658	Moreover variants on the gene cluster CHRNA3 <strong>CHRNB4</strong> CHRNA5 are associated with <b>nicotine</b> addiction antismoking therapy and antismoking therapy side effects.
+CHRNB4	addiction	addiction	23061658	Moreover variants on the gene cluster CHRNA3 <strong>CHRNB4</strong> CHRNA5 are associated with nicotine <b>addiction</b> antismoking therapy and antismoking therapy side effects.
+CHRNB4	drug	nicotine	23029550	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster on 15q25 has consistently been associated with <b>smoking</b> quantity, <b>nicotine</b> dependence and lung cancer.
+CHRNB4	addiction	dependence	23029550	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster on 15q25 has consistently been associated with smoking quantity, nicotine <b>dependence</b> and lung cancer.
+CHRNB4	drug	nicotine	22945651	Single nucleotide polymorphisms rs421629 on 5p15.33 and rs1948, rs660652, rs8040868 and rs2036527 on 15q25.1, previously identified as lung cancer risk or <b>nicotine</b> addiction modifiers, were associated with tumor DNA methylation levels in the promoters of TERT and <strong>CHRNB4</strong> (P<0.001), respectively, in two independent sample sets (n=82; n=150).
+CHRNB4	addiction	addiction	22945651	Single nucleotide polymorphisms rs421629 on 5p15.33 and rs1948, rs660652, rs8040868 and rs2036527 on 15q25.1, previously identified as lung cancer risk or nicotine <b>addiction</b> modifiers, were associated with tumor DNA methylation levels in the promoters of TERT and <strong>CHRNB4</strong> (P<0.001), respectively, in two independent sample sets (n=82; n=150).
+CHRNB4	drug	nicotine	22884254	Several genetic variants within the nicotinic cholinergic receptor gene cluster, CHRNA5 CHRNA3 <strong>CHRNB4</strong> have been reported to be associated with <b>nicotine</b> dependence (ND), and this association has been validated in multiple studies.
+CHRNB4	addiction	dependence	22884254	Several genetic variants within the nicotinic cholinergic receptor gene cluster, CHRNA5 CHRNA3 <strong>CHRNB4</strong> have been reported to be associated with nicotine <b>dependence</b> (ND), and this association has been validated in multiple studies.
+CHRNB4	drug	nicotine	22648373	Interplay of genetic risk factors (CHRNA5 CHRNA3 <strong>CHRNB4</strong>) and cessation treatments in <b>smoking</b> cessation success.
+CHRNB4	drug	nicotine	22648373	This study tested whether variants in the nicotinic receptor gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong> predict age at <b>smoking</b> cessation and relapse after an attempt to quit <b>smoking</b>.
+CHRNB4	addiction	relapse	22648373	This study tested whether variants in the nicotinic receptor gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong> predict age at smoking cessation and <b>relapse</b> after an attempt to quit smoking.
+CHRNB4	drug	nicotine	22648373	In a community based, crosssectional study (N=5,216) and a randomized comparative effectiveness <b>smoking</b> cessation trial (N=1,073), the authors used Cox proportional hazard models and logistic regression to model the relationships of <b>smoking</b> cessation (self reported quit age in the community study and point prevalence abstinence at the end of treatment in the clinical trial) to three common haplotypes in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> region defined by rs16969968 and rs680244.
+CHRNB4	drug	nicotine	22648373	The genetic variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> region that predict <b>nicotine</b> dependence also predicted a later age at <b>smoking</b> cessation in the community sample.
+CHRNB4	addiction	dependence	22648373	The genetic variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> region that predict nicotine <b>dependence</b> also predicted a later age at smoking cessation in the community sample.
+CHRNB4	drug	nicotine	22438940	Variants located upstream of <strong>CHRNB4</strong> on chromosome 15q25.1 are associated with age at onset of daily <b>smoking</b> and habitual <b>smoking</b>.
+CHRNB4	drug	alcohol	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster) with <b>alcohol</b> dependence, nicotine dependence and smoking related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNB4	drug	nicotine	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster) with alcohol dependence, <b>nicotine</b> dependence and <b>smoking</b> related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNB4	addiction	dependence	22438940	Several genome wide association and candidate gene studies have linked chromosome 15q24 q25.1 (a region including the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster) with alcohol <b>dependence</b>, nicotine <b>dependence</b> and smoking related illnesses such as lung cancer and chronic obstructive pulmonary disease.
+CHRNB4	drug	alcohol	22438940	To further examine the impact of these genes on the development of substance use disorders, we tested whether variants within and flanking the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster affect the transition to daily smoking (individuals who smoked cigarettes 4 or more days per week) in a cross sectional sample of adolescents and young adults from the COGA (Collaborative Study of the Genetics of <b>Alcoholism</b>) families.
+CHRNB4	drug	nicotine	22438940	To further examine the impact of these genes on the development of substance use disorders, we tested whether variants within and flanking the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster affect the transition to daily <b>smoking</b> (individuals who smoked cigarettes 4 or more days per week) in a cross sectional sample of adolescents and young adults from the COGA (Collaborative Study of the Genetics of Alcoholism) families.
+CHRNB4	drug	nicotine	22438940	Using the Quantitative trait disequilibrium test (QTDT) significant association was detected between age at onset of daily <b>smoking</b> and variants located upstream of <strong>CHRNB4</strong>.
+CHRNB4	drug	nicotine	22438940	The data suggests that an age associated relationship underlies the association of SNPs in <strong>CHRNB4</strong> with onset of chronic <b>smoking</b> behaviors in adolescents and young adults and may improve genetic information that will lead to better prevention and intervention for substance use disorders among adolescents and young adults.
+CHRNB4	drug	nicotine	22241830	Analysis of detailed phenotype profiles reveals CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster association with several <b>nicotine</b> dependence traits.
+CHRNB4	addiction	dependence	22241830	Analysis of detailed phenotype profiles reveals CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster association with several nicotine <b>dependence</b> traits.
+CHRNB4	drug	nicotine	22241830	In this study, we included all 15 tagging single nucleotide polymorphisms (SNPs) within the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster and tested associations with 30 <b>smoking</b> related phenotypes.
+CHRNB4	drug	nicotine	22241830	DSM IV ND symptoms associated significantly with the proxy SNP Locus 1 (rs2036527, p = .000009) and Locus 2 (rs578776, p = .0001) and tolerance factor of the <b>Nicotine</b> Dependence Syndrome Scale (NDSS) showed suggestive association to rs11636753 (p = .0059), rs11634351 (p = .0069), and rs1948 (p = .0071) in <strong>CHRNB4</strong>.
+CHRNB4	addiction	dependence	22241830	DSM IV ND symptoms associated significantly with the proxy SNP Locus 1 (rs2036527, p = .000009) and Locus 2 (rs578776, p = .0001) and tolerance factor of the Nicotine <b>Dependence</b> Syndrome Scale (NDSS) showed suggestive association to rs11636753 (p = .0059), rs11634351 (p = .0069), and rs1948 (p = .0071) in <strong>CHRNB4</strong>.
+CHRNB4	drug	nicotine	22042774	Rare missense variants in <strong>CHRNB4</strong> are associated with reduced risk of <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	22042774	Rare missense variants in <strong>CHRNB4</strong> are associated with reduced risk of nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	22042774	Genome wide association studies have identified common variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> and CHRNA6 CHRNB3 gene clusters that contribute to <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	22042774	Genome wide association studies have identified common variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> and CHRNA6 CHRNB3 gene clusters that contribute to nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, <strong>CHRNB4</strong>, CHRNA6 and CHRNB3 genes in African American and European American <b>nicotine</b> dependent <b>smokers</b> and <b>smokers</b> without symptoms of dependence.
+CHRNB4	addiction	dependence	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, <strong>CHRNB4</strong>, CHRNA6 and CHRNB3 genes in African American and European American nicotine dependent smokers and smokers without symptoms of <b>dependence</b>.
+CHRNB4	drug	nicotine	22042774	Missense variants at conserved residues in <strong>CHRNB4</strong> are associated with lower risk for <b>nicotine</b> dependence in African Americans and European Americans (AA P = 0.0025, odds ratio (OR) = 0.31, 95% confidence interval (CI) = 0.31 0.72; EA P = 0.023, OR = 0.69, 95% CI = 0.50 0.95).
+CHRNB4	addiction	dependence	22042774	Missense variants at conserved residues in <strong>CHRNB4</strong> are associated with lower risk for nicotine <b>dependence</b> in African Americans and European Americans (AA P = 0.0025, odds ratio (OR) = 0.31, 95% confidence interval (CI) = 0.31 0.72; EA P = 0.023, OR = 0.69, 95% CI = 0.50 0.95).
+CHRNB4	drug	nicotine	22042774	The minor allele of each polymorphism increased cellular response to <b>nicotine</b> (T375I P = 0.01, T91I P = 0.02, R37H P = 0.003), but the largest effect on in vitro receptor activity was seen in the presence of both <strong>CHRNB4</strong> T91I and CHRNA3 R37H (P = 2 × 10( 6)).
+CHRNB4	drug	nicotine	22042234	Genetic variation in the CHRNA5/CHRNA3/<strong>CHRNB4</strong> gene cluster has been associated with early substance experimentation, <b>nicotine</b> dependence, and other drug behaviors.
+CHRNB4	addiction	dependence	22042234	Genetic variation in the CHRNA5/CHRNA3/<strong>CHRNB4</strong> gene cluster has been associated with early substance experimentation, nicotine <b>dependence</b>, and other drug behaviors.
+CHRNB4	drug	nicotine	21747048	Relationship between CYP2A6 and CHRNA5 CHRNA3 <strong>CHRNB4</strong> variation and <b>smoking</b> behaviors and lung cancer risk.
+CHRNB4	drug	nicotine	21747048	Genetic variations in the CYP2A6 <b>nicotine</b> metabolic gene and the CHRNA5 CHRNA3 <strong>CHRNB4</strong> (CHRNA5 A3 B4) nicotinic gene cluster have been independently associated with lung cancer.
+CHRNB4	drug	nicotine	21740894	Consistent with this possibility, human genome wide association studies have shown that genetic variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster located in chromosome region 15q25, which encode the α5, α3 and β4 nAChR subunits, respectively, increases vulnerability to <b>tobacco</b> addiction and <b>smoking</b> related diseases.
+CHRNB4	addiction	addiction	21740894	Consistent with this possibility, human genome wide association studies have shown that genetic variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster located in chromosome region 15q25, which encode the α5, α3 and β4 nAChR subunits, respectively, increases vulnerability to tobacco <b>addiction</b> and smoking related diseases.
+CHRNB4	drug	nicotine	21555077	<b>Nicotine</b> dependence is linked to single nucleotide polymorphisms in the <strong>CHRNB4</strong> CHRNA3 CHRNA5 gene cluster encoding the α3β4α5 nicotinic acetylcholine receptor (nAChR).
+CHRNB4	addiction	dependence	21555077	Nicotine <b>dependence</b> is linked to single nucleotide polymorphisms in the <strong>CHRNB4</strong> CHRNA3 CHRNA5 gene cluster encoding the α3β4α5 nicotinic acetylcholine receptor (nAChR).
+CHRNB4	drug	nicotine	21555077	Transgenic mice with targeted overexpression of <strong>Chrnb4</strong> to endogenous sites display a strong aversion to <b>nicotine</b> that can be reversed by viral mediated expression of the α5 D398N variant in the medial habenula (MHb).
+CHRNB4	addiction	aversion	21555077	Transgenic mice with targeted overexpression of <strong>Chrnb4</strong> to endogenous sites display a strong <b>aversion</b> to nicotine that can be reversed by viral mediated expression of the α5 D398N variant in the medial habenula (MHb).
+CHRNB4	drug	nicotine	21511889	Common variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene region is robustly associated with <b>smoking</b> quantity.
+CHRNB4	drug	nicotine	21498873	As the physiological effects of <b>nicotine</b> are mediated by nicotinic acetylcholine receptors (nAChRs), we aimed at examining whether single nucleotide polymorphisms (SNPs) residing in nAChR subunit (CHRN) genes, other than CHRNA3/CHRNA5/<strong>CHRNB4</strong> gene cluster previously showing association in our sample, are associated with <b>smoking</b> quantity or serum cotinine levels.
+CHRNB4	drug	nicotine	21268243	We focused on eight SNPs in the 15q24 region, which contains the genes for the nicotinic cholinergic receptor subunits CHRNA5, CHRNA3, and <strong>CHRNB4</strong>, and has previously been implicated in <b>nicotine</b> addiction and <b>smoking</b> cessation.
+CHRNB4	addiction	addiction	21268243	We focused on eight SNPs in the 15q24 region, which contains the genes for the nicotinic cholinergic receptor subunits CHRNA5, CHRNA3, and <strong>CHRNB4</strong>, and has previously been implicated in nicotine <b>addiction</b> and smoking cessation.
+CHRNB4	drug	nicotine	21228559	An exploratory study on the CHRNA3 CHRNA5 <strong>CHRNB4</strong> cluster, <b>smoking</b>, and Parkinson's disease.
+CHRNB4	drug	nicotine	21228559	Recent genome wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the CHRNA3 CHRNA5 <strong>CHRNB4</strong> cluster on chromosome 15.q25 to <b>smoking</b> behaviors and <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	21228559	Recent genome wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the CHRNA3 CHRNA5 <strong>CHRNB4</strong> cluster on chromosome 15.q25 to smoking behaviors and nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	21228559	Four SNPs in linkage disequilibrium from the CHRNA3 CHRNA5 <strong>CHRNB4</strong> cluster were associated with <b>smoking</b> duration (OR >1.3, p < 0.05).
+CHRNB4	drug	nicotine	21168125	TTC12 ANKK1 DRD2 and CHRNA5 CHRNA3 <strong>CHRNB4</strong> influence different pathways leading to <b>smoking</b> behavior from adolescence to mid adulthood.
+CHRNB4	drug	nicotine	21168125	CHRNA5 CHRNA3 <strong>CHRNB4</strong> and TTC12 ANKK1 DRD2 gene clusters influence <b>smoking</b> behavior.
+CHRNB4	drug	nicotine	21168125	In contrast, CHRNA5 CHRNA3 <strong>CHRNB4</strong> is involved in the transition toward heavy <b>smoking</b> in mid adulthood and in <b>smoking</b> persistence.
+CHRNB4	drug	alcohol	21048701	Recent human genetic association studies have implicated the gene cluster CHRNA3 CHRNA5 <strong>CHRNB4</strong> encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop nicotine and <b>alcohol</b> dependence; however, their role in <b>ethanol</b> mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNB4	drug	nicotine	21048701	Recent human genetic association studies have implicated the gene cluster CHRNA3 CHRNA5 <strong>CHRNB4</strong> encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop <b>nicotine</b> and alcohol dependence; however, their role in ethanol mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNB4	addiction	dependence	21048701	Recent human genetic association studies have implicated the gene cluster CHRNA3 CHRNA5 <strong>CHRNB4</strong> encoding the α3, α5, and β4 subunits of the nAChR in susceptibility to develop nicotine and alcohol <b>dependence</b>; however, their role in ethanol mediated behaviors is unknown due to the lack of suitable and selective research tools.
+CHRNB4	drug	alcohol	21048701	Together, these data provide further support for the human genetic association studies, implicating CHRNA3 and <strong>CHRNB4</strong> genes in <b>ethanol</b> mediated behaviors.
+CHRNB4	drug	nicotine	20886544	Risk gene variants for <b>nicotine</b> dependence in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster are associated with cognitive performance.
+CHRNB4	addiction	dependence	20886544	Risk gene variants for nicotine <b>dependence</b> in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster are associated with cognitive performance.
+CHRNB4	drug	nicotine	20886544	Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong> with <b>nicotine</b> dependence (ND).
+CHRNB4	addiction	dependence	20886544	Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong> with nicotine <b>dependence</b> (ND).
+CHRNB4	drug	nicotine	20808433	Multiple genome wide and targeted association studies reveal a significant association of variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> (CHRNA5/A3/B4) gene cluster on chromosome 15 with <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	20808433	Multiple genome wide and targeted association studies reveal a significant association of variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> (CHRNA5/A3/B4) gene cluster on chromosome 15 with nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	20808433	A spectrum of haplotypes formed by three consecutive SNPs located between rs16969948 in CHRNA5 and rs6495316 in the intergenic region downstream from the 5' end of <strong>CHRNB4</strong> was associated with these three <b>smoking</b> related phenotypes in both the total and the male sample.
+CHRNB4	drug	nicotine	20700436	Recently, genetic association findings for <b>nicotine</b> dependence, <b>smoking</b> behavior, and <b>smoking</b> related diseases converged to implicate the chromosome 15q25.1 region, which includes the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cholinergic nicotinic receptor subunit genes.
+CHRNB4	addiction	dependence	20700436	Recently, genetic association findings for nicotine <b>dependence</b>, smoking behavior, and smoking related diseases converged to implicate the chromosome 15q25.1 region, which includes the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cholinergic nicotinic receptor subunit genes.
+CHRNB4	drug	nicotine	20696214	<strong>CHRNB4</strong>, which encodes the nAChR β4 subunit, plays a major role in the molecular mechanisms that govern <b>nicotine</b> withdrawal.
+CHRNB4	addiction	withdrawal	20696214	<strong>CHRNB4</strong>, which encodes the nAChR β4 subunit, plays a major role in the molecular mechanisms that govern nicotine <b>withdrawal</b>.
+CHRNB4	drug	nicotine	20631687	Variation in the nicotinic acetylcholine receptor gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong> and its interaction with recent <b>tobacco</b> use influence cognitive flexibility.
+CHRNB4	drug	nicotine	20631687	Variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster have been associated with <b>nicotine</b> dependence (ND) and ND related traits.
+CHRNB4	addiction	dependence	20631687	Variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster have been associated with nicotine <b>dependence</b> (ND) and ND related traits.
+CHRNB4	drug	nicotine	20631687	These findings suggest that variation in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster influences cognitive flexibility differentially in AAs and EAs and that current <b>smoking</b> moderates this effect.
+CHRNB4	drug	nicotine	20584212	Several independent studies show that the chromosome 15q25.1 region, which contains the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, harbors variants strongly associated with <b>nicotine</b> dependence, other <b>smoking</b> behaviors, lung cancer and chronic obstructive pulmonary disease.
+CHRNB4	addiction	dependence	20584212	Several independent studies show that the chromosome 15q25.1 region, which contains the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, harbors variants strongly associated with nicotine <b>dependence</b>, other smoking behaviors, lung cancer and chronic obstructive pulmonary disease.
+CHRNB4	drug	alcohol	20496163	This report explores the association between six nAChR subunit genes (Chrna3, Chrna4, <strong>Chrnb4</strong>, Chrnb2, Chrna5, and Chrna7) with <b>alcohol</b> preference (AP) using co segregation of AP with nAChR subunit genotypes in a F(2) population produced from reciprocal crosses of <b>alcohol</b> preferring C57BL/6J (B6) and <b>alcohol</b> avoiding DBA/2J (D2) strains of mice.
+CHRNB4	drug	alcohol	20496163	Further, the <strong>Chrnb4</strong> and Chrna5 genes showed expression differences between B6 and D2 mice, which is compatible with their involvement in AP in mice and, potentially, <b>alcohol</b> abuse in humans.
+CHRNB4	drug	nicotine	19859904	Association and interaction analysis of variants in CHRNA5/CHRNA3/<strong>CHRNB4</strong> gene cluster with <b>nicotine</b> dependence in African and European Americans.
+CHRNB4	addiction	dependence	19859904	Association and interaction analysis of variants in CHRNA5/CHRNA3/<strong>CHRNB4</strong> gene cluster with nicotine <b>dependence</b> in African and European Americans.
+CHRNB4	drug	nicotine	19859904	Several previous genome wide and targeted association studies revealed that variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> (CHRNA5/A3/B4) gene cluster on chromosome 15 that encode the alpha5, alpha3, and beta4 subunits of the nicotinic acetylcholine receptors (nAChRs) are associated with <b>nicotine</b> dependence (ND) in European Americans (EAs) or others of European origin.
+CHRNB4	addiction	dependence	19859904	Several previous genome wide and targeted association studies revealed that variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> (CHRNA5/A3/B4) gene cluster on chromosome 15 that encode the alpha5, alpha3, and beta4 subunits of the nicotinic acetylcholine receptors (nAChRs) are associated with nicotine <b>dependence</b> (ND) in European Americans (EAs) or others of European origin.
+CHRNB4	drug	nicotine	19706762	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> nicotinic receptor subunit gene cluster affects risk for <b>nicotine</b> dependence in African Americans and in European Americans.
+CHRNB4	addiction	dependence	19706762	The CHRNA5 CHRNA3 <strong>CHRNB4</strong> nicotinic receptor subunit gene cluster affects risk for nicotine <b>dependence</b> in African Americans and in European Americans.
+CHRNB4	drug	nicotine	19706762	Genetic association studies have shown the importance of variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cholinergic nicotinic receptor subunit gene cluster on chromosome 15q24 25.1 for the risk of <b>nicotine</b> dependence, <b>smoking</b>, and lung cancer in populations of European descent.
+CHRNB4	addiction	dependence	19706762	Genetic association studies have shown the importance of variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cholinergic nicotinic receptor subunit gene cluster on chromosome 15q24 25.1 for the risk of nicotine <b>dependence</b>, smoking, and lung cancer in populations of European descent.
+CHRNB4	drug	nicotine	19696770	Role of genetic variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster in <b>nicotine</b> dependence risk: importance of gene environment interplay.
+CHRNB4	addiction	dependence	19696770	Role of genetic variants in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> cluster in nicotine <b>dependence</b> risk: importance of gene environment interplay.
+CHRNB4	drug	nicotine	19628476	A cluster of three nicotinic acetylcholine receptor genes on chromosome 15 (CHRNA5/CHRNA3/<strong>CHRNB4</strong>) has been shown to be associated with <b>nicotine</b> dependence and <b>smoking</b> quantity.
+CHRNB4	addiction	dependence	19628476	A cluster of three nicotinic acetylcholine receptor genes on chromosome 15 (CHRNA5/CHRNA3/<strong>CHRNB4</strong>) has been shown to be associated with nicotine <b>dependence</b> and smoking quantity.
+CHRNB4	drug	nicotine	19628476	Variation at CHRNA5/CHRNA3/<strong>CHRNB4</strong> cluster influences <b>nicotine</b> level, measured as cotinine, more strongly than <b>smoking</b> quantity, measured by CPD, and appears thus to be involved in regulation of <b>nicotine</b> levels among <b>smokers</b>.
+CHRNB4	drug	nicotine	19443489	<b>Nicotine</b> dependence risk and lung cancer risk are associated with variants in a region of chromosome 15 encompassing genes encoding the nicotinic receptor subunits CHRNA5, CHRNA3 and <strong>CHRNB4</strong>.
+CHRNB4	addiction	dependence	19443489	Nicotine <b>dependence</b> risk and lung cancer risk are associated with variants in a region of chromosome 15 encompassing genes encoding the nicotinic receptor subunits CHRNA5, CHRNA3 and <strong>CHRNB4</strong>.
+CHRNB4	drug	nicotine	19429911	A common genetic variant in the 15q24 nicotinic acetylcholine receptor gene cluster (CHRNA5 CHRNA3 <strong>CHRNB4</strong>) is associated with a reduced ability of women to quit <b>smoking</b> in pregnancy.
+CHRNB4	drug	nicotine	19429911	A recent genome wide association study demonstrated an association between a common polymorphism (rs1051730) in the nicotinic acetylcholine receptor gene cluster (CHRNA5 CHRNA3 <strong>CHRNB4</strong>) and both <b>smoking</b> quantity and <b>nicotine</b> dependence.
+CHRNB4	addiction	dependence	19429911	A recent genome wide association study demonstrated an association between a common polymorphism (rs1051730) in the nicotinic acetylcholine receptor gene cluster (CHRNA5 CHRNA3 <strong>CHRNB4</strong>) and both smoking quantity and nicotine <b>dependence</b>.
+CHRNB4	drug	nicotine	19064933	Genetic association studies indicate that a genetic locus, which includes the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, plays a role in <b>nicotine</b> consumption and dependence.
+CHRNB4	addiction	dependence	19064933	Genetic association studies indicate that a genetic locus, which includes the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster, plays a role in nicotine consumption and <b>dependence</b>.
+CHRNB4	drug	nicotine	19029397	Compared with the most common allele, two separate groups of single nucleotide polymorphisms (SNP) in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster were associated with heavy <b>smoking</b> with a very high statistical significance.
+CHRNB4	drug	nicotine	19029397	Our findings identify two loci in the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster that predict <b>smoking</b> behavior and provide strong evidence for the involvement of the alpha5 nicotinic receptor in heavy <b>smoking</b>.
+CHRNB4	drug	cocaine	18759969	We applied this method to correlated SNPs in the cholinergic nicotinic receptor gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong>, in a case control study of <b>cocaine</b> dependence composed of 504 European American and 583 African American samples.
+CHRNB4	addiction	dependence	18759969	We applied this method to correlated SNPs in the cholinergic nicotinic receptor gene cluster CHRNA5 CHRNA3 <strong>CHRNB4</strong>, in a case control study of cocaine <b>dependence</b> composed of 504 European American and 583 African American samples.
+CHRNB4	drug	nicotine	18519524	The purpose of this study was to replicate these findings in an independent data set and more thoroughly investigate the role of genetic variation in the cluster of physically linked nicotinic receptors, CHRNA5 CHRNA3 <strong>CHRNB4</strong>, and the risk of <b>smoking</b>.
+CHRNB4	drug	alcohol	18414406	In this study we performed a comprehensive association analysis of the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster in the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) families to investigate the role of genetic variants in risk for <b>alcohol</b> dependence.
+CHRNB4	addiction	dependence	18414406	In this study we performed a comprehensive association analysis of the CHRNA5 CHRNA3 <strong>CHRNB4</strong> gene cluster in the Collaborative Study on the Genetics of Alcoholism (COGA) families to investigate the role of genetic variants in risk for alcohol <b>dependence</b>.
+CHRNB4	drug	nicotine	17503330	We applied our proposed method to a genetics study of four genes that were reported to be associated with <b>nicotine</b> dependence and found significant joint action between <strong>CHRNB4</strong> and NTRK2.
+CHRNB4	addiction	dependence	17503330	We applied our proposed method to a genetics study of four genes that were reported to be associated with nicotine <b>dependence</b> and found significant joint action between <strong>CHRNB4</strong> and NTRK2.
+ADH1C	drug	alcohol	31074035	<b>Alcohol</b> dehydrogenase 1C (<strong>ADH1C</strong>) and secreted phosphoprotein 1 (SPP1) were finally identified correlating with the LUAD survival through least absolute shrinkage and selection operator penalized Cox proportion hazards regression model, and applied to build a 2 gene signature related to prognosis in training set.
+ADH1C	drug	alcohol	30320893	Other ADH and ALDH variants, including functional variations in <strong>ADH1C</strong>, have also been implicated in affecting drinking behavior and risk for <b>alcoholism</b>.
+ADH1C	drug	alcohol	29438797	Previous studies have investigated the association between <strong>ADH1C</strong> *1/*2 polymorphism and <b>alcohol</b> dependence (AD), but have yielded controversial results in Turkey.
+ADH1C	addiction	dependence	29438797	Previous studies have investigated the association between <strong>ADH1C</strong> *1/*2 polymorphism and alcohol <b>dependence</b> (AD), but have yielded controversial results in Turkey.
+ADH1C	drug	alcohol	29084628	We evaluated the presence of SNPs in the ADH (ADH1B, <strong>ADH1C</strong>, and ADH4) and ALDH (ALDH2) genes in <b>alcohol</b> users of Goiânia, State of Goiás   Brazil, and then we established a possible relationship with AUD by allelic and genotypic study.
+ADH1C	drug	alcohol	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, <strong>ADH1C</strong>, OPRM1, DRD2, BDNF, and ALDH2 genes on <b>alcohol</b> dependence in a Caucasian population.
+ADH1C	addiction	dependence	28805974	Effect of single nucleotide polymorphisms in ADH1B, ADH4, <strong>ADH1C</strong>, OPRM1, DRD2, BDNF, and ALDH2 genes on alcohol <b>dependence</b> in a Caucasian population.
+ADH1C	drug	alcohol	27172571	The interactions of religious involvement with ADH1B rs2066702, <strong>ADH1C</strong> rs698, and ADH4 rs1042364 were significantly associated with maximum drinks and <b>alcohol</b> dependence symptoms.
+ADH1C	addiction	dependence	27172571	The interactions of religious involvement with ADH1B rs2066702, <strong>ADH1C</strong> rs698, and ADH4 rs1042364 were significantly associated with maximum drinks and alcohol <b>dependence</b> symptoms.
+ADH1C	drug	alcohol	27163368	Certain genetic variants (i.e., alleles)  particularly the ADH1B*2, ADH1B*3, <strong>ADH1C</strong>*1, and ALDH2*2 alleles  have been associated with lower rates of <b>alcohol</b> dependence.
+ADH1C	addiction	dependence	27163368	Certain genetic variants (i.e., alleles)  particularly the ADH1B*2, ADH1B*3, <strong>ADH1C</strong>*1, and ALDH2*2 alleles  have been associated with lower rates of alcohol <b>dependence</b>.
+ADH1C	drug	cannabinoid	27151647	Two QTSs within or near <strong>ADH1C</strong> showed very strong association in a dominance inheritance mode and increased the phenotype value of ADSC when the effect of co morbid opiate or <b>marijuana</b> dependence was controlled.
+ADH1C	addiction	dependence	27151647	Two QTSs within or near <strong>ADH1C</strong> showed very strong association in a dominance inheritance mode and increased the phenotype value of ADSC when the effect of co morbid opiate or marijuana <b>dependence</b> was controlled.
+ADH1C	drug	alcohol	26848198	Characterization of polymorphisms of genes ADH2, <strong>ADH3</strong>, ALDH2 and CYP2E1 and relationship to the <b>alcoholism</b> in a Colombian population.
+ADH1C	drug	alcohol	26848198	Identify and characterize polymorphisms of genes ADH2, <strong>ADH3</strong>, ALDH2 and CYP2E1 in a Colombian population residing in the city of Bogotá and determine its possible relationship to the <b>alcoholism</b>.
+ADH1C	drug	alcohol	26848198	ADH2, <strong>ADH3</strong>, ALDH2, and CYP2E1 genotypes a population of 148 individuals with non problematic <b>alcohol</b> and 65 individuals with <b>alcoholism</b> were determined with TaqMan probes and PCR RFLP.
+ADH1C	drug	alcohol	26848198	Se determinaron los genotipos ADH2, <strong>ADH3</strong>, ALDH2 y CYP2E1 a una población de 148 individuos con un consumo no problemático de <b>alcohol</b> y 65 individuos con alcoholismo.
+ADH1C	drug	alcohol	25958762	Variants of ADH1B and <strong>ADH1C</strong> genes encoding <b>alcohol</b> dehydrogenases enzymes have also been consistently associated, this time with <b>alcohol</b> dependence (AD).
+ADH1C	addiction	dependence	25958762	Variants of ADH1B and <strong>ADH1C</strong> genes encoding alcohol dehydrogenases enzymes have also been consistently associated, this time with alcohol <b>dependence</b> (AD).
+ADH1C	drug	alcohol	25535445	The genes for <b>alcohol</b> metabolizing enzymes: <b>Alcohol</b> dehydrogenase (ADH2 and <strong>ADH3</strong>) and aldehyde dehydrogenase (ALDH2) exhibit functional polymorphisms.
+ADH1C	drug	alcohol	25535445	To determine whether any association exists between polymorphisms of ADH2, <strong>ADH3</strong> and ALDH2 and <b>alcohol</b> dependence syndrome in a group of Asian Indians.
+ADH1C	addiction	dependence	25535445	To determine whether any association exists between polymorphisms of ADH2, <strong>ADH3</strong> and ALDH2 and alcohol <b>dependence</b> syndrome in a group of Asian Indians.
+ADH1C	drug	alcohol	25535445	Allele frequencies of ADH2*2 (0.50), <strong>ADH3</strong>*1 (0.67) and ALSH2*2 (0.09) were significantly low in the <b>alcohol</b> dependent subjects.
+ADH1C	drug	alcohol	25372623	Association between <strong>ADH1C</strong> and ALDH2 polymorphisms and <b>alcoholism</b> in a Turkish sample.
+ADH1C	drug	alcohol	25372623	To evaluate the association between the <b>alcohol</b> dehydrogenase 1C (<strong>ADH1C</strong>) Ile350Val and aldehyde dehydrogenase 2 (ALDH2) Glu504Lys polymorphisms and <b>alcohol</b> dependence in a Turkish sample.
+ADH1C	addiction	dependence	25372623	To evaluate the association between the alcohol dehydrogenase 1C (<strong>ADH1C</strong>) Ile350Val and aldehyde dehydrogenase 2 (ALDH2) Glu504Lys polymorphisms and alcohol <b>dependence</b> in a Turkish sample.
+ADH1C	drug	alcohol	25372623	235 individuals (115 <b>alcohol</b> dependent patients and 120 controls) were genotyped for <strong>ADH1C</strong> and ALDH2 with PCR RFLP (polymerase chain reaction restriction fragment length polymorphism).
+ADH1C	drug	alcohol	25372623	The  350Val allele for <strong>ADH1C</strong> (<strong>ADH1C</strong>*2) was increased in <b>alcohol</b> dependent patients (P = 0.05).
+ADH1C	drug	alcohol	25372623	These findings suggest that <strong>ADH1C</strong>*2 is associated with <b>alcohol</b> dependence in the Turkish population displaying a dominant inheritance model.
+ADH1C	addiction	dependence	25372623	These findings suggest that <strong>ADH1C</strong>*2 is associated with alcohol <b>dependence</b> in the Turkish population displaying a dominant inheritance model.
+ADH1C	drug	alcohol	25372623	<strong>ADH1C</strong>*2 allele may contribute to the variance in heritability of <b>alcohol</b> dependence.
+ADH1C	addiction	dependence	25372623	<strong>ADH1C</strong>*2 allele may contribute to the variance in heritability of alcohol <b>dependence</b>.
+ADH1C	drug	alcohol	25208201	Regular male drinkers without <b>alcohol</b> dependence (n = 112) ages 18 25 years participated in <b>alcohol</b> challenge sessions consisting of placebo and two doses of <b>alcohol</b> (target BrAC: 0 g/dl for placebo, .04 g/dl low dose, and .08 g/dl high dose) and genotyped for variants in ADH1B*3 and <strong>ADH1C</strong>*2.
+ADH1C	addiction	dependence	25208201	Regular male drinkers without alcohol <b>dependence</b> (n = 112) ages 18 25 years participated in alcohol challenge sessions consisting of placebo and two doses of alcohol (target BrAC: 0 g/dl for placebo, .04 g/dl low dose, and .08 g/dl high dose) and genotyped for variants in ADH1B*3 and <strong>ADH1C</strong>*2.
+ADH1C	drug	alcohol	25208201	Higher responses on the SHAS items muddle/confused and nauseated were significantly associated with the presence of at least one ADH1B*3 allele following the high dose of <b>alcohol</b> in Afro T. Indo T with at least one <strong>ADH1C</strong>*2 allele displayed significantly different Drug × Time interactions for the SHAS item effects of <b>alcohol</b> at the low dose and for the SHAS items clumsy, muddle/confused, effects of <b>alcohol</b>, floating, drunk, and total at the high dose from Indo T with two <strong>ADH1C</strong>*1 alleles.
+ADH1C	drug	alcohol	25208201	Indo T with at least one <strong>ADH1C</strong>*2 allele may be at higher risk for heavy drinking by feeling less of the effects of <b>alcohol</b>, including nausea.
+ADH1C	drug	alcohol	24735490	Genetic variants in or near ADH1B and <strong>ADH1C</strong> affect susceptibility to <b>alcohol</b> dependence in a British and Irish population.
+ADH1C	addiction	dependence	24735490	Genetic variants in or near ADH1B and <strong>ADH1C</strong> affect susceptibility to alcohol <b>dependence</b> in a British and Irish population.
+ADH1C	drug	alcohol	24505444	We investigated six variants known to influence nicotine addiction or <b>alcohol</b> metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (<strong>ADH1C</strong>), rs1573496 (ADH7), and rs4767364 (ALDH2).
+ADH1C	drug	nicotine	24505444	We investigated six variants known to influence <b>nicotine</b> addiction or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (<strong>ADH1C</strong>), rs1573496 (ADH7), and rs4767364 (ALDH2).
+ADH1C	addiction	addiction	24505444	We investigated six variants known to influence nicotine <b>addiction</b> or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (<strong>ADH1C</strong>), rs1573496 (ADH7), and rs4767364 (ALDH2).
+ADH1C	drug	alcohol	24166409	We confirmed well known risk loci mapped to <b>alcohol</b> metabolizing enzyme genes, notably ADH1B (EAs: Arg48His, P=1.17 × 10( 31); AAs: Arg369Cys, P=6.33 × 10( 17)) and <strong>ADH1C</strong> in AAs (Thr151Thr, P=4.94 × 10( 10)), and identified novel risk loci mapping to the ADH gene cluster on chromosome 4 and extending centromerically beyond it to include GWS associations at LOC100507053 in AAs (P=2.63 × 10( 11)), PDLIM5 in EAs (P=2.01 × 10( 8)), and METAP in AAs (P=3.35 × 10( 8)).
+ADH1C	drug	alcohol	23516558	Replication of genome wide association studies of <b>alcohol</b> dependence: support for association with variation in <strong>ADH1C</strong>.
+ADH1C	addiction	dependence	23516558	Replication of genome wide association studies of alcohol <b>dependence</b>: support for association with variation in <strong>ADH1C</strong>.
+ADH1C	drug	alcohol	23516558	Our analysis of 808 <b>alcohol</b> dependent cases and 1,248 controls provided evidence of association of <b>alcohol</b> dependence with SNP rs1614972 in the <strong>ADH1C</strong> gene (unadjusted p = 0.0017).
+ADH1C	addiction	dependence	23516558	Our analysis of 808 alcohol dependent cases and 1,248 controls provided evidence of association of alcohol <b>dependence</b> with SNP rs1614972 in the <strong>ADH1C</strong> gene (unadjusted p = 0.0017).
+ADH1C	drug	alcohol	23516558	Despite a number of potential differences between the samples investigated by the prior GWAS and the current study, data presented here provide additional support for the association of SNP rs1614972 in <strong>ADH1C</strong> with <b>alcohol</b> dependence and extend this finding by demonstrating association with consumption levels in both non <b>alcoholic</b> and <b>alcohol</b> dependent populations.
+ADH1C	addiction	dependence	23516558	Despite a number of potential differences between the samples investigated by the prior GWAS and the current study, data presented here provide additional support for the association of SNP rs1614972 in <strong>ADH1C</strong> with alcohol <b>dependence</b> and extend this finding by demonstrating association with consumption levels in both non alcoholic and alcohol dependent populations.
+ADH1C	drug	alcohol	23468174	Humans express at least seven <b>alcohol</b> dehydrogenase (ADH) isoforms that are encoded by ADH gene cluster (ADH7 <strong>ADH1C</strong> ADH1B ADH1A ADH6 ADH4 ADH5) at chromosome 4.
+ADH1C	drug	alcohol	23134050	For example, certain ADH1B and <strong>ADH1C</strong> variants that are commonly found in East Asian populations lead to more rapid <b>ethanol</b> breakdown and acetaldehyde accumulation in the body.
+ADH1C	drug	alcohol	23019235	ADH1B*2, ADH1B*3 and <strong>ADH1C</strong>*2) that significantly affect the risk of <b>alcohol</b> dependence are rare variants in most populations.
+ADH1C	addiction	dependence	23019235	ADH1B*2, ADH1B*3 and <strong>ADH1C</strong>*2) that significantly affect the risk of alcohol <b>dependence</b> are rare variants in most populations.
+ADH1C	drug	alcohol	22931071	Associations between <b>alcohol</b> dependence and polymorphisms in ADH1B, <strong>ADH1C</strong>, and ALDH2 were compared in a community sample of Native Americans (n 791) living on reservations and Mexican Americans (n 391) living within the same county.
+ADH1C	addiction	dependence	22931071	Associations between alcohol <b>dependence</b> and polymorphisms in ADH1B, <strong>ADH1C</strong>, and ALDH2 were compared in a community sample of Native Americans (n 791) living on reservations and Mexican Americans (n 391) living within the same county.
+ADH1C	drug	alcohol	22931071	No associations between <b>alcohol</b> dependence and polymorphisms in <strong>ADH1C</strong> were found.
+ADH1C	addiction	dependence	22931071	No associations between alcohol <b>dependence</b> and polymorphisms in <strong>ADH1C</strong> were found.
+ADH1C	drug	alcohol	22476623	Further clarification of the contribution of the <strong>ADH1C</strong> gene to vulnerability of <b>alcoholism</b> and selected liver diseases.
+ADH1C	drug	alcohol	22476623	The <b>alcohol</b> dehydrogenase 1C (<strong>ADH1C</strong>) subunit is an important member of the <b>alcohol</b> dehydrogenase family, a set of genes that plays a major role in the catabolism of <b>ethanol</b>.
+ADH1C	drug	alcohol	22476623	Numerous association studies have provided compelling evidence that <strong>ADH1C</strong> gene variation (formerly ADH3) is associated with altered genetic susceptibility to <b>alcoholism</b> and <b>alcohol</b> related liver disease, cirrhosis, or pancreatitis.
+ADH1C	drug	alcohol	22476623	Numerous association studies have provided compelling evidence that <strong>ADH1C</strong> gene variation (formerly <strong>ADH3</strong>) is associated with altered genetic susceptibility to <b>alcoholism</b> and <b>alcohol</b> related liver disease, cirrhosis, or pancreatitis.
+ADH1C	drug	alcohol	22476623	The results showed strong evidence of association between <strong>ADH1C</strong> Ile350Val (rs698, formerly <strong>ADH1C</strong> *1/*2) and <b>alcohol</b> dependence (AD) and abuse in the combined studies.
+ADH1C	addiction	dependence	22476623	The results showed strong evidence of association between <strong>ADH1C</strong> Ile350Val (rs698, formerly <strong>ADH1C</strong> *1/*2) and alcohol <b>dependence</b> (AD) and abuse in the combined studies.
+ADH1C	drug	alcohol	22476623	Our findings support that <strong>ADH1C</strong> Ile may lower the risk of AD and <b>alcohol</b> abuse as well as <b>alcohol</b> related cirrhosis in pooled populations, with the strongest and most consistent effects in Asians.
+ADH1C	drug	alcohol	22414625	Association of a genetic polymorphism of the <b>alcohol</b> metabolizing enzyme <strong>ADH1C</strong> with <b>alcohol</b> dependence: results of a case control study.
+ADH1C	addiction	dependence	22414625	Association of a genetic polymorphism of the alcohol metabolizing enzyme <strong>ADH1C</strong> with alcohol <b>dependence</b>: results of a case control study.
+ADH1C	drug	alcohol	22414625	The aim was to investigate the allelic and genotypic difference in distribution of a polymorphism in <b>alcohol</b> dehydrogenase 1C gene (<strong>ADH1C</strong>) between <b>alcohol</b> dependent individuals and controls, and to examine if these genotypes were associated with the age at which the patient became <b>alcohol</b> dependent.
+ADH1C	drug	alcohol	22414625	The <strong>ADH1C</strong>*1 allele frequencies were 0.89 (95% CI 0.84 0.91) in controls and 0.68 (95% CI 0.61 0.74) in <b>alcohol</b> dependent patients.
+ADH1C	drug	alcohol	22414625	The frequencies of the <strong>ADH1C</strong>*2 allele were 0.11 (95% CI 0.07 0.14) and 0.32 (95% CI 0.25 0.38) among controls and <b>alcohol</b> dependent patients, respectively (p < 0.0001).
+ADH1C	drug	alcohol	22414625	The <strong>ADH1C</strong>*1/*1 genotype frequency was significantly higher in the control group (77%) compared to that of the <b>alcohol</b> dependents (51%, p < 0.0001).
+ADH1C	drug	alcohol	22414625	The <strong>ADH1C</strong>*1/*2 genotype frequency was significantly lower in the control group (23%) compared to that of the <b>alcohol</b> dependents (42%, p < 0.0001).
+ADH1C	drug	alcohol	22414625	These findings suggest that a significantly higher presence of <strong>ADH1C</strong>*2 allele is associated with <b>alcohol</b> dependence in a Turkish population.
+ADH1C	addiction	dependence	22414625	These findings suggest that a significantly higher presence of <strong>ADH1C</strong>*2 allele is associated with alcohol <b>dependence</b> in a Turkish population.
+ADH1C	drug	alcohol	22414625	Studies with other related polymorphisms are needed to more precisely estimate the association of <b>alcohol</b> dependence with <strong>ADH1C</strong>.
+ADH1C	addiction	dependence	22414625	Studies with other related polymorphisms are needed to more precisely estimate the association of alcohol <b>dependence</b> with <strong>ADH1C</strong>.
+ADH1C	drug	alcohol	22325912	Determination of the effects of <b>alcohol</b> dehydrogenase (ADH) 1B and <strong>ADH1C</strong> polymorphisms on <b>alcohol</b> dependence in Turkey.
+ADH1C	addiction	dependence	22325912	Determination of the effects of alcohol dehydrogenase (ADH) 1B and <strong>ADH1C</strong> polymorphisms on alcohol <b>dependence</b> in Turkey.
+ADH1C	drug	alcohol	22325912	No profound connection between <b>alcohol</b> dependence and <strong>ADH1C</strong> Ile350Val gene polymorphism was detected.
+ADH1C	addiction	dependence	22325912	No profound connection between alcohol <b>dependence</b> and <strong>ADH1C</strong> Ile350Val gene polymorphism was detected.
+ADH1C	drug	alcohol	22048268	Combined effect of ADH1B RS1229984, RS2066702 and <strong>ADH1C</strong> RS1693482/ RS698 alleles on <b>alcoholism</b> and chronic liver diseases.
+ADH1C	drug	alcohol	22048268	The aim of this study was to analyze the combined effect of the most frequent <b>alcohol</b> dehydrogenase polymorphisms (Arg48His and Arg370Cys in ADH1B, Arg272Gln and Ile350Val in <strong>ADH1C</strong>) on the <b>alcohol</b> use habits, <b>alcohol</b> dependence and chronic liver diseases in Hungary.
+ADH1C	addiction	dependence	22048268	The aim of this study was to analyze the combined effect of the most frequent alcohol dehydrogenase polymorphisms (Arg48His and Arg370Cys in ADH1B, Arg272Gln and Ile350Val in <strong>ADH1C</strong>) on the alcohol use habits, alcohol <b>dependence</b> and chronic liver diseases in Hungary.
+ADH1C	drug	alcohol	22004471	The SNP rs1789891 is in complete linkage disequilibrium with the functional Arg272Gln variant (P = 1.24E 7, OR = 1.31) of the <strong>ADH1C</strong> gene, which has been reported to modify the rate of <b>ethanol</b> oxidation to acetaldehyde in vitro.
+ADH1C	drug	alcohol	20714161	We develop a pharmacokinetic model describing how genetic variations in ADH1B, <strong>ADH1C</strong>, ADH7, ALDH2, and TAS2R38 affect consumption behavior, and <b>alcohol</b> and acetaldehyde levels over time in various tissues of individuals with a particular genotype to predict their susceptibility to <b>alcohol</b> dependence.
+ADH1C	addiction	dependence	20714161	We develop a pharmacokinetic model describing how genetic variations in ADH1B, <strong>ADH1C</strong>, ADH7, ALDH2, and TAS2R38 affect consumption behavior, and alcohol and acetaldehyde levels over time in various tissues of individuals with a particular genotype to predict their susceptibility to alcohol <b>dependence</b>.
+ADH1C	drug	alcohol	20617019	A new view of <b>alcohol</b> metabolism and <b>alcoholism</b>  role of the high Km Class III <b>alcohol</b> dehydrogenase (<strong>ADH3</strong>).
+ADH1C	drug	alcohol	20617019	Recently, using <strong>ADH3</strong> null mutant mice, we demonstrated that <strong>ADH3</strong> (Class III), which has a high K(m) and is a ubiquitous enzyme of ancient origin, contributes to systemic <b>alcohol</b> metabolism in a dose dependent manner, thereby diminishing acute <b>alcohol</b> intoxication.
+ADH1C	addiction	intoxication	20617019	Recently, using <strong>ADH3</strong> null mutant mice, we demonstrated that <strong>ADH3</strong> (Class III), which has a high K(m) and is a ubiquitous enzyme of ancient origin, contributes to systemic alcohol metabolism in a dose dependent manner, thereby diminishing acute alcohol <b>intoxication</b>.
+ADH1C	drug	alcohol	20617019	Although the activity of <strong>ADH3</strong> toward <b>ethanol</b> is usually low in vitro due to its very high K(m), the catalytic efficiency (k(cat)/K(m)) is markedly enhanced when the solution hydrophobicity of the reaction medium increases.
+ADH1C	drug	alcohol	20617019	When various doses of <b>ethanol</b> are administered to mice, liver <strong>ADH3</strong> activity is dynamically regulated through induction or kinetic activation, while ADH1 activity is markedly lower at high doses (3 5 g/kg).
+ADH1C	drug	alcohol	20617019	These data suggest that <strong>ADH3</strong> plays a dynamic role in <b>alcohol</b> metabolism, either collaborating with ADH1 or compensating for the reduced role of ADH1.
+ADH1C	drug	alcohol	20617019	A complex two ADH model that ascribes total liver ADH activity to both ADH1 and <strong>ADH3</strong> explains the dose dependent changes in the pharmacokinetic parameters (beta, CL(T), AUC) of blood <b>ethanol</b> very well, suggesting that <b>alcohol</b> metabolism in mice is primarily governed by these two ADHs.
+ADH1C	drug	alcohol	20617019	In patients with <b>alcoholic</b> liver disease, liver <strong>ADH3</strong> activity increases, while ADH1 activity decreases, as <b>alcohol</b> intake increases.
+ADH1C	drug	alcohol	20617019	These data suggest that chronic binge drinking and the resulting liver disease shifts the key enzyme in <b>alcohol</b> metabolism from low K(m) ADH1 to high K(m) <strong>ADH3</strong>, thereby reducing the rate of <b>alcohol</b> metabolism.
+ADH1C	addiction	intoxication	20617019	These data suggest that chronic <b>binge</b> drinking and the resulting liver disease shifts the key enzyme in alcohol metabolism from low K(m) ADH1 to high K(m) <strong>ADH3</strong>, thereby reducing the rate of alcohol metabolism.
+ADH1C	drug	alcohol	20617019	The interdependent increase in the <strong>ADH3</strong>/ADH1 activity ratio and AUC may be a factor in the development of <b>alcoholic</b> liver disease.
+ADH1C	drug	alcohol	20617019	However, the adaptive increase in <strong>ADH3</strong> sustains <b>alcohol</b> metabolism, even in patients with <b>alcoholic</b> liver cirrhosis, which makes it possible for them to drink themselves to death.
+ADH1C	drug	alcohol	20617019	Thus, the regulation of <strong>ADH3</strong> activity may be important in preventing <b>alcoholism</b> development.
+ADH1C	drug	alcohol	20401433	The purpose of this study was to investigate the differences, if present, in the allele and genotype frequency of <b>alcohol</b> dehydrogenase 1B (ADH1B), <strong>ADH1C</strong> and the microsomal <b>ethanol</b> oxidizing system (MEOS/CYP2E1) between <b>alcohol</b> dependent individuals and controls and also to determine if these genotypes cause a difference in the age at which the patients become <b>alcohol</b> dependent.
+ADH1C	drug	alcohol	20401433	The allele and genotype frequencies of ADH1B, <strong>ADH1C</strong>, and CYP2E1 were determined in 204 <b>alcohol</b> dependent men and 172 healthy volunteers who do not drink <b>alcohol</b> (control group).
+ADH1C	drug	alcohol	20401433	ADH1B*1 (99.3%) and <strong>ADH1C</strong>*1 (62.5%) alleles and ADH1B*1/*1 (N = 201) and <strong>ADH1C</strong>*1/*1 (N = 85) genotypes were statistically more frequent among <b>alcohol</b> dependent subjects than among controls (99.3 and 62.5%, N = 201 and 85 vs 94.5 and 40.7%, N = 153 and 32, respectively).
+ADH1C	drug	alcohol	20401433	The persons with <strong>ADH1C</strong>*1/*1 and CYP2E1*c1/*c2 genotypes became <b>alcohol</b> dependent at a considerably younger age than the subjects with <strong>ADH1C</strong>*1/*2, <strong>ADH1C</strong>*2/*2 and CYP2E1*c1/*c1 genotypes (28.08, 25.67 years vs 36.0, 45.05, 34.45 years, respectively).
+ADH1C	drug	alcohol	20401433	In the Polish men examined, <strong>ADH1C</strong>*1 and ADH1B*1 alleles and <strong>ADH1C</strong>*1/*1 and ADH1B*1/*1 genotypes favor <b>alcohol</b> dependence.
+ADH1C	addiction	dependence	20401433	In the Polish men examined, <strong>ADH1C</strong>*1 and ADH1B*1 alleles and <strong>ADH1C</strong>*1/*1 and ADH1B*1/*1 genotypes favor alcohol <b>dependence</b>.
+ADH1C	drug	alcohol	20401433	However, subjects with <strong>ADH1C</strong>*1/*1 and CYP2E1*c1/*c2 genotypes become <b>alcohol</b> dependent at a considerably younger age than the subjects with <strong>ADH1C</strong>*1/*2, <strong>ADH1C</strong>*2/*2 and CYP2E1*c1/*c1 genotypes.
+ADH1C	drug	alcohol	19581569	Nine SNPs were located in genes, including the CDH13 and <strong>ADH1C</strong> genes, that have been reported to be associated with <b>alcohol</b> dependence.
+ADH1C	addiction	dependence	19581569	Nine SNPs were located in genes, including the CDH13 and <strong>ADH1C</strong> genes, that have been reported to be associated with alcohol <b>dependence</b>.
+ADH1C	drug	alcohol	19489444	[A new sight on <b>alcohol</b> metabolism and <b>alcoholism</b>  role of high Km <b>alcohol</b> dehydrogenase <strong>ADH3</strong> (Class III)].
+ADH1C	drug	alcohol	19489444	Recently, we used <strong>ADH3</strong> null mutant mice to demonstrate that high Km <strong>ADH3</strong> (Class III), a ubiquitous enzyme of ancient origin, contributes to systemic <b>alcohol</b> metabolism dose dependently resulting in a diminution of acute <b>alcohol</b> intoxication.
+ADH1C	addiction	intoxication	19489444	Recently, we used <strong>ADH3</strong> null mutant mice to demonstrate that high Km <strong>ADH3</strong> (Class III), a ubiquitous enzyme of ancient origin, contributes to systemic alcohol metabolism dose dependently resulting in a diminution of acute alcohol <b>intoxication</b>.
+ADH1C	drug	alcohol	19489444	Although the <b>ethanol</b> activity of <strong>ADH3</strong> in vitro is usually low due to its very high Km, the catalytic efficiency (k(cat)/Km) was markedly enhanced when the solution hydrophobicity of the reaction medium was increased.
+ADH1C	drug	alcohol	19489444	By acute administrations of <b>ethanol</b> to mice at various doses, liver <strong>ADH3</strong> activity was dynamically regulated through induction or kinetic activation, though ADH1 activity was markedly decreased at higher doses (3   5 g/kg).
+ADH1C	drug	alcohol	19489444	These data suggest that <strong>ADH3</strong> plays a dynamical share in <b>alcohol</b> metabolism with ADH1, collaborating with it or supplementing the decreased role of ADH1.
+ADH1C	drug	alcohol	19489444	The two ADH complex model, which ascribes total liver ADH activity to both ADH1 and <strong>ADH3</strong>, explained well the dose dependent changes in pharmacokinetic parameters (beta, CL(T), AUC) of blood <b>ethanol</b>, suggesting that <b>alcohol</b> metabolism in mice is primarily governed by the two ADHs.
+ADH1C	drug	alcohol	19489444	In patients with <b>alcoholic</b> liver diseases, the liver <strong>ADH3</strong> activity increased but the ADH1 activity decreased with an increase in <b>alcohol</b> intake.
+ADH1C	drug	alcohol	19489444	These data suggest that heavy and chronic drinking shifts the main enzyme in <b>alcohol</b> metabolism from low Km ADH1 to high Km <strong>ADH3</strong> to develop <b>alcoholic</b> liver diseases by the nonlinear increase in AUC due to the decrease of the metabolic rate.
+ADH1C	drug	alcohol	19489444	However, the adaptively increased <strong>ADH3</strong> keeps the ability of <b>alcohol</b> metabolism even in patients with <b>alcoholic</b> liver cirrhosis and make possible for them to keep drinking to death.
+ADH1C	drug	alcohol	19489444	Therefore, the regulation of <strong>ADH3</strong> activity may be important to prevent the development of <b>alcoholism</b>.
+ADH1C	drug	alcohol	18996923	After controlling for rs1229984, an independent association was observed between rs1042026 (ADH1B) and <b>alcohol</b> intake (P=4.7 x 10( 5)) and suggestive associations (P<0.001) between <b>alcohol</b> consumption phenotypes and rs1693482 (<strong>ADH1C</strong>), rs1230165 (ADH5) and rs3762894 (ADH4).
+ADH1C	drug	alcohol	17885622	The subjects were divided into 3 combinatorial genotypic groups of <b>alcohol</b> dehydrogenase (ADH) and ALDH, that is, ALDH2*1/*1 ADH1B*1/*1 <strong>ADH1C</strong>*1/*1 (n=8), ALDH2*1/*1 ADH1B*2/*2 <strong>ADH1C</strong>*1/*1 (n=8), and ALDH2*1/*2 ADH1B*2/*2 <strong>ADH1C</strong>*1/*1 (n=16).
+ADH1C	drug	alcohol	17718398	Studies have demonstrated that a certain variant of the gene encoding ADH1B (ADH1B*3) is associated with a reduced risk of <b>alcoholism</b> in Afro Trinidadians, as is a variant of the gene encoding <strong>ADH1C</strong> (i.e., <strong>ADH1C</strong>*1) in Indo Trinidadians.
+ADH1C	drug	alcohol	17718397	Variants of three genes encoding <b>alcohol</b> metabolizing enzymes, the aldehyde dehydrogenase gene ALDH2 and the <b>alcohol</b> dehydrogenase genes ADH1B and <strong>ADH1C</strong>, have been associated with reduced rates of <b>alcohol</b> dependence.
+ADH1C	addiction	dependence	17718397	Variants of three genes encoding alcohol metabolizing enzymes, the aldehyde dehydrogenase gene ALDH2 and the alcohol dehydrogenase genes ADH1B and <strong>ADH1C</strong>, have been associated with reduced rates of alcohol <b>dependence</b>.
+ADH1C	drug	alcohol	17629074	The aim of the present study was to find in the Polish population the <strong>ADH3</strong> genotypes, which are likely to be responsible for higher susceptibility to <b>alcohol</b> disease of the liver and chronic <b>alcohol</b> pancreatitis.
+ADH1C	drug	alcohol	17629074	The genotype <strong>ADH3</strong>*1/<strong>ADH3</strong>*1 was found to be significantly more frequent in <b>alcohol</b> abusers compared to non drinkers.
+ADH1C	drug	alcohol	17629074	The examinations of the group of <b>alcohol</b> abusers showed that the genotype <strong>ADH3</strong>*2/<strong>ADH3</strong>*2 occurred statistically significantly less frequently in patients with chronic pancreatitis than those without alimentary lesions and patients with cirrhosis.
+ADH1C	drug	alcohol	17454860	We determined the allele and genotype of ADH2, <strong>ADH3</strong> and ALDH2 in 198 subjects: 57 with <b>alcohol</b> cirrhosis, 44 with <b>alcohol</b> chronic pancreatitis and 43 "healthy <b>alcoholics</b>"; 54 healthy non drinkers served as controls.
+ADH1C	drug	alcohol	17454860	The ADH2*1 and the <strong>ADH3</strong>*1 alleles were statistically more common among patients who abuse <b>alcohol</b> in comparison with the controls.
+ADH1C	drug	alcohol	17454860	The ADH2*1/*1 and the <strong>ADH3</strong>*1/*1 genotypes were statistically significantly more common among the patients who abuse <b>alcohol</b> than in the control group.
+ADH1C	drug	alcohol	17454860	Patients with the <strong>ADH3</strong>*1 allele and the <strong>ADH3</strong>*1/*1 genotype started to abuse <b>alcohol</b> significantly earlier in comparison to the patients with the <strong>ADH3</strong>*2 allele and the <strong>ADH3</strong>*2 /*2 genotype.
+ADH1C	drug	alcohol	17454860	In the Polish population examined, the <strong>ADH3</strong>*1 allele and the <strong>ADH3</strong>*1/*1 genotype are conducive to the development of <b>alcoholism</b>, <b>alcohol</b> liver cirrhosis and <b>alcohol</b> chronic pancreatitis.
+ADH1C	drug	alcohol	17454860	The <strong>ADH3</strong>*1 allele and the <strong>ADH3</strong>*1/*1 genotype are conducive to <b>alcohol</b> abuse starting at a younger age.
+ADH1C	drug	alcohol	17250612	Two of the class I <b>alcohol</b> dehydrogenase (ADH) genes located on chromosome 4 (ADH1B and <strong>ADH1C</strong>) encode for multiple isozymes that differ in their kinetic properties.
+ADH1C	drug	alcohol	17134660	<strong>ADH1C</strong>*2 allele is associated with <b>alcohol</b> dependence and elevated liver enzymes in Trinidad and Tobago.
+ADH1C	addiction	dependence	17134660	<strong>ADH1C</strong>*2 allele is associated with alcohol <b>dependence</b> and elevated liver enzymes in Trinidad and Tobago.
+ADH1C	drug	alcohol	17134660	This study sought to determine whether an association exists between ADH (<strong>ADH1C</strong> previously ADH3, ADH1B*2 previously ADH2*2) genotypes, <b>alcohol</b> dependence, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH1C	addiction	dependence	17134660	This study sought to determine whether an association exists between ADH (<strong>ADH1C</strong> previously ADH3, ADH1B*2 previously ADH2*2) genotypes, alcohol <b>dependence</b>, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH1C	drug	alcohol	17134660	This study sought to determine whether an association exists between ADH (<strong>ADH1C</strong> previously <strong>ADH3</strong>, ADH1B*2 previously ADH2*2) genotypes, <b>alcohol</b> dependence, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH1C	addiction	dependence	17134660	This study sought to determine whether an association exists between ADH (<strong>ADH1C</strong> previously <strong>ADH3</strong>, ADH1B*2 previously ADH2*2) genotypes, alcohol <b>dependence</b>, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH1C	drug	alcohol	17134660	The <strong>ADH1C</strong>*2 allele was significantly associated with <b>alcohol</b> dependence overall and within Indo TT ancestry, however, it was not associated with current or heaviest <b>alcohol</b> consumption levels.
+ADH1C	addiction	dependence	17134660	The <strong>ADH1C</strong>*2 allele was significantly associated with alcohol <b>dependence</b> overall and within Indo TT ancestry, however, it was not associated with current or heaviest alcohol consumption levels.
+ADH1C	drug	alcohol	17134660	Additionally, GGT levels were also found to be elevated (P<.02) within Indo TT <b>alcohol</b> dependents with at least one <strong>ADH1C</strong>*2 allele but not within the Afro TT <b>alcohol</b> dependents with that allele.
+ADH1C	drug	alcohol	17134660	A linear regression that included <b>alcohol</b> dependence and levels of <b>alcohol</b> consumption confirmed that levels of serum GGT were significantly associated with the <strong>ADH1C</strong>*2 genotype.
+ADH1C	addiction	dependence	17134660	A linear regression that included alcohol <b>dependence</b> and levels of alcohol consumption confirmed that levels of serum GGT were significantly associated with the <strong>ADH1C</strong>*2 genotype.
+ADH1C	drug	alcohol	17134660	These results suggest that <strong>ADH1C</strong> polymorphisms are associated with <b>alcohol</b> dependence and <b>alcohol</b> associated elevations of liver enzymes in a population with a low frequency of ADH1B2 alleles.
+ADH1C	addiction	dependence	17134660	These results suggest that <strong>ADH1C</strong> polymorphisms are associated with alcohol <b>dependence</b> and alcohol associated elevations of liver enzymes in a population with a low frequency of ADH1B2 alleles.
+ADH1C	drug	alcohol	16930209	Variations in the ADH1B and <strong>ADH1C</strong> genes may influence the LR to <b>alcohol</b> by increasing levels of acetaldehyde during <b>alcohol</b> metabolism, although most data on this question come from Asian populations.
+ADH1C	drug	alcohol	16431092	In vivo contribution of Class III <b>alcohol</b> dehydrogenase (<strong>ADH3</strong>) to <b>alcohol</b> metabolism through activation by cytoplasmic solution hydrophobicity.
+ADH1C	drug	alcohol	16431092	In this study, we used <strong>Adh3</strong> null mutant mice to demonstrate that Class III ADH (<strong>ADH3</strong>), a ubiquitous enzyme of ancient origin, contributes to <b>alcohol</b> metabolism in vivo dose dependently resulting in a diminution of acute <b>alcohol</b> intoxication.
+ADH1C	addiction	intoxication	16431092	In this study, we used <strong>Adh3</strong> null mutant mice to demonstrate that Class III ADH (<strong>ADH3</strong>), a ubiquitous enzyme of ancient origin, contributes to alcohol metabolism in vivo dose dependently resulting in a diminution of acute alcohol <b>intoxication</b>.
+ADH1C	drug	alcohol	16431092	Although the <b>ethanol</b> oxidation activity of <strong>ADH3</strong> in vitro is low due to its very high Km, it was found to exhibit a markedly enhanced catalytic efficiency (kcat/Km) toward <b>ethanol</b> when the solution hydrophobicity of the reaction medium was increased with a hydrophobic substance.
+ADH1C	drug	alcohol	16431092	So, the in vivo contribution of high Km <strong>ADH3</strong> to <b>alcohol</b> metabolism is likely to involve activation in a hydrophobic solution.
+ADH1C	drug	alcohol	16431092	Thus, the present study demonstrated that <strong>ADH3</strong> plays an important role in systemic <b>ethanol</b> metabolism at higher levels of blood <b>ethanol</b> through activation by cytoplasmic solution hydrophobicity.
+ADH1C	drug	alcohol	16404797	Two <b>alcohol</b> dehydrogenase genes (ADHIB and <strong>ADH1C</strong> on chromosome 4) and one aldehyde dehydrogenase gene (ALDH2 on chromosome 12) exhibit functional polymorphisms that are associated with lower rates of <b>alcohol</b> dependence.
+ADH1C	addiction	dependence	16404797	Two alcohol dehydrogenase genes (ADHIB and <strong>ADH1C</strong> on chromosome 4) and one aldehyde dehydrogenase gene (ALDH2 on chromosome 12) exhibit functional polymorphisms that are associated with lower rates of alcohol <b>dependence</b>.
+ADH1C	drug	alcohol	16404797	Studies of the ADHIBand <strong>ADH1C</strong> haplotypes, however, have shown that <strong>ADH1C</strong>*I is in linkage disequilibrium with ADHiB*2, and the <strong>ADH1C</strong>*i allele does not appear to have significant unique associations with <b>alcohol</b> dependence.
+ADH1C	addiction	dependence	16404797	Studies of the ADHIBand <strong>ADH1C</strong> haplotypes, however, have shown that <strong>ADH1C</strong>*I is in linkage disequilibrium with ADHiB*2, and the <strong>ADH1C</strong>*i allele does not appear to have significant unique associations with alcohol <b>dependence</b>.
+ADH1C	drug	alcohol	16239350	To find the <strong>ADH3</strong> genotypes in the Polish population likely to be responsible for higher susceptibility to <b>alcohol</b> disease of the liver and chronic <b>alcohol</b> pancreatitis.
+ADH1C	drug	alcohol	16239350	The genotype <strong>ADH3</strong>*1/<strong>ADH3</strong>*1 was found to be significantly more frequent in <b>alcohol</b> abusers compared with non drinkers.
+ADH1C	drug	alcohol	16239350	The examinations of the group of <b>alcohol</b> abusers showed that the genotype <strong>ADH3</strong>*2/<strong>ADH3</strong>*2 occurred statistically significantly less frequently in patients with chronic pancreatitis than in those without alimentary lesions (healthy drinkers).
+ADH1C	drug	alcohol	16239350	Variations in <strong>ADH3</strong> genotypes may account for some of the differences in prevalence of <b>alcohol</b> dependence between genders in the Polish population.
+ADH1C	addiction	dependence	16239350	Variations in <strong>ADH3</strong> genotypes may account for some of the differences in prevalence of alcohol <b>dependence</b> between genders in the Polish population.
+ADH1C	drug	alcohol	16184481	Genetic time series analysis identifies a major QTL for in vivo <b>alcohol</b> metabolism not predicted by in vitro studies of structural protein polymorphism at the ADH1B or <strong>ADH1C</strong> loci.
+ADH1C	drug	alcohol	15863807	The authors examined the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 and 3 (ADH2 and <strong>ADH3</strong>) and aldehyde dehydrogenase (ALDH2) in patients diagnosed as having Cloninger's type I or type II <b>alcoholism</b>.
+ADH1C	drug	alcohol	15863807	Seventy two <b>alcoholic</b> men and 38 nonalcoholic, healthy men were tested for the distribution of genotypes and alleles of ADH2, <strong>ADH3</strong>, and ALDH2.
+ADH1C	drug	alcohol	15863807	The frequencies of ADH2*1 and <strong>ADH3</strong>*2 alleles were significantly higher in men with type II <b>alcoholism</b> than in men with type I <b>alcoholism</b> and healthy men.
+ADH1C	drug	alcohol	15542698	The genotype for the most active <b>alcohol</b> dehydrogenase enzyme <strong>ADH1C</strong> was associated with a lower risk of <b>alcoholism</b> (P = .026) and was less prevalent in <b>alcoholics</b> with DRD2TaqIA2/A2 (P = .047), GABAA beta2 1412C/C (P = .01), or EAAT2 603G/A (P = .022) genotypes.
+ADH1C	drug	alcohol	12884000	Allelic variation at <b>alcohol</b> metabolism genes (ADH1B, <strong>ADH1C</strong>, ALDH2) and <b>alcohol</b> dependence in an American Indian population.
+ADH1C	addiction	dependence	12884000	Allelic variation at alcohol metabolism genes (ADH1B, <strong>ADH1C</strong>, ALDH2) and alcohol <b>dependence</b> in an American Indian population.
+ADH1C	drug	alcohol	12884000	In the current study, variants at ADH1B (previously ADH2), <strong>ADH1C</strong> (previously ADH3), and ALDH2 were assayed in DNA extracts from participants belonging to a Southwest American Indian tribe (n=490) with a high prevalence of <b>alcoholism</b>.
+ADH1C	drug	alcohol	12884000	In the current study, variants at ADH1B (previously ADH2), <strong>ADH1C</strong> (previously <strong>ADH3</strong>), and ALDH2 were assayed in DNA extracts from participants belonging to a Southwest American Indian tribe (n=490) with a high prevalence of <b>alcoholism</b>.
+ADH1C	drug	alcohol	12884000	Both linkage and association analysis identified several <strong>ADH1C</strong> alleles and a neighboring microsatellite marker that affected risk of <b>alcohol</b> dependence and were also related to binge drinking.
+ADH1C	addiction	dependence	12884000	Both linkage and association analysis identified several <strong>ADH1C</strong> alleles and a neighboring microsatellite marker that affected risk of alcohol <b>dependence</b> and were also related to binge drinking.
+ADH1C	addiction	intoxication	12884000	Both linkage and association analysis identified several <strong>ADH1C</strong> alleles and a neighboring microsatellite marker that affected risk of alcohol dependence and were also related to <b>binge</b> drinking.
+ADH1C	drug	alcohol	12750236	<b>Alcohol</b> is a probable risk factor with regard to colorectal neoplasm and is metabolized to the carcinogen acetaldehyde by the genetically polymorphic <b>alcohol</b> dehydrogenase 3 (<strong>ADH3</strong>) enzyme.
+ADH1C	drug	alcohol	12750236	We evaluated whether the association between <b>alcohol</b> and colorectal adenomas is modified by <strong>ADH3</strong> polymorphism.
+ADH1C	drug	alcohol	12750236	Among subjects in the highest tertile of <b>alcohol</b> consumption, those with the <strong>ADH3</strong>*1/*1 genotype were at higher risk (OR, 1.8; 95% CI, 1.0 3.1) than those with other <strong>ADH3</strong> genotypes (OR, 1.2; 95% CI, 0.7 1.9) when compared with those in the lowest tertile with <strong>ADH3</strong>*1/*2 or <strong>ADH3</strong>*2/*2 genotypes.
+ADH1C	drug	alcohol	12750236	<strong>ADH3</strong> polymorphism may modify the association between <b>alcohol</b> consumption and colorectal adenomas.
+ADH1C	drug	alcohol	12710951	The <strong>ADH3</strong>*2 and CYP2E1 c2 alleles increase the risk of <b>alcoholism</b> in Mexican American men.
+ADH1C	drug	alcohol	12710951	To identify the association between the polymorphisms of genes encoding <b>alcohol</b> metabolizing enzymes and <b>alcoholism</b>, the <b>alcohol</b> dehydrogenase 2 (ADH2), <b>alcohol</b> dehydrogenase 3 (<strong>ADH3</strong>), aldehyde dehydrogenase 2 (ALDH2), and cytochrome P450 2E1 (CYP2E1) genes were studied in 101 male Mexican American <b>alcoholics</b>.
+ADH1C	drug	alcohol	12710951	A strong association was found between <strong>ADH3</strong> genotype and <b>alcoholism</b>; the percentage of subjects who carry the <strong>ADH3</strong>*2 allele was significantly higher in <b>alcoholics</b> (64.4%) than controls (50%).
+ADH1C	drug	alcohol	12710951	Among 101 <b>alcoholics</b>, only 18 subjects carry neither <strong>ADH3</strong>*2 nor CYP2E1 c2 alleles.
+ADH1C	drug	alcohol	12710951	Taken together, <strong>ADH3</strong>*2 and CYP2E1 c2/C alleles might independently contribute to the development of <b>alcoholism</b> in Mexican American men.
+ADH1C	drug	alcohol	12505800	Two <b>alcohol</b> dehydrogenase genes (ADH2 and <strong>ADH3</strong> on chromosome 4) and one aldehyde dehydrogenase gene (ALDH2 on chromosome 12) exhibit functional polymorphisms.
+ADH1C	drug	alcohol	12505800	The goal of this study was to determine whether any associations exist between the ADH2, <strong>ADH3</strong>, and ALDH2 polymorphisms and <b>alcohol</b> dependence in a group of Native Americans.
+ADH1C	addiction	dependence	12505800	The goal of this study was to determine whether any associations exist between the ADH2, <strong>ADH3</strong>, and ALDH2 polymorphisms and alcohol <b>dependence</b> in a group of Native Americans.
+ADH1C	drug	alcohol	11752857	<b>Alcohol</b> dehydrogenase type 3 (<strong>ADH3</strong>) and the risk of bladder cancer.
+ADH1C	drug	alcohol	11752857	After correction for sex, age and smoking, ORs for <strong>ADH3</strong> genotype and <b>alcohol</b> intake were 2.10 (1.05 4.22) and 1.21 (0.60 2.44), respectively.
+ADH1C	drug	nicotine	11752857	After correction for sex, age and <b>smoking</b>, ORs for <strong>ADH3</strong> genotype and alcohol intake were 2.10 (1.05 4.22) and 1.21 (0.60 2.44), respectively.
+ADH1C	drug	alcohol	11752857	Although moderate drinkers with the gamma1gamma1 genotype seem to have the highest risk, we did not get a clear indication that <strong>ADH3</strong> genotype modifies the relationship between <b>alcohol</b> intake and bladder cancer.
+ADH1C	drug	alcohol	11584143	In view of this association and the known genetic influences on both <b>alcohol</b> pharmacokinetics and <b>alcohol</b> dependence, it is probable that part of the heritability of dependence is mediated by genes (other than the known ADH2 and <strong>ADH3</strong> polymorphisms) affecting <b>alcohol</b> metabolism.
+ADH1C	addiction	dependence	11584143	In view of this association and the known genetic influences on both alcohol pharmacokinetics and alcohol <b>dependence</b>, it is probable that part of the heritability of <b>dependence</b> is mediated by genes (other than the known ADH2 and <strong>ADH3</strong> polymorphisms) affecting alcohol metabolism.
+ADH1C	drug	alcohol	10630602	An <b>alcohol</b> dependent patient was identified to be ALDH2*2/*2, ADH2*2/*2, and <strong>ADH3</strong>*1/*2.
+ADH1C	drug	alcohol	10597438	Evidence for linkage to the ALDX1 <b>alcoholism</b> phenotype at the <strong>ADH3</strong> functional candidate gene was increased in the late onset subgroup (Bonferroni corrected significance level < 0.002), as compared with the unstratified sample that replicated COGA linkage obtained in the same analysis; there was no evidence for linkage at this locus in the early onset subgroup.
+ADH1C	drug	alcohol	10597410	For the "<b>alcoholism</b> free" outcome, we found significant linkage signals at D4S2457, D41651 (both flank <strong>ADH3</strong>), D11S2359, and D16S47 and significant linkage disequilibrium signals at D4S2361, FABP2, D11S2359, D19S431 and D19S47 D19S198 D19S601.
+ADH1C	drug	alcohol	10235293	The different genotypes at the genes encoding the enzymes involved in <b>alcohol</b> metabolism, class one <b>alcohol</b> dehydrogenase (ADH2 and <strong>ADH3</strong>) and mitochondrial aldehyde dehydrogenase (ALDH2), have previously been shown to confer different predispositions to the development of <b>alcoholism</b> in Chinese Han males (Thomasson et al., 1991; Chen WJ et al., 1996; Chen CC et al., unpublished data).
+ADH1C	drug	alcohol	10235293	Therefore, association studies of <b>alcoholism</b> in Chinese Han might be more sensitive if controlled for the genotypes of ADH2,<strong>ADH3</strong>, and ALDH2, when other loci, such as DRD2, are examined.
+ADH1C	drug	alcohol	10235293	These tests included considering the high risk (ADH2*1/*1; *1/*2; <strong>ADH3</strong>*1/*2; *2/*2; and ALDH2*1/*1) and the low risk (ADH2*2/*2; <strong>ADH3</strong>*1/*1; and ALDH2*1/*2; *2/*2) groups of <b>alcoholics</b>, as well as nonalcoholic controls.
+ADH1C	drug	alcohol	10235293	After stratification by the relevant genotypes of ADH2, <strong>ADH3</strong>, and ALDH2 no significant association exists between the genetic variants at the DRD2 locus and <b>alcoholism</b> in the Chinese Han population.
+ADH1C	drug	alcohol	9731720	Caucasians are polymorphic at only two of these gene loci  cytochrome P450 2E1 (CYP2E1) and <b>alcohol</b> dehydrogenase 3 (<strong>ADH3</strong>).
+ADH1C	drug	alcohol	9731720	We examined the frequency of the RsaI polymorphism of CYP2E1 and <strong>ADH3</strong> genotype in 264 patients with <b>alcoholic</b> liver disease and 121 local control individuals.
+ADH1C	drug	alcohol	9731720	This risk appears to be particularly manifest in individuals carrying the <strong>ADH3</strong>*2 allele, presumably reflecting increased metabolism of <b>ethanol</b> by CYP2E1.
+ADH1C	drug	alcohol	9731720	In the absence of the c2 allele, <strong>ADH3</strong> genotype does not influence the risk of advanced <b>alcoholic</b> liver disease but, in males at least, may influence the risk of <b>alcoholism</b>.
+ADH1C	drug	alcohol	9373704	The purpose of this paper is to assemble and evaluate existing data on the effect of genetic variation in ADH2 and <strong>ADH3</strong> on the risk of <b>alcohol</b> dependence, and on the risk of <b>alcoholic</b> liver disease.
+ADH1C	addiction	dependence	9373704	The purpose of this paper is to assemble and evaluate existing data on the effect of genetic variation in ADH2 and <strong>ADH3</strong> on the risk of alcohol <b>dependence</b>, and on the risk of alcoholic liver disease.
+ADH1C	drug	alcohol	9373704	<strong>ADH3</strong> variation also has significant effects on <b>alcohol</b> dependence, which may be due to linkage to ADH2; the <strong>ADH3</strong> effect differs significantly between Asian and European subjects.
+ADH1C	addiction	dependence	9373704	<strong>ADH3</strong> variation also has significant effects on alcohol <b>dependence</b>, which may be due to linkage to ADH2; the <strong>ADH3</strong> effect differs significantly between Asian and European subjects.
+ADH1C	drug	alcohol	9066994	In this report we determined the genotypes for three genes, ADH2, <strong>ADH3</strong>, and ALDH2 among subjects with <b>alcohol</b> dependence (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ADH1C	addiction	dependence	9066994	In this report we determined the genotypes for three genes, ADH2, <strong>ADH3</strong>, and ALDH2 among subjects with alcohol <b>dependence</b> (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ADH1C	drug	alcohol	8904964	The influences of estimated body water, recent drinking history, recent smoking history, polymorphism at the ADH2 and <strong>ADH3</strong> loci, family history of <b>alcoholism</b>, and percentage Native American heritage on <b>alcohol</b> elimination rate were determined using multiple regression analyses.
+ADH1C	drug	nicotine	8904964	The influences of estimated body water, recent drinking history, recent <b>smoking</b> history, polymorphism at the ADH2 and <strong>ADH3</strong> loci, family history of alcoholism, and percentage Native American heritage on alcohol elimination rate were determined using multiple regression analyses.
+ADH1C	drug	alcohol	8773821	<b>Alcohol</b> metabolising genes and <b>alcoholism</b> among Taiwanese Han men: independent effect of ADH2, <strong>ADH3</strong> and ALDH2.
+ADH1C	drug	alcohol	8773821	The association of ALDH2 and ADH2 with the development of <b>alcoholism</b> was found to be independent of each other and has been replicated in different Asian populations, while the effect of <strong>ADH3</strong> is less studied.
+ADH1C	drug	alcohol	8773821	Multiple logistic regression was then applied to assess the contribution of <strong>ADH3</strong> to <b>alcoholism</b> by controlling the effect of ALDH2 and ADH2.
+ADH1C	drug	alcohol	8773821	The results of multivariate analyses demonstrated that the odds ratios for an increment of one allele of ADH2*1, <strong>ADH3</strong>*2 and ALDH2*1 in the development of <b>alcoholism</b> were 4.18, 3.82, and 6.89, respectively.
+ADH1C	drug	alcohol	8651462	A comparison of the genotypes of ALDH2, ADH2, <strong>ADH3</strong>, and cytochrome P 4502E1 between <b>alcoholics</b> and nonalcoholics.
+ADH1C	drug	alcohol	8651462	We examined the genotypes of the aldehyde dehydrogenase (ALDH) 2, <b>alcohol</b> dehydrogenase (ADH) 2, <strong>ADH3</strong>, and P 4502E1 loci of 53 <b>alcoholics</b> and 97 nonalcoholics.
+ADH1C	drug	alcohol	8651462	Our study revealed differences in the allelic frequencies of the ALDH2, ADH2, and <strong>ADH3</strong> loci between <b>alcoholics</b> and nonalcoholics.
+ADH1C	drug	alcohol	8651462	For <b>alcoholics</b> with both homozygous ALDH2*1/1 and heterozygous ALDH2*1/2 genotypes, it was found that ADH2 and <strong>ADH3</strong> played important rates.
+ADH1C	drug	alcohol	7943668	Genetic variation at two polymorphic <b>alcohol</b> dehydrogenase loci, ADH2 and <strong>ADH3</strong>, and at the polymorphic mitochondrial aldehyde dehydrogenase locus, ALDH2, may influence the risk of developing <b>alcoholism</b> by modulating the rate of elimination of <b>ethanol</b> and the rate of formation and elimination of acetaldehyde.
+ACHE	drug	cannabinoid	32414087	<b>Cannabis</b> Constituents and Acetylcholinesterase Interaction: Molecular Docking, In Vitro Studies and Association with CNR1 rs806368 and <strong>ACHE</strong> rs17228602.
+ACHE	drug	cannabinoid	32414087	The study documented here was aimed to find the molecular interactions of some of the <b>cannabinoid</b> constituents of <b>cannabis</b> with acetylcholinesterase (<strong>AChE</strong>).
+ACHE	drug	cannabinoid	32414087	<strong>AChE</strong> enzyme activity was measured in the blood of <b>cannabis</b> addicted human subjects.
+ACHE	drug	cannabinoid	32414087	Further, genetic predisposition to <b>cannabis</b> addiction was investigated by association analysis of <b>cannabinoid</b> receptor 1 (CNR1) single nucleotide polymorphism (SNP) rs806368 and <strong>ACHE</strong> rs17228602 using restriction fragment length polymorphism (RFLP) method.
+ACHE	addiction	addiction	32414087	Further, genetic predisposition to cannabis <b>addiction</b> was investigated by association analysis of cannabinoid receptor 1 (CNR1) single nucleotide polymorphism (SNP) rs806368 and <strong>ACHE</strong> rs17228602 using restriction fragment length polymorphism (RFLP) method.
+ACHE	drug	cannabinoid	32414087	All the understudied <b>cannabis</b> constituents showed promising binding affinities with <strong>AChE</strong> and are lipophilic in nature.
+ACHE	drug	cannabinoid	32414087	The <strong>AChE</strong> activity was observed to be indifferent in <b>cannabis</b> addicted and non addicted healthy controls.
+ACHE	drug	cannabinoid	32414087	Further studies to explore the inhibitory potential of different <b>cannabis</b> constituents for intended <strong>AChE</strong> inhibitor based drug are warranted.
+ACHE	drug	benzodiazepine	31879781	The primary therapeutic strategy employed in the United States to treat OP intoxication includes reactivation of inhibited <strong>AChE</strong> with the oxime pralidoxime (2 PAM) along with the muscarinic acetylcholine receptor antagonist atropine and the <b>benzodiazepine</b>, <b>diazepam</b>.
+ACHE	addiction	intoxication	31879781	The primary therapeutic strategy employed in the United States to treat OP <b>intoxication</b> includes reactivation of inhibited <strong>AChE</strong> with the oxime pralidoxime (2 PAM) along with the muscarinic acetylcholine receptor antagonist atropine and the benzodiazepine, diazepam.
+ACHE	drug	alcohol	31660828	<b>Ethanol</b> and methanol showed no anti <strong>AChE</strong> activity up to 0.29% (v/v) and 0.23% (v/v), respectively.
+ACHE	drug	nicotine	31646410	<b>Nicotine</b> induced oxidative stress, testis injury, <strong>AChE</strong> inhibition and brain damage alleviated by Mentha spicata.
+ACHE	drug	nicotine	31646410	In addition, exposure to <b>nicotine</b> significantly (p < 0.01) increased acetylcholinesterase level (<strong>AChE</strong>) in brain, lipid peroxidation level in brain and testis as compared to control group.
+ACHE	addiction	addiction	31129131	Association of status of acetylcholinesterase and <strong>ACHE</strong> gene 3' UTR variants (rs17228602, rs17228616) with drug <b>addiction</b> vulnerability in pakistani population.
+ACHE	addiction	addiction	31129131	Acetylecholine (ACh), a cholinergic neurotransmitter hydrolyzed by acetylcholinesterase (<strong>AChE</strong>), is an essential neurotransmitter and neuromodulator in central and peripheral nervous system and has regulatory influence on numerous neuronal functions including <b>addiction</b>.
+ACHE	drug	opioid	31129131	The present study was carried out to investigate the role of acetylcholinesterase (<strong>AChE</strong>) in addiction through measurement of enzyme activity and to find potential association of <strong>ACHE</strong> gene 3'UTR variants rs17228602 and rs17228616 in <b>heroin</b>, hashish and poly drug addicts.
+ACHE	addiction	addiction	31129131	The present study was carried out to investigate the role of acetylcholinesterase (<strong>AChE</strong>) in <b>addiction</b> through measurement of enzyme activity and to find potential association of <strong>ACHE</strong> gene 3'UTR variants rs17228602 and rs17228616 in heroin, hashish and poly drug addicts.
+ACHE	addiction	addiction	31129131	A statistically significant association of <strong>ACHE</strong> rs17228602 SNP with <b>addiction</b> vulnerability in dominant (DM: Odd's ratio OR = 2.095, 95% CI = 1.157 3.807 p = 0.009) and allelic genetic models (OR = 1.854 95% CI = 1.082 3.187, p = 0.016) was observed.
+ACHE	addiction	addiction	31129131	The data presented here shows that <strong>AChE</strong> could play significant role in substance <b>addiction</b>.
+ACHE	addiction	addiction	31129131	Further studies with larger sample size and other variants of <strong>AChE</strong> are recommended to identify novel therapeutic approaches for cholinergic based treatment of <b>addiction</b>.
+ACHE	drug	nicotine	30712397	Acetylcholinesterase (<strong>AChE</strong>) inhibitors and positive allosteric nicotinic acetylcholine receptor (nAChR) modulators are potential pharmacotherapies for <b>nicotine</b> dependence.
+ACHE	addiction	dependence	30712397	Acetylcholinesterase (<strong>AChE</strong>) inhibitors and positive allosteric nicotinic acetylcholine receptor (nAChR) modulators are potential pharmacotherapies for nicotine <b>dependence</b>.
+ACHE	drug	nicotine	30712397	varenicline) appear to work by mimicking the effects of <b>nicotine</b>, we used drug discrimination to examine whether <strong>AChE</strong> inhibitors and nAChR allosteric modulators mimic the effects of <b>nicotine</b>.
+ACHE	drug	nicotine	30712397	<b>Nicotine</b> and the <strong>AChE</strong> inhibitors donepezil and galantamine dose dependently increased responding on the <b>nicotine</b> appropriate lever with ED50 values of 0.35, 0.22, and 0.77 mg/kg, respectively.
+ACHE	drug	nicotine	30712397	Oxotremorine, a muscarinic acetylcholine receptor agonist that was used to explore the extent to which muscarinic receptor agonism might contribute to the effects of <strong>AChE</strong> inhibitors, produced 94% <b>nicotine</b> lever responding (ED50 value 0.013 mg/kg).
+ACHE	drug	nicotine	30712397	Collectively, these results suggest that <strong>AChE</strong> inhibitors can mimic the effects of <b>nicotine</b> by indirectly stimulating both nicotinic and muscarinic receptors.
+ACHE	drug	nicotine	30712397	Inasmuch as some <b>smoking</b> cessation aids work by exerting <b>nicotine</b> like effects, the current results are consistent with the potential use of <strong>AChE</strong> inhibitors as novel <b>smoking</b> cessation aids.
+ACHE	drug	nicotine	30099467	In addition, curcuminoid significantly suppressed the priming effects of <b>nicotine</b> and inhibited acetylcholinesterase (<strong>AChE</strong>) activity.
+ACHE	drug	nicotine	30099467	Taken together, curcuminoid ameliorates <b>nicotine</b> dependence and relapse, in part via the inhibition of the <strong>AChE</strong> activity in the brain.
+ACHE	addiction	dependence	30099467	Taken together, curcuminoid ameliorates nicotine <b>dependence</b> and relapse, in part via the inhibition of the <strong>AChE</strong> activity in the brain.
+ACHE	addiction	relapse	30099467	Taken together, curcuminoid ameliorates nicotine dependence and <b>relapse</b>, in part via the inhibition of the <strong>AChE</strong> activity in the brain.
+ACHE	drug	nicotine	29750975	Here, we evaluated whether <b>nicotine</b> enhances contextual fear responses in zebrafish and investigated a putative involvement of brain acetylcholinesterase (<strong>AChE</strong>) in associative learning.
+ACHE	drug	nicotine	29750975	<b>Nicotine</b> also stimulated brain <strong>AChE</strong> activity in CAS exposed animals reintroduced in tanks with similar context.
+ACHE	drug	alcohol	29626671	This study aims at associating the digestion related ethno uses of Plectranthus species decoctions to molecular mechanism that might explain them: easing digestion (<strong>AChE</strong> inhibition) and treating hangover (ADH inhibition) MATERIAL AND METHODS: Decoctions from Plectranthus species were analysed for their <b>alcohol</b> dehydrogenase (ADH) inhibition and acetylcholinesterase (<strong>AChE</strong>) inhibition, related with <b>alcohol</b> metabolism and intestinal motility, respectively.
+ACHE	drug	opioid	28461881	To determine the effect of the most commonly abused drugs (<b>tramadol</b> and <b>morphine</b>), on acetylcholine esterase (<strong>AChE</strong>), Na+/K+ ATPase activities and related parameters, Na+ and K+ as biomarkers of neurotoxicity.
+ACHE	drug	opioid	28461881	Acetylcholine esterase (<strong>AChE</strong>) activity in the brain cerebral cortex increased after the administration of therapeutic repeated doses of either <b>tramadol</b> (20 mg/kg b.w.)
+ACHE	drug	benzodiazepine	27705071	The standard treatment for sarin like nerve agent exposure is post exposure injection of atropine, a muscarinic receptor antagonist, accompanied by an oxime, an <strong>AChE</strong> reactivator, and <b>diazepam</b>.
+ACHE	drug	psychedelics	26232639	The aim of the present study was to evaluate the efficacy of type I and II PAMs, N (5 chloro 2,4 dimethoxyphenyl) N' (5 methyl 3 isoxazolyl)urea (PNU 120596) and N (4 chlorophenyl) [[(4 chlorophenyl)amino]methylene] 3 methyl 5 isoxazoleacet amide (CCMI), respectively, and galantamine, an acetylcholinesterase inhibitor (<strong>AChE</strong>) that also allosterically modulates nAChRs, against <b>ketamine</b> induced cognitive deficits and social withdrawal in rats.
+ACHE	addiction	withdrawal	26232639	The aim of the present study was to evaluate the efficacy of type I and II PAMs, N (5 chloro 2,4 dimethoxyphenyl) N' (5 methyl 3 isoxazolyl)urea (PNU 120596) and N (4 chlorophenyl) [[(4 chlorophenyl)amino]methylene] 3 methyl 5 isoxazoleacet amide (CCMI), respectively, and galantamine, an acetylcholinesterase inhibitor (<strong>AChE</strong>) that also allosterically modulates nAChRs, against ketamine induced cognitive deficits and social <b>withdrawal</b> in rats.
+ACHE	drug	alcohol	26180599	These data suggested that the extract improved memory deficit in <b>alcoholic</b> rats partly via the decreased oxidative stress and the suppression of <strong>AChE</strong>.
+ACHE	drug	amphetamine	25518108	[Effect of manual acupuncture stimulation of "Baihui" (GV 20) and "Dazhui" (GV 14) on contents of 5 HT, dopamine and ACh and expression of 5 HT mRNA, DA mRNA and <strong>AChE</strong> mRNA in the hippocampus in <b>methamphetamine</b> addiction rats].
+ACHE	addiction	addiction	25518108	[Effect of manual acupuncture stimulation of "Baihui" (GV 20) and "Dazhui" (GV 14) on contents of 5 HT, dopamine and ACh and expression of 5 HT mRNA, DA mRNA and <strong>AChE</strong> mRNA in the hippocampus in methamphetamine <b>addiction</b> rats].
+ACHE	drug	amphetamine	25518108	To observe the effect of manual acupuncture stimulation on changes of hippocampal monoamine neurotransmitter levels and expression of 5 hydorxytryptamine (5 HT) mRNA, dopamine (DA) mRNA and acetylcholine esterase (<strong>AChE</strong>) mRNA in <b>methamphetamine</b> addiction rats, so as to explore its mechanism underlying improvement of drug addiction.
+ACHE	addiction	addiction	25518108	To observe the effect of manual acupuncture stimulation on changes of hippocampal monoamine neurotransmitter levels and expression of 5 hydorxytryptamine (5 HT) mRNA, dopamine (DA) mRNA and acetylcholine esterase (<strong>AChE</strong>) mRNA in methamphetamine <b>addiction</b> rats, so as to explore its mechanism underlying improvement of drug <b>addiction</b>.
+ACHE	drug	amphetamine	25518108	Manual acupuncture stimulation of GV 20 and GV 14 can adjust <b>methamphetamine</b> addiction induced changes of some hippocampal monoa  mine neurotransmitters and expression levels of 5 HT, DA and <strong>AChE</strong> genes.
+ACHE	addiction	addiction	25518108	Manual acupuncture stimulation of GV 20 and GV 14 can adjust methamphetamine <b>addiction</b> induced changes of some hippocampal monoa  mine neurotransmitters and expression levels of 5 HT, DA and <strong>AChE</strong> genes.
+ACHE	drug	nicotine	24854235	Following 14 days of <b>nicotine</b> exposure, the NAc was dissected and acetylcholinesterase (<strong>AChE</strong>) activity was compared across groups.
+ACHE	drug	nicotine	24854235	The second study revealed that <b>nicotine</b> exposure increased <strong>AChE</strong> activity in the NAc to a greater extent in adolescent versus adult rats.
+ACHE	addiction	intoxication	23959117	Acetylcholinesterase (<strong>AChE</strong>) reactivators were developed for the treatment of organophosphate <b>intoxication</b>.
+ACHE	drug	benzodiazepine	23959117	Standard care involves the use of anticonvulsants (e.g., <b>diazepam</b>), parasympatolytics (e.g., atropine) and oximes that restore <strong>AChE</strong> activity.
+ACHE	drug	nicotine	23836027	Rat offspring exposed perinatally to a HFD or chow diet were characterized in terms of their <b>nicotine</b> self administration behavior in a series of operant response experiments and the activity of acetylcholinesterase (<strong>AChE</strong>) and density of nicotinic ACh receptors (nAChRs) in different brain areas.
+ACHE	addiction	reward	23836027	Rat offspring exposed perinatally to a HFD or chow diet were characterized in terms of their nicotine self administration behavior in a series of <b>operant</b> response experiments and the activity of acetylcholinesterase (<strong>AChE</strong>) and density of nicotinic ACh receptors (nAChRs) in different brain areas.
+ACHE	drug	alcohol	23797318	Results demonstrated that <strong>AChE</strong> activity increased in the Cd/<b>ethanol</b> group when compared to saline/<b>ethanol</b> group.
+ACHE	drug	alcohol	23797318	Treatment with quercetin prevented the increase in <strong>AChE</strong> activity when compared to Cd/<b>ethanol</b> group.
+ACHE	drug	opioid	23651795	Acetylcholinesterase (<strong>AChE</strong>) activity and [³H] epibatidine binding were evaluated in order to determine if <b>morphine</b> dependence and withdrawal induces alterations in cholinergic signaling or expression of high affinity nicotinic acetylcholine receptors (nAChRs) in the midbrain (MB), medial habenula (MHb) and interpeduncular nucleus (IPN).
+ACHE	addiction	dependence	23651795	Acetylcholinesterase (<strong>AChE</strong>) activity and [³H] epibatidine binding were evaluated in order to determine if morphine <b>dependence</b> and withdrawal induces alterations in cholinergic signaling or expression of high affinity nicotinic acetylcholine receptors (nAChRs) in the midbrain (MB), medial habenula (MHb) and interpeduncular nucleus (IPN).
+ACHE	addiction	withdrawal	23651795	Acetylcholinesterase (<strong>AChE</strong>) activity and [³H] epibatidine binding were evaluated in order to determine if morphine dependence and <b>withdrawal</b> induces alterations in cholinergic signaling or expression of high affinity nicotinic acetylcholine receptors (nAChRs) in the midbrain (MB), medial habenula (MHb) and interpeduncular nucleus (IPN).
+ACHE	drug	opioid	23651795	Chronic <b>morphine</b> administration decreased <strong>AChE</strong> activity in MB and MHb, an effect that was no longer present following precipitated withdrawal.
+ACHE	addiction	withdrawal	23651795	Chronic morphine administration decreased <strong>AChE</strong> activity in MB and MHb, an effect that was no longer present following precipitated <b>withdrawal</b>.
+ACHE	drug	amphetamine	23245536	The present study aims to investigate the effects of mood stabilizers, lithium (Li) and valproate (VPA), on acetylcholinesterase (<strong>AChE</strong>) activity in the brains of rats subjected to an animal model of mania induced by D <b>amphetamine</b> (D <b>AMPH</b>).
+ACHE	drug	amphetamine	23245536	However, D <b>AMPH</b> decreased activity of <strong>AChE</strong> in the striatum of rats in both the reversion and prevention treatments.
+ACHE	addiction	reward	23245536	Our findings further support the notion that the mechanisms of mood stabilizers also involve changes in <strong>AChE</strong> activity, thus <b>reinforcing</b> the need for more studies to better characterize the role of acetylcholine in bipolar disorder.
+ACHE	drug	psychedelics	22200647	The question of whether <b>ibogaine</b> inhibits acetylcholinesterase (<strong>AChE</strong>) is of pharmacological and toxicological significance.
+ACHE	drug	psychedelics	22200647	<b>Ibogaine</b> inhibited <strong>AChE</strong> with an IC(50) of 520±40 μM.
+ACHE	drug	psychedelics	22200647	<b>Ibogaine</b>'s inhibition of <strong>AChE</strong> is physiologically negligible, and does not appear to account for observations of functional effects in animals and humans that might otherwise suggest the possible involvement of pathways linked to muscarinic acetylcholine transmission.
+ACHE	drug	cocaine	22173266	This study was carried out to evaluate the effects of donepezil (which selectively inhibits <strong>AChE</strong>) and rivastigmine (which inhibits both <strong>AChE</strong> and butyrylcholinesterase) on <b>cocaine</b> self administration.
+ACHE	drug	benzodiazepine	21971501	Therapeutic treatment comprising of HI 6, atropine and <b>diazepam</b> has completely protected animals from death and reactivated soman inhibited <strong>AChE</strong> up to 40% in the plasma and RBC.
+ACHE	addiction	withdrawal	21633116	Effects on ChAT and <strong>AChE</strong> were dependent on the brain region and restricted to the <b>withdrawal</b> period: There were increased activities in the midbrain on PN30.
+ACHE	drug	nicotine	21116174	The purpose of this study was to investigate whether <strong>AChE</strong> Is with nicotinic acetylcholine receptor positive allosteric modulator properties generalize to the discriminative stimulus effect of <b>nicotine</b> in rats.
+ACHE	drug	nicotine	21116174	Our study showed that these three <strong>AChE</strong> Is partially generalized to the <b>nicotine</b> stimulus without a significant distinction between <strong>AChE</strong> Is with or without APL properties.
+ACHE	drug	benzodiazepine	20929049	Standard treatment for acute poisoning involves administration of intravenous atropine, oxime 2 PAM to counter <strong>AChE</strong> inhibition and <b>diazepam</b> for CNS protection.
+ACHE	drug	nicotine	20309727	The present study extends that finding by examining the effects of <b>nicotine</b> (Nic), Alc, and their combination on ChAT and acetylcholinesterase (<strong>AChE</strong>) in the frontal cortex and hippocampus of rat.
+ACHE	drug	cocaine	19836169	Because <strong>AChE</strong> inhibitors have been shown to decrease the reinforcing effects of <b>cocaine</b> in animals, our hypothesis was that pretreatment with donepezil would attenuate the perceived value and other positive subjective effects of <b>cocaine</b>.
+ACHE	addiction	reward	19836169	Because <strong>AChE</strong> inhibitors have been shown to decrease the <b>reinforcing</b> effects of cocaine in animals, our hypothesis was that pretreatment with donepezil would attenuate the perceived value and other positive subjective effects of cocaine.
+ACHE	drug	alcohol	19576740	The ethyl acetate fraction of the <b>alcohol</b> extract (IC50 53.00 +/  17.33microg/ml), and total alkaloid fraction (IC50 9.23+/ 6.08microg/ml) showed potential <strong>AChE</strong> inhibition.
+ACHE	addiction	intoxication	18784370	Management of this <b>intoxication</b> includes: (i) pretreatment with reversible blockers of <strong>AChE</strong>, (ii) blockade of muscarinic receptors with atropine, and (iii) facilitation of GABA(A) receptor signal transduction by benzodiazepines.
+ACHE	drug	nicotine	18776044	In summary, we found that <b>nicotine</b> acts as an anxiolytic in TgR mice but not in control mice and that continuously overexpressed <strong>AChE</strong> R regulates striatal gene expression, modulating cholinergic signaling and stress related pathways.
+ACHE	addiction	intoxication	18465647	Cholinergic drugs are currently in use, or in advanced stages of development, for the chronic treatment of Alzheimer's disease (AD) and myasthenia gravis, as well as for the treatment of acute <b>intoxication</b> with organophosphate or carbamate inhibitors of the ACh hydrolyzing enzyme acetyl cholinesterase (<strong>AChE</strong>).
+ACHE	drug	amphetamine	18248689	Of interest, recent data suggest that acetylcholinesterase (<strong>AChE</strong>) inhibitors attenuate <b>Meth</b> seeking behaviour in rats.
+ACHE	addiction	relapse	18248689	Of interest, recent data suggest that acetylcholinesterase (<strong>AChE</strong>) inhibitors attenuate Meth <b>seeking</b> behaviour in rats.
+ACHE	drug	amphetamine	18248689	We conducted this study in order to determine the safety (adverse events, mood changes, cardiovascular effects) and preliminary efficacy (subjective effects) of the <strong>AChE</strong> inhibitor rivastigmine (Riv) when tested in combination with <b>Meth</b>.
+ACHE	drug	amphetamine	18207225	We conducted a double blind, placebo controlled, between groups investigation of the acetylcholinesterase (<strong>AChE</strong>) inhibitor rivastigmine in non treatment seeking volunteers who met criteria for <b>methamphetamine</b> abuse or dependence.
+ACHE	addiction	dependence	18207225	We conducted a double blind, placebo controlled, between groups investigation of the acetylcholinesterase (<strong>AChE</strong>) inhibitor rivastigmine in non treatment seeking volunteers who met criteria for methamphetamine abuse or <b>dependence</b>.
+ACHE	addiction	relapse	18207225	We conducted a double blind, placebo controlled, between groups investigation of the acetylcholinesterase (<strong>AChE</strong>) inhibitor rivastigmine in non treatment <b>seeking</b> volunteers who met criteria for methamphetamine abuse or dependence.
+ACHE	drug	alcohol	17888594	Here we investigated the in vitro and in vivo effects promoted by <b>ethanol</b> and its metabolites on zebrafish brain acetylcholinesterase (<strong>AChE</strong>).
+ACHE	drug	alcohol	17888594	There was a significant increase of <strong>AChE</strong> (33%) activity after acute 1% <b>ethanol</b> exposure.
+ACHE	drug	alcohol	17888594	However, <b>ethanol</b> in vitro did not alter <strong>AChE</strong> activity.
+ACHE	drug	alcohol	17888594	Furthermore, the acute <b>ethanol</b> exposure was able to inhibit <strong>AChE</strong> transcripts at 0.5% and 1%.
+ACHE	drug	alcohol	17888594	These findings suggest that the alterations on zebrafish <strong>AChE</strong> could reveal molecular mechanisms related to cholinergic signaling in <b>alcoholism</b>.
+ACHE	addiction	intoxication	17289099	In this study, we have evaluated donepezil hydrochloride, a partial reversible inhibitor of acetylcholinesterase (<strong>AChE</strong>) clinically used for treating Alzheimer's disease, in combination with procyclidine, used in treatment of Parkinson's disease and schizophrenia, as prophylaxis against <b>intoxication</b> by the nerve agent soman.
+ACHE	addiction	intoxication	17289099	The ACh concentration had returned to basal levels 24 h after soman <b>intoxication</b>, while <strong>AChE</strong> activity had recovered to 20% of control.
+ACHE	drug	amphetamine	16470869	Genetic identification of <strong>AChE</strong> as a positive modulator of addiction to the psychostimulant D <b>amphetamine</b> in zebrafish.
+ACHE	addiction	addiction	16470869	Genetic identification of <strong>AChE</strong> as a positive modulator of <b>addiction</b> to the psychostimulant D amphetamine in zebrafish.
+ACHE	addiction	addiction	16470869	Our observations demonstrate that the cholinergic system modulates drug induced reward in zebrafish, and identify genetically <strong>AChE</strong> as a promising target for systemic therapies against <b>addiction</b> to psychostimulants.
+ACHE	addiction	reward	16470869	Our observations demonstrate that the cholinergic system modulates drug induced <b>reward</b> in zebrafish, and identify genetically <strong>AChE</strong> as a promising target for systemic therapies against addiction to psychostimulants.
+ACHE	addiction	intoxication	15521192	For nerve agent <b>intoxication</b>, <strong>AChE</strong> in the red blood cell is more diagnostically important than BuChE activity in the plasma.
+ACHE	drug	benzodiazepine	15036754	The rats received <strong>AChE</strong> reactivator pralidoxime 2 chloride (2PAM) (30.0 mg/kg BW), anticonvulsant <b>diazepam</b> (2.0 mg/kg BW), A(1) adenosine receptor agonist N(6) cyclopentyl adenosine (CPA) (2.0 mg/kg BW), NMDA receptor antagonist dizocilpine maleate (+ MK801 hydrogen maleate) (2.0 mg/kg BW) or their combinations with cholinolytic drug atropine sulfate (50.0 mg/kg BW) immediately or 30 min after the single SC injection of DFP.
+ACHE	drug	cocaine	12721372	Remarkably, acetylcholinesterase (<strong>AChE</strong>) inhibitors that act on the brain <strong>AChE</strong> suppressed both <b>cocaine</b>  and morphine induced conditioned place preference and blocked the induction and persistence of <b>cocaine</b> evoked hyperlocomotion.
+ACHE	drug	opioid	12721372	Remarkably, acetylcholinesterase (<strong>AChE</strong>) inhibitors that act on the brain <strong>AChE</strong> suppressed both cocaine  and <b>morphine</b> induced conditioned place preference and blocked the induction and persistence of cocaine evoked hyperlocomotion.
+ACHE	drug	cocaine	12721372	These results demonstrate that centrally active <strong>AChE</strong> inhibitors prevent long lasting behavioral abnormalities associated with <b>cocaine</b> and morphine addictions by potentiating the actions of ACh released from the NAc cholinergic neurons.
+ACHE	drug	opioid	12721372	These results demonstrate that centrally active <strong>AChE</strong> inhibitors prevent long lasting behavioral abnormalities associated with cocaine and <b>morphine</b> addictions by potentiating the actions of ACh released from the NAc cholinergic neurons.
+ACHE	addiction	addiction	12721372	Centrally active <strong>AChE</strong> inhibitors could thus be approached as novel and potential therapeutic agents for drug <b>addiction</b>.
+ACHE	drug	opioid	12185962	For example, anisodamine possesses good effects in the treatment of septic shock and <b>morphine</b> addiction; 3 n butylphthalide isolated from seeds of celery was shown to be a new cerebral anti ischemic agent; indirubin was identified as an anti leukemic drug with no inhibition of bone marrow; huperzine is a potent and reversible inhibitor of acetylcholinesterase (<strong>AChE</strong>) and its selective action is superior to that of donepezil; clausenamide was shown to be a potassium channel blocker, its nootropic effect was 50 100 times more potent than that of piracetam; bicyclol was synthesized from schizandrin C isolated from Fructus schizandrae.
+ACHE	addiction	addiction	12185962	For example, anisodamine possesses good effects in the treatment of septic shock and morphine <b>addiction</b>; 3 n butylphthalide isolated from seeds of celery was shown to be a new cerebral anti ischemic agent; indirubin was identified as an anti leukemic drug with no inhibition of bone marrow; huperzine is a potent and reversible inhibitor of acetylcholinesterase (<strong>AChE</strong>) and its selective action is superior to that of donepezil; clausenamide was shown to be a potassium channel blocker, its nootropic effect was 50 100 times more potent than that of piracetam; bicyclol was synthesized from schizandrin C isolated from Fructus schizandrae.
+ACHE	drug	nicotine	10939190	A bivaried analysis was used to analyse the <strong>AchE</strong> activity and its association with gestational age, body mass index, <b>tobacco</b> addiction, and use of pesticides at home, and hemoglobin concentration.
+ACHE	addiction	addiction	10939190	A bivaried analysis was used to analyse the <strong>AchE</strong> activity and its association with gestational age, body mass index, tobacco <b>addiction</b>, and use of pesticides at home, and hemoglobin concentration.
+ACHE	drug	nicotine	10939190	There was no difference in <strong>AchE</strong> activity by <b>tobacco</b> addiction, hemoglobin levels, and use of insecticides at home.
+ACHE	addiction	addiction	10939190	There was no difference in <strong>AchE</strong> activity by tobacco <b>addiction</b>, hemoglobin levels, and use of insecticides at home.
+ACHE	drug	nicotine	10939190	We determined that possible confounding factors like <b>tobacco</b> addiction and use of pesticides at home have no significant effects over <strong>AchE</strong> activity.
+ACHE	addiction	addiction	10939190	We determined that possible confounding factors like tobacco <b>addiction</b> and use of pesticides at home have no significant effects over <strong>AchE</strong> activity.
+ACHE	drug	opioid	10661498	In separate groups of rats, non toxic doses (50 and 250 microg/kg) of the acetylcholinesterase (<strong>AChE</strong>) inhibitor, diisopropylflurophosphate (DFP) were administered as single daily injections concomitant with the <b>morphine</b> infusion.
+ACHE	addiction	withdrawal	10661498	The apparent anti <b>withdrawal</b> effect of DFP was not reproduced by the selective peripherally acting <strong>AChE</strong> inhibitor, echothiophate, although both compounds effectively reduced the expression of certain other <b>withdrawal</b> symptoms.
+ACHE	drug	opioid	8149590	The effect of prenatal exposure to <b>methadone</b> via maternal osmotic minipumps on the expression of acetylcholinesterase (<strong>AChE</strong>) and choline acetyltransferase (ChAT) has been studied by light microscopy in the striatum of male and female rats.
+ACHE	addiction	intoxication	1631893	In a second experiment similarly treated marmosets were euthanized at 5 min (three saline treated animals) or at 10 min (three HI 6 treated animals) after the soman <b>intoxication</b> to enable the determination of acetylcholinesterase (<strong>AChE</strong>) activities in diaphragm and brain tissue.
+ACHE	drug	alcohol	1786855	Depending on the hydrophobicity and the site specificity of an inhibitor, striking differences were found in <b>ethanol</b> acetylcholinesterase (<strong>AChE</strong>) inhibitor interactions.
+ACHE	drug	alcohol	1786855	Their abilities to inhibit <strong>AChE</strong> activity were enhanced by <b>ethanol</b>.
+ACHE	drug	alcohol	1786855	Such an enhancement could not result from combining individual perturbations from <b>ethanol</b> and propidium or edrophonium, since <b>ethanol</b> itself increased the <strong>AChE</strong> activity.
+ACHE	drug	benzodiazepine	2364909	<b>Diazepam</b> (50 mg/kg, ip) slightly modified <strong>AchE</strong> and abolished hyperglycemia, hyperlactacidemia, and glycogenolytic effects.
+ACHE	addiction	sensitization	2474836	Iodide exerted a modest inhibition of photohemolysis and loss of <strong>AchE</strong> sensitized by E16, but had virtually no influence on <b>sensitization</b> by EYMA.
+ACHE	drug	alcohol	3683767	Changes in the activity of acetylcholinesterase (<strong>AChE</strong>) of the isolated vas deferens from normal, castrated, morphine and <b>ethanol</b> tolerant rats were studied.
+ACHE	drug	opioid	3683767	Changes in the activity of acetylcholinesterase (<strong>AChE</strong>) of the isolated vas deferens from normal, castrated, <b>morphine</b> and ethanol tolerant rats were studied.
+ACHE	drug	alcohol	3683767	Three days after the termination of treatment with morphine and on the last day of treatment with <b>ethanol</b>, a significant inhibition of the activity of <strong>AChE</strong> was detected.
+ACHE	drug	opioid	3683767	Three days after the termination of treatment with <b>morphine</b> and on the last day of treatment with ethanol, a significant inhibition of the activity of <strong>AChE</strong> was detected.
+ACHE	drug	opioid	3683767	This reduction in the enzymatic activity persisted in <b>morphine</b> tolerant rats for 15 days, but not for 30 days, at which time the levels of <strong>AChE</strong> were determined to be normal.
+ACHE	drug	alcohol	3683767	During withdrawal from morphine or <b>ethanol</b>, the levels of <strong>AChE</strong> were significantly increased.
+ACHE	drug	opioid	3683767	During withdrawal from <b>morphine</b> or ethanol, the levels of <strong>AChE</strong> were significantly increased.
+ACHE	addiction	withdrawal	3683767	During <b>withdrawal</b> from morphine or ethanol, the levels of <strong>AChE</strong> were significantly increased.
+ACHE	drug	alcohol	3683767	The results indicate that morphine and <b>ethanol</b> may be inducing changes in the feedback mechanism which regulates the levels of <strong>AChE</strong> at post synaptic sites, and these changes could play an important role in the development of tolerance to morphine and to <b>ethanol</b>.
+ACHE	drug	opioid	3683767	The results indicate that <b>morphine</b> and ethanol may be inducing changes in the feedback mechanism which regulates the levels of <strong>AChE</strong> at post synaptic sites, and these changes could play an important role in the development of tolerance to <b>morphine</b> and to ethanol.
+ACHE	drug	benzodiazepine	3004260	The effective dose range for physostigmine, 3 12 mumol/kg, is close to concentrations of this agent that inhibit activity in solubilized preparations of <strong>AChE</strong> from rabbit cortex, 1 3 X 10( 8) M. However, physostigmine, 10( 9)  10( 4) M, failed to displace 3H <b>flunitrazepam</b> from specific binding sites on membranes prepared from rabbit cerebral cortex.
+ACHE	drug	alcohol	6123169	Albino mongrel rats were used for the determination of the gamma glutamyl transferase (gamma GTF) and acetylcholine esterase (<strong>AChE</strong>) activities in various brain areas (cerebral hemispheres, cerebellum, hippocampus, brain stem) during acute (1.5; 4 and 6 g/kg i. p.) and chronic (15 months) <b>alcoholic</b> intoxication and <b>alcohol</b> withdrawal (24 48 h, 4 and 8 days).
+ACHE	addiction	intoxication	6123169	Albino mongrel rats were used for the determination of the gamma glutamyl transferase (gamma GTF) and acetylcholine esterase (<strong>AChE</strong>) activities in various brain areas (cerebral hemispheres, cerebellum, hippocampus, brain stem) during acute (1.5; 4 and 6 g/kg i. p.) and chronic (15 months) alcoholic <b>intoxication</b> and alcohol withdrawal (24 48 h, 4 and 8 days).
+ACHE	addiction	withdrawal	6123169	Albino mongrel rats were used for the determination of the gamma glutamyl transferase (gamma GTF) and acetylcholine esterase (<strong>AChE</strong>) activities in various brain areas (cerebral hemispheres, cerebellum, hippocampus, brain stem) during acute (1.5; 4 and 6 g/kg i. p.) and chronic (15 months) alcoholic intoxication and alcohol <b>withdrawal</b> (24 48 h, 4 and 8 days).
+ACHE	drug	alcohol	6123169	The activity of gamma GTF grew in all brain areas during chronic <b>ethanol</b> intoxication; the activity of <strong>AChE</strong> was also enhanced in three brain areas but it was diminished in cerebral hemispheres.
+ACHE	addiction	intoxication	6123169	The activity of gamma GTF grew in all brain areas during chronic ethanol <b>intoxication</b>; the activity of <strong>AChE</strong> was also enhanced in three brain areas but it was diminished in cerebral hemispheres.
+ACHE	drug	alcohol	6123169	A tendency to normalization of the gamma GTF and <strong>AChE</strong> activities is manifested 4 8 days after <b>alcohol</b> withdrawal.
+ACHE	addiction	withdrawal	6123169	A tendency to normalization of the gamma GTF and <strong>AChE</strong> activities is manifested 4 8 days after alcohol <b>withdrawal</b>.
+ACHE	drug	alcohol	7198309	The activities of acetylcholinesterase (<strong>AChE</strong>) and choline acetyltransferase (ChaT) in the cerebral cortex, cerebellum, hypothalamus, hippocampus, midbrain and pons of adult, male mice injected with 2 g/kg <b>ethanol</b> and of control mice injected with physiological saline, were determined by spectrophotometric methods.
+ACHE	drug	alcohol	7198309	All animals were killed 30 min after injection between 11.00 h and 12.00 h. Results show that the acute dose of <b>ethanol</b> significantly decreased <strong>AChE</strong> activity only in the cerebral cortex whereas ChaT activity was reduced in the cerebral cortex, hypothalamus and hippocampus.
+ACHE	drug	alcohol	7198309	These findings show that the effect of an acute dose of <b>ethanol</b> on the cholinergic system of mouse brain is mediated through its effect on <strong>AChE</strong> and ChaT in specific regions.
+ACHE	drug	alcohol	7300947	This difference between fast and slow synapses was more pronounced after <strong>AChE</strong> inhibition or after <b>ethanol</b> treatment.
+ACHE	drug	nicotine	6156227	The content of acetylcholine (ACh) and activities of the cholinergic enzymes choline (acetyltransferase (CAT) and ACh esterase (<strong>AChE</strong>) were studied in intact and crushed rat sciatic nerve after chronic <b>nicotine</b> administration and withdrawal 2 days before the final experiment.
+ACHE	addiction	withdrawal	6156227	The content of acetylcholine (ACh) and activities of the cholinergic enzymes choline (acetyltransferase (CAT) and ACh esterase (<strong>AChE</strong>) were studied in intact and crushed rat sciatic nerve after chronic nicotine administration and <b>withdrawal</b> 2 days before the final experiment.
+ACHE	drug	nicotine	6156227	In the chronic <b>nicotine</b> group, ACh levels and <strong>AChE</strong> activity of uncrushed nerve were significantly decreased as compared to the controls.
+ACHE	drug	nicotine	6156227	After withdrawal of <b>nicotine</b> for 2 days the ACh content of both uncrushed and 12 hours crushed nerves were further decreased, while <strong>AChE</strong> was instead increased to control (uncrushed) or even supranormal (18 hour crush) levels.
+ACHE	addiction	withdrawal	6156227	After <b>withdrawal</b> of nicotine for 2 days the ACh content of both uncrushed and 12 hours crushed nerves were further decreased, while <strong>AChE</strong> was instead increased to control (uncrushed) or even supranormal (18 hour crush) levels.
+RTN4	drug	nicotine	32608084	Eighty four never <b>smoking</b> adolescents (nonexposed = 32, exposed = 52) performed a <b>smoking</b> cue reactivity, a Go/<strong>NoGo</strong>, and a monetary incentive delay (MID) task while ERPs were measured.
+RTN4	addiction	reward	32608084	Eighty four never smoking adolescents (nonexposed = 32, exposed = 52) performed a smoking cue reactivity, a Go/<strong>NoGo</strong>, and a monetary <b>incentive</b> delay (MID) task while ERPs were measured.
+RTN4	drug	alcohol	32581896	Sixty seven (36 females) first year university students, classified as BDs (n = 32) or controls (n = 35), underwent fMRI as they performed an <b>alcohol</b> cued Go/<strong>NoGo</strong> task in which pictures of <b>alcoholic</b> or non <b>alcoholic</b> beverages were presented as Go or <strong>NoGo</strong> stimuli.
+RTN4	drug	alcohol	32276071	We addressed these issues using a double blind, randomized, parallel, placebo controlled experimental design comparing the behavioral and electrical neuroimaging acute effects of 0.6 vs 0.02 ​g/kg <b>alcohol</b> intake recorded in 65 healthy adults during an inhibitory control Go/<strong>NoGo</strong> task.
+RTN4	drug	nicotine	31995811	<b>Nicotine</b> dependence (trait) and acute nicotinic stimulation (state) modulate attention but not inhibitory control: converging fMRI evidence from Go <strong>Nogo</strong> and Flanker tasks.
+RTN4	addiction	dependence	31995811	Nicotine <b>dependence</b> (trait) and acute nicotinic stimulation (state) modulate attention but not inhibitory control: converging fMRI evidence from Go <strong>Nogo</strong> and Flanker tasks.
+RTN4	drug	nicotine	31995811	Here we examine the effects of <b>nicotine</b> dependence (trait; <b>smokers</b> (n = 24) vs. non <b>smoking</b> controls; n = 20) and acute nicotinic stimulation (state; administration of <b>nicotine</b> and varenicline, two FDA approved <b>smoking</b> cessation aids, during abstinence), on two well established tests of inhibitory control, the Go <strong>Nogo</strong> task and the Flanker task, during fMRI scanning.
+RTN4	addiction	dependence	31995811	Here we examine the effects of nicotine <b>dependence</b> (trait; smokers (n = 24) vs. non smoking controls; n = 20) and acute nicotinic stimulation (state; administration of nicotine and varenicline, two FDA approved smoking cessation aids, during abstinence), on two well established tests of inhibitory control, the Go <strong>Nogo</strong> task and the Flanker task, during fMRI scanning.
+RTN4	drug	nicotine	31995811	Go <strong>Nogo</strong> fMRI results showed decreased inhibition related neural activity in right anterior insula and right putamen in <b>smokers</b> and decreased dorsal anterior cingulate cortex activity on <b>nicotine</b> across groups.
+RTN4	drug	opioid	31915860	Sixty seven male HAs performed a modified Go/<strong>NoGo</strong> task in which a motor response to frequent Go targets and no response to rare <strong>NoGo</strong> targets were required and a Go or <strong>NoGo</strong> target was displayed after either a <b>heroin</b> related or a neutral picture presented for the 200 ms and 600 ms SOAs.
+RTN4	drug	alcohol	31866805	<b>Alcohol</b> use disorder (AUD) is characterized by increased impulsivity, which is multifactorial and can be assessed by tests like the delay discounting, Go <strong>Nogo</strong>, and stop signal task (SST).
+RTN4	drug	alcohol	31864068	Following real and sham tDCS placing the anode over the right and cathode over the left DLPFC, a rewarded Go/<strong>NoGo</strong> paradigm was administrated to provoke behavioral biases (irrespective of the task goal) After the cognitive paradigm, <b>alcohol</b> consumption was examined using a beer taste test.
+RTN4	drug	alcohol	31752082	Electrophysiological Correlates of an <b>Alcohol</b> Cued Go/<strong>NoGo</strong> Task: A Dual Process Approach to Binge Drinking in University Students.
+RTN4	addiction	intoxication	31752082	Electrophysiological Correlates of an Alcohol Cued Go/<strong>NoGo</strong> Task: A Dual Process Approach to <b>Binge</b> Drinking in University Students.
+RTN4	drug	alcohol	31752082	First year university students (n = 151, 54 % females) classified as binge drinkers (n = 71, ≥6 binge drinking episodes, defined as 5/7 standard drinks per occasion in the last 180 days) and controls (n = 80, <6 binge drinking episodes in the last 180 days) performed a beverage Go/<strong>NoGo</strong> task (pictures of <b>alcoholic</b> and nonalcoholic drinks were presented according to the condition as Go or <strong>NoGo</strong> stimuli; Go probability = 0.75) during event related potential recording.
+RTN4	addiction	intoxication	31752082	First year university students (n = 151, 54 % females) classified as <b>binge</b> drinkers (n = 71, ≥6 <b>binge</b> drinking episodes, defined as 5/7 standard drinks per occasion in the last 180 days) and controls (n = 80, <6 <b>binge</b> drinking episodes in the last 180 days) performed a beverage Go/<strong>NoGo</strong> task (pictures of alcoholic and nonalcoholic drinks were presented according to the condition as Go or <strong>NoGo</strong> stimuli; Go probability = 0.75) during event related potential recording.
+RTN4	drug	alcohol	31752082	In binge drinkers but not controls, the amplitude of the anterior N2 <strong>NoGo</strong> was larger in response to nonalcohol than in response to <b>alcohol</b> pictures.
+RTN4	addiction	intoxication	31752082	In <b>binge</b> drinkers but not controls, the amplitude of the anterior N2 <strong>NoGo</strong> was larger in response to nonalcohol than in response to alcohol pictures.
+RTN4	drug	alcohol	31611789	In experiment 1, we validated our experimental paradigm (electroencephalography combined with a modified Go/<strong>NoGo</strong> task using images of <b>alcoholic</b> and nonalcoholic drinks as prime stimuli) in 20 healthy adults to ensure that our protocol is suitable for assessing the behavioral and neural aspects of executive control.
+RTN4	drug	nicotine	31474901	12 h Abstinence Induced ERP Changes in Young <b>Smokers</b>: Electrophysiological Evidence From a Go/<strong>NoGo</strong> Study.
+RTN4	drug	nicotine	31474901	No significant changes were found in the number of <strong>NoGo</strong> errors and the response time of Go in young <b>smokers</b> after 12 h of abstinence.
+RTN4	drug	alcohol	31277683	After baseline assessment, participants are randomly assigned to one of three computerized Go <strong>NoGo</strong> based inhibition training interventions (two <b>alcohol</b> specific versions with different Go/<strong>NoGo</strong> ratios, or neutral control training) and one of two intervention times (morning/afternoon), resulting in six study arms.
+RTN4	drug	nicotine	31069895	In addition, greater commission errors on the Go/<strong>NoGo</strong> task were correlated with reduced neural response to <b>smoking</b> cues in the right dlPFC only among those with obesity.
+RTN4	drug	alcohol	30376829	To test this, 108 participants (Mean age = 21.7, range = 16 27), whom were both drinkers and non drinkers performed a modified Go/<strong>NoGo</strong> task tailored to measure distraction and response inhibition in the presence of <b>alcohol</b> cues relative to neutral stimuli.
+RTN4	drug	nicotine	29450255	In the current study, <b>tobacco</b> <b>smokers</b> (SMK; n = 22) and non <b>smoking</b> controls (CON; n = 19) completed a Go/<strong>NoGo</strong> task involving <b>smoking</b> cues during a functional magnetic resonance imaging (fMRI) scan.
+RTN4	drug	nicotine	29450255	We evaluated pre cessation brain activity during <strong>NoGo</strong> trials in <b>smokers</b> who were versus were not able to quit <b>smoking</b>.
+RTN4	drug	nicotine	29450255	However, compared to SMK who relapsed, SMK who attained biochemically validated abstinence at the end of the <b>smoking</b> cessation trial had greater neural activation in the anterior insula during <strong>NoGo</strong> trials specifically with <b>smoking</b> related cues.
+RTN4	drug	nicotine	29402679	This study quantified the effects of age of <b>smoking</b> onset on response impulsivity and inhibitory control using a novel <b>smoking</b> Go/<strong>NoGo</strong> task (Luijten et al., 2011).
+RTN4	drug	nicotine	29402679	<b>Nicotine</b> deprived adult EOS (n = 10) and LOS (n = 10) and adult healthy non <b>smokers</b> (HNS; n = 10) were shown <b>smoking</b> related and neutral images with either a blue (Go) or yellow (<strong>NoGo</strong>) frame.
+RTN4	drug	nicotine	29402679	EOS also made more errors in inhibiting responses to <b>smoking</b> related (p ≤ 0.02) and neutral (p ≤ 0.02) <strong>NoGo</strong> trials.
+RTN4	drug	nicotine	29402679	EOS exhibited greater difficulty than LOS in responding accurately to Go stimuli and withholding responses to both <b>smoking</b> and neutral <strong>NoGo</strong> stimuli, indicating greater response impulsivity, poor attention, and deficits in response inhibition.
+RTN4	drug	nicotine	29370256	Immediately after this, they performed a <b>smoking</b> Go/<strong>NoGo</strong> task, while their brain activity was recorded.
+RTN4	drug	nicotine	29193059	Male adolescent rats were trained on the Go/<strong>NoGo</strong> task, then subjected to <b>nicotine</b> CPP, and then randomly separated into four groups: sedentary (SED), high  (HE), moderate  (ME), and low intensity (LE) exercise.
+RTN4	addiction	reward	29193059	Male adolescent rats were trained on the Go/<strong>NoGo</strong> task, then subjected to nicotine <b>CPP</b>, and then randomly separated into four groups: sedentary (SED), high  (HE), moderate  (ME), and low intensity (LE) exercise.
+RTN4	addiction	reward	29193059	MEs and HEs showed higher performance accuracy on <strong>NoGo</strong> and lower scores on <b>CPP</b> tasks.
+RTN4	addiction	reward	29193059	Expression of α7 nicotinic acetylcholine receptors (nAChRs) and downstream signaling molecules increased in MEs in prefrontal cortex but not hippocampus, with α7 nAChRs expression positively associated with <strong>NoGo</strong> accuracy and MWM probe test performance, but negatively correlated with <b>CPP</b> scores.
+RTN4	drug	alcohol	29044574	All subjects performed a Go/<strong>NoGo</strong> task involving neutral and <b>alcohol</b> related <strong>NoGo</strong> trials, while their brain activity was recorded using multichannel electroencephalography.
+RTN4	drug	alcohol	29044574	In subjects with strong craving, the conflict reflected in the <strong>NoGo</strong> N2 was enhanced in the <b>alcohol</b> related context.
+RTN4	addiction	relapse	29044574	In subjects with strong <b>craving</b>, the conflict reflected in the <strong>NoGo</strong> N2 was enhanced in the alcohol related context.
+RTN4	drug	nicotine	28826017	A <b>smoking</b> related background helps moderate <b>smokers</b> to focus: An event related potential study using a Go <strong>NoGo</strong> task.
+RTN4	drug	nicotine	28826017	ERPs were recorded during a visual Go <strong>NoGo</strong> task performed by 18 <b>smokers</b> and 23 controls, in which either a frequent Go signal (letter "M") or a rare No Go signal ("letter W") were superimposed on three different long lasting background contexts: black neutral, <b>smoking</b> related and non <b>smoking</b> related.
+RTN4	drug	nicotine	28826017	(1) <b>Smokers</b> performed worse and had an earlier <strong>NoGo</strong> N2 latency as compared to controls and independently of context, suggesting a general inhibition impairment; (2) with <b>smoking</b> related backgrounds specifically, <b>smokers</b> made fewer mistakes than they did in other contexts and displayed a larger <strong>NoGo</strong> P3 amplitude.
+RTN4	drug	nicotine	28440102	Thirty two <b>smokers</b> (17 low dependent and 15 dependent; cut off FTND of 4) and 28 non <b>smokers</b> performed a modified Go/<strong>NoGo</strong> task using <b>tobacco</b> related words and neutral words as stimuli.
+RTN4	drug	alcohol	28168896	Findings are congruent with event related oscillation studies showing reduced delta and/or theta oscillations in <b>alcoholics</b> during Go/<strong>NoGo</strong> tasks.
+RTN4	drug	nicotine	27917562	The present study is the first to delineate functional networks of the anterior and posterior putamen in a Go <strong>NoGo</strong> response inhibition task, and to examine differences between <b>smokers</b> (n = 25) and non <b>smokers</b> (n = 23) within these networks.
+RTN4	drug	cocaine	26037156	Compared with a placebo, <b>cocaine</b> yielded improved accuracy, quicker reaction times and an increased prefrontal <strong>NoGo</strong> P3 ERP.
+RTN4	drug	cannabinoid	26037156	<b>Cannabis</b> produced opposing results; slower reaction times, impaired accuracy and a reduction in the amplitude of the prefrontal <strong>NoGo</strong> P3.
+RTN4	drug	alcohol	27410426	Future studies may adapt the auditory Go/<strong>NoGo</strong> paradigm with specific acoustic stimuli (e.g., sound of opening a bottle) in order to address cognitive biases in particular disorders (e.g., <b>alcohol</b> dependence).
+RTN4	addiction	dependence	27410426	Future studies may adapt the auditory Go/<strong>NoGo</strong> paradigm with specific acoustic stimuli (e.g., sound of opening a bottle) in order to address cognitive biases in particular disorders (e.g., alcohol <b>dependence</b>).
+RTN4	drug	nicotine	27277662	Seventy two <b>smokers</b> viewed <b>smoking</b> and neutral pictures and performed a Go <strong>NoGo</strong> and an Eriksen Flanker task, while ERPs were measured using electroencephalography.
+RTN4	drug	alcohol	27000120	Thirty recently detoxified patients with <b>alcohol</b> addiction, and 31 healthy control subjects, were assessed in a Go and a <strong>NoGo</strong> condition, each using three visual stimuli: tea, juice and beer.
+RTN4	addiction	addiction	27000120	Thirty recently detoxified patients with alcohol <b>addiction</b>, and 31 healthy control subjects, were assessed in a Go and a <strong>NoGo</strong> condition, each using three visual stimuli: tea, juice and beer.
+RTN4	drug	alcohol	27000120	Additionally, patients' heightened N170 amplitudes in response to the <b>alcohol</b> related (beer) stimulus were found only under the <strong>NoGo</strong> condition, where subjects had to react to the frequent tea stimulus and ignore the beer and the juice stimuli, thus resulting in a condition x stimulus x group interaction.
+RTN4	drug	alcohol	27000120	Patients reporting relapse in a 3 month follow up assessment showed larger <strong>NoGo</strong> N170 <b>alcohol</b> cue related ERP amplitudes and increased depression scores as compared to patients who stayed abstinent.
+RTN4	addiction	relapse	27000120	Patients reporting <b>relapse</b> in a 3 month follow up assessment showed larger <strong>NoGo</strong> N170 alcohol cue related ERP amplitudes and increased depression scores as compared to patients who stayed abstinent.
+RTN4	drug	opioid	26625401	As a case study, the method was applied to electroencephalography (EEG) data collected during a GO/<strong>NOGO</strong> cognitive task performed by untreated opiate addicts, those undergoing <b>methadone</b> maintenance treatment (MMT) for opiate dependence and a healthy control group.
+RTN4	addiction	dependence	26625401	As a case study, the method was applied to electroencephalography (EEG) data collected during a GO/<strong>NOGO</strong> cognitive task performed by untreated opiate addicts, those undergoing methadone maintenance treatment (MMT) for opiate <b>dependence</b> and a healthy control group.
+RTN4	drug	nicotine	26528200	A number of studies involving the use of Go/<strong>NoGo</strong> and stop signal paradigms have shown that <b>smokers</b> have reduced response inhibition for cigarette related cues.
+RTN4	drug	nicotine	26093534	Inhibition control impairments in adolescent <b>smokers</b>: electrophysiological evidence from a Go/<strong>NoGo</strong> study.
+RTN4	drug	nicotine	26093534	By using relatively homogenous groups of adolescent <b>smokers</b> (n = 18) and matched nonsmokers (n = 18), we employed event related potentials (ERP) to investigate the N200 and P300 amplitude and latency differences during a Go/<strong>NoGo</strong> task between the adolescent <b>smokers</b> and nonsmokers.
+RTN4	drug	nicotine	26093534	Relative to nonsmokers, more <strong>NoGo</strong> response errors, reduced <strong>NoGo</strong> P300 amplitude, and longer P300 latency were observed in adolescent <b>smokers</b>.
+RTN4	drug	nicotine	26093534	Correlation analysis revealed that the <strong>NoGo</strong> P300 amplitudes were significantly correlated with <strong>NoGo</strong> errors in both adolescent <b>smokers</b> and nonsmokers.
+RTN4	drug	opioid	28911381	In order to investigate the response inhibition functions in <b>heroin</b> addicts who were treated with <b>methadone</b> maintenance, electroencephalography (EEG) was used to examine 14 <b>heroin</b> addicts treated with <b>methadone</b> maintenance (HDM), 17 <b>heroin</b> addicts (HD), and 18 healthy controls (HC) in an equiprobability Go∖<strong>NoGo</strong> task.
+RTN4	addiction	aversion	25805975	This task presented emotional distractor pictures (<b>aversive</b> vs. neutral) simultaneously with Go/<strong>NoGo</strong> stimuli (square vs. circle) that required a button press or withholding of the press, respectively.
+RTN4	drug	nicotine	25542919	Reduced Influence of Monetary Incentives on Go/<strong>NoGo</strong> Performance During <b>Smoking</b> Abstinence.
+RTN4	drug	nicotine	25542919	Eighteen <b>smokers</b> performed an incentivized Go/<strong>NoGo</strong> task on 2 occasions, once after <b>smoking</b> as usual prior to the session, and once after undergoing 12 hr abstinence.
+RTN4	addiction	reward	25542919	Participants could earn up to $5.00 ($2.50 per session) based on their performance on <b>reward</b> blocks of the Go/<strong>NoGo</strong> task.
+RTN4	addiction	addiction	25195081	The meta analysis used fixed effects models to integrate results from 97 studies that compared groups with heavy substance use or <b>addiction</b> like behaviours with healthy control participants on two experimental paradigms commonly used to assess response inhibition: the Go/<strong>NoGo</strong> task, and the Stop Signal Task (SST).
+RTN4	drug	alcohol	25189856	The <strong>NoGo</strong> N2 was larger for <b>alcohol</b> cues and acute <b>alcohol</b> decreased the amplitude of the <strong>NoGo</strong> N2 for <b>alcohol</b> cues.
+RTN4	drug	opioid	25171718	Participants with histories of illicit <b>heroin</b> use (n = 24), former <b>heroin</b> users stabilized on prescribed <b>methadone</b> (<b>methadone</b> maintenance treatment; MMT) (n = 29), licit <b>opioid</b> prescriptions for chronic pain without history of abuse or dependence (n = 28) and healthy controls (n = 28) were recruited and tested on a task battery that included measures of cognitive impulsivity (Cambridge Gambling Task, CGT), motor impulsivity (Affective Go/<strong>NoGo</strong>, AGN) and non planning impulsivity (Stockings of Cambridge, SOC).
+RTN4	addiction	dependence	25171718	Participants with histories of illicit heroin use (n = 24), former heroin users stabilized on prescribed methadone (methadone maintenance treatment; MMT) (n = 29), licit opioid prescriptions for chronic pain without history of abuse or <b>dependence</b> (n = 28) and healthy controls (n = 28) were recruited and tested on a task battery that included measures of cognitive impulsivity (Cambridge Gambling Task, CGT), motor impulsivity (Affective Go/<strong>NoGo</strong>, AGN) and non planning impulsivity (Stockings of Cambridge, SOC).
+RTN4	drug	alcohol	24835220	Event related potentials (ERPs) elicited by a Go/<strong>NoGo</strong> task were recorded twice within a 2 year interval in 57 undergraduate students (25 controls, 22 binge drinkers, and 10 ex binge drinkers) with no personal or family history of <b>alcoholism</b> or psychopathological disorders.
+RTN4	addiction	intoxication	24835220	Event related potentials (ERPs) elicited by a Go/<strong>NoGo</strong> task were recorded twice within a 2 year interval in 57 undergraduate students (25 controls, 22 <b>binge</b> drinkers, and 10 ex <b>binge</b> drinkers) with no personal or family history of alcoholism or psychopathological disorders.
+RTN4	drug	alcohol	24835220	The results showed that the amplitude of <strong>NoGo</strong> P3 over the frontal region correlated with an earlier age of onset of regular drinking as well as with greater quantity and speed of <b>alcohol</b> consumption.
+RTN4	drug	alcohol	24835220	Regression analysis showed that <strong>NoGo</strong> P3 amplitude was significantly predicted by the speed of <b>alcohol</b> intake and the age of onset of regular drinking.
+RTN4	addiction	intoxication	24835220	The group comparisons showed that, after maintaining a <b>binge</b> drinking pattern for at least 2 years, <b>binge</b> drinkers displayed significantly larger <strong>NoGo</strong> P3 amplitudes than controls, whereas ex <b>binge</b> drinkers were in an intermediate position between the two other groups (with no significant differences with respect to controls or <b>binge</b> drinkers).
+RTN4	drug	nicotine	24828276	Participants prenatally exposed to <b>nicotine</b> exhibited a weaker response in the anterior cingulate cortex (t168 = 4.46; peak Montreal Neurological Institute [MNI] coordinates x =  2, y = 20, z = 30; familywise error [FWE] corrected P = .003), the right inferior frontal gyrus (t168 = 3.65; peak MNI coordinates x = 44, y = 38, z = 12; FWE corrected P = .04), the left inferior frontal gyrus (t168 = 4.09; peak MNI coordinates x =  38, y = 36, z = 8; FWE corrected P = .009), and the supramarginal gyrus (t168 = 5.03; peak MNI coordinates x = 64, y =  28, z = 22; FWE corrected P = .02) during the processing of the <strong>NoGo</strong> compared to neutral stimuli, while presenting a decreased volume in the right inferior frontal gyrus.
+RTN4	drug	opioid	24750243	Using cognitive modelling to investigate the psychological processes of the Go/<strong>NoGo</strong> discrimination task in male abstinent <b>heroin</b> misusers.
+RTN4	drug	opioid	24750243	Four parameters representing the attention to wins, learning rate, response sensitivity and incentive of <b>heroin</b> related stimuli from the modified Go/<strong>NoGo</strong> discrimination task.
+RTN4	addiction	reward	24750243	Four parameters representing the attention to wins, learning rate, response sensitivity and <b>incentive</b> of heroin related stimuli from the modified Go/<strong>NoGo</strong> discrimination task.
+RTN4	drug	nicotine	24380760	The present study measured inhibitory control using a flanker task and a go <strong>nogo</strong> continuous performance tasks in daily dependent <b>smokers</b>, intermittent non dependent <b>smokers</b>, and nonsmokers.
+RTN4	addiction	addiction	23773427	The Monetary Incentive Go/<strong>NoGo</strong> (MI Go/<strong>NoGo</strong>) task was administered that provided three types of reward outcomes contingent upon inhibitory control performance over rewarding stimuli: inhibition failure was either followed by no monetary reward (neutral condition), a small monetary reward with immediate feedback (reward condition) or immediate monetary <b>punishment</b> (<b>punishment</b> condition).
+RTN4	addiction	reward	23773427	The Monetary <b>Incentive</b> Go/<strong>NoGo</strong> (MI Go/<strong>NoGo</strong>) task was administered that provided three types of <b>reward</b> outcomes contingent upon inhibitory control performance over rewarding stimuli: inhibition failure was either followed by no monetary <b>reward</b> (neutral condition), a small monetary <b>reward</b> with immediate feedback (<b>reward</b> condition) or immediate monetary punishment (punishment condition).
+RTN4	drug	amphetamine	23770273	Dynamic downregulation of <strong>Nogo</strong> receptor expression in the rat forebrain by <b>amphetamine</b>.
+RTN4	drug	alcohol	23709633	Reduced intra individual reaction time variability during a Go <strong>NoGo</strong> task in detoxified <b>alcohol</b> dependent patients after one right sided dorsolateral prefrontal HF rTMS session.
+RTN4	drug	alcohol	23709633	We examined the effect of a single right DLPFC HF rTMS session on commission errors, mean reaction times (RTs) and intra individual reaction time variability (IIRTV) during a Go <strong>NoGo</strong> task (50% Go/50% <strong>NoGo</strong> condition) in 29 <b>alcohol</b> dependent patients.
+RTN4	drug	alcohol	23200160	One hundred sixty four individuals with a range of drinking from non treatment seeking adults with problematic <b>alcohol</b> use to treatment seeking adults with <b>alcohol</b> dependence completed a Go/<strong>NoGo</strong> task while undergoing functional magnetic resonance imaging.
+RTN4	addiction	dependence	23200160	One hundred sixty four individuals with a range of drinking from non treatment seeking adults with problematic alcohol use to treatment seeking adults with alcohol <b>dependence</b> completed a Go/<strong>NoGo</strong> task while undergoing functional magnetic resonance imaging.
+RTN4	addiction	relapse	23200160	One hundred sixty four individuals with a range of drinking from non treatment <b>seeking</b> adults with problematic alcohol use to treatment <b>seeking</b> adults with alcohol dependence completed a Go/<strong>NoGo</strong> task while undergoing functional magnetic resonance imaging.
+RTN4	drug	nicotine	23194834	Haloperidol (2 mg), a dopamine D2/D3 receptor antagonist, and placebo were administered to 25 <b>smokers</b> and 25 non <b>smoking</b> controls in a double blind randomized cross over design while performing a Go/<strong>NoGo</strong> task during fMRI scanning.
+RTN4	drug	nicotine	23194834	In addition, <b>smokers</b> showed behavioral deficits on the Go/<strong>NoGo</strong> task as well as hypoactivity in the left IFG, right MFG and ACC after placebo, supporting the hypothesis of a hypoactive prefrontal system in <b>smokers</b>.
+RTN4	drug	nicotine	21526125	Deficits in inhibitory control in <b>smokers</b> during a Go/<strong>NoGo</strong> task: an investigation using event related brain potentials.
+RTN4	drug	nicotine	21526125	Participants (19 <b>smokers</b> and 20 non <b>smoking</b> controls) performed a <b>smoking</b> Go/<strong>NoGo</strong> task.
+RTN4	drug	nicotine	21526125	Reduced <strong>NoGo</strong> N2 amplitudes in <b>smokers</b> relative to controls were accompanied by decreased task performance, whereas no differences between groups were found in P3 amplitudes.
+RTN4	drug	cocaine	19830263	This study used a flanker task with <strong>NoGo</strong> elements to investigate frontal executive function deficits in 19 <b>cocaine</b> abusers.
+RTN4	drug	cocaine	19501630	<b>cocaine</b>) rewards were examined in four rhesus monkeys performing a visual Go <strong>Nogo</strong> decision task.
+RTN4	addiction	reward	19501630	Task related striatal neurons increased firing to one or more of the specific events that occurred within a trial represented by (1) Target stimuli (Go trials) or (2) Nogotarget stimuli (<strong>Nogo</strong> trials), and (3) <b>Reward</b> delivery for correct performance.
+RTN4	drug	alcohol	19250950	Only the <strong>NoGo</strong> P3 reduction was correlated with <b>alcohol</b> consumption.
+RTN4	drug	nicotine	19220487	This study examined differences in attentional processing between nonsmokers, satiated <b>smokers</b> and overnight <b>nicotine</b> deprived <b>smokers</b> by comparing the amplitude of the P300 (P3) component of the event related brain potential (ERP) elicited during a go <strong>nogo</strong> task.
+RTN4	drug	nicotine	19220487	Nonsmokers relative to <b>smokers</b> had greater <strong>nogo</strong> P3 amplitude.
+RTN4	addiction	withdrawal	19220487	Carrying the A1 allele at the dopamine receptor D2 (DRD2) Taq1A polymorphism site moderated the effects of <b>withdrawal</b> on <strong>nogo</strong> P3 amplitude, suggesting the A1 allele is a vulnerability marker for <b>withdrawal</b> related attentional deficits.
+RTN4	drug	opioid	18485592	We used functional magnetic resonance imaging (fMRI) to examine the neural substrates of response inhibition and competition in 18 healthy controls and assess the frontal neurocognition in 30 abstinent <b>heroin</b> dependents (AHD) as they performed a Go/<strong>NoGo</strong> Association task with reaction times recorded spontaneously.
+RTN4	drug	alcohol	18373725	Impulsive errors on a Go <strong>NoGo</strong> reaction time task: disinhibitory traits in relation to a family history of <b>alcoholism</b>.
+RTN4	drug	alcohol	18373725	We predicted that healthy young adults with a family history of <b>alcoholism</b> (FH+) who also displayed externalizing behavior characteristics (low scores on the California Psychological Inventory Sociability Scale; CPI So) would exhibit more impulsive responding (false alarms) on a Go <strong>NoGo</strong> reaction time task.
+RTN4	drug	alcohol	17826793	Sixteen healthy volunteers and 16 detoxified <b>alcohol</b> dependent patients completed an auditory go/<strong>nogo</strong> paradigm.
+RTN4	drug	cocaine	15590917	Using a GO <strong>NOGO</strong> response inhibition task in which working memory (WM) demands can be varied, we demonstrate that the compromised abilities of <b>cocaine</b> users to exert control over strong prepotent urges are associated with reduced activity in anterior cingulate and right prefrontal cortices, two regions thought to be critical for implementing cognitive control.
+RTN4	drug	cocaine	12944513	Cingulate hypoactivity in <b>cocaine</b> users during a GO <strong>NOGO</strong> task as revealed by event related functional magnetic resonance imaging.
+RTN4	drug	alcohol	12909389	The cognitive event related potentials were studied in a group of 55 <b>alcoholic</b> patients, paired in age and sex with a group of 18 control subjects, using a protocol oddball (visual and auditory) and a protocol VCN Go/<strong>Nogo</strong>.
+RTN4	drug	alcohol	12909389	Using a Go/<strong>Nogo</strong> paradigm, a significant difference on the final part of the VCN appears between <b>alcoholic</b> and pilot subjects.
+RTN4	drug	alcohol	9811199	The ERP field differed between <b>alcoholics</b> and controls in the Go condition (P < 0.05) and <strong>NoGo</strong> anteriorization in <b>alcoholics</b> was correlated inversely with Novelty Seeking in Cloninger's Temperament and Character Inventory (r= 0.67, P < 0.01).
+RTN4	addiction	relapse	9811199	The ERP field differed between alcoholics and controls in the Go condition (P < 0.05) and <strong>NoGo</strong> anteriorization in alcoholics was correlated inversely with Novelty <b>Seeking</b> in Cloninger's Temperament and Character Inventory (r= 0.67, P < 0.01).
+RTN4	drug	nicotine	8880370	<b>Smoking</b> did not differentially affect the dominance groups unless gender was taken into account, and the most striking interactions between <b>smoking</b> and dominance groups were noted for the <strong>NoGo</strong> trials.
+RTN4	drug	nicotine	8880370	As expected, <b>smoking</b> decreased the amplitude of the early component of the <strong>NoGo</strong> CNV for telic dominant women, but increased it for paratelic dominant women; no significant differences were found for the late component.
+RTN4	drug	benzodiazepine	6198668	<b>Chlordiazepoxide</b>, go <strong>nogo</strong> successive discrimination and brain biogenic amines in cats.
+RTN4	drug	benzodiazepine	6198668	<b>Chlordiazepoxide</b> (CDP; 0.4 mg/kg/day, per os) was administered to cats during either the acquisition (CDP 21 22 days) of a go <strong>nogo</strong> successive discrimination task (SD) or the performance (CDP 10 days) of the previously learned SD task.
+MCOLN1	drug	opioid	30835647	Case: The patient is a 56 year old Caucasian male with a history of opiate use disorder on treatment with <b>buprenorphine</b>/<b>naloxone</b> 8/2 <strong>mg 2</strong> times a day (BID) who was followed in an outpatient general psychiatry clinic that specializes in patients with co occurring substance use disorders.
+MCOLN1	drug	opioid	10098365	Conservative management including eliminating multiple nonessential medications (including the prochlorperazine); changing her <b>opioid</b> analgesic; providing a 24 hour companion: and administering low doses of haloperidol (0.5 <strong>mg 2</strong>.0 mg) were not effective in treating the patient's delirium.
+MCOLN1	drug	opioid	2308760	Eight patients with established lower limb postamputation stump pain were given lumbar intrathecal <b>fentanyl</b> 25 micrograms and lidocaine 70 <strong>mg 2</strong> weeks apart in an attempt to better understand the role of peripheral and central mechanisms in this condition.
+PSENEN	drug	opioid	24120272	The selective DOR agonist [d <strong>pen2</strong>, 5] enkephalin (DPDPE) significantly increased EAAT3 expression in C6δ cells and even reversed the decreased EAAT3 expression caused by chronic <b>morphine</b> exposure.
+PSENEN	drug	opioid	21983967	We also tested the effects of intrathecal <b>morphine</b> (μ agonist), DPDPE ([D <strong>Pen2</strong>, D Pen5] enkephalin, a δ agonist), U50488H (trans(+) 3,4 dichloro N methyl N [2 (1 pyrrolidinyl) cyclohexyl] benzacetamide methane sulfonate salt, a κ agonist), and ST 91 (2 [2,6 diethyl phenylamino] 2 imidazoline, an α(2) agonist) on PWL.
+PSENEN	drug	opioid	18598850	Drugs included the mu <b>opioid</b> agonists <b>morphine</b> and DAMGO ([d Ala2,NMePhe4,Gly ol5] enkephalin), the kappa <b>opioid</b> agonists spiradoline, bremazocine, and U69,593, and the delta <b>opioid</b> agonists BW 373U86 and DPDPE ([D <strong>Pen2</strong>, D Pen5] enkephalin).
+PSENEN	drug	opioid	16472257	Somatostatin acting via G(i)1 coupled sstr3 receptor, DPDPE ([D <strong>Pen2</strong>,D Pen5]enkephalin; where Pen is penicillamine) acting via G(i)2 coupled delta <b>opioid</b> receptors, and cyclopentyl adenosine acting via G(i)3 coupled adenosine A1 receptors preferentially activated PI3K (phosphoinositide 3 kinase) and ILK (integrin linked kinase), whereas ACh (acetylcholine) acting via G(i)3 coupled M2 receptors preferentially activated PI3K, Cdc42 (cell division cycle 42)/Rac1, PAK1 (p21 activated kinase 1) and p38 MAPK (mitogen activated protein kinase).
+PSENEN	drug	opioid	16290012	The present investigation evaluated the proactive influence of an intracerebroventricular injection of the <b>opioid</b> receptor agonist D <strong>Pen2</strong>, D Pen5 enkephalin (DPDPE) (0 microg, 0.005 microg, 1.0 microg or 2.5 microg) on locomotor behavior of mice following uncontrollable footshock (Shock) or novel shock chamber exposure (No Shock).
+PSENEN	drug	opioid	12903471	DPDPE(D <strong>Pen2</strong>, D Pen5 enkephalin), a delta <b>opioid</b> receptor agonist, and <b>morphine</b> acutely induced the increase in [Ca2+]i of NG LNCXiNOS cells.
+PSENEN	drug	opioid	12672796	Endogenous human delta <b>opioid</b> receptors (hDOR) are differentially regulated in terms of desensitization by peptide ([d <strong>Pen2</strong>,5]enkephalin (DPDPE) and Deltorphin I) and alkaloid (etorphine) agonists in the neuroblastoma cell line SK N BE (Allouche, S., Roussel, M., Marie, N., and Jauzac, P. (1999) Eur.
+PSENEN	drug	opioid	12660310	Maximal forskolin stimulated cAMP formation in hDOR/CHO cells increased by 472 +/  91, 399 +/  2, and 433 +/  73% after chronic treatment with the delta <b>opioid</b> agonists (+) 4 [(alphaR) alpha ((2S,5R) 4 allyl 2,5 dimethyl 1 piperazinyl) 3 methoxy benzyl] N,N diethyl benzamide (SNC 80), [d <strong>Pen2</strong>,d Pen5] enkephalin, and deltorphin II, respectively.
+PSENEN	drug	opioid	12503000	In the present study, the authors determined the role of spinal endogenous NO in the antinociceptive effect of intrathecal [D <strong>Pen2</strong>, D Pen5 ] enkephalin (DPDPE), a delta <b>opioid</b> receptor agonist, in normal rats and a rat model of diabetic neuropathic pain.
+PSENEN	drug	opioid	9809857	), and the delta <b>opioid</b> receptor agonist [D <strong>Pen2</strong>,5] enkephalin (DPDPE; 10 100 microg i.c.v.)
+PSENEN	drug	opioid	9776518	Of 127 neurones tested, the large majority were inhibited in a dose dependent manner by the delta <b>opioid</b> receptor agonists [D Ala2, D Leu5] enkephalin (DADLE) and [D <strong>Pen2</strong>, Pen5] enkephalin (DPLPE).
+PSENEN	drug	opioid	9493866	Acute cross tolerance to the delta <b>opioid</b> receptor directed agonist DPDPE, [D <strong>Pen2</strong>, D Pen5]enkephalin, was also found.
+PSENEN	drug	opioid	9476973	Similar to several other <b>fentanyl</b> derivatives with clinical potential, OHM3507 had the highest affinity (IC50 = 10 nM) for mu ([3H]D Ala2,N Me Phe4,Gly5 OH labeled) receptors with 6  and 176 fold lower affinity for delta ([3H]D <strong>Pen2</strong> D Pen5 labeled), and kappa ([3H]ethylketocyclazocine labeled) receptors, respectively.
+PSENEN	drug	opioid	9359460	The more specific agonists of <b>opioid</b> receptors such as <b>morphine</b>, [D Ala2, N Me Phe4, Gly5 ol] enkephalin (DAGO), [D <strong>Pen2</strong>, D Pen5] enkephalin (DPDPE), dynorphin A and nociceptin/orphanin FQ did not show similar toxic activities under the same conditions.
+PSENEN	drug	opioid	9298512	<b>Morphine</b> (0, 0.5, 5 micrograms/0.5 microliter), the mu agonist D Ala2, NMe Phe4, Glyo 15 enkephalin (DAMGO; 0, 0.025, 0.25 and 2.5 micrograms/0.5 microliter), the delta agonist D <strong>Pen2</strong>,5 enkephalin (DPEN; 0, 0.031, 0.31, 3.1 micrograms/0.5 microliter), and the kappa agonists U50488H (0, 0.0186, 0.186, 1.86 micrograms/0.5 microliter), and dynorphin (0, 0.05, 0.5, 5 micrograms/0.5 microliter) were microinfused into Acb.
+PSENEN	drug	opioid	9271350	With a 3 hr pretreatment protocol, the delta selective agonists [D <strong>Pen2</strong>,D Pen5]enkephalin, [D Ala2,D Leu5]enkephalin, and [D Ser2,Leu5]enkephalin Thr and the nonselective <b>opioids</b> levorphanol, etorphine, and ethylketocyclazocine were found to desensitize delta receptors.
+PSENEN	drug	opioid	9262340	In adult female and male Sprague Dawley rats, time effect curves were obtained for vehicle and three doses each of the mu agonists <b>fentanyl</b> and <b>buprenorphine</b>, the kappa agonists (5alpha,7alpha,8alpha) ( ) N methyl [7 (1 pyrrolidinyl) 1 oxaspiro (4,5)dec 8 yl]benzeneacetamide (U69,593) and bremazocine and the delta agonists [D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE) and deltorphin on the 52 degrees C hot plate and tail withdrawal (immersion) assays.
+PSENEN	addiction	withdrawal	9262340	In adult female and male Sprague Dawley rats, time effect curves were obtained for vehicle and three doses each of the mu agonists fentanyl and buprenorphine, the kappa agonists (5alpha,7alpha,8alpha) ( ) N methyl [7 (1 pyrrolidinyl) 1 oxaspiro (4,5)dec 8 yl]benzeneacetamide (U69,593) and bremazocine and the delta agonists [D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE) and deltorphin on the 52 degrees C hot plate and tail <b>withdrawal</b> (immersion) assays.
+PSENEN	drug	opioid	9106462	To determine whether these effects are mediated via <b>opioid</b> receptor systems, the effects of ibogaine and its metabolite, noribogaine on the antinociceptive actions of <b>morphine</b>, U 50,488H and [D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE) which are mu  kappa  and delta <b>opioid</b> receptor agonists, respectively, were determined in male Swiss Webster mice.
+PSENEN	drug	psychedelics	9106462	To determine whether these effects are mediated via opioid receptor systems, the effects of <b>ibogaine</b> and its metabolite, noribogaine on the antinociceptive actions of morphine, U 50,488H and [D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE) which are mu  kappa  and delta opioid receptor agonists, respectively, were determined in male Swiss Webster mice.
+PSENEN	drug	opioid	9067332	The potencies of <b>opioids</b> binding the mu OR, [D Ala2,N MePhe4,Gly ol5]enkephalin and <b>morphine</b> were significantly attenuated in mice injected with ODNs to this receptor, an effect not seen for the delta OR binding agonists, [D <strong>Pen2</strong>,5]enkephalin and [D Ala2]deltorphin II.
+PSENEN	drug	opioid	9067332	The ODN directed to nucleotides 7 26 of the delta OR mRNA selectively impaired antinociception induced by [D Ala2]deltorphin II (delta 2), but not that of [D <strong>Pen2</strong>,5]enkephalin (delta 1) or <b>morphine</b>.
+PSENEN	drug	opioid	9437726	Effect of chronic administration of <b>morphine</b>, U 50, 488H and [D <strong>Pen2</strong>, D Pen5]enkephalin on the concentration of cGMP in brain regions and spinal cord of the mouse.
+PSENEN	drug	opioid	9437722	We have studied the binding of highly selective [3H]labeled ligands of mu ([D Ala2, MePhe4, Gly ol5]enkephalin; DAMGO), delta ([D <strong>Pen2</strong>, D Pen5]enkephalin; DPDPE), and kappa (U 69,593) <b>opioid</b> receptors to membranes of trachea, main bronchus, lung parenchyma and pulmonary artery obtained from normal (unsensitized) and actively IgE sensitized rats acutely challenged with the specific antigen.
+PSENEN	drug	opioid	9016945	The goal of this study was to determine the relative contribution of entropy and enthalpy to the free energies of binding to recombinant mouse delta <b>opioid</b> receptors for the peptide agonist, DPDPE ([D <strong>Pen2</strong>,D Pen5]enkephalin), the peptide antagonist, TIPP(psi) (Tyr Tic(psi)[CH2NH]Phe Phe OH), the nonpeptide agonist, SNC80 ((+) 4 [(alphaR) alpha ((2S,5R) 4 allyl 2,5 dimethyl 1 piperazinyl) 3 methoxybenzyl] N,N diethylbenzamide), and the nonpeptide antagonist, naltrindole.
+PSENEN	drug	opioid	8982679	A rate free method of determining brain stimulation reward thresholds was used to identify the rewarding effects of the delta <b>opioid</b> receptor and mu <b>opioid</b> receptor agonist peptides, [D <strong>Pen2</strong>, D Pen5]enkephalin (DPDPE) and [D Ala2 MePhe4 Gly(o1)5]enkephalin (DAMGO).
+PSENEN	addiction	reward	8982679	A rate free method of determining brain stimulation <b>reward</b> thresholds was used to identify the rewarding effects of the delta opioid receptor and mu opioid receptor agonist peptides, [D <strong>Pen2</strong>, D Pen5]enkephalin (DPDPE) and [D Ala2 MePhe4 Gly(o1)5]enkephalin (DAMGO).
+PSENEN	drug	opioid	8912400	Discriminative stimulus effects of a centrally administered, delta <b>opioid</b> peptide (D <strong>Pen2</strong> D Pen5 enkephalin) in pigeons.
+PSENEN	drug	opioid	8912400	The present study assessed the discriminative stimulus effects of the delta <b>opioid</b> agonist [D <strong>Pen2</strong> D Pen5]enkephalin (DPDPE) in pigeons.
+PSENEN	addiction	reward	8912400	Food restricted pigeons were trained to discriminate between i.c.v injections of 100 micrograms [D <strong>Pen2</strong> D Pen5]enkephalin (DPDPE) and saline in a two key <b>operant</b> procedure; acquisition of discriminative control was rapid (14 28 daily sessions).
+PSENEN	drug	opioid	7861658	[D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE: a delta 1 <b>opioid</b> receptor agonist) and [D Ala2,Glu4]deltorphin (deltorphin II: a delta 2 <b>opioid</b> receptor agonist) induced a significant place preference in ddY mice, but not in CXBK mice.
+PSENEN	drug	opioid	8158252	Independent groups were allowed to lever press for ventral tegmental area (VTA) microinfusions of <b>morphine</b>, the selective mu agonist [D Ala2,N Me Phe4 Gly5 ol] enkephalin (DAMGO), the selective delta agonist [D <strong>Pen2</strong>,D Pen5] enkephalin (DPDPE), or ineffective drug vehicle.
+PSENEN	drug	opioid	8301589	Selected compounds also were studied for their binding affinities at mu [[3H](D Ala2 Me Phe4,Glyol5)enkephalin], kappa ([3H]U 69,593) and delta [[3H](D <strong>Pen2</strong> D Pen5) enkephalin], <b>opioid</b> receptors in monkey brain membranes.
+PSENEN	drug	opioid	8246165	The relative pA2 and pKB values of quadazocine in antagonizing the rate decreasing effects of mu, kappa and delta <b>opioid</b> agonists corresponded to the relative potency of quadazocine in displacing the specific binding of the mu agonist [3H]Tyr D Ala Gly (Me) Phe Gly ol (IC50 = 0.080 nM), the kappa agonist [3H]U69,593 (IC50 = 0.52 nM) and the delta agonist [D <strong>Pen2</strong>,D Pen5] [3H]enkephalin (IC50 = 4.6 nM) from binding sites in membranes from monkey brain cortex.
+PSENEN	drug	opioid	8394181	Thirty minutes later, localization of binding of highly specific ligands (([D Ala2, Gly ol] enkephalin ([3H]DAGO) for mu (mu) receptor sites, [D <strong>Pen2</strong>,D Pen5] enkephalin ([3H] DPDPE) for delta (delta) sites, and [3H] U  69593 for kappa (kappa 1) sites) to <b>opioid</b> receptors in various regions of the forebrain of methyl anthranilate trained (M ) and control (water trained (W )) chicks was determined using quantitative receptor autoradiography.
+PSENEN	drug	opioid	1422864	Separate groups of animals received 4 day intra accumbens treatment with either saline, <b>morphine</b> (0.5 microgram/0.5 microliter), [D Ala2 NMe Phe4 Gly ol5] Enkephalin (DAMGO; 1.0 micrograms/0.5 microliter), or [D <strong>Pen2</strong>,5] Enkephalin (DPEN; 2.0 micrograms/0.5 microliter).
+PSENEN	drug	opioid	1358641	In contrast, intrathecal injection of the <b>opioid</b> receptor agonists, [D Ala2,MePhe4,Gly ol5]enkephalin (DAMGO, mu selective) and [D <strong>Pen2</strong>,D Pen5] enkephalin (DPDPE, delta selective), produced antinociception in both injected and non injected paws.
+PSENEN	drug	opioid	1323677	In order to develop systemically active <b>opioid</b> peptides, the delta selective, <b>opioid</b> pentapeptide [D <strong>Pen2</strong>,D Pen5] enkephalin (DPDPE) was modified by esterification and by substitution of 2',6' dimethyltyrosine for tyrosine to yield 4.
+PSENEN	drug	opioid	1380079	Pretreatment with TAMO for 24 hr antagonized antinociception produced by both H2BAMO and <b>morphine</b>, as well as TAMO itself, but not that of the delta selective agonist [D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE) or U50,488, a kappa selective agonist.
+PSENEN	drug	opioid	1659256	To gain better understanding of this phenomenon, this study evaluated the effects on the thermally evoked hind paw withdrawal latency produced by the intrathecal administration of <b>morphine</b>, U 50 488H (U 50), (D <strong>Pen2</strong>, D Pen5) enkephalin (DPDPE), ST 91, baclofen, muscimol, and 5' N ethylcarboxamide adenosine (NECA) in normal rats and in rats with a hind paw rendered unilaterally hyperesthetic by the unilateral application of loose ligatures to the sciatic nerve.
+PSENEN	addiction	withdrawal	1659256	To gain better understanding of this phenomenon, this study evaluated the effects on the thermally evoked hind paw <b>withdrawal</b> latency produced by the intrathecal administration of morphine, U 50 488H (U 50), (D <strong>Pen2</strong>, D Pen5) enkephalin (DPDPE), ST 91, baclofen, muscimol, and 5' N ethylcarboxamide adenosine (NECA) in normal rats and in rats with a hind paw rendered unilaterally hyperesthetic by the unilateral application of loose ligatures to the sciatic nerve.
+PSENEN	drug	opioid	1660817	Differences in the binding of [3H][D Ser2,Thr6]leucine enkephalin and [3H][D <strong>Pen2</strong>,D Pen5]enkephalin to brain membranes of <b>morphine</b> tolerant dependent rats.
+PSENEN	drug	opioid	1650700	The enhancement in the binding affinity of DAMGO and <b>naloxone</b> and the increased density of DADLE binding sites paralleled the development of <b>morphine</b> tolerance and dependence and [D <strong>Pen2</strong>,D Pen5]enkephalin cross tolerance in whole animals.
+PSENEN	addiction	dependence	1650700	The enhancement in the binding affinity of DAMGO and naloxone and the increased density of DADLE binding sites paralleled the development of morphine tolerance and <b>dependence</b> and [D <strong>Pen2</strong>,D Pen5]enkephalin cross tolerance in whole animals.
+PSENEN	drug	opioid	1673249	We used this strategy to study operant behavioral effects of the <b>opioid</b> peptides, [D Ala2, NMePhe4, Gly ol5]enkephalin (DAGO), [D <strong>Pen2</strong>.5] enkephalin (DPDPE) and dynorphin, agonists highly selective for mu, delta, and kappa receptors, respectively.
+PSENEN	addiction	reward	1673249	We used this strategy to study <b>operant</b> behavioral effects of the opioid peptides, [D Ala2, NMePhe4, Gly ol5]enkephalin (DAGO), [D <strong>Pen2</strong>.5] enkephalin (DPDPE) and dynorphin, agonists highly selective for mu, delta, and kappa receptors, respectively.
+PSENEN	drug	opioid	1976759	administration of selective mu <b>opioid</b> [D Ala2, N methyl Phe4, Gly5 ol] enkephalin (DAMGO) or delta <b>opioid</b> [D <strong>Pen2</strong>, D Pen5] enkephalin (DPDPE) agonists, at doses that function as positive reinforcers in rats, resulted in an immediate and significant increase in extracellular DA.
+PSENEN	drug	opioid	2155044	This study evaluated the interaction of the analgesic effects of a selective kappa  (U50, 488H) and a selective delta  ([D <strong>Pen2</strong>,5]enkephalin, DPDPE) <b>opioid</b> agonist, co injected intrathecally, using the Randall Selitto paw withdrawal test, in the rat.
+PSENEN	addiction	withdrawal	2155044	This study evaluated the interaction of the analgesic effects of a selective kappa  (U50, 488H) and a selective delta  ([D <strong>Pen2</strong>,5]enkephalin, DPDPE) opioid agonist, co injected intrathecally, using the Randall Selitto paw <b>withdrawal</b> test, in the rat.
+PSENEN	drug	alcohol	2405152	Neither chlordiazepoxide nor [D <strong>pen2</strong>, D pen5]enkephalin pretreatments appreciably altered the effects of <b>naltrexone</b>.
+PSENEN	drug	benzodiazepine	2405152	Neither <b>chlordiazepoxide</b> nor [D <strong>pen2</strong>, D pen5]enkephalin pretreatments appreciably altered the effects of naltrexone.
+PSENEN	drug	opioid	2553917	<b>Morphine</b> treatment resulted in a decrease in the maximal excitation produced by both mu and delta selective agonists, [N MePhe3,D Pro4] morphiceptin and [D <strong>Pen2</strong>,L Pen5] enkephalin.
+PSENEN	drug	opioid	2901490	The objective of this study was to describe, quantitate and compare <b>naloxone</b> induced abstinence syndromes in rats infused centrally (Sylvian aqueduct) with agonists that are currently the most selective for mu [(D Ala2, MePhe4, Gly ol5]enkephalin), delta [(D <strong>Pen2</strong>, D Pen5]enkephalin) and kappa (3,4 dichloro N methyl N [2 (1 pyrrolidinyl) cyclohexyl]benzeneacetamide) (U 50,488H) <b>opioid</b> receptors, respectively.
+PSENEN	drug	opioid	2901490	After 70 hr of infusion from s.c. implanted osmotic minipumps, three levels of abstinence were associated with the injection of <b>naloxone</b> (3 mg/kg s.c.): 1) negligible syndromes (scores of less than 21) were obtained in rats on water or the kappa directed ligands, U 50,488H and dynorphin A; 2) a low to moderate abstinence score (37 38) was recorded with rats receiving [D <strong>Pen2</strong>, D Pen5]enkephalin and ethylketazocine; and 3) a high abstinence score (64 73) was obtained with rats on <b>morphine</b> and DAGO.
+PSENEN	drug	opioid	2843384	Analgesic and tolerance inducing effects of the highly selective delta <b>opioid</b> agonist [D <strong>Pen2</strong>,D Pen5]enkephalin in mice.
+PSENEN	drug	opioid	2843384	The novel and highly selective, conformationally restricted enkephalin analogue for delta <b>opioid</b> receptors, [D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE; Pen = penicillamine), was studied in various in vivo tests for analgesia, tolerance and physical dependence.
+PSENEN	addiction	dependence	2843384	The novel and highly selective, conformationally restricted enkephalin analogue for delta opioid receptors, [D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE; Pen = penicillamine), was studied in various in vivo tests for analgesia, tolerance and physical <b>dependence</b>.
+PSENEN	drug	opioid	3401719	Contraversive circling induced by ventral tegmental microinjections of moderate doses of <b>morphine</b> and [D <strong>Pen2</strong>, D Pen5]enkephalin.
+PSENEN	drug	opioid	3401719	Unilateral ventral tegmental area (VTA) injections of <b>morphine</b> and [D <strong>Pen2</strong>,D Pen5]enkephalin (DPDPE), caused contraversive circling at doses of 1.2, 12, and 24 nmol.
+PSENEN	drug	opioid	2823990	Rats were trained to lever press for lateral hypothalamic electrical stimulation, and tested following ventral tegmental microinjections of <b>morphine</b>, delta ([D <strong>Pen2</strong>,D Pen5]enkephalin: DPDPE), or kappa (U 50, 488H) receptor agonists or saline.
+PSENEN	drug	opioid	2823970	Antinociceptive dose response curves were constructed for mu ([D Ala2,NMePhe4,Gly ol]enkephalin, DAGO; <b>morphine</b>) and delta ([D <strong>Pen2</strong>,D Pen5]enkephalin, DPDPE) agonists in the absence, and in the presence of the mu non surmountable antagonist, beta funaltrexamine (beta FNA) or the delta antagonist ICI 174,864 (N,N diallyl Tyr Aib Aib Phe Leu OH, where Aib is alpha amino isobutyric acid).
+PSENEN	drug	opioid	3033214	The <b>opioid</b> receptors involved in the supraspinal and spinal actions of [D <strong>Pen2</strong>, D Pen5]enkephalin (DPDPE) for production and/or modulation of analgesia were investigated in two thermal analgesic tests, the mouse warm water (55 degrees C) tail withdrawal assay and the radiant heat tail flick test.
+PSENEN	addiction	withdrawal	3033214	The opioid receptors involved in the supraspinal and spinal actions of [D <strong>Pen2</strong>, D Pen5]enkephalin (DPDPE) for production and/or modulation of analgesia were investigated in two thermal analgesic tests, the mouse warm water (55 degrees C) tail <b>withdrawal</b> assay and the radiant heat tail flick test.
+PSENEN	drug	opioid	3033214	Two approaches were used at supraspinal and spinal sites: determination of possible cross tolerance between <b>morphine</b> and a variety of receptor selective/nonselective agonists (DPDPE, [D <strong>Pen2</strong>, L Pen5]enkephalin (DPLPE), [D Ala2, MePhe4, Gly ol]enkephalin, [D Ala2, Met5]enkephalin amide, [D Ser2, Leu5, Thr6]enkephalin and [D Thr2 Leu, Thr6]enkephalin) and possible potentiation of <b>morphine</b> (mu) analgesia by proposed delta agonists (DPDPE, DPLPE and [D Ala2, D Leu5]enkephalin) in naive and <b>morphine</b> tolerant mice.
+PSENEN	drug	opioid	3022095	The apparent affinity of <b>naloxone</b> at cerebral and spinal sites was estimated using selective mu [D Ala2, Gly o15] enkephalin (DAGO) and delta [D <strong>Pen2</strong>, D Pen5]enkephalin] (DPDPE) <b>opioid</b> agonists in the mouse warm water tail withdrawal test in vivo; the mu agonist <b>morphine</b> was employed as a reference compound.
+PSENEN	addiction	withdrawal	3022095	The apparent affinity of naloxone at cerebral and spinal sites was estimated using selective mu [D Ala2, Gly o15] enkephalin (DAGO) and delta [D <strong>Pen2</strong>, D Pen5]enkephalin] (DPDPE) opioid agonists in the mouse warm water tail <b>withdrawal</b> test in vivo; the mu agonist morphine was employed as a reference compound.
+PSENEN	drug	opioid	6735586	The conformational basis for the differing <b>opioid</b> receptor selectivities of the cyclic cystine containing analogs, [D Cys2, D(or L) Cys5] enkephalinamide and the related penicillamine containing analogs, [D <strong>Pen2</strong>, D(or L) Cys5] enkephalinamide (penicillamine = beta, beta dimethylcysteine) was investigated by 1H n.m.r.
+SH2D3C	drug	alcohol	32607619	Replicated preclinical data has indicated that adolescent exposure to binge like levels of <b>alcohol</b> results in a reduction of choline acetyltransferase (<strong>ChAT</strong>) and an upregulation in the α7 nicotinic receptor (α7).
+SH2D3C	addiction	intoxication	32607619	Replicated preclinical data has indicated that adolescent exposure to <b>binge</b> like levels of alcohol results in a reduction of choline acetyltransferase (<strong>ChAT</strong>) and an upregulation in the α7 nicotinic receptor (α7).
+SH2D3C	drug	nicotine	31796061	Effectiveness of a <strong>chat</strong> bot for the adult population to quit <b>smoking</b>: protocol of a pragmatic clinical trial in primary care (Dejal@).
+SH2D3C	drug	nicotine	31796061	Thus, the purpose of this study is to assess the effectiveness of an intervention that helps people cease <b>smoking</b> and increase their <b>nicotine</b> abstinence rates in the long term via a <strong>chat</strong> bot, compared to usual practice, utilizing a chemical validation at 6 months.
+SH2D3C	drug	nicotine	31796061	Intervention group: use of a <strong>chat</strong> bot with evidence based contents to help quit <b>smoking</b>.
+SH2D3C	drug	alcohol	31634498	In the present study, we have examined, using stereological methods, the effects of chronic <b>alcohol</b> consumption (6 months) and subsequent withdrawal (2 months) on the total number and size of PPT and LDT choline acetyltransferase (<strong>ChAT</strong>) immunoreactive neurons.
+SH2D3C	addiction	withdrawal	31634498	In the present study, we have examined, using stereological methods, the effects of chronic alcohol consumption (6 months) and subsequent <b>withdrawal</b> (2 months) on the total number and size of PPT and LDT choline acetyltransferase (<strong>ChAT</strong>) immunoreactive neurons.
+SH2D3C	drug	alcohol	31634498	The total number of PPT and LDT <strong>ChAT</strong> immunoreactive neurons was unchanged in <b>ethanol</b> treated and withdrawn rats.
+SH2D3C	drug	alcohol	31634498	However, <strong>ChAT</strong> immunoreactive neurons were significantly hypertrophied in <b>ethanol</b> treated rats, an alteration that did not revert 2 months after <b>ethanol</b> withdrawal.
+SH2D3C	addiction	withdrawal	31634498	However, <strong>ChAT</strong> immunoreactive neurons were significantly hypertrophied in ethanol treated rats, an alteration that did not revert 2 months after ethanol <b>withdrawal</b>.
+SH2D3C	drug	cocaine	31193584	Web based self help with and without <strong>chat</strong> counseling to reduce <b>cocaine</b> use in <b>cocaine</b> misusers: Results of a three arm randomized controlled trial.
+SH2D3C	drug	cocaine	31193584	To test the efficacy of a web based self help intervention, with and without <strong>chat</strong> counseling, grounded in CBT, at reducing <b>cocaine</b> use in <b>cocaine</b> misusers not in treatment for a substance use disorder.
+SH2D3C	drug	alcohol	30779268	Preclinical rodent studies using the adolescent intermittent <b>ethanol</b> (AIE; 5.0 g/kg, i.g., 2 day on/2 day off from postnatal day [P]25 to P55) model of human adolescent binge drinking report decreased basal forebrain cholinergic (ie, <strong>ChAT</strong>+) neurons that persist into adulthood (ie, P56 P220).
+SH2D3C	addiction	intoxication	30779268	Preclinical rodent studies using the adolescent intermittent ethanol (AIE; 5.0 g/kg, i.g., 2 day on/2 day off from postnatal day [P]25 to P55) model of human adolescent <b>binge</b> drinking report decreased basal forebrain cholinergic (ie, <strong>ChAT</strong>+) neurons that persist into adulthood (ie, P56 P220).
+SH2D3C	drug	alcohol	30779268	Adolescent intermittent <b>ethanol</b> caused a persistent increase in adult H3K9me2 and DNA methylation at promoter regions of <strong>Chat</strong> and H3K9me2 of Trka, which was restored by wheel running.
+SH2D3C	drug	nicotine	30702431	Exploring Community <b>Smokers</b>' Perspectives for Developing a <strong>Chat</strong> Based <b>Smoking</b> Cessation Intervention Delivered Through Mobile Instant Messaging: Qualitative Study.
+SH2D3C	drug	nicotine	30702431	This study aims to explore the perception of using mobile IM as a modality to deliver a proposed <strong>chat</strong> intervention for <b>smoking</b> cessation in community <b>smokers</b> in Hong Kong, where the proportion of smartphone use is among the highest in the world.
+SH2D3C	drug	nicotine	30702431	Furthermore, the findings inform the development of a <strong>chat</strong> based, IM <b>smoking</b> cessation program being evaluated in a community trial.
+SH2D3C	drug	nicotine	30593882	<strong>Chat</strong> based instant messaging support combined with brief <b>smoking</b> cessation interventions for Chinese community <b>smokers</b> in Hong Kong: Rationale and study protocol for a pragmatic, cluster randomized controlled trial.
+SH2D3C	drug	nicotine	30593882	This paper presents the rationale and study design of a trial which aims to evaluate the effectiveness of a <strong>chat</strong> based intervention using mobile instant messaging combined with brief interventions for community <b>smokers</b>.
+SH2D3C	drug	nicotine	30593882	Subjects in intervention group received three months of <strong>chat</strong> based, instant messaging support guided by acceptance and commitment therapy and other behavioural change techniques, integrated with brief advice and active referral to a <b>smoking</b> cessation service using the AWARD (Ask, Warn, Advise, Refer, Do it again) intervention model.
+SH2D3C	drug	alcohol	30296276	Adolescent intermittent <b>ethanol</b> exposure also reduces basal forebrain expression of choline acetyltransferase (<strong>ChAT</strong>), an enzyme critical for acetylcholine synthesis in cholinergic neurons similar to findings in the post mortem human <b>alcoholic</b> basal forebrain.
+SH2D3C	drug	alcohol	30296276	We report here that AIE decreases basal forebrain <strong>ChAT</strong>+IR neurons in both adult female and male Wistar rats following early or late adolescent <b>ethanol</b> exposure.
+SH2D3C	addiction	reward	29740282	Here we study the function of muscarinic M4 receptors (M4Rs) in dopamine D1 receptor (D1R) expressing neurons and cholinergic neurons (expressing choline acetyltransferase; <strong>ChAT</strong>), during various <b>reward</b> enforced behaviors and in a "waiting" impulsivity test.
+SH2D3C	drug	cannabinoid	29739738	Effects of Treatment Length and <strong>Chat</strong> Based Counseling in a Web Based Intervention for <b>Cannabis</b> Users: Randomized Factorial Trial.
+SH2D3C	drug	nicotine	29371319	Altered Baseline and <b>Nicotine</b> Mediated Behavioral and Cholinergic Profiles in <strong>ChAT</strong> Cre Mouse Lines.
+SH2D3C	drug	nicotine	29371319	<strong>ChAT</strong>(BAC) Cre transgenic and wild type mice did not differ in general locomotor behavior, anxiety measures, drug induced cataplexy, <b>nicotine</b> mediated hypolocomotion, or operant food training.
+SH2D3C	addiction	reward	29371319	<strong>ChAT</strong>(BAC) Cre transgenic and wild type mice did not differ in general locomotor behavior, anxiety measures, drug induced cataplexy, nicotine mediated hypolocomotion, or <b>operant</b> food training.
+SH2D3C	drug	nicotine	29371319	However, <strong>ChAT</strong>(BAC) Cre transgenic mice did exhibit significant deficits in intravenous <b>nicotine</b> self administration, which paralleled an increase in vesicular acetylcholine transporter and choline acetyltransferase (<strong>ChAT</strong>) hippocampal expression.
+SH2D3C	drug	nicotine	29371319	For the <strong>ChAT</strong>(IRES) Cre line, transgenic mice exhibited deficits in baseline locomotor, <b>nicotine</b> mediated hypolocomotion, and operant food training compared with wild type and hemizygous littermates.
+SH2D3C	addiction	reward	29371319	For the <strong>ChAT</strong>(IRES) Cre line, transgenic mice exhibited deficits in baseline locomotor, nicotine mediated hypolocomotion, and <b>operant</b> food training compared with wild type and hemizygous littermates.
+SH2D3C	drug	nicotine	29371319	No differences among <strong>ChAT</strong>(IRES) Cre wild type, hemizygous, and transgenic littermates were found in anxiety measures, drug induced cataplexy, and <b>nicotine</b> self administration.
+SH2D3C	drug	nicotine	29371319	As such, interpretation of data derived from <strong>ChAT</strong> Cre rodents must consider potential limitations dependent on the line and/or genotype used in research investigations.SIGNIFICANCE STATEMENT Altered baseline and/or <b>nicotine</b> mediated behavioral profiles were discovered in transgenic mice from the <strong>ChAT</strong>(BAC) Cre and <strong>ChAT</strong>(IRES) Cre lines.
+SH2D3C	addiction	intoxication	28807788	These results indicate that early adolescent <b>binge</b> EtOH exposure leads to a long lasting frontocortical functional cholinergic deficit, driven by a loss of <strong>ChAT</strong>+/nestin+ neurons in the NbM, which was associated with impaired cognitive flexibility during adulthood.
+SH2D3C	drug	amphetamine	28628197	Previous experiments established that <strong>ChAT</strong> ChR2 mice display an increased sensitivity to <b>amphetamine</b> induced locomotor activity and stereotypes.
+SH2D3C	drug	cocaine	28628197	<strong>ChAT</strong> ChR2 mice displayed increased locomotor sensitization in response to low dose of <b>cocaine</b>.
+SH2D3C	addiction	sensitization	28628197	<strong>ChAT</strong> ChR2 mice displayed increased locomotor <b>sensitization</b> in response to low dose of cocaine.
+SH2D3C	drug	cocaine	28628197	These findings demonstrate that <strong>ChAT</strong> ChR2 mice present major alterations of CIN neuronal morphology and increased behavioral sensitization to <b>cocaine</b>, supporting the notion that the increased levels of VAChT observed in these mice make them fundamentally different from wild type mice.
+SH2D3C	addiction	sensitization	28628197	These findings demonstrate that <strong>ChAT</strong> ChR2 mice present major alterations of CIN neuronal morphology and increased behavioral <b>sensitization</b> to cocaine, supporting the notion that the increased levels of VAChT observed in these mice make them fundamentally different from wild type mice.
+SH2D3C	addiction	relapse	27707896	Participants were telephone interviewed and assessed using the Case finding and Help Assessment Tool (<strong>CHAT</strong>) with employee lifestyle risk factors, mental health issues and help <b>seeking</b> intentions screened across eight industries.
+SH2D3C	drug	nicotine	26623516	Mice lacking <strong>CHAT</strong> in habenular neurons were insensitive to <b>nicotine</b> conditioned reward and withdrawal.
+SH2D3C	addiction	reward	26623516	Mice lacking <strong>CHAT</strong> in habenular neurons were insensitive to nicotine conditioned <b>reward</b> and withdrawal.
+SH2D3C	addiction	withdrawal	26623516	Mice lacking <strong>CHAT</strong> in habenular neurons were insensitive to nicotine conditioned reward and <b>withdrawal</b>.
+SH2D3C	drug	cannabinoid	26462848	A Web Based Self Help Intervention With and Without <strong>Chat</strong> Counseling to Reduce <b>Cannabis</b> Use in Problematic <b>Cannabis</b> Users: Three Arm Randomized Controlled Trial.
+SH2D3C	drug	cannabinoid	26462848	To test the efficacy of a Web based self help intervention with and without <strong>chat</strong> counseling Can Reduce in reducing the <b>cannabis</b> use of problematic <b>cannabis</b> users as an alternative to outpatient treatment services.
+SH2D3C	drug	cannabinoid	26462848	The change in the mean number of <b>cannabis</b> use days per week at 3 months differed between self help without <strong>chat</strong> (mean change 0.7, SD  0.2) and self help with <strong>chat</strong> (mean change 1.4, SD  0.5; beta= 0.75, SE=0.32, t= 2.39, P=.02, d=0.34, 95% CI 0.07 0.61), as well as between self help with <strong>chat</strong> and waiting list (mean change 1.0, SD  0.8; beta=0.70, SE=0.32, t=2.16, P=.03, d=0.20, 95% CI  0.07 to 0.47).
+SH2D3C	drug	cannabinoid	26462848	Web based self help interventions supplemented by brief <strong>chat</strong> counseling are an effective alternative to face to face treatment and can reach a group of <b>cannabis</b> users who differ in their use and sociodemographic characteristics from those who enter outpatient addiction treatment.
+SH2D3C	addiction	addiction	26462848	Web based self help interventions supplemented by brief <strong>chat</strong> counseling are an effective alternative to face to face treatment and can reach a group of cannabis users who differ in their use and sociodemographic characteristics from those who enter outpatient <b>addiction</b> treatment.
+SH2D3C	drug	cocaine	26159624	Evaluating the efficacy of a web based self help intervention with and without <strong>chat</strong> counseling in reducing the <b>cocaine</b> use of problematic <b>cocaine</b> users: the study protocol of a pragmatic three arm randomized controlled trial.
+SH2D3C	drug	cocaine	26159624	The study will use a three arm randomized controlled trial (RCT) design to test the efficacy of a web based self help intervention with or without guided <strong>chat</strong> counseling compared with that of a waiting list control condition in reducing or stopping <b>cocaine</b> use.
+SH2D3C	addiction	relapse	26159624	The three individual <strong>chat</strong> therapy sessions will be based on the same therapy approaches and will be tailored to participants' self help data and aim to assist the <b>reinstatement</b> of social rewards and the improvement of social support and relationships.
+SH2D3C	drug	cocaine	26159624	This study will be the first RCT to test the effectiveness of a web based self help intervention in combination with or without <strong>chat</strong> counseling in reducing <b>cocaine</b> use.
+SH2D3C	drug	cocaine	26059306	In particular, p11 in the <strong>ChAT</strong>+ cells or DRD1+ MSN of the NAc, controls depressive like behavior or <b>cocaine</b> reward, respectively.
+SH2D3C	addiction	reward	26059306	In particular, p11 in the <strong>ChAT</strong>+ cells or DRD1+ MSN of the NAc, controls depressive like behavior or cocaine <b>reward</b>, respectively.
+SH2D3C	addiction	reward	25586659	Rats bearing bilateral lesions of cholinergic pPPTg neurons (>90% <strong>ChAT</strong>+ neuronal loss) displayed no deficits in the learning or performance of fixed and variable ratio schedules of <b>reinforcement</b> for pellet <b>reward</b>.
+SH2D3C	drug	alcohol	25405505	In Experiment 1, adolescent intermittent <b>ethanol</b> (AIE; 5.0 g/kg, i.g., 2 day on/2 day off from postnatal day [P] 25 to P55) treatment led to persistent, global reductions of choline acetyltransferase (<strong>ChAT</strong>) expression.
+SH2D3C	drug	alcohol	25405505	To determine if the binge <b>ethanol</b> induced <strong>ChAT</strong> decline was unique to the adolescent, Experiment 2 examined <strong>ChAT</strong>+IR in the basal forebrain following adolescent (P28 P48) and adult (P70 P90) binge <b>ethanol</b> exposure.
+SH2D3C	addiction	intoxication	25405505	To determine if the <b>binge</b> ethanol induced <strong>ChAT</strong> decline was unique to the adolescent, Experiment 2 examined <strong>ChAT</strong>+IR in the basal forebrain following adolescent (P28 P48) and adult (P70 P90) <b>binge</b> ethanol exposure.
+SH2D3C	drug	alcohol	25405505	Twenty five days later, <strong>ChAT</strong> expression was reduced in adolescent, but not adult, binge <b>ethanol</b> exposed animals.
+SH2D3C	addiction	intoxication	25405505	Twenty five days later, <strong>ChAT</strong> expression was reduced in adolescent, but not adult, <b>binge</b> ethanol exposed animals.
+SH2D3C	drug	alcohol	25405505	In Experiment 3, expression of <strong>ChAT</strong> and vesicular acetylcholine transporter expression was found to be significantly reduced in the <b>alcoholic</b> basal forebrain relative to moderate drinking controls.
+SH2D3C	drug	alcohol	25405505	Together, these data suggest that adolescent binge <b>ethanol</b> decreases adult <strong>ChAT</strong> expression, possibly through neuroimmune mechanisms, which might impact adult cognition, arousal, or reward sensitivity.
+SH2D3C	addiction	intoxication	25405505	Together, these data suggest that adolescent <b>binge</b> ethanol decreases adult <strong>ChAT</strong> expression, possibly through neuroimmune mechanisms, which might impact adult cognition, arousal, or reward sensitivity.
+SH2D3C	addiction	reward	25405505	Together, these data suggest that adolescent binge ethanol decreases adult <strong>ChAT</strong> expression, possibly through neuroimmune mechanisms, which might impact adult cognition, arousal, or <b>reward</b> sensitivity.
+SH2D3C	drug	alcohol	24893293	Conversely, the number and the size of cholinergic interneurons, and the amount of <strong>ChAT</strong> were unchanged in <b>ethanol</b> treated and withdrawn rats, but the density of cholinergic varicosities was reduced by 50% during <b>alcohol</b> consumption and by 64% after withdrawal.
+SH2D3C	addiction	withdrawal	24893293	Conversely, the number and the size of cholinergic interneurons, and the amount of <strong>ChAT</strong> were unchanged in ethanol treated and withdrawn rats, but the density of cholinergic varicosities was reduced by 50% during alcohol consumption and by 64% after <b>withdrawal</b>.
+SH2D3C	drug	cannabinoid	24228630	Can reduce  the effects of <strong>chat</strong> counseling and web based self help, web based self help alone and a waiting list control program on <b>cannabis</b> use in problematic <b>cannabis</b> users: a randomized controlled trial.
+SH2D3C	drug	cannabinoid	24228630	The offer of a combined web based self help and <strong>chat</strong> counseling treatment could potentially also reach those users who hesitate to approach such treatment centers and help them to reduce their <b>cannabis</b> use.
+SH2D3C	drug	cannabinoid	24228630	This paper presents the protocol for a three armed randomized controlled trial that will test the effectiveness of a web based self help intervention in combination with, or independent of, tailored <strong>chat</strong> counseling compared to a waiting list in reducing or enabling the abstention from <b>cannabis</b> use in problematic users.
+SH2D3C	drug	cannabinoid	24228630	To the best of our knowledge, this will be the first randomized controlled trial to test the effectiveness of online self help therapy in combination or without <strong>chat</strong> counseling in reducing or enabling the abstention from <b>cannabis</b> use.
+SH2D3C	drug	nicotine	24076142	Recently, we reported that several polymorphisms and haplotypes in the choline acetyltransferase gene (<strong>ChAT</strong>) are associated with <b>nicotine</b> dependence (ND).
+SH2D3C	addiction	dependence	24076142	Recently, we reported that several polymorphisms and haplotypes in the choline acetyltransferase gene (<strong>ChAT</strong>) are associated with nicotine <b>dependence</b> (ND).
+SH2D3C	drug	nicotine	23222296	<b>Nicotine</b> induced ACh production was mediated by α7 , α3β2 , and β3 nAChRs, <strong>ChAT</strong> and VAChT pathways.
+SH2D3C	drug	nicotine	23222296	We observed that <b>nicotine</b> upregulated <strong>ChAT</strong> and VAChT.
+SH2D3C	drug	alcohol	22033458	Periadolescent <b>ethanol</b> exposure reduces adult forebrain <strong>ChAT</strong>+IR neurons: correlation with behavioral pathology.
+SH2D3C	drug	alcohol	22033458	In the present study, immunohistochemistry for choline acetyltransferase (<strong>ChAT</strong>) was determined to assess forebrain cholinergic neurons (Ch1 4), and behavioral changes following periadolescent <b>alcohol</b> exposure.
+SH2D3C	drug	alcohol	22033458	Quantitative analyses of <strong>ChAT</strong> immunoreactivity revealed a significant reduction in cell counts in the Ch1 2 and Ch3 4 regions of the basal forebrain in <b>ethanol</b> vapor exposed rats.
+SH2D3C	drug	alcohol	22033458	These studies demonstrate that behavioral measures of arousal, affective state, disinhibitory behavior, and <strong>ChAT</strong>+IR, are all significantly impacted by periadolescent <b>ethanol</b> exposure and withdrawal in Wistar rats.
+SH2D3C	addiction	withdrawal	22033458	These studies demonstrate that behavioral measures of arousal, affective state, disinhibitory behavior, and <strong>ChAT</strong>+IR, are all significantly impacted by periadolescent ethanol exposure and <b>withdrawal</b> in Wistar rats.
+SH2D3C	drug	opioid	21967037	Moreover, the time course of PEBP expression changes and <strong>ChAT</strong> activity was investigated during chronic <b>morphine</b> treatment and withdrawal.
+SH2D3C	addiction	withdrawal	21967037	Moreover, the time course of PEBP expression changes and <strong>ChAT</strong> activity was investigated during chronic morphine treatment and <b>withdrawal</b>.
+SH2D3C	addiction	withdrawal	21633116	Effects on <strong>ChAT</strong> and AChE were dependent on the brain region and restricted to the <b>withdrawal</b> period: There were increased activities in the midbrain on PN30.
+SH2D3C	drug	nicotine	20383528	We recently reported association of the encoding gene <strong>ChAT</strong> with both <b>smoking</b> cessation and <b>nicotine</b> dependence (ND) in two independent European American (EA) samples; however, in the replication sample, only limited SNPs partially covering the gene were examined.
+SH2D3C	addiction	dependence	20383528	We recently reported association of the encoding gene <strong>ChAT</strong> with both smoking cessation and nicotine <b>dependence</b> (ND) in two independent European American (EA) samples; however, in the replication sample, only limited SNPs partially covering the gene were examined.
+SH2D3C	drug	alcohol	20309727	Acute <b>alcohol</b> (Alc) intoxication has been shown to decrease choline acetyltransferase (<strong>ChAT</strong>) in the rat brain.
+SH2D3C	addiction	intoxication	20309727	Acute alcohol (Alc) <b>intoxication</b> has been shown to decrease choline acetyltransferase (<strong>ChAT</strong>) in the rat brain.
+SH2D3C	drug	nicotine	20309727	The present study extends that finding by examining the effects of <b>nicotine</b> (Nic), Alc, and their combination on <strong>ChAT</strong> and acetylcholinesterase (AChE) in the frontal cortex and hippocampus of rat.
+SH2D3C	drug	nicotine	20147892	Single SNPs in <strong>ChAT</strong> haplotype block 2 were also associated with pretreatment levels of <b>nicotine</b> dependence in this cohort.
+SH2D3C	addiction	dependence	20147892	Single SNPs in <strong>ChAT</strong> haplotype block 2 were also associated with pretreatment levels of nicotine <b>dependence</b> in this cohort.
+SH2D3C	drug	nicotine	20147892	To replicate associations of SNPs in haplotype blocks 2 and 6 of <strong>ChAT</strong> with <b>nicotine</b> dependence in a non treatment seeking cohort, we used data from an independent community based sample of 629 <b>smokers</b> representing 200 families of European ancestry.
+SH2D3C	addiction	dependence	20147892	To replicate associations of SNPs in haplotype blocks 2 and 6 of <strong>ChAT</strong> with nicotine <b>dependence</b> in a non treatment seeking cohort, we used data from an independent community based sample of 629 smokers representing 200 families of European ancestry.
+SH2D3C	addiction	relapse	20147892	To replicate associations of SNPs in haplotype blocks 2 and 6 of <strong>ChAT</strong> with nicotine dependence in a non treatment <b>seeking</b> cohort, we used data from an independent community based sample of 629 smokers representing 200 families of European ancestry.
+SH2D3C	drug	nicotine	20147892	Although the effect sizes in both cohorts are modest, converging data across cohorts and phenotypes suggest that <strong>ChAT</strong> may be involved in <b>nicotine</b> dependence and ability to quit <b>smoking</b>.
+SH2D3C	addiction	dependence	20147892	Although the effect sizes in both cohorts are modest, converging data across cohorts and phenotypes suggest that <strong>ChAT</strong> may be involved in nicotine <b>dependence</b> and ability to quit smoking.
+SH2D3C	drug	nicotine	20147892	Additional sequencing and characterization of <strong>ChAT</strong> may reveal functional variants that contribute to <b>nicotine</b> dependence and <b>smoking</b> cessation.
+SH2D3C	addiction	dependence	20147892	Additional sequencing and characterization of <strong>ChAT</strong> may reveal functional variants that contribute to nicotine <b>dependence</b> and smoking cessation.
+SH2D3C	addiction	withdrawal	19465085	We assessed nAChR binding, choline acetyltransferase (<strong>ChAT</strong>) activity and [(3)H]hemicholinium 3 (HC 3) binding in the cerebral cortex and midbrain of mice at short (PN50) and long term (PN75) <b>withdrawal</b>.
+SH2D3C	addiction	withdrawal	19465085	NIC short term <b>withdrawal</b> elicited an increase in <strong>ChAT</strong> activity that was reversed by ETOH <b>withdrawal</b>.
+SH2D3C	addiction	withdrawal	19465085	In addition, NIC+ETOH elicited a decrease in <strong>ChAT</strong> activity at long term <b>withdrawal</b>.
+SH2D3C	drug	alcohol	19433841	The short, validated, self administered, Case finding and Help Assessment Tool (<strong>CHAT</strong>) for lifestyle and mental health assessment of adult patients in primary health care addresses inactivity, tobacco use, <b>alcohol</b> and other drug misuse, problem gambling, depression, anxiety and stress, abuse, and anger problems.
+SH2D3C	drug	nicotine	19433841	The short, validated, self administered, Case finding and Help Assessment Tool (<strong>CHAT</strong>) for lifestyle and mental health assessment of adult patients in primary health care addresses inactivity, <b>tobacco</b> use, alcohol and other drug misuse, problem gambling, depression, anxiety and stress, abuse, and anger problems.
+SH2D3C	drug	nicotine	18395624	By itself, adolescent <b>nicotine</b> exposure evoked sex selective deficits in cerebrocortical HC3 binding while elevating <strong>ChAT</strong> in young adulthood in striatum and midbrain.
+SH2D3C	addiction	withdrawal	18088441	When mice were treated with an antisense oligodeoxynucleotide (AS ODN) against <strong>ChAT</strong>, which decreased <strong>ChAT</strong> signals in the dorsal horn and DRG, but not in motor neurons, they showed a significant decrease in nociceptive thresholds in paw pressure and thermal paw <b>withdrawal</b> tests.
+SH2D3C	drug	amphetamine	17711382	Characteristics of a sample of men who have sex with men, recruited from gay bars and Internet <strong>chat</strong> rooms, who report <b>methamphetamine</b> use.
+SH2D3C	drug	nicotine	15066159	Animals neonatally treated with quinpirole demonstrated a significant 36% decrease of <strong>ChAT</strong> in the hippocampus compared to saline controls that was partially eliminated by <b>nicotine</b>.
+SH2D3C	drug	nicotine	14970833	Prenatal <b>nicotine</b> exposure had only minor effects on nAChRs but produced persistent cholinergic hypoactivity (reduced HC 3 binding relative to <strong>ChAT</strong>) throughout adolescence and into adulthood (PN75).
+SH2D3C	drug	alcohol	12831864	In addition, the somatic size of <strong>ChAT</strong> IR neurons was reduced by <b>ethanol</b> intake, and withdrawal further aggravated neuronal atrophy.
+SH2D3C	addiction	withdrawal	12831864	In addition, the somatic size of <strong>ChAT</strong> IR neurons was reduced by ethanol intake, and <b>withdrawal</b> further aggravated neuronal atrophy.
+SH2D3C	drug	nicotine	12784097	Adolescent <b>nicotine</b> treatment also produced lasting decrements in HC 3 binding that were separable from effects on <strong>ChAT</strong>, suggesting cholinergic synaptic impairment.
+SH2D3C	drug	nicotine	10915806	During <b>nicotine</b> treatment and for 1 month after the termination of treatment, <strong>ChAT</strong> activity was reduced significantly in the midbrain but not in the other regions.
+SH2D3C	addiction	withdrawal	10487390	There were no significant differences in the density of the <strong>ChAT</strong> IR hippocampal fiber network when the pure <b>withdrawal</b> and <b>withdrawal</b> + vehicle groups were compared to the <b>withdrawal</b> + GM1 or <b>withdrawal</b> + piracetam groups.
+SH2D3C	addiction	withdrawal	10487390	In contrast, the number of <strong>ChAT</strong> IR interneurons in the hippocampal formation was higher in the <b>withdrawal</b> + GM1 or <b>withdrawal</b> + piracetam groups than in the pure <b>withdrawal</b> and <b>withdrawal</b> + vehicle groups.
+SH2D3C	drug	cocaine	7877755	Choline acetyltransferase (<strong>ChAT</strong>) activity was measured in discrete areas of rat brain after chronic, unlimited access to self administration of <b>cocaine</b>.
+SH2D3C	drug	cocaine	7877755	Mean activity of <strong>ChAT</strong> was reduced by approximately 30% in the nucleus accumbens, both on the last day of <b>cocaine</b> access and after 3 weeks <b>cocaine</b> withdrawal.
+SH2D3C	addiction	withdrawal	7877755	Mean activity of <strong>ChAT</strong> was reduced by approximately 30% in the nucleus accumbens, both on the last day of cocaine access and after 3 weeks cocaine <b>withdrawal</b>.
+SH2D3C	drug	opioid	8149590	The effect of prenatal exposure to <b>methadone</b> via maternal osmotic minipumps on the expression of acetylcholinesterase (AChE) and choline acetyltransferase (<strong>ChAT</strong>) has been studied by light microscopy in the striatum of male and female rats.
+SH2D3C	drug	opioid	8149590	At postnatal day 10, rats of both sexes exhibit reduced intensity of <strong>ChAT</strong> immunoreactive staining in striatal neurons in the <b>methadone</b> treated group in comparison to either untreated or water treated controls.
+SH2D3C	drug	opioid	8149590	Although the number and distribution of <strong>ChAT</strong> immunoreactive neurons appear to be similar across all three groups, the size (cross sectional area) of these neurons is significantly smaller in the <b>methadone</b> treated animals.
+SH2D3C	drug	opioid	8149590	By postnatal day 22, there are no differences in the <strong>ChAT</strong> immunoreactivity of striatal neurons between the water treated and <b>methadone</b> treated animals.
+SH2D3C	drug	opioid	8149590	Thus, prenatal exposure to <b>methadone</b> appears to produce a delay in the expression of <strong>ChAT</strong> in striatal neurons.
+SH2D3C	drug	alcohol	7748324	Specific activity of GAD but not <strong>ChAT</strong> was found to be significantly decreased in hippocampi of <b>ethanol</b> dependent animals following injection of NMDA, suggesting that chronic <b>ethanol</b> administration sensitizes GABAergic neurons to the toxic effects of excitatory amino acid transmitters.
+SH2D3C	drug	nicotine	4064913	No significant change in cholineacetyltransferase (<strong>ChAT</strong>) activity or number of muscarinic binding sites in brain was observed after 9 or 41 weeks of <b>nicotine</b> treatment.
+SH2D3C	drug	opioid	6685808	The results demonstrate that neither short nor long term <b>morphine</b> treatment had an effect on choline acetyltransferase (<strong>ChAT</strong>) activity or 3H quinuclidinylbenzilate (3HQNB) binding in discrete striatal regions of the rat brain.
+SH2D3C	drug	alcohol	7198309	The activities of acetylcholinesterase (AChE) and choline acetyltransferase (<strong>ChaT</strong>) in the cerebral cortex, cerebellum, hypothalamus, hippocampus, midbrain and pons of adult, male mice injected with 2 g/kg <b>ethanol</b> and of control mice injected with physiological saline, were determined by spectrophotometric methods.
+SH2D3C	drug	alcohol	7198309	All animals were killed 30 min after injection between 11.00 h and 12.00 h. Results show that the acute dose of <b>ethanol</b> significantly decreased AChE activity only in the cerebral cortex whereas <strong>ChaT</strong> activity was reduced in the cerebral cortex, hypothalamus and hippocampus.
+SH2D3C	drug	alcohol	7198309	These findings show that the effect of an acute dose of <b>ethanol</b> on the cholinergic system of mouse brain is mediated through its effect on AChE and <strong>ChaT</strong> in specific regions.
+SH2D3C	drug	alcohol	6994921	Eighteen weeks of <b>ethanol</b> consumption in a liquid diet reduced rat striatal and mammillary body choline acetylase (<strong>ChAT</strong>) by 53% and 58%, respectively.
+IL1B	drug	opioid	32733481	<b>Opioids</b> non stereoselectively activate the TLR4 pathway, and together with the subsequent release of pro inflammatory cytokines such as <strong>IL 1</strong> by glia, this TLR4 signaling initiates the central immune signaling response and modifies <b>opioid</b> pharmacodynamics.
+IL1B	drug	alcohol	31854009	C57BL/6J male and female mice were provided a 2 bottle choice of <b>alcohol</b> at increasing concentrations (3, 6, 9, and 12%, 4 days each) or water, and some were treated with daily injections of an NLRP3 inhibitor (MCC950), a caspase 1 inhibitor (VX765), <strong>IL 1</strong> receptor antagonist (IL 1ra; anakinra), or vehicle injection.
+IL1B	drug	cocaine	31704270	<b>Cocaine</b> induces neuroinflammatory response and <strong>interleukin 1 beta</strong> (IL1β) is suggested a final effector for many <b>cocaine</b> induced inflammatory signals.
+IL1B	drug	alcohol	30791967	Human genetic and preclinical studies suggest a critical role for IL 1β signaling in <b>ethanol</b> drinking and dependence, but little is known about the effects of chronic <b>ethanol</b> on the <strong>IL 1</strong> system in addiction related brain regions such as the central amygdala (CeA).
+IL1B	addiction	addiction	30791967	Human genetic and preclinical studies suggest a critical role for IL 1β signaling in ethanol drinking and dependence, but little is known about the effects of chronic ethanol on the <strong>IL 1</strong> system in <b>addiction</b> related brain regions such as the central amygdala (CeA).
+IL1B	addiction	dependence	30791967	Human genetic and preclinical studies suggest a critical role for IL 1β signaling in ethanol drinking and <b>dependence</b>, but little is known about the effects of chronic ethanol on the <strong>IL 1</strong> system in addiction related brain regions such as the central amygdala (CeA).
+IL1B	drug	alcohol	30791967	In this study, we generated naïve, non dependent (Non Dep) and dependent (Dep) male mice using a paradigm of chronic intermittent <b>ethanol</b> vapor exposure interspersed with two bottle choice to examine 1) the expression of IL 1β, 2) the role of the <strong>IL 1</strong> system on GABAergic transmission, and 3) the potential interaction with the acute effects of <b>ethanol</b> in the CeA.
+IL1B	drug	cannabinoid	30584942	In addition, mechanistically at the molecular level, these effects are elicited via up regulation of the <b>cannabinoid</b> type 2 receptor, up regulating the level of β endorphin, and reducing the levels of <strong>IL 1</strong>, NO and PGE2.
+IL1B	addiction	reward	30075289	Furthermore, it has not been evaluated whether the involvement of <strong>IL 1</strong> in associative learning extends to classically conditioned appetitive behaviors, such as conditioned place preference (<b>CPP</b>).
+IL1B	drug	cannabinoid	30046349	Δ9 <b>THC</b>/sesame oil therapy showed similar effects to MTX in neutralizing the inflammatory process of AIA, through attenuating erythrocyte sedimentation rate (ESR) scores and proinflammatory cytokines, including tumor necrosis factor alpha (TNF α), <strong>interleukin 1 beta</strong> (IL 1β), and interleukin 6 (IL 6) levels, to normal values.
+IL1B	drug	alcohol	29178411	We found that during abstinence, <b>alcohol</b> binge drinkers had elevated plasma levels of oleoylethanolamide, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (TLR4), pro inflammatory cytokines/chemokines <strong>interleukin 1 beta</strong>, interleukin 6 and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+IL1B	drug	cannabinoid	29178411	We found that during abstinence, alcohol binge drinkers had elevated plasma levels of <b>oleoylethanolamide</b>, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (TLR4), pro inflammatory cytokines/chemokines <strong>interleukin 1 beta</strong>, interleukin 6 and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+IL1B	addiction	intoxication	29178411	We found that during abstinence, alcohol <b>binge</b> drinkers had elevated plasma levels of oleoylethanolamide, palmitoleoylethanolamide, arachidonoylethanolamide, dihomo γ linolenoyl ethanolamide and linoleoyl ethanolamide, which positively correlated with changes in the mRNA expression of key inflammatory markers in peripheral blood mononuclear cells, such as toll like receptors (TLR4), pro inflammatory cytokines/chemokines <strong>interleukin 1 beta</strong>, interleukin 6 and monocyte chemoattractant protein 1, and cyclooxygenase 2.
+IL1B	drug	opioid	29111854	We observed differential methylation of Bdnf and Il6 in the pons, Nr3c1 in the cerebellum, and <strong>Il1b</strong> in the hippocampus in response to acute <b>morphine</b> exposure (all P value < 0.05).
+IL1B	drug	opioid	28178176	In response to LPS, there was a significant increase in the expression of the pro inflammatory cytokine/chemokine genes <strong>interleukin 1 beta</strong> (Il 1β), interleukin 6 (Il 6), C C motif chemokine ligand 2 (Ccl2), C C motif chemokine ligand 7 (Ccl7), C X C motif chemokine ligand 1 (Cxcl1), and C X C motif chemokine ligand 3 (Cxcl3) and a significant decrease in the anti inflammatory NLRP12 gene in both <b>morphine</b> tolerant and placebo control rats compared to saline treated rats, although the changes were greater in the placebo control animals.
+IL1B	drug	alcohol	28095363	Also, <b>alcohol</b> administration augmented lipid peroxidation, mitochondrial oxidized glutathione (GSSG), <strong>interleukin 1 beta</strong> (IL 1β), tumor necrosis factor alpha (TNF α) and Bax levels in isolated hippocampal tissues.
+IL1B	addiction	withdrawal	27430907	Further, Pinellia ternata treatment reversed budesonide <b>withdrawal</b> induced increase of interleukin 1[Formula: see text] (<strong>IL 1</strong>[Formula: see text] and tumor necrosis factor [Formula: see text] (TNF [Formula: see text]) levels in bronchoalveolar lavage fluid (BALF).
+IL1B	drug	alcohol	27273552	Here, we examined the role of interleukin 1 (<strong>IL 1</strong>) and tumor necrosis factor α (TNF α) in regulation of voluntary <b>alcohol</b> consumption, <b>alcohol</b> reward and stress induced drinking.
+IL1B	addiction	reward	27273552	Here, we examined the role of interleukin 1 (<strong>IL 1</strong>) and tumor necrosis factor α (TNF α) in regulation of voluntary alcohol consumption, alcohol <b>reward</b> and stress induced drinking.
+IL1B	drug	alcohol	27273552	Mice with a deletion of the <strong>IL 1</strong> receptor I gene (IL 1RI KO) exhibited modestly decreased <b>alcohol</b> consumption.
+IL1B	addiction	sensitization	26773297	This <b>sensitization</b> enhances the production of various proinflammatory cytokines such as interleukin 1 (<strong>IL 1</strong>) and tumor necrosis factor alpha, thereby contributing to hepatocyte dysfunction, necrosis, and apoptosis and the generation of extracellular matrix proteins leading to fibrosis/cirrhosis.
+IL1B	drug	alcohol	26773297	As <strong>IL 1</strong> is clearly linked to key clinical symptoms of acute <b>alcoholic</b> hepatitis such as fever, neutrophilia, and wasting, interfering with the <strong>IL 1</strong> pathway might be an attractive treatment strategy in the future.
+IL1B	drug	alcohol	26365025	<strong>IL 1</strong> receptor signaling in the basolateral amygdala modulates binge like <b>ethanol</b> consumption in male C57BL/6J mice.
+IL1B	addiction	intoxication	26365025	<strong>IL 1</strong> receptor signaling in the basolateral amygdala modulates <b>binge</b> like ethanol consumption in male C57BL/6J mice.
+IL1B	drug	alcohol	26365025	Moreover, the role of <strong>IL 1</strong> receptor signaling in the amygdala on <b>ethanol</b> consumption was assessed.
+IL1B	drug	alcohol	26365025	Bilateral infusions of <strong>IL 1</strong> receptor antagonist (IL 1Ra) reduced <b>ethanol</b> consumption when infused into the BLA but not the CeA.
+IL1B	drug	alcohol	26365025	The current findings highlight a specific role for <strong>IL 1</strong> receptor signaling in modulating binge like <b>ethanol</b> consumption and indicate that proinflammatory cytokines can be induced prior to dependence or any evidence of neuronal cell death.
+IL1B	addiction	dependence	26365025	The current findings highlight a specific role for <strong>IL 1</strong> receptor signaling in modulating binge like ethanol consumption and indicate that proinflammatory cytokines can be induced prior to <b>dependence</b> or any evidence of neuronal cell death.
+IL1B	addiction	intoxication	26365025	The current findings highlight a specific role for <strong>IL 1</strong> receptor signaling in modulating <b>binge</b> like ethanol consumption and indicate that proinflammatory cytokines can be induced prior to dependence or any evidence of neuronal cell death.
+IL1B	drug	opioid	26363312	No difference in cortisol production was initially observed between the two groups, however, when participants were separated based on their genotype for two single nucleotide polymorphisms in the promoter of the <strong>IL1B</strong> gene, which have been shown to occur at a higher frequency in <b>opioid</b> dependent populations, individuals carrying the  511T and  31 C alleles ( 511 C/T,  31 C/T or  511 T/T,  31 C/C) had a significantly (p<0.05) higher cortisol levels compared to individuals homozygous for the  511 C and  31T alleles.
+IL1B	drug	alcohol	25930080	In vivo depletion of Kupffer cells (KCs) by liposomal clodronate reduced liver injury and the expression of <strong>Il1b</strong>, but not Cxcl1, Cxcl2, and Cxcl5, suggesting that KCs are partly associated with liver injury, but not neutrophil recruitment, in a chronic binge <b>ethanol</b> feeding model.
+IL1B	addiction	intoxication	25930080	In vivo depletion of Kupffer cells (KCs) by liposomal clodronate reduced liver injury and the expression of <strong>Il1b</strong>, but not Cxcl1, Cxcl2, and Cxcl5, suggesting that KCs are partly associated with liver injury, but not neutrophil recruitment, in a chronic <b>binge</b> ethanol feeding model.
+IL1B	drug	nicotine	25858413	Moreover, recent studies suggested that <strong>IL 1</strong> participates in the progression of lung disease in <b>smokers</b>, which are overrepresented in schizophrenia.
+IL1B	drug	alcohol	25852553	<strong>IL 1</strong> interacts with <b>ethanol</b> effects on GABAergic transmission in the mouse central amygdala.
+IL1B	drug	alcohol	25852553	Overall, our data suggest that the <strong>IL 1</strong> system is involved in basal GABAergic transmission and that IL 1β interacts with the <b>ethanol</b> induced facilitation of CeA GABAergic transmission.
+IL1B	drug	alcohol	25839897	Gene expression studies identified the interleukin 1 receptor type I (IL 1R1) as part of a pathway associated with a genetic predisposition to high <b>alcohol</b> consumption, and lack of the endogenous <strong>IL 1</strong> receptor antagonist (IL 1ra) strongly reduced <b>ethanol</b> intake in mice.
+IL1B	drug	alcohol	25839897	Conversely, deletion of Il1r1 (the gene encoding the <strong>IL 1</strong> receptor type I, IL 1R1) reduces sensitivity to the sedative effects of <b>ethanol</b> and flurazepam and increases the severity of acute <b>ethanol</b> withdrawal.
+IL1B	drug	benzodiazepine	25839897	Conversely, deletion of Il1r1 (the gene encoding the <strong>IL 1</strong> receptor type I, IL 1R1) reduces sensitivity to the sedative effects of ethanol and <b>flurazepam</b> and increases the severity of acute ethanol withdrawal.
+IL1B	addiction	withdrawal	25839897	Conversely, deletion of Il1r1 (the gene encoding the <strong>IL 1</strong> receptor type I, IL 1R1) reduces sensitivity to the sedative effects of ethanol and flurazepam and increases the severity of acute ethanol <b>withdrawal</b>.
+IL1B	drug	cocaine	25762940	The plasma concentrations of <strong>interleukin 1 beta</strong> (IL 1β), IL 6, IL 10, and tumor necrosis factor alpha (TNFα) were affected by history of <b>cocaine</b> addiction and sex.
+IL1B	addiction	addiction	25762940	The plasma concentrations of <strong>interleukin 1 beta</strong> (IL 1β), IL 6, IL 10, and tumor necrosis factor alpha (TNFα) were affected by history of cocaine <b>addiction</b> and sex.
+IL1B	drug	alcohol	25708278	<b>Alcohol</b> induces widespread changes in cytokine expression, with recent data from our laboratory having demonstrated that, during acute <b>ethanol</b> intoxication, adult rats exhibit consistent increases in interleukin (IL) 6 mRNA expression in several brain regions, while showing reductions in <strong>IL 1</strong> and TNFα expression.
+IL1B	addiction	intoxication	25708278	Alcohol induces widespread changes in cytokine expression, with recent data from our laboratory having demonstrated that, during acute ethanol <b>intoxication</b>, adult rats exhibit consistent increases in interleukin (IL) 6 mRNA expression in several brain regions, while showing reductions in <strong>IL 1</strong> and TNFα expression.
+IL1B	drug	alcohol	25582105	Kupffer cells and IL 1β were required for the hepatic iNKT accumulation, as either blocking IL 1β signaling with a recombinant <strong>IL 1</strong> receptor antagonist (IL 1Ra), depleting Kupffer cells by clodronate liposomes, or specifically silencing IL 1β in Kupffer cells by nanoparticle encapsulated siRNA, resulted in inhibited hepatic iNKT cell accumulation and activation, as well as amelioration of <b>alcoholic</b> fatty liver.
+IL1B	addiction	intoxication	25156612	Although cytokine  and region dependent central IL 6 expression was generally increased and tumor necrosis factor alpha decreased during <b>intoxication</b>, <strong>IL 1</strong> expression exhibited increases during withdrawal.
+IL1B	addiction	withdrawal	25156612	Although cytokine  and region dependent central IL 6 expression was generally increased and tumor necrosis factor alpha decreased during intoxication, <strong>IL 1</strong> expression exhibited increases during <b>withdrawal</b>.
+IL1B	drug	cocaine	24854157	<strong>Interleukin 1 beta</strong> (IL 1β), chemokine (C X3 C motif) ligand 1 (CX3CL1)/fractalkine and CXCL12/SDF 1 positively correlated with the <b>cocaine</b> symptom severity when using the DSM IV TR criteria for <b>cocaine</b> abuse/dependence.
+IL1B	addiction	dependence	24854157	<strong>Interleukin 1 beta</strong> (IL 1β), chemokine (C X3 C motif) ligand 1 (CX3CL1)/fractalkine and CXCL12/SDF 1 positively correlated with the cocaine symptom severity when using the DSM IV TR criteria for cocaine abuse/<b>dependence</b>.
+IL1B	drug	opioid	24121451	In this study we investigated the neurodegenerative effects of <b>morphine</b> through its effects on Toll Like Receptor 4 (TLR4) in the male rat hippocampus and evaluated the level of <strong>Interleukin 1 beta</strong> (IL 1β).
+IL1B	drug	alcohol	23206318	<b>Ethanol</b> treatment of brain slice culture released HMGB1 into the media and induced the proinflammatory cytokine, <strong>interleukin 1 beta</strong> (IL 1β).
+IL1B	drug	alcohol	22921768	Taken together, these studies demonstrate that the behavioral sequelae of acute illness and <b>ethanol</b> withdrawal are similar in nature, while antagonist studies suggest that these behavioral alterations are not reversed by blockade of <strong>IL 1</strong> receptors or inhibition of prostaglandin synthesis.
+IL1B	addiction	withdrawal	22921768	Taken together, these studies demonstrate that the behavioral sequelae of acute illness and ethanol <b>withdrawal</b> are similar in nature, while antagonist studies suggest that these behavioral alterations are not reversed by blockade of <strong>IL 1</strong> receptors or inhibition of prostaglandin synthesis.
+IL1B	addiction	sensitization	22820848	Local effects of C5a or <strong>IL 1</strong> receptor antagonists PMX 53 and anakinra on <b>sensitization</b> after neutrophil depletion were examined.
+IL1B	drug	alcohol	19764937	Polymorphisms of the <strong>IL 1</strong> gene complex are associated with <b>alcohol</b> dependence in Spanish Caucasians: data from an association study.
+IL1B	addiction	dependence	19764937	Polymorphisms of the <strong>IL 1</strong> gene complex are associated with alcohol <b>dependence</b> in Spanish Caucasians: data from an association study.
+IL1B	drug	alcohol	19764937	The aim of this study was to investigate whether 4 functionally relevant polymorphisms of the interleukin 1 (<strong>IL 1</strong>) and tumor necrosis factor alpha genes were associated with <b>alcohol</b> dependence and with measures of clinical severity and treatment outcome.
+IL1B	addiction	dependence	19764937	The aim of this study was to investigate whether 4 functionally relevant polymorphisms of the interleukin 1 (<strong>IL 1</strong>) and tumor necrosis factor alpha genes were associated with alcohol <b>dependence</b> and with measures of clinical severity and treatment outcome.
+IL1B	drug	alcohol	19764937	Our findings provide further tentative evidence of the role of <strong>IL 1</strong> in <b>alcohol</b> dependence as well as evidence that the nature of the associations may be direct, gender specific, or involve haplotype effects.
+IL1B	addiction	dependence	19764937	Our findings provide further tentative evidence of the role of <strong>IL 1</strong> in alcohol <b>dependence</b> as well as evidence that the nature of the associations may be direct, gender specific, or involve haplotype effects.
+IL1B	drug	alcohol	19742166	Epistasis between IL1A, <strong>IL1B</strong>, TNF, HTR2A, 5 HTTLPR and TPH2 variations does not impact <b>alcohol</b> dependence disorder features.
+IL1B	addiction	dependence	19742166	Epistasis between IL1A, <strong>IL1B</strong>, TNF, HTR2A, 5 HTTLPR and TPH2 variations does not impact alcohol <b>dependence</b> disorder features.
+IL1B	drug	alcohol	19742166	In both groups we genotyped 11 genetic variations (rs1800587; rs3087258; rs1799724; 5 HTTLPR; rs1386493; rs1386494; rs1487275; rs1843809; rs4570625; rs2129575; rs6313) located in genes whose impact on <b>alcohol</b> related behaviors and disorders has been hypothesized (IL1A, <strong>IL1B</strong>, TNF, 5 HTTLPR, TPH2 and HTR2A).
+IL1B	drug	alcohol	17551540	administrations of the cytokines <strong>IL 1</strong> beta, CCL2 (MCP 1) or TNFalpha (cytokine/withdrawal protocol) before exposure and withdrawal from a 5 day cycle of chronic <b>ethanol</b> diet.
+IL1B	addiction	withdrawal	17551540	administrations of the cytokines <strong>IL 1</strong> beta, CCL2 (MCP 1) or TNFalpha (cytokine/<b>withdrawal</b> protocol) before exposure and <b>withdrawal</b> from a 5 day cycle of chronic ethanol diet.
+IL1B	drug	alcohol	17386065	Conversely, patients with ALC and at least 1 year of <b>alcohol</b> withdrawal (ALCAW group) showed a decreased number of total circulating DC, whereas ALC patients with active EtOH intake (ALCET group) had an abnormally low production of <strong>IL1beta</strong> and TNFalpha by PB DC.
+IL1B	addiction	withdrawal	17386065	Conversely, patients with ALC and at least 1 year of alcohol <b>withdrawal</b> (ALCAW group) showed a decreased number of total circulating DC, whereas ALC patients with active EtOH intake (ALCET group) had an abnormally low production of <strong>IL1beta</strong> and TNFalpha by PB DC.
+IL1B	drug	alcohol	17386065	Conversely, patients with ALC and at least 1 year of <b>alcohol</b> withdrawal (ALCAW group) showed a decreased number of total circulating DC, whereas ALC patients with active EtOH intake (ALCET group) had an abnormally low production of <strong><strong>IL1beta</strong></strong> and TNFalpha by PB DC.
+IL1B	addiction	withdrawal	17386065	Conversely, patients with ALC and at least 1 year of alcohol <b>withdrawal</b> (ALCAW group) showed a decreased number of total circulating DC, whereas ALC patients with active EtOH intake (ALCET group) had an abnormally low production of <strong><strong>IL1beta</strong></strong> and TNFalpha by PB DC.
+IL1B	drug	alcohol	17374050	While T x Hem did not prevent LPS induced release of TNF alpha, IL 1alpha, IL 6, or IL 10 at 6 or 24 hours, <b>alcohol</b> binge suppressed TNF alpha, <strong>IL 1</strong> and IL 6 release, without altering IL 10 response in cells isolated from blood and pleural compartment.
+IL1B	addiction	intoxication	17374050	While T x Hem did not prevent LPS induced release of TNF alpha, IL 1alpha, IL 6, or IL 10 at 6 or 24 hours, alcohol <b>binge</b> suppressed TNF alpha, <strong>IL 1</strong> and IL 6 release, without altering IL 10 response in cells isolated from blood and pleural compartment.
+IL1B	drug	alcohol	17105669	<strong>IL 1</strong> levels were significantly reduced in the <b>alcohol</b> plus resveratrol group compared with the <b>alcohol</b> group (p < 0.05).
+IL1B	drug	benzodiazepine	15713338	Effects of HI 6, <b>diazepam</b> and atropine on soman induced <strong>IL 1</strong> beta protein in rat brain.
+IL1B	drug	alcohol	15289211	In 36 <b>alcoholics</b> without liver disease, at the point of commencing withdrawal from <b>alcohol</b>, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, <strong>IL1beta</strong>, IL1RA, IL4, IL6, IL8, IL10 and IL12).
+IL1B	addiction	withdrawal	15289211	In 36 alcoholics without liver disease, at the point of commencing <b>withdrawal</b> from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, <strong>IL1beta</strong>, IL1RA, IL4, IL6, IL8, IL10 and IL12).
+IL1B	drug	alcohol	15289211	In 36 <b>alcoholics</b> without liver disease, at the point of commencing withdrawal from <b>alcohol</b>, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, <strong><strong>IL1beta</strong></strong>, IL1RA, IL4, IL6, IL8, IL10 and IL12).
+IL1B	addiction	withdrawal	15289211	In 36 alcoholics without liver disease, at the point of commencing <b>withdrawal</b> from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, <strong><strong>IL1beta</strong></strong>, IL1RA, IL4, IL6, IL8, IL10 and IL12).
+IL1B	drug	amphetamine	12542666	Single administration of the cytokine interleukin 1 alpha (<strong>IL 1</strong>), or the psychostimulant <b>amphetamine</b>, enhanced adrenocorticotropin hormone and corticosterone responses to a stress challenge weeks later.
+IL1B	drug	amphetamine	12542666	Three weeks later, <strong>IL 1</strong> and <b>amphetamine</b> primed rats showed enhanced adrenocorticotropin hormone and corticosterone responses to an <b>amphetamine</b> challenge.
+IL1B	drug	amphetamine	12542666	Single administration of either <strong>IL 1</strong> or <b>amphetamine</b> causes three weeks later a selective decrease in relative DBH innervation density in those subnuclei of the PVN that contain high numbers of corticotrophin releasing hormone (CRH) producing neurons: the dorsal parvocellular and medial parvocellular PVN.
+IL1B	drug	amphetamine	12542666	We conclude that (1) long lasting sensitization induced by single exposure to <strong>IL 1</strong> and <b>amphetamine</b> induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative DBH innervation density in CRH rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.
+IL1B	addiction	sensitization	12542666	We conclude that (1) long lasting <b>sensitization</b> induced by single exposure to <strong>IL 1</strong> and amphetamine induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative DBH innervation density in CRH rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.
+IL1B	drug	opioid	12200111	These results suggest that <strong>IL 1</strong> beta produces antinociceptive effect by binding <strong>IL 1</strong> receptor at the spinal level, and is related to the activation of <b>opioid</b> and 5 HT systems.
+IL1B	drug	nicotine	11579484	The present investigation was conducted to determine the HP infection rate with reference to the <strong>Interleukin 1 beta</strong> gene (IL 1B) polymorphism and assess the interactions with <b>smoking</b> reported for outpatients.
+IL1B	drug	amphetamine	11403685	Single administration of the cytokine interleukin 1beta (<strong>IL 1</strong>) or the psychostimulant <b>amphetamine</b> causes long term sensitization of the hypothalamus pituitary adrenal (HPA) axis, i.e.
+IL1B	addiction	sensitization	11403685	Single administration of the cytokine interleukin 1beta (<strong>IL 1</strong>) or the psychostimulant amphetamine causes long term <b>sensitization</b> of the hypothalamus pituitary adrenal (HPA) axis, i.e.
+IL1B	drug	amphetamine	11403685	Single exposure to <strong>IL 1</strong> or <b>amphetamine</b> induced cross sensitization of ACTH and corticosterone responses 11 and 22 days later, but not after 42 days.
+IL1B	addiction	sensitization	11403685	Single exposure to <strong>IL 1</strong> or amphetamine induced cross <b>sensitization</b> of ACTH and corticosterone responses 11 and 22 days later, but not after 42 days.
+IL1B	drug	amphetamine	11403685	<b>Amphetamine</b> induced HPA sensitization was not accompanied by increased costorage of arginine vasopressin (AVP) in CRH terminals, as found previously after <strong>IL 1</strong> pretreatment.
+IL1B	addiction	sensitization	11403685	Amphetamine induced HPA <b>sensitization</b> was not accompanied by increased costorage of arginine vasopressin (AVP) in CRH terminals, as found previously after <strong>IL 1</strong> pretreatment.
+IL1B	drug	amphetamine	11403685	Single administration of <b>amphetamine</b> and <strong>IL 1</strong> induced a long lasting (up to 22 days) increase (up to 165%) of evoked noradrenaline release.
+IL1B	drug	amphetamine	11403685	This common, long lasting functional change may underlie, at least in part, <strong>IL 1</strong>  and <b>amphetamine</b> induced HPA cross sensitization.
+IL1B	addiction	sensitization	11403685	This common, long lasting functional change may underlie, at least in part, <strong>IL 1</strong>  and amphetamine induced HPA cross <b>sensitization</b>.
+IL1B	drug	amphetamine	11403685	In addition, increased AVP signalling by hypothalamic CRH neurons appears to play a role in <strong>IL 1</strong> induced, but not in <b>amphetamine</b> induced, HPA sensitization.
+IL1B	addiction	sensitization	11403685	In addition, increased AVP signalling by hypothalamic CRH neurons appears to play a role in <strong>IL 1</strong> induced, but not in amphetamine induced, HPA <b>sensitization</b>.
+IL1B	drug	alcohol	10417056	During chronic <b>alcohol</b> intoxication, increased levels of serum endotoxin, TNF, <strong>IL 1</strong>, and transaminase were observed and hepatic superoxide anion release was present.
+IL1B	addiction	intoxication	10417056	During chronic alcohol <b>intoxication</b>, increased levels of serum endotoxin, TNF, <strong>IL 1</strong>, and transaminase were observed and hepatic superoxide anion release was present.
+IL1B	drug	alcohol	9895030	This study examines i) the activity of serum prolyl endopeptidase (PEP) and dipeptidlyl peptidase IV (DPP IV) in detoxified <b>alcohol</b> dependent patients without liver disease versus normal controls, and ii) the relationships between serum DPP IV and PEP activity and the production of cytokines or cytokine receptors, such as interleukin 6 (IL 6), tumor necrosis factor alpha (TNF alpha), interferon y (IFN y), <strong>IL 1</strong> receptor antagonist (IL 1RA), and IL 10, and granulocyte macrophage colony stimulatory factor (GM CSF).
+IL1B	drug	opioid	8814911	Chronic exposure to <b>morphine</b> attenuates expression of <strong>interleukin 1 beta</strong> in the rat hippocampus.
+IL1B	drug	opioid	8814911	Alteration of <strong>IL 1</strong> beta expression by exogenous factors, such as <b>morphine</b>, may affect the neuro endocrine immune axis.
+IL1B	drug	opioid	8814911	Brain sections from male rats implanted with either <b>morphine</b> or placebo pellets were stained for <strong>IL 1</strong> beta immunoreactivity.
+IL1B	drug	opioid	8814911	The results showed pronounced attenuation of <strong>IL 1</strong> beta immuno reactivity in the dentate gyrus and the CA1 CA3 fields of the hippocampus in <b>morphine</b> implanted rats compared to placebo controls.
+IL1B	drug	opioid	8814911	Attenuation of <strong>IL 1</strong> beta expression in the hippocampus by chronic exposure to <b>morphine</b> may be one of the mechanisms underlying the neuro endocrine immune modulatory effects of opiate addiction.
+IL1B	addiction	addiction	8814911	Attenuation of <strong>IL 1</strong> beta expression in the hippocampus by chronic exposure to morphine may be one of the mechanisms underlying the neuro endocrine immune modulatory effects of opiate <b>addiction</b>.
+IL1B	drug	opioid	8590986	administration of interleukin 1 beta (<strong>IL 1</strong> beta) attenuates <b>naloxone</b> precipitated withdrawal jumps in <b>morphine</b> dependent mice, and the effect was partly mediated by the corticotropin releasing factor.
+IL1B	addiction	withdrawal	8590986	administration of interleukin 1 beta (<strong>IL 1</strong> beta) attenuates naloxone precipitated <b>withdrawal</b> jumps in morphine dependent mice, and the effect was partly mediated by the corticotropin releasing factor.
+IL1B	drug	opioid	8590986	administration of <strong>interleukin 1 beta</strong> (<strong>IL 1</strong> beta) attenuates <b>naloxone</b> precipitated withdrawal jumps in <b>morphine</b> dependent mice, and the effect was partly mediated by the corticotropin releasing factor.
+IL1B	addiction	withdrawal	8590986	administration of <strong>interleukin 1 beta</strong> (<strong>IL 1</strong> beta) attenuates naloxone precipitated <b>withdrawal</b> jumps in morphine dependent mice, and the effect was partly mediated by the corticotropin releasing factor.
+IL1B	drug	opioid	8590986	To elucidate further other possible mechanisms involved in the inhibitory effect of <strong>IL 1</strong> beta on <b>morphine</b> withdrawal jumping behaviour, in this study, we examined the involvement of the prostaglandin synthesis pathway, because prostaglandins have been shown to mediate the several central effects of <strong>IL 1</strong>.
+IL1B	addiction	withdrawal	8590986	To elucidate further other possible mechanisms involved in the inhibitory effect of <strong>IL 1</strong> beta on morphine <b>withdrawal</b> jumping behaviour, in this study, we examined the involvement of the prostaglandin synthesis pathway, because prostaglandins have been shown to mediate the several central effects of <strong>IL 1</strong>.
+IL1B	drug	opioid	8590986	The inhibitory effect of <strong>IL 1</strong> beta (1 ng/mouse) administered intracisternally 30 min before <b>naloxone</b> (10 mg kg 1, i.p.)
+IL1B	drug	opioid	8590986	administration of vehicle instead of <strong>IL 1</strong> beta did not significantly change the number of jumps precipitated by <b>naloxone</b>.
+IL1B	drug	opioid	8590986	These results indicate that the prostaglandin synthesis pathway is, at least in part, involved in the inhibitory effect of <strong>IL 1</strong> beta on <b>naloxone</b> precipitated withdrawal jumps in <b>morphine</b> dependent mice, and that the prostaglandin synthesized in the brain suppresses the <b>morphine</b> withdrawal jumping behaviour via the EP3 receptor, but not via the EP1 , EP2 , IP  or FP receptor.
+IL1B	addiction	withdrawal	8590986	These results indicate that the prostaglandin synthesis pathway is, at least in part, involved in the inhibitory effect of <strong>IL 1</strong> beta on naloxone precipitated <b>withdrawal</b> jumps in morphine dependent mice, and that the prostaglandin synthesized in the brain suppresses the morphine <b>withdrawal</b> jumping behaviour via the EP3 receptor, but not via the EP1 , EP2 , IP  or FP receptor.
+IL1B	drug	opioid	7671998	Intracisternal administration of <strong>interleukin 1 beta</strong> attenuates <b>naloxone</b> precipitated withdrawal in <b>morphine</b> dependent mice.
+IL1B	addiction	withdrawal	7671998	Intracisternal administration of <strong>interleukin 1 beta</strong> attenuates naloxone precipitated <b>withdrawal</b> in morphine dependent mice.
+IL1B	drug	opioid	7671998	The effect of central administration of <strong>interleukin 1 beta</strong> on <b>naloxone</b> precipitated withdrawal in <b>morphine</b> dependent mice was studied.
+IL1B	addiction	withdrawal	7671998	The effect of central administration of <strong>interleukin 1 beta</strong> on naloxone precipitated <b>withdrawal</b> in morphine dependent mice was studied.
+IL1B	drug	opioid	7671998	administration of <strong>interleukin 1 beta</strong> (0.01 1 ng/5 microliters per mouse) to <b>morphine</b> dependent mice 30 min prior to the injection of <b>naloxone</b> (10 mg/kg i.p.)
+IL1B	drug	opioid	7671998	These results suggest that centrally administered <strong>interleukin 1 beta</strong> could attenuate <b>naloxone</b> precipitated withdrawal in <b>morphine</b> dependent mice via interleukin 1 receptors in the brain.
+IL1B	addiction	withdrawal	7671998	These results suggest that centrally administered <strong>interleukin 1 beta</strong> could attenuate naloxone precipitated <b>withdrawal</b> in morphine dependent mice via interleukin 1 receptors in the brain.
+IL1B	drug	opioid	8231628	Since <strong>IL 1</strong> alone did not induce analgesia, we tested its capacity to potentiate <b>morphine</b> analgesia.
+IL1B	drug	opioid	8231628	<b>Morphine</b> (5.0 and 10 micrograms, icv) induced analgesia in the CWT (32.7 and 61.8% maximum analgesia, respectively); however, there was no significant effect of <strong>IL 1</strong> beta on <b>morphine</b> induced analgesia.
+IL1B	drug	opioid	8231628	In summary, we failed to find an analgesic effect of <strong>IL 1</strong>, alone or in combination with <b>morphine</b>, at doses which clearly had a physiological effect; this is in contrast to the reports cited above.
+IL1B	addiction	dependence	2115435	We then studied the ability of the most potent lymphokine in this system, interleukin 1 beta (<strong>Il 1</strong> beta), to interfere with the proestrous LH surge and ovulation in the intact female rat as well as the <b>dependence</b> of this effect on the activation of opiate receptors.
+IL1B	addiction	dependence	2115435	We then studied the ability of the most potent lymphokine in this system, <strong>interleukin 1 beta</strong> (<strong>Il 1</strong> beta), to interfere with the proestrous LH surge and ovulation in the intact female rat as well as the <b>dependence</b> of this effect on the activation of opiate receptors.
+IL1B	drug	opioid	2115435	The possible involvement of opiate dependent pathways in mediating the inhibitory action of <strong>Il 1</strong> beta on reproductive processes was tested by implanting <b>naloxone</b> pellets 16 24 h before lymphokine treatment.
+IL1B	drug	opioid	2115435	When given before icv <strong>Il 1</strong> beta, all <b>naloxone</b> regimens countered the effect of the cytokine, with the 800 micrograms/h dose restoring ovulation in eight of nine rats.
+CHAT	drug	alcohol	32607619	Replicated preclinical data has indicated that adolescent exposure to binge like levels of <b>alcohol</b> results in a reduction of choline acetyltransferase (<strong>ChAT</strong>) and an upregulation in the α7 nicotinic receptor (α7).
+CHAT	addiction	intoxication	32607619	Replicated preclinical data has indicated that adolescent exposure to <b>binge</b> like levels of alcohol results in a reduction of choline acetyltransferase (<strong>ChAT</strong>) and an upregulation in the α7 nicotinic receptor (α7).
+CHAT	drug	nicotine	31796061	Effectiveness of a <strong>chat</strong> bot for the adult population to quit <b>smoking</b>: protocol of a pragmatic clinical trial in primary care (Dejal@).
+CHAT	drug	nicotine	31796061	Thus, the purpose of this study is to assess the effectiveness of an intervention that helps people cease <b>smoking</b> and increase their <b>nicotine</b> abstinence rates in the long term via a <strong>chat</strong> bot, compared to usual practice, utilizing a chemical validation at 6 months.
+CHAT	drug	nicotine	31796061	Intervention group: use of a <strong>chat</strong> bot with evidence based contents to help quit <b>smoking</b>.
+CHAT	drug	alcohol	31634498	In the present study, we have examined, using stereological methods, the effects of chronic <b>alcohol</b> consumption (6 months) and subsequent withdrawal (2 months) on the total number and size of PPT and LDT choline acetyltransferase (<strong>ChAT</strong>) immunoreactive neurons.
+CHAT	addiction	withdrawal	31634498	In the present study, we have examined, using stereological methods, the effects of chronic alcohol consumption (6 months) and subsequent <b>withdrawal</b> (2 months) on the total number and size of PPT and LDT choline acetyltransferase (<strong>ChAT</strong>) immunoreactive neurons.
+CHAT	drug	alcohol	31634498	The total number of PPT and LDT <strong>ChAT</strong> immunoreactive neurons was unchanged in <b>ethanol</b> treated and withdrawn rats.
+CHAT	drug	alcohol	31634498	However, <strong>ChAT</strong> immunoreactive neurons were significantly hypertrophied in <b>ethanol</b> treated rats, an alteration that did not revert 2 months after <b>ethanol</b> withdrawal.
+CHAT	addiction	withdrawal	31634498	However, <strong>ChAT</strong> immunoreactive neurons were significantly hypertrophied in ethanol treated rats, an alteration that did not revert 2 months after ethanol <b>withdrawal</b>.
+CHAT	drug	cocaine	31193584	Web based self help with and without <strong>chat</strong> counseling to reduce <b>cocaine</b> use in <b>cocaine</b> misusers: Results of a three arm randomized controlled trial.
+CHAT	drug	cocaine	31193584	To test the efficacy of a web based self help intervention, with and without <strong>chat</strong> counseling, grounded in CBT, at reducing <b>cocaine</b> use in <b>cocaine</b> misusers not in treatment for a substance use disorder.
+CHAT	drug	alcohol	30779268	Preclinical rodent studies using the adolescent intermittent <b>ethanol</b> (AIE; 5.0 g/kg, i.g., 2 day on/2 day off from postnatal day [P]25 to P55) model of human adolescent binge drinking report decreased basal forebrain cholinergic (ie, <strong>ChAT</strong>+) neurons that persist into adulthood (ie, P56 P220).
+CHAT	addiction	intoxication	30779268	Preclinical rodent studies using the adolescent intermittent ethanol (AIE; 5.0 g/kg, i.g., 2 day on/2 day off from postnatal day [P]25 to P55) model of human adolescent <b>binge</b> drinking report decreased basal forebrain cholinergic (ie, <strong>ChAT</strong>+) neurons that persist into adulthood (ie, P56 P220).
+CHAT	drug	alcohol	30779268	Adolescent intermittent <b>ethanol</b> caused a persistent increase in adult H3K9me2 and DNA methylation at promoter regions of <strong>Chat</strong> and H3K9me2 of Trka, which was restored by wheel running.
+CHAT	drug	nicotine	30702431	Exploring Community <b>Smokers</b>' Perspectives for Developing a <strong>Chat</strong> Based <b>Smoking</b> Cessation Intervention Delivered Through Mobile Instant Messaging: Qualitative Study.
+CHAT	drug	nicotine	30702431	This study aims to explore the perception of using mobile IM as a modality to deliver a proposed <strong>chat</strong> intervention for <b>smoking</b> cessation in community <b>smokers</b> in Hong Kong, where the proportion of smartphone use is among the highest in the world.
+CHAT	drug	nicotine	30702431	Furthermore, the findings inform the development of a <strong>chat</strong> based, IM <b>smoking</b> cessation program being evaluated in a community trial.
+CHAT	drug	nicotine	30593882	<strong>Chat</strong> based instant messaging support combined with brief <b>smoking</b> cessation interventions for Chinese community <b>smokers</b> in Hong Kong: Rationale and study protocol for a pragmatic, cluster randomized controlled trial.
+CHAT	drug	nicotine	30593882	This paper presents the rationale and study design of a trial which aims to evaluate the effectiveness of a <strong>chat</strong> based intervention using mobile instant messaging combined with brief interventions for community <b>smokers</b>.
+CHAT	drug	nicotine	30593882	Subjects in intervention group received three months of <strong>chat</strong> based, instant messaging support guided by acceptance and commitment therapy and other behavioural change techniques, integrated with brief advice and active referral to a <b>smoking</b> cessation service using the AWARD (Ask, Warn, Advise, Refer, Do it again) intervention model.
+CHAT	drug	alcohol	30296276	Adolescent intermittent <b>ethanol</b> exposure also reduces basal forebrain expression of choline acetyltransferase (<strong>ChAT</strong>), an enzyme critical for acetylcholine synthesis in cholinergic neurons similar to findings in the post mortem human <b>alcoholic</b> basal forebrain.
+CHAT	drug	alcohol	30296276	We report here that AIE decreases basal forebrain <strong>ChAT</strong>+IR neurons in both adult female and male Wistar rats following early or late adolescent <b>ethanol</b> exposure.
+CHAT	addiction	reward	29740282	Here we study the function of muscarinic M4 receptors (M4Rs) in dopamine D1 receptor (D1R) expressing neurons and cholinergic neurons (expressing choline acetyltransferase; <strong>ChAT</strong>), during various <b>reward</b> enforced behaviors and in a "waiting" impulsivity test.
+CHAT	drug	cannabinoid	29739738	Effects of Treatment Length and <strong>Chat</strong> Based Counseling in a Web Based Intervention for <b>Cannabis</b> Users: Randomized Factorial Trial.
+CHAT	drug	nicotine	29371319	Altered Baseline and <b>Nicotine</b> Mediated Behavioral and Cholinergic Profiles in <strong>ChAT</strong> Cre Mouse Lines.
+CHAT	drug	nicotine	29371319	<strong>ChAT</strong>(BAC) Cre transgenic and wild type mice did not differ in general locomotor behavior, anxiety measures, drug induced cataplexy, <b>nicotine</b> mediated hypolocomotion, or operant food training.
+CHAT	addiction	reward	29371319	<strong>ChAT</strong>(BAC) Cre transgenic and wild type mice did not differ in general locomotor behavior, anxiety measures, drug induced cataplexy, nicotine mediated hypolocomotion, or <b>operant</b> food training.
+CHAT	drug	nicotine	29371319	However, <strong>ChAT</strong>(BAC) Cre transgenic mice did exhibit significant deficits in intravenous <b>nicotine</b> self administration, which paralleled an increase in vesicular acetylcholine transporter and choline acetyltransferase (<strong>ChAT</strong>) hippocampal expression.
+CHAT	drug	nicotine	29371319	For the <strong>ChAT</strong>(IRES) Cre line, transgenic mice exhibited deficits in baseline locomotor, <b>nicotine</b> mediated hypolocomotion, and operant food training compared with wild type and hemizygous littermates.
+CHAT	addiction	reward	29371319	For the <strong>ChAT</strong>(IRES) Cre line, transgenic mice exhibited deficits in baseline locomotor, nicotine mediated hypolocomotion, and <b>operant</b> food training compared with wild type and hemizygous littermates.
+CHAT	drug	nicotine	29371319	No differences among <strong>ChAT</strong>(IRES) Cre wild type, hemizygous, and transgenic littermates were found in anxiety measures, drug induced cataplexy, and <b>nicotine</b> self administration.
+CHAT	drug	nicotine	29371319	As such, interpretation of data derived from <strong>ChAT</strong> Cre rodents must consider potential limitations dependent on the line and/or genotype used in research investigations.SIGNIFICANCE STATEMENT Altered baseline and/or <b>nicotine</b> mediated behavioral profiles were discovered in transgenic mice from the <strong>ChAT</strong>(BAC) Cre and <strong>ChAT</strong>(IRES) Cre lines.
+CHAT	addiction	intoxication	28807788	These results indicate that early adolescent <b>binge</b> EtOH exposure leads to a long lasting frontocortical functional cholinergic deficit, driven by a loss of <strong>ChAT</strong>+/nestin+ neurons in the NbM, which was associated with impaired cognitive flexibility during adulthood.
+CHAT	drug	amphetamine	28628197	Previous experiments established that <strong>ChAT</strong> ChR2 mice display an increased sensitivity to <b>amphetamine</b> induced locomotor activity and stereotypes.
+CHAT	drug	cocaine	28628197	<strong>ChAT</strong> ChR2 mice displayed increased locomotor sensitization in response to low dose of <b>cocaine</b>.
+CHAT	addiction	sensitization	28628197	<strong>ChAT</strong> ChR2 mice displayed increased locomotor <b>sensitization</b> in response to low dose of cocaine.
+CHAT	drug	cocaine	28628197	These findings demonstrate that <strong>ChAT</strong> ChR2 mice present major alterations of CIN neuronal morphology and increased behavioral sensitization to <b>cocaine</b>, supporting the notion that the increased levels of VAChT observed in these mice make them fundamentally different from wild type mice.
+CHAT	addiction	sensitization	28628197	These findings demonstrate that <strong>ChAT</strong> ChR2 mice present major alterations of CIN neuronal morphology and increased behavioral <b>sensitization</b> to cocaine, supporting the notion that the increased levels of VAChT observed in these mice make them fundamentally different from wild type mice.
+CHAT	addiction	relapse	27707896	Participants were telephone interviewed and assessed using the Case finding and Help Assessment Tool (<strong>CHAT</strong>) with employee lifestyle risk factors, mental health issues and help <b>seeking</b> intentions screened across eight industries.
+CHAT	drug	nicotine	26623516	Mice lacking <strong>CHAT</strong> in habenular neurons were insensitive to <b>nicotine</b> conditioned reward and withdrawal.
+CHAT	addiction	reward	26623516	Mice lacking <strong>CHAT</strong> in habenular neurons were insensitive to nicotine conditioned <b>reward</b> and withdrawal.
+CHAT	addiction	withdrawal	26623516	Mice lacking <strong>CHAT</strong> in habenular neurons were insensitive to nicotine conditioned reward and <b>withdrawal</b>.
+CHAT	drug	cannabinoid	26462848	A Web Based Self Help Intervention With and Without <strong>Chat</strong> Counseling to Reduce <b>Cannabis</b> Use in Problematic <b>Cannabis</b> Users: Three Arm Randomized Controlled Trial.
+CHAT	drug	cannabinoid	26462848	To test the efficacy of a Web based self help intervention with and without <strong>chat</strong> counseling Can Reduce in reducing the <b>cannabis</b> use of problematic <b>cannabis</b> users as an alternative to outpatient treatment services.
+CHAT	drug	cannabinoid	26462848	The change in the mean number of <b>cannabis</b> use days per week at 3 months differed between self help without <strong>chat</strong> (mean change 0.7, SD  0.2) and self help with <strong>chat</strong> (mean change 1.4, SD  0.5; beta= 0.75, SE=0.32, t= 2.39, P=.02, d=0.34, 95% CI 0.07 0.61), as well as between self help with <strong>chat</strong> and waiting list (mean change 1.0, SD  0.8; beta=0.70, SE=0.32, t=2.16, P=.03, d=0.20, 95% CI  0.07 to 0.47).
+CHAT	drug	cannabinoid	26462848	Web based self help interventions supplemented by brief <strong>chat</strong> counseling are an effective alternative to face to face treatment and can reach a group of <b>cannabis</b> users who differ in their use and sociodemographic characteristics from those who enter outpatient addiction treatment.
+CHAT	addiction	addiction	26462848	Web based self help interventions supplemented by brief <strong>chat</strong> counseling are an effective alternative to face to face treatment and can reach a group of cannabis users who differ in their use and sociodemographic characteristics from those who enter outpatient <b>addiction</b> treatment.
+CHAT	drug	cocaine	26159624	Evaluating the efficacy of a web based self help intervention with and without <strong>chat</strong> counseling in reducing the <b>cocaine</b> use of problematic <b>cocaine</b> users: the study protocol of a pragmatic three arm randomized controlled trial.
+CHAT	drug	cocaine	26159624	The study will use a three arm randomized controlled trial (RCT) design to test the efficacy of a web based self help intervention with or without guided <strong>chat</strong> counseling compared with that of a waiting list control condition in reducing or stopping <b>cocaine</b> use.
+CHAT	addiction	relapse	26159624	The three individual <strong>chat</strong> therapy sessions will be based on the same therapy approaches and will be tailored to participants' self help data and aim to assist the <b>reinstatement</b> of social rewards and the improvement of social support and relationships.
+CHAT	drug	cocaine	26159624	This study will be the first RCT to test the effectiveness of a web based self help intervention in combination with or without <strong>chat</strong> counseling in reducing <b>cocaine</b> use.
+CHAT	drug	cocaine	26059306	In particular, p11 in the <strong>ChAT</strong>+ cells or DRD1+ MSN of the NAc, controls depressive like behavior or <b>cocaine</b> reward, respectively.
+CHAT	addiction	reward	26059306	In particular, p11 in the <strong>ChAT</strong>+ cells or DRD1+ MSN of the NAc, controls depressive like behavior or cocaine <b>reward</b>, respectively.
+CHAT	addiction	reward	25586659	Rats bearing bilateral lesions of cholinergic pPPTg neurons (>90% <strong>ChAT</strong>+ neuronal loss) displayed no deficits in the learning or performance of fixed and variable ratio schedules of <b>reinforcement</b> for pellet <b>reward</b>.
+CHAT	drug	alcohol	25405505	In Experiment 1, adolescent intermittent <b>ethanol</b> (AIE; 5.0 g/kg, i.g., 2 day on/2 day off from postnatal day [P] 25 to P55) treatment led to persistent, global reductions of choline acetyltransferase (<strong>ChAT</strong>) expression.
+CHAT	drug	alcohol	25405505	To determine if the binge <b>ethanol</b> induced <strong>ChAT</strong> decline was unique to the adolescent, Experiment 2 examined <strong>ChAT</strong>+IR in the basal forebrain following adolescent (P28 P48) and adult (P70 P90) binge <b>ethanol</b> exposure.
+CHAT	addiction	intoxication	25405505	To determine if the <b>binge</b> ethanol induced <strong>ChAT</strong> decline was unique to the adolescent, Experiment 2 examined <strong>ChAT</strong>+IR in the basal forebrain following adolescent (P28 P48) and adult (P70 P90) <b>binge</b> ethanol exposure.
+CHAT	drug	alcohol	25405505	Twenty five days later, <strong>ChAT</strong> expression was reduced in adolescent, but not adult, binge <b>ethanol</b> exposed animals.
+CHAT	addiction	intoxication	25405505	Twenty five days later, <strong>ChAT</strong> expression was reduced in adolescent, but not adult, <b>binge</b> ethanol exposed animals.
+CHAT	drug	alcohol	25405505	In Experiment 3, expression of <strong>ChAT</strong> and vesicular acetylcholine transporter expression was found to be significantly reduced in the <b>alcoholic</b> basal forebrain relative to moderate drinking controls.
+CHAT	drug	alcohol	25405505	Together, these data suggest that adolescent binge <b>ethanol</b> decreases adult <strong>ChAT</strong> expression, possibly through neuroimmune mechanisms, which might impact adult cognition, arousal, or reward sensitivity.
+CHAT	addiction	intoxication	25405505	Together, these data suggest that adolescent <b>binge</b> ethanol decreases adult <strong>ChAT</strong> expression, possibly through neuroimmune mechanisms, which might impact adult cognition, arousal, or reward sensitivity.
+CHAT	addiction	reward	25405505	Together, these data suggest that adolescent binge ethanol decreases adult <strong>ChAT</strong> expression, possibly through neuroimmune mechanisms, which might impact adult cognition, arousal, or <b>reward</b> sensitivity.
+CHAT	drug	alcohol	24893293	Conversely, the number and the size of cholinergic interneurons, and the amount of <strong>ChAT</strong> were unchanged in <b>ethanol</b> treated and withdrawn rats, but the density of cholinergic varicosities was reduced by 50% during <b>alcohol</b> consumption and by 64% after withdrawal.
+CHAT	addiction	withdrawal	24893293	Conversely, the number and the size of cholinergic interneurons, and the amount of <strong>ChAT</strong> were unchanged in ethanol treated and withdrawn rats, but the density of cholinergic varicosities was reduced by 50% during alcohol consumption and by 64% after <b>withdrawal</b>.
+CHAT	drug	cannabinoid	24228630	Can reduce  the effects of <strong>chat</strong> counseling and web based self help, web based self help alone and a waiting list control program on <b>cannabis</b> use in problematic <b>cannabis</b> users: a randomized controlled trial.
+CHAT	drug	cannabinoid	24228630	The offer of a combined web based self help and <strong>chat</strong> counseling treatment could potentially also reach those users who hesitate to approach such treatment centers and help them to reduce their <b>cannabis</b> use.
+CHAT	drug	cannabinoid	24228630	This paper presents the protocol for a three armed randomized controlled trial that will test the effectiveness of a web based self help intervention in combination with, or independent of, tailored <strong>chat</strong> counseling compared to a waiting list in reducing or enabling the abstention from <b>cannabis</b> use in problematic users.
+CHAT	drug	cannabinoid	24228630	To the best of our knowledge, this will be the first randomized controlled trial to test the effectiveness of online self help therapy in combination or without <strong>chat</strong> counseling in reducing or enabling the abstention from <b>cannabis</b> use.
+CHAT	drug	nicotine	24076142	Recently, we reported that several polymorphisms and haplotypes in the choline acetyltransferase gene (<strong>ChAT</strong>) are associated with <b>nicotine</b> dependence (ND).
+CHAT	addiction	dependence	24076142	Recently, we reported that several polymorphisms and haplotypes in the choline acetyltransferase gene (<strong>ChAT</strong>) are associated with nicotine <b>dependence</b> (ND).
+CHAT	drug	nicotine	23222296	<b>Nicotine</b> induced ACh production was mediated by α7 , α3β2 , and β3 nAChRs, <strong>ChAT</strong> and VAChT pathways.
+CHAT	drug	nicotine	23222296	We observed that <b>nicotine</b> upregulated <strong>ChAT</strong> and VAChT.
+CHAT	drug	alcohol	22033458	Periadolescent <b>ethanol</b> exposure reduces adult forebrain <strong>ChAT</strong>+IR neurons: correlation with behavioral pathology.
+CHAT	drug	alcohol	22033458	In the present study, immunohistochemistry for choline acetyltransferase (<strong>ChAT</strong>) was determined to assess forebrain cholinergic neurons (Ch1 4), and behavioral changes following periadolescent <b>alcohol</b> exposure.
+CHAT	drug	alcohol	22033458	Quantitative analyses of <strong>ChAT</strong> immunoreactivity revealed a significant reduction in cell counts in the Ch1 2 and Ch3 4 regions of the basal forebrain in <b>ethanol</b> vapor exposed rats.
+CHAT	drug	alcohol	22033458	These studies demonstrate that behavioral measures of arousal, affective state, disinhibitory behavior, and <strong>ChAT</strong>+IR, are all significantly impacted by periadolescent <b>ethanol</b> exposure and withdrawal in Wistar rats.
+CHAT	addiction	withdrawal	22033458	These studies demonstrate that behavioral measures of arousal, affective state, disinhibitory behavior, and <strong>ChAT</strong>+IR, are all significantly impacted by periadolescent ethanol exposure and <b>withdrawal</b> in Wistar rats.
+CHAT	drug	opioid	21967037	Moreover, the time course of PEBP expression changes and <strong>ChAT</strong> activity was investigated during chronic <b>morphine</b> treatment and withdrawal.
+CHAT	addiction	withdrawal	21967037	Moreover, the time course of PEBP expression changes and <strong>ChAT</strong> activity was investigated during chronic morphine treatment and <b>withdrawal</b>.
+CHAT	addiction	withdrawal	21633116	Effects on <strong>ChAT</strong> and AChE were dependent on the brain region and restricted to the <b>withdrawal</b> period: There were increased activities in the midbrain on PN30.
+CHAT	drug	nicotine	20383528	We recently reported association of the encoding gene <strong>ChAT</strong> with both <b>smoking</b> cessation and <b>nicotine</b> dependence (ND) in two independent European American (EA) samples; however, in the replication sample, only limited SNPs partially covering the gene were examined.
+CHAT	addiction	dependence	20383528	We recently reported association of the encoding gene <strong>ChAT</strong> with both smoking cessation and nicotine <b>dependence</b> (ND) in two independent European American (EA) samples; however, in the replication sample, only limited SNPs partially covering the gene were examined.
+CHAT	drug	alcohol	20309727	Acute <b>alcohol</b> (Alc) intoxication has been shown to decrease choline acetyltransferase (<strong>ChAT</strong>) in the rat brain.
+CHAT	addiction	intoxication	20309727	Acute alcohol (Alc) <b>intoxication</b> has been shown to decrease choline acetyltransferase (<strong>ChAT</strong>) in the rat brain.
+CHAT	drug	nicotine	20309727	The present study extends that finding by examining the effects of <b>nicotine</b> (Nic), Alc, and their combination on <strong>ChAT</strong> and acetylcholinesterase (AChE) in the frontal cortex and hippocampus of rat.
+CHAT	drug	nicotine	20147892	Single SNPs in <strong>ChAT</strong> haplotype block 2 were also associated with pretreatment levels of <b>nicotine</b> dependence in this cohort.
+CHAT	addiction	dependence	20147892	Single SNPs in <strong>ChAT</strong> haplotype block 2 were also associated with pretreatment levels of nicotine <b>dependence</b> in this cohort.
+CHAT	drug	nicotine	20147892	To replicate associations of SNPs in haplotype blocks 2 and 6 of <strong>ChAT</strong> with <b>nicotine</b> dependence in a non treatment seeking cohort, we used data from an independent community based sample of 629 <b>smokers</b> representing 200 families of European ancestry.
+CHAT	addiction	dependence	20147892	To replicate associations of SNPs in haplotype blocks 2 and 6 of <strong>ChAT</strong> with nicotine <b>dependence</b> in a non treatment seeking cohort, we used data from an independent community based sample of 629 smokers representing 200 families of European ancestry.
+CHAT	addiction	relapse	20147892	To replicate associations of SNPs in haplotype blocks 2 and 6 of <strong>ChAT</strong> with nicotine dependence in a non treatment <b>seeking</b> cohort, we used data from an independent community based sample of 629 smokers representing 200 families of European ancestry.
+CHAT	drug	nicotine	20147892	Although the effect sizes in both cohorts are modest, converging data across cohorts and phenotypes suggest that <strong>ChAT</strong> may be involved in <b>nicotine</b> dependence and ability to quit <b>smoking</b>.
+CHAT	addiction	dependence	20147892	Although the effect sizes in both cohorts are modest, converging data across cohorts and phenotypes suggest that <strong>ChAT</strong> may be involved in nicotine <b>dependence</b> and ability to quit smoking.
+CHAT	drug	nicotine	20147892	Additional sequencing and characterization of <strong>ChAT</strong> may reveal functional variants that contribute to <b>nicotine</b> dependence and <b>smoking</b> cessation.
+CHAT	addiction	dependence	20147892	Additional sequencing and characterization of <strong>ChAT</strong> may reveal functional variants that contribute to nicotine <b>dependence</b> and smoking cessation.
+CHAT	addiction	withdrawal	19465085	We assessed nAChR binding, choline acetyltransferase (<strong>ChAT</strong>) activity and [(3)H]hemicholinium 3 (HC 3) binding in the cerebral cortex and midbrain of mice at short (PN50) and long term (PN75) <b>withdrawal</b>.
+CHAT	addiction	withdrawal	19465085	NIC short term <b>withdrawal</b> elicited an increase in <strong>ChAT</strong> activity that was reversed by ETOH <b>withdrawal</b>.
+CHAT	addiction	withdrawal	19465085	In addition, NIC+ETOH elicited a decrease in <strong>ChAT</strong> activity at long term <b>withdrawal</b>.
+CHAT	drug	alcohol	19433841	The short, validated, self administered, Case finding and Help Assessment Tool (<strong>CHAT</strong>) for lifestyle and mental health assessment of adult patients in primary health care addresses inactivity, tobacco use, <b>alcohol</b> and other drug misuse, problem gambling, depression, anxiety and stress, abuse, and anger problems.
+CHAT	drug	nicotine	19433841	The short, validated, self administered, Case finding and Help Assessment Tool (<strong>CHAT</strong>) for lifestyle and mental health assessment of adult patients in primary health care addresses inactivity, <b>tobacco</b> use, alcohol and other drug misuse, problem gambling, depression, anxiety and stress, abuse, and anger problems.
+CHAT	drug	nicotine	18395624	By itself, adolescent <b>nicotine</b> exposure evoked sex selective deficits in cerebrocortical HC3 binding while elevating <strong>ChAT</strong> in young adulthood in striatum and midbrain.
+CHAT	addiction	withdrawal	18088441	When mice were treated with an antisense oligodeoxynucleotide (AS ODN) against <strong>ChAT</strong>, which decreased <strong>ChAT</strong> signals in the dorsal horn and DRG, but not in motor neurons, they showed a significant decrease in nociceptive thresholds in paw pressure and thermal paw <b>withdrawal</b> tests.
+CHAT	drug	amphetamine	17711382	Characteristics of a sample of men who have sex with men, recruited from gay bars and Internet <strong>chat</strong> rooms, who report <b>methamphetamine</b> use.
+CHAT	drug	nicotine	15066159	Animals neonatally treated with quinpirole demonstrated a significant 36% decrease of <strong>ChAT</strong> in the hippocampus compared to saline controls that was partially eliminated by <b>nicotine</b>.
+CHAT	drug	nicotine	14970833	Prenatal <b>nicotine</b> exposure had only minor effects on nAChRs but produced persistent cholinergic hypoactivity (reduced HC 3 binding relative to <strong>ChAT</strong>) throughout adolescence and into adulthood (PN75).
+CHAT	drug	alcohol	12831864	In addition, the somatic size of <strong>ChAT</strong> IR neurons was reduced by <b>ethanol</b> intake, and withdrawal further aggravated neuronal atrophy.
+CHAT	addiction	withdrawal	12831864	In addition, the somatic size of <strong>ChAT</strong> IR neurons was reduced by ethanol intake, and <b>withdrawal</b> further aggravated neuronal atrophy.
+CHAT	drug	nicotine	12784097	Adolescent <b>nicotine</b> treatment also produced lasting decrements in HC 3 binding that were separable from effects on <strong>ChAT</strong>, suggesting cholinergic synaptic impairment.
+CHAT	drug	nicotine	10915806	During <b>nicotine</b> treatment and for 1 month after the termination of treatment, <strong>ChAT</strong> activity was reduced significantly in the midbrain but not in the other regions.
+CHAT	addiction	withdrawal	10487390	There were no significant differences in the density of the <strong>ChAT</strong> IR hippocampal fiber network when the pure <b>withdrawal</b> and <b>withdrawal</b> + vehicle groups were compared to the <b>withdrawal</b> + GM1 or <b>withdrawal</b> + piracetam groups.
+CHAT	addiction	withdrawal	10487390	In contrast, the number of <strong>ChAT</strong> IR interneurons in the hippocampal formation was higher in the <b>withdrawal</b> + GM1 or <b>withdrawal</b> + piracetam groups than in the pure <b>withdrawal</b> and <b>withdrawal</b> + vehicle groups.
+CHAT	drug	cocaine	7877755	Choline acetyltransferase (<strong>ChAT</strong>) activity was measured in discrete areas of rat brain after chronic, unlimited access to self administration of <b>cocaine</b>.
+CHAT	drug	cocaine	7877755	Mean activity of <strong>ChAT</strong> was reduced by approximately 30% in the nucleus accumbens, both on the last day of <b>cocaine</b> access and after 3 weeks <b>cocaine</b> withdrawal.
+CHAT	addiction	withdrawal	7877755	Mean activity of <strong>ChAT</strong> was reduced by approximately 30% in the nucleus accumbens, both on the last day of cocaine access and after 3 weeks cocaine <b>withdrawal</b>.
+CHAT	drug	opioid	8149590	The effect of prenatal exposure to <b>methadone</b> via maternal osmotic minipumps on the expression of acetylcholinesterase (AChE) and choline acetyltransferase (<strong>ChAT</strong>) has been studied by light microscopy in the striatum of male and female rats.
+CHAT	drug	opioid	8149590	At postnatal day 10, rats of both sexes exhibit reduced intensity of <strong>ChAT</strong> immunoreactive staining in striatal neurons in the <b>methadone</b> treated group in comparison to either untreated or water treated controls.
+CHAT	drug	opioid	8149590	Although the number and distribution of <strong>ChAT</strong> immunoreactive neurons appear to be similar across all three groups, the size (cross sectional area) of these neurons is significantly smaller in the <b>methadone</b> treated animals.
+CHAT	drug	opioid	8149590	By postnatal day 22, there are no differences in the <strong>ChAT</strong> immunoreactivity of striatal neurons between the water treated and <b>methadone</b> treated animals.
+CHAT	drug	opioid	8149590	Thus, prenatal exposure to <b>methadone</b> appears to produce a delay in the expression of <strong>ChAT</strong> in striatal neurons.
+CHAT	drug	alcohol	7748324	Specific activity of GAD but not <strong>ChAT</strong> was found to be significantly decreased in hippocampi of <b>ethanol</b> dependent animals following injection of NMDA, suggesting that chronic <b>ethanol</b> administration sensitizes GABAergic neurons to the toxic effects of excitatory amino acid transmitters.
+CHAT	drug	nicotine	4064913	No significant change in cholineacetyltransferase (<strong>ChAT</strong>) activity or number of muscarinic binding sites in brain was observed after 9 or 41 weeks of <b>nicotine</b> treatment.
+CHAT	drug	opioid	6685808	The results demonstrate that neither short nor long term <b>morphine</b> treatment had an effect on choline acetyltransferase (<strong>ChAT</strong>) activity or 3H quinuclidinylbenzilate (3HQNB) binding in discrete striatal regions of the rat brain.
+CHAT	drug	alcohol	7198309	The activities of acetylcholinesterase (AChE) and choline acetyltransferase (<strong>ChaT</strong>) in the cerebral cortex, cerebellum, hypothalamus, hippocampus, midbrain and pons of adult, male mice injected with 2 g/kg <b>ethanol</b> and of control mice injected with physiological saline, were determined by spectrophotometric methods.
+CHAT	drug	alcohol	7198309	All animals were killed 30 min after injection between 11.00 h and 12.00 h. Results show that the acute dose of <b>ethanol</b> significantly decreased AChE activity only in the cerebral cortex whereas <strong>ChaT</strong> activity was reduced in the cerebral cortex, hypothalamus and hippocampus.
+CHAT	drug	alcohol	7198309	These findings show that the effect of an acute dose of <b>ethanol</b> on the cholinergic system of mouse brain is mediated through its effect on AChE and <strong>ChaT</strong> in specific regions.
+CHAT	drug	alcohol	6994921	Eighteen weeks of <b>ethanol</b> consumption in a liquid diet reduced rat striatal and mammillary body choline acetylase (<strong>ChAT</strong>) by 53% and 58%, respectively.
+HTR3A	drug	nicotine	30797147	Potential roles of 5 HT3 receptor (<strong>5 HT3R</strong>) antagonists in modulating the effects of <b>nicotine</b>.
+HTR3A	drug	nicotine	30797147	This review gathered existing studies conducted investigating the potential of " setron" class of <strong>5 HT3R</strong> antagonists in modulating <b>nicotine</b> effects.
+HTR3A	drug	nicotine	30797147	We proposed that the mechanism where <strong>5 HT3R</strong> antagonists mediate the effects of <b>nicotine</b> could be attributed by both direct at <strong>5 HT3R</strong> and indirect mechanism in <b>nicotine</b> addiction downstream regulation.
+HTR3A	addiction	addiction	30797147	We proposed that the mechanism where <strong>5 HT3R</strong> antagonists mediate the effects of nicotine could be attributed by both direct at <strong>5 HT3R</strong> and indirect mechanism in nicotine <b>addiction</b> downstream regulation.
+HTR3A	drug	alcohol	27144979	The association of <strong>HTR3A</strong> mRNA expression and craving in Han Chinese <b>alcohol</b> dependent patients: a preliminary study.
+HTR3A	addiction	relapse	27144979	The association of <strong>HTR3A</strong> mRNA expression and <b>craving</b> in Han Chinese alcohol dependent patients: a preliminary study.
+HTR3A	drug	alcohol	27144979	<strong>HTR3A</strong> mRNA expression levels and acetylation levels of H3K9 in the <strong>HTR3A</strong> promoter region were significantly higher in the <b>alcohol</b> dependent patients.
+HTR3A	drug	alcohol	27144979	The current findings suggest that <strong>HTR3A</strong> mRNA expression levels were positively correlated with craving in Han Chinese <b>alcohol</b> dependent patients.
+HTR3A	addiction	relapse	27144979	The current findings suggest that <strong>HTR3A</strong> mRNA expression levels were positively correlated with <b>craving</b> in Han Chinese alcohol dependent patients.
+HTR3A	drug	alcohol	27144979	The regulation of H3K9 histone acetylation in <strong>HTR3A</strong> promoter region may offer a target for the treatment of <b>alcohol</b> dependence.
+HTR3A	addiction	dependence	27144979	The regulation of H3K9 histone acetylation in <strong>HTR3A</strong> promoter region may offer a target for the treatment of alcohol <b>dependence</b>.
+HTR3A	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., <strong>HTR3A</strong>, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+HTR3A	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., <strong>HTR3A</strong>, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+HTR3A	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., <strong>HTR3A</strong>, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+HTR3A	drug	alcohol	24590108	Previous studies have implicated genes encoding the 5 HT3AB receptors (<strong>HTR3A</strong> and HTR3B) and the serotonin transporter (SLC6A4), both independently and interactively, in <b>alcohol</b> (AD), cocaine (CD), and nicotine dependence (ND).
+HTR3A	drug	cocaine	24590108	Previous studies have implicated genes encoding the 5 HT3AB receptors (<strong>HTR3A</strong> and HTR3B) and the serotonin transporter (SLC6A4), both independently and interactively, in alcohol (AD), <b>cocaine</b> (CD), and nicotine dependence (ND).
+HTR3A	drug	nicotine	24590108	Previous studies have implicated genes encoding the 5 HT3AB receptors (<strong>HTR3A</strong> and HTR3B) and the serotonin transporter (SLC6A4), both independently and interactively, in alcohol (AD), cocaine (CD), and <b>nicotine</b> dependence (ND).
+HTR3A	addiction	dependence	24590108	Previous studies have implicated genes encoding the 5 HT3AB receptors (<strong>HTR3A</strong> and HTR3B) and the serotonin transporter (SLC6A4), both independently and interactively, in alcohol (AD), cocaine (CD), and nicotine <b>dependence</b> (ND).
+HTR3A	drug	nicotine	24590108	We used 1,136 African American (AA) and 2,428 European American (EA) subjects from the Study of Addiction: Genetics and Environment (SAGE) to determine associations between 88 genotyped or imputed variants within <strong>HTR3A</strong>, HTR3B, and SLC6A4 and three types of addictions, which were measured by DSM IV diagnoses of AD, CD, and ND and the Fagerström Test for <b>Nicotine</b> Dependence (FTND), an independent measure of ND commonly used in <b>tobacco</b> research.
+HTR3A	addiction	addiction	24590108	We used 1,136 African American (AA) and 2,428 European American (EA) subjects from the Study of <b>Addiction</b>: Genetics and Environment (SAGE) to determine associations between 88 genotyped or imputed variants within <strong>HTR3A</strong>, HTR3B, and SLC6A4 and three types of addictions, which were measured by DSM IV diagnoses of AD, CD, and ND and the Fagerström Test for Nicotine Dependence (FTND), an independent measure of ND commonly used in tobacco research.
+HTR3A	addiction	dependence	24590108	We used 1,136 African American (AA) and 2,428 European American (EA) subjects from the Study of Addiction: Genetics and Environment (SAGE) to determine associations between 88 genotyped or imputed variants within <strong>HTR3A</strong>, HTR3B, and SLC6A4 and three types of addictions, which were measured by DSM IV diagnoses of AD, CD, and ND and the Fagerström Test for Nicotine <b>Dependence</b> (FTND), an independent measure of ND commonly used in tobacco research.
+HTR3A	addiction	addiction	24590108	Interestingly, most of the SNPs included in the genetic interaction model(s) for each <b>addictive</b> phenotype are either overlapped or in high linkage disequilibrium for both AA and EA samples, suggesting these detected variants in <strong>HTR3A</strong>, HTR3B, and SLC6A4 are interactively contributing to etiology of the three <b>addictive</b> phenotypes examined in this study.
+HTR3A	drug	alcohol	23897038	In this study, they explored additional markers of ondansetron treatment response in <b>alcoholics</b> by examining polymorphisms in the <strong>HTR3A</strong> and HTR3B genes, which regulate directly the function and binding of 5 HT3 receptors to ondansetron.
+HTR3A	drug	alcohol	23757001	On the basis of the converging evidence showing regulation of drinking behavior by 5 HT3AB receptors and the serotonin transporter, we hypothesized that the interactive effects of genetic variations in the genes <strong>HTR3A</strong>, HTR3B, and SLC6A4 confer greater susceptibility to <b>alcohol</b> dependence (AD) than do their effects individually.
+HTR3A	addiction	dependence	23757001	On the basis of the converging evidence showing regulation of drinking behavior by 5 HT3AB receptors and the serotonin transporter, we hypothesized that the interactive effects of genetic variations in the genes <strong>HTR3A</strong>, HTR3B, and SLC6A4 confer greater susceptibility to alcohol <b>dependence</b> (AD) than do their effects individually.
+HTR3A	addiction	dependence	23377636	Other candidate genes associated with substance <b>dependence</b> phenotypes in Native Americans include OPRM1, CRN1, COMT, GABRA2, MAOA, and <strong>HTR3</strong> B.
+HTR3A	drug	nicotine	23290502	Pharmacologic studies implicate a significant role of genes encoding the serotonin transporter (SLC6A4) and the 5 HT3AB subunits <strong>HTR3A</strong> and HTR3B in <b>nicotine</b> dependence (ND).
+HTR3A	addiction	dependence	23290502	Pharmacologic studies implicate a significant role of genes encoding the serotonin transporter (SLC6A4) and the 5 HT3AB subunits <strong>HTR3A</strong> and HTR3B in nicotine <b>dependence</b> (ND).
+HTR3A	drug	alcohol	22834954	<b>Ethanol</b> induced <strong>Htr3a</strong> promoter methylation changes in mouse blood and brain.
+HTR3A	drug	alcohol	22834954	We investigated <b>ethanol</b> (EtOH) induced DNA methylation changes in mouse serotonin receptor 3a gene (<strong>Htr3a</strong>).
+HTR3A	drug	alcohol	22834954	Additionally, the expression level of <strong>Htr3a</strong> in the DMSTR was 1.43 fold higher in <b>alcohol</b> drinking mice than in water drinking mice (p = 0.044).
+HTR3A	drug	alcohol	22834954	Our findings indicate that <b>alcohol</b> consumption may induce tissue specific DNA methylation changes and further suggest that <strong>Htr3a</strong> promoter methylation levels may be reversely correlated with <strong>Htr3a</strong> expression levels in specific brain regions such as DMSTR.
+HTR3A	drug	alcohol	25722691	Histone acetylation of the <strong>htr3a</strong> gene in the prefrontal cortex of Wistar rats regulates <b>ethanol</b> seeking behavior.
+HTR3A	addiction	relapse	25722691	Histone acetylation of the <strong>htr3a</strong> gene in the prefrontal cortex of Wistar rats regulates ethanol <b>seeking</b> behavior.
+HTR3A	drug	alcohol	25722691	Previous reports showed that decreased histone deacetylase activity significantly potentiated the rewarding effects of psychostimulants, and that encoding of the 5 HT3 receptor by the <strong>htr3a</strong> gene was related to <b>ethanol</b> seeking behavior.
+HTR3A	addiction	relapse	25722691	Previous reports showed that decreased histone deacetylase activity significantly potentiated the rewarding effects of psychostimulants, and that encoding of the 5 HT3 receptor by the <strong>htr3a</strong> gene was related to ethanol <b>seeking</b> behavior.
+HTR3A	drug	alcohol	25722691	However, the effects of a histone deacetylase inhibitor on <b>ethanol</b> seeking behavior and epigenetic regulation of <strong>htr3a</strong> mRNA expression after chronic <b>ethanol</b> exposure are not fully understood.
+HTR3A	addiction	relapse	25722691	However, the effects of a histone deacetylase inhibitor on ethanol <b>seeking</b> behavior and epigenetic regulation of <strong>htr3a</strong> mRNA expression after chronic ethanol exposure are not fully understood.
+HTR3A	drug	alcohol	25722691	Using quantitative reverse transcription polymerase chain reaction and chromatin immunoprecipitation analysis, we investigated the effects of chronic <b>ethanol</b> exposure and its interaction with a histone deacetylase inhibitor on histone acetylation mediated changes in <strong>htr3a</strong> mRNA expression in the <strong>htr3a</strong> promoter region.
+HTR3A	drug	alcohol	25722691	In the prefrontal cortex, the acetylation of H3K9 and <strong>htr3a</strong> mRNA expression in the <strong>htr3a</strong> promoter region were significantly higher in the <b>ethanol</b> group than in the saline group.
+HTR3A	drug	alcohol	25722691	The histone deacetylase inhibitor sodium butyrate potentiated the effects of <b>ethanol</b> on <strong>htr3a</strong> mRNA expression and enhanced <b>ethanol</b> induced conditioned place preferences.
+HTR3A	drug	alcohol	25722691	These results suggest that <b>ethanol</b> upregulates <strong>htr3a</strong> levels through mechanisms involving H3K9 acetylation, and that histone acetylation may be a therapeutic target for treating <b>ethanol</b> abuse.
+HTR3A	drug	alcohol	22140596	In this study, we used a PCR array containing 46 primer pairs of selected genes to compare mRNA expression in the spleen, an immune system organ, of adolescent rats following binge drinking of <b>alcohol</b> solutions containing either 20% or 52% <b>ethanol</b> (v/v, 4.8 g/kg daily dosage), or water (control) for 3 d. We found that, expression of IL 1β, IL 6, CCL2, and GABA(A) receptor α2 subunit in the spleen were decreased, and mGluR5 and <strong>5 HT3A</strong> receptor expression were increased after administration of an <b>ethanol</b> solution containing 52% <b>ethanol</b>, but not one with 20% <b>ethanol</b>.
+HTR3A	addiction	intoxication	22140596	In this study, we used a PCR array containing 46 primer pairs of selected genes to compare mRNA expression in the spleen, an immune system organ, of adolescent rats following <b>binge</b> drinking of alcohol solutions containing either 20% or 52% ethanol (v/v, 4.8 g/kg daily dosage), or water (control) for 3 d. We found that, expression of IL 1β, IL 6, CCL2, and GABA(A) receptor α2 subunit in the spleen were decreased, and mGluR5 and <strong>5 HT3A</strong> receptor expression were increased after administration of an ethanol solution containing 52% ethanol, but not one with 20% ethanol.
+HTR3A	drug	alcohol	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of <b>alcohol</b>, cocaine and heroin dependence and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (SLC6A4) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and <strong>HTR3A</strong>, genes encoding 5 HT3 receptors.
+HTR3A	drug	cocaine	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, <b>cocaine</b> and heroin dependence and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (SLC6A4) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and <strong>HTR3A</strong>, genes encoding 5 HT3 receptors.
+HTR3A	drug	opioid	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and <b>heroin</b> dependence and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (SLC6A4) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and <strong>HTR3A</strong>, genes encoding 5 HT3 receptors.
+HTR3A	addiction	dependence	20838391	In this study, 360 treatment seeking African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and heroin <b>dependence</b> and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (SLC6A4) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and <strong>HTR3A</strong>, genes encoding 5 HT3 receptors.
+HTR3A	addiction	relapse	20838391	In this study, 360 treatment <b>seeking</b> African American male patients with single and comorbid DSM IV lifetime diagnoses of alcohol, cocaine and heroin dependence and 187 African American male controls were genotyped for the triallelic 5 HTTLPR functional polymorphism in the 5 HT transporter gene (SLC6A4) and 16 haplotype tagging single nucleotide polymorphisms (SNPs) across HTR3B (including the functional rs1176744 Tyr129Ser) and <strong>HTR3A</strong>, genes encoding 5 HT3 receptors.
+HTR3A	drug	amphetamine	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), <strong>Htr3a</strong> (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and Fos (cFos), represent candidates whose expression levels may predict <b>methamphetamine</b> consumption and susceptibility to <b>methamphetamine</b> reward and aversion.
+HTR3A	addiction	aversion	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), <strong>Htr3a</strong> (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and Fos (cFos), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine reward and <b>aversion</b>.
+HTR3A	addiction	reward	19689456	Genes differentially expressed in the drug naï ve state, including Slc6a4 (serotonin transporter), <strong>Htr3a</strong> (serotonin receptor 3A), Rela [nuclear factor kappaB (NFkappaB)] and Fos (cFos), represent candidates whose expression levels may predict methamphetamine consumption and susceptibility to methamphetamine <b>reward</b> and aversion.
+HTR3A	drug	alcohol	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (<strong>HTR3A</strong>) as well as <b>alcohol</b> dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and diazepam binding inhibitor (DBI).
+HTR3A	drug	benzodiazepine	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (<strong>HTR3A</strong>) as well as alcohol dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and <b>diazepam</b> binding inhibitor (DBI).
+HTR3A	drug	opioid	19214139	<b>Morphine</b> strongly regulated the expression of the <strong>Htr3a</strong> gene in various central nervous system regions including the amygdala, dorsal raphe, and periaqueductal gray nuclei, which have been linked to <b>opioid</b> dependence in previous studies.
+HTR3A	addiction	dependence	19214139	Morphine strongly regulated the expression of the <strong>Htr3a</strong> gene in various central nervous system regions including the amygdala, dorsal raphe, and periaqueductal gray nuclei, which have been linked to opioid <b>dependence</b> in previous studies.
+HTR3A	drug	alcohol	19185213	<strong>5 HT3R</strong> might contribute to the imbalance between excitation and inhibition that characterize the brain of <b>alcoholics</b>.
+HTR3A	drug	alcohol	11274721	<strong>5 HT 3</strong> receptor antagonist ICS 205 930 alters the discriminative effects of <b>ethanol</b>.
+HTR3A	drug	alcohol	8000444	Studies on the effects of certain <strong>5 HT 3</strong> receptor antagonists on <b>ethanol</b> preference and withdrawal seizures in the rat.
+HTR3A	addiction	withdrawal	8000444	Studies on the effects of certain <strong>5 HT 3</strong> receptor antagonists on ethanol preference and <b>withdrawal</b> seizures in the rat.
+HTR3A	drug	alcohol	8000444	We tested how certain antagonists of <strong>5 HT 3</strong> receptors affect <b>ethanol</b> consumption and withdrawal seizures in <b>ethanol</b> dependent Wistar male rats.
+HTR3A	addiction	withdrawal	8000444	We tested how certain antagonists of <strong>5 HT 3</strong> receptors affect ethanol consumption and <b>withdrawal</b> seizures in ethanol dependent Wistar male rats.
+HDAC9	drug	cocaine	31998092	Here, we investigated garcinol's effect on <b>cocaine</b> cue memory reconsolidation when administered to the lateral nucleus of the amygdala (LA), as well as its epigenetic activity following systemic garcinol administration and also when given in conjunction with trichostatin A (TSA), a histone deacetylase (<strong>HDAC</strong>) inhibitor.
+HDAC9	drug	alcohol	31398085	In vitro <b>ethanol</b> (ETOH) treatment increased <strong>HDAC</strong> expression during differentiation and decreased differentiation potential of myoblasts.
+HDAC9	drug	alcohol	31398085	These findings suggest that an <b>alcohol</b> mediated increase in Class IIA <strong>HDAC</strong> expression contributes to decreased myoblast differentiation by downregulating MEF2C, a transcription factor critical for myogenesis.
+HDAC9	drug	amphetamine	31343201	This study examined the effects of environmental condition on <b>amphetamine</b> self administration, and whether drug taking and drug seeking behaviors could be influenced through inhibition of an epigenetic regulator, histone deacetylase (<strong>HDAC</strong>).
+HDAC9	addiction	relapse	31343201	This study examined the effects of environmental condition on amphetamine self administration, and whether drug taking and drug <b>seeking</b> behaviors could be influenced through inhibition of an epigenetic regulator, histone deacetylase (<strong>HDAC</strong>).
+HDAC9	addiction	reward	31343201	The <strong>HDAC</strong> inhibitor, Trichostatin A (TsA; 0.3 mg/kg, IV), was injected 30 min prior to <b>operant</b> sessions.
+HDAC9	drug	amphetamine	31343201	<strong>HDAC</strong> inhibition decreases cue induced reinstatement of <b>amphetamine</b> seeking in IC rats.
+HDAC9	addiction	relapse	31343201	<strong>HDAC</strong> inhibition decreases cue induced <b>reinstatement</b> of amphetamine <b>seeking</b> in IC rats.
+HDAC9	drug	alcohol	31294671	Such findings support the participation of <strong>HDAC</strong> enzymes in cognitive and emotional alterations induced by binge <b>alcohol</b> consumption during gestation and lactation and would indicate potential benefits of <strong>HDAC</strong> inhibitors for some aspects of foetal <b>alcohol</b> spectrum disorders.
+HDAC9	addiction	intoxication	31294671	Such findings support the participation of <strong>HDAC</strong> enzymes in cognitive and emotional alterations induced by <b>binge</b> alcohol consumption during gestation and lactation and would indicate potential benefits of <strong>HDAC</strong> inhibitors for some aspects of foetal alcohol spectrum disorders.
+HDAC9	drug	alcohol	31029598	Moreover, histone deacetylase (<strong>HDAC</strong>) inhibitors restrain the activity of <strong>HDAC</strong> and cause increased histone acetylation, which may be related to <b>alcohol</b> dependence.
+HDAC9	addiction	dependence	31029598	Moreover, histone deacetylase (<strong>HDAC</strong>) inhibitors restrain the activity of <strong>HDAC</strong> and cause increased histone acetylation, which may be related to alcohol <b>dependence</b>.
+HDAC9	addiction	withdrawal	30851364	Rats were treated with the <strong>HDAC</strong> inhibitor, suberoylanilide hydroxamic acid (SAHA), during <b>withdrawal</b> and were tested for depression like behavior.
+HDAC9	addiction	withdrawal	30851364	Treatment with an <strong>HDAC</strong> inhibitor can correct this state and alleviate depression like symptoms developed during <b>withdrawal</b>.
+HDAC9	drug	amphetamine	30811820	<strong>HDAC</strong> superfamily promoters acetylation is differentially regulated by modafinil and <b>methamphetamine</b> in the mouse medial prefrontal cortex.
+HDAC9	drug	amphetamine	30811820	For mRNA, single dose <b>METH</b> increased Hdac4 and modafinil increased <strong>Hdac7</strong> expression.
+HDAC9	drug	amphetamine	30811820	Our results suggest that <strong>HDAC</strong> targets linked to the effects of modafinil and <b>METH</b> may be related to the cognitive enhancing vs cognitive impairing effects of these psychostimulants.
+HDAC9	drug	alcohol	29713786	Recent preclinical research suggested that histone deacetylase inhibitors (HDACIs) and specifically class I <strong>HDAC</strong> selective inhibitors might be useful to treat <b>alcohol</b> use disorders (AUDs).
+HDAC9	drug	alcohol	29713786	Our study demonstrated that a new compound designed to target <strong>HDAC</strong> 1 is effective in reducing <b>ethanol</b> intake and relapse in rats and further confirm the interest of pursuing research to study the exact mechanism by which such inhibitor may be useful to treat AUDs.
+HDAC9	addiction	relapse	29713786	Our study demonstrated that a new compound designed to target <strong>HDAC</strong> 1 is effective in reducing ethanol intake and <b>relapse</b> in rats and further confirm the interest of pursuing research to study the exact mechanism by which such inhibitor may be useful to treat AUDs.
+HDAC9	drug	alcohol	29520058	Administration of the <strong>HDAC</strong> inhibitor trichostatin A (TSA) after chronic <b>ethanol</b> exposure prevents the decrease in Gabra1 expression and function as well as the increase in Hdac2 and Hdac3 expression in both the cortex and the medial prefrontal cortex (mPFC).
+HDAC9	drug	cocaine	29109977	Decreased nuclear <strong>HDAC</strong> activity results in global H3 acetylation, creating a permissive environment for <b>cocaine</b> induced gene expression.
+HDAC9	drug	cocaine	29109977	We also find that selective degradation of HDAC4 and HDAC5, facilitated by the class II specific <strong>HDAC</strong> inhibitor MC1568, enhances compulsive <b>cocaine</b> self administration.
+HDAC9	addiction	addiction	29109977	We also find that selective degradation of HDAC4 and HDAC5, facilitated by the class II specific <strong>HDAC</strong> inhibitor MC1568, enhances <b>compulsive</b> cocaine self administration.
+HDAC9	drug	cocaine	29109977	These results parallel our previously reported findings that the gateway drug nicotine enhances the behavioral effects of <b>cocaine</b> via <strong>HDAC</strong> inhibition.
+HDAC9	drug	nicotine	29109977	These results parallel our previously reported findings that the gateway drug <b>nicotine</b> enhances the behavioral effects of cocaine via <strong>HDAC</strong> inhibition.
+HDAC9	drug	alcohol	28771357	Class I <strong>HDAC</strong> Inhibitors: Potential New Epigenetic Therapeutics for <b>Alcohol</b> Use Disorder (AUD).
+HDAC9	drug	alcohol	28771357	<b>Alcohol</b> exposure has been widely demonstrated to modulate epigenetic mechanisms, such as histone acetylation/deacetylation balance, in part via histone deacetylase (<strong>HDAC</strong>) inhibition.
+HDAC9	drug	alcohol	28682229	Furthermore, we recently showed that a single <b>ethanol</b> exposure inhibits <strong>HDAC</strong> activity and increases both H3 and H4 histone acetylation within the amygdala of rats.
+HDAC9	drug	alcohol	28682229	In neuronal cell line culture, <b>ethanol</b> was shown to induce <strong>HDAC</strong> expression.
+HDAC9	drug	alcohol	28682229	Numerous studies have shown that <strong>HDAC</strong> inhibitors are able to counter <b>ethanol</b> induced behaviors and the <b>ethanol</b> induced changes in the levels of <strong>HDAC</strong> and/or levels of acetylated <strong>HDAC</strong>.
+HDAC9	drug	alcohol	28682229	For example, trichostatin A (TSA) treatment caused the reversal of <b>ethanol</b> induced tolerance, anxiety, and <b>ethanol</b> drinking by inhibiting <strong>HDAC</strong> activity, thereby increasing histone acetylation in the amygdala of rats.
+HDAC9	drug	alcohol	28682229	Another study demonstrated that TSA prevented the development of <b>ethanol</b> withdrawal induced anxiety in rats by rescuing deficits in histone acetylation induced by increased <strong>HDAC</strong> activity in the amygdala.
+HDAC9	addiction	withdrawal	28682229	Another study demonstrated that TSA prevented the development of ethanol <b>withdrawal</b> induced anxiety in rats by rescuing deficits in histone acetylation induced by increased <strong>HDAC</strong> activity in the amygdala.
+HDAC9	drug	alcohol	28682229	We have demonstrated that treatment with the <strong>HDAC</strong> inhibitor sodium butyrate blocks both the development and the expression of <b>ethanol</b> induced behavioral sensitization in mice.
+HDAC9	addiction	sensitization	28682229	We have demonstrated that treatment with the <strong>HDAC</strong> inhibitor sodium butyrate blocks both the development and the expression of ethanol induced behavioral <b>sensitization</b> in mice.
+HDAC9	drug	alcohol	28682229	In this context, converging evidence indicates that <strong>HDAC</strong> inhibitors could be useful in counteracting <b>ethanol</b> induced gene regulations via epigenetic mechanisms, that is, <strong>HDAC</strong> inhibitors could affect different acetylation sites and may also alter the expression of different genes that could in turn counteract the effect of <b>ethanol</b>.
+HDAC9	drug	alcohol	28682229	Recent work in rodents has shown that systemic administration of pan HDAC class I and II inhibitors, TSA and N hydroxy N phenyl octanediamide [SuberoylAnilide Hydroxamic Acid] (SAHA), and of the more selective inhibitor (mainly HDAC1 and <strong>HDAC9</strong>) MS 275, decrease binge like <b>alcohol</b> drinking in mice.
+HDAC9	addiction	intoxication	28682229	Recent work in rodents has shown that systemic administration of pan HDAC class I and II inhibitors, TSA and N hydroxy N phenyl octanediamide [SuberoylAnilide Hydroxamic Acid] (SAHA), and of the more selective inhibitor (mainly HDAC1 and <strong>HDAC9</strong>) MS 275, decrease <b>binge</b> like alcohol drinking in mice.
+HDAC9	drug	alcohol	28682229	Recent work in rodents has shown that systemic administration of pan <strong>HDAC</strong> class I and II inhibitors, TSA and N hydroxy N phenyl octanediamide [SuberoylAnilide Hydroxamic Acid] (SAHA), and of the more selective inhibitor (mainly HDAC1 and <strong>HDAC9</strong>) MS 275, decrease binge like <b>alcohol</b> drinking in mice.
+HDAC9	addiction	intoxication	28682229	Recent work in rodents has shown that systemic administration of pan <strong>HDAC</strong> class I and II inhibitors, TSA and N hydroxy N phenyl octanediamide [SuberoylAnilide Hydroxamic Acid] (SAHA), and of the more selective inhibitor (mainly HDAC1 and <strong>HDAC9</strong>) MS 275, decrease <b>binge</b> like alcohol drinking in mice.
+HDAC9	drug	alcohol	28433417	There is growing evidence that small molecule inhibitors of epigenetic modulators, such as histone deacetylases (<strong>HDAC</strong>) and DNA methyltransferases (DNMT), can reduce voluntary <b>ethanol</b> consumption in animal models, but molecular and cellular processes underlying this behavioral effect are poorly understood.
+HDAC9	drug	alcohol	28433417	We used C57BL/6J male mice to investigate the effects of two FDA approved drugs, decitabine (a DNMT inhibitor) and SAHA (an <strong>HDAC</strong> inhibitor), on <b>ethanol</b> consumption using two tests: binge like drinking in the dark (DID) and chronic intermittent every other day (EOD) drinking.
+HDAC9	addiction	intoxication	28433417	We used C57BL/6J male mice to investigate the effects of two FDA approved drugs, decitabine (a DNMT inhibitor) and SAHA (an <strong>HDAC</strong> inhibitor), on ethanol consumption using two tests: <b>binge</b> like drinking in the dark (DID) and chronic intermittent every other day (EOD) drinking.
+HDAC9	addiction	addiction	28255755	Furthermore, this review also reports on the advancement of interventions for drug <b>addiction</b> and takes into account the emerging roles of histone deacetylase (<strong>HDAC</strong>) inhibitors in the etiology of drug <b>addiction</b> and that <strong>HDAC</strong> may be a potential therapeutic target at nucleosomal level to improve treatment outcomes.
+HDAC9	drug	opioid	28243713	The objective of this study is to characterize the role of the clock gene mPer1 in the development of <b>morphine</b> induced behaviors and a possible link to histone deacetylase (<strong>HDAC</strong>) activity.
+HDAC9	drug	opioid	28243713	Because a very similar dissociation between tolerance and dependence vs. sensitization and CPP was recently observed after the co administration of <b>morphine</b> and the <strong>HDAC</strong> inhibitor sodium butyrate (NaBut), we studied a possible link between mPer1 and <strong>HDAC</strong> activity.
+HDAC9	addiction	dependence	28243713	Because a very similar dissociation between tolerance and <b>dependence</b> vs. sensitization and CPP was recently observed after the co administration of morphine and the <strong>HDAC</strong> inhibitor sodium butyrate (NaBut), we studied a possible link between mPer1 and <strong>HDAC</strong> activity.
+HDAC9	addiction	reward	28243713	Because a very similar dissociation between tolerance and dependence vs. sensitization and <b>CPP</b> was recently observed after the co administration of morphine and the <strong>HDAC</strong> inhibitor sodium butyrate (NaBut), we studied a possible link between mPer1 and <strong>HDAC</strong> activity.
+HDAC9	addiction	sensitization	28243713	Because a very similar dissociation between tolerance and dependence vs. <b>sensitization</b> and CPP was recently observed after the co administration of morphine and the <strong>HDAC</strong> inhibitor sodium butyrate (NaBut), we studied a possible link between mPer1 and <strong>HDAC</strong> activity.
+HDAC9	drug	opioid	28243713	As opposed to WT controls, Per1 Brdm1 mutant mice showed significantly enhanced striatal global <strong>HDAC</strong> activity within the striatum when exposed to a locomotor sensitizing <b>morphine</b> administration regimen.
+HDAC9	drug	opioid	28243713	Furthermore, the administration of the <strong>HDAC</strong> inhibitor NaBut restored the ability of <b>morphine</b> to promote locomotor sensitization and reward in Per1 Brdm1 mutant mice.
+HDAC9	addiction	reward	28243713	Furthermore, the administration of the <strong>HDAC</strong> inhibitor NaBut restored the ability of morphine to promote locomotor sensitization and <b>reward</b> in Per1 Brdm1 mutant mice.
+HDAC9	addiction	sensitization	28243713	Furthermore, the administration of the <strong>HDAC</strong> inhibitor NaBut restored the ability of morphine to promote locomotor <b>sensitization</b> and reward in Per1 Brdm1 mutant mice.
+HDAC9	drug	opioid	28243713	Our results reveal that although the mPer1 gene does not alter <b>morphine</b> induced antinociception nor withdrawal, it plays a prominent role in the development of <b>morphine</b> induced behavioral sensitization and reward via inhibitory modulation of striatal <strong>HDAC</strong> activity.
+HDAC9	addiction	reward	28243713	Our results reveal that although the mPer1 gene does not alter morphine induced antinociception nor withdrawal, it plays a prominent role in the development of morphine induced behavioral sensitization and <b>reward</b> via inhibitory modulation of striatal <strong>HDAC</strong> activity.
+HDAC9	addiction	sensitization	28243713	Our results reveal that although the mPer1 gene does not alter morphine induced antinociception nor withdrawal, it plays a prominent role in the development of morphine induced behavioral <b>sensitization</b> and reward via inhibitory modulation of striatal <strong>HDAC</strong> activity.
+HDAC9	addiction	withdrawal	28243713	Our results reveal that although the mPer1 gene does not alter morphine induced antinociception nor <b>withdrawal</b>, it plays a prominent role in the development of morphine induced behavioral sensitization and reward via inhibitory modulation of striatal <strong>HDAC</strong> activity.
+HDAC9	drug	alcohol	28174112	Acute <b>alcohol</b> exposure produces an anxiolytic response which is associated with the opening of chromatin due to increased histone acetylation, increased CREB binding protein (CBP) levels, and histone deacetylase (<strong>HDAC</strong>) inhibition.
+HDAC9	addiction	withdrawal	28174112	However, during <b>withdrawal</b>, histone acetylation decreases due to increased <strong>HDAC</strong> activity and decreased CBP levels in the amygdala circuitry leading to the development of anxiety like behaviors.
+HDAC9	drug	opioid	27742468	Inhibition of histone deacetylases (<strong>HDAC</strong>) activity results in the change of some drug induced behaviors，however, relatively little is known about the effects of <strong>HDAC</strong> inhibitors on <b>heroin</b> seeking behavior.
+HDAC9	addiction	relapse	27742468	Inhibition of histone deacetylases (<strong>HDAC</strong>) activity results in the change of some drug induced behaviors，however, relatively little is known about the effects of <strong>HDAC</strong> inhibitors on heroin <b>seeking</b> behavior.
+HDAC9	drug	opioid	27742468	), an inhibitor of <strong>HDAC</strong>, failed to affect <b>heroin</b> self administration.
+HDAC9	drug	opioid	27312092	Since addiction and stress memories share some common pathways, the present study was designed to investigate the role of histone deacetylase (<strong>HDAC</strong>) activity in the VLO during <b>morphine</b> induced behavioral sensitization.
+HDAC9	addiction	addiction	27312092	Since <b>addiction</b> and stress memories share some common pathways, the present study was designed to investigate the role of histone deacetylase (<strong>HDAC</strong>) activity in the VLO during morphine induced behavioral sensitization.
+HDAC9	addiction	sensitization	27312092	Since addiction and stress memories share some common pathways, the present study was designed to investigate the role of histone deacetylase (<strong>HDAC</strong>) activity in the VLO during morphine induced behavioral <b>sensitization</b>.
+HDAC9	drug	opioid	27312092	The effect of <strong>HDAC</strong> activity in the VLO in <b>morphine</b> induced behavioral sensitization was examined by microinjection of <strong>HDAC</strong> inhibitor Trichostatin A (TSA).
+HDAC9	addiction	sensitization	27312092	The effect of <strong>HDAC</strong> activity in the VLO in morphine induced behavioral <b>sensitization</b> was examined by microinjection of <strong>HDAC</strong> inhibitor Trichostatin A (TSA).
+HDAC9	drug	opioid	27312092	Our findings suggest that <strong>HDAC</strong> activity in the VLO could potentiate <b>morphine</b> induced behavioral sensitization.
+HDAC9	addiction	sensitization	27312092	Our findings suggest that <strong>HDAC</strong> activity in the VLO could potentiate morphine induced behavioral <b>sensitization</b>.
+HDAC9	drug	opioid	27306674	<b>Morphine</b> induced synaptic plasticity in the VTA is reversed by <strong>HDAC</strong> inhibition.
+HDAC9	drug	opioid	27306674	Here we investigated the function of histone acetylation and histone deacetylase (<strong>HDAC</strong>)2 in the VTA in recovery of <b>morphine</b> induced synaptic modifications following a single in vivo exposure to <b>morphine</b>.
+HDAC9	drug	alcohol	27238566	<b>Alcohol</b> increased <strong>Hdac</strong> gene expression in blood and nalmefene prevented the increases in Hdacs 3, 8, 5, 7, 9, 6 and 10.
+HDAC9	drug	alcohol	27238566	In the other tissues, <b>alcohol</b> and nalmefene either did not alter the gene expression of Hdacs, as in the prefrontal cortex, or a tissue <strong>Hdac</strong> specific effect was observed.
+HDAC9	drug	cocaine	27180319	Inhibition of HAT by curcumin (100mg/kg) before each SD blocked the increase in the conditioned reinforcing effects of 1mg/kg of <b>cocaine</b>, while inhibition of <strong>HDAC</strong> by valproic acid (500mg/kg) before social stress potentiated <b>cocaine</b> induced CPP.
+HDAC9	addiction	reward	27180319	Inhibition of HAT by curcumin (100mg/kg) before each SD blocked the increase in the conditioned <b>reinforcing</b> effects of 1mg/kg of cocaine, while inhibition of <strong>HDAC</strong> by valproic acid (500mg/kg) before social stress potentiated cocaine induced <b>CPP</b>.
+HDAC9	drug	cocaine	26554014	However, on stimulation by agonists such as <b>cocaine</b>, Sig 1Rs translocate from ER to the NE, where Sig 1Rs bind NE protein emerin and recruit chromatin remodeling molecules, including lamin A/C, barrier to autointegration factor (BAF), and histone deacetylase (<strong>HDAC</strong>), to form a complex with the gene repressor specific protein 3 (Sp3).
+HDAC9	drug	alcohol	26509893	When fetal <b>alcohol</b> exposed rats were treated neonatally with a DNA methylation inhibitor 5 Aza deoxycytidine and/or a <strong>HDAC</strong> inhibitor trichostatin A their pituitary D2R mRNA, pituitary weights and plasma PRL levels were normalized.
+HDAC9	drug	alcohol	26365275	This study aimed to characterize the gene expression patterns of <strong>Hdac</strong> 1 11 in samples of rat peripheral blood, liver, heart, prefrontal cortex, and amygdala following repeated binge <b>alcohol</b> consumption and to determine the parallelism of <strong>Hdac</strong> gene expression between rats and humans in peripheral blood.
+HDAC9	addiction	intoxication	26365275	This study aimed to characterize the gene expression patterns of <strong>Hdac</strong> 1 11 in samples of rat peripheral blood, liver, heart, prefrontal cortex, and amygdala following repeated <b>binge</b> alcohol consumption and to determine the parallelism of <strong>Hdac</strong> gene expression between rats and humans in peripheral blood.
+HDAC9	drug	alcohol	26365275	To accomplish this goal, we examined <strong>Hdac</strong> gene expression following 1, 4, or 8 <b>alcohol</b> binges (3 g/kg, orally) in the rat, in patients who were admitted to the hospital emergency department for acute <b>alcohol</b> intoxication, and in rats trained in daily operant <b>alcohol</b> self administration.
+HDAC9	addiction	intoxication	26365275	To accomplish this goal, we examined <strong>Hdac</strong> gene expression following 1, 4, or 8 alcohol binges (3 g/kg, orally) in the rat, in patients who were admitted to the hospital emergency department for acute alcohol <b>intoxication</b>, and in rats trained in daily operant alcohol self administration.
+HDAC9	addiction	reward	26365275	To accomplish this goal, we examined <strong>Hdac</strong> gene expression following 1, 4, or 8 alcohol binges (3 g/kg, orally) in the rat, in patients who were admitted to the hospital emergency department for acute alcohol intoxication, and in rats trained in daily <b>operant</b> alcohol self administration.
+HDAC9	drug	alcohol	26365275	Finally, both binge consumption of <b>alcohol</b> in humans and daily operant <b>alcohol</b> self administration in rats increased <strong>Hdac</strong> gene expression in peripheral blood.
+HDAC9	addiction	intoxication	26365275	Finally, both <b>binge</b> consumption of alcohol in humans and daily operant alcohol self administration in rats increased <strong>Hdac</strong> gene expression in peripheral blood.
+HDAC9	addiction	reward	26365275	Finally, both binge consumption of alcohol in humans and daily <b>operant</b> alcohol self administration in rats increased <strong>Hdac</strong> gene expression in peripheral blood.
+HDAC9	drug	alcohol	26365275	Our results suggest that increases in <strong>HDAC</strong> gene expression within the peripheral blood are associated with chronic <b>alcohol</b> consumption, whereas <strong>HDAC</strong> gene expression is reduced following initial exposure to <b>alcohol</b>.
+HDAC9	addiction	addiction	26361715	We investigated the effects induced by acute EtOH exposure on the protein levels of class I <strong>HDAC</strong> 1 3 isoforms of wild type (WT) and BDNF heterozygous mice (BDNF(+/ )), in nuclear and cytoplasmic extracts of specific brain regions associated with EtOH <b>addiction</b>.
+HDAC9	drug	nicotine	25880762	The present series of experiments aimed to examine the effect of histone deacetylase (<strong>HDAC</strong>) inhibition on the extinction and reinstatement of <b>nicotine</b> self administration.
+HDAC9	addiction	relapse	25880762	The present series of experiments aimed to examine the effect of histone deacetylase (<strong>HDAC</strong>) inhibition on the extinction and <b>reinstatement</b> of nicotine self administration.
+HDAC9	addiction	addiction	25880762	These results provide the first demonstration that <strong>HDAC</strong> inhibition facilitates the extinction of responding for an intravenously self administered drug of abuse and further highlight the potential of <strong>HDAC</strong> inhibitors in the treatment of drug <b>addiction</b>.
+HDAC9	drug	alcohol	25814047	The effects of AIE on anxiety like and <b>alcohol</b> drinking behaviors in adulthood were measured with or without treatment with the histone deacetylase (<strong>HDAC</strong>) inhibitor, trichostatin A (TSA).
+HDAC9	drug	alcohol	25762717	The Class I Specific <strong>HDAC</strong> Inhibitor MS 275 Decreases Motivation to Consume <b>Alcohol</b> and Relapse in Heavy Drinking Rats.
+HDAC9	addiction	relapse	25762717	The Class I Specific <strong>HDAC</strong> Inhibitor MS 275 Decreases Motivation to Consume Alcohol and <b>Relapse</b> in Heavy Drinking Rats.
+HDAC9	drug	amphetamine	25452209	We found that <b>METH</b> did produce significant decreases in the mRNA expression of HDAC8, which is a class I <strong>HDAC</strong>.
+HDAC9	drug	amphetamine	25452209	<b>METH</b> also decreased expression of HDAC6, <strong>HDAC9</strong>, and HDAC10 that are class II HDACs.
+HDAC9	drug	amphetamine	25452209	The expression of the class IV <strong>HDAC</strong>, HDAC11, was also suppressed by <b>METH</b>.
+HDAC9	drug	amphetamine	25452209	Our findings implicate changes in <strong>HDAC</strong> expression may be an early indicator of impending <b>METH</b> induced neurotoxicity in the striatum.
+HDAC9	drug	alcohol	25108044	The histone deacetylase (<strong>HDAC</strong>) inhibitor valproic acid reduces <b>ethanol</b> consumption and <b>ethanol</b> conditioned place preference in rats.
+HDAC9	drug	alcohol	25108044	In the current study, we studied the effects of systemic injection of the histone deacetylase (<strong>HDAC</strong>) inhibitor, valproic acid (VPA) on <b>ethanol</b> consumption and <b>ethanol</b> elicited conditioned place preference (CPP).
+HDAC9	addiction	reward	25108044	In the current study, we studied the effects of systemic injection of the histone deacetylase (<strong>HDAC</strong>) inhibitor, valproic acid (VPA) on ethanol consumption and ethanol elicited conditioned place preference (<b>CPP</b>).
+HDAC9	drug	alcohol	25108044	Taken together, our results implicated <strong>HDAC</strong> inhibition in the behavioral and reinforcement related effects of <b>alcohol</b> and raise the question of whether specific drugs that target <strong>HDAC</strong> could potentially help to tackle <b>alcoholism</b> in humans.
+HDAC9	addiction	reward	25108044	Taken together, our results implicated <strong>HDAC</strong> inhibition in the behavioral and <b>reinforcement</b> related effects of alcohol and raise the question of whether specific drugs that target <strong>HDAC</strong> could potentially help to tackle alcoholism in humans.
+HDAC9	drug	alcohol	25041570	No study has addressed whether histone deacetylase (<strong>HDAC</strong>) inhibitors (HDACi) can reduce excessive <b>ethanol</b> intake or prevent relapse in <b>alcohol</b> dependent animals.
+HDAC9	addiction	relapse	25041570	No study has addressed whether histone deacetylase (<strong>HDAC</strong>) inhibitors (HDACi) can reduce excessive ethanol intake or prevent <b>relapse</b> in alcohol dependent animals.
+HDAC9	drug	alcohol	24968059	We investigated the effects of acute <b>ethanol</b> exposure on anxiety measures and function of histone deacetylases (<strong>HDAC</strong>) and DNA methyltransferases (DNMT) in the amygdala and bed nucleus of stria terminalis (BNST) of adolescent rats.
+HDAC9	drug	alcohol	24968059	The lower dose of <b>ethanol</b> (1 g/kg) produced neither anxiolysis, nor inhibited the <strong>HDAC</strong> and DNMT activities in the amygdala and BNST, except DNMT activity in BNST was attenuated.
+HDAC9	drug	alcohol	24968059	DNMT activity in the amygdala and BNST, and nuclear <strong>HDAC</strong> activity in the amygdala, but not in the BNST were also inhibited by these doses of <b>ethanol</b>.
+HDAC9	drug	alcohol	24968059	A lack of tolerance was observed on <b>ethanol</b> induced inhibition of DNMT activity in the amygdala and BNST, and nuclear <strong>HDAC</strong> activity in the amygdala, as well to anxiolysis produced by <b>ethanol</b> (2 g/kg).
+HDAC9	drug	alcohol	24968059	These results suggest that reduced sensitivity to anxiolysis and the lack of rapid tolerance to the anxiolytic effects of <b>ethanol</b> and inhibition of <strong>HDAC</strong> and DNMT functions may play a role in engaging adolescents in binge drinking patterns.
+HDAC9	addiction	intoxication	24968059	These results suggest that reduced sensitivity to anxiolysis and the lack of rapid tolerance to the anxiolytic effects of ethanol and inhibition of <strong>HDAC</strong> and DNMT functions may play a role in engaging adolescents in <b>binge</b> drinking patterns.
+HDAC9	drug	opioid	24829091	However, the behavioral effect of histone deacetylase (<strong>HDAC</strong>) inhibition in the BLA and the underlying molecular alterations at different phases of <b>morphine</b> induced conditioned place preference (CPP) has not been investigated.
+HDAC9	addiction	reward	24829091	However, the behavioral effect of histone deacetylase (<strong>HDAC</strong>) inhibition in the BLA and the underlying molecular alterations at different phases of morphine induced conditioned place preference (<b>CPP</b>) has not been investigated.
+HDAC9	drug	opioid	24829091	In this study, we measured the expression, extinction, and reinstatement of <b>morphine</b> induced place preference in rats pretreated with trichostatin A (TSA), an <strong>HDAC</strong> inhibitor.
+HDAC9	addiction	relapse	24829091	In this study, we measured the expression, extinction, and <b>reinstatement</b> of morphine induced place preference in rats pretreated with trichostatin A (TSA), an <strong>HDAC</strong> inhibitor.
+HDAC9	drug	alcohol	24551070	Release of neuronal HMGB1 by <b>ethanol</b> through decreased <strong>HDAC</strong> activity activates brain neuroimmune signaling.
+HDAC9	drug	alcohol	24551070	These results suggest decreased <strong>HDAC</strong> activity may be critical in regulating acetylated HMGB1 release from neurons in response to <b>ethanol</b>.
+HDAC9	drug	alcohol	24103311	Reversal of deficits in dendritic spines, BDNF and Arc expression in the amygdala during <b>alcohol</b> dependence by <strong>HDAC</strong> inhibitor treatment.
+HDAC9	addiction	dependence	24103311	Reversal of deficits in dendritic spines, BDNF and Arc expression in the amygdala during alcohol <b>dependence</b> by <strong>HDAC</strong> inhibitor treatment.
+HDAC9	drug	alcohol	24103311	Development of anxiety like behaviours during <b>ethanol</b> withdrawal has been correlated with increased histone deacetylase (<strong>HDAC</strong>) activity and decreased brain derived neurotrophic factor (BDNF) and activity regulated cytoskeleton associated protein (Arc) gene expression in the amygdala.
+HDAC9	addiction	withdrawal	24103311	Development of anxiety like behaviours during ethanol <b>withdrawal</b> has been correlated with increased histone deacetylase (<strong>HDAC</strong>) activity and decreased brain derived neurotrophic factor (BDNF) and activity regulated cytoskeleton associated protein (Arc) gene expression in the amygdala.
+HDAC9	drug	alcohol	24103311	In this study we used the <strong>HDAC</strong> inhibitor trichostatin A (TSA) to determine whether <strong>HDAC</strong> inhibition could prevent <b>ethanol</b> withdrawal induced deficits in dendritic spine density (DSD), BDNF or Arc expression in the amygdala of rats.
+HDAC9	addiction	withdrawal	24103311	In this study we used the <strong>HDAC</strong> inhibitor trichostatin A (TSA) to determine whether <strong>HDAC</strong> inhibition could prevent ethanol <b>withdrawal</b> induced deficits in dendritic spine density (DSD), BDNF or Arc expression in the amygdala of rats.
+HDAC9	drug	alcohol	23905631	Recently, we have demonstrated that acute <b>alcohol</b> exposure due to binge drinking leads to hepatic steatosis with the deregulation of hepatic histone deacetylase (<strong>HDAC</strong>) expression.
+HDAC9	addiction	intoxication	23905631	Recently, we have demonstrated that acute alcohol exposure due to <b>binge</b> drinking leads to hepatic steatosis with the deregulation of hepatic histone deacetylase (<strong>HDAC</strong>) expression.
+HDAC9	addiction	intoxication	23905631	The <b>binge</b> EtOH mediated increase in HDAC3 was prevented by simultaneous administration of <strong>HDAC</strong> inhibitor, TSA, which markedly attenuated hepatic steatosis and injury.
+HDAC9	drug	alcohol	23485013	However, the epigenetic basis and role of specific histone deacetylase (<strong>HDAC</strong>) isoforms in the genetic predisposition to anxiety and <b>alcoholism</b> is unknown.
+HDAC9	drug	alcohol	23485013	We measured amygdaloid <strong>HDAC</strong> activity, levels of <strong>HDAC</strong> isoforms, and histone H3 acetylation in selectively bred <b>alcohol</b> preferring (P) and  nonpreferring (NP) rats.
+HDAC9	drug	alcohol	23485013	Acute <b>ethanol</b> exposure decreased amygdaloid <strong>HDAC</strong> activity and HDAC2 protein levels, increased global and gene (Bdnf and Arc) specific histone acetylation, and attenuated anxiety like behaviors in P rats but had no effects in NP rats.
+HDAC9	drug	cocaine	23475113	Class I <strong>HDAC</strong> inhibition blocks <b>cocaine</b> induced plasticity by targeted changes in histone methylation.
+HDAC9	drug	cocaine	23475113	Histone deacetylases (HDACs) tightly regulate the acetylation of histone tails, but little is known about the functional specificity of different <strong>HDAC</strong> isoforms in the development and maintenance of <b>cocaine</b> induced plasticity, and previous studies of <strong>HDAC</strong> inhibitors report conflicting effects on <b>cocaine</b> elicited behavioral adaptations.
+HDAC9	drug	cocaine	23475113	Our findings suggest a new mechanism by which prolonged and selective <strong>HDAC</strong> inhibition can alter behavioral and molecular adaptations to <b>cocaine</b> and inform the development of therapeutics for <b>cocaine</b> addiction.
+HDAC9	addiction	addiction	23475113	Our findings suggest a new mechanism by which prolonged and selective <strong>HDAC</strong> inhibition can alter behavioral and molecular adaptations to cocaine and inform the development of therapeutics for cocaine <b>addiction</b>.
+HDAC9	addiction	withdrawal	23474591	Whether <strong>HDAC</strong> induced histone modifications regulate changes in GABA sensitivity of VTA pDAergic neurons during <b>withdrawal</b> is unknown.
+HDAC9	drug	alcohol	23474591	Here, we investigated modulation of withdrawal induced changes in GABA sensitivity of pDAergic VTA neurons by <strong>HDAC</strong> inhibitors (HDACi), and also measured the levels of HDAC2, histone (H3 K9) acetylation, and GABA Aα1 receptor (GABA (A α1) R) subunit in VTA during <b>ethanol</b> withdrawal.
+HDAC9	addiction	withdrawal	23474591	Here, we investigated modulation of <b>withdrawal</b> induced changes in GABA sensitivity of pDAergic VTA neurons by <strong>HDAC</strong> inhibitors (HDACi), and also measured the levels of HDAC2, histone (H3 K9) acetylation, and GABA Aα1 receptor (GABA (A α1) R) subunit in VTA during ethanol <b>withdrawal</b>.
+HDAC9	drug	cocaine	23454534	Here, we investigate the effects of the histone deacetylase (<strong>HDAC</strong>) inhibitor sodium butyrate (NaBut) on <b>cocaine</b> induced conditioned place preference (CPP) in C57BL/6 mice.
+HDAC9	addiction	reward	23454534	Here, we investigate the effects of the histone deacetylase (<strong>HDAC</strong>) inhibitor sodium butyrate (NaBut) on cocaine induced conditioned place preference (<b>CPP</b>) in C57BL/6 mice.
+HDAC9	drug	cocaine	23454534	These findings suggest that <strong>HDAC</strong> inhibition may have dose dependent effects on different components of <b>cocaine</b> CPP, with implications for (1) involvement of histone acetylation in context drug learning, (2) interpretation of acute and chronic drug effects, and (3) the targeting of different types of learning in therapeutic application of <strong>HDAC</strong> inhibitors.
+HDAC9	addiction	reward	23454534	These findings suggest that <strong>HDAC</strong> inhibition may have dose dependent effects on different components of cocaine <b>CPP</b>, with implications for (1) involvement of histone acetylation in context drug learning, (2) interpretation of acute and chronic drug effects, and (3) the targeting of different types of learning in therapeutic application of <strong>HDAC</strong> inhibitors.
+HDAC9	drug	alcohol	23423140	Similarly, we find that increasing histone acetylation via systemic treatment with several histone deacetylase (<strong>HDAC</strong>) inhibitors reduces mice binge like <b>alcohol</b> drinking.
+HDAC9	addiction	intoxication	23423140	Similarly, we find that increasing histone acetylation via systemic treatment with several histone deacetylase (<strong>HDAC</strong>) inhibitors reduces mice <b>binge</b> like alcohol drinking.
+HDAC9	drug	alcohol	23423140	We further report that systemic administration of the FDA approved <strong>HDAC</strong> inhibitor, SAHA, inhibits the motivation of rats to seek <b>alcohol</b>.
+HDAC9	drug	alcohol	23423140	Importantly, the actions of both DNMT and <strong>HDAC</strong> inhibitors are specific for <b>alcohol</b>, as no changes in saccharin or sucrose intake were observed.
+HDAC9	drug	alcohol	23423140	Our study therefore highlights the possibility that DNMT and <strong>HDAC</strong> inhibitors can be used to treat harmful <b>alcohol</b> abuse.
+HDAC9	addiction	relapse	23297220	Nonspecific histone deacetylase (<strong>HDAC</strong>) inhibition has been shown to facilitate the extinction of drug <b>seeking</b> behavior in a manner resistant to <b>reinstatement</b>.
+HDAC9	addiction	relapse	23297220	A key open question is which specific <strong>HDAC</strong> is involved in the extinction of drug <b>seeking</b> behavior.
+HDAC9	drug	opioid	23273833	In the current work we explored how the balance of histone acetyltransferase (HAT) versus histone deacetylase (<strong>HDAC</strong>) might regulate these <b>morphine</b> induced changes.
+HDAC9	drug	opioid	23273833	Moreover, we observed a decrease in <strong>HDAC</strong> activity in the spinal cords of <b>morphine</b> treated mice while overall HAT activity was unchanged, suggesting a shift toward a state of enhanced histone acetylation.
+HDAC9	drug	alcohol	23110077	Brains were then removed 30 min after a saline or 2 g/kg <b>ethanol</b> challenge to assess i) gene expression using PCR array targeting 84 epigenetic related genes and ii) histone deacetylases (<strong>HDAC</strong>), histone acetylases (HAT) and DNA methyltransferases (DNMT) activities as well as H4K12 acetylation.
+HDAC9	drug	alcohol	23110077	Whereas global HAT or DNMT activity was not affected, global <strong>HDAC</strong> activity was reduced after an acute <b>ethanol</b> injection.
+HDAC9	drug	alcohol	23110077	<strong>HDAC</strong> inhibition occurred in all <b>ethanol</b> treated mice but with a lesser extent in sensitized animals.
+HDAC9	drug	opioid	23035088	We found that CPA extinction training induced an increase in recruiting cAMP response element binding protein (CREB) to and acetylation of histone H3 at the promoters of BDNF exon I transcript and increased BDNF mRNA and protein expression in the ventromedial prefrontal cortex (vmPFC) of acute <b>morphine</b> dependent rats and that such epigenetic regulation of BDNF gene transcription could be facilitated or diminished by intra vmPFC infusion of <strong>HDAC</strong> inhibitor trichostatin A or extracellular signal regulated kinase (ERK) inhibitor U0126 (1,4 diamino 2,3 dicyano 1,4 bis(methylthio)butadiene) before extinction training.
+HDAC9	addiction	addiction	22796363	Recent studies have also implicated histone deacetylases (HDACs) and acetyltransferases (HATS) in regulation of drug <b>addiction</b>, and <strong>HDAC</strong> inhibitors (HDACi) have been reported as transcriptional modulators of monoaminergic neurotransmission.
+HDAC9	drug	alcohol	22796363	The effects of <b>ethanol</b> on serotonin and 5 HT3, and the role HDACs, <strong>HDAC</strong> activity and the HDACi, trichostatin A (TSA), play in <b>alcohol</b> induced serotonergic effects were studied.
+HDAC9	drug	alcohol	22796363	Further, <b>ethanol</b> significantly increased HDACs 1 and 3 genes accompanied by an increased in <strong>HDAC</strong> activity while TSA significantly inhibited HDACs.
+HDAC9	drug	alcohol	22796363	In summary, our studies demonstrate some of the novel properties of <strong>HDAC</strong> inhibitors and contribute to the understanding of the mechanisms involve in <b>alcohol</b> serotonergic modulation in the CNS.
+HDAC9	drug	amphetamine	22470541	These results suggest that <b>METH</b> induced alterations in global gene expression seen in rat NAC might be related, in part, to <b>METH</b> induced changes in histone acetylation secondary to changes in HAT and <strong>HDAC</strong> expression.
+HDAC9	drug	alcohol	22375794	Binge <b>alcohol</b> induced microvesicular liver steatosis and injury are associated with down regulation of hepatic <strong>Hdac</strong> 1, 7, 9, 10, 11 and up regulation of <strong>Hdac</strong> 3.
+HDAC9	addiction	intoxication	22375794	<b>Binge</b> alcohol induced microvesicular liver steatosis and injury are associated with down regulation of hepatic <strong>Hdac</strong> 1, 7, 9, 10, 11 and up regulation of <strong>Hdac</strong> 3.
+HDAC9	drug	alcohol	22375794	Binge <b>alcohol</b> exposure resulted in alterations of hepatic <strong>Hdac</strong> mRNA levels.
+HDAC9	addiction	intoxication	22375794	<b>Binge</b> alcohol exposure resulted in alterations of hepatic <strong>Hdac</strong> mRNA levels.
+HDAC9	addiction	intoxication	22375794	Fas promoter analysis revealed that <b>binge</b> EtOH treatment decreased <strong>HDAC</strong> 9 occupancy at the Fas promoter resulting in its transcriptional activation.
+HDAC9	drug	alcohol	22375794	Deregulation of hepatic <strong>Hdac</strong> expression likely plays a major role in the binge <b>alcohol</b> induced hepatic steatosis and liver injury by affecting lipogenesis and fatty acid β oxidation.
+HDAC9	addiction	intoxication	22375794	Deregulation of hepatic <strong>Hdac</strong> expression likely plays a major role in the <b>binge</b> alcohol induced hepatic steatosis and liver injury by affecting lipogenesis and fatty acid β oxidation.
+HDAC9	drug	cocaine	21886555	We have previously demonstrated that pretreatment with histone deacetylase (<strong>HDAC</strong>) inhibitors reduces the <b>cocaine</b> reinforcing properties as well as the motivation of rats for <b>cocaine</b>.
+HDAC9	addiction	reward	21886555	We have previously demonstrated that pretreatment with histone deacetylase (<strong>HDAC</strong>) inhibitors reduces the cocaine <b>reinforcing</b> properties as well as the motivation of rats for cocaine.
+HDAC9	drug	cocaine	21886555	We show here that the same <strong>HDAC</strong> inhibitors, trichostatin A and phenylbutyrate, significantly reduced the <b>cocaine</b> seeking behavior induced by the combination of a <b>cocaine</b> injection together with the exposure to a light cue previously associated with <b>cocaine</b> taking.
+HDAC9	addiction	relapse	21886555	We show here that the same <strong>HDAC</strong> inhibitors, trichostatin A and phenylbutyrate, significantly reduced the cocaine <b>seeking</b> behavior induced by the combination of a cocaine injection together with the exposure to a light cue previously associated with cocaine taking.
+HDAC9	addiction	addiction	21886555	Our results suggest that pharmacological treatment aimed at modulating epigenetic regulation, and particularly treatment that would inhibit <strong>HDAC</strong> activity, could reduce the risk of relapse, a major drawback in the treatment of drug <b>addiction</b>.
+HDAC9	addiction	relapse	21886555	Our results suggest that pharmacological treatment aimed at modulating epigenetic regulation, and particularly treatment that would inhibit <strong>HDAC</strong> activity, could reduce the risk of <b>relapse</b>, a major drawback in the treatment of drug addiction.
+HDAC9	addiction	addiction	21447001	Previous studies have implicated histone deacetylases (HDACs) and <strong>HDAC</strong> inhibitors (HDIs) such as trichostatin A (TSA) in the regulation of gene expression during drug <b>addiction</b>.
+HDAC9	drug	opioid	20691756	In this study, we will examine the effect of histone deacetylase (<strong>HDAC</strong>) inhibitors on extinction of <b>morphine</b> induced conditioned place preference (CPP).
+HDAC9	addiction	reward	20691756	In this study, we will examine the effect of histone deacetylase (<strong>HDAC</strong>) inhibitors on extinction of morphine induced conditioned place preference (<b>CPP</b>).
+HDAC9	drug	opioid	20691756	We found that <strong>HDAC</strong> inhibition during nonconfined extinction or confined extinction consolidation can facilitate extinction of <b>morphine</b> induced CPP.
+HDAC9	addiction	reward	20691756	We found that <strong>HDAC</strong> inhibition during nonconfined extinction or confined extinction consolidation can facilitate extinction of morphine induced <b>CPP</b>.
+HDAC9	addiction	relapse	20691756	We also showed that the extinction of drug <b>seeking</b> via <strong>HDAC</strong> inhibition modulates extinction learning such that <b>reinstatement</b> behavior is significantly attenuated.
+HDAC9	drug	cocaine	20383415	Male Sprague Dawley rats (n=160) were tested by conditioned place preference (CPP) procedure, to evaluate the effects of inhibitors of histone deacetylase (<strong>HDAC</strong>) and histone acetyltransferase (HAT) on the conditioned effects of <b>cocaine</b>.
+HDAC9	addiction	reward	20383415	Male Sprague Dawley rats (n=160) were tested by conditioned place preference (<b>CPP</b>) procedure, to evaluate the effects of inhibitors of histone deacetylase (<strong>HDAC</strong>) and histone acetyltransferase (HAT) on the conditioned effects of cocaine.
+HDAC9	drug	cocaine	20383415	For each conditioning session, rats were injected with either <strong>HDAC</strong> (or HAT) inhibitors or saline in home cages, followed by <b>cocaine</b> (intraperitoneally [ip]) or saline (ip) 30 minutes later, and then immediately confined for 50 minutes in the cue specific chamber.
+HDAC9	drug	cocaine	20383415	Our results showed that pretreatment with <strong>HDAC</strong> inhibitor (sodium butyrate), potentiated <b>cocaine</b> induced CPP, but did not itself lead to conditioned preferences, or aversions.
+HDAC9	addiction	reward	20383415	Our results showed that pretreatment with <strong>HDAC</strong> inhibitor (sodium butyrate), potentiated cocaine induced <b>CPP</b>, but did not itself lead to conditioned preferences, or aversions.
+HDAC9	drug	cocaine	20010550	The effect of the <strong>HDAC</strong> inhibitor is attributed to the increased elevation of histone acetylation induced by chronic, but not acute, <b>cocaine</b> experience.
+HDAC9	drug	cocaine	19765687	In this study, we examined the ability of histone deacetylase (<strong>HDAC</strong>) inhibitors to facilitate extinction and attenuate reinstatement of <b>cocaine</b> induced conditioned place preference (CPP).
+HDAC9	addiction	relapse	19765687	In this study, we examined the ability of histone deacetylase (<strong>HDAC</strong>) inhibitors to facilitate extinction and attenuate <b>reinstatement</b> of cocaine induced conditioned place preference (CPP).
+HDAC9	addiction	reward	19765687	In this study, we examined the ability of histone deacetylase (<strong>HDAC</strong>) inhibitors to facilitate extinction and attenuate reinstatement of cocaine induced conditioned place preference (<b>CPP</b>).
+HDAC9	drug	cocaine	19765687	We demonstrate that <strong>HDAC</strong> inhibition during extinction consolidation can facilitate extinction of <b>cocaine</b> induced CPP.
+HDAC9	addiction	reward	19765687	We demonstrate that <strong>HDAC</strong> inhibition during extinction consolidation can facilitate extinction of cocaine induced <b>CPP</b>.
+HDAC9	drug	cocaine	19765687	Animals treated with an <strong>HDAC</strong> inhibitor extinguished <b>cocaine</b> induced CPP both more quickly and to a greater extent than did vehicle treated animals.
+HDAC9	addiction	reward	19765687	Animals treated with an <strong>HDAC</strong> inhibitor extinguished cocaine induced <b>CPP</b> both more quickly and to a greater extent than did vehicle treated animals.
+HDAC9	drug	cocaine	19765687	We also show that the extinction of <b>cocaine</b> seeking via <strong>HDAC</strong> inhibition modulates extinction learning such that reinstatement behavior is significantly attenuated.
+HDAC9	addiction	relapse	19765687	We also show that the extinction of cocaine <b>seeking</b> via <strong>HDAC</strong> inhibition modulates extinction learning such that <b>reinstatement</b> behavior is significantly attenuated.
+HDAC9	drug	opioid	19727068	In this study, we extend those seminal findings by showing that the administration of the <strong>HDAC</strong> inhibitor sodium butyrate enhances <b>morphine</b> induced locomotor sensitization and conditioned place preference.
+HDAC9	addiction	sensitization	19727068	In this study, we extend those seminal findings by showing that the administration of the <strong>HDAC</strong> inhibitor sodium butyrate enhances morphine induced locomotor <b>sensitization</b> and conditioned place preference.
+HDAC9	addiction	sensitization	18848971	Histone deacetylase (<strong>HDAC</strong>) plays an important role in chromatin remodeling in response to a variety of neurochemical signalings and behavioral manipulations, and may be a therapeutic target for modulation of psychostimulant behavioral <b>sensitization</b>.
+HDAC9	addiction	sensitization	18848971	Thus, HDACi may interact additively with psychostimulants at both histone acetylation and CREB phosphorylation through the CREB:<strong>HDAC</strong> protein complex in the striatum to modulate DeltaFosB protein levels and psychomotor behavioral <b>sensitization</b>.
+HDAC9	drug	cocaine	18799668	Using the fixed ratio 1 schedule, we found that the histone deacetylase (<strong>HDAC</strong>) inhibitors trichostatin A and phenylbutyrate dose dependently reduced <b>cocaine</b> self administration.
+HDAC9	drug	cocaine	18799668	Under the progressive ratio schedule, both trichostatin A and depudecin significantly reduced the breaking point, indicating that <strong>HDAC</strong> inhibition attenuated the motivation of rats for <b>cocaine</b>.
+HDAC9	drug	cocaine	18799668	This observation was correlated with measurements of <strong>HDAC</strong> activity in the frontal cortex, which was inhibited in response to <b>cocaine</b>, but not to sucrose self administration.
+HDAC9	addiction	dependence	18799668	Together, the data show that epigenetic regulation of gene transcription in adult brain is able to influence a motivated behavior and suggest that <strong>HDAC</strong> inhibition may counteract the neural sensitization leading to drug <b>dependence</b>.
+HDAC9	addiction	sensitization	18799668	Together, the data show that epigenetic regulation of gene transcription in adult brain is able to influence a motivated behavior and suggest that <strong>HDAC</strong> inhibition may counteract the neural <b>sensitization</b> leading to drug dependence.
+HDAC9	drug	alcohol	18385331	We found that the anxiolytic effects produced by acute <b>alcohol</b> were associated with a decrease in histone deacetylase (<strong>HDAC</strong>) activity and increases in acetylation of histones (H3 and H4), levels of CREB (cAMP responsive element binding) binding protein (CBP), and neuropeptide Y (NPY) expression in the amygdaloid brain regions of rats.
+HDAC9	drug	alcohol	18385331	However, the anxiety like behaviors during withdrawal after chronic <b>alcohol</b> exposure were associated with an increase in <strong>HDAC</strong> activity and decreases in acetylation of H3 and H4, and levels of both CBP and NPY in the amygdala.
+HDAC9	addiction	withdrawal	18385331	However, the anxiety like behaviors during <b>withdrawal</b> after chronic alcohol exposure were associated with an increase in <strong>HDAC</strong> activity and decreases in acetylation of H3 and H4, and levels of both CBP and NPY in the amygdala.
+HDAC9	drug	alcohol	18385331	Blocking the observed increase in <strong>HDAC</strong> activity during <b>alcohol</b> withdrawal with the <strong>HDAC</strong> inhibitor, trichostatin A, rescued the deficits in H3 and H4 acetylation and NPY expression (mRNA and protein levels) in the amygdala (central and medial nucleus of amygdala) and prevented the development of <b>alcohol</b> withdrawal related anxiety in rats as measured by the elevated plus maze and light/dark box exploration tests.
+HDAC9	addiction	withdrawal	18385331	Blocking the observed increase in <strong>HDAC</strong> activity during alcohol <b>withdrawal</b> with the <strong>HDAC</strong> inhibitor, trichostatin A, rescued the deficits in H3 and H4 acetylation and NPY expression (mRNA and protein levels) in the amygdala (central and medial nucleus of amygdala) and prevented the development of alcohol <b>withdrawal</b> related anxiety in rats as measured by the elevated plus maze and light/dark box exploration tests.
+HDAC9	drug	alcohol	18385331	These results reveal a novel role for amygdaloid chromatin remodeling in the process of <b>alcohol</b> addiction and further suggest that <strong>HDAC</strong> inhibitors may be potential therapeutic agents in treating <b>alcohol</b> withdrawal symptoms.
+HDAC9	addiction	addiction	18385331	These results reveal a novel role for amygdaloid chromatin remodeling in the process of alcohol <b>addiction</b> and further suggest that <strong>HDAC</strong> inhibitors may be potential therapeutic agents in treating alcohol withdrawal symptoms.
+HDAC9	addiction	withdrawal	18385331	These results reveal a novel role for amygdaloid chromatin remodeling in the process of alcohol addiction and further suggest that <strong>HDAC</strong> inhibitors may be potential therapeutic agents in treating alcohol <b>withdrawal</b> symptoms.
+HDAC9	drug	amphetamine	17477979	We then administered the <strong>HDAC</strong> inhibitors after treatment with <b>amphetamine</b> for 8 days to establish locomotor sensitization.
+HDAC9	addiction	sensitization	17477979	We then administered the <strong>HDAC</strong> inhibitors after treatment with amphetamine for 8 days to establish locomotor <b>sensitization</b>.
+HDAC9	drug	amphetamine	17477979	Finally, in a context specific model we studied the effect of <strong>HDAC</strong> inhibitors on <b>amphetamine</b> induced association of the treatment environment (associative learning).
+HDAC9	drug	amphetamine	17477979	Thus, <strong>HDAC</strong> inhibitors differentially modulate the induction and expression of <b>amphetamine</b> induced effects.
+TRH	drug	alcohol	25433251	A few studies have suggested a relationship between thyroid hormones and <b>alcohol</b> dependence (AD) such as a blunted increase of thyroid stimulating hormone (TSH) in response to thyrotropin releasing hormone (<strong>TRH</strong>), lower levels of circulating free triiodothyronine (fT3) and free thyroxine (fT4) levels and down regulation of the <strong>TRH</strong> receptors.
+TRH	addiction	dependence	25433251	A few studies have suggested a relationship between thyroid hormones and alcohol <b>dependence</b> (AD) such as a blunted increase of thyroid stimulating hormone (TSH) in response to thyrotropin releasing hormone (<strong>TRH</strong>), lower levels of circulating free triiodothyronine (fT3) and free thyroxine (fT4) levels and down regulation of the <strong>TRH</strong> receptors.
+TRH	drug	alcohol	25433251	A few studies have suggested a relationship between thyroid hormones and <b>alcohol</b> dependence (AD) such as a blunted increase of thyroid stimulating hormone (TSH) in response to <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), lower levels of circulating free triiodothyronine (fT3) and free thyroxine (fT4) levels and down regulation of the <strong>TRH</strong> receptors.
+TRH	addiction	dependence	25433251	A few studies have suggested a relationship between thyroid hormones and alcohol <b>dependence</b> (AD) such as a blunted increase of thyroid stimulating hormone (TSH) in response to <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), lower levels of circulating free triiodothyronine (fT3) and free thyroxine (fT4) levels and down regulation of the <strong>TRH</strong> receptors.
+TRH	drug	opioid	18771713	Specific radioimmunoassays demonstrated that the increase in PC1/3 and PC2 levels following long term <b>morphine</b> led to increased <strong>TRH</strong> biosynthesis as evidence by increased <strong>TRH</strong>/5.4 kDa C terminal proTRH derived peptide ratios in the median eminence.
+TRH	drug	opioid	18771713	Specific radioimmunoassays demonstrated that the increase in PC1/3 and PC2 levels following long term <b>morphine</b> led to increased <strong>TRH</strong> biosynthesis as evidence by increased <strong>TRH</strong>/5.4 kDa C terminal <strong>proTRH</strong> derived peptide ratios in the median eminence.
+TRH	drug	alcohol	15680480	Chronic <b>ethanol</b> or glucose consumption alter <strong>TRH</strong> content and pyroglutamyl aminopeptidase II activity in rat limbic regions.
+TRH	drug	alcohol	15680480	Nutritional changes or acute <b>ethanol</b> administration in male rats differentially modulate <strong>TRH</strong> or PPII expression.
+TRH	drug	alcohol	15680480	<b>Ethanol</b> consumption decreased <strong>TRH</strong> content and PPII activity in frontal cortex of male rats after 3 6 weeks.
+TRH	drug	alcohol	15680480	Withdrawal at 24 h after 3 week <b>ethanol</b> ingestion decreased <strong>TRH</strong> content in amygdala and PPII activity in n. accumbens, while withdrawal from glucose reverted some of the effects produced by chronic glucose ingestion.
+TRH	addiction	withdrawal	15680480	<b>Withdrawal</b> at 24 h after 3 week ethanol ingestion decreased <strong>TRH</strong> content in amygdala and PPII activity in n. accumbens, while <b>withdrawal</b> from glucose reverted some of the effects produced by chronic glucose ingestion.
+TRH	addiction	withdrawal	15025564	<strong>TRH</strong> caused a 5 25 fold increase in receptor protein during 48 h, which was half maximal at 1 nM and was slowly reversible after hormone <b>withdrawal</b>.
+TRH	drug	cocaine	15003716	Effect of <strong>thyrotropin releasing hormone</strong> on the locomotor and sensitizing effects of <b>cocaine</b> in rats.
+TRH	drug	cocaine	15003716	The present study was designed to find out whether single and repeated treatment with thyrotropin releasing hormone (<strong>TRH</strong>) changed the <b>cocaine</b> evoked hyperactivation or sensitization, and whether cross sensitization occurred between <strong>TRH</strong> and <b>cocaine</b>.
+TRH	addiction	sensitization	15003716	The present study was designed to find out whether single and repeated treatment with thyrotropin releasing hormone (<strong>TRH</strong>) changed the cocaine evoked hyperactivation or <b>sensitization</b>, and whether cross <b>sensitization</b> occurred between <strong>TRH</strong> and cocaine.
+TRH	drug	cocaine	15003716	The present study was designed to find out whether single and repeated treatment with <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) changed the <b>cocaine</b> evoked hyperactivation or sensitization, and whether cross sensitization occurred between <strong>TRH</strong> and <b>cocaine</b>.
+TRH	addiction	sensitization	15003716	The present study was designed to find out whether single and repeated treatment with <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) changed the cocaine evoked hyperactivation or <b>sensitization</b>, and whether cross <b>sensitization</b> occurred between <strong>TRH</strong> and cocaine.
+TRH	drug	cocaine	15003716	Like <b>cocaine</b> (10 mg/kg), <strong>TRH</strong> (10 mg/kg) increased the basal activation of rats; however, when given in combination with <b>cocaine</b> (10 mg/kg), <strong>TRH</strong> (5 10 mg/kg) did not change the locomotor effect of <b>cocaine</b>.
+TRH	drug	cocaine	15003716	When co administered with <b>cocaine</b> for 5 days during the development of sensitization, <strong>TRH</strong> (10 mg/kg) enhanced the effect of the challenge dose of <b>cocaine</b> (10 mg/kg) following a 5 day withdrawal.
+TRH	addiction	sensitization	15003716	When co administered with cocaine for 5 days during the development of <b>sensitization</b>, <strong>TRH</strong> (10 mg/kg) enhanced the effect of the challenge dose of cocaine (10 mg/kg) following a 5 day withdrawal.
+TRH	addiction	withdrawal	15003716	When co administered with cocaine for 5 days during the development of sensitization, <strong>TRH</strong> (10 mg/kg) enhanced the effect of the challenge dose of cocaine (10 mg/kg) following a 5 day <b>withdrawal</b>.
+TRH	drug	cocaine	15003716	Given acutely with <b>cocaine</b> on day 10 to <b>cocaine</b> treated animals, <strong>TRH</strong> (5 10 mg/kg) did not change the expression of <b>cocaine</b> sensitization.
+TRH	addiction	sensitization	15003716	Given acutely with cocaine on day 10 to cocaine treated animals, <strong>TRH</strong> (5 10 mg/kg) did not change the expression of cocaine <b>sensitization</b>.
+TRH	drug	cocaine	15003716	The response to <strong>TRH</strong> (5 10 mg/kg) was stronger in repeated <b>cocaine</b> treated rats than in saline injected ones; similarly, the response to <b>cocaine</b> (10 mg/kg) was more potent in <strong>TRH</strong> treated animals compared to saline injected ones (cross sensitization).
+TRH	addiction	sensitization	15003716	The response to <strong>TRH</strong> (5 10 mg/kg) was stronger in repeated cocaine treated rats than in saline injected ones; similarly, the response to cocaine (10 mg/kg) was more potent in <strong>TRH</strong> treated animals compared to saline injected ones (cross <b>sensitization</b>).
+TRH	addiction	sensitization	15003716	In conclusion, our results indicate that exposure to <strong>TRH</strong> induces <b>sensitization</b> to its locomotor hyperactivity effect.
+TRH	drug	cocaine	15003716	They also show that <strong>TRH</strong> enhances the development of <b>cocaine</b> sensitization, but affects neither the expression phase of the phenomenon nor the locomotor hyperactivity induced by a single dose of <b>cocaine</b>.
+TRH	addiction	sensitization	15003716	They also show that <strong>TRH</strong> enhances the development of cocaine <b>sensitization</b>, but affects neither the expression phase of the phenomenon nor the locomotor hyperactivity induced by a single dose of cocaine.
+TRH	drug	cocaine	15003716	Moreover, cross sensitization between <b>cocaine</b> and <strong>TRH</strong> has also been demonstrated.
+TRH	addiction	sensitization	15003716	Moreover, cross <b>sensitization</b> between cocaine and <strong>TRH</strong> has also been demonstrated.
+TRH	drug	cocaine	15003716	These findings also may provide an insight into the relationship between <strong>TRH</strong> and <b>cocaine</b> in humans exposed to the psychostimulant.
+TRH	drug	alcohol	12410778	About one third of all <b>alcoholics</b> also displayed a blunted thyroid stimulation hormone (TSH) response in the thyrotrophin releasing hormone test (<strong>TRH</strong> test).
+TRH	drug	alcohol	12410778	We suggest that a reduction in peripheral thyroid hormones may be caused by a direct toxic effect of <b>alcohol</b> on the thyroid gland, which induces a central compensatory activation of the hypothalamic pituitary axis with an increased <strong>TRH</strong> release.
+TRH	drug	cocaine	12213229	<b>Cocaine</b> regulates <strong>TRH</strong> related peptides in rat brain.
+TRH	drug	cocaine	12213229	<b>Cocaine</b> administration has previously been reported to alter the levels of prepro <strong>TRH</strong> mRNA and <strong>TRH</strong> (pGlu His Pro NH(2)) in the limbic system of rats (J. Neurochem.
+TRH	drug	cocaine	12213229	We have now demonstrated that a previously unrecognized family of <strong>TRH</strong> like peptides is involved in the actions of <b>cocaine</b>.
+TRH	drug	cocaine	12213229	Acute <b>cocaine</b> produced a 4.1 fold increase in Val(2) <strong>TRH</strong> level in medulla while Val(2) <strong>TRH</strong> and Tyr(2) <strong>TRH</strong>, increased 6.2  and 2.9 fold, respectively in pyriform cortex PYR.
+TRH	drug	cocaine	12213229	<strong>TRH</strong> and Leu(2) <strong>TRH</strong>, decreased 47 and 93%, respectively in the nucleus accumbens (AM) while other EEP IR peaks decreased 50 100% consistent with the significant decrease in total EEP IR in the AMs following acute <b>cocaine</b> treatment.
+TRH	drug	cocaine	12213229	Because 2h is too short a time to alter levels of neuropeptides via changes in the rate of biosynthesis, the acute <b>cocaine</b> induced elevation or reduction in <strong>TRH</strong> and related peptides is most likely due to suppression or stimulation, respectively, of the corresponding peptide secretion rate.
+TRH	drug	cocaine	12213229	Because <strong>TRH</strong> and <strong>TRH</strong> like peptides have antidepressant, analeptic and euphorigenic properties, we conclude that these endogenous substances are potential mediators of both the <b>cocaine</b> "high" and withdrawal symptoms.
+TRH	addiction	withdrawal	12213229	Because <strong>TRH</strong> and <strong>TRH</strong> like peptides have antidepressant, analeptic and euphorigenic properties, we conclude that these endogenous substances are potential mediators of both the cocaine "high" and <b>withdrawal</b> symptoms.
+TRH	drug	opioid	11948251	Effect of precipitated <b>morphine</b> withdrawal on post translational processing of prothyrotropin releasing hormone (<strong>proTRH</strong>) in the ventrolateral column of the midbrain periaqueductal gray.
+TRH	addiction	withdrawal	11948251	Effect of precipitated morphine <b>withdrawal</b> on post translational processing of prothyrotropin releasing hormone (<strong>proTRH</strong>) in the ventrolateral column of the midbrain periaqueductal gray.
+TRH	addiction	withdrawal	11948251	We have demonstrated that during opiate <b>withdrawal</b>, preprothyrotropin releasing hormone (preproTRH) mRNA is increased in neurons of the midbrain periaqueductal gray matter (PAG) while the concentration of <strong>TRH</strong> remained unaltered, suggesting that the processing of proTRH may be different in this region of the brain.
+TRH	addiction	withdrawal	11948251	We have demonstrated that during opiate <b>withdrawal</b>, preprothyrotropin releasing hormone (preproTRH) mRNA is increased in neurons of the midbrain periaqueductal gray matter (PAG) while the concentration of <strong>TRH</strong> remained unaltered, suggesting that the processing of <strong>proTRH</strong> may be different in this region of the brain.
+TRH	addiction	withdrawal	11948251	The aim of the present study was to determine which of the <strong>proTRH</strong> derived peptides are affected by opiate <b>withdrawal</b> in the PAG.
+TRH	addiction	withdrawal	11948251	Opiate <b>withdrawal</b> caused a significant change in the level of some post translational processing products derived from the <strong>TRH</strong> precursor.
+TRH	addiction	withdrawal	11948251	In the PAG, opiate <b>withdrawal</b> resulted in an accumulation of the intervening preproTRH(83 106) peptide from the N terminal side of the prohormone, while the levels of the C terminal preproTRH(208 285) peptide were reduced, with no change in preproTRH(25 50) or <strong>TRH</strong>, itself, as compared to control animals.
+TRH	addiction	withdrawal	11948251	Opiate <b>withdrawal</b> in the lateral hypothalamus, unlike from the PAG, was accompanied by an increase in the concentration of <strong>TRH</strong>.
+TRH	addiction	withdrawal	11948251	Thus, these results demonstrate a region specific regulation of <strong>TRH</strong> prohormone processing in the brain, which may engage PC2, further suggesting a role for specific proTRH derived peptides in the manifestations of opiate <b>withdrawal</b>.
+TRH	addiction	withdrawal	11948251	Thus, these results demonstrate a region specific regulation of <strong>TRH</strong> prohormone processing in the brain, which may engage PC2, further suggesting a role for specific <strong>proTRH</strong> derived peptides in the manifestations of opiate <b>withdrawal</b>.
+TRH	drug	opioid	11701131	Our previous study has shown that prothyrotropin releasing hormone (<strong>proTRH</strong>) gene expression is increased in the ventrolateral periaqueductal gray (PAG) neurons following precipitated <b>morphine</b> withdrawal and continues to be activated even 24 h after withdrawal.
+TRH	addiction	withdrawal	11701131	Our previous study has shown that prothyrotropin releasing hormone (<strong>proTRH</strong>) gene expression is increased in the ventrolateral periaqueductal gray (PAG) neurons following precipitated morphine <b>withdrawal</b> and continues to be activated even 24 h after <b>withdrawal</b>.
+TRH	drug	opioid	11701131	We have hypothesized that peptide products of <strong>proTRH</strong> may participate in the recovery from <b>morphine</b> withdrawal.
+TRH	addiction	withdrawal	11701131	We have hypothesized that peptide products of <strong>proTRH</strong> may participate in the recovery from morphine <b>withdrawal</b>.
+TRH	addiction	withdrawal	11701131	These studies demonstrate that <strong>proTRH</strong> neurons in the ventrolateral PAG project to several regions of the brain that are involved in autonomic and behavioral regulation and thereby, may function as an integrating center to coordinate responses to opiate <b>withdrawal</b>.
+TRH	drug	amphetamine	11104823	Cocaine  and <b>amphetamine</b> regulated transcript peptide (55 102) and <strong>thyrotropin releasing hormone</strong> inhibit hypothalamic dopamine release.
+TRH	drug	cocaine	11104823	<b>Cocaine</b>  and amphetamine regulated transcript peptide (55 102) and <strong>thyrotropin releasing hormone</strong> inhibit hypothalamic dopamine release.
+TRH	drug	amphetamine	11104823	Cocaine  and <b>amphetamine</b> regulated transcript (CART) peptide (55 102) and thyrotropin releasing hormone (<strong>TRH</strong>) play an anorectic role in the hypothalamus.
+TRH	drug	cocaine	11104823	<b>Cocaine</b>  and amphetamine regulated transcript (CART) peptide (55 102) and thyrotropin releasing hormone (<strong>TRH</strong>) play an anorectic role in the hypothalamus.
+TRH	drug	amphetamine	11104823	Cocaine  and <b>amphetamine</b> regulated transcript (CART) peptide (55 102) and <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) play an anorectic role in the hypothalamus.
+TRH	drug	cocaine	11104823	<b>Cocaine</b>  and amphetamine regulated transcript (CART) peptide (55 102) and <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) play an anorectic role in the hypothalamus.
+TRH	addiction	reward	11104823	Considering the role played by dopamine in the central mechanisms of <b>reward</b>, these findings suggest that the inhibition of dopamine release could underlie the decreased appetitive behaviour induced by CART peptide (55 102) and <strong>TRH</strong>.
+TRH	drug	alcohol	10871700	Acute <b>ethanol</b> administration induces changes in <strong>TRH</strong> and proenkephalin expression in hypothalamic and limbic regions of rat brain.
+TRH	drug	alcohol	10871700	We measured <strong>TRH</strong> content and the levels of its mRNA in hypothalamic and limbic zones 1 24 h after acute <b>ethanol</b> injection.
+TRH	drug	alcohol	10871700	Wistar rats were administered one dose of <b>ethanol</b> (intraperitoneal, 3 g/kg body weight) and brains dissected in hypothalamus, hippocampus, amygdala, n. accumbens and frontal cortex, for <strong>TRH</strong> quantification by radioimmunoassay or for proTRH mRNA measurement by RT PCR.
+TRH	drug	alcohol	10871700	Wistar rats were administered one dose of <b>ethanol</b> (intraperitoneal, 3 g/kg body weight) and brains dissected in hypothalamus, hippocampus, amygdala, n. accumbens and frontal cortex, for <strong>TRH</strong> quantification by radioimmunoassay or for <strong>proTRH</strong> mRNA measurement by RT PCR.
+TRH	drug	alcohol	10871700	The effect of <b>ethanol</b> was also studied in primary culture of hypothalamic cells; a fast and transient increase in <strong>proTRH</strong> mRNA was observed at 1 h of incubation (0.001% final <b>ethanol</b> concentration).
+TRH	drug	alcohol	10871700	Changes in the mRNA levels of <strong>proTRH</strong> and proenkephalin were quantified by in situ hybridization in rats administered <b>ethanol</b> intragastrically (2.5 g/kg).
+TRH	drug	alcohol	10871700	These results give support for <strong>TRH</strong> and enkephalin neurons as targets of <b>ethanol</b> and, as possible mediators of some of its observed behavioral effects.
+TRH	drug	alcohol	10684782	Combination pharmacotherapy: a mixture of small doses of <b>naltrexone</b>, fluoxetine, and a <strong>thyrotropin releasing hormone</strong> analogue reduces <b>alcohol</b> intake in three strains of <b>alcohol</b> preferring rats.
+TRH	drug	alcohol	10684782	injections of relatively low doses of either <b>naltrexone</b> (2.0 mg/kg), fluoxetine (1.0 mg/kg), the <strong>thyrotropin releasing hormone</strong> analogue TA 0910 (0.2 mg/kg), a mixture of all three drugs, or the vehicle at 09:30.
+TRH	drug	cocaine	10657535	<strong>Thyrotropin releasing hormone</strong> induced GH release after <b>cocaine</b> withdrawal in <b>cocaine</b> addicts.
+TRH	addiction	withdrawal	10657535	<strong>Thyrotropin releasing hormone</strong> induced GH release after cocaine <b>withdrawal</b> in cocaine addicts.
+TRH	drug	cocaine	10657535	During <b>cocaine</b> addiction the hypothalamus pituitary axis is widely affected and a blunted response of thyroid stimulating hormone (TSH) to thyroid releasing hormone (<strong>TRH</strong>) consistent with a hyperthyroid state has been observed.
+TRH	addiction	addiction	10657535	During cocaine <b>addiction</b> the hypothalamus pituitary axis is widely affected and a blunted response of thyroid stimulating hormone (TSH) to thyroid releasing hormone (<strong>TRH</strong>) consistent with a hyperthyroid state has been observed.
+TRH	drug	cocaine	10657535	Since the thyroid status can affect the release of growth hormone (GH) the authors evaluated TSH and GH responses to <strong>TRH</strong> in <b>cocaine</b> addicts at the time of drug withdrawal and 30 days after.
+TRH	addiction	withdrawal	10657535	Since the thyroid status can affect the release of growth hormone (GH) the authors evaluated TSH and GH responses to <strong>TRH</strong> in cocaine addicts at the time of drug <b>withdrawal</b> and 30 days after.
+TRH	addiction	withdrawal	10657535	<strong>TRH</strong> and placebo tests were performed at random at 5 day intervals at the time of drug <b>withdrawal</b> and after 30 days.
+TRH	drug	cocaine	10657535	After 30 days of <b>cocaine</b> abstinence basal freeT4 plasma levels were significantly lower, and TSH levels and the TSH response to <strong>TRH</strong> were higher than in the first test.
+TRH	drug	cocaine	10657535	At the first examination, basal GH concentrations were similar in <b>cocaine</b> addicts and in control subjects and GH did not respond to <strong>TRH</strong>.
+TRH	drug	cocaine	10657535	After 30 days of abstinence, basal GH plasma levels were unmodified, but the <strong>TRH</strong> became stimulatory of GH release in <b>cocaine</b> deprived, but not in control subjects.
+TRH	drug	cocaine	10657535	In conclusion, in <b>cocaine</b> addicts, drug withdrawal is associated with a condition of subclinical hypothyroidism that makes the GH releasing machinery sensitive to <strong>TRH</strong>.
+TRH	addiction	withdrawal	10657535	In conclusion, in cocaine addicts, drug <b>withdrawal</b> is associated with a condition of subclinical hypothyroidism that makes the GH releasing machinery sensitive to <strong>TRH</strong>.
+TRH	drug	opioid	10323386	<b>Naloxone</b> had no effect on the TSH responses to <strong>TRH</strong>, neither during hypo  nor during normocortisolism.
+TRH	drug	opioid	10323386	The PRL responses to <strong>TRH</strong> were similar during hypo  and normocortisolism and without any change during <b>opioid</b> receptor blockade.
+TRH	drug	alcohol	9347094	Effect of pyridostigmine on the thyroid stimulating hormone response to <strong>thyrotropin releasing hormone</strong> in abstinent <b>alcoholics</b>.
+TRH	drug	alcohol	9347094	<b>Alcoholism</b> is sometimes associated with a blunted thyroid stimulating hormone (TSH) response to thyrotropin releasing hormone (<strong>TRH</strong>; peak minus baseline < 5 mIU/liter), despite basal TSH and thyroid hormone levels within the normal range.
+TRH	drug	alcohol	9347094	<b>Alcoholism</b> is sometimes associated with a blunted thyroid stimulating hormone (TSH) response to <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>; peak minus baseline < 5 mIU/liter), despite basal TSH and thyroid hormone levels within the normal range.
+TRH	drug	alcohol	9347094	To answer this question, 16 euthyroid male <b>alcoholics</b> (aged 38 to 50 years) with normal [n = 8; normal responder <b>alcoholics</b> (NRAs)] or blunted [n = 8; low responder <b>alcoholics</b> (LRAs)] TSH response to <strong>TRH</strong> were selected in a preliminary <strong>TRH</strong> test (200 micrograms in an intravenous bolus).
+TRH	drug	alcohol	9347094	These data argue against the possibility that an enhanced somatostatinergic tone is responsible for the blunted TSH response to <strong>TRH</strong> observed in some <b>alcoholic</b> patients.
+TRH	drug	psychedelics	9252236	The drugs used were the N methyl D aspartate receptor channel blocker <b>ketamine</b>; the competitive antagonists, 3 ((R) 2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (D CPP) and D 2 amino 5 phosphonopentanoic acid (D AP5), and the positive modulator <strong>thyrotropin releasing hormone</strong>.
+TRH	addiction	reward	9252236	The drugs used were the N methyl D aspartate receptor channel blocker ketamine; the competitive antagonists, 3 ((R) 2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (D <b>CPP</b>) and D 2 amino 5 phosphonopentanoic acid (D AP5), and the positive modulator <strong>thyrotropin releasing hormone</strong>.
+TRH	drug	cocaine	9243522	Effects of repeated <b>cocaine</b> administration on the <strong>thyrotropin releasing hormone</strong> level and receptors in the rat brain.
+TRH	drug	cocaine	9243522	The effects of single and repeated administration of <b>cocaine</b> on the thyrotropin releasing hormone (<strong>TRH</strong>) level and receptors in discrete rat brain structures were evaluated.
+TRH	drug	cocaine	9243522	The effects of single and repeated administration of <b>cocaine</b> on the <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) level and receptors in discrete rat brain structures were evaluated.
+TRH	drug	cocaine	9243522	A radioimmunoassay (RIA) study showed that a single dose of <b>cocaine</b> increased the <strong>TRH</strong> level in the striatum by 68%, but had no significant effect on the peptide content in the nucleus accumbens, hippocampus, amygdala, septum, hypothalamus, frontal and prefrontal cortex at 45 min after the drug injection.
+TRH	drug	cocaine	9243522	Repeated administration of <b>cocaine</b> increased the <strong>TRH</strong> level in the striatum by 89% at 45 min, and in the hippocampus by 26% at 72 h after the last dose.
+TRH	drug	cocaine	9243522	In vitro <b>cocaine</b> (10( 6) 10( 4) M) inhibited the K(+) stimulated release in a concentration dependent manner, but had no effect on the basal release of <strong>TRH</strong> from the striatum and nucleus accumbens of naive rats.
+TRH	drug	cocaine	9243522	Acute <b>cocaine</b> decreased the Bmax of <strong>TRH</strong> receptors in the striatum, but had no effect on the density and affinity of <strong>TRH</strong> receptors in other brain regions.
+TRH	drug	cocaine	9243522	Repeated administration of <b>cocaine</b> evoked a long lasting decrease in the Bmax of <strong>TRH</strong> receptors in the striatum (by c. 30%), whereas an increase in that parameter was observed in the frontal cortex.
+TRH	drug	cocaine	9243522	The Bmax and affinity of <strong>TRH</strong> receptors following repeated <b>cocaine</b> remained unchanged in the nucleus accumbens.
+TRH	drug	cocaine	9243522	The results obtained indicate that <b>cocaine</b> affects the <strong>TRH</strong> system mainly in the striatum, and to a lesser extent in the nucleus accumbens, cortex and hippocampus.
+TRH	drug	amphetamine	9243522	Furthermore, the above changes do not resemble those induced by <b>amphetamine</b>, which points to certain differences in adaptation of the <strong>TRH</strong> neuronal system to these psychostimulants.
+TRH	drug	cocaine	9243522	On the other hand, the increase in the hippocampal <strong>TRH</strong> level during both chronic <b>cocaine</b> and morphine withdrawal is a common feature of the mechanism of dependence on these drugs.
+TRH	drug	opioid	9243522	On the other hand, the increase in the hippocampal <strong>TRH</strong> level during both chronic cocaine and <b>morphine</b> withdrawal is a common feature of the mechanism of dependence on these drugs.
+TRH	addiction	dependence	9243522	On the other hand, the increase in the hippocampal <strong>TRH</strong> level during both chronic cocaine and morphine withdrawal is a common feature of the mechanism of <b>dependence</b> on these drugs.
+TRH	addiction	withdrawal	9243522	On the other hand, the increase in the hippocampal <strong>TRH</strong> level during both chronic cocaine and morphine <b>withdrawal</b> is a common feature of the mechanism of dependence on these drugs.
+TRH	drug	alcohol	9211435	On different days <b>alcoholics</b> were tested with <strong>TRH</strong> to evaluate possible alterations in the PRL pituitary reserve.
+TRH	drug	alcohol	8949950	Contrary to expectations, both PTU and <strong>TRH</strong> administration attenuated the transient rise in plasma T4 levels at postnatal days 10 16 in LS mice and in both instances this was associated with decreased CNS <b>ethanol</b> sensitivity (sleep time and hypothermia) in adults.
+TRH	drug	alcohol	8949950	However, the observation that neonatal administration of both <strong>TRH</strong> and PTU blunted the postnatal rise in thyroid levels in LS mice, yet both treatments resulted in a decrease in adult <b>ethanol</b> sensitivity in LS mice, indicates that the relationship between postnatal thyroid development and CNS <b>ethanol</b> sensitivity is more complex than originally hypothesized.
+TRH	addiction	withdrawal	8874872	Opiate <b>withdrawal</b> increases <strong>ProTRH</strong> gene expression in the ventrolateral column of the midbrain periaqueductal gray.
+TRH	drug	alcohol	8874872	We report a nearly 5 fold increase in <strong>proTRH</strong> gene expression in neurons of the ventrolateral column of the PAG following <b>naltrexone</b> precipitated morphine withdrawal.
+TRH	drug	opioid	8874872	We report a nearly 5 fold increase in <strong>proTRH</strong> gene expression in neurons of the ventrolateral column of the PAG following naltrexone precipitated <b>morphine</b> withdrawal.
+TRH	addiction	withdrawal	8874872	We report a nearly 5 fold increase in <strong>proTRH</strong> gene expression in neurons of the ventrolateral column of the PAG following naltrexone precipitated morphine <b>withdrawal</b>.
+TRH	addiction	withdrawal	8874872	These findings indicate that <strong>proTRH</strong> derived peptides synthesized in neurons of the ventrolateral PAG may function as modifiers of opiate <b>withdrawal</b> responses.
+TRH	addiction	dependence	8819143	Furthermore, systemic administration of thyrotropin releasing hormone (<strong>TRH</strong>) inhibits the development of opiate <b>dependence</b> in rats.
+TRH	addiction	dependence	8819143	Furthermore, systemic administration of <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) inhibits the development of opiate <b>dependence</b> in rats.
+TRH	drug	opioid	8819143	To elucidate the link between <strong>TRH</strong> and opiate withdrawal, we examined the regulation of ppTRH mRNA in the central gray of rats made dependent on <b>morphine</b>, and during opiate withdrawal, using quantitative in situ hybridization.
+TRH	addiction	withdrawal	8819143	To elucidate the link between <strong>TRH</strong> and opiate <b>withdrawal</b>, we examined the regulation of ppTRH mRNA in the central gray of rats made dependent on morphine, and during opiate <b>withdrawal</b>, using quantitative in situ hybridization.
+TRH	drug	opioid	8819143	These findings support a role for <strong>TRH</strong> or other ppTRH derived peptides in the central gray during <b>morphine</b> withdrawal.
+TRH	addiction	withdrawal	8819143	These findings support a role for <strong>TRH</strong> or other ppTRH derived peptides in the central gray during morphine <b>withdrawal</b>.
+TRH	drug	alcohol	8800390	Dose response studies with <strong>thyrotropin releasing hormone</strong>: evidence for differential pituitary responses in men with major depression, <b>alcoholism</b>, or no psychopathology.
+TRH	drug	alcohol	8800390	A reduced thyrotropin (TSH) response to thyrotropin releasing hormone (<strong>TRH</strong>) has been reported in both <b>alcoholic</b> and depressed men.
+TRH	drug	alcohol	8800390	A reduced thyrotropin (TSH) response to <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) has been reported in both <b>alcoholic</b> and depressed men.
+TRH	drug	alcohol	8800390	To discern whether the pathophysiological basis of a reduced TSH response is similar in these two disorders, the present study compares the dose response patterns of TSH and prolactin (PRL) to <strong>TRH</strong> in depressed, <b>alcoholic</b>, and control men.
+TRH	drug	alcohol	8800390	Four doses of <strong>TRH</strong> (25, 100, 500, and 800 micrograms) were given at several day intervals to 6 men with major depression, 8 men with <b>alcohol</b> dependence, and 7 control men.
+TRH	addiction	dependence	8800390	Four doses of <strong>TRH</strong> (25, 100, 500, and 800 micrograms) were given at several day intervals to 6 men with major depression, 8 men with alcohol <b>dependence</b>, and 7 control men.
+TRH	drug	alcohol	8800390	Examination of the pattern of <strong>TRH</strong> induced TSH and PRL response revealed differences for each paired group comparison: depressed versus control, depressed versus <b>alcoholic</b>, and <b>alcoholic</b> versus control.
+TRH	drug	alcohol	8800390	Compared with controls, depressed men had low TSH and low PRL responses to <strong>TRH</strong>, whereas <b>alcoholic</b> men had low TSH responses and normal PRL responses.
+TRH	drug	alcohol	8800390	These findings suggest that the pathophysiological basis of a reduced TSH response to <strong>TRH</strong> is different in <b>alcoholism</b>, compared with depression.
+TRH	drug	opioid	8585307	[The modulating effect of the <strong>thyrotropin releasing hormone</strong> on genetically induced mechanisms of <b>morphine</b> sensitivity].
+TRH	drug	opioid	8585307	The influence of thyrotropin releasing hormone (<strong>TRH</strong>) on <b>morphine</b> induced analgesic and reinforced responses was studied in two inbred strains of rats, Fischer 344 (F344) and Wistar Albino Glaxo/GSto (WAG).
+TRH	drug	opioid	8585307	The influence of <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) on <b>morphine</b> induced analgesic and reinforced responses was studied in two inbred strains of rats, Fischer 344 (F344) and Wistar Albino Glaxo/GSto (WAG).
+TRH	drug	opioid	8585307	Administration of <strong>TRH</strong> in combination with <b>morphine</b> significantly stronger potentiated the effect of the latter in WAG than in F344 rats.
+TRH	drug	alcohol	8554651	The <strong>thyrotropin releasing hormone</strong> stimulation test in <b>alcoholism</b>.
+TRH	drug	alcohol	8554651	The mechanism for a blunted thyroid stimulating hormone (TSH) response to thyrotropin releasing hormone (<strong>TRH</strong>) in <b>alcoholics</b> is not known.
+TRH	drug	alcohol	8554651	The mechanism for a blunted thyroid stimulating hormone (TSH) response to <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) in <b>alcoholics</b> is not known.
+TRH	drug	alcohol	8554651	We performed a combined <strong>TRH</strong> and gonadoliberin stimulation test on three well defined groups of nondepressed <b>alcoholic</b> men.
+TRH	addiction	withdrawal	8554651	We conclude that <strong>TRH</strong> stimulation test blunting appears to be related to factors operating in the <b>withdrawal</b> state and improves with continued abstinence.
+TRH	drug	opioid	8162104	In experiments on different species of animals respiratory stimulating effects of <b>naloxone</b>, <strong>TRH</strong> and its analogue RGH 2202 during respiratory rhythmogenesis disturbances, evoked by hyperventilation of lungs, bleeding and intoxication with cyanides or opiates, were investigated.
+TRH	addiction	intoxication	8162104	In experiments on different species of animals respiratory stimulating effects of naloxone, <strong>TRH</strong> and its analogue RGH 2202 during respiratory rhythmogenesis disturbances, evoked by hyperventilation of lungs, bleeding and <b>intoxication</b> with cyanides or opiates, were investigated.
+TRH	drug	cocaine	8436966	Clinical and preclinical evidence supports a possible role for thyrotropin releasing hormone (<strong>TRH</strong>) in <b>cocaine</b> action.
+TRH	drug	cocaine	8436966	Clinical and preclinical evidence supports a possible role for <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) in <b>cocaine</b> action.
+TRH	drug	cocaine	8436966	However, the interaction between <b>cocaine</b> and <strong>TRH</strong> has not been directly examined.
+TRH	drug	cocaine	8436966	These studies support the hypothesis that <strong>TRH</strong> or other ppTRH derived peptides are involved in <b>cocaine</b> action, especially in the extrahypothalamic regions of the amygdala and hippocampus.
+TRH	drug	alcohol	1335721	The clinical significance of the <strong>thyrotropin releasing hormone</strong> test in <b>alcoholic</b> men.
+TRH	drug	alcohol	1335721	Sixty six <b>alcoholic</b> men who had been abstinent from <b>alcohol</b> for at least four weeks were assessed clinically and then investigated in terms of Thyroid Stimulating Hormone (TSH) and prolactin responses to a Thyrotropin Releasing Hormone (<strong>TRH</strong>) challenge.
+TRH	drug	alcohol	1335721	Sixty six <b>alcoholic</b> men who had been abstinent from <b>alcohol</b> for at least four weeks were assessed clinically and then investigated in terms of Thyroid Stimulating Hormone (TSH) and prolactin responses to a <strong>Thyrotropin Releasing Hormone</strong> (<strong>TRH</strong>) challenge.
+TRH	drug	alcohol	1467129	The TSH and PRL responses after the administration of 50 or 200 micrograms <strong>TRH</strong> were higher in <b>alcoholics</b> than in controls, while a blunted response is known to occur in depression.
+TRH	drug	opioid	1797554	The effect of treatment with thyrotropin releasing hormone (<strong>TRH</strong>) or <b>naloxone</b> on the neurologic impairment after spinal cord injury was studied in rats with the severest neurologic impairment (complete paraplegia, no withdrawal response upon tail pinching, and urinary incontinence) 24 h and 7 days after injury.
+TRH	addiction	withdrawal	1797554	The effect of treatment with thyrotropin releasing hormone (<strong>TRH</strong>) or naloxone on the neurologic impairment after spinal cord injury was studied in rats with the severest neurologic impairment (complete paraplegia, no <b>withdrawal</b> response upon tail pinching, and urinary incontinence) 24 h and 7 days after injury.
+TRH	drug	opioid	1797554	The effect of treatment with <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) or <b>naloxone</b> on the neurologic impairment after spinal cord injury was studied in rats with the severest neurologic impairment (complete paraplegia, no withdrawal response upon tail pinching, and urinary incontinence) 24 h and 7 days after injury.
+TRH	addiction	withdrawal	1797554	The effect of treatment with <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) or naloxone on the neurologic impairment after spinal cord injury was studied in rats with the severest neurologic impairment (complete paraplegia, no <b>withdrawal</b> response upon tail pinching, and urinary incontinence) 24 h and 7 days after injury.
+TRH	drug	opioid	1797554	These results indicate that <strong>TRH</strong> but not <b>naloxone</b> treatment starting 24 h and as late as 7 days after injury is effective in rats with the severest neurologic impairment following spinal cord injury.
+TRH	drug	opioid	1797554	Thus, it is suggested that the duration of the effectiveness of late treatment with <strong>TRH</strong> on the neurologic impairment in rats with spinal cord injury is more than 1 week, while the duration with <b>naloxone</b> is less than 24 h.
+TRH	drug	alcohol	1827638	Serum thyrotropin responses to <strong>thyrotropin releasing hormone</strong> in <b>alcohol</b> dependent patients with and without depression.
+TRH	drug	opioid	2172939	Spinal cord <strong>thyrotropin releasing hormone</strong> receptors of <b>morphine</b> tolerant dependent and abstinent rats.
+TRH	drug	opioid	2172939	The effect of chronic administration of <b>morphine</b> and its withdrawal on the binding of 3H [3 MeHis2]<strong>thyrotropin releasing hormone</strong> (3H MeTRH) to membranes of the spinal cord of the rat was determined.
+TRH	addiction	withdrawal	2172939	The effect of chronic administration of morphine and its <b>withdrawal</b> on the binding of 3H [3 MeHis2]<strong>thyrotropin releasing hormone</strong> (3H MeTRH) to membranes of the spinal cord of the rat was determined.
+TRH	drug	opioid	2172939	Previous studies from this laboratory indicate that <strong>TRH</strong> can inhibit <b>morphine</b> tolerance dependence and abstinence processes without modifying brain <strong>TRH</strong> receptors.
+TRH	addiction	dependence	2172939	Previous studies from this laboratory indicate that <strong>TRH</strong> can inhibit morphine tolerance <b>dependence</b> and abstinence processes without modifying brain <strong>TRH</strong> receptors.
+TRH	drug	opioid	2172939	Together with the present results, it appears that the inhibitory effect of <strong>TRH</strong> on <b>morphine</b> tolerance dependence and abstinence is probably not mediated via central <strong>TRH</strong> receptors but may be due to its interaction with other neurotransmitter systems.
+TRH	addiction	dependence	2172939	Together with the present results, it appears that the inhibitory effect of <strong>TRH</strong> on morphine tolerance <b>dependence</b> and abstinence is probably not mediated via central <strong>TRH</strong> receptors but may be due to its interaction with other neurotransmitter systems.
+TRH	drug	opioid	2516632	The binding of 3H (3 MeHis2) <strong>thyrotropin releasing hormone</strong> to brain and pituitary membranes of <b>morphine</b> tolerant dependent and abstinent rats.
+TRH	drug	opioid	2516632	The effect of chronic administration of <b>morphine</b> and subsequent withdrawal on brain and pituitary receptors for thyrotropin releasing hormone (<strong>TRH</strong>) was investigated in Sprague Dawley rats.
+TRH	addiction	withdrawal	2516632	The effect of chronic administration of morphine and subsequent <b>withdrawal</b> on brain and pituitary receptors for thyrotropin releasing hormone (<strong>TRH</strong>) was investigated in Sprague Dawley rats.
+TRH	drug	opioid	2516632	The effect of chronic administration of <b>morphine</b> and subsequent withdrawal on brain and pituitary receptors for <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) was investigated in Sprague Dawley rats.
+TRH	addiction	withdrawal	2516632	The effect of chronic administration of morphine and subsequent <b>withdrawal</b> on brain and pituitary receptors for <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) was investigated in Sprague Dawley rats.
+TRH	drug	amphetamine	2539202	Reduction of rat striatal <strong>thyrotropin releasing hormone</strong> receptors produced by repeated <b>methamphetamine</b> administration.
+TRH	addiction	sensitization	2539202	These results suggest that repeated MAP administration caused lasting dysfunction in the brain <strong>TRH</strong> system, which may be implicated in the behavioral <b>sensitization</b>.
+TRH	drug	alcohol	2543997	The results of the <strong>TRH</strong> test and the DST point to similar endocrinological patterns in <b>alcoholics</b> as in depressive patients and thus support the hypothesis of a link between <b>alcoholism</b> and depression.
+TRH	drug	alcohol	2839819	<strong>TRH</strong> and naloxone influence on the clinical hormonal manifestations of the <b>alcohol</b> withdrawal syndrome (AWS) was studied.
+TRH	drug	opioid	2839819	<strong>TRH</strong> and <b>naloxone</b> influence on the clinical hormonal manifestations of the alcohol withdrawal syndrome (AWS) was studied.
+TRH	addiction	withdrawal	2839819	<strong>TRH</strong> and naloxone influence on the clinical hormonal manifestations of the alcohol <b>withdrawal</b> syndrome (AWS) was studied.
+TRH	drug	opioid	2839819	It should be noted that symptoms like depression, sleep disturbances and headaches happened to be more sensitive to <strong>TRH</strong> while sweating is more sensitive to <b>naloxone</b>.
+TRH	drug	alcohol	3620000	Basal TSH levels and TSH responses to cold were as a rule decreased in the course of <b>ethanol</b> intake and abstinence, whereas the <strong>TRH</strong> induced TSH elevation became more consistent than before <b>ethanol</b>.
+TRH	drug	alcohol	3107289	In a double blind diagnostic study of the reserve thyrotropic function of the hypophysis, the authors have investigated the effect of the thyrotropic releasing hormone (<strong>TRH</strong>) versus placebo on the clinical manifestations of the <b>alcohol</b> abstinence syndrome in 60 patients with stage 2 chronic <b>alcoholism</b>.
+TRH	drug	alcohol	3107289	<strong>TRH</strong> has a positive effect on some psychopathological and somatovegetative manifestations of <b>alcohol</b> abstinence.
+TRH	drug	alcohol	3107289	It is suggested that the use of <strong>TRH</strong>, in addition to its therapeutic and diagnostic value, will help to better study at the clinical level the role of the peptidergic system in the pathogenesis of <b>alcohol</b> induced disorders.
+TRH	drug	amphetamine	3774630	Org 8282 did not affect the reserpine induced hypothermia, hypoactivity and ptosis, did not modify the apomorphine induced hypothermia and the <strong>TRH</strong> induced hyperthermia in mice, did not change the motor stimulation and stereotypy produced by <b>amphetamine</b>.
+TRH	drug	alcohol	3092267	<strong>TRH</strong> induced thyrotropin (TSH), prolactin (PRL), and growth hormone (GH) responses were investigated together with a dexamethasone suppression test in female psychiatric inpatients with major melancholic depression (n = 21), schizophrenic disorder (n = 20), <b>alcohol</b> dependence (n = 11), and adjustment disorder with predominantly depressed mood (n = 13), as well as in 15 healthy women.
+TRH	addiction	dependence	3092267	<strong>TRH</strong> induced thyrotropin (TSH), prolactin (PRL), and growth hormone (GH) responses were investigated together with a dexamethasone suppression test in female psychiatric inpatients with major melancholic depression (n = 21), schizophrenic disorder (n = 20), alcohol <b>dependence</b> (n = 11), and adjustment disorder with predominantly depressed mood (n = 13), as well as in 15 healthy women.
+TRH	drug	cocaine	3090273	Diagnosing depression with the DST and <strong>TRH</strong> in <b>cocaine</b> and opioid abusers.
+TRH	drug	opioid	3090273	Diagnosing depression with the DST and <strong>TRH</strong> in cocaine and <b>opioid</b> abusers.
+TRH	drug	alcohol	3090273	Studies in <b>alcoholics</b> have been contradictory, but two recent studies using the DST in opiate addicts and the <strong>TRH</strong> in cocaine abusers may be relevant to clinical practice and future studies.
+TRH	drug	cocaine	3090273	Studies in alcoholics have been contradictory, but two recent studies using the DST in opiate addicts and the <strong>TRH</strong> in <b>cocaine</b> abusers may be relevant to clinical practice and future studies.
+TRH	drug	alcohol	3010391	Other CNS compounds that may play a role in <b>alcohol</b> withdrawal are prolactin, thyrotropin releasing hormone (<strong>TRH</strong>), vasopressin, cyclic 3'5' adenosine monophophate (cAMP), Delta sleep inducing peptide (DSIP), and iron.
+TRH	addiction	withdrawal	3010391	Other CNS compounds that may play a role in alcohol <b>withdrawal</b> are prolactin, thyrotropin releasing hormone (<strong>TRH</strong>), vasopressin, cyclic 3'5' adenosine monophophate (cAMP), Delta sleep inducing peptide (DSIP), and iron.
+TRH	drug	alcohol	3010391	Other CNS compounds that may play a role in <b>alcohol</b> withdrawal are prolactin, <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), vasopressin, cyclic 3'5' adenosine monophophate (cAMP), Delta sleep inducing peptide (DSIP), and iron.
+TRH	addiction	withdrawal	3010391	Other CNS compounds that may play a role in alcohol <b>withdrawal</b> are prolactin, <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), vasopressin, cyclic 3'5' adenosine monophophate (cAMP), Delta sleep inducing peptide (DSIP), and iron.
+TRH	addiction	withdrawal	3010391	Perturbation studies with corticotropin releasing factor (CRF) and <strong>TRH</strong> (with measures of ACTH and cortisol and TSH and prolactin, respectively), may identify patients with <b>withdrawal</b> related autonomic dysfunction.
+TRH	drug	alcohol	3930250	Baseline and <strong>TRH</strong> induced changes of thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) were measured in 15 healthy control subjects and 63 psychiatric inpatients with DSM III diagnoses of major depression (n = 19), schizophrenic disorder (n = 20), <b>alcohol</b> dependence (n = 10), and adjustment disorder (n = 14); baseline and postdexamethasone cortisol (CS) were also determined 3 6 days after the <strong>TRH</strong> challenge.
+TRH	addiction	dependence	3930250	Baseline and <strong>TRH</strong> induced changes of thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) were measured in 15 healthy control subjects and 63 psychiatric inpatients with DSM III diagnoses of major depression (n = 19), schizophrenic disorder (n = 20), alcohol <b>dependence</b> (n = 10), and adjustment disorder (n = 14); baseline and postdexamethasone cortisol (CS) were also determined 3 6 days after the <strong>TRH</strong> challenge.
+TRH	drug	alcohol	3930250	Baseline TSH and PRL were lower in depression, <strong>TRH</strong> induced TSH and PRL responses were lower in the whole patient group, but most markedly in depression and <b>alcohol</b> dependence.
+TRH	addiction	dependence	3930250	Baseline TSH and PRL were lower in depression, <strong>TRH</strong> induced TSH and PRL responses were lower in the whole patient group, but most markedly in depression and alcohol <b>dependence</b>.
+TRH	drug	opioid	2996045	Comparative effects of <strong>thyrotropin releasing hormone</strong>, MK 771 and DN 1417 on <b>morphine</b> abstinence syndrome.
+TRH	drug	opioid	2996045	The effects of thyrotropin releasing hormone (<strong>TRH</strong>) were compared with two of its analogs, L N (2 oxopiperidine 6 yl carbonyl) L histidyl L thiazolidine 4 carbo xam ide (MK 771) and gamma butyrolactone 4 carboxyl histidyl prolineamide (DN 1417) on the abrupt and <b>naloxone</b> precipitated abstinence symptoms in <b>morphine</b> dependent male Swiss Wester mice.
+TRH	drug	opioid	2996045	The effects of <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) were compared with two of its analogs, L N (2 oxopiperidine 6 yl carbonyl) L histidyl L thiazolidine 4 carbo xam ide (MK 771) and gamma butyrolactone 4 carboxyl histidyl prolineamide (DN 1417) on the abrupt and <b>naloxone</b> precipitated abstinence symptoms in <b>morphine</b> dependent male Swiss Wester mice.
+TRH	drug	opioid	2996045	<strong>TRH</strong> at all doses employed prevented the hypothermia observed during abrupt withdrawal of <b>morphine</b> (pellet removal).
+TRH	addiction	withdrawal	2996045	<strong>TRH</strong> at all doses employed prevented the hypothermia observed during abrupt <b>withdrawal</b> of morphine (pellet removal).
+TRH	drug	opioid	2996045	However, both <strong>TRH</strong> analogs produced long lasting antagonism of withdrawal hypothermia in mice from which <b>morphine</b> pellets had been removed.
+TRH	addiction	withdrawal	2996045	However, both <strong>TRH</strong> analogs produced long lasting antagonism of <b>withdrawal</b> hypothermia in mice from which morphine pellets had been removed.
+TRH	drug	opioid	2996045	<strong>TRH</strong> and its analogs had no effect on the body weight loss observed during abrupt withdrawal of <b>morphine</b>.
+TRH	addiction	withdrawal	2996045	<strong>TRH</strong> and its analogs had no effect on the body weight loss observed during abrupt <b>withdrawal</b> of morphine.
+TRH	drug	opioid	2996045	Intracerebral administration of 10 micrograms <strong>TRH</strong> and its analogs inhibited the <b>naloxone</b> induced jumping response as evidenced by increases in <b>naloxone</b> ED50 values to elicit this response.
+TRH	addiction	withdrawal	2996045	It is concluded that <strong>TRH</strong> and its analogs may be useful in combating some of the <b>withdrawal</b> symptoms in opiate dependent subjects.
+TRH	drug	benzodiazepine	2985852	On the other hand, radiolabeled ligand binding to CNS receptors in the <b>benzodiazepine</b> (BDZ) , muscarinic cholinergic (mACh) , methionine enkephalin (ENK)  and thyrotropin releasing hormone (<strong>TRH</strong>) RRA systems was not inhibited even by the addition of HOPA up to 100 microM.
+TRH	drug	benzodiazepine	2985852	On the other hand, radiolabeled ligand binding to CNS receptors in the <b>benzodiazepine</b> (BDZ) , muscarinic cholinergic (mACh) , methionine enkephalin (ENK)  and <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) RRA systems was not inhibited even by the addition of HOPA up to 100 microM.
+TRH	addiction	reward	2417253	Studies employing conditioned <b>operant</b> behavior of squirrel monkeys, rabbits and pigeons have demonstrated that the neuroactive peptides thyrotropin releasing hormone (<strong>TRH</strong>), substance P (SP) and neurotensin (NT) produce marked behavioral effects under a wide range of procedures.
+TRH	addiction	reward	2417253	Studies employing conditioned <b>operant</b> behavior of squirrel monkeys, rabbits and pigeons have demonstrated that the neuroactive peptides <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), substance P (SP) and neurotensin (NT) produce marked behavioral effects under a wide range of procedures.
+TRH	drug	alcohol	2417253	The co administration of <strong>TRH</strong> with chlordiazepoxide, pentobarbital and <b>ethanol</b> potentiates the effects of these agents on punished behavior.
+TRH	drug	benzodiazepine	2417253	The co administration of <strong>TRH</strong> with <b>chlordiazepoxide</b>, pentobarbital and ethanol potentiates the effects of these agents on punished behavior.
+TRH	drug	alcohol	6437146	Fifteen healthy women and 64 female psychiatric inpatients (major depression: 17, schizophrenia: 24, <b>alcohol</b> dependence: 9, and adjustment disorder: 14 cases) without identifiable thyroid dysfunction were investigated with the <strong>TRH</strong> test under comparable circumstances.
+TRH	addiction	dependence	6437146	Fifteen healthy women and 64 female psychiatric inpatients (major depression: 17, schizophrenia: 24, alcohol <b>dependence</b>: 9, and adjustment disorder: 14 cases) without identifiable thyroid dysfunction were investigated with the <strong>TRH</strong> test under comparable circumstances.
+TRH	drug	alcohol	6437146	Women with <b>alcohol</b> dependence (in the early withdrawal period) showed significantly decreased TSH responses to <strong>TRH</strong> but only a weak tendency to lower basal TSH levels.
+TRH	addiction	dependence	6437146	Women with alcohol <b>dependence</b> (in the early withdrawal period) showed significantly decreased TSH responses to <strong>TRH</strong> but only a weak tendency to lower basal TSH levels.
+TRH	addiction	withdrawal	6437146	Women with alcohol dependence (in the early <b>withdrawal</b> period) showed significantly decreased TSH responses to <strong>TRH</strong> but only a weak tendency to lower basal TSH levels.
+TRH	drug	alcohol	6437146	The <strong>TRH</strong> test, using only 0.2 mg <strong>TRH</strong> for stimulation, seemed to be useful for identifying major depression and showed that early withdrawal from <b>alcohol</b> may be a factor to be considered in similar studies.
+TRH	addiction	withdrawal	6437146	The <strong>TRH</strong> test, using only 0.2 mg <strong>TRH</strong> for stimulation, seemed to be useful for identifying major depression and showed that early <b>withdrawal</b> from alcohol may be a factor to be considered in similar studies.
+TRH	drug	alcohol	6434573	Prolactin and thyrotropin responses to <strong>thyrotropin releasing hormone</strong> and metoclopramide in men with chronic <b>alcoholism</b>.
+TRH	drug	alcohol	6434573	Twenty five micrograms of <strong>TRH</strong>, injected iv in six <b>alcoholic</b> men during acute withdrawal, raised TSH by 1.6 +/  0.8 (SEM) microU/ml and PRL by 18 +/  7 ng/ml.
+TRH	addiction	withdrawal	6434573	Twenty five micrograms of <strong>TRH</strong>, injected iv in six alcoholic men during acute <b>withdrawal</b>, raised TSH by 1.6 +/  0.8 (SEM) microU/ml and PRL by 18 +/  7 ng/ml.
+TRH	drug	alcohol	6434573	Furthermore, <strong>TRH</strong>, injected 90 min after oral priming with metoclopramide in six additional <b>alcoholics</b>, elicited TSH and PRL increments in the acute withdrawal state which did not differ significantly from those obtained in the late withdrawal state (TSH, 3.5 +/  0.9 vs. 4.1 +/  1.2 microU/ml; PRL, 27 +/  3 vs. 24 +/  6 ng/ml).
+TRH	addiction	withdrawal	6434573	Furthermore, <strong>TRH</strong>, injected 90 min after oral priming with metoclopramide in six additional alcoholics, elicited TSH and PRL increments in the acute <b>withdrawal</b> state which did not differ significantly from those obtained in the late <b>withdrawal</b> state (TSH, 3.5 +/  0.9 vs. 4.1 +/  1.2 microU/ml; PRL, 27 +/  3 vs. 24 +/  6 ng/ml).
+TRH	drug	alcohol	6434573	These findings suggest that dopaminergic inhibition of the thyrotrophs and lactotrophs may be responsible for the blunted TSH and PRL responses to <strong>TRH</strong> during the acute withdrawal period in chronic <b>alcoholic</b> patients.
+TRH	addiction	withdrawal	6434573	These findings suggest that dopaminergic inhibition of the thyrotrophs and lactotrophs may be responsible for the blunted TSH and PRL responses to <strong>TRH</strong> during the acute <b>withdrawal</b> period in chronic alcoholic patients.
+TRH	drug	alcohol	6424482	Specificity of the DST and the <strong>TRH</strong> test for major depression in <b>alcoholics</b>.
+TRH	drug	alcohol	6424482	The authors examined dexamethasone suppression test (DST) and thyrotropin releasing hormone (<strong>TRH</strong>) test results in 32 chronic <b>alcoholics</b> without depression or hepatic disease to see if <b>alcoholism</b> alone might lead to positive test results.
+TRH	drug	alcohol	6424482	The authors examined dexamethasone suppression test (DST) and <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) test results in 32 chronic <b>alcoholics</b> without depression or hepatic disease to see if <b>alcoholism</b> alone might lead to positive test results.
+TRH	drug	alcohol	6424482	After 3 weeks of sobriety there were no DST abnormalities, but blunted <strong>TRH</strong> test results were observed in eight of the 32 <b>alcoholics</b>.
+TRH	drug	alcohol	6424482	More of the 15 patients also tested during <b>alcohol</b> withdrawal than of the 20 normal subjects or the 32 <b>alcoholics</b> without <b>alcohol</b> withdrawal had DST and <strong>TRH</strong> test abnormalities.
+TRH	addiction	withdrawal	6424482	More of the 15 patients also tested during alcohol <b>withdrawal</b> than of the 20 normal subjects or the 32 alcoholics without alcohol <b>withdrawal</b> had DST and <strong>TRH</strong> test abnormalities.
+TRH	drug	alcohol	6424482	When performed after 3 weeks of sobriety, the DST but not the <strong>TRH</strong> test has potential as a specific laboratory adjunct in the diagnosis of depression in <b>alcoholics</b>.
+TRH	addiction	aversion	6422515	Central administration of <strong>thyrotropin releasing hormone</strong> and histidyl proline diketopiperazine disrupts the acquisition of a food rewarded task by a non <b>aversive</b> action.
+TRH	addiction	reward	6422515	The effects of thyrotropin releasing hormone (<strong>TRH</strong>) and its metabolites on <b>operant</b> behaviour have rarely been explored.
+TRH	addiction	reward	6422515	The effects of <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) and its metabolites on <b>operant</b> behaviour have rarely been explored.
+TRH	drug	opioid	6307193	Behavioral studies of shaking behavior induced by <strong>thyrotropin releasing hormone</strong> and <b>morphine</b> withdrawal in rats.
+TRH	addiction	withdrawal	6307193	Behavioral studies of shaking behavior induced by <strong>thyrotropin releasing hormone</strong> and morphine <b>withdrawal</b> in rats.
+TRH	drug	opioid	6307193	The <b>morphine</b> withdrawal body shaking was antagonized by pretreatment with <strong>TRH</strong> in the doses (10, 20 mg/kg, i.p.)
+TRH	addiction	withdrawal	6307193	The morphine <b>withdrawal</b> body shaking was antagonized by pretreatment with <strong>TRH</strong> in the doses (10, 20 mg/kg, i.p.)
+TRH	drug	opioid	6307193	The present results imply that <strong>TRH</strong> induced body shaking is not associated with the increased activity of serotonergic, cholinergic and enkephalinergic neurons in the brain, and also its mechanisms seem to be different from that of <b>morphine</b> withdrawal body shaking.
+TRH	addiction	withdrawal	6307193	The present results imply that <strong>TRH</strong> induced body shaking is not associated with the increased activity of serotonergic, cholinergic and enkephalinergic neurons in the brain, and also its mechanisms seem to be different from that of morphine <b>withdrawal</b> body shaking.
+TRH	addiction	dependence	6141121	<strong>Thyrotropin releasing hormone</strong> and related compounds appear to (a) antagonize hypothermia, respiratory depression, locomotor depression and catalepsy but not the analgesia induced by opiates, (b) inhibit the development of tolerance to the analgesic effect but not to the hypothermic effect of opiates, (c) inhibit the development of physical <b>dependence</b> on opiates as evidenced by the inhibition of development of certain withdrawal symptoms, and (d) suppress the abstinence syndrome in opiate dependent rodents.
+TRH	addiction	withdrawal	6141121	<strong>Thyrotropin releasing hormone</strong> and related compounds appear to (a) antagonize hypothermia, respiratory depression, locomotor depression and catalepsy but not the analgesia induced by opiates, (b) inhibit the development of tolerance to the analgesic effect but not to the hypothermic effect of opiates, (c) inhibit the development of physical dependence on opiates as evidenced by the inhibition of development of certain <b>withdrawal</b> symptoms, and (d) suppress the abstinence syndrome in opiate dependent rodents.
+TRH	drug	alcohol	7197560	It has been shown that <b>alcohol</b> motivated Wistar female rats after 10 days of repeated <b>ethanol</b> administration have a decreased cold  or <strong>TRH</strong> stimulated TSH level in the blood serum under physical dependence and abstinence.
+TRH	addiction	dependence	7197560	It has been shown that alcohol motivated Wistar female rats after 10 days of repeated ethanol administration have a decreased cold  or <strong>TRH</strong> stimulated TSH level in the blood serum under physical <b>dependence</b> and abstinence.
+TRH	drug	alcohol	7197560	It is suggested that repeated <b>ethanol</b> administration causes hypofunction of both hypothalamic <strong>TRH</strong> neurons and anterior pituitary thyrotropic cells.
+TRH	addiction	withdrawal	6783443	RX 336 M (7,8 dihydro 5',6' dimethylcyclohex 5' eno 1',2',8',14 codeinone) and four other chemically diverse agents  AG 3 5 (1 [2 hydroxyphenyl] 4 [3 nitrophenyl] 1,2,3,6 tetrahydropyrimidine 2 one), Sgd 8473 (alpha [4 chlorobenzylideneamino) oxy] isobutyric acid), thyrotropin releasing hormone (<strong>TRH</strong>), and sodium valproate  each induce signs of <b>withdrawal</b>, most notably 'wet dog' shaking, after acute i.p.
+TRH	addiction	withdrawal	6783443	RX 336 M (7,8 dihydro 5',6' dimethylcyclohex 5' eno 1',2',8',14 codeinone) and four other chemically diverse agents  AG 3 5 (1 [2 hydroxyphenyl] 4 [3 nitrophenyl] 1,2,3,6 tetrahydropyrimidine 2 one), Sgd 8473 (alpha [4 chlorobenzylideneamino) oxy] isobutyric acid), <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), and sodium valproate  each induce signs of <b>withdrawal</b>, most notably 'wet dog' shaking, after acute i.p.
+TRH	drug	opioid	6260535	Pharmacological aspects of shaking behavior produced by <strong>TRH</strong>, AG 3 5, and <b>morphine</b> withdrawal.
+TRH	addiction	withdrawal	6260535	Pharmacological aspects of shaking behavior produced by <strong>TRH</strong>, AG 3 5, and morphine <b>withdrawal</b>.
+TRH	drug	opioid	6260535	<strong>Thyrotropin releasing hormone</strong>, injected centrally at submicrogram doses, produced in nondependent, barbiturate anesthetized animals, shaking behavior identical in its general features to that of <b>morphine</b> withdrawal.
+TRH	addiction	withdrawal	6260535	<strong>Thyrotropin releasing hormone</strong>, injected centrally at submicrogram doses, produced in nondependent, barbiturate anesthetized animals, shaking behavior identical in its general features to that of morphine <b>withdrawal</b>.
+TRH	drug	alcohol	6799971	[Endocrinal changes observed by <strong>TRH</strong> (thyrotropin releasing hormone) test in <b>alcohol</b> withdrawal syndrome (author's transl)].
+TRH	addiction	withdrawal	6799971	[Endocrinal changes observed by <strong>TRH</strong> (thyrotropin releasing hormone) test in alcohol <b>withdrawal</b> syndrome (author's transl)].
+TRH	drug	alcohol	6799971	[Endocrinal changes observed by <strong>TRH</strong> (<strong>thyrotropin releasing hormone</strong>) test in <b>alcohol</b> withdrawal syndrome (author's transl)].
+TRH	addiction	withdrawal	6799971	[Endocrinal changes observed by <strong>TRH</strong> (<strong>thyrotropin releasing hormone</strong>) test in alcohol <b>withdrawal</b> syndrome (author's transl)].
+TRH	drug	alcohol	6792942	Differential effects of <strong>TRH</strong>, amphetamine, naloxone, and fenmetozole on <b>ethanol</b> actions: attenuation of the effects of punishment and impairment of aerial righting reflex.
+TRH	drug	amphetamine	6792942	Differential effects of <strong>TRH</strong>, <b>amphetamine</b>, naloxone, and fenmetozole on ethanol actions: attenuation of the effects of punishment and impairment of aerial righting reflex.
+TRH	drug	opioid	6792942	Differential effects of <strong>TRH</strong>, amphetamine, <b>naloxone</b>, and fenmetozole on ethanol actions: attenuation of the effects of punishment and impairment of aerial righting reflex.
+TRH	addiction	addiction	6792942	Differential effects of <strong>TRH</strong>, amphetamine, naloxone, and fenmetozole on ethanol actions: attenuation of the effects of <b>punishment</b> and impairment of aerial righting reflex.
+TRH	drug	alcohol	6792942	The effects of four putative <b>ethanol</b> antagonists [thyrotropin releasing hormone (<strong>TRH</strong>), naloxone, d amphetamine, and fenmetozole] on two distinct behavioral actions of <b>ethanol</b> were compared.
+TRH	drug	amphetamine	6792942	The effects of four putative ethanol antagonists [thyrotropin releasing hormone (<strong>TRH</strong>), naloxone, d <b>amphetamine</b>, and fenmetozole] on two distinct behavioral actions of ethanol were compared.
+TRH	drug	opioid	6792942	The effects of four putative ethanol antagonists [thyrotropin releasing hormone (<strong>TRH</strong>), <b>naloxone</b>, d amphetamine, and fenmetozole] on two distinct behavioral actions of ethanol were compared.
+TRH	drug	alcohol	6792942	The effects of four putative <b>ethanol</b> antagonists [<strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), naloxone, d amphetamine, and fenmetozole] on two distinct behavioral actions of <b>ethanol</b> were compared.
+TRH	drug	amphetamine	6792942	The effects of four putative ethanol antagonists [<strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), naloxone, d <b>amphetamine</b>, and fenmetozole] on two distinct behavioral actions of ethanol were compared.
+TRH	drug	opioid	6792942	The effects of four putative ethanol antagonists [<strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>), <b>naloxone</b>, d amphetamine, and fenmetozole] on two distinct behavioral actions of ethanol were compared.
+TRH	drug	alcohol	6792942	<strong>TRH</strong> (20 40 mg/kg) reduced <b>ethanol</b> induced impairment of the aerial righting reflex (ARR) but enhanced the <b>ethanol</b> induced increase in punished drinking (anticonflict effect).
+TRH	drug	alcohol	6267562	Simultaneous treatment with <b>ethanol</b> (4.0 g/kg, IP) and thyrotropin releasing hormone (<strong>TRH</strong>, 3.0 30 micrograms, IC) caused less impairment of this measure than <b>ethanol</b> alone.
+TRH	drug	alcohol	6267562	Simultaneous treatment with <b>ethanol</b> (4.0 g/kg, IP) and <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>, 3.0 30 micrograms, IC) caused less impairment of this measure than <b>ethanol</b> alone.
+TRH	drug	alcohol	6267562	Unexpectedly, <strong>TRH</strong> (20 and 40 mg/kg, IP) potentiated the action of <b>ethanol</b> by increasing punished licking in water deprived rats, rather than antagonizing this acute action of <b>ethanol</b>.
+TRH	drug	alcohol	6267562	<strong>TRH</strong> (10 100 micrograms, IC, or 1 40 mg/kg, IV) and neurotensin (10 100 micrograms, IC) had no effect on these <b>ethanol</b> withdrawal signs.
+TRH	addiction	withdrawal	6267562	<strong>TRH</strong> (10 100 micrograms, IC, or 1 40 mg/kg, IV) and neurotensin (10 100 micrograms, IC) had no effect on these ethanol <b>withdrawal</b> signs.
+TRH	drug	alcohol	6267562	Because <strong>TRH</strong>, neurotensin, bombesin and beta endorphin do not alter all actions of <b>ethanol</b> in the same way, an interaction of <b>ethanol</b> with many functionally independent neuronal circuits is suggested.
+TRH	drug	alcohol	6123410	The initial sensitivity of an animal to <b>ethanol</b> can also be affected by peptides, notably thyrotropin releasing hormone (thyroliberin, <strong>TRH</strong>).
+TRH	drug	alcohol	6123410	The initial sensitivity of an animal to <b>ethanol</b> can also be affected by peptides, notably <strong>thyrotropin releasing hormone</strong> (thyroliberin, <strong>TRH</strong>).
+TRH	drug	alcohol	6123410	<strong>TRH</strong> antagonizes many of the initial responses to <b>ethanol</b>, perhaps by non specific means.
+TRH	drug	benzodiazepine	6768086	Drugs that failed to show dose related generalization included phenethylamine, <strong>thyrotropin releasing hormone</strong>, imipramine, nortriptyline, amitriptyline, desipramine, mianserin, <b>chlordiazepoxide</b>, <b>diazepam</b>, scopolamine, phenobarbital, and morphine.
+TRH	drug	opioid	6768086	Drugs that failed to show dose related generalization included phenethylamine, <strong>thyrotropin releasing hormone</strong>, imipramine, nortriptyline, amitriptyline, desipramine, mianserin, chlordiazepoxide, diazepam, scopolamine, phenobarbital, and <b>morphine</b>.
+TRH	drug	alcohol	7017756	<strong>TRH</strong> induced secretion of prolactin is increased during <b>alcohol</b> intoxication and inhibited during hangover and withdrawal.
+TRH	addiction	intoxication	7017756	<strong>TRH</strong> induced secretion of prolactin is increased during alcohol <b>intoxication</b> and inhibited during hangover and withdrawal.
+TRH	addiction	withdrawal	7017756	<strong>TRH</strong> induced secretion of prolactin is increased during alcohol intoxication and inhibited during hangover and <b>withdrawal</b>.
+TRH	drug	opioid	6776564	The effects of <strong>thyrotropin releasing hormone</strong> on the central nervous system responses to chronic <b>morphine</b> administration.
+TRH	drug	opioid	6776564	The effects of thyrotropin releasing hormone (<strong>TRH</strong>) on abrupt and <b>naloxone</b> precipitated abstinence symptoms were determined in male Swiss Webster mice rendered dependent on <b>morphine</b> by SC implantation of <b>morphine</b> pellets.
+TRH	drug	opioid	6776564	The effects of <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) on abrupt and <b>naloxone</b> precipitated abstinence symptoms were determined in male Swiss Webster mice rendered dependent on <b>morphine</b> by SC implantation of <b>morphine</b> pellets.
+TRH	drug	opioid	6776564	Intracerebral (IC) administration of <strong>TRH</strong> inhibited the hypothermic response observed during abrupt (removal of <b>morphine</b> pellets) and <b>naloxone</b> (0.1 mg/kg SC) precipitated withdrawal.
+TRH	addiction	withdrawal	6776564	Intracerebral (IC) administration of <strong>TRH</strong> inhibited the hypothermic response observed during abrupt (removal of morphine pellets) and naloxone (0.1 mg/kg SC) precipitated <b>withdrawal</b>.
+TRH	drug	opioid	6776564	IC injection of <strong>TRH</strong> also inhibited the <b>naloxone</b> precipitated withdrawal jumping response as evidenced by increases in the dose of <b>naloxone</b> required to elicit the response.
+TRH	addiction	withdrawal	6776564	IC injection of <strong>TRH</strong> also inhibited the naloxone precipitated <b>withdrawal</b> jumping response as evidenced by increases in the dose of naloxone required to elicit the response.
+TRH	drug	opioid	6776564	The effects of <strong>TRH</strong> on the development of <b>morphine</b> dependence were also investigated.
+TRH	addiction	dependence	6776564	The effects of <strong>TRH</strong> on the development of morphine <b>dependence</b> were also investigated.
+TRH	drug	opioid	6776564	A single SC injection of <strong>TRH</strong> (4 16 mg/kg) did not modify development of <b>morphine</b> dependence.
+TRH	addiction	dependence	6776564	A single SC injection of <strong>TRH</strong> (4 16 mg/kg) did not modify development of morphine <b>dependence</b>.
+TRH	drug	opioid	6776564	Administration of <strong>TRH</strong> prior to and during <b>morphine</b> pellet implantation inhibited the development of dependence as evidenced by inhibition in the development of abrupt and <b>naloxone</b> induced withdrawal hypothermia.
+TRH	addiction	dependence	6776564	Administration of <strong>TRH</strong> prior to and during morphine pellet implantation inhibited the development of <b>dependence</b> as evidenced by inhibition in the development of abrupt and naloxone induced withdrawal hypothermia.
+TRH	addiction	withdrawal	6776564	Administration of <strong>TRH</strong> prior to and during morphine pellet implantation inhibited the development of dependence as evidenced by inhibition in the development of abrupt and naloxone induced <b>withdrawal</b> hypothermia.
+TRH	drug	opioid	6776564	Even though the hypothermic response was blocked, multiple SC administration of <strong>TRH</strong> failed to modify <b>naloxone</b> induced stereotyped jumping response.
+TRH	drug	opioid	6776564	These studies indicate that <strong>TRH</strong> administration can modify central nervous system responses to chronic <b>morphine</b> treatment and that separate sites may initiate withdrawal jumping behavior and affect temperature regulation during abrupt and antagonist induced abstinence.
+TRH	addiction	withdrawal	6776564	These studies indicate that <strong>TRH</strong> administration can modify central nervous system responses to chronic morphine treatment and that separate sites may initiate <b>withdrawal</b> jumping behavior and affect temperature regulation during abrupt and antagonist induced abstinence.
+TRH	drug	opioid	6769068	Growth hormone response to <strong>thyrotropin releasing hormone</strong> and gonadotropin releasing hormone stimulation in <b>heroin</b> addicts.
+TRH	drug	opioid	6769068	Since the response of the pituitary to nonspecific stimuli is considered an expression of hypothalamic dysfunction, indicating a disconnection between the central nervous system and the anterior pituitary, we thought it worthwhile to study the GH response to stimulation with thyrotropin releasing hormone (<strong>TRH</strong>) or gonadotropin releasing hormone (GnRH) in <b>heroin</b> addicts.
+TRH	drug	opioid	6769068	Since the response of the pituitary to nonspecific stimuli is considered an expression of hypothalamic dysfunction, indicating a disconnection between the central nervous system and the anterior pituitary, we thought it worthwhile to study the GH response to stimulation with <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) or gonadotropin releasing hormone (GnRH) in <b>heroin</b> addicts.
+TRH	drug	benzodiazepine	6243358	Attenuation of the effect of punishment by <strong>thyrotropin releasing hormone</strong>: comparisons with <b>chlordiazepoxide</b>.
+TRH	addiction	addiction	6243358	Attenuation of the effect of <b>punishment</b> by <strong>thyrotropin releasing hormone</strong>: comparisons with chlordiazepoxide.
+TRH	drug	alcohol	6154298	However, at doses that did not disrupt performance, <strong>TRH</strong>, HP, and OHT did not affect the stimulus properties of <b>ethanol</b> at any dose tested, nor did they change the stimulus properties of saline.
+TRH	drug	alcohol	107908	<strong>TRH</strong> (protirelin) in depressed <b>alcoholic</b> men.
+TRH	addiction	reward	104325	Male Sprague Dawley rats were trained in a two lever <b>operant</b> discrimination task using 20 mg/kg thyrotropin releasing hormone (<strong>TRH</strong>) and saline as cues.
+TRH	addiction	reward	104325	Male Sprague Dawley rats were trained in a two lever <b>operant</b> discrimination task using 20 mg/kg <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) and saline as cues.
+TRH	drug	amphetamine	104325	However, animals failed to show generalization between the training drug (20 mg/kg <strong>TRH</strong>) and d <b>amphetamine</b> sulfate (0.8, 1.6, or 2.4 mg/kg); likewise, animals trained to discriminate d <b>amphetamine</b> (0.8 or 1.6 mg/kg) from saline failed to show generalization between d <b>amphetamine</b> and <strong>TRH</strong> (10, 20, OR 30 MG/KG).
+TRH	drug	alcohol	122287	The effects of <strong>TRH</strong> and LRH on the secretion of TSH, PRL, and LH were studied in these subjects once during the period of acute <b>alcohol</b> intoxication (4 h after the start of drinking) and once during the hangover period (14 h after the start of drinking).
+TRH	addiction	intoxication	122287	The effects of <strong>TRH</strong> and LRH on the secretion of TSH, PRL, and LH were studied in these subjects once during the period of acute alcohol <b>intoxication</b> (4 h after the start of drinking) and once during the hangover period (14 h after the start of drinking).
+TRH	drug	alcohol	122287	<b>Alcohol</b> also did not significantly alter the effects of <strong>TRH</strong> and LRH on plasma TSH and LH levels at 4 and 14 h. During the hangover period, the PRL response to <strong>TRH</strong> was totally blocked, but during <b>alcohol</b> intoxication, there was a slight increase in the PRL response to <strong>TRH</strong>.
+TRH	addiction	intoxication	122287	Alcohol also did not significantly alter the effects of <strong>TRH</strong> and LRH on plasma TSH and LH levels at 4 and 14 h. During the hangover period, the PRL response to <strong>TRH</strong> was totally blocked, but during alcohol <b>intoxication</b>, there was a slight increase in the PRL response to <strong>TRH</strong>.
+TRH	addiction	withdrawal	122287	The lack of response of PRL to <strong>TRH</strong> during the hangover suggests that <b>withdrawal</b> symptoms are associated with increased dopaminergic activity in the hypothalamus.
+TRH	drug	opioid	402526	Interactions of <strong>thyrotropin releasing hormone</strong> and <b>morphine</b> sulfate in rodents.
+TRH	drug	alcohol	822858	[The influence of thyrotrophin releasing hormone (<strong>TRH</strong>) on depression in the <b>alcohol</b> withdrawal syndrome (author's transl)].
+TRH	addiction	withdrawal	822858	[The influence of thyrotrophin releasing hormone (<strong>TRH</strong>) on depression in the alcohol <b>withdrawal</b> syndrome (author's transl)].
+TRH	drug	alcohol	822858	A single injection of thyrotrophin releasing hormone (<strong>TRH</strong>) was compared to injection of nicotinic acid or saline in <b>alcohol</b> withdrawal syndrome.
+TRH	addiction	withdrawal	822858	A single injection of thyrotrophin releasing hormone (<strong>TRH</strong>) was compared to injection of nicotinic acid or saline in alcohol <b>withdrawal</b> syndrome.
+TRH	addiction	addiction	138141	Thyrotropin releasing hormone (<strong>TRH</strong>) administered intraventricularly to rabbits produces tachypnea, hyperthermia, behavioral excitation and, with larger doses, <b>compulsive</b> scratching.
+TRH	addiction	addiction	138141	<strong>Thyrotropin releasing hormone</strong> (<strong>TRH</strong>) administered intraventricularly to rabbits produces tachypnea, hyperthermia, behavioral excitation and, with larger doses, <b>compulsive</b> scratching.
+TRH	drug	opioid	138141	<b>Morphine</b> actually appeared to antagonize the excitatory actions of <strong>TRH</strong>.
+TRH	addiction	addiction	817376	The intraventricular administration of thyrotropin releasing hormone (<strong>TRH</strong>) to conscious rabbits produces a dose related increase in body temperature, a <b>compulsive</b> scratching syndrome, and behavioral excitation.
+TRH	addiction	addiction	817376	The intraventricular administration of <strong>thyrotropin releasing hormone</strong> (<strong>TRH</strong>) to conscious rabbits produces a dose related increase in body temperature, a <b>compulsive</b> scratching syndrome, and behavioral excitation.
+TRH	drug	opioid	817376	Of all the depressants tested, only <b>morphine</b> was resistant to the analeptic effect of <strong>TRH</strong>, although the <b>morphine</b> induced hypothermia was reversed.
+TRH	drug	alcohol	804705	Preliminary studies on the use of <strong>thyrotropin releasing hormone</strong> in manic states, depression, and the dysphoria of <b>alcohol</b> withdrawal.
+TRH	addiction	withdrawal	804705	Preliminary studies on the use of <strong>thyrotropin releasing hormone</strong> in manic states, depression, and the dysphoria of alcohol <b>withdrawal</b>.
+GDNF	drug	psychedelics	31829932	Finally, we show how <b>ibogaine</b> could exert its anti addictive properties through a completely different neurotrophic factor than other <b>psychedelic</b> drugs, the glial cell line derived neurotrophic factor (<strong>GDNF</strong>).
+GDNF	addiction	addiction	31829932	Finally, we show how ibogaine could exert its anti <b>addictive</b> properties through a completely different neurotrophic factor than other psychedelic drugs, the glial cell line derived neurotrophic factor (<strong>GDNF</strong>).
+GDNF	drug	alcohol	31710958	<b>Alcohol</b> consumption alters <strong>Gdnf</strong> promoter methylation and expression in rats.
+GDNF	drug	alcohol	31710958	Glial cell derived neurotrophic factor (<strong>Gdnf</strong>) shows promising results concerning the inhibition of <b>alcohol</b> consumption in rodent models.
+GDNF	drug	alcohol	31710958	<strong>Glial cell derived neurotrophic factor</strong> (<strong>Gdnf</strong>) shows promising results concerning the inhibition of <b>alcohol</b> consumption in rodent models.
+GDNF	drug	alcohol	31710958	We investigated the epigenetic regulation of <strong>Gdnf</strong> following <b>ethanol</b> consumption and withdrawal in a rat model.
+GDNF	addiction	withdrawal	31710958	We investigated the epigenetic regulation of <strong>Gdnf</strong> following ethanol consumption and <b>withdrawal</b> in a rat model.
+GDNF	drug	nicotine	31694445	NQ treated animals conditioned to <b>nicotine</b> resulted in an increase of NAcc <strong>GDNF</strong>, but this was eliminated by CGS 21680.
+GDNF	addiction	reward	31694445	Both BDNF and <strong>GDNF</strong> correlated with <b>CPP</b> performance.
+GDNF	addiction	addiction	31446765	This pilot study provides further support for the role of <strong>GDNF</strong> and CNTNAP2 in <b>addiction</b> behaviors.
+GDNF	drug	psychedelics	30890941	<b>Ibogaine</b> Administration Modifies <strong>GDNF</strong> and BDNF Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits.
+GDNF	drug	alcohol	30890941	Recent work has suggested that ibogaine effects on <b>alcohol</b> self administration in rats are related to the release of Glial cell Derived Neurotrophic Factor (<strong>GDNF</strong>) in the Ventral Tegmental Area (VTA), a mesencephalic region which hosts the soma of dopaminergic neurons.
+GDNF	drug	psychedelics	30890941	Recent work has suggested that <b>ibogaine</b> effects on alcohol self administration in rats are related to the release of Glial cell Derived Neurotrophic Factor (<strong>GDNF</strong>) in the Ventral Tegmental Area (VTA), a mesencephalic region which hosts the soma of dopaminergic neurons.
+GDNF	drug	alcohol	30890941	Recent work has suggested that ibogaine effects on <b>alcohol</b> self administration in rats are related to the release of <strong>Glial cell Derived Neurotrophic Factor</strong> (<strong>GDNF</strong>) in the Ventral Tegmental Area (VTA), a mesencephalic region which hosts the soma of dopaminergic neurons.
+GDNF	drug	psychedelics	30890941	Recent work has suggested that <b>ibogaine</b> effects on alcohol self administration in rats are related to the release of <strong>Glial cell Derived Neurotrophic Factor</strong> (<strong>GDNF</strong>) in the Ventral Tegmental Area (VTA), a mesencephalic region which hosts the soma of dopaminergic neurons.
+GDNF	drug	psychedelics	30890941	Although previous reports have shown <b>ibogaine</b>'s ability to induce <strong>GDNF</strong> expression in rat midbrain, there are no studies addressing its effect on the expression of <strong>GDNF</strong> and other neurotrophic factors (NFs) such as Brain Derived Neurotrophic Factor (BDNF) or Nerve Growth Factor (NGF) in distinct brain regions containing dopaminergic neurons.
+GDNF	drug	amphetamine	30699853	BDNF, NGF, and <strong>GDNF</strong> levels were decreased, while NT 3 and NT 4 levels were increased in brains after d <b>AMPH</b> sensitization.
+GDNF	addiction	sensitization	30699853	BDNF, NGF, and <strong>GDNF</strong> levels were decreased, while NT 3 and NT 4 levels were increased in brains after d AMPH <b>sensitization</b>.
+GDNF	drug	alcohol	29726054	<strong>GDNF</strong> and <b>alcohol</b> use disorder.
+GDNF	drug	alcohol	29726054	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) has been extensively studied for its role in the development and maintenance of the midbrain dopaminergic system, although evidence suggests that <strong>GDNF</strong> also plays a role in drug and <b>alcohol</b> addiction.
+GDNF	addiction	addiction	29726054	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) has been extensively studied for its role in the development and maintenance of the midbrain dopaminergic system, although evidence suggests that <strong>GDNF</strong> also plays a role in drug and alcohol <b>addiction</b>.
+GDNF	drug	alcohol	29726054	This review focuses on the unique actions of <strong>GDNF</strong> in the mechanisms that prevent the transition from recreational <b>alcohol</b> use to abuse.
+GDNF	drug	alcohol	29726054	Specifically, we describe studies in rodents suggesting that <b>alcohol</b> acutely increases <strong>GDNF</strong> expression in the ventral tegmental area, which enables the activation of the mitogen activated protein kinase signaling pathway and the gating of <b>alcohol</b> intake.
+GDNF	drug	alcohol	29726054	We further provide evidence to suggest that <strong>GDNF</strong> acts in the ventral tegmental area via both nongenomic and genomic mechanisms to suppress <b>alcohol</b> consumption.
+GDNF	drug	alcohol	29726054	Finally, we describe the potential use of <strong>GDNF</strong> inducers as a novel therapeutic approach to treat <b>alcohol</b> use disorder.
+GDNF	drug	nicotine	29444518	Results were complex, and revealed that NAcc <strong>GDNF</strong> was increased in animals given <b>nicotine</b>, regardless of housing condition.
+GDNF	drug	nicotine	29444518	Further, enrichment increased <strong>GDNF</strong> in NQ rats regardless of adolescent drug treatment and in NS treated rats given <b>nicotine</b>, but did not increase <strong>GDNF</strong> in NS treated controls compared to the isolated housing condition.
+GDNF	drug	cocaine	29066725	The ability of the HS binding neuropeptide glial cell line derived neurotrophic factor (<strong>GDNF</strong>) to increase <b>cocaine</b> intake was potentiated by a deletion that abolished its HS binding.
+GDNF	addiction	addiction	29031851	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) is an important regulator of midbrain dopamine neurons, and may play a mechanistic role in <b>addiction</b> related behaviors.
+GDNF	drug	amphetamine	29031851	To elucidate the components of <strong>GDNF</strong> signaling that contribute to addiction related behaviors of place preference and its extinction, we utilized two genetically modified <strong>GDNF</strong> mouse models in an <b>amphetamine</b> induced conditioned place preference (CPP) paradigm and evaluated how the behavioral findings correlate with dopamine signaling in the dorsal and ventral striatum.
+GDNF	addiction	addiction	29031851	To elucidate the components of <strong>GDNF</strong> signaling that contribute to <b>addiction</b> related behaviors of place preference and its extinction, we utilized two genetically modified <strong>GDNF</strong> mouse models in an amphetamine induced conditioned place preference (CPP) paradigm and evaluated how the behavioral findings correlate with dopamine signaling in the dorsal and ventral striatum.
+GDNF	addiction	reward	29031851	To elucidate the components of <strong>GDNF</strong> signaling that contribute to addiction related behaviors of place preference and its extinction, we utilized two genetically modified <strong>GDNF</strong> mouse models in an amphetamine induced conditioned place preference (<b>CPP</b>) paradigm and evaluated how the behavioral findings correlate with dopamine signaling in the dorsal and ventral striatum.
+GDNF	drug	amphetamine	29031851	The duration of <b>amphetamine</b> induced CPP was greatly enhanced in MEN2B mice, but not in the <strong>GDNF</strong> hypermorphic mice.
+GDNF	addiction	reward	29031851	The duration of amphetamine induced <b>CPP</b> was greatly enhanced in MEN2B mice, but not in the <strong>GDNF</strong> hypermorphic mice.
+GDNF	addiction	relapse	29031851	Together, our results suggest that downstream components of <strong>GDNF</strong> signaling, in this case Ret, may mediate persistent drug <b>seeking</b> behavior through increased TH expression and dopamine levels in the mesolimbic dopamine neurons.
+GDNF	drug	opioid	28847022	This study was aimed to investigate the attenuation effect of Cerebrolysin, a mixture of potent growth factors (BDNF, <strong>GDNF</strong>, NGF, CNTF etc,), on the development of <b>Morphine</b> induced dependence and tolerance.
+GDNF	addiction	dependence	28847022	This study was aimed to investigate the attenuation effect of Cerebrolysin, a mixture of potent growth factors (BDNF, <strong>GDNF</strong>, NGF, CNTF etc,), on the development of Morphine induced <b>dependence</b> and tolerance.
+GDNF	drug	alcohol	28559549	Furthermore, re exposure to the nicotine associated context in adult rats led to a decrease in glial cell line derived neurotrophic factor (<strong>Gdnf</strong>) mRNA expression in the ventral tegmental area, an effect that leads to increased <b>alcohol</b> consumption, as we have previously reported.
+GDNF	drug	nicotine	28559549	Furthermore, re exposure to the <b>nicotine</b> associated context in adult rats led to a decrease in glial cell line derived neurotrophic factor (<strong>Gdnf</strong>) mRNA expression in the ventral tegmental area, an effect that leads to increased alcohol consumption, as we have previously reported.
+GDNF	drug	alcohol	28559549	Our findings suggest that retrieval of nicotine associated contextual memories from adolescence may gate <b>alcohol</b> intake in adulthood, with a possible involvement of <strong>GDNF</strong>.
+GDNF	drug	nicotine	28559549	Our findings suggest that retrieval of <b>nicotine</b> associated contextual memories from adolescence may gate alcohol intake in adulthood, with a possible involvement of <strong>GDNF</strong>.
+GDNF	drug	nicotine	28314679	An analysis of the rewarding and aversive associative properties of <b>nicotine</b> in the neonatal quinpirole model: Effects on glial cell line derived neurotrophic factor (<strong>GDNF</strong>).
+GDNF	addiction	aversion	28314679	An analysis of the rewarding and <b>aversive</b> associative properties of nicotine in the neonatal quinpirole model: Effects on glial cell line derived neurotrophic factor (<strong>GDNF</strong>).
+GDNF	drug	nicotine	28314679	NQ increased accumbal <strong>GDNF</strong> which was sensitized in NQ rats conditioned to <b>nicotine</b> in Experiment 1, but the aversive dose of <b>nicotine</b> reduced <strong>GDNF</strong> in NQ animals in Experiment 2.
+GDNF	addiction	aversion	28314679	NQ increased accumbal <strong>GDNF</strong> which was sensitized in NQ rats conditioned to nicotine in Experiment 1, but the <b>aversive</b> dose of nicotine reduced <strong>GDNF</strong> in NQ animals in Experiment 2.
+GDNF	drug	nicotine	28314679	Both antipsychotics in combination with the aversive dose of <b>nicotine</b> decreased accumbal <strong>GDNF</strong>.
+GDNF	addiction	aversion	28314679	Both antipsychotics in combination with the <b>aversive</b> dose of nicotine decreased accumbal <strong>GDNF</strong>.
+GDNF	drug	nicotine	28314679	In sum, increased D2 receptor sensitivity influenced the associative properties and <strong>GDNF</strong> response to <b>nicotine</b> which has implications towards pharmacological targets for <b>smoking</b> cessation in schizophrenia.
+GDNF	drug	amphetamine	28096470	Dampened <b>Amphetamine</b> Stimulated Behavior and Altered Dopamine Transporter Function in the Absence of Brain <strong>GDNF</strong>.
+GDNF	drug	amphetamine	28096470	Using conditional <strong>Gdnf</strong> knock out mice, we found that endogenous <strong>GDNF</strong> affects striatal dopamine homeostasis and regulates <b>amphetamine</b> induced behaviors by regulating the level and function of dopamine transporters.
+GDNF	drug	nicotine	27994179	Since the role of dopamine system in <b>smoking</b> is well established, we hypothesized that <strong>GDNF</strong> gene variants may affect <b>smoking</b> behaviour.
+GDNF	drug	nicotine	27994179	Allele wise association analyses of the eight <strong>GDNF</strong> SNPs provided a significant association between <b>smoking</b> behaviour and rs3096140 (P=0.0039).
+GDNF	drug	amphetamine	27994179	Although previous data demonstrated an association between <strong>GDNF</strong> rs2910704 and severity of <b>methamphetamine</b> use to the best of our knowledge, this is the first study on the role of <strong>GDNF</strong> genetic variations in smoking behaviour.
+GDNF	drug	nicotine	27994179	Although previous data demonstrated an association between <strong>GDNF</strong> rs2910704 and severity of methamphetamine use to the best of our knowledge, this is the first study on the role of <strong>GDNF</strong> genetic variations in <b>smoking</b> behaviour.
+GDNF	drug	nicotine	27994179	Our results suggest that <strong>GDNF</strong> rs3096140 might be involved in the genetic background of <b>smoking</b>, independent of anxiety characteristics.
+GDNF	drug	alcohol	26517751	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>), in particular, has been implicated in marked reduction of <b>alcohol</b> consumption in rodent addiction models, and the natural product ibogaine, a substance used traditionally in ritualistic ceremonies, has been suggested to increase the synthesis and release of <strong>GDNF</strong> in the dopaminergic system in rats.
+GDNF	drug	psychedelics	26517751	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>), in particular, has been implicated in marked reduction of alcohol consumption in rodent addiction models, and the natural product <b>ibogaine</b>, a substance used traditionally in ritualistic ceremonies, has been suggested to increase the synthesis and release of <strong>GDNF</strong> in the dopaminergic system in rats.
+GDNF	addiction	addiction	26517751	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>), in particular, has been implicated in marked reduction of alcohol consumption in rodent <b>addiction</b> models, and the natural product ibogaine, a substance used traditionally in ritualistic ceremonies, has been suggested to increase the synthesis and release of <strong>GDNF</strong> in the dopaminergic system in rats.
+GDNF	drug	opioid	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of <b>morphine</b> dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (<strong>GDNF</strong>), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous <b>morphine</b> withdrawal in dependent animals.
+GDNF	addiction	dependence	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine <b>dependence</b> on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (<strong>GDNF</strong>), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine withdrawal in dependent animals.
+GDNF	addiction	withdrawal	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (<strong>GDNF</strong>), nerve growth factor (NGF), and insulin like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine <b>withdrawal</b> in dependent animals.
+GDNF	drug	opioid	26346883	The expression of the BDNF, <strong>GDNF</strong>, NGF, IGF1, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after <b>morphine</b> withdrawal.
+GDNF	addiction	withdrawal	26346883	The expression of the BDNF, <strong>GDNF</strong>, NGF, IGF1, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after morphine <b>withdrawal</b>.
+GDNF	drug	alcohol	25638740	A comparison of dexmedetomidine and placebo on the plasma concentrations of NGF, BDNF, <strong>GDNF</strong>, and epinephrine during severe <b>alcohol</b> withdrawal.
+GDNF	addiction	withdrawal	25638740	A comparison of dexmedetomidine and placebo on the plasma concentrations of NGF, BDNF, <strong>GDNF</strong>, and epinephrine during severe alcohol <b>withdrawal</b>.
+GDNF	drug	alcohol	25638740	<b>Alcohol</b> withdrawal and therapies may affect nerve growth factor (NGF), brain derived neurotrophic growth factor (BDNF), glial derived neurotrophic growth factor (<strong>GDNF</strong>), and epinephrine (EPI).
+GDNF	addiction	withdrawal	25638740	Alcohol <b>withdrawal</b> and therapies may affect nerve growth factor (NGF), brain derived neurotrophic growth factor (BDNF), glial derived neurotrophic growth factor (<strong>GDNF</strong>), and epinephrine (EPI).
+GDNF	drug	alcohol	25638740	This study evaluated dexmedetomidine (DEX) on NGF, BDNF, <strong>GDNF</strong>, and EPI in severe <b>alcohol</b> withdrawal and related their plasma concentrations to DEX concentrations.
+GDNF	addiction	withdrawal	25638740	This study evaluated dexmedetomidine (DEX) on NGF, BDNF, <strong>GDNF</strong>, and EPI in severe alcohol <b>withdrawal</b> and related their plasma concentrations to DEX concentrations.
+GDNF	drug	alcohol	25638740	In summary, the plasma concentrations of NGF, BDNF, <strong>GDNF</strong>, and EPI during <b>alcohol</b> withdrawal are variable and the effects of DEX were marginal.
+GDNF	addiction	withdrawal	25638740	In summary, the plasma concentrations of NGF, BDNF, <strong>GDNF</strong>, and EPI during alcohol <b>withdrawal</b> are variable and the effects of DEX were marginal.
+GDNF	drug	alcohol	25623403	The aim of this study was to investigate the alterations in serum neurotrophin levels (brain derived neurotrophic factor [BDNF], glial derived neurotrophic factor [<strong>GDNF</strong>], and nerve growth factor [NGF]) in <b>alcohol</b> use disorder in a young population, and thus possibly representing the early stages of the illness.
+GDNF	drug	opioid	25611164	As the effect of Lvs siGDNF to relieve pain was similar to <b>morphine</b>, but it is not a narcotic, the use of <strong>GDNF</strong> RNA interference may be considered as a new therapeutic strategy for the treatment of bone cancer pain in the future.
+GDNF	drug	cocaine	25576963	On PND 56, rats treated with <b>cocaine</b> or methylphenidate from PND 14 through PND 35 exhibited increased hippocampal glial cell derived neurotrophic factor (<strong>GDNF</strong>) mRNA levels, after 21 withdrawal days, compared to the saline treated rats.
+GDNF	addiction	withdrawal	25576963	On PND 56, rats treated with cocaine or methylphenidate from PND 14 through PND 35 exhibited increased hippocampal glial cell derived neurotrophic factor (<strong>GDNF</strong>) mRNA levels, after 21 <b>withdrawal</b> days, compared to the saline treated rats.
+GDNF	drug	cocaine	25576963	On PND 56, rats treated with <b>cocaine</b> or methylphenidate from PND 14 through PND 35 exhibited increased hippocampal <strong>glial cell derived neurotrophic factor</strong> (<strong>GDNF</strong>) mRNA levels, after 21 withdrawal days, compared to the saline treated rats.
+GDNF	addiction	withdrawal	25576963	On PND 56, rats treated with cocaine or methylphenidate from PND 14 through PND 35 exhibited increased hippocampal <strong>glial cell derived neurotrophic factor</strong> (<strong>GDNF</strong>) mRNA levels, after 21 <b>withdrawal</b> days, compared to the saline treated rats.
+GDNF	addiction	relapse	25576963	It is possible that the increased hippocampal <strong>GDNF</strong> mRNA levels, may be relevant to the reduced rate of drug <b>seeking</b> behavior in ADHD adolescence that were maintained from childhood on methylphenidate.
+GDNF	drug	alcohol	25155311	EtOH and nicotine directly administered into the pVTA resulted in alterations in gene expression in the AcbSh (50.8 fold increase in brain derived neurotrophic factor (BDNF), 2.4 fold decrease in glial cell line derived neurotrophic factor (<strong>GDNF</strong>), 10.3 fold increase in vesicular glutamate transporter 1 (Vglut1)) that were not observed following microinjections of equivalent concentrations/doses of <b>ethanol</b> or nicotine.
+GDNF	drug	nicotine	25155311	EtOH and <b>nicotine</b> directly administered into the pVTA resulted in alterations in gene expression in the AcbSh (50.8 fold increase in brain derived neurotrophic factor (BDNF), 2.4 fold decrease in glial cell line derived neurotrophic factor (<strong>GDNF</strong>), 10.3 fold increase in vesicular glutamate transporter 1 (Vglut1)) that were not observed following microinjections of equivalent concentrations/doses of ethanol or <b>nicotine</b>.
+GDNF	drug	alcohol	24801661	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) is an endogenous protector in the mesolimbic system against excessive <b>alcohol</b> consumption and relapse.
+GDNF	addiction	relapse	24801661	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) is an endogenous protector in the mesolimbic system against excessive alcohol consumption and <b>relapse</b>.
+GDNF	drug	alcohol	24801661	We found that <strong>GDNF</strong> knockdown, by infecting rat Acb neurons with a small hairpin RNA (shRNA) targeting the <strong>GDNF</strong> gene, produced a rapid escalation to excessive <b>alcohol</b> consumption and enhanced relapse to <b>alcohol</b> drinking.
+GDNF	addiction	addiction	24801661	We found that <strong>GDNF</strong> knockdown, by infecting rat Acb neurons with a small hairpin RNA (shRNA) targeting the <strong>GDNF</strong> gene, produced a rapid <b>escalation</b> to excessive alcohol consumption and enhanced relapse to alcohol drinking.
+GDNF	addiction	relapse	24801661	We found that <strong>GDNF</strong> knockdown, by infecting rat Acb neurons with a small hairpin RNA (shRNA) targeting the <strong>GDNF</strong> gene, produced a rapid escalation to excessive alcohol consumption and enhanced <b>relapse</b> to alcohol drinking.
+GDNF	drug	alcohol	24801661	To access the mechanism underlying <strong>GDNF</strong>'s actions, we measured the firing rate of dopaminergic (DAergic) neurons in the VTA after a history of excessive <b>alcohol</b> intake with or without elevating <strong>GDNF</strong> levels.
+GDNF	drug	alcohol	24801661	We found that the spontaneous firing rate of DAergic neurons in the VTA was reduced during <b>alcohol</b> withdrawal and that <strong>GDNF</strong> reversed this <b>alcohol</b> induced DA deficiency.
+GDNF	addiction	withdrawal	24801661	We found that the spontaneous firing rate of DAergic neurons in the VTA was reduced during alcohol <b>withdrawal</b> and that <strong>GDNF</strong> reversed this alcohol induced DA deficiency.
+GDNF	drug	alcohol	24801661	Together, our results suggest that endogenous <strong>GDNF</strong> in the mesolimbic system controls the transition from moderate to excessive <b>alcohol</b> drinking and relapse via reversal of <b>alcohol</b> dependent neuro adaptations in DAergic VTA neurons.
+GDNF	addiction	relapse	24801661	Together, our results suggest that endogenous <strong>GDNF</strong> in the mesolimbic system controls the transition from moderate to excessive alcohol drinking and <b>relapse</b> via reversal of alcohol dependent neuro adaptations in DAergic VTA neurons.
+GDNF	drug	opioid	24399412	NCAM signaling mediates the effects of <strong>GDNF</strong> on chronic <b>morphine</b> induced neuroadaptations.
+GDNF	addiction	addiction	24399412	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) is a potent neurotrophic factor for midbrain dopamine (DA) neurons, while the DA neurons in the ventral tegmental area (VTA) is a crucial part of the neural circuits associated with drug <b>addiction</b>.
+GDNF	addiction	addiction	24399412	Recently, more and more evidence suggests that <strong>GDNF</strong> plays an important role in negatively regulating the neuroadaptations induced by chronic exposure to drugs, which was thought to be the neurobiological basis of drug <b>addiction</b>, but the underlying mechanism is still unknown.
+GDNF	drug	opioid	24399412	The purpose of this study was to investigate whether NCAM was involved in the effects of <strong>GDNF</strong> on the neuroadaptations induced by chronic <b>morphine</b> exposure.
+GDNF	drug	opioid	24399412	Moreover, pre treatment with the antibody could antagonize the effect of <strong>GDNF</strong> on inhibiting the neuroadaptations induced by chronic <b>morphine</b> exposure, including the decreases of the number and length of neurites and the size of cell bodies of VTA dopamine neurons, as well as the increase of tyrosine hydroxylase in the VTA dopamine neurons.
+GDNF	drug	opioid	24399412	These results suggest that NCAM signaling is involved in the negative regulatory effects of <strong>GDNF</strong> on chronic <b>morphine</b> induced neuroadaptations.
+GDNF	drug	alcohol	24061482	Our primary interest is the examination of how regions that receive BF cholinergic projections are influenced by short term <b>ethanol</b> exposure through alterations in the mRNA levels of neurotrophic factors [nerve growth factor/TrkA, brain derived neurotrophic factor/TrkB, and glial derived neurotrophic factor (<strong>GDNF</strong>)/<strong>GDNF</strong> family receptor α1].
+GDNF	drug	opioid	24022000	Association of the <strong>GDNF</strong> gene with depression and <b>heroin</b> dependence, but not schizophrenia, in a Chinese population.
+GDNF	addiction	dependence	24022000	Association of the <strong>GDNF</strong> gene with depression and heroin <b>dependence</b>, but not schizophrenia, in a Chinese population.
+GDNF	drug	opioid	24022000	The association of seven <strong>GDNF</strong> tag SNPs with depression, <b>heroin</b> dependence (HD) and schizophrenia was evaluated in Chinese.
+GDNF	addiction	dependence	24022000	The association of seven <strong>GDNF</strong> tag SNPs with depression, heroin <b>dependence</b> (HD) and schizophrenia was evaluated in Chinese.
+GDNF	drug	alcohol	23588198	Binge <b>alcohol</b> induced alterations in BDNF and <strong>GDNF</strong> expression in central extended amygdala and pyriform cortex on infant rats.
+GDNF	addiction	intoxication	23588198	<b>Binge</b> alcohol induced alterations in BDNF and <strong>GDNF</strong> expression in central extended amygdala and pyriform cortex on infant rats.
+GDNF	drug	alcohol	23588198	Our goal was to study whether brain derived neurotrophic factor (BDNF) and glial derived neurotrophic factor (<strong>GDNF</strong>) expression were affected by <b>alcohol</b> in central extended amygdala (CEXA) and pyriform cortex (Pyr), structures strongly involved in emotional/social behaviors.
+GDNF	drug	alcohol	23588198	Results showed: (1) <b>alcohol</b> induced enhancement of BDNF positive cells on PND 7 and 20, a decrease on PND 15 in the CEXA, and no changes in the Pyr on PND 7 and 20, but a diminished on PND 15; (2) <strong>GDNF</strong> positive cells rise after <b>alcohol</b> administration for the three ages in the CEXA and Pyr except on PND 15, where there was a decline; and (3) pharmacokinetics analysis demonstrated age related differences showing equal BALs on PND 7 and 20 but higher BALs on PND 15.
+GDNF	drug	amphetamine	23432945	Intrastriatal gene delivery of <strong>GDNF</strong> persistently attenuates <b>methamphetamine</b> self administration and relapse in mice.
+GDNF	addiction	relapse	23432945	Intrastriatal gene delivery of <strong>GDNF</strong> persistently attenuates methamphetamine self administration and <b>relapse</b> in mice.
+GDNF	drug	amphetamine	23432945	In our well established mouse models of <b>methamphetamine</b> (<b>Meth</b>) self administration and reinstatement, bilateral microinjection of adeno associated virus vectors expressing <strong>GDNF</strong> (AAV <strong>Gdnf</strong>) into the striatum significantly reduced <b>Meth</b> self administration, without affecting locomotor activity.
+GDNF	addiction	relapse	23432945	In our well established mouse models of methamphetamine (Meth) self administration and <b>reinstatement</b>, bilateral microinjection of adeno associated virus vectors expressing <strong>GDNF</strong> (AAV <strong>Gdnf</strong>) into the striatum significantly reduced Meth self administration, without affecting locomotor activity.
+GDNF	drug	amphetamine	23432945	Moreover, the intrastriatal AAV <strong>Gdnf</strong> attenuated cue induced reinstatement of <b>Meth</b> seeking behaviour in a sustainable manner.
+GDNF	addiction	relapse	23432945	Moreover, the intrastriatal AAV <strong>Gdnf</strong> attenuated cue induced <b>reinstatement</b> of Meth <b>seeking</b> behaviour in a sustainable manner.
+GDNF	drug	amphetamine	23432945	These findings suggest that the AAV vector mediated <strong>Gdnf</strong> gene transfer into the striatum is an effective and sustainable approach to attenuate <b>Meth</b> self administration and <b>Meth</b> associated cue induced relapsing behaviour and that the AAV mediated <strong>Gdnf</strong> gene transfer in the brain may be a valuable gene therapy against drug dependence and protracted relapse in clinical settings.
+GDNF	addiction	dependence	23432945	These findings suggest that the AAV vector mediated <strong>Gdnf</strong> gene transfer into the striatum is an effective and sustainable approach to attenuate Meth self administration and Meth associated cue induced relapsing behaviour and that the AAV mediated <strong>Gdnf</strong> gene transfer in the brain may be a valuable gene therapy against drug <b>dependence</b> and protracted relapse in clinical settings.
+GDNF	addiction	relapse	23432945	These findings suggest that the AAV vector mediated <strong>Gdnf</strong> gene transfer into the striatum is an effective and sustainable approach to attenuate Meth self administration and Meth associated cue induced relapsing behaviour and that the AAV mediated <strong>Gdnf</strong> gene transfer in the brain may be a valuable gene therapy against drug dependence and protracted <b>relapse</b> in clinical settings.
+GDNF	drug	alcohol	23298382	<strong>GDNF</strong> is a novel <b>ethanol</b> responsive gene in the VTA: implications for the development and persistence of excessive drinking.
+GDNF	drug	alcohol	23298382	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) is a potent inhibitor of <b>ethanol</b> consumption and relapse, and <strong>GDNF</strong> heterozygous knockout mice display increased reward sensitivity to <b>ethanol</b> and consume more <b>ethanol</b> after a period of abstinence than their wild type littermates.
+GDNF	addiction	relapse	23298382	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) is a potent inhibitor of ethanol consumption and <b>relapse</b>, and <strong>GDNF</strong> heterozygous knockout mice display increased reward sensitivity to ethanol and consume more ethanol after a period of abstinence than their wild type littermates.
+GDNF	addiction	reward	23298382	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) is a potent inhibitor of ethanol consumption and relapse, and <strong>GDNF</strong> heterozygous knockout mice display increased <b>reward</b> sensitivity to ethanol and consume more ethanol after a period of abstinence than their wild type littermates.
+GDNF	drug	alcohol	23298382	Here, we tested whether <b>ethanol</b> alters <strong>GDNF</strong> expression in the ventral tegmental area (VTA; <strong>GDNF</strong>'s site of action) and/or the nucleus accumbens (NAc; the main source of <strong>GDNF</strong>), and if so, determine the role of the endogenous growth factor in the regulation of <b>ethanol</b> consumption.
+GDNF	drug	alcohol	23298382	Systemic administration of <b>ethanol</b> increased <strong>GDNF</strong> expression and protein levels in the VTA, but not the NAc.
+GDNF	drug	alcohol	23298382	Additionally, <strong>GDNF</strong> levels were elevated after an <b>ethanol</b> drinking session in rats that consumed <b>ethanol</b> in the intermittent access two bottle choice procedure for 1 week, but not 7 weeks.
+GDNF	drug	alcohol	23298382	Deprivation following 7 weeks of excessive <b>ethanol</b> intake reduced <strong>GDNF</strong> levels, while a short <b>ethanol</b> binge drinking period following deprivation upregulated <strong>GDNF</strong> expression.
+GDNF	addiction	intoxication	23298382	Deprivation following 7 weeks of excessive ethanol intake reduced <strong>GDNF</strong> levels, while a short ethanol <b>binge</b> drinking period following deprivation upregulated <strong>GDNF</strong> expression.
+GDNF	drug	alcohol	23298382	Importantly, knockdown of <strong>GDNF</strong> within the VTA using adenovirus expressing short hairpin RNA facilitated the escalation of <b>ethanol</b> drinking by <b>ethanol</b> naïve rats, but not by rats with a history of excessive <b>ethanol</b> consumption.
+GDNF	addiction	addiction	23298382	Importantly, knockdown of <strong>GDNF</strong> within the VTA using adenovirus expressing short hairpin RNA facilitated the <b>escalation</b> of ethanol drinking by ethanol naïve rats, but not by rats with a history of excessive ethanol consumption.
+GDNF	drug	alcohol	23298382	These results suggest that during initial <b>ethanol</b> drinking experiences, <strong>GDNF</strong> in the VTA is increased and protects against the development of excessive <b>ethanol</b> intake.
+GDNF	drug	amphetamine	22470541	Our study investigated the effects of a non toxic <b>METH</b> injection (20 mg/kg) on gene expression, histone acetylation, and the expression of the histone acetyltransferase (HAT), <strong>ATF2</strong>, and of the histone deacetylases (HDACs), HDAC1 and HDAC2, in that structure.
+GDNF	drug	amphetamine	22470541	The histone acetyltransferase, <strong>ATF2</strong>, showed significant <b>METH</b> induced increased in protein expression.
+GDNF	drug	alcohol	22238721	Positive autoregulation of <strong>GDNF</strong> levels in the ventral tegmental area mediates long lasting inhibition of excessive <b>alcohol</b> consumption.
+GDNF	drug	alcohol	22238721	Activation of the <strong>GDNF</strong> pathway in the ventral tegmental area (VTA), where the <strong>GDNF</strong> receptors are expressed, produces a long lasting suppression of excessive <b>alcohol</b> consumption in rats.
+GDNF	drug	alcohol	22238721	Here we determined whether <strong>GDNF</strong> activates a positive autoregulatory feedback loop in vivo within the VTA, and if so, whether this mechanism underlies the long lasting suppressive effects of the growth factor on excessive <b>alcohol</b> consumption.
+GDNF	drug	alcohol	22238721	Importantly, we report that the <strong>GDNF</strong> mediated positive autoregulatory feedback loop accounts for the long lasting inhibitory actions of <strong>GDNF</strong> in the VTA on excessive <b>alcohol</b> consumption.
+GDNF	drug	alcohol	22238721	Specifically, the long lasting suppressive effects of a single rGDNF infusion into the VTA on excessive <b>alcohol</b> consumption were prevented when protein synthesis was inhibited, as well as when the upregulation of <strong>GDNF</strong> expression was prevented using short hairpin RNA to focally knock down <strong>GDNF</strong> mRNA in the VTA.
+GDNF	addiction	addiction	22238721	Our results could have implications for the development of long lasting treatments for disorders in which <strong>GDNF</strong> has a beneficial role, including drug <b>addiction</b>, chronic stress and Parkinson's disease.
+GDNF	drug	amphetamine	22174933	<b>METH</b> also caused up regulation of ER stress genes, <strong>Atf2</strong>, Atf3, Atf4, CHOP/Gadd153 and Gadd34.
+GDNF	drug	alcohol	22016515	<b>Alcohol</b> reward, dopamine depletion, and <strong>GDNF</strong>.
+GDNF	addiction	reward	22016515	Alcohol <b>reward</b>, dopamine depletion, and <strong>GDNF</strong>.
+GDNF	addiction	addiction	21890593	Preclinical study results suggest that brain derived neurotrophic factor (BDNF) and glial cell line derived neurotrophic factor (<strong>GDNF</strong>) are involved in the modulation of <b>addictive</b> behaviour.
+GDNF	drug	opioid	21890593	BDNF serum levels were significantly associated with craving for <b>heroin</b> (measured by the <b>Heroin</b> Craving Questionnaire (r = 0.420, p = 0.029) and by the General Craving Scale (r = 0.457, p = 0.016), whereas <strong>GDNF</strong> serum levels were not associated with psychometric dimensions of <b>heroin</b> craving.
+GDNF	addiction	relapse	21890593	BDNF serum levels were significantly associated with <b>craving</b> for heroin (measured by the Heroin <b>Craving</b> Questionnaire (r = 0.420, p = 0.029) and by the General <b>Craving</b> Scale (r = 0.457, p = 0.016), whereas <strong>GDNF</strong> serum levels were not associated with psychometric dimensions of heroin <b>craving</b>.
+GDNF	drug	opioid	21886595	Since activation of pain pathways result in exhaustion of growth factors, we examined the influence of cerebrolysin, a mixture of potent growth factors (BDNF, <strong>GDNF</strong>, NGF, CNTF etc,) on <b>morphine</b> induced HSP expression.
+GDNF	drug	alcohol	21734280	We previously showed that infusion of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) into the ventral tegmental area (VTA) rapidly reduces <b>alcohol</b> intake and relapse (Carnicella et al., 2008, 2009a), and increases dopamine (DA) levels in the nucleus accumbens (NAc) of <b>alcohol</b> naive rats (Wang et al., 2010).
+GDNF	addiction	relapse	21734280	We previously showed that infusion of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) into the ventral tegmental area (VTA) rapidly reduces alcohol intake and <b>relapse</b> (Carnicella et al., 2008, 2009a), and increases dopamine (DA) levels in the nucleus accumbens (NAc) of alcohol naive rats (Wang et al., 2010).
+GDNF	drug	alcohol	21734280	We therefore tested whether <strong>GDNF</strong> in the VTA reverses <b>alcohol</b> withdrawal associated DA deficiency and/or possesses rewarding properties.
+GDNF	addiction	withdrawal	21734280	We therefore tested whether <strong>GDNF</strong> in the VTA reverses alcohol <b>withdrawal</b> associated DA deficiency and/or possesses rewarding properties.
+GDNF	drug	alcohol	21734280	Using in vivo microdialysis, we show that 24 h withdrawal from <b>alcohol</b> causes a substantial reduction in NAc DA overflow, which was reversed by intra VTA <strong>GDNF</strong> infusion.
+GDNF	addiction	withdrawal	21734280	Using in vivo microdialysis, we show that 24 h <b>withdrawal</b> from alcohol causes a substantial reduction in NAc DA overflow, which was reversed by intra VTA <strong>GDNF</strong> infusion.
+GDNF	addiction	reward	21734280	Using conditioned place preference (<b>CPP</b>) paradigm, we observed that <strong>GDNF</strong> on its own does not induce <b>CPP</b>, suggesting that the growth factor is not rewarding.
+GDNF	drug	alcohol	21734280	However, <strong>GDNF</strong> blocked acquisition and expression of <b>alcohol</b> CPP.
+GDNF	addiction	reward	21734280	However, <strong>GDNF</strong> blocked acquisition and expression of alcohol <b>CPP</b>.
+GDNF	drug	alcohol	21734280	In addition, <strong>GDNF</strong> induced a downward shift in the dose response curve for operant self administration of <b>alcohol</b>, further suggesting that <strong>GDNF</strong> suppresses, rather than substitutes for, the reinforcing effects of <b>alcohol</b>.
+GDNF	addiction	reward	21734280	In addition, <strong>GDNF</strong> induced a downward shift in the dose response curve for <b>operant</b> self administration of alcohol, further suggesting that <strong>GDNF</strong> suppresses, rather than substitutes for, the <b>reinforcing</b> effects of alcohol.
+GDNF	drug	alcohol	21734280	Our findings suggest that <strong>GDNF</strong> reduces <b>alcohol</b> drinking behaviors by reversing an <b>alcohol</b> induced allostatic DA deficiency in the mesolimbic system.
+GDNF	drug	alcohol	21734280	In addition, as it lacks abuse liability, the study further highlights <strong>GDNF</strong> as a promising target for treatment of <b>alcohol</b> use/abuse disorders.
+GDNF	drug	amphetamine	21514351	Association analysis of the <strong>GDNF</strong> gene with <b>methamphetamine</b> use disorder in a Japanese population.
+GDNF	addiction	dependence	21514351	In this study, we examined the association between <strong>GDNF</strong> and MAP <b>dependence</b> using a Japanese population based sample.
+GDNF	addiction	addiction	21375485	This review discusses targeting growth factors such as glial derived neurotrophic factor (<strong>GDNF</strong>) and brain derived neurotrophic factor (BDNF) to treat Parkinson's disease and/or drug <b>addiction</b> and compiles recent evidences to propose the pleiotrophin/receptor protein tyrosine phosphatase β/ζ signaling pathway as a new therapeutic target to treat Parkinson's disease and to prevent drug of abuse induced neurotoxicity and <b>addictive</b> effects.
+GDNF	drug	opioid	21182575	Endogenous <strong>GDNF</strong> in ventral tegmental area and nucleus accumbens does not play a role in the incubation of <b>heroin</b> craving.
+GDNF	addiction	relapse	21182575	Endogenous <strong>GDNF</strong> in ventral tegmental area and nucleus accumbens does not play a role in the incubation of heroin <b>craving</b>.
+GDNF	drug	cocaine	21182575	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) activity in ventral tegmental area (VTA) mediates the time dependent increases in cue induced <b>cocaine</b> seeking after withdrawal (incubation of <b>cocaine</b> craving).
+GDNF	addiction	relapse	21182575	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) activity in ventral tegmental area (VTA) mediates the time dependent increases in cue induced cocaine <b>seeking</b> after withdrawal (incubation of cocaine <b>craving</b>).
+GDNF	addiction	withdrawal	21182575	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) activity in ventral tegmental area (VTA) mediates the time dependent increases in cue induced cocaine seeking after <b>withdrawal</b> (incubation of cocaine craving).
+GDNF	drug	opioid	21182575	Cue induced <b>heroin</b> seeking was higher after 11 or 30 days than after 1 day (incubation of <b>heroin</b> craving), and the time dependent increases in extinction responding were associated with time dependent changes in <strong>GDNF</strong> mRNA expression in VTA and nucleus accumbens.
+GDNF	addiction	relapse	21182575	Cue induced heroin <b>seeking</b> was higher after 11 or 30 days than after 1 day (incubation of heroin <b>craving</b>), and the time dependent increases in extinction responding were associated with time dependent changes in <strong>GDNF</strong> mRNA expression in VTA and nucleus accumbens.
+GDNF	drug	opioid	21182575	Additionally, acute accumbens (but not VTA) <strong>GDNF</strong> injections (12.5 µg/side) administered 1 3 hours after the last <b>heroin</b> self administration training session enhanced the time dependent increases in extinction responding after withdrawal.
+GDNF	addiction	withdrawal	21182575	Additionally, acute accumbens (but not VTA) <strong>GDNF</strong> injections (12.5 µg/side) administered 1 3 hours after the last heroin self administration training session enhanced the time dependent increases in extinction responding after <b>withdrawal</b>.
+GDNF	addiction	withdrawal	21182575	However, the time dependent increases in extinction responding after <b>withdrawal</b> were not associated with changes in <strong>GDNF</strong> protein expression in VTA and accumbens.
+GDNF	drug	opioid	21182575	In summary, <b>heroin</b> self administration and withdrawal regulate VTA and accumbens <strong>GDNF</strong> mRNA expression in a time dependent manner, and exogenous <strong>GDNF</strong> administration into accumbens but not VTA potentiates cue induced <b>heroin</b> seeking.
+GDNF	addiction	relapse	21182575	In summary, heroin self administration and withdrawal regulate VTA and accumbens <strong>GDNF</strong> mRNA expression in a time dependent manner, and exogenous <strong>GDNF</strong> administration into accumbens but not VTA potentiates cue induced heroin <b>seeking</b>.
+GDNF	addiction	withdrawal	21182575	In summary, heroin self administration and <b>withdrawal</b> regulate VTA and accumbens <strong>GDNF</strong> mRNA expression in a time dependent manner, and exogenous <strong>GDNF</strong> administration into accumbens but not VTA potentiates cue induced heroin seeking.
+GDNF	drug	opioid	21182575	However, based on the <strong>GDNF</strong> protein expression and the anti <strong>GDNF</strong> monoclonal neutralizing antibodies manipulation data, we conclude that neither accumbens nor VTA endogenous <strong>GDNF</strong> mediates the incubation of <b>heroin</b> craving.
+GDNF	addiction	relapse	21182575	However, based on the <strong>GDNF</strong> protein expression and the anti <strong>GDNF</strong> monoclonal neutralizing antibodies manipulation data, we conclude that neither accumbens nor VTA endogenous <strong>GDNF</strong> mediates the incubation of heroin <b>craving</b>.
+GDNF	drug	alcohol	21040239	Noribogaine, but not 18 MC, exhibits similar actions as ibogaine on <strong>GDNF</strong> expression and <b>ethanol</b> self administration.
+GDNF	drug	psychedelics	21040239	Noribogaine, but not 18 MC, exhibits similar actions as <b>ibogaine</b> on <strong>GDNF</strong> expression and ethanol self administration.
+GDNF	drug	alcohol	21040239	Previously, we reported that the desirable actions of ibogaine to reduce self administration of, and relapse to, <b>alcohol</b> consumption are mediated via the upregulation of the expression of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in the midbrain ventral tegmental area (VTA), and the consequent activation of the <strong>GDNF</strong> pathway.
+GDNF	drug	psychedelics	21040239	Previously, we reported that the desirable actions of <b>ibogaine</b> to reduce self administration of, and relapse to, alcohol consumption are mediated via the upregulation of the expression of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in the midbrain ventral tegmental area (VTA), and the consequent activation of the <strong>GDNF</strong> pathway.
+GDNF	addiction	relapse	21040239	Previously, we reported that the desirable actions of ibogaine to reduce self administration of, and <b>relapse</b> to, alcohol consumption are mediated via the upregulation of the expression of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in the midbrain ventral tegmental area (VTA), and the consequent activation of the <strong>GDNF</strong> pathway.
+GDNF	drug	alcohol	21040239	Here, we determined whether noribogaine and/or 18 MC, like ibogaine, increase <strong>GDNF</strong> expression, and whether their site of action to reduce <b>alcohol</b> consumption is the VTA.
+GDNF	drug	psychedelics	21040239	Here, we determined whether noribogaine and/or 18 MC, like <b>ibogaine</b>, increase <strong>GDNF</strong> expression, and whether their site of action to reduce alcohol consumption is the VTA.
+GDNF	drug	psychedelics	21040239	We used SH SY5Y cells as a cell culture model and found that noribogaine, like <b>ibogaine</b>, but not 18 MC, induces a robust increase in <strong>GDNF</strong> mRNA levels.
+GDNF	drug	alcohol	20553781	BDNF and <strong>GDNF</strong> serum levels in <b>alcohol</b> dependent patients during withdrawal.
+GDNF	addiction	withdrawal	20553781	BDNF and <strong>GDNF</strong> serum levels in alcohol dependent patients during <b>withdrawal</b>.
+GDNF	addiction	addiction	20553781	Preclinical study results suggest that brain derived neurotrophic factor (BDNF) and glial cell line derived neurotrophic factor (<strong>GDNF</strong>) modulate <b>addictive</b> behaviour.
+GDNF	drug	alcohol	20553781	Therefore we investigated alterations in BDNF (81 male patients) and <strong>GDNF</strong> serum levels (52 male patients) in <b>alcohol</b> dependent patients during <b>alcohol</b> withdrawal (day 1, 7 and 14) in comparison to healthy controls (41 male controls).
+GDNF	addiction	withdrawal	20553781	Therefore we investigated alterations in BDNF (81 male patients) and <strong>GDNF</strong> serum levels (52 male patients) in alcohol dependent patients during alcohol <b>withdrawal</b> (day 1, 7 and 14) in comparison to healthy controls (41 male controls).
+GDNF	drug	alcohol	20553781	<strong>GDNF</strong> serum levels were significantly reduced in the <b>alcohol</b> dependent patients (p<0.001).
+GDNF	drug	alcohol	20553781	BDNF (p=0.265) and <strong>GDNF</strong> (p=0.255) serum levels did not change significantly during <b>alcohol</b> withdrawal.
+GDNF	addiction	withdrawal	20553781	BDNF (p=0.265) and <strong>GDNF</strong> (p=0.255) serum levels did not change significantly during alcohol <b>withdrawal</b>.
+GDNF	drug	alcohol	20553781	<strong>GDNF</strong> serum levels were significantly negatively associated with individual estimation of <b>alcohol</b> tolerance (SESA XT score, p=0.028).
+GDNF	drug	alcohol	20553781	In conclusion we found that <strong>GDNF</strong> serum levels are significantly reduced in <b>alcohol</b> dependent patients.
+GDNF	drug	alcohol	20553781	<strong>GDNF</strong> serum levels were negatively associated with <b>alcohol</b> tolerance.
+GDNF	drug	cannabinoid	20482506	A variety of systems have been investigated, such as the <b>endocannabinoid</b> system, modulators of glutamatergic transmission, corticotropin releasing factor (CRF), neuropeptide Y (NPY), nociceptin, glial cell line derived neurotrophic factor (<strong>GDNF</strong>), acetaldehyde (ACD), substance P and Neurokinin 1 (NK1) receptor, nicotinic acetylcholine receptors (nAchRs), alpha adrenergic receptor, and many others.
+GDNF	drug	amphetamine	20399770	Human brain microglial activation has been linked with <b>methamphetamine</b> abuse, and inhibitors of glial cell activation, certain phosphodiesterase (PDE) inhibitors, and glial cell derived neurotrophic factor (<strong>GDNF</strong>) have been reported to modulate drug abuse effects.
+GDNF	drug	amphetamine	20399770	Human brain microglial activation has been linked with <b>methamphetamine</b> abuse, and inhibitors of glial cell activation, certain phosphodiesterase (PDE) inhibitors, and <strong>glial cell derived neurotrophic factor</strong> (<strong>GDNF</strong>) have been reported to modulate drug abuse effects.
+GDNF	drug	amphetamine	20399770	Our objective was to determine whether the glial cell attenuator, 3 isobutyryl 2 isopropylpyrazolo [1,5 a]pyridine (AV411, ibudilast), a non selective PDE inhibitor and promoter of <strong>GDNF</strong>, could reduce stress  and <b>methamphetamine</b> prime induced reinstatement of <b>methamphetamine</b> seeking behavior.
+GDNF	addiction	relapse	20399770	Our objective was to determine whether the glial cell attenuator, 3 isobutyryl 2 isopropylpyrazolo [1,5 a]pyridine (AV411, ibudilast), a non selective PDE inhibitor and promoter of <strong>GDNF</strong>, could reduce stress  and methamphetamine prime induced <b>reinstatement</b> of methamphetamine <b>seeking</b> behavior.
+GDNF	drug	opioid	19995896	Moreover, <b>morphine</b> treatment significantly inhibited the S. pneumoniae induced phosphorylation of interferon response factor 3 (IRF3), <strong>ATF2</strong>, and NF kappaBp65.
+GDNF	drug	amphetamine	19562947	We have demonstrated that systemic administration of dipeptide Leu Ile increases BDNF and <strong>GDNF</strong> production in the brain, and has a protective role in <b>methamphetamine</b> and morphine dependence.
+GDNF	drug	opioid	19562947	We have demonstrated that systemic administration of dipeptide Leu Ile increases BDNF and <strong>GDNF</strong> production in the brain, and has a protective role in methamphetamine and <b>morphine</b> dependence.
+GDNF	addiction	dependence	19562947	We have demonstrated that systemic administration of dipeptide Leu Ile increases BDNF and <strong>GDNF</strong> production in the brain, and has a protective role in methamphetamine and morphine <b>dependence</b>.
+GDNF	drug	cocaine	19345340	Here, we studied the role of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in incubation of <b>cocaine</b> craving because, like BDNF, <strong>GDNF</strong> provides trophic support to midbrain dopamine neurons.
+GDNF	addiction	relapse	19345340	Here, we studied the role of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in incubation of cocaine <b>craving</b> because, like BDNF, <strong>GDNF</strong> provides trophic support to midbrain dopamine neurons.
+GDNF	drug	cocaine	19345340	We then manipulated VTA <strong>GDNF</strong> function and assessed cue induced <b>cocaine</b> seeking in extinction tests after withdrawal from <b>cocaine</b>.
+GDNF	addiction	relapse	19345340	We then manipulated VTA <strong>GDNF</strong> function and assessed cue induced cocaine <b>seeking</b> in extinction tests after withdrawal from cocaine.
+GDNF	addiction	withdrawal	19345340	We then manipulated VTA <strong>GDNF</strong> function and assessed cue induced cocaine seeking in extinction tests after <b>withdrawal</b> from cocaine.
+GDNF	drug	cocaine	19345340	VTA injections of an adeno associated virus (AAV) vector containing rat <strong>GDNF</strong> cDNA (5 x 10(8) viral genomes) on withdrawal Day 1 increased cue induced <b>cocaine</b> seeking on withdrawal days 11 and 31; this effect was not observed after VTA injections of an AAV viral vector containing red fluorescent protein (RFP).
+GDNF	addiction	relapse	19345340	VTA injections of an adeno associated virus (AAV) vector containing rat <strong>GDNF</strong> cDNA (5 x 10(8) viral genomes) on withdrawal Day 1 increased cue induced cocaine <b>seeking</b> on withdrawal days 11 and 31; this effect was not observed after VTA injections of an AAV viral vector containing red fluorescent protein (RFP).
+GDNF	addiction	withdrawal	19345340	VTA injections of an adeno associated virus (AAV) vector containing rat <strong>GDNF</strong> cDNA (5 x 10(8) viral genomes) on <b>withdrawal</b> Day 1 increased cue induced cocaine seeking on <b>withdrawal</b> days 11 and 31; this effect was not observed after VTA injections of an AAV viral vector containing red fluorescent protein (RFP).
+GDNF	drug	cocaine	19345340	Additionally, VTA, but not substantial nigra (SN), <strong>GDNF</strong> injections (1.25 microg or 12.5 microg/side) immediately after the last <b>cocaine</b> self administration session increased cue induced drug seeking on withdrawal days 3 and 10; this effect was reversed by VTA injections of U0126, which inhibits the activity of extracellular signal regulated kinases (ERK).
+GDNF	addiction	relapse	19345340	Additionally, VTA, but not substantial nigra (SN), <strong>GDNF</strong> injections (1.25 microg or 12.5 microg/side) immediately after the last cocaine self administration session increased cue induced drug <b>seeking</b> on withdrawal days 3 and 10; this effect was reversed by VTA injections of U0126, which inhibits the activity of extracellular signal regulated kinases (ERK).
+GDNF	addiction	withdrawal	19345340	Additionally, VTA, but not substantial nigra (SN), <strong>GDNF</strong> injections (1.25 microg or 12.5 microg/side) immediately after the last cocaine self administration session increased cue induced drug seeking on <b>withdrawal</b> days 3 and 10; this effect was reversed by VTA injections of U0126, which inhibits the activity of extracellular signal regulated kinases (ERK).
+GDNF	drug	cocaine	19345340	Finally, interfering with VTA <strong>GDNF</strong> function by chronic delivery of anti <strong>GDNF</strong> monoclonal neutralizing antibodies via minipumps (600 ng/side/d) during withdrawal Days 1 14 prevented the time dependent increases in cue induced <b>cocaine</b> seeking on withdrawal days 11 and 31.
+GDNF	addiction	relapse	19345340	Finally, interfering with VTA <strong>GDNF</strong> function by chronic delivery of anti <strong>GDNF</strong> monoclonal neutralizing antibodies via minipumps (600 ng/side/d) during withdrawal Days 1 14 prevented the time dependent increases in cue induced cocaine <b>seeking</b> on withdrawal days 11 and 31.
+GDNF	addiction	withdrawal	19345340	Finally, interfering with VTA <strong>GDNF</strong> function by chronic delivery of anti <strong>GDNF</strong> monoclonal neutralizing antibodies via minipumps (600 ng/side/d) during <b>withdrawal</b> Days 1 14 prevented the time dependent increases in cue induced cocaine seeking on <b>withdrawal</b> days 11 and 31.
+GDNF	drug	cocaine	19345340	Our results indicate that during the first weeks of withdrawal from <b>cocaine</b> self administration, <strong>GDNF</strong> dependent neuroadaptations in midbrain VTA neurons play an important role in the development of incubation of <b>cocaine</b> craving.
+GDNF	addiction	relapse	19345340	Our results indicate that during the first weeks of withdrawal from cocaine self administration, <strong>GDNF</strong> dependent neuroadaptations in midbrain VTA neurons play an important role in the development of incubation of cocaine <b>craving</b>.
+GDNF	addiction	withdrawal	19345340	Our results indicate that during the first weeks of <b>withdrawal</b> from cocaine self administration, <strong>GDNF</strong> dependent neuroadaptations in midbrain VTA neurons play an important role in the development of incubation of cocaine craving.
+GDNF	drug	alcohol	19302086	<strong>GDNF</strong> is an endogenous negative regulator of <b>ethanol</b> mediated reward and of <b>ethanol</b> consumption after a period of abstinence.
+GDNF	addiction	reward	19302086	<strong>GDNF</strong> is an endogenous negative regulator of ethanol mediated <b>reward</b> and of ethanol consumption after a period of abstinence.
+GDNF	drug	alcohol	19302086	We previously found that activation of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) pathway in the ventral tegmental area (VTA) reduces <b>ethanol</b> drinking behaviors.
+GDNF	drug	alcohol	19302086	In this study, we set out to assess the contribution of endogenous <strong>GDNF</strong> or its receptor GFRalpha1 to the regulation of <b>ethanol</b> related behaviors.
+GDNF	drug	alcohol	19302086	We observed no differences between the <strong>GDNF</strong> HET and WT mice in the level of locomotor activity or in sensitization to <b>ethanol</b> induced hyperlocomotion after systemic injection of a nonhypnotic dose of <b>ethanol</b> and in BEC.
+GDNF	addiction	sensitization	19302086	We observed no differences between the <strong>GDNF</strong> HET and WT mice in the level of locomotor activity or in <b>sensitization</b> to ethanol induced hyperlocomotion after systemic injection of a nonhypnotic dose of ethanol and in BEC.
+GDNF	drug	alcohol	19302086	However, <strong>GDNF</strong> and GFRalpha1 mice exhibited increased place preference to <b>ethanol</b> as compared with their WT littermates.
+GDNF	drug	alcohol	19302086	The levels of voluntary <b>ethanol</b> or quinine consumption were similar in the <strong>GDNF</strong> HET and WT mice, however, a small but significant increase in saccharin intake was observed in the <strong>GDNF</strong> HET mice.
+GDNF	drug	alcohol	19302086	Interestingly, however, both the <strong>GDNF</strong> and GFRalpha1 HET mice consumed much larger quantities of <b>ethanol</b> after a period of abstinence from <b>ethanol</b> as compared with their WT littermates.
+GDNF	drug	alcohol	19302086	Furthermore, the increase in <b>ethanol</b> consumption after abstinence was found to be specific for <b>ethanol</b> as similar levels of saccharin intake were measured in the <strong>GDNF</strong> and GFRalpha1 HET and WT mice after abstinence.
+GDNF	drug	alcohol	19302086	Our results suggest that endogenous <strong>GDNF</strong> negatively regulates the rewarding effect of <b>ethanol</b> and <b>ethanol</b> drinking behaviors after a period of abstinence.
+GDNF	drug	alcohol	19232578	We recently showed that <strong>GDNF</strong> in the ventral tegmental area (VTA) reduces the motivation to consume <b>alcohol</b>.
+GDNF	drug	alcohol	19232578	We therefore set out to determine whether cabergoline administration decreases <b>alcohol</b> drinking and  seeking behaviors via <strong>GDNF</strong>.
+GDNF	addiction	relapse	19232578	We therefore set out to determine whether cabergoline administration decreases alcohol drinking and  <b>seeking</b> behaviors via <strong>GDNF</strong>.
+GDNF	drug	alcohol	19232578	Finally, the increase in <strong>GDNF</strong> expression and the decrease in <b>alcohol</b> consumption by cabergoline were abolished in <strong>GDNF</strong> heterozygous knockout mice.
+GDNF	drug	alcohol	19232578	Together, these findings suggest that cabergoline mediated upregulation of the <strong>GDNF</strong> pathway attenuates <b>alcohol</b> drinking behaviors and relapse.
+GDNF	addiction	relapse	19232578	Together, these findings suggest that cabergoline mediated upregulation of the <strong>GDNF</strong> pathway attenuates alcohol drinking behaviors and <b>relapse</b>.
+GDNF	drug	alcohol	19185208	We previously found that activation of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) pathway in the ventral tegmental area (VTA) reduces moderate <b>alcohol</b> (<b>ethanol</b>) intake in a rat operant self administration paradigm.
+GDNF	addiction	reward	19185208	We previously found that activation of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) pathway in the ventral tegmental area (VTA) reduces moderate alcohol (ethanol) intake in a rat <b>operant</b> self administration paradigm.
+GDNF	drug	alcohol	19185208	Here, we set out to assess the effect of <strong>GDNF</strong> in the VTA on excessive voluntary consumption of <b>ethanol</b>.
+GDNF	drug	alcohol	19185208	The rats were given three 24 h sessions per week, and <strong>GDNF</strong>'s actions were measured when rats achieved a baseline of <b>ethanol</b> consumption of 5.5g/kg/24h.
+GDNF	drug	alcohol	19185208	We found that microinjection of <strong>GDNF</strong> into the VTA 10min before the beginning of an <b>ethanol</b> drinking session significantly reduced <b>ethanol</b> intake and preference, but did not affect total fluid intake.
+GDNF	drug	alcohol	19185208	We further show that <strong>GDNF</strong> greatly decreased both the first bout of excessive <b>ethanol</b> intake at the beginning of the session, and the later consummatory activity occurring during the dark cycle.
+GDNF	drug	alcohol	19185208	These data suggest that <strong>GDNF</strong> is a rapid and long lasting inhibitor of "binge like" <b>ethanol</b> consumption.
+GDNF	addiction	intoxication	19185208	These data suggest that <strong>GDNF</strong> is a rapid and long lasting inhibitor of "<b>binge</b> like" ethanol consumption.
+GDNF	drug	amphetamine	19110059	Minocycline restores striatal tyrosine hydroxylase in <strong>GDNF</strong> heterozygous mice but not in <b>methamphetamine</b> treated mice.
+GDNF	drug	amphetamine	19110059	Microglial activation in the substantia nigra and a tyrosine hydroxylase deficit in the striatum of 3 month old <strong>GDNF</strong> heterozygous (<strong>GDNF</strong>(+/ )) mice were previously reported and both were exacerbated by a toxic <b>methamphetamine</b> binge.
+GDNF	addiction	intoxication	19110059	Microglial activation in the substantia nigra and a tyrosine hydroxylase deficit in the striatum of 3 month old <strong>GDNF</strong> heterozygous (<strong>GDNF</strong>(+/ )) mice were previously reported and both were exacerbated by a toxic methamphetamine <b>binge</b>.
+GDNF	drug	amphetamine	19110059	Minocycline (45 mg/kg, i.p.x 14 days post <b>methamphetamine</b> or saline injections) reduced microglial activation and phospho p38 MAPK in the substantia nigra of saline treated <strong>GDNF</strong>(+/ ) mice and in <b>methamphetamine</b> treated wildtype and <strong>GDNF</strong>(+/ ) mice.
+GDNF	drug	amphetamine	19110059	Although minocycline increased tyrosine hydroxylase immunoreactivity in <strong>GDNF</strong>(+/ ) mice, it did not attenuate the <b>methamphetamine</b> induced reduction of tyrosine hydroxylase.
+GDNF	drug	amphetamine	19110059	The results suggest that neuroinflammation is deleterious to the dopamine system of <strong>GDNF</strong>(+/ ) mice but is not the primary cause of <b>methamphetamine</b> induced damage to the dopamine system in either <strong>GDNF</strong>(+/ ) or wildtype mice.
+GDNF	drug	alcohol	18541917	<strong>GDNF</strong> is a fast acting potent inhibitor of <b>alcohol</b> consumption and relapse.
+GDNF	addiction	relapse	18541917	<strong>GDNF</strong> is a fast acting potent inhibitor of alcohol consumption and <b>relapse</b>.
+GDNF	drug	alcohol	18541917	Previously, we demonstrated that the action of the natural alkaloid, ibogaine, to reduce <b>alcohol</b> (<b>ethanol</b>) consumption is mediated by the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in the ventral tegmental area (VTA).
+GDNF	drug	psychedelics	18541917	Previously, we demonstrated that the action of the natural alkaloid, <b>ibogaine</b>, to reduce alcohol (ethanol) consumption is mediated by the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in the ventral tegmental area (VTA).
+GDNF	drug	alcohol	18541917	Here we set out to test the actions of <strong>GDNF</strong> in the VTA on <b>ethanol</b> drinking behaviors.
+GDNF	drug	alcohol	18541917	We found that <strong>GDNF</strong> infusion very rapidly and dose dependently reduced rat <b>ethanol</b>, but not sucrose, operant self administration.
+GDNF	addiction	reward	18541917	We found that <strong>GDNF</strong> infusion very rapidly and dose dependently reduced rat ethanol, but not sucrose, <b>operant</b> self administration.
+GDNF	drug	alcohol	18541917	A <strong>GDNF</strong> mediated decrease in <b>ethanol</b> consumption was also observed in rats with a history of high voluntary <b>ethanol</b> intake.
+GDNF	drug	alcohol	18541917	We found that the action of <strong>GDNF</strong> on <b>ethanol</b> consumption was specific to the VTA as infusion of the growth factor into the neighboring substantia nigra did not affect operant responses for <b>ethanol</b>.
+GDNF	addiction	reward	18541917	We found that the action of <strong>GDNF</strong> on ethanol consumption was specific to the VTA as infusion of the growth factor into the neighboring substantia nigra did not affect <b>operant</b> responses for ethanol.
+GDNF	drug	alcohol	18541917	We further show that intra VTA <strong>GDNF</strong> administration rapidly activated the MAPK signaling pathway in the VTA and that inhibition of the MAPK pathway in the VTA blocked the reduction of <b>ethanol</b> self administration by <strong>GDNF</strong>.
+GDNF	addiction	relapse	18541917	Importantly, we demonstrate that <strong>GDNF</strong> infused into the VTA alters rats' responses in a model of <b>relapse</b>.
+GDNF	drug	alcohol	18541917	Specifically, <strong>GDNF</strong> application blocked reacquisition of <b>ethanol</b> self administration after extinction.
+GDNF	drug	alcohol	18541917	Together, these results suggest that <strong>GDNF</strong>, via activation of the MAPK pathway, is a fast acting selective agent to reduce the motivation to consume and seek <b>alcohol</b>.
+GDNF	drug	amphetamine	17699663	Administration of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) protects dopamine neurons from the toxic effects of <b>methamphetamine</b> in animal models.
+GDNF	drug	amphetamine	17699663	Therefore, we hypothesized that a partial <strong>GDNF</strong> gene deletion would increase the susceptibility of mice to <b>methamphetamine</b> neurotoxicity during young adulthood and possibly increase age related deterioration of behavior and dopamine function.
+GDNF	drug	amphetamine	17699663	Two weeks after a <b>methamphetamine</b> binge (4 x 10 mg/kg, i.p., at 2 h intervals), <strong>GDNF</strong>(+/ ) mice had a significantly greater reduction of tyrosine hydroxylase immunoreactivity in the medial striatum, a proportionally greater depletion of dopamine and 3,4 dihydroxyphenylacetic acid (DOPAC) levels in the striatum, and a greater increase in activated microglia in the substantia nigra than wild type mice.
+GDNF	addiction	intoxication	17699663	Two weeks after a methamphetamine <b>binge</b> (4 x 10 mg/kg, i.p., at 2 h intervals), <strong>GDNF</strong>(+/ ) mice had a significantly greater reduction of tyrosine hydroxylase immunoreactivity in the medial striatum, a proportionally greater depletion of dopamine and 3,4 dihydroxyphenylacetic acid (DOPAC) levels in the striatum, and a greater increase in activated microglia in the substantia nigra than wild type mice.
+GDNF	drug	amphetamine	17699663	At 12 months of age, <b>methamphetamine</b> treated <strong>GDNF</strong>(+/ ) mice exhibited less motor activity and lower levels of tyrosine hydroxylase immunoreactivity, dopamine, DOPAC, and serotonin than wild type mice.
+GDNF	drug	amphetamine	17699663	Greater striatal dopamine transporter activity in <strong>GDNF</strong>(+/ ) mice may underlie their differential response to <b>methamphetamine</b>.
+GDNF	drug	amphetamine	17699663	These data suggest the possibility that <b>methamphetamine</b> use in young adults, when combined with lower levels of <strong>GDNF</strong> throughout life, may precipitate the appearance of parkinsonian like behaviors during aging.
+GDNF	addiction	dependence	17538232	In this article, the roles of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) and tumor necrosis factor alpha (TNF alpha) in drug <b>dependence</b> are discussed.
+GDNF	drug	cocaine	17538232	<strong>GDNF</strong> inhibits the <b>cocaine</b> induced upregulation of tyrosine hydroxylase activity in the ventral tegmental area and blocks behavioral responses to <b>cocaine</b>.
+GDNF	addiction	dependence	17538232	Moreover, we mentioned the potential of Leu Ile, which induces the expression of <strong>GDNF</strong> and TNF alpha, as a novel therapeutic agent for drug <b>dependence</b>.
+GDNF	drug	amphetamine	17538232	The inhibitory effect of Leu Ile on <b>METH</b>  or MOR induced place preference is not observed in <strong>GDNF</strong> heterozygous and TNF alpha knockout mice.
+GDNF	drug	amphetamine	17538232	Leu Ile inhibits <b>METH</b>  or MOR induced place preference and sensitization by attenuating the <b>METH</b>  or MOR induced increase in extracellular dopamine levels in the nucleus accumbens via the induction of <strong>GDNF</strong> and TNF alpha expression.
+GDNF	addiction	sensitization	17538232	Leu Ile inhibits METH  or MOR induced place preference and <b>sensitization</b> by attenuating the METH  or MOR induced increase in extracellular dopamine levels in the nucleus accumbens via the induction of <strong>GDNF</strong> and TNF alpha expression.
+GDNF	drug	amphetamine	17356005	Using a mouse model of reinstatement, which models relapse of drug seeking behavior in addicts, we provide evidence that a partial reduction in the expression of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) potentiates <b>methamphetamine</b> (<b>METH</b>) self administration, enhances motivation to take <b>METH</b>, increases vulnerability to drug primed reinstatement, and prolongs cue induced reinstatement of extinguished <b>METH</b> seeking behavior.
+GDNF	addiction	relapse	17356005	Using a mouse model of <b>reinstatement</b>, which models <b>relapse</b> of drug <b>seeking</b> behavior in addicts, we provide evidence that a partial reduction in the expression of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) potentiates methamphetamine (METH) self administration, enhances motivation to take METH, increases vulnerability to drug primed <b>reinstatement</b>, and prolongs cue induced <b>reinstatement</b> of extinguished METH <b>seeking</b> behavior.
+GDNF	drug	amphetamine	17356005	In contrast, there was no significant difference in novelty responses, <b>METH</b> stimulated hyperlocomotion and locomotor sensitization, food reinforced operant behavior and motivation, or reinstatement of food seeking behavior between <strong>GDNF</strong> heterozygous knockout mice and wild type littermates.
+GDNF	addiction	relapse	17356005	In contrast, there was no significant difference in novelty responses, METH stimulated hyperlocomotion and locomotor sensitization, food reinforced operant behavior and motivation, or <b>reinstatement</b> of food <b>seeking</b> behavior between <strong>GDNF</strong> heterozygous knockout mice and wild type littermates.
+GDNF	addiction	reward	17356005	In contrast, there was no significant difference in novelty responses, METH stimulated hyperlocomotion and locomotor sensitization, food reinforced <b>operant</b> behavior and motivation, or reinstatement of food seeking behavior between <strong>GDNF</strong> heterozygous knockout mice and wild type littermates.
+GDNF	addiction	sensitization	17356005	In contrast, there was no significant difference in novelty responses, METH stimulated hyperlocomotion and locomotor <b>sensitization</b>, food reinforced operant behavior and motivation, or reinstatement of food seeking behavior between <strong>GDNF</strong> heterozygous knockout mice and wild type littermates.
+GDNF	drug	amphetamine	17356005	These findings suggest that <strong>GDNF</strong> may be associated with enduring vulnerability to reinstatement of <b>METH</b> seeking behavior and a potential target in the development of therapies to control relapse.
+GDNF	addiction	relapse	17356005	These findings suggest that <strong>GDNF</strong> may be associated with enduring vulnerability to <b>reinstatement</b> of METH <b>seeking</b> behavior and a potential target in the development of therapies to control <b>relapse</b>.
+GDNF	drug	amphetamine	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only tumor necrosis factor alpha (TNF alpha) but also glial cell line derived neurotrophic factor (<strong>GDNF</strong>), inhibits <b>methamphetamine</b> (<b>METH</b>) and morphine (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of TNF alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for <b>METH</b> and MOR induced dependence.
+GDNF	drug	opioid	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only tumor necrosis factor alpha (TNF alpha) but also glial cell line derived neurotrophic factor (<strong>GDNF</strong>), inhibits methamphetamine (METH) and <b>morphine</b> (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of TNF alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced dependence.
+GDNF	addiction	dependence	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only tumor necrosis factor alpha (TNF alpha) but also glial cell line derived neurotrophic factor (<strong>GDNF</strong>), inhibits methamphetamine (METH) and morphine (MOR) induced sensitization and rewarding effects by regulating extracellular dopamine levels via the induction of TNF alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced <b>dependence</b>.
+GDNF	addiction	sensitization	17331595	We have previously demonstrated that Leu Ile, which induces the expression of not only tumor necrosis factor alpha (TNF alpha) but also glial cell line derived neurotrophic factor (<strong>GDNF</strong>), inhibits methamphetamine (METH) and morphine (MOR) induced <b>sensitization</b> and rewarding effects by regulating extracellular dopamine levels via the induction of TNF alpha expression, and indicated the potential of Leu Ile as a novel therapeutic agent for METH and MOR induced dependence.
+GDNF	addiction	sensitization	17331595	In the present study, we investigated the involvement of <strong>GDNF</strong> in inhibitory effects of Leu Ile on MOR induced <b>sensitization</b> and rewarding effects.
+GDNF	addiction	sensitization	17331595	Repeated treatment with MOR for 9 days, which results in an enhancement of the locomotor stimulating effects (<b>sensitization</b>) of MOR, increased <strong>GDNF</strong> levels in the nucleus accumbens compared with those in saline treated mice.
+GDNF	addiction	sensitization	17331595	These results suggest that <strong>GDNF</strong> is involved in the inhibitory effects of Leu Ile on MOR induced <b>sensitization</b> and rewarding effects.
+GDNF	drug	amphetamine	17046726	We investigated the potential of Leu Ile, which induces the expression of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) and tumor necrosis factor alpha (TNF alpha), as a novel therapeutic agent for <b>methamphetamine</b> (<b>METH</b>) induced dependence.
+GDNF	addiction	dependence	17046726	We investigated the potential of Leu Ile, which induces the expression of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) and tumor necrosis factor alpha (TNF alpha), as a novel therapeutic agent for methamphetamine (METH) induced <b>dependence</b>.
+GDNF	drug	amphetamine	17046726	An inhibitory effect of Leu Ile on <b>METH</b> induced place preference was observed in neither <strong>GDNF</strong> heterozygous nor TNF alpha knockout mice.
+GDNF	drug	amphetamine	17046726	These results suggest that Leu Ile inhibits <b>METH</b> induced rewarding effects and sensitization by regulating extracellular DA levels via the induction of <strong>GDNF</strong> and TNF alpha expression.
+GDNF	addiction	sensitization	17046726	These results suggest that Leu Ile inhibits METH induced rewarding effects and <b>sensitization</b> by regulating extracellular DA levels via the induction of <strong>GDNF</strong> and TNF alpha expression.
+GDNF	drug	alcohol	17023388	We recently showed that the up regulation of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) pathway in the midbrain, is the molecular mechanism by which the putative anti addiction drug Ibogaine mediates its desirable action of reducing <b>alcohol</b> consumption.
+GDNF	drug	psychedelics	17023388	We recently showed that the up regulation of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) pathway in the midbrain, is the molecular mechanism by which the putative anti addiction drug <b>Ibogaine</b> mediates its desirable action of reducing alcohol consumption.
+GDNF	addiction	addiction	17023388	We recently showed that the up regulation of the glial cell line derived neurotrophic factor (<strong>GDNF</strong>) pathway in the midbrain, is the molecular mechanism by which the putative anti <b>addiction</b> drug Ibogaine mediates its desirable action of reducing alcohol consumption.
+GDNF	drug	psychedelics	17023388	Here we determine whether, and how, <b>Ibogaine</b> exerts its long lasting actions on <strong>GDNF</strong> expression and signaling.
+GDNF	drug	psychedelics	17023388	Using the dopaminergic like SHSY5Y cell line as a culture model, we observed that short term <b>Ibogaine</b> exposure results in a sustained increase in <strong>GDNF</strong> expression that is mediated via the induction of a long lasting autoregulatory cycle by which <strong>GDNF</strong> positively regulates its own expression.
+GDNF	drug	psychedelics	17023388	We show that the initial exposure of cells to <b>Ibogaine</b> or <strong>GDNF</strong> results in an increase in <strong>GDNF</strong> mRNA, leading to protein expression and to the corresponding activation of the <strong>GDNF</strong> signaling pathway.
+GDNF	addiction	addiction	17023388	The identification of a <strong>GDNF</strong> mediated, autoregulatory long lasting feedback loop could have important implications for <strong>GDNF</strong>'s potential value as a treatment for <b>addiction</b> and neurodegenerative diseases.
+GDNF	drug	opioid	16879618	To study the effects of reduced <strong>GDNF</strong> on dopaminergic behaviour related to addiction, we compared the effects of <b>morphine</b> on locomotor activity, conditioned place preference (CPP) and extracellular accumbal dopamine in heterozygous <strong>GDNF</strong> knockout mice (<strong>GDNF</strong>+/ ) with those in their wild type (Wt) littermates.
+GDNF	addiction	addiction	16879618	To study the effects of reduced <strong>GDNF</strong> on dopaminergic behaviour related to <b>addiction</b>, we compared the effects of morphine on locomotor activity, conditioned place preference (CPP) and extracellular accumbal dopamine in heterozygous <strong>GDNF</strong> knockout mice (<strong>GDNF</strong>+/ ) with those in their wild type (Wt) littermates.
+GDNF	addiction	reward	16879618	To study the effects of reduced <strong>GDNF</strong> on dopaminergic behaviour related to addiction, we compared the effects of morphine on locomotor activity, conditioned place preference (<b>CPP</b>) and extracellular accumbal dopamine in heterozygous <strong>GDNF</strong> knockout mice (<strong>GDNF</strong>+/ ) with those in their wild type (Wt) littermates.
+GDNF	drug	opioid	16879618	When <b>morphine</b> 30 mg/kg was administered daily for 4 days, tolerance developed towards its locomotor stimulatory action only in the <strong>GDNF</strong>+/  mice.
+GDNF	drug	opioid	16879618	A <b>morphine</b> 5 mg/kg challenge dose stimulated locomotor activity only in the <strong>GDNF</strong>+/  mice withdrawn for 96 h from repeated <b>morphine</b> treatment, whereas clear and similar sensitization of the locomotor response was seen after a 10 mg/kg challenge dose in mice of both genotypes.
+GDNF	addiction	sensitization	16879618	A morphine 5 mg/kg challenge dose stimulated locomotor activity only in the <strong>GDNF</strong>+/  mice withdrawn for 96 h from repeated morphine treatment, whereas clear and similar <b>sensitization</b> of the locomotor response was seen after a 10 mg/kg challenge dose in mice of both genotypes.
+GDNF	drug	opioid	16879618	<b>Morphine</b> induced CPP developed initially similarly in Wt and <strong>GDNF</strong>+/  mice, but it lasted longer in the Wt mice.
+GDNF	addiction	reward	16879618	Morphine induced <b>CPP</b> developed initially similarly in Wt and <strong>GDNF</strong>+/  mice, but it lasted longer in the Wt mice.
+GDNF	drug	opioid	16879618	The small challenge dose of <b>morphine</b> increased accumbal dopamine output slightly more in the <strong>GDNF</strong>+/  mice than in the Wt mice, but doubling the challenge dose caused a dose dependent response only in the Wt mice.
+GDNF	drug	opioid	16879618	In addition, repeated <b>morphine</b> treatment counteracted the increase in the accumbal extracellular dopamine concentration we previously found in drug naive <strong>GDNF</strong>+/  mice.
+GDNF	drug	opioid	16879618	Thus, reduced endogenous <strong>GDNF</strong> level alters the dopaminergic behavioural effects to repeatedly administered <b>morphine</b>, emphasizing the involvement of <strong>GDNF</strong> in the neuroplastic changes related to long term effects of drugs of abuse.
+GDNF	addiction	addiction	16519005	<strong>GDNF</strong> and <b>addiction</b>.
+GDNF	drug	alcohol	16519005	Behavioral effects of drugs of abuse such as cocaine and <b>alcohol</b> are also negatively regulated by <strong>GDNF</strong>: inhibition of the endogenous <strong>GDNF</strong> pathway enhances the activity of drugs of abuse, while administration of <strong>GDNF</strong> reduces the severity of the effects.
+GDNF	drug	cocaine	16519005	Behavioral effects of drugs of abuse such as <b>cocaine</b> and alcohol are also negatively regulated by <strong>GDNF</strong>: inhibition of the endogenous <strong>GDNF</strong> pathway enhances the activity of drugs of abuse, while administration of <strong>GDNF</strong> reduces the severity of the effects.
+GDNF	drug	alcohol	16519005	In this review, we summarize the data implicating <strong>GDNF</strong> as a negative regulator of drug and <b>alcohol</b> addiction.
+GDNF	addiction	addiction	16519005	In this review, we summarize the data implicating <strong>GDNF</strong> as a negative regulator of drug and alcohol <b>addiction</b>.
+GDNF	drug	alcohol	16519005	We also provide evidence to suggest that therapies that activate <strong>GDNF</strong> signaling may be useful for the treatment of drug and <b>alcohol</b> addiction.
+GDNF	addiction	addiction	16519005	We also provide evidence to suggest that therapies that activate <strong>GDNF</strong> signaling may be useful for the treatment of drug and alcohol <b>addiction</b>.
+GDNF	drug	alcohol	16441270	BIG news in <b>alcohol</b> addiction: new findings on growth factor pathways BDNF, insulin, and <strong>GDNF</strong>.
+GDNF	addiction	addiction	16441270	BIG news in alcohol <b>addiction</b>: new findings on growth factor pathways BDNF, insulin, and <strong>GDNF</strong>.
+GDNF	drug	alcohol	16441270	The 4 speakers showed that the behavioral effects of <b>alcohol</b> in the adult are regulated by 3 growth factors, insulin, glial cell line derived neurotrophic factor (<strong>GDNF</strong>), and brain derived neurotrophic factor (BDNF).
+GDNF	drug	alcohol	16441270	Finally, Dr. Janak presented evidence that increases in the expression of <strong>GDNF</strong> in the midbrain reduce <b>alcohol</b> self administration in rats.
+GDNF	addiction	reward	16364262	Partial deletion of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in mice: Effects on sucrose <b>reward</b> and striatal <strong>GDNF</strong> concentrations.
+GDNF	drug	alcohol	16364262	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) has been reported to alter the reward value of abused substances such as <b>alcohol</b> and cocaine as well as neural circuitry underlying reward.
+GDNF	drug	cocaine	16364262	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) has been reported to alter the reward value of abused substances such as alcohol and <b>cocaine</b> as well as neural circuitry underlying reward.
+GDNF	addiction	reward	16364262	Glial cell line derived neurotrophic factor (<strong>GDNF</strong>) has been reported to alter the <b>reward</b> value of abused substances such as alcohol and cocaine as well as neural circuitry underlying <b>reward</b>.
+GDNF	addiction	reward	16364262	The role of <strong>GDNF</strong> in <b>reward</b> was further characterized in the present study using <b>operant</b> procedures to determine the value of a natural <b>reward</b>, sucrose, in <strong>GDNF</strong> heterozygous (<strong>GDNF</strong>+/ ) mice versus wild type (WT) mice.
+GDNF	addiction	reward	16364262	<strong>GDNF</strong>+/  mice emitted more responses than WT mice for sucrose, suggesting enhanced <b>reward</b> value of sucrose in these mice.
+GDNF	addiction	reward	16364262	Together, the results are consistent with an emerging literature indicating that reduced <strong>GDNF</strong> levels augment <b>reward</b> and increased <strong>GDNF</strong> levels attenuate <b>reward</b>, suggesting that <strong>GDNF</strong> plays an important role in neural systems mediating <b>reward</b>.
+GDNF	drug	opioid	16044914	[Intrathecal injection of muscarinic receptors or <strong>GDNF</strong> antisense oligonucleotides inhibits the increase of c Fos expression in locus coeruleus of <b>morphine</b> withdrawal rats].
+GDNF	addiction	withdrawal	16044914	[Intrathecal injection of muscarinic receptors or <strong>GDNF</strong> antisense oligonucleotides inhibits the increase of c Fos expression in locus coeruleus of morphine <b>withdrawal</b> rats].
+GDNF	drug	opioid	16044914	The antisense approach and immunohistochemistry were used to study the effects of different muscarinic receptor (M) subtypes and glial cell derived neurotrophic factor (<strong>GDNF</strong>) on the scores of <b>morphine</b> withdrawal syndrome and the expression of c Fos in locus coeruleus (LC).
+GDNF	addiction	withdrawal	16044914	The antisense approach and immunohistochemistry were used to study the effects of different muscarinic receptor (M) subtypes and glial cell derived neurotrophic factor (<strong>GDNF</strong>) on the scores of morphine <b>withdrawal</b> syndrome and the expression of c Fos in locus coeruleus (LC).
+GDNF	drug	opioid	16044914	The antisense approach and immunohistochemistry were used to study the effects of different muscarinic receptor (M) subtypes and <strong>glial cell derived neurotrophic factor</strong> (<strong>GDNF</strong>) on the scores of <b>morphine</b> withdrawal syndrome and the expression of c Fos in locus coeruleus (LC).
+GDNF	addiction	withdrawal	16044914	The antisense approach and immunohistochemistry were used to study the effects of different muscarinic receptor (M) subtypes and <strong>glial cell derived neurotrophic factor</strong> (<strong>GDNF</strong>) on the scores of morphine <b>withdrawal</b> syndrome and the expression of c Fos in locus coeruleus (LC).
+GDNF	drug	opioid	16044914	Intrathecal injection of M2 receptor antisense oligonucleotides (M2AS oligo) or <strong>GDNF</strong> antisense oligonucleotides (GDNFAS oligo) decreased the scores of <b>morphine</b> withdrawal syndrome.
+GDNF	addiction	withdrawal	16044914	Intrathecal injection of M2 receptor antisense oligonucleotides (M2AS oligo) or <strong>GDNF</strong> antisense oligonucleotides (GDNFAS oligo) decreased the scores of morphine <b>withdrawal</b> syndrome.
+GDNF	drug	cocaine	15899247	The neurotrophic factor glial cell line derived neurotrophic factor (<strong>GDNF</strong>) may have therapeutic potential for preventing and treating <b>cocaine</b> addiction.
+GDNF	addiction	addiction	15899247	The neurotrophic factor glial cell line derived neurotrophic factor (<strong>GDNF</strong>) may have therapeutic potential for preventing and treating cocaine <b>addiction</b>.
+GDNF	drug	cocaine	15899247	Previously, we found that transplantation of a <strong>GDNF</strong> expressing astrocyte cell line into the striatum and nucleus accumbens attenuates <b>cocaine</b> seeking behavior in Sprague Dawley rats.
+GDNF	addiction	relapse	15899247	Previously, we found that transplantation of a <strong>GDNF</strong> expressing astrocyte cell line into the striatum and nucleus accumbens attenuates cocaine <b>seeking</b> behavior in Sprague Dawley rats.
+GDNF	drug	cocaine	15899247	Therefore, we examined the effect of <strong>GDNF</strong> conjugated nanoparticles microinjected into the striatum and nucleus accumbens on <b>cocaine</b> self administration in rats.
+GDNF	drug	cocaine	15899247	<strong>GDNF</strong> conjugated nanoparticles blocked the acquisition of <b>cocaine</b> self administration compared to control treatments.
+GDNF	drug	cocaine	15899247	Furthermore, a <b>cocaine</b> dose response demonstrated that decreased lever response in rats that received <strong>GDNF</strong> conjugated nanoparticles persisted after substitution with different <b>cocaine</b> doses.
+GDNF	addiction	addiction	15899247	These findings suggest that <strong>GDNF</strong> conjugated nanoparticles may serve as a novel potential treatment for drug <b>addiction</b>.
+GDNF	drug	alcohol	15659598	Microinjection of ibogaine into the ventral tegmental area (VTA), but not the substantia nigra, reduced self administration of <b>ethanol</b>, and systemic administration of ibogaine increased the expression of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in a midbrain region that includes the VTA.
+GDNF	drug	psychedelics	15659598	Microinjection of <b>ibogaine</b> into the ventral tegmental area (VTA), but not the substantia nigra, reduced self administration of ethanol, and systemic administration of <b>ibogaine</b> increased the expression of glial cell line derived neurotrophic factor (<strong>GDNF</strong>) in a midbrain region that includes the VTA.
+GDNF	drug	psychedelics	15659598	In dopaminergic neuron like SHSY5Y cells, <b>ibogaine</b> treatment upregulated the <strong>GDNF</strong> pathway as indicated by increases in phosphorylation of the <strong>GDNF</strong> receptor, Ret, and the downstream kinase, ERK1 (extracellular signal regulated kinase 1).
+GDNF	drug	alcohol	15659598	Finally, the ibogaine mediated decrease in <b>ethanol</b> self administration was mimicked by intra VTA microinjection of <strong>GDNF</strong> and was reduced by intra VTA delivery of anti <strong>GDNF</strong> neutralizing antibodies.
+GDNF	drug	psychedelics	15659598	Finally, the <b>ibogaine</b> mediated decrease in ethanol self administration was mimicked by intra VTA microinjection of <strong>GDNF</strong> and was reduced by intra VTA delivery of anti <strong>GDNF</strong> neutralizing antibodies.
+GDNF	drug	alcohol	15659598	Together, these results suggest that <strong>GDNF</strong> in the VTA mediates the action of ibogaine on <b>ethanol</b> consumption.
+GDNF	drug	psychedelics	15659598	Together, these results suggest that <strong>GDNF</strong> in the VTA mediates the action of <b>ibogaine</b> on ethanol consumption.
+GDNF	drug	alcohol	15659598	These findings highlight the importance of <strong>GDNF</strong> as a new target for drug development for <b>alcoholism</b> that may mimic the effect of ibogaine against <b>alcohol</b> consumption but avoid the negative side effects.
+GDNF	drug	psychedelics	15659598	These findings highlight the importance of <strong>GDNF</strong> as a new target for drug development for alcoholism that may mimic the effect of <b>ibogaine</b> against alcohol consumption but avoid the negative side effects.
+GDNF	addiction	addiction	14622243	Neurotrophic factors, such as glial cell line derived neurotrophic factor (<strong>GDNF</strong>), may play a role in drug induced biochemical and behavioural adaptations that characterize <b>addiction</b>.
+GDNF	drug	cocaine	14622243	We found that <strong>GDNF</strong> mRNA levels are lower in the striatum of rats that chronically self administered <b>cocaine</b>.
+GDNF	drug	cocaine	14622243	Therefore, we examined the effect of transplanted cells used as a biodelivery system for <strong>GDNF</strong> on <b>cocaine</b> self administration in rats.
+GDNF	drug	cocaine	14622243	Moreover, rats that received a chronic infusion of <strong>GDNF</strong> via a micro osmotic pump also exhibited weak <b>cocaine</b> self administration.
+GDNF	drug	cocaine	14622243	Therefore, we conclude that exogenous augmentation of <strong>GDNF</strong> repositories may be useful in suppressing <b>cocaine</b> self administration.
+GDNF	drug	opioid	11798749	[The expression of <strong>glial cell derived neurotrophic factor</strong> and its receptor GDNFR alpha and GDNFR beta mRNA in spinal cord, brainstem and frontal cortex during <b>morphine</b> withdrawal in rats].
+GDNF	addiction	withdrawal	11798749	[The expression of <strong>glial cell derived neurotrophic factor</strong> and its receptor GDNFR alpha and GDNFR beta mRNA in spinal cord, brainstem and frontal cortex during morphine <b>withdrawal</b> in rats].
+GDNF	drug	opioid	11798749	To investigate the expression of glial cell derived neurotrophic factor (<strong>GDNF</strong>) and its receptor GDNFR alpha (GFRalpha 1) and GDNFR beta (Ret) genes and the effects of muscarinic receptor antagonists, NMDA receptor antagonist, inhibitor of nitric oxide synthase on the expression of these genes in the spinal cord, brainstem and frontal cortex during <b>morphine</b> withdrawal, and to observe the effects of <strong>GDNF</strong> antisense oligoneucleotide (i.c.v) on the <b>morphine</b> withdrawal symptoms in rats.
+GDNF	addiction	withdrawal	11798749	To investigate the expression of glial cell derived neurotrophic factor (<strong>GDNF</strong>) and its receptor GDNFR alpha (GFRalpha 1) and GDNFR beta (Ret) genes and the effects of muscarinic receptor antagonists, NMDA receptor antagonist, inhibitor of nitric oxide synthase on the expression of these genes in the spinal cord, brainstem and frontal cortex during morphine <b>withdrawal</b>, and to observe the effects of <strong>GDNF</strong> antisense oligoneucleotide (i.c.v) on the morphine <b>withdrawal</b> symptoms in rats.
+GDNF	drug	opioid	11798749	To investigate the expression of <strong>glial cell derived neurotrophic factor</strong> (<strong>GDNF</strong>) and its receptor GDNFR alpha (GFRalpha 1) and GDNFR beta (Ret) genes and the effects of muscarinic receptor antagonists, NMDA receptor antagonist, inhibitor of nitric oxide synthase on the expression of these genes in the spinal cord, brainstem and frontal cortex during <b>morphine</b> withdrawal, and to observe the effects of <strong>GDNF</strong> antisense oligoneucleotide (i.c.v) on the <b>morphine</b> withdrawal symptoms in rats.
+GDNF	addiction	withdrawal	11798749	To investigate the expression of <strong>glial cell derived neurotrophic factor</strong> (<strong>GDNF</strong>) and its receptor GDNFR alpha (GFRalpha 1) and GDNFR beta (Ret) genes and the effects of muscarinic receptor antagonists, NMDA receptor antagonist, inhibitor of nitric oxide synthase on the expression of these genes in the spinal cord, brainstem and frontal cortex during morphine <b>withdrawal</b>, and to observe the effects of <strong>GDNF</strong> antisense oligoneucleotide (i.c.v) on the morphine <b>withdrawal</b> symptoms in rats.
+GDNF	drug	opioid	11798749	The <strong>GDNF</strong> mRNA levels were increased, and GDNFR alpha and GDNFR beta mRNA levels was slightly increased in the spinal cord and brainstem during <b>morphine</b> dependence.
+GDNF	addiction	dependence	11798749	The <strong>GDNF</strong> mRNA levels were increased, and GDNFR alpha and GDNFR beta mRNA levels was slightly increased in the spinal cord and brainstem during morphine <b>dependence</b>.
+GDNF	drug	opioid	11798749	While the <strong>GDNF</strong>, GDNFR alpha and GDNFR beta levels in the frontal cortex were increased significantly at 1, 2 and 4 h after the injection of <b>naloxone</b> during <b>morphine</b> withdrawal.
+GDNF	addiction	withdrawal	11798749	While the <strong>GDNF</strong>, GDNFR alpha and GDNFR beta levels in the frontal cortex were increased significantly at 1, 2 and 4 h after the injection of naloxone during morphine <b>withdrawal</b>.
+GDNF	drug	opioid	11798749	Moreover, the <b>morphine</b> withdrawal symptoms were attenuated by intracerebroven tricular injection of <strong>GDNF</strong> antisense oligoneucleotide in 6 hour and 24 hour before <b>naloxone</b> administration in <b>morphine</b> dependent rats.
+GDNF	addiction	withdrawal	11798749	Moreover, the morphine <b>withdrawal</b> symptoms were attenuated by intracerebroven tricular injection of <strong>GDNF</strong> antisense oligoneucleotide in 6 hour and 24 hour before naloxone administration in morphine dependent rats.
+GDNF	drug	opioid	11798749	The results not only provide direct evidence that the expressions of <strong>GDNF</strong> and its receptors mRNA in glial cells play an important role in mediating the process of <b>morphine</b> dependence and may be account for the long term neuro adaptation associated with <b>morphine</b> dependence, but also suggest that muscarinic receptor, NMDA receptor and nitric oxide pathways may be involved in the expression of <strong>GDNF</strong> and <strong>GDNF</strong> receptor genes during <b>morphine</b> withdrawal.
+GDNF	addiction	dependence	11798749	The results not only provide direct evidence that the expressions of <strong>GDNF</strong> and its receptors mRNA in glial cells play an important role in mediating the process of morphine <b>dependence</b> and may be account for the long term neuro adaptation associated with morphine <b>dependence</b>, but also suggest that muscarinic receptor, NMDA receptor and nitric oxide pathways may be involved in the expression of <strong>GDNF</strong> and <strong>GDNF</strong> receptor genes during morphine withdrawal.
+GDNF	addiction	withdrawal	11798749	The results not only provide direct evidence that the expressions of <strong>GDNF</strong> and its receptors mRNA in glial cells play an important role in mediating the process of morphine dependence and may be account for the long term neuro adaptation associated with morphine dependence, but also suggest that muscarinic receptor, NMDA receptor and nitric oxide pathways may be involved in the expression of <strong>GDNF</strong> and <strong>GDNF</strong> receptor genes during morphine <b>withdrawal</b>.
+GDNF	addiction	withdrawal	11595754	<strong>GDNF</strong> release continued for 24 h following <b>withdrawal</b> of amitriptyline.
+GDNF	drug	benzodiazepine	11595754	Furthermore, following treatment with antidepressants belonging to several different classes (amitriptyline, clomipramine, mianserin, fluoxetine and paroxetine) significantly increased <strong>GDNF</strong> release, but which did not occur after treatment with non antidepressant psychotropic drugs (haloperidol, <b>diazepam</b> and diphenhydramine).
+GDNF	drug	amphetamine	11328352	Ventricular <strong>GDNF</strong> infusion completely blocked the late degenerating neurons in the caudal SN and had long lasting behavioural effects on the stepping test and <b>amphetamine</b> rotation, extending to 6 weeks after withdrawal of the factor.
+GDNF	addiction	withdrawal	11328352	Ventricular <strong>GDNF</strong> infusion completely blocked the late degenerating neurons in the caudal SN and had long lasting behavioural effects on the stepping test and amphetamine rotation, extending to 6 weeks after <b>withdrawal</b> of the factor.
+GDNF	drug	cocaine	10798408	Infusion of <strong>GDNF</strong> into the ventral tegmental area (VTA), a dopaminergic brain region important for addiction, blocks certain biochemical adaptations to chronic <b>cocaine</b> or morphine as well as the rewarding effects of <b>cocaine</b>.
+GDNF	drug	opioid	10798408	Infusion of <strong>GDNF</strong> into the ventral tegmental area (VTA), a dopaminergic brain region important for addiction, blocks certain biochemical adaptations to chronic cocaine or <b>morphine</b> as well as the rewarding effects of cocaine.
+GDNF	addiction	addiction	10798408	Infusion of <strong>GDNF</strong> into the ventral tegmental area (VTA), a dopaminergic brain region important for <b>addiction</b>, blocks certain biochemical adaptations to chronic cocaine or morphine as well as the rewarding effects of cocaine.
+GDNF	drug	cocaine	10798408	Conversely, responses to <b>cocaine</b> are enhanced in rats by intra VTA infusion of an anti <strong>GDNF</strong> antibody and in mice heterozygous for a null mutation in the <strong>GDNF</strong> gene.
+GDNF	drug	cocaine	10798408	Chronic morphine or <b>cocaine</b> exposure decreases levels of phosphoRet, the protein kinase that mediates <strong>GDNF</strong> signaling, in the VTA.
+GDNF	drug	opioid	10798408	Chronic <b>morphine</b> or cocaine exposure decreases levels of phosphoRet, the protein kinase that mediates <strong>GDNF</strong> signaling, in the VTA.
+PPP1R1B	drug	opioid	32440365	According to IPA Canonical Pathways Analysis, Gamma aminobutyric Acid (GABA) Receptor Signaling, Neuroinflammation Signaling Pathway, <b>Opioid</b> Signaling Pathway and Dopamine <strong>DARPP32</strong> Feedback in cAMP Signaling are potential contributors to the interaction of AUD and OUD.
+PPP1R1B	drug	cocaine	29354053	Activation of Dopamine D1 D2 Receptor Complex Attenuates <b>Cocaine</b> Reward and Reinstatement of <b>Cocaine</b> Seeking through Inhibition of <strong>DARPP 32</strong>, ERK, and ΔFosB.
+PPP1R1B	addiction	relapse	29354053	Activation of Dopamine D1 D2 Receptor Complex Attenuates Cocaine Reward and <b>Reinstatement</b> of Cocaine <b>Seeking</b> through Inhibition of <strong>DARPP 32</strong>, ERK, and ΔFosB.
+PPP1R1B	addiction	reward	29354053	Activation of Dopamine D1 D2 Receptor Complex Attenuates Cocaine <b>Reward</b> and Reinstatement of Cocaine Seeking through Inhibition of <strong>DARPP 32</strong>, ERK, and ΔFosB.
+PPP1R1B	drug	cocaine	29354053	The D1 D2 heteromer activated Cdk5/Thr75 <strong>DARPP 32</strong> and attenuated <b>cocaine</b> induced pERK and ΔFosB accumulation, together with inhibition of <b>cocaine</b> enhanced local field potentials in NAc, blocking thus the signaling pathway activated by <b>cocaine</b>: D1R/cAMP/PKA/Thr34 <strong>DARPP 32</strong>/pERK with ΔFosB accumulation.
+PPP1R1B	drug	cannabinoid	29082320	Phosphorylation of glycogen synthase kinase 3β (GSK3β), a Cdk5 target, was reduced in PFC after repeated <b>THC</b> treatment regardless of <b>THC</b> history, and phosphorylation of dopamine  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>) at the Cdk5 regulated threonine 75 site was unchanged.
+PPP1R1B	drug	amphetamine	30462388	For example, a <b>methamphetamine</b> monoclonal antibody, a new chemical acting on <strong>DARPP 32</strong> (dopamine and c AMP regulated phophoprotein 32), a galanin analogue, oxytocin, and others are included in such attempt.
+PPP1R1B	drug	alcohol	27650828	Erratum to: The melanin concentrating hormone 1 receptor modulates <b>alcohol</b> induced reward and <strong>DARPP 32</strong> phosphorylation.
+PPP1R1B	addiction	reward	27650828	Erratum to: The melanin concentrating hormone 1 receptor modulates alcohol induced <b>reward</b> and <strong>DARPP 32</strong> phosphorylation.
+PPP1R1B	drug	alcohol	27044354	The melanin concentrating hormone 1 receptor modulates <b>alcohol</b> induced reward and <strong>DARPP 32</strong> phosphorylation.
+PPP1R1B	addiction	reward	27044354	The melanin concentrating hormone 1 receptor modulates alcohol induced <b>reward</b> and <strong>DARPP 32</strong> phosphorylation.
+PPP1R1B	drug	alcohol	27044354	The increase in <strong>DARPP 32</strong> phosphorylation seen in wildtype (WT) mice after acute <b>alcohol</b> administration in the NAcSh was markedly reduced in MCH1 R knock out (KO) mice.
+PPP1R1B	drug	amphetamine	26947946	Genetic inactivation of the protein phosphatase 1 inhibitor, dopamine  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>), reduces the phosphorylation of H3K27me3S28 produced by <b>amphetamine</b> and haloperidol.
+PPP1R1B	drug	alcohol	26304024	A case control study of the association between <strong>DARPP 32</strong> gene polymorphisms and <b>alcohol</b> dependence in Chinese Han subjects.
+PPP1R1B	addiction	dependence	26304024	A case control study of the association between <strong>DARPP 32</strong> gene polymorphisms and alcohol <b>dependence</b> in Chinese Han subjects.
+PPP1R1B	drug	amphetamine	26146906	Conversely, <b>methamphetamine</b> induced locomotor activity was attenuated in DKO mice, accompanied by reductions in dopamine and HVA content and impaired <strong>DARPP 32</strong> activation.
+PPP1R1B	addiction	addiction	26041984	Gene expression networks consisted of recognized substrates for <b>addiction</b>, such as the dopamine  and cAMP regulated neuronal phosphoprotein <strong>PPP1R1B</strong>/DARPP 32 and the vesicular glutamate transporter SLC17A7/VGLUT1 as well as potentially novel molecular targets for substance abuse.
+PPP1R1B	addiction	addiction	26041984	Gene expression networks consisted of recognized substrates for <b>addiction</b>, such as the dopamine  and cAMP regulated neuronal phosphoprotein <strong>PPP1R1B</strong>/<strong>DARPP 32</strong> and the vesicular glutamate transporter SLC17A7/VGLUT1 as well as potentially novel molecular targets for substance abuse.
+PPP1R1B	drug	opioid	25521358	CSNK1E interacts with circadian rhythms and <strong>DARPP 32</strong> and has been implicated in negative regulation of sensitivity to <b>opioids</b> in rodents.
+PPP1R1B	drug	opioid	25311134	These effects are associated with a marked reduction of <b>heroin</b> induced increase in phosphorylation of <strong>DARPP 32</strong> protein in the nucleus accumbens (NAc) and with a marked and selective reduction of acute <b>heroin</b> induced elevation of extracellular dopamine (DA) levels in the NAc shell, as measured by in vivo microdialysis.
+PPP1R1B	drug	alcohol	24919054	Individual differences in <b>ethanol</b> locomotor sensitization are associated with dopamine D1 receptor intra cellular signaling of <strong>DARPP 32</strong> in the nucleus accumbens.
+PPP1R1B	addiction	sensitization	24919054	Individual differences in ethanol locomotor <b>sensitization</b> are associated with dopamine D1 receptor intra cellular signaling of <strong>DARPP 32</strong> in the nucleus accumbens.
+PPP1R1B	drug	alcohol	24919054	Here we investigated if the functional hyperresponsiveness of D1 receptors observed in <b>ethanol</b> sensitized mice leads to an increased activation of <strong>DARPP 32</strong>, a central regulatory protein in medium spiny neurons, in the nucleus accumbens   a brain region known to play a role in drug reinforcement.
+PPP1R1B	addiction	reward	24919054	Here we investigated if the functional hyperresponsiveness of D1 receptors observed in ethanol sensitized mice leads to an increased activation of <strong>DARPP 32</strong>, a central regulatory protein in medium spiny neurons, in the nucleus accumbens   a brain region known to play a role in drug <b>reinforcement</b>.
+PPP1R1B	drug	cocaine	23786641	Biochemical studies in the ventral striatum show that phosphorylation of <strong>DARPP 32</strong>(Thr) ( 34) and GluR1(Ser) ( 845) is diminished in MC4R null mice after chronic <b>cocaine</b> administration but rescued in MC4R/D1R mice.
+PPP1R1B	drug	cocaine	23499958	Treatment with resveratrol (50μM for 30min) enhanced <b>cocaine</b> induced increases in the phosphorylation of <strong>DARPP 32</strong> at Thr34 and GluA1 at Ser845, postsynaptic substrates for dopamine/D1 receptor/PKA signaling, and a <b>cocaine</b> induced decrease in the phosphorylation of tyrosine hydroxylase at Ser40, a presynaptic substrate for dopamine/D2 receptor signaling.
+PPP1R1B	drug	cocaine	23499958	The inhibition of both MAO A and MAO B by clorgyline and pargyline, respectively, enhanced the effects of <b>cocaine</b> on <strong>DARPP 32</strong> phosphorylation.
+PPP1R1B	drug	cocaine	23499958	The acute effect of resveratrol on <b>cocaine</b> induced <strong>DARPP 32</strong> phosphorylation was occluded with inhibition of MAO A and MAO B.
+PPP1R1B	drug	nicotine	22952905	Environmental enrichment alters <b>nicotine</b> mediated locomotor sensitization and phosphorylation of <strong>DARPP 32</strong> and CREB in rat prefrontal cortex.
+PPP1R1B	addiction	sensitization	22952905	Environmental enrichment alters nicotine mediated locomotor <b>sensitization</b> and phosphorylation of <strong>DARPP 32</strong> and CREB in rat prefrontal cortex.
+PPP1R1B	drug	nicotine	22952905	The current study determined activation of <strong>DARPP 32</strong> (dopamine  and cAMP regulated phosphoprotein 32) and CREB (cAMP response element binding protein), and locomotor activity in rats raised in enriched (EC), impoverished (IC), and standard (SC) conditions following repeated administration of <b>nicotine</b> or saline.
+PPP1R1B	drug	cocaine	21925237	In the PFC of <b>cocaine</b> abusers, several signaling molecules associated with <b>cocaine</b>/dopamine and/or apoptotic pathways were not significantly altered, with the exception of anti apoptotic truncated <strong>DARPP 32</strong> (t DARPP), a truncated isoform of dopamine  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>), whose content was decreased ( 28%).
+PPP1R1B	drug	alcohol	21843598	<strong>DARPP 32</strong> and Akt regulation in <b>ethanol</b> preferring AA and <b>ethanol</b> avoiding ANA rats.
+PPP1R1B	drug	alcohol	21843598	The present experiments characterized the regulation of three key signaling molecules, <strong>DARPP 32</strong> (dopamine and cAMP regulated phosphoprotein, 32kDa), Akt kinase and ERK1/2 (extracellular signal regulated kinase 1 and 2) in <b>ethanol</b> preferring AA (Alko, <b>alcohol</b>) and <b>ethanol</b> avoiding ANA (Alko, non <b>alcohol</b>) rat lines.
+PPP1R1B	drug	alcohol	21843598	<b>Ethanol</b> (1.5g/kg) increased phosphorylation of <strong>DARPP 32</strong> at threonine 34 in both AA and in ANA rats indicating that acute <b>ethanol</b> activates <strong>DARPP 32</strong> similarly in these rat lines.
+PPP1R1B	drug	alcohol	21843598	Our findings suggest that <strong>DARPP 32</strong> and Akt are regulated by <b>ethanol</b> and differences in the regulation of these molecules might contribute to the dramatically different <b>ethanol</b> drinking patterns seen in AA and ANA rats.
+PPP1R1B	drug	opioid	21600884	We further demonstrated that the <b>morphine</b> induced DOR expression, while activation of <strong>DARPP 32</strong> and MAP kinase was suppressed by JWA knockdown.
+PPP1R1B	drug	amphetamine	21564097	Inhibiting Csnk1δ/ε in the NAcc with the selective inhibitor PF 670462 blocks <b>amphetamine</b> induced locomotion and its ability to increase phosphorylation of <strong>Darpp 32</strong> at S137 and T34, decrease PP1 activity and increase phosphorylation of the AMPA receptor subunit at S845.
+PPP1R1B	drug	opioid	20731628	The levels of phosphorylated <strong>DARPP32</strong> (Thr34) and phosphorylated CREB (Ser133) were increased in the ACG of rats that had maintained the <b>morphine</b> induced place preference, whereas the increases of these levels induced by <b>morphine</b> were blocked by pre treatment of a selective dopamine D1 receptor antagonist SCH23390.
+PPP1R1B	drug	opioid	20731628	The activation of <strong>DARPP32</strong> and CREB through dopamine D1 receptors in the ACG could be implicated in the maintenance of μ <b>opioid</b> induced place preference.
+PPP1R1B	drug	cocaine	20519061	Thus, since behavioural <b>cocaine</b> sensitization is characterized by tonically increased levels of phospho Thr75 <strong>DARPP 32</strong> that is a potent PKA inhibitor, we hypothesized that <b>cocaine</b> sensitized rats might reveal deficits in palatable food responding.
+PPP1R1B	addiction	sensitization	20519061	Thus, since behavioural cocaine <b>sensitization</b> is characterized by tonically increased levels of phospho Thr75 <strong>DARPP 32</strong> that is a potent PKA inhibitor, we hypothesized that cocaine sensitized rats might reveal deficits in palatable food responding.
+PPP1R1B	drug	cocaine	20519061	Indeed, non food deprived <b>cocaine</b> sensitized rats showed no interest in palatable food, no dopaminergic response after a palatable meal in terms of increased dopamine output and <strong>DARPP 32</strong> phosphorylation changes, and no ability to acquire a palatable food sustained instrumental behaviour.
+PPP1R1B	drug	alcohol	20456289	<b>Ethanol</b> induced activation of AKT and <strong>DARPP 32</strong> in the mouse striatum mediated by opioid receptors.
+PPP1R1B	drug	opioid	20456289	Ethanol induced activation of AKT and <strong>DARPP 32</strong> in the mouse striatum mediated by <b>opioid</b> receptors.
+PPP1R1B	drug	alcohol	20456289	Here we report that an acute <b>ethanol</b> challenge induces a robust phosphorylation of two key signal transduction kinases, AKT and <strong>DARPP 32</strong>, in the striatum of mice.
+PPP1R1B	drug	nicotine	20384816	In this study we used an animal model of <b>nicotine</b> addiction to examine the possibility that changes in insular cortex levels of dopamine (DA)  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>), a phosphoprotein enriched in DA neurons containing DA D1 receptors, may be associated with changes in vulnerability to <b>nicotine</b> addiction.
+PPP1R1B	addiction	addiction	20384816	In this study we used an animal model of nicotine <b>addiction</b> to examine the possibility that changes in insular cortex levels of dopamine (DA)  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>), a phosphoprotein enriched in DA neurons containing DA D1 receptors, may be associated with changes in vulnerability to nicotine <b>addiction</b>.
+PPP1R1B	drug	nicotine	20384816	<b>Nicotine</b> seeking, as assessed under a cue induced reinstatement paradigm, and markers of <strong>DARPP 32</strong> signaling, as assessed using western blot analysis, were examined in separate groups of rats at two different abstinent intervals: 1 and 7 days.
+PPP1R1B	addiction	relapse	20384816	Nicotine <b>seeking</b>, as assessed under a cue induced <b>reinstatement</b> paradigm, and markers of <strong>DARPP 32</strong> signaling, as assessed using western blot analysis, were examined in separate groups of rats at two different abstinent intervals: 1 and 7 days.
+PPP1R1B	drug	nicotine	20384816	These results demonstrate incubation of drug seeking following extended access to <b>nicotine</b> self administration and suggest that enhanced protein kinase A signaling in the insular cortex via phosphorylation of <strong>DARPP 32</strong> at Thr34 is associated with this effect.
+PPP1R1B	addiction	relapse	20384816	These results demonstrate incubation of drug <b>seeking</b> following extended access to nicotine self administration and suggest that enhanced protein kinase A signaling in the insular cortex via phosphorylation of <strong>DARPP 32</strong> at Thr34 is associated with this effect.
+PPP1R1B	addiction	addiction	19897079	Therapeutic targeting of "<strong>DARPP 32</strong>": a key signaling molecule in the dopiminergic pathway for the treatment of opiate <b>addiction</b>.
+PPP1R1B	addiction	addiction	19897079	The 32 kDa dopamine  and adenosine 3',5' monophosphate regulated phosphoprotein (<strong>DARPP 32</strong>) is recognized to be critical to the pathogenesis of drug <b>addiction</b>.
+PPP1R1B	addiction	addiction	19897079	Silencing of <strong>DARPP 32</strong> using an siRNA against <strong>DARPP 32</strong> may provide a novel gene therapy strategy to overcome drug <b>addiction</b>.
+PPP1R1B	drug	opioid	19897079	In this study, we investigated the effect of the opiate (<b>heroin</b>) on D1 receptor (D1R) and <strong>DARPP 32</strong> expression and additionally, evaluated the effects of <strong>DARPP 32</strong> siRNA gene silencing on protein phosphatase 1 (PP 1), ERK, and cAMP response element binding (CREB) gene expression in primary normal human astrocytes (NHA) cells in vitro.
+PPP1R1B	drug	opioid	19897079	Our results indicate that <b>heroin</b> significantly upregulated both D1R and <strong>DARPP 32</strong> gene expression, and that <strong>DARPP 32</strong> silencing in the NHA cells resulted in the significant modulation of the activity of downstream effector molecules such as PP 1, ERK, and CREB which are known to play an important role in opiate abuse induced changes in long term neural plasticity.
+PPP1R1B	addiction	addiction	19897079	These findings have the potential to facilitate the development of <strong>DARPP32</strong> siRNA based therapeutics against drug <b>addiction</b>.
+PPP1R1B	drug	opioid	19759531	Sensitization to <b>morphine</b> injection was prevented in knockin mutant mice bearing a Thr 34 Ala mutation of <strong>DARPP 32</strong>, which suppresses its ability to inhibit protein phosphatase 1 (PP1), but not mutation of Thr 75 or Ser 130.
+PPP1R1B	addiction	sensitization	19759531	<b>Sensitization</b> to morphine injection was prevented in knockin mutant mice bearing a Thr 34 Ala mutation of <strong>DARPP 32</strong>, which suppresses its ability to inhibit protein phosphatase 1 (PP1), but not mutation of Thr 75 or Ser 130.
+PPP1R1B	drug	cocaine	19580849	<strong>DARPP 32</strong> was unchanged by housing or <b>cocaine</b>, while phospho Thr(34) <strong>DARPP 32</strong> was increased by <b>cocaine</b> treatment across conditions.
+PPP1R1B	drug	opioid	19559764	Acute <b>morphine</b> administration induced an early increase and delayed decrease in phospho threonine (Thr)34 <strong>DARPP 32</strong> levels accompanied by a delayed increase in phospho Thr75 <strong>DARPP 32</strong> levels in the nucleus accumbens and caudate putamen of sensitized rats, while it had no effects in control animals.
+PPP1R1B	drug	cocaine	19348873	Sixty minutes of <b>cocaine</b> administration increased p thr34 <strong>DARPP 32</strong> levels in the NAc of rats during estrus and proestrus and in the CPu of rats in diestrus.
+PPP1R1B	drug	cocaine	19181855	Compared with WT mice, tPA /  mice injected with <b>cocaine</b> displayed attenuated phosphorylation of ERK, cAMP response element binding protein (CREB), and dopamine and cAMP regulated phosphoprotein 32 kDa (<strong>DARPP 32</strong>) and blunted induction of immediate early genes (IEGs) c Fos, Egr 1, and Homer 1a in the amygdala and the nucleus accumbens (NAc).
+PPP1R1B	addiction	dependence	18991847	CKIepsilon phosphorylates and activates <strong>DARPP 32</strong>, a key molecule in various complex signaling pathways, including dopamine and glutamine signaling, which have both been demonstrated to be main pathways in substance <b>dependence</b>.
+PPP1R1B	drug	cocaine	18985320	Basal and <b>cocaine</b> induced sex differences in the <strong>DARPP 32</strong> mediated signaling pathway.
+PPP1R1B	drug	cocaine	18985320	Activation of the dopamine  and cAMP regulated phosphoprotein of Mr 32 kDa (<strong>DARPP 32</strong>) intracellular cascade mediates responses to <b>cocaine</b>.
+PPP1R1B	drug	cocaine	18985320	To examine the possibility that acute <b>cocaine</b> administration alters the <strong>DARPP 32</strong> cascade in a sexually dimorphic pattern.
+PPP1R1B	drug	cocaine	18985320	In females, <b>cocaine</b> administration significantly decreased protein levels of <strong>DARPP 32</strong>, P Thr34 <strong>DARPP 32</strong>, and CaN A at 45 min but increased PP 1 protein levels at 30 min.
+PPP1R1B	drug	cocaine	18985320	Overall, males had higher activation of the <strong>DARPP 32</strong> pathway after <b>cocaine</b> administration than did females.
+PPP1R1B	drug	cocaine	18985320	These novel results show that basal and <b>cocaine</b> induced sex differences in the <strong>DARPP 32</strong>/PP 1 cascade may be responsible for the sexual dimorphism in acute <b>cocaine</b> induced behavioral responses.
+PPP1R1B	drug	cocaine	18554320	Enhanced CREB and <strong>DARPP 32</strong> phosphorylation in the nucleus accumbens and CREB, ERK, and GluR1 phosphorylation in the dorsal hippocampus is associated with <b>cocaine</b> conditioned place preference behavior.
+PPP1R1B	drug	cocaine	18554320	To better understand the mechanism of <b>cocaine</b> conditioned place preference we have used western blot analysis to examine changes in phosphorylation of cAMP response element binding protein (CREB), dopamine  and cyclic AMP regulated phosphoprotein 32 (<strong>DARPP 32</strong>), extracellular signal regulated kinase (ERK) and GluR1, key molecular substrates altered by <b>cocaine</b>, in the nucleus accumbens (NAc) and dorsal hippocampus (DHC) of C57BL/6 mice.
+PPP1R1B	drug	cocaine	18554320	Our studies revealed that re exposing mice to an environment in which they were previously given <b>cocaine</b> resulted in increased levels of Ser133 phospho CREB and Thr34 phospho <strong>DARPP 32</strong> with a corresponding decrease in Thr75 phospho <strong>DARPP 32</strong> in the NAc.
+PPP1R1B	addiction	reward	18554320	These data suggest that the formation of contextual drug <b>reward</b> associations involves recruitment of the DHC NAc circuit with activation of the <strong>DARPP 32</strong>/CREB pathway in the NAc and the ERK/CREB pathway in the DHC.
+PPP1R1B	drug	cocaine	18234897	Postweanling, periadolescent, and adult male CD 1 mice were exposed to <b>cocaine</b> (20 mg/kg) for 7 d. The rewarding effects of <b>cocaine</b> were assessed, as were the response to a Trk antagonist and the regulation of dopamine and cAMP regulated phosphoprotein, 32 kDa (<strong>DARPP 32</strong>).
+PPP1R1B	drug	cocaine	18234897	<strong>DARPP 32</strong> protein levels were significantly upregulated in the lateral region of the caudate putamen exclusively in postweanling mice after chronic <b>cocaine</b>.
+PPP1R1B	drug	cocaine	18234897	These data indicate that Trk neurotransmission plays a role in age specific behavioral and molecular responses to <b>cocaine</b> and concurrently modulates <strong>DARPP 32</strong> levels.
+PPP1R1B	drug	amphetamine	17953657	The role of the cannabinoid type 1 receptor and down stream cAMP/<strong>DARPP 32</strong> signal in the nucleus accumbens of <b>methamphetamine</b> sensitized rats.
+PPP1R1B	drug	cannabinoid	17953657	The role of the <b>cannabinoid</b> type 1 receptor and down stream cAMP/<strong>DARPP 32</strong> signal in the nucleus accumbens of methamphetamine sensitized rats.
+PPP1R1B	drug	amphetamine	17953657	Overall, we demonstrated that brain CB(1) receptor and its down stream cAMP/<strong>DARPP 32</strong>/T34/PP 2B signaling are profoundly altered in <b>methamphetamine</b> sensitized animals.
+PPP1R1B	drug	nicotine	17687035	Systemic cyclosporine administration decreased calcineurin activity in the brain, attenuated <b>nicotine</b> mediated locomotor sensitization, and blocked the effects of <b>nicotine</b> on <strong>DARPP32</strong> (dopamine  and cAMP regulated phosphoprotein 32) activation in the striatum.
+PPP1R1B	addiction	sensitization	17687035	Systemic cyclosporine administration decreased calcineurin activity in the brain, attenuated nicotine mediated locomotor <b>sensitization</b>, and blocked the effects of nicotine on <strong>DARPP32</strong> (dopamine  and cAMP regulated phosphoprotein 32) activation in the striatum.
+PPP1R1B	drug	cocaine	17680995	Behavioral expression of <b>cocaine</b> sensitization in rats is accompanied by a distinct pattern of modifications in the PKA/<strong>DARPP 32</strong> signaling pathway.
+PPP1R1B	addiction	sensitization	17680995	Behavioral expression of cocaine <b>sensitization</b> in rats is accompanied by a distinct pattern of modifications in the PKA/<strong>DARPP 32</strong> signaling pathway.
+PPP1R1B	drug	cocaine	17680995	Repeated <b>cocaine</b> administration induces behavioral sensitization and modifications in the phosphorylation pattern of dopamine and cAMP regulated phosphoprotein of Mr 32,000 (<strong>DARPP 32</strong>), characterized by a tonic increase in the Thr75 phosphorylated form, and a decrease in the Thr34 phosphorylated form.
+PPP1R1B	addiction	sensitization	17680995	Repeated cocaine administration induces behavioral <b>sensitization</b> and modifications in the phosphorylation pattern of dopamine and cAMP regulated phosphoprotein of Mr 32,000 (<strong>DARPP 32</strong>), characterized by a tonic increase in the Thr75 phosphorylated form, and a decrease in the Thr34 phosphorylated form.
+PPP1R1B	drug	cocaine	17680995	This study further investigated the correlations between <b>cocaine</b> sensitization and modifications in the <strong>DARPP 32</strong> phosphorylation pattern, cAMP dependent protein kinase (PKA) activity, and mGluR5 tone in the medial prefrontal cortex and nucleus accumbens.
+PPP1R1B	addiction	sensitization	17680995	This study further investigated the correlations between cocaine <b>sensitization</b> and modifications in the <strong>DARPP 32</strong> phosphorylation pattern, cAMP dependent protein kinase (PKA) activity, and mGluR5 tone in the medial prefrontal cortex and nucleus accumbens.
+PPP1R1B	drug	cocaine	17680995	Moreover, in sensitized rats acute <b>cocaine</b> administration modified phosphorylation levels of Thr75  and Thr34 <strong>DARPP 32</strong>, GluR1, and NR1 subunits in the nucleus accumbens only at a dose double the efficacious dose in control rats.
+PPP1R1B	drug	cocaine	17680995	Furthermore, in sensitized rats the acute administration of 6 methyl 2 (phenylethynyl) pyridine, a mGluR5 antagonist, reinstated the phosphorylation levels of Thr75  and Thr34 <strong>DARPP 32</strong>, GluR1, and NR1 to control values, and a subsequent <b>cocaine</b> challenge did not elicit a sensitized response.
+PPP1R1B	drug	cocaine	17680995	These data suggest that a tonic increase in mGluR5 transmission in <b>cocaine</b> sensitized rats sustains both the increase in phospho Thr75 <strong>DARPP 32</strong> levels and the expression of behavioral sensitization.
+PPP1R1B	addiction	sensitization	17680995	These data suggest that a tonic increase in mGluR5 transmission in cocaine sensitized rats sustains both the increase in phospho Thr75 <strong>DARPP 32</strong> levels and the expression of behavioral <b>sensitization</b>.
+PPP1R1B	drug	opioid	17251906	Activation of the cAMP/PKA/<strong>DARPP 32</strong> signaling pathway is required for <b>morphine</b> psychomotor stimulation but not for <b>morphine</b> reward.
+PPP1R1B	addiction	reward	17251906	Activation of the cAMP/PKA/<strong>DARPP 32</strong> signaling pathway is required for morphine psychomotor stimulation but not for morphine <b>reward</b>.
+PPP1R1B	drug	opioid	17251906	Here, we show that, in the mouse nucleus accumbens and dorsal striatum, acute administration of <b>morphine</b> resulted in an increase in the state of phosphorylation of the dopamine  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>) at Thr34, without affecting phosphorylation at Thr75.
+PPP1R1B	drug	opioid	17251906	<strong>DARPP 32</strong> knockout mice and T34A <strong>DARPP 32</strong> mutant mice displayed a lower hyperlocomotor response to a single injection of <b>morphine</b> than wild type controls.
+PPP1R1B	drug	opioid	17251906	In contrast, in T75A <strong>DARPP 32</strong> mutant mice, <b>morphine</b> induced psychomotor activation was indistinguishable from that of wild type littermates.
+PPP1R1B	drug	opioid	17251906	In spite of their reduced response to the acute hyperlocomotor effect of <b>morphine</b>, <strong>DARPP 32</strong> knockout mice and T34A <strong>DARPP 32</strong> mutant mice were able to develop behavioral sensitization to <b>morphine</b> comparable to that of wild type controls and to display <b>morphine</b> conditioned place preference.
+PPP1R1B	addiction	sensitization	17251906	In spite of their reduced response to the acute hyperlocomotor effect of morphine, <strong>DARPP 32</strong> knockout mice and T34A <strong>DARPP 32</strong> mutant mice were able to develop behavioral <b>sensitization</b> to morphine comparable to that of wild type controls and to display morphine conditioned place preference.
+PPP1R1B	drug	opioid	17251906	These results demonstrate that dopamine D1 receptor mediated activation of the cAMP/<strong>DARPP 32</strong> cascade in striatal medium spiny neurons is involved in the psychomotor action, but not in the rewarding properties, of <b>morphine</b>.
+PPP1R1B	drug	cocaine	17180335	<strong>DARPP 32</strong> phosphorylation was also increased as a consequence of <b>cocaine</b> when tested after a 0 day abstinence period in male rats but not female rats.
+PPP1R1B	drug	nicotine	17171661	Association analysis of the protein phosphatase 1 regulatory subunit 1B (<strong>PPP1R1B</strong>) gene with <b>nicotine</b> dependence in European  and African American <b>smokers</b>.
+PPP1R1B	addiction	dependence	17171661	Association analysis of the protein phosphatase 1 regulatory subunit 1B (<strong>PPP1R1B</strong>) gene with nicotine <b>dependence</b> in European  and African American smokers.
+PPP1R1B	drug	nicotine	17171661	Because the mesolimbic dopaminergic system is implicated in the reinforcing effects of many drugs, including <b>nicotine</b>, <strong>PPP1R1B</strong> is considered a plausible candidate for involvement in the development of vulnerability to <b>nicotine</b> dependence (ND).
+PPP1R1B	addiction	dependence	17171661	Because the mesolimbic dopaminergic system is implicated in the reinforcing effects of many drugs, including nicotine, <strong>PPP1R1B</strong> is considered a plausible candidate for involvement in the development of vulnerability to nicotine <b>dependence</b> (ND).
+PPP1R1B	addiction	reward	17171661	Because the mesolimbic dopaminergic system is implicated in the <b>reinforcing</b> effects of many drugs, including nicotine, <strong>PPP1R1B</strong> is considered a plausible candidate for involvement in the development of vulnerability to nicotine dependence (ND).
+PPP1R1B	drug	nicotine	17171661	In the present study, we analyzed six single nucleotide polymorphisms (SNPs) within <strong>PPP1R1B</strong> for association with three ND measures: <b>smoking</b> quantity (SQ), the heaviness of <b>smoking</b> index (HSI), and the Fagerström Test for ND (FTND) score.
+PPP1R1B	drug	alcohol	16764827	Prior activation of D1 signaling cascade through the cAMP regulated phosphoprotein 32kD (<strong>DARPP 32</strong>) and protein phosphatase 1 (PP 1) pathway significantly attenuates <b>ethanol</b> inhibition of NMDA receptor function.
+PPP1R1B	drug	cocaine	16710312	Chronic <b>cocaine</b> induces the accumulation of the transcription factor deltaFosB and upregulates cAMP response element binding protein (CREB) and dopamine  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>).
+PPP1R1B	drug	cocaine	16525043	<b>Cocaine</b> self administration in mice is inversely related to phosphorylation at Thr34 (protein kinase A site) and Ser130 (kinase CK1 site) of <strong>DARPP 32</strong>.
+PPP1R1B	drug	cocaine	16525043	<b>Cocaine</b> self administration and striatal levels of dopamine after acute "binge" <b>cocaine</b> administration were measured in separate lines of mice with alanine mutations introduced into <strong>DARPP 32</strong> at either Thr34 (protein kinase A site, Thr34A), Thr75, (cyclin dependent kinase 5 site, Thr75A), Ser97 (kinase CK2 site, Ser97A), or Ser130 (kinase CK1 site, Ser130A).
+PPP1R1B	addiction	intoxication	16525043	Cocaine self administration and striatal levels of dopamine after acute "<b>binge</b>" cocaine administration were measured in separate lines of mice with alanine mutations introduced into <strong>DARPP 32</strong> at either Thr34 (protein kinase A site, Thr34A), Thr75, (cyclin dependent kinase 5 site, Thr75A), Ser97 (kinase CK2 site, Ser97A), or Ser130 (kinase CK1 site, Ser130A).
+PPP1R1B	drug	cocaine	16525043	Both Thr34A  and Ser130A <strong>DARPP 32</strong> mutant mice self administered more <b>cocaine</b> than their respective wild type controls.
+PPP1R1B	drug	cocaine	16525043	Also, <b>cocaine</b> induced increases of dopamine in dorsal striatum were attenuated in the Thr34A  and Ser130A <strong>DARPP 32</strong> phosphomutant mice compared with wild type mice.
+PPP1R1B	drug	cocaine	16525043	Notably, levels of P Thr34  and P Ser130 <strong>DARPP 32</strong> were reduced after self administration of <b>cocaine</b> in wild type mice.
+PPP1R1B	drug	cocaine	16525043	Thus, phosphorylation states of Thr34  and Ser130 <strong>DARPP 32</strong> play important roles in modulating the reinforcing effects of <b>cocaine</b>.
+PPP1R1B	addiction	reward	16525043	Thus, phosphorylation states of Thr34  and Ser130 <strong>DARPP 32</strong> play important roles in modulating the <b>reinforcing</b> effects of cocaine.
+PPP1R1B	drug	cocaine	16123776	Phosphorylation of <strong>DARPP 32</strong> at Threonine 34 is required for <b>cocaine</b> action.
+PPP1R1B	drug	cocaine	16123776	Mice lacking <strong>DARPP 32</strong>, a striatal enriched phosphoprotein, show abnormal behavioral and biochemical responses to <b>cocaine</b>, but the role of individual phosphorylation sites in <strong>DARPP 32</strong> in these responses is unknown.
+PPP1R1B	drug	cocaine	16123776	We show here that mutation of Thr 34 in <strong>DARPP 32</strong> mimicked the behavioral phenotype of the constitutive <strong>DARPP 32</strong> knockout in <b>cocaine</b> induced place conditioning, locomotor activity, and sensitization paradigms.
+PPP1R1B	addiction	sensitization	16123776	We show here that mutation of Thr 34 in <strong>DARPP 32</strong> mimicked the behavioral phenotype of the constitutive <strong>DARPP 32</strong> knockout in cocaine induced place conditioning, locomotor activity, and <b>sensitization</b> paradigms.
+PPP1R1B	drug	cocaine	16123776	In contrast, mutations of Thr75 did not affect conditioned place preference or the acute locomotor response to <b>cocaine</b>, but <strong>DARPP 32</strong> Thr 75 mutants showed no locomotor sensitization in response to repeated <b>cocaine</b> administration.
+PPP1R1B	addiction	sensitization	16123776	In contrast, mutations of Thr75 did not affect conditioned place preference or the acute locomotor response to cocaine, but <strong>DARPP 32</strong> Thr 75 mutants showed no locomotor <b>sensitization</b> in response to repeated cocaine administration.
+PPP1R1B	drug	cocaine	16123776	Consistent with these behavioral findings, we found that <b>cocaine</b> regulation of gene expression in striatum, including the acute induction of the immediate early genes c fos and arc (activity regulated cytoskeletal associated gene), was abolished in <strong>DARPP 32</strong> Thr 34 mutants, but not in Thr 75 mutants.
+PPP1R1B	drug	cocaine	16123776	These findings highlight distinct roles of the Thr 34 and Thr 75 phosphorylation sites of <strong>DARPP 32</strong> in mediating short  and long term behavioral and biochemical actions of <b>cocaine</b>.
+PPP1R1B	drug	nicotine	16084497	<strong>DARPP 32</strong> phosphorylation opposes the behavioral effects of <b>nicotine</b>.
+PPP1R1B	drug	nicotine	16084497	Because post synaptic neurons within the striatum contain high levels of the dopamine  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>), we hypothesized that <strong>DARPP 32</strong> may functionally contribute to the behavioral effects of <b>nicotine</b>.
+PPP1R1B	drug	nicotine	16084497	We examined the behavioral effects of <b>nicotine</b> and the phosphorylation state of <strong>DARPP 32</strong> in wild type (WT) and <strong>DARPP 32</strong> knockout (KO) mice.
+PPP1R1B	drug	nicotine	16084497	Systemic injections of <b>nicotine</b> resulted in increased striatal <strong>DARPP 32</strong> phosphorylation at threonine34 and threonine75.
+PPP1R1B	drug	nicotine	16084497	<strong>DARPP 32</strong> opposes the behavioral effects of <b>nicotine</b> possibly via concurrent phosphorylation at the two threonine sites.
+PPP1R1B	drug	alcohol	16037948	Previously, we reported that D(1) like dopamine receptors activate a postsynaptic cAMP/PKA/<strong>DARPP 32</strong> signaling cascade culminating in phosphorylation of SER897 NR1 subunits and a reduction in the sensitivity to <b>ethanol</b> of NMDA receptor mediated synaptic transmission.
+PPP1R1B	drug	amphetamine	15608059	Activation of ERK by d <b>amphetamine</b> or by widely abused drugs, including cocaine, nicotine, morphine, and Delta(9) tetrahydrocannabinol was absent in mice lacking dopamine  and cAMP regulated phosphoprotein of M(r) 32,000 (<strong>DARPP 32</strong>).
+PPP1R1B	drug	cannabinoid	15608059	Activation of ERK by d amphetamine or by widely abused drugs, including cocaine, nicotine, morphine, and Delta(9) <b>tetrahydrocannabinol</b> was absent in mice lacking dopamine  and cAMP regulated phosphoprotein of M(r) 32,000 (<strong>DARPP 32</strong>).
+PPP1R1B	drug	cocaine	15608059	Activation of ERK by d amphetamine or by widely abused drugs, including <b>cocaine</b>, nicotine, morphine, and Delta(9) tetrahydrocannabinol was absent in mice lacking dopamine  and cAMP regulated phosphoprotein of M(r) 32,000 (<strong>DARPP 32</strong>).
+PPP1R1B	drug	nicotine	15608059	Activation of ERK by d amphetamine or by widely abused drugs, including cocaine, <b>nicotine</b>, morphine, and Delta(9) tetrahydrocannabinol was absent in mice lacking dopamine  and cAMP regulated phosphoprotein of M(r) 32,000 (<strong>DARPP 32</strong>).
+PPP1R1B	drug	opioid	15608059	Activation of ERK by d amphetamine or by widely abused drugs, including cocaine, nicotine, <b>morphine</b>, and Delta(9) tetrahydrocannabinol was absent in mice lacking dopamine  and cAMP regulated phosphoprotein of M(r) 32,000 (<strong>DARPP 32</strong>).
+PPP1R1B	drug	amphetamine	15608059	The effects of d <b>amphetamine</b> or cocaine on ERK activation in the striatum, but not in the prefrontal cortex, were prevented by point mutation of Thr 34, a <strong>DARPP 32</strong> residue specifically involved in protein phosphatase 1 inhibition.
+PPP1R1B	drug	cocaine	15608059	The effects of d amphetamine or <b>cocaine</b> on ERK activation in the striatum, but not in the prefrontal cortex, were prevented by point mutation of Thr 34, a <strong>DARPP 32</strong> residue specifically involved in protein phosphatase 1 inhibition.
+PPP1R1B	addiction	sensitization	15608059	Blockade of the ERK pathway or mutation of <strong>DARPP 32</strong> altered locomotor <b>sensitization</b> induced by a single injection of psychostimulants, demonstrating the functional relevance of this regulation.
+PPP1R1B	drug	cocaine	15536496	The cyclin dependent kinase Cdk5 and <strong>DARPP 32</strong> (dopamine  and cAMP regulated phosphoprotein of Mr 32 kDa) dependent signaling have been implicated in the regulation of dopaminergic neurotransmission after chronic <b>cocaine</b> treatment.
+PPP1R1B	drug	amphetamine	15536496	The phosphorylation of <strong>DARPP 32</strong> at both Thr75 and Thr34 was differentially regulated after acute <b>METH</b> treatment, but the levels of total Cdk5, p35, and <strong>DARPP 32</strong> remained the same.
+PPP1R1B	addiction	reward	15447670	Within the <b>reward</b>/motor circuitry of the basal ganglia, Cdk5 regulates dopamine neurotransmission via phosphorylation of the postsynaptic signal transduction pathway integrator, <strong>DARPP 32</strong> (dopamine  and cyclic AMP regulated phosphoprotein, M(r) 32,000).
+PPP1R1B	drug	cocaine	15287884	<b>Cocaine</b> sensitized rats showed increased phosphorylation of dopamine  and cyclic AMP regulated phosphoprotein Mr 32 kDa (<strong>DARPP 32</strong>) at threonine 75 (Thr75) and decreased <strong>DARPP 32</strong> phosphorylation at Thr34, in the caudate putamen (CPu) and nucleus accumbens (NAc) 7 days after sensitization assessment.
+PPP1R1B	addiction	sensitization	15287884	Cocaine sensitized rats showed increased phosphorylation of dopamine  and cyclic AMP regulated phosphoprotein Mr 32 kDa (<strong>DARPP 32</strong>) at threonine 75 (Thr75) and decreased <strong>DARPP 32</strong> phosphorylation at Thr34, in the caudate putamen (CPu) and nucleus accumbens (NAc) 7 days after <b>sensitization</b> assessment.
+PPP1R1B	drug	opioid	15287884	Conversely, in <b>morphine</b> sensitized rats, no apparent modifications in <strong>DARPP 32</strong> phosphorylation pattern were observed.
+PPP1R1B	drug	opioid	15287884	Thus, the <strong>DARPP 32</strong> phosphorylation pattern was studied in <b>morphine</b> sensitized rats at different times after <b>morphine</b> challenge.
+PPP1R1B	drug	opioid	15287884	<b>Morphine</b> challenge increased levels of phospho Thr75 <strong>DARPP 32</strong> and decreased levels of phospho Thr34 <strong>DARPP 32</strong> in a time dependent manner in the CPu and NAc.
+PPP1R1B	drug	opioid	15287884	The phosphorylation levels of GluR1 and NR1 subunits decreased in parallel with those of phospho Thr 34 <strong>DARPP 32</strong>, supporting the hypothesis that <b>morphine</b> challenge elicited a decrease in PKA activity in <b>morphine</b> sensitized rats.
+PPP1R1B	drug	cocaine	15066157	Repeated acetyl l carnitine administration increases phospho Thr34 <strong>DARPP 32</strong> levels and antagonizes <b>cocaine</b> induced increase in Cdk5 and phospho Thr75 <strong>DARPP 32</strong> levels in rat striatum.
+PPP1R1B	drug	cocaine	15066157	Abstract Acute <b>cocaine</b> administration increases phosphorylation of dopamine and cAMP regulated phosphoprotein (M(r) 32 kDa) (<strong>DARPP 32</strong>) at threonine (Thr) 34, whereas repeated <b>cocaine</b> administration increases <strong>DARPP 32</strong> phosphorylation at Thr 75 in Sprague Dawley rat striatum.
+PPP1R1B	drug	cocaine	15066157	We compared the effects of repeated <b>cocaine</b> and repeated ALCAR administrations on the behavioural response to <b>cocaine</b> challenge and on the <strong>DARPP 32</strong> phosphorylation pattern and cyclin dependent kinase 5 (Cdk5) levels in the striatum.
+PPP1R1B	drug	cocaine	15066157	A week after the <b>cocaine</b> challenge, the two drugs had induced opposite modifications in <strong>DARPP 32</strong> phosphorylation, as <b>cocaine</b> increased phosphorylation at Thr 75, while ALCAR increased phosphorylation at Thr 34.
+PPP1R1B	drug	cocaine	15066157	In <b>cocaine</b> plus ALCAR treated rats, irrespective of treatment order, ALCAR administration antagonized <b>cocaine</b> effects on <strong>DARPP 32</strong> phosphorylation.
+PPP1R1B	addiction	sensitization	12642909	As to subcellular neurochemical mechanisms of <b>sensitization</b>, the activation of three main cascades is indispensable, 1) D1 dopamine (DA) receptors/PKA/phospho 34Thr <strong>DARPP 32</strong>/PP 1 cascade activated by psychostimulant induced enhancement of DA release in the accumbens, 2) NMDA receptors and CaM KII activated by enhanced release of glutamate, 3) activation of MAP kinase cascade by BDNF and beta 1 subunit of G protein.
+PPP1R1B	drug	alcohol	12068305	<strong>DARPP 32</strong> and regulation of the <b>ethanol</b> sensitivity of NMDA receptors in the nucleus accumbens.
+PPP1R1B	drug	alcohol	12068305	Here we investigate how dopaminergic inputs alter the <b>ethanol</b> sensitivity of NMDA receptors in rats and mice and report that previous dopamine receptor 1 (D1) activation, culminating in dopamine and cAMP regulated phosphoprotein 32 kD (<strong>DARPP 32</strong>) and NMDA receptor subunit 1 (NR1) NMDA receptor phosphorylation, strongly decreases <b>ethanol</b> inhibition of NMDA responses.
+PPP1R1B	drug	alcohol	12068305	The regulation of <b>ethanol</b> sensitivity of NMDA receptors by D1 receptors was absent in <strong>DARPP 32</strong> knockout mice.
+PPP1R1B	drug	alcohol	12068305	We propose that <strong>DARPP 32</strong> mediated blunting of the response to <b>ethanol</b> subsequent to activation of ventral tegmental area dopaminergic neurons initiates molecular alterations that influence synaptic plasticity in this circuit, thereby promoting the development of <b>ethanol</b> reinforcement.
+PPP1R1B	addiction	reward	12068305	We propose that <strong>DARPP 32</strong> mediated blunting of the response to ethanol subsequent to activation of ventral tegmental area dopaminergic neurons initiates molecular alterations that influence synaptic plasticity in this circuit, thereby promoting the development of ethanol <b>reinforcement</b>.
+PPP1R1B	drug	cocaine	11955461	Reduction of <b>cocaine</b> place preference in mice lacking the protein phosphatase 1 inhibitors <strong>DARPP 32</strong> or Inhibitor 1.
+PPP1R1B	drug	cocaine	11955461	In contrast, conditioned place preference to <b>cocaine</b> is reduced in mice lacking <strong>DARPP 32</strong>, I 1, or both phosphoproteins.
+PPP1R1B	drug	cocaine	11955461	These data imply that increased PP 1 function as a result of deficits in <strong>DARPP 32</strong> or I 1 is sufficient to decrease the rewarding properties of <b>cocaine</b>.
+PPP1R1B	drug	alcohol	11150351	Motivational effects of <b>ethanol</b> in <strong>DARPP 32</strong> knock out mice.
+PPP1R1B	drug	alcohol	11150351	<strong>DARPP 32</strong> (dopamine and adenosine 3',5' monophosphate regulated phosphoprotein, 32 kDa) is an important component of dopaminergic function in brain areas thought to be important for drug and <b>alcohol</b> addiction.
+PPP1R1B	addiction	addiction	11150351	<strong>DARPP 32</strong> (dopamine and adenosine 3',5' monophosphate regulated phosphoprotein, 32 kDa) is an important component of dopaminergic function in brain areas thought to be important for drug and alcohol <b>addiction</b>.
+PPP1R1B	drug	alcohol	11150351	The present experiments characterized the acquisition of <b>ethanol</b> induced conditioned taste aversion, <b>ethanol</b> induced conditioned place preference, and <b>ethanol</b> self administration in <strong>DARPP 32</strong> knock out (KO) mice compared to wild type (WT) controls.
+PPP1R1B	addiction	aversion	11150351	The present experiments characterized the acquisition of ethanol induced conditioned taste <b>aversion</b>, ethanol induced conditioned place preference, and ethanol self administration in <strong>DARPP 32</strong> knock out (KO) mice compared to wild type (WT) controls.
+PPP1R1B	drug	amphetamine	20575854	Here we document the involvement of the dopaminoceptive phosphoprotein, <strong>DARPP 32</strong>, the fos related antigen, FRA 2, and the growth associated protein kinase, MAP kinase, in the neurotoxic action of known dopaminergic neurotoxicants, including <b>methamphetamine</b>.
+PPP1R1B	drug	cocaine	10516482	Effects of chronic 'Binge' <b>cocaine</b> administration on plasma ACTH and corticosterone levels in mice deficient in <strong>DARPP 32</strong>.
+PPP1R1B	addiction	intoxication	10516482	Effects of chronic '<b>Binge</b>' cocaine administration on plasma ACTH and corticosterone levels in mice deficient in <strong>DARPP 32</strong>.
+PPP1R1B	drug	cocaine	10516482	We determined the effects of chronic 'binge' pattern <b>cocaine</b> on HPA activity in mice containing a targeted disruption of the <strong>DARPP 32</strong> gene.
+PPP1R1B	addiction	intoxication	10516482	We determined the effects of chronic '<b>binge</b>' pattern cocaine on HPA activity in mice containing a targeted disruption of the <strong>DARPP 32</strong> gene.
+PPP1R1B	drug	cocaine	10516482	In contrast, <strong>DARPP 32</strong> deficient mice failed to show a significant elevation of either plasma ACTH or corticosterone levels following 'binge' <b>cocaine</b>.
+PPP1R1B	addiction	intoxication	10516482	In contrast, <strong>DARPP 32</strong> deficient mice failed to show a significant elevation of either plasma ACTH or corticosterone levels following '<b>binge</b>' cocaine.
+PPP1R1B	drug	cocaine	10516482	The results indicate that <strong>DARPP 32</strong> plays a role in mediating the stimulatory effects of <b>cocaine</b> on the HPA axis.
+PPP1R1B	drug	cocaine	10103106	We investigated the role of the protein phosphatase inhibitor, dopamine  and cAMP regulated phosphoprotein of 32 kDa (<strong>DARPP 32</strong>), in the expression of striatal neuropeptides and in biochemical and behavioural responses to repeated <b>cocaine</b> administration, using <strong>DARPP 32</strong> knock out mice.
+PPP1R1B	drug	cocaine	10103106	Repeated <b>cocaine</b> administration increased levels of DeltaFosB, a Fos family transcription factor, in the striatum of wild type mice, and this increase was abolished in <strong>DARPP 32</strong> mutant mice.
+PPP1R1B	drug	cocaine	10103106	These data show that <strong>DARPP 32</strong> is involved in regulating substance P expression in the striatonigral pathway, and in biochemical and behavioural plasticity with chronic administration of <b>cocaine</b>.
+HOMER1	drug	alcohol	32338122	Following in utero THC exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and aversive limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for NPY neurons and the PSD proteins <strong>Homer</strong> 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, <b>alcohol</b> taking, relapse and conflict behaviour in the operant chamber throughout adolescence until early adulthood (cohort 2).
+HOMER1	drug	cannabinoid	32338122	Following in utero <b>THC</b> exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and aversive limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for NPY neurons and the PSD proteins <strong>Homer</strong> 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, alcohol taking, relapse and conflict behaviour in the operant chamber throughout adolescence until early adulthood (cohort 2).
+HOMER1	addiction	aversion	32338122	Following in utero THC exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and <b>aversive</b> limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for NPY neurons and the PSD proteins <strong>Homer</strong> 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, alcohol taking, relapse and conflict behaviour in the operant chamber throughout adolescence until early adulthood (cohort 2).
+HOMER1	addiction	relapse	32338122	Following in utero THC exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and aversive limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for NPY neurons and the PSD proteins <strong>Homer</strong> 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, alcohol taking, <b>relapse</b> and conflict behaviour in the operant chamber throughout adolescence until early adulthood (cohort 2).
+HOMER1	addiction	reward	32338122	Following in utero THC exposure (2 mg/kg delivered subcutaneously), preadolescent male rat offspring were assessed for: behavioural reactivity in the open field test, neutral declarative memory and aversive limbic memory in the Novel Object and Emotional Object Recognition tests, immunofluorescence for NPY neurons and the PSD proteins <strong>Homer</strong> 1, 1b/c and 2 in the prefrontal cortex, amygdala and nucleus accumbens at adolescence (cohort 1); and instrumental learning, alcohol taking, relapse and conflict behaviour in the <b>operant</b> chamber throughout adolescence until early adulthood (cohort 2).
+HOMER1	drug	alcohol	32338122	In utero THC exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired aversive limbic memory; (d) decreased NPY positive neurons in limbic regions; (e) region specific variations in <strong>Homer</strong> 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased <b>alcohol</b> drinking, relapse and conflict behaviour in the operant chamber.
+HOMER1	drug	cannabinoid	32338122	In utero <b>THC</b> exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired aversive limbic memory; (d) decreased NPY positive neurons in limbic regions; (e) region specific variations in <strong>Homer</strong> 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased alcohol drinking, relapse and conflict behaviour in the operant chamber.
+HOMER1	addiction	aversion	32338122	In utero THC exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired <b>aversive</b> limbic memory; (d) decreased NPY positive neurons in limbic regions; (e) region specific variations in <strong>Homer</strong> 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased alcohol drinking, relapse and conflict behaviour in the operant chamber.
+HOMER1	addiction	relapse	32338122	In utero THC exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired aversive limbic memory; (d) decreased NPY positive neurons in limbic regions; (e) region specific variations in <strong>Homer</strong> 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased alcohol drinking, <b>relapse</b> and conflict behaviour in the operant chamber.
+HOMER1	addiction	reward	32338122	In utero THC exposed adolescent rats showed: (a) increased locomotor activity; (b) no alteration in neutral declarative memory; (c) impaired aversive limbic memory; (d) decreased NPY positive neurons in limbic regions; (e) region specific variations in <strong>Homer</strong> 1, 1b/c and 2 immunoreactivity; (f) decreased instrumental learning and increased alcohol drinking, relapse and conflict behaviour in the <b>operant</b> chamber.
+HOMER1	drug	cocaine	31653935	Consistent with this in vivo observation, we found that lack of Rhes in mice caused a greater increase in striatal <b>cocaine</b> dependent D1R/cAMP/PKA signaling, along with considerable enhancement of Arc, zif268, and <strong>Homer1</strong> mRNA expression.
+HOMER1	drug	amphetamine	31146278	Here, we observed no change in surface or total mGlu1 protein or its coupling to <strong>Homer</strong> scaffolding proteins after <b>methamphetamine</b> withdrawal, nor did elevation of mGlu1 tone through repeated injections of an mGlu1 positive allosteric modulator delay incubation of craving.
+HOMER1	addiction	relapse	31146278	Here, we observed no change in surface or total mGlu1 protein or its coupling to <strong>Homer</strong> scaffolding proteins after methamphetamine withdrawal, nor did elevation of mGlu1 tone through repeated injections of an mGlu1 positive allosteric modulator delay incubation of <b>craving</b>.
+HOMER1	addiction	withdrawal	31146278	Here, we observed no change in surface or total mGlu1 protein or its coupling to <strong>Homer</strong> scaffolding proteins after methamphetamine <b>withdrawal</b>, nor did elevation of mGlu1 tone through repeated injections of an mGlu1 positive allosteric modulator delay incubation of craving.
+HOMER1	drug	cocaine	30946882	Further, we found that dysregulated metabolic activity and mGlu5 receptor signaling in the PrL of <b>cocaine</b> rats correlated with past working memory performance and/or drug seeking, as indicated by the analysis of cytochrome oxidase reactivity, mGlu5 and <strong>Homer</strong> 1b/c protein expression, as well as Arc mRNA expression in mGlu5 positive cells.
+HOMER1	addiction	relapse	30946882	Further, we found that dysregulated metabolic activity and mGlu5 receptor signaling in the PrL of cocaine rats correlated with past working memory performance and/or drug <b>seeking</b>, as indicated by the analysis of cytochrome oxidase reactivity, mGlu5 and <strong>Homer</strong> 1b/c protein expression, as well as Arc mRNA expression in mGlu5 positive cells.
+HOMER1	drug	alcohol	29580163	From <strong>Homer</strong> and Hippocrates to modern personalized medicine: is there a role for pharmacoepigenomics in the treatment of <b>alcohol</b> addiction?
+HOMER1	addiction	addiction	29580163	From <strong>Homer</strong> and Hippocrates to modern personalized medicine: is there a role for pharmacoepigenomics in the treatment of alcohol <b>addiction</b>?
+HOMER1	drug	alcohol	29249995	The consequences of repeated <b>alcohol</b> administration on the expression of the <strong>Homer</strong> family proteins demonstrate a crucial and active role, particularly for the expression of Homer2 isoform, in regulating <b>alcohol</b> induced behavioral and cellular neuroplasticity.
+HOMER1	drug	cocaine	29163080	Earlier studies of <strong>Homer1</strong> gene knock out (KO) mice indicated active, but distinct, roles for IEG and constitutively expressed <strong>Homer1</strong> gene products in regulating cognitive, emotional, motivational and sensorimotor processing, as well as behavioral and neurochemical sensitivity to <b>cocaine</b>.
+HOMER1	drug	cocaine	29163080	More recent characterization of transgenic mice engineered to prevent generation of the IEG form (a.k.a <strong>Homer1a</strong> KO) pose a critical role for <strong>Homer1a</strong> in <b>cocaine</b> induced behavioral and neurochemical sensitization of relevance to drug addiction and related neuropsychiatric disorders.
+HOMER1	addiction	addiction	29163080	More recent characterization of transgenic mice engineered to prevent generation of the IEG form (a.k.a <strong>Homer1a</strong> KO) pose a critical role for <strong>Homer1a</strong> in cocaine induced behavioral and neurochemical sensitization of relevance to drug <b>addiction</b> and related neuropsychiatric disorders.
+HOMER1	addiction	sensitization	29163080	More recent characterization of transgenic mice engineered to prevent generation of the IEG form (a.k.a <strong>Homer1a</strong> KO) pose a critical role for <strong>Homer1a</strong> in cocaine induced behavioral and neurochemical <b>sensitization</b> of relevance to drug addiction and related neuropsychiatric disorders.
+HOMER1	drug	cocaine	29163080	Here, we extend our characterization of the <strong>Homer1a</strong> KO mouse and report a modest pro depressant phenotype, but no deleterious effects of the KO upon spatial learning/memory, prepulse inhibition, or <b>cocaine</b> induced place conditioning.
+HOMER1	drug	cocaine	29163080	As we reported previously, <strong>Homer1a</strong> KO mice did not develop <b>cocaine</b> induced behavioral or neurochemical sensitization within the nucleus accumbens; however, virus mediated <strong>Homer1a</strong> over expression within the nucleus accumbens reversed the sensitization phenotype of KO mice.
+HOMER1	addiction	sensitization	29163080	As we reported previously, <strong>Homer1a</strong> KO mice did not develop cocaine induced behavioral or neurochemical <b>sensitization</b> within the nucleus accumbens; however, virus mediated <strong>Homer1a</strong> over expression within the nucleus accumbens reversed the <b>sensitization</b> phenotype of KO mice.
+HOMER1	drug	cocaine	29163080	Moreover, the data indicate a specific role for <strong>Homer1a</strong> in regulating <b>cocaine</b> induced behavioral and neurochemical sensitization of potential relevance to the psychotogenic properties of this drug.
+HOMER1	addiction	sensitization	29163080	Moreover, the data indicate a specific role for <strong>Homer1a</strong> in regulating cocaine induced behavioral and neurochemical <b>sensitization</b> of potential relevance to the psychotogenic properties of this drug.
+HOMER1	drug	cocaine	29055697	<b>Cocaine</b> alters <strong>Homer1</strong> natural antisense transcript in the nucleus accumbens.
+HOMER1	drug	cocaine	29055697	We found that 22% of the genes examined contain NATs and that expression of <strong>Homer1</strong> natural antisense transcript (<strong>Homer1</strong> AS) was altered in the nucleus accumbens (NAc) of mice 2h and 10days following repeated <b>cocaine</b> administration.
+HOMER1	drug	cocaine	29055697	Future in vivo studies are needed to definitely determine a role for <strong>Homer1</strong> AS in <b>cocaine</b> induced behavioral and molecular adaptations.
+HOMER1	drug	alcohol	27180911	However, genetic variations in ANKK1 (rs1800497) and <strong>HOMER1</strong> (rs7713917) play an equal role in predicting <b>alcohol</b> drinking two years later and are most important in predicting the increase in <b>alcohol</b> consumption.
+HOMER1	drug	alcohol	26791202	mTORC1 is critically involved in RNA to protein translation, and we found that the first <b>alcohol</b> session rapidly activated mTORC1 in NAc shell D1+ neurons and increased synaptic expression of the AMPAR subunit GluA1 and the scaffolding protein <strong>Homer</strong>.
+HOMER1	drug	cocaine	26598422	Increased expression after <b>cocaine</b> self administration was found for 6 IEGs in dorsal and ventral striatum (c fos, Mkp1, Fosb/ΔFosb, Egr2, Egr4, and Arc) and 10 IEGs in mPFC (same 6 IEGs as in striatum, plus Bdnf, <strong>Homer1</strong>, Sgk1 and Rgs2).
+HOMER1	drug	alcohol	25743187	In the medial prefrontal cortex, 2.5g/kg <b>ethanol</b> decreased mRNA expression of brain derived neurotrophic factor, NMDA NR2A subunit, mGluR8 receptor, <strong>Homer1</strong>, the glutamate transporters SLC1a1 and SLC1a6 and Srr.
+HOMER1	drug	cocaine	25530939	Thus, we measured the effects of a 6 day repeated treatment with methylphenidate (5 mg/kg), fluoxetine (5 mg/kg) or their combination on the inducibility (by <b>cocaine</b>) of neuroplasticity related IEGs (Zif268, <strong>Homer1a</strong>) in the striatum, by in situ hybridization histochemistry.
+HOMER1	drug	cocaine	25408547	Our results showed that both contingent and non contingent <b>cocaine</b> administration produces numerous, brain region specific, alterations in the mGluR(5), NMDA, and <strong>Homer1b</strong>/1c protein expression which are dependent on the modality of <b>cocaine</b> administration.
+HOMER1	drug	cocaine	24118426	<b>Cocaine</b> elicited imbalances in ventromedial prefrontal cortex <strong>Homer1</strong> versus Homer2 expression: implications for relapse.
+HOMER1	addiction	relapse	24118426	Cocaine elicited imbalances in ventromedial prefrontal cortex <strong>Homer1</strong> versus Homer2 expression: implications for <b>relapse</b>.
+HOMER1	drug	cocaine	24118426	Withdrawal from a history of extended access to self administered <b>cocaine</b> produces a time dependent intensification of drug seeking, which might relate to a <b>cocaine</b> induced imbalance in the relative expression of constitutively expressed <strong>Homer1</strong> versus Homer2 isoforms within the ventromedial aspect of the prefrontal cortex (vmPFC).
+HOMER1	addiction	relapse	24118426	Withdrawal from a history of extended access to self administered cocaine produces a time dependent intensification of drug <b>seeking</b>, which might relate to a cocaine induced imbalance in the relative expression of constitutively expressed <strong>Homer1</strong> versus Homer2 isoforms within the ventromedial aspect of the prefrontal cortex (vmPFC).
+HOMER1	addiction	withdrawal	24118426	<b>Withdrawal</b> from a history of extended access to self administered cocaine produces a time dependent intensification of drug seeking, which might relate to a cocaine induced imbalance in the relative expression of constitutively expressed <strong>Homer1</strong> versus Homer2 isoforms within the ventromedial aspect of the prefrontal cortex (vmPFC).
+HOMER1	drug	cocaine	24118426	Thus, we employed immunoblotting to examine the relation between cue reinforced lever pressing at 3  versus 30 day withdrawal from a 10 day history of extended access (6 hours/day) to intravenous <b>cocaine</b> (0.25 mg/infusion) or saline (Sal6h), and the expression of <strong>Homer1b</strong>/c and Homer2a/b within the vmPFC versus the more dorsomedial aspect of this structure (dmPFC).
+HOMER1	addiction	withdrawal	24118426	Thus, we employed immunoblotting to examine the relation between cue reinforced lever pressing at 3  versus 30 day <b>withdrawal</b> from a 10 day history of extended access (6 hours/day) to intravenous cocaine (0.25 mg/infusion) or saline (Sal6h), and the expression of <strong>Homer1b</strong>/c and Homer2a/b within the vmPFC versus the more dorsomedial aspect of this structure (dmPFC).
+HOMER1	drug	cocaine	24118426	Behavioral studies employed adeno associated virus (AAV) vectors to reverse <b>cocaine</b> elicited changes in the relative expression of <strong>Homer1</strong> versus Homer2 isoforms and tested animals for <b>cocaine</b> prime , and cue induced responding following extinction training.
+HOMER1	drug	cocaine	24118426	<b>Cocaine</b> self administration elevated both <strong>Homer1b</strong>/c and Homer2a/b levels within the vmPFC at 3 day withdrawal, and the rise in Homer2a/b persisted for at least 30 days.
+HOMER1	addiction	withdrawal	24118426	Cocaine self administration elevated both <strong>Homer1b</strong>/c and Homer2a/b levels within the vmPFC at 3 day <b>withdrawal</b>, and the rise in Homer2a/b persisted for at least 30 days.
+HOMER1	drug	cocaine	24118426	Reversing the relative increase in Homer2 versus <strong>Homer1</strong> expression via Homer1c overexpression or Homer2b knockdown failed to influence cue reinforced lever pressing when animals were tested in a drug free state, but both AAV treatments prevented <b>cocaine</b> primed reinstatement of lever pressing behavior.
+HOMER1	addiction	relapse	24118426	Reversing the relative increase in Homer2 versus <strong>Homer1</strong> expression via Homer1c overexpression or Homer2b knockdown failed to influence cue reinforced lever pressing when animals were tested in a drug free state, but both AAV treatments prevented cocaine primed <b>reinstatement</b> of lever pressing behavior.
+HOMER1	drug	cocaine	24118426	Reversing the relative increase in Homer2 versus <strong>Homer1</strong> expression via <strong>Homer1c</strong> overexpression or Homer2b knockdown failed to influence cue reinforced lever pressing when animals were tested in a drug free state, but both AAV treatments prevented <b>cocaine</b> primed reinstatement of lever pressing behavior.
+HOMER1	addiction	relapse	24118426	Reversing the relative increase in Homer2 versus <strong>Homer1</strong> expression via <strong>Homer1c</strong> overexpression or Homer2b knockdown failed to influence cue reinforced lever pressing when animals were tested in a drug free state, but both AAV treatments prevented cocaine primed <b>reinstatement</b> of lever pressing behavior.
+HOMER1	drug	cocaine	24118426	These data suggest that a <b>cocaine</b> elicited imbalance in the relative expression of constitutively expressed Homer2 versus <strong>Homer1</strong> within the vmPFC is necessary for the capacity of <b>cocaine</b> to reinstate drug seeking behavior, posing drug induced changes in vmPFC Homer expression as a molecular trigger contributing to drug elicited relapse.
+HOMER1	addiction	relapse	24118426	These data suggest that a cocaine elicited imbalance in the relative expression of constitutively expressed Homer2 versus <strong>Homer1</strong> within the vmPFC is necessary for the capacity of cocaine to reinstate drug <b>seeking</b> behavior, posing drug induced changes in vmPFC Homer expression as a molecular trigger contributing to drug elicited <b>relapse</b>.
+HOMER1	drug	cocaine	24118426	These data suggest that a <b>cocaine</b> elicited imbalance in the relative expression of constitutively expressed Homer2 versus <strong>Homer1</strong> within the vmPFC is necessary for the capacity of <b>cocaine</b> to reinstate drug seeking behavior, posing drug induced changes in vmPFC <strong>Homer</strong> expression as a molecular trigger contributing to drug elicited relapse.
+HOMER1	addiction	relapse	24118426	These data suggest that a cocaine elicited imbalance in the relative expression of constitutively expressed Homer2 versus <strong>Homer1</strong> within the vmPFC is necessary for the capacity of cocaine to reinstate drug <b>seeking</b> behavior, posing drug induced changes in vmPFC <strong>Homer</strong> expression as a molecular trigger contributing to drug elicited <b>relapse</b>.
+HOMER1	drug	amphetamine	23895375	<b>Methamphetamine</b> induced 3 20 fold increases of immediate early genes arc, <strong>homer</strong> 2, c fos, fosB, and its isoforms (ΔfosB and a novel isoform ΔfosB 2) in Fos positive but not Fos negative neurons.
+HOMER1	drug	cocaine	23763573	We measured, by in situ hybridization histochemistry, the effects of a 5 day repeated treatment with methylphenidate (5 mg/kg), fluoxetine (5 mg/kg) or a combination on the inducibility (by <b>cocaine</b>) of neuroplasticity related genes (Zif268, <strong>Homer1a</strong>) in the striatum.
+HOMER1	addiction	addiction	23761764	<strong>Homer</strong> proteins, and their associated glutamate receptors, regulate behavioral sensitivity to various <b>addictive</b> drugs.
+HOMER1	drug	opioid	23761764	Null mutations of Homer1a, <strong>Homer1</strong>, and Homer2, as well as transgenic disruption of mGluR5 Homer interactions, either attenuated or completely blocked low dose <b>heroin</b> CPP, and none of the CCI mutant strains exhibited <b>heroin</b> induced CPA.
+HOMER1	addiction	reward	23761764	Null mutations of Homer1a, <strong>Homer1</strong>, and Homer2, as well as transgenic disruption of mGluR5 Homer interactions, either attenuated or completely blocked low dose heroin <b>CPP</b>, and none of the CCI mutant strains exhibited heroin induced CPA.
+HOMER1	drug	opioid	23761764	Null mutations of Homer1a, <strong>Homer1</strong>, and Homer2, as well as transgenic disruption of mGluR5 <strong>Homer</strong> interactions, either attenuated or completely blocked low dose <b>heroin</b> CPP, and none of the CCI mutant strains exhibited <b>heroin</b> induced CPA.
+HOMER1	addiction	reward	23761764	Null mutations of Homer1a, <strong>Homer1</strong>, and Homer2, as well as transgenic disruption of mGluR5 <strong>Homer</strong> interactions, either attenuated or completely blocked low dose heroin <b>CPP</b>, and none of the CCI mutant strains exhibited heroin induced CPA.
+HOMER1	drug	opioid	23761764	Null mutations of <strong>Homer1a</strong>, <strong>Homer1</strong>, and Homer2, as well as transgenic disruption of mGluR5 <strong>Homer</strong> interactions, either attenuated or completely blocked low dose <b>heroin</b> CPP, and none of the CCI mutant strains exhibited <b>heroin</b> induced CPA.
+HOMER1	addiction	reward	23761764	Null mutations of <strong>Homer1a</strong>, <strong>Homer1</strong>, and Homer2, as well as transgenic disruption of mGluR5 <strong>Homer</strong> interactions, either attenuated or completely blocked low dose heroin <b>CPP</b>, and none of the CCI mutant strains exhibited heroin induced CPA.
+HOMER1	drug	opioid	23761764	However, <b>heroin</b> CPP did not depend upon full Homer1c expression within the nucleus accumbens (NAC), as CPP occurred in controls infused locally with small hairpin RNA Homer1c, although intra NAC and/or intrathecal cDNA Homer1c,  <strong>Homer1a</strong>, and  Homer2b infusions (to best mimic CCI's effects) were sufficient to blunt <b>heroin</b> CPP in uninjured mice.
+HOMER1	addiction	reward	23761764	However, heroin <b>CPP</b> did not depend upon full Homer1c expression within the nucleus accumbens (NAC), as <b>CPP</b> occurred in controls infused locally with small hairpin RNA Homer1c, although intra NAC and/or intrathecal cDNA Homer1c,  <strong>Homer1a</strong>, and  Homer2b infusions (to best mimic CCI's effects) were sufficient to blunt heroin <b>CPP</b> in uninjured mice.
+HOMER1	drug	opioid	23761764	However, <b>heroin</b> CPP did not depend upon full <strong>Homer1c</strong> expression within the nucleus accumbens (NAC), as CPP occurred in controls infused locally with small hairpin RNA <strong>Homer1c</strong>, although intra NAC and/or intrathecal cDNA <strong>Homer1c</strong>,  <strong>Homer1a</strong>, and  Homer2b infusions (to best mimic CCI's effects) were sufficient to blunt <b>heroin</b> CPP in uninjured mice.
+HOMER1	addiction	reward	23761764	However, heroin <b>CPP</b> did not depend upon full <strong>Homer1c</strong> expression within the nucleus accumbens (NAC), as <b>CPP</b> occurred in controls infused locally with small hairpin RNA <strong>Homer1c</strong>, although intra NAC and/or intrathecal cDNA <strong>Homer1c</strong>,  <strong>Homer1a</strong>, and  Homer2b infusions (to best mimic CCI's effects) were sufficient to blunt heroin <b>CPP</b> in uninjured mice.
+HOMER1	drug	opioid	23761764	However, arguing against a simple role for CCI induced increases in either spinal or NAC <strong>Homer</strong> expression for <b>heroin</b> CPA, cDNA infusion of our various cDNA constructs either did not affect (intrathecal) or attenuated (NAC) <b>heroin</b> CPA.
+HOMER1	drug	opioid	23761764	Together, these data implicate increases in glutamate receptor/<strong>Homer</strong>/kinase activity within limbic structures, perhaps outside the NAC, as possibly critical for switching the incentive motivational properties of <b>heroin</b> following nerve injury, which has relevance for <b>opioid</b> psychopharmacology in individuals suffering from neuropathic pain.
+HOMER1	addiction	reward	23761764	Together, these data implicate increases in glutamate receptor/<strong>Homer</strong>/kinase activity within limbic structures, perhaps outside the NAC, as possibly critical for switching the <b>incentive</b> motivational properties of heroin following nerve injury, which has relevance for opioid psychopharmacology in individuals suffering from neuropathic pain.
+HOMER1	drug	cocaine	23658151	Imbalances in prefrontal cortex CC <strong>Homer1</strong> versus CC Homer2 expression promote <b>cocaine</b> preference.
+HOMER1	addiction	addiction	23658151	<strong>Homer</strong> postsynaptic scaffolding proteins regulate forebrain glutamate transmission and thus, are likely molecular candidates mediating hypofrontality in <b>addiction</b>.
+HOMER1	drug	cocaine	23658151	Protracted withdrawal from <b>cocaine</b> experience increases the relative expression of Homer2 versus <strong>Homer1</strong> isoforms within medial prefrontal cortex (mPFC).
+HOMER1	addiction	withdrawal	23658151	Protracted <b>withdrawal</b> from cocaine experience increases the relative expression of Homer2 versus <strong>Homer1</strong> isoforms within medial prefrontal cortex (mPFC).
+HOMER1	drug	cocaine	23658151	In contrast, elevating the relative expression of Homer2b versus <strong>Homer1</strong> within mPFC, by overexpressing Homer2b or knocking down Homer1c, shifted the dose response function for <b>cocaine</b> conditioned reward to the left, without affecting <b>cocaine</b> locomotion or sensitization.
+HOMER1	addiction	reward	23658151	In contrast, elevating the relative expression of Homer2b versus <strong>Homer1</strong> within mPFC, by overexpressing Homer2b or knocking down Homer1c, shifted the dose response function for cocaine conditioned <b>reward</b> to the left, without affecting cocaine locomotion or sensitization.
+HOMER1	addiction	sensitization	23658151	In contrast, elevating the relative expression of Homer2b versus <strong>Homer1</strong> within mPFC, by overexpressing Homer2b or knocking down Homer1c, shifted the dose response function for cocaine conditioned reward to the left, without affecting cocaine locomotion or <b>sensitization</b>.
+HOMER1	drug	cocaine	23658151	In contrast, elevating the relative expression of Homer2b versus <strong>Homer1</strong> within mPFC, by overexpressing Homer2b or knocking down <strong>Homer1c</strong>, shifted the dose response function for <b>cocaine</b> conditioned reward to the left, without affecting <b>cocaine</b> locomotion or sensitization.
+HOMER1	addiction	reward	23658151	In contrast, elevating the relative expression of Homer2b versus <strong>Homer1</strong> within mPFC, by overexpressing Homer2b or knocking down <strong>Homer1c</strong>, shifted the dose response function for cocaine conditioned <b>reward</b> to the left, without affecting cocaine locomotion or sensitization.
+HOMER1	addiction	sensitization	23658151	In contrast, elevating the relative expression of Homer2b versus <strong>Homer1</strong> within mPFC, by overexpressing Homer2b or knocking down <strong>Homer1c</strong>, shifted the dose response function for cocaine conditioned reward to the left, without affecting cocaine locomotion or <b>sensitization</b>.
+HOMER1	drug	cocaine	23658151	Intriguingly, both these transgenic manipulations produced glutamate anomalies within the nucleus accumbens (NAC) of <b>cocaine</b> naive animals that are reminiscent of those observed in <b>cocaine</b> experienced animals, including reduced basal extracellular glutamate content, reduced <strong>Homer1</strong>/2 and glutamate receptor expression, and augmented <b>cocaine</b> elicited glutamate release.
+HOMER1	drug	cocaine	23658151	Together, these data provide novel evidence in support of opposing roles for constitutively expressed <strong>Homer1</strong> and Homer2 isoforms in regulating mPFC glutamate transmission in vivo and support the hypothesis that <b>cocaine</b> elicited increases in the relative amount of mPFC Homer2 versus <strong>Homer1</strong> signaling produces abnormalities in NAC glutamate transmission that enhance vulnerability to <b>cocaine</b> reward.
+HOMER1	addiction	reward	23658151	Together, these data provide novel evidence in support of opposing roles for constitutively expressed <strong>Homer1</strong> and Homer2 isoforms in regulating mPFC glutamate transmission in vivo and support the hypothesis that cocaine elicited increases in the relative amount of mPFC Homer2 versus <strong>Homer1</strong> signaling produces abnormalities in NAC glutamate transmission that enhance vulnerability to cocaine <b>reward</b>.
+HOMER1	drug	alcohol	22749946	Chronic self administration of <b>ethanol</b> reduced the expression of the C fos gene 4  to 12 fold and increased expression of the COX 2 (up to 4 fold) and <strong>Homer1a</strong> genes in the rat prefrontal cortex.
+HOMER1	drug	alcohol	22432643	Intra NAC shell blockade of mGluR5, Homer2, or PI3K signaling, as well as transgenic disruption of the <strong>Homer</strong> binding site on mGluR5, decreased <b>alcohol</b> consumption in B6 mice.
+HOMER1	drug	cocaine	22340009	Microinjecting a membrane permeable peptide antagonist of <strong>Homer</strong> binding to mGluR5 into the NAcore also inhibited cue  and <b>cocaine</b> reinstated lever pressing.
+HOMER1	drug	cocaine	22340009	Taken together, these data show that mGluR5 inhibition and stimulation in the NAcore can regulate <b>cocaine</b> seeking, and demonstrate that one mechanism for this effect is via interactions with <strong>Homer</strong> proteins.
+HOMER1	addiction	relapse	22340009	Taken together, these data show that mGluR5 inhibition and stimulation in the NAcore can regulate cocaine <b>seeking</b>, and demonstrate that one mechanism for this effect is via interactions with <strong>Homer</strong> proteins.
+HOMER1	drug	cocaine	21126734	In line with the GluA1 PSD 95 implications of enhanced synaptic plasticity, <strong>Homer</strong> 1b/c protein expression was increased in both heroin and <b>cocaine</b> users as was its binding partner, dynamin 3.
+HOMER1	drug	opioid	21126734	In line with the GluA1 PSD 95 implications of enhanced synaptic plasticity, <strong>Homer</strong> 1b/c protein expression was increased in both <b>heroin</b> and cocaine users as was its binding partner, dynamin 3.
+HOMER1	drug	alcohol	21041654	We further show that the protein expression levels of GluR1 and <strong>Homer</strong>, two synaptic proteins whose translation has been shown to be modulated by mTORC1, are up regulated in the NAc of rodents with a history of excessive <b>alcohol</b> consumption.
+HOMER1	drug	amphetamine	20649838	Furthermore, <b>amphetamine</b> but not cocaine treatment maintained the ratio between the glutamate receptor mGluR1/5 interacting proteins <strong>Homer</strong> and Homer1a in the knockouts thereby sustaining the direct pathway.
+HOMER1	drug	cocaine	20649838	Furthermore, amphetamine but not <b>cocaine</b> treatment maintained the ratio between the glutamate receptor mGluR1/5 interacting proteins <strong>Homer</strong> and Homer1a in the knockouts thereby sustaining the direct pathway.
+HOMER1	drug	amphetamine	20649838	Furthermore, <b>amphetamine</b> but not cocaine treatment maintained the ratio between the glutamate receptor mGluR1/5 interacting proteins <strong>Homer</strong> and <strong>Homer1a</strong> in the knockouts thereby sustaining the direct pathway.
+HOMER1	drug	cocaine	20649838	Furthermore, amphetamine but not <b>cocaine</b> treatment maintained the ratio between the glutamate receptor mGluR1/5 interacting proteins <strong>Homer</strong> and <strong>Homer1a</strong> in the knockouts thereby sustaining the direct pathway.
+HOMER1	drug	cocaine	20534846	Accordingly, when <strong>Homer1c</strong> was overexpressed in the core of <b>cocaine</b> naive rats with an adenoassociated virus, long term depression was inhibited.
+HOMER1	drug	cocaine	20534846	This mechanism may contribute to the inhibition of <b>cocaine</b> seeking by extinction training because overexpression of <strong>Homer1c</strong> in the core also inhibited cue induced reinstatement of <b>cocaine</b> seeking.
+HOMER1	addiction	relapse	20534846	This mechanism may contribute to the inhibition of cocaine <b>seeking</b> by extinction training because overexpression of <strong>Homer1c</strong> in the core also inhibited cue induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+HOMER1	drug	alcohol	20333726	No association of <b>alcohol</b> dependence with <strong>HOMER</strong> 1 and 2 genetic variants.
+HOMER1	addiction	dependence	20333726	No association of alcohol <b>dependence</b> with <strong>HOMER</strong> 1 and 2 genetic variants.
+HOMER1	drug	alcohol	20333726	<strong>HOMER</strong> 1 and 2 have been reported to contribute to chronic <b>alcohol</b> induced long term neurochemical changes in the endogenous reward system.
+HOMER1	addiction	reward	20333726	<strong>HOMER</strong> 1 and 2 have been reported to contribute to chronic alcohol induced long term neurochemical changes in the endogenous <b>reward</b> system.
+HOMER1	drug	alcohol	20333726	Data from animal models suggest a potential role of the <strong>Homer</strong> protein family in the development of <b>alcohol</b> and substance use.
+HOMER1	drug	alcohol	20333726	The aim of this study is to assess potential associations between <strong>HOMER</strong> 1 and 2 genetic variants in a larger sample of <b>alcohol</b> dependent individuals and unrelated controls.
+HOMER1	drug	alcohol	20333726	Five genetic variants of <strong>HOMER</strong> 1 and 3 of <strong>HOMER</strong> 2 were genotyped in a multi site sample of 1,923 German healthy controls and 2,039 <b>alcohol</b> dependent subjects.
+HOMER1	drug	alcohol	20333726	While most of the <strong>HOMER</strong> 1 and 2 SNPs are in low to moderate linkage disequilibrium, three major haplotypes of <strong>HOMER</strong> 1 and 4 haplotypes of <strong>HOMER</strong> 2 are present in the majority of <b>alcohol</b> dependent and control subjects.
+HOMER1	drug	alcohol	19673743	Differential effects of chronic <b>ethanol</b> consumption and withdrawal on <strong>homer</strong>/glutamate receptor expression in subregions of the accumbens and amygdala of P rats.
+HOMER1	addiction	withdrawal	19673743	Differential effects of chronic ethanol consumption and <b>withdrawal</b> on <strong>homer</strong>/glutamate receptor expression in subregions of the accumbens and amygdala of P rats.
+HOMER1	drug	alcohol	19673743	In this study, we examined the effects of short versus long term withdrawal from chronic <b>ethanol</b> consumption on <strong>Homer</strong> and glutamate receptor protein expression within striatal and amygdala subregions of selectively bred, <b>alcohol</b> preferring P rats.
+HOMER1	addiction	withdrawal	19673743	In this study, we examined the effects of short versus long term <b>withdrawal</b> from chronic ethanol consumption on <strong>Homer</strong> and glutamate receptor protein expression within striatal and amygdala subregions of selectively bred, alcohol preferring P rats.
+HOMER1	drug	alcohol	19673743	Rats were killed 24 hours (short withdrawal: SW) or 4 weeks (long withdrawal: LW) after termination of <b>ethanol</b> access, subregions of interest were micropunched and tissue processed for detection of Group1 mGluRs, NR2 subunits of the NMDA receptor and <strong>Homer</strong> protein expression.
+HOMER1	addiction	withdrawal	19673743	Rats were killed 24 hours (short <b>withdrawal</b>: SW) or 4 weeks (long <b>withdrawal</b>: LW) after termination of ethanol access, subregions of interest were micropunched and tissue processed for detection of Group1 mGluRs, NR2 subunits of the NMDA receptor and <strong>Homer</strong> protein expression.
+HOMER1	drug	alcohol	19587272	Moreover, when compared with wild type littermates, transgenic mice with an F1128R point mutation in mGluR5 that markedly reduces <strong>Homer</strong> binding exhibited a 50% reduction in binge <b>alcohol</b> drinking, which was related to reduced NAC basal PI3K activity.
+HOMER1	addiction	intoxication	19587272	Moreover, when compared with wild type littermates, transgenic mice with an F1128R point mutation in mGluR5 that markedly reduces <strong>Homer</strong> binding exhibited a 50% reduction in <b>binge</b> alcohol drinking, which was related to reduced NAC basal PI3K activity.
+HOMER1	drug	alcohol	19587272	Consistent with the hypothesis that mGluR5 <strong>Homer</strong> PI3K signaling may be a mechanism governing excessive <b>alcohol</b> intake, the "anti binge" effects of MPEP and wortmannin were not additive, nor were they observed in the mGluR5(F1128R) transgenic mice.
+HOMER1	addiction	intoxication	19587272	Consistent with the hypothesis that mGluR5 <strong>Homer</strong> PI3K signaling may be a mechanism governing excessive alcohol intake, the "anti <b>binge</b>" effects of MPEP and wortmannin were not additive, nor were they observed in the mGluR5(F1128R) transgenic mice.
+HOMER1	drug	alcohol	19426165	Electroacupuncture inhibits <b>ethanol</b> induced locomotor sensitization and alters <strong>homer1A</strong> mRNA expression in mice.
+HOMER1	addiction	sensitization	19426165	Electroacupuncture inhibits ethanol induced locomotor <b>sensitization</b> and alters <strong>homer1A</strong> mRNA expression in mice.
+HOMER1	drug	alcohol	19426165	One hour after the challenge with <b>ethanol</b>, the animals were decapitated, the hippocampus, striatum, and prefrontal cortex were dissected, and the expression of <strong>homer1A</strong> mRNA assessed by PCR.
+HOMER1	drug	alcohol	19426165	In addition, electroacupuncture blocked the diminution of <strong>homer1A</strong> mRNA expression triggered by <b>ethanol</b> in the acquisition (striatum and prefrontal cortex), expression (hippocampus), and in the maintenance (hippocampus and prefrontal cortex) phases.
+HOMER1	drug	alcohol	19426165	We suggest that electroacupuncture effects over <b>ethanol</b> induced locomotor sensitization are associated to its ability to modulate <strong>homer1A</strong> expression and glutamatergic plasticity.
+HOMER1	addiction	sensitization	19426165	We suggest that electroacupuncture effects over ethanol induced locomotor <b>sensitization</b> are associated to its ability to modulate <strong>homer1A</strong> expression and glutamatergic plasticity.
+HOMER1	drug	cocaine	19419424	Long lasting dysregulation of gene expression in corticostriatal circuits after repeated <b>cocaine</b> treatment in adult rats: effects on zif 268 and <strong>homer</strong> 1a.
+HOMER1	drug	cocaine	19419424	We employed gene markers (zif 268 and <strong>homer</strong> 1a) that offer a high anatomical resolution to map <b>cocaine</b> induced changes in 22 cortical areas and 23 functionally related striatal sectors, in order to determine the corticostriatal circuits altered by repeated <b>cocaine</b> exposure (25 mg/kg, 5 days).
+HOMER1	drug	cocaine	19419424	Repeated <b>cocaine</b> resulted in blunted inducibility of both zif 268 and <strong>homer</strong> 1a, changes that were still very robust 3 weeks later.
+HOMER1	drug	cocaine	19306440	Extended daily access to <b>cocaine</b> results in distinct alterations in <strong>Homer</strong> 1b/c and NMDA receptor subunit expression within the medial prefrontal cortex.
+HOMER1	drug	cocaine	19306440	In contrast, extended access to <b>cocaine</b> resulted in distinct and long lasting alterations of protein expression within the mPFC that included: increased levels of <strong>Homer1b</strong>/c at 1 day, NR2b at 14 days, and NR2a at 60 days, of withdrawal.
+HOMER1	addiction	withdrawal	19306440	In contrast, extended access to cocaine resulted in distinct and long lasting alterations of protein expression within the mPFC that included: increased levels of <strong>Homer1b</strong>/c at 1 day, NR2b at 14 days, and NR2a at 60 days, of <b>withdrawal</b>.
+HOMER1	drug	cocaine	19181855	Compared with WT mice, tPA /  mice injected with <b>cocaine</b> displayed attenuated phosphorylation of ERK, cAMP response element binding protein (CREB), and dopamine and cAMP regulated phosphoprotein 32 kDa (DARPP 32) and blunted induction of immediate early genes (IEGs) c Fos, Egr 1, and <strong>Homer</strong> 1a in the amygdala and the nucleus accumbens (NAc).
+HOMER1	drug	cocaine	19128205	Future pharmacotherapy may focus on manipulating signal transduction proteins and pathways, which include <strong>Homer</strong>/N methyl D aspartic acid complexes, to provide effective treatment for <b>cocaine</b> addiction.
+HOMER1	addiction	addiction	19128205	Future pharmacotherapy may focus on manipulating signal transduction proteins and pathways, which include <strong>Homer</strong>/N methyl D aspartic acid complexes, to provide effective treatment for cocaine <b>addiction</b>.
+HOMER1	drug	cocaine	19118598	Neuroadaptations in the cellular and postsynaptic group 1 metabotropic glutamate receptor mGluR5 and <strong>Homer</strong> proteins following extinction of <b>cocaine</b> self administration.
+HOMER1	drug	cocaine	19118598	This study examined the role of group1 metabotropic glutamate receptor mGluR5 and associated postsynaptic scaffolding protein <strong>Homer1b</strong>/c in behavioral plasticity after three withdrawal treatments from <b>cocaine</b> self administration.
+HOMER1	addiction	withdrawal	19118598	This study examined the role of group1 metabotropic glutamate receptor mGluR5 and associated postsynaptic scaffolding protein <strong>Homer1b</strong>/c in behavioral plasticity after three <b>withdrawal</b> treatments from cocaine self administration.
+HOMER1	addiction	withdrawal	19105975	At 21 days of <b>withdrawal</b>, there was a decrease in the expression of mGluR2/3 protein in core and shell, an increase in GluR1 and a decrease in <strong>Homer1b</strong>/c proteins in the nucleus accumbens core tissue.
+HOMER1	drug	cocaine	18932227	<b>Cocaine</b> activates <strong>Homer1</strong> immediate early gene transcription in the mesocorticolimbic circuit: differential regulation by dopamine and glutamate signaling.
+HOMER1	drug	cocaine	18932227	<strong>Homer</strong> proteins have been implicated in synaptic and behavioral plasticity, including drug seeking behavior after <b>cocaine</b> treatment.
+HOMER1	addiction	relapse	18932227	<strong>Homer</strong> proteins have been implicated in synaptic and behavioral plasticity, including drug <b>seeking</b> behavior after cocaine treatment.
+HOMER1	drug	cocaine	18932227	In this study, using RT PCR, activation of <strong>Homer1a</strong> mRNA transcription in response to acute and repeated administration of <b>cocaine</b> was characterized in prefrontal cortex, nucleus accumbens, and ventral tegmental area, three mesocorticolimbic nuclei of the rat brain.
+HOMER1	drug	cocaine	18932227	Moreover, the dopaminergic and glutamatergic regulation of <strong>Homer1</strong> gene activation by <b>cocaine</b> was investigated.
+HOMER1	drug	cocaine	18932227	Acute <b>cocaine</b> rapidly and transiently activated transcription of <strong>Homer1a</strong> mRNA in all three nuclei.
+HOMER1	drug	cocaine	18932227	However, repeated administration of <b>cocaine</b> was not effective in inducing the <strong>Homer1a</strong> mRNA transcription after various withdrawal times ranging from 2 h to 3 weeks.
+HOMER1	addiction	withdrawal	18932227	However, repeated administration of cocaine was not effective in inducing the <strong>Homer1a</strong> mRNA transcription after various <b>withdrawal</b> times ranging from 2 h to 3 weeks.
+HOMER1	drug	cocaine	18932227	The acute <b>cocaine</b> mediated activation of <strong>Homer1</strong> gene was regulated by D1 but not D2 dopamine receptors.
+HOMER1	drug	cocaine	18932227	The blockade of AMPA or NMDA glutamate receptors did not prevent <b>cocaine</b> mediated activation of <strong>Homer1</strong> gene in the three mesocorticolimbic nuclei.
+HOMER1	drug	cocaine	18932227	These data indicate that acute administration of <b>cocaine</b> transiently activates <strong>Homer1</strong> gene producing the immediate early gene Homer1a mRNA in the three mesocorticolimbic nuclei of the rat brain.
+HOMER1	drug	cocaine	18932227	These data indicate that acute administration of <b>cocaine</b> transiently activates <strong>Homer1</strong> gene producing the immediate early gene <strong>Homer1a</strong> mRNA in the three mesocorticolimbic nuclei of the rat brain.
+HOMER1	drug	cocaine	18932227	Activation of <strong>Homer1</strong> gene may contribute to the <b>cocaine</b> mediated synaptic and behavioral plasticity.
+HOMER1	drug	alcohol	18690104	This review summarizes the existing data derived from our studies using adeno associated viral vector mediated neuronal targeting of <strong>Homer</strong> in rodents, implicating this family of proteins in drug and <b>alcohol</b> addiction, learning/memory and emotional processing.
+HOMER1	addiction	addiction	18690104	This review summarizes the existing data derived from our studies using adeno associated viral vector mediated neuronal targeting of <strong>Homer</strong> in rodents, implicating this family of proteins in drug and alcohol <b>addiction</b>, learning/memory and emotional processing.
+HOMER1	drug	opioid	18466961	<strong>Homer</strong> 1 b/c decreased after 14 days of enforced abstinence in rats that received non contingent <b>heroin</b>.
+HOMER1	drug	amphetamine	17963850	Other effects, notably those on the expression of opioid peptides and postsynaptic density molecules (<strong>Homer</strong> 1a), differ between methylphenidate and cocaine or <b>amphetamine</b> treatment.
+HOMER1	drug	cocaine	17963850	Other effects, notably those on the expression of opioid peptides and postsynaptic density molecules (<strong>Homer</strong> 1a), differ between methylphenidate and <b>cocaine</b> or amphetamine treatment.
+HOMER1	drug	opioid	17963850	Other effects, notably those on the expression of <b>opioid</b> peptides and postsynaptic density molecules (<strong>Homer</strong> 1a), differ between methylphenidate and cocaine or amphetamine treatment.
+HOMER1	drug	cocaine	17950706	Regional differences in the effects of withdrawal from repeated <b>cocaine</b> upon <strong>Homer</strong> and glutamate receptor expression: a two species comparison.
+HOMER1	addiction	withdrawal	17950706	Regional differences in the effects of <b>withdrawal</b> from repeated cocaine upon <strong>Homer</strong> and glutamate receptor expression: a two species comparison.
+HOMER1	drug	cocaine	17950706	The constitutively expressed (CC) <strong>Homer</strong> protein Homer2a/b actively regulates behavioral and neurochemical sensitivity to <b>cocaine</b> in both rats and mice.
+HOMER1	drug	cocaine	17950706	The present study employed standard immunoblotting techniques to compare the effects of withdrawal from repeated <b>cocaine</b> (7 x 30 mg/kg) upon the protein expression of Homer2a/b with a related CC <strong>Homer</strong> protein Homer1b/c, as well as their associated glutamate receptors, within brain regions implicated in <b>cocaine</b> addiction.
+HOMER1	addiction	addiction	17950706	The present study employed standard immunoblotting techniques to compare the effects of withdrawal from repeated cocaine (7 x 30 mg/kg) upon the protein expression of Homer2a/b with a related CC <strong>Homer</strong> protein Homer1b/c, as well as their associated glutamate receptors, within brain regions implicated in cocaine <b>addiction</b>.
+HOMER1	addiction	withdrawal	17950706	The present study employed standard immunoblotting techniques to compare the effects of <b>withdrawal</b> from repeated cocaine (7 x 30 mg/kg) upon the protein expression of Homer2a/b with a related CC <strong>Homer</strong> protein Homer1b/c, as well as their associated glutamate receptors, within brain regions implicated in cocaine addiction.
+HOMER1	drug	cocaine	17950706	The present study employed standard immunoblotting techniques to compare the effects of withdrawal from repeated <b>cocaine</b> (7 x 30 mg/kg) upon the protein expression of Homer2a/b with a related CC <strong>Homer</strong> protein <strong>Homer1b</strong>/c, as well as their associated glutamate receptors, within brain regions implicated in <b>cocaine</b> addiction.
+HOMER1	addiction	addiction	17950706	The present study employed standard immunoblotting techniques to compare the effects of withdrawal from repeated cocaine (7 x 30 mg/kg) upon the protein expression of Homer2a/b with a related CC <strong>Homer</strong> protein <strong>Homer1b</strong>/c, as well as their associated glutamate receptors, within brain regions implicated in cocaine <b>addiction</b>.
+HOMER1	addiction	withdrawal	17950706	The present study employed standard immunoblotting techniques to compare the effects of <b>withdrawal</b> from repeated cocaine (7 x 30 mg/kg) upon the protein expression of Homer2a/b with a related CC <strong>Homer</strong> protein <strong>Homer1b</strong>/c, as well as their associated glutamate receptors, within brain regions implicated in cocaine addiction.
+HOMER1	drug	cocaine	17950706	To determine whether or not the observed <b>cocaine</b> induced changes in <strong>Homer</strong> and glutamate receptor expression generalized across mammalian species, immunoblotting was conducted on tissue derived from both male Sprague Dawley rats and male C57BL/6J mice.
+HOMER1	drug	cocaine	17950706	In both species, withdrawal from repeated <b>cocaine</b> administration down regulated Homer1b/c and Homer2a/b within the shell, but not the core, of the nucleus accumbens (NAC), and the reduced <strong>Homer</strong> levels were accompanied by decreases in mGluR1a, NR2a and NR2b.
+HOMER1	addiction	withdrawal	17950706	In both species, <b>withdrawal</b> from repeated cocaine administration down regulated Homer1b/c and Homer2a/b within the shell, but not the core, of the nucleus accumbens (NAC), and the reduced <strong>Homer</strong> levels were accompanied by decreases in mGluR1a, NR2a and NR2b.
+HOMER1	drug	cocaine	17950706	In both species, withdrawal from repeated <b>cocaine</b> administration down regulated <strong>Homer1b</strong>/c and Homer2a/b within the shell, but not the core, of the nucleus accumbens (NAC), and the reduced <strong>Homer</strong> levels were accompanied by decreases in mGluR1a, NR2a and NR2b.
+HOMER1	addiction	withdrawal	17950706	In both species, <b>withdrawal</b> from repeated cocaine administration down regulated <strong>Homer1b</strong>/c and Homer2a/b within the shell, but not the core, of the nucleus accumbens (NAC), and the reduced <strong>Homer</strong> levels were accompanied by decreases in mGluR1a, NR2a and NR2b.
+HOMER1	drug	cocaine	17950706	In the PFC, repeated <b>cocaine</b> up regulated Homer2a/b, mGluR1 and NR2b expression, without affecting <strong>Homer1b</strong>/c levels.
+HOMER1	drug	cocaine	17950706	<b>Cocaine</b> induced increases in Homer1b/c, Homer2a/b, mGluR1a and NR2a were observed in the hippocampus of both rats and mice, while in dorsal striatum, NR2a levels were elevated but <strong>Homer</strong> and Group1 mGluR levels were unchanged.
+HOMER1	drug	cocaine	17950706	<b>Cocaine</b> induced increases in <strong>Homer1b</strong>/c, Homer2a/b, mGluR1a and NR2a were observed in the hippocampus of both rats and mice, while in dorsal striatum, NR2a levels were elevated but <strong>Homer</strong> and Group1 mGluR levels were unchanged.
+HOMER1	drug	cocaine	17950706	Thus, withdrawal from repeated <b>cocaine</b> alters the expression of CC <strong>Homer</strong> isoforms and their associated glutamate receptors in a regionally distinct manner.
+HOMER1	addiction	withdrawal	17950706	Thus, <b>withdrawal</b> from repeated cocaine alters the expression of CC <strong>Homer</strong> isoforms and their associated glutamate receptors in a regionally distinct manner.
+HOMER1	drug	cocaine	17950706	As CC <strong>Homer</strong> proteins, Group1 mGluRs and NMDA receptors actively regulate <b>cocaine</b> induced neuroplasticity in vivo, these data support the hypothesis that <b>cocaine</b> induced changes in mGluR <strong>Homer</strong> NMDA signaling pathways may be important neuroadaptations mediating the enduring changes in behavior produced by repeated <b>cocaine</b> experience.
+HOMER1	drug	alcohol	17568396	<strong>Homer</strong> proteins are integral components of the postsynaptic density that are necessary for <b>alcohol</b> induced neuroplasticity within the nucleus accumbens (NAC).
+HOMER1	drug	alcohol	17568396	In this report, we describe the effects of chronic <b>alcohol</b> consumption upon NAC <strong>Homer</strong> expression and investigate the functional consequences of mimicking the <b>alcohol</b> induced changes in <strong>Homer</strong> expression vis à vis <b>alcohol</b> induced changes in NAC neurochemistry and behavior.
+HOMER1	drug	alcohol	16704932	Converging preclinical observations indicate a potential role for both immediate early gene <strong>Homer</strong> isoforms and constitutively expressed <strong>Homer</strong> isoforms in behavioral pathologies associated with neuropsychiatric disorders, such as addiction and/or <b>alcoholism</b>, depression, anxiety, epilepsy and schizophrenia.
+HOMER1	addiction	addiction	16704932	Converging preclinical observations indicate a potential role for both immediate early gene <strong>Homer</strong> isoforms and constitutively expressed <strong>Homer</strong> isoforms in behavioral pathologies associated with neuropsychiatric disorders, such as <b>addiction</b> and/or alcoholism, depression, anxiety, epilepsy and schizophrenia.
+HOMER1	drug	cocaine	16314758	Association of a polymorphism in the <strong>Homer1</strong> gene with <b>cocaine</b> dependence in an African American population.
+HOMER1	addiction	dependence	16314758	Association of a polymorphism in the <strong>Homer1</strong> gene with cocaine <b>dependence</b> in an African American population.
+HOMER1	drug	cocaine	16314758	The purpose of this study is to determine whether single nucleotide polymorphisms in the <strong>Homer1</strong> and Homer2 genes associate with the <b>cocaine</b> dependent phenotype in an African American population.
+HOMER1	drug	cocaine	16314758	This study utilized a case control design in which the genotype and allele frequencies for four single nucleotide polymorphisms in the <strong>Homer1</strong> gene and three single nucleotide polymorphisms in the Homer2 gene were compared between African American individuals with a diagnosis of <b>cocaine</b> dependence (n=170) and African American individuals with no history of substance abuse (n=90).
+HOMER1	addiction	dependence	16314758	This study utilized a case control design in which the genotype and allele frequencies for four single nucleotide polymorphisms in the <strong>Homer1</strong> gene and three single nucleotide polymorphisms in the Homer2 gene were compared between African American individuals with a diagnosis of cocaine <b>dependence</b> (n=170) and African American individuals with no history of substance abuse (n=90).
+HOMER1	drug	cocaine	16314758	The data indicate that one single nucleotide polymorphism, rs6871510, located in intron 1 of the <strong>Homer1</strong> gene significantly (P=0.029) associates with <b>cocaine</b> dependence at the genotype level, and trends toward a significant association at the allele frequency level (chi=2.62, df=1, P=0.106, OR=1.71).
+HOMER1	addiction	dependence	16314758	The data indicate that one single nucleotide polymorphism, rs6871510, located in intron 1 of the <strong>Homer1</strong> gene significantly (P=0.029) associates with cocaine <b>dependence</b> at the genotype level, and trends toward a significant association at the allele frequency level (chi=2.62, df=1, P=0.106, OR=1.71).
+HOMER1	drug	cocaine	16314758	The results of this study suggest that a polymorphism in the <strong>Homer1</strong> gene, rs6871510, is a potential risk factor for the development of <b>cocaine</b> dependence in an African American population, whereas polymorphisms in the Homer2 gene are not.
+HOMER1	addiction	dependence	16314758	The results of this study suggest that a polymorphism in the <strong>Homer1</strong> gene, rs6871510, is a potential risk factor for the development of cocaine <b>dependence</b> in an African American population, whereas polymorphisms in the Homer2 gene are not.
+HOMER1	drug	cocaine	16160706	<strong>Homer</strong> isoforms differentially regulate <b>cocaine</b> induced neuroplasticity.
+HOMER1	drug	cocaine	16160706	<strong>Homer</strong> proteins modulate neuroplasticity in excitatory synapses and are dynamically regulated by <b>cocaine</b>.
+HOMER1	drug	cocaine	16160706	Whereas acute <b>cocaine</b> elevates immediate early gene (short) isoforms of <strong>Homer1</strong> in the nucleus accumbens, withdrawal from repeated <b>cocaine</b> administration downregulates the expression of constitutive <strong>Homer1</strong> isoforms.
+HOMER1	addiction	withdrawal	16160706	Whereas acute cocaine elevates immediate early gene (short) isoforms of <strong>Homer1</strong> in the nucleus accumbens, <b>withdrawal</b> from repeated cocaine administration downregulates the expression of constitutive <strong>Homer1</strong> isoforms.
+HOMER1	drug	cocaine	16160706	The present study determined whether or not this downregulation in constitutive <strong>Homer</strong> expression in the accumbens is necessary for enduring alterations in <b>cocaine</b> induced changes in the brain and behavior.
+HOMER1	drug	cocaine	16160706	The long vs short <strong>Homer</strong> isoforms were overexpressed in the rat nucleus accumbens during drug abstinence, and the adaptations elicited by repeated <b>cocaine</b> on glutamate transmission and motor behavior were measured.
+HOMER1	drug	cocaine	16160706	It was found that both chronic and acute overexpression of constitutive, but not short, <strong>Homer</strong> isoforms abolished <b>cocaine</b> induced sensitization of locomotor hyperactivity and prevented the development of glutamate abnormalities in the accumbens, including the reduction in basal extracellular glutamate content and the sensitized glutamate response to a subsequent <b>cocaine</b> challenge injection.
+HOMER1	addiction	sensitization	16160706	It was found that both chronic and acute overexpression of constitutive, but not short, <strong>Homer</strong> isoforms abolished cocaine induced <b>sensitization</b> of locomotor hyperactivity and prevented the development of glutamate abnormalities in the accumbens, including the reduction in basal extracellular glutamate content and the sensitized glutamate response to a subsequent cocaine challenge injection.
+HOMER1	drug	cocaine	16160706	Together, these data indicate that the enduring reduction of long <strong>Homer</strong> isoforms in the nucleus accumbens of <b>cocaine</b> withdrawn rats is necessary for the expression of <b>cocaine</b> induced neuroplasticity.
+HOMER1	drug	alcohol	16049182	Constitutive Homer2 gene deletion [knock out (KO)] and rescue with adeno associated viral (AAV) transfection of Homer2b was used to demonstrate the importance of <strong>Homer</strong> proteins in neuroplasticity produced by repeated <b>ethanol</b> (EtOH) administration.
+HOMER1	addiction	addiction	16011574	<strong>Homer</strong> proteins are involved in the functional assembly of postsynaptic density proteins at glutamatergic synapses and are implicated in learning, memory and drug <b>addiction</b>.
+HOMER1	drug	amphetamine	16011574	Relative to wild type mice, <strong>Homer1</strong> KO mice exhibited deficits in radial arm maze performance, impaired prepulse inhibition, enhanced 'behavioral despair', increased anxiety in a novel objects test, enhanced reactivity to novel environments, decreased instrumental responding for sucrose and enhanced MK 801  and <b>methamphetamine</b> stimulated motor behavior.
+HOMER1	drug	cocaine	16011574	Moreover, in <strong>Homer1</strong> KO mice, <b>cocaine</b> did not stimulate a rise in frontal cortex extracellular glutamate levels, suggesting hypofrontality.
+HOMER1	drug	cocaine	15545022	The parallel between the effect of Homer2 gene deletion and chronic <b>cocaine</b> administration on behavioral and glutamatergic neurochemical responses to <b>cocaine</b> supports involvement of <strong>Homer</strong> proteins and glutamate transmission in the sensitization of behavior produced by repeated <b>cocaine</b>.
+HOMER1	addiction	sensitization	15545022	The parallel between the effect of Homer2 gene deletion and chronic cocaine administration on behavioral and glutamatergic neurochemical responses to cocaine supports involvement of <strong>Homer</strong> proteins and glutamate transmission in the <b>sensitization</b> of behavior produced by repeated cocaine.
+HOMER1	drug	cocaine	15295029	We found that the <b>cocaine</b> induced blockade of retrograde signaling was correlated with enhanced expression levels of <strong>Homer</strong> scaffolding proteins containing the coiled coil domain and accompanied by a strong reduction of mGluR5 surface expression.
+HOMER1	drug	cocaine	15294147	<strong>Homer</strong> proteins regulate sensitivity to <b>cocaine</b>.
+HOMER1	drug	cocaine	15294147	Members of the <strong>Homer</strong> gene family are regulated by acute and chronic <b>cocaine</b> administration.
+HOMER1	drug	cocaine	15294147	Here, we report that deletion of <strong>Homer1</strong> or Homer2 in mice caused the same increase in sensitivity to <b>cocaine</b> induced locomotion, conditioned reward, and augmented extracellular glutamate in nucleus accumbens as that elicited by withdrawal from repeated <b>cocaine</b> administration.
+HOMER1	addiction	reward	15294147	Here, we report that deletion of <strong>Homer1</strong> or Homer2 in mice caused the same increase in sensitivity to cocaine induced locomotion, conditioned <b>reward</b>, and augmented extracellular glutamate in nucleus accumbens as that elicited by withdrawal from repeated cocaine administration.
+HOMER1	addiction	withdrawal	15294147	Here, we report that deletion of <strong>Homer1</strong> or Homer2 in mice caused the same increase in sensitivity to cocaine induced locomotion, conditioned reward, and augmented extracellular glutamate in nucleus accumbens as that elicited by <b>withdrawal</b> from repeated cocaine administration.
+HOMER1	drug	cocaine	15294147	These data show that <strong>Homer</strong> deletion mimics the behavioral and neurochemical phenotype produced by repeated <b>cocaine</b> administration and implicate <strong>Homer</strong> in regulating addiction to <b>cocaine</b>.
+HOMER1	addiction	addiction	15294147	These data show that <strong>Homer</strong> deletion mimics the behavioral and neurochemical phenotype produced by repeated cocaine administration and implicate <strong>Homer</strong> in regulating <b>addiction</b> to cocaine.
+HOMER1	drug	cocaine	14684470	Nucleus accumbens <strong>Homer</strong> proteins regulate behavioral sensitization to <b>cocaine</b>.
+HOMER1	addiction	sensitization	14684470	Nucleus accumbens <strong>Homer</strong> proteins regulate behavioral <b>sensitization</b> to cocaine.
+HOMER1	drug	cocaine	14684444	(4) <strong>Homer1</strong> protein is reduced in the nucleus accumbens, and Homer2 knockout mice show enhanced responsiveness to <b>cocaine</b>.
+HOMER1	drug	cocaine	14511343	<strong>Homer1</strong> proteins and AMPA receptors modulate <b>cocaine</b> induced behavioural plasticity.
+HOMER1	drug	cocaine	14511343	<strong>Homer</strong> proteins form functional assemblies in the excitatory postsynaptic density, and withdrawal from repeated <b>cocaine</b> administration reduces the expression of Homer1b/c in the nucleus accumbens.
+HOMER1	addiction	withdrawal	14511343	<strong>Homer</strong> proteins form functional assemblies in the excitatory postsynaptic density, and <b>withdrawal</b> from repeated cocaine administration reduces the expression of Homer1b/c in the nucleus accumbens.
+HOMER1	drug	cocaine	14511343	<strong>Homer</strong> proteins form functional assemblies in the excitatory postsynaptic density, and withdrawal from repeated <b>cocaine</b> administration reduces the expression of <strong>Homer1b</strong>/c in the nucleus accumbens.
+HOMER1	addiction	withdrawal	14511343	<strong>Homer</strong> proteins form functional assemblies in the excitatory postsynaptic density, and <b>withdrawal</b> from repeated cocaine administration reduces the expression of <strong>Homer1b</strong>/c in the nucleus accumbens.
+HOMER1	drug	cocaine	14511343	To determine if the reduction in Homer1b/c may be contributing to <b>cocaine</b> induced behavioural sensitization, antisense oligonucleotides were infused over two weeks into the nucleus accumbens of rats to reduce <strong>Homer1</strong> gene expression by approximately 35%.
+HOMER1	addiction	sensitization	14511343	To determine if the reduction in Homer1b/c may be contributing to cocaine induced behavioural <b>sensitization</b>, antisense oligonucleotides were infused over two weeks into the nucleus accumbens of rats to reduce <strong>Homer1</strong> gene expression by approximately 35%.
+HOMER1	drug	cocaine	14511343	To determine if the reduction in <strong>Homer1b</strong>/c may be contributing to <b>cocaine</b> induced behavioural sensitization, antisense oligonucleotides were infused over two weeks into the nucleus accumbens of rats to reduce <strong>Homer1</strong> gene expression by approximately 35%.
+HOMER1	addiction	sensitization	14511343	To determine if the reduction in <strong>Homer1b</strong>/c may be contributing to cocaine induced behavioural <b>sensitization</b>, antisense oligonucleotides were infused over two weeks into the nucleus accumbens of rats to reduce <strong>Homer1</strong> gene expression by approximately 35%.
+HOMER1	addiction	sensitization	14511343	These data indicate that the expression of behavioural <b>sensitization</b> arises in part from a reduction in <strong>Homer1</strong> gene products in the accumbens, while the development of <b>sensitization</b> requires stimulation of AMPA/kainate receptors.
+HOMER1	drug	amphetamine	12774298	Differential regulation by stimulants of neocortical expression of mrt1, arc, and <strong>homer1a</strong> mRNA in the rats treated with repeated <b>methamphetamine</b>.
+HOMER1	drug	cocaine	12774298	In contrast, the basal expression of other stimulant inducible and plasticity related genes arc and <strong>homer1a</strong> and the ability of MAP or <b>cocaine</b> challenge to augment the amounts of their transcripts were not affected by the repeated MAP regimen in the cortical area.
+HOMER1	addiction	sensitization	12774298	These findings suggest the differential regulation by stimulant of neocortical mrt1, arc, and <strong>homer1a</strong> expression in the behaviorally sensitized animals and supports the view that stimulant induction of mrt1 may be involved in the early molecular signalings for stimulant <b>sensitization</b>.
+HOMER1	drug	cocaine	12687634	Many genes upregulated in the CPu by <b>cocaine</b> were immediate early genes for transcription factors and for "effector" proteins (e.g., vesl/<strong>Homer1a</strong>, Arc, synaptotagmin IV).
+CALCA	drug	opioid	31794788	The rest of the 5 brainstem tissues were then used to measure CCK, <strong>CGRP</strong>, and <b>opioid</b> peptide receptor (DORR) levels by western blotting(WB).
+CALCA	addiction	sensitization	31551772	TRPV1 contributes to peripheral <b>sensitization</b> and hyperalgesia, in part, via triggering the release of proinflammatory peptides, such as calcitonin gene related peptide (<strong>CGRP</strong>), both locally and at the dorsal horn of the spinal cord.
+CALCA	drug	opioid	31551772	Blocking TRPV1, but not <b>opioid</b> receptors, attenuated the onset of analgesia and capsaicin induced <strong>CGRP</strong> release.
+CALCA	drug	opioid	31010055	We evaluated the mechanical paw withdrawal threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) <b>opioid</b> receptor, brain derived neurotrophic factor (BDNF), Substance P, and calcitonin gene related peptide (<strong>CGRP</strong>) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real time quantitative polymerase chain reaction (RT PCR).
+CALCA	addiction	withdrawal	31010055	We evaluated the mechanical paw <b>withdrawal</b> threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) opioid receptor, brain derived neurotrophic factor (BDNF), Substance P, and calcitonin gene related peptide (<strong>CGRP</strong>) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real time quantitative polymerase chain reaction (RT PCR).
+CALCA	addiction	sensitization	30706780	On the basis of their anatomic location, transient receptor potential ion channels (TRPV1, TRPV2 and TRPM8), Piezo 2, acid sensing ion channels (ASICs), purinergic (P2X and P2Y), bradykinin (B1 and B2), α amino 3 hydroxy 5  methylisoxazole 4 propionate (AMPA), N methyl D aspartate (NMDA), metabotropic glutamate (mGlu), neurokinin 1 (NK1) and calcitonin gene related peptide (<strong>CGRP</strong>) receptors are activated during pain <b>sensitization</b>.
+CALCA	drug	cannabinoid	30342013	They include peptides targeting Ca2+, Na+ and K+ voltage gated ion channels, the neuronal nicotinic receptors (nAChR), transient receptor potential channels (TRP), and different non opioid G protein coupled receptors (GPCRs), like the calcitonin gen related peptide (<strong>CGRP</strong>), <b>cannabinoid</b>, bradykinin and neurotensin receptors, among others.
+CALCA	drug	opioid	30342013	They include peptides targeting Ca2+, Na+ and K+ voltage gated ion channels, the neuronal nicotinic receptors (nAChR), transient receptor potential channels (TRP), and different non <b>opioid</b> G protein coupled receptors (GPCRs), like the calcitonin gen related peptide (<strong>CGRP</strong>), cannabinoid, bradykinin and neurotensin receptors, among others.
+CALCA	drug	opioid	29148033	Given that growing evidence indicates that calcitonin gene related peptide (<strong>CGRP</strong>) plays a key role in the development of peripheral sensitization and is associated with enhanced pain, we hypothesized that <strong>CGRP</strong> 4218T/C polymorphism is associated with the variability in <b>fentanyl</b> consumption for post cesarean analgesia.
+CALCA	addiction	sensitization	29148033	Given that growing evidence indicates that calcitonin gene related peptide (<strong>CGRP</strong>) plays a key role in the development of peripheral <b>sensitization</b> and is associated with enhanced pain, we hypothesized that <strong>CGRP</strong> 4218T/C polymorphism is associated with the variability in fentanyl consumption for post cesarean analgesia.
+CALCA	drug	opioid	29148033	We examined the association of <strong>CGRP</strong> 4218T/C polymorphism and post operative <b>fentanyl</b> consumption for analgesia as well as adverse reactions to <b>fentanyl</b> in those patients who received cesarean section surgeries.
+CALCA	drug	opioid	29148033	We found that the <strong>CGRP</strong> 4218T/C polymorphism has a significant effect on pain perception, analgesic requirement, and nausea and vomiting for the first 24 h after cesarean delivery in patients who received PCEA <b>fentanyl</b>.
+CALCA	drug	cannabinoid	28492437	<b>Cannabinoid</b> receptors were expressed not only in IB4 (isolectin B4) and <strong>CGRP</strong> (calcitonin gene related peptide) dorsal root ganglion neurons, their central terminals, and peripheral axons, but also in neurons, microglia, and astrocytes in spinal cord.
+CALCA	drug	opioid	28049076	Both the orbitofrontal cortex and amygdala are involved in the processing of olfactory information, and olfactory deficits may be also influenced by endogenous <b>opioids</b> and calcitonin gene related peptide (<strong>CGRP</strong>), which is probably involved in dopaminergic transmission.
+CALCA	drug	opioid	26748051	At doses providing equal or greater antinociception than <b>morphine</b> in the rat, the analogs showed reduced a) respiratory depression, b) impairment of motor coordination, c) tolerance and hyperalgesia, d) glial p38/<strong>CGRP</strong>/P2X7 receptor signaling, and e) reward/abuse potential in both conditioned place preference and self administration tests.
+CALCA	addiction	reward	26748051	At doses providing equal or greater antinociception than morphine in the rat, the analogs showed reduced a) respiratory depression, b) impairment of motor coordination, c) tolerance and hyperalgesia, d) glial p38/<strong>CGRP</strong>/P2X7 receptor signaling, and e) <b>reward</b>/abuse potential in both conditioned place preference and self administration tests.
+CALCA	drug	opioid	24824948	RT PCR and Western blot analysis showed that NaHS significantly reversed the gene and protein expression of up regulated spinal calcitonin gene related peptide (<strong>CGRP</strong>) in <b>naloxone</b> treated animals.
+CALCA	drug	opioid	24824948	Our data suggest that H2S prevents the development of <b>opioid</b> withdrawal induced hyperalgesia via suppression of synthesis of <strong>CGRP</strong> in spine through inhibition of AC/cAMP and PKC/Raf 1/ERK pathways.
+CALCA	addiction	withdrawal	24824948	Our data suggest that H2S prevents the development of opioid <b>withdrawal</b> induced hyperalgesia via suppression of synthesis of <strong>CGRP</strong> in spine through inhibition of AC/cAMP and PKC/Raf 1/ERK pathways.
+CALCA	drug	opioid	23244430	The present review discusses the neurobiology of <b>opioid</b> withdrawal syndrome and its therapeutic target recptors like calcitonin gene related peptide receptors (<strong>CGRP</strong>), N methyl D aspartate (NMDA) receptors, gamma aminobutyric acid receptors (GABA), G proteingated inwardly rectifying potassium (GIRK) channels and calcium channels.
+CALCA	addiction	withdrawal	23244430	The present review discusses the neurobiology of opioid <b>withdrawal</b> syndrome and its therapeutic target recptors like calcitonin gene related peptide receptors (<strong>CGRP</strong>), N methyl D aspartate (NMDA) receptors, gamma aminobutyric acid receptors (GABA), G proteingated inwardly rectifying potassium (GIRK) channels and calcium channels.
+CALCA	drug	cannabinoid	21631400	The present review discusses these therapeutic targets including noradrenaline and 5 HT reuptake inhibitors; sodium, calcium and potassium channels; inhibitory and excitatory neurotransmitters; neuropeptides including bradykinin, tachykinin, cholecystokinin, neuropeptide Y, vasoactive intestinal peptide, and <strong>CGRP</strong>; pro inflammatory cytokines; MAP kinases; PPAR γ; Na(+)/Ca(2+) exchanger; nitric oxide; purinergic receptors; neuronal nicotinic receptors; cation dependent chloride transporters; oxidative stress; matrix metalloproteinase and plasminogen activators; growth factors; transient receptor potential (TRP) channels; <b>endocannabinoids</b>; histamine receptors; dopamine; sigma receptors, beta adrenergic receptors, endothelins, and D amino acid oxidase.
+CALCA	drug	opioid	21571003	Sustained <b>morphine</b> treatment has been shown to produce paradoxical pain sensitization (<b>opioid</b> induced hyperalgesia) and also causes increase in spinal pain neurotransmitter, such as calcitonin gene related peptide (<strong>CGRP</strong>), concentration in experimental animals.
+CALCA	addiction	sensitization	21571003	Sustained morphine treatment has been shown to produce paradoxical pain <b>sensitization</b> (opioid induced hyperalgesia) and also causes increase in spinal pain neurotransmitter, such as calcitonin gene related peptide (<strong>CGRP</strong>), concentration in experimental animals.
+CALCA	drug	opioid	21571003	We have previously shown that in cultured primary sensory dorsal root ganglion (DRG) neurons sustained in vitro <b>opioid</b> agonist treatment upregulates cAMP levels (adenylyl cyclase (AC) superactivation) and augments basal and capsaicin evoked <strong>CGRP</strong> release in a PKA dependent manner.
+CALCA	drug	opioid	21571003	pretreatment of rats with a PKA selective small interference RNA (siRNA) mixture significantly attenuates sustained <b>morphine</b> mediated augmentation of spinal <strong>CGRP</strong> immunoreactivity, thermal hyperalgesia, mechanical allodynia and antinociceptive tolerance.
+CALCA	drug	opioid	20970925	The present study examines the effects of intraplantar injection of the μ  and δ <b>opioid</b> receptor agonists, <b>morphine</b> and deltorphin, alone and in combination on behavioral tests of nociception in naïve rats and on potassium evoked release of <strong>CGRP</strong> from sciatic nerves of naïve rats.
+CALCA	drug	opioid	20970925	Similarly, concentration dependent inhibition of <strong>CGRP</strong> release was observed when deltorphin and <b>morphine</b> were administered in sequence prior to potassium stimulation.
+CALCA	drug	opioid	20826131	In the present work we investigated the hypothesis that <b>morphine</b> pretreatment also sensitizes ACs toward Gs protein coupled excitatory modulators (such as PGE₂), leading to augmented PKA dependent <strong>CGRP</strong> release from PGE₂ stimulated primary sensory dorsal root ganglion (DRG) neurons.
+CALCA	drug	opioid	20826131	Our results show that sustained <b>morphine</b> treatment potentiated PGE₂ mediated cAMP formation and augmented PGE₂ evoked <strong>CGRP</strong> release from cultured primary sensory neurons in a PKA dependent manner.
+CALCA	drug	opioid	20727859	Induction of viscerosomatic hypersensitivity resulted in an increased labeling of <strong>CGRP</strong> , but not substance P positive cells in the lumbar dorsal root ganglia; increased labeling was not affected by prior exposure to <b>morphine</b>.
+CALCA	drug	opioid	20718739	Long term <b>morphine</b> treatment enhances pain neurotransmitter [such as calcitonin gene related peptide (<strong>CGRP</strong>)] levels in the spinal cord.
+CALCA	drug	opioid	20718739	It has been suggested previously that increased spinal <strong>CGRP</strong> may contribute to sustained <b>morphine</b> mediated paradoxical pain sensitization and antinociceptive tolerance.
+CALCA	addiction	sensitization	20718739	It has been suggested previously that increased spinal <strong>CGRP</strong> may contribute to sustained morphine mediated paradoxical pain <b>sensitization</b> and antinociceptive tolerance.
+CALCA	drug	opioid	20718739	Previous in vitro studies from our group indicated that Raf 1 kinase mediated adenylyl cyclase superactivation played a crucial role in sustained <b>morphine</b> mediated augmentation of basal and evoked <strong>CGRP</strong> release from cultured primary sensory neurons.
+CALCA	drug	opioid	20718739	Selective knockdown of spinal Raf 1 protein levels by i.th Raf 1 selective siRNA pretreatment significantly attenuated sustained <b>morphine</b> mediated up regulation of <strong>CGRP</strong> immunoreactivity in the spinal cord of rats and prevented the development of thermal hyperalgesia, mechanical allodynia and antinociceptive tolerance.
+CALCA	drug	opioid	20659434	Involvement of <b>opioid</b> receptors in the <strong>CGRP</strong> induced antinociception in the nucleus accumbens of rats.
+CALCA	drug	opioid	20659434	The present study is performed to explore the possible involvement of <b>opioid</b> receptors in the <strong>CGRP</strong> induced antinociception in the NAc of rats.
+CALCA	addiction	withdrawal	20659434	Intra NAc administration of <strong>CGRP</strong> induces significant increases in the hindpaw <b>withdrawal</b> latency (HWL) to noxious thermal and mechanical stimulation in rats.
+CALCA	drug	opioid	20659434	Interestingly, the <strong>CGRP</strong> induced antinociceptive effects are inhibited by following intra NAc injection of the <b>opioid</b> receptor antagonist <b>naloxone</b>, suggesting that the <b>opioid</b> receptors are involved in the <strong>CGRP</strong> induced antinociception in the NAc of rats.
+CALCA	drug	opioid	20659434	Furthermore, the <strong>CGRP</strong> induced antinociception is attenuated by intra NAc injection of mu <b>opioid</b> receptor (MOR) antagonist beta funaltrexamine (beta FNA) and kappa <b>opioid</b> receptor (KOR) antagonist nor binaltorphimine (nor BNI), but not by delta receptor (DOR) antagonist naltrindole.
+CALCA	drug	opioid	20659434	In the present study, we also demonstrated that there was no significant difference between the <strong>CGRP</strong> induced antinociception and the <b>morphine</b> induced antinociception in the NAc in rats.
+CALCA	drug	opioid	20659434	The results of the present study demonstrate that both mu  and kappa <b>opioid</b> receptors are involved in the <strong>CGRP</strong> induced antinociception in the NAc of rats.
+CALCA	drug	opioid	20359526	Several groups maintain that <b>morphine</b> tolerance and dependence correlate with increased activity of protein kinases ERK1/2 and P38 MAPK and PKC as well as elevated levels of the neuropeptides dynorphin (DYN), substance P (sP), and calcitonin gene related peptide (<strong>CGRP</strong>) in spinal cord dorsal horn (SCDH).
+CALCA	addiction	dependence	20359526	Several groups maintain that morphine tolerance and <b>dependence</b> correlate with increased activity of protein kinases ERK1/2 and P38 MAPK and PKC as well as elevated levels of the neuropeptides dynorphin (DYN), substance P (sP), and calcitonin gene related peptide (<strong>CGRP</strong>) in spinal cord dorsal horn (SCDH).
+CALCA	drug	opioid	20359526	In contrast, while <b>morphine</b> increased spinal DYN and <strong>CGRP</strong> in WT mice, DYN remained unchanged and <strong>CGRP</strong> was reduced in GluR5 KO mice.
+CALCA	drug	opioid	20359526	These observations suggest that spinal ERK2, P38 and PKCgamma are likely involved in multiple adaptive responses following systemic <b>morphine</b> administration, whereas DYN and <strong>CGRP</strong> may contribute selectively to the development of antinociceptive tolerance.
+CALCA	drug	opioid	19491327	It was shown previously (J Neurosci 22:6747 6755, 2002) that sustained <b>morphine</b> exposure augments pain neurotransmitter [such as calcitonin gene related peptide (<strong>CGRP</strong>)] release in the dorsal horn of the spinal cord in response to the heat sensing transient receptor potential vanilloid 1 receptor agonist 8 methyl N vanillyl 6 nonenamide (capsaicin).
+CALCA	drug	opioid	19491327	In the present study, we demonstrate that sustained <b>morphine</b> mediated augmentation of <strong>CGRP</strong> release from isolated primary sensory dorsal root ganglion neurons is dependent on protein kinase A and Raf 1 kinase.
+CALCA	drug	cannabinoid	19387418	Sustained <b>cannabinoid</b> agonist treatment augments <strong>CGRP</strong> release in a PKA dependent manner.
+CALCA	addiction	sensitization	19387418	It has been suggested that augmented release of pain neurotransmitters (such as calcitonin gene related peptide, <strong>CGRP</strong>) might be responsible for this abnormal pain <b>sensitization</b>.
+CALCA	drug	cannabinoid	19387418	We hypothesize that intracellular adaptations upon sustained <b>cannabinoid</b> treatment causes augmented release of <strong>CGRP</strong> from primary nociceptors leading to increased pain sensitivity.
+CALCA	drug	cannabinoid	19387418	We show that sustained (24 h) <b>cannabinoid</b> agonist [(+)WIN 55,212 2] treatment of 7 day old neonatal rat dorsal root ganglion neurons significantly augments basal <strong>CGRP</strong> release from these cells in a protein kinase A dependent manner.
+CALCA	drug	opioid	18976650	Enhanced excitatory pain neurotransmitter (such as calcitonin gene related peptide (<strong>CGRP</strong>)) release in the dorsal horn of the spinal cord may play a role in sustained <b>morphine</b> mediated paradoxical pain.
+CALCA	drug	opioid	18976650	Recently we have demonstrated that inhibition of Raf 1 attenuates sustained <b>morphine</b> treatment mediated augmentation of <strong>CGRP</strong> release in vitro, in cultured primary sensory neurons.
+CALCA	drug	opioid	18328477	Sustained <b>morphine</b> treatment augments basal <strong>CGRP</strong> release from cultured primary sensory neurons in a Raf 1 dependent manner.
+CALCA	drug	opioid	18328477	The intracellular signal transduction pathways involved in sustained <b>opioid</b> mediated augmentation of spinal pain neurotransmitter (such as calcitonin gene related peptide (<strong>CGRP</strong>)) release are not fully clarified.
+CALCA	drug	opioid	18328477	Therefore, in the present study we examined the role of Raf 1 in sustained <b>morphine</b> mediated regulation of cAMP formation and basal <strong>CGRP</strong> release in vitro, in cultured neonatal rat dorsal root ganglion (DRG) neurons.
+CALCA	drug	opioid	18328477	We found that sustained <b>morphine</b> treatment significantly augments intracellular cAMP production as well as basal <strong>CGRP</strong> release from cultured neonatal rat DRG neurons.
+CALCA	drug	opioid	18328477	The selective PKA inhibitor, H 89, attenuates the sustained <b>morphine</b> mediated augmentation of basal <strong>CGRP</strong> release, indicating that the cAMP/PKA pathway plays an important role in regulation of <strong>CGRP</strong> release from sensory neurons.
+CALCA	drug	opioid	18328477	Since our present data also demonstrated that selective Raf 1 inhibitor, GW 5074, attenuated both the cAMP overshoot and the augmentation of <strong>CGRP</strong> release mediated by sustained <b>morphine</b> in neonatal rat DRG neurons, we suggest that Raf 1 mediated sensitization of the intracellular cAMP formation may play an important role in sustained <b>morphine</b> mediated augmentation of spinal pain neurotransmitter release.
+CALCA	addiction	sensitization	18328477	Since our present data also demonstrated that selective Raf 1 inhibitor, GW 5074, attenuated both the cAMP overshoot and the augmentation of <strong>CGRP</strong> release mediated by sustained morphine in neonatal rat DRG neurons, we suggest that Raf 1 mediated <b>sensitization</b> of the intracellular cAMP formation may play an important role in sustained morphine mediated augmentation of spinal pain neurotransmitter release.
+CALCA	addiction	sensitization	17693023	As the anti NGF antibody does not appreciably cross the blood brain barrier, the present data suggest that the anti hyperalgesic action of anti NGF therapy results from blockade of activation and/or <b>sensitization</b> of the <strong>CGRP</strong>/trkA positive fibers that normally constitute the majority of sensory fibers that innervate the bone.
+CALCA	drug	opioid	17498818	The chronic administration of butoxamine with <b>morphine</b> reduced or eliminated the normally observed up regulation of <strong>CGRP</strong> and SP in spinal cord and DRG tissues.
+CALCA	drug	opioid	17395382	Sustained exposure to <b>opioid</b> agonists such as <b>morphine</b> increases levels of calcitonin gene related peptide (<strong>CGRP</strong>) in the spinal dorsal horn, a response implicated in the development of <b>opioid</b> tolerance and physical dependence.
+CALCA	addiction	dependence	17395382	Sustained exposure to opioid agonists such as morphine increases levels of calcitonin gene related peptide (<strong>CGRP</strong>) in the spinal dorsal horn, a response implicated in the development of opioid tolerance and physical <b>dependence</b>.
+CALCA	drug	cannabinoid	17395382	Recent evidence suggests that both the opioid induced increase in <strong>CGRP</strong> and the development of opioid physical dependence are suppressed by blockade of spinal <b>cannabinoid</b> (CB1) receptors.
+CALCA	drug	opioid	17395382	Recent evidence suggests that both the <b>opioid</b> induced increase in <strong>CGRP</strong> and the development of <b>opioid</b> physical dependence are suppressed by blockade of spinal cannabinoid (CB1) receptors.
+CALCA	addiction	dependence	17395382	Recent evidence suggests that both the opioid induced increase in <strong>CGRP</strong> and the development of opioid physical <b>dependence</b> are suppressed by blockade of spinal cannabinoid (CB1) receptors.
+CALCA	drug	opioid	17395382	In another set of experiments, chronic administration of spinal <b>morphine</b> (15 microg) once daily for 5 days produced a similar loss of analgesic effect and a marked increase in <strong>CGRP</strong> immunoreactivity in the superficial laminae of the dorsal horn.
+CALCA	drug	opioid	17395382	Consistent with the in vivo findings, primary cultures of adult dorsal root ganglion (DRG) neurons exposed to <b>morphine</b> for 5 days showed a significant increase in the number of <strong>CGRP</strong> immunoreactive neurons.
+CALCA	drug	opioid	17395382	Co administration with AM 251 attenuated the <b>morphine</b> induced increase in <strong>CGRP</strong> immunoreactivity in the spinal cord and in DRG cultured neurons.
+CALCA	drug	cannabinoid	17395382	Collectively, the results of this study suggest that activity of <b>endocannabinoids</b>, mediated via CB1 receptors, contributes to both the development and maintenance of opioid tolerance by influencing the opioid induced increase in spinal <strong>CGRP</strong>.
+CALCA	drug	opioid	17395382	Collectively, the results of this study suggest that activity of endocannabinoids, mediated via CB1 receptors, contributes to both the development and maintenance of <b>opioid</b> tolerance by influencing the <b>opioid</b> induced increase in spinal <strong>CGRP</strong>.
+CALCA	drug	opioid	16935424	Previous evidence suggests that spinal release of calcitonin gene related peptide (<strong>CGRP</strong>) and activation of its receptors contribute to <b>opioid</b> physical dependence.
+CALCA	addiction	dependence	16935424	Previous evidence suggests that spinal release of calcitonin gene related peptide (<strong>CGRP</strong>) and activation of its receptors contribute to opioid physical <b>dependence</b>.
+CALCA	drug	cannabinoid	16935424	The release of <strong>CGRP</strong> at the spinal level is modulated by <b>cannabinoid</b> (CB1) receptors.
+CALCA	drug	opioid	16935424	Thus, this study examined whether CB1 receptor activity mediates changes in <strong>CGRP</strong> underlying development of <b>opioid</b> physical dependence.
+CALCA	addiction	dependence	16935424	Thus, this study examined whether CB1 receptor activity mediates changes in <strong>CGRP</strong> underlying development of opioid physical <b>dependence</b>.
+CALCA	drug	opioid	16935424	Systemic <b>morphine</b> administration for 5 days elevated <strong>CGRP</strong> immunoreactivity in the rat spinal dorsal horn.
+CALCA	drug	opioid	16935424	In situ hybridization of dorsal root ganglion (DRG) neurons revealed an increase in <strong>CGRP</strong> mRNA during initial (day 1 3) but not later phase (day 4 5) of <b>morphine</b> treatment.
+CALCA	drug	opioid	16935424	<strong>CGRP</strong> immunoreactivity in DRG neurons, however, was increased in the later phase of <b>morphine</b> treatment.
+CALCA	drug	opioid	16935424	<b>Naloxone</b> challenge to <b>morphine</b> treated animals precipitated an intense withdrawal syndrome that depleted <strong>CGRP</strong> immunoreactivity and increased Fos expression in the dorsal horn.
+CALCA	addiction	withdrawal	16935424	Naloxone challenge to morphine treated animals precipitated an intense <b>withdrawal</b> syndrome that depleted <strong>CGRP</strong> immunoreactivity and increased Fos expression in the dorsal horn.
+CALCA	addiction	withdrawal	16935424	The Fos response primarily occurred in neurons that expressed <strong>CGRP</strong> receptor component protein (RCP) suggesting <strong>CGRP</strong> activity contributes to neuronal activation during precipitated <b>withdrawal</b>.
+CALCA	drug	opioid	16935424	Spinal slices obtained from <b>morphine</b> treated animals showed higher levels of <strong>CGRP</strong> release than from saline controls.
+CALCA	drug	cannabinoid	16935424	Altogether, this study suggests that <b>endocannabinoid</b> activity, expressed via CB1 receptors, contributes to the induction of opioid physical dependence through spinal modulation of <strong>CGRP</strong>.
+CALCA	drug	opioid	16935424	Altogether, this study suggests that endocannabinoid activity, expressed via CB1 receptors, contributes to the induction of <b>opioid</b> physical dependence through spinal modulation of <strong>CGRP</strong>.
+CALCA	addiction	dependence	16935424	Altogether, this study suggests that endocannabinoid activity, expressed via CB1 receptors, contributes to the induction of opioid physical <b>dependence</b> through spinal modulation of <strong>CGRP</strong>.
+CALCA	drug	opioid	16215302	A non inclusive list of examples of substances reported to block or reverse <b>opioid</b> antinociceptive tolerance include: substance P receptor (NK 1) antagonists, calcitonin gene related peptide (<strong>CGRP</strong>) receptor antagonists, nitric oxide (NO) synthase inhibitors, calcium channel blockers, cyclooxygenase (COX) inhibitors, protein kinase C inhibitors, competitive and non competitive antagonists of the NMDA (N methyl D aspartate) receptor, AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid) antagonists, anti dynorphin antiserum, and cholecystokinin (CCK) receptor antagonists.
+CALCA	drug	cannabinoid	16042975	The mechanisms underlying tolerance dependence are not entirely clear, however, recent evidence suggests that spinal adaptations leading to increased activity of sensory neuropeptides (calcitonin gene related peptide (<strong>CGRP</strong>), substance P) and their downstream signaling messengers derived from metabolism of arachidonic acid: prostaglandins (PG), lipoxygenase (LOX) metabolites, and <b>endocannabinoids</b>, plays an important role in this phenomenon.
+CALCA	addiction	dependence	16042975	The mechanisms underlying tolerance <b>dependence</b> are not entirely clear, however, recent evidence suggests that spinal adaptations leading to increased activity of sensory neuropeptides (calcitonin gene related peptide (<strong>CGRP</strong>), substance P) and their downstream signaling messengers derived from metabolism of arachidonic acid: prostaglandins (PG), lipoxygenase (LOX) metabolites, and endocannabinoids, plays an important role in this phenomenon.
+CALCA	addiction	sensitization	15836976	Mechanistically, the great majority of sensory fibers that innervate the bone are <strong>CGRP</strong>/TrkA expressing fibers, and if the <b>sensitization</b> and activation of these fibers is blocked by anti NGF therapy there would not be another population of nociceptors, such as the non peptidergic IB4/RET IR nerve fibers, to take their place in signaling nociceptive events.
+CALCA	drug	opioid	14598307	The present study was undertaken to investigate the plasticity of calcitonin gene related peptide (<strong>CGRP</strong>) in antinociception after <b>morphine</b> tolerance in rats.
+CALCA	drug	opioid	14598307	The hindpaw withdrawal latencies (HWLs) to both thermal and mechanical stimulation increased significantly after intracerebroventricular injection of 2.5 nmol of <strong>CGRP</strong> in <b>opioid</b> naive rats, indicating that <strong>CGRP</strong> produces an antinociceptive effect in the brain.
+CALCA	addiction	withdrawal	14598307	The hindpaw <b>withdrawal</b> latencies (HWLs) to both thermal and mechanical stimulation increased significantly after intracerebroventricular injection of 2.5 nmol of <strong>CGRP</strong> in opioid naive rats, indicating that <strong>CGRP</strong> produces an antinociceptive effect in the brain.
+CALCA	drug	opioid	14598307	Furthermore, there was an antinociceptive effect after intracerebroventricular injection of 2.5 nmol of <strong>CGRP</strong> in <b>morphine</b> tolerant rats.
+CALCA	drug	opioid	14598307	Interestingly, the antinociceptive effect induced by intracerebroventricular injection of <strong>CGRP</strong> was lower in <b>morphine</b> tolerant rats than that in <b>opioid</b> naive rats at the same dose.
+CALCA	drug	opioid	14598307	At the same time, there was downregulation of <strong>CGRP</strong> like immunoreactivity in both lateral septal nucleus and central nucleus of amygdala tested by immunohistochemical methods, whereas no significant changes were observed in arcuate nucleus of hypothalamus and periaqueductal gray after <b>morphine</b> treatment in rats.
+CALCA	drug	opioid	14598307	The present study demonstrates plastic changes in both <strong>CGRP</strong> induced antinociception and <strong>CGRP</strong> like immunoreactivity in rat brain after <b>morphine</b> tolerance, suggesting that <strong>CGRP</strong> may play an important role in <b>morphine</b> tolerance.
+CALCA	drug	alcohol	13129832	Investigation of DUSP8 and <strong>CALCA</strong> in <b>alcohol</b> dependence.
+CALCA	addiction	dependence	13129832	Investigation of DUSP8 and <strong>CALCA</strong> in alcohol <b>dependence</b>.
+CALCA	drug	opioid	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of <b>opioid</b> physical dependence using behavioural assessment of withdrawal and immunostaining for <strong>CGRP</strong> and Fos protein expression in the spinal cord.
+CALCA	addiction	dependence	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of opioid physical <b>dependence</b> using behavioural assessment of withdrawal and immunostaining for <strong>CGRP</strong> and Fos protein expression in the spinal cord.
+CALCA	addiction	withdrawal	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of opioid physical dependence using behavioural assessment of <b>withdrawal</b> and immunostaining for <strong>CGRP</strong> and Fos protein expression in the spinal cord.
+CALCA	drug	opioid	12970109	of <b>morphine</b> for 5 days markedly elevated <strong>CGRP</strong> like immunoreactivity in the dorsal horn of the rat spinal cord.
+CALCA	addiction	withdrawal	12970109	challenge precipitated a robust <b>withdrawal</b> syndrome that depleted <strong>CGRP</strong> like immunoreactivity and increased the number of Fos like immunoreactive neurons in the dorsal horn.
+CALCA	drug	opioid	12970109	Intrathecal administration of NDGA (10, 20 microg), a nonselective LOX inhibitor, AA 861 (1.5, 3 microg), a 5 LOX selective inhibitor, or baicalein (1.4, 2.8 microg), a 12 LOX selective inhibitor, concurrently with systemic <b>morphine</b> for 5 days or as a single injection immediately preceding <b>naloxone</b> challenge, blocked the depletion of <strong>CGRP</strong> like immunoreactivity, prevented increase in the number of Fos like immunoreactive neurons in the dorsal horn, and significantly attenuated the <b>morphine</b> withdrawal syndrome.
+CALCA	addiction	withdrawal	12970109	Intrathecal administration of NDGA (10, 20 microg), a nonselective LOX inhibitor, AA 861 (1.5, 3 microg), a 5 LOX selective inhibitor, or baicalein (1.4, 2.8 microg), a 12 LOX selective inhibitor, concurrently with systemic morphine for 5 days or as a single injection immediately preceding naloxone challenge, blocked the depletion of <strong>CGRP</strong> like immunoreactivity, prevented increase in the number of Fos like immunoreactive neurons in the dorsal horn, and significantly attenuated the morphine <b>withdrawal</b> syndrome.
+CALCA	addiction	withdrawal	12732246	Intra CeA injection of <strong>CGRP</strong> induced dose dependent increases in the hind paw <b>withdrawal</b> latency tested by hotplate test and Randall Selitto Test, indicating an antinociceptive effect of <strong>CGRP</strong> in CeA.
+CALCA	drug	opioid	12732246	The <strong>CGRP</strong> induced antinociception was attenuated by s.c. injection of the <b>opioid</b> antagonist <b>naloxone</b>, suggesting an involvement of endogenous <b>opioid</b> systems in <strong>CGRP</strong> induced antinociception.
+CALCA	drug	opioid	12732246	Moreover, it was demonstrated that <b>opioid</b> receptors in the periaqueductal gray, but not in CeA, contributed to the <strong>CGRP</strong> induced antinociception, indicating the importance of the pathway between CeA and the periaqueductal gray in <strong>CGRP</strong> induced antinociception.
+CALCA	drug	opioid	11976266	This study examined the role of spinal calcitonin gene related peptide (<strong>CGRP</strong>), substance P, and prostaglandins in the development and expression of <b>opioid</b> physical dependence.
+CALCA	addiction	dependence	11976266	This study examined the role of spinal calcitonin gene related peptide (<strong>CGRP</strong>), substance P, and prostaglandins in the development and expression of opioid physical <b>dependence</b>.
+CALCA	drug	opioid	11976266	of <b>morphine</b> for 7 days markedly elevated <strong>CGRP</strong> and substance P  immunoreactivity in the dorsal horn of the rat spinal cord.
+CALCA	addiction	withdrawal	11976266	challenge decreased both <strong>CGRP</strong> and substance P immunoreactivity and precipitated a robust <b>withdrawal</b> syndrome.
+CALCA	drug	opioid	11976266	Acute intrathecal pre treatment with a <strong>CGRP</strong> receptor antagonist, <strong>CGRP</strong>(8   37) (4, 8 microg), a substance P receptor antagonist, SR 140333 (1.4, 2.8 microg), a cyclo oxygenase (COX) inhibitor, ketorolac (30, 45 microg), and COX 2 selective inhibitors, DuP 697 (10, 30 microg) and nimesulide (30 microg), 30 min before <b>naloxone</b> challenge, partially attenuated the symptoms of <b>morphine</b> withdrawal.
+CALCA	addiction	withdrawal	11976266	Acute intrathecal pre treatment with a <strong>CGRP</strong> receptor antagonist, <strong>CGRP</strong>(8   37) (4, 8 microg), a substance P receptor antagonist, SR 140333 (1.4, 2.8 microg), a cyclo oxygenase (COX) inhibitor, ketorolac (30, 45 microg), and COX 2 selective inhibitors, DuP 697 (10, 30 microg) and nimesulide (30 microg), 30 min before naloxone challenge, partially attenuated the symptoms of morphine <b>withdrawal</b>.
+CALCA	drug	opioid	11976266	Chronic intrathecal treatment with <strong>CGRP</strong>(8   37) (4, 8 microg), SR 140333 (1.4 microg), ketorolac (15, 30 microg), DuP 697 (10, 30micro g), and nimesulide (30 microg), delivered with daily <b>morphine</b> injection significantly attenuated both the symptoms of withdrawal and the decrease in <strong>CGRP</strong> but not substance P immunoreactivity.
+CALCA	addiction	withdrawal	11976266	Chronic intrathecal treatment with <strong>CGRP</strong>(8   37) (4, 8 microg), SR 140333 (1.4 microg), ketorolac (15, 30 microg), DuP 697 (10, 30micro g), and nimesulide (30 microg), delivered with daily morphine injection significantly attenuated both the symptoms of <b>withdrawal</b> and the decrease in <strong>CGRP</strong> but not substance P immunoreactivity.
+CALCA	drug	opioid	11976266	The results of this study suggest that activation of <strong>CGRP</strong> and substance P receptors, at the spinal level, contributes to the induction and expression of <b>opioid</b> physical dependence and that this activity may be partially expressed through the intermediary actions of prostaglandins.
+CALCA	addiction	dependence	11976266	The results of this study suggest that activation of <strong>CGRP</strong> and substance P receptors, at the spinal level, contributes to the induction and expression of opioid physical <b>dependence</b> and that this activity may be partially expressed through the intermediary actions of prostaglandins.
+CALCA	drug	opioid	11454653	<b>Morphine</b> had no effect on <strong>CGRP</strong> evoked dural vasodilation.
+CALCA	drug	opioid	11454653	<b>Morphine</b> (3 mg kg( 1)) also inhibited the TNC neuronal sensitization following <strong>CGRP</strong> evoked dilation.
+CALCA	addiction	sensitization	11454653	Morphine (3 mg kg( 1)) also inhibited the TNC neuronal <b>sensitization</b> following <strong>CGRP</strong> evoked dilation.
+CALCA	drug	opioid	11353815	In contrast, the mu <b>opioid</b> agonist <b>fentanyl</b> elicited a 74 +/  4% reduction in <strong>CGRP</strong> levels.
+CALCA	addiction	dependence	11353815	Taken together, the present data confirm the PKA <b>dependence</b> of forskolin stimulated <strong>CGRP</strong> release and suggest that A(1) adenosine agonists may warrant further investigation in models of migraine and neurogenic inflammation.
+CALCA	drug	alcohol	11281986	Calcitonin gene related peptide (<strong>CGRP</strong>) levels and <b>alcohol</b>.
+CALCA	drug	alcohol	11281986	Since <b>alcohol</b> consumption may be related to <b>alcohol</b>'s anxiolytic properties, the present study sought to determine if brain <strong>CGRP</strong> levels were correlated with genetic differences in preference for drinking <b>alcohol</b> and/or affected by <b>alcohol</b> exposure/withdrawal.
+CALCA	addiction	withdrawal	11281986	Since alcohol consumption may be related to alcohol's anxiolytic properties, the present study sought to determine if brain <strong>CGRP</strong> levels were correlated with genetic differences in preference for drinking alcohol and/or affected by alcohol exposure/<b>withdrawal</b>.
+CALCA	drug	alcohol	11281986	In the first experiment, <strong>CGRP</strong> LI was compared in <b>alcohol</b> naive rats [preferring (P) and non preferring (NP)], lower concentrations were found in the hippocampus (U = 153.5; d.f.
+CALCA	drug	alcohol	11281986	However, at 4 wk following <b>ethanol</b> withdrawal, higher concentrations of <strong>CGRP</strong> LI were found in the hippocampus (U = 26.5; d.f.
+CALCA	addiction	withdrawal	11281986	However, at 4 wk following ethanol <b>withdrawal</b>, higher concentrations of <strong>CGRP</strong> LI were found in the hippocampus (U = 26.5; d.f.
+CALCA	drug	alcohol	11281986	These studies suggest that <strong>CGRP</strong> may modulate <b>alcohol</b> preference and additionally, that exposure/withdrawal from <b>ethanol</b> produces long lasting effects on <strong>CGRP</strong> LI.
+CALCA	addiction	withdrawal	11281986	These studies suggest that <strong>CGRP</strong> may modulate alcohol preference and additionally, that exposure/<b>withdrawal</b> from ethanol produces long lasting effects on <strong>CGRP</strong> LI.
+CALCA	addiction	dependence	11276224	Altered neuroadaptation in opiate <b>dependence</b> and neurogenic inflammatory nociception in alpha <strong>CGRP</strong> deficient mice.
+CALCA	drug	opioid	11276224	Furthermore, alpha <strong>CGRP</strong>( / ) mice do not show changes in <b>heroin</b> self administration or <b>morphine</b> tolerance, but display a marked decrease in <b>morphine</b> withdrawal signs, suggesting an important contribution of alpha <strong>CGRP</strong> to opiate withdrawal.
+CALCA	addiction	withdrawal	11276224	Furthermore, alpha <strong>CGRP</strong>( / ) mice do not show changes in heroin self administration or morphine tolerance, but display a marked decrease in morphine <b>withdrawal</b> signs, suggesting an important contribution of alpha <strong>CGRP</strong> to opiate <b>withdrawal</b>.
+CALCA	drug	alcohol	11208722	Exposure of <b>ethanol</b> after 1 mol/L NaCl increased intragastric <strong>CGRP</strong> levels from 166 +/  27 to 713 +/  55 pg/2 min (n = 4, P < 0.05), and the protective action of 1 mol/L NaCl was inhibited by indomethacin treatment.
+CALCA	drug	alcohol	11208722	Intragastric perfusion of 50% <b>ethanol</b> after administration of PGI(2), but not of PGE(2), increased <strong>CGRP</strong> levels.
+CALCA	drug	alcohol	11208722	<strong>CGRP</strong> level during <b>ethanol</b> perfusion was not increased in IP( / ) but was increased in EP3( / ) and wild type counterparts after preperfusion of 1 mol/L NaCl.
+CALCA	drug	opioid	10915810	The present study investigated the role of calcitonin gene related peptide (<strong>CGRP</strong>) on nociception in nucleus raphe magnus (NRM) and the interaction between <strong>CGRP</strong> and <b>opioid</b> peptides in NRM of rats.
+CALCA	addiction	withdrawal	10915810	The hindpaw <b>withdrawal</b> latency (HWL) to thermal and mechanical stimulation increased significantly after intra NRM administration of 0.5 or 1 nmol of <strong>CGRP</strong> in rats, but not 0.25 nmol.
+CALCA	drug	opioid	10915810	Furthermore, the <strong>CGRP</strong> induced anti nociceptive effect was attenuated by following intra NRM administration of 6 nmol of <b>naloxone</b>.
+CALCA	drug	opioid	10915810	The results indicate that <strong>CGRP</strong> and its receptors play an important role in anti nociception, and there is a possible interaction between <strong>CGRP</strong> and <b>opioid</b> peptides in NRM of rats.
+CALCA	addiction	withdrawal	9574827	Intrathecal <strong>CGRP</strong>(8 37) results in a bilateral increase in hindpaw <b>withdrawal</b> latency in rats with a unilateral thermal injury.
+CALCA	addiction	withdrawal	9574827	The present study was performed to explore the effects of intrathecal administration of calcitonin gene related peptide8 37 (<strong>CGRP</strong>(8 37)) on the hindpaw <b>withdrawal</b> latency (HWL) to pressure in rats with one thermally injured hindpaw.
+CALCA	drug	opioid	9574827	Furthermore, the interaction of <strong>CGRP</strong>(8 37)and <b>naloxone</b> was studied.
+CALCA	drug	opioid	9574827	The effect of <strong>CGRP</strong>(8 37) was partly reversed by intrathecal injection of <b>naloxone</b> at a dose of 32 and 64 microg respectively.
+CALCA	drug	opioid	9574827	Furthermore, our findings suggest that <b>opioids</b> can modulate <strong>CGRP</strong> related effects in the spinal cord.
+CALCA	addiction	withdrawal	8825341	Recent work in our laboratory has demonstrated that intrathecal administration of a selective antagonist of calcitonin gene related peptide (<strong>CGRP</strong>), CGRP8 37, increased the hindpaw <b>withdrawal</b> latency (HWL) to thermal stimulation and hindpaw <b>withdrawal</b> threshold (HWT) to pressure in normal rats, and that these effects were more pronounced than in rats with mononeuropathy.
+CALCA	drug	opioid	8825341	Furthermore, our findings suggest that <b>opioids</b> can modulate <strong>CGRP</strong> related effects in the spinal cord.
+CALCA	addiction	withdrawal	8581488	We recently demonstrated that intrathecal administration of calcitonin gene related peptide 8 37 (CGRP8 37), a selective antagonist of calcitonin gene related peptide receptors, dose dependently increased the latency to hindpaw <b>withdrawal</b> responses induced by both thermal and mechanical stimulation in intact rats, indicating a role for <strong>CGRP</strong> and its receptors in the transmission of presumed nociceptive information in the spinal cord.
+CALCA	drug	opioid	8581488	The present study was performed to explore the interaction between <strong>CGRP</strong> and <b>opioids</b> in the spinal cord of rats.
+CALCA	drug	opioid	8581488	These results indicate that mu and delta, but not kappa, <b>opioid</b> receptors are involved in the modulation of post synaptic effects and/or release of <strong>CGRP</strong> and other neurotransmitters.
+CALCA	drug	opioid	8545480	The aim of this study was to investigate the possible interaction of <strong>CGRP</strong> with <b>morphine</b> on nociception in adult male NMRI mice after central administration of the peptide.
+CALCA	drug	opioid	8545480	<strong>CGRP</strong> (20 or 200 ng) did not itself modify pain sensitivity in the tail flick test and did not affect the acute antinociceptive action of a single dose of <b>morphine</b> in the same test.
+CALCA	drug	opioid	8545480	However, <strong>CGRP</strong> suppressed the development of rapid tolerance to <b>morphine</b> in a dose dependent manner, but had no action on the development of chronic tolerance to <b>morphine</b> and on manifestations of <b>naloxone</b> precipitated withdrawal syndrome.
+CALCA	addiction	withdrawal	8545480	However, <strong>CGRP</strong> suppressed the development of rapid tolerance to morphine in a dose dependent manner, but had no action on the development of chronic tolerance to morphine and on manifestations of naloxone precipitated <b>withdrawal</b> syndrome.
+CALCA	drug	opioid	8336518	Previously we have shown that calcitonin gene related peptide (<strong>CGRP</strong>) modulates nociception and the effect of <b>opioid</b> analgesics in the central nervous system of mice.
+CALCA	addiction	withdrawal	8336518	Subcutaneous injection of <strong>CGRP</strong> produced a modest elevation of <b>withdrawal</b> latency time at doses that were two orders of magnitude greater than the physiologic levels determined in naive animals by radioimmunoassay.
+CALCA	addiction	withdrawal	8336518	These results indicate that subcutaneous injection of <strong>CGRP</strong> into the dorsal hindpaw skin of the mouse produces a modest increase in paw <b>withdrawal</b> latency times at high, non physiologic doses.
+CALCA	drug	opioid	1335576	Acute administration of <b>morphine</b> decreases levels of <strong>CGRP</strong> in rat corpus striatum.
+CALCA	drug	opioid	1335576	Tolerance to <b>morphine</b> did not alter the levels of <strong>CGRP</strong> in any brain region or in the spinal cord of the rat.
+CALCA	drug	opioid	1335576	<strong>CGRP</strong> did not alter the tolerance to the antinociceptive effects of <b>morphine</b>.
+CALCA	drug	alcohol	1335576	Chronic <b>naltrexone</b> increased the levels of <strong>CGRP</strong> in the hypothalamus.
+CALCA	drug	alcohol	1335576	Concurrent chronic administration of <b>naltrexone</b> plus morphine raised the levels of <strong>CGRP</strong> in the medulla, midbrain, and spinal cord.
+CALCA	drug	opioid	1335576	Concurrent chronic administration of naltrexone plus <b>morphine</b> raised the levels of <strong>CGRP</strong> in the medulla, midbrain, and spinal cord.
+CALCA	drug	opioid	1335576	<strong>CGRP</strong> enhances <b>naloxone</b> precipitated withdrawal jumping in mice.
+CALCA	addiction	withdrawal	1335576	<strong>CGRP</strong> enhances naloxone precipitated <b>withdrawal</b> jumping in mice.
+CALCA	addiction	withdrawal	1335576	In rats, during <b>withdrawal</b> the levels of <strong>CGRP</strong> were tripled in the corpus striatum and significantly reduced in the hippocampus and hypothalamus.
+CALCA	drug	opioid	1335576	These data are consistent with the hypothesis that <strong>CGRP</strong> acts as a modulatory peptide in opiate sensitive systems and tonic <b>opioid</b> control of <strong>CGRP</strong> levels exists in brain.
+CALCA	drug	opioid	1382137	In this study, we examined the effects of dependence on and withdrawal from <b>morphine</b> and <b>methadone</b> on brain SP and <strong>CGRP</strong> content.
+CALCA	addiction	dependence	1382137	In this study, we examined the effects of <b>dependence</b> on and withdrawal from morphine and methadone on brain SP and <strong>CGRP</strong> content.
+CALCA	addiction	withdrawal	1382137	In this study, we examined the effects of dependence on and <b>withdrawal</b> from morphine and methadone on brain SP and <strong>CGRP</strong> content.
+ADH4	drug	alcohol	31989819	Native <b>ethanol</b> dehydrogenase <strong>ADH2</strong> and acetaldehyde dehydrogenase ADA from Dickeya zeae were further overexpressed, which enhanced the capability to utilize <b>ethanol</b> for squalene synthesis and endowed the engineered strain with greater adaptability to high <b>ethanol</b> concentrations.
+ADH4	drug	alcohol	29084628	We evaluated the presence of SNPs in the ADH (ADH1B, ADH1C, and <strong>ADH4</strong>) and ALDH (ALDH2) genes in <b>alcohol</b> users of Goiânia, State of Goiás   Brazil, and then we established a possible relationship with AUD by allelic and genotypic study.
+ADH4	drug	alcohol	28805974	Effect of single nucleotide polymorphisms in ADH1B, <strong>ADH4</strong>, ADH1C, OPRM1, DRD2, BDNF, and ALDH2 genes on <b>alcohol</b> dependence in a Caucasian population.
+ADH4	addiction	dependence	28805974	Effect of single nucleotide polymorphisms in ADH1B, <strong>ADH4</strong>, ADH1C, OPRM1, DRD2, BDNF, and ALDH2 genes on alcohol <b>dependence</b> in a Caucasian population.
+ADH4	drug	alcohol	27172571	The interactions of religious involvement with ADH1B rs2066702, ADH1C rs698, and <strong>ADH4</strong> rs1042364 were significantly associated with maximum drinks and <b>alcohol</b> dependence symptoms.
+ADH4	addiction	dependence	27172571	The interactions of religious involvement with ADH1B rs2066702, ADH1C rs698, and <strong>ADH4</strong> rs1042364 were significantly associated with maximum drinks and alcohol <b>dependence</b> symptoms.
+ADH4	drug	alcohol	26848198	Characterization of polymorphisms of genes <strong>ADH2</strong>, ADH3, ALDH2 and CYP2E1 and relationship to the <b>alcoholism</b> in a Colombian population.
+ADH4	drug	alcohol	26848198	Identify and characterize polymorphisms of genes <strong>ADH2</strong>, ADH3, ALDH2 and CYP2E1 in a Colombian population residing in the city of Bogotá and determine its possible relationship to the <b>alcoholism</b>.
+ADH4	drug	alcohol	26848198	<strong>ADH2</strong>, ADH3, ALDH2, and CYP2E1 genotypes a population of 148 individuals with non problematic <b>alcohol</b> and 65 individuals with <b>alcoholism</b> were determined with TaqMan probes and PCR RFLP.
+ADH4	drug	alcohol	26848198	Since substance dependence requires interaction of multiple genes, the combination of genotypes <strong>ADH2</strong> * 2, CYP2E1 * 1 combined with genotype homozygous ALDH2 * 1 found in this study could be leading to the population to a potential risk to <b>alcoholism</b>.
+ADH4	addiction	dependence	26848198	Since substance <b>dependence</b> requires interaction of multiple genes, the combination of genotypes <strong>ADH2</strong> * 2, CYP2E1 * 1 combined with genotype homozygous ALDH2 * 1 found in this study could be leading to the population to a potential risk to alcoholism.
+ADH4	drug	alcohol	26848198	Se determinaron los genotipos <strong>ADH2</strong>, ADH3, ALDH2 y CYP2E1 a una población de 148 individuos con un consumo no problemático de <b>alcohol</b> y 65 individuos con alcoholismo.
+ADH4	drug	alcohol	26230553	Alleles involved in inefficient (ADH1B2*2 and ALDH2*2) or efficient (SNP6, <strong>ADH4</strong> gene) <b>alcohol</b> metabolism may influence the risk of <b>alcoholism</b>.
+ADH4	drug	alcohol	25535445	The genes for <b>alcohol</b> metabolizing enzymes: <b>Alcohol</b> dehydrogenase (<strong>ADH2</strong> and ADH3) and aldehyde dehydrogenase (ALDH2) exhibit functional polymorphisms.
+ADH4	drug	alcohol	25535445	To determine whether any association exists between polymorphisms of <strong>ADH2</strong>, ADH3 and ALDH2 and <b>alcohol</b> dependence syndrome in a group of Asian Indians.
+ADH4	addiction	dependence	25535445	To determine whether any association exists between polymorphisms of <strong>ADH2</strong>, ADH3 and ALDH2 and alcohol <b>dependence</b> syndrome in a group of Asian Indians.
+ADH4	drug	alcohol	25535445	Allele frequencies of <strong>ADH2</strong>*2 (0.50), ADH3*1 (0.67) and ALSH2*2 (0.09) were significantly low in the <b>alcohol</b> dependent subjects.
+ADH4	drug	alcohol	24889829	Rs1800759 (previously known to be associated to AD) and CpG cg12011299 (distance: 37 bp) are both located in <b>alcohol</b> dehydrogenase (ADH) 4 gene (<strong>ADH4</strong>) promoter region.
+ADH4	drug	alcohol	24692236	Linkage studies of <b>alcoholism</b> have implicated several chromosome regions, leading to the successful identification of susceptibility genes, including <strong>ADH4</strong> and GABRA2 on chromosome 4.
+ADH4	drug	alcohol	23468174	Humans express at least seven <b>alcohol</b> dehydrogenase (ADH) isoforms that are encoded by ADH gene cluster (ADH7 ADH1C ADH1B ADH1A ADH6 <strong>ADH4</strong> ADH5) at chromosome 4.
+ADH4	drug	alcohol	22232963	[Research on associations between selected polymorphisms of genes DRD2, 5HTT, GRIK3, <strong>ADH4</strong> and <b>alcohol</b> dependence syndrome].
+ADH4	addiction	dependence	22232963	[Research on associations between selected polymorphisms of genes DRD2, 5HTT, GRIK3, <strong>ADH4</strong> and alcohol <b>dependence</b> syndrome].
+ADH4	drug	alcohol	22232963	The aim of this study was to assess the relation between the <b>alcohol</b> dependence syndrome (ADS) and the polymorphism of the selected genes (GRIK3, 5HTT, ANKK1, <strong>ADH4</strong>).
+ADH4	addiction	dependence	22232963	The aim of this study was to assess the relation between the alcohol <b>dependence</b> syndrome (ADS) and the polymorphism of the selected genes (GRIK3, 5HTT, ANKK1, <strong>ADH4</strong>).
+ADH4	drug	alcohol	22232963	Comparison between the patients with ADS and the patients from the control group demonstrated statistically significant association of <strong>ADH4</strong> (rs1800759) with the <b>alcohol</b> dependence syndrome.
+ADH4	addiction	dependence	22232963	Comparison between the patients with ADS and the patients from the control group demonstrated statistically significant association of <strong>ADH4</strong> (rs1800759) with the alcohol <b>dependence</b> syndrome.
+ADH4	drug	alcohol	22232963	Our results suggest that the analysed polymorphisms ofANKK1 and <strong>ADH4</strong> can play an important part in the pathogenesis of <b>alcohol</b> abuse.
+ADH4	drug	alcohol	22044940	<strong>ADH4</strong> intronic variations are associated with <b>alcohol</b> dependence: results from an Italian case control association study.
+ADH4	addiction	dependence	22044940	<strong>ADH4</strong> intronic variations are associated with alcohol <b>dependence</b>: results from an Italian case control association study.
+ADH4	drug	alcohol	22044940	This study investigated the involvement of <strong>ADH4</strong> gene polymorphisms in the susceptibility to <b>alcohol</b> use disorders.
+ADH4	drug	alcohol	22044940	Thirty eight single nucleotide polymorphisms (SNPs) in and around the <strong>ADH4</strong> gene were investigated in 136 Italian <b>alcoholics</b> and 276 healthy controls.
+ADH4	drug	alcohol	22044940	Case control comparisons for allele and genotype frequencies showed that <strong>ADH4</strong> SNPs were associated with <b>alcohol</b> dependence but not with <b>alcohol</b> abuse.
+ADH4	addiction	dependence	22044940	Case control comparisons for allele and genotype frequencies showed that <strong>ADH4</strong> SNPs were associated with alcohol <b>dependence</b> but not with alcohol abuse.
+ADH4	drug	alcohol	22044940	A logistic regression analysis confirmed the association between <strong>ADH4</strong> variants and <b>alcohol</b> dependence when sex, age, years of education, marital status and the allele genotype, haplotype and diplotype data of the six haplotype tag SNP were considered.
+ADH4	addiction	dependence	22044940	A logistic regression analysis confirmed the association between <strong>ADH4</strong> variants and alcohol <b>dependence</b> when sex, age, years of education, marital status and the allele genotype, haplotype and diplotype data of the six haplotype tag SNP were considered.
+ADH4	drug	alcohol	22044940	These data suggest that <strong>ADH4</strong> intronic variants play a role in <b>alcohol</b> dependence susceptibility in Italian populations.
+ADH4	addiction	dependence	22044940	These data suggest that <strong>ADH4</strong> intronic variants play a role in alcohol <b>dependence</b> susceptibility in Italian populations.
+ADH4	drug	alcohol	21635275	No evidence for association with the <b>alcohol</b> dependence diagnosis was observed, but an SNP in exon 9 of ADH1B (rs2066702; ADH1B*3) and an SNP at the 5' end of <strong>ADH4</strong> (rs3762894) showed significant evidence of association with the presence of withdrawal symptoms (p = 0.0018 and 0.0012, respectively).
+ADH4	addiction	dependence	21635275	No evidence for association with the alcohol <b>dependence</b> diagnosis was observed, but an SNP in exon 9 of ADH1B (rs2066702; ADH1B*3) and an SNP at the 5' end of <strong>ADH4</strong> (rs3762894) showed significant evidence of association with the presence of withdrawal symptoms (p = 0.0018 and 0.0012, respectively).
+ADH4	addiction	withdrawal	21635275	No evidence for association with the alcohol dependence diagnosis was observed, but an SNP in exon 9 of ADH1B (rs2066702; ADH1B*3) and an SNP at the 5' end of <strong>ADH4</strong> (rs3762894) showed significant evidence of association with the presence of <b>withdrawal</b> symptoms (p = 0.0018 and 0.0012, respectively).
+ADH4	drug	alcohol	21635275	These results suggest that variants in the ADH1B and <strong>ADH4</strong> genes may be protective against the development of some symptoms associated with <b>alcohol</b> dependence.
+ADH4	addiction	dependence	21635275	These results suggest that variants in the ADH1B and <strong>ADH4</strong> genes may be protective against the development of some symptoms associated with alcohol <b>dependence</b>.
+ADH4	drug	alcohol	21083667	The systematic evaluation of <b>alcohol</b> metabolizing genes in four non East Asian populations has shown only modest associations with AD, largely for ALDH1A1 and <strong>ADH4</strong>.
+ADH4	drug	alcohol	20626721	Association of <strong>ADH4</strong> genetic variants with <b>alcohol</b> dependence risk and related phenotypes: results from a larger multicenter association study.
+ADH4	addiction	dependence	20626721	Association of <strong>ADH4</strong> genetic variants with alcohol <b>dependence</b> risk and related phenotypes: results from a larger multicenter association study.
+ADH4	drug	alcohol	20626721	Genetic variants of the <b>alcohol</b> metabolizing enzyme <strong>ADH4</strong>, located on chromosome 4q22 4q23, have been related to <b>alcohol</b> dependence (AD) risk in previous research.
+ADH4	addiction	dependence	20626721	Genetic variants of the alcohol metabolizing enzyme <strong>ADH4</strong>, located on chromosome 4q22 4q23, have been related to alcohol <b>dependence</b> (AD) risk in previous research.
+ADH4	drug	alcohol	20626721	The aim of this association study in a large multicenter sample of <b>alcohol</b> dependent individuals and controls is to confirm <strong>ADH4</strong> single nucleotide polymorphism (SNP) and haplotype association with AD and relevant related phenotypes.
+ADH4	drug	alcohol	20077761	The genotype frequencies of the <strong>ADH2</strong> and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu opioid receptor gene (OPRM1) in Korean men and women with <b>alcohol</b> dependence (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for <b>alcoholism</b>.
+ADH4	drug	opioid	20077761	The genotype frequencies of the <strong>ADH2</strong> and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu <b>opioid</b> receptor gene (OPRM1) in Korean men and women with alcohol dependence (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for alcoholism.
+ADH4	addiction	dependence	20077761	The genotype frequencies of the <strong>ADH2</strong> and ALDH2 gene polymorphisms as well as the A118G polymorphism of the mu opioid receptor gene (OPRM1) in Korean men and women with alcohol <b>dependence</b> (AD) were compared with those of normal healthy (NH) Korean men and women at a low risk for alcoholism.
+ADH4	drug	alcohol	20077761	These results suggest that, while the risk of <b>alcoholism</b> in Korean men is predominantly affected by the presence of the ALDH2 1/1 genotype, the risk of <b>alcoholism</b> in Korean women is primarily associated with the <strong>ADH2</strong> 1/1 genotype and G carrier genotype of the OPRM1 A118G polymorphism.
+ADH4	drug	alcohol	20025435	The association between two functional polymorphisms in <b>alcohol</b> dehydrogenase (<strong>ADH2</strong>/ADH1B) and aldehyde dehydrogenase (ALDH2) genes and <b>alcohol</b> dependence was examined in 182 Chinese and Indian patients undergoing treatment for <b>alcohol</b> dependence and 184 screened control subjects from Singapore.
+ADH4	addiction	dependence	20025435	The association between two functional polymorphisms in alcohol dehydrogenase (<strong>ADH2</strong>/ADH1B) and aldehyde dehydrogenase (ALDH2) genes and alcohol <b>dependence</b> was examined in 182 Chinese and Indian patients undergoing treatment for alcohol <b>dependence</b> and 184 screened control subjects from Singapore.
+ADH4	drug	alcohol	19193628	Alleles of ADH7 SNPs were associated with the early stages of <b>alcohol</b> metabolism, with additional effects in the ADH1A, ADH1B and <strong>ADH4</strong> regions.
+ADH4	drug	alcohol	19182438	Polymorphisms in the promoter region of the human class II <b>alcohol</b> dehydrogenase (<strong>ADH4</strong>) gene affect both transcriptional activity and <b>ethanol</b> metabolism in Japanese subjects.
+ADH4	drug	alcohol	19182438	Class II <b>alcohol</b> dehydrogenase (pi ADH), encoded by <b>alcohol</b> dehydrogenase (<strong>ADH4</strong>), is considered to contribute to <b>ethanol</b> (EtOH) oxidation in the liver at high concentration.
+ADH4	drug	alcohol	19182438	These results suggested that the SNP at  136bp in the <strong>ADH4</strong> promoter had an effect on transcriptional regulation, and that the higher activity of the  136A allele compared with the  136C allele caused a lower level of blood EtOH after <b>alcohol</b> ingestion; that is, individuals with the  136A allele may consume more EtOH and might have a higher risk for development of <b>alcohol</b> dependence than those without the  136A allele.
+ADH4	addiction	dependence	19182438	These results suggested that the SNP at  136bp in the <strong>ADH4</strong> promoter had an effect on transcriptional regulation, and that the higher activity of the  136A allele compared with the  136C allele caused a lower level of blood EtOH after alcohol ingestion; that is, individuals with the  136A allele may consume more EtOH and might have a higher risk for development of alcohol <b>dependence</b> than those without the  136A allele.
+ADH4	drug	alcohol	18996923	After controlling for rs1229984, an independent association was observed between rs1042026 (ADH1B) and <b>alcohol</b> intake (P=4.7 x 10( 5)) and suggestive associations (P<0.001) between <b>alcohol</b> consumption phenotypes and rs1693482 (ADH1C), rs1230165 (ADH5) and rs3762894 (<strong>ADH4</strong>).
+ADH4	addiction	dependence	18801187	Recessive genetic mode of an <strong>ADH4</strong> variant in substance <b>dependence</b> in African Americans: A model of utility of the HWD test.
+ADH4	drug	alcohol	18801187	In our previous studies, we reported positive associations between seven <strong>ADH4</strong> polymorphisms and substance dependence [i.e., <b>alcohol</b> dependence (AD) and/or drug dependence (DD)] in European Americans (EAs).
+ADH4	addiction	dependence	18801187	In our previous studies, we reported positive associations between seven <strong>ADH4</strong> polymorphisms and substance <b>dependence</b> [i.e., alcohol <b>dependence</b> (AD) and/or drug <b>dependence</b> (DD)] in European Americans (EAs).
+ADH4	addiction	dependence	18801187	In the present study, we address the relationship between <strong>ADH4</strong> variation and substance <b>dependence</b> in an African American (AA) population, and report evidence that supports an association between a different <strong>ADH4</strong> polymorphism (rs2226896) and these phenotypes in AAs.
+ADH4	addiction	dependence	18801187	Two family based association study methods, i.e., TDT and FBAT, were applied to test the relationship between <strong>ADH4</strong> variation and substance <b>dependence</b> in Sample 3 (112 small nuclear families) and in Sample 4 (632 pedigrees), respectively.
+ADH4	addiction	dependence	18801187	<strong>ADH4</strong> variation might play a role in risk for substance <b>dependence</b> in AAs, potentially via a recessive mechanism.
+ADH4	drug	alcohol	17454860	We determined the allele and genotype of <strong>ADH2</strong>, ADH3 and ALDH2 in 198 subjects: 57 with <b>alcohol</b> cirrhosis, 44 with <b>alcohol</b> chronic pancreatitis and 43 "healthy <b>alcoholics</b>"; 54 healthy non drinkers served as controls.
+ADH4	drug	alcohol	17454860	The <strong>ADH2</strong>*1 and the ADH3*1 alleles were statistically more common among patients who abuse <b>alcohol</b> in comparison with the controls.
+ADH4	drug	alcohol	17454860	The <strong>ADH2</strong>*2 allele was not detected in any of the patients with chronic <b>alcohol</b> pancreatitis.
+ADH4	drug	alcohol	17454860	The <strong>ADH2</strong>*1/*1 and the ADH3*1/*1 genotypes were statistically significantly more common among the patients who abuse <b>alcohol</b> than in the control group.
+ADH4	drug	alcohol	17134660	This study sought to determine whether an association exists between ADH (ADH1C previously ADH3, ADH1B*2 previously <strong>ADH2</strong>*2) genotypes, <b>alcohol</b> dependence, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH4	addiction	dependence	17134660	This study sought to determine whether an association exists between ADH (ADH1C previously ADH3, ADH1B*2 previously <strong>ADH2</strong>*2) genotypes, alcohol <b>dependence</b>, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH4	drug	alcohol	16571603	There was strong evidence that variations in <strong>ADH4</strong> are associated with <b>alcoholism</b>: 12 SNPs were significantly associated.
+ADH4	drug	alcohol	16571603	Haplotype tag SNPs were selected for the block in the <strong>ADH4</strong> gene that provided evidence of association and subsequently used in association analysis; the haplotype was significantly associated with <b>alcoholism</b> (P=0.01) There was weaker evidence that variations in ADH1A and ADH1B might also play a role in modifying risk.
+ADH4	drug	alcohol	16237392	<strong>ADH4</strong> gene variation is associated with <b>alcohol</b> dependence and drug dependence in European Americans: results from HWD tests and case control association studies.
+ADH4	addiction	dependence	16237392	<strong>ADH4</strong> gene variation is associated with alcohol <b>dependence</b> and drug <b>dependence</b> in European Americans: results from HWD tests and case control association studies.
+ADH4	drug	alcohol	16237392	The <strong>ADH4</strong> gene, an important member of this family, is a functional and positional candidate for <b>alcohol</b> dependence.
+ADH4	addiction	dependence	16237392	The <strong>ADH4</strong> gene, an important member of this family, is a functional and positional candidate for alcohol <b>dependence</b>.
+ADH4	drug	alcohol	16237392	The present study aimed to investigate the relationship between <strong>ADH4</strong> gene variation and <b>alcohol</b> dependence and drug dependence in European Americans (EAs) and African Americans (AAs).
+ADH4	addiction	dependence	16237392	The present study aimed to investigate the relationship between <strong>ADH4</strong> gene variation and alcohol <b>dependence</b> and drug <b>dependence</b> in European Americans (EAs) and African Americans (AAs).
+ADH4	drug	alcohol	16237392	Seven single nucleotide polymorphisms (SNPs) spanning the <strong>ADH4</strong> gene were genotyped in 365 healthy controls (317 EAs and 48 AAs) and 561 subjects (400 EAs and 161 AAs) affected with <b>alcohol</b> dependence and/or drug dependence (436 with <b>alcohol</b> dependence; 356 with drug dependence).
+ADH4	addiction	dependence	16237392	Seven single nucleotide polymorphisms (SNPs) spanning the <strong>ADH4</strong> gene were genotyped in 365 healthy controls (317 EAs and 48 AAs) and 561 subjects (400 EAs and 161 AAs) affected with alcohol <b>dependence</b> and/or drug <b>dependence</b> (436 with alcohol <b>dependence</b>; 356 with drug <b>dependence</b>).
+ADH4	drug	alcohol	16237392	These findings suggest that <strong>ADH4</strong> genotypes predispose to <b>alcohol</b> dependence and drug dependence in a recessive manner, a predisposition that is population specific.
+ADH4	addiction	dependence	16237392	These findings suggest that <strong>ADH4</strong> genotypes predispose to alcohol <b>dependence</b> and drug <b>dependence</b> in a recessive manner, a predisposition that is population specific.
+ADH4	drug	alcohol	16220108	<strong>ADH4</strong> gene variation is associated with <b>alcohol</b> and drug dependence: results from family controlled and population structured association studies.
+ADH4	addiction	dependence	16220108	<strong>ADH4</strong> gene variation is associated with alcohol and drug <b>dependence</b>: results from family controlled and population structured association studies.
+ADH4	drug	alcohol	16220108	We found strong associations between <strong>ADH4</strong> gene variation and <b>alcohol</b> and drug dependence by the Hardy Weinberg Disequilibrium (HWD) test and case control association analysis in an initial study.
+ADH4	addiction	dependence	16220108	We found strong associations between <strong>ADH4</strong> gene variation and alcohol and drug <b>dependence</b> by the Hardy Weinberg Disequilibrium (HWD) test and case control association analysis in an initial study.
+ADH4	drug	alcohol	16220108	Structured association analysis demonstrated that the genotypes of six <strong>ADH4</strong> markers were associated with <b>alcohol</b> dependence, and all seven <strong>ADH4</strong> markers were associated with drug dependence (P=10 0.047).
+ADH4	addiction	dependence	16220108	Structured association analysis demonstrated that the genotypes of six <strong>ADH4</strong> markers were associated with alcohol <b>dependence</b>, and all seven <strong>ADH4</strong> markers were associated with drug <b>dependence</b> (P=10 0.047).
+ADH4	drug	alcohol	16220108	Transmission disequilibrium test, haplotype based haplotype relative risk and genotype based haplotype relative risk analyses all confirmed the association of the <strong>ADH4</strong> markers with <b>alcohol</b> dependence and drug dependence.
+ADH4	addiction	dependence	16220108	Transmission disequilibrium test, haplotype based haplotype relative risk and genotype based haplotype relative risk analyses all confirmed the association of the <strong>ADH4</strong> markers with alcohol <b>dependence</b> and drug <b>dependence</b>.
+ADH4	drug	alcohol	16220108	Using rigorous study designs that account for possible population stratification, these findings confirm and extend our original observations indicating that variation at <strong>ADH4</strong> predisposes to <b>alcohol</b> and drug dependence.
+ADH4	addiction	dependence	16220108	Using rigorous study designs that account for possible population stratification, these findings confirm and extend our original observations indicating that variation at <strong>ADH4</strong> predisposes to alcohol and drug <b>dependence</b>.
+ADH4	drug	alcohol	16125912	One hundred and eleven male patients with <b>alcohol</b> dependence and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 (<strong>ADH2</strong>), aldehyde dehydrogenase 2 (ALDH2), serotonin transporter (5 HTT) and dopamine transporter (DAT1).
+ADH4	addiction	dependence	16125912	One hundred and eleven male patients with alcohol <b>dependence</b> and 123 nonalcoholic healthy men were tested for the genetic polymorphisms of alcohol dehydrogenase 2 (<strong>ADH2</strong>), aldehyde dehydrogenase 2 (ALDH2), serotonin transporter (5 HTT) and dopamine transporter (DAT1).
+ADH4	drug	alcohol	16125912	There were significant differences in genotype frequencies of <strong>ADH2</strong> C992G and A13543G SNPs between <b>alcoholic</b> patients with family history of <b>alcohol</b> dependence (familial) and <b>alcoholic</b> patients without family history (non familial).
+ADH4	addiction	dependence	16125912	There were significant differences in genotype frequencies of <strong>ADH2</strong> C992G and A13543G SNPs between alcoholic patients with family history of alcohol <b>dependence</b> (familial) and alcoholic patients without family history (non familial).
+ADH4	drug	alcohol	23105541	Subtypes of <strong>ADH2</strong> gene in <b>alcoholics</b>.
+ADH4	drug	alcohol	23105541	In the present study, genetic variation was detected in the subtypes of gene, coding for the <b>alcohol</b> metabolizing enzyme <b>Alcohol</b> Dehydrogenase 2 (<strong>ADH2</strong>).
+ADH4	drug	alcohol	23105541	Blood samples were collected from the <b>alcoholic</b> and non <b>alcoholic</b> subjects and genotyping was performed using PCR RFLP (Polymerase Chain Reaction Restriction Fragment Length Polymorphism), analysis to determine genetic polymorphisms in the <strong>ADH2</strong> gene subtypes.
+ADH4	drug	alcohol	23105541	The three subtypes of <strong>ADH2</strong> gene (<strong>ADH2</strong>.1, <strong>ADH2</strong>.2 and <strong>ADH2</strong>.3) were found in both <b>alcoholics</b> (Family History Positive and Family History Negative) as well as non <b>alcoholics</b>.
+ADH4	drug	alcohol	15863808	The authors evaluated the association of three functional promoter polymorphisms of the <strong>ADH4</strong> gene with <b>alcohol</b> dependence.
+ADH4	addiction	dependence	15863808	The authors evaluated the association of three functional promoter polymorphisms of the <strong>ADH4</strong> gene with alcohol <b>dependence</b>.
+ADH4	drug	alcohol	15863808	These preliminary results suggest that <strong>ADH4</strong> may play a role in the etiology of <b>alcohol</b> dependence.
+ADH4	addiction	dependence	15863808	These preliminary results suggest that <strong>ADH4</strong> may play a role in the etiology of alcohol <b>dependence</b>.
+ADH4	drug	alcohol	15863807	The authors examined the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 and 3 (<strong>ADH2</strong> and ADH3) and aldehyde dehydrogenase (ALDH2) in patients diagnosed as having Cloninger's type I or type II <b>alcoholism</b>.
+ADH4	drug	alcohol	15863807	Seventy two <b>alcoholic</b> men and 38 nonalcoholic, healthy men were tested for the distribution of genotypes and alleles of <strong>ADH2</strong>, ADH3, and ALDH2.
+ADH4	drug	alcohol	15863807	The frequencies of <strong>ADH2</strong>*1 and ADH3*2 alleles were significantly higher in men with type II <b>alcoholism</b> than in men with type I <b>alcoholism</b> and healthy men.
+ADH4	drug	alcohol	15842823	To study the distribution of genotypes about <b>alcohol</b> dehydrogenase 2 (<strong>ADH2</strong>) and aldehyde dehydrogenase 2 (ALDH2) and its relationship with drinking behaviors in Chinese Han healthy population as to providing a theoretic direction for filtering out high risk and sensitive individuals and taking preventive measures to decrease the <b>alcohol</b> related diseases.
+ADH4	drug	alcohol	15842823	Correlation between genotypes of <strong>ADH2</strong> and ALDH2 and <b>alcohol</b> related diseases should be more important.
+ADH4	drug	alcohol	15542751	The results revealed that (1) the less active allele of the <strong>ADH2</strong> gene (<strong>ADH2</strong>*1) is associated with an increased risk for <b>alcohol</b> dependence, <b>alcohol</b> induced persistent amnestic disorder, <b>alcohol</b> withdrawal syndrome, and cancer of the upper GI tract; (2) the inactive allele of the ALDH2 gene (ALDH2*2) is associated with a decreased risk for <b>alcohol</b> dependence, and an increased risk for <b>alcoholic</b> polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of <b>alcohol</b> dependence.
+ADH4	addiction	dependence	15542751	The results revealed that (1) the less active allele of the <strong>ADH2</strong> gene (<strong>ADH2</strong>*1) is associated with an increased risk for alcohol <b>dependence</b>, alcohol induced persistent amnestic disorder, alcohol withdrawal syndrome, and cancer of the upper GI tract; (2) the inactive allele of the ALDH2 gene (ALDH2*2) is associated with a decreased risk for alcohol <b>dependence</b>, and an increased risk for alcoholic polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of alcohol <b>dependence</b>.
+ADH4	addiction	withdrawal	15542751	The results revealed that (1) the less active allele of the <strong>ADH2</strong> gene (<strong>ADH2</strong>*1) is associated with an increased risk for alcohol dependence, alcohol induced persistent amnestic disorder, alcohol <b>withdrawal</b> syndrome, and cancer of the upper GI tract; (2) the inactive allele of the ALDH2 gene (ALDH2*2) is associated with a decreased risk for alcohol dependence, and an increased risk for alcoholic polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of alcohol dependence.
+ADH4	drug	alcohol	15122947	This study examined aldehyde dehydrogense (ALDH2) gene status, <b>alcohol</b> dehydrogense (<strong>ADH2</strong>) gene status, conduct disorder, and <b>alcohol</b> dependence in Chinese, Korean, and White American college students.
+ADH4	addiction	dependence	15122947	This study examined aldehyde dehydrogense (ALDH2) gene status, alcohol dehydrogense (<strong>ADH2</strong>) gene status, conduct disorder, and alcohol <b>dependence</b> in Chinese, Korean, and White American college students.
+ADH4	drug	alcohol	15122947	<strong>ADH2</strong> status was not related to <b>alcohol</b> dependence with ALDH2 included, and no interactions were significant.
+ADH4	addiction	dependence	15122947	<strong>ADH2</strong> status was not related to alcohol <b>dependence</b> with ALDH2 included, and no interactions were significant.
+ADH4	drug	alcohol	15112932	Mr. Cook's and Dr. Wall's paper adds another dimension to this article by presenting research on both the aldehyde dehydrogenase (ALDH2) and <b>alcohol</b> dehydrogenase (<strong>ADH2</strong>) genetic variants and their association with the <b>alcohol</b> related flushing response that is prevalent in Asian populations.
+ADH4	drug	alcohol	15041893	Among the multiple factors which influence these variations, genetic factors especially those related to the different alleles of <strong>ADH2</strong> and ALDH2, are the most well known and are related to the development of <b>alcohol</b> dependence, particularly in some populations such as those of Asian origin.
+ADH4	addiction	dependence	15041893	Among the multiple factors which influence these variations, genetic factors especially those related to the different alleles of <strong>ADH2</strong> and ALDH2, are the most well known and are related to the development of alcohol <b>dependence</b>, particularly in some populations such as those of Asian origin.
+ADH4	drug	alcohol	14745297	There is growing evidence of a functional role of the <strong>ADH2</strong>*2 allele in <b>alcohol</b> drinking patterns among Jews, who have traditionally exhibited low rates of <b>alcoholism</b> and <b>alcohol</b> related problems.
+ADH4	drug	alcohol	14745297	This study examined the effect of <strong>ADH2</strong>*2 on <b>alcohol</b> elimination rates (AER) under experimental conditions.
+ADH4	drug	alcohol	14745297	The rate of <b>alcohol</b> elimination is significantly associated with the <strong>ADH2</strong> genotype of Jewish males.
+ADH4	drug	alcohol	12884000	Specifically, ADH1B*47His (previously <strong>ADH2</strong> 2) and ALDH2 2 have been shown to confer protection against <b>alcoholism</b>, presumably through accumulation of acetaldehyde in the blood and a resultant 'flushing response' to <b>alcohol</b> consumption.
+ADH4	drug	alcohol	12884000	In the current study, variants at ADH1B (previously <strong>ADH2</strong>), ADH1C (previously ADH3), and ALDH2 were assayed in DNA extracts from participants belonging to a Southwest American Indian tribe (n=490) with a high prevalence of <b>alcoholism</b>.
+ADH4	drug	alcohol	12824808	In Taiwan, about 70% of the Han Chinese population have the <strong>ADH2</strong>*2 allele and 50% show ALDH2*1/*2 or ALDH2*2/*2 genotypes, which offer protection against drinking behavior and the risk of developing <b>alcoholism</b>.
+ADH4	drug	alcohol	12710951	To identify the association between the polymorphisms of genes encoding <b>alcohol</b> metabolizing enzymes and <b>alcoholism</b>, the <b>alcohol</b> dehydrogenase 2 (<strong>ADH2</strong>), <b>alcohol</b> dehydrogenase 3 (ADH3), aldehyde dehydrogenase 2 (ALDH2), and cytochrome P450 2E1 (CYP2E1) genes were studied in 101 male Mexican American <b>alcoholics</b>.
+ADH4	drug	alcohol	12710951	The allele frequency of <strong>ADH2</strong>*2 (4.3%) and ALDH2*2 (0%), which are considered as protective alleles against <b>alcohol</b> drinking, is very low in Mexican Americans and no association is found between these alleles and <b>alcohol</b> dependence.
+ADH4	addiction	dependence	12710951	The allele frequency of <strong>ADH2</strong>*2 (4.3%) and ALDH2*2 (0%), which are considered as protective alleles against alcohol drinking, is very low in Mexican Americans and no association is found between these alleles and alcohol <b>dependence</b>.
+ADH4	drug	alcohol	12505800	Two <b>alcohol</b> dehydrogenase genes (<strong>ADH2</strong> and ADH3 on chromosome 4) and one aldehyde dehydrogenase gene (ALDH2 on chromosome 12) exhibit functional polymorphisms.
+ADH4	drug	alcohol	12505800	The goal of this study was to determine whether any associations exist between the <strong>ADH2</strong>, ADH3, and ALDH2 polymorphisms and <b>alcohol</b> dependence in a group of Native Americans.
+ADH4	addiction	dependence	12505800	The goal of this study was to determine whether any associations exist between the <strong>ADH2</strong>, ADH3, and ALDH2 polymorphisms and alcohol <b>dependence</b> in a group of Native Americans.
+ADH4	drug	alcohol	12505800	A significant difference in the <strong>ADH2</strong> allele distributions was found between <b>alcohol</b> dependent and non <b>alcohol</b> dependent participants.
+ADH4	drug	alcohol	12505800	Those with <b>alcohol</b> dependence were significantly less likely to have the <strong>ADH2</strong>*3 allele (odds ratio=0.28) and significantly more likely to have the <strong>ADH2</strong>*1 allele (odds ratio=2.00) than those who were not <b>alcohol</b> dependent.
+ADH4	addiction	dependence	12505800	Those with alcohol <b>dependence</b> were significantly less likely to have the <strong>ADH2</strong>*3 allele (odds ratio=0.28) and significantly more likely to have the <strong>ADH2</strong>*1 allele (odds ratio=2.00) than those who were not alcohol dependent.
+ADH4	drug	alcohol	12505800	These results are consistent with genetic linkage studies showing protective associations for <b>alcohol</b> dependence and related behavior on chromosome 4 and suggest that <strong>ADH2</strong> polymorphisms may account for these findings.
+ADH4	addiction	dependence	12505800	These results are consistent with genetic linkage studies showing protective associations for alcohol <b>dependence</b> and related behavior on chromosome 4 and suggest that <strong>ADH2</strong> polymorphisms may account for these findings.
+ADH4	drug	alcohol	12500100	All participants completed the Time Line Follow Back, had blood drawn for genotyping at the <b>alcohol</b> dehydrogenase locus <strong>ADH2</strong>, and reported their religious affiliation and the number of religious services attended in the past year.
+ADH4	drug	alcohol	12500100	In the total sample, individuals who possessed a variant <b>alcohol</b> dehydrogenase allele <strong>ADH2</strong>*2 were approximately half as likely to binge drink as those who did not possess this allele.
+ADH4	addiction	intoxication	12500100	In the total sample, individuals who possessed a variant alcohol dehydrogenase allele <strong>ADH2</strong>*2 were approximately half as likely to <b>binge</b> drink as those who did not possess this allele.
+ADH4	drug	alcohol	12351924	The <strong>ADH2</strong>*2 allele of the <b>alcohol</b> dehydrogenase 2 (<strong>ADH2</strong>) gene protects against <b>alcoholism</b> in Asians and is found in approximately 20% of Jews.
+ADH4	addiction	dependence	12351924	We studied the relationship of <strong>ADH2</strong>*2 to DSM IV <b>dependence</b> severity in a random community sample of Israeli Ashkenazis, recent Russian immigrants (also Ashkenazis), and Sephardics.
+ADH4	drug	alcohol	12351924	Controlling for group and other potentially confounding factors, <strong>ADH2</strong>*2 was associated with a lower lifetime DSM IV <b>alcohol</b> dependence severity, although this differed somewhat within groups.
+ADH4	addiction	dependence	12351924	Controlling for group and other potentially confounding factors, <strong>ADH2</strong>*2 was associated with a lower lifetime DSM IV alcohol <b>dependence</b> severity, although this differed somewhat within groups.
+ADH4	addiction	dependence	12351924	<strong>ADH2</strong>*2 protects against <b>dependence</b> severity in Jewish samples.
+ADH4	drug	alcohol	12351924	Future work in larger samples should address genetic and environmental factors that affect the relationship of <strong>ADH2</strong>*2 to <b>alcohol</b> consumption and dependence.
+ADH4	addiction	dependence	12351924	Future work in larger samples should address genetic and environmental factors that affect the relationship of <strong>ADH2</strong>*2 to alcohol consumption and <b>dependence</b>.
+ADH4	drug	alcohol	11900616	<b>Alcohol</b> dehydrogenase <strong>ADH2</strong> 1 and <strong>ADH2</strong> 2 allelic isoforms in the Russian population correlate with type of <b>alcoholic</b> disease.
+ADH4	drug	alcohol	11900616	The frequency <strong>ADH2</strong> 2 allele in the Moscow urban population and a correlation between the <strong>ADH2</strong> 2 allele, <b>alcoholic</b> dependence without cirrhosis, symptomatic <b>alcoholic</b> cirrhosis and status on hepatitis B and C infection have been studied.
+ADH4	addiction	dependence	11900616	The frequency <strong>ADH2</strong> 2 allele in the Moscow urban population and a correlation between the <strong>ADH2</strong> 2 allele, alcoholic <b>dependence</b> without cirrhosis, symptomatic alcoholic cirrhosis and status on hepatitis B and C infection have been studied.
+ADH4	drug	alcohol	11900616	There is a negative correlation between the <strong>ADH2</strong> 2 allele and <b>alcohol</b> misuse (both <b>alcoholic</b> dependence and <b>alcoholic</b> cirrhosis).
+ADH4	addiction	dependence	11900616	There is a negative correlation between the <strong>ADH2</strong> 2 allele and alcohol misuse (both alcoholic <b>dependence</b> and alcoholic cirrhosis).
+ADH4	drug	alcohol	11900616	In spite of the possession of the <strong>ADH2</strong> 2 allele (or genotype <strong>ADH2</strong> 1/2), <b>alcohol</b> misuse increases the risk of cirrhosis.
+ADH4	drug	alcohol	11900616	At the same time, positive status for active hepatitis B, C or combined infection B + C (replication markers HBV DNA or HCV RNA) increases the risk for symptomatic <b>alcoholic</b> cirrhosis in <b>alcohol</b> abusing patients, independently of <strong>ADH2</strong> genotype.
+ADH4	drug	alcohol	11584143	In view of this association and the known genetic influences on both <b>alcohol</b> pharmacokinetics and <b>alcohol</b> dependence, it is probable that part of the heritability of dependence is mediated by genes (other than the known <strong>ADH2</strong> and ADH3 polymorphisms) affecting <b>alcohol</b> metabolism.
+ADH4	addiction	dependence	11584143	In view of this association and the known genetic influences on both alcohol pharmacokinetics and alcohol <b>dependence</b>, it is probable that part of the heritability of <b>dependence</b> is mediated by genes (other than the known <strong>ADH2</strong> and ADH3 polymorphisms) affecting alcohol metabolism.
+ADH4	drug	alcohol	11545539	<strong>ADH2</strong> and <b>alcohol</b> related phenotypes in Ashkenazic Jewish American college students.
+ADH4	drug	alcohol	11545539	In Asians, variation in the <b>alcohol</b> dehydrogenase (<strong>ADH2</strong>) gene relates to <b>alcohol</b> dependence, <b>alcohol</b> consumption, and reported <b>alcohol</b> related symptoms, even after controlling for variation in the aldehyde dehydrogenase (ALDH2) gene.
+ADH4	addiction	dependence	11545539	In Asians, variation in the alcohol dehydrogenase (<strong>ADH2</strong>) gene relates to alcohol <b>dependence</b>, alcohol consumption, and reported alcohol related symptoms, even after controlling for variation in the aldehyde dehydrogenase (ALDH2) gene.
+ADH4	drug	alcohol	11545539	The association of <strong>ADH2</strong> polymorphisms with <b>alcohol</b> related behavior, however, has not been well characterized in non Asians.
+ADH4	drug	alcohol	11545539	<strong>ADH2</strong>*2, however, was not related to <b>alcohol</b> use disorders, <b>alcohol</b> induced flushing and associated symptoms, number of binge drinking episodes in the past 90 days, maximum number of drinks ever consumed, or self reported levels of response to <b>alcohol</b>.
+ADH4	addiction	intoxication	11545539	<strong>ADH2</strong>*2, however, was not related to alcohol use disorders, alcohol induced flushing and associated symptoms, number of <b>binge</b> drinking episodes in the past 90 days, maximum number of drinks ever consumed, or self reported levels of response to alcohol.
+ADH4	drug	alcohol	11545539	Results suggest that Ashkenazic Jewish Americans with <strong>ADH2</strong>*2 alleles drink less frequently, which might contribute, in part, to the overall lower rates of <b>alcoholism</b> in this population.
+ADH4	drug	alcohol	11315223	In men, effects of <b>alcohol</b> dehydrogenase <strong>ADH2</strong>*1/*2 genotype or high <b>alcohol</b> sensitivity (risk decreasing), and of history of childhood conduct disorder, or having monozygotic co twin or twin sister with AlcD (risk increasing) were significant and comparable in magnitude.
+ADH4	drug	alcohol	10630602	An <b>alcohol</b> dependent patient was identified to be ALDH2*2/*2, <strong>ADH2</strong>*2/*2, and ADH3*1/*2.
+ADH4	drug	alcohol	10630602	Logistic regression analysis of the combinatorial genotypes of <strong>ADH2</strong> and ALDH2 in 420 <b>alcohol</b> dependent and 689 nonalcohol dependent subjects indicated that risk for <b>alcoholism</b> was 100 fold lower for the <strong>ADH2</strong>*2/*2 ALDH2*2/*2 individuals than the <strong>ADH2</strong>*1/*1 ALDH2*1/*1 individuals.
+ADH4	drug	alcohol	10235293	The different genotypes at the genes encoding the enzymes involved in <b>alcohol</b> metabolism, class one <b>alcohol</b> dehydrogenase (<strong>ADH2</strong> and ADH3) and mitochondrial aldehyde dehydrogenase (ALDH2), have previously been shown to confer different predispositions to the development of <b>alcoholism</b> in Chinese Han males (Thomasson et al., 1991; Chen WJ et al., 1996; Chen CC et al., unpublished data).
+ADH4	drug	alcohol	10235293	Therefore, association studies of <b>alcoholism</b> in Chinese Han might be more sensitive if controlled for the genotypes of <strong>ADH2</strong>,ADH3, and ALDH2, when other loci, such as DRD2, are examined.
+ADH4	drug	alcohol	10235293	These tests included considering the high risk (<strong>ADH2</strong>*1/*1; *1/*2; ADH3*1/*2; *2/*2; and ALDH2*1/*1) and the low risk (<strong>ADH2</strong>*2/*2; ADH3*1/*1; and ALDH2*1/*2; *2/*2) groups of <b>alcoholics</b>, as well as nonalcoholic controls.
+ADH4	drug	alcohol	10235293	After stratification by the relevant genotypes of <strong>ADH2</strong>, ADH3, and ALDH2 no significant association exists between the genetic variants at the DRD2 locus and <b>alcoholism</b> in the Chinese Han population.
+ADH4	addiction	dependence	9802529	<strong>ADH2</strong> genotype had significant effects on both consumption and <b>dependence</b> in the men, but not in the women.
+ADH4	drug	alcohol	9509496	Men with an <strong>ADH2</strong> x 3 allele had significantly higher amplitude P3 components at placebo and also demonstrated more <b>alcohol</b> induced reductions in P3 amplitude than men with <strong>ADH2</strong> x 1 alleles only.
+ADH4	drug	alcohol	9373704	The purpose of this paper is to assemble and evaluate existing data on the effect of genetic variation in <strong>ADH2</strong> and ADH3 on the risk of <b>alcohol</b> dependence, and on the risk of <b>alcoholic</b> liver disease.
+ADH4	addiction	dependence	9373704	The purpose of this paper is to assemble and evaluate existing data on the effect of genetic variation in <strong>ADH2</strong> and ADH3 on the risk of alcohol <b>dependence</b>, and on the risk of alcoholic liver disease.
+ADH4	drug	alcohol	9373704	It is clear that possession of the <strong>ADH2</strong> 2 allele decreases the risk of <b>alcohol</b> dependence, but it increases the risk of <b>alcoholic</b> liver disease among <b>alcoholics</b>.
+ADH4	addiction	dependence	9373704	It is clear that possession of the <strong>ADH2</strong> 2 allele decreases the risk of alcohol <b>dependence</b>, but it increases the risk of alcoholic liver disease among alcoholics.
+ADH4	drug	alcohol	9373704	ADH3 variation also has significant effects on <b>alcohol</b> dependence, which may be due to linkage to <strong>ADH2</strong>; the ADH3 effect differs significantly between Asian and European subjects.
+ADH4	addiction	dependence	9373704	ADH3 variation also has significant effects on alcohol <b>dependence</b>, which may be due to linkage to <strong>ADH2</strong>; the ADH3 effect differs significantly between Asian and European subjects.
+ADH4	drug	alcohol	9066994	In this report we determined the genotypes for three genes, <strong>ADH2</strong>, ADH3, and ALDH2 among subjects with <b>alcohol</b> dependence (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ADH4	addiction	dependence	9066994	In this report we determined the genotypes for three genes, <strong>ADH2</strong>, ADH3, and ALDH2 among subjects with alcohol <b>dependence</b> (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ADH4	drug	alcohol	9066994	On an individual level, however, the genotypes controlling <b>alcohol</b> metabolism did not account for intragroup differences in vulnerability to <b>alcoholism</b> except in the case of <strong>ADH2</strong> for the Ami ethnic group.
+ADH4	drug	alcohol	8904964	The influences of estimated body water, recent drinking history, recent smoking history, polymorphism at the <strong>ADH2</strong> and ADH3 loci, family history of <b>alcoholism</b>, and percentage Native American heritage on <b>alcohol</b> elimination rate were determined using multiple regression analyses.
+ADH4	drug	nicotine	8904964	The influences of estimated body water, recent drinking history, recent <b>smoking</b> history, polymorphism at the <strong>ADH2</strong> and ADH3 loci, family history of alcoholism, and percentage Native American heritage on alcohol elimination rate were determined using multiple regression analyses.
+ADH4	drug	alcohol	8904964	There was also a nonsignificant trend for subjects with an <strong>ADH2</strong>*3 allele (n = 6) to have faster rates of <b>alcohol</b> elimination than those with <strong>ADH2</strong>*1 alleles only (n = 33).
+ADH4	drug	alcohol	8773821	<b>Alcohol</b> metabolising genes and <b>alcoholism</b> among Taiwanese Han men: independent effect of <strong>ADH2</strong>, ADH3 and ALDH2.
+ADH4	drug	alcohol	8773821	The association of ALDH2 and <strong>ADH2</strong> with the development of <b>alcoholism</b> was found to be independent of each other and has been replicated in different Asian populations, while the effect of ADH3 is less studied.
+ADH4	drug	alcohol	8773821	Multiple logistic regression was then applied to assess the contribution of ADH3 to <b>alcoholism</b> by controlling the effect of ALDH2 and <strong>ADH2</strong>.
+ADH4	drug	alcohol	8773821	The results of multivariate analyses demonstrated that the odds ratios for an increment of one allele of <strong>ADH2</strong>*1, ADH3*2 and ALDH2*1 in the development of <b>alcoholism</b> were 4.18, 3.82, and 6.89, respectively.
+ADH4	drug	alcohol	8651462	A comparison of the genotypes of ALDH2, <strong>ADH2</strong>, ADH3, and cytochrome P 4502E1 between <b>alcoholics</b> and nonalcoholics.
+ADH4	drug	alcohol	8651462	Our study revealed differences in the allelic frequencies of the ALDH2, <strong>ADH2</strong>, and ADH3 loci between <b>alcoholics</b> and nonalcoholics.
+ADH4	drug	alcohol	8651462	For <b>alcoholics</b> with both homozygous ALDH2*1/1 and heterozygous ALDH2*1/2 genotypes, it was found that <strong>ADH2</strong> and ADH3 played important rates.
+ADH4	drug	alcohol	8651462	<b>Alcoholics</b> with the heterozygous ALDH2*1/2 genotype showed a significantly higher frequency of <strong>ADH2</strong>*1/1 than ones with the homozygous ALDH2*1/1 genotype.
+ADH4	drug	alcohol	8651462	We assume <strong>ADH2</strong>*1 plays an important role in the development of <b>alcoholism</b> in <b>alcoholics</b> with the heterozygous ALDH2*1/2 genotype.
+ADH4	drug	alcohol	8591846	High incidence of <strong>ADH2</strong>*1/ALDH2*1 genes among Japanese <b>alcohol</b> dependents and patients with <b>alcoholic</b> liver disease.
+ADH4	drug	alcohol	8591846	Genetic polymorphism of <strong>ADH2</strong>/ALDH2 in 66 cases of normal subjects, 90 cases of <b>alcohol</b> dependent, and 31 patients with <b>alcoholic</b> liver disease among Japanese has been analyzed using a polymerase chain reaction assay followed by a direct sequencing method, because <b>ethanol</b> is mainly catabolized by ADH and ALDH and less by cytochrome P450IIE1 and catalase.
+ADH4	drug	alcohol	8591846	The incidence of both <strong>ADH2</strong>*1/*1 and ALDH2*1/*1 was significantly higher in patients with <b>alcohol</b> dependence and in patients with <b>alcoholic</b> liver disease when compared with that in control subjects.
+ADH4	addiction	dependence	8591846	The incidence of both <strong>ADH2</strong>*1/*1 and ALDH2*1/*1 was significantly higher in patients with alcohol <b>dependence</b> and in patients with alcoholic liver disease when compared with that in control subjects.
+ADH4	drug	alcohol	8591846	Genetic polymorphism of <strong>ADH2</strong>/ALDH2 in patients with <b>alcoholic</b> liver disease was not different from that of <b>alcohol</b> dependents.
+ADH4	drug	alcohol	8591846	According to these results, not only ALDH2 gene, often claimed to be responsible for <b>alcohol</b> dependence among Japanese, but also <strong>ADH2</strong> gene polymorphism, which modulates the metabolism of <b>ethanol</b>, play important roles in habitual <b>alcohol</b> intake behavior in Japanese patients and in some patients leads to <b>alcoholic</b> liver diseases.
+ADH4	addiction	dependence	8591846	According to these results, not only ALDH2 gene, often claimed to be responsible for alcohol <b>dependence</b> among Japanese, but also <strong>ADH2</strong> gene polymorphism, which modulates the metabolism of ethanol, play important roles in habitual alcohol intake behavior in Japanese patients and in some patients leads to alcoholic liver diseases.
+ADH4	drug	alcohol	7943668	Low frequency of the <strong>ADH2</strong>*2 allele among Atayal natives of Taiwan with <b>alcohol</b> use disorders.
+ADH4	drug	alcohol	7943668	Genetic variation at two polymorphic <b>alcohol</b> dehydrogenase loci, <strong>ADH2</strong> and ADH3, and at the polymorphic mitochondrial aldehyde dehydrogenase locus, ALDH2, may influence the risk of developing <b>alcoholism</b> by modulating the rate of elimination of <b>ethanol</b> and the rate of formation and elimination of acetaldehyde.
+ADH4	drug	alcohol	7943668	Among the Atayal, the group with <b>alcohol</b> use disorders (<b>alcohol</b> dependence and <b>alcohol</b> abuse) had a significantly lower frequency of the <strong>ADH2</strong>*2 allele (0.82) than those without <b>alcohol</b> use disorders (0.91).
+ADH4	addiction	dependence	7943668	Among the Atayal, the group with alcohol use disorders (alcohol <b>dependence</b> and alcohol abuse) had a significantly lower frequency of the <strong>ADH2</strong>*2 allele (0.82) than those without alcohol use disorders (0.91).
+ADH4	drug	alcohol	7943668	The <strong>ADH2</strong>*2 allele encodes the beta 2 subunit; isozymes containing beta 2 subunits oxidize <b>alcohol</b> faster in vitro than the beta 1 beta 1 isozyme encoded by <strong>ADH2</strong>*1.
+ADH4	drug	alcohol	3189338	Genetic polymorphisms of two major <b>alcohol</b> metabolizing enzymes i.e., one of the class I <b>alcohol</b> dehydrogenase isozymes (<strong>ADH2</strong>) and the mitochondrial aldehyde dehydrogenase (ALDH2) exist in Japanese and other Orientals but not in Caucasians.
+ADH4	drug	alcohol	3189338	We determined, by means of hybridization of genomic DNA samples with allele specific synthetic oligonucleotide probes, genotypes of the <strong>ADH2</strong> and the ALDH2 loci of Japanese with <b>alcoholic</b> liver diseases and of control subjects.
+ADH4	drug	alcohol	2940107	Starch gel electrophoresis of rat ocular tissues shows two anodic isoenzymes of <b>alcohol</b> dehydrogenase (ADH), designated as ADH 1 and <strong>ADH 2</strong>, ADH 1 is characteristic of the ocular tissues, and corresponds to more than 95% of all ADH activity in the eye.
+ADH4	drug	alcohol	6321953	Seven cis dominant mutations leading to the overproduction of the glucose repressible <b>alcohol</b> dehydrogenase isozyme ADHII (structural gene, <strong>ADH2</strong>) in Saccharomyces cerevisiae have previously been shown to be due to insertion of a transposable element, Ty, in the 5' regulatory region of the <strong>ADH2</strong> gene.
+S100A12	drug	opioid	31794788	The rest of the 5 brainstem tissues were then used to measure CCK, <strong>CGRP</strong>, and <b>opioid</b> peptide receptor (DORR) levels by western blotting(WB).
+S100A12	addiction	sensitization	31551772	TRPV1 contributes to peripheral <b>sensitization</b> and hyperalgesia, in part, via triggering the release of proinflammatory peptides, such as calcitonin gene related peptide (<strong>CGRP</strong>), both locally and at the dorsal horn of the spinal cord.
+S100A12	drug	opioid	31551772	Blocking TRPV1, but not <b>opioid</b> receptors, attenuated the onset of analgesia and capsaicin induced <strong>CGRP</strong> release.
+S100A12	drug	opioid	31010055	We evaluated the mechanical paw withdrawal threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) <b>opioid</b> receptor, brain derived neurotrophic factor (BDNF), Substance P, and calcitonin gene related peptide (<strong>CGRP</strong>) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real time quantitative polymerase chain reaction (RT PCR).
+S100A12	addiction	withdrawal	31010055	We evaluated the mechanical paw <b>withdrawal</b> threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) opioid receptor, brain derived neurotrophic factor (BDNF), Substance P, and calcitonin gene related peptide (<strong>CGRP</strong>) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real time quantitative polymerase chain reaction (RT PCR).
+S100A12	addiction	sensitization	30706780	On the basis of their anatomic location, transient receptor potential ion channels (TRPV1, TRPV2 and TRPM8), Piezo 2, acid sensing ion channels (ASICs), purinergic (P2X and P2Y), bradykinin (B1 and B2), α amino 3 hydroxy 5  methylisoxazole 4 propionate (AMPA), N methyl D aspartate (NMDA), metabotropic glutamate (mGlu), neurokinin 1 (NK1) and calcitonin gene related peptide (<strong>CGRP</strong>) receptors are activated during pain <b>sensitization</b>.
+S100A12	drug	cannabinoid	30342013	They include peptides targeting Ca2+, Na+ and K+ voltage gated ion channels, the neuronal nicotinic receptors (nAChR), transient receptor potential channels (TRP), and different non opioid G protein coupled receptors (GPCRs), like the calcitonin gen related peptide (<strong>CGRP</strong>), <b>cannabinoid</b>, bradykinin and neurotensin receptors, among others.
+S100A12	drug	opioid	30342013	They include peptides targeting Ca2+, Na+ and K+ voltage gated ion channels, the neuronal nicotinic receptors (nAChR), transient receptor potential channels (TRP), and different non <b>opioid</b> G protein coupled receptors (GPCRs), like the calcitonin gen related peptide (<strong>CGRP</strong>), cannabinoid, bradykinin and neurotensin receptors, among others.
+S100A12	drug	opioid	29148033	Given that growing evidence indicates that calcitonin gene related peptide (<strong>CGRP</strong>) plays a key role in the development of peripheral sensitization and is associated with enhanced pain, we hypothesized that <strong>CGRP</strong> 4218T/C polymorphism is associated with the variability in <b>fentanyl</b> consumption for post cesarean analgesia.
+S100A12	addiction	sensitization	29148033	Given that growing evidence indicates that calcitonin gene related peptide (<strong>CGRP</strong>) plays a key role in the development of peripheral <b>sensitization</b> and is associated with enhanced pain, we hypothesized that <strong>CGRP</strong> 4218T/C polymorphism is associated with the variability in fentanyl consumption for post cesarean analgesia.
+S100A12	drug	opioid	29148033	We examined the association of <strong>CGRP</strong> 4218T/C polymorphism and post operative <b>fentanyl</b> consumption for analgesia as well as adverse reactions to <b>fentanyl</b> in those patients who received cesarean section surgeries.
+S100A12	drug	opioid	29148033	We found that the <strong>CGRP</strong> 4218T/C polymorphism has a significant effect on pain perception, analgesic requirement, and nausea and vomiting for the first 24 h after cesarean delivery in patients who received PCEA <b>fentanyl</b>.
+S100A12	drug	cannabinoid	28492437	<b>Cannabinoid</b> receptors were expressed not only in IB4 (isolectin B4) and <strong>CGRP</strong> (calcitonin gene related peptide) dorsal root ganglion neurons, their central terminals, and peripheral axons, but also in neurons, microglia, and astrocytes in spinal cord.
+S100A12	drug	opioid	28049076	Both the orbitofrontal cortex and amygdala are involved in the processing of olfactory information, and olfactory deficits may be also influenced by endogenous <b>opioids</b> and calcitonin gene related peptide (<strong>CGRP</strong>), which is probably involved in dopaminergic transmission.
+S100A12	drug	opioid	26748051	At doses providing equal or greater antinociception than <b>morphine</b> in the rat, the analogs showed reduced a) respiratory depression, b) impairment of motor coordination, c) tolerance and hyperalgesia, d) glial p38/<strong>CGRP</strong>/P2X7 receptor signaling, and e) reward/abuse potential in both conditioned place preference and self administration tests.
+S100A12	addiction	reward	26748051	At doses providing equal or greater antinociception than morphine in the rat, the analogs showed reduced a) respiratory depression, b) impairment of motor coordination, c) tolerance and hyperalgesia, d) glial p38/<strong>CGRP</strong>/P2X7 receptor signaling, and e) <b>reward</b>/abuse potential in both conditioned place preference and self administration tests.
+S100A12	drug	opioid	24824948	RT PCR and Western blot analysis showed that NaHS significantly reversed the gene and protein expression of up regulated spinal calcitonin gene related peptide (<strong>CGRP</strong>) in <b>naloxone</b> treated animals.
+S100A12	drug	opioid	24824948	Our data suggest that H2S prevents the development of <b>opioid</b> withdrawal induced hyperalgesia via suppression of synthesis of <strong>CGRP</strong> in spine through inhibition of AC/cAMP and PKC/Raf 1/ERK pathways.
+S100A12	addiction	withdrawal	24824948	Our data suggest that H2S prevents the development of opioid <b>withdrawal</b> induced hyperalgesia via suppression of synthesis of <strong>CGRP</strong> in spine through inhibition of AC/cAMP and PKC/Raf 1/ERK pathways.
+S100A12	drug	opioid	23244430	The present review discusses the neurobiology of <b>opioid</b> withdrawal syndrome and its therapeutic target recptors like calcitonin gene related peptide receptors (<strong>CGRP</strong>), N methyl D aspartate (NMDA) receptors, gamma aminobutyric acid receptors (GABA), G proteingated inwardly rectifying potassium (GIRK) channels and calcium channels.
+S100A12	addiction	withdrawal	23244430	The present review discusses the neurobiology of opioid <b>withdrawal</b> syndrome and its therapeutic target recptors like calcitonin gene related peptide receptors (<strong>CGRP</strong>), N methyl D aspartate (NMDA) receptors, gamma aminobutyric acid receptors (GABA), G proteingated inwardly rectifying potassium (GIRK) channels and calcium channels.
+S100A12	drug	cannabinoid	21631400	The present review discusses these therapeutic targets including noradrenaline and 5 HT reuptake inhibitors; sodium, calcium and potassium channels; inhibitory and excitatory neurotransmitters; neuropeptides including bradykinin, tachykinin, cholecystokinin, neuropeptide Y, vasoactive intestinal peptide, and <strong>CGRP</strong>; pro inflammatory cytokines; MAP kinases; PPAR γ; Na(+)/Ca(2+) exchanger; nitric oxide; purinergic receptors; neuronal nicotinic receptors; cation dependent chloride transporters; oxidative stress; matrix metalloproteinase and plasminogen activators; growth factors; transient receptor potential (TRP) channels; <b>endocannabinoids</b>; histamine receptors; dopamine; sigma receptors, beta adrenergic receptors, endothelins, and D amino acid oxidase.
+S100A12	drug	opioid	21571003	Sustained <b>morphine</b> treatment has been shown to produce paradoxical pain sensitization (<b>opioid</b> induced hyperalgesia) and also causes increase in spinal pain neurotransmitter, such as calcitonin gene related peptide (<strong>CGRP</strong>), concentration in experimental animals.
+S100A12	addiction	sensitization	21571003	Sustained morphine treatment has been shown to produce paradoxical pain <b>sensitization</b> (opioid induced hyperalgesia) and also causes increase in spinal pain neurotransmitter, such as calcitonin gene related peptide (<strong>CGRP</strong>), concentration in experimental animals.
+S100A12	drug	opioid	21571003	We have previously shown that in cultured primary sensory dorsal root ganglion (DRG) neurons sustained in vitro <b>opioid</b> agonist treatment upregulates cAMP levels (adenylyl cyclase (AC) superactivation) and augments basal and capsaicin evoked <strong>CGRP</strong> release in a PKA dependent manner.
+S100A12	drug	opioid	21571003	pretreatment of rats with a PKA selective small interference RNA (siRNA) mixture significantly attenuates sustained <b>morphine</b> mediated augmentation of spinal <strong>CGRP</strong> immunoreactivity, thermal hyperalgesia, mechanical allodynia and antinociceptive tolerance.
+S100A12	drug	opioid	20970925	The present study examines the effects of intraplantar injection of the μ  and δ <b>opioid</b> receptor agonists, <b>morphine</b> and deltorphin, alone and in combination on behavioral tests of nociception in naïve rats and on potassium evoked release of <strong>CGRP</strong> from sciatic nerves of naïve rats.
+S100A12	drug	opioid	20970925	Similarly, concentration dependent inhibition of <strong>CGRP</strong> release was observed when deltorphin and <b>morphine</b> were administered in sequence prior to potassium stimulation.
+S100A12	drug	opioid	20826131	In the present work we investigated the hypothesis that <b>morphine</b> pretreatment also sensitizes ACs toward Gs protein coupled excitatory modulators (such as PGE₂), leading to augmented PKA dependent <strong>CGRP</strong> release from PGE₂ stimulated primary sensory dorsal root ganglion (DRG) neurons.
+S100A12	drug	opioid	20826131	Our results show that sustained <b>morphine</b> treatment potentiated PGE₂ mediated cAMP formation and augmented PGE₂ evoked <strong>CGRP</strong> release from cultured primary sensory neurons in a PKA dependent manner.
+S100A12	drug	opioid	20727859	Induction of viscerosomatic hypersensitivity resulted in an increased labeling of <strong>CGRP</strong> , but not substance P positive cells in the lumbar dorsal root ganglia; increased labeling was not affected by prior exposure to <b>morphine</b>.
+S100A12	drug	opioid	20718739	Long term <b>morphine</b> treatment enhances pain neurotransmitter [such as calcitonin gene related peptide (<strong>CGRP</strong>)] levels in the spinal cord.
+S100A12	drug	opioid	20718739	It has been suggested previously that increased spinal <strong>CGRP</strong> may contribute to sustained <b>morphine</b> mediated paradoxical pain sensitization and antinociceptive tolerance.
+S100A12	addiction	sensitization	20718739	It has been suggested previously that increased spinal <strong>CGRP</strong> may contribute to sustained morphine mediated paradoxical pain <b>sensitization</b> and antinociceptive tolerance.
+S100A12	drug	opioid	20718739	Previous in vitro studies from our group indicated that Raf 1 kinase mediated adenylyl cyclase superactivation played a crucial role in sustained <b>morphine</b> mediated augmentation of basal and evoked <strong>CGRP</strong> release from cultured primary sensory neurons.
+S100A12	drug	opioid	20718739	Selective knockdown of spinal Raf 1 protein levels by i.th Raf 1 selective siRNA pretreatment significantly attenuated sustained <b>morphine</b> mediated up regulation of <strong>CGRP</strong> immunoreactivity in the spinal cord of rats and prevented the development of thermal hyperalgesia, mechanical allodynia and antinociceptive tolerance.
+S100A12	drug	opioid	20659434	Involvement of <b>opioid</b> receptors in the <strong>CGRP</strong> induced antinociception in the nucleus accumbens of rats.
+S100A12	drug	opioid	20659434	The present study is performed to explore the possible involvement of <b>opioid</b> receptors in the <strong>CGRP</strong> induced antinociception in the NAc of rats.
+S100A12	addiction	withdrawal	20659434	Intra NAc administration of <strong>CGRP</strong> induces significant increases in the hindpaw <b>withdrawal</b> latency (HWL) to noxious thermal and mechanical stimulation in rats.
+S100A12	drug	opioid	20659434	Interestingly, the <strong>CGRP</strong> induced antinociceptive effects are inhibited by following intra NAc injection of the <b>opioid</b> receptor antagonist <b>naloxone</b>, suggesting that the <b>opioid</b> receptors are involved in the <strong>CGRP</strong> induced antinociception in the NAc of rats.
+S100A12	drug	opioid	20659434	Furthermore, the <strong>CGRP</strong> induced antinociception is attenuated by intra NAc injection of mu <b>opioid</b> receptor (MOR) antagonist beta funaltrexamine (beta FNA) and kappa <b>opioid</b> receptor (KOR) antagonist nor binaltorphimine (nor BNI), but not by delta receptor (DOR) antagonist naltrindole.
+S100A12	drug	opioid	20659434	In the present study, we also demonstrated that there was no significant difference between the <strong>CGRP</strong> induced antinociception and the <b>morphine</b> induced antinociception in the NAc in rats.
+S100A12	drug	opioid	20659434	The results of the present study demonstrate that both mu  and kappa <b>opioid</b> receptors are involved in the <strong>CGRP</strong> induced antinociception in the NAc of rats.
+S100A12	drug	opioid	20359526	Several groups maintain that <b>morphine</b> tolerance and dependence correlate with increased activity of protein kinases ERK1/2 and P38 MAPK and PKC as well as elevated levels of the neuropeptides dynorphin (DYN), substance P (sP), and calcitonin gene related peptide (<strong>CGRP</strong>) in spinal cord dorsal horn (SCDH).
+S100A12	addiction	dependence	20359526	Several groups maintain that morphine tolerance and <b>dependence</b> correlate with increased activity of protein kinases ERK1/2 and P38 MAPK and PKC as well as elevated levels of the neuropeptides dynorphin (DYN), substance P (sP), and calcitonin gene related peptide (<strong>CGRP</strong>) in spinal cord dorsal horn (SCDH).
+S100A12	drug	opioid	20359526	In contrast, while <b>morphine</b> increased spinal DYN and <strong>CGRP</strong> in WT mice, DYN remained unchanged and <strong>CGRP</strong> was reduced in GluR5 KO mice.
+S100A12	drug	opioid	20359526	These observations suggest that spinal ERK2, P38 and PKCgamma are likely involved in multiple adaptive responses following systemic <b>morphine</b> administration, whereas DYN and <strong>CGRP</strong> may contribute selectively to the development of antinociceptive tolerance.
+S100A12	drug	opioid	19491327	It was shown previously (J Neurosci 22:6747 6755, 2002) that sustained <b>morphine</b> exposure augments pain neurotransmitter [such as calcitonin gene related peptide (<strong>CGRP</strong>)] release in the dorsal horn of the spinal cord in response to the heat sensing transient receptor potential vanilloid 1 receptor agonist 8 methyl N vanillyl 6 nonenamide (capsaicin).
+S100A12	drug	opioid	19491327	In the present study, we demonstrate that sustained <b>morphine</b> mediated augmentation of <strong>CGRP</strong> release from isolated primary sensory dorsal root ganglion neurons is dependent on protein kinase A and Raf 1 kinase.
+S100A12	drug	cannabinoid	19387418	Sustained <b>cannabinoid</b> agonist treatment augments <strong>CGRP</strong> release in a PKA dependent manner.
+S100A12	addiction	sensitization	19387418	It has been suggested that augmented release of pain neurotransmitters (such as calcitonin gene related peptide, <strong>CGRP</strong>) might be responsible for this abnormal pain <b>sensitization</b>.
+S100A12	drug	cannabinoid	19387418	We hypothesize that intracellular adaptations upon sustained <b>cannabinoid</b> treatment causes augmented release of <strong>CGRP</strong> from primary nociceptors leading to increased pain sensitivity.
+S100A12	drug	cannabinoid	19387418	We show that sustained (24 h) <b>cannabinoid</b> agonist [(+)WIN 55,212 2] treatment of 7 day old neonatal rat dorsal root ganglion neurons significantly augments basal <strong>CGRP</strong> release from these cells in a protein kinase A dependent manner.
+S100A12	drug	opioid	18976650	Enhanced excitatory pain neurotransmitter (such as calcitonin gene related peptide (<strong>CGRP</strong>)) release in the dorsal horn of the spinal cord may play a role in sustained <b>morphine</b> mediated paradoxical pain.
+S100A12	drug	opioid	18976650	Recently we have demonstrated that inhibition of Raf 1 attenuates sustained <b>morphine</b> treatment mediated augmentation of <strong>CGRP</strong> release in vitro, in cultured primary sensory neurons.
+S100A12	drug	opioid	18328477	Sustained <b>morphine</b> treatment augments basal <strong>CGRP</strong> release from cultured primary sensory neurons in a Raf 1 dependent manner.
+S100A12	drug	opioid	18328477	The intracellular signal transduction pathways involved in sustained <b>opioid</b> mediated augmentation of spinal pain neurotransmitter (such as calcitonin gene related peptide (<strong>CGRP</strong>)) release are not fully clarified.
+S100A12	drug	opioid	18328477	Therefore, in the present study we examined the role of Raf 1 in sustained <b>morphine</b> mediated regulation of cAMP formation and basal <strong>CGRP</strong> release in vitro, in cultured neonatal rat dorsal root ganglion (DRG) neurons.
+S100A12	drug	opioid	18328477	We found that sustained <b>morphine</b> treatment significantly augments intracellular cAMP production as well as basal <strong>CGRP</strong> release from cultured neonatal rat DRG neurons.
+S100A12	drug	opioid	18328477	The selective PKA inhibitor, H 89, attenuates the sustained <b>morphine</b> mediated augmentation of basal <strong>CGRP</strong> release, indicating that the cAMP/PKA pathway plays an important role in regulation of <strong>CGRP</strong> release from sensory neurons.
+S100A12	drug	opioid	18328477	Since our present data also demonstrated that selective Raf 1 inhibitor, GW 5074, attenuated both the cAMP overshoot and the augmentation of <strong>CGRP</strong> release mediated by sustained <b>morphine</b> in neonatal rat DRG neurons, we suggest that Raf 1 mediated sensitization of the intracellular cAMP formation may play an important role in sustained <b>morphine</b> mediated augmentation of spinal pain neurotransmitter release.
+S100A12	addiction	sensitization	18328477	Since our present data also demonstrated that selective Raf 1 inhibitor, GW 5074, attenuated both the cAMP overshoot and the augmentation of <strong>CGRP</strong> release mediated by sustained morphine in neonatal rat DRG neurons, we suggest that Raf 1 mediated <b>sensitization</b> of the intracellular cAMP formation may play an important role in sustained morphine mediated augmentation of spinal pain neurotransmitter release.
+S100A12	addiction	sensitization	17693023	As the anti NGF antibody does not appreciably cross the blood brain barrier, the present data suggest that the anti hyperalgesic action of anti NGF therapy results from blockade of activation and/or <b>sensitization</b> of the <strong>CGRP</strong>/trkA positive fibers that normally constitute the majority of sensory fibers that innervate the bone.
+S100A12	drug	opioid	17498818	The chronic administration of butoxamine with <b>morphine</b> reduced or eliminated the normally observed up regulation of <strong>CGRP</strong> and SP in spinal cord and DRG tissues.
+S100A12	drug	opioid	17395382	Sustained exposure to <b>opioid</b> agonists such as <b>morphine</b> increases levels of calcitonin gene related peptide (<strong>CGRP</strong>) in the spinal dorsal horn, a response implicated in the development of <b>opioid</b> tolerance and physical dependence.
+S100A12	addiction	dependence	17395382	Sustained exposure to opioid agonists such as morphine increases levels of calcitonin gene related peptide (<strong>CGRP</strong>) in the spinal dorsal horn, a response implicated in the development of opioid tolerance and physical <b>dependence</b>.
+S100A12	drug	cannabinoid	17395382	Recent evidence suggests that both the opioid induced increase in <strong>CGRP</strong> and the development of opioid physical dependence are suppressed by blockade of spinal <b>cannabinoid</b> (CB1) receptors.
+S100A12	drug	opioid	17395382	Recent evidence suggests that both the <b>opioid</b> induced increase in <strong>CGRP</strong> and the development of <b>opioid</b> physical dependence are suppressed by blockade of spinal cannabinoid (CB1) receptors.
+S100A12	addiction	dependence	17395382	Recent evidence suggests that both the opioid induced increase in <strong>CGRP</strong> and the development of opioid physical <b>dependence</b> are suppressed by blockade of spinal cannabinoid (CB1) receptors.
+S100A12	drug	opioid	17395382	In another set of experiments, chronic administration of spinal <b>morphine</b> (15 microg) once daily for 5 days produced a similar loss of analgesic effect and a marked increase in <strong>CGRP</strong> immunoreactivity in the superficial laminae of the dorsal horn.
+S100A12	drug	opioid	17395382	Consistent with the in vivo findings, primary cultures of adult dorsal root ganglion (DRG) neurons exposed to <b>morphine</b> for 5 days showed a significant increase in the number of <strong>CGRP</strong> immunoreactive neurons.
+S100A12	drug	opioid	17395382	Co administration with AM 251 attenuated the <b>morphine</b> induced increase in <strong>CGRP</strong> immunoreactivity in the spinal cord and in DRG cultured neurons.
+S100A12	drug	cannabinoid	17395382	Collectively, the results of this study suggest that activity of <b>endocannabinoids</b>, mediated via CB1 receptors, contributes to both the development and maintenance of opioid tolerance by influencing the opioid induced increase in spinal <strong>CGRP</strong>.
+S100A12	drug	opioid	17395382	Collectively, the results of this study suggest that activity of endocannabinoids, mediated via CB1 receptors, contributes to both the development and maintenance of <b>opioid</b> tolerance by influencing the <b>opioid</b> induced increase in spinal <strong>CGRP</strong>.
+S100A12	drug	opioid	16935424	Previous evidence suggests that spinal release of calcitonin gene related peptide (<strong>CGRP</strong>) and activation of its receptors contribute to <b>opioid</b> physical dependence.
+S100A12	addiction	dependence	16935424	Previous evidence suggests that spinal release of calcitonin gene related peptide (<strong>CGRP</strong>) and activation of its receptors contribute to opioid physical <b>dependence</b>.
+S100A12	drug	cannabinoid	16935424	The release of <strong>CGRP</strong> at the spinal level is modulated by <b>cannabinoid</b> (CB1) receptors.
+S100A12	drug	opioid	16935424	Thus, this study examined whether CB1 receptor activity mediates changes in <strong>CGRP</strong> underlying development of <b>opioid</b> physical dependence.
+S100A12	addiction	dependence	16935424	Thus, this study examined whether CB1 receptor activity mediates changes in <strong>CGRP</strong> underlying development of opioid physical <b>dependence</b>.
+S100A12	drug	opioid	16935424	Systemic <b>morphine</b> administration for 5 days elevated <strong>CGRP</strong> immunoreactivity in the rat spinal dorsal horn.
+S100A12	drug	opioid	16935424	In situ hybridization of dorsal root ganglion (DRG) neurons revealed an increase in <strong>CGRP</strong> mRNA during initial (day 1 3) but not later phase (day 4 5) of <b>morphine</b> treatment.
+S100A12	drug	opioid	16935424	<strong>CGRP</strong> immunoreactivity in DRG neurons, however, was increased in the later phase of <b>morphine</b> treatment.
+S100A12	drug	opioid	16935424	<b>Naloxone</b> challenge to <b>morphine</b> treated animals precipitated an intense withdrawal syndrome that depleted <strong>CGRP</strong> immunoreactivity and increased Fos expression in the dorsal horn.
+S100A12	addiction	withdrawal	16935424	Naloxone challenge to morphine treated animals precipitated an intense <b>withdrawal</b> syndrome that depleted <strong>CGRP</strong> immunoreactivity and increased Fos expression in the dorsal horn.
+S100A12	addiction	withdrawal	16935424	The Fos response primarily occurred in neurons that expressed <strong>CGRP</strong> receptor component protein (RCP) suggesting <strong>CGRP</strong> activity contributes to neuronal activation during precipitated <b>withdrawal</b>.
+S100A12	drug	opioid	16935424	Spinal slices obtained from <b>morphine</b> treated animals showed higher levels of <strong>CGRP</strong> release than from saline controls.
+S100A12	drug	cannabinoid	16935424	Altogether, this study suggests that <b>endocannabinoid</b> activity, expressed via CB1 receptors, contributes to the induction of opioid physical dependence through spinal modulation of <strong>CGRP</strong>.
+S100A12	drug	opioid	16935424	Altogether, this study suggests that endocannabinoid activity, expressed via CB1 receptors, contributes to the induction of <b>opioid</b> physical dependence through spinal modulation of <strong>CGRP</strong>.
+S100A12	addiction	dependence	16935424	Altogether, this study suggests that endocannabinoid activity, expressed via CB1 receptors, contributes to the induction of opioid physical <b>dependence</b> through spinal modulation of <strong>CGRP</strong>.
+S100A12	drug	opioid	16215302	A non inclusive list of examples of substances reported to block or reverse <b>opioid</b> antinociceptive tolerance include: substance P receptor (NK 1) antagonists, calcitonin gene related peptide (<strong>CGRP</strong>) receptor antagonists, nitric oxide (NO) synthase inhibitors, calcium channel blockers, cyclooxygenase (COX) inhibitors, protein kinase C inhibitors, competitive and non competitive antagonists of the NMDA (N methyl D aspartate) receptor, AMPA (alpha amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid) antagonists, anti dynorphin antiserum, and cholecystokinin (CCK) receptor antagonists.
+S100A12	drug	cannabinoid	16042975	The mechanisms underlying tolerance dependence are not entirely clear, however, recent evidence suggests that spinal adaptations leading to increased activity of sensory neuropeptides (calcitonin gene related peptide (<strong>CGRP</strong>), substance P) and their downstream signaling messengers derived from metabolism of arachidonic acid: prostaglandins (PG), lipoxygenase (LOX) metabolites, and <b>endocannabinoids</b>, plays an important role in this phenomenon.
+S100A12	addiction	dependence	16042975	The mechanisms underlying tolerance <b>dependence</b> are not entirely clear, however, recent evidence suggests that spinal adaptations leading to increased activity of sensory neuropeptides (calcitonin gene related peptide (<strong>CGRP</strong>), substance P) and their downstream signaling messengers derived from metabolism of arachidonic acid: prostaglandins (PG), lipoxygenase (LOX) metabolites, and endocannabinoids, plays an important role in this phenomenon.
+S100A12	addiction	sensitization	15836976	Mechanistically, the great majority of sensory fibers that innervate the bone are <strong>CGRP</strong>/TrkA expressing fibers, and if the <b>sensitization</b> and activation of these fibers is blocked by anti NGF therapy there would not be another population of nociceptors, such as the non peptidergic IB4/RET IR nerve fibers, to take their place in signaling nociceptive events.
+S100A12	drug	opioid	14598307	The present study was undertaken to investigate the plasticity of calcitonin gene related peptide (<strong>CGRP</strong>) in antinociception after <b>morphine</b> tolerance in rats.
+S100A12	drug	opioid	14598307	The hindpaw withdrawal latencies (HWLs) to both thermal and mechanical stimulation increased significantly after intracerebroventricular injection of 2.5 nmol of <strong>CGRP</strong> in <b>opioid</b> naive rats, indicating that <strong>CGRP</strong> produces an antinociceptive effect in the brain.
+S100A12	addiction	withdrawal	14598307	The hindpaw <b>withdrawal</b> latencies (HWLs) to both thermal and mechanical stimulation increased significantly after intracerebroventricular injection of 2.5 nmol of <strong>CGRP</strong> in opioid naive rats, indicating that <strong>CGRP</strong> produces an antinociceptive effect in the brain.
+S100A12	drug	opioid	14598307	Furthermore, there was an antinociceptive effect after intracerebroventricular injection of 2.5 nmol of <strong>CGRP</strong> in <b>morphine</b> tolerant rats.
+S100A12	drug	opioid	14598307	Interestingly, the antinociceptive effect induced by intracerebroventricular injection of <strong>CGRP</strong> was lower in <b>morphine</b> tolerant rats than that in <b>opioid</b> naive rats at the same dose.
+S100A12	drug	opioid	14598307	At the same time, there was downregulation of <strong>CGRP</strong> like immunoreactivity in both lateral septal nucleus and central nucleus of amygdala tested by immunohistochemical methods, whereas no significant changes were observed in arcuate nucleus of hypothalamus and periaqueductal gray after <b>morphine</b> treatment in rats.
+S100A12	drug	opioid	14598307	The present study demonstrates plastic changes in both <strong>CGRP</strong> induced antinociception and <strong>CGRP</strong> like immunoreactivity in rat brain after <b>morphine</b> tolerance, suggesting that <strong>CGRP</strong> may play an important role in <b>morphine</b> tolerance.
+S100A12	drug	opioid	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of <b>opioid</b> physical dependence using behavioural assessment of withdrawal and immunostaining for <strong>CGRP</strong> and Fos protein expression in the spinal cord.
+S100A12	addiction	dependence	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of opioid physical <b>dependence</b> using behavioural assessment of withdrawal and immunostaining for <strong>CGRP</strong> and Fos protein expression in the spinal cord.
+S100A12	addiction	withdrawal	12970109	This study investigated the role of spinal lipoxygenase (LOX) products in the induction and expression of opioid physical dependence using behavioural assessment of <b>withdrawal</b> and immunostaining for <strong>CGRP</strong> and Fos protein expression in the spinal cord.
+S100A12	drug	opioid	12970109	of <b>morphine</b> for 5 days markedly elevated <strong>CGRP</strong> like immunoreactivity in the dorsal horn of the rat spinal cord.
+S100A12	addiction	withdrawal	12970109	challenge precipitated a robust <b>withdrawal</b> syndrome that depleted <strong>CGRP</strong> like immunoreactivity and increased the number of Fos like immunoreactive neurons in the dorsal horn.
+S100A12	drug	opioid	12970109	Intrathecal administration of NDGA (10, 20 microg), a nonselective LOX inhibitor, AA 861 (1.5, 3 microg), a 5 LOX selective inhibitor, or baicalein (1.4, 2.8 microg), a 12 LOX selective inhibitor, concurrently with systemic <b>morphine</b> for 5 days or as a single injection immediately preceding <b>naloxone</b> challenge, blocked the depletion of <strong>CGRP</strong> like immunoreactivity, prevented increase in the number of Fos like immunoreactive neurons in the dorsal horn, and significantly attenuated the <b>morphine</b> withdrawal syndrome.
+S100A12	addiction	withdrawal	12970109	Intrathecal administration of NDGA (10, 20 microg), a nonselective LOX inhibitor, AA 861 (1.5, 3 microg), a 5 LOX selective inhibitor, or baicalein (1.4, 2.8 microg), a 12 LOX selective inhibitor, concurrently with systemic morphine for 5 days or as a single injection immediately preceding naloxone challenge, blocked the depletion of <strong>CGRP</strong> like immunoreactivity, prevented increase in the number of Fos like immunoreactive neurons in the dorsal horn, and significantly attenuated the morphine <b>withdrawal</b> syndrome.
+S100A12	addiction	withdrawal	12732246	Intra CeA injection of <strong>CGRP</strong> induced dose dependent increases in the hind paw <b>withdrawal</b> latency tested by hotplate test and Randall Selitto Test, indicating an antinociceptive effect of <strong>CGRP</strong> in CeA.
+S100A12	drug	opioid	12732246	The <strong>CGRP</strong> induced antinociception was attenuated by s.c. injection of the <b>opioid</b> antagonist <b>naloxone</b>, suggesting an involvement of endogenous <b>opioid</b> systems in <strong>CGRP</strong> induced antinociception.
+S100A12	drug	opioid	12732246	Moreover, it was demonstrated that <b>opioid</b> receptors in the periaqueductal gray, but not in CeA, contributed to the <strong>CGRP</strong> induced antinociception, indicating the importance of the pathway between CeA and the periaqueductal gray in <strong>CGRP</strong> induced antinociception.
+S100A12	drug	opioid	11976266	This study examined the role of spinal calcitonin gene related peptide (<strong>CGRP</strong>), substance P, and prostaglandins in the development and expression of <b>opioid</b> physical dependence.
+S100A12	addiction	dependence	11976266	This study examined the role of spinal calcitonin gene related peptide (<strong>CGRP</strong>), substance P, and prostaglandins in the development and expression of opioid physical <b>dependence</b>.
+S100A12	drug	opioid	11976266	of <b>morphine</b> for 7 days markedly elevated <strong>CGRP</strong> and substance P  immunoreactivity in the dorsal horn of the rat spinal cord.
+S100A12	addiction	withdrawal	11976266	challenge decreased both <strong>CGRP</strong> and substance P immunoreactivity and precipitated a robust <b>withdrawal</b> syndrome.
+S100A12	drug	opioid	11976266	Acute intrathecal pre treatment with a <strong>CGRP</strong> receptor antagonist, <strong>CGRP</strong>(8   37) (4, 8 microg), a substance P receptor antagonist, SR 140333 (1.4, 2.8 microg), a cyclo oxygenase (COX) inhibitor, ketorolac (30, 45 microg), and COX 2 selective inhibitors, DuP 697 (10, 30 microg) and nimesulide (30 microg), 30 min before <b>naloxone</b> challenge, partially attenuated the symptoms of <b>morphine</b> withdrawal.
+S100A12	addiction	withdrawal	11976266	Acute intrathecal pre treatment with a <strong>CGRP</strong> receptor antagonist, <strong>CGRP</strong>(8   37) (4, 8 microg), a substance P receptor antagonist, SR 140333 (1.4, 2.8 microg), a cyclo oxygenase (COX) inhibitor, ketorolac (30, 45 microg), and COX 2 selective inhibitors, DuP 697 (10, 30 microg) and nimesulide (30 microg), 30 min before naloxone challenge, partially attenuated the symptoms of morphine <b>withdrawal</b>.
+S100A12	drug	opioid	11976266	Chronic intrathecal treatment with <strong>CGRP</strong>(8   37) (4, 8 microg), SR 140333 (1.4 microg), ketorolac (15, 30 microg), DuP 697 (10, 30micro g), and nimesulide (30 microg), delivered with daily <b>morphine</b> injection significantly attenuated both the symptoms of withdrawal and the decrease in <strong>CGRP</strong> but not substance P immunoreactivity.
+S100A12	addiction	withdrawal	11976266	Chronic intrathecal treatment with <strong>CGRP</strong>(8   37) (4, 8 microg), SR 140333 (1.4 microg), ketorolac (15, 30 microg), DuP 697 (10, 30micro g), and nimesulide (30 microg), delivered with daily morphine injection significantly attenuated both the symptoms of <b>withdrawal</b> and the decrease in <strong>CGRP</strong> but not substance P immunoreactivity.
+S100A12	drug	opioid	11976266	The results of this study suggest that activation of <strong>CGRP</strong> and substance P receptors, at the spinal level, contributes to the induction and expression of <b>opioid</b> physical dependence and that this activity may be partially expressed through the intermediary actions of prostaglandins.
+S100A12	addiction	dependence	11976266	The results of this study suggest that activation of <strong>CGRP</strong> and substance P receptors, at the spinal level, contributes to the induction and expression of opioid physical <b>dependence</b> and that this activity may be partially expressed through the intermediary actions of prostaglandins.
+S100A12	drug	opioid	11454653	<b>Morphine</b> had no effect on <strong>CGRP</strong> evoked dural vasodilation.
+S100A12	drug	opioid	11454653	<b>Morphine</b> (3 mg kg( 1)) also inhibited the TNC neuronal sensitization following <strong>CGRP</strong> evoked dilation.
+S100A12	addiction	sensitization	11454653	Morphine (3 mg kg( 1)) also inhibited the TNC neuronal <b>sensitization</b> following <strong>CGRP</strong> evoked dilation.
+S100A12	drug	opioid	11353815	In contrast, the mu <b>opioid</b> agonist <b>fentanyl</b> elicited a 74 +/  4% reduction in <strong>CGRP</strong> levels.
+S100A12	addiction	dependence	11353815	Taken together, the present data confirm the PKA <b>dependence</b> of forskolin stimulated <strong>CGRP</strong> release and suggest that A(1) adenosine agonists may warrant further investigation in models of migraine and neurogenic inflammation.
+S100A12	drug	alcohol	11281986	Calcitonin gene related peptide (<strong>CGRP</strong>) levels and <b>alcohol</b>.
+S100A12	drug	alcohol	11281986	Since <b>alcohol</b> consumption may be related to <b>alcohol</b>'s anxiolytic properties, the present study sought to determine if brain <strong>CGRP</strong> levels were correlated with genetic differences in preference for drinking <b>alcohol</b> and/or affected by <b>alcohol</b> exposure/withdrawal.
+S100A12	addiction	withdrawal	11281986	Since alcohol consumption may be related to alcohol's anxiolytic properties, the present study sought to determine if brain <strong>CGRP</strong> levels were correlated with genetic differences in preference for drinking alcohol and/or affected by alcohol exposure/<b>withdrawal</b>.
+S100A12	drug	alcohol	11281986	In the first experiment, <strong>CGRP</strong> LI was compared in <b>alcohol</b> naive rats [preferring (P) and non preferring (NP)], lower concentrations were found in the hippocampus (U = 153.5; d.f.
+S100A12	drug	alcohol	11281986	However, at 4 wk following <b>ethanol</b> withdrawal, higher concentrations of <strong>CGRP</strong> LI were found in the hippocampus (U = 26.5; d.f.
+S100A12	addiction	withdrawal	11281986	However, at 4 wk following ethanol <b>withdrawal</b>, higher concentrations of <strong>CGRP</strong> LI were found in the hippocampus (U = 26.5; d.f.
+S100A12	drug	alcohol	11281986	These studies suggest that <strong>CGRP</strong> may modulate <b>alcohol</b> preference and additionally, that exposure/withdrawal from <b>ethanol</b> produces long lasting effects on <strong>CGRP</strong> LI.
+S100A12	addiction	withdrawal	11281986	These studies suggest that <strong>CGRP</strong> may modulate alcohol preference and additionally, that exposure/<b>withdrawal</b> from ethanol produces long lasting effects on <strong>CGRP</strong> LI.
+S100A12	addiction	dependence	11276224	Altered neuroadaptation in opiate <b>dependence</b> and neurogenic inflammatory nociception in alpha <strong>CGRP</strong> deficient mice.
+S100A12	drug	opioid	11276224	Furthermore, alpha <strong>CGRP</strong>( / ) mice do not show changes in <b>heroin</b> self administration or <b>morphine</b> tolerance, but display a marked decrease in <b>morphine</b> withdrawal signs, suggesting an important contribution of alpha <strong>CGRP</strong> to opiate withdrawal.
+S100A12	addiction	withdrawal	11276224	Furthermore, alpha <strong>CGRP</strong>( / ) mice do not show changes in heroin self administration or morphine tolerance, but display a marked decrease in morphine <b>withdrawal</b> signs, suggesting an important contribution of alpha <strong>CGRP</strong> to opiate <b>withdrawal</b>.
+S100A12	drug	alcohol	11208722	Exposure of <b>ethanol</b> after 1 mol/L NaCl increased intragastric <strong>CGRP</strong> levels from 166 +/  27 to 713 +/  55 pg/2 min (n = 4, P < 0.05), and the protective action of 1 mol/L NaCl was inhibited by indomethacin treatment.
+S100A12	drug	alcohol	11208722	Intragastric perfusion of 50% <b>ethanol</b> after administration of PGI(2), but not of PGE(2), increased <strong>CGRP</strong> levels.
+S100A12	drug	alcohol	11208722	<strong>CGRP</strong> level during <b>ethanol</b> perfusion was not increased in IP( / ) but was increased in EP3( / ) and wild type counterparts after preperfusion of 1 mol/L NaCl.
+S100A12	drug	opioid	10915810	The present study investigated the role of calcitonin gene related peptide (<strong>CGRP</strong>) on nociception in nucleus raphe magnus (NRM) and the interaction between <strong>CGRP</strong> and <b>opioid</b> peptides in NRM of rats.
+S100A12	addiction	withdrawal	10915810	The hindpaw <b>withdrawal</b> latency (HWL) to thermal and mechanical stimulation increased significantly after intra NRM administration of 0.5 or 1 nmol of <strong>CGRP</strong> in rats, but not 0.25 nmol.
+S100A12	drug	opioid	10915810	Furthermore, the <strong>CGRP</strong> induced anti nociceptive effect was attenuated by following intra NRM administration of 6 nmol of <b>naloxone</b>.
+S100A12	drug	opioid	10915810	The results indicate that <strong>CGRP</strong> and its receptors play an important role in anti nociception, and there is a possible interaction between <strong>CGRP</strong> and <b>opioid</b> peptides in NRM of rats.
+S100A12	addiction	withdrawal	9574827	Intrathecal <strong>CGRP</strong>(8 37) results in a bilateral increase in hindpaw <b>withdrawal</b> latency in rats with a unilateral thermal injury.
+S100A12	addiction	withdrawal	9574827	The present study was performed to explore the effects of intrathecal administration of calcitonin gene related peptide8 37 (<strong>CGRP</strong>(8 37)) on the hindpaw <b>withdrawal</b> latency (HWL) to pressure in rats with one thermally injured hindpaw.
+S100A12	drug	opioid	9574827	Furthermore, the interaction of <strong>CGRP</strong>(8 37)and <b>naloxone</b> was studied.
+S100A12	drug	opioid	9574827	The effect of <strong>CGRP</strong>(8 37) was partly reversed by intrathecal injection of <b>naloxone</b> at a dose of 32 and 64 microg respectively.
+S100A12	drug	opioid	9574827	Furthermore, our findings suggest that <b>opioids</b> can modulate <strong>CGRP</strong> related effects in the spinal cord.
+S100A12	addiction	withdrawal	8825341	Recent work in our laboratory has demonstrated that intrathecal administration of a selective antagonist of calcitonin gene related peptide (<strong>CGRP</strong>), CGRP8 37, increased the hindpaw <b>withdrawal</b> latency (HWL) to thermal stimulation and hindpaw <b>withdrawal</b> threshold (HWT) to pressure in normal rats, and that these effects were more pronounced than in rats with mononeuropathy.
+S100A12	drug	opioid	8825341	Furthermore, our findings suggest that <b>opioids</b> can modulate <strong>CGRP</strong> related effects in the spinal cord.
+S100A12	addiction	withdrawal	8581488	We recently demonstrated that intrathecal administration of calcitonin gene related peptide 8 37 (CGRP8 37), a selective antagonist of calcitonin gene related peptide receptors, dose dependently increased the latency to hindpaw <b>withdrawal</b> responses induced by both thermal and mechanical stimulation in intact rats, indicating a role for <strong>CGRP</strong> and its receptors in the transmission of presumed nociceptive information in the spinal cord.
+S100A12	drug	opioid	8581488	The present study was performed to explore the interaction between <strong>CGRP</strong> and <b>opioids</b> in the spinal cord of rats.
+S100A12	drug	opioid	8581488	These results indicate that mu and delta, but not kappa, <b>opioid</b> receptors are involved in the modulation of post synaptic effects and/or release of <strong>CGRP</strong> and other neurotransmitters.
+S100A12	drug	opioid	8545480	The aim of this study was to investigate the possible interaction of <strong>CGRP</strong> with <b>morphine</b> on nociception in adult male NMRI mice after central administration of the peptide.
+S100A12	drug	opioid	8545480	<strong>CGRP</strong> (20 or 200 ng) did not itself modify pain sensitivity in the tail flick test and did not affect the acute antinociceptive action of a single dose of <b>morphine</b> in the same test.
+S100A12	drug	opioid	8545480	However, <strong>CGRP</strong> suppressed the development of rapid tolerance to <b>morphine</b> in a dose dependent manner, but had no action on the development of chronic tolerance to <b>morphine</b> and on manifestations of <b>naloxone</b> precipitated withdrawal syndrome.
+S100A12	addiction	withdrawal	8545480	However, <strong>CGRP</strong> suppressed the development of rapid tolerance to morphine in a dose dependent manner, but had no action on the development of chronic tolerance to morphine and on manifestations of naloxone precipitated <b>withdrawal</b> syndrome.
+S100A12	drug	opioid	8336518	Previously we have shown that calcitonin gene related peptide (<strong>CGRP</strong>) modulates nociception and the effect of <b>opioid</b> analgesics in the central nervous system of mice.
+S100A12	addiction	withdrawal	8336518	Subcutaneous injection of <strong>CGRP</strong> produced a modest elevation of <b>withdrawal</b> latency time at doses that were two orders of magnitude greater than the physiologic levels determined in naive animals by radioimmunoassay.
+S100A12	addiction	withdrawal	8336518	These results indicate that subcutaneous injection of <strong>CGRP</strong> into the dorsal hindpaw skin of the mouse produces a modest increase in paw <b>withdrawal</b> latency times at high, non physiologic doses.
+S100A12	drug	opioid	1335576	Acute administration of <b>morphine</b> decreases levels of <strong>CGRP</strong> in rat corpus striatum.
+S100A12	drug	opioid	1335576	Tolerance to <b>morphine</b> did not alter the levels of <strong>CGRP</strong> in any brain region or in the spinal cord of the rat.
+S100A12	drug	opioid	1335576	<strong>CGRP</strong> did not alter the tolerance to the antinociceptive effects of <b>morphine</b>.
+S100A12	drug	alcohol	1335576	Chronic <b>naltrexone</b> increased the levels of <strong>CGRP</strong> in the hypothalamus.
+S100A12	drug	alcohol	1335576	Concurrent chronic administration of <b>naltrexone</b> plus morphine raised the levels of <strong>CGRP</strong> in the medulla, midbrain, and spinal cord.
+S100A12	drug	opioid	1335576	Concurrent chronic administration of naltrexone plus <b>morphine</b> raised the levels of <strong>CGRP</strong> in the medulla, midbrain, and spinal cord.
+S100A12	drug	opioid	1335576	<strong>CGRP</strong> enhances <b>naloxone</b> precipitated withdrawal jumping in mice.
+S100A12	addiction	withdrawal	1335576	<strong>CGRP</strong> enhances naloxone precipitated <b>withdrawal</b> jumping in mice.
+S100A12	addiction	withdrawal	1335576	In rats, during <b>withdrawal</b> the levels of <strong>CGRP</strong> were tripled in the corpus striatum and significantly reduced in the hippocampus and hypothalamus.
+S100A12	drug	opioid	1335576	These data are consistent with the hypothesis that <strong>CGRP</strong> acts as a modulatory peptide in opiate sensitive systems and tonic <b>opioid</b> control of <strong>CGRP</strong> levels exists in brain.
+S100A12	drug	opioid	1382137	In this study, we examined the effects of dependence on and withdrawal from <b>morphine</b> and <b>methadone</b> on brain SP and <strong>CGRP</strong> content.
+S100A12	addiction	dependence	1382137	In this study, we examined the effects of <b>dependence</b> on and withdrawal from morphine and methadone on brain SP and <strong>CGRP</strong> content.
+S100A12	addiction	withdrawal	1382137	In this study, we examined the effects of dependence on and <b>withdrawal</b> from morphine and methadone on brain SP and <strong>CGRP</strong> content.
+BCHE	drug	cocaine	32387315	In particular, rational design and site directed mutagenesis transformed human serum recombinant butyrylcholinesterase (<strong>BChE</strong>) into a highly efficient <b>cocaine</b> hydrolase with drastically improved catalytic efficiency toward ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	32387315	In particular, rational design and site directed mutagenesis transformed human serum recombinant <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) into a highly efficient <b>cocaine</b> hydrolase with drastically improved catalytic efficiency toward ( ) <b>cocaine</b>.
+BCHE	drug	cannabinoid	31898159	Here, we have evaluated the effects of two in house designed <b>cannabinoid</b> receptors (CB) agonists showing inhibitory actions on β secretase 1 (BACE 1) (NP137) and BACE 1/<strong>butyrylcholinesterase</strong> (BuChE) (NP148), on cellular models of AD, including immortalized lymphocytes from late onset AD patients.
+BCHE	drug	cocaine	31754920	As a promising therapeutic strategy for treatment of <b>cocaine</b> toxicity and addiction to develop a highly efficient <b>cocaine</b> hydrolase (CocH) capable of accelerating <b>cocaine</b> metabolism to produce physiologically/biologically inactive metabolites, our previously designed A199S/S287G/A328W/Y332G mutant of human butyrylcholinesterase (<strong>BChE</strong>), known as <b>cocaine</b> hydrolase 1 (CocH1), possesses the desirably high catalytic activity against <b>cocaine</b>.
+BCHE	addiction	addiction	31754920	As a promising therapeutic strategy for treatment of cocaine toxicity and <b>addiction</b> to develop a highly efficient cocaine hydrolase (CocH) capable of accelerating cocaine metabolism to produce physiologically/biologically inactive metabolites, our previously designed A199S/S287G/A328W/Y332G mutant of human butyrylcholinesterase (<strong>BChE</strong>), known as cocaine hydrolase 1 (CocH1), possesses the desirably high catalytic activity against cocaine.
+BCHE	drug	cocaine	31754920	As a promising therapeutic strategy for treatment of <b>cocaine</b> toxicity and addiction to develop a highly efficient <b>cocaine</b> hydrolase (CocH) capable of accelerating <b>cocaine</b> metabolism to produce physiologically/biologically inactive metabolites, our previously designed A199S/S287G/A328W/Y332G mutant of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), known as <b>cocaine</b> hydrolase 1 (CocH1), possesses the desirably high catalytic activity against <b>cocaine</b>.
+BCHE	addiction	addiction	31754920	As a promising therapeutic strategy for treatment of cocaine toxicity and <b>addiction</b> to develop a highly efficient cocaine hydrolase (CocH) capable of accelerating cocaine metabolism to produce physiologically/biologically inactive metabolites, our previously designed A199S/S287G/A328W/Y332G mutant of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), known as cocaine hydrolase 1 (CocH1), possesses the desirably high catalytic activity against cocaine.
+BCHE	drug	cocaine	31702488	The substrate scope of <strong>butyrylcholinesterase</strong> was recently found to include <b>cocaine</b>, as well as ghrelin, the "hunger hormone".
+BCHE	drug	cocaine	31702488	These findings led to the development of recombinant <strong>butyrylcholinesterase</strong> mutants and viral gene therapy to combat <b>cocaine</b> addiction, along with in depth studies on the significance of <strong>butyrylcholinesterase</strong> in obesity.
+BCHE	addiction	addiction	31702488	These findings led to the development of recombinant <strong>butyrylcholinesterase</strong> mutants and viral gene therapy to combat cocaine <b>addiction</b>, along with in depth studies on the significance of <strong>butyrylcholinesterase</strong> in obesity.
+BCHE	drug	alcohol	31660828	Similarly, <b>ethanol</b> up to 0.33% (v/v) and methanol up to 0.29% (v/v) did not inhibit the activity of <strong>BChE</strong>.
+BCHE	drug	cocaine	30986387	A199S/F227A/S287G/A328W/Y332G mutant of human <strong>BChE</strong>), which has a ~2000 fold improved catalytic activity against <b>cocaine</b> compared to wild type <strong>BChE</strong>, we designed an N terminal fusion protein, Fc(M3) (PAPAP)2 CocH3, which was constructed by fusing Fc of human IgG1 to the N terminal of CocH3 and further optimized by inserting a linker between the two protein domains.
+BCHE	drug	cocaine	30899600	Here, we show that the transplantation, into mice, of skin cells modified to express an enhanced form of <strong>butyrylcholinesterase</strong>, an enzyme that hydrolyzes <b>cocaine</b>, enables the long term release of the enzyme and efficiently protects the mice from <b>cocaine</b> seeking behavior and <b>cocaine</b> overdose.
+BCHE	addiction	relapse	30899600	Here, we show that the transplantation, into mice, of skin cells modified to express an enhanced form of <strong>butyrylcholinesterase</strong>, an enzyme that hydrolyzes cocaine, enables the long term release of the enzyme and efficiently protects the mice from cocaine <b>seeking</b> behavior and cocaine overdose.
+BCHE	drug	cocaine	30707402	Butyrylcholinesterase (<strong>BChE</strong>), a cholinergic enzyme, has been implicated in the metabolism of various drugs, including <b>cocaine</b>, and an association between single nucleotide polymorphisms (SNPs) of the butyrylcholinesterase gene (<strong>BCHE</strong>) and neuronal disorders has been reported.
+BCHE	drug	cocaine	30707402	<strong>Butyrylcholinesterase</strong> (<strong>BChE</strong>), a cholinergic enzyme, has been implicated in the metabolism of various drugs, including <b>cocaine</b>, and an association between single nucleotide polymorphisms (SNPs) of the <strong>butyrylcholinesterase</strong> gene (<strong>BCHE</strong>) and neuronal disorders has been reported.
+BCHE	drug	opioid	30707402	We report here the first investigation to be conducted on the status of <strong>BChE</strong> activity and the potential association of two <strong>BCHE</strong> gene SNPs, rs3495 (c.*189G > A) and rs1803274 (c.1699G>A, p.Ala567Thr, K variant), with addiction vulnerability in <b>heroin</b>, hashish and polydrug users.
+BCHE	addiction	addiction	30707402	We report here the first investigation to be conducted on the status of <strong>BChE</strong> activity and the potential association of two <strong>BCHE</strong> gene SNPs, rs3495 (c.*189G > A) and rs1803274 (c.1699G>A, p.Ala567Thr, K variant), with <b>addiction</b> vulnerability in heroin, hashish and polydrug users.
+BCHE	addiction	addiction	30707402	The authors conclude that <strong>BChE</strong> plays significant roles in <b>addiction</b> pathophysiology as increased <strong>BChE</strong> activity in blood samples obtained from the cohorts with <b>addiction</b> was evident.
+BCHE	drug	cocaine	29807217	TV 1380 is a rationally mutated, human <strong>BChE</strong> fused to human serum albumin that has high hydrolytic enzymatic activity against <b>cocaine</b> and as well as an extended elimination half life.
+BCHE	drug	alcohol	29807217	The results of this study demonstrate that TV 1380 not only accelerates the elimination of cocaine, but also protects the treated animal from the cardiac effects of cocaine, and inhibits the formation of the toxic cocaethylene metabolite when cocaine is given together with <b>ethanol</b>, supporting further clinical development of modified <strong>BChE</strong> products as possible treatments for cocaine abuse.
+BCHE	drug	cocaine	29807217	The results of this study demonstrate that TV 1380 not only accelerates the elimination of <b>cocaine</b>, but also protects the treated animal from the cardiac effects of <b>cocaine</b>, and inhibits the formation of the toxic cocaethylene metabolite when <b>cocaine</b> is given together with ethanol, supporting further clinical development of modified <strong>BChE</strong> products as possible treatments for <b>cocaine</b> abuse.
+BCHE	drug	cocaine	29535625	Treating <b>Cocaine</b> Addiction, Obesity, and Emotional Disorders by Viral Gene Transfer of <strong>Butyrylcholinesterase</strong>.
+BCHE	addiction	addiction	29535625	Treating Cocaine <b>Addiction</b>, Obesity, and Emotional Disorders by Viral Gene Transfer of <strong>Butyrylcholinesterase</strong>.
+BCHE	drug	cocaine	29535625	However, very recent studies at Mayo Clinic have amassed support for the concept that <strong>BChE</strong> does have a true physiological role as a "ghrelin hydrolase" and, pharmacologically, as a <b>cocaine</b> hydrolase.
+BCHE	drug	cocaine	29535625	This brief review examines some key phenomena and considers means of modulating <strong>BChE</strong> as treatments for <b>cocaine</b> addiction, anxiety, aggression, and obesity.
+BCHE	addiction	addiction	29535625	This brief review examines some key phenomena and considers means of modulating <strong>BChE</strong> as treatments for cocaine <b>addiction</b>, anxiety, aggression, and obesity.
+BCHE	drug	cocaine	28874829	Plant expressed <b>cocaine</b> hydrolase variants of <strong>butyrylcholinesterase</strong> exhibit altered allosteric effects of cholinesterase activity and increased inhibitor sensitivity.
+BCHE	drug	cocaine	28874829	Variants of <strong>BChE</strong> were rationally designed to increase the enzyme's ability to hydrolyze the psychoactive enantiomer of <b>cocaine</b>.
+BCHE	drug	cocaine	27394932	TV 1380 (AlbuChE) is a novel recombinant fusion protein of mutated butyrylcholinesterase (<strong>BChE</strong>) that has increased catalytic efficiency for <b>cocaine</b> metabolism compared to wild type <strong>BChE</strong>.
+BCHE	drug	cocaine	27394932	TV 1380 (AlbuChE) is a novel recombinant fusion protein of mutated <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) that has increased catalytic efficiency for <b>cocaine</b> metabolism compared to wild type <strong>BChE</strong>.
+BCHE	drug	cocaine	27392137	Nonetheless, <b>cocaine</b> is metabolized by <strong>butyrylcholinesterase</strong> (BuChE), raising concerns that cholinesterase inhibition could increase its peripheral concentrations, perhaps augmenting toxicity.
+BCHE	drug	cocaine	27224254	Here, through combined computational modeling and experimental studies, we demonstrate for the first time that human butyrylcholinesterase (<strong>BChE</strong>) is actually active against benzoylecgonine, and that a rationally designed <strong>BChE</strong> mutant can not only more efficiently accelerate <b>cocaine</b> hydrolysis but also significantly hydrolyze benzoylecgonine in vitro and in vivo.
+BCHE	drug	cocaine	27224254	Here, through combined computational modeling and experimental studies, we demonstrate for the first time that human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) is actually active against benzoylecgonine, and that a rationally designed <strong>BChE</strong> mutant can not only more efficiently accelerate <b>cocaine</b> hydrolysis but also significantly hydrolyze benzoylecgonine in vitro and in vivo.
+BCHE	drug	cocaine	27154495	Effects of a <b>cocaine</b> hydrolase engineered from human <strong>butyrylcholinesterase</strong> on metabolic profile of <b>cocaine</b> in rats.
+BCHE	drug	cocaine	27154495	Our more recently designed A199S/F227A/S287G/A328W/Y332G mutant of human <strong>BChE</strong>, denoted as <b>cocaine</b> hydrolase 3 (CocH3), has a considerably improved catalytic efficiency against <b>cocaine</b> and has been proven active in blocking <b>cocaine</b> induced toxicity and physiological effects.
+BCHE	drug	alcohol	27097732	The present study examined the influence of the cholinesterase inhibitors donepezil (a selective inhibitor of acetylcholinesterase) and rivastigmine (also an inhibitor of <strong>butyrylcholinesterase</strong>) on the acquisition and reinstatement of <b>ethanol</b> induced conditioned place preference (CPP) in rats.
+BCHE	addiction	relapse	27097732	The present study examined the influence of the cholinesterase inhibitors donepezil (a selective inhibitor of acetylcholinesterase) and rivastigmine (also an inhibitor of <strong>butyrylcholinesterase</strong>) on the acquisition and <b>reinstatement</b> of ethanol induced conditioned place preference (CPP) in rats.
+BCHE	addiction	reward	27097732	The present study examined the influence of the cholinesterase inhibitors donepezil (a selective inhibitor of acetylcholinesterase) and rivastigmine (also an inhibitor of <strong>butyrylcholinesterase</strong>) on the acquisition and reinstatement of ethanol induced conditioned place preference (<b>CPP</b>) in rats.
+BCHE	drug	cocaine	26968195	A promising approach in treating <b>cocaine</b> abuse is to metabolize <b>cocaine</b> in the blood using a mutated butyrylcholinesterase (<strong>BChE</strong>) that functions as a <b>cocaine</b> hydrolase (CocH).
+BCHE	drug	cocaine	26968195	A promising approach in treating <b>cocaine</b> abuse is to metabolize <b>cocaine</b> in the blood using a mutated <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) that functions as a <b>cocaine</b> hydrolase (CocH).
+BCHE	drug	cocaine	28250715	A recently designed and discovered <b>cocaine</b> hydrolase (CocH), engineered from human butyrylcholinesterase (<strong>BChE</strong>), has been proven promising as a novel enzyme therapy for treatment of <b>cocaine</b> overdose and addiction because it is highly efficient in catalyzing hydrolysis of naturally occurring ( ) <b>cocaine</b>.
+BCHE	addiction	addiction	28250715	A recently designed and discovered cocaine hydrolase (CocH), engineered from human butyrylcholinesterase (<strong>BChE</strong>), has been proven promising as a novel enzyme therapy for treatment of cocaine overdose and <b>addiction</b> because it is highly efficient in catalyzing hydrolysis of naturally occurring ( ) cocaine.
+BCHE	drug	cocaine	28250715	A recently designed and discovered <b>cocaine</b> hydrolase (CocH), engineered from human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), has been proven promising as a novel enzyme therapy for treatment of <b>cocaine</b> overdose and addiction because it is highly efficient in catalyzing hydrolysis of naturally occurring ( ) <b>cocaine</b>.
+BCHE	addiction	addiction	28250715	A recently designed and discovered cocaine hydrolase (CocH), engineered from human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), has been proven promising as a novel enzyme therapy for treatment of cocaine overdose and <b>addiction</b> because it is highly efficient in catalyzing hydrolysis of naturally occurring ( ) cocaine.
+BCHE	drug	cocaine	26669428	Viral gene transfer of <b>cocaine</b> hydrolase engineered from <strong>butyrylcholinesterase</strong> offers therapeutic promise for treatment seeking drug users.
+BCHE	addiction	relapse	26669428	Viral gene transfer of cocaine hydrolase engineered from <strong>butyrylcholinesterase</strong> offers therapeutic promise for treatment <b>seeking</b> drug users.
+BCHE	drug	cocaine	26082975	Assessment of Pharmacokinetic and Pharmacodynamic Interactions Between Albumin Fused Mutated <strong>Butyrylcholinesterase</strong> and Intravenously Administered <b>Cocaine</b> in Recreational <b>Cocaine</b> Users.
+BCHE	drug	cocaine	26082975	TV 1380 is a novel recombinant albumin fused mutated butyrylcholinesterase (Albu <strong>BChE</strong>) that has increased catalytic efficiency for <b>cocaine</b> compared with wild type <strong>BChE</strong> and therefore has the potential to facilitate abstinence in <b>cocaine</b> dependent subjects by decreasing exposure to <b>cocaine</b> and its reinforcing effects.
+BCHE	addiction	reward	26082975	TV 1380 is a novel recombinant albumin fused mutated butyrylcholinesterase (Albu <strong>BChE</strong>) that has increased catalytic efficiency for cocaine compared with wild type <strong>BChE</strong> and therefore has the potential to facilitate abstinence in cocaine dependent subjects by decreasing exposure to cocaine and its <b>reinforcing</b> effects.
+BCHE	drug	cocaine	26082975	TV 1380 is a novel recombinant albumin fused mutated <strong>butyrylcholinesterase</strong> (Albu <strong>BChE</strong>) that has increased catalytic efficiency for <b>cocaine</b> compared with wild type <strong>BChE</strong> and therefore has the potential to facilitate abstinence in <b>cocaine</b> dependent subjects by decreasing exposure to <b>cocaine</b> and its reinforcing effects.
+BCHE	addiction	reward	26082975	TV 1380 is a novel recombinant albumin fused mutated <strong>butyrylcholinesterase</strong> (Albu <strong>BChE</strong>) that has increased catalytic efficiency for cocaine compared with wild type <strong>BChE</strong> and therefore has the potential to facilitate abstinence in cocaine dependent subjects by decreasing exposure to cocaine and its <b>reinforcing</b> effects.
+BCHE	drug	cocaine	26082975	This randomized, double blind, placebo controlled, parallel group study in nondependent <b>cocaine</b> users was conducted to evaluate the effect of a single intramuscular dose of Albu <strong>BChE</strong> (50, 100, and 300 mg) on the pharmacokinetic and metabolic profile of intravenous <b>cocaine</b> infusions (40 mg) administered at baseline and at 24, 96, and 168 hours after Albu <strong>BChE</strong> dosing, to assess safety of coadministering Albu <strong>BChE</strong> and <b>cocaine</b>, and to explore the subjective responses to <b>cocaine</b> infusions after Albu <strong>BChE</strong> dosing.
+BCHE	drug	cocaine	26082975	Administration of Albu <strong>BChE</strong> resulted in significant dose dependent reductions in <b>cocaine</b> exposure (maximum concentration, area under the curve) and half life.
+BCHE	drug	cocaine	26082975	Spearman correlations indicated a significant negative relationship between Albu <strong>BChE</strong> concentration and <b>cocaine</b> clearance and exposure.
+BCHE	drug	cocaine	26082975	Consistent with its mechanism of action, Albu <strong>BChE</strong> also shifted <b>cocaine</b> metabolism toward preferential formation of ecgonine methyl ester.
+BCHE	drug	cocaine	26082975	Administration of Albu <strong>BChE</strong> was associated with modest decreases in subjective reports of feeling high and willingness to take <b>cocaine</b> again after <b>cocaine</b> infusion.
+BCHE	drug	cocaine	26082975	Coadministration of Albu <strong>BChE</strong> and <b>cocaine</b> was safe and well tolerated.
+BCHE	drug	cocaine	26082975	Administration of Albu <strong>BChE</strong> at single doses of 50, 100, and 300 mg safely resulted in long lasting decreases in <b>cocaine</b> exposure in recreational <b>cocaine</b> users.
+BCHE	drug	cocaine	25814464	Butyrylcholinesterase (<strong>BChE</strong>) gene therapy is emerging as a promising concept for treatment of <b>cocaine</b> addiction.
+BCHE	addiction	addiction	25814464	Butyrylcholinesterase (<strong>BChE</strong>) gene therapy is emerging as a promising concept for treatment of cocaine <b>addiction</b>.
+BCHE	drug	cocaine	25814464	<strong>Butyrylcholinesterase</strong> (<strong>BChE</strong>) gene therapy is emerging as a promising concept for treatment of <b>cocaine</b> addiction.
+BCHE	addiction	addiction	25814464	<strong>Butyrylcholinesterase</strong> (<strong>BChE</strong>) gene therapy is emerging as a promising concept for treatment of cocaine <b>addiction</b>.
+BCHE	drug	cocaine	25814464	For months or years, gene transfer of a <strong>BChE</strong> mutated into a <b>cocaine</b> hydrolase (CocH) can maintain enzyme levels that destroy <b>cocaine</b> within seconds after appearance in the blood stream, allowing little to reach the brain.
+BCHE	drug	cocaine	25524052	Safety, pharmacokinetics, and pharmacodynamics of TV 1380, a novel mutated <strong>butyrylcholinesterase</strong> treatment for <b>cocaine</b> addiction, after single and multiple intramuscular injections in healthy subjects.
+BCHE	addiction	addiction	25524052	Safety, pharmacokinetics, and pharmacodynamics of TV 1380, a novel mutated <strong>butyrylcholinesterase</strong> treatment for cocaine <b>addiction</b>, after single and multiple intramuscular injections in healthy subjects.
+BCHE	drug	cocaine	25524052	Human plasma butyrylcholinesterase (<strong>BChE</strong>) contributes to <b>cocaine</b> metabolism and has been considered for use in treating <b>cocaine</b> addiction and <b>cocaine</b> overdose.
+BCHE	addiction	addiction	25524052	Human plasma butyrylcholinesterase (<strong>BChE</strong>) contributes to cocaine metabolism and has been considered for use in treating cocaine <b>addiction</b> and cocaine overdose.
+BCHE	drug	cocaine	25524052	Human plasma <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) contributes to <b>cocaine</b> metabolism and has been considered for use in treating <b>cocaine</b> addiction and <b>cocaine</b> overdose.
+BCHE	addiction	addiction	25524052	Human plasma <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) contributes to cocaine metabolism and has been considered for use in treating cocaine <b>addiction</b> and cocaine overdose.
+BCHE	drug	cocaine	25448037	A recombinant mutant of <strong>BChE</strong> that rapidly inactivates <b>cocaine</b> is being developed as a treatment to help recovering <b>cocaine</b> addicts avoid relapse into drug taking.
+BCHE	addiction	relapse	25448037	A recombinant mutant of <strong>BChE</strong> that rapidly inactivates cocaine is being developed as a treatment to help recovering cocaine addicts avoid <b>relapse</b> into drug taking.
+BCHE	drug	cocaine	25321637	<strong>Butyrylcholinesterase</strong> levels and subjective effects of smoked <b>cocaine</b> in healthy <b>cocaine</b> users.
+BCHE	drug	cocaine	25321637	Butyrylcholinesterase (<strong>BChE</strong>) is beginning to attract attention as a possible target for <b>cocaine</b> abuse treatment because of its role in metabolizing <b>cocaine</b>.
+BCHE	drug	cocaine	25321637	<strong>Butyrylcholinesterase</strong> (<strong>BChE</strong>) is beginning to attract attention as a possible target for <b>cocaine</b> abuse treatment because of its role in metabolizing <b>cocaine</b>.
+BCHE	drug	cocaine	25321637	The purpose of this analysis was to assess whether endogenous <strong>BChE</strong> levels are associated with the subjective effects of <b>cocaine</b>.
+BCHE	drug	cocaine	25321637	After controlling for age, sex, total years of <b>cocaine</b> use, total milligrams of <b>cocaine</b> administered before the 25 mg dose being analyzed, and baseline diastolic blood pressure, endogenous <strong>BChE</strong> was not significantly associated with any of the nine change in VAS ratings.
+BCHE	drug	cocaine	25321637	Though <strong>BChE</strong> appears to be a possible target for <b>cocaine</b> abuse treatment, these data suggest that endogenous levels of <strong>BChE</strong> may not play a role in modifying the subjective effects of <b>cocaine</b>.
+BCHE	drug	cocaine	25321637	Future larger studies of <strong>BChE</strong> in respect to the subjective effects produced by <b>cocaine</b> are needed to confirm or refute these findings.
+BCHE	drug	cocaine	24892251	In continuing efforts to develop gene transfer of human butyrylcholinesterase (<strong>BChE</strong>) as therapy for <b>cocaine</b> addiction, we conducted wide ranging studies of physiological and metabolic safety.
+BCHE	addiction	addiction	24892251	In continuing efforts to develop gene transfer of human butyrylcholinesterase (<strong>BChE</strong>) as therapy for cocaine <b>addiction</b>, we conducted wide ranging studies of physiological and metabolic safety.
+BCHE	drug	cocaine	24892251	In continuing efforts to develop gene transfer of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) as therapy for <b>cocaine</b> addiction, we conducted wide ranging studies of physiological and metabolic safety.
+BCHE	addiction	addiction	24892251	In continuing efforts to develop gene transfer of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) as therapy for cocaine <b>addiction</b>, we conducted wide ranging studies of physiological and metabolic safety.
+BCHE	drug	cocaine	24892251	For that purpose, mice were given injections of adeno associated virus (AAV) vector or helper dependent adenoviral (hdAD) vector encoding human or mouse <strong>BChE</strong> mutated for optimal <b>cocaine</b> hydrolysis.
+BCHE	drug	cocaine	24892251	We conclude that neither the tested vectors nor great excesses of circulating <strong>BChE</strong> affect general physiology directly, while they protect mice from disturbance by <b>cocaine</b>.
+BCHE	drug	cocaine	24892251	Hence, viral gene transfer of <strong>BChE</strong> appears benign and worth exploring as a therapy for <b>cocaine</b> abuse and possibly other disorders as well.
+BCHE	drug	opioid	24755308	Additionally, this study aimed to compare the effects of donepezil, which selectively inhibits acetylcholinesterase, and rivastigmine, which inhibits both acetylcholinesterase and <strong>butyrylcholinesterase</strong> on <b>morphine</b> reward.
+BCHE	addiction	reward	24755308	Additionally, this study aimed to compare the effects of donepezil, which selectively inhibits acetylcholinesterase, and rivastigmine, which inhibits both acetylcholinesterase and <strong>butyrylcholinesterase</strong> on morphine <b>reward</b>.
+BCHE	drug	cocaine	24582612	Our recently designed and discovered <b>cocaine</b> hydrolase, particularly E12 7 engineered from human butyrylcholinesterase (<strong>BChE</strong>), has the promise of becoming a valuable <b>cocaine</b> abuse treatment.
+BCHE	drug	cocaine	24582612	Our recently designed and discovered <b>cocaine</b> hydrolase, particularly E12 7 engineered from human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), has the promise of becoming a valuable <b>cocaine</b> abuse treatment.
+BCHE	drug	cocaine	24407266	A new pharmacokinetic approach treating <b>cocaine</b> addiction involves rapidly metabolizing <b>cocaine</b> before it reaches brain reward centers using mutated human butyrylcholinesterase (<strong>BChE</strong>) or <b>cocaine</b> hydrolase (CocH).
+BCHE	addiction	addiction	24407266	A new pharmacokinetic approach treating cocaine <b>addiction</b> involves rapidly metabolizing cocaine before it reaches brain reward centers using mutated human butyrylcholinesterase (<strong>BChE</strong>) or cocaine hydrolase (CocH).
+BCHE	addiction	reward	24407266	A new pharmacokinetic approach treating cocaine addiction involves rapidly metabolizing cocaine before it reaches brain <b>reward</b> centers using mutated human butyrylcholinesterase (<strong>BChE</strong>) or cocaine hydrolase (CocH).
+BCHE	drug	cocaine	24407266	A new pharmacokinetic approach treating <b>cocaine</b> addiction involves rapidly metabolizing <b>cocaine</b> before it reaches brain reward centers using mutated human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) or <b>cocaine</b> hydrolase (CocH).
+BCHE	addiction	addiction	24407266	A new pharmacokinetic approach treating cocaine <b>addiction</b> involves rapidly metabolizing cocaine before it reaches brain reward centers using mutated human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) or cocaine hydrolase (CocH).
+BCHE	addiction	reward	24407266	A new pharmacokinetic approach treating cocaine addiction involves rapidly metabolizing cocaine before it reaches brain <b>reward</b> centers using mutated human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) or cocaine hydrolase (CocH).
+BCHE	drug	cocaine	24407266	Pretreatment with the selective <strong>BChE</strong> and CocH inhibitor iso OMPA (1.5 mg/kg) restored <b>cocaine</b> intake; therefore, the decline in self administration was likely due to rapid CocH mediated <b>cocaine</b> metabolism.
+BCHE	drug	cocaine	24327294	Human butyrylcholinesterase (<strong>BChE</strong>) and its mutants have shown great potential in treating <b>cocaine</b> overdose and addiction.
+BCHE	addiction	addiction	24327294	Human butyrylcholinesterase (<strong>BChE</strong>) and its mutants have shown great potential in treating cocaine overdose and <b>addiction</b>.
+BCHE	drug	cocaine	24327294	Human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) and its mutants have shown great potential in treating <b>cocaine</b> overdose and addiction.
+BCHE	addiction	addiction	24327294	Human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) and its mutants have shown great potential in treating cocaine overdose and <b>addiction</b>.
+BCHE	drug	cocaine	24312228	<strong>Butyrylcholinesterase</strong> genetic variants: association with <b>cocaine</b> dependence and related phenotypes.
+BCHE	addiction	dependence	24312228	<strong>Butyrylcholinesterase</strong> genetic variants: association with cocaine <b>dependence</b> and related phenotypes.
+BCHE	drug	cocaine	24312228	Butyrylcholinesterase (<strong>BChE</strong>) metabolizes <b>cocaine</b>, and genetic variants of the <strong>BChE</strong> gene (<strong>BCHE</strong>) alter its catalytic activity.
+BCHE	drug	cocaine	24312228	<strong>Butyrylcholinesterase</strong> (<strong>BChE</strong>) metabolizes <b>cocaine</b>, and genetic variants of the <strong>BChE</strong> gene (<strong>BCHE</strong>) alter its catalytic activity.
+BCHE	drug	cocaine	24312228	Therefore, we hypothesize that <b>cocaine</b> users with polymorphisms in <strong>BCHE</strong> can show diverse addictive behaviors due to differences in effective plasma concentrations of <b>cocaine</b>.
+BCHE	addiction	addiction	24312228	Therefore, we hypothesize that cocaine users with polymorphisms in <strong>BCHE</strong> can show diverse <b>addictive</b> behaviors due to differences in effective plasma concentrations of cocaine.
+BCHE	drug	cocaine	24312228	The present work investigates polymorphisms in <strong>BCHE</strong> and if those genetic variants constitute risk factors for <b>cocaine</b> dependence and for crack <b>cocaine</b> use.
+BCHE	addiction	dependence	24312228	The present work investigates polymorphisms in <strong>BCHE</strong> and if those genetic variants constitute risk factors for cocaine <b>dependence</b> and for crack cocaine use.
+BCHE	drug	cocaine	24312228	A total of 1,436 individuals (698 <b>cocaine</b> dependent patients and 738 controls) were genotyped for three single nucleotide polymorphisms (SNPs) in <strong>BCHE</strong>: rs1803274, rs4263329, and rs4680662.
+BCHE	drug	cocaine	24312228	Further studies are needed in order to confirm this preliminary result and clarify the role of <strong>BCHE</strong> and its variants in <b>cocaine</b> dependence.
+BCHE	addiction	dependence	24312228	Further studies are needed in order to confirm this preliminary result and clarify the role of <strong>BCHE</strong> and its variants in cocaine <b>dependence</b>.
+BCHE	drug	cocaine	24085526	<b>Cocaine</b> hydrolase gene transfer of mutated human butyrylcholinesterase (<strong>BChE</strong>) is evolving as a promising therapy for <b>cocaine</b> addiction.
+BCHE	addiction	addiction	24085526	Cocaine hydrolase gene transfer of mutated human butyrylcholinesterase (<strong>BChE</strong>) is evolving as a promising therapy for cocaine <b>addiction</b>.
+BCHE	drug	cocaine	24085526	<b>Cocaine</b> hydrolase gene transfer of mutated human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) is evolving as a promising therapy for <b>cocaine</b> addiction.
+BCHE	addiction	addiction	24085526	Cocaine hydrolase gene transfer of mutated human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) is evolving as a promising therapy for cocaine <b>addiction</b>.
+BCHE	drug	cocaine	24085526	BALB/c mice were given adeno associated virus vector or helper dependent adenoviral vector encoding mouse or human <strong>BChE</strong> optimized for <b>cocaine</b>.
+BCHE	drug	cocaine	24077614	<b>cocaine</b> hydrolysis catalyzed by butyrylcholinesterase (<strong>BChE</strong>) in plasma.
+BCHE	drug	cocaine	24077614	<b>cocaine</b> hydrolysis catalyzed by <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) in plasma.
+BCHE	drug	cocaine	24077614	However, the native <strong>BChE</strong> has a low catalytic efficiency against the abused <b>cocaine</b>, i.e.
+BCHE	drug	cocaine	24077614	Our recently designed and discovered A199S/F227A/S287G/A328W/Y332G mutant and other mutants of human <strong>BChE</strong> have a considerably improved catalytic efficiency against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	24077614	In the present study, we carried out both computational modeling and experimental kinetic analysis on the catalytic activities of these promising new <strong>BChE</strong> mutants against other known substrates, including neurotransmitter acetylcholine (ACh), acetylthiocholine (ATC), butyrylthiocholine (BTC), and (+) <b>cocaine</b>, in comparison with the corresponding catalytic activity against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	24077614	Both the computational modeling and kinetic analysis have consistently revealed that all the examined amino acid mutations only considerably improve the catalytic efficiency of human <strong>BChE</strong> against ( ) <b>cocaine</b>, without significantly improving the catalytic efficiency of the enzyme against any of the other substrates examined.
+BCHE	drug	cocaine	24077614	This observation gives us confidence in developing an anti <b>cocaine</b> enzyme therapy by using one of these <strong>BChE</strong> mutants, particularly the A199S/F227A/S287G/A328W/Y332G mutant.
+BCHE	drug	cocaine	23840704	Gene transfer of a human <b>cocaine</b> hydrolase (hCocH) derived from butyrylcholinesterase (<strong>BChE</strong>) by 5 mutations (A199S/F227A/S287G/A328W/Y332G) has shown promise in animal studies for treatment of <b>cocaine</b> addiction.
+BCHE	addiction	addiction	23840704	Gene transfer of a human cocaine hydrolase (hCocH) derived from butyrylcholinesterase (<strong>BChE</strong>) by 5 mutations (A199S/F227A/S287G/A328W/Y332G) has shown promise in animal studies for treatment of cocaine <b>addiction</b>.
+BCHE	drug	cocaine	23840704	Gene transfer of a human <b>cocaine</b> hydrolase (hCocH) derived from <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) by 5 mutations (A199S/F227A/S287G/A328W/Y332G) has shown promise in animal studies for treatment of <b>cocaine</b> addiction.
+BCHE	addiction	addiction	23840704	Gene transfer of a human cocaine hydrolase (hCocH) derived from <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) by 5 mutations (A199S/F227A/S287G/A328W/Y332G) has shown promise in animal studies for treatment of cocaine <b>addiction</b>.
+BCHE	drug	cocaine	23840704	Experiments on substrate kinetics of purified mCocH expressed in HEK293T cells showed 30 fold higher activity (U/mg) with (3)H <b>cocaine</b> and 25% lower activity with butyrylthiocholine, compared with wild type <strong>BChE</strong>.
+BCHE	drug	cocaine	23000451	Plants as a source of <strong>butyrylcholinesterase</strong> variants designed for enhanced <b>cocaine</b> hydrolase activity.
+BCHE	drug	cocaine	23000451	Recent studies, however, have demonstrated a promising potential treatment option with the help of the serum enzyme butyrylcholinesterase (<strong>BChE</strong>), which is capable of breaking down naturally occurring ( ) <b>cocaine</b> before the drug can influence the reward centers of the brain or affect other areas of the body.
+BCHE	addiction	reward	23000451	Recent studies, however, have demonstrated a promising potential treatment option with the help of the serum enzyme butyrylcholinesterase (<strong>BChE</strong>), which is capable of breaking down naturally occurring ( ) cocaine before the drug can influence the <b>reward</b> centers of the brain or affect other areas of the body.
+BCHE	drug	cocaine	23000451	Recent studies, however, have demonstrated a promising potential treatment option with the help of the serum enzyme <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), which is capable of breaking down naturally occurring ( ) <b>cocaine</b> before the drug can influence the reward centers of the brain or affect other areas of the body.
+BCHE	addiction	reward	23000451	Recent studies, however, have demonstrated a promising potential treatment option with the help of the serum enzyme <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), which is capable of breaking down naturally occurring ( ) cocaine before the drug can influence the <b>reward</b> centers of the brain or affect other areas of the body.
+BCHE	drug	cocaine	23000451	This prompted the design of variants of <strong>BChE</strong> which exhibit significantly improved catalytic activity against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	23000451	Plants are a promising means to produce large amounts of these <b>cocaine</b> hydrolase variants of <strong>BChE</strong>, cheaply, safely with no concerns regarding human pathogens and functionally equivalent to enzymes derived from other sources.
+BCHE	drug	cocaine	23000451	Here, in expressing <b>cocaine</b> hydrolyzing mutants of <strong>BChE</strong> in Nicotiana benthamiana using the MagnICON virus assisted transient expression system, and in reporting their initial biochemical analysis, we provide proof of principle that plants can express engineered <strong>BChE</strong> proteins with desired properties.
+BCHE	drug	cocaine	22960160	Anti <b>cocaine</b> antibody and <strong>butyrylcholinesterase</strong> derived <b>cocaine</b> hydrolase exert cooperative effects on <b>cocaine</b> pharmacokinetics and <b>cocaine</b> induced locomotor activity in mice.
+BCHE	drug	cocaine	22960160	We are investigating treatments for <b>cocaine</b> abuse based on viral gene transfer of a <b>cocaine</b> hydrolase (CocH) derived from human <strong>butyrylcholinesterase</strong>, which can reduce <b>cocaine</b> stimulated locomotion and <b>cocaine</b> primed reinstatement of drug seeking behavior in rats for many months.
+BCHE	addiction	relapse	22960160	We are investigating treatments for cocaine abuse based on viral gene transfer of a cocaine hydrolase (CocH) derived from human <strong>butyrylcholinesterase</strong>, which can reduce cocaine stimulated locomotion and cocaine primed <b>reinstatement</b> of drug <b>seeking</b> behavior in rats for many months.
+BCHE	drug	cocaine	22935511	In developing an vivo drug interception therapy to treat <b>cocaine</b> abuse and hinder relapse into drug seeking provoked by re encounter with <b>cocaine</b>, two promising agents are: (1) a <b>cocaine</b> hydrolase enzyme (CocH) derived from human <strong>butyrylcholinesterase</strong> and delivered by gene transfer; (2) an anti <b>cocaine</b> antibody elicited by vaccination.
+BCHE	addiction	relapse	22935511	In developing an vivo drug interception therapy to treat cocaine abuse and hinder <b>relapse</b> into drug <b>seeking</b> provoked by re encounter with cocaine, two promising agents are: (1) a cocaine hydrolase enzyme (CocH) derived from human <strong>butyrylcholinesterase</strong> and delivered by gene transfer; (2) an anti cocaine antibody elicited by vaccination.
+BCHE	drug	cocaine	22912888	Mice and rats were tested for reduced sensitivity to <b>cocaine</b> induced hyper locomotion after pretreatment with anti <b>cocaine</b> antibody or <b>cocaine</b> hydrolase (CocH) derived from human butyrylcholinesterase (<strong>BChE</strong>).
+BCHE	drug	cocaine	22912888	Mice and rats were tested for reduced sensitivity to <b>cocaine</b> induced hyper locomotion after pretreatment with anti <b>cocaine</b> antibody or <b>cocaine</b> hydrolase (CocH) derived from human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>).
+BCHE	drug	amphetamine	22300100	Monoclonal antibodies against cocaine, <b>methamphetamine</b> and phencyclidine have shown promise in animal studies, as has enhancing cocaine metabolism with genetic variants of human <strong>butyrylcholinesterase</strong>, with a bacterial esterase, and with catalytic monoclonal antibodies.
+BCHE	drug	cocaine	22300100	Monoclonal antibodies against <b>cocaine</b>, methamphetamine and phencyclidine have shown promise in animal studies, as has enhancing <b>cocaine</b> metabolism with genetic variants of human <strong>butyrylcholinesterase</strong>, with a bacterial esterase, and with catalytic monoclonal antibodies.
+BCHE	drug	cocaine	22300095	Rapid progress in the past decade with re engineering of human plasma <strong>butyrylcholinesterase</strong> has led to enzymes that destroy <b>cocaine</b> so efficiently that they prevent or interrupt drug actions in the CNS even though confined to the blood stream.
+BCHE	drug	cocaine	22264200	Albu CocH was developed from successive mutations of human butyrylcholinesterase (<strong>BChE</strong>) and has 1000 fold greater catalytic activity against <b>cocaine</b> than naturally occurring <strong>BChE</strong>.
+BCHE	drug	cocaine	22264200	Albu CocH was developed from successive mutations of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) and has 1000 fold greater catalytic activity against <b>cocaine</b> than naturally occurring <strong>BChE</strong>.
+BCHE	drug	cocaine	22264200	The ability of Albu CocH to attenuate the abuse related effects of <b>cocaine</b> in squirrel monkeys indicates that further investigation of <strong>BChE</strong> mutants as potential treatment for <b>cocaine</b> abuse and toxicity is warranted.
+BCHE	drug	cocaine	22229308	Recent progress in enzyme engineering has led to versions of human butyrylcholinesterase (<strong>BChE</strong>) that hydrolyze <b>cocaine</b> efficiently in plasma, reduce concentrations reaching reward neurocircuity in the brain, and weaken behavioral responses to this drug.
+BCHE	addiction	reward	22229308	Recent progress in enzyme engineering has led to versions of human butyrylcholinesterase (<strong>BChE</strong>) that hydrolyze cocaine efficiently in plasma, reduce concentrations reaching <b>reward</b> neurocircuity in the brain, and weaken behavioral responses to this drug.
+BCHE	drug	cocaine	22229308	Recent progress in enzyme engineering has led to versions of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) that hydrolyze <b>cocaine</b> efficiently in plasma, reduce concentrations reaching reward neurocircuity in the brain, and weaken behavioral responses to this drug.
+BCHE	addiction	reward	22229308	Recent progress in enzyme engineering has led to versions of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) that hydrolyze cocaine efficiently in plasma, reduce concentrations reaching <b>reward</b> neurocircuity in the brain, and weaken behavioral responses to this drug.
+BCHE	drug	cocaine	22209637	In a previous study, direct administration of a quadruple mutant albumin fused <strong>butyrylcholinesterase</strong> that efficiently catalyzes hydrolysis of <b>cocaine</b> to benzoic acid and ecgonine methyl ester acutely blocked <b>cocaine</b> seeking in an animal model of relapse.
+BCHE	addiction	relapse	22209637	In a previous study, direct administration of a quadruple mutant albumin fused <strong>butyrylcholinesterase</strong> that efficiently catalyzes hydrolysis of cocaine to benzoic acid and ecgonine methyl ester acutely blocked cocaine <b>seeking</b> in an animal model of <b>relapse</b>.
+BCHE	drug	cocaine	22209637	In the present experiments, these results were extended to achieve a long duration blockade of <b>cocaine</b> seeking with a gene transfer paradigm using a related <strong>butyrylcholinesterase</strong> based <b>cocaine</b> hydrolase (CocH).
+BCHE	addiction	relapse	22209637	In the present experiments, these results were extended to achieve a long duration blockade of cocaine <b>seeking</b> with a gene transfer paradigm using a related <strong>butyrylcholinesterase</strong> based cocaine hydrolase (CocH).
+BCHE	drug	cocaine	22173266	This study was carried out to evaluate the effects of donepezil (which selectively inhibits AChE) and rivastigmine (which inhibits both AChE and <strong>butyrylcholinesterase</strong>) on <b>cocaine</b> self administration.
+BCHE	drug	cocaine	20972552	Previously, Albu CocH, a <b>cocaine</b> hydrolase derived from human <strong>butyrylcholinesterase</strong>, blocked <b>cocaine</b> induced reinstatement of drug seeking in rats.
+BCHE	addiction	relapse	20972552	Previously, Albu CocH, a cocaine hydrolase derived from human <strong>butyrylcholinesterase</strong>, blocked cocaine induced <b>reinstatement</b> of drug <b>seeking</b> in rats.
+BCHE	drug	cocaine	20161378	The structure  and mechanism based computational design efforts have led to the discovery of high activity mutants of <strong>butyrylcholinesterase</strong> and thermostable mutants of <b>cocaine</b> esterase as promising anti <b>cocaine</b> therapeutics.
+BCHE	drug	cocaine	20060817	Characterization of a high activity mutant of human <strong>butyrylcholinesterase</strong> against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	20060817	Our recently designed and discovered high activity mutant (A199S/S287G/A328W/Y332G) of human butyrylcholinesterase (<strong>BChE</strong>) has been recognized to be worth exploring for clinical application in humans as a potential anti <b>cocaine</b> medication.
+BCHE	drug	cocaine	20060817	Our recently designed and discovered high activity mutant (A199S/S287G/A328W/Y332G) of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) has been recognized to be worth exploring for clinical application in humans as a potential anti <b>cocaine</b> medication.
+BCHE	drug	cocaine	20060817	The catalytic rate constant (k(cat)) and Michaelis Menten constant (K(M)) for ( ) <b>cocaine</b> hydrolysis catalyzed by A199S/S287G/A328W/Y332G <strong>BChE</strong> (without fusion with any other peptide) have been determined to be 3,060 min( 1) and 3.1 microM, respectively, in the present study.
+BCHE	drug	cocaine	20060817	The determined kinetic parameters reveal that the un fused A199S/S287G/A328W/Y332G mutant has a approximately 1,080 fold improved catalytic efficiency (k(cat)/K(M)) against ( ) <b>cocaine</b> compared to the wild type <strong>BChE</strong>.
+BCHE	drug	cocaine	20060817	It has been shown that the A199S/S287G/A328W/Y332G mutations actually decreased the catalytic efficiencies of <strong>BChE</strong> against ATC and BTC, while considerably improving the catalytic efficiency of <strong>BChE</strong> against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	19478136	We previously found that a quadruple mutant <b>cocaine</b> hydrolase derived from human <strong>butyrylcholinesterase</strong> [termed <b>cocaine</b> esterase (CocE)] can suppress or reverse <b>cocaine</b> toxicity and abolish drug primed reinstatement in rats.
+BCHE	addiction	relapse	19478136	We previously found that a quadruple mutant cocaine hydrolase derived from human <strong>butyrylcholinesterase</strong> [termed cocaine esterase (CocE)] can suppress or reverse cocaine toxicity and abolish drug primed <b>reinstatement</b> in rats.
+BCHE	drug	cocaine	18710224	It has been recognized that an ideal anticocaine medication is one that accelerates <b>cocaine</b> metabolism producing biologically inactive metabolites via a route similar to the primary <b>cocaine</b> metabolizing pathway, i.e., <b>cocaine</b> hydrolysis catalyzed by plasma enzyme butyrylcholinesterase (<strong>BChE</strong>).
+BCHE	drug	cocaine	18710224	It has been recognized that an ideal anticocaine medication is one that accelerates <b>cocaine</b> metabolism producing biologically inactive metabolites via a route similar to the primary <b>cocaine</b> metabolizing pathway, i.e., <b>cocaine</b> hydrolysis catalyzed by plasma enzyme <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>).
+BCHE	drug	cocaine	18710224	However, wild type <strong>BChE</strong> has a low catalytic efficiency against the abused <b>cocaine</b>.
+BCHE	drug	cocaine	18710224	The novel computational design approach has led to discovery of the most efficient <b>cocaine</b> hydrolase, i.e., a human <strong>BChE</strong> mutant with an approximately 2000 fold improved catalytic efficiency, promising for therapeutic treatment of <b>cocaine</b> overdose and addiction as an exogenous enzyme in human.
+BCHE	addiction	addiction	18710224	The novel computational design approach has led to discovery of the most efficient cocaine hydrolase, i.e., a human <strong>BChE</strong> mutant with an approximately 2000 fold improved catalytic efficiency, promising for therapeutic treatment of cocaine overdose and <b>addiction</b> as an exogenous enzyme in human.
+BCHE	drug	cocaine	18514640	An albumin <strong>butyrylcholinesterase</strong> for <b>cocaine</b> toxicity and addiction: catalytic and pharmacokinetic properties.
+BCHE	addiction	addiction	18514640	An albumin <strong>butyrylcholinesterase</strong> for cocaine toxicity and <b>addiction</b>: catalytic and pharmacokinetic properties.
+BCHE	drug	cocaine	18514640	Butyrylcholinesterase (<strong>BChE</strong>, EC 3.1.1.8) is important in human <b>cocaine</b> metabolism despite its limited ability to hydrolyze this drug.
+BCHE	drug	cocaine	18514640	<strong>Butyrylcholinesterase</strong> (<strong>BChE</strong>, EC 3.1.1.8) is important in human <b>cocaine</b> metabolism despite its limited ability to hydrolyze this drug.
+BCHE	drug	cocaine	18499092	Human serum butyrylcholinesterase (Hu <strong>BChE</strong>) is a promising therapeutic against the toxicity of chemical warfare nerve agents, pesticide intoxication, and <b>cocaine</b> overdose.
+BCHE	addiction	intoxication	18499092	Human serum butyrylcholinesterase (Hu <strong>BChE</strong>) is a promising therapeutic against the toxicity of chemical warfare nerve agents, pesticide <b>intoxication</b>, and cocaine overdose.
+BCHE	drug	cocaine	18499092	Human serum <strong>butyrylcholinesterase</strong> (Hu <strong>BChE</strong>) is a promising therapeutic against the toxicity of chemical warfare nerve agents, pesticide intoxication, and <b>cocaine</b> overdose.
+BCHE	addiction	intoxication	18499092	Human serum <strong>butyrylcholinesterase</strong> (Hu <strong>BChE</strong>) is a promising therapeutic against the toxicity of chemical warfare nerve agents, pesticide <b>intoxication</b>, and cocaine overdose.
+BCHE	drug	amphetamine	24422652	Also showing promise in animal studies are monoclonal antibodies against cocaine, <b>methamphetamine</b> and phencyclidine, as well as the enhancment of cocaine metabolism with genetic variants of human <strong>butyrylcholinesterase</strong>, using a bacterial esterase or catalytic monoclonal antibodies.
+BCHE	drug	cocaine	24422652	Also showing promise in animal studies are monoclonal antibodies against <b>cocaine</b>, methamphetamine and phencyclidine, as well as the enhancment of <b>cocaine</b> metabolism with genetic variants of human <strong>butyrylcholinesterase</strong>, using a bacterial esterase or catalytic monoclonal antibodies.
+BCHE	drug	cocaine	18292872	Promising agents, such as anti <b>cocaine</b> catalytic antibodies and high activity mutants of human butyrylcholinesterase (<strong>BChE</strong>), for therapeutic treatment of <b>cocaine</b> overdose have been developed through structure and mechanism based design and discovery.
+BCHE	drug	cocaine	18292872	Promising agents, such as anti <b>cocaine</b> catalytic antibodies and high activity mutants of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), for therapeutic treatment of <b>cocaine</b> overdose have been developed through structure and mechanism based design and discovery.
+BCHE	drug	cocaine	18292872	One of the discovered high activity mutants of <strong>BChE</strong> has a approximately 456 fold improved catalytic efficiency against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	18199998	A <b>cocaine</b> hydrolase engineered from human <strong>butyrylcholinesterase</strong> selectively blocks <b>cocaine</b> toxicity and reinstatement of drug seeking in rats.
+BCHE	addiction	relapse	18199998	A cocaine hydrolase engineered from human <strong>butyrylcholinesterase</strong> selectively blocks cocaine toxicity and <b>reinstatement</b> of drug <b>seeking</b> in rats.
+BCHE	drug	cocaine	18199998	Successive rational mutations of human butyrylcholinesterase (<strong>BChE</strong>) followed by fusion to human serum albumin have yielded an efficient hydrolase that offers realistic options for therapy of <b>cocaine</b> overdose and abuse.
+BCHE	drug	cocaine	18199998	Successive rational mutations of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) followed by fusion to human serum albumin have yielded an efficient hydrolase that offers realistic options for therapy of <b>cocaine</b> overdose and abuse.
+BCHE	drug	cocaine	18199998	This albumin <strong>BChE</strong> prevented seizures in rats given a normally lethal <b>cocaine</b> injection (100 mg/kg, i.p.
+BCHE	drug	cocaine	17989928	Reviewed in this article is the state of the art computational design of high activity mutants of human butyrylcholinesterase (<strong>BChE</strong>) against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	17989928	Reviewed in this article is the state of the art computational design of high activity mutants of human <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	17989928	The computational design of <strong>BChE</strong> mutants have been based on not only the structure of the enzyme, but also the detailed catalytic mechanisms for <strong>BChE</strong> catalyzed hydrolysis of ( ) <b>cocaine</b> and (+) <b>cocaine</b>.
+BCHE	drug	cocaine	17989928	By using the computational insights into the catalytic mechanisms, a recently developed unique computational design strategy based on the simulation of the rate determining transition state has been employed to design high activity mutants of human <strong>BChE</strong> for hydrolysis of ( ) <b>cocaine</b>, leading to the exciting discovery of <strong>BChE</strong> mutants with a considerably improved catalytic efficiency against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	17989928	One of the discovered <strong>BChE</strong> mutants (i.e., A199S/S287G/A328W/Y332G) has a approximately 456 fold improved catalytic efficiency against ( ) <b>cocaine</b>.
+BCHE	drug	cocaine	16708286	Site directed mutagenesis of human plasma <strong>butyrylcholinesterase</strong> has led to novel hydrolases that rapidly destroy <b>cocaine</b>.
+BCHE	drug	cocaine	16243302	Visualizing viral transduction of a <b>cocaine</b> hydrolyzing, human <strong>butyrylcholinesterase</strong> in rats.
+BCHE	drug	cocaine	16243302	Human plasma butyrylcholinesterase (<strong>BChE</strong>) is essential for <b>cocaine</b> detoxification even though its catalytic efficiency for that substrate is relatively poor.
+BCHE	drug	cocaine	16243302	Human plasma <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) is essential for <b>cocaine</b> detoxification even though its catalytic efficiency for that substrate is relatively poor.
+BCHE	drug	cocaine	15967428	Intravenous <strong>butyrylcholinesterase</strong> administration and plasma and brain levels of <b>cocaine</b> and metabolites in rats.
+BCHE	drug	cocaine	15967428	<strong>Butyrylcholinesterase</strong> is a major <b>cocaine</b> metabolizing enzyme in humans and other primates, catalyzing hydrolysis to ecgonine methylester.
+BCHE	drug	cocaine	15967428	Increasing <strong>butyrylcholinesterase</strong> activity may be a treatment for <b>cocaine</b> addiction.
+BCHE	addiction	addiction	15967428	Increasing <strong>butyrylcholinesterase</strong> activity may be a treatment for cocaine <b>addiction</b>.
+BCHE	drug	cocaine	15967428	<strong>Butyrylcholinesterase</strong> significantly increased plasma and brain ecgonine methylester levels and decreased <b>cocaine</b> plasma half life from 26.2 min (saline) to 16.4 min (15,000 U).
+BCHE	drug	cocaine	15967428	<strong>Butyrylcholinesterase</strong> had no significant effect on plasma or brain <b>cocaine</b> or benzoylecgonine levels.
+BCHE	drug	cocaine	15967428	These findings suggest that <strong>butyrylcholinesterase</strong> treatment may have benefits in enhancing <b>cocaine</b> metabolism and in increasing levels of ecgonine methylester, which may have a protective action against <b>cocaine</b>.
+BCHE	drug	cocaine	15233592	This is being explored in animals using the natural <b>cocaine</b> metabolising enzyme <strong>butyrylcholinesterase</strong> (or recombinant versions with enhanced capabilities), catalytic antibodies, and passive or active immunisation to produce anti <b>cocaine</b> binding antibodies.
+BCHE	drug	cocaine	10681384	<strong>Butyrylcholinesterase</strong> accelerates <b>cocaine</b> metabolism: in vitro and in vivo effects in nonhuman primates and humans.
+BCHE	drug	cocaine	10681384	Butyrylcholinesterase (<strong>BChE</strong>) is known to metabolize <b>cocaine</b> in humans.
+BCHE	drug	cocaine	10681384	<strong>Butyrylcholinesterase</strong> (<strong>BChE</strong>) is known to metabolize <b>cocaine</b> in humans.
+BCHE	drug	cocaine	10681384	In the present study, three different experiments were performed to determine whether the addition of horse serum derived <strong>BChE</strong> would accelerate the metabolism of <b>cocaine</b>.
+BCHE	drug	cocaine	10681384	In the first experiment, the addition of <strong>BChE</strong> to squirrel monkey plasma in vitro reduced the half life of <b>cocaine</b> by over 80%, decreased the production of the metabolic product benzoylecgonine, and increased ecgonine methyl ester formation.
+BCHE	drug	cocaine	10681384	The effect of <strong>BChE</strong> on <b>cocaine</b> metabolism was reversed by a specific <strong>BChE</strong> inhibitor.
+BCHE	drug	cocaine	10681384	In the second, in vivo, experiment, exogenously administered <strong>BChE</strong> reduced peak <b>cocaine</b> concentrations when given to anesthetized squirrel monkeys.
+BCHE	drug	cocaine	10681384	Finally, incubation of <b>cocaine</b> with added <strong>BChE</strong> in human plasma in vitro resulted in a decrease in <b>cocaine</b> half life similar to that observed with squirrel monkey plasma.
+BCHE	drug	cocaine	10681384	The magnitude of the decrease in <b>cocaine</b> half life was proportional to the amount of added <strong>BChE</strong>.
+BCHE	drug	cocaine	10681384	Together, these results indicate that exogenously administered <strong>BChE</strong> can accelerate <b>cocaine</b> metabolism in such a way as to potentially lessen the behavioral and toxic effects of <b>cocaine</b>.
+BCHE	drug	cocaine	10681384	Therefore, <strong>BChE</strong> may be useful as a treatment for <b>cocaine</b> addiction and toxicity.
+BCHE	addiction	addiction	10681384	Therefore, <strong>BChE</strong> may be useful as a treatment for cocaine <b>addiction</b> and toxicity.
+BCHE	drug	cocaine	10192412	Amitriptyline (AMI) and procainamide (PA) have been reported to inhibit the activity of human plasma <strong>butyrylcholinesterase</strong>, an enzyme important in the metabolic degradation of <b>cocaine</b> (COC) and its ethyl analogue cocaethylene (CE).
+BCHE	drug	cocaine	9882701	An improved <b>cocaine</b> hydrolase: the A328Y mutant of human <strong>butyrylcholinesterase</strong> is 4 fold more efficient.
+BCHE	drug	cocaine	9882701	Butyrylcholinesterase (<strong>BChE</strong>) has a major role in <b>cocaine</b> detoxication.
+BCHE	drug	cocaine	9882701	<strong>Butyrylcholinesterase</strong> (<strong>BChE</strong>) has a major role in <b>cocaine</b> detoxication.
+BCHE	drug	cocaine	9882701	The rate at which human <strong>BChE</strong> hydrolyzes <b>cocaine</b> is slow, with a kcat of 3.9 min( 1) and Km of 14 microM.
+BCHE	drug	cocaine	9882701	<strong>BChE</strong> purified from plasma of cat, horse, and chicken was tested for <b>cocaine</b> hydrolase activity.
+BCHE	drug	cocaine	9882701	Naturally occurring genetic variants of human <strong>BChE</strong> were tested for <b>cocaine</b> hydrolase activity.
+BCHE	drug	cocaine	9882701	The atypical variant (D70G) had a 10 fold lower binding affinity for <b>cocaine</b>, suggesting that persons with the atypical variant of <strong>BChE</strong> may experience severe or fatal <b>cocaine</b> intoxication when administered a dose of <b>cocaine</b> that is not harmful to others.
+BCHE	addiction	intoxication	9882701	The atypical variant (D70G) had a 10 fold lower binding affinity for cocaine, suggesting that persons with the atypical variant of <strong>BChE</strong> may experience severe or fatal cocaine <b>intoxication</b> when administered a dose of cocaine that is not harmful to others.
+BCHE	drug	cocaine	9673783	The influence of plasma <strong>butyrylcholinesterase</strong> concentration on the in vitro hydrolysis of <b>cocaine</b> in human plasma.
+BCHE	drug	cocaine	9673783	In humans, the plasma enzyme butyrylcholinesterase, <strong>BChE</strong> (EC 3.1.1.8), mediates the in vivo plasma hydrolysis of <b>cocaine</b> to the pharmacologically inactive metabolite ecgonine methyl ester, EME.
+BCHE	drug	cocaine	9673783	In humans, the plasma enzyme <strong>butyrylcholinesterase</strong>, <strong>BChE</strong> (EC 3.1.1.8), mediates the in vivo plasma hydrolysis of <b>cocaine</b> to the pharmacologically inactive metabolite ecgonine methyl ester, EME.
+BCHE	drug	cocaine	9673783	<b>Cocaine</b> (2.1 micrograms mL 1) was incubated in plasma with a <strong>BChE</strong> concentration in the normal range (3.02 micrograms mL 1) and in plasma with enhanced <strong>BChE</strong> concentrations of 9.14, 20.8 and 37.8 micrograms mL 1, respectively for time periods up to 120 min.
+BCHE	drug	cocaine	9673783	The enhancement of plasma <strong>BChE</strong> concentration resulted in a dramatic increase in the rate of hydrolysis of <b>cocaine</b>.
+BCHE	drug	cocaine	9673783	Accordingly, the half life of <b>cocaine</b> in plasma decreased significantly with enhanced <strong>BChE</strong> concentration.
+BCHE	drug	cocaine	9673783	The marked reduction in <b>cocaine</b> half life provides evidence supporting the potential therapeutic use of <strong>BChE</strong> for the treatment of <b>cocaine</b> intoxication.
+BCHE	addiction	intoxication	9673783	The marked reduction in cocaine half life provides evidence supporting the potential therapeutic use of <strong>BChE</strong> for the treatment of cocaine <b>intoxication</b>.
+BCHE	drug	cocaine	26734822	<strong>Butyrylcholinesterase</strong>: an enzyme antidote for <b>cocaine</b> intoxication.
+BCHE	addiction	intoxication	26734822	<strong>Butyrylcholinesterase</strong>: an enzyme antidote for cocaine <b>intoxication</b>.
+BCHE	drug	cocaine	26734822	Since the primary route of <b>cocaine</b> inactivation is enzymatic degradation by butyrylcholinesterase (<strong>BChE</strong>), we sought to determine if the administration of purified human enzyme would ameliorate the lethal effects of <b>cocaine</b>.
+BCHE	drug	cocaine	26734822	Since the primary route of <b>cocaine</b> inactivation is enzymatic degradation by <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>), we sought to determine if the administration of purified human enzyme would ameliorate the lethal effects of <b>cocaine</b>.
+BCHE	drug	cocaine	26734822	While the cardiovascular, autonomic or central nervous systems were unaffected by <strong>BChE</strong>, the enzyme reduced the adverse effects of <b>cocaine</b> including hypertension, hyperactivity and convulsions.
+BCHE	drug	cocaine	26734822	<strong>BChE</strong> decreased both the brain and blood levels of <b>cocaine</b> and shifted the metabolites towards the production of the inactive product ecgonine methyl ester and away from the physiologically active metabolites, norcocaine and benzoylecgonine.
+BCHE	drug	cocaine	26734822	We conclude that <strong>BChE</strong> would appear to be an ideal antidote in the treatment of <b>cocaine</b> intoxication and has potential therapeutic application.
+BCHE	addiction	intoxication	26734822	We conclude that <strong>BChE</strong> would appear to be an ideal antidote in the treatment of cocaine <b>intoxication</b> and has potential therapeutic application.
+BCHE	drug	cocaine	9266811	Therapeutic use of <strong>butyrylcholinesterase</strong> for <b>cocaine</b> intoxication.
+BCHE	addiction	intoxication	9266811	Therapeutic use of <strong>butyrylcholinesterase</strong> for cocaine <b>intoxication</b>.
+BCHE	drug	cocaine	9266811	In humans, decreased levels of butyrylcholinesterase (<strong>BChE</strong>) (EC 3.1.1.8) have been associated with sustained effects of <b>cocaine</b> and life threatening complications.
+BCHE	drug	cocaine	9266811	In humans, decreased levels of <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) (EC 3.1.1.8) have been associated with sustained effects of <b>cocaine</b> and life threatening complications.
+BCHE	drug	cocaine	9266811	Administration of purified human <strong>BChE</strong> has previously been demonstrated to protect against <b>cocaine</b> associated cardiovascular toxicity in rats.
+BCHE	drug	cocaine	9266811	Plasma and brain concentrations of <b>cocaine</b> were lowered by 80% after <strong>BChE</strong> administration.
+BCHE	drug	cocaine	9266811	<b>Cocaine</b> associated effects upon the central nervous system were also shown to be reduced by administration of <strong>BChE</strong> to conscious rats.
+BCHE	drug	cocaine	9266811	Furthermore, our studies in the cat have also shown that purified <strong>BChE</strong> shifts the metabolic profile of <b>cocaine</b> (1 mg/kg) to the pharmacologically inactive products ecgonine methylester and ecgonine.
+BCHE	drug	cocaine	9266811	Pretreatment with <strong>BChE</strong> (0.27, 1.0, and 10.0 mg/kg) ameliorated the hypertensive effects of <b>cocaine</b> (1 mg/kg) by reducing the duration and the extent of BP elevation by 66%.
+BCHE	drug	cocaine	9266811	These results suggest that <strong>BChE</strong> could be an effective and rapid therapy for the treatment of life threatening <b>cocaine</b> induced cardiovascular effects in human while clearing the total body burden of <b>cocaine</b>.
+BCHE	drug	cocaine	9266810	<b>Cocaine</b> detoxification by human plasma <strong>butyrylcholinesterase</strong>.
+BCHE	drug	cocaine	9266810	The ability of human plasma butyrylcholinesterase (<strong>BChE</strong>) to detoxify <b>cocaine</b> in vivo was evaluated.
+BCHE	drug	cocaine	9266810	The ability of human plasma <strong>butyrylcholinesterase</strong> (<strong>BChE</strong>) to detoxify <b>cocaine</b> in vivo was evaluated.
+BCHE	drug	cocaine	9266810	Pretreatment of chloralose urethane anesthetized rats with <strong>BChE</strong>, 0.1 7.8 mg/kg, decreased the hypertensive and arrhythmogenic effects produced by <b>cocaine</b> and increased the lethal dose of <b>cocaine</b> by three  to fourfold.
+BCHE	drug	cocaine	9266810	Treatment of conscious rats with 1 and 10 mg/kg <strong>BChE</strong> decreased the incidence of seizures and deaths produced by a prior dose of <b>cocaine</b> (80 mg/kg, i.p.).
+BCHE	drug	cocaine	9266810	These results suggest that <strong>BChE</strong> would provide a safe and highly efficacious treatment for <b>cocaine</b> intoxication.
+BCHE	addiction	intoxication	9266810	These results suggest that <strong>BChE</strong> would provide a safe and highly efficacious treatment for cocaine <b>intoxication</b>.
+JUNB	drug	cocaine	32457073	We identified 133 genes differentially expressed between CUD case patients and <b>cocaine</b> free control subjects, including previously implicated candidates for <b>cocaine</b> use/addiction (FOSB, ARC, KCNJ9/GIRK3, NR4A2, <strong>JUNB</strong>, and MECP2).
+JUNB	addiction	addiction	32457073	We identified 133 genes differentially expressed between CUD case patients and cocaine free control subjects, including previously implicated candidates for cocaine use/<b>addiction</b> (FOSB, ARC, KCNJ9/GIRK3, NR4A2, <strong>JUNB</strong>, and MECP2).
+JUNB	drug	cocaine	28710498	In particular, we identified an <strong>AP 1</strong> regulated transcriptional network in dlPFC neurons associated with <b>cocaine</b> use disorder that contains several differentially expressed hub genes.
+JUNB	drug	opioid	23238466	Among them, a cluster of 8 genes, including 6 inducible transcription factors (c fos, fra 2, <strong>junB</strong>, zif268 (egr1), egr2, NGFI B) and 2 effector IEG (arc and mkp1) seemed to be regulated in concert in response to <b>morphine</b>.
+JUNB	drug	alcohol	22020770	To our surprise, the impairment of <strong>AP 1</strong> activation was sufficient to mediate a severe and dose dependent phenotype in human monocytes in vitro at <b>alcohol</b> concentrations as low as 0.16% (or 26 mM).
+JUNB	drug	alcohol	21338584	Prodynorphin promoter SNP associated with <b>alcohol</b> dependence forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+JUNB	addiction	dependence	21338584	Prodynorphin promoter SNP associated with alcohol <b>dependence</b> forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+JUNB	drug	amphetamine	21229349	Acute injection of <b>METH</b> increased c fos, fosB, fra2, <strong>junB</strong>, Egr1 3, Nr4a1 (Nur77), and Nr4a3 (Nor 1) mRNA levels in the striatum of saline pretreated rats.
+JUNB	drug	alcohol	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after <b>ethanol</b> withdrawal.
+JUNB	addiction	withdrawal	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after ethanol <b>withdrawal</b>.
+JUNB	drug	cocaine	18991842	We found that the composition of <strong>AP 1</strong> transcription complexes and expression levels of <strong>AP 1</strong> complexes, and several transcription factors, neurotransmitter receptors as well as intracellular signaling molecules following repeated <b>cocaine</b> administration are altered in Fos deficient brains.
+JUNB	drug	cocaine	18355967	These results indicate that <strong>AP 1</strong> suppresses this behavioral response to <b>cocaine</b>.
+JUNB	drug	opioid	18184800	In contrast to PENK, no association was detected between PDYN genotype (68 bp repeat element containing one to four copies of <strong>AP 1</strong> binding sites in the promoter region) and <b>heroin</b> abuse, although there was a clear functional association with striatal PDYN mRNA expression: an increased number of inducible repeats (three and four) correlated with higher PDYN levels than adult or fetal subjects with noninducible (one and two) alleles.
+JUNB	drug	alcohol	17851539	<b>Alcohol</b> relapse induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+JUNB	addiction	relapse	17851539	Alcohol <b>relapse</b> induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+JUNB	drug	alcohol	17127267	Recent findings indicate that low concentrations of <b>ethanol</b> (10 mM) promote inflammatory processes in brain and in glial cells by up regulating cytokines and inflammatory mediators (iNOS, NO, COX 2), and by activating signaling pathways (IKK, MAPKs) and transcriptional factors (NF kappaB, <strong>AP 1</strong>) implicated in inflammatory injury.
+JUNB	drug	amphetamine	16855532	Forty three genes exhibited significant differences in expression in HR vs LR 24 h after <b>METH</b> treatment including a group of immediate early genes (IEGs) (eg, c fos, <strong>junB</strong>, NGFI B, serum regulated glucocorticoid kinase).
+JUNB	drug	cocaine	16263220	SL327 pre treatment, however, reduces the DNA binding activity of the activator protein 1 complex induced six hours after an acute <b>cocaine</b> treatment as well as one hour after the last of the chronic <b>cocaine</b> injections, a phenomenon that results from the concomitant reduction of all <b>cocaine</b> induced proteins (c Fos, FosB, deltaFosB, <strong>JunB</strong>).
+JUNB	drug	cocaine	16115217	The patterns of <b>cocaine</b> induced c Fos, <strong>JunB</strong> and Zif268 protein expression were investigated, using an immunohistochemical approach, within distinct nuclei of the amygdala, either in the presence or absence of a selective inhibitor of the ERK pathway, SL327.
+JUNB	drug	cocaine	16115217	In particular, whereas c Fos and <strong>JunB</strong> expressions were augmented following chronic <b>cocaine</b> treatment, as compared with acute treatment, Zif268 expression was decreased by this chronic treatment.
+JUNB	drug	cocaine	16115217	Additionally, chronic blocking of ERK activation affected <b>cocaine</b> induced c Fos and <strong>JunB</strong> but not Zif268 expression.
+JUNB	drug	amphetamine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of <b>amphetamine</b> or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUNB	drug	cocaine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or <b>cocaine</b> (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUNB	addiction	addiction	15814102	In order to approach the astroglial implication of <b>addictive</b> and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUNB	addiction	dependence	15814102	Because astrocytes interact extensively with the neurons in the brain, our data led us to conclude that oxidation regulated <strong>AP 1</strong> target genes may represent one of the molecular mechanisms underlying neuronal adaptation associated with psychostimulant <b>dependence</b>.
+JUNB	drug	cocaine	15770241	These results suggest that genes encoding certain extracellular factors, membrane receptors and modulators, and intracellular signaling molecules, among others, are regulated by <b>cocaine</b> via the D1 receptor, and these <strong>AP 1</strong> transcription complex regulated genes might contribute to persistent <b>cocaine</b> induced behavioral changes.
+JUNB	drug	amphetamine	15680202	Ginsenosides attenuate <b>methamphetamine</b> induced behavioral side effects in mice via activation of adenosine A2A receptors: possible involvements of the striatal reduction in <strong>AP 1</strong> DNA binding activity and proenkephalin gene expression.
+JUNB	drug	cocaine	15464827	<b>Cocaine</b> induced behavioral effects (hyperlocomotion and CPP) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+JUNB	addiction	reward	15464827	Cocaine induced behavioral effects (hyperlocomotion and <b>CPP</b>) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+JUNB	drug	opioid	15287893	Activation of <strong>AP 1</strong> and CRE dependent gene expression via mu <b>opioid</b> receptor.
+JUNB	drug	opioid	15287893	Transcription factors Ca2+/cAMP responsive element binding protein (CREB) and activator protein 1 (<strong>AP 1</strong>) may constitute a direct link between the <b>opioid</b> regulated signal transduction pathways and modulation of gene expression.
+JUNB	drug	opioid	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during withdrawal from the <b>opioid</b>.
+JUNB	addiction	withdrawal	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during <b>withdrawal</b> from the opioid.
+JUNB	drug	alcohol	14576487	The injurious effects of <b>ethanol</b> on the pancreas may be mediated through (1) sensitization of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) sensitization of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+JUNB	addiction	sensitization	14576487	The injurious effects of ethanol on the pancreas may be mediated through (1) <b>sensitization</b> of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) <b>sensitization</b> of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+JUNB	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for <strong>AP 1</strong> in the NAc: the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+JUNB	drug	cocaine	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying <b>cocaine</b> addiction.
+JUNB	addiction	addiction	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying cocaine <b>addiction</b>.
+JUNB	drug	amphetamine	12504868	In addition, DNA binding activities of NF kappaB, <strong>AP 1</strong>, and CREB in the frontal cortex and hippocampus were more pronounced in mice injected with Tat plus <b>METH</b> compared to the effects of Tat or <b>METH</b> alone.
+JUNB	drug	alcohol	12482856	Up regulation of CD14 in liver caused by acute <b>ethanol</b> involves oxidant dependent <strong>AP 1</strong> pathway.
+JUNB	drug	alcohol	12482856	Additionally, overexpression of SOD also blunted <b>ethanol</b> induced activation of redox sensitive transcription factors NFkappaB and <strong>AP 1</strong> and production of cytokines.
+JUNB	drug	alcohol	12482856	However, only inhibition of <strong>AP 1</strong> with dominant negative TAK1 but not NFkappaB by dominant negative IkappaBalpha significantly blunted <b>ethanol</b> induced increases in CD14, suggesting that <strong>AP 1</strong> is important for CD14 transcriptional regulation.
+JUNB	drug	amphetamine	12112395	Similarly, in the second experiment it was found that the D1R dependent induction by <b>AMPH</b> of Fos, FosB, and <strong>JunB</strong>, but not NGFI A, in the NAc was enhanced in rats exposed 1 week earlier to repeated VTA <b>AMPH</b>.
+JUNB	drug	alcohol	12045006	Chronic <b>alcohol</b> intoxication was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+JUNB	addiction	intoxication	12045006	Chronic alcohol <b>intoxication</b> was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+JUNB	drug	alcohol	12045006	Chronic <b>ethanol</b> feeding significantly enhanced MNP 1 binding, but not those of NF kappaB and <strong>AP 1</strong> in endothelial cells.
+JUNB	drug	opioid	11605942	Activation of mu <b>opioid</b> receptor induces expression of c fos and <strong>junB</strong> via mitogen activated protein kinase cascade.
+JUNB	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induced c fos and <strong>junB</strong> messenger RNAs, which were inhibited by pretreatment of the cells with pertussis toxin and PD98059, an inhibitor of extracellular signal regulated kinase cascade.
+JUNB	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induces c fos and <strong>junB</strong> expression and elevates AP 1 mediated transcriptional activities via the mitogen activated protein kinase cascade.
+JUNB	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induces c fos and <strong>junB</strong> expression and elevates <strong>AP 1</strong> mediated transcriptional activities via the mitogen activated protein kinase cascade.
+JUNB	drug	nicotine	10555165	The influence of <b>nicotine</b> on the expression of Fos family proteins, which specifically formed complexes with the <strong>AP 1</strong> sequence, was assessed.
+JUNB	drug	nicotine	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during <b>nicotine</b> dependence.
+JUNB	addiction	dependence	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during nicotine <b>dependence</b>.
+JUNB	drug	nicotine	10320004	The effects of acute and chronic <b>nicotine</b> treatment on activator protein 1 (<strong>AP 1</strong>) gene transcription factor binding activity in the rat cortex were investigated.
+JUNB	drug	nicotine	10320004	It was observed that 1 h after acute <b>nicotine</b> treatment (single injection) <strong>AP 1</strong> DNA binding activity was significantly increased in the rat cortex.
+JUNB	drug	nicotine	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of <b>nicotine</b> withdrawal after repeated <b>nicotine</b> treatment (10 days).
+JUNB	addiction	withdrawal	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of nicotine <b>withdrawal</b> after repeated nicotine treatment (10 days).
+JUNB	drug	nicotine	10320004	However, at 18 and 24 h of <b>nicotine</b> withdrawal after 10 days of <b>nicotine</b> treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+JUNB	addiction	withdrawal	10320004	However, at 18 and 24 h of nicotine <b>withdrawal</b> after 10 days of nicotine treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+JUNB	drug	nicotine	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to <b>nicotine</b> dependence.
+JUNB	addiction	dependence	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to nicotine <b>dependence</b>.
+JUNB	drug	amphetamine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered Fos like proteins in brain by chronic cocaine and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on <b>methamphetamine</b> induced stereotypy in mice, Jpn.
+JUNB	drug	cocaine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered Fos like proteins in brain by chronic <b>cocaine</b> and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on methamphetamine induced stereotypy in mice, Jpn.
+JUNB	drug	alcohol	9918601	This investigation examined the effects of acute and chronic <b>ethanol</b> exposure and its withdrawal on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+JUNB	addiction	withdrawal	9918601	This investigation examined the effects of acute and chronic ethanol exposure and its <b>withdrawal</b> on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+JUNB	drug	alcohol	9918601	It was observed that acute <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+JUNB	addiction	withdrawal	9918601	It was observed that acute ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+JUNB	drug	alcohol	9918601	It was also found that chronic <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+JUNB	addiction	withdrawal	9918601	It was also found that chronic ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+JUNB	drug	cocaine	9668659	<b>Cocaine</b> and the <strong>AP 1</strong> transcription factor complex.
+JUNB	drug	cocaine	9668659	We presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain
+JUNB	drug	cocaine	29090793	<b>Cocaine</b> and the <strong>AP 1</strong> Transcription Factor Complex.
+JUNB	drug	cocaine	29090793	We are presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain.
+JUNB	drug	alcohol	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during <b>ethanol</b> withdrawal.
+JUNB	addiction	withdrawal	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during ethanol <b>withdrawal</b>.
+JUNB	drug	alcohol	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during <b>ethanol</b> withdrawal.
+JUNB	addiction	withdrawal	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during ethanol <b>withdrawal</b>.
+JUNB	addiction	withdrawal	9202324	The AP 1 DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of FosB, c Jun, <strong>JunB</strong>, and JunD.
+JUNB	addiction	withdrawal	9202324	The <strong>AP 1</strong> DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of FosB, c Jun, <strong>JunB</strong>, and JunD.
+JUNB	addiction	withdrawal	9202324	<b>Withdrawal</b> severity did not affect the composition of the <strong>AP 1</strong> DNA binding activities.
+JUNB	drug	amphetamine	9070635	Thus, <b>amphetamine</b> sensitization is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+JUNB	addiction	sensitization	9070635	Thus, amphetamine <b>sensitization</b> is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+JUNB	drug	amphetamine	8962158	We show here that deletion of the D1 dopamine receptor produces a neural phenotype in which <b>amphetamine</b> and cocaine, two addictive psychomotor stimulants, can no longer stimulate neurons in the striatum to express cFos or <strong>JunB</strong> or to regulate dynorphin.
+JUNB	drug	cocaine	8962158	We show here that deletion of the D1 dopamine receptor produces a neural phenotype in which amphetamine and <b>cocaine</b>, two addictive psychomotor stimulants, can no longer stimulate neurons in the striatum to express cFos or <strong>JunB</strong> or to regulate dynorphin.
+JUNB	addiction	addiction	8962158	We show here that deletion of the D1 dopamine receptor produces a neural phenotype in which amphetamine and cocaine, two <b>addictive</b> psychomotor stimulants, can no longer stimulate neurons in the striatum to express cFos or <strong>JunB</strong> or to regulate dynorphin.
+JUNB	drug	cocaine	8959019	However, the induction of the chronic <strong>AP 1</strong> complex and the chronic Fras provides a mechanism capable of underlying long lasting alterations in gene expression following chronic <b>cocaine</b> treatment.
+JUNB	drug	opioid	8843097	A mu receptor <b>opioid</b> agonist induces <strong>AP 1</strong> and NF kappa B transcription factor activity in primary cultures of rat cortical neurons.
+JUNB	drug	opioid	8843097	The specific mu receptor <b>opioid</b> agonist, Tyr, D Ala2, Gly, N Me Phe4, Gly ol5 (DAMGO), was found to increase <strong>AP 1</strong> and NF kappa B activity in primary cultures of neurons from rat cerebral cortex.
+JUNB	drug	opioid	8843097	Acute (2 h, 4 h) and long term (72 h) treatment with DAMGO time dependently increased the DNA binding activity of both <strong>AP 1</strong> and NF kappa B and the stimulation could be abolished or inhibited by concurrent incubation with <b>naloxone</b>.
+JUNB	drug	opioid	8843097	However, acute <b>naloxone</b> precipitated withdrawal did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+JUNB	addiction	withdrawal	8843097	However, acute naloxone precipitated <b>withdrawal</b> did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+JUNB	drug	opioid	8843097	These results indicate a mu <b>opioid</b> receptor related co induction of <strong>AP 1</strong> and NF kappa B transcription factors in cultured cortical neurons.
+JUNB	drug	opioid	8609891	After 5 days of <b>morphine</b> treatment, we observed increased levels of the chronic Fras and of <strong>AP 1</strong> binding activity in rat striatum and nucleus accumbens, effects that were not seen in most other brain regions that we studied.
+JUNB	drug	opioid	7755894	NMDA and D1 receptors mediate induction of c fos and <strong>junB</strong> genes in striatum following <b>morphine</b> administration: implications for studies of memory.
+JUNB	drug	opioid	7755894	The c fos and <strong>junB</strong> immediate early genes (IEGs) were induced in neurons of the medial and ventral striatum following administration of <b>morphine</b>.
+JUNB	drug	opioid	7755894	The striatal induction of c fos and <strong>junB</strong> mRNA and Fos protein was blocked by <b>naloxone</b>, the D1 dopamine (DA) receptor antagonists, SCH23390 and SCH39166, and the N methyl D aspartate (NMDA) glutamate receptor antagonist, MK801.
+JUNB	drug	opioid	7755894	SCH23390 and MK801 did not block <b>morphine</b> induction of c fos and <strong>junB</strong> in septum.
+JUNB	drug	amphetamine	7755894	Since the pattern of the morphine induction of c fos and <strong>junB</strong> in striatum and nucleus accumbens was similar to that observed with cocaine and <b>amphetamine</b> [2,18,45,51], these data support current concepts that limbic striatum and nucleus accumbens are among the brain regions that mediate drug abuse [9,10,23,27,49].
+JUNB	drug	cocaine	7755894	Since the pattern of the morphine induction of c fos and <strong>junB</strong> in striatum and nucleus accumbens was similar to that observed with <b>cocaine</b> and amphetamine [2,18,45,51], these data support current concepts that limbic striatum and nucleus accumbens are among the brain regions that mediate drug abuse [9,10,23,27,49].
+JUNB	drug	opioid	7755894	Since the pattern of the <b>morphine</b> induction of c fos and <strong>junB</strong> in striatum and nucleus accumbens was similar to that observed with cocaine and amphetamine [2,18,45,51], these data support current concepts that limbic striatum and nucleus accumbens are among the brain regions that mediate drug abuse [9,10,23,27,49].
+JUNB	drug	opioid	7838131	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal, a model of <b>opioid</b> dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUNB	addiction	dependence	7838131	Naloxone precipitated morphine withdrawal, a model of opioid <b>dependence</b>, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUNB	addiction	withdrawal	7838131	Naloxone precipitated morphine <b>withdrawal</b>, a model of opioid dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUNB	addiction	withdrawal	7838131	<strong>AP 1</strong> DNA binding activity and dimer composition also exhibited regulation after <b>withdrawal</b>, presumably as a result of both transcriptional and post translational events.
+JUNB	drug	opioid	7838131	Thus, <b>morphine</b> dependence results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+JUNB	addiction	dependence	7838131	Thus, morphine <b>dependence</b> results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+JUNB	drug	cocaine	7969045	One early cellular response to <b>cocaine</b> administration is a brain region specific alteration in the transcriptional pattern of immediate early genes belonging to the Fos/Jun family of nucleotide sequence specific [activator protein 1 (<strong>AP 1</strong>)] DNA binding proteins.
+JUNB	drug	cocaine	7969045	The work described here compares <b>cocaine</b> induced transcriptional regulation of immediate early gene mRNA levels, as well as <strong>AP 1</strong> DNA binding activity, within the striatum and cerebellum.
+JUNB	drug	cocaine	7969045	Gel retention analysis using antibodies to the various Fos and Jun proteins was used to characterize <b>cocaine</b> dependent alterations in the composition of striatal and cerebellar <strong>AP 1</strong> DNA binding complexes.
+JUNB	drug	cocaine	7969045	In striatum, <b>cocaine</b> increases the relative levels of c Fos, Fos B, Jun B, and Jun D proteins that bind the <strong>AP 1</strong> DNA sequence element, whereas in the cerebellum only c Fos and Jun D binding activities are increased.
+JUNB	drug	opioid	8078918	<b>Morphine</b> induces c fos and <strong>junB</strong> in striatum and nucleus accumbens via D1 and N methyl D aspartate receptors.
+JUNB	drug	opioid	8078918	<b>Morphine</b> induced the c fos and <strong>junB</strong> immediate early genes in neurons of the medial and ventral striatum and nucleus accumbens.
+JUNB	drug	opioid	8078918	Induction of c fos and <strong>junB</strong> mRNA and Fos protein was blocked by <b>naloxone</b>, the D1 dopamine (DA) receptor antagonists SCH23390 and SCH39166, and the N methyl D aspartate (NMDA) glutamate receptor antagonist MK801.
+JUNB	drug	opioid	8078918	SCH23390 attenuated <b>morphine</b> induction of AP 1 binding in striatum, suggesting that c fos and <strong>junB</strong> contribute to AP 1 binding.
+JUNB	drug	opioid	8078918	SCH23390 attenuated <b>morphine</b> induction of <strong>AP 1</strong> binding in striatum, suggesting that c fos and <strong>junB</strong> contribute to <strong>AP 1</strong> binding.
+JUNB	drug	opioid	8078918	SCH23390 and MK801 did not block <b>morphine</b> induction of c fos and <strong>junB</strong> in septum.
+JUNB	drug	amphetamine	8078918	Since the morphine induction of c fos and <strong>junB</strong> in striatum and nucleus accumbens (NA) was similar to that observed with cocaine and <b>amphetamine</b>, these data support current concepts that limbic striatum and NA are among the brain regions that mediate drug abuse.
+JUNB	drug	cocaine	8078918	Since the morphine induction of c fos and <strong>junB</strong> in striatum and nucleus accumbens (NA) was similar to that observed with <b>cocaine</b> and amphetamine, these data support current concepts that limbic striatum and NA are among the brain regions that mediate drug abuse.
+JUNB	drug	opioid	8078918	Since the <b>morphine</b> induction of c fos and <strong>junB</strong> in striatum and nucleus accumbens (NA) was similar to that observed with cocaine and amphetamine, these data support current concepts that limbic striatum and NA are among the brain regions that mediate drug abuse.
+JUNB	addiction	reward	8078918	Furthermore, since DA and NMDA receptors may mediate opiate <b>reward</b> and opiate induction of c fos and <strong>junB</strong>, the DA/NMDA regulation of c fos and <strong>junB</strong> and their target genes may produce long term changes in the striatal and NA circuits that contribute to opiate drug abuse.
+JUNB	drug	amphetamine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with <b>methamphetamine</b>, cocaine and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of <b>methamphetamine</b> and cocaine, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+JUNB	drug	cocaine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, <b>cocaine</b> and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and <b>cocaine</b>, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+JUNB	drug	opioid	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, cocaine and <b>morphine</b>: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and cocaine, 2) CRE binding activity was decreased by chronic <b>morphine</b> treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic <b>morphine</b> treatment in the mouse cerebellum.
+JUNB	drug	alcohol	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during <b>ethanol</b> withdrawal.
+JUNB	addiction	withdrawal	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during ethanol <b>withdrawal</b>.
+JUNB	drug	alcohol	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing <b>ethanol</b> withdrawal.
+JUNB	addiction	withdrawal	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing ethanol <b>withdrawal</b>.
+JUNB	drug	alcohol	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>ethanol</b> withdrawal.
+JUNB	addiction	withdrawal	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after ethanol <b>withdrawal</b>.
+JUNB	drug	alcohol	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of <b>ethanol</b> withdrawal.
+JUNB	addiction	withdrawal	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of ethanol <b>withdrawal</b>.
+JUNB	addiction	withdrawal	8974322	Gel shift assays indicated the formation of <strong>AP 1</strong> binding factors in nuclear extracts of the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>withdrawal</b>.
+JUNB	drug	cocaine	1631058	Regulation of immediate early gene expression and <strong>AP 1</strong> binding in the rat nucleus accumbens by chronic <b>cocaine</b>.
+JUNB	drug	cocaine	1631058	We therefore examined changes in the mRNA levels for the IEGs c fos, c jun, fosB, <strong>junB</strong>, and zif268 in the NAc of rats treated acutely and chronically with <b>cocaine</b>.
+JUNB	drug	cocaine	1631058	As would be expected from the RNA data and immunohistochemistry, acute <b>cocaine</b> administration increased <strong>AP 1</strong> binding activity in the NAc, an effect that reverted completely to control levels within 8 12 hr.
+JUNB	drug	cocaine	1631058	In contrast, <strong>AP 1</strong> binding activity in the NAc of animals treated chronically with <b>cocaine</b> remained elevated at acute levels 18 hr after the last chronic injection, a time at which c fos and c jun mRNA levels and Fos like immunoreactivity had returned to control values.
+JUNB	drug	cocaine	1631058	An additional acute <b>cocaine</b> challenge did not further increase <strong>AP 1</strong> binding.
+JUNB	drug	cocaine	1631058	The data suggest that chronic <b>cocaine</b> treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of <b>cocaine</b> addiction.
+JUNB	addiction	addiction	1631058	The data suggest that chronic cocaine treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of cocaine <b>addiction</b>.
+GRIN2A	drug	cocaine	32751823	We found an up regulation of the accumbal levels of GluN1 and <strong>GluN2A</strong> following <b>cocaine</b> self administration that was paralleled by an increase of Munc13 and RIM1 levels.
+GRIN2A	drug	opioid	32032749	To explore the potential mechanism of <b>heroin</b> dependence, this study examined changes in the expression levels of NR2 subunits <strong>NR2A</strong> D in the prelimbic (PL) region of the medial prefrontal cortex (mPFC) after repeated <b>heroin</b> administration and subsequent abstinence.
+GRIN2A	addiction	dependence	32032749	To explore the potential mechanism of heroin <b>dependence</b>, this study examined changes in the expression levels of NR2 subunits <strong>NR2A</strong> D in the prelimbic (PL) region of the medial prefrontal cortex (mPFC) after repeated heroin administration and subsequent abstinence.
+GRIN2A	drug	opioid	32032749	Western blotting and qRT PCR revealed no differences in <strong>NR2A</strong> subunit expression among <b>heroin</b> exposure, <b>heroin</b> withdrawal, and control group rats; in contrast, expression of NR2B was significantly higher in the <b>heroin</b> exposure group, whereas expression levels of NR2C and NR2D were significantly higher in the <b>heroin</b> withdrawal group relative to the controls.
+GRIN2A	addiction	withdrawal	32032749	Western blotting and qRT PCR revealed no differences in <strong>NR2A</strong> subunit expression among heroin exposure, heroin <b>withdrawal</b>, and control group rats; in contrast, expression of NR2B was significantly higher in the heroin exposure group, whereas expression levels of NR2C and NR2D were significantly higher in the heroin <b>withdrawal</b> group relative to the controls.
+GRIN2A	drug	alcohol	31978422	Results showed that the mRNA levels of <strong>GluN2A</strong> but not GluN1 in NAc are higher after <b>ethanol</b> CPP.
+GRIN2A	addiction	reward	31978422	Results showed that the mRNA levels of <strong>GluN2A</strong> but not GluN1 in NAc are higher after ethanol <b>CPP</b>.
+GRIN2A	drug	opioid	31941720	<strong>NR2A</strong> NMDA receptor blockade reverses the lack of <b>morphine</b> analgesia without affecting chronic pain status in fibromyalgia like mouse model.
+GRIN2A	drug	opioid	31941720	On the other hand, the lack of <b>morphine</b> analgesia was abolished in <strong>NR2A</strong> NMDA receptor KO (<strong>NR2A</strong> / ) mice, and blocked by intracerebroventricular (i.c,v,) injection of (R) CPP, an <strong>NR2A</strong> antagonist or by microinjection of siRNA for <strong>NR2A</strong> into PAG region, while no change was observed with Ro 04 5595, an NR2B antagonist (i.c.v.).
+GRIN2A	addiction	reward	31941720	On the other hand, the lack of morphine analgesia was abolished in <strong>NR2A</strong> NMDA receptor KO (<strong>NR2A</strong> / ) mice, and blocked by intracerebroventricular (i.c,v,) injection of (R) <b>CPP</b>, an <strong>NR2A</strong> antagonist or by microinjection of siRNA for <strong>NR2A</strong> into PAG region, while no change was observed with Ro 04 5595, an NR2B antagonist (i.c.v.).
+GRIN2A	drug	opioid	31941720	All these results suggest that chronic pain status and lack of <b>morphine</b> analgesia are independent to each other, and the lack of <b>morphine</b> analgesia is mediated by an activation of <strong>NR2A</strong> NMDA receptor system.
+GRIN2A	drug	alcohol	31473305	However, we observed a correlation of α1 and γ2 subunits induced by taurine, while in the <b>alcohol</b> group there was a correlation between α4 and <strong>GluN2A</strong>.
+GRIN2A	drug	alcohol	31473305	In the group treated with <b>alcohol</b> and taurine, we observed an extra correlation, between α1 and <strong>GluN2A</strong>.
+GRIN2A	addiction	withdrawal	31473305	After 5 days of <b>withdrawal</b>, a correlation observed in the control group, between δ and <strong>GluN2A</strong>, was reestablished.
+GRIN2A	drug	cocaine	31361029	Activation of GSK3β induced by recall of <b>cocaine</b> reward memories is dependent on <strong>GluN2A</strong>/B NMDA receptor signaling.
+GRIN2A	addiction	reward	31361029	Activation of GSK3β induced by recall of cocaine <b>reward</b> memories is dependent on <strong>GluN2A</strong>/B NMDA receptor signaling.
+GRIN2A	drug	cocaine	31361029	Administration of the <strong>GluN2A</strong>  and GluN2B NMDA receptor antagonists, NVP AAM077 and ifenprodil, respectively, immediately following recall abrogated an established <b>cocaine</b> place preference, while preventing the activation of GSK3β in the amygdala, nucleus accumbens, and hippocampus during <b>cocaine</b> memory reactivation.
+GRIN2A	addiction	intoxication	31056842	Memory and plasticity impairment after <b>binge</b> drinking in adolescent rat hippocampus: <strong>GluN2A</strong>/GluN2B NMDA receptor subunits imbalance through HDAC2.
+GRIN2A	addiction	intoxication	31056842	In conclusion, the memory impairing effects of two <b>binge</b> like EtOH exposure involve NMDA receptor dependent LTD deficits due to a <strong>GluN2A</strong>/GluN2B imbalance resulting from changes in GluN2B expression induced by HDAC2.
+GRIN2A	addiction	withdrawal	30733663	We then analyzed the expression levels of presynaptic (vGlut1, vGlut2, CB1 receptor, synaptophysin) and postsynaptic (PSD95, GluN1, <strong>GluN2A</strong>, GluN2B, GluA1, GluA2, mGluR1 and mGluR5) proteins after 7 days EtOH incubation or after EtOH <b>withdrawal</b>.
+GRIN2A	drug	cocaine	30165076	Injection of GSK J4 selectively reversed this <b>cocaine</b> induced increase of <strong>NR2A</strong> expression and synaptic function, suggesting that mal adaptation of <b>cocaine</b> induced synaptic plasticity in mPFC largely underlies KDM6B mediated <b>cocaine</b> associated memory.
+GRIN2A	drug	cocaine	30144237	In <b>cocaine</b> naïve animals, SERT removal led to reduced baseline Hb mRNA levels of critical determinants of glutamate transmission, such as SLC1A2, the main glutamate transporter and N methyl D aspartate (Grin1, <strong>Grin2A</strong> and Grin2B) as well as α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (Gria1 and Gria2) receptor subunits, with no changes in the scaffolding protein Dlg4.
+GRIN2A	drug	alcohol	29953905	NMDA receptor <strong>GluN2A</strong> subunit deletion protects against dependence like <b>ethanol</b> drinking.
+GRIN2A	addiction	dependence	29953905	NMDA receptor <strong>GluN2A</strong> subunit deletion protects against <b>dependence</b> like ethanol drinking.
+GRIN2A	drug	alcohol	29953905	The N methyl D aspartate receptor (NMDAR) is mechanistically involved in the behavioral and neurophysiological effects of <b>alcohol</b>, but the specific role of the <strong>GluN2A</strong> subunit remains unclear.
+GRIN2A	drug	alcohol	29953905	Here, we exposed mice with constitutive <strong>GluN2A</strong> gene knockout (KO) to chronic intermittent <b>ethanol</b> vapor (CIE) and tested for EtOH consumption/preference using a two bottle choice paradigm, as well as NMDAR mediated transmission at basolateral amygdala synapses via ex vivo slice electrophysiology.
+GRIN2A	addiction	dependence	29953905	Taken together, these data add to mounting evidence supporting <strong>GluN2A</strong> containing NMDARs as a mechanism underlying relative risk for developing EtOH <b>dependence</b> after repeated EtOH exposure.
+GRIN2A	drug	opioid	29788757	Discussion and conclusions Transcriptional levels of <strong>GluN2A</strong> and GluN2D subunits in online computer game addicts are similar to our previously reported data of <b>opioid</b> addiction and are not different from the control group.
+GRIN2A	addiction	addiction	29788757	Discussion and conclusions Transcriptional levels of <strong>GluN2A</strong> and GluN2D subunits in online computer game addicts are similar to our previously reported data of opioid <b>addiction</b> and are not different from the control group.
+GRIN2A	addiction	addiction	29766293	Data obtained using Western blotting technique showed a significant increase in the level of GluN1 and GluN2B, but not in <strong>GluN2A</strong> subunits in all the three regions (mPFC, lPFC, and OFC) of men whom suffered from <b>addiction</b> as compared to the appropriate controls.
+GRIN2A	addiction	addiction	29766293	These findings showed a novel role for GluN1, GluN2B subunits, rather than the <strong>GluN2A</strong> subunit of NMDARs, in the pathophysiology of <b>addiction</b> and suggested their role in the drug induced plasticity of NMDARs.
+GRIN2A	drug	opioid	29754475	The results of this study show that the NAc specific knockdown of RGS4 significantly increased the behaviors associated with <b>morphine</b> and did so by phosphorylation of the GluR1 (Ser831) and <strong>NR2A</strong> (Tyr1325) glutamate receptors in the NAc.
+GRIN2A	drug	opioid	29754475	Furthermore, the knock down of RGS4 enhanced the phosphorylation of the GluR1 and <strong>NR2A</strong> glutamate receptors in the primary NAc/striatal neurons during spontaneous <b>morphine</b> withdrawal.
+GRIN2A	addiction	withdrawal	29754475	Furthermore, the knock down of RGS4 enhanced the phosphorylation of the GluR1 and <strong>NR2A</strong> glutamate receptors in the primary NAc/striatal neurons during spontaneous morphine <b>withdrawal</b>.
+GRIN2A	drug	alcohol	29704590	Protective influences of N acetylcysteine against <b>alcohol</b> abstinence induced depression by regulating biochemical and <strong>GRIN2A</strong>, GRIN2B gene expression of NMDA receptor signaling pathway in rats.
+GRIN2A	drug	alcohol	29704590	The increased expression levels of <strong>GRIN2A</strong> and GRIN2B following <b>ethanol</b> abstinence were reversed with a higher dose of NAC (100 mg/kg) treatment.
+GRIN2A	drug	alcohol	29704590	In conclusion, the results of the study reveal that NAC has remarkable protective effects in the <b>alcohol</b> abstinence induced depression by modulating <b>alcohol</b> markers, serotonin levels and <strong>GRIN2A</strong>, GRIN2B gene expression of NMDAR signaling pathway in rats.
+GRIN2A	drug	amphetamine	29441405	In rats that reinstated <b>methamphetamine</b> seeking, these altered electrophysiological properties of GCNs were associated with enhanced expression of Fos, <strong>GluN2A</strong> subunits and PSD95 and reduced expression of GABAA subunits in the DG and enhanced expression of synaptic PSD in the molecular layer.
+GRIN2A	addiction	relapse	29441405	In rats that reinstated methamphetamine <b>seeking</b>, these altered electrophysiological properties of GCNs were associated with enhanced expression of Fos, <strong>GluN2A</strong> subunits and PSD95 and reduced expression of GABAA subunits in the DG and enhanced expression of synaptic PSD in the molecular layer.
+GRIN2A	drug	psychedelics	29305627	Since <b>ketamine</b> equally blocks <strong>NR2A</strong>  and NR2B containing NMDAR, and has affinity to other receptors, NR2B selective drugs might have improved therapeutic efficiency and side effect profile.
+GRIN2A	drug	cocaine	28585567	Role of Src Family Kinases in BDNF Mediated Suppression of <b>Cocaine</b> Seeking and Prevention of <b>Cocaine</b> Induced ERK, <strong>GluN2A</strong>, and GluN2B Dephosphorylation in the Prelimbic Cortex.
+GRIN2A	addiction	relapse	28585567	Role of Src Family Kinases in BDNF Mediated Suppression of Cocaine <b>Seeking</b> and Prevention of Cocaine Induced ERK, <strong>GluN2A</strong>, and GluN2B Dephosphorylation in the Prelimbic Cortex.
+GRIN2A	drug	cocaine	28585567	As previously reported, infusion of BDNF into the PrL cortex blocked <b>cocaine</b> SA induced dephosphorylation of ERK, <strong>GluN2A</strong>, and GluN2B containing receptors.
+GRIN2A	drug	cocaine	28123030	We further show that the <b>cocaine</b> facilitation of t LTP induction is caused by sensitized D1 cAMP/protein kinase A dopamine signaling in pyramidal neurons, which then pathologically recruits voltage gated l type Ca2+ channels that synergize with <strong>GluN2A</strong> containing NMDA receptors to drive t LTP at extended timing.
+GRIN2A	drug	cocaine	28042872	Infralimbic <strong>GluN2A</strong> Containing NMDA Receptors Modulate Reconsolidation of <b>Cocaine</b> Self Administration Memory.
+GRIN2A	addiction	relapse	28042872	These results indicate that IL mPFC <strong>GluN2A</strong> containing NMDArs modulate reconsolidation, and suggest a novel treatment strategy, as reducing cue reactivity could limit <b>relapse</b> susceptibility.
+GRIN2A	addiction	reward	27267684	During a first testing phase, adult male rats implanted with bilateral ventral midbrain cannulae were injected every second day for three days with D [Tyr11]neurotensin (1.5 nmol/side), the preferred NMDA <strong>GluN2A</strong>/B antagonist, <b>CPP</b> (40 or 120 pmol/side), the selective GluN2B antagonist, Ro04 5595 (200 or 1200 pmol/side), <b>CPP</b> (40 or 120 pmol/side) + D [Tyr11]neurotensin (1.5 nmol/side) or Ro04 5595 (200 or 1200 pmol/side) + D [Tyr11]neurotensin (1.5 nmol/side) and locomotor activity was measured immediately after the injection.
+GRIN2A	drug	amphetamine	27267684	These results support the hypothesis that neurotensin is stimulating glutamate neurotransmission to initiate neural changes that sub serve <b>amphetamine</b> sensitization and that glutamate is acting on NMDA receptors that are mostly likely composed of <strong>GluN2A</strong>, but not GluN2B, subunits.
+GRIN2A	addiction	sensitization	27267684	These results support the hypothesis that neurotensin is stimulating glutamate neurotransmission to initiate neural changes that sub serve amphetamine <b>sensitization</b> and that glutamate is acting on NMDA receptors that are mostly likely composed of <strong>GluN2A</strong>, but not GluN2B, subunits.
+GRIN2A	drug	cocaine	27765467	In the present study, infusion of the <strong>GluN2A</strong> containing NMDA receptor antagonist, TCN 201, or the GluN2B containing NMDA receptor antagonist, Ro 25 6981, into the prelimbic cortex of rats blocked the suppressive effect of BDNF on <b>cocaine</b> seeking.
+GRIN2A	addiction	relapse	27765467	In the present study, infusion of the <strong>GluN2A</strong> containing NMDA receptor antagonist, TCN 201, or the GluN2B containing NMDA receptor antagonist, Ro 25 6981, into the prelimbic cortex of rats blocked the suppressive effect of BDNF on cocaine <b>seeking</b>.
+GRIN2A	drug	cocaine	27765467	During early withdrawal from <b>cocaine</b> self administration, tyrosine phosphorylation of ERK, <strong>GluN2A</strong>, and GluN2B in the prelimbic cortex was reduced and this reduction of phospho proteins was prevented by intra prelimbic BDNF infusion.
+GRIN2A	addiction	withdrawal	27765467	During early <b>withdrawal</b> from cocaine self administration, tyrosine phosphorylation of ERK, <strong>GluN2A</strong>, and GluN2B in the prelimbic cortex was reduced and this reduction of phospho proteins was prevented by intra prelimbic BDNF infusion.
+GRIN2A	drug	cocaine	27765467	These data demonstrate that BDNF mediated activation of <strong>GluN2A</strong>  and GluN2B containing NMDA receptors underlies ERK activation in the prelimbic cortex during early withdrawal, preventing subsequent relapse to <b>cocaine</b> seeking.
+GRIN2A	addiction	relapse	27765467	These data demonstrate that BDNF mediated activation of <strong>GluN2A</strong>  and GluN2B containing NMDA receptors underlies ERK activation in the prelimbic cortex during early withdrawal, preventing subsequent <b>relapse</b> to cocaine <b>seeking</b>.
+GRIN2A	addiction	withdrawal	27765467	These data demonstrate that BDNF mediated activation of <strong>GluN2A</strong>  and GluN2B containing NMDA receptors underlies ERK activation in the prelimbic cortex during early <b>withdrawal</b>, preventing subsequent relapse to cocaine seeking.
+GRIN2A	addiction	reward	27531839	We found that destabilization of MeAM <b>CPP</b> after the application of ANI was blocked by the N methyl d aspartate receptor (NMDAR) antagonist MK 801 and the NR2B antagonist ifenprodil (IFN) but not by the <strong>NR2A</strong> antagonist NVP AAM077 (NVP).
+GRIN2A	drug	cocaine	27478879	As NMDA receptor function is regulated critically by its GluN2 subunits, herein, we assayed the relation between incubated cue elicited <b>cocaine</b> seeking following extended access to intravenous <b>cocaine</b> (6 h/d; 0.25 mg/infusion for 10 d) and the expression of <strong>GluN2A</strong>/B receptor subunits within PFC sub regions during early versus late withdrawal (respectively, 3 vs. 30 days).
+GRIN2A	addiction	relapse	27478879	As NMDA receptor function is regulated critically by its GluN2 subunits, herein, we assayed the relation between incubated cue elicited cocaine <b>seeking</b> following extended access to intravenous cocaine (6 h/d; 0.25 mg/infusion for 10 d) and the expression of <strong>GluN2A</strong>/B receptor subunits within PFC sub regions during early versus late withdrawal (respectively, 3 vs. 30 days).
+GRIN2A	addiction	withdrawal	27478879	As NMDA receptor function is regulated critically by its GluN2 subunits, herein, we assayed the relation between incubated cue elicited cocaine seeking following extended access to intravenous cocaine (6 h/d; 0.25 mg/infusion for 10 d) and the expression of <strong>GluN2A</strong>/B receptor subunits within PFC sub regions during early versus late <b>withdrawal</b> (respectively, 3 vs. 30 days).
+GRIN2A	drug	opioid	27457480	Antisense oligodeoxynucleotides of NMDA receptor subunits NR1, <strong>NR2A</strong>, NR2B significantly enhanced the inhibition of paeoniflorin on excitatory amino acid and high dose <b>morphine</b> induced nociception.
+GRIN2A	addiction	withdrawal	27038592	Incubation with chronic EtOH for 7 days and its removal from the medium induced a significant decrease in GluA1 and GluA2 expression levels; a significant reduction in the expression of synaptophysin and <strong>GluN2A</strong> was observed only after EtOH <b>withdrawal</b>.
+GRIN2A	addiction	withdrawal	26777139	Impaired hippocampal synaptic plasticity and <strong>NR2A</strong>/2B expression ratio in remifentanil <b>withdrawal</b> rats.
+GRIN2A	drug	alcohol	26773198	Expression of genes encoding mGlu1, mGlu5, the <strong>NR2A</strong> subunit of the NMDA receptor, and Homer2 were all decreased by binge <b>alcohol</b> consumption in males, while females were relatively resistant (only phosphoinositide dependent protein kinase 1 was decreased).
+GRIN2A	addiction	intoxication	26773198	Expression of genes encoding mGlu1, mGlu5, the <strong>NR2A</strong> subunit of the NMDA receptor, and Homer2 were all decreased by <b>binge</b> alcohol consumption in males, while females were relatively resistant (only phosphoinositide dependent protein kinase 1 was decreased).
+GRIN2A	addiction	relapse	26687341	Ex vivo reverse transcription polymerase chain reaction analysis of brain tissue found reduced sensitivity to punished EtOH <b>seeking</b> after CIE exposure was accompanied by a significant increase in gene expression of the GluN1 and <strong>GluN2A</strong> subunits of the N methyl d aspartate receptor, specifically in the medial orbitofrontal cortex.
+GRIN2A	drug	amphetamine	26366944	Moreover, <b>METH</b> inhibited mitogen activated protein kinase (MAPK) signaling activity and altered expression of the N methyl d aspartate (NMDA) receptor subunits <strong>NR2A</strong> and NR2B as well as calcium/calmodulin dependent protein kinase II (CaMKII).
+GRIN2A	drug	alcohol	26289945	The aim of the current study was to determine genotype effects of four single nucleotide polymorphisms (SNPs) in the genes of the N Methyl d aspartate receptor (GRIN1, <strong>GRIN2A</strong>, GRIN2C) and kainate receptor (GRIK1), which have been previously associated with <b>alcoholism</b>, on behavior, neural cue reactivity and drinking outcome.
+GRIN2A	addiction	addiction	26277529	In addition, SNPs GABRB3 rs7165224; DBI rs12613135; GAD1 SNPs rs2058725, rs1978340, rs2241164; and <strong>GRIN2A</strong> rs1650420 were previously reported in associations with drug <b>addiction</b> or related phenotypes.
+GRIN2A	drug	alcohol	26266540	In the present study, we used human embryonic stem cell (hESC) derived cortical neurons as in vitro cellular models to investigate <b>alcohol</b> induced expression changes of genes involved in <b>alcohol</b> metabolism (ALDH2), anti apoptosis (BCL2 and CCND2), neurotransmission (NMDA receptor subunit genes: GRIN1, <strong>GRIN2A</strong>, GRIN2B, and GRIN2D), calcium channel activity (ITPR2), or transcriptional repression (JARID2).
+GRIN2A	drug	alcohol	26266540	After a 7 day <b>ethanol</b> (50 mM) exposure followed by a 24 hour <b>ethanol</b> withdrawal treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93 fold, P = 0.003; <strong>GRIN2A</strong>: 1.40 fold, P = 0.003; GRIN2B: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; BCL2: 1.34 fold, P = 0.031), and the results of GRIN1, <strong>GRIN2A</strong>, and GRIN2B survived multiple comparison correction.
+GRIN2A	addiction	withdrawal	26266540	After a 7 day ethanol (50 mM) exposure followed by a 24 hour ethanol <b>withdrawal</b> treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93 fold, P = 0.003; <strong>GRIN2A</strong>: 1.40 fold, P = 0.003; GRIN2B: 1.75 fold, P = 0.002; GRIN2D: 1.86 fold, P = 0.048; BCL2: 1.34 fold, P = 0.031), and the results of GRIN1, <strong>GRIN2A</strong>, and GRIN2B survived multiple comparison correction.
+GRIN2A	drug	cocaine	26202103	Finally, we evaluated the effects of intra DH PEAQX (2.5 μg per 0.5 μl per hemisphere), a <strong>GluN2A</strong> subunit selective NMDAR antagonist, following, or in the absence of, <b>cocaine</b> memory reactivation on subsequent drug context induced <b>cocaine</b> seeking behavior.
+GRIN2A	addiction	relapse	26202103	Finally, we evaluated the effects of intra DH PEAQX (2.5 μg per 0.5 μl per hemisphere), a <strong>GluN2A</strong> subunit selective NMDAR antagonist, following, or in the absence of, cocaine memory reactivation on subsequent drug context induced cocaine <b>seeking</b> behavior.
+GRIN2A	addiction	relapse	25855177	Context induced <b>reinstatement</b> was associated with increased expression of the immediate early genes Fos and FosB and the NMDA receptor subunit gene <strong>Grin2a</strong> in only Fos positive neurons.
+GRIN2A	drug	alcohol	25800798	On the other hand <b>ethanol</b> significantly decreased <strong>NR2A</strong> and NR2B mRNAs expression, and increase GABAA mRNA expression.
+GRIN2A	drug	amphetamine	25752339	We also found that <b>METH</b> altered the expression of the N methyl d aspartate (NMDA) receptor subunits <strong>NR2A</strong> (79.6%) and NR2B (126.7%) and Ca(2+) /calmodulin dependent protein kinase II (CAMKII) (74.0%).
+GRIN2A	drug	alcohol	25743187	In the medial prefrontal cortex, 2.5g/kg <b>ethanol</b> decreased mRNA expression of brain derived neurotrophic factor, NMDA <strong>NR2A</strong> subunit, mGluR8 receptor, Homer1, the glutamate transporters SLC1a1 and SLC1a6 and Srr.
+GRIN2A	drug	cocaine	25539508	An overall decrease was observed in the mRNA expression of the glutamate synthesizing gene kidney type glutaminase (KGA), the metabotropic glutamate receptors (mGluR3 and GluR), and subunits of NMDA ionotropic receptors (NR1, <strong>NR2A</strong>, NR2B and NR2C) after acute <b>cocaine</b> administration, while mice repeatedly exposed to <b>cocaine</b> only displayed an increase in NR2C.
+GRIN2A	drug	alcohol	25538565	Thus, in the caudate we found reduced levels of mRNAs encoding the <strong>GluN2A</strong> glutamate receptor and the δ, ε, and ρ2 GABA A receptor subunits, and increased levels of the mRNAs encoding GluD1, GluD2, and GABA A γ1 subunits in the <b>alcoholics</b> as compared to controls.
+GRIN2A	drug	cocaine	25408547	The present study focused on metabotropic glutamatergic receptors type 5 (mGluR(5)) and N methyl D aspartate receptor subunits (NMDAR: GluN1, <strong>GluN2A</strong>, GluN2B) proteins during <b>cocaine</b> self administration and after 10 day of extinction training in rats.
+GRIN2A	drug	cocaine	25408547	Our results revealed that <b>cocaine</b> self administration selectively increased GluN1 and <strong>GluN2A</strong> subunit in the rat hippocampus and dorsal striatum, respectively, while mGluR(5) protein expression was similarly increased in the dorsal striatum of both experimental groups.
+GRIN2A	drug	cocaine	25408547	Withdrawal from both contingent and non contingent <b>cocaine</b> delivery induced parallel increases in prefrontal cortical <strong>GluN2A</strong> protein expression, hippocampal mGluR(5), and GluN1 protein expression as well as in accumbal GluN1 subunit expression, while the mGluR(5) expression was reduced in the prefrontal cortex.
+GRIN2A	addiction	withdrawal	25408547	<b>Withdrawal</b> from both contingent and non contingent cocaine delivery induced parallel increases in prefrontal cortical <strong>GluN2A</strong> protein expression, hippocampal mGluR(5), and GluN1 protein expression as well as in accumbal GluN1 subunit expression, while the mGluR(5) expression was reduced in the prefrontal cortex.
+GRIN2A	drug	cocaine	25408547	Extinction training in animals with a history of <b>cocaine</b> self administration resulted in an elevation of the hippocampal <strong>GluN2A</strong>/GluN2B subunits and accumbal mGluR(5), and in a 50 % decrease of mGluR(5) protein expression in the dorsal striatum.
+GRIN2A	drug	opioid	25366762	Genetic polymorphisms in functional regions of the glutamate receptor, N methyl D aspartate 2A (<strong>GRIN2A</strong>) gene, which encodes the 2A subunit of the N methyl D aspartate (NMDA) receptor, may modulate the risk of <b>heroin</b> addiction.
+GRIN2A	addiction	addiction	25366762	Genetic polymorphisms in functional regions of the glutamate receptor, N methyl D aspartate 2A (<strong>GRIN2A</strong>) gene, which encodes the 2A subunit of the N methyl D aspartate (NMDA) receptor, may modulate the risk of heroin <b>addiction</b>.
+GRIN2A	drug	opioid	25366762	We investigated the potential association between 8 single nucleotide polymorphisms (SNPs) of the <strong>GRIN2A</strong> gene (SNPs rs3219790, rs1014531, rs8044472, rs8045712, rs9933624, rs9940680, rs1420040, and rs767749) and <b>heroin</b> addiction using the MassARRAY system and GeneScan.
+GRIN2A	addiction	addiction	25366762	We investigated the potential association between 8 single nucleotide polymorphisms (SNPs) of the <strong>GRIN2A</strong> gene (SNPs rs3219790, rs1014531, rs8044472, rs8045712, rs9933624, rs9940680, rs1420040, and rs767749) and heroin <b>addiction</b> using the MassARRAY system and GeneScan.
+GRIN2A	drug	opioid	25366762	These data suggest that <strong>GRIN2A</strong> gene polymorphisms confer susceptibility to <b>heroin</b> addiction and support the hypothesis that dysfunction of <strong>GRIN2A</strong> is involved in the pathophysiological process of <b>heroin</b> addiction.
+GRIN2A	addiction	addiction	25366762	These data suggest that <strong>GRIN2A</strong> gene polymorphisms confer susceptibility to heroin <b>addiction</b> and support the hypothesis that dysfunction of <strong>GRIN2A</strong> is involved in the pathophysiological process of heroin <b>addiction</b>.
+GRIN2A	drug	opioid	25121622	Activation of the D1 receptors inhibits the long term potentiation in vivo induced by acute <b>morphine</b> administration through a D1 <strong>GluN2A</strong> interaction in the nucleus accumbens.
+GRIN2A	drug	opioid	25121622	Here, we report that acute in vivo <b>morphine</b> administration induces the long term potentiation (Mor LTP) of field excitatory postsynaptic potentials at the prefrontal cortex to nucleus accumbens shell synapses, and this process requires the activation of <strong>GluN2A</strong> containing N methyl D aspartate receptors.
+GRIN2A	addiction	addiction	25121622	These results indicate that the activation of D1 receptors modulates Mor LTP by the direct D1 <strong>GluN2A</strong> interaction at the prefrontal cortex to nucleus accumbens shell synapses and might play a role in <b>addiction</b> related plastic alterations.
+GRIN2A	drug	cocaine	24847958	However, both <strong>GluN2A</strong> and GluN2B subunit expression in the nucleus accumbens increased following <b>cocaine</b> self administration, and this increased expression was relatively resistant to modulation by extinction.
+GRIN2A	drug	cocaine	24832868	In addition, repeated <b>cocaine</b> altered NMDA receptor subunit expression in the ventral hippocampus, reducing the <strong>NR2A</strong> : NR2B subunit ratio.
+GRIN2A	drug	cocaine	24832868	This was associated with reduced ventral hippocampal <strong>NR2A</strong>:NR2B subunit ratio, suggesting that repeated exposure to <b>cocaine</b> produces changes in hippocampal NMDA receptor composition that lead to enhanced ventral hippocampus nucleus accumbens communication.
+GRIN2A	drug	alcohol	24523671	Out of the 16 glutamate receptor subunits, mRNAs encoding two AMPA [2 amino 3 (3 hydroxy 5 methyl isoxazol 4 yl)propanoic acid] receptor subunits GluA2 and GluA3; three kainate receptor subunits GluK2, GluK3 and GluK5 and five NMDA (N methyl D aspartate) receptor subunits GluN1, <strong>GluN2A</strong>, GluN2C, GluN2D, and GluN3A were significantly increased in the HP DG region in <b>alcoholics</b>.
+GRIN2A	drug	alcohol	24397780	Tolerance to <b>ethanol</b> intoxication after chronic <b>ethanol</b>: role of <strong>GluN2A</strong> and PSD 95.
+GRIN2A	addiction	intoxication	24397780	Tolerance to ethanol <b>intoxication</b> after chronic ethanol: role of <strong>GluN2A</strong> and PSD 95.
+GRIN2A	drug	alcohol	24397780	The <strong>GluN2A</strong> N methyl D aspartate receptors (NMDAR) subunit and the NMDAR anchoring protein PSD 95 mediate acute <b>alcohol</b> intoxication and represent putative mechanisms mediating tolerance.
+GRIN2A	addiction	intoxication	24397780	The <strong>GluN2A</strong> N methyl D aspartate receptors (NMDAR) subunit and the NMDAR anchoring protein PSD 95 mediate acute alcohol <b>intoxication</b> and represent putative mechanisms mediating tolerance.
+GRIN2A	drug	alcohol	24397780	We found that chronic intermittent <b>ethanol</b> exposure (CIE) did not produce tolerance [loss of righting reflex (LORR)] or withdrawal anxiety in C57BL/6J, <strong>GluN2A</strong> or PSD 95 knockout mice assayed 2 3 days later.
+GRIN2A	addiction	withdrawal	24397780	We found that chronic intermittent ethanol exposure (CIE) did not produce tolerance [loss of righting reflex (LORR)] or <b>withdrawal</b> anxiety in C57BL/6J, <strong>GluN2A</strong> or PSD 95 knockout mice assayed 2 3 days later.
+GRIN2A	drug	alcohol	24397780	These data suggest a role for <strong>GluN2A</strong> in tolerance, extending evidence that human <strong>GluN2A</strong> gene variation is involved in <b>alcohol</b> dependence.
+GRIN2A	addiction	dependence	24397780	These data suggest a role for <strong>GluN2A</strong> in tolerance, extending evidence that human <strong>GluN2A</strong> gene variation is involved in alcohol <b>dependence</b>.
+GRIN2A	addiction	reward	24373903	The NMDA evoked [(3)H]dopamine outflow was blocked by MK801 (1 μM) and inhibited by the selective GluN2B selective antagonists ifenprodil (1 μM) and RO 25 6981 (1 μM), but not by the <strong>GluN2A</strong> preferring antagonists <b>CPP</b> 19755 (1 μM) and ZnCl2 (1 nM).
+GRIN2A	addiction	sensitization	24315834	We examined NR1, <strong>NR2A</strong>, and NR2B expression throughout the brain during the development phase of EtOH <b>sensitization</b>, as well as after a 14 day withdrawal period.
+GRIN2A	addiction	withdrawal	24315834	We examined NR1, <strong>NR2A</strong>, and NR2B expression throughout the brain during the development phase of EtOH sensitization, as well as after a 14 day <b>withdrawal</b> period.
+GRIN2A	drug	opioid	23940648	Analysis of variations in the glutamate receptor, N methyl D aspartate 2A (<strong>GRIN2A</strong>) gene reveals their relative importance as genetic susceptibility factors for <b>heroin</b> addiction.
+GRIN2A	addiction	addiction	23940648	Analysis of variations in the glutamate receptor, N methyl D aspartate 2A (<strong>GRIN2A</strong>) gene reveals their relative importance as genetic susceptibility factors for heroin <b>addiction</b>.
+GRIN2A	addiction	addiction	23940648	The glutamate receptor, N methyl D aspartate 2A (<strong>GRIN2A</strong>) gene that encodes the 2A subunit of the N methyl D aspartate (NMDA) receptor was recently shown to be involved in the development of opiate <b>addiction</b>.
+GRIN2A	drug	opioid	23940648	Genetic polymorphisms in <strong>GRIN2A</strong> have a plausible role in modulating the risk of <b>heroin</b> addiction.
+GRIN2A	addiction	addiction	23940648	Genetic polymorphisms in <strong>GRIN2A</strong> have a plausible role in modulating the risk of heroin <b>addiction</b>.
+GRIN2A	drug	opioid	23940648	An association of <strong>GRIN2A</strong> single nucleotide polymorphisms (SNPs) with <b>heroin</b> addiction was found earlier in African Americans.
+GRIN2A	addiction	addiction	23940648	An association of <strong>GRIN2A</strong> single nucleotide polymorphisms (SNPs) with heroin <b>addiction</b> was found earlier in African Americans.
+GRIN2A	drug	opioid	23940648	To identify markers that contribute to the genetic susceptibility to <b>heroin</b> addiction, we examined the potential association between <b>heroin</b> addiction and forty polymorphisms of the <strong>GRIN2A</strong> gene using the MassARRAY system and GeneScan in this study.
+GRIN2A	addiction	addiction	23940648	To identify markers that contribute to the genetic susceptibility to heroin <b>addiction</b>, we examined the potential association between heroin <b>addiction</b> and forty polymorphisms of the <strong>GRIN2A</strong> gene using the MassARRAY system and GeneScan in this study.
+GRIN2A	drug	opioid	23940648	These findings point to a role for <strong>GRIN2A</strong> polymorphisms in <b>heroin</b> addiction among the Han Chinese from Shaanxi province, and may be informative for future genetic or neurobiological studies on <b>heroin</b> addiction.
+GRIN2A	addiction	addiction	23940648	These findings point to a role for <strong>GRIN2A</strong> polymorphisms in heroin <b>addiction</b> among the Han Chinese from Shaanxi province, and may be informative for future genetic or neurobiological studies on heroin <b>addiction</b>.
+GRIN2A	drug	alcohol	23693003	In the present study we report reduced amygdala activity during the acquisition of conditioned fear in healthy carriers of a risk variant for <b>alcoholism</b> (rs2072450) in the <strong>NR2A</strong> subunit containing N methyl d aspartate (NMDA) receptor.
+GRIN2A	drug	nicotine	23671067	In support of this hypothesis, we found that pharmacological inhibition of <strong>GluN2A</strong> with 3 Chloro 4 fluoro N [4 [[2 (phenylcarbonyl)hydrazino]carbonyl]benzyl]benzenesulfonamide (TCN 201) or GluN2B with ifenprodil abolished reinstated <b>nicotine</b> seeking.
+GRIN2A	addiction	relapse	23671067	In support of this hypothesis, we found that pharmacological inhibition of <strong>GluN2A</strong> with 3 Chloro 4 fluoro N [4 [[2 (phenylcarbonyl)hydrazino]carbonyl]benzyl]benzenesulfonamide (TCN 201) or GluN2B with ifenprodil abolished reinstated nicotine <b>seeking</b>.
+GRIN2A	drug	nicotine	23671067	These results indicate that up regulated <strong>GluN2A</strong>, GluN2B, and rapid synaptic potentiation in the accumbens contribute to cue induced relapse to <b>nicotine</b> use.
+GRIN2A	addiction	relapse	23671067	These results indicate that up regulated <strong>GluN2A</strong>, GluN2B, and rapid synaptic potentiation in the accumbens contribute to cue induced <b>relapse</b> to nicotine use.
+GRIN2A	drug	opioid	23242725	Furthermore, exogenous H2S can decrease the high level of p NR1 and can increase the low levels of p <strong>NR2A</strong> and p NR2B caused by <b>heroin</b>.
+GRIN2A	drug	amphetamine	23195702	This study investigated the involvements of dopaminergic and glutamatergic transmission in the development of <b>Meth</b> psychosis and dependence by using tyrosine hydroxylase heterozygous mutant (TH+/ ) mice and N methyl d aspartate receptor knockout (<strong>NR2A</strong> / ) mice.
+GRIN2A	addiction	dependence	23195702	This study investigated the involvements of dopaminergic and glutamatergic transmission in the development of Meth psychosis and <b>dependence</b> by using tyrosine hydroxylase heterozygous mutant (TH+/ ) mice and N methyl d aspartate receptor knockout (<strong>NR2A</strong> / ) mice.
+GRIN2A	drug	alcohol	22486492	Finally, we examined changes in mRNA expression of the NMDA receptor subunit genes GRIN1, <strong>GRIN2A</strong>, GRIN2B, and GRIN2D after 7 days of <b>alcohol</b> exposure and after 24 hour withdrawal from chronic <b>alcohol</b> exposure.
+GRIN2A	addiction	withdrawal	22486492	Finally, we examined changes in mRNA expression of the NMDA receptor subunit genes GRIN1, <strong>GRIN2A</strong>, GRIN2B, and GRIN2D after 7 days of alcohol exposure and after 24 hour <b>withdrawal</b> from chronic alcohol exposure.
+GRIN2A	drug	alcohol	22486492	After 7 days of chronic <b>alcohol</b> exposure, there were significant increases in mRNA expression of GRIN1, <strong>GRIN2A</strong>, and GRIN2D in cultures derived from <b>alcoholic</b> subjects but not in cultures derived from nonalcoholics.
+GRIN2A	drug	alcohol	21886913	<b>Ethanol</b> withdrawal increased N methyl D aspartate (NMDA) evoked neuronal death, probably by altering the ratio between <strong>GluN2A</strong> and GluN2B NMDA receptor subunits.
+GRIN2A	addiction	withdrawal	21886913	Ethanol <b>withdrawal</b> increased N methyl D aspartate (NMDA) evoked neuronal death, probably by altering the ratio between <strong>GluN2A</strong> and GluN2B NMDA receptor subunits.
+GRIN2A	drug	alcohol	21507155	Association between a polymorphism in the promoter of a glutamate receptor subunit gene (<strong>GRIN2A</strong>) and <b>alcoholism</b>.
+GRIN2A	drug	alcohol	21163614	The mutant NR1(S890D) showed greater <b>ethanol</b> inhibition than NR1(890A) containing receptors, although this was only observed when it was combined with the <strong>NR2A</strong> subunit.
+GRIN2A	drug	alcohol	21163614	<b>Ethanol</b> inhibition was increased when T900E was added to the five serine /threonine substituted mutants, but again this was selective for <strong>NR2A</strong> containing receptors.
+GRIN2A	drug	opioid	21114966	When <b>naloxone</b>, an <b>opioid</b> receptor antagonist, was given systemically following the MK801 microinjection, the TPDNs' responsiveness was rekindled and expression levels of NR2D and <strong>NR2A</strong> mRNAs were increased.
+GRIN2A	drug	benzodiazepine	20853509	Immunogold electron microscopic evidence of differential regulation of GluN1, <strong>GluN2A</strong>, and GluN2B, NMDA type glutamate receptor subunits in rat hippocampal CA1 synapses during <b>benzodiazepine</b> withdrawal.
+GRIN2A	addiction	withdrawal	20853509	Immunogold electron microscopic evidence of differential regulation of GluN1, <strong>GluN2A</strong>, and GluN2B, NMDA type glutamate receptor subunits in rat hippocampal CA1 synapses during benzodiazepine <b>withdrawal</b>.
+GRIN2A	drug	benzodiazepine	20853509	Therefore, in this study ultrastructural evidence for possible reductions in NMDAR GluN1, <strong>GluN2A</strong>, and GluN2B subunits was sought at CA1 stratum radiatum synapses in proximal dendrites using postembedding immunogold labeling of tissues from rats withdrawn for 2 days from 1 week daily oral administration of the <b>benzodiazepine</b>, <b>flurazepam</b> (FZP).
+GRIN2A	addiction	withdrawal	20853509	The data therefore provide direct evidence for reduced synaptic GluN1/GluN2B receptors and preservation of GluN1/<strong>GluN2A</strong> receptors in the CA1 stratum radiatum region during BZ <b>withdrawal</b>.
+GRIN2A	drug	alcohol	20807241	Repeated <b>alcohol</b> treatment (8 × 2 g/kg) increased the expression of Group1 metabotropic glutamate receptors, the <strong>NR2a</strong>/b subunits of the N methyl D aspartate receptor, Homer2a/b, as well as the activated forms of protein kinase C (PKC) epsilon and phosphoinositol 3 kinase within ventral, but not dorsal, striatum.
+GRIN2A	drug	alcohol	20807241	Regardless of prior <b>alcohol</b> experience, C57BL/6J mice exhibited higher accumbens levels of mGluR1/5, Homer2a/b, <strong>NR2a</strong> and activated kinases vs. DBA2/J mice, whereas an <b>alcohol</b> induced rise in dorsal striatum mGluR1/5 expression was observed only in C57BL/6J mice.
+GRIN2A	drug	alcohol	20603193	After 2 weeks of <b>ethanol</b> vapor exposure N methyl d aspartate receptor NR1 subunit (NR1), N methyl d aspartate receptor <strong>NR2A</strong> subunit (<strong>NR2A</strong>), and N methyl d aspartate receptor NR2B subunit (NR2B) subunit expression was found to be increased in hippocampus of the adults.
+GRIN2A	drug	alcohol	20603193	In contrast, 2 weeks of <b>ethanol</b> exposure resulted in no significant changes in NR1 and NR2B subunits and a reduction <strong>NR2A</strong> subunit expression in hippocampus in adolescents.
+GRIN2A	drug	alcohol	20603193	Twenty four h and 2 weeks following withdrawal from <b>ethanol</b> vapor NR1 and <strong>NR2A</strong> subunit expression in hippocampus was decreased in adolescents, whereas in adults it had returned to control levels.
+GRIN2A	addiction	withdrawal	20603193	Twenty four h and 2 weeks following <b>withdrawal</b> from ethanol vapor NR1 and <strong>NR2A</strong> subunit expression in hippocampus was decreased in adolescents, whereas in adults it had returned to control levels.
+GRIN2A	drug	alcohol	20603193	In frontal cortex, 2 weeks of chronic <b>ethanol</b> exposure produced decreases in NR1 subunit expression in both adults and adolescents but also produced decreases in <strong>NR2A</strong> and NR2B subunit expression in adults that returned or exceeded control levels by 2 weeks following withdrawal from <b>ethanol</b> vapor.
+GRIN2A	addiction	withdrawal	20603193	In frontal cortex, 2 weeks of chronic ethanol exposure produced decreases in NR1 subunit expression in both adults and adolescents but also produced decreases in <strong>NR2A</strong> and NR2B subunit expression in adults that returned or exceeded control levels by 2 weeks following <b>withdrawal</b> from ethanol vapor.
+GRIN2A	drug	opioid	20420822	This study was designed to evaluate the possibility of using the mRNA expression state of <strong>NR2A</strong> and NR3A subunits of NMDA receptors in human peripheral blood lymphocytes as a peripheral marker in <b>opioid</b> addiction studies.
+GRIN2A	addiction	addiction	20420822	This study was designed to evaluate the possibility of using the mRNA expression state of <strong>NR2A</strong> and NR3A subunits of NMDA receptors in human peripheral blood lymphocytes as a peripheral marker in opioid <b>addiction</b> studies.
+GRIN2A	drug	cocaine	19524640	<strong>NR2A</strong>/B containing NMDA receptors mediate <b>cocaine</b> induced synaptic plasticity in the VTA and <b>cocaine</b> psychomotor sensitization.
+GRIN2A	addiction	sensitization	19524640	<strong>NR2A</strong>/B containing NMDA receptors mediate cocaine induced synaptic plasticity in the VTA and cocaine psychomotor <b>sensitization</b>.
+GRIN2A	drug	cocaine	19524640	We found that inhibition of <strong>NR2A</strong> containing NMDARs by NVP AAM077, or NR2B containing receptors by ifenprodil, blocked <b>cocaine</b> induced increase in the AMPAR/NMDAR currents ratio, a measure of long term potentiation (LTP) in vivo, in VTA neurons 24h following a single <b>cocaine</b> injection.
+GRIN2A	drug	cocaine	19524640	Furthermore, inhibition of the <strong>NR2A</strong> subunit during the development of psychomotor sensitization attenuated the enhanced locomotor activity following repeated <b>cocaine</b> injections.
+GRIN2A	addiction	sensitization	19524640	Furthermore, inhibition of the <strong>NR2A</strong> subunit during the development of psychomotor <b>sensitization</b> attenuated the enhanced locomotor activity following repeated cocaine injections.
+GRIN2A	drug	alcohol	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (<strong>GRIN2A</strong>) and serotonin (HTR3A) as well as <b>alcohol</b> dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and diazepam binding inhibitor (DBI).
+GRIN2A	drug	benzodiazepine	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (<strong>GRIN2A</strong>) and serotonin (HTR3A) as well as alcohol dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and <b>diazepam</b> binding inhibitor (DBI).
+GRIN2A	drug	cocaine	19474322	Here, we show that repeated noncontingent <b>cocaine</b> injections increased NAc NMDAR subunits, NR1, <strong>NR2A</strong>, and NR2B 21 d, but not 1 d, after withdrawal from <b>cocaine</b>.
+GRIN2A	addiction	withdrawal	19474322	Here, we show that repeated noncontingent cocaine injections increased NAc NMDAR subunits, NR1, <strong>NR2A</strong>, and NR2B 21 d, but not 1 d, after <b>withdrawal</b> from cocaine.
+GRIN2A	drug	cocaine	19306440	In contrast, extended access to <b>cocaine</b> resulted in distinct and long lasting alterations of protein expression within the mPFC that included: increased levels of Homer1b/c at 1 day, NR2b at 14 days, and <strong>NR2a</strong> at 60 days, of withdrawal.
+GRIN2A	addiction	withdrawal	19306440	In contrast, extended access to cocaine resulted in distinct and long lasting alterations of protein expression within the mPFC that included: increased levels of Homer1b/c at 1 day, NR2b at 14 days, and <strong>NR2a</strong> at 60 days, of <b>withdrawal</b>.
+GRIN2A	drug	cocaine	19046409	Here we show that application of <b>cocaine</b> both in slices and in vivo induced an increase in tyrosine phosphorylation of the <strong>NR2A</strong>, but not the NR2B subunit of the NMDAR in juvenile rats.
+GRIN2A	drug	cocaine	19046409	<b>Cocaine</b> induced an increase in the activity of both Fyn and Src kinases, and the Src protein tyrosine kinase (Src PTKs) inhibitor, 4 amino 5 (4 chlorophenyl) 7 (t butyl)pyrazolo[3,4 d]pyrimidine (PP2), abolished both <b>cocaine</b> induced increase in tyrosine phosphorylation of the <strong>NR2A</strong> subunit and the increase in the expression of NR1, <strong>NR2A</strong>, and NR2B in the VTA.
+GRIN2A	drug	cocaine	19046409	Taken together, these results suggest that acute <b>cocaine</b> induced an increase in the expression of NMDAR subunits and enhanced tyrosine phosphorylation of <strong>NR2A</strong> containing NMDAR through members of the Src PTKs.
+GRIN2A	drug	alcohol	18938187	A significant decrease was observed in GABA(A) alpha(1), GAD(67), and CRF, but not <strong>NR2A</strong>, mRNAs in adult rats that consumed <b>ethanol</b> in comparison to controls.
+GRIN2A	drug	opioid	18851757	Distinct expression of synaptic <strong>NR2A</strong> and NR2B in the central nervous system and impaired <b>morphine</b> tolerance and physical dependence in mice deficient in postsynaptic density 93 protein.
+GRIN2A	addiction	dependence	18851757	Distinct expression of synaptic <strong>NR2A</strong> and NR2B in the central nervous system and impaired morphine tolerance and physical <b>dependence</b> in mice deficient in postsynaptic density 93 protein.
+GRIN2A	drug	opioid	18851757	These findings indicate that impaired NMDAR dependent neuronal plasticity following repeated <b>morphine</b> injection in PSD 93 knockout mice is attributed to PSD 93 deletion induced alterations of synaptic <strong>NR2A</strong> and NR2B expression in dorsal horn and forebrain cortex neurons.
+GRIN2A	drug	alcohol	18849153	Fyn tyrosine kinase is a member of the Scr family that phosphorylates the <strong>NR2A</strong> and NR2B subunits of the NMDA receptors reducing the inhibitory effects of <b>ethanol</b> and therefore may regulate the individual sensitivity to <b>ethanol</b>.
+GRIN2A	drug	alcohol	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, <strong>NR2A</strong>, and NR2B; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with <b>alcohol</b> dependence using multivariate statistical analysis.
+GRIN2A	addiction	dependence	18606955	Genotype profiles for GLAST; N methyl d aspartate receptor subunits NR1, <strong>NR2A</strong>, and NR2B; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with alcohol <b>dependence</b> using multivariate statistical analysis.
+GRIN2A	drug	alcohol	18606955	Analysis of study 1 revealed that <strong>NR2A</strong> and MGLUR5 have the greatest relevance for human <b>alcohol</b> dependence among the genes selected with odds ratios of 2.35 and 1.69, respectively.
+GRIN2A	addiction	dependence	18606955	Analysis of study 1 revealed that <strong>NR2A</strong> and MGLUR5 have the greatest relevance for human alcohol <b>dependence</b> among the genes selected with odds ratios of 2.35 and 1.69, respectively.
+GRIN2A	drug	alcohol	18606955	Replication analysis in study 2 confirmed an association of <b>alcohol</b> dependence with <strong>NR2A</strong> (odds ratio, 2.01) but showed no association with MGLUR5.
+GRIN2A	addiction	dependence	18606955	Replication analysis in study 2 confirmed an association of alcohol <b>dependence</b> with <strong>NR2A</strong> (odds ratio, 2.01) but showed no association with MGLUR5.
+GRIN2A	drug	alcohol	18606955	Combined analysis of study 1 and study 2 exhibited a more significant association on the Cochran Mantel Haenszel test (P < .001) for <strong>NR2A</strong>; <strong>NR2A</strong> was associated with positive family history, early onset of <b>alcoholism</b>, and maximum number of drinks in adults as well as risky drinking patterns in adolescents.
+GRIN2A	drug	alcohol	18606955	Genetic variations in <strong>NR2A</strong> have the greatest relevance for human <b>alcohol</b> dependence among the glutamatergic genes selected for their known alteration of <b>alcohol</b> effects in animal models.
+GRIN2A	addiction	dependence	18606955	Genetic variations in <strong>NR2A</strong> have the greatest relevance for human alcohol <b>dependence</b> among the glutamatergic genes selected for their known alteration of alcohol effects in animal models.
+GRIN2A	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, GluR3), the glutamate receptor subunits of NMDA (NR1, <strong>NR2A</strong> and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRIN2A	drug	opioid	18391508	In the genetic section of the study, results of quantitative real time RT PCR clearly indicated that <b>morphine</b> sensitization increased the expression of NMDA receptor subunits mRNA in the amygdala (NR1 by 104% and <strong>NR2A</strong> by 85%), while the other areas of the brain were unaffected.
+GRIN2A	addiction	sensitization	18391508	In the genetic section of the study, results of quantitative real time RT PCR clearly indicated that morphine <b>sensitization</b> increased the expression of NMDA receptor subunits mRNA in the amygdala (NR1 by 104% and <strong>NR2A</strong> by 85%), while the other areas of the brain were unaffected.
+GRIN2A	drug	opioid	18374314	<b>Morphine</b> withdrawal affects both delayed escape behaviour in Morris water maze and hippocampal <strong>NR2A</strong>/2B expression ratio.
+GRIN2A	addiction	withdrawal	18374314	Morphine <b>withdrawal</b> affects both delayed escape behaviour in Morris water maze and hippocampal <strong>NR2A</strong>/2B expression ratio.
+GRIN2A	drug	opioid	18374314	Here, we examined whether and how <b>morphine</b> withdrawal influenced delayed escape behaviour and <strong>NR2A</strong>/2B expression ratio of hippocampal synaptosomes.
+GRIN2A	addiction	withdrawal	18374314	Here, we examined whether and how morphine <b>withdrawal</b> influenced delayed escape behaviour and <strong>NR2A</strong>/2B expression ratio of hippocampal synaptosomes.
+GRIN2A	addiction	withdrawal	18374314	We found that both delayed escape behaviour and <strong>NR2A</strong>/2B expression ratio showed an inverted U curve and peaked on 4 day <b>withdrawal</b> during a 20 day <b>withdrawal</b> period.
+GRIN2A	addiction	withdrawal	18374314	Furthermore, treatment of the glucocorticoid receptor antagonist RU38486 for 3 days reduced delayed escape behaviour and <strong>NR2A</strong>/2B ratio on 4 day <b>withdrawal</b> to a level similar to those of 18 h <b>withdrawal</b>.
+GRIN2A	addiction	withdrawal	18374314	In contrast, elevated platform stress enabled delayed escape behaviour of 18 h <b>withdrawal</b> to a higher level similar to that of 4 day <b>withdrawal</b>, but had no significant effect on the <strong>NR2A</strong>/2B ratio.
+GRIN2A	drug	alcohol	18358639	The relative mRNA expression of exon 5 inclusion/exclusion variants of the NR1 subunit, and the relative expression of <strong>NR2A</strong>, NR2B and NR2C subunits was examined in rats subjected to long term free choice, <b>alcohol</b> self administration with repeated <b>alcohol</b> deprivation phases.
+GRIN2A	drug	cocaine	17950706	In both species, withdrawal from repeated <b>cocaine</b> administration down regulated Homer1b/c and Homer2a/b within the shell, but not the core, of the nucleus accumbens (NAC), and the reduced Homer levels were accompanied by decreases in mGluR1a, <strong>NR2a</strong> and NR2b.
+GRIN2A	addiction	withdrawal	17950706	In both species, <b>withdrawal</b> from repeated cocaine administration down regulated Homer1b/c and Homer2a/b within the shell, but not the core, of the nucleus accumbens (NAC), and the reduced Homer levels were accompanied by decreases in mGluR1a, <strong>NR2a</strong> and NR2b.
+GRIN2A	drug	cocaine	17950706	<b>Cocaine</b> induced increases in Homer1b/c, Homer2a/b, mGluR1a and <strong>NR2a</strong> were observed in the hippocampus of both rats and mice, while in dorsal striatum, <strong>NR2a</strong> levels were elevated but Homer and Group1 mGluR levels were unchanged.
+GRIN2A	drug	alcohol	17625498	While genetic removal of <strong>NR2A</strong> did not alter the magnitude of <b>ethanol</b> inhibition, pharmacological blockade of NR2B rendered synaptically activated NMDARs insensitive to <b>ethanol</b> inhibition.
+GRIN2A	drug	opioid	17321516	We have previously shown, using radioligand binding studies, that N methyl d aspartate (NMDA) NR1 and <strong>NR2A</strong> receptor subunits density was decreased in the forebrain of <b>morphine</b> dependent rats.
+GRIN2A	drug	opioid	17321516	In <b>morphine</b> dependent rats, the expression of NR1 and <strong>NR2A</strong> subunits protein, as determined by Western blotting with NMDA receptor subunit antibodies, were decreased in frontal cortex and hippocampus but significantly increased in the nucleus accumbens.
+GRIN2A	drug	alcohol	17156796	Under these conditions, mRNA and protein levels of NR1, <strong>NR2A</strong> and NR2B subunits did not change in the spinal cord of chronic <b>ethanol</b> fed rats.
+GRIN2A	drug	alcohol	16835771	<b>Ethanol</b> related behaviors in mice lacking the NMDA receptor <strong>NR2A</strong> subunit.
+GRIN2A	drug	alcohol	16835771	In the current study, we assessed the relative roles of NMDA subunits via phenotypic assessment of <b>ethanol</b> related behaviors in <strong>NR2A</strong> knockout (KO) mice.
+GRIN2A	drug	alcohol	16835771	Results demonstrated that <strong>NR2A</strong> KO and heterozygous mice failed to show evidence of <b>ethanol</b> induced conditioned place preference.
+GRIN2A	drug	alcohol	16835771	Results suggest that the loss of <strong>NR2A</strong> subunit containing NMDA receptors impairs the ability to form or express learned reward related responses to <b>ethanol</b> and causes deficits in motor coordination.
+GRIN2A	addiction	reward	16835771	Results suggest that the loss of <strong>NR2A</strong> subunit containing NMDA receptors impairs the ability to form or express learned <b>reward</b> related responses to ethanol and causes deficits in motor coordination.
+GRIN2A	drug	alcohol	16835771	However, the loss of <strong>NR2A</strong> does not alter other measures of acute <b>ethanol</b> intoxication or <b>ethanol</b> consumption, possibly implicating other NMDA subunits in these effects.
+GRIN2A	addiction	intoxication	16835771	However, the loss of <strong>NR2A</strong> does not alter other measures of acute ethanol <b>intoxication</b> or ethanol consumption, possibly implicating other NMDA subunits in these effects.
+GRIN2A	drug	opioid	16453311	In this study we examined the effects of chronic <b>morphine</b> administration on gene and protein expression of three major NMDA receptors subunits (NR1, <strong>NR2A</strong>, and NR2B) in NAcc and CeA.
+GRIN2A	drug	alcohol	16396741	There were also no significant changes observed in any of the NMDA subunit mRNAs, although there was a trend toward greater <strong>NR2A</strong> mRNA expression during chronic <b>ethanol</b> exposure.
+GRIN2A	drug	alcohol	16396741	Like the mRNA measures, chronic <b>ethanol</b> exposure did influence <strong>NR2A</strong> protein levels but the effects were modest.
+GRIN2A	drug	alcohol	16009711	Here we show that exposure of hippocampal neurons to <b>ethanol</b> increases the internalization of the <strong>NR2A</strong> but not NR2B subunit of the NMDAR via the endocytic pathway.
+GRIN2A	drug	alcohol	16009711	We further observed that <b>ethanol</b> exposure results in <strong>NR2A</strong> endocytosis through the activation of H Ras and the inhibition of the tyrosine kinase Src.
+GRIN2A	drug	alcohol	16009711	Importantly, <b>ethanol</b> treatment alters functional subunit composition from <strong>NR2A</strong>/NR2B  to mainly NR2B containing NMDARs.
+GRIN2A	drug	alcohol	16009352	The <b>ethanol</b> sensitive NMDA receptor subunits NR1, <strong>NR2A</strong> and NR2B were quantified by Western immunoblot analysis.
+GRIN2A	drug	alcohol	16009352	Exposure to <b>ethanol</b> (50 mM) caused an increase in the levels of NR1 (137 +/  11% of untreated control, P = 0.009), <strong>NR2A</strong> (128 +/  14%, P = 0.022) and NR2B (136 +/  19%, P = 0.012).
+GRIN2A	drug	alcohol	16009352	Coincubation with memantine (10 microM) completely blocked the <b>ethanol</b> induced up regulation of NR1 (102 +/  4%), <strong>NR2A</strong> (95 +/  7%) and NR2B (105 +/  13%).
+GRIN2A	drug	cocaine	15953359	In the basolateral amygdala, GluR1 but not GluR2 levels were increased on days 1 and 30, <strong>NR2A</strong> levels were increased on day 1, and NR2B levels were decreased on day 30 of withdrawal from <b>cocaine</b>.
+GRIN2A	addiction	withdrawal	15953359	In the basolateral amygdala, GluR1 but not GluR2 levels were increased on days 1 and 30, <strong>NR2A</strong> levels were increased on day 1, and NR2B levels were decreased on day 30 of <b>withdrawal</b> from cocaine.
+GRIN2A	drug	cocaine	15953359	In the central amygdala, GluR2 but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and <strong>NR2A</strong> or NR2B levels were not altered after withdrawal from <b>cocaine</b>.
+GRIN2A	addiction	withdrawal	15953359	In the central amygdala, GluR2 but not GluR1 levels were increased on days 1 and 30, NR1 levels were increased on day 30 and <strong>NR2A</strong> or NR2B levels were not altered after <b>withdrawal</b> from cocaine.
+GRIN2A	addiction	withdrawal	15919065	Western blot analysis of NMDA receptor subunit expression showed that, at 7 days of <b>withdrawal</b>, the level of protein for <strong>NR2A</strong> and NR2B subunits was elevated in the CA1 region of hippocampal slices from CIE treated animals compared with slices from age matched controls.
+GRIN2A	drug	alcohol	15902902	Fyn kinase does not reduce <b>ethanol</b> inhibition of zinc insensitive <strong>NR2A</strong> containing N methyl D aspartate receptors.
+GRIN2A	drug	opioid	15542739	By a novel electroporation technique to deliver the receptor into the brain of knockout mice, we succeeded in determining the specific locus for the site of anti <b>opioid</b> (through GluRepsilon1 or <strong>NR2A</strong>) action.
+GRIN2A	drug	opioid	15464026	The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (<strong>NR2A</strong>) protein, phosphorylated Ca(2+)/calmodulin kinase II (p CaMKII) protein, c fos mRNA, c Fos protein, are observed in the specific brain areas of mice and/or rats showing signs of <b>naloxone</b> precipitated withdrawal.
+GRIN2A	addiction	withdrawal	15464026	The increased levels of extracellular glutamate, NMDA receptor zeta subunit (NR1) mRNA, NMDA receptor epsilon 1 subunit (<strong>NR2A</strong>) protein, phosphorylated Ca(2+)/calmodulin kinase II (p CaMKII) protein, c fos mRNA, c Fos protein, are observed in the specific brain areas of mice and/or rats showing signs of naloxone precipitated <b>withdrawal</b>.
+GRIN2A	drug	opioid	15464026	In the NMDA receptor deficient mice, the <strong>NR2A</strong> knockout mice show the marked loss of typical withdrawal abstinence behaviors precipitated by <b>naloxone</b>.
+GRIN2A	addiction	withdrawal	15464026	In the NMDA receptor deficient mice, the <strong>NR2A</strong> knockout mice show the marked loss of typical <b>withdrawal</b> abstinence behaviors precipitated by naloxone.
+GRIN2A	drug	opioid	15263066	Taken together with our recent molecular studies, our data are consistent with a shift away from NMDA receptor subunit (NR) NR2B and 2C function toward increased <strong>NR2A</strong> subunit expression or function after chronic <b>morphine</b>, a process that could alter excitability and integrative properties and may represent a neuroadaptation of NAcc medium spiny neurons underlying <b>morphine</b> dependence.
+GRIN2A	addiction	dependence	15263066	Taken together with our recent molecular studies, our data are consistent with a shift away from NMDA receptor subunit (NR) NR2B and 2C function toward increased <strong>NR2A</strong> subunit expression or function after chronic morphine, a process that could alter excitability and integrative properties and may represent a neuroadaptation of NAcc medium spiny neurons underlying morphine <b>dependence</b>.
+GRIN2A	addiction	withdrawal	14745308	The up regulation of <strong>NR2A</strong> during EtOH <b>withdrawal</b> is consistent with compensatory changes to prolonged inhibition of the NMDAR.
+GRIN2A	drug	opioid	14684447	Therefore, we examined the effects of <b>morphine</b> dependence on electrophysiological properties of NMDARs in freshly isolated NAcc neurons and on expression of mRNA coding for <strong>NR2A</strong> C subunits using single cell RT PCR.
+GRIN2A	addiction	dependence	14684447	Therefore, we examined the effects of morphine <b>dependence</b> on electrophysiological properties of NMDARs in freshly isolated NAcc neurons and on expression of mRNA coding for <strong>NR2A</strong> C subunits using single cell RT PCR.
+GRIN2A	drug	nicotine	14666123	NMDA <strong>NR2A</strong>/B subunits were affected by <b>nicotine</b>, but without age related differences.
+GRIN2A	drug	alcohol	14615013	<b>Ethanol</b> inhibition of recombinant NR1/2A receptors: effects of heavy metal chelators and a zinc insensitive <strong>NR2A</strong> mutant.
+GRIN2A	drug	alcohol	14615013	Results from previous studies with recombinant NMDA receptors have demonstrated that subunit composition influences the <b>ethanol</b> sensitivity of NMDA receptors, with <strong>NR2A</strong> containing receptors often showing greater inhibition by <b>ethanol</b> than shown by those containing other NR2 subunits.
+GRIN2A	drug	alcohol	14615013	In this study, we examined the effects of <b>ethanol</b> on NR1/<strong>NR2A</strong> receptors expressed in human embryonic kidney 293 (HEK 293) cells recorded under conditions in which the effects of zinc are minimized.
+GRIN2A	drug	alcohol	14615013	These results support the suggestion that low levels of zinc present in experimental solutions may affect the apparent <b>ethanol</b> sensitivity of NMDA receptors containing the <strong>NR2A</strong> subunit.
+GRIN2A	drug	alcohol	14534353	Most GAD , presumed projection neurons expressed both <strong>NR2A</strong> and NR2B mRNAs, and this profile did not change during chronic <b>ethanol</b> exposure.
+GRIN2A	drug	cocaine	12325043	Repeated <b>cocaine</b> administration differentially affects NMDA receptor subunit (NR1, <strong>NR2A</strong> C) mRNAs in rat brain.
+GRIN2A	drug	cocaine	12325043	injections of <b>cocaine</b> (20 mg/kg) on subunit mRNAs of N methyl D aspartate (NMDA) receptors (NR1/<strong>NR2A</strong> 2C) in the rat brain by in situ hybridization using phosphor screen analysis.
+GRIN2A	drug	alcohol	11696675	Unexpectedly, we found that expression of NR1 (including the expression of NR1 subunits containing the N1, C1, and C2 inserts), <strong>NR2A</strong>, NR2B, NR2C, GluR1, GluR2/3, GluR5, GluR6/7, and KA2 subunits was not altered in hippocampal homogenates from <b>ethanol</b> exposed rats.
+GRIN2A	drug	alcohol	11530236	Altered effects of <b>ethanol</b> in <strong>NR2A</strong>(DeltaC/DeltaC) mice expressing C terminally truncated <strong>NR2A</strong> subunit of NMDA receptor.
+GRIN2A	drug	alcohol	11530236	To investigate whether the C terminus of the <strong>NR2A</strong> subunit is involved in determining the sensitivity of NMDA receptors to <b>ethanol</b> we compared the effects of <b>ethanol</b> in vitro on NMDA mediated field excitatory postsynaptic potentials (fEPSPs) in the CA1 and dentate gyrus (DG) of adult male <strong>NR2A</strong>(DeltaC/DeltaC) mice lacking the C terminus of <strong>NR2A</strong> subunit and in their parental strain C57Bl/6.
+GRIN2A	drug	alcohol	11530236	We also tested the in vivo effects of a hypnotic dose of <b>ethanol</b> in C57Bl/6 and <strong>NR2A</strong>(DeltaC/DeltaC) mice and their F2 offspring.
+GRIN2A	drug	alcohol	11530236	<b>Ethanol</b> (100 mM) in the presence of ifenprodil inhibited the CA1 <strong>NR2A</strong> mediated component of NMDA fEPSPs two times more in <strong>NR2A</strong>(DeltaC/DeltaC) than in C57Bl/6.
+GRIN2A	drug	alcohol	11530236	<b>Ethanol</b> inhibition of the CA1 NR2B mediated component was five to seven times lower in <strong>NR2A</strong>(DeltaC/DeltaC) than in C57Bl/6.
+GRIN2A	drug	alcohol	11530236	A second administration of <b>ethanol</b> 7 days after the initial injection revealed an increased <b>ethanol</b> sensitivity of <strong>NR2A</strong>(DeltaC/DeltaC) and F2(DeltaC/DeltaC) mice including a shortened time to loss of righting reflex and an increased sleep time.
+GRIN2A	drug	alcohol	11530236	The sensitization of <strong>NR2A</strong>(DeltaC/DeltaC) mice to <b>alcohol</b> was not accompanied by an altered <b>ethanol</b> sensitivity of NMDA fEPSPs recorded in vitro.
+GRIN2A	addiction	sensitization	11530236	The <b>sensitization</b> of <strong>NR2A</strong>(DeltaC/DeltaC) mice to alcohol was not accompanied by an altered ethanol sensitivity of NMDA fEPSPs recorded in vitro.
+GRIN2A	drug	alcohol	11530236	Our data are consistent with the inhibitory action of <b>ethanol</b> on NMDA receptors being mediated by a site other than the intracellular C terminus of the <strong>NR2A</strong> subunit.
+GRIN2A	drug	alcohol	11530236	The altered sensitivities to <b>ethanol</b> of both <strong>NR2A</strong>  and NR2B mediated responses in the CA1 of <strong>NR2A</strong>(DeltaC/DeltaC) imply that <strong>NR2A</strong>  and NR2B subunit containing NMDA receptors may be linked by a common target of <b>ethanol</b>.
+GRIN2A	drug	psychedelics	11438305	These results suggest that NR1/<strong>NR2A</strong> subunit containing NMDA antagonism may be critical for the production of the <b>ketamine</b> cue.
+GRIN2A	drug	alcohol	11369029	In HEK 293 cells, <b>acamprosate</b> showed almost no effect on NR1 1a/<strong>NR2A</strong> or NR1 1a/NR2B recombinants (IC(50)s not calculated).
+GRIN2A	drug	opioid	11233291	treatment with a specific antibody against the carboxyl terminal region of the NR2B subunit abolishes the <b>morphine</b> induced place preference, whereas antibodies against the NR1 and <strong>NR2A</strong> subunits do not affect the rewarding effect of <b>morphine</b>, indicating that the blockade of the NR2B subunit suppresses the development of the <b>morphine</b> induced rewarding effect.
+GRIN2A	addiction	withdrawal	11152389	The <strong>NR2A</strong> mRNA was significantly decreased in the CA1 and CA3 of hippocampus in tolerant rats and increased in the cerebral cortex and dentate gyrus in butorphanol <b>withdrawal</b> rats.
+GRIN2A	addiction	withdrawal	11152389	No changes of NR1, <strong>NR2A</strong>, NR2C subunit mRNA in the cerebellar granule cell layer were observed in either butorphanol tolerant or <b>withdrawal</b> rats.
+GRIN2A	drug	alcohol	10405999	The NR1/<strong>NR2A</strong> and NR1/NR2B combinations are preferentially sensitive to <b>ethanol</b> inhibition.
+GRIN2A	drug	alcohol	10225371	<strong>NR2A</strong> subunit levels were significantly increased only in hippocampus from <b>ethanol</b> dependent male rats, whereas NR2B subunit levels significantly increased in cerebral cortex of both female and male rats.
+GRIN2A	drug	alcohol	10082858	Levels of <strong>NR2A</strong>, NR2C, NR1 pan and both 3' NR1 insert mRNAs from the <b>ethanol</b> treated groups did not alter compared with the pair fed control group.
+GRIN2A	drug	opioid	9988122	Using in situ hybridization techniques, the effects of chronic <b>morphine</b> treatment on the expression of mRNAs encoding the NMDA receptor subunits NRI, <strong>NR2A</strong>, and NR2B were investigated.
+GRIN2A	drug	opioid	9988122	The expression of <strong>NR2A</strong> and NR2B subunit mRNAs did not change after <b>morphine</b> treatment in any brain region.
+GRIN2A	drug	alcohol	9685652	We investigated the effect of chronic <b>ethanol</b> administration and its withdrawal on the polypeptide levels of NMDA receptor subunits such as NR1, <strong>NR2A</strong>, and NR2B in the rat cerebral cortex and hippocampus using Western blot analysis technique.
+GRIN2A	addiction	withdrawal	9685652	We investigated the effect of chronic ethanol administration and its <b>withdrawal</b> on the polypeptide levels of NMDA receptor subunits such as NR1, <strong>NR2A</strong>, and NR2B in the rat cerebral cortex and hippocampus using Western blot analysis technique.
+GRIN2A	drug	alcohol	9685652	Our results indicate that chronic <b>ethanol</b> treatment upregulates NMDA receptor subunits NR1, <strong>NR2A</strong>, and NR2B (approximately 35%).
+GRIN2A	drug	benzodiazepine	9543260	The protein levels of the NR1 and NR2B, but not <strong>NR2A</strong>, subunits were significantly increased in <b>diazepam</b> withdrawn rats compared to those in control rats.
+GRIN2A	drug	alcohol	9145911	Immunoblot analysis of expression of NR1, <strong>NR2A</strong>, and NR2B receptor subunits showed no difference between control and chronic <b>ethanol</b> treated cultures.
+GRIN2A	drug	alcohol	8840015	Our current work demonstrates that chronic <b>ethanol</b> ingestion by mice, which results in the generation of physical dependence, also produces increases in the NMDA receptor NR1 subunit protein in the hippocampus and cerebellum (approximately 50% and 95%, respectively), and produces increases in the <strong>NR2A</strong> subunit protein in the hippocampus and cortex (approximately 25% and 40%, respectively).
+GRIN2A	addiction	dependence	8840015	Our current work demonstrates that chronic ethanol ingestion by mice, which results in the generation of physical <b>dependence</b>, also produces increases in the NMDA receptor NR1 subunit protein in the hippocampus and cerebellum (approximately 50% and 95%, respectively), and produces increases in the <strong>NR2A</strong> subunit protein in the hippocampus and cortex (approximately 25% and 40%, respectively).
+CYP2B6	drug	nicotine	32573327	One susceptibility gene for <b>nicotine</b> dependence is Cytochrome <strong>P450</strong> (CYP) 2A6, an enzyme responsible for the conversion of <b>nicotine</b> to cotinine and <b>nicotine</b> clearance in the liver.
+CYP2B6	addiction	dependence	32573327	One susceptibility gene for nicotine <b>dependence</b> is Cytochrome <strong>P450</strong> (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine and nicotine clearance in the liver.
+CYP2B6	drug	opioid	32416296	An indicator for cytochrome <strong>P450</strong> enzymes which have the most fundamental role in <b>methadone</b> metabolism in the liver.
+CYP2B6	drug	benzodiazepine	32354497	To clarify the cause of cardiogenic shock, we performed whole exome sequencing and screened relative single nucleotide variants of 2 cytochrome <strong>P450</strong> (CYP) isoforms, CYP3A4 and CYP3A5, which play a dominant role in the metabolic elimination of <b>midazolam</b>.
+CYP2B6	drug	opioid	32302325	Although CYP3A4 was conventionally considered the principal <b>methadone</b> metabolizing enzyme, more recent data have identified <strong>CYP2B6</strong> as the principal enzyme.
+CYP2B6	drug	opioid	32302325	We assessed hepatic fibrosis and steatosis by transient elastography and <strong>CYP2B6</strong> alleles, principally responsible for <b>methadone</b> metabolism.
+CYP2B6	drug	opioid	32302325	<strong>CYP2B6</strong> loss of function (LOF) alleles significantly affected (S) <b>methadone</b> metabolism (p = 0.012).
+CYP2B6	drug	opioid	32302325	Although the principal <b>methadone</b> metabolizing enzyme remains controversial, our results suggest that sex, <strong>CYP2B6</strong> genotype, and BMI should be incorporated into multivariate models to create <b>methadone</b> dosing algorithms.
+CYP2B6	drug	nicotine	32247097	<b>Nicotine</b> is mainly metabolized (C oxidation) in the liver to cotinine by the cytochrome <strong>P450</strong> enzyme system.
+CYP2B6	drug	opioid	31820437	The data suggest that <strong>P450</strong> enzymatic activity impacts the clearance of <b>methadone</b> in virtual adults and neonates, while the contribution of cardiac output may be negligible.
+CYP2B6	drug	opioid	31820437	Understanding maturational and/or pharmacogenetic changes in cytochrome <strong>P450</strong> enzymatic activity may further explain the large PK variability of <b>methadone</b> in newborns with NAS and will help individualized treatment.
+CYP2B6	drug	alcohol	31646907	The role of oxidative metabolism of <b>ethanol</b> by <b>alcohol</b> dehydrogenase, cytochrome <strong>P450</strong> 2E1, and aldehyde dehydrogenase, as well as the impact of genetic polymorphism in its physiopathology are also highlighted.
+CYP2B6	drug	nicotine	31628204	During <b>tobacco</b> and e cigarette use, <b>nicotine</b> is mainly metabolized in the human liver by cytochrome <strong>P450</strong> 2A6 (CYP2A6).
+CYP2B6	drug	opioid	31263758	We find that mitragynine is converted in vitro in both mouse and human liver preparations to the much more potent mu <b>opioid</b> receptor agonist 7 hydroxymitragynine and that this conversion is mediated by cytochrome <strong>P450</strong> 3A isoforms.
+CYP2B6	drug	nicotine	31241144	Pharmacogenomics of <b>Nicotine</b> Metabolism: Novel CYP2A6 and <strong>CYP2B6</strong> Genetic Variation Patterns in Alaska Native and American Indian Populations.
+CYP2B6	drug	nicotine	31241144	Diverse CYP2A6 and <strong>CYP2B6</strong> variation among the subgroups highlight the need for comprehensive pharmacogenetic testing to guide <b>tobacco</b> cessation therapy for AN/AI populations.
+CYP2B6	drug	alcohol	31220535	Carvacrol inhibits cytochrome <strong>P450</strong> and protects against binge <b>alcohol</b> induced liver toxicity.
+CYP2B6	addiction	intoxication	31220535	Carvacrol inhibits cytochrome <strong>P450</strong> and protects against <b>binge</b> alcohol induced liver toxicity.
+CYP2B6	drug	opioid	31206401	<b>Methadone</b> is metabolized by several cytochrome P450 isoenzymes; primarily CYP3A4, <strong>CYP2B6</strong>, and CYP2D6 before renal and fecal elimination.
+CYP2B6	drug	opioid	31206401	<b>Methadone</b> is metabolized by several cytochrome <strong>P450</strong> isoenzymes; primarily CYP3A4, <strong>CYP2B6</strong>, and CYP2D6 before renal and fecal elimination.
+CYP2B6	drug	nicotine	31187118	Prolonging the Reduction of <b>Nicotine</b> Self Administration in Rats by Coadministering Chronic <b>Nicotine</b> With Amitifadine, a Triple Monoamine Reuptake Inhibitor With <strong>CYP2B6</strong> Inhibitory Actions.
+CYP2B6	drug	nicotine	31187118	This study was conducted to determine if the combination of chronic <b>nicotine</b> with amitifadine, a triple monoamine reuptake inhibitor with <strong>CYP2B</strong> inhibitory effects, would reduce <b>nicotine</b> self administration to a greater extent than either alone or placebo.
+CYP2B6	drug	nicotine	31187118	The improved efficacy of the amitifadine and <b>nicotine</b> combination may be potentiated by amitifadine's inhibitory effects on <strong>CYP2B</strong>, which slows <b>nicotine</b> metabolism.
+CYP2B6	drug	benzodiazepine	31147443	Simulation of the binding of the ligands <b>midazolam</b>, bromocriptine, testosterone, and ketoconazole to <strong>P450</strong> 3A4 was consistent with an induced fit or a conformational selection model, but the concentration dependence of binding rates for varying both <strong>P450</strong> 3A4 and <b>midazolam</b> concentrations revealed discordance in the parameters, indicative of conformational selection.
+CYP2B6	addiction	dependence	31147443	Simulation of the binding of the ligands midazolam, bromocriptine, testosterone, and ketoconazole to <strong>P450</strong> 3A4 was consistent with an induced fit or a conformational selection model, but the concentration <b>dependence</b> of binding rates for varying both <strong>P450</strong> 3A4 and midazolam concentrations revealed discordance in the parameters, indicative of conformational selection.
+CYP2B6	drug	benzodiazepine	31023150	As <b>midazolam</b> is an established marker substance for cytochrome <strong>P450</strong> 3A activity, this single arm prospective trial was designed to obtain a 4 h pharmacokinetic profile of <b>midazolam</b> after oral administration of a 10 µg dose from each enrolled patient.
+CYP2B6	drug	opioid	31005596	<b>Tramadol</b> labeling indicates cytochrome <strong>P450</strong> (CYP) isozyme 2D6 ultrarapid metabolizer can produce dangerous (+) M1 levels, and CYP2D6 poor metabolizers insufficient (+) M1 for analgesia.
+CYP2B6	drug	alcohol	30931596	The <strong>P450</strong> CYP2E1 *5 c2, an inducible microsomal oxidase, upregulated by <b>ethanol</b> and by formation of acetaldehyde and reactive oxygen species, increases liver toxicity.
+CYP2B6	drug	opioid	30907440	Relevance of <strong>CYP2B6</strong> and CYP2D6 genotypes to <b>methadone</b> pharmacokinetics and response in the OPAL study.
+CYP2B6	drug	opioid	30907440	Our study aimed to evaluate the impacts of the cytochrome <strong>P450</strong> (CYP) 2B6 G516T and CYP2D6 genetic polymorphisms on pharmacokinetic and clinical parameters in patients receiving <b>methadone</b> maintenance treatment.
+CYP2B6	drug	opioid	30907440	When comparing the three <strong>CYP2B6</strong> genotype groups, the <b>methadone</b> (R)  and (S) <b>methadone</b> enantiomer concentrations/doses (concentrations relative to doses) were different (P = .029, P = .0019).
+CYP2B6	drug	opioid	30907440	On multivariate analysis, neither the <strong>CYP2B6</strong> genotype nor the CYP2D6 phenotype explained the (R) <b>methadone</b> concentration/dose values (P = .92; P = .86); the (S) <b>methadone</b> concentration/dose values (P = .052; P = .95 [although there was a difference between the TT group and GT and GG groups {P = .019}]); or opiate cessation (P = .12; P = .90).
+CYP2B6	drug	opioid	30907440	The genotyping of <strong>CYP2B6</strong> G516T could be an interesting tool to explore <b>methadone</b> intervariability.
+CYP2B6	drug	alcohol	30603740	Induction of the cytochrome <strong>P450</strong> 2E1 (CYP2E1) enzyme by chronic and excessive <b>alcohol</b> intake is known to play a role in the pathogenesis of ALD.
+CYP2B6	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome <strong>P450</strong> 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+CYP2B6	drug	opioid	30508992	Clinically actionable polymorphisms in CYP2D6 (cytochrome <strong>p450</strong> 2D6) and OPRM1 (mu 1 <b>opioid</b> receptor), the most important gene coding, respectively, for a metabolizing enzyme and receptor for <b>opioids</b> are reviewed, and functional effects described.
+CYP2B6	drug	alcohol	30301883	We used HepG2 cells that do not metabolize EtOH and its engineered clone that expresses EtOH metabolizing Cytochrome <strong>P450</strong> E2 and <b>alcohol</b> dehydrogenase (VL 17A cells).
+CYP2B6	drug	alcohol	30237578	The <b>ethanol</b> induced expression of cytochrome <strong>P450</strong> 2E1 (CYP2E1), pro inflammatory proteins, cytokines, chemokines and reactive oxygen species (ROS) levels were also reduced in the livers of AXT administrated group.
+CYP2B6	drug	opioid	30205091	<b>Methadone</b> undergoes N demethylation by multiple cytochrome P450 (CYP) enzymes including CYP3A4, <strong>CYP2B6</strong>, CYP2C19, CYP2D6, CYP2C9, and CYP2C8.
+CYP2B6	drug	opioid	30205091	<b>Methadone</b> undergoes N demethylation by multiple cytochrome <strong>P450</strong> (CYP) enzymes including CYP3A4, <strong>CYP2B6</strong>, CYP2C19, CYP2D6, CYP2C9, and CYP2C8.
+CYP2B6	drug	opioid	30205091	In vivo, polymorphism effects on <b>methadone</b> systemic exposure have been noted for <strong>CYP2B6</strong>, CYP3A4, and CYP2D6.
+CYP2B6	drug	alcohol	30035739	It is indicated that polypharmacy   the joint use of statins with such drugs as anti inflammatory (glucocorticoids), immunosuppressants (cyclosporine), antipsychotics, antiviral (protease inhibitors), macrolides, antifungal, lipid modifying (gemfibrozole), cytochrome <strong>P450</strong> inhibitors and substances causing dependence (<b>alcohol</b>, opioids) may contribute to the development of statin associated myopathy.
+CYP2B6	drug	opioid	30035739	It is indicated that polypharmacy   the joint use of statins with such drugs as anti inflammatory (glucocorticoids), immunosuppressants (cyclosporine), antipsychotics, antiviral (protease inhibitors), macrolides, antifungal, lipid modifying (gemfibrozole), cytochrome <strong>P450</strong> inhibitors and substances causing dependence (alcohol, <b>opioids</b>) may contribute to the development of statin associated myopathy.
+CYP2B6	addiction	dependence	30035739	It is indicated that polypharmacy   the joint use of statins with such drugs as anti inflammatory (glucocorticoids), immunosuppressants (cyclosporine), antipsychotics, antiviral (protease inhibitors), macrolides, antifungal, lipid modifying (gemfibrozole), cytochrome <strong>P450</strong> inhibitors and substances causing <b>dependence</b> (alcohol, opioids) may contribute to the development of statin associated myopathy.
+CYP2B6	drug	psychedelics	30030374	Cytochrome <strong>P450</strong> and O methyltransferase catalyze the final steps in the biosynthesis of the anti addictive alkaloid <b>ibogaine</b> from Tabernanthe iboga.
+CYP2B6	addiction	addiction	30030374	Cytochrome <strong>P450</strong> and O methyltransferase catalyze the final steps in the biosynthesis of the anti <b>addictive</b> alkaloid ibogaine from Tabernanthe iboga.
+CYP2B6	addiction	sensitization	29671087	A number of mechanisms could be responsible for his increased sensitivity to chemicals following exposure to fluconazole/ketoconazole, including inhibition of <strong>P450</strong> and other detoxification enzymes, acetaldehyde buildup, and neurogenic <b>sensitization</b>.
+CYP2B6	drug	alcohol	29588096	Cytochrome <strong>P450</strong> 2E1 (CYP2E1) gene is one of the candidate genes for <b>alcohol</b> dependence (AD).
+CYP2B6	addiction	dependence	29588096	Cytochrome <strong>P450</strong> 2E1 (CYP2E1) gene is one of the candidate genes for alcohol <b>dependence</b> (AD).
+CYP2B6	drug	opioid	29450233	Pharmacogenetic testing revealed that the patient exhibited a cytochrome <strong>P450</strong> 3A4 ultrarapid metabolizer phenotype, which necessitated a higher than recommended daily dose of <b>buprenorphine</b> (32 mg) for adequate OUD management.
+CYP2B6	drug	alcohol	29404485	Increased <b>ethanol</b> inducible cytochrome <strong>P450</strong> 2E1 and cytochrome <strong>P450</strong> isoforms in exosomes of <b>alcohol</b> exposed rodents and patients with <b>alcoholism</b> through oxidative and endoplasmic reticulum stress.
+CYP2B6	drug	alcohol	29404485	This study investigated the role of <b>ethanol</b> inducible cytochrome <strong>P450</strong> 2E1 (CYP2E1) in enhancing CYP2E1 and other <strong>P450</strong> proteins in extracellular vesicles (EVs) from <b>alcohol</b> exposed rodents and human patients with <b>alcoholism</b> and their effects on oxidative hepatocyte injury.
+CYP2B6	drug	alcohol	29404485	The number of EVs and EV <strong>P450</strong> proteins were significantly reduced in <b>ethanol</b> exposed rats fed a diet containing polyunsaturated fatty acids.
+CYP2B6	drug	alcohol	29404485	The increased number of EVs and EV CYP2E1 and other <strong>P450</strong> isoforms in <b>alcohol</b> exposed wild types were significantly reduced in the corresponding Cyp2e1 null mice.
+CYP2B6	drug	opioid	29333880	Variants in six pharmacokinetic genes (CYP1A2, <strong>CYP2B6</strong>, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+CYP2B6	addiction	dependence	29333880	Variants in six pharmacokinetic genes (CYP1A2, <strong>CYP2B6</strong>, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+CYP2B6	drug	opioid	29302220	In pharmacogenetics of <b>opioid</b> addictions, <b>methadone</b> dose may be regulated by variants in cytochrome P450 2B6 (<strong>CYP2B6</strong>), a <b>methadone</b> metabolizing enzyme, and by a locus 300 kb 5' to OPRM1.
+CYP2B6	drug	opioid	29302220	In pharmacogenetics of <b>opioid</b> addictions, <b>methadone</b> dose may be regulated by variants in cytochrome <strong>P450</strong> 2B6 (<strong>CYP2B6</strong>), a <b>methadone</b> metabolizing enzyme, and by a locus 300 kb 5' to OPRM1.
+CYP2B6	addiction	addiction	29302220	Dans la pharmacogénétique de l'<b>addiction</b> aux opioïdes, la dose de méthadone peut être régulée par des variants du cytochrome P450 2B6 (<strong>CYP2B6</strong>), une enzyme métabolisant la méthadone, et par le locus situé à 300 kb en en amont du gène OPRM1.
+CYP2B6	addiction	addiction	29302220	Dans la pharmacogénétique de l'<b>addiction</b> aux opioïdes, la dose de méthadone peut être régulée par des variants du cytochrome <strong>P450</strong> 2B6 (<strong>CYP2B6</strong>), une enzyme métabolisant la méthadone, et par le locus situé à 300 kb en en amont du gène OPRM1.
+CYP2B6	drug	nicotine	29048184	<b>Nicotine</b> is metabolized into cotinine and then into trans 3' hydroxycotinine, mainly by cytochrome <strong>P450</strong> 2A6.
+CYP2B6	drug	benzodiazepine	28958437	Given that <b>clobazam</b> is primarily demethylated to N CLB by cytochrome <strong>P450</strong> (CYP) enzyme, CYP3A4, the mean plasma time concentration profile of <b>clobazam</b> was unchanged with the exclusion of CYP2C19 poor metabolizers.
+CYP2B6	drug	psychedelics	28917081	<b>MDMA</b> exerted greater inhibitory effects on cytochrome <strong>P450</strong> 3A4 (CYP3A4) than on cytochrome <strong>P450</strong> 2D6 (CYP2D6).
+CYP2B6	drug	opioid	28699698	This study discovered that the estrogen response element single nucleotide polymorphism (ERE SNP; rs16974799, C/T) of cytochrome 2B6 gene (<strong>cyp2b6</strong>; <b>methadone</b> catabolic enzyme) responded differently to MMT dosing.
+CYP2B6	drug	nicotine	28542511	In most <b>smokers</b>, cytochrome <strong>P450</strong> 2A6 (CYP2A6) catalyzed C oxidation accounts for >75% of <b>nicotine</b> metabolism, and the activity of this enzyme has been shown to correlate with the amount of <b>nicotine</b> and carcinogens drawn from cigarettes.
+CYP2B6	drug	nicotine	28472995	Interaction between cytochrome <strong>P450</strong> 2A6 and Catechol O Methyltransferase genes and their association with <b>smoking</b> risk in young men.
+CYP2B6	drug	nicotine	28472995	Although some effects of gene gene interactions on <b>nicotine</b> dopamine metabolism for <b>smoking</b> behavior have been reported, polymorphisms of cytochrome <strong>P450</strong> (CYP) 2A6 and catechol O methyltransferase (COMT) have not been studied together to determine their effects on <b>smokers</b>.
+CYP2B6	drug	opioid	28263461	However, <strong>CYP2B6</strong> is also a major catalyst of <b>methadone</b> metabolism in vitro.
+CYP2B6	drug	opioid	28263461	It has now been unequivocally established that <strong>CYP2B6</strong>, not CYP3A4, is the principal determinant of <b>methadone</b> metabolism, clearance, elimination, and plasma concentrations in humans.
+CYP2B6	drug	opioid	28263461	<strong>CYP2B6</strong> genetics also influences <b>methadone</b> metabolism and clearance, which were diminished in <strong>CYP2B6</strong>*6 carriers and increased in <strong>CYP2B6</strong>*4 carriers.
+CYP2B6	drug	opioid	28263461	<strong>CYP2B6</strong> genetics can explain, in part, interindividual variability in <b>methadone</b> metabolism and clearance.
+CYP2B6	drug	opioid	28263461	Thus, both constitutive variability due to <strong>CYP2B6</strong> genetics, and <strong>CYP2B6</strong> mediated drug interactions, can alter <b>methadone</b> disposition, clinical effect, and drug safety.
+CYP2B6	drug	nicotine	28092945	<b>Nicotine</b> Metabolism and <b>Smoking</b>: Ethnic Differences in the Role of <strong>P450</strong> 2A6.
+CYP2B6	drug	nicotine	28092945	<b>Nicotine</b> is the primary addictive agent in <b>tobacco</b>, and <strong>P450</strong> 2A6 (gene name: CYP2A6) is the primary catalyst of <b>nicotine</b> metabolism.
+CYP2B6	addiction	addiction	28092945	Nicotine is the primary <b>addictive</b> agent in tobacco, and <strong>P450</strong> 2A6 (gene name: CYP2A6) is the primary catalyst of nicotine metabolism.
+CYP2B6	drug	nicotine	28092945	In other ethnic groups, it has been challenging to confirm a direct link between <strong>P450</strong> 2A6 mediated <b>nicotine</b> metabolism and the risk of lung cancer.
+CYP2B6	drug	nicotine	28092945	This challenge is due in part to the difficulty in accurately quantifying <b>smoking</b> dose and accurately predicting or measuring <strong>P450</strong> 2A6 mediated <b>nicotine</b> metabolism.
+CYP2B6	drug	nicotine	28092945	Biomarkers of <b>nicotine</b> metabolism and <b>smoking</b> exposure, including the ratio of trans 3 hydroxycotine to cotinine, a measure of <strong>P450</strong> 2A6 activity and plasma cotinine, or urinary total <b>nicotine</b> equivalents (the sum of <b>nicotine</b> and six metabolites) as measures of exposure are useful for addressing this challenge.
+CYP2B6	drug	nicotine	28092945	Variation in metabolism pathways, other than those catalyzed by <strong>P450</strong> 2A6, can impact biomarkers of both <b>nicotine</b> metabolism and dose.
+CYP2B6	drug	nicotine	28032407	Cytochrome <strong>P450</strong> 2A6 (CYP2A6) encodes the enzyme responsible for the majority of <b>nicotine</b> metabolism.
+CYP2B6	drug	opioid	27861439	It is a prodrug that is metabolized by cytochrome <strong>P450</strong> (CYP) enzymes CYP2D6 and CYP3A4 to its more potent <b>opioid</b> analgesic metabolites, particularly the O demethylation product M1.
+CYP2B6	drug	cocaine	27568835	However, these potentiating effects of thioperamide do not necessarily result from H3 receptor blockade since thioperamide is an imidazole based compound capable of enhancing plasma <b>cocaine</b> concentrations by blocking cytochrome <strong>P450</strong> activity.
+CYP2B6	drug	cannabinoid	27106177	Both <b>marijuana</b> and tobacco smoking induce cytochrome <strong>P450</strong> (CYP) 1A2 through activation of the aromatic hydrocarbon receptor, and the induction effect between the two products is additive.
+CYP2B6	drug	nicotine	27106177	Both marijuana and <b>tobacco</b> <b>smoking</b> induce cytochrome <strong>P450</strong> (CYP) 1A2 through activation of the aromatic hydrocarbon receptor, and the induction effect between the two products is additive.
+CYP2B6	drug	cannabinoid	27683558	The remainder pertains to various <b>cannabis</b> controversies that certainly require closer examination if the scientific, consumer, and governmental stakeholders are ever to reach consensus on safety issues, specifically: whether botanical <b>cannabis</b> displays herbal synergy of its components, pharmacokinetics of <b>cannabis</b> and dose titration, whether <b>cannabis</b> medicines produce cyclo oxygenase inhibition, <b>cannabis</b> drug interactions, and cytochrome <strong>P450</strong> issues, whether <b>cannabis</b> randomized clinical trials are properly blinded, combatting the placebo effect in those trials via new approaches, the drug abuse liability (DAL) of <b>cannabis</b> based medicines and their regulatory scheduling, their effects on cognitive function and psychiatric sequelae, immunological effects, <b>cannabis</b> and driving safety, youth usage, issues related to <b>cannabis</b> smoking and vaporization, <b>cannabis</b> concentrates and vape pens, and laboratory analysis for contamination with bacteria and heavy metals.
+CYP2B6	drug	nicotine	27683558	The remainder pertains to various cannabis controversies that certainly require closer examination if the scientific, consumer, and governmental stakeholders are ever to reach consensus on safety issues, specifically: whether botanical cannabis displays herbal synergy of its components, pharmacokinetics of cannabis and dose titration, whether cannabis medicines produce cyclo oxygenase inhibition, cannabis drug interactions, and cytochrome <strong>P450</strong> issues, whether cannabis randomized clinical trials are properly blinded, combatting the placebo effect in those trials via new approaches, the drug abuse liability (DAL) of cannabis based medicines and their regulatory scheduling, their effects on cognitive function and psychiatric sequelae, immunological effects, cannabis and driving safety, youth usage, issues related to cannabis <b>smoking</b> and vaporization, cannabis concentrates and vape pens, and laboratory analysis for contamination with bacteria and heavy metals.
+CYP2B6	drug	cannabinoid	27670094	Three weeks later, saline or the cytochrome <strong>P450</strong> inhibitor proadifen (25mg/kg; to block <b>THC</b> metabolism and boost <b>THC</b>'s effects) was injected i.p.
+CYP2B6	drug	opioid	27515451	<strong>CYP2B6</strong> and OPRM1 Receptor Polymorphisms at <b>Methadone</b> Clinics And Novel OPRM1 Haplotypes: A Cross Sectional Study.
+CYP2B6	drug	opioid	27515451	This study sought to detect <strong>CYP2B6</strong> and OPRM1 variants and their genotypes, as major contributors to inter variability in <b>methadone</b> responsiveness and <b>methadone</b> dose requirements.
+CYP2B6	drug	psychedelics	27400739	Characterization of the hepatic cytochrome <strong>P450</strong> enzymes involved in the metabolism of 25I <b>NBOMe</b> and 25I NBOH.
+CYP2B6	drug	psychedelics	27400739	The aim of this study was to determine the importance of the different cytochrome <strong>P450</strong> enzymes (CYP) involved in the metabolism of 2 (4 iodo 2,5 dimethoxyphenyl) N (2methoxybenzyl)ethanamine (25I <b>NBOMe</b>) and 2 [[2 (4 iodo 2,5dimethoxyphenyl)ethylamino]methyl]phenol (25I NBOH) and to characterize the metabolites.
+CYP2B6	drug	alcohol	27375174	Indices of liver injury (alanine and aspartate aminotransferases [ALT and AST]; cytochrome <strong>p450</strong> 2E1 [CYP2E1]; <b>alcohol</b> dehydrogenase [ADH]; Oil Red O and triglyceride content; lipid peroxidation; inflammatory cytokine expression; and macrophage infiltration), and lung inflammatory cell count, proinflammatory cytokine expression, and lipid peroxidation were measured.
+CYP2B6	drug	opioid	27320437	The main mechanism for <b>methadone</b> metabolism is hepatic through the cytochrome <strong>P450</strong>, specifically isoenzymes 2B6, 3A4 and 2D6.
+CYP2B6	drug	opioid	27289271	Relationship between <strong>CYP2B6</strong>*6 and cold pressor pain sensitivity in <b>opioid</b> dependent patients on <b>methadone</b> maintenance therapy (MMT).
+CYP2B6	drug	opioid	27289271	<strong>CYP2B6</strong> polymorphisms contribute to inter individual variations in pharmacokinetics of <b>methadone</b>.
+CYP2B6	drug	opioid	27289271	It is possible, therefore, that genetic polymorphisms in <strong>CYP2B6</strong>, which affects the metabolism of <b>methadone</b>, influence pain sensitivity among patients on MMT.
+CYP2B6	drug	opioid	27289271	Our study indicates that the <strong>CYP2B6</strong>*6 allele is associated with a lower pain threshold and lower pain tolerance among males with <b>opioid</b> dependence on MMT.
+CYP2B6	addiction	dependence	27289271	Our study indicates that the <strong>CYP2B6</strong>*6 allele is associated with a lower pain threshold and lower pain tolerance among males with opioid <b>dependence</b> on MMT.
+CYP2B6	drug	opioid	27289271	The <strong>CYP2B6</strong>*6 allele may provide a mechanistic explanation for clinical observations of heightened pain sensitivity among <b>opioid</b> dependent patients receiving MMT.
+CYP2B6	drug	opioid	27286724	(S) <b>methadone</b> clearance was influenced by cytochrome P450 (CYP) 2B6 activity, ABCB1 3435C>T, and α 1 acid glycoprotein level, while (R) <b>methadone</b> clearance was influenced by <strong>CYP2B6</strong> activity, POR*28, and CYP3A4*22.
+CYP2B6	drug	opioid	27286724	(S) <b>methadone</b> clearance was influenced by cytochrome <strong>P450</strong> (CYP) 2B6 activity, ABCB1 3435C>T, and α 1 acid glycoprotein level, while (R) <b>methadone</b> clearance was influenced by <strong>CYP2B6</strong> activity, POR*28, and CYP3A4*22.
+CYP2B6	drug	nicotine	27230546	Brain <strong>CYP2B</strong> induction can decrease <b>nicotine</b> levels in the brain.
+CYP2B6	drug	nicotine	27230546	<b>Nicotine</b> can be metabolized by the enzyme <strong>CYP2B</strong>; brain <strong>CYP2B</strong> is higher in rats and monkeys treated with <b>nicotine</b>, and in human <b>smokers</b>.
+CYP2B6	drug	nicotine	27230546	A 7 day <b>nicotine</b> treatment increased <strong>CYP2B</strong> expression in rat brain but not liver, and decreased the behavioral response and brain levels (ex vivo) to the <strong>CYP2B</strong> substrate propofol.
+CYP2B6	drug	nicotine	27230546	However, the effect of <strong>CYP2B</strong> induction on the time course and levels of circulating brain <b>nicotine</b> in vivo has not been demonstrated.
+CYP2B6	drug	nicotine	27230546	There was a significant time x treatment interaction (p = 0.01); peak <b>nicotine</b> levels (15 45 minutes post injection) were lower after treatment (p = 0.04) consistent with <strong>CYP2B</strong> induction.
+CYP2B6	drug	nicotine	27230546	Following a two week washout period, brain <b>nicotine</b> levels increased to day one levels (p = 0.02), consistent with brain <strong>CYP2B</strong> levels returning to baseline.
+CYP2B6	drug	nicotine	27230546	Brain pretreatment of the <strong>CYP2B</strong> inhibitor, C8 xanthate, increased brain <b>nicotine</b> levels acutely and after 7 day <b>nicotine</b> treatment, indicating the alterations in brain <b>nicotine</b> levels were due to changes in brain <strong>CYP2B</strong> activity.
+CYP2B6	drug	nicotine	27230546	These results demonstrate that chronic <b>nicotine</b>, by increasing brain <strong>CYP2B</strong> activity, reduces brain <b>nicotine</b> levels, which could alter <b>nicotine</b>'s reinforcing effects.
+CYP2B6	addiction	reward	27230546	These results demonstrate that chronic nicotine, by increasing brain <strong>CYP2B</strong> activity, reduces brain nicotine levels, which could alter nicotine's <b>reinforcing</b> effects.
+CYP2B6	drug	nicotine	27230546	Higher brain <strong>CYP2B</strong> levels in <b>smokers</b> could lower brain <b>nicotine</b> levels; as this induction would occur following continued <b>nicotine</b> exposure it could increase withdrawal symptoms and contribute to sustaining <b>smoking</b> behavior.
+CYP2B6	addiction	withdrawal	27230546	Higher brain <strong>CYP2B</strong> levels in smokers could lower brain nicotine levels; as this induction would occur following continued nicotine exposure it could increase <b>withdrawal</b> symptoms and contribute to sustaining smoking behavior.
+CYP2B6	drug	opioid	27061230	To examine whether certain genotypes were associated with this, we examined the frequencies of 29 SNPs located in candidate genes related to <b>opioid</b> pharmacology: ABCB1, OPRM1, UGT2B7, CYP3A5, <strong>CYP2B6</strong>, CYP2C19, CYP2D6, COMT, KCNJ6 and SCN9A in 274 deceased patients with OA (DOA), 309 living patients with OA (LOA) and in 394 healthy volunteers (HV).
+CYP2B6	drug	opioid	27042732	The potency of <b>codeine</b> and <b>tramadol</b> is strongly influenced by the cytochrome <strong>P450</strong> isoenzyme CYP2D6 genotype, which varies widely from one person to another.
+CYP2B6	drug	opioid	27010727	Genome Wide Pharmacogenomic Study on <b>Methadone</b> Maintenance Treatment Identifies SNP rs17180299 and Multiple Haplotypes on <strong>CYP2B6</strong>, SPON1, and GSG1L Associated with Plasma Concentrations of <b>Methadone</b> R  and S enantiomers in <b>Heroin</b> Dependent Patients.
+CYP2B6	drug	opioid	27010727	The association between the S <b>methadone</b> plasma concentration and <strong>CYP2B6</strong>, SPON1, and GSG1L were replicated in another independent study.
+CYP2B6	drug	nicotine	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 addiction genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to <b>smoking</b> behavior and <b>nicotine</b> metabolism: CHRNA5 CHRNA3 CHRNB4 and CYP2A6 <strong>CYP2B6</strong>.
+CYP2B6	addiction	addiction	26921259	The array design covers genome wide common variation (65.67, 82.37, and 90.72% in African (YRI), East Asian (ASN), and European (EUR) respectively); most of the variation with a minor allele frequency ≥ 0.01 in 1014 <b>addiction</b> genes (85.16, 89.51, and 90.49% for YRI, ASN, and EUR respectively); and nearly all variation from the 1000 Genomes Project Phase 1, NHLBI GO Exome Sequencing Project and HapMap databases in the regions related to smoking behavior and nicotine metabolism: CHRNA5 CHRNA3 CHRNB4 and CYP2A6 <strong>CYP2B6</strong>.
+CYP2B6	drug	alcohol	26804639	Both studies enrolled healthy volunteers, aged 18 to 55 years, who received concurrent oral <b>naltrexone</b> to reduce adverse events (AEs); subjects with a history or evidence of substance abuse or current use of any product affecting cytochrome <strong>P450</strong> 3A4 activity were excluded.
+CYP2B6	drug	nicotine	26644138	<b>Smoking</b> is influenced by genetic factors including variation in CYP2A6 and <strong>CYP2B6</strong>, which encode <b>nicotine</b> metabolizing enzymes.
+CYP2B6	drug	nicotine	26644138	Here we extend this work by examining associations of CYP2A6 and <strong>CYP2B6</strong> with <b>tobacco</b> dependence acquisition in a larger sample of <b>smokers</b> followed throughout adolescence.
+CYP2B6	addiction	dependence	26644138	Here we extend this work by examining associations of CYP2A6 and <strong>CYP2B6</strong> with tobacco <b>dependence</b> acquisition in a larger sample of smokers followed throughout adolescence.
+CYP2B6	drug	nicotine	26644138	Cox's proportional hazards models compared the risk of ICD 10 <b>tobacco</b> dependence acquisition (score 3+) for CYP2A6 and <strong>CYP2B6</strong> metabolism groups.
+CYP2B6	addiction	dependence	26644138	Cox's proportional hazards models compared the risk of ICD 10 tobacco <b>dependence</b> acquisition (score 3+) for CYP2A6 and <strong>CYP2B6</strong> metabolism groups.
+CYP2B6	addiction	dependence	26644138	In those who initiated inhalation during follow up, CYP2A6 slow (vs. normal) metabolizers were at greater risk of <b>dependence</b> (hazards ratio (HR)=2.3; 95% CI=1.1, 4.8); <strong>CYP2B6</strong> slow (vs. normal) metabolizers had non significantly greater risk (HR=1.5; 95% CI=0.8, 2.6).
+CYP2B6	drug	nicotine	26644138	Variation in CYP2A6 or <strong>CYP2B6</strong> was not significantly associated with early <b>smoking</b> symptoms or cigarette consumption at end of follow up.
+CYP2B6	drug	nicotine	26644138	Our findings extend previous work indicating that slow <b>nicotine</b> metabolism mediated by CYP2A6, and perhaps <strong>CYP2B6</strong>, increases risk for <b>tobacco</b> dependence throughout adolescence.
+CYP2B6	addiction	dependence	26644138	Our findings extend previous work indicating that slow nicotine metabolism mediated by CYP2A6, and perhaps <strong>CYP2B6</strong>, increases risk for tobacco <b>dependence</b> throughout adolescence.
+CYP2B6	drug	opioid	26396499	The most common mechanisms eliciting drug drug interactions were alteration of <b>opioid</b> metabolism by inhibiting the activity of cytochrome <strong>P450</strong> 3A4 and pharmacodynamic interactions due to the combined effect on <b>opioid</b>, dopaminergic, cholinergic, and serotonergic activity in the central nervous system.
+CYP2B6	drug	nicotine	26375198	Opioids and compounds in <b>tobacco</b>, including <b>nicotine</b>, are metabolized by the cytochrome <strong>P450</strong> enzyme system, but the metabolism of opioids and <b>tobacco</b> products can be complicated.
+CYP2B6	drug	opioid	26375198	<b>Opioids</b> and compounds in tobacco, including nicotine, are metabolized by the cytochrome <strong>P450</strong> enzyme system, but the metabolism of <b>opioids</b> and tobacco products can be complicated.
+CYP2B6	addiction	dependence	26290405	Buffer conditions in in vitro metabolism studies using human liver microsomes (HLM) have been reported to affect the metabolic activities of several cytochrome <strong>P450</strong> (CYP) isozymes in different ways, although there are no reports about the <b>dependence</b> of CYP2C8 activity on buffer conditions.
+CYP2B6	drug	nicotine	26153084	<strong>CYP2B6</strong> rs2279343 polymorphism is associated with <b>smoking</b> cessation success in bupropion therapy.
+CYP2B6	drug	nicotine	26153084	Thus, the aim of the present study was to evaluate whether the <strong>CYP2B6</strong> and ANKK1 polymorphisms are associated with the response to <b>smoking</b> cessation therapies in patients from a <b>smoking</b> cessation assistance program.
+CYP2B6	drug	alcohol	26109895	The present work reports the effects of chronic <b>alcoholism</b> on contents of free amino acids, levels of cytochrome <strong>P450</strong> 3A2 (CYP3A2) mRNA expression and DNA fragmentation, as well as on contents of different cholesterol fractions and protein thiol groups in rat testes.
+CYP2B6	drug	nicotine	26081405	[Association of cytochrome <strong>P450</strong> 2A6 gene polymorphisms with <b>smoking</b> behaviors:a Meta analysis].
+CYP2B6	drug	nicotine	26081405	A Meta analysis was performed to assess the association of defective hepatic cytochrome <strong>P450</strong> 2A6 (CYP2A6) gene with <b>smoking</b> behaviors.
+CYP2B6	drug	nicotine	26081405	All eligible studies published up to 2014 were searched out from PubMed, China National Knowledge Internet (CNKI), ISI Web of knowledge (ISI), vip citation databases (VIP), Chinese BioMedical Literature (CBM) and Elsevier Science Direct, searching words were "smok*","<b>nicotine</b> dependence","CYP2A6","cytochrome <strong>P450</strong> 2A6","polymorphism","mut*"and"varia*", while 436 articles were concluded.
+CYP2B6	addiction	dependence	26081405	All eligible studies published up to 2014 were searched out from PubMed, China National Knowledge Internet (CNKI), ISI Web of knowledge (ISI), vip citation databases (VIP), Chinese BioMedical Literature (CBM) and Elsevier Science Direct, searching words were "smok*","nicotine <b>dependence</b>","CYP2A6","cytochrome <strong>P450</strong> 2A6","polymorphism","mut*"and"varia*", while 436 articles were concluded.
+CYP2B6	drug	nicotine	25895022	For <b>nicotine</b> and metabolite levels, function of the cytochrome <strong>P450</strong> 2A6 liver enzyme, which can be assessed with the <b>nicotine</b> metabolite ratio or via genotype, has been found to predict response, with slow <b>nicotine</b> metabolizers having less severe <b>nicotine</b> dependence and a greater likelihood of quitting with NRT than normal metabolizers.
+CYP2B6	addiction	dependence	25895022	For nicotine and metabolite levels, function of the cytochrome <strong>P450</strong> 2A6 liver enzyme, which can be assessed with the nicotine metabolite ratio or via genotype, has been found to predict response, with slow nicotine metabolizers having less severe nicotine <b>dependence</b> and a greater likelihood of quitting with NRT than normal metabolizers.
+CYP2B6	drug	alcohol	25872594	The tissue specific expression of cytochrome <strong>P450</strong> enzymes (CYP, <strong>P450</strong>) in the human brain may influence the therapeutic response to, and side effects of, neuroactive drugs including <b>alcohol</b>.
+CYP2B6	drug	alcohol	25872594	These brain regions were selected as they mediate the addictive effects of cigarette smoking and <b>alcohol</b> consumption, substances known to modulate <strong>P450</strong> expression in other tissues.
+CYP2B6	drug	nicotine	25872594	These brain regions were selected as they mediate the addictive effects of cigarette <b>smoking</b> and alcohol consumption, substances known to modulate <strong>P450</strong> expression in other tissues.
+CYP2B6	addiction	addiction	25872594	These brain regions were selected as they mediate the <b>addictive</b> effects of cigarette smoking and alcohol consumption, substances known to modulate <strong>P450</strong> expression in other tissues.
+CYP2B6	drug	nicotine	25857233	Inhibition effects of Vernonia cinerea active compounds against cytochrome <strong>P450</strong> 2A6 and human monoamine oxidases, possible targets for reduction of <b>tobacco</b> dependence.
+CYP2B6	addiction	dependence	25857233	Inhibition effects of Vernonia cinerea active compounds against cytochrome <strong>P450</strong> 2A6 and human monoamine oxidases, possible targets for reduction of tobacco <b>dependence</b>.
+CYP2B6	drug	nicotine	25857233	The human cytochrome <strong>P450</strong> 2A6 (CYP2A6) and monoamine oxidases (MAO A and MAO B), catalyzing <b>nicotine</b> and dopamine metabolisms, respectively, are two therapeutic targets of <b>nicotine</b> dependence.
+CYP2B6	addiction	dependence	25857233	The human cytochrome <strong>P450</strong> 2A6 (CYP2A6) and monoamine oxidases (MAO A and MAO B), catalyzing nicotine and dopamine metabolisms, respectively, are two therapeutic targets of nicotine <b>dependence</b>.
+CYP2B6	drug	opioid	25825958	This study investigated the influence of human cytochrome <strong>P450</strong> 2D6 (CYP2D6) gene polymorphism in gastric cancer (GC) patients to understand the pharmacogenomic basis for patient response to postoperative <b>fentanyl</b> analgesia.
+CYP2B6	drug	amphetamine	25671639	This pathogenic cascade is triggered by reactive oxygen species, likely generated through <b>methamphetamine</b> metabolism via cytochrome <strong>P450</strong>, and involves the recruitment of nuclear factor κB (NF κB) to induce expression of enzymes in the de novo pathway of ceramide biosynthesis.
+CYP2B6	drug	nicotine	25655887	<b>Nicotine</b>, the major psychoactive compound in cigarette smoke, is metabolized by a number of enzymes, including CYP2A6, <strong>CYP2B6</strong>, FMOs, and UGTs, among others.
+CYP2B6	drug	nicotine	25652250	Effect of Brain <strong>CYP2B</strong> Inhibition on Brain <b>Nicotine</b> Levels and <b>Nicotine</b> Self Administration.
+CYP2B6	drug	nicotine	25652250	<strong>CYP2B</strong> can metabolize <b>nicotine</b>, the main psychoactive ingredient in cigarettes; if altered brain <strong>CYP2B</strong> activity can influence <b>nicotine</b> brain levels, it could influence <b>nicotine</b> mediated behaviors.
+CYP2B6	drug	nicotine	25652250	To investigate this, a mechanism based inhibitor selective for <strong>CYP2B</strong>, C8 xanthate (20 μg), was administered intracerebroventricularly (ICV) into the brain of rats, and 22 h later, <b>nicotine</b> levels were measured by in vivo microdialysis following <b>nicotine</b> (150 μg/kg intravenous).
+CYP2B6	drug	nicotine	25652250	Together these data demonstrate that the brain <strong>CYP2B</strong> activity can influence <b>nicotine</b> brain levels and subsequent behaviors independent of hepatic metabolism.
+CYP2B6	drug	nicotine	25652250	This suggests that human <b>smokers</b> with variable <strong>CYP2B</strong> brain levels could have different <b>nicotine</b> levels and reinforcement, which might have a role in <b>smoking</b> behaviors and dependence.
+CYP2B6	addiction	dependence	25652250	This suggests that human smokers with variable <strong>CYP2B</strong> brain levels could have different nicotine levels and reinforcement, which might have a role in smoking behaviors and <b>dependence</b>.
+CYP2B6	addiction	reward	25652250	This suggests that human smokers with variable <strong>CYP2B</strong> brain levels could have different nicotine levels and <b>reinforcement</b>, which might have a role in smoking behaviors and dependence.
+CYP2B6	drug	benzodiazepine	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) methadone), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the <b>midazolam</b> test, R,S methadone trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, ABCB1, <strong>CYP2B6</strong>, CYP3A5, CYP2C19 and CYP2D6 genes.
+CYP2B6	drug	opioid	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) <b>methadone</b>), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the midazolam test, R,S <b>methadone</b> trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, ABCB1, <strong>CYP2B6</strong>, CYP3A5, CYP2C19 and CYP2D6 genes.
+CYP2B6	drug	benzodiazepine	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) methadone), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome <strong>P450</strong> (CYP) 3A4 activity measured by the <b>midazolam</b> test, R,S methadone trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, ABCB1, <strong>CYP2B6</strong>, CYP3A5, CYP2C19 and CYP2D6 genes.
+CYP2B6	drug	opioid	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) <b>methadone</b>), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome <strong>P450</strong> (CYP) 3A4 activity measured by the midazolam test, R,S <b>methadone</b> trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, ABCB1, <strong>CYP2B6</strong>, CYP3A5, CYP2C19 and CYP2D6 genes.
+CYP2B6	addiction	dependence	32733675	Cytochrome <strong>P450</strong> (CYP) activity, another critical marker of hepatocytes, displayed a strong <b>dependence</b> on substrate stiffness, wherein hepatocytes on soft substrates retained 2.7 fold higher CYP activity on day 7 in culture, as compared to TCPS.
+CYP2B6	drug	nicotine	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (ANKK1), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (SLC6A3) and cytochrome <strong>P450</strong> 2A6 (CYP2A6) genes influence <b>smoking</b> cessation and <b>nicotine</b> dependence in a Japanese population.
+CYP2B6	addiction	dependence	25526961	This study investigated whether polymorphisms of the ankyrin repeat and kinase domain containing 1 gene (ANKK1), which is adjacent to the dopamine D2 receptor gene (DRD2), and the dopamine transporter (SLC6A3) and cytochrome <strong>P450</strong> 2A6 (CYP2A6) genes influence smoking cessation and nicotine <b>dependence</b> in a Japanese population.
+CYP2B6	drug	nicotine	25489907	<strong>CYP2B6</strong> gene single nucleotide polymorphisms in an Italian population sample and relationship with <b>nicotine</b> dependence.
+CYP2B6	addiction	dependence	25489907	<strong>CYP2B6</strong> gene single nucleotide polymorphisms in an Italian population sample and relationship with nicotine <b>dependence</b>.
+CYP2B6	drug	nicotine	25489907	The extensively polymorphic <strong>CYP2B6</strong> gene metabolizes endogenous and exogenous compounds, among which are <b>nicotine</b> and bupropion, although its contribution to the systemic metabolism of <b>nicotine</b> still remains controversial.
+CYP2B6	drug	nicotine	25489907	In the present study, the distribution of the <strong>CYP2B6</strong> variant and genotype frequencies were analyzed in a sample of 202 Italian individuals who were also invited to answer the Fagerström test for <b>nicotine</b> dependence (FTND), in an effort to assess the involvement of <strong>CYP2B6</strong> polymorphisms in <b>nicotine</b> dependence.
+CYP2B6	addiction	dependence	25489907	In the present study, the distribution of the <strong>CYP2B6</strong> variant and genotype frequencies were analyzed in a sample of 202 Italian individuals who were also invited to answer the Fagerström test for nicotine <b>dependence</b> (FTND), in an effort to assess the involvement of <strong>CYP2B6</strong> polymorphisms in nicotine <b>dependence</b>.
+CYP2B6	drug	nicotine	25489907	The reduced activity of the <strong>CYP2B6</strong>*6 variant was significantly (p=0.025) distributed among the <b>nicotine</b> dependent individuals compared to non <b>nicotine</b> dependents.
+CYP2B6	drug	nicotine	25489907	Also, the <strong>CYP2B6</strong>*1/*6 genotype achieved statistical significance (p=0.016) within the <b>nicotine</b> dependent individuals.
+CYP2B6	drug	nicotine	25489907	The high occurrence of <strong>CYP2B6</strong>*6 carriers among <b>nicotine</b> dependent individuals may suggest a possible involvement in <b>nicotine</b> dependence, with a potential impact on <b>smoking</b> cessation treatments tailored to the individual <b>smoker</b>'s genotype.
+CYP2B6	addiction	dependence	25489907	The high occurrence of <strong>CYP2B6</strong>*6 carriers among nicotine dependent individuals may suggest a possible involvement in nicotine <b>dependence</b>, with a potential impact on smoking cessation treatments tailored to the individual smoker's genotype.
+CYP2B6	drug	alcohol	25455889	Either the total cytochrome <strong>P450</strong> 2E1 or the mitochondria located cytochrome <strong>P450</strong> 2E1, which is implicated in <b>ethanol</b> mediated oxidative stress, was suppressed by berberine.
+CYP2B6	drug	alcohol	25427919	The primary enzymes involved in <b>ethanol</b> metabolism include <b>alcohol</b> dehydrogenase (ADH), cytochrome <strong>P450</strong> isoform 2E1, (CYP2E1), catalase (CAT), and aldehyde dehydrogenases (ALDH).
+CYP2B6	drug	nicotine	25414797	However, these differences also covaried with cigarette <b>smoking</b> status (not balanced between groups), and <b>nicotine</b> <b>smoking</b> is known to alter caffeine/paraxanthine metabolism via cytochrome <strong>P450</strong> enzymes.
+CYP2B6	drug	nicotine	25352656	It is important to consider the blood to liver transport of <b>nicotine</b> to understand the <b>nicotine</b> elimination from the body because most of the <b>nicotine</b> is converted to inactive metabolites by cytochrome <strong>P450</strong> localized in the endoplasmic reticulum of the hepatocytes.
+CYP2B6	drug	opioid	25288149	The metabolism of all other <b>opioids</b> requires specific Cytochrome <strong>P450</strong> (CYP) isoenzymes.
+CYP2B6	drug	opioid	25278738	Genes encoding the liver cytochrome P 450 (CYP) enzymes that are involved with the metabolism of <b>methadone</b> (<strong>CYP2B6</strong>, 3A4 and 2C19) were selected and genotyped in this cohort.
+CYP2B6	drug	opioid	25278738	We found that the SNPs on <strong>CYP2B6</strong> were associated with plasma S <b>methadone</b> concentration; SNPs on CYP3A4 were associated with withdrawal symptoms and side effects; and SNPs on CYP2C19 were associated with <b>methadone</b> dose.
+CYP2B6	addiction	withdrawal	25278738	We found that the SNPs on <strong>CYP2B6</strong> were associated with plasma S methadone concentration; SNPs on CYP3A4 were associated with <b>withdrawal</b> symptoms and side effects; and SNPs on CYP2C19 were associated with methadone dose.
+CYP2B6	drug	alcohol	25236742	Binge <b>alcohol</b> promoted acute liver injury in mice with elevated levels of <b>ethanol</b> inducible cytochrome <strong>P450</strong> 2E1 (CYP2E1) and hypoxia, both of which were colocalized in the centrilobular areas.
+CYP2B6	addiction	intoxication	25236742	<b>Binge</b> alcohol promoted acute liver injury in mice with elevated levels of ethanol inducible cytochrome <strong>P450</strong> 2E1 (CYP2E1) and hypoxia, both of which were colocalized in the centrilobular areas.
+CYP2B6	drug	opioid	25148377	Cytochrome <strong>P450</strong> epoxygenase dependence of <b>opioid</b> analgesia: fluconazole does not interfere with remifentanil mediated analgesia in human subjects.
+CYP2B6	addiction	dependence	25148377	Cytochrome <strong>P450</strong> epoxygenase <b>dependence</b> of opioid analgesia: fluconazole does not interfere with remifentanil mediated analgesia in human subjects.
+CYP2B6	drug	opioid	25148377	Cytochrome <strong>P450</strong> (CYP) inhibitors may reduce <b>opioid</b> analgesia by inhibiting CYP activity dependent post <b>opioid</b> receptor signaling pathways in the brain.
+CYP2B6	drug	opioid	25148377	This suggestion was predicated on observations of highly attenuated <b>morphine</b> antinociception in rodents after intracerebroventricular injection of fluconazole or carrying a neuron specific deletion of the cytochrome <strong>P450</strong> reductase.
+CYP2B6	drug	opioid	25062792	Deficits in neuronal cytochrome <strong>P450</strong> activity attenuate <b>opioid</b> analgesia but not <b>opioid</b> side effects.
+CYP2B6	drug	opioid	25062792	The analgesic properties of <b>morphine</b> were recently shown to require the activity of a brain neuronal cytochrome <strong>P450</strong> epoxygenase, but the significance of this pathway for <b>opioid</b> side effects is unknown.
+CYP2B6	drug	opioid	25062792	Here we show that brain <strong>P450</strong> activity is not required for three of <b>morphine</b>׳s major side effects (respiratory depression, constipation, and locomotor stimulation).
+CYP2B6	drug	opioid	25062792	Following systemic or intracerebroventricular administration of <b>morphine</b>, transgenic mice with brain neuron   specific reductions in <strong>P450</strong> activity showed highly attenuated analgesic responses as compared with wild type (control) mice.
+CYP2B6	drug	opioid	25062792	However, brain <strong>P450</strong> deficient mice showed normal <b>morphine</b> induced side effects (respiratory depression, locomotor stimulation, and inhibition of intestinal motility).
+CYP2B6	drug	opioid	25062792	Pretreatment of control mice with the <strong>P450</strong> inhibitor CC12 similarly reduced the analgesia, but not these side effects of <b>morphine</b>.
+CYP2B6	drug	opioid	24956254	Nevertheless many genetic factors have been investigated including those affecting its metabolism (<strong>CYP2B6</strong> consistent results), efflux transport (P gp inconsistent results), target μ <b>opioid</b> receptor (μ <b>opioid</b> receptor inconsistent results) and a host of other receptors (DRD2) and signaling elements (GIRK2 and ARRB2; not replicated).
+CYP2B6	drug	alcohol	24863043	Induction of brain cytochrome <strong>P450</strong> 2E1 boosts the locomotor stimulating effects of <b>ethanol</b> in mice.
+CYP2B6	drug	alcohol	24760842	Overexpression of the steroidogenic enzyme cytochrome <strong>P450</strong> side chain cleavage in the ventral tegmental area increases 3α,5α THP and reduces long term operant <b>ethanol</b> self administration.
+CYP2B6	addiction	reward	24760842	Overexpression of the steroidogenic enzyme cytochrome <strong>P450</strong> side chain cleavage in the ventral tegmental area increases 3α,5α THP and reduces long term <b>operant</b> ethanol self administration.
+CYP2B6	drug	opioid	26574964	Blood samples were taken for the determination of serum levels of racemic <b>methadone</b> and its R and S enantiomers, and for typing of candidate alleles of POR, <strong>CYP2B6</strong>, ABCB1, GRIN1, OPRM1, SLC6A3, DßH and ARRB2 genes, all associated with the metabolism, tissue distribution and mechanism of action of <b>methadone</b>.
+CYP2B6	drug	alcohol	24625836	Several fold increases for cytochrome <strong>P450</strong> 2E1, caspase 8 and caspase 3 found in the lungs of <b>ethanol</b> fed mice as compared to pair fed controls suggest role of oxidative stress in <b>ethanol</b> induced lung injury.
+CYP2B6	drug	alcohol	24618581	Depolarization was linked to <b>ethanol</b> metabolism, since deficiency of <b>alcohol</b> dehydrogenase and cytochrome <strong>P450</strong> 2E1 (CYP2E1), the major <b>ethanol</b> metabolizing enzymes, decreased mitochondrial depolarization by ∼ 70% and ∼ 20%, respectively.
+CYP2B6	drug	nicotine	24527722	Electrochemical detection of human cytochrome <strong>P450</strong> 2A6 inhibition: a step toward reducing dependence on <b>smoking</b>.
+CYP2B6	addiction	dependence	24527722	Electrochemical detection of human cytochrome <strong>P450</strong> 2A6 inhibition: a step toward reducing <b>dependence</b> on smoking.
+CYP2B6	drug	nicotine	24527722	Inhibition of human cytochrome <strong>P450</strong> 2A6 has been demonstrated to play an important role in <b>nicotine</b> metabolism and consequent <b>smoking</b> habits.
+CYP2B6	drug	opioid	24489693	Impact of ABCB1 and <strong>CYP2B6</strong> genetic polymorphisms on <b>methadone</b> metabolism, dose and treatment response in patients with <b>opioid</b> addiction: a systematic review and meta analysis.
+CYP2B6	addiction	addiction	24489693	Impact of ABCB1 and <strong>CYP2B6</strong> genetic polymorphisms on methadone metabolism, dose and treatment response in patients with opioid <b>addiction</b>: a systematic review and meta analysis.
+CYP2B6	drug	opioid	24489693	To determine whether the <strong>CYP2B6</strong>*6 or ABCB1 (rs1045642) polymorphisms are associated with variation in <b>methadone</b> response (plasma concentration, dose, or response to treatment).
+CYP2B6	drug	opioid	24489693	We included studies that reported <b>methadone</b> plasma concentration, <b>methadone</b> response, or <b>methadone</b> dose in relation to the <strong>CYP2B6</strong>*6 or ABCB1 polymorphisms.
+CYP2B6	drug	opioid	24489693	Trough (R) <b>methadone</b> plasma concentration was significantly higher in <strong>CYP2B6</strong>*6 homozygous carriers when compared to non carriers (standardized mean difference [SMD] = 0.53, 95% confidence interval [CI], 0.05 1.00, p = 0.03) with minimal heterogeneity (I(2) = 0%).
+CYP2B6	drug	opioid	24489693	Although the number of studies included and sample size were modest, this is the first meta analysis to show participants homozygous for the <strong>CYP2B6</strong>*6 genotype have higher trough (R) and (S) <b>methadone</b> plasma concentrations, suggesting that <b>methadone</b> metabolism is significantly slower in *6 homozygous carriers.
+CYP2B6	drug	alcohol	24307790	Thus, genes related to <b>alcohol</b> addiction, such as dopamine receptor D2 in the brain, or liver <b>alcohol</b> metabolizing enzymes, such as <b>alcohol</b> dehydrogenase class I polypeptide B, cytochrome <strong>P450</strong> 2E1 and aldehyde dehydrogenase class 2, may vary from one individual to another.
+CYP2B6	addiction	addiction	24307790	Thus, genes related to alcohol <b>addiction</b>, such as dopamine receptor D2 in the brain, or liver alcohol metabolizing enzymes, such as alcohol dehydrogenase class I polypeptide B, cytochrome <strong>P450</strong> 2E1 and aldehyde dehydrogenase class 2, may vary from one individual to another.
+CYP2B6	drug	nicotine	24305170	Variants were introduced into a bi cistronic cDNA expression construct containing CYP2A6 and <strong>P450</strong> oxidoreductase and assessed for protein expression, enzymatic activity and stability as evaluated using western blotting and <b>nicotine</b> metabolism.
+CYP2B6	drug	nicotine	24305170	The variants showed significantly lower protein expression (P<0.001) when compared with the wild type as well as reduced metabolism of <b>nicotine</b> to cotinine when controlling for cDNA expression using <strong>P450</strong> oxidoreductase (P<0.001).
+CYP2B6	drug	amphetamine	24113184	HIV gp120  and <b>methamphetamine</b> mediated oxidative stress induces astrocyte apoptosis via cytochrome <strong>P450</strong> 2E1.
+CYP2B6	drug	amphetamine	24113184	In the present study, we demonstrate that gp120 and <b>methamphetamine</b> (MA) causes apoptotic cell death by inducing oxidative stress through the cytochrome <strong>P450</strong> (CYP) and NADPH oxidase (NOX) pathways.
+CYP2B6	drug	alcohol	24064383	<b>Ethanol</b> inducible cytochrome <strong>P450</strong> 2E1 (CYP2E1) contributes to increased oxidative stress and steatosis in chronic <b>alcohol</b> exposure models.
+CYP2B6	drug	nicotine	24045421	As a key step toward testing this hypothesis, we have studied <b>nicotine</b> metabolism and <b>nicotine</b>'s pharmacological and behavioral effects in a novel knockout mouse model [named Cyp2a(4/5)bgs null] lacking a number of cytochrome P450 genes known to be or possibly involved in <b>nicotine</b> metabolism, including two Cyp2a and all <strong>Cyp2b</strong> genes.
+CYP2B6	drug	nicotine	24045421	As a key step toward testing this hypothesis, we have studied <b>nicotine</b> metabolism and <b>nicotine</b>'s pharmacological and behavioral effects in a novel knockout mouse model [named Cyp2a(4/5)bgs null] lacking a number of cytochrome <strong>P450</strong> genes known to be or possibly involved in <b>nicotine</b> metabolism, including two Cyp2a and all <strong>Cyp2b</strong> genes.
+CYP2B6	drug	nicotine	24045421	Further comparisons of <b>nicotine</b> metabolism between Cyp2a(4/5)bgs null and Cyp2a5 null mice revealed significant roles of both CYP2A5 and <strong>CYP2B</strong> enzymes in <b>nicotine</b> clearance.
+CYP2B6	drug	nicotine	24033696	Evidence suggests that both the nicotinic receptor α5 subunit (CHRNA5) and Cytochrome <strong>P450</strong> 2A6 (CYP2A6) genotypes influence <b>smoking</b> cessation success and response to pharmacotherapy.
+CYP2B6	drug	nicotine	23983622	In general, over 70% absorbed <b>nicotine</b> is metabolized to cotinine and trans 3' hydroxycotinine by cytochrome oxidase <strong>P450</strong>, and <b>nicotine</b> is also a major addictive and the psychoactive component in cigarettes.
+CYP2B6	addiction	addiction	23983622	In general, over 70% absorbed nicotine is metabolized to cotinine and trans 3' hydroxycotinine by cytochrome oxidase <strong>P450</strong>, and nicotine is also a major <b>addictive</b> and the psychoactive component in cigarettes.
+CYP2B6	drug	alcohol	23958860	Activities of several other XME were below detection, namely the investigated cytochrome <strong>P450</strong> dependent alkylresorufin O dealkylases 7 ethylresorufin O deethylase, 7 benzylresorufin O debenzylase and 7 pentylresorufin O depentylase (while NADPH cytochrome c reductase activities were much above the limit of quantification), the flavin containing monooxygenase, the <b>alcohol</b> dehydrogenase as well as the UDP glucuronosyl transferase activities.
+CYP2B6	drug	nicotine	23807309	More importantly, the ratio of 3HC to cotinine is a good indicator to phenotype individuals for cytochrome <strong>P450</strong> 2A6 activity and to individualize pharmacotherapy for <b>tobacco</b> addiction.
+CYP2B6	addiction	addiction	23807309	More importantly, the ratio of 3HC to cotinine is a good indicator to phenotype individuals for cytochrome <strong>P450</strong> 2A6 activity and to individualize pharmacotherapy for tobacco <b>addiction</b>.
+CYP2B6	drug	alcohol	23639433	<b>Ethanol</b> self administration and nicotine treatment induce brain levels of <strong>CYP2B6</strong> and CYP2E1 in African green monkeys.
+CYP2B6	drug	nicotine	23639433	Ethanol self administration and <b>nicotine</b> treatment induce brain levels of <strong>CYP2B6</strong> and CYP2E1 in African green monkeys.
+CYP2B6	drug	alcohol	23639433	Human smokers and <b>alcoholics</b> have elevated levels of <strong>CYP2B6</strong> and CYP2E1 in certain brain regions, which may contribute to altered drug efficacy, neurotoxicity and metabolic tolerance.
+CYP2B6	drug	nicotine	23639433	Human <b>smokers</b> and alcoholics have elevated levels of <strong>CYP2B6</strong> and CYP2E1 in certain brain regions, which may contribute to altered drug efficacy, neurotoxicity and metabolic tolerance.
+CYP2B6	drug	alcohol	23639433	The objective of this study was to determine the effects of <b>ethanol</b> self administration and nicotine treatment, alone and in combination, on brain <strong>CYP2B6</strong> and CYP2E1 levels in monkeys.
+CYP2B6	drug	nicotine	23639433	The objective of this study was to determine the effects of ethanol self administration and <b>nicotine</b> treatment, alone and in combination, on brain <strong>CYP2B6</strong> and CYP2E1 levels in monkeys.
+CYP2B6	drug	alcohol	23639433	Immunocytochemistry revealed induction of both <strong>CYP2B6</strong> and CYP2E1 protein in certain brain regions and cells within monkey brain as a result of <b>ethanol</b> self administration, nicotine treatment and combined exposure to both drugs.
+CYP2B6	drug	nicotine	23639433	Immunocytochemistry revealed induction of both <strong>CYP2B6</strong> and CYP2E1 protein in certain brain regions and cells within monkey brain as a result of ethanol self administration, <b>nicotine</b> treatment and combined exposure to both drugs.
+CYP2B6	drug	alcohol	23639433	Immunoblotting analyses demonstrated <strong>CYP2B6</strong> induction by <b>ethanol</b> in the caudate, putamen and cerebellum (1.5 3.2 fold, P < 0.05), and CYP2E1 induction by nicotine in the frontal cortex and putamen (1.6 2.0 fold, P < 0.05).
+CYP2B6	drug	nicotine	23639433	Immunoblotting analyses demonstrated <strong>CYP2B6</strong> induction by ethanol in the caudate, putamen and cerebellum (1.5 3.2 fold, P < 0.05), and CYP2E1 induction by <b>nicotine</b> in the frontal cortex and putamen (1.6 2.0 fold, P < 0.05).
+CYP2B6	drug	alcohol	23639433	Combined <b>ethanol</b> and nicotine exposure induced <strong>CYP2B6</strong> in the caudate, putamen, thalamus and cerebellum (1.4 2.4 fold, P < 0.05), and CYP2E1 in the frontal cortex and putamen (1.5 1.8, P < 0.05).
+CYP2B6	drug	nicotine	23639433	Combined ethanol and <b>nicotine</b> exposure induced <strong>CYP2B6</strong> in the caudate, putamen, thalamus and cerebellum (1.4 2.4 fold, P < 0.05), and CYP2E1 in the frontal cortex and putamen (1.5 1.8, P < 0.05).
+CYP2B6	drug	alcohol	23639433	<strong>CYP2B6</strong> and CYP2E1 mRNA levels were unaffected by <b>ethanol</b> or nicotine exposure.
+CYP2B6	drug	nicotine	23639433	<strong>CYP2B6</strong> and CYP2E1 mRNA levels were unaffected by ethanol or <b>nicotine</b> exposure.
+CYP2B6	drug	alcohol	23639433	In summary, <b>ethanol</b> and nicotine can induce <strong>CYP2B6</strong> and CYP2E1 protein in the primate brain, which could potentially result in altered sensitivity to centrally acting drugs and toxins.
+CYP2B6	drug	nicotine	23639433	In summary, ethanol and <b>nicotine</b> can induce <strong>CYP2B6</strong> and CYP2E1 protein in the primate brain, which could potentially result in altered sensitivity to centrally acting drugs and toxins.
+CYP2B6	drug	opioid	23527673	Pharmacogenomics is of growing relevance to the pain field, for example cytochrome <strong>P450</strong> 2D6 (CYP2D6) polymorphisms with resulting variation in degree of CYP2D6 expression may affect <b>codeine</b> analgesia.
+CYP2B6	drug	alcohol	23400924	Catalase and cytochrome <strong>P450</strong> 2E1 (CYP2E1) represent the major enzymes in the CNS that catalyze <b>ethanol</b> oxidation.
+CYP2B6	drug	alcohol	23352848	However, sodium azide, a catalase inhibitor, and allyl sulfide, an inhibitor of cytochrome <strong>P450</strong> 2E1 (CYP2E1), failed to overcome LTP inhibition by 60mM <b>ethanol</b>.
+CYP2B6	drug	alcohol	23118795	In addition; levels of <b>alcohol</b> dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), the activities of cytochrome <strong>P450</strong> 2E1 (CYP2E1), selected antioxidative enzymes, and the contents of malonaldehyde (MDA) were measured.
+CYP2B6	drug	alcohol	22935730	Differential effects of nicotine treatment and <b>ethanol</b> self administration on CYP2A6, <strong>CYP2B6</strong> and nicotine pharmacokinetics in African green monkeys.
+CYP2B6	drug	nicotine	22935730	Differential effects of <b>nicotine</b> treatment and ethanol self administration on CYP2A6, <strong>CYP2B6</strong> and <b>nicotine</b> pharmacokinetics in African green monkeys.
+CYP2B6	drug	nicotine	22935730	In primates, <b>nicotine</b> is metabolically inactivated in the liver by CYP2A6 and possibly <strong>CYP2B6</strong>.
+CYP2B6	drug	nicotine	22935730	s.c.) on hepatic CYP2A6 and <strong>CYP2B6</strong> levels (mRNA, protein, and enzymatic activity), in vitro <b>nicotine</b> metabolism, and in vivo <b>nicotine</b> pharmacokinetics in monkeys.
+CYP2B6	drug	alcohol	22935730	<strong>CYP2B6</strong> protein levels and in vitro bupropion (selective <strong>CYP2B6</strong> substrate) metabolism were increased by <b>ethanol</b> but unaffected by nicotine treatment; <strong>CYP2B6</strong> mRNA levels were unaltered by either treatment.
+CYP2B6	drug	nicotine	22935730	<strong>CYP2B6</strong> protein levels and in vitro bupropion (selective <strong>CYP2B6</strong> substrate) metabolism were increased by ethanol but unaffected by <b>nicotine</b> treatment; <strong>CYP2B6</strong> mRNA levels were unaltered by either treatment.
+CYP2B6	drug	alcohol	22935730	Combined <b>ethanol</b> and nicotine exposure decreased CYP2A6 mRNA and protein levels, as well as in vitro coumarin and nicotine metabolism, and increased <strong>CYP2B6</strong> protein levels and in vitro bupropion metabolism, with no change in <strong>CYP2B6</strong> mRNA levels.
+CYP2B6	drug	nicotine	22935730	Combined ethanol and <b>nicotine</b> exposure decreased CYP2A6 mRNA and protein levels, as well as in vitro coumarin and <b>nicotine</b> metabolism, and increased <strong>CYP2B6</strong> protein levels and in vitro bupropion metabolism, with no change in <strong>CYP2B6</strong> mRNA levels.
+CYP2B6	drug	alcohol	22935730	Thus, nicotine can decrease hepatic CYP2A6, reducing the metabolism of its substrates, including nicotine, whereas <b>ethanol</b> can increase hepatic <strong>CYP2B6</strong>, increasing the metabolism of <strong>CYP2B6</strong> substrates.
+CYP2B6	drug	nicotine	22935730	Thus, <b>nicotine</b> can decrease hepatic CYP2A6, reducing the metabolism of its substrates, including <b>nicotine</b>, whereas ethanol can increase hepatic <strong>CYP2B6</strong>, increasing the metabolism of <strong>CYP2B6</strong> substrates.
+CYP2B6	drug	opioid	22926004	Study goals were to (1) characterize changes in <b>methadone</b> dose across childbearing, (2) determine enantiomer specific <b>methadone</b> withdrawal kinetics from steady state during late pregnancy, (3) assess enantiomer specific changes in <b>methadone</b> level/dose (L/D) ratios across childbearing, and (4) explore relationships between <strong>CYP2B6</strong>, CYP2C19, and CYP3A4 single nucleotide polymorphisms and maternal dose, plasma concentration, and L/D.
+CYP2B6	addiction	withdrawal	22926004	Study goals were to (1) characterize changes in methadone dose across childbearing, (2) determine enantiomer specific methadone <b>withdrawal</b> kinetics from steady state during late pregnancy, (3) assess enantiomer specific changes in methadone level/dose (L/D) ratios across childbearing, and (4) explore relationships between <strong>CYP2B6</strong>, CYP2C19, and CYP3A4 single nucleotide polymorphisms and maternal dose, plasma concentration, and L/D.
+CYP2B6	drug	opioid	22926004	Women with the <strong>CYP2B6</strong> Q172 variant GT genotype have consistently higher L/D values for S <b>methadone</b> across both pregnancy and postpartum.
+CYP2B6	drug	opioid	22722506	The complete metabolic disposition of <b>methadone</b> is likely to involve a number of enzymes, including specifically <strong>CYP2B6</strong>.
+CYP2B6	drug	nicotine	22700965	<b>Nicotine</b> and 4 (methylnitrosamino) 1 (3 pyridyl) 1 butanone binding and access channel in human cytochrome <strong>P450</strong> 2A6 and 2A13 enzymes.
+CYP2B6	drug	nicotine	22700965	Cytochromes <strong>P450</strong> (CYP) from the 2A subfamily are known for their roles in the metabolism of <b>nicotine</b>, the addictive agent in <b>tobacco</b>, and activation of the <b>tobacco</b> procarcinogen 4 (methylnitrosamino) 1 (3 pyridyl) 1 butanone (NNK).
+CYP2B6	addiction	addiction	22700965	Cytochromes <strong>P450</strong> (CYP) from the 2A subfamily are known for their roles in the metabolism of nicotine, the <b>addictive</b> agent in tobacco, and activation of the tobacco procarcinogen 4 (methylnitrosamino) 1 (3 pyridyl) 1 butanone (NNK).
+CYP2B6	drug	opioid	22685215	Mechanism based inactivation of cytochrome <strong>P450</strong> 2B6 by <b>methadone</b> through destruction of prosthetic heme.
+CYP2B6	drug	opioid	22685215	<b>Methadone</b> is metabolized predominantly in the liver by cytochromes <strong>P450</strong> to its pharmacologically inactive primary metabolite 2 ethylidene 1,5 dimethyl 3,3 diphenylpyrrolidine.
+CYP2B6	drug	opioid	22685215	However, recent clinical data have indicated that <strong>CYP2B6</strong> is actually the major isoform responsible for <b>methadone</b> metabolism and clearance in vivo.
+CYP2B6	drug	opioid	22685215	In this study, <b>methadone</b> was shown to act as a mechanism based inactivator of <strong>CYP2B6</strong>.
+CYP2B6	drug	opioid	22685215	<b>Methadone</b> inactivates <strong>CYP2B6</strong> in a time , concentration , and NADPH dependent manner with a K(I) = 10.0 μM and k(inact) = 0.027 min⁻¹.
+CYP2B6	drug	opioid	22685215	The loss of <strong>CYP2B6</strong> activity in the presence of <b>methadone</b> and NADPH occurred with concomitant loss of the reduced CO spectrum of the P450.
+CYP2B6	drug	opioid	22685215	The loss of <strong>CYP2B6</strong> activity in the presence of <b>methadone</b> and NADPH occurred with concomitant loss of the reduced CO spectrum of the <strong>P450</strong>.
+CYP2B6	drug	opioid	22685215	The evidence strongly suggests that destruction of prosthetic heme is the underlying mechanism leading to the inactivation of <strong>CYP2B6</strong> by <b>methadone</b>.
+CYP2B6	drug	nicotine	22676413	Cytochrome <strong>P450</strong> catalyzed degradation of <b>nicotine</b>: fundamental parameters determining hydroxylation by cytochrome <strong>P450</strong> 2A6 at the 5' carbon or the n methyl carbon.
+CYP2B6	drug	nicotine	22676413	The oxidation of (2'S) <b>nicotine</b> in the active site of human cytochrome <strong>P450</strong> 2A6 has been subjected to a detailed analysis by theoretical quantum mechanical/molecular mechanical (QM/MM) calculations linked with a theoretical and experimental study of the associated isotope effects.
+CYP2B6	drug	alcohol	22534656	<b>Disulfiram</b> has complex pharmacokinetics with rapid metabolism to active metabolites, including S methyl N,N diethylthiocarbamate (DET Me) which is formed from cytochrome <strong>P450</strong> (CYP450).
+CYP2B6	drug	opioid	22511698	<b>Methadone</b> is primarily metabolized by N demethylation to an inactive metabolite 2 ethylidene 1,5 dimethyl 3,3 diphenylpyrrolidene (EDDP) by CYP3A4 and <strong>CYP2B6</strong>.
+CYP2B6	drug	nicotine	22451501	Previous investigations of the relationship between Cytochrome <strong>P450</strong> 2A6 (CYP2A6) genotype and <b>smoking</b> phenotypes made comparisons by dividing subjects into broad categories based on assumptions that simplify the range of function of different CYP2A6 alleles, their numerous possible diplotype combinations and non additive allele effects.
+CYP2B6	drug	opioid	22381725	Nearly 20 studies showed a prolonged QT interval secondary to <b>methadone</b> in patients exhibiting the following features: (1) patients with cardiac pathologies, notably bradycardia, congenital long QT interval, myocardial pathologies related to AIDS and electrolyte disturbances; (2) patients receiving concomitant treatment with substances known to prolong QT interval, such as psychoactive stimulants, narcoleptics, tricyclic antidepressants, antiarrhythmic agents, macrolids, quinolones, non diuretic hypokalemiants and certain corticoids; (3) patients receiving treatments that inhibit <b>methadone</b>'s metabolism, particularly those that act on the cytochrome <strong>P450</strong> 3A4 such as SSRI, antifungal agents, some macrolids and some retroviral agents.
+CYP2B6	drug	opioid	22352453	By means of a generic modeling approach integrating prior physiologic knowledge, we systematically investigated the complex dependence of <b>opioid</b> exposure on cytochrome <strong>P450</strong> 2D6 and 3A4 (CYP2D6 and CYP3A4), and uridine diphosphate glucuronosyltransferase 2B7 (UGT2B7) activity, as well as renal function, by means of a virtual clinical trial.
+CYP2B6	addiction	dependence	22352453	By means of a generic modeling approach integrating prior physiologic knowledge, we systematically investigated the complex <b>dependence</b> of opioid exposure on cytochrome <strong>P450</strong> 2D6 and 3A4 (CYP2D6 and CYP3A4), and uridine diphosphate glucuronosyltransferase 2B7 (UGT2B7) activity, as well as renal function, by means of a virtual clinical trial.
+CYP2B6	drug	alcohol	22289614	The mRNA levels of cytochrome <strong>P450</strong> 2E1, NF κB, TNF α and transforming growth factor β1 were found to be increased in the <b>alcohol</b> treated rats, and their expressions were found to be decreased in the co administered group.
+CYP2B6	drug	nicotine	22073590	Absorbed <b>nicotine</b> through <b>smoking</b> into the body is mainly metabolized by cytochrome <strong>P450</strong> (CYP) 2A6.
+CYP2B6	drug	nicotine	22046326	The purpose of this study was to analyse the association of <b>smoking</b> status and <b>smoking</b> related phenotypes (included <b>nicotine</b> dependence) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], <strong>CYP2B6</strong>*4 (785A>G), <strong>CYP2B6</strong>*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CYP2B6	addiction	dependence	22046326	The purpose of this study was to analyse the association of smoking status and smoking related phenotypes (included nicotine <b>dependence</b>) with 17 candidate genetic variants: CYP2A6*1×2, CYP2A6*2 (1799T>A) [rs1801272], CYP2A6*9 ( 48T>G) [rs28399433], CYP2A6*12, CYP2A13*2 (3375C>T) [rs8192789], CYP2A13*3 (7520C>G), CYP2A13*4 (579G>A), CYP2A13*7 (578C>T) [rs72552266], <strong>CYP2B6</strong>*4 (785A>G), <strong>CYP2B6</strong>*9 (516G>T), CHRNA3 546C>T [rs578776], CHRNA5 1192G>A [rs16969968], CNR1 3764C>G [rs6928499], DRD2 ANKK1 2137G>A (Taq1A) [rs1800497], 5HTT LPR, HTR2A  1438A>G [rs6311] and OPRM1 118A>G [rs1799971].
+CYP2B6	drug	nicotine	22046326	We found a significant genotype effect (all P≤0.017) for the following <b>smoking</b> related phenotypes: (i) cigarettes smoked per day and CYP2A13*3; (ii) pack years smoked and CYP2A6*2, CYP2A6*1×2, CYP2A13*7, <strong>CYP2B6</strong>*4 and DRD2 ANKK1 2137G>A (Taq1A); (iii) <b>nicotine</b> dependence (assessed with the Fagestrom test) and CYP2A6*9.
+CYP2B6	addiction	dependence	22046326	We found a significant genotype effect (all P≤0.017) for the following smoking related phenotypes: (i) cigarettes smoked per day and CYP2A13*3; (ii) pack years smoked and CYP2A6*2, CYP2A6*1×2, CYP2A13*7, <strong>CYP2B6</strong>*4 and DRD2 ANKK1 2137G>A (Taq1A); (iii) nicotine <b>dependence</b> (assessed with the Fagestrom test) and CYP2A6*9.
+CYP2B6	drug	opioid	22035341	<b>Methadone</b> is extensively metabolized by cytochrome <strong>P450</strong> (CYP) 3A4 and to a lesser extent by CYP 1A2, 2D6, 2D8, 2C9/2C8, 2C19, and 2B6.
+CYP2B6	drug	opioid	22035341	Keywords that included <b>methadone</b>, drug drug interactions, CYP <strong>P450</strong> and AGP identified a total of 7709 papers.
+CYP2B6	drug	opioid	21902501	The isozyme CYP3A4 of the CYP system is one of the metabolic enzymes, as well as <strong>CYP2B6</strong>, responsible for the metabolism of <b>methadone</b>.
+CYP2B6	drug	opioid	21871151	The prevalence of <strong>CYP2B6</strong> and μ <b>opioid</b> receptor (OPRM1) gene variations were examined between a postmortem population where the deaths were associated with <b>methadone</b> and a live nondrug using control population using Taqman™ SNP Genotyping assays.
+CYP2B6	drug	opioid	21871151	Individual susceptibility to <b>methadone</b> may be determined by screening for <strong>CYP2B6</strong>*6.
+CYP2B6	drug	alcohol	21868470	Cytochrome <strong>P450</strong> 2E1 metabolizes <b>ethanol</b> and also bioactivates many toxins and procarcinogens.
+CYP2B6	drug	opioid	21790905	<strong>CYP2B6</strong> SNPs are associated with <b>methadone</b> dose required for effective treatment of <b>opioid</b> addiction.
+CYP2B6	addiction	addiction	21790905	<strong>CYP2B6</strong> SNPs are associated with methadone dose required for effective treatment of opioid <b>addiction</b>.
+CYP2B6	drug	opioid	21790905	<b>Methadone</b> metabolism is attributed primarily to cytochrome P450 enzymes CYP3A4, <strong>CYP2B6</strong> and CYP2D6.
+CYP2B6	drug	opioid	21790905	<b>Methadone</b> metabolism is attributed primarily to cytochrome <strong>P450</strong> enzymes CYP3A4, <strong>CYP2B6</strong> and CYP2D6.
+CYP2B6	drug	opioid	21790905	The <strong>CYP2B6</strong>*6 allele [single nucleotide polymorphisms (SNPs) 785A>G (rs2279343) and 516G>T (rs3745274)] was associated with slow <b>methadone</b> metabolism.
+CYP2B6	drug	opioid	21790905	To explore the effects of <strong>CYP2B6</strong>*6 allele on <b>methadone</b> dose requirement, it was genotyped in a well characterized sample of 74 Israeli former <b>heroin</b> addicts in MMT.
+CYP2B6	drug	opioid	21790905	The mean <b>methadone</b> doses required by subjects homozygous for the variant alleles of the <strong>CYP2B6</strong> SNPs 785A>G and 516G>T (88, 96mg, respectively) were significantly lower than those of the heterozygotes (133, 129mg, respectively) and the non carriers (150, 151mg, respectively) (nominal P=0.012, 0.048, respectively).
+CYP2B6	drug	cocaine	21705300	In the combination group, nifedipine decreased the nNOS activity in respect to the <b>cocaine</b> only group.In the liver, <b>cocaine</b> significantly decreased and nifedipine significantly increased cytochrome <strong>P450</strong>, ethylmorphine N demethylase, and anilinehydroxylase in respect to control.
+CYP2B6	drug	opioid	21691803	The marketed <b>tramadol</b> is a racemic mixture containing 50% (+)<b>tramadol</b> and 50% ( )<b>tramadol</b> and is mainly metabolized to O desmethyltramadol (M1) by the cytochrome <strong>P450</strong> CYP2D6.
+CYP2B6	drug	opioid	21589866	Contribution of cytochrome <strong>P450</strong> and ABCB1 genetic variability on <b>methadone</b> pharmacokinetics, dose requirements, and response.
+CYP2B6	drug	opioid	21589866	Patients were clinically assessed and blood samples were obtained to determine plasma concentrations of (R,S) , (R) and (S) <b>methadone</b> and to study allelic variants of genes encoding CYP3A5, CYP2D6, <strong>CYP2B6</strong>, CYP2C9, CYP2C19, and P glycoprotein.
+CYP2B6	drug	nicotine	21540762	To identify genetic polymorphisms that contribute to <b>nicotine</b> dependence, our group undertook a genetic association study including three enzyme families that potentially influence <b>nicotine</b> metabolism: cytochrome <strong>P450</strong> enzymes, flavin monooxygenases (FMOs), and UDP glucuronosyl transferases.
+CYP2B6	addiction	dependence	21540762	To identify genetic polymorphisms that contribute to nicotine <b>dependence</b>, our group undertook a genetic association study including three enzyme families that potentially influence nicotine metabolism: cytochrome <strong>P450</strong> enzymes, flavin monooxygenases (FMOs), and UDP glucuronosyl transferases.
+CYP2B6	drug	opioid	21411146	He was taking a relatively high dose of <b>methadone</b> but was not taking any concomitant cytochrome <strong>P450</strong> inhibitor or QT prolonging drugs.
+CYP2B6	drug	alcohol	21357267	This impairment of myeloid progenitor cell proliferation was not attenuated by inhibition of <b>alcohol</b> metabolism through either the <b>alcohol</b> dehydrogenase pathway or the cytochrome <strong>P450</strong> system.
+CYP2B6	drug	nicotine	21266057	Participants responded to survey items and provided blood samples for evaluation of phenotype and genotype of CYP2A6 and <strong>CYP2B6</strong> enzymes involved in <b>nicotine</b> and bupropion metabolism.
+CYP2B6	drug	nicotine	21266057	KIS III is the first study designed to examine both <b>nicotine</b> and bupropion metabolism, evaluating CYP2A6 and <strong>CYP2B6</strong> phenotype and genotype in conjunction with psychosocial factors, in the context of treatment of African American light <b>smokers</b>.
+CYP2B6	drug	opioid	21241245	Genetic transmission of cytochrome <strong>P450</strong> 2D6 (CYP2D6) ultrarapid metabolism: implications for breastfeeding women taking <b>codeine</b>.
+CYP2B6	drug	opioid	21241245	The safety of <b>codeine</b> during breastfeeding is related in part to the extent of the active <b>morphine</b> metabolite catalyzed from <b>codeine</b> via the cytochrome <strong>P450</strong> 2D6 (CYP2D6) enzyme.
+CYP2B6	drug	nicotine	21208832	Determination of the <b>nicotine</b> metabolites cotinine and trans 3' hydroxycotinine in biologic fluids of <b>smokers</b> and non <b>smokers</b> using liquid chromatography tandem mass spectrometry: biomarkers for <b>tobacco</b> smoke exposure and for phenotyping cytochrome <strong>P450</strong> 2A6 activity.
+CYP2B6	drug	nicotine	21208832	The ratio of another <b>nicotine</b> metabolite, trans 3' hydroxycotinine, to cotinine in biofluids is highly correlated with the rate of <b>nicotine</b> metabolism, which is catalyzed mainly by cytochrome <strong>P450</strong> 2A6 (CYP2A6).
+CYP2B6	drug	alcohol	20958327	The inhibitor of cytochrome <strong>P450</strong> 2E1 (CYP2E1) had no effect on <b>ethanol</b> induced DNA damage, and CYP2E1 mRNA expression was not affected by <b>ethanol</b>.
+CYP2B6	drug	opioid	20829393	In HepG2 cells, <b>buprenorphine</b> significantly increased human PXR mediated <strong>CYP2B6</strong> and CYP3A4 reporter activities.
+CYP2B6	drug	opioid	20829393	<strong>CYP2B6</strong> reporter activity was also enhanced by <b>buprenorphine</b> in HepG2 cells cotransfected with a chemical responsive human CAR variant.
+CYP2B6	drug	opioid	20829393	However, treatment with the same concentrations of <b>buprenorphine</b> in HPHs resulted in literally no induction of CYP3A4 or <strong>CYP2B6</strong> expression.
+CYP2B6	drug	opioid	20829393	Further studies indicated that <b>buprenorphine</b> could neither translocate human CAR to the nucleus nor activate <strong>CYP2B6</strong>/CYP3A4 reporter activities in transfected HPHs.
+CYP2B6	drug	alcohol	20828554	The <b>ethanol</b> elimination rate is regulated by <b>alcohol</b> metabolizing enzymes, primarily <b>alcohol</b> dehydrogenase (ADH1), acetaldehyde dehydrogenase (ALDH), and cytochrome <strong>P450</strong> (CYP2E1).
+CYP2B6	drug	amphetamine	20727252	Cytochrome <strong>P450</strong> 2D6 extensive metabolizers are more vulnerable to <b>methamphetamine</b> associated neurocognitive impairment: preliminary findings.
+CYP2B6	drug	amphetamine	20727252	One source of differential vulnerability could come from genotypic variability in metabolic clearance of <b>meth</b>, dependent on the activity of cytochrome <strong>P450</strong> 2D6 (CYP2D6).
+CYP2B6	drug	opioid	20668445	OPRM1 and <strong>CYP2B6</strong> gene variants as risk factors in <b>methadone</b> related deaths.
+CYP2B6	drug	opioid	20668445	We have examined the association between <strong>CYP2B6</strong> and micro <b>opioid</b> receptor (OPRM1) gene variations and apparent susceptibility to <b>methadone</b> poisoning.
+CYP2B6	drug	opioid	20668445	<strong>CYP2B6</strong> *4, *9, and *6 alleles were found to be associated with higher postmortem <b>methadone</b> concentrations in blood (P < or = 0.05).
+CYP2B6	drug	opioid	20668445	The risk of a <b>methadone</b> related fatality during treatment may be evaluated in part by screening for <strong>CYP2B6</strong>*6 and A118G.
+CYP2B6	drug	alcohol	20598484	The most well known metabolic pathways from <b>ethanol</b> to acetaldehyde include <b>alcohol</b> dehydrogenase (ADH) and the microsomal <b>ethanol</b> oxidizing system that involves cytochrome <strong>P450</strong> 2E1 (CYP2E1).
+CYP2B6	drug	nicotine	20418888	Among the genes at the two newly associated loci are genes encoding <b>nicotine</b> metabolizing enzymes (CYP2A6 and <strong>CYP2B6</strong>) and nicotinic acetylcholine receptor subunits (CHRNB3 and CHRNA6), all of which have been highlighted in previous studies of <b>smoking</b> and <b>nicotine</b> dependence.
+CYP2B6	addiction	dependence	20418888	Among the genes at the two newly associated loci are genes encoding nicotine metabolizing enzymes (CYP2A6 and <strong>CYP2B6</strong>) and nicotinic acetylcholine receptor subunits (CHRNB3 and CHRNA6), all of which have been highlighted in previous studies of smoking and nicotine <b>dependence</b>.
+CYP2B6	drug	alcohol	20021565	The inhibition of ACTH release, de novo adrenal StAR synthesis or cytochrome <strong>P450</strong> side chain cleavage activity prevents <b>ethanol</b> induced increases in GABAergic steroids in plasma and brain.
+CYP2B6	addiction	withdrawal	19924124	We aimed to assess the effect of coadministration and <b>withdrawal</b> of a potent cytochrome <strong>P450</strong> 3A (CYP3A) inhibitor (ritonavir) and a potent CYP3A inducer (St John's wort) on CYP3A enzyme activity in an open, fixed sequence study design.
+CYP2B6	drug	benzodiazepine	19884365	A cytochrome <strong>P450</strong> 3A (CYP3A) substudy with <b>midazolam</b> was conducted with the 25 mg dose.
+CYP2B6	drug	alcohol	19883652	These data indicate that <b>alcohol</b> dehydrogenase, and probably catalase and cytochrome <strong>P450</strong> monooxygenase oxidize methanol to formaldehyde, catalase and cytochrome <strong>P450</strong> monooxygenase catalyze formaldehyde to formic acid, water and carbon dioxide, and carboxylesterase may have a minor effect.
+CYP2B6	drug	psychedelics	19702527	<strong>CYP2B6</strong> can metabolise approximately 8% of clinically used drugs (n > 60), including cyclophosphamide, ifosfamide, tamoxifen, <b>ketamine</b>, artemisinin, nevirapine, efavirenz, bupropion, sibutramine, and propofol.
+CYP2B6	drug	nicotine	19702527	<b>Smokers</b> with the 1459C>T (R487C) variant of <strong>CYP2B6</strong> may be more vulnerable to abstinence symptoms and relapse following treatment with bupropion as a <b>smoking</b> cessation agent.
+CYP2B6	addiction	relapse	19702527	Smokers with the 1459C>T (R487C) variant of <strong>CYP2B6</strong> may be more vulnerable to abstinence symptoms and <b>relapse</b> following treatment with bupropion as a smoking cessation agent.
+CYP2B6	drug	nicotine	19563927	Polymorphisms of cytochrome <strong>P450</strong> 1A1, cigarette <b>smoking</b> and risk of coronary artery disease.
+CYP2B6	drug	nicotine	19563927	Cytochrome <strong>P450</strong> 1A1 (CYP1A1) is a key enzyme that metabolizes the cigarette toxin relevant to <b>smoking</b> induced atherogenesis.
+CYP2B6	addiction	sensitization	19480554	The results also indicate that skin <b>sensitization</b> and irritation reactions not only can be explained by the frequently in literature reported auto oxidation of tea tree resulting in bioactive oxidized products, but also now by the formation of epoxide intermediates resulting from catalysed arene epoxidation reactions by selected human cytochrome <strong>P450</strong> enzymes which are also located in different organs in humans.
+CYP2B6	drug	nicotine	19415821	In this study, we investigated the association and multilocus gene gene interactions of cytochrome <strong>P450</strong> 2A6 (CYP2A6), dopamine beta hydroxylase (DBH), catechol O methyl transferase (COMT), and monoamine oxidase A (MAOA) polymorphisms with <b>smoking</b> behavior in a community based Chinese male population.
+CYP2B6	drug	nicotine	19279561	Cytochrome <strong>P450</strong> 2A6 (CYP2A6) is the main <b>nicotine</b> (NIC) metabolizing enzyme in humans.
+CYP2B6	drug	nicotine	19251795	Recently, it has been shown that genetic variants in the dopaminergic system, opioid receptors, the bupropion metabolising enzyme <strong>CYP2B6</strong> and the <b>nicotine</b> metabolising enzyme CYP2A6 may play an important role in predicting <b>smoking</b> cessation responses to <b>nicotine</b> replacement therapy and bupropion treatment.
+CYP2B6	drug	opioid	19251795	Recently, it has been shown that genetic variants in the dopaminergic system, <b>opioid</b> receptors, the bupropion metabolising enzyme <strong>CYP2B6</strong> and the nicotine metabolising enzyme CYP2A6 may play an important role in predicting smoking cessation responses to nicotine replacement therapy and bupropion treatment.
+CYP2B6	drug	alcohol	19177030	Recent studies, however, suggest that cytochrome, in particular the isoform <strong>P450</strong> 2E1, can also contribute to the central metabolism of <b>ethanol</b>.
+CYP2B6	drug	nicotine	19169923	<b>Nicotine</b> metabolism is mediated primarily by cytochrome <strong>P450</strong> 2A6 (CYP2A6).
+CYP2B6	drug	nicotine	19169923	Inherited variation in the <strong>CYP2B6</strong> enzyme is also associated with response to bupropion treatment and counseling alone for <b>smoking</b> cessation.
+CYP2B6	drug	opioid	19133059	To investigate the influence of different cytochrome <strong>P450</strong> (CYP) activities and other potential covariates on the disposition of <b>methadone</b> in patients on <b>methadone</b> maintenance therapy (MMT).
+CYP2B6	drug	opioid	22190985	The pronounced inhibitory impact of voriconazole on <b>methadone</b> metabolism via the cytochrome <strong>P450</strong> (CYP)2B6 isoenzyme was identified as a probable cause of the arrhythmia.
+CYP2B6	addiction	addiction	19004845	Published data and data obtained from the drug's manufacturer implies that the dose <b>escalation</b> after 48 hours is to compensate for fomepizole induced increased body clearance resulting from autoinduction of the cytochrome <strong>P450</strong> (CYP) drug metabolizing enzyme CYP2E1.
+CYP2B6	drug	nicotine	18666753	The idea that the liver enzyme cytochrome <strong>P450</strong> 2A6 (CYP2A6), known also as <b>nicotine</b> C oxidase, is one of the determinants of <b>smoking</b> addiction and <b>smoking</b> behavior is primarily based on its role in <b>nicotine</b> metabolism and disposition.
+CYP2B6	addiction	addiction	18666753	The idea that the liver enzyme cytochrome <strong>P450</strong> 2A6 (CYP2A6), known also as nicotine C oxidase, is one of the determinants of smoking <b>addiction</b> and smoking behavior is primarily based on its role in nicotine metabolism and disposition.
+CYP2B6	drug	nicotine	18484799	This article focuses on a range of novel pharmacological approaches for the treatment of <b>tobacco</b> dependence and/or withdrawal, including oral and pulmonary <b>nicotine</b> delivery and the following non nicotinic medications: antidepressants, an alpha4beta2 <b>nicotine</b> partial agonist, an alpha2 noradrenergic agonist, cytochrome <strong>P450</strong> (CYP) 2A6 inhibitors, opioid antagonists and GABAergic medications.
+CYP2B6	drug	opioid	18484799	This article focuses on a range of novel pharmacological approaches for the treatment of tobacco dependence and/or withdrawal, including oral and pulmonary nicotine delivery and the following non nicotinic medications: antidepressants, an alpha4beta2 nicotine partial agonist, an alpha2 noradrenergic agonist, cytochrome <strong>P450</strong> (CYP) 2A6 inhibitors, <b>opioid</b> antagonists and GABAergic medications.
+CYP2B6	addiction	dependence	18484799	This article focuses on a range of novel pharmacological approaches for the treatment of tobacco <b>dependence</b> and/or withdrawal, including oral and pulmonary nicotine delivery and the following non nicotinic medications: antidepressants, an alpha4beta2 nicotine partial agonist, an alpha2 noradrenergic agonist, cytochrome <strong>P450</strong> (CYP) 2A6 inhibitors, opioid antagonists and GABAergic medications.
+CYP2B6	addiction	withdrawal	18484799	This article focuses on a range of novel pharmacological approaches for the treatment of tobacco dependence and/or <b>withdrawal</b>, including oral and pulmonary nicotine delivery and the following non nicotinic medications: antidepressants, an alpha4beta2 nicotine partial agonist, an alpha2 noradrenergic agonist, cytochrome <strong>P450</strong> (CYP) 2A6 inhibitors, opioid antagonists and GABAergic medications.
+CYP2B6	drug	alcohol	18424410	The review focuses on several related genes that control <b>alcohol</b> metabolism such as <b>alcohol</b> dehydrogenase, aldehyde dehydrogenase, cytochrome <strong>P450</strong> 2E1 and regulate neurotransmission such as catechol O methyltransferase, dopamine receptors D2 and D4, and mu opioid receptor.
+CYP2B6	drug	opioid	18424410	The review focuses on several related genes that control alcohol metabolism such as alcohol dehydrogenase, aldehyde dehydrogenase, cytochrome <strong>P450</strong> 2E1 and regulate neurotransmission such as catechol O methyltransferase, dopamine receptors D2 and D4, and mu <b>opioid</b> receptor.
+CYP2B6	drug	opioid	18422375	Cytochrome <strong>P450</strong> (CYP) 3A4 and 2B6 have been identified as the main CYP isoforms involved in <b>methadone</b> metabolism.
+CYP2B6	drug	opioid	18294936	Since <b>buprenorphine</b> is metabolized through cytochrome <strong>P450</strong> 3A4, we genotyped six genetic polymorphisms previously described in poor metabolizers but could not confirm these pharmacogenetic bases in this case.
+CYP2B6	drug	opioid	18202730	<b>Buprenorphine</b> is metabolized in the liver by cytochrome <strong>P450</strong> to the active metabolite norbuprenorphine, and further to <b>buprenorphine</b> glucuronide and norbuprenorphine glucuronide.
+CYP2B6	drug	cannabinoid	18201292	The present investigation evaluated associations between the P350 and <strong>P450</strong> components of the event related potential (ERP) elicited by affective stimuli, and <b>marijuana</b> dependence in a population of Southwest California (SWC) Indian adults.
+CYP2B6	addiction	dependence	18201292	The present investigation evaluated associations between the P350 and <strong>P450</strong> components of the event related potential (ERP) elicited by affective stimuli, and marijuana <b>dependence</b> in a population of Southwest California (SWC) Indian adults.
+CYP2B6	drug	cannabinoid	18201292	Increases in the latency of both the P350 and <strong>P450</strong> component peaks were found to be associated with the diagnosis of <b>marijuana</b> dependence and <b>marijuana</b> dependence co morbid with other drug dependence.
+CYP2B6	addiction	dependence	18201292	Increases in the latency of both the P350 and <strong>P450</strong> component peaks were found to be associated with the diagnosis of marijuana <b>dependence</b> and marijuana <b>dependence</b> co morbid with other drug <b>dependence</b>.
+CYP2B6	drug	alcohol	18046720	Chronic <b>alcohol</b> consumption induces cytochrome <strong>P450</strong> 2E1, a microsomal enzyme that metabolizes <b>alcohol</b> at high concentrations and also metabolizes medications such as acetaminophen and protease inhibitors.
+CYP2B6	drug	nicotine	18033154	Interactions between <b>smoking</b> and antipsychotic medication   <b>Smoking</b> increases the metabolism of the antipsychotic medications by inducing the cytochrome <strong>P450</strong> 1A2 isoform.
+CYP2B6	drug	nicotine	18004205	Gene gene interactions between <strong>CYP2B6</strong> and CYP2A6 in <b>nicotine</b> metabolism.
+CYP2B6	drug	nicotine	18004205	We investigated the influence of genetic variation in another potential <b>nicotine</b> metabolizing enzyme, <strong>CYP2B6</strong>, and its interaction with CYP2A6, on the metabolism of <b>nicotine</b>.
+CYP2B6	drug	nicotine	18004205	We observed that the <strong>CYP2B6</strong>*6 haplotype (defined as having both Q172 H and K262R variants) was associated with faster <b>nicotine</b> and cotinine clearance, and that such associations were more prominent among individuals having decreased activity CYP2A6 genotypes.
+CYP2B6	drug	nicotine	18004205	Statistically significant interactions between <strong>CYP2B6</strong> and CYP2A6 genotypes were observed (P<0.003 for <b>nicotine</b> clearance and P<0.002 for cotinine clearance).
+CYP2B6	drug	nicotine	18004205	Our results indicate that <strong>CYP2B6</strong> genetic variation is associated with the metabolism of <b>nicotine</b> and cotinine among individuals with decreased CYP2A6 activity.
+CYP2B6	drug	nicotine	18004205	Further investigation of the roles of <strong>CYP2B6</strong> and the interaction between <strong>CYP2B6</strong> and CYP2A6 genotypes in mediating <b>nicotine</b> dependence and <b>tobacco</b> related diseases is merited.
+CYP2B6	addiction	dependence	18004205	Further investigation of the roles of <strong>CYP2B6</strong> and the interaction between <strong>CYP2B6</strong> and CYP2A6 genotypes in mediating nicotine <b>dependence</b> and tobacco related diseases is merited.
+CYP2B6	drug	nicotine	17979512	Cytochrome <strong>P450</strong> (CYP)2A6 is the human hepatic enzyme that mediates most of <b>nicotine</b>'s metabolic inactivation to cotinine.
+CYP2B6	drug	alcohol	17960299	The present investigation evaluated associations between the P350 and <strong>P450</strong> components of the event related potential (ERP) elicited by affective stimuli and potential vulnerability factors associated with risk of <b>alcohol</b> dependence in Southwest California (SWC) Indian adults.
+CYP2B6	addiction	dependence	17960299	The present investigation evaluated associations between the P350 and <strong>P450</strong> components of the event related potential (ERP) elicited by affective stimuli and potential vulnerability factors associated with risk of alcohol <b>dependence</b> in Southwest California (SWC) Indian adults.
+CYP2B6	drug	alcohol	17960299	<strong>P450</strong> amplitudes were significantly reduced in participants who met lifetime Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, criteria for <b>alcohol</b> dependence in centroparietal leads.
+CYP2B6	addiction	dependence	17960299	<strong>P450</strong> amplitudes were significantly reduced in participants who met lifetime Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, criteria for alcohol <b>dependence</b> in centroparietal leads.
+CYP2B6	drug	alcohol	17960299	Neither P350 nor <strong>P450</strong> component amplitudes were significantly altered based on a family history of <b>alcohol</b> dependence, a personal history of antisocial personality disorder/conduct disorder, or the presence of drug dependence other than <b>alcohol</b>.
+CYP2B6	addiction	dependence	17960299	Neither P350 nor <strong>P450</strong> component amplitudes were significantly altered based on a family history of alcohol <b>dependence</b>, a personal history of antisocial personality disorder/conduct disorder, or the presence of drug <b>dependence</b> other than alcohol.
+CYP2B6	drug	alcohol	17960299	These findings suggest, in this select population, that <strong>P450</strong> amplitudes are selectively affected by both <b>alcohol</b> dependence and affective disorder.
+CYP2B6	addiction	dependence	17960299	These findings suggest, in this select population, that <strong>P450</strong> amplitudes are selectively affected by both alcohol <b>dependence</b> and affective disorder.
+CYP2B6	drug	alcohol	17960299	However, reductions in <strong>P450</strong> amplitude were restricted to those participants with <b>alcohol</b> dependence, confirming that it may be an important putative endophenotype for genetic studies of that disorder in this high risk population.
+CYP2B6	addiction	dependence	17960299	However, reductions in <strong>P450</strong> amplitude were restricted to those participants with alcohol <b>dependence</b>, confirming that it may be an important putative endophenotype for genetic studies of that disorder in this high risk population.
+CYP2B6	drug	nicotine	17923852	<b>Nicotine</b> is eliminated by metabolism through the cytochrome <strong>P450</strong> 2A6 (CYP2A6) enzyme in liver.
+CYP2B6	drug	alcohol	17764730	The relationship between the <strong>P450</strong> component elicited by affective stimuli and: a personal history of <b>alcohol</b> dependence, antisocial personality disorder/conduct disorder (ASPD/CD) or affective anxiety disorders (ANYAXAF) was examined in Mexican Americans, a group with high rates of heavy drinking.
+CYP2B6	addiction	dependence	17764730	The relationship between the <strong>P450</strong> component elicited by affective stimuli and: a personal history of alcohol <b>dependence</b>, antisocial personality disorder/conduct disorder (ASPD/CD) or affective anxiety disorders (ANYAXAF) was examined in Mexican Americans, a group with high rates of heavy drinking.
+CYP2B6	drug	alcohol	17764730	No significant associations were seen between the <strong>P450</strong> amplitude and the diagnosis of <b>alcohol</b> dependence.
+CYP2B6	addiction	dependence	17764730	No significant associations were seen between the <strong>P450</strong> amplitude and the diagnosis of alcohol <b>dependence</b>.
+CYP2B6	drug	alcohol	17718403	The primary enzymes involved are aldehyde dehydrogenase (ALDH), <b>alcohol</b> dehydrogenase (ADH), cytochrome <strong>P450</strong> (CYP2E1), and catalase.
+CYP2B6	drug	nicotine	17654295	<b>Smokers</b> of European ancestry (N = 291), who were randomized to receive bupropion or placebo (12 weeks) plus counseling, were genotyped for the dopamine D2 receptor (DRD2 Taq1A), dopamine transporter (SLC6A3 3' VNTR), and cytochrome P450 2B6 (<strong>CYP2B6</strong> 1459 CT) polymorphisms.
+CYP2B6	drug	nicotine	17654295	<b>Smokers</b> of European ancestry (N = 291), who were randomized to receive bupropion or placebo (12 weeks) plus counseling, were genotyped for the dopamine D2 receptor (DRD2 Taq1A), dopamine transporter (SLC6A3 3' VNTR), and cytochrome <strong>P450</strong> 2B6 (<strong>CYP2B6</strong> 1459 CT) polymorphisms.
+CYP2B6	drug	alcohol	17614007	Study on the cytochrome <strong>P450</strong> mediated oxidative metabolism of the terpene <b>alcohol</b> linalool: indication of biological epoxidation.
+CYP2B6	drug	alcohol	17614007	The cytochrome <strong>P450</strong> mediated oxidative metabolism of the terpene <b>alcohol</b> linalool was studied in vitro by enzymatic assays using recombinant human cytochrome <strong>P450</strong> enzymes.
+CYP2B6	addiction	sensitization	17614007	The results indicate that the electrophilic oxidation products of linalool such as 6,7 epoxy linalool which may cause <b>sensitization</b> and irritational skin reactions are not only produced by auto oxidation reactions in the presence of air oxygen as published in the past, but also by <strong>P450</strong> mediated oxidative biological transformation.
+CYP2B6	drug	nicotine	17454707	<b>Nicotine</b> is metabolized into biologically inactive cotinine primarily by the cytochrome <strong>P450</strong> enzyme CYP2A6.
+CYP2B6	drug	alcohol	17392391	CYP2E1 is widely accepted as the sole form of cytochrome <strong>P450</strong> responsible for <b>alcohol</b> mediated increases in acetaminophen (APAP) hepatotoxicity.
+CYP2B6	drug	nicotine	17372541	Some variants of the cytochrome <strong>P450</strong> seem to be more frequent among dependent <b>smokers</b> than controls or ever <b>smokers</b> (CYP2A6) and heavier <b>smokers</b> (CYP2D6).
+CYP2B6	drug	alcohol	17343998	Minor metabolic <b>alcohol</b> pathways include oxidation through the cytochrome <strong>P450</strong> system and catalase.
+CYP2B6	addiction	dependence	17284003	Cytochrome <strong>P450</strong> 3A4 (CYP3A4) is a key enzyme responsible for the metabolism of 50% of all orally administered drugs which exhibit an intriguing kinetic behavior typified by a sigmoidal <b>dependence</b> of the reaction velocity on the substrate concentration.
+CYP2B6	drug	nicotine	17223085	<strong>CYP2B6</strong> genotype alters abstinence rates in a bupropion <b>smoking</b> cessation trial.
+CYP2B6	drug	nicotine	17223085	Among <b>smokers</b> in the <strong>CYP2B6</strong>*6 group (<strong>CYP2B6</strong>*1/*6 or <strong>CYP2B6</strong>*6/*6 genotype, n = 147, 45% of the population), bupropion produced significantly higher abstinence rates than placebo at the end of treatment (32.5% vs. 14.3%, p = .01) and at the 6 month follow up (31.2% vs. 12.9%, p = .008).
+CYP2B6	drug	nicotine	17223085	In contrast, bupropion was no more effective than placebo for <b>smokers</b> in the <strong>CYP2B6</strong>*1 group (<strong>CYP2B6</strong>*1/*1, n = 179) at the end of treatment (31.0% vs. 31.6%, p = .93) or at the 6 month follow up (22.0% vs. 21.5%, p = .94).
+CYP2B6	drug	nicotine	17223085	These data suggest that <b>smokers</b> with the <strong>CYP2B6</strong>*6 genotype have a higher liability to relapse on placebo and that they may be good candidates for bupropion treatment for <b>smoking</b> cessation.
+CYP2B6	addiction	relapse	17223085	These data suggest that smokers with the <strong>CYP2B6</strong>*6 genotype have a higher liability to <b>relapse</b> on placebo and that they may be good candidates for bupropion treatment for smoking cessation.
+CYP2B6	drug	alcohol	17196788	Decreases in a later component amplitude (<strong>P450</strong>) were also found in young adults exposed to <b>alcohol</b>, and those exposed to <b>alcohol</b> and drugs.
+CYP2B6	drug	opioid	17187532	This would include the effects <b>methadone</b> has on N methyl D aspartate (NMDA) in addition to the impact of <b>methadone</b> on the cytochrome <strong>P450</strong> enzyme system.
+CYP2B6	drug	opioid	17084876	In contrast, norbuprenorphine, the <b>buprenorphine</b> major cytochrome <strong>P450</strong> (CYP) 3A derived metabolite, is a potent respiratory depressant.
+CYP2B6	drug	opioid	17084876	We investigated the effects on ventilation of 30 mg kg( 1) <b>buprenorphine</b> alone or following cytochrome <strong>P450</strong> (CYP) 3A induction with dexamethasone, using whole body plethysmography (N=24) and arterial blood gases (N=12).
+CYP2B6	drug	nicotine	17015050	Studies on cytochrome <strong>P450</strong> (CYP) 2A6 suggest that genotype affects the rate of <b>nicotine</b> metabolism and, consequently, cigarette consumption.
+CYP2B6	drug	nicotine	17015050	The <b>nicotine</b> metabolite ratio was associated with sex (P < .0001), CYP2A6 genotype (*1B, *2, *4, *9, and *12) (P < .0001), <strong>CYP2B6</strong> haplotype (*4 dominant) (P = .02), plasma <b>nicotine</b> concentration (P < .0001), and age (P = .02) but was not associated with dependence score (P > .20).
+CYP2B6	addiction	dependence	17015050	The nicotine metabolite ratio was associated with sex (P < .0001), CYP2A6 genotype (*1B, *2, *4, *9, and *12) (P < .0001), <strong>CYP2B6</strong> haplotype (*4 dominant) (P = .02), plasma nicotine concentration (P < .0001), and age (P = .02) but was not associated with <b>dependence</b> score (P > .20).
+CYP2B6	drug	nicotine	17015050	In this cohort the rate of <b>nicotine</b> metabolism is related to age, sex, CYP2A6 genotype, and <strong>CYP2B6</strong> genotype and may affect the level of <b>tobacco</b> consumption.
+CYP2B6	drug	nicotine	16952495	Human cytochrome <strong>P450</strong> (CYP) 2A6 metabolizes <b>nicotine</b> to cotinine and is a possible modulator of <b>nicotine</b> addiction.
+CYP2B6	addiction	addiction	16952495	Human cytochrome <strong>P450</strong> (CYP) 2A6 metabolizes nicotine to cotinine and is a possible modulator of nicotine <b>addiction</b>.
+CYP2B6	drug	alcohol	16923312	<b>Ethanol</b> induced oxidative stress is the result of the combined impairment of antioxidant defences and the production of reactive oxygen species by the mitochondrial electron transport chain, the <b>alcohol</b> inducible cytochrome <strong>P450</strong> (CYP) 2E1 and activated phagocytes.
+CYP2B6	drug	nicotine	16891249	The genetically polymorphic cytochrome <strong>P450</strong> (CYP) 2A6 is the major <b>nicotine</b> oxidase in humans that may contribute to <b>nicotine</b> dependence and cancer susceptibility.
+CYP2B6	addiction	dependence	16891249	The genetically polymorphic cytochrome <strong>P450</strong> (CYP) 2A6 is the major nicotine oxidase in humans that may contribute to nicotine <b>dependence</b> and cancer susceptibility.
+CYP2B6	drug	opioid	16785264	Candidate genes include those involved in central mechanisms (such as genes encoding the nicotinic acetylcholine receptors, dopamine receptors, dopamine transporters and <b>opioid</b> receptors) and peripheral mechanisms (such as genes encoding the drug metabolizing enzymes CYP2A6 and <strong>CYP2B6</strong>).
+CYP2B6	drug	nicotine	16784837	The association between current <b>smoking</b> and heavy caffeine intake may be partly explained by a pharmacokinetic effect: <b>tobacco</b> smoke compounds induce caffeine metabolism by the cytochrome <strong>P450</strong> 1A2.
+CYP2B6	drug	nicotine	16765148	<b>Nicotine</b> is metabolized to cotinine, and cotinine is metabolized to 3' hydroxycotinine (3 HC) by the liver enzyme cytochrome <strong>P450</strong> (CYP) 2A6.
+CYP2B6	drug	nicotine	16599377	To investigate the potential mechanism of previously documented lower <b>smoking</b> rates among African American adolescent <b>smokers</b> seeking cessation treatment, we measured <b>nicotine</b> metabolite ratios as markers of the metabolic disposition of <b>nicotine</b>, which is generally considered to be under the influence of cytochrome <strong>P450</strong> (CYP) 2A6.
+CYP2B6	addiction	relapse	16599377	To investigate the potential mechanism of previously documented lower smoking rates among African American adolescent smokers <b>seeking</b> cessation treatment, we measured nicotine metabolite ratios as markers of the metabolic disposition of nicotine, which is generally considered to be under the influence of cytochrome <strong>P450</strong> (CYP) 2A6.
+CYP2B6	drug	alcohol	16549397	Induction of cytochrome <strong>P450</strong> 2E1 by <b>ethanol</b> is believed to be one of the central pathways by which <b>ethanol</b> generates a state of oxidative stress and causes hepatotoxicity.
+CYP2B6	drug	opioid	16431829	The pharmacokinetics of <b>methadone</b> differ from those of <b>morphine</b> in that <b>methadone</b> has a higher bioavailability, a much longer half life, and is hepatically metabolized by cytochrome <strong>P450</strong> enzymes.
+CYP2B6	drug	alcohol	16337197	<b>Ethanol</b> increases mitochondrial cytochrome <strong>P450</strong> 2E1 in mouse liver and rat hepatocytes.
+CYP2B6	drug	amphetamine	16250257	It is metabolized in the organism with a reaction that is catalyzed by cytochrome <strong>P450</strong>, mainly by the CYP2D and CYP3A subfamily, 4 hydroxyamphetamine and <b>amphetamine</b> being dominant metabolites.
+CYP2B6	drug	alcohol	16226717	We report here the unexpected finding that recombinant or hepatic microsomal NADPH cytochrome <strong>P450</strong> reductase catalyzes the oxidative deformylation of a model xenobiotic aldehyde, 2 phenylpropionaldehyde, to the n 1 <b>alcohol</b>, 1 phenylethanol, in the absence of cytochrome <strong>P450</strong>.
+CYP2B6	drug	opioid	16184033	To determine if atazanavir, a once daily protease inhibitor and moderate inhibitor of <strong>P450</strong> CYP3A4, exhibited pharmacokinetic interactions with (R) <b>methadone</b>.
+CYP2B6	drug	nicotine	16174803	<b>Nicotine</b> and 4 (methylnitrosamino) 1 (3 pyridyl) butanone metabolism by cytochrome <strong>P450</strong> 2B6.
+CYP2B6	drug	nicotine	16174803	4 (Methylnitrosamine) 1 (3 pyridyl) 1 butanone (NNK), a potent lung carcinogen generated from <b>nicotine</b> during the curing of <b>tobacco</b>, is metabolically activated by <strong>P450</strong> enzymes.
+CYP2B6	drug	nicotine	16174803	<strong>P450</strong> 2A6 is the primary hepatic catalyst of <b>nicotine</b> metabolism and also catalyzes NNK alpha hydroxylation, albeit less efficiently.
+CYP2B6	drug	nicotine	16174803	It was previously reported that <strong>P450</strong> 2B6 catalyzed <b>nicotine</b> 5' oxidation.
+CYP2B6	drug	nicotine	16174803	The studies presented here investigate the relative importance of <strong>P450</strong> 2B6 as a catalyst of <b>nicotine</b> 5' oxidation and NNK alpha hydroxylation by human liver microsomes (HLMs).
+CYP2B6	drug	nicotine	16174803	The primary product of <strong>P450</strong> 2B6 catalyzed <b>nicotine</b> metabolism was the delta1'(5') iminium ion.
+CYP2B6	drug	nicotine	16174803	We determined that <strong>P450</strong> 2B6 was a much less efficient catalyst of <b>nicotine</b> 5' oxidation than previously reported, with an estimated K(m) of 820 microM.
+CYP2B6	drug	nicotine	16174803	Experiments with <strong>P450</strong> 2A6  and <strong>P450</strong> 2B6 selective inhibitory antibodies did not support <strong>P450</strong> 2B6 as a significant catalyst of <b>nicotine</b> 5' oxidation by HLMs, and it is unlikely that this enzyme contributes to <b>nicotine</b> metabolism in <b>smokers</b> who express <strong>P450</strong> 2A6.
+CYP2B6	drug	alcohol	16126318	Chronic <b>ethanol</b> exposure downregulates hepatic expression of pregnane X receptor and <strong>P450</strong> 3A11 in female ICR mice.
+CYP2B6	drug	alcohol	16126318	In this study, we investigated the effects of chronic <b>ethanol</b> exposure on PXR and <strong>P450</strong> 3A11 gene expression in mouse liver.
+CYP2B6	drug	alcohol	16126318	Results showed that chronic <b>ethanol</b> exposure markedly decreased hepatic PXR and <strong>P450</strong> 3A11 mRNA levels.
+CYP2B6	drug	alcohol	16126318	Consistent with downregulation of <strong>P450</strong> 3A11 mRNA, chronic <b>ethanol</b> exposure significantly decreased ERND activity in a dose dependent manner.
+CYP2B6	drug	alcohol	16126318	These results indicated that activation of Kupffer cells by gut derived endotoxin contributes to downregulation of hepatic PXR and <strong>P450</strong> 3A11 expression during chronic <b>alcohol</b> intoxication.
+CYP2B6	addiction	intoxication	16126318	These results indicated that activation of Kupffer cells by gut derived endotoxin contributes to downregulation of hepatic PXR and <strong>P450</strong> 3A11 expression during chronic alcohol <b>intoxication</b>.
+CYP2B6	drug	alcohol	16054976	Chronic <b>ethanol</b> consumption may promote carcinogenesis by (1) production of acetaldehyde, which is a weak mutagen and carcinogen; (2) induction of cytochrome <strong>P450</strong> 2E1 and associated oxidative stress and conversion of procarcinogens to carcinogens; (3) depletion of S adenosylmethionine and, consequently, induction of global DNA hypomethylation; (4) induction of increased production of inhibitory guanine nucleotide regulatory proteins and components of extracellular signal regulated kinase mitogen activated protein kinase signaling; (5) accumulation of iron and associated oxidative stress; (6) inactivation of the tumor suppressor gene BRCA1 and increased estrogen responsiveness (primarily in breast); and (7) impairment of retinoic acid metabolism.
+CYP2B6	drug	nicotine	15735610	Influence of menstrual cycle on cytochrome <strong>P450</strong> 2A6 activity and cardiovascular effects of <b>nicotine</b>.
+CYP2B6	drug	nicotine	15735610	Cytochrome <strong>P450</strong> (CYP) 2A6 is primarily responsible for the metabolism of <b>nicotine</b>.
+CYP2B6	drug	nicotine	15735609	In this review we summarize <b>nicotine</b> dependence and the genetics of <b>smoking</b> in brief before focusing on cytochrome <strong>P450</strong> (CYP) 2A6.
+CYP2B6	addiction	dependence	15735609	In this review we summarize nicotine <b>dependence</b> and the genetics of smoking in brief before focusing on cytochrome <strong>P450</strong> (CYP) 2A6.
+CYP2B6	drug	nicotine	15734728	<b>Nicotine</b> is of importance as the addictive chemical in <b>tobacco</b>, pharmacotherapy for <b>smoking</b> cessation, a potential medication for several diseases, and a useful probe drug for phenotyping cytochrome <strong>P450</strong> 2A6 (CYP2A6).
+CYP2B6	addiction	addiction	15734728	Nicotine is of importance as the <b>addictive</b> chemical in tobacco, pharmacotherapy for smoking cessation, a potential medication for several diseases, and a useful probe drug for phenotyping cytochrome <strong>P450</strong> 2A6 (CYP2A6).
+CYP2B6	drug	nicotine	15734728	Enzymes involved in <b>nicotine</b> metabolism including cytochrome <strong>P450</strong> enzymes, aldehyde oxidase, flavin containing monooxygenase 3, amine N methyltransferase, and UDP glucuronosyltransferases are represented, as well as factors affecting metabolism, such as genetic variations in metabolic enzymes, effects of diet, age, gender, pregnancy, liver and kidney diseases, and racial and ethnic differences.
+CYP2B6	drug	alcohol	15633127	Hepatitis C virus core protein, cytochrome <strong>P450</strong> 2E1, and <b>alcohol</b> produce combined mitochondrial injury and cytotoxicity in hepatoma cells.
+CYP2B6	drug	alcohol	15633127	The aim of this study was to determine whether hepatitis C virus core protein and <b>alcohol</b> inducible cytochrome <strong>P450</strong> 2E1 contribute to reactive oxygen species production and cytotoxicity in human hepatoma cells.
+CYP2B6	drug	alcohol	15633127	Huh 7 cells expressing core protein, cytochrome <strong>P450</strong> 2E1, or both were exposed to 0.1 mmol/L tertiary butyl hydroperoxide, tumor necrosis factor alpha, and/or 25 mmol/L <b>ethanol</b>.
+CYP2B6	drug	opioid	15605124	The quantity of liver cytochrome <strong>P450</strong>, after multiple coadministration of <b>morphine</b> and nifedipine, was also increased.
+CYP2B6	drug	opioid	15605124	The quantity of brain cytochrome <strong>P450</strong> was not significantly changed by <b>morphine</b> and nifedipine alone or in combination.
+CYP2B6	drug	opioid	15568612	Moreover, the use of <b>methadone</b> associated with other inhibitors of cytochrome <strong>P450</strong> might increase plasma concentrations and contribute to <b>methadone</b> cardiac toxicity.
+CYP2B6	drug	nicotine	15564629	Case control studies in adults suggest that defective alleles in the gene that codes for the hepatic cytochrome <strong>P450</strong> 2A6 (CYP2A6) protect against <b>nicotine</b> dependence (ND) and higher levels of cigarette consumption.
+CYP2B6	addiction	dependence	15564629	Case control studies in adults suggest that defective alleles in the gene that codes for the hepatic cytochrome <strong>P450</strong> 2A6 (CYP2A6) protect against nicotine <b>dependence</b> (ND) and higher levels of cigarette consumption.
+CYP2B6	drug	nicotine	15534625	We investigated polymorphisms of cytochrome <strong>P450</strong> 2A6 (CYP2A6) and its association with <b>smoking</b> habits in 412 healthy Brazilians, self recognized as white (n=147), black (n=123) and intermediate (n=142), and classified as <b>smokers</b> (n=205, including 61 ex <b>smokers</b>) and nonsmokers (n=207).
+CYP2B6	drug	nicotine	15528319	Metabolism of <b>nicotine</b> and cotinine by human cytochrome <strong>P450</strong> 2A13.
+CYP2B6	drug	opioid	15509185	The O demethylation of <b>tramadol</b> to M1, the main analgesic effective metabolite, is catalysed by cytochrome P450 (CYP) 2D6, whereas N demethylation to M2 is catalysed by <strong>CYP2B6</strong> and CYP3A4.
+CYP2B6	drug	opioid	15509185	The O demethylation of <b>tramadol</b> to M1, the main analgesic effective metabolite, is catalysed by cytochrome <strong>P450</strong> (CYP) 2D6, whereas N demethylation to M2 is catalysed by <strong>CYP2B6</strong> and CYP3A4.
+CYP2B6	drug	opioid	15504834	<b>Methadone</b> is metabolized by various isoforms of the cytochrome <strong>P450</strong> family, which can be induced by many drugs, including nevirapine.
+CYP2B6	addiction	addiction	15453622	In addition no significant correlation was found between dose <b>escalation</b> and concomitant drugs that either inhibited or induced the <strong>P450</strong> system.
+CYP2B6	drug	opioid	15371986	Role of hepatic and intestinal cytochrome <strong>P450</strong> 3A and 2B6 in the metabolism, disposition, and miotic effects of <b>methadone</b>.
+CYP2B6	drug	opioid	15371986	<b>Methadone</b> undergoes N  demethylation to the primary metabolite 2 ethyl 1,5 dimethyl 3,3 diphenylpyrrolinium (EDDP), catalyzed in vitro by intestinal, hepatic, and expressed cytochrome <strong>P450</strong> (CYP) 3A4.
+CYP2B6	drug	opioid	15371986	In vitro experiments showed a predominant role for both CYP3A4 and <strong>CYP2B6</strong> in liver microsomal <b>methadone</b> N  demethylation.
+CYP2B6	drug	opioid	15371986	Greater rifampin effects, compared with troleandomycin and grapefruit juice, on <b>methadone</b> disposition suggest a major role for intestinal transporters and for other CYPs, such as <strong>CYP2B6</strong>.
+CYP2B6	drug	opioid	15371986	Interindividual variability and drug interactions affecting intestinal transporter and hepatic CYP3A and <strong>CYP2B6</strong> activity may alter <b>methadone</b> disposition.
+CYP2B6	drug	nicotine	15364541	<b>Nicotine</b>, the psychoactive and addictive chemical in cigarettes, and a known inducer of brain <strong>CYP2B6</strong>, was an efficacious activator of PXR and inducer of CYP3A4 transcription.
+CYP2B6	addiction	addiction	15364541	Nicotine, the psychoactive and <b>addictive</b> chemical in cigarettes, and a known inducer of brain <strong>CYP2B6</strong>, was an efficacious activator of PXR and inducer of CYP3A4 transcription.
+CYP2B6	drug	cannabinoid	15302113	Delta(9) <b>THC</b> induced antinociception (50 degrees C warm water tail withdrawal assay) and catalepsy (bar test) were compared in male and female rats following pretreatment with saline or SKF525A, a cytochrome <strong>P450</strong> inhibitor.
+CYP2B6	addiction	withdrawal	15302113	Delta(9) THC induced antinociception (50 degrees C warm water tail <b>withdrawal</b> assay) and catalepsy (bar test) were compared in male and female rats following pretreatment with saline or SKF525A, a cytochrome <strong>P450</strong> inhibitor.
+CYP2B6	drug	nicotine	15229465	<b>Nicotine</b> metabolite ratio as an index of cytochrome <strong>P450</strong> 2A6 metabolic activity.
+CYP2B6	drug	nicotine	15229465	<b>Nicotine</b> and a variety of other drugs and toxins are metabolized by cytochrome <strong>P450</strong> (CYP) 2A6.
+CYP2B6	drug	alcohol	15119458	It is contraindicated in patients who are pregnant, breast feeding, and those concomitantly taking <b>ethanol</b>, macrolid antibiotics, some protease inhibitors, psychotropic medications, ketoconazole, itraconazole, nefaxodone, or other medications that impair oxidative metabolism mediated by cytochrome <strong>P450</strong> 3A (CYP 3A).
+CYP2B6	drug	alcohol	14992787	The cellular mechanisms impacted by combined smoking and <b>alcohol</b> exposure are poorly understood, but molecular epidemiology approaches are providing insights regarding the importance of effects on oxidant/antioxidant pathways and on metabolic pathways involving the cytochrome <strong>P450</strong> system.
+CYP2B6	drug	nicotine	14992787	The cellular mechanisms impacted by combined <b>smoking</b> and alcohol exposure are poorly understood, but molecular epidemiology approaches are providing insights regarding the importance of effects on oxidant/antioxidant pathways and on metabolic pathways involving the cytochrome <strong>P450</strong> system.
+CYP2B6	drug	alcohol	14724834	rats; however, the <b>ethanol</b> binge increased cytochrome <strong>P450</strong> 2E1 in both genotypes.
+CYP2B6	addiction	intoxication	14724834	rats; however, the ethanol <b>binge</b> increased cytochrome <strong>P450</strong> 2E1 in both genotypes.
+CYP2B6	drug	alcohol	14695664	Hepatitis C virus (HCV) and HCV core protein are hypothesized to induce hepatic oxidative stress and exacerbate injury caused by other toxins such as <b>ethanol</b> that induce the cytochrome <strong>P450</strong> enzyme, CYP2E1.
+CYP2B6	drug	nicotine	14668073	<b>Nicotine</b> is metabolized to the inactive metabolite cotinine by cytochrome <strong>P450</strong> 2A6.
+CYP2B6	drug	benzodiazepine	14586385	Cytochrome <strong>p450</strong> 3A4 messenger ribonucleic acid induction by rifampin in human peripheral blood mononuclear cells: correlation with <b>alprazolam</b> pharmacokinetics.
+CYP2B6	drug	nicotine	12818518	Current treatments are outlined and we highlight new strategies that are based on the manipulation of cytochrome <strong>P450</strong> 2A6 (CYP2A6) activity, which is responsible for the metabolism of <b>nicotine</b>.
+CYP2B6	drug	nicotine	12740294	Candidate gene studies have detected functional polymorphisms in genes coding for the cytochrome <strong>P450</strong> enzymes, and variations in these genes that lead to more rapid <b>nicotine</b> metabolism have been implicated in <b>smoking</b>.
+CYP2B6	drug	alcohol	12710951	To identify the association between the polymorphisms of genes encoding <b>alcohol</b> metabolizing enzymes and <b>alcoholism</b>, the <b>alcohol</b> dehydrogenase 2 (ADH2), <b>alcohol</b> dehydrogenase 3 (ADH3), aldehyde dehydrogenase 2 (ALDH2), and cytochrome <strong>P450</strong> 2E1 (CYP2E1) genes were studied in 101 male Mexican American <b>alcoholics</b>.
+CYP2B6	addiction	dependence	12676880	In addition to the multidrug resistance associated protein mediated efflux, cytochrome <strong>P450</strong> (<strong>P450</strong>) mediated metabolism could be a possible mechanism to explain the inconsistencies in the site <b>dependence</b> of tacrolimus absorption.
+CYP2B6	drug	benzodiazepine	12676880	Two enzyme inhibitors, ketoconazole and <b>midazolam</b>, were coperfused in rat intestinal lumen with tacrolimus to specify the effect of P gp and <strong>P450</strong>.
+CYP2B6	drug	nicotine	12618594	The effect of <b>smoking</b> and cytochrome <strong>P450</strong> CYP1A2 genetic polymorphism on clozapine clearance and dose requirement.
+CYP2B6	drug	alcohol	12462420	One group consisted of oxidoreductases, including ceruloplasmin, uricase, branched chain alpha keto acid dehydrogenase, NADH ubiquinone oxidoreductase, <strong>P450</strong>, NAD+ isocitrate dehydrogenase, and cytochrome c oxidase, which may be related to <b>ethanol</b> induced oxidative stress.
+CYP2B6	drug	nicotine	12439223	The <strong>CYP2B6</strong> gene has been implicated in bupropion kinetics and <b>nicotine</b> metabolism, and is a plausible candidate for pharmacogenetic studies of treatment response.
+CYP2B6	drug	nicotine	12439223	We investigated whether a functional genetic polymorphism in the <strong>CYP2B6</strong> gene predicts <b>smoking</b> outcomes in a placebo controlled randomized trial.
+CYP2B6	drug	nicotine	12439223	<b>Smokers</b> with a decreased activity variant of <strong>CYP2B6</strong> reported greater increases in cravings for cigarettes following the target quit date and had higher relapse rates.
+CYP2B6	addiction	relapse	12439223	Smokers with a decreased activity variant of <strong>CYP2B6</strong> reported greater increases in cravings for cigarettes following the target quit date and had higher <b>relapse</b> rates.
+CYP2B6	drug	nicotine	12439223	We conclude that <b>smokers</b> with the <strong>CYP2B6</strong> variant may be more vulnerable to abstinence symptoms and relapse.
+CYP2B6	addiction	relapse	12439223	We conclude that smokers with the <strong>CYP2B6</strong> variant may be more vulnerable to abstinence symptoms and <b>relapse</b>.
+CYP2B6	drug	opioid	12405865	Cytochrome <strong>P450</strong> (CYP) 3A4 and to a lesser extent 2D6 are probably the main isoforms involved in <b>methadone</b> metabolism.
+CYP2B6	drug	benzodiazepine	12397859	A case is presented of a patient who experienced <b>benzodiazepine</b> withdrawal symptoms on discontinuation of nefazodone, an antidepressant that inhibits the cytochrome <strong>P450</strong> 3A4 isoenzyme.
+CYP2B6	addiction	withdrawal	12397859	A case is presented of a patient who experienced benzodiazepine <b>withdrawal</b> symptoms on discontinuation of nefazodone, an antidepressant that inhibits the cytochrome <strong>P450</strong> 3A4 isoenzyme.
+CYP2B6	addiction	intoxication	12189363	Severe 2,3,7,8 tetrachlorodibenzo p dioxin (TCDD) <b>intoxication</b>: insights into the measurement of hepatic cytochrome <strong>P450</strong> 1A2 induction.
+CYP2B6	drug	alcohol	12023540	The <b>alcohol</b> treated group had the highest hepatic alpha(1) acid glycoprotein, microsomal protein (MP), and cytochrome <strong>P450</strong> (<strong>P450</strong>) concentrations.
+CYP2B6	drug	alcohol	12023540	Various pharmacokinetic parameters could be related to the octanol water partition coefficient (log P(app)) of the drug as a surrogate for plasma membrane partition coefficient and affinity for MP or <strong>P450</strong>, the dependence being lower in the CCl(4) treated group and higher in the <b>alcohol</b> treated group relative to controls.
+CYP2B6	addiction	dependence	12023540	Various pharmacokinetic parameters could be related to the octanol water partition coefficient (log P(app)) of the drug as a surrogate for plasma membrane partition coefficient and affinity for MP or <strong>P450</strong>, the <b>dependence</b> being lower in the CCl(4) treated group and higher in the alcohol treated group relative to controls.
+CYP2B6	drug	opioid	12006904	Treatment of <b>codeine</b> dependence with inhibitors of cytochrome <strong>P450</strong> 2D6.
+CYP2B6	addiction	dependence	12006904	Treatment of codeine <b>dependence</b> with inhibitors of cytochrome <strong>P450</strong> 2D6.
+CYP2B6	drug	opioid	12006904	<b>Codeine</b> is O demethylated by cytochrome <strong>P450</strong> 2D6 (CYP2D6) to form the more potent drug <b>morphine</b>, accounting for much of <b>codeine</b>'s analgesic and dependence producing properties.
+CYP2B6	addiction	dependence	12006904	Codeine is O demethylated by cytochrome <strong>P450</strong> 2D6 (CYP2D6) to form the more potent drug morphine, accounting for much of codeine's analgesic and <b>dependence</b> producing properties.
+CYP2B6	addiction	dependence	11972441	The role of pharmacogenetically variable cytochrome <strong>P450</strong> enzymes in drug abuse and <b>dependence</b>.
+CYP2B6	drug	alcohol	11960985	Studies on the mechanism have shown that chronic <b>ethanol</b> consumption induces <strong>P450</strong> enzymes that increase RA degradation, thus accounting for much but not all of the observed decrease in RA.
+CYP2B6	drug	opioid	11825096	Acceleration of <b>methadone</b> metabolism caused by cytochrome <strong>P450</strong> (CYP) 3A4 induction by antiretroviral drugs or rifampicin (rifampin) has caused <b>methadone</b> withdrawal symptoms.
+CYP2B6	addiction	withdrawal	11825096	Acceleration of methadone metabolism caused by cytochrome <strong>P450</strong> (CYP) 3A4 induction by antiretroviral drugs or rifampicin (rifampin) has caused methadone <b>withdrawal</b> symptoms.
+CYP2B6	drug	alcohol	11812920	The liver expresses many cytochrome <strong>P450</strong> isoforms, including <b>ethanol</b> induced CYP2E1.
+CYP2B6	drug	alcohol	11762131	This pathway involves enzymes that belong to the super family of cytochrome <strong>P450</strong> and allows to explain a lot of pharmacokinetic or toxic interactions between <b>alcohol</b> and xenobiotics.
+CYP2B6	drug	alcohol	11762131	Cytochrome <strong>P450</strong> 2E1 (CYP2E1) is the key enzyme of the microsomal pathway of <b>ethanol</b> oxidation.
+CYP2B6	drug	alcohol	11762131	This induction involves to a lesser extent cytochromes <strong>P450</strong> 3A4 and 1A2 and contributes to the metabolic tolerance of <b>alcohol</b> and drugs observed in <b>alcoholics</b>.
+CYP2B6	drug	opioid	11513833	The role of metabolic polymorphism in the development of physical dependence to <b>codeine</b> was assessed in cytochrome <strong>P450</strong> 2D2 (CYP2D2) deficient Dark Agouti and CYP2D2 intact Sprague Dawley rats by assessment of the severity of <b>naloxone</b> precipitated withdrawal after <b>codeine</b> and <b>morphine</b> administration.
+CYP2B6	addiction	dependence	11513833	The role of metabolic polymorphism in the development of physical <b>dependence</b> to codeine was assessed in cytochrome <strong>P450</strong> 2D2 (CYP2D2) deficient Dark Agouti and CYP2D2 intact Sprague Dawley rats by assessment of the severity of naloxone precipitated withdrawal after codeine and morphine administration.
+CYP2B6	addiction	withdrawal	11513833	The role of metabolic polymorphism in the development of physical dependence to codeine was assessed in cytochrome <strong>P450</strong> 2D2 (CYP2D2) deficient Dark Agouti and CYP2D2 intact Sprague Dawley rats by assessment of the severity of naloxone precipitated <b>withdrawal</b> after codeine and morphine administration.
+CYP2B6	drug	opioid	11504799	Metabolism of <b>methadone</b> and levo alpha acetylmethadol (LAAM) by human intestinal cytochrome <strong>P450</strong> 3A4 (CYP3A4): potential contribution of intestinal metabolism to presystemic clearance and bioactivation.
+CYP2B6	drug	opioid	11504799	We conclude that <b>methadone</b>, LAAM, and nor LAAM are metabolized by human intestinal microsomes; CYP3A4 is the predominant cytochrome <strong>P450</strong> isoform; CYP3A4 catalyzed <b>methadone</b>, LAAM, and nor LAAM metabolism is characterized by noncooperative, multisite kinetics; and intestinal metabolism may contribute to presystemic <b>methadone</b> inactivation and LAAM bioactivation.
+CYP2B6	drug	alcohol	11432125	<b>Alcohol</b> dehydrogenase (ADH), acetaldehydede hydrogenase (ALDH) and cytochrome <strong>P450</strong> 2E1 are the enzymes responsible for the metabolism of <b>ethanol</b>.
+CYP2B6	drug	alcohol	11398342	The cytochrome <strong>P450</strong> 2E1 (CYP2E1) gene, which is mapped to chromosome 10q24.3 qter contributes also the conversion of <b>ethanol</b> to acetaldehyde.
+CYP2B6	drug	opioid	11366210	<b>Methadone</b> is metabolized by the cytochrome <strong>P450</strong> system, and NRTIs do not appear to be inducers or inhibitors of the cytochrome <strong>P450</strong> system.
+CYP2B6	drug	opioid	11298066	<b>Methadone</b> is predominantly metabolized by cytochrome <strong>P450</strong> 3A4 and the non nucleoside reverse transcriptase inhibitor (NNRTI) efavirenz is a recognized inducer of this enzyme.
+CYP2B6	drug	nicotine	11286758	Functional polymorphisms in CYTOCHROME <strong>P450</strong> monooxygenases that metabolize <b>nicotine</b> have now been defined and it should soon be possible to identify fast <b>nicotine</b> metabolizers by DNA analysis.
+CYP2B6	drug	opioid	11270921	Cytochrome <strong>P450</strong> 2D6 genotype and <b>methadone</b> steady state concentrations.
+CYP2B6	drug	opioid	11270921	These results confirm the involvement of cytochrome <strong>P450</strong> 2D6 in <b>methadone</b> metabolism.
+CYP2B6	drug	nicotine	11207029	Cytochrome <strong>P450</strong> 2A6 (CYP2A6) is involved in the C oxidation of <b>nicotine</b> and in the metabolic activation of <b>tobacco</b> nitrosamines.
+CYP2B6	drug	alcohol	11173983	<b>Disulfiram</b>, the parent compound of DETC MeSO, also inhibits glutamate receptors partially in vivo; however, it fails to inhibit glutamate receptors in mice pretreated with N butyl imidazole, a cytochrome <strong>P450</strong> enzyme inhibitor, implicating the need for bioactivation of <b>disulfiram</b> to be an effective antagonist.
+CYP2B6	drug	opioid	11064491	<b>Methadone</b> is metabolized primarily in the liver, by up to five cytochrome <strong>P450</strong> isoforms, and individual differences in enzyme activity help explain wide ranges of active R enantiomer concentrations in patients given identical doses of racemic <b>methadone</b>.
+CYP2B6	drug	nicotine	10945314	Inhibition of cytochrome <strong>P450</strong> 2A6 increases <b>nicotine</b>'s oral bioavailability and decreases <b>smoking</b>.
+CYP2B6	drug	alcohol	10759684	The paracetamol <b>ethanol</b> interaction is not specific for any one isoform of cytochrome <strong>P450</strong>, and it seems that isoenzymes other than CYP2E1 are primarily responsible for the oxidative metabolism of paracetamol in man.
+CYP2B6	drug	opioid	10745087	These opiates, in contrast to their 3 O demethylated metabolites <b>morphine</b> and dihydromorphine (formed by cytochrome <strong>P450</strong> 2D6), demonstrated neither acute inhibition nor chronic induced superactivation.
+CYP2B6	drug	nicotine	10667460	Major classes of carcinogens present in <b>tobacco</b> and <b>tobacco</b> smoke are converted into DNA reactive metabolites by cytochrome <strong>P450</strong> (CYP) related enzymes, several of which display genetic polymorphism.
+CYP2B6	drug	opioid	10653207	Cytochrome <strong>P450</strong> 2D6 and treatment of <b>codeine</b> dependence.
+CYP2B6	addiction	dependence	10653207	Cytochrome <strong>P450</strong> 2D6 and treatment of codeine <b>dependence</b>.
+CYP2B6	drug	opioid	10653207	<b>Codeine</b> is a substrate of CYP2D6, a genetically polymorphic <strong>P450</strong> enzyme, and is metabolized to the more potent drug <b>morphine</b>.
+CYP2B6	drug	opioid	10641980	<b>Methadone</b> metabolism is affected by cytochrome <strong>P450</strong> (CYP) 3A4 inhibitors or inducers.
+CYP2B6	drug	nicotine	10544257	The polymorphic human cytochrome <strong>P450</strong> 2A6 (CYP2A6) metabolises a number of drugs, activates a variety of precarcinogens and constitutes the major <b>nicotine</b> C oxidase.
+CYP2B6	drug	opioid	10506872	PHARMACOKINETICS PHARMACODYNAMICS: <b>Methadone</b> is metabolized by cytochrome <strong>P450</strong> enzymes in the liver microsomes and binds selectively to mu opiate receptors.
+CYP2B6	drug	alcohol	10456581	Two days following <b>alcohol</b> withdrawal, the apparent activity of the <b>alcohol</b> inducible form of cytochrome <strong>P450</strong> (CYP2E1) was unchanged although total cytochrome <strong>P450</strong> content was increased.
+CYP2B6	addiction	withdrawal	10456581	Two days following alcohol <b>withdrawal</b>, the apparent activity of the alcohol inducible form of cytochrome <strong>P450</strong> (CYP2E1) was unchanged although total cytochrome <strong>P450</strong> content was increased.
+CYP2B6	drug	opioid	10372797	Inhibitors of cytochrome <strong>P450</strong> differentially modify discriminative stimulus and antinociceptive effects of <b>hydrocodone</b> and <b>hydromorphone</b> in rhesus monkeys.
+CYP2B6	drug	opioid	10372797	The present study was conducted to investigate the role of cytochrome <strong>P450</strong> in the discriminative stimulus and antinociceptive effects of <b>hydrocodone</b> (HC) and <b>hydromorphone</b> (HM) in rhesus monkeys.
+CYP2B6	drug	alcohol	10333489	Relationship between cytochrome <strong>P450</strong> catalytic cycling and stability: fast degradation of <b>ethanol</b> inducible cytochrome <strong>P450</strong> 2E1 (CYP2E1) in hepatoma cells is abolished by inactivation of its electron donor NADPH cytochrome <strong>P450</strong> reductase.
+CYP2B6	drug	alcohol	10333489	<b>Ethanol</b> inducible cytochrome <strong>P450</strong> 2E1 (CYP2E1) involved in the metabolism of gluconeogenetic precursors and some cytotoxins is distinguished from other cytochrome <strong>P450</strong> enzymes by its rapid turnover (in vivo half life of 4 7 h), with ligands to the haem iron, both substrates and inhibitors, stabilizing the protein.
+CYP2B6	addiction	withdrawal	10333489	Fao hepatoma cells, where CYP2E1 showed a half life of 4 h upon serum <b>withdrawal</b>, were treated for 1 h with 0.3 microM diphenylene iodonium (DPI), a suicide inhibitor of flavoenzymes, which resulted in approximately 90% inhibition of the microsomal NADPH cytochrome <strong>P450</strong> reductase and CYP2E1 dependent chlorzoxazone hydroxylase activities.
+CYP2B6	drug	alcohol	9731720	Caucasians are polymorphic at only two of these gene loci  cytochrome <strong>P450</strong> 2E1 (CYP2E1) and <b>alcohol</b> dehydrogenase 3 (ADH3).
+CYP2B6	drug	psychedelics	9698290	In hepatic microsomes from a panel of human donors, the low KMapp <b>ibogaine</b> O demethylase activity correlated with CYP2D6 catalyzed bufuralol 1' hydroxylase activity but not with other <strong>P450</strong> isoform specific activities.
+CYP2B6	drug	psychedelics	9698290	Quinidine, a CYP2D6 specific inhibitor, inhibited <b>ibogaine</b> O demethylase (IC50 = 0.2 microM), whereas other <strong>P450</strong> isoform specific inhibitors did not inhibit this activity.
+CYP2B6	drug	psychedelics	9698290	Also, of a battery of recombinant heterologously expressed human <strong>P450</strong> isoforms, only rCYP2D6 possessed significant <b>ibogaine</b> O demethylase activity.
+CYP2B6	drug	amphetamine	9638684	d <b>Methamphetamine</b> (MA) is one of more than two dozen drugs included in the cytochrome <strong>P450</strong> mediated "debrisoquine oxidation polymorphism" panel.
+CYP2B6	drug	alcohol	9633991	Previous experiments implicating CYP2E in <b>alcohol</b> mediated increases in acetaminophen hepatotoxicity have used inhibitors of this form of <strong>P450</strong> that are now proving to be non specific.
+CYP2B6	drug	opioid	9565774	<b>Methadone</b> and <b>buprenorphine</b>, widely used in the treatment of <b>opioid</b> abuse, are metabolized by cytochrome <strong>P450</strong> 3A4, while fluoxetine and fluvoxamine, both selective serotonin reuptake inhibitors, are known to be <strong>P450</strong> 2D6 and 3A4 inhibitors in vitro.
+CYP2B6	drug	alcohol	9478048	At E7.5, two other mouse enzymes known to metabolize <b>ethanol</b> (ADH I and <strong>P450</strong> 2E1) are not expressed, indicating that ADH IV may be the only enzyme available at this stage to metabolize both <b>ethanol</b> and retinol.
+CYP2B6	drug	alcohol	9391747	Of these the effect of long term <b>alcohol</b> consumption in increasing the hepatotoxicity of paracetamol and of cytochrome <strong>P450</strong> 3A microsomal enzyme stimulating drugs in diminishing the efficacy of methadone are the most commonly encountered.
+CYP2B6	drug	opioid	9391747	Of these the effect of long term alcohol consumption in increasing the hepatotoxicity of paracetamol and of cytochrome <strong>P450</strong> 3A microsomal enzyme stimulating drugs in diminishing the efficacy of <b>methadone</b> are the most commonly encountered.
+CYP2B6	addiction	dependence	9352573	This is the first investigation and demonstration of differences in genetically determined <strong>P450</strong> metabolism influencing risk for substance <b>dependence</b> and we suggest that these differences may influence the risk for <b>dependence</b> of other substrate drugs, and may occur with other genetically variable P450s.
+CYP2B6	drug	alcohol	9328319	Because it had been reported that chlormethiazole inhibits the <b>alcohol</b> inducible cytochrome <strong>P450</strong> 2E1 in rat liver, we investigated the in vivo and in vitro effect of this drug on cytochrome <strong>P450</strong> 2E1 in human beings.
+CYP2B6	drug	alcohol	9328319	The 6 hydroxychlorzoxazone chlorzoxazone blood concentration ratio, reflecting the cytochrome <strong>P450</strong> 2E1 activity, was determined in 10 controls and in 24 <b>alcoholic</b> patients who had entered a hospital for detoxification.
+CYP2B6	drug	alcohol	9328319	Cytochrome <strong>P450</strong> 2E1 activity was significantly increased in <b>alcoholic</b> patients treated with chlorazepate (1.16 +/  0.40 vs. 0.27 +/  0.03, P < .05).
+CYP2B6	drug	alcohol	9328319	Because cytochrome <strong>P450</strong> 2E1 induction after chronic <b>ethanol</b> consumption has detrimental effects on the liver through free radical formation, treatment of <b>alcohol</b> detoxification with chlormethiazole may be beneficial.
+CYP2B6	drug	alcohol	26735944	The brain <b>alcohol</b> dehydrogenase and microsomal <b>ethanol</b> oxidizing systems, including cytochrome <strong>P450</strong> II E1 and catalase are considered.
+CYP2B6	drug	alcohol	9160798	<b>Ethanol</b> is metabolized in the brain by catalase/H2O2 to yield acetaldehyde and by an <b>ethanol</b> inducible form of cytochrome <strong>P450</strong> (<strong>P450</strong> IIE1) in a reaction that yields oxygen radicals.
+CYP2B6	drug	alcohol	9144448	CYP2E is considered the only form of cytochrome <strong>P450</strong> responsible for <b>ethanol</b> mediated increases in acetaminophen hepatotoxicity.
+CYP2B6	drug	opioid	9067326	Effect of cytochrome <strong>P450</strong> 2D1 inhibition on <b>hydrocodone</b> metabolism and its behavioral consequences in rats.
+CYP2B6	drug	opioid	9067326	Humans that lack cytochrome <strong>P450</strong> 2D6 (CYP2D6) activity may have an altered risk of drug dependence or abuse because this enzyme is important in the metabolism of some drugs of abuse, including <b>hydrocodone</b>.
+CYP2B6	addiction	dependence	9067326	Humans that lack cytochrome <strong>P450</strong> 2D6 (CYP2D6) activity may have an altered risk of drug <b>dependence</b> or abuse because this enzyme is important in the metabolism of some drugs of abuse, including hydrocodone.
+CYP2B6	drug	opioid	9190321	The rate of production of this M1 derivative (O demethyl <b>tramadol</b>), is influenced by a polymorphic isoenzyme of the debrisoquine type, cytochrome <strong>P450</strong> 2D6 (CYP2D6).
+CYP2B6	drug	benzodiazepine	9118585	<b>alprazolam</b>, <b>triazolam</b> and <b>midazolam</b>) are metabolised by the cytochrome <strong>P450</strong> (CYP)3A subfamily.
+CYP2B6	addiction	intoxication	8937429	These data indicate that YH439 suppresses the expression of <strong>P450</strong> 2E1 and protects the liver against chemical induced hepatic injury and that the selective modulation of detoxifying enzymes by YH439 may contribute to the protection of liver from xenobiotic induced <b>intoxication</b>.
+CYP2B6	drug	alcohol	8876971	Therefore, PGE1 affects on both, <b>ethanol</b> inducible IIE1 and phenobarbital inducible <strong>IIB1</strong> isoforms.
+CYP2B6	drug	alcohol	9054307	The <b>ethanol</b> inducible cytochrome <strong>P450</strong> 2E1 plays a key role in its generation, favoured itself by an increase in the "redox active" fraction of intracellular non heme iron.
+CYP2B6	drug	alcohol	8812268	Metabolism of 1,2 difluoroethane by cytochrome <strong>P450</strong> (most likely CYP2E1) is suspected because pretreatment of rats or mice with SKF 525F, <b>disulfiram</b>, or dimethyl sulfoxide prevented or delayed the toxicity observed in rats not pretreated.
+CYP2B6	drug	alcohol	8691480	Recent evidence suggests that intraneuronal metabolism of <b>ethanol</b> by catalase/H2O2 and an <b>ethanol</b> inducible form of cytochrome <strong>P450</strong> together generate acetaldehyde and oxygen radicals including the hydroxyl radical (HO.).
+CYP2B6	drug	alcohol	8705373	The <b>ethanol</b> inducible cytochrome <strong>P450</strong> 2E1 plays a key role in its generation, favoured itself by an increase in the "redox active " fraction of intracellular non heme iron.
+CYP2B6	drug	nicotine	8573960	Pharmacokinetic interactions may cause <b>smokers</b> to require a larger dosage of certain drugs through an increase in plasma clearance, a decrease in absorption, an induction of cytochrome <strong>P450</strong> enzymes, or a combination of these factors.
+CYP2B6	drug	alcohol	7786308	Rapid changes in cytochrome P4502E1 (CYP2E1) activity and other <strong>P450</strong> isozymes following <b>ethanol</b> withdrawal in rats.
+CYP2B6	addiction	withdrawal	7786308	Rapid changes in cytochrome P4502E1 (CYP2E1) activity and other <strong>P450</strong> isozymes following ethanol <b>withdrawal</b> in rats.
+CYP2B6	addiction	withdrawal	7786308	Of the other parameters investigated in this study, total cytochrome <strong>P450</strong> content was increased 2.5 fold after ETOH feeding, with levels dropping markedly 24 hr post <b>withdrawal</b>.
+CYP2B6	addiction	withdrawal	7786308	Induction of these <strong>P450</strong> isoforms persisted for several days following <b>withdrawal</b>.
+CYP2B6	addiction	intoxication	7655131	This man's delirium is consistent with fluoxetine <b>intoxication</b>, which appears to have resulted from inhibition of hepatic cytochrome <strong>P450</strong> metabolism by clarithromycin.
+CYP2B6	drug	alcohol	8014872	<b>Ethanol</b> inducible cytochrome <strong>P450</strong> (CYP) 2E1 (CYP2E1) is responsible for the metabolism of many xenobiotics which exert toxic effects in humans.
+CYP2B6	drug	cocaine	8277979	Some exceptions to this rule were found: HCBD significantly increased T15 alpha OH, PROD and EROD activities in C57Bl/6 mice, whereas <b>cocaine</b> caused a significant stimulation of T15 alpha OH and PROD in DBA/2 mice, It is concluded that i) different hepatoxins cause different types of liver injury and responses of the monooxygenase complex ("hepatotoxinspecific finger prints"), ii) although DBA/2 and C57Bl/6 mice responded rather similarly to hepatotoxins, also with respect to <strong>P450</strong> content and most MO activities, they displayed a profound difference in the behaviour of COH activity, and iii) within the <strong>P450</strong> superfamily, the regulation of COH activity seems to be rather unique, also when compared to its structurally close enzyme, testosterone 15 alpha hydroxylase.
+CYP2B6	drug	alcohol	1443429	The addition of 4 methyl pyrazole (an <b>alcohol</b> dehydrogenase inhibitor) or metyrapone (a cytochrome <strong>P450</strong> inhibitor) had no effect on the amount of recovered AcHO.
+CYP2B6	drug	nicotine	1674558	To investigate whether genetic factors are involved in the maintenance of <b>smoking</b> habits, we examined restriction fragment length polymorphisms of cytochrome P 450 gene (P450 <strong>IIB1</strong>), one of the metabolizing enzymes of <b>nicotine</b>.
+CYP2B6	drug	nicotine	1674558	To investigate whether genetic factors are involved in the maintenance of <b>smoking</b> habits, we examined restriction fragment length polymorphisms of cytochrome P 450 gene (<strong>P450</strong> <strong>IIB1</strong>), one of the metabolizing enzymes of <b>nicotine</b>.
+CYP2B6	drug	alcohol	1811956	Most notably, THF is an inhibitor of a number of cytochrome <strong>P450</strong> (<strong>P450</strong>) dependent mixed function oxidase activities, with a particular affinity for the <b>alcohol</b> induced isozyme (P450IIE1).
+CYP2B6	drug	opioid	2178849	The majority of these interactions arise because phenytoin is a potent inducer of cytochrome <strong>P450</strong> microsomal enzymes, and therefore may increase the clearance of drugs which are extensively metabolised; drugs affected include carbamazepine, theophylline, <b>methadone</b>, prednisolone, dexamethasone, metyrapone and several cardiac antiarrhythmic agents.
+CYP2B6	drug	alcohol	2537602	Temperature dependence of the microsomal oxidation of <b>ethanol</b> by cytochrome <strong>P450</strong> and hydroxyl radical dependent reactions.
+CYP2B6	addiction	dependence	2537602	Temperature <b>dependence</b> of the microsomal oxidation of ethanol by cytochrome <strong>P450</strong> and hydroxyl radical dependent reactions.
+CYP2B6	drug	alcohol	2537602	Arrhenius plots of the .OH dependent oxidation of <b>ethanol</b> by both microsomal preparations were linear with energies of activation (about 7 kcal/mol) that were considerably lower than values found for the <strong>P450</strong> dependent pathway.
+CYP2B6	drug	alcohol	2537602	These results suggest that, at least in terms of activation energy, the increase in microsomal <b>ethanol</b> oxidation by pyrazole treatment is not associated with any apparent change in the overall mechanism or rate limiting step for <b>ethanol</b> oxidation but likely reflects induction of a <strong>P450</strong> isozyme with increased activity toward <b>ethanol</b>.
+CYP2B6	drug	alcohol	2537602	The lower activation energy for the .OH dependent oxidation of <b>ethanol</b> suggests that different steps are rate limiting for oxidation of <b>ethanol</b> by .OH and by <strong>P450</strong>, which may reflect the different enzyme components of the microsomal electron transfer system involved in these reactions.
+CYP2B6	drug	opioid	4817249	Proceedings: The relation between cytochrome <strong>P450</strong> in liver biopsies and drug metabolism in patients with liver disease and in <b>morphine</b> addiction.
+CYP2B6	addiction	addiction	4817249	Proceedings: The relation between cytochrome <strong>P450</strong> in liver biopsies and drug metabolism in patients with liver disease and in morphine <b>addiction</b>.
+MGLL	drug	alcohol	32738384	We have closely monitored the critical indicators reflecting changes of ECS during the whole process from <b>alcohol</b> absorption to its metabolization after acute <b>alcohol</b> (4.5 g/kg) intake by intragastric administration, including two key endocannabinoids (AEA and 2 AG) and their hydrolytic enzymes (FAAH and <strong>MAGL</strong>), as well as two crucial receptors (CB1R and CB2R) of ECS in blood and three brain regions.
+MGLL	drug	cannabinoid	32738384	We have closely monitored the critical indicators reflecting changes of ECS during the whole process from alcohol absorption to its metabolization after acute alcohol (4.5 g/kg) intake by intragastric administration, including two key <b>endocannabinoids</b> (AEA and 2 AG) and their hydrolytic enzymes (FAAH and <strong>MAGL</strong>), as well as two crucial receptors (CB1R and CB2R) of ECS in blood and three brain regions.
+MGLL	drug	nicotine	32479813	Contrary to our hypothesis, we found that inhibition of monoacylglycerol lipase (<strong>MAGL</strong>), the primary catabolic enzyme of 2 AG, attenuates <b>nicotine</b> conditioned place preference (CPP) in mice, through a non CB1 receptor mediated mechanism.
+MGLL	addiction	reward	32479813	Contrary to our hypothesis, we found that inhibition of monoacylglycerol lipase (<strong>MAGL</strong>), the primary catabolic enzyme of 2 AG, attenuates nicotine conditioned place preference (<b>CPP</b>) in mice, through a non CB1 receptor mediated mechanism.
+MGLL	addiction	aversion	32479813	<strong>MAGL</strong> inhibition did not alter palatable food reward or Lithium Chloride (LiCl) <b>aversion</b>.
+MGLL	addiction	reward	32479813	<strong>MAGL</strong> inhibition did not alter palatable food <b>reward</b> or Lithium Chloride (LiCl) aversion.
+MGLL	addiction	reward	32479813	To explore the potential mechanism of action, we investigated if <strong>MAGL</strong> inhibition affected other fatty acid levels in our <b>CPP</b> paradigm.
+MGLL	drug	nicotine	32479813	Collectively, these findings, along with our reported studies on <b>nicotine</b> withdrawal, suggest that inhibition of <strong>MAGL</strong> represents a promising new target for the development of pharmacotherapies to treat <b>nicotine</b> dependence.
+MGLL	addiction	dependence	32479813	Collectively, these findings, along with our reported studies on nicotine withdrawal, suggest that inhibition of <strong>MAGL</strong> represents a promising new target for the development of pharmacotherapies to treat nicotine <b>dependence</b>.
+MGLL	addiction	withdrawal	32479813	Collectively, these findings, along with our reported studies on nicotine <b>withdrawal</b>, suggest that inhibition of <strong>MAGL</strong> represents a promising new target for the development of pharmacotherapies to treat nicotine dependence.
+MGLL	drug	cannabinoid	32057593	In the mPFC and hippocampus, EtOH rats had significantly higher mRNA expression of <b>endocannabinoid</b> signaling (mPFC: Ppara, Dagla, Daglb and Napepld; and hippocampus: Cnr2, Dagla and <strong>Mgll</strong>) and neuroinflammation associated genes (mPFC: Gfap; and hippocampus: Aif1) than in controls.
+MGLL	drug	cannabinoid	32043730	At 6 and 12 months of age, we evaluated hippocampal dependent learning and memory: β amyloid concentrations and RNA and protein levels of <b>cannabinoid</b> type 2 receptors (CB2), diacylglycerol lipase α (DAGLα), and monoacylglycerol lipase (<strong>MAGL</strong>) in the hippocampus.
+MGLL	drug	cannabinoid	31695165	Brain structural changes in <b>cannabis</b> dependence: association with <strong>MAGL</strong>.
+MGLL	addiction	dependence	31695165	Brain structural changes in cannabis <b>dependence</b>: association with <strong>MAGL</strong>.
+MGLL	drug	cannabinoid	31695165	Regions with high <strong>MAGL</strong> expression, and therefore with potentially physiologically restricted endogenous <b>cannabinoid</b> signaling, may be more vulnerable to the effects of chronic <b>cannabis</b> use on cortical thickness.
+MGLL	addiction	reward	31628934	The novel <strong>MAGL</strong> inhibitor MJN110 enhances responding to <b>reward</b> predictive <b>incentive</b> cues by activation of CB1 receptors.
+MGLL	drug	cannabinoid	31628934	Conversely, enhancing <b>endocannabinoid</b> signaling, particularly 2 arachidonyl glycerol (2 AG), by inhibition of monoacyl glycerol lipase (<strong>MAGL</strong>), may facilitate some aspects of reward seeking.
+MGLL	addiction	relapse	31628934	Conversely, enhancing endocannabinoid signaling, particularly 2 arachidonyl glycerol (2 AG), by inhibition of monoacyl glycerol lipase (<strong>MAGL</strong>), may facilitate some aspects of reward <b>seeking</b>.
+MGLL	addiction	reward	31628934	Conversely, enhancing endocannabinoid signaling, particularly 2 arachidonyl glycerol (2 AG), by inhibition of monoacyl glycerol lipase (<strong>MAGL</strong>), may facilitate some aspects of <b>reward</b> seeking.
+MGLL	addiction	relapse	31628934	Using a modified version of the task, the novel <strong>MAGL</strong> inhibitor MJN110 increased the response ratio, decreased the latencies to respond to the IC and enhanced active nosepokes per IC, indicating a facilitation of cue induced reward <b>seeking</b>.
+MGLL	addiction	reward	31628934	Using a modified version of the task, the novel <strong>MAGL</strong> inhibitor MJN110 increased the response ratio, decreased the latencies to respond to the IC and enhanced active nosepokes per IC, indicating a facilitation of cue induced <b>reward</b> seeking.
+MGLL	drug	cannabinoid	31549358	Since then, much research interest has shifted to other <b>cannabinoid</b> based strategies, such as peripheral CB1R antagonists/inverse agonists, neutral CB1R antagonists, allosteric CB1R modulators, CB2R agonists, fatty acid amide hydrolase (FAAH) inhibitors, monoacylglycerol lipase (<strong>MAGL</strong>) inhibitors, fatty acid binding protein (FABP) inhibitors, or nonaddictive phytocannabinoids with CB1R or CB2R binding profiles, as new therapeutics for SUDs.
+MGLL	drug	alcohol	30553937	In the brainstem, ETS exposure decreased cannabinoid 1 (CB1) receptor, CB2 receptor, N arachidonoyl phosphatidyl <b>ethanol</b> specific phospholipase D (NAPE PLD), and fatty acid amino hydrolase (FAAH) levels and increased in diacylglycerol lipase (DAGL) and monoacylglycerol lipase (<strong>MAGL</strong>) levels during infancy and decreased CB2 and FAAH levels during adulthood.
+MGLL	drug	cannabinoid	30553937	In the brainstem, ETS exposure decreased <b>cannabinoid</b> 1 (CB1) receptor, CB2 receptor, N arachidonoyl phosphatidyl ethanol specific phospholipase D (NAPE PLD), and fatty acid amino hydrolase (FAAH) levels and increased in diacylglycerol lipase (DAGL) and monoacylglycerol lipase (<strong>MAGL</strong>) levels during infancy and decreased CB2 and FAAH levels during adulthood.
+MGLL	drug	alcohol	29748627	Additionally, we evaluated the inhibition of endocannabinoids clearance enzymes [monoacylglycerol lipase (<strong>MAGL</strong>) and fatty acid amide hydrolase] on anxiety like behavior and <b>alcohol</b> consumption in <b>alcohol</b> dependent rats and mice.
+MGLL	drug	cannabinoid	29748627	Additionally, we evaluated the inhibition of <b>endocannabinoids</b> clearance enzymes [monoacylglycerol lipase (<strong>MAGL</strong>) and fatty acid amide hydrolase] on anxiety like behavior and alcohol consumption in alcohol dependent rats and mice.
+MGLL	drug	alcohol	29748627	Pharmacological studies in rats and mice showed that anxiety like behavior and <b>alcohol</b> consumption were increased in <b>alcohol</b> dependent animals, and these behavioral effects were attenuated mainly by <strong>MAGL</strong> inhibitors [MJN110 (10 and 20 mg/kg) in rats and JZL184 (1 and 3 mg/kg) in mice].
+MGLL	drug	cannabinoid	29540562	As inhibitors of monoacylglycerol lipase (<strong>MAGL</strong>), the primary hydrolytic enzyme of the endogenous <b>cannabinoid</b>, 2 arachidonyolglycerol, produces antinociceptive effects in numerous rodent models of pain, we investigated whether inhibitors of this enzyme (i.e., JZL184 and MJN110) would reverse paclitaxel induced mechanical allodynia in mice.
+MGLL	drug	cannabinoid	29503395	The present study used inferior orbital nerve (ION) injured mice to investigate the effect of inhibiting monoacylglycerol lipase (<strong>MAGL</strong>), an enzyme that degrades the major <b>endocannabinoid</b> 2 arachydonoylgycerol (2 AG) in orofacial neuropathic pain.
+MGLL	addiction	withdrawal	29503395	Injection of JZL184, a selective inhibitor of <strong>MAGL</strong>, on day 7 after ION injury attenuated the reduction in head <b>withdrawal</b> threshold at 2 h after administration.
+MGLL	drug	cannabinoid	29481079	Monoacylglycerol lipase (<strong>MAGL</strong>) is the principle enzyme for metabolizing endogenous <b>cannabinoid</b> ligand 2 arachidonoyglycerol (2 AG).
+MGLL	drug	cannabinoid	29481079	Blockade of <strong>MAGL</strong> increases 2 AG levels, resulting in subsequent activation of the <b>endocannabinoid</b> system, and has emerged as a novel therapeutic strategy to treat drug addiction, inflammation, and neurodegenerative diseases.
+MGLL	addiction	addiction	29481079	Blockade of <strong>MAGL</strong> increases 2 AG levels, resulting in subsequent activation of the endocannabinoid system, and has emerged as a novel therapeutic strategy to treat drug <b>addiction</b>, inflammation, and neurodegenerative diseases.
+MGLL	drug	opioid	28714716	As well, when administered systemically or by infusion into the basolateral nucleus of the amygdala (BLA) or the interoceptive insular cortex, the monoaclyglycerol lipase (<strong>MAGL</strong>) inhibitor, MJN110 (which elevates 2 arachidonlyglycerol), also prevented a <b>naloxone</b> precipitated MWD induced place aversion.
+MGLL	addiction	aversion	28714716	As well, when administered systemically or by infusion into the basolateral nucleus of the amygdala (BLA) or the interoceptive insular cortex, the monoaclyglycerol lipase (<strong>MAGL</strong>) inhibitor, MJN110 (which elevates 2 arachidonlyglycerol), also prevented a naloxone precipitated MWD induced place <b>aversion</b>.
+MGLL	drug	cannabinoid	28192193	We found that expression of morphine CPP was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (fatty acid amide hydrolase [FAAH] and monoacylglycerol lipase [<strong>MAGL</strong>], respectively), but with reductions in <b>cannabinoid</b> 1 receptors (CB1R) and CB2R in dorsal hippocampus following the expression of CPP.
+MGLL	drug	opioid	28192193	We found that expression of <b>morphine</b> CPP was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (fatty acid amide hydrolase [FAAH] and monoacylglycerol lipase [<strong>MAGL</strong>], respectively), but with reductions in cannabinoid 1 receptors (CB1R) and CB2R in dorsal hippocampus following the expression of CPP.
+MGLL	addiction	reward	28192193	We found that expression of morphine <b>CPP</b> was associated with significant increases in mRNA expression for the primary clearance routes for anandamide (AEA) and 2 AG (fatty acid amide hydrolase [FAAH] and monoacylglycerol lipase [<strong>MAGL</strong>], respectively), but with reductions in cannabinoid 1 receptors (CB1R) and CB2R in dorsal hippocampus following the expression of <b>CPP</b>.
+MGLL	drug	opioid	28192193	However, our results indicated that decreased in <strong>MAGL</strong> and increased CB1R mRNA levels were accompanied with <b>morphine</b> CPP reinstatement.
+MGLL	addiction	relapse	28192193	However, our results indicated that decreased in <strong>MAGL</strong> and increased CB1R mRNA levels were accompanied with morphine CPP <b>reinstatement</b>.
+MGLL	addiction	reward	28192193	However, our results indicated that decreased in <strong>MAGL</strong> and increased CB1R mRNA levels were accompanied with morphine <b>CPP</b> reinstatement.
+MGLL	drug	cannabinoid	27890603	Wilkerson and colleagues, in this issue, examine SA 57, an inhibitor of two different <b>endocannabinoid</b> catabolic enzymes FAAH and <strong>MAGL</strong>, demonstrating its analgesic effectiveness and morphine sparing properties in a chronic pain model, as well as its ability to reduce heroin seeking behavior in a self administration paradigm in mice.
+MGLL	drug	opioid	27890603	Wilkerson and colleagues, in this issue, examine SA 57, an inhibitor of two different endocannabinoid catabolic enzymes FAAH and <strong>MAGL</strong>, demonstrating its analgesic effectiveness and <b>morphine</b> sparing properties in a chronic pain model, as well as its ability to reduce <b>heroin</b> seeking behavior in a self administration paradigm in mice.
+MGLL	addiction	relapse	27890603	Wilkerson and colleagues, in this issue, examine SA 57, an inhibitor of two different endocannabinoid catabolic enzymes FAAH and <strong>MAGL</strong>, demonstrating its analgesic effectiveness and morphine sparing properties in a chronic pain model, as well as its ability to reduce heroin <b>seeking</b> behavior in a self administration paradigm in mice.
+MGLL	drug	cannabinoid	27890602	Inhibitors of the primary <b>endocannabinoid</b> catabolic enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>) show opioid sparing effects in preclinical models of pain.
+MGLL	drug	opioid	27890602	Inhibitors of the primary endocannabinoid catabolic enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>) show <b>opioid</b> sparing effects in preclinical models of pain.
+MGLL	drug	opioid	27890602	As simultaneous inhibition of these enzymes elicits enhanced antinociceptive effects compared with single enzyme inhibition, the present study tested whether the dual FAAH <strong>MAGL</strong> inhibitor SA 57 [4 [2 (4 chlorophenyl)ethyl] 1 piperidinecarboxylic acid 2 (methylamino) 2 oxoethyl ester] produces <b>morphine</b> sparing antinociceptive effects, without major side effects associated with either drug class.
+MGLL	drug	alcohol	27578612	Male rats exposed to six weeks of CIA showed escalated <b>alcohol</b> consumption during acute withdrawal and reductions in NAc N acyl phosphatidylethanolamine phospholipase D (NAPEPLD), DAG lipase alpha (DAGLα), and monoacylglycerol lipase (<strong>MAGL</strong>) mRNA.
+MGLL	addiction	withdrawal	27578612	Male rats exposed to six weeks of CIA showed escalated alcohol consumption during acute <b>withdrawal</b> and reductions in NAc N acyl phosphatidylethanolamine phospholipase D (NAPEPLD), DAG lipase alpha (DAGLα), and monoacylglycerol lipase (<strong>MAGL</strong>) mRNA.
+MGLL	drug	alcohol	27578612	However, when these data were analyzed according to estrous stage, significant differences in NAPEPLD and <strong>MAGL</strong> mRNA expression emerged in the NAc of air exposed control rats, which were absent in <b>alcohol</b> dependent females.
+MGLL	drug	cannabinoid	27394933	Five genes known to play a role in the <b>endocannabinoid</b> system and CUDs were examined in a community sample of young adult Mexican Americans (MAs): CNR1, <strong>MGLL</strong>, FAAH, DAGLA, and DAGLB.
+MGLL	drug	cannabinoid	26791602	Here, we tested whether elevating the endogenous <b>cannabinoid</b> 2 arachidonoylglycerol through the inhibition of its primary hydrolytic enzyme monoacylglycerol lipase (<strong>MAGL</strong>), will produce opioid sparing effects in the mouse chronic constriction injury (CCI) of the sciatic nerve model of neuropathic pain.
+MGLL	drug	opioid	26791602	Here, we tested whether elevating the endogenous cannabinoid 2 arachidonoylglycerol through the inhibition of its primary hydrolytic enzyme monoacylglycerol lipase (<strong>MAGL</strong>), will produce <b>opioid</b> sparing effects in the mouse chronic constriction injury (CCI) of the sciatic nerve model of neuropathic pain.
+MGLL	drug	opioid	26791602	administration of <b>morphine</b> and the selective <strong>MAGL</strong> inhibitor 2,5 dioxopyrrolidin 1 yl 4 (bis(4 chlorophenyl)methyl)piperazine 1 carboxylate (MJN110) were tested alone and in combination at equieffective doses for reversal of CCI induced mechanical allodynia and thermal hyperalgesia.
+MGLL	addiction	aversion	26647976	Systemic pretreatment with the <strong>MAGL</strong> inhibitor, MJN110, prevented the <b>aversive</b> effects of acute MWD by a CB1 receptor dependent mechanism.
+MGLL	drug	cannabinoid	26628106	This <b>endocannabinoid</b> and its hydrolyzing enzyme, monoacylglycerol lipase (<strong>MAGL</strong>), are present in encephalic regions related to psychiatric disorders, including the midbrain dorsolateral periaqueductal grey (dlPAG).
+MGLL	drug	cannabinoid	26595473	Monoacylglycerol lipase (<strong>MGLL</strong>) polymorphism rs604300 interacts with childhood adversity to predict <b>cannabis</b> dependence symptoms and amygdala habituation: Evidence from an <b>endocannabinoid</b> system level analysis.
+MGLL	addiction	dependence	26595473	Monoacylglycerol lipase (<strong>MGLL</strong>) polymorphism rs604300 interacts with childhood adversity to predict cannabis <b>dependence</b> symptoms and amygdala habituation: Evidence from an endocannabinoid system level analysis.
+MGLL	drug	cannabinoid	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism: <strong>MGLL</strong>, FAAH; binding: CNR1; SNPs N = 65) and childhood sexual abuse (CSA) predict <b>cannabis</b> dependence symptoms.
+MGLL	addiction	dependence	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism: <strong>MGLL</strong>, FAAH; binding: CNR1; SNPs N = 65) and childhood sexual abuse (CSA) predict cannabis <b>dependence</b> symptoms.
+MGLL	drug	cannabinoid	26595473	These results are consistent with rodent models implicating 2 arachidonoylglycerol (2 AG), an endogenous <b>cannabinoid</b> metabolized by the enzyme encoded by <strong>MGLL</strong>, in the etiology of stress adaptation related to <b>cannabis</b> dependence, but require further replication.
+MGLL	addiction	dependence	26595473	These results are consistent with rodent models implicating 2 arachidonoylglycerol (2 AG), an endogenous cannabinoid metabolized by the enzyme encoded by <strong>MGLL</strong>, in the etiology of stress adaptation related to cannabis <b>dependence</b>, but require further replication.
+MGLL	drug	nicotine	26490035	Inhibition of monoacylglycerol lipase (<strong>MAGL</strong>) enhances cue induced reinstatement of <b>nicotine</b> seeking behavior in mice.
+MGLL	addiction	relapse	26490035	Inhibition of monoacylglycerol lipase (<strong>MAGL</strong>) enhances cue induced <b>reinstatement</b> of nicotine <b>seeking</b> behavior in mice.
+MGLL	drug	cannabinoid	26490035	There are two main <b>endocannabinoids</b>: anandamide degraded by fatty acid amide hydrolase (FAAH) and 2 arachidonoylglycerol (2 AG) degraded by monoacylglycerol lipase (<strong>MAGL</strong>).
+MGLL	drug	nicotine	26490035	The role of <strong>MAGL</strong> has only been explored recently, and so far, no study have been performed to evaluate the effects of <strong>MAGL</strong> inhibitor on <b>nicotine</b> reinforcing properties and cue induced reinstatement of <b>nicotine</b> seeking.
+MGLL	addiction	relapse	26490035	The role of <strong>MAGL</strong> has only been explored recently, and so far, no study have been performed to evaluate the effects of <strong>MAGL</strong> inhibitor on nicotine reinforcing properties and cue induced <b>reinstatement</b> of nicotine <b>seeking</b>.
+MGLL	addiction	reward	26490035	The role of <strong>MAGL</strong> has only been explored recently, and so far, no study have been performed to evaluate the effects of <strong>MAGL</strong> inhibitor on nicotine <b>reinforcing</b> properties and cue induced reinstatement of nicotine seeking.
+MGLL	drug	nicotine	26490035	Here, we investigated the effects of the <strong>MAGL</strong> inhibitor JZL184 on <b>nicotine</b> self administration under fixed and progressive ratio schedules of reinforcement and on cue induced reinstatement of <b>nicotine</b> seeking in mice.
+MGLL	addiction	relapse	26490035	Here, we investigated the effects of the <strong>MAGL</strong> inhibitor JZL184 on nicotine self administration under fixed and progressive ratio schedules of reinforcement and on cue induced <b>reinstatement</b> of nicotine <b>seeking</b> in mice.
+MGLL	addiction	reward	26490035	Here, we investigated the effects of the <strong>MAGL</strong> inhibitor JZL184 on nicotine self administration under fixed and progressive ratio schedules of <b>reinforcement</b> and on cue induced reinstatement of nicotine seeking in mice.
+MGLL	drug	nicotine	26490035	<strong>MAGL</strong> inhibition by JZL184 (16 mg/kg) increased reinstatement of previously extinguished <b>nicotine</b> seeking induced by presentation of <b>nicotine</b> associated cues, but did not produce reinstatement on its own.
+MGLL	addiction	relapse	26490035	<strong>MAGL</strong> inhibition by JZL184 (16 mg/kg) increased <b>reinstatement</b> of previously extinguished nicotine <b>seeking</b> induced by presentation of nicotine associated cues, but did not produce <b>reinstatement</b> on its own.
+MGLL	addiction	addiction	26223500	The impairment of CB1 R signaling in <strong>MAGL</strong> /  mice was also accompanied by enhanced excitatory drive in the basolateral amygdala (BLA) mPFC circuit, with subsequent elevation of glutamate release to the mPFC and anxiety like and obsessive <b>compulsive</b> behaviors, as assessed by the light/dark box and marble burying tests, respectively.
+MGLL	drug	cannabinoid	25539508	In addition, acute cocaine administration (10 mg/kg) in cocaine sensitized mice (referred to as cocaine priming) induced a selective increase in the <b>endocannabinoid</b> degrading enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>).
+MGLL	drug	cocaine	25539508	In addition, acute <b>cocaine</b> administration (10 mg/kg) in <b>cocaine</b> sensitized mice (referred to as <b>cocaine</b> priming) induced a selective increase in the endocannabinoid degrading enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>).
+MGLL	drug	cannabinoid	25539508	These protein changes were accompanied by an overall decrease in the ratios of <b>endocannabinoid</b> synthesis/degradation, especially the N acyl phosphatidylethanolamine phospholipase D/FAAH and diacylglycerol lipase alpha/<strong>MAGL</strong> ratios.
+MGLL	drug	cannabinoid	25479915	Inhibition of <b>endocannabinoid</b> catabolic enzymes fatty acid amide hydrolase (FAAH) and/or monoacylglycerol lipase (<strong>MAGL</strong>) reduces somatic morphine withdrawal signs, but its effects on aversive aspects of withdrawal are unknown.
+MGLL	drug	opioid	25479915	Inhibition of endocannabinoid catabolic enzymes fatty acid amide hydrolase (FAAH) and/or monoacylglycerol lipase (<strong>MAGL</strong>) reduces somatic <b>morphine</b> withdrawal signs, but its effects on aversive aspects of withdrawal are unknown.
+MGLL	addiction	aversion	25479915	Inhibition of endocannabinoid catabolic enzymes fatty acid amide hydrolase (FAAH) and/or monoacylglycerol lipase (<strong>MAGL</strong>) reduces somatic morphine withdrawal signs, but its effects on <b>aversive</b> aspects of withdrawal are unknown.
+MGLL	addiction	withdrawal	25479915	Inhibition of endocannabinoid catabolic enzymes fatty acid amide hydrolase (FAAH) and/or monoacylglycerol lipase (<strong>MAGL</strong>) reduces somatic morphine <b>withdrawal</b> signs, but its effects on aversive aspects of <b>withdrawal</b> are unknown.
+MGLL	drug	cannabinoid	25479915	The present study investigated whether Δ(9) <b>tetrahydrocannabinol</b> (<b>THC</b>), the <strong>MAGL</strong> inhibitor JZL184, the FAAH inhibitor PF 3845, or the dual FAAH/<strong>MAGL</strong> inhibitor SA 57 would reduce acquisition of morphine withdrawal induced conditioned place avoidance (CPA) and jumping.
+MGLL	drug	opioid	25479915	The present study investigated whether Δ(9) tetrahydrocannabinol (THC), the <strong>MAGL</strong> inhibitor JZL184, the FAAH inhibitor PF 3845, or the dual FAAH/<strong>MAGL</strong> inhibitor SA 57 would reduce acquisition of <b>morphine</b> withdrawal induced conditioned place avoidance (CPA) and jumping.
+MGLL	addiction	withdrawal	25479915	The present study investigated whether Δ(9) tetrahydrocannabinol (THC), the <strong>MAGL</strong> inhibitor JZL184, the FAAH inhibitor PF 3845, or the dual FAAH/<strong>MAGL</strong> inhibitor SA 57 would reduce acquisition of morphine <b>withdrawal</b> induced conditioned place avoidance (CPA) and jumping.
+MGLL	drug	cannabinoid	25398241	In this study, we investigated the impact of <b>THC</b> and inhibitors of the <b>endocannabinoid</b> hydrolytic enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>) on operant responding for electrical stimulation of the medial forebrain bundle [intracranial self stimulation (ICSS)], which is known to activate the mesolimbic dopamine system.
+MGLL	addiction	reward	25398241	In this study, we investigated the impact of THC and inhibitors of the endocannabinoid hydrolytic enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>) on <b>operant</b> responding for electrical stimulation of the medial forebrain bundle [intracranial self stimulation (<b>ICSS</b>)], which is known to activate the mesolimbic dopamine system.
+MGLL	drug	cannabinoid	25398241	<b>THC</b> and the <strong>MAGL</strong> inhibitor JZL184 (4 [bis(1,3 benzodioxol 5 yl)hydroxymethyl] 1 piperidinecarboxylic acid 4 nitrophenyl ester) attenuated operant responding for ICSS and food, and also reduced spontaneous locomotor activity.
+MGLL	addiction	reward	25398241	THC and the <strong>MAGL</strong> inhibitor JZL184 (4 [bis(1,3 benzodioxol 5 yl)hydroxymethyl] 1 piperidinecarboxylic acid 4 nitrophenyl ester) attenuated <b>operant</b> responding for <b>ICSS</b> and food, and also reduced spontaneous locomotor activity.
+MGLL	drug	cannabinoid	25398241	Consistent with previous studies showing that combined inhibition of FAAH and <strong>MAGL</strong> produces a substantially greater cannabimimetic profile than single enzyme inhibition, the dual FAAH <strong>MAGL</strong> inhibitor SA 57 (4 [2 (4 chlorophenyl)ethyl] 1 piperidinecarboxylic acid 2 (methylamino) 2 oxoethyl ester) produced a similar magnitude of ICSS depression as that produced by <b>THC</b>.
+MGLL	addiction	reward	25398241	Consistent with previous studies showing that combined inhibition of FAAH and <strong>MAGL</strong> produces a substantially greater cannabimimetic profile than single enzyme inhibition, the dual FAAH <strong>MAGL</strong> inhibitor SA 57 (4 [2 (4 chlorophenyl)ethyl] 1 piperidinecarboxylic acid 2 (methylamino) 2 oxoethyl ester) produced a similar magnitude of <b>ICSS</b> depression as that produced by THC.
+MGLL	drug	cannabinoid	25398241	Thus, <b>THC</b>, <strong>MAGL</strong> inhibition, and dual FAAH <strong>MAGL</strong> inhibition not only reduce ICSS, but also decrease other reinforced and nonreinforced behaviors.
+MGLL	addiction	reward	25398241	Thus, THC, <strong>MAGL</strong> inhibition, and dual FAAH <strong>MAGL</strong> inhibition not only reduce <b>ICSS</b>, but also decrease other reinforced and nonreinforced behaviors.
+MGLL	drug	cannabinoid	25258021	While blockade of fatty acid amide hydrolase, the primary catabolic enzyme of the <b>endocannabinoid</b> arachidonoylethanolamine (anandamide), exacerbates withdrawal responses in nicotine dependent mice, the role of monoacylglycerol lipase (<strong>MAGL</strong>), the main hydrolytic enzyme of a second <b>endocannabinoid</b> 2 arachidonylglycerol (2 AG), in nicotine withdrawal remains unexplored.
+MGLL	drug	nicotine	25258021	While blockade of fatty acid amide hydrolase, the primary catabolic enzyme of the endocannabinoid arachidonoylethanolamine (anandamide), exacerbates withdrawal responses in <b>nicotine</b> dependent mice, the role of monoacylglycerol lipase (<strong>MAGL</strong>), the main hydrolytic enzyme of a second endocannabinoid 2 arachidonylglycerol (2 AG), in <b>nicotine</b> withdrawal remains unexplored.
+MGLL	addiction	withdrawal	25258021	While blockade of fatty acid amide hydrolase, the primary catabolic enzyme of the endocannabinoid arachidonoylethanolamine (anandamide), exacerbates <b>withdrawal</b> responses in nicotine dependent mice, the role of monoacylglycerol lipase (<strong>MAGL</strong>), the main hydrolytic enzyme of a second endocannabinoid 2 arachidonylglycerol (2 AG), in nicotine <b>withdrawal</b> remains unexplored.
+MGLL	drug	nicotine	25258021	To evaluate the role of <strong>MAGL</strong> enzyme inhibition in <b>nicotine</b> withdrawal, we initially performed a genetic correlation approach using the BXD recombinant inbred mouse panel.
+MGLL	addiction	withdrawal	25258021	To evaluate the role of <strong>MAGL</strong> enzyme inhibition in nicotine <b>withdrawal</b>, we initially performed a genetic correlation approach using the BXD recombinant inbred mouse panel.
+MGLL	drug	nicotine	25258021	We then assessed <b>nicotine</b> withdrawal intensity in the mouse after treatment with the selective <strong>MAGL</strong> inhibitor, JZL184, and after genetic deletion of the enzyme.
+MGLL	addiction	withdrawal	25258021	We then assessed nicotine <b>withdrawal</b> intensity in the mouse after treatment with the selective <strong>MAGL</strong> inhibitor, JZL184, and after genetic deletion of the enzyme.
+MGLL	drug	nicotine	25258021	BXD mice displayed significant positive correlations between basal <strong>MAGL</strong> mRNA expression and <b>nicotine</b> withdrawal responses, consistent with the idea that increased 2 AG brain levels may attenuate withdrawal responses.
+MGLL	addiction	withdrawal	25258021	BXD mice displayed significant positive correlations between basal <strong>MAGL</strong> mRNA expression and nicotine <b>withdrawal</b> responses, consistent with the idea that increased 2 AG brain levels may attenuate <b>withdrawal</b> responses.
+MGLL	drug	cannabinoid	25258021	Strikingly, the <strong>MAGL</strong> inhibitor, JZL184, dose dependently reduced somatic and aversive withdrawal signs, which was blocked by <b>rimonabant</b>, indicating a CB1 receptor dependent mechanism.
+MGLL	addiction	aversion	25258021	Strikingly, the <strong>MAGL</strong> inhibitor, JZL184, dose dependently reduced somatic and <b>aversive</b> withdrawal signs, which was blocked by rimonabant, indicating a CB1 receptor dependent mechanism.
+MGLL	addiction	withdrawal	25258021	Strikingly, the <strong>MAGL</strong> inhibitor, JZL184, dose dependently reduced somatic and aversive <b>withdrawal</b> signs, which was blocked by rimonabant, indicating a CB1 receptor dependent mechanism.
+MGLL	drug	nicotine	25258021	<strong>MAGL</strong> knockout mice also showed attenuated <b>nicotine</b> withdrawal.
+MGLL	addiction	withdrawal	25258021	<strong>MAGL</strong> knockout mice also showed attenuated nicotine <b>withdrawal</b>.
+MGLL	drug	nicotine	25258021	Lastly, genetic analyses in humans revealed associations of the <strong>MAGL</strong> gene with <b>smoking</b> withdrawal in humans.
+MGLL	addiction	withdrawal	25258021	Lastly, genetic analyses in humans revealed associations of the <strong>MAGL</strong> gene with smoking <b>withdrawal</b> in humans.
+MGLL	drug	nicotine	25258021	Overall, our findings suggest that <strong>MAGL</strong> inhibition maybe a promising target for treatment of <b>nicotine</b> dependence.
+MGLL	addiction	dependence	25258021	Overall, our findings suggest that <strong>MAGL</strong> inhibition maybe a promising target for treatment of nicotine <b>dependence</b>.
+MGLL	drug	cannabinoid	25083569	The <b>endocannabinoid</b> system comprises the CB1 and CB2 receptors (the targets of the <b>Cannabis</b> sativa compound delta 9 <b>tetrahydrocannabinol</b>), the endogenous ligands (<b>endocannabinoids</b>) arachidonoyl ethanolamide (anandamide) and 2 arachidonoyl glycerol, their synthesizing machinery and membrane transport system, and the hydrolyzing enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>), respectively.
+MGLL	drug	cannabinoid	25083569	Understanding the pharmacological properties of FAAH and <strong>MAGL</strong> inhibitors may contribute toward the development of new anxiolytic interventions based on the <b>endocannabinoid</b> system.
+MGLL	drug	alcohol	25041461	The aim of the present study was to assess the state of the CB1 receptor, the enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>), and the extracellular signal regulated kinase (ERK) and cyclic AMP response element binding protein (CREB) in the post mortem prefrontal cortex of <b>alcoholic</b> subjects.
+MGLL	drug	alcohol	25041461	In parallel, <b>alcoholic</b> subjects presented lower levels of <strong>MAGL</strong> activity, regardless of the cause of death.
+MGLL	drug	cannabinoid	24849924	Complementary genetic and pharmacological approaches to inhibit monoacylglycerol lipase (<strong>MAGL</strong>) and fatty acid amide hydrolase (FAAH), the primary hydrolytic enzymes of the respective endogenous <b>cannabinoids</b> 2 arachidonoylglycerol (2 AG) and N arachidonoylethanolamine, enable the exploration of potential therapeutic applications and physiologic roles of these enzymes.
+MGLL	drug	cannabinoid	24849924	While <b>cannabinoid</b> receptor type 1 (CB1) function is maintained following chronic FAAH inactivation, prolonged excessive elevation of brain 2 AG levels, via <strong>MAGL</strong> inhibition, elicits both behavioral and molecular signs of <b>cannabinoid</b> tolerance and dependence.
+MGLL	addiction	dependence	24849924	While cannabinoid receptor type 1 (CB1) function is maintained following chronic FAAH inactivation, prolonged excessive elevation of brain 2 AG levels, via <strong>MAGL</strong> inhibition, elicits both behavioral and molecular signs of cannabinoid tolerance and <b>dependence</b>.
+MGLL	drug	cannabinoid	24849924	Together, these data suggest that simultaneous elevation of both <b>endocannabinoids</b> elicits enhanced cannabimimetic activity but <strong>MAGL</strong> inhibition drives CB1 receptor functional tolerance and <b>cannabinoid</b> dependence.
+MGLL	addiction	dependence	24849924	Together, these data suggest that simultaneous elevation of both endocannabinoids elicits enhanced cannabimimetic activity but <strong>MAGL</strong> inhibition drives CB1 receptor functional tolerance and cannabinoid <b>dependence</b>.
+MGLL	drug	cannabinoid	24634647	To this end, we investigated whether eCB signaling related gene and protein expression {<b>cannabinoid</b> receptor type 1 receptors and enzymes that produce [diacylglycerol lipase alpha/beta (DAGLα/β) and N acyl phosphatidylethanolamine phospholipase D (NAPE PLD)] and degrade [monoacylglycerol lipase (<strong>MAGL</strong>) and fatty acid amino hydrolase (FAAH)] eCB} were altered.
+MGLL	drug	cocaine	24634647	The acquisition of conditioned locomotion and sensitization after repeated <b>cocaine</b> exposure were associated with an increased NAPE PLD/FAAH ratio, suggesting enhanced anandamide production, and a decreased DAGLβ/<strong>MAGL</strong> ratio, suggesting decreased 2 AG generation.
+MGLL	addiction	sensitization	24634647	The acquisition of conditioned locomotion and <b>sensitization</b> after repeated cocaine exposure were associated with an increased NAPE PLD/FAAH ratio, suggesting enhanced anandamide production, and a decreased DAGLβ/<strong>MAGL</strong> ratio, suggesting decreased 2 AG generation.
+MGLL	drug	cannabinoid	23909864	Also, the effect of JZL184, an inhibitor of monoacylglycerol lipase (<strong>MAGL</strong>) which is reported to mobilize AA from <b>endocannabinoids</b> during neuroinflammatory insults, was examined.
+MGLL	addiction	addiction	23512546	In this review, we will discuss the development of FAAH and <strong>MAGL</strong> inhibitors and their pharmacological application to investigate the function of anandamide and 2 AG signaling pathways in preclinical models of neurobehavioral processes, such as pain, anxiety, and <b>addiction</b>.
+MGLL	drug	cannabinoid	23412396	Taken together, these results indicate that prolonged, partial <strong>MAGL</strong> inhibition maintains potentially beneficial antinociceptive and anti inflammatory effects, without producing functional CB1 receptor tachyphylaxis/tolerance or <b>cannabinoid</b> dependence.
+MGLL	addiction	dependence	23412396	Taken together, these results indicate that prolonged, partial <strong>MAGL</strong> inhibition maintains potentially beneficial antinociceptive and anti inflammatory effects, without producing functional CB1 receptor tachyphylaxis/tolerance or cannabinoid <b>dependence</b>.
+MGLL	drug	cannabinoid	23303065	Inhibition of the <b>endocannabinoid</b> catabolic enzymes, monoacylglycerol lipase (<strong>MAGL</strong>) or fatty acid amide hydrolase (FAAH) attenuates naloxone precipitated opioid withdrawal signs in mice via activation of CB1 receptors.
+MGLL	drug	opioid	23303065	Inhibition of the endocannabinoid catabolic enzymes, monoacylglycerol lipase (<strong>MAGL</strong>) or fatty acid amide hydrolase (FAAH) attenuates <b>naloxone</b> precipitated <b>opioid</b> withdrawal signs in mice via activation of CB1 receptors.
+MGLL	addiction	withdrawal	23303065	Inhibition of the endocannabinoid catabolic enzymes, monoacylglycerol lipase (<strong>MAGL</strong>) or fatty acid amide hydrolase (FAAH) attenuates naloxone precipitated opioid <b>withdrawal</b> signs in mice via activation of CB1 receptors.
+MGLL	addiction	withdrawal	23303065	Complete FAAH inhibition blocks only a subset of <b>withdrawal</b> signs, whereas complete <strong>MAGL</strong> inhibition elicits enhanced antiwithdrawal efficacy, but is accompanied with some cannabimimetic side effects.
+MGLL	drug	opioid	23303065	Thus, the primary objective of the present study was to determine whether combined, full FAAH inhibition and partial <strong>MAGL</strong> represents an optimal strategy to reduce <b>opioid</b> withdrawal.
+MGLL	addiction	withdrawal	23303065	Thus, the primary objective of the present study was to determine whether combined, full FAAH inhibition and partial <strong>MAGL</strong> represents an optimal strategy to reduce opioid <b>withdrawal</b>.
+MGLL	drug	opioid	23303065	To test this hypothesis, we examined whether combined administration of high dose of the FAAH inhibitor PF 3845 and low dose of the <strong>MAGL</strong> inhibitor JZL184, as well as the novel dual FAAH <strong>MAGL</strong> inhibitor SA 57, which is 100 fold more potent in inhibiting FAAH than <strong>MAGL</strong>, would prevent spontaneous withdrawal in <b>morphine</b> dependent mice, a model with greater face validity than precipitating withdrawal with μ <b>opioid</b> receptor antagonists.
+MGLL	addiction	withdrawal	23303065	To test this hypothesis, we examined whether combined administration of high dose of the FAAH inhibitor PF 3845 and low dose of the <strong>MAGL</strong> inhibitor JZL184, as well as the novel dual FAAH <strong>MAGL</strong> inhibitor SA 57, which is 100 fold more potent in inhibiting FAAH than <strong>MAGL</strong>, would prevent spontaneous <b>withdrawal</b> in morphine dependent mice, a model with greater face validity than precipitating <b>withdrawal</b> with μ opioid receptor antagonists.
+MGLL	drug	opioid	23303065	More generally, these findings support the idea that joint <strong>MAGL</strong> and FAAH inhibition represents a promising approach for the treatment of <b>opioid</b> dependence.
+MGLL	addiction	dependence	23303065	More generally, these findings support the idea that joint <strong>MAGL</strong> and FAAH inhibition represents a promising approach for the treatment of opioid <b>dependence</b>.
+MGLL	drug	cannabinoid	23142242	Recent studies have uncovered that the serine hydrolase monoacylglycerol lipase (<strong>MAGL</strong>) links the <b>endocannabinoid</b> and eicosanoid systems together through hydrolysis of the <b>endocannabinoid</b> 2 arachidonoylglycerol (2 AG) to provide the major arachidonic acid (AA) precursor pools for pro inflammatory eicosanoid synthesis in specific tissues.
+MGLL	drug	cannabinoid	23142242	Studies in recent years have shown that <strong>MAGL</strong> inhibitors elicit anti nociceptive, anxiolytic, and anti emetic responses and attenuate precipitated withdrawal symptoms in addiction paradigms through enhancing <b>endocannabinoid</b> signaling.
+MGLL	addiction	addiction	23142242	Studies in recent years have shown that <strong>MAGL</strong> inhibitors elicit anti nociceptive, anxiolytic, and anti emetic responses and attenuate precipitated withdrawal symptoms in <b>addiction</b> paradigms through enhancing endocannabinoid signaling.
+MGLL	addiction	withdrawal	23142242	Studies in recent years have shown that <strong>MAGL</strong> inhibitors elicit anti nociceptive, anxiolytic, and anti emetic responses and attenuate precipitated <b>withdrawal</b> symptoms in addiction paradigms through enhancing endocannabinoid signaling.
+MGLL	drug	cannabinoid	23142242	In cancer, <strong>MAGL</strong> inhibitors have been shown to have anti cancer properties not only through modulating the <b>endocannabinoid</b> eicosanoid network, but also by controlling fatty acid release for the synthesis of protumorigenic signaling lipids.
+MGLL	drug	cannabinoid	22924700	The <b>cannabinoid</b> receptor mediated analgesic effects of 2 arachidonoylglycerol (2 AG) are limited by monoacylglycerol lipase (<strong>MAGL</strong>).
+MGLL	drug	cannabinoid	22647577	We analysed the effects of inhibition of the two main <b>endocannabinoid</b> degradation enzymes: fatty acid amide hydrolase (FAAH), using inhibitor URB597 (1 mg/kg); monoacylglycerol lipase (<strong>MAGL</strong>), using inhibitor URB602 (10 mg/kg).
+MGLL	drug	cocaine	22647577	Administration of FAAH or <strong>MAGL</strong> inhibitors did not attenuate the acute effects of <b>cocaine</b>.
+MGLL	drug	cocaine	22647577	Only <strong>MAGL</strong> inhibition attenuated the expression of an already acquired <b>cocaine</b> induced behavioural sensitization.
+MGLL	addiction	sensitization	22647577	Only <strong>MAGL</strong> inhibition attenuated the expression of an already acquired cocaine induced behavioural <b>sensitization</b>.
+MGLL	drug	cannabinoid	22141465	Although similar alterations in FAAH mRNA were evident following either continuous or intermittent EtOH exposure, alterations in <strong>MAGL</strong> and <b>cannabinoid</b> receptor related mRNA (e.g., CB(1) , CB(2) , GPR55) were more pronounced following intermittent exposure.
+MGLL	drug	cannabinoid	21719468	The endogenous <b>cannabinoids</b>, N arachidonoylethanolamine (anandamide; AEA) and 2 arachidonylglycerol (2 AG), activate both <b>cannabinoid</b> receptors but are rapidly metabolized by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>), respectively.
+MGLL	drug	cannabinoid	21719468	<b>THC</b> and the <strong>MAGL</strong> inhibitor 4 nitrophenyl 4 (dibenzo[d][1,3]dioxol 5 yl(hydroxy)methyl)piperidine 1 carboxylate (JZL184) dose dependently reduced the intensity of most measures through the activation of CB(1) receptors.
+MGLL	addiction	addiction	21145341	In the present study, we investigated the effects of inhibiting FAAH or <strong>MAGL</strong> on anxiety like behavior in marble burying, a model of repetitive, <b>compulsive</b> behaviors germane to anxiety disorders such as obsessive <b>compulsive</b> disorder.
+MGLL	drug	benzodiazepine	21145341	The FAAH inhibitor PF 3845, the <strong>MAGL</strong> inhibitor JZL184, and the <b>benzodiazepine</b> <b>diazepam</b> decreased marble burying at doses that did not affect locomotor activity.
+MGLL	drug	benzodiazepine	21145341	The CB1 cannabinoid receptor antagonist rimonabant blocked the reduction in marble burying caused by FAAH and <strong>MAGL</strong> inhibitors, but not by <b>diazepam</b>, indicating a CB1 receptor mechanism of action.
+MGLL	drug	cannabinoid	21145341	The CB1 <b>cannabinoid</b> receptor antagonist <b>rimonabant</b> blocked the reduction in marble burying caused by FAAH and <strong>MAGL</strong> inhibitors, but not by diazepam, indicating a CB1 receptor mechanism of action.
+MGLL	drug	cannabinoid	20855465	2 Arachidonoylglycerol (2 AG) is the most abundant <b>endocannabinoid</b> in the brain and is believed to be hydrolyzed primarily by the serine hydrolase monoacylglycerol lipase (<strong>MAGL</strong>).
+MGLL	drug	cannabinoid	20855465	These findings provide the first genetic in vivo evidence that <strong>MAGL</strong> is the major regulator of 2 AG levels and signaling and reveal a pivotal role for 2 AG in modulating CB1 receptor sensitization and <b>endocannabinoid</b> tone.
+MGLL	addiction	sensitization	20855465	These findings provide the first genetic in vivo evidence that <strong>MAGL</strong> is the major regulator of 2 AG levels and signaling and reveal a pivotal role for 2 AG in modulating CB1 receptor <b>sensitization</b> and endocannabinoid tone.
+MGLL	drug	cannabinoid	20729846	We found that a similar form of functional antagonism was produced by sustained inactivation of monoacylglycerol lipase (<strong>MAGL</strong>), the principal degradative enzyme for the <b>endocannabinoid</b> 2 arachidonoylglycerol.
+MGLL	drug	cannabinoid	20729846	After repeated administration, the MAGL inhibitor JZL184 lost its analgesic activity and produced cross tolerance to <b>cannabinoid</b> receptor (CB1) agonists in mice, effects that were phenocopied by genetic disruption of <strong>Mgll</strong> (encoding MAGL).
+MGLL	drug	cannabinoid	20729846	After repeated administration, the <strong>MAGL</strong> inhibitor JZL184 lost its analgesic activity and produced cross tolerance to <b>cannabinoid</b> receptor (CB1) agonists in mice, effects that were phenocopied by genetic disruption of <strong>Mgll</strong> (encoding <strong>MAGL</strong>).
+MGLL	drug	cannabinoid	20729846	Chronic <strong>MAGL</strong> blockade also caused physical dependence, impaired <b>endocannabinoid</b> dependent synaptic plasticity and desensitized brain CB1 receptors.
+MGLL	addiction	dependence	20729846	Chronic <strong>MAGL</strong> blockade also caused physical <b>dependence</b>, impaired endocannabinoid dependent synaptic plasticity and desensitized brain CB1 receptors.
+MGLL	drug	amphetamine	20590579	Seven days after neurotoxic <b>METH</b>, the following biochemical determinations were carried out in limbic forebrain: CB(1) receptor density and stimulated activity, 2 arachidonoyl glycerol (2 AG) and monoacylglycerol lipase (<strong>MAGL</strong>) activity, dopamine levels and dopamine transporter density.
+MGLL	drug	amphetamine	20590579	The CB(1) receptor antagonist AM251 prevented the <b>METH</b> induced increase in EtOH consumption and preference, while N arachidonoyl maleimide, an inhibitor of <strong>MAGL</strong>, increased EtOH consumption and preference in both saline  and <b>METH</b> treated mice.
+MGLL	drug	amphetamine	20590579	An increase in endocannabinoid tone may be involved in the increased consumption of and preference for EtOH displayed by <b>METH</b> lesioned mice as blockade of the CB(1) receptor decreased EtOH seeking behaviours, whereas the <strong>MAGL</strong> inhibitor increased EtOH consumption.
+MGLL	drug	cannabinoid	20590579	An increase in <b>endocannabinoid</b> tone may be involved in the increased consumption of and preference for EtOH displayed by METH lesioned mice as blockade of the CB(1) receptor decreased EtOH seeking behaviours, whereas the <strong>MAGL</strong> inhibitor increased EtOH consumption.
+MGLL	addiction	relapse	20590579	An increase in endocannabinoid tone may be involved in the increased consumption of and preference for EtOH displayed by METH lesioned mice as blockade of the CB(1) receptor decreased EtOH <b>seeking</b> behaviours, whereas the <strong>MAGL</strong> inhibitor increased EtOH consumption.
+MGLL	drug	cannabinoid	19918051	Dual blockade of FAAH and <strong>MAGL</strong> identifies behavioral processes regulated by <b>endocannabinoid</b> crosstalk in vivo.
+MGLL	drug	cannabinoid	19918051	Why, however, this full spectrum of activities is not observed upon pharmacological inhibition or genetic deletion of either fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (<strong>MAGL</strong>), enzymes that regulate the two major <b>endocannabinoids</b> anandamide (AEA) and 2 arachidonoylglycerol (2 AG), respectively, has remained unclear.
+MGLL	drug	cannabinoid	19918051	Comparison of JZL195 to specific FAAH and <strong>MAGL</strong> inhibitors identified behavioral processes that were regulated by a single <b>endocannabinoid</b> pathway (e.g., hypomotility by the 2 AG/<strong>MAGL</strong> pathway) and, interestingly, those where disruption of both FAAH and <strong>MAGL</strong> produced additive effects that were reversed by a CB1 antagonist.
+MGLL	drug	cannabinoid	19918051	Falling into this latter category was drug discrimination behavior, where dual FAAH/<strong>MAGL</strong> blockade, but not disruption of either FAAH or <strong>MAGL</strong> alone, produced <b>THC</b> like responses that were reversed by a CB1 antagonist.
+MGLL	drug	cannabinoid	19675519	<b>Endocannabinoids</b> are transported into cells by a specific uptake system and degraded by the enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (<strong>MAGL</strong>).
+MGLL	drug	cannabinoid	19430909	However, new genetic and pharmacological tools are available to increase <b>endocannabinoid</b> levels by targeting fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (<strong>MAGL</strong>), the enzymes responsible for the degradation of the endogenous <b>cannabinoid</b> ligands anandamide and 2 arachidonoylglycerol, respectively.
+MGLL	drug	cannabinoid	19430909	In the present study, we investigated whether increasing endogenous <b>cannabinoids</b> levels, through the use of FAAH ( / ) mice as well as the FAAH inhibitor URB597 or the <strong>MAGL</strong> inhibitor JZL184, would reduce the intensity of withdrawal signs precipitated by the CB(1) receptor antagonist <b>rimonabant</b> in <b>THC</b> dependent mice.
+MGLL	addiction	withdrawal	19430909	In the present study, we investigated whether increasing endogenous cannabinoids levels, through the use of FAAH ( / ) mice as well as the FAAH inhibitor URB597 or the <strong>MAGL</strong> inhibitor JZL184, would reduce the intensity of <b>withdrawal</b> signs precipitated by the CB(1) receptor antagonist rimonabant in THC dependent mice.
+MGLL	drug	cannabinoid	19335651	Gene association studies are presented for (a) genes posited to have specific influences on <b>cannabis</b> use disorders: CNR1, CB2, FAAH, <strong>MGLL</strong>, TRPV1 and GPR55 and (b) genes from various neurotransmitter systems that are likely to exert a non specific influence on risk of <b>cannabis</b> use disorders, e.g.
+MGLL	drug	alcohol	17621164	Association study between <b>alcoholism</b> and endocannabinoid metabolic enzyme genes encoding fatty acid amide hydrolase and <strong>monoglyceride lipase</strong> in a Japanese population.
+MGLL	drug	cannabinoid	17621164	Association study between alcoholism and <b>endocannabinoid</b> metabolic enzyme genes encoding fatty acid amide hydrolase and <strong>monoglyceride lipase</strong> in a Japanese population.
+MGLL	drug	cannabinoid	17621164	Fatty acid amide hydrolase (FAAH) and monoglyceride lipase (<strong>MGLL</strong>) are the major <b>endocannabinoid</b> metabolic enzymes.
+MGLL	drug	cannabinoid	17621164	Fatty acid amide hydrolase (FAAH) and <strong>monoglyceride lipase</strong> (<strong>MGLL</strong>) are the major <b>endocannabinoid</b> metabolic enzymes.
+MGLL	drug	alcohol	17621164	To determine whether the single nucleodtide polymorphisms of the FAAH and <strong>MGLL</strong> genes are associated with <b>alcoholism</b> in a Japanese population.
+GLP1R	addiction	reward	32388229	The gut brain peptide glucagon like peptide 1 (<strong>GLP 1</strong>) reduces <b>reward</b> from palatable food and drugs of abuse.
+GLP1R	drug	alcohol	32388229	Recent rodent studies show that activation of <strong>GLP 1</strong> receptors (GLP 1R) within the nucleus of the solitary tract (NTS) not only suppresses the motivation and intake of palatable food, but also reduces <b>alcohol</b> related behaviors.
+GLP1R	drug	alcohol	32388229	Recent rodent studies show that activation of <strong>GLP 1</strong> receptors (<strong>GLP 1R</strong>) within the nucleus of the solitary tract (NTS) not only suppresses the motivation and intake of palatable food, but also reduces <b>alcohol</b> related behaviors.
+GLP1R	addiction	addiction	32388229	As reward induced by <b>addictive</b> drugs and sexual behaviors involve similar neurocircuits, we hypothesized that activation of <strong>GLP 1R</strong> suppresses sexual behavior in sexually naïve male mice.
+GLP1R	addiction	reward	32388229	As <b>reward</b> induced by addictive drugs and sexual behaviors involve similar neurocircuits, we hypothesized that activation of <strong>GLP 1R</strong> suppresses sexual behavior in sexually naïve male mice.
+GLP1R	addiction	reward	32388229	Collectively, these data highlight that activation of <strong>GLP 1R</strong>, specifically those in the NTS, reduces sexual interaction behaviors in sexually naïve male mice and further provide a link between NTS <strong>GLP 1R</strong> activation and <b>reward</b> related behaviors.
+GLP1R	drug	alcohol	31759971	Further studies established that Ex4 modulates <b>alcohol</b> mediated behaviours via activation of <strong>GLP 1</strong> receptors in reward related areas and an area of the hindbrain.
+GLP1R	addiction	reward	31759971	Further studies established that Ex4 modulates alcohol mediated behaviours via activation of <strong>GLP 1</strong> receptors in <b>reward</b> related areas and an area of the hindbrain.
+GLP1R	drug	alcohol	31759971	Finally, another <strong>GLP 1</strong> receptor agonist, AC3174, counteracts relapse drinking to <b>alcohol</b>.
+GLP1R	addiction	relapse	31759971	Finally, another <strong>GLP 1</strong> receptor agonist, AC3174, counteracts <b>relapse</b> drinking to alcohol.
+GLP1R	drug	alcohol	31759971	Furthermore, a polymorphism in the <strong>GLP 1</strong> receptor gene is associated with enhanced intravenous self administration of <b>alcohol</b> in social drinkers and higher response in globus pallidus following high monetary reward.
+GLP1R	addiction	reward	31759971	Furthermore, a polymorphism in the <strong>GLP 1</strong> receptor gene is associated with enhanced intravenous self administration of alcohol in social drinkers and higher response in globus pallidus following high monetary <b>reward</b>.
+GLP1R	drug	alcohol	31759971	Collectively, these data provide evidence that up coming clinical trials should evaluate the effect of these <strong>GLP 1</strong> receptor agonists on <b>alcohol</b> intake in patients with AUD.
+GLP1R	drug	opioid	31581176	Activation of <strong>GLP 1</strong> receptors attenuates <b>oxycodone</b> taking and seeking without compromising the antinociceptive effects of <b>oxycodone</b> in rats.
+GLP1R	addiction	relapse	31581176	Activation of <strong>GLP 1</strong> receptors attenuates oxycodone taking and <b>seeking</b> without compromising the antinociceptive effects of oxycodone in rats.
+GLP1R	addiction	reward	31581176	A growing body of preclinical evidence indicates that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists reduce drug <b>reinforcement</b>.
+GLP1R	drug	opioid	31581176	However, the efficacy of <strong>GLP 1</strong> receptor agonists in attenuating <b>opioid</b> mediated behaviors has not been thoroughly investigated.
+GLP1R	drug	opioid	31581176	Using recently established models of <b>opioid</b> taking and  seeking behaviors, we showed that systemic administration of the <strong>GLP 1</strong> receptor agonist exendin 4 reduced <b>oxycodone</b> self administration and the reinstatement of <b>oxycodone</b> seeking behavior in rats.
+GLP1R	addiction	relapse	31581176	Using recently established models of opioid taking and  <b>seeking</b> behaviors, we showed that systemic administration of the <strong>GLP 1</strong> receptor agonist exendin 4 reduced oxycodone self administration and the <b>reinstatement</b> of oxycodone <b>seeking</b> behavior in rats.
+GLP1R	drug	opioid	31581176	Finally, exendin 4 did not alter the analgesic effects of <b>oxycodone</b>, suggesting that activation of <strong>GLP 1</strong> receptors attenuated <b>opioid</b> reinforcement without reducing the thermal antinociceptive effects of <b>oxycodone</b>.
+GLP1R	addiction	reward	31581176	Finally, exendin 4 did not alter the analgesic effects of oxycodone, suggesting that activation of <strong>GLP 1</strong> receptors attenuated opioid <b>reinforcement</b> without reducing the thermal antinociceptive effects of oxycodone.
+GLP1R	drug	opioid	31581176	Taken together, these findings suggest that <strong>GLP 1</strong> receptors could serve as potential molecular targets for pharmacotherapies aimed at reducing <b>opioid</b> use disorder.
+GLP1R	drug	opioid	31058214	<strong>Glucagon Like Peptide 1 Receptor</strong> Agonist Treatment Does Not Reduce Abuse Related Effects of <b>Opioid</b> Drugs.
+GLP1R	drug	alcohol	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of <b>alcohol</b>, cocaine, amphetamine, and nicotine in rodents.
+GLP1R	drug	amphetamine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, cocaine, <b>amphetamine</b>, and nicotine in rodents.
+GLP1R	drug	cocaine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, <b>cocaine</b>, amphetamine, and nicotine in rodents.
+GLP1R	drug	nicotine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, cocaine, amphetamine, and <b>nicotine</b> in rodents.
+GLP1R	addiction	reward	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the <b>reinforcing</b> and rewarding effects of alcohol, cocaine, amphetamine, and nicotine in rodents.
+GLP1R	drug	opioid	31058214	Investigations on effects of <strong>GLP 1</strong> analogs on <b>opioid</b> reward and reinforcement have not been reported.
+GLP1R	addiction	reward	31058214	Investigations on effects of <strong>GLP 1</strong> analogs on opioid <b>reward</b> and <b>reinforcement</b> have not been reported.
+GLP1R	drug	alcohol	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, <b>naltrexone</b> precipitated morphine withdrawal, morphine analgesia (male and female mice), and locomotor activity.
+GLP1R	drug	opioid	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on <b>opioid</b> related behaviors in male mice, i.e., <b>morphine</b> conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic <b>opioid</b> remifentanil, naltrexone precipitated <b>morphine</b> withdrawal, <b>morphine</b> analgesia (male and female mice), and locomotor activity.
+GLP1R	addiction	reward	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (<b>CPP</b>), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, naltrexone precipitated morphine withdrawal, morphine analgesia (male and female mice), and locomotor activity.
+GLP1R	addiction	withdrawal	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, naltrexone precipitated morphine <b>withdrawal</b>, morphine analgesia (male and female mice), and locomotor activity.
+GLP1R	drug	opioid	31058214	Taken together, Ex4 did not attenuate the addiction related behavioral effects of <b>opioids</b>, indicating that <strong>GLP 1</strong> analogs would not be useful medications in the treatment of <b>opioid</b> addiction.
+GLP1R	addiction	addiction	31058214	Taken together, Ex4 did not attenuate the <b>addiction</b> related behavioral effects of opioids, indicating that <strong>GLP 1</strong> analogs would not be useful medications in the treatment of opioid <b>addiction</b>.
+GLP1R	drug	alcohol	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of <b>alcohol</b>, central stimulants, and nicotine.
+GLP1R	drug	nicotine	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of alcohol, central stimulants, and <b>nicotine</b>.
+GLP1R	drug	opioid	31058214	This difference between <b>opioids</b> and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of alcohol, central stimulants, and nicotine.
+GLP1R	addiction	addiction	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the <b>addictive</b> effects of alcohol, central stimulants, and nicotine.
+GLP1R	drug	cocaine	30930091	Central <strong>GLP 1</strong> receptors: Novel molecular targets for <b>cocaine</b> use disorder.
+GLP1R	drug	cocaine	30930091	Recent preclinical evidence suggests that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists could be re purposed to treat <b>cocaine</b> craving induced relapse.
+GLP1R	addiction	relapse	30930091	Recent preclinical evidence suggests that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists could be re purposed to treat cocaine <b>craving</b> induced <b>relapse</b>.
+GLP1R	drug	cocaine	30930091	This review endeavors to comprehensively summarize the current literature investigating the efficacy of <strong>GLP 1</strong> receptor agonists in reducing the rewarding and reinforcing effects of <b>cocaine</b> in animal models of <b>cocaine</b> use disorder.
+GLP1R	addiction	reward	30930091	This review endeavors to comprehensively summarize the current literature investigating the efficacy of <strong>GLP 1</strong> receptor agonists in reducing the rewarding and <b>reinforcing</b> effects of cocaine in animal models of cocaine use disorder.
+GLP1R	drug	cocaine	30930091	The role of central endogenous <strong>GLP 1</strong> circuits in voluntary <b>cocaine</b> taking and seeking is also discussed.
+GLP1R	addiction	relapse	30930091	The role of central endogenous <strong>GLP 1</strong> circuits in voluntary cocaine taking and <b>seeking</b> is also discussed.
+GLP1R	addiction	addiction	30930091	Behavioral, neurochemical, electrophysiological and molecular biology studies indicate that central <strong>GLP 1</strong> receptor activation functionally modulates the mesolimbic reward system and decreases <b>addiction</b> like phenotypes in rodents.
+GLP1R	addiction	reward	30930091	Behavioral, neurochemical, electrophysiological and molecular biology studies indicate that central <strong>GLP 1</strong> receptor activation functionally modulates the mesolimbic <b>reward</b> system and decreases addiction like phenotypes in rodents.
+GLP1R	drug	cocaine	30930091	Overall, an emerging preclinical literature provides compelling evidence to advance <strong>GLP 1</strong> receptor agonists into clinical trials testing the efficacy of these medications in preventing <b>cocaine</b> craving induced relapse.
+GLP1R	addiction	relapse	30930091	Overall, an emerging preclinical literature provides compelling evidence to advance <strong>GLP 1</strong> receptor agonists into clinical trials testing the efficacy of these medications in preventing cocaine <b>craving</b> induced <b>relapse</b>.
+GLP1R	drug	amphetamine	30831183	Stress responsive prolactin releasing peptide (PrRP) positive noradrenergic and glucagon like peptide 1 (<strong>GLP 1</strong>) positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating <b>amph</b> induced hypophagia and CTA.
+GLP1R	addiction	aversion	30831183	Stress responsive prolactin releasing peptide (PrRP) positive noradrenergic and glucagon like peptide 1 (<strong>GLP 1</strong>) positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating amph induced hypophagia and <b>CTA</b>.
+GLP1R	drug	amphetamine	30831183	Compared to control saline treatment, <b>amph</b> activated significantly more cNTS neurons, including PrRP negative noradrenergic (NA) neurons, GABAergic neurons, and glutamatergic neurons, but not PrRP or <strong>GLP 1</strong> neurons.
+GLP1R	drug	alcohol	30772374	It has also been demonstrated that systemic administration of <strong>GLP 1R</strong> agonists attenuates <b>alcohol</b> mediated behaviors via, to date, unknown mechanisms.
+GLP1R	drug	alcohol	30772374	Therefore, we evaluated the effects of NTS <strong>GLP 1R</strong> activation by exendin 4 (Ex4) on <b>alcohol</b> induced locomotor stimulation, accumbal dopamine release and memory of <b>alcohol</b> reward in the conditioned place preference (CPP) model in mice.
+GLP1R	addiction	reward	30772374	Therefore, we evaluated the effects of NTS <strong>GLP 1R</strong> activation by exendin 4 (Ex4) on alcohol induced locomotor stimulation, accumbal dopamine release and memory of alcohol <b>reward</b> in the conditioned place preference (<b>CPP</b>) model in mice.
+GLP1R	drug	alcohol	30772374	Pharmacological suppression of <strong>GLP 1R</strong> in the NTS prevents the ability of systemic Ex4 to block the <b>alcohol</b> induced locomotor stimulation in mice.
+GLP1R	drug	alcohol	30772374	These data add a functional role of <strong>GLP 1R</strong> within the NTS, involving <b>alcohol</b> related behaviors.
+GLP1R	drug	alcohol	30772374	In addition, they may provide insight into the <strong>GLP 1R</strong> containing brain areas that modulate the ability of <strong>GLP 1R</strong> agonists to reduce <b>alcohol</b> reinforcement.
+GLP1R	addiction	reward	30772374	In addition, they may provide insight into the <strong>GLP 1R</strong> containing brain areas that modulate the ability of <strong>GLP 1R</strong> agonists to reduce alcohol <b>reinforcement</b>.
+GLP1R	drug	alcohol	30772374	Collectively, this further supports <strong>GLP 1R</strong> as potential treatment targets for <b>alcohol</b> use disorder.
+GLP1R	drug	alcohol	30771711	Glucagon like peptide 1 (<strong>GLP 1</strong>), an incretin hormone that reduces food intake, was recently established as a novel regulator of <b>alcohol</b> mediated behaviors.
+GLP1R	drug	alcohol	30771711	Clinically available analogues pass freely into the brain, but the mechanisms underlying <strong>GLP 1</strong> modulated <b>alcohol</b> reward remains largely unclear.
+GLP1R	addiction	reward	30771711	Clinically available analogues pass freely into the brain, but the mechanisms underlying <strong>GLP 1</strong> modulated alcohol <b>reward</b> remains largely unclear.
+GLP1R	drug	alcohol	30771711	<strong>GLP 1</strong> receptors (GLP 1R) are expressed throughout the nuclei of importance for acute and chronic effects of <b>alcohol</b>, such as the laterodorsal tegmental area (LDTg), the ventral tegmental area (VTA) and the nucleus accumbens (NAc).
+GLP1R	drug	alcohol	30771711	<strong>GLP 1</strong> receptors (<strong>GLP 1R</strong>) are expressed throughout the nuclei of importance for acute and chronic effects of <b>alcohol</b>, such as the laterodorsal tegmental area (LDTg), the ventral tegmental area (VTA) and the nucleus accumbens (NAc).
+GLP1R	drug	alcohol	30771711	We therefore evaluated the effects of bilateral infusion of the <strong>GLP 1R</strong> agonist exendin 4 (Ex4) into NAc shell, anterior (aVTA), posterior (pVTA) or LDTg on the acute <b>alcohol</b> induced locomotor stimulation and memory of <b>alcohol</b> reward in the conditioned place preference (CPP) model in mice, as well as on <b>alcohol</b> intake in rats consuming high amounts of <b>alcohol</b> for 12 weeks.
+GLP1R	addiction	reward	30771711	We therefore evaluated the effects of bilateral infusion of the <strong>GLP 1R</strong> agonist exendin 4 (Ex4) into NAc shell, anterior (aVTA), posterior (pVTA) or LDTg on the acute alcohol induced locomotor stimulation and memory of alcohol <b>reward</b> in the conditioned place preference (<b>CPP</b>) model in mice, as well as on alcohol intake in rats consuming high amounts of alcohol for 12 weeks.
+GLP1R	drug	alcohol	30771711	The <strong>GLP 1R</strong> expression in NAc is elevated in high compared to low <b>alcohol</b> consuming rats.
+GLP1R	drug	alcohol	30771711	On the contrary, <strong>GLP 1R</strong> activation in the aVTA does not modulate <b>alcohol</b> induced behaviors.
+GLP1R	drug	alcohol	30771711	Collectively, these data provide additional knowledge of the functional role of <strong>GLP 1R</strong> in reward related areas for <b>alcohol</b> mediated behaviors and further support <strong>GLP 1R</strong> as a potential treatment target for <b>alcohol</b> use disorder.
+GLP1R	addiction	reward	30771711	Collectively, these data provide additional knowledge of the functional role of <strong>GLP 1R</strong> in <b>reward</b> related areas for alcohol mediated behaviors and further support <strong>GLP 1R</strong> as a potential treatment target for alcohol use disorder.
+GLP1R	drug	alcohol	30439457	The present review therefore summarizes the current studies investigating the ability of the gut brain peptides ghrelin, glucagon like peptide 1 (<strong>GLP 1</strong>), amylin and neuromedin U (NMU) to modulate <b>alcohol</b>  and drug related behaviors in rodents and humans.
+GLP1R	drug	alcohol	30439457	On the other hand, the anorexigenic peptides <strong>GLP 1</strong>, amylin and NMU independently inhibits reward from <b>alcohol</b> and drugs of abuse in rodents.
+GLP1R	addiction	reward	30439457	On the other hand, the anorexigenic peptides <strong>GLP 1</strong>, amylin and NMU independently inhibits <b>reward</b> from alcohol and drugs of abuse in rodents.
+GLP1R	addiction	addiction	30439457	Collectively, these rodent and human studies imply that central ghrelin, <strong>GLP 1</strong>, amylin and NMU signaling may contribute to <b>addiction</b> processes.
+GLP1R	drug	cocaine	30414405	<b>Cocaine</b> and <b>cocaine</b> expectancy increase growth hormone, ghrelin, <strong>GLP 1</strong>, IGF 1, adiponectin, and corticosterone while decreasing leptin, insulin, GIP, and prolactin.
+GLP1R	drug	cocaine	30414405	During <b>cocaine</b> taking, growth hormone and acetylated ghrelin increased 10 fold; glucagon like peptide 1 (<strong>GLP 1</strong>) doubled; non acetylated ghrelin, insulin like growth factor 1 (IGF 1), and corticosterone increased by 50% and adiponectin increased by 17%.
+GLP1R	drug	alcohol	30012779	Does glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist stimulation reduce <b>alcohol</b> intake in patients with <b>alcohol</b> dependence: study protocol of a randomised, double blinded, placebo controlled clinical trial.
+GLP1R	addiction	dependence	30012779	Does glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist stimulation reduce alcohol intake in patients with alcohol <b>dependence</b>: study protocol of a randomised, double blinded, placebo controlled clinical trial.
+GLP1R	drug	alcohol	30012779	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor stimulation has proven to reduce <b>alcohol</b> consumption in preclinical experiments.
+GLP1R	drug	alcohol	29927808	The present study investigated the relationship between accumbal ghrelin and glucagon like peptide 1 (<strong>GLP 1</strong>) signaling in <b>alcohol</b> reward in female rats.
+GLP1R	addiction	reward	29927808	The present study investigated the relationship between accumbal ghrelin and glucagon like peptide 1 (<strong>GLP 1</strong>) signaling in alcohol <b>reward</b> in female rats.
+GLP1R	drug	alcohol	29927808	Overall, these findings demonstrate the importance of accumbal ghrelin and <strong>GLP 1</strong> signaling in <b>alcohol</b> reward and appetitive motivation.
+GLP1R	addiction	reward	29927808	Overall, these findings demonstrate the importance of accumbal ghrelin and <strong>GLP 1</strong> signaling in alcohol <b>reward</b> and appetitive motivation.
+GLP1R	drug	cocaine	29497166	<strong>Glucagon like peptide 1 receptor</strong> activation in the ventral tegmental area attenuates <b>cocaine</b> seeking in rats.
+GLP1R	addiction	relapse	29497166	<strong>Glucagon like peptide 1 receptor</strong> activation in the ventral tegmental area attenuates cocaine <b>seeking</b> in rats.
+GLP1R	drug	cocaine	29497166	Here we investigated a role for glucagon like peptide 1 (<strong>GLP 1</strong>) receptors in the reinstatement of <b>cocaine</b> seeking behavior, an animal model of relapse.
+GLP1R	addiction	relapse	29497166	Here we investigated a role for glucagon like peptide 1 (<strong>GLP 1</strong>) receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior, an animal model of <b>relapse</b>.
+GLP1R	drug	cocaine	29497166	We showed that peripheral administration of the <strong>GLP 1</strong> receptor agonist exendin 4 dose dependently reduced <b>cocaine</b> seeking in rats at doses that did not affect ad libitum food intake, meal patterns or body weight.
+GLP1R	addiction	relapse	29497166	We showed that peripheral administration of the <strong>GLP 1</strong> receptor agonist exendin 4 dose dependently reduced cocaine <b>seeking</b> in rats at doses that did not affect ad libitum food intake, meal patterns or body weight.
+GLP1R	drug	cocaine	29497166	The effects of systemic exendin 4 on <b>cocaine</b> reinstatement were attenuated in rats pretreated with intra VTA infusions of the <strong>GLP 1</strong> receptor antagonist exendin (9 39), indicating that the suppressive effects of systemic exendin 4 on <b>cocaine</b> seeking were due, in part, to activation of <strong>GLP 1</strong> receptors in the VTA.
+GLP1R	addiction	relapse	29497166	The effects of systemic exendin 4 on cocaine <b>reinstatement</b> were attenuated in rats pretreated with intra VTA infusions of the <strong>GLP 1</strong> receptor antagonist exendin (9 39), indicating that the suppressive effects of systemic exendin 4 on cocaine <b>seeking</b> were due, in part, to activation of <strong>GLP 1</strong> receptors in the VTA.
+GLP1R	drug	cocaine	29497166	Thus, our study demonstrated a novel role for <strong>GLP 1</strong> receptors in the reinstatement of <b>cocaine</b> seeking behavior and identified behaviorally relevant doses of a <strong>GLP 1</strong> receptor agonist that selectively reduced <b>cocaine</b> seeking and did not produce adverse effects.
+GLP1R	addiction	relapse	29497166	Thus, our study demonstrated a novel role for <strong>GLP 1</strong> receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior and identified behaviorally relevant doses of a <strong>GLP 1</strong> receptor agonist that selectively reduced cocaine <b>seeking</b> and did not produce adverse effects.
+GLP1R	drug	alcohol	29480848	A novel approach might use glucagon like peptide 1 (<strong>GLP 1</strong>) agonists, which reduce <b>alcohol</b> and drug use in preclinical studies.
+GLP1R	drug	nicotine	29480848	Several <strong>GLP 1</strong> agonists are used clinically to treat type 2 diabetes and obesity, but none have been tested in humans to reduce <b>smoking</b>.
+GLP1R	drug	alcohol	29337226	<strong>GLP 1</strong> signaling and <b>alcohol</b> mediated behaviors; preclinical and clinical evidence.
+GLP1R	drug	alcohol	29337226	One of these gut brain peptides is the annorexigenic peptide glucagon like peptide 1 (<strong>GLP 1</strong>), Preclinical studies show that <strong>GLP 1</strong> receptor activation, either by <strong>GLP 1</strong> or analogues, attenuate the ability of <b>alcohol</b> to activate the mesolimbic dopamine system as well as decrease <b>alcohol</b> consumption and operant self administration.
+GLP1R	addiction	reward	29337226	One of these gut brain peptides is the annorexigenic peptide glucagon like peptide 1 (<strong>GLP 1</strong>), Preclinical studies show that <strong>GLP 1</strong> receptor activation, either by <strong>GLP 1</strong> or analogues, attenuate the ability of alcohol to activate the mesolimbic dopamine system as well as decrease alcohol consumption and <b>operant</b> self administration.
+GLP1R	drug	alcohol	29337226	In further support for the endogenous <strong>GLP 1</strong> system in addiction processes are the experimental data showing that a <strong>GLP 1</strong> receptor antagonist increases <b>alcohol</b> intake.
+GLP1R	addiction	addiction	29337226	In further support for the endogenous <strong>GLP 1</strong> system in <b>addiction</b> processes are the experimental data showing that a <strong>GLP 1</strong> receptor antagonist increases alcohol intake.
+GLP1R	addiction	addiction	29337226	Moreover, <strong>GLP 1</strong> receptor agonists prevent the ability of other <b>addictive</b> drugs to activate the mesolimbic dopamine system.
+GLP1R	drug	alcohol	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with <b>alcohol</b> addiction as well as increased <b>alcohol</b> infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of cocaine and iii) that a <strong>GLP 1</strong> receptor agonist reduces <b>alcohol</b> intake in patients with type 2 diabetes mellitus.
+GLP1R	drug	cocaine	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with alcohol addiction as well as increased alcohol infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of <b>cocaine</b> and iii) that a <strong>GLP 1</strong> receptor agonist reduces alcohol intake in patients with type 2 diabetes mellitus.
+GLP1R	addiction	addiction	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with alcohol <b>addiction</b> as well as increased alcohol infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of cocaine and iii) that a <strong>GLP 1</strong> receptor agonist reduces alcohol intake in patients with type 2 diabetes mellitus.
+GLP1R	drug	alcohol	29337226	These experimental and clinical studies raises the concern that clinically available <strong>GLP 1</strong> receptor agonists deserves to be tested as potential treatments of patients with addictive disorders including <b>alcohol</b> addiction.
+GLP1R	addiction	addiction	29337226	These experimental and clinical studies raises the concern that clinically available <strong>GLP 1</strong> receptor agonists deserves to be tested as potential treatments of patients with <b>addictive</b> disorders including alcohol <b>addiction</b>.
+GLP1R	drug	cannabinoid	29231147	Inclusion criteria were: 1) full text available in English; 2) published in a peerreviewed journal and using the following keywords: neurotransmitters (AgRP, BDNF, αMSH, NP Y, <b>endocannabinoids</b>, adiponectin, CCK, ghrelin, <strong>GLP 1</strong>, insulin, leptin, PP, PYY), hormones (FSH, LH, estrogen, progesterone, testosterone) and bulimia nervosa, eating disorders.
+GLP1R	drug	cocaine	29226617	Recent evidence indicates that activation of glucagon like peptide 1 (<strong>GLP 1</strong>) receptors reduces <b>cocaine</b> mediated behaviors and <b>cocaine</b> evoked dopamine release in the nucleus accumbens (NAc).
+GLP1R	drug	cocaine	29226617	However, no studies have examined the role of NAc <strong>GLP 1</strong> receptors in the reinstatement of <b>cocaine</b> seeking behavior, an animal model of relapse.
+GLP1R	addiction	relapse	29226617	However, no studies have examined the role of NAc <strong>GLP 1</strong> receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior, an animal model of <b>relapse</b>.
+GLP1R	drug	cocaine	29226617	To determine the effects of <strong>GLP 1</strong> receptor activation on neuronal excitability, exendin 4 was bath applied to ex vivo NAc slices from <b>cocaine</b> experienced and saline experienced rats following extinction of <b>cocaine</b> taking behavior.
+GLP1R	drug	cocaine	29226617	These effects were not associated with altered expression of <strong>GLP 1</strong> receptors in the NAc following <b>cocaine</b> self administration.
+GLP1R	drug	cocaine	29226617	Taken together, these findings indicate that increased activation of <strong>GLP 1</strong> receptors in the NAc during <b>cocaine</b> abstinence increases intrinsic, but not synaptic, excitability of medium spiny neurons and is sufficient to reduce <b>cocaine</b> seeking behavior.
+GLP1R	addiction	relapse	29226617	Taken together, these findings indicate that increased activation of <strong>GLP 1</strong> receptors in the NAc during cocaine abstinence increases intrinsic, but not synaptic, excitability of medium spiny neurons and is sufficient to reduce cocaine <b>seeking</b> behavior.
+GLP1R	addiction	relapse	28778739	The <strong>glucagon like peptide 1 receptor</strong> agonist Exendin 4 decreases <b>relapse</b> like drinking in socially housed mice.
+GLP1R	drug	alcohol	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for <b>alcohol</b> and drug reward, and for the development of addiction.
+GLP1R	addiction	addiction	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for alcohol and drug reward, and for the development of <b>addiction</b>.
+GLP1R	addiction	reward	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for alcohol and drug <b>reward</b>, and for the development of addiction.
+GLP1R	drug	alcohol	28778739	<strong>GLP 1</strong> receptor agonists can decrease <b>alcohol</b> intake acutely in rodents.
+GLP1R	addiction	relapse	28778739	Here, we assessed the effect of daily treatment with the <strong>GLP 1</strong> receptor agonist Exendin 4 in an assay of <b>relapse</b> like drinking in socially housed mice.
+GLP1R	drug	alcohol	28778739	These findings support the possible use of <strong>GLP 1</strong> receptor agonists in the treatment of <b>alcohol</b> use disorder.
+GLP1R	addiction	withdrawal	28664354	After pioglitazone <b>withdrawal</b>, case reports increased for dipeptidyl peptidase 4 (DPP 4) inhibitors, glinides, and glucagon like peptide 1 (<strong>GLP 1</strong>) analogues (+84%, +22% and +5%, respectively) and reimbursements (+55, +11 and +50%, respectively); both decreased for sulfonylureas (case reports:  6%, reimbursements:  2%).
+GLP1R	drug	nicotine	28368384	<strong>GLP 1</strong> acts on habenular avoidance circuits to control <b>nicotine</b> intake.
+GLP1R	drug	nicotine	28368384	Here we show that <b>nicotine</b> activates glucagon like peptide 1 (<strong>GLP 1</strong>) neurons in the nucleus tractus solitarius (NTS).
+GLP1R	drug	nicotine	28368384	The antidiabetic drugs sitagliptin and exenatide, which inhibit <strong>GLP 1</strong> breakdown and stimulate <strong>GLP 1</strong> receptors, respectively, decreased <b>nicotine</b> intake in mice.
+GLP1R	drug	nicotine	28368384	Chemogenetic activation of <strong>GLP 1</strong> neurons in NTS similarly decreased <b>nicotine</b> intake.
+GLP1R	drug	nicotine	28368384	Conversely, <strong>Glp1r</strong> knockout mice consumed greater quantities of <b>nicotine</b> than wild type mice.
+GLP1R	drug	nicotine	28368384	Activation of <strong>GLP 1</strong> receptors in the MHb IPN circuit abolished <b>nicotine</b> reward and decreased <b>nicotine</b> intake, whereas their knockdown or pharmacological blockade increased intake.
+GLP1R	addiction	reward	28368384	Activation of <strong>GLP 1</strong> receptors in the MHb IPN circuit abolished nicotine <b>reward</b> and decreased nicotine intake, whereas their knockdown or pharmacological blockade increased intake.
+GLP1R	drug	nicotine	28368384	<strong>GLP 1</strong> neurons may therefore serve as 'satiety sensors' for <b>nicotine</b> that stimulate habenular systems to promote <b>nicotine</b> avoidance before its aversive effects are encountered.
+GLP1R	addiction	aversion	28368384	<strong>GLP 1</strong> neurons may therefore serve as 'satiety sensors' for nicotine that stimulate habenular systems to promote nicotine avoidance before its <b>aversive</b> effects are encountered.
+GLP1R	drug	cocaine	28315693	Central <strong>GLP 1</strong> receptor activation modulates <b>cocaine</b> evoked phasic dopamine signaling in the nucleus accumbens core.
+GLP1R	drug	cocaine	28315693	Recently, metabolic regulatory peptides, including the satiety signal glucagon like peptide 1 (<strong>GLP 1</strong>), have been shown to modulate <b>cocaine</b> reward driven behavior and sustained dopamine levels after <b>cocaine</b> administration.
+GLP1R	addiction	reward	28315693	Recently, metabolic regulatory peptides, including the satiety signal glucagon like peptide 1 (<strong>GLP 1</strong>), have been shown to modulate cocaine <b>reward</b> driven behavior and sustained dopamine levels after cocaine administration.
+GLP1R	drug	cocaine	28315693	Here, we use fast scan cyclic voltammetry (FSCV) to explore <strong>GLP 1</strong> receptor (GLP 1R) modulation of dynamic dopamine release in the nucleus accumbens (NAc) during <b>cocaine</b> administration.
+GLP1R	drug	cocaine	28315693	Here, we use fast scan cyclic voltammetry (FSCV) to explore <strong>GLP 1</strong> receptor (<strong>GLP 1R</strong>) modulation of dynamic dopamine release in the nucleus accumbens (NAc) during <b>cocaine</b> administration.
+GLP1R	drug	cocaine	28315693	We found that central delivery of the <strong>GLP 1R</strong> agonist Exendin 4 suppressed the induction of phasic dopamine release events by intravenous <b>cocaine</b>.
+GLP1R	drug	cocaine	28315693	Given the role of NAc core dopamine in the generation of conditioned responses based on associative learning, suppression of <b>cocaine</b> induced dopamine signaling in this subregion by <strong>GLP 1R</strong> agonism may decrease the reinforcing properties of <b>cocaine</b>.
+GLP1R	addiction	reward	28315693	Given the role of NAc core dopamine in the generation of conditioned responses based on associative learning, suppression of cocaine induced dopamine signaling in this subregion by <strong>GLP 1R</strong> agonism may decrease the <b>reinforcing</b> properties of cocaine.
+GLP1R	drug	alcohol	27579999	Effects of the <strong>GLP 1</strong> Agonist Exendin 4 on Intravenous <b>Ethanol</b> Self Administration in Mice.
+GLP1R	drug	alcohol	27579999	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists have been shown to decrease <b>ethanol</b> (EtOH) drinking in rodent assays.
+GLP1R	addiction	reward	27579999	To begin to understand the neurobiological mechanisms by which <strong>GLP 1</strong> receptor ligands may be able to control EtOH intake, it is important to ascertain whether they can modulate the direct <b>reinforcing</b> effects of EtOH, without the confound of effects on ingestive behaviors generally.
+GLP1R	addiction	reward	27579999	Second, <strong>GLP 1</strong> receptor agonists can powerfully attenuate voluntary EtOH intake by directly modulating the <b>reinforcing</b> effects of EtOH.
+GLP1R	drug	alcohol	27579999	These findings support the potential usefulness of <strong>GLP 1</strong> receptor ligands in the treatment of <b>alcohol</b> use disorder.
+GLP1R	drug	cocaine	27187231	<strong>Glucagon like peptide 1 receptor</strong> activation regulates <b>cocaine</b> actions and dopamine homeostasis in the lateral septum by decreasing arachidonic acid levels.
+GLP1R	drug	cocaine	27187231	Agonism of the glucagon like peptide 1 (<strong>GLP 1</strong>) receptor (GLP 1R) has been effective at treating aspects of addictive behavior for a number of abused substances, including <b>cocaine</b>.
+GLP1R	addiction	addiction	27187231	Agonism of the glucagon like peptide 1 (<strong>GLP 1</strong>) receptor (GLP 1R) has been effective at treating aspects of <b>addictive</b> behavior for a number of abused substances, including cocaine.
+GLP1R	drug	cocaine	27187231	Agonism of the glucagon like peptide 1 (<strong>GLP 1</strong>) receptor (<strong>GLP 1R</strong>) has been effective at treating aspects of addictive behavior for a number of abused substances, including <b>cocaine</b>.
+GLP1R	addiction	addiction	27187231	Agonism of the glucagon like peptide 1 (<strong>GLP 1</strong>) receptor (<strong>GLP 1R</strong>) has been effective at treating aspects of <b>addictive</b> behavior for a number of abused substances, including cocaine.
+GLP1R	drug	cocaine	27187231	However, the molecular mechanisms and brain circuits underlying the therapeutic effects of <strong>GLP 1R</strong> signaling on <b>cocaine</b> actions remain elusive.
+GLP1R	drug	cocaine	27187231	Recent evidence has revealed that endogenous signaling at the <strong>GLP 1R</strong> within the forebrain lateral septum (LS) acts to reduce <b>cocaine</b> induced locomotion and <b>cocaine</b> conditioned place preference, both considered dopamine (DA) associated behaviors.
+GLP1R	drug	cocaine	27187231	Therefore, <strong>GLP 1R</strong> signaling might exert effects on DAT to account for its regulation of <b>cocaine</b> induced behaviors.
+GLP1R	drug	cocaine	27187231	Exenatide (Ex 4), a long lasting synthetic analog of <strong>GLP 1</strong> abolished <b>cocaine</b> induced elevation of DA.
+GLP1R	drug	cocaine	27187231	These results support a mechanism in which postsynaptic septal <strong>GLP 1R</strong> activation regulates 2 AG levels to alter presynaptic DA homeostasis and <b>cocaine</b> actions through AA.
+GLP1R	addiction	addiction	27072507	Central & peripheral <strong>glucagon like peptide 1 receptor</strong> signaling differentially regulate <b>addictive</b> behaviors.
+GLP1R	drug	alcohol	27072507	Recent data implicate glucagon like peptide 1 (<strong>GLP 1</strong>), a potent anorexigenic peptide released in response to nutrient intake, as a regulator for the reinforcing properties of food, <b>alcohol</b> and psychostimulants.
+GLP1R	addiction	reward	27072507	Recent data implicate glucagon like peptide 1 (<strong>GLP 1</strong>), a potent anorexigenic peptide released in response to nutrient intake, as a regulator for the <b>reinforcing</b> properties of food, alcohol and psychostimulants.
+GLP1R	addiction	reward	27072507	While, both central and peripheral mechanisms mediate effects of <strong>GLP 1R</strong> signaling on food intake, the extent to which central or peripheral <strong>GLP 1R</strong> signaling regulates <b>reinforcing</b> properties of drugs of abuse is unknown.
+GLP1R	drug	alcohol	27072507	Here, we examined amphetamine reinforcement, <b>alcohol</b> intake and hedonic feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+GLP1R	drug	amphetamine	27072507	Here, we examined <b>amphetamine</b> reinforcement, alcohol intake and hedonic feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+GLP1R	addiction	reward	27072507	Here, we examined amphetamine <b>reinforcement</b>, alcohol intake and <b>hedonic</b> feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+GLP1R	drug	alcohol	27072507	Here, we examined amphetamine reinforcement, <b>alcohol</b> intake and hedonic feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and <strong>GLP 1R</strong> KD(Nestin) (<strong>GLP 1R</strong> selectively ablated from the central nervous system) mice (n=13/group).
+GLP1R	drug	amphetamine	27072507	Here, we examined <b>amphetamine</b> reinforcement, alcohol intake and hedonic feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and <strong>GLP 1R</strong> KD(Nestin) (<strong>GLP 1R</strong> selectively ablated from the central nervous system) mice (n=13/group).
+GLP1R	addiction	reward	27072507	Here, we examined amphetamine <b>reinforcement</b>, alcohol intake and <b>hedonic</b> feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and <strong>GLP 1R</strong> KD(Nestin) (<strong>GLP 1R</strong> selectively ablated from the central nervous system) mice (n=13/group).
+GLP1R	drug	amphetamine	27072507	First, the effect of EX 4 pretreatment on the expression of <b>amphetamine</b> induced conditioned place preference (Amp CPP) was examined in the FLOX and <strong>GLP 1R</strong> KD(Nestin) mice.
+GLP1R	addiction	reward	27072507	First, the effect of EX 4 pretreatment on the expression of amphetamine induced conditioned place preference (Amp <b>CPP</b>) was examined in the FLOX and <strong>GLP 1R</strong> KD(Nestin) mice.
+GLP1R	drug	alcohol	27072507	Next, <b>alcohol</b> intake (10% v/v) was evaluated in FLOX and <strong>GLP 1R</strong> KD(Nestin) mice following saline or EX 4 injections.
+GLP1R	addiction	reward	27072507	Results indicate that Amp <b>CPP</b> was completely blocked in the FLOX mice, but not in the <strong>GLP 1R</strong> KD(Nestin) mice following EX 4 pretreatment.
+GLP1R	drug	alcohol	27072507	Ex 4 pretreatment selectively blocked <b>alcohol</b> consumption in the FLOX mice, but was ineffective in altering <b>alcohol</b> intake in the <strong>GLP 1R</strong> KD(Nestin) mice.
+GLP1R	addiction	reward	27072507	Notably, <b>hedonic</b> feeding was partially blocked in the <strong>GLP 1R</strong> KD(Nestin) mice, whereas it was abolished in the FLOX mice.
+GLP1R	addiction	addiction	27072507	The present study provides critical insights regarding the nature by which <strong>GLP 1</strong> signaling controls reinforced behaviors and underscores the importance of both peripheral and central GLP 1R signaling for the regulation of <b>addictive</b> disorders.
+GLP1R	addiction	addiction	27072507	The present study provides critical insights regarding the nature by which <strong>GLP 1</strong> signaling controls reinforced behaviors and underscores the importance of both peripheral and central <strong>GLP 1R</strong> signaling for the regulation of <b>addictive</b> disorders.
+GLP1R	addiction	reward	27066524	<strong>GLP 1</strong> influences food and drug <b>reward</b>.
+GLP1R	addiction	reward	27066524	That the neuropeptide glucagon like peptide 1 (<strong>GLP 1</strong>) is under investigation for both the homeostatic and <b>hedonic</b> controls of feeding is not surprising or novel.
+GLP1R	addiction	reward	27066524	However, if the neural substrates that underline food <b>reward</b> are shared with other <b>reward</b> related behaviors generally, then future research should investigate and embrace the likelihood that endogenous and exogenous <strong>GLP 1</strong> receptor activation may influence multiple <b>reward</b> related behaviors.
+GLP1R	drug	alcohol	27066524	An emerging literature demonstrates a role for the <strong>GLP 1</strong> system in modulating maladaptive reward behaviors, including drug and <b>alcohol</b> consumption.
+GLP1R	addiction	reward	27066524	An emerging literature demonstrates a role for the <strong>GLP 1</strong> system in modulating maladaptive <b>reward</b> behaviors, including drug and alcohol consumption.
+GLP1R	addiction	addiction	27066524	Thus, if <strong>GLP 1</strong> based pharmacotherapies are to be used to treat drug <b>addiction</b> and other diseases associated with maladaptive reward behaviors (e.g.
+GLP1R	addiction	reward	27066524	Thus, if <strong>GLP 1</strong> based pharmacotherapies are to be used to treat drug addiction and other diseases associated with maladaptive <b>reward</b> behaviors (e.g.
+GLP1R	addiction	reward	27066524	Equally as likely, non selective effects on natural <b>reward</b> and maladaptive <b>reward</b> behaviors may be observed for <strong>GLP 1</strong> based pharmacotherapies.
+GLP1R	addiction	dependence	27066524	In this case, a better understanding of the effects of increased central <strong>GLP 1R</strong> activation on motivated behaviors will aid in clinical approaches toward treating aberrant feeding behaviors and/or drug <b>dependence</b>.
+GLP1R	drug	cocaine	26675243	<strong>Glucagon Like Peptide 1 Receptor</strong> Activation in the Ventral Tegmental Area Decreases the Reinforcing Efficacy of <b>Cocaine</b>.
+GLP1R	addiction	reward	26675243	<strong>Glucagon Like Peptide 1 Receptor</strong> Activation in the Ventral Tegmental Area Decreases the <b>Reinforcing</b> Efficacy of Cocaine.
+GLP1R	drug	cocaine	26675243	As the neural circuits and neurobiological mechanisms underlying drug taking overlap to some degree with those regulating food intake, these findings suggest that activation of central <strong>GLP 1</strong> receptors may also attenuate <b>cocaine</b> taking.
+GLP1R	drug	cocaine	26675243	Here, we show that intra VTA administration of the <strong>GLP 1</strong> receptor agonist exendin 4 (0.05 μg) significantly reduced <b>cocaine</b>, but not sucrose, self administration in rats.
+GLP1R	drug	cocaine	26675243	We also demonstrate that <b>cocaine</b> taking is associated with elevated plasma corticosterone levels and that systemic infusion of <b>cocaine</b> activates <strong>GLP 1</strong> expressing neurons in the nucleus tractus solitarius (NTS), a hindbrain nucleus that projects monosynaptically to the VTA.
+GLP1R	drug	cocaine	26675243	To determine the potential mechanisms by which <b>cocaine</b> activates NTS <strong>GLP 1</strong> expressing neurons, we microinjected corticosterone (0.5 μg) directly into the hindbrain fourth ventricle.
+GLP1R	drug	cocaine	26675243	Intraventricular corticosterone attenuated <b>cocaine</b> self administration and this effect was blocked in animals pretreated with the <strong>GLP 1</strong> receptor antagonist exendin (9 39) (10 μg) in the VTA.
+GLP1R	drug	cocaine	26675243	Finally, AAV shRNA mediated knockdown of VTA <strong>GLP 1</strong> receptors was sufficient to augment <b>cocaine</b> self administration.
+GLP1R	drug	cocaine	26675243	Taken together, these findings indicate that increased activation of NTS <strong>GLP 1</strong> expressing neurons by corticosterone may represent a homeostatic response to <b>cocaine</b> taking, thereby reducing the reinforcing efficacy of <b>cocaine</b>.
+GLP1R	addiction	reward	26675243	Taken together, these findings indicate that increased activation of NTS <strong>GLP 1</strong> expressing neurons by corticosterone may represent a homeostatic response to cocaine taking, thereby reducing the <b>reinforcing</b> efficacy of cocaine.
+GLP1R	drug	cocaine	26675243	Therefore, central <strong>GLP 1</strong> receptors may represent a novel target for <b>cocaine</b> addiction pharmacotherapies.
+GLP1R	addiction	addiction	26675243	Therefore, central <strong>GLP 1</strong> receptors may represent a novel target for cocaine <b>addiction</b> pharmacotherapies.
+GLP1R	drug	cannabinoid	26546790	To explore the role of some gastrointestinal orexigenic and anorexigenic peptides and <b>endocannabinoids</b> (and some related congeners) in chocolate consumption, we measured changes in circulating levels of ghrelin, glucagon like peptide 1 (<strong>GLP 1</strong>), peptide YY (PYY), anandamide (AEA), 2 AG, <b>palmitoylethanolamide</b> (PEA), and <b>oleoylethanolamide</b> (OEA) in 10 satiated severely obese subjects after consumption of chocolate and, on a separate day, of a non palatable isocaloric food with the same bromatologic composition.
+GLP1R	drug	alcohol	26303264	The <strong>glucagon like peptide 1 receptor</strong> agonist liraglutide attenuates the reinforcing properties of <b>alcohol</b> in rodents.
+GLP1R	addiction	reward	26303264	The <strong>glucagon like peptide 1 receptor</strong> agonist liraglutide attenuates the <b>reinforcing</b> properties of alcohol in rodents.
+GLP1R	drug	alcohol	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several <b>alcohol</b> mediated behaviors as well as amphetamine induced, cocaine induced and nicotine induced reward.
+GLP1R	drug	amphetamine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as <b>amphetamine</b> induced, cocaine induced and nicotine induced reward.
+GLP1R	drug	cocaine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, <b>cocaine</b> induced and nicotine induced reward.
+GLP1R	drug	nicotine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, cocaine induced and <b>nicotine</b> induced reward.
+GLP1R	addiction	reward	26303264	<strong>GLP 1</strong> receptors are expressed in <b>reward</b> related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, cocaine induced and nicotine induced <b>reward</b>.
+GLP1R	drug	alcohol	26303264	The present series of experiments were undertaken to investigate the effect of the <strong>GLP 1</strong> receptor agonist, liraglutide, on several <b>alcohol</b> related behaviors in rats that model different aspects of <b>alcohol</b> use disorder in humans.
+GLP1R	drug	alcohol	26303264	Collectively, these data suggest that <strong>GLP 1</strong> receptor agonists could be tested for treatment of <b>alcohol</b> dependence in humans.
+GLP1R	addiction	dependence	26303264	Collectively, these data suggest that <strong>GLP 1</strong> receptor agonists could be tested for treatment of alcohol <b>dependence</b> in humans.
+GLP1R	addiction	aversion	26211731	The <b>Aversive</b> Agent Lithium Chloride Suppresses Phasic Dopamine Release Through Central <strong>GLP 1</strong> Receptors.
+GLP1R	drug	opioid	26211731	Pretreatment with Ex 9 did not, however, affect the suppression of phasic dopamine release by the kappa <b>opioid</b> receptor agonist, salvinorin A, supporting a selective effect of <strong>GLP 1R</strong> stimulation in LiCl induced dopamine suppression.
+GLP1R	drug	alcohol	26080318	The <strong>glucagon like peptide 1 receptor</strong> as a potential treatment target in <b>alcohol</b> use disorder: evidence from human genetic association studies and a mouse model of <b>alcohol</b> dependence.
+GLP1R	addiction	dependence	26080318	The <strong>glucagon like peptide 1 receptor</strong> as a potential treatment target in alcohol use disorder: evidence from human genetic association studies and a mouse model of alcohol <b>dependence</b>.
+GLP1R	drug	alcohol	26080318	<strong>GLP 1</strong> receptor (GLP 1R) activation also attenuates the reinforcing properties of <b>alcohol</b> in rodents.
+GLP1R	addiction	reward	26080318	<strong>GLP 1</strong> receptor (GLP 1R) activation also attenuates the <b>reinforcing</b> properties of alcohol in rodents.
+GLP1R	drug	alcohol	26080318	<strong>GLP 1</strong> receptor (<strong>GLP 1R</strong>) activation also attenuates the reinforcing properties of <b>alcohol</b> in rodents.
+GLP1R	addiction	reward	26080318	<strong>GLP 1</strong> receptor (<strong>GLP 1R</strong>) activation also attenuates the <b>reinforcing</b> properties of alcohol in rodents.
+GLP1R	drug	alcohol	26080318	The present translational study is based on four human genetic association studies and one preclinical study providing data that support the hypothesis that <strong>GLP 1R</strong> may have a role in the pathophysiology of <b>alcohol</b> use disorder (AUD).
+GLP1R	drug	alcohol	26080318	In the preclinical study, a <strong>GLP 1R</strong> agonist was evaluated in a mouse model of <b>alcohol</b> dependence to demonstrate the role of <strong>GLP 1R</strong> for <b>alcohol</b> consumption.
+GLP1R	addiction	dependence	26080318	In the preclinical study, a <strong>GLP 1R</strong> agonist was evaluated in a mouse model of alcohol <b>dependence</b> to demonstrate the role of <strong>GLP 1R</strong> for alcohol consumption.
+GLP1R	drug	alcohol	26080318	Finally, <strong>GLP 1R</strong> agonism significantly reduced <b>alcohol</b> consumption in a mouse model of <b>alcohol</b> dependence.
+GLP1R	addiction	dependence	26080318	Finally, <strong>GLP 1R</strong> agonism significantly reduced alcohol consumption in a mouse model of alcohol <b>dependence</b>.
+GLP1R	drug	cocaine	26072178	The glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist exendin 4 reduces <b>cocaine</b> self administration in mice.
+GLP1R	drug	cocaine	26072178	Based on the anatomical distribution of <strong>GLP 1</strong> receptors in the brain and the well established effects of <strong>GLP 1</strong> on food reward, we decided to investigate the effect of the <strong>GLP 1</strong> analogue exendin 4 on <b>cocaine</b>  and dopamine D1 receptor agonist induced hyperlocomotion, on acute and chronic <b>cocaine</b> self administration, on <b>cocaine</b> induced striatal dopamine release in mice and on <b>cocaine</b> induced c fos activation.
+GLP1R	addiction	reward	26072178	Based on the anatomical distribution of <strong>GLP 1</strong> receptors in the brain and the well established effects of <strong>GLP 1</strong> on food <b>reward</b>, we decided to investigate the effect of the <strong>GLP 1</strong> analogue exendin 4 on cocaine  and dopamine D1 receptor agonist induced hyperlocomotion, on acute and chronic cocaine self administration, on cocaine induced striatal dopamine release in mice and on cocaine induced c fos activation.
+GLP1R	drug	cocaine	26072178	Here, we report that <strong>GLP 1</strong> receptor stimulation reduces acute and chronic <b>cocaine</b> self administration and attenuates <b>cocaine</b> induced hyperlocomotion.
+GLP1R	drug	cocaine	26072178	In addition, we show that peripheral administration of exendin 4 reduces <b>cocaine</b> induced elevation of striatal dopamine levels and striatal c fos expression implicating central <strong>GLP 1</strong> receptors in these responses.
+GLP1R	drug	cocaine	26072178	The present results demonstrate that the <strong>GLP 1</strong> system modulates <b>cocaine</b>'s effects on behavior and dopamine homeostasis, indicating that the <strong>GLP 1</strong> receptor may be a novel target for the pharmacological treatment of drug addiction.
+GLP1R	addiction	addiction	26072178	The present results demonstrate that the <strong>GLP 1</strong> system modulates cocaine's effects on behavior and dopamine homeostasis, indicating that the <strong>GLP 1</strong> receptor may be a novel target for the pharmacological treatment of drug <b>addiction</b>.
+GLP1R	drug	cocaine	25669605	Septal <strong>Glucagon Like Peptide 1 Receptor</strong> Expression Determines Suppression of <b>Cocaine</b> Induced Behavior.
+GLP1R	addiction	addiction	25669605	Both palatable food and illicit drugs activate brain reward circuitries, and pharmacological studies suggest that central nervous system <strong>GLP 1</strong> signaling holds potential for the treatment of <b>addiction</b>.
+GLP1R	addiction	reward	25669605	Both palatable food and illicit drugs activate brain <b>reward</b> circuitries, and pharmacological studies suggest that central nervous system <strong>GLP 1</strong> signaling holds potential for the treatment of addiction.
+GLP1R	addiction	reward	25669605	However, the role of endogenous <strong>GLP 1</strong> in the attenuation of <b>reward</b> oriented behavior, and the essential domains of the mesolimbic system mediating these beneficial effects, are largely unknown.
+GLP1R	drug	cocaine	25669605	Here, we show that <strong>Glp 1r</strong> deficient (<strong>Glp 1r</strong>( / )) mice have greatly augmented <b>cocaine</b> induced locomotor responses and enhanced conditional place preference compared with wild type (<strong>Glp 1r</strong>(+/+)) controls.
+GLP1R	addiction	reward	25669605	Employing mRNA in situ hybridization we located peak <strong>Glp 1r</strong> mRNA expression in GABAergic neurons of the dorsal lateral septum, an anatomical site with a crucial function in <b>reward</b> perception.
+GLP1R	drug	cocaine	25669605	Viral vector mediated <strong>Glp 1r</strong> gene delivery to the dorsal lateral septum of <strong>Glp 1r</strong>( / ) animals reduced <b>cocaine</b> induced locomotion and conditional place preference to wild type levels.
+GLP1R	drug	cocaine	25669605	These data reveal a novel role of <strong>GLP 1R</strong> in dorsal lateral septum function driving behavioral responses to <b>cocaine</b>.
+GLP1R	drug	alcohol	25380665	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist prevents development of tolerance to anti anxiety effect of <b>ethanol</b> and withdrawal induced anxiety in rats.
+GLP1R	addiction	withdrawal	25380665	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist prevents development of tolerance to anti anxiety effect of ethanol and <b>withdrawal</b> induced anxiety in rats.
+GLP1R	drug	alcohol	25380665	We recently reported that inhibition of dipeptidyl peptidase IV (DPP IV), an enzyme responsible for metabolism of endogenous glucagon like peptide 1 (<strong>GLP 1</strong>), delays tolerance to anti anxiety effect of <b>ethanol</b> and withdrawal induced anxiety in rats.
+GLP1R	addiction	withdrawal	25380665	We recently reported that inhibition of dipeptidyl peptidase IV (DPP IV), an enzyme responsible for metabolism of endogenous glucagon like peptide 1 (<strong>GLP 1</strong>), delays tolerance to anti anxiety effect of ethanol and <b>withdrawal</b> induced anxiety in rats.
+GLP1R	drug	alcohol	25380665	Intrigued with this report, present study examined the role of glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist, liraglutide in (1) acute anti anxiety effect of <b>ethanol</b>; (2) tolerance to <b>ethanol</b>'s anti anxiety effect and (3) <b>ethanol</b> withdrawal induced anxiety using elevated plus maze (EPM) test in rats.
+GLP1R	addiction	withdrawal	25380665	Intrigued with this report, present study examined the role of glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist, liraglutide in (1) acute anti anxiety effect of ethanol; (2) tolerance to ethanol's anti anxiety effect and (3) ethanol <b>withdrawal</b> induced anxiety using elevated plus maze (EPM) test in rats.
+GLP1R	drug	alcohol	25380665	(1) <strong>GLP 1</strong> agonist, liraglutide exhibited anti anxiety effect per se; (2) potentiated anti anxiety effect of <b>ethanol</b>; (3) prevented development tolerance to anti anxiety effect of <b>ethanol</b> and (4) prevented withdrawal induced anxiety.
+GLP1R	addiction	withdrawal	25380665	(1) <strong>GLP 1</strong> agonist, liraglutide exhibited anti anxiety effect per se; (2) potentiated anti anxiety effect of ethanol; (3) prevented development tolerance to anti anxiety effect of ethanol and (4) prevented <b>withdrawal</b> induced anxiety.
+GLP1R	drug	alcohol	25380665	Further studies examining intracellular cascade of events contributing to these effects may help to improve understanding about role of <strong>GLP 1</strong> receptors in <b>ethanol</b> mediated behaviors.
+GLP1R	drug	cannabinoid	25361428	<b>Cannabinoid</b> receptor 1 antagonist treatment induces glucagon release and shows an additive therapeutic effect with <strong>GLP 1</strong> agonist in diet induced obese mice.
+GLP1R	drug	cannabinoid	25361428	We hypothesized that the insulin secretagogue effect of <strong>GLP 1</strong> agonist exendin 4 may synergize with the insulin sensitizing action of <b>rimonabant</b>.
+GLP1R	addiction	reward	24958205	However, <strong>GLP 1</strong> receptors are expressed in areas intimately associated with <b>reward</b> regulation.
+GLP1R	addiction	reward	24958205	Given that regulation of food and drug intake share common neurobiological substrates, the possibility that ghrelin and <strong>GLP 1</strong> play an important role in <b>reward</b> regulation should be considered.
+GLP1R	drug	alcohol	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by <b>alcohol</b>, amphetamine, cocaine and nicotine in rodents are overviewed herein.
+GLP1R	drug	amphetamine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, <b>amphetamine</b>, cocaine and nicotine in rodents are overviewed herein.
+GLP1R	drug	cocaine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, amphetamine, <b>cocaine</b> and nicotine in rodents are overviewed herein.
+GLP1R	drug	nicotine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, amphetamine, cocaine and <b>nicotine</b> in rodents are overviewed herein.
+GLP1R	addiction	reward	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls <b>reward</b> induced by alcohol, amphetamine, cocaine and nicotine in rodents are overviewed herein.
+GLP1R	drug	alcohol	24958205	Collectively, these data suggest that ghrelin and <strong>GLP 1</strong> receptors may be novel targets for development of pharmacological treatments of <b>alcohol</b> and drug dependence.
+GLP1R	addiction	dependence	24958205	Collectively, these data suggest that ghrelin and <strong>GLP 1</strong> receptors may be novel targets for development of pharmacological treatments of alcohol and drug <b>dependence</b>.
+GLP1R	addiction	reward	24204788	The findings that <strong>GLP 1</strong> targets <b>reward</b> related areas including mesolimbic dopamine areas indicate that the physiological role of <strong>GLP 1</strong> extends beyond food intake and glucose homeostasis control to include <b>reward</b> regulation.
+GLP1R	drug	nicotine	24204788	The present series of experiments was therefore designed to investigate the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on established <b>nicotine</b> induced effects on the mesolimbic dopamine system in mice.
+GLP1R	drug	nicotine	24204788	Given that development of <b>nicotine</b> addiction largely depends on the effects of <b>nicotine</b> on the mesolimbic dopamine system these findings indicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for <b>nicotine</b> cessations in humans.
+GLP1R	addiction	addiction	24204788	Given that development of nicotine <b>addiction</b> largely depends on the effects of nicotine on the mesolimbic dopamine system these findings indicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for nicotine cessations in humans.
+GLP1R	addiction	reward	24140429	However, emerging data indicate that <strong>GLP 1</strong> also contributes to non homeostatic regulation of food <b>reward</b> and motivated behaviors in brain <b>reward</b> centers, including the ventral tegmental area and nucleus accumbens.
+GLP1R	drug	alcohol	24140429	The hypothesis that <strong>GLP 1</strong> signaling modulates reward circuitry has provided the impetus for studies demonstrating that <strong>GLP 1</strong> attenuates reward for psychostimulants and <b>alcohol</b>.
+GLP1R	addiction	reward	24140429	The hypothesis that <strong>GLP 1</strong> signaling modulates <b>reward</b> circuitry has provided the impetus for studies demonstrating that <strong>GLP 1</strong> attenuates <b>reward</b> for psychostimulants and alcohol.
+GLP1R	addiction	reward	24140429	Here, we examine current evidence for <strong>GLP 1</strong> mediated regulation of food and drug <b>reward</b> and use these findings to hypothesize mechanisms of action within brain <b>reward</b> centers.
+GLP1R	addiction	reward	24133407	The central <strong>GLP 1</strong>: implications for food and drug <b>reward</b>.
+GLP1R	addiction	reward	24133407	Results reviewed here support the idea that mesolimbic <strong>GLP 1R</strong> are sufficient to reduce hunger driven feeding, the <b>hedonic</b> value of food and food motivation.
+GLP1R	drug	alcohol	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to cocaine, amphetamine, and <b>alcohol</b> reward.
+GLP1R	drug	amphetamine	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to cocaine, <b>amphetamine</b>, and alcohol reward.
+GLP1R	drug	cocaine	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to <b>cocaine</b>, amphetamine, and alcohol reward.
+GLP1R	addiction	reward	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on <b>reward</b> behavior is not limited to food derived <b>reward</b> but extends to cocaine, amphetamine, and alcohol <b>reward</b>.
+GLP1R	addiction	reward	24133407	The new discoveries concerning <strong>GLP 1</strong> action on the mesolimbic <b>reward</b> system significantly extend the potential therapeutic range of this drug target.
+GLP1R	addiction	reward	23874851	Given that <strong>GLP 1</strong> receptors are expressed in <b>reward</b> areas, such as the nucleus accumbens and ventral tegmental area, and that common mechanisms regulate food and drug induced <b>reward</b> we hypothesize that <strong>GLP 1</strong> receptors are involved in <b>reward</b> regulation.
+GLP1R	drug	amphetamine	23874851	Herein the effect of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4), on <b>amphetamine</b>  and cocaine induced activation of the mesolimbic dopamine system was investigated in mice.
+GLP1R	drug	cocaine	23874851	Herein the effect of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4), on amphetamine  and <b>cocaine</b> induced activation of the mesolimbic dopamine system was investigated in mice.
+GLP1R	addiction	reward	23874851	Collectively these data propose a role for <strong>GLP 1</strong> receptors in regulating drug <b>reward</b>.
+GLP1R	addiction	addiction	23874851	Moreover, the <strong>GLP 1</strong> signaling system may be involved in the development of drug dependence since the rewarding effects of <b>addictive</b> drugs involves interferences with the mesolimbic dopamine system.
+GLP1R	addiction	dependence	23874851	Moreover, the <strong>GLP 1</strong> signaling system may be involved in the development of drug <b>dependence</b> since the rewarding effects of addictive drugs involves interferences with the mesolimbic dopamine system.
+GLP1R	addiction	dependence	23874851	Given that <strong>GLP 1</strong> analogues, such as exenatide and liraglutide, are clinically available for treatment of type II diabetes, we propose that these should be elucidated as treatments of drug <b>dependence</b>.
+GLP1R	drug	alcohol	23613987	Gut peptide <strong>GLP 1</strong> and its analogue, Exendin 4, decrease <b>alcohol</b> intake and reward.
+GLP1R	addiction	reward	23613987	Gut peptide <strong>GLP 1</strong> and its analogue, Exendin 4, decrease alcohol intake and <b>reward</b>.
+GLP1R	addiction	reward	23613987	Interestingly, <strong>GLP 1</strong> receptors (GLP 1R) are expressed in key mesolimbic <b>reward</b> areas (including the ventral tegmental area, VTA), innervated by hindbrain <strong>GLP 1</strong> neurons.
+GLP1R	addiction	reward	23613987	Interestingly, <strong>GLP 1</strong> receptors (<strong>GLP 1R</strong>) are expressed in key mesolimbic <b>reward</b> areas (including the ventral tegmental area, VTA), innervated by hindbrain <strong>GLP 1</strong> neurons.
+GLP1R	addiction	reward	23613987	Recently <strong>GLP 1</strong> has emerged as a potential regulator of food <b>reward</b> behavior, an effect driven by the mesolimbic GLP 1Rs.
+GLP1R	drug	alcohol	23613987	Since a considerable overlap has been suggested for circuitry controlling reward behavior derived from food and <b>alcohol</b> we hypothesized that <strong>GLP 1</strong> and GLP 1Rs could regulate <b>alcohol</b> intake and <b>alcohol</b> reward.
+GLP1R	addiction	reward	23613987	Since a considerable overlap has been suggested for circuitry controlling <b>reward</b> behavior derived from food and alcohol we hypothesized that <strong>GLP 1</strong> and GLP 1Rs could regulate alcohol intake and alcohol <b>reward</b>.
+GLP1R	drug	alcohol	23613987	We sought to determine whether <strong>GLP 1</strong> or its clinically safe stable analogue, Exendin 4, reduce <b>alcohol</b> intake and reward.
+GLP1R	addiction	reward	23613987	We sought to determine whether <strong>GLP 1</strong> or its clinically safe stable analogue, Exendin 4, reduce alcohol intake and <b>reward</b>.
+GLP1R	drug	alcohol	23613987	To determine the potential role of the endogenous <strong>GLP 1</strong> in <b>alcohol</b> intake we evaluated whether GLP 1R antagonist, Exendin 9 39, can increase <b>alcohol</b> intake.
+GLP1R	drug	alcohol	23613987	To determine the potential role of the endogenous <strong>GLP 1</strong> in <b>alcohol</b> intake we evaluated whether <strong>GLP 1R</strong> antagonist, Exendin 9 39, can increase <b>alcohol</b> intake.
+GLP1R	drug	alcohol	23613987	Furthermore, we set out to evaluate whether VTA <strong>GLP 1R</strong> activation is sufficient to reduce <b>alcohol</b> intake.
+GLP1R	drug	alcohol	23613987	Male Wistar rats injected peripherally with <strong>GLP 1</strong> or Exendin 4 reduced their <b>alcohol</b> intake in an intermittent access two bottle free choice drinking model.
+GLP1R	drug	alcohol	23613987	Importantly, a contribution of endogenously released <strong>GLP 1</strong> is highlighted by our observation that blockade of <strong>GLP 1</strong> receptors alone resulted in an increased <b>alcohol</b> intake.
+GLP1R	drug	alcohol	23613987	Furthermore, <strong>GLP 1</strong> injection reduced <b>alcohol</b> reward in the <b>alcohol</b> conditioned place preference test in mice.
+GLP1R	addiction	reward	23613987	Furthermore, <strong>GLP 1</strong> injection reduced alcohol <b>reward</b> in the alcohol conditioned place preference test in mice.
+GLP1R	drug	alcohol	23613987	To evaluate the neuroanatomical substrate linking <strong>GLP 1</strong> with <b>alcohol</b> intake/reward, we selectively microinjected <strong>GLP 1</strong> or Exendin 4 into the VTA.
+GLP1R	addiction	reward	23613987	To evaluate the neuroanatomical substrate linking <strong>GLP 1</strong> with alcohol intake/<b>reward</b>, we selectively microinjected <strong>GLP 1</strong> or Exendin 4 into the VTA.
+GLP1R	drug	alcohol	23613987	This direct stimulation of the VTA <strong>GLP 1</strong> receptors potently reduced <b>alcohol</b> intake.
+GLP1R	drug	alcohol	23613987	Our findings implicate <strong>GLP 1R</strong> signaling as a novel modulator of <b>alcohol</b> intake and reward.
+GLP1R	addiction	reward	23613987	Our findings implicate <strong>GLP 1R</strong> signaling as a novel modulator of alcohol intake and <b>reward</b>.
+GLP1R	drug	alcohol	23613987	We show for the first time that VTA <strong>GLP 1R</strong> stimulation leads to reduced <b>alcohol</b> intake.
+GLP1R	drug	alcohol	23613987	Considering that <strong>GLP 1</strong> analogues are already approved for clinical use, this places the GLP system as an exciting new potential therapeutic target for <b>alcohol</b> use disorders.
+GLP1R	addiction	reward	23219472	Glucagon like peptide 1 (<strong>GLP 1</strong>), a gastrointestinal peptide regulating food intake and glucose homeostasis, has recently been shown to target central brain areas involved in <b>reward</b> and motivation, including the ventral tegmental area and nucleus accumbens.
+GLP1R	drug	alcohol	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of <b>alcohol</b> induced reward as well as on <b>alcohol</b> intake and <b>alcohol</b> seeking behavior in rodents.
+GLP1R	addiction	relapse	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of alcohol induced reward as well as on alcohol intake and alcohol <b>seeking</b> behavior in rodents.
+GLP1R	addiction	reward	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of alcohol induced <b>reward</b> as well as on alcohol intake and alcohol seeking behavior in rodents.
+GLP1R	drug	alcohol	23219472	These novel findings indicate that <strong>GLP 1</strong> signaling attenuates the reinforcing properties of <b>alcohol</b> implying that the physiological role of <strong>GLP 1</strong> extends beyond glucose homeostasis and food intake regulation.
+GLP1R	addiction	reward	23219472	These novel findings indicate that <strong>GLP 1</strong> signaling attenuates the <b>reinforcing</b> properties of alcohol implying that the physiological role of <strong>GLP 1</strong> extends beyond glucose homeostasis and food intake regulation.
+GLP1R	drug	alcohol	23219472	Collectively these findings implicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for <b>alcohol</b> use disorders.
+GLP1R	drug	cocaine	23089631	<strong>GLP 1</strong> analog attenuates <b>cocaine</b> reward.
+GLP1R	addiction	reward	23089631	<strong>GLP 1</strong> analog attenuates cocaine <b>reward</b>.
+GLP1R	drug	opioid	22541480	Injection of <b>naloxone</b> decreased plasma glucagon like peptide 1 (<strong>GLP 1</strong>) in NAL calves.
+GLP1R	drug	opioid	22541480	Blocking <b>opioid</b> receptors reduced intake the first 2 h after <b>naloxone</b> injection in FED calves, altered oro sensorial preferences, and reduced plasma <strong>GLP 1</strong> concentration.
+GLP1R	drug	amphetamine	22465309	Here, we identify the <strong>GLP 1R</strong> agonist exendin 4 (Ex 4) as a modulator of behavioral activation by <b>AMPH</b>.
+GLP1R	drug	alcohol	22444202	Notably, the attenuating effect of RYGB surgery on <b>ethanol</b> consumption was associated with <b>ethanol</b> induced increases in the gut hormone glucagon like peptide 1 (<strong>GLP 1</strong>).
+GLP1R	drug	alcohol	22444202	Pharmacologic administration of <strong>GLP 1</strong> agonists attenuated <b>ethanol</b> consumption in sham P rats.
+GLP1R	addiction	reward	22444202	Furthermore, our data indicate that this regulation is achieved, in part, through reduction of <b>reward</b> and is modified by the gut hormones <strong>GLP 1</strong> and ghrelin.
+GLP1R	drug	alcohol	21696355	Products at preclinical and clinical stages include formulations of <b>naltrexone</b> and buprenorphine for <b>alcoholism</b>/drug abuse, <strong>GLP 1</strong> peptides for diabetes, r hFSH for fertility, dopamine for nerve growth, dexamethasone for ocular treatment, melanotan for cancer prevention, plasmid DNA for cancer prevention, a variety of vaccines, octreotide generics, etc.
+GLP1R	drug	opioid	21696355	Products at preclinical and clinical stages include formulations of naltrexone and <b>buprenorphine</b> for alcoholism/drug abuse, <strong>GLP 1</strong> peptides for diabetes, r hFSH for fertility, dopamine for nerve growth, dexamethasone for ocular treatment, melanotan for cancer prevention, plasmid DNA for cancer prevention, a variety of vaccines, octreotide generics, etc.
+GLP1R	drug	cannabinoid	20462703	It is suggested that neurobiological substrates such as adiponectin, dopamine (D2 receptors), <b>endocannabinoids</b>, ghrelin, leptin, nesfatin 1, norepinephrine, orexin, oxytocin, serotonin, vasopressin, CCK, <strong>GLP 1</strong>, MCH, PYY, and stress hormones (e.g., CRF) in the brain (e.g., OFC, VTA, NAcc, and the hypothalamus) may determine parameters in the economic theory of obesity.
+DRD3	drug	amphetamine	31417344	Significant changes were observed in the cocaine  and <b>amphetamine</b> regulated transcript prepropeptide, tachykinin receptor 3, <strong>dopamine receptor D3</strong> gene expression in the striatum regions, in the glucocorticoid nuclear receptor Nr3c1 gene expression in the prefrontal cortex and in the carboxylesterase 2 gene expression in the hippocampus of prenatally <b>METH</b> exposed rats.
+DRD3	drug	cocaine	31417344	Significant changes were observed in the <b>cocaine</b>  and amphetamine regulated transcript prepropeptide, tachykinin receptor 3, <strong>dopamine receptor D3</strong> gene expression in the striatum regions, in the glucocorticoid nuclear receptor Nr3c1 gene expression in the prefrontal cortex and in the carboxylesterase 2 gene expression in the hippocampus of prenatally METH exposed rats.
+DRD3	drug	opioid	31192519	Substance use, DD, and genotype data (DRD1 rs686 and rs5326, <strong>DRD3</strong> rs6280, COMT rs4680) were obtained from 106 current <b>heroin</b> users.
+DRD3	drug	opioid	30268777	<strong>DRD3</strong> level decreased in all the brain regions except in the amygdala of <b>opioid</b> abusers in comparison with the control group.
+DRD3	drug	amphetamine	30005280	Differential effect of the <strong>DRD3</strong> genotype on inflammatory cytokine responses during abstinence in <b>amphetamine</b> dependent women.
+DRD3	drug	amphetamine	30005280	<b>Amphetamine</b> exposure impacts on innate and adaptive immunity and <strong>DRD3</strong> may modulate the effect of <b>amphetamine</b> on the immune response.
+DRD3	drug	alcohol	29357295	Association study of BDNF and <strong>DRD3</strong> genes with <b>alcohol</b> use disorder in Schizophrenia.
+DRD3	drug	alcohol	29357295	The brain derived neurotrophic factor (BDNF) and dopamine D3 receptor (<strong>DRD3</strong>) have been implicated in <b>alcohol</b> drinking behaviour.
+DRD3	drug	alcohol	29357295	Previous genetic studies of the BDNF and <strong>DRD3</strong> genes produced mixed findings; however, only one study investigated two BDNF genetic markers with <b>alcohol</b> dependence in schizophrenia patients.
+DRD3	addiction	dependence	29357295	Previous genetic studies of the BDNF and <strong>DRD3</strong> genes produced mixed findings; however, only one study investigated two BDNF genetic markers with alcohol <b>dependence</b> in schizophrenia patients.
+DRD3	drug	alcohol	29357295	We investigated 15 single nucleotide polymorphisms (SNPs) in <strong>DRD3</strong> and four SNPs in BDNF for possible association with <b>alcohol</b> abuse or dependence in schizophrenia patients of European ancestry (N = 195).
+DRD3	addiction	dependence	29357295	We investigated 15 single nucleotide polymorphisms (SNPs) in <strong>DRD3</strong> and four SNPs in BDNF for possible association with alcohol abuse or <b>dependence</b> in schizophrenia patients of European ancestry (N = 195).
+DRD3	drug	amphetamine	28621212	However, the abovementioned effects induced by <b>Meth</b> were abolished by the addition of <strong>dopamine receptor D3</strong> antagonist.
+DRD3	addiction	reward	28042871	We used functional magnetic resonance imaging to investigate the acute effects of the <strong>DRD3</strong> antagonist GSK598809 on anticipatory <b>reward</b> processing, using the monetary <b>incentive</b> delay task (MIDT), and response inhibition using the Go/No Go task (GNGT).
+DRD3	addiction	reward	28042871	GSK598809 normalized ventral striatal <b>reward</b> response and enhanced response in the <strong>DRD3</strong> rich regions of the ventral pallidum and substantia nigra.
+DRD3	addiction	addiction	28042871	GSK598809 modulated the neural network underlying reward anticipation but not response inhibition, suggesting that <strong>DRD3</strong> antagonists may restore reward deficits in <b>addiction</b>.
+DRD3	addiction	reward	28042871	GSK598809 modulated the neural network underlying <b>reward</b> anticipation but not response inhibition, suggesting that <strong>DRD3</strong> antagonists may restore <b>reward</b> deficits in addiction.
+DRD3	drug	amphetamine	28028606	Novelty seeking mediates the effect of <strong>DRD3</strong> variation on onset age of <b>amphetamine</b> dependence in Han Chinese population.
+DRD3	addiction	dependence	28028606	Novelty seeking mediates the effect of <strong>DRD3</strong> variation on onset age of amphetamine <b>dependence</b> in Han Chinese population.
+DRD3	addiction	relapse	28028606	Novelty <b>seeking</b> mediates the effect of <strong>DRD3</strong> variation on onset age of amphetamine dependence in Han Chinese population.
+DRD3	drug	amphetamine	28028606	The dopamine receptor D3 (<strong>DRD3</strong>) gene, one of the candidate genes for <b>amphetamine</b> dependence (AD), is involved in the mesolimbic dopaminergic system, implicated as the underlying mechanism of addiction.
+DRD3	addiction	addiction	28028606	The dopamine receptor D3 (<strong>DRD3</strong>) gene, one of the candidate genes for amphetamine dependence (AD), is involved in the mesolimbic dopaminergic system, implicated as the underlying mechanism of <b>addiction</b>.
+DRD3	addiction	dependence	28028606	The dopamine receptor D3 (<strong>DRD3</strong>) gene, one of the candidate genes for amphetamine <b>dependence</b> (AD), is involved in the mesolimbic dopaminergic system, implicated as the underlying mechanism of addiction.
+DRD3	drug	amphetamine	28028606	The <strong>dopamine receptor D3</strong> (<strong>DRD3</strong>) gene, one of the candidate genes for <b>amphetamine</b> dependence (AD), is involved in the mesolimbic dopaminergic system, implicated as the underlying mechanism of addiction.
+DRD3	addiction	addiction	28028606	The <strong>dopamine receptor D3</strong> (<strong>DRD3</strong>) gene, one of the candidate genes for amphetamine dependence (AD), is involved in the mesolimbic dopaminergic system, implicated as the underlying mechanism of <b>addiction</b>.
+DRD3	addiction	dependence	28028606	The <strong>dopamine receptor D3</strong> (<strong>DRD3</strong>) gene, one of the candidate genes for amphetamine <b>dependence</b> (AD), is involved in the mesolimbic dopaminergic system, implicated as the underlying mechanism of addiction.
+DRD3	addiction	relapse	28028606	In addition, <strong>DRD3</strong> rs9825563 may influence onset age of drug use, partially mediated by novelty <b>seeking</b> in the non psychosis AD group.
+DRD3	addiction	relapse	28028606	In conclusion, <strong>DRD3</strong> is a potential genetic factor in the susceptibility to AD and is associated with onset age of drug use through interaction with novelty <b>seeking</b> in a specific patient group in the Han Chinese population.
+DRD3	drug	alcohol	27447243	Association study of DRD2 A2/A1, <strong>DRD3</strong> Ser9Gly, DβH  1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A polymorphisms with <b>alcohol</b> dependence.
+DRD3	addiction	dependence	27447243	Association study of DRD2 A2/A1, <strong>DRD3</strong> Ser9Gly, DβH  1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A polymorphisms with alcohol <b>dependence</b>.
+DRD3	drug	opioid	27447243	Genes of dopaminergic (DRD2, <strong>DRD3</strong> and DβH), <b>opioid</b> (OPRM1) and glutaminergic (GRIK1) systems mediate the dependent behavior via different mechanisms; however, they all target the serotonergic and dopaminergic pathways in the ventral tegmental area.
+DRD3	drug	alcohol	27447243	In the present study, DRD2 A2/A1, <strong>DRD3</strong> Ser9Gly, DβH  1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A polymorphisms and their interactions were analyzed in 72 <b>alcohol</b> dependent patients and 74 controls of Greek Cypriot origin, using the PCR RFLP method.
+DRD3	drug	alcohol	27447243	No differences were found in the genotype or allele distribution of DRD2 A2/A1, <strong>DRD3</strong> Ser9Gly, DβH  1021C>T, OPRM1 A118G and GRIK1 rs2832407C>A between <b>alcohol</b> dependent patients and controls.
+DRD3	drug	alcohol	26621272	The results indicate that <b>alcohol</b> dependence is associated with high expression of SNCA and DRD4 (signifi cantly higher than in the control group) and is not associated with changes in the work of NR4A2 and <strong>DRD3</strong> genes.
+DRD3	addiction	dependence	26621272	The results indicate that alcohol <b>dependence</b> is associated with high expression of SNCA and DRD4 (signifi cantly higher than in the control group) and is not associated with changes in the work of NR4A2 and <strong>DRD3</strong> genes.
+DRD3	drug	nicotine	26279138	We and others have proposed that targeting the dopamine D3 receptor (<strong>DRD3</strong>) may be a good strategy for treatment of <b>nicotine</b> dependence.
+DRD3	addiction	dependence	26279138	We and others have proposed that targeting the dopamine D3 receptor (<strong>DRD3</strong>) may be a good strategy for treatment of nicotine <b>dependence</b>.
+DRD3	drug	nicotine	26279138	As the role of <strong>DRD3</strong> in context induced reinstatement of <b>nicotine</b> seeking has not yet been explored, we investigated the effects of different doses of the selective <strong>DRD3</strong> antagonist SB 277011 A on this reinstatement.
+DRD3	addiction	relapse	26279138	As the role of <strong>DRD3</strong> in context induced <b>reinstatement</b> of nicotine <b>seeking</b> has not yet been explored, we investigated the effects of different doses of the selective <strong>DRD3</strong> antagonist SB 277011 A on this <b>reinstatement</b>.
+DRD3	drug	nicotine	26279138	Our results support a role for <strong>DRD3</strong> mediating context induced reinstatement of <b>nicotine</b> seeking, but these effects may not be sustained over time.
+DRD3	addiction	relapse	26279138	Our results support a role for <strong>DRD3</strong> mediating context induced <b>reinstatement</b> of nicotine <b>seeking</b>, but these effects may not be sustained over time.
+DRD3	drug	alcohol	26246443	Pharmacological modulation of reward, impulsivity and emotional reactivity were investigated in a monetary incentive delay task, an inhibitory control task, and an evocative images task, using selective antagonists for µ opioid, dopamine D3 receptor (<strong>DRD3</strong>) and neurokinin 1 (NK1) receptors (<b>naltrexone</b>, GSK598809, vofopitant/aprepitant), in a placebo controlled, randomised, crossover design.
+DRD3	drug	opioid	26246443	Pharmacological modulation of reward, impulsivity and emotional reactivity were investigated in a monetary incentive delay task, an inhibitory control task, and an evocative images task, using selective antagonists for µ <b>opioid</b>, dopamine D3 receptor (<strong>DRD3</strong>) and neurokinin 1 (NK1) receptors (naltrexone, GSK598809, vofopitant/aprepitant), in a placebo controlled, randomised, crossover design.
+DRD3	addiction	reward	26246443	Pharmacological modulation of <b>reward</b>, impulsivity and emotional reactivity were investigated in a monetary <b>incentive</b> delay task, an inhibitory control task, and an evocative images task, using selective antagonists for µ opioid, dopamine D3 receptor (<strong>DRD3</strong>) and neurokinin 1 (NK1) receptors (naltrexone, GSK598809, vofopitant/aprepitant), in a placebo controlled, randomised, crossover design.
+DRD3	addiction	reward	26228024	The D3 receptor antagonist SB 277011A and the BDNF receptor antagonist ANA 12 completely prevented <b>CPP</b> as well as the increases in <strong>Drd3</strong> in all groups.
+DRD3	drug	nicotine	25907750	Interestingly, polymorphisms of the dopamine D3 receptor (<strong>DRD3</strong>) gene have been associated with <b>smoking</b> behavior, and the receptor is expressed in an age  and brain region dependent manner that suggests relevance to addiction.
+DRD3	addiction	addiction	25907750	Interestingly, polymorphisms of the dopamine D3 receptor (<strong>DRD3</strong>) gene have been associated with smoking behavior, and the receptor is expressed in an age  and brain region dependent manner that suggests relevance to <b>addiction</b>.
+DRD3	drug	nicotine	25907750	Here, we investigate the possible role of dopamine related receptors, including <strong>DRD3</strong> and an intriguing splice variant known as D3nf, in <b>nicotine</b> induced sensitization.
+DRD3	addiction	sensitization	25907750	Here, we investigate the possible role of dopamine related receptors, including <strong>DRD3</strong> and an intriguing splice variant known as D3nf, in nicotine induced <b>sensitization</b>.
+DRD3	drug	nicotine	25907750	In adolescent and adult male rats, we examined (1) alterations occurring in dopamine receptor related mRNAs (DRD1, DRD2, <strong>DRD3</strong> and D3nf) at two time points during a sensitizing regimen of <b>nicotine</b> and (2) whether <strong>DRD3</strong> antagonism either during the initial treatment (induction) or at a later challenge exposure (expression) is able to block <b>nicotine</b> sensitization.
+DRD3	addiction	sensitization	25907750	In adolescent and adult male rats, we examined (1) alterations occurring in dopamine receptor related mRNAs (DRD1, DRD2, <strong>DRD3</strong> and D3nf) at two time points during a sensitizing regimen of nicotine and (2) whether <strong>DRD3</strong> antagonism either during the initial treatment (induction) or at a later challenge exposure (expression) is able to block nicotine <b>sensitization</b>.
+DRD3	drug	nicotine	25907750	<b>Nicotine</b> induced changes were seen for <strong>DRD3</strong> and D3nf mRNAs in the nucleus accumbens shell early in repeated exposure in both age groups.
+DRD3	addiction	sensitization	25907750	<strong>DRD3</strong> antagonism only blocked the induction of <b>sensitization</b> in adolescents and did not block the expression of <b>sensitization</b> in either age group.
+DRD3	drug	nicotine	25907750	These data reveal important age dependent regulation of DRD1  and <strong>DRD3</strong> related mRNAs during the course of <b>nicotine</b> exposure.
+DRD3	drug	nicotine	25907750	Furthermore, they highlight a requirement for <strong>DRD3</strong> signaling in the development of adolescent <b>nicotine</b> sensitization, suggesting it may represent an appropriate target in the prevention of <b>nicotine</b> dependence initiated at this age.
+DRD3	addiction	dependence	25907750	Furthermore, they highlight a requirement for <strong>DRD3</strong> signaling in the development of adolescent nicotine sensitization, suggesting it may represent an appropriate target in the prevention of nicotine <b>dependence</b> initiated at this age.
+DRD3	addiction	sensitization	25907750	Furthermore, they highlight a requirement for <strong>DRD3</strong> signaling in the development of adolescent nicotine <b>sensitization</b>, suggesting it may represent an appropriate target in the prevention of nicotine dependence initiated at this age.
+DRD3	drug	nicotine	25762751	During <b>nicotine</b> exposure, intact females displayed a decrease in CRF R1, CRF R2, <strong>Drd3</strong>, and Esr2 gene expression and an increase in CRF BP.
+DRD3	drug	alcohol	25660313	Meta analysis of six genes (BDNF, DRD1, <strong>DRD3</strong>, DRD4, GRIN2B and MAOA) involved in neuroplasticity and the risk for <b>alcohol</b> dependence.
+DRD3	addiction	dependence	25660313	Meta analysis of six genes (BDNF, DRD1, <strong>DRD3</strong>, DRD4, GRIN2B and MAOA) involved in neuroplasticity and the risk for alcohol <b>dependence</b>.
+DRD3	drug	cocaine	25444159	Direct regulation of diurnal <strong>Drd3</strong> expression and <b>cocaine</b> reward by NPAS2.
+DRD3	addiction	reward	25444159	Direct regulation of diurnal <strong>Drd3</strong> expression and cocaine <b>reward</b> by NPAS2.
+DRD3	drug	cocaine	25444159	Chronic <b>cocaine</b> treatment likewise disrupts the normal rhythm in Npas2 and <strong>Drd3</strong> expression in the NAc, which may underlie behavioral plasticity in response to <b>cocaine</b>.
+DRD3	drug	nicotine	24927283	Role of <b>nicotine</b> dependence in the association between the dopamine receptor gene <strong>DRD3</strong> and major depressive disorder.
+DRD3	addiction	dependence	24927283	Role of nicotine <b>dependence</b> in the association between the dopamine receptor gene <strong>DRD3</strong> and major depressive disorder.
+DRD3	drug	nicotine	24927283	Our results further suggest that <b>nicotine</b> dependence may potentiate the influence of the <strong>DRD3</strong> genetic variant on MDD.
+DRD3	addiction	dependence	24927283	Our results further suggest that nicotine <b>dependence</b> may potentiate the influence of the <strong>DRD3</strong> genetic variant on MDD.
+DRD3	drug	alcohol	24776816	<strong>DRD3</strong> gene rs6280 polymorphism may be associated with <b>alcohol</b> dependence overall and with Lesch type I <b>alcohol</b> dependence in Koreans.
+DRD3	addiction	dependence	24776816	<strong>DRD3</strong> gene rs6280 polymorphism may be associated with alcohol <b>dependence</b> overall and with Lesch type I alcohol <b>dependence</b> in Koreans.
+DRD3	drug	alcohol	24776816	Several polymorphisms of the dopamine D3 receptor (<strong>DRD3</strong>) gene are reported to be involved in the susceptibility to <b>alcoholism</b>.
+DRD3	drug	alcohol	24776816	Although the <strong>DRD3</strong> rs6280 (Ser9Gly) polymorphism plays an important role in various psychiatric disorders, findings regarding the association between this single nucleotide polymorphism (SNP) and <b>alcohol</b> dependence (AD) have been inconsistent.
+DRD3	addiction	dependence	24776816	Although the <strong>DRD3</strong> rs6280 (Ser9Gly) polymorphism plays an important role in various psychiatric disorders, findings regarding the association between this single nucleotide polymorphism (SNP) and alcohol <b>dependence</b> (AD) have been inconsistent.
+DRD3	drug	alcohol	24469594	Animal studies support the role of the dopamine D3 receptor (<strong>DRD3</strong>) in <b>alcohol</b> reinforcement or liking.
+DRD3	addiction	reward	24469594	Animal studies support the role of the dopamine D3 receptor (<strong>DRD3</strong>) in alcohol <b>reinforcement</b> or liking.
+DRD3	drug	alcohol	24469594	Sustained voluntary <b>alcohol</b> drinking in rats has been associated with an upregulation of striatal <strong>DRD3</strong> gene expression and selective blockade of <strong>DRD3</strong> reduces <b>ethanol</b> preference, consumption, and cue induced reinstatement.
+DRD3	addiction	relapse	24469594	Sustained voluntary alcohol drinking in rats has been associated with an upregulation of striatal <strong>DRD3</strong> gene expression and selective blockade of <strong>DRD3</strong> reduces ethanol preference, consumption, and cue induced <b>reinstatement</b>.
+DRD3	drug	alcohol	24469594	In this study, <strong>DRD3</strong> status was assessed for the first time in human <b>alcohol</b> addiction.
+DRD3	addiction	addiction	24469594	In this study, <strong>DRD3</strong> status was assessed for the first time in human alcohol <b>addiction</b>.
+DRD3	drug	alcohol	24469594	Brain <strong>DRD3</strong> availability was compared between 16 male abstinent <b>alcohol</b> dependent patients and 13 healthy non dependent age matched males using the <strong>DRD3</strong> preferring agonist positron emission tomography (PET) radioligand [(11)C]PHNO with and without blockade with a selective <strong>DRD3</strong> antagonist (GSK598809 60 mg p.o.).
+DRD3	drug	alcohol	24469594	However, baseline [(11)C]PHNO binding was higher in <b>alcohol</b> dependent patients in hypothalamus (VT: 16.5 ± 4 vs 13.7 ± 2.9, p = 0.040), a region in which the [(11)C]PHNO signal almost entirely reflects <strong>DRD3</strong> availability.
+DRD3	drug	alcohol	24469594	There were no differences in regional changes in VT following <strong>DRD3</strong> blockade between the two groups, indicating that the regional fractions of <strong>DRD3</strong> are similar in the two groups, and the increased [(11)C]PHNO binding in the hypothalamus in <b>alcohol</b> dependent patients is explained by elevated <strong>DRD3</strong> in this group.
+DRD3	drug	alcohol	24469594	Although we found no difference between <b>alcohol</b> dependent patients and controls in striatal <strong>DRD3</strong> levels, increased <strong>DRD3</strong> binding in the hypothalamus of <b>alcohol</b> dependent patients was observed.
+DRD3	drug	opioid	24398431	<strong>DRD3</strong> variation associates with early onset <b>heroin</b> dependence, but not specific personality traits.
+DRD3	addiction	dependence	24398431	<strong>DRD3</strong> variation associates with early onset heroin <b>dependence</b>, but not specific personality traits.
+DRD3	drug	opioid	24398431	The aim of this study was to examine whether the corresponding gene, <strong>DRD3</strong>, is associated with the development of <b>heroin</b> dependence and specific personality traits in HD patients.
+DRD3	addiction	dependence	24398431	The aim of this study was to examine whether the corresponding gene, <strong>DRD3</strong>, is associated with the development of heroin <b>dependence</b> and specific personality traits in HD patients.
+DRD3	drug	opioid	24398431	Eight polymorphisms in <strong>DRD3</strong> were analyzed in 1067 unrelated Han Chinese subjects (566 <b>heroin</b> dependence patients and 501 controls).
+DRD3	addiction	dependence	24398431	Eight polymorphisms in <strong>DRD3</strong> were analyzed in 1067 unrelated Han Chinese subjects (566 heroin <b>dependence</b> patients and 501 controls).
+DRD3	addiction	relapse	24398431	In addition, these <strong>DRD3</strong> polymorphisms did not influence novelty <b>seeking</b> and harm avoidance scores in HD patients.
+DRD3	drug	opioid	24398431	<strong>DRD3</strong> is possibly a genetic factor in the development of early onset <b>heroin</b> dependence, but is not associated with specific personality traits in these patients among the Han Chinese population.
+DRD3	addiction	dependence	24398431	<strong>DRD3</strong> is possibly a genetic factor in the development of early onset heroin <b>dependence</b>, but is not associated with specific personality traits in these patients among the Han Chinese population.
+DRD3	drug	cocaine	23285158	These embryos were exposed to <b>cocaine</b> hydrochloride (HCl) at 5 hours post fertilization (hpf) and were then collected at 8, 16, 24, 48 and 72 hpf to study the expression of dopamine receptors, drd1, drd2a, drd2b and <strong>drd3</strong>, by quantitative real time PCR (qPCR) and in situ hybridization (ISH, only at 24 hpf).
+DRD3	drug	alcohol	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, DRD2, <strong>DRD3</strong>, DRD4) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of craving, as well as alpha synuclein (SNCA), which has been previously found to be associated with craving, were associated with <b>alcohol</b> craving in this sample.
+DRD3	addiction	relapse	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, DRD2, <strong>DRD3</strong>, DRD4) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of <b>craving</b>, as well as alpha synuclein (SNCA), which has been previously found to be associated with <b>craving</b>, were associated with alcohol <b>craving</b> in this sample.
+DRD3	addiction	relapse	22481050	When examining genes in the dopamine pathway, single nucleotide polymorphisms (SNPs) in <strong>DRD3</strong> and SNCA were associated with <b>craving</b> (p<0.05).
+DRD3	drug	nicotine	22309839	Our results provided confirmation of the previous findings that DRD2, <strong>DRD3</strong>, DDC, CHRNB3, GABBR2 and CHRNA4 are associated with <b>nicotine</b> dependence.
+DRD3	addiction	dependence	22309839	Our results provided confirmation of the previous findings that DRD2, <strong>DRD3</strong>, DDC, CHRNB3, GABBR2 and CHRNA4 are associated with nicotine <b>dependence</b>.
+DRD3	drug	amphetamine	21491142	<strong>Dopamine receptor D3</strong> genetic polymorphism (rs6280TC) is associated with rates of cognitive impairment in <b>methamphetamine</b> dependent men with HIV: preliminary findings.
+DRD3	drug	amphetamine	21491142	A single nucleotide polymorphism (SNP) of the <strong>DRD3</strong> gene (rs6280TC) modulates its dopamine binding affinity, resulting in the possibility that inheriting a variant of this SNP increases macrophage susceptibility to HIV infection in the presence of <b>METH</b> and DA, particularly in the CNS where <b>METH</b> is sequestered, leading to cognitive impairment (CI).
+DRD3	drug	amphetamine	21491142	We hypothesized that only HIV positive/<b>METH</b> positive carriers of the C allele, which increases the <strong>DRD3</strong>'s binding to DA, would be more likely to develop CI.
+DRD3	drug	opioid	21277174	The present study used a conditioning procedure to assess the roles of BDNF, <strong>Drd3</strong>, and their interactions in the NAc in the expression of <b>morphine</b> induced context specific locomotor sensitization.
+DRD3	addiction	sensitization	21277174	The present study used a conditioning procedure to assess the roles of BDNF, <strong>Drd3</strong>, and their interactions in the NAc in the expression of morphine induced context specific locomotor <b>sensitization</b>.
+DRD3	drug	opioid	21277174	We showed that the expression of locomotor sensitization in the <b>morphine</b> paired environment was accompanied by significantly increased expression of <strong>Drd3</strong> mRNA and BDNF mRNA and protein levels.
+DRD3	addiction	sensitization	21277174	We showed that the expression of locomotor <b>sensitization</b> in the morphine paired environment was accompanied by significantly increased expression of <strong>Drd3</strong> mRNA and BDNF mRNA and protein levels.
+DRD3	drug	opioid	21277174	Both sensitized locomotion in <b>morphine</b> paired rats and enhanced <strong>Drd3</strong> mRNA were suppressed by intra NAc infusion of anti tyrosine kinase receptor B (TrkB) IgG.
+DRD3	addiction	sensitization	21277174	Furthermore, intra NAc infusion of the <strong>Drd3</strong> selective antagonist SB 277011A significantly decreased the expression of context specific locomotor <b>sensitization</b> and upregulated BDNF mRNA.
+DRD3	drug	opioid	21277174	Altogether, these results suggest that BDNF/TrkB signaling and activation of <strong>Drd3</strong> in the NAc are required for the expression of <b>morphine</b> induced context specific locomotor sensitization.
+DRD3	addiction	sensitization	21277174	Altogether, these results suggest that BDNF/TrkB signaling and activation of <strong>Drd3</strong> in the NAc are required for the expression of morphine induced context specific locomotor <b>sensitization</b>.
+DRD3	drug	nicotine	20456319	Association of polymorphisms in the BDNF, DRD1 and <strong>DRD3</strong> genes with <b>tobacco</b> <b>smoking</b> in schizophrenia.
+DRD3	drug	nicotine	20456319	Emerging evidence indicates that the DRD1 BDNF <strong>DRD3</strong> cluster plays an important role in <b>nicotine</b> addiction.
+DRD3	addiction	addiction	20456319	Emerging evidence indicates that the DRD1 BDNF <strong>DRD3</strong> cluster plays an important role in nicotine <b>addiction</b>.
+DRD3	drug	nicotine	20456319	Both DRD1 markers tested (rs4532 and rs686) and the <strong>DRD3</strong> marker (rs1025398) showed association with quantity of <b>tobacco</b> smoked (p = 0.01, 0.005 and 0.002, respectively).
+DRD3	drug	nicotine	20456319	Our findings are preliminary; however, they support the involvement of the DRD1, BDNF and <strong>DRD3</strong> genes in <b>smoking</b> behaviour.
+DRD3	addiction	relapse	19995481	The dopamine D3 receptor (<strong>DRD3</strong>) has been suggested to be involved in the mechanisms underlying stimulus controlled drug <b>seeking</b> behaviour.
+DRD3	drug	nicotine	19995481	SB 277011 A (1 10 mg/kg) was able to block cue induced reinstatement of <b>nicotine</b> seeking, indicating that <strong>DRD3</strong> selective antagonism may be an effective approach to prevent relapse for <b>nicotine</b>.
+DRD3	addiction	relapse	19995481	SB 277011 A (1 10 mg/kg) was able to block cue induced <b>reinstatement</b> of nicotine <b>seeking</b>, indicating that <strong>DRD3</strong> selective antagonism may be an effective approach to prevent <b>relapse</b> for nicotine.
+DRD3	drug	nicotine	19995481	These findings validate the role of <strong>DRD3</strong> on reactivity to drug associated stimuli and suggest that the <strong>DRD3</strong> antagonist, but perhaps not the <strong>DRD3</strong> partial agonist, could be used to prevent relapse in <b>tobacco</b> <b>smokers</b>.
+DRD3	addiction	relapse	19995481	These findings validate the role of <strong>DRD3</strong> on reactivity to drug associated stimuli and suggest that the <strong>DRD3</strong> antagonist, but perhaps not the <strong>DRD3</strong> partial agonist, could be used to prevent <b>relapse</b> in tobacco smokers.
+DRD3	drug	cannabinoid	19931559	(3) Feeding motivation  and reward related systems (opioids, OPRD1, <b>cannabinoids</b> (anandamide (AEA), <b>THC</b>, CBR1), dopamine, DRD2, <strong>DRD3</strong>, DRD4, catecholamine O methyl transferase (COMT).
+DRD3	drug	opioid	19931559	(3) Feeding motivation  and reward related systems (<b>opioids</b>, OPRD1, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, <strong>DRD3</strong>, DRD4, catecholamine O methyl transferase (COMT).
+DRD3	addiction	reward	19931559	(3) Feeding motivation  and <b>reward</b> related systems (opioids, OPRD1, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, <strong>DRD3</strong>, DRD4, catecholamine O methyl transferase (COMT).
+DRD3	drug	cocaine	19503018	Association analysis between polymorphisms in the dopamine D3 receptor (<strong>DRD3</strong>) gene and <b>cocaine</b> dependence.
+DRD3	addiction	dependence	19503018	Association analysis between polymorphisms in the dopamine D3 receptor (<strong>DRD3</strong>) gene and cocaine <b>dependence</b>.
+DRD3	drug	amphetamine	19275926	To test this hypothesis, 6 putatively functional polymorphisms of D2 like receptors,  141C Ins/Del, Ser311Cys and TaqIA of the DRD2 gene, Ser9Gly of the <strong>DRD3</strong> gene, and  521C>T and a variable number of tandem repeats in exon 3 of the DRD4 gene, were analyzed in 202 patients with <b>methamphetamine</b> dependence and/or psychosis and 243 healthy controls in a Japanese population.
+DRD3	addiction	dependence	19275926	To test this hypothesis, 6 putatively functional polymorphisms of D2 like receptors,  141C Ins/Del, Ser311Cys and TaqIA of the DRD2 gene, Ser9Gly of the <strong>DRD3</strong> gene, and  521C>T and a variable number of tandem repeats in exon 3 of the DRD4 gene, were analyzed in 202 patients with methamphetamine <b>dependence</b> and/or psychosis and 243 healthy controls in a Japanese population.
+DRD3	drug	amphetamine	19275926	These findings revealed that genetic variants of DRD2, but not <strong>DRD3</strong> or DRD4, confer individual risks for rapid onset, prolonged duration, and spontaneous relapse of <b>methamphetamine</b> psychosis.
+DRD3	addiction	relapse	19275926	These findings revealed that genetic variants of DRD2, but not <strong>DRD3</strong> or DRD4, confer individual risks for rapid onset, prolonged duration, and spontaneous <b>relapse</b> of methamphetamine psychosis.
+DRD3	drug	alcohol	19219710	Two studies reported a significant association of <b>alcohol</b> withdrawal delirium with the dopamine transporter gene (SLC6A3) and the dopamine receptor 3 (<strong>DRD3</strong>).
+DRD3	addiction	withdrawal	19219710	Two studies reported a significant association of alcohol <b>withdrawal</b> delirium with the dopamine transporter gene (SLC6A3) and the dopamine receptor 3 (<strong>DRD3</strong>).
+DRD3	addiction	addiction	19179847	Here, we will review the information collected implicating the receptors of the D1 family (DRD1 and DRD5) and of the D2 family (DRD2, <strong>DRD3</strong> and DRD4) in drug <b>addiction</b>.
+DRD3	addiction	reward	18790725	Dopamine D(3) receptors (<strong>Drd3</strong>) have been implicated in the control of responding by drug related conditioned <b>incentive</b> stimuli.
+DRD3	drug	alcohol	18790725	We review recent studies of the effects of <strong>Drd3</strong> antagonists or partial agonists on the control of self administration of intravenous (IV) cocaine, IV morphine and oral <b>ethanol</b> on reward rich and lean schedules, in reinstatement tests, on second order schedules and on the acquisition and expression of conditioned place preference (CPP) and conditioned motor activity.
+DRD3	drug	cocaine	18790725	We review recent studies of the effects of <strong>Drd3</strong> antagonists or partial agonists on the control of self administration of intravenous (IV) <b>cocaine</b>, IV morphine and oral ethanol on reward rich and lean schedules, in reinstatement tests, on second order schedules and on the acquisition and expression of conditioned place preference (CPP) and conditioned motor activity.
+DRD3	drug	opioid	18790725	We review recent studies of the effects of <strong>Drd3</strong> antagonists or partial agonists on the control of self administration of intravenous (IV) cocaine, IV <b>morphine</b> and oral ethanol on reward rich and lean schedules, in reinstatement tests, on second order schedules and on the acquisition and expression of conditioned place preference (CPP) and conditioned motor activity.
+DRD3	addiction	relapse	18790725	We review recent studies of the effects of <strong>Drd3</strong> antagonists or partial agonists on the control of self administration of intravenous (IV) cocaine, IV morphine and oral ethanol on reward rich and lean schedules, in <b>reinstatement</b> tests, on second order schedules and on the acquisition and expression of conditioned place preference (CPP) and conditioned motor activity.
+DRD3	addiction	reward	18790725	We review recent studies of the effects of <strong>Drd3</strong> antagonists or partial agonists on the control of self administration of intravenous (IV) cocaine, IV morphine and oral ethanol on <b>reward</b> rich and lean schedules, in reinstatement tests, on second order schedules and on the acquisition and expression of conditioned place preference (<b>CPP</b>) and conditioned motor activity.
+DRD3	drug	cocaine	18790725	<strong>Drd3</strong> agents also block the ability of conditioned cues to reinstate responding for <b>cocaine</b> or food.
+DRD3	addiction	reward	18790725	Published results suggest that <strong>Drd3</strong> plays a more important role in the expression than in the acquisition of a <b>CPP</b> or conditioned motor activity.
+DRD3	addiction	reward	18790725	The mechanism mediating the role of <strong>Drd3</strong> in the control of responding by conditioned <b>incentive</b> stimuli remains unknown but it has been found that <strong>Drd3</strong> receptors increase in number in the nucleus accumbens during conditioning.
+DRD3	addiction	reward	18790725	Perhaps <strong>Drd3</strong> participates in the molecular mechanisms underlying the role of dopamine and of dopamine receptor subtypes in <b>reward</b> related <b>incentive</b> learning.
+DRD3	drug	alcohol	18552399	The aim of this study was to investigate the potential association between functional polymorphisms of dopaminergic [dopamine receptor D2 (DRD2), dopamine receptor D3 (<strong>DRD3</strong>) and dopamine transporter (SLC6A3)] and serotonergic [serotonin 2A receptor (HTR2A) and serotonin transporter (SLC6A4)] genes and treatment outcome in <b>alcohol</b> dependent patients.
+DRD3	drug	alcohol	18552399	The aim of this study was to investigate the potential association between functional polymorphisms of dopaminergic [dopamine receptor D2 (DRD2), <strong>dopamine receptor D3</strong> (<strong>DRD3</strong>) and dopamine transporter (SLC6A3)] and serotonergic [serotonin 2A receptor (HTR2A) and serotonin transporter (SLC6A4)] genes and treatment outcome in <b>alcohol</b> dependent patients.
+DRD3	drug	nicotine	18348205	A functional polymorphism, rs6280, in <strong>DRD3</strong> is significantly associated with <b>nicotine</b> dependence in European American <b>smokers</b>.
+DRD3	addiction	dependence	18348205	A functional polymorphism, rs6280, in <strong>DRD3</strong> is significantly associated with nicotine <b>dependence</b> in European American smokers.
+DRD3	drug	cocaine	17671965	Polymorphisms TaqI A of the DRD2, BalI of the <strong>DRD3</strong>, exon III repeat of the DRD4, and 3' UTR VNTR of the DAT: association with childhood ADHD in male African Caribbean <b>cocaine</b> dependents?
+DRD3	drug	cocaine	17671965	The potential association of the variants TaqI A of the DRD2, BalI of the <strong>DRD3</strong>, exon III repeat of the DRD4, and 3' UTR VNTR of the DAT was examined in African Caribbean males, smoked <b>cocaine</b> dependents.
+DRD3	drug	nicotine	17407504	Dopamine receptor genes (DRD2, <strong>DRD3</strong> and DRD4) and gene gene interactions associated with <b>smoking</b> related behaviors.
+DRD3	drug	nicotine	17407504	Cigarette <b>smoking</b>, like many addictive behaviors, has a genetic component, and the dopamine D2 like receptor genes (DRD2, <strong>DRD3</strong> and DRD4) are candidates for contributing to these behaviors.
+DRD3	addiction	addiction	17407504	Cigarette smoking, like many <b>addictive</b> behaviors, has a genetic component, and the dopamine D2 like receptor genes (DRD2, <strong>DRD3</strong> and DRD4) are candidates for contributing to these behaviors.
+DRD3	drug	nicotine	17407504	The presence of the glycine allele at the S9G polymorphism of the <strong>DRD3</strong> gene was associated with frequency/quantity measures of <b>smoking</b> [log transformed time to first cigarette (P = 0.031) and heaviness of <b>smoking</b> index (P = 0.035)].
+DRD3	drug	cannabinoid	17209799	Other therapeutic drugs that are under development include <b>rimonabant</b>, mecamylamine, monoamine oxidase inhibitors, and <strong>dopamine receptor D3</strong> antagonists.
+DRD3	drug	nicotine	17155853	This review considers the potential use of the dopamine D(3) receptor (<strong>DRD3</strong>) as a novel therapeutic target for the treatment of <b>tobacco</b> dependence.
+DRD3	addiction	dependence	17155853	This review considers the potential use of the dopamine D(3) receptor (<strong>DRD3</strong>) as a novel therapeutic target for the treatment of tobacco <b>dependence</b>.
+DRD3	addiction	relapse	17155853	Among the 5 dopamine receptors identified, the <strong>DRD3</strong> is located in the nucleus accumbens, ventral tegmental area and amygdala: 3 brain structures that are implicated in the motivational control of drug <b>seeking</b> behaviour and drug conditioning processes.
+DRD3	addiction	dependence	17155853	Several highly selective <strong>DRD3</strong> ligands have recently been evaluated in preclinical models of drug <b>dependence</b>.
+DRD3	drug	nicotine	17155853	In contrast to <b>nicotine</b> replacement therapy, varenicline and bupropion (which are currently used for the treatment of <b>smokers</b>), <strong>DRD3</strong> antagonists do not seem to produce <b>nicotine</b> like effects in experimental animals and, therefore, may not substitute for <b>nicotine</b> or alleviate <b>nicotine</b> withdrawal symptoms in human <b>smokers</b>.
+DRD3	addiction	withdrawal	17155853	In contrast to nicotine replacement therapy, varenicline and bupropion (which are currently used for the treatment of smokers), <strong>DRD3</strong> antagonists do not seem to produce nicotine like effects in experimental animals and, therefore, may not substitute for nicotine or alleviate nicotine <b>withdrawal</b> symptoms in human smokers.
+DRD3	drug	cannabinoid	17155853	This behavioural profile, which was also reported recently with <b>cannabinoid</b> CB(1) receptor antagonists, may result from effects on specific brain pathways that express <strong>DRD3</strong> receptors and are involved in relapse and conditioning processes.
+DRD3	addiction	relapse	17155853	This behavioural profile, which was also reported recently with cannabinoid CB(1) receptor antagonists, may result from effects on specific brain pathways that express <strong>DRD3</strong> receptors and are involved in <b>relapse</b> and conditioning processes.
+DRD3	addiction	relapse	17155853	These preclinical studies suggest that the clinical evaluation of <strong>DRD3</strong> ligands should be performed with clinical trials designed specifically to evaluate the <b>relapse</b> phenomena.
+DRD3	drug	alcohol	16759339	No association of dopamine receptor sensitivity in vivo with genetic predisposition for <b>alcoholism</b> and DRD2/<strong>DRD3</strong> gene polymorphisms in <b>alcohol</b> dependence.
+DRD3	addiction	dependence	16759339	No association of dopamine receptor sensitivity in vivo with genetic predisposition for alcoholism and DRD2/<strong>DRD3</strong> gene polymorphisms in alcohol <b>dependence</b>.
+DRD3	drug	alcohol	16759339	This study sought to examine dopamine receptor sensitivity among <b>alcoholics</b> in vivo and to explore whether this sensitivity might be associated with functional variations of dopamine D2 (DRD2) and D3 (<strong>DRD3</strong>) receptor genes along with a genetic predisposition for <b>alcoholism</b> as reflected by an <b>alcohol</b> dependent first degree relative.
+DRD3	drug	alcohol	16759339	We analyzed the  141C Ins/Del polymorphism in the promoter region of the DRD2 gene and the Ser9Gly (BalI) polymorphism in exon 1 of the <strong>DRD3</strong> gene in 74 <b>alcohol</b> dependent Caucasian men with or without genetic predisposition for <b>alcoholism</b>.
+DRD3	drug	alcohol	16759339	Given the explorative and preliminary character of this investigation, we cannot provide evidence that in <b>alcohol</b> dependent Caucasian men a genetic predisposition for <b>alcoholism</b> along with functional variants of the DRD2 and <strong>DRD3</strong> genes are associated with differences in dopamine receptor sensitivity.
+DRD3	addiction	dependence	15963538	Dopamine D(3) receptors (<strong>DRD3</strong>) are predominantly expressed in the nucleus accumbens, but also in the ventral tegmental area and in the amygdala, brain structures implicated in drug <b>dependence</b>.
+DRD3	addiction	dependence	15963538	Moreover, converging pharmacological, human post mortem and genetic studies have suggested the involvement of the <strong>DRD3</strong> in drug <b>dependence</b>.
+DRD3	addiction	reward	15963538	However, recent studies using highly selective <strong>DRD3</strong> ligands and the <strong>DRD3</strong> deficient mice have revealed that the <strong>DRD3</strong> is not implicated in the direct <b>reinforcing</b> effects of drugs of abuse.
+DRD3	addiction	relapse	15963538	The <strong>DRD3</strong> strongly modulates the influence of these environmental stimuli on drug <b>seeking</b> behavior.
+DRD3	addiction	relapse	15963538	All these findings suggest that <strong>DRD3</strong> ligands may represent a useful strategy for decreasing <b>relapse</b> in abstinent drug abusers.
+DRD3	drug	alcohol	15935433	Association between <strong>dopamine receptor D3</strong> gene BalI polymorphism and cognitive impulsiveness in <b>alcohol</b> dependent men.
+DRD3	addiction	addiction	15935433	The gene coding for the dopamine receptor D3 (<strong>DRD3</strong>) is considered as a major candidate gene in various <b>addictive</b> disorders.
+DRD3	addiction	addiction	15935433	The gene coding for the <strong>dopamine receptor D3</strong> (<strong>DRD3</strong>) is considered as a major candidate gene in various <b>addictive</b> disorders.
+DRD3	addiction	addiction	15935433	the <strong>DRD3</strong> gene is a vulnerability gene in a specific subgroup of patients only) could explain these spurious findings, focusing on a core dimension of <b>addictive</b> disorders, namely impulsiveness.
+DRD3	drug	cocaine	15671872	Acute <b>cocaine</b> produced a transient increase in BDNF mRNA in the prefrontal cortex, associated with a long lasting increase in <strong>drd3</strong> mRNA, and a delayed and long lasting increase in <strong>Drd3</strong> protein in the nucleus accumbens.
+DRD3	drug	opioid	15371743	Role of <strong>DRD3</strong> in <b>morphine</b> induced conditioned place preference using <strong>drd3</strong> knockout mice.
+DRD3	drug	opioid	15371743	CPP was obtained at <b>morphine</b> doses of 16 and 32 mg/kg in wild type (<strong>drd3</strong>+/+) mice and 8, 16 and 32 mg/kg in <strong>DRD3</strong> knockout (<strong>drd3</strong> / ) mice.
+DRD3	addiction	reward	15371743	<b>CPP</b> was obtained at morphine doses of 16 and 32 mg/kg in wild type (<strong>drd3</strong>+/+) mice and 8, 16 and 32 mg/kg in <strong>DRD3</strong> knockout (<strong>drd3</strong> / ) mice.
+DRD3	drug	opioid	15371743	BP897, a <strong>DRD3</strong> selective partial agonist, inhibited the expression of <b>morphine</b> CPP in <strong>drd3</strong>+/+, but not <strong>drd3</strong> /  mice.
+DRD3	addiction	reward	15371743	BP897, a <strong>DRD3</strong> selective partial agonist, inhibited the expression of morphine <b>CPP</b> in <strong>drd3</strong>+/+, but not <strong>drd3</strong> /  mice.
+DRD3	addiction	reward	15371743	BP 897 reduced brain regional activation, measured by c fos imaging after the <b>CPP</b> test session, in the somatosensory cortex of <strong>drd3</strong>+/+, but not <strong>drd3</strong> /  mice.
+DRD3	drug	opioid	15371743	These results confirm the role of <strong>DRD3</strong> in the expression of conditioned effects of <b>morphine</b> and the participation of the somatosensory cortex in these effects.
+DRD3	drug	opioid	15288384	Psychiatry 3 (1998) 333] in French <b>Heroin</b> addicts, found a significant association with homozygotes alleles of the <strong>DRD3</strong> Bal 1.
+DRD3	drug	nicotine	14982687	Dopamine receptor D(3) (<strong>DRD3</strong>) and D(4) (DRD4) mRNA expression in PBLs was measured by real time polymerase chain reaction in <b>smokers</b> (n=26) and former <b>smokers</b> (n=14), compared with nonsmoking control subjects (n=35).
+DRD3	drug	nicotine	14982687	A significant (p=.032, Bonferroni corrected) 30% reduction of <strong>DRD3</strong> mRNA expression in PBLs was found in <b>smokers</b> but not former <b>smokers</b> in comparison with controls.
+DRD3	drug	nicotine	14982687	<strong>DRD3</strong> mRNA expression in PBLs in <b>smokers</b> but not former <b>smokers</b> was negatively correlated with daily number of cigarettes consumed (Pearson correlation coefficient r= .54, p=.005).
+DRD3	drug	nicotine	14982687	These data suggest a selective inhibiting effect of <b>smoking</b> on <strong>DRD3</strong> mRNA expression and, with the known involvement of <strong>DRD3</strong> in reward mediation, indicates a vicious cycle explanation for the motivation for continued <b>smoking</b>.
+DRD3	addiction	reward	14982687	These data suggest a selective inhibiting effect of smoking on <strong>DRD3</strong> mRNA expression and, with the known involvement of <strong>DRD3</strong> in <b>reward</b> mediation, indicates a vicious cycle explanation for the motivation for continued smoking.
+DRD3	drug	alcohol	12218663	So we compared the distribution of genotypes and frequencies of BalI polymorphism of the <strong>DRD3</strong> gene in <b>alcoholics</b> and controls to assess the role of the <strong>DRD3</strong> gene in Korean <b>alcoholism</b>.
+DRD3	drug	alcohol	12218663	No evidence for an allelic association was found between the A1 allele of <strong>DRD3</strong> and <b>alcoholism</b> in a Korean population.
+DRD3	drug	alcohol	12082567	The dopamine D(3) receptor gene (<strong>DRD3</strong>) is a candidate for a number of psychiatric conditions including schizophrenia, bipolar disorder and <b>alcohol</b> and drug abuse.
+DRD3	addiction	relapse	11762133	Furthermore, a previous collaborative study showed that homozygosity for the Ball <strong>DRD3</strong> locus was more frequently observed in opiate dependent patients with high sensation <b>seeking</b> scores.
+DRD3	drug	alcohol	11762133	In this study, we analyzed the distribution of Ball <strong>DRD3</strong> polymorphism in a new sample of 131 French male <b>alcoholic</b> patients (DSM III R criteria) and 68 healthy controls matched for sex and origins.
+DRD3	drug	alcohol	11762133	Although we replicated the higher sensation seeking score in <b>alcohol</b> dependent patients with comorbid dependence, we found no significant difference in the <strong>DRD3</strong> gene polymorphism between controls and <b>alcoholic</b> patients, regardless of sensation seeking score, addictive or psychiatric comorbidity, <b>alcoholism</b> typology, and clinical specificities of <b>alcoholism</b>.
+DRD3	addiction	addiction	11762133	Although we replicated the higher sensation seeking score in alcohol dependent patients with comorbid dependence, we found no significant difference in the <strong>DRD3</strong> gene polymorphism between controls and alcoholic patients, regardless of sensation seeking score, <b>addictive</b> or psychiatric comorbidity, alcoholism typology, and clinical specificities of alcoholism.
+DRD3	addiction	dependence	11762133	Although we replicated the higher sensation seeking score in alcohol dependent patients with comorbid <b>dependence</b>, we found no significant difference in the <strong>DRD3</strong> gene polymorphism between controls and alcoholic patients, regardless of sensation seeking score, addictive or psychiatric comorbidity, alcoholism typology, and clinical specificities of alcoholism.
+DRD3	addiction	relapse	11762133	Although we replicated the higher sensation <b>seeking</b> score in alcohol dependent patients with comorbid dependence, we found no significant difference in the <strong>DRD3</strong> gene polymorphism between controls and alcoholic patients, regardless of sensation <b>seeking</b> score, addictive or psychiatric comorbidity, alcoholism typology, and clinical specificities of alcoholism.
+DRD3	drug	alcohol	11762133	There is good evidence that gene coding for the <strong>dopamine receptor D3</strong> does not play a major role in the genetic vulnerability to <b>alcoholism</b>.
+DRD3	drug	cocaine	10523822	Homozygosity at the dopamine <strong>DRD3</strong> receptor gene in <b>cocaine</b> dependence.
+DRD3	addiction	dependence	10523822	Homozygosity at the dopamine <strong>DRD3</strong> receptor gene in cocaine <b>dependence</b>.
+DRD3	drug	cocaine	10523822	We examined the hypothesis that the dopamine D3 receptor gene (<strong>DRD3</strong>) is a susceptibility factor for <b>cocaine</b> dependence.
+DRD3	addiction	dependence	10523822	We examined the hypothesis that the dopamine D3 receptor gene (<strong>DRD3</strong>) is a susceptibility factor for cocaine <b>dependence</b>.
+DRD3	drug	cocaine	10523822	The MscI/BalI polymorphism of the <strong>DRD3</strong> gene was examined in 47 Caucasian subjects with <b>cocaine</b> dependence and 305 Caucasian controls.
+DRD3	addiction	dependence	10523822	The MscI/BalI polymorphism of the <strong>DRD3</strong> gene was examined in 47 Caucasian subjects with cocaine <b>dependence</b> and 305 Caucasian controls.
+DRD3	drug	cocaine	10523822	The <strong>DRD3</strong> gene accounted for 1.64% of the variance of <b>cocaine</b> dependence.
+DRD3	addiction	dependence	10523822	The <strong>DRD3</strong> gene accounted for 1.64% of the variance of cocaine <b>dependence</b>.
+DRD3	drug	cocaine	10523822	These findings support a modest role of the <strong>DRD3</strong> gene in susceptibility to <b>cocaine</b> dependence.
+DRD3	addiction	dependence	10523822	These findings support a modest role of the <strong>DRD3</strong> gene in susceptibility to cocaine <b>dependence</b>.
+DRD3	drug	opioid	10483044	No association between the serotonin transporter promoter region (5 HTTLPR) and the dopamine D3 receptor (BalI <strong>D3DR</strong>) polymorphisms and <b>heroin</b> addiction.
+DRD3	addiction	addiction	10483044	No association between the serotonin transporter promoter region (5 HTTLPR) and the dopamine D3 receptor (BalI <strong>D3DR</strong>) polymorphisms and heroin <b>addiction</b>.
+DRD3	drug	opioid	9790747	Population studies of polymorphisms at loci of neuropsychiatric interest (tryptophan hydroxylase (TPH), dopamine transporter protein (SLC6A3), D3 dopamine receptor (<strong>DRD3</strong>), apolipoprotein E (APOE), mu <b>opioid</b> receptor (OPRM1), and ciliary neurotrophic factor (CNTF)).
+DRD3	drug	opioid	9790747	We determined allele frequencies for polymorphisms at several loci of interest in neuropsychiatry tryptophan hydroxylase (TPH), dopamine transporter protein (SLC6A3), D3 dopamine receptor (<strong>DRD3</strong>), apolipoprotein E (APOE), ciliary neurotrophic factor (CNTF), and the mu <b>opioid</b> receptor (OPRM1) in samples of individuals from populations in several different parts of the world.
+DRD3	drug	cocaine	9790747	Associations with psychiatric illness have been proposed for specific polymorphisms at TPH (suicide related behaviors and impulsivity), <strong>DRD3</strong> (schizophrenia and bipolar affective disorder), SLC6A3 (susceptibility to <b>cocaine</b> induced paranoia and attention deficit disorder), CNTF (psychosis), and OPRM1 (substance dependence).
+DRD3	addiction	dependence	9790747	Associations with psychiatric illness have been proposed for specific polymorphisms at TPH (suicide related behaviors and impulsivity), <strong>DRD3</strong> (schizophrenia and bipolar affective disorder), SLC6A3 (susceptibility to cocaine induced paranoia and attention deficit disorder), CNTF (psychosis), and OPRM1 (substance <b>dependence</b>).
+DRD3	drug	cocaine	12893467	No association between D3 dopamine receptor (<strong>DRD3</strong>) alleles and <b>cocaine</b> dependence.
+DRD3	addiction	dependence	12893467	No association between D3 dopamine receptor (<strong>DRD3</strong>) alleles and cocaine <b>dependence</b>.
+DRD3	drug	cocaine	12893467	The dopamine D3 receptor (genetic locus <strong>DRD3</strong>) is localized to brain regions that have been implicated in the reinforcing effects of a number of substances of abuse, including <b>cocaine</b>.
+DRD3	addiction	reward	12893467	The dopamine D3 receptor (genetic locus <strong>DRD3</strong>) is localized to brain regions that have been implicated in the <b>reinforcing</b> effects of a number of substances of abuse, including cocaine.
+DRD3	drug	cocaine	12893467	We examined alleles of the <strong>DRD3</strong> gene in <b>cocaine</b> dependence using a genetic association strategy in samples of 62 white and 62 black <b>cocaine</b> dependent individuals.
+DRD3	addiction	dependence	12893467	We examined alleles of the <strong>DRD3</strong> gene in cocaine <b>dependence</b> using a genetic association strategy in samples of 62 white and 62 black cocaine dependent individuals.
+DRD3	drug	cocaine	12893467	No association was found between <b>cocaine</b> dependence and <strong>DRD3</strong> alleles in either group (Bonferroni corrected).
+DRD3	addiction	dependence	12893467	No association was found between cocaine <b>dependence</b> and <strong>DRD3</strong> alleles in either group (Bonferroni corrected).
+DRD3	addiction	addiction	8825889	Another receptor, the D3 dopamine receptor (<strong>DRD3</strong>), may be of additional interest since it is specifically located in the limbic area, and in particular in the nucleus accumbens which plays a significant role in the reward process of <b>addiction</b> behavior.
+DRD3	addiction	reward	8825889	Another receptor, the D3 dopamine receptor (<strong>DRD3</strong>), may be of additional interest since it is specifically located in the limbic area, and in particular in the nucleus accumbens which plays a significant role in the <b>reward</b> process of addiction behavior.
+DRD3	drug	alcohol	8825889	No difference in the <strong>DRD3</strong> gene polymorphism emerged between controls and <b>alcoholic</b> patients, regardless of their origin, inclusion criteria, or presence or absence of the DRD2 TaqI A1 allele.
+DRD3	drug	alcohol	8825889	Despite the fact that more information could have been considered and that association studies provide limited information, there is good evidence that this <strong>DRD3</strong> polymorphism does not play a major role in the genetic component of <b>alcoholism</b>.
+DRD3	drug	alcohol	8750359	Without correction for multiple testing, we found a significantly increased allele frequency of a common <strong>DRD3</strong> gene variant expressing a serine at position 9 in the extracellular N terminal part of the receptor protein in 55 <b>alcohol</b> dependent individuals with delirium (chi 2 = 4.1, df = 1, p = 0.042).
+ABCB1	drug	alcohol	32613204	Our findings include compounds that killed by inducing PDE3A SLFN12 complex formation; vanadium containing compounds whose killing depended on the sulfate transporter SLC26A2; the <b>alcohol</b> dependence drug <b>disulfiram</b>, which killed cells with low expression of metallothioneins; and the anti inflammatory drug tepoxalin, which killed via the multi drug resistance protein <strong>ABCB1</strong>.
+ABCB1	addiction	dependence	32613204	Our findings include compounds that killed by inducing PDE3A SLFN12 complex formation; vanadium containing compounds whose killing depended on the sulfate transporter SLC26A2; the alcohol <b>dependence</b> drug disulfiram, which killed cells with low expression of metallothioneins; and the anti inflammatory drug tepoxalin, which killed via the multi drug resistance protein <strong>ABCB1</strong>.
+ABCB1	drug	opioid	31743739	Though in vitro bidirectional transport studies showed that NFP might be a <strong>P gp</strong> substrate, in warm water tail withdrawal assays it was able to antagonize the antinociceptive effects of <b>morphine</b> indicating its potential central nervous system activity.
+ABCB1	addiction	withdrawal	31743739	Though in vitro bidirectional transport studies showed that NFP might be a <strong>P gp</strong> substrate, in warm water tail <b>withdrawal</b> assays it was able to antagonize the antinociceptive effects of morphine indicating its potential central nervous system activity.
+ABCB1	drug	cocaine	31257858	Sequentially, we looked into the detail of (1) the addiction to <b>cocaine</b> and fentanyl by binding to the dopamine transporter and the μ opioid receptor (DAT and μOR, respectively), (2) the potential drug drug interaction of <b>cocaine</b> and fentanyl via p glycoprotein (<strong>P gp</strong>) efflux, (3) the metabolism of <b>cocaine</b> and fentanyl in CYP3A4, and (4) the physiologically based pharmacokinetic (PBPK) model for two drugs and their drug drug interaction at the absorption, distribution, metabolism, and excretion (ADME) level.
+ABCB1	drug	opioid	31257858	Sequentially, we looked into the detail of (1) the addiction to cocaine and <b>fentanyl</b> by binding to the dopamine transporter and the μ <b>opioid</b> receptor (DAT and μOR, respectively), (2) the potential drug drug interaction of cocaine and <b>fentanyl</b> via p glycoprotein (<strong>P gp</strong>) efflux, (3) the metabolism of cocaine and <b>fentanyl</b> in CYP3A4, and (4) the physiologically based pharmacokinetic (PBPK) model for two drugs and their drug drug interaction at the absorption, distribution, metabolism, and excretion (ADME) level.
+ABCB1	addiction	addiction	31257858	Sequentially, we looked into the detail of (1) the <b>addiction</b> to cocaine and fentanyl by binding to the dopamine transporter and the μ opioid receptor (DAT and μOR, respectively), (2) the potential drug drug interaction of cocaine and fentanyl via p glycoprotein (<strong>P gp</strong>) efflux, (3) the metabolism of cocaine and fentanyl in CYP3A4, and (4) the physiologically based pharmacokinetic (PBPK) model for two drugs and their drug drug interaction at the absorption, distribution, metabolism, and excretion (ADME) level.
+ABCB1	drug	nicotine	31237077	Furthermore, neither <b>nicotine</b>, cotinine nor OH cotinine inhibited MRP2 4, BCRP or <strong>MDR1</strong>.
+ABCB1	drug	opioid	30420869	Objective: To explore the association between <b>methadone</b> dosage, plasma drug concentration, SNPs of μ <b>opioid</b> receptor gene (OPRM1), ATP binding cassette subfamily B member 1 gene (<strong>ABCB1</strong>), and <b>methadone</b> maintenance treatment (MMT) response.
+ABCB1	drug	opioid	30420869	Objective: To explore the association between <b>methadone</b> dosage, plasma drug concentration, SNPs of μ <b>opioid</b> receptor gene (OPRM1), <strong>ATP binding cassette subfamily B member 1</strong> gene (<strong>ABCB1</strong>), and <b>methadone</b> maintenance treatment (MMT) response.
+ABCB1	drug	opioid	30420869	Nine single nucleotide polymorphisms (SNPs) of the OPRM1 gene and three SNPs of the <strong>ABCB1</strong> gene were genotyped, plasma <b>methadone</b> concentration was detected, and a <b>morphine</b> urine test was taken from all subjects.
+ABCB1	drug	alcohol	29978425	<b>Alcohol</b> and Cocaine Exposure Modulates <strong>ABCB1</strong> and ABCG2 Transporters in Male <b>Alcohol</b> Preferring Rats.
+ABCB1	drug	cocaine	29978425	Alcohol and <b>Cocaine</b> Exposure Modulates <strong>ABCB1</strong> and ABCG2 Transporters in Male Alcohol Preferring Rats.
+ABCB1	addiction	dependence	29978425	However, whether <strong>ABCB1</strong> or ABCG2 has any link with drug <b>dependence</b>, drug withdrawal effects, or the incidence of adverse effects in drug abuser is not known.
+ABCB1	addiction	withdrawal	29978425	However, whether <strong>ABCB1</strong> or ABCG2 has any link with drug dependence, drug <b>withdrawal</b> effects, or the incidence of adverse effects in drug abuser is not known.
+ABCB1	drug	alcohol	29978425	In this study, we determined the effects of voluntary <b>ethanol</b> consumption following repeated exposure to cocaine or vehicle on the relative mRNA and protein expression of Abcg2/ABCG2 and <strong>Abcb1</strong>/<strong>ABCB1</strong> in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) of male <b>alcohol</b> preferring (P) rats.
+ABCB1	drug	cocaine	29978425	In this study, we determined the effects of voluntary ethanol consumption following repeated exposure to <b>cocaine</b> or vehicle on the relative mRNA and protein expression of Abcg2/ABCG2 and <strong>Abcb1</strong>/<strong>ABCB1</strong> in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) of male alcohol preferring (P) rats.
+ABCB1	drug	alcohol	29978425	The relative mRNA and protein expression of <strong>Abcb1</strong>/<strong>ABCB1</strong> and Abcg2/ABCG2 in the NAc and mPFC were significantly decreased in <b>ethanol</b> saline  and <b>ethanol</b> cocaine exposed rats compared to control rats that received neither <b>ethanol</b> nor cocaine.
+ABCB1	drug	cocaine	29978425	The relative mRNA and protein expression of <strong>Abcb1</strong>/<strong>ABCB1</strong> and Abcg2/ABCG2 in the NAc and mPFC were significantly decreased in ethanol saline  and ethanol <b>cocaine</b> exposed rats compared to control rats that received neither ethanol nor <b>cocaine</b>.
+ABCB1	drug	alcohol	29978425	Thus, prolonged exposure to commonly abused drugs, <b>ethanol</b> and cocaine, alters the expression of <strong>Abcb1</strong>/<strong>ABCB1</strong> and Abcg2/ABCG2 mRNA and protein levels in brain areas that play a role in drug dependence.
+ABCB1	drug	cocaine	29978425	Thus, prolonged exposure to commonly abused drugs, ethanol and <b>cocaine</b>, alters the expression of <strong>Abcb1</strong>/<strong>ABCB1</strong> and Abcg2/ABCG2 mRNA and protein levels in brain areas that play a role in drug dependence.
+ABCB1	addiction	dependence	29978425	Thus, prolonged exposure to commonly abused drugs, ethanol and cocaine, alters the expression of <strong>Abcb1</strong>/<strong>ABCB1</strong> and Abcg2/ABCG2 mRNA and protein levels in brain areas that play a role in drug <b>dependence</b>.
+ABCB1	drug	opioid	29414996	Many <b>opioids</b> are a substrate for p glycoprotein (<strong>p gp</strong>), an efflux transporter at the blood brain barrier (BBB).
+ABCB1	drug	opioid	29414996	Increased <strong>p gp</strong> is associated with a decreased central nervous system uptake and analgesic efficacy of <b>morphine</b>.
+ABCB1	drug	opioid	29414996	Our laboratory previously found that acute peripheral inflammatory pain (PIP) induces <strong>p gp</strong> trafficking from the nucleus to the luminal surface of endothelial cells making up the BBB concomitant with increased <strong>p gp</strong> activity and decreased <b>morphine</b> analgesic efficacy.
+ABCB1	drug	opioid	29414996	In the current study, we tested whether PIP induced <strong>p gp</strong> trafficking could contribute to decreased <b>opioid</b> efficacy in <b>morphine</b> tolerant rats.
+ABCB1	drug	opioid	29414996	PIP induced <strong>p gp</strong> trafficking away from nuclear stores showed a 2 fold increase in <b>morphine</b> tolerant rats.
+ABCB1	drug	opioid	29414996	This observation suggests that <strong>p gp</strong> trafficking contributes to the decreased <b>morphine</b> analgesic effects in <b>morphine</b> tolerant rats experiencing an acute pain stimulus.
+ABCB1	drug	opioid	29414996	Attenuating <strong>p gp</strong> trafficking during an acute pain stimulus could improve pain management by increasing the amount of <b>opioid</b> that could reach CNS analgesic targets and decrease the need for the dose escalation that is a serious challenge in pain management.
+ABCB1	addiction	addiction	29414996	Attenuating <strong>p gp</strong> trafficking during an acute pain stimulus could improve pain management by increasing the amount of opioid that could reach CNS analgesic targets and decrease the need for the dose <b>escalation</b> that is a serious challenge in pain management.
+ABCB1	drug	cannabinoid	28917442	<strong>ABCB1</strong> C3435T polymorphism is associated with <b>tetrahydrocannabinol</b> blood levels in heavy <b>cannabis</b> users.
+ABCB1	drug	cannabinoid	28917442	<strong>ABCB1</strong> polymorphisms are known to modify drug pharmacokinetics but have yet to be studied for their role in generating and maintaining <b>cannabis</b> dependence.
+ABCB1	addiction	dependence	28917442	<strong>ABCB1</strong> polymorphisms are known to modify drug pharmacokinetics but have yet to be studied for their role in generating and maintaining cannabis <b>dependence</b>.
+ABCB1	drug	cannabinoid	28917442	The objective of this study is to determine if <strong>ABCB1</strong> C3435T (rs1045642) polymorphism may modulate Δ9 <b>Tetrahydrocannabinol</b> (<b>THC</b>) blood levels in a sample of heavy <b>cannabis</b> users.
+ABCB1	drug	cannabinoid	28917442	Each underwent clinical evaluation, <b>cannabis</b> blood metabolite dosage (<b>THC</b>, 11 OH <b>THC</b>, and <b>THC</b> COOH) and genotyping of <strong>ABCB1</strong> C3435T polymorphism.
+ABCB1	drug	cannabinoid	28917442	Our results show that <strong>ABCB1</strong> C3435T polymorphism may modulate serum <b>THC</b> levels in chronic heavy <b>cannabis</b> users.
+ABCB1	drug	amphetamine	28893794	Transporter function was examined after exposure of Tat with or without <b>methamphetamine</b> using the <strong>P gp</strong> substrate rhodamine 123 and also using the dual <strong>P gp</strong>/MRP 1 substrate and protease inhibitor atazanavir.
+ABCB1	drug	amphetamine	28893794	Neither Tat nor <b>methamphetamine</b> significantly altered <strong>P gp</strong> expression.
+ABCB1	drug	amphetamine	28893794	However, Tat plus <b>methamphetamine</b> exposure significantly increased rhodamine 123 accumulation within brain endothelial cells, suggesting that treatment inhibited or impaired <strong>P gp</strong> function.
+ABCB1	drug	cannabinoid	28272498	As risperidone and its active metabolite are excellent substrates of the ABC transporter P glycoprotein (<strong>P gp</strong>), we hypothesized that <b>THC</b> might increase <strong>P gp</strong> expression at the blood brain barrier (BBB) and thus enhance efflux of risperidone and its metabolite from brain tissue.
+ABCB1	drug	cannabinoid	28272498	Furthermore, we demonstrated that <b>THC</b> exposure increased <strong>P gp</strong> expression in various brain regions important to risperidone's antipsychotic action.
+ABCB1	drug	cannabinoid	28272498	Our results imply that clozapine or non <strong>P gp</strong> substrate antipsychotic drugs may be better first line treatments for schizophrenia patients with a history of <b>cannabis</b> use.
+ABCB1	drug	opioid	28252574	<strong>ABCB1</strong> Polymorphisms and Cold Pressor Pain Responses: <b>Opioid</b> Dependent Patients on <b>Methadone</b> Maintenance Therapy.
+ABCB1	drug	opioid	28252574	<b>Methadone</b> is a substrate of the P glycoprotein efflux transporter, which is encoded by <strong>ABCB1</strong> (MDR1), and thus, <strong>ABCB1</strong> polymorphisms may influence the transport of <b>methadone</b> at the blood brain barrier, affecting its adverse effects.
+ABCB1	drug	opioid	28252574	<b>Methadone</b> is a substrate of the P glycoprotein efflux transporter, which is encoded by <strong>ABCB1</strong> (<strong>MDR1</strong>), and thus, <strong>ABCB1</strong> polymorphisms may influence the transport of <b>methadone</b> at the blood brain barrier, affecting its adverse effects.
+ABCB1	drug	opioid	28252574	This study investigated the association between <strong>ABCB1</strong> polymorphisms and cold pressor pain responses among <b>opioid</b> dependent patients on <b>methadone</b> maintenance therapy (MMT).
+ABCB1	drug	opioid	28252574	To the best of our knowledge, this study provides the first evidence that <strong>ABCB1</strong> polymorphisms are associated with cold pressor pain responses among Malay male patients with <b>opioid</b> dependence on MMT.
+ABCB1	addiction	dependence	28252574	To the best of our knowledge, this study provides the first evidence that <strong>ABCB1</strong> polymorphisms are associated with cold pressor pain responses among Malay male patients with opioid <b>dependence</b> on MMT.
+ABCB1	drug	opioid	28111265	Previous studies have shown that norbuprenorphine, but not <b>buprenorphine</b>, is a <strong>P gp</strong> substrate.
+ABCB1	drug	opioid	27286724	(S) <b>methadone</b> clearance was influenced by cytochrome P450 (CYP) 2B6 activity, <strong>ABCB1</strong> 3435C>T, and α 1 acid glycoprotein level, while (R) <b>methadone</b> clearance was influenced by CYP2B6 activity, POR*28, and CYP3A4*22.
+ABCB1	drug	opioid	27284701	Relationship between <strong>ABCB1</strong> polymorphisms and serum <b>methadone</b> concentration in patients undergoing <b>methadone</b> maintenance therapy (MMT).
+ABCB1	drug	opioid	27284701	<b>Methadone</b> is a substrate of the permeability glycoprotein (P gp) efflux transporter, which is encoded by the <strong>ABCB1</strong> (MDR1) gene.
+ABCB1	drug	opioid	27284701	<b>Methadone</b> is a substrate of the permeability glycoprotein (P gp) efflux transporter, which is encoded by the <strong>ABCB1</strong> (<strong>MDR1</strong>) gene.
+ABCB1	drug	opioid	27284701	<b>Methadone</b> is a substrate of the permeability glycoprotein (<strong>P gp</strong>) efflux transporter, which is encoded by the <strong>ABCB1</strong> (<strong>MDR1</strong>) gene.
+ABCB1	drug	opioid	27284701	Genetic variations in <strong>ABCB1</strong> gene may be responsible for the variability in observed <b>methadone</b> concentrations.
+ABCB1	drug	opioid	27284701	This study investigated the associations of <strong>ABCB1</strong> polymorphisms and serum <b>methadone</b> concentration over the 24 hour dosing interval in <b>opioid</b> dependent patients on <b>methadone</b> maintenance therapy (MMT).
+ABCB1	drug	opioid	27284701	There was an association between the CGC/TTT diplotype of <strong>ABCB1</strong> polymorphisms and serum <b>methadone</b> concentration over the 24 hour dosing interval among patients on MMT.
+ABCB1	drug	opioid	27284701	Genotyping of <strong>ABCB1</strong> among <b>opioid</b> dependent patients on MMT may help individualize and optimize <b>methadone</b> substitution treatment.
+ABCB1	drug	opioid	27061230	The <strong>ABCB1</strong>, rs9282564, AG and TT Genotypes and the COMT, rs4680, AA Genotype are Less Frequent in Deceased Patients with <b>Opioid</b> Addiction than in Living Patients with <b>Opioid</b> Addiction.
+ABCB1	addiction	addiction	27061230	The <strong>ABCB1</strong>, rs9282564, AG and TT Genotypes and the COMT, rs4680, AA Genotype are Less Frequent in Deceased Patients with Opioid <b>Addiction</b> than in Living Patients with Opioid <b>Addiction</b>.
+ABCB1	drug	opioid	27061230	To examine whether certain genotypes were associated with this, we examined the frequencies of 29 SNPs located in candidate genes related to <b>opioid</b> pharmacology: <strong>ABCB1</strong>, OPRM1, UGT2B7, CYP3A5, CYP2B6, CYP2C19, CYP2D6, COMT, KCNJ6 and SCN9A in 274 deceased patients with OA (DOA), 309 living patients with OA (LOA) and in 394 healthy volunteers (HV).
+ABCB1	drug	opioid	27061230	The main hypothesis of the study was that subjects homozygous for the variant 3435T in <strong>ABCB1</strong> (rs1045642) occur more frequently in DOA than in LOA and HV because <b>morphine</b> and <b>methadone</b> more readily cross the blood barrier in these subjects due to a lower efflux transporter activity of the <strong>ABCB1</strong> (p glycoprotein) transporter.
+ABCB1	drug	opioid	26554626	Effect of Subchronic Intravenous <b>Morphine</b> Infusion and <b>Naloxone</b> Precipitated <b>Morphine</b> Withdrawal on <strong>P gp</strong> and Bcrp at the Rat Blood Brain Barrier.
+ABCB1	addiction	withdrawal	26554626	Effect of Subchronic Intravenous Morphine Infusion and Naloxone Precipitated Morphine <b>Withdrawal</b> on <strong>P gp</strong> and Bcrp at the Rat Blood Brain Barrier.
+ABCB1	drug	opioid	26554626	Chronic <b>morphine</b> regimen increases P glycoprotein (<strong>P gp</strong>) and breast cancer resistance protein (Bcrp) expressions at the rat blood–brain barrier (BBB) but what drives this effect is poorly understood.
+ABCB1	drug	opioid	26554626	The objective of this study is to assess subchronic continuous <b>morphine</b> infusion and <b>naloxone</b> precipitated <b>morphine</b> withdrawal effects on <strong>P gp</strong>/Bcrp contents and activities at the rat BBB.
+ABCB1	addiction	withdrawal	26554626	The objective of this study is to assess subchronic continuous morphine infusion and naloxone precipitated morphine <b>withdrawal</b> effects on <strong>P gp</strong>/Bcrp contents and activities at the rat BBB.
+ABCB1	drug	opioid	26554626	<b>morphine</b> did not change <strong>P gp</strong>/Bcrp protein levels in rat brain microvessels, whereas <b>naloxone</b> precipitated withdrawal after escalating or chronic <b>morphine</b> dose regimen increased Mdr1a and Bcrp mRNA levels by 1.4 fold and 2.4 fold, respectively.
+ABCB1	addiction	withdrawal	26554626	morphine did not change <strong>P gp</strong>/Bcrp protein levels in rat brain microvessels, whereas naloxone precipitated <b>withdrawal</b> after escalating or chronic morphine dose regimen increased Mdr1a and Bcrp mRNA levels by 1.4 fold and 2.4 fold, respectively.
+ABCB1	drug	opioid	26554626	Conversely, <strong>P gp</strong>/Bcrp protein expressions remained unchanged after <b>naloxone</b> administration, and brain uptake of [3H] verapamil (<strong>P gp</strong>) and [3H] mitoxantrone (Bcrp) was not altered.
+ABCB1	drug	opioid	26554626	The study concludes subchronic <b>morphine</b> infusion and <b>naloxone</b> precipitated <b>morphine</b> withdrawal have poor effect on <strong>P gp</strong>/Bcrp levels at the rat BBB.
+ABCB1	addiction	withdrawal	26554626	The study concludes subchronic morphine infusion and naloxone precipitated morphine <b>withdrawal</b> have poor effect on <strong>P gp</strong>/Bcrp levels at the rat BBB.
+ABCB1	addiction	aversion	26327575	Haplotype analysis of <strong>ABCB1</strong> indicated that <b>CTA</b> (rs1045642C rs1128503T rs1202184A) haplotype frequencies in the effective group were significantly lower than the ineffective group (p = 0.022), but TCG (rs1045642T rs1128503C rs1202184G) haplotype frequencies in the effective group were significantly higher than the ineffective group (p = 0.048).
+ABCB1	drug	nicotine	26327575	<strong>ABCB1</strong> rs1045642C > T polymorphism and CTA/TCG haplotypes, as well as <b>smoking</b> history may influence the efficacy of SFC inhalation therapy in stable COPD patients in the Chinese Han population.
+ABCB1	addiction	aversion	26327575	<strong>ABCB1</strong> rs1045642C > T polymorphism and <b>CTA</b>/TCG haplotypes, as well as smoking history may influence the efficacy of SFC inhalation therapy in stable COPD patients in the Chinese Han population.
+ABCB1	drug	opioid	26062728	Butorphanol, a synthetic <b>opioid</b>, sensitizes <strong>ABCB1</strong> mediated multidrug resistance via inhibition of the efflux function of <strong>ABCB1</strong> in leukemia cells.
+ABCB1	addiction	relapse	26062728	ATP binding cassette subfamily B member 1 (<strong>ABCB1</strong>) is a recognized factor which causes MDR and is closely related to poor outcome and <b>relapse</b> in leukemia.
+ABCB1	addiction	relapse	26062728	<strong>ATP binding cassette subfamily B member 1</strong> (<strong>ABCB1</strong>) is a recognized factor which causes MDR and is closely related to poor outcome and <b>relapse</b> in leukemia.
+ABCB1	drug	alcohol	25918995	<strong>ABCB1</strong> has been implicated in substance use, and in post hoc tests we found that variation in <strong>ABCB1</strong> was associated with DSM IV <b>alcohol</b> and cocaine dependence criterion counts.
+ABCB1	drug	cocaine	25918995	<strong>ABCB1</strong> has been implicated in substance use, and in post hoc tests we found that variation in <strong>ABCB1</strong> was associated with DSM IV alcohol and <b>cocaine</b> dependence criterion counts.
+ABCB1	addiction	dependence	25918995	<strong>ABCB1</strong> has been implicated in substance use, and in post hoc tests we found that variation in <strong>ABCB1</strong> was associated with DSM IV alcohol and cocaine <b>dependence</b> criterion counts.
+ABCB1	drug	opioid	25832841	The ADR and clinical response of <b>fentanyl</b> were affected by polymorphisms of CYP3A5 and <strong>ABCB1</strong>.
+ABCB1	drug	benzodiazepine	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) methadone), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the <b>midazolam</b> test, R,S methadone trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, <strong>ABCB1</strong>, CYP2B6, CYP3A5, CYP2C19 and CYP2D6 genes.
+ABCB1	drug	opioid	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) <b>methadone</b>), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the midazolam test, R,S <b>methadone</b> trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, <strong>ABCB1</strong>, CYP2B6, CYP3A5, CYP2C19 and CYP2D6 genes.
+ABCB1	drug	opioid	24956254	Nevertheless many genetic factors have been investigated including those affecting its metabolism (CYP2B6 consistent results), efflux transport (<strong>P gp</strong> inconsistent results), target μ <b>opioid</b> receptor (μ <b>opioid</b> receptor inconsistent results) and a host of other receptors (DRD2) and signaling elements (GIRK2 and ARRB2; not replicated).
+ABCB1	drug	opioid	24950410	Higher frequency of C.3435 of the <strong>ABCB1</strong> gene in patients with <b>tramadol</b> dependence disorder.
+ABCB1	addiction	dependence	24950410	Higher frequency of C.3435 of the <strong>ABCB1</strong> gene in patients with tramadol <b>dependence</b> disorder.
+ABCB1	drug	opioid	24950410	A significant association was found between the <strong>ABCB1</strong> gene T allele at the polymorphic site 3435 and <b>tramadol</b> dependence.
+ABCB1	addiction	dependence	24950410	A significant association was found between the <strong>ABCB1</strong> gene T allele at the polymorphic site 3435 and tramadol <b>dependence</b>.
+ABCB1	drug	opioid	24950410	The high frequency of <strong>ABCB1</strong> gene T allele present at the polymorphic site 3435 could provide a protective mechanism from <b>tramadol</b> dependence disorder.
+ABCB1	addiction	dependence	24950410	The high frequency of <strong>ABCB1</strong> gene T allele present at the polymorphic site 3435 could provide a protective mechanism from tramadol <b>dependence</b> disorder.
+ABCB1	drug	opioid	24705903	<b>Morphine</b> is a known substrate of P glycoprotein (<strong>P gp</strong>) at the blood brain barrier (BBB) however, little is known about the interaction of <b>heroin</b> and 6 MAM with <strong>P gp</strong>.
+ABCB1	drug	opioid	24705903	The objective of this paper is to study the role of the <strong>P gp</strong> mediated efflux at the BBB in the behavioral and molecular effects of <b>heroin</b> and <b>morphine</b>.
+ABCB1	drug	opioid	24705903	We then examined the effect of inhibition of <strong>P gp</strong> on the acute nociception, locomotor activity, and gene expression modulations induced by <b>heroin</b> and <b>morphine</b>.
+ABCB1	drug	opioid	24705903	The effect of <strong>P gp</strong> inhibition during the acquisition of <b>morphine</b> induced place preference was also studied.
+ABCB1	drug	opioid	24705903	Inhibition of <strong>P gp</strong> significantly increased the uptake of <b>morphine</b> but not that of <b>heroin</b> nor 6 MAM.
+ABCB1	drug	opioid	24705903	Inhibition of <strong>P gp</strong> significantly increased <b>morphine</b> induced acute analgesia and locomotor activity but did not affect the behavioral effects of <b>heroin</b>; in addition, acute transcriptional responses to <b>morphine</b> were selectively modulated in the nucleus accumbens.
+ABCB1	drug	opioid	24705903	The present study demonstrated that acute inhibition of <strong>P gp</strong> not only modulates <b>morphine</b> induced behavioral effects but also its transcriptional effects and reinforcing properties.
+ABCB1	addiction	reward	24705903	The present study demonstrated that acute inhibition of <strong>P gp</strong> not only modulates morphine induced behavioral effects but also its transcriptional effects and <b>reinforcing</b> properties.
+ABCB1	drug	opioid	26574964	Blood samples were taken for the determination of serum levels of racemic <b>methadone</b> and its R and S enantiomers, and for typing of candidate alleles of POR, CYP2B6, <strong>ABCB1</strong>, GRIN1, OPRM1, SLC6A3, DßH and ARRB2 genes, all associated with the metabolism, tissue distribution and mechanism of action of <b>methadone</b>.
+ABCB1	drug	opioid	24489693	Impact of <strong>ABCB1</strong> and CYP2B6 genetic polymorphisms on <b>methadone</b> metabolism, dose and treatment response in patients with <b>opioid</b> addiction: a systematic review and meta analysis.
+ABCB1	addiction	addiction	24489693	Impact of <strong>ABCB1</strong> and CYP2B6 genetic polymorphisms on methadone metabolism, dose and treatment response in patients with opioid <b>addiction</b>: a systematic review and meta analysis.
+ABCB1	drug	opioid	24489693	To determine whether the CYP2B6*6 or <strong>ABCB1</strong> (rs1045642) polymorphisms are associated with variation in <b>methadone</b> response (plasma concentration, dose, or response to treatment).
+ABCB1	drug	opioid	24489693	We included studies that reported <b>methadone</b> plasma concentration, <b>methadone</b> response, or <b>methadone</b> dose in relation to the CYP2B6*6 or <strong>ABCB1</strong> polymorphisms.
+ABCB1	drug	opioid	24489693	We found no significant association between the <strong>ABCB1</strong> polymorphism and the trough (R), (S) plasma concentrations, <b>methadone</b> dose, or <b>methadone</b> response.
+ABCB1	drug	opioid	24086514	Association of polymorphisms in pharmacogenetic candidate genes (OPRD1, GAL, <strong>ABCB1</strong>, OPRM1) with <b>opioid</b> dependence in European population: a case control study.
+ABCB1	addiction	dependence	24086514	Association of polymorphisms in pharmacogenetic candidate genes (OPRD1, GAL, <strong>ABCB1</strong>, OPRM1) with opioid <b>dependence</b> in European population: a case control study.
+ABCB1	drug	opioid	24086514	Moreover, an association of the ATP binding cassette transporter 1 (<strong>ABCB1</strong>) variant rs1045642 and the Mu <b>Opioid</b> receptor (OPRM1) variant rs9479757 with <b>opioid</b> addiction was observed.
+ABCB1	addiction	addiction	24086514	Moreover, an association of the ATP binding cassette transporter 1 (<strong>ABCB1</strong>) variant rs1045642 and the Mu Opioid receptor (OPRM1) variant rs9479757 with opioid <b>addiction</b> was observed.
+ABCB1	drug	opioid	23803057	Gene polymorphisms of OPRM1 A118G and <strong>ABCB1</strong> C3435T may influence <b>opioid</b> requirements in Chinese patients with cancer pain.
+ABCB1	drug	opioid	23803057	Polymorphisms of OPRM1 A118G and <strong>ABCB1</strong> C3435T have been suggested to contribute to inter individual variability regarding pain sensitivity, <b>opioid</b> usage, tolerance and dependence and incidence of adverse effects in patients with chronic pain.
+ABCB1	addiction	dependence	23803057	Polymorphisms of OPRM1 A118G and <strong>ABCB1</strong> C3435T have been suggested to contribute to inter individual variability regarding pain sensitivity, opioid usage, tolerance and <b>dependence</b> and incidence of adverse effects in patients with chronic pain.
+ABCB1	drug	opioid	23803057	Compared with CC/CT, patients with <strong>ABCB1</strong> TT genotype received higher 24h  and weight surface area adjusted 24h  <b>opioids</b> doses (P=0.057 and 0.028, respectively).
+ABCB1	drug	opioid	23632726	Single nucleotide polymorphisms (SNPs) in the μ <b>opioid</b> receptor (OPRM1), multidrug resistance (<strong>ABCB1</strong>), and catechol o methyltransferase (COMT) genes are associated with risk for <b>opioid</b> addiction in adults.
+ABCB1	addiction	addiction	23632726	Single nucleotide polymorphisms (SNPs) in the μ opioid receptor (OPRM1), multidrug resistance (<strong>ABCB1</strong>), and catechol o methyltransferase (COMT) genes are associated with risk for opioid <b>addiction</b> in adults.
+ABCB1	drug	opioid	23527191	Functional impact of <strong>ABCB1</strong> variants on interactions between P glycoprotein and <b>methadone</b>.
+ABCB1	drug	opioid	23527191	Large inter individual variability has been observed in <b>methadone</b> maintenance dosages and P glycoprotein (<strong>P gp</strong>) was considered to be one of the major contributors.
+ABCB1	drug	opioid	23527191	To investigate the mechanism of <strong>P gp</strong>'s interaction with <b>methadone</b>, as well as the effect of genetic variants on the interaction, Flp In™ 293 cells stably transfected with various genotypes of human <strong>P gp</strong> were established in the present study.
+ABCB1	drug	opioid	23527191	Utilizing rhodamine 123 efflux assay and calcein AM uptake study, <b>methadone</b> was demonstrated to be an inhibitor of wild type human <strong>P gp</strong> via non competitive kinetic (IC50 = 2.17±0.10 µM), while the variant type human <strong>P gp</strong>, <strong>P gp</strong> with 1236T 2677T 3435T genotype and <strong>P gp</strong> with 1236T 2677A 3435T genotype, showed less inhibition potency (IC50 = 2.97±0.09 µM and 4.43±1.10 µM, respectively) via uncompetitive kinetics.
+ABCB1	drug	opioid	23527191	<b>Methadone</b> also stimulated <strong>P gp</strong> ATPase and inhibited verapamil stimulated <strong>P gp</strong> ATPase activity under therapeutic concentrations.
+ABCB1	drug	opioid	23527191	These results may provide a possible explanation for higher <b>methadone</b> dosage requirements in patients carrying variant type of <strong>P gp</strong> and revealed the possible drug drug interactions in patients who receive concomitant drugs which are also <strong>P gp</strong> substrates.
+ABCB1	drug	cocaine	24892317	The present results indicate that the VNTR  6R polymorphism of the gene SLC6A3 and the genotype 3435CC in the <strong>ABCB1</strong> gene, are both associated with addictive behavior to heroin or <b>cocaine</b>.
+ABCB1	drug	opioid	24892317	The present results indicate that the VNTR  6R polymorphism of the gene SLC6A3 and the genotype 3435CC in the <strong>ABCB1</strong> gene, are both associated with addictive behavior to <b>heroin</b> or cocaine.
+ABCB1	addiction	addiction	24892317	The present results indicate that the VNTR  6R polymorphism of the gene SLC6A3 and the genotype 3435CC in the <strong>ABCB1</strong> gene, are both associated with <b>addictive</b> behavior to heroin or cocaine.
+ABCB1	drug	nicotine	23212563	Studies on knockout mice showed that the OCT Oct1 3, <strong>P gp</strong>, and Bcrp did not alter [(3)H] <b>nicotine</b> transport at the BBB.
+ABCB1	drug	opioid	26019822	Acute kidney injury in a preterm infant homozygous for the C3435T polymorphism in the <strong>ABCB1</strong> gene given oral <b>morphine</b>.
+ABCB1	drug	opioid	22845665	Subchronic <b>morphine</b> treatment induces P glycoprotein (<strong>P gp</strong>) up regulation at the blood brain barrier.
+ABCB1	drug	opioid	22845665	This study investigates the rate and extent to which <strong>P gp</strong> and breast cancer resistance protein (Bcrp) increase at the rat blood brain barrier following subchronic <b>morphine</b> treatment.
+ABCB1	drug	opioid	22845665	The gene and protein expression of <strong>P gp</strong> and Bcrp in <b>morphine</b> treated and control rats were compared by qRT PCR and western blotting.
+ABCB1	drug	opioid	22845665	The levels of Mdr1a and Bcrp mRNAs were not significantly modified 6 h post <b>morphine</b>, but the Mdr1a mRNA increased 1.4 fold and Bcrp mRNA 2.4 fold at 24 h. <strong>P gp</strong> and Bcrp protein expression in brain microvessels was unchanged 6 h post <b>morphine</b> and increased 1.5 fold at 24 h. This effect was more pronounced in large vessels than in microvessels.
+ABCB1	drug	opioid	22845665	However, extracellular <b>morphine</b> concentrations of 0.01 10 μM did not modify the expressions of the <strong>MDR1</strong> and BCRP genes in hCMEC/D3 human endothelial brain cells in vitro.
+ABCB1	drug	opioid	22845665	MK 801 (NMDA antagonist) and meloxicam (cyclo oxygenase 2 inhibitor) given after <b>morphine</b> treatment completely blocked <strong>P gp</strong> and Bcrp up regulation.
+ABCB1	drug	opioid	22845665	Thus, <b>morphine</b> does not directly stimulate <strong>P gp</strong> and Bcrp expression by the brain endothelium, but glutamate released during <b>morphine</b> withdrawal may do so by activating the NMDA/cyclo oxygenase 2 cascade.
+ABCB1	addiction	withdrawal	22845665	Thus, morphine does not directly stimulate <strong>P gp</strong> and Bcrp expression by the brain endothelium, but glutamate released during morphine <b>withdrawal</b> may do so by activating the NMDA/cyclo oxygenase 2 cascade.
+ABCB1	drug	amphetamine	22426312	Apolipoprotein E controls adenosine triphosphate binding cassette transporters <strong>ABCB1</strong> and ABCC1 on cerebral microvessels after <b>methamphetamine</b> intoxication.
+ABCB1	addiction	intoxication	22426312	Apolipoprotein E controls adenosine triphosphate binding cassette transporters <strong>ABCB1</strong> and ABCC1 on cerebral microvessels after methamphetamine <b>intoxication</b>.
+ABCB1	drug	amphetamine	22426312	<b>Methamphetamine</b> transiently increased the expression of the luminal adenosine triphosphate binding cassette transporter <strong>ABCB1</strong> on cerebral microvessels and reduced the expression of the abluminal transporter ABCC1.
+ABCB1	drug	amphetamine	22426312	Elevated expression of ApoE was noted in the brain parenchyma by <b>methamphetamine</b>, activating ApoE receptor 2 on brain capillaries, deactivating c Jun N terminal kinase 1/2 and c Jun, and regulating <strong>ABCB1</strong> and ABCC1 expression.
+ABCB1	drug	opioid	21790905	The results remain significant after controlling for age, sex and the <strong>ABCB1</strong> SNP 1236C>T (rs1128503), which was previously shown to be associated with high <b>methadone</b> dose requirement in this population (P=0.006, 0.030, respectively).
+ABCB1	drug	opioid	21589866	Contribution of cytochrome P450 and <strong>ABCB1</strong> genetic variability on <b>methadone</b> pharmacokinetics, dose requirements, and response.
+ABCB1	drug	opioid	21209234	The aim of this study was to evaluate the plasma dispositions of <b>oxycodone</b> and its demethylates and dose escalation based on genetic polymorphisms of CYP2D6, CYP3A5, <strong>ABCB1</strong>, and OPRM1 in cancer patients receiving <b>oxycodone</b>.
+ABCB1	addiction	addiction	21209234	The aim of this study was to evaluate the plasma dispositions of oxycodone and its demethylates and dose <b>escalation</b> based on genetic polymorphisms of CYP2D6, CYP3A5, <strong>ABCB1</strong>, and OPRM1 in cancer patients receiving oxycodone.
+ABCB1	drug	opioid	21050174	A growing body of evidence suggests that P glycoprotein (<strong>P gp</strong>), an efflux transporter, may contribute a systems level approach to the development of <b>opioid</b> tolerance.
+ABCB1	drug	opioid	21050174	Herein, we describe current in vitro and in vivo methodology available to analyze interactions between <b>opioids</b> and <strong>P gp</strong> and critically analyze <strong>P gp</strong> data associated with six commonly used mu <b>opioids</b> to include <b>morphine</b>, <b>methadone</b>, loperamide, meperidine, <b>oxycodone</b>, and <b>fentanyl</b>.
+ABCB1	drug	opioid	21050174	Recent studies focused on the development of <b>opioids</b> lacking <strong>P gp</strong> substrate activity are explored, concentrating on structure activity relationships to develop an optimal <b>opioid</b> analgesic lacking this systems level contribution to tolerance development.
+ABCB1	drug	opioid	21050174	Continued work in this area will potentially allow for delineation of the mechanism responsible for <b>opioid</b> related <strong>P gp</strong> up regulation and provide further support for evidence based medicine supporting clinical <b>opioid</b> rotation.
+ABCB1	drug	opioid	20201854	In addition, we provide the first evidence of a cis acting polymorphism and a functional haplotype in the PDYN gene, of significantly higher DNA methylation rate of the OPRM1 gene in the lymphocytes of <b>heroin</b> addicts, and significant differences in genotype frequencies of three single nucleotide polymorphisms of the P glycoprotein gene (<strong>ABCB1</strong>) between "higher" and "lower" <b>methadone</b> doses in <b>methadone</b> maintained patients.
+ABCB1	drug	cannabinoid	19887017	The limited data obtained using in vitro models indicate that methadone, buprenorphine, and <b>cannabinoids</b> may interact with human <strong>P gp</strong>; but almost nothing is known about drugs of abuse and BCRP.
+ABCB1	drug	opioid	19887017	The limited data obtained using in vitro models indicate that <b>methadone</b>, <b>buprenorphine</b>, and cannabinoids may interact with human <strong>P gp</strong>; but almost nothing is known about drugs of abuse and BCRP.
+ABCB1	drug	amphetamine	19887017	We used in vitro <strong>P gp</strong> and BCRP inhibition flow cytometric assays with hMDR1  and hBCRP transfected HEK293 cells to test 14 compounds or metabolites frequently involved in addiction, including buprenorphine, norbuprenorphine, methadone, ibogaine, cocaine, cocaethylene, <b>amphetamine</b>, N methyl 3,4 methylenedioxyamphetamine, 3,4 methylenedioxyamphetamine, nicotine, ketamine, Delta9 tetrahydrocannabinol (THC), naloxone, and morphine.
+ABCB1	drug	cannabinoid	19887017	We used in vitro <strong>P gp</strong> and BCRP inhibition flow cytometric assays with hMDR1  and hBCRP transfected HEK293 cells to test 14 compounds or metabolites frequently involved in addiction, including buprenorphine, norbuprenorphine, methadone, ibogaine, cocaine, cocaethylene, amphetamine, N methyl 3,4 methylenedioxyamphetamine, 3,4 methylenedioxyamphetamine, nicotine, ketamine, Delta9 <b>tetrahydrocannabinol</b> (<b>THC</b>), naloxone, and morphine.
+ABCB1	drug	cocaine	19887017	We used in vitro <strong>P gp</strong> and BCRP inhibition flow cytometric assays with hMDR1  and hBCRP transfected HEK293 cells to test 14 compounds or metabolites frequently involved in addiction, including buprenorphine, norbuprenorphine, methadone, ibogaine, <b>cocaine</b>, cocaethylene, amphetamine, N methyl 3,4 methylenedioxyamphetamine, 3,4 methylenedioxyamphetamine, nicotine, ketamine, Delta9 tetrahydrocannabinol (THC), naloxone, and morphine.
+ABCB1	drug	nicotine	19887017	We used in vitro <strong>P gp</strong> and BCRP inhibition flow cytometric assays with hMDR1  and hBCRP transfected HEK293 cells to test 14 compounds or metabolites frequently involved in addiction, including buprenorphine, norbuprenorphine, methadone, ibogaine, cocaine, cocaethylene, amphetamine, N methyl 3,4 methylenedioxyamphetamine, 3,4 methylenedioxyamphetamine, <b>nicotine</b>, ketamine, Delta9 tetrahydrocannabinol (THC), naloxone, and morphine.
+ABCB1	drug	opioid	19887017	We used in vitro <strong>P gp</strong> and BCRP inhibition flow cytometric assays with hMDR1  and hBCRP transfected HEK293 cells to test 14 compounds or metabolites frequently involved in addiction, including <b>buprenorphine</b>, norbuprenorphine, <b>methadone</b>, ibogaine, cocaine, cocaethylene, amphetamine, N methyl 3,4 methylenedioxyamphetamine, 3,4 methylenedioxyamphetamine, nicotine, ketamine, Delta9 tetrahydrocannabinol (THC), <b>naloxone</b>, and <b>morphine</b>.
+ABCB1	drug	psychedelics	19887017	We used in vitro <strong>P gp</strong> and BCRP inhibition flow cytometric assays with hMDR1  and hBCRP transfected HEK293 cells to test 14 compounds or metabolites frequently involved in addiction, including buprenorphine, norbuprenorphine, methadone, <b>ibogaine</b>, cocaine, cocaethylene, amphetamine, N methyl 3,4 methylenedioxyamphetamine, 3,4 methylenedioxyamphetamine, nicotine, <b>ketamine</b>, Delta9 tetrahydrocannabinol (THC), naloxone, and morphine.
+ABCB1	addiction	addiction	19887017	We used in vitro <strong>P gp</strong> and BCRP inhibition flow cytometric assays with hMDR1  and hBCRP transfected HEK293 cells to test 14 compounds or metabolites frequently involved in <b>addiction</b>, including buprenorphine, norbuprenorphine, methadone, ibogaine, cocaine, cocaethylene, amphetamine, N methyl 3,4 methylenedioxyamphetamine, 3,4 methylenedioxyamphetamine, nicotine, ketamine, Delta9 tetrahydrocannabinol (THC), naloxone, and morphine.
+ABCB1	drug	cannabinoid	19887017	Human <strong>P gp</strong> was significantly inhibited in a concentration dependent manner by norbuprenorphine>buprenorphine>methadone>ibogaine and <b>THC</b>.
+ABCB1	drug	opioid	19887017	Human <strong>P gp</strong> was significantly inhibited in a concentration dependent manner by norbuprenorphine><b>buprenorphine</b>><b>methadone</b>>ibogaine and THC.
+ABCB1	drug	psychedelics	19887017	Human <strong>P gp</strong> was significantly inhibited in a concentration dependent manner by norbuprenorphine>buprenorphine>methadone><b>ibogaine</b> and THC.
+ABCB1	drug	opioid	19887017	Norbuprenorphine (transport efflux ratio approoximately 11) and <b>methadone</b> (transport efflux ratio approoximately 1.9) transport was <strong>P gp</strong> mediated; however, with no significant stereo selectivity regarding <b>methadone</b> enantiomers.
+ABCB1	drug	cannabinoid	19625010	Association between <strong>ABCB1</strong> C3435T polymorphism and increased risk of <b>cannabis</b> dependence.
+ABCB1	addiction	dependence	19625010	Association between <strong>ABCB1</strong> C3435T polymorphism and increased risk of cannabis <b>dependence</b>.
+ABCB1	drug	cannabinoid	19625010	<strong>ABCB1</strong> polymorphisms are known to modify drug pharmacokinetics but have yet to be studied for their role in generating and maintaining <b>cannabis</b> dependence.
+ABCB1	addiction	dependence	19625010	<strong>ABCB1</strong> polymorphisms are known to modify drug pharmacokinetics but have yet to be studied for their role in generating and maintaining cannabis <b>dependence</b>.
+ABCB1	drug	cannabinoid	19625010	The objective of this study is to determine if <strong>ABCB1</strong> C3435T polymorphism may represent an independent genetic marker for <b>cannabis</b> dependence risk.
+ABCB1	addiction	dependence	19625010	The objective of this study is to determine if <strong>ABCB1</strong> C3435T polymorphism may represent an independent genetic marker for cannabis <b>dependence</b> risk.
+ABCB1	drug	cannabinoid	19625010	Independent association between <strong>ABCB1</strong> C3435T SNP marker and <b>cannabis</b> dependence was evaluated using multiple logistic regression analysis.
+ABCB1	addiction	dependence	19625010	Independent association between <strong>ABCB1</strong> C3435T SNP marker and cannabis <b>dependence</b> was evaluated using multiple logistic regression analysis.
+ABCB1	addiction	dependence	19625010	<strong>ABCB1</strong> polymorphisms may alter Delta9THC distribution, its psychoactive effects and individual vulnerability to <b>dependence</b>.
+ABCB1	drug	opioid	19370547	Differential involvement of P glycoprotein (<strong>ABCB1</strong>) in permeability, tissue distribution, and antinociceptive activity of <b>methadone</b>, <b>buprenorphine</b>, and diprenorphine: in vitro and in vivo evaluation.
+ABCB1	drug	opioid	19370547	Conclusions based on either in vitro or in vivo approach to evaluate the <strong>P gp</strong> affinity status of <b>opioids</b> may be misleading.
+ABCB1	drug	opioid	19370547	For example, in vitro studies indicated that <b>fentanyl</b> is a <strong>P gp</strong> inhibitor while in vivo studies indicated that it is a <strong>P gp</strong> substrate.
+ABCB1	drug	opioid	19370547	The objective of this study was to evaluate the <strong>P gp</strong> affinity status of <b>methadone</b>, <b>buprenorphine</b> and diprenorphine to predict <strong>P gp</strong> mediated drug drug interactions and to determine a better candidate for management of <b>opioid</b> dependence.
+ABCB1	addiction	dependence	19370547	The objective of this study was to evaluate the <strong>P gp</strong> affinity status of methadone, buprenorphine and diprenorphine to predict <strong>P gp</strong> mediated drug drug interactions and to determine a better candidate for management of opioid <b>dependence</b>.
+ABCB1	drug	opioid	19370547	<b>Methadone</b> stimulated the <strong>P gp</strong> ATPase activity only at higher concentrations, while verapamil and GF120918 inhibited its efflux (p < 0.05).
+ABCB1	drug	opioid	19370547	The brain distribution and antinociceptive activity of <b>methadone</b> were enhanced (p < 0.05) in <strong>P gp</strong> knockout mice.
+ABCB1	drug	opioid	19370547	<strong>P gp</strong> can affect the PK/PD of <b>methadone</b>, but not <b>buprenorphine</b> or diprenorphine.
+ABCB1	drug	opioid	19370547	<b>Buprenorphine</b> most likely is not a <strong>P gp</strong> substrate and concerns regarding <strong>P gp</strong> mediated drug drug interaction are not expected.
+ABCB1	drug	opioid	18424454	<strong>ABCB1</strong> (MDR1) genetic variants are associated with <b>methadone</b> doses required for effective treatment of <b>heroin</b> dependence.
+ABCB1	addiction	dependence	18424454	<strong>ABCB1</strong> (MDR1) genetic variants are associated with methadone doses required for effective treatment of heroin <b>dependence</b>.
+ABCB1	drug	opioid	18424454	<strong>ABCB1</strong> (<strong>MDR1</strong>) genetic variants are associated with <b>methadone</b> doses required for effective treatment of <b>heroin</b> dependence.
+ABCB1	addiction	dependence	18424454	<strong>ABCB1</strong> (<strong>MDR1</strong>) genetic variants are associated with methadone doses required for effective treatment of heroin <b>dependence</b>.
+ABCB1	drug	opioid	18424454	<b>Methadone</b> is a substrate of the transporter P glycoprotein (P gp) 170 that is encoded by the <strong>ABCB1</strong> (MDR1) gene.
+ABCB1	drug	opioid	18424454	<b>Methadone</b> is a substrate of the transporter P glycoprotein (P gp) 170 that is encoded by the <strong>ABCB1</strong> (<strong>MDR1</strong>) gene.
+ABCB1	drug	opioid	18424454	<b>Methadone</b> is a substrate of the transporter P glycoprotein (<strong>P gp</strong>) 170 that is encoded by the <strong>ABCB1</strong> (<strong>MDR1</strong>) gene.
+ABCB1	drug	opioid	18424454	Thus, <strong>P gp</strong> variants may play a role in <b>methadone</b> absorption and distribution.
+ABCB1	drug	opioid	18424454	We assessed the association between <strong>ABCB1</strong> polymorphisms and <b>methadone</b> dose requirements in 98 <b>methadone</b> maintained patients.
+ABCB1	drug	opioid	18424454	These data suggest that specific <strong>ABCB1</strong> variants may have clinical relevance by influencing the <b>methadone</b> dose required to prevent withdrawal symptoms and relapse in this population.
+ABCB1	addiction	relapse	18424454	These data suggest that specific <strong>ABCB1</strong> variants may have clinical relevance by influencing the methadone dose required to prevent withdrawal symptoms and <b>relapse</b> in this population.
+ABCB1	addiction	withdrawal	18424454	These data suggest that specific <strong>ABCB1</strong> variants may have clinical relevance by influencing the methadone dose required to prevent <b>withdrawal</b> symptoms and relapse in this population.
+ABCB1	drug	opioid	18422375	Genetic polymorphisms in genes coding for <b>methadone</b> metabolizing enzymes, transporter proteins (p glycoprotein; <strong>P gp</strong>), and mu <b>opioid</b> receptors may explain part of the observed interindividual variation in the pharmacokinetics and pharmacodynamics of <b>methadone</b>.
+ABCB1	drug	opioid	18422375	<b>Methadone</b> is a P gp substrate, and, although there are inconsistent reports, <strong>ABCB1</strong> genetic polymorphisms also contribute slightly to the interindividual variability of <b>methadone</b> kinetics and influence dose requirements.
+ABCB1	drug	opioid	18422375	<b>Methadone</b> is a <strong>P gp</strong> substrate, and, although there are inconsistent reports, <strong>ABCB1</strong> genetic polymorphisms also contribute slightly to the interindividual variability of <b>methadone</b> kinetics and influence dose requirements.
+ABCB1	drug	opioid	17690563	Using a cellular model, we aimed to determine if <b>methadone</b>, LAAM and their main metabolites are substrates of the human P glycoprotein transporter (P gp), which is encoded by the <strong>ABCB1</strong> gene, and whether <b>methadone</b> transport exhibits stereoselectivity.
+ABCB1	drug	opioid	17690563	Using a cellular model, we aimed to determine if <b>methadone</b>, LAAM and their main metabolites are substrates of the human P glycoprotein transporter (<strong>P gp</strong>), which is encoded by the <strong>ABCB1</strong> gene, and whether <b>methadone</b> transport exhibits stereoselectivity.
+ABCB1	drug	opioid	17690563	Pig kidney epithelial cells (control) and human <strong>ABCB1</strong> transfected cells were incubated with <b>methadone</b>, LAAM and their metabolites, and their intra  and extracellular concentrations were measured.
+ABCB1	drug	opioid	17690563	The intra  to extracellular ratios of <b>methadone</b>, LAAM and their metabolites were all decreased in <strong>ABCB1</strong> transfected cells compared to controls (p < 0.05), thus indicating that they are substrates of P gp.
+ABCB1	drug	opioid	17690563	The intra  to extracellular ratios of <b>methadone</b>, LAAM and their metabolites were all decreased in <strong>ABCB1</strong> transfected cells compared to controls (p < 0.05), thus indicating that they are substrates of <strong>P gp</strong>.
+ABCB1	drug	opioid	17690563	<strong>P gp</strong> may therefore affect the pharmacokinetics and pharmacodynamics of <b>methadone</b> and LAAM.
+ABCB1	drug	opioid	17339873	Some <b>opioids</b> are P glycoprotein substrates, whereas, <strong>ABCB1</strong> genotypes inconsistently influence <b>opioid</b> pharmacodynamics and dosage requirements.
+ABCB1	drug	opioid	17178268	<strong>ABCB1</strong> genetic variability and <b>methadone</b> dosage requirements in <b>opioid</b> dependent individuals.
+ABCB1	drug	opioid	17178268	<b>Methadone</b> is a substrate for the P glycoprotein transporter, encoded by the <strong>ABCB1</strong> gene, which regulates central nervous system exposure.
+ABCB1	drug	opioid	17178268	This retrospective study aimed to investigate the influence of <strong>ABCB1</strong> genetic variability on <b>methadone</b> dose requirements.
+ABCB1	drug	opioid	17178268	<strong>ABCB1</strong> genetic variability influenced daily <b>methadone</b> dose requirements, such that subjects carrying 2 copies of the wild type haplotype required higher doses compared with those with 1 copy and those with no copies (98.3 +/  10.4, 58.6 +/  20.9, and 55.4 +/  26.1 mg/d, respectively; P = .029).
+ABCB1	drug	opioid	17178268	Although <strong>ABCB1</strong> genetic variability is not related to the development of <b>opioid</b> dependence, identification of variant haplotypes may, after larger prospective studies have been performed, provide clinicians with a tool for <b>methadone</b> dosage individualization.
+ABCB1	addiction	dependence	17178268	Although <strong>ABCB1</strong> genetic variability is not related to the development of opioid <b>dependence</b>, identification of variant haplotypes may, after larger prospective studies have been performed, provide clinicians with a tool for methadone dosage individualization.
+ABCB1	addiction	dependence	12721332	The objective of the present study was to examine the time course and concentration <b>dependence</b> of modulation of P glycoprotein (<strong>P gp</strong>) activity in the blood brain barrier (BBB) with consequent influence on substrate uptake into brain tissue.
+ABCB1	drug	opioid	12721332	Potential <strong>P gp</strong> inducers (rifampin and <b>morphine</b>) were administered subchorionically to <strong>P gp</strong> competent [mdr1a(+/+)] mice to induce <strong>P gp</strong> expression in brain; the impact of rifampin pretreatment on brain penetration of verapamil also was evaluated with an in situ brain perfusion technique.
+ABCB1	drug	opioid	12721332	Chronic exposure to rifampin or <b>morphine</b> induced <strong>P gp</strong> expression in mouse brain to a modest extent.
+ABCB1	drug	benzodiazepine	12676880	Two enzyme inhibitors, ketoconazole and <b>midazolam</b>, were coperfused in rat intestinal lumen with tacrolimus to specify the effect of <strong>P gp</strong> and P450.
+ABCB1	drug	benzodiazepine	12676880	However, <b>midazolam</b> failed to enhance the absorption of tacrolimus, indicating the dominant role of P glycoprotein (<strong>P gp</strong>) mediated efflux in the lower region.
+ABCB1	drug	opioid	11964599	The transcellular movement of the various <b>opioids</b>, including loperamide and <b>morphine</b>, was assessed in L <strong>MDR1</strong> (expressing P glycoprotein) and LLC PK1 cell monolayers (P glycoprotein expression absent).
+ABCB1	drug	opioid	11964599	<b>Morphine</b> also showed a basal to apical gradient in the L <strong>MDR1</strong> cell monolayer, indicating that it too is a P glycoprotein substrate, but with less dependence than loperamide in that only 1.5 fold greater basal apical directional transport was observed.
+ABCB1	addiction	dependence	11964599	Morphine also showed a basal to apical gradient in the L <strong>MDR1</strong> cell monolayer, indicating that it too is a P glycoprotein substrate, but with less <b>dependence</b> than loperamide in that only 1.5 fold greater basal apical directional transport was observed.
+ABCB1	drug	alcohol	1360981	Lower doses of A2C (0.6 microM) and benzyl <b>alcohol</b> (1 mM) failed to influence either lipid fluidity or <strong>P gp</strong> mediated drug accumulation.
+ARGININE\ VASOPRESSIN	drug	alcohol	31386210	Amygdala <strong>Arginine Vasopressin</strong> Modulates Chronic <b>Ethanol</b> Withdrawal Anxiety Like Behavior in the Social Interaction Task.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	31386210	Amygdala <strong>Arginine Vasopressin</strong> Modulates Chronic Ethanol <b>Withdrawal</b> Anxiety Like Behavior in the Social Interaction Task.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	31386210	The central nucleus of the amygdala (CEA) regulates anxiety like behavior induced by <b>withdrawal</b> from chronic intermittent EtOH (CIE) exposure, and the <strong>arginine vasopressin</strong> (AVP) system within the CEA regulates many anxiety like behaviors.
+ARGININE\ VASOPRESSIN	drug	alcohol	31339663	For stress genes, nPE1 /  had lowered basal Oxt (oxytocin) and Avp (<strong>arginine vasopressin</strong>) that were restored by low <b>alcohol</b> intake to basal levels of nPE1+/+ .
+ARGININE\ VASOPRESSIN	drug	alcohol	29669731	Addiction to specific drugs such as <b>alcohol</b>, psychostimulants, and opioids shares some common direct or downstream effects on the brain's stress responsive systems, including <strong>arginine vasopressin</strong> and its V1b receptors, dynorphin and the κ opioid receptors, pro opiomelanocortin/β endorphin and the μ opioid receptors, and the endocannabinoids.
+ARGININE\ VASOPRESSIN	drug	cannabinoid	29669731	Addiction to specific drugs such as alcohol, psychostimulants, and opioids shares some common direct or downstream effects on the brain's stress responsive systems, including <strong>arginine vasopressin</strong> and its V1b receptors, dynorphin and the κ opioid receptors, pro opiomelanocortin/β endorphin and the μ opioid receptors, and the <b>endocannabinoids</b>.
+ARGININE\ VASOPRESSIN	drug	opioid	29669731	Addiction to specific drugs such as alcohol, psychostimulants, and <b>opioids</b> shares some common direct or downstream effects on the brain's stress responsive systems, including <strong>arginine vasopressin</strong> and its V1b receptors, dynorphin and the κ <b>opioid</b> receptors, pro opiomelanocortin/β endorphin and the μ <b>opioid</b> receptors, and the endocannabinoids.
+ARGININE\ VASOPRESSIN	addiction	addiction	29669731	<b>Addiction</b> to specific drugs such as alcohol, psychostimulants, and opioids shares some common direct or downstream effects on the brain's stress responsive systems, including <strong>arginine vasopressin</strong> and its V1b receptors, dynorphin and the κ opioid receptors, pro opiomelanocortin/β endorphin and the μ opioid receptors, and the endocannabinoids.
+ARGININE\ VASOPRESSIN	drug	psychedelics	28855876	The Non Peptide <strong>Arginine Vasopressin</strong> v1a Selective Receptor Antagonist, SR49059, Blocks the Rewarding, Prosocial, and Anxiolytic Effects of 3,4 <b>Methylenedioxymethamphetamine</b> and Its Derivatives in Zebra Fish.
+ARGININE\ VASOPRESSIN	drug	amphetamine	28842817	Here, we show that <b>METH</b> administration produced time dependent increases in the expression of corticotropin releasing hormone (Crh/Crf), <strong>arginine vasopressin</strong> (Avp), and cocaine  and <b>amphetamine</b> regulated transcript prepropeptide (Cartpt) mRNAs in the rat nucleus accumbens (NAc).
+ARGININE\ VASOPRESSIN	drug	cocaine	28842817	Here, we show that METH administration produced time dependent increases in the expression of corticotropin releasing hormone (Crh/Crf), <strong>arginine vasopressin</strong> (Avp), and <b>cocaine</b>  and amphetamine regulated transcript prepropeptide (Cartpt) mRNAs in the rat nucleus accumbens (NAc).
+ARGININE\ VASOPRESSIN	drug	alcohol	26969417	Single Dose Interaction Study of the <strong>Arginine Vasopressin</strong> Type 1B Receptor Antagonist ABT 436 and <b>Alcohol</b> in Moderate <b>Alcohol</b> Drinkers.
+ARGININE\ VASOPRESSIN	drug	opioid	25446223	<strong>Arginine vasopressin</strong> (AVP) and its V1b receptor, components of the brain stress responsive systems, play a role in <b>heroin</b> seeking behavior triggered by foot shock (FS) stress in rats.
+ARGININE\ VASOPRESSIN	addiction	relapse	25446223	<strong>Arginine vasopressin</strong> (AVP) and its V1b receptor, components of the brain stress responsive systems, play a role in heroin <b>seeking</b> behavior triggered by foot shock (FS) stress in rats.
+ARGININE\ VASOPRESSIN	drug	alcohol	24002017	Acute <b>ethanol</b> intoxication (AEI) attenuates the <strong>arginine vasopressin</strong> (AVP) response to hemorrhage leading to impaired hemodynamic counter regulation and accentuated hemodynamic stability.
+ARGININE\ VASOPRESSIN	addiction	intoxication	24002017	Acute ethanol <b>intoxication</b> (AEI) attenuates the <strong>arginine vasopressin</strong> (AVP) response to hemorrhage leading to impaired hemodynamic counter regulation and accentuated hemodynamic stability.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	23805290	Neuropeptide Y (NPY) and <strong>arginine vasopressin</strong> (AVP) mRNA levels were transiently increased during opiate <b>withdrawal</b>.
+ARGININE\ VASOPRESSIN	addiction	addiction	23406607	Apart from cortisol, <strong>arginine vasopressin</strong> peptide (AVP), and atrial natriuretic peptide (ANP) are known to directly impact upon the HPA axis in <b>addictive</b> behavior.
+ARGININE\ VASOPRESSIN	drug	alcohol	23147176	Acute <b>alcohol</b> intoxication (AAI) impairs the hemodynamic and <strong>arginine vasopressin</strong> (AVP) counter regulation to hemorrhagic shock (HS) and lactated Ringer's solution (LR) fluid resuscitation (FR).
+ARGININE\ VASOPRESSIN	addiction	intoxication	23147176	Acute alcohol <b>intoxication</b> (AAI) impairs the hemodynamic and <strong>arginine vasopressin</strong> (AVP) counter regulation to hemorrhagic shock (HS) and lactated Ringer's solution (LR) fluid resuscitation (FR).
+ARGININE\ VASOPRESSIN	drug	alcohol	22384198	We have previously shown that repeated binge pattern <b>alcohol</b> exposure increased the expression of two critical central regulators of stress and anxiety, corticotrophin releasing hormone (CRH) and <strong>arginine vasopressin</strong> (AVP), in adolescent male rats.
+ARGININE\ VASOPRESSIN	addiction	intoxication	22384198	We have previously shown that repeated <b>binge</b> pattern alcohol exposure increased the expression of two critical central regulators of stress and anxiety, corticotrophin releasing hormone (CRH) and <strong>arginine vasopressin</strong> (AVP), in adolescent male rats.
+ARGININE\ VASOPRESSIN	drug	cocaine	21677651	Persistent increase in hypothalamic <strong>arginine vasopressin</strong> gene expression during protracted withdrawal from chronic escalating dose <b>cocaine</b> in rodents.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	21677651	Persistent increase in hypothalamic <strong>arginine vasopressin</strong> gene expression during protracted <b>withdrawal</b> from chronic escalating dose cocaine in rodents.
+ARGININE\ VASOPRESSIN	drug	alcohol	21575018	Involvement of <strong>arginine vasopressin</strong> and V1b receptor in <b>alcohol</b> drinking in Sardinian <b>alcohol</b> preferring rats.
+ARGININE\ VASOPRESSIN	drug	cocaine	21575018	Recent animal studies have shown that the level of stress responsive <strong>arginine vasopressin</strong> (AVP) gene expression in the amygdala is increased during early withdrawal from long term heroin or <b>cocaine</b> administration.
+ARGININE\ VASOPRESSIN	drug	opioid	21575018	Recent animal studies have shown that the level of stress responsive <strong>arginine vasopressin</strong> (AVP) gene expression in the amygdala is increased during early withdrawal from long term <b>heroin</b> or cocaine administration.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	21575018	Recent animal studies have shown that the level of stress responsive <strong>arginine vasopressin</strong> (AVP) gene expression in the amygdala is increased during early <b>withdrawal</b> from long term heroin or cocaine administration.
+ARGININE\ VASOPRESSIN	drug	alcohol	21533237	Our previous studies showed that binge pattern <b>ethanol</b> (EtOH) treatment during pubertal development negatively dysregulated the responsiveness of the hypothalamo pituitary adrenal (HPA) axis, as manifested by alterations in corticotrophin releasing hormone (CRH), <strong>arginine vasopressin</strong> (AVP), and corticosterone (CORT) during this time period.
+ARGININE\ VASOPRESSIN	addiction	intoxication	21533237	Our previous studies showed that <b>binge</b> pattern ethanol (EtOH) treatment during pubertal development negatively dysregulated the responsiveness of the hypothalamo pituitary adrenal (HPA) axis, as manifested by alterations in corticotrophin releasing hormone (CRH), <strong>arginine vasopressin</strong> (AVP), and corticosterone (CORT) during this time period.
+ARGININE\ VASOPRESSIN	drug	opioid	20458554	We developed a new model of traumatic complete cervical SCI in piglets and measured acute hemodynamic variables and serum <strong>arginine vasopressin</strong> (AVP) concentrations at baseline and for 4 h after SCI under <b>fentanyl</b> anesthesia.
+ARGININE\ VASOPRESSIN	drug	alcohol	19952347	In this study, we determined the effects of binge <b>ethanol</b> exposure during puberty on two critical central regulators of stress and anxiety behavior: corticotrophin releasing hormone (CRH) and <strong>arginine vasopressin</strong> (AVP).
+ARGININE\ VASOPRESSIN	addiction	intoxication	19952347	In this study, we determined the effects of <b>binge</b> ethanol exposure during puberty on two critical central regulators of stress and anxiety behavior: corticotrophin releasing hormone (CRH) and <strong>arginine vasopressin</strong> (AVP).
+ARGININE\ VASOPRESSIN	drug	cocaine	19596360	<strong>Arginine vasopressin</strong> gene expression changes within the nucleus accumbens during environment elicited <b>cocaine</b> conditioned response in rats.
+ARGININE\ VASOPRESSIN	drug	cocaine	19596360	We found that the gene for <strong>arginine vasopressin</strong> (AVP) was differentially expressed on experimental subjects during all stages of environment elicited <b>cocaine</b> conditioning.
+ARGININE\ VASOPRESSIN	drug	alcohol	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), <strong>arginine vasopressin</strong> (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as <b>alcohol</b> dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and diazepam binding inhibitor (DBI).
+ARGININE\ VASOPRESSIN	drug	benzodiazepine	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), <strong>arginine vasopressin</strong> (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as alcohol dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and <b>diazepam</b> binding inhibitor (DBI).
+ARGININE\ VASOPRESSIN	drug	cocaine	19155191	orexin, <strong>arginine vasopressin</strong>, V1b receptor, and corticotropin releasing factor), hypothalamic pituitary adrenal axis, and neurotransmitters (especially dopamine), in response to both chronic <b>cocaine</b> or opiate exposure and to drug withdrawal, using several newly developed animal models and molecular approaches.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	19155191	orexin, <strong>arginine vasopressin</strong>, V1b receptor, and corticotropin releasing factor), hypothalamic pituitary adrenal axis, and neurotransmitters (especially dopamine), in response to both chronic cocaine or opiate exposure and to drug <b>withdrawal</b>, using several newly developed animal models and molecular approaches.
+ARGININE\ VASOPRESSIN	drug	nicotine	18337407	<b>Nicotine</b> self administration differentially regulates hypothalamic corticotropin releasing factor and <strong>arginine vasopressin</strong> mRNAs and facilitates stress induced neuronal activation.
+ARGININE\ VASOPRESSIN	drug	nicotine	18337407	To identify underlying mechanisms, we investigated (1) the effects of chronic <b>nicotine</b> SA on the coexpression of corticotropin releasing factor (CRF) and <strong>arginine vasopressin</strong> (AVP) mRNAs, the primary hypothalamic neuropeptides regulating ACTH release, in the parvocellular division of paraventricular nucleus (pcPVN), and (2) mFSS induced activation of these neurons during <b>nicotine</b> SA.
+ARGININE\ VASOPRESSIN	drug	opioid	17443128	Involvement of <strong>arginine vasopressin</strong> and V1b receptor in <b>heroin</b> withdrawal and <b>heroin</b> seeking precipitated by stress and by <b>heroin</b>.
+ARGININE\ VASOPRESSIN	addiction	relapse	17443128	Involvement of <strong>arginine vasopressin</strong> and V1b receptor in heroin withdrawal and heroin <b>seeking</b> precipitated by stress and by heroin.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	17443128	Involvement of <strong>arginine vasopressin</strong> and V1b receptor in heroin <b>withdrawal</b> and heroin seeking precipitated by stress and by heroin.
+ARGININE\ VASOPRESSIN	drug	cocaine	17443128	A previous study has shown that the stress responsive neurohormone <strong>arginine vasopressin</strong> (AVP) is activated in the amygdala during early withdrawal from <b>cocaine</b>.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	17443128	A previous study has shown that the stress responsive neurohormone <strong>arginine vasopressin</strong> (AVP) is activated in the amygdala during early <b>withdrawal</b> from cocaine.
+ARGININE\ VASOPRESSIN	drug	opioid	17286593	To reveal secretory, activational and transcriptional changes in the hypothalamus of <b>morphine</b> dependent rats during <b>naloxone</b> precipitated <b>opioid</b> withdrawal, we measured corticosterone secretion, c Fos induction and heteronuclear (hn)RNA levels of corticotropin releasing hormone (CRH) and <strong>arginine vasopressin</strong> (AVP) in naïve and <b>morphine</b> dependent animals injected with saline or 5 mg/kg <b>naloxone</b>.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	17286593	To reveal secretory, activational and transcriptional changes in the hypothalamus of morphine dependent rats during naloxone precipitated opioid <b>withdrawal</b>, we measured corticosterone secretion, c Fos induction and heteronuclear (hn)RNA levels of corticotropin releasing hormone (CRH) and <strong>arginine vasopressin</strong> (AVP) in naïve and morphine dependent animals injected with saline or 5 mg/kg naloxone.
+ARGININE\ VASOPRESSIN	addiction	relapse	16297621	Our efforts in <b>seeking</b> low molecular weight agonists of the antidiuretic peptide hormone <strong>arginine vasopressin</strong> (AVP) have led to the identification of the clinical candidate WAY 151932 (VNA 932).
+ARGININE\ VASOPRESSIN	drug	cocaine	16039786	The present studies were undertaken to determine whether: (1) 14 day (chronic) "binge" pattern <b>cocaine</b> administration (45 mg/kg/day) or its withdrawal for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters <strong>arginine vasopressin</strong> mRNA levels in amygdala or hypothalamus; (2) the opioid receptor antagonist naloxone (1mg/kg) alters <strong>arginine vasopressin</strong> mRNA or hypothalamic pituitary adrenal hormonal responses in acute <b>cocaine</b> withdrawal; and (3) there are associated changes of mu opioid receptor or proopiomelanocortin mRNA levels.
+ARGININE\ VASOPRESSIN	drug	opioid	16039786	The present studies were undertaken to determine whether: (1) 14 day (chronic) "binge" pattern cocaine administration (45 mg/kg/day) or its withdrawal for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters <strong>arginine vasopressin</strong> mRNA levels in amygdala or hypothalamus; (2) the <b>opioid</b> receptor antagonist <b>naloxone</b> (1mg/kg) alters <strong>arginine vasopressin</strong> mRNA or hypothalamic pituitary adrenal hormonal responses in acute cocaine withdrawal; and (3) there are associated changes of mu <b>opioid</b> receptor or proopiomelanocortin mRNA levels.
+ARGININE\ VASOPRESSIN	addiction	intoxication	16039786	The present studies were undertaken to determine whether: (1) 14 day (chronic) "<b>binge</b>" pattern cocaine administration (45 mg/kg/day) or its withdrawal for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters <strong>arginine vasopressin</strong> mRNA levels in amygdala or hypothalamus; (2) the opioid receptor antagonist naloxone (1mg/kg) alters <strong>arginine vasopressin</strong> mRNA or hypothalamic pituitary adrenal hormonal responses in acute cocaine withdrawal; and (3) there are associated changes of mu opioid receptor or proopiomelanocortin mRNA levels.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	16039786	The present studies were undertaken to determine whether: (1) 14 day (chronic) "binge" pattern cocaine administration (45 mg/kg/day) or its <b>withdrawal</b> for 3 h (acute), 1 day (subacute) or 10 days (chronic) alters <strong>arginine vasopressin</strong> mRNA levels in amygdala or hypothalamus; (2) the opioid receptor antagonist naloxone (1mg/kg) alters <strong>arginine vasopressin</strong> mRNA or hypothalamic pituitary adrenal hormonal responses in acute cocaine <b>withdrawal</b>; and (3) there are associated changes of mu opioid receptor or proopiomelanocortin mRNA levels.
+ARGININE\ VASOPRESSIN	drug	cocaine	16039786	In amygdala, <strong>arginine vasopressin</strong> mRNA levels were unchanged after chronic "binge" <b>cocaine</b>, but were increased during acute <b>cocaine</b> withdrawal.
+ARGININE\ VASOPRESSIN	addiction	intoxication	16039786	In amygdala, <strong>arginine vasopressin</strong> mRNA levels were unchanged after chronic "<b>binge</b>" cocaine, but were increased during acute cocaine withdrawal.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	16039786	In amygdala, <strong>arginine vasopressin</strong> mRNA levels were unchanged after chronic "binge" cocaine, but were increased during acute cocaine <b>withdrawal</b>.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	16039786	The increase in amygdalar <strong>arginine vasopressin</strong> mRNA levels was still observed after subacute <b>withdrawal</b>, but not after chronic <b>withdrawal</b>.
+ARGININE\ VASOPRESSIN	drug	cocaine	16039786	In hypothalamus, neither chronic <b>cocaine</b> nor acute withdrawal altered <strong>arginine vasopressin</strong>, proopiomelanocortin or mu opioid receptor mRNA levels.
+ARGININE\ VASOPRESSIN	drug	opioid	16039786	In hypothalamus, neither chronic cocaine nor acute withdrawal altered <strong>arginine vasopressin</strong>, proopiomelanocortin or mu <b>opioid</b> receptor mRNA levels.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	16039786	In hypothalamus, neither chronic cocaine nor acute <b>withdrawal</b> altered <strong>arginine vasopressin</strong>, proopiomelanocortin or mu opioid receptor mRNA levels.
+ARGININE\ VASOPRESSIN	drug	cocaine	16039786	These results show that: (1) opioid receptors mediate increased amygdalar <strong>arginine vasopressin</strong> gene expression during acute <b>cocaine</b> withdrawal, and (2) <b>cocaine</b> withdrawal renders the hypothalamic pituitary adrenal axis insensitive to naloxone.
+ARGININE\ VASOPRESSIN	drug	opioid	16039786	These results show that: (1) <b>opioid</b> receptors mediate increased amygdalar <strong>arginine vasopressin</strong> gene expression during acute cocaine withdrawal, and (2) cocaine withdrawal renders the hypothalamic pituitary adrenal axis insensitive to <b>naloxone</b>.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	16039786	These results show that: (1) opioid receptors mediate increased amygdalar <strong>arginine vasopressin</strong> gene expression during acute cocaine <b>withdrawal</b>, and (2) cocaine <b>withdrawal</b> renders the hypothalamic pituitary adrenal axis insensitive to naloxone.
+ARGININE\ VASOPRESSIN	drug	cocaine	16039786	Our findings suggest a potential role for amygdalar <strong>arginine vasopressin</strong> in the aversive consequences of early <b>cocaine</b> withdrawal.
+ARGININE\ VASOPRESSIN	addiction	aversion	16039786	Our findings suggest a potential role for amygdalar <strong>arginine vasopressin</strong> in the <b>aversive</b> consequences of early cocaine withdrawal.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	16039786	Our findings suggest a potential role for amygdalar <strong>arginine vasopressin</strong> in the aversive consequences of early cocaine <b>withdrawal</b>.
+ARGININE\ VASOPRESSIN	drug	alcohol	15203290	<strong>Arginine vasopressin</strong> and adrenocorticotropin secretion in response to psychosocial stress is attenuated by <b>ethanol</b> in sons of <b>alcohol</b> dependent fathers.
+ARGININE\ VASOPRESSIN	drug	amphetamine	11403685	<b>Amphetamine</b> induced HPA sensitization was not accompanied by increased costorage of <strong>arginine vasopressin</strong> (AVP) in CRH terminals, as found previously after IL 1 pretreatment.
+ARGININE\ VASOPRESSIN	addiction	sensitization	11403685	Amphetamine induced HPA <b>sensitization</b> was not accompanied by increased costorage of <strong>arginine vasopressin</strong> (AVP) in CRH terminals, as found previously after IL 1 pretreatment.
+ARGININE\ VASOPRESSIN	drug	alcohol	8666023	In the present work, the effects of neurotrophins on <b>ethanol</b> tolerance were compared to the effect of the neuropeptide, <strong>arginine vasopressin</strong>, which maintains (reduces the rate of dissipation of) both <b>ethanol</b> tolerance and memory.
+ARGININE\ VASOPRESSIN	drug	alcohol	7573805	During the <b>alcohol</b> induced diuresis, the plasma <strong>arginine vasopressin</strong> levels did not differ from the control experiment, but were higher during the phase of antidiuresis from 10 PM to 6 AM (p < 0.05  < 0.01).
+ARGININE\ VASOPRESSIN	drug	alcohol	7521910	Ingestion of <b>ethanol</b> results in a decreased level of plasma vasopressin, which appears to be caused by inhibition of <strong>arginine vasopressin</strong> (AVP) release from the neurohypophysis.
+ARGININE\ VASOPRESSIN	drug	opioid	1606493	Dependency on the brain function of <strong>arginine vasopressin</strong> system of the development to and recovery from analgesic tolerance to <b>morphine</b>.
+ARGININE\ VASOPRESSIN	drug	opioid	1606493	injection of anti <strong>arginine vasopressin</strong> (AVP) antiserum dose dependently suppressed the development of analgesic tolerance to daily <b>morphine</b>, 10 mg/kg, s.c., in mice.
+ARGININE\ VASOPRESSIN	drug	alcohol	1747746	Endogenous <strong>arginine vasopressin</strong> was previously shown to modulate the rate of loss of functional (CNS) tolerance to <b>ethanol</b>, suggesting that chronic <b>ethanol</b> ingestion might alter vasopressin synthesis and/or release.
+ARGININE\ VASOPRESSIN	drug	opioid	2187076	The aim of the study was to examine regional changes in sympathetic nerve activity (SNA) and baroreceptor function and arterial plasma catecholamines, <strong>arginine vasopressin</strong> (AVP) and plasma renin activity during <b>morphine</b> withdrawal in chloralose anesthetized rats.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	2187076	The aim of the study was to examine regional changes in sympathetic nerve activity (SNA) and baroreceptor function and arterial plasma catecholamines, <strong>arginine vasopressin</strong> (AVP) and plasma renin activity during morphine <b>withdrawal</b> in chloralose anesthetized rats.
+ARGININE\ VASOPRESSIN	drug	alcohol	2757699	Functional tolerance to <b>ethanol</b> can be prolonged by administration of the neuropeptide <strong>arginine vasopressin</strong> (AVP), which acts at specific CNS receptors.
+ARGININE\ VASOPRESSIN	addiction	dependence	3370533	The relative <b>dependence</b> or independence of the secretion of the neurohypophysial hormones, <strong>arginine vasopressin</strong> and oxytocin, was investigated using a wide variety of stimuli reported to cause the secretion of one or the other hormone.
+ARGININE\ VASOPRESSIN	drug	alcohol	3444873	Compared with age and sex matched healthy volunteers (n = 14), <b>alcoholics</b> in withdrawal (n = 17) exhibited lower cumulative urine output (p = 0.0001), higher minimum urine osmolality (p = 0.0001), lower serum sodium (p = 0.0024 before loading) and elevated plasma <strong>arginine vasopressin</strong> levels (p = 0.0045 before loading).
+ARGININE\ VASOPRESSIN	addiction	withdrawal	3444873	Compared with age and sex matched healthy volunteers (n = 14), alcoholics in <b>withdrawal</b> (n = 17) exhibited lower cumulative urine output (p = 0.0001), higher minimum urine osmolality (p = 0.0001), lower serum sodium (p = 0.0024 before loading) and elevated plasma <strong>arginine vasopressin</strong> levels (p = 0.0045 before loading).
+ARGININE\ VASOPRESSIN	drug	alcohol	3426715	Retention of <b>ethanol</b> tolerance by desglycinamide <strong>arginine vasopressin</strong> occurs in the absence of changes in hippocampal serotonin synthesis.
+ARGININE\ VASOPRESSIN	drug	alcohol	3426715	Central tolerance to the effects of <b>ethanol</b> in rats can be prolonged beyond its normal time of disappearance by administration of vasopressin (AVP) or desglycinamide <strong>arginine vasopressin</strong> (DGAVP) after <b>ethanol</b> withdrawal.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	3426715	Central tolerance to the effects of ethanol in rats can be prolonged beyond its normal time of disappearance by administration of vasopressin (AVP) or desglycinamide <strong>arginine vasopressin</strong> (DGAVP) after ethanol <b>withdrawal</b>.
+ARGININE\ VASOPRESSIN	drug	amphetamine	3122257	The effects of peripherally injected <strong>arginine vasopressin</strong> (AVP: 0 25 micrograms/kg), its desglycinamide analogue (DGAVP: 0 25 micrograms/kg), which is practically devoid of pressor activity, and d <b>amphetamine</b> (AMP: 0 1.25 mg/kg) were studied using a delayed (0 32 s) matching to position task (Dunnett 1985).
+ARGININE\ VASOPRESSIN	drug	alcohol	2431418	Central tolerance to the effects of <b>ethanol</b> in rats can be prolonged beyond its normal time of disappearance by administration of vasopressin (AVP) or desglycinamide <strong>arginine vasopressin</strong> (DGAVP) after <b>ethanol</b> withdrawal.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	2431418	Central tolerance to the effects of ethanol in rats can be prolonged beyond its normal time of disappearance by administration of vasopressin (AVP) or desglycinamide <strong>arginine vasopressin</strong> (DGAVP) after ethanol <b>withdrawal</b>.
+ARGININE\ VASOPRESSIN	drug	nicotine	3697900	Correlation of cigarette induced increase in serum <b>nicotine</b> levels with <strong>arginine vasopressin</strong> concentrations in the syndrome of self induced water intoxication and psychosis (SIWIP).
+ARGININE\ VASOPRESSIN	addiction	intoxication	3697900	Correlation of cigarette induced increase in serum nicotine levels with <strong>arginine vasopressin</strong> concentrations in the syndrome of self induced water <b>intoxication</b> and psychosis (SIWIP).
+ARGININE\ VASOPRESSIN	drug	alcohol	3834412	The role of <strong>arginine vasopressin</strong> in <b>alcohol</b> dependence and withdrawal.
+ARGININE\ VASOPRESSIN	addiction	dependence	3834412	The role of <strong>arginine vasopressin</strong> in alcohol <b>dependence</b> and withdrawal.
+ARGININE\ VASOPRESSIN	addiction	withdrawal	3834412	The role of <strong>arginine vasopressin</strong> in alcohol dependence and <b>withdrawal</b>.
+ARGININE\ VASOPRESSIN	drug	alcohol	3834412	The development and maintenance of tolerance to the physiological and behavioral effects of repeated exposure to <b>ethanol</b> can be altered markedly by the presence of <strong>arginine vasopressin</strong> (AVP).
+ARGININE\ VASOPRESSIN	drug	alcohol	4038620	Site of interaction of serotonin and desglycinamide <strong>arginine vasopressin</strong> in maintenance of <b>ethanol</b> tolerance.
+ARGININE\ VASOPRESSIN	drug	alcohol	6519181	Intraventricular <strong>arginine vasopressin</strong> maintains <b>ethanol</b> tolerance.
+ARGININE\ VASOPRESSIN	drug	alcohol	6519181	Tolerance to the hypnotic effect of <b>ethanol</b> in mice is prolonged by once daily intraventricular injections of <strong>arginine vasopressin</strong>.
+ARGININE\ VASOPRESSIN	drug	nicotine	6314418	In the high <b>nicotine</b> (2.87 mg) condition, there were significant positive correlations between integrated plasma <b>nicotine</b> and plasma <strong>arginine vasopressin</strong> (r = +0.985), its carrier protein neurophysin I (r = +0.944), and beta endorphin beta lipotropin (r = +0.977), but not adrenocorticotropic hormone.
+ARGININE\ VASOPRESSIN	drug	alcohol	6123410	Among the many factors that may influence the development or expression of functional tolerance to or physical dependence on <b>ethanol</b> is the neurohypophyseal hormone, <strong>arginine vasopressin</strong> (AVP).
+ARGININE\ VASOPRESSIN	addiction	dependence	6123410	Among the many factors that may influence the development or expression of functional tolerance to or physical <b>dependence</b> on ethanol is the neurohypophyseal hormone, <strong>arginine vasopressin</strong> (AVP).
+ARGININE\ VASOPRESSIN	drug	alcohol	573677	The influence of <strong>arginine vasopressin</strong> and oxytocin on <b>ethanol</b> dependence and tolerance.
+ARGININE\ VASOPRESSIN	addiction	dependence	573677	The influence of <strong>arginine vasopressin</strong> and oxytocin on ethanol <b>dependence</b> and tolerance.
+ARGININE\ VASOPRESSIN	drug	alcohol	362827	The effect of <b>ethanol</b> intoxication and hangover on immunoreactive plasma <strong>arginine vasopressin</strong> (AVP) concentration was studied in 7 healthy supine men in controlled clinical conditions.
+ARGININE\ VASOPRESSIN	addiction	intoxication	362827	The effect of ethanol <b>intoxication</b> and hangover on immunoreactive plasma <strong>arginine vasopressin</strong> (AVP) concentration was studied in 7 healthy supine men in controlled clinical conditions.
+ADORA2A	addiction	addiction	32492952	In this review, we updated the view on the brain D2 receptor complexes with adenosine (A)2A receptors (<strong>A2AR</strong>) and discussed the role of <strong>A2AR</strong> in different aspects of <b>addiction</b> phenotypes in laboratory animal procedures that permit the highly complex syndrome of human drug <b>addiction</b>.
+ADORA2A	drug	cocaine	32492952	We presented the current knowledge on the neurochemical in vivo and ex vivo mechanisms related to <b>cocaine</b> use disorder (CUD) and discussed future research directions for <strong>A2AR</strong> heteromeric complexes in SUD.
+ADORA2A	drug	cocaine	32338111	Furthermore, <b>cocaine</b> exposure differentially altered promoter methylation levels of <strong>A2AR</strong>, Ppp1cc, and Taar7b in the NAc and LHb of HE  and LE rats.
+ADORA2A	drug	cocaine	32124388	Upon <b>cocaine</b> self administration, this antagonistic <strong>A2AR</strong> D2R interaction disappeared in the dorsal striatum.
+ADORA2A	drug	cocaine	32124388	In the current experiments, it was tested whether such modifications in the antagonistic <strong>A2AR</strong> D2R receptor receptor interactions can develop also after an acute systemic injection of a low <b>cocaine</b> dose (1 mg/kg; sc).
+ADORA2A	drug	cocaine	32124388	Competition dopamine receptor binding experiments demonstrated that in the acute <b>cocaine</b> group, the <strong>A2AR</strong> agonist CGS 21680 produced significantly larger increases in the D2R Ki, High values (reduction of high affinity) versus the saline injected (i.e.
+ADORA2A	drug	cocaine	32124388	The molecular mechanism involved in the acute <b>cocaine</b> induced increase in the antagonistic allosteric <strong>A2AR</strong> D2R receptor receptor interactions may be an increased formation of higher order complexes <strong>A2AR</strong> D2R sigma1R in which <b>cocaine</b> by binding to the sigma1R protomer also allosterically enhances the inhibitory <strong>A2AR</strong> D2R interaction in this receptor complex.
+ADORA2A	drug	cannabinoid	31973708	It has been hypothesized that heteromers of adenosine A2A receptors (<strong>A2AR</strong>) and <b>cannabinoid</b> CB1 receptors (CB1R) localized in glutamatergic nerve terminals mediate the integration of adenosine and <b>endocannabinoid</b> signaling involved in the modulation of striatal excitatory neurotransmission.
+ADORA2A	addiction	dependence	31973708	A <b>dependence</b> of <strong>A2AR</strong> signaling for the Gi protein mediated CB1R signaling was described as one of its main biochemical characteristics.
+ADORA2A	drug	cannabinoid	31973708	We demonstrate that the well established <b>cannabinoid</b> induced inhibition of striatal glutamate release can mostly be explained by a CB1R mediated counteraction of the <strong>A2AR</strong> mediated constitutive activation of adenylyl cyclase in the <strong>A2AR</strong> CB1R heteromer.
+ADORA2A	drug	cocaine	31816953	<strong>A2AR</strong> Transmembrane 2 Peptide Administration Disrupts the <strong>A2AR</strong> <strong>A2AR</strong> Homoreceptor but Not the <strong>A2AR</strong> D2R Heteroreceptor Complex: Lack of Actions on Rodent <b>Cocaine</b> Self Administration.
+ADORA2A	drug	cocaine	31816953	It was previously demonstrated that rat adenosine <strong>A2AR</strong> transmembrane V peptide administration into the nucleus accumbens enhances <b>cocaine</b> self administration through disruption of the <strong>A2AR</strong> dopamine (D2R) heteroreceptor complex of this region.
+ADORA2A	drug	cocaine	31816953	<strong>A2AR</strong> TM2 was proposed to be part of the of the receptor interface of the <strong>A2AR</strong> homomer instead and was therefore tested in the current article for effects on rat <b>cocaine</b> self administration using rat <strong>A2AR</strong> synthetic TM2 peptide bilaterally injected into the nucleus accumbens.
+ADORA2A	drug	cocaine	31816953	The injected <strong>A2AR</strong> TM2 peptide failed to significantly counteract the inhibitory action of the <strong>A2AR</strong> agonist CGS 21680 (0.1 mg/Kg) on <b>cocaine</b> self administration.
+ADORA2A	drug	cocaine	31816953	The results indicate that the accumbal <strong>A2AR</strong> <strong>A2AR</strong> homomeric complexes are not involved in mediating the <strong>A2AR</strong> agonist induced inhibition of <b>cocaine</b> self administration.
+ADORA2A	drug	cocaine	31782100	In <b>cocaine</b> self administration, highly significant increases were also induced by OSU 6162 in the <strong>A2AR</strong> D2R heteroreceptor complexes in the nucleus accumbens shell versus vehicle treated rats.
+ADORA2A	drug	cocaine	31782100	Furthermore, ex vivo, the <strong>A2AR</strong> agonist CGS21680 (100 nM) produced a marked and significant increase of the D2R Ki high values in the OSU 6162 treated versus vehicle treated rats under maintenance of <b>cocaine</b> self administration.
+ADORA2A	drug	cocaine	31782100	These results indicate a substantial increase in the inhibitory allosteric <strong>A2AR</strong> D2R interactions following <b>cocaine</b> self administration upon activation by the <strong>A2AR</strong> agonist ex vivo.
+ADORA2A	drug	cocaine	31782100	The current results indicate that OSU 6162 via its high affinity for the Sigma1R may increase the number of accumbal shell D2R Sigma1R and <strong>A2AR</strong> D2R heteroreceptor complexes associated with further increases in the antagonistic <strong>A2AR</strong> D2R interactions in <b>cocaine</b> self administration.
+ADORA2A	drug	alcohol	31499144	However, under unrestricted access conditions caffeine and the <strong>adenosine A2A receptor</strong> antagonist increased <b>ethanol</b> intake.
+ADORA2A	drug	alcohol	31409667	We previously found that adenosine A2A receptor (<strong>A2AR</strong>) activation dampens <b>ethanol</b> drinking behaviors in equilibrative nucleoside transporter 1 (ENT1) knockout mice, and <strong>A2AR</strong> inhibition augments reward seeking behavior in wild type mice.
+ADORA2A	addiction	relapse	31409667	We previously found that adenosine A2A receptor (<strong>A2AR</strong>) activation dampens ethanol drinking behaviors in equilibrative nucleoside transporter 1 (ENT1) knockout mice, and <strong>A2AR</strong> inhibition augments reward <b>seeking</b> behavior in wild type mice.
+ADORA2A	addiction	reward	31409667	We previously found that adenosine A2A receptor (<strong>A2AR</strong>) activation dampens ethanol drinking behaviors in equilibrative nucleoside transporter 1 (ENT1) knockout mice, and <strong>A2AR</strong> inhibition augments <b>reward</b> seeking behavior in wild type mice.
+ADORA2A	drug	alcohol	31409667	We previously found that <strong>adenosine A2A receptor</strong> (<strong>A2AR</strong>) activation dampens <b>ethanol</b> drinking behaviors in equilibrative nucleoside transporter 1 (ENT1) knockout mice, and <strong>A2AR</strong> inhibition augments reward seeking behavior in wild type mice.
+ADORA2A	addiction	relapse	31409667	We previously found that <strong>adenosine A2A receptor</strong> (<strong>A2AR</strong>) activation dampens ethanol drinking behaviors in equilibrative nucleoside transporter 1 (ENT1) knockout mice, and <strong>A2AR</strong> inhibition augments reward <b>seeking</b> behavior in wild type mice.
+ADORA2A	addiction	reward	31409667	We previously found that <strong>adenosine A2A receptor</strong> (<strong>A2AR</strong>) activation dampens ethanol drinking behaviors in equilibrative nucleoside transporter 1 (ENT1) knockout mice, and <strong>A2AR</strong> inhibition augments <b>reward</b> seeking behavior in wild type mice.
+ADORA2A	drug	alcohol	31409667	Taken together, NHBA through <strong>A2AR</strong> activation and ENT1 modulation may dampen <b>ethanol</b> drinking and seeking behaviors, suggesting that NHBA is a potential therapeutic agent for treating <b>alcohol</b> use disorder.
+ADORA2A	addiction	relapse	31409667	Taken together, NHBA through <strong>A2AR</strong> activation and ENT1 modulation may dampen ethanol drinking and <b>seeking</b> behaviors, suggesting that NHBA is a potential therapeutic agent for treating alcohol use disorder.
+ADORA2A	drug	alcohol	31409667	SIGNIFICANCE STATEMENT: Our work highlights that <strong>A2AR</strong> activation and ENT1 inhibition by a novel adenosine analog isolated from Gastrodia elata, N6 (4 hydroxybenzyl) adenosine, decreases <b>ethanol</b> drinking and seeking behaviors.
+ADORA2A	addiction	relapse	31409667	SIGNIFICANCE STATEMENT: Our work highlights that <strong>A2AR</strong> activation and ENT1 inhibition by a novel adenosine analog isolated from Gastrodia elata, N6 (4 hydroxybenzyl) adenosine, decreases ethanol drinking and <b>seeking</b> behaviors.
+ADORA2A	addiction	relapse	31315945	Adenosine 2A receptor (<strong>A2AR</strong>) containing indirect medium spiny neurons (iMSNs) in the dorsomedial striatum (DMS) contribute to reward <b>seeking</b> behaviors.
+ADORA2A	addiction	reward	31315945	Adenosine 2A receptor (<strong>A2AR</strong>) containing indirect medium spiny neurons (iMSNs) in the dorsomedial striatum (DMS) contribute to <b>reward</b> seeking behaviors.
+ADORA2A	drug	alcohol	31315945	DMS <strong>A2AR</strong> activation dampened operant conditioning induced <b>ethanol</b> containing reward, whereas <strong>A2AR</strong> antagonist abolished the effects of the <strong>A2AR</strong> agonist and restored <b>ethanol</b> containing reward seeking.
+ADORA2A	addiction	relapse	31315945	DMS <strong>A2AR</strong> activation dampened operant conditioning induced ethanol containing reward, whereas <strong>A2AR</strong> antagonist abolished the effects of the <strong>A2AR</strong> agonist and restored ethanol containing reward <b>seeking</b>.
+ADORA2A	addiction	reward	31315945	DMS <strong>A2AR</strong> activation dampened <b>operant</b> conditioning induced ethanol containing <b>reward</b>, whereas <strong>A2AR</strong> antagonist abolished the effects of the <strong>A2AR</strong> agonist and restored ethanol containing <b>reward</b> seeking.
+ADORA2A	drug	alcohol	31315945	Moreover, pre <b>ethanol</b> exposure potentiated the <strong>A2AR</strong> dependent reward seeking.
+ADORA2A	addiction	relapse	31315945	Moreover, pre ethanol exposure potentiated the <strong>A2AR</strong> dependent reward <b>seeking</b>.
+ADORA2A	addiction	reward	31315945	Moreover, pre ethanol exposure potentiated the <strong>A2AR</strong> dependent <b>reward</b> seeking.
+ADORA2A	drug	alcohol	31315945	Together, our study demonstrates that DMS <strong>A2AR</strong> and iMSNs regulate <b>ethanol</b> containing reward seeking behaviors.SIGNIFICANCE STATEMENT Our findings highlight the mechanisms of how operant conditioning develops the preference of <b>ethanol</b> containing conditioned reward.
+ADORA2A	addiction	relapse	31315945	Together, our study demonstrates that DMS <strong>A2AR</strong> and iMSNs regulate ethanol containing reward <b>seeking</b> behaviors.SIGNIFICANCE STATEMENT Our findings highlight the mechanisms of how operant conditioning develops the preference of ethanol containing conditioned reward.
+ADORA2A	addiction	reward	31315945	Together, our study demonstrates that DMS <strong>A2AR</strong> and iMSNs regulate ethanol containing <b>reward</b> seeking behaviors.SIGNIFICANCE STATEMENT Our findings highlight the mechanisms of how <b>operant</b> conditioning develops the preference of ethanol containing conditioned <b>reward</b>.
+ADORA2A	drug	alcohol	31315945	Pharmacological activation of adenosine A2A receptor (<strong>A2AR</strong>) or optogenetic activation of indirect medium spiny neurons dampened operant conditioned <b>ethanol</b> containing reward seeking, whereas inhibiting this neuronal activity restored <b>ethanol</b> containing reward seeking.
+ADORA2A	addiction	relapse	31315945	Pharmacological activation of adenosine A2A receptor (<strong>A2AR</strong>) or optogenetic activation of indirect medium spiny neurons dampened operant conditioned ethanol containing reward <b>seeking</b>, whereas inhibiting this neuronal activity restored ethanol containing reward <b>seeking</b>.
+ADORA2A	addiction	reward	31315945	Pharmacological activation of adenosine A2A receptor (<strong>A2AR</strong>) or optogenetic activation of indirect medium spiny neurons dampened <b>operant</b> conditioned ethanol containing <b>reward</b> seeking, whereas inhibiting this neuronal activity restored ethanol containing <b>reward</b> seeking.
+ADORA2A	drug	alcohol	31315945	Pharmacological activation of <strong>adenosine A2A receptor</strong> (<strong>A2AR</strong>) or optogenetic activation of indirect medium spiny neurons dampened operant conditioned <b>ethanol</b> containing reward seeking, whereas inhibiting this neuronal activity restored <b>ethanol</b> containing reward seeking.
+ADORA2A	addiction	relapse	31315945	Pharmacological activation of <strong>adenosine A2A receptor</strong> (<strong>A2AR</strong>) or optogenetic activation of indirect medium spiny neurons dampened operant conditioned ethanol containing reward <b>seeking</b>, whereas inhibiting this neuronal activity restored ethanol containing reward <b>seeking</b>.
+ADORA2A	addiction	reward	31315945	Pharmacological activation of <strong>adenosine A2A receptor</strong> (<strong>A2AR</strong>) or optogenetic activation of indirect medium spiny neurons dampened <b>operant</b> conditioned ethanol containing <b>reward</b> seeking, whereas inhibiting this neuronal activity restored ethanol containing <b>reward</b> seeking.
+ADORA2A	drug	alcohol	31315945	Furthermore, repeated intermittent <b>ethanol</b> exposure potentiated <strong>A2AR</strong> dependent reward seeking.
+ADORA2A	addiction	relapse	31315945	Furthermore, repeated intermittent ethanol exposure potentiated <strong>A2AR</strong> dependent reward <b>seeking</b>.
+ADORA2A	addiction	reward	31315945	Furthermore, repeated intermittent ethanol exposure potentiated <strong>A2AR</strong> dependent <b>reward</b> seeking.
+ADORA2A	drug	alcohol	31315945	Therefore, our finding suggests that <strong>A2AR</strong> containing indirect medium spiny neuronal activation reduces <b>ethanol</b> containing reward seeking, which may provide a potential therapeutic target for <b>alcohol</b> use disorder.
+ADORA2A	addiction	relapse	31315945	Therefore, our finding suggests that <strong>A2AR</strong> containing indirect medium spiny neuronal activation reduces ethanol containing reward <b>seeking</b>, which may provide a potential therapeutic target for alcohol use disorder.
+ADORA2A	addiction	reward	31315945	Therefore, our finding suggests that <strong>A2AR</strong> containing indirect medium spiny neuronal activation reduces ethanol containing <b>reward</b> seeking, which may provide a potential therapeutic target for alcohol use disorder.
+ADORA2A	drug	amphetamine	31245856	In contrast, D1R SPNs of the intermingled and D2R/<strong>A2aR</strong> lacking areas were strongly activated by both D1R agonists and psychostimulant drugs (d <b>amphetamine</b>, cocaine, 3,4 methyl enedioxy <b>methamphetamine</b>, or methylphenidate), but not by hallucinogens.
+ADORA2A	drug	cocaine	31245856	In contrast, D1R SPNs of the intermingled and D2R/<strong>A2aR</strong> lacking areas were strongly activated by both D1R agonists and psychostimulant drugs (d amphetamine, <b>cocaine</b>, 3,4 methyl enedioxy methamphetamine, or methylphenidate), but not by hallucinogens.
+ADORA2A	drug	amphetamine	30783122	<strong>A2aR</strong>) in the brain responsible for restlessness and painlessness, may attenuate the behavioral sensitization caused by <b>Amphetamine</b>.
+ADORA2A	addiction	sensitization	30783122	<strong>A2aR</strong>) in the brain responsible for restlessness and painlessness, may attenuate the behavioral <b>sensitization</b> caused by Amphetamine.
+ADORA2A	drug	cocaine	30392131	Effects of <strong>adenosine A2A receptor</strong> antagonists on <b>cocaine</b> induced locomotion and <b>cocaine</b> seeking.
+ADORA2A	addiction	relapse	30392131	Effects of <strong>adenosine A2A receptor</strong> antagonists on cocaine induced locomotion and cocaine <b>seeking</b>.
+ADORA2A	drug	cocaine	30392131	These studies sought to elucidate how two <strong>A2AR</strong> antagonists distinguished by their antagonist effects at presynaptic and postsynaptic <strong>A2AR</strong> influence <b>cocaine</b> induced locomotion and <b>cocaine</b> seeking.
+ADORA2A	addiction	relapse	30392131	These studies sought to elucidate how two <strong>A2AR</strong> antagonists distinguished by their antagonist effects at presynaptic and postsynaptic <strong>A2AR</strong> influence cocaine induced locomotion and cocaine <b>seeking</b>.
+ADORA2A	drug	cocaine	30392131	We assessed the effects of the <strong>A2AR</strong> antagonists to induce <b>cocaine</b> seeking when administered alone and their effects on <b>cocaine</b> seeking induced by a <b>cocaine</b> priming injection.
+ADORA2A	addiction	relapse	30392131	We assessed the effects of the <strong>A2AR</strong> antagonists to induce cocaine <b>seeking</b> when administered alone and their effects on cocaine <b>seeking</b> induced by a cocaine priming injection.
+ADORA2A	drug	cocaine	30392131	These findings demonstrate differential effects of two <strong>A2AR</strong> antagonists distinguished by their effects at pre  and postsynaptic <strong>A2AR</strong> on <b>cocaine</b> induced behaviors.
+ADORA2A	drug	cocaine	30384981	<strong>A2AR</strong> D2R Heteroreceptor Complexes in <b>Cocaine</b> Reward and Addiction.
+ADORA2A	addiction	addiction	30384981	<strong>A2AR</strong> D2R Heteroreceptor Complexes in Cocaine Reward and <b>Addiction</b>.
+ADORA2A	addiction	reward	30384981	<strong>A2AR</strong> D2R Heteroreceptor Complexes in Cocaine <b>Reward</b> and Addiction.
+ADORA2A	drug	cocaine	30384981	Among the receptor complexes, disruption of the A2A receptor dopamine D2 receptor (<strong>A2AR</strong> D2R) complex by an <strong>A2AR</strong> agonist has been shown to fully block the inhibition of <b>cocaine</b> self administration.
+ADORA2A	drug	cocaine	30384981	<b>Cocaine</b> induced pathological <strong>A2AR</strong> D2R Sigma1R complexes may form a long term memory with a strong and permanent D2R brake, leading to <b>cocaine</b> addiction.
+ADORA2A	addiction	addiction	30384981	Cocaine induced pathological <strong>A2AR</strong> D2R Sigma1R complexes may form a long term memory with a strong and permanent D2R brake, leading to cocaine <b>addiction</b>.
+ADORA2A	drug	cocaine	30384981	These heteroreceptor complexes can potentially be targeted for future pharmacotherapy of <b>cocaine</b> addiction by using heterobivalent compounds or <strong>A2AR</strong> D2R receptor interface interfering peptides that disrupt the <strong>A2AR</strong> D2R Sigma1R complexes.
+ADORA2A	addiction	addiction	30384981	These heteroreceptor complexes can potentially be targeted for future pharmacotherapy of cocaine <b>addiction</b> by using heterobivalent compounds or <strong>A2AR</strong> D2R receptor interface interfering peptides that disrupt the <strong>A2AR</strong> D2R Sigma1R complexes.
+ADORA2A	drug	cannabinoid	29740319	The adenosine receptors (namely <strong>A2AR</strong> and A1R), with their high expression pattern in the striatum and abilities to interact and integrate dopamine, glutamate and <b>cannabinoid</b> signals in the striatum, may represent novel therapeutic targets for modulating instrumental behavior.
+ADORA2A	addiction	addiction	29740319	These findings provide pharmacological evidence for a potential therapeutic strategy to control abnormal instrumental behaviors associated with drug <b>addiction</b> and obsessive <b>compulsive</b> disorder by targeting the <strong>A2AR</strong>.
+ADORA2A	drug	cocaine	29383683	Disruption of <strong>A2AR</strong> D2R Heteroreceptor Complexes After <strong>A2AR</strong> Transmembrane 5 Peptide Administration Enhances <b>Cocaine</b> Self Administration in Rats.
+ADORA2A	drug	cocaine	29383683	Antagonistic allosteric <strong>A2AR</strong> D2R receptor receptor interactions in heteroreceptor complexes counteract <b>cocaine</b> self administration and <b>cocaine</b> seeking in rats as seen in biochemical and behavioral experiments.
+ADORA2A	addiction	relapse	29383683	Antagonistic allosteric <strong>A2AR</strong> D2R receptor receptor interactions in heteroreceptor complexes counteract cocaine self administration and cocaine <b>seeking</b> in rats as seen in biochemical and behavioral experiments.
+ADORA2A	drug	cocaine	29383683	Rat <strong>A2AR</strong> synthTM5 peptide, microinjected into the nucleus accumbens, produced a complete counteraction of the inhibitory effects of the <strong>A2AR</strong> agonist CGS21680 on <b>cocaine</b> self administration.
+ADORA2A	drug	cocaine	29383683	Evidence is provided that accumbal <strong>A2AR</strong> D2R like heteroreceptor complexes with their antagonistic receptor receptor interactions can be major targets for treatment of <b>cocaine</b> use disorder.
+ADORA2A	drug	cannabinoid	29338068	<b>Cannabinoid</b> withdrawal signs were assessed following precipitated withdrawal by acute administration of the CB1 receptor antagonist <b>SR141716</b>, the 5 HT1A receptor antagonist WAY100635, the TRPV1 receptor antagonist capsazepine or the <strong>adenosine A2A receptor</strong> antagonist SCH58261.
+ADORA2A	addiction	withdrawal	29338068	Cannabinoid <b>withdrawal</b> signs were assessed following precipitated <b>withdrawal</b> by acute administration of the CB1 receptor antagonist SR141716, the 5 HT1A receptor antagonist WAY100635, the TRPV1 receptor antagonist capsazepine or the <strong>adenosine A2A receptor</strong> antagonist SCH58261.
+ADORA2A	drug	alcohol	29205397	<b>Alcohol</b> drinking also reduced the striatal density of D2R D2R homoreceptor complexes, increased the density of <strong>A2AR</strong> D2R heteroreceptor complexes in the NAc shell and the dorsal striatum, and decreased the density of sigma1R D2R heteroreceptor complexes in the dorsal striatum.
+ADORA2A	addiction	dependence	28779351	Accordingly, here we aimed to demonstrate the <strong>A2AR</strong> <b>dependence</b> of D2R/β arrestin signaling.
+ADORA2A	drug	amphetamine	28779351	Subsequently, the role of <strong>A2AR</strong> in the antipsychotic like activity of UNC9994 was assessed in wild type and <strong>A2AR</strong> /  mice administered with phencyclidine (PCP) or <b>amphetamine</b> (<b>AMPH</b>).
+ADORA2A	drug	amphetamine	28779351	Interestingly, while UNC9994 reduced hyperlocomotion in wild type animals treated either with PCP or <b>AMPH</b>, in <strong>A2AR</strong> /  mice, it failed to reduce PCP induced hyperlocomotion or produced only a moderate reduction of <b>AMPH</b> mediated hyperlocomotion.
+ADORA2A	drug	cannabinoid	28734904	Using genetic and candidate gene approaches, we show that among a variety of protein, Wls interacts with the dopamine transporter (target of cocaine), <b>cannabinoid</b> receptors (target of <b>THC</b>), <strong>Adenosine A2A receptor</strong> (target of caffeine), and SGIP1 (endocytic regulator of <b>cannabinoid</b> receptors).
+ADORA2A	drug	cocaine	28734904	Using genetic and candidate gene approaches, we show that among a variety of protein, Wls interacts with the dopamine transporter (target of <b>cocaine</b>), cannabinoid receptors (target of THC), <strong>Adenosine A2A receptor</strong> (target of caffeine), and SGIP1 (endocytic regulator of cannabinoid receptors).
+ADORA2A	drug	cocaine	28300546	<b>Cocaine</b> self administration specifically increases <strong>A2AR</strong> D2R and D2R sigma1R heteroreceptor complexes in the rat nucleus accumbens shell.
+ADORA2A	drug	cocaine	28300546	Adenosine 2A receptor (<strong>A2AR</strong>) agonists were indicated to reduce <b>cocaine</b> reward and <b>cocaine</b> seeking mainly through activation of antagonistic allosteric <strong>A2AR</strong> dopamine D2R (D2R) interactions in <strong>A2AR</strong> D2R heteroreceptor complexes.
+ADORA2A	addiction	relapse	28300546	Adenosine 2A receptor (<strong>A2AR</strong>) agonists were indicated to reduce cocaine reward and cocaine <b>seeking</b> mainly through activation of antagonistic allosteric <strong>A2AR</strong> dopamine D2R (D2R) interactions in <strong>A2AR</strong> D2R heteroreceptor complexes.
+ADORA2A	addiction	reward	28300546	Adenosine 2A receptor (<strong>A2AR</strong>) agonists were indicated to reduce cocaine <b>reward</b> and cocaine seeking mainly through activation of antagonistic allosteric <strong>A2AR</strong> dopamine D2R (D2R) interactions in <strong>A2AR</strong> D2R heteroreceptor complexes.
+ADORA2A	drug	cocaine	28300546	Furthermore, it was shown that modulation of <b>cocaine</b> reward involves antagonistic <strong>A2AR</strong> D2R interactions in the ventral but not the dorsal striatum in rats.
+ADORA2A	addiction	reward	28300546	Furthermore, it was shown that modulation of cocaine <b>reward</b> involves antagonistic <strong>A2AR</strong> D2R interactions in the ventral but not the dorsal striatum in rats.
+ADORA2A	drug	cocaine	28300546	In the current work the proximity ligation assay (PLA) was used to further study the <strong>A2AR</strong> D2R heteroreceptor complexes in the nucleus accumbens shell and core as well as the dorsal striatum under the influence of <b>cocaine</b> self administration in rats.
+ADORA2A	drug	cocaine	28300546	The results suggest that <b>cocaine</b> self administration can reorganize <strong>A2AR</strong> and D2R into increased <strong>A2AR</strong> D2R heteroreceptor complexes in the nucleus accumbens shell associated with increases in the D2R sigma1R heteroreceptor complexes in this region.
+ADORA2A	drug	cocaine	28300546	This reorganization can contribute to the demonstrated anti <b>cocaine</b> actions of A2A receptor agonists and the putative formation of <strong>A2AR</strong> D2R sigma1R heterocomplexes.
+ADORA2A	drug	cocaine	28270751	Neuromodulation of neuronal networks in <b>cocaine</b> use disorder via dopamine (DA) and adenosine signals involve <strong>A2AR</strong> D2R and <strong>A2AR</strong> D2R Sigma1R heteroreceptor complexes in the dorsal and ventral striatum.
+ADORA2A	drug	cocaine	28270751	The excitatory modulation by <strong>A2AR</strong> agonists of the ventral striato pallidal GABA anti reward system via targeting the <strong>A2AR</strong> D2R and <strong>A2AR</strong> D2R Sigma1R heteroreceptor complex holds high promise as a new way to treat <b>cocaine</b> use disorders.
+ADORA2A	addiction	reward	28270751	The excitatory modulation by <strong>A2AR</strong> agonists of the ventral striato pallidal GABA anti <b>reward</b> system via targeting the <strong>A2AR</strong> D2R and <strong>A2AR</strong> D2R Sigma1R heteroreceptor complex holds high promise as a new way to treat cocaine use disorders.
+ADORA2A	drug	cocaine	27872762	This principle is illustrated by showing how <b>cocaine</b> abuse can alter the adenosine <strong>A2AR</strong> dopamine D2R heterocomplexes and their receptor receptor interactions and hereby induce neural plasticity in the basal ganglia.
+ADORA2A	drug	cocaine	27872762	Studies with <strong>A2AR</strong> ligands using <b>cocaine</b> self administration procedures indicate that antagonistic allosteric <strong>A2AR</strong> D2R heterocomplexes of the ventral striatopallidal GABA antireward pathway play a significant role in reducing <b>cocaine</b> induced reward, motivation, and <b>cocaine</b> seeking.
+ADORA2A	addiction	relapse	27872762	Studies with <strong>A2AR</strong> ligands using cocaine self administration procedures indicate that antagonistic allosteric <strong>A2AR</strong> D2R heterocomplexes of the ventral striatopallidal GABA antireward pathway play a significant role in reducing cocaine induced reward, motivation, and cocaine <b>seeking</b>.
+ADORA2A	addiction	reward	27872762	Studies with <strong>A2AR</strong> ligands using cocaine self administration procedures indicate that antagonistic allosteric <strong>A2AR</strong> D2R heterocomplexes of the ventral striatopallidal GABA antireward pathway play a significant role in reducing cocaine induced <b>reward</b>, motivation, and cocaine seeking.
+ADORA2A	drug	cocaine	27872762	In contrast, the allosteric brake on the D2R protomer signaling in the <strong>A2AR</strong> D2R heterocomplex of the dorsal striatopallidal GABA neurons is lost upon <b>cocaine</b> self administration.
+ADORA2A	drug	cocaine	26987369	In the current study behavioral and biochemical experiments were performed to study changes in the allosteric <strong>A2AR</strong> D2R interactions in the ventral and dorsal striatum after <b>cocaine</b> self administration versus corresponding yoked saline control.
+ADORA2A	drug	cocaine	26987369	The results therefore support the hypothesis that <strong>A2AR</strong> agonists can at least in part counteract the motivational actions of <b>cocaine</b>.
+ADORA2A	drug	cocaine	26987369	In contrast, in the dorsal striatum the CGS 21680 induced antagonistic modulation in the D2 likeR agonist high affinity state was abolished after <b>cocaine</b> self administration versus the yoked saline group probably due to a local dysfunction/disruption of the <strong>A2AR</strong> D2 like R heteroreceptor complexes.
+ADORA2A	drug	cocaine	26987369	Potential differences in the composition and stoichiometry of the <strong>A2AR</strong> D2R heteroreceptor complexes, including differential recruitment of sigma 1 receptor, in the ventral and dorsal striatum may explain the differential regional changes observed in the A2A D2 likeR interactions after <b>cocaine</b> self administration.
+ADORA2A	drug	psychedelics	25702084	The anti immobility effect of creatine (1 mg/kg, po) or <b>ketamine</b> (a fast acting antidepressant, 1 mg/kg, ip) in the TST was prevented by pretreatment of mice with caffeine (3 mg/kg, ip, nonselective adenosine receptor antagonist), 8 cyclopentyl 1,3 dipropylxanthine (DPCPX) (2 mg/kg, ip, selective adenosine A1 receptor antagonist), and 4 (2 [7 amino 2 {2 furyl}{1,2,4}triazolo {2,3 a}{1,3,5}triazin 5 yl amino]ethyl) phenol (ZM241385) (1 mg/kg, ip, selective <strong>adenosine A2A receptor</strong> antagonist).
+ADORA2A	drug	psychedelics	25702084	Moreover, the administration of subeffective doses of creatine or <b>ketamine</b> combined with N 6 cyclohexyladenosine (CHA) (0.05 mg/kg, ip, selective adenosine A1 receptor agonist), N 6 [2 (3,5 dimethoxyphenyl) 2 (methylphenyl)ethyl]adenosine (DPMA) (0.1 mg/kg, ip, selective <strong>adenosine A2A receptor</strong> agonist), or dipyridamole (0.1 μg/mouse, icv, adenosine transporter inhibitor) produced a synergistic antidepressant like effect in the TST.
+ADORA2A	drug	cannabinoid	24806674	Differential effects of presynaptic versus postsynaptic <strong>adenosine A2A receptor</strong> blockade on Δ9 <b>tetrahydrocannabinol</b> (<b>THC</b>) self administration in squirrel monkeys.
+ADORA2A	drug	cannabinoid	24806674	Different doses of an <strong>adenosine A2A receptor</strong> antagonist MSX 3 [3,7 dihydro 8 [(1E) 2 (3 ethoxyphenyl)ethenyl] 7 methyl 3 [3 (phosphooxy)propyl 1 (2 propynil) 1H purine 2,6 dione] were found previously to either decrease or increase self administration of <b>cannabinoids</b> delta 9 <b>tetrahydrocannabinol</b> (<b>THC</b>) or anandamide in squirrel monkeys.
+ADORA2A	addiction	withdrawal	24562064	Following a 1 week <b>withdrawal</b>, the direct effects of adenosine receptor modulation were tested by administering the adenosine A1 receptor agonist, N(6) cyclopentyladenosine (CPA, 0.03 and 0.1 mg/kg), the adenosine A2A agonist, CGS 21680 (0.03 and 0.1 mg/kg), the presynaptic <strong>adenosine A2A receptor</strong> antagonist, SCH 442416 (0.3, 1, and 3 mg/kg), or vehicle prior to each of six daily extinction sessions.
+ADORA2A	addiction	relapse	24562064	Interestingly, adenosine A1 receptor stimulation or presynaptic <strong>adenosine A2A receptor</strong> blockade during extinction produces lasting changes in <b>relapse</b> susceptibility.
+ADORA2A	drug	alcohol	23912595	Numerous studies have indicated a role for A1 receptors (A1R) in acute <b>ethanol</b> induced motor incoordination, while A2A receptors (<strong>A2AR</strong>) mainly regulate the rewarding effect of <b>ethanol</b> in mice.
+ADORA2A	drug	alcohol	23912595	Recent findings have demonstrated that dampened <strong>A2AR</strong> mediated signaling in the dorsomedial striatum (DMS) promotes <b>ethanol</b> seeking behaviors.
+ADORA2A	addiction	relapse	23912595	Recent findings have demonstrated that dampened <strong>A2AR</strong> mediated signaling in the dorsomedial striatum (DMS) promotes ethanol <b>seeking</b> behaviors.
+ADORA2A	drug	alcohol	23912595	Moreover, decreased <strong>A2AR</strong> function is associated with decreased CREB activity in the DMS, which enhances goal oriented behaviors and contributes to excessive <b>ethanol</b> drinking in mice.
+ADORA2A	drug	alcohol	23912595	Furthermore, based on the fact that <strong>A2AR</strong> activity plays a role in goal directed behavior, caffeine may also promote <b>ethanol</b> seeking behavior.
+ADORA2A	addiction	relapse	23912595	Furthermore, based on the fact that <strong>A2AR</strong> activity plays a role in goal directed behavior, caffeine may also promote ethanol <b>seeking</b> behavior.
+ADORA2A	drug	amphetamine	23843511	Moreover, CD73 KO mice displayed increased working memory performance and a blunted <b>amphetamine</b> induced sensitization, mimicking the phenotype of global or forebrain <strong>A2AR</strong> KO mice, as well as upon pharmacological <strong>A2AR</strong> blockade.
+ADORA2A	addiction	sensitization	23843511	Moreover, CD73 KO mice displayed increased working memory performance and a blunted amphetamine induced <b>sensitization</b>, mimicking the phenotype of global or forebrain <strong>A2AR</strong> KO mice, as well as upon pharmacological <strong>A2AR</strong> blockade.
+ADORA2A	drug	amphetamine	23680573	Chronic <b>methamphetamine</b> treatment induces oxytocin receptor up regulation in the amygdala and hypothalamus via an <strong>adenosine A2A receptor</strong> independent mechanism.
+ADORA2A	drug	cocaine	23469532	Our findings suggest that sleep disorder caused by subacute and subchronic <b>cocaine</b> abstinence may be associated with over expression of <strong>adenosine A2A receptor</strong> in rat hypothalamus to some extent.
+ADORA2A	drug	alcohol	23467349	Striatal adenosine A2A receptors (<strong>A2AR</strong>) play an essential role in both <b>ethanol</b> drinking and the shift from goal directed action to habitual behavior.
+ADORA2A	drug	alcohol	23467349	However, direct evidence for a role of striatal <strong>A2AR</strong> signaling in <b>ethanol</b> drinking and habit development has not been established.
+ADORA2A	drug	alcohol	23467349	In the present study, we found that decreased <strong>A2AR</strong> mediated CREB activity in the dorsomedial striatum (DMS) enhanced initial behavioral acquisition of goal directed behaviors and the vulnerability to progress to excessive <b>ethanol</b> drinking during operant conditioning in mice lacking <b>ethanol</b> sensitive adenosine transporter ENT1 (ENT1( / )).
+ADORA2A	addiction	reward	23467349	In the present study, we found that decreased <strong>A2AR</strong> mediated CREB activity in the dorsomedial striatum (DMS) enhanced initial behavioral acquisition of goal directed behaviors and the vulnerability to progress to excessive ethanol drinking during <b>operant</b> conditioning in mice lacking ethanol sensitive adenosine transporter ENT1 (ENT1( / )).
+ADORA2A	drug	alcohol	23467349	Using mice expressing β galactosidase (lacZ) under the control of seven repeated CRE sites in both genotypes (CRE lacZ/ENT1(+/+) mice and CRE lacZ/ENT1( / ) mice) and the dominant negative form of CREB, we found that reduced CREB activity in the DMS was causally associated with decreased <strong>A2AR</strong> signaling and increased goal directed <b>ethanol</b> drinking.
+ADORA2A	drug	alcohol	23467349	Finally, we have demonstrated that the <strong>A2AR</strong> antagonist ZM241385 dampened protein kinase A activity mediated signaling in the DMS and promoted excessive <b>ethanol</b> drinking in ENT1(+/+) mice, but not in ENT1( / ) mice.
+ADORA2A	drug	alcohol	23467349	Our results indicate that <strong>A2AR</strong> mediated CREB signaling in the DMS is a key determinant in enhancing the development of goal directed <b>ethanol</b> drinking in mice.
+ADORA2A	drug	alcohol	23301633	The <strong>adenosine A2A receptor</strong> agonist CGS 21680 decreases <b>ethanol</b> self administration in both non dependent and dependent animals.
+ADORA2A	drug	alcohol	23301633	We have already demonstrated the involvement of A2A receptors (<strong>A2AR</strong>) in <b>ethanol</b> related behaviours in mice.
+ADORA2A	drug	alcohol	23301633	Here, we investigated whether the <strong>A2AR</strong> agonist CGS 21680 can reduce <b>ethanol</b> operant self administration in both non dependent and <b>ethanol</b> dependent Wistar rats.
+ADORA2A	addiction	reward	23301633	Here, we investigated whether the <strong>A2AR</strong> agonist CGS 21680 can reduce ethanol <b>operant</b> self administration in both non dependent and ethanol dependent Wistar rats.
+ADORA2A	drug	alcohol	23301633	These results suggest that the <strong>A2AR</strong> are involved in CGS 21680 effects since the reduction of <b>ethanol</b> self administration was not dependent upon the presence of A1R in mice.
+ADORA2A	drug	alcohol	23301633	In conclusion, our findings demonstrated the effectiveness of the <strong>A2AR</strong> agonist CGS 21680 in a preclinical model of <b>alcohol</b> addiction and suggested that the adenosinergic pathway is a promising target to treat <b>alcohol</b> addiction.
+ADORA2A	addiction	addiction	23301633	In conclusion, our findings demonstrated the effectiveness of the <strong>A2AR</strong> agonist CGS 21680 in a preclinical model of alcohol <b>addiction</b> and suggested that the adenosinergic pathway is a promising target to treat alcohol <b>addiction</b>.
+ADORA2A	drug	cocaine	21816123	mGlu5 and <strong>adenosine A2A receptor</strong> interactions regulate the conditioned effects of <b>cocaine</b>.
+ADORA2A	drug	cannabinoid	21054689	Reinforcing and neurochemical effects of <b>cannabinoid</b> CB1 receptor agonists, but not cocaine, are altered by an <strong>adenosine A2A receptor</strong> antagonist.
+ADORA2A	drug	cocaine	21054689	Reinforcing and neurochemical effects of cannabinoid CB1 receptor agonists, but not <b>cocaine</b>, are altered by an <strong>adenosine A2A receptor</strong> antagonist.
+ADORA2A	addiction	reward	21054689	<b>Reinforcing</b> and neurochemical effects of cannabinoid CB1 receptor agonists, but not cocaine, are altered by an <strong>adenosine A2A receptor</strong> antagonist.
+ADORA2A	drug	amphetamine	20799992	The <strong>adenosine A2A receptor</strong> is associated with <b>methamphetamine</b> dependence/psychosis in the Japanese population.
+ADORA2A	addiction	dependence	20799992	The <strong>adenosine A2A receptor</strong> is associated with methamphetamine <b>dependence</b>/psychosis in the Japanese population.
+ADORA2A	drug	amphetamine	20799992	We therefore hypothesized that variations in the A2A adenosine receptor (<strong>ADORA2A</strong>) gene modify genetic susceptibility to <b>METH</b> dependence/psychosis.
+ADORA2A	addiction	dependence	20799992	We therefore hypothesized that variations in the A2A adenosine receptor (<strong>ADORA2A</strong>) gene modify genetic susceptibility to METH <b>dependence</b>/psychosis.
+ADORA2A	drug	amphetamine	20799992	We first analyzed variations in the exons and exon intron boundaries of the <strong>ADORA2A</strong> gene in <b>METH</b> dependent/psychotic patients.
+ADORA2A	drug	amphetamine	20799992	These results suggest that the <strong>ADORA2A</strong> gene could be a vulnerability factor for <b>METH</b> dependence/psychosis, especially in females and/or in patients using only <b>METH</b>.
+ADORA2A	addiction	dependence	20799992	These results suggest that the <strong>ADORA2A</strong> gene could be a vulnerability factor for METH <b>dependence</b>/psychosis, especially in females and/or in patients using only METH.
+ADORA2A	drug	cocaine	19641899	Effects of <strong>adenosine A2A receptor</strong> stimulation on <b>cocaine</b> seeking behavior in rats.
+ADORA2A	addiction	relapse	19641899	Effects of <strong>adenosine A2A receptor</strong> stimulation on cocaine <b>seeking</b> behavior in rats.
+ADORA2A	drug	alcohol	19097273	We have shown previously that mice lacking the adenosine A2A receptor (<strong>A2AR</strong>) generated on a CD1 background self administer more <b>ethanol</b> and exhibit hyposensitivity to acute <b>ethanol</b>.
+ADORA2A	drug	alcohol	19097273	We have shown previously that mice lacking the <strong>adenosine A2A receptor</strong> (<strong>A2AR</strong>) generated on a CD1 background self administer more <b>ethanol</b> and exhibit hyposensitivity to acute <b>ethanol</b>.
+ADORA2A	drug	alcohol	19097273	Finally, the <strong>A2AR</strong> agonist, 2 p (2 carboxyethyl) phenylethylamino 50 N ethylcarboxamidoadenosine hydrochloride (CGS 21680), reduced <b>ethanol</b> consumption and preference in C57BL/6J mice.
+ADORA2A	drug	alcohol	19097273	In conclusion, <strong>A2AR</strong> deficiency in mice generated on a CD1 background leads to high <b>ethanol</b> consumption that is associated with an increased sensitivity to the locomotor stimulant/anxiolytic effects of <b>ethanol</b> and a decrease in <b>ethanol</b> induced CPP.
+ADORA2A	addiction	reward	19097273	In conclusion, <strong>A2AR</strong> deficiency in mice generated on a CD1 background leads to high ethanol consumption that is associated with an increased sensitivity to the locomotor stimulant/anxiolytic effects of ethanol and a decrease in ethanol induced <b>CPP</b>.
+ADORA2A	drug	opioid	19066414	The results indicate that stimulation of the <strong>adenosine A2A receptor</strong> plays some role in modulating the neuroadaptive changes appearing during chronic <b>opioid</b> treatment and that <strong>adenosine A2A receptor</strong> agonists may serve as useful drugs in relapse protection.
+ADORA2A	addiction	relapse	19066414	The results indicate that stimulation of the <strong>adenosine A2A receptor</strong> plays some role in modulating the neuroadaptive changes appearing during chronic opioid treatment and that <strong>adenosine A2A receptor</strong> agonists may serve as useful drugs in <b>relapse</b> protection.
+ADORA2A	drug	alcohol	18640664	<b>Alcohol</b> exposure also resulted in an increase in maximal vessel response to CGS 21680, an <strong>adenosine A2A receptor</strong> agonist, but did not alter the concentration dependent response curves to adenosine.
+ADORA2A	addiction	relapse	18536706	A differential role for the <strong>adenosine A2A receptor</strong> in opiate reinforcement vs opiate <b>seeking</b> behavior.
+ADORA2A	addiction	reward	18536706	A differential role for the <strong>adenosine A2A receptor</strong> in opiate <b>reinforcement</b> vs opiate seeking behavior.
+ADORA2A	drug	nicotine	17616786	Persons with the <strong>ADORA2A</strong> TT genotype also were significantly more likely to consume less caffeine (ie, <100 mg/d) than were carriers of the C allele [P=0.011 (nonsmokers), P=0.008 (<b>smokers</b>)].
+ADORA2A	drug	alcohol	17550371	Effect of the <strong>adenosine A2a receptor</strong> antagonist 3,7 dimethyl propargylxanthine on anxiety like and depression like behavior and <b>alcohol</b> consumption in Wistar Rats.
+ADORA2A	drug	alcohol	17550371	We therefore examined the effect of the <strong>adenosine A2a receptor</strong> antagonist 3,7 dimethylpropargylxanthine (DMPX, 3, and 10 mg/kg intraperitoneal) on <b>alcohol</b> reinforcement, anxiety related, depression, and rewarding behaviors in nonselected Wistar rats.
+ADORA2A	addiction	reward	17550371	We therefore examined the effect of the <strong>adenosine A2a receptor</strong> antagonist 3,7 dimethylpropargylxanthine (DMPX, 3, and 10 mg/kg intraperitoneal) on alcohol <b>reinforcement</b>, anxiety related, depression, and rewarding behaviors in nonselected Wistar rats.
+ADORA2A	drug	alcohol	17517168	Administration of the selective <strong>adenosine A2A receptor</strong> antagonist, SCH 58261, reduced fixed ratio responding for <b>alcohol</b> in iP rats in a dose related manner.
+ADORA2A	drug	cocaine	16516871	Recent data indicate that <b>cocaine</b> locomotor responses may be influenced by dopamine (DA) neurotransmission and adenosine neuromodulation involving the A2A receptor (<strong>A2AR</strong>).
+ADORA2A	drug	cocaine	16516871	Male Wistar rats were injected with MSX 3 (1 25 mg/kg; an antagonist of <strong>A2AR</strong>), CGS 21680 (0.05 0.2 mg/kg; an agonist of <strong>A2AR</strong>), SCH 23390 (0.125 0.25 mg/kg; an antagonist of DA D1/5R), raclopride (0.1 0.8 mg/kg; an antagonist of DA D2/3R), nafadotride (0.2 0.4 mg/kg; an antagonist of DA D3R) or 7 OH PIPAT (0.01 1 mg/kg; an agonist of DA D3R) to verify the hypothesis that adenosine <strong>A2AR</strong> and DA receptors and their antagonistic interactions may control locomotor and sensitizing effects of <b>cocaine</b>.
+ADORA2A	drug	cocaine	16516871	Pharmacological stimulation of adenosine A2ARs protected against both the development and expression of <b>cocaine</b> sensitization, which may offer a therapeutic potential of <strong>A2AR</strong> agonists in the treatment of <b>cocaine</b> dependence.
+ADORA2A	addiction	dependence	16516871	Pharmacological stimulation of adenosine A2ARs protected against both the development and expression of cocaine sensitization, which may offer a therapeutic potential of <strong>A2AR</strong> agonists in the treatment of cocaine <b>dependence</b>.
+ADORA2A	addiction	sensitization	16516871	Pharmacological stimulation of adenosine A2ARs protected against both the development and expression of cocaine <b>sensitization</b>, which may offer a therapeutic potential of <strong>A2AR</strong> agonists in the treatment of cocaine dependence.
+ADORA2A	drug	opioid	16470403	Absence of quasi <b>morphine</b> withdrawal syndrome in <strong>adenosine A2A receptor</strong> knockout mice.
+ADORA2A	addiction	withdrawal	16470403	Absence of quasi morphine <b>withdrawal</b> syndrome in <strong>adenosine A2A receptor</strong> knockout mice.
+ADORA2A	addiction	withdrawal	16407902	The acute administration of 'nonanxiolytic' doses of adenosine and the selective adenosine A1 receptor agonist 2 chloro N6 cyclopentyladenosine (CCPA), but not the <strong>adenosine A2A receptor</strong> agonist N6 [2 (3,5 dimethoxyphenyl) 2 (2 methylphenyl)ethyl]adenosine (DPMA), at the onset of peak <b>withdrawal</b> (18 h), reduced this anxiogenic like response.
+ADORA2A	drug	alcohol	15983797	In connection with the rota rod apparatus, the effects of acute administration of the adenosine receptor antagonists caffeine (non selective), 8 cyclopentyl 1,3 dipropylxanthine (DPCPX, adenosine A1 receptor antagonist) and 4 (2 [7 amino 2 {2 furyl}{1,2,4}triazolo {2,3 a}{1,3,5}triazin 5 yl amino]ethyl)phenol (ZM241385, <strong>adenosine A2A receptor</strong> antagonist), together with R(+) 7 chloro 8 hydroxy 3 methyl 1 phenyl 2,3,4,5 tetrahydro 1H 3 benzazepine (SCH23390, dopamine D1 receptor antagonist) and sulpiride (dopamine D2 receptor antagonist), alone or in combination with <b>ethanol</b> (2.25 g/kg, i.p.
+ADORA2A	drug	cocaine	15464827	Our results suggest that PTE prevents <b>cocaine</b> induced behavioral effects, at least in part, via the activation of the <strong>adenosine A2A receptor</strong>.
+ADORA2A	addiction	sensitization	14663016	The unique neuronal localization of the <strong>adenosine A2A receptor</strong> in the basal ganglia and its extensive interactions with dopaminergic and glutamatergic systems led the authors to investigate a potential role of the A2A receptor in the development of behavioral <b>sensitization</b> in response to repeated dopaminergic stimulation.
+ADORA2A	drug	alcohol	12451148	We have shown previously that the severity of handling induced convulsions during <b>ethanol</b> withdrawal was reduced in A2A receptor knock out (<strong>A2AR</strong> / ) mice.
+ADORA2A	addiction	withdrawal	12451148	We have shown previously that the severity of handling induced convulsions during ethanol <b>withdrawal</b> was reduced in A2A receptor knock out (<strong>A2AR</strong> / ) mice.
+ADORA2A	drug	alcohol	12451148	Male <strong>A2AR</strong> /  mice showed increased consumption of solutions containing 6 and 20% (v/v) <b>ethanol</b> compared with wild type (<strong>A2AR</strong>+/+) control mice; female <strong>A2AR</strong> /  mice showed increased consumption of solutions containing 6 and 10% <b>ethanol</b>.
+ADORA2A	drug	alcohol	12451148	Relative to <strong>A2AR</strong>+/+ mice, <strong>A2AR</strong> /  mice were found to be less sensitive to the sedative effect of 3.0 gm/kg <b>ethanol</b>, as measured by more rapid recovery from <b>ethanol</b> induced loss of righting reflex, and to the hypothermic effects of 1.5, 3.0, and 4.0 gm/kg <b>ethanol</b>, although plasma <b>ethanol</b> levels did not differ significantly between the two genotypes.
+ADORA2A	drug	alcohol	12451148	The selective <strong>adenosine A2A receptor</strong> antagonist ZM 241385 (4 (2 [7 amino 2 (2 furyl)[1,2,4]triazolo[2,3 a][1,3,5]triazin 5 ylamino]ethyl)phenol) (10 30 mg/kg) significantly attenuated <b>ethanol</b> induced (4.0 gm/kg) hypothermia in CD1 mice.
+ADORA2A	drug	alcohol	12451148	To assess whether <b>ethanol</b> administration would induce differential tolerance in <strong>A2AR</strong> /  and wild type mice, we administered <b>ethanol</b> (3.0 gm/kg) over 4 consecutive days and found no difference in the development of tolerance; however, female <strong>A2AR</strong> /  mice showed a lower tolerance acquisition rate.
+ADORA2A	drug	opioid	10714888	The same effect was induced by the adenosine A1 receptor agonist, N6 Cyclopentyladenosine (CPA) whereas the selective <strong>adenosine A2A receptor</strong> agonist CGS 21680 increased the <b>naloxone</b> precipitated withdrawal phenomenon.
+ADORA2A	addiction	withdrawal	10714888	The same effect was induced by the adenosine A1 receptor agonist, N6 Cyclopentyladenosine (CPA) whereas the selective <strong>adenosine A2A receptor</strong> agonist CGS 21680 increased the naloxone precipitated <b>withdrawal</b> phenomenon.
+ADORA2A	drug	opioid	8788434	However, the <strong>adenosine A2A receptor</strong> agonist 2 p (carboxyethyl) phenylamino 5' N ethylcarboxamidoadenosine (CGS 21680) had a greater effect on blood pressure in <b>morphine</b> dependent rats compared to opiate naive rats.
+ZGLP1	addiction	reward	32388229	The gut brain peptide glucagon like peptide 1 (<strong>GLP 1</strong>) reduces <b>reward</b> from palatable food and drugs of abuse.
+ZGLP1	drug	alcohol	32388229	Recent rodent studies show that activation of <strong>GLP 1</strong> receptors (GLP 1R) within the nucleus of the solitary tract (NTS) not only suppresses the motivation and intake of palatable food, but also reduces <b>alcohol</b> related behaviors.
+ZGLP1	drug	alcohol	31759971	Further studies established that Ex4 modulates <b>alcohol</b> mediated behaviours via activation of <strong>GLP 1</strong> receptors in reward related areas and an area of the hindbrain.
+ZGLP1	addiction	reward	31759971	Further studies established that Ex4 modulates alcohol mediated behaviours via activation of <strong>GLP 1</strong> receptors in <b>reward</b> related areas and an area of the hindbrain.
+ZGLP1	drug	alcohol	31759971	Finally, another <strong>GLP 1</strong> receptor agonist, AC3174, counteracts relapse drinking to <b>alcohol</b>.
+ZGLP1	addiction	relapse	31759971	Finally, another <strong>GLP 1</strong> receptor agonist, AC3174, counteracts <b>relapse</b> drinking to alcohol.
+ZGLP1	drug	alcohol	31759971	Furthermore, a polymorphism in the <strong>GLP 1</strong> receptor gene is associated with enhanced intravenous self administration of <b>alcohol</b> in social drinkers and higher response in globus pallidus following high monetary reward.
+ZGLP1	addiction	reward	31759971	Furthermore, a polymorphism in the <strong>GLP 1</strong> receptor gene is associated with enhanced intravenous self administration of alcohol in social drinkers and higher response in globus pallidus following high monetary <b>reward</b>.
+ZGLP1	drug	alcohol	31759971	Collectively, these data provide evidence that up coming clinical trials should evaluate the effect of these <strong>GLP 1</strong> receptor agonists on <b>alcohol</b> intake in patients with AUD.
+ZGLP1	drug	opioid	31581176	Activation of <strong>GLP 1</strong> receptors attenuates <b>oxycodone</b> taking and seeking without compromising the antinociceptive effects of <b>oxycodone</b> in rats.
+ZGLP1	addiction	relapse	31581176	Activation of <strong>GLP 1</strong> receptors attenuates oxycodone taking and <b>seeking</b> without compromising the antinociceptive effects of oxycodone in rats.
+ZGLP1	addiction	reward	31581176	A growing body of preclinical evidence indicates that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists reduce drug <b>reinforcement</b>.
+ZGLP1	drug	opioid	31581176	However, the efficacy of <strong>GLP 1</strong> receptor agonists in attenuating <b>opioid</b> mediated behaviors has not been thoroughly investigated.
+ZGLP1	drug	opioid	31581176	Using recently established models of <b>opioid</b> taking and  seeking behaviors, we showed that systemic administration of the <strong>GLP 1</strong> receptor agonist exendin 4 reduced <b>oxycodone</b> self administration and the reinstatement of <b>oxycodone</b> seeking behavior in rats.
+ZGLP1	addiction	relapse	31581176	Using recently established models of opioid taking and  <b>seeking</b> behaviors, we showed that systemic administration of the <strong>GLP 1</strong> receptor agonist exendin 4 reduced oxycodone self administration and the <b>reinstatement</b> of oxycodone <b>seeking</b> behavior in rats.
+ZGLP1	drug	opioid	31581176	Finally, exendin 4 did not alter the analgesic effects of <b>oxycodone</b>, suggesting that activation of <strong>GLP 1</strong> receptors attenuated <b>opioid</b> reinforcement without reducing the thermal antinociceptive effects of <b>oxycodone</b>.
+ZGLP1	addiction	reward	31581176	Finally, exendin 4 did not alter the analgesic effects of oxycodone, suggesting that activation of <strong>GLP 1</strong> receptors attenuated opioid <b>reinforcement</b> without reducing the thermal antinociceptive effects of oxycodone.
+ZGLP1	drug	opioid	31581176	Taken together, these findings suggest that <strong>GLP 1</strong> receptors could serve as potential molecular targets for pharmacotherapies aimed at reducing <b>opioid</b> use disorder.
+ZGLP1	drug	alcohol	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of <b>alcohol</b>, cocaine, amphetamine, and nicotine in rodents.
+ZGLP1	drug	amphetamine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, cocaine, <b>amphetamine</b>, and nicotine in rodents.
+ZGLP1	drug	cocaine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, <b>cocaine</b>, amphetamine, and nicotine in rodents.
+ZGLP1	drug	nicotine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, cocaine, amphetamine, and <b>nicotine</b> in rodents.
+ZGLP1	addiction	reward	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the <b>reinforcing</b> and rewarding effects of alcohol, cocaine, amphetamine, and nicotine in rodents.
+ZGLP1	drug	opioid	31058214	Investigations on effects of <strong>GLP 1</strong> analogs on <b>opioid</b> reward and reinforcement have not been reported.
+ZGLP1	addiction	reward	31058214	Investigations on effects of <strong>GLP 1</strong> analogs on opioid <b>reward</b> and <b>reinforcement</b> have not been reported.
+ZGLP1	drug	alcohol	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, <b>naltrexone</b> precipitated morphine withdrawal, morphine analgesia (male and female mice), and locomotor activity.
+ZGLP1	drug	opioid	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on <b>opioid</b> related behaviors in male mice, i.e., <b>morphine</b> conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic <b>opioid</b> remifentanil, naltrexone precipitated <b>morphine</b> withdrawal, <b>morphine</b> analgesia (male and female mice), and locomotor activity.
+ZGLP1	addiction	reward	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (<b>CPP</b>), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, naltrexone precipitated morphine withdrawal, morphine analgesia (male and female mice), and locomotor activity.
+ZGLP1	addiction	withdrawal	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, naltrexone precipitated morphine <b>withdrawal</b>, morphine analgesia (male and female mice), and locomotor activity.
+ZGLP1	drug	opioid	31058214	Taken together, Ex4 did not attenuate the addiction related behavioral effects of <b>opioids</b>, indicating that <strong>GLP 1</strong> analogs would not be useful medications in the treatment of <b>opioid</b> addiction.
+ZGLP1	addiction	addiction	31058214	Taken together, Ex4 did not attenuate the <b>addiction</b> related behavioral effects of opioids, indicating that <strong>GLP 1</strong> analogs would not be useful medications in the treatment of opioid <b>addiction</b>.
+ZGLP1	drug	alcohol	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of <b>alcohol</b>, central stimulants, and nicotine.
+ZGLP1	drug	nicotine	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of alcohol, central stimulants, and <b>nicotine</b>.
+ZGLP1	drug	opioid	31058214	This difference between <b>opioids</b> and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of alcohol, central stimulants, and nicotine.
+ZGLP1	addiction	addiction	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the <b>addictive</b> effects of alcohol, central stimulants, and nicotine.
+ZGLP1	drug	cocaine	30930091	Central <strong>GLP 1</strong> receptors: Novel molecular targets for <b>cocaine</b> use disorder.
+ZGLP1	drug	cocaine	30930091	Recent preclinical evidence suggests that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists could be re purposed to treat <b>cocaine</b> craving induced relapse.
+ZGLP1	addiction	relapse	30930091	Recent preclinical evidence suggests that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists could be re purposed to treat cocaine <b>craving</b> induced <b>relapse</b>.
+ZGLP1	drug	cocaine	30930091	This review endeavors to comprehensively summarize the current literature investigating the efficacy of <strong>GLP 1</strong> receptor agonists in reducing the rewarding and reinforcing effects of <b>cocaine</b> in animal models of <b>cocaine</b> use disorder.
+ZGLP1	addiction	reward	30930091	This review endeavors to comprehensively summarize the current literature investigating the efficacy of <strong>GLP 1</strong> receptor agonists in reducing the rewarding and <b>reinforcing</b> effects of cocaine in animal models of cocaine use disorder.
+ZGLP1	drug	cocaine	30930091	The role of central endogenous <strong>GLP 1</strong> circuits in voluntary <b>cocaine</b> taking and seeking is also discussed.
+ZGLP1	addiction	relapse	30930091	The role of central endogenous <strong>GLP 1</strong> circuits in voluntary cocaine taking and <b>seeking</b> is also discussed.
+ZGLP1	addiction	addiction	30930091	Behavioral, neurochemical, electrophysiological and molecular biology studies indicate that central <strong>GLP 1</strong> receptor activation functionally modulates the mesolimbic reward system and decreases <b>addiction</b> like phenotypes in rodents.
+ZGLP1	addiction	reward	30930091	Behavioral, neurochemical, electrophysiological and molecular biology studies indicate that central <strong>GLP 1</strong> receptor activation functionally modulates the mesolimbic <b>reward</b> system and decreases addiction like phenotypes in rodents.
+ZGLP1	drug	cocaine	30930091	Overall, an emerging preclinical literature provides compelling evidence to advance <strong>GLP 1</strong> receptor agonists into clinical trials testing the efficacy of these medications in preventing <b>cocaine</b> craving induced relapse.
+ZGLP1	addiction	relapse	30930091	Overall, an emerging preclinical literature provides compelling evidence to advance <strong>GLP 1</strong> receptor agonists into clinical trials testing the efficacy of these medications in preventing cocaine <b>craving</b> induced <b>relapse</b>.
+ZGLP1	drug	amphetamine	30831183	Stress responsive prolactin releasing peptide (PrRP) positive noradrenergic and glucagon like peptide 1 (<strong>GLP 1</strong>) positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating <b>amph</b> induced hypophagia and CTA.
+ZGLP1	addiction	aversion	30831183	Stress responsive prolactin releasing peptide (PrRP) positive noradrenergic and glucagon like peptide 1 (<strong>GLP 1</strong>) positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating amph induced hypophagia and <b>CTA</b>.
+ZGLP1	drug	amphetamine	30831183	Compared to control saline treatment, <b>amph</b> activated significantly more cNTS neurons, including PrRP negative noradrenergic (NA) neurons, GABAergic neurons, and glutamatergic neurons, but not PrRP or <strong>GLP 1</strong> neurons.
+ZGLP1	drug	alcohol	30771711	Glucagon like peptide 1 (<strong>GLP 1</strong>), an incretin hormone that reduces food intake, was recently established as a novel regulator of <b>alcohol</b> mediated behaviors.
+ZGLP1	drug	alcohol	30771711	Clinically available analogues pass freely into the brain, but the mechanisms underlying <strong>GLP 1</strong> modulated <b>alcohol</b> reward remains largely unclear.
+ZGLP1	addiction	reward	30771711	Clinically available analogues pass freely into the brain, but the mechanisms underlying <strong>GLP 1</strong> modulated alcohol <b>reward</b> remains largely unclear.
+ZGLP1	drug	alcohol	30771711	<strong>GLP 1</strong> receptors (GLP 1R) are expressed throughout the nuclei of importance for acute and chronic effects of <b>alcohol</b>, such as the laterodorsal tegmental area (LDTg), the ventral tegmental area (VTA) and the nucleus accumbens (NAc).
+ZGLP1	drug	alcohol	30439457	The present review therefore summarizes the current studies investigating the ability of the gut brain peptides ghrelin, glucagon like peptide 1 (<strong>GLP 1</strong>), amylin and neuromedin U (NMU) to modulate <b>alcohol</b>  and drug related behaviors in rodents and humans.
+ZGLP1	drug	alcohol	30439457	On the other hand, the anorexigenic peptides <strong>GLP 1</strong>, amylin and NMU independently inhibits reward from <b>alcohol</b> and drugs of abuse in rodents.
+ZGLP1	addiction	reward	30439457	On the other hand, the anorexigenic peptides <strong>GLP 1</strong>, amylin and NMU independently inhibits <b>reward</b> from alcohol and drugs of abuse in rodents.
+ZGLP1	addiction	addiction	30439457	Collectively, these rodent and human studies imply that central ghrelin, <strong>GLP 1</strong>, amylin and NMU signaling may contribute to <b>addiction</b> processes.
+ZGLP1	drug	cocaine	30414405	<b>Cocaine</b> and <b>cocaine</b> expectancy increase growth hormone, ghrelin, <strong>GLP 1</strong>, IGF 1, adiponectin, and corticosterone while decreasing leptin, insulin, GIP, and prolactin.
+ZGLP1	drug	cocaine	30414405	During <b>cocaine</b> taking, growth hormone and acetylated ghrelin increased 10 fold; glucagon like peptide 1 (<strong>GLP 1</strong>) doubled; non acetylated ghrelin, insulin like growth factor 1 (IGF 1), and corticosterone increased by 50% and adiponectin increased by 17%.
+ZGLP1	drug	alcohol	30012779	Does glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist stimulation reduce <b>alcohol</b> intake in patients with <b>alcohol</b> dependence: study protocol of a randomised, double blinded, placebo controlled clinical trial.
+ZGLP1	addiction	dependence	30012779	Does glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist stimulation reduce alcohol intake in patients with alcohol <b>dependence</b>: study protocol of a randomised, double blinded, placebo controlled clinical trial.
+ZGLP1	drug	alcohol	30012779	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor stimulation has proven to reduce <b>alcohol</b> consumption in preclinical experiments.
+ZGLP1	drug	alcohol	29927808	The present study investigated the relationship between accumbal ghrelin and glucagon like peptide 1 (<strong>GLP 1</strong>) signaling in <b>alcohol</b> reward in female rats.
+ZGLP1	addiction	reward	29927808	The present study investigated the relationship between accumbal ghrelin and glucagon like peptide 1 (<strong>GLP 1</strong>) signaling in alcohol <b>reward</b> in female rats.
+ZGLP1	drug	alcohol	29927808	Overall, these findings demonstrate the importance of accumbal ghrelin and <strong>GLP 1</strong> signaling in <b>alcohol</b> reward and appetitive motivation.
+ZGLP1	addiction	reward	29927808	Overall, these findings demonstrate the importance of accumbal ghrelin and <strong>GLP 1</strong> signaling in alcohol <b>reward</b> and appetitive motivation.
+ZGLP1	drug	cocaine	29497166	Here we investigated a role for glucagon like peptide 1 (<strong>GLP 1</strong>) receptors in the reinstatement of <b>cocaine</b> seeking behavior, an animal model of relapse.
+ZGLP1	addiction	relapse	29497166	Here we investigated a role for glucagon like peptide 1 (<strong>GLP 1</strong>) receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior, an animal model of <b>relapse</b>.
+ZGLP1	drug	cocaine	29497166	We showed that peripheral administration of the <strong>GLP 1</strong> receptor agonist exendin 4 dose dependently reduced <b>cocaine</b> seeking in rats at doses that did not affect ad libitum food intake, meal patterns or body weight.
+ZGLP1	addiction	relapse	29497166	We showed that peripheral administration of the <strong>GLP 1</strong> receptor agonist exendin 4 dose dependently reduced cocaine <b>seeking</b> in rats at doses that did not affect ad libitum food intake, meal patterns or body weight.
+ZGLP1	drug	cocaine	29497166	The effects of systemic exendin 4 on <b>cocaine</b> reinstatement were attenuated in rats pretreated with intra VTA infusions of the <strong>GLP 1</strong> receptor antagonist exendin (9 39), indicating that the suppressive effects of systemic exendin 4 on <b>cocaine</b> seeking were due, in part, to activation of <strong>GLP 1</strong> receptors in the VTA.
+ZGLP1	addiction	relapse	29497166	The effects of systemic exendin 4 on cocaine <b>reinstatement</b> were attenuated in rats pretreated with intra VTA infusions of the <strong>GLP 1</strong> receptor antagonist exendin (9 39), indicating that the suppressive effects of systemic exendin 4 on cocaine <b>seeking</b> were due, in part, to activation of <strong>GLP 1</strong> receptors in the VTA.
+ZGLP1	drug	cocaine	29497166	Thus, our study demonstrated a novel role for <strong>GLP 1</strong> receptors in the reinstatement of <b>cocaine</b> seeking behavior and identified behaviorally relevant doses of a <strong>GLP 1</strong> receptor agonist that selectively reduced <b>cocaine</b> seeking and did not produce adverse effects.
+ZGLP1	addiction	relapse	29497166	Thus, our study demonstrated a novel role for <strong>GLP 1</strong> receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior and identified behaviorally relevant doses of a <strong>GLP 1</strong> receptor agonist that selectively reduced cocaine <b>seeking</b> and did not produce adverse effects.
+ZGLP1	drug	alcohol	29480848	A novel approach might use glucagon like peptide 1 (<strong>GLP 1</strong>) agonists, which reduce <b>alcohol</b> and drug use in preclinical studies.
+ZGLP1	drug	nicotine	29480848	Several <strong>GLP 1</strong> agonists are used clinically to treat type 2 diabetes and obesity, but none have been tested in humans to reduce <b>smoking</b>.
+ZGLP1	drug	alcohol	29337226	<strong>GLP 1</strong> signaling and <b>alcohol</b> mediated behaviors; preclinical and clinical evidence.
+ZGLP1	drug	alcohol	29337226	One of these gut brain peptides is the annorexigenic peptide glucagon like peptide 1 (<strong>GLP 1</strong>), Preclinical studies show that <strong>GLP 1</strong> receptor activation, either by <strong>GLP 1</strong> or analogues, attenuate the ability of <b>alcohol</b> to activate the mesolimbic dopamine system as well as decrease <b>alcohol</b> consumption and operant self administration.
+ZGLP1	addiction	reward	29337226	One of these gut brain peptides is the annorexigenic peptide glucagon like peptide 1 (<strong>GLP 1</strong>), Preclinical studies show that <strong>GLP 1</strong> receptor activation, either by <strong>GLP 1</strong> or analogues, attenuate the ability of alcohol to activate the mesolimbic dopamine system as well as decrease alcohol consumption and <b>operant</b> self administration.
+ZGLP1	drug	alcohol	29337226	In further support for the endogenous <strong>GLP 1</strong> system in addiction processes are the experimental data showing that a <strong>GLP 1</strong> receptor antagonist increases <b>alcohol</b> intake.
+ZGLP1	addiction	addiction	29337226	In further support for the endogenous <strong>GLP 1</strong> system in <b>addiction</b> processes are the experimental data showing that a <strong>GLP 1</strong> receptor antagonist increases alcohol intake.
+ZGLP1	addiction	addiction	29337226	Moreover, <strong>GLP 1</strong> receptor agonists prevent the ability of other <b>addictive</b> drugs to activate the mesolimbic dopamine system.
+ZGLP1	drug	alcohol	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with <b>alcohol</b> addiction as well as increased <b>alcohol</b> infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of cocaine and iii) that a <strong>GLP 1</strong> receptor agonist reduces <b>alcohol</b> intake in patients with type 2 diabetes mellitus.
+ZGLP1	drug	cocaine	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with alcohol addiction as well as increased alcohol infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of <b>cocaine</b> and iii) that a <strong>GLP 1</strong> receptor agonist reduces alcohol intake in patients with type 2 diabetes mellitus.
+ZGLP1	addiction	addiction	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with alcohol <b>addiction</b> as well as increased alcohol infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of cocaine and iii) that a <strong>GLP 1</strong> receptor agonist reduces alcohol intake in patients with type 2 diabetes mellitus.
+ZGLP1	drug	alcohol	29337226	These experimental and clinical studies raises the concern that clinically available <strong>GLP 1</strong> receptor agonists deserves to be tested as potential treatments of patients with addictive disorders including <b>alcohol</b> addiction.
+ZGLP1	addiction	addiction	29337226	These experimental and clinical studies raises the concern that clinically available <strong>GLP 1</strong> receptor agonists deserves to be tested as potential treatments of patients with <b>addictive</b> disorders including alcohol <b>addiction</b>.
+ZGLP1	drug	cannabinoid	29231147	Inclusion criteria were: 1) full text available in English; 2) published in a peerreviewed journal and using the following keywords: neurotransmitters (AgRP, BDNF, αMSH, NP Y, <b>endocannabinoids</b>, adiponectin, CCK, ghrelin, <strong>GLP 1</strong>, insulin, leptin, PP, PYY), hormones (FSH, LH, estrogen, progesterone, testosterone) and bulimia nervosa, eating disorders.
+ZGLP1	drug	cocaine	29226617	Recent evidence indicates that activation of glucagon like peptide 1 (<strong>GLP 1</strong>) receptors reduces <b>cocaine</b> mediated behaviors and <b>cocaine</b> evoked dopamine release in the nucleus accumbens (NAc).
+ZGLP1	drug	cocaine	29226617	However, no studies have examined the role of NAc <strong>GLP 1</strong> receptors in the reinstatement of <b>cocaine</b> seeking behavior, an animal model of relapse.
+ZGLP1	addiction	relapse	29226617	However, no studies have examined the role of NAc <strong>GLP 1</strong> receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior, an animal model of <b>relapse</b>.
+ZGLP1	drug	cocaine	29226617	To determine the effects of <strong>GLP 1</strong> receptor activation on neuronal excitability, exendin 4 was bath applied to ex vivo NAc slices from <b>cocaine</b> experienced and saline experienced rats following extinction of <b>cocaine</b> taking behavior.
+ZGLP1	drug	cocaine	29226617	These effects were not associated with altered expression of <strong>GLP 1</strong> receptors in the NAc following <b>cocaine</b> self administration.
+ZGLP1	drug	cocaine	29226617	Taken together, these findings indicate that increased activation of <strong>GLP 1</strong> receptors in the NAc during <b>cocaine</b> abstinence increases intrinsic, but not synaptic, excitability of medium spiny neurons and is sufficient to reduce <b>cocaine</b> seeking behavior.
+ZGLP1	addiction	relapse	29226617	Taken together, these findings indicate that increased activation of <strong>GLP 1</strong> receptors in the NAc during cocaine abstinence increases intrinsic, but not synaptic, excitability of medium spiny neurons and is sufficient to reduce cocaine <b>seeking</b> behavior.
+ZGLP1	drug	alcohol	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for <b>alcohol</b> and drug reward, and for the development of addiction.
+ZGLP1	addiction	addiction	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for alcohol and drug reward, and for the development of <b>addiction</b>.
+ZGLP1	addiction	reward	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for alcohol and drug <b>reward</b>, and for the development of addiction.
+ZGLP1	drug	alcohol	28778739	<strong>GLP 1</strong> receptor agonists can decrease <b>alcohol</b> intake acutely in rodents.
+ZGLP1	addiction	relapse	28778739	Here, we assessed the effect of daily treatment with the <strong>GLP 1</strong> receptor agonist Exendin 4 in an assay of <b>relapse</b> like drinking in socially housed mice.
+ZGLP1	drug	alcohol	28778739	These findings support the possible use of <strong>GLP 1</strong> receptor agonists in the treatment of <b>alcohol</b> use disorder.
+ZGLP1	addiction	withdrawal	28664354	After pioglitazone <b>withdrawal</b>, case reports increased for dipeptidyl peptidase 4 (DPP 4) inhibitors, glinides, and glucagon like peptide 1 (<strong>GLP 1</strong>) analogues (+84%, +22% and +5%, respectively) and reimbursements (+55, +11 and +50%, respectively); both decreased for sulfonylureas (case reports:  6%, reimbursements:  2%).
+ZGLP1	drug	nicotine	28368384	<strong>GLP 1</strong> acts on habenular avoidance circuits to control <b>nicotine</b> intake.
+ZGLP1	drug	nicotine	28368384	Here we show that <b>nicotine</b> activates glucagon like peptide 1 (<strong>GLP 1</strong>) neurons in the nucleus tractus solitarius (NTS).
+ZGLP1	drug	nicotine	28368384	The antidiabetic drugs sitagliptin and exenatide, which inhibit <strong>GLP 1</strong> breakdown and stimulate <strong>GLP 1</strong> receptors, respectively, decreased <b>nicotine</b> intake in mice.
+ZGLP1	drug	nicotine	28368384	Chemogenetic activation of <strong>GLP 1</strong> neurons in NTS similarly decreased <b>nicotine</b> intake.
+ZGLP1	drug	nicotine	28368384	Activation of <strong>GLP 1</strong> receptors in the MHb IPN circuit abolished <b>nicotine</b> reward and decreased <b>nicotine</b> intake, whereas their knockdown or pharmacological blockade increased intake.
+ZGLP1	addiction	reward	28368384	Activation of <strong>GLP 1</strong> receptors in the MHb IPN circuit abolished nicotine <b>reward</b> and decreased nicotine intake, whereas their knockdown or pharmacological blockade increased intake.
+ZGLP1	drug	nicotine	28368384	<strong>GLP 1</strong> neurons may therefore serve as 'satiety sensors' for <b>nicotine</b> that stimulate habenular systems to promote <b>nicotine</b> avoidance before its aversive effects are encountered.
+ZGLP1	addiction	aversion	28368384	<strong>GLP 1</strong> neurons may therefore serve as 'satiety sensors' for nicotine that stimulate habenular systems to promote nicotine avoidance before its <b>aversive</b> effects are encountered.
+ZGLP1	drug	cocaine	28315693	Central <strong>GLP 1</strong> receptor activation modulates <b>cocaine</b> evoked phasic dopamine signaling in the nucleus accumbens core.
+ZGLP1	drug	cocaine	28315693	Recently, metabolic regulatory peptides, including the satiety signal glucagon like peptide 1 (<strong>GLP 1</strong>), have been shown to modulate <b>cocaine</b> reward driven behavior and sustained dopamine levels after <b>cocaine</b> administration.
+ZGLP1	addiction	reward	28315693	Recently, metabolic regulatory peptides, including the satiety signal glucagon like peptide 1 (<strong>GLP 1</strong>), have been shown to modulate cocaine <b>reward</b> driven behavior and sustained dopamine levels after cocaine administration.
+ZGLP1	drug	cocaine	28315693	Here, we use fast scan cyclic voltammetry (FSCV) to explore <strong>GLP 1</strong> receptor (GLP 1R) modulation of dynamic dopamine release in the nucleus accumbens (NAc) during <b>cocaine</b> administration.
+ZGLP1	drug	alcohol	27579999	Effects of the <strong>GLP 1</strong> Agonist Exendin 4 on Intravenous <b>Ethanol</b> Self Administration in Mice.
+ZGLP1	drug	alcohol	27579999	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists have been shown to decrease <b>ethanol</b> (EtOH) drinking in rodent assays.
+ZGLP1	addiction	reward	27579999	To begin to understand the neurobiological mechanisms by which <strong>GLP 1</strong> receptor ligands may be able to control EtOH intake, it is important to ascertain whether they can modulate the direct <b>reinforcing</b> effects of EtOH, without the confound of effects on ingestive behaviors generally.
+ZGLP1	addiction	reward	27579999	Second, <strong>GLP 1</strong> receptor agonists can powerfully attenuate voluntary EtOH intake by directly modulating the <b>reinforcing</b> effects of EtOH.
+ZGLP1	drug	alcohol	27579999	These findings support the potential usefulness of <strong>GLP 1</strong> receptor ligands in the treatment of <b>alcohol</b> use disorder.
+ZGLP1	drug	cocaine	27187231	Agonism of the glucagon like peptide 1 (<strong>GLP 1</strong>) receptor (GLP 1R) has been effective at treating aspects of addictive behavior for a number of abused substances, including <b>cocaine</b>.
+ZGLP1	addiction	addiction	27187231	Agonism of the glucagon like peptide 1 (<strong>GLP 1</strong>) receptor (GLP 1R) has been effective at treating aspects of <b>addictive</b> behavior for a number of abused substances, including cocaine.
+ZGLP1	drug	cocaine	27187231	Exenatide (Ex 4), a long lasting synthetic analog of <strong>GLP 1</strong> abolished <b>cocaine</b> induced elevation of DA.
+ZGLP1	drug	alcohol	27072507	Recent data implicate glucagon like peptide 1 (<strong>GLP 1</strong>), a potent anorexigenic peptide released in response to nutrient intake, as a regulator for the reinforcing properties of food, <b>alcohol</b> and psychostimulants.
+ZGLP1	addiction	reward	27072507	Recent data implicate glucagon like peptide 1 (<strong>GLP 1</strong>), a potent anorexigenic peptide released in response to nutrient intake, as a regulator for the <b>reinforcing</b> properties of food, alcohol and psychostimulants.
+ZGLP1	drug	alcohol	27072507	Here, we examined amphetamine reinforcement, <b>alcohol</b> intake and hedonic feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+ZGLP1	drug	amphetamine	27072507	Here, we examined <b>amphetamine</b> reinforcement, alcohol intake and hedonic feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+ZGLP1	addiction	reward	27072507	Here, we examined amphetamine <b>reinforcement</b>, alcohol intake and <b>hedonic</b> feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+ZGLP1	addiction	addiction	27072507	The present study provides critical insights regarding the nature by which <strong>GLP 1</strong> signaling controls reinforced behaviors and underscores the importance of both peripheral and central GLP 1R signaling for the regulation of <b>addictive</b> disorders.
+ZGLP1	addiction	reward	27066524	<strong>GLP 1</strong> influences food and drug <b>reward</b>.
+ZGLP1	addiction	reward	27066524	That the neuropeptide glucagon like peptide 1 (<strong>GLP 1</strong>) is under investigation for both the homeostatic and <b>hedonic</b> controls of feeding is not surprising or novel.
+ZGLP1	addiction	reward	27066524	However, if the neural substrates that underline food <b>reward</b> are shared with other <b>reward</b> related behaviors generally, then future research should investigate and embrace the likelihood that endogenous and exogenous <strong>GLP 1</strong> receptor activation may influence multiple <b>reward</b> related behaviors.
+ZGLP1	drug	alcohol	27066524	An emerging literature demonstrates a role for the <strong>GLP 1</strong> system in modulating maladaptive reward behaviors, including drug and <b>alcohol</b> consumption.
+ZGLP1	addiction	reward	27066524	An emerging literature demonstrates a role for the <strong>GLP 1</strong> system in modulating maladaptive <b>reward</b> behaviors, including drug and alcohol consumption.
+ZGLP1	addiction	addiction	27066524	Thus, if <strong>GLP 1</strong> based pharmacotherapies are to be used to treat drug <b>addiction</b> and other diseases associated with maladaptive reward behaviors (e.g.
+ZGLP1	addiction	reward	27066524	Thus, if <strong>GLP 1</strong> based pharmacotherapies are to be used to treat drug addiction and other diseases associated with maladaptive <b>reward</b> behaviors (e.g.
+ZGLP1	addiction	reward	27066524	Equally as likely, non selective effects on natural <b>reward</b> and maladaptive <b>reward</b> behaviors may be observed for <strong>GLP 1</strong> based pharmacotherapies.
+ZGLP1	drug	cocaine	26675243	As the neural circuits and neurobiological mechanisms underlying drug taking overlap to some degree with those regulating food intake, these findings suggest that activation of central <strong>GLP 1</strong> receptors may also attenuate <b>cocaine</b> taking.
+ZGLP1	drug	cocaine	26675243	Here, we show that intra VTA administration of the <strong>GLP 1</strong> receptor agonist exendin 4 (0.05 μg) significantly reduced <b>cocaine</b>, but not sucrose, self administration in rats.
+ZGLP1	drug	cocaine	26675243	We also demonstrate that <b>cocaine</b> taking is associated with elevated plasma corticosterone levels and that systemic infusion of <b>cocaine</b> activates <strong>GLP 1</strong> expressing neurons in the nucleus tractus solitarius (NTS), a hindbrain nucleus that projects monosynaptically to the VTA.
+ZGLP1	drug	cocaine	26675243	To determine the potential mechanisms by which <b>cocaine</b> activates NTS <strong>GLP 1</strong> expressing neurons, we microinjected corticosterone (0.5 μg) directly into the hindbrain fourth ventricle.
+ZGLP1	drug	cocaine	26675243	Intraventricular corticosterone attenuated <b>cocaine</b> self administration and this effect was blocked in animals pretreated with the <strong>GLP 1</strong> receptor antagonist exendin (9 39) (10 μg) in the VTA.
+ZGLP1	drug	cocaine	26675243	Finally, AAV shRNA mediated knockdown of VTA <strong>GLP 1</strong> receptors was sufficient to augment <b>cocaine</b> self administration.
+ZGLP1	drug	cocaine	26675243	Taken together, these findings indicate that increased activation of NTS <strong>GLP 1</strong> expressing neurons by corticosterone may represent a homeostatic response to <b>cocaine</b> taking, thereby reducing the reinforcing efficacy of <b>cocaine</b>.
+ZGLP1	addiction	reward	26675243	Taken together, these findings indicate that increased activation of NTS <strong>GLP 1</strong> expressing neurons by corticosterone may represent a homeostatic response to cocaine taking, thereby reducing the <b>reinforcing</b> efficacy of cocaine.
+ZGLP1	drug	cocaine	26675243	Therefore, central <strong>GLP 1</strong> receptors may represent a novel target for <b>cocaine</b> addiction pharmacotherapies.
+ZGLP1	addiction	addiction	26675243	Therefore, central <strong>GLP 1</strong> receptors may represent a novel target for cocaine <b>addiction</b> pharmacotherapies.
+ZGLP1	drug	cannabinoid	26546790	To explore the role of some gastrointestinal orexigenic and anorexigenic peptides and <b>endocannabinoids</b> (and some related congeners) in chocolate consumption, we measured changes in circulating levels of ghrelin, glucagon like peptide 1 (<strong>GLP 1</strong>), peptide YY (PYY), anandamide (AEA), 2 AG, <b>palmitoylethanolamide</b> (PEA), and <b>oleoylethanolamide</b> (OEA) in 10 satiated severely obese subjects after consumption of chocolate and, on a separate day, of a non palatable isocaloric food with the same bromatologic composition.
+ZGLP1	drug	alcohol	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several <b>alcohol</b> mediated behaviors as well as amphetamine induced, cocaine induced and nicotine induced reward.
+ZGLP1	drug	amphetamine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as <b>amphetamine</b> induced, cocaine induced and nicotine induced reward.
+ZGLP1	drug	cocaine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, <b>cocaine</b> induced and nicotine induced reward.
+ZGLP1	drug	nicotine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, cocaine induced and <b>nicotine</b> induced reward.
+ZGLP1	addiction	reward	26303264	<strong>GLP 1</strong> receptors are expressed in <b>reward</b> related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, cocaine induced and nicotine induced <b>reward</b>.
+ZGLP1	drug	alcohol	26303264	The present series of experiments were undertaken to investigate the effect of the <strong>GLP 1</strong> receptor agonist, liraglutide, on several <b>alcohol</b> related behaviors in rats that model different aspects of <b>alcohol</b> use disorder in humans.
+ZGLP1	drug	alcohol	26303264	Collectively, these data suggest that <strong>GLP 1</strong> receptor agonists could be tested for treatment of <b>alcohol</b> dependence in humans.
+ZGLP1	addiction	dependence	26303264	Collectively, these data suggest that <strong>GLP 1</strong> receptor agonists could be tested for treatment of alcohol <b>dependence</b> in humans.
+ZGLP1	addiction	aversion	26211731	The <b>Aversive</b> Agent Lithium Chloride Suppresses Phasic Dopamine Release Through Central <strong>GLP 1</strong> Receptors.
+ZGLP1	drug	alcohol	26080318	<strong>GLP 1</strong> receptor (GLP 1R) activation also attenuates the reinforcing properties of <b>alcohol</b> in rodents.
+ZGLP1	addiction	reward	26080318	<strong>GLP 1</strong> receptor (GLP 1R) activation also attenuates the <b>reinforcing</b> properties of alcohol in rodents.
+ZGLP1	drug	cocaine	26072178	The glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist exendin 4 reduces <b>cocaine</b> self administration in mice.
+ZGLP1	drug	cocaine	26072178	Based on the anatomical distribution of <strong>GLP 1</strong> receptors in the brain and the well established effects of <strong>GLP 1</strong> on food reward, we decided to investigate the effect of the <strong>GLP 1</strong> analogue exendin 4 on <b>cocaine</b>  and dopamine D1 receptor agonist induced hyperlocomotion, on acute and chronic <b>cocaine</b> self administration, on <b>cocaine</b> induced striatal dopamine release in mice and on <b>cocaine</b> induced c fos activation.
+ZGLP1	addiction	reward	26072178	Based on the anatomical distribution of <strong>GLP 1</strong> receptors in the brain and the well established effects of <strong>GLP 1</strong> on food <b>reward</b>, we decided to investigate the effect of the <strong>GLP 1</strong> analogue exendin 4 on cocaine  and dopamine D1 receptor agonist induced hyperlocomotion, on acute and chronic cocaine self administration, on cocaine induced striatal dopamine release in mice and on cocaine induced c fos activation.
+ZGLP1	drug	cocaine	26072178	Here, we report that <strong>GLP 1</strong> receptor stimulation reduces acute and chronic <b>cocaine</b> self administration and attenuates <b>cocaine</b> induced hyperlocomotion.
+ZGLP1	drug	cocaine	26072178	In addition, we show that peripheral administration of exendin 4 reduces <b>cocaine</b> induced elevation of striatal dopamine levels and striatal c fos expression implicating central <strong>GLP 1</strong> receptors in these responses.
+ZGLP1	drug	cocaine	26072178	The present results demonstrate that the <strong>GLP 1</strong> system modulates <b>cocaine</b>'s effects on behavior and dopamine homeostasis, indicating that the <strong>GLP 1</strong> receptor may be a novel target for the pharmacological treatment of drug addiction.
+ZGLP1	addiction	addiction	26072178	The present results demonstrate that the <strong>GLP 1</strong> system modulates cocaine's effects on behavior and dopamine homeostasis, indicating that the <strong>GLP 1</strong> receptor may be a novel target for the pharmacological treatment of drug <b>addiction</b>.
+ZGLP1	addiction	addiction	25669605	Both palatable food and illicit drugs activate brain reward circuitries, and pharmacological studies suggest that central nervous system <strong>GLP 1</strong> signaling holds potential for the treatment of <b>addiction</b>.
+ZGLP1	addiction	reward	25669605	Both palatable food and illicit drugs activate brain <b>reward</b> circuitries, and pharmacological studies suggest that central nervous system <strong>GLP 1</strong> signaling holds potential for the treatment of addiction.
+ZGLP1	addiction	reward	25669605	However, the role of endogenous <strong>GLP 1</strong> in the attenuation of <b>reward</b> oriented behavior, and the essential domains of the mesolimbic system mediating these beneficial effects, are largely unknown.
+ZGLP1	drug	alcohol	25380665	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist prevents development of tolerance to anti anxiety effect of <b>ethanol</b> and withdrawal induced anxiety in rats.
+ZGLP1	addiction	withdrawal	25380665	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist prevents development of tolerance to anti anxiety effect of ethanol and <b>withdrawal</b> induced anxiety in rats.
+ZGLP1	drug	alcohol	25380665	We recently reported that inhibition of dipeptidyl peptidase IV (DPP IV), an enzyme responsible for metabolism of endogenous glucagon like peptide 1 (<strong>GLP 1</strong>), delays tolerance to anti anxiety effect of <b>ethanol</b> and withdrawal induced anxiety in rats.
+ZGLP1	addiction	withdrawal	25380665	We recently reported that inhibition of dipeptidyl peptidase IV (DPP IV), an enzyme responsible for metabolism of endogenous glucagon like peptide 1 (<strong>GLP 1</strong>), delays tolerance to anti anxiety effect of ethanol and <b>withdrawal</b> induced anxiety in rats.
+ZGLP1	drug	alcohol	25380665	Intrigued with this report, present study examined the role of glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist, liraglutide in (1) acute anti anxiety effect of <b>ethanol</b>; (2) tolerance to <b>ethanol</b>'s anti anxiety effect and (3) <b>ethanol</b> withdrawal induced anxiety using elevated plus maze (EPM) test in rats.
+ZGLP1	addiction	withdrawal	25380665	Intrigued with this report, present study examined the role of glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist, liraglutide in (1) acute anti anxiety effect of ethanol; (2) tolerance to ethanol's anti anxiety effect and (3) ethanol <b>withdrawal</b> induced anxiety using elevated plus maze (EPM) test in rats.
+ZGLP1	drug	alcohol	25380665	(1) <strong>GLP 1</strong> agonist, liraglutide exhibited anti anxiety effect per se; (2) potentiated anti anxiety effect of <b>ethanol</b>; (3) prevented development tolerance to anti anxiety effect of <b>ethanol</b> and (4) prevented withdrawal induced anxiety.
+ZGLP1	addiction	withdrawal	25380665	(1) <strong>GLP 1</strong> agonist, liraglutide exhibited anti anxiety effect per se; (2) potentiated anti anxiety effect of ethanol; (3) prevented development tolerance to anti anxiety effect of ethanol and (4) prevented <b>withdrawal</b> induced anxiety.
+ZGLP1	drug	alcohol	25380665	Further studies examining intracellular cascade of events contributing to these effects may help to improve understanding about role of <strong>GLP 1</strong> receptors in <b>ethanol</b> mediated behaviors.
+ZGLP1	drug	cannabinoid	25361428	<b>Cannabinoid</b> receptor 1 antagonist treatment induces glucagon release and shows an additive therapeutic effect with <strong>GLP 1</strong> agonist in diet induced obese mice.
+ZGLP1	drug	cannabinoid	25361428	We hypothesized that the insulin secretagogue effect of <strong>GLP 1</strong> agonist exendin 4 may synergize with the insulin sensitizing action of <b>rimonabant</b>.
+ZGLP1	addiction	reward	24958205	However, <strong>GLP 1</strong> receptors are expressed in areas intimately associated with <b>reward</b> regulation.
+ZGLP1	addiction	reward	24958205	Given that regulation of food and drug intake share common neurobiological substrates, the possibility that ghrelin and <strong>GLP 1</strong> play an important role in <b>reward</b> regulation should be considered.
+ZGLP1	drug	alcohol	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by <b>alcohol</b>, amphetamine, cocaine and nicotine in rodents are overviewed herein.
+ZGLP1	drug	amphetamine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, <b>amphetamine</b>, cocaine and nicotine in rodents are overviewed herein.
+ZGLP1	drug	cocaine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, amphetamine, <b>cocaine</b> and nicotine in rodents are overviewed herein.
+ZGLP1	drug	nicotine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, amphetamine, cocaine and <b>nicotine</b> in rodents are overviewed herein.
+ZGLP1	addiction	reward	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls <b>reward</b> induced by alcohol, amphetamine, cocaine and nicotine in rodents are overviewed herein.
+ZGLP1	drug	alcohol	24958205	Collectively, these data suggest that ghrelin and <strong>GLP 1</strong> receptors may be novel targets for development of pharmacological treatments of <b>alcohol</b> and drug dependence.
+ZGLP1	addiction	dependence	24958205	Collectively, these data suggest that ghrelin and <strong>GLP 1</strong> receptors may be novel targets for development of pharmacological treatments of alcohol and drug <b>dependence</b>.
+ZGLP1	addiction	reward	24204788	The findings that <strong>GLP 1</strong> targets <b>reward</b> related areas including mesolimbic dopamine areas indicate that the physiological role of <strong>GLP 1</strong> extends beyond food intake and glucose homeostasis control to include <b>reward</b> regulation.
+ZGLP1	drug	nicotine	24204788	The present series of experiments was therefore designed to investigate the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on established <b>nicotine</b> induced effects on the mesolimbic dopamine system in mice.
+ZGLP1	drug	nicotine	24204788	Given that development of <b>nicotine</b> addiction largely depends on the effects of <b>nicotine</b> on the mesolimbic dopamine system these findings indicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for <b>nicotine</b> cessations in humans.
+ZGLP1	addiction	addiction	24204788	Given that development of nicotine <b>addiction</b> largely depends on the effects of nicotine on the mesolimbic dopamine system these findings indicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for nicotine cessations in humans.
+ZGLP1	addiction	reward	24140429	However, emerging data indicate that <strong>GLP 1</strong> also contributes to non homeostatic regulation of food <b>reward</b> and motivated behaviors in brain <b>reward</b> centers, including the ventral tegmental area and nucleus accumbens.
+ZGLP1	drug	alcohol	24140429	The hypothesis that <strong>GLP 1</strong> signaling modulates reward circuitry has provided the impetus for studies demonstrating that <strong>GLP 1</strong> attenuates reward for psychostimulants and <b>alcohol</b>.
+ZGLP1	addiction	reward	24140429	The hypothesis that <strong>GLP 1</strong> signaling modulates <b>reward</b> circuitry has provided the impetus for studies demonstrating that <strong>GLP 1</strong> attenuates <b>reward</b> for psychostimulants and alcohol.
+ZGLP1	addiction	reward	24140429	Here, we examine current evidence for <strong>GLP 1</strong> mediated regulation of food and drug <b>reward</b> and use these findings to hypothesize mechanisms of action within brain <b>reward</b> centers.
+ZGLP1	addiction	reward	24133407	The central <strong>GLP 1</strong>: implications for food and drug <b>reward</b>.
+ZGLP1	drug	alcohol	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to cocaine, amphetamine, and <b>alcohol</b> reward.
+ZGLP1	drug	amphetamine	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to cocaine, <b>amphetamine</b>, and alcohol reward.
+ZGLP1	drug	cocaine	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to <b>cocaine</b>, amphetamine, and alcohol reward.
+ZGLP1	addiction	reward	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on <b>reward</b> behavior is not limited to food derived <b>reward</b> but extends to cocaine, amphetamine, and alcohol <b>reward</b>.
+ZGLP1	addiction	reward	24133407	The new discoveries concerning <strong>GLP 1</strong> action on the mesolimbic <b>reward</b> system significantly extend the potential therapeutic range of this drug target.
+ZGLP1	addiction	reward	23874851	Given that <strong>GLP 1</strong> receptors are expressed in <b>reward</b> areas, such as the nucleus accumbens and ventral tegmental area, and that common mechanisms regulate food and drug induced <b>reward</b> we hypothesize that <strong>GLP 1</strong> receptors are involved in <b>reward</b> regulation.
+ZGLP1	drug	amphetamine	23874851	Herein the effect of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4), on <b>amphetamine</b>  and cocaine induced activation of the mesolimbic dopamine system was investigated in mice.
+ZGLP1	drug	cocaine	23874851	Herein the effect of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4), on amphetamine  and <b>cocaine</b> induced activation of the mesolimbic dopamine system was investigated in mice.
+ZGLP1	addiction	reward	23874851	Collectively these data propose a role for <strong>GLP 1</strong> receptors in regulating drug <b>reward</b>.
+ZGLP1	addiction	addiction	23874851	Moreover, the <strong>GLP 1</strong> signaling system may be involved in the development of drug dependence since the rewarding effects of <b>addictive</b> drugs involves interferences with the mesolimbic dopamine system.
+ZGLP1	addiction	dependence	23874851	Moreover, the <strong>GLP 1</strong> signaling system may be involved in the development of drug <b>dependence</b> since the rewarding effects of addictive drugs involves interferences with the mesolimbic dopamine system.
+ZGLP1	addiction	dependence	23874851	Given that <strong>GLP 1</strong> analogues, such as exenatide and liraglutide, are clinically available for treatment of type II diabetes, we propose that these should be elucidated as treatments of drug <b>dependence</b>.
+ZGLP1	drug	alcohol	23613987	Gut peptide <strong>GLP 1</strong> and its analogue, Exendin 4, decrease <b>alcohol</b> intake and reward.
+ZGLP1	addiction	reward	23613987	Gut peptide <strong>GLP 1</strong> and its analogue, Exendin 4, decrease alcohol intake and <b>reward</b>.
+ZGLP1	addiction	reward	23613987	Interestingly, <strong>GLP 1</strong> receptors (GLP 1R) are expressed in key mesolimbic <b>reward</b> areas (including the ventral tegmental area, VTA), innervated by hindbrain <strong>GLP 1</strong> neurons.
+ZGLP1	addiction	reward	23613987	Recently <strong>GLP 1</strong> has emerged as a potential regulator of food <b>reward</b> behavior, an effect driven by the mesolimbic GLP 1Rs.
+ZGLP1	drug	alcohol	23613987	Since a considerable overlap has been suggested for circuitry controlling reward behavior derived from food and <b>alcohol</b> we hypothesized that <strong>GLP 1</strong> and GLP 1Rs could regulate <b>alcohol</b> intake and <b>alcohol</b> reward.
+ZGLP1	addiction	reward	23613987	Since a considerable overlap has been suggested for circuitry controlling <b>reward</b> behavior derived from food and alcohol we hypothesized that <strong>GLP 1</strong> and GLP 1Rs could regulate alcohol intake and alcohol <b>reward</b>.
+ZGLP1	drug	alcohol	23613987	We sought to determine whether <strong>GLP 1</strong> or its clinically safe stable analogue, Exendin 4, reduce <b>alcohol</b> intake and reward.
+ZGLP1	addiction	reward	23613987	We sought to determine whether <strong>GLP 1</strong> or its clinically safe stable analogue, Exendin 4, reduce alcohol intake and <b>reward</b>.
+ZGLP1	drug	alcohol	23613987	To determine the potential role of the endogenous <strong>GLP 1</strong> in <b>alcohol</b> intake we evaluated whether GLP 1R antagonist, Exendin 9 39, can increase <b>alcohol</b> intake.
+ZGLP1	drug	alcohol	23613987	Male Wistar rats injected peripherally with <strong>GLP 1</strong> or Exendin 4 reduced their <b>alcohol</b> intake in an intermittent access two bottle free choice drinking model.
+ZGLP1	drug	alcohol	23613987	Importantly, a contribution of endogenously released <strong>GLP 1</strong> is highlighted by our observation that blockade of <strong>GLP 1</strong> receptors alone resulted in an increased <b>alcohol</b> intake.
+ZGLP1	drug	alcohol	23613987	Furthermore, <strong>GLP 1</strong> injection reduced <b>alcohol</b> reward in the <b>alcohol</b> conditioned place preference test in mice.
+ZGLP1	addiction	reward	23613987	Furthermore, <strong>GLP 1</strong> injection reduced alcohol <b>reward</b> in the alcohol conditioned place preference test in mice.
+ZGLP1	drug	alcohol	23613987	To evaluate the neuroanatomical substrate linking <strong>GLP 1</strong> with <b>alcohol</b> intake/reward, we selectively microinjected <strong>GLP 1</strong> or Exendin 4 into the VTA.
+ZGLP1	addiction	reward	23613987	To evaluate the neuroanatomical substrate linking <strong>GLP 1</strong> with alcohol intake/<b>reward</b>, we selectively microinjected <strong>GLP 1</strong> or Exendin 4 into the VTA.
+ZGLP1	drug	alcohol	23613987	This direct stimulation of the VTA <strong>GLP 1</strong> receptors potently reduced <b>alcohol</b> intake.
+ZGLP1	drug	alcohol	23613987	Considering that <strong>GLP 1</strong> analogues are already approved for clinical use, this places the GLP system as an exciting new potential therapeutic target for <b>alcohol</b> use disorders.
+ZGLP1	addiction	reward	23219472	Glucagon like peptide 1 (<strong>GLP 1</strong>), a gastrointestinal peptide regulating food intake and glucose homeostasis, has recently been shown to target central brain areas involved in <b>reward</b> and motivation, including the ventral tegmental area and nucleus accumbens.
+ZGLP1	drug	alcohol	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of <b>alcohol</b> induced reward as well as on <b>alcohol</b> intake and <b>alcohol</b> seeking behavior in rodents.
+ZGLP1	addiction	relapse	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of alcohol induced reward as well as on alcohol intake and alcohol <b>seeking</b> behavior in rodents.
+ZGLP1	addiction	reward	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of alcohol induced <b>reward</b> as well as on alcohol intake and alcohol seeking behavior in rodents.
+ZGLP1	drug	alcohol	23219472	These novel findings indicate that <strong>GLP 1</strong> signaling attenuates the reinforcing properties of <b>alcohol</b> implying that the physiological role of <strong>GLP 1</strong> extends beyond glucose homeostasis and food intake regulation.
+ZGLP1	addiction	reward	23219472	These novel findings indicate that <strong>GLP 1</strong> signaling attenuates the <b>reinforcing</b> properties of alcohol implying that the physiological role of <strong>GLP 1</strong> extends beyond glucose homeostasis and food intake regulation.
+ZGLP1	drug	alcohol	23219472	Collectively these findings implicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for <b>alcohol</b> use disorders.
+ZGLP1	drug	cocaine	23089631	<strong>GLP 1</strong> analog attenuates <b>cocaine</b> reward.
+ZGLP1	addiction	reward	23089631	<strong>GLP 1</strong> analog attenuates cocaine <b>reward</b>.
+ZGLP1	drug	opioid	22541480	Injection of <b>naloxone</b> decreased plasma glucagon like peptide 1 (<strong>GLP 1</strong>) in NAL calves.
+ZGLP1	drug	opioid	22541480	Blocking <b>opioid</b> receptors reduced intake the first 2 h after <b>naloxone</b> injection in FED calves, altered oro sensorial preferences, and reduced plasma <strong>GLP 1</strong> concentration.
+ZGLP1	drug	alcohol	22444202	Notably, the attenuating effect of RYGB surgery on <b>ethanol</b> consumption was associated with <b>ethanol</b> induced increases in the gut hormone glucagon like peptide 1 (<strong>GLP 1</strong>).
+ZGLP1	drug	alcohol	22444202	Pharmacologic administration of <strong>GLP 1</strong> agonists attenuated <b>ethanol</b> consumption in sham P rats.
+ZGLP1	addiction	reward	22444202	Furthermore, our data indicate that this regulation is achieved, in part, through reduction of <b>reward</b> and is modified by the gut hormones <strong>GLP 1</strong> and ghrelin.
+ZGLP1	drug	alcohol	21696355	Products at preclinical and clinical stages include formulations of <b>naltrexone</b> and buprenorphine for <b>alcoholism</b>/drug abuse, <strong>GLP 1</strong> peptides for diabetes, r hFSH for fertility, dopamine for nerve growth, dexamethasone for ocular treatment, melanotan for cancer prevention, plasmid DNA for cancer prevention, a variety of vaccines, octreotide generics, etc.
+ZGLP1	drug	opioid	21696355	Products at preclinical and clinical stages include formulations of naltrexone and <b>buprenorphine</b> for alcoholism/drug abuse, <strong>GLP 1</strong> peptides for diabetes, r hFSH for fertility, dopamine for nerve growth, dexamethasone for ocular treatment, melanotan for cancer prevention, plasmid DNA for cancer prevention, a variety of vaccines, octreotide generics, etc.
+ZGLP1	drug	cannabinoid	20462703	It is suggested that neurobiological substrates such as adiponectin, dopamine (D2 receptors), <b>endocannabinoids</b>, ghrelin, leptin, nesfatin 1, norepinephrine, orexin, oxytocin, serotonin, vasopressin, CCK, <strong>GLP 1</strong>, MCH, PYY, and stress hormones (e.g., CRF) in the brain (e.g., OFC, VTA, NAcc, and the hypothalamus) may determine parameters in the economic theory of obesity.
+GLP\ 1	addiction	reward	32388229	The gut brain peptide glucagon like peptide 1 (<strong>GLP 1</strong>) reduces <b>reward</b> from palatable food and drugs of abuse.
+GLP\ 1	drug	alcohol	32388229	Recent rodent studies show that activation of <strong>GLP 1</strong> receptors (GLP 1R) within the nucleus of the solitary tract (NTS) not only suppresses the motivation and intake of palatable food, but also reduces <b>alcohol</b> related behaviors.
+GLP\ 1	drug	alcohol	31759971	Further studies established that Ex4 modulates <b>alcohol</b> mediated behaviours via activation of <strong>GLP 1</strong> receptors in reward related areas and an area of the hindbrain.
+GLP\ 1	addiction	reward	31759971	Further studies established that Ex4 modulates alcohol mediated behaviours via activation of <strong>GLP 1</strong> receptors in <b>reward</b> related areas and an area of the hindbrain.
+GLP\ 1	drug	alcohol	31759971	Finally, another <strong>GLP 1</strong> receptor agonist, AC3174, counteracts relapse drinking to <b>alcohol</b>.
+GLP\ 1	addiction	relapse	31759971	Finally, another <strong>GLP 1</strong> receptor agonist, AC3174, counteracts <b>relapse</b> drinking to alcohol.
+GLP\ 1	drug	alcohol	31759971	Furthermore, a polymorphism in the <strong>GLP 1</strong> receptor gene is associated with enhanced intravenous self administration of <b>alcohol</b> in social drinkers and higher response in globus pallidus following high monetary reward.
+GLP\ 1	addiction	reward	31759971	Furthermore, a polymorphism in the <strong>GLP 1</strong> receptor gene is associated with enhanced intravenous self administration of alcohol in social drinkers and higher response in globus pallidus following high monetary <b>reward</b>.
+GLP\ 1	drug	alcohol	31759971	Collectively, these data provide evidence that up coming clinical trials should evaluate the effect of these <strong>GLP 1</strong> receptor agonists on <b>alcohol</b> intake in patients with AUD.
+GLP\ 1	drug	opioid	31581176	Activation of <strong>GLP 1</strong> receptors attenuates <b>oxycodone</b> taking and seeking without compromising the antinociceptive effects of <b>oxycodone</b> in rats.
+GLP\ 1	addiction	relapse	31581176	Activation of <strong>GLP 1</strong> receptors attenuates oxycodone taking and <b>seeking</b> without compromising the antinociceptive effects of oxycodone in rats.
+GLP\ 1	addiction	reward	31581176	A growing body of preclinical evidence indicates that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists reduce drug <b>reinforcement</b>.
+GLP\ 1	drug	opioid	31581176	However, the efficacy of <strong>GLP 1</strong> receptor agonists in attenuating <b>opioid</b> mediated behaviors has not been thoroughly investigated.
+GLP\ 1	drug	opioid	31581176	Using recently established models of <b>opioid</b> taking and  seeking behaviors, we showed that systemic administration of the <strong>GLP 1</strong> receptor agonist exendin 4 reduced <b>oxycodone</b> self administration and the reinstatement of <b>oxycodone</b> seeking behavior in rats.
+GLP\ 1	addiction	relapse	31581176	Using recently established models of opioid taking and  <b>seeking</b> behaviors, we showed that systemic administration of the <strong>GLP 1</strong> receptor agonist exendin 4 reduced oxycodone self administration and the <b>reinstatement</b> of oxycodone <b>seeking</b> behavior in rats.
+GLP\ 1	drug	opioid	31581176	Finally, exendin 4 did not alter the analgesic effects of <b>oxycodone</b>, suggesting that activation of <strong>GLP 1</strong> receptors attenuated <b>opioid</b> reinforcement without reducing the thermal antinociceptive effects of <b>oxycodone</b>.
+GLP\ 1	addiction	reward	31581176	Finally, exendin 4 did not alter the analgesic effects of oxycodone, suggesting that activation of <strong>GLP 1</strong> receptors attenuated opioid <b>reinforcement</b> without reducing the thermal antinociceptive effects of oxycodone.
+GLP\ 1	drug	opioid	31581176	Taken together, these findings suggest that <strong>GLP 1</strong> receptors could serve as potential molecular targets for pharmacotherapies aimed at reducing <b>opioid</b> use disorder.
+GLP\ 1	drug	alcohol	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of <b>alcohol</b>, cocaine, amphetamine, and nicotine in rodents.
+GLP\ 1	drug	amphetamine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, cocaine, <b>amphetamine</b>, and nicotine in rodents.
+GLP\ 1	drug	cocaine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, <b>cocaine</b>, amphetamine, and nicotine in rodents.
+GLP\ 1	drug	nicotine	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, cocaine, amphetamine, and <b>nicotine</b> in rodents.
+GLP\ 1	addiction	reward	31058214	<strong>GLP 1</strong> analogs, which are approved diabetes medications, can reduce the <b>reinforcing</b> and rewarding effects of alcohol, cocaine, amphetamine, and nicotine in rodents.
+GLP\ 1	drug	opioid	31058214	Investigations on effects of <strong>GLP 1</strong> analogs on <b>opioid</b> reward and reinforcement have not been reported.
+GLP\ 1	addiction	reward	31058214	Investigations on effects of <strong>GLP 1</strong> analogs on opioid <b>reward</b> and <b>reinforcement</b> have not been reported.
+GLP\ 1	drug	alcohol	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, <b>naltrexone</b> precipitated morphine withdrawal, morphine analgesia (male and female mice), and locomotor activity.
+GLP\ 1	drug	opioid	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on <b>opioid</b> related behaviors in male mice, i.e., <b>morphine</b> conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic <b>opioid</b> remifentanil, naltrexone precipitated <b>morphine</b> withdrawal, <b>morphine</b> analgesia (male and female mice), and locomotor activity.
+GLP\ 1	addiction	reward	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (<b>CPP</b>), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, naltrexone precipitated morphine withdrawal, morphine analgesia (male and female mice), and locomotor activity.
+GLP\ 1	addiction	withdrawal	31058214	We assessed the effects of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4) on opioid related behaviors in male mice, i.e., morphine conditioned place preference (CPP), intravenous self administration (IVSA) of the short acting synthetic opioid remifentanil, naltrexone precipitated morphine <b>withdrawal</b>, morphine analgesia (male and female mice), and locomotor activity.
+GLP\ 1	drug	opioid	31058214	Taken together, Ex4 did not attenuate the addiction related behavioral effects of <b>opioids</b>, indicating that <strong>GLP 1</strong> analogs would not be useful medications in the treatment of <b>opioid</b> addiction.
+GLP\ 1	addiction	addiction	31058214	Taken together, Ex4 did not attenuate the <b>addiction</b> related behavioral effects of opioids, indicating that <strong>GLP 1</strong> analogs would not be useful medications in the treatment of opioid <b>addiction</b>.
+GLP\ 1	drug	alcohol	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of <b>alcohol</b>, central stimulants, and nicotine.
+GLP\ 1	drug	nicotine	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of alcohol, central stimulants, and <b>nicotine</b>.
+GLP\ 1	drug	opioid	31058214	This difference between <b>opioids</b> and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the addictive effects of alcohol, central stimulants, and nicotine.
+GLP\ 1	addiction	addiction	31058214	This difference between opioids and other drug classes investigated to date may shed light on the mechanism of action of <strong>GLP 1</strong> receptor treatment in the <b>addictive</b> effects of alcohol, central stimulants, and nicotine.
+GLP\ 1	drug	cocaine	30930091	Central <strong>GLP 1</strong> receptors: Novel molecular targets for <b>cocaine</b> use disorder.
+GLP\ 1	drug	cocaine	30930091	Recent preclinical evidence suggests that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists could be re purposed to treat <b>cocaine</b> craving induced relapse.
+GLP\ 1	addiction	relapse	30930091	Recent preclinical evidence suggests that glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists could be re purposed to treat cocaine <b>craving</b> induced <b>relapse</b>.
+GLP\ 1	drug	cocaine	30930091	This review endeavors to comprehensively summarize the current literature investigating the efficacy of <strong>GLP 1</strong> receptor agonists in reducing the rewarding and reinforcing effects of <b>cocaine</b> in animal models of <b>cocaine</b> use disorder.
+GLP\ 1	addiction	reward	30930091	This review endeavors to comprehensively summarize the current literature investigating the efficacy of <strong>GLP 1</strong> receptor agonists in reducing the rewarding and <b>reinforcing</b> effects of cocaine in animal models of cocaine use disorder.
+GLP\ 1	drug	cocaine	30930091	The role of central endogenous <strong>GLP 1</strong> circuits in voluntary <b>cocaine</b> taking and seeking is also discussed.
+GLP\ 1	addiction	relapse	30930091	The role of central endogenous <strong>GLP 1</strong> circuits in voluntary cocaine taking and <b>seeking</b> is also discussed.
+GLP\ 1	addiction	addiction	30930091	Behavioral, neurochemical, electrophysiological and molecular biology studies indicate that central <strong>GLP 1</strong> receptor activation functionally modulates the mesolimbic reward system and decreases <b>addiction</b> like phenotypes in rodents.
+GLP\ 1	addiction	reward	30930091	Behavioral, neurochemical, electrophysiological and molecular biology studies indicate that central <strong>GLP 1</strong> receptor activation functionally modulates the mesolimbic <b>reward</b> system and decreases addiction like phenotypes in rodents.
+GLP\ 1	drug	cocaine	30930091	Overall, an emerging preclinical literature provides compelling evidence to advance <strong>GLP 1</strong> receptor agonists into clinical trials testing the efficacy of these medications in preventing <b>cocaine</b> craving induced relapse.
+GLP\ 1	addiction	relapse	30930091	Overall, an emerging preclinical literature provides compelling evidence to advance <strong>GLP 1</strong> receptor agonists into clinical trials testing the efficacy of these medications in preventing cocaine <b>craving</b> induced <b>relapse</b>.
+GLP\ 1	drug	amphetamine	30831183	Stress responsive prolactin releasing peptide (PrRP) positive noradrenergic and glucagon like peptide 1 (<strong>GLP 1</strong>) positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating <b>amph</b> induced hypophagia and CTA.
+GLP\ 1	addiction	aversion	30831183	Stress responsive prolactin releasing peptide (PrRP) positive noradrenergic and glucagon like peptide 1 (<strong>GLP 1</strong>) positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating amph induced hypophagia and <b>CTA</b>.
+GLP\ 1	drug	amphetamine	30831183	Compared to control saline treatment, <b>amph</b> activated significantly more cNTS neurons, including PrRP negative noradrenergic (NA) neurons, GABAergic neurons, and glutamatergic neurons, but not PrRP or <strong>GLP 1</strong> neurons.
+GLP\ 1	drug	alcohol	30771711	Glucagon like peptide 1 (<strong>GLP 1</strong>), an incretin hormone that reduces food intake, was recently established as a novel regulator of <b>alcohol</b> mediated behaviors.
+GLP\ 1	drug	alcohol	30771711	Clinically available analogues pass freely into the brain, but the mechanisms underlying <strong>GLP 1</strong> modulated <b>alcohol</b> reward remains largely unclear.
+GLP\ 1	addiction	reward	30771711	Clinically available analogues pass freely into the brain, but the mechanisms underlying <strong>GLP 1</strong> modulated alcohol <b>reward</b> remains largely unclear.
+GLP\ 1	drug	alcohol	30771711	<strong>GLP 1</strong> receptors (GLP 1R) are expressed throughout the nuclei of importance for acute and chronic effects of <b>alcohol</b>, such as the laterodorsal tegmental area (LDTg), the ventral tegmental area (VTA) and the nucleus accumbens (NAc).
+GLP\ 1	drug	alcohol	30439457	The present review therefore summarizes the current studies investigating the ability of the gut brain peptides ghrelin, glucagon like peptide 1 (<strong>GLP 1</strong>), amylin and neuromedin U (NMU) to modulate <b>alcohol</b>  and drug related behaviors in rodents and humans.
+GLP\ 1	drug	alcohol	30439457	On the other hand, the anorexigenic peptides <strong>GLP 1</strong>, amylin and NMU independently inhibits reward from <b>alcohol</b> and drugs of abuse in rodents.
+GLP\ 1	addiction	reward	30439457	On the other hand, the anorexigenic peptides <strong>GLP 1</strong>, amylin and NMU independently inhibits <b>reward</b> from alcohol and drugs of abuse in rodents.
+GLP\ 1	addiction	addiction	30439457	Collectively, these rodent and human studies imply that central ghrelin, <strong>GLP 1</strong>, amylin and NMU signaling may contribute to <b>addiction</b> processes.
+GLP\ 1	drug	cocaine	30414405	<b>Cocaine</b> and <b>cocaine</b> expectancy increase growth hormone, ghrelin, <strong>GLP 1</strong>, IGF 1, adiponectin, and corticosterone while decreasing leptin, insulin, GIP, and prolactin.
+GLP\ 1	drug	cocaine	30414405	During <b>cocaine</b> taking, growth hormone and acetylated ghrelin increased 10 fold; glucagon like peptide 1 (<strong>GLP 1</strong>) doubled; non acetylated ghrelin, insulin like growth factor 1 (IGF 1), and corticosterone increased by 50% and adiponectin increased by 17%.
+GLP\ 1	drug	alcohol	30012779	Does glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist stimulation reduce <b>alcohol</b> intake in patients with <b>alcohol</b> dependence: study protocol of a randomised, double blinded, placebo controlled clinical trial.
+GLP\ 1	addiction	dependence	30012779	Does glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist stimulation reduce alcohol intake in patients with alcohol <b>dependence</b>: study protocol of a randomised, double blinded, placebo controlled clinical trial.
+GLP\ 1	drug	alcohol	30012779	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor stimulation has proven to reduce <b>alcohol</b> consumption in preclinical experiments.
+GLP\ 1	drug	alcohol	29927808	The present study investigated the relationship between accumbal ghrelin and glucagon like peptide 1 (<strong>GLP 1</strong>) signaling in <b>alcohol</b> reward in female rats.
+GLP\ 1	addiction	reward	29927808	The present study investigated the relationship between accumbal ghrelin and glucagon like peptide 1 (<strong>GLP 1</strong>) signaling in alcohol <b>reward</b> in female rats.
+GLP\ 1	drug	alcohol	29927808	Overall, these findings demonstrate the importance of accumbal ghrelin and <strong>GLP 1</strong> signaling in <b>alcohol</b> reward and appetitive motivation.
+GLP\ 1	addiction	reward	29927808	Overall, these findings demonstrate the importance of accumbal ghrelin and <strong>GLP 1</strong> signaling in alcohol <b>reward</b> and appetitive motivation.
+GLP\ 1	drug	cocaine	29497166	Here we investigated a role for glucagon like peptide 1 (<strong>GLP 1</strong>) receptors in the reinstatement of <b>cocaine</b> seeking behavior, an animal model of relapse.
+GLP\ 1	addiction	relapse	29497166	Here we investigated a role for glucagon like peptide 1 (<strong>GLP 1</strong>) receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior, an animal model of <b>relapse</b>.
+GLP\ 1	drug	cocaine	29497166	We showed that peripheral administration of the <strong>GLP 1</strong> receptor agonist exendin 4 dose dependently reduced <b>cocaine</b> seeking in rats at doses that did not affect ad libitum food intake, meal patterns or body weight.
+GLP\ 1	addiction	relapse	29497166	We showed that peripheral administration of the <strong>GLP 1</strong> receptor agonist exendin 4 dose dependently reduced cocaine <b>seeking</b> in rats at doses that did not affect ad libitum food intake, meal patterns or body weight.
+GLP\ 1	drug	cocaine	29497166	The effects of systemic exendin 4 on <b>cocaine</b> reinstatement were attenuated in rats pretreated with intra VTA infusions of the <strong>GLP 1</strong> receptor antagonist exendin (9 39), indicating that the suppressive effects of systemic exendin 4 on <b>cocaine</b> seeking were due, in part, to activation of <strong>GLP 1</strong> receptors in the VTA.
+GLP\ 1	addiction	relapse	29497166	The effects of systemic exendin 4 on cocaine <b>reinstatement</b> were attenuated in rats pretreated with intra VTA infusions of the <strong>GLP 1</strong> receptor antagonist exendin (9 39), indicating that the suppressive effects of systemic exendin 4 on cocaine <b>seeking</b> were due, in part, to activation of <strong>GLP 1</strong> receptors in the VTA.
+GLP\ 1	drug	cocaine	29497166	Thus, our study demonstrated a novel role for <strong>GLP 1</strong> receptors in the reinstatement of <b>cocaine</b> seeking behavior and identified behaviorally relevant doses of a <strong>GLP 1</strong> receptor agonist that selectively reduced <b>cocaine</b> seeking and did not produce adverse effects.
+GLP\ 1	addiction	relapse	29497166	Thus, our study demonstrated a novel role for <strong>GLP 1</strong> receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior and identified behaviorally relevant doses of a <strong>GLP 1</strong> receptor agonist that selectively reduced cocaine <b>seeking</b> and did not produce adverse effects.
+GLP\ 1	drug	alcohol	29480848	A novel approach might use glucagon like peptide 1 (<strong>GLP 1</strong>) agonists, which reduce <b>alcohol</b> and drug use in preclinical studies.
+GLP\ 1	drug	nicotine	29480848	Several <strong>GLP 1</strong> agonists are used clinically to treat type 2 diabetes and obesity, but none have been tested in humans to reduce <b>smoking</b>.
+GLP\ 1	drug	alcohol	29337226	<strong>GLP 1</strong> signaling and <b>alcohol</b> mediated behaviors; preclinical and clinical evidence.
+GLP\ 1	drug	alcohol	29337226	One of these gut brain peptides is the annorexigenic peptide glucagon like peptide 1 (<strong>GLP 1</strong>), Preclinical studies show that <strong>GLP 1</strong> receptor activation, either by <strong>GLP 1</strong> or analogues, attenuate the ability of <b>alcohol</b> to activate the mesolimbic dopamine system as well as decrease <b>alcohol</b> consumption and operant self administration.
+GLP\ 1	addiction	reward	29337226	One of these gut brain peptides is the annorexigenic peptide glucagon like peptide 1 (<strong>GLP 1</strong>), Preclinical studies show that <strong>GLP 1</strong> receptor activation, either by <strong>GLP 1</strong> or analogues, attenuate the ability of alcohol to activate the mesolimbic dopamine system as well as decrease alcohol consumption and <b>operant</b> self administration.
+GLP\ 1	drug	alcohol	29337226	In further support for the endogenous <strong>GLP 1</strong> system in addiction processes are the experimental data showing that a <strong>GLP 1</strong> receptor antagonist increases <b>alcohol</b> intake.
+GLP\ 1	addiction	addiction	29337226	In further support for the endogenous <strong>GLP 1</strong> system in <b>addiction</b> processes are the experimental data showing that a <strong>GLP 1</strong> receptor antagonist increases alcohol intake.
+GLP\ 1	addiction	addiction	29337226	Moreover, <strong>GLP 1</strong> receptor agonists prevent the ability of other <b>addictive</b> drugs to activate the mesolimbic dopamine system.
+GLP\ 1	drug	alcohol	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with <b>alcohol</b> addiction as well as increased <b>alcohol</b> infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of cocaine and iii) that a <strong>GLP 1</strong> receptor agonist reduces <b>alcohol</b> intake in patients with type 2 diabetes mellitus.
+GLP\ 1	drug	cocaine	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with alcohol addiction as well as increased alcohol infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of <b>cocaine</b> and iii) that a <strong>GLP 1</strong> receptor agonist reduces alcohol intake in patients with type 2 diabetes mellitus.
+GLP\ 1	addiction	addiction	29337226	The number of clinical studies is limited, but show i) that genetic variation in the <strong>GLP 1</strong> receptor gene is associated with alcohol <b>addiction</b> as well as increased alcohol infusion in humans, ii) that plasma levels of <strong>GLP 1</strong> are associated with the subjective experience of cocaine and iii) that a <strong>GLP 1</strong> receptor agonist reduces alcohol intake in patients with type 2 diabetes mellitus.
+GLP\ 1	drug	alcohol	29337226	These experimental and clinical studies raises the concern that clinically available <strong>GLP 1</strong> receptor agonists deserves to be tested as potential treatments of patients with addictive disorders including <b>alcohol</b> addiction.
+GLP\ 1	addiction	addiction	29337226	These experimental and clinical studies raises the concern that clinically available <strong>GLP 1</strong> receptor agonists deserves to be tested as potential treatments of patients with <b>addictive</b> disorders including alcohol <b>addiction</b>.
+GLP\ 1	drug	cannabinoid	29231147	Inclusion criteria were: 1) full text available in English; 2) published in a peerreviewed journal and using the following keywords: neurotransmitters (AgRP, BDNF, αMSH, NP Y, <b>endocannabinoids</b>, adiponectin, CCK, ghrelin, <strong>GLP 1</strong>, insulin, leptin, PP, PYY), hormones (FSH, LH, estrogen, progesterone, testosterone) and bulimia nervosa, eating disorders.
+GLP\ 1	drug	cocaine	29226617	Recent evidence indicates that activation of glucagon like peptide 1 (<strong>GLP 1</strong>) receptors reduces <b>cocaine</b> mediated behaviors and <b>cocaine</b> evoked dopamine release in the nucleus accumbens (NAc).
+GLP\ 1	drug	cocaine	29226617	However, no studies have examined the role of NAc <strong>GLP 1</strong> receptors in the reinstatement of <b>cocaine</b> seeking behavior, an animal model of relapse.
+GLP\ 1	addiction	relapse	29226617	However, no studies have examined the role of NAc <strong>GLP 1</strong> receptors in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior, an animal model of <b>relapse</b>.
+GLP\ 1	drug	cocaine	29226617	To determine the effects of <strong>GLP 1</strong> receptor activation on neuronal excitability, exendin 4 was bath applied to ex vivo NAc slices from <b>cocaine</b> experienced and saline experienced rats following extinction of <b>cocaine</b> taking behavior.
+GLP\ 1	drug	cocaine	29226617	These effects were not associated with altered expression of <strong>GLP 1</strong> receptors in the NAc following <b>cocaine</b> self administration.
+GLP\ 1	drug	cocaine	29226617	Taken together, these findings indicate that increased activation of <strong>GLP 1</strong> receptors in the NAc during <b>cocaine</b> abstinence increases intrinsic, but not synaptic, excitability of medium spiny neurons and is sufficient to reduce <b>cocaine</b> seeking behavior.
+GLP\ 1	addiction	relapse	29226617	Taken together, these findings indicate that increased activation of <strong>GLP 1</strong> receptors in the NAc during cocaine abstinence increases intrinsic, but not synaptic, excitability of medium spiny neurons and is sufficient to reduce cocaine <b>seeking</b> behavior.
+GLP\ 1	drug	alcohol	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for <b>alcohol</b> and drug reward, and for the development of addiction.
+GLP\ 1	addiction	addiction	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for alcohol and drug reward, and for the development of <b>addiction</b>.
+GLP\ 1	addiction	reward	28778739	<strong>GLP 1</strong> is also produced and released in the brain, and <strong>GLP 1</strong> receptors are expressed in brain regions important for alcohol and drug <b>reward</b>, and for the development of addiction.
+GLP\ 1	drug	alcohol	28778739	<strong>GLP 1</strong> receptor agonists can decrease <b>alcohol</b> intake acutely in rodents.
+GLP\ 1	addiction	relapse	28778739	Here, we assessed the effect of daily treatment with the <strong>GLP 1</strong> receptor agonist Exendin 4 in an assay of <b>relapse</b> like drinking in socially housed mice.
+GLP\ 1	drug	alcohol	28778739	These findings support the possible use of <strong>GLP 1</strong> receptor agonists in the treatment of <b>alcohol</b> use disorder.
+GLP\ 1	addiction	withdrawal	28664354	After pioglitazone <b>withdrawal</b>, case reports increased for dipeptidyl peptidase 4 (DPP 4) inhibitors, glinides, and glucagon like peptide 1 (<strong>GLP 1</strong>) analogues (+84%, +22% and +5%, respectively) and reimbursements (+55, +11 and +50%, respectively); both decreased for sulfonylureas (case reports:  6%, reimbursements:  2%).
+GLP\ 1	drug	nicotine	28368384	<strong>GLP 1</strong> acts on habenular avoidance circuits to control <b>nicotine</b> intake.
+GLP\ 1	drug	nicotine	28368384	Here we show that <b>nicotine</b> activates glucagon like peptide 1 (<strong>GLP 1</strong>) neurons in the nucleus tractus solitarius (NTS).
+GLP\ 1	drug	nicotine	28368384	The antidiabetic drugs sitagliptin and exenatide, which inhibit <strong>GLP 1</strong> breakdown and stimulate <strong>GLP 1</strong> receptors, respectively, decreased <b>nicotine</b> intake in mice.
+GLP\ 1	drug	nicotine	28368384	Chemogenetic activation of <strong>GLP 1</strong> neurons in NTS similarly decreased <b>nicotine</b> intake.
+GLP\ 1	drug	nicotine	28368384	Activation of <strong>GLP 1</strong> receptors in the MHb IPN circuit abolished <b>nicotine</b> reward and decreased <b>nicotine</b> intake, whereas their knockdown or pharmacological blockade increased intake.
+GLP\ 1	addiction	reward	28368384	Activation of <strong>GLP 1</strong> receptors in the MHb IPN circuit abolished nicotine <b>reward</b> and decreased nicotine intake, whereas their knockdown or pharmacological blockade increased intake.
+GLP\ 1	drug	nicotine	28368384	<strong>GLP 1</strong> neurons may therefore serve as 'satiety sensors' for <b>nicotine</b> that stimulate habenular systems to promote <b>nicotine</b> avoidance before its aversive effects are encountered.
+GLP\ 1	addiction	aversion	28368384	<strong>GLP 1</strong> neurons may therefore serve as 'satiety sensors' for nicotine that stimulate habenular systems to promote nicotine avoidance before its <b>aversive</b> effects are encountered.
+GLP\ 1	drug	cocaine	28315693	Central <strong>GLP 1</strong> receptor activation modulates <b>cocaine</b> evoked phasic dopamine signaling in the nucleus accumbens core.
+GLP\ 1	drug	cocaine	28315693	Recently, metabolic regulatory peptides, including the satiety signal glucagon like peptide 1 (<strong>GLP 1</strong>), have been shown to modulate <b>cocaine</b> reward driven behavior and sustained dopamine levels after <b>cocaine</b> administration.
+GLP\ 1	addiction	reward	28315693	Recently, metabolic regulatory peptides, including the satiety signal glucagon like peptide 1 (<strong>GLP 1</strong>), have been shown to modulate cocaine <b>reward</b> driven behavior and sustained dopamine levels after cocaine administration.
+GLP\ 1	drug	cocaine	28315693	Here, we use fast scan cyclic voltammetry (FSCV) to explore <strong>GLP 1</strong> receptor (GLP 1R) modulation of dynamic dopamine release in the nucleus accumbens (NAc) during <b>cocaine</b> administration.
+GLP\ 1	drug	alcohol	27579999	Effects of the <strong>GLP 1</strong> Agonist Exendin 4 on Intravenous <b>Ethanol</b> Self Administration in Mice.
+GLP\ 1	drug	alcohol	27579999	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonists have been shown to decrease <b>ethanol</b> (EtOH) drinking in rodent assays.
+GLP\ 1	addiction	reward	27579999	To begin to understand the neurobiological mechanisms by which <strong>GLP 1</strong> receptor ligands may be able to control EtOH intake, it is important to ascertain whether they can modulate the direct <b>reinforcing</b> effects of EtOH, without the confound of effects on ingestive behaviors generally.
+GLP\ 1	addiction	reward	27579999	Second, <strong>GLP 1</strong> receptor agonists can powerfully attenuate voluntary EtOH intake by directly modulating the <b>reinforcing</b> effects of EtOH.
+GLP\ 1	drug	alcohol	27579999	These findings support the potential usefulness of <strong>GLP 1</strong> receptor ligands in the treatment of <b>alcohol</b> use disorder.
+GLP\ 1	drug	cocaine	27187231	Agonism of the glucagon like peptide 1 (<strong>GLP 1</strong>) receptor (GLP 1R) has been effective at treating aspects of addictive behavior for a number of abused substances, including <b>cocaine</b>.
+GLP\ 1	addiction	addiction	27187231	Agonism of the glucagon like peptide 1 (<strong>GLP 1</strong>) receptor (GLP 1R) has been effective at treating aspects of <b>addictive</b> behavior for a number of abused substances, including cocaine.
+GLP\ 1	drug	cocaine	27187231	Exenatide (Ex 4), a long lasting synthetic analog of <strong>GLP 1</strong> abolished <b>cocaine</b> induced elevation of DA.
+GLP\ 1	drug	alcohol	27072507	Recent data implicate glucagon like peptide 1 (<strong>GLP 1</strong>), a potent anorexigenic peptide released in response to nutrient intake, as a regulator for the reinforcing properties of food, <b>alcohol</b> and psychostimulants.
+GLP\ 1	addiction	reward	27072507	Recent data implicate glucagon like peptide 1 (<strong>GLP 1</strong>), a potent anorexigenic peptide released in response to nutrient intake, as a regulator for the <b>reinforcing</b> properties of food, alcohol and psychostimulants.
+GLP\ 1	drug	alcohol	27072507	Here, we examined amphetamine reinforcement, <b>alcohol</b> intake and hedonic feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+GLP\ 1	drug	amphetamine	27072507	Here, we examined <b>amphetamine</b> reinforcement, alcohol intake and hedonic feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+GLP\ 1	addiction	reward	27072507	Here, we examined amphetamine <b>reinforcement</b>, alcohol intake and <b>hedonic</b> feeding following peripheral administration of EX 4 (a <strong>GLP 1</strong> analog) in FLOX and GLP 1R KD(Nestin) (GLP 1R selectively ablated from the central nervous system) mice (n=13/group).
+GLP\ 1	addiction	addiction	27072507	The present study provides critical insights regarding the nature by which <strong>GLP 1</strong> signaling controls reinforced behaviors and underscores the importance of both peripheral and central GLP 1R signaling for the regulation of <b>addictive</b> disorders.
+GLP\ 1	addiction	reward	27066524	<strong>GLP 1</strong> influences food and drug <b>reward</b>.
+GLP\ 1	addiction	reward	27066524	That the neuropeptide glucagon like peptide 1 (<strong>GLP 1</strong>) is under investigation for both the homeostatic and <b>hedonic</b> controls of feeding is not surprising or novel.
+GLP\ 1	addiction	reward	27066524	However, if the neural substrates that underline food <b>reward</b> are shared with other <b>reward</b> related behaviors generally, then future research should investigate and embrace the likelihood that endogenous and exogenous <strong>GLP 1</strong> receptor activation may influence multiple <b>reward</b> related behaviors.
+GLP\ 1	drug	alcohol	27066524	An emerging literature demonstrates a role for the <strong>GLP 1</strong> system in modulating maladaptive reward behaviors, including drug and <b>alcohol</b> consumption.
+GLP\ 1	addiction	reward	27066524	An emerging literature demonstrates a role for the <strong>GLP 1</strong> system in modulating maladaptive <b>reward</b> behaviors, including drug and alcohol consumption.
+GLP\ 1	addiction	addiction	27066524	Thus, if <strong>GLP 1</strong> based pharmacotherapies are to be used to treat drug <b>addiction</b> and other diseases associated with maladaptive reward behaviors (e.g.
+GLP\ 1	addiction	reward	27066524	Thus, if <strong>GLP 1</strong> based pharmacotherapies are to be used to treat drug addiction and other diseases associated with maladaptive <b>reward</b> behaviors (e.g.
+GLP\ 1	addiction	reward	27066524	Equally as likely, non selective effects on natural <b>reward</b> and maladaptive <b>reward</b> behaviors may be observed for <strong>GLP 1</strong> based pharmacotherapies.
+GLP\ 1	drug	cocaine	26675243	As the neural circuits and neurobiological mechanisms underlying drug taking overlap to some degree with those regulating food intake, these findings suggest that activation of central <strong>GLP 1</strong> receptors may also attenuate <b>cocaine</b> taking.
+GLP\ 1	drug	cocaine	26675243	Here, we show that intra VTA administration of the <strong>GLP 1</strong> receptor agonist exendin 4 (0.05 μg) significantly reduced <b>cocaine</b>, but not sucrose, self administration in rats.
+GLP\ 1	drug	cocaine	26675243	We also demonstrate that <b>cocaine</b> taking is associated with elevated plasma corticosterone levels and that systemic infusion of <b>cocaine</b> activates <strong>GLP 1</strong> expressing neurons in the nucleus tractus solitarius (NTS), a hindbrain nucleus that projects monosynaptically to the VTA.
+GLP\ 1	drug	cocaine	26675243	To determine the potential mechanisms by which <b>cocaine</b> activates NTS <strong>GLP 1</strong> expressing neurons, we microinjected corticosterone (0.5 μg) directly into the hindbrain fourth ventricle.
+GLP\ 1	drug	cocaine	26675243	Intraventricular corticosterone attenuated <b>cocaine</b> self administration and this effect was blocked in animals pretreated with the <strong>GLP 1</strong> receptor antagonist exendin (9 39) (10 μg) in the VTA.
+GLP\ 1	drug	cocaine	26675243	Finally, AAV shRNA mediated knockdown of VTA <strong>GLP 1</strong> receptors was sufficient to augment <b>cocaine</b> self administration.
+GLP\ 1	drug	cocaine	26675243	Taken together, these findings indicate that increased activation of NTS <strong>GLP 1</strong> expressing neurons by corticosterone may represent a homeostatic response to <b>cocaine</b> taking, thereby reducing the reinforcing efficacy of <b>cocaine</b>.
+GLP\ 1	addiction	reward	26675243	Taken together, these findings indicate that increased activation of NTS <strong>GLP 1</strong> expressing neurons by corticosterone may represent a homeostatic response to cocaine taking, thereby reducing the <b>reinforcing</b> efficacy of cocaine.
+GLP\ 1	drug	cocaine	26675243	Therefore, central <strong>GLP 1</strong> receptors may represent a novel target for <b>cocaine</b> addiction pharmacotherapies.
+GLP\ 1	addiction	addiction	26675243	Therefore, central <strong>GLP 1</strong> receptors may represent a novel target for cocaine <b>addiction</b> pharmacotherapies.
+GLP\ 1	drug	cannabinoid	26546790	To explore the role of some gastrointestinal orexigenic and anorexigenic peptides and <b>endocannabinoids</b> (and some related congeners) in chocolate consumption, we measured changes in circulating levels of ghrelin, glucagon like peptide 1 (<strong>GLP 1</strong>), peptide YY (PYY), anandamide (AEA), 2 AG, <b>palmitoylethanolamide</b> (PEA), and <b>oleoylethanolamide</b> (OEA) in 10 satiated severely obese subjects after consumption of chocolate and, on a separate day, of a non palatable isocaloric food with the same bromatologic composition.
+GLP\ 1	drug	alcohol	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several <b>alcohol</b> mediated behaviors as well as amphetamine induced, cocaine induced and nicotine induced reward.
+GLP\ 1	drug	amphetamine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as <b>amphetamine</b> induced, cocaine induced and nicotine induced reward.
+GLP\ 1	drug	cocaine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, <b>cocaine</b> induced and nicotine induced reward.
+GLP\ 1	drug	nicotine	26303264	<strong>GLP 1</strong> receptors are expressed in reward related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, cocaine induced and <b>nicotine</b> induced reward.
+GLP\ 1	addiction	reward	26303264	<strong>GLP 1</strong> receptors are expressed in <b>reward</b> related areas such as the ventral tegmental area and nucleus accumbens, and <strong>GLP 1</strong> was recently shown to regulate several alcohol mediated behaviors as well as amphetamine induced, cocaine induced and nicotine induced <b>reward</b>.
+GLP\ 1	drug	alcohol	26303264	The present series of experiments were undertaken to investigate the effect of the <strong>GLP 1</strong> receptor agonist, liraglutide, on several <b>alcohol</b> related behaviors in rats that model different aspects of <b>alcohol</b> use disorder in humans.
+GLP\ 1	drug	alcohol	26303264	Collectively, these data suggest that <strong>GLP 1</strong> receptor agonists could be tested for treatment of <b>alcohol</b> dependence in humans.
+GLP\ 1	addiction	dependence	26303264	Collectively, these data suggest that <strong>GLP 1</strong> receptor agonists could be tested for treatment of alcohol <b>dependence</b> in humans.
+GLP\ 1	addiction	aversion	26211731	The <b>Aversive</b> Agent Lithium Chloride Suppresses Phasic Dopamine Release Through Central <strong>GLP 1</strong> Receptors.
+GLP\ 1	drug	alcohol	26080318	<strong>GLP 1</strong> receptor (GLP 1R) activation also attenuates the reinforcing properties of <b>alcohol</b> in rodents.
+GLP\ 1	addiction	reward	26080318	<strong>GLP 1</strong> receptor (GLP 1R) activation also attenuates the <b>reinforcing</b> properties of alcohol in rodents.
+GLP\ 1	drug	cocaine	26072178	The glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist exendin 4 reduces <b>cocaine</b> self administration in mice.
+GLP\ 1	drug	cocaine	26072178	Based on the anatomical distribution of <strong>GLP 1</strong> receptors in the brain and the well established effects of <strong>GLP 1</strong> on food reward, we decided to investigate the effect of the <strong>GLP 1</strong> analogue exendin 4 on <b>cocaine</b>  and dopamine D1 receptor agonist induced hyperlocomotion, on acute and chronic <b>cocaine</b> self administration, on <b>cocaine</b> induced striatal dopamine release in mice and on <b>cocaine</b> induced c fos activation.
+GLP\ 1	addiction	reward	26072178	Based on the anatomical distribution of <strong>GLP 1</strong> receptors in the brain and the well established effects of <strong>GLP 1</strong> on food <b>reward</b>, we decided to investigate the effect of the <strong>GLP 1</strong> analogue exendin 4 on cocaine  and dopamine D1 receptor agonist induced hyperlocomotion, on acute and chronic cocaine self administration, on cocaine induced striatal dopamine release in mice and on cocaine induced c fos activation.
+GLP\ 1	drug	cocaine	26072178	Here, we report that <strong>GLP 1</strong> receptor stimulation reduces acute and chronic <b>cocaine</b> self administration and attenuates <b>cocaine</b> induced hyperlocomotion.
+GLP\ 1	drug	cocaine	26072178	In addition, we show that peripheral administration of exendin 4 reduces <b>cocaine</b> induced elevation of striatal dopamine levels and striatal c fos expression implicating central <strong>GLP 1</strong> receptors in these responses.
+GLP\ 1	drug	cocaine	26072178	The present results demonstrate that the <strong>GLP 1</strong> system modulates <b>cocaine</b>'s effects on behavior and dopamine homeostasis, indicating that the <strong>GLP 1</strong> receptor may be a novel target for the pharmacological treatment of drug addiction.
+GLP\ 1	addiction	addiction	26072178	The present results demonstrate that the <strong>GLP 1</strong> system modulates cocaine's effects on behavior and dopamine homeostasis, indicating that the <strong>GLP 1</strong> receptor may be a novel target for the pharmacological treatment of drug <b>addiction</b>.
+GLP\ 1	addiction	addiction	25669605	Both palatable food and illicit drugs activate brain reward circuitries, and pharmacological studies suggest that central nervous system <strong>GLP 1</strong> signaling holds potential for the treatment of <b>addiction</b>.
+GLP\ 1	addiction	reward	25669605	Both palatable food and illicit drugs activate brain <b>reward</b> circuitries, and pharmacological studies suggest that central nervous system <strong>GLP 1</strong> signaling holds potential for the treatment of addiction.
+GLP\ 1	addiction	reward	25669605	However, the role of endogenous <strong>GLP 1</strong> in the attenuation of <b>reward</b> oriented behavior, and the essential domains of the mesolimbic system mediating these beneficial effects, are largely unknown.
+GLP\ 1	drug	alcohol	25380665	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist prevents development of tolerance to anti anxiety effect of <b>ethanol</b> and withdrawal induced anxiety in rats.
+GLP\ 1	addiction	withdrawal	25380665	Glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist prevents development of tolerance to anti anxiety effect of ethanol and <b>withdrawal</b> induced anxiety in rats.
+GLP\ 1	drug	alcohol	25380665	We recently reported that inhibition of dipeptidyl peptidase IV (DPP IV), an enzyme responsible for metabolism of endogenous glucagon like peptide 1 (<strong>GLP 1</strong>), delays tolerance to anti anxiety effect of <b>ethanol</b> and withdrawal induced anxiety in rats.
+GLP\ 1	addiction	withdrawal	25380665	We recently reported that inhibition of dipeptidyl peptidase IV (DPP IV), an enzyme responsible for metabolism of endogenous glucagon like peptide 1 (<strong>GLP 1</strong>), delays tolerance to anti anxiety effect of ethanol and <b>withdrawal</b> induced anxiety in rats.
+GLP\ 1	drug	alcohol	25380665	Intrigued with this report, present study examined the role of glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist, liraglutide in (1) acute anti anxiety effect of <b>ethanol</b>; (2) tolerance to <b>ethanol</b>'s anti anxiety effect and (3) <b>ethanol</b> withdrawal induced anxiety using elevated plus maze (EPM) test in rats.
+GLP\ 1	addiction	withdrawal	25380665	Intrigued with this report, present study examined the role of glucagon like peptide 1 (<strong>GLP 1</strong>) receptor agonist, liraglutide in (1) acute anti anxiety effect of ethanol; (2) tolerance to ethanol's anti anxiety effect and (3) ethanol <b>withdrawal</b> induced anxiety using elevated plus maze (EPM) test in rats.
+GLP\ 1	drug	alcohol	25380665	(1) <strong>GLP 1</strong> agonist, liraglutide exhibited anti anxiety effect per se; (2) potentiated anti anxiety effect of <b>ethanol</b>; (3) prevented development tolerance to anti anxiety effect of <b>ethanol</b> and (4) prevented withdrawal induced anxiety.
+GLP\ 1	addiction	withdrawal	25380665	(1) <strong>GLP 1</strong> agonist, liraglutide exhibited anti anxiety effect per se; (2) potentiated anti anxiety effect of ethanol; (3) prevented development tolerance to anti anxiety effect of ethanol and (4) prevented <b>withdrawal</b> induced anxiety.
+GLP\ 1	drug	alcohol	25380665	Further studies examining intracellular cascade of events contributing to these effects may help to improve understanding about role of <strong>GLP 1</strong> receptors in <b>ethanol</b> mediated behaviors.
+GLP\ 1	drug	cannabinoid	25361428	<b>Cannabinoid</b> receptor 1 antagonist treatment induces glucagon release and shows an additive therapeutic effect with <strong>GLP 1</strong> agonist in diet induced obese mice.
+GLP\ 1	drug	cannabinoid	25361428	We hypothesized that the insulin secretagogue effect of <strong>GLP 1</strong> agonist exendin 4 may synergize with the insulin sensitizing action of <b>rimonabant</b>.
+GLP\ 1	addiction	reward	24958205	However, <strong>GLP 1</strong> receptors are expressed in areas intimately associated with <b>reward</b> regulation.
+GLP\ 1	addiction	reward	24958205	Given that regulation of food and drug intake share common neurobiological substrates, the possibility that ghrelin and <strong>GLP 1</strong> play an important role in <b>reward</b> regulation should be considered.
+GLP\ 1	drug	alcohol	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by <b>alcohol</b>, amphetamine, cocaine and nicotine in rodents are overviewed herein.
+GLP\ 1	drug	amphetamine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, <b>amphetamine</b>, cocaine and nicotine in rodents are overviewed herein.
+GLP\ 1	drug	cocaine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, amphetamine, <b>cocaine</b> and nicotine in rodents are overviewed herein.
+GLP\ 1	drug	nicotine	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls reward induced by alcohol, amphetamine, cocaine and <b>nicotine</b> in rodents are overviewed herein.
+GLP\ 1	addiction	reward	24958205	In addition, the recent findings showing that <strong>GLP 1</strong> controls <b>reward</b> induced by alcohol, amphetamine, cocaine and nicotine in rodents are overviewed herein.
+GLP\ 1	drug	alcohol	24958205	Collectively, these data suggest that ghrelin and <strong>GLP 1</strong> receptors may be novel targets for development of pharmacological treatments of <b>alcohol</b> and drug dependence.
+GLP\ 1	addiction	dependence	24958205	Collectively, these data suggest that ghrelin and <strong>GLP 1</strong> receptors may be novel targets for development of pharmacological treatments of alcohol and drug <b>dependence</b>.
+GLP\ 1	addiction	reward	24204788	The findings that <strong>GLP 1</strong> targets <b>reward</b> related areas including mesolimbic dopamine areas indicate that the physiological role of <strong>GLP 1</strong> extends beyond food intake and glucose homeostasis control to include <b>reward</b> regulation.
+GLP\ 1	drug	nicotine	24204788	The present series of experiments was therefore designed to investigate the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on established <b>nicotine</b> induced effects on the mesolimbic dopamine system in mice.
+GLP\ 1	drug	nicotine	24204788	Given that development of <b>nicotine</b> addiction largely depends on the effects of <b>nicotine</b> on the mesolimbic dopamine system these findings indicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for <b>nicotine</b> cessations in humans.
+GLP\ 1	addiction	addiction	24204788	Given that development of nicotine <b>addiction</b> largely depends on the effects of nicotine on the mesolimbic dopamine system these findings indicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for nicotine cessations in humans.
+GLP\ 1	addiction	reward	24140429	However, emerging data indicate that <strong>GLP 1</strong> also contributes to non homeostatic regulation of food <b>reward</b> and motivated behaviors in brain <b>reward</b> centers, including the ventral tegmental area and nucleus accumbens.
+GLP\ 1	drug	alcohol	24140429	The hypothesis that <strong>GLP 1</strong> signaling modulates reward circuitry has provided the impetus for studies demonstrating that <strong>GLP 1</strong> attenuates reward for psychostimulants and <b>alcohol</b>.
+GLP\ 1	addiction	reward	24140429	The hypothesis that <strong>GLP 1</strong> signaling modulates <b>reward</b> circuitry has provided the impetus for studies demonstrating that <strong>GLP 1</strong> attenuates <b>reward</b> for psychostimulants and alcohol.
+GLP\ 1	addiction	reward	24140429	Here, we examine current evidence for <strong>GLP 1</strong> mediated regulation of food and drug <b>reward</b> and use these findings to hypothesize mechanisms of action within brain <b>reward</b> centers.
+GLP\ 1	addiction	reward	24133407	The central <strong>GLP 1</strong>: implications for food and drug <b>reward</b>.
+GLP\ 1	drug	alcohol	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to cocaine, amphetamine, and <b>alcohol</b> reward.
+GLP\ 1	drug	amphetamine	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to cocaine, <b>amphetamine</b>, and alcohol reward.
+GLP\ 1	drug	cocaine	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on reward behavior is not limited to food derived reward but extends to <b>cocaine</b>, amphetamine, and alcohol reward.
+GLP\ 1	addiction	reward	24133407	In parallel, emerging evidence suggests that the range of action of <strong>GLP 1</strong> on <b>reward</b> behavior is not limited to food derived <b>reward</b> but extends to cocaine, amphetamine, and alcohol <b>reward</b>.
+GLP\ 1	addiction	reward	24133407	The new discoveries concerning <strong>GLP 1</strong> action on the mesolimbic <b>reward</b> system significantly extend the potential therapeutic range of this drug target.
+GLP\ 1	addiction	reward	23874851	Given that <strong>GLP 1</strong> receptors are expressed in <b>reward</b> areas, such as the nucleus accumbens and ventral tegmental area, and that common mechanisms regulate food and drug induced <b>reward</b> we hypothesize that <strong>GLP 1</strong> receptors are involved in <b>reward</b> regulation.
+GLP\ 1	drug	amphetamine	23874851	Herein the effect of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4), on <b>amphetamine</b>  and cocaine induced activation of the mesolimbic dopamine system was investigated in mice.
+GLP\ 1	drug	cocaine	23874851	Herein the effect of the <strong>GLP 1</strong> receptor agonist Exendin 4 (Ex4), on amphetamine  and <b>cocaine</b> induced activation of the mesolimbic dopamine system was investigated in mice.
+GLP\ 1	addiction	reward	23874851	Collectively these data propose a role for <strong>GLP 1</strong> receptors in regulating drug <b>reward</b>.
+GLP\ 1	addiction	addiction	23874851	Moreover, the <strong>GLP 1</strong> signaling system may be involved in the development of drug dependence since the rewarding effects of <b>addictive</b> drugs involves interferences with the mesolimbic dopamine system.
+GLP\ 1	addiction	dependence	23874851	Moreover, the <strong>GLP 1</strong> signaling system may be involved in the development of drug <b>dependence</b> since the rewarding effects of addictive drugs involves interferences with the mesolimbic dopamine system.
+GLP\ 1	addiction	dependence	23874851	Given that <strong>GLP 1</strong> analogues, such as exenatide and liraglutide, are clinically available for treatment of type II diabetes, we propose that these should be elucidated as treatments of drug <b>dependence</b>.
+GLP\ 1	drug	alcohol	23613987	Gut peptide <strong>GLP 1</strong> and its analogue, Exendin 4, decrease <b>alcohol</b> intake and reward.
+GLP\ 1	addiction	reward	23613987	Gut peptide <strong>GLP 1</strong> and its analogue, Exendin 4, decrease alcohol intake and <b>reward</b>.
+GLP\ 1	addiction	reward	23613987	Interestingly, <strong>GLP 1</strong> receptors (GLP 1R) are expressed in key mesolimbic <b>reward</b> areas (including the ventral tegmental area, VTA), innervated by hindbrain <strong>GLP 1</strong> neurons.
+GLP\ 1	addiction	reward	23613987	Recently <strong>GLP 1</strong> has emerged as a potential regulator of food <b>reward</b> behavior, an effect driven by the mesolimbic GLP 1Rs.
+GLP\ 1	drug	alcohol	23613987	Since a considerable overlap has been suggested for circuitry controlling reward behavior derived from food and <b>alcohol</b> we hypothesized that <strong>GLP 1</strong> and GLP 1Rs could regulate <b>alcohol</b> intake and <b>alcohol</b> reward.
+GLP\ 1	addiction	reward	23613987	Since a considerable overlap has been suggested for circuitry controlling <b>reward</b> behavior derived from food and alcohol we hypothesized that <strong>GLP 1</strong> and GLP 1Rs could regulate alcohol intake and alcohol <b>reward</b>.
+GLP\ 1	drug	alcohol	23613987	We sought to determine whether <strong>GLP 1</strong> or its clinically safe stable analogue, Exendin 4, reduce <b>alcohol</b> intake and reward.
+GLP\ 1	addiction	reward	23613987	We sought to determine whether <strong>GLP 1</strong> or its clinically safe stable analogue, Exendin 4, reduce alcohol intake and <b>reward</b>.
+GLP\ 1	drug	alcohol	23613987	To determine the potential role of the endogenous <strong>GLP 1</strong> in <b>alcohol</b> intake we evaluated whether GLP 1R antagonist, Exendin 9 39, can increase <b>alcohol</b> intake.
+GLP\ 1	drug	alcohol	23613987	Male Wistar rats injected peripherally with <strong>GLP 1</strong> or Exendin 4 reduced their <b>alcohol</b> intake in an intermittent access two bottle free choice drinking model.
+GLP\ 1	drug	alcohol	23613987	Importantly, a contribution of endogenously released <strong>GLP 1</strong> is highlighted by our observation that blockade of <strong>GLP 1</strong> receptors alone resulted in an increased <b>alcohol</b> intake.
+GLP\ 1	drug	alcohol	23613987	Furthermore, <strong>GLP 1</strong> injection reduced <b>alcohol</b> reward in the <b>alcohol</b> conditioned place preference test in mice.
+GLP\ 1	addiction	reward	23613987	Furthermore, <strong>GLP 1</strong> injection reduced alcohol <b>reward</b> in the alcohol conditioned place preference test in mice.
+GLP\ 1	drug	alcohol	23613987	To evaluate the neuroanatomical substrate linking <strong>GLP 1</strong> with <b>alcohol</b> intake/reward, we selectively microinjected <strong>GLP 1</strong> or Exendin 4 into the VTA.
+GLP\ 1	addiction	reward	23613987	To evaluate the neuroanatomical substrate linking <strong>GLP 1</strong> with alcohol intake/<b>reward</b>, we selectively microinjected <strong>GLP 1</strong> or Exendin 4 into the VTA.
+GLP\ 1	drug	alcohol	23613987	This direct stimulation of the VTA <strong>GLP 1</strong> receptors potently reduced <b>alcohol</b> intake.
+GLP\ 1	drug	alcohol	23613987	Considering that <strong>GLP 1</strong> analogues are already approved for clinical use, this places the GLP system as an exciting new potential therapeutic target for <b>alcohol</b> use disorders.
+GLP\ 1	addiction	reward	23219472	Glucagon like peptide 1 (<strong>GLP 1</strong>), a gastrointestinal peptide regulating food intake and glucose homeostasis, has recently been shown to target central brain areas involved in <b>reward</b> and motivation, including the ventral tegmental area and nucleus accumbens.
+GLP\ 1	drug	alcohol	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of <b>alcohol</b> induced reward as well as on <b>alcohol</b> intake and <b>alcohol</b> seeking behavior in rodents.
+GLP\ 1	addiction	relapse	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of alcohol induced reward as well as on alcohol intake and alcohol <b>seeking</b> behavior in rodents.
+GLP\ 1	addiction	reward	23219472	Herein we investigated the effects of the <strong>GLP 1</strong> receptor agonist, Exendin 4 (Ex4), on various measures of alcohol induced <b>reward</b> as well as on alcohol intake and alcohol seeking behavior in rodents.
+GLP\ 1	drug	alcohol	23219472	These novel findings indicate that <strong>GLP 1</strong> signaling attenuates the reinforcing properties of <b>alcohol</b> implying that the physiological role of <strong>GLP 1</strong> extends beyond glucose homeostasis and food intake regulation.
+GLP\ 1	addiction	reward	23219472	These novel findings indicate that <strong>GLP 1</strong> signaling attenuates the <b>reinforcing</b> properties of alcohol implying that the physiological role of <strong>GLP 1</strong> extends beyond glucose homeostasis and food intake regulation.
+GLP\ 1	drug	alcohol	23219472	Collectively these findings implicate that the <strong>GLP 1</strong> receptor may be a potential target for the development of novel treatment strategies for <b>alcohol</b> use disorders.
+GLP\ 1	drug	cocaine	23089631	<strong>GLP 1</strong> analog attenuates <b>cocaine</b> reward.
+GLP\ 1	addiction	reward	23089631	<strong>GLP 1</strong> analog attenuates cocaine <b>reward</b>.
+GLP\ 1	drug	opioid	22541480	Injection of <b>naloxone</b> decreased plasma glucagon like peptide 1 (<strong>GLP 1</strong>) in NAL calves.
+GLP\ 1	drug	opioid	22541480	Blocking <b>opioid</b> receptors reduced intake the first 2 h after <b>naloxone</b> injection in FED calves, altered oro sensorial preferences, and reduced plasma <strong>GLP 1</strong> concentration.
+GLP\ 1	drug	alcohol	22444202	Notably, the attenuating effect of RYGB surgery on <b>ethanol</b> consumption was associated with <b>ethanol</b> induced increases in the gut hormone glucagon like peptide 1 (<strong>GLP 1</strong>).
+GLP\ 1	drug	alcohol	22444202	Pharmacologic administration of <strong>GLP 1</strong> agonists attenuated <b>ethanol</b> consumption in sham P rats.
+GLP\ 1	addiction	reward	22444202	Furthermore, our data indicate that this regulation is achieved, in part, through reduction of <b>reward</b> and is modified by the gut hormones <strong>GLP 1</strong> and ghrelin.
+GLP\ 1	drug	alcohol	21696355	Products at preclinical and clinical stages include formulations of <b>naltrexone</b> and buprenorphine for <b>alcoholism</b>/drug abuse, <strong>GLP 1</strong> peptides for diabetes, r hFSH for fertility, dopamine for nerve growth, dexamethasone for ocular treatment, melanotan for cancer prevention, plasmid DNA for cancer prevention, a variety of vaccines, octreotide generics, etc.
+GLP\ 1	drug	opioid	21696355	Products at preclinical and clinical stages include formulations of naltrexone and <b>buprenorphine</b> for alcoholism/drug abuse, <strong>GLP 1</strong> peptides for diabetes, r hFSH for fertility, dopamine for nerve growth, dexamethasone for ocular treatment, melanotan for cancer prevention, plasmid DNA for cancer prevention, a variety of vaccines, octreotide generics, etc.
+GLP\ 1	drug	cannabinoid	20462703	It is suggested that neurobiological substrates such as adiponectin, dopamine (D2 receptors), <b>endocannabinoids</b>, ghrelin, leptin, nesfatin 1, norepinephrine, orexin, oxytocin, serotonin, vasopressin, CCK, <strong>GLP 1</strong>, MCH, PYY, and stress hormones (e.g., CRF) in the brain (e.g., OFC, VTA, NAcc, and the hypothalamus) may determine parameters in the economic theory of obesity.
+OPRK1	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (Oprm), delta (Oprd), and kappa (<strong>Oprk</strong>), and their endogenous opioid peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+OPRK1	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (Oprm), delta (Oprd), and kappa (<strong>Oprk</strong>), and their endogenous <b>opioid</b> peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+OPRK1	drug	cocaine	32730947	We found that <b>cocaine</b> self administration significantly increased the mRNA levels of Oprm and Oprd in both the CPu and PFC, but had no effect on <strong>Oprk</strong> mRNA levels in either brain region.
+OPRK1	drug	opioid	31940240	The κ <b>opioid</b> receptor 1 (<strong>OPRK1</strong>) is critically involved in abstinence and remission.
+OPRK1	drug	opioid	31940240	Results: The <strong>OPRK1</strong> rs3802279, rs3802281, and rs963549 genotypes were significantly associated with <b>methadone</b> dosage analyzed by Pearson's chi square test or binary logistic regression to correct for covariates.
+OPRK1	drug	opioid	31940240	Conclusion: These findings support an important role of the <strong>OPRK1</strong> polymorphism in determining the daily <b>methadone</b> dose and may guide future studies in identifying additional genetic risk factors for HUD.
+OPRK1	drug	alcohol	31339663	nPE1 /  had lower basal Pomc and Pdyn (prodynorphin) levels compared to nPE1+/+ , coupled with increased basal Oprm1 and <strong>Oprk1</strong> (kappa opioid receptor) levels, and low <b>alcohol</b> drinking increased Pomc and Pdyn to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and <strong>Oprk1</strong>.
+OPRK1	drug	opioid	31339663	nPE1 /  had lower basal Pomc and Pdyn (prodynorphin) levels compared to nPE1+/+ , coupled with increased basal Oprm1 and <strong>Oprk1</strong> (kappa <b>opioid</b> receptor) levels, and low alcohol drinking increased Pomc and Pdyn to the basal levels of nPE1+/+ in the water group, without significant effects on Oprm1 and <strong>Oprk1</strong>.
+OPRK1	drug	alcohol	31339663	In nPE1+/+ , excessive <b>alcohol</b> intake increased Pomc and Oprm1, with no effect on Pdyn or <strong>Oprk1</strong>.
+OPRK1	drug	opioid	31004399	Three μ <b>opioid</b> receptor gene (OPRM1) variants and two κ <b>opioid</b> receptor gene (<strong>OPRK1</strong>) variants were examined in 314 male patients with AUD and 324 male controls.
+OPRK1	drug	alcohol	31004399	However, <strong>OPRK1</strong> SNP rs6473797 was significantly related to the severity of <b>alcohol</b> related symptoms as measured by AUDIT and OCDS and a haplotype containing rs6473797 was also related to OCDS scores in AUD patients.
+OPRK1	drug	opioid	30210591	However, the potential correlation between the κ1 <b>opioid</b> receptor (<strong>OPRK1</strong>) and drug addiction has not yet been characterized.
+OPRK1	addiction	addiction	30210591	However, the potential correlation between the κ1 opioid receptor (<strong>OPRK1</strong>) and drug <b>addiction</b> has not yet been characterized.
+OPRK1	drug	amphetamine	30210591	Bisulfite pyrosequencing technology was used to determine the levels of <strong>OPRK1</strong> promoter methylation in 60 drug abusers (30 heroin and 30 <b>METH</b> addicts) and 52 controls, observed to exhibit no significant differences in age or gender.
+OPRK1	drug	opioid	30210591	Bisulfite pyrosequencing technology was used to determine the levels of <strong>OPRK1</strong> promoter methylation in 60 drug abusers (30 <b>heroin</b> and 30 METH addicts) and 52 controls, observed to exhibit no significant differences in age or gender.
+OPRK1	drug	opioid	30210591	Significant correlations between <strong>OPRK1</strong> promoter methylation and the length and frequency of drug use were also observed in male <b>heroin</b> addicts (length: r=0.661, P=0.007; frequency: r= 0.684, P=0.005).
+OPRK1	addiction	addiction	30210591	In conclusion, results of the present study indicate that methylation of the <strong>OPRK1</strong> promoter contributes to the pathophysiology of drug <b>addiction</b>.
+OPRK1	drug	opioid	30171993	<b>Opioid</b> related genes, including OPRM1, OPRD1, <strong>OPRK1</strong>, and POMC, are obvious candidates for HD.
+OPRK1	drug	opioid	30138645	Prodynorphin (PDYN) binds to k <b>opioid</b> receptors (KOPr; encoded by <strong>OPRK1</strong>) and is known to regulate dopaminergic tone, making this system important for drugs addiction.
+OPRK1	addiction	addiction	30138645	Prodynorphin (PDYN) binds to k opioid receptors (KOPr; encoded by <strong>OPRK1</strong>) and is known to regulate dopaminergic tone, making this system important for drugs <b>addiction</b>.
+OPRK1	drug	alcohol	30075159	The current experiments were designed to assess dysregulation of the BNST DYN/KOR system by evaluating <b>alcohol</b> dependence induced changes in DYN/KOR gene expression (Pdyn and <strong>Oprk1</strong>, respectively), and the sensitivity of <b>alcohol</b> self administration, negative affective like behavior and physiological withdrawal to intra BNST KOR antagonism during acute withdrawal.
+OPRK1	addiction	dependence	30075159	The current experiments were designed to assess dysregulation of the BNST DYN/KOR system by evaluating alcohol <b>dependence</b> induced changes in DYN/KOR gene expression (Pdyn and <strong>Oprk1</strong>, respectively), and the sensitivity of alcohol self administration, negative affective like behavior and physiological withdrawal to intra BNST KOR antagonism during acute withdrawal.
+OPRK1	addiction	withdrawal	30075159	The current experiments were designed to assess dysregulation of the BNST DYN/KOR system by evaluating alcohol dependence induced changes in DYN/KOR gene expression (Pdyn and <strong>Oprk1</strong>, respectively), and the sensitivity of alcohol self administration, negative affective like behavior and physiological <b>withdrawal</b> to intra BNST KOR antagonism during acute <b>withdrawal</b>.
+OPRK1	addiction	dependence	30075159	BNST micropunches from air  and vapor exposed animals were analyzed using RT qPCR to quantify <b>dependence</b> induced changes in Pdyn and <strong>Oprk1</strong> mRNA expression.
+OPRK1	drug	alcohol	30075159	During acute withdrawal, following <b>alcohol</b> dependence induction, there was an upregulation in <strong>Oprk1</strong> mRNA expression in <b>alcohol</b> self administering animals, but not non <b>alcohol</b> self administering animals, that confirmed dysregulation of the KOR/DYN system within the BNST.
+OPRK1	addiction	dependence	30075159	During acute withdrawal, following alcohol <b>dependence</b> induction, there was an upregulation in <strong>Oprk1</strong> mRNA expression in alcohol self administering animals, but not non alcohol self administering animals, that confirmed dysregulation of the KOR/DYN system within the BNST.
+OPRK1	addiction	withdrawal	30075159	During acute <b>withdrawal</b>, following alcohol dependence induction, there was an upregulation in <strong>Oprk1</strong> mRNA expression in alcohol self administering animals, but not non alcohol self administering animals, that confirmed dysregulation of the KOR/DYN system within the BNST.
+OPRK1	drug	alcohol	29925858	We addressed this hypothesis by comparing the expression levels and co expression (transcriptionally coordinated) patterns of PDYN and KOR (<strong>OPRK1</strong>) genes in dorsolateral prefrontal cortex (dlPFC) between human <b>alcoholics</b> and controls.
+OPRK1	drug	alcohol	29925858	PDYN was found to be downregulated in dlPFC of <b>alcoholics</b>, while <strong>OPRK1</strong> transcription was not altered.
+OPRK1	drug	alcohol	29925858	Absolute expression levels of PDYN were lower compared to those of <strong>OPRK1</strong>, suggesting that PDYN expression is a limiting factor in the DYN/KOR signaling, and that the PDYN downregulation diminishes efficacy of DYN/KOR signaling in dlPFC of human <b>alcoholics</b>.
+OPRK1	drug	opioid	29878268	In contrast, in rats adapted to an HP diet compared with an NP diet, energy intake was lower; and in the NAcc, meal induced c Fos protein expression was 20% lower, and mRNA expression was 17% higher for dopamine receptor 2 (Drd2) receptors and 38% lower for κ <b>opioid</b> receptor (<strong>Oprk1</strong>) receptors.
+OPRK1	drug	opioid	29852138	Changes in expression of the Pdyn and κ <b>opioid</b> receptor (<strong>Oprk1</strong>) genes were coordinated between the ipsi  and contralateral sides.
+OPRK1	drug	opioid	29430855	The present study aimed to investigate whether neuropathic pain is accompanied by prodynorphin (Pdyn) and κ <b>opioid</b> receptor (<strong>Oprk1</strong>) gene expression alterations in selected mouse brain areas.
+OPRK1	drug	alcohol	29383684	We here analyzed post mortem NAc samples of human <b>alcoholics</b> to assess changes in prodynorphin (PDYN) and KOR (<strong>OPRK1</strong>) gene expression and co expression (transcriptionally coordinated) patterns.
+OPRK1	drug	alcohol	29383684	No significant differences in PDYN and <strong>OPRK1</strong> gene expression levels between <b>alcoholics</b> and controls were evident.
+OPRK1	drug	alcohol	29383684	However, PDYN and <strong>OPRK1</strong> showed transcriptionally coordinated pattern that was significantly different between <b>alcoholics</b> and controls.
+OPRK1	drug	opioid	29259946	This prospective association study investigated seven variations in the OPRM1, <strong>OPRK1</strong> and COMT gene, which encode Mu and KAPPA <b>opioid</b> receptors, and Catechol O methyltransferase enzyme respectively, in a cohort of 129 Tunisian cancer pain patients under oral <b>morphine</b> treatment.
+OPRK1	drug	opioid	29055075	The aim of this study was to investigate if genetic variants of mu, kappa, and delta <b>opioid</b> receptor genes (OPRM1, <strong>OPRK1</strong>, and OPRD1) and the catechol O methyltransferase gene (COMT) influenced the pain phenotype in patients with osteoarthritis.
+OPRK1	drug	opioid	28786760	Association of <strong>OPRK1</strong> gene polymorphisms with <b>opioid</b> dependence in addicted men undergoing <b>methadone</b> treatment in an Iranian population.
+OPRK1	addiction	dependence	28786760	Association of <strong>OPRK1</strong> gene polymorphisms with opioid <b>dependence</b> in addicted men undergoing methadone treatment in an Iranian population.
+OPRK1	drug	opioid	28786760	Previous studies have shown significant associations between <strong>OPRK1</strong> and susceptibility to <b>opioid</b> dependence and the relationships between libido dysfunction and insomnia among opium addicts who underwent <b>methadone</b> maintenance treatment.
+OPRK1	addiction	dependence	28786760	Previous studies have shown significant associations between <strong>OPRK1</strong> and susceptibility to opioid <b>dependence</b> and the relationships between libido dysfunction and insomnia among opium addicts who underwent methadone maintenance treatment.
+OPRK1	drug	opioid	28786760	The <strong>OPRK1</strong> gene variants showed significant association with susceptibility to <b>opioid</b> dependence among Iranians.
+OPRK1	addiction	dependence	28786760	The <strong>OPRK1</strong> gene variants showed significant association with susceptibility to opioid <b>dependence</b> among Iranians.
+OPRK1	drug	opioid	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the <b>opioid</b> receptor genes (OPRM1, OPRD1, and <strong>OPRK1</strong>), have been implicated in drug dependence, but relatively little is known on their contributions to <b>heroin</b> dependence in populations worldwide.
+OPRK1	addiction	dependence	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the opioid receptor genes (OPRM1, OPRD1, and <strong>OPRK1</strong>), have been implicated in drug <b>dependence</b>, but relatively little is known on their contributions to heroin <b>dependence</b> in populations worldwide.
+OPRK1	addiction	reward	28692418	<b>Reward</b>  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the opioid receptor genes (OPRM1, OPRD1, and <strong>OPRK1</strong>), have been implicated in drug dependence, but relatively little is known on their contributions to heroin dependence in populations worldwide.
+OPRK1	drug	opioid	28656735	Drug addiction is a novelty seeking personality trait that is associated with the candidate genes OPRD1 (<b>opioid</b> delta receptors), <strong>OPRK1</strong> (<b>opioid</b> kappa receptors) and PDYN (prodynorphin).
+OPRK1	addiction	addiction	28656735	Drug <b>addiction</b> is a novelty seeking personality trait that is associated with the candidate genes OPRD1 (opioid delta receptors), <strong>OPRK1</strong> (opioid kappa receptors) and PDYN (prodynorphin).
+OPRK1	addiction	relapse	28656735	Drug addiction is a novelty <b>seeking</b> personality trait that is associated with the candidate genes OPRD1 (opioid delta receptors), <strong>OPRK1</strong> (opioid kappa receptors) and PDYN (prodynorphin).
+OPRK1	addiction	relapse	28656735	However, associations between single nucleotide polymorphisms (SNPs) rs1042114 (80G>T) of the OPRD1 gene, rs702764 (843 A>G) of the <strong>OPRK1</strong> gene, and rs910080 (3' UTR _743T>C), rs1997794 (5' UTR  381A>G) and rs1022563 (3' UTR) of the PDYN gene and novelty <b>seeking</b> remain controversial as reported results have not been reproducible.
+OPRK1	drug	opioid	28656735	Polymorphic alleles at SNP rs702764 of <strong>OPRK1</strong> were not associated with <b>opioid</b> dependence.
+OPRK1	addiction	dependence	28656735	Polymorphic alleles at SNP rs702764 of <strong>OPRK1</strong> were not associated with opioid <b>dependence</b>.
+OPRK1	drug	opioid	28511993	Rats exposed to early life stress (MS360) had increased <b>opioid</b> receptor gene (Oprm1, Oprd1 and <strong>Oprk1</strong>) expression in the dorsal striatum.
+OPRK1	drug	alcohol	28511993	<b>Ethanol</b> drinking was associated with lower striatal Oprd1 and <strong>Oprk1</strong> expression solely in rats exposed to early life stress.
+OPRK1	drug	opioid	27725223	Next generation sequencing (NGS) workflow was based on a custom AmpliSeq™ panel and designed for sequencing of human genes related to the <b>opioid</b> receptor group (OPRM1, OPRD1, <strong>OPRK1</strong>, SIGMA1, OPRL1) on an Ion PGM™ Sequencer.
+OPRK1	drug	opioid	27061086	<b>Opioid</b> genes (e.g., <strong>Oprk1</strong>, Oprm1) and genes for neuropeptides linked to anxiety and panic behaviors (e.g., Npy1r) had mostly decreased expression.
+OPRK1	drug	cocaine	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, Penk, Pdyn) and cognate receptors (Oprm, <strong>Oprk</strong> and Oprd) in reward related brain regions, after exposure to either <b>cocaine</b> self administration or yoked saline, in the aforementioned translational paradigm.
+OPRK1	drug	opioid	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous <b>opioid</b> peptides (Pomc, Penk, Pdyn) and cognate receptors (Oprm, <strong>Oprk</strong> and Oprd) in reward related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+OPRK1	addiction	reward	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, Penk, Pdyn) and cognate receptors (Oprm, <strong>Oprk</strong> and Oprd) in <b>reward</b> related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+OPRK1	drug	cocaine	26777278	Also, different strain specific <b>cocaine</b> induced mRNA expression of Oprm and <strong>Oprk</strong> was found in DS.
+OPRK1	drug	cocaine	26777278	Moreover, gene expression level of Pdyn, Penk, <strong>Oprk</strong>, and Oprm in the DS was significantly correlated with <b>cocaine</b> intake only in Fischer rats.
+OPRK1	drug	opioid	28300812	All enrolled participants were genotyped for polymorphisms in the following genes: mu  (OPRM1), kappa <b>opioid</b> receptors (<strong>OPRK1</strong>), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (SLC6A3, DAT1) and alpha 2 adrenoreceptor (ADRA2A) a pharmacological target of guanfacine.
+OPRK1	addiction	withdrawal	26692286	The total <b>withdrawal</b> severity score (based on the COWS) from this procedure was correlated with genotype information for variants of OPRM1 (rs1799971; rs6848893), OPRD1 (rs10753331; rs2234918; rs581111; rs678849; rs1042114), and <strong>OPRK1</strong> (rs6473797; rs963549).
+OPRK1	drug	opioid	26692286	For participants who underwent <b>naloxone</b> precipitated withdrawal (n = 29) only <strong>OPRK1</strong> rs6473797 ( .23) was significant in the bivariate analysis, though not retained in the final model.
+OPRK1	addiction	withdrawal	26692286	For participants who underwent naloxone precipitated <b>withdrawal</b> (n = 29) only <strong>OPRK1</strong> rs6473797 ( .23) was significant in the bivariate analysis, though not retained in the final model.
+OPRK1	drug	opioid	26288297	It was genotyped polymorphisms in the following genes: mu <b>opioid</b> receptor (OPRM1), kappa <b>opioid</b> receptor (<strong>OPRK1</strong>), catechol O methyltransferase (COMT), dopamine receptors types 2 (DRD2) and 4 (DRD4), dopamine beta hydroxylase, and dopamine transporter (DAT1).
+OPRK1	addiction	relapse	26288297	Regardless of treatment several polymorphisms of these genes were associated with high risk of <b>relapse</b>: an allele L (2R) DRD4 120bp (p=0.05; OR (95% CI)=3.3(1.1 10.1)); an allele С DRD2 NcoI (р=0,051; OR (95% CI)=2,86 (1,09 7,52)); the genotype 9.9 DAT VNTR 40bp (р=0,04; OR (95% CI)=1,4 (1,3 1,5)); on the contrary, (СС+СТ) (ТТ)) variants of <strong>OPRK1</strong> DRD2Ncol increased a chance to complete treatment program (р=0,004; OR (95% CI)=7.4 (1.8 30.4)), Kaplan Meier survival analysis (р=0,016).
+OPRK1	drug	alcohol	25823631	The genetic variability of μ , δ  and κ opioid receptors genes OPRM1, OPRD1, and <strong>OPRK1</strong> modulates the efficacy of opioid antagonist treatments such as <b>naltrexone</b> and methadone, as well as the cocaine vaccine.
+OPRK1	drug	cocaine	25823631	The genetic variability of μ , δ  and κ opioid receptors genes OPRM1, OPRD1, and <strong>OPRK1</strong> modulates the efficacy of opioid antagonist treatments such as naltrexone and methadone, as well as the <b>cocaine</b> vaccine.
+OPRK1	drug	opioid	25823631	The genetic variability of μ , δ  and κ <b>opioid</b> receptors genes OPRM1, OPRD1, and <strong>OPRK1</strong> modulates the efficacy of <b>opioid</b> antagonist treatments such as naltrexone and <b>methadone</b>, as well as the cocaine vaccine.
+OPRK1	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and <strong>OPRK1</strong>) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+OPRK1	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and <strong>OPRK1</strong>) pathways which presumably impact reinforcing properties of alcohol.
+OPRK1	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and <strong>OPRK1</strong>) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+OPRK1	drug	alcohol	25177835	A molecular prospective provides new insights into implication of PDYN and <strong>OPRK1</strong> genes in <b>alcohol</b> dependence.
+OPRK1	addiction	dependence	25177835	A molecular prospective provides new insights into implication of PDYN and <strong>OPRK1</strong> genes in alcohol <b>dependence</b>.
+OPRK1	drug	alcohol	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for <b>alcohol</b> dependence by remodeling DNA protein interaction patterns in prodynorphin (PDYN) and the κ opioid receptor (<strong>OPRK1</strong>) genes.
+OPRK1	drug	opioid	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for alcohol dependence by remodeling DNA protein interaction patterns in prodynorphin (PDYN) and the κ <b>opioid</b> receptor (<strong>OPRK1</strong>) genes.
+OPRK1	addiction	dependence	25177835	These genetic variations, SNPs, may alter an individual׳s susceptibility for alcohol <b>dependence</b> by remodeling DNA protein interaction patterns in prodynorphin (PDYN) and the κ opioid receptor (<strong>OPRK1</strong>) genes.
+OPRK1	drug	alcohol	25177835	In order to elaborate the underlying molecular mechanism behind these susceptibility differences we used bioinformatics tools to retrieve differential DNA protein interactions at PDYN and <strong>OPRK1</strong> SNPs significantly associated with <b>alcohol</b> dependence.
+OPRK1	addiction	dependence	25177835	In order to elaborate the underlying molecular mechanism behind these susceptibility differences we used bioinformatics tools to retrieve differential DNA protein interactions at PDYN and <strong>OPRK1</strong> SNPs significantly associated with alcohol <b>dependence</b>.
+OPRK1	drug	alcohol	25177835	In a nutshell, transition of a single nucleotide may modify differential DNA protein interactions at <strong>OPRK1</strong> and PDYN׳s SNPs, significantly associated with pathology that may lead to altered individual vulnerability for <b>alcohol</b> dependence.
+OPRK1	addiction	dependence	25177835	In a nutshell, transition of a single nucleotide may modify differential DNA protein interactions at <strong>OPRK1</strong> and PDYN׳s SNPs, significantly associated with pathology that may lead to altered individual vulnerability for alcohol <b>dependence</b>.
+OPRK1	addiction	addiction	24690494	The research community has increasingly focused on the development of <strong>OPRK</strong> antagonists as pharmacotherapies for the treatment of depression, anxiety, <b>addictive</b> disorders and other psychiatric conditions produced or exacerbated by stress.
+OPRK1	drug	alcohol	24533225	Polymorphisms in the μ , δ  and κ opioid receptor genes (OPRM1, OPRD1 and <strong>OPRK1</strong>) have been reported to be associated with substance (<b>alcohol</b> or drug) dependence.
+OPRK1	drug	opioid	24533225	Polymorphisms in the μ , δ  and κ <b>opioid</b> receptor genes (OPRM1, OPRD1 and <strong>OPRK1</strong>) have been reported to be associated with substance (alcohol or drug) dependence.
+OPRK1	addiction	dependence	24533225	Polymorphisms in the μ , δ  and κ opioid receptor genes (OPRM1, OPRD1 and <strong>OPRK1</strong>) have been reported to be associated with substance (alcohol or drug) <b>dependence</b>.
+OPRK1	drug	alcohol	24533225	Genotype data for 13 OPRM1 Single Nucleotide Polymorphisms (SNPs), 11 OPRD1 SNPs and seven <strong>OPRK1</strong> SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with <b>Alcohol</b> Dependence (AD), 171 with Cocaine Dependence (CD), and 91 with Opioid Dependence (OD)] and 338 EA control subjects.
+OPRK1	drug	cocaine	24533225	Genotype data for 13 OPRM1 Single Nucleotide Polymorphisms (SNPs), 11 OPRD1 SNPs and seven <strong>OPRK1</strong> SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with Alcohol Dependence (AD), 171 with <b>Cocaine</b> Dependence (CD), and 91 with Opioid Dependence (OD)] and 338 EA control subjects.
+OPRK1	drug	opioid	24533225	Genotype data for 13 OPRM1 Single Nucleotide Polymorphisms (SNPs), 11 OPRD1 SNPs and seven <strong>OPRK1</strong> SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with Alcohol Dependence (AD), 171 with Cocaine Dependence (CD), and 91 with <b>Opioid</b> Dependence (OD)] and 338 EA control subjects.
+OPRK1	addiction	dependence	24533225	Genotype data for 13 OPRM1 Single Nucleotide Polymorphisms (SNPs), 11 OPRD1 SNPs and seven <strong>OPRK1</strong> SNPs were obtained from 382 European Americans (EAs) affected with substance <b>dependence</b> [among them, 318 with Alcohol <b>Dependence</b> (AD), 171 with Cocaine <b>Dependence</b> (CD), and 91 with Opioid <b>Dependence</b> (OD)] and 338 EA control subjects.
+OPRK1	drug	opioid	24525640	This study tested the hypotheses that the genetic polymorphisms in the κ <b>opioid</b> receptor 1 (<strong>OPRK1</strong>) gene region are associated with <b>methadone</b> treatment responses in a Taiwan <b>methadone</b> maintenance treatment (MMT) cohort.
+OPRK1	drug	alcohol	24525640	The findings suggest that genetic polymorphisms in <strong>OPRK1</strong> were associated with the body weight, <b>alcohol</b> use, and opioid withdrawal symptoms in MMT patients.
+OPRK1	drug	opioid	24525640	The findings suggest that genetic polymorphisms in <strong>OPRK1</strong> were associated with the body weight, alcohol use, and <b>opioid</b> withdrawal symptoms in MMT patients.
+OPRK1	addiction	withdrawal	24525640	The findings suggest that genetic polymorphisms in <strong>OPRK1</strong> were associated with the body weight, alcohol use, and opioid <b>withdrawal</b> symptoms in MMT patients.
+OPRK1	drug	opioid	24274990	No difference was evidenced between responders and non responders to BUP in the frequency of kappa <b>opioid</b> receptor (<strong>OPRK1</strong>) 36G>T SNP.
+OPRK1	drug	alcohol	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (<strong>OPRK1</strong>) opioid receptors and precursors of their ligands   proopiomelanocortin (POMC), coding for beta endorphin and prodynorphin (PDYN) coding for dynorphins, were analyzed in a case control study that included 354 male <b>alcohol</b> dependent and 357 male control subjects from Croatian population.
+OPRK1	drug	opioid	24035285	In this study, single nucleotide polymorphisms within the genes for mu (OPRM1) and kappa (<strong>OPRK1</strong>) <b>opioid</b> receptors and precursors of their ligands   proopiomelanocortin (POMC), coding for beta endorphin and prodynorphin (PDYN) coding for dynorphins, were analyzed in a case control study that included 354 male alcohol dependent and 357 male control subjects from Croatian population.
+OPRK1	drug	alcohol	24035285	Thus, the data obtained suggest no association of the selected polymorphisms of the genes OPRM1/POMC and <strong>OPRK1</strong>/PDYN with <b>alcoholism</b> in Croatian population.
+OPRK1	drug	cocaine	23995774	We examined the pharmacogenetic association between a variant in the κ opioid receptor (<strong>OPRK1</strong>) gene and the response to treatment with a <b>cocaine</b> vaccine tested in a recent clinical trial (October 2003 to April 2005).
+OPRK1	drug	opioid	23995774	We examined the pharmacogenetic association between a variant in the κ <b>opioid</b> receptor (<strong>OPRK1</strong>) gene and the response to treatment with a cocaine vaccine tested in a recent clinical trial (October 2003 to April 2005).
+OPRK1	drug	cocaine	23995774	We genotyped 66 of these patients for the rs6473797 variant of the <strong>OPRK1</strong> gene and compared vaccine patients with placebo patients in terms of <b>cocaine</b> free urines over time.
+OPRK1	drug	cocaine	23995774	Using repeated measures analysis of variance corrected for population structure, it was seen that vaccine pharmacotherapy reduced <b>cocaine</b> positive urines significantly on the basis of the <strong>OPRK1</strong> genotype.
+OPRK1	drug	cocaine	23995774	This study indicates that a patient's <strong>OPRK1</strong> genotype could be used to identify a subset of individuals for whom vaccine treatment may be an effective pharmacotherapy for <b>cocaine</b> dependence.
+OPRK1	addiction	dependence	23995774	This study indicates that a patient's <strong>OPRK1</strong> genotype could be used to identify a subset of individuals for whom vaccine treatment may be an effective pharmacotherapy for cocaine <b>dependence</b>.
+OPRK1	drug	cocaine	23962922	A variant on the kappa opioid receptor gene (<strong>OPRK1</strong>) is associated with stress response and related drug craving, limbic brain activation and <b>cocaine</b> relapse risk.
+OPRK1	drug	opioid	23962922	A variant on the kappa <b>opioid</b> receptor gene (<strong>OPRK1</strong>) is associated with stress response and related drug craving, limbic brain activation and cocaine relapse risk.
+OPRK1	addiction	relapse	23962922	A variant on the kappa opioid receptor gene (<strong>OPRK1</strong>) is associated with stress response and related drug <b>craving</b>, limbic brain activation and cocaine <b>relapse</b> risk.
+OPRK1	drug	opioid	23962922	The kappa <b>opioid</b> receptor gene (<strong>OPRK1</strong>) mediates stress responses.
+OPRK1	drug	cocaine	23962922	Here, we examined whether the <strong>OPRK1</strong> rs6989250 C>G affects stress induced <b>cocaine</b> craving and cortisol responses, subsequent <b>cocaine</b> relapse risk and the neural response to stress using functional magnetic resonance imaging (fMRI) in <b>cocaine</b> dependence.
+OPRK1	addiction	dependence	23962922	Here, we examined whether the <strong>OPRK1</strong> rs6989250 C>G affects stress induced cocaine craving and cortisol responses, subsequent cocaine relapse risk and the neural response to stress using functional magnetic resonance imaging (fMRI) in cocaine <b>dependence</b>.
+OPRK1	addiction	relapse	23962922	Here, we examined whether the <strong>OPRK1</strong> rs6989250 C>G affects stress induced cocaine <b>craving</b> and cortisol responses, subsequent cocaine <b>relapse</b> risk and the neural response to stress using functional magnetic resonance imaging (fMRI) in cocaine dependence.
+OPRK1	drug	cocaine	23962922	These results suggest that <strong>OPRK1</strong> is associated with stress induced craving and cortisol, hyperactive hypothalamus/thalamus midbrain cerebellum responses, and also associated with greater subsequent <b>cocaine</b> relapse risk.
+OPRK1	addiction	relapse	23962922	These results suggest that <strong>OPRK1</strong> is associated with stress induced <b>craving</b> and cortisol, hyperactive hypothalamus/thalamus midbrain cerebellum responses, and also associated with greater subsequent cocaine <b>relapse</b> risk.
+OPRK1	drug	opioid	23277131	Two primary gene candidates were supported by the linkage association, gene expression profiling, and network analysis: neurotrophic tyrosine kinase receptor, type 2 (NTRK2), and the <b>opioid</b> receptor, κ1 (<strong>OPRK1</strong>).
+OPRK1	drug	alcohol	23101464	Synthetic κ opioid receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (<strong>OPRK1</strong>) and prodynorphin (PDYN) genes have been shown to be associated with <b>alcohol</b> dependence.
+OPRK1	drug	opioid	23101464	Synthetic κ <b>opioid</b> receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (<strong>OPRK1</strong>) and prodynorphin (PDYN) genes have been shown to be associated with alcohol dependence.
+OPRK1	addiction	dependence	23101464	Synthetic κ opioid receptor (KOR) agonists induce dysphoric and pro depressive effects and variations in the KOR (<strong>OPRK1</strong>) and prodynorphin (PDYN) genes have been shown to be associated with alcohol <b>dependence</b>.
+OPRK1	drug	alcohol	23101464	We genotyped 23 single nucleotide polymorphisms (SNPs) in the PDYN and <strong>OPRK1</strong> genes in 816 <b>alcohol</b> dependent subjects and investigated their association with: (1) negative craving measured by a subscale of the Inventory of Drug Taking Situations; (2) a self reported history of depression; (3) the intensity of depressive symptoms measured by the Beck Depression Inventory II.
+OPRK1	addiction	relapse	23101464	We genotyped 23 single nucleotide polymorphisms (SNPs) in the PDYN and <strong>OPRK1</strong> genes in 816 alcohol dependent subjects and investigated their association with: (1) negative <b>craving</b> measured by a subscale of the Inventory of Drug Taking Situations; (2) a self reported history of depression; (3) the intensity of depressive symptoms measured by the Beck Depression Inventory II.
+OPRK1	drug	alcohol	23101464	In addition, 13 of the 23 PDYN and <strong>OPRK1</strong> SNPs, which were previously genotyped in a set of 1248 controls, were used to evaluate association with <b>alcohol</b> dependence.
+OPRK1	addiction	dependence	23101464	In addition, 13 of the 23 PDYN and <strong>OPRK1</strong> SNPs, which were previously genotyped in a set of 1248 controls, were used to evaluate association with alcohol <b>dependence</b>.
+OPRK1	drug	alcohol	23101464	No associations of <strong>OPRK1</strong> gene variation with <b>alcohol</b> dependence or other studied phenotypes were found.
+OPRK1	addiction	dependence	23101464	No associations of <strong>OPRK1</strong> gene variation with alcohol <b>dependence</b> or other studied phenotypes were found.
+OPRK1	drug	alcohol	22954510	This alternate binding presents the possibility that single nucleotide polymorphisms (SNPs) in the kappa and delta opioid receptor (<strong>OPRK1</strong> and OPRD1) genes may contribute to <b>naltrexone</b> pharmacogenetics.
+OPRK1	drug	opioid	22954510	This alternate binding presents the possibility that single nucleotide polymorphisms (SNPs) in the kappa and delta <b>opioid</b> receptor (<strong>OPRK1</strong> and OPRD1) genes may contribute to naltrexone pharmacogenetics.
+OPRK1	drug	alcohol	22954510	Multilevel models revealed a significant <b>Naltrexone</b>×<strong>OPRK1</strong> Genotype (rs997917) interaction predicting <b>alcohol</b> induced sedation, such that TT homozygotes reported lower <b>naltrexone</b> induced <b>alcohol</b> sedation as compared to carriers of the C allele.
+OPRK1	drug	cocaine	22709632	κ Opioid receptors (KOPr; encoded by <strong>OPRK1</strong>), and their endogenous agonists, the dynorphins (encoded by PDYN), have counter modulatory effects on reward caused by <b>cocaine</b> or MOPr agonist exposure, and exhibit plasticity in addictive like states.
+OPRK1	drug	opioid	22709632	κ <b>Opioid</b> receptors (KOPr; encoded by <strong>OPRK1</strong>), and their endogenous agonists, the dynorphins (encoded by PDYN), have counter modulatory effects on reward caused by cocaine or MOPr agonist exposure, and exhibit plasticity in addictive like states.
+OPRK1	addiction	addiction	22709632	κ Opioid receptors (KOPr; encoded by <strong>OPRK1</strong>), and their endogenous agonists, the dynorphins (encoded by PDYN), have counter modulatory effects on reward caused by cocaine or MOPr agonist exposure, and exhibit plasticity in <b>addictive</b> like states.
+OPRK1	addiction	reward	22709632	κ Opioid receptors (KOPr; encoded by <strong>OPRK1</strong>), and their endogenous agonists, the dynorphins (encoded by PDYN), have counter modulatory effects on <b>reward</b> caused by cocaine or MOPr agonist exposure, and exhibit plasticity in addictive like states.
+OPRK1	addiction	addiction	22709632	Vulnerability and resilience can be due to pre existing (e.g., genetic) factors, or epigenetic modifications of the <strong>OPRK1</strong> or PDYN genes during the <b>addiction</b> cycle.
+OPRK1	drug	opioid	22500942	Genes encoding the <b>opioid</b> receptors (OPRM1, OPRD1 and <strong>OPRK1</strong>) are obvious candidates for involvement in risk for <b>heroin</b> dependence.
+OPRK1	addiction	dependence	22500942	Genes encoding the opioid receptors (OPRM1, OPRD1 and <strong>OPRK1</strong>) are obvious candidates for involvement in risk for heroin <b>dependence</b>.
+OPRK1	drug	alcohol	22138325	A study was undertaken to identify the single nucleotide polymorphisms (SNP) at selective areas of kappa opioid receptor 1 (<strong>OPRK1</strong>) gene in heroin as well as in <b>alcohol</b> addicts and to compare them with that in control population.
+OPRK1	drug	opioid	22138325	A study was undertaken to identify the single nucleotide polymorphisms (SNP) at selective areas of kappa <b>opioid</b> receptor 1 (<strong>OPRK1</strong>) gene in <b>heroin</b> as well as in alcohol addicts and to compare them with that in control population.
+OPRK1	drug	opioid	22138325	Exons 3 and 4 of <strong>OPRK1</strong> and the SNP, A118G of mu <b>opioid</b> receptor 1 (OPRM1) in the DNA samples were genotyped by sequencing and restriction fragment length polymorphism respectively.
+OPRK1	addiction	addiction	22138325	Three SNPs of <strong>OPRK1</strong>, rs16918875, rs702764 and rs963549, were identified in the population, none of which showed significant association with <b>addiction</b>.
+OPRK1	drug	alcohol	22138325	A potential SNP SNP interaction showed that the odds of being addicted was 2.51 fold in heroin subjects [CI (95%)=1.1524 to 5.4947, P=0.0206] and 2.31 fold in <b>alcoholics</b> [CI (95%)=1.025 to 5.24, P=0.0433] with the <strong>OPRK1</strong> (rs16918875) and A118G risk alleles than without either.
+OPRK1	drug	opioid	22138325	A potential SNP SNP interaction showed that the odds of being addicted was 2.51 fold in <b>heroin</b> subjects [CI (95%)=1.1524 to 5.4947, P=0.0206] and 2.31 fold in alcoholics [CI (95%)=1.025 to 5.24, P=0.0433] with the <strong>OPRK1</strong> (rs16918875) and A118G risk alleles than without either.
+OPRK1	drug	opioid	21807019	Within strains, complex patterns of <b>heroin</b> dose dependent changes in the levels of Oprm1, <strong>Oprk1</strong> and Oprd1 mRNAs were observed in the SN/VTA.
+OPRK1	drug	alcohol	19393386	<b>Naltrexone</b> is a competitive antagonist of opioid receptors OPRM1, OPRD1 and <strong>OPRK1</strong>.
+OPRK1	drug	opioid	19393386	Naltrexone is a competitive antagonist of <b>opioid</b> receptors OPRM1, OPRD1 and <strong>OPRK1</strong>.
+OPRK1	drug	opioid	18518925	These variants were in noncoding regions of the genes encoding the mu (OPRM1; rs510769 and rs3778151), kappa (<strong>OPRK1</strong>; rs6473797) and delta (OPRD1; rs2236861, rs2236857 and rs3766951) <b>opioid</b> receptors; the neuropeptide galanin (GAL; rs694066); the serotonin receptor subtype 3B (HTR3B; rs3758987) and the casein kinase 1 isoform epsilon (CSNK1E; rs1534891).
+OPRK1	drug	alcohol	18319328	A regulatory variation in <strong>OPRK1</strong>, the gene encoding the kappa opioid receptor, is associated with <b>alcohol</b> dependence.
+OPRK1	drug	opioid	18319328	A regulatory variation in <strong>OPRK1</strong>, the gene encoding the kappa <b>opioid</b> receptor, is associated with alcohol dependence.
+OPRK1	addiction	dependence	18319328	A regulatory variation in <strong>OPRK1</strong>, the gene encoding the kappa opioid receptor, is associated with alcohol <b>dependence</b>.
+OPRK1	drug	alcohol	18319328	Variations in <strong>OPRK1</strong>, which encodes the kappa opioid receptor, are associated with the risk for <b>alcohol</b> dependence.
+OPRK1	drug	opioid	18319328	Variations in <strong>OPRK1</strong>, which encodes the kappa <b>opioid</b> receptor, are associated with the risk for alcohol dependence.
+OPRK1	addiction	dependence	18319328	Variations in <strong>OPRK1</strong>, which encodes the kappa opioid receptor, are associated with the risk for alcohol <b>dependence</b>.
+OPRK1	drug	alcohol	18319328	This indel is, therefore, a functional regulatory variation likely to explain at least part of the association of <strong>OPRK1</strong> with <b>alcohol</b> dependence.
+OPRK1	addiction	dependence	18319328	This indel is, therefore, a functional regulatory variation likely to explain at least part of the association of <strong>OPRK1</strong> with alcohol <b>dependence</b>.
+OPRK1	drug	alcohol	17622222	The OPRD1 and <strong>OPRK1</strong> loci in <b>alcohol</b> or drug dependence: OPRD1 variation modulates substance dependence risk.
+OPRK1	addiction	dependence	17622222	The OPRD1 and <strong>OPRK1</strong> loci in alcohol or drug <b>dependence</b>: OPRD1 variation modulates substance <b>dependence</b> risk.
+OPRK1	drug	alcohol	17503481	In an earlier study, we reported that variation in the genes encoding the kappa opioid receptor (<strong>OPRK1</strong>) and its peptide ligand (PDYN) were associated with the risk for <b>alcoholism</b>.
+OPRK1	drug	opioid	17503481	In an earlier study, we reported that variation in the genes encoding the kappa <b>opioid</b> receptor (<strong>OPRK1</strong>) and its peptide ligand (PDYN) were associated with the risk for alcoholism.
+OPRK1	drug	alcohol	17374034	Opioid receptor gene (OPRM1, <strong>OPRK1</strong>, and OPRD1) variants and response to <b>naltrexone</b> treatment for <b>alcohol</b> dependence: results from the VA Cooperative Study.
+OPRK1	drug	opioid	17374034	<b>Opioid</b> receptor gene (OPRM1, <strong>OPRK1</strong>, and OPRD1) variants and response to naltrexone treatment for alcohol dependence: results from the VA Cooperative Study.
+OPRK1	addiction	dependence	17374034	Opioid receptor gene (OPRM1, <strong>OPRK1</strong>, and OPRD1) variants and response to naltrexone treatment for alcohol <b>dependence</b>: results from the VA Cooperative Study.
+OPRK1	drug	alcohol	17374034	We studied polymorphic variants at each of the 3 opioid receptor genes  OPRM1, OPRD1, and <strong>OPRK1</strong>, which encode the mu, delta, and kappa opioid receptors, respectively  including the OPRM1 Asn40Asp variant  as predictors of response to NTX or placebo in 215 <b>alcohol</b> dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "<b>Naltrexone</b> in the Treatment of <b>Alcohol</b> Dependence."
+OPRK1	drug	opioid	17374034	We studied polymorphic variants at each of the 3 <b>opioid</b> receptor genes  OPRM1, OPRD1, and <strong>OPRK1</strong>, which encode the mu, delta, and kappa <b>opioid</b> receptors, respectively  including the OPRM1 Asn40Asp variant  as predictors of response to NTX or placebo in 215 alcohol dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "Naltrexone in the Treatment of Alcohol Dependence."
+OPRK1	addiction	dependence	17374034	We studied polymorphic variants at each of the 3 opioid receptor genes  OPRM1, OPRD1, and <strong>OPRK1</strong>, which encode the mu, delta, and kappa opioid receptors, respectively  including the OPRM1 Asn40Asp variant  as predictors of response to NTX or placebo in 215 alcohol dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "Naltrexone in the Treatment of Alcohol <b>Dependence</b>."
+OPRK1	drug	opioid	17373729	Human kappa <b>opioid</b> receptor gene (<strong>OPRK1</strong>) polymorphism is associated with opiate addiction.
+OPRK1	addiction	addiction	17373729	Human kappa opioid receptor gene (<strong>OPRK1</strong>) polymorphism is associated with opiate <b>addiction</b>.
+OPRK1	drug	alcohol	16924269	We genotyped SNPs throughout <strong>OPRK1</strong>, encoding the kappa opioid receptor, and PDYN, which encodes its ligand prodynorphin, in a group of 1860 European American individuals from 219 multiplex <b>alcohol</b> dependent families.
+OPRK1	drug	opioid	16924269	We genotyped SNPs throughout <strong>OPRK1</strong>, encoding the kappa <b>opioid</b> receptor, and PDYN, which encodes its ligand prodynorphin, in a group of 1860 European American individuals from 219 multiplex alcohol dependent families.
+OPRK1	drug	alcohol	16924269	Family based analyses demonstrated associations between <b>alcohol</b> dependence and multiple SNPs in the promoter and 3' end of PDYN, and in intron 2 of <strong>OPRK1</strong>.
+OPRK1	addiction	dependence	16924269	Family based analyses demonstrated associations between alcohol <b>dependence</b> and multiple SNPs in the promoter and 3' end of PDYN, and in intron 2 of <strong>OPRK1</strong>.
+OPRK1	drug	alcohol	16924269	Thus, variations in the genes encoding both the kappa opioid receptor and its ligand, <strong>OPRK1</strong> and PDYN, are associated with the risk for <b>alcohol</b> dependence; this makes biological sense as variations in either should affect signaling through the kappa opioid system.
+OPRK1	drug	opioid	16924269	Thus, variations in the genes encoding both the kappa <b>opioid</b> receptor and its ligand, <strong>OPRK1</strong> and PDYN, are associated with the risk for alcohol dependence; this makes biological sense as variations in either should affect signaling through the kappa <b>opioid</b> system.
+OPRK1	addiction	dependence	16924269	Thus, variations in the genes encoding both the kappa opioid receptor and its ligand, <strong>OPRK1</strong> and PDYN, are associated with the risk for alcohol <b>dependence</b>; this makes biological sense as variations in either should affect signaling through the kappa opioid system.
+OPRK1	drug	opioid	16753266	In chronic treatment, both <strong>Oprk1</strong> and Oprm1 expression levels, that encoded kappa and mu <b>opioid</b> receptor respectively, showed significant decreases in the periaqueductal gray and striatum.
+OPRK1	drug	cocaine	15901784	Genetic and pharmacological approaches were used to examine kappa opioid receptor (<strong>KOR 1</strong>) regulation of dopamine (DA) dynamics in the nucleus accumbens and vulnerability to <b>cocaine</b>.
+OPRK1	drug	opioid	15901784	Genetic and pharmacological approaches were used to examine kappa <b>opioid</b> receptor (<strong>KOR 1</strong>) regulation of dopamine (DA) dynamics in the nucleus accumbens and vulnerability to cocaine.
+OPRK1	drug	cocaine	15901784	Its loss induces neuroadaptations characteristic of "<b>cocaine</b> sensitized" animals, indicating a critical role of <strong>KOR 1</strong> in attenuating responsiveness to <b>cocaine</b>.
+OPRK1	drug	opioid	15608558	Redefinition of the human kappa <b>opioid</b> receptor gene (<strong>OPRK1</strong>) structure and association of haplotypes with opiate addiction.
+OPRK1	addiction	addiction	15608558	Redefinition of the human kappa opioid receptor gene (<strong>OPRK1</strong>) structure and association of haplotypes with opiate <b>addiction</b>.
+OPRK1	drug	alcohol	14745298	Nonselective opioid antagonists reduce <b>alcohol</b> consumption under various experimental situations, and several association studies have examined possible roles of opioid receptor mu (OPRM), delta (OPRD), and kappa (<strong>OPRK</strong>) genes in the development of <b>alcohol</b> dependence.
+OPRK1	drug	opioid	14745298	Nonselective <b>opioid</b> antagonists reduce alcohol consumption under various experimental situations, and several association studies have examined possible roles of <b>opioid</b> receptor mu (OPRM), delta (OPRD), and kappa (<strong>OPRK</strong>) genes in the development of alcohol dependence.
+OPRK1	addiction	dependence	14745298	Nonselective opioid antagonists reduce alcohol consumption under various experimental situations, and several association studies have examined possible roles of opioid receptor mu (OPRM), delta (OPRD), and kappa (<strong>OPRK</strong>) genes in the development of alcohol <b>dependence</b>.
+OPRK1	drug	alcohol	14745298	We examined 20 single nucleotide polymorphisms (SNPs) across the OPRM, OPRD, and <strong>OPRK</strong> genes in 158 <b>alcohol</b> dependent subjects and 149 controls.
+OPRK1	drug	opioid	10835636	The mu , delta  and kappa  <b>opioid</b> receptors (encoded by Oprm, Oprd1 and <strong>Oprk1</strong>, respectively) mediate the biological activity of <b>opioids</b>.
+OPRK1	drug	opioid	10835636	Our data show no detectable phenotype in <strong>Oprk1</strong> /  mutants, suggesting that kappa receptors do not have a role in this aspect of <b>opioid</b> function; opposing phenotypes in Oprm /  and Oprd1 /  mutants which contrasts with the classical notion of similar activities of mu  and delta receptors; and consistent anxiogenic  and depressive like responses in Oprd1 /  mice, indicating that delta receptor activity contributes to improvement of mood states.
+OPRK1	drug	opioid	7752808	In this study, we completed the localization on mouse chromosomes of the genes encoding mu (Oprm) and kappa (<strong>Oprk</strong>) receptors, as well as the genes for the <b>opioid</b> propeptides proenkephalin (Penk) and prodynorphin (Pdyn).
+JUND	drug	cocaine	30089879	We identify the <strong>JUND</strong> transcription factor as a key regulator of <b>cocaine</b> action and confirmed, by use of viral mediated gene transfer, that <strong>JUND</strong> activity in somatostatin interneurons influences behavioral responses to <b>cocaine</b>.
+JUND	drug	cocaine	28710498	In particular, we identified an <strong>AP 1</strong> regulated transcriptional network in dlPFC neurons associated with <b>cocaine</b> use disorder that contains several differentially expressed hub genes.
+JUND	drug	amphetamine	24939695	After a 30 day withdrawal from <b>methamphetamine</b> self administration, however, there was mostly decreased expression of transcription factors including <strong>junD</strong>.
+JUND	addiction	withdrawal	24939695	After a 30 day <b>withdrawal</b> from methamphetamine self administration, however, there was mostly decreased expression of transcription factors including <strong>junD</strong>.
+JUND	drug	alcohol	22020770	To our surprise, the impairment of <strong>AP 1</strong> activation was sufficient to mediate a severe and dose dependent phenotype in human monocytes in vitro at <b>alcohol</b> concentrations as low as 0.16% (or 26 mM).
+JUND	drug	alcohol	21338584	Prodynorphin promoter SNP associated with <b>alcohol</b> dependence forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+JUND	addiction	dependence	21338584	Prodynorphin promoter SNP associated with alcohol <b>dependence</b> forms noncanonical <strong>AP 1</strong> binding site that may influence gene expression in human brain.
+JUND	drug	amphetamine	20680358	Repeated administration of <b>methamphetamine</b> blocked cholecystokinin octapeptide injection induced c fos mRNA expression without change in capsaicin induced <strong>junD</strong> mRNA expression in rat cerebellum.
+JUND	drug	amphetamine	20680358	Third, capsaicin injections (physical stress) into a hind limb of the rat increased <strong>junD</strong> mRNA expression with no effect on c fos mRNA expression, and repeated <b>methamphetamine</b> injections had no effect on the capsaicin induced expression of <strong>junD</strong> mRNA.
+JUND	drug	alcohol	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after <b>ethanol</b> withdrawal.
+JUND	addiction	withdrawal	20098704	The CIE induced demethylation is characterized by being located near certain transcription factor binding sequences, <strong>AP 1</strong> and CRE, and occurred during treatment as well as after ethanol <b>withdrawal</b>.
+JUND	drug	cocaine	18991842	We found that the composition of <strong>AP 1</strong> transcription complexes and expression levels of <strong>AP 1</strong> complexes, and several transcription factors, neurotransmitter receptors as well as intracellular signaling molecules following repeated <b>cocaine</b> administration are altered in Fos deficient brains.
+JUND	drug	cocaine	18355967	These results indicate that <strong>AP 1</strong> suppresses this behavioral response to <b>cocaine</b>.
+JUND	drug	opioid	18184800	In contrast to PENK, no association was detected between PDYN genotype (68 bp repeat element containing one to four copies of <strong>AP 1</strong> binding sites in the promoter region) and <b>heroin</b> abuse, although there was a clear functional association with striatal PDYN mRNA expression: an increased number of inducible repeats (three and four) correlated with higher PDYN levels than adult or fetal subjects with noninducible (one and two) alleles.
+JUND	drug	alcohol	17851539	<b>Alcohol</b> relapse induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+JUND	addiction	relapse	17851539	Alcohol <b>relapse</b> induced by discrete cues activates components of <strong>AP 1</strong> transcription factor and ERK pathway in the rat basolateral and central amygdala.
+JUND	drug	alcohol	17127267	Recent findings indicate that low concentrations of <b>ethanol</b> (10 mM) promote inflammatory processes in brain and in glial cells by up regulating cytokines and inflammatory mediators (iNOS, NO, COX 2), and by activating signaling pathways (IKK, MAPKs) and transcriptional factors (NF kappaB, <strong>AP 1</strong>) implicated in inflammatory injury.
+JUND	drug	amphetamine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of <b>amphetamine</b> or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUND	drug	cocaine	15814102	In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or <b>cocaine</b> (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUND	addiction	addiction	15814102	In order to approach the astroglial implication of <b>addictive</b> and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or cocaine (1 100 microM) on redox status, <strong>AP 1</strong> transcription factor and pro enkephalin, an <strong>AP 1</strong> target gene, were investigated in the human astrocyte like U373 MG cells.
+JUND	addiction	dependence	15814102	Because astrocytes interact extensively with the neurons in the brain, our data led us to conclude that oxidation regulated <strong>AP 1</strong> target genes may represent one of the molecular mechanisms underlying neuronal adaptation associated with psychostimulant <b>dependence</b>.
+JUND	drug	cocaine	15770241	These results suggest that genes encoding certain extracellular factors, membrane receptors and modulators, and intracellular signaling molecules, among others, are regulated by <b>cocaine</b> via the D1 receptor, and these <strong>AP 1</strong> transcription complex regulated genes might contribute to persistent <b>cocaine</b> induced behavioral changes.
+JUND	drug	amphetamine	15680202	Ginsenosides attenuate <b>methamphetamine</b> induced behavioral side effects in mice via activation of adenosine A2A receptors: possible involvements of the striatal reduction in <strong>AP 1</strong> DNA binding activity and proenkephalin gene expression.
+JUND	drug	cocaine	15464827	<b>Cocaine</b> induced behavioral effects (hyperlocomotion and CPP) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+JUND	addiction	reward	15464827	Cocaine induced behavioral effects (hyperlocomotion and <b>CPP</b>) occurred in parallel with increases in FRA IR and <strong>AP 1</strong> DNA binding activity in the nucleus accumbens.
+JUND	drug	opioid	15287893	Activation of <strong>AP 1</strong> and CRE dependent gene expression via mu <b>opioid</b> receptor.
+JUND	drug	opioid	15287893	Transcription factors Ca2+/cAMP responsive element binding protein (CREB) and activator protein 1 (<strong>AP 1</strong>) may constitute a direct link between the <b>opioid</b> regulated signal transduction pathways and modulation of gene expression.
+JUND	drug	opioid	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during withdrawal from the <b>opioid</b>.
+JUND	addiction	withdrawal	15287893	Along with CREB, <strong>AP 1</strong> binding activity and <strong>AP 1</strong> directed transcription were stimulated after single administration and during <b>withdrawal</b> from the opioid.
+JUND	drug	alcohol	14576487	The injurious effects of <b>ethanol</b> on the pancreas may be mediated through (1) sensitization of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) sensitization of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+JUND	addiction	sensitization	14576487	The injurious effects of ethanol on the pancreas may be mediated through (1) <b>sensitization</b> of acinar cells to CCK induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF kappaB) and activating protein 1 (<strong>AP 1</strong>); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) <b>sensitization</b> of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
+JUND	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for <strong>AP 1</strong> in the NAc: the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase Cdk5, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+JUND	drug	cocaine	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying <b>cocaine</b> addiction.
+JUND	addiction	addiction	12706249	Taken together, these results provide further support for an important role of <strong>AP 1</strong> mediated transcription in some of the behavioral and molecular mechanisms underlying cocaine <b>addiction</b>.
+JUND	drug	amphetamine	12504868	In addition, DNA binding activities of NF kappaB, <strong>AP 1</strong>, and CREB in the frontal cortex and hippocampus were more pronounced in mice injected with Tat plus <b>METH</b> compared to the effects of Tat or <b>METH</b> alone.
+JUND	drug	alcohol	12482856	Up regulation of CD14 in liver caused by acute <b>ethanol</b> involves oxidant dependent <strong>AP 1</strong> pathway.
+JUND	drug	alcohol	12482856	Additionally, overexpression of SOD also blunted <b>ethanol</b> induced activation of redox sensitive transcription factors NFkappaB and <strong>AP 1</strong> and production of cytokines.
+JUND	drug	alcohol	12482856	However, only inhibition of <strong>AP 1</strong> with dominant negative TAK1 but not NFkappaB by dominant negative IkappaBalpha significantly blunted <b>ethanol</b> induced increases in CD14, suggesting that <strong>AP 1</strong> is important for CD14 transcriptional regulation.
+JUND	drug	alcohol	12045006	Chronic <b>alcohol</b> intoxication was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+JUND	addiction	intoxication	12045006	Chronic alcohol <b>intoxication</b> was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF kappaB, <strong>AP 1</strong> and MNP 1 in Kupffer Cells.
+JUND	drug	alcohol	12045006	Chronic <b>ethanol</b> feeding significantly enhanced MNP 1 binding, but not those of NF kappaB and <strong>AP 1</strong> in endothelial cells.
+JUND	drug	opioid	11605942	Mu <b>opioid</b> receptor activation induces c fos and junB expression and elevates <strong>AP 1</strong> mediated transcriptional activities via the mitogen activated protein kinase cascade.
+JUND	drug	nicotine	10555165	The influence of <b>nicotine</b> on the expression of Fos family proteins, which specifically formed complexes with the <strong>AP 1</strong> sequence, was assessed.
+JUND	drug	nicotine	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during <b>nicotine</b> dependence.
+JUND	addiction	dependence	10320004	Regulation of <strong>AP 1</strong> gene transcription factor binding activity in the rat brain during nicotine <b>dependence</b>.
+JUND	drug	nicotine	10320004	The effects of acute and chronic <b>nicotine</b> treatment on activator protein 1 (<strong>AP 1</strong>) gene transcription factor binding activity in the rat cortex were investigated.
+JUND	drug	nicotine	10320004	It was observed that 1 h after acute <b>nicotine</b> treatment (single injection) <strong>AP 1</strong> DNA binding activity was significantly increased in the rat cortex.
+JUND	drug	nicotine	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of <b>nicotine</b> withdrawal after repeated <b>nicotine</b> treatment (10 days).
+JUND	addiction	withdrawal	10320004	On the other hand, <strong>AP 1</strong> DNA binding activity in the rat cortex was not altered at 1 and 8 h of nicotine <b>withdrawal</b> after repeated nicotine treatment (10 days).
+JUND	drug	nicotine	10320004	However, at 18 and 24 h of <b>nicotine</b> withdrawal after 10 days of <b>nicotine</b> treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+JUND	addiction	withdrawal	10320004	However, at 18 and 24 h of nicotine <b>withdrawal</b> after 10 days of nicotine treatment, <strong>AP 1</strong> DNA binding activity was significantly decreased in the rat cortex.
+JUND	drug	nicotine	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to <b>nicotine</b> dependence.
+JUND	addiction	dependence	10320004	Thus, these findings suggest that desensitization of cortical <strong>AP 1</strong> DNA binding activity may be involved in the neuroadaptational mechanisms to nicotine <b>dependence</b>.
+JUND	drug	amphetamine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered Fos like proteins in brain by chronic cocaine and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on <b>methamphetamine</b> induced stereotypy in mice, Jpn.
+JUND	drug	cocaine	10234448	Nestler, Induction of a long lasting <strong>AP 1</strong> complex composed of altered Fos like proteins in brain by chronic <b>cocaine</b> and other chronic treatments, Neuron 13 (1994) 1235 1244 [10]; T. Miyauchi, K. Kikuchi, S. Satoh, Further studies on the potentiating effect of lithium chloride on methamphetamine induced stereotypy in mice, Jpn.
+JUND	drug	alcohol	9918601	This investigation examined the effects of acute and chronic <b>ethanol</b> exposure and its withdrawal on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+JUND	addiction	withdrawal	9918601	This investigation examined the effects of acute and chronic ethanol exposure and its <b>withdrawal</b> on the cAMP responsive element binding protein (CREB) and the activator protein 1 (<strong>AP 1</strong>) gene transcription factors in the rat brain.
+JUND	drug	alcohol	9918601	It was observed that acute <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+JUND	addiction	withdrawal	9918601	It was observed that acute ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on CRE  or <strong>AP 1</strong> DNA binding activities in the rat cortex as determined by the electrophoretic gel mobility shift assay.
+JUND	drug	alcohol	9918601	It was also found that chronic <b>ethanol</b> treatment and its withdrawal (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+JUND	addiction	withdrawal	9918601	It was also found that chronic ethanol treatment and its <b>withdrawal</b> (24 h) had no effect on <strong>AP 1</strong> DNA binding activity in the rat cortex.
+JUND	drug	cocaine	9668659	<b>Cocaine</b> and the <strong>AP 1</strong> transcription factor complex.
+JUND	drug	cocaine	9668659	We presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain
+JUND	drug	cocaine	29090793	<b>Cocaine</b> and the <strong>AP 1</strong> Transcription Factor Complex.
+JUND	drug	cocaine	29090793	We are presently purifying the chronic Fras to obtain amino acid sequence in order to directly examine our hypothesis about the effects of repeated <b>cocaine</b> administration on <strong>AP 1</strong> dependent transcription and gene expression in the brain.
+JUND	drug	alcohol	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during <b>ethanol</b> withdrawal.
+JUND	addiction	withdrawal	9202324	<strong>AP 1</strong> and Egr DNA binding activities are increased in rat brain during ethanol <b>withdrawal</b>.
+JUND	drug	alcohol	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during <b>ethanol</b> withdrawal.
+JUND	addiction	withdrawal	9202324	The DNA binding activities of <strong>AP 1</strong> and Egr proteins were investigated in nuclear extracts of rat brain regions during ethanol <b>withdrawal</b>.
+JUND	addiction	withdrawal	9202324	The AP 1 DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of FosB, c Jun, JunB, and <strong>JunD</strong>.
+JUND	addiction	withdrawal	9202324	The <strong>AP 1</strong> DNA binding activities in all regions at all times after <b>withdrawal</b> were composed of FosB, c Jun, JunB, and <strong>JunD</strong>.
+JUND	addiction	withdrawal	9202324	<b>Withdrawal</b> severity did not affect the composition of the <strong>AP 1</strong> DNA binding activities.
+JUND	drug	amphetamine	9070635	Thus, <b>amphetamine</b> sensitization is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+JUND	addiction	sensitization	9070635	Thus, amphetamine <b>sensitization</b> is accompanied by alterations in the composition of the <strong>AP 1</strong> DNA binding complex.
+JUND	drug	cocaine	8959019	However, the induction of the chronic <strong>AP 1</strong> complex and the chronic Fras provides a mechanism capable of underlying long lasting alterations in gene expression following chronic <b>cocaine</b> treatment.
+JUND	drug	opioid	8843097	A mu receptor <b>opioid</b> agonist induces <strong>AP 1</strong> and NF kappa B transcription factor activity in primary cultures of rat cortical neurons.
+JUND	drug	opioid	8843097	The specific mu receptor <b>opioid</b> agonist, Tyr, D Ala2, Gly, N Me Phe4, Gly ol5 (DAMGO), was found to increase <strong>AP 1</strong> and NF kappa B activity in primary cultures of neurons from rat cerebral cortex.
+JUND	drug	opioid	8843097	Acute (2 h, 4 h) and long term (72 h) treatment with DAMGO time dependently increased the DNA binding activity of both <strong>AP 1</strong> and NF kappa B and the stimulation could be abolished or inhibited by concurrent incubation with <b>naloxone</b>.
+JUND	drug	opioid	8843097	However, acute <b>naloxone</b> precipitated withdrawal did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+JUND	addiction	withdrawal	8843097	However, acute naloxone precipitated <b>withdrawal</b> did not significantly change <strong>AP 1</strong> or NF kappa B activity.
+JUND	drug	opioid	8843097	These results indicate a mu <b>opioid</b> receptor related co induction of <strong>AP 1</strong> and NF kappa B transcription factors in cultured cortical neurons.
+JUND	drug	opioid	8609891	After 5 days of <b>morphine</b> treatment, we observed increased levels of the chronic Fras and of <strong>AP 1</strong> binding activity in rat striatum and nucleus accumbens, effects that were not seen in most other brain regions that we studied.
+JUND	drug	opioid	7838131	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal, a model of <b>opioid</b> dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUND	addiction	dependence	7838131	Naloxone precipitated morphine withdrawal, a model of opioid <b>dependence</b>, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUND	addiction	withdrawal	7838131	Naloxone precipitated morphine <b>withdrawal</b>, a model of opioid dependence, induces brain region specific changes in activator protein 1 (<strong>AP 1</strong>) transcription factor gene expression.
+JUND	addiction	withdrawal	7838131	<strong>AP 1</strong> DNA binding activity and dimer composition also exhibited regulation after <b>withdrawal</b>, presumably as a result of both transcriptional and post translational events.
+JUND	drug	opioid	7838131	Thus, <b>morphine</b> dependence results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+JUND	addiction	dependence	7838131	Thus, morphine <b>dependence</b> results in the alteration of diverse, brain region specific, signal transcription pathways involving <strong>AP 1</strong> transcription factors.
+JUND	drug	cocaine	7969045	One early cellular response to <b>cocaine</b> administration is a brain region specific alteration in the transcriptional pattern of immediate early genes belonging to the Fos/Jun family of nucleotide sequence specific [activator protein 1 (<strong>AP 1</strong>)] DNA binding proteins.
+JUND	drug	cocaine	7969045	The work described here compares <b>cocaine</b> induced transcriptional regulation of immediate early gene mRNA levels, as well as <strong>AP 1</strong> DNA binding activity, within the striatum and cerebellum.
+JUND	drug	cocaine	7969045	Gel retention analysis using antibodies to the various Fos and Jun proteins was used to characterize <b>cocaine</b> dependent alterations in the composition of striatal and cerebellar <strong>AP 1</strong> DNA binding complexes.
+JUND	drug	cocaine	7969045	In striatum, <b>cocaine</b> increases the relative levels of c Fos, Fos B, Jun B, and Jun D proteins that bind the <strong>AP 1</strong> DNA sequence element, whereas in the cerebellum only c Fos and Jun D binding activities are increased.
+JUND	drug	opioid	8078918	SCH23390 attenuated <b>morphine</b> induction of <strong>AP 1</strong> binding in striatum, suggesting that c fos and junB contribute to <strong>AP 1</strong> binding.
+JUND	drug	amphetamine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with <b>methamphetamine</b>, cocaine and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of <b>methamphetamine</b> and cocaine, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+JUND	drug	cocaine	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, <b>cocaine</b> and morphine: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and <b>cocaine</b>, 2) CRE binding activity was decreased by chronic morphine treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic morphine treatment in the mouse cerebellum.
+JUND	drug	opioid	7975924	Our studies showed that the binding activity of nuclear factors to several DNA sequences is altered by long term treatment with methamphetamine, cocaine and <b>morphine</b>: 1) the binding activity of <strong>AP 1</strong> increased markedly in the mouse brain after administration of methamphetamine and cocaine, 2) CRE binding activity was decreased by chronic <b>morphine</b> treatment in the amygdala complex, cerebral cortex and hypothalamus of the mouse brain, and 3) the binding activity of single stranded CRE binding proteins was decreased by chronic <b>morphine</b> treatment in the mouse cerebellum.
+JUND	drug	alcohol	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during <b>ethanol</b> withdrawal.
+JUND	addiction	withdrawal	8974340	Elevated <strong>AP 1</strong> DNA binding activity in rat brain during ethanol <b>withdrawal</b>.
+JUND	drug	alcohol	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing <b>ethanol</b> withdrawal.
+JUND	addiction	withdrawal	8974340	The DNA binding activity of the transcription factors <strong>AP 1</strong>, CREB and OCT was investigated in nuclear extracts of brains from rats undergoing ethanol <b>withdrawal</b>.
+JUND	drug	alcohol	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>ethanol</b> withdrawal.
+JUND	addiction	withdrawal	8974340	<strong>AP 1</strong> DNA binding activity but not that of CREB or OCT was increased in the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after ethanol <b>withdrawal</b>.
+JUND	drug	alcohol	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of <b>ethanol</b> withdrawal.
+JUND	addiction	withdrawal	8974340	A similar increase in <strong>AP 1</strong> binding activity was observed in subcortical structures at 17 hr of ethanol <b>withdrawal</b>.
+JUND	addiction	withdrawal	8974322	Gel shift assays indicated the formation of <strong>AP 1</strong> binding factors in nuclear extracts of the cerebral cortex, hippocampus and cerebellum 15 and 17 hr after <b>withdrawal</b>.
+JUND	drug	cocaine	1631058	Regulation of immediate early gene expression and <strong>AP 1</strong> binding in the rat nucleus accumbens by chronic <b>cocaine</b>.
+JUND	drug	cocaine	1631058	As would be expected from the RNA data and immunohistochemistry, acute <b>cocaine</b> administration increased <strong>AP 1</strong> binding activity in the NAc, an effect that reverted completely to control levels within 8 12 hr.
+JUND	drug	cocaine	1631058	In contrast, <strong>AP 1</strong> binding activity in the NAc of animals treated chronically with <b>cocaine</b> remained elevated at acute levels 18 hr after the last chronic injection, a time at which c fos and c jun mRNA levels and Fos like immunoreactivity had returned to control values.
+JUND	drug	cocaine	1631058	An additional acute <b>cocaine</b> challenge did not further increase <strong>AP 1</strong> binding.
+JUND	drug	cocaine	1631058	The data suggest that chronic <b>cocaine</b> treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of <b>cocaine</b> addiction.
+JUND	addiction	addiction	1631058	The data suggest that chronic cocaine treatment leads to a persistent increase in <strong>AP 1</strong> binding activity, which may be involved in some of the physiological and behavioral aspects of cocaine <b>addiction</b>.
+CCKBR	drug	opioid	30147637	Therefore, CCK1R and <strong>CCK2R</strong> function differently in chronic <b>morphine</b> dependence, but the mechanism is still unclear.
+CCKBR	addiction	dependence	30147637	Therefore, CCK1R and <strong>CCK2R</strong> function differently in chronic morphine <b>dependence</b>, but the mechanism is still unclear.
+CCKBR	drug	opioid	30147637	In this study, HEK 293 cells co transfected with µ <b>opioid</b> receptors (HEK293 hMOR) and CCK1R or <strong>CCK2R</strong> were established.
+CCKBR	drug	opioid	30147637	While over expression of <strong>CCK2R</strong> promoted <b>morphine</b> dependence, which was related with phosphorylation of CREB but not ERK1/2 signaling activation.
+CCKBR	addiction	dependence	30147637	While over expression of <strong>CCK2R</strong> promoted morphine <b>dependence</b>, which was related with phosphorylation of CREB but not ERK1/2 signaling activation.
+CCKBR	drug	cocaine	29923314	A <strong>cholecystokinin B receptor</strong> antagonist and <b>cocaine</b> interaction, phase I study.
+CCKBR	drug	opioid	19944533	In the same animals we show that spinal blockade of CCK A receptors prevents cross tolerance at spinal delta <b>opioid</b> receptors that normally occurs with high frequency TENS; and blockade of <strong>CCK B</strong> receptors prevents cross tolerance at spinal mu <b>opioid</b> receptors that normally occurs with low frequency TENS.
+CCKBR	drug	cocaine	12393241	), 30 min before <b>cocaine</b> priming, significantly attenuated <b>cocaine</b> induced reinstatement of CPP, while <strong>CCK B</strong> receptor antagonist, L365,260 (0.1 and 1 mg/kg, i.p.
+CCKBR	addiction	relapse	12393241	), 30 min before cocaine priming, significantly attenuated cocaine induced <b>reinstatement</b> of CPP, while <strong>CCK B</strong> receptor antagonist, L365,260 (0.1 and 1 mg/kg, i.p.
+CCKBR	addiction	reward	12393241	), 30 min before cocaine priming, significantly attenuated cocaine induced reinstatement of <b>CPP</b>, while <strong>CCK B</strong> receptor antagonist, L365,260 (0.1 and 1 mg/kg, i.p.
+CCKBR	addiction	relapse	12393241	<strong>CCK B</strong> receptor antagonists might be of some value in the treatment and prevention of <b>relapse</b> to stress induced to drug <b>craving</b> following long term detoxification.
+CCKBR	drug	alcohol	12198366	We previously reported genetic variations in the promoter and coding regions of the CCKA receptor (CCKAR), <strong>CCKBR</strong>, and CCK genes and a possible association between polymorphisms of the CCKAR gene and <b>alcoholism</b>.
+CCKBR	drug	benzodiazepine	11812248	It explores the risk benefit profiles of putative therapies for BZ withdrawal, including drugs acting via <b>benzodiazepine</b> receptors, serotonergic and noradrenergic agents, <strong>cholecystokinin B receptor</strong> antagonists, calcium channel blockers, N methyl D aspartate (NMDA) antagonists, and other miscellaneous agents.
+CCKBR	addiction	withdrawal	11812248	It explores the risk benefit profiles of putative therapies for BZ <b>withdrawal</b>, including drugs acting via benzodiazepine receptors, serotonergic and noradrenergic agents, <strong>cholecystokinin B receptor</strong> antagonists, calcium channel blockers, N methyl D aspartate (NMDA) antagonists, and other miscellaneous agents.
+CCKBR	drug	alcohol	11513220	Polymorphisms of the CCK, CCKAR and <strong>CCKBR</strong> genes: an association with <b>alcoholism</b> study.
+CCKBR	drug	alcohol	11513220	We analyzed genetic variations in the promoter and coding regions of the CCK, CCKA receptor (CCKAR) and CCKB receptor (<strong>CCKBR</strong>) genes, and performed association analyses with <b>alcoholism</b>.
+CCKBR	drug	alcohol	11513220	We analyzed genetic variations in the promoter and coding regions of the CCK, CCKA receptor (CCKAR) and <strong>CCKB</strong> receptor (<strong>CCKBR</strong>) genes, and performed association analyses with <b>alcoholism</b>.
+CCKBR	drug	alcohol	11513220	Our data suggest that polymorphisms of the CCK, CCKAR and <strong>CCKBR</strong> genes do not play a major role in <b>alcohol</b> withdrawal symptoms (even though significant associations were found among polymorphisms at the  388 and  333 loci of the CCKAR gene and hallucinations, the rate was nonsignificant after Bonferroni correction).
+CCKBR	addiction	withdrawal	11513220	Our data suggest that polymorphisms of the CCK, CCKAR and <strong>CCKBR</strong> genes do not play a major role in alcohol <b>withdrawal</b> symptoms (even though significant associations were found among polymorphisms at the  388 and  333 loci of the CCKAR gene and hallucinations, the rate was nonsignificant after Bonferroni correction).
+CCKBR	drug	benzodiazepine	11420071	To further examine the relationship between cholecystokinin (CCK) and GABA, the present study assessed the ability of the CCK A antagonist devazepide and the <strong>CCK B</strong> antagonist L 365,260 to substitute for the stimulus effects of <b>chlordiazepoxide</b> (CDP), as well as the ability of CCK 8s to block these effects, in female Long Evans rats within the conditioned taste aversion baseline of drug discrimination learning.
+CCKBR	addiction	aversion	11420071	To further examine the relationship between cholecystokinin (CCK) and GABA, the present study assessed the ability of the CCK A antagonist devazepide and the <strong>CCK B</strong> antagonist L 365,260 to substitute for the stimulus effects of chlordiazepoxide (CDP), as well as the ability of CCK 8s to block these effects, in female Long Evans rats within the conditioned taste <b>aversion</b> baseline of drug discrimination learning.
+CCKBR	drug	alcohol	11368834	The results suggest that CCK  45C>T and <strong>CCKBR</strong> Val125Ile polymorphisms do not have a major role in <b>alcohol</b> dependence in the population studied.
+CCKBR	addiction	dependence	11368834	The results suggest that CCK  45C>T and <strong>CCKBR</strong> Val125Ile polymorphisms do not have a major role in alcohol <b>dependence</b> in the population studied.
+CCKBR	drug	opioid	11173090	Different role of cholecystokinin (CCK) A and <strong>CCK B</strong> receptors in relapse to <b>morphine</b> dependence in rats.
+CCKBR	addiction	dependence	11173090	Different role of cholecystokinin (CCK) A and <strong>CCK B</strong> receptors in relapse to morphine <b>dependence</b> in rats.
+CCKBR	addiction	relapse	11173090	Different role of cholecystokinin (CCK) A and <strong>CCK B</strong> receptors in <b>relapse</b> to morphine dependence in rats.
+CCKBR	drug	opioid	11173090	The present study demonstrated that <strong>CCK B</strong> receptor but not CCK A receptor is involved in the maintenance and reactivation of <b>morphine</b> CPP.
+CCKBR	addiction	reward	11173090	The present study demonstrated that <strong>CCK B</strong> receptor but not CCK A receptor is involved in the maintenance and reactivation of morphine <b>CPP</b>.
+CCKBR	addiction	dependence	11173090	These findings suggest that <strong>CCK B</strong> receptor antagonists might be of some value in the treatment and prevention of relapse to drug <b>dependence</b> long after detoxification.
+CCKBR	addiction	relapse	11173090	These findings suggest that <strong>CCK B</strong> receptor antagonists might be of some value in the treatment and prevention of <b>relapse</b> to drug dependence long after detoxification.
+CCKBR	drug	opioid	10757528	<strong>Cholecystokinin B receptor</strong> antagonists attenuate <b>morphine</b> dependence and withdrawal in rats.
+CCKBR	addiction	dependence	10757528	<strong>Cholecystokinin B receptor</strong> antagonists attenuate morphine <b>dependence</b> and withdrawal in rats.
+CCKBR	addiction	withdrawal	10757528	<strong>Cholecystokinin B receptor</strong> antagonists attenuate morphine dependence and <b>withdrawal</b> in rats.
+CCKBR	addiction	dependence	10757528	The present study demonstrated CCK, acting on <strong>CCK B</strong> receptors, participates in the development of the opiate <b>dependence</b>.
+CCKBR	addiction	relapse	10757528	These findings suggest that <strong>CCK B</strong> receptor antagonists might be of some value in the treatment and prevention the <b>relapse</b> of opiate addicts.
+CCKBR	drug	amphetamine	10639694	Self administration of intravenous <b>amphetamine</b>: effect of nucleus accumbens <strong>CCKB</strong> receptor activation on fixed ratio responding.
+CCKBR	drug	amphetamine	10639694	The present experiment was designed to examine the effects of intra NAcc <strong>CCKB</strong> receptor stimulation on fixed ratio (FR) <b>amphetamine</b> self administration.
+CCKBR	drug	amphetamine	10639694	These results are consistent with the notion that NAcc <strong>CCKB</strong> receptor activation attenuates <b>amphetamine</b> reward.
+CCKBR	addiction	reward	10639694	These results are consistent with the notion that NAcc <strong>CCKB</strong> receptor activation attenuates amphetamine <b>reward</b>.
+CCKBR	drug	opioid	10319787	<strong>Cholecystokinin B receptor</strong> activation has been reported to reduce <b>morphine</b> analgesia.
+CCKBR	drug	opioid	10319787	The authors evaluated the role of the spinal <strong>cholecystokinin B receptor</strong> on <b>morphine</b> analgesia in two rat neuropathic pain models: chronic constriction injury and partial sciatic nerve injury.
+CCKBR	drug	opioid	10319787	PD135158, a <strong>cholecystokinin B receptor</strong> antagonist, potentiated the analgesic effect of <b>morphine</b> on injured and uninjured paws.
+CCKBR	drug	opioid	10319787	The role of the <strong>cholecystokinin B receptor</strong> in <b>morphine</b> analgesia in thermal hyperalgesia after nerve injury also depends on the type of nerve injury.
+CCKBR	drug	alcohol	9922984	The role of cholecystokinin (CCK), CCK A or <strong>CCK B</strong> receptor antagonists in the spontaneous preference for drugs of abuse (<b>alcohol</b> or cocaine) in naive rats.
+CCKBR	drug	cocaine	9922984	The role of cholecystokinin (CCK), CCK A or <strong>CCK B</strong> receptor antagonists in the spontaneous preference for drugs of abuse (alcohol or <b>cocaine</b>) in naive rats.
+CCKBR	drug	alcohol	9922984	In particular, the data imply a CCK A receptor mechanism in the regulation of individual sensitivity towards <b>ethanol</b> and a <strong>CCK B</strong> receptor mechanism in the regulation of individual sensitivity towards cocaine.
+CCKBR	drug	cocaine	9922984	In particular, the data imply a CCK A receptor mechanism in the regulation of individual sensitivity towards ethanol and a <strong>CCK B</strong> receptor mechanism in the regulation of individual sensitivity towards <b>cocaine</b>.
+CCKBR	drug	alcohol	9922984	Thus, a potential therapeutic role for CCK A antagonists in the treatment of <b>ethanol</b> abuse and for <strong>CCK B</strong> antagonists in the treatment of cocaine abuse is proposed.
+CCKBR	drug	cocaine	9922984	Thus, a potential therapeutic role for CCK A antagonists in the treatment of ethanol abuse and for <strong>CCK B</strong> antagonists in the treatment of <b>cocaine</b> abuse is proposed.
+CCKBR	drug	benzodiazepine	9832933	The effects of CR 2945, an antranilic acid derivative member of a novel family of non peptide <strong>CCKB</strong> receptor antagonists, have been compared with those of CAM 1028, an analogue of the <strong>CCKB</strong> receptor antagonist CI 988, L 365,260 a <b>benzodiazepine</b> derivative <strong>CCKB</strong> antagonist, CR 1795, an analogue of the CCKA receptor antagonist lorglumide and <b>diazepam</b>, a <b>benzodiazepine</b> receptor agonist, in several rodent screens sensitive to conventional anxiolytics.
+CCKBR	drug	opioid	9578139	Several cholecystokinin ligands were chronically administered during the development of <b>morphine</b> dependence: the CCKA antagonist devazepide, the <strong>CCKB</strong> antagonists PD 134,308 and L 365,260, and the <strong>CCKB</strong> agonist BC 264.
+CCKBR	addiction	dependence	9578139	Several cholecystokinin ligands were chronically administered during the development of morphine <b>dependence</b>: the CCKA antagonist devazepide, the <strong>CCKB</strong> antagonists PD 134,308 and L 365,260, and the <strong>CCKB</strong> agonist BC 264.
+CCKBR	drug	opioid	9578139	The <strong>CCK B</strong> antagonists L 365,260 and PD 134,308 decreased and completely blocked (respectively) the place aversion induced by <b>naloxone</b> in <b>morphine</b> dependent animals whereas BC 264 and devazepide were inactive in this model.
+CCKBR	addiction	aversion	9578139	The <strong>CCK B</strong> antagonists L 365,260 and PD 134,308 decreased and completely blocked (respectively) the place <b>aversion</b> induced by naloxone in morphine dependent animals whereas BC 264 and devazepide were inactive in this model.
+CCKBR	addiction	withdrawal	9489608	When the <strong>CCKB</strong> antagonist, CI988, was added to the bathing medium, at 1 microM, there were small, but significant decreases in the <b>withdrawal</b> hyperexcitability.
+CCKBR	addiction	dependence	9276016	Binding affinity for the CCK A vs <strong>CCK B</strong> receptor showed little <b>dependence</b> on the structure of the C3 moiety but was affected by the nature of the second substituent at C3.
+CCKBR	drug	opioid	9181639	The attenuation of <b>morphine</b> conditioned place preference following chronic mild stress is reversed by a <strong>CCKB</strong> receptor antagonist.
+CCKBR	drug	opioid	9181639	When the <strong>CCKB</strong> receptor antagonist PD 134,308 was co administered with <b>morphine</b> in stressed animals during the conditioning period, the preference for the <b>morphine</b> paired compartment was also re established.
+CCKBR	drug	opioid	8947930	Association of enkephalin catabolism inhibitors and <strong>CCK B</strong> antagonists: a potential use in the management of pain and <b>opioid</b> addiction.
+CCKBR	addiction	addiction	8947930	Association of enkephalin catabolism inhibitors and <strong>CCK B</strong> antagonists: a potential use in the management of pain and opioid <b>addiction</b>.
+CCKBR	drug	opioid	8947930	The overlapping distribution of <b>opioid</b> and cholecystokinin (CCK) peptides and their receptors (mu and delta <b>opioid</b> receptors; CCK A and <strong>CCK B</strong> receptors) in the central nervous system have led to a large number of studies aimed at clarifying the functional relationships between these two neuropeptides.
+CCKBR	drug	opioid	8947930	Recently the existence of regulatory mechanisms between both systems have been proposed, and the physiological antagonism between CCK and endogenous <b>opioid</b> systems has been definitely demonstrated by coadministration of <strong>CCK B</strong> selective antagonists with RB 101, a systemically active inhibitor, which fully protects enkephalins from their degradation.
+CCKBR	drug	opioid	8947930	This article will review the experimental pharmacology of association of enkephalin degrading enzyme inhibitors and <strong>CCK B</strong> antagonists to demonstrate the interest of these molecules in the management of both pain and <b>opioid</b> addiction.
+CCKBR	addiction	addiction	8947930	This article will review the experimental pharmacology of association of enkephalin degrading enzyme inhibitors and <strong>CCK B</strong> antagonists to demonstrate the interest of these molecules in the management of both pain and opioid <b>addiction</b>.
+CCKBR	drug	opioid	8872371	In this study we have investigated the effects induced by RB 101 given alone, or with the <strong>CCKB</strong> antagonist, PD 134,308, on a model of spontaneous <b>morphine</b> withdrawal and substitutive maintenance in rats.
+CCKBR	addiction	withdrawal	8872371	In this study we have investigated the effects induced by RB 101 given alone, or with the <strong>CCKB</strong> antagonist, PD 134,308, on a model of spontaneous morphine <b>withdrawal</b> and substitutive maintenance in rats.
+CCKBR	drug	opioid	8836616	It is argued that the effect of PD 142898 in the conditioned place preference test involves antagonism of CCKA receptors, whilst the potentiation of the antinociceptive action of <b>morphine</b> is mediated via blockade of <strong>CCKB</strong> receptors.
+CCKBR	drug	opioid	8818359	The ability of a selective CCKA receptor antagonist PD 140548 and a selective <strong>CCKB</strong> receptor antagonist CI 988 (formerly PD 134308) to modulate the various in vivo properties of <b>morphine</b> was investigated in the rat.
+CCKBR	drug	opioid	8818359	In conclusion, the results of the present study indicate that CCKA and <strong>CCKB</strong> receptors modulate different properties of <b>morphine</b>.
+CCKBR	drug	opioid	8818359	Thus, whilst a selective CCKA receptor antagonist blocked the rewarding properties of <b>morphine</b>, a selective <strong>CCKB</strong> receptor antagonist potentiated the antinociceptive action.
+CCKBR	addiction	reward	8761988	The present experiment examines whether the blockade of <strong>CCKB</strong> receptors in the NAC with microinjection of PD 135158 (10 micrograms in 0.5 microliter) potentiates bar pressing for stimuli previously associated with food <b>reward</b>.
+CCKBR	addiction	reward	8761988	These findings suggest that endogenous <strong>CCKB</strong> mechanisms in the NAC may normally inhibit dopamine function in <b>reward</b> related behaviors.
+CCKBR	drug	nicotine	8804049	The <strong>CCK B</strong> antagonist LY288513 blocks the effects of <b>nicotine</b> withdrawal on auditory startle.
+CCKBR	addiction	withdrawal	8804049	The <strong>CCK B</strong> antagonist LY288513 blocks the effects of nicotine <b>withdrawal</b> on auditory startle.
+CCKBR	drug	nicotine	8804049	In order to explore the potential clinical utility of <strong>CCK B</strong> antagonists for the treatment of <b>nicotine</b> withdrawal symptoms, the auditory startle reflex was examined in rats undergoing withdrawal from the chronic administration of <b>nicotine</b>.
+CCKBR	addiction	withdrawal	8804049	In order to explore the potential clinical utility of <strong>CCK B</strong> antagonists for the treatment of nicotine <b>withdrawal</b> symptoms, the auditory startle reflex was examined in rats undergoing <b>withdrawal</b> from the chronic administration of nicotine.
+CCKBR	drug	nicotine	8804049	Acute treatment with the <strong>CCK B</strong> antagonist LY288513, at doses that have no effect on startle responses in naive rats, blocked the <b>nicotine</b> withdrawal induced increase in the acoustic startle reflex.
+CCKBR	addiction	withdrawal	8804049	Acute treatment with the <strong>CCK B</strong> antagonist LY288513, at doses that have no effect on startle responses in naive rats, blocked the nicotine <b>withdrawal</b> induced increase in the acoustic startle reflex.
+CCKBR	drug	nicotine	8804049	These results indicate that <strong>CCK B</strong> antagonists may be an efficacious treatment for some <b>nicotine</b> withdrawal symptoms in man and may represent a novel pharmacotherapy for <b>smoking</b> cessation.
+CCKBR	addiction	withdrawal	8804049	These results indicate that <strong>CCK B</strong> antagonists may be an efficacious treatment for some nicotine <b>withdrawal</b> symptoms in man and may represent a novel pharmacotherapy for smoking cessation.
+CCKBR	addiction	reward	8741936	In contrast, experiment 2 showed that the development of conditioned <b>reward</b> was not affected by similar administration of the <strong>CCKB</strong> selective antagonist, L 365,260 (0, 0.001, 0.01, or 0.1 mg/kg).
+CCKBR	addiction	aversion	8741934	Pretreatment with the <strong>CCKB</strong> antagonist PD 134,308 (0.1, 0.3, 1 and 3 mg/kg, IP) alone failed to produce a reliable <b>aversion</b> or preference on the paradigm studied.
+CCKBR	drug	opioid	8741934	When PD 134,308 (0.3 mg/kg, IP) was coadministered with a subthreshold dose of <b>morphine</b> (0.6 mg/kg, SC) or RB 101 (5 mg/kg, IP), a conditioned place preference was observed, indicating that the <strong>CCKB</strong> antagonist facilitated the motivational responses induced by endogenous enkephalins as compared to <b>morphine</b>.
+CCKBR	addiction	aversion	8735976	Several roles of CCKA and <strong>CCKB</strong> receptor subtypes in CCK 8 induced and LiCl induced taste <b>aversion</b> conditioning.
+CCKBR	drug	benzodiazepine	8735976	Because the CCK antagonists affected TAC like <b>chlordiazepoxide</b>, blockade of CCKA and <strong>CCKB</strong> mechanisms may produce a mild anxiolytic effect.
+CCKBR	drug	opioid	7780637	Inhibition of <b>morphine</b> withdrawal by the association of RB 101, an inhibitor of enkephalin catabolism, and the <strong>CCKB</strong> antagonist PD 134,308.
+CCKBR	addiction	withdrawal	7780637	Inhibition of morphine <b>withdrawal</b> by the association of RB 101, an inhibitor of enkephalin catabolism, and the <strong>CCKB</strong> antagonist PD 134,308.
+CCKBR	drug	opioid	7780637	The effects induced in rats on <b>naloxone</b> precipitated <b>morphine</b> withdrawal syndrome by the new mixed inhibitor of enkephalin catabolism able to cross the blood brain barrier RB 101 (N ((R,S) 2 benzyl 3[(S)(2 amino 4 methylthio)butyl dithio] 1 ox opropyl L phenylalanine benzyl ester) given alone or associated with the selective <strong>CCKB</strong> antagonist, PD 134,308, were investigated.
+CCKBR	addiction	withdrawal	7780637	The effects induced in rats on naloxone precipitated morphine <b>withdrawal</b> syndrome by the new mixed inhibitor of enkephalin catabolism able to cross the blood brain barrier RB 101 (N ((R,S) 2 benzyl 3[(S)(2 amino 4 methylthio)butyl dithio] 1 ox opropyl L phenylalanine benzyl ester) given alone or associated with the selective <strong>CCKB</strong> antagonist, PD 134,308, were investigated.
+CCKBR	addiction	withdrawal	7780637	<strong>CCKB</strong> antagonists, such as PD 134,308 may be useful in potentiating this anti <b>withdrawal</b> effect.
+CCKBR	drug	benzodiazepine	7597123	Effects of the <strong>CCKB</strong> antagonist L 365, 260 on <b>benzodiazepine</b> withdrawal induced hypophagia in rats.
+CCKBR	addiction	withdrawal	7597123	Effects of the <strong>CCKB</strong> antagonist L 365, 260 on benzodiazepine <b>withdrawal</b> induced hypophagia in rats.
+CCKBR	drug	benzodiazepine	7597123	The effect of the selective <strong>CCKB</strong> antagonist L 365, 260 on <b>chlordiazepoxide</b> (CDP) withdrawal induced hypophagia was assessed in two related studies in rats pretreated for 21 days with CDP at doses escalated from 10 to 30 mg/kg per day (b.i.d).
+CCKBR	addiction	withdrawal	7597123	The effect of the selective <strong>CCKB</strong> antagonist L 365, 260 on chlordiazepoxide (CDP) <b>withdrawal</b> induced hypophagia was assessed in two related studies in rats pretreated for 21 days with CDP at doses escalated from 10 to 30 mg/kg per day (b.i.d).
+CCKBR	drug	benzodiazepine	7597123	These data contrast with reports that <strong>CCKB</strong> antagonists alleviate behavioural <b>benzodiazepine</b> (BZ) withdrawal symptoms considered to be indicative of "anxiogenesis".
+CCKBR	addiction	withdrawal	7597123	These data contrast with reports that <strong>CCKB</strong> antagonists alleviate behavioural benzodiazepine (BZ) <b>withdrawal</b> symptoms considered to be indicative of "anxiogenesis".
+CCKBR	addiction	withdrawal	7597123	Presumably, such positive effects of <strong>CCKB</strong> antagonists are due to "functional antagonism", with enhanced anxiety during BZ <b>withdrawal</b> being attenuated by anxiolytic actions of <strong>CCKB</strong> antagonists.
+CCKBR	addiction	withdrawal	7597123	Collectively, studies with <strong>CCKB</strong> antagonists and other agents involving a number of different BZ <b>withdrawal</b> signs suggest that BZ <b>withdrawal</b> is a heterogeneous syndrome, with various different underlying mechanisms.
+CCKBR	addiction	withdrawal	7597123	<strong>CCKB</strong> antagonists appear to alleviate only a subset of possible BZ <b>withdrawal</b> signs.
+CCKBR	drug	opioid	8742781	The <strong>CCKB</strong> receptor antagonist enhances <b>morphine</b> analgesia and blocks tolerance to <b>morphine</b> but has no effect on the development of dependence on <b>morphine</b>.
+CCKBR	addiction	dependence	8742781	The <strong>CCKB</strong> receptor antagonist enhances morphine analgesia and blocks tolerance to morphine but has no effect on the development of <b>dependence</b> on morphine.
+CCKBR	drug	opioid	8617406	For example, CCK appears to exert its anti <b>opioid</b> actions mainly through the activation of <strong>CCK B</strong> receptors, whereas its <b>opioid</b> like effects seem to result from the stimulation of CCK A receptors.
+CCKBR	drug	amphetamine	7479342	Interaction of <strong>CCKB</strong> receptors with <b>amphetamine</b> in responding for conditioned rewards.
+CCKBR	addiction	reward	7479342	The present experiment tested the whether blockade of endogenous <strong>CCKB</strong> receptors with L 365,260 (0.1 mg/kg, IP) potentiates bar pressing for stimuli previously associated with food <b>reward</b>.
+CCKBR	addiction	reward	7479342	These findings suggest that endogenous <strong>CCKB</strong> mechanisms may normally inhibit DA function in <b>reward</b> related behaviors.
+CCKBR	drug	opioid	8090802	Effects induced by BC 264, a selective agonist of <strong>CCK B</strong> receptors, on <b>morphine</b> dependent rats.
+CCKBR	drug	opioid	8090802	Rats were made dependent to <b>morphine</b> and the ability of cholecystokinin octapeptide (CCK 8) and Tyr(SO3H) gNle mGly Trp (NMe)Nle Asp Phe NH2 (BC 264), a selective agonist of <strong>CCK B</strong> receptors, to induce signs of <b>morphine</b> withdrawal after ICV injection was tested.
+CCKBR	addiction	withdrawal	8090802	Rats were made dependent to morphine and the ability of cholecystokinin octapeptide (CCK 8) and Tyr(SO3H) gNle mGly Trp (NMe)Nle Asp Phe NH2 (BC 264), a selective agonist of <strong>CCK B</strong> receptors, to induce signs of morphine <b>withdrawal</b> after ICV injection was tested.
+CCKBR	addiction	reward	8065550	An investigation into the discriminative stimulus and <b>reinforcing</b> properties of the <strong>CCKB</strong> receptor antagonist, L 365,260 in rats.
+CCKBR	drug	benzodiazepine	8065550	The discriminative stimulus properties of the selective <strong>CCKB</strong> receptor antagonist, L 365,260 were evaluated in rats trained to discriminate <b>diazepam</b> (2 mg/kg) or morphine (5 mg/kg) from vehicle, using a two lever food reinforced technique.
+CCKBR	drug	opioid	8065550	The discriminative stimulus properties of the selective <strong>CCKB</strong> receptor antagonist, L 365,260 were evaluated in rats trained to discriminate diazepam (2 mg/kg) or <b>morphine</b> (5 mg/kg) from vehicle, using a two lever food reinforced technique.
+CCKBR	drug	benzodiazepine	8185192	The <strong>CCK B</strong> antagonist LY288513 blocks <b>diazepam</b> withdrawal induced increases in auditory startle response.
+CCKBR	addiction	withdrawal	8185192	The <strong>CCK B</strong> antagonist LY288513 blocks diazepam <b>withdrawal</b> induced increases in auditory startle response.
+CCKBR	drug	opioid	8004452	In a final study the <strong>CCKB</strong> antagonist L365 260 was also found not to affect an <b>opioid</b> discriminative cue.
+CCKBR	drug	opioid	8004452	The present results therefore cast doubt on the potential utility of selective CCKA antagonists as treatments for <b>opioid</b> abuse, and further suggest that <strong>CCKB</strong> antagonists may not potentiate the subjective effects of <b>opioids</b>, an important finding considering that such drugs have been proposed as adjuncts to <b>opioid</b> therapy for the treatment of pain relief.
+CCKBR	drug	benzodiazepine	8111002	The <strong>CCK B</strong> antagonist LY288513 blocks effects of <b>diazepam</b> withdrawal on auditory startle.
+CCKBR	addiction	withdrawal	8111002	The <strong>CCK B</strong> antagonist LY288513 blocks effects of diazepam <b>withdrawal</b> on auditory startle.
+CCKBR	drug	benzodiazepine	8111002	In order to explore the potential clinical utility of <strong>CCK B</strong> antagonists for the treatment of <b>benzodiazepine</b> withdrawal symptoms, the auditory startle reflex was examined in rats undergoing withdrawal from the chronic administration of <b>diazepam</b>.
+CCKBR	addiction	withdrawal	8111002	In order to explore the potential clinical utility of <strong>CCK B</strong> antagonists for the treatment of benzodiazepine <b>withdrawal</b> symptoms, the auditory startle reflex was examined in rats undergoing <b>withdrawal</b> from the chronic administration of diazepam.
+CCKBR	drug	benzodiazepine	8111002	Acute pretreatment with either <b>diazepam</b> or the selective <strong>CCK B</strong> antagonist LY288513 dose dependently blocked withdrawal induced increases in the auditory startle response.
+CCKBR	addiction	withdrawal	8111002	Acute pretreatment with either diazepam or the selective <strong>CCK B</strong> antagonist LY288513 dose dependently blocked <b>withdrawal</b> induced increases in the auditory startle response.
+CCKBR	drug	benzodiazepine	8111002	These results support the hypothesis that the selective <strong>CCK B</strong> antagonist LY288513 may be an effective treatment for alleviating at least some <b>benzodiazepine</b> withdrawal symptoms in man.
+CCKBR	addiction	withdrawal	8111002	These results support the hypothesis that the selective <strong>CCK B</strong> antagonist LY288513 may be an effective treatment for alleviating at least some benzodiazepine <b>withdrawal</b> symptoms in man.
+CCKBR	drug	opioid	1628146	The effect of chronic treatment with CI988, a recently developed selective antagonist of cholecystokinin type B receptors (<strong>CCKB</strong> receptors) on the tolerance to <b>morphine</b> analgesia was studied in rats with the hot plate test.
+CCKBR	drug	opioid	1628146	The present results provide evidence that chronic treatment with a selective <strong>CCKB</strong> receptor antagonist could prevent tolerance to the analgesic effect of <b>morphine</b> without affecting <b>morphine</b> induced physical dependence.
+CCKBR	addiction	dependence	1628146	The present results provide evidence that chronic treatment with a selective <strong>CCKB</strong> receptor antagonist could prevent tolerance to the analgesic effect of morphine without affecting morphine induced physical <b>dependence</b>.
+CCKBR	drug	opioid	1611514	<b>Morphine</b> place conditioning is differentially affected by CCKA and <strong>CCKB</strong> receptor antagonists.
+CCKBR	drug	opioid	1611514	In the present study we have examined the interaction between the selective cholecystokinin (CCK)A and <strong>CCKB</strong> receptor antagonists, devazepide and L365 260 on <b>morphine</b> conditioned place preference (CPP).
+CCKBR	addiction	reward	1611514	In the present study we have examined the interaction between the selective cholecystokinin (CCK)A and <strong>CCKB</strong> receptor antagonists, devazepide and L365 260 on morphine conditioned place preference (<b>CPP</b>).
+CCKBR	drug	opioid	1611514	The <strong>CCKB</strong> antagonist L365 260 (0.000001 0.01 mg/kg) failed to antagonize the <b>morphine</b> CPP, if anything a mild potentiation was observed.
+CCKBR	addiction	reward	1611514	The <strong>CCKB</strong> antagonist L365 260 (0.000001 0.01 mg/kg) failed to antagonize the morphine <b>CPP</b>, if anything a mild potentiation was observed.
+CCKBR	drug	opioid	1316755	Thus high efficacy kappa <b>opioid</b> receptor agonists such as CI 977 (enadoline) have potential for the treatment of pain and stroke whilst the development of highly selective and bioavailable cholecystokinin B (<strong>CCK B</strong>) antagonists such as CI 988 ([R (R*,R*)] 4 [[2 [[3 (1H indol 3 yl) 2 methyl 1 ox6 2  [[tricyclo[3.3.1.1.3.1]dec 2 yloxy)carbonyl]amino]propyl]ami no] 1 phenethyl]amino 4 oxobutanoic acid) have offered new insights into the mechanisms underlying and the treatment of anxiety disorders and drug abuse.
+CCKBR	drug	benzodiazepine	1350747	The ability of a selective cholecystokininB (<strong>CCKB</strong>) receptor antagonist, CI 988, to block <b>benzodiazepine</b> withdrawal effects was examined in mice.
+CCKBR	addiction	withdrawal	1350747	The ability of a selective cholecystokininB (<strong>CCKB</strong>) receptor antagonist, CI 988, to block benzodiazepine <b>withdrawal</b> effects was examined in mice.
+CCKBR	addiction	aversion	1679211	PD134308 and PD135158 are highly selective <strong>CCK B</strong> receptor antagonists and were used to investigate the role of <strong>CCK B</strong> receptors in <b>aversive</b> responding in rodent and primate models of anxiety.
+CCKBR	drug	benzodiazepine	1679211	However, the <strong>CCK B</strong> antagonists were much more potent than <b>diazepam</b> and their effects were recorded over an extensive dose range.
+CCKBR	addiction	aversion	1679211	It is concluded that <strong>CCK B</strong> receptors are involved in <b>aversive</b> anxiety responding and that <strong>CCK B</strong> receptor antagonists may provide a novel and improved approach to the treatment of anxiety and withdrawal from drugs of abuse.
+CCKBR	addiction	withdrawal	1679211	It is concluded that <strong>CCK B</strong> receptors are involved in aversive anxiety responding and that <strong>CCK B</strong> receptor antagonists may provide a novel and improved approach to the treatment of anxiety and <b>withdrawal</b> from drugs of abuse.
+CCKBR	drug	benzodiazepine	1975695	Both <strong>CCK B</strong> antagonists were able to suppress the withdrawal anxiogenesis and produce an anxiolytic effect in mice previously made tolerant to <b>diazepam</b>.
+CCKBR	addiction	withdrawal	1975695	Both <strong>CCK B</strong> antagonists were able to suppress the <b>withdrawal</b> anxiogenesis and produce an anxiolytic effect in mice previously made tolerant to diazepam.
+CCKBR	drug	opioid	2311658	The selective <strong>CCK B</strong> receptor antagonist L 365,260 enhances <b>morphine</b> analgesia and prevents <b>morphine</b> tolerance in the rat.
+CCKBR	drug	opioid	2311658	The effects of the selective CCK A antagonist L 365,031 and the selective <strong>CCK B</strong> antagonist L 365,260 on <b>morphine</b> analgesia and opiate tolerance and dependence in rats were examined.
+CCKBR	addiction	dependence	2311658	The effects of the selective CCK A antagonist L 365,031 and the selective <strong>CCK B</strong> antagonist L 365,260 on morphine analgesia and opiate tolerance and <b>dependence</b> in rats were examined.
+NODAL	drug	alcohol	32319345	Mechanistically, <b>alcohol</b> inhibited extracellular signal related kinase activity, a <strong>nodal</strong> signaling kinase activating physiology hypertrophy.
+NODAL	addiction	relapse	31710020	In multivariable analysis, surgical procedure, tumor size, <strong>nodal</strong> stage, and subtype were still significant factors for <b>relapse</b> free survival (RFS) while only subtype acted as the significant factor for overall survival (OS).
+NODAL	drug	alcohol	31315270	Confocal analysis of <strong>nodal</strong> domains, flanked by immunofluorescent labeled contactin associated protein (Caspr) clusters, indicated that <b>alcohol</b> drinking reduced <strong>nodal</strong> length to width ratios in layers II/III of the Cg1 in both sexes.
+NODAL	drug	alcohol	31315270	Despite sex differences in the underlying cause (larger diameter axons after <b>alcohol</b> in males vs. shorter <strong>nodal</strong> lengths after <b>alcohol</b> in females), reduced <strong>nodal</strong> ratios could have important implications for the speed and integrity of neural transmission along these axons in both males and females.
+NODAL	drug	nicotine	29850577	The intratumoral density of CD204 was correlated with T stage, <strong>nodal</strong> involvement, lymphovascular invasion, and cancer relapse after the surgery, but not with age, gender, or <b>smoking</b> history.
+NODAL	addiction	relapse	29850577	The intratumoral density of CD204 was correlated with T stage, <strong>nodal</strong> involvement, lymphovascular invasion, and cancer <b>relapse</b> after the surgery, but not with age, gender, or smoking history.
+NODAL	addiction	relapse	29496037	There was no difference in <strong>nodal</strong> <b>relapse</b> rate in patients with <strong>nodal</strong> CR vs. <strong>nodal</strong> ER/IR.
+NODAL	addiction	reward	29305627	At the <strong>nodal</strong> level, all compounds induced increased connectivity of the regions mediating <b>reward</b> and cognitive aspects of emotional processing, such as ventromedial prefrontal cortex, septal nuclei, and nucleus accumbens.
+NODAL	addiction	reward	29280246	We also found rank ordered differences (Control > Sibling > AUD) for both <strong>nodal</strong> clustering coefficient and <strong>nodal</strong> local efficiency in <b>reward</b> system nodes, particularly left caudate, right putamen and left hippocampus.
+NODAL	drug	alcohol	29020937	Pretreatment ADC values were determined and compared with patients' age, gender, <b>alcohol</b> intake, smoking, tumor volume, pathological type, tumor stage, and <strong>nodal</strong> stage.
+NODAL	drug	nicotine	29020937	Pretreatment ADC values were determined and compared with patients' age, gender, alcohol intake, <b>smoking</b>, tumor volume, pathological type, tumor stage, and <strong>nodal</strong> stage.
+NODAL	drug	nicotine	28290074	In addition, the increased <strong>nodal</strong> efficiency predominately was located in frontal cortex, striatum and anterior cingulate gyrus (ACG) in <b>smokers</b>.
+NODAL	drug	nicotine	28290074	Meanwhile, the network parameters were correlated with the <b>nicotine</b> dependence severity (FTND) scores, and the <strong>nodal</strong> efficiency of orbitofrontal cortex was positive correlation with the cigarette per day (CPD) in young <b>smokers</b>.
+NODAL	addiction	dependence	28290074	Meanwhile, the network parameters were correlated with the nicotine <b>dependence</b> severity (FTND) scores, and the <strong>nodal</strong> efficiency of orbitofrontal cortex was positive correlation with the cigarette per day (CPD) in young smokers.
+NODAL	addiction	addiction	27872524	HPV positivity did not find any statistical correlation with age, gender, residence, <b>addiction</b> habit, stage, tumor size, <strong>nodal</strong> status, tumor grade, and number of sexual contacts.
+NODAL	drug	nicotine	27209503	E6 high maintained statistical significance in multivariate regression models balancing surgery, chemotherapy, <strong>nodal</strong> stage, and <b>smoking</b> status.
+NODAL	drug	nicotine	26937365	Significant association of GLUT 1 expression was found with history of <b>tobacco</b> (p < 0.001), Bryne's grade (p < 0.001), tumour size (p = 0.001), <strong>nodal</strong> metastasis (p = 0.022) and stage (p < 0.001).
+NODAL	drug	opioid	26922239	In a multivariable model including confounding variables of concurrent chemotherapy and involved <strong>nodal</strong> disease, comprehensive head and neck radiation therapy using proton therapy was associated with a lower <b>opioid</b> pain requirement at the completion of radiation and a lower rate of gastrostomy tube dependence by the completion of radiation therapy and at 3 months after radiation compared to IMRT.
+NODAL	addiction	dependence	26922239	In a multivariable model including confounding variables of concurrent chemotherapy and involved <strong>nodal</strong> disease, comprehensive head and neck radiation therapy using proton therapy was associated with a lower opioid pain requirement at the completion of radiation and a lower rate of gastrostomy tube <b>dependence</b> by the completion of radiation therapy and at 3 months after radiation compared to IMRT.
+NODAL	drug	nicotine	26487998	Of 182 patients, 78% were p16 positive, were younger (predominantly male), mostly former or non <b>smokers</b>, and had a more advanced <strong>nodal</strong> stage.
+NODAL	drug	nicotine	25001635	Patient age, gender, <b>smoking</b> history, human papillomavirus (HPV) status, T  and N category, lowest involved <strong>nodal</strong> level and gross tumour volume of the primary (GTV p) and <strong>nodal</strong> (GTV n) disease were analysed in relation to LRR, distant relapse and death by way of univariate and multivariate analysis.
+NODAL	addiction	relapse	25001635	Patient age, gender, smoking history, human papillomavirus (HPV) status, T  and N category, lowest involved <strong>nodal</strong> level and gross tumour volume of the primary (GTV p) and <strong>nodal</strong> (GTV n) disease were analysed in relation to LRR, distant <b>relapse</b> and death by way of univariate and multivariate analysis.
+NODAL	drug	nicotine	24962385	Furthermore, heavy <b>smokers</b> demonstrated decreased <strong>nodal</strong> global efficiency mainly in brain regions within the default mode network, whereas increased <strong>nodal</strong> local efficiency predominated in the visual related regions.
+NODAL	drug	opioid	24358220	Moreover, <strong>nodal</strong> centralities in the left hippocampus were positively correlated with the duration of <b>heroin</b> addiction.
+NODAL	addiction	addiction	24358220	Moreover, <strong>nodal</strong> centralities in the left hippocampus were positively correlated with the duration of heroin <b>addiction</b>.
+NODAL	drug	nicotine	23775406	Positive ANCCA expression was significantly associated with male sex, <b>smokers</b>, poorly differentiated tumors, nonlepidic predominant subtype, more advanced T stage, lymph <strong>nodal</strong> metastasis and late disease stage.
+NODAL	drug	nicotine	19104841	Poor patients' outcome was predicted in the cases with alteration of ROBO1/DUTT1 along with <b>tobacco</b> addiction and <strong>nodal</strong> involvement.
+NODAL	addiction	addiction	19104841	Poor patients' outcome was predicted in the cases with alteration of ROBO1/DUTT1 along with tobacco <b>addiction</b> and <strong>nodal</strong> involvement.
+NODAL	drug	nicotine	18983643	A 58 year old, non <b>smoking</b> female of Philippine origin presented with painful thoracic and neck <strong>nodal</strong> relapse of lung adenocarcinoma almost 5 years after left pneumonectomy for stage II non small cell lung cancer.
+NODAL	addiction	relapse	18983643	A 58 year old, non smoking female of Philippine origin presented with painful thoracic and neck <strong>nodal</strong> <b>relapse</b> of lung adenocarcinoma almost 5 years after left pneumonectomy for stage II non small cell lung cancer.
+NODAL	drug	amphetamine	10461823	A 13 year old African American female taking sertraline for obsessive compulsive disorder was diagnosed with her first episode of atrioventricular (AV) <strong>nodal</strong> re entrant tachycardia five days after beginning Mixed Salts of a Single Entity <b>Amphetamine</b> Product (Adderall) for treatment of attention deficit hyperactivity disorder (ADHD).
+NODAL	addiction	addiction	10461823	A 13 year old African American female taking sertraline for obsessive <b>compulsive</b> disorder was diagnosed with her first episode of atrioventricular (AV) <strong>nodal</strong> re entrant tachycardia five days after beginning Mixed Salts of a Single Entity Amphetamine Product (Adderall) for treatment of attention deficit hyperactivity disorder (ADHD).
+CCL4	drug	alcohol	32390833	The present study aimed to explore the hepatoprotective effects of acidic hydrolysates of polysaccharide extracted from the marine clam M. veneriformis (Ah MVPS) against <b>ethanol</b>  and <strong>CCl4</strong> induced liver damage.
+CCL4	drug	alcohol	32390833	They can suppress membrane destruction in boundaries and the collapse of reticular scaffolds of injured mouse hepatocytes and can substantially reduce the inflammatory extent of liver tissue aroused by excessive intake of <b>ethanol</b> or <strong>CCl4</strong>.
+CCL4	addiction	intoxication	32050489	This study confirms the ability of quercetin loaded niosomes to reverse <strong>CCl4</strong> <b>intoxication</b> and to carry out an antioxidant effect.
+CCL4	drug	alcohol	31919559	Genome wide expression and TRN analysis were performed time dependently in mouse liver after acute injury by <strong>CCl4</strong> (2 h, 8 h, 1, 2, 4, 6, 8, 16 days), as well as lipopolysaccharide (LPS, 24 h) and compared to publicly available data after tunicamycin exposure (mouse, 6 h), hepatocellular carcinoma (HCC, mouse), and human chronic liver disease (non <b>alcoholic</b> fatty liver, HBV infection and HCC).
+CCL4	addiction	intoxication	31919559	Acute <strong>CCl4</strong> <b>intoxication</b> induced expression of gene clusters enriched for inflammation and stress signaling that peaked between 2 and 24 h, accompanied by a decrease of mature liver functions, particularly metabolic genes.
+CCL4	drug	alcohol	31870920	In addition, chronic <strong>CCl4</strong> and acute LPS treatment inhibited hepatic ADH1 expression and activity, leading to increases in blood and liver <b>ethanol</b> concentrations.
+CCL4	drug	cocaine	31557508	In rats treated repeatedly with <b>cocaine</b> (10 mg/kg × 4 days, IP), CCR5 gene expression was upregulated in the nucleus accumbens and ventral tegmental area but mRNA levels of CCR5 ligands (i.e., CCL3, <strong>CCL4</strong> and CCL5) were not affected.
+CCL4	drug	alcohol	31188634	Combination of <strong>CCl4</strong> with <b>alcoholic</b> and metabolic injuries mimics human liver fibrosis.
+CCL4	drug	alcohol	31188634	<b>Ethanol</b> in drinking water (16%) or Western diet (WD) were administered for 7 wk in mice either alone or in combination with <strong>CCl4</strong> intoxications.
+CCL4	drug	alcohol	31188634	Combination of <strong>CCl4</strong> and <b>ethanol</b> induced the strongest inflammation, with significant liver fibrosis and moderate steatosis.
+CCL4	drug	alcohol	31188634	The relationship pattern between fibrosis, proliferation, and inflammation of human ALD was mostly similar in mice treated with <strong>CCl4</strong> and <b>ethanol</b>.
+CCL4	addiction	intoxication	31188634	The combination of <strong>CCl4</strong> <b>intoxication</b> with WD validates previous data suggesting it as an appropriate model for human nonalcoholic steatohepatitis.
+CCL4	drug	alcohol	31188634	Especially, <strong>CCl4</strong> plus <b>ethanol</b> for 7 wk induces ALD in mice, providing a model suitable for further basic research and drug testing.NEW & NOTEWORTHY <b>Alcoholic</b> fatty liver disease with significant fibrosis is generated within 7 wk using carbon tetrachloride as a fibrosis accelerator and administering gradually <b>ethanol</b> (up to 16%) in mice.
+CCL4	drug	alcohol	30787972	112 male C57BL/6 mice were randomly divided into 14 groups: control group (CG), <strong>CCL4</strong> group (CTG), low/medium/high dose of Euonymus alatus <b>ethanol</b> extracts (EAE), catechin (CA), dihydroquercetin (DHQ) and kaempferol (KA) groups.
+CCL4	addiction	dependence	30787972	Results showed that EAE/CA/DHQ/KA prevented increases in liver index, ALT, AST, α SMA, collagen I, TβR1, Smad2/3, TNF α and p NF κB caused by <strong>CCL4</strong> in dose <b>dependence</b>, they also improved the liver morphology, decreased inflammatory cell infiltration and collagenous fiber in dose <b>dependence</b>, CA' efficacy was best in mice; in LX 2, CA also decreased the expression of α SMA, collagen I, TGF β, Smad2/3.
+CCL4	drug	alcohol	30529260	Despite its low bioavailability, its hepatoprotective effects have been studied in various protocols of hepatotoxicity including acetaminophen, <b>alcohol</b>, lindane, carbon tetrachloride (<strong>CCL4</strong>), diethylnitrosamine and heavy metals induced hepatotoxicities.
+CCL4	drug	alcohol	29862216	Metadoxine (pyridoxine pyrrolidone carboxylate) is considered to be a beneficial agent for the treatment of experimental hepatotoxicity due to <b>alcohol</b>, <strong>CCl4</strong>, and bile duct ligation.
+CCL4	addiction	intoxication	29404036	The extract and silymarin treated animal groups showed significant decrease in activities of different biochemical parameters like serum glutamic oxaloacetic transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP), which were elevated by carbon tetrachloride (<strong>CCl4</strong>) <b>intoxication</b>.
+CCL4	drug	alcohol	29274031	After <b>alcohol</b> exposure, C C motif chemokine ligand 4 (<strong>CCL4</strong>) was significantly increased in female AE pups on PD5 and PD8.
+CCL4	drug	alcohol	29274031	After <b>alcohol</b> exposure, <strong>C C motif chemokine ligand 4</strong> (<strong>CCL4</strong>) was significantly increased in female AE pups on PD5 and PD8.
+CCL4	drug	opioid	29146238	Protein array analyses revealed only minor changes to cytokine profiles when <b>morphine</b> was administered acutely or repeatedly; however, 24 h post <b>morphine</b> administration, the expression of several cytokines was greatly increased, including endogenous CCR5 chemokine ligands (CCL3, <strong>CCL4</strong>, and CCL5), as well as CCL2.
+CCL4	addiction	intoxication	28706418	NAR administration prevented increases in ALT, AP, γ GTP, and GPx enzymatic activity; depletion of GSH and glycogen; and increases in LPO and collagen produced by chronic <strong>CCl4</strong> <b>intoxication</b> (P < 0.05).
+CCL4	addiction	intoxication	28653915	Hepatoprotective and reno potective effect of Sargassum species was investigated in rats against carbon tetrachloride (<strong>CCl4</strong>) and acetaminophen (AAP) <b>intoxication</b>.
+CCL4	addiction	intoxication	28587348	The effects of EC and PA2 on liver cell regenerative activity were investigated using a scratch wound healing assay and flow cytometric cell cycle analysis; the results of which demonstrated that LPE protected BNL from <strong>CCl4</strong> <b>intoxication</b>.
+CCL4	drug	alcohol	28501008	<b>Ethanol</b> extract and its dichloromethane fraction of Alpinia oxyphylla Miquel exhibited hepatoprotective effects against <strong>CCl4</strong> induced oxidative damage in vitro and in vivo with the involvement of Nrf2.
+CCL4	drug	alcohol	28501008	This study aimed to investigate the protective effects of <b>ethanol</b> extract (EE) and its dichloromethane fraction (DM) of A. oxyphylla, which are rich in phenolic compounds, against <strong>CCl4</strong> induced hepatic injury in vitro and in vivo.
+CCL4	addiction	intoxication	28501008	Liver histopathology revealed that EE and DM attenuated the incidence of liver lesions triggered by <strong>CCl4</strong> <b>intoxication</b>.
+CCL4	drug	alcohol	28489378	Efficient reduction of <strong>CCl4</strong> took place upon exposure to 350 nm photons of aqueous solutions containing sulfonated poly(ether etherketone) (SPEEK) as a sensitizer and either poly(vinyl <b>alcohol</b>) (PVA) or HCO2H/HCO2  buffer.
+CCL4	addiction	dependence	28489378	The <b>dependence</b> of r(Cl ) on (I0)1/2, where I0 is the light intensity, and the occurrence of postirradiation formation of Cl  through the reduction of <strong>CCl4</strong> in the dark are further evidence that the photoreaction proceeded by a chain process.
+CCL4	addiction	intoxication	28100224	It left beyond doubt that a flower of L. speciosa is a reservoir of antioxidant and hepatoprotective agents capable of reversing the damage inflicted by <strong>CCl4</strong> <b>intoxication</b>.
+CCL4	drug	alcohol	26996510	Furthermore, both <b>alcohol</b> exposed and SI animals had increased levels of pro inflammatory cytokines IL 1β, TNF α, CD11b, and <strong>CCL4</strong>; in addition, <strong>CCL4</strong> was significantly increased in <b>alcohol</b> exposed animals compared to SI as well.
+CCL4	drug	alcohol	23683793	Among the 75 patients in each group the percentage still retained on <b>naltrexone</b> treatment at six months was: N/<strong>G 26</strong>.7%, N/P 19.7% (p=0.258 to N/G), P/G 6.7% (p<0.05 to both N groups), and P/P 10.7% (p=0.013 to N+G).
+CCL4	drug	alcohol	24363682	After inducing hepatic damage, group III served as control for <strong>CCl4</strong>; and groups IV  VI received different doses of Ficus carica <b>ethanol</b> extract (200, 400 and 800 mg/kg) prior to intoxication with <strong>CCl4</strong>.
+CCL4	addiction	intoxication	24363682	After inducing hepatic damage, group III served as control for <strong>CCl4</strong>; and groups IV  VI received different doses of Ficus carica ethanol extract (200, 400 and 800 mg/kg) prior to <b>intoxication</b> with <strong>CCl4</strong>.
+CCL4	drug	alcohol	15992118	Liver injury caused by hepatotoxins, such as carbon tetrachloride (<strong>CCl4</strong>), <b>ethanol</b>, and acetaminophen (APAP), is characterised by varying degrees of hepatocyte degeneration and cell death via either apoptosis or necrosis.
+CCL4	drug	alcohol	15945353	Preventive administration of the balm and hydrolysates to animals subjected to an intoxications by 40% <b>alcohol</b> and <strong>CCl4</strong> normalized clinical diagnostic parameters of liver and blood plasma of experimental animals.
+CCL4	drug	nicotine	11762131	Drugs currently used such as paracetamol, anesthetics (enflurane, halothane), industrial solvents (benzene or its derivatives), halogenated solvents (<strong>CCl4</strong>, trichlorethylene) and nitrosamines which are present in food or <b>tobacco</b> smoke are included.
+CCL4	drug	alcohol	11450593	Since the authors reported the presence of collagenase in the liver as well as its increased activity in the early stage of hepatic fibrosis and its reduced activity in advanced fibrosis in rats induced by chronic <strong>CCl4</strong> intoxication, in baboons fed <b>alcohol</b> chronically and in patients with <b>alcoholic</b> fibrosis, other investigators have demonstrated the same tendency of collagenase activity biologically and histochemically.
+CCL4	addiction	intoxication	11450593	Since the authors reported the presence of collagenase in the liver as well as its increased activity in the early stage of hepatic fibrosis and its reduced activity in advanced fibrosis in rats induced by chronic <strong>CCl4</strong> <b>intoxication</b>, in baboons fed alcohol chronically and in patients with alcoholic fibrosis, other investigators have demonstrated the same tendency of collagenase activity biologically and histochemically.
+CCL4	drug	alcohol	11327524	ES of Nux MT in <strong>CCl4</strong> showed a red shift when 90% <b>ethanol</b> was added indicating molecular complexation and charge transfer interaction between <b>ethanol</b> and Nux compounds.
+CCL4	drug	alcohol	10759217	Since authors first reported increased activity of interstitial collagenase in the early stage of hepatic fibrosis in rats induced by chronic <strong>CCl4</strong> intoxication, in baboons fed <b>alcohol</b> chronically and in patients with <b>alcoholic</b> fibrosis, other investigators have also demonstrated increased activity biologically and histochemically.
+CCL4	addiction	intoxication	10759217	Since authors first reported increased activity of interstitial collagenase in the early stage of hepatic fibrosis in rats induced by chronic <strong>CCl4</strong> <b>intoxication</b>, in baboons fed alcohol chronically and in patients with alcoholic fibrosis, other investigators have also demonstrated increased activity biologically and histochemically.
+CCL4	drug	opioid	10654191	In this study, chemotaxis of monkey leukocytes was evaluated using human chemokines IL 8 (interleukin 8), <strong>MIP 1 beta</strong> and RANTES as the chemoattractants, and the effects of micro <b>opioid</b> receptor agonists, <b>morphine</b>, DAMGO, <b>methadone</b> and endomorphine, on the efficiency of chemotaxis were examined.
+CCL4	addiction	intoxication	10467456	The n BuOH and EtOAc fractions had the greatest hepatoprotective effects on <strong>CCl4</strong> induced liver injury; in contrast, the CHCl3 fraction was most potent against D GalN <b>intoxication</b>, which is comparable to silymarin, as a recognized hepatoprotective drug.
+CCL4	drug	alcohol	8948088	We have studied the hepatic microsomal metabolism of <b>ethanol</b> (MEOS), CYP2E1 expression and catalytic activity, and the response to phenobarbital (PB) induction or <strong>CCl4</strong> challenge in rats of either sex genetically selected for their preference (P) or aversion (NP) for <b>ethanol</b>.
+CCL4	addiction	aversion	8948088	We have studied the hepatic microsomal metabolism of ethanol (MEOS), CYP2E1 expression and catalytic activity, and the response to phenobarbital (PB) induction or <strong>CCl4</strong> challenge in rats of either sex genetically selected for their preference (P) or <b>aversion</b> (NP) for ethanol.
+CCL4	drug	alcohol	8937429	Animals treated with <strong>CCl4</strong> and <b>ethanol</b> for 9 weeks showed hepatic injury as demonstrated by 2.5  and 2 fold increases in serum alanine aminotransferase and alkaline phosphatase activities, respectively.
+CCL4	drug	alcohol	7487375	Group IV was treated with <strong>CCl4</strong> as group III, but drinking water was substituted by <b>ethanol</b> solutions with increasing concentrations as in the group II.
+CCL4	addiction	intoxication	7487375	Samples of blood, liver and spleen were taken 24 h after the third acute <strong>CCl4</strong> <b>intoxication</b>.
+CCL4	addiction	intoxication	7487375	Acute <strong>CCl4</strong> <b>intoxication</b> (group III) significantly decreased IFN production in liver and spleen cells isolated 24 h after the last <strong>CCl4</strong> injection.
+CCL4	drug	alcohol	7487375	Combined <strong>CCl4</strong> and <b>ethanol</b> administration affected very strongly IFN production (group IV).
+CCL4	drug	alcohol	8277979	Acute effects of a single intraperitoneal dose of allyl <b>alcohol</b> (AA, 64 mg/kg), dimethylnitrosamine (DMNA, 30 mg/kg), hexachlorobutadiene (HCBD, 50 mg/kg), carbon tetrachloride (<strong>CCl4</strong>, 24 mg/kg), cocaine (60 mg/kg) and pyrazole (300 mg/kg) on the hepatic histology and monooxygenases in DBA/2 and C57Bl/6 strains of mice were investigated.
+CCL4	drug	cocaine	8277979	Acute effects of a single intraperitoneal dose of allyl alcohol (AA, 64 mg/kg), dimethylnitrosamine (DMNA, 30 mg/kg), hexachlorobutadiene (HCBD, 50 mg/kg), carbon tetrachloride (<strong>CCl4</strong>, 24 mg/kg), <b>cocaine</b> (60 mg/kg) and pyrazole (300 mg/kg) on the hepatic histology and monooxygenases in DBA/2 and C57Bl/6 strains of mice were investigated.
+CCL4	drug	cocaine	8277979	In DBA/2 strain, coumarin 7 hydroxylase (COH) activity was increased from 3  to 5 fold by pyrazole, <b>cocaine</b>, HCBD and <strong>CCl4</strong>.
+CCL4	drug	alcohol	8286481	FL can be induced by either acute or chronic administration of <b>ethanol</b> (EtOH), and/or several haloalkanes (carbon tetrachloride, <strong>CCl4</strong>; 1.2 dichloroethane, DCE; 1.1.2.2 tetrachloroethane, TTCE), both in laboratory animals and in man.
+CCL4	drug	alcohol	1446373	The plasma AGP concentration in carbon tetrachloride (<strong>CCl4</strong>), allyl <b>alcohol</b>, bromobenzene, acetaminophen or N nitrosodimethylamine induced liver injury was increased to 2 3.5 times the normal level at 24 h after the intoxication.
+CCL4	addiction	intoxication	1446373	The plasma AGP concentration in carbon tetrachloride (<strong>CCl4</strong>), allyl alcohol, bromobenzene, acetaminophen or N nitrosodimethylamine induced liver injury was increased to 2 3.5 times the normal level at 24 h after the <b>intoxication</b>.
+CCL4	addiction	withdrawal	2136321	In the EtOH drinking group previously treated with <strong>CCl4</strong> we found that irrespective of the time of EtOH <b>withdrawal</b>, EtOH elimination did not differ from that in the respective <strong>CCl4</strong> treated group, only 12 hours after its <b>withdrawal</b> EtOH elimination was decreased in livers injured with <strong>CCl4</strong> in dose of 5 mmoles/kg.
+CCL4	drug	alcohol	2137379	The derangement to the Ca2(+) ATPase seems to be independent on a 'solvent effect' of the agent since the in vitro addition of increasing concentrations of either <strong>CCl4</strong> or <b>ethanol</b> to control plasma membranes does not affect the enzymatic activity.
+CCL4	addiction	intoxication	2137379	The same procedure is however able to affort a significant protection against the exacerbation of the damage to the Ca2(+) ATPase becoming evident late during the course of <strong>CCl4</strong> <b>intoxication</b>.
+CCL4	drug	alcohol	2739484	6 pigs (19.75 27.0 kg) were intoxicated with different dosages of <strong>CCl4</strong> and <b>ethanol</b>.
+CCL4	drug	alcohol	2739484	Three different regimens of <strong>CCl4</strong> and C2H5OH applications were used: <strong>CCl4</strong> was administered intragastrically alone (group 1) or combined with <b>ethanol</b> (group 2), and <strong>CCl4</strong> was given intragastrically and <b>ethanol</b> intravenously (group 3).
+CCL4	addiction	intoxication	2739484	<strong>CCl4</strong> and C2H5OH <b>intoxication</b> in pigs causes effects that are different from those described in humans or laboratory rats.
+CCL4	addiction	intoxication	2684438	Of course both phenomena produce cell damage as in the case of <strong>CCl4</strong> or BrCCl3 <b>intoxication</b>.
+CCL4	drug	alcohol	2574105	Beta hexosaminidase activity in <b>alcoholic</b> fatty liver and in <strong>CCl4</strong> induced liver fibrosis of the rat.
+CCL4	drug	alcohol	2574105	beta Hexosaminidase (Hex) activity was previously found to be increased in the sera of patients with liver cirrhosis, cholestasis and acute <b>alcohol</b> intoxication, as well as in rats with <strong>CCl4</strong> induced liver cirrhosis.
+CCL4	addiction	intoxication	2574105	beta Hexosaminidase (Hex) activity was previously found to be increased in the sera of patients with liver cirrhosis, cholestasis and acute alcohol <b>intoxication</b>, as well as in rats with <strong>CCl4</strong> induced liver cirrhosis.
+CCL4	drug	alcohol	2574105	We studied this enzymatic activity in the sera and liver tissue of rats with <b>alcoholic</b> fatty liver due to prolonged <b>alcohol</b> intake and <strong>CCl4</strong> induced liver fibrosis in association with moderate alterations in liver function tests.
+CCL4	drug	alcohol	3583469	Both <strong>CCl4</strong> and <b>ethanol</b> produce a liver damage by free radical mechanisms causing a lesion of liver cell endoplasmic reticulum.
+CCL4	drug	alcohol	3583469	Protective effects of antioxidants on <strong>CCl4</strong> or <b>ethanol</b> induced liver damage were investigated on this basis in adult Wistar rats.
+CCL4	addiction	intoxication	3583469	In conclusion <strong>CCl4</strong> <b>intoxication</b> is a suitable model for studying radical initiated liver injuries.
+CCL4	drug	alcohol	3792537	Some methionine derivatives with the amine group acylated with an aliphatic group bearing a free, esterified or etherified thiol group in the omega position were prepared and tested for protection against <strong>CCl4</strong>, paracetamol, ethyl <b>alcohol</b> and ethionine intoxication.
+CCL4	addiction	intoxication	3792537	Some methionine derivatives with the amine group acylated with an aliphatic group bearing a free, esterified or etherified thiol group in the omega position were prepared and tested for protection against <strong>CCl4</strong>, paracetamol, ethyl alcohol and ethionine <b>intoxication</b>.
+CCL4	addiction	intoxication	4080564	The activities of an endogenous inhibitor and of a stimulator of cell proliferation were assayed in the livers of sham operated (SO) or partially hepatectomized (PH) adult rats; rats fed a choline supplemented (CS) or a choline devoid (CD) diet; the same diets followed by acute <strong>CCl4</strong> <b>intoxication</b>; the same diets supplemented with phenobarbital (PHB); or a CD diet containing DL ethionine (ETH).
+CCL4	addiction	intoxication	4080564	Following PH, a CD diet, or <strong>CCl4</strong> <b>intoxication</b> the inhibitor activity was suppressed, and there was a simultaneous appearance of a stimulator activity.
+CCL4	addiction	intoxication	4080564	Thus, PH, a CD diet, and <strong>CCl4</strong> <b>intoxication</b> cause similar cellular (loss and regeneration) and humoral homeostatic changes in adult rat livers.
+CCL4	drug	alcohol	6532381	To study the effect of an acute dose of <b>ethanol</b> on carbon tetrachloride (<strong>CCl4</strong>) concentration and hepatotoxicity, female rats received <b>ethanol</b> (2.5 ml/kg body wt.)
+CCL4	drug	alcohol	6532381	Three hours after acute <strong>CCl4</strong> intoxication there was a striking increase in <strong>CCl4</strong> concentration in animals treated simultaneously with <b>ethanol</b> intragastrically compared to those receiving <b>ethanol</b> intraperitoneally.
+CCL4	addiction	intoxication	6532381	Three hours after acute <strong>CCl4</strong> <b>intoxication</b> there was a striking increase in <strong>CCl4</strong> concentration in animals treated simultaneously with ethanol intragastrically compared to those receiving ethanol intraperitoneally.
+CCL4	drug	alcohol	6532381	Serum activities of glutamate oxalacetate transaminase, glutamate pyruvate transaminase and glutamate dehydrogenase were found to be considerably higher in animals treated with the combination of <strong>CCl4</strong> and <b>ethanol</b> when compared to those receiving <strong>CCl4</strong> alone, showing that <b>ethanol</b> given intraperitoneally or intragastrically enhances <strong>CCl4</strong> hepatotoxicity.
+CCL4	drug	alcohol	6532381	Since the intraperitoneal administration of <b>ethanol</b> led to a reduction rather than an increase in <strong>CCl4</strong> concentration in the early phase of intoxication, additional mechanisms independent of actual levels of <strong>CCl4</strong>, such as direct effects of <b>ethanol</b> on the <strong>CCl4</strong> metabolizing enzyme of the membrane of the endoplasmic reticulum, have to be implicated in the pathogenesis of the potentiation of <strong>CCl4</strong> hepatotoxicity by <b>ethanol</b>.
+CCL4	addiction	intoxication	6532381	Since the intraperitoneal administration of ethanol led to a reduction rather than an increase in <strong>CCl4</strong> concentration in the early phase of <b>intoxication</b>, additional mechanisms independent of actual levels of <strong>CCl4</strong>, such as direct effects of ethanol on the <strong>CCl4</strong> metabolizing enzyme of the membrane of the endoplasmic reticulum, have to be implicated in the pathogenesis of the potentiation of <strong>CCl4</strong> hepatotoxicity by ethanol.
+CCL4	drug	alcohol	6882388	Second derivative spectroscopy was used to determine the conjugated diene shift that measures the extent of the first step of lipid peroxidation after carbon tetrachloride (<strong>CCl4</strong>), bromotrichloromethane (BrCCl3) and <b>ethanol</b> intoxication.
+CCL4	addiction	intoxication	6882388	Second derivative spectroscopy was used to determine the conjugated diene shift that measures the extent of the first step of lipid peroxidation after carbon tetrachloride (<strong>CCl4</strong>), bromotrichloromethane (BrCCl3) and ethanol <b>intoxication</b>.
+CCL4	drug	alcohol	6877050	To study the effect of an acute dose of <b>alcohol</b> on the hepatotoxicity due to <strong>CCl4</strong>, rats received <b>alcohol</b> (4 g/kg BW) and/or <strong>CCl4</strong> (1.5 ml/kg BW) by concomitant intragastric intubation.
+CCL4	drug	alcohol	6877050	Compared to animals receiving <strong>CCl4</strong> alone, the simultaneous application of <strong>CCl4</strong> and <b>alcohol</b> resulted 12 h after administration in significantly lower serum activities of glutamate oxalacetate transaminase (1005 +/  70 vs 739 +/  47; p less than 0.01) and glutamate pyruvate transaminase (746 +/  10 vs 330 +/  41; p less than 0.01), whereas 36 h after administration, an increase of serum enzyme activities was observed.
+CCL4	drug	alcohol	6877050	By histological assessment, liver damage was also much less pronounced 12 h after combined administration of <strong>CCl4</strong> and <b>ethanol</b>, compared to <strong>CCl4</strong> alone, whereas the reversed constellation could be demonstrated 36 h after administration.
+CCL4	drug	alcohol	6877050	These results therefore show that in the early phase of <strong>CCl4</strong> intoxication an acute dose of <b>alcohol</b> may partially protect from <strong>CCl4</strong> hepatotoxicity, whereas potentiation was observed under these experimental conditions in the late phase of <strong>CCl4</strong> intoxication.
+CCL4	addiction	intoxication	6877050	These results therefore show that in the early phase of <strong>CCl4</strong> <b>intoxication</b> an acute dose of alcohol may partially protect from <strong>CCl4</strong> hepatotoxicity, whereas potentiation was observed under these experimental conditions in the late phase of <strong>CCl4</strong> <b>intoxication</b>.
+CCL4	addiction	intoxication	6178134	The occurrence of AFP was studied in normal and diseased livers of mice and rats: (a) fetal and neonatal livers; (b) liver regeneration after <strong>CCl4</strong> <b>intoxication</b>; (c) chemical hepatocarcinogenesis.
+CCL4	addiction	intoxication	6178134	After <strong>CCl4</strong> <b>intoxication</b> of low and high AFP producing mouse strains, cellular AFP is found in hepatocytes of portal, periportal and intermediate zones.
+CCL4	drug	opioid	710265	Furthermore, the analysis revealed the time lag relationships between components  "new admissions to <b>methadone</b> treatment" <strong>lag 1</strong>  2 years behind the "street" component; "readmissions to <b>methadone</b> treatment" <strong>lag 1</strong>  3 years behind the "new admissions" component.
+CDK5	drug	alcohol	31403700	Chronic exposure to <b>ethanol</b> (EtOH) and other drugs of abuse can alter the expression and activity of cyclin dependent kinase 5 (<strong>CDK5</strong>) and its cofactor p35, but the functional implication of <strong>CDK5</strong> signaling in the regulation of EtOH related behaviors remains unknown.
+CDK5	drug	alcohol	31403700	Chronic exposure to <b>ethanol</b> (EtOH) and other drugs of abuse can alter the expression and activity of <strong>cyclin dependent kinase 5</strong> (<strong>CDK5</strong>) and its cofactor p35, but the functional implication of <strong>CDK5</strong> signaling in the regulation of EtOH related behaviors remains unknown.
+CDK5	addiction	addiction	31403700	In the present study, we sought to determine whether <strong>CDK5</strong> activity plays a role in the <b>escalation</b> of EtOH self administration triggered by dependence.
+CDK5	addiction	dependence	31403700	In the present study, we sought to determine whether <strong>CDK5</strong> activity plays a role in the escalation of EtOH self administration triggered by <b>dependence</b>.
+CDK5	addiction	dependence	31403700	In the bed nucleus of the stria terminalis, <strong>CDK5</strong> abundance was negatively correlated with intoxication levels during EtOH vapor exposure but there was no effect of <b>dependence</b> on the phosphorylation ratio of <strong>CDK5</strong> substrates.
+CDK5	addiction	intoxication	31403700	In the bed nucleus of the stria terminalis, <strong>CDK5</strong> abundance was negatively correlated with <b>intoxication</b> levels during EtOH vapor exposure but there was no effect of dependence on the phosphorylation ratio of <strong>CDK5</strong> substrates.
+CDK5	drug	alcohol	31403700	However, increased activity of CDKs other than <strong>CDK5</strong> in the BLA may contribute to excessive EtOH consumption in <b>alcohol</b> dependence.
+CDK5	addiction	dependence	31403700	However, increased activity of CDKs other than <strong>CDK5</strong> in the BLA may contribute to excessive EtOH consumption in alcohol <b>dependence</b>.
+CDK5	drug	cocaine	30622460	Furthermore, we highlight future directions to elucidate the interaction between the prefrontal cortex (PFC) and key intermediaries including ΔFosB, cAMP response element binding protein (CREB) and cyclin dependent kinase 5 (<strong>CDK5</strong>) to highlight possible mechanisms that underlie stress induced acceleration of the progression to a <b>cocaine</b> use disorder diagnosis.
+CDK5	drug	cocaine	30622460	Furthermore, we highlight future directions to elucidate the interaction between the prefrontal cortex (PFC) and key intermediaries including ΔFosB, cAMP response element binding protein (CREB) and <strong>cyclin dependent kinase 5</strong> (<strong>CDK5</strong>) to highlight possible mechanisms that underlie stress induced acceleration of the progression to a <b>cocaine</b> use disorder diagnosis.
+CDK5	drug	cocaine	30321610	Increased expression of Arc, <strong>CDK5</strong> and TH, and decrease in DAT protein levels persisted longer after withdrawal, pointing to a neuroplastic lasting effect similar to that involved in <b>cocaine</b> addiction.
+CDK5	addiction	addiction	30321610	Increased expression of Arc, <strong>CDK5</strong> and TH, and decrease in DAT protein levels persisted longer after withdrawal, pointing to a neuroplastic lasting effect similar to that involved in cocaine <b>addiction</b>.
+CDK5	addiction	withdrawal	30321610	Increased expression of Arc, <strong>CDK5</strong> and TH, and decrease in DAT protein levels persisted longer after <b>withdrawal</b>, pointing to a neuroplastic lasting effect similar to that involved in cocaine addiction.
+CDK5	drug	cocaine	29354053	The D1 D2 heteromer activated <strong>Cdk5</strong>/Thr75 DARPP 32 and attenuated <b>cocaine</b> induced pERK and ΔFosB accumulation, together with inhibition of <b>cocaine</b> enhanced local field potentials in NAc, blocking thus the signaling pathway activated by <b>cocaine</b>: D1R/cAMP/PKA/Thr34 DARPP 32/pERK with ΔFosB accumulation.
+CDK5	drug	amphetamine	29225566	<strong>Cdk5</strong> Is Essential for <b>Amphetamine</b> to Increase Dendritic Spine Density in Hippocampal Pyramidal Neurons.
+CDK5	addiction	addiction	29225566	Recent reports suggest that <strong>Cdk5</strong> plays an important role in drug <b>addiction</b>, but its role in psychostimulant's effects on dendritic spines in hippocampus remain unknown.
+CDK5	drug	amphetamine	29225566	Primary cultures and organotypic slice cultures were used for cellular, molecular, pharmacological and biochemical analyses of the role of <strong>Cdk5</strong>/p25 in <b>amphetamine</b> induced dendritic spine formation.
+CDK5	drug	amphetamine	29225566	Either genetic or pharmacological inhibition of <strong>Cdk5</strong> activity prevented the <b>amphetamine</b> induced increase in dendritic spine density.
+CDK5	drug	amphetamine	29225566	<b>Amphetamine</b> also increased spine density in neurons overexpressing the strong <strong>Cdk5</strong> activator p25.
+CDK5	drug	amphetamine	29225566	Moreover, we show that the <strong>Cdk5</strong>/p25 signaling and calpain activity are both necessary for the effect of <b>amphetamine</b> on dendritic spine density.
+CDK5	drug	cannabinoid	29082320	<b>THC</b> injection in mice with a history of repeated <b>THC</b> treatment increased expression of cyclin dependent kinase 5 (<strong>Cdk5</strong>) and its regulatory protein p35 only in the PFC.
+CDK5	drug	cannabinoid	29082320	<b>THC</b> injection in mice with a history of repeated <b>THC</b> treatment increased expression of <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) and its regulatory protein p35 only in the PFC.
+CDK5	drug	cannabinoid	29082320	This increase in <strong>Cdk5</strong> and p35 expression in PFC was also found in mice that had only received repeated <b>THC</b> administration, suggesting that this effect might be due to induction of ΔFosB.
+CDK5	drug	cannabinoid	29082320	Phosphorylation of glycogen synthase kinase 3β (GSK3β), a <strong>Cdk5</strong> target, was reduced in PFC after repeated <b>THC</b> treatment regardless of <b>THC</b> history, and phosphorylation of dopamine  and cAMP regulated phosphoprotein of 32 kDa (DARPP 32) at the <strong>Cdk5</strong> regulated threonine 75 site was unchanged.
+CDK5	drug	cannabinoid	29082320	Conclusion: These results suggest that a history of repeated <b>THC</b> administration primes <b>THC</b> mediated induction of ΔFosB in the NAc and PFC, and that expression of both downstream targets of ΔFosB (e.g., <strong>Cdk5</strong> and p35) and upstream activators (e.g., pERK) in the PFC is dependent on <b>THC</b> history, which might have functional implications in addiction and neuropsychiatric disease.
+CDK5	addiction	addiction	29082320	Conclusion: These results suggest that a history of repeated THC administration primes THC mediated induction of ΔFosB in the NAc and PFC, and that expression of both downstream targets of ΔFosB (e.g., <strong>Cdk5</strong> and p35) and upstream activators (e.g., pERK) in the PFC is dependent on THC history, which might have functional implications in <b>addiction</b> and neuropsychiatric disease.
+CDK5	drug	benzodiazepine	29031852	Enhancement of GABA signaling by <b>diazepam</b> impeded ocular dominance plasticity rescued by <strong>Cdk5</strong> inhibition.
+CDK5	drug	nicotine	28857504	In contrast, <b>nicotine</b> self administration alone, resulted in a significant decrease in histone methylation at the H3K27me3 and H3K9me2 marks in the promoter regions of BDNF exon IV and <strong>cyclin dependent kinase 5</strong> (Cdk 5).
+CDK5	drug	amphetamine	28782589	In this study, we examined the rewarding effect after <b>METH</b> administration by conditioned place preference (CPP) of mice, and detected the levels of dopamine and the activity of cAMP responsive element binding protein (CREB), the expressions of ΔFosB and cyclin dependent kinase 5 (<strong>CDK5</strong>) in the ventral tegmental area (VTA) and nucleus accumbens (NAc) in mice.
+CDK5	addiction	reward	28782589	In this study, we examined the rewarding effect after METH administration by conditioned place preference (<b>CPP</b>) of mice, and detected the levels of dopamine and the activity of cAMP responsive element binding protein (CREB), the expressions of ΔFosB and cyclin dependent kinase 5 (<strong>CDK5</strong>) in the ventral tegmental area (VTA) and nucleus accumbens (NAc) in mice.
+CDK5	drug	amphetamine	28782589	In this study, we examined the rewarding effect after <b>METH</b> administration by conditioned place preference (CPP) of mice, and detected the levels of dopamine and the activity of cAMP responsive element binding protein (CREB), the expressions of ΔFosB and <strong>cyclin dependent kinase 5</strong> (<strong>CDK5</strong>) in the ventral tegmental area (VTA) and nucleus accumbens (NAc) in mice.
+CDK5	addiction	reward	28782589	In this study, we examined the rewarding effect after METH administration by conditioned place preference (<b>CPP</b>) of mice, and detected the levels of dopamine and the activity of cAMP responsive element binding protein (CREB), the expressions of ΔFosB and <strong>cyclin dependent kinase 5</strong> (<strong>CDK5</strong>) in the ventral tegmental area (VTA) and nucleus accumbens (NAc) in mice.
+CDK5	drug	amphetamine	28782589	The activity of CREB and the expressions of ΔFosB and <strong>CDK5</strong> were increased by <b>METH</b> in wile type mice, which were not further increased in TG mice.
+CDK5	drug	cocaine	27734601	Similarly, NGB2904 and SCH23390 showed opposite/differential effects on <b>cocaine</b> induced structural plasticity, conditioned place preference and locomotor activity and signaling activation, including the activation of ERK, CREB and NR1 and the expression of c fos and <strong>Cdk5</strong>.
+CDK5	drug	opioid	27549397	Dissociative role for dorsal hippocampus in mediating <b>heroin</b> self administration and relapse through <strong>CDK5</strong> and RhoB signaling revealed by proteomic analysis.
+CDK5	addiction	relapse	27549397	Dissociative role for dorsal hippocampus in mediating heroin self administration and <b>relapse</b> through <strong>CDK5</strong> and RhoB signaling revealed by proteomic analysis.
+CDK5	drug	opioid	27549397	Among them, cyclin dependent kinase 5 (<strong>CDK5</strong>) and ras homolog family member B (RhoB) were up regulated in rats with a history of extended access to <b>heroin</b>.
+CDK5	drug	opioid	27549397	Among them, <strong>cyclin dependent kinase 5</strong> (<strong>CDK5</strong>) and ras homolog family member B (RhoB) were up regulated in rats with a history of extended access to <b>heroin</b>.
+CDK5	drug	opioid	27549397	Functionally, inhibition of <strong>CDK5</strong> in the DH enhanced <b>heroin</b> self administration, indicating that <strong>CDK5</strong> signaling in the DH acts as a homeostatic compensatory mechanism to limit <b>heroin</b> taking behavior, whereas blockade of the Rho Rho kinase (ROCK) pathway attenuated context induced <b>heroin</b> relapse, indicating that RhoB signaling in the DH is required for the retrieval (recall) of addiction memory.
+CDK5	addiction	addiction	27549397	Functionally, inhibition of <strong>CDK5</strong> in the DH enhanced heroin self administration, indicating that <strong>CDK5</strong> signaling in the DH acts as a homeostatic compensatory mechanism to limit heroin taking behavior, whereas blockade of the Rho Rho kinase (ROCK) pathway attenuated context induced heroin relapse, indicating that RhoB signaling in the DH is required for the retrieval (recall) of <b>addiction</b> memory.
+CDK5	addiction	relapse	27549397	Functionally, inhibition of <strong>CDK5</strong> in the DH enhanced heroin self administration, indicating that <strong>CDK5</strong> signaling in the DH acts as a homeostatic compensatory mechanism to limit heroin taking behavior, whereas blockade of the Rho Rho kinase (ROCK) pathway attenuated context induced heroin <b>relapse</b>, indicating that RhoB signaling in the DH is required for the retrieval (recall) of addiction memory.
+CDK5	addiction	relapse	27549397	Our findings suggest that manipulation of <strong>CDK5</strong> signaling in the DH may be essential in determining vulnerability to opiate taking, whereas manipulation of RhoB signaling in the DH may be essential in determining vulnerability to <b>relapse</b>.
+CDK5	drug	opioid	27549397	Overall, the present study suggests that the DH can exert dissociative effects on <b>heroin</b> addiction through <strong>CDK5</strong> and RhoB signaling.
+CDK5	addiction	addiction	27549397	Overall, the present study suggests that the DH can exert dissociative effects on heroin <b>addiction</b> through <strong>CDK5</strong> and RhoB signaling.
+CDK5	drug	cocaine	27122028	Targeted Epigenetic Remodeling of the <strong>Cdk5</strong> Gene in Nucleus Accumbens Regulates <b>Cocaine</b>  and Stress Evoked Behavior.
+CDK5	addiction	reward	27122028	We sought to examine the role of histone modifications at the murine <strong>Cdk5</strong> (cyclin dependent kinase 5) locus, given growing evidence of <strong>Cdk5</strong> expression in nucleus accumbens (NAc) influencing <b>reward</b> related behaviors.
+CDK5	addiction	reward	27122028	We sought to examine the role of histone modifications at the murine <strong>Cdk5</strong> (<strong>cyclin dependent kinase 5</strong>) locus, given growing evidence of <strong>Cdk5</strong> expression in nucleus accumbens (NAc) influencing <b>reward</b> related behaviors.
+CDK5	drug	cocaine	27122028	We examined the behavioral consequences of this epigenetic remodeling and found that <strong>Cdk5</strong> targeted H3K9/14ac increased <b>cocaine</b> induced locomotor behavior, as well as resilience to social stress.
+CDK5	drug	cocaine	27122028	Conversely, <strong>Cdk5</strong> targeted H3K9me2 attenuated both <b>cocaine</b> induced locomotor behavior and conditioned place preference, but had no effect on stress induced social avoidance behavior.
+CDK5	addiction	reward	27122028	The current study provides evidence for the causal role of <strong>Cdk5</strong> epigenetic remodeling in NAc in <strong>Cdk5</strong> gene expression and in the control of <b>reward</b> and stress responses.
+CDK5	drug	cocaine	27122028	In particular, epigenetic regulation of the <strong>Cdk5</strong> gene alters responses to <b>cocaine</b> and stress in mouse and rat models.
+CDK5	drug	cocaine	27122028	We found that this is sufficient to regulate the expression of <strong>Cdk5</strong> and results in altered behavioral responses to <b>cocaine</b> and social stress.
+CDK5	addiction	addiction	27056740	The effects of these drugs of abuse in different animal models of drug reward, dependence and <b>addiction</b> are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), cyclin dependent kinase 5 (<strong>Cdk5</strong>), heat shock proteins (Hsp) and other enzymes and proteins.
+CDK5	addiction	dependence	27056740	The effects of these drugs of abuse in different animal models of drug reward, <b>dependence</b> and addiction are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), cyclin dependent kinase 5 (<strong>Cdk5</strong>), heat shock proteins (Hsp) and other enzymes and proteins.
+CDK5	addiction	reward	27056740	The effects of these drugs of abuse in different animal models of drug <b>reward</b>, dependence and addiction are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), cyclin dependent kinase 5 (<strong>Cdk5</strong>), heat shock proteins (Hsp) and other enzymes and proteins.
+CDK5	addiction	addiction	27056740	The effects of these drugs of abuse in different animal models of drug reward, dependence and <b>addiction</b> are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>), heat shock proteins (Hsp) and other enzymes and proteins.
+CDK5	addiction	dependence	27056740	The effects of these drugs of abuse in different animal models of drug reward, <b>dependence</b> and addiction are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>), heat shock proteins (Hsp) and other enzymes and proteins.
+CDK5	addiction	reward	27056740	The effects of these drugs of abuse in different animal models of drug <b>reward</b>, dependence and addiction are altered by manipulation of the mitogen activated protein kinase (MAPK) family, particularly extracellular signal regulated kinase (ERK), calcium/calmodulin dependent kinase II (CaMKII), the protein kinase C (PKC) family (including PKMζ), cAMP dependent protein kinase A (PKA), cGMP dependent protein kinase G (PKG), the phosphatidylinositol 3 kinase (PI3K) pathway and its downstream target mammalian target of Rapamycin (mTOR), <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>), heat shock proteins (Hsp) and other enzymes and proteins.
+CDK5	drug	amphetamine	26692451	Association between the expression of <b>amphetamine</b> induced behavioral sensitization and <strong>Cdk5</strong>/p35 activity in dorsal striatum.
+CDK5	addiction	sensitization	26692451	Association between the expression of amphetamine induced behavioral <b>sensitization</b> and <strong>Cdk5</strong>/p35 activity in dorsal striatum.
+CDK5	drug	amphetamine	26692451	Our findings provide clear behavioral and neurochemical evidence of a specific association between increased p35 and <strong>Cdk5</strong> activity in the dorsal striatum and the expression of <b>amphetamine</b> behavioral sensitization, allowing us to propose p35 as a biochemical marker of behavioral sensitization to <b>amphetamine</b>.
+CDK5	addiction	sensitization	26692451	Our findings provide clear behavioral and neurochemical evidence of a specific association between increased p35 and <strong>Cdk5</strong> activity in the dorsal striatum and the expression of amphetamine behavioral <b>sensitization</b>, allowing us to propose p35 as a biochemical marker of behavioral <b>sensitization</b> to amphetamine.
+CDK5	drug	alcohol	26617831	<strong>Cdk5</strong> kinase activity and cell survival rate in primary hippocampal neuron cultures treated with <b>ethanol</b> or <b>ethanol</b> and polydatin were measured in the in vitro study.
+CDK5	drug	alcohol	26617831	Polydatin reversed the performance impairments in chronic <b>ethanol</b> treated rats in Morris water maze test, and decreased unregulated <strong>Cdk5</strong> expression.
+CDK5	drug	alcohol	26617831	Moreover, polydatin increased cell survival rate, and decreased <strong>Cdk5</strong> activity in the <b>ethanol</b> treated primary culture of hippocampal neurons.
+CDK5	drug	alcohol	26617831	The study results suggest that polydatin exhibits neuroprotective potential for <b>ethanol</b> induced neurotoxicity, both in vivo and in vitro, which is most likely related to its ability to target <strong>Cdk5</strong> in neurons.
+CDK5	drug	cocaine	26377474	We also found that H4R3me2a is upregulated in NAc after repeated <b>cocaine</b> administration, and that H4R3me2a upregulation in turn controls the expression of <strong>Cdk5</strong> and CaMKII.
+CDK5	drug	cocaine	26377474	Additionally, the suppression of PRMT1 in NAc with lentiviral short hairpin PMRT1 decreases levels of CaMKII and <strong>Cdk5</strong> in the <b>cocaine</b> treated group, demonstrating that PRMT1 affects the ability of <b>cocaine</b> to induce CaMKII and <strong>Cdk5</strong> in NAc.
+CDK5	drug	cocaine	26377474	This study also showed that H4R3me2a controlled transcriptions of <strong>Cdk5</strong> and CaMKII, and that PRMT1 negatively affected the ability of <b>cocaine</b> to induce CaMKII and <strong>Cdk5</strong> in NAc.
+CDK5	drug	alcohol	26248414	[Effects of polydatin on learning and memory and <strong>Cdk5</strong> kinase activity in the hippocampus of rats with chronic <b>alcoholism</b>].
+CDK5	drug	alcohol	26248414	To observe the effects of polydatin on learning and memory and cyclin dependent kinase 5 (<strong>Cdk5</strong>) kinase activity in the hippocampus of rats with chronic <b>alcoholism</b>.
+CDK5	drug	alcohol	26248414	To observe the effects of polydatin on learning and memory and <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) kinase activity in the hippocampus of rats with chronic <b>alcoholism</b>.
+CDK5	addiction	withdrawal	26248414	The abstinence scoring was used to evaluate the rats <b>withdrawal</b> symptoms; cognitive function was measured by Morris water maze experiment; <strong>Cdk5</strong> protein expression in the hippocampus was detected by immunofluorescence; <strong>Cdk5</strong> kinase activity in the hippocampus was detected by liquid scintillation counting method.
+CDK5	drug	alcohol	26248414	The abstinence score, escape latency, <strong>Cdk5</strong> kinase activity in chronic <b>alcoholism</b> group rats were significantly higher than those of control group (P < 0.05).
+CDK5	drug	alcohol	26248414	The abstinence score, escape latency in high polydatin group rats were significantly lower than those of chronic <b>alcoholism</b> group (P < 0.05); <strong>Cdk5</strong> kinase activity in high and low polydatin group rats was significantly lower than that of chronic <b>alcoholism</b> group(P < 0.05); immunofluorescence showed that the <strong>Cdk5</strong> positive cells of chronic <b>alcoholism</b> group were significantly increased compared with control group (P < 0.05), and the <strong>Cdk5</strong> positive cells of polydatin groups were significantly decreased compared with chronic <b>alcoholism</b> group (P < 0.05).
+CDK5	drug	alcohol	26248414	Polydatin reduced the chronic <b>alcoholism</b> damage may interrelate with regulation of <strong>Cdk5</strong> kinase activity.
+CDK5	drug	cocaine	26019323	Treatment with an intra NAc injection of the ESR1 agonist propyl pyrazole triol (10 nm) or the <strong>CDK5</strong> inhibitor roscovitine (28 μm) on day 30 of withdrawal significantly decreased cue induced <b>cocaine</b> seeking.
+CDK5	addiction	relapse	26019323	Treatment with an intra NAc injection of the ESR1 agonist propyl pyrazole triol (10 nm) or the <strong>CDK5</strong> inhibitor roscovitine (28 μm) on day 30 of withdrawal significantly decreased cue induced cocaine <b>seeking</b>.
+CDK5	addiction	withdrawal	26019323	Treatment with an intra NAc injection of the ESR1 agonist propyl pyrazole triol (10 nm) or the <strong>CDK5</strong> inhibitor roscovitine (28 μm) on day 30 of <b>withdrawal</b> significantly decreased cue induced cocaine seeking.
+CDK5	drug	amphetamine	24939858	Locomotor conditioning by <b>amphetamine</b> requires <strong>cyclin dependent kinase 5</strong> signaling in the nucleus accumbens.
+CDK5	drug	cocaine	24939858	Pharmacological inhibition of <strong>Cdk5</strong> in the NAcc prevents the increases in dendritic spine density normally observed in this site following repeated <b>cocaine</b>.
+CDK5	drug	amphetamine	24939858	In the present experiments, blockade in rats of NAcc <strong>Cdk5</strong> activity with roscovitine (40 nmol/0.5 μl/side) prior to each of 4 injections of <b>amphetamine</b> (1.5 mg/kg; i.p.)
+CDK5	drug	amphetamine	24939858	Similarly, transient viral expression in the NAcc exclusively during <b>amphetamine</b> exposure of a threonine alanine mutant form of Kal7 [mKal7(T1590A)] that is not phosphorylated by <strong>Cdk5</strong> also prevented the accrual of contextual conditioning and spared the induction of sensitization.
+CDK5	addiction	sensitization	24939858	Similarly, transient viral expression in the NAcc exclusively during amphetamine exposure of a threonine alanine mutant form of Kal7 [mKal7(T1590A)] that is not phosphorylated by <strong>Cdk5</strong> also prevented the accrual of contextual conditioning and spared the induction of <b>sensitization</b>.
+CDK5	drug	opioid	23153991	Differential regulation of <strong>CDK5</strong> and c Fos expression by <b>morphine</b> in the brain of Lewis and Fischer 344 rat strains.
+CDK5	drug	opioid	23153991	The aim of this study was to comparatively study cyclin dependent kinase 5 (<strong>CDK5</strong>) and c Fos regulation by <b>morphine</b> in the brains of Lewis and Fischer 344 (F344) rats, which are known to differ in their behavioral sensitivities to several drugs of abuse.
+CDK5	drug	opioid	23153991	The aim of this study was to comparatively study <strong>cyclin dependent kinase 5</strong> (<strong>CDK5</strong>) and c Fos regulation by <b>morphine</b> in the brains of Lewis and Fischer 344 (F344) rats, which are known to differ in their behavioral sensitivities to several drugs of abuse.
+CDK5	drug	opioid	23153991	<b>Morphine</b> upregulated <strong>CDK5</strong> with a varying pattern depending on the strain and brain area.
+CDK5	drug	opioid	23153991	We propose that the acute <b>morphine</b> regulation of <strong>CDK5</strong> expression in the NAC may predict the rate of drug intake and/or extinction of drug seeking, while the pattern of c Fos activation may be more related to the differential acquisition of <b>morphine</b> seeking behaviors.
+CDK5	addiction	relapse	23153991	We propose that the acute morphine regulation of <strong>CDK5</strong> expression in the NAC may predict the rate of drug intake and/or extinction of drug <b>seeking</b>, while the pattern of c Fos activation may be more related to the differential acquisition of morphine <b>seeking</b> behaviors.
+CDK5	drug	alcohol	23020045	Chronic cocaine and <b>alcohol</b> treatment activate and repress many genes such as FosB, <strong>Cdk5</strong>, and Bdnf, where their dysregulation, at the chromatin level, contribute to the development and maintenance of addiction.
+CDK5	drug	cocaine	23020045	Chronic <b>cocaine</b> and alcohol treatment activate and repress many genes such as FosB, <strong>Cdk5</strong>, and Bdnf, where their dysregulation, at the chromatin level, contribute to the development and maintenance of addiction.
+CDK5	addiction	addiction	23020045	Chronic cocaine and alcohol treatment activate and repress many genes such as FosB, <strong>Cdk5</strong>, and Bdnf, where their dysregulation, at the chromatin level, contribute to the development and maintenance of <b>addiction</b>.
+CDK5	drug	opioid	22466129	Our previous study identified Threonine 161 (Thr 161), located in the second intracellular loop of the δ <b>opioid</b> receptor (DOR), as the only consensus phosphorylation site for cyclin dependent kinase 5 (<strong>Cdk5</strong>).
+CDK5	drug	opioid	22466129	Our previous study identified Threonine 161 (Thr 161), located in the second intracellular loop of the δ <b>opioid</b> receptor (DOR), as the only consensus phosphorylation site for <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>).
+CDK5	drug	opioid	22466129	The aim of this study was to assess the function of DOR phosphorylation by <strong>Cdk5</strong> in complete Freund's adjuvant (CFA) induced inflammatory pain and <b>morphine</b> tolerance.
+CDK5	drug	opioid	22466129	Phosphorylation of DOR at Thr 161 by <strong>Cdk5</strong> attenuates hypersensitivity and potentiates <b>morphine</b> tolerance in rats with CFA induced inflammatory pain, while disruption of the phosphorylation of DOR at Thr 161 attenuates <b>morphine</b> tolerance.
+CDK5	drug	alcohol	22349397	After treating juvenile and adult rats with intermittent <b>ethanol</b> administration, we found that <b>ethanol</b> treatment upregulates histone acetyl transferase (HAT) activity in adolescent prefrontal cortex and increases histone (H3 or H4) acetylation and H3(K4) dimethylation in the promoter region of cFos, <strong>Cdk5</strong> and FosB.
+CDK5	drug	alcohol	22349397	Inhibition of histone deacetylase by sodium butyrate before <b>ethanol</b> injection enhances both up regulation of HAT activity and histone acetylation of cFos, <strong>Cdk5</strong> and FosB.
+CDK5	drug	opioid	22285390	Furthermore, the activation of cAMP responsive element binding protein and the expression of ΔFosB and <strong>cyclin dependent kinase 5</strong> were decreased in the nucleus accumbens by GGA treatment after <b>morphine</b> withdrawal.
+CDK5	addiction	withdrawal	22285390	Furthermore, the activation of cAMP responsive element binding protein and the expression of ΔFosB and <strong>cyclin dependent kinase 5</strong> were decreased in the nucleus accumbens by GGA treatment after morphine <b>withdrawal</b>.
+CDK5	addiction	reward	20832057	Mice lacking the <strong>Cdk5</strong> activating cofactor p35 are deficient in cortical lamination, suggesting altered motor/<b>reward</b> circuitry.
+CDK5	drug	cocaine	20685978	Basolateral amygdala <strong>cdk5</strong> activity mediates consolidation and reconsolidation of memories for <b>cocaine</b> cues.
+CDK5	drug	cocaine	20685978	We used a conditioned place preference (CPP) procedure in rats to study the role of neuronal protein kinase cyclin dependent kinase 5 (<strong>Cdk5</strong>) in consolidation and reconsolidation of <b>cocaine</b> cue memories.
+CDK5	addiction	reward	20685978	We used a conditioned place preference (<b>CPP</b>) procedure in rats to study the role of neuronal protein kinase cyclin dependent kinase 5 (<strong>Cdk5</strong>) in consolidation and reconsolidation of cocaine cue memories.
+CDK5	drug	cocaine	20685978	We used a conditioned place preference (CPP) procedure in rats to study the role of neuronal protein kinase <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) in consolidation and reconsolidation of <b>cocaine</b> cue memories.
+CDK5	addiction	reward	20685978	We used a conditioned place preference (<b>CPP</b>) procedure in rats to study the role of neuronal protein kinase <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) in consolidation and reconsolidation of cocaine cue memories.
+CDK5	drug	cocaine	20685978	We found that the expression of <b>cocaine</b> CPP in drug free tests 1 d after CPP training (four pairings of 10 mg/kg <b>cocaine</b> with one context and four pairings of saline with a different context) increased <strong>Cdk5</strong> activity, and levels of the <strong>Cdk5</strong> activator p35 in basolateral but not central amygdala.
+CDK5	addiction	reward	20685978	We found that the expression of cocaine <b>CPP</b> in drug free tests 1 d after <b>CPP</b> training (four pairings of 10 mg/kg cocaine with one context and four pairings of saline with a different context) increased <strong>Cdk5</strong> activity, and levels of the <strong>Cdk5</strong> activator p35 in basolateral but not central amygdala.
+CDK5	drug	cocaine	20685978	We also found that basolateral (but not central) amygdala injections of the <strong>Cdk5</strong> inhibitor beta butyrolactone (100 ng/side) immediately (but not 6 h) after <b>cocaine</b> context pairings during training prevented subsequent <b>cocaine</b> CPP expression.
+CDK5	addiction	reward	20685978	We also found that basolateral (but not central) amygdala injections of the <strong>Cdk5</strong> inhibitor beta butyrolactone (100 ng/side) immediately (but not 6 h) after cocaine context pairings during training prevented subsequent cocaine <b>CPP</b> expression.
+CDK5	drug	cocaine	20685978	Results indicate that basolateral amygdala <strong>Cdk5</strong> activity is critical for consolidation and reconsolidation of the memories of <b>cocaine</b> associated environmental cues.
+CDK5	drug	cocaine	19017804	Striatal dysregulation of <strong>Cdk5</strong> alters locomotor responses to <b>cocaine</b>, motor learning, and dendritic morphology.
+CDK5	drug	cocaine	19017804	Cyclin dependent kinase 5 (<strong>Cdk5</strong>) regulates striatal dopamine neurotransmission and behavioral responses to <b>cocaine</b>.
+CDK5	drug	cocaine	19017804	<strong>Cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) regulates striatal dopamine neurotransmission and behavioral responses to <b>cocaine</b>.
+CDK5	drug	amphetamine	18991853	Transient enhanced expression of <strong>Cdk5</strong> activator p25 after acute and chronic d <b>amphetamine</b> administration.
+CDK5	drug	cocaine	18991853	Recently, chronic treatment with <b>cocaine</b> has been shown to upregulate the expression of cyclin dependent kinase 5 (<strong>cdk5</strong>) and its specific activator, p35, in the striatum, as a downstream target gene of DeltaFosB, and has been implicated in compensatory adaptive changes associated with psychostimulants.
+CDK5	drug	cocaine	18991853	Recently, chronic treatment with <b>cocaine</b> has been shown to upregulate the expression of <strong>cyclin dependent kinase 5</strong> (<strong>cdk5</strong>) and its specific activator, p35, in the striatum, as a downstream target gene of DeltaFosB, and has been implicated in compensatory adaptive changes associated with psychostimulants.
+CDK5	drug	amphetamine	18991853	In this study we report that the <strong>cdk5</strong>/p35 complex participates in acute and chronic d <b>amphetamine</b> (<b>AMPH</b>) evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic <b>AMPH</b> administration.
+CDK5	drug	amphetamine	18991853	Pak1, a substrate for <strong>cdk5</strong>, is also enriched in the synaptosomal fraction of acute <b>AMPH</b> treated rats.
+CDK5	addiction	sensitization	18991853	Our data suggest that the transient upregulation of p25 may regulate the activity of <strong>cdk5</strong> in phosphorylating particular substrates, such as Pak1, implicated in the compensatory adaptive morphophysiologic changes associated with the process of behavioral <b>sensitization</b> to psychostimulants.
+CDK5	drug	opioid	18082850	<b>Morphine</b> induced analgesic tolerance, locomotor sensitization and physical dependence do not require modification of mu <b>opioid</b> receptor, <strong>cdk5</strong> and adenylate cyclase activity.
+CDK5	addiction	dependence	18082850	Morphine induced analgesic tolerance, locomotor sensitization and physical <b>dependence</b> do not require modification of mu opioid receptor, <strong>cdk5</strong> and adenylate cyclase activity.
+CDK5	addiction	sensitization	18082850	Morphine induced analgesic tolerance, locomotor <b>sensitization</b> and physical dependence do not require modification of mu opioid receptor, <strong>cdk5</strong> and adenylate cyclase activity.
+CDK5	addiction	sensitization	18082850	Second, <strong>cdk5</strong> and p35 protein levels were unchanged in caudate putamen, nucleus accumbens and prefrontal cortex of mice displaying locomotor <b>sensitization</b>.
+CDK5	drug	opioid	18082850	Therefore, the expression of behavioral adaptations to chronic <b>morphine</b> treatment was not associated with the regulation of micro <b>opioid</b> receptor, <strong>cdk5</strong> or adenylate cyclase activity in relevant brain areas.
+CDK5	drug	cocaine	18032670	<strong>Cdk5</strong> modulates <b>cocaine</b> reward, motivation, and striatal neuron excitability.
+CDK5	addiction	reward	18032670	<strong>Cdk5</strong> modulates cocaine <b>reward</b>, motivation, and striatal neuron excitability.
+CDK5	drug	cocaine	18032670	In this model system, loss of <strong>Cdk5</strong> in the adult forebrain increased the psychomotor activating effects of <b>cocaine</b>.
+CDK5	addiction	reward	18032670	Additionally, these CaMKII Cre <strong>Cdk5</strong> cKO mice show enhanced <b>incentive</b> motivation for food as assessed by instrumental responding on a progressive ratio schedule of <b>reinforcement</b>.
+CDK5	drug	cocaine	18032670	Targeted knock out of <strong>Cdk5</strong> in the NAc facilitated <b>cocaine</b> induced locomotor sensitization and conditioned place preference for <b>cocaine</b>.
+CDK5	addiction	sensitization	18032670	Targeted knock out of <strong>Cdk5</strong> in the NAc facilitated cocaine induced locomotor <b>sensitization</b> and conditioned place preference for cocaine.
+CDK5	drug	cocaine	18032670	These results suggest that <strong>Cdk5</strong> acts as a negative regulator of neuronal excitability in the NAc and that <strong>Cdk5</strong> may govern the behavioral effects of <b>cocaine</b> and motivation for reinforcement.
+CDK5	addiction	reward	18032670	These results suggest that <strong>Cdk5</strong> acts as a negative regulator of neuronal excitability in the NAc and that <strong>Cdk5</strong> may govern the behavioral effects of cocaine and motivation for <b>reinforcement</b>.
+CDK5	drug	cocaine	17360491	Inhibition of <strong>Cdk5</strong> in the nucleus accumbens enhances the locomotor activating and incentive motivational effects of <b>cocaine</b>.
+CDK5	addiction	reward	17360491	Inhibition of <strong>Cdk5</strong> in the nucleus accumbens enhances the locomotor activating and <b>incentive</b> motivational effects of cocaine.
+CDK5	drug	cocaine	17360491	Cyclin dependent kinase 5 (<strong>Cdk5</strong>) regulates striatal dopamine signaling and is a downstream target gene of the transcription factor DeltaFosB, which accumulates in striatal neurons after chronic <b>cocaine</b> exposure.
+CDK5	drug	cocaine	17360491	<strong>Cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) regulates striatal dopamine signaling and is a downstream target gene of the transcription factor DeltaFosB, which accumulates in striatal neurons after chronic <b>cocaine</b> exposure.
+CDK5	drug	cocaine	17360491	Here we investigated the role of <strong>Cdk5</strong> activity in the nucleus accumbens (NAc) on <b>cocaine</b> induced locomotor sensitization, responding for reward associated stimuli (conditioned reinforcement), and <b>cocaine</b> self administration under a progressive ratio schedule.
+CDK5	addiction	reward	17360491	Here we investigated the role of <strong>Cdk5</strong> activity in the nucleus accumbens (NAc) on cocaine induced locomotor sensitization, responding for <b>reward</b> associated stimuli (conditioned <b>reinforcement</b>), and cocaine self administration under a progressive ratio schedule.
+CDK5	addiction	sensitization	17360491	Here we investigated the role of <strong>Cdk5</strong> activity in the nucleus accumbens (NAc) on cocaine induced locomotor <b>sensitization</b>, responding for reward associated stimuli (conditioned reinforcement), and cocaine self administration under a progressive ratio schedule.
+CDK5	drug	cocaine	17360491	Repeated infusions of the <strong>Cdk5</strong> inhibitor roscovitine into the NAc before <b>cocaine</b> injections augmented both the development and expression of <b>cocaine</b> sensitization without having any intrinsic stimulant actions of its own.
+CDK5	addiction	sensitization	17360491	Repeated infusions of the <strong>Cdk5</strong> inhibitor roscovitine into the NAc before cocaine injections augmented both the development and expression of cocaine <b>sensitization</b> without having any intrinsic stimulant actions of its own.
+CDK5	drug	cocaine	17360491	Repeated inhibition of <strong>Cdk5</strong> within the NAc also robustly enhanced the incentive motivational effects of <b>cocaine</b>, similar to the effect of prior repeated <b>cocaine</b> exposure.
+CDK5	addiction	reward	17360491	Repeated inhibition of <strong>Cdk5</strong> within the NAc also robustly enhanced the <b>incentive</b> motivational effects of cocaine, similar to the effect of prior repeated cocaine exposure.
+CDK5	drug	cocaine	17360491	These results demonstrate profound and persistent effects of NAc <strong>Cdk5</strong> inhibition on locomotor sensitization and incentive motivational processes and provide direct evidence for a role for striatal <strong>Cdk5</strong> induced alterations in the brain's long term adaptations to <b>cocaine</b>.
+CDK5	addiction	reward	17360491	These results demonstrate profound and persistent effects of NAc <strong>Cdk5</strong> inhibition on locomotor sensitization and <b>incentive</b> motivational processes and provide direct evidence for a role for striatal <strong>Cdk5</strong> induced alterations in the brain's long term adaptations to cocaine.
+CDK5	addiction	sensitization	17360491	These results demonstrate profound and persistent effects of NAc <strong>Cdk5</strong> inhibition on locomotor <b>sensitization</b> and incentive motivational processes and provide direct evidence for a role for striatal <strong>Cdk5</strong> induced alterations in the brain's long term adaptations to cocaine.
+CDK5	drug	cocaine	17339080	Increased accumbens <strong>Cdk5</strong> expression in rats after short access to self administered <b>cocaine</b>, but not after long access sessions.
+CDK5	drug	cocaine	17339080	Upregulation of cyclin dependent kinase 5 (<strong>Cdk5</strong>) after chronic <b>cocaine</b> administration has led to speculation that <strong>Cdk5</strong> plays an important role in drug addiction.
+CDK5	addiction	addiction	17339080	Upregulation of cyclin dependent kinase 5 (<strong>Cdk5</strong>) after chronic cocaine administration has led to speculation that <strong>Cdk5</strong> plays an important role in drug <b>addiction</b>.
+CDK5	drug	cocaine	17339080	Upregulation of <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) after chronic <b>cocaine</b> administration has led to speculation that <strong>Cdk5</strong> plays an important role in drug addiction.
+CDK5	addiction	addiction	17339080	Upregulation of <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) after chronic cocaine administration has led to speculation that <strong>Cdk5</strong> plays an important role in drug <b>addiction</b>.
+CDK5	drug	cocaine	17339080	The present study utilized <b>cocaine</b> self administration and food reinforced operant procedures to assess possible relationships between <b>cocaine</b> intake, food reinforced operant responding, behavioral activity, and <strong>Cdk5</strong> levels in the nucleus accumbens (NAcc), ventral tegmental area (VTA), and prefrontal cortex (PFC) in rats.
+CDK5	addiction	reward	17339080	The present study utilized cocaine self administration and food reinforced <b>operant</b> procedures to assess possible relationships between cocaine intake, food reinforced <b>operant</b> responding, behavioral activity, and <strong>Cdk5</strong> levels in the nucleus accumbens (NAcc), ventral tegmental area (VTA), and prefrontal cortex (PFC) in rats.
+CDK5	drug	cocaine	17339080	In Experiment 1, animals undergoing daily <b>cocaine</b> self administration (1 h/30 days) or food reinforced operant sessions (20 min/30 days) showed significant between group differences in operant responding and behavioral activity, but no significant differences in NAcc, VTA or PFC <strong>Cdk5</strong> levels compared to a Handled Control group.
+CDK5	addiction	reward	17339080	In Experiment 1, animals undergoing daily cocaine self administration (1 h/30 days) or food reinforced <b>operant</b> sessions (20 min/30 days) showed significant between group differences in <b>operant</b> responding and behavioral activity, but no significant differences in NAcc, VTA or PFC <strong>Cdk5</strong> levels compared to a Handled Control group.
+CDK5	drug	cocaine	17339080	In Experiment 2, animals that had self administered <b>cocaine</b> in 10 daily 1 h sessions (Short Access <b>Cocaine</b>) showed significantly greater NAcc <strong>Cdk5</strong> expression compared to an Unhandled Control group, and no evidence of <b>cocaine</b> induced behavioral sensitization.
+CDK5	addiction	sensitization	17339080	In Experiment 2, animals that had self administered cocaine in 10 daily 1 h sessions (Short Access Cocaine) showed significantly greater NAcc <strong>Cdk5</strong> expression compared to an Unhandled Control group, and no evidence of cocaine induced behavioral <b>sensitization</b>.
+CDK5	drug	cocaine	17339080	Animals given 4 h daily access to <b>cocaine</b> over the same number of sessions (Long Access <b>Cocaine</b>) showed significantly enhanced <b>cocaine</b> reinforced responding and locomotor activation by the end of the sessions, but no significant differences in <strong>Cdk5</strong> expression compared to Control animals.
+CDK5	drug	cocaine	17339080	These findings suggest that overexpression of <strong>Cdk5</strong> may be a transient adaptation to <b>cocaine</b> experience that subsides with increased <b>cocaine</b> exposure and does not correspond with measures of <b>cocaine</b> induced behavioral sensitization.
+CDK5	addiction	sensitization	17339080	These findings suggest that overexpression of <strong>Cdk5</strong> may be a transient adaptation to cocaine experience that subsides with increased cocaine exposure and does not correspond with measures of cocaine induced behavioral <b>sensitization</b>.
+CDK5	drug	alcohol	16899035	Neuroadaptations of <strong>Cdk5</strong> in cholinergic interneurons of the nucleus accumbens and prefrontal cortex of inbred <b>alcohol</b> preferring rats following voluntary <b>alcohol</b> drinking.
+CDK5	drug	alcohol	16899035	Cyclin dependent kinase 5 (<strong>Cdk5</strong>) immunoreactivity (IR), a marker of neuronal plasticity, was examined in cholinergic neurons of the nucleus accumbens (NuAcc) and prefrontal cortex (PFC) and other brain areas implicated in <b>alcohol</b> drinking, using dual immunocytochemical (ICC) procedures.
+CDK5	drug	alcohol	16899035	<strong>Cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) immunoreactivity (IR), a marker of neuronal plasticity, was examined in cholinergic neurons of the nucleus accumbens (NuAcc) and prefrontal cortex (PFC) and other brain areas implicated in <b>alcohol</b> drinking, using dual immunocytochemical (ICC) procedures.
+CDK5	drug	alcohol	16899035	Single <strong>Cdk5</strong> IR was also examined in several brain areas implicated in <b>alcohol</b> drinking.
+CDK5	drug	alcohol	16899035	<b>Alcohol</b> drinking resulted in a 51% increase in <strong>Cdk5</strong> IR cholinergic interneurons in the shell NuAcc, while in the PFC there was a 51% decrease in the percent of <strong>Cdk5</strong> IR cholinergic interneurons in the infralimbic region and a 46% decrease in <strong>Cdk5</strong> IR cholinergic interneurons in the prelimbic region.
+CDK5	drug	alcohol	16899035	This study identified <strong>Cdk5</strong> neuroadaptation in cholinergic interneurons of the NuAcc and PFC and in other neurons of the CNA following 1 month of <b>alcohol</b> drinking.
+CDK5	drug	opioid	16637594	We also report here that protein kinase C, Janus kinase/signal transducer and activator of transcription pathway, <strong>cyclin dependent kinase 5</strong> and tyrosine kinase cascade are directly involved in the neuron glia communication during the development of synaptic plasticity induced by chronic <b>morphine</b> treatment.
+CDK5	drug	cocaine	16525043	<b>Cocaine</b> self administration and striatal levels of dopamine after acute "binge" <b>cocaine</b> administration were measured in separate lines of mice with alanine mutations introduced into DARPP 32 at either Thr34 (protein kinase A site, Thr34A), Thr75, (<strong>cyclin dependent kinase 5</strong> site, Thr75A), Ser97 (kinase CK2 site, Ser97A), or Ser130 (kinase CK1 site, Ser130A).
+CDK5	addiction	intoxication	16525043	Cocaine self administration and striatal levels of dopamine after acute "<b>binge</b>" cocaine administration were measured in separate lines of mice with alanine mutations introduced into DARPP 32 at either Thr34 (protein kinase A site, Thr34A), Thr75, (<strong>cyclin dependent kinase 5</strong> site, Thr75A), Ser97 (kinase CK2 site, Ser97A), or Ser130 (kinase CK1 site, Ser130A).
+CDK5	drug	cocaine	16476411	The effect of <b>cocaine</b> on depotentiation was prevented by D1 but not D2 dopamine receptor antagonists and was mimicked by pharmacological inhibition of <strong>cyclin dependent kinase 5</strong>, to enhance D1 receptor associated intracellular signaling.
+CDK5	drug	cocaine	16263094	The effect of 'binge' <b>cocaine</b> administration on the expression of <strong>cyclin dependent kinase 5</strong> and its activator p35 in various regions of rat brain.
+CDK5	addiction	intoxication	16263094	The effect of '<b>binge</b>' cocaine administration on the expression of <strong>cyclin dependent kinase 5</strong> and its activator p35 in various regions of rat brain.
+CDK5	drug	cocaine	16263094	The present study was aimed at determining whether the administration of <b>cocaine</b> in 'binge' pattern regimen that evoked tolerance to the locomotor stimulant effects of <b>cocaine</b> also influenced the expression of cyclin dependent kinase 5 (<strong>Cdk5</strong>) and its activator p35 in the amygdala, medial prefrontal cortex, nucleus accumbens septi and caudate putamen.
+CDK5	addiction	intoxication	16263094	The present study was aimed at determining whether the administration of cocaine in '<b>binge</b>' pattern regimen that evoked tolerance to the locomotor stimulant effects of cocaine also influenced the expression of cyclin dependent kinase 5 (<strong>Cdk5</strong>) and its activator p35 in the amygdala, medial prefrontal cortex, nucleus accumbens septi and caudate putamen.
+CDK5	drug	cocaine	16263094	The present study was aimed at determining whether the administration of <b>cocaine</b> in 'binge' pattern regimen that evoked tolerance to the locomotor stimulant effects of <b>cocaine</b> also influenced the expression of <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) and its activator p35 in the amygdala, medial prefrontal cortex, nucleus accumbens septi and caudate putamen.
+CDK5	addiction	intoxication	16263094	The present study was aimed at determining whether the administration of cocaine in '<b>binge</b>' pattern regimen that evoked tolerance to the locomotor stimulant effects of cocaine also influenced the expression of <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) and its activator p35 in the amygdala, medial prefrontal cortex, nucleus accumbens septi and caudate putamen.
+CDK5	drug	cocaine	16263094	Western blot techniques revealed that acute and repeated 'binge' <b>cocaine</b> decreased expression of the <strong>Cdk5</strong> protein in the amygdala.
+CDK5	addiction	intoxication	16263094	Western blot techniques revealed that acute and repeated '<b>binge</b>' cocaine decreased expression of the <strong>Cdk5</strong> protein in the amygdala.
+CDK5	drug	cocaine	16263094	In the medial prefrontal cortex, only exposure to repeated 'binge' <b>cocaine</b> decreased the content of the <strong>Cdk5</strong> protein.
+CDK5	addiction	intoxication	16263094	In the medial prefrontal cortex, only exposure to repeated '<b>binge</b>' cocaine decreased the content of the <strong>Cdk5</strong> protein.
+CDK5	drug	cocaine	16263094	'Binge' <b>cocaine</b> administration also altered the expression of <strong>Cdk5</strong> activator p35 protein.
+CDK5	addiction	intoxication	16263094	'<b>Binge</b>' cocaine administration also altered the expression of <strong>Cdk5</strong> activator p35 protein.
+CDK5	drug	cocaine	16263094	In neither the nucleus accumbens septi nor the caudate putamen acute or repeated 'binge' <b>cocaine</b> modified the expression of <strong>Cdk5</strong> and p35.
+CDK5	addiction	intoxication	16263094	In neither the nucleus accumbens septi nor the caudate putamen acute or repeated '<b>binge</b>' cocaine modified the expression of <strong>Cdk5</strong> and p35.
+CDK5	drug	cocaine	16263094	The above data indicate that in contrast to sensitizing doses of <b>cocaine</b>, a single and repeated binge of <b>cocaine</b>, which evoked tolerance to its locomotor stimulant effects, decreases expression of <strong>Cdk5</strong> and p35 and possibly decreases the efficacy of neurotransmission or induces brain plastic changes regulated by <strong>Cdk5</strong> and its activator p35.
+CDK5	addiction	intoxication	16263094	The above data indicate that in contrast to sensitizing doses of cocaine, a single and repeated <b>binge</b> of cocaine, which evoked tolerance to its locomotor stimulant effects, decreases expression of <strong>Cdk5</strong> and p35 and possibly decreases the efficacy of neurotransmission or induces brain plastic changes regulated by <strong>Cdk5</strong> and its activator p35.
+CDK5	drug	opioid	15935062	Implication of <strong>cyclin dependent kinase 5</strong> in the development of psychological dependence on and behavioral sensitization to <b>morphine</b>.
+CDK5	addiction	dependence	15935062	Implication of <strong>cyclin dependent kinase 5</strong> in the development of psychological <b>dependence</b> on and behavioral sensitization to morphine.
+CDK5	addiction	sensitization	15935062	Implication of <strong>cyclin dependent kinase 5</strong> in the development of psychological dependence on and behavioral <b>sensitization</b> to morphine.
+CDK5	drug	opioid	15935062	In the present study, we investigated the role of cyclin dependent kinase 5 (<strong>cdk5</strong>) in the brain dynamics changed by repeated in vivo treatment with <b>morphine</b>.
+CDK5	drug	opioid	15935062	In the present study, we investigated the role of <strong>cyclin dependent kinase 5</strong> (<strong>cdk5</strong>) in the brain dynamics changed by repeated in vivo treatment with <b>morphine</b>.
+CDK5	drug	opioid	15935062	The level of phosphorylated <strong>cdk5</strong> was significantly increased in the cingulate cortex of mice showing the <b>morphine</b> induced rewarding effect.
+CDK5	drug	opioid	15935062	In addition, the dose response effect of the <b>morphine</b> induced rewarding effect was dramatically attenuated in <strong>cdk5</strong> heterozygous (+/ ) knockout mice.
+CDK5	drug	opioid	15935062	Furthermore, the development of behavioral sensitization by intermittent administration of <b>morphine</b> was virtually abolished in <strong>cdk5</strong> (+/ ) mice.
+CDK5	addiction	sensitization	15935062	Furthermore, the development of behavioral <b>sensitization</b> by intermittent administration of morphine was virtually abolished in <strong>cdk5</strong> (+/ ) mice.
+CDK5	drug	opioid	15935062	These findings suggest that the induction and/or activation of <strong>cdk5</strong> are implicated in the development of psychological dependence on <b>morphine</b>.
+CDK5	addiction	dependence	15935062	These findings suggest that the induction and/or activation of <strong>cdk5</strong> are implicated in the development of psychological <b>dependence</b> on morphine.
+CDK5	drug	cocaine	15665076	Increased activity of <strong>cyclin dependent kinase 5</strong> leads to attenuation of <b>cocaine</b> mediated dopamine signaling.
+CDK5	drug	cocaine	15665076	Cyclin dependent kinase 5 (<strong>Cdk5</strong>) and its activator p35, proteins involved in phosphorylation of substrates in postmitotic neurons, have been found to be up regulated after chronic exposure to <b>cocaine</b>.
+CDK5	drug	cocaine	15665076	<strong>Cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) and its activator p35, proteins involved in phosphorylation of substrates in postmitotic neurons, have been found to be up regulated after chronic exposure to <b>cocaine</b>.
+CDK5	drug	cocaine	15665076	We report here that increased <strong>Cdk5</strong> activity, as a result of p35 but not of <strong>Cdk5</strong> overexpression, leads to attenuation of <b>cocaine</b> mediated dopamine signaling.
+CDK5	drug	cocaine	15665076	These results support the idea that <strong>Cdk5</strong> activity is involved in altered gene expression after chronic exposure to <b>cocaine</b> and hence impacts the long lasting changes in neuronal function underlying <b>cocaine</b> addiction.
+CDK5	addiction	addiction	15665076	These results support the idea that <strong>Cdk5</strong> activity is involved in altered gene expression after chronic exposure to cocaine and hence impacts the long lasting changes in neuronal function underlying cocaine <b>addiction</b>.
+CDK5	drug	cocaine	15659224	Neuroadaptations of total levels of adenylate cyclase, protein kinase A, tyrosine hydroxylase, <strong>cdk5</strong> and neurofilaments in the nucleus accumbens and ventral tegmental area do not correlate with expression of sensitized or tolerant locomotor responses to <b>cocaine</b>.
+CDK5	drug	cocaine	15542734	Furthermore, the morphological changes associated with chronic <b>cocaine</b> exposure are dependent on <strong>Cdk5</strong>.
+CDK5	drug	amphetamine	15536496	Enhanced <strong>Cdk5</strong> activity and p35 translocation in the ventral striatum of acute and chronic <b>methamphetamine</b> treated rats.
+CDK5	drug	cocaine	15536496	The cyclin dependent kinase <strong>Cdk5</strong> and DARPP 32 (dopamine  and cAMP regulated phosphoprotein of Mr 32 kDa) dependent signaling have been implicated in the regulation of dopaminergic neurotransmission after chronic <b>cocaine</b> treatment.
+CDK5	drug	amphetamine	15536496	In this study, we examined if <strong>Cdk5</strong> signaling participates in the behavioral and biochemical effect of acute and chronic <b>methamphetamine</b> (<b>METH</b>) treatment.
+CDK5	drug	amphetamine	15536496	We found that <strong>Cdk5</strong> activity and the membrane fraction of p35 protein, a <strong>Cdk5</strong> activator, in the ventral striatum increased transiently after an injection of 4 mg/kg <b>METH</b>, while intra accumbens treatment with a <strong>Cdk5</strong> inhibitor, roscovitine, prevented the acute <b>METH</b> induced locomotor activation.
+CDK5	drug	amphetamine	15536496	The phosphorylation of DARPP 32 at both Thr75 and Thr34 was differentially regulated after acute <b>METH</b> treatment, but the levels of total <strong>Cdk5</strong>, p35, and DARPP 32 remained the same.
+CDK5	drug	amphetamine	15536496	To determine if <strong>Cdk5</strong> signaling was associated with behavior sensitization to <b>METH</b>, rats that received repetitive injections of <b>METH</b> (4 mg/kg) for 14 consecutive days were analyzed at withdrawal day 7.
+CDK5	addiction	sensitization	15536496	To determine if <strong>Cdk5</strong> signaling was associated with behavior <b>sensitization</b> to METH, rats that received repetitive injections of METH (4 mg/kg) for 14 consecutive days were analyzed at withdrawal day 7.
+CDK5	addiction	withdrawal	15536496	To determine if <strong>Cdk5</strong> signaling was associated with behavior sensitization to METH, rats that received repetitive injections of METH (4 mg/kg) for 14 consecutive days were analyzed at <b>withdrawal</b> day 7.
+CDK5	drug	amphetamine	15536496	The results indicate that <strong>Cdk5</strong> activity and p35 translocation in the ventral striatum were upregulated in <b>METH</b> sensitized rats; treatment with roscovitine in the nucleus accumbens effectively suppressed the 1 mg/kg <b>METH</b> induced behavioral sensitization.
+CDK5	addiction	sensitization	15536496	The results indicate that <strong>Cdk5</strong> activity and p35 translocation in the ventral striatum were upregulated in METH sensitized rats; treatment with roscovitine in the nucleus accumbens effectively suppressed the 1 mg/kg METH induced behavioral <b>sensitization</b>.
+CDK5	drug	amphetamine	15536496	The overall results demonstrate that <strong>Cdk5</strong>/p35 and downstream signaling in the ventral striatum play a critical role in the effects of acute <b>METH</b> treatment as well as the development of behavioral <b>METH</b> sensitization.
+CDK5	addiction	sensitization	15536496	The overall results demonstrate that <strong>Cdk5</strong>/p35 and downstream signaling in the ventral striatum play a critical role in the effects of acute METH treatment as well as the development of behavioral METH <b>sensitization</b>.
+CDK5	addiction	reward	15447670	Within the <b>reward</b>/motor circuitry of the basal ganglia, <strong>Cdk5</strong> regulates dopamine neurotransmission via phosphorylation of the postsynaptic signal transduction pathway integrator, DARPP 32 (dopamine  and cyclic AMP regulated phosphoprotein, M(r) 32,000).
+CDK5	drug	cocaine	15447670	These results demonstrate direct and indirect regulation of the phosphorylation state of a <strong>Cdk5</strong>/ERK1/2 site on TH and suggest a role for these pathways in the neuroadaptive changes associated with chronic <b>cocaine</b> exposure.
+CDK5	drug	cocaine	15066157	Repeated acetyl l carnitine administration increases phospho Thr34 DARPP 32 levels and antagonizes <b>cocaine</b> induced increase in <strong>Cdk5</strong> and phospho Thr75 DARPP 32 levels in rat striatum.
+CDK5	drug	cocaine	15066157	We compared the effects of repeated <b>cocaine</b> and repeated ALCAR administrations on the behavioural response to <b>cocaine</b> challenge and on the DARPP 32 phosphorylation pattern and cyclin dependent kinase 5 (<strong>Cdk5</strong>) levels in the striatum.
+CDK5	drug	cocaine	15066157	We compared the effects of repeated <b>cocaine</b> and repeated ALCAR administrations on the behavioural response to <b>cocaine</b> challenge and on the DARPP 32 phosphorylation pattern and <strong>cyclin dependent kinase 5</strong> (<strong>Cdk5</strong>) levels in the striatum.
+CDK5	drug	cocaine	15066157	Moreover, <b>cocaine</b>, but not ALCAR, increased DeltaFosB and <strong>Cdk5</strong> expression, and the increase in <strong>Cdk5</strong> was antagonized by ALCAR administration in rats receiving combined treatments.
+CDK5	drug	cocaine	14769920	Inhibitors of <strong>CDK5</strong> increase evoked dopamine release in a way that is additive to that of <b>cocaine</b>.
+CDK5	drug	cocaine	14749431	The N terminal domain of PSD 95 contains three consensus phosphorylation sites for cyclin dependent kinase 5 (<strong>cdk5</strong>), a proline directed serine threonine kinase essential for brain development and implicated in synaptic plasticity, dopamine signaling, <b>cocaine</b> addiction, and neurodegenerative disorders.
+CDK5	addiction	addiction	14749431	The N terminal domain of PSD 95 contains three consensus phosphorylation sites for cyclin dependent kinase 5 (<strong>cdk5</strong>), a proline directed serine threonine kinase essential for brain development and implicated in synaptic plasticity, dopamine signaling, cocaine <b>addiction</b>, and neurodegenerative disorders.
+CDK5	drug	cocaine	14749431	The N terminal domain of PSD 95 contains three consensus phosphorylation sites for <strong>cyclin dependent kinase 5</strong> (<strong>cdk5</strong>), a proline directed serine threonine kinase essential for brain development and implicated in synaptic plasticity, dopamine signaling, <b>cocaine</b> addiction, and neurodegenerative disorders.
+CDK5	addiction	addiction	14749431	The N terminal domain of PSD 95 contains three consensus phosphorylation sites for <strong>cyclin dependent kinase 5</strong> (<strong>cdk5</strong>), a proline directed serine threonine kinase essential for brain development and implicated in synaptic plasticity, dopamine signaling, cocaine <b>addiction</b>, and neurodegenerative disorders.
+CDK5	drug	cocaine	12787079	In the accumbens of <b>cocaine</b> trained rats, GluR1 and NMDAR1 levels were increased on days 1 and 90, while GluR2 levels were increased on days 1 and 30, but not day 90; PKA activity levels were increased on days 1 and 30, but not day 90, while AC activity, TH and <strong>cdk5</strong> levels were unaltered.
+CDK5	drug	cocaine	12787079	In the VTA of <b>cocaine</b> trained rats, NMDAR1 levels were increased for up to 90 days, while GluR2 levels were increased only on day 1; TH and <strong>Cdk5</strong> levels were increased only on day 1, while PKA and AC activity levels were unaltered.
+CDK5	drug	cocaine	12706249	However, expression of Deltac Jun in adult mice blocked the ability of chronic <b>cocaine</b> administration to induce three known targets for AP 1 in the NAc: the AMPA glutamate receptor subunit GluR2, the cyclin dependent protein kinase <strong>Cdk5</strong>, and the transcription factor nuclear factor kappaB (NFkappaB), without affecting several other proteins examined for comparison.
+CDK5	drug	opioid	12637947	Downregulation of neuronal <strong>cdk5</strong>/p35 in <b>opioid</b> addicts and opiate treated rats: relation to neurofilament phosphorylation.
+CDK5	drug	opioid	12637947	Since <b>opioid</b> addiction was associated with hyperphosphorylation of neurofilament (NF) in postmortem human brains, this study was undertaken to assess the status of the <strong>cdk5</strong>/p35 complex and its relation with NF H phosphorylation in brains of chronic <b>opioid</b> abusers.
+CDK5	addiction	addiction	12637947	Since opioid <b>addiction</b> was associated with hyperphosphorylation of neurofilament (NF) in postmortem human brains, this study was undertaken to assess the status of the <strong>cdk5</strong>/p35 complex and its relation with NF H phosphorylation in brains of chronic opioid abusers.
+CDK5	drug	opioid	12637947	Decreased immunodensities of <strong>cdk5</strong> (18%) and p35 (26 44%) were found in the prefrontal cortex of <b>opioid</b> addicts compared with matched controls.
+CDK5	drug	opioid	12637947	Acute treatment of rats with <b>morphine</b> (30 mg/kg, 2 h) increased the density of <strong>cdk5</strong> (35%), but not that of p35, in the cerebral cortex.
+CDK5	drug	opioid	12637947	In contrast, chronic <b>morphine</b> (10 100 mg/kg for 5 days) induced marked decreases in <strong>cdk5</strong> (40%) and p35 (47%) in rat brain.
+CDK5	addiction	addiction	12637947	The results suggest that opiate <b>addiction</b> is associated with downregulation of <strong>cdk5</strong>/p35 levels in the brain.
+CDK5	drug	cocaine	11268215	Effects of chronic exposure to <b>cocaine</b> are regulated by the neuronal protein <strong>Cdk5</strong>.
+CDK5	drug	cocaine	11268215	Overexpression of DeltaFosB, or chronic <b>cocaine</b> administration, raised levels of <strong>Cdk5</strong> messenger RNA, protein, and activity in the striatum.
+CDK5	drug	cocaine	11268215	Moreover, injection of <strong>Cdk5</strong> inhibitors into the striatum potentiated behavioural effects of repeated <b>cocaine</b> administration.
+CDK5	drug	cocaine	11268215	Our results suggest that changes in <strong>Cdk5</strong> levels mediated by DeltaFosB, and resulting alterations in signalling involving D1 dopamine receptors, contribute to adaptive changes in the brain related to <b>cocaine</b> addiction.
+CDK5	addiction	addiction	11268215	Our results suggest that changes in <strong>Cdk5</strong> levels mediated by DeltaFosB, and resulting alterations in signalling involving D1 dopamine receptors, contribute to adaptive changes in the brain related to cocaine <b>addiction</b>.
+SRC	addiction	sensitization	32579948	A <strong>Src</strong> family kinase maintains latent <b>sensitization</b> in rats, a model of inflammatory and neuropathic pain.
+SRC	addiction	sensitization	32579948	We hypothesized that <strong>Src</strong> family kinases (SFKs) maintain latent <b>sensitization</b> and tested this hypothesis by inducing latent <b>sensitization</b> in rats with complete Freund's adjuvant (CFA) or spared nerve injury.
+SRC	drug	cocaine	31092585	Synaptic Microtubule Associated Protein EB3 and <strong>SRC</strong> Phosphorylation Mediate Structural and Behavioral Adaptations During Withdrawal From <b>Cocaine</b> Self Administration.
+SRC	addiction	withdrawal	31092585	Synaptic Microtubule Associated Protein EB3 and <strong>SRC</strong> Phosphorylation Mediate Structural and Behavioral Adaptations During <b>Withdrawal</b> From Cocaine Self Administration.
+SRC	drug	cocaine	31092585	We then investigated the roles of microtubule end binding protein 3 (EB3) and <strong>SRC</strong> kinase in the neuronal and behavioral responses to volitionally administered <b>cocaine</b>.
+SRC	addiction	withdrawal	31092585	In synaptoneurosomal fractions from the NAc of self administering male rats, the phosphorylation of <strong>SRC</strong> at an activating site was induced after 1 d of <b>withdrawal</b>, while EB3 levels were increased only after 30 d of <b>withdrawal</b>.
+SRC	drug	cocaine	31092585	Blocking <strong>SRC</strong> phosphorylation during early withdrawal by virally overexpressing SRCIN1, a negative regulator of <strong>SRC</strong> activity known to interact with EB3, abolished the incubation of <b>cocaine</b> craving in both male and female rats.
+SRC	addiction	relapse	31092585	Blocking <strong>SRC</strong> phosphorylation during early withdrawal by virally overexpressing SRCIN1, a negative regulator of <strong>SRC</strong> activity known to interact with EB3, abolished the incubation of cocaine <b>craving</b> in both male and female rats.
+SRC	addiction	withdrawal	31092585	Blocking <strong>SRC</strong> phosphorylation during early <b>withdrawal</b> by virally overexpressing SRCIN1, a negative regulator of <strong>SRC</strong> activity known to interact with EB3, abolished the incubation of cocaine craving in both male and female rats.
+SRC	drug	cocaine	31092585	These findings suggest that microtubule associated signaling proteins such as EB3 cooperate with actin remodeling pathways, notably <strong>SRC</strong> kinase activity, to establish and maintain long lasting cellular and behavioral alterations following <b>cocaine</b> self administration.SIGNIFICANCE STATEMENT Drug induced morphological restructuring of dendritic spines of nucleus accumbens neurons is thought to be one of the cellular substrates of long lasting drug associated memories.
+SRC	drug	opioid	30983591	Alternative approaches include inhibition of peripheral μ <b>opioid</b> receptors and blockade of downstream signalling mechanisms, such as the non receptor tyrosine kinase <strong>Src</strong> or N methyl D aspartate receptors.
+SRC	drug	amphetamine	30599269	The mGlu1/5 agonist stimulated <strong>Src</strong> kinase phosphorylation was also augmented in rats treated with <b>amphetamine</b>.
+SRC	drug	alcohol	30536923	Fyn is a member of the <strong>Src</strong> family of protein tyrosine kinases (PTKs) that plays an important role not only in normal synaptic functions but also in brain pathologies including <b>alcohol</b> use disorder.
+SRC	drug	alcohol	30536923	Here, we used AZD0530, a CNS penetrable inhibitor of <strong>Src</strong> PTKs developed for the treatment of Alzheimer disease and cancer and tested its efficacy to suppress <b>alcohol</b> dependent molecular and behavioral effects.
+SRC	drug	opioid	28855588	<b>Morphine</b> activation of mu <b>opioid</b> receptors causes disinhibition of neurons in the ventral tegmental area mediated by β arrestin2 and c <strong>Src</strong>.
+SRC	drug	opioid	28855588	The tyrosine kinase, c <strong>Src</strong>, participates in mu <b>opioid</b> receptor (MOP) mediated inhibition in sensory neurons in which β arrestin2 (β arr2) is implicated in its recruitment.
+SRC	drug	opioid	28855588	Mice lacking β arr2 exhibit increased sensitivity to <b>morphine</b> reinforcement; however, whether β arr2 and/or c <strong>Src</strong> participate in the actions of <b>opioids</b> in neurons within the reward pathway is unknown.
+SRC	addiction	reward	28855588	Mice lacking β arr2 exhibit increased sensitivity to morphine <b>reinforcement</b>; however, whether β arr2 and/or c <strong>Src</strong> participate in the actions of opioids in neurons within the <b>reward</b> pathway is unknown.
+SRC	drug	opioid	28855588	We examined the involvement of MOPs, DOPs, β arr2 and c <strong>Src</strong> in the inhibition by <b>morphine</b> of GABAergic inhibitory postsynaptic currents (IPSCs) recorded from neurons in the mouse ventral tegmental area.
+SRC	drug	opioid	28855588	The application of the c <strong>Src</strong> inhibitor, PP2, to WT neurons also reduced inhibition by <b>morphine</b>, while the inactive PP3, and the MEK inhibitor, SL327, had no effect.
+SRC	drug	opioid	28855588	These data suggest that inhibition of IPSCs by <b>morphine</b> involves a β arr2/c <strong>Src</strong> mediated mechanism.
+SRC	drug	opioid	28820778	<strong>Src</strong> Kinase Inhibition Attenuates <b>Morphine</b> Tolerance without Affecting Reinforcement or Psychomotor Stimulation.
+SRC	addiction	reward	28820778	<strong>Src</strong> Kinase Inhibition Attenuates Morphine Tolerance without Affecting <b>Reinforcement</b> or Psychomotor Stimulation.
+SRC	drug	opioid	28820778	We explored the role of <strong>Src</strong> kinase in <b>morphine</b> analgesic tolerance, locomotor stimulation, and reinforcement in C57BL/6 mice.
+SRC	addiction	reward	28820778	We explored the role of <strong>Src</strong> kinase in morphine analgesic tolerance, locomotor stimulation, and <b>reinforcement</b> in C57BL/6 mice.
+SRC	drug	opioid	28820778	By contrast, c <strong>Src</strong> inhibition affected neither <b>morphine</b> evoked locomotor stimulation nor reinforcement.
+SRC	addiction	reward	28820778	By contrast, c <strong>Src</strong> inhibition affected neither morphine evoked locomotor stimulation nor <b>reinforcement</b>.
+SRC	drug	opioid	28820778	The ability of c <strong>Src</strong> inhibitors to inhibit tolerance, thereby restoring analgesia, without altering the hedonic effect of <b>morphine</b>, makes c <strong>Src</strong> inhibitors promising candidates as adjuncts to <b>opioid</b> analgesics.
+SRC	addiction	reward	28820778	The ability of c <strong>Src</strong> inhibitors to inhibit tolerance, thereby restoring analgesia, without altering the <b>hedonic</b> effect of morphine, makes c <strong>Src</strong> inhibitors promising candidates as adjuncts to opioid analgesics.
+SRC	drug	opioid	28818835	<strong>Src</strong> dependent phosphorylation of μ <b>opioid</b> receptor at Tyr336 modulates opiate withdrawal.
+SRC	addiction	withdrawal	28818835	<strong>Src</strong> dependent phosphorylation of μ opioid receptor at Tyr336 modulates opiate <b>withdrawal</b>.
+SRC	drug	opioid	28818835	This increase requires the phosphorylation of μ <b>opioid</b> receptor (MOR) at Tyr336 by <strong>Src</strong> after prolonged opiate treatment in vitro Here, we report that the <strong>Src</strong> mediated MOR phosphorylation at Tyr336 is a prerequisite for opiate withdrawal in mice.
+SRC	addiction	withdrawal	28818835	This increase requires the phosphorylation of μ opioid receptor (MOR) at Tyr336 by <strong>Src</strong> after prolonged opiate treatment in vitro Here, we report that the <strong>Src</strong> mediated MOR phosphorylation at Tyr336 is a prerequisite for opiate <b>withdrawal</b> in mice.
+SRC	drug	opioid	28818835	We observed the recruitment of <strong>Src</strong> in the vicinity of MOR and an increase in phosphorylated Tyr336 (pY336) levels during <b>naloxone</b> precipitated withdrawal.
+SRC	addiction	withdrawal	28818835	We observed the recruitment of <strong>Src</strong> in the vicinity of MOR and an increase in phosphorylated Tyr336 (pY336) levels during naloxone precipitated <b>withdrawal</b>.
+SRC	addiction	withdrawal	28818835	The intracerebroventricular or stereotaxic injection of a <strong>Src</strong> inhibitor (AZD0530), or <strong>Src</strong> shRNA viruses attenuated pY336 levels, and several somatic <b>withdrawal</b> signs.
+SRC	drug	cocaine	28585567	Role of <strong>Src</strong> Family Kinases in BDNF Mediated Suppression of <b>Cocaine</b> Seeking and Prevention of <b>Cocaine</b> Induced ERK, GluN2A, and GluN2B Dephosphorylation in the Prelimbic Cortex.
+SRC	addiction	relapse	28585567	Role of <strong>Src</strong> Family Kinases in BDNF Mediated Suppression of Cocaine <b>Seeking</b> and Prevention of Cocaine Induced ERK, GluN2A, and GluN2B Dephosphorylation in the Prelimbic Cortex.
+SRC	addiction	sensitization	28306605	These findings demonstrate that the maintenance of DAMGO induced type II priming, and latent <b>sensitization</b> is mediated by an interaction between, <strong>Src</strong> and MAP kinases, which in females is GPR30 dependent.
+SRC	drug	cocaine	27506785	Using ChIP seq, we identified <strong>Src</strong> kinase signaling inhibitor 1 (Srcin1; also referred to as p140Cap) as a key gene target for reduced H3R2me2a binding, and found that consequent Srcin1 induction in the NAc decreases <strong>Src</strong> signaling, <b>cocaine</b> reward, and the motivation to self administer <b>cocaine</b>.
+SRC	addiction	reward	27506785	Using ChIP seq, we identified <strong>Src</strong> kinase signaling inhibitor 1 (Srcin1; also referred to as p140Cap) as a key gene target for reduced H3R2me2a binding, and found that consequent Srcin1 induction in the NAc decreases <strong>Src</strong> signaling, cocaine <b>reward</b>, and the motivation to self administer cocaine.
+SRC	drug	cocaine	27506785	Taken together, these findings suggest that suppression of <strong>Src</strong> signaling in NAc D2 MSNs, via PRMT6 and H3R2me2a down regulation, functions as a homeostatic brake to restrain <b>cocaine</b> action, and provide novel candidates for the development of treatments for <b>cocaine</b> addiction.
+SRC	addiction	addiction	27506785	Taken together, these findings suggest that suppression of <strong>Src</strong> signaling in NAc D2 MSNs, via PRMT6 and H3R2me2a down regulation, functions as a homeostatic brake to restrain cocaine action, and provide novel candidates for the development of treatments for cocaine <b>addiction</b>.
+SRC	drug	nicotine	27228072	Treatment of cells with <b>nicotine</b> induced the mRNA and protein levels of α7 nAChR; this could be abrogated by treatment with inhibitors targeting <strong>Src</strong>, PI3K, MEK, α7 nAChR, CDK4/6 or a disruptor of the Rb Raf 1 interaction.
+SRC	drug	cocaine	26202103	Here, we used the rat extinction reinstatement procedure to test the hypothesis that the <strong>Src</strong> family of tyrosine kinases (SFK) in the dorsal hippocampus (DH) critically controls contextual <b>cocaine</b> memory reconsolidation.
+SRC	addiction	relapse	26202103	Here, we used the rat extinction <b>reinstatement</b> procedure to test the hypothesis that the <strong>Src</strong> family of tyrosine kinases (SFK) in the dorsal hippocampus (DH) critically controls contextual cocaine memory reconsolidation.
+SRC	addiction	withdrawal	26004981	We also showed reduced expression of the GR co chaperone FKBP51, that normally keeps the receptor in the cytoplasm, and increased expression of <strong>Src1</strong>, which cooperates in the activation of GR transcriptional activity, revealing that short <b>withdrawal</b> alters the finely tuned mechanisms regulating GR action.
+SRC	drug	alcohol	24904439	Attentional bias for <b>alcohol</b> was assessed with a Visual Probe Test; approach bias toward <b>alcohol</b> was assessed with a Stimulus Response Compatibility (<strong>SRC</strong>) Test; and memory associations with <b>alcohol</b> were assessed with an Implicit Association Test (IAT) and a Word Association Test.
+SRC	drug	alcohol	24904439	Moreover, <strong>SRC</strong> scores predicted changes in <b>alcohol</b> use only when negative expectancies were low.
+SRC	drug	cocaine	23872878	Role of a hippocampal <strong>SRC</strong> family kinase mediated glutamatergic mechanism in drug context induced <b>cocaine</b> seeking.
+SRC	addiction	relapse	23872878	Role of a hippocampal <strong>SRC</strong> family kinase mediated glutamatergic mechanism in drug context induced cocaine <b>seeking</b>.
+SRC	drug	cocaine	23872878	Thus, <strong>Src</strong> family kinases in the DH may similarly control contextual <b>cocaine</b> seeking behavior.
+SRC	addiction	relapse	23872878	Thus, <strong>Src</strong> family kinases in the DH may similarly control contextual cocaine <b>seeking</b> behavior.
+SRC	drug	cocaine	23872878	<b>Cocaine</b> seeking behavior (non reinforced active lever pressing) was then assessed in the previously <b>cocaine</b> paired and extinction contexts after AP5 (N methyl D aspartate glutamate (NMDA) receptor (NMDAR) antagonist; 0.25 or 2.5 μg/0.5 μl/hemisphere), PP2 (<strong>Src</strong> family kinase inhibitor; 6.25 or 62.5 ng/0.5 μl/hemisphere), Ro25 6981 (NR2B subunit containing NMDAR antagonist; 0.2 or 2 μg/0.5 μl/hemisphere), or vehicle administration into the DH.
+SRC	addiction	relapse	23872878	Cocaine <b>seeking</b> behavior (non reinforced active lever pressing) was then assessed in the previously cocaine paired and extinction contexts after AP5 (N methyl D aspartate glutamate (NMDA) receptor (NMDAR) antagonist; 0.25 or 2.5 μg/0.5 μl/hemisphere), PP2 (<strong>Src</strong> family kinase inhibitor; 6.25 or 62.5 ng/0.5 μl/hemisphere), Ro25 6981 (NR2B subunit containing NMDAR antagonist; 0.2 or 2 μg/0.5 μl/hemisphere), or vehicle administration into the DH.
+SRC	drug	cocaine	23872878	Together, these findings suggest that <strong>Src</strong> family kinase activation, NMDAR stimulation, and likely <strong>Src</strong> family kinase mediated NR2B subunit containing NMDAR activation in the DH are necessary for incentive motivational and/or memory processes that promote contextual <b>cocaine</b> seeking behavior.
+SRC	addiction	relapse	23872878	Together, these findings suggest that <strong>Src</strong> family kinase activation, NMDAR stimulation, and likely <strong>Src</strong> family kinase mediated NR2B subunit containing NMDAR activation in the DH are necessary for incentive motivational and/or memory processes that promote contextual cocaine <b>seeking</b> behavior.
+SRC	addiction	reward	23872878	Together, these findings suggest that <strong>Src</strong> family kinase activation, NMDAR stimulation, and likely <strong>Src</strong> family kinase mediated NR2B subunit containing NMDAR activation in the DH are necessary for <b>incentive</b> motivational and/or memory processes that promote contextual cocaine seeking behavior.
+SRC	drug	nicotine	23308043	<b>Nicotine</b> induces inhibitor of differentiation 1 in a <strong>Src</strong> dependent pathway promoting metastasis and chemoresistance in pancreatic adenocarcinoma.
+SRC	drug	nicotine	23308043	Here, we show that stimulation of pancreatic cancer cells with <b>nicotine</b> concentrations that are within the range of human exposure results in activation of <strong>Src</strong> kinase, which facilitated the induction of the inhibitor of differentiation 1 (Id1) transcription factor.
+SRC	drug	nicotine	23308043	<b>Nicotine</b> could also confer resistance to apoptosis induced by gemcitabine in pancreatic cancer cells in vitro and depletion of <strong>Src</strong> or Id1 rendered the cells sensitive to gemcitabine.
+SRC	drug	opioid	23244430	The present review further details the potential role of second messengers like calcium (Ca2+) / calmodulin dependent protein kinase (CaMKII), nitric oxide synthase, cytokines, arachidonic acid metabolites, corticotropin releasing factor, fos and <strong>src</strong> kinases in causing <b>opioid</b> withdrawal syndrome.
+SRC	addiction	withdrawal	23244430	The present review further details the potential role of second messengers like calcium (Ca2+) / calmodulin dependent protein kinase (CaMKII), nitric oxide synthase, cytokines, arachidonic acid metabolites, corticotropin releasing factor, fos and <strong>src</strong> kinases in causing opioid <b>withdrawal</b> syndrome.
+SRC	drug	opioid	23142605	Compensatory adenylyl cyclase (AC) superactivation has been postulated to be responsible for the development of <b>morphine</b> tolerance and dependence, the underlying mechanism was demonstrated to comprise c <strong>Src</strong> dependent upregulation of AC5 within the lipid rafts.
+SRC	addiction	dependence	23142605	Compensatory adenylyl cyclase (AC) superactivation has been postulated to be responsible for the development of morphine tolerance and <b>dependence</b>, the underlying mechanism was demonstrated to comprise c <strong>Src</strong> dependent upregulation of AC5 within the lipid rafts.
+SRC	drug	alcohol	22960456	In this paper, a life cycle assessment (LCA) study was developed to evaluate the environmental implications of the production of <b>ethanol</b> from a fast growing short rotation crop (<strong>SRC</strong>): eucalyptus as well as its use in a flexi fuel vehicle (FFV).
+SRC	drug	cannabinoid	22957019	Using functional Magnetic Resonance Imaging (fMRI), neural approach bias activations were measured with a Stimulus Response Compatibility task (<strong>SRC</strong>) and compared between 33 heavy <b>cannabis</b> users and 36 matched controls.
+SRC	drug	nicotine	22791813	The resulting increase in catecholamine production was associated with significant inductions in the phosphorylation of signaling proteins ERK, CREB, <strong>Src</strong> and AKT, upregulated protein expression of nAChR subunits α3, α4, α5 and α7 and increased responsiveness to <b>nicotine</b> in 3 (4,5 dimethylthiazole 2 yl) 2,5 diphenyl tetrazolium bromide and cell migration assays.
+SRC	drug	nicotine	22240023	<b>Nicotine</b> mediated induction of E selectin in aortic endothelial cells requires <strong>Src</strong> kinase and E2F1 transcriptional activity.
+SRC	drug	nicotine	22240023	Here we demonstrate that <b>nicotine</b> induced E selectin transcription in human aortic endothelial cells (HAECs) could be significantly blocked by α7 nAChR subunit inhibitor, α BT, <strong>Src</strong> kinase inhibitor, PP2, or siRNAs against <strong>Src</strong> or β Arrestin 1 (β Arr1).
+SRC	drug	nicotine	22240023	Similarly, depletion of E2F1 or <strong>Src</strong> using RNAi blocked the increased adhesion of monocytes to <b>nicotine</b> stimulated HAECs.
+SRC	drug	nicotine	22240023	These results suggest that <b>nicotine</b> stimulated adhesion of monocytes to endothelial cells is dependent on the activation of α7 nAChRs, β Arr1 and <strong>cSrc</strong> regulated increase in E2F1 mediated transcription of E selectin gene.
+SRC	drug	alcohol	22182418	Eighty heavy social drinkers (46 female) initially completed measures of automatic approach tendencies (stimulus response compatibility [<strong>SRC</strong>] task) and attentional bias (visual probe task) elicited by <b>alcohol</b> related cues.
+SRC	drug	nicotine	22102627	SU 6656, a selective <strong>Src</strong> kinase inhibitor, attenuates mecamylamine precipitated <b>nicotine</b> withdrawal syndrome in mice.
+SRC	addiction	withdrawal	22102627	SU 6656, a selective <strong>Src</strong> kinase inhibitor, attenuates mecamylamine precipitated nicotine <b>withdrawal</b> syndrome in mice.
+SRC	drug	nicotine	22102627	<strong>Src</strong> kinase is reported to regulate neuronal nicotinic acetylcholine receptor activity, which is among the principal receptor systems acted upon by <b>nicotine</b>.
+SRC	addiction	dependence	22102627	<strong>Src</strong> kinase is documented to mediate the pathogenesis of substance <b>dependence</b>.
+SRC	drug	nicotine	22102627	Therefore, the present study has been designed to investigate the effect of SU 6656, selective <strong>src</strong> kinase inhibitor, on the development of <b>nicotine</b> dependence in a mouse model of mecamylamine induced <b>nicotine</b> withdrawal syndrome.
+SRC	addiction	dependence	22102627	Therefore, the present study has been designed to investigate the effect of SU 6656, selective <strong>src</strong> kinase inhibitor, on the development of nicotine <b>dependence</b> in a mouse model of mecamylamine induced nicotine withdrawal syndrome.
+SRC	addiction	withdrawal	22102627	Therefore, the present study has been designed to investigate the effect of SU 6656, selective <strong>src</strong> kinase inhibitor, on the development of nicotine dependence in a mouse model of mecamylamine induced nicotine <b>withdrawal</b> syndrome.
+SRC	drug	nicotine	22102627	Thus, it is suggested that <strong>src</strong> kinase is involved in the development of <b>nicotine</b> dependence induced precipitation of its withdrawal syndrome and thus may serve as a viable pharmacological target to tackle the problem of <b>nicotine</b> addiction.
+SRC	addiction	addiction	22102627	Thus, it is suggested that <strong>src</strong> kinase is involved in the development of nicotine dependence induced precipitation of its withdrawal syndrome and thus may serve as a viable pharmacological target to tackle the problem of nicotine <b>addiction</b>.
+SRC	addiction	dependence	22102627	Thus, it is suggested that <strong>src</strong> kinase is involved in the development of nicotine <b>dependence</b> induced precipitation of its withdrawal syndrome and thus may serve as a viable pharmacological target to tackle the problem of nicotine addiction.
+SRC	addiction	withdrawal	22102627	Thus, it is suggested that <strong>src</strong> kinase is involved in the development of nicotine dependence induced precipitation of its <b>withdrawal</b> syndrome and thus may serve as a viable pharmacological target to tackle the problem of nicotine addiction.
+SRC	drug	nicotine	22085699	In this study, we demonstrated a novel signaling mechanism by which <b>nicotine</b> exposure activated <strong>Src</strong> to sensitize epidermal growth factor receptor (EGFR) mediated pathways for breast cancer cell growth promotion.
+SRC	drug	nicotine	22085699	Subsequently, <strong>Src</strong>, Akt and ERK1/2 were phosphorylated at different time points following <b>nicotine</b> treatment.
+SRC	drug	nicotine	22085699	We further demonstrated that through <strong>Src</strong>, the ligation of <b>nicotine</b> with nAChR stimulated the EGFR/ERK1/2 pathway for the activation of E2F1 and further cell progression.
+SRC	drug	nicotine	22085699	Our study reveals the existence of a potential, regulatory network governed by the interaction of <b>nicotine</b> and nAChR that integrates the conventional, mitogenic <strong>Src</strong> and EGFR signals for breast cancer development.
+SRC	drug	alcohol	21895719	A total of 63 <b>alcohol</b> dependent patients undergoing detoxification and 64 light drinking controls completed a stimulus response compatibility (<strong>SRC</strong>) task, which assesses the speed of categorization of <b>alcohol</b> related pictures by making symbolic approach and avoidance movements.
+SRC	drug	alcohol	21895719	We also included modified versions of the <strong>SRC</strong> task to assess automatic motivational conflict, that is, strong approach and avoidance tendencies elicited simultaneously by <b>alcohol</b> related cues.
+SRC	drug	alcohol	21895719	There were no differences between <b>alcohol</b> dependent patients and controls on the <strong>SRC</strong> task, although individual differences in the quantity of <b>alcohol</b> consumed before entering treatment were significantly positively correlated with the strength of approach (but not avoidance) tendencies elicited by <b>alcohol</b> related cues.
+SRC	drug	alcohol	21307254	We report here that the <strong>Src</strong> family tyrosine kinase Lyn negatively regulates the release of dopamine (DA) in the mesolimbic system, as well as the rewarding properties of <b>alcohol</b>.
+SRC	drug	opioid	21285874	Modulation of <strong>src</strong> kinase attenuates <b>naloxone</b> precipitated <b>opioid</b> withdrawal syndrome in mice.
+SRC	addiction	withdrawal	21285874	Modulation of <strong>src</strong> kinase attenuates naloxone precipitated opioid <b>withdrawal</b> syndrome in mice.
+SRC	drug	opioid	21285874	This study was designed to investigate the effect of 2,3 dihydro N, N dimethyl 2 oxo 3 [(4,5,6,7 tetrahydro 1H indol 2 yl)methylene] 1H indole 5 sulfonamide (SU 6656), a selective inhibitor of <strong>src</strong> family kinase, on the development of <b>naloxone</b> induced <b>opioid</b> withdrawal syndrome in mice.
+SRC	addiction	withdrawal	21285874	This study was designed to investigate the effect of 2,3 dihydro N, N dimethyl 2 oxo 3 [(4,5,6,7 tetrahydro 1H indol 2 yl)methylene] 1H indole 5 sulfonamide (SU 6656), a selective inhibitor of <strong>src</strong> family kinase, on the development of naloxone induced opioid <b>withdrawal</b> syndrome in mice.
+SRC	drug	opioid	21285874	Therefore, it seems that an <strong>src</strong> family kinase linked mechanism is involved in the development of physiological <b>opioid</b> dependence; thus, <strong>src</strong> family kinase may serve as a potential target to address the pathological condition of physiological dependence and abstinence associated with continuous <b>opioid</b> usage.
+SRC	addiction	dependence	21285874	Therefore, it seems that an <strong>src</strong> family kinase linked mechanism is involved in the development of physiological opioid <b>dependence</b>; thus, <strong>src</strong> family kinase may serve as a potential target to address the pathological condition of physiological <b>dependence</b> and abstinence associated with continuous opioid usage.
+SRC	drug	cocaine	21055728	We also demonstrate that the D1R/<strong>Src</strong> family kinases/NR2B pathway is responsible for ERK activation by <b>cocaine</b> in vivo.
+SRC	drug	alcohol	20668202	We previously observed that ex vivo acute exposure of the dorsal striatum to, and withdrawal from, <b>alcohol</b> induces long term facilitation (LTF) of the activity of NR2B containing NMDA receptors (NR2B NMDARs) in a mechanism that requires the <strong>Src</strong> family protein tyrosine kinase (PTK), Fyn (Wang et al., 2007).
+SRC	addiction	withdrawal	20668202	We previously observed that ex vivo acute exposure of the dorsal striatum to, and <b>withdrawal</b> from, alcohol induces long term facilitation (LTF) of the activity of NR2B containing NMDA receptors (NR2B NMDARs) in a mechanism that requires the <strong>Src</strong> family protein tyrosine kinase (PTK), Fyn (Wang et al., 2007).
+SRC	drug	alcohol	20668202	Finally, we show that inhibition of NR2B NMDARs or <strong>Src</strong> family PTKs in the DMS, but not in the DLS, significantly decreases operant self administration of <b>alcohol</b> and reduces <b>alcohol</b> priming induced reinstatement of <b>alcohol</b> seeking.
+SRC	addiction	relapse	20668202	Finally, we show that inhibition of NR2B NMDARs or <strong>Src</strong> family PTKs in the DMS, but not in the DLS, significantly decreases operant self administration of alcohol and reduces alcohol priming induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+SRC	addiction	reward	20668202	Finally, we show that inhibition of NR2B NMDARs or <strong>Src</strong> family PTKs in the DMS, but not in the DLS, significantly decreases <b>operant</b> self administration of alcohol and reduces alcohol priming induced reinstatement of alcohol seeking.
+SRC	drug	opioid	20483033	RACK1 inhibits <b>morphine</b> re exposure via inhibition of <strong>Src</strong>.
+SRC	drug	opioid	20483033	In the present study, we examined the role of <strong>Src</strong> in regulating the inhibition of p ERK in the brain following RACK1 over expression during <b>morphine</b> reward.
+SRC	addiction	reward	20483033	In the present study, we examined the role of <strong>Src</strong> in regulating the inhibition of p ERK in the brain following RACK1 over expression during morphine <b>reward</b>.
+SRC	drug	opioid	20483033	Chronic <b>morphine</b> injection increased <strong>Src</strong> and p ERK expression in cortex and hippocampus, and mice exhibited increased place preference.
+SRC	drug	opioid	20483033	Intraventricular administration of RACK1 reduced <strong>Src</strong> and p ERK levels in cortex and hippocampus, as well as <b>morphine</b> reward.
+SRC	addiction	reward	20483033	Intraventricular administration of RACK1 reduced <strong>Src</strong> and p ERK levels in cortex and hippocampus, as well as morphine <b>reward</b>.
+SRC	drug	opioid	20483033	At 7 days of final RACK1 administration, the effects of RACK1 on <strong>Src</strong> and p ERK disappeared, and <b>morphine</b> place preference was restored.
+SRC	drug	opioid	20483033	We demonstrated that RACK1 acts on ERK activation via <strong>Src</strong> in <b>morphine</b> reward in mice.
+SRC	addiction	reward	20483033	We demonstrated that RACK1 acts on ERK activation via <strong>Src</strong> in morphine <b>reward</b> in mice.
+SRC	drug	cocaine	19046409	<strong>Src</strong> protein tyrosine kinases are required for <b>cocaine</b> induced increase in the expression and function of the NMDA receptor in the ventral tegmental area.
+SRC	drug	cocaine	19046409	<b>Cocaine</b> induced an increase in the activity of both Fyn and <strong>Src</strong> kinases, and the <strong>Src</strong> protein tyrosine kinase (<strong>Src</strong> PTKs) inhibitor, 4 amino 5 (4 chlorophenyl) 7 (t butyl)pyrazolo[3,4 d]pyrimidine (PP2), abolished both <b>cocaine</b> induced increase in tyrosine phosphorylation of the NR2A subunit and the increase in the expression of NR1, NR2A, and NR2B in the VTA.
+SRC	drug	cocaine	19046409	Taken together, these results suggest that acute <b>cocaine</b> induced an increase in the expression of NMDAR subunits and enhanced tyrosine phosphorylation of NR2A containing NMDAR through members of the <strong>Src</strong> PTKs.
+SRC	drug	alcohol	17640615	Participants completed a stimulus response compatibility (<strong>SRC</strong>) task, which requires participants to move a manikin towards or away from <b>alcohol</b> related and matched control pictures, together with self report measures of <b>alcohol</b> consumption and craving.
+SRC	addiction	relapse	17640615	Participants completed a stimulus response compatibility (<strong>SRC</strong>) task, which requires participants to move a manikin towards or away from alcohol related and matched control pictures, together with self report measures of alcohol consumption and <b>craving</b>.
+SRC	drug	alcohol	17640615	Results demonstrated that heavy drinkers, but not light drinkers, were faster to approach than avoid <b>alcohol</b> pictures on the <strong>SRC</strong> task.
+SRC	drug	nicotine	17179996	Within this region, the gene encoding <strong>Src</strong> homology 2 domain containing transforming protein C3 (SHC3) represents a plausible candidate for association with ND, assessed by <b>smoking</b> quantity (SQ), the Heaviness of <b>Smoking</b> Index (HSI) and the Fagerström Test for ND (FTND).
+SRC	drug	nicotine	17102610	Analysis of the molecular mechanisms underlying <b>nicotine</b> mediated cell proliferation showed the involvement of <strong>Src</strong> kinase and the scaffolding protein beta arrestin 1.
+SRC	drug	alcohol	16009711	We further observed that <b>ethanol</b> exposure results in NR2A endocytosis through the activation of H Ras and the inhibition of the tyrosine kinase <strong>Src</strong>.
+SRC	drug	nicotine	15075624	We also obtained explicit and implicit measures of the valence of the <b>smoking</b> related pictures from pleasantness ratings and from behavioural responses on a stimulus response compatibility (<strong>SRC</strong>) task.
+SRC	drug	cannabinoid	12657697	The <b>endocannabinoid</b> induced stimulation of ERK was lost in Fyn knock out mice, in slices and in vivo, although it was insensitive to inhibitors of <strong>Src</strong> family tyrosine kinases in vitro, suggesting a noncatalytic role of Fyn.
+SRC	drug	opioid	11602657	Dependence of delta1 <b>opioid</b> receptor induced cardioprotection on a tyrosine kinase dependent but not a <strong>Src</strong> dependent pathway.
+SRC	addiction	dependence	11602657	<b>Dependence</b> of delta1 opioid receptor induced cardioprotection on a tyrosine kinase dependent but not a <strong>Src</strong> dependent pathway.
+SRC	drug	opioid	11602657	These data suggest that a TK, but most likely not an <strong>Src</strong>/EGF receptor TK, is important in cardioprotection via <b>opioid</b> receptor stimulation and that the pathway for TK activation is downstream from or parallel to PKC activation in the in situ rat heart since genistein could not affect PKC translocation of selective isoforms induced by TAN 67 and assessed by immunohistochemistry.
+IFI6	drug	alcohol	32593842	In a cross sectional community based survey, we randomly selected 4133 <b>alcoholic</b> parents and their children aged between <strong>6 16</strong> years from seven districts of Kerala, south India.
+IFI6	drug	nicotine	26751933	The questionnaires were then analysed by SPSS 20 software The prevalence of <b>smoking</b>, always in the form of cigarettes, was 13.4% (C/95%: 10.<strong>6 16</strong>.1) among college students.
+IFI6	drug	alcohol	26573323	The proportion of 60+ years with excessive <b>alcohol</b> intake varies in western countries between <strong>6 16</strong> % among men and 2 7 % among women.
+IFI6	drug	alcohol	24485061	The median follow up after admission to treatment was 11.6 years (IQR: 6.<strong>6 16</strong>.1), 6.5 years (IQR: 3.9 10.6), and 4.8 years (IQR: 3.1 7.8) for the heroin , cocaine , and <b>alcohol</b> dependent patients, respectively.
+IFI6	drug	cocaine	24485061	The median follow up after admission to treatment was 11.6 years (IQR: 6.<strong>6 16</strong>.1), 6.5 years (IQR: 3.9 10.6), and 4.8 years (IQR: 3.1 7.8) for the heroin , <b>cocaine</b> , and alcohol dependent patients, respectively.
+IFI6	drug	opioid	24485061	The median follow up after admission to treatment was 11.6 years (IQR: 6.<strong>6 16</strong>.1), 6.5 years (IQR: 3.9 10.6), and 4.8 years (IQR: 3.1 7.8) for the <b>heroin</b> , cocaine , and alcohol dependent patients, respectively.
+IFI6	addiction	withdrawal	18838937	A total of 1040 <b>withdrawal</b> symptom assessments were completed, with a median (interquartile range) of 11 (<strong>6 16</strong>) per patient over 6.6 (4.8 11) days.
+IFI6	drug	nicotine	15175538	Total <b>nicotine</b> content was between <strong>6 16</strong> mg/g.
+IFI6	addiction	reward	14755004	EM 1 (1.<strong>6 16</strong>.3 nmol) microinjected into the VTA produced <b>CPP</b>, whereas EM 2 (8.7 and 17.5 nmol) given into the same VTA site did not produce any effect, but at a high dose (35 nmol) produced <b>CPP</b>.
+IFI6	drug	alcohol	14502238	The cell death process occurs over a <strong>6 16</strong> h period following <b>ethanol</b> administration, is accompanied by a robust display of caspase 3 enzyme activation, and meets ultrastructural criteria for apoptosis.
+IFI6	drug	nicotine	11209912	8.<strong>6 16</strong>.08) as was sibling <b>smoking</b> (O.R.
+ECT	drug	alcohol	32733110	There was no significant difference between the two groups in terms of DSM  IV based psychiatric diagnosis distributions, the existence of complete recovery periods during the course of the disease; total duration of APD use for at least 10 years; APD holidays; regular APD use; history of <strong>ECT</strong> and smoking or <b>alcohol</b> and substance abuse/addiction.
+ECT	drug	nicotine	32733110	There was no significant difference between the two groups in terms of DSM  IV based psychiatric diagnosis distributions, the existence of complete recovery periods during the course of the disease; total duration of APD use for at least 10 years; APD holidays; regular APD use; history of <strong>ECT</strong> and <b>smoking</b> or alcohol and substance abuse/addiction.
+ECT	addiction	addiction	32733110	There was no significant difference between the two groups in terms of DSM  IV based psychiatric diagnosis distributions, the existence of complete recovery periods during the course of the disease; total duration of APD use for at least 10 years; APD holidays; regular APD use; history of <strong>ECT</strong> and smoking or alcohol and substance abuse/<b>addiction</b>.
+ECT	drug	psychedelics	31913927	It remains controversial whether a subanesthetic dose of <b>ketamine</b> could modulate the antidepressant effect of electroconvulsive therapy (<strong>ECT</strong>) in patients with major depressive disorder.
+ECT	drug	psychedelics	31913927	We investigated the effect of <b>ketamine</b> on accelerating the antidepressant efficacy of <strong>ECT</strong>.
+ECT	drug	psychedelics	31913927	The study group received 0.3 mg/kg <b>ketamine</b>, and the control group received an isovolumetric dose of normal saline before undergoing <strong>ECT</strong> under propofol anesthesia.
+ECT	drug	psychedelics	31913927	Low dose <b>ketamine</b> (0.3 mg/kg) could modulate the antidepressant efficacy of <strong>ECT</strong> via accelerating the onset of its effects and reducing the number of <strong>ECT</strong> sessions required to obtain response, remission, and SI reduction, without influencing the relapse rates in remitting patients after <strong>ECT</strong> treatment.
+ECT	addiction	relapse	31913927	Low dose ketamine (0.3 mg/kg) could modulate the antidepressant efficacy of <strong>ECT</strong> via accelerating the onset of its effects and reducing the number of <strong>ECT</strong> sessions required to obtain response, remission, and SI reduction, without influencing the <b>relapse</b> rates in remitting patients after <strong>ECT</strong> treatment.
+ECT	drug	nicotine	31865511	Variables significantly correlated with patients' LOS included gender, age, employment status, marital status, number of divorces, disability rate, discharge diagnosis, physical comorbidity, number of previous hospitalizations, suicide ideation, number of suicide attempts, history of assault, <b>tobacco</b> consumption, a history of narcotic drug abuse and number of <strong>ECT</strong> sessions.
+ECT	drug	cannabinoid	31642158	To describe the use of extracorporeal therapy (<strong>ECT</strong>) to treat severe <b>cannabinoid</b> intoxication in a dog with severe hyperlipidemia.
+ECT	addiction	intoxication	31642158	To describe the use of extracorporeal therapy (<strong>ECT</strong>) to treat severe cannabinoid <b>intoxication</b> in a dog with severe hyperlipidemia.
+ECT	drug	cannabinoid	31642158	To the authors' knowledge, this is the first published report to document <strong>ECT</strong> to treat <b>THC</b> intoxication in veterinary medicine.
+ECT	addiction	intoxication	31642158	To the authors' knowledge, this is the first published report to document <strong>ECT</strong> to treat THC <b>intoxication</b> in veterinary medicine.
+ECT	drug	cannabinoid	31642158	<strong>ECT</strong> may be considered as a treatment option for severe <b>THC</b> intoxication that is refractory to standard therapy or where severe hyperlipidemia precludes use of IV lipid emulsions.
+ECT	addiction	intoxication	31642158	<strong>ECT</strong> may be considered as a treatment option for severe THC <b>intoxication</b> that is refractory to standard therapy or where severe hyperlipidemia precludes use of IV lipid emulsions.
+ECT	drug	benzodiazepine	31170309	Although there is no consensus about the treatment of Persistent Genital Arousal Disorder in the psychiatric literature, there are some case reports about the use of pregabaline, clomipramine, duloxetine, <b>clonazepam</b>, varenicline, olanzapine, risperidone in addition to the case reports on treatment with hypnotherapy, pelvic floor physiotherapy and electroconvulsive therapy (<strong>ECT</strong>).
+ECT	drug	psychedelics	30614886	For inpatients with severe melancholic depression and acute safety concerns, electroconvulsive therapy (or <b>ketamine</b> if <strong>ECT</strong> refused or ineffective) may be the first line treatment.
+ECT	drug	psychedelics	30572160	ELEctroconvulsive therapy (<strong>ECT</strong>) vs. <b>Ketamine</b> in patients with Treatment resistant Depression: The ELEKT D study protocol.
+ECT	drug	psychedelics	30572160	While response rates are similar between <strong>ECT</strong> and <b>ketamine</b> in clinical trials, these treatments have never been compared head to head in a sufficiently large, well powered randomized study.
+ECT	drug	psychedelics	30572160	Here we describe the study protocol for ELEctroconvulsive therapy (<strong>ECT</strong>) vs. <b>Ketamine</b> in patients with Treatment resistant Depression (ELEKT D), a non inferiority, comparative effectiveness trial.
+ECT	drug	psychedelics	30572160	Patients with TRD seeking clinical treatment are randomized (1:1) to receive <strong>ECT</strong> (thrice weekly) or intravenous <b>ketamine</b> (twice weekly) for 3 5 weeks.
+ECT	addiction	relapse	30572160	Patients with TRD <b>seeking</b> clinical treatment are randomized (1:1) to receive <strong>ECT</strong> (thrice weekly) or intravenous ketamine (twice weekly) for 3 5 weeks.
+ECT	drug	psychedelics	30572160	The study is powered such that the non inferiority margin allows for <b>ketamine</b> to retain 90% of the <strong>ECT</strong> treatment effect, with a projected sample size of 400 patients (200 per group).
+ECT	addiction	relapse	30531397	Depression <b>relapse</b> after electroconvulsive therapy (<strong>ECT</strong>) is common (40% at 6 months).
+ECT	addiction	relapse	30531397	Participants were followed up for 6 months after <strong>ECT</strong> to assess for <b>relapse</b>.
+ECT	drug	benzodiazepine	28615768	Patients who did not respond to <b>lorazepam</b> trial were given <strong>ECT</strong>.
+ECT	drug	benzodiazepine	28615768	Younger age group patients were mainly responded to <b>lorazepam</b> only, whereas older age group patients responded to both <strong>ECT</strong> and <b>lorazepam</b>.
+ECT	drug	benzodiazepine	28615768	This study has came out with very important insights in the age of incidence, phenomenology, clinical profile, source of referral, diagnostic break up and treatment response with <b>lorazepam</b> and <strong>ECT</strong> in catatonic patients following mental disorder.
+ECT	drug	benzodiazepine	28463343	The following searches were used in PubMed to obtain the most relevant advances in treating schizophrenia or bipolar disorder with acute agitation and aggression: (agitation, agitated, aggression, aggressive, hostile, hostility, violent, or violence) and (schizophr*, psychosis, psychot*, psychos*, mania, manic, or bipolar) and (*pharmacologic, antipsychotic*, neuroleptic*, antiepileptic*, anti seizure*, mood stabilizer*, lithium, <b>benzodiazepine</b>*, beta blocker, beta blocker, alpha2, alpha 2, *histamine*, electroconvulsive, <strong>ECT</strong>, shock, or transcranial).
+ECT	drug	alcohol	28055126	The goal of this review is to explore alternative neurological therapies in the treatment of <b>alcohol</b> use disorder; including transcranial direct current stimulation (tDCS), transcranial magnetic stimulation, deep brain stimulation (DBS), electroconvulsive therapy (<strong>ECT</strong>), and the off label use of the GABAB receptor agonist baclofen.
+ECT	addiction	relapse	27965856	However, <b>relapse</b> rates are high following <strong>ECT</strong> 38 % after 6 months.
+ECT	drug	psychedelics	27965856	The main objective of this study is to conduct a randomised controlled pilot trial (n = 40) of a 4 week course of once weekly <b>ketamine</b> infusions for relapse prevention following <strong>ECT</strong> for depression to assess trial procedures that will inform a future definitive trial.
+ECT	addiction	relapse	27965856	The main objective of this study is to conduct a randomised controlled pilot trial (n = 40) of a 4 week course of once weekly ketamine infusions for <b>relapse</b> prevention following <strong>ECT</strong> for depression to assess trial procedures that will inform a future definitive trial.
+ECT	drug	benzodiazepine	27965856	Those who meet standard response criteria will be invited, on completing <strong>ECT</strong>, to be randomised in a 1:1 ratio to a course of four once weekly infusions of ketamine or an active comparator <b>midazolam</b>, which mimics some of the effects of ketamine and may improve blinding over inactive placebo.
+ECT	drug	psychedelics	27965856	Those who meet standard response criteria will be invited, on completing <strong>ECT</strong>, to be randomised in a 1:1 ratio to a course of four once weekly infusions of <b>ketamine</b> or an active comparator midazolam, which mimics some of the effects of <b>ketamine</b> and may improve blinding over inactive placebo.
+ECT	drug	amphetamine	26834801	The aim of this study is to describe the use of electroconvulsive therapy (<strong>ECT</strong>) in the treatment of <b>methamphetamine</b> induced withdrawal delirium and craving in a single case.
+ECT	addiction	relapse	26834801	The aim of this study is to describe the use of electroconvulsive therapy (<strong>ECT</strong>) in the treatment of methamphetamine induced withdrawal delirium and <b>craving</b> in a single case.
+ECT	addiction	withdrawal	26834801	The aim of this study is to describe the use of electroconvulsive therapy (<strong>ECT</strong>) in the treatment of methamphetamine induced <b>withdrawal</b> delirium and craving in a single case.
+ECT	drug	amphetamine	26834801	A 44 year old male presented to the hospital in Fars province, Iran, with <b>Methamphetamine</b> Induced Withdrawal Delirium who responded to <strong>ECT</strong>.
+ECT	addiction	withdrawal	26834801	A 44 year old male presented to the hospital in Fars province, Iran, with Methamphetamine Induced <b>Withdrawal</b> Delirium who responded to <strong>ECT</strong>.
+ECT	drug	psychedelics	26721476	The augmentative effect of sub anesthetic S <b>ketamine</b> on <strong>ECT</strong> is discussed.
+ECT	drug	amphetamine	25561962	Treatment of <b>Methamphetamine</b> Dependence with Electroconvulsive Therapy (<strong>ECT</strong>) in Iran: A Critical Note.
+ECT	addiction	dependence	25561962	Treatment of Methamphetamine <b>Dependence</b> with Electroconvulsive Therapy (<strong>ECT</strong>) in Iran: A Critical Note.
+ECT	drug	amphetamine	25561962	This comment article reviews the literature to explore whether the use of <strong>ECT</strong> for the treatment of <b>methamphetamine</b> dependence can be justified by scientific rationale and/or evidence.
+ECT	addiction	dependence	25561962	This comment article reviews the literature to explore whether the use of <strong>ECT</strong> for the treatment of methamphetamine <b>dependence</b> can be justified by scientific rationale and/or evidence.
+ECT	addiction	addiction	25561962	This article reviews the literature on the use of <strong>ECT</strong> in <b>addictive</b> disorders.
+ECT	drug	amphetamine	25561962	It describes a patient with <b>methamphetamine</b> dependence treated with <strong>ECT</strong>.
+ECT	addiction	dependence	25561962	It describes a patient with methamphetamine <b>dependence</b> treated with <strong>ECT</strong>.
+ECT	drug	amphetamine	25561962	We found no scientific evidence or justification for <strong>ECT</strong> as a treatment of <b>methamphetamine</b> dependence or as the first line treatment for <b>methamphetamine</b> induced psychiatric comorbidities.
+ECT	addiction	dependence	25561962	We found no scientific evidence or justification for <strong>ECT</strong> as a treatment of methamphetamine <b>dependence</b> or as the first line treatment for methamphetamine induced psychiatric comorbidities.
+ECT	addiction	addiction	25561962	the current available evidence does not support using <strong>ECT</strong> for the treatment of <b>addictive</b> disorders, and hence is unethical, unacceptable and inhumane and warrants immediate social and political attention.
+ECT	drug	benzodiazepine	25553236	After seven years a <b>lorazepam</b> provocation test was performed as he had a new relapse after 3 weeks without <strong>ECT</strong>.
+ECT	addiction	relapse	25553236	After seven years a lorazepam provocation test was performed as he had a new <b>relapse</b> after 3 weeks without <strong>ECT</strong>.
+ECT	drug	benzodiazepine	24901428	It initially responded to a <b>lorazepam</b> challenge; however, a complicated hospital course and deterioration of the patient's condition, including septic shock, delirium, and continued catatonic symptoms, led to the pursuit of <strong>ECT</strong> to treat her symptoms.
+ECT	drug	benzodiazepine	24459371	Majority of patients responded to therapy either by <b>lorazepam</b> alone or to its augmentation with modified <strong>ECT</strong>.
+ECT	drug	benzodiazepine	24416611	Some improvement was achieved through supportive therapy, high dose of <b>lorazepam</b>, and a series of 10 <strong>ECT</strong> sessions.
+ECT	drug	alcohol	23859979	However, similar to most antidepressant trials, patients with depression and comorbid <b>alcohol</b> and substance abuse are excluded from <strong>ECT</strong> efficacy studies.
+ECT	drug	alcohol	23859979	Through a retrospective chart review, we compared response to <strong>ECT</strong> in patients with mood disorder and comorbid <b>alcohol</b> and drug abuse to those with mood disorder only.
+ECT	drug	alcohol	23859979	There was no difference in <strong>ECT</strong> outcome between those with comorbid <b>alcohol</b> abuse and those without based on percent decrease in pre  and post <strong>ECT</strong> symptom scores (abuse: mean [SD], 0.89 [0.2] vs nonabuse: mean [SD], 0.93 [0.16]; Wilcoxon, 1332; P = 0.086).
+ECT	drug	alcohol	23859979	Our results indicate that comorbid <b>alcohol</b> and drug abuse may influence the response to <strong>ECT</strong> in the treatment of mood disorders.
+ECT	drug	benzodiazepine	23228156	Factors independently associated with a statistically significant increased time to regained occupational functioning were longer duration of sick leave pre <strong>ECT</strong>, milder depression pre <strong>ECT</strong>, less complete improvement with <strong>ECT</strong>, <b>benzodiazepine</b> treatment after <strong>ECT</strong> and co morbid substance dependence.
+ECT	addiction	dependence	23228156	Factors independently associated with a statistically significant increased time to regained occupational functioning were longer duration of sick leave pre <strong>ECT</strong>, milder depression pre <strong>ECT</strong>, less complete improvement with <strong>ECT</strong>, benzodiazepine treatment after <strong>ECT</strong> and co morbid substance <b>dependence</b>.
+ECT	drug	alcohol	22945180	Here, the efficacy of different neuromodulation techniques in <b>alcohol</b> addiction, such as transcranial direct current stimulation (tDCS), repetitive transcranial magnetic stimulation (rTMS), deep brain stimulation (DBS), vagal nerve stimulation (VNS) and electroconvulsive therapy (<strong>ECT</strong>) is critically evaluated.
+ECT	addiction	addiction	22945180	Here, the efficacy of different neuromodulation techniques in alcohol <b>addiction</b>, such as transcranial direct current stimulation (tDCS), repetitive transcranial magnetic stimulation (rTMS), deep brain stimulation (DBS), vagal nerve stimulation (VNS) and electroconvulsive therapy (<strong>ECT</strong>) is critically evaluated.
+ECT	drug	alcohol	22945180	The use of VNS and <strong>ECT</strong> has yet to be investigated in <b>alcohol</b> dependent patients.
+ECT	drug	alcohol	23137143	We selected 20 PETs and identified the following commonly used exclusion criteria: 'a baseline severity threshold of HAM D≤14', 'current or past abuse or dependence of <b>alcohol</b> and/or drugs' and 'previous use of medication or <strong>ECT</strong>'.
+ECT	addiction	dependence	23137143	We selected 20 PETs and identified the following commonly used exclusion criteria: 'a baseline severity threshold of HAM D≤14', 'current or past abuse or <b>dependence</b> of alcohol and/or drugs' and 'previous use of medication or <strong>ECT</strong>'.
+ECT	drug	benzodiazepine	22914637	Here, we report a case of the use of the <b>benzodiazepine</b> antagonist flumazenil before <strong>ECT</strong> to facilitate the simultaneous use of <b>lorazepam</b> and <strong>ECT</strong> for the treatment of co occurring catatonia and obsessive compulsive disorder.
+ECT	addiction	addiction	22914637	Here, we report a case of the use of the benzodiazepine antagonist flumazenil before <strong>ECT</strong> to facilitate the simultaneous use of lorazepam and <strong>ECT</strong> for the treatment of co occurring catatonia and obsessive <b>compulsive</b> disorder.
+ECT	drug	nicotine	22216822	However, there was no correlation found between <b>smoking</b> and gender, and no cause eff <strong>ect</strong> relationship between <b>smoking</b> and hard dental tissues status as defined by DMF, DMFs values and their components.
+ECT	drug	amphetamine	22037141	Our findings suggest electroconvulsive therapy (<strong>ECT</strong>) may have potential applications with regard to the treatment of <b>methamphetamine</b> psychosis and addiction.
+ECT	addiction	addiction	22037141	Our findings suggest electroconvulsive therapy (<strong>ECT</strong>) may have potential applications with regard to the treatment of methamphetamine psychosis and <b>addiction</b>.
+ECT	drug	benzodiazepine	20851717	<b>Midazolam</b> administration into the <strong>Ect</strong>, Per, and Ent reduced freezing responses.
+ECT	drug	benzodiazepine	20159196	The interest of this report is (1) it reinforces the need to be cautious before prescribing neuroleptics in adolescents presenting with symptoms of catatonia; (2) the complete recovery from catatonia after treatment with intensive care and more than three weeks of intravenous <b>clonazepam</b> without the use of <strong>ECT</strong> and (3) the effectiveness of carbamazepine over a long period of follow up.
+ECT	addiction	withdrawal	19686432	Based on the patient's bipolar disorder, the mechanism of action of <strong>ECT</strong> and the observation of <strong>ECT</strong> effectiveness on her PGAD, we hypothesize the following: (i) bipolar disorder led to central hyperactive dopamine release, an important component in the pathophysiology of her PGAD; (ii) central serotonin deficiency after selective serotonin reuptake inhibitor (SSRI) <b>withdrawal</b> resulted in a lack of inhibition of sexual excitement; (iii) <strong>ECT</strong> resulted in lowering of the hyperstimulated central dopamine release; and (iv) <strong>ECT</strong> led to an increase in sexual inhibition by stimulating serotonin activity.
+ECT	drug	benzodiazepine	12506260	If necessary, the patient could receive 3 mg/day with a 6 day full dose treatment and then, treatment would progressively be reduced; 4) If the patient failed to respond to <b>lorazepam</b>, <strong>ECT</strong> are needed; 5) Earlier use of <strong>ECT</strong> is recommended if autonomic instability or hyperthermia appears and malignant catatonia is suspected.
+ECT	drug	benzodiazepine	9661088	The use of flumazenil in the anxious and <b>benzodiazepine</b> dependent <strong>ECT</strong> patient.
+ECT	drug	benzodiazepine	9661088	Many patients who receive electroconvulsive therapy (<strong>ECT</strong>) are <b>benzodiazepine</b> dependent or are anxious and require <b>benzodiazepine</b> drugs.
+ECT	drug	benzodiazepine	9661088	Because these agents may diminish the therapeutic effectiveness of <strong>ECT</strong>, we explored the dosing, safety, and efficacy of pre <strong>ECT</strong> flumazenil administration, a <b>benzodiazepine</b> competitive antagonist, in patients receiving <b>benzodiazepine</b> medications.
+ECT	drug	benzodiazepine	9661088	We report our experience with 35 patients who received both flumazenil and <b>benzodiazepine</b> drugs during their <strong>ECT</strong> course.
+ECT	drug	benzodiazepine	9661088	Flumazenil offers the promise of safe and effective <strong>ECT</strong> in patients receiving <b>benzodiazepine</b> drugs.
+ECT	drug	benzodiazepine	9661088	In addition, the direct effect of <b>benzodiazepine</b> drugs and the flumazenil/<b>benzodiazepine</b> combination on <strong>ECT</strong> seizures remains to be determined.
+ECT	drug	benzodiazepine	9283923	<b>Diazepam</b>, carbamazepine, antidepressants or electroconvulsive therapy (<strong>ECT</strong>).
+ECT	drug	benzodiazepine	1571756	A 67 year old anxious and depressed woman was withdrawn from a long term course of a <b>benzodiazepine</b> and soon after was given <strong>ECT</strong>.
+ECT	drug	benzodiazepine	1571756	It is suggested that the chronic administration of the <b>benzodiazepine</b> may have induced changes in the brain that interfered with <strong>ECT</strong>.
+ECT	drug	benzodiazepine	1974219	Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of <b>lorazepam</b> if catatonic symptoms persist, or of electroconvulsive therapy (<strong>ECT</strong>) if psychotic symptoms persist.
+ECT	drug	opioid	7045089	Methods reviewed include the Towns Lambert belladonna treatment, sodium thiocyanate, bromide sleep treatment, Narcosan, insulin, autogenous serum, <strong>ECT</strong>, hibernation, <b>methadone</b>, phenothiazines, propranolol, propoxyphene, acupuncture, vitamin C, and the <b>naloxone</b> flush.
+TANK	drug	alcohol	32639005	DNMT3b mediated methylation of ZSWIM3 enhances inflammation in <b>alcohol</b> induced liver injury via regulating <strong>TRAF2</strong> mediated NF κB pathway.
+TANK	drug	nicotine	31941548	In an online experiment, participants were randomly assigned to view one of four videos, which included <b>smoking</b>, vaping (cigalike or <strong>tank</strong> system), or neutral cues.
+TANK	addiction	relapse	31888637	Compared with modular devices (18.9% <b>relapse</b>), <strong>tank</strong> models (45.6%; adjOR = 3.63; 95% CI, 1.33 9.95) were associated with increased <b>relapse</b>; evidence was unclear for disposable/cartridge refillable devices (41.9%; adjOR = 2.83; 95% CI, 0.90 8.95).
+TANK	drug	nicotine	31837232	Compared to cigarette <b>smoking</b>, <b>nicotine</b> exposure for variable power <strong>tank</strong> users was similar, while cig a like (t(30) = 2.71, P = 0.011, d = 0.745) and fixed power <strong>tank</strong> users (t(30) = 3.37, P = 0.002, d = 0.993) were exposed to less <b>nicotine</b>.
+TANK	drug	nicotine	31837232	During a 24 hour period in a hospital setting in the United States, <b>nicotine</b> exposure for dual users of e cigarettes and cigarettes was similar when using cigarettes or variable power <strong>tank</strong> devices only but was lower for those using cig a like or fixed power devices only.
+TANK	drug	nicotine	31538804	Electronic <b>nicotine</b> delivery systems (ENDS) are devices that contain a power source, a heating element, and a <strong>tank</strong> or cartridge containing an "e liquid," which is a mixture of <b>nicotine</b> and flavoring in a glycerol propylene glycol vehicle.
+TANK	drug	alcohol	30946939	Animals were exposed to <b>ethanol</b> (1% v/v, 20 min) or control water, followed by treatment with NAC (1 mg/L, 10 min) or control water daily for 8 days; 24 h later, experimental animals were submitted to the novel <strong>tank</strong> test (NTT).
+TANK	drug	alcohol	30721969	The Cortical Neuroimmune Regulator <strong>TANK</strong> Affects Emotional Processing and Enhances <b>Alcohol</b> Drinking: A Translational Study.
+TANK	drug	alcohol	30721969	In this report, we analyse how the gene "TRAF family member associated NF κB activator" (<strong>TANK</strong>) affects <b>alcohol</b> drinking behavior.
+TANK	drug	alcohol	30721969	Based on our recent discovery in a large GWAS dataset that suggested an association of <strong>TANK</strong>, SNP rs197273, with <b>alcohol</b> drinking, we report that SNP rs197273 in <strong>TANK</strong> is associated both with gene expression (P = 1.16 × 10 19) and regional methylation (P = 5.90 × 10 25).
+TANK	drug	alcohol	30721969	A <strong>tank</strong> knock out mouse model suggests a role of <strong>TANK</strong> in <b>alcohol</b> drinking, anxiety related behavior, as well as <b>alcohol</b> exposure induced activation of insular cortex NF κB.
+TANK	addiction	aversion	30721969	Functional and structural neuroimaging studies among up to 1896 adolescents reveal that <strong>TANK</strong> is involved in the control of brain activity in areas of <b>aversive</b> interoceptive processing, including the insular cortex, but not in areas related to reinforcement, reward processing or impulsiveness.
+TANK	addiction	reward	30721969	Functional and structural neuroimaging studies among up to 1896 adolescents reveal that <strong>TANK</strong> is involved in the control of brain activity in areas of aversive interoceptive processing, including the insular cortex, but not in areas related to <b>reinforcement</b>, <b>reward</b> processing or impulsiveness.
+TANK	drug	alcohol	30721969	Our findings suggest that the cortical neuroimmune regulator <strong>TANK</strong> is associated with enhanced aversive emotional processing that better protects from the establishment of <b>alcohol</b> drinking behavior.
+TANK	addiction	aversion	30721969	Our findings suggest that the cortical neuroimmune regulator <strong>TANK</strong> is associated with enhanced <b>aversive</b> emotional processing that better protects from the establishment of alcohol drinking behavior.
+TANK	drug	nicotine	29481898	Here we evaluated the rewarding effects of <b>nicotine</b> and caffeine using a <strong>tank</strong> with five arms distributed radially from a central chamber that we have denoted Fish <strong>Tank</strong> Radial Maze (FTRM).
+TANK	drug	nicotine	29129555	To address this issue, we monitored blood <b>nicotine</b> levels during the acute phase in volunteers using disposable cigalikes (CLs) and a <strong>tank</strong> model (TM) and compared them with blood <b>nicotine</b> levels in subjects using a <b>tobacco</b> cigarette (TC).
+TANK	drug	psychedelics	28855876	In this study, <b>MDMA</b> (2.5 10 mg/kg), DOB (0.5 mg/kg), or PMA (0.005, 0.1, or 0.25 mg/kg) were administered intramuscularly to adult zebra fish, alone or in combination with the V1a vasopressin antagonist, SR49059 (0.01 1 ng/kg), before carrying out conditioned place preference (CPP), social preference, novel <strong>tank</strong> diving, and light dark tests in order to evaluate subsequent rewarding, social, and emotional like behavior.
+TANK	addiction	reward	28855876	In this study, MDMA (2.5 10 mg/kg), DOB (0.5 mg/kg), or PMA (0.005, 0.1, or 0.25 mg/kg) were administered intramuscularly to adult zebra fish, alone or in combination with the V1a vasopressin antagonist, SR49059 (0.01 1 ng/kg), before carrying out conditioned place preference (<b>CPP</b>), social preference, novel <strong>tank</strong> diving, and light dark tests in order to evaluate subsequent rewarding, social, and emotional like behavior.
+TANK	addiction	reward	28855876	The combination of SR49059 and each drug progressively blocked: (1) rewarding behavior as measured by <b>CPP</b> in terms of time spent in drug paired compartment; (2) prosocial effects measured on the basis of the time spent in the proximity of a nacre fish picture; and (3) anxiolytic effects in terms of the time spent in the upper half of the novel <strong>tank</strong> and in the white compartment of the <strong>tank</strong> used for the light dark test.
+TANK	drug	alcohol	28797598	In this study, <b>ethanol</b> induced change in time spent by zebrafish on the initially non preferred <strong>tank</strong> side was studied by conditioning adult zebrafish to <b>ethanol</b> dissolved in water (0.00% 1.00%; 1.25%; 1.50%; 1.60%; 1.75% vol/vol) paired with an initially non preferred environment.
+TANK	drug	alcohol	28714785	Zebrafish were initially exposed to different <b>alcohol</b> treatments and submitted to an inhibitory avoidance protocol, where an electroshock was applied to the fish as they swam from the white to the black side of a shuttle box <strong>tank</strong> (naturally preferred environment of zebrafish).
+TANK	drug	alcohol	28714785	Animals from the control and 0.5% acute <b>alcohol</b> groups exhibited high latency to enter the black side of the <strong>tank</strong> after the first exposure to electroshock, in addition to higher freezing and a shorter distance from the bottom of the <strong>tank</strong>, suggesting acute <b>alcohol</b> exposure did not affect aversive learning in zebrafish.
+TANK	addiction	aversion	28714785	Animals from the control and 0.5% acute alcohol groups exhibited high latency to enter the black side of the <strong>tank</strong> after the first exposure to electroshock, in addition to higher freezing and a shorter distance from the bottom of the <strong>tank</strong>, suggesting acute alcohol exposure did not affect <b>aversive</b> learning in zebrafish.
+TANK	drug	benzodiazepine	28645783	Adult zebrafish were treated with M. angolensis extract, fluoxetine, desipramine, and <b>diazepam</b> followed by testing in the novel <strong>tank</strong> and light dark tests.
+TANK	drug	nicotine	28393086	Among the 8 <strong>tank</strong> users, number of puffs was positively correlated with amount of <b>nicotine</b> inhaled, Cmax, and area under the plasma <b>nicotine</b> concentration time curve (AUC0→90min) while interpuff interval was negatively correlated with Cmax and AUC0→90.
+TANK	drug	alcohol	28092494	In the current study, we analyzed the time course of <b>alcohol</b> induced behavioral changes of zebrafish while being immersed in <b>alcohol</b> solution in a 1.5 L <strong>tank</strong>.
+TANK	drug	benzodiazepine	27061599	Successively, they explored the relationship between the internal concentrations of <b>oxazepam</b> and the effects on fish exploratory behavior quantified by performing 2 types of behavioral tests, the novel <strong>tank</strong> diving test and the shelter seeking test.
+TANK	addiction	relapse	27061599	Successively, they explored the relationship between the internal concentrations of oxazepam and the effects on fish exploratory behavior quantified by performing 2 types of behavioral tests, the novel <strong>tank</strong> diving test and the shelter <b>seeking</b> test.
+TANK	drug	alcohol	26781213	We utilized the zebrafish model system to address the effect of chronic <b>alcohol</b> exposure (0.5% <b>alcohol</b> in the holding <strong>tank</strong> for 9 weeks) on reproductive capacity.
+TANK	drug	alcohol	26781213	In agreement with observations on fecundity, the chronic <b>alcohol</b> exposure leads to increased anxiety, as measured by the novel <strong>tank</strong> diving assay.
+TANK	drug	amphetamine	26433144	In the novel <strong>tank</strong> test, acute administration of <b>METH</b> (2 mg/L) induced a significant decrease in the number of total vertical transitions and time spent in the upper zone.
+TANK	drug	nicotine	25643654	We also found that chronic exposure to <b>nicotine</b> evokes robust anxiogenic behavioral responses in zebrafish tested in the novel <strong>tank</strong> test paradigm.
+TANK	addiction	aversion	25599606	Habituation to a repeated environmental stimulus and overall sensorimotor function were assessed using a tap startle test; measurements of anxiety and exploration behavior were made following introduction to a novel <strong>tank</strong>; and spatial discrimination learning was assessed using <b>aversive</b> control in a three chambered apparatus.
+TANK	drug	alcohol	25599606	<b>Ethanol</b> treated fish were more active both at baseline and following a tap stimulus compared to the control fish and were hyperactive when placed in a novel <strong>tank</strong>.
+TANK	drug	nicotine	26946554	Aims of the study were to (1) measure and compare <b>nicotine</b> concentration in e liquids to values reported by manufacturers on packaging labels; (2) assess the precision of <b>nicotine</b> delivery from <strong>tank</strong> during aerosol formation.
+TANK	drug	alcohol	24922137	In this case study, we examined how SABMiller engaged the think <strong>tank</strong> Demos to produce reports on binge drinking, which were heavily promoted among policymakers at crucial stages in the development of the UK government's 2012 <b>alcohol</b> strategy.
+TANK	addiction	intoxication	24922137	In this case study, we examined how SABMiller engaged the think <strong>tank</strong> Demos to produce reports on <b>binge</b> drinking, which were heavily promoted among policymakers at crucial stages in the development of the UK government's 2012 alcohol strategy.
+TANK	drug	nicotine	24922137	In this instance, the perceived independence of an influential think <strong>tank</strong> was used to promote industry interests in tactics similar to those of transnational <b>tobacco</b> corporations.
+TANK	drug	alcohol	24681197	For the drug seeking behavior, we used a place preference paradigm (shuttle box <strong>tank</strong>) before and after <b>alcohol</b> exposure in acute (single exposure) and chronic (7 days) treatments.
+TANK	addiction	relapse	24681197	For the drug <b>seeking</b> behavior, we used a place preference paradigm (shuttle box <strong>tank</strong>) before and after alcohol exposure in acute (single exposure) and chronic (7 days) treatments.
+TANK	drug	cannabinoid	24216135	Here, we explore the effects of acute 20 min exposure to two commonly abused psychotropic compounds, Δ(9) <b>tetrahydrocannabinol</b> (<b>THC</b>) and heroin, on adult zebrafish behavior in the novel <strong>tank</strong> test.
+TANK	drug	opioid	24216135	Here, we explore the effects of acute 20 min exposure to two commonly abused psychotropic compounds, Δ(9) tetrahydrocannabinol (THC) and <b>heroin</b>, on adult zebrafish behavior in the novel <strong>tank</strong> test.
+TANK	drug	nicotine	23869690	Here, we tested adult zebrafish from the casper line, as well as wild type (Tübingen, TU) and wild types treated as embryos with PTU on three commonly used behavioural endpoints in neuroscience: novel <strong>tank</strong> test (similar to open field in rodents), conditioned place preference for <b>nicotine</b>, and social cohesion (using a new method of cluster analysis).
+TANK	drug	alcohol	23658154	The novel gene <strong>tank</strong>, a tumor suppressor homolog, regulates <b>ethanol</b> sensitivity in Drosophila.
+TANK	drug	alcohol	23658154	Based on a previous genetic screen in Drosophila for <b>ethanol</b> sedation mutants, we identified a novel gene, <strong>tank</strong> (CG15626), the homolog of the mammalian tumor suppressor EI24/PIG8, which has a strong role in regulating <b>ethanol</b> sedation sensitivity.
+TANK	drug	alcohol	23658154	Genetic and behavioral analyses revealed that <strong>tank</strong> acts in the adult nervous system to promote <b>ethanol</b> sensitivity.
+TANK	drug	alcohol	23658154	We localized the function of <strong>tank</strong> in regulating <b>ethanol</b> sensitivity to neurons within the pars intercerebralis that have not been implicated previously in <b>ethanol</b> responses.
+TANK	drug	alcohol	23658154	We show that acutely manipulating the activity of all <strong>tank</strong> expressing neurons, or of pars intercerebralis neurons in particular, alters <b>ethanol</b> sensitivity in a sexually dimorphic manner, since neuronal activation enhanced <b>ethanol</b> sedation in males, but not females.
+TANK	drug	alcohol	23658154	Finally, we provide anatomical evidence that <strong>tank</strong> expressing neurons form likely synaptic connections with neurons expressing the neural sex determination factor fruitless (fru), which have been implicated recently in the regulation of <b>ethanol</b> sensitivity.
+TANK	drug	alcohol	23558086	We assessed the effects of withdrawal from chronic <b>ethanol</b> exposure, and subsequent administration of fluoxetine (Prozac®), buspirone (Buspar®), and diazepam (Valium) using two behavioral paradigms; the Novel <strong>Tank</strong> Diving Test and the Light/Dark Choice Assay.
+TANK	drug	benzodiazepine	23558086	We assessed the effects of withdrawal from chronic ethanol exposure, and subsequent administration of fluoxetine (Prozac®), buspirone (Buspar®), and <b>diazepam</b> (<b>Valium</b>) using two behavioral paradigms; the Novel <strong>Tank</strong> Diving Test and the Light/Dark Choice Assay.
+TANK	addiction	withdrawal	23558086	We assessed the effects of <b>withdrawal</b> from chronic ethanol exposure, and subsequent administration of fluoxetine (Prozac®), buspirone (Buspar®), and diazepam (Valium) using two behavioral paradigms; the Novel <strong>Tank</strong> Diving Test and the Light/Dark Choice Assay.
+TANK	drug	alcohol	23558086	Following withdrawal from chronic <b>ethanol</b> exposure, zebrafish exhibited dose/time dependent anxiogenic effects; including reduced exploration and freezing behavior in the Novel <strong>Tank</strong> Diving Test, and preference for the dark area for the Light/Dark Choice Assay.
+TANK	addiction	withdrawal	23558086	Following <b>withdrawal</b> from chronic ethanol exposure, zebrafish exhibited dose/time dependent anxiogenic effects; including reduced exploration and freezing behavior in the Novel <strong>Tank</strong> Diving Test, and preference for the dark area for the Light/Dark Choice Assay.
+TANK	drug	alcohol	22266470	Animated bird silhouette above the <strong>tank</strong>: acute <b>alcohol</b> diminishes fear responses in zebrafish.
+TANK	drug	alcohol	22266470	The fear inducing stimulus was found to decrease the distance of the zebrafish from the bottom of the <strong>tank</strong>, to increase number of erratic movements, and to increase the number of jumps in <b>alcohol</b> exposed fish (versus control fish).
+TANK	drug	opioid	22205946	Using the novel <strong>tank</strong> diving tests, we first showed that <b>morphine</b> withdrawn zebrafish display anxiety related swimming behaviors such as decreased exploratory behavior and increased erratic movement.
+TANK	drug	alcohol	21255611	In this study, we assess the effects of both acute and chronic <b>ethanol</b> exposure on anxiety like behaviors in zebrafish, using two behavioral paradigms, the Novel <strong>Tank</strong> Diving Test and the Light/Dark Choice Assay.
+TANK	drug	alcohol	20974186	The largest increase in preference is in response to a 1.5% <b>ethanol</b> administered in the <strong>tank</strong> water.
+TANK	drug	alcohol	9392779	In Experiment 2, either 4.5 or 5.25 g/kg/day of <b>ethanol</b> was administered on PD 7 9 and place learning was tested in a 171 cm diameter <strong>tank</strong>.
+CHRNA4	drug	nicotine	31402126	Gene polymorphisms of CHRNA3 (rs578776) and <strong>CHRNA4</strong> (rs1044396 and rs2229959) were associated with the success of <b>smoking</b> cessation after the diagnosis of lung cancer, which should be considered in the management of <b>smoking</b> cessation after patients are diagnosed with lung cancer.
+CHRNA4	drug	alcohol	31294817	Candidates supported by both FTND and TTFC (<strong>CHRNA4</strong>, THSD7B, RBFOX1, and ZNF804A) were associated with addiction to <b>alcohol</b>, cocaine, and heroin, and were associated with autism and schizophrenia.
+CHRNA4	drug	cocaine	31294817	Candidates supported by both FTND and TTFC (<strong>CHRNA4</strong>, THSD7B, RBFOX1, and ZNF804A) were associated with addiction to alcohol, <b>cocaine</b>, and heroin, and were associated with autism and schizophrenia.
+CHRNA4	drug	opioid	31294817	Candidates supported by both FTND and TTFC (<strong>CHRNA4</strong>, THSD7B, RBFOX1, and ZNF804A) were associated with addiction to alcohol, cocaine, and <b>heroin</b>, and were associated with autism and schizophrenia.
+CHRNA4	addiction	addiction	31294817	Candidates supported by both FTND and TTFC (<strong>CHRNA4</strong>, THSD7B, RBFOX1, and ZNF804A) were associated with <b>addiction</b> to alcohol, cocaine, and heroin, and were associated with autism and schizophrenia.
+CHRNA4	drug	nicotine	29411706	Our results confirmed the genetic effect of <strong>CHRNA4</strong> and CHRNB2 on <b>smoking</b> related depression.
+CHRNA4	drug	nicotine	28583088	Finally, we found that liver specific <strong>CHRNA4</strong> transcription was highly correlated with genes involved in the <b>nicotine</b> metabolism, including CYP2A6, UGT2B7, and FMO3.
+CHRNA4	drug	nicotine	27611310	<strong>CHRNA4</strong> and ANKK1 Polymorphisms Influence <b>Smoking</b> Induced Nicotinic Acetylcholine Receptor Upregulation.
+CHRNA4	drug	nicotine	27611310	The <strong>CHRNA4</strong> SNP rs2236196 and ANKK1 SNP rs4938015 were associated with significantly higher cerebellar and cortical β2* nAChR availability in <b>smokers</b> versus nonsmokers for specific genotypes.
+CHRNA4	drug	nicotine	27611310	This study provides evidence for genetic regulation of <b>tobacco</b> <b>smoking</b> induced changes in β2* nAChR availability and suggests that β2* nAChR availability could be an endophenotype mediating influences of <strong>CHRNA4</strong> variants on <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	27611310	This study provides evidence for genetic regulation of tobacco smoking induced changes in β2* nAChR availability and suggests that β2* nAChR availability could be an endophenotype mediating influences of <strong>CHRNA4</strong> variants on nicotine <b>dependence</b>.
+CHRNA4	drug	nicotine	27428758	In the cholinergic system, regional differences in Chnrb2 and Chrna5, sex differences in <strong>Chrna4</strong> and Chrna5, and <b>nicotine</b> preference effects in the expression of all subunits except α4 were observed.
+CHRNA4	drug	nicotine	27327258	Besides the <strong>CHRNA4</strong>, CHRNB2 and CHRNA5/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the CHRNB3 CHRNA6 gene cluster on chromosome 8 in <b>nicotine</b> dependence (ND).
+CHRNA4	addiction	dependence	27327258	Besides the <strong>CHRNA4</strong>, CHRNB2 and CHRNA5/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the CHRNB3 CHRNA6 gene cluster on chromosome 8 in nicotine <b>dependence</b> (ND).
+CHRNA4	drug	nicotine	27054571	Single nucleotide polymorphisms (SNPs) in the <strong>CHRNA4</strong> gene that codes for the alpha4 subunit of alpha4/beta2 containing receptors have previously been implicated in aspects of (mostly visual) attention and <b>smoking</b> related behavioral measures.
+CHRNA4	drug	nicotine	26952864	A rare missense mutation in <strong>CHRNA4</strong> associates with <b>smoking</b> behavior and its consequences.
+CHRNA4	drug	nicotine	26952864	Using Icelandic whole genome sequence data and an imputation approach we searched for rare sequence variants in <strong>CHRNA4</strong> and tested them for association with <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	26952864	Using Icelandic whole genome sequence data and an imputation approach we searched for rare sequence variants in <strong>CHRNA4</strong> and tested them for association with nicotine <b>dependence</b>.
+CHRNA4	drug	nicotine	26952864	We show that carriers of a rare missense variant (allele frequency=0.24%) within <strong>CHRNA4</strong>, encoding an R336C substitution, have greater risk of <b>nicotine</b> addiction than non carriers as assessed by the Fagerstrom Test for <b>Nicotine</b> Dependence (P=1.2 × 10( 4)).
+CHRNA4	addiction	addiction	26952864	We show that carriers of a rare missense variant (allele frequency=0.24%) within <strong>CHRNA4</strong>, encoding an R336C substitution, have greater risk of nicotine <b>addiction</b> than non carriers as assessed by the Fagerstrom Test for Nicotine Dependence (P=1.2 × 10( 4)).
+CHRNA4	addiction	dependence	26952864	We show that carriers of a rare missense variant (allele frequency=0.24%) within <strong>CHRNA4</strong>, encoding an R336C substitution, have greater risk of nicotine addiction than non carriers as assessed by the Fagerstrom Test for Nicotine <b>Dependence</b> (P=1.2 × 10( 4)).
+CHRNA4	drug	nicotine	26440539	Genome wide meta analysis reveals common splice site acceptor variant in <strong>CHRNA4</strong> associated with <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	26440539	Genome wide meta analysis reveals common splice site acceptor variant in <strong>CHRNA4</strong> associated with nicotine <b>dependence</b>.
+CHRNA4	addiction	dependence	26440539	We identified genome wide significant association in the alpha 4 nicotinic receptor subunit (<strong>CHRNA4</strong>) gene on chromosome 20q13: lowest P=8.0 × 10( 9) across all the samples for rs2273500 C (frequency=0.15; odds ratio=1.12 and 95% confidence interval=1.08 1.17 for severe vs mild <b>dependence</b>).
+CHRNA4	drug	nicotine	26440539	Using criteria for <b>smoking</b> behavior that encompass more than the single 'cigarettes per day' item, we identified a common <strong>CHRNA4</strong> variant with important regulatory properties that contributes to <b>nicotine</b> dependence and <b>smoking</b> related consequences.
+CHRNA4	addiction	dependence	26440539	Using criteria for smoking behavior that encompass more than the single 'cigarettes per day' item, we identified a common <strong>CHRNA4</strong> variant with important regulatory properties that contributes to nicotine <b>dependence</b> and smoking related consequences.
+CHRNA4	drug	nicotine	26416825	Three hundred sixty four Mexican Mestizo Mexico City residents from 87 families with at least one <b>smoker</b> were assessed for association of 12 gene variants of six candidate genes (<strong>CHRNA4</strong>, CHRNB2, DRD2, ANKK1, SLC6A3, and CYP2A6) with cigarette consumption, age of initiation and <b>smoking</b> duration.
+CHRNA4	drug	nicotine	25774163	<strong>CHRNA4</strong> rs1044396 is associated with <b>smoking</b> cessation in varenicline therapy.
+CHRNA4	drug	nicotine	25774163	In the context of personalized medicine, the main aim of the present study was to evaluate whether the <strong>CHRNA4</strong> and CHRNB2 polymorphisms are associated with response to <b>smoking</b> cessation therapies in patients from a <b>smoker</b> assistance program.
+CHRNA4	drug	nicotine	25774163	The <strong>CHRNA4</strong> rs1044396 is associated with <b>smoking</b> cessation in individuals on varenicline therapy.
+CHRNA4	drug	nicotine	25498233	As an example of the ability of a natural genetic variant to modify the effect of an engineered mutation, data will be presented that demonstrate that the effect of Chrna5 deletion on oral <b>nicotine</b> intake is dependent upon naturally occurring variant alleles of <strong>Chrna4</strong>.
+CHRNA4	drug	nicotine	24498031	Massive withdrawal symptoms and affective vulnerability are associated with variants of the <strong>CHRNA4</strong> gene in a subgroup of <b>smokers</b>.
+CHRNA4	addiction	withdrawal	24498031	Massive <b>withdrawal</b> symptoms and affective vulnerability are associated with variants of the <strong>CHRNA4</strong> gene in a subgroup of smokers.
+CHRNA4	drug	nicotine	24498031	This is the first report on a significant association between <strong>CHRNA4</strong> variants and a subgroup of <b>smokers</b> characterized by massive withdrawal symptoms and affective vulnerability.
+CHRNA4	addiction	withdrawal	24498031	This is the first report on a significant association between <strong>CHRNA4</strong> variants and a subgroup of smokers characterized by massive <b>withdrawal</b> symptoms and affective vulnerability.
+CHRNA4	addiction	intoxication	24428733	Association of the <strong>CHRNA4</strong> neuronal nicotinic receptor subunit gene with frequency of <b>binge</b> drinking in young adults.
+CHRNA4	drug	alcohol	24428733	Frequency of binge drinking and other correlated <b>alcohol</b> consumption measures were significantly associated with SNPs in <strong>CHRNA4</strong> (p values ranged from 0.0003 to 0.02), but not with SNPs in other CHRNs.
+CHRNA4	addiction	intoxication	24428733	Frequency of <b>binge</b> drinking and other correlated alcohol consumption measures were significantly associated with SNPs in <strong>CHRNA4</strong> (p values ranged from 0.0003 to 0.02), but not with SNPs in other CHRNs.
+CHRNA4	addiction	intoxication	24428733	Variants in <strong>CHRNA4</strong> may contribute to risk of <b>binge</b> drinking in young adults in this cohort.
+CHRNA4	drug	nicotine	24385388	A number of rare variants in the <strong>CHRNA4</strong> gene that encode the α4 nAChR subunit have been identified in human subjects and appear to be underrepresented in a cohort of <b>smokers</b>.
+CHRNA4	drug	nicotine	24385388	Taken together, these experiments suggest that genetic variation at <strong>CHRNA4</strong> alters the assembly and expression of human α4β2 nAChRs, resulting in receptors that are more sensitive to <b>nicotine</b> exposure than those assembled with the common α4 variant.
+CHRNA4	drug	nicotine	24057800	In application to a real dataset, we detected one significant tetragenic interaction among <strong>CHRNA4</strong>, CHRNB2, BDNF, and NTRK2 associated with <b>nicotine</b> dependence in the Study of Addiction: Genetics and Environment sample, suggesting the biological role of these genes in <b>nicotine</b> dependence development.
+CHRNA4	addiction	addiction	24057800	In application to a real dataset, we detected one significant tetragenic interaction among <strong>CHRNA4</strong>, CHRNB2, BDNF, and NTRK2 associated with nicotine dependence in the Study of <b>Addiction</b>: Genetics and Environment sample, suggesting the biological role of these genes in nicotine dependence development.
+CHRNA4	addiction	dependence	24057800	In application to a real dataset, we detected one significant tetragenic interaction among <strong>CHRNA4</strong>, CHRNB2, BDNF, and NTRK2 associated with nicotine <b>dependence</b> in the Study of Addiction: Genetics and Environment sample, suggesting the biological role of these genes in nicotine <b>dependence</b> development.
+CHRNA4	drug	nicotine	23553665	We investigated whether <b>nicotine</b> dependence affects these endophenotypes in Japanese schizophrenia patients and whether alpha4 and beta2 subunits of neuronal nicotinic acetylcholine receptor genes (alpha4 subunit of the nAChR gene (<strong>CHRNA4</strong>)/beta2 subunit of the nAChR gene (CHRNB2)) were associated with <b>nicotine</b> dependence in patients (n = 100) and healthy controls (n = 107).
+CHRNA4	addiction	dependence	23553665	We investigated whether nicotine <b>dependence</b> affects these endophenotypes in Japanese schizophrenia patients and whether alpha4 and beta2 subunits of neuronal nicotinic acetylcholine receptor genes (alpha4 subunit of the nAChR gene (<strong>CHRNA4</strong>)/beta2 subunit of the nAChR gene (CHRNB2)) were associated with nicotine <b>dependence</b> in patients (n = 100) and healthy controls (n = 107).
+CHRNA4	drug	nicotine	23553665	Finally, using 12 tagging single nucleotide polymorphisms in each the <strong>CHRNA4</strong>/CHRNB2, we used multiple linear regression analysis to examine the association between <b>nicotine</b> dependence measures and each selected single nucleotide polymorphism.
+CHRNA4	addiction	dependence	23553665	Finally, using 12 tagging single nucleotide polymorphisms in each the <strong>CHRNA4</strong>/CHRNB2, we used multiple linear regression analysis to examine the association between nicotine <b>dependence</b> measures and each selected single nucleotide polymorphism.
+CHRNA4	drug	nicotine	23553665	In addition, rs755203 and rs1044397 in <strong>CHRNA4</strong> were associated with <b>nicotine</b> dependence in healthy controls.
+CHRNA4	addiction	dependence	23553665	In addition, rs755203 and rs1044397 in <strong>CHRNA4</strong> were associated with nicotine <b>dependence</b> in healthy controls.
+CHRNA4	drug	nicotine	23553665	In addition, rs755203 and rs1044397 in <strong>CHRNA4</strong> might play a role in the pathophysiology of <b>nicotine</b> dependence in healthy controls in the Japanese population.
+CHRNA4	addiction	dependence	23553665	In addition, rs755203 and rs1044397 in <strong>CHRNA4</strong> might play a role in the pathophysiology of nicotine <b>dependence</b> in healthy controls in the Japanese population.
+CHRNA4	drug	nicotine	23350800	Nominal association with <strong>CHRNA4</strong> variants and <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	23350800	Nominal association with <strong>CHRNA4</strong> variants and nicotine <b>dependence</b>.
+CHRNA4	drug	nicotine	23037950	Possible association of nicotinic acetylcholine receptor gene (<strong>CHRNA4</strong> and CHRNB2) polymorphisms with <b>nicotine</b> dependence in Japanese males: an exploratory study.
+CHRNA4	addiction	dependence	23037950	Possible association of nicotinic acetylcholine receptor gene (<strong>CHRNA4</strong> and CHRNB2) polymorphisms with nicotine <b>dependence</b> in Japanese males: an exploratory study.
+CHRNA4	drug	nicotine	23037950	It has been reported that the nicotinic acetylcholine receptor (<strong>CHRNA4</strong> and CHRNB2) genes might be associated with <b>smoking</b> behavior in several ethnic populations.
+CHRNA4	drug	nicotine	23037950	Furthermore, we demonstrated a possible gene gene interaction of <strong>CHRNA4</strong> and CHRNB2 on ND in a dose dependent manner: those <b>smokers</b> with <strong>CHRNA4</strong> rs1044397 GG or GA genotypes along with CHRNB2 rs4845652 CC genotype are likely to demonstrate higher ND scores.
+CHRNA4	drug	nicotine	22309839	Our results provided confirmation of the previous findings that DRD2, DRD3, DDC, CHRNB3, GABBR2 and <strong>CHRNA4</strong> are associated with <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	22309839	Our results provided confirmation of the previous findings that DRD2, DRD3, DDC, CHRNB3, GABBR2 and <strong>CHRNA4</strong> are associated with nicotine <b>dependence</b>.
+CHRNA4	drug	nicotine	26451072	Gamma aminobutyric acid B receptor 2 (GABBR2), dopa decarboxylase (DDC), and cholinergic receptor nicotinic alpha 4 (<strong>CHRNA4</strong>) are three examples of genes that have previously shown strong associations with <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	26451072	Gamma aminobutyric acid B receptor 2 (GABBR2), dopa decarboxylase (DDC), and cholinergic receptor nicotinic alpha 4 (<strong>CHRNA4</strong>) are three examples of genes that have previously shown strong associations with nicotine <b>dependence</b>.
+CHRNA4	drug	nicotine	26451072	We used a population based sample of 377 case parent trios of cleft lip with or without cleft palate (CL/P) and 762 control parent trios from Norway (1996 2001) to investigate whether variants in GABBR2, DDC and <strong>CHRNA4</strong> are associated with maternal first trimester <b>smoking</b> and with clefting risk.
+CHRNA4	drug	nicotine	26451072	Despite strong associations previously reported between <b>nicotine</b> dependence and variants in GABBR2, DDC and <strong>CHRNA4</strong>, these genes were poor predictors of maternal first trimester <b>smoking</b> in our data.
+CHRNA4	addiction	dependence	26451072	Despite strong associations previously reported between nicotine <b>dependence</b> and variants in GABBR2, DDC and <strong>CHRNA4</strong>, these genes were poor predictors of maternal first trimester smoking in our data.
+CHRNA4	drug	nicotine	21740768	It has been reported that the nicotinic acetylcholine receptor subunit α4 gene (<strong>CHRNA4</strong>) might be associated with <b>smoking</b> behaviors in the previous studies.
+CHRNA4	drug	nicotine	21740768	Up to now, there are few reports on the relationship between <strong>CHRNA4</strong> and <b>smoking</b> initiation.
+CHRNA4	drug	nicotine	21740768	In this study, we tried to explore the role of two polymorphisms in <strong>CHRNA4</strong> (rs1044396 and rs1044397) in <b>smoking</b> initiation and <b>nicotine</b> dependence in Chinese male <b>smokers</b>.
+CHRNA4	addiction	dependence	21740768	In this study, we tried to explore the role of two polymorphisms in <strong>CHRNA4</strong> (rs1044396 and rs1044397) in smoking initiation and nicotine <b>dependence</b> in Chinese male smokers.
+CHRNA4	drug	nicotine	21740768	These findings suggest that <strong>CHRNA4</strong> may be associated with <b>smoking</b> initiation and the C G haplotype of rs1044396 rs1044397 might increase the vulnerability to <b>nicotine</b> dependence in Chinese male <b>smokers</b>.
+CHRNA4	addiction	dependence	21740768	These findings suggest that <strong>CHRNA4</strong> may be associated with smoking initiation and the C G haplotype of rs1044396 rs1044397 might increase the vulnerability to nicotine <b>dependence</b> in Chinese male smokers.
+CHRNA4	drug	nicotine	21683344	Several studies report association of alpha 4 nicotinic acetylcholine receptors (encoded by <strong>CHRNA4</strong>) with <b>nicotine</b> dependence (ND).
+CHRNA4	addiction	dependence	21683344	Several studies report association of alpha 4 nicotinic acetylcholine receptors (encoded by <strong>CHRNA4</strong>) with nicotine <b>dependence</b> (ND).
+CHRNA4	drug	nicotine	21445957	Association of <strong>CHRNA4</strong> polymorphisms with <b>smoking</b> behavior in two populations.
+CHRNA4	drug	nicotine	21445957	<strong>CHRNA4</strong>, the gene that encodes the nicotinic acetylcholine receptor α(4) subunit, is a potential candidate gene for <b>nicotine</b> dependence (ND).
+CHRNA4	addiction	dependence	21445957	<strong>CHRNA4</strong>, the gene that encodes the nicotinic acetylcholine receptor α(4) subunit, is a potential candidate gene for nicotine <b>dependence</b> (ND).
+CHRNA4	drug	nicotine	21445957	Our meta analysis of linkage studies of <b>smoking</b> behavior identified a genome wide significant linkage of the phenotype maximum number of cigarettes smoked in a 24 hour period to a region (20q13.12 q13.32) harboring <strong>CHRNA4</strong>.
+CHRNA4	drug	nicotine	21445957	This motivated us to examine the association of <strong>CHRNA4</strong> with <b>smoking</b> behavior in two independent samples.
+CHRNA4	drug	nicotine	21445957	In this study, we examined five single nucleotide polymorphisms (SNPs) within <strong>CHRNA4</strong> and three <b>smoking</b> related behaviors: one quantitative trait [cigarettes smoked per day (CPD)], and two binary traits [DSM IV diagnosis of ND and dichotomized Fagerstrom test of ND (FTND)], in 1,249 unrelated European Americans (EAs) and 1,790 unrelated African Americans (AAs).
+CHRNA4	drug	nicotine	20736995	Exons of 10 genes were resequenced with next generation sequencing technology in 448 European American participants of a <b>smoking</b> cessation trial, and CHRNB2 and <strong>CHRNA4</strong> were resequenced by Sanger technology to improve sequence coverage.
+CHRNA4	drug	alcohol	20496163	This report explores the association between six nAChR subunit genes (Chrna3, <strong>Chrna4</strong>, Chrnb4, Chrnb2, Chrna5, and Chrna7) with <b>alcohol</b> preference (AP) using co segregation of AP with nAChR subunit genotypes in a F(2) population produced from reciprocal crosses of <b>alcohol</b> preferring C57BL/6J (B6) and <b>alcohol</b> avoiding DBA/2J (D2) strains of mice.
+CHRNA4	drug	nicotine	20061993	<strong>Chrna4</strong> A529 knock in mice exhibit altered <b>nicotine</b> sensitivity.
+CHRNA4	drug	nicotine	20061993	However, one genetic variant has been implicated in altering <b>nicotine</b> sensitivity in mice is a T529A polymorphism in <strong>Chrna4</strong>, the gene that encodes the nicotinic receptor (nAChR) alpha4 subunit.
+CHRNA4	drug	nicotine	20061993	To more definitively address whether the <strong>Chrna4</strong> T529A polymorphism does, in fact, influence sensitivity to <b>nicotine</b>, knock in mice were generated in which the threonine codon at position 529 was mutated to an alanine codon.
+CHRNA4	drug	nicotine	20061993	Compared with <strong>Chrna4</strong> T529 littermate controls, the <strong>Chrna4</strong> A529 knock in mice exhibited greater sensitivity to the hypothermic effects of <b>nicotine</b>, reduced oral <b>nicotine</b> consumption and did not develop conditioned place preference to <b>nicotine</b>.
+CHRNA4	drug	nicotine	19819424	Subgroup analysis of MaxCigs24 (966 families with 3273 subjects) identified a genome wide significant linkage in 20q13.12 q13.32 (p(SR) = .00041, p(OR) = .048), where a strongly supported <b>nicotine</b> dependence candidate gene, <strong>CHRNA4</strong>, is located.
+CHRNA4	addiction	dependence	19819424	Subgroup analysis of MaxCigs24 (966 families with 3273 subjects) identified a genome wide significant linkage in 20q13.12 q13.32 (p(SR) = .00041, p(OR) = .048), where a strongly supported nicotine <b>dependence</b> candidate gene, <strong>CHRNA4</strong>, is located.
+CHRNA4	drug	alcohol	19698703	Moreover, one haplotype of the <strong>CHRNA4</strong> (GGTG) was associated with increased body weight as compared to non carriers of this haplotype, especially in the heavy consumers of <b>alcohol</b> (p=0.004).The present findings are the first to disclose a haplotype association between the CHRNA6 gene and heavy <b>alcohol</b> use as well as an association of the <strong>CHRNA4</strong> gene with increased body mass in heavy consumers of <b>alcohol</b>.
+CHRNA4	drug	nicotine	19693267	Financial and psychological risk attitudes associated with two single nucleotide polymorphisms in the <b>nicotine</b> receptor (<strong>CHRNA4</strong>) gene.
+CHRNA4	drug	nicotine	19693267	Analysis of the genotyping data identified two single nucleotide polymorphisms (SNPs) in the gene encoding the alpha 4 <b>nicotine</b> receptor (<strong>CHRNA4</strong>, rs4603829 and rs4522666) that are significantly associated with harm avoidance, a risk attitude measurement drawn from the psychology literature.
+CHRNA4	addiction	relapse	19482438	There were possible associations between the temperament trait novelty <b>seeking</b> and <strong>CHRNA4</strong> rs1044396, CHRNA5 rs16969968 and CHRNB2 rs4845378, but these associations were not robust to correction for multiple testing.
+CHRNA4	drug	nicotine	19482438	We conclude that the analysis of polymorphisms in genes coding for four nicotinic acetylcholine receptor subunits (<strong>CHRNA4</strong>, CHRNA5, CHRNB2 and CHRNB3) and several <b>smoking</b> related phenotypes revealed no statistically significant association.
+CHRNA4	drug	nicotine	19290018	Polymorphisms in the <strong>CHRNA4</strong> gene coding the nicotinic acetylcholine receptor subunit alpha 4 have recently been suggested to play a role in the determination of <b>smoking</b> related phenotypes.
+CHRNA4	drug	nicotine	19290018	Five single nucleotide polymorphisms in <strong>CHRNA4</strong> were genotyped in 5561 participants, including 2707 heavily <b>smoking</b> cases (regularly <b>smoking</b> at least 20 cigarettes per day) and 2399 never <b>smoking</b> controls (<or=100 cigarettes over lifetime).
+CHRNA4	drug	nicotine	19290018	The consistent effect estimates across three independent cohorts elaborate on recently published functional studies of rs2236196 from the <strong>CHRNA4</strong> 3' untranslated region and seem to converge with accumulating evidence to firmly implicate the variant G allele of this polymorphism in the intensification of <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	19290018	The consistent effect estimates across three independent cohorts elaborate on recently published functional studies of rs2236196 from the <strong>CHRNA4</strong> 3' untranslated region and seem to converge with accumulating evidence to firmly implicate the variant G allele of this polymorphism in the intensification of nicotine <b>dependence</b>.
+CHRNA4	drug	amphetamine	18991851	Therefore, we conducted a genetic association analysis of the alpha4 gene (<strong>CHRNA4</strong>) and beta2 gene (CHRNB2) with <b>methamphetamine</b> (<b>METH</b>) use disorder (191 cases and 753 controls).
+CHRNA4	drug	amphetamine	18991851	In conclusion, our results suggest that neither <strong>CHRNA4</strong> nor CHRNB2 plays a major role in Japanese <b>METH</b> use disorder.
+CHRNA4	drug	nicotine	18534558	Gene gene interactions among <strong>CHRNA4</strong>, CHRNB2, BDNF, and NTRK2 in <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	18534558	Gene gene interactions among <strong>CHRNA4</strong>, CHRNB2, BDNF, and NTRK2 in nicotine <b>dependence</b>.
+CHRNA4	drug	nicotine	18534558	To determine if gene gene interactions exist among the four genes, we genotyped six single nucleotide polymorphisms (SNPs) for <strong>CHRNA4</strong> and BDNF, nine SNPs for NTRK2, and four SNPs for CHRNB2 in a case control sample containing 275 unrelated <b>smokers</b> with a Fagerström Test for <b>Nicotine</b> Dependence score of 4.0 or more and 348 unrelated nonsmokers.
+CHRNA4	addiction	dependence	18534558	To determine if gene gene interactions exist among the four genes, we genotyped six single nucleotide polymorphisms (SNPs) for <strong>CHRNA4</strong> and BDNF, nine SNPs for NTRK2, and four SNPs for CHRNB2 in a case control sample containing 275 unrelated smokers with a Fagerström Test for Nicotine <b>Dependence</b> score of 4.0 or more and 348 unrelated nonsmokers.
+CHRNA4	drug	nicotine	17768273	<strong>CHRNA4</strong> and <b>tobacco</b> dependence: from gene regulation to treatment outcome.
+CHRNA4	addiction	dependence	17768273	<strong>CHRNA4</strong> and tobacco <b>dependence</b>: from gene regulation to treatment outcome.
+CHRNA4	drug	nicotine	17768273	Given the probable importance of the alpha4 subunit of the neuronal nicotinic acetylcholine receptor, the gene that codes for this subunit (<strong>CHRNA4</strong>) represents an excellent starting point for a genetic investigation of <b>smoking</b> behavior.
+CHRNA4	drug	nicotine	17768273	Bioinformatics analyses, cell culture experiments, and analyses of <strong>CHRNA4</strong> expression and <b>nicotine</b> binding in postmortem human brain tissue advanced 2 single nucleotide polymorphisms (rs6122429 and rs2236196).
+CHRNA4	drug	nicotine	17768273	Results of analyses ranging from basic biological approaches to clinical outcome data provide consistent evidence that 2 single nucleotide polymorphisms in <strong>CHRNA4</strong> are functional at a biological level and are associated with <b>nicotine</b> dependence phenotypes.
+CHRNA4	addiction	dependence	17768273	Results of analyses ranging from basic biological approaches to clinical outcome data provide consistent evidence that 2 single nucleotide polymorphisms in <strong>CHRNA4</strong> are functional at a biological level and are associated with nicotine <b>dependence</b> phenotypes.
+CHRNA4	drug	nicotine	17613539	Mutational analyses in xenopus oocyte and mice models indicate that the positive effect of <b>nicotine</b> on attention may be modulated by genetic variations within exon 5 of the alpha4 subunit of the nicotinergic acetylcholine receptor gene <strong>CHRNA4</strong>.
+CHRNA4	drug	alcohol	17226798	We have examined two neuronal nicotinic receptor subunit genes (<strong>CHRNA4</strong> and CHRNB2) for possible associations with nicotine and <b>alcohol</b> phenotypes, including measures of frequency of use and measures of initial subjective response in the period shortly after first using the drugs.
+CHRNA4	drug	nicotine	17226798	We have examined two neuronal nicotinic receptor subunit genes (<strong>CHRNA4</strong> and CHRNB2) for possible associations with <b>nicotine</b> and alcohol phenotypes, including measures of frequency of use and measures of initial subjective response in the period shortly after first using the drugs.
+CHRNA4	drug	alcohol	17226798	Analysis of six SNPs in the <strong>CHRNA4</strong> gene provided modest support for an association with past 6 month use of <b>alcohol</b> in Caucasians (three SNPs with P < 0.08), but no evidence for an association with tobacco and <strong>CHRNA4</strong> was detected.
+CHRNA4	drug	nicotine	17226798	Analysis of six SNPs in the <strong>CHRNA4</strong> gene provided modest support for an association with past 6 month use of alcohol in Caucasians (three SNPs with P < 0.08), but no evidence for an association with <b>tobacco</b> and <strong>CHRNA4</strong> was detected.
+CHRNA4	drug	nicotine	15790597	Ethnic  and gender specific association of the nicotinic acetylcholine receptor alpha4 subunit gene (<strong>CHRNA4</strong>) with <b>nicotine</b> dependence.
+CHRNA4	addiction	dependence	15790597	Ethnic  and gender specific association of the nicotinic acetylcholine receptor alpha4 subunit gene (<strong>CHRNA4</strong>) with nicotine <b>dependence</b>.
+CHRNA4	drug	nicotine	15790597	We tested six single nucleotide polymorphisms (SNPs) in the alpha4 subunit gene (<strong>CHRNA4</strong>) and four SNPs in the beta2 subunit gene (CHRNB2) of nicotinic acetylcholine receptors (nAChRs) for association with <b>nicotine</b> dependence (ND), which was assessed by <b>smoking</b> quantity (SQ), the heaviness of <b>smoking</b> index (HSI) and the Fagerstrom test for ND (FTND) in 2037 subjects from 602 nuclear families of either European American (EA) or African American (AA) ancestry.
+CHRNA4	addiction	dependence	15790597	We tested six single nucleotide polymorphisms (SNPs) in the alpha4 subunit gene (<strong>CHRNA4</strong>) and four SNPs in the beta2 subunit gene (CHRNB2) of nicotinic acetylcholine receptors (nAChRs) for association with nicotine <b>dependence</b> (ND), which was assessed by smoking quantity (SQ), the heaviness of smoking index (HSI) and the Fagerstrom test for ND (FTND) in 2037 subjects from 602 nuclear families of either European American (EA) or African American (AA) ancestry.
+CHRNA4	drug	alcohol	15617774	A polymorphism in the nicotinic receptor alpha4 subunit gene, <strong>Chrna4</strong>, showed a trend with nicotine consumption and a significant association with <b>alcohol</b> consumption in female but not male mice.
+CHRNA4	drug	nicotine	15617774	A polymorphism in the nicotinic receptor alpha4 subunit gene, <strong>Chrna4</strong>, showed a trend with <b>nicotine</b> consumption and a significant association with alcohol consumption in female but not male mice.
+CHRNA4	drug	nicotine	15154117	We studied six single nucleotide polymorphisms (SNPs) in the <strong>CHRNA4</strong> gene and four SNPs in the CHRNB2 gene with respect to <b>nicotine</b> dependence in a collection of 901 subjects (815 siblings and 86 parents) from 222 nuclear families with multiple <b>nicotine</b> addicted siblings.
+CHRNA4	addiction	dependence	15154117	We studied six single nucleotide polymorphisms (SNPs) in the <strong>CHRNA4</strong> gene and four SNPs in the CHRNB2 gene with respect to nicotine <b>dependence</b> in a collection of 901 subjects (815 siblings and 86 parents) from 222 nuclear families with multiple nicotine addicted siblings.
+CHRNA4	drug	nicotine	15154117	Univariate (single marker) family based association tests (FBATs) demonstrated that variant alleles at two SNPs, rs1044396 and rs1044397, in exon 5 of the <strong>CHRNA4</strong> gene were significantly associated with a protective effect against <b>nicotine</b> addiction as either a dichotomized trait or a quantitative phenotype (i.e., age adjusted FTND and RTQ scores), which was consistent with the results of the global haplotype FBAT.
+CHRNA4	addiction	addiction	15154117	Univariate (single marker) family based association tests (FBATs) demonstrated that variant alleles at two SNPs, rs1044396 and rs1044397, in exon 5 of the <strong>CHRNA4</strong> gene were significantly associated with a protective effect against nicotine <b>addiction</b> as either a dichotomized trait or a quantitative phenotype (i.e., age adjusted FTND and RTQ scores), which was consistent with the results of the global haplotype FBAT.
+CHRNA4	drug	nicotine	15154117	Furthermore, the haplotype specific FBAT showed a common (22.5%) <strong>CHRNA4</strong> haplotype, GCTATA, which was significantly associated with both a protective effect against <b>nicotine</b> addiction as a dichotomized trait (Z= 3.04, P<.005) and significant decreases of age adjusted FTND (Z= 3.31, P<.005) or RTQ scores (Z= 2.73, P=.006).
+CHRNA4	addiction	addiction	15154117	Furthermore, the haplotype specific FBAT showed a common (22.5%) <strong>CHRNA4</strong> haplotype, GCTATA, which was significantly associated with both a protective effect against nicotine <b>addiction</b> as a dichotomized trait (Z= 3.04, P<.005) and significant decreases of age adjusted FTND (Z= 3.31, P<.005) or RTQ scores (Z= 2.73, P=.006).
+CHRNA4	drug	nicotine	15154117	Our findings provide strong evidence suggesting a common <strong>CHRNA4</strong> haplotype might be protective against vulnerability to <b>nicotine</b> addiction in men.
+CHRNA4	addiction	addiction	15154117	Our findings provide strong evidence suggesting a common <strong>CHRNA4</strong> haplotype might be protective against vulnerability to nicotine <b>addiction</b> in men.
+CHRNA4	drug	alcohol	14610221	Furthermore, some <b>ethanol</b> related behaviors are associated with a region of mouse chromosome 2 that contains the gene encoding the alpha4 subunit of the nAChR (<strong>Chrna4</strong>).
+PENK	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous opioid peptide precursors including proopiomelanocortin (Pomc), proenkephalin (<strong>Penk</strong>), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+PENK	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous <b>opioid</b> peptide precursors including proopiomelanocortin (Pomc), proenkephalin (<strong>Penk</strong>), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+PENK	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous opioid peptide precursors including proopiomelanocortin (Pomc), <strong>proenkephalin</strong> (<strong>Penk</strong>), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+PENK	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (Oprm), delta (Oprd), and kappa (Oprk), and their endogenous <b>opioid</b> peptide precursors including proopiomelanocortin (Pomc), <strong>proenkephalin</strong> (<strong>Penk</strong>), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+PENK	drug	cocaine	32730947	In the CPu, <b>cocaine</b> self administration significantly increased the mRNA levels of <strong>Penk</strong> and Pdyn and abolished the mRNA levels of Pomc.
+PENK	drug	cocaine	32730947	In the PFC, <b>cocaine</b> self administration only increased Pdyn mRNA levels without changing the mRNA levels of Pomc and <strong>Penk</strong>.
+PENK	drug	opioid	32487735	Since then, ~20 peptides with <b>opioid</b> receptor activity have been discovered, all of which are generated from three precursors (<strong>proenkephalin</strong>, prodynorphin, and proopiomelanocortin) by sequential proteolytic processing by prohormone convertases and carboxypeptidase E. Each of these peptides bind to all three of the <b>opioid</b> receptor types (mu, delta, kappa), albeit with differing affinities.
+PENK	drug	opioid	32393639	It is generally thought that the three types of <b>opioid</b> receptors (μ, δ, κ) are activated by endogenous peptides derived from three different precursors: Proopiomelanocortin, <strong>proenkephalin</strong>, and prodynorphin.
+PENK	drug	cannabinoid	30664203	In addition, kininogen 1, lysophosphatidic acid receptor 5, formyl peptide receptor (FPR) 2, adenylate cyclase 2, γ‑aminobutyric acid type B receptor subunit 2, FPR1, hydroxycarboxylic acid receptor 1, prostaglandin E receptor 3, <b>cannabinoid</b> receptor 1 and <strong>proenkephalin</strong> were identified as the top 10 hub genes.
+PENK	drug	opioid	30326159	Evidence for roles for <b>opioid</b> related genes <b>opioid</b> receptor, delta 1 (Oprd1) and preproenkephalin (<strong>Penk</strong>) was also found.
+PENK	drug	opioid	30028550	The evidence for roles for <b>opioid</b> related genes <b>opioid</b> receptor, delta 1 (Oprd1) and preproenkephalin (<strong>Penk</strong>) was also found.
+PENK	drug	opioid	29852138	Prodynorphin (Pdyn) expression was upregulated in the ipsilateral dorsal domains by each the left and right side SNL, while changes in expression of μ <b>opioid</b> receptor (Oprm1) and proenkephalin (<strong>Penk</strong>) genes were dependent on the SNL side.
+PENK	drug	opioid	29852138	Prodynorphin (Pdyn) expression was upregulated in the ipsilateral dorsal domains by each the left and right side SNL, while changes in expression of μ <b>opioid</b> receptor (Oprm1) and <strong>proenkephalin</strong> (<strong>Penk</strong>) genes were dependent on the SNL side.
+PENK	drug	nicotine	28509375	Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN) derived opioid peptides are proposed as important mediators of <b>nicotine</b> reward.
+PENK	drug	opioid	28509375	Delta and kappa <b>opioid</b> receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN) derived <b>opioid</b> peptides are proposed as important mediators of nicotine reward.
+PENK	addiction	reward	28509375	Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN) derived opioid peptides are proposed as important mediators of nicotine <b>reward</b>.
+PENK	drug	nicotine	28509375	Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN) derived opioid peptides are proposed as important mediators of <b>nicotine</b> reward.
+PENK	drug	opioid	28509375	Delta and kappa <b>opioid</b> receptors (DOR and KOR, respectively) and their endogenous ligands, <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN) derived <b>opioid</b> peptides are proposed as important mediators of nicotine reward.
+PENK	addiction	reward	28509375	Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN) derived opioid peptides are proposed as important mediators of nicotine <b>reward</b>.
+PENK	drug	nicotine	28509375	This study investigated the regulatory effect of chronic <b>nicotine</b> treatment on the gene expression of DOR, KOR, <strong>PENK</strong> and PDYN in the mesocorticolimbic system.
+PENK	drug	nicotine	28509375	<b>Nicotine</b> did not regulate <strong>PENK</strong> mRNA in any brain region studied.
+PENK	drug	amphetamine	27841313	Increased expression of <strong>proenkephalin</strong> and prodynorphin mRNAs in the nucleus accumbens of compulsive <b>methamphetamine</b> taking rats.
+PENK	addiction	addiction	27841313	Increased expression of <strong>proenkephalin</strong> and prodynorphin mRNAs in the nucleus accumbens of <b>compulsive</b> methamphetamine taking rats.
+PENK	drug	amphetamine	27841313	Because PDYN and <strong>PENK</strong> are expressed in dopamine D1  and D2 containing NAc neurons, respectively, these findings suggest that mechanisms, which impact both cell types may play a role in the regulation of compulsive <b>methamphetamine</b> taking by rats.
+PENK	addiction	addiction	27841313	Because PDYN and <strong>PENK</strong> are expressed in dopamine D1  and D2 containing NAc neurons, respectively, these findings suggest that mechanisms, which impact both cell types may play a role in the regulation of <b>compulsive</b> methamphetamine taking by rats.
+PENK	drug	cocaine	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, <strong>Penk</strong>, Pdyn) and cognate receptors (Oprm, Oprk and Oprd) in reward related brain regions, after exposure to either <b>cocaine</b> self administration or yoked saline, in the aforementioned translational paradigm.
+PENK	drug	opioid	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous <b>opioid</b> peptides (Pomc, <strong>Penk</strong>, Pdyn) and cognate receptors (Oprm, Oprk and Oprd) in reward related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+PENK	addiction	reward	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, <strong>Penk</strong>, Pdyn) and cognate receptors (Oprm, Oprk and Oprd) in <b>reward</b> related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+PENK	drug	cocaine	26777278	Moreover, gene expression level of Pdyn, <strong>Penk</strong>, Oprk, and Oprm in the DS was significantly correlated with <b>cocaine</b> intake only in Fischer rats.
+PENK	drug	nicotine	26520239	After <b>nicotine</b> administration, there was a positive shift in correlation of mass/charge peak expression levels with substance P and <strong>proenkephalin</strong> A (218 228).
+PENK	drug	cocaine	26164485	Effects of an opioid (<strong>proenkephalin</strong>) polymorphism on neural response to errors in health and <b>cocaine</b> use disorder.
+PENK	drug	opioid	26164485	Effects of an <b>opioid</b> (<strong>proenkephalin</strong>) polymorphism on neural response to errors in health and cocaine use disorder.
+PENK	drug	cannabinoid	26164485	In the current imaging genetics study, we investigated a single nucleotide polymorphism (SNP) of the protein coding proenkephalin gene (<strong>PENK</strong>: rs2609997, recently shown to be associated with <b>cannabis</b> dependence) in 55 individuals with cocaine use disorder and 37 healthy controls.
+PENK	drug	cocaine	26164485	In the current imaging genetics study, we investigated a single nucleotide polymorphism (SNP) of the protein coding proenkephalin gene (<strong>PENK</strong>: rs2609997, recently shown to be associated with cannabis dependence) in 55 individuals with <b>cocaine</b> use disorder and 37 healthy controls.
+PENK	addiction	dependence	26164485	In the current imaging genetics study, we investigated a single nucleotide polymorphism (SNP) of the protein coding proenkephalin gene (<strong>PENK</strong>: rs2609997, recently shown to be associated with cannabis <b>dependence</b>) in 55 individuals with cocaine use disorder and 37 healthy controls.
+PENK	drug	cannabinoid	26164485	In the current imaging genetics study, we investigated a single nucleotide polymorphism (SNP) of the protein coding <strong>proenkephalin</strong> gene (<strong>PENK</strong>: rs2609997, recently shown to be associated with <b>cannabis</b> dependence) in 55 individuals with cocaine use disorder and 37 healthy controls.
+PENK	drug	cocaine	26164485	In the current imaging genetics study, we investigated a single nucleotide polymorphism (SNP) of the protein coding <strong>proenkephalin</strong> gene (<strong>PENK</strong>: rs2609997, recently shown to be associated with cannabis dependence) in 55 individuals with <b>cocaine</b> use disorder and 37 healthy controls.
+PENK	addiction	dependence	26164485	In the current imaging genetics study, we investigated a single nucleotide polymorphism (SNP) of the protein coding <strong>proenkephalin</strong> gene (<strong>PENK</strong>: rs2609997, recently shown to be associated with cannabis <b>dependence</b>) in 55 individuals with cocaine use disorder and 37 healthy controls.
+PENK	drug	cocaine	26164485	Analyses tested for <strong>PENK</strong> associations with fMRI response to error (during a classical color word Stroop task) and gray matter volume (voxel based morphometry) as a function of Diagnosis (<b>cocaine</b>, control).
+PENK	drug	cocaine	26164485	These interactions were driven by differences between individuals with <b>cocaine</b> use disorders and controls that were accentuated in individuals carrying the higher risk <strong>PENK</strong> C allele.
+PENK	drug	opioid	26164485	Taken together, the <strong>PENK</strong> polymorphism and potentially <b>opioid</b> neurotransmission more generally modulates functioning and structural integrity of brain regions previously implicated in error related processing.
+PENK	drug	cocaine	26164485	<strong>PENK</strong> could potentially render a subgroup of individuals with <b>cocaine</b> use disorder (i.e., C allele carriers) more sensitive to mistakes or other related challenges; in future studies, these results could contribute to the development of individualized genetics informed treatments.
+PENK	drug	alcohol	26029055	We compared the levels of prodynorphin (PDYN) and proenkephalin (<strong>PENK</strong>) mRNAs (by qRT PCR), and dynorphins and enkephalins (by radioimmunoassay) in the caudate nucleus and putamen between <b>alcoholics</b> and control subjects.
+PENK	drug	alcohol	26029055	We compared the levels of prodynorphin (PDYN) and <strong>proenkephalin</strong> (<strong>PENK</strong>) mRNAs (by qRT PCR), and dynorphins and enkephalins (by radioimmunoassay) in the caudate nucleus and putamen between <b>alcoholics</b> and control subjects.
+PENK	drug	alcohol	26029055	PDYN mRNA and Met enkephalin Arg Phe, a marker of <strong>PENK</strong> were downregulated in the caudate of <b>alcoholics</b>, while PDYN mRNA and Leu enkephalin Arg, a marker of PDYN were decreased in the putamen of <b>alcoholics</b> carrying high risk rs1997794 C allele.
+PENK	drug	opioid	26019998	Additionally, the molecular mechanisms of lappaconitine's analgesic effects may be related to affect the expression levels of endogenous <b>opioid</b> system genes (POMC, <strong>PENK</strong> and MOR), as well as apoptosis related genes (Xiap, Smac, Bim, NF κB and p53).
+PENK	drug	opioid	25521590	We used quantitative real time PCR to measure expression of the enkephalin <b>opioid</b> precursor preproenkephalin (<strong>PENK</strong>) and mu <b>opioid</b> receptors (MOR) in the medial preoptic nucleus (POM; a region in which <b>opioids</b> are implicated in both reward and starling fall song) and additionally the song control region HVC as a control.
+PENK	addiction	reward	25521590	We used quantitative real time PCR to measure expression of the enkephalin opioid precursor preproenkephalin (<strong>PENK</strong>) and mu opioid receptors (MOR) in the medial preoptic nucleus (POM; a region in which opioids are implicated in both <b>reward</b> and starling fall song) and additionally the song control region HVC as a control.
+PENK	addiction	reward	25521590	Both <strong>PENK</strong> and MOR mRNA expression in the POM, but not HVC, correlated positively with both individual <b>reward</b> state (as reflected in <b>CPP</b>) and undirected singing behavior.
+PENK	drug	cocaine	25431310	Wild type (WT) and <strong>proenkephalin</strong> KO mice were treated with <b>cocaine</b> once daily for 9 days to induce sensitization.
+PENK	addiction	sensitization	25431310	Wild type (WT) and <strong>proenkephalin</strong> KO mice were treated with cocaine once daily for 9 days to induce <b>sensitization</b>.
+PENK	drug	cocaine	25431310	We show for first time that the <strong>proenkephalin</strong> system is essential in regulating long lasting pivotal neuroadaptations in the NAc underlying behavioral sensitization to <b>cocaine</b>.
+PENK	addiction	sensitization	25431310	We show for first time that the <strong>proenkephalin</strong> system is essential in regulating long lasting pivotal neuroadaptations in the NAc underlying behavioral <b>sensitization</b> to cocaine.
+PENK	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, <strong>Penk</strong>, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+PENK	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, <strong>Penk</strong>, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+PENK	drug	cocaine	24943644	We have used genetically modified mice to evaluate the involvement of μ opioid receptor (MOR) and δ opioid receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN), in the reinstatement of <b>cocaine</b> seeking behavior.
+PENK	drug	opioid	24943644	We have used genetically modified mice to evaluate the involvement of μ <b>opioid</b> receptor (MOR) and δ <b>opioid</b> receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN), in the reinstatement of cocaine seeking behavior.
+PENK	addiction	relapse	24943644	We have used genetically modified mice to evaluate the involvement of μ opioid receptor (MOR) and δ opioid receptor (DOR) and their main endogenous ligands, the enkephalins derived from proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN), in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+PENK	drug	cocaine	24943644	We have used genetically modified mice to evaluate the involvement of μ opioid receptor (MOR) and δ opioid receptor (DOR) and their main endogenous ligands, the enkephalins derived from <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN), in the reinstatement of <b>cocaine</b> seeking behavior.
+PENK	drug	opioid	24943644	We have used genetically modified mice to evaluate the involvement of μ <b>opioid</b> receptor (MOR) and δ <b>opioid</b> receptor (DOR) and their main endogenous ligands, the enkephalins derived from <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN), in the reinstatement of cocaine seeking behavior.
+PENK	addiction	relapse	24943644	We have used genetically modified mice to evaluate the involvement of μ opioid receptor (MOR) and δ opioid receptor (DOR) and their main endogenous ligands, the enkephalins derived from <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN), in the <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+PENK	drug	cocaine	24943644	Constitutive knockout mice of MOR, DOR, <strong>PENK</strong>, and PDYN, and their wild type littermates were trained to self administer <b>cocaine</b> or to seek for palatable food, followed by a period of extinction and finally tested on a cue induced reinstatement of seeking behavior.
+PENK	addiction	relapse	24943644	Constitutive knockout mice of MOR, DOR, <strong>PENK</strong>, and PDYN, and their wild type littermates were trained to self administer cocaine or to seek for palatable food, followed by a period of extinction and finally tested on a cue induced <b>reinstatement</b> of <b>seeking</b> behavior.
+PENK	drug	cocaine	24943644	The four lines of knockout mice acquired operant <b>cocaine</b> self administration behavior, although DOR and <strong>PENK</strong> knockout mice showed less motivation for <b>cocaine</b> than wild type littermates.
+PENK	addiction	reward	24943644	The four lines of knockout mice acquired <b>operant</b> cocaine self administration behavior, although DOR and <strong>PENK</strong> knockout mice showed less motivation for cocaine than wild type littermates.
+PENK	drug	opioid	24727340	We measured mRNA expression of key components of the reward pathway (mu <b>opioid</b> receptor, <strong>proenkephalin</strong>, tyrosine hydroxylase, D1 and D2 receptors and the dopamine active transporter (DAT)) in the nucleus accumbens (NAc) and ventral tegmental area (VTA) of the offspring of control and cafeteria fed (JF) dams at weaning and after a 10 day <b>naloxone</b> treatment post weaning and determined food preferences in adulthood in the remaining offspring.
+PENK	addiction	reward	24727340	We measured mRNA expression of key components of the <b>reward</b> pathway (mu opioid receptor, <strong>proenkephalin</strong>, tyrosine hydroxylase, D1 and D2 receptors and the dopamine active transporter (DAT)) in the nucleus accumbens (NAc) and ventral tegmental area (VTA) of the offspring of control and cafeteria fed (JF) dams at weaning and after a 10 day naloxone treatment post weaning and determined food preferences in adulthood in the remaining offspring.
+PENK	drug	opioid	24727340	<strong>Proenkephalin</strong> mRNA expression was higher in the NAc of female JF offspring compared to controls, independent of <b>naloxone</b> treatment (P<0.05).
+PENK	drug	opioid	24035914	This neuromodulator system is composed of three receptors, mu, delta and kappa, interacting with a family of <b>opioid</b> peptides derived from POMC (β endorphin), preproenkephalin (<strong>pEnk</strong>) and preprodynorphin (pDyn) precursors.
+PENK	drug	alcohol	24035914	<strong>pEnk</strong> is involved in these processes and delta/<strong>pEnk</strong> signaling likely regulates <b>alcohol</b> intake.
+PENK	drug	opioid	23924601	Expression of the mu <b>opioid</b> receptor (MOR), preproenkephalin (<strong>PENK</strong>), and the dopamine transporter was evaluated in the hypothalamus and reward circuitry (ventral tegmental area, prefrontal cortex, and nucleus accumbens) in adult and late embryonic brains.
+PENK	addiction	reward	23924601	Expression of the mu opioid receptor (MOR), preproenkephalin (<strong>PENK</strong>), and the dopamine transporter was evaluated in the hypothalamus and <b>reward</b> circuitry (ventral tegmental area, prefrontal cortex, and nucleus accumbens) in adult and late embryonic brains.
+PENK	drug	alcohol	23770261	Female mice lacking beta endorphin and/or the <strong>proenkephalin</strong> gene as well as their respective wild type controls were tested for baseline place preference on day 1, conditioned with <b>ethanol</b> versus saline on days 2 4 and were then tested under a drug free state for postconditioning place preference on day 5.
+PENK	drug	opioid	23346966	Finally, we assessed the expression of the genes proopiomelanocortin (POMC), pro dynorphin (PDyn) and pro enkephalin (<strong>PEnk</strong>), coding for the <b>opioids</b> peptides in the NAcc and the mPFC in both groups.
+PENK	drug	alcohol	23287538	This vulnerability to <b>ethanol</b> abuse was associated with a lower c Fos immunoreactivity in the Nac and enduring alterations of the expression of <strong>Penk</strong> and Slc6a4, 2 neurotransmission related genes that have been shown to play critical roles in the behavioral effects of <b>ethanol</b> and <b>alcoholism</b>.
+PENK	drug	cannabinoid	22745721	<b>Cannabis</b> dependence risk relates to synergism between neuroticism and <strong>proenkephalin</strong> SNPs associated with amygdala gene expression: case control study.
+PENK	addiction	dependence	22745721	Cannabis <b>dependence</b> risk relates to synergism between neuroticism and <strong>proenkephalin</strong> SNPs associated with amygdala gene expression: case control study.
+PENK	drug	cannabinoid	22745721	Dopamine receptor D2 (DRD2) and proenkephalin (<strong>PENK</strong>) genes have been implicated in animal studies with <b>cannabis</b> exposure.
+PENK	drug	cannabinoid	22745721	Dopamine receptor D2 (DRD2) and <strong>proenkephalin</strong> (<strong>PENK</strong>) genes have been implicated in animal studies with <b>cannabis</b> exposure.
+PENK	drug	cannabinoid	22745721	Healthy young adults (18 27 years) with <b>cannabis</b> dependence and without a dependence diagnosis were studied (N = 50/group) in relation to a priori determined single nucleotide polymorphisms (SNPs) of the DRD2 and <strong>PENK</strong> genes.
+PENK	addiction	dependence	22745721	Healthy young adults (18 27 years) with cannabis <b>dependence</b> and without a <b>dependence</b> diagnosis were studied (N = 50/group) in relation to a priori determined single nucleotide polymorphisms (SNPs) of the DRD2 and <strong>PENK</strong> genes.
+PENK	drug	cannabinoid	22745721	Moreover, <strong>PENK</strong> variants (rs2576573 and rs2609997) significantly related to Neuroticism and <b>cannabis</b> dependence.
+PENK	addiction	dependence	22745721	Moreover, <strong>PENK</strong> variants (rs2576573 and rs2609997) significantly related to Neuroticism and cannabis <b>dependence</b>.
+PENK	drug	cannabinoid	22745721	Cigarette smoking is common in <b>cannabis</b> users, but it was not associated to <strong>PENK</strong> SNPs as also validated in another cohort (N = 247 smokers, N = 312 non smokers).
+PENK	drug	nicotine	22745721	Cigarette <b>smoking</b> is common in cannabis users, but it was not associated to <strong>PENK</strong> SNPs as also validated in another cohort (N = 247 <b>smokers</b>, N = 312 non <b>smokers</b>).
+PENK	drug	cannabinoid	22745721	Overall, the findings suggest an important role for Neuroticism as an endophenotype linking <strong>PENK</strong> polymorphisms to <b>cannabis</b> dependence vulnerability synergistically amplifying the apparent genetic risk.
+PENK	addiction	dependence	22745721	Overall, the findings suggest an important role for Neuroticism as an endophenotype linking <strong>PENK</strong> polymorphisms to cannabis <b>dependence</b> vulnerability synergistically amplifying the apparent genetic risk.
+PENK	drug	cannabinoid	22683090	<strong>Proenkephalin</strong> mediates the enduring effects of adolescent <b>cannabis</b> exposure associated with adult opiate vulnerability.
+PENK	drug	opioid	22683090	However, a causal link between proenkephalin (<strong>Penk</strong>) expression and vulnerability to <b>heroin</b> has yet to be established.
+PENK	drug	opioid	22683090	However, a causal link between <strong>proenkephalin</strong> (<strong>Penk</strong>) expression and vulnerability to <b>heroin</b> has yet to be established.
+PENK	drug	opioid	22683090	To investigate the functional significance of NAcsh <strong>Penk</strong> tone, selective viral mediated knockdown and overexpression of <strong>Penk</strong> was performed, followed by analysis of subsequent <b>heroin</b> SA behavior.
+PENK	drug	cannabinoid	22683090	To determine whether adolescent <b>THC</b> exposure was associated with chromatin alteration, we analyzed levels of histone H3 methylation in the NAcsh via chromatin immunoprecipitation at five sites flanking the <strong>Penk</strong> gene transcription start site.
+PENK	drug	opioid	22683090	Here we show that regulation of the <strong>Penk</strong> <b>opioid</b> neuropeptide gene in NAcsh directly regulates <b>heroin</b> SA behavior.
+PENK	drug	cannabinoid	22683090	Selective viral mediated knockdown of <strong>Penk</strong> in striatopallidal neurons attenuates heroin SA in adolescent <b>THC</b> exposed rats, whereas <strong>Penk</strong> overexpression potentiates heroin SA in <b>THC</b> naïve rats.
+PENK	drug	opioid	22683090	Selective viral mediated knockdown of <strong>Penk</strong> in striatopallidal neurons attenuates <b>heroin</b> SA in adolescent THC exposed rats, whereas <strong>Penk</strong> overexpression potentiates <b>heroin</b> SA in THC naïve rats.
+PENK	drug	cannabinoid	22683090	Furthermore, we report that adolescent <b>THC</b> exposure mediates <strong>Penk</strong> upregulation through reduction of histone H3 lysine 9 (H3K9) methylation in the NAcsh, thereby disrupting the normal developmental pattern of H3K9 methylation.
+PENK	drug	cannabinoid	22683090	These data establish a direct association between <b>THC</b> induced NAcsh <strong>Penk</strong> upregulation and heroin SA and indicate that epigenetic dysregulation of <strong>Penk</strong> underlies the long term effects of <b>THC</b>.
+PENK	drug	opioid	22683090	These data establish a direct association between THC induced NAcsh <strong>Penk</strong> upregulation and <b>heroin</b> SA and indicate that epigenetic dysregulation of <strong>Penk</strong> underlies the long term effects of THC.
+PENK	drug	cocaine	22504589	Furthermore, preproenkephalin (<strong>Penk</strong>) mRNA levels in caudate putamen were significantly higher in mice that received 14 day withdrawal from escalating dose binge <b>cocaine</b> before the CPP procedure (tested 24 days post binge) than those that received 1 day withdrawal (tested 10 days post binge).
+PENK	addiction	intoxication	22504589	Furthermore, preproenkephalin (<strong>Penk</strong>) mRNA levels in caudate putamen were significantly higher in mice that received 14 day withdrawal from escalating dose <b>binge</b> cocaine before the CPP procedure (tested 24 days post <b>binge</b>) than those that received 1 day withdrawal (tested 10 days post <b>binge</b>).
+PENK	addiction	reward	22504589	Furthermore, preproenkephalin (<strong>Penk</strong>) mRNA levels in caudate putamen were significantly higher in mice that received 14 day withdrawal from escalating dose binge cocaine before the <b>CPP</b> procedure (tested 24 days post binge) than those that received 1 day withdrawal (tested 10 days post binge).
+PENK	addiction	withdrawal	22504589	Furthermore, preproenkephalin (<strong>Penk</strong>) mRNA levels in caudate putamen were significantly higher in mice that received 14 day <b>withdrawal</b> from escalating dose binge cocaine before the CPP procedure (tested 24 days post binge) than those that received 1 day <b>withdrawal</b> (tested 10 days post binge).
+PENK	drug	cocaine	22387539	As TOP can be implicated in the processing of many neuropeptides, and previous studies have shown that <b>cocaine</b> also alters the gene expression of <strong>proenkephalin</strong> and prodynorphin in the striatum, the present findings suggest that TOP changes in the brain could play important role in the balance of neuropeptide level correlated with <b>cocaine</b> effects.
+PENK	drug	alcohol	21966993	Handling induced convulsion (HIC) associated to <b>alcohol</b>, <b>alcohol</b> induced loss of righting reflex (LORR), hypothermic effects in response to acute <b>ethanol</b> challenge, blood <b>ethanol</b> levels (BELs), conditioned place preference, voluntary <b>ethanol</b> consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and proenkephalin (<strong>PENK</strong>) gene expression, and µ , δ  and κ opioid agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild type (WT) mice.
+PENK	drug	opioid	21966993	Handling induced convulsion (HIC) associated to alcohol, alcohol induced loss of righting reflex (LORR), hypothermic effects in response to acute ethanol challenge, blood ethanol levels (BELs), conditioned place preference, voluntary ethanol consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and proenkephalin (<strong>PENK</strong>) gene expression, and µ , δ  and κ <b>opioid</b> agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild type (WT) mice.
+PENK	drug	alcohol	21966993	Handling induced convulsion (HIC) associated to <b>alcohol</b>, <b>alcohol</b> induced loss of righting reflex (LORR), hypothermic effects in response to acute <b>ethanol</b> challenge, blood <b>ethanol</b> levels (BELs), conditioned place preference, voluntary <b>ethanol</b> consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and <strong>proenkephalin</strong> (<strong>PENK</strong>) gene expression, and µ , δ  and κ opioid agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild type (WT) mice.
+PENK	drug	opioid	21966993	Handling induced convulsion (HIC) associated to alcohol, alcohol induced loss of righting reflex (LORR), hypothermic effects in response to acute ethanol challenge, blood ethanol levels (BELs), conditioned place preference, voluntary ethanol consumption and preference, tyrosine hydroxylase (TH), dopamine transporter (DAT) and <strong>proenkephalin</strong> (<strong>PENK</strong>) gene expression, and µ , δ  and κ <b>opioid</b> agonist stimulated [S(35) ]  guanosine 5' triphosphate binding autoradiography were studied in prodynorphin knockout (PDYN KO) and wild type (WT) mice.
+PENK	drug	alcohol	21966993	These results suggest that deletion of the PDYN gene increased vulnerability for <b>ethanol</b> consumption by altering, at least in part, <strong>PENK</strong>, TH and DAT gene expression, and µ , δ  and κ opioid receptor functional activity in brain areas closely related to <b>ethanol</b> reinforcement.
+PENK	drug	opioid	21966993	These results suggest that deletion of the PDYN gene increased vulnerability for ethanol consumption by altering, at least in part, <strong>PENK</strong>, TH and DAT gene expression, and µ , δ  and κ <b>opioid</b> receptor functional activity in brain areas closely related to ethanol reinforcement.
+PENK	addiction	reward	21966993	These results suggest that deletion of the PDYN gene increased vulnerability for ethanol consumption by altering, at least in part, <strong>PENK</strong>, TH and DAT gene expression, and µ , δ  and κ opioid receptor functional activity in brain areas closely related to ethanol <b>reinforcement</b>.
+PENK	drug	opioid	21955155	No significant changes in expression of <strong>proenkephalin</strong>, and µ  and δ <b>opioid</b> receptors were evident; pro opiomelanocortin mRNA levels were below the detection limit.
+PENK	addiction	addiction	21796661	We conducted a multicenter, dose <b>escalation</b>, phase I clinical trial of NP2, a replication defective HSV based vector expressing human preproenkephalin (<strong>PENK</strong>) in subjects with intractable focal pain caused by cancer.
+PENK	addiction	relapse	21161187	Extinction and <b>reinstatement</b> of this operant response enhanced <strong>proenkephalin</strong> mRNA in the dorsal striatum and/or the nucleus accumbens core.
+PENK	addiction	reward	21161187	Extinction and reinstatement of this <b>operant</b> response enhanced <strong>proenkephalin</strong> mRNA in the dorsal striatum and/or the nucleus accumbens core.
+PENK	drug	opioid	20685869	Additionally, expression of both μ <b>opioid</b> receptor (MOR) and preproenkephalin (<strong>PENK</strong>) was increased in nucleus accumbens, prefrontal cortex, and hypothalamus of mice from dams that consumed the HF diet.
+PENK	drug	opioid	20651230	Moreover, Tat expression widely disrupted the endogenous <b>opioid</b> system, altering mu and kappa, but not delta, <b>opioid</b> receptor and proopiomelanocortin, <strong>proenkephalin</strong>, and prodynorphin transcript levels in cortex, hippocampus, and striatum.
+PENK	drug	opioid	20494127	The mu <b>opioid</b> receptor and the cognate <b>opioid</b> neuropeptides from <strong>proenkephalin</strong> and proopiomelancortin are members of a superfamily of <b>opioid</b> systems, each with unique and still to be defined roles in the central nervous system.
+PENK	drug	opioid	19997907	Forebrain <strong>PENK</strong> and PDYN gene expression levels in three inbred strains of mice and their relationship to genotype dependent <b>morphine</b> reward sensitivity.
+PENK	addiction	reward	19997907	Forebrain <strong>PENK</strong> and PDYN gene expression levels in three inbred strains of mice and their relationship to genotype dependent morphine <b>reward</b> sensitivity.
+PENK	addiction	addiction	19997907	Proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN) gene expression was measured by in situ hybridization in brain regions implicated in <b>addiction</b>.
+PENK	addiction	addiction	19997907	<strong>Proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN) gene expression was measured by in situ hybridization in brain regions implicated in <b>addiction</b>.
+PENK	drug	opioid	19997907	Our results demonstrate that inter strain differences in <strong>PENK</strong> and PDYN genes expression in the nucleus accumbens parallel sensitivity of the selected mouse strains to rewarding effects of <b>morphine</b>.
+PENK	drug	opioid	19789384	The <b>opioid</b> system consists of three receptors, mu, delta, and kappa, which are activated by endogenous <b>opioid</b> peptides processed from three protein precursors, proopiomelanocortin, <strong>proenkephalin</strong>, and prodynorphin.
+PENK	drug	opioid	19674841	The anti nociceptive effects of PAR(1) agonist were mediated by endogenous <b>opioids</b>, as this effect was inhibited by local injection of <b>naloxone</b> methiodide, and because intraplantar injection of PAR(1) agonist increased mRNA expression of the endogenous <b>opioid</b> precursor <strong>proenkephalin</strong>.
+PENK	drug	psychedelics	19523041	Moreover, the consequences of acute and chronic <b>MDMA</b> administration on pro enkephalin (<strong>Penk</strong>) and pro opiomelanocortin (Pomc) gene expression were assessed by real time quantitative polymerase chain reaction (QPCR).
+PENK	drug	psychedelics	19523041	<strong>Penk</strong> gene expression was not modulated by acute <b>MDMA</b>, but a decrease of Pomc gene expression was observed, which was not antagonized by NTI.
+PENK	drug	opioid	19481570	Besides actions of peptides from all three classical <b>opioid</b> precursors (<strong>proenkephalin</strong>, prodynorphin, proopiomelanocortin) on the three classical <b>opioid</b> receptors (delta, mu and kappa), dynorphins were also shown to exert non <b>opioid</b> effects mainly through direct effects on NMDA receptors.
+PENK	drug	nicotine	19376143	Thus, micro opioid receptor and the endogenous opioids derived from <strong>proenkephalin</strong> are involved in the central effects of <b>nicotine</b>.
+PENK	drug	opioid	19376143	Thus, micro <b>opioid</b> receptor and the endogenous <b>opioids</b> derived from <strong>proenkephalin</strong> are involved in the central effects of nicotine.
+PENK	drug	opioid	19100723	Opiate induced alterations in the gene expression of the <b>opioid</b> propeptides prodynorphin (PDYN) and proenkephalin (<strong>PENK</strong>) in the brain have previously been described.
+PENK	drug	opioid	19100723	Opiate induced alterations in the gene expression of the <b>opioid</b> propeptides prodynorphin (PDYN) and <strong>proenkephalin</strong> (<strong>PENK</strong>) in the brain have previously been described.
+PENK	drug	opioid	19100723	In our study, using in situ hybridization, we measured PDYN and <strong>PENK</strong> mRNA levels in the dorsal striatum, central nucleus of amygdala (CEA), and nucleus accumbens (NAcc) shell and core in rats after 6 weeks of <b>heroin</b> self administration (fixed ratio 5, 0.02 mg/kg/infusion of <b>heroin</b> i.v.)
+PENK	drug	opioid	19100723	Our results show an increase in the PDYN mRNA level in the CEA and NAcc shell and no changes of <strong>PENK</strong> gene expression after <b>heroin</b> self administration.
+PENK	drug	opioid	19100723	In addition, to dissociate pharmacological effects of <b>heroin</b> from those produced by motivational processes driving active <b>heroin</b> intake on the PDYN and <strong>PENK</strong> gene expression, we compared effects of response dependent (contingent) and response independent (noncontingent  "yoked" <b>heroin</b> control) <b>heroin</b> administration.
+PENK	drug	opioid	19100723	In conclusion, our results indicate neuroadaptations in the PDYN but not <strong>PENK</strong> gene expression in rat limbic forebrain during <b>heroin</b> self administration.
+PENK	drug	opioid	19058913	Using a mouse model of postoperative pain, we assessed the expression of MOR and delta <b>opioid</b> receptors (DORs) and the efficacy of Herpes Simplex vector mediated <strong>proenkephalin</strong> release (SHPE) preventing postoperative nociceptive sensitization induced by remifentanil or surgical incision.
+PENK	addiction	sensitization	19058913	Using a mouse model of postoperative pain, we assessed the expression of MOR and delta opioid receptors (DORs) and the efficacy of Herpes Simplex vector mediated <strong>proenkephalin</strong> release (SHPE) preventing postoperative nociceptive <b>sensitization</b> induced by remifentanil or surgical incision.
+PENK	drug	opioid	18761380	In order to investigate the role of spinal <b>opioid</b> peptide in the phenomenon of <b>naloxone</b> precipitated withdrawal we examined the effect of herpes simplex virus vector mediated overexpression of <strong>proenkephalin</strong> in lumbar dorsal root ganglia in rats with neuropathic pain treated with <b>morphine</b>.
+PENK	addiction	withdrawal	18761380	In order to investigate the role of spinal opioid peptide in the phenomenon of naloxone precipitated <b>withdrawal</b> we examined the effect of herpes simplex virus vector mediated overexpression of <strong>proenkephalin</strong> in lumbar dorsal root ganglia in rats with neuropathic pain treated with morphine.
+PENK	drug	opioid	18761380	Rats with neuropathic pain inoculated subcutaneously with the vector mediated overexpression of <strong>proenkephalin</strong> showed a significant reduction in jumps, 'wet dog' shakes, diarrhea and ptosis precipitated by <b>naloxone</b> after 2 weeks of <b>morphine</b> treatment.
+PENK	addiction	withdrawal	18761380	The global <b>withdrawal</b> score was also reduced significantly by vector mediated overexpression of <strong>proenkephalin</strong>.
+PENK	drug	alcohol	18227978	<b>Ethanol</b> induced changes in <strong>proenkephalin</strong> mRNA expression in the rat nigrostriatal pathway.
+PENK	drug	alcohol	18227978	The aim of this work was to study the effects of acute <b>ethanol</b> administration on <strong>proenkephalin</strong> (proenk) mRNA expression in the rat substantia nigra and caudate putamen (CP) for up to 24 h post treatment.
+PENK	drug	opioid	18184800	<b>Opioid</b> neuropeptide genotypes in relation to <b>heroin</b> abuse: dopamine tone contributes to reversed mesolimbic <strong>proenkephalin</strong> expression.
+PENK	drug	opioid	18184800	We examined polymorphisms of proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN) genes in relation to <b>heroin</b> abuse and gene expression in the human striatum and the relevance of genetic dopaminergic tone, critical for drug reward and striatal function.
+PENK	addiction	reward	18184800	We examined polymorphisms of proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN) genes in relation to heroin abuse and gene expression in the human striatum and the relevance of genetic dopaminergic tone, critical for drug <b>reward</b> and striatal function.
+PENK	drug	opioid	18184800	We examined polymorphisms of <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN) genes in relation to <b>heroin</b> abuse and gene expression in the human striatum and the relevance of genetic dopaminergic tone, critical for drug reward and striatal function.
+PENK	addiction	reward	18184800	We examined polymorphisms of <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN) genes in relation to heroin abuse and gene expression in the human striatum and the relevance of genetic dopaminergic tone, critical for drug <b>reward</b> and striatal function.
+PENK	drug	opioid	18184800	<b>Heroin</b> abuse was significantly associated with <strong>PENK</strong> polymorphic 3' UTR dinucleotide (CA) repeats; 79% of subjects homozygous for the 79 bp allele were <b>heroin</b> abusers.
+PENK	drug	opioid	18184800	Control Met/Met individuals expressed lower <strong>PENK</strong> mRNA than Val carriers, a pattern reversed in <b>heroin</b> users.
+PENK	drug	opioid	18184800	Up regulation of NAc <strong>PENK</strong> in Met/Met <b>heroin</b> abusers was accompanied by impaired tyrosine hydroxylase (TH) mRNA expression in mesolimbic dopamine neurons.
+PENK	drug	opioid	18184800	In contrast to <strong>PENK</strong>, no association was detected between PDYN genotype (68 bp repeat element containing one to four copies of AP 1 binding sites in the promoter region) and <b>heroin</b> abuse, although there was a clear functional association with striatal PDYN mRNA expression: an increased number of inducible repeats (three and four) correlated with higher PDYN levels than adult or fetal subjects with noninducible (one and two) alleles.
+PENK	drug	opioid	18184800	Altogether, the data suggest that dysfunction of the <b>opioid</b> reward system is significantly linked to opiate abuse vulnerability and that <b>heroin</b> use alters the apparent influence of heritable dopamine tone on mesolimbic <strong>PENK</strong> and TH function.
+PENK	addiction	reward	18184800	Altogether, the data suggest that dysfunction of the opioid <b>reward</b> system is significantly linked to opiate abuse vulnerability and that heroin use alters the apparent influence of heritable dopamine tone on mesolimbic <strong>PENK</strong> and TH function.
+PENK	drug	amphetamine	18093743	The expression patterns of nerve growth factor inducible clone A (NGFI A), secretogranin, post synaptic density protein of 95 Kd (PSD 95), prodynorphin and <strong>proenkephalin</strong> mRNA were also analyzed using in situ hybridization, after the challenge with <b>amphetamine</b>.
+PENK	drug	opioid	17944864	The CB(1) receptor and <strong>proenkephalin</strong> gene expressions, and CB(1) receptor and mu <b>opioid</b> (MO) receptor mediated G protein activation were found to be significantly lower in the caudate putamen, nucleus accumbens core and shell of FAAH  /  than +/+ mice.
+PENK	drug	opioid	17934066	We observed a significant decrease in the expression of <b>opioid</b> peptide precursors (proopiomelanocortin, <strong>proenkephalin</strong>, and prodynorphin) and of the kappa <b>opioid</b> receptor after 48 and 72 h of EtOH exposure (10 and 40 mM).
+PENK	drug	opioid	17934066	We observed the same pattern of changes for prodynorphin, <strong>proenkephalin</strong>, and the kappa <b>opioid</b> receptor as after 72 h exposure to EtOH.
+PENK	drug	opioid	17905519	We sought additional evidence for the role of constitutively active MORs in this <b>morphine</b> induced enhancement using the pro enkephalin knockout (<strong>pENK</strong>( )/( )) mouse, which is devoid of <b>naloxone</b> CPA in the <b>morphine</b> naive state.
+PENK	drug	opioid	17905519	<b>Naloxone</b>, but not the neutral antagonist, 6 beta naloxol, produced CPA and physical withdrawal signs in <strong>pENK</strong>( )/( ) mice when administered 2 h, but not 20 h, after <b>morphine</b> administration.
+PENK	addiction	withdrawal	17905519	Naloxone, but not the neutral antagonist, 6 beta naloxol, produced CPA and physical <b>withdrawal</b> signs in <strong>pENK</strong>( )/( ) mice when administered 2 h, but not 20 h, after morphine administration.
+PENK	drug	opioid	17905519	<b>Naloxone</b> precipitated physical withdrawal signs were attenuated in the <strong>pENK</strong>( )/( ) mice relative to wild type (WT) animals.
+PENK	addiction	withdrawal	17905519	Naloxone precipitated physical <b>withdrawal</b> signs were attenuated in the <strong>pENK</strong>( )/( ) mice relative to wild type (WT) animals.
+PENK	drug	opioid	17905519	In both WT and <strong>pENK</strong>( )/( ) mice, <b>naloxone</b> precipitated withdrawal jumping was greatest when <b>naloxone</b> was administered 2 h after <b>morphine</b> treatment and diminished at 3 h, in agreement with previous estimates of the time course for <b>morphine</b> induced MOR constitutive activity in vitro.
+PENK	addiction	withdrawal	17905519	In both WT and <strong>pENK</strong>( )/( ) mice, naloxone precipitated <b>withdrawal</b> jumping was greatest when naloxone was administered 2 h after morphine treatment and diminished at 3 h, in agreement with previous estimates of the time course for morphine induced MOR constitutive activity in vitro.
+PENK	drug	opioid	17905519	However, <b>naloxone</b> regained an ability to precipitate physical withdrawal in the WT, but not the <strong>pENK</strong>( )/( ) mice when administered 4.5 h after <b>morphine</b> administration.
+PENK	addiction	withdrawal	17905519	However, naloxone regained an ability to precipitate physical <b>withdrawal</b> in the WT, but not the <strong>pENK</strong>( )/( ) mice when administered 4.5 h after morphine administration.
+PENK	drug	amphetamine	17537495	Changes in <strong>Proenkephalin</strong> mRNA expression in forebrain areas after <b>amphetamine</b> induced behavioural sensitization.
+PENK	addiction	sensitization	17537495	Changes in <strong>Proenkephalin</strong> mRNA expression in forebrain areas after amphetamine induced behavioural <b>sensitization</b>.
+PENK	drug	amphetamine	17537495	In order to investigate a possible involvement of opioid systems in <b>amphetamine</b> (<b>AMPH</b>) behavioural sensitization, we studied the <b>AMPH</b> induced changes in <strong>Proenkephalin</strong> (Pro Enk) mRNA expression in forebrain areas in both drug naïve and <b>AMPH</b> sensitized rats.
+PENK	drug	opioid	17537495	In order to investigate a possible involvement of <b>opioid</b> systems in amphetamine (AMPH) behavioural sensitization, we studied the AMPH induced changes in <strong>Proenkephalin</strong> (Pro Enk) mRNA expression in forebrain areas in both drug naïve and AMPH sensitized rats.
+PENK	addiction	sensitization	17537495	In order to investigate a possible involvement of opioid systems in amphetamine (AMPH) behavioural <b>sensitization</b>, we studied the AMPH induced changes in <strong>Proenkephalin</strong> (Pro Enk) mRNA expression in forebrain areas in both drug naïve and AMPH sensitized rats.
+PENK	drug	alcohol	17503481	We analyzed 18 OPRM1 SNPs, 18 OPRD1 SNPs, 7 <strong>PENK</strong> SNPs, and 7 POMC SNPs in a sample of 1923 European Americans from 219 multiplex <b>alcohol</b> dependent families.
+PENK	drug	opioid	17503481	Secondary analyses employing the narrower phenotype of <b>opioid</b> dependence (83 affected individuals) demonstrated association with SNPs in <strong>PENK</strong> and POMC, but not in OPRM1 or OPRD1.
+PENK	addiction	dependence	17503481	Secondary analyses employing the narrower phenotype of opioid <b>dependence</b> (83 affected individuals) demonstrated association with SNPs in <strong>PENK</strong> and POMC, but not in OPRM1 or OPRD1.
+PENK	drug	opioid	17503481	Haplotype analyses provided further support for the association of <strong>PENK</strong> and POMC with <b>opioid</b> dependence.
+PENK	addiction	dependence	17503481	Haplotype analyses provided further support for the association of <strong>PENK</strong> and POMC with opioid <b>dependence</b>.
+PENK	drug	alcohol	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, OPRD1, <strong>PENK</strong> and POMC are associated with <b>alcohol</b> dependence or general illicit drug dependence, but variations in <strong>PENK</strong> and POMC appear to be associated with the narrower phenotype of opioid dependence in these families.
+PENK	drug	opioid	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, OPRD1, <strong>PENK</strong> and POMC are associated with alcohol dependence or general illicit drug dependence, but variations in <strong>PENK</strong> and POMC appear to be associated with the narrower phenotype of <b>opioid</b> dependence in these families.
+PENK	addiction	dependence	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, OPRD1, <strong>PENK</strong> and POMC are associated with alcohol <b>dependence</b> or general illicit drug <b>dependence</b>, but variations in <strong>PENK</strong> and POMC appear to be associated with the narrower phenotype of opioid <b>dependence</b> in these families.
+PENK	drug	opioid	17493673	Mild postnatal manipulation reduces <strong>proenkephalin</strong> mRNA in the striatum in developing mice and increases <b>morphine</b> conditioned place preference in adulthood.
+PENK	drug	opioid	17493673	Therefore, in the present study, we assessed activity levels, emotionality, sensitivity to the effects of <b>morphine</b>, as well as expression of <strong>proenkephalin</strong> and prodynorphin in several brain regions in 35 and 90 day old male mice, subjected to postnatal manipulation consisting in brief exposures to clean bedding (CB).
+PENK	drug	opioid	17467916	In contrast gene deletion of either <strong>proenkephalin</strong> or prodynorphin <b>opioids</b> did not block the effects of pSNL.
+PENK	drug	opioid	17173187	Bovine adrenal medulla 22 (BAM22), an endogenous <b>opioid</b> peptide, is one of the cleavage products of <strong>proenkephalin</strong> A.
+PENK	drug	opioid	17161852	In this study, after animals of both strains self administered <b>morphine</b> (1mg/kg) or extinguished this behaviour for 3, 7 or 15days, we measured the binding to, and functional state of mu <b>opioid</b> receptors (MORs) as well as proenkephalin (<strong>PENK</strong>) mRNA content in several brain regions.
+PENK	drug	opioid	17161852	In this study, after animals of both strains self administered <b>morphine</b> (1mg/kg) or extinguished this behaviour for 3, 7 or 15days, we measured the binding to, and functional state of mu <b>opioid</b> receptors (MORs) as well as <strong>proenkephalin</strong> (<strong>PENK</strong>) mRNA content in several brain regions.
+PENK	drug	alcohol	17063152	Voluntary <b>ethanol</b> consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, proenkephalin (<strong>PENK</strong>) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+PENK	drug	cannabinoid	17063152	Voluntary ethanol consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, proenkephalin (<strong>PENK</strong>) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, <b>cannabinoid</b> CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+PENK	drug	opioid	17063152	Voluntary ethanol consumption altered mu <b>opioid</b> receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, proenkephalin (<strong>PENK</strong>) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+PENK	drug	alcohol	17063152	Voluntary <b>ethanol</b> consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, <strong>proenkephalin</strong> (<strong>PENK</strong>) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+PENK	drug	cannabinoid	17063152	Voluntary ethanol consumption altered mu opioid receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, <strong>proenkephalin</strong> (<strong>PENK</strong>) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, <b>cannabinoid</b> CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+PENK	drug	opioid	17063152	Voluntary ethanol consumption altered mu <b>opioid</b> receptor function in the cingulate cortex, caudate putamen (CPu), nucleus accumbens core (Acb C) and shell (Acb S), the expression of tyrosine hydroxylase (TH) in the ventral tegmental area and substantia nigra, <strong>proenkephalin</strong> (<strong>PENK</strong>) in the piriform cortex, olfactory tubercle, CPu, Acb C and Acb S, ventromedial nucleus (VMN) and paraventricular nucleus (PVN) of the hypothalamus, corticotropin releasing factor (CRF) in PVN, cannabinoid CB(1) receptor (CB1 R) in the CPu, hippocampus and VMN, and serotonin transporter (5 HTT) in the dorsal and median raphe nuclei.
+PENK	drug	alcohol	17063152	These results point to a role for the mu opioid receptor, TH, <strong>PENK</strong>, CRF, CB1 R, and 5 HTT genes in specific brain regions in the modulation of neuroadaptative mechanisms associated to the decrease of <b>ethanol</b> intake induced by <b>naltrexone</b>.
+PENK	drug	opioid	17063152	These results point to a role for the mu <b>opioid</b> receptor, TH, <strong>PENK</strong>, CRF, CB1 R, and 5 HTT genes in specific brain regions in the modulation of neuroadaptative mechanisms associated to the decrease of ethanol intake induced by naltrexone.
+PENK	drug	amphetamine	16904191	We analyzed effects of <b>amphetamine</b> on <strong>proenkephalin</strong> derived peptides in brain areas and immune cells in rats.
+PENK	drug	cannabinoid	16876136	<b>THC</b> exposure reduced preproenkephalin (<strong>PENK</strong>) mRNA expression in the nucleus accumbens during early development, but was elevated in adulthood; no adult striatal changes on preprodynorphin mRNA or <strong>PENK</strong> in caudate putamen.
+PENK	drug	cannabinoid	16876136	<strong>PENK</strong> mRNA was also increased in the central and medial amygdala in adult <b>THC</b> exposed animals.
+PENK	drug	cannabinoid	16876136	This study demonstrates enduring effects of prenatal <b>THC</b> exposure into adulthood that is evident on heroin seeking behavior during extinction and allostatic changes in mesocorticolimbic <strong>PENK</strong> systems relevant to drug motivation/reward and stress response.
+PENK	drug	opioid	16876136	This study demonstrates enduring effects of prenatal THC exposure into adulthood that is evident on <b>heroin</b> seeking behavior during extinction and allostatic changes in mesocorticolimbic <strong>PENK</strong> systems relevant to drug motivation/reward and stress response.
+PENK	addiction	relapse	16876136	This study demonstrates enduring effects of prenatal THC exposure into adulthood that is evident on heroin <b>seeking</b> behavior during extinction and allostatic changes in mesocorticolimbic <strong>PENK</strong> systems relevant to drug motivation/reward and stress response.
+PENK	addiction	reward	16876136	This study demonstrates enduring effects of prenatal THC exposure into adulthood that is evident on heroin seeking behavior during extinction and allostatic changes in mesocorticolimbic <strong>PENK</strong> systems relevant to drug motivation/<b>reward</b> and stress response.
+PENK	drug	opioid	16861111	In situ hybridization histochemistry was used to study mRNA expression levels of dopamine (e.g., D2 receptor, dopamine transporter) and <b>opioid</b> (e.g., <strong>proenkephalin</strong>) related markers in various structures in relation to brain pH.
+PENK	drug	cocaine	16412997	Contingency does not contribute to the effects of <b>cocaine</b> self administration on prodynorphin and <strong>proenkephalin</strong> gene expression in the rat forebrain.
+PENK	drug	opioid	16412997	Although regulation of the gene expression of the <b>opioid</b> propeptides proenkephalin (<strong>PENK</strong>) and prodynorphin (PDYN) by psychostimulants has previously been described, little attention has been paid to dissociating effects of pharmacological actions of the drugs from those produced by motivational processes driving active drug intake in self administration paradigms.
+PENK	drug	opioid	16412997	Although regulation of the gene expression of the <b>opioid</b> propeptides <strong>proenkephalin</strong> (<strong>PENK</strong>) and prodynorphin (PDYN) by psychostimulants has previously been described, little attention has been paid to dissociating effects of pharmacological actions of the drugs from those produced by motivational processes driving active drug intake in self administration paradigms.
+PENK	drug	cocaine	16412997	In the present study, effects of response dependent (contingent) and response independent (noncontingent) <b>cocaine</b> administration on the <strong>PENK</strong> and PDYN gene expression in the rat forebrain have been directly compared using the "yoked" self administration procedure.
+PENK	drug	cocaine	16412997	Levels of the <strong>PENK</strong> mRNA remained unaltered in all the above mentioned forebrain regions of rats receiving contingent or noncontingent <b>cocaine</b> injections.
+PENK	drug	opioid	15874900	We surmise that <b>opioid</b> peptides, i.e., methionine enkephalin, first arose during evolution as modulators of cellular immune function given their immune actions and the presence of enkelytin, a potent antibacterial peptide, and its precursor <strong>proenkephalin</strong> in animals 500 million years divergent in evolution.
+PENK	drug	amphetamine	15680202	Ginsenosides attenuate <b>methamphetamine</b> induced behavioral side effects in mice via activation of adenosine A2A receptors: possible involvements of the striatal reduction in AP 1 DNA binding activity and <strong>proenkephalin</strong> gene expression.
+PENK	drug	cannabinoid	15545023	These disturbances are likely originated by the capability of <b>cannabinoids</b> to influence the expression of key genes for both neurotransmitters, in particular, the enzyme tyrosine hydroxylase and the opioid precursor <strong>proenkephalin</strong>.
+PENK	drug	opioid	15545023	These disturbances are likely originated by the capability of cannabinoids to influence the expression of key genes for both neurotransmitters, in particular, the enzyme tyrosine hydroxylase and the <b>opioid</b> precursor <strong>proenkephalin</strong>.
+PENK	drug	alcohol	15544578	Mice lacking a functional copy of G protein gated potassium channel subunit 2 (Girk2) show a decrease in the aversive effects of <b>ethanol</b>, whereas preproenkephalin (<strong>Penk</strong>) null mutant mice show the opposite response.
+PENK	addiction	aversion	15544578	Mice lacking a functional copy of G protein gated potassium channel subunit 2 (Girk2) show a decrease in the <b>aversive</b> effects of ethanol, whereas preproenkephalin (<strong>Penk</strong>) null mutant mice show the opposite response.
+PENK	drug	opioid	14525992	Cloning and characterization of Xen dorphin prohormone from Xenopus laevis: a new <b>opioid</b> like prohormone distinct from <strong>proenkephalin</strong> and prodynorphin.
+PENK	drug	cannabinoid	12641731	Spontaneous <b>cannabinoid</b> withdrawal produced time related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (TH) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (<strong>PENK</strong>) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus.
+PENK	addiction	withdrawal	12641731	Spontaneous cannabinoid <b>withdrawal</b> produced time related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (TH) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (<strong>PENK</strong>) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus.
+PENK	drug	cannabinoid	12641731	Spontaneous <b>cannabinoid</b> withdrawal produced time related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (TH) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased <strong>proenkephalin</strong> (<strong>PENK</strong>) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus.
+PENK	addiction	withdrawal	12641731	Spontaneous cannabinoid <b>withdrawal</b> produced time related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (TH) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased <strong>proenkephalin</strong> (<strong>PENK</strong>) gene expression more than 100% in caudate putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20 40%) pro opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus.
+PENK	drug	amphetamine	12542667	Ciproxifan strongly potentiated the decrease of <strong>proenkephalin</strong> mRNA expression induced by <b>methamphetamine</b>.
+PENK	drug	amphetamine	12523490	Effect of cocaine and <b>amphetamine</b> on biosynthesis of <strong>proenkephalin</strong> and prodynorphin in some regions of the rat limbic system.
+PENK	drug	cocaine	12523490	Effect of <b>cocaine</b> and amphetamine on biosynthesis of <strong>proenkephalin</strong> and prodynorphin in some regions of the rat limbic system.
+PENK	drug	amphetamine	12523490	The goal of the present study was to investigate the influence of acutely and chronically administered drugs of abuse, cocaine and <b>amphetamine</b> on biosynthesis of prodynorphin and <strong>proenkephalin</strong> in the rat amygdala, the structure involved in the mechanism of drug addiction.
+PENK	drug	cocaine	12523490	The goal of the present study was to investigate the influence of acutely and chronically administered drugs of abuse, <b>cocaine</b> and amphetamine on biosynthesis of prodynorphin and <strong>proenkephalin</strong> in the rat amygdala, the structure involved in the mechanism of drug addiction.
+PENK	addiction	addiction	12523490	The goal of the present study was to investigate the influence of acutely and chronically administered drugs of abuse, cocaine and amphetamine on biosynthesis of prodynorphin and <strong>proenkephalin</strong> in the rat amygdala, the structure involved in the mechanism of drug <b>addiction</b>.
+PENK	drug	amphetamine	12523490	Acute injection of cocaine (20 mg/kg ip every hour for 3 h) or <b>amphetamine</b> (2.5 mg/kg) did not changed or decreased the level of <strong>proenkephalin</strong> mRNA in the central nucleus of the amygdala.
+PENK	drug	cocaine	12523490	Acute injection of <b>cocaine</b> (20 mg/kg ip every hour for 3 h) or amphetamine (2.5 mg/kg) did not changed or decreased the level of <strong>proenkephalin</strong> mRNA in the central nucleus of the amygdala.
+PENK	drug	cocaine	12523490	Repeated <b>cocaine</b> administration (20 mg/kg ip every hour for 3 h, for 5 days) had no effect on the <strong>proenkephalin</strong> and prodynorphin mRNA in the central nucleus of the amygdala.
+PENK	drug	amphetamine	12523490	Chronic <b>amphetamine</b> (2.5 mg/kg twice daily for 5 days) administration decreased <strong>proenkephalin</strong> and increased prodynorphin mRNA level in the central nucleus of the amygdala (at 24 and 48 h).
+PENK	drug	alcohol	12044625	To ascertain the role of the enkephalinergic opioid peptide system in these processes, we examined voluntary <b>ethanol</b> consumption patterns in mice lacking the preproenkephalin (<strong>Penk</strong>) gene using a two bottle choice paradigm with free access to water and increasing concentrations of <b>ethanol</b> (2, 4, 8, and 10% v/v).
+PENK	drug	opioid	12044625	To ascertain the role of the enkephalinergic <b>opioid</b> peptide system in these processes, we examined voluntary ethanol consumption patterns in mice lacking the preproenkephalin (<strong>Penk</strong>) gene using a two bottle choice paradigm with free access to water and increasing concentrations of ethanol (2, 4, 8, and 10% v/v).
+PENK	drug	alcohol	12044625	No differences in <b>ethanol</b> consumption or preference were observed between wildtypes and <strong>Penk</strong> null mutant mice.
+PENK	drug	opioid	12015197	The endogenous <b>opioid</b> system consists of three <b>opioid</b> peptide precursor genes encoding enkephalins (preproenkephalin, <strong>Penk</strong>), dynorphins (preprodynorphin, Pdyn) and beta endorphin (betaend), proopiomelanocortin (POMC) and three receptor genes encoding mu opiod receptor (MOR), delta opiod receptor (DOR) and kappa opiod receptor (KOR).
+PENK	drug	cocaine	11425502	Extinction of <b>cocaine</b> self administration produces a differential time related regulation of <strong>proenkephalin</strong> gene expression in rat brain.
+PENK	drug	cocaine	11425502	The purpose of this study was to examine the time course effects of extinction of <b>cocaine</b> self administration behavior on proenkephalin (<strong>PENK</strong>) gene expression in caudate putamen nucleus (ST), nucleus accumbens (Acc), olfactory tubercle (Tu), piriform cortex (Pir), ventromedial hypothalamic nucleus (VMN), and central amygdala (Ce) as measured by in situ hybridization histochemistry.
+PENK	drug	cocaine	11425502	The purpose of this study was to examine the time course effects of extinction of <b>cocaine</b> self administration behavior on <strong>proenkephalin</strong> (<strong>PENK</strong>) gene expression in caudate putamen nucleus (ST), nucleus accumbens (Acc), olfactory tubercle (Tu), piriform cortex (Pir), ventromedial hypothalamic nucleus (VMN), and central amygdala (Ce) as measured by in situ hybridization histochemistry.
+PENK	drug	cocaine	11425502	<strong>PENK</strong> mRNA levels were significantly higher in the <b>cocaine</b> groups when compared with SALINE group in the ST, Acc, Pir, and Tu regions on days 0, 1, 5, and 10 of the extinction and lower in the Ce region of CONT group when compared to NONCONT and SALINE groups on days 1, 5, and 10 of the extinction period.
+PENK	drug	cocaine	11425502	These results suggest that changes in <strong>PENK</strong> gene expression after contingent <b>cocaine</b> administration might be involved in <b>cocaine</b> withdrawal states.
+PENK	addiction	withdrawal	11425502	These results suggest that changes in <strong>PENK</strong> gene expression after contingent cocaine administration might be involved in cocaine <b>withdrawal</b> states.
+PENK	drug	alcohol	10871700	Acute <b>ethanol</b> administration induces changes in TRH and <strong>proenkephalin</strong> expression in hypothalamic and limbic regions of rat brain.
+PENK	drug	alcohol	10871700	Changes in the mRNA levels of proTRH and <strong>proenkephalin</strong> were quantified by in situ hybridization in rats administered <b>ethanol</b> intragastrically (2.5 g/kg).
+PENK	addiction	addiction	10821116	In situ hybridization was used to compare the content of proopiomelanocortin, <strong>proenkephalin</strong> and prodynorphin mRNA in distinct brain regions known to be involved in the reinforcing properties of <b>addictive</b> drugs, between rats from each line.
+PENK	addiction	reward	10821116	In situ hybridization was used to compare the content of proopiomelanocortin, <strong>proenkephalin</strong> and prodynorphin mRNA in distinct brain regions known to be involved in the <b>reinforcing</b> properties of addictive drugs, between rats from each line.
+PENK	drug	cannabinoid	10727732	Prenatal Delta(9) <b>tetrahydrocannabinol</b> exposure modifies <strong>proenkephalin</strong> gene expression in the fetal rat brain: sex dependent differences.
+PENK	drug	cannabinoid	10727732	Perinatal Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>) exposure in rats resulted in enhanced morphine self administration behavior, naloxone precipitated withdrawal signs or changes in pain sensitivity, which have been related to changes in micro opioid receptor binding and/or <strong>proenkephalin</strong> mRNA levels in several brain regions.
+PENK	drug	opioid	10727732	Perinatal Delta(9) tetrahydrocannabinol (Delta(9) THC) exposure in rats resulted in enhanced <b>morphine</b> self administration behavior, <b>naloxone</b> precipitated withdrawal signs or changes in pain sensitivity, which have been related to changes in micro <b>opioid</b> receptor binding and/or <strong>proenkephalin</strong> mRNA levels in several brain regions.
+PENK	addiction	withdrawal	10727732	Perinatal Delta(9) tetrahydrocannabinol (Delta(9) THC) exposure in rats resulted in enhanced morphine self administration behavior, naloxone precipitated <b>withdrawal</b> signs or changes in pain sensitivity, which have been related to changes in micro opioid receptor binding and/or <strong>proenkephalin</strong> mRNA levels in several brain regions.
+PENK	drug	cannabinoid	10727732	The purpose of the present study was to examine the changes in <strong>proenkephalin</strong> mRNA levels, measured by using in situ hybridization, in several brain nuclei of rat fetuses that had been daily exposed to Delta(9) <b>THC</b> from the 5th day of gestation.
+PENK	drug	cannabinoid	10727732	Prenatal Delta(9) <b>THC</b> exposure altered <strong>proenkephalin</strong> mRNA levels in most of the brain areas studied at different fetal ages, but the effects were different between sexes.
+PENK	drug	cannabinoid	10727732	Thus, <strong>proenkephalin</strong> mRNA levels increased in females, but decreased in males that had been prenatally exposed to Delta(9) <b>THC</b>.
+PENK	drug	cannabinoid	10727732	In summary, prenatal Delta(9) <b>THC</b> exposure produced a sex dependent effect in <strong>proenkephalin</strong> mRNA levels in several brain structures of rat fetuses.
+PENK	drug	cannabinoid	11125007	<b>Cannabinoid</b> withdrawal syndrome is reduced in pre <strong>proenkephalin</strong> knock out mice.
+PENK	addiction	withdrawal	11125007	Cannabinoid <b>withdrawal</b> syndrome is reduced in pre <strong>proenkephalin</strong> knock out mice.
+PENK	drug	cannabinoid	11125007	The functional interactions between the endogenous <b>cannabinoid</b> and opioid systems were evaluated in pre <strong>proenkephalin</strong> deficient mice.
+PENK	drug	opioid	11125007	The functional interactions between the endogenous cannabinoid and <b>opioid</b> systems were evaluated in pre <strong>proenkephalin</strong> deficient mice.
+PENK	drug	opioid	10321497	The proenkephalin gene (<strong>PENK</strong>) and <b>opioid</b> dependence.
+PENK	addiction	dependence	10321497	The proenkephalin gene (<strong>PENK</strong>) and opioid <b>dependence</b>.
+PENK	drug	opioid	10321497	The <strong>proenkephalin</strong> gene (<strong>PENK</strong>) and <b>opioid</b> dependence.
+PENK	addiction	dependence	10321497	The <strong>proenkephalin</strong> gene (<strong>PENK</strong>) and opioid <b>dependence</b>.
+PENK	drug	opioid	10321497	We tested the hypothesis that the alleles at the (CA)n repeat of the proenkephalin gene (<strong>PENK</strong>) might be associated with <b>opioid</b> addiction in 31 non Hispanic Caucasian subjects with <b>opioid</b> dependence (<b>heroin</b>), 89 ethnically matched subjects with substance dependence other than <b>opioid</b> dependence and 132 controls.
+PENK	addiction	addiction	10321497	We tested the hypothesis that the alleles at the (CA)n repeat of the proenkephalin gene (<strong>PENK</strong>) might be associated with opioid <b>addiction</b> in 31 non Hispanic Caucasian subjects with opioid dependence (heroin), 89 ethnically matched subjects with substance dependence other than opioid dependence and 132 controls.
+PENK	addiction	dependence	10321497	We tested the hypothesis that the alleles at the (CA)n repeat of the proenkephalin gene (<strong>PENK</strong>) might be associated with opioid addiction in 31 non Hispanic Caucasian subjects with opioid <b>dependence</b> (heroin), 89 ethnically matched subjects with substance <b>dependence</b> other than opioid <b>dependence</b> and 132 controls.
+PENK	drug	opioid	10321497	We tested the hypothesis that the alleles at the (CA)n repeat of the <strong>proenkephalin</strong> gene (<strong>PENK</strong>) might be associated with <b>opioid</b> addiction in 31 non Hispanic Caucasian subjects with <b>opioid</b> dependence (<b>heroin</b>), 89 ethnically matched subjects with substance dependence other than <b>opioid</b> dependence and 132 controls.
+PENK	addiction	addiction	10321497	We tested the hypothesis that the alleles at the (CA)n repeat of the <strong>proenkephalin</strong> gene (<strong>PENK</strong>) might be associated with opioid <b>addiction</b> in 31 non Hispanic Caucasian subjects with opioid dependence (heroin), 89 ethnically matched subjects with substance dependence other than opioid dependence and 132 controls.
+PENK	addiction	dependence	10321497	We tested the hypothesis that the alleles at the (CA)n repeat of the <strong>proenkephalin</strong> gene (<strong>PENK</strong>) might be associated with opioid addiction in 31 non Hispanic Caucasian subjects with opioid <b>dependence</b> (heroin), 89 ethnically matched subjects with substance <b>dependence</b> other than opioid <b>dependence</b> and 132 controls.
+PENK	drug	opioid	10321497	These results are consistent with a role of the <strong>PENK</strong> gene in <b>opioid</b> dependence.
+PENK	addiction	dependence	10321497	These results are consistent with a role of the <strong>PENK</strong> gene in opioid <b>dependence</b>.
+PENK	drug	cannabinoid	10219981	Repeated administration of delta9 <b>tetrahydrocannabinol</b> produces a differential time related responsiveness on <strong>proenkephalin</strong>, proopiomelanocortin and corticotropin releasing factor gene expression in the hypothalamus and pituitary gland of the rat.
+PENK	addiction	withdrawal	10077663	Baseline foot <b>withdrawal</b> responses to noxious radiant heat mediated by Adelta and C fibers were similar in animals infected with <strong>proenkephalin</strong> encoding and beta galactosidase encoding viruses.
+PENK	addiction	sensitization	10077663	<b>Sensitization</b> of the foot withdrawal response after application of capsaicin (C fibers) or dimethyl sulfoxide (Adelta fibers) observed in control animals was reduced or eliminated in animals infected with the <strong>proenkephalin</strong> encoding virus for at least 7 weeks postinfection.
+PENK	addiction	withdrawal	10077663	Sensitization of the foot <b>withdrawal</b> response after application of capsaicin (C fibers) or dimethyl sulfoxide (Adelta fibers) observed in control animals was reduced or eliminated in animals infected with the <strong>proenkephalin</strong> encoding virus for at least 7 weeks postinfection.
+PENK	drug	opioid	10064821	Differential basal <strong>proenkephalin</strong> gene expression in dorsal striatum and nucleus accumbens, and vulnerability to <b>morphine</b> self administration in Fischer 344 and Lewis rats.
+PENK	drug	opioid	10064821	Taken together, these results reveal a strain difference in the reinforcing efficacy of <b>morphine</b> and in the basal <strong>PENK</strong> gene expression in brain regions involved in the reinforcing actions of opiates.
+PENK	addiction	reward	10064821	Taken together, these results reveal a strain difference in the <b>reinforcing</b> efficacy of morphine and in the basal <strong>PENK</strong> gene expression in brain regions involved in the <b>reinforcing</b> actions of opiates.
+PENK	drug	cannabinoid	9734704	Perinatal delta9 <b>tetrahydrocannabinol</b> exposure reduces <strong>proenkephalin</strong> gene expression in the caudate putamen of adult female rats.
+PENK	drug	cannabinoid	9734704	The results showed a marked reduction in <strong>proenkephalin</strong> mRNA levels in the caudate putamen of delta9 <b>THC</b> exposed females as compared to oil exposed females, whereas no changes were observed between delta9 <b>THC</b>  and oil exposed males.
+PENK	drug	cannabinoid	9734704	There were no differences in <strong>proenkephalin</strong> mRNA levels in the nucleus accumbens, central amygdala and prefrontal cingulate cortex between males and females perinatally exposed to delta9 <b>THC</b> and their respective controls, although a certain trend to decrease was observed in delta9 <b>THC</b> exposed females.
+PENK	drug	cannabinoid	9734704	In summary, perinatal exposure to delta9 <b>THC</b> exposure decreased <strong>proenkephalin</strong> gene expression in the caudate putamen of adult rats, although this effect exhibited a marked sexual dimorphism since it was only seen in females.
+PENK	drug	nicotine	9675304	One transmitter that may relate to long term <b>nicotine</b> use and its withdrawal is enkephalin, a five amino acid opioid peptide derived from the <strong>proenkephalin</strong> A family.
+PENK	drug	opioid	9675304	One transmitter that may relate to long term nicotine use and its withdrawal is enkephalin, a five amino acid <b>opioid</b> peptide derived from the <strong>proenkephalin</strong> A family.
+PENK	addiction	withdrawal	9675304	One transmitter that may relate to long term nicotine use and its <b>withdrawal</b> is enkephalin, a five amino acid opioid peptide derived from the <strong>proenkephalin</strong> A family.
+PENK	drug	cannabinoid	9645967	Chronic administration of <b>cannabinoids</b> regulates <strong>proenkephalin</strong> mRNA levels in selected regions of the rat brain.
+PENK	drug	cannabinoid	9645967	of delta 9  <b>tetrahydrocannabinol</b> (<b>THC</b>) or R methanandamide (AM356) and chronic (18 days) administration with the synthetic <b>cannabinoid</b> receptor agonist CP 55,940 (1 mg.kg 1.day 1; i.p) on proenkephalin (<strong>PENK</strong>) mRNA levels in several brain regions of the rat.
+PENK	drug	cannabinoid	9645967	of delta 9  <b>tetrahydrocannabinol</b> (<b>THC</b>) or R methanandamide (AM356) and chronic (18 days) administration with the synthetic <b>cannabinoid</b> receptor agonist CP 55,940 (1 mg.kg 1.day 1; i.p) on <strong>proenkephalin</strong> (<strong>PENK</strong>) mRNA levels in several brain regions of the rat.
+PENK	drug	cannabinoid	9645967	Subchronic administration of <b>THC</b> or AM356 increased <strong>PENK</strong> mRNA levels in the ventromedial nucleus of the hypothalamus, (82%) and (39%), in the periaqueductal grey matter, (97%) and (49%), and mammillary nucleus, (43%) and (9%), respectively.
+PENK	drug	alcohol	9630499	Enhanced sensitivity of the nucleus accumbens <strong>proenkephalin</strong> system to <b>alcohol</b> in rats selectively bred for <b>alcohol</b> preference.
+PENK	drug	opioid	9602109	In the present study, the mRNA expression of the dopamine receptors, D1 and D2, and the <b>opioid</b> peptides, prodynorphin and <strong>proenkephalin</strong>, were analyzed in the rat striatum using in situ hybridization histochemistry.
+PENK	drug	cocaine	9602109	<strong>Proenkephalin</strong> and the D2 receptor mRNAs were not altered during <b>cocaine</b> abstinence, though <strong>proenkephalin</strong> was elevated following acute but not repeated <b>cocaine</b> administration.
+PENK	drug	alcohol	9581644	Gel retardation assays with oligomers encoding the rat <strong>proenkephalin</strong> CRE 1 and CRE 2 were performed to determine the effects of <b>ethanol</b> on CRE binding activity.
+PENK	drug	alcohol	9464643	An in situ hybridization study showed an increase in the prodynorphin mRNA level at 24 and 48 h (by 189 and 146%, respectively) after <b>ethanol</b> withdrawal, whereas the <strong>proenkephalin</strong> mRNA level remained unchanged.
+PENK	addiction	withdrawal	9464643	An in situ hybridization study showed an increase in the prodynorphin mRNA level at 24 and 48 h (by 189 and 146%, respectively) after ethanol <b>withdrawal</b>, whereas the <strong>proenkephalin</strong> mRNA level remained unchanged.
+PENK	drug	opioid	9453554	<strong>Proenkephalin</strong> gene regulation in the paraventricular nucleus by GABA: interactions with <b>opioid</b> systems in a transgenic model.
+PENK	drug	cocaine	9030708	Prodynorphin, <strong>proenkephalin</strong> and kappa opioid receptor mRNA responses to acute "binge" <b>cocaine</b>.
+PENK	drug	opioid	9030708	Prodynorphin, <strong>proenkephalin</strong> and kappa <b>opioid</b> receptor mRNA responses to acute "binge" cocaine.
+PENK	addiction	intoxication	9030708	Prodynorphin, <strong>proenkephalin</strong> and kappa opioid receptor mRNA responses to acute "<b>binge</b>" cocaine.
+PENK	drug	opioid	9227847	Effect of <b>morphine</b> on <strong>proenkephalin</strong> gene expression in the rat brain.
+PENK	drug	opioid	9227847	Therefore, in situ hybridization with probes directed against intronic sequences to measure the primary transcript of <strong>proenkephalin</strong> (PPE) mRNA (heteronucleic RNA, hnRNA) in the rat brain following <b>morphine</b> administration was used in this study.
+PENK	drug	opioid	9157322	Using in situ hybridization histochemistry, the messenger RNA expression of the <b>opioid</b> precursors, prodynorphin and <strong>proenkephalin</strong>, was studied in whole hemisphere human brain tissue.
+PENK	drug	opioid	9157322	The marked anatomical dissociation between the expression of these two <b>opioid</b> peptide genes, seen clearly in whole hemisphere sections, indicates that distinct functions must be subserved by the prodynorphin and <strong>proenkephalin</strong> systems in the human brain.
+PENK	drug	cocaine	8998398	Adaptive changes in the <strong>proenkephalin</strong> and D2 dopamine receptor mRNA expression after chronic <b>cocaine</b> in the nucleus accumbens and striatum of the rat.
+PENK	drug	cocaine	8998398	The effects of single and repeated <b>cocaine</b> administration on proenkephalin (<strong>PENK</strong>) and D2 dopamine receptor mRNA expression in the nucleus accumbens and striatum of the rat were studied.
+PENK	drug	cocaine	8998398	The effects of single and repeated <b>cocaine</b> administration on <strong>proenkephalin</strong> (<strong>PENK</strong>) and D2 dopamine receptor mRNA expression in the nucleus accumbens and striatum of the rat were studied.
+PENK	drug	cocaine	8998398	Acute <b>cocaine</b> administration increased <strong>PENK</strong> expression of mRNA in the striatum and decreased it in both those structures after 24 and 48 h. D2 receptor expression of mRNA fell after 3 h, returned to the control value after 24 h and rose after 48 h in both those brain regions following single <b>cocaine</b> injection.
+PENK	drug	cocaine	8998398	Repeated <b>cocaine</b> increased <strong>PENK</strong> expression of mRNA after 3 h, but after 24 and 48 h depletion of mRNA expression was observed.
+PENK	drug	cocaine	8998398	The obtained results suggest that in the nucleus accumbens and striatum there is an opposite regulation between <strong>PENK</strong> and D2 receptor gene expression a short time after single and chronic <b>cocaine</b> administration.
+PENK	drug	cocaine	8998398	Hence, these data provide further evidence for the significance of the <strong>PENK</strong> and dopamine systems in the neurochemical mechanism of <b>cocaine</b>.
+PENK	drug	opioid	8750881	Prenatal <b>morphine</b> treatment significantly increased <strong>proenkephalin</strong> mRNA levels and decreased met enkephalin levels in striatum of newborns.
+PENK	drug	opioid	7552341	Leu enkephalin, which derives from both prodynorphin and <strong>proenkephalin</strong>, and Met enkephalin, which derives from <strong>proenkephalin</strong>, were affected by chronic <b>morphine</b> mainly in Fischer rats, increasing levels in most of the brain areas examined.
+PENK	drug	opioid	7552341	The results in this study show (1) strain differences in basal levels of prodynorphin derived <b>opioid</b> peptides, (2) the prodynorphin system to be differently influenced by <b>morphine</b> in Lewis rats than in Fischer rats and 3) the <strong>proenkephalin</strong> system to be influenced by chronic <b>morphine</b> in brain areas related to reward processes only in Fischer rats.
+PENK	addiction	reward	7552341	The results in this study show (1) strain differences in basal levels of prodynorphin derived opioid peptides, (2) the prodynorphin system to be differently influenced by morphine in Lewis rats than in Fischer rats and 3) the <strong>proenkephalin</strong> system to be influenced by chronic morphine in brain areas related to <b>reward</b> processes only in Fischer rats.
+PENK	drug	opioid	7640004	The co secreted <b>opioids</b> include products of pro dynorphin (released by both vasopressin and oxytocin terminals) and <strong>proenkephalin</strong> (released by oxytocin terminals).
+PENK	drug	opioid	7568625	The effect of <b>morphine</b> tolerance and withdrawal on prodynorphin peptides was studied in relevant brain areas and in the pituitary gland of male Sprague Dawley rats, and compared with effects on the <strong>proenkephalin</strong> derived peptide Met enkephalin.
+PENK	addiction	withdrawal	7568625	The effect of morphine tolerance and <b>withdrawal</b> on prodynorphin peptides was studied in relevant brain areas and in the pituitary gland of male Sprague Dawley rats, and compared with effects on the <strong>proenkephalin</strong> derived peptide Met enkephalin.
+PENK	drug	opioid	7752808	In this study, we completed the localization on mouse chromosomes of the genes encoding mu (Oprm) and kappa (Oprk) receptors, as well as the genes for the <b>opioid</b> propeptides proenkephalin (<strong>Penk</strong>) and prodynorphin (Pdyn).
+PENK	drug	opioid	7752808	In this study, we completed the localization on mouse chromosomes of the genes encoding mu (Oprm) and kappa (Oprk) receptors, as well as the genes for the <b>opioid</b> propeptides <strong>proenkephalin</strong> (<strong>Penk</strong>) and prodynorphin (Pdyn).
+PENK	drug	alcohol	7847619	Differences between <b>alcohol</b> preferring (AA) and <b>alcohol</b> avoiding (ANA) rats in the prodynorphin and <strong>proenkephalin</strong> systems.
+PENK	drug	alcohol	7943650	Allele frequencies of the preproenkephalin A (<strong>PENK</strong>) gene CA repeat in Asians, African Americans, and Caucasians: lack of evidence for different allele frequencies in <b>alcoholics</b>.
+PENK	drug	opioid	7908338	We investigated the changes in the levels of mRNA of <strong>proenkephalin</strong> (PPE) and prodynorphin (DYN) and the stimulatory G protein alpha subunit (G alpha s) in adult <b>morphine</b> tolerant rats.
+PENK	drug	opioid	1491720	Data presented here indicate that the gene encoding the <b>opioid</b> precursor <strong>proenkephalin</strong> is highly regulated by neural activity, second messenger pathways, and PKA.
+PENK	addiction	withdrawal	1684735	In this study, the cerebrospinal fluid content of a <strong>proenkephalin</strong> derivative, Met5 enkephalin Arg6 Gly7 Leu8 (MERGL), was found in significantly low concentrations in parkinsonian patients following overnight <b>withdrawal</b> of all medications compared with control subjects, and failed to change after at least 16 h of steady state, optimal doses of levodopa infusion intravenously.
+PENK	drug	opioid	1645431	Rapid changes in the content of <strong>proenkephalin</strong> A and corticotrophin releasing hormone mRNAs in the paraventricular nucleus during <b>morphine</b> withdrawal in urethane anaesthetized rats.
+PENK	addiction	withdrawal	1645431	Rapid changes in the content of <strong>proenkephalin</strong> A and corticotrophin releasing hormone mRNAs in the paraventricular nucleus during morphine <b>withdrawal</b> in urethane anaesthetized rats.
+PENK	drug	opioid	1645431	<b>morphine</b> infused rats <strong>proenkephalin</strong> a mRNA in the PVN was significantly less than in controls.
+PENK	drug	opioid	1645431	<b>morphine</b> infused rats resulted in a doubling of hybridization to <strong>proenkephalin</strong> mRNA in the PVN which was significantly greater than that seen in the i.c.v.
+PENK	drug	opioid	3111927	Striking dynamic alterations include a pronounced increase in levels of <strong>proenkephalin</strong> mRNA in the corpus striatum after blockade of dopamine receptors, but changes in <b>opioid</b> peptide mRNA after opiate addiction are less clear.
+PENK	addiction	addiction	3111927	Striking dynamic alterations include a pronounced increase in levels of <strong>proenkephalin</strong> mRNA in the corpus striatum after blockade of dopamine receptors, but changes in opioid peptide mRNA after opiate <b>addiction</b> are less clear.
+IFNG	drug	alcohol	29976100	Objective <b>Alcohol</b> is a hypnotic that modifies immune function, specifically the cytokines <strong>interferon gamma</strong> (IFN γ) and interleukin 2 (IL 2).
+IFNG	drug	opioid	27622168	Effect of Moderate Exercise on Serum <strong>Interferon Gamma</strong> and Interleukin 17 Levels in the <b>Morphine</b> Withdrawal Period.
+IFNG	addiction	withdrawal	27622168	Effect of Moderate Exercise on Serum <strong>Interferon Gamma</strong> and Interleukin 17 Levels in the Morphine <b>Withdrawal</b> Period.
+IFNG	drug	opioid	27622168	This study aimed to investigate the changes in serum levels of <strong>interferon gamma</strong> (IFN γ) and interleukin 17 (IL 17) during the <b>morphine</b> withdrawal syndrome induced by 8 weeks of moderate exercise and their effects on the immune system function.
+IFNG	addiction	withdrawal	27622168	This study aimed to investigate the changes in serum levels of <strong>interferon gamma</strong> (IFN γ) and interleukin 17 (IL 17) during the morphine <b>withdrawal</b> syndrome induced by 8 weeks of moderate exercise and their effects on the immune system function.
+IFNG	drug	cocaine	18719314	<b>Cocaine</b> self administered for 18 days induced a significant increase in spleen weight, plasma corticosterone levels, interleukin (IL) 10, and tumor necrosis factor alpha production, while concanavalin A stimulated proliferation responses of peripheral blood T lymphocytes and <strong>interferon gamma</strong> production by splenic lymphocytes were not altered.
+IFNG	drug	opioid	18040852	The splenocytes from protected mice and <b>morphine</b> low concentration treated infected PM, elaborated significantly (p < 0.05) enhanced levels of interleukin 12, <strong>interferon gamma</strong>, tumor necrosis factor alpha, granulocyte macrophage colony stimulating factor and nitrite in the culture medium; a high dose/concentration suppressed their elaboration.
+IFNG	drug	opioid	17993452	This study was performed to investigate the in vitro production of <strong>interferon gamma</strong> and interleukin 10 after antigenic stimulation of cells using whole blood from <b>opioid</b> addicts.
+IFNG	drug	opioid	17993452	The results demonstrated a significant decrease in <strong>interferon gamma</strong> production and an increase in interleukin 10 secretion in <b>heroin</b> addicts, relative to the control group (35.9+/ 26.3 versus 110.2+/ 60.3 pg/mL, p<0.01 and 71.8+/ 28.4 versus 17.1+/ 13.5 pg/mL, p<0.01, respectively), however the changes in these values in opium addicts were not significant compared to healthy individuals.
+IFNG	drug	alcohol	16792568	Efficacy of AM pretreatment with <strong>interferon gamma</strong> (IFN gamma) on IL 23 expression before <b>ethanol</b> exposure and infection was evaluated.
+IFNG	drug	alcohol	16792568	<strong>Interferon gamma</strong> pretreatment strongly inhibits AM IL 23 production in both the presence and absence of <b>alcohol</b>.
+IFNG	addiction	intoxication	16792568	<strong>Interferon gamma</strong> priming antagonizes IL 23 and is, therefore, not likely to be a useful adjuvant therapy in restoring IL 23/IL 17 responses during infection and <b>intoxication</b>.
+IFNG	drug	nicotine	12907840	We provided a self administered questionnaire to evaluate sleep habits, <b>smoking</b> and medical disorders to 578 men without any toxic exposure (20 64 years old), and measured natural killer (NK) cell activity in 324 men and production of <strong>interferon gamma</strong> (IFN gamma) and interleukin 4 (IL 4) after stimulation with phytohemagglutinin in 254 men.
+IFNG	drug	alcohol	11505051	The ratio of IL 4 to <strong>interferon gamma</strong> production by phytohemagglutinin stimulated PBMCs (as an approach to Th2/Th1 balance) was significantly lower in <b>alcoholics</b> than in healthy controls, both in the atopic and in the nonatopic group.
+IFNG	drug	alcohol	11454939	The current work shows <b>ethanol</b> also suppresses cytokine induced iNOS expression and reduces interleukin 1beta and tumor necrosis factor alpha potency without affecting <strong>interferon gamma</strong> potency.
+IFNG	drug	alcohol	11454939	Furthermore, <b>ethanol</b> inhibition of the 526 base fragment activity, which lacks <strong>interferon gamma</strong> enhancement of lipopolysaccharide induced luciferase activity, confirmed that <strong>interferon gamma</strong> responsive elements do not participate in acute <b>ethanol</b> induced inhibition of rat iNOS gene transcription.
+IFNG	drug	alcohol	9514301	Adenoviral mediated <strong>interferon gamma</strong> gene therapy augments pulmonary host defense of <b>ethanol</b> treated rats.
+IFNG	addiction	aversion	9394782	This <b>aversive</b> conditioned stimulus induces a reduction in splenic natural killer cell activity, splenocyte proliferation in response to mitogens, and diminished levels of <strong>interferon gamma</strong> (IFN gamma) production by splenocytes.
+IFNG	drug	alcohol	9347083	Alterations in tumor necrosis factor alpha, <strong>interferon gamma</strong>, and interleukin 6 production by natural killer cell enriched peripheral blood mononuclear cells in chronic <b>alcoholism</b>: relationship with liver disease and <b>ethanol</b> intake.
+IFNG	drug	opioid	9296419	Results show that <b>morphine</b>'s immunomodulatory effects on NK cell activity begin within 30 min, continue for at least 12 h, and return to control values by 24 h. In contrast, proliferation of splenic T and B cells and <strong>interferon gamma</strong> production are not altered within 30 min; maximal suppression occurs at 1 h, and recovery begins within 2 h. In all immune measures, therefore, maximal suppression is present at the 1 h time point, and recovery is complete within 24 h. <b>Morphine</b> induces antinociception 30 min to 2 h after drug administration; recovery is complete within 6 h. These results suggest the possibility that different mechanisms modulate <b>morphine</b>'s immunologic and analgesic effects.
+IFNG	drug	opioid	8632330	A second experiment showed that s.c. doses of N methylnaltrexone that do not gain access to the CNS, as determined by the tail withdrawal assay, do not antagonize the suppressive effects of a single, s.c. injection of <b>morphine</b> on the mitogen stimulated proliferation of splenic and blood lymphocytes, splenic natural killer cell activity and the production of <strong>interferon gamma</strong> by stimulated splenocytes.
+IFNG	addiction	withdrawal	8632330	A second experiment showed that s.c. doses of N methylnaltrexone that do not gain access to the CNS, as determined by the tail <b>withdrawal</b> assay, do not antagonize the suppressive effects of a single, s.c. injection of morphine on the mitogen stimulated proliferation of splenic and blood lymphocytes, splenic natural killer cell activity and the production of <strong>interferon gamma</strong> by stimulated splenocytes.
+IFNG	drug	alcohol	1662988	In addition, although <b>ethanol</b> had no effect on TNF binding to resting macrophages and to macrophages infected with M. avium, <b>ethanol</b> significantly reduced the expression of TNF receptors on <strong>interferon gamma</strong> stimulated macrophages.
+IFNG	drug	opioid	3040807	<b>Opioid</b> mediated suppression of <strong>interferon gamma</strong> production by cultured peripheral blood mononuclear cells.
+IFNG	drug	opioid	3040807	We tested the hypothesis that <b>morphine</b> and the endogenous <b>opioid</b> beta endorphin (beta END), a pituitary peptide released in increased concentrations during stress, can suppress the production of the key macrophage activating lymphokine <strong>interferon gamma</strong> (IFN gamma) by cultured human peripheral blood mononuclear cells (PBMNC).
+FEV	addiction	dependence	31513741	Acid pKa <b>Dependence</b> in O O Bond Heterolysis of a Nonheme FeIII OOH Intermediate To Form a Potent <strong>FeV</strong>═O Oxidant with Heme Compound I Like Reactivity.
+FEV	drug	nicotine	23424753	Reduced lung function (<strong>FEV</strong>, < 80%) occurred in <b>smokers</b> more often than in nonsmokers (30% versus 21%).
+FEV	drug	nicotine	23155143	An interaction (multiplicative effect) was present between asthma and active <b>smoking</b> as it relates to the ratio of post bronchodilator <strong>FEV</strong>(1)/FVC, but only among those with atopic sensitization.
+FEV	addiction	sensitization	23155143	An interaction (multiplicative effect) was present between asthma and active smoking as it relates to the ratio of post bronchodilator <strong>FEV</strong>(1)/FVC, but only among those with atopic <b>sensitization</b>.
+FEV	drug	nicotine	22970659	Both <b>smokers</b> and non <b>smokers</b> were similar in age and baseline <strong>FEV</strong>(1).
+FEV	drug	nicotine	22970659	<b>Smoking</b> yielded considerably reduced mean change in <strong>FEV</strong>(1) [SMD =  0.197, 95% CI: ( 0.327,  0.066), p = 0.003], morning PEF [SMD =  0.796, 95% CI: ( 1.047,  0.545), p < 0.001], night time PEF [SMD =  0.501, 95% CI: ( 0.797,  0.204), p = 0.001] and post treatment <strong>FEV</strong>(1) [SMD =  0.178, 95% CI: ( 0.309,  0.046), p = 0.008] and increased use of concomitant medications [SMD = 0.537, 95% CI: (0.166, 0.908), p = 0.005] in <b>smokers</b>, but not non <b>smokers</b> with asthma, although there was no statistical difference in allergy related endpoints and asthma score (ACQ 5).
+FEV	drug	nicotine	22441734	In homozygous (11%), heterozygous (44%) and noncarrier (45%) ever <b>smokers</b>, forced expiratory volume in 1 s (<strong>FEV</strong>(1)) was 94.1% predicted, 95.3% pred and 96.5% pred, forced vital capacity (FVC) was 97.1% pred, 97.5% pred and 98.3% pred, and <strong>FEV</strong>(1)/FVC was 0.770, 0.773 and 0.777, respectively (all p<0.001 for trend).
+FEV	drug	nicotine	22441734	<b>Smoking</b> interacted with genotype on <strong>FEV</strong>(1) % pred and <strong>FEV</strong>(1)/FVC (both p<0.001).
+FEV	addiction	sensitization	22017462	The rs8034191 SNP genotyped in 551 children from the environment and childhood asthma (ECA) birth cohort study in Oslo, Norway, and in 516 families from six European centers [the Genetics of Asthma International Network (GAIN) study] was tested for genotypic or allelic associations to current or history of asthma, allergic <b>sensitization</b> (≥ one positive skin prick tests), bronchial hyperresponsiveness (BHR), and lung function (<strong>FEV</strong>(1%) of predicted and <strong>FEV</strong>(1) /FVC ratio over/ below the 5th percentile).
+FEV	drug	nicotine	21845038	Demographics were balanced between the D (n = 5846) and ND (n = 6317) groups, except for higher cumulative <b>smoking</b> (56 pack years versus 48 pack years), lower forced expiratory volume in one second (<strong>FEV</strong>(1))/forced vital capacity (43% versus 48%), and lower baseline <strong>FEV</strong>(1) (35.8% predicted versus 42.4% predicted) in the D group.
+FEV	drug	nicotine	21624643	Factors (f) (fII, fV, fVII, fVIII, fIX, fX), antithrombin, protein C (PC) and free tissue factor pathway inhibitor (fTFPI) from 60 COPD patients (aged 64.2 ± 10.1 years; a mean forced expiratory volume in 1 second [<strong>FEV</strong>(1)], 55.6 ± 15.8% of predicted values) were compared with those for 43 controls matched for age, sex, weight and <b>smoking</b>.
+FEV	addiction	dependence	21486723	For simplicity analysis of age and height <b>dependence</b> of investigated respiratory parameters (VC, FVC, <strong>FEV</strong>⊂1, <strong>FEV</strong>⊂1%FVC, PEF, MEF⊂75,50,25) can be described by linear functions (y = a * height ?
+FEV	addiction	dependence	20971276	Independent predictors of mortality by multivariable analysis were ventilator <b>dependence</b> (p = 0.038) and peak <strong>FEV</strong>(1) (p < 0.0001); normal SE was associated with improved survival (hazard ratio 0.13; confidence interval 0.03 to 0.54, p = 0.03).
+FEV	addiction	dependence	20156745	For analysis age and height <b>dependence</b> of investigated respiratory parameters (VC, FVC, <strong>FEV</strong>(1), <strong>FEV</strong>(1) %FVC, PEF, MEF(75,50,25)) can for simplicity be described by linear functions (y = a .
+FEV	drug	nicotine	20456673	In contrast, persons exposed to environmental <b>tobacco</b> smoke for >5 h/day had a significantly increased risk of 'wheeze' (OR 1.69, 95% CI: 1.24 2.30) and 'chronic cough' (OR 1.57, 95% CI: 1.12 2.20), as well as decreased lung function (<strong>FEV</strong>(1)% predicted), compared with those who were not exposed.
+FEV	drug	nicotine	19710291	The corresponding effect in pre bronchodilator therapy <strong>FEV</strong>(1) was 118.1 mL (p = 0.002) in <b>smokers</b> and 72.9 mL (p < 0.001) in nonsmokers.
+FEV	drug	nicotine	19614600	In addition, 392 twins have been invited to a clinical investigation to evaluate: (i) to what extent genetic factors contribute to individual differences (variation) in <strong>FEV</strong>(1) (forced expiratory volume in 1 s), vital capacity and DL(CO) (diffusion capacity), taking sex into consideration, and (ii) whether <b>smoking</b> behaviour and respiratory symptoms influence these estimates.
+FEV	addiction	dependence	19343615	The age <b>dependence</b> of respiratory parameters (VC, FVC, <strong>FEV</strong> (1), <strong>FEV</strong> (1) %FVC, PEF, MEF (75,50,25)) for the healthy subjects can be described with a linear function (y =   m x age + n).
+FEV	drug	nicotine	19210360	<b>Smoking</b> was a risk factor for a lower <strong>FEV</strong>(1).
+FEV	drug	nicotine	19136238	A population sample of 2402 Chinese aged >or=55 with and without COPD (characteristic symptoms of chronic cough, sputum or breathlessness and airflow obstruction and <strong>FEV</strong>(1)/FVC<0.70) was assessed on Geriatric Depression Scale (score>or=5), dependence on basic activities of daily living (ADL), SF 12 health status, <b>smoking</b> and medication behaviour.
+FEV	addiction	dependence	19136238	A population sample of 2402 Chinese aged >or=55 with and without COPD (characteristic symptoms of chronic cough, sputum or breathlessness and airflow obstruction and <strong>FEV</strong>(1)/FVC<0.70) was assessed on Geriatric Depression Scale (score>or=5), <b>dependence</b> on basic activities of daily living (ADL), SF 12 health status, smoking and medication behaviour.
+FEV	addiction	reward	17356080	There is controversy about whether therapy with inhaled corticosteroids (<b>ICSs</b>) modifies the natural history of COPD, characterized by an accelerated decline in <strong>FEV</strong>(1).
+FEV	drug	nicotine	17356080	We aimed to determine whether the regular use of ICSs vs placebo improves <strong>FEV</strong>(1) decline in COPD patients, and whether this relationship is modified by gender and <b>smoking</b>.
+FEV	addiction	reward	17356080	We aimed to determine whether the regular use of <b>ICSs</b> vs placebo improves <strong>FEV</strong>(1) decline in COPD patients, and whether this relationship is modified by gender and smoking.
+FEV	drug	nicotine	17356080	<b>Smokers</b> who continued to smoke had a smaller increase in <strong>FEV</strong>(1) during the first 6 months than did ex <b>smokers</b>.
+FEV	drug	nicotine	17356080	Female ex <b>smokers</b> had a larger increase in <strong>FEV</strong>(1) with ICS therapy than did male ex <b>smokers</b>.
+FEV	addiction	reward	17258304	To evaluate whether prolonged treatment with <b>ICSs</b> is associated with <strong>FEV</strong>(1) decline in adults with asthma.
+FEV	drug	nicotine	17258304	<strong>FEV</strong>(1) decline was analyzed according to age, sex, height, body mass index, total IgE, time of ICS use, and <b>smoking</b>, while adjusting for potential confounders.
+FEV	drug	nicotine	15557134	Factors related to asthma severity and BMI such as <b>smoking</b>, <strong>FEV</strong>(1), bronchial hyperresponsiveness, and dyspnea were taken into account.
+FEV	drug	nicotine	15557134	In women, the association remained after adjustment for age, <strong>FEV</strong>(1), <b>smoking</b> habits, and BMI adjusted dyspnea and taking into account familial dependence (p = 0.0001).
+FEV	addiction	dependence	15557134	In women, the association remained after adjustment for age, <strong>FEV</strong>(1), smoking habits, and BMI adjusted dyspnea and taking into account familial <b>dependence</b> (p = 0.0001).
+FEV	drug	nicotine	14519147	We retrospectively evaluated two groups of non <b>smoking</b> asthmatics (forced expiratory volume in 1 s (<strong>FEV</strong>)1>/=60% predicted) who were reactive (responders) or unreactive (controls) to inhaled AMP.
+FEV	drug	nicotine	10722765	In utero exposure to maternal <b>smoking</b> was associated with reduced peak expiratory flow rate (PEFR) ( 3.0%, 95% CI  4.4 to  1.4), mean mid expiratory flow (MMEF) ( 4.6%, 95% CI  7.0 to  2.3), and forced expiratory flow (FEF(75)) ( 6.2%, 95% CI  9.1 to  3.1), but not forced expiratory volume in one second (<strong>FEV</strong>(1)).
+FEV	drug	nicotine	10556107	Twenty six Danish and 30 Dutch ex <b>smokers</b> with alpha(1) antitrypsin deficiency of PI*ZZ phenotype and moderate emphysema (<strong>FEV</strong>(1) between 30% and 80% of predicted) participated in a double blind trial of alpha(1) antitrypsin augmentation therapy.
+FEV	addiction	dependence	6648052	Density <b>dependence</b> variables (helium to air difference in forced expiratory flows at 50 and 25% vital capacity and volume of isoflow) were compared with spirographic performance (vital capacity, <strong>FEV</strong> 1.0) in 76 men aged 33 56 years.
+CRHR2	drug	alcohol	31666410	[<b>Ethanol</b> withdrawal leads to an increase in the <strong>CRFR2</strong> mRNA level in the ventricular tegmental region of the rat brain].
+CRHR2	addiction	withdrawal	31666410	[Ethanol <b>withdrawal</b> leads to an increase in the <strong>CRFR2</strong> mRNA level in the ventricular tegmental region of the rat brain].
+CRHR2	drug	alcohol	31666410	During the period of <b>alcohol</b> withdrawal, the level of <strong>CRFR2</strong> mRNA in the ventral tegmental area of the brain on the seventh day of abstinence was significantly increased in comparison with the control group.
+CRHR2	addiction	withdrawal	31666410	During the period of alcohol <b>withdrawal</b>, the level of <strong>CRFR2</strong> mRNA in the ventral tegmental area of the brain on the seventh day of abstinence was significantly increased in comparison with the control group.
+CRHR2	drug	amphetamine	31562746	Moreover, there were significant correlations between nucleus accumbens Hcrtr1, Hcrtr2, <strong>Crhr2</strong>, and Avpr1b mRNA levels and cue induced <b>METH</b> seeking only in female rats.
+CRHR2	addiction	relapse	31562746	Moreover, there were significant correlations between nucleus accumbens Hcrtr1, Hcrtr2, <strong>Crhr2</strong>, and Avpr1b mRNA levels and cue induced METH <b>seeking</b> only in female rats.
+CRHR2	drug	opioid	31071414	<b>Oxycodone</b> CPP females have: a) increases in ARC (activity regulated cytoskeletal associated protein) immunoreactivity (ir) in CA3 pyramidal cells; b) decreases in Npy (neuropeptide Y) gene expression in the medial hippocampus but higher numbers of NPY containing hilar interneurons compared to males; c) increases in <strong>Crhr2</strong> (corticotropin releasing factor receptor 2) expression in CA2/3; d) increases in Akt1 (AKT serine/threonine kinase 1) expression in medial hippocampus; and e) decreases in phosphorylated MAPK (mitogen activated protein kinase) ir in CA1 and dentate gyrus.
+CRHR2	addiction	reward	31071414	Oxycodone <b>CPP</b> females have: a) increases in ARC (activity regulated cytoskeletal associated protein) immunoreactivity (ir) in CA3 pyramidal cells; b) decreases in Npy (neuropeptide Y) gene expression in the medial hippocampus but higher numbers of NPY containing hilar interneurons compared to males; c) increases in <strong>Crhr2</strong> (corticotropin releasing factor receptor 2) expression in CA2/3; d) increases in Akt1 (AKT serine/threonine kinase 1) expression in medial hippocampus; and e) decreases in phosphorylated MAPK (mitogen activated protein kinase) ir in CA1 and dentate gyrus.
+CRHR2	drug	nicotine	30722977	Changes in striatal dopamine release and locomotor activity following acute withdrawal from chronic <b>nicotine</b> are mediated by CRF1, but not <strong>CRF2</strong>, receptors.
+CRHR2	addiction	withdrawal	30722977	Changes in striatal dopamine release and locomotor activity following acute <b>withdrawal</b> from chronic nicotine are mediated by CRF1, but not <strong>CRF2</strong>, receptors.
+CRHR2	drug	nicotine	30722977	The aim of the present study was to investigate the participation of corticotropin releasing factor (CRF) receptors (CRF1 and <strong>CRF2</strong>) in the alterations of the dorsal and ventral striatal dopamine release and the vertical and horizontal locomotor activity observed in rats following chronic <b>nicotine</b> treatment and consequent acute withdrawal.
+CRHR2	addiction	withdrawal	30722977	The aim of the present study was to investigate the participation of corticotropin releasing factor (CRF) receptors (CRF1 and <strong>CRF2</strong>) in the alterations of the dorsal and ventral striatal dopamine release and the vertical and horizontal locomotor activity observed in rats following chronic nicotine treatment and consequent acute <b>withdrawal</b>.
+CRHR2	drug	nicotine	30722977	The present study demonstrates that the changes of striatal dopamine release and locomotor activity observed following chronic <b>nicotine</b> treatment and consequent acute withdrawal are mediated by CRF1, but not <strong>CRF2</strong>, receptor.
+CRHR2	addiction	withdrawal	30722977	The present study demonstrates that the changes of striatal dopamine release and locomotor activity observed following chronic nicotine treatment and consequent acute <b>withdrawal</b> are mediated by CRF1, but not <strong>CRF2</strong>, receptor.
+CRHR2	drug	amphetamine	30465812	Differential effect of <b>amphetamine</b> over the corticotropin releasing factor <strong>CRF2</strong> receptor, the orexin OX1 receptor and the <strong>CRF2</strong> OX1 heteroreceptor complex.
+CRHR2	drug	amphetamine	30465812	Moreover, we show that <b>amphetamine</b> effect on <strong>CRF2</strong> receptors was mediated by σ1R whereas the effect on OX1 receptors was mediated by σ2R.
+CRHR2	drug	amphetamine	30465812	<b>Amphetamine</b> did potentiate the negative cross talk occurring within the <strong>CRF2</strong> OX1 receptor heteromer context, likely by a macromolecular complex involving the two sigma receptors and the two GPCRs.
+CRHR2	drug	opioid	29953524	A non coding <strong>CRHR2</strong> SNP rs255105, a cis eQTL for a downstream lincRNA AC005154.6, is associated with <b>heroin</b> addiction.
+CRHR2	addiction	addiction	29953524	A non coding <strong>CRHR2</strong> SNP rs255105, a cis eQTL for a downstream lincRNA AC005154.6, is associated with heroin <b>addiction</b>.
+CRHR2	addiction	sensitization	29857328	Significantly higher CRF1 and <strong>CRF2</strong> receptor levels after <b>sensitization</b> were detected in the Hip.
+CRHR2	addiction	sensitization	29857328	Additionally, <strong>CRF2</strong> receptor levels were augmented by <b>sensitization</b> in the PFCx, and treatment and time induced increases were detected in the DS.
+CRHR2	drug	cocaine	29406581	In the present study we investigated the role of the <strong>CRF2</strong> receptor in social behaviour deficits, vulnerability to stress and related brain alterations induced by <b>cocaine</b> administration and withdrawal.
+CRHR2	addiction	withdrawal	29406581	In the present study we investigated the role of the <strong>CRF2</strong> receptor in social behaviour deficits, vulnerability to stress and related brain alterations induced by cocaine administration and <b>withdrawal</b>.
+CRHR2	drug	cocaine	29406581	<strong>CRF2</strong> receptor deficiency eliminated the sociability deficit induced by <b>cocaine</b> withdrawal.
+CRHR2	addiction	withdrawal	29406581	<strong>CRF2</strong> receptor deficiency eliminated the sociability deficit induced by cocaine <b>withdrawal</b>.
+CRHR2	drug	cocaine	29406581	Moreover, <strong>CRF2</strong>  /  mice did not show either the stress induced sociability deficit or the increased AVP and OT expression associated with long term <b>cocaine</b> withdrawal, indicating resilience to stress.
+CRHR2	addiction	withdrawal	29406581	Moreover, <strong>CRF2</strong>  /  mice did not show either the stress induced sociability deficit or the increased AVP and OT expression associated with long term cocaine <b>withdrawal</b>, indicating resilience to stress.
+CRHR2	drug	cocaine	29406581	Throughout, wild type and <strong>CRF2</strong>  /  mice displayed SNP, suggesting that <b>cocaine</b> withdrawal induced sociability deficits were not due to impaired detection of social stimuli.
+CRHR2	addiction	withdrawal	29406581	Throughout, wild type and <strong>CRF2</strong>  /  mice displayed SNP, suggesting that cocaine <b>withdrawal</b> induced sociability deficits were not due to impaired detection of social stimuli.
+CRHR2	drug	cocaine	29406581	These findings demonstrate a central role for the <strong>CRF2</strong> receptor in social behaviour deficits and biomarkers of vulnerability induced by <b>cocaine</b> withdrawal, suggesting new therapeutic strategies for stimulant use disorders.
+CRHR2	addiction	withdrawal	29406581	These findings demonstrate a central role for the <strong>CRF2</strong> receptor in social behaviour deficits and biomarkers of vulnerability induced by cocaine <b>withdrawal</b>, suggesting new therapeutic strategies for stimulant use disorders.
+CRHR2	drug	cocaine	29391155	The effect of RSD on <b>cocaine</b> sensitization was again blocked by the corticotropin releasing factor CRF1 receptor antagonist, while peripheral <strong>CRF2</strong> receptor antagonist did not show effect.
+CRHR2	addiction	sensitization	29391155	The effect of RSD on cocaine <b>sensitization</b> was again blocked by the corticotropin releasing factor CRF1 receptor antagonist, while peripheral <strong>CRF2</strong> receptor antagonist did not show effect.
+CRHR2	drug	alcohol	29118713	After having had continuous access to <b>ethanol</b> (20% weight/volume) for 4 weeks, control and stressed mice had CRF type 1 (CRFR1) or type 2 (<strong>CRFR2</strong>) receptor antagonists infused into the BNST and then had access to <b>ethanol</b> for 24 h. In separate cohorts of control and stressed mice, we assessed mRNA levels of BNST CRF, CRFR1 and <strong>CRFR2</strong>.
+CRHR2	drug	alcohol	29118713	The selective blockade of BNST CRFR1 with CP376,395 effectively reduced <b>alcohol</b> drinking in non stressed mice, whereas the selective <strong>CRFR2</strong> antagonist astressin2B produced a dose dependent increase in <b>ethanol</b> consumption in both non stressed controls and stressed mice.
+CRHR2	drug	alcohol	29118713	CRF CRFR1 signaling in the BNST seems to underlie <b>ethanol</b> intake in non stressed mice, whereas <strong>CRFR2</strong> modulates <b>alcohol</b> consumption in both socially defeated and non stressed mice with a history of chronic intake.
+CRHR2	drug	alcohol	28807676	Therefore, in this study we used in vitro slice electrophysiology to investigate the effects of CRF and its receptor subtype (CRF1 and <strong>CRF2</strong>) antagonists on both evoked and spontaneous action potential independent glutamatergic transmission in the CeA of naive and <b>ethanol</b> dependent Sprague Dawley rats.
+CRHR2	drug	nicotine	28222901	In the present review, we analyze reports studying the role of Corticotropin Releasing Factor (CRF), the principle neuroendocrine mediator of the stress response and its two receptors (CRF1 and <strong>CRF2</strong>) in the withdrawal phase as well as in the abstinence from <b>nicotine</b> use.
+CRHR2	addiction	withdrawal	28222901	In the present review, we analyze reports studying the role of Corticotropin Releasing Factor (CRF), the principle neuroendocrine mediator of the stress response and its two receptors (CRF1 and <strong>CRF2</strong>) in the <b>withdrawal</b> phase as well as in the abstinence from nicotine use.
+CRHR2	addiction	reward	27818644	This review will further discuss a putative role for other components of the CRF system that contribute for the overall balance of CRF function in <b>reward</b> and stress pathways, including <strong>CRF2</strong> receptors, CRF binding protein, and urocortins, a family of CRF related peptides.
+CRHR2	drug	nicotine	27693397	Selective <strong>CRF2</strong> receptor agonists ameliorate the anxiety  and depression like state developed during chronic <b>nicotine</b> treatment and consequent acute withdrawal in mice.
+CRHR2	addiction	withdrawal	27693397	Selective <strong>CRF2</strong> receptor agonists ameliorate the anxiety  and depression like state developed during chronic nicotine treatment and consequent acute <b>withdrawal</b> in mice.
+CRHR2	drug	nicotine	27693397	The present study suggests that selective <strong>CRF2</strong> receptor agonists could be used as a therapy in <b>nicotine</b> addiction.
+CRHR2	addiction	addiction	27693397	The present study suggests that selective <strong>CRF2</strong> receptor agonists could be used as a therapy in nicotine <b>addiction</b>.
+CRHR2	drug	nicotine	27461514	In conclusion, the overexpression of CRF in the BNST prevents the dysphoria like state associated with <b>nicotine</b> withdrawal and increases the <strong>CRF2</strong>/CRF1 receptor ratio, which may diminish the negative effects of CRF on mood.
+CRHR2	addiction	withdrawal	27461514	In conclusion, the overexpression of CRF in the BNST prevents the dysphoria like state associated with nicotine <b>withdrawal</b> and increases the <strong>CRF2</strong>/CRF1 receptor ratio, which may diminish the negative effects of CRF on mood.
+CRHR2	drug	alcohol	27440230	Therefore, in <b>alcohol</b> preferring rats, we examined the effect of bilateral injections into the NI of the CRF1 receptor antagonist, CP376395 or the <strong>CRF2</strong> receptor antagonist, astressin 2B on yohimbine induced reinstatement of <b>alcohol</b> seeking.
+CRHR2	addiction	relapse	27440230	Therefore, in alcohol preferring rats, we examined the effect of bilateral injections into the NI of the CRF1 receptor antagonist, CP376395 or the <strong>CRF2</strong> receptor antagonist, astressin 2B on yohimbine induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+CRHR2	drug	alcohol	27440230	In line with these data, CRF1 , but not <strong>CRF2</strong> , receptor mRNA was upregulated in the NI following chronic <b>ethanol</b> intake.
+CRHR2	addiction	withdrawal	26907806	The CRF1 and the <strong>CRF2</strong> receptor mediate recognition memory deficits and vulnerability induced by opiate <b>withdrawal</b>.
+CRHR2	drug	opioid	26907806	In the present study, CRF1 / , <strong>CRF2</strong> /  and their respective wild type mice are injected with escalating doses of <b>morphine</b> and cognitive function assessed by the novel object recognition (NOR) memory task throughout relatively long periods of opiate withdrawal.
+CRHR2	addiction	withdrawal	26907806	In the present study, CRF1 / , <strong>CRF2</strong> /  and their respective wild type mice are injected with escalating doses of morphine and cognitive function assessed by the novel object recognition (NOR) memory task throughout relatively long periods of opiate <b>withdrawal</b>.
+CRHR2	addiction	withdrawal	26907806	Early (2 days) phases of opiate <b>withdrawal</b> impair NOR memory in wild type, CRF1 /  and <strong>CRF2</strong> /  mice.
+CRHR2	addiction	withdrawal	26907806	However, the duration of opiate <b>withdrawal</b> induced NOR memory deficits is prolonged in CRF1 /  but shortened in <strong>CRF2</strong> /  mice, as compared to their respective wild type mice, indicating opposite roles for the two CRF receptor subtypes.
+CRHR2	drug	alcohol	26247973	Corticotropin Releasing Factor Binding Protein and <strong>CRF2</strong> Receptors in the Ventral Tegmental Area: Modulation of <b>Ethanol</b> Binge Drinking in C57BL/6J Mice.
+CRHR2	addiction	intoxication	26247973	Corticotropin Releasing Factor Binding Protein and <strong>CRF2</strong> Receptors in the Ventral Tegmental Area: Modulation of Ethanol <b>Binge</b> Drinking in C57BL/6J Mice.
+CRHR2	drug	alcohol	26247973	Most studies with corticotropin releasing factor (CRF) and <b>ethanol</b> (EtOH) consumption have focused on CRF type 1 (CRF1) receptors; less is known about other components of the CRF system, such as the CRF type 2 (<strong>CRF2</strong>) receptors and the CRF binding protein (CRFBP).
+CRHR2	addiction	intoxication	26247973	Potential interactions between VTA CRFBP and <strong>CRF2</strong> receptors on EtOH <b>binge</b> drinking were also assessed.
+CRHR2	addiction	withdrawal	25672976	<strong>CRF2</strong> Receptor Deficiency Eliminates the Long Lasting Vulnerability of Motivational States Induced by Opiate <b>Withdrawal</b>.
+CRHR2	drug	opioid	25672976	In this study, we report that genetic inactivation of the stress responsive corticotropin releasing factor receptor 2 (<strong>CRF2</strong> / ) completely eliminates the reemergence of increased nonrewarded nose pokes, reflecting up shifted motivational states, triggered by ethological environmental stressors long after cessation of <b>morphine</b> administration in mice.
+CRHR2	addiction	withdrawal	25672976	Accordingly, <strong>CRF2</strong> receptor deficiency completely abolishes the increase in biomarkers of synthesis of major brain motivational substrates, such as ventral tegmental area (VTA) dopamine (DA) and amygdala γ aminobutyric acid (GABA) systems, associated with the stress induced reemergence of up shifted motivational states long after opiate <b>withdrawal</b>.
+CRHR2	addiction	withdrawal	25672976	Nevertheless, neither <strong>CRF2</strong> receptor deficiency nor long term opiate <b>withdrawal</b> affects amygdala CRF or hypothalamus CRF expression, indicating preserved brain stress coping systems.
+CRHR2	addiction	withdrawal	25672976	Moreover, <strong>CRF2</strong> receptor deficiency does not influence the locomotor or the anxiety like effect of long term opiate <b>withdrawal</b>.
+CRHR2	addiction	withdrawal	25672976	Thus, the present results reveal an essential and specific role for the <strong>CRF2</strong> receptor in the stress induced reemergence of up shifted motivational states and related alterations in brain motivational systems long after opiate <b>withdrawal</b>.
+CRHR2	drug	amphetamine	25205625	Central <strong>CRF2</strong> receptor antagonism reduces anxiety states during <b>amphetamine</b> withdrawal.
+CRHR2	addiction	withdrawal	25205625	Central <strong>CRF2</strong> receptor antagonism reduces anxiety states during amphetamine <b>withdrawal</b>.
+CRHR2	drug	amphetamine	25205625	Anxiety like behaviors observed during <b>amphetamine</b> withdrawal are mediated by increased expression and activity of corticotropin releasing factor type 2 (<strong>CRF2</strong>) receptors in the dorsal raphe nucleus (dRN).
+CRHR2	addiction	withdrawal	25205625	Anxiety like behaviors observed during amphetamine <b>withdrawal</b> are mediated by increased expression and activity of corticotropin releasing factor type 2 (<strong>CRF2</strong>) receptors in the dorsal raphe nucleus (dRN).
+CRHR2	addiction	withdrawal	25205625	Anxiety like behavior of rats during <b>withdrawal</b> can be reversed by <strong>CRF2</strong> receptor antagonism in the dRN, but the efficacy of global central <strong>CRF2</strong> receptor antagonism is unknown.
+CRHR2	addiction	withdrawal	25205625	Rats undergoing <b>withdrawal</b> showed increased anxiety like behavior, which was reduced by ventricular infusion of the <strong>CRF2</strong> antagonist antisauvagine 30 (ASV 2 μg/2 μl).
+CRHR2	drug	amphetamine	25205625	Overall, these results suggest that central <strong>CRF2</strong> antagonism reduces anxiety states during <b>amphetamine</b> withdrawal, and that behavioral effects may be dependent upon the balance of CRF1 and <strong>CRF2</strong> receptor activity in anxiety related regions.
+CRHR2	addiction	withdrawal	25205625	Overall, these results suggest that central <strong>CRF2</strong> antagonism reduces anxiety states during amphetamine <b>withdrawal</b>, and that behavioral effects may be dependent upon the balance of CRF1 and <strong>CRF2</strong> receptor activity in anxiety related regions.
+CRHR2	drug	cocaine	25073922	Repeated treatment with <b>cocaine</b> potentiates glutamatergic transmission in the rat basolateral amygdala/cortex pathway through a synergistic action of D1  like dopamine receptors and CRH type 2α receptors (<strong>CRF2</strong> α receptors).
+CRHR2	addiction	addiction	25073922	D1 /<strong>CRF2</strong> α receptor heteromerization might account, at least in part, for the complex physiological interactions established between dopamine and CRH in normal and pathological conditions such as <b>addiction</b>, representing a new potential pharmacological target.
+CRHR2	drug	opioid	24845178	Nineteen single nucleotide polymorphisms (SNPs) in 9 genes (AVP, AVPR1A, CRHR1, <strong>CRHR2</strong>, FKBP5, GAL, GLRA1, NPY1R and NR3C2) showed nominally significant association with <b>heroin</b> addiction.
+CRHR2	addiction	addiction	24845178	Nineteen single nucleotide polymorphisms (SNPs) in 9 genes (AVP, AVPR1A, CRHR1, <strong>CRHR2</strong>, FKBP5, GAL, GLRA1, NPY1R and NR3C2) showed nominally significant association with heroin <b>addiction</b>.
+CRHR2	drug	cocaine	24806691	This study investigated whether injecting either a CRFR1 or <strong>CRFR2</strong> antagonist directly into the VTA before each social defeat would prevent the development of later (1) locomotor sensitization, (2) dopaminergic sensitization, and (3) escalated <b>cocaine</b> self administration in rats.
+CRHR2	addiction	sensitization	24806691	This study investigated whether injecting either a CRFR1 or <strong>CRFR2</strong> antagonist directly into the VTA before each social defeat would prevent the development of later (1) locomotor <b>sensitization</b>, (2) dopaminergic <b>sensitization</b>, and (3) escalated cocaine self administration in rats.
+CRHR2	drug	cocaine	24806691	Intra VTA antagonism of CRFR1, but not <strong>CRFR2</strong>, inhibited the induction of locomotor cross sensitization to <b>cocaine</b>, whereas both prevented dopaminergic cross sensitization and escalated <b>cocaine</b> self administration during a 24 h "binge."
+CRHR2	addiction	intoxication	24806691	Intra VTA antagonism of CRFR1, but not <strong>CRFR2</strong>, inhibited the induction of locomotor cross sensitization to cocaine, whereas both prevented dopaminergic cross sensitization and escalated cocaine self administration during a 24 h "<b>binge</b>."
+CRHR2	addiction	sensitization	24806691	Intra VTA antagonism of CRFR1, but not <strong>CRFR2</strong>, inhibited the induction of locomotor cross <b>sensitization</b> to cocaine, whereas both prevented dopaminergic cross <b>sensitization</b> and escalated cocaine self administration during a 24 h "binge."
+CRHR2	drug	cocaine	24800964	In the present study, wild type and <strong>CRF2</strong> /  mice are injected with <b>cocaine</b> and memory assessed by the novel object recognition (NOR) task throughout relatively long periods of drug withdrawal.
+CRHR2	addiction	withdrawal	24800964	In the present study, wild type and <strong>CRF2</strong> /  mice are injected with cocaine and memory assessed by the novel object recognition (NOR) task throughout relatively long periods of drug <b>withdrawal</b>.
+CRHR2	drug	cocaine	24800964	<b>Cocaine</b> impairs NOR memory in wild type and <strong>CRF2</strong> /  mice.
+CRHR2	drug	cocaine	24800964	However, following <b>cocaine</b> withdrawal NOR memory deficits last less time in <strong>CRF2</strong> /  than in wild type mice.
+CRHR2	addiction	withdrawal	24800964	However, following cocaine <b>withdrawal</b> NOR memory deficits last less time in <strong>CRF2</strong> /  than in wild type mice.
+CRHR2	drug	cocaine	24800964	Furthermore, a relatively mild stressor induces the re emergence of NOR deficits in long term <b>cocaine</b> withdrawn wild type but not <strong>CRF2</strong> /  mice.
+CRHR2	drug	cocaine	24800964	These data indicate a new role for the <strong>CRF2</strong> receptor in cognitive deficits induced by <b>cocaine</b> withdrawal, both as regards to their duration and their re induction by stress.
+CRHR2	addiction	withdrawal	24800964	These data indicate a new role for the <strong>CRF2</strong> receptor in cognitive deficits induced by cocaine <b>withdrawal</b>, both as regards to their duration and their re induction by stress.
+CRHR2	drug	nicotine	24755994	In conclusion, the overexpression of CRF in the CeA diminishes the dysphoric like state associated with <b>nicotine</b> withdrawal and this might be driven by neuroadaptive changes in CRF1 and <strong>CRF2</strong> receptor gene expression.
+CRHR2	addiction	withdrawal	24755994	In conclusion, the overexpression of CRF in the CeA diminishes the dysphoric like state associated with nicotine <b>withdrawal</b> and this might be driven by neuroadaptive changes in CRF1 and <strong>CRF2</strong> receptor gene expression.
+CRHR2	drug	cocaine	24144545	Here we explored the in vivo role of brain corticotropin releasing factor receptor type 2 (<strong>CRFR2</strong>) in <b>cocaine</b> primed reinstatement of drug seeking.
+CRHR2	addiction	relapse	24144545	Here we explored the in vivo role of brain corticotropin releasing factor receptor type 2 (<strong>CRFR2</strong>) in cocaine primed <b>reinstatement</b> of drug <b>seeking</b>.
+CRHR2	drug	cocaine	24144545	First, expressions of <strong>CRFR2</strong> were shown to be affected in a brain region specific manner within <b>cocaine</b> induced CPP and <b>cocaine</b> extinct CPP models.
+CRHR2	addiction	reward	24144545	First, expressions of <strong>CRFR2</strong> were shown to be affected in a brain region specific manner within cocaine induced <b>CPP</b> and cocaine extinct <b>CPP</b> models.
+CRHR2	drug	cocaine	24144545	Bilateral blockade of <strong>CRFR2</strong> in the dorsal portion of the medial prefrontal cortex (mPFC), or hippocampus (HP) was partially inhibited, but in the dorsal striatum (DS) did not affect, the <b>cocaine</b> primed reinstatement of <b>cocaine</b> CPP.
+CRHR2	addiction	relapse	24144545	Bilateral blockade of <strong>CRFR2</strong> in the dorsal portion of the medial prefrontal cortex (mPFC), or hippocampus (HP) was partially inhibited, but in the dorsal striatum (DS) did not affect, the cocaine primed <b>reinstatement</b> of cocaine CPP.
+CRHR2	addiction	reward	24144545	Bilateral blockade of <strong>CRFR2</strong> in the dorsal portion of the medial prefrontal cortex (mPFC), or hippocampus (HP) was partially inhibited, but in the dorsal striatum (DS) did not affect, the cocaine primed reinstatement of cocaine <b>CPP</b>.
+CRHR2	drug	alcohol	22444954	While dependence induced and binge drinking rely on the actions of CRF on CRFR1 receptors, <b>alcohol</b> consumption in models of these behaviors is inhibited by actions of Ucns on <strong>CRFR2</strong>.
+CRHR2	addiction	dependence	22444954	While <b>dependence</b> induced and binge drinking rely on the actions of CRF on CRFR1 receptors, alcohol consumption in models of these behaviors is inhibited by actions of Ucns on <strong>CRFR2</strong>.
+CRHR2	addiction	intoxication	22444954	While dependence induced and <b>binge</b> drinking rely on the actions of CRF on CRFR1 receptors, alcohol consumption in models of these behaviors is inhibited by actions of Ucns on <strong>CRFR2</strong>.
+CRHR2	drug	alcohol	22444954	In contrast, <b>alcohol</b> preference is positively influenced by actions of Ucn1, which is capable of acting on both CRFR1 and <strong>CRFR2</strong>.
+CRHR2	drug	alcohol	21895713	To avoid the potential nonspecific effects of antagonists, in this study, we tested <b>alcohol</b> drinking in CRFR1, <strong>CRFR2</strong>, CRF, and urocortin 1 (Ucn1) KO and corresponding wild type (WT) littermates using the DID paradigm.
+CRHR2	drug	alcohol	21895713	On days 1 to 3, the CRFR1, <strong>CRFR2</strong>, Ucn1, and CRF KO mice and their respective WT littermates were provided with 20% <b>ethanol</b> or 10% sucrose for 2 hours with water available at all other times.
+CRHR2	drug	alcohol	21895713	In contrast, <strong>CRFR2</strong> KO mice, while having reduced intakes initially, had similar <b>alcohol</b> intakes on days 2 to 4 and similar BECs as the WTs.
+CRHR2	drug	cocaine	21843515	More recently, the role of type 2 CRF (<strong>CRF2</strong>) receptors in stress induced relapse to <b>cocaine</b> seeking has also has been documented.
+CRHR2	addiction	relapse	21843515	More recently, the role of type 2 CRF (<strong>CRF2</strong>) receptors in stress induced <b>relapse</b> to cocaine <b>seeking</b> has also has been documented.
+CRHR2	drug	cocaine	21843515	The new information involving <strong>CRF2</strong> receptors in stress induced relapse to <b>cocaine</b> seeking has generated a need for a reappraisal of the existing anatomical and pharmacological evidence that have been used to support the critical role of CRF1 receptors.
+CRHR2	addiction	relapse	21843515	The new information involving <strong>CRF2</strong> receptors in stress induced <b>relapse</b> to cocaine <b>seeking</b> has generated a need for a reappraisal of the existing anatomical and pharmacological evidence that have been used to support the critical role of CRF1 receptors.
+CRHR2	addiction	relapse	21843515	The role of <strong>CRF2</strong> receptors in stress induced <b>relapse</b> to drug <b>seeking</b> also opens the question of the putative role of the other peptides of the CRH family (urocotin 1, urocortin 2 and urocortin 3) that have high affinity for <strong>CRF2</strong> receptors.
+CRHR2	addiction	relapse	21843515	In this commentary, the available evidence supporting the role of both CRF1 and <strong>CRF2</strong> receptors in stress induced <b>relapse</b> to drug <b>seeking</b> is reviewed.
+CRHR2	drug	amphetamine	19958793	Increased anxiety like behavior of rats during <b>amphetamine</b> withdrawal is reversed by <strong>CRF2</strong> receptor antagonism.
+CRHR2	addiction	withdrawal	19958793	Increased anxiety like behavior of rats during amphetamine <b>withdrawal</b> is reversed by <strong>CRF2</strong> receptor antagonism.
+CRHR2	drug	nicotine	19217073	Previous research has shown that blockade of corticotropin releasing factor (CRF) receptors with a nonspecific CRF1/<strong>CRF2</strong> receptor antagonist prevents the deficit in brain reward function associated with <b>nicotine</b> withdrawal and stress induced reinstatement of extinguished <b>nicotine</b> seeking in rats.
+CRHR2	addiction	relapse	19217073	Previous research has shown that blockade of corticotropin releasing factor (CRF) receptors with a nonspecific CRF1/<strong>CRF2</strong> receptor antagonist prevents the deficit in brain reward function associated with nicotine withdrawal and stress induced <b>reinstatement</b> of extinguished nicotine <b>seeking</b> in rats.
+CRHR2	addiction	reward	19217073	Previous research has shown that blockade of corticotropin releasing factor (CRF) receptors with a nonspecific CRF1/<strong>CRF2</strong> receptor antagonist prevents the deficit in brain <b>reward</b> function associated with nicotine withdrawal and stress induced reinstatement of extinguished nicotine seeking in rats.
+CRHR2	addiction	withdrawal	19217073	Previous research has shown that blockade of corticotropin releasing factor (CRF) receptors with a nonspecific CRF1/<strong>CRF2</strong> receptor antagonist prevents the deficit in brain reward function associated with nicotine <b>withdrawal</b> and stress induced reinstatement of extinguished nicotine seeking in rats.
+CRHR2	drug	nicotine	19217073	The aim of these studies was to investigate the role of CRF1 and <strong>CRF2</strong> receptors in the deficit in brain reward function associated with precipitated <b>nicotine</b> withdrawal and stress induced reinstatement of <b>nicotine</b> seeking.
+CRHR2	addiction	relapse	19217073	The aim of these studies was to investigate the role of CRF1 and <strong>CRF2</strong> receptors in the deficit in brain reward function associated with precipitated nicotine withdrawal and stress induced <b>reinstatement</b> of nicotine <b>seeking</b>.
+CRHR2	addiction	reward	19217073	The aim of these studies was to investigate the role of CRF1 and <strong>CRF2</strong> receptors in the deficit in brain <b>reward</b> function associated with precipitated nicotine withdrawal and stress induced reinstatement of nicotine seeking.
+CRHR2	addiction	withdrawal	19217073	The aim of these studies was to investigate the role of CRF1 and <strong>CRF2</strong> receptors in the deficit in brain reward function associated with precipitated nicotine <b>withdrawal</b> and stress induced reinstatement of nicotine seeking.
+CRHR2	drug	nicotine	19217073	The CRF1 receptor antagonist R278995/CRA0450 but not the <strong>CRF2</strong> receptor antagonist astressin 2B prevented the elevations in brain reward thresholds associated with precipitated <b>nicotine</b> withdrawal.
+CRHR2	addiction	reward	19217073	The CRF1 receptor antagonist R278995/CRA0450 but not the <strong>CRF2</strong> receptor antagonist astressin 2B prevented the elevations in brain <b>reward</b> thresholds associated with precipitated nicotine withdrawal.
+CRHR2	addiction	withdrawal	19217073	The CRF1 receptor antagonist R278995/CRA0450 but not the <strong>CRF2</strong> receptor antagonist astressin 2B prevented the elevations in brain reward thresholds associated with precipitated nicotine <b>withdrawal</b>.
+CRHR2	drug	alcohol	19151899	We recently reported that the <b>ethanol</b> augmentation of GABAergic synaptic transmission in rat CeA involves CRF1 receptors, because both CRF and <b>ethanol</b> significantly enhanced the amplitude of evoked GABAergic inhibitory postsynaptic currents (IPSCs) in CeA neurons from wild type (WT) and <strong>CRF2</strong> knockout (KO) mice, but not in neurons of CRF1 KO mice.
+CRHR2	drug	alcohol	19151899	A CRF1 (but not <strong>CRF2</strong>) KO construct and the CRF1 selective nonpeptide antagonist NIH 3 (LWH 63) blocked the augmenting effect of both CRF and <b>ethanol</b> on evoked IPSCs.
+CRHR2	addiction	sensitization	18591672	Deletion of <strong>CRF2</strong> receptors alone did not prevent <b>sensitization</b>.
+CRHR2	drug	cocaine	18184795	Now, activation of either D(1/5) or <strong>CRF2</strong> receptors increased the <b>cocaine</b> induced, depressed EPSCs.
+CRHR2	drug	cocaine	18184795	Also unmasked after acute withdrawal from chronic <b>cocaine</b> are endogenous, tonic inhibitory D2 like and tonic facilitatory <strong>CRF2</strong> receptor actions.
+CRHR2	addiction	withdrawal	18184795	Also unmasked after acute <b>withdrawal</b> from chronic cocaine are endogenous, tonic inhibitory D2 like and tonic facilitatory <strong>CRF2</strong> receptor actions.
+CRHR2	addiction	aversion	18184783	CRF induced place <b>aversion</b> was blocked by the <strong>CRF2</strong> receptor antagonist antisauvigine 30, but not by the CRF1 receptor antagonist antalarmin.
+CRHR2	addiction	aversion	18184783	These results suggest that the <b>aversive</b> effects of stress were mediated by <strong>CRF2</strong> receptor stimulation of dynorphin release and subsequent KOR activation.
+CRHR2	drug	cocaine	17004937	After prolonged withdrawal, CRF induced LTP was dependent on activation of <strong>CRF2</strong>, CaV2.3 (R type) calcium channels and intracellular signalling through protein kinase C in both saline  and <b>cocaine</b> treated groups.
+CRHR2	addiction	withdrawal	17004937	After prolonged <b>withdrawal</b>, CRF induced LTP was dependent on activation of <strong>CRF2</strong>, CaV2.3 (R type) calcium channels and intracellular signalling through protein kinase C in both saline  and cocaine treated groups.
+CRHR2	drug	alcohol	16205360	The objective of these studies was to examine the effect of corticotropin releasing factor receptor type 2 (<strong>CRF2</strong>) on <b>ethanol</b> consumption, conditioned taste aversion, sedation, and hypothermia.
+CRHR2	addiction	aversion	16205360	The objective of these studies was to examine the effect of corticotropin releasing factor receptor type 2 (<strong>CRF2</strong>) on ethanol consumption, conditioned taste <b>aversion</b>, sedation, and hypothermia.
+CRHR2	drug	alcohol	16205360	<strong>CRF2</strong> null mutant or knock out (KO), and wild type (WT) mice were used to assess consumption of increasing concentrations of <b>ethanol</b> in a two bottle, 24 hr test and during daily limited access sessions.
+CRHR2	drug	alcohol	16205360	<b>Ethanol</b> induced conditioned taste aversion (CTA), loss of righting reflex (LORR), hypothermia, and <b>ethanol</b> metabolism kinetics were also examined in the <strong>CRF2</strong> KO and WT mice.
+CRHR2	addiction	aversion	16205360	Ethanol induced conditioned taste <b>aversion</b> (<b>CTA</b>), loss of righting reflex (LORR), hypothermia, and ethanol metabolism kinetics were also examined in the <strong>CRF2</strong> KO and WT mice.
+CRHR2	drug	alcohol	16205360	<strong>CRF2</strong> KO mice did not differ from WT mice in sensitivity to <b>ethanol</b> induced CTA, LORR, hypothermia, or <b>ethanol</b> metabolism kinetics.
+CRHR2	addiction	aversion	16205360	<strong>CRF2</strong> KO mice did not differ from WT mice in sensitivity to ethanol induced <b>CTA</b>, LORR, hypothermia, or ethanol metabolism kinetics.
+CRHR2	drug	alcohol	16205360	<strong>CRF2</strong> deficiency had little effect on several <b>ethanol</b> associated behaviors in <strong>CRF2</strong> null mutant compared with WT mice, suggesting that this receptor does not have a primary role in modulating these behaviors.
+CRHR2	drug	alcohol	16205360	Evidence of a role for this receptor in neural circuits subserving stress coping behaviors suggest that future studies should focus on the role of endogenous <strong>CRF2</strong> in <b>ethanol</b> associated behaviors in mice that are stressed or withdrawing from dependence on <b>ethanol</b>.
+CRHR2	addiction	dependence	16205360	Evidence of a role for this receptor in neural circuits subserving stress coping behaviors suggest that future studies should focus on the role of endogenous <strong>CRF2</strong> in ethanol associated behaviors in mice that are stressed or withdrawing from <b>dependence</b> on ethanol.
+CRHR2	drug	cocaine	15659593	After acute withdrawal from a chronic <b>cocaine</b> administration regimen, CRF1 activation remained facilitatory, but <strong>CRF2</strong> activation facilitated rather than depressed LSMLN EPSCs.
+CRHR2	addiction	withdrawal	15659593	After acute <b>withdrawal</b> from a chronic cocaine administration regimen, CRF1 activation remained facilitatory, but <strong>CRF2</strong> activation facilitated rather than depressed LSMLN EPSCs.
+CRHR2	drug	cocaine	15659593	In saline treated rats, CRF1 and <strong>CRF2</strong> coupled predominantly to protein kinase A signaling pathways, whereas after <b>cocaine</b> withdrawal, protein kinase C activity was more prominent and likely contributed to the <strong>CRF2</strong> mediated presynaptic facilitation.
+CRHR2	addiction	withdrawal	15659593	In saline treated rats, CRF1 and <strong>CRF2</strong> coupled predominantly to protein kinase A signaling pathways, whereas after cocaine <b>withdrawal</b>, protein kinase C activity was more prominent and likely contributed to the <strong>CRF2</strong> mediated presynaptic facilitation.
+CRHR2	drug	alcohol	15201629	Given the behavioral characterization of these receptors, the objective of the following experiments was to characterize the role of <strong>CRF2</strong> receptors in the interaction between <b>alcohol</b> and stress by examining the effects of <strong>CRF2</strong> receptor activation in the behavioral stress response and <b>ethanol</b> self administration during early <b>ethanol</b> withdrawal in dependent rats.
+CRHR2	addiction	withdrawal	15201629	Given the behavioral characterization of these receptors, the objective of the following experiments was to characterize the role of <strong>CRF2</strong> receptors in the interaction between alcohol and stress by examining the effects of <strong>CRF2</strong> receptor activation in the behavioral stress response and ethanol self administration during early ethanol <b>withdrawal</b> in dependent rats.
+CRHR2	addiction	withdrawal	15201629	The role of the <strong>CRF2</strong> receptor in the regulation of these behaviors during the early stages of <b>withdrawal</b> was examined via central injection of the highly selective <strong>CRF2</strong> receptor agonist urocortin 3.
+CRHR2	drug	alcohol	15201629	These data suggest that activation of the <strong>CRF2</strong> receptor may provide a novel target in the attenuation of the stress response characteristic of the early stages of <b>ethanol</b> withdrawal.
+CRHR2	addiction	withdrawal	15201629	These data suggest that activation of the <strong>CRF2</strong> receptor may provide a novel target in the attenuation of the stress response characteristic of the early stages of ethanol <b>withdrawal</b>.
+OXTR	addiction	aversion	32304701	In addition to dopamine neurons that project from ventral tegmental area (VTA) to nucleus accumbens (NAc) to signal positively reinforcing events, OT receptors (<strong>OxTR</strong>) are also expressed by dopamine neurons that project from VTA to brain regions that can convey <b>aversive</b> properties of a stimulus.
+OXTR	addiction	reward	32304701	In addition to dopamine neurons that project from ventral tegmental area (VTA) to nucleus accumbens (NAc) to signal positively <b>reinforcing</b> events, OT receptors (<strong>OxTR</strong>) are also expressed by dopamine neurons that project from VTA to brain regions that can convey aversive properties of a stimulus.
+OXTR	drug	alcohol	32304701	Moreover, <strong>OxTR</strong> are expressed by non dopaminergic neurons in the VTA, such as GABA and glutamate neurons, which can both modulate the activity of dopamine VTA neurons locally (in opposite directions) or can project to other brain regions, including the NAc, where it can alter either positive reinforcement or aversion caused by <b>ethanol</b>.
+OXTR	addiction	aversion	32304701	Moreover, <strong>OxTR</strong> are expressed by non dopaminergic neurons in the VTA, such as GABA and glutamate neurons, which can both modulate the activity of dopamine VTA neurons locally (in opposite directions) or can project to other brain regions, including the NAc, where it can alter either positive reinforcement or <b>aversion</b> caused by ethanol.
+OXTR	addiction	reward	32304701	Moreover, <strong>OxTR</strong> are expressed by non dopaminergic neurons in the VTA, such as GABA and glutamate neurons, which can both modulate the activity of dopamine VTA neurons locally (in opposite directions) or can project to other brain regions, including the NAc, where it can alter either positive <b>reinforcement</b> or aversion caused by ethanol.
+OXTR	drug	opioid	31609135	Augmentation of <b>morphine</b> conditioned place preference by food restriction is associated with alterations in the oxytocin/<strong>oxytocin receptor</strong> in rat models.
+OXTR	drug	opioid	31609135	Conclusion: We propose the inclusion of OXT and <strong>OXTR</strong> alterations in the enhancement of <b>morphine</b> induced CPP and addiction vulnerability following FR.
+OXTR	addiction	addiction	31609135	Conclusion: We propose the inclusion of OXT and <strong>OXTR</strong> alterations in the enhancement of morphine induced CPP and <b>addiction</b> vulnerability following FR.
+OXTR	addiction	reward	31609135	Conclusion: We propose the inclusion of OXT and <strong>OXTR</strong> alterations in the enhancement of morphine induced <b>CPP</b> and addiction vulnerability following FR.
+OXTR	addiction	withdrawal	31386210	The V1b receptor antagonist, but not an <strong>oxytocin receptor</strong> agonist, into the CEA during the first 2 <b>withdrawal</b> cycles suppressed anxiety.
+OXTR	drug	alcohol	30990816	In dependent rats, intracerebroventricular administration of oxytocin or the <strong>oxytocin receptor</strong> agonist PF 06655075, which does not cross the blood brain barrier (i.e., it would not diffuse to the periphery), but not systemic administration of PF 06655075 (i.e., it would not reach the brain), decreased <b>alcohol</b> drinking.
+OXTR	drug	alcohol	30990816	Administration of a peripherally restricted <strong>oxytocin receptor</strong> antagonist did not reverse the effect of intranasal oxytocin on <b>alcohol</b> drinking.
+OXTR	drug	nicotine	30218618	Chronic <b>nicotine</b> administration restores brain region specific upregulation of <strong>oxytocin receptor</strong> binding levels in a G72 mouse model of schizophrenia.
+OXTR	drug	nicotine	30218618	Therefore, we sought to investigate the effects of chronic <b>nicotine</b> administration on <strong>oxytocin receptor</strong> (OTR) binding in the brain of a transgenic mouse model of schizophrenia that carries a bacterial artificial chromosome of the human G72/G30 locus (G72Tg).
+OXTR	addiction	addiction	30193705	We then posit several theories about how oxytocin interacts with both drug and social reward, as well as presenting a mechanistic account of how specific <strong>oxytocin receptor</strong> localization may contribute to oxytocin's efficacy as an <b>addiction</b> therapeutic.
+OXTR	addiction	reward	30193705	We then posit several theories about how oxytocin interacts with both drug and social <b>reward</b>, as well as presenting a mechanistic account of how specific <strong>oxytocin receptor</strong> localization may contribute to oxytocin's efficacy as an addiction therapeutic.
+OXTR	drug	alcohol	30110605	Prenatal <b>alcohol</b> exposure disrupts male adolescent social behavior and <strong>oxytocin receptor</strong> binding in rodents.
+OXTR	drug	opioid	29679881	Antiallodynia induced by oxytocin (20 ng/site) was inhibited by prior intra VLOC administration of atosiban (an <strong>oxytocin receptor</strong> antagonist, 100 ng/site) and <b>naloxone</b> (an <b>opioid</b> receptor antagonist, 500 ng/site).
+OXTR	drug	amphetamine	29353054	The nucleus accumbens core (NAcc) has been identified as an important site for oxytocin to inhibit <b>METH</b> behaviours, although previous findings suggest that the effects of oxytocin in the NAcc are mediated by receptors other than the <strong>oxytocin receptor</strong> (OTR).
+OXTR	drug	alcohol	27716573	<strong>Oxytocin receptor</strong> gene variation rs53576 and <b>alcohol</b> abuse in a longitudinal population representative study.
+OXTR	drug	alcohol	27716573	We examined the association of a variance in the oxytocin receptor gene (<strong>OXTR</strong> rs53576 polymorphism) with <b>alcohol</b> use in a population representative sample, and potential moderation by social functioning.
+OXTR	drug	alcohol	27716573	We examined the association of a variance in the <strong>oxytocin receptor</strong> gene (<strong>OXTR</strong> rs53576 polymorphism) with <b>alcohol</b> use in a population representative sample, and potential moderation by social functioning.
+OXTR	drug	alcohol	27716573	<b>Alcohol</b> use was not associated with the <strong>OXTR</strong> genotype in females.
+OXTR	drug	alcohol	27716573	<strong>OXTR</strong> rs53576 polymorphism is associated with <b>alcohol</b> use and prevalence of <b>alcohol</b> use disorders in males, and this may be moderated by inferior interpersonal relationships.
+OXTR	drug	cocaine	27453431	<b>Cocaine</b> abstinence induces emotional impairment and brain region specific upregulation of the <strong>oxytocin receptor</strong> binding.
+OXTR	drug	cocaine	27453431	Fourteen day escalating dose <b>cocaine</b> administration (3 × 15 30 mg/kg/day) and 14 day withdrawal increased plasma corticosterone levels and <strong>oxytocin receptor</strong> (OTR) binding in piriform cortex, lateral septum and amygdala.
+OXTR	addiction	withdrawal	27453431	Fourteen day escalating dose cocaine administration (3 × 15 30 mg/kg/day) and 14 day <b>withdrawal</b> increased plasma corticosterone levels and <strong>oxytocin receptor</strong> (OTR) binding in piriform cortex, lateral septum and amygdala.
+OXTR	drug	alcohol	27306084	Nucleus accumbens lentiviral mediated gain of function of the <strong>oxytocin receptor</strong> regulates anxiety  and <b>ethanol</b> related behaviors in adult mice.
+OXTR	drug	alcohol	27306084	Our previous study implicated a potential role for the oxytocin receptor (<strong>OxtR</strong>) in regulating <b>ethanol</b> conditioned place preference.
+OXTR	drug	alcohol	27306084	Our previous study implicated a potential role for the <strong>oxytocin receptor</strong> (<strong>OxtR</strong>) in regulating <b>ethanol</b> conditioned place preference.
+OXTR	drug	alcohol	27306084	Here, we examined anxiety and the behavioral responses to <b>ethanol</b> in C57BL/6 mice stereotaxically injected in the nucleus accumbens (NAcc) with lentiviral vectors expressing an empty vector (Mock) or the <strong>OxtR</strong> cDNA.
+OXTR	drug	alcohol	27306084	Most importantly, we found that, relative to Mock controls, increased expression of the <strong>OxtR</strong> in the NAcc led to decreased <b>ethanol</b> consumption and preference in the two bottle choice protocol and increased resistance to <b>ethanol</b> induced sedation.
+OXTR	drug	alcohol	27306084	These results provide further evidence that the oxytocin system contributes to the regulation of <b>ethanol</b> drinking and sensitivity and position <strong>OxtR</strong> as a central molecular mediator of <b>ethanol</b>'s effects within the mesolimbic system.
+OXTR	drug	alcohol	27306084	Taken together, the current findings suggest that <strong>OxtR</strong> manipulation may be a relevant strategy to address <b>ethanol</b> use disorders.
+OXTR	drug	amphetamine	26563756	Chronic <b>Methamphetamine</b> Self Administration Dysregulates Oxytocin Plasma Levels and <strong>Oxytocin Receptor</strong> Fibre Density in the Nucleus Accumbens Core and Subthalamic Nucleus of the Rat.
+OXTR	drug	amphetamine	26563756	Surprisingly, the <strong>oxytocin receptor</strong> (OTR) is only modestly involved in both regions in oxytocin attenuation of <b>METH</b> primed reinstatement.
+OXTR	addiction	relapse	26563756	Surprisingly, the <strong>oxytocin receptor</strong> (OTR) is only modestly involved in both regions in oxytocin attenuation of METH primed <b>reinstatement</b>.
+OXTR	drug	opioid	26475574	In addition, given recent evidence suggesting the presence of <strong>oxytocin receptor</strong> (OTR) μ <b>opioid</b> receptor (MOPr) interactions in the brain, we further explored these interactions by carrying out OTR autoradiographic binding in brain of mice lacking MOPr.
+OXTR	drug	amphetamine	26284529	However, it is unclear if oxytocin acts in this region to attenuate relapse to <b>METH</b> seeking behaviour, and if this action is through the <strong>oxytocin receptor</strong>.
+OXTR	addiction	relapse	26284529	However, it is unclear if oxytocin acts in this region to attenuate <b>relapse</b> to METH <b>seeking</b> behaviour, and if this action is through the <strong>oxytocin receptor</strong>.
+OXTR	drug	amphetamine	26284529	We aimed to determine whether oxytocin pretreatment administered into the STh would reduce reinstatement to <b>METH</b> use in rats experienced at <b>METH</b> self administration, and if this could be reversed by the co administration of the <strong>oxytocin receptor</strong> antagonist desGly NH2,d(CH2)5[D Tyr2,Thr4]OVT.
+OXTR	addiction	relapse	26284529	We aimed to determine whether oxytocin pretreatment administered into the STh would reduce <b>reinstatement</b> to METH use in rats experienced at METH self administration, and if this could be reversed by the co administration of the <strong>oxytocin receptor</strong> antagonist desGly NH2,d(CH2)5[D Tyr2,Thr4]OVT.
+OXTR	drug	alcohol	26282397	Because oxytocin (OXT) and vasopressin (AVP) contribute to rewarding social behavior, the present study utilized a genetic strategy to determine whether OXT and AVP receptors (<strong>OXTR</strong>, AVPR1a) are essential for female mice to demonstrate a conditioned social preference for <b>ethanol</b>.
+OXTR	drug	alcohol	26282397	The results suggest that <strong>Oxtr</strong> and Avpr1a are required for conditioned effects of an <b>ethanol</b> associated social stimulus.
+OXTR	drug	nicotine	26037668	Region specific up regulation of <strong>oxytocin receptor</strong> binding in the brain of mice following chronic <b>nicotine</b> administration.
+OXTR	drug	nicotine	26037668	Chronic <b>nicotine</b> administration induced a marked region specific upregulation of the <strong>oxytocin receptor</strong> binding in the amygdala, a brain region involved in stress and emotional regulation.
+OXTR	drug	alcohol	25713389	Here, we demonstrate that oxytocin selectively attenuates <b>ethanol</b> induced motor impairment and <b>ethanol</b> induced increases in GABAergic activity at δ GABA(A)Rs and that this effect does not involve the <strong>oxytocin receptor</strong>.
+OXTR	drug	opioid	25618594	Intracerebroventricular (ICV) administration of oxytocin (0.2μg) or the specific <strong>oxytocin receptor</strong> antagonist (OTA), desGly NH2, d(CH2)5[Tyr(Me)(2), Thr(4)] OVT, (0.75μg), on the conditioning days did not affect the acquisition of <b>morphine</b> induced CPP.
+OXTR	addiction	reward	25618594	Intracerebroventricular (ICV) administration of oxytocin (0.2μg) or the specific <strong>oxytocin receptor</strong> antagonist (OTA), desGly NH2, d(CH2)5[Tyr(Me)(2), Thr(4)] OVT, (0.75μg), on the conditioning days did not affect the acquisition of morphine induced <b>CPP</b>.
+OXTR	drug	cocaine	25539504	Immunoprecipitation of <strong>oxytocin receptor</strong> and GluA1 subunit receptors further demonstrated a physical interaction between these 2 receptors, although the interaction was not influenced by chronic <b>cocaine</b> or oxytocin treatment.
+OXTR	drug	cocaine	25522112	Given the evidence implicating the metabotropic glutamate receptor 5 (mGlu5 R), μ opioid receptor (MOPr), κ opioid receptor (ΚOPr) and <strong>oxytocin receptor</strong> (OTR) systems in <b>cocaine</b> addiction and relapse, our aim was to assess the modulation of these receptors using a mouse model of cue  and priming induced reinstatement of <b>cocaine</b> seeking.
+OXTR	drug	opioid	25522112	Given the evidence implicating the metabotropic glutamate receptor 5 (mGlu5 R), μ <b>opioid</b> receptor (MOPr), κ <b>opioid</b> receptor (ΚOPr) and <strong>oxytocin receptor</strong> (OTR) systems in cocaine addiction and relapse, our aim was to assess the modulation of these receptors using a mouse model of cue  and priming induced reinstatement of cocaine seeking.
+OXTR	addiction	addiction	25522112	Given the evidence implicating the metabotropic glutamate receptor 5 (mGlu5 R), μ opioid receptor (MOPr), κ opioid receptor (ΚOPr) and <strong>oxytocin receptor</strong> (OTR) systems in cocaine <b>addiction</b> and relapse, our aim was to assess the modulation of these receptors using a mouse model of cue  and priming induced reinstatement of cocaine seeking.
+OXTR	addiction	relapse	25522112	Given the evidence implicating the metabotropic glutamate receptor 5 (mGlu5 R), μ opioid receptor (MOPr), κ opioid receptor (ΚOPr) and <strong>oxytocin receptor</strong> (OTR) systems in cocaine addiction and <b>relapse</b>, our aim was to assess the modulation of these receptors using a mouse model of cue  and priming induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+OXTR	drug	alcohol	25449413	The <strong>oxytocin receptor</strong> impairs <b>ethanol</b> reward in mice.
+OXTR	addiction	reward	25449413	The <strong>oxytocin receptor</strong> impairs ethanol <b>reward</b> in mice.
+OXTR	drug	alcohol	25449413	It is well established that oxytocin, and its receptor (<strong>OxtR</strong>), play a crucial role in addiction and that the stimulation of oxytocin neurotransmission reduces addictive behaviors to <b>ethanol</b> in laboratory animals.
+OXTR	addiction	addiction	25449413	It is well established that oxytocin, and its receptor (<strong>OxtR</strong>), play a crucial role in <b>addiction</b> and that the stimulation of oxytocin neurotransmission reduces <b>addictive</b> behaviors to ethanol in laboratory animals.
+OXTR	drug	alcohol	25449413	However, the impact of <strong>OxtR</strong> modulation on acquisition, extinction and reinstatement of drug elicited <b>ethanol</b> conditioned place preference (EtOH CPP) has not yet been investigated.
+OXTR	addiction	relapse	25449413	However, the impact of <strong>OxtR</strong> modulation on acquisition, extinction and <b>reinstatement</b> of drug elicited ethanol conditioned place preference (EtOH CPP) has not yet been investigated.
+OXTR	addiction	reward	25449413	However, the impact of <strong>OxtR</strong> modulation on acquisition, extinction and reinstatement of drug elicited ethanol conditioned place preference (EtOH <b>CPP</b>) has not yet been investigated.
+OXTR	addiction	relapse	25449413	In this study, we evaluated the effects of <strong>OxtR</strong> pharmacological modulation, using the oxytocin analog Carbetocin, and genetic overexpression in the nucleus accumbens (NAcc), using lentiviral mediated gene transfer technology, of the <strong>OxtR</strong> on acquisition, extinction and <b>reinstatement</b> of drug elicited EtOH CPP in mice.
+OXTR	addiction	reward	25449413	In this study, we evaluated the effects of <strong>OxtR</strong> pharmacological modulation, using the oxytocin analog Carbetocin, and genetic overexpression in the nucleus accumbens (NAcc), using lentiviral mediated gene transfer technology, of the <strong>OxtR</strong> on acquisition, extinction and reinstatement of drug elicited EtOH <b>CPP</b> in mice.
+OXTR	addiction	reward	25449413	In the first experiment, results showed that Carbetocin administration and NAcc <strong>OxtR</strong> overexpression (LV <strong>OxtR</strong>) reduced EtOH <b>CPP</b> establishment.
+OXTR	drug	alcohol	25449413	In the second experiment, systemic Carbetocin treatment and <strong>OxtR</strong> overexpression resulted in decreased time spent in the <b>ethanol</b> paired compartment following completion of a 7 day extinction protocol.
+OXTR	addiction	relapse	25449413	Finally, the third experiment showed that Carbetocin and LV <strong>OxtR</strong> suppressed primed <b>reinstatement</b> of EtOH CPP.
+OXTR	addiction	reward	25449413	Finally, the third experiment showed that Carbetocin and LV <strong>OxtR</strong> suppressed primed reinstatement of EtOH <b>CPP</b>.
+OXTR	drug	alcohol	25449413	It is concluded that pharmacological and genetic modulation of the <strong>OxtR</strong> can modulate the acquisition, extinction, and reinstatement of conditioned reinforcing effects of <b>ethanol</b>.
+OXTR	addiction	relapse	25449413	It is concluded that pharmacological and genetic modulation of the <strong>OxtR</strong> can modulate the acquisition, extinction, and <b>reinstatement</b> of conditioned reinforcing effects of ethanol.
+OXTR	addiction	reward	25449413	It is concluded that pharmacological and genetic modulation of the <strong>OxtR</strong> can modulate the acquisition, extinction, and reinstatement of conditioned <b>reinforcing</b> effects of ethanol.
+OXTR	drug	amphetamine	25399704	Using the drug reinstatement paradigm in rats experienced at <b>METH</b> self administration, we aimed to determine whether oxytocin pre treatment within the NAc core would reduce relapse to <b>METH</b> use and if this could be reversed by the co administration of the <strong>oxytocin receptor</strong> (OTR) antagonist desGly NH2,d(CH2)5[D Tyr2,Thr4]OVT.
+OXTR	addiction	relapse	25399704	Using the drug <b>reinstatement</b> paradigm in rats experienced at METH self administration, we aimed to determine whether oxytocin pre treatment within the NAc core would reduce <b>relapse</b> to METH use and if this could be reversed by the co administration of the <strong>oxytocin receptor</strong> (OTR) antagonist desGly NH2,d(CH2)5[D Tyr2,Thr4]OVT.
+OXTR	drug	opioid	25225634	To better understand the <b>opioid</b> OXT interplay in the central nervous system, we first determined the expression of the oxytocin receptor (<strong>OXTR</strong>) in the brain of WT C57BL6/J mice by quantitative autoradiography; we then evaluated <strong>OXTR</strong> regional alterations in Oprm1 ( / ) mice.
+OXTR	drug	opioid	25225634	To better understand the <b>opioid</b> OXT interplay in the central nervous system, we first determined the expression of the <strong>oxytocin receptor</strong> (<strong>OXTR</strong>) in the brain of WT C57BL6/J mice by quantitative autoradiography; we then evaluated <strong>OXTR</strong> regional alterations in Oprm1 ( / ) mice.
+OXTR	drug	cocaine	24766650	Thirteen SNPs showed association with <b>cocaine</b> addiction, including the synonymous SNPs rs237902, in the oxytocin receptor gene (<strong>OXTR</strong>), and rs5374 in GALR1.
+OXTR	addiction	addiction	24766650	Thirteen SNPs showed association with cocaine <b>addiction</b>, including the synonymous SNPs rs237902, in the oxytocin receptor gene (<strong>OXTR</strong>), and rs5374 in GALR1.
+OXTR	drug	cocaine	24766650	Thirteen SNPs showed association with <b>cocaine</b> addiction, including the synonymous SNPs rs237902, in the <strong>oxytocin receptor</strong> gene (<strong>OXTR</strong>), and rs5374 in GALR1.
+OXTR	addiction	addiction	24766650	Thirteen SNPs showed association with cocaine <b>addiction</b>, including the synonymous SNPs rs237902, in the <strong>oxytocin receptor</strong> gene (<strong>OXTR</strong>), and rs5374 in GALR1.
+OXTR	drug	amphetamine	24183790	KD of Mll1 reduced H3K4me3, Fos and <strong>Oxtr</strong> levels and disrupted <b>METH</b> associated memory.
+OXTR	addiction	withdrawal	24129263	Seven days <b>withdrawal</b> from this administration paradigm induced a decrease of hypothalamic OT levels and a concomitant increase of <strong>oxytocin receptor</strong> (OTR) binding in the lateral septum and amygdala.
+OXTR	drug	psychedelics	23872370	In our second study we investigated whether <strong>oxytocin receptor</strong> activation might be implicated in the interoceptive effects experienced with the popular party drug, <b>MDMA</b> ('<b>ecstasy</b>').
+OXTR	drug	psychedelics	23872370	Carbetocin partially substituted for <b>MDMA</b>, while atosiban interfered with <b>MDMA</b> discrimination, suggesting that <strong>oxytocin receptor</strong> activation contributes to <b>MDMA</b> related interoceptive cues.
+OXTR	drug	amphetamine	23680573	Chronic <b>methamphetamine</b> treatment induces <strong>oxytocin receptor</strong> up regulation in the amygdala and hypothalamus via an adenosine A2A receptor independent mechanism.
+OXTR	drug	amphetamine	23680573	We tested this hypothesis by examining the effect of chronic <b>methamphetamine</b> administration on <strong>oxytocin receptor</strong> density in mice brains with the use of quantitative receptor autoradiographic binding.
+OXTR	drug	amphetamine	23680573	Chronic <b>methamphetamine</b> administration induced a region specific upregulation of <strong>oxytocin receptor</strong> density in the amygdala and hypothalamus, but not in the nucleus accumbens and caudate putamen.
+OXTR	drug	amphetamine	23680573	To test this hypothesis, autoradiographic <strong>oxytocin receptor</strong> binding was carried out in brain sections of male CD1 mice lacking A2A receptors which were chronically treated with <b>methamphetamine</b> (1mg/kg/day, i.p.
+OXTR	drug	amphetamine	23680573	Similar to wild type animals, chronic <b>methamphetamine</b> administration induced a region specific upregulation of <strong>oxytocin receptor</strong> binding in the amygdala and hypothalamus of A2A receptor knockout mice and no genotype effect was observed.
+OXTR	addiction	reward	23238104	Results showed that male Sprague Dawley rats i) formed a preference for the context paired with dopamine (100 nmol/side) administration into the STh, which was prevented by co administration of ii) the mixed dopamine receptor antagonist fluphenazine (10 nmol/side) or iii) oxytocin (0.6 pmol/side), [corrected] with the oxytocin effect on dopamine <b>CPP</b> reversed by the co administration of the <strong>oxytocin receptor</strong> antagonist (3 nmol/side).
+OXTR	drug	alcohol	22008269	<b>Alcohol</b> and aggressive behavior in men  moderating effects of oxytocin receptor gene (<strong>OXTR</strong>) polymorphisms.
+OXTR	drug	alcohol	22008269	<b>Alcohol</b> and aggressive behavior in men  moderating effects of <strong>oxytocin receptor</strong> gene (<strong>OXTR</strong>) polymorphisms.
+OXTR	drug	alcohol	22008269	We explored if the disposition to react with aggression while <b>alcohol</b> intoxicated was moderated by polymorphic variants of the oxytocin receptor gene (<strong>OXTR</strong>).
+OXTR	drug	alcohol	22008269	We explored if the disposition to react with aggression while <b>alcohol</b> intoxicated was moderated by polymorphic variants of the <strong>oxytocin receptor</strong> gene (<strong>OXTR</strong>).
+OXTR	drug	alcohol	22008269	Twelve <strong>OXTR</strong> polymorphisms were genotyped in 116 Finnish men [aged 18 30, M = 22.7, standard deviation (SD) = 2.4] who were randomly assigned to an <b>alcohol</b> condition in which they received an <b>alcohol</b> dose of 0.7 g pure <b>ethanol</b>/kg body weight or a placebo condition.
+OXTR	drug	alcohol	22008269	The interactive effects between <b>alcohol</b> and two of the <strong>OXTR</strong> polymorphisms (rs4564970 and rs1488467) on aggressive behavior were nominally significant and remained significant for the rs4564970 when controlled for multiple tests.
+OXTR	drug	psychedelics	20730418	However, <b>MDMA</b> pre exposure increased hypothalamic oxytocin mRNA while GHB pre exposure upregulated <strong>oxytocin receptor</strong> mRNA.
+OXTR	drug	cannabinoid	15380376	Rats were habituated to the test environment and injection procedure, and then received intracerebroventricular (ICV) injections of various combinations of the <strong>oxytocin receptor</strong> antagonist tocinoic acid, the cannabionid receptor agonist delta(9) <b>tetrahydrocannabinol</b> (<b>THC</b>), oxytocin, or the <b>cannabinoid</b> receptor antagonist SR 141716.
+LPA	drug	alcohol	32159228	None of the RCTs comparing non manualized AA/TSF to other clinical interventions assessed <strong>LPA</strong>, <b>alcohol</b> related consequences, or <b>alcohol</b> addiction severity.
+LPA	addiction	addiction	32159228	None of the RCTs comparing non manualized AA/TSF to other clinical interventions assessed <strong>LPA</strong>, alcohol related consequences, or alcohol <b>addiction</b> severity.
+LPA	drug	nicotine	32109881	Participants with <strong>LPA</strong> had significantly higher chance of cigarette <b>smoking</b>, diabetes, overweight/obesity, hypertension, and opium addiction.
+LPA	addiction	addiction	32109881	Participants with <strong>LPA</strong> had significantly higher chance of cigarette smoking, diabetes, overweight/obesity, hypertension, and opium <b>addiction</b>.
+LPA	addiction	dependence	31961165	<strong>LPA</strong> identified 6 classes of college student drinkers: light drinkers with minor problems, moderate drinkers with mild problems, moderate drinkers with severe problems, heavy drinkers with mild problems, heavy drinkers with severe problems, and heavy drinkers with physical <b>dependence</b>.
+LPA	drug	alcohol	30689405	<strong>LPA</strong> characterized the variability across substance use (<b>alcohol</b> consumption, cigarette smoking, marijuana use), criminal behavior, peer impairment, educational attainment, maternal relationship, financial dependence, and sexual activity among young adults with childhood ADHD.
+LPA	drug	cannabinoid	30689405	<strong>LPA</strong> characterized the variability across substance use (alcohol consumption, cigarette smoking, <b>marijuana</b> use), criminal behavior, peer impairment, educational attainment, maternal relationship, financial dependence, and sexual activity among young adults with childhood ADHD.
+LPA	drug	nicotine	30689405	<strong>LPA</strong> characterized the variability across substance use (alcohol consumption, cigarette <b>smoking</b>, marijuana use), criminal behavior, peer impairment, educational attainment, maternal relationship, financial dependence, and sexual activity among young adults with childhood ADHD.
+LPA	addiction	dependence	30689405	<strong>LPA</strong> characterized the variability across substance use (alcohol consumption, cigarette smoking, marijuana use), criminal behavior, peer impairment, educational attainment, maternal relationship, financial <b>dependence</b>, and sexual activity among young adults with childhood ADHD.
+LPA	drug	cocaine	29480526	To investigate whether increasing AHN prompted the forgetting of previous contextual <b>cocaine</b> associations, mice trained in a <b>cocaine</b> induced conditioned place preference (CPP) paradigm were administered chronic intracerebroventricular infusions of lysophosphatidic acid (<strong>LPA</strong>, an endogenous lysophospholipid with pro neurogenic actions), ki16425 (an LPA1/3 receptor antagonist) or a vehicle solution, and they were tested 23 days later for CPP retention and extinction.
+LPA	addiction	reward	29480526	To investigate whether increasing AHN prompted the forgetting of previous contextual cocaine associations, mice trained in a cocaine induced conditioned place preference (<b>CPP</b>) paradigm were administered chronic intracerebroventricular infusions of lysophosphatidic acid (<strong>LPA</strong>, an endogenous lysophospholipid with pro neurogenic actions), ki16425 (an LPA1/3 receptor antagonist) or a vehicle solution, and they were tested 23 days later for <b>CPP</b> retention and extinction.
+LPA	addiction	reward	29480526	The results of immunohistochemical experiments showed that the <strong>LPA</strong> treated mice exhibited reduced long term <b>CPP</b> retention and an approximately twofold increase in the number of adult born hippocampal cells that differentiated into mature neurons.
+LPA	drug	cocaine	29480526	These results suggest that the <strong>LPA</strong>/LPA1 pathway acts as a potent in vivo modulator of AHN and highlight the potential usefulness of pro AHN strategies to treat aberrant cognition in those addicted to <b>cocaine</b>.
+LPA	drug	cocaine	29478874	Secondary outcomes at the 1 month follow up were percentage days abstinent (PDA) from <b>cocaine</b>, and longest period (days) of continuous abstinence (<strong>LPA</strong>) in the prior 28days.
+LPA	drug	alcohol	29378212	In these animals, ki16425 modulated the expression of glutamate related genes in brain limbic regions after <b>ethanol</b> exposure; and peripheral <strong>LPA</strong> signaling was dysregulated by either ki16425 or <b>ethanol</b>.
+LPA	drug	alcohol	28755778	Given the demonstrated benefits of exercise for decreasing depression, negative affect, and urges to drink, helping women engage in a lifestyle physical activity (<strong>LPA</strong>) intervention in early recovery may provide them a tool they can utilize "in the moment" in order to cope with negative emotional states and <b>alcohol</b> craving when relapse risk is highest.
+LPA	addiction	relapse	28755778	Given the demonstrated benefits of exercise for decreasing depression, negative affect, and urges to drink, helping women engage in a lifestyle physical activity (<strong>LPA</strong>) intervention in early recovery may provide them a tool they can utilize "in the moment" in order to cope with negative emotional states and alcohol <b>craving</b> when <b>relapse</b> risk is highest.
+LPA	drug	alcohol	28755778	We piloted a 12 week <strong>LPA</strong>+Fitbit intervention focused on strategically using bouts of PA to cope with affect and <b>alcohol</b> cravings to prevent relapse in 20 depressed women (mean age=39.5years) in <b>alcohol</b> treatment.
+LPA	addiction	relapse	28755778	We piloted a 12 week <strong>LPA</strong>+Fitbit intervention focused on strategically using bouts of PA to cope with affect and alcohol cravings to prevent <b>relapse</b> in 20 depressed women (mean age=39.5years) in alcohol treatment.
+LPA	drug	alcohol	28755778	If the <strong>LPA</strong>+Fitbit intervention proves to be helpful during early recovery, this simple, low cost and easily transported intervention can provide a much needed alternate coping strategy to help reduce relapse risk among women in <b>alcohol</b> treatment.
+LPA	addiction	relapse	28755778	If the <strong>LPA</strong>+Fitbit intervention proves to be helpful during early recovery, this simple, low cost and easily transported intervention can provide a much needed alternate coping strategy to help reduce <b>relapse</b> risk among women in alcohol treatment.
+LPA	drug	alcohol	28343281	We applied latent profile analysis (<strong>LPA</strong>) to p values resulting from genome wide association studies across three phenotypes: symptom counts of <b>alcohol</b> dependence (AD), antisocial personality disorder (ASP), and major depression (MD), using the European American case control genome wide association study subsample of the collaborative study on the genetics of <b>alcoholism</b> (N = 1399).
+LPA	addiction	dependence	28343281	We applied latent profile analysis (<strong>LPA</strong>) to p values resulting from genome wide association studies across three phenotypes: symptom counts of alcohol <b>dependence</b> (AD), antisocial personality disorder (ASP), and major depression (MD), using the European American case control genome wide association study subsample of the collaborative study on the genetics of alcoholism (N = 1399).
+LPA	drug	alcohol	26700247	Results suggest a relevant role for the <strong>LPA</strong>/LPA1 signaling system in <b>alcoholism</b>.
+LPA	drug	cannabinoid	23574441	The main lipid transmitters reviewed here include a) acylethanolamides and acylglycerols acting on <b>cannabinoid</b> receptors, such as anandamide and 2 arachidonoylglycerol; b) acylethanolamides that do not act on <b>cannabinoid</b> receptors, such as <b>oleoylethanolamide</b>; c) eicosanoids derived from arachidonic acid, including prostaglandins; and d) lysophosphatidic acid, focusing on the role of its <strong>LPA</strong> 1 receptor.
+LPA	drug	cannabinoid	22820167	Interestingly, 2 arachidonyl glycerol (2 AG), an endogenous ligand for <b>cannabinoid</b> receptors, can be metabolized to 2 arachidonoyl <strong>LPA</strong> through the action of a monoacylglycerol kinase; the reverse reaction has also been demonstrated.
+LPA	drug	amphetamine	22691016	The present pilot study hypothesized that degree of exposure to prenatal testosterone interacts with a history of lifetime physical abuse (<strong>LPA</strong>) to predict the cognitive (anger rumination) and behavioral (intimate partner and interpersonal violence) components of aggression within incarcerated <b>methamphetamine</b> (MA) users.
+LPA	drug	opioid	22337641	nor <b>morphine</b> (0.3 3 mg/kg, s.c.) did, which indicates that <strong>LPA</strong> induced pain consists mostly of neuropathic rather than inflammatory pain.
+LPA	addiction	sensitization	22337641	The <strong>LPA</strong> induced pain model described here mimics aspects of the neuropathic pain state, including the <b>sensitization</b> of VGCC, and may be useful for the early assessment of drug candidates to treat neuropathic pain.
+LPA	drug	opioid	21453194	The aim was to evaluate the frequency in serum lipid disturbances of hepatitis C virus (HCV) seronegative <b>heroin</b> addicts; the capacity of high density lipoprotein (HDL) C and apolipoprotein B (apoB)/apolipoprotein A I (<strong>apoA</strong> I) for predicting hypertriglyceridemia/low HDL C profile; correlation of HDL C with the apoB/<strong>apoA</strong> I and their correlation to plasma apo/lipoproteins.
+LPA	drug	opioid	21453194	ApoB/<strong>apoA</strong> I showed stronger correlation with the observed apo/lipoproteins than the HDL C. The logistic regression model showed that apoB/<strong>apoA</strong> I index (OR 89.1, 95% CI 1.3 5971.2) is more significant predictor in developing hypertriglyceridemia/low HDL profile than HDL C. <b>Heroin</b> addiction is associated with decreased plasma concentrations of HDL C, <strong>apoA</strong> I, apoB, and increased TGL concentrations.
+LPA	addiction	addiction	21453194	ApoB/<strong>apoA</strong> I showed stronger correlation with the observed apo/lipoproteins than the HDL C. The logistic regression model showed that apoB/<strong>apoA</strong> I index (OR 89.1, 95% CI 1.3 5971.2) is more significant predictor in developing hypertriglyceridemia/low HDL profile than HDL C. Heroin <b>addiction</b> is associated with decreased plasma concentrations of HDL C, <strong>apoA</strong> I, apoB, and increased TGL concentrations.
+LPA	drug	opioid	21453194	In <b>heroin</b> addicts, HDL C concentrations are significantly associated with the apoB/<strong>apoA</strong> I index, which correlates to all lipid fractions and is a stronger predictor of metabolic syndrome lipid profile in <b>heroin</b> addicts.
+LPA	drug	alcohol	21301951	<strong>LPA</strong> generated three psychiatric symptom profiles: Low , High  <b>Alcohol</b> , and High  Internalizing Symptoms profiles.
+LPA	drug	alcohol	17429021	We applied latent profile analysis (<strong>LPA</strong>) to determine meaningful subgroups of women based on interrelationships among factors that contextualize women's vulnerability to sexual assault, including prior victimization, <b>alcohol</b> consumption, relationship expectancies of the assailant, and assertive precautionary habits.
+LPA	drug	alcohol	16739925	<b>Ethanol</b> inhibited LCAT and LPL activities, and increased <strong>apoA</strong> containing LP in blood serum.
+LPA	drug	alcohol	12916168	The 14th day after <b>alcohol</b> abolition was characterized by tendency to normalization of these disturbances, but at the 30th day of soberness a recurrence growing the changes of <strong>apoA</strong> containing lipoproteins transformation was observed.
+LPA	drug	alcohol	12916168	In the patients under intoxication period and first 3 days after <b>alcohol</b> abolition a significant increase of quantity of all the <strong>apoA</strong> containing lipoprotein populations took place which was restored completely in remission.
+LPA	addiction	intoxication	12916168	In the patients under <b>intoxication</b> period and first 3 days after alcohol abolition a significant increase of quantity of all the <strong>apoA</strong> containing lipoprotein populations took place which was restored completely in remission.
+LPA	addiction	dependence	12695531	The inhibitory effect of FAP showed a strong hydrocarbon chain length <b>dependence</b> with C12 being optimum in the Xenopus laevis oocytes and in <strong>LPA</strong>(3) expressing RH7777 cells.
+LPA	addiction	sensitization	12486210	It is concluded that troglitazone doses known to achieve insulin <b>sensitization</b> did not enhance rat <strong>apoA</strong> I promoter activity sufficiently to result in an increased <strong>apoA</strong> I mRNA or protein expression in the intact rat.
+LPA	drug	alcohol	11981126	ApoE genotypes and concentrations of serum cholesterol, triglyceride, and Lps containing <strong>apoA</strong> I, A II, B, E, and C III were determined in 84 male <b>alcohol</b> abusers before and after 3 weeks of abstinence.
+LPA	addiction	withdrawal	11981126	After <b>withdrawal</b>, concentrations of serum apoA I, <strong>LpA</strong> I, <strong>LpA</strong> I/A II, apoC III, LpC III non B, apoE, and LpE non B significantly decreased, whereas those of triglycerides and apoB increased; levels of cholesterol, LpC III:B, and LpB:E were not affected.
+LPA	addiction	withdrawal	11981126	After <b>withdrawal</b>, concentrations of serum <strong>apoA</strong> I, <strong>LpA</strong> I, <strong>LpA</strong> I/A II, apoC III, LpC III non B, apoE, and LpE non B significantly decreased, whereas those of triglycerides and apoB increased; levels of cholesterol, LpC III:B, and LpB:E were not affected.
+LPA	drug	alcohol	8855152	Serum concentrations of apo A I, <strong>LpA</strong> I, <strong>LpA</strong> I:A II, apo C III, and LpC III significantly (P </= 0.01) increased with <b>alcohol</b> intake (mean +/  SE in low drinkers vs in <b>alcoholics</b>)  1.45 +/  0.03 vs 1.78 +/  0.05 g/L; 0.45 +/  0.02 vs 0.56 +/  0.02 g/L; 0.99 +/  0.02 vs 1.22 +/  0.04 g/L; 27.6 +/  1.5 vs 39.7 +/  1.7 mg/L; and 8.4 +/  0.9 vs 24.7 +/  1.7 mg/L, respectively whereas apo B and LpC III:B concentrations tended to decrease  1.20 +/  0.04 vs 1.06 +/  0.04 g/L and 19.3 +/  1.2 vs 14.9 +/  1.0 mg/L, respectively.
+LPA	addiction	withdrawal	8855152	After <b>withdrawal</b>, the concentrations of serum apo A I, apo C III, <strong>LpA</strong> I, <strong>LpA</strong> I:A II, and LpC III decreased significantly (P </= 0.01), reaching values comparable with those in low drinkers; concentrations of triglycerides, apo B, apo E, and Lp(a) rose; and cholesterol concentration was unaffected.
+LPA	drug	alcohol	8855152	In multiple regression analysis, after adjustment for serum concentrations of albumin, aspartate aminotransferase, and gamma glutamyltransferase and for the Quetelet index, <b>alcohol</b> consumption remained positively correlated to apo A I, <strong>LpA</strong> I:A II, apo C III, and LpC III concentrations.
+LPA	drug	alcohol	3517775	STA, <strong>apoA</strong> lipoprotein, HDL cholesterol, total cholesterol and triglycerides were tested in 44 men dealt in 4 groups (subjects with normal or elevated STA, <b>alcoholic</b> or withdrawn).
+ADA	drug	alcohol	31989819	Native <b>ethanol</b> dehydrogenase ADH2 and acetaldehyde dehydrogenase <strong>ADA</strong> from Dickeya zeae were further overexpressed, which enhanced the capability to utilize <b>ethanol</b> for squalene synthesis and endowed the engineered strain with greater adaptability to high <b>ethanol</b> concentrations.
+ADA	drug	alcohol	30991909	The protections afforded by the <strong>ADA</strong> for individuals with substance use disorders are restricted by what appears to be the statute's moralizing on drug and <b>alcohol</b> use and those who use these substances.
+ADA	drug	alcohol	30697154	To investigate the involvement of NAc RNA editing in <b>alcohol</b> addiction, we generated NAc specific knockout mice of the double stranded RNA specific <strong>adenosine deaminase</strong> ADAR2 using AAV GFP/Cre and conducted a battery of behavioral tests including anxiety  and depression like behaviors.
+ADA	addiction	addiction	30697154	To investigate the involvement of NAc RNA editing in alcohol <b>addiction</b>, we generated NAc specific knockout mice of the double stranded RNA specific <strong>adenosine deaminase</strong> ADAR2 using AAV GFP/Cre and conducted a battery of behavioral tests including anxiety  and depression like behaviors.
+ADA	drug	nicotine	29176829	Using the Truth <b>Tobacco</b> Industry Documents Library and Congressional records, we examined the <b>tobacco</b> industry's involvement with the 1990 Americans with Disabilities Act (<strong>ADA</strong>).
+ADA	drug	nicotine	29176829	During legislative drafting of the <strong>ADA</strong> (1989 1990), the <b>Tobacco</b> Institute, the <b>tobacco</b> industry's lobbying and public relations arm at the time, worked with industry lawyers and civil rights groups to include <b>smoking</b> in the <strong>ADA</strong>'s definition of "disability."
+ADA	drug	nicotine	29176829	Language that would have explicitly excluded <b>smoking</b> from <strong>ADA</strong> coverage was weakened or omitted.
+ADA	drug	nicotine	29176829	<b>Tobacco</b> Institute lawyers did not think the argument that <b>smokers</b> are "disabled" would convince the courts, so in the two years after the <strong>ADA</strong> was signed into law, the <b>Tobacco</b> Institute paid a lawyer to conduct media tours, seminars, and write articles to convince employers that hiring only non <b>smokers</b> would violate the <strong>ADA</strong>.
+ADA	drug	nicotine	29176829	Employers and policy makers need to be aware that <b>tobacco</b> use is not protected by the <strong>ADA</strong> and should not be misled by <b>tobacco</b> industry efforts to insinuate otherwise.
+ADA	addiction	withdrawal	29142516	A total of 54 CD patients, with follow up of more than 6 months after the <b>withdrawal</b> of <strong>ADA</strong>, were enrolled.
+ADA	addiction	relapse	29142516	After discontinuing <strong>ADA</strong>, 59.3% patients suffered a clinical <b>relapse</b>.
+ADA	addiction	relapse	29142516	Fifty nine percent of patients experienced a <b>relapse</b> after discontinuing the limited period of <strong>ADA</strong> treatment, and most of them occurred within 1 year following cessation.
+ADA	addiction	relapse	29142516	Though 60.4% of the <b>relapse</b> patients responded to <strong>ADA</strong> again.
+ADA	drug	alcohol	29122710	<strong>Adenosine deaminase</strong> activity and gene expression patterns are altered after chronic <b>ethanol</b> exposure in zebrafish brain.
+ADA	drug	alcohol	29122710	However, we verified a decrease of <strong>ADA</strong> activity in membrane fraction after 28days (44%) of <b>ethanol</b> exposure.
+ADA	drug	alcohol	29122710	Altogether, the purine catabolism promoted by <strong>ADA</strong> may be an important target of the chronic toxicity induced for <b>ethanol</b>.
+ADA	drug	alcohol	28449374	Genetic Variability in <strong>Adenosine Deaminase</strong> Like Contributes to Variation in <b>Alcohol</b> Preference in Mice.
+ADA	drug	alcohol	28449374	Moreover, we found that the <strong>adenosine deaminase</strong> inhibitor EHNA reduced the difference in <b>alcohol</b> preference between CSS 2 and C57BL/6J mice.
+ADA	drug	alcohol	27838211	The activity of XO and <strong>ADA</strong> increased, and their mRNA expression was enhanced in the <b>alcohol</b> dependence group, but there was no significant difference in the activity of RPPPK and GPRPPAT in the liver, small intestine, and muscle; furthermore, no significant difference in the activity of HGPRT and APRT was observed in the brain.
+ADA	addiction	dependence	27838211	The activity of XO and <strong>ADA</strong> increased, and their mRNA expression was enhanced in the alcohol <b>dependence</b> group, but there was no significant difference in the activity of RPPPK and GPRPPAT in the liver, small intestine, and muscle; furthermore, no significant difference in the activity of HGPRT and APRT was observed in the brain.
+ADA	drug	alcohol	27838211	These results indicate that chronic <b>alcohol</b> administration might enhance the catabolism of purine nucleotides in tissues by inducing gene expression of <strong>ADA</strong> and XO, leading to elevation of plasma uric acid levels.
+ADA	drug	alcohol	23797318	Quercetin treatment prevented the cadmium induced increase in NTPDase, 5 nucleotidase, and <strong>ADA</strong> activities in Cd/<b>ethanol</b> group when compared to saline/<b>ethanol</b> group.
+ADA	drug	cocaine	22749927	Following one week withdrawal, the effects of intra NAc microinjections of the adenosine kinase inhibitor (ABT 702), the <strong>adenosine deaminase</strong> inhibitor (deoxycoformycin; DCF), the specific A(1) receptor agonist (CPA) and the specific A(2A) receptor agonist (CGS 21680) were tested on the behavioral expression of <b>cocaine</b> sensitization.
+ADA	addiction	sensitization	22749927	Following one week withdrawal, the effects of intra NAc microinjections of the adenosine kinase inhibitor (ABT 702), the <strong>adenosine deaminase</strong> inhibitor (deoxycoformycin; DCF), the specific A(1) receptor agonist (CPA) and the specific A(2A) receptor agonist (CGS 21680) were tested on the behavioral expression of cocaine <b>sensitization</b>.
+ADA	addiction	withdrawal	22749927	Following one week <b>withdrawal</b>, the effects of intra NAc microinjections of the adenosine kinase inhibitor (ABT 702), the <strong>adenosine deaminase</strong> inhibitor (deoxycoformycin; DCF), the specific A(1) receptor agonist (CPA) and the specific A(2A) receptor agonist (CGS 21680) were tested on the behavioral expression of cocaine sensitization.
+ADA	drug	opioid	22019714	Compared with those in the saline group, the content of AMP and GTP of <b>heroin</b> group decreased significantly; the UA concentration in plasma, <strong>ADA</strong> and XO activities and the mRNA level of <strong>ADA</strong> and XO in brain tissues in <b>heroin</b> group increased significantly; the mRNA level of AK, APRT and HGPRT in brain tissues in <b>heroin</b> group decreased significantly (P<0.01).
+ADA	addiction	withdrawal	21951369	This review looks into the application of acute drug administration (<strong>ADA</strong>) against febrile and prolonged nonfebrile seizures in children, seizure clustering (habitual or at drug <b>withdrawal</b>), catamenial epilepsy, response to seizure "warnings", and prophylaxis of seizures at perceived increased risk (reflex epilepsies, long distance travel, lifestyle, and social occasions).
+ADA	drug	benzodiazepine	21951369	The drugs most commonly used for <strong>ADA</strong> are the benzodiazepines <b>diazepam</b> (oral or rectal), <b>clobazam</b> and buccal or nasal <b>midazolam</b>, and <b>lorazepam</b>.
+ADA	drug	nicotine	21456032	In all, 41% of CD patients required <strong>ADA</strong> DE, with shorter time to DE in <b>smokers</b>, men, and patients with isolated colonic disease.
+ADA	drug	opioid	22876215	The paper also draws parallels between <b>methadone</b> and other medical conditions and analyzes the problem in the context of disabilities encompassed in the <strong>ADA</strong>.
+ADA	drug	alcohol	17763121	Specific questions were how personality traits changed after a first episode of <b>alcohol</b> dependence/abuse (<strong>ADA</strong>), anxiety or depression disorders and after remission of an episode.
+ADA	addiction	dependence	17763121	Specific questions were how personality traits changed after a first episode of alcohol <b>dependence</b>/abuse (<strong>ADA</strong>), anxiety or depression disorders and after remission of an episode.
+ADA	drug	opioid	17640470	(i) the concentration of plasma uric acid in the <b>morphine</b> administered group was significantly higher (P<0.05) than the control group; (ii) during <b>morphine</b> administration and withdrawal periods, the <strong>ADA</strong> and XO concentrations in the plasma increased significantly (P<0.05); (iii) the amount of <strong>ADA</strong> and XO in the parietal lobe, liver, small intestine, and skeletal muscles of the <b>morphine</b> administered groups increased, while the level of <strong>ADA</strong> and XO in those tissues of the withdrawal groups decreased; (iv) the transcripts of the <strong>ADA</strong> and XO genes in the parietal lobe, liver, small intestine, and skeletal muscles were higher in the <b>morphine</b> administered group.
+ADA	addiction	withdrawal	17640470	(i) the concentration of plasma uric acid in the morphine administered group was significantly higher (P<0.05) than the control group; (ii) during morphine administration and <b>withdrawal</b> periods, the <strong>ADA</strong> and XO concentrations in the plasma increased significantly (P<0.05); (iii) the amount of <strong>ADA</strong> and XO in the parietal lobe, liver, small intestine, and skeletal muscles of the morphine administered groups increased, while the level of <strong>ADA</strong> and XO in those tissues of the <b>withdrawal</b> groups decreased; (iv) the transcripts of the <strong>ADA</strong> and XO genes in the parietal lobe, liver, small intestine, and skeletal muscles were higher in the morphine administered group.
+ADA	drug	opioid	17640470	The expression of the <strong>ADA</strong> and XO genes in those tissues returned to the control level during <b>morphine</b> withdrawal, with the exception of the skeletal muscles; and (v) the upregulation of the expression of the <strong>ADA</strong> and XO genes induced by <b>morphine</b> treatment could be reversed by <b>naloxone</b>.
+ADA	addiction	withdrawal	17640470	The expression of the <strong>ADA</strong> and XO genes in those tissues returned to the control level during morphine <b>withdrawal</b>, with the exception of the skeletal muscles; and (v) the upregulation of the expression of the <strong>ADA</strong> and XO genes induced by morphine treatment could be reversed by naloxone.
+ADA	drug	alcohol	17468300	Furthermore, subthreshold concentrations of nicotine with <b>ethanol</b> increased gene expression in cocultures, and this increase was blocked by nACh, D(2) or adenosine A(2A) receptor antagonists, Gbetagamma or protein kinase A (PKA) inhibitors, and <strong>adenosine deaminase</strong>.
+ADA	drug	nicotine	17468300	Furthermore, subthreshold concentrations of <b>nicotine</b> with ethanol increased gene expression in cocultures, and this increase was blocked by nACh, D(2) or adenosine A(2A) receptor antagonists, Gbetagamma or protein kinase A (PKA) inhibitors, and <strong>adenosine deaminase</strong>.
+ADA	drug	opioid	16223513	When two <b>heroin</b> administration groups were compared with the control group, the concentrations of plasma uric acid and <strong>ADA</strong> in plasma, brain, liver, and small intestine increased, whereas the plasma urea nitrogen concentrations in two <b>heroin</b> administration groups and the plasma creatinine concentration in the 3 day <b>heroin</b> administration group did not increase.
+ADA	drug	opioid	16223513	When two withdrawal groups were compared with two <b>heroin</b> administration groups, the concentrations of plasma uric acid and <strong>ADA</strong> in liver and small intestine decreased, but there was no significant reduction in <strong>ADA</strong> concentrations of the brain, while the plasma <strong>ADA</strong> concentrations in the two withdrawal groups were significantly higher than those of two <b>heroin</b> administration groups.
+ADA	addiction	withdrawal	16223513	When two <b>withdrawal</b> groups were compared with two heroin administration groups, the concentrations of plasma uric acid and <strong>ADA</strong> in liver and small intestine decreased, but there was no significant reduction in <strong>ADA</strong> concentrations of the brain, while the plasma <strong>ADA</strong> concentrations in the two <b>withdrawal</b> groups were significantly higher than those of two heroin administration groups.
+ADA	addiction	withdrawal	16223513	When the two <b>withdrawal</b> groups were compared with the control group, there was no significant difference in the concentrations of plasma uric acid and <strong>ADA</strong> in liver and small intestine, while the concentrations of <strong>ADA</strong> in plasma and brain were still higher than those of the control group.
+ADA	drug	opioid	16223513	The results imply that <b>heroin</b> administration may enhance the catabolism of purine nucleotides in the brain and other tissues by increased concentration of <strong>ADA</strong> and the effect may last for a long time in the brain.
+ADA	drug	alcohol	15462231	This study investigates relationships between personality traits, <b>alcohol</b> dependence and abuse (<strong>ADA</strong>), and psychiatric comorbidity in a general population sample of women.
+ADA	addiction	dependence	15462231	This study investigates relationships between personality traits, alcohol <b>dependence</b> and abuse (<strong>ADA</strong>), and psychiatric comorbidity in a general population sample of women.
+ADA	drug	opioid	14560041	MNTX also inhibited the R5 strain (<strong>ADA</strong>) envelope pseudotyped HIV replication induced by <b>morphine</b>.
+ADA	drug	alcohol	12529074	The <b>alcohol</b> response was quantified as an initial response (ira = B1 B0) and an adaptive response (<strong>ada</strong> = B2 B1).
+ADA	drug	alcohol	12227975	For analyses in this study the following variables were selected from the interview protocol: childhood and adolescence, education, employment, social class, self rated physical health and <b>alcohol</b> dependence or abuse (<strong>ADA</strong>), with diagnoses assessed according to DSM III R. Information on disability pension and sickness absence was obtained from the local Social Insurance Office.
+ADA	addiction	dependence	12227975	For analyses in this study the following variables were selected from the interview protocol: childhood and adolescence, education, employment, social class, self rated physical health and alcohol <b>dependence</b> or abuse (<strong>ADA</strong>), with diagnoses assessed according to DSM III R. Information on disability pension and sickness absence was obtained from the local Social Insurance Office.
+ADA	drug	alcohol	12111341	Such thoughts were acknowledged by 24.2% of the women with a depressive disorder, 20% of the women with an anxiety disorder and 22.7% of those with <b>alcohol</b> dependence/abuse (<strong>ADA</strong>) during the past year.
+ADA	addiction	dependence	12111341	Such thoughts were acknowledged by 24.2% of the women with a depressive disorder, 20% of the women with an anxiety disorder and 22.7% of those with alcohol <b>dependence</b>/abuse (<strong>ADA</strong>) during the past year.
+ADA	drug	alcohol	11831580	Are the federal <b>Alcohol</b> and Drug Abuse (<strong>ADA</strong>) block grant funds substituting for or supplementing state and local government spending on substance abuse?
+ADA	drug	alcohol	11696668	Crude and adjusted odds ratios (ORs) were calculated for <b>alcohol</b> dependence/abuse (<strong>ADA</strong>) and physical or sexual assault by a current partner or someone other than a current partner.
+ADA	addiction	dependence	11696668	Crude and adjusted odds ratios (ORs) were calculated for alcohol <b>dependence</b>/abuse (<strong>ADA</strong>) and physical or sexual assault by a current partner or someone other than a current partner.
+ADA	drug	alcohol	11521552	Disability insurance  <strong>ADA</strong>  benefits for mental disability, <b>alcoholism</b> and drug abuse.
+ADA	drug	alcohol	11301978	The aim was to find out more about risk factors for <b>alcohol</b> dependence and abuse (<strong>ADA</strong>) among women in the general population, as well as social conditions and life style among these women.
+ADA	addiction	dependence	11301978	The aim was to find out more about risk factors for alcohol <b>dependence</b> and abuse (<strong>ADA</strong>) among women in the general population, as well as social conditions and life style among these women.
+ADA	drug	alcohol	11301977	Prevalence of <b>alcohol</b> dependence and abuse (<strong>ADA</strong>) was determined in a cohort of women selected by stratified random sampling from the general population in Gothenburg.
+ADA	addiction	dependence	11301977	Prevalence of alcohol <b>dependence</b> and abuse (<strong>ADA</strong>) was determined in a cohort of women selected by stratified random sampling from the general population in Gothenburg.
+ADA	drug	alcohol	11301977	In a follow up five years after base line, the prevalence of <strong>ADA</strong> was unchanged, while indicators of high <b>alcohol</b> consumption and high episodic drinking showed reduced levels of problem drinking.
+ADA	drug	alcohol	11022027	The aims of this study were to: (1) document women's <b>alcohol</b> use over a 5 year period; (2) compare different measures of <b>alcohol</b> consumption such as high <b>alcohol</b> consumption (HAC) and high episodic drinking (HED); (3) to follow the incidence and course of <b>alcohol</b> dependence and abuse (<strong>ADA</strong>).
+ADA	addiction	dependence	11022027	The aims of this study were to: (1) document women's alcohol use over a 5 year period; (2) compare different measures of alcohol consumption such as high alcohol consumption (HAC) and high episodic drinking (HED); (3) to follow the incidence and course of alcohol <b>dependence</b> and abuse (<strong>ADA</strong>).
+ADA	drug	alcohol	10892609	Our aims were to study associations between depressive disorders and <b>alcohol</b> dependence/abuse (<strong>ADA</strong>) in a female population based sample, and to identify risk indicators common to both depressive disorders and <strong>ADA</strong>.
+ADA	addiction	dependence	10892609	Our aims were to study associations between depressive disorders and alcohol <b>dependence</b>/abuse (<strong>ADA</strong>) in a female population based sample, and to identify risk indicators common to both depressive disorders and <strong>ADA</strong>.
+ADA	drug	alcohol	10892609	<b>Alcohol</b> intoxication before the age of 15 and psychological and/or psychiatric problems before the age of 18 years increased the risk for <strong>ADA</strong> and depressive disorders in our study.
+ADA	addiction	intoxication	10892609	Alcohol <b>intoxication</b> before the age of 15 and psychological and/or psychiatric problems before the age of 18 years increased the risk for <strong>ADA</strong> and depressive disorders in our study.
+ADA	drug	alcohol	9926542	(1) To study the prevalence of childhood sexual abuse before the age of 18 years (CSA) and life time sexual abuse (LSA) in a Swedish female, general population, (2) to analyse associations between CSA and life time <b>alcohol</b> dependence or abuse (<strong>ADA</strong>), and (3) to identify possible confounding factors.
+ADA	addiction	dependence	9926542	(1) To study the prevalence of childhood sexual abuse before the age of 18 years (CSA) and life time sexual abuse (LSA) in a Swedish female, general population, (2) to analyse associations between CSA and life time alcohol <b>dependence</b> or abuse (<strong>ADA</strong>), and (3) to identify possible confounding factors.
+ADA	drug	alcohol	9857794	The study objective was to assess sick leave among women investigated in a general population survey of <b>alcohol</b> dependence/abuse (<strong>ADA</strong>).
+ADA	addiction	dependence	9857794	The study objective was to assess sick leave among women investigated in a general population survey of alcohol <b>dependence</b>/abuse (<strong>ADA</strong>).
+ADA	drug	alcohol	9766171	As outcome measures we used <b>alcohol</b> dependence and abuse (<strong>ADA</strong>), diagnosed in a clinical interview according to the Diagnostic and Statistical Manual of Mental Disorders, Third Edition Revised (DSM III R).
+ADA	addiction	dependence	9766171	As outcome measures we used alcohol <b>dependence</b> and abuse (<strong>ADA</strong>), diagnosed in a clinical interview according to the Diagnostic and Statistical Manual of Mental Disorders, Third Edition Revised (DSM III R).
+ADA	drug	alcohol	9199727	The aim was to assess risk factors during childhood and youth for <b>alcohol</b> dependence/abuse (<strong>ADA</strong>) in a population based study of Swedish women.
+ADA	addiction	dependence	9199727	The aim was to assess risk factors during childhood and youth for alcohol <b>dependence</b>/abuse (<strong>ADA</strong>) in a population based study of Swedish women.
+ADA	drug	alcohol	9199727	Experiences of sexual abuse before the age of 13 years, a history of psychological or psychiatric problems, early deviant behaviour and an episode of <b>alcohol</b> intoxication before the age of 15 years were significantly associated with <strong>ADA</strong> in a logistic model.
+ADA	addiction	intoxication	9199727	Experiences of sexual abuse before the age of 13 years, a history of psychological or psychiatric problems, early deviant behaviour and an episode of alcohol <b>intoxication</b> before the age of 15 years were significantly associated with <strong>ADA</strong> in a logistic model.
+ADA	drug	alcohol	8686488	In a multi purpose two phase general population survey of female <b>alcoholism</b>/<b>alcohol</b> problems, unknown <b>alcohol</b> dependence and abuse (<strong>ADA</strong>) was estimated with interviews and by search of medical and National Insurance Office records.
+ADA	addiction	dependence	8686488	In a multi purpose two phase general population survey of female alcoholism/alcohol problems, unknown alcohol <b>dependence</b> and abuse (<strong>ADA</strong>) was estimated with interviews and by search of medical and National Insurance Office records.
+ADA	drug	alcohol	7541691	Inclusion of adenosine deaminase (<strong>ADA</strong>; 1 unit ml 1) during the incubation period to measure cyclic AMP accumulation completely abolished the increase in basal accumulation following chronic <b>ethanol</b>, but did not affect the increase in iloprost stimulation.
+ADA	drug	alcohol	7541691	Inclusion of <strong>adenosine deaminase</strong> (<strong>ADA</strong>; 1 unit ml 1) during the incubation period to measure cyclic AMP accumulation completely abolished the increase in basal accumulation following chronic <b>ethanol</b>, but did not affect the increase in iloprost stimulation.
+ADA	drug	alcohol	7541691	On the other hand <strong>ADA</strong> partially reversed the increase in forskolin stimulation following chronic <b>ethanol</b>, but even in the presence of high concentrations of <strong>ADA</strong> (5 units ml 1) the forskolin stimulation remained elevated above control.
+ADA	drug	alcohol	7998934	When cells were cultured with 2 units/ml <strong>adenosine deaminase</strong>, to degrade extracellular adenosine, <b>ethanol</b> induced increases in cyclic AMP production were completely prevented.
+ADA	drug	alcohol	7998934	Treatment with <strong>adenosine deaminase</strong> or CPDX also prevented the decrease in quantity of the alpha subunit protein of G(i) observed in hepatocytes after chronic treatment with <b>ethanol</b>.
+ADA	drug	alcohol	3827998	In addition, neither the <strong>adenosine deaminase</strong> inhibitor erythro 9 (2 hydroxy 3 nonyl) adenine nor the adenosine uptake inhibitor dipyridamole were able to enhance the level of <b>ethanol</b> appropriate responding seen after a low dose of <b>ethanol</b>.
+ADA	addiction	sensitization	3888866	While even a single application of <strong>ADA</strong> 202 718 at the time of <b>sensitization</b> resulted in a stimulation of the hypersensitivity reaction, administration of the compound at the time of challenge was without effect.
+ADA	drug	alcohol	2992340	We determined the activities of adenosine deaminase (<strong>ADA</strong>) and ecto 5' nucleotidase (ecto 5'N) in lymphocytes from 54 subjects: 15 healthy controls, 28 non cirrhotic <b>alcoholics</b>, 8 <b>alcoholic</b> cirrhotics and 3 non <b>alcoholic</b> cirrhotics.
+ADA	drug	alcohol	2992340	We determined the activities of <strong>adenosine deaminase</strong> (<strong>ADA</strong>) and ecto 5' nucleotidase (ecto 5'N) in lymphocytes from 54 subjects: 15 healthy controls, 28 non cirrhotic <b>alcoholics</b>, 8 <b>alcoholic</b> cirrhotics and 3 non <b>alcoholic</b> cirrhotics.
+ADA	drug	alcohol	2992340	Whereas <strong>ADA</strong> activity was the same for all 54 subjects, ecto 5'N activity was in general lower in <b>alcoholic</b> subjects after cessation of <b>alcohol</b> intake.
+TUBB3	drug	alcohol	22459873	Transgenic over expression of nicotinic receptor alpha 5, alpha 3, and <strong>beta 4</strong> subunit genes reduces <b>ethanol</b> intake in mice.
+TUBB3	drug	alcohol	22459873	We tested mice with transgenic over expression of the alpha 5, alpha 3, <strong>beta 4</strong> receptor subunit genes, which lie in a cluster on human chromosome 15, that were previously shown to have increased nicotine self administration, for several responses to <b>ethanol</b>.
+TUBB3	drug	nicotine	22459873	We tested mice with transgenic over expression of the alpha 5, alpha 3, <strong>beta 4</strong> receptor subunit genes, which lie in a cluster on human chromosome 15, that were previously shown to have increased <b>nicotine</b> self administration, for several responses to ethanol.
+TUBB3	drug	nicotine	20114055	Structural differences determine the relative selectivity of nicotinic compounds for native alpha 4 beta 2* , alpha 6 beta 2* , alpha 3 <strong>beta 4</strong>*  and alpha 7 <b>nicotine</b> acetylcholine receptors.
+TUBB3	drug	nicotine	18996504	<b>Smoking</b> cessation and variations in nicotinic acetylcholine receptor subunits alpha 5, alpha 3, and <strong>beta 4</strong> genes.
+TUBB3	drug	nicotine	18996504	Evidence has recently accumulated that single nucleotide polymorphisms in the genetic region encoding the nicotinic acetylcholine receptor subunits alpha 5, alpha 3, and <strong>beta 4</strong> are associated with <b>smoking</b> and <b>nicotine</b> dependence.
+TUBB3	addiction	dependence	18996504	Evidence has recently accumulated that single nucleotide polymorphisms in the genetic region encoding the nicotinic acetylcholine receptor subunits alpha 5, alpha 3, and <strong>beta 4</strong> are associated with smoking and nicotine <b>dependence</b>.
+TUBB3	drug	nicotine	12144940	Modulation of <b>nicotine</b> self administration in rats by combination therapy with agents blocking alpha 3 <strong>beta 4</strong> nicotinic receptors.
+TUBB3	drug	opioid	11906717	Antagonism of alpha 3 <strong>beta 4</strong> nicotinic receptors as a strategy to reduce <b>opioid</b> and stimulant self administration.
+TUBB3	drug	psychedelics	11906717	Both <b>ibogaine</b> and 18 methoxycoronaridine were antagonists at alpha 3 <strong>beta 4</strong> nicotinic receptors and both agents were more potent at this site than at alpha 4 beta 2 nicotinic receptors or at NMDA or 5 HT(3) receptors; 18 methoxycoronaridine was more selective in this regard than <b>ibogaine</b>.
+TUBB3	addiction	relapse	11906717	The data are consistent with the hypothesis that antagonism at alpha 3 <strong>beta 4</strong> receptors is a potential mechanism to modulate drug <b>seeking</b> behavior.
+TUBB3	drug	nicotine	11854451	There were no changes in the levels of alpha 4, alpha 5, alpha 6, alpha 7, beta 2, and <strong>beta 4</strong> mRNA, or in [(125)I]epibatidine and [(3)H]<b>nicotine</b> binding between +/T and +/+ mice.
+TUBB3	drug	alcohol	9422812	In some cells, agonist induced current responses with the alpha 3 <strong>beta 4</strong> subunit combination could be either significantly potentiated or inhibited (range 25% to 237% of control response) by low <b>ethanol</b> concentrations (1 30 mM).
+TUBB3	drug	alcohol	9422812	In general, the alpha 3 beta 2, alpha 4 1 beta 2 and alpha 4 1 <strong>beta 4</strong> subunit combinations were less sensitive to low concentrations of <b>ethanol</b>, but respectively showed potentiations of up to 178%, 226% and 154% at high EtOH concentrations.
+OPRD1	drug	cocaine	32730947	We then examined the mRNA levels of opioid receptors including mu (Oprm), delta (<strong>Oprd</strong>), and kappa (Oprk), and their endogenous opioid peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last <b>cocaine</b> infusion.
+OPRD1	drug	opioid	32730947	We then examined the mRNA levels of <b>opioid</b> receptors including mu (Oprm), delta (<strong>Oprd</strong>), and kappa (Oprk), and their endogenous <b>opioid</b> peptide precursors including proopiomelanocortin (Pomc), proenkephalin (Penk), prodynorphin (Pdyn) in the dorsal striatum (CPu) and the prefrontal cortex (PFC) 18 hrs after the last cocaine infusion.
+OPRD1	drug	cocaine	32730947	We found that <b>cocaine</b> self administration significantly increased the mRNA levels of Oprm and <strong>Oprd</strong> in both the CPu and PFC, but had no effect on Oprk mRNA levels in either brain region.
+OPRD1	drug	opioid	31907389	Genetic polymorphisms in the <b>opioid</b> receptor delta 1 (<strong>OPRD1</strong>) gene are associated with <b>methadone</b> dose in <b>methadone</b> maintenance treatment for <b>heroin</b> dependence.
+OPRD1	addiction	dependence	31907389	Genetic polymorphisms in the opioid receptor delta 1 (<strong>OPRD1</strong>) gene are associated with methadone dose in methadone maintenance treatment for heroin <b>dependence</b>.
+OPRD1	drug	opioid	31907389	Genetic polymorphisms in the <strong><b>opioid</b> receptor delta 1</strong> (<strong>OPRD1</strong>) gene are associated with <b>methadone</b> dose in <b>methadone</b> maintenance treatment for <b>heroin</b> dependence.
+OPRD1	addiction	dependence	31907389	Genetic polymorphisms in the <strong>opioid receptor delta 1</strong> (<strong>OPRD1</strong>) gene are associated with methadone dose in methadone maintenance treatment for heroin <b>dependence</b>.
+OPRD1	drug	opioid	31907389	This study tested the hypothesis that single nucleotide polymorphisms (SNPs) in the <b>opioid</b> receptor delta 1 (<strong>OPRD1</strong>) gene coding region are associated with treatment responses in a <b>methadone</b> maintenance therapy (MMT) cohort in Taiwan.
+OPRD1	drug	opioid	31907389	The results indicated that <strong>OPRD1</strong> genetic variants were associated with <b>methadone</b> dosage and <b>methadone</b> plasma concentration in MMT patients with a negative <b>morphine</b> test result.
+OPRD1	drug	opioid	30599218	Interestingly, <b>naloxone</b>, β funaltrexamine, naloxonazine, and naltrindole, but not nor binaltorphimine, could also antagonize the antinociceptive effect markedly, suggesting that OPRM (primary μ1 subtype) and <strong>OPRD</strong> were involved in the antinociceptive response induced by ghrelin(1 7) NH2.
+OPRD1	drug	opioid	30326159	Evidence for roles for <b>opioid</b> related genes <b>opioid</b> receptor, delta 1 (<strong>Oprd1</strong>) and preproenkephalin (Penk) was also found.
+OPRD1	drug	opioid	30171993	<strong>OPRD1</strong> gene affects disease vulnerability and environmental stress in patients with <b>heroin</b> dependence in Han Chinese.
+OPRD1	addiction	dependence	30171993	<strong>OPRD1</strong> gene affects disease vulnerability and environmental stress in patients with heroin <b>dependence</b> in Han Chinese.
+OPRD1	drug	opioid	30171993	<b>Opioid</b> related genes, including OPRM1, <strong>OPRD1</strong>, OPRK1, and POMC, are obvious candidates for HD.
+OPRD1	drug	opioid	30118972	The most studied candidate genes have included the mu <b>opioid</b> receptor (OPRM1), the delta <b>opioid</b> receptor (<strong>OPRD1</strong>), the dopamine D2 receptor (DRD2), and brain derived neurotrophic factor (BDNF).
+OPRD1	drug	opioid	30028550	The evidence for roles for <b>opioid</b> related genes <b>opioid</b> receptor, delta 1 (<strong>Oprd1</strong>) and preproenkephalin (Penk) was also found.
+OPRD1	drug	opioid	29055075	The aim of this study was to investigate if genetic variants of mu, kappa, and delta <b>opioid</b> receptor genes (OPRM1, OPRK1, and <strong>OPRD1</strong>) and the catechol O methyltransferase gene (COMT) influenced the pain phenotype in patients with osteoarthritis.
+OPRD1	drug	opioid	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the <b>opioid</b> receptor genes (OPRM1, <strong>OPRD1</strong>, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to <b>heroin</b> dependence in populations worldwide.
+OPRD1	addiction	dependence	28692418	Reward  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the opioid receptor genes (OPRM1, <strong>OPRD1</strong>, and OPRK1), have been implicated in drug <b>dependence</b>, but relatively little is known on their contributions to heroin <b>dependence</b> in populations worldwide.
+OPRD1	addiction	reward	28692418	<b>Reward</b>  and memory related candidate genes dopamine D2 receptor (DRD2) and brain derived neurotrophic factor (BDNF), as well as the opioid receptor genes (OPRM1, <strong>OPRD1</strong>, and OPRK1), have been implicated in drug dependence, but relatively little is known on their contributions to heroin dependence in populations worldwide.
+OPRD1	drug	opioid	28692418	The G allele of rs4654327 (<strong>OPRD1</strong>), DRD2 haplotype block CCGCCGTT (rs6277 rs1076560 rs2283265 rs2734833 rs2075652 rs1079596 rs4436578 rs11214607), and <strong>OPRD1</strong> haplotypes TACG (rs6669447 rs2236857 rs508448 rs4654327), CG (rs508448 rs4654327), and TG (rs6669447 rs4654327) were significantly associated with <b>heroin</b> dependence phenotype.
+OPRD1	addiction	dependence	28692418	The G allele of rs4654327 (<strong>OPRD1</strong>), DRD2 haplotype block CCGCCGTT (rs6277 rs1076560 rs2283265 rs2734833 rs2075652 rs1079596 rs4436578 rs11214607), and <strong>OPRD1</strong> haplotypes TACG (rs6669447 rs2236857 rs508448 rs4654327), CG (rs508448 rs4654327), and TG (rs6669447 rs4654327) were significantly associated with heroin <b>dependence</b> phenotype.
+OPRD1	drug	opioid	28692418	Homozygotes AA at rs6265 (BDNF), TT at rs16917234 (BDNF), and CC at rs508448 (<strong>OPRD1</strong>) also appeared as risk factors for the endophenotype earlier age of onset for <b>heroin</b> use.
+OPRD1	drug	opioid	28656735	Drug addiction is a novelty seeking personality trait that is associated with the candidate genes <strong>OPRD1</strong> (<b>opioid</b> delta receptors), OPRK1 (<b>opioid</b> kappa receptors) and PDYN (prodynorphin).
+OPRD1	addiction	addiction	28656735	Drug <b>addiction</b> is a novelty seeking personality trait that is associated with the candidate genes <strong>OPRD1</strong> (opioid delta receptors), OPRK1 (opioid kappa receptors) and PDYN (prodynorphin).
+OPRD1	addiction	relapse	28656735	Drug addiction is a novelty <b>seeking</b> personality trait that is associated with the candidate genes <strong>OPRD1</strong> (opioid delta receptors), OPRK1 (opioid kappa receptors) and PDYN (prodynorphin).
+OPRD1	addiction	relapse	28656735	However, associations between single nucleotide polymorphisms (SNPs) rs1042114 (80G>T) of the <strong>OPRD1</strong> gene, rs702764 (843 A>G) of the OPRK1 gene, and rs910080 (3' UTR _743T>C), rs1997794 (5' UTR  381A>G) and rs1022563 (3' UTR) of the PDYN gene and novelty <b>seeking</b> remain controversial as reported results have not been reproducible.
+OPRD1	addiction	addiction	28656735	SNP rs1042114 in the <strong>OPRD1</strong> gene is strongly associated with opiate <b>addiction</b> (P=.0001).
+OPRD1	drug	opioid	28632076	Association of <strong>OPRD1</strong> Gene Variants with <b>Opioid</b> Dependence in Addicted Male Individuals Undergoing <b>Methadone</b> Treatment in the North of Iran.
+OPRD1	addiction	dependence	28632076	Association of <strong>OPRD1</strong> Gene Variants with Opioid <b>Dependence</b> in Addicted Male Individuals Undergoing Methadone Treatment in the North of Iran.
+OPRD1	drug	opioid	28632076	In conclusion, the four studied <strong>OPRD1</strong> gene variants and their haplotypes can play important roles in susceptibility to <b>opioid</b> dependence.
+OPRD1	addiction	dependence	28632076	In conclusion, the four studied <strong>OPRD1</strong> gene variants and their haplotypes can play important roles in susceptibility to opioid <b>dependence</b>.
+OPRD1	drug	opioid	28511993	Rats exposed to early life stress (MS360) had increased <b>opioid</b> receptor gene (Oprm1, <strong>Oprd1</strong> and Oprk1) expression in the dorsal striatum.
+OPRD1	drug	alcohol	28511993	<b>Ethanol</b> drinking was associated with lower striatal <strong>Oprd1</strong> and Oprk1 expression solely in rats exposed to early life stress.
+OPRD1	drug	opioid	28035534	The <strong>OPRD1</strong> gene encodes the delta <b>opioid</b> receptor, which has multiple functions including regulating reward pathways.
+OPRD1	addiction	reward	28035534	The <strong>OPRD1</strong> gene encodes the delta opioid receptor, which has multiple functions including regulating <b>reward</b> pathways.
+OPRD1	drug	opioid	27725223	Next generation sequencing (NGS) workflow was based on a custom AmpliSeq™ panel and designed for sequencing of human genes related to the <b>opioid</b> receptor group (OPRM1, <strong>OPRD1</strong>, OPRK1, SIGMA1, OPRL1) on an Ion PGM™ Sequencer.
+OPRD1	drug	opioid	27664554	The association of the delta <b>opioid</b> receptor (<strong>OPRD1</strong>) intronic SNP rs2236861 with non dependent <b>opioid</b> use (HC vs. NOD) remained significant after correction for multiple testing (OR=0.032; pcorrected=0.015).
+OPRD1	drug	cocaine	27449273	An intronic polymorphism in the delta opioid receptor gene (<strong>OPRD1</strong>) was previously associated with <b>cocaine</b> dependence in African Americans.
+OPRD1	drug	opioid	27449273	An intronic polymorphism in the delta <b>opioid</b> receptor gene (<strong>OPRD1</strong>) was previously associated with cocaine dependence in African Americans.
+OPRD1	addiction	dependence	27449273	An intronic polymorphism in the delta opioid receptor gene (<strong>OPRD1</strong>) was previously associated with cocaine <b>dependence</b> in African Americans.
+OPRD1	drug	cocaine	27449273	A polymorphism in <strong>OPRD1</strong> appears to be associated with both <b>cocaine</b> dependence and <b>cocaine</b> use during treatment in African Americans.
+OPRD1	addiction	dependence	27449273	A polymorphism in <strong>OPRD1</strong> appears to be associated with both cocaine <b>dependence</b> and cocaine use during treatment in African Americans.
+OPRD1	drug	cocaine	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, Penk, Pdyn) and cognate receptors (Oprm, Oprk and <strong>Oprd</strong>) in reward related brain regions, after exposure to either <b>cocaine</b> self administration or yoked saline, in the aforementioned translational paradigm.
+OPRD1	drug	opioid	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous <b>opioid</b> peptides (Pomc, Penk, Pdyn) and cognate receptors (Oprm, Oprk and <strong>Oprd</strong>) in reward related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+OPRD1	addiction	reward	26777278	We compare here Fischer and Lewis rats in the gene expression of endogenous opioid peptides (Pomc, Penk, Pdyn) and cognate receptors (Oprm, Oprk and <strong>Oprd</strong>) in <b>reward</b> related brain regions, after exposure to either cocaine self administration or yoked saline, in the aforementioned translational paradigm.
+OPRD1	addiction	withdrawal	26692286	The total <b>withdrawal</b> severity score (based on the COWS) from this procedure was correlated with genotype information for variants of OPRM1 (rs1799971; rs6848893), <strong>OPRD1</strong> (rs10753331; rs2234918; rs581111; rs678849; rs1042114), and OPRK1 (rs6473797; rs963549).
+OPRD1	addiction	withdrawal	26692286	Three polymorphisms were significantly associated with severity of abstinence induced <b>withdrawal</b> (n = 19) in the bivariate analysis (R): OPRM1 rs6848893 (.45), <strong>OPRD1</strong> rs10753331 (.03), and rs678849 (.08), but only the OPRM1 rs6848893 was retained in the multivariate model (p < .001).
+OPRD1	drug	alcohol	25823631	The genetic variability of μ , δ  and κ opioid receptors genes OPRM1, <strong>OPRD1</strong>, and OPRK1 modulates the efficacy of opioid antagonist treatments such as <b>naltrexone</b> and methadone, as well as the cocaine vaccine.
+OPRD1	drug	cocaine	25823631	The genetic variability of μ , δ  and κ opioid receptors genes OPRM1, <strong>OPRD1</strong>, and OPRK1 modulates the efficacy of opioid antagonist treatments such as naltrexone and methadone, as well as the <b>cocaine</b> vaccine.
+OPRD1	drug	opioid	25823631	The genetic variability of μ , δ  and κ <b>opioid</b> receptors genes OPRM1, <strong>OPRD1</strong>, and OPRK1 modulates the efficacy of <b>opioid</b> antagonist treatments such as naltrexone and <b>methadone</b>, as well as the cocaine vaccine.
+OPRD1	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, <strong>OPRD1</strong>, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+OPRD1	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, <strong>OPRD1</strong>, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+OPRD1	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, <strong>OPRD1</strong>, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+OPRD1	drug	cannabinoid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ opioid receptor (<strong>OPRD1</strong>), <b>cannabinoid</b> receptor 1 (CNR1), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+OPRD1	drug	opioid	25418810	The overexpression of four genes, DNA methyltransferase 1 (DNMT1), δ <b>opioid</b> receptor (<strong>OPRD1</strong>), cannabinoid receptor 1 (CNR1), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+OPRD1	drug	alcohol	24533225	Polymorphisms in the μ , δ  and κ opioid receptor genes (OPRM1, <strong>OPRD1</strong> and OPRK1) have been reported to be associated with substance (<b>alcohol</b> or drug) dependence.
+OPRD1	drug	opioid	24533225	Polymorphisms in the μ , δ  and κ <b>opioid</b> receptor genes (OPRM1, <strong>OPRD1</strong> and OPRK1) have been reported to be associated with substance (alcohol or drug) dependence.
+OPRD1	addiction	dependence	24533225	Polymorphisms in the μ , δ  and κ opioid receptor genes (OPRM1, <strong>OPRD1</strong> and OPRK1) have been reported to be associated with substance (alcohol or drug) <b>dependence</b>.
+OPRD1	drug	alcohol	24533225	Genotype data for 13 OPRM1 Single Nucleotide Polymorphisms (SNPs), 11 <strong>OPRD1</strong> SNPs and seven OPRK1 SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with <b>Alcohol</b> Dependence (AD), 171 with Cocaine Dependence (CD), and 91 with Opioid Dependence (OD)] and 338 EA control subjects.
+OPRD1	drug	cocaine	24533225	Genotype data for 13 OPRM1 Single Nucleotide Polymorphisms (SNPs), 11 <strong>OPRD1</strong> SNPs and seven OPRK1 SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with Alcohol Dependence (AD), 171 with <b>Cocaine</b> Dependence (CD), and 91 with Opioid Dependence (OD)] and 338 EA control subjects.
+OPRD1	drug	opioid	24533225	Genotype data for 13 OPRM1 Single Nucleotide Polymorphisms (SNPs), 11 <strong>OPRD1</strong> SNPs and seven OPRK1 SNPs were obtained from 382 European Americans (EAs) affected with substance dependence [among them, 318 with Alcohol Dependence (AD), 171 with Cocaine Dependence (CD), and 91 with <b>Opioid</b> Dependence (OD)] and 338 EA control subjects.
+OPRD1	addiction	dependence	24533225	Genotype data for 13 OPRM1 Single Nucleotide Polymorphisms (SNPs), 11 <strong>OPRD1</strong> SNPs and seven OPRK1 SNPs were obtained from 382 European Americans (EAs) affected with substance <b>dependence</b> [among them, 318 with Alcohol <b>Dependence</b> (AD), 171 with Cocaine <b>Dependence</b> (CD), and 91 with Opioid <b>Dependence</b> (OD)] and 338 EA control subjects.
+OPRD1	drug	opioid	24126707	Genetic variation in <strong>OPRD1</strong> and the response to treatment for <b>opioid</b> dependence with <b>buprenorphine</b> in European American females.
+OPRD1	addiction	dependence	24126707	Genetic variation in <strong>OPRD1</strong> and the response to treatment for opioid <b>dependence</b> with buprenorphine in European American females.
+OPRD1	drug	opioid	24126707	This study analyses the pharmacogenetic association of six polymorphisms in <strong>OPRD1</strong>, the gene encoding the delta <b>opioid</b> receptor, on treatment outcome in 582 <b>opioid</b> addicted European Americans randomized to either <b>methadone</b> or <b>buprenorphine</b>/<b>naloxone</b> (<b>Suboxone</b>) over the course of a 24 week open label clinical trial.
+OPRD1	drug	opioid	24086514	Association of polymorphisms in pharmacogenetic candidate genes (<strong>OPRD1</strong>, GAL, ABCB1, OPRM1) with <b>opioid</b> dependence in European population: a case control study.
+OPRD1	addiction	dependence	24086514	Association of polymorphisms in pharmacogenetic candidate genes (<strong>OPRD1</strong>, GAL, ABCB1, OPRM1) with opioid <b>dependence</b> in European population: a case control study.
+OPRD1	drug	opioid	24086514	The most significant associations with <b>opioid</b> addiction (remaining significant after adjustment for multiple testing) were observed for the rs948854 SNP in the galanin gene (GAL, p = 0.001) and the rs2236861 SNP in the delta <b>opioid</b> receptor gene (<strong>OPRD1</strong>, p = 0.001).
+OPRD1	addiction	addiction	24086514	The most significant associations with opioid <b>addiction</b> (remaining significant after adjustment for multiple testing) were observed for the rs948854 SNP in the galanin gene (GAL, p = 0.001) and the rs2236861 SNP in the delta opioid receptor gene (<strong>OPRD1</strong>, p = 0.001).
+OPRD1	drug	opioid	24086514	The present study provides further support for a contribution of GAL and <strong>OPRD1</strong> variants to the development of <b>opioid</b> addiction.
+OPRD1	addiction	addiction	24086514	The present study provides further support for a contribution of GAL and <strong>OPRD1</strong> variants to the development of opioid <b>addiction</b>.
+OPRD1	drug	opioid	23612435	An intronic variant in <strong>OPRD1</strong> predicts treatment outcome for <b>opioid</b> dependence in African Americans.
+OPRD1	addiction	dependence	23612435	An intronic variant in <strong>OPRD1</strong> predicts treatment outcome for opioid <b>dependence</b> in African Americans.
+OPRD1	drug	opioid	23612435	This study is a pharmacogenetic analysis of the effects of genetic variants in <strong>OPRD1</strong>, the gene encoding the δ <b>opioid</b> receptor, on the prevalence of <b>opioid</b> positive urine tests in African Americans (n=77) or European Americans (n=566) undergoing treatment for <b>opioid</b> dependence.
+OPRD1	addiction	dependence	23612435	This study is a pharmacogenetic analysis of the effects of genetic variants in <strong>OPRD1</strong>, the gene encoding the δ opioid receptor, on the prevalence of opioid positive urine tests in African Americans (n=77) or European Americans (n=566) undergoing treatment for opioid <b>dependence</b>.
+OPRD1	drug	opioid	23427138	A commonly carried genetic variant in the delta <b>opioid</b> receptor gene, <strong>OPRD1</strong>, is associated with smaller regional brain volumes: replication in elderly and young populations.
+OPRD1	drug	opioid	23427138	These receptors play a key role in the reinforcing properties of drugs of abuse, and polymorphisms in <strong>OPRD1</strong> (the gene encoding delta <b>opioid</b> receptors) are associated with drug addiction.
+OPRD1	addiction	addiction	23427138	These receptors play a key role in the reinforcing properties of drugs of abuse, and polymorphisms in <strong>OPRD1</strong> (the gene encoding delta opioid receptors) are associated with drug <b>addiction</b>.
+OPRD1	addiction	reward	23427138	These receptors play a key role in the <b>reinforcing</b> properties of drugs of abuse, and polymorphisms in <strong>OPRD1</strong> (the gene encoding delta opioid receptors) are associated with drug addiction.
+OPRD1	addiction	addiction	23427138	We hypothesized that common variants in <strong>OPRD1</strong> would be associated with differences in brain structure, particularly in regions relevant to <b>addictive</b> and neurodegenerative disorders.
+OPRD1	drug	alcohol	22954510	This alternate binding presents the possibility that single nucleotide polymorphisms (SNPs) in the kappa and delta opioid receptor (OPRK1 and <strong>OPRD1</strong>) genes may contribute to <b>naltrexone</b> pharmacogenetics.
+OPRD1	drug	opioid	22954510	This alternate binding presents the possibility that single nucleotide polymorphisms (SNPs) in the kappa and delta <b>opioid</b> receptor (OPRK1 and <strong>OPRD1</strong>) genes may contribute to naltrexone pharmacogenetics.
+OPRD1	drug	alcohol	22954510	Moreover, there was a significant <b>Naltrexone</b>×<strong>OPRD1</strong> Genotype (rs4654327) interaction predicting <b>alcohol</b> induced stimulation and craving, such that carriers of the A allele at this locus reported greater <b>naltrexone</b> induced blunting of <b>alcohol</b> stimulation and <b>alcohol</b> craving compared to GG homozygotes.
+OPRD1	addiction	relapse	22954510	Moreover, there was a significant Naltrexone×<strong>OPRD1</strong> Genotype (rs4654327) interaction predicting alcohol induced stimulation and <b>craving</b>, such that carriers of the A allele at this locus reported greater naltrexone induced blunting of alcohol stimulation and alcohol <b>craving</b> compared to GG homozygotes.
+OPRD1	drug	cocaine	22795689	Case control association analysis of polymorphisms in the δ opioid receptor, <strong>OPRD1</strong>, with <b>cocaine</b> and opioid addicted populations.
+OPRD1	drug	opioid	22795689	Case control association analysis of polymorphisms in the δ <b>opioid</b> receptor, <strong>OPRD1</strong>, with cocaine and <b>opioid</b> addicted populations.
+OPRD1	drug	cocaine	22795689	The present study evaluated the contribution of <strong>OPRD1</strong>, the gene encoding the DOR, to the risk of addiction to opioids and <b>cocaine</b>.
+OPRD1	drug	opioid	22795689	The present study evaluated the contribution of <strong>OPRD1</strong>, the gene encoding the DOR, to the risk of addiction to <b>opioids</b> and cocaine.
+OPRD1	addiction	addiction	22795689	The present study evaluated the contribution of <strong>OPRD1</strong>, the gene encoding the DOR, to the risk of <b>addiction</b> to opioids and cocaine.
+OPRD1	drug	cocaine	22795689	The association of <strong>OPRD1</strong> polymorphisms with both opioid addiction (OA) and <b>cocaine</b> addiction (CA) was analyzed in African American (OA n=336, CA n=503) and European American (OA n=1007, CA n=336) populations.
+OPRD1	drug	opioid	22795689	The association of <strong>OPRD1</strong> polymorphisms with both <b>opioid</b> addiction (OA) and cocaine addiction (CA) was analyzed in African American (OA n=336, CA n=503) and European American (OA n=1007, CA n=336) populations.
+OPRD1	addiction	addiction	22795689	The association of <strong>OPRD1</strong> polymorphisms with both opioid <b>addiction</b> (OA) and cocaine <b>addiction</b> (CA) was analyzed in African American (OA n=336, CA n=503) and European American (OA n=1007, CA n=336) populations.
+OPRD1	drug	cocaine	22795689	The present study suggests that polymorphisms in <strong>OPRD1</strong> are relevant for <b>cocaine</b> addiction in the African American population and provides additional support for a broad role for <strong>OPRD1</strong> variants in drug dependence.
+OPRD1	addiction	addiction	22795689	The present study suggests that polymorphisms in <strong>OPRD1</strong> are relevant for cocaine <b>addiction</b> in the African American population and provides additional support for a broad role for <strong>OPRD1</strong> variants in drug dependence.
+OPRD1	addiction	dependence	22795689	The present study suggests that polymorphisms in <strong>OPRD1</strong> are relevant for cocaine addiction in the African American population and provides additional support for a broad role for <strong>OPRD1</strong> variants in drug <b>dependence</b>.
+OPRD1	drug	opioid	22526530	Under classical experimental conditions, <b>morphine</b> induced CPP is decreased in mice lacking delta <b>opioid</b> receptors (<strong>Oprd1</strong> ( / )).
+OPRD1	addiction	reward	22526530	Under classical experimental conditions, morphine induced <b>CPP</b> is decreased in mice lacking delta opioid receptors (<strong>Oprd1</strong> ( / )).
+OPRD1	drug	opioid	22526530	We first identified experimental conditions under which <strong>Oprd1</strong> ( / ) mice are able to express CPP to <b>morphine</b> (5, 10 or 20 mg/kg) in a drug free state and observed that, in this paradigm, CPP was dependent on circadian time conditions.
+OPRD1	addiction	reward	22526530	We first identified experimental conditions under which <strong>Oprd1</strong> ( / ) mice are able to express <b>CPP</b> to morphine (5, 10 or 20 mg/kg) in a drug free state and observed that, in this paradigm, <b>CPP</b> was dependent on circadian time conditions.
+OPRD1	drug	opioid	22526530	We then took advantage of this particularity to assess the ability of various cues (internal or discrete), predicting either drug or food reward, to restore CPP induced by <b>morphine</b> (10 mg/kg) in <strong>Oprd1</strong> ( / ) mice in conditions under which they normally fail to express CPP.
+OPRD1	addiction	reward	22526530	We then took advantage of this particularity to assess the ability of various cues (internal or discrete), predicting either drug or food <b>reward</b>, to restore <b>CPP</b> induced by morphine (10 mg/kg) in <strong>Oprd1</strong> ( / ) mice in conditions under which they normally fail to express <b>CPP</b>.
+OPRD1	drug	opioid	22526530	We found that presentation of circadian, drug or auditory cues, predicting <b>morphine</b> or food reward, restored <b>morphine</b> CPP in <strong>Oprd1</strong> ( / ) mice, which then performed as well as control mice.
+OPRD1	addiction	reward	22526530	We found that presentation of circadian, drug or auditory cues, predicting morphine or food <b>reward</b>, restored morphine <b>CPP</b> in <strong>Oprd1</strong> ( / ) mice, which then performed as well as control mice.
+OPRD1	drug	opioid	22526530	This study reveals that, in contrast to spatial cues, internal or discrete <b>morphine</b> predicting stimuli permit full expression of <b>morphine</b> CPP in <strong>Oprd1</strong> ( / ) mice.
+OPRD1	addiction	reward	22526530	This study reveals that, in contrast to spatial cues, internal or discrete morphine predicting stimuli permit full expression of morphine <b>CPP</b> in <strong>Oprd1</strong> ( / ) mice.
+OPRD1	drug	opioid	22500942	Association of <strong>OPRD1</strong> polymorphisms with <b>heroin</b> dependence in a large case control series.
+OPRD1	addiction	dependence	22500942	Association of <strong>OPRD1</strong> polymorphisms with heroin <b>dependence</b> in a large case control series.
+OPRD1	drug	opioid	22500942	Genes encoding the <b>opioid</b> receptors (OPRM1, <strong>OPRD1</strong> and OPRK1) are obvious candidates for involvement in risk for <b>heroin</b> dependence.
+OPRD1	addiction	dependence	22500942	Genes encoding the opioid receptors (OPRM1, <strong>OPRD1</strong> and OPRK1) are obvious candidates for involvement in risk for heroin <b>dependence</b>.
+OPRD1	drug	opioid	22500942	Our results replicate a prior report providing strong evidence implicating <strong>OPRD1</strong> SNPs and, in particular, the two SNP (rs2236857 and rs581111) GA haplotype in liability for <b>heroin</b> dependence.
+OPRD1	addiction	dependence	22500942	Our results replicate a prior report providing strong evidence implicating <strong>OPRD1</strong> SNPs and, in particular, the two SNP (rs2236857 and rs581111) GA haplotype in liability for heroin <b>dependence</b>.
+OPRD1	drug	opioid	21807019	Within strains, complex patterns of <b>heroin</b> dose dependent changes in the levels of Oprm1, Oprk1 and <strong>Oprd1</strong> mRNAs were observed in the SN/VTA.
+OPRD1	drug	alcohol	20605909	We find here that the relative specificity of DOR agonists for <strong>DOR1</strong> or DOR2 can greatly affect the effects they exert on <b>ethanol</b> consumption and anxiety.
+OPRD1	drug	alcohol	20605909	The <strong>DOR1</strong> agonist 2 methyl 4aα (3 hydroxyphenyl) 1,2,3,4,4a,5,12,12aα octahydro quinolino[2,3,30g]isoquinoline (TAN 67), although not effective in decreasing anxiety like behavior in naive mice, has anxiolytic like properties in <b>ethanol</b> withdrawn mice.
+OPRD1	drug	alcohol	20605909	We believe the dual efficacy of <strong>DOR1</strong> agonists makes these receptors an interesting therapeutic target for treatment seeking <b>alcoholics</b>.
+OPRD1	addiction	relapse	20605909	We believe the dual efficacy of <strong>DOR1</strong> agonists makes these receptors an interesting therapeutic target for treatment <b>seeking</b> alcoholics.
+OPRD1	drug	opioid	20300121	We reported an increased frequency of the minor G allele of single nucleotide polymorphism (SNP) rs569356 (the only variant identified so far in the promoter region of the delta <b>opioid</b> receptor gene (<strong>OPRD1</strong>)) in subjects with <b>opioid</b> dependence.
+OPRD1	addiction	dependence	20300121	We reported an increased frequency of the minor G allele of single nucleotide polymorphism (SNP) rs569356 (the only variant identified so far in the promoter region of the delta opioid receptor gene (<strong>OPRD1</strong>)) in subjects with opioid <b>dependence</b>.
+OPRD1	drug	cannabinoid	19931559	(3) Feeding motivation  and reward related systems (opioids, <strong>OPRD1</strong>, <b>cannabinoids</b> (anandamide (AEA), <b>THC</b>, CBR1), dopamine, DRD2, DRD3, DRD4, catecholamine O methyl transferase (COMT).
+OPRD1	drug	opioid	19931559	(3) Feeding motivation  and reward related systems (<b>opioids</b>, <strong>OPRD1</strong>, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, DRD3, DRD4, catecholamine O methyl transferase (COMT).
+OPRD1	addiction	reward	19931559	(3) Feeding motivation  and <b>reward</b> related systems (opioids, <strong>OPRD1</strong>, cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, DRD3, DRD4, catecholamine O methyl transferase (COMT).
+OPRD1	drug	alcohol	19393386	<b>Naltrexone</b> is a competitive antagonist of opioid receptors OPRM1, <strong>OPRD1</strong> and OPRK1.
+OPRD1	drug	opioid	19393386	Naltrexone is a competitive antagonist of <b>opioid</b> receptors OPRM1, <strong>OPRD1</strong> and OPRK1.
+OPRD1	drug	opioid	19198656	We examine, for the first time, the role of <b>opioid</b> systems in impulsivity by testing whether inactivation of the mu  (Oprm1) or delta  (<strong>Oprd1</strong>) <b>opioid</b> receptor gene alters motor impulsivity in mice.
+OPRD1	drug	opioid	18518925	These variants were in noncoding regions of the genes encoding the mu (OPRM1; rs510769 and rs3778151), kappa (OPRK1; rs6473797) and delta (<strong>OPRD1</strong>; rs2236861, rs2236857 and rs3766951) <b>opioid</b> receptors; the neuropeptide galanin (GAL; rs694066); the serotonin receptor subtype 3B (HTR3B; rs3758987) and the casein kinase 1 isoform epsilon (CSNK1E; rs1534891).
+OPRD1	drug	opioid	18518925	Analysis of a combined effect of OPRM1 and <strong>OPRD1</strong> showed that rs510769 and rs2236861 increase the risk of <b>heroin</b> addiction (P = 0.0005).
+OPRD1	addiction	addiction	18518925	Analysis of a combined effect of OPRM1 and <strong>OPRD1</strong> showed that rs510769 and rs2236861 increase the risk of heroin <b>addiction</b> (P = 0.0005).
+OPRD1	drug	alcohol	17622222	The <strong>OPRD1</strong> and OPRK1 loci in <b>alcohol</b> or drug dependence: <strong>OPRD1</strong> variation modulates substance dependence risk.
+OPRD1	addiction	dependence	17622222	The <strong>OPRD1</strong> and OPRK1 loci in alcohol or drug <b>dependence</b>: <strong>OPRD1</strong> variation modulates substance <b>dependence</b> risk.
+OPRD1	drug	alcohol	17622222	Eleven single nucleotide polymorphisms (SNPs) spanning <strong>OPRD1</strong> were examined in 1063 European Americans (EAs) (620 cases with substance dependence (SD), including 557 with <b>alcohol</b> dependence (AD), 225 with cocaine dependence (CD) and 111 with opioid dependence (OD), and 443 controls).
+OPRD1	drug	cocaine	17622222	Eleven single nucleotide polymorphisms (SNPs) spanning <strong>OPRD1</strong> were examined in 1063 European Americans (EAs) (620 cases with substance dependence (SD), including 557 with alcohol dependence (AD), 225 with <b>cocaine</b> dependence (CD) and 111 with opioid dependence (OD), and 443 controls).
+OPRD1	drug	opioid	17622222	Eleven single nucleotide polymorphisms (SNPs) spanning <strong>OPRD1</strong> were examined in 1063 European Americans (EAs) (620 cases with substance dependence (SD), including 557 with alcohol dependence (AD), 225 with cocaine dependence (CD) and 111 with <b>opioid</b> dependence (OD), and 443 controls).
+OPRD1	addiction	dependence	17622222	Eleven single nucleotide polymorphisms (SNPs) spanning <strong>OPRD1</strong> were examined in 1063 European Americans (EAs) (620 cases with substance <b>dependence</b> (SD), including 557 with alcohol <b>dependence</b> (AD), 225 with cocaine <b>dependence</b> (CD) and 111 with opioid <b>dependence</b> (OD), and 443 controls).
+OPRD1	drug	alcohol	17503481	We analyzed 18 OPRM1 SNPs, 18 <strong>OPRD1</strong> SNPs, 7 PENK SNPs, and 7 POMC SNPs in a sample of 1923 European Americans from 219 multiplex <b>alcohol</b> dependent families.
+OPRD1	drug	opioid	17503481	Secondary analyses employing the narrower phenotype of <b>opioid</b> dependence (83 affected individuals) demonstrated association with SNPs in PENK and POMC, but not in OPRM1 or <strong>OPRD1</strong>.
+OPRD1	addiction	dependence	17503481	Secondary analyses employing the narrower phenotype of opioid <b>dependence</b> (83 affected individuals) demonstrated association with SNPs in PENK and POMC, but not in OPRM1 or <strong>OPRD1</strong>.
+OPRD1	drug	alcohol	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, <strong>OPRD1</strong>, PENK and POMC are associated with <b>alcohol</b> dependence or general illicit drug dependence, but variations in PENK and POMC appear to be associated with the narrower phenotype of opioid dependence in these families.
+OPRD1	drug	opioid	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, <strong>OPRD1</strong>, PENK and POMC are associated with alcohol dependence or general illicit drug dependence, but variations in PENK and POMC appear to be associated with the narrower phenotype of <b>opioid</b> dependence in these families.
+OPRD1	addiction	dependence	17503481	Therefore, our data provide no support for the idea that variations in OPRM1, <strong>OPRD1</strong>, PENK and POMC are associated with alcohol <b>dependence</b> or general illicit drug <b>dependence</b>, but variations in PENK and POMC appear to be associated with the narrower phenotype of opioid <b>dependence</b> in these families.
+OPRD1	drug	alcohol	17374034	Opioid receptor gene (OPRM1, OPRK1, and <strong>OPRD1</strong>) variants and response to <b>naltrexone</b> treatment for <b>alcohol</b> dependence: results from the VA Cooperative Study.
+OPRD1	drug	opioid	17374034	<b>Opioid</b> receptor gene (OPRM1, OPRK1, and <strong>OPRD1</strong>) variants and response to naltrexone treatment for alcohol dependence: results from the VA Cooperative Study.
+OPRD1	addiction	dependence	17374034	Opioid receptor gene (OPRM1, OPRK1, and <strong>OPRD1</strong>) variants and response to naltrexone treatment for alcohol <b>dependence</b>: results from the VA Cooperative Study.
+OPRD1	drug	alcohol	17374034	We studied polymorphic variants at each of the 3 opioid receptor genes  OPRM1, <strong>OPRD1</strong>, and OPRK1, which encode the mu, delta, and kappa opioid receptors, respectively  including the OPRM1 Asn40Asp variant  as predictors of response to NTX or placebo in 215 <b>alcohol</b> dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "<b>Naltrexone</b> in the Treatment of <b>Alcohol</b> Dependence."
+OPRD1	drug	opioid	17374034	We studied polymorphic variants at each of the 3 <b>opioid</b> receptor genes  OPRM1, <strong>OPRD1</strong>, and OPRK1, which encode the mu, delta, and kappa <b>opioid</b> receptors, respectively  including the OPRM1 Asn40Asp variant  as predictors of response to NTX or placebo in 215 alcohol dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "Naltrexone in the Treatment of Alcohol Dependence."
+OPRD1	addiction	dependence	17374034	We studied polymorphic variants at each of the 3 opioid receptor genes  OPRM1, <strong>OPRD1</strong>, and OPRK1, which encode the mu, delta, and kappa opioid receptors, respectively  including the OPRM1 Asn40Asp variant  as predictors of response to NTX or placebo in 215 alcohol dependent male subjects who participated in Veterans Affairs Cooperative Study 425, "Naltrexone in the Treatment of Alcohol <b>Dependence</b>."
+OPRD1	drug	opioid	16806108	These data suggest that polymorphisms in both the serotonin 1D (HTR1D) and <b>opioid</b> delta 1 (<strong>OPRD1</strong>) receptor genes show a significant association with restricting AN (RAN).
+OPRD1	addiction	intoxication	16806108	3 SNPs were found to be associated with both RAN and <b>binge</b> purge AN (BPAN) within the gene for <strong>OPRD1</strong>.
+OPRD1	drug	amphetamine	16741914	The role of the delta opioid receptor (<strong>OPRD1</strong>) in <b>methamphetamine</b> (MAP) addiction was investigated using association analysis between <strong>OPRD1</strong> gene polymorphisms and MAP dependence/psychosis.
+OPRD1	drug	opioid	16741914	The role of the delta <b>opioid</b> receptor (<strong>OPRD1</strong>) in methamphetamine (MAP) addiction was investigated using association analysis between <strong>OPRD1</strong> gene polymorphisms and MAP dependence/psychosis.
+OPRD1	addiction	addiction	16741914	The role of the delta opioid receptor (<strong>OPRD1</strong>) in methamphetamine (MAP) <b>addiction</b> was investigated using association analysis between <strong>OPRD1</strong> gene polymorphisms and MAP dependence/psychosis.
+OPRD1	addiction	dependence	16741914	The role of the delta opioid receptor (<strong>OPRD1</strong>) in methamphetamine (MAP) addiction was investigated using association analysis between <strong>OPRD1</strong> gene polymorphisms and MAP <b>dependence</b>/psychosis.
+OPRD1	addiction	dependence	16741914	DNA samples from Japanese patients with MAP <b>dependence</b>/psychosis were analyzed to find polymorphisms in <strong>OPRD1</strong> gene exons and exon intron boundaries.
+OPRD1	addiction	dependence	16741914	These results suggest that the <strong>OPRD1</strong> gene variants may not be a factor in vulnerability to MAP <b>dependence</b>/psychosis.
+OPRD1	drug	opioid	15157710	Loci in the vanilloid receptor subtype 1 gene (TRPV1), delta <b>opioid</b> receptor subtype 1 gene (<strong>OPRD1</strong>) and catechol O methyltransferase gene (COMT) were genotyped using 5' nuclease assays.
+OPRD1	drug	alcohol	14745298	Nonselective opioid antagonists reduce <b>alcohol</b> consumption under various experimental situations, and several association studies have examined possible roles of opioid receptor mu (OPRM), delta (<strong>OPRD</strong>), and kappa (OPRK) genes in the development of <b>alcohol</b> dependence.
+OPRD1	drug	opioid	14745298	Nonselective <b>opioid</b> antagonists reduce alcohol consumption under various experimental situations, and several association studies have examined possible roles of <b>opioid</b> receptor mu (OPRM), delta (<strong>OPRD</strong>), and kappa (OPRK) genes in the development of alcohol dependence.
+OPRD1	addiction	dependence	14745298	Nonselective opioid antagonists reduce alcohol consumption under various experimental situations, and several association studies have examined possible roles of opioid receptor mu (OPRM), delta (<strong>OPRD</strong>), and kappa (OPRK) genes in the development of alcohol <b>dependence</b>.
+OPRD1	drug	alcohol	14745298	We examined 20 single nucleotide polymorphisms (SNPs) across the OPRM, <strong>OPRD</strong>, and OPRK genes in 158 <b>alcohol</b> dependent subjects and 149 controls.
+OPRD1	drug	opioid	12116270	Previously, two single nucleotide polymorphisms (SNPs), <strong>OPRD1</strong> 921T > C and 80G > T, of the human delta <b>opioid</b> receptor gene were used in population based studies of <b>heroin</b> dependence.
+OPRD1	addiction	dependence	12116270	Previously, two single nucleotide polymorphisms (SNPs), <strong>OPRD1</strong> 921T > C and 80G > T, of the human delta opioid receptor gene were used in population based studies of heroin <b>dependence</b>.
+OPRD1	drug	opioid	12116270	One study in a German population found that <strong>OPRD1</strong> 921T > C was associated with <b>heroin</b> dependence.
+OPRD1	addiction	dependence	12116270	One study in a German population found that <strong>OPRD1</strong> 921T > C was associated with heroin <b>dependence</b>.
+OPRD1	drug	opioid	12116270	To test the hypothesis that <strong>OPRD1</strong> or a closely linked gene is associated with <b>heroin</b> dependence, we used 5' nuclease assays to genotype both <strong>OPRD1</strong> SNPs in 450 Chinese <b>heroin</b> dependent patients and 304 unaffected controls from the same population.
+OPRD1	addiction	dependence	12116270	To test the hypothesis that <strong>OPRD1</strong> or a closely linked gene is associated with heroin <b>dependence</b>, we used 5' nuclease assays to genotype both <strong>OPRD1</strong> SNPs in 450 Chinese heroin dependent patients and 304 unaffected controls from the same population.
+OPRD1	drug	opioid	12116270	Genotype and allele frequencies at <strong>OPRD1</strong> 921T > C were not significantly different, and the <strong>OPRD1</strong> 80G was absent from both Chinese <b>opioid</b> dependence patients and controls.
+OPRD1	addiction	dependence	12116270	Genotype and allele frequencies at <strong>OPRD1</strong> 921T > C were not significantly different, and the <strong>OPRD1</strong> 80G was absent from both Chinese opioid <b>dependence</b> patients and controls.
+OPRD1	drug	opioid	12116270	Based on the genotype and allele frequencies of the genomic control loci, there was no evidence for stratification bias capable of masking an association of <strong>OPRD1</strong> to <b>heroin</b> dependence in this large and homogenous Chinese sample.
+OPRD1	addiction	dependence	12116270	Based on the genotype and allele frequencies of the genomic control loci, there was no evidence for stratification bias capable of masking an association of <strong>OPRD1</strong> to heroin <b>dependence</b> in this large and homogenous Chinese sample.
+OPRD1	drug	opioid	12116270	Therefore, these data do not support an association between the <strong>OPRD1</strong> gene and <b>heroin</b> dependence in the Chinese population.
+OPRD1	addiction	dependence	12116270	Therefore, these data do not support an association between the <strong>OPRD1</strong> gene and heroin <b>dependence</b> in the Chinese population.
+OPRD1	drug	opioid	10982041	Variant detection at the delta <b>opioid</b> receptor (<strong>OPRD1</strong>) locus and population genetics of a novel variant affecting protein sequence.
+OPRD1	drug	opioid	10982041	The three <b>opioid</b> receptor genes, and in particular the mu and delta loci (OPRM1 and <strong>OPRD1</strong>, respectively), are compelling candidates to influence risk for substance dependence.
+OPRD1	addiction	dependence	10982041	The three opioid receptor genes, and in particular the mu and delta loci (OPRM1 and <strong>OPRD1</strong>, respectively), are compelling candidates to influence risk for substance <b>dependence</b>.
+OPRD1	drug	opioid	10982041	Previous study of a variant at the <strong>OPRD1</strong> locus, T921C, has shown association with <b>opioid</b> dependence.
+OPRD1	addiction	dependence	10982041	Previous study of a variant at the <strong>OPRD1</strong> locus, T921C, has shown association with opioid <b>dependence</b>.
+OPRD1	drug	opioid	10835636	The mu , delta  and kappa  <b>opioid</b> receptors (encoded by Oprm, <strong>Oprd1</strong> and Oprk1, respectively) mediate the biological activity of <b>opioids</b>.
+OPRD1	drug	opioid	10835636	Our data show no detectable phenotype in Oprk1 /  mutants, suggesting that kappa receptors do not have a role in this aspect of <b>opioid</b> function; opposing phenotypes in Oprm /  and <strong>Oprd1</strong> /  mutants which contrasts with the classical notion of similar activities of mu  and delta receptors; and consistent anxiogenic  and depressive like responses in <strong>Oprd1</strong> /  mice, indicating that delta receptor activity contributes to improvement of mood states.
+OPRD1	addiction	addiction	10835636	We conclude that the <strong>Oprd1</strong> encoded receptor, which has been proposed to be a promising target for the clinical management of pain, should also be considered in the treatment of drug <b>addiction</b> and other mood related disorders.
+C6	drug	amphetamine	31253835	Identification of cytotoxic markers in <b>methamphetamine</b> treated rat <strong>C6</strong> astroglia like cells.
+C6	drug	amphetamine	31253835	The present study aimed to assess <b>METH</b> toxicity in differentiated <strong>C6</strong> astroglia like cells through biochemical and toxicity markers with acute (1 h) and chronic (48 h) treatments.
+C6	drug	nicotine	31011457	We present a case of a 39 year old male patient, <b>smoker</b>, diagnosed with multiple cervical disc herniations, who underwent Anterior Cervical Discectomy and Fusion (ACDF) for C3 C4, C4 C5, and C5 <strong>C6</strong>.
+C6	drug	alcohol	30732651	BmoR, an <b>alcohol</b> regulated transcription factor, mediates a σ54 dependent promoter Pbmo of alkane monooxygenase in n alkane metabolism of Thauera butanivorans and displays high sensitivity to C4 <strong>C6</strong> linear alcohols and C3 C5 branched chain alcohols.
+C6	drug	cannabinoid	29492979	Moreover, the intracellular GSH was also decreased in the <b>THC</b> co treated <strong>C6</strong> cells.
+C6	drug	cocaine	29475069	For that, we used a <strong>C6</strong> glioblastoma cells and evaluated cell death, oxygen reactive species induction, oxidation of macromolecules as membrane lipids and DNA and loss of mitochondrial membrane potential after <b>cocaine</b> exposure.
+C6	drug	cocaine	29475069	The results showed that <b>cocaine</b> can decrease cellular viability in a dose dependent way in the <strong>C6</strong> cell immortalized and astrocytes primary culture.
+C6	drug	opioid	25330195	In this work, a therapeutic concentration of <b>morphine</b> partially protected the cellular viability of cells from a <strong>C6</strong> glioma cell line exposed to methylmercury.
+C6	drug	cocaine	25174449	Milk thistle seed extract protects rat <strong>C6</strong> astroglial cells from acute <b>cocaine</b> toxicity.
+C6	drug	opioid	24462800	Using this approach, we studied naïve and activated B cells specific for structurally related model haptens based on derivatization of the morphinan structure at the <strong>C6</strong> position on <b>oxycodone</b> or at the C8 position on <b>hydrocodone</b>, and showing different pre clinical efficacy against the prescription <b>opioid</b> <b>oxycodone</b>.
+C6	drug	opioid	24462800	Prior to vaccination, naïve B cells exhibited relatively higher affinity for the more effective <strong>C6</strong> derivatized <b>oxycodone</b> based hapten (6OXY) and the 6OXY specific naïve B cell population contained a higher number of B cells with greater affinity for free <b>oxycodone</b>.
+C6	drug	cocaine	22735768	Effects of chronic <b>cocaine</b> in rat <strong>C6</strong> astroglial cells.
+C6	drug	opioid	22583811	<b>Morphine</b> (M) and <b>oxycodone</b> (OXY) haptens were conjugated to keyhole limpet hemocyanin (KLH) through tetraglycine (Gly)(4) linkers at the <strong>C6</strong> position.
+C6	drug	cocaine	21545090	First syntheses of <strong>C6</strong>,7 and C7 enantiopure <b>cocaine</b> analogues were achieved from D ( ) ribose via a trans acetonide controlled endo selective intramolecular nitrone alkene cycloaddition (INAC) as the key step.
+C6	drug	alcohol	20837132	Acute <b>ethanol</b> exposure disrupts actin cytoskeleton and generates reactive oxygen species in <strong>c6</strong> cells.
+C6	drug	alcohol	20837132	Therefore the aim of the present study was to analyze the short term effects of <b>ethanol</b> (50, 100 and 200 mM) on the cytoskeleton of <strong>C6</strong> glioma cells.
+C6	drug	alcohol	20837132	Here we report that acute <b>ethanol</b> exposure profoundly disrupts the actin cytoskeleton in <strong>C6</strong> cells decreasing stress fiber formation and downregulating RhoA and vinculin immunocontent.
+C6	drug	alcohol	20837132	Our results show that <b>ethanol</b> at concentrations described to be toxic to the central nervous system was able to target the cytoskeleton of <strong>C6</strong> cells and this effect could be related with increased ROS generation.
+C6	drug	cocaine	19757036	<b>Cocaine</b> induces alterations in mitochondrial membrane potential and dual cell cycle arrest in rat <strong>c6</strong> astroglioma cells.
+C6	drug	opioid	19368530	examined whether treatment of <strong>C6</strong> glioma cells with mu <b>opioid</b> receptor agonists produced constitutively active mu <b>opioid</b> receptors or other commonly reported adaptations to prolonged agonist treatment.
+C6	drug	alcohol	19220294	Neutral antagonist activity of <b>naltrexone</b> and 6beta naltrexol in naïve and opioid dependent <strong>C6</strong> cells expressing a mu opioid receptor.
+C6	drug	opioid	19220294	Neutral antagonist activity of naltrexone and 6beta naltrexol in naïve and <b>opioid</b> dependent <strong>C6</strong> cells expressing a mu <b>opioid</b> receptor.
+C6	drug	opioid	19220294	<strong>C6</strong> glioma and HEK293 cells expressing mu <b>opioid</b> receptors were used.
+C6	drug	nicotine	18460644	The current study evaluated a new series of N,N' alkane diyl bis 3 picolinium (bAPi) analogs with <strong>C6</strong> C12 methylene linkers as nicotinic acetylcholine receptor (nAChR) antagonists, for <b>nicotine</b> evoked [3H]dopamine (DA) overflow, for blood brain barrier choline transporter affinity, and for attenuation of discriminative stimulus and locomotor stimulant effects of <b>nicotine</b>.
+C6	drug	nicotine	18460644	With the exception of <strong>C6</strong>, all analogs inhibited <b>nicotine</b> evoked [3H]DA overflow (IC50 = 2 nM 6 microM; Imax = 54 64%), with N,N' dodecane 1,12 diyl bis 3 picolinium dibromide (bPiDDB; C12) being most potent.
+C6	drug	opioid	17640470	The rat model of <b>morphine</b> dependence and withdrawal and rat <strong>C6</strong> glioma cells in culture were used.
+C6	addiction	dependence	17640470	The rat model of morphine <b>dependence</b> and withdrawal and rat <strong>C6</strong> glioma cells in culture were used.
+C6	addiction	withdrawal	17640470	The rat model of morphine dependence and <b>withdrawal</b> and rat <strong>C6</strong> glioma cells in culture were used.
+C6	drug	alcohol	17267582	Moreover, agonist pretreatment converts the neutral antagonists naloxone and <b>naltrexone</b> into inverse agonists, suppressing basal signaling, whereas analogs with reduced <strong>C6</strong> position, e.g., 6beta naltrexol, remain neutral antagonists at MOR under any condition.
+C6	drug	opioid	17267582	Moreover, agonist pretreatment converts the neutral antagonists <b>naloxone</b> and naltrexone into inverse agonists, suppressing basal signaling, whereas analogs with reduced <strong>C6</strong> position, e.g., 6beta naltrexol, remain neutral antagonists at MOR under any condition.
+C6	drug	opioid	17230639	Galpha , G , G or G were individually transiently transfected into <strong>C6</strong> glioma cells stably expressing the mu <b>opioid</b> receptor, or transiently co expressed with the mu <b>opioid</b> receptor into human embryonic kidney (HEK)293T cells.
+C6	drug	opioid	16291875	The potency to stimulate guanosine 5' O (3 [35 S]thio)triphosphate ([35S]GTPgammaS) binding and binding affinity of the various morphinans was compared in rat glioma <strong>C6</strong> cells expressing the rat mu <b>opioid</b> receptor; relative efficacy was also compared by stimulation of [35S]GTPgammaS binding in slices of rat brain thalamus.
+C6	drug	opioid	15014136	In this article, we use <strong>C6</strong> glioma cells expressing the rat mu <b>opioid</b> receptor (C6mu) to examine the hypothesis that Galphao alone can mediate mu <b>opioid</b> agonist induced adenylyl cyclase supersensitivity and that endogenous RGS proteins serve to limit the extent of this supersensitization.
+C6	drug	nicotine	14622092	The mechanism of TNFalpha mediated neuroprotection and antagonism by <b>nicotine</b> was independent of caspase 8 activation or nuclear factor kappa B translocation in neurons but <strong>C6</strong> ceramide addition to neuronal cultures subsequently exposed to NMDA mimicked the neuroprotective effect of TNFalpha and, like TNFalpha, it was antagonized by cotreatment with <b>nicotine</b>.
+C6	drug	alcohol	11454939	Cytokine induced iNOS expression in <strong>C6</strong> glial cells: transcriptional inhibition by <b>ethanol</b>.
+C6	drug	alcohol	11454939	The effect of cytokines, lipopolysaccharide, and <b>ethanol</b> on inducible nitric oxide synthase (iNOS) expression was studied in <strong>C6</strong> glial cells.
+C6	drug	alcohol	11454939	<b>Ethanol</b> is known to suppress iNOS expression in <strong>C6</strong> cells induced by a phorbol ester plus lipopolysaccharide.
+C6	drug	alcohol	11454939	Therefore, <strong>C6</strong> cells stably expressing 1846 and 526 base fragments of the rat iNOS gene promoter fused to a luciferase reporter gene were prepared and characterized and used to study the effect of <b>ethanol</b> on iNOS promoter activity.
+C6	drug	alcohol	11454939	Promoter activity in stable transfected <strong>C6</strong> cells was inhibited by <b>ethanol</b> exposure with a similar concentration dependence as observed for inhibition of nitrite production, indicating that iNOS inhibition by <b>ethanol</b> is transcriptional.
+C6	addiction	dependence	11454939	Promoter activity in stable transfected <strong>C6</strong> cells was inhibited by ethanol exposure with a similar concentration <b>dependence</b> as observed for inhibition of nitrite production, indicating that iNOS inhibition by ethanol is transcriptional.
+C6	drug	alcohol	10099327	Concerning the specificity behavior of the enzyme, a bimodal pattern was observed for the deacylation rate dependence on the <b>alcohol</b> chain length, with the highest values for hexanol (<strong>C6</strong>) and decanol (C10).
+C6	addiction	dependence	10099327	Concerning the specificity behavior of the enzyme, a bimodal pattern was observed for the deacylation rate <b>dependence</b> on the alcohol chain length, with the highest values for hexanol (<strong>C6</strong>) and decanol (C10).
+C6	drug	opioid	9366464	In addition, <strong>C6</strong> glioma cells with either mu, delta, or kappa receptors stably introduced were exposed to <b>opioids</b> and MAPK activation determined by in vitro activation assay or antibody detection of activated forms.
+C6	drug	alcohol	1530131	<b>Ethanol</b> inhibits <strong>C6</strong> cell growth: fetal <b>alcohol</b> syndrome model.
+C6	drug	alcohol	1530131	We report the dose dependent inhibition by <b>ethanol</b> of the growth of a glioma derived cell line, <strong>C6</strong> cells; the effects occur at <b>ethanol</b> concentrations commonly encountered in the blood during human intoxication.
+C6	addiction	intoxication	1530131	We report the dose dependent inhibition by ethanol of the growth of a glioma derived cell line, <strong>C6</strong> cells; the effects occur at ethanol concentrations commonly encountered in the blood during human <b>intoxication</b>.
+C6	drug	alcohol	1530131	The results demonstrate that <strong>C6</strong> cells are a model for the study of the effects of <b>ethanol</b> on nervous system cell growth.
+C6	drug	opioid	1804344	Effect of <b>morphine</b> applied to the spinal cord segments L4 S2 or <strong>C6</strong> tI on pressor reflexes evoked by supramaximal stimulation of radial and tibial nerve with low frequency (I 2 Hz) was studied in anesthetized cats.
+C6	drug	opioid	1804344	When applied to <strong>C6</strong> tI segments, <b>morphine</b> did not suppress the pressor reflexes to the tibial nerve stimulation while reflexes to the radial nerve signals were decreased considerably.
+C6	drug	opioid	2823987	Influence of <b>opioids</b> on beta receptors down regulation: studies in cultured <strong>C6</strong> glioma cells.
+C6	drug	opioid	2823987	Rat <strong>C6</strong> glioma cells do not have <b>opioid</b> receptors or, at least, the number of these receptors is very low, but cell exposure to desmethylimipramine (DMI) causes expression of functional <b>opioid</b> receptors as indicated by the increased [3H]DHM binding and by the acquired ability of <b>opioids</b> to inhibit ISO stimulated cAMP accumulation.
+C6	drug	nicotine	3110835	Clinical evidence suggests that <b>smoking</b> cessation would be facilitated by the administration of a nicotinic antagonist having a selective action on central nicotinic cholinoceptors of the <strong>C6</strong> (ganglionic) type.
+NDUFS7	drug	opioid	31689290	There were 15,143 respondents (27.5% [95% CI 27.0 28.0], corresponding to 32.8 million individuals) who used prescription <b>opioids</b> in the previous year, including 21.0% (95% <strong>CI 20</strong>.4 21.6) of adolescents and 32.2% (95% CI 31.4 33.0) of young adults.
+NDUFS7	drug	nicotine	30637110	Nearly one in four (23.8%, 95% <strong>CI 20</strong>.2 27.8%) male drinkers screened positive for AUD, and AUDIT scores were associated with age, caste, marital status, occupation, <b>tobacco</b> use, depression, functional status and suicidal ideation.
+NDUFS7	drug	alcohol	25735959	Specifically, the highest mean prevalence of current psychiatric disorders was for nicotine dependence (56.4%, 95% CI 35.7 75.2) and major depressive disorder (29.9%, 95% <strong>CI 20</strong>.5 41.3), with smaller estimates for <b>alcohol</b> abuse (18.2%, 95% CI 13.4 24.2), <b>alcohol</b> dependence (15.2%, 95% CI 10.2 22.0), social phobia (14.9%, 95% CI 2.0 59.8), generalised anxiety disorder (14.4%, 95% CI 3.9 40.8), panic disorder (13.7%, 95% CI 6.7 26.0), post traumatic stress disorder (12.3%, 95% CI 3.4 35.7), cannabis use disorder (11.5%, 95% CI 4.8 25.0), attention deficit hyperactivity disorder (9.3%, 95% CI 4.1 19.6), adjustment disorder (9.2%, 95% CI 4.8 17.2), bipolar disorder (8.8%, 95% CI 4.4 17.1) and obsessive compulsive disorder (8.2%, 95% CI 3.4 18.6).
+NDUFS7	drug	cannabinoid	25735959	Specifically, the highest mean prevalence of current psychiatric disorders was for nicotine dependence (56.4%, 95% CI 35.7 75.2) and major depressive disorder (29.9%, 95% <strong>CI 20</strong>.5 41.3), with smaller estimates for alcohol abuse (18.2%, 95% CI 13.4 24.2), alcohol dependence (15.2%, 95% CI 10.2 22.0), social phobia (14.9%, 95% CI 2.0 59.8), generalised anxiety disorder (14.4%, 95% CI 3.9 40.8), panic disorder (13.7%, 95% CI 6.7 26.0), post traumatic stress disorder (12.3%, 95% CI 3.4 35.7), <b>cannabis</b> use disorder (11.5%, 95% CI 4.8 25.0), attention deficit hyperactivity disorder (9.3%, 95% CI 4.1 19.6), adjustment disorder (9.2%, 95% CI 4.8 17.2), bipolar disorder (8.8%, 95% CI 4.4 17.1) and obsessive compulsive disorder (8.2%, 95% CI 3.4 18.6).
+NDUFS7	drug	nicotine	25735959	Specifically, the highest mean prevalence of current psychiatric disorders was for <b>nicotine</b> dependence (56.4%, 95% CI 35.7 75.2) and major depressive disorder (29.9%, 95% <strong>CI 20</strong>.5 41.3), with smaller estimates for alcohol abuse (18.2%, 95% CI 13.4 24.2), alcohol dependence (15.2%, 95% CI 10.2 22.0), social phobia (14.9%, 95% CI 2.0 59.8), generalised anxiety disorder (14.4%, 95% CI 3.9 40.8), panic disorder (13.7%, 95% CI 6.7 26.0), post traumatic stress disorder (12.3%, 95% CI 3.4 35.7), cannabis use disorder (11.5%, 95% CI 4.8 25.0), attention deficit hyperactivity disorder (9.3%, 95% CI 4.1 19.6), adjustment disorder (9.2%, 95% CI 4.8 17.2), bipolar disorder (8.8%, 95% CI 4.4 17.1) and obsessive compulsive disorder (8.2%, 95% CI 3.4 18.6).
+NDUFS7	addiction	addiction	25735959	Specifically, the highest mean prevalence of current psychiatric disorders was for nicotine dependence (56.4%, 95% CI 35.7 75.2) and major depressive disorder (29.9%, 95% <strong>CI 20</strong>.5 41.3), with smaller estimates for alcohol abuse (18.2%, 95% CI 13.4 24.2), alcohol dependence (15.2%, 95% CI 10.2 22.0), social phobia (14.9%, 95% CI 2.0 59.8), generalised anxiety disorder (14.4%, 95% CI 3.9 40.8), panic disorder (13.7%, 95% CI 6.7 26.0), post traumatic stress disorder (12.3%, 95% CI 3.4 35.7), cannabis use disorder (11.5%, 95% CI 4.8 25.0), attention deficit hyperactivity disorder (9.3%, 95% CI 4.1 19.6), adjustment disorder (9.2%, 95% CI 4.8 17.2), bipolar disorder (8.8%, 95% CI 4.4 17.1) and obsessive <b>compulsive</b> disorder (8.2%, 95% CI 3.4 18.6).
+NDUFS7	addiction	dependence	25735959	Specifically, the highest mean prevalence of current psychiatric disorders was for nicotine <b>dependence</b> (56.4%, 95% CI 35.7 75.2) and major depressive disorder (29.9%, 95% <strong>CI 20</strong>.5 41.3), with smaller estimates for alcohol abuse (18.2%, 95% CI 13.4 24.2), alcohol <b>dependence</b> (15.2%, 95% CI 10.2 22.0), social phobia (14.9%, 95% CI 2.0 59.8), generalised anxiety disorder (14.4%, 95% CI 3.9 40.8), panic disorder (13.7%, 95% CI 6.7 26.0), post traumatic stress disorder (12.3%, 95% CI 3.4 35.7), cannabis use disorder (11.5%, 95% CI 4.8 25.0), attention deficit hyperactivity disorder (9.3%, 95% CI 4.1 19.6), adjustment disorder (9.2%, 95% CI 4.8 17.2), bipolar disorder (8.8%, 95% CI 4.4 17.1) and obsessive compulsive disorder (8.2%, 95% CI 3.4 18.6).
+NDUFS7	addiction	sensitization	15005763	SM <b>sensitization</b> was found in 104 cases (weighted value 24.4%, 95% <strong>CI 20</strong>.6 28.2).
+NDUFS7	drug	alcohol	14672249	Compared with their non psychotic counterparts, these MAMP users were younger at first MAMP use, used larger amounts of MAMP, had a significantly higher mean <strong>PSST</strong> score, and higher rates of major depressive disorder, <b>alcohol</b> dependence and antisocial personality disorder.
+NDUFS7	addiction	dependence	14672249	Compared with their non psychotic counterparts, these MAMP users were younger at first MAMP use, used larger amounts of MAMP, had a significantly higher mean <strong>PSST</strong> score, and higher rates of major depressive disorder, alcohol <b>dependence</b> and antisocial personality disorder.
+MECP2	drug	cocaine	32457807	However, increasing reports indicate that some <strong>MECP2</strong> mutations may also present various neuropsychiatric phenotypes, including intellectual disability, autism spectrum disorder, depression, <b>cocaine</b> addiction, and schizophrenia in both males and females, suggesting varied clinical expressivity in some <strong>MECP2</strong> mutations.
+MECP2	addiction	addiction	32457807	However, increasing reports indicate that some <strong>MECP2</strong> mutations may also present various neuropsychiatric phenotypes, including intellectual disability, autism spectrum disorder, depression, cocaine <b>addiction</b>, and schizophrenia in both males and females, suggesting varied clinical expressivity in some <strong>MECP2</strong> mutations.
+MECP2	drug	cocaine	32457073	We identified 133 genes differentially expressed between CUD case patients and <b>cocaine</b> free control subjects, including previously implicated candidates for <b>cocaine</b> use/addiction (FOSB, ARC, KCNJ9/GIRK3, NR4A2, JUNB, and <strong>MECP2</strong>).
+MECP2	addiction	addiction	32457073	We identified 133 genes differentially expressed between CUD case patients and cocaine free control subjects, including previously implicated candidates for cocaine use/<b>addiction</b> (FOSB, ARC, KCNJ9/GIRK3, NR4A2, JUNB, and <strong>MECP2</strong>).
+MECP2	drug	cocaine	29859319	<b>Cocaine</b> mediated activation of microglia and microglial <strong>MeCP2</strong> and BDNF production.
+MECP2	drug	cocaine	29859319	Methyl CpG binding protein 2 (<strong>MeCP2</strong>) binds to the promoter region of BDNF to negatively regulate its expression and <b>cocaine</b> can recruit <strong>MeCP2</strong> to alter the expression of genes such as BDNF that are involved in synaptic plasticity.
+MECP2	drug	cocaine	29859319	<strong>Methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) binds to the promoter region of BDNF to negatively regulate its expression and <b>cocaine</b> can recruit <strong>MeCP2</strong> to alter the expression of genes such as BDNF that are involved in synaptic plasticity.
+MECP2	drug	cocaine	29859319	The current study assessed the effects of intravenous <b>cocaine</b> self administration on microglial activation, and <strong>MeCP2</strong> and BDNF expression in reward regions of the brain in vivo, as well as determined specific effects of <b>cocaine</b> exposure on <strong>MeCP2</strong> and BDNF expression in human primary neurons and microglia.
+MECP2	addiction	reward	29859319	The current study assessed the effects of intravenous cocaine self administration on microglial activation, and <strong>MeCP2</strong> and BDNF expression in <b>reward</b> regions of the brain in vivo, as well as determined specific effects of cocaine exposure on <strong>MeCP2</strong> and BDNF expression in human primary neurons and microglia.
+MECP2	drug	cocaine	29859319	The results from this study highlight a distinct molecular pathway in microglia through which <b>cocaine</b> increases BDNF, including the phosphorylation of <strong>MeCP2</strong> its subsequent translocation from the nucleus to the cytosol, which frees the BDNF promoter and permits its transcriptional activation.
+MECP2	drug	cocaine	29859319	Results from these studies show for the first time that <b>cocaine</b> self administration increases microglial activation, and that microglial <strong>MeCP2</strong> is a sensitive target of <b>cocaine</b> resulting in increased release of BDNF from microglia, and possibly contributing to <b>cocaine</b> induced synaptic plasticity.
+MECP2	addiction	aversion	28116477	Regulation and function of <strong>MeCP2</strong> Ser421 phosphorylation in U50488 induced conditioned place <b>aversion</b> in mice.
+MECP2	addiction	reward	28116477	Phosphorylation of the methyl DNA binding protein <strong>MeCP2</strong> at Ser421 (pMeCP2 S421) is induced in corticolimbic brain regions during exposure to drugs of abuse and modulates <b>reward</b> driven behaviors.
+MECP2	drug	opioid	28074855	MiR 218 targets <strong>MeCP2</strong> and inhibits <b>heroin</b> seeking behavior.
+MECP2	addiction	relapse	28074855	MiR 218 targets <strong>MeCP2</strong> and inhibits heroin <b>seeking</b> behavior.
+MECP2	drug	opioid	28074855	These data reveal a functional role of miR 218 and its target, <strong>MeCP2</strong>, in the regulation of <b>heroin</b> induced behavioral plasticity.
+MECP2	drug	cocaine	27392631	Increased <b>cocaine</b> induced conditioned place preference during periadolescence in maternally separated male BALB/c mice: the role of cortical BDNF, microRNA 212, and <strong>MeCP2</strong>.
+MECP2	drug	cocaine	27392631	MicroRNA 212 (miR 212) and methyl CpG binding protein 2 (<strong>MeCP2</strong>) have recently emerged as key regulators of brain derived neurotrophic factor (BDNF) signaling during the acquisition and maintenance of <b>cocaine</b> seeking behaviors.
+MECP2	addiction	relapse	27392631	MicroRNA 212 (miR 212) and methyl CpG binding protein 2 (<strong>MeCP2</strong>) have recently emerged as key regulators of brain derived neurotrophic factor (BDNF) signaling during the acquisition and maintenance of cocaine <b>seeking</b> behaviors.
+MECP2	drug	cocaine	27392631	MicroRNA 212 (miR 212) and <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) have recently emerged as key regulators of brain derived neurotrophic factor (BDNF) signaling during the acquisition and maintenance of <b>cocaine</b> seeking behaviors.
+MECP2	addiction	relapse	27392631	MicroRNA 212 (miR 212) and <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) have recently emerged as key regulators of brain derived neurotrophic factor (BDNF) signaling during the acquisition and maintenance of cocaine <b>seeking</b> behaviors.
+MECP2	drug	cocaine	27392631	We therefore investigated the effect of maternal separation (MS) on <b>cocaine</b> induced conditioned place preference (CPP) during periadolescence and how this influences miR 212, <strong>Mecp2</strong>, and Bdnf expressions in the prefrontal cortex.
+MECP2	addiction	reward	27392631	We therefore investigated the effect of maternal separation (MS) on cocaine induced conditioned place preference (<b>CPP</b>) during periadolescence and how this influences miR 212, <strong>Mecp2</strong>, and Bdnf expressions in the prefrontal cortex.
+MECP2	drug	cocaine	27392631	In contrast, increased <strong>Mecp2</strong> expression was found after CPP test, suggesting an opposing relationship between miR 212 and <strong>Mecp2</strong> expression following <b>cocaine</b> place preference acquisition.
+MECP2	addiction	reward	27392631	In contrast, increased <strong>Mecp2</strong> expression was found after <b>CPP</b> test, suggesting an opposing relationship between miR 212 and <strong>Mecp2</strong> expression following cocaine place preference acquisition.
+MECP2	drug	cocaine	27392631	Together, our results suggest that early life stress can enhance the motivational salience for <b>cocaine</b> paired cues during periadolescence, and that altered expression of miR 212, <strong>Mecp2</strong>, and Bdnf in the prefrontal cortex is involved in this process.
+MECP2	drug	opioid	27380026	Moreover, the regulation of both oprm1 and of the cluster promoter is mediated by <strong>MeCP2</strong>, acting as a transcriptional repressor on methylated DNA after prolonged <b>morphine</b> administration.
+MECP2	drug	amphetamine	27312406	Interactions between Early Life Stress, Nucleus Accumbens <strong>MeCP2</strong> Expression, and <b>Methamphetamine</b> Self Administration in Male Rats.
+MECP2	drug	amphetamine	27312406	In addition, we show new evidence that both ELS and <b>methamphetamine</b> SA alter the expression of the epigenetic regulator methyl CpG binding protein 2 (<strong>MeCP2</strong>) in key brain reward regions, particularly in the nucleus accumbens (NAc) core.
+MECP2	addiction	reward	27312406	In addition, we show new evidence that both ELS and methamphetamine SA alter the expression of the epigenetic regulator methyl CpG binding protein 2 (<strong>MeCP2</strong>) in key brain <b>reward</b> regions, particularly in the nucleus accumbens (NAc) core.
+MECP2	drug	amphetamine	27312406	In addition, we show new evidence that both ELS and <b>methamphetamine</b> SA alter the expression of the epigenetic regulator <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) in key brain reward regions, particularly in the nucleus accumbens (NAc) core.
+MECP2	addiction	reward	27312406	In addition, we show new evidence that both ELS and methamphetamine SA alter the expression of the epigenetic regulator <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) in key brain <b>reward</b> regions, particularly in the nucleus accumbens (NAc) core.
+MECP2	drug	amphetamine	27312406	In turn, viral mediated knockdown of <strong>MeCP2</strong> expression in the NAc core reduces <b>methamphetamine</b> SA, as well as saccharin intake.
+MECP2	drug	amphetamine	27312406	Furthermore, NAc core <strong>MeCP2</strong> knockdown reduces <b>methamphetamine</b>, but not saccharin, SA on a progressive ratio schedule of reinforcement.
+MECP2	addiction	reward	27312406	Furthermore, NAc core <strong>MeCP2</strong> knockdown reduces methamphetamine, but not saccharin, SA on a progressive ratio schedule of <b>reinforcement</b>.
+MECP2	drug	amphetamine	27312406	These data suggest that NAc core <strong>MeCP2</strong> may be recruited by both ELS and <b>methamphetamine</b> SA and promote the development of certain aspects of drug abuse related behavior.
+MECP2	drug	amphetamine	27312406	Taken together, functional interactions between ELS, <b>methamphetamine</b> SA, and the expression of <strong>MeCP2</strong> in the NAc may represent novel mechanisms that can ultimately be targeted for intervention in individuals with adverse early life experiences who are at risk for developing substance use disorders.
+MECP2	drug	cocaine	27213019	We showcase all of the above in two particular important neurological functional alterations in the brain: depression (major depressive disorder [MDD]) and <b>cocaine</b> addiction, both of which affect the <strong>MeCP2</strong> homeostasis and result in significant changes in the overall levels of these epigenetic marks.
+MECP2	addiction	addiction	27213019	We showcase all of the above in two particular important neurological functional alterations in the brain: depression (major depressive disorder [MDD]) and cocaine <b>addiction</b>, both of which affect the <strong>MeCP2</strong> homeostasis and result in significant changes in the overall levels of these epigenetic marks.
+MECP2	drug	alcohol	26610727	Rats exposed to ELS were more sensitive to <b>ethanol</b> induced changes in Vglut expression in the VTA, Acb, and dStr and in Dnmt1 and <strong>Mecp2</strong> expression in the striatal regions.
+MECP2	drug	amphetamine	26416230	Melatonin treatment during the incubation of sensitization attenuates <b>methamphetamine</b> induced locomotor sensitization and <strong>MeCP2</strong> expression.
+MECP2	addiction	sensitization	26416230	Melatonin treatment during the incubation of <b>sensitization</b> attenuates methamphetamine induced locomotor <b>sensitization</b> and <strong>MeCP2</strong> expression.
+MECP2	addiction	sensitization	26416230	Our results suggest that melatonin treatment during the incubation of <b>sensitization</b> attenuates MA induced expression of <b>sensitization</b> and decreases <strong>MeCP2</strong> expression in vivo.
+MECP2	drug	opioid	25716866	Persistent pain maintains <b>morphine</b> seeking behavior after <b>morphine</b> withdrawal through reduced <strong>MeCP2</strong> repression of GluA1 in rat central amygdala.
+MECP2	addiction	relapse	25716866	Persistent pain maintains morphine <b>seeking</b> behavior after morphine withdrawal through reduced <strong>MeCP2</strong> repression of GluA1 in rat central amygdala.
+MECP2	addiction	withdrawal	25716866	Persistent pain maintains morphine seeking behavior after morphine <b>withdrawal</b> through reduced <strong>MeCP2</strong> repression of GluA1 in rat central amygdala.
+MECP2	drug	opioid	25716866	Furthermore, viral overexpression of CeA <strong>MeCP2</strong> repressed the GluA1 level and eliminated the maintenance of <b>morphine</b> seeking behavior after <b>morphine</b> withdrawal.
+MECP2	addiction	relapse	25716866	Furthermore, viral overexpression of CeA <strong>MeCP2</strong> repressed the GluA1 level and eliminated the maintenance of morphine <b>seeking</b> behavior after morphine withdrawal.
+MECP2	addiction	withdrawal	25716866	Furthermore, viral overexpression of CeA <strong>MeCP2</strong> repressed the GluA1 level and eliminated the maintenance of morphine seeking behavior after morphine <b>withdrawal</b>.
+MECP2	drug	opioid	25716866	These results suggest direct <strong>MeCp2</strong> repression of GluA1 function as a likely mechanism for <b>morphine</b> seeking behavior maintained by long lasting affective pain after <b>morphine</b> withdrawal.
+MECP2	addiction	relapse	25716866	These results suggest direct <strong>MeCp2</strong> repression of GluA1 function as a likely mechanism for morphine <b>seeking</b> behavior maintained by long lasting affective pain after morphine withdrawal.
+MECP2	addiction	withdrawal	25716866	These results suggest direct <strong>MeCp2</strong> repression of GluA1 function as a likely mechanism for morphine seeking behavior maintained by long lasting affective pain after morphine <b>withdrawal</b>.
+MECP2	drug	alcohol	25656446	Changes in the methylation status of DAT, SERT, and <strong>MeCP2</strong> gene promoters in the blood cell in families exposed to <b>alcohol</b> during the periconceptional period.
+MECP2	drug	alcohol	25656446	These findings suggest that periconceptional <b>alcohol</b> intake may cause epigenetic changes in specific locus of parental and newborn genomes as follows: <b>Alcohol</b> consumption decreases the methylation level of the DAT promoter region of the parent themselves, maternal <b>alcohol</b> drinking during the periconceptional period decreases the methylation level of the SERT promoter region of newborns, and maternal <b>alcohol</b> consumption increases the methylation level of the <strong>MeCP2</strong> promoter region of newborns.
+MECP2	drug	alcohol	25620416	<b>Ethanol</b> deregulates <strong>Mecp2</strong>/<strong>MeCP2</strong> in differentiating neural stem cells via interplay between 5 methylcytosine and 5 hydroxymethylcytosine at the <strong>Mecp2</strong> regulatory elements.
+MECP2	drug	alcohol	25620416	<strong>MeCP2</strong> expression is affected by different environmental insults including <b>alcohol</b> exposure.
+MECP2	drug	alcohol	25620416	Accumulating evidence supports the role of aberrant <strong>MeCP2</strong> expression in <b>ethanol</b> exposure induced neurological symptoms.
+MECP2	drug	alcohol	25620416	However, the underlying molecular mechanisms of <b>ethanol</b> induced <strong>MeCP2</strong> deregulation remain elusive.
+MECP2	drug	alcohol	25620416	To study the effect of <b>ethanol</b> on <strong>Mecp2</strong>/<strong>MeCP2</strong> expression during neurodifferentiation, we established an in vitro model of <b>ethanol</b> exposure, using differentiating embryonic brain derived neural stem cells (NSC).
+MECP2	drug	alcohol	25620416	Here, we studied whether altered DNA methylation at these REs is associated with the <strong>Mecp2</strong>/<strong>MeCP2</strong> misexpression induced by <b>ethanol</b>.
+MECP2	drug	alcohol	25620416	Binge like and continuous <b>ethanol</b> exposure upregulated <strong>Mecp2</strong>/<strong>MeCP2</strong>, while <b>ethanol</b> withdrawal downregulated its expression.
+MECP2	addiction	intoxication	25620416	<b>Binge</b> like and continuous ethanol exposure upregulated <strong>Mecp2</strong>/<strong>MeCP2</strong>, while ethanol withdrawal downregulated its expression.
+MECP2	addiction	withdrawal	25620416	Binge like and continuous ethanol exposure upregulated <strong>Mecp2</strong>/<strong>MeCP2</strong>, while ethanol <b>withdrawal</b> downregulated its expression.
+MECP2	drug	alcohol	25620416	DNA methylation analysis by methylated DNA immunoprecipitation indicated that increased 5 hydroxymethylcytosine (5hmC) and decreased 5 methylcytosine (5mC) enrichment at specific REs were associated with upregulated <strong>Mecp2</strong>/<strong>MeCP2</strong> following continuous <b>ethanol</b> exposure.
+MECP2	drug	alcohol	25620416	The reduced <strong>Mecp2</strong>/<strong>MeCP2</strong> expression upon <b>ethanol</b> withdrawal was associated with reduced 5hmC and increased 5mC enrichment at these REs.
+MECP2	addiction	withdrawal	25620416	The reduced <strong>Mecp2</strong>/<strong>MeCP2</strong> expression upon ethanol <b>withdrawal</b> was associated with reduced 5hmC and increased 5mC enrichment at these REs.
+MECP2	drug	alcohol	25620416	Taken together, our data represent an epigenetic mechanism for <b>ethanol</b> mediated misexpression of <strong>Mecp2</strong>/<strong>MeCP2</strong> in differentiating embryonic brain cells.
+MECP2	drug	alcohol	25620416	We also show the potential role of DNA methylation and <strong>MeCP2</strong> in <b>alcohol</b> related neurological disorders, specifically Fetal <b>Alcohol</b> Spectrum Disorders.
+MECP2	drug	opioid	25392083	The association of <strong>MeCP2</strong> with BDNF promoters during spontaneous <b>morphine</b> withdrawal did not change.
+MECP2	addiction	withdrawal	25392083	The association of <strong>MeCP2</strong> with BDNF promoters during spontaneous morphine <b>withdrawal</b> did not change.
+MECP2	drug	opioid	24990928	<strong>MeCP2</strong> repression of G9a in regulation of pain and <b>morphine</b> reward.
+MECP2	addiction	reward	24990928	<strong>MeCP2</strong> repression of G9a in regulation of pain and morphine <b>reward</b>.
+MECP2	drug	opioid	24990928	Both persistent pain and repeated <b>morphine</b> upregulated the transcriptional regulator <strong>MeCP2</strong> in mouse central nucleus of the amygdala (CeA).
+MECP2	drug	opioid	24990928	These results suggest that <strong>MeCP2</strong> directly represses G9a as a shared mechanism in central amygdala for regulation of emotional responses to pain and <b>opioid</b> reward, and for their behavioral interaction.
+MECP2	addiction	reward	24990928	These results suggest that <strong>MeCP2</strong> directly represses G9a as a shared mechanism in central amygdala for regulation of emotional responses to pain and opioid <b>reward</b>, and for their behavioral interaction.
+MECP2	drug	cocaine	24936739	Differential regulation of <strong>MeCP2</strong> and PP1 in passive or voluntary administration of <b>cocaine</b> or food.
+MECP2	drug	cocaine	24936739	We have initially shown that <b>cocaine</b> increases the expression of the chromatin remodeling protein methyl CpG binding protein 2 (<strong>MeCP2</strong>) and characterized the protein phosphatase 1Cβ (PP1Cβ) gene, as repressed by passive i.p.
+MECP2	drug	cocaine	24936739	We have initially shown that <b>cocaine</b> increases the expression of the chromatin remodeling protein <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) and characterized the protein phosphatase 1Cβ (PP1Cβ) gene, as repressed by passive i.p.
+MECP2	drug	cocaine	24936739	<b>cocaine</b> injections through a <strong>Mecp2</strong> mediated mechanism involving de novo DNA methylation.
+MECP2	drug	cocaine	24936739	<b>cocaine</b> intake was found to induce <strong>Mecp2</strong> and to repress PP1Cβ in the prefrontal cortex and the caudate putamen.
+MECP2	addiction	reward	24671997	The methyl DNA binding protein <strong>MeCP2</strong> is emerging as an important regulator of drug <b>reinforcement</b> processes.
+MECP2	addiction	addiction	24671997	Psychostimulants induce phosphorylation of <strong>MeCP2</strong> at Ser421; however, the functional significance of this posttranslational modification for <b>addictive</b> like behaviors was unknown.
+MECP2	drug	amphetamine	24671997	Here we show that <strong>MeCP2</strong> Ser421Ala knock in mice display both a reduced threshold for the induction of locomotor sensitization by investigator administered <b>amphetamine</b> and enhanced behavioral sensitivity to the reinforcing properties of self administered cocaine.
+MECP2	drug	cocaine	24671997	Here we show that <strong>MeCP2</strong> Ser421Ala knock in mice display both a reduced threshold for the induction of locomotor sensitization by investigator administered amphetamine and enhanced behavioral sensitivity to the reinforcing properties of self administered <b>cocaine</b>.
+MECP2	addiction	reward	24671997	Here we show that <strong>MeCP2</strong> Ser421Ala knock in mice display both a reduced threshold for the induction of locomotor sensitization by investigator administered amphetamine and enhanced behavioral sensitivity to the <b>reinforcing</b> properties of self administered cocaine.
+MECP2	addiction	sensitization	24671997	Here we show that <strong>MeCP2</strong> Ser421Ala knock in mice display both a reduced threshold for the induction of locomotor <b>sensitization</b> by investigator administered amphetamine and enhanced behavioral sensitivity to the reinforcing properties of self administered cocaine.
+MECP2	addiction	addiction	24671997	These data show that phosphorylation of <strong>MeCP2</strong> at Ser421 functions to limit the circuit plasticities in the nucleus accumbens that underlie <b>addictive</b> like behaviors.
+MECP2	drug	amphetamine	23785337	The Effects of Maternal Separation on Adult <b>Methamphetamine</b> Self Administration, Extinction, Reinstatement, and <strong>MeCP2</strong> Immunoreactivity in the Nucleus Accumbens.
+MECP2	addiction	relapse	23785337	The Effects of Maternal Separation on Adult Methamphetamine Self Administration, Extinction, <b>Reinstatement</b>, and <strong>MeCP2</strong> Immunoreactivity in the Nucleus Accumbens.
+MECP2	drug	cocaine	23717324	Second, miR 212 was also shown to regulate <b>cocaine</b> intake by repressing striatal expression of methyl CpG binding protein 2 (<strong>MeCP2</strong>), consequently decreasing protein levels of brain derived neurotrophic factor (BDNF).
+MECP2	drug	cocaine	23717324	Second, miR 212 was also shown to regulate <b>cocaine</b> intake by repressing striatal expression of <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>), consequently decreasing protein levels of brain derived neurotrophic factor (BDNF).
+MECP2	drug	cocaine	23717324	The concerted actions of miR 212 on striatal CREB and <strong>MeCP2</strong>/BDNF activity greatly attenuate the motivational effects of <b>cocaine</b>.
+MECP2	drug	cocaine	23688924	<b>Cocaine</b> represses protein phosphatase 1Cβ through DNA methylation and <strong>Methyl CpG Binding Protein 2</strong> recruitment in adult rat brain.
+MECP2	drug	cocaine	23688924	Repeated <b>cocaine</b> administration was found to increase DNA methylation at the PP1Cβ gene together with its binding to <strong>Mecp2</strong> in rat caudate putamen, establishing a link between two genes involved in <b>cocaine</b> related effects and in learning and memory processes.
+MECP2	drug	alcohol	23448145	<strong>MeCP2</strong> regulates <b>ethanol</b> sensitivity and intake.
+MECP2	addiction	dependence	23448145	We observed that the methyl CpG binding protein 2 (<strong>MeCP2</strong>) was one of the few chromatin regulating genes to be differentially regulated by a history of <b>dependence</b>.
+MECP2	addiction	dependence	23448145	We observed that the <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) was one of the few chromatin regulating genes to be differentially regulated by a history of <b>dependence</b>.
+MECP2	drug	alcohol	23448145	As <strong>MeCP2</strong> has the potential of acting as a broad gene regulator, we investigated sensitivity to <b>ethanol</b> and <b>ethanol</b> drinking in <strong>MeCP2</strong>(308/) (Y) mice, which harbor a truncated <strong>MeCP2</strong> allele but have a milder phenotype than <strong>MeCP2</strong> null mice.
+MECP2	drug	alcohol	23448145	We observed that <strong>MeCP2</strong>(308/) (Y) mice were more sensitive to <b>ethanol</b>'s stimulatory and sedative effects than wild type (WT) mice, drank less <b>ethanol</b> in a limited access 2 bottle choice paradigm and did not show increased drinking after induction of dependence with exposure to CIE vapors.
+MECP2	addiction	dependence	23448145	We observed that <strong>MeCP2</strong>(308/) (Y) mice were more sensitive to ethanol's stimulatory and sedative effects than wild type (WT) mice, drank less ethanol in a limited access 2 bottle choice paradigm and did not show increased drinking after induction of <b>dependence</b> with exposure to CIE vapors.
+MECP2	drug	alcohol	23448145	<b>Alcohol</b> metabolism did not differ in <strong>MeCP2</strong>(308/) (Y) and WT mice.
+MECP2	drug	alcohol	23448145	Additionally, <strong>MeCP2</strong>(308/) (Y) mice did not differ from WT mice in <b>ethanol</b> preference in a 24 hour paradigm nor in their intake of graded solutions of saccharin or quinine, suggesting that the <strong>MeCP2</strong>(308/) (Y) mutation did not alter taste function.
+MECP2	drug	alcohol	23448145	Lastly, using the Gene Set Enrichment Analysis algorithm, we found a significant overlap in the genes regulated by <b>alcohol</b> and by <strong>MeCP2</strong>.
+MECP2	drug	alcohol	23448145	Together, these results suggest that <strong>MeCP2</strong> contributes to the regulation of <b>ethanol</b> sensitivity and drinking.
+MECP2	drug	cocaine	23375146	Decrease in <b>cocaine</b> self administration was accompanied with reduced expression of the epigenetic markers methyl CpG binding protein 2 (<strong>MeCP2</strong>) and histone deacetylase 2 (HDAC2) in dopaminergic projection areas.
+MECP2	drug	cocaine	23375146	Decrease in <b>cocaine</b> self administration was accompanied with reduced expression of the epigenetic markers <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) and histone deacetylase 2 (HDAC2) in dopaminergic projection areas.
+MECP2	drug	cocaine	23375146	Since <strong>MeCP2</strong> and HDAC2 are known to modulate dynamic functions in the adult brain, such as synaptic plasticity, our results showing that activation of the cGMP signal transduction pathway decreased both <b>cocaine</b> intake and expression of the epigenetic markers strongly suggest that the <strong>MeCP2</strong>/HDAC2 complex is involved in the analysis of the reinforcing properties of <b>cocaine</b> in the prefrontal cortex.
+MECP2	addiction	reward	23375146	Since <strong>MeCP2</strong> and HDAC2 are known to modulate dynamic functions in the adult brain, such as synaptic plasticity, our results showing that activation of the cGMP signal transduction pathway decreased both cocaine intake and expression of the epigenetic markers strongly suggest that the <strong>MeCP2</strong>/HDAC2 complex is involved in the analysis of the <b>reinforcing</b> properties of cocaine in the prefrontal cortex.
+MECP2	drug	opioid	23347952	<b>Morphine</b> withdrawal induced the phosphorylation of the epigenetic factor methyl CpG binding protein 2 (<strong>MeCP2</strong>) in Ser421 both in the LS and the NAc shell.
+MECP2	addiction	withdrawal	23347952	Morphine <b>withdrawal</b> induced the phosphorylation of the epigenetic factor methyl CpG binding protein 2 (<strong>MeCP2</strong>) in Ser421 both in the LS and the NAc shell.
+MECP2	drug	opioid	23347952	<b>Morphine</b> withdrawal induced the phosphorylation of the epigenetic factor <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) in Ser421 both in the LS and the NAc shell.
+MECP2	addiction	withdrawal	23347952	Morphine <b>withdrawal</b> induced the phosphorylation of the epigenetic factor <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) in Ser421 both in the LS and the NAc shell.
+MECP2	drug	opioid	22790874	Association of time dependent changes in mu <b>opioid</b> receptor mRNA, but not BDNF, TrkB, or <strong>MeCP2</strong> mRNA and protein expression in the rat nucleus accumbens with incubation of <b>heroin</b> craving.
+MECP2	addiction	relapse	22790874	Association of time dependent changes in mu opioid receptor mRNA, but not BDNF, TrkB, or <strong>MeCP2</strong> mRNA and protein expression in the rat nucleus accumbens with incubation of heroin <b>craving</b>.
+MECP2	drug	opioid	22790874	We investigated whether this incubation is associated with time dependent changes in brain derived neurotrophic factor (BDNF) and methyl CpG binding protein 2 (<strong>MeCP2</strong>) signaling and mu <b>opioid</b> receptor (MOR) expression in nucleus accumbens (NAc), dorsal striatum (DS), and medial prefrontal cortex (mPFC).
+MECP2	drug	opioid	22790874	We investigated whether this incubation is associated with time dependent changes in brain derived neurotrophic factor (BDNF) and <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) signaling and mu <b>opioid</b> receptor (MOR) expression in nucleus accumbens (NAc), dorsal striatum (DS), and medial prefrontal cortex (mPFC).
+MECP2	drug	opioid	22790874	We trained rats to self administer <b>heroin</b> or saline for 9 10 days and then dissected the NAc, DS, and mPFC at different abstinence days and measured mRNA and protein levels of BDNF, TrkB, and <strong>MeCP2</strong>, as well as MOR mRNA (Oprm1).
+MECP2	drug	cocaine	21704097	<b>Cocaine</b> increases phosphorylation of <strong>MeCP2</strong> in the rat striatum in vivo: a differential role of NMDA receptors.
+MECP2	addiction	addiction	21704097	As a transcriptional repressor densely expressed in limbic reward circuits of adult mammalian brains, <strong>MeCP2</strong> is recently emerging as a critical epigenetic factor in experience dependent neural plasticity and psychostimulant <b>addiction</b>.
+MECP2	addiction	reward	21704097	As a transcriptional repressor densely expressed in limbic <b>reward</b> circuits of adult mammalian brains, <strong>MeCP2</strong> is recently emerging as a critical epigenetic factor in experience dependent neural plasticity and psychostimulant addiction.
+MECP2	drug	cocaine	21704097	In this study, we investigated the regulation of <strong>MeCP2</strong> phosphorylation in the rat striatum by the psychostimulant <b>cocaine</b> in vivo.
+MECP2	drug	cocaine	21704097	We found that acute systemic injection of <b>cocaine</b> increased <strong>MeCP2</strong> phosphorylation at S421 in the rat striatum, including both the caudate putamen and the nucleus accumbens, while <b>cocaine</b> did not affect <strong>MeCP2</strong> phosphorylation in the medial prefrontal cortex.
+MECP2	drug	cocaine	21704097	The <b>cocaine</b> stimulated <strong>MeCP2</strong> phosphorylation in the nucleus accumbens was a rapid and transient event, as it was evident at 20 min and returned to normal levels 3h after drug injection.
+MECP2	drug	cocaine	21704097	Pretreatment with an N methyl d aspartate (NMDA) glutamate receptor antagonist significantly reduced the <b>cocaine</b> stimulated <strong>MeCP2</strong> phosphorylation in the caudate putamen, although not in the nucleus accumbens.
+MECP2	drug	cocaine	21704097	NMDA receptors play a region specific role in linking <b>cocaine</b> to <strong>MeCP2</strong> phosphorylation in striatal neurons in vivo.
+MECP2	addiction	reward	21326195	Methyl CpG binding protein 2 (<strong>MeCP2</strong>) can bind methylated DNA and repress transcription, and DIO mice showed increased binding of <strong>MeCP2</strong> to the MOR promoter in <b>reward</b> related regions of the brain.
+MECP2	addiction	reward	21326195	<strong>Methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) can bind methylated DNA and repress transcription, and DIO mice showed increased binding of <strong>MeCP2</strong> to the MOR promoter in <b>reward</b> related regions of the brain.
+MECP2	drug	nicotine	21166804	We measured immunohistochemically the acetylation of lysine 9 of histone H3, and the expression of phosphorylated cAMP response element binding protein, HDAC2 and <strong>methyl CpG binding protein 2</strong> in the striatum and prefrontal cortex of rats displaying <b>nicotine</b> preference or aversion and treated with phenylbutyrate.
+MECP2	addiction	aversion	21166804	We measured immunohistochemically the acetylation of lysine 9 of histone H3, and the expression of phosphorylated cAMP response element binding protein, HDAC2 and <strong>methyl CpG binding protein 2</strong> in the striatum and prefrontal cortex of rats displaying nicotine preference or <b>aversion</b> and treated with phenylbutyrate.
+MECP2	drug	cocaine	20810894	In contrast, there was decreased methyl CpG binding protein 2 (<strong>MeCP2</strong>) association with BDNF promoter IV in the mPFC of rats that previously self administered <b>cocaine</b>.
+MECP2	drug	cocaine	20810894	In contrast, there was decreased <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) association with BDNF promoter IV in the mPFC of rats that previously self administered <b>cocaine</b>.
+MECP2	drug	cocaine	20810894	Together, these results indicate that <b>cocaine</b> induced increases in BDNF promoter IV transcript in the mPFC are driven by increased binding of AcH3 and pCREB as well as decreased <strong>MeCP2</strong> binding at this BDNF promoter.
+MECP2	drug	cocaine	20720536	Using methylated DNA immunoprecipitation, DNA bisulfite modification, and chromatin immunoprecipitation assays, we observed that <b>cocaine</b> treatment resulted in DNA hypermethylation and increased binding of methyl CpG binding protein 2 (<strong>MeCP2</strong>) at the protein phosphatase 1 catalytic subunit (PP1c) promoter.
+MECP2	drug	cocaine	20720536	Using methylated DNA immunoprecipitation, DNA bisulfite modification, and chromatin immunoprecipitation assays, we observed that <b>cocaine</b> treatment resulted in DNA hypermethylation and increased binding of <strong>methyl CpG binding protein 2</strong> (<strong>MeCP2</strong>) at the protein phosphatase 1 catalytic subunit (PP1c) promoter.
+MECP2	drug	cocaine	20720536	In contrast, acute and repeated <b>cocaine</b> administrations induced hypomethylation and decreased binding of <strong>MeCP2</strong> at the fosB promoter, and these are associated with transcriptional upregulation of fosB in NAc.
+MECP2	drug	amphetamine	20711186	Here we show that acute viral manipulation of <strong>MeCP2</strong> expression in the nucleus accumbens (NAc) bidirectionally modulates <b>amphetamine</b> (<b>AMPH</b>) induced conditioned place preference.
+MECP2	drug	amphetamine	20711186	<strong>Mecp2</strong> hypomorphic mutant mice have more NAc GABAergic synapses and show deficient <b>AMPH</b> induced structural plasticity of NAc dendritic spines.
+MECP2	drug	cocaine	20711185	<strong>MeCP2</strong> controls BDNF expression and <b>cocaine</b> intake through homeostatic interactions with microRNA 212.
+MECP2	drug	cocaine	20711185	<b>Cocaine</b> addiction is commonly viewed as a disorder of neuroplasticity, but the potential involvement of <strong>MeCP2</strong> has not been explored.
+MECP2	addiction	addiction	20711185	Cocaine <b>addiction</b> is commonly viewed as a disorder of neuroplasticity, but the potential involvement of <strong>MeCP2</strong> has not been explored.
+MECP2	drug	cocaine	20711185	Here we identify a key role for <strong>MeCP2</strong> in the dorsal striatum in the escalating <b>cocaine</b> intake seen in rats with extended access to the drug, a process that mimics the increasingly uncontrolled <b>cocaine</b> use seen in addicted humans.
+MECP2	drug	cocaine	20711185	<strong>MeCP2</strong> regulates <b>cocaine</b> intake through homeostatic interactions with microRNA 212 (miR 212) to control the effects of <b>cocaine</b> on striatal brain derived neurotrophic factor (BDNF) levels.
+MECP2	drug	cocaine	20711185	These data suggest that homeostatic interactions between <strong>MeCP2</strong> and miR 212 in dorsal striatum may be important in regulating vulnerability to <b>cocaine</b> addiction.
+MECP2	addiction	addiction	20711185	These data suggest that homeostatic interactions between <strong>MeCP2</strong> and miR 212 in dorsal striatum may be important in regulating vulnerability to cocaine <b>addiction</b>.
+MECP2	drug	cocaine	19939859	<b>Cocaine</b> self administration was accompanied by an increased synthesis of <strong>Mecp2</strong>, HDAC2 and HDAC11 and by a decreased nuclear localization of HDAC5 and of the phospho form of HDAC5, suggesting a nuclear export of this protein in response to the drug.
+MECP2	drug	cocaine	19939859	Among the genes we examined, treatment with trichostatin A before each <b>cocaine</b> self administration session was found to mostly affect <strong>Mecp2</strong> and HDAC11 expression.
+MECP2	drug	cocaine	19939859	A correlation was found between the modification of <strong>Mecp2</strong> and MEF2C gene expression and the reinforcing property of <b>cocaine</b>.
+MECP2	addiction	reward	19939859	A correlation was found between the modification of <strong>Mecp2</strong> and MEF2C gene expression and the <b>reinforcing</b> property of cocaine.
+CHRFAM7A	drug	alcohol	32569950	We administered (per os) for 60 <strong>d 10</strong> mg · kg 1 · d 1 of resveratrol in <b>alcoholic</b> adult male mice.
+CHRFAM7A	drug	nicotine	30089821	Genetic variation in CHRNA7 and <strong>CHRFAM7A</strong> is associated with <b>nicotine</b> dependence and response to varenicline treatment.
+CHRFAM7A	addiction	dependence	30089821	Genetic variation in CHRNA7 and <strong>CHRFAM7A</strong> is associated with nicotine <b>dependence</b> and response to varenicline treatment.
+CHRFAM7A	drug	nicotine	30089821	Genetic variation in <strong>CHRNA7</strong> and <strong>CHRFAM7A</strong> is associated with <b>nicotine</b> dependence and response to varenicline treatment.
+CHRFAM7A	addiction	dependence	30089821	Genetic variation in <strong>CHRNA7</strong> and <strong>CHRFAM7A</strong> is associated with nicotine <b>dependence</b> and response to varenicline treatment.
+CHRFAM7A	drug	nicotine	30089821	The role of nicotinic acetylcholine receptors (nAChR) in <b>nicotine</b> dependence (ND) is well established; <strong>CHRNA7</strong>, encoding the α7 subunit, has a still uncertain role in ND, although it is implicated in a wide range of neuropsychiatric conditions.
+CHRFAM7A	addiction	dependence	30089821	The role of nicotinic acetylcholine receptors (nAChR) in nicotine <b>dependence</b> (ND) is well established; <strong>CHRNA7</strong>, encoding the α7 subunit, has a still uncertain role in ND, although it is implicated in a wide range of neuropsychiatric conditions.
+CHRFAM7A	drug	nicotine	30089821	The aim of this study was to investigate the role of CHRNA7 and <strong>CHRFAM7A</strong> genetic variants in ND and to test the hypothesis that α7 nAChR variation may modulate the efficacy of varenicline treatment in <b>smoking</b> cessation.
+CHRFAM7A	drug	nicotine	30089821	The aim of this study was to investigate the role of <strong>CHRNA7</strong> and <strong>CHRFAM7A</strong> genetic variants in ND and to test the hypothesis that α7 nAChR variation may modulate the efficacy of varenicline treatment in <b>smoking</b> cessation.
+CHRFAM7A	drug	nicotine	30089821	We assessed CHRNA7 and <strong>CHRFAM7A</strong> copy number, <strong>CHRFAM7A</strong> exon 6 ∆2 bp polymorphism, and sequence variants in the CHRNA7 proximal promoter in an Italian sample of 408 treatment seeking <b>smokers</b>.
+CHRFAM7A	addiction	relapse	30089821	We assessed CHRNA7 and <strong>CHRFAM7A</strong> copy number, <strong>CHRFAM7A</strong> exon 6 ∆2 bp polymorphism, and sequence variants in the CHRNA7 proximal promoter in an Italian sample of 408 treatment <b>seeking</b> smokers.
+CHRFAM7A	drug	nicotine	30089821	We assessed <strong>CHRNA7</strong> and <strong>CHRFAM7A</strong> copy number, <strong>CHRFAM7A</strong> exon 6 ∆2 bp polymorphism, and sequence variants in the <strong>CHRNA7</strong> proximal promoter in an Italian sample of 408 treatment seeking <b>smokers</b>.
+CHRFAM7A	addiction	relapse	30089821	We assessed <strong>CHRNA7</strong> and <strong>CHRFAM7A</strong> copy number, <strong>CHRFAM7A</strong> exon 6 ∆2 bp polymorphism, and sequence variants in the <strong>CHRNA7</strong> proximal promoter in an Italian sample of 408 treatment <b>seeking</b> smokers.
+CHRFAM7A	drug	nicotine	30089821	The <strong>CHRNA7</strong> promoter variant rs28531779 showed association with both <b>smoking</b> quantitative measures (FNTD p = 0.026, β = 0.89, 95% CI 0.11 1.67; CPD p = 0.006, β = 4.82 95% CI 1.42 8.22).
+CHRFAM7A	drug	nicotine	30089821	Moreover, in the varenicline treated subgroup we observed association of <strong>CHRFAM7A</strong> copy number with 6 months <b>smoking</b> abstinence (p = 0.035, OR = 3.18, 95% CI = 1.09 9.30).
+CHRFAM7A	drug	nicotine	30089821	Thus, our study points to a possible role of genetic variation in CHRNA7 and <strong>CHRFAM7A</strong> in <b>tobacco</b> addiction mechanisms and response to varenicline treatment.
+CHRFAM7A	addiction	addiction	30089821	Thus, our study points to a possible role of genetic variation in CHRNA7 and <strong>CHRFAM7A</strong> in tobacco <b>addiction</b> mechanisms and response to varenicline treatment.
+CHRFAM7A	drug	nicotine	30089821	Thus, our study points to a possible role of genetic variation in <strong>CHRNA7</strong> and <strong>CHRFAM7A</strong> in <b>tobacco</b> addiction mechanisms and response to varenicline treatment.
+CHRFAM7A	addiction	addiction	30089821	Thus, our study points to a possible role of genetic variation in <strong>CHRNA7</strong> and <strong>CHRFAM7A</strong> in tobacco <b>addiction</b> mechanisms and response to varenicline treatment.
+CHRFAM7A	drug	nicotine	29666375	Association and cis mQTL analysis of variants in CHRNA3 A5, <strong>CHRNA7</strong>, CHRNB2, and CHRNB4 in relation to <b>nicotine</b> dependence in a Chinese Han population.
+CHRFAM7A	addiction	dependence	29666375	Association and cis mQTL analysis of variants in CHRNA3 A5, <strong>CHRNA7</strong>, CHRNB2, and CHRNB4 in relation to nicotine <b>dependence</b> in a Chinese Han population.
+CHRFAM7A	drug	nicotine	27428758	<b>Nicotine</b> intake is correlated negatively with Chrnb2, <strong>Chrna7</strong> and positively with Drd1 expression.
+CHRFAM7A	drug	nicotine	24289814	Genetic variation within the <strong>Chrna7</strong> gene modulates <b>nicotine</b> reward like phenotypes in mice.
+CHRFAM7A	addiction	reward	24289814	Genetic variation within the <strong>Chrna7</strong> gene modulates nicotine <b>reward</b> like phenotypes in mice.
+CHRFAM7A	drug	nicotine	24289814	Genetic analysis of gene expression and behavior identified <strong>Chrna7</strong> as potentially modulating <b>nicotine</b> place conditioning in the BXD panel of inbred mice.
+CHRFAM7A	drug	nicotine	24289814	We used gene targeting and pharmacological tools to confirm the role of <strong>Chrna7</strong> in <b>nicotine</b> conditioned place preference (CPP).
+CHRFAM7A	addiction	reward	24289814	We used gene targeting and pharmacological tools to confirm the role of <strong>Chrna7</strong> in nicotine conditioned place preference (<b>CPP</b>).
+CHRFAM7A	drug	nicotine	24289814	To identify molecular events downstream of <strong>Chrna7</strong> that may modulate <b>nicotine</b> preference, we performed microarray analysis of α7 knock out (KO) and wild type (WT) nucleus accumbens (NAc) tissue, followed by confirmation with quantitative polymerase chain reaction (PCR) and immunoblotting.
+CHRFAM7A	drug	nicotine	24289814	In the BXD panel, we found a putative cis expression quantitative trait loci (eQTL) for <strong>Chrna7</strong> in NAc that correlated inversely to <b>nicotine</b> CPP.
+CHRFAM7A	addiction	reward	24289814	In the BXD panel, we found a putative cis expression quantitative trait loci (eQTL) for <strong>Chrna7</strong> in NAc that correlated inversely to nicotine <b>CPP</b>.
+CHRFAM7A	drug	nicotine	24289814	Mice lacking <strong>Chrna7</strong> demonstrate increased insulin signaling in the NAc, which may modulate <b>nicotine</b> place preference.
+CHRFAM7A	drug	opioid	23373221	The CPP model was established by injecting <b>morphine</b> in rats with a increasing dose for 10 days, with the initial dose of 10 g x kg( 1) and the final dose of 100 g x kg( 1), 10 mg x kg( 1) was increased each day, thus 100 mg x kg( 1) was injected by <strong>d 10</strong>.
+CHRFAM7A	addiction	reward	23373221	The <b>CPP</b> model was established by injecting morphine in rats with a increasing dose for 10 days, with the initial dose of 10 g x kg( 1) and the final dose of 100 g x kg( 1), 10 mg x kg( 1) was increased each day, thus 100 mg x kg( 1) was injected by <strong>d 10</strong>.
+CHRFAM7A	drug	nicotine	20584212	Variants in or near CHRND CHRNG, <strong>CHRNA7</strong> and CHRNA10 show modest association with <b>nicotine</b> dependence risk in the AA sample.
+CHRFAM7A	addiction	dependence	20584212	Variants in or near CHRND CHRNG, <strong>CHRNA7</strong> and CHRNA10 show modest association with nicotine <b>dependence</b> risk in the AA sample.
+CHRFAM7A	drug	alcohol	20496163	This report explores the association between six nAChR subunit genes (Chrna3, Chrna4, Chrnb4, Chrnb2, Chrna5, and <strong>Chrna7</strong>) with <b>alcohol</b> preference (AP) using co segregation of AP with nAChR subunit genotypes in a F(2) population produced from reciprocal crosses of <b>alcohol</b> preferring C57BL/6J (B6) and <b>alcohol</b> avoiding DBA/2J (D2) strains of mice.
+CHRFAM7A	drug	nicotine	19307444	We found evidence that genetic variation at CHRNA1, CHRNA2, <strong>CHRNA7</strong>, and CHRNB1 alters susceptibility to <b>nicotine</b> dependence, but we did not replicate any of the most significant single nucleotide polymorphism associations from the NICSNP high density association study.
+CHRFAM7A	addiction	dependence	19307444	We found evidence that genetic variation at CHRNA1, CHRNA2, <strong>CHRNA7</strong>, and CHRNB1 alters susceptibility to nicotine <b>dependence</b>, but we did not replicate any of the most significant single nucleotide polymorphism associations from the NICSNP high density association study.
+CHRFAM7A	drug	nicotine	19082523	Differentiating <b>nicotine</b>  versus schizophrenia associated decreases of the alpha7 nicotinic acetylcholine receptor transcript, <strong>CHRFAM7A</strong>, in peripheral blood lymphocytes.
+CHRFAM7A	drug	nicotine	19082523	In 20 <b>smoking</b> matched people (n = 10 schizophrenia, n = 10 controls), we found significantly lower <strong>CHRFAM7A</strong> in cotinine and self reported <b>smokers</b> versus nonsmokers (p <or= 0.001 0.03) and an inverse correlation of cotinine with <strong>CHRFAM7A</strong> (p <or= 0.04) in regression models.
+CHRFAM7A	drug	nicotine	16314871	We found nominally significant (P<0.05) allelic and genotypic association with <b>smoking</b> initiation of SNP rs2072660 and multilocus haplotypes (P<0.007 0.05) in CHRNB2 and nominal (P<0.05) allelic or genotypic association of SNPs in <strong>CHRNA7</strong> (rs1909884), CHRNA9 (rs4861065) and CHRNB3 (rs9298629) with <b>nicotine</b> dependence.
+CHRFAM7A	addiction	dependence	16314871	We found nominally significant (P<0.05) allelic and genotypic association with smoking initiation of SNP rs2072660 and multilocus haplotypes (P<0.007 0.05) in CHRNB2 and nominal (P<0.05) allelic or genotypic association of SNPs in <strong>CHRNA7</strong> (rs1909884), CHRNA9 (rs4861065) and CHRNB3 (rs9298629) with nicotine <b>dependence</b>.
+CHRFAM7A	drug	nicotine	16314871	For severity of <b>nicotine</b> dependence, two SNPs in <strong>CHRNA7</strong> (rs1909884 and rs883473), one SNP in CHRNA5 (rs680244) and the interaction of a SNP in <strong>CHRNA7</strong> (rs2337980) with neuroticism, were included in the model (P=2.24 x 10( 7), Nagelkerke r(2)=0.40).
+CHRFAM7A	addiction	dependence	16314871	For severity of nicotine <b>dependence</b>, two SNPs in <strong>CHRNA7</strong> (rs1909884 and rs883473), one SNP in CHRNA5 (rs680244) and the interaction of a SNP in <strong>CHRNA7</strong> (rs2337980) with neuroticism, were included in the model (P=2.24 x 10( 7), Nagelkerke r(2)=0.40).
+ADH5	drug	alcohol	26848198	Characterization of polymorphisms of genes ADH2, <strong>ADH3</strong>, ALDH2 and CYP2E1 and relationship to the <b>alcoholism</b> in a Colombian population.
+ADH5	drug	alcohol	26848198	Identify and characterize polymorphisms of genes ADH2, <strong>ADH3</strong>, ALDH2 and CYP2E1 in a Colombian population residing in the city of Bogotá and determine its possible relationship to the <b>alcoholism</b>.
+ADH5	drug	alcohol	26848198	ADH2, <strong>ADH3</strong>, ALDH2, and CYP2E1 genotypes a population of 148 individuals with non problematic <b>alcohol</b> and 65 individuals with <b>alcoholism</b> were determined with TaqMan probes and PCR RFLP.
+ADH5	drug	alcohol	26848198	Se determinaron los genotipos ADH2, <strong>ADH3</strong>, ALDH2 y CYP2E1 a una población de 148 individuos con un consumo no problemático de <b>alcohol</b> y 65 individuos con alcoholismo.
+ADH5	drug	alcohol	25535445	The genes for <b>alcohol</b> metabolizing enzymes: <b>Alcohol</b> dehydrogenase (ADH2 and <strong>ADH3</strong>) and aldehyde dehydrogenase (ALDH2) exhibit functional polymorphisms.
+ADH5	drug	alcohol	25535445	To determine whether any association exists between polymorphisms of ADH2, <strong>ADH3</strong> and ALDH2 and <b>alcohol</b> dependence syndrome in a group of Asian Indians.
+ADH5	addiction	dependence	25535445	To determine whether any association exists between polymorphisms of ADH2, <strong>ADH3</strong> and ALDH2 and alcohol <b>dependence</b> syndrome in a group of Asian Indians.
+ADH5	drug	alcohol	25535445	Allele frequencies of ADH2*2 (0.50), <strong>ADH3</strong>*1 (0.67) and ALSH2*2 (0.09) were significantly low in the <b>alcohol</b> dependent subjects.
+ADH5	drug	alcohol	23468174	Humans express at least seven <b>alcohol</b> dehydrogenase (ADH) isoforms that are encoded by ADH gene cluster (ADH7 ADH1C ADH1B ADH1A ADH6 ADH4 <strong>ADH5</strong>) at chromosome 4.
+ADH5	drug	alcohol	22476623	Numerous association studies have provided compelling evidence that ADH1C gene variation (formerly <strong>ADH3</strong>) is associated with altered genetic susceptibility to <b>alcoholism</b> and <b>alcohol</b> related liver disease, cirrhosis, or pancreatitis.
+ADH5	drug	alcohol	20617019	A new view of <b>alcohol</b> metabolism and <b>alcoholism</b>  role of the high Km Class III <b>alcohol</b> dehydrogenase (<strong>ADH3</strong>).
+ADH5	drug	alcohol	20617019	Recently, using <strong>ADH3</strong> null mutant mice, we demonstrated that <strong>ADH3</strong> (Class III), which has a high K(m) and is a ubiquitous enzyme of ancient origin, contributes to systemic <b>alcohol</b> metabolism in a dose dependent manner, thereby diminishing acute <b>alcohol</b> intoxication.
+ADH5	addiction	intoxication	20617019	Recently, using <strong>ADH3</strong> null mutant mice, we demonstrated that <strong>ADH3</strong> (Class III), which has a high K(m) and is a ubiquitous enzyme of ancient origin, contributes to systemic alcohol metabolism in a dose dependent manner, thereby diminishing acute alcohol <b>intoxication</b>.
+ADH5	drug	alcohol	20617019	Although the activity of <strong>ADH3</strong> toward <b>ethanol</b> is usually low in vitro due to its very high K(m), the catalytic efficiency (k(cat)/K(m)) is markedly enhanced when the solution hydrophobicity of the reaction medium increases.
+ADH5	drug	alcohol	20617019	When various doses of <b>ethanol</b> are administered to mice, liver <strong>ADH3</strong> activity is dynamically regulated through induction or kinetic activation, while ADH1 activity is markedly lower at high doses (3 5 g/kg).
+ADH5	drug	alcohol	20617019	These data suggest that <strong>ADH3</strong> plays a dynamic role in <b>alcohol</b> metabolism, either collaborating with ADH1 or compensating for the reduced role of ADH1.
+ADH5	drug	alcohol	20617019	A complex two ADH model that ascribes total liver ADH activity to both ADH1 and <strong>ADH3</strong> explains the dose dependent changes in the pharmacokinetic parameters (beta, CL(T), AUC) of blood <b>ethanol</b> very well, suggesting that <b>alcohol</b> metabolism in mice is primarily governed by these two ADHs.
+ADH5	drug	alcohol	20617019	In patients with <b>alcoholic</b> liver disease, liver <strong>ADH3</strong> activity increases, while ADH1 activity decreases, as <b>alcohol</b> intake increases.
+ADH5	drug	alcohol	20617019	These data suggest that chronic binge drinking and the resulting liver disease shifts the key enzyme in <b>alcohol</b> metabolism from low K(m) ADH1 to high K(m) <strong>ADH3</strong>, thereby reducing the rate of <b>alcohol</b> metabolism.
+ADH5	addiction	intoxication	20617019	These data suggest that chronic <b>binge</b> drinking and the resulting liver disease shifts the key enzyme in alcohol metabolism from low K(m) ADH1 to high K(m) <strong>ADH3</strong>, thereby reducing the rate of alcohol metabolism.
+ADH5	drug	alcohol	20617019	The interdependent increase in the <strong>ADH3</strong>/ADH1 activity ratio and AUC may be a factor in the development of <b>alcoholic</b> liver disease.
+ADH5	drug	alcohol	20617019	However, the adaptive increase in <strong>ADH3</strong> sustains <b>alcohol</b> metabolism, even in patients with <b>alcoholic</b> liver cirrhosis, which makes it possible for them to drink themselves to death.
+ADH5	drug	alcohol	20617019	Thus, the regulation of <strong>ADH3</strong> activity may be important in preventing <b>alcoholism</b> development.
+ADH5	drug	alcohol	19489444	[A new sight on <b>alcohol</b> metabolism and <b>alcoholism</b>  role of high Km <b>alcohol</b> dehydrogenase <strong>ADH3</strong> (Class III)].
+ADH5	drug	alcohol	19489444	Recently, we used <strong>ADH3</strong> null mutant mice to demonstrate that high Km <strong>ADH3</strong> (Class III), a ubiquitous enzyme of ancient origin, contributes to systemic <b>alcohol</b> metabolism dose dependently resulting in a diminution of acute <b>alcohol</b> intoxication.
+ADH5	addiction	intoxication	19489444	Recently, we used <strong>ADH3</strong> null mutant mice to demonstrate that high Km <strong>ADH3</strong> (Class III), a ubiquitous enzyme of ancient origin, contributes to systemic alcohol metabolism dose dependently resulting in a diminution of acute alcohol <b>intoxication</b>.
+ADH5	drug	alcohol	19489444	Although the <b>ethanol</b> activity of <strong>ADH3</strong> in vitro is usually low due to its very high Km, the catalytic efficiency (k(cat)/Km) was markedly enhanced when the solution hydrophobicity of the reaction medium was increased.
+ADH5	drug	alcohol	19489444	By acute administrations of <b>ethanol</b> to mice at various doses, liver <strong>ADH3</strong> activity was dynamically regulated through induction or kinetic activation, though ADH1 activity was markedly decreased at higher doses (3   5 g/kg).
+ADH5	drug	alcohol	19489444	These data suggest that <strong>ADH3</strong> plays a dynamical share in <b>alcohol</b> metabolism with ADH1, collaborating with it or supplementing the decreased role of ADH1.
+ADH5	drug	alcohol	19489444	The two ADH complex model, which ascribes total liver ADH activity to both ADH1 and <strong>ADH3</strong>, explained well the dose dependent changes in pharmacokinetic parameters (beta, CL(T), AUC) of blood <b>ethanol</b>, suggesting that <b>alcohol</b> metabolism in mice is primarily governed by the two ADHs.
+ADH5	drug	alcohol	19489444	In patients with <b>alcoholic</b> liver diseases, the liver <strong>ADH3</strong> activity increased but the ADH1 activity decreased with an increase in <b>alcohol</b> intake.
+ADH5	drug	alcohol	19489444	These data suggest that heavy and chronic drinking shifts the main enzyme in <b>alcohol</b> metabolism from low Km ADH1 to high Km <strong>ADH3</strong> to develop <b>alcoholic</b> liver diseases by the nonlinear increase in AUC due to the decrease of the metabolic rate.
+ADH5	drug	alcohol	19489444	However, the adaptively increased <strong>ADH3</strong> keeps the ability of <b>alcohol</b> metabolism even in patients with <b>alcoholic</b> liver cirrhosis and make possible for them to keep drinking to death.
+ADH5	drug	alcohol	19489444	Therefore, the regulation of <strong>ADH3</strong> activity may be important to prevent the development of <b>alcoholism</b>.
+ADH5	drug	alcohol	18996923	After controlling for rs1229984, an independent association was observed between rs1042026 (ADH1B) and <b>alcohol</b> intake (P=4.7 x 10( 5)) and suggestive associations (P<0.001) between <b>alcohol</b> consumption phenotypes and rs1693482 (ADH1C), rs1230165 (<strong>ADH5</strong>) and rs3762894 (ADH4).
+ADH5	drug	alcohol	18207224	The primary isozyme of <b>alcohol</b> dehydrogenase (ADH) in rat liver, <strong>ADH 3</strong>, had a similar Km and higher activity in liver preparations from juveniles.
+ADH5	drug	alcohol	17629074	The aim of the present study was to find in the Polish population the <strong>ADH3</strong> genotypes, which are likely to be responsible for higher susceptibility to <b>alcohol</b> disease of the liver and chronic <b>alcohol</b> pancreatitis.
+ADH5	drug	alcohol	17629074	The genotype <strong>ADH3</strong>*1/<strong>ADH3</strong>*1 was found to be significantly more frequent in <b>alcohol</b> abusers compared to non drinkers.
+ADH5	drug	alcohol	17629074	The examinations of the group of <b>alcohol</b> abusers showed that the genotype <strong>ADH3</strong>*2/<strong>ADH3</strong>*2 occurred statistically significantly less frequently in patients with chronic pancreatitis than those without alimentary lesions and patients with cirrhosis.
+ADH5	drug	alcohol	17454860	We determined the allele and genotype of ADH2, <strong>ADH3</strong> and ALDH2 in 198 subjects: 57 with <b>alcohol</b> cirrhosis, 44 with <b>alcohol</b> chronic pancreatitis and 43 "healthy <b>alcoholics</b>"; 54 healthy non drinkers served as controls.
+ADH5	drug	alcohol	17454860	The ADH2*1 and the <strong>ADH3</strong>*1 alleles were statistically more common among patients who abuse <b>alcohol</b> in comparison with the controls.
+ADH5	drug	alcohol	17454860	The ADH2*1/*1 and the <strong>ADH3</strong>*1/*1 genotypes were statistically significantly more common among the patients who abuse <b>alcohol</b> than in the control group.
+ADH5	drug	alcohol	17454860	Patients with the <strong>ADH3</strong>*1 allele and the <strong>ADH3</strong>*1/*1 genotype started to abuse <b>alcohol</b> significantly earlier in comparison to the patients with the <strong>ADH3</strong>*2 allele and the <strong>ADH3</strong>*2 /*2 genotype.
+ADH5	drug	alcohol	17454860	In the Polish population examined, the <strong>ADH3</strong>*1 allele and the <strong>ADH3</strong>*1/*1 genotype are conducive to the development of <b>alcoholism</b>, <b>alcohol</b> liver cirrhosis and <b>alcohol</b> chronic pancreatitis.
+ADH5	drug	alcohol	17454860	The <strong>ADH3</strong>*1 allele and the <strong>ADH3</strong>*1/*1 genotype are conducive to <b>alcohol</b> abuse starting at a younger age.
+ADH5	drug	alcohol	17134660	This study sought to determine whether an association exists between ADH (ADH1C previously <strong>ADH3</strong>, ADH1B*2 previously ADH2*2) genotypes, <b>alcohol</b> dependence, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH5	addiction	dependence	17134660	This study sought to determine whether an association exists between ADH (ADH1C previously <strong>ADH3</strong>, ADH1B*2 previously ADH2*2) genotypes, alcohol <b>dependence</b>, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ADH5	drug	alcohol	16431092	In vivo contribution of Class III <b>alcohol</b> dehydrogenase (<strong>ADH3</strong>) to <b>alcohol</b> metabolism through activation by cytoplasmic solution hydrophobicity.
+ADH5	drug	alcohol	16431092	In this study, we used <strong>Adh3</strong> null mutant mice to demonstrate that Class III ADH (<strong>ADH3</strong>), a ubiquitous enzyme of ancient origin, contributes to <b>alcohol</b> metabolism in vivo dose dependently resulting in a diminution of acute <b>alcohol</b> intoxication.
+ADH5	addiction	intoxication	16431092	In this study, we used <strong>Adh3</strong> null mutant mice to demonstrate that Class III ADH (<strong>ADH3</strong>), a ubiquitous enzyme of ancient origin, contributes to alcohol metabolism in vivo dose dependently resulting in a diminution of acute alcohol <b>intoxication</b>.
+ADH5	drug	alcohol	16431092	Although the <b>ethanol</b> oxidation activity of <strong>ADH3</strong> in vitro is low due to its very high Km, it was found to exhibit a markedly enhanced catalytic efficiency (kcat/Km) toward <b>ethanol</b> when the solution hydrophobicity of the reaction medium was increased with a hydrophobic substance.
+ADH5	drug	alcohol	16431092	So, the in vivo contribution of high Km <strong>ADH3</strong> to <b>alcohol</b> metabolism is likely to involve activation in a hydrophobic solution.
+ADH5	drug	alcohol	16431092	Thus, the present study demonstrated that <strong>ADH3</strong> plays an important role in systemic <b>ethanol</b> metabolism at higher levels of blood <b>ethanol</b> through activation by cytoplasmic solution hydrophobicity.
+ADH5	drug	alcohol	16239350	To find the <strong>ADH3</strong> genotypes in the Polish population likely to be responsible for higher susceptibility to <b>alcohol</b> disease of the liver and chronic <b>alcohol</b> pancreatitis.
+ADH5	drug	alcohol	16239350	The genotype <strong>ADH3</strong>*1/<strong>ADH3</strong>*1 was found to be significantly more frequent in <b>alcohol</b> abusers compared with non drinkers.
+ADH5	drug	alcohol	16239350	The examinations of the group of <b>alcohol</b> abusers showed that the genotype <strong>ADH3</strong>*2/<strong>ADH3</strong>*2 occurred statistically significantly less frequently in patients with chronic pancreatitis than in those without alimentary lesions (healthy drinkers).
+ADH5	drug	alcohol	16239350	Variations in <strong>ADH3</strong> genotypes may account for some of the differences in prevalence of <b>alcohol</b> dependence between genders in the Polish population.
+ADH5	addiction	dependence	16239350	Variations in <strong>ADH3</strong> genotypes may account for some of the differences in prevalence of alcohol <b>dependence</b> between genders in the Polish population.
+ADH5	drug	alcohol	15863807	The authors examined the genetic polymorphisms of <b>alcohol</b> dehydrogenase 2 and 3 (ADH2 and <strong>ADH3</strong>) and aldehyde dehydrogenase (ALDH2) in patients diagnosed as having Cloninger's type I or type II <b>alcoholism</b>.
+ADH5	drug	alcohol	15863807	Seventy two <b>alcoholic</b> men and 38 nonalcoholic, healthy men were tested for the distribution of genotypes and alleles of ADH2, <strong>ADH3</strong>, and ALDH2.
+ADH5	drug	alcohol	15863807	The frequencies of ADH2*1 and <strong>ADH3</strong>*2 alleles were significantly higher in men with type II <b>alcoholism</b> than in men with type I <b>alcoholism</b> and healthy men.
+ADH5	drug	alcohol	12884000	In the current study, variants at ADH1B (previously ADH2), ADH1C (previously <strong>ADH3</strong>), and ALDH2 were assayed in DNA extracts from participants belonging to a Southwest American Indian tribe (n=490) with a high prevalence of <b>alcoholism</b>.
+ADH5	drug	alcohol	12750236	<b>Alcohol</b> is a probable risk factor with regard to colorectal neoplasm and is metabolized to the carcinogen acetaldehyde by the genetically polymorphic <b>alcohol</b> dehydrogenase 3 (<strong>ADH3</strong>) enzyme.
+ADH5	drug	alcohol	12750236	We evaluated whether the association between <b>alcohol</b> and colorectal adenomas is modified by <strong>ADH3</strong> polymorphism.
+ADH5	drug	alcohol	12750236	Among subjects in the highest tertile of <b>alcohol</b> consumption, those with the <strong>ADH3</strong>*1/*1 genotype were at higher risk (OR, 1.8; 95% CI, 1.0 3.1) than those with other <strong>ADH3</strong> genotypes (OR, 1.2; 95% CI, 0.7 1.9) when compared with those in the lowest tertile with <strong>ADH3</strong>*1/*2 or <strong>ADH3</strong>*2/*2 genotypes.
+ADH5	drug	alcohol	12750236	<strong>ADH3</strong> polymorphism may modify the association between <b>alcohol</b> consumption and colorectal adenomas.
+ADH5	drug	alcohol	12710951	The <strong>ADH3</strong>*2 and CYP2E1 c2 alleles increase the risk of <b>alcoholism</b> in Mexican American men.
+ADH5	drug	alcohol	12710951	To identify the association between the polymorphisms of genes encoding <b>alcohol</b> metabolizing enzymes and <b>alcoholism</b>, the <b>alcohol</b> dehydrogenase 2 (ADH2), <b>alcohol</b> dehydrogenase 3 (<strong>ADH3</strong>), aldehyde dehydrogenase 2 (ALDH2), and cytochrome P450 2E1 (CYP2E1) genes were studied in 101 male Mexican American <b>alcoholics</b>.
+ADH5	drug	alcohol	12710951	A strong association was found between <strong>ADH3</strong> genotype and <b>alcoholism</b>; the percentage of subjects who carry the <strong>ADH3</strong>*2 allele was significantly higher in <b>alcoholics</b> (64.4%) than controls (50%).
+ADH5	drug	alcohol	12710951	Among 101 <b>alcoholics</b>, only 18 subjects carry neither <strong>ADH3</strong>*2 nor CYP2E1 c2 alleles.
+ADH5	drug	alcohol	12710951	Taken together, <strong>ADH3</strong>*2 and CYP2E1 c2/C alleles might independently contribute to the development of <b>alcoholism</b> in Mexican American men.
+ADH5	drug	alcohol	12505800	Two <b>alcohol</b> dehydrogenase genes (ADH2 and <strong>ADH3</strong> on chromosome 4) and one aldehyde dehydrogenase gene (ALDH2 on chromosome 12) exhibit functional polymorphisms.
+ADH5	drug	alcohol	12505800	The goal of this study was to determine whether any associations exist between the ADH2, <strong>ADH3</strong>, and ALDH2 polymorphisms and <b>alcohol</b> dependence in a group of Native Americans.
+ADH5	addiction	dependence	12505800	The goal of this study was to determine whether any associations exist between the ADH2, <strong>ADH3</strong>, and ALDH2 polymorphisms and alcohol <b>dependence</b> in a group of Native Americans.
+ADH5	drug	alcohol	11752857	<b>Alcohol</b> dehydrogenase type 3 (<strong>ADH3</strong>) and the risk of bladder cancer.
+ADH5	drug	alcohol	11752857	After correction for sex, age and smoking, ORs for <strong>ADH3</strong> genotype and <b>alcohol</b> intake were 2.10 (1.05 4.22) and 1.21 (0.60 2.44), respectively.
+ADH5	drug	nicotine	11752857	After correction for sex, age and <b>smoking</b>, ORs for <strong>ADH3</strong> genotype and alcohol intake were 2.10 (1.05 4.22) and 1.21 (0.60 2.44), respectively.
+ADH5	drug	alcohol	11752857	Although moderate drinkers with the gamma1gamma1 genotype seem to have the highest risk, we did not get a clear indication that <strong>ADH3</strong> genotype modifies the relationship between <b>alcohol</b> intake and bladder cancer.
+ADH5	drug	alcohol	11584143	In view of this association and the known genetic influences on both <b>alcohol</b> pharmacokinetics and <b>alcohol</b> dependence, it is probable that part of the heritability of dependence is mediated by genes (other than the known ADH2 and <strong>ADH3</strong> polymorphisms) affecting <b>alcohol</b> metabolism.
+ADH5	addiction	dependence	11584143	In view of this association and the known genetic influences on both alcohol pharmacokinetics and alcohol <b>dependence</b>, it is probable that part of the heritability of <b>dependence</b> is mediated by genes (other than the known ADH2 and <strong>ADH3</strong> polymorphisms) affecting alcohol metabolism.
+ADH5	drug	alcohol	10630602	An <b>alcohol</b> dependent patient was identified to be ALDH2*2/*2, ADH2*2/*2, and <strong>ADH3</strong>*1/*2.
+ADH5	drug	alcohol	10597438	Evidence for linkage to the ALDX1 <b>alcoholism</b> phenotype at the <strong>ADH3</strong> functional candidate gene was increased in the late onset subgroup (Bonferroni corrected significance level < 0.002), as compared with the unstratified sample that replicated COGA linkage obtained in the same analysis; there was no evidence for linkage at this locus in the early onset subgroup.
+ADH5	drug	alcohol	10597410	For the "<b>alcoholism</b> free" outcome, we found significant linkage signals at D4S2457, D41651 (both flank <strong>ADH3</strong>), D11S2359, and D16S47 and significant linkage disequilibrium signals at D4S2361, FABP2, D11S2359, D19S431 and D19S47 D19S198 D19S601.
+ADH5	drug	alcohol	10235293	The different genotypes at the genes encoding the enzymes involved in <b>alcohol</b> metabolism, class one <b>alcohol</b> dehydrogenase (ADH2 and <strong>ADH3</strong>) and mitochondrial aldehyde dehydrogenase (ALDH2), have previously been shown to confer different predispositions to the development of <b>alcoholism</b> in Chinese Han males (Thomasson et al., 1991; Chen WJ et al., 1996; Chen CC et al., unpublished data).
+ADH5	drug	alcohol	10235293	Therefore, association studies of <b>alcoholism</b> in Chinese Han might be more sensitive if controlled for the genotypes of ADH2,<strong>ADH3</strong>, and ALDH2, when other loci, such as DRD2, are examined.
+ADH5	drug	alcohol	10235293	These tests included considering the high risk (ADH2*1/*1; *1/*2; <strong>ADH3</strong>*1/*2; *2/*2; and ALDH2*1/*1) and the low risk (ADH2*2/*2; <strong>ADH3</strong>*1/*1; and ALDH2*1/*2; *2/*2) groups of <b>alcoholics</b>, as well as nonalcoholic controls.
+ADH5	drug	alcohol	10235293	After stratification by the relevant genotypes of ADH2, <strong>ADH3</strong>, and ALDH2 no significant association exists between the genetic variants at the DRD2 locus and <b>alcoholism</b> in the Chinese Han population.
+ADH5	drug	alcohol	9731720	Caucasians are polymorphic at only two of these gene loci  cytochrome P450 2E1 (CYP2E1) and <b>alcohol</b> dehydrogenase 3 (<strong>ADH3</strong>).
+ADH5	drug	alcohol	9731720	We examined the frequency of the RsaI polymorphism of CYP2E1 and <strong>ADH3</strong> genotype in 264 patients with <b>alcoholic</b> liver disease and 121 local control individuals.
+ADH5	drug	alcohol	9731720	This risk appears to be particularly manifest in individuals carrying the <strong>ADH3</strong>*2 allele, presumably reflecting increased metabolism of <b>ethanol</b> by CYP2E1.
+ADH5	drug	alcohol	9731720	In the absence of the c2 allele, <strong>ADH3</strong> genotype does not influence the risk of advanced <b>alcoholic</b> liver disease but, in males at least, may influence the risk of <b>alcoholism</b>.
+ADH5	drug	alcohol	9373704	The purpose of this paper is to assemble and evaluate existing data on the effect of genetic variation in ADH2 and <strong>ADH3</strong> on the risk of <b>alcohol</b> dependence, and on the risk of <b>alcoholic</b> liver disease.
+ADH5	addiction	dependence	9373704	The purpose of this paper is to assemble and evaluate existing data on the effect of genetic variation in ADH2 and <strong>ADH3</strong> on the risk of alcohol <b>dependence</b>, and on the risk of alcoholic liver disease.
+ADH5	drug	alcohol	9373704	<strong>ADH3</strong> variation also has significant effects on <b>alcohol</b> dependence, which may be due to linkage to ADH2; the <strong>ADH3</strong> effect differs significantly between Asian and European subjects.
+ADH5	addiction	dependence	9373704	<strong>ADH3</strong> variation also has significant effects on alcohol <b>dependence</b>, which may be due to linkage to ADH2; the <strong>ADH3</strong> effect differs significantly between Asian and European subjects.
+ADH5	drug	alcohol	9066994	In this report we determined the genotypes for three genes, ADH2, <strong>ADH3</strong>, and ALDH2 among subjects with <b>alcohol</b> dependence (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ADH5	addiction	dependence	9066994	In this report we determined the genotypes for three genes, ADH2, <strong>ADH3</strong>, and ALDH2 among subjects with alcohol <b>dependence</b> (n = 159) and ethnically matched normal controls (n = 149) for the four largest aboriginal groups (Atayal, Ami, Bunun, and Paiwan) in Taiwan.
+ADH5	drug	alcohol	8904964	The influences of estimated body water, recent drinking history, recent smoking history, polymorphism at the ADH2 and <strong>ADH3</strong> loci, family history of <b>alcoholism</b>, and percentage Native American heritage on <b>alcohol</b> elimination rate were determined using multiple regression analyses.
+ADH5	drug	nicotine	8904964	The influences of estimated body water, recent drinking history, recent <b>smoking</b> history, polymorphism at the ADH2 and <strong>ADH3</strong> loci, family history of alcoholism, and percentage Native American heritage on alcohol elimination rate were determined using multiple regression analyses.
+ADH5	drug	alcohol	8773821	<b>Alcohol</b> metabolising genes and <b>alcoholism</b> among Taiwanese Han men: independent effect of ADH2, <strong>ADH3</strong> and ALDH2.
+ADH5	drug	alcohol	8773821	The association of ALDH2 and ADH2 with the development of <b>alcoholism</b> was found to be independent of each other and has been replicated in different Asian populations, while the effect of <strong>ADH3</strong> is less studied.
+ADH5	drug	alcohol	8773821	Multiple logistic regression was then applied to assess the contribution of <strong>ADH3</strong> to <b>alcoholism</b> by controlling the effect of ALDH2 and ADH2.
+ADH5	drug	alcohol	8773821	The results of multivariate analyses demonstrated that the odds ratios for an increment of one allele of ADH2*1, <strong>ADH3</strong>*2 and ALDH2*1 in the development of <b>alcoholism</b> were 4.18, 3.82, and 6.89, respectively.
+ADH5	drug	alcohol	8651462	A comparison of the genotypes of ALDH2, ADH2, <strong>ADH3</strong>, and cytochrome P 4502E1 between <b>alcoholics</b> and nonalcoholics.
+ADH5	drug	alcohol	8651462	We examined the genotypes of the aldehyde dehydrogenase (ALDH) 2, <b>alcohol</b> dehydrogenase (ADH) 2, <strong>ADH3</strong>, and P 4502E1 loci of 53 <b>alcoholics</b> and 97 nonalcoholics.
+ADH5	drug	alcohol	8651462	Our study revealed differences in the allelic frequencies of the ALDH2, ADH2, and <strong>ADH3</strong> loci between <b>alcoholics</b> and nonalcoholics.
+ADH5	drug	alcohol	8651462	For <b>alcoholics</b> with both homozygous ALDH2*1/1 and heterozygous ALDH2*1/2 genotypes, it was found that ADH2 and <strong>ADH3</strong> played important rates.
+ADH5	drug	alcohol	7943668	Genetic variation at two polymorphic <b>alcohol</b> dehydrogenase loci, ADH2 and <strong>ADH3</strong>, and at the polymorphic mitochondrial aldehyde dehydrogenase locus, ALDH2, may influence the risk of developing <b>alcoholism</b> by modulating the rate of elimination of <b>ethanol</b> and the rate of formation and elimination of acetaldehyde.
+ADH5	drug	alcohol	8462548	These results allow us to assume an important role of rat liver <strong>ADH 3</strong> in the mechanism of <b>alcohol</b> addiction.
+ADH5	addiction	addiction	8462548	These results allow us to assume an important role of rat liver <strong>ADH 3</strong> in the mechanism of alcohol <b>addiction</b>.
+TRD	addiction	relapse	32616208	While standard antidepressants are at least partly effective for the short term treatment of acute depressive episodes of MDD, many patients <b>relapse</b> within 6 months of apparent clinical remission, with faster and higher rates observed in those with treatment resistant depression (<strong>TRD</strong>).
+TRD	drug	psychedelics	32616208	More recently, maintenance of antidepressant effects beyond the initial acute (induction) treatment period has been shown with esketamine nasal spray, an enantiomer of <b>ketamine</b>, in conjunction with an oral antidepressant in three phase 2/3 registration studies (SYNAPSE, SUSTAIN 1, SUSTAIN 2) of adult patients with <strong>TRD</strong>.
+TRD	drug	psychedelics	32446640	"Remote Monitoring of Intranasal <b>Ketamine</b> Self Administration as Maintenance Therapy in Treatment Resistant Depression (<strong>TRD</strong>): A Novel Strategy for Vulnerable and At Risk Populations to COVID 19?"
+TRD	addiction	withdrawal	32331032	No indication of drug specific <b>withdrawal</b> symptoms was seen after stopping up to 1 year of intermittent treatment with ESK nasal spray for <strong>TRD</strong>.
+TRD	drug	psychedelics	32240970	Intravenous <b>ketamine</b>, a dissociative anesthetic that induces complex downstream effects via NMDARs, rapidly reduces depressive and suicidal symptoms in treatment resistant depression (<strong>TRD</strong>), as demonstrated by several trials.
+TRD	drug	psychedelics	32240970	Recently, the United States Food and Drug Administration (FDA) approved an intranasal version of <b>ketamine</b> (esketamine) for <strong>TRD</strong>.
+TRD	drug	psychedelics	32061748	<b>Ketamine</b>, a dissociative anesthetic and <b>psychedelic</b> compound, has revolutionized the field of psychopharmacology by showing robust, and rapid acting antidepressant activity in patients suffering from major depressive disorder (MDD), suicidal tendencies, and treatment resistant depression (<strong>TRD</strong>).
+TRD	drug	benzodiazepine	31759333	Thirty seven participants with treatment resistant depression (<strong>TRD</strong>) and baseline SI first received a single ketamine infusion during a randomized, double blind crossover with <b>midazolam</b>.
+TRD	drug	psychedelics	31759333	Thirty seven participants with treatment resistant depression (<strong>TRD</strong>) and baseline SI first received a single <b>ketamine</b> infusion during a randomized, double blind crossover with midazolam.
+TRD	drug	psychedelics	31759333	In <strong>TRD</strong>, single and repeated <b>ketamine</b> infusions resulted in decreases in SI which were maintained with once weekly maintenance infusions.
+TRD	drug	alcohol	31656053	Increased risks for <strong>TRD</strong> were found ≤ 180 days before treatment start for the subcategories of sedative use (aOR = 2.37; 1.88 2.99), opioids (aOR = 2.02; 1.48 2.75), <b>alcohol</b> (aOR = 1.77; CI = 1.59 1.98) and combined substance use (aOR = 2.31; 1.87 2.99).
+TRD	drug	opioid	31656053	Increased risks for <strong>TRD</strong> were found ≤ 180 days before treatment start for the subcategories of sedative use (aOR = 2.37; 1.88 2.99), <b>opioids</b> (aOR = 2.02; 1.48 2.75), alcohol (aOR = 1.77; CI = 1.59 1.98) and combined substance use (aOR = 2.31; 1.87 2.99).
+TRD	drug	psychedelics	31514448	The N methyl D aspartate receptor (NDMAR) antagonist <b>ketamine</b> has been shown to rapidly improve symptoms of depression in patients with <strong>TRD</strong>.
+TRD	drug	psychedelics	31514448	We examined the relationship between childhood maltreatment using the Childhood Trauma Questionnaire (CTQ) and treatment response using the Quick Inventory of Depressive Symptoms Self Report (QIDS SR) in <strong>TRD</strong> patients receiving intravenous <b>ketamine</b> at a community outpatient clinic.
+TRD	drug	psychedelics	31514448	In contrast to conventional antidepressants, <b>ketamine</b> could be more effective in <strong>TRD</strong> patients with more childhood trauma burden, perhaps due to <b>ketamine</b>'s proposed ability to block trauma associated behavioral sensitization.
+TRD	addiction	sensitization	31514448	In contrast to conventional antidepressants, ketamine could be more effective in <strong>TRD</strong> patients with more childhood trauma burden, perhaps due to ketamine's proposed ability to block trauma associated behavioral <b>sensitization</b>.
+TRD	drug	psychedelics	31494365	To examine the rate and time to relapse for remitters and responders to <b>ketamine</b> in treatment resistant depression (<strong>TRD</strong>).
+TRD	addiction	relapse	31494365	To examine the rate and time to <b>relapse</b> for remitters and responders to ketamine in treatment resistant depression (<strong>TRD</strong>).
+TRD	drug	benzodiazepine	31494365	Subjects with <strong>TRD</strong> were randomized to a single infusion of one of several doses of intravenous ketamine, or <b>midazolam</b>.
+TRD	drug	psychedelics	31494365	Subjects with <strong>TRD</strong> were randomized to a single infusion of one of several doses of intravenous <b>ketamine</b>, or midazolam.
+TRD	drug	psychedelics	31374046	A recent striking advance in the treatment of depression has been the finding of rapid antidepressant effects in over 70% of patients with treatment resistant depression (<strong>TRD</strong>) using <b>ketamine</b>.
+TRD	drug	psychedelics	31282772	While the efficacy of esketamine compared to off label use of racemic <b>ketamine</b> remains unclear, both esketamine's approval for use in <strong>TRD</strong> and longer term safety data may position it preferentially above racemic <b>ketamine</b>, although factors such as cost and monitoring requirements may limit its use.
+TRD	addiction	addiction	31282772	While questions remain regarding duration and frequency of treatment, as well as <b>addictive</b> potential, esketamine is a novel treatment option offering new hope for <strong>TRD</strong>.
+TRD	drug	psychedelics	30858518	The N methyl D aspartate (NMDA) receptor antagonist <b>ketamine</b> is associated with rapid but transient antidepressant effects in patients with treatment resistant unipolar depression (<strong>TRD</strong>).
+TRD	drug	psychedelics	30858518	Based on work suggesting that <b>ketamine</b> and lithium may share overlapping mechanisms of action, we tested lithium compared to placebo as a continuation strategy following <b>ketamine</b> in subjects with <strong>TRD</strong>.
+TRD	drug	psychedelics	30858518	Forty seven participants with <strong>TRD</strong> were enrolled in the study and underwent an initial <b>ketamine</b> infusion, of whom 34 participants were deemed to have at least a partial antidepressant response and were eligible for randomization.
+TRD	drug	psychedelics	30572160	Patients with <strong>TRD</strong> seeking clinical treatment are randomized (1:1) to receive ECT (thrice weekly) or intravenous <b>ketamine</b> (twice weekly) for 3 5 weeks.
+TRD	addiction	relapse	30572160	Patients with <strong>TRD</strong> <b>seeking</b> clinical treatment are randomized (1:1) to receive ECT (thrice weekly) or intravenous ketamine (twice weekly) for 3 5 weeks.
+TRD	drug	psychedelics	30450382	In this review, we will discuss the safety of repeated treatments with <b>ketamine</b> for patients with treatment resistant depression (<strong>TRD</strong>), a condition in which patients with major depression do not show any clinical improvements following treatments with at least two antidepressant drugs.
+TRD	drug	psychedelics	30450382	Numerous small clinical studies have shown that a single, low dose <b>ketamine</b> infusion can rapidly alleviate depressive symptoms and thoughts of suicidality in patients with <strong>TRD</strong>, and these effects can last for about one week.
+TRD	drug	psychedelics	30450382	Additionally, during <b>ketamine</b> infusions, many <strong>TRD</strong> patients report hallucinations and feelings of dissociation and depersonalization, and therefore the effects of repeated treatments of <b>ketamine</b> on cognition must be further examined.
+TRD	drug	psychedelics	30450382	Although more work about the safety of <b>ketamine</b> is warranted, we hope this review will bring some answers about the safety of treating <strong>TRD</strong> with repeated <b>ketamine</b> infusions.
+TRD	drug	psychedelics	30427812	However, the evidence for long term maintenance <b>ketamine</b> therapy for treatment resistant depression (<strong>TRD</strong>) and suicidal behavior is limited.
+TRD	drug	psychedelics	30427812	Two cases of <strong>TRD</strong> achieved functional remission with long term maintenance <b>ketamine</b> treatment.
+TRD	drug	benzodiazepine	30427812	Factors that may contribute to lack of effectiveness of serial ketamine include inadequate mood stabilization in <strong>TRD</strong> in bipolar spectrum diagnoses, concomitant <b>benzodiazepine</b> use, complex comorbidities, and adverse effects such as significant hypertension and severe dissociation.
+TRD	drug	psychedelics	30427812	Factors that may contribute to lack of effectiveness of serial <b>ketamine</b> include inadequate mood stabilization in <strong>TRD</strong> in bipolar spectrum diagnoses, concomitant benzodiazepine use, complex comorbidities, and adverse effects such as significant hypertension and severe dissociation.
+TRD	drug	psychedelics	30427812	Future systematic controlled studies are warranted to establish the efficacy and safety profile of long term <b>ketamine</b> as maintenance therapy for <strong>TRD</strong> with suicidal behavior.
+TRD	addiction	relapse	30055578	Time from <b>relapse</b> to death (<strong>TRD</strong>) was calculated from date of recurrence to date of death.
+TRD	drug	psychedelics	30004254	<b>Ketamine</b> has been studied in adults with <strong>TRD</strong>, but little information is available for adolescents.
+TRD	drug	psychedelics	30004254	This study investigated efficacy and tolerability of intravenous <b>ketamine</b> in adolescents with <strong>TRD</strong>, and explored clinical response predictors.
+TRD	drug	psychedelics	30004254	Adolescents, 12 18 years of age, with <strong>TRD</strong> (failure to respond to two previous antidepressant trials) were administered six <b>ketamine</b> (0.5 mg/kg) infusions over 2 weeks.
+TRD	drug	psychedelics	30004254	These results demonstrate the potential role for <b>ketamine</b> in treating adolescents with <strong>TRD</strong>.
+TRD	drug	psychedelics	29727073	The present study examined the efficacy, safety, and durability of repeated <b>ketamine</b> infusions for the treatment of comorbid posttraumatic stress disorder (PTSD) and treatment resistant depression (<strong>TRD</strong>) in a sample of veterans.
+TRD	drug	psychedelics	29727073	This report suggests that repeated <b>ketamine</b> treatments are safe and may represent an efficacious treatment for individuals with comorbid PTSD and <strong>TRD</strong>.
+TRD	drug	psychedelics	29542371	The drug formulation, the delivery device, the insufflation technique and individual patient factors play an important role in tolerability and efficacy when using IN <b>ketamine</b> for <strong>TRD</strong>.
+TRD	drug	psychedelics	28124853	While the molecular basis of <b>ketamine</b>'s therapeutic effect has not been fully determined, it has shown to effectively and swiftly mitigate the symptoms of <strong>TRD</strong>.
+TRD	drug	psychedelics	28124853	Despite this, <b>ketamine</b> remains a promising pharmacotherapy for <strong>TRD</strong> and further investigation is required.
+TRD	drug	psychedelics	27189960	<b>Ketamine</b> is a rapidly acting antidepressant in patients with treatment resistant depression (<strong>TRD</strong>).
+TRD	drug	psychedelics	27189960	Preclinical data suggest that blockade of metabotropic glutamate (mGlu2/3) receptors shares many overlapping features and mechanisms with <b>ketamine</b> and may also provide rapid efficacy for <strong>TRD</strong> patients.
+TRD	drug	psychedelics	26509083	<b>Ketamine</b> and repetitive transcranial magnetic stimulation (rTMS) have useful roles in <strong>TRD</strong>, but their utility in long term is unknown.
+TRD	drug	psychedelics	26509083	Considering the limitations of existing treatment options, including those of <b>ketamine</b> and rTMS when used as the sole modality of treatment, we suggest a "tiered approach for <strong>TRD</strong>" by combining <b>ketamine</b> and rTMS (alone or along with antidepressants) for rapid remission of acute depression symptoms and to use DepS Y MBCT for maintaining remission and preventing relapse.
+TRD	addiction	relapse	26509083	Considering the limitations of existing treatment options, including those of ketamine and rTMS when used as the sole modality of treatment, we suggest a "tiered approach for <strong>TRD</strong>" by combining ketamine and rTMS (alone or along with antidepressants) for rapid remission of acute depression symptoms and to use DepS Y MBCT for maintaining remission and preventing <b>relapse</b>.
+TRD	drug	psychedelics	25539512	A single subanesthetic infusion of the N methyl D aspartate (NMDA) receptor antagonist <b>ketamine</b> has rapid and potent antidepressant properties in treatment resistant major depressive disorder (<strong>TRD</strong>).
+TRD	drug	psychedelics	25539512	Fifty two <strong>TRD</strong> subjects received an open label infusion of <b>ketamine</b> (0.5mg/kg over 40 minutes), and, four to six hours post infusion, were randomized to either flexible dose (100 200mg/day) riluzole or placebo in the following proportions: Family History Positive (FHP) riluzole (n = 10), FHP placebo (n = 9), Family History Negative (FHN) riluzole (n = 16), and FHN placebo (n = 17).
+TRD	drug	psychedelics	25539512	<b>Ketamine</b>'s extended antidepressant durability in FHP <strong>TRD</strong> should be considered in the design and analysis of <b>ketamine</b> depression trials.
+TRD	drug	psychedelics	24963561	The N methyl D aspartate glutamate receptor antagonist <b>ketamine</b> has demonstrated rapid antidepressant effects in treatment resistant depression (<strong>TRD</strong>).
+TRD	drug	psychedelics	24963561	However, evaluation of <b>ketamine</b>'s neurocognitive aspects in <strong>TRD</strong> has started to be explored.
+TRD	drug	psychedelics	24963561	Six IV infusions of 0.5 mg/Kg <b>ketamine</b> over 40 min were conducted on a Monday Wednesday Friday schedule during a 12 d period on 15 patients with <strong>TRD</strong> followed by a 4 wk observational period.
+TRD	drug	psychedelics	24963561	Our findings suggest a potential baseline neurocognitive predictor of <b>ketamine</b> response and the apparently lack of short term neurocognitive impairment after completion of six <b>ketamine</b> infusions in <strong>TRD</strong>.
+TRD	drug	psychedelics	24434008	The recent discovery of <b>ketamine</b>'s unique antidepressant properties, with rapid onset of response and high rate of responders opens new perspectives for treatment resistant depression (<strong>TRD</strong>).
+TRD	drug	psychedelics	24268616	Safety and efficacy of repeated <b>ketamine</b> infusions were attained without medication free state in patients with <strong>TRD</strong>.
+TRD	drug	psychedelics	22840761	A previous report including 10 participants with treatment resistant major depression (<strong>TRD</strong>) found that six <b>ketamine</b> infusions resulted in a sustained antidepressant effect.
+TRD	drug	psychedelics	22840761	Participants with <strong>TRD</strong> (n = 24) underwent a washout of antidepressant medication followed by a series of up to six IV infusions of <b>ketamine</b> (.5 mg/kg) administered open label three times weekly over a 12 day period.
+TRD	drug	psychedelics	22840761	<b>Ketamine</b> was associated with a rapid antidepressant effect in <strong>TRD</strong> that was predictive of a sustained effect.
+TRD	drug	psychedelics	22303887	The first generation of studies in patients with treatment resistant depression (<strong>TRD</strong>) reported the safety and acute efficacy of a single subanaesthetic dose (0.5 mg/kg) of intravenous <b>ketamine</b>.
+TRD	drug	psychedelics	22303887	Given the potential risks of <b>ketamine</b>, safety considerations will ultimately determine whether this old drug is successfully repositioned as a new therapy for <strong>TRD</strong>.
+TRD	drug	psychedelics	22298121	The N methyl D aspartate antagonist <b>ketamine</b> has rapid antidepressant effects in patients with treatment resistant major depression (<strong>TRD</strong>); these effects have been reported to last for 1 week in some patients.
+TRD	drug	psychedelics	22298121	Forty two subjects (18 65) with <strong>TRD</strong> and a Montgomery Asberg Depression Rating Scale (MADRS) score of ≥ 22 received a single intravenous infusion of <b>ketamine</b> (0.5 mg/kg).
+TRD	drug	psychedelics	19897179	A single subanesthetic (intravenous) IV dose of <b>ketamine</b> might have rapid but transient antidepressant effects in patients with treatment resistant depression (<strong>TRD</strong>).
+TRD	drug	psychedelics	19897179	Here we tested the tolerability, safety, and efficacy of repeated dose open label IV <b>ketamine</b> (six infusions over 12 days) in 10 medication free symptomatic patients with <strong>TRD</strong> who had previously shown a meaningful antidepressant response to a single dose.
+TRD	drug	psychedelics	19897179	These pilot findings suggest feasibility of repeated dose IV <b>ketamine</b> for the acute treatment of <strong>TRD</strong>.
+TRD	drug	psychedelics	19288975	<b>ketamine</b> is well tolerated in <strong>TRD</strong>, and may have rapid and sustained antidepressant properties.
+TRD	addiction	reward	17689921	To assess strain differences in temporal processing, males and females of the SHR, Wistar Kyoto (WKY), and Sprague Dawley (SD) strains were compared on two timing tasks: one requiring maintenance of a lever press for 10 14 s (<strong>TRD</strong>, temporal response differentiation) and the other requiring withholding of a lever press for 10 14 s (DRL, differential <b>reinforcement</b> of low rates).
+TRD	addiction	reward	11704259	As adults, subjects were tested under one of two paradigms   a differential <b>reinforcement</b> of low response rate (DRL) task requiring that subjects withhold a lever press response for 10 14 s or a temporal response differentiation (<strong>TRD</strong>) task requiring that subjects maintain a lever press response for 10 14 s. Training and steady state performance of the DRL and <strong>TRD</strong> tasks were not significantly altered by DFMO treatment.
+TRD	drug	opioid	11124404	The present series of experiments compared the effects of physostigmine, caffeine, pentobarbital, <b>morphine</b>, and <b>naloxone</b> on the performance of a differential reinforcement of low rates with limited hold (DRL LH) and a temporal response differentiation (<strong>TRD</strong>) task.
+TRD	addiction	reward	11124404	The present series of experiments compared the effects of physostigmine, caffeine, pentobarbital, morphine, and naloxone on the performance of a differential <b>reinforcement</b> of low rates with limited hold (DRL LH) and a temporal response differentiation (<strong>TRD</strong>) task.
+TRD	addiction	reward	10719798	Tasks included: temporal response differentiation (<strong>TRD</strong>) to assess timing behavior; differential <b>reinforcement</b> of low response rates (DRL) to assess timing and response inhibition; incremental repeated acquisition (IRA) to assess learning; conditioned position responding (CPR) to assess auditory, visual, and position discrimination; and progressive ratio (PR) to assess motivation.
+TRD	drug	alcohol	10719798	<b>Ethanol</b> (0.0, 0.5, 1.0, 1.5, 2.0, and 3.0 g/kg via orogastric gavage) reduced accuracy and/or percent task completed for the <strong>TRD</strong>, DRL, and CPR tasks.
+TRD	drug	nicotine	10672976	The present experiment assessed <b>nicotine</b>'s effects on complex cognitive processes using a variety of operant tasks in rats, including incremental repeated acquisition (IRA) to assess learning; conditioned position responding (CPR) to assess auditory, visual, and position discrimination; progressive ratio (PR) to assess motivation; temporal response differentiation (<strong>TRD</strong>) to assess timing; and differential reinforcement of low response rates (DRL) to assess timing and response inhibition.
+TRD	addiction	reward	10672976	The present experiment assessed nicotine's effects on complex cognitive processes using a variety of <b>operant</b> tasks in rats, including incremental repeated acquisition (IRA) to assess learning; conditioned position responding (CPR) to assess auditory, visual, and position discrimination; progressive ratio (PR) to assess motivation; temporal response differentiation (<strong>TRD</strong>) to assess timing; and differential <b>reinforcement</b> of low response rates (DRL) to assess timing and response inhibition.
+TRD	drug	nicotine	10672976	For <strong>TRD</strong>, <b>nicotine</b> had a U shaped dose effect on accuracy, but failed to shift the mode of the <strong>TRD</strong> response distribution.
+TRD	drug	benzodiazepine	8848440	Acute administration of <b>diazepam</b> (0.25 4.0 mg/kg, IP) altered <strong>TRD</strong> performance only.
+TRD	addiction	reward	8516351	The effects of acute pentobarbital treatment were assessed using a complex <b>operant</b> test battery containing five tasks in which correct performance is thought to depend upon processes associated with short term memory and attention [delayed matching to sample (DMTS)], color and position discrimination [conditioned position responding (CPR)], motivation [progressive ratio (PR)], time perception [temporal response differentiation (<strong>TRD</strong>)], and learning [incremental repeated acquisition (IRA)].
+TRD	drug	opioid	2017457	The acute effects of <b>morphine</b> sulfate were assessed using a battery of complex food reinforced operant tasks that included temporal response differentiation (<strong>TRD</strong>, n = 5), delayed matching to sample (DMTS, n = 6), progressive ratio (PR, n = 9), incremental repeated acquisition (IRA, n = 9), and conditioned position responding (CPR, n = 7) tasks.
+TRD	addiction	reward	2017457	The acute effects of morphine sulfate were assessed using a battery of complex food reinforced <b>operant</b> tasks that included temporal response differentiation (<strong>TRD</strong>, n = 5), delayed matching to sample (DMTS, n = 6), progressive ratio (PR, n = 9), incremental repeated acquisition (IRA, n = 9), and conditioned position responding (CPR, n = 7) tasks.
+TRD	drug	opioid	2017457	These results indicate that in monkeys, the performance of operant tasks designed to model learning ability (IRA), time perception (<strong>TRD</strong>) and motivation (PR) are more sensitive to the disruptive effects of <b>morphine</b> than is performance in tasks designed to model short term memory and attention (DMTS).
+TRD	addiction	reward	2017457	These results indicate that in monkeys, the performance of <b>operant</b> tasks designed to model learning ability (IRA), time perception (<strong>TRD</strong>) and motivation (PR) are more sensitive to the disruptive effects of morphine than is performance in tasks designed to model short term memory and attention (DMTS).
+TRD	drug	amphetamine	2345755	The acute effects of d <b>amphetamine</b> were assessed using a battery of complex food reinforced operant tasks that included responding in delayed matching to sample (DMTS, n = 6), conditioned position responding (CPR, n = 7), progressive ratio (PR, n = 8), temporal response differentiation (<strong>TRD</strong>, n = 4), and incremental repeated acquisition (IRA, n = 9) tasks.
+TRD	addiction	reward	2345755	The acute effects of d amphetamine were assessed using a battery of complex food reinforced <b>operant</b> tasks that included responding in delayed matching to sample (DMTS, n = 6), conditioned position responding (CPR, n = 7), progressive ratio (PR, n = 8), temporal response differentiation (<strong>TRD</strong>, n = 4), and incremental repeated acquisition (IRA, n = 9) tasks.
+TRD	drug	amphetamine	2345755	Thus, the relative sensitivities of these tasks for detecting d <b>amphetamine</b> behavioral effects were IRA = <strong>TRD</strong> greater than PR = DMTS greater than CPR.
+TRD	drug	benzodiazepine	2626452	The acute effects of <b>diazepam</b> (<b>Valium</b>) were assessed using a battery of complex food reinforced operant tasks that included responding in delayed matching to sample (DMTS, n = 5), conditioned position response (CPR, n = 7) progressive ratio (PR, n = 8), temporal response differentiation (<strong>TRD</strong>, n = 4), and incremental repeated acquisition (IRA, n = 9) tests.
+TRD	addiction	reward	2626452	The acute effects of diazepam (Valium) were assessed using a battery of complex food reinforced <b>operant</b> tasks that included responding in delayed matching to sample (DMTS, n = 5), conditioned position response (CPR, n = 7) progressive ratio (PR, n = 8), temporal response differentiation (<strong>TRD</strong>, n = 4), and incremental repeated acquisition (IRA, n = 9) tests.
+TRD	drug	benzodiazepine	2626452	<b>Diazepam</b> (0.25 4.0 mg/kg IV) produced significant dose dependent decreases in the number of reinforcers obtained in the <strong>TRD</strong> and IRA tasks only.
+TRD	drug	cannabinoid	2770412	The acute behavioral effects of <b>marijuana</b> smoke were assessed in rhesus monkeys using a battery of food reinforced complex operant tasks that included incremental repeated acquisition (IRA, n = 9), conditioned position responding (CPR, n = 8), progressive ratio (PR, n = 8), delayed matching to sample (DMTS, n = 6), and temporal response differentiation responding (<strong>TRD</strong>, n = 3).
+TRD	addiction	reward	2770412	The acute behavioral effects of marijuana smoke were assessed in rhesus monkeys using a battery of food reinforced complex <b>operant</b> tasks that included incremental repeated acquisition (IRA, n = 9), conditioned position responding (CPR, n = 8), progressive ratio (PR, n = 8), delayed matching to sample (DMTS, n = 6), and temporal response differentiation responding (<strong>TRD</strong>, n = 3).
+TRD	drug	cannabinoid	2770412	In the three animals performing under all five schedules, the relative sensitivities for detecting <b>marijuana</b> behavioral effects were DMTS = <strong>TRD</strong> greater than IRA = CPR greater than PR.
+TRD	drug	cannabinoid	2834536	Acute effects of delta 9 <b>tetrahydrocannabinol</b> (<b>THC</b>) were assessed using a battery of food reinforced complex operant tasks that included responding under delayed matching to sample (DMTS, n = 6), conditioned position response (CPR, n = 8) progressive ratio (PR, n = 8), temporal response differentiation (<strong>TRD</strong>, n = 3) and incremental repeated acquisition (IRA, n = 9) tasks.
+TRD	addiction	reward	2834536	Acute effects of delta 9 tetrahydrocannabinol (THC) were assessed using a battery of food reinforced complex <b>operant</b> tasks that included responding under delayed matching to sample (DMTS, n = 6), conditioned position response (CPR, n = 8) progressive ratio (PR, n = 8), temporal response differentiation (<strong>TRD</strong>, n = 3) and incremental repeated acquisition (IRA, n = 9) tasks.
+TRD	drug	cannabinoid	2834536	The relative sensitivities of these tests for detecting <b>THC</b> behavioral effects were thus <strong>TRD</strong> greater than IRA = DMTS = CPR greater than PR.
+TAAR1	drug	amphetamine	32424970	Trace amine associated receptor 1 (<strong>Taar1</strong>) impacts <b>methamphetamine</b> (MA) intake.
+TAAR1	drug	amphetamine	32424970	<strong>Trace amine associated receptor 1</strong> (<strong>Taar1</strong>) impacts <b>methamphetamine</b> (MA) intake.
+TAAR1	drug	alcohol	32407821	Effects of a <strong>trace amine associated receptor 1</strong> agonist RO 5263397 on <b>ethanol</b> induced behavioral sensitization.
+TAAR1	addiction	sensitization	32407821	Effects of a <strong>trace amine associated receptor 1</strong> agonist RO 5263397 on ethanol induced behavioral <b>sensitization</b>.
+TAAR1	drug	alcohol	32407821	While <strong>TAAR1</strong> is critically involved in the modulation of dopamine, there is little evidence indicating that <strong>TAAR1</strong> could play a role in behavioral effects of <b>ethanol</b>.
+TAAR1	drug	alcohol	32407821	By using the animal model of behavioral sensitization induced by <b>ethanol</b> in mice, the present study was performed to investigate whether the activation of <strong>TAAR1</strong> would affect the behavioral plasticity of <b>ethanol</b>.
+TAAR1	addiction	sensitization	32407821	By using the animal model of behavioral <b>sensitization</b> induced by ethanol in mice, the present study was performed to investigate whether the activation of <strong>TAAR1</strong> would affect the behavioral plasticity of ethanol.
+TAAR1	drug	alcohol	32407821	The <strong>TAAR1</strong> agonist RO5263397 significantly decreased the expression of <b>ethanol</b> induced behavioral sensitization both in male and female WT mice (0.1 and 0.32 mg/kg).
+TAAR1	addiction	sensitization	32407821	The <strong>TAAR1</strong> agonist RO5263397 significantly decreased the expression of ethanol induced behavioral <b>sensitization</b> both in male and female WT mice (0.1 and 0.32 mg/kg).
+TAAR1	drug	alcohol	32407821	Moreover, while <strong>TAAR1</strong> KO mice developed normal levels of <b>ethanol</b> induced behavioral sensitization, RO5263397 did not affect this behavior in <strong>TAAR1</strong> KO mice.
+TAAR1	addiction	sensitization	32407821	Moreover, while <strong>TAAR1</strong> KO mice developed normal levels of ethanol induced behavioral <b>sensitization</b>, RO5263397 did not affect this behavior in <strong>TAAR1</strong> KO mice.
+TAAR1	drug	alcohol	32407821	These results indicated that the <strong>TAAR1</strong> agonist RO5263397 negatively regulated the expression and development of <b>ethanol</b> elicited behavioral sensitization in WT but not in <strong>TAAR1</strong> KO mice.
+TAAR1	addiction	sensitization	32407821	These results indicated that the <strong>TAAR1</strong> agonist RO5263397 negatively regulated the expression and development of ethanol elicited behavioral <b>sensitization</b> in WT but not in <strong>TAAR1</strong> KO mice.
+TAAR1	drug	alcohol	32407821	The present study suggests that <strong>TAAR1</strong> is probably involved in certain addiction like effects of <b>alcohol</b> and could be a useful drug target for the development of new medications to treat <b>alcohol</b> dependence.
+TAAR1	addiction	addiction	32407821	The present study suggests that <strong>TAAR1</strong> is probably involved in certain <b>addiction</b> like effects of alcohol and could be a useful drug target for the development of new medications to treat alcohol dependence.
+TAAR1	addiction	dependence	32407821	The present study suggests that <strong>TAAR1</strong> is probably involved in certain addiction like effects of alcohol and could be a useful drug target for the development of new medications to treat alcohol <b>dependence</b>.
+TAAR1	drug	cocaine	32246467	<strong>TAAR1</strong> agonists attenuate extended access <b>cocaine</b> self administration and yohimbine induced reinstatement of <b>cocaine</b> seeking.
+TAAR1	addiction	relapse	32246467	<strong>TAAR1</strong> agonists attenuate extended access cocaine self administration and yohimbine induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+TAAR1	drug	cocaine	32246467	Our previous studies demonstrated that <strong>TAAR1</strong> agonists attenuated cue  and drug induced <b>cocaine</b> seeking and increased the elasticity of the <b>cocaine</b> demand curve, in the short access <b>cocaine</b> self administration model.
+TAAR1	addiction	relapse	32246467	Our previous studies demonstrated that <strong>TAAR1</strong> agonists attenuated cue  and drug induced cocaine <b>seeking</b> and increased the elasticity of the cocaine demand curve, in the short access cocaine self administration model.
+TAAR1	drug	cocaine	32246467	To characterize the role of <strong>TAAR1</strong> in compulsive <b>cocaine</b> use, we evaluated the effects of activation of <strong>TAAR1</strong> on <b>cocaine</b> intake, <b>cocaine</b> binge and cue induced <b>cocaine</b> seeking using the extended access <b>cocaine</b> self administration model in adult male Sprague Dawley rats.
+TAAR1	addiction	addiction	32246467	To characterize the role of <strong>TAAR1</strong> in <b>compulsive</b> cocaine use, we evaluated the effects of activation of <strong>TAAR1</strong> on cocaine intake, cocaine binge and cue induced cocaine seeking using the extended access cocaine self administration model in adult male Sprague Dawley rats.
+TAAR1	addiction	intoxication	32246467	To characterize the role of <strong>TAAR1</strong> in compulsive cocaine use, we evaluated the effects of activation of <strong>TAAR1</strong> on cocaine intake, cocaine <b>binge</b> and cue induced cocaine seeking using the extended access cocaine self administration model in adult male Sprague Dawley rats.
+TAAR1	addiction	relapse	32246467	To characterize the role of <strong>TAAR1</strong> in compulsive cocaine use, we evaluated the effects of activation of <strong>TAAR1</strong> on cocaine intake, cocaine binge and cue induced cocaine <b>seeking</b> using the extended access cocaine self administration model in adult male Sprague Dawley rats.
+TAAR1	drug	cocaine	32246467	We also investigated the role of <strong>TAAR1</strong> in stress triggered <b>cocaine</b> relapse by using the α2  adrenoceptor antagonist yohimbine induced reinstatement of <b>cocaine</b> seeking.
+TAAR1	addiction	relapse	32246467	We also investigated the role of <strong>TAAR1</strong> in stress triggered cocaine <b>relapse</b> by using the α2  adrenoceptor antagonist yohimbine induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+TAAR1	drug	cocaine	32246467	The selective <strong>TAAR1</strong> partial agonist RO5263397 attenuated <b>cocaine</b> intake and did not develop tolerance during the 10 day extended access <b>cocaine</b> self administration.
+TAAR1	drug	cocaine	32246467	Furthermore, RO5263397 and the selective <strong>TAAR1</strong> full agonist RO5166017 reduced yohimbine induced reinstatement of <b>cocaine</b> seeking behaviour.
+TAAR1	addiction	relapse	32246467	Furthermore, RO5263397 and the selective <strong>TAAR1</strong> full agonist RO5166017 reduced yohimbine induced <b>reinstatement</b> of cocaine <b>seeking</b> behaviour.
+TAAR1	drug	cocaine	32246467	Activation of <strong>TAAR1</strong> attenuated extended access <b>cocaine</b> self administration and stress induced <b>cocaine</b> reinstatement.
+TAAR1	addiction	relapse	32246467	Activation of <strong>TAAR1</strong> attenuated extended access cocaine self administration and stress induced cocaine <b>reinstatement</b>.
+TAAR1	drug	cocaine	32246467	These results suggest that <strong>TAAR1</strong> agonists are promising pharmacological interventions to treat <b>cocaine</b> use disorder and relapse.
+TAAR1	addiction	relapse	32246467	These results suggest that <strong>TAAR1</strong> agonists are promising pharmacological interventions to treat cocaine use disorder and <b>relapse</b>.
+TAAR1	addiction	addiction	31974906	<strong>TAAR1</strong> and Psychostimulant <b>Addiction</b>.
+TAAR1	addiction	addiction	31974906	In the last decade, many preclinical models of psychostimulant <b>addiction</b> such as drug induced behavioral sensitization, drug induced conditioned place preference, drug self administration, drug discrimination, and relapse models were used to assess the effects of <strong>TAAR1</strong> agonists on psychostimulants' behavioral effects.
+TAAR1	addiction	relapse	31974906	In the last decade, many preclinical models of psychostimulant addiction such as drug induced behavioral sensitization, drug induced conditioned place preference, drug self administration, drug discrimination, and <b>relapse</b> models were used to assess the effects of <strong>TAAR1</strong> agonists on psychostimulants' behavioral effects.
+TAAR1	addiction	sensitization	31974906	In the last decade, many preclinical models of psychostimulant addiction such as drug induced behavioral <b>sensitization</b>, drug induced conditioned place preference, drug self administration, drug discrimination, and relapse models were used to assess the effects of <strong>TAAR1</strong> agonists on psychostimulants' behavioral effects.
+TAAR1	addiction	addiction	31974906	Here, we review the advances in <strong>TAAR1</strong> and its agonists in modulating psychostimulant <b>addiction</b>.
+TAAR1	addiction	addiction	31974906	In conclusion, although further investigations are in need to address certain concerns and the underlying neural mechanisms, <strong>TAAR1</strong> agonists appear to be a promising pharmacotherapy to treat psychostimulant <b>addiction</b> and prevent relapse.
+TAAR1	addiction	relapse	31974906	In conclusion, although further investigations are in need to address certain concerns and the underlying neural mechanisms, <strong>TAAR1</strong> agonists appear to be a promising pharmacotherapy to treat psychostimulant addiction and prevent <b>relapse</b>.
+TAAR1	drug	opioid	31925906	Data from a family of recombinant inbred mouse strains support the influence of Oprm1 genotype, but not <strong>Taar1</strong> genotype, on thermal response to <b>morphine</b>.
+TAAR1	drug	amphetamine	31912366	We previously found that the biochemical cascade leading to this cellular process involves entry of <b>AMPH</b> into the cell through the DAT, stimulation of an intracellular trace amine associated receptor, <strong>TAAR1</strong>, and activation of the small GTPase, RhoA.
+TAAR1	drug	amphetamine	31600226	<b>Methamphetamine</b> (MA) is a potent agonist at the trace amine associated receptor 1 (<strong>TAAR1</strong>).
+TAAR1	drug	amphetamine	31600226	<b>Methamphetamine</b> (MA) is a potent agonist at the <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>).
+TAAR1	addiction	dependence	31600226	This study evaluated a common variant (CV) in the human <strong>TAAR1</strong> gene, synonymous single nucleotide polymorphism (SNP) V288V, to determine the involvement of <strong>TAAR1</strong> in MA <b>dependence</b>.
+TAAR1	addiction	relapse	31600226	Analyses of study group and <strong>TAAR1</strong> genotype revealed a significant interaction for PC3 (<b>craving</b> response) (p = 0.003).
+TAAR1	addiction	relapse	31600226	The control group showed no difference in PC3 associated with <strong>TAAR1</strong>, while adjusted mean <b>craving</b> for the MA ACT and MA REM groups, among those with at least one copy of V288V, was estimated to be, respectively, 1.55 (p = 0.036) and 1.77 (p = 0.071) times the adjusted mean <b>craving</b> for those without the <strong>TAAR1</strong> SNP.
+TAAR1	addiction	relapse	31600226	Neuroadaptation to chronic MA use may be altered by <strong>TAAR1</strong> genotype and result in increased dopamine signaling and <b>craving</b> in individuals with the V288V genotype.
+TAAR1	drug	amphetamine	31409621	SIGNIFICANCE STATEMENT: <b>Methamphetamine</b> stimulates <strong>TAAR1</strong>, a G protein coupled receptor.
+TAAR1	drug	amphetamine	31409621	The role and mechanisms for <strong>TAAR1</strong> in <b>methamphetamine</b> induced neurotoxicity are not known.
+TAAR1	drug	amphetamine	31320495	The Role of Biogenic Amine Transporters in <strong>Trace Amine Associated Receptor 1</strong> Regulation of <b>Methamphetamine</b> Induced Neurotoxicity.
+TAAR1	addiction	intoxication	31320495	To investigate interactions among <strong>TAAR1</strong>, VMAT2, and DAT, transporter function and expression were measured in transgenic <strong>Taar1</strong> knockout (KO) and wild type (WT) mice 24 hours following a <b>binge</b> like regimen (four intraperitoneal injections, 2 hours apart) of MA (5 mg/kg) or the same schedule of saline treatment.
+TAAR1	drug	amphetamine	31320495	SIGNIFICANCE STATEMENT: <b>Methamphetamine</b> stimulates the G protein coupled receptor <strong>TAAR1</strong> to affect dopaminergic function and neurotoxicity.
+TAAR1	drug	amphetamine	31320495	Here we demonstrate that a functional <strong>TAAR1</strong> protects a specific subcellular fraction of VMAT2, but not the dopamine transporter, from <b>methamphetamine</b> induced effects, suggesting new directions in pharmacotherapeutic development for neurodegenerative disorders.
+TAAR1	drug	amphetamine	31274109	<strong>Taar1</strong> gene variants have a causal role in <b>methamphetamine</b> intake and response and interact with Oprm1.
+TAAR1	drug	opioid	31274109	We nominated the trace amine associated receptor 1 gene, <strong>Taar1</strong>, as the strongest candidate and identified regulation of the mu <b>opioid</b> receptor 1 gene, Oprm1, as another contributor.
+TAAR1	drug	opioid	31274109	We nominated the <strong>trace amine associated receptor 1</strong> gene, <strong>Taar1</strong>, as the strongest candidate and identified regulation of the mu <b>opioid</b> receptor 1 gene, Oprm1, as another contributor.
+TAAR1	drug	amphetamine	31274109	This study exploited CRISPR Cas9 to test the causal role of <strong>Taar1</strong> in <b>methamphetamine</b> intake and a genetically associated thermal response to <b>methamphetamine</b>.
+TAAR1	drug	amphetamine	31274109	Both <b>methamphetamine</b> intake and the thermal response mapped to <strong>Taar1</strong> and the independent effect of <strong>Taar1</strong> was dependent on genotype at Oprm1.
+TAAR1	drug	amphetamine	31274109	Our findings encourage investigation of the contribution of <strong>Taar1</strong> and Oprm1 variants to human <b>methamphetamine</b> addiction.
+TAAR1	addiction	addiction	31274109	Our findings encourage investigation of the contribution of <strong>Taar1</strong> and Oprm1 variants to human methamphetamine <b>addiction</b>.
+TAAR1	drug	amphetamine	30783122	Of note, <b>Amphetamine</b>, an agonist for trace amine associated receptor 1 (<strong>TAAR1</strong>) with enhancing dopamine signaling (increase of irritability, aggression, etc.
+TAAR1	drug	amphetamine	30783122	Of note, <b>Amphetamine</b>, an agonist for <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) with enhancing dopamine signaling (increase of irritability, aggression, etc.
+TAAR1	drug	amphetamine	30783122	We carried out further molecular docking modeling and molecular dynamics simulation to explore the molecular interactions between <b>Amphetamine</b> and Theophylline and their important GPCRs targets, including <strong>TAAR1</strong> and adenosine receptors.
+TAAR1	drug	nicotine	29681856	<strong>Trace Amine Associated Receptor 1</strong> Modulates the Locomotor and Sensitization Effects of <b>Nicotine</b>.
+TAAR1	addiction	sensitization	29681856	<strong>Trace Amine Associated Receptor 1</strong> Modulates the Locomotor and <b>Sensitization</b> Effects of Nicotine.
+TAAR1	addiction	addiction	29681856	Trace amine associated receptor 1 (<strong>TAAR1</strong>) has emerged as a promising target for <b>addiction</b> treatments because it affects dopamine transmission in the mesolimbic pathway.
+TAAR1	addiction	addiction	29681856	<strong>Trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) has emerged as a promising target for <b>addiction</b> treatments because it affects dopamine transmission in the mesolimbic pathway.
+TAAR1	drug	alcohol	29681856	<strong>TAAR1</strong> is involved in the effects of addictive drugs, such as amphetamines, cocaine and <b>ethanol</b>, but the impact of <strong>TAAR1</strong> on the effects of nicotine, the psychoactive drug responsible for the development and maintenance of tobacco smoking, has not yet been studied.
+TAAR1	drug	cocaine	29681856	<strong>TAAR1</strong> is involved in the effects of addictive drugs, such as amphetamines, <b>cocaine</b> and ethanol, but the impact of <strong>TAAR1</strong> on the effects of nicotine, the psychoactive drug responsible for the development and maintenance of tobacco smoking, has not yet been studied.
+TAAR1	drug	nicotine	29681856	<strong>TAAR1</strong> is involved in the effects of addictive drugs, such as amphetamines, cocaine and ethanol, but the impact of <strong>TAAR1</strong> on the effects of <b>nicotine</b>, the psychoactive drug responsible for the development and maintenance of <b>tobacco</b> <b>smoking</b>, has not yet been studied.
+TAAR1	addiction	addiction	29681856	<strong>TAAR1</strong> is involved in the effects of <b>addictive</b> drugs, such as amphetamines, cocaine and ethanol, but the impact of <strong>TAAR1</strong> on the effects of nicotine, the psychoactive drug responsible for the development and maintenance of tobacco smoking, has not yet been studied.
+TAAR1	drug	nicotine	29681856	This study was performed to investigate the possible modulatory action of <strong>TAAR1</strong> on the effects of <b>nicotine</b> on locomotor behaviors in rats and mice.
+TAAR1	drug	nicotine	29681856	Pretreatment with the <strong>TAAR1</strong> agonist RO5263397 dose dependently decreased <b>nicotine</b> induced hyperlocomotion in rats habituated to locomotor boxes, prevented the development of <b>nicotine</b> sensitization and blocked hypermotility in <b>nicotine</b> sensitized rats at the highest tested dose (10 mg/kg).
+TAAR1	addiction	sensitization	29681856	Pretreatment with the <strong>TAAR1</strong> agonist RO5263397 dose dependently decreased nicotine induced hyperlocomotion in rats habituated to locomotor boxes, prevented the development of nicotine <b>sensitization</b> and blocked hypermotility in nicotine sensitized rats at the highest tested dose (10 mg/kg).
+TAAR1	drug	nicotine	29681856	The lack of <strong>TAAR1</strong> failed to affect the effects of <b>nicotine</b> on the locomotion of mutant mice.
+TAAR1	drug	nicotine	29681856	Based on the results of the present study, <strong>TAAR1</strong> activation attenuates the locomotion stimulating effects of <b>nicotine</b> on rats.
+TAAR1	addiction	addiction	29681856	These results further support the previously proposed hypothesis that <strong>TAAR1</strong> is a promising target for the prevention and treatment of drug <b>addiction</b>.
+TAAR1	drug	nicotine	29681856	Further studies aimed at analyzing the effects of <strong>TAAR1</strong> agonists on animal models of <b>nicotine</b> addiction are warranted.
+TAAR1	addiction	addiction	29681856	Further studies aimed at analyzing the effects of <strong>TAAR1</strong> agonists on animal models of nicotine <b>addiction</b> are warranted.
+TAAR1	drug	amphetamine	29520239	Moreover, during the IDT, we tested the effects of <b>amphetamine</b> (<b>AMPH</b>) and RO 5203648, a trace amine associated receptor 1 (<strong>TAAR1</strong>) partial agonist.
+TAAR1	drug	amphetamine	29520239	Moreover, during the IDT, we tested the effects of <b>amphetamine</b> (<b>AMPH</b>) and RO 5203648, a <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) partial agonist.
+TAAR1	drug	nicotine	29472642	Role of <strong>trace amine associated receptor 1</strong> in <b>nicotine</b>'s behavioral and neurochemical effects.
+TAAR1	addiction	addiction	29472642	Trace amine associated receptor 1 (<strong>TAAR1</strong>) is thought to directly modulate dopaminergic system and are thought to be a neural substrate underlying <b>addictive</b> like behaviors.
+TAAR1	addiction	addiction	29472642	<strong>Trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) is thought to directly modulate dopaminergic system and are thought to be a neural substrate underlying <b>addictive</b> like behaviors.
+TAAR1	drug	nicotine	29472642	We aimed to investigate the role of <strong>TAAR1</strong> in <b>nicotine</b> addictive like behaviors.
+TAAR1	addiction	addiction	29472642	We aimed to investigate the role of <strong>TAAR1</strong> in nicotine <b>addictive</b> like behaviors.
+TAAR1	drug	nicotine	29472642	<strong>TAAR1</strong> expression after <b>nicotine</b> treatment was evaluated by western blotting.
+TAAR1	drug	nicotine	29472642	We then thoroughly and systematically examined the role of <strong>TAAR1</strong> in mediating <b>nicotine</b> induced sensitization, <b>nicotine</b> discrimination, <b>nicotine</b> self administration, <b>nicotine</b> demand curve, and the reinstatement of <b>nicotine</b> seeking.
+TAAR1	addiction	relapse	29472642	We then thoroughly and systematically examined the role of <strong>TAAR1</strong> in mediating nicotine induced sensitization, nicotine discrimination, nicotine self administration, nicotine demand curve, and the <b>reinstatement</b> of nicotine <b>seeking</b>.
+TAAR1	addiction	sensitization	29472642	We then thoroughly and systematically examined the role of <strong>TAAR1</strong> in mediating nicotine induced <b>sensitization</b>, nicotine discrimination, nicotine self administration, nicotine demand curve, and the reinstatement of nicotine seeking.
+TAAR1	drug	nicotine	29472642	Local pharmacological manipulation was conducted to determine the role of <strong>TAAR1</strong> in the nucleus accumbens (NAcs) in the reinstatement of <b>nicotine</b> seeking.
+TAAR1	addiction	relapse	29472642	Local pharmacological manipulation was conducted to determine the role of <strong>TAAR1</strong> in the nucleus accumbens (NAcs) in the <b>reinstatement</b> of nicotine <b>seeking</b>.
+TAAR1	drug	nicotine	29472642	<strong>TAAR1</strong> activation was sufficient to block <b>nicotine</b> induced c Fos expression in the NAc, while also reducing <b>nicotine</b> induced dopamine release in the NAc.
+TAAR1	drug	nicotine	29472642	Systemic administration of <strong>TAAR1</strong> agonists attenuated the expression and development of <b>nicotine</b> induced sensitization, <b>nicotine</b> self administration, the reinstatement of <b>nicotine</b> seeking, and increased the elasticity of <b>nicotine</b> demand curve, while intra NAc infusions of a <strong>TAAR1</strong> agonist was sufficient to attenuate <b>nicotine</b> reinstatement.
+TAAR1	addiction	relapse	29472642	Systemic administration of <strong>TAAR1</strong> agonists attenuated the expression and development of nicotine induced sensitization, nicotine self administration, the <b>reinstatement</b> of nicotine <b>seeking</b>, and increased the elasticity of nicotine demand curve, while intra NAc infusions of a <strong>TAAR1</strong> agonist was sufficient to attenuate nicotine <b>reinstatement</b>.
+TAAR1	addiction	sensitization	29472642	Systemic administration of <strong>TAAR1</strong> agonists attenuated the expression and development of nicotine induced <b>sensitization</b>, nicotine self administration, the reinstatement of nicotine seeking, and increased the elasticity of nicotine demand curve, while intra NAc infusions of a <strong>TAAR1</strong> agonist was sufficient to attenuate nicotine reinstatement.
+TAAR1	drug	nicotine	29472642	Moreover, <strong>TAAR1</strong> knockout rats showed augmented cue induced and drug induced reinstatement of <b>nicotine</b> seeking.
+TAAR1	addiction	relapse	29472642	Moreover, <strong>TAAR1</strong> knockout rats showed augmented cue induced and drug induced <b>reinstatement</b> of nicotine <b>seeking</b>.
+TAAR1	drug	nicotine	29472642	These results indicated that modulation of <strong>TAAR1</strong> activity regulates <b>nicotine</b> addictive like behaviors and <strong>TAAR1</strong> represents a novel target towards the treatment of <b>nicotine</b> addiction.
+TAAR1	addiction	addiction	29472642	These results indicated that modulation of <strong>TAAR1</strong> activity regulates nicotine <b>addictive</b> like behaviors and <strong>TAAR1</strong> represents a novel target towards the treatment of nicotine <b>addiction</b>.
+TAAR1	drug	amphetamine	29403379	A Spontaneous Mutation in <strong>Taar1</strong> Impacts <b>Methamphetamine</b> Related Traits Exclusively in DBA/2 Mice from a Single Vendor.
+TAAR1	drug	amphetamine	29403379	Previous findings in <b>methamphetamine</b> drinking (MADR) lines of mice, bred for high or low voluntary MA intake, and in null mutants demonstrate a major impact of the trace amine associated receptor 1 (<strong>Taar1</strong>) gene on a triad of MA related traits: MA consumption, MA induced conditioned taste aversion and MA induced hypothermia.
+TAAR1	addiction	aversion	29403379	Previous findings in methamphetamine drinking (MADR) lines of mice, bred for high or low voluntary MA intake, and in null mutants demonstrate a major impact of the trace amine associated receptor 1 (<strong>Taar1</strong>) gene on a triad of MA related traits: MA consumption, MA induced conditioned taste <b>aversion</b> and MA induced hypothermia.
+TAAR1	drug	amphetamine	29403379	Previous findings in <b>methamphetamine</b> drinking (MADR) lines of mice, bred for high or low voluntary MA intake, and in null mutants demonstrate a major impact of the <strong>trace amine associated receptor 1</strong> (<strong>Taar1</strong>) gene on a triad of MA related traits: MA consumption, MA induced conditioned taste aversion and MA induced hypothermia.
+TAAR1	addiction	aversion	29403379	Previous findings in methamphetamine drinking (MADR) lines of mice, bred for high or low voluntary MA intake, and in null mutants demonstrate a major impact of the <strong>trace amine associated receptor 1</strong> (<strong>Taar1</strong>) gene on a triad of MA related traits: MA consumption, MA induced conditioned taste <b>aversion</b> and MA induced hypothermia.
+TAAR1	addiction	addiction	29375386	<strong>TAAR1</strong> is widely expressed across the mammalian brain, particularly in limbic and monoaminergic areas, allegedly involved in mood, attention, memory, fear, and <b>addiction</b>.
+TAAR1	drug	alcohol	29375386	<strong>TAAR1</strong> knock out mice show a worse performance in anxiety and working memory tests, and they are more prone to develop <b>ethanol</b> addiction.
+TAAR1	addiction	addiction	29375386	<strong>TAAR1</strong> knock out mice show a worse performance in anxiety and working memory tests, and they are more prone to develop ethanol <b>addiction</b>.
+TAAR1	drug	amphetamine	29348190	Hyperactivity of DAT KO rats can be counteracted by <b>amphetamine</b>, methylphenidate, the partial Trace Amine Associated Receptor 1 (<strong>TAAR1</strong>) agonist RO5203648 ((S) 4 (3,4 Dichloro phenyl) 4,5 dihydro oxazol 2 ylamine) and haloperidol.
+TAAR1	drug	amphetamine	29348190	Hyperactivity of DAT KO rats can be counteracted by <b>amphetamine</b>, methylphenidate, the partial <strong>Trace Amine Associated Receptor 1</strong> (<strong>TAAR1</strong>) agonist RO5203648 ((S) 4 (3,4 Dichloro phenyl) 4,5 dihydro oxazol 2 ylamine) and haloperidol.
+TAAR1	drug	amphetamine	29128305	We also examined whether the trace amine associated receptor 1 (<strong>TAAR1</strong>) agonist RO5263397 attenuated <b>methamphetamine</b> induced effects in parallel tests.
+TAAR1	drug	amphetamine	29128305	We also examined whether the <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) agonist RO5263397 attenuated <b>methamphetamine</b> induced effects in parallel tests.
+TAAR1	drug	amphetamine	29128305	These results suggest that acute discontinuation from prolonged <b>methamphetamine</b> treatment increases impulsivity, which can be reduced by a <strong>TAAR1</strong> agonist.
+TAAR1	drug	cocaine	28123023	Role of <strong>TAAR1</strong> within the Subregions of the Mesocorticolimbic Dopaminergic System in <b>Cocaine</b> Seeking Behavior.
+TAAR1	addiction	relapse	28123023	Role of <strong>TAAR1</strong> within the Subregions of the Mesocorticolimbic Dopaminergic System in Cocaine <b>Seeking</b> Behavior.
+TAAR1	addiction	relapse	28123023	A novel G protein coupled receptor, trace amine associated receptor 1 (<strong>TAAR1</strong>), has been shown to be a promising target to prevent stimulant <b>relapse</b>.
+TAAR1	addiction	relapse	28123023	A novel G protein coupled receptor, <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>), has been shown to be a promising target to prevent stimulant <b>relapse</b>.
+TAAR1	drug	cocaine	28123023	Our recent studies showed that systemic administration of <strong>TAAR1</strong> agonists decreased abuse related behaviors of <b>cocaine</b>.
+TAAR1	addiction	addiction	28123023	However, the role of <strong>TAAR1</strong> in specific subregions of the reward system in drug <b>addiction</b> is unknown.
+TAAR1	addiction	reward	28123023	However, the role of <strong>TAAR1</strong> in specific subregions of the <b>reward</b> system in drug addiction is unknown.
+TAAR1	drug	cocaine	28123023	Here, using a local pharmacological activation method, we assessed the role of <strong>TAAR1</strong> within the subregions of the mesocorticolimbic system: that is, the VTA, the prelimbic cortex (PrL), and infralimbic cortex of medial prefrontal cortex, the core and shell of NAc, BLA, and CeA, on cue  and drug induced <b>cocaine</b> seeking in the rat <b>cocaine</b> reinstatement model.
+TAAR1	addiction	relapse	28123023	Here, using a local pharmacological activation method, we assessed the role of <strong>TAAR1</strong> within the subregions of the mesocorticolimbic system: that is, the VTA, the prelimbic cortex (PrL), and infralimbic cortex of medial prefrontal cortex, the core and shell of NAc, BLA, and CeA, on cue  and drug induced cocaine <b>seeking</b> in the rat cocaine <b>reinstatement</b> model.
+TAAR1	drug	cocaine	28123023	Together, these results indicate that <strong>TAAR1</strong> in different subregions of the mesocorticolimbic system distinctly contributes to cue  and drug induced reinstatement of <b>cocaine</b> seeking behavior.
+TAAR1	addiction	relapse	28123023	Together, these results indicate that <strong>TAAR1</strong> in different subregions of the mesocorticolimbic system distinctly contributes to cue  and drug induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+TAAR1	drug	cocaine	28123023	Previous research showed that systemic administration of <strong>TAAR1</strong> agonists could attenuate <b>cocaine</b> related behaviors, suggesting that <strong>TAAR1</strong> may be a promising drug target for the treatment of <b>cocaine</b> addiction.
+TAAR1	addiction	addiction	28123023	Previous research showed that systemic administration of <strong>TAAR1</strong> agonists could attenuate cocaine related behaviors, suggesting that <strong>TAAR1</strong> may be a promising drug target for the treatment of cocaine <b>addiction</b>.
+TAAR1	addiction	addiction	28123023	However, the specific role of <strong>TAAR1</strong> in subregions of the mesocorticolimbic system in drug <b>addiction</b> is unknown.
+TAAR1	drug	cocaine	28123023	Then, by using a local pharmacological activation method, we demonstrated that <strong>TAAR1</strong> in different subregions of the mesocorticolimbic system distinctly contributes to cue  and drug induced reinstatement of <b>cocaine</b> seeking behavior.
+TAAR1	addiction	relapse	28123023	Then, by using a local pharmacological activation method, we demonstrated that <strong>TAAR1</strong> in different subregions of the mesocorticolimbic system distinctly contributes to cue  and drug induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+TAAR1	drug	amphetamine	27193165	A partial <strong>trace amine associated receptor 1</strong> agonist exhibits properties consistent with a <b>methamphetamine</b> substitution treatment.
+TAAR1	drug	cocaine	27193165	Several selective <strong>TAAR1</strong> agonists have previously shown efficacy in models of <b>cocaine</b> addiction.
+TAAR1	addiction	addiction	27193165	Several selective <strong>TAAR1</strong> agonists have previously shown efficacy in models of cocaine <b>addiction</b>.
+TAAR1	drug	amphetamine	27193165	However, the effects of <strong>TAAR1</strong> activation on <b>methamphetamine</b> (<b>METH</b>) induced behaviours are less well understood, as indeed are the underlying neurochemical mechanisms mediating potential interactions between <strong>TAAR1</strong> and <b>METH</b>.
+TAAR1	drug	amphetamine	27193165	Here, in a progressive ratio schedule of reinforcement the partial <strong>TAAR1</strong> agonist, RO5263397, reduced the break point for <b>METH</b> self administration, while significantly increasing responding maintained by food reward.
+TAAR1	addiction	reward	27193165	Here, in a progressive ratio schedule of <b>reinforcement</b> the partial <strong>TAAR1</strong> agonist, RO5263397, reduced the break point for METH self administration, while significantly increasing responding maintained by food <b>reward</b>.
+TAAR1	drug	amphetamine	27193165	Collectively, the present observations demonstrate that partial <strong>TAAR1</strong> activation decreases the motivation to self administer <b>METH</b>, blocks <b>METH</b> primed reinstatement of <b>METH</b> seeking and prevents <b>METH</b> induced DA elevations in the nucleus accumbens, and strongly support the candidacy of <strong>TAAR1</strong> based medications as potential substitute treatment in <b>METH</b> addiction.
+TAAR1	addiction	addiction	27193165	Collectively, the present observations demonstrate that partial <strong>TAAR1</strong> activation decreases the motivation to self administer METH, blocks METH primed reinstatement of METH seeking and prevents METH induced DA elevations in the nucleus accumbens, and strongly support the candidacy of <strong>TAAR1</strong> based medications as potential substitute treatment in METH <b>addiction</b>.
+TAAR1	addiction	relapse	27193165	Collectively, the present observations demonstrate that partial <strong>TAAR1</strong> activation decreases the motivation to self administer METH, blocks METH primed <b>reinstatement</b> of METH <b>seeking</b> and prevents METH induced DA elevations in the nucleus accumbens, and strongly support the candidacy of <strong>TAAR1</strong> based medications as potential substitute treatment in METH addiction.
+TAAR1	drug	amphetamine	27055611	In addition, mice that consume high levels of <b>methamphetamine</b> were found to possess a nonfunctional form of the trace amine associated receptor 1 (<strong>TAAR1</strong>).
+TAAR1	drug	amphetamine	27055611	In addition, mice that consume high levels of <b>methamphetamine</b> were found to possess a nonfunctional form of the <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>).
+TAAR1	drug	amphetamine	27055611	The <strong>Taar1</strong> gene is within a mouse chromosome 10 quantitative trait locus for <b>methamphetamine</b> consumption, and <strong>TAAR1</strong> function determines sensitivity to aversive effects of <b>methamphetamine</b> that may curb intake.
+TAAR1	addiction	aversion	27055611	The <strong>Taar1</strong> gene is within a mouse chromosome 10 quantitative trait locus for methamphetamine consumption, and <strong>TAAR1</strong> function determines sensitivity to <b>aversive</b> effects of methamphetamine that may curb intake.
+TAAR1	drug	amphetamine	27031617	<b>Methamphetamine</b> (MA) and neurotransmitter precursors and metabolites such as tyramine, octopamine, and β phenethylamine stimulate the G protein coupled trace amine associated receptor 1 (<strong>TAAR1</strong>).
+TAAR1	drug	amphetamine	27031617	<b>Methamphetamine</b> (MA) and neurotransmitter precursors and metabolites such as tyramine, octopamine, and β phenethylamine stimulate the G protein coupled <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>).
+TAAR1	addiction	addiction	27031617	<strong>TAAR1</strong> has been implicated in human conditions including obesity, schizophrenia, depression, fibromyalgia, migraine, and <b>addiction</b>.
+TAAR1	addiction	aversion	27031617	<strong>Taar1</strong> knockout mice orally self administer more MA than wild type and are insensitive to its <b>aversive</b> effects.
+TAAR1	drug	cocaine	26822713	Effects of <strong>Trace Amine associated Receptor 1</strong> Agonists on the Expression, Reconsolidation, and Extinction of <b>Cocaine</b> Reward Memory.
+TAAR1	addiction	reward	26822713	Effects of <strong>Trace Amine associated Receptor 1</strong> Agonists on the Expression, Reconsolidation, and Extinction of Cocaine <b>Reward</b> Memory.
+TAAR1	drug	cocaine	26822713	It has been demonstrated that activation of <strong>trace amine associated receptor 1</strong> decreased the abuse related behaviors of <b>cocaine</b> in rats.
+TAAR1	drug	cocaine	26822713	However, the role of <strong>trace amine associated receptor 1</strong> in specific stages of <b>cocaine</b> reward memory is still unclear.
+TAAR1	addiction	reward	26822713	However, the role of <strong>trace amine associated receptor 1</strong> in specific stages of cocaine <b>reward</b> memory is still unclear.
+TAAR1	drug	cocaine	26822713	Here, using a <b>cocaine</b> induced conditioned place preference model, we tested the effects of a selective <strong>trace amine associated receptor 1</strong> agonist RO5166017 on the expression, reconsolidation, and extinction of <b>cocaine</b> reward memory.
+TAAR1	addiction	reward	26822713	Here, using a cocaine induced conditioned place preference model, we tested the effects of a selective <strong>trace amine associated receptor 1</strong> agonist RO5166017 on the expression, reconsolidation, and extinction of cocaine <b>reward</b> memory.
+TAAR1	drug	cocaine	26822713	self administration model, we found that the combined <strong>trace amine associated receptor 1</strong> partial agonist RO5263397 with extinction had no effect on the following cue  and drug induced reinstatement of <b>cocaine</b> seeking behavior.
+TAAR1	addiction	relapse	26822713	self administration model, we found that the combined <strong>trace amine associated receptor 1</strong> partial agonist RO5263397 with extinction had no effect on the following cue  and drug induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+TAAR1	drug	cocaine	26822713	Repeated administration of the <strong>trace amine associated receptor 1</strong> agonist during extinction showed a continually inhibitory effect on the expression of <b>cocaine</b> reward memory both in <b>cocaine</b> induced conditioned place preference and <b>cocaine</b> self administration models.
+TAAR1	addiction	reward	26822713	Repeated administration of the <strong>trace amine associated receptor 1</strong> agonist during extinction showed a continually inhibitory effect on the expression of cocaine <b>reward</b> memory both in cocaine induced conditioned place preference and cocaine self administration models.
+TAAR1	drug	cocaine	26822713	Taken together, these results indicate that activation of <strong>trace amine associated receptor 1</strong> specifically inhibited the expression of <b>cocaine</b> reward memory.
+TAAR1	addiction	reward	26822713	Taken together, these results indicate that activation of <strong>trace amine associated receptor 1</strong> specifically inhibited the expression of cocaine <b>reward</b> memory.
+TAAR1	drug	cocaine	26822713	The inhibitory effect of <strong>trace amine associated receptor 1</strong> agonists on <b>cocaine</b> reward memory suggests that <strong>trace amine associated receptor 1</strong> agonists could be a promising agent to prevent <b>cocaine</b> relapse.
+TAAR1	addiction	relapse	26822713	The inhibitory effect of <strong>trace amine associated receptor 1</strong> agonists on cocaine reward memory suggests that <strong>trace amine associated receptor 1</strong> agonists could be a promising agent to prevent cocaine <b>relapse</b>.
+TAAR1	addiction	reward	26822713	The inhibitory effect of <strong>trace amine associated receptor 1</strong> agonists on cocaine <b>reward</b> memory suggests that <strong>trace amine associated receptor 1</strong> agonists could be a promising agent to prevent cocaine relapse.
+TAAR1	drug	amphetamine	26791601	Trace amine associated receptor 1 (<strong>TAAR1</strong>) has been implicated in the behavioral effects of <b>amphetamine</b> type stimulant drugs in rodents.
+TAAR1	drug	amphetamine	26791601	<strong>Trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) has been implicated in the behavioral effects of <b>amphetamine</b> type stimulant drugs in rodents.
+TAAR1	addiction	addiction	26791601	<strong>TAAR1</strong> has also been suggested as a target for novel medications to treat psychostimulant <b>addiction</b>.
+TAAR1	addiction	relapse	28317038	Hypothesizing that, A Pro Dopamine Regulator (KB220Z) Should Optimize, but Not Hyper Activate the Activity of <strong>Trace Amine Associated Receptor 1</strong> (TAAR 1) and Induce Anti <b>Craving</b> of Psychostimulants in the Long Term.
+TAAR1	drug	cocaine	28317038	<strong>TAAR1</strong> agonists reduce the neurochemical effects of <b>cocaine</b> and amphetamines as well as attenuate addiction and abuse associated with these two psychostimulants.
+TAAR1	addiction	addiction	28317038	<strong>TAAR1</strong> agonists reduce the neurochemical effects of cocaine and amphetamines as well as attenuate <b>addiction</b> and abuse associated with these two psychostimulants.
+TAAR1	addiction	relapse	28317038	Hyper activation instead of optimizing the <strong>TAAR1</strong> system unfortunately will lead to a prolonged hypodopaminergic state and as such, will cause enhanced <b>craving</b> for not only psychoactive substances, but also other drug related and even non drug related RDS behaviors.
+TAAR1	addiction	addiction	26644139	In keeping with the free thinking tradition San Antonians are known for, the Scientific Program Committee of the Behavior, Biology and Chemistry: Translational Research in <b>Addiction</b> Conference chose trace amine associated receptor 1 (<strong>TAAR1</strong>) as the focus of the plenary symposium for its 7th annual meeting held at the University of Texas Health Science Center at San Antonio on March 14 and 15, 2015.
+TAAR1	addiction	addiction	26644139	In keeping with the free thinking tradition San Antonians are known for, the Scientific Program Committee of the Behavior, Biology and Chemistry: Translational Research in <b>Addiction</b> Conference chose <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) as the focus of the plenary symposium for its 7th annual meeting held at the University of Texas Health Science Center at San Antonio on March 14 and 15, 2015.
+TAAR1	drug	amphetamine	26644139	The consensus was that <strong>TAAR1</strong> is a DA and <b>methamphetamine</b> receptor, interacts with DAT and DA D2 receptors, and is essential in modulating addiction related effects of psychostimulants.
+TAAR1	addiction	addiction	26644139	The consensus was that <strong>TAAR1</strong> is a DA and methamphetamine receptor, interacts with DAT and DA D2 receptors, and is essential in modulating <b>addiction</b> related effects of psychostimulants.
+TAAR1	drug	amphetamine	26640076	Increased context dependent conditioning to <b>amphetamine</b> in mice lacking <strong>TAAR1</strong>.
+TAAR1	drug	amphetamine	26640076	Given the recent evidence indicating that <b>amphetamine</b> derivatives may also act as direct agonists of the G protein coupled trace amine associated receptor 1 (<strong>TAAR1</strong>), we hypothesized that <strong>TAAR1</strong> could contribute to the reinforcing and addictive properties of amphetamines.
+TAAR1	addiction	addiction	26640076	Given the recent evidence indicating that amphetamine derivatives may also act as direct agonists of the G protein coupled trace amine associated receptor 1 (<strong>TAAR1</strong>), we hypothesized that <strong>TAAR1</strong> could contribute to the reinforcing and <b>addictive</b> properties of amphetamines.
+TAAR1	addiction	reward	26640076	Given the recent evidence indicating that amphetamine derivatives may also act as direct agonists of the G protein coupled trace amine associated receptor 1 (<strong>TAAR1</strong>), we hypothesized that <strong>TAAR1</strong> could contribute to the <b>reinforcing</b> and addictive properties of amphetamines.
+TAAR1	drug	amphetamine	26640076	Given the recent evidence indicating that <b>amphetamine</b> derivatives may also act as direct agonists of the G protein coupled <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>), we hypothesized that <strong>TAAR1</strong> could contribute to the reinforcing and addictive properties of amphetamines.
+TAAR1	addiction	addiction	26640076	Given the recent evidence indicating that amphetamine derivatives may also act as direct agonists of the G protein coupled <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>), we hypothesized that <strong>TAAR1</strong> could contribute to the reinforcing and <b>addictive</b> properties of amphetamines.
+TAAR1	addiction	reward	26640076	Given the recent evidence indicating that amphetamine derivatives may also act as direct agonists of the G protein coupled <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>), we hypothesized that <strong>TAAR1</strong> could contribute to the <b>reinforcing</b> and addictive properties of amphetamines.
+TAAR1	drug	amphetamine	26640076	Accordingly, the present study aimed to investigate the role of <strong>TAAR1</strong> in the effects of psychostimulants by analyzing context dependent sensitization and conditioned place preference (CPP) to d <b>amphetamine</b> (<b>AMPH</b>) in <strong>TAAR1</strong> KO mice.
+TAAR1	addiction	reward	26640076	Accordingly, the present study aimed to investigate the role of <strong>TAAR1</strong> in the effects of psychostimulants by analyzing context dependent sensitization and conditioned place preference (<b>CPP</b>) to d amphetamine (AMPH) in <strong>TAAR1</strong> KO mice.
+TAAR1	addiction	sensitization	26640076	Accordingly, the present study aimed to investigate the role of <strong>TAAR1</strong> in the effects of psychostimulants by analyzing context dependent <b>sensitization</b> and conditioned place preference (CPP) to d amphetamine (AMPH) in <strong>TAAR1</strong> KO mice.
+TAAR1	addiction	sensitization	26640076	In context dependent <b>sensitization</b> experiment, <strong>TAAR1</strong> KO mice showed higher conditioned locomotor responses compared to wild type mice.
+TAAR1	drug	amphetamine	26640076	In the CPP test, <strong>TAAR1</strong> KO animals were also more sensitive to priming induced reinstatement of <b>AMPH</b> induced conditioned place preference (CPP) than wild type mice.
+TAAR1	addiction	relapse	26640076	In the CPP test, <strong>TAAR1</strong> KO animals were also more sensitive to priming induced <b>reinstatement</b> of AMPH induced conditioned place preference (CPP) than wild type mice.
+TAAR1	addiction	reward	26640076	In the <b>CPP</b> test, <strong>TAAR1</strong> KO animals were also more sensitive to priming induced reinstatement of AMPH induced conditioned place preference (<b>CPP</b>) than wild type mice.
+TAAR1	drug	amphetamine	26640076	Importantly, saline treated and <b>AMPH</b> treated mice lacking <strong>TAAR1</strong> demonstrated significant alterations in the total levels and phosphorylation of the critical subunit of NMDA glutamate receptors, GluN1, in the striatum, suggesting a role of <strong>TAAR1</strong> in the modulation of frontostriatal glutamate transmission; this effect could underlie the observed alterations in conditioning processes.
+TAAR1	drug	amphetamine	26640076	In conclusion, our data suggest that <strong>TAAR1</strong> receptors play an inhibitory role with respect to conditioned responses to <b>AMPH</b> by modulating, at least in part, corticostriatal glutamate transmission.
+TAAR1	addiction	intoxication	26441502	Future directions include the development of a <b>binge</b> model of MA intake, examining the effect of withdrawal from chronic MA on MA intake, and studying potential <strong>Taar1</strong> gene × gene and gene × environment interactions.
+TAAR1	addiction	withdrawal	26441502	Future directions include the development of a binge model of MA intake, examining the effect of <b>withdrawal</b> from chronic MA on MA intake, and studying potential <strong>Taar1</strong> gene × gene and gene × environment interactions.
+TAAR1	drug	amphetamine	26302754	<b>Methamphetamine</b> induces trace amine associated receptor 1 (<strong>TAAR1</strong>) expression in human T lymphocytes: role in immunomodulation.
+TAAR1	drug	amphetamine	26302754	<b>Methamphetamine</b> induces <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) expression in human T lymphocytes: role in immunomodulation.
+TAAR1	drug	amphetamine	26302754	For the first time, our studies have illustrated that there is an induction of <strong>TAAR1</strong> mRNA expression in resting T lymphocytes in response to <b>methamphetamine</b>.
+TAAR1	drug	amphetamine	26302754	<b>Methamphetamine</b> treatment for 6 h significantly increased <strong>TAAR1</strong> mRNA expression (P < 0.001) and protein expression (P < 0.01) at 24 h. With the use of <strong>TAAR1</strong> gene silencing, we demonstrate that <b>methamphetamine</b> induced cAMP, a classic response to <b>methamphetamine</b> stimulation, is regulated via <strong>TAAR1</strong>.
+TAAR1	drug	amphetamine	26302754	We also show by <strong>TAAR1</strong> knockdown that the down regulation of IL 2 in T cells by <b>methamphetamine</b>, which we reported earlier, is indeed regulated by <strong>TAAR1</strong>.
+TAAR1	drug	amphetamine	26302754	Our results also show the presence of <strong>TAAR1</strong> in human lymph nodes from HIV 1 infected patients, with or without a history of <b>methamphetamine</b> abuse.
+TAAR1	drug	amphetamine	26302754	<strong>TAAR1</strong> expression on lymphocytes was largely in the paracortical lymphoid area of the lymph nodes with enhanced expression in lymph nodes of HIV 1 infected <b>methamphetamine</b> abusers rather than infected only subjects.
+TAAR1	drug	amphetamine	26302754	In vitro analysis of HIV 1 infection of human PBMCs revealed increased <strong>TAAR1</strong> expression in the presence of <b>methamphetamine</b>.
+TAAR1	drug	amphetamine	26302754	In summary, the ability of <b>methamphetamine</b> to activate trace <strong>TAAR1</strong> in vitro and to regulate important T cell functions, such as cAMP activation and IL 2 production; the expression of <strong>TAAR1</strong> in T lymphocytes in peripheral lymphoid organs, such as lymph nodes; and our in vitro HIV 1 infection model in PBMCs suggests that <strong>TAAR1</strong> may play an important role in <b>methamphetamine</b>  mediated immune modulatory responses.
+TAAR1	addiction	addiction	26092759	<strong>Trace amine associated receptor 1</strong>: A promising target for the treatment of psychostimulant <b>addiction</b>.
+TAAR1	drug	cocaine	26048337	Selective activation of the <strong>trace amine associated receptor 1</strong> decreases <b>cocaine</b>'s reinforcing efficacy and prevents <b>cocaine</b> induced changes in brain reward thresholds.
+TAAR1	addiction	reward	26048337	Selective activation of the <strong>trace amine associated receptor 1</strong> decreases cocaine's <b>reinforcing</b> efficacy and prevents cocaine induced changes in brain <b>reward</b> thresholds.
+TAAR1	addiction	addiction	26048337	The newly discovered trace amine associated receptor 1 (<strong>TAAR1</strong>) has emerged as a promising target for medication development in stimulant <b>addiction</b> due to its ability to regulate dopamine (DA) function and modulate stimulants' effects.
+TAAR1	addiction	addiction	26048337	The newly discovered <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) has emerged as a promising target for medication development in stimulant <b>addiction</b> due to its ability to regulate dopamine (DA) function and modulate stimulants' effects.
+TAAR1	drug	cocaine	26048337	Recent findings indicate that <strong>TAAR1</strong> activation blocks some of the abuse related physiological and behavioral effects of <b>cocaine</b>.
+TAAR1	drug	cocaine	26048337	Here, in order to shed light on the influence of <strong>TAAR1</strong> on <b>cocaine</b>'s reward and reinforcement, we studied the effects of partial and full activation of TAAR1on (1) the dose response curve for <b>cocaine</b> self administration and (2) <b>cocaine</b> induced changes in intracranial self stimulation (ICSS).
+TAAR1	addiction	reward	26048337	Here, in order to shed light on the influence of <strong>TAAR1</strong> on cocaine's <b>reward</b> and <b>reinforcement</b>, we studied the effects of partial and full activation of TAAR1on (1) the dose response curve for cocaine self administration and (2) cocaine induced changes in intracranial self stimulation (<b>ICSS</b>).
+TAAR1	drug	cocaine	26048337	In the first experiment, we examined the effects of the selective full and partial <strong>TAAR1</strong> agonists, RO5256390 and RO5203648, on self administration of five unit injection doses of <b>cocaine</b> (0.03, 0.1, 0.2, 0.45, and 1mg/kg/infusion).
+TAAR1	drug	cocaine	26048337	Both agonists induced dose dependent downward shifts in the <b>cocaine</b> dose response curve, indicating that both partial and full <strong>TAAR1</strong> activation decrease <b>cocaine</b>, reinforcing efficacy.
+TAAR1	addiction	reward	26048337	Both agonists induced dose dependent downward shifts in the cocaine dose response curve, indicating that both partial and full <strong>TAAR1</strong> activation decrease cocaine, <b>reinforcing</b> efficacy.
+TAAR1	drug	cocaine	26048337	Taken together, these data demonstrated that <strong>TAAR1</strong> stimulation effectively suppresses the rewarding and reinforcing effects of <b>cocaine</b> in self administration and ICSS models, supporting the candidacy of <strong>TAAR1</strong> as a drug discovery target for <b>cocaine</b> addiction.
+TAAR1	addiction	addiction	26048337	Taken together, these data demonstrated that <strong>TAAR1</strong> stimulation effectively suppresses the rewarding and reinforcing effects of cocaine in self administration and ICSS models, supporting the candidacy of <strong>TAAR1</strong> as a drug discovery target for cocaine <b>addiction</b>.
+TAAR1	addiction	reward	26048337	Taken together, these data demonstrated that <strong>TAAR1</strong> stimulation effectively suppresses the rewarding and <b>reinforcing</b> effects of cocaine in self administration and <b>ICSS</b> models, supporting the candidacy of <strong>TAAR1</strong> as a drug discovery target for cocaine addiction.
+TAAR1	drug	amphetamine	25762894	The <strong>trace amine associated receptor 1</strong> modulates <b>methamphetamine</b>'s neurochemical and behavioral effects.
+TAAR1	drug	amphetamine	25762894	Here, we tested in rats the ability of RO5203648, a selective <strong>TAAR1</strong> partial agonist, to modulate the physiological and behavioral effects of <b>methamphetamine</b> (<b>METH</b>).
+TAAR1	drug	amphetamine	25762894	Taken together, these data highlight the significant potential of <strong>TAAR1</strong> to modulate <b>METH</b>'s neurochemical and behavioral effects.
+TAAR1	drug	amphetamine	25740289	<strong>Trace Amine Associated Receptor 1</strong> Regulation of <b>Methamphetamine</b> Intake and Related Traits.
+TAAR1	addiction	aversion	25740289	We demonstrate the existence of a non functional allele of <strong>Taar1</strong> in the DBA/2J mouse strain, one of the founder strains of the selected lines, and show that this non functional allele co segregates with high MA drinking and with reduced sensitivity to MA induced conditioned taste <b>aversion</b> (<b>CTA</b>) and hypothermia.
+TAAR1	addiction	aversion	25740289	The functional <strong>Taar1</strong> allele, derived from the other founder strain, C57BL/6J, segregates with low MA drinking and heightened sensitivity to MA induced <b>CTA</b> and hypothermia.
+TAAR1	addiction	aversion	25740289	A role for <strong>TAAR1</strong> in these phenotypes is corroborated in <strong>Taar1</strong> transgenic mice: <strong>Taar1</strong> knockout mice consume more MA and exhibit insensitivity to MA induced <b>CTA</b> and hypothermia, compared with <strong>Taar1</strong> wild type mice.
+TAAR1	addiction	aversion	25740289	Behavioral and physiological studies indicate that <strong>TAAR1</strong> function increases sensitivity to <b>aversive</b> effects of MA, and may thereby protect against MA use.
+TAAR1	drug	amphetamine	25522401	Effects of the <strong>trace amine associated receptor 1</strong> agonist RO5263397 on abuse related behavioral indices of <b>methamphetamine</b> in rats.
+TAAR1	drug	cocaine	25522401	<strong>Trace amine associated receptor 1</strong> is implicated in <b>cocaine</b> addiction and represents a potential therapeutic target.
+TAAR1	addiction	addiction	25522401	<strong>Trace amine associated receptor 1</strong> is implicated in cocaine <b>addiction</b> and represents a potential therapeutic target.
+TAAR1	drug	amphetamine	25522401	However, the effects of <strong>trace amine associated receptor 1</strong> agonists on addiction related behavioral effects of <b>methamphetamine</b> are unknown.
+TAAR1	addiction	addiction	25522401	However, the effects of <strong>trace amine associated receptor 1</strong> agonists on <b>addiction</b> related behavioral effects of methamphetamine are unknown.
+TAAR1	drug	amphetamine	25522401	This study examined the effects of a <strong>trace amine associated receptor 1</strong> agonist RO5263397 on <b>methamphetamine</b> induced behavioral sensitization, <b>methamphetamine</b> self administration, cue  and <b>methamphetamine</b> induced reinstatement of drug seeking, and cue induced reinstatement of sucrose seeking behaviors in rats.
+TAAR1	addiction	relapse	25522401	This study examined the effects of a <strong>trace amine associated receptor 1</strong> agonist RO5263397 on methamphetamine induced behavioral sensitization, methamphetamine self administration, cue  and methamphetamine induced <b>reinstatement</b> of drug <b>seeking</b>, and cue induced <b>reinstatement</b> of sucrose <b>seeking</b> behaviors in rats.
+TAAR1	addiction	sensitization	25522401	This study examined the effects of a <strong>trace amine associated receptor 1</strong> agonist RO5263397 on methamphetamine induced behavioral <b>sensitization</b>, methamphetamine self administration, cue  and methamphetamine induced reinstatement of drug seeking, and cue induced reinstatement of sucrose seeking behaviors in rats.
+TAAR1	drug	amphetamine	25522401	Male Sprague Dawley rats were used to examine the effects of <b>methamphetamine</b> alone and in combination with the <strong>trace amine associated receptor 1</strong> agonist RO5263397 (3.2 10mg/kg).
+TAAR1	drug	amphetamine	25522401	Taken together, <strong>trace amine associated receptor 1</strong> agonists attenuate some abuse related behavioral effects of <b>methamphetamine</b>, strongly suggesting that drugs activating <strong>trace amine associated receptor 1</strong> may be potentially useful for the treatment of <b>methamphetamine</b> addiction and warrant further studies.
+TAAR1	addiction	addiction	25522401	Taken together, <strong>trace amine associated receptor 1</strong> agonists attenuate some abuse related behavioral effects of methamphetamine, strongly suggesting that drugs activating <strong>trace amine associated receptor 1</strong> may be potentially useful for the treatment of methamphetamine <b>addiction</b> and warrant further studies.
+TAAR1	drug	cocaine	24743376	Effects of the <strong>trace amine associated receptor 1</strong> agonist RO5263397 on abuse related effects of <b>cocaine</b> in rats.
+TAAR1	drug	cocaine	24722355	Activation of the <strong>trace amine associated receptor 1</strong> prevents relapse to <b>cocaine</b> seeking.
+TAAR1	addiction	relapse	24722355	Activation of the <strong>trace amine associated receptor 1</strong> prevents <b>relapse</b> to cocaine <b>seeking</b>.
+TAAR1	addiction	addiction	24722355	The trace amine associated receptor 1 (<strong>TAAR1</strong>) has emerged as a promising target for medication development in <b>addiction</b> because of its ability to regulate dopamine (DA) transmission.
+TAAR1	addiction	addiction	24722355	The <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) has emerged as a promising target for medication development in <b>addiction</b> because of its ability to regulate dopamine (DA) transmission.
+TAAR1	drug	cocaine	24722355	We tested in rats the efficacy of RO5203648 and RO5256390, partial and full <strong>TAAR1</strong> agonists, respectively, in models of <b>cocaine</b> relapse.
+TAAR1	addiction	relapse	24722355	We tested in rats the efficacy of RO5203648 and RO5256390, partial and full <strong>TAAR1</strong> agonists, respectively, in models of cocaine <b>relapse</b>.
+TAAR1	drug	cocaine	24722355	Moreover, fast scan cyclic voltammetry data showed that RO5203648 prevented <b>cocaine</b> induced DA overflow in the nucleus accumbens without altering DA half life, suggesting that the partial <strong>TAAR1</strong> agonist attenuated <b>cocaine</b> stimulated DA overflow by mechanisms other than direct interference with DA uptake.
+TAAR1	drug	cocaine	24722355	Collectively, these data provide strong evidence in support of <strong>TAAR1</strong> as a neuropharmacological target for the treatment of <b>cocaine</b> addiction.
+TAAR1	addiction	addiction	24722355	Collectively, these data provide strong evidence in support of <strong>TAAR1</strong> as a neuropharmacological target for the treatment of cocaine <b>addiction</b>.
+TAAR1	drug	cocaine	24561093	The <strong>trace amine associated receptor 1</strong> agonist RO5263397 attenuates the induction of <b>cocaine</b> behavioral sensitization in rats.
+TAAR1	addiction	sensitization	24561093	The <strong>trace amine associated receptor 1</strong> agonist RO5263397 attenuates the induction of cocaine behavioral <b>sensitization</b> in rats.
+TAAR1	drug	alcohol	23861588	<strong>Trace amine associated receptor 1</strong> modulates behavioral effects of <b>ethanol</b>.
+TAAR1	drug	alcohol	23861588	Here, we assessed whether trace amine associated receptor 1 (<strong>TAAR1</strong>), a modulator of brain monoamine systems, is involved in the behavioral and reinforcement related effects of <b>ethanol</b> and whether it could potentially serve as a therapeutic target.
+TAAR1	addiction	reward	23861588	Here, we assessed whether trace amine associated receptor 1 (<strong>TAAR1</strong>), a modulator of brain monoamine systems, is involved in the behavioral and <b>reinforcement</b> related effects of ethanol and whether it could potentially serve as a therapeutic target.
+TAAR1	drug	alcohol	23861588	Here, we assessed whether <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>), a modulator of brain monoamine systems, is involved in the behavioral and reinforcement related effects of <b>ethanol</b> and whether it could potentially serve as a therapeutic target.
+TAAR1	addiction	reward	23861588	Here, we assessed whether <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>), a modulator of brain monoamine systems, is involved in the behavioral and <b>reinforcement</b> related effects of ethanol and whether it could potentially serve as a therapeutic target.
+TAAR1	drug	alcohol	23861588	Wild type (WT) and <strong>TAAR1</strong> knockout (KO) mice (75% C57J/BL6 and 25% 129S1/Sv background) were compared in tests of <b>ethanol</b> consumption (two bottle choice [TBC]), motor impairment (loss of righting reflex, [LORR], locomotor activity) and <b>ethanol</b> clearance (blood <b>ethanol</b> level [BEL]).
+TAAR1	drug	alcohol	23861588	The present findings are the first to implicate <strong>TAAR1</strong> in the behavioral and reinforcement related effects of <b>ethanol</b> and raise the question of whether specific drugs that target <strong>TAAR1</strong> could potentially reduce <b>alcohol</b> consumption in humans with AUDs.
+TAAR1	addiction	reward	23861588	The present findings are the first to implicate <strong>TAAR1</strong> in the behavioral and <b>reinforcement</b> related effects of ethanol and raise the question of whether specific drugs that target <strong>TAAR1</strong> could potentially reduce alcohol consumption in humans with AUDs.
+TAAR1	drug	amphetamine	22079347	Augmentation of <b>methamphetamine</b> induced behaviors in transgenic mice lacking the <strong>trace amine associated receptor 1</strong>.
+TAAR1	drug	amphetamine	22079347	The trace amine associated receptor 1 (<strong>TAAR1</strong>) is a G protein coupled receptor that is functionally activated by <b>amphetamine</b> based psychostimulants, including <b>amphetamine</b>, <b>methamphetamine</b> and MDMA.
+TAAR1	drug	psychedelics	22079347	The trace amine associated receptor 1 (<strong>TAAR1</strong>) is a G protein coupled receptor that is functionally activated by amphetamine based psychostimulants, including amphetamine, methamphetamine and <b>MDMA</b>.
+TAAR1	drug	amphetamine	22079347	The <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) is a G protein coupled receptor that is functionally activated by <b>amphetamine</b> based psychostimulants, including <b>amphetamine</b>, <b>methamphetamine</b> and MDMA.
+TAAR1	drug	psychedelics	22079347	The <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) is a G protein coupled receptor that is functionally activated by amphetamine based psychostimulants, including amphetamine, methamphetamine and <b>MDMA</b>.
+TAAR1	drug	amphetamine	22079347	Previous studies have shown that in transgenic mice lacking the <strong>TAAR1</strong> gene (<strong>TAAR1</strong> knockout; KO) a single injection of <b>amphetamine</b> can produce enhanced behavioral responses compared to responses evoked in wild type (WT) mice.
+TAAR1	drug	cocaine	22079347	Further, the psychostimulant effects of <b>cocaine</b> can be diminished by selective activation of <strong>TAAR1</strong>.
+TAAR1	drug	amphetamine	22079347	To investigate the role of <strong>TAAR1</strong> in the rewarding effects of drugs of abuse, the psychomotor stimulating effects of <b>amphetamine</b> and <b>methamphetamine</b> and the conditioned rewarding effects of <b>methamphetamine</b> and morphine were compared between WT and <strong>TAAR1</strong> KO mice.
+TAAR1	drug	opioid	22079347	To investigate the role of <strong>TAAR1</strong> in the rewarding effects of drugs of abuse, the psychomotor stimulating effects of amphetamine and methamphetamine and the conditioned rewarding effects of methamphetamine and <b>morphine</b> were compared between WT and <strong>TAAR1</strong> KO mice.
+TAAR1	drug	amphetamine	22079347	In locomotor activity studies, both single and repeated exposure to d <b>amphetamine</b> or <b>methamphetamine</b> generated significantly higher levels of total distance traveled in <strong>TAAR1</strong> KO mice compared to WT mice.
+TAAR1	drug	amphetamine	22079347	In conditioned place preference (CPP) studies, <strong>TAAR1</strong> KO mice acquired <b>methamphetamine</b> induced CPP earlier than WT mice and retained CPP longer during extinction training.
+TAAR1	addiction	reward	22079347	In conditioned place preference (<b>CPP</b>) studies, <strong>TAAR1</strong> KO mice acquired methamphetamine induced <b>CPP</b> earlier than WT mice and retained <b>CPP</b> longer during extinction training.
+TAAR1	drug	amphetamine	22079347	Results from locomotor activity studies suggest that <strong>TAAR1</strong> may have a modulatory role in the behavioral sensitization to <b>amphetamine</b> based psychostimulants.
+TAAR1	addiction	sensitization	22079347	Results from locomotor activity studies suggest that <strong>TAAR1</strong> may have a modulatory role in the behavioral <b>sensitization</b> to amphetamine based psychostimulants.
+TAAR1	drug	amphetamine	22079347	That <b>methamphetamine</b> but not morphine induced CPP was augmented in <strong>TAAR1</strong> KO mice suggests a selective role of <strong>TAAR1</strong> in the conditioned reinforcing effects of <b>methamphetamine</b>.
+TAAR1	drug	opioid	22079347	That methamphetamine but not <b>morphine</b> induced CPP was augmented in <strong>TAAR1</strong> KO mice suggests a selective role of <strong>TAAR1</strong> in the conditioned reinforcing effects of methamphetamine.
+TAAR1	addiction	reward	22079347	That methamphetamine but not morphine induced <b>CPP</b> was augmented in <strong>TAAR1</strong> KO mice suggests a selective role of <strong>TAAR1</strong> in the conditioned <b>reinforcing</b> effects of methamphetamine.
+TAAR1	drug	amphetamine	22079347	Collectively, these findings provide support for a regulatory role of <strong>TAAR1</strong> in <b>methamphetamine</b> signaling.
+TAAR1	drug	amphetamine	21073468	It is now recognized that trace amine associated receptor 1 (<strong>TAAR1</strong>) plays a functional role in the regulation of brain monoamines and the mediation of action of <b>amphetamine</b> like psychostimulants.
+TAAR1	drug	amphetamine	21073468	It is now recognized that <strong>trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) plays a functional role in the regulation of brain monoamines and the mediation of action of <b>amphetamine</b> like psychostimulants.
+TAAR1	addiction	addiction	21073468	Accordingly, research on <strong>TAAR1</strong> opens the door to a new avenue of approach for medications development to treat drug <b>addiction</b> as well as the spectrum of neuropsychiatric disorders hallmarked by aberrant regulation of brain monoamines.
+TAAR1	drug	amphetamine	19482011	<strong>TAAR1</strong> activation by the common biogenic amines, the trace amine beta phenylethylamine and <b>methamphetamine</b> alters the monoamine transporter function in both mouse and rhesus monkey brain synaptosomes, suggesting a modulatory role for this receptor in the presynaptic regulation of monoaminergic activity.
+TAAR1	drug	amphetamine	19364908	Trace amine associated receptor 1 (<strong>TAAR1</strong>) is expressed in brain dopaminergic nuclei and is activated by <b>methamphetamine</b> in vitro.
+TAAR1	drug	amphetamine	19364908	<strong>Trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) is expressed in brain dopaminergic nuclei and is activated by <b>methamphetamine</b> in vitro.
+TAAR1	drug	amphetamine	19364908	Here, we show that <b>methamphetamine</b> interaction with <strong>TAAR1</strong> inhibits [(3)H]dopamine uptake, enhances or induces [(3)H]dopamine efflux, and triggers DAT internalization.
+TAAR1	drug	amphetamine	19364908	In time course assays in which <b>methamphetamine</b> and [(3)H]dopamine were concurrently loaded into cells or synaptosomes or in pretreatment assays in which <b>methamphetamine</b> was washed away before [(3)H]dopamine loading, <b>methamphetamine</b> caused a distinct inhibition in [(3)H]dopamine uptake in <strong>TAAR1</strong> + DAT cotransfected cells and in wild type mouse and rhesus monkey striatal synaptosomes.
+TAAR1	drug	amphetamine	19364908	In [(3)H]dopamine efflux assays using the same cell and synaptosome preparations, <b>methamphetamine</b> enhanced [(3)H]dopamine efflux at a high loading concentration of [(3)H]dopamine (1 muM) or induced [(3)H]dopamine efflux at a low loading concentration of [(3)H]dopamine (10 nM) in a <strong>TAAR1</strong> dependent manner.
+TAAR1	drug	amphetamine	19364908	In DAT biotinylation assays using the same cell and synaptosome preparations, we observed that 1 muM <b>methamphetamine</b> induced DAT internalization in a <strong>TAAR1</strong> dependent manner.
+TAAR1	drug	amphetamine	19364908	All these <strong>TAAR1</strong> mediated effects of <b>methamphetamine</b> were blocked by the protein kinase inhibitors H89 [N [2 (4 bromocinnamylamino)ethyl] 5 isoquinoline] and/or 2 {8 [(dimethylamino) methyl] 6,7,8,9 tetrahydropyrido[1,2 a]indol 3 yl} 3 (1 methylindol 3 yl)maleimide (Ro32 0432), suggesting that <b>methamphetamine</b> interaction with <strong>TAAR1</strong> triggers cellular phosphorylation cascades and leads to the observed effects of <b>methamphetamine</b> on DAT.
+TAAR1	drug	amphetamine	19364908	These findings demonstrate a mediatory role of <strong>TAAR1</strong> in <b>methamphetamine</b> action in DAT regulation and implicate this receptor as a potential target of therapeutics drugs for <b>methamphetamine</b> addiction.
+TAAR1	addiction	addiction	19364908	These findings demonstrate a mediatory role of <strong>TAAR1</strong> in methamphetamine action in DAT regulation and implicate this receptor as a potential target of therapeutics drugs for methamphetamine <b>addiction</b>.
+TAAR1	drug	amphetamine	17234899	Trace amine associated receptor 1 (<strong>TAAR1</strong>) is a G protein coupled receptor activated by a broad range of monoamines and <b>amphetamine</b> related psychostimulants.
+TAAR1	drug	amphetamine	17234899	<strong>Trace amine associated receptor 1</strong> (<strong>TAAR1</strong>) is a G protein coupled receptor activated by a broad range of monoamines and <b>amphetamine</b> related psychostimulants.
+TAAR1	drug	amphetamine	17234899	Rhesus monkey <strong>TAAR1</strong> expressed with DAT in human embryonic kidney 293 cells was dose dependently activated by dopamine or (+) <b>methamphetamine</b>.
+TAAR1	drug	amphetamine	17234899	[3H]Dopamine efflux assays performed in Dulbecco's modified Eagle's medium displayed a <strong>TAAR1</strong> dependent spontaneous [3H]dopamine efflux that was dose dependently augmented by dopamine or (+) <b>methamphetamine</b> and that was blocked by either methylphenidate or a PKC inhibitor.
+TAAR1	drug	amphetamine	17234899	Taken together, this study provides evidence that <strong>TAAR1</strong> is involved in functional regulation of DAT and suggests that <strong>TAAR1</strong> is a potentially important target for therapeutics for <b>methamphetamine</b> addiction.
+TAAR1	addiction	addiction	17234899	Taken together, this study provides evidence that <strong>TAAR1</strong> is involved in functional regulation of DAT and suggests that <strong>TAAR1</strong> is a potentially important target for therapeutics for methamphetamine <b>addiction</b>.
+SIGMAR1	drug	amphetamine	32670551	Cannabidiol attenuates <b>methamphetamine</b> induced conditioned place preference via the <strong>Sigma1R</strong>/AKT/GSK 3β/CREB signaling pathway in rats.
+SIGMAR1	drug	cannabinoid	32670551	<b>Cannabidiol</b> attenuates methamphetamine induced conditioned place preference via the <strong>Sigma1R</strong>/AKT/GSK 3β/CREB signaling pathway in rats.
+SIGMAR1	drug	amphetamine	32670551	The present study examines whether CBD has a protective effect on <b>METH</b> induced conditioned place preference (CPP) in rats by regulating the <strong>Sigma1R</strong> and AKT GSK3β CREB signaling pathway.
+SIGMAR1	addiction	reward	32670551	The present study examines whether CBD has a protective effect on METH induced conditioned place preference (<b>CPP</b>) in rats by regulating the <strong>Sigma1R</strong> and AKT GSK3β CREB signaling pathway.
+SIGMAR1	drug	amphetamine	32670551	The expression levels of <strong>Sigma1R</strong>, p AKT, p GSK3β, and p CREB increased significantly in the <b>METH</b> induced CPP model.
+SIGMAR1	addiction	reward	32670551	The expression levels of <strong>Sigma1R</strong>, p AKT, p GSK3β, and p CREB increased significantly in the METH induced <b>CPP</b> model.
+SIGMAR1	drug	amphetamine	32670551	When a pretreatment of CBD is applied, the CBD can weaken CPP in <b>METH</b> induced rats by regulating the <strong>SigmaR1</strong>/AKT/GSK 3β/CREB signaling pathway.
+SIGMAR1	addiction	reward	32670551	When a pretreatment of CBD is applied, the CBD can weaken <b>CPP</b> in METH induced rats by regulating the <strong>SigmaR1</strong>/AKT/GSK 3β/CREB signaling pathway.
+SIGMAR1	drug	cocaine	32124388	The molecular mechanism involved in the acute <b>cocaine</b> induced increase in the antagonistic allosteric A2AR D2R receptor receptor interactions may be an increased formation of higher order complexes A2AR D2R <strong>sigma1R</strong> in which <b>cocaine</b> by binding to the <strong>sigma1R</strong> protomer also allosterically enhances the inhibitory A2AR D2R interaction in this receptor complex.
+SIGMAR1	drug	cocaine	31782100	OSU 6162, a <strong>Sigma1R</strong> Ligand in Low Doses, Can Further Increase the Effects of <b>Cocaine</b> Self Administration on Accumbal D2R Heteroreceptor Complexes.
+SIGMAR1	drug	cocaine	31782100	<b>Cocaine</b> was previously shown to act at the <strong>Sigma1R</strong> which is a target for counteracting <b>cocaine</b> actions.
+SIGMAR1	drug	cocaine	31782100	It therefore becomes of interest to test if the monoamine stabilizer ( ) OSU 6162 (OSU 6162) with a nanomolar affinity for the <strong>Sigma1R</strong> can acutely modulate in low doses the effects of <b>cocaine</b> self administration.
+SIGMAR1	drug	cocaine	31782100	In contrast, in maintenance of <b>cocaine</b> self administration, the proximity ligation assay performed on brains from rats pretreated with OSU 6162 showed highly significant increases in the density of the D2R <strong>Sigma1R</strong> heteroreceptor complexes in the shell of the nucleus accumbens versus OSU 6162 induced increases in this region of yoked saline rats.
+SIGMAR1	drug	cocaine	31782100	The current results indicate that OSU 6162 via its high affinity for the <strong>Sigma1R</strong> may increase the number of accumbal shell D2R <strong>Sigma1R</strong> and A2AR D2R heteroreceptor complexes associated with further increases in the antagonistic A2AR D2R interactions in <b>cocaine</b> self administration.
+SIGMAR1	drug	cocaine	31596232	In NG108 cells and mouse midbrain tissue, we find that 2 AG is localized in non synaptic extracellular vesicles (EVs) that are secreted in the presence of <b>cocaine</b> via interaction with the chaperone protein sigma 1 receptor (<strong>Sig 1R</strong>).
+SIGMAR1	drug	cocaine	31596232	The release of EVs occurs when <b>cocaine</b> causes dissociation of the <strong>Sig 1R</strong> from ADP ribosylation factor (ARF6), a G protein regulating EV trafficking, leading to activation of myosin light chain kinase (MLCK).
+SIGMAR1	drug	cocaine	31596232	Blockade of <strong>Sig 1R</strong> function, or inhibition of ARF6 or MLCK also prevented <b>cocaine</b> induced EV release and <b>cocaine</b> stimulated 2 AG modulation of inhibitory synapses in DA neurons.
+SIGMAR1	drug	cocaine	31596232	Our results implicate the <strong>Sig 1R</strong> ARF6 complex in control of EV release and demonstrate that <b>cocaine</b> mediated 2 AG release can occur via EVs.
+SIGMAR1	drug	cocaine	30384981	<b>Cocaine</b> induced pathological A2AR D2R <strong>Sigma1R</strong> complexes may form a long term memory with a strong and permanent D2R brake, leading to <b>cocaine</b> addiction.
+SIGMAR1	addiction	addiction	30384981	Cocaine induced pathological A2AR D2R <strong>Sigma1R</strong> complexes may form a long term memory with a strong and permanent D2R brake, leading to cocaine <b>addiction</b>.
+SIGMAR1	drug	cocaine	30384981	These heteroreceptor complexes can potentially be targeted for future pharmacotherapy of <b>cocaine</b> addiction by using heterobivalent compounds or A2AR D2R receptor interface interfering peptides that disrupt the A2AR D2R <strong>Sigma1R</strong> complexes.
+SIGMAR1	addiction	addiction	30384981	These heteroreceptor complexes can potentially be targeted for future pharmacotherapy of cocaine <b>addiction</b> by using heterobivalent compounds or A2AR D2R receptor interface interfering peptides that disrupt the A2AR D2R <strong>Sigma1R</strong> complexes.
+SIGMAR1	drug	psychedelics	29674970	N,N Dimethyltryptamine (DMT, one of the alkaloids in <b>Ayahuasca</b>) activates sigma 1 receptor (<strong>SIGMAR1</strong>) and others.
+SIGMAR1	drug	psychedelics	29674970	Since traumatic memories in post traumatic stress disorder (PTSD) are often characterised by "repression" and PTSD patients ingesting <b>Ayahuasca</b> report the retrieval of such memories, it cannot be excluded that DMT mediated <strong>SIGMAR1</strong> activation and the concomitant MAOIs effects during <b>Ayahuasca</b> ingestion might mediate such "anti amnesic" process.
+SIGMAR1	drug	psychedelics	29674970	Here I hypothesise that <b>Ayahuasca</b>, via hyperactivation of trauma and emotional memory related centres, and via its concomitant <strong>SIGMAR1</strong>  and MAOIs  induced anti amnesic effects, facilitates the retrieval of traumatic memories, in turn making them labile (destabilised).
+SIGMAR1	addiction	addiction	29674970	Lastly, since <strong>SIGMAR1</strong> activation triggers both epigenetic and immunomodulatory programmes, the mechanism here presented could help understanding and treating other conditions in which the cellular memory is dysregulated, such as cancer, diabetes, autoimmune and neurodegenerative pathologies and substance <b>addiction</b>.
+SIGMAR1	drug	alcohol	29205397	<b>Alcohol</b> drinking also reduced the striatal density of D2R D2R homoreceptor complexes, increased the density of A2AR D2R heteroreceptor complexes in the NAc shell and the dorsal striatum, and decreased the density of <strong>sigma1R</strong> D2R heteroreceptor complexes in the dorsal striatum.
+SIGMAR1	drug	opioid	28786753	Here, we have shown that the circular RNA HIPK2 (circHIPK2) functions as an endogenous microRNA 124 (MIR124 2HG) sponge to sequester MIR124 2HG and inhibit its activity, resulting in increased sigma non <b>opioid</b> intracellular receptor 1 (<strong>SIGMAR1</strong>/OPRS1) expression.
+SIGMAR1	drug	opioid	28786753	Here, we have shown that the circular RNA HIPK2 (circHIPK2) functions as an endogenous microRNA 124 (MIR124 2HG) sponge to sequester MIR124 2HG and inhibit its activity, resulting in increased sigma non <b>opioid</b> intracellular receptor 1 (<strong>SIGMAR1</strong>/<strong>OPRS1</strong>) expression.
+SIGMAR1	drug	cocaine	28300546	<b>Cocaine</b> self administration specifically increases A2AR D2R and D2R <strong>sigma1R</strong> heteroreceptor complexes in the rat nucleus accumbens shell.
+SIGMAR1	drug	cocaine	28300546	Additionally, <b>cocaine</b> self administration evoked a selective and significant increase in the density of D2R <strong>sigma1R</strong> positive clusters in the nucleus accumbens shell vs yoked saline controls, while a significant reduction of the density of the D2R <strong>sigma1R</strong> positive clusters was found in the dorsal part of the dorsal striatum.
+SIGMAR1	drug	cocaine	28300546	The results suggest that <b>cocaine</b> self administration can reorganize A2AR and D2R into increased A2AR D2R heteroreceptor complexes in the nucleus accumbens shell associated with increases in the D2R <strong>sigma1R</strong> heteroreceptor complexes in this region.
+SIGMAR1	drug	cocaine	28300546	This reorganization can contribute to the demonstrated anti <b>cocaine</b> actions of A2A receptor agonists and the putative formation of A2AR D2R <strong>sigma1R</strong> heterocomplexes.
+SIGMAR1	drug	cocaine	28270751	Neuromodulation of neuronal networks in <b>cocaine</b> use disorder via dopamine (DA) and adenosine signals involve A2AR D2R and A2AR D2R <strong>Sigma1R</strong> heteroreceptor complexes in the dorsal and ventral striatum.
+SIGMAR1	drug	cocaine	28270751	The excitatory modulation by A2AR agonists of the ventral striato pallidal GABA anti reward system via targeting the A2AR D2R and A2AR D2R <strong>Sigma1R</strong> heteroreceptor complex holds high promise as a new way to treat <b>cocaine</b> use disorders.
+SIGMAR1	addiction	reward	28270751	The excitatory modulation by A2AR agonists of the ventral striato pallidal GABA anti <b>reward</b> system via targeting the A2AR D2R and A2AR D2R <strong>Sigma1R</strong> heteroreceptor complex holds high promise as a new way to treat cocaine use disorders.
+SIGMAR1	drug	amphetamine	27088037	The <strong>Sig 1R</strong> has been shown to bind psychostimulants including cocaine and <b>methamphetamine</b> (<b>METH</b>) and thus has been implicated in the actions of those psychostimulants.
+SIGMAR1	drug	cocaine	27088037	The <strong>Sig 1R</strong> has been shown to bind psychostimulants including <b>cocaine</b> and methamphetamine (METH) and thus has been implicated in the actions of those psychostimulants.
+SIGMAR1	drug	amphetamine	27088037	In this review, we will focus on the molecular mechanisms of the <strong>Sig 1R</strong> and discuss in such a manner with a hope to further understand or unveil unexplored relations between the <strong>Sig 1R</strong> and the actions of cocaine and <b>METH</b>, particularly in the context of cellular biological relevance.
+SIGMAR1	drug	cocaine	27088037	In this review, we will focus on the molecular mechanisms of the <strong>Sig 1R</strong> and discuss in such a manner with a hope to further understand or unveil unexplored relations between the <strong>Sig 1R</strong> and the actions of <b>cocaine</b> and METH, particularly in the context of cellular biological relevance.
+SIGMAR1	drug	psychedelics	26973523	A growing number of studies indicate that the psychotherapeutic potential of <b>ayahuasca</b> is based mostly on the strong serotonergic effects, whereas the sigma 1 receptor (<strong>Sig 1R</strong>) agonist effect of its active ingredient dimethyltryptamine raises the possibility that the ethnomedical observations on the diversity of treated conditions can be scientifically verified.
+SIGMAR1	drug	psychedelics	26973523	This article has two important take home messages: (1) the therapeutic effects of <b>ayahuasca</b> are best understood from a bio psycho socio spiritual model, and (2) on the biological level <b>ayahuasca</b> may act against chronic low grade inflammation and oxidative stress via the <strong>Sig 1R</strong> which can explain its widespread therapeutic indications.
+SIGMAR1	drug	cocaine	26554014	<b>Cocaine</b> was found to suppress the gene expression of monoamine oxidase B (MAOB) in the brain of wild type but not <strong>Sig 1R</strong> knockout mouse.
+SIGMAR1	drug	cocaine	26554014	Our results demonstrate a role of <strong>Sig 1R</strong> in transcriptional regulation and suggest <b>cocaine</b> may work through this newly discovered genomic action to achieve its addictive action.
+SIGMAR1	addiction	addiction	26554014	Our results demonstrate a role of <strong>Sig 1R</strong> in transcriptional regulation and suggest cocaine may work through this newly discovered genomic action to achieve its <b>addictive</b> action.
+SIGMAR1	addiction	addiction	26462569	The Sigma 1 receptor (<strong>Sig 1R</strong>) is a chaperone protein that has been implicated in drug abuse and <b>addiction</b>.
+SIGMAR1	drug	alcohol	26462569	Multiple studies have characterized the role the <strong>Sig 1R</strong> plays in psychostimulant addiction; however, fewer studies have specifically investigated its role in <b>alcohol</b> addiction.
+SIGMAR1	addiction	addiction	26462569	Multiple studies have characterized the role the <strong>Sig 1R</strong> plays in psychostimulant <b>addiction</b>; however, fewer studies have specifically investigated its role in alcohol <b>addiction</b>.
+SIGMAR1	addiction	intoxication	26462569	We have previously shown that antagonism of the <strong>Sig 1R</strong> reduces excessive drinking and motivation to drink, whereas agonism induces <b>binge</b> like drinking in rodents.
+SIGMAR1	drug	alcohol	26462569	The objectives of these studies were to investigate the impact of <strong>Sig 1R</strong> gene deletion in C57Bl/6J mice on <b>ethanol</b> drinking and other <b>ethanol</b> related behaviors.
+SIGMAR1	drug	alcohol	26462569	We used an extensive panel of behavioral tests to examine <b>ethanol</b> actions in male, adult mice lacking <strong>Oprs1</strong>, the gene encoding the Sig 1R.
+SIGMAR1	drug	alcohol	26462569	We used an extensive panel of behavioral tests to examine <b>ethanol</b> actions in male, adult mice lacking <strong>Oprs1</strong>, the gene encoding the <strong>Sig 1R</strong>.
+SIGMAR1	drug	alcohol	26462569	<strong>Sig 1R</strong> KO mice displayed higher <b>ethanol</b> intake compared to WT mice; the two genotypes did not differ in their sweet or bitter taste perception.
+SIGMAR1	drug	alcohol	26462569	<strong>Sig 1R</strong> KO mice showed lower sensitivity to <b>ethanol</b> stimulant effects, but greater sensitivity to its taste aversive effects.
+SIGMAR1	addiction	aversion	26462569	<strong>Sig 1R</strong> KO mice showed lower sensitivity to ethanol stimulant effects, but greater sensitivity to its taste <b>aversive</b> effects.
+SIGMAR1	drug	alcohol	26462569	Our results prove that the deletion of the <strong>Sig 1R</strong> increases <b>ethanol</b> consumption, likely by decreasing its rewarding effects, and therefore indicating that the <strong>Sig 1R</strong> is involved in modulation of the reinforcing effects of <b>alcohol</b>.
+SIGMAR1	addiction	reward	26462569	Our results prove that the deletion of the <strong>Sig 1R</strong> increases ethanol consumption, likely by decreasing its rewarding effects, and therefore indicating that the <strong>Sig 1R</strong> is involved in modulation of the <b>reinforcing</b> effects of alcohol.
+SIGMAR1	drug	alcohol	25848705	Sigma 1 receptor (<strong>Sig 1R</strong>) has been proposed as a novel therapeutic target for drug and <b>alcohol</b> addiction.
+SIGMAR1	addiction	addiction	25848705	Sigma 1 receptor (<strong>Sig 1R</strong>) has been proposed as a novel therapeutic target for drug and alcohol <b>addiction</b>.
+SIGMAR1	drug	alcohol	25848705	We have shown previously that <strong>Sig 1R</strong> agonists facilitate the reinforcing effects of <b>ethanol</b> and induce binge like drinking, while <strong>Sig 1R</strong> antagonists on the other hand block excessive drinking in genetic and environmental models of <b>alcoholism</b>, without affecting intake in outbred non dependent rats.
+SIGMAR1	addiction	intoxication	25848705	We have shown previously that <strong>Sig 1R</strong> agonists facilitate the reinforcing effects of ethanol and induce <b>binge</b> like drinking, while <strong>Sig 1R</strong> antagonists on the other hand block excessive drinking in genetic and environmental models of alcoholism, without affecting intake in outbred non dependent rats.
+SIGMAR1	addiction	reward	25848705	We have shown previously that <strong>Sig 1R</strong> agonists facilitate the <b>reinforcing</b> effects of ethanol and induce binge like drinking, while <strong>Sig 1R</strong> antagonists on the other hand block excessive drinking in genetic and environmental models of alcoholism, without affecting intake in outbred non dependent rats.
+SIGMAR1	drug	alcohol	25848705	Even though significant progress has been made in understanding the function of <strong>Sig 1R</strong> in <b>alcohol</b> reinforcement, its role in the early and late stage of <b>alcohol</b> addiction remains unclear.
+SIGMAR1	addiction	addiction	25848705	Even though significant progress has been made in understanding the function of <strong>Sig 1R</strong> in alcohol reinforcement, its role in the early and late stage of alcohol <b>addiction</b> remains unclear.
+SIGMAR1	addiction	reward	25848705	Even though significant progress has been made in understanding the function of <strong>Sig 1R</strong> in alcohol <b>reinforcement</b>, its role in the early and late stage of alcohol addiction remains unclear.
+SIGMAR1	drug	alcohol	25848705	Administration of the selective <strong>Sig 1R</strong> antagonist BD 1063 dramatically reduced the acquisition of <b>alcohol</b> drinking behavior as well as the preference for <b>alcohol</b> in genetically selected TSRI Sardinian <b>alcohol</b> preferring (Scr:sP) rats; the treatment had instead no effect on total fluid intake, food intake or body weight gain, proving selectivity of action.
+SIGMAR1	drug	alcohol	25848705	Finally, an innate elevation in <strong>Sig 1R</strong> protein levels was found in the nucleus accumbens of <b>alcohol</b> preferring Scr:sP rats, compared to outbred Wistar rats, alteration which was normalized by chronic, voluntary <b>alcohol</b> drinking.
+SIGMAR1	drug	alcohol	25848705	Taken together these findings demonstrate that <strong>Sig 1R</strong> blockade reduces the propensity to both acquire <b>alcohol</b> drinking and to seek <b>alcohol</b>, and point to the nucleus accumbens as a potential key region for the effects observed.
+SIGMAR1	drug	alcohol	25848705	Our data suggest that <strong>Sig 1R</strong> antagonists may have therapeutic potential in multiple stages of <b>alcohol</b> addiction.
+SIGMAR1	addiction	addiction	25848705	Our data suggest that <strong>Sig 1R</strong> antagonists may have therapeutic potential in multiple stages of alcohol <b>addiction</b>.
+SIGMAR1	addiction	relapse	23332758	The sigma 1 receptor (<strong>Sig 1R</strong>), an endoplasmic reticulum (ER) chaperone protein, is an interorganelle signaling modulator that potentially plays a role in drug <b>seeking</b> behaviors.
+SIGMAR1	drug	cocaine	23332758	We found that <b>cocaine</b> exposure triggers a <strong>Sig 1R</strong> dependent upregulation of D type K(+) current in the nucleus accumbens (NAc) that results in neuronal hypoactivity and thereby enhances behavioral <b>cocaine</b> response.
+SIGMAR1	drug	cocaine	23332758	In conclusion, the dynamic <strong>Sig 1R</strong> Kv1.2 complex represents a mechanism that shapes neuronal and behavioral response to <b>cocaine</b>.
+SIGMAR1	drug	amphetamine	22934790	Previous findings have shown that sigma 1 receptors (Sig 1Rs) are upregulated by the self administration of <b>methamphetamine</b>, whereas <strong>Sig 1R</strong> antisense can attenuate the behavioral effects of psychostimulants in rodents.
+SIGMAR1	drug	amphetamine	22934790	Therefore, we examined the effects of selective <strong>Sig 1R</strong> agonists, such as SA4503 and (+) pentazocine, on the rewarding effects of abused drugs such as <b>methamphetamine</b>, cocaine and morphine in rats, as measured by the conditioned place preference.
+SIGMAR1	drug	cocaine	22934790	Therefore, we examined the effects of selective <strong>Sig 1R</strong> agonists, such as SA4503 and (+) pentazocine, on the rewarding effects of abused drugs such as methamphetamine, <b>cocaine</b> and morphine in rats, as measured by the conditioned place preference.
+SIGMAR1	drug	opioid	22934790	Therefore, we examined the effects of selective <strong>Sig 1R</strong> agonists, such as SA4503 and (+) pentazocine, on the rewarding effects of abused drugs such as methamphetamine, cocaine and <b>morphine</b> in rats, as measured by the conditioned place preference.
+SIGMAR1	drug	alcohol	18946467	The effects of subcutaneous treatment with the potent, selective <strong>Sig 1R</strong> antagonist BD 1063 on operant <b>ethanol</b> self administration were studied in two models of excessive drinking Sardinian <b>alcohol</b> preferring (sP) rats and acutely withdrawn <b>ethanol</b> dependent Wistar rats and compared to <b>ethanol</b> self administration in nondependent Wistar controls.
+SIGMAR1	addiction	reward	18946467	The effects of subcutaneous treatment with the potent, selective <strong>Sig 1R</strong> antagonist BD 1063 on <b>operant</b> ethanol self administration were studied in two models of excessive drinking Sardinian alcohol preferring (sP) rats and acutely withdrawn ethanol dependent Wistar rats and compared to ethanol self administration in nondependent Wistar controls.
+SIGMAR1	drug	alcohol	18946467	Gene expression of <strong>Sig 1R</strong> in reward related brain areas implicated in <b>ethanol</b> reinforcement was compared between <b>ethanol</b> naive sP and Wistar rats and withdrawn <b>ethanol</b> dependent Wistar rats.
+SIGMAR1	addiction	reward	18946467	Gene expression of <strong>Sig 1R</strong> in <b>reward</b> related brain areas implicated in ethanol <b>reinforcement</b> was compared between ethanol naive sP and Wistar rats and withdrawn ethanol dependent Wistar rats.
+SIGMAR1	drug	alcohol	18946467	<b>Ethanol</b> naive sP rats and 24 h withdrawn, dependent Wistar rats showed reduced <strong>Sig 1R</strong> mRNA expression in the nucleus accumbens.
+SIGMAR1	drug	amphetamine	17050780	The sigma 1 receptor (<strong>Sig 1R</strong>) can bind psychostimulants and was shown to be up regulated in the brain of <b>methamphetamine</b> self administering rats.
+SIGMAR1	addiction	addiction	17050780	Results also suggest that psychostimulants may manipulate the cAMP PKA <strong>Sig 1R</strong> and/or the cAMP ERK <strong>Sig 1R</strong> pathways to achieve a neuroplasticity that favors <b>addictive</b> behaviors.
+SIGMAR1	addiction	sensitization	15029471	Sigma(1) receptors (<strong>Sig 1R</strong>) are implicated in behavioral <b>sensitization</b>, conditioned place preference, and cellular restructuring induced by psychostimulants.
+SIGMAR1	drug	amphetamine	15029471	This study examined neuroadaptive changes in <strong>Sig 1R</strong> in the brains of rats self administering <b>methamphetamine</b>.
+SIGMAR1	drug	amphetamine	15029471	There was a marked upregulation of <strong>Sig 1R</strong> proteins (50%) in the midbrain and altered levels of <strong>Sig 1R</strong> mRNA in the frontal cortex and hippocampus of rats that learned to actively self administer <b>methamphetamine</b>, but not in yoked <b>methamphetamine</b>  or saline control rats.
+SIGMAR1	drug	amphetamine	15029471	Neuroadaptive increases in <strong>Sig 1R</strong> seen in this study may contribute to the reinforcing effects of <b>methamphetamine</b>.
+SIGMAR1	addiction	reward	15029471	Neuroadaptive increases in <strong>Sig 1R</strong> seen in this study may contribute to the <b>reinforcing</b> effects of methamphetamine.
+SIGMAR1	drug	alcohol	14706429	To investigate the role of <strong>SIGMAR1</strong> in conveying susceptibility to <b>alcoholism</b>, we performed a functional analysis of polymorphisms in the <strong>SIGMAR1</strong> and a case control study.
+SIGMAR1	drug	alcohol	14706429	The distribution of <strong>SIGMAR1</strong> polymorphisms was analyzed in 307 <b>alcoholic</b> and 302 control subjects.
+NPFF	drug	opioid	31226311	Previous study has indicated that this peptide displays neuropeptide FF (<strong>NPFF</strong>) like anti <b>opioid</b> activity.
+NPFF	drug	opioid	31226311	Thus, KSO inhibited the <b>morphine</b> induced CPP mainly by involving specific activation of <strong>NPFF</strong> receptors.
+NPFF	addiction	reward	31226311	Thus, KSO inhibited the morphine induced <b>CPP</b> mainly by involving specific activation of <strong>NPFF</strong> receptors.
+NPFF	drug	alcohol	30981809	Neuropeptide FF (<strong>NPFF</strong>) has been described as an anti opioid peptide because, in many cases, it inhibits opioid and <b>ethanol</b> effects in rodents.
+NPFF	drug	opioid	30981809	Neuropeptide FF (<strong>NPFF</strong>) has been described as an anti <b>opioid</b> peptide because, in many cases, it inhibits <b>opioid</b> and ethanol effects in rodents.
+NPFF	addiction	dependence	29981879	Considerable evidence suggests the Neuropeptide FF (<strong>NPFF</strong>) and related peptides exert pro nociceptive and anti opiate actions, particularly at the supra spinal level, which may contribute to opiate <b>dependence</b>.
+NPFF	drug	nicotine	29981879	Taken together, these findings suggest that <strong>NPFF</strong> or related neuropeptides contribute to opiate, as well as <b>nicotine</b>, dependence and withdrawal syndrome through the FF1 receptor.
+NPFF	addiction	dependence	29981879	Taken together, these findings suggest that <strong>NPFF</strong> or related neuropeptides contribute to opiate, as well as nicotine, <b>dependence</b> and withdrawal syndrome through the FF1 receptor.
+NPFF	addiction	withdrawal	29981879	Taken together, these findings suggest that <strong>NPFF</strong> or related neuropeptides contribute to opiate, as well as nicotine, dependence and <b>withdrawal</b> syndrome through the FF1 receptor.
+NPFF	drug	opioid	29708942	Neuropeptide FF (<strong>NPFF</strong>) and its receptors (NPFF1R and NPFF2R) are recognized as an important pronociceptive system involved in <b>opioid</b> induced hyperalgesia and analgesic tolerance.
+NPFF	drug	alcohol	28965655	This peptide possesses neuropeptide FF (<strong>NPFF</strong>) like biological activity in vitro; <strong>NPFF</strong>, in many cases, inhibits opioid and <b>ethanol</b> effects in rodents.
+NPFF	drug	opioid	28965655	This peptide possesses neuropeptide FF (<strong>NPFF</strong>) like biological activity in vitro; <strong>NPFF</strong>, in many cases, inhibits <b>opioid</b> and ethanol effects in rodents.
+NPFF	drug	opioid	28965655	Thus, KSO possesses <strong>NPFF</strong> like anti <b>opioid</b> activity in these behavioral studies.
+NPFF	drug	opioid	27018797	Neuropeptide FF (<strong>NPFF</strong>) behaves as an endogenous <b>opioid</b> modulating peptide.
+NPFF	drug	opioid	27018797	In the present study, the <b>opioid</b> and <strong>NPFF</strong> pharmacophore containing chimeric peptide BN 9 was synthesized and pharmacologically characterized.
+NPFF	drug	opioid	27018797	Agonist activities of BN 9 at <b>opioid</b> and <strong>NPFF</strong> receptors were characterized in in vitro cAMP assays.
+NPFF	drug	opioid	27018797	As BN 9 is able to activate both <b>opioid</b> and <strong>NPFF</strong> systems, this provides an interesting approach for the development of novel analgesics with minimal side effects.
+NPFF	drug	opioid	26970017	Mounting evidences indicate the functional interactions between neuropeptide FF (<strong>NPFF</strong>) and <b>opioids</b>, including the endogenous <b>opioids</b>.
+NPFF	drug	opioid	26970017	In the present work, EN 9, a chimeric peptide containing the functional domains of the endogenous <b>opioid</b> endomorphin 2 (EM 2) and <strong>NPFF</strong>, was synthesized and pharmacologically characterized.
+NPFF	drug	opioid	26970017	Furthermore, the experiments using the antagonists of <b>opioid</b> and <strong>NPFF</strong> receptors indicated that the central antinociception of EN 9 was mainly mediated by κ <b>opioid</b> receptor, independently on <strong>NPFF</strong> receptors.
+NPFF	drug	opioid	26970017	Taken together, the multifunctional agonist of κ <b>opioid</b> and <strong>NPFF</strong> receptors EN 9 produced a potent, non tolerance forming antinociception with limited side effects.
+NPFF	drug	opioid	25268943	Neuropeptide FF1 and FF2 receptors (NPFF1 R and NPFF2 R), and their endogenous ligand <strong>NPFF</strong>, are one of only several systems responsible for mediating <b>opioid</b> induced hyperalgesia, tolerance, and dependence.
+NPFF	addiction	dependence	25268943	Neuropeptide FF1 and FF2 receptors (NPFF1 R and NPFF2 R), and their endogenous ligand <strong>NPFF</strong>, are one of only several systems responsible for mediating opioid induced hyperalgesia, tolerance, and <b>dependence</b>.
+NPFF	addiction	withdrawal	25268943	Testing of 46 alone was without effect in the mouse 48 °C warm water tail <b>withdrawal</b> test, but pretreatment with 46 prevented <strong>NPFF</strong> induced hyperalgesia.
+NPFF	drug	opioid	23578757	Neuropeptide FF (<strong>NPFF</strong>) was reported to act as a functional antagonist of mu <b>opioid</b> receptor and to exert <b>opioid</b> modulating activities.
+NPFF	addiction	reward	23578757	The present study examined the influence of <strong>NPFF</strong> on the rewarding action of EM 2, using the unbiased conditioned place preference (<b>CPP</b>) paradigm.
+NPFF	addiction	reward	23578757	To explore the effect of <strong>NPFF</strong> on the expression of EM 2 induced CPA, EM 2 was administered alone on the conditioning days, and <strong>NPFF</strong> was given 5 min before placement in the <b>CPP</b> apparatus on the test day.
+NPFF	drug	opioid	23578757	These data provide the first evidence for a functional interaction of the endogenous ligands for <strong>NPFF</strong> and MOP receptors, and further support an anti <b>opioid</b> character of <strong>NPFF</strong> system.
+NPFF	drug	amphetamine	22197492	Modulation of neuropeptide FF (<strong>NPFF</strong>) receptors influences the expression of <b>amphetamine</b> induced conditioned place preference and <b>amphetamine</b> withdrawal anxiety like behavior in rats.
+NPFF	addiction	withdrawal	22197492	Modulation of neuropeptide FF (<strong>NPFF</strong>) receptors influences the expression of amphetamine induced conditioned place preference and amphetamine <b>withdrawal</b> anxiety like behavior in rats.
+NPFF	drug	opioid	22197492	Neuropeptide FF (<strong>NPFF</strong>) possesses <b>opioid</b> modulating properties.
+NPFF	drug	amphetamine	22197492	The aim of the present study was to determine whether pharmacological modulation of <strong>NPFF</strong> receptors modify the expression of <b>amphetamine</b> induced conditioned place preference (CPP) and <b>amphetamine</b> withdrawal anxiety like behavior, both processes relevant to drug addiction/abuse.
+NPFF	addiction	addiction	22197492	The aim of the present study was to determine whether pharmacological modulation of <strong>NPFF</strong> receptors modify the expression of amphetamine induced conditioned place preference (CPP) and amphetamine withdrawal anxiety like behavior, both processes relevant to drug <b>addiction</b>/abuse.
+NPFF	addiction	reward	22197492	The aim of the present study was to determine whether pharmacological modulation of <strong>NPFF</strong> receptors modify the expression of amphetamine induced conditioned place preference (<b>CPP</b>) and amphetamine withdrawal anxiety like behavior, both processes relevant to drug addiction/abuse.
+NPFF	addiction	withdrawal	22197492	The aim of the present study was to determine whether pharmacological modulation of <strong>NPFF</strong> receptors modify the expression of amphetamine induced conditioned place preference (CPP) and amphetamine <b>withdrawal</b> anxiety like behavior, both processes relevant to drug addiction/abuse.
+NPFF	drug	amphetamine	22197492	injection of <strong>NPFF</strong> (5, 10, and 20 nmol) inhibited the expression of <b>amphetamine</b> CPP at the doses of 10 and 20 nmol.
+NPFF	addiction	reward	22197492	injection of <strong>NPFF</strong> (5, 10, and 20 nmol) inhibited the expression of amphetamine <b>CPP</b> at the doses of 10 and 20 nmol.
+NPFF	drug	amphetamine	22197492	Our results indicated that stimulation or inhibition of <strong>NPFF</strong> receptors decrease the expression of <b>amphetamine</b> CPP and <b>amphetamine</b> withdrawal anxiety, respectively.
+NPFF	addiction	reward	22197492	Our results indicated that stimulation or inhibition of <strong>NPFF</strong> receptors decrease the expression of amphetamine <b>CPP</b> and amphetamine withdrawal anxiety, respectively.
+NPFF	addiction	withdrawal	22197492	Our results indicated that stimulation or inhibition of <strong>NPFF</strong> receptors decrease the expression of amphetamine CPP and amphetamine <b>withdrawal</b> anxiety, respectively.
+NPFF	drug	opioid	21718302	In this study, we investigated the consequences of <strong>NPFF</strong> receptor blockade on acute and chronic stimulation of <b>opioid</b> receptors in mice by using RF9, a potent and selective antagonist of <strong>NPFF</strong> receptors that can be administered systemically.
+NPFF	addiction	dependence	21718302	CONCLUSION AND IMPLICATIONS The <strong>NPFF</strong> system is involved in the development of two major undesirable effects: tolerance and <b>dependence</b>, which are clinically associated with prolonged exposure to opiates.
+NPFF	drug	opioid	21718302	Our findings suggest that <strong>NPFF</strong> receptors are interesting therapeutic targets to improve the analgesic efficacy of opiates by limiting the development of tolerance, and for the treatment of <b>opioid</b> dependence.
+NPFF	addiction	dependence	21718302	Our findings suggest that <strong>NPFF</strong> receptors are interesting therapeutic targets to improve the analgesic efficacy of opiates by limiting the development of tolerance, and for the treatment of opioid <b>dependence</b>.
+NPFF	drug	opioid	20381562	Distribution of neuropeptide FF (<strong>NPFF</strong>) receptors in correlation with <b>morphine</b> induced reward in the rat brain.
+NPFF	addiction	reward	20381562	Distribution of neuropeptide FF (<strong>NPFF</strong>) receptors in correlation with morphine induced <b>reward</b> in the rat brain.
+NPFF	drug	opioid	20381562	Neuropeptide FF (<strong>NPFF</strong>) exhibited anti /pro <b>opioid</b> effects when centrally injected.
+NPFF	drug	opioid	20381562	It was proved to bind to its own receptors, namely <strong>NPFF</strong>(1) and <strong>NPFF</strong>(2) receptors, but did not bind to <b>opioid</b> receptors.
+NPFF	drug	opioid	20381562	injected <strong>NPFF</strong> suppressed <b>morphine</b> induced conditioned place preference (CPP) in rats, which indicated that <strong>NPFF</strong> may play a role in the modulation of <b>morphine</b> induced reward.
+NPFF	addiction	reward	20381562	injected <strong>NPFF</strong> suppressed morphine induced conditioned place preference (<b>CPP</b>) in rats, which indicated that <strong>NPFF</strong> may play a role in the modulation of morphine induced <b>reward</b>.
+NPFF	drug	opioid	20381562	In the present study, we further investigated the action site of <strong>NPFF</strong> to attenuate <b>morphine</b> induced reward.
+NPFF	addiction	reward	20381562	In the present study, we further investigated the action site of <strong>NPFF</strong> to attenuate morphine induced <b>reward</b>.
+NPFF	drug	opioid	20381562	Bilateral intra VTA (ventral tegmental area) and intra NAc (nucleus accumbens) injections of <strong>NPFF</strong> both blocked the CPP caused by <b>morphine</b> in rats.
+NPFF	addiction	reward	20381562	Bilateral intra VTA (ventral tegmental area) and intra NAc (nucleus accumbens) injections of <strong>NPFF</strong> both blocked the <b>CPP</b> caused by morphine in rats.
+NPFF	addiction	sensitization	20381562	This suggests that <strong>NPFF</strong> may act at both VTA and NAc to inhibit the <b>sensitization</b> of the mesocorticolimbic dopaminergic pathway.
+NPFF	drug	opioid	20381562	Neurochemical analyses support that <strong>NPFF</strong> could be acting through the inhibition of the mesocorticolimbic dopaminergic activity increased by <b>morphine</b>.
+NPFF	drug	opioid	20381562	Taken together, our study should be helpful for clarifying the possible mechanisms of <strong>NPFF</strong> system to modulate <b>morphine</b> induced reward.
+NPFF	addiction	reward	20381562	Taken together, our study should be helpful for clarifying the possible mechanisms of <strong>NPFF</strong> system to modulate morphine induced <b>reward</b>.
+NPFF	drug	opioid	20336629	Modulation of basal and <b>morphine</b> induced neuronal activity by a <strong>NPFF</strong>(2) selective agonist measured by c Fos mapping of the mouse brain.
+NPFF	drug	opioid	20336629	Neuropeptide FF (<strong>NPFF</strong>) is a neurotransmitter known to modulate <b>opioid</b> induced analgesia, sensitization, and reward.
+NPFF	addiction	reward	20336629	Neuropeptide FF (<strong>NPFF</strong>) is a neurotransmitter known to modulate opioid induced analgesia, sensitization, and <b>reward</b>.
+NPFF	addiction	sensitization	20336629	Neuropeptide FF (<strong>NPFF</strong>) is a neurotransmitter known to modulate opioid induced analgesia, <b>sensitization</b>, and reward.
+NPFF	drug	opioid	20336629	The expression of the immediate early gene c Fos was analyzed to map the distribution of neurons whose activity is regulated by central administration of the <strong>NPFF</strong>(2) selective agonist dNPA in naive mice and in animals who had received a systemic injection of <b>morphine</b>.
+NPFF	drug	opioid	20336629	Moreover, our study identified the nucleus accumbens shell and ventral pallidum as putative sites of interaction between <strong>NPFF</strong> and <b>opioid</b> systems in relation with the modulation of acute <b>morphine</b> rewarding and locomotor effects.
+NPFF	drug	alcohol	19463751	Dansyl PQRamide, a putative antagonist of <strong>NPFF</strong> receptors, reduces anxiety like behavior of <b>ethanol</b> withdrawal in a plus maze test in rats.
+NPFF	addiction	withdrawal	19463751	Dansyl PQRamide, a putative antagonist of <strong>NPFF</strong> receptors, reduces anxiety like behavior of ethanol <b>withdrawal</b> in a plus maze test in rats.
+NPFF	drug	alcohol	19463751	The aim of the present study was to determine whether dansyl PQR amide, a putative antagonist of receptors for an anti opioid peptide neuropeptide FF (<strong>NPFF</strong>) could affect anxiety like behavior measured during withdrawal from acute , and chronic <b>ethanol</b> administration in the elevated plus maze test in rats.
+NPFF	drug	opioid	19463751	The aim of the present study was to determine whether dansyl PQR amide, a putative antagonist of receptors for an anti <b>opioid</b> peptide neuropeptide FF (<strong>NPFF</strong>) could affect anxiety like behavior measured during withdrawal from acute , and chronic ethanol administration in the elevated plus maze test in rats.
+NPFF	addiction	withdrawal	19463751	The aim of the present study was to determine whether dansyl PQR amide, a putative antagonist of receptors for an anti opioid peptide neuropeptide FF (<strong>NPFF</strong>) could affect anxiety like behavior measured during <b>withdrawal</b> from acute , and chronic ethanol administration in the elevated plus maze test in rats.
+NPFF	drug	opioid	19463751	Dansyl PQR amide, <strong>NPFF</strong> and <b>naloxone</b> given alone to naive rats did not have influence on spontaneous locomotor activity of animals.
+NPFF	drug	alcohol	19463751	Furthermore, <strong>NPFF</strong> potentiated anxiety like behavior during withdrawal from chronic, but not acute, <b>ethanol</b> administration in rats.
+NPFF	addiction	withdrawal	19463751	Furthermore, <strong>NPFF</strong> potentiated anxiety like behavior during <b>withdrawal</b> from chronic, but not acute, ethanol administration in rats.
+NPFF	drug	alcohol	19463751	Our data suggest that <strong>NPFF</strong> system is involved in regulation of affective symptoms of <b>ethanol</b> withdrawal.
+NPFF	addiction	withdrawal	19463751	Our data suggest that <strong>NPFF</strong> system is involved in regulation of affective symptoms of ethanol <b>withdrawal</b>.
+NPFF	drug	alcohol	19463751	It seems that involvement of the <strong>NPFF</strong> system in <b>ethanol</b> withdrawal anxiety like behavior is associated with regulation of the opioid system activity.
+NPFF	drug	opioid	19463751	It seems that involvement of the <strong>NPFF</strong> system in ethanol withdrawal anxiety like behavior is associated with regulation of the <b>opioid</b> system activity.
+NPFF	addiction	withdrawal	19463751	It seems that involvement of the <strong>NPFF</strong> system in ethanol <b>withdrawal</b> anxiety like behavior is associated with regulation of the opioid system activity.
+NPFF	drug	opioid	18706462	Recently, we reported the discovery of a novel amino acid sequence derived from the <strong>NPFF</strong> precursor NAWGPWSKEQLSPQA, which blocked the expression of conditioned place preference induced by <b>morphine</b> and reversed the antinociceptive activity of <b>morphine</b> (5mg/kg, s.c.) in the tail immersion test in rats.
+NPFF	drug	cocaine	18295932	Neuropeptide FF (<strong>NPFF</strong>) reduces the expression of <b>cocaine</b> induced conditioned place preference and <b>cocaine</b> induced sensitization in animals.
+NPFF	addiction	sensitization	18295932	Neuropeptide FF (<strong>NPFF</strong>) reduces the expression of cocaine induced conditioned place preference and cocaine induced <b>sensitization</b> in animals.
+NPFF	drug	cocaine	18295932	The aim of the present study was to indicate whether the anti opioid peptide, neuropeptide FF (<strong>NPFF</strong>; FLFQPQRF NH2) was able to modify the rewarding effect of <b>cocaine</b> (5 mg/kg) measured in the expression of conditioned place preference (CPP) test in rats and the expression of sensitization to hyperlocomotor effect of <b>cocaine</b> (10 mg/kg) in mice.
+NPFF	drug	opioid	18295932	The aim of the present study was to indicate whether the anti <b>opioid</b> peptide, neuropeptide FF (<strong>NPFF</strong>; FLFQPQRF NH2) was able to modify the rewarding effect of cocaine (5 mg/kg) measured in the expression of conditioned place preference (CPP) test in rats and the expression of sensitization to hyperlocomotor effect of cocaine (10 mg/kg) in mice.
+NPFF	addiction	reward	18295932	The aim of the present study was to indicate whether the anti opioid peptide, neuropeptide FF (<strong>NPFF</strong>; FLFQPQRF NH2) was able to modify the rewarding effect of cocaine (5 mg/kg) measured in the expression of conditioned place preference (<b>CPP</b>) test in rats and the expression of sensitization to hyperlocomotor effect of cocaine (10 mg/kg) in mice.
+NPFF	addiction	sensitization	18295932	The aim of the present study was to indicate whether the anti opioid peptide, neuropeptide FF (<strong>NPFF</strong>; FLFQPQRF NH2) was able to modify the rewarding effect of cocaine (5 mg/kg) measured in the expression of conditioned place preference (CPP) test in rats and the expression of <b>sensitization</b> to hyperlocomotor effect of cocaine (10 mg/kg) in mice.
+NPFF	drug	cocaine	18295932	Moreover, <strong>NPFF</strong> inhibited the expression of <b>cocaine</b> induced sensitization to its hyperlocomotor effect at the dose of 20 nmol (P<0.05) and acute hyperlocomotor effect of <b>cocaine</b> at doses of 5 nmol (P<0.01), 10 nmol (P<0.01), and 20 nmol (P<0.05).
+NPFF	addiction	sensitization	18295932	Moreover, <strong>NPFF</strong> inhibited the expression of cocaine induced <b>sensitization</b> to its hyperlocomotor effect at the dose of 20 nmol (P<0.05) and acute hyperlocomotor effect of cocaine at doses of 5 nmol (P<0.01), 10 nmol (P<0.01), and 20 nmol (P<0.05).
+NPFF	drug	cocaine	18295932	Our study suggests that <strong>NPFF</strong> may participate in a rewarding effect of <b>cocaine</b> measured in the CPP paradigm.
+NPFF	addiction	reward	18295932	Our study suggests that <strong>NPFF</strong> may participate in a rewarding effect of cocaine measured in the <b>CPP</b> paradigm.
+NPFF	drug	cocaine	18295932	On the other hand, our experiments indicate that <strong>NPFF</strong> is involved in the mechanism of expression of sensitization to <b>cocaine</b> hyperlocomotion but this effect seems to be non specific because <strong>NPFF</strong> also inhibited the acute hyperlocomotor effect of <b>cocaine</b>.
+NPFF	addiction	sensitization	18295932	On the other hand, our experiments indicate that <strong>NPFF</strong> is involved in the mechanism of expression of <b>sensitization</b> to cocaine hyperlocomotion but this effect seems to be non specific because <strong>NPFF</strong> also inhibited the acute hyperlocomotor effect of cocaine.
+NPFF	drug	alcohol	17884254	Neuropeptide FF (<strong>NPFF</strong>) reduces the expression of morphine  but not of <b>ethanol</b> induced conditioned place preference in rats.
+NPFF	drug	opioid	17884254	Neuropeptide FF (<strong>NPFF</strong>) reduces the expression of <b>morphine</b>  but not of ethanol induced conditioned place preference in rats.
+NPFF	drug	opioid	17884254	Neuropeptide FF (<strong>NPFF</strong>) has been described as an anti <b>opioid</b> peptide.
+NPFF	drug	alcohol	17884254	Previous study has indicated that 1DMe ([D Tyr(1), (NMe)Phe(3)]<strong>NPFF</strong>), a stable analog of <strong>NPFF</strong>, inhibits acquisition of the rewarding effect of morphine but not of <b>ethanol</b> in mice.
+NPFF	drug	opioid	17884254	Previous study has indicated that 1DMe ([D Tyr(1), (NMe)Phe(3)]<strong>NPFF</strong>), a stable analog of <strong>NPFF</strong>, inhibits acquisition of the rewarding effect of <b>morphine</b> but not of ethanol in mice.
+NPFF	drug	alcohol	17884254	The present study examines the influence of <strong>NPFF</strong> on the expression of morphine  and <b>ethanol</b> induced CPP in the biased procedure in rats.
+NPFF	drug	opioid	17884254	The present study examines the influence of <strong>NPFF</strong> on the expression of <b>morphine</b>  and ethanol induced CPP in the biased procedure in rats.
+NPFF	addiction	reward	17884254	The present study examines the influence of <strong>NPFF</strong> on the expression of morphine  and ethanol induced <b>CPP</b> in the biased procedure in rats.
+NPFF	addiction	aversion	17884254	<strong>NPFF</strong> gave itself, neither induced place preference nor <b>aversion</b>, although a tendency to <b>aversive</b> effect was seen at the highest dose of 20 nmol.
+NPFF	drug	alcohol	17884254	However, <strong>NPFF</strong> was unable to inhibit the expression of <b>ethanol</b> induced CPP.
+NPFF	addiction	reward	17884254	However, <strong>NPFF</strong> was unable to inhibit the expression of ethanol induced <b>CPP</b>.
+NPFF	drug	opioid	17884254	These results suggest that <strong>NPFF</strong> is involved in the expression of <b>morphine</b> reward.
+NPFF	addiction	reward	17884254	These results suggest that <strong>NPFF</strong> is involved in the expression of morphine <b>reward</b>.
+NPFF	drug	alcohol	17107711	The role of neuropeptide FF (<strong>NPFF</strong>) in the expression of sensitization to hyperlocomotor effect of morphine and <b>ethanol</b>.
+NPFF	drug	opioid	17107711	The role of neuropeptide FF (<strong>NPFF</strong>) in the expression of sensitization to hyperlocomotor effect of <b>morphine</b> and ethanol.
+NPFF	addiction	sensitization	17107711	The role of neuropeptide FF (<strong>NPFF</strong>) in the expression of <b>sensitization</b> to hyperlocomotor effect of morphine and ethanol.
+NPFF	drug	opioid	17107711	Neuropeptide FF (<strong>NPFF</strong>) has been characterized as an endogenous anti <b>opioid</b> peptide because its intraventricular injection (icv) reversed <b>morphine</b>  and stress induced analgesia, and precipitates withdrawal syndrome in <b>morphine</b> dependent rats.
+NPFF	addiction	withdrawal	17107711	Neuropeptide FF (<strong>NPFF</strong>) has been characterized as an endogenous anti opioid peptide because its intraventricular injection (icv) reversed morphine  and stress induced analgesia, and precipitates <b>withdrawal</b> syndrome in morphine dependent rats.
+NPFF	addiction	dependence	17107711	The role of <strong>NPFF</strong> in other aspects of drug <b>dependence</b> is unknown.
+NPFF	drug	opioid	17107711	Therefore, the aim of this study was to determine <strong>NPFF</strong> influence on the expression of sensitization to the <b>morphine</b> induced hyperlocomotion.
+NPFF	addiction	sensitization	17107711	Therefore, the aim of this study was to determine <strong>NPFF</strong> influence on the expression of <b>sensitization</b> to the morphine induced hyperlocomotion.
+NPFF	drug	alcohol	17107711	As the opioid system plays a role in <b>ethanol</b> effects, the influence of <strong>NPFF</strong> on the expression of sensitization to hyperlocomotor effect of <b>ethanol</b> was also investigated.
+NPFF	drug	opioid	17107711	As the <b>opioid</b> system plays a role in ethanol effects, the influence of <strong>NPFF</strong> on the expression of sensitization to hyperlocomotor effect of ethanol was also investigated.
+NPFF	addiction	sensitization	17107711	As the opioid system plays a role in ethanol effects, the influence of <strong>NPFF</strong> on the expression of <b>sensitization</b> to hyperlocomotor effect of ethanol was also investigated.
+NPFF	drug	alcohol	17107711	Our study indicated that acute administration of <strong>NPFF</strong> (5, 10, 20nmol, icv) inhibited the expression of morphine induced sensitization at doses of 10 (P<0.05) and 20nmol (P<0.01), and also inhibited <b>ethanol</b> induced sensitization at a dose of 20nmol (P<0.01).
+NPFF	drug	opioid	17107711	Our study indicated that acute administration of <strong>NPFF</strong> (5, 10, 20nmol, icv) inhibited the expression of <b>morphine</b> induced sensitization at doses of 10 (P<0.05) and 20nmol (P<0.01), and also inhibited ethanol induced sensitization at a dose of 20nmol (P<0.01).
+NPFF	addiction	sensitization	17107711	Our study indicated that acute administration of <strong>NPFF</strong> (5, 10, 20nmol, icv) inhibited the expression of morphine induced <b>sensitization</b> at doses of 10 (P<0.05) and 20nmol (P<0.01), and also inhibited ethanol induced <b>sensitization</b> at a dose of 20nmol (P<0.01).
+NPFF	drug	alcohol	17107711	Furthermore, <strong>NPFF</strong> inhibited the acute locomotor effect of morphine (10 and 20nmol) but not that of <b>ethanol</b>.
+NPFF	drug	opioid	17107711	Furthermore, <strong>NPFF</strong> inhibited the acute locomotor effect of <b>morphine</b> (10 and 20nmol) but not that of ethanol.
+NPFF	drug	opioid	17107711	In conclusion, our experiments indicated that <strong>NPFF</strong> attenuated the acute <b>morphine</b> locomotion and the expression of sensitization to locomotion.
+NPFF	addiction	sensitization	17107711	In conclusion, our experiments indicated that <strong>NPFF</strong> attenuated the acute morphine locomotion and the expression of <b>sensitization</b> to locomotion.
+NPFF	drug	opioid	16529722	Immunohistochemical distribution patterns of neuropeptide FF (<strong>NPFF</strong>) and neuropeptide tyrosine (NPY) were studied in the brain of rats submitted to two different protocols of <b>heroin</b> treatment.
+NPFF	drug	opioid	16529722	In drug naive rats, acutely injected <b>heroin</b> significantly depleted <strong>NPFF</strong> immunoreactive material within the neurons of the nucleus of solitary tract (NTS), significantly decreased the density of <strong>NPFF</strong> immunoreactive nerve fibers within the median eminence, pituitary stalk, and neurohypophysis, and markedly increased NPY immunoreactive neurons and nerve fibers in the thalamic paraventricular nucleus and bed nucleus of stria terminalis.
+NPFF	drug	opioid	16529722	In drug sensitized rats, <b>heroin</b> significantly increased the number and immunostaining intensity of the <strong>NPFF</strong> immunoreactive neurons within the NTS and induced minor changes in the <strong>NPFF</strong> immunoreactive nerve fiber network of the median eminence, pituitary stalk, and neurohypophysis and a relatively minor increase in NPY neurons in the thalamic paraventricular nucleus and bed nucleus of stria terminalis.
+NPFF	drug	opioid	16529722	These <b>heroin</b> induced changes suggest that <strong>NPFF</strong> is involved in regulating the effects of the <b>heroin</b> injection and in the mechanisms underlying behavioral sensitization.
+NPFF	addiction	sensitization	16529722	These heroin induced changes suggest that <strong>NPFF</strong> is involved in regulating the effects of the heroin injection and in the mechanisms underlying behavioral <b>sensitization</b>.
+NPFF	drug	alcohol	16494968	injections of 1DMe (D Tyr1(NMe)Phe3]<strong>NPFF</strong>), a stable agonist of the neuropeptide FF system, on the acquisition of place conditioning by morphine or <b>alcohol</b> (<b>ethanol</b>).
+NPFF	drug	opioid	16494968	injections of 1DMe (D Tyr1(NMe)Phe3]<strong>NPFF</strong>), a stable agonist of the neuropeptide FF system, on the acquisition of place conditioning by <b>morphine</b> or alcohol (ethanol).
+NPFF	drug	opioid	16490283	Neuropeptide FF (<strong>NPFF</strong>) participates in many physiological functions associated with <b>opioids</b> in the mammalian CNS.
+NPFF	drug	opioid	12126738	Pharmacological studies have implicated the anti <b>opioid</b> neuropeptide FF (<strong>NPFF</strong>) in the modulation of pain transmission.
+NPFF	drug	opioid	12126738	Our results evidence a physiological interplay between <strong>NPFF</strong> and <b>opioid</b> systems and further support the use of PNA as effective antisense agents, for studying gene function in vivo.
+NPFF	drug	opioid	11835998	Neuropeptide FF (<strong>NPFF</strong>) is an endogenous anti <b>opioid</b> peptide.
+NPFF	drug	opioid	11835998	<strong>NPFF</strong> could potentiate the <b>naloxone</b> precipitated <b>morphine</b> withdrawal syndromes in <b>morphine</b> dependent rats, indicating the possible involvement of the endogenous <strong>NPFF</strong> system in <b>opioid</b> analgesia and dependence.
+NPFF	addiction	dependence	11835998	<strong>NPFF</strong> could potentiate the naloxone precipitated morphine withdrawal syndromes in morphine dependent rats, indicating the possible involvement of the endogenous <strong>NPFF</strong> system in opioid analgesia and <b>dependence</b>.
+NPFF	addiction	withdrawal	11835998	<strong>NPFF</strong> could potentiate the naloxone precipitated morphine <b>withdrawal</b> syndromes in morphine dependent rats, indicating the possible involvement of the endogenous <strong>NPFF</strong> system in opioid analgesia and dependence.
+NPFF	drug	opioid	11835998	The present study was performed to examine the effects of dansyl PQRamide (dns PQRa), a putative <strong>NPFF</strong> antagonist, on conditioned place preference (CPP), in addition, its interaction with the <b>opioid</b> system.
+NPFF	addiction	reward	11835998	The present study was performed to examine the effects of dansyl PQRamide (dns PQRa), a putative <strong>NPFF</strong> antagonist, on conditioned place preference (<b>CPP</b>), in addition, its interaction with the opioid system.
+NPFF	drug	opioid	11835998	These results suggest that blockade of the <strong>NPFF</strong> system produces rewarding, possibly via an inhibition of the anti <b>opioid</b> action of <strong>NPFF</strong>.
+NPFF	drug	opioid	10851242	The anti opiate neuropeptides FF and AF (<strong>NPFF</strong> and NPAF) have been implicated in pain modulation as well as in <b>opioid</b> tolerance and may play a critical role in this process, although their mechanism of action has remained unknown.
+NPFF	drug	opioid	10698116	In this study, we investigated the effects of chronically infused alpha melanocyte stimulating hormone (alpha MSH), dynorphin(1 8) (DYN(1 8)), dynorphin A (DYNA), and <strong>NPFF</strong> antibodies on delta <b>opioid</b> receptor expression in rat brains.
+NPFF	drug	opioid	10573293	Neuropeptide FF (<strong>NPFF</strong>) has been reported to be an endogenous anti <b>opioid</b> peptide that has significant effects on <b>morphine</b> tolerance and dependence.
+NPFF	addiction	dependence	10573293	Neuropeptide FF (<strong>NPFF</strong>) has been reported to be an endogenous anti opioid peptide that has significant effects on morphine tolerance and <b>dependence</b>.
+NPFF	drug	opioid	10573293	In the present study, we examined the chronic effects of <strong>NPFF</strong> and its synthetic analogs: the putative agonist, PFRFamide, and the putative antagonists, dansyl PQRamide and PFR(Tic)amide on <b>naloxone</b> precipitated <b>morphine</b> withdrawal syndromes in rats.
+NPFF	addiction	withdrawal	10573293	In the present study, we examined the chronic effects of <strong>NPFF</strong> and its synthetic analogs: the putative agonist, PFRFamide, and the putative antagonists, dansyl PQRamide and PFR(Tic)amide on naloxone precipitated morphine <b>withdrawal</b> syndromes in rats.
+NPFF	drug	opioid	10573293	Our results revealed that <strong>NPFF</strong> significantly potentiated the overall <b>morphine</b> withdrawal syndromes and, on the contrary, dansyl PQRamide attenuated these syndromes.
+NPFF	addiction	withdrawal	10573293	Our results revealed that <strong>NPFF</strong> significantly potentiated the overall morphine <b>withdrawal</b> syndromes and, on the contrary, dansyl PQRamide attenuated these syndromes.
+NPFF	addiction	dependence	10573293	These results clearly indicate that modulation of the <strong>NPFF</strong> system in the mammalian central nervous system has significant effects on opiate <b>dependence</b>.
+NPFF	drug	opioid	10573293	In addition, <b>morphine</b> withdrawal syndromes could be practically applied as a valid parameter to functionally characterize the putative <strong>NPFF</strong> agonists and antagonists.
+NPFF	addiction	withdrawal	10573293	In addition, morphine <b>withdrawal</b> syndromes could be practically applied as a valid parameter to functionally characterize the putative <strong>NPFF</strong> agonists and antagonists.
+NPFF	drug	amphetamine	9878747	We have demonstrated that chronic administration of neuropeptide FF (<strong>NPFF</strong>) into the lateral ventricle potentiated the behavioral sensitization to <b>amphetamine</b>.
+NPFF	addiction	sensitization	9878747	We have demonstrated that chronic administration of neuropeptide FF (<strong>NPFF</strong>) into the lateral ventricle potentiated the behavioral <b>sensitization</b> to amphetamine.
+NPFF	drug	amphetamine	9878747	Further, the treatment with <strong>NPFF</strong> decreased the levels of serotonin, and increased the glutamate and GABA content in the medial prefrontal cortex of <b>amphetamine</b> sensitized rats.
+NPFF	drug	amphetamine	9878747	The results suggest that <strong>NPFF</strong> may modulate the neuronal process of <b>amphetamine</b> addiction.
+NPFF	addiction	addiction	9878747	The results suggest that <strong>NPFF</strong> may modulate the neuronal process of amphetamine <b>addiction</b>.
+NPFF	drug	opioid	9845244	Neuropeptide FF (<strong>NPFF</strong>), a <b>morphine</b> modulatory peptide, is localized within discrete autonomic regions including the brainstem nucleus tractus solitarius (NTS) and the parabrachial nucleus (PBN).
+NPFF	addiction	withdrawal	9845244	We investigated the activation of <strong>NPFF</strong> neurons in the NTS of rats induced by cardiovascular challenge and centrally generated opiate <b>withdrawal</b>.
+NPFF	addiction	withdrawal	9845244	However, following opiate <b>withdrawal</b>, virtually no Fos expression was observed in <strong>NPFF</strong> neurons.
+NPFF	addiction	withdrawal	9845244	This study shows that <strong>NPFF</strong> neurons in NTS that project to the PBN respond selectively to NP as opposed to other cardiovascular challenges or opiate <b>withdrawal</b>.
+NPFF	drug	nicotine	8743632	Might <strong>NPFF</strong> also play a role in <b>nicotine</b> dependence?
+NPFF	addiction	dependence	8743632	Might <strong>NPFF</strong> also play a role in nicotine <b>dependence</b>?
+NPFF	addiction	dependence	8746922	There is evidence that neuropeptide FF (<strong>NPFF</strong>) has antiopiate activity and may play a role in opiate <b>dependence</b> and subsequent abstinence syndrome.
+NPFF	drug	opioid	8746922	Third ventricle administration of the resulting compound, dansyl PQRamide (0.75 microgram and 1 microgram), dose dependently antagonized the quasi <b>morphine</b> abstinence activity of <strong>NPFF</strong> (10 micrograms) in opiate naive rats.
+NPFF	drug	opioid	8617406	"Anti <b>opioid</b>" properties have been attributed to various peptides, especially cholecystokinin (CCK), neuropeptide FF (<strong>NPFF</strong>) and melanocyte inhibiting factor (MIF) related peptides.
+NPFF	drug	opioid	8617406	In fact, CCK, <strong>NPFF</strong> and the MIF family of peptides have complex properties and can act as <b>opioid</b> like as well as anti <b>opioid</b> peptides.
+NPFF	drug	opioid	8617406	CCK  and <strong>NPFF</strong> related drugs have potential therapeutic interest as adjuncts to <b>opioids</b> for alleviating pain and/or for the treatment of <b>opioid</b> abuse.
+NPFF	drug	opioid	8545244	It is possible to speculate that the administration of <b>morphine</b> stimulates antiopioid systems such as neuropeptide FF (<strong>NPFF</strong>), as part of an homeostatic mechanism contributing to the development of tolerance.
+NPFF	drug	opioid	8545244	To test this hypothesis, pain sensitivity, opiate dependence, and CNS <strong>NPFF</strong> IR levels were estimated at different times after implantation of <b>morphine</b> pellets (2 x 75 mg; NIDA).
+NPFF	addiction	dependence	8545244	To test this hypothesis, pain sensitivity, opiate <b>dependence</b>, and CNS <strong>NPFF</strong> IR levels were estimated at different times after implantation of morphine pellets (2 x 75 mg; NIDA).
+NPFF	drug	opioid	8545244	Three hours after <b>morphine</b> pellet treatment the analgesic effect was maximum and it decreased rapidly during the following 12 h. <b>Naloxone</b> precipitated withdrawal syndrome was detected as soon as 3 h after <b>morphine</b> pellet implantation and was maximal after 24 h. <strong>NPFF</strong> IR levels were measured in the spinal cord, brain stem, and hypothalamus.
+NPFF	addiction	withdrawal	8545244	Three hours after morphine pellet treatment the analgesic effect was maximum and it decreased rapidly during the following 12 h. Naloxone precipitated <b>withdrawal</b> syndrome was detected as soon as 3 h after morphine pellet implantation and was maximal after 24 h. <strong>NPFF</strong> IR levels were measured in the spinal cord, brain stem, and hypothalamus.
+NPFF	drug	opioid	8545244	A significant decrease of <strong>NPFF</strong> IR was observed 1 h after <b>morphine</b> pellet implantation ( 25% to  45% depending on the structures) followed by a drastic increase of <strong>NPFF</strong> IR levels (+60 to +140%) between 3 and 6 h. <strong>NPFF</strong> IR levels rapidly returned to baseline after 24 36 h. It is suggested that the activity of these <strong>NPFF</strong> IR neurones may increase gradually as a consequence of the continuous stimulation of opiate receptors and be part of an adaptive process that is able to counteract <b>morphine</b> effects and to induce dependence and tolerance to the analgesic effects of opiates.
+NPFF	addiction	dependence	8545244	A significant decrease of <strong>NPFF</strong> IR was observed 1 h after morphine pellet implantation ( 25% to  45% depending on the structures) followed by a drastic increase of <strong>NPFF</strong> IR levels (+60 to +140%) between 3 and 6 h. <strong>NPFF</strong> IR levels rapidly returned to baseline after 24 36 h. It is suggested that the activity of these <strong>NPFF</strong> IR neurones may increase gradually as a consequence of the continuous stimulation of opiate receptors and be part of an adaptive process that is able to counteract morphine effects and to induce <b>dependence</b> and tolerance to the analgesic effects of opiates.
+NPFF	drug	opioid	8134310	Chronic intracerebroventricular infusion of the antiopioid peptide, Phe Leu Phe Gln Pro Gln Arg Phe NH2 (<strong>NPFF</strong>), downregulates mu <b>opioid</b> binding sites in rat brain.
+NPFF	drug	opioid	8134310	Phe Leu Phe Gln Pro Gln Arg Phe NH2 (<strong>NPFF</strong>), an endogenous mammalian antiopioid peptide, has been shown by other laboratories to attenuate the acute antinociceptive effects of <b>morphine</b>, the development of <b>morphine</b> tolerance, and <b>naloxone</b> induced withdrawal in <b>morphine</b> dependent rats.
+NPFF	addiction	withdrawal	8134310	Phe Leu Phe Gln Pro Gln Arg Phe NH2 (<strong>NPFF</strong>), an endogenous mammalian antiopioid peptide, has been shown by other laboratories to attenuate the acute antinociceptive effects of morphine, the development of morphine tolerance, and naloxone induced <b>withdrawal</b> in morphine dependent rats.
+NPFF	drug	opioid	8134310	The present study determined the effect of chronic <strong>NPFF</strong> on mu <b>opioid</b> receptors and mRNA for the endogenous <b>opioids</b> dynorphin and enkephalin.
+NPFF	drug	opioid	8134310	Chronic administration of <strong>NPFF</strong> concurrently with <b>morphine</b> sulfate did not significantly alter <b>naloxone</b> induced withdrawal signs or the development of <b>morphine</b> tolerance.
+NPFF	addiction	withdrawal	8134310	Chronic administration of <strong>NPFF</strong> concurrently with morphine sulfate did not significantly alter naloxone induced <b>withdrawal</b> signs or the development of morphine tolerance.
+NPFF	drug	opioid	8229791	Neuropeptide FF (FLFQPQRFamide, <strong>NPFF</strong>) is an octapeptide implicated in <b>morphine</b> analgesia, tolerance and dependence.
+NPFF	addiction	dependence	8229791	Neuropeptide FF (FLFQPQRFamide, <strong>NPFF</strong>) is an octapeptide implicated in morphine analgesia, tolerance and <b>dependence</b>.
+NPFF	drug	opioid	8229791	The radioligand binding and G protein coupling of <strong>NPFF</strong> receptors were not altered by chronic <b>morphine</b> treatment.
+NPFF	drug	opioid	8284250	We studied the ability of <strong>NPFF</strong>, a FMRFamide like peptide with certain antiopiate properties, to affect the inhibitory effect of <b>morphine</b> on the electrically induced contraction of guinea pig ileum.
+NPFF	drug	opioid	8284250	These results suggest that <strong>NPFF</strong> receptors exist in guinea pig ileum in association with opiate receptors, and that endogenous <strong>NPFF</strong> may play a role in the diarrhea observed in the <b>morphine</b> withdrawal syndrome.
+NPFF	addiction	withdrawal	8284250	These results suggest that <strong>NPFF</strong> receptors exist in guinea pig ileum in association with opiate receptors, and that endogenous <strong>NPFF</strong> may play a role in the diarrhea observed in the morphine <b>withdrawal</b> syndrome.
+NPFF	drug	opioid	8412495	Neuropeptide FF (<strong>NPFF</strong>) has been shown to exert various antiopiate actions, including precipitation of opiate abstinence syndrome by third ventricle injection in <b>morphine</b> dependent rats.
+NPFF	drug	opioid	8412495	In the present study, dansyl Pro Gln Arg Phe amide, a lipophilic analog of <strong>NPFF</strong>, was injected into <b>morphine</b> dependent rats and appropriate sham controls at a dose of 9 mg/kg s.c.
+NPFF	drug	opioid	8412495	The <strong>NPFF</strong> analog precipitated a vigorous opiate abstinence syndrome in <b>morphine</b> dependent rats, but not in sham controls.
+NPFF	addiction	dependence	1491790	Previous studies suggest that neuropeptide FF (<strong>NPFF</strong>) plays a role in opiate <b>dependence</b> and subsequent abstinence syndrome.
+NPFF	drug	opioid	1491790	Endogenous <strong>NPFF</strong> also appears to play a role in opiate tolerance since third ventricle injection of IgG from <strong>NPFF</strong> antiserum selectively restores <b>morphine</b> sensitivity in <b>morphine</b> tolerant rats.
+NPFF	drug	opioid	1491790	The <strong>NPFF</strong> analog, desamino YFLFQPQRamide (daY8Ra) has previously antagonized behavioral effects of <strong>NPFF</strong> and has attenuated <b>morphine</b> dependence.
+NPFF	addiction	dependence	1491790	The <strong>NPFF</strong> analog, desamino YFLFQPQRamide (daY8Ra) has previously antagonized behavioral effects of <strong>NPFF</strong> and has attenuated morphine <b>dependence</b>.
+NPFF	addiction	dependence	1787914	Previous studies suggest that neuropeptide FF (<strong>NPFF</strong>) plays a role in opiate <b>dependence</b> and subsequent abstinence syndrome.
+NPFF	drug	opioid	1787914	Thus, immunoneutralization of <strong>NPFF</strong> appears to selectively restore <b>morphine</b> sensitivity in opiate tolerant animals.
+NPFF	drug	opioid	1800944	Previously, <strong>NPFF</strong> precipitated opiate abstinence syndrome, while IgG from <strong>NPFF</strong> antiserum attenuated subsequent <b>naloxone</b> precipitated abstinence signs in dependent rats.
+NPFF	drug	opioid	1800944	Pretreatment with 600 ng of <strong>NPFF</strong> itself, or of <strong>NPFF</strong> modified at the N terminal only (daY9Fa), failed to attenuate subsequent <b>naloxone</b> precipitated abstinence, suggesting that the C terminal modification is critical for <strong>NPFF</strong> antagonist activity.
+HOMER2	drug	amphetamine	32116834	Transgenic Analyses of <strong>Homer2</strong> Function Within Nucleus Accumbens Subregions in the Regulation of <b>Methamphetamine</b> Reward and Reinforcement in Mice.
+HOMER2	addiction	reward	32116834	Transgenic Analyses of <strong>Homer2</strong> Function Within Nucleus Accumbens Subregions in the Regulation of Methamphetamine <b>Reward</b> and <b>Reinforcement</b> in Mice.
+HOMER2	addiction	reward	32116834	Recently, we discovered an association between genetic vulnerability to MA taking and increased expression of the glutamate receptor scaffolding protein <strong>Homer2</strong> within both the shell and core subregions of the nucleus accumbens (NAC) and demonstrated a necessary role for <strong>Homer2</strong> within the shell subregion in MA <b>reward</b> and <b>reinforcement</b> in mice.
+HOMER2	addiction	reward	32116834	This report extends our earlier work by interrogating the functional relevance of <strong>Homer2</strong> within the NAC core for the conditioned rewarding and <b>reinforcing</b> properties of MA.
+HOMER2	addiction	reward	32116834	To determine whether Homer2b within NAC subregions played an active role in regulating MA <b>reward</b> and <b>reinforcement</b>, we characterized the MA phenotype of constitutive <strong>Homer2</strong> knockout (KO) mice and then assayed the effects of virus mediated overexpression of Homer2b within the NAC shell and core of wild type and KO mice.
+HOMER2	addiction	relapse	32116834	In line with the results of NAC core knockdown, <strong>Homer2</strong> deletion potentiated MA induced CPP, MA reinforced responding and intake, as well as both cue  and MA primed <b>reinstatement</b> of MA <b>seeking</b> following extinction.
+HOMER2	addiction	reward	32116834	In line with the results of NAC core knockdown, <strong>Homer2</strong> deletion potentiated MA induced <b>CPP</b>, MA reinforced responding and intake, as well as both cue  and MA primed reinstatement of MA seeking following extinction.
+HOMER2	addiction	addiction	32116834	These data provide new evidence indicating a globally suppressive role for <strong>Homer2</strong> in MA seeking and MA taking but argue against specific NAC subregions as the neural loci through which <strong>Homer2</strong> actively regulates MA <b>addiction</b> related behaviors.
+HOMER2	addiction	relapse	32116834	These data provide new evidence indicating a globally suppressive role for <strong>Homer2</strong> in MA <b>seeking</b> and MA taking but argue against specific NAC subregions as the neural loci through which <strong>Homer2</strong> actively regulates MA addiction related behaviors.
+HOMER2	drug	alcohol	30737312	Our studies demonstrate that, in male mice, a history of chronic binge <b>alcohol</b> drinking elevates BNST levels of the mGlu5 scaffolding protein <strong>Homer2</strong> and activated extracellular signal regulated kinase (ERK) in an adaptive response to limit <b>alcohol</b> consumption.
+HOMER2	addiction	intoxication	30737312	Our studies demonstrate that, in male mice, a history of chronic <b>binge</b> alcohol drinking elevates BNST levels of the mGlu5 scaffolding protein <strong>Homer2</strong> and activated extracellular signal regulated kinase (ERK) in an adaptive response to limit alcohol consumption.
+HOMER2	drug	cocaine	30268522	Prolonged access to <b>cocaine</b> induces distinct <strong>Homer2</strong> DNA methylation, hydroxymethylation, and transcriptional profiles in the dorsomedial prefrontal cortex of Male Sprague Dawley rats.
+HOMER2	addiction	withdrawal	30267744	Likewise, mice receiving the MA <b>withdrawal</b> regimen had high expression in mGluR5 protein but unaltered EAAT3, <strong>Homer2</strong> expression in hippocampal tissues.
+HOMER2	drug	alcohol	29249995	<strong>Homer2</strong> and <b>Alcohol</b>: A Mutual Interaction.
+HOMER2	drug	alcohol	29249995	The consequences of repeated <b>alcohol</b> administration on the expression of the Homer family proteins demonstrate a crucial and active role, particularly for the expression of <strong>Homer2</strong> isoform, in regulating <b>alcohol</b> induced behavioral and cellular neuroplasticity.
+HOMER2	drug	alcohol	29249995	The interaction between <strong>Homer2</strong> and <b>alcohol</b> can be defined as a mutual relation: <b>alcohol</b> consumption enhances the expression of <strong>Homer2</strong> protein isoform within the nucleus accumbens and the extended amygdala, cerebral areas where, in turn, <strong>Homer2</strong> is able to mediate the development of the "pro <b>alcoholic</b>" behavioral phenotype, as a consequence of the morpho functional synaptic adaptations.
+HOMER2	addiction	addiction	29234834	One day after the final self administration session, the rats were euthanized and the dmPFC was removed for quantification of mRNA expression of critical glutamatergic signaling genes, <strong>Homer2</strong>, Grin1, and Dlg4, as these genes and brain region have been previously implicated in <b>addiction</b>, learning, and memory.
+HOMER2	drug	cocaine	29234834	Lastly, <strong>Homer2</strong>, Grin1, and Dlg4 mRNA were impacted by both duration and mode of <b>cocaine</b> exposure.
+HOMER2	addiction	intoxication	29109058	<strong>Homer2</strong> within the central nucleus of the amygdala modulates withdrawal induced anxiety in a mouse model of <b>binge</b> drinking.
+HOMER2	addiction	withdrawal	29109058	<strong>Homer2</strong> within the central nucleus of the amygdala modulates <b>withdrawal</b> induced anxiety in a mouse model of binge drinking.
+HOMER2	addiction	intoxication	29109058	A history of <b>binge</b> drinking decreases protein expression of the glutamate related scaffolding protein <strong>Homer2</strong> within the central nucleus of the amygdala (CEA), coinciding with behavioral signs of negative affect.
+HOMER2	addiction	withdrawal	29109058	To assess the functional relevance of this protein change for <b>withdrawal</b> induced hyper anxiety, adult (PND 56) and adolescent (PND 28) male C57BL/6J mice were administered an intra CEA infusion of an adeno associated viral vector (AAV) carrying either cDNA to express <strong>Homer2</strong> (H2 cDNA) or GFP as control.
+HOMER2	drug	alcohol	29109058	Following behavioral testing, all animals experienced 5 days of drinking to evaluate the effects of prior <b>alcohol</b> experience and <strong>Homer2</strong> manipulation on subsequent <b>alcohol</b> consumption.
+HOMER2	drug	alcohol	29109058	<strong>Homer2</strong> cDNA infusion in adolescent onset <b>alcohol</b> drinking animals was anxiolytic and reduced subsequent <b>alcohol</b> consumption.
+HOMER2	addiction	intoxication	29109058	Nevertheless, the present results provide novel cause effect evidence supporting a role for CEA <strong>Homer2</strong> in the regulation of both basal anxiety and the time dependent intensification of negative affective states in individuals with a history of <b>binge</b> drinking during adolescence.
+HOMER2	addiction	aversion	27890469	Neuropharmacological and <strong>Homer2</strong> knockdown approaches were also used in C57BL/6J mice to confirm the role for nucleus accumbens (NAC) glutamate/<strong>Homer2</strong> expression in MA preference/<b>aversion</b>.
+HOMER2	addiction	withdrawal	27890469	We also confirmed that subchronic subtoxic MA experience elicits a hyperglutamatergic state within the NAC during protracted <b>withdrawal</b>, characterized by elevated metabotropic glutamate 1/5 receptor function and <strong>Homer2</strong> receptor scaffolding protein expression.
+HOMER2	drug	alcohol	26773198	Expression of genes encoding mGlu1, mGlu5, the NR2A subunit of the NMDA receptor, and <strong>Homer2</strong> were all decreased by binge <b>alcohol</b> consumption in males, while females were relatively resistant (only phosphoinositide dependent protein kinase 1 was decreased).
+HOMER2	addiction	intoxication	26773198	Expression of genes encoding mGlu1, mGlu5, the NR2A subunit of the NMDA receptor, and <strong>Homer2</strong> were all decreased by <b>binge</b> alcohol consumption in males, while females were relatively resistant (only phosphoinositide dependent protein kinase 1 was decreased).
+HOMER2	drug	alcohol	26426435	The postsynaptic scaffolding protein <strong>Homer2</strong> can regulate the cell surface expression of NMDA receptors in vivo, and mice with a null mutation of the <strong>Homer2</strong> gene exhibit an <b>alcohol</b> avoiding and  intolerant phenotype that is accompanied by a lack of <b>ethanol</b> induced glutamate sensitization.
+HOMER2	addiction	sensitization	26426435	The postsynaptic scaffolding protein <strong>Homer2</strong> can regulate the cell surface expression of NMDA receptors in vivo, and mice with a null mutation of the <strong>Homer2</strong> gene exhibit an alcohol avoiding and  intolerant phenotype that is accompanied by a lack of ethanol induced glutamate <b>sensitization</b>.
+HOMER2	drug	alcohol	26426435	Thus, <strong>Homer2</strong> deletion may perturb the function or acute <b>ethanol</b> sensitivity of the NMDA receptor.
+HOMER2	drug	alcohol	26426435	In this study, the function and <b>ethanol</b> sensitivity of glutamate receptors in cultured hippocampal neurons from wild type (WT) and <strong>Homer2</strong> knock out (KO) mice were examined at 7 and 14 days in vitro (DIV) using standard whole cell voltage clamp electrophysiology.
+HOMER2	drug	alcohol	26426435	In conclusion, NMDA receptor function, but not <b>ethanol</b> sensitivity, is reduced in hippocampal neurons lacking the <strong>Homer2</strong> gene.
+HOMER2	drug	alcohol	26254965	<strong>Homer2</strong> within the nucleus accumbens core bidirectionally regulates <b>alcohol</b> intake by both P and Wistar rats.
+HOMER2	drug	alcohol	26254965	In murine models of <b>alcoholism</b>, the glutamate receptor scaffolding protein <strong>Homer2</strong> bidirectionally regulates <b>alcohol</b> intake.
+HOMER2	drug	alcohol	26254965	Although chronic <b>alcohol</b> drinking increases <strong>Homer2</strong> expression within the core subregion of the nucleus accumbens (NAc) of <b>alcohol</b> preferring P rats, the relevance of this neuroadaptation for <b>alcohol</b> intake has yet to be determined in rats.
+HOMER2	drug	alcohol	26254965	No net flux in vivo microdialysis was conducted for glutamate in the NAc to relate <strong>Homer2</strong> dependent changes in <b>alcohol</b> intake to extracellular levels of glutamate.
+HOMER2	drug	alcohol	26101849	Importantly, the association between several genetic variants within the mGluR eEF2 AMPAR pathway and <b>alcohol</b> use behavior (i.e., consumption and <b>alcohol</b> related problems) replicated in the Grady Trauma Project (GTP), an independent sample of adults living in Atlanta, Georgia (n = 1034; 95% African American), including individual variants in GRM1, GRM5, EEF2, MTOR, GRIA1, GRIA4 and <strong>HOMER2</strong> (P < 0.05).
+HOMER2	drug	alcohol	25916683	<strong>Homer2</strong> regulates <b>alcohol</b> and stress cross sensitization.
+HOMER2	addiction	sensitization	25916683	<strong>Homer2</strong> regulates alcohol and stress cross <b>sensitization</b>.
+HOMER2	drug	alcohol	25916683	Regardless of prior <b>alcohol</b> injection (2 g/kg), UCMS mice exhibited elevated NAC shell levels of mGlu1α, GluN2b and <strong>Homer2</strong>, as well as lower phospholipase Cβ within this subregion.
+HOMER2	drug	alcohol	25916683	As <strong>Homer2</strong> regulates <b>alcohol</b> sensitization, we assayed also for locomotor cross sensitization in <strong>Homer2</strong> wild type (WT) and knock out (KO) mice.
+HOMER2	addiction	sensitization	25916683	As <strong>Homer2</strong> regulates alcohol <b>sensitization</b>, we assayed also for locomotor cross <b>sensitization</b> in <strong>Homer2</strong> wild type (WT) and knock out (KO) mice.
+HOMER2	drug	alcohol	25861702	Finally, neuropharmacologic inhibition of PKCε translocation within both regions reduced binge <b>alcohol</b> consumption in a manner requiring intact group 1 metabotropic glutamate receptors, <strong>Homer2</strong>, phospholipase C, and/or phosphotidylinositide 3 kinase function.
+HOMER2	addiction	intoxication	25861702	Finally, neuropharmacologic inhibition of PKCε translocation within both regions reduced <b>binge</b> alcohol consumption in a manner requiring intact group 1 metabotropic glutamate receptors, <strong>Homer2</strong>, phospholipase C, and/or phosphotidylinositide 3 kinase function.
+HOMER2	drug	alcohol	25755642	<strong>Homer2</strong> deletion alters dendritic spine morphology but not <b>alcohol</b> associated adaptations in GluN2B containing N methyl D aspartate receptors in the nucleus accumbens.
+HOMER2	drug	alcohol	25755642	<strong>Homer2</strong> is a member of a family of postsynaptic density (PSD) scaffolding proteins that functions in part to cluster N methyl D aspartate (NMDA) signaling complexes in the PSD, and has been shown to be critically important for plasticity in multiple models of drug and <b>alcohol</b> abuse.
+HOMER2	drug	alcohol	25755642	Here we used <strong>Homer2</strong> knockout (KO) mice and a chronic intermittent intraperitoneal (IP) <b>ethanol</b> injection model to investigate a potential role for the protein in <b>ethanol</b> induced adaptations in dendritic spine morphology and PSD protein expression.
+HOMER2	drug	alcohol	25755642	While deletion of <strong>Homer2</strong> was associated with increased density of long spines on medium spiny neurons of the NAc core of saline treated mice, <b>ethanol</b> exposure had no effect on dendritic spine morphology in either wild type (WT) or <strong>Homer2</strong> KO mice.
+HOMER2	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, <strong>Homer2</strong>, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+HOMER2	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, <strong>Homer2</strong>, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+HOMER2	drug	alcohol	24467847	Intra NAC JNJ 16259685 infusion dose dependently reduced <b>alcohol</b> consumption by C57BL/6J mice; this effect was not additive with that produced by U 73122, nor was it present in <strong>Homer2</strong> KO animals.
+HOMER2	drug	alcohol	24467847	These data provide novel evidence in support of a critical role for mGluR1 PLC signaling, scaffolded by <strong>Homer2</strong>, within the NAC shell, in maintaining <b>alcohol</b> consumption under limited access procedures.
+HOMER2	drug	cocaine	24118426	<b>Cocaine</b> elicited imbalances in ventromedial prefrontal cortex Homer1 versus <strong>Homer2</strong> expression: implications for relapse.
+HOMER2	addiction	relapse	24118426	Cocaine elicited imbalances in ventromedial prefrontal cortex Homer1 versus <strong>Homer2</strong> expression: implications for <b>relapse</b>.
+HOMER2	drug	cocaine	24118426	Withdrawal from a history of extended access to self administered <b>cocaine</b> produces a time dependent intensification of drug seeking, which might relate to a <b>cocaine</b> induced imbalance in the relative expression of constitutively expressed Homer1 versus <strong>Homer2</strong> isoforms within the ventromedial aspect of the prefrontal cortex (vmPFC).
+HOMER2	addiction	relapse	24118426	Withdrawal from a history of extended access to self administered cocaine produces a time dependent intensification of drug <b>seeking</b>, which might relate to a cocaine induced imbalance in the relative expression of constitutively expressed Homer1 versus <strong>Homer2</strong> isoforms within the ventromedial aspect of the prefrontal cortex (vmPFC).
+HOMER2	addiction	withdrawal	24118426	<b>Withdrawal</b> from a history of extended access to self administered cocaine produces a time dependent intensification of drug seeking, which might relate to a cocaine induced imbalance in the relative expression of constitutively expressed Homer1 versus <strong>Homer2</strong> isoforms within the ventromedial aspect of the prefrontal cortex (vmPFC).
+HOMER2	drug	cocaine	24118426	Behavioral studies employed adeno associated virus (AAV) vectors to reverse <b>cocaine</b> elicited changes in the relative expression of Homer1 versus <strong>Homer2</strong> isoforms and tested animals for <b>cocaine</b> prime , and cue induced responding following extinction training.
+HOMER2	drug	cocaine	24118426	Reversing the relative increase in <strong>Homer2</strong> versus Homer1 expression via Homer1c overexpression or Homer2b knockdown failed to influence cue reinforced lever pressing when animals were tested in a drug free state, but both AAV treatments prevented <b>cocaine</b> primed reinstatement of lever pressing behavior.
+HOMER2	addiction	relapse	24118426	Reversing the relative increase in <strong>Homer2</strong> versus Homer1 expression via Homer1c overexpression or Homer2b knockdown failed to influence cue reinforced lever pressing when animals were tested in a drug free state, but both AAV treatments prevented cocaine primed <b>reinstatement</b> of lever pressing behavior.
+HOMER2	drug	cocaine	24118426	These data suggest that a <b>cocaine</b> elicited imbalance in the relative expression of constitutively expressed <strong>Homer2</strong> versus Homer1 within the vmPFC is necessary for the capacity of <b>cocaine</b> to reinstate drug seeking behavior, posing drug induced changes in vmPFC Homer expression as a molecular trigger contributing to drug elicited relapse.
+HOMER2	addiction	relapse	24118426	These data suggest that a cocaine elicited imbalance in the relative expression of constitutively expressed <strong>Homer2</strong> versus Homer1 within the vmPFC is necessary for the capacity of cocaine to reinstate drug <b>seeking</b> behavior, posing drug induced changes in vmPFC Homer expression as a molecular trigger contributing to drug elicited <b>relapse</b>.
+HOMER2	addiction	intoxication	23966068	The efficacy of mGluR1, mGluR5 and PLC inhibitors to reduce <b>binge</b> intake depended upon intact <strong>Homer2</strong> expression as revealed through neuropharmacological studies of <strong>Homer2</strong> null mutant mice.
+HOMER2	drug	amphetamine	23895375	<b>Methamphetamine</b> induced 3 20 fold increases of immediate early genes arc, <strong>homer 2</strong>, c fos, fosB, and its isoforms (ΔfosB and a novel isoform ΔfosB 2) in Fos positive but not Fos negative neurons.
+HOMER2	drug	opioid	23761764	Null mutations of Homer1a, Homer1, and <strong>Homer2</strong>, as well as transgenic disruption of mGluR5 Homer interactions, either attenuated or completely blocked low dose <b>heroin</b> CPP, and none of the CCI mutant strains exhibited <b>heroin</b> induced CPA.
+HOMER2	addiction	reward	23761764	Null mutations of Homer1a, Homer1, and <strong>Homer2</strong>, as well as transgenic disruption of mGluR5 Homer interactions, either attenuated or completely blocked low dose heroin <b>CPP</b>, and none of the CCI mutant strains exhibited heroin induced CPA.
+HOMER2	drug	cocaine	23658151	Imbalances in prefrontal cortex CC Homer1 versus CC <strong>Homer2</strong> expression promote <b>cocaine</b> preference.
+HOMER2	drug	cocaine	23658151	Protracted withdrawal from <b>cocaine</b> experience increases the relative expression of <strong>Homer2</strong> versus Homer1 isoforms within medial prefrontal cortex (mPFC).
+HOMER2	addiction	withdrawal	23658151	Protracted <b>withdrawal</b> from cocaine experience increases the relative expression of <strong>Homer2</strong> versus Homer1 isoforms within medial prefrontal cortex (mPFC).
+HOMER2	drug	cocaine	23658151	Together, these data provide novel evidence in support of opposing roles for constitutively expressed Homer1 and <strong>Homer2</strong> isoforms in regulating mPFC glutamate transmission in vivo and support the hypothesis that <b>cocaine</b> elicited increases in the relative amount of mPFC <strong>Homer2</strong> versus Homer1 signaling produces abnormalities in NAC glutamate transmission that enhance vulnerability to <b>cocaine</b> reward.
+HOMER2	addiction	reward	23658151	Together, these data provide novel evidence in support of opposing roles for constitutively expressed Homer1 and <strong>Homer2</strong> isoforms in regulating mPFC glutamate transmission in vivo and support the hypothesis that cocaine elicited increases in the relative amount of mPFC <strong>Homer2</strong> versus Homer1 signaling produces abnormalities in NAC glutamate transmission that enhance vulnerability to cocaine <b>reward</b>.
+HOMER2	drug	alcohol	22432643	<b>Alcohol</b> increases the expression of Group 1 metabotropic glutamate receptors (mGluRs) and their associated scaffolding protein <strong>Homer2</strong> and stimulates phosphatidylinositol 3 kinase (PI3K) within the nucleus accumbens (NAC).
+HOMER2	drug	alcohol	22432643	Moreover, functional studies suggest that NAC Group 1 mGluR/<strong>Homer2</strong>/PI3K signaling may be a potential target for pharmacotherapeutic intervention in <b>alcoholism</b>.
+HOMER2	drug	alcohol	22432643	Follow up behavioral studies examined the importance of Group 1 mGluR/<strong>Homer2</strong>/PI3K signaling within the NAC shell for limited access <b>alcohol</b> drinking.
+HOMER2	drug	alcohol	22432643	Limited access <b>alcohol</b> drinking under DID procedures up regulated NAC shell <strong>Homer2</strong> levels, concomitant with increases in mGluR5 and NR2B.
+HOMER2	drug	alcohol	22432643	Intra NAC shell blockade of mGluR5, <strong>Homer2</strong>, or PI3K signaling, as well as transgenic disruption of the Homer binding site on mGluR5, decreased <b>alcohol</b> consumption in B6 mice.
+HOMER2	drug	alcohol	22432643	Taken together, these data further implicate Group 1 mGluR signaling through <strong>Homer2</strong> within the NAC in excessive <b>alcohol</b> consumption.
+HOMER2	drug	alcohol	20807241	Accumbens <strong>Homer2</strong> mediated signaling: a factor contributing to mouse strain differences in <b>alcohol</b> drinking?
+HOMER2	drug	alcohol	20807241	We next employed virus mediated gene transfer approaches to ascertain the functional relevance of the observed strain difference in accumbens <strong>Homer2</strong> expression for B6/D2 differences in <b>alcohol</b> induced glutamate sensitization, as well as <b>alcohol</b> preference/intake.
+HOMER2	addiction	sensitization	20807241	We next employed virus mediated gene transfer approaches to ascertain the functional relevance of the observed strain difference in accumbens <strong>Homer2</strong> expression for B6/D2 differences in alcohol induced glutamate <b>sensitization</b>, as well as alcohol preference/intake.
+HOMER2	drug	alcohol	20807241	These data support the over arching hypothesis that augmented accumbens <strong>Homer2</strong> mediated glutamate signaling may be an endophenotype related to genetic variance in <b>alcohol</b> consumption.
+HOMER2	drug	alcohol	20807241	If relevant to humans, such data pose polymorphisms affecting glutamate receptor/<strong>Homer2</strong> signaling in the etiology of <b>alcoholism</b>.
+HOMER2	drug	alcohol	20333726	Five genetic variants of HOMER 1 and 3 of <strong>HOMER 2</strong> were genotyped in a multi site sample of 1,923 German healthy controls and 2,039 <b>alcohol</b> dependent subjects.
+HOMER2	drug	alcohol	20333726	While most of the HOMER 1 and 2 SNPs are in low to moderate linkage disequilibrium, three major haplotypes of HOMER 1 and 4 haplotypes of <strong>HOMER 2</strong> are present in the majority of <b>alcohol</b> dependent and control subjects.
+HOMER2	drug	alcohol	19673743	Overall, these subregion specific, <b>ethanol</b> induced increases in mGluR/<strong>Homer2</strong>/NR2 expression within the NAC and amygdala suggest changes in glutamatergic plasticity had taken place.
+HOMER2	drug	alcohol	19587272	Binge drinking upregulates accumbens mGluR5 <strong>Homer2</strong> PI3K signaling: functional implications for <b>alcoholism</b>.
+HOMER2	addiction	intoxication	19587272	<b>Binge</b> drinking upregulates accumbens mGluR5 <strong>Homer2</strong> PI3K signaling: functional implications for alcoholism.
+HOMER2	drug	alcohol	19587272	The glutamate receptor associated protein <strong>Homer2</strong> regulates <b>alcohol</b> induced neuroplasticity within the nucleus accumbens (NAC), but the precise intracellular signaling cascades involved are not known.
+HOMER2	drug	alcohol	19587272	This study examined the role for NAC metabotropic glutamate receptor (mGluR) <strong>Homer2</strong> phosphatidylinositol 3 kinase (PI3K) signaling in regulating excessive <b>alcohol</b> consumption within the context of the scheduled high <b>alcohol</b> consumption (SHAC) model of binge <b>alcohol</b> drinking.
+HOMER2	addiction	intoxication	19587272	This study examined the role for NAC metabotropic glutamate receptor (mGluR) <strong>Homer2</strong> phosphatidylinositol 3 kinase (PI3K) signaling in regulating excessive alcohol consumption within the context of the scheduled high alcohol consumption (SHAC) model of <b>binge</b> alcohol drinking.
+HOMER2	drug	alcohol	19587272	Virus mediated knockdown of NAC Homer2b expression attenuated <b>alcohol</b> intake, as did an intra NAC infusion of the mGluR5 antagonist MPEP [2 methyl 6 (phenylethynyl)pyridine hydrochloride] (0.1 1 microg/side) and the PI3K antagonist wortmannin (50 ng/side), supporting necessary roles for mGluR5/<strong>Homer2</strong>/PI3K in binge <b>alcohol</b> drinking.
+HOMER2	addiction	intoxication	19587272	Virus mediated knockdown of NAC Homer2b expression attenuated alcohol intake, as did an intra NAC infusion of the mGluR5 antagonist MPEP [2 methyl 6 (phenylethynyl)pyridine hydrochloride] (0.1 1 microg/side) and the PI3K antagonist wortmannin (50 ng/side), supporting necessary roles for mGluR5/<strong>Homer2</strong>/PI3K in <b>binge</b> alcohol drinking.
+HOMER2	drug	alcohol	19587272	Finally, mice genetically selected for a high versus low SHAC phenotype differed in NAC mGluR, <strong>Homer2</strong>, and PI3K activity, consistent with the hypothesis that augmented NAC mGluR5 <strong>Homer2</strong> PI3K signaling predisposes a high binge <b>alcohol</b> drinking phenotype.
+HOMER2	addiction	intoxication	19587272	Finally, mice genetically selected for a high versus low SHAC phenotype differed in NAC mGluR, <strong>Homer2</strong>, and PI3K activity, consistent with the hypothesis that augmented NAC mGluR5 <strong>Homer2</strong> PI3K signaling predisposes a high <b>binge</b> alcohol drinking phenotype.
+HOMER2	drug	alcohol	19587272	Together, these data point to an important role for NAC mGluR5 <strong>Homer2</strong> PI3K signaling in regulating binge like <b>alcohol</b> consumption that has relevance for our understanding of the neurobiology of <b>alcoholism</b> and its pharmacotherapy.
+HOMER2	addiction	intoxication	19587272	Together, these data point to an important role for NAC mGluR5 <strong>Homer2</strong> PI3K signaling in regulating <b>binge</b> like alcohol consumption that has relevance for our understanding of the neurobiology of alcoholism and its pharmacotherapy.
+HOMER2	drug	alcohol	17568396	Accumbens <strong>Homer2</strong> overexpression facilitates <b>alcohol</b> induced neuroplasticity in C57BL/6J mice.
+HOMER2	drug	alcohol	17568396	Chronic <b>alcohol</b> consumption under continuous access (3 months; daily intake approximately 11.2+/ 1.5 g/kg/day) produced a robust increase in NAC <strong>Homer2</strong> protein levels that was apparent at 2 days, 2 weeks, and 2 months following withdrawal from <b>alcohol</b> drinking.
+HOMER2	addiction	withdrawal	17568396	Chronic alcohol consumption under continuous access (3 months; daily intake approximately 11.2+/ 1.5 g/kg/day) produced a robust increase in NAC <strong>Homer2</strong> protein levels that was apparent at 2 days, 2 weeks, and 2 months following <b>withdrawal</b> from alcohol drinking.
+HOMER2	drug	alcohol	17568396	Mimicking the <b>alcohol</b> induced increase in <strong>Homer2</strong> levels by viral transfection of NAC neurons in <b>alcohol</b> preferring C57BL/6J inbred mice enhanced behavioral output for <b>alcohol</b> reinforcement and increased <b>alcohol</b> intake under both preprandial and postprandial conditions.
+HOMER2	addiction	reward	17568396	Mimicking the alcohol induced increase in <strong>Homer2</strong> levels by viral transfection of NAC neurons in alcohol preferring C57BL/6J inbred mice enhanced behavioral output for alcohol <b>reinforcement</b> and increased alcohol intake under both preprandial and postprandial conditions.
+HOMER2	drug	alcohol	17568396	Moreover, NAC <strong>Homer2</strong> overexpression facilitated the expression of an <b>alcohol</b> conditioned place preference, as well as the development of motor tolerance.
+HOMER2	drug	alcohol	17568396	Finally, NAC <strong>Homer2</strong> overexpression facilitated NAC glutamate and dopamine release following an acute <b>alcohol</b> injection and augmented <b>alcohol</b> induced dopamine and glutamate sensitization, but did not affect NAC gamma aminobutyric acid levels.
+HOMER2	addiction	sensitization	17568396	Finally, NAC <strong>Homer2</strong> overexpression facilitated NAC glutamate and dopamine release following an acute alcohol injection and augmented alcohol induced dopamine and glutamate <b>sensitization</b>, but did not affect NAC gamma aminobutyric acid levels.
+HOMER2	drug	alcohol	17568396	Thus, an upregulation in NAC mGluR <strong>Homer2</strong> N methyl D aspartic acid receptor signaling appears to be an important molecular adaptation to <b>alcohol</b> that promotes neuroplasticity facilitating motivational drive for <b>alcohol</b> and the development of <b>alcoholism</b> related behaviors.
+HOMER2	drug	alcohol	16441286	The presentations were (1) Chronic <b>Ethanol</b> Exposure, N Methyl D Aspartate (NMDA) Receptor Dynamics, and Withdrawal Hyperexcitability, by Adam Hendricson, Regina Maldve, and Richard Morrisett; (2) <b>Ethanol</b> Induced Synaptic Targeting of NMDA Receptors Is Associated With Enhanced Postsynaptic Density 95 Clustering and Spine Size, by Judson Chandler and Ezekiel Carpenter Hyland; (3) Presynaptic and Postsynaptic Alterations in the Nucleus Accumbens Following Chronic <b>Alcohol</b> Exposure, by Feng Zhou, Youssef Sari, and Richard Bell; and (4) An Active Role for Accumbens <strong>Homer2</strong> Expression in <b>Alcohol</b> Induced Neural Plasticity, by Karen Szumlinski.
+HOMER2	addiction	withdrawal	16441286	The presentations were (1) Chronic Ethanol Exposure, N Methyl D Aspartate (NMDA) Receptor Dynamics, and <b>Withdrawal</b> Hyperexcitability, by Adam Hendricson, Regina Maldve, and Richard Morrisett; (2) Ethanol Induced Synaptic Targeting of NMDA Receptors Is Associated With Enhanced Postsynaptic Density 95 Clustering and Spine Size, by Judson Chandler and Ezekiel Carpenter Hyland; (3) Presynaptic and Postsynaptic Alterations in the Nucleus Accumbens Following Chronic Alcohol Exposure, by Feng Zhou, Youssef Sari, and Richard Bell; and (4) An Active Role for Accumbens <strong>Homer2</strong> Expression in Alcohol Induced Neural Plasticity, by Karen Szumlinski.
+HOMER2	drug	cocaine	16314758	The purpose of this study is to determine whether single nucleotide polymorphisms in the Homer1 and <strong>Homer2</strong> genes associate with the <b>cocaine</b> dependent phenotype in an African American population.
+HOMER2	drug	cocaine	16314758	This study utilized a case control design in which the genotype and allele frequencies for four single nucleotide polymorphisms in the Homer1 gene and three single nucleotide polymorphisms in the <strong>Homer2</strong> gene were compared between African American individuals with a diagnosis of <b>cocaine</b> dependence (n=170) and African American individuals with no history of substance abuse (n=90).
+HOMER2	addiction	dependence	16314758	This study utilized a case control design in which the genotype and allele frequencies for four single nucleotide polymorphisms in the Homer1 gene and three single nucleotide polymorphisms in the <strong>Homer2</strong> gene were compared between African American individuals with a diagnosis of cocaine <b>dependence</b> (n=170) and African American individuals with no history of substance abuse (n=90).
+HOMER2	drug	cocaine	16314758	None of the single nucleotide polymorphisms analyzed in the <strong>Homer2</strong> gene associates with <b>cocaine</b> dependence.
+HOMER2	addiction	dependence	16314758	None of the single nucleotide polymorphisms analyzed in the <strong>Homer2</strong> gene associates with cocaine <b>dependence</b>.
+HOMER2	drug	cocaine	16314758	The results of this study suggest that a polymorphism in the Homer1 gene, rs6871510, is a potential risk factor for the development of <b>cocaine</b> dependence in an African American population, whereas polymorphisms in the <strong>Homer2</strong> gene are not.
+HOMER2	addiction	dependence	16314758	The results of this study suggest that a polymorphism in the Homer1 gene, rs6871510, is a potential risk factor for the development of cocaine <b>dependence</b> in an African American population, whereas polymorphisms in the <strong>Homer2</strong> gene are not.
+HOMER2	drug	alcohol	16049182	Constitutive <strong>Homer2</strong> gene deletion [knock out (KO)] and rescue with adeno associated viral (AAV) transfection of Homer2b was used to demonstrate the importance of Homer proteins in neuroplasticity produced by repeated <b>ethanol</b> (EtOH) administration.
+HOMER2	addiction	sensitization	16049182	<strong>Homer2</strong> KO mice avoided drinking high concentrations of EtOH and did not develop place preference or locomotor <b>sensitization</b> after repeated EtOH administration.
+HOMER2	drug	cocaine	15580483	To evaluate the hypothesis that repeated intra VTA microinjections of the ionotropic glutamate agonist, AMPA, or the metabotropic glutamate agonist, t <strong>ACPD</strong>, augment the behavioral hyperactivity induced by a subsequent challenge injection of <b>cocaine</b>.
+HOMER2	drug	cocaine	15580483	Following the <b>cocaine</b> challenge injection, there was an augmentation of <b>cocaine</b> induced behavioral hyperactivity in the groups pretreated with AMPA or t <strong>ACPD</strong> but not in the animals administered t <strong>ACPD</strong> plus KN 93.
+HOMER2	drug	cocaine	15545022	<strong>Homer2</strong> gene deletion in mice produces a phenotype similar to chronic <b>cocaine</b> treated rats.
+HOMER2	drug	cocaine	15545022	In this report we summarize the behavioral and neurochemical effects of <strong>Homer2</strong> gene deletion in mice and compare this with the effects of chronic <b>cocaine</b> treatment in rats.
+HOMER2	drug	cocaine	15545022	It was shown that <strong>Homer2</strong> KO mice demonstrate enhanced locomotor stimulant and conditioned place preference responses to <b>cocaine</b>.
+HOMER2	drug	cocaine	15545022	<strong>Homer2</strong> deletion also caused mice to show reduced basal extracellular glutamate in the nucleus accumbens and a sensitized increase in extracellular glutamate in response to a <b>cocaine</b> injection.
+HOMER2	drug	cocaine	15545022	In contrast to glutamate, <strong>Homer2</strong> KO mice showed a normal increase in extracellular dopamine following a <b>cocaine</b> challenge injection.
+HOMER2	drug	cocaine	15545022	The parallel between the effect of <strong>Homer2</strong> gene deletion and chronic <b>cocaine</b> administration on behavioral and glutamatergic neurochemical responses to <b>cocaine</b> supports involvement of Homer proteins and glutamate transmission in the sensitization of behavior produced by repeated <b>cocaine</b>.
+HOMER2	addiction	sensitization	15545022	The parallel between the effect of <strong>Homer2</strong> gene deletion and chronic cocaine administration on behavioral and glutamatergic neurochemical responses to cocaine supports involvement of Homer proteins and glutamate transmission in the <b>sensitization</b> of behavior produced by repeated cocaine.
+HOMER2	drug	cocaine	15294147	Here, we report that deletion of Homer1 or <strong>Homer2</strong> in mice caused the same increase in sensitivity to <b>cocaine</b> induced locomotion, conditioned reward, and augmented extracellular glutamate in nucleus accumbens as that elicited by withdrawal from repeated <b>cocaine</b> administration.
+HOMER2	addiction	reward	15294147	Here, we report that deletion of Homer1 or <strong>Homer2</strong> in mice caused the same increase in sensitivity to cocaine induced locomotion, conditioned <b>reward</b>, and augmented extracellular glutamate in nucleus accumbens as that elicited by withdrawal from repeated cocaine administration.
+HOMER2	addiction	withdrawal	15294147	Here, we report that deletion of Homer1 or <strong>Homer2</strong> in mice caused the same increase in sensitivity to cocaine induced locomotion, conditioned reward, and augmented extracellular glutamate in nucleus accumbens as that elicited by <b>withdrawal</b> from repeated cocaine administration.
+HOMER2	drug	cocaine	15294147	Moreover, adeno associated virus mediated restoration of <strong>Homer2</strong> in the accumbens of <strong>Homer2</strong> KO mice reversed the <b>cocaine</b> sensitized phenotype.
+HOMER2	drug	cocaine	15294147	Further analysis of <strong>Homer2</strong> KO mice revealed extensive additional behavioral and neurochemical similarities to <b>cocaine</b> sensitized animals, including accelerated acquisition of <b>cocaine</b> self administration and altered regulation of glutamate by metabotropic glutamate receptors and cystine/glutamate exchange.
+HOMER2	drug	cocaine	14684444	(4) Homer1 protein is reduced in the nucleus accumbens, and <strong>Homer2</strong> knockout mice show enhanced responsiveness to <b>cocaine</b>.
+HOMER2	drug	alcohol	12500101	<b>Acamprosate</b> inhibits the binding and neurotoxic effects of trans <strong>ACPD</strong>, suggesting a novel site of action at metabotropic glutamate receptors.
+HOMER2	drug	alcohol	12500101	The following experiments were performed to determine whether <b>acamprosate</b> could compete with trnas <strong>ACPD</strong> (+/  1 aminocyclopentane trans 1,3 dicarboxylic acid, an equimolecular mixture of 1S, 3R and 1R, 3S <strong>ACPD</strong> and an agonist at both group I and group II mGluRs) sensitive binding sites and protect against trans <strong>ACPD</strong> induced neurotoxicity in organotypic hippocampal slice cultures.
+HOMER2	drug	alcohol	12500101	A P2 membrane preparation of cortices, cerebellums, and hippocampi of adult, male Sprague Dawley rats was used to determine the abilities of N methyl D aspartic acid (NMDA) and trans <strong>ACPD</strong> to displace [3H]glutamate in both the absence and the presence of the sodium salt of <b>acamprosate</b> (sodium mono N acetyl homotaurine or Na <b>acamprosate</b>).
+HOMER2	drug	alcohol	12500101	A comparison of the effects of 100 microM guanosine 5' triphosphate on unlabeled glutamate, trans <strong>ACPD</strong>, and Na <b>acamprosate</b> was performed in the same paradigm.
+HOMER2	drug	alcohol	12500101	Na <b>acamprosate</b> displayed total competition with trans <strong>ACPD</strong>.
+HOMER2	drug	alcohol	12500101	The presence of 100 microM guanosine 5' triphosphate differentially altered the displacing capabilities of the two mGluR agonists, unlabeled glutamate and trans <strong>ACPD</strong>, as compared with Na <b>acamprosate</b>.
+HOMER2	drug	alcohol	12500101	Na <b>acamprosate</b> (200 1000 microM) and SIB 1893 (20 500 microM) both were neuroprotective against trans <strong>ACPD</strong> induced neurotoxicity that likely results from mGluR potentiation of NMDARs.
+HOMER2	drug	alcohol	11923593	Chronic <b>ethanol</b> treatment and withdrawal alter <strong>ACPD</strong> evoked calcium signals in developing Purkinje neurons.
+HOMER2	addiction	withdrawal	11923593	Chronic ethanol treatment and <b>withdrawal</b> alter <strong>ACPD</strong> evoked calcium signals in developing Purkinje neurons.
+HOMER2	drug	alcohol	11923593	After the <b>ethanol</b> treatment, the response of Purkinje neurons to the selective metabotropic glutamate receptor (mGluR) agonist (1S,3R) 1 aminocyclopentane 1,3 dicarboxylic acid (<strong>ACPD</strong>; 300 microM) was examined in parallel fura 2 Ca2+ imaging and current clamp experiments.
+HOMER2	drug	alcohol	11923593	In Ca2+ imaging studies, the mean peak amplitude of <strong>ACPD</strong> evoked Ca2+ signals was depressed in the dendritic region of chronic <b>ethanol</b> treated Purkinje neurons compared with control neurons (p < 0.05, unpaired t test), whereas there was no apparent difference in the somatic region.
+HOMER2	drug	alcohol	11923593	Parallel current clamp studies showed no consistent effect of chronic <b>ethanol</b> treatment or <b>ethanol</b> withdrawal on the membrane response to <strong>ACPD</strong>.
+HOMER2	addiction	withdrawal	11923593	Parallel current clamp studies showed no consistent effect of chronic ethanol treatment or ethanol <b>withdrawal</b> on the membrane response to <strong>ACPD</strong>.
+HOMER2	drug	amphetamine	9680243	While (1S,3R) <strong>ACPD</strong> increased locomotor activity when injected into the NAcc, no significant difference between saline and <b>AMPH</b> pre exposed rats was observed.
+HOMER2	addiction	withdrawal	9179394	administration of the non selective mGluR agonist 1 aminocyclopentane 1,3 dicarboxylic acid ((1S,3R) <strong>ACPD</strong>), as well as the group II selective agonist (2S,1'R,2'R,3'R) 2 (2'.3' dicarboxycyclopropyl)glycine (DCG IV), significantly attenuated the severity of precipitated <b>withdrawal</b> symptoms.
+HOMER2	drug	amphetamine	9152375	Extracellular single cell recording and microiontophoresis were used to investigate possible alterations in the ability of glutamate agonists [(S) alpha amino 3  hydroxy 5 methyl 4 isoxazole propionate (AMPA), N methyl D aspartate (NMDA), and (1S,3R) 1 aminocyclopentane 1,3 dicarboxylic acid (1S,3R t <strong>ACPD</strong>)] to stimulate the firing of VTA DA neurons after 3 days of withdrawal from repeated administration of saline, cocaine or <b>amphetamine</b>.
+HOMER2	drug	cocaine	9152375	Extracellular single cell recording and microiontophoresis were used to investigate possible alterations in the ability of glutamate agonists [(S) alpha amino 3  hydroxy 5 methyl 4 isoxazole propionate (AMPA), N methyl D aspartate (NMDA), and (1S,3R) 1 aminocyclopentane 1,3 dicarboxylic acid (1S,3R t <strong>ACPD</strong>)] to stimulate the firing of VTA DA neurons after 3 days of withdrawal from repeated administration of saline, <b>cocaine</b> or amphetamine.
+HOMER2	addiction	withdrawal	9152375	Extracellular single cell recording and microiontophoresis were used to investigate possible alterations in the ability of glutamate agonists [(S) alpha amino 3  hydroxy 5 methyl 4 isoxazole propionate (AMPA), N methyl D aspartate (NMDA), and (1S,3R) 1 aminocyclopentane 1,3 dicarboxylic acid (1S,3R t <strong>ACPD</strong>)] to stimulate the firing of VTA DA neurons after 3 days of <b>withdrawal</b> from repeated administration of saline, cocaine or amphetamine.
+HOMER2	drug	amphetamine	9152375	Current response curves showed that responses to iontophoretic AMPA, but not NMDA or 1S,3R t <strong>ACPD</strong> were significantly enhanced in cocaine  or <b>amphetamine</b> pretreated rats in that neurons entered into a state of apparent depolarization block at significantly lower iontophoretic currents.
+HOMER2	drug	cocaine	9152375	Current response curves showed that responses to iontophoretic AMPA, but not NMDA or 1S,3R t <strong>ACPD</strong> were significantly enhanced in <b>cocaine</b>  or amphetamine pretreated rats in that neurons entered into a state of apparent depolarization block at significantly lower iontophoretic currents.
+HOMER2	addiction	withdrawal	9127819	After a 6 day <b>withdrawal</b>, DA release from striatal slices evoked by +/  ( )1 aminocyclopentane trans 1,3 dicarboxylic acid (trans <strong>ACPD</strong>) was measured, trans <strong>ACPD</strong> induced DA release was significantly enhanced in MAP sensitized rats, but the inactive form of trans <strong>ACPD</strong> (1R,3S <strong>ACPD</strong>) did not enhance DA release.
+HOMER2	drug	benzodiazepine	7616393	Dose response curves for stimulation of phosphoinositide (PI) hydrolysis by the selective metabotropic glutamate receptor (mGluR) agonist, (1S,3R) 1 aminocyclopentane dicarboxylic acid [(1S,3R) <strong>ACPD</strong>] were performed with cortical slices from mice treated with <b>lorazepam</b> or vehicle for 7 days and subject to 0, 1, 2, 3, 4 and 7 days of withdrawal.
+HOMER2	addiction	withdrawal	7616393	Dose response curves for stimulation of phosphoinositide (PI) hydrolysis by the selective metabotropic glutamate receptor (mGluR) agonist, (1S,3R) 1 aminocyclopentane dicarboxylic acid [(1S,3R) <strong>ACPD</strong>] were performed with cortical slices from mice treated with lorazepam or vehicle for 7 days and subject to 0, 1, 2, 3, 4 and 7 days of <b>withdrawal</b>.
+HOMER2	drug	benzodiazepine	7616393	The efficacy of (1S,3R) <strong>ACPD</strong> to stimulate PI hydrolysis was increased significantly at 2 and 3 days of <b>lorazepam</b> withdrawal when compared with responses in control slices.
+HOMER2	addiction	withdrawal	7616393	The efficacy of (1S,3R) <strong>ACPD</strong> to stimulate PI hydrolysis was increased significantly at 2 and 3 days of lorazepam <b>withdrawal</b> when compared with responses in control slices.
+HOMER2	drug	alcohol	7893331	Exposure in utero to <b>ethanol</b> did not affect PPI hydrolysis stimulated by a selective metabotropic glutamate receptor agonist, trans (+/ ) l amino 1,3 cyclopentanedicarboxylic acid (t <strong>ACPD</strong>).
+HOMER2	drug	alcohol	7893331	Although the PPI hydrolysis stimulated by t <strong>ACPD</strong> could be blocked by (RS) alpha methyl 4 carboxyphenylglycine (MCPG), an antagonist of the metabotropic glutamate receptor, MCPG was incapable of affecting QA induced PPI hydrolysis and the suppressive effects of prenatal <b>ethanol</b> exposure on this hydrolysis.
+HOMER2	drug	alcohol	7893331	Taken together, the data suggest that the long lasting suppressive effects of prenatal <b>ethanol</b> exposure on QA stimulated PPI hydrolysis in cerebellar granule cell cultures is through a metabotropic QA receptor pathway that may be different from the one activated by t <strong>ACPD</strong>.
+GNRH1	drug	amphetamine	28681200	Canonical pathway analysis revealed that a high number of <b>METH</b> addiction related miRNAs play important roles in the MAPK, CREB, G Protein Couple Receptor and <strong>GnRH</strong> Signaling pathways.
+GNRH1	addiction	addiction	28681200	Canonical pathway analysis revealed that a high number of METH <b>addiction</b> related miRNAs play important roles in the MAPK, CREB, G Protein Couple Receptor and <strong>GnRH</strong> Signaling pathways.
+GNRH1	drug	cannabinoid	27354844	Evidence suggests that <b>marijuana</b> can reduce female fertility by disrupting hypothalamic release of gonadotropin releasing hormone (<strong>GnRH</strong>), leading to reduced estrogen and progesterone production and anovulatory menstrual cycles.
+GNRH1	drug	opioid	22183092	Search from databases Pubmed, SciFinder, and Medline with search words <b>opioid</b> antagonists, hormones, LH, testosterone, and <strong>GnRH</strong>, in different combinations.
+GNRH1	drug	opioid	22183092	<b>Opioid</b> antagonists seem to increase the secretion of <strong>GnRH</strong> in the hypothalamus which then causes a pulsatile release of LH in the pituitary and secretion of testosterone.
+GNRH1	drug	alcohol	20034543	Since <b>alcohol</b> (ALC) blocks IGF 1 induced <strong>LHRH</strong> release acutely, we assessed whether this drug could affect IGF 1 stimulated prepubertal KiSS 1 gene expression following a binge type of exposure.
+GNRH1	addiction	intoxication	20034543	Since alcohol (ALC) blocks IGF 1 induced <strong>LHRH</strong> release acutely, we assessed whether this drug could affect IGF 1 stimulated prepubertal KiSS 1 gene expression following a <b>binge</b> type of exposure.
+GNRH1	drug	alcohol	18448097	<b>Ethanol</b> is known to reduce hypothalamic synthesis, release, and mRNA expression of gonadotropin releasing hormone (<strong>GnRH</strong>) that modulates serotonergic, dopaminergic, and glutamatergic systems, which experience adaptive changes on chronic exposure to <b>ethanol</b>.
+GNRH1	drug	alcohol	18448097	Therefore, it was proposed to investigate the effect of <b>ethanol</b> withdrawal on marble burying behavior in mice, particularly because it simulates some aspects of obsessive compulsive behavior; further, the influence of <strong>GnRH</strong> agonist was studied on the same.
+GNRH1	addiction	addiction	18448097	Therefore, it was proposed to investigate the effect of ethanol withdrawal on marble burying behavior in mice, particularly because it simulates some aspects of obsessive <b>compulsive</b> behavior; further, the influence of <strong>GnRH</strong> agonist was studied on the same.
+GNRH1	addiction	withdrawal	18448097	Therefore, it was proposed to investigate the effect of ethanol <b>withdrawal</b> on marble burying behavior in mice, particularly because it simulates some aspects of obsessive compulsive behavior; further, the influence of <strong>GnRH</strong> agonist was studied on the same.
+GNRH1	drug	psychedelics	18309234	Here, we hypothesized that the recreational drug (+/ ) 3,4 <b>methylenedioxymethamphetamine</b> (<b>MDMA</b>; '<b>ecstasy</b>'), which acts through several of the neurotransmitter systems that affect <strong>GnRH</strong> neurons, suppresses the hypothalamic pituitary gonadal reproductive axis of male rats.
+GNRH1	drug	psychedelics	18309234	The results indicate that the hypothalamic and gonadal levels of the hypothalamic pituitary gonadal axis are significantly altered by <b>MDMA</b>, with <strong>GnRH</strong> mRNA and serum testosterone levels suppressed in rats administered <b>MDMA</b> compared to saline.
+GNRH1	drug	psychedelics	18309234	Furthermore, our finding that hypothalamic <strong>GnRH</strong> mRNA levels are suppressed in the context of low testosterone concentrations suggests that the central <strong>GnRH</strong> neurosecretory system may be a primary target of inhibitory regulation by <b>MDMA</b> usage.
+GNRH1	drug	alcohol	18280564	<b>Ethanol</b> inhibits the synthesis, content and release of hypothalamic luteinizing hormone releasing hormone (<strong>LHRH</strong>), and <strong>LHRH</strong> modulates the activity of several neurotransmitters that experience adaptive changes on chronic exposure to <b>ethanol</b>, and also implicate in <b>ethanol</b> dependence.
+GNRH1	addiction	dependence	18280564	Ethanol inhibits the synthesis, content and release of hypothalamic luteinizing hormone releasing hormone (<strong>LHRH</strong>), and <strong>LHRH</strong> modulates the activity of several neurotransmitters that experience adaptive changes on chronic exposure to ethanol, and also implicate in ethanol <b>dependence</b>.
+GNRH1	drug	alcohol	18280564	Hence, it was contemplated that <strong>LHRH</strong> agonist such as leuprolide may influence the behavioral consequences of withdrawing <b>ethanol</b> in dependent state.
+GNRH1	addiction	withdrawal	10818386	Puberty results from <b>withdrawal</b> of the "gonadostat" mechanisms and from increased gonadotropin sensitivity to <strong>GnRH</strong>.
+GNRH1	drug	opioid	10818386	Neuropeptides mainly involved in the control of <strong>GnRH</strong> release are <b>opioids</b>, neuropeptide Y (NPY), galanin, and corticotropin releasing factor (CRF), whereas neurotransmitters are noradrenaline, dopamine, serotonin, melatonin and gamma aminobutyric acid (GABA).
+GNRH1	drug	alcohol	9037095	Inhibition of the PLD pathway by <b>ethanol</b> and propranolol reduced diacylglycerol production and caused a concomitant fall in <strong>GnRH</strong> release.
+GNRH1	addiction	withdrawal	9014843	Concentration of <strong>GnRH</strong> receptor and <strong>GnRH</strong> receptor mRNA in pituitary tissue of orchidectomized sheep: effect of oestradiol, progesterone, and progesterone <b>withdrawal</b>.
+GNRH1	addiction	withdrawal	9014843	The effect of progesterone (P4) and P4 <b>withdrawal</b> on oestradiol (E2) induced change in gonadotrope responsiveness (GR) and concentration of <strong>GnRH</strong> receptor and <strong>GnRH</strong> receptor mRNA in pituitary tissue of orchidectomized sheep (wethers) was determined.
+GNRH1	addiction	withdrawal	9014843	This P4 induced decrease in tissue concentration of <strong>GnRH</strong> receptor and <strong>GnRH</strong> receptor mRNA was not reversed during the 24 h period after P4 <b>withdrawal</b>.
+GNRH1	addiction	withdrawal	9014843	However, the magnitude of oestrogen induced increase in tissue concentrations of <strong>GnRH</strong> receptor mRNA was not significantly affected by P4 or P4 <b>withdrawal</b>.
+GNRH1	addiction	withdrawal	9014843	This P4 induced suppression of <strong>GnRH</strong> receptor activity is not reversed within 24 h of P4 <b>withdrawal</b>.
+GNRH1	drug	opioid	8828858	However, our observation that Nmf accelerated the reinstatement of ovarian cycles after surgery, when circulating E2 and P4 were very low, suggests that <strong>GnRH</strong> secretions are influenced by activation of different <b>opioid</b> receptor subtypes in response to different stresses.
+GNRH1	addiction	relapse	8828858	However, our observation that Nmf accelerated the <b>reinstatement</b> of ovarian cycles after surgery, when circulating E2 and P4 were very low, suggests that <strong>GnRH</strong> secretions are influenced by activation of different opioid receptor subtypes in response to different stresses.
+GNRH1	drug	opioid	8828858	Some of these <strong>GnRH</strong>/<b>opioid</b> interactions are independent of P4.
+GNRH1	addiction	withdrawal	8788193	The effects of estradiol (E2) and E2 <b>withdrawal</b> on tissue concentrations of <strong>GnRH</strong> receptor mRNA were assessed in orchidectomized sheep (wethers).
+GNRH1	addiction	withdrawal	8788193	These data suggest that the dynamic changes in tissue concentrations of <strong>GnRH</strong> receptor mRNA during the periovulatory period may be due to the inductive effects of gonadal steroids from the developing follicle and to the combined suppressive effects of the increased <strong>GnRH</strong> stimulation and E2 <b>withdrawal</b> that are associated with the gonadotropin surge.
+GNRH1	drug	alcohol	7579706	Also, phospholipase D activity, estimated by the production of phosphatidylethanol from phosphatidylcholine in the presence of <b>ethanol</b>, was stimulated by <strong>GnRH</strong> but not ET 1.
+GNRH1	drug	alcohol	7579706	Inhibition of PA phosphohydrolase activity by propranolol also decreased <strong>GnRH</strong> induced DG production and, in contrast to <b>ethanol</b>, increased PA and cytidine diphosphate diacylglycerol levels.
+GNRH1	drug	alcohol	7579706	The fall in DG production caused by <b>ethanol</b> and propranolol was accompanied by inhibition of <strong>GnRH</strong> induced c fos expression, whereas agonist induced luteinizing hormone release was not affected.
+GNRH1	drug	alcohol	7579706	In contrast to their inhibitory actions on <strong>GnRH</strong> induced early gene expression, neither <b>ethanol</b> nor propranolol affected ET 1 induced c fos expression, or <strong>GnRH</strong>  and ET 1 induced inositol trisphosphate/Ca2+ signaling.
+GNRH1	drug	alcohol	7883843	In each subject, LH pulsatility (10 min blood drawing for 8 h) and the pituitary LH response to a 10 micrograms <strong>GnRH</strong> stimulus were investigated at baseline and on the fifth day of placebo/<b>naltrexone</b> administration.
+GNRH1	drug	alcohol	7883843	The same occurred after <b>naltrexone</b> treatment, when significant increases in both mean LH levels (P < 0.02) and LH response to <strong>GnRH</strong> (P < 0.025) were observed.
+GNRH1	drug	alcohol	7883843	The same occurred after <b>naltrexone</b> treatment, when significant decreases in both the amplitude of LH pulses (P < 0.05) and the LH response to <strong>GnRH</strong> (P < 0.05) were observed.
+GNRH1	drug	opioid	7852517	Short term <b>naloxone</b> infusion studies have suggested that enhanced endogenous <b>opioid</b> activity may play a role in inhibiting <strong>GnRH</strong> and gonadotropin secretion in hyperprolactinemic patients.
+GNRH1	drug	opioid	7956937	The aim of the present study was, using an in vitro superfusion approach, to perform a detailed study of the effects of <b>opioid</b> receptor activation and blockade on the dimensions of pulsatile <strong>GnRH</strong> release from the isolated medial basal hypothalamus of the adult male guinea pig.
+GNRH1	drug	opioid	7956937	<b>Morphine</b> suppressed total <strong>GnRH</strong> output from the medial basal hypothalami (P < or = 0.01 at 10( 3) M and 10( 6) M; P = NS at 10( 9) M), with mean pulse frequency, mean amplitude of all pulses, and mean sum of pulse amplitudes being significantly inhibited at all <b>morphine</b> concentrations, whether pulse analysis (Ultra pulse analysis algorithm) was performed at a two coefficient of variation (2CV; P < or = 0.05, P < or = 0.01, and P < or = 0.01, respectively) or a 3CV (P < or = 0.05, P < or = 0.05, and P < or = 0.01, respectively) threshold.
+GNRH1	drug	opioid	7956937	A different set of experiments (n = 14), with exposure to 10( 3) M <b>morphine</b> during the second of three consecutive 3 h observation periods, indicated that after <b>morphine</b> withdrawal a gradual recovery of <strong>GnRH</strong> output and pulse frequency to pretreatment values occurred, whereas pulse amplitude remained significantly suppressed during the posttreatment observation period.
+GNRH1	addiction	withdrawal	7956937	A different set of experiments (n = 14), with exposure to 10( 3) M morphine during the second of three consecutive 3 h observation periods, indicated that after morphine <b>withdrawal</b> a gradual recovery of <strong>GnRH</strong> output and pulse frequency to pretreatment values occurred, whereas pulse amplitude remained significantly suppressed during the posttreatment observation period.
+GNRH1	drug	opioid	7956937	Total <strong>GnRH</strong> output (P < or = 0.05), mean pulse frequency (P < or = 0.05), mean amplitude of all pulses (P < or = 0.05), and mean of the sum of pulse amplitudes (P < or = 0.01) were increased during <b>opioid</b> blockade with 10( 3) M and 10( 9) M <b>naloxone</b> (either 2CV or 3CV threshold for pulse analysis).
+GNRH1	drug	opioid	7956937	A similar trend for 10( 6) M <b>naloxone</b> was only apparent after the exclusion of two outliers with unusually high basal <strong>GnRH</strong> release.
+GNRH1	drug	opioid	7926138	The mode of action of the drug in <strong>GnRH</strong> a treated patients and possible interactions with endogenous <b>opioid</b> peptides need further elucidation.
+GNRH1	drug	alcohol	8119185	However, the ability of <strong>GnRH</strong> to stimulate phosphatidylethanol (PEt) in the presence of <b>ethanol</b> suggested that phospholipase D may also participate in DG formation.
+GNRH1	drug	alcohol	8286567	The magnitude of <strong>GnRH</strong> induced (1600 ng/hourly pulse for 24 h) preovulatory surge like secretion of LH was assessed in orchidectomized sheep (wethers) during infusion of estradiol (E2, 5 micrograms/h in 10% <b>ethanol</b> saline [vehicle]) or at 0, 12, 24, or 48 h after E2 withdrawal (n = 6 wethers/group).
+GNRH1	addiction	withdrawal	8286567	The magnitude of <strong>GnRH</strong> induced (1600 ng/hourly pulse for 24 h) preovulatory surge like secretion of LH was assessed in orchidectomized sheep (wethers) during infusion of estradiol (E2, 5 micrograms/h in 10% ethanol saline [vehicle]) or at 0, 12, 24, or 48 h after E2 <b>withdrawal</b> (n = 6 wethers/group).
+GNRH1	drug	opioid	1359599	Because hypothalamic <b>opioids</b> are believed to modulate <strong>GnRH</strong> secretion, in part under the influence of ovarian steroids, we performed longitudinal studies of gonadotropin and ovarian steroid secretion across ovulatory, symptomatic cycles of 17 PMS patients and 8 normal volunteers.
+GNRH1	drug	alcohol	2508387	The cells of chambers I + II had been pretreated with medium containing vehicle (0.1% <b>ethanol</b>), those of chambers III + IV with medium containing 1 nmol/l estradiol for 48 h. After perfusion was started, each of the chambers was challenged with an initial 2 min <strong>GnRH</strong> (1 nmol/l) pulse.
+GNRH1	drug	alcohol	2573815	On the basis of their properties of noradrenergic and/or thromboxane inhibition, or on their activation of the dopaminergic reward system and/or beta endorphin, the following substances or treatments are predicted to be effective in treating <b>alcohol</b> or drug addiction: ginger; carbon dioxide; dietary sulfur; methionine; calcium; <strong>LHRH</strong>; high intensity light; interferon; negative ions; serotonin antagonists such as methysergide and cyproheptadine; guanabenz and guenfacine; antihistamines; head out water immersion; X irradiation; and forced unilateral left nostril breathing.
+GNRH1	addiction	addiction	2573815	On the basis of their properties of noradrenergic and/or thromboxane inhibition, or on their activation of the dopaminergic reward system and/or beta endorphin, the following substances or treatments are predicted to be effective in treating alcohol or drug <b>addiction</b>: ginger; carbon dioxide; dietary sulfur; methionine; calcium; <strong>LHRH</strong>; high intensity light; interferon; negative ions; serotonin antagonists such as methysergide and cyproheptadine; guanabenz and guenfacine; antihistamines; head out water immersion; X irradiation; and forced unilateral left nostril breathing.
+GNRH1	addiction	reward	2573815	On the basis of their properties of noradrenergic and/or thromboxane inhibition, or on their activation of the dopaminergic <b>reward</b> system and/or beta endorphin, the following substances or treatments are predicted to be effective in treating alcohol or drug addiction: ginger; carbon dioxide; dietary sulfur; methionine; calcium; <strong>LHRH</strong>; high intensity light; interferon; negative ions; serotonin antagonists such as methysergide and cyproheptadine; guanabenz and guenfacine; antihistamines; head out water immersion; X irradiation; and forced unilateral left nostril breathing.
+GNRH1	drug	opioid	2643703	In contrast to these results, adult rats showed only transient effects (less than 1 week) of <b>morphine</b> on certain reproductive endocrine parameters (e.g., serum LH, testosterone and the weights of the seminal vesicles) and no effects on others (e.g., testes weights and hypothalamic <strong>LHRH</strong>).
+GNRH1	drug	alcohol	3122772	In men, provocative tests of gonadotropin response to <strong>LHRH</strong> stimulation were normal during periods of intoxication and hangover, indicating that <b>ethanol</b> has no significant direct effect on LH secretion at the pituitary level.
+GNRH1	addiction	intoxication	3122772	In men, provocative tests of gonadotropin response to <strong>LHRH</strong> stimulation were normal during periods of <b>intoxication</b> and hangover, indicating that ethanol has no significant direct effect on LH secretion at the pituitary level.
+GNRH1	drug	opioid	3100869	Withdrawal of the gonadal steroids has been reported to cause a rapid loss of the tonic inhibitory control of the opiate system on <strong>LHRH</strong> secretion as revealed by a lack of response to <b>naloxone</b>.
+GNRH1	addiction	withdrawal	3100869	<b>Withdrawal</b> of the gonadal steroids has been reported to cause a rapid loss of the tonic inhibitory control of the opiate system on <strong>LHRH</strong> secretion as revealed by a lack of response to naloxone.
+GNRH1	drug	opioid	6769068	Since the response of the pituitary to nonspecific stimuli is considered an expression of hypothalamic dysfunction, indicating a disconnection between the central nervous system and the anterior pituitary, we thought it worthwhile to study the GH response to stimulation with thyrotropin releasing hormone (TRH) or gonadotropin releasing hormone (<strong>GnRH</strong>) in <b>heroin</b> addicts.
+GNRH1	drug	opioid	569031	Normal basal and <strong>LHRH</strong> stimulated LH and FSH levels suggest that chronic <b>heroin</b> abuse depressed testicular function via the hypothalamus or higher centres.
+GNRH1	drug	opioid	356791	Time course of effects of <b>morphine</b> on hypothalamic content of <strong>LHRH</strong> and serum testosterone and LH levels of <b>morphine</b> tolerant and nontolerant male rats.
+GNRH1	drug	opioid	356791	Time course of the effects of <b>morphine</b> on the hypothalamic content of <strong>LHRH</strong> in both nontolerant and <b>morphine</b> tolerant male rats was investigated in relation to the temporal changes of serum testosterone and LH levels.
+GNRH1	drug	opioid	356791	The hypothalamic <strong>LHRH</strong> content of the nontolerant rats was increased 8 hr after the administration of <b>morphine</b> (100 mg/kg) when serum testosterone levels were depressed.
+GNRH1	drug	opioid	356791	The <strong>LHRH</strong> content of the tolerant rats was decreased during withdrawal of <b>morphine</b> for 48 hr when the lowered serum testosterone and LH levels had returned to within the control levels.
+GNRH1	addiction	withdrawal	356791	The <strong>LHRH</strong> content of the tolerant rats was decreased during <b>withdrawal</b> of morphine for 48 hr when the lowered serum testosterone and LH levels had returned to within the control levels.
+GNRH1	drug	opioid	356791	Although the hypothalamic <strong>LHRH</strong> content does not necessarily reflect the release of <strong>LHRH</strong>, these results are in favour of the hypothesis that the release of hypothalamic <strong>LHRH</strong> is inhibited by the administration of <b>morphine</b> and is restored by the withdrawal of the narcotic.
+GNRH1	addiction	withdrawal	356791	Although the hypothalamic <strong>LHRH</strong> content does not necessarily reflect the release of <strong>LHRH</strong>, these results are in favour of the hypothesis that the release of hypothalamic <strong>LHRH</strong> is inhibited by the administration of morphine and is restored by the <b>withdrawal</b> of the narcotic.
+KCNK15	drug	cocaine	23761390	On day 1 (acute phase), escitalopram produced a significantly greater decrease from baseline than placebo in attentional bias measured by <b>cocaine</b> Stroop <strong>task 5</strong> hours post dose.
+PTH	drug	alcohol	30708098	The expression of HSP27, pHSP27, Trx 1, total TH and <strong>pTH</strong> in the right ventricle was increased after binge <b>ethanol</b> or MDMA alone.
+PTH	drug	psychedelics	30708098	The expression of HSP27, pHSP27, Trx 1, total TH and <strong>pTH</strong> in the right ventricle was increased after binge ethanol or <b>MDMA</b> alone.
+PTH	addiction	intoxication	30708098	The expression of HSP27, pHSP27, Trx 1, total TH and <strong>pTH</strong> in the right ventricle was increased after <b>binge</b> ethanol or MDMA alone.
+PTH	drug	alcohol	27890540	47 inpatient <b>alcohol</b> dependent patients undergoing detoxification treatment underwent laboratory testing, including calcium, sodium, liver enzymes as well as serum concentrations of calcitonin, <strong>parathyroid hormone</strong> and vitamin D. The psychometric dimension of craving was analyzed with the Obsessive Compulsive Drinking Scale (OCDS).
+PTH	addiction	addiction	27890540	47 inpatient alcohol dependent patients undergoing detoxification treatment underwent laboratory testing, including calcium, sodium, liver enzymes as well as serum concentrations of calcitonin, <strong>parathyroid hormone</strong> and vitamin D. The psychometric dimension of craving was analyzed with the Obsessive <b>Compulsive</b> Drinking Scale (OCDS).
+PTH	addiction	relapse	27890540	47 inpatient alcohol dependent patients undergoing detoxification treatment underwent laboratory testing, including calcium, sodium, liver enzymes as well as serum concentrations of calcitonin, <strong>parathyroid hormone</strong> and vitamin D. The psychometric dimension of <b>craving</b> was analyzed with the Obsessive Compulsive Drinking Scale (OCDS).
+PTH	drug	amphetamine	26946780	Moreover, phosphorylated tyrosine hydroxylase serine40 (<strong>pTH</strong> Ser40) levels in the ventral tegmental area (VTA) were increased by <b>methamphetamine</b>.
+PTH	drug	amphetamine	26946780	The increment of <strong>pTH</strong> Ser40 levels in the VTA by <b>methamphetamine</b> was attenuated by RS504393, a selective CC chemokine receptor 2 (CCR2) antagonist, indicating that the increased CCL2 activates the brain reward system via CCR2 activation.
+PTH	addiction	reward	26946780	The increment of <strong>pTH</strong> Ser40 levels in the VTA by methamphetamine was attenuated by RS504393, a selective CC chemokine receptor 2 (CCR2) antagonist, indicating that the increased CCL2 activates the brain <b>reward</b> system via CCR2 activation.
+PTH	drug	opioid	26461969	Furthermore, in <b>opioid</b> dependent subjects the values of <strong>PTH</strong> were lower, while those of PINP were higher, in comparison to healthy individuals.
+PTH	drug	amphetamine	24748435	Moreover, <b>methamphetamine</b> increased phosphorylated tyrosine hydroxylase (<strong>pTH</strong>) levels in the ventral tegmental area (VTA).
+PTH	drug	amphetamine	24748435	Increased levels of <strong>pTH</strong> in the VTA by <b>methamphetamine</b> was also suppressed by RS504393.
+PTH	drug	cocaine	24672596	We also reviewed the clinical use of <strong>PTH</strong> in relation to <b>cocaine</b>.
+PTH	drug	opioid	22396106	In the present study, we measured dynamic changes in TH and phosphorylated TH serine 40 (<strong>pTH</strong> Ser(40)) and <strong>pTH</strong> Ser(31) proteins in the VTA, and DA concentrations in the NAc at 5 min intervals during a 30 min <b>morphine</b> induced CPP test.
+PTH	addiction	reward	22396106	In the present study, we measured dynamic changes in TH and phosphorylated TH serine 40 (<strong>pTH</strong> Ser(40)) and <strong>pTH</strong> Ser(31) proteins in the VTA, and DA concentrations in the NAc at 5 min intervals during a 30 min morphine induced <b>CPP</b> test.
+PTH	addiction	reward	22396106	TH and <strong>pTH</strong> Ser(40) levels, but not <strong>pTH</strong> Ser(31) levels, in the VTA were enhanced during the <b>CPP</b> test.
+PTH	drug	alcohol	19330277	The expression of key bone formation related marker genes such as osteocalcin and alkaline phosphatase were significantly reduced (P < 0.05) after acute binge <b>alcohol</b> exposure, and expression of regulators of osteoblast activity such as bone morphogenetic proteins and <strong>parathyroid hormone</strong> receptor displayed significantly (P < 0.05) decreased differential expression.
+PTH	addiction	intoxication	19330277	The expression of key bone formation related marker genes such as osteocalcin and alkaline phosphatase were significantly reduced (P < 0.05) after acute <b>binge</b> alcohol exposure, and expression of regulators of osteoblast activity such as bone morphogenetic proteins and <strong>parathyroid hormone</strong> receptor displayed significantly (P < 0.05) decreased differential expression.
+PTH	drug	nicotine	19187564	Patients with <strong>PTH</strong> levels in the second to fourth quartiles had higher odds of prevalent MS (odds ratio 1.47 [95% CI 0.92 2.35], 2.33 [95% CI 1.40 3.87] and 2.09 [95% CI 1.23 3.56], respectively), after adjustment for 25(OH)D, magnesium, calcium, phosphate, creatinine, age, gender, season of serum sampling, BMI, current <b>smoking</b>, albuminuria, CRP, insulin resistance and type 2 diabetes.
+PTH	addiction	relapse	19187564	The <strong>PTH</strong> level, but not the vitamin D level, is an independent predictor of MS in treatment <b>seeking</b> morbidly obese Caucasian women and men.
+PTH	drug	alcohol	17855333	Serum insulin like growth factor 1 (IGF 1), interleukin (IL) 6, IL 8, IL 10, TNF alpha, <strong>PTH</strong>, estradiol, free testosterone, and corticosterone were measured in 36 <b>alcoholics</b>, ten of them cirrhotics, who also underwent brain CT, which recorded the presence of cortical atrophy or cerebellar atrophy, Evan's, Huckmann's, cella media, bicaudate, cortical atrophy, bifrontal, and ventricular indices, and diameter of the third ventricle; subjective nutritional assessment, midarm anthropometry, and evaluation of liver function.
+PTH	addiction	addiction	17855333	Patients showed marked alterations of all the CT indices compared with 12 controls, but poor relations between these indices and the other parameters analysed (IGF 1, handgrip strength and years of <b>addiction</b> with bifrontal index (P < 0.025 in all cases); <strong>PTH</strong> and Evan's index (r = 0.36, P = 0.032); mean corpuscular volume with cella index and cortical atrophy (P < 0.05).
+PTH	drug	alcohol	17643361	We previously reported that binge <b>alcohol</b> treatment increases bone resorption and that <b>alcohol</b> induced damage can be prevented by treatments with intermittent <strong>parathyroid hormone</strong> and bisphosphonates.
+PTH	addiction	intoxication	17643361	We previously reported that <b>binge</b> alcohol treatment increases bone resorption and that alcohol induced damage can be prevented by treatments with intermittent <strong>parathyroid hormone</strong> and bisphosphonates.
+PTH	drug	alcohol	17204460	Effects of <strong>parathyroid hormone</strong> (1 34) on tibia in an adult rat model for chronic <b>alcohol</b> abuse.
+PTH	drug	alcohol	17204460	The purpose of the present study was to determine whether <strong>PTH</strong> is effective in increasing bone formation and bone mass in a rat model for established osteopenia caused by chronic <b>alcohol</b> abuse.
+PTH	drug	alcohol	17204460	High dose <strong>PTH</strong> (80 microg/kg/day) was administered 5 days/week for 6 weeks to establish the differential efficacy of hormone therapy on bone formation in <b>alcohol</b> consuming and <b>alcohol</b> withdrawn rats.
+PTH	drug	alcohol	17204460	The effects of <b>alcohol</b> and <strong>PTH</strong> on cancellous and cortical bone mass, architecture and turnover were determined by densitometry and histomorphometry.
+PTH	drug	alcohol	17204460	<strong>PTH</strong> treatment increased bone mineral content and density, bone formation rates, cortical bone area, cancellous bone area and trabecular number and thickness, but several indices of bone formation were reduced in the presence of continued <b>alcohol</b> consumption.
+PTH	drug	alcohol	17204460	These results suggest that <b>alcohol</b> consumption, in addition to inducing bone loss, may reduce the efficacy of <strong>PTH</strong> therapy to reverse osteoporosis.
+PTH	drug	alcohol	16573585	Binge <b>alcohol</b> treatment increases vertebral bone loss following ovariectomy: compensation by intermittent <strong>parathyroid hormone</strong>.
+PTH	addiction	intoxication	16573585	<b>Binge</b> alcohol treatment increases vertebral bone loss following ovariectomy: compensation by intermittent <strong>parathyroid hormone</strong>.
+PTH	drug	alcohol	16573585	Ninety six adult (400 g) female Sprague Dawley rats (48 sham operated and 48 OVX, pair fed) were randomly divided into 4 treatment groups: (a) saline treated, (b) binge <b>alcohol</b> treated (3 g/kg <b>alcohol</b> as a 20% weight to volume <b>alcohol</b>/saline solution, intraperitoneal (IP), 3 times per week), (c) parathyroid hormone (<strong>PTH</strong>) treated (80 microg/kg, SC, 5 d/wk), and (d) binge <b>alcohol</b> plus <strong>PTH</strong>.
+PTH	addiction	intoxication	16573585	Ninety six adult (400 g) female Sprague Dawley rats (48 sham operated and 48 OVX, pair fed) were randomly divided into 4 treatment groups: (a) saline treated, (b) <b>binge</b> alcohol treated (3 g/kg alcohol as a 20% weight to volume alcohol/saline solution, intraperitoneal (IP), 3 times per week), (c) parathyroid hormone (<strong>PTH</strong>) treated (80 microg/kg, SC, 5 d/wk), and (d) <b>binge</b> alcohol plus <strong>PTH</strong>.
+PTH	drug	alcohol	16573585	Ninety six adult (400 g) female Sprague Dawley rats (48 sham operated and 48 OVX, pair fed) were randomly divided into 4 treatment groups: (a) saline treated, (b) binge <b>alcohol</b> treated (3 g/kg <b>alcohol</b> as a 20% weight to volume <b>alcohol</b>/saline solution, intraperitoneal (IP), 3 times per week), (c) <strong>parathyroid hormone</strong> (<strong>PTH</strong>) treated (80 microg/kg, SC, 5 d/wk), and (d) binge <b>alcohol</b> plus <strong>PTH</strong>.
+PTH	addiction	intoxication	16573585	Ninety six adult (400 g) female Sprague Dawley rats (48 sham operated and 48 OVX, pair fed) were randomly divided into 4 treatment groups: (a) saline treated, (b) <b>binge</b> alcohol treated (3 g/kg alcohol as a 20% weight to volume alcohol/saline solution, intraperitoneal (IP), 3 times per week), (c) <strong>parathyroid hormone</strong> (<strong>PTH</strong>) treated (80 microg/kg, SC, 5 d/wk), and (d) <b>binge</b> alcohol plus <strong>PTH</strong>.
+PTH	drug	alcohol	16573585	Intermittent <strong>PTH</strong> administration compensated for losses of BMD, compressive strength, and restored BV/TV deficits caused by OVX, <b>alcohol</b>, or their combination.
+PTH	drug	alcohol	16573585	The effects of <b>alcohol</b> and OVX are compensated by concurrent intermittent treatment with <strong>PTH</strong>.
+PTH	drug	nicotine	11685424	<b>Nicotine</b> induced treatment differences were not detected in serum calcium, 25 hydroxyvitamin D, and 1,25 dihydroxyvitamin D. However, serum phosphorus and parathyroid hormone (<strong>PTH</strong>) were higher in rats treated with high dose <b>nicotine</b>, and serum calcitonin was lower in rats treated with both high  and low dose <b>nicotine</b> than in control rats.
+PTH	drug	nicotine	11685424	<b>Nicotine</b> induced treatment differences were not detected in serum calcium, 25 hydroxyvitamin D, and 1,25 dihydroxyvitamin D. However, serum phosphorus and <strong>parathyroid hormone</strong> (<strong>PTH</strong>) were higher in rats treated with high dose <b>nicotine</b>, and serum calcitonin was lower in rats treated with both high  and low dose <b>nicotine</b> than in control rats.
+PTH	drug	alcohol	10548155	Premenstrual tension headache (<strong>PTH</strong>) and its exacerbation by <b>alcohol</b> in women is also accompanied by deficits in IMg2+, and elevation in serum ICa2+/IMg2+; IV MgSO4 corrects the <strong>PTH</strong> and the serum deficit in IMg2+.
+PTH	addiction	withdrawal	9755018	Normally innocuous low intensity tactile stimuli applied to inflamed tissue induce a progressive decrease in the mechanical flexion <b>withdrawal</b> threshold, the phenomenon of progressive tactile hypersensitivity (<strong>PTH</strong>).
+PTH	drug	opioid	9755018	The effects of the mu <b>opioid</b> receptor agonist <b>morphine</b>, the non competitive NMDA receptor antagonist MK801 and the tachykinin NK1 receptor antagonist RP67580 on the development and maintenance of <strong>PTH</strong> has now been investigated behaviourally in rats inflamed 48 h earlier by intraplantar complete Freund's adjuvant injection.
+PTH	drug	opioid	9755018	At 0.5 mg/kg, <b>morphine</b> prevented the establishment of <strong>PTH</strong> without changing baseline thresholds.
+PTH	drug	alcohol	7715435	The effect of <b>alcoholism</b> on calciotropic hormones includes fall of <strong>PTH</strong> serum levels after an acute or moderate <b>alcohol</b> intake, causing transient hypoparathyroidism.
+PTH	drug	alcohol	7992017	An acute intoxication result in transitory hypoparatthyreoidism, while chronic <b>ethanol</b> intake make grow the <strong>PTH</strong> level and decreases the level of D vitamin metabolises.
+PTH	addiction	intoxication	7992017	An acute <b>intoxication</b> result in transitory hypoparatthyreoidism, while chronic ethanol intake make grow the <strong>PTH</strong> level and decreases the level of D vitamin metabolises.
+PTH	drug	alcohol	1422307	We measured the serum concentrations of intact parathyroid hormone (<strong>PTH</strong>), and serum and urine calcium and magnesium in six normal men before and at intervals up to 6 h after the ingestion of fruit juice (control) and 0.5, 1.0 and 1.3 g of <b>alcohol</b> per kg of body weight.
+PTH	drug	alcohol	1422307	We measured the serum concentrations of intact <strong>parathyroid hormone</strong> (<strong>PTH</strong>), and serum and urine calcium and magnesium in six normal men before and at intervals up to 6 h after the ingestion of fruit juice (control) and 0.5, 1.0 and 1.3 g of <b>alcohol</b> per kg of body weight.
+PTH	drug	alcohol	1422307	As compared with the control experiment the maximum reductions in the mean <strong>PTH</strong> concentration were 31% (P = 0.19), 31% (P = 0.20) and 45% (P = 0.01) with the three <b>alcohol</b> doses, respectively.
+PTH	drug	alcohol	1308958	With this study, the authors investigated parathyroid hormone (<strong>PTH</strong>) behaviour in thirteen selected patients with <b>alcohol</b> abuse, free from any clinical or humoral sign of hepatopathy, and in ten healthy subjects as a control group.
+PTH	drug	alcohol	1308958	With this study, the authors investigated <strong>parathyroid hormone</strong> (<strong>PTH</strong>) behaviour in thirteen selected patients with <b>alcohol</b> abuse, free from any clinical or humoral sign of hepatopathy, and in ten healthy subjects as a control group.
+PTH	drug	alcohol	1308958	In <b>alcohol</b> abusers a significant reduction of plasmatic <strong>PTH</strong>, compared to normal calcium levels were found.
+PTH	drug	alcohol	1308958	A possible direct interaction effect between ethyl <b>alcohol</b> and <strong>PTH</strong> may be suggested, even if further studies are required.
+PTH	drug	alcohol	1609627	Our <b>alcoholic</b> patients presented with (1) decreased serum concentrations of bone gla protein (BGP), suggesting decreased bone formation; (2) increased urinary excretion of hydroxyproline, suggesting increased bone resorption; (3) increased renal threshold of phosphate excretion without modification of serum <strong>PTH</strong> concentration, suggesting a direct effect of <b>ethanol</b> on the renal handling of phosphate.
+PTH	drug	alcohol	1997837	In the women, serum <strong>parathyroid hormone</strong> levels decreased from 29.2 +/  2.8 to 17.3 +/  2.6 ng per liter two hours after the administration of <b>alcohol</b> was begun (P less than 0.001) and increased above base line values during the last four hours of the study period.
+PTH	drug	alcohol	1997837	This decline in the secretion of <strong>parathyroid hormone</strong> accounts at least in part for the transient hypocalcemia, hypercalciuria, and hypermagnesuria that follow <b>alcohol</b> ingestion.
+PTH	drug	alcohol	1933604	Prolonged moderate drinking elevates serum parathyroid hormone (<strong>PTH</strong>) levels, whereas chronic <b>alcoholics</b> are characterized by low serum levels of vitamin D metabolites with resultant malabsorption of calcium, hypocalcemia, and hypocalciuria.
+PTH	drug	alcohol	1933604	Prolonged moderate drinking elevates serum <strong>parathyroid hormone</strong> (<strong>PTH</strong>) levels, whereas chronic <b>alcoholics</b> are characterized by low serum levels of vitamin D metabolites with resultant malabsorption of calcium, hypocalcemia, and hypocalciuria.
+PRKAB1	drug	alcohol	32113062	Longer periods of <b>ethanol</b> exposure and associated chronic suppression of <strong>AMPK</strong> activity activates regulatory mechanisms, including gene expression, that operate over longer time scales, both in onset and reversal.
+PRKAB1	drug	opioid	31756370	Activation of the <strong>AMPK</strong> pathway inhibits mTOR and p38 MAPK ameliorating neuroinflammation and tolerance induced by <b>morphine</b>.
+PRKAB1	drug	alcohol	31734306	Repeated <b>ethanol</b> exposure influences key enzymes in cholesterol and lipid homeostasis via the <strong>AMPK</strong> pathway in the rat prefrontal cortex.
+PRKAB1	drug	alcohol	31734306	Similarly, the phosphorylation of <strong>AMPK</strong> and the upstream regulators, LKB1 and CaMK4, were transiently increased only in chronically <b>ethanol</b> treated animals.
+PRKAB1	drug	alcohol	31734306	The phosphorylation of TAK1, another upstream kinase of <strong>AMPK</strong>, was increased only from 30 min to 24 h after the chronic treatment with <b>ethanol</b>.
+PRKAB1	drug	alcohol	31734306	This effect seems to be mediated by the <strong>AMPK</strong> system, and may contribute to the long lasting neuroadaptation involved in the development of <b>alcohol</b> dependence.
+PRKAB1	addiction	dependence	31734306	This effect seems to be mediated by the <strong>AMPK</strong> system, and may contribute to the long lasting neuroadaptation involved in the development of alcohol <b>dependence</b>.
+PRKAB1	drug	alcohol	31199934	Behavioral cross sensitization between cocaine and <b>ethanol</b> is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAB1	drug	cocaine	31199934	Behavioral cross sensitization between <b>cocaine</b> and ethanol is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAB1	addiction	sensitization	31199934	Behavioral cross <b>sensitization</b> between cocaine and ethanol is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAB1	drug	alcohol	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross sensitization between cocaine and <b>ethanol</b> in the rat prefrontal cortex and dorsal striatum.
+PRKAB1	drug	cocaine	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross sensitization between <b>cocaine</b> and ethanol in the rat prefrontal cortex and dorsal striatum.
+PRKAB1	addiction	sensitization	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross <b>sensitization</b> between cocaine and ethanol in the rat prefrontal cortex and dorsal striatum.
+PRKAB1	drug	alcohol	31199934	Although the same changes were found for two upstream kinases of <strong>AMPK</strong> (LKB1 and CaMK4), TAK1 responded differently and was not affected by acute challenges from either cocaine or <b>ethanol</b>.
+PRKAB1	drug	cocaine	31199934	Although the same changes were found for two upstream kinases of <strong>AMPK</strong> (LKB1 and CaMK4), TAK1 responded differently and was not affected by acute challenges from either <b>cocaine</b> or ethanol.
+PRKAB1	drug	alcohol	31195351	In addition, PLE obviously suppressed the expression of SREBP1 and enhanced phosphorylation of <strong>AMPK</strong> compared with chronic <b>ethanol</b> administration.
+PRKAB1	drug	alcohol	31195351	AML12 cells were pretreated with different concentrations of PLE for 2 h and then exposed to <b>ethanol</b> for 48 h. PLE suppressed the expression of SREBP1 and enhanced phosphorylation of <strong>AMPK</strong> in AML12 cells exposed to <b>ethanol</b>.
+PRKAB1	drug	alcohol	31195351	<strong>AMPK</strong> interference confirms that PLE downregulation SREBP1 and F4/80 depending on <strong>AMPK</strong> activation in <b>ethanol</b> treated AML12 cells.
+PRKAB1	drug	alcohol	31167126	CD74 knockout attenuates <b>alcohol</b> intake induced cardiac dysfunction through <strong>AMPK</strong> Skp2 mediated regulation of autophagy.
+PRKAB1	drug	alcohol	31167126	<b>Ethanol</b> challenge upregulated autophagy (p < 0.001), promoted <strong>AMPK</strong> phosphorylation and Sirt1 levels (p < 0.003) while suppressing mTOR phosphorylation and Skp2 levels (p < 0.02).
+PRKAB1	drug	alcohol	31167126	Moreover, the CD74 ablation offered beneficial effects against <b>ethanol</b> induced cardiomyocyte dysfunction, and GFP Puncta formation were nullified by the <strong>AMPK</strong> activator AICAR, the Skp2 inhibitor C1 or the Sirt1 activator SRT1720 (p < 0.0001).
+PRKAB1	drug	alcohol	31167126	Taken together, our data revealed that CD74 ablation counteracts acute <b>ethanol</b> challenge induced myocardial dysfunction, inflammation and apoptosis possibly through an <strong>AMPK</strong> mTOR Skp2 mediated regulation of autophagy.
+PRKAB1	drug	alcohol	30836218	While, the PUE+SIL treatment showed the most effective protection, which was associated with reducing <b>alcohol</b> induced hepatic steatosis via upregulating LKB1/<strong>AMPK</strong>/ACC signaling, and inhibiting hepatic inflammation via LPS triggered TLR4 mediated NF κB signaling pathway.
+PRKAB1	drug	cocaine	30788886	Activation of <strong>AMPK</strong> dependent autophagy in the nucleus accumbens opposes <b>cocaine</b> induced behaviors of mice.
+PRKAB1	drug	cocaine	30788886	Here, we reported that D1 receptor  CaMKII <strong>AMPK</strong> FoxO3a signaling pathway was involved in acute <b>cocaine</b> application induced autophagy in the nucleus accumbens (NAc) both in vitro and in vivo.
+PRKAB1	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase <strong>AMPK</strong> AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+PRKAB1	drug	alcohol	30200508	Finally, GN administration promoted hepatic sirtuin1 (SIRT1) AMP activated protein kinase (<strong>AMPK</strong>) signaling in <b>ethanol</b> fed mice.
+PRKAB1	drug	alcohol	30200508	Moreover, GN prevented <b>ethanol</b> mediated reduction in SIRT1 and phosphorylated <strong>AMPK</strong>.
+PRKAB1	drug	opioid	30146703	We examined the effects of chronic treatment of <b>morphine</b> and/or <b>methadone</b> in the presence or absence of metformin with or without <strong>AMPK</strong> inhibitor (dorsomorphin hydrochloride) on levels of nitric oxide and cyclic adenosine monophosphate (cAMP), phosphorylated and dephosphorylated ribosomal protein S6 kinase β 1 (S6K1) and 4E binding protein 1 (4E BP1) in T98G cells.
+PRKAB1	drug	opioid	30146703	Pretreatment of cells with metformin (40 µM) with or without <strong>AMPK</strong> inhibitor (dorsomorphin hydrochloride; 1 µM) before adding of <b>morphine</b> (2.5 µM) or <b>methadone</b> (1 µM) revealed a protective effects on the development of <b>opioid</b> tolerance.
+PRKAB1	drug	alcohol	29906537	Phenolic acid and flavonoid rich fraction of Sasa quelpaertensis Nakai leaves prevent <b>alcohol</b> induced fatty liver through <strong>AMPK</strong> activation.
+PRKAB1	drug	nicotine	29610348	Activation of <strong>AMPK</strong> by metformin improves withdrawal signs precipitated by <b>nicotine</b> withdrawal.
+PRKAB1	addiction	withdrawal	29610348	Activation of <strong>AMPK</strong> by metformin improves <b>withdrawal</b> signs precipitated by nicotine <b>withdrawal</b>.
+PRKAB1	drug	nicotine	29610348	Here we show that the AMP activated protein kinase (<strong>AMPK</strong>) pathway in the hippocampus is activated following chronic <b>nicotine</b> use, an effect that is rapidly reversed by <b>nicotine</b> withdrawal.
+PRKAB1	addiction	withdrawal	29610348	Here we show that the AMP activated protein kinase (<strong>AMPK</strong>) pathway in the hippocampus is activated following chronic nicotine use, an effect that is rapidly reversed by nicotine <b>withdrawal</b>.
+PRKAB1	drug	nicotine	29610348	Increasing pAMPK levels and, consequently, downstream <strong>AMPK</strong> signaling pharmacologically attenuate anxiety like behavior following <b>nicotine</b> withdrawal.
+PRKAB1	addiction	withdrawal	29610348	Increasing pAMPK levels and, consequently, downstream <strong>AMPK</strong> signaling pharmacologically attenuate anxiety like behavior following nicotine <b>withdrawal</b>.
+PRKAB1	addiction	withdrawal	29610348	We show that metformin, a known <strong>AMPK</strong> activator in the periphery, reduces <b>withdrawal</b> symptoms through a mechanism dependent on the presence of the AMPKα subunits within the hippocampus.
+PRKAB1	drug	nicotine	29610348	This study provides evidence of a direct effect of <strong>AMPK</strong> modulation on <b>nicotine</b> withdrawal symptoms and suggests central <strong>AMPK</strong> activation as a therapeutic target for <b>smoking</b> cessation.
+PRKAB1	addiction	withdrawal	29610348	This study provides evidence of a direct effect of <strong>AMPK</strong> modulation on nicotine <b>withdrawal</b> symptoms and suggests central <strong>AMPK</strong> activation as a therapeutic target for smoking cessation.
+PRKAB1	drug	amphetamine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, neuropeptide Y, pro opiomelanocortin, and cocaine  and <b>amphetamine</b> related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (<strong>AMPK</strong>), mechanistic target of rapamycin and cAMP response element binding protein (CREB).
+PRKAB1	drug	cocaine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, neuropeptide Y, pro opiomelanocortin, and <b>cocaine</b>  and amphetamine related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (<strong>AMPK</strong>), mechanistic target of rapamycin and cAMP response element binding protein (CREB).
+PRKAB1	drug	alcohol	29338075	Up regulated SREBP1, down regulated PPARα and phosphorylated acetyl CoA carboxylase caused by acute and chronic <b>alcohol</b> feeding were modulated by gentiopicroside, through the elevation of LKB1 and <strong>AMPK</strong>.
+PRKAB1	drug	alcohol	29338075	Genetic or pharmacological blockade of P2X7 receptors enhanced <strong>AMPK</strong> activity and reduced SREBP1 expression in <b>ethanol</b> treated HepG2 cells.
+PRKAB1	drug	alcohol	29338075	Activation of LKB1/<strong>AMPK</strong> signalling by gentiopicroside was mediated by the P2X7 receptor NLRP3 inflammasome, suggesting the therapeutic value of blocking P2X7 receptors in the treatment of <b>alcoholic</b> hepatosteatosis.
+PRKAB1	drug	alcohol	29091708	Chronic <b>alcohol</b> consumption causes <b>alcohol</b> induced lipogenesis and promotes hepatic injury by preventing the oxidation of hepatocellular fatty acids through the suppression of the activation of AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAB1	drug	alcohol	28847514	Our results demonstrated that endogenous and exogenous n 3 PUFA enrichment ameliorates <b>ethanol</b> stimulated adipose lipolysis by increasing PDE3B activity and reducing cAMP accumulation in adipocyte, which was associated with activation of GPR120 and regulation of Ca2+/CaMKKβ/<strong>AMPK</strong> signaling, resultantly blocking fatty acid trafficking from adipose tissue to the liver, which contributing to ameliorating <b>ethanol</b> induced adipose dysfunction and liver injury.
+PRKAB1	drug	cocaine	28432301	<strong>AMPK</strong> signaling in the nucleus accumbens core mediates cue induced reinstatement of <b>cocaine</b> seeking.
+PRKAB1	addiction	relapse	28432301	<strong>AMPK</strong> signaling in the nucleus accumbens core mediates cue induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+PRKAB1	drug	cocaine	28432301	Here, we investigated the role of <strong>AMPK</strong> activity in the nucleus accumbens (NAc) in relapse to <b>cocaine</b> seeking.
+PRKAB1	addiction	relapse	28432301	Here, we investigated the role of <strong>AMPK</strong> activity in the nucleus accumbens (NAc) in <b>relapse</b> to cocaine <b>seeking</b>.
+PRKAB1	drug	cocaine	28432301	We found that exposure to drug related cues reinstated <b>cocaine</b> seeking behavior and increased <strong>AMPK</strong> and p70s6k phosphorylation in the NAc core but not shell.
+PRKAB1	addiction	relapse	28432301	We found that exposure to drug related cues reinstated cocaine <b>seeking</b> behavior and increased <strong>AMPK</strong> and p70s6k phosphorylation in the NAc core but not shell.
+PRKAB1	drug	cocaine	28432301	Augmenting <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> activator 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide (AICAR) or adenovirus expressing constitutively active subunits of <strong>AMPK</strong> decreased cue induced reinstatement of <b>cocaine</b> seeking and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal regulated kinase 1/2 (ERK1/2) pathways.
+PRKAB1	addiction	relapse	28432301	Augmenting <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> activator 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide (AICAR) or adenovirus expressing constitutively active subunits of <strong>AMPK</strong> decreased cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal regulated kinase 1/2 (ERK1/2) pathways.
+PRKAB1	drug	cocaine	28432301	In contrast, inhibition of <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> inhibitor compound C or adenovirus expressing dominant negative subunits of <strong>AMPK</strong> increased cue induced reinstatement of <b>cocaine</b> seeking and enhanced mTORC1 and ERK1/2 activity.
+PRKAB1	addiction	relapse	28432301	In contrast, inhibition of <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> inhibitor compound C or adenovirus expressing dominant negative subunits of <strong>AMPK</strong> increased cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and enhanced mTORC1 and ERK1/2 activity.
+PRKAB1	drug	cocaine	28432301	The regulation of <strong>AMPK</strong> activity in the NAc shell had no effect on cue induced <b>cocaine</b> seeking.
+PRKAB1	addiction	relapse	28432301	The regulation of <strong>AMPK</strong> activity in the NAc shell had no effect on cue induced cocaine <b>seeking</b>.
+PRKAB1	drug	cocaine	28432301	Altogether, these results indicate that <strong>AMPK</strong> activity in the NAc core is critical for the cue induced reinstatement of <b>cocaine</b> seeking, which may be mediated by mTORC1 and ERK1/2 signaling.
+PRKAB1	addiction	relapse	28432301	Altogether, these results indicate that <strong>AMPK</strong> activity in the NAc core is critical for the cue induced <b>reinstatement</b> of cocaine <b>seeking</b>, which may be mediated by mTORC1 and ERK1/2 signaling.
+PRKAB1	drug	alcohol	27901267	Binge <b>Alcohol</b> Intake After Hypergravity Stress Sustainably Decreases <strong>AMPK</strong> and Transcription Factors Necessary for Hepatocyte Survival.
+PRKAB1	addiction	intoxication	27901267	<b>Binge</b> Alcohol Intake After Hypergravity Stress Sustainably Decreases <strong>AMPK</strong> and Transcription Factors Necessary for Hepatocyte Survival.
+PRKAB1	drug	alcohol	27901267	This study investigated whether a combination of hypergravity stress and binge <b>alcohol</b> intake has a detrimental effect on AMP activated protein kinase (<strong>AMPK</strong>) and other molecules necessary for hepatocyte survival.
+PRKAB1	addiction	intoxication	27901267	This study investigated whether a combination of hypergravity stress and <b>binge</b> alcohol intake has a detrimental effect on AMP activated protein kinase (<strong>AMPK</strong>) and other molecules necessary for hepatocyte survival.
+PRKAB1	drug	cocaine	27132751	Region specific activation of the <strong>AMPK</strong> system by <b>cocaine</b>: The role of D1 and D2 receptors.
+PRKAB1	drug	cocaine	27132751	Thus, the present study examined whether the sensitizing effects of <b>cocaine</b> could be observed in the <strong>AMPK</strong> system and aimed to determine whether these effects were mediated by dopamine (DA) D1 or D2 receptors.
+PRKAB1	drug	cocaine	27132751	In the drug naïve state, acute treatment with <b>cocaine</b> produced an increase in locomotor activity and increased <strong>AMPK</strong> phosphorylation in the frontal cortex but decreased it in the dorsal striatum.
+PRKAB1	drug	cocaine	27132751	In the drug sensitized state (following repeated treatment), the behavioral responsiveness to <b>cocaine</b> was augmented and accompanied by alterations in <strong>AMPK</strong> activity.
+PRKAB1	drug	cocaine	27132751	The opposite effects induced by <b>cocaine</b> in the <strong>AMPK</strong> system in the dorsal striatum and frontal cortex may be explained by the differential activations of DA D1 and D2 receptors in these brain regions.
+PRKAB1	drug	alcohol	26776965	Betulin alleviated <b>ethanol</b> induced <b>alcoholic</b> liver injury via SIRT1/<strong>AMPK</strong> signaling pathway.
+PRKAB1	drug	alcohol	26776965	Betulin suppressed the expression of sterol regulatory element binding protein 1 (SREBP 1), and genetic deletion of <strong>AMPK</strong> blocked the effect of betulin on SREBP 1 in <b>ethanol</b> treated LX 2 cells.
+PRKAB1	drug	alcohol	26776965	In vivo, betulin attenuated the increases in serum aminotransferase and triglyceride levels in the mice fed with chronic binge <b>ethanol</b>, while significantly inhibited SREBP 1 expression and activated LKB1 <strong>AMPK</strong> phosphorylation.
+PRKAB1	addiction	intoxication	26776965	In vivo, betulin attenuated the increases in serum aminotransferase and triglyceride levels in the mice fed with chronic <b>binge</b> ethanol, while significantly inhibited SREBP 1 expression and activated LKB1 <strong>AMPK</strong> phosphorylation.
+PRKAB1	drug	alcohol	26776965	Taken together, betulin alleviates <b>alcoholic</b> liver injury possibly through blocking the regulation of SREBP 1 on fatty acid synthesis and activating SIRT1 LKB1 <strong>AMPK</strong> signaling pathway.
+PRKAB1	drug	opioid	26378398	Activation of adenosine monophosphate activated kinase (<strong>AMPK</strong>) has been associated with the inhibition of inflammatory nociception and the attenuation of <b>morphine</b> antinociceptive tolerance.
+PRKAB1	addiction	withdrawal	26378398	Resveratrol and 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide, the <strong>AMPK</strong> activators, significantly attenuated bone cancer pain in rats with tumor cell implantation (TCI; threshold of mechanical <b>withdrawal</b>, resveratrol vs. vehicle: 10.1 ± 0.56 vs. 4.1 ± 0.37; 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide vs. vehicle: 8.2 ± 0.17 vs. 4.1 ± 0.37, mean ± SEM); these effects were reversed by the <strong>AMPK</strong> inhibitor compound C (compound C vs. resveratrol: 6.2 ± 1.35 vs. 10.1 ± 0.56, mean ± SEM).
+PRKAB1	drug	alcohol	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates <b>ethanol</b> induced liver injury through modulation of <strong>AMPK</strong> and Nrf2 related signals in a binge drinking mouse model.
+PRKAB1	addiction	intoxication	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates ethanol induced liver injury through modulation of <strong>AMPK</strong> and Nrf2 related signals in a <b>binge</b> drinking mouse model.
+PRKAB1	drug	alcohol	25703252	The adiponectin SIRT1 <strong>AMPK</strong> pathway in <b>alcoholic</b> fatty liver disease in the rat.
+PRKAB1	addiction	intoxication	25703252	Our previous work showed that <b>binge</b> drinking in the rat induced hepatic steatosis which correlated with reduced expression of AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAB1	drug	alcohol	25703252	The serum Adip and tumor necrosis factor alpha (TNF α) as well as liver Adip receptors (AdipoR1 and AdipoR2) SIRT1, <strong>AMPK</strong>, phosphorylated <strong>AMPK</strong> (p <strong>AMPK</strong>), sterol regulatory element binding proteins (SREBPs), acetyl CoA carboxylase (ACC), LIP 1, lipocalin 2 (LCN2), and serum amyloid A1 were assessed in the rat model where 16 weeks of gavaged <b>alcohol</b> were administered.
+PRKAB1	drug	alcohol	25703252	Our present observations demonstrate that the impaired Adip SIRT1 <strong>AMPK</strong> signaling pathway contributes, at least in part, to the development of <b>alcoholic</b> fatty liver disease in EtOH binge rats.
+PRKAB1	addiction	intoxication	25703252	Our present observations demonstrate that the impaired Adip SIRT1 <strong>AMPK</strong> signaling pathway contributes, at least in part, to the development of alcoholic fatty liver disease in EtOH <b>binge</b> rats.
+PRKAB1	drug	alcohol	24283421	<b>Ethanol</b> intoxication altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (<strong>AMPK</strong>), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (TNF α) expression.
+PRKAB1	addiction	intoxication	24283421	Ethanol <b>intoxication</b> altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (<strong>AMPK</strong>), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (TNF α) expression.
+PRKAB1	drug	alcohol	22563259	These results demonstrated that cilostazol effectively decrease the <b>ethanol</b> mediated TNFα production both in murine macrophage and in liver from binge drinking mice and <strong>AMPK</strong> may be responsible for the inhibition of TNFα production by cilostazol.
+PRKAB1	addiction	intoxication	22563259	These results demonstrated that cilostazol effectively decrease the ethanol mediated TNFα production both in murine macrophage and in liver from <b>binge</b> drinking mice and <strong>AMPK</strong> may be responsible for the inhibition of TNFα production by cilostazol.
+PRKAB1	drug	alcohol	22451512	Deficiency in <strong>AMPK</strong> attenuates <b>ethanol</b> induced cardiac contractile dysfunction through inhibition of autophagosome formation.
+PRKAB1	addiction	intoxication	22451512	<b>Binge</b> drinking often triggers compromised myocardial contractile function while activating AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAB1	drug	alcohol	22451512	Given the role of <strong>AMPK</strong> in the initiation of autophagy through the mammalian target of rapamycin complex 1 (mTORC1) and Unc51 like kinase (ULK1), this study was designed to examine the impact of <strong>AMPK</strong> deficiency on cardiac function and the mechanism involved with a focus on autophagy following an acute <b>ethanol</b> challenge.
+PRKAB1	drug	alcohol	22451512	Wild type (WT) and transgenic mice overexpressing a kinase dead (KD) α2 isoform (K45R mutation) of <strong>AMPK</strong> were challenged with <b>ethanol</b>.
+PRKAB1	drug	alcohol	22451512	<b>Ethanol</b> exposure triggered glucose intolerance and compromised cardiac contraction accompanied by increased phosphorylation of <strong>AMPK</strong> and ACC as well as autophagosome accumulation (increased LC3II and p62), the effects of which were attenuated or mitigated by <strong>AMPK</strong> deficiency or inhibition.
+PRKAB1	drug	alcohol	22451512	<b>Ethanol</b> dampened and stimulated, respectively, the phosphorylation of mTOR and Raptor, the effects of which were abolished by <strong>AMPK</strong> deficiency.
+PRKAB1	drug	alcohol	22451512	ULK1 phosphorylation at Ser(757) and Ser(777) was down regulated and up regulated, respectively, by <b>ethanol</b>, the effect of which was nullified by <strong>AMPK</strong> deficiency or inhibition.
+PRKAB1	drug	alcohol	22451512	Moreover, the <b>ethanol</b> challenge enhanced LC3 puncta in H9c2 cells and promoted cardiac contractile dysfunction, and these effects were ablated by the inhibition of autophagy or <strong>AMPK</strong>.
+PRKAB1	drug	alcohol	22451512	In summary, these data suggest that <b>ethanol</b> exposure may trigger myocardial dysfunction through a mechanism associated with <strong>AMPK</strong> mTORC1 ULK1 mediated autophagy.
+PRKAB1	drug	nicotine	22315316	The aim of this study was to investigate the effect of <b>nicotine</b> on hypothalamic AMP activated protein kinase (<strong>AMPK</strong>) and its effect on energy balance.
+PRKAB1	drug	nicotine	22315316	Here we demonstrate that <b>nicotine</b> induced weight loss is associated with inactivation of hypothalamic <strong>AMPK</strong>, decreased orexigenic signaling in the hypothalamus, increased energy expenditure as a result of increased locomotor activity, increased thermogenesis in brown adipose tissue (BAT), and alterations in fuel substrate utilization.
+PRKAB1	drug	nicotine	22315316	Conversely, <b>nicotine</b> withdrawal or genetic activation of hypothalamic <strong>AMPK</strong> in the ventromedial nucleus of the hypothalamus reversed <b>nicotine</b> induced negative energy balance.
+PRKAB1	addiction	withdrawal	22315316	Conversely, nicotine <b>withdrawal</b> or genetic activation of hypothalamic <strong>AMPK</strong> in the ventromedial nucleus of the hypothalamus reversed nicotine induced negative energy balance.
+PRKAB1	drug	nicotine	22315316	Overall these data demonstrate that the effects of <b>nicotine</b> on energy balance involve specific modulation of the hypothalamic <strong>AMPK</strong> BAT axis.
+PRKAB1	drug	alcohol	22272351	In primary rat alveolar type II cells <b>alcohol</b> and adenosine decreased the abundance of the Na,K ATPase at the basolateral membrane via a mechanism that required activation of the <strong>AMPK</strong>.
+PRKAB1	drug	alcohol	21062897	Moreover, activation of <strong>AMPK</strong>, a known positive modulator of sirtuin activity, prevented the <b>ethanol</b> induced suppression of sirtuin 3 activity and the attendant increase of cyclophilin D acetylation, activity and association with ANT 1.
+PRKAB1	drug	alcohol	21062897	Additionally, <strong>AMPK</strong> reactivation of sirtuin 3 prevented the sensitization to the MPT and the enhancement of cell killing by TNF in cells exposed to <b>ethanol</b>.
+PRKAB1	addiction	sensitization	21062897	Additionally, <strong>AMPK</strong> reactivation of sirtuin 3 prevented the <b>sensitization</b> to the MPT and the enhancement of cell killing by TNF in cells exposed to ethanol.
+PRKAB1	drug	alcohol	20585647	Involvement of <strong>AMPK</strong> in <b>alcohol</b> dehydrogenase accentuated myocardial dysfunction following acute <b>ethanol</b> challenge in mice.
+PRKAB1	drug	alcohol	20585647	This study was designed to examine the impact of cardiac specific overexpression of <b>alcohol</b> dehydrogenase (ADH) on <b>ethanol</b> induced change in cardiac contractile function, intracellular Ca(2+) homeostasis, insulin and AMP dependent kinase (<strong>AMPK</strong>) signaling.
+PRKAB1	drug	alcohol	20585647	<b>Ethanol</b> exposure led to glucose intolerance, elevated plasma insulin, compromised cardiac contractile and intracellular Ca(2+) properties, downregulated protein phosphatase PP2A subunit and PPAR gamma, as well as phosphorylation of <strong>AMPK</strong>, ACC and LKB1, all of which except plasma insulin were overtly accentuated by ADH transgene.
+PRKAB1	drug	alcohol	20585647	In addition, the <strong>AMPK</strong> inhibitor compound C (10 microM) abrogated acute <b>ethanol</b> exposure elicited cardiomyocyte mechanical dysfunction.
+PRKAB1	drug	alcohol	20585647	In summary, these data suggest that the ADH transgene exacerbated acute <b>ethanol</b> toxicity induced myocardial contractile dysfunction, intracellular Ca(2+) mishandling and glucose intolerance, indicating a role of ADH in acute <b>ethanol</b> toxicity induced cardiac dysfunction possibly related to altered cellular fuel <strong>AMPK</strong> signaling cascade.
+PRKAB1	drug	alcohol	19942091	<b>Ethanol</b> treatment dampened phosphorylation of Akt and <strong>AMPK</strong> associated with up regulated PP2A and PP2C, which was abrogated by ALDH2.
+PRKAB1	drug	alcohol	19942091	ALDH2 significantly attenuated <b>ethanol</b> induced decrease in Akt  and <strong>AMPK</strong> stimulated phosphorylation of Foxo3 at Thr32 and Ser413, respectively.
+PRKAB1	drug	alcohol	19942091	Our results suggest that ALDH2 is cardioprotective against acute <b>ethanol</b> toxicity, possibly through inhibition of protein phosphatases, leading to enhanced Akt and <strong>AMPK</strong> activation, and subsequently, inhibition of Foxo3, apoptosis, and mitochondrial dysfunction.
+PRKAA2	drug	alcohol	32113062	Longer periods of <b>ethanol</b> exposure and associated chronic suppression of <strong>AMPK</strong> activity activates regulatory mechanisms, including gene expression, that operate over longer time scales, both in onset and reversal.
+PRKAA2	drug	opioid	31756370	Activation of the <strong>AMPK</strong> pathway inhibits mTOR and p38 MAPK ameliorating neuroinflammation and tolerance induced by <b>morphine</b>.
+PRKAA2	drug	alcohol	31734306	Repeated <b>ethanol</b> exposure influences key enzymes in cholesterol and lipid homeostasis via the <strong>AMPK</strong> pathway in the rat prefrontal cortex.
+PRKAA2	drug	alcohol	31734306	Similarly, the phosphorylation of <strong>AMPK</strong> and the upstream regulators, LKB1 and CaMK4, were transiently increased only in chronically <b>ethanol</b> treated animals.
+PRKAA2	drug	alcohol	31734306	The phosphorylation of TAK1, another upstream kinase of <strong>AMPK</strong>, was increased only from 30 min to 24 h after the chronic treatment with <b>ethanol</b>.
+PRKAA2	drug	alcohol	31734306	This effect seems to be mediated by the <strong>AMPK</strong> system, and may contribute to the long lasting neuroadaptation involved in the development of <b>alcohol</b> dependence.
+PRKAA2	addiction	dependence	31734306	This effect seems to be mediated by the <strong>AMPK</strong> system, and may contribute to the long lasting neuroadaptation involved in the development of alcohol <b>dependence</b>.
+PRKAA2	drug	alcohol	31199934	Behavioral cross sensitization between cocaine and <b>ethanol</b> is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAA2	drug	cocaine	31199934	Behavioral cross sensitization between <b>cocaine</b> and ethanol is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAA2	addiction	sensitization	31199934	Behavioral cross <b>sensitization</b> between cocaine and ethanol is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAA2	drug	alcohol	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross sensitization between cocaine and <b>ethanol</b> in the rat prefrontal cortex and dorsal striatum.
+PRKAA2	drug	cocaine	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross sensitization between <b>cocaine</b> and ethanol in the rat prefrontal cortex and dorsal striatum.
+PRKAA2	addiction	sensitization	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross <b>sensitization</b> between cocaine and ethanol in the rat prefrontal cortex and dorsal striatum.
+PRKAA2	drug	alcohol	31199934	Although the same changes were found for two upstream kinases of <strong>AMPK</strong> (LKB1 and CaMK4), TAK1 responded differently and was not affected by acute challenges from either cocaine or <b>ethanol</b>.
+PRKAA2	drug	cocaine	31199934	Although the same changes were found for two upstream kinases of <strong>AMPK</strong> (LKB1 and CaMK4), TAK1 responded differently and was not affected by acute challenges from either <b>cocaine</b> or ethanol.
+PRKAA2	drug	alcohol	31195351	In addition, PLE obviously suppressed the expression of SREBP1 and enhanced phosphorylation of <strong>AMPK</strong> compared with chronic <b>ethanol</b> administration.
+PRKAA2	drug	alcohol	31195351	AML12 cells were pretreated with different concentrations of PLE for 2 h and then exposed to <b>ethanol</b> for 48 h. PLE suppressed the expression of SREBP1 and enhanced phosphorylation of <strong>AMPK</strong> in AML12 cells exposed to <b>ethanol</b>.
+PRKAA2	drug	alcohol	31195351	<strong>AMPK</strong> interference confirms that PLE downregulation SREBP1 and F4/80 depending on <strong>AMPK</strong> activation in <b>ethanol</b> treated AML12 cells.
+PRKAA2	drug	alcohol	31167126	CD74 knockout attenuates <b>alcohol</b> intake induced cardiac dysfunction through <strong>AMPK</strong> Skp2 mediated regulation of autophagy.
+PRKAA2	drug	alcohol	31167126	<b>Ethanol</b> challenge upregulated autophagy (p < 0.001), promoted <strong>AMPK</strong> phosphorylation and Sirt1 levels (p < 0.003) while suppressing mTOR phosphorylation and Skp2 levels (p < 0.02).
+PRKAA2	drug	alcohol	31167126	Moreover, the CD74 ablation offered beneficial effects against <b>ethanol</b> induced cardiomyocyte dysfunction, and GFP Puncta formation were nullified by the <strong>AMPK</strong> activator AICAR, the Skp2 inhibitor C1 or the Sirt1 activator SRT1720 (p < 0.0001).
+PRKAA2	drug	alcohol	31167126	Taken together, our data revealed that CD74 ablation counteracts acute <b>ethanol</b> challenge induced myocardial dysfunction, inflammation and apoptosis possibly through an <strong>AMPK</strong> mTOR Skp2 mediated regulation of autophagy.
+PRKAA2	drug	alcohol	30836218	While, the PUE+SIL treatment showed the most effective protection, which was associated with reducing <b>alcohol</b> induced hepatic steatosis via upregulating LKB1/<strong>AMPK</strong>/ACC signaling, and inhibiting hepatic inflammation via LPS triggered TLR4 mediated NF κB signaling pathway.
+PRKAA2	drug	cocaine	30788886	Activation of <strong>AMPK</strong> dependent autophagy in the nucleus accumbens opposes <b>cocaine</b> induced behaviors of mice.
+PRKAA2	drug	cocaine	30788886	Here, we reported that D1 receptor  CaMKII <strong>AMPK</strong> FoxO3a signaling pathway was involved in acute <b>cocaine</b> application induced autophagy in the nucleus accumbens (NAc) both in vitro and in vivo.
+PRKAA2	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase <strong>AMPK</strong> AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+PRKAA2	drug	alcohol	30200508	Finally, GN administration promoted hepatic sirtuin1 (SIRT1) AMP activated protein kinase (<strong>AMPK</strong>) signaling in <b>ethanol</b> fed mice.
+PRKAA2	drug	alcohol	30200508	Moreover, GN prevented <b>ethanol</b> mediated reduction in SIRT1 and phosphorylated <strong>AMPK</strong>.
+PRKAA2	drug	opioid	30146703	We examined the effects of chronic treatment of <b>morphine</b> and/or <b>methadone</b> in the presence or absence of metformin with or without <strong>AMPK</strong> inhibitor (dorsomorphin hydrochloride) on levels of nitric oxide and cyclic adenosine monophosphate (cAMP), phosphorylated and dephosphorylated ribosomal protein S6 kinase β 1 (S6K1) and 4E binding protein 1 (4E BP1) in T98G cells.
+PRKAA2	drug	opioid	30146703	Pretreatment of cells with metformin (40 µM) with or without <strong>AMPK</strong> inhibitor (dorsomorphin hydrochloride; 1 µM) before adding of <b>morphine</b> (2.5 µM) or <b>methadone</b> (1 µM) revealed a protective effects on the development of <b>opioid</b> tolerance.
+PRKAA2	drug	alcohol	29906537	Phenolic acid and flavonoid rich fraction of Sasa quelpaertensis Nakai leaves prevent <b>alcohol</b> induced fatty liver through <strong>AMPK</strong> activation.
+PRKAA2	drug	nicotine	29610348	Activation of <strong>AMPK</strong> by metformin improves withdrawal signs precipitated by <b>nicotine</b> withdrawal.
+PRKAA2	addiction	withdrawal	29610348	Activation of <strong>AMPK</strong> by metformin improves <b>withdrawal</b> signs precipitated by nicotine <b>withdrawal</b>.
+PRKAA2	drug	nicotine	29610348	Here we show that the AMP activated protein kinase (<strong>AMPK</strong>) pathway in the hippocampus is activated following chronic <b>nicotine</b> use, an effect that is rapidly reversed by <b>nicotine</b> withdrawal.
+PRKAA2	addiction	withdrawal	29610348	Here we show that the AMP activated protein kinase (<strong>AMPK</strong>) pathway in the hippocampus is activated following chronic nicotine use, an effect that is rapidly reversed by nicotine <b>withdrawal</b>.
+PRKAA2	drug	nicotine	29610348	Increasing pAMPK levels and, consequently, downstream <strong>AMPK</strong> signaling pharmacologically attenuate anxiety like behavior following <b>nicotine</b> withdrawal.
+PRKAA2	addiction	withdrawal	29610348	Increasing pAMPK levels and, consequently, downstream <strong>AMPK</strong> signaling pharmacologically attenuate anxiety like behavior following nicotine <b>withdrawal</b>.
+PRKAA2	addiction	withdrawal	29610348	We show that metformin, a known <strong>AMPK</strong> activator in the periphery, reduces <b>withdrawal</b> symptoms through a mechanism dependent on the presence of the AMPKα subunits within the hippocampus.
+PRKAA2	drug	nicotine	29610348	This study provides evidence of a direct effect of <strong>AMPK</strong> modulation on <b>nicotine</b> withdrawal symptoms and suggests central <strong>AMPK</strong> activation as a therapeutic target for <b>smoking</b> cessation.
+PRKAA2	addiction	withdrawal	29610348	This study provides evidence of a direct effect of <strong>AMPK</strong> modulation on nicotine <b>withdrawal</b> symptoms and suggests central <strong>AMPK</strong> activation as a therapeutic target for smoking cessation.
+PRKAA2	drug	amphetamine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, neuropeptide Y, pro opiomelanocortin, and cocaine  and <b>amphetamine</b> related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (<strong>AMPK</strong>), mechanistic target of rapamycin and cAMP response element binding protein (CREB).
+PRKAA2	drug	cocaine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, neuropeptide Y, pro opiomelanocortin, and <b>cocaine</b>  and amphetamine related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (<strong>AMPK</strong>), mechanistic target of rapamycin and cAMP response element binding protein (CREB).
+PRKAA2	drug	alcohol	29338075	Up regulated SREBP1, down regulated PPARα and phosphorylated acetyl CoA carboxylase caused by acute and chronic <b>alcohol</b> feeding were modulated by gentiopicroside, through the elevation of LKB1 and <strong>AMPK</strong>.
+PRKAA2	drug	alcohol	29338075	Genetic or pharmacological blockade of P2X7 receptors enhanced <strong>AMPK</strong> activity and reduced SREBP1 expression in <b>ethanol</b> treated HepG2 cells.
+PRKAA2	drug	alcohol	29338075	Activation of LKB1/<strong>AMPK</strong> signalling by gentiopicroside was mediated by the P2X7 receptor NLRP3 inflammasome, suggesting the therapeutic value of blocking P2X7 receptors in the treatment of <b>alcoholic</b> hepatosteatosis.
+PRKAA2	drug	alcohol	29091708	Chronic <b>alcohol</b> consumption causes <b>alcohol</b> induced lipogenesis and promotes hepatic injury by preventing the oxidation of hepatocellular fatty acids through the suppression of the activation of AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAA2	drug	alcohol	28847514	Our results demonstrated that endogenous and exogenous n 3 PUFA enrichment ameliorates <b>ethanol</b> stimulated adipose lipolysis by increasing PDE3B activity and reducing cAMP accumulation in adipocyte, which was associated with activation of GPR120 and regulation of Ca2+/CaMKKβ/<strong>AMPK</strong> signaling, resultantly blocking fatty acid trafficking from adipose tissue to the liver, which contributing to ameliorating <b>ethanol</b> induced adipose dysfunction and liver injury.
+PRKAA2	drug	cocaine	28432301	<strong>AMPK</strong> signaling in the nucleus accumbens core mediates cue induced reinstatement of <b>cocaine</b> seeking.
+PRKAA2	addiction	relapse	28432301	<strong>AMPK</strong> signaling in the nucleus accumbens core mediates cue induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+PRKAA2	drug	cocaine	28432301	Here, we investigated the role of <strong>AMPK</strong> activity in the nucleus accumbens (NAc) in relapse to <b>cocaine</b> seeking.
+PRKAA2	addiction	relapse	28432301	Here, we investigated the role of <strong>AMPK</strong> activity in the nucleus accumbens (NAc) in <b>relapse</b> to cocaine <b>seeking</b>.
+PRKAA2	drug	cocaine	28432301	We found that exposure to drug related cues reinstated <b>cocaine</b> seeking behavior and increased <strong>AMPK</strong> and p70s6k phosphorylation in the NAc core but not shell.
+PRKAA2	addiction	relapse	28432301	We found that exposure to drug related cues reinstated cocaine <b>seeking</b> behavior and increased <strong>AMPK</strong> and p70s6k phosphorylation in the NAc core but not shell.
+PRKAA2	drug	cocaine	28432301	Augmenting <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> activator 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide (AICAR) or adenovirus expressing constitutively active subunits of <strong>AMPK</strong> decreased cue induced reinstatement of <b>cocaine</b> seeking and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal regulated kinase 1/2 (ERK1/2) pathways.
+PRKAA2	addiction	relapse	28432301	Augmenting <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> activator 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide (AICAR) or adenovirus expressing constitutively active subunits of <strong>AMPK</strong> decreased cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal regulated kinase 1/2 (ERK1/2) pathways.
+PRKAA2	drug	cocaine	28432301	In contrast, inhibition of <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> inhibitor compound C or adenovirus expressing dominant negative subunits of <strong>AMPK</strong> increased cue induced reinstatement of <b>cocaine</b> seeking and enhanced mTORC1 and ERK1/2 activity.
+PRKAA2	addiction	relapse	28432301	In contrast, inhibition of <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> inhibitor compound C or adenovirus expressing dominant negative subunits of <strong>AMPK</strong> increased cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and enhanced mTORC1 and ERK1/2 activity.
+PRKAA2	drug	cocaine	28432301	The regulation of <strong>AMPK</strong> activity in the NAc shell had no effect on cue induced <b>cocaine</b> seeking.
+PRKAA2	addiction	relapse	28432301	The regulation of <strong>AMPK</strong> activity in the NAc shell had no effect on cue induced cocaine <b>seeking</b>.
+PRKAA2	drug	cocaine	28432301	Altogether, these results indicate that <strong>AMPK</strong> activity in the NAc core is critical for the cue induced reinstatement of <b>cocaine</b> seeking, which may be mediated by mTORC1 and ERK1/2 signaling.
+PRKAA2	addiction	relapse	28432301	Altogether, these results indicate that <strong>AMPK</strong> activity in the NAc core is critical for the cue induced <b>reinstatement</b> of cocaine <b>seeking</b>, which may be mediated by mTORC1 and ERK1/2 signaling.
+PRKAA2	drug	alcohol	27901267	Binge <b>Alcohol</b> Intake After Hypergravity Stress Sustainably Decreases <strong>AMPK</strong> and Transcription Factors Necessary for Hepatocyte Survival.
+PRKAA2	addiction	intoxication	27901267	<b>Binge</b> Alcohol Intake After Hypergravity Stress Sustainably Decreases <strong>AMPK</strong> and Transcription Factors Necessary for Hepatocyte Survival.
+PRKAA2	drug	alcohol	27901267	This study investigated whether a combination of hypergravity stress and binge <b>alcohol</b> intake has a detrimental effect on AMP activated protein kinase (<strong>AMPK</strong>) and other molecules necessary for hepatocyte survival.
+PRKAA2	addiction	intoxication	27901267	This study investigated whether a combination of hypergravity stress and <b>binge</b> alcohol intake has a detrimental effect on AMP activated protein kinase (<strong>AMPK</strong>) and other molecules necessary for hepatocyte survival.
+PRKAA2	drug	cocaine	27132751	Region specific activation of the <strong>AMPK</strong> system by <b>cocaine</b>: The role of D1 and D2 receptors.
+PRKAA2	drug	cocaine	27132751	Thus, the present study examined whether the sensitizing effects of <b>cocaine</b> could be observed in the <strong>AMPK</strong> system and aimed to determine whether these effects were mediated by dopamine (DA) D1 or D2 receptors.
+PRKAA2	drug	cocaine	27132751	In the drug naïve state, acute treatment with <b>cocaine</b> produced an increase in locomotor activity and increased <strong>AMPK</strong> phosphorylation in the frontal cortex but decreased it in the dorsal striatum.
+PRKAA2	drug	cocaine	27132751	In the drug sensitized state (following repeated treatment), the behavioral responsiveness to <b>cocaine</b> was augmented and accompanied by alterations in <strong>AMPK</strong> activity.
+PRKAA2	drug	cocaine	27132751	The opposite effects induced by <b>cocaine</b> in the <strong>AMPK</strong> system in the dorsal striatum and frontal cortex may be explained by the differential activations of DA D1 and D2 receptors in these brain regions.
+PRKAA2	drug	alcohol	26776965	Betulin alleviated <b>ethanol</b> induced <b>alcoholic</b> liver injury via SIRT1/<strong>AMPK</strong> signaling pathway.
+PRKAA2	drug	alcohol	26776965	Betulin suppressed the expression of sterol regulatory element binding protein 1 (SREBP 1), and genetic deletion of <strong>AMPK</strong> blocked the effect of betulin on SREBP 1 in <b>ethanol</b> treated LX 2 cells.
+PRKAA2	drug	alcohol	26776965	In vivo, betulin attenuated the increases in serum aminotransferase and triglyceride levels in the mice fed with chronic binge <b>ethanol</b>, while significantly inhibited SREBP 1 expression and activated LKB1 <strong>AMPK</strong> phosphorylation.
+PRKAA2	addiction	intoxication	26776965	In vivo, betulin attenuated the increases in serum aminotransferase and triglyceride levels in the mice fed with chronic <b>binge</b> ethanol, while significantly inhibited SREBP 1 expression and activated LKB1 <strong>AMPK</strong> phosphorylation.
+PRKAA2	drug	alcohol	26776965	Taken together, betulin alleviates <b>alcoholic</b> liver injury possibly through blocking the regulation of SREBP 1 on fatty acid synthesis and activating SIRT1 LKB1 <strong>AMPK</strong> signaling pathway.
+PRKAA2	drug	opioid	26378398	Activation of adenosine monophosphate activated kinase (<strong>AMPK</strong>) has been associated with the inhibition of inflammatory nociception and the attenuation of <b>morphine</b> antinociceptive tolerance.
+PRKAA2	addiction	withdrawal	26378398	Resveratrol and 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide, the <strong>AMPK</strong> activators, significantly attenuated bone cancer pain in rats with tumor cell implantation (TCI; threshold of mechanical <b>withdrawal</b>, resveratrol vs. vehicle: 10.1 ± 0.56 vs. 4.1 ± 0.37; 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide vs. vehicle: 8.2 ± 0.17 vs. 4.1 ± 0.37, mean ± SEM); these effects were reversed by the <strong>AMPK</strong> inhibitor compound C (compound C vs. resveratrol: 6.2 ± 1.35 vs. 10.1 ± 0.56, mean ± SEM).
+PRKAA2	drug	alcohol	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates <b>ethanol</b> induced liver injury through modulation of <strong>AMPK</strong> and Nrf2 related signals in a binge drinking mouse model.
+PRKAA2	addiction	intoxication	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates ethanol induced liver injury through modulation of <strong>AMPK</strong> and Nrf2 related signals in a <b>binge</b> drinking mouse model.
+PRKAA2	drug	alcohol	25703252	The adiponectin SIRT1 <strong>AMPK</strong> pathway in <b>alcoholic</b> fatty liver disease in the rat.
+PRKAA2	addiction	intoxication	25703252	Our previous work showed that <b>binge</b> drinking in the rat induced hepatic steatosis which correlated with reduced expression of AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAA2	drug	alcohol	25703252	The serum Adip and tumor necrosis factor alpha (TNF α) as well as liver Adip receptors (AdipoR1 and AdipoR2) SIRT1, <strong>AMPK</strong>, phosphorylated <strong>AMPK</strong> (p <strong>AMPK</strong>), sterol regulatory element binding proteins (SREBPs), acetyl CoA carboxylase (ACC), LIP 1, lipocalin 2 (LCN2), and serum amyloid A1 were assessed in the rat model where 16 weeks of gavaged <b>alcohol</b> were administered.
+PRKAA2	drug	alcohol	25703252	Our present observations demonstrate that the impaired Adip SIRT1 <strong>AMPK</strong> signaling pathway contributes, at least in part, to the development of <b>alcoholic</b> fatty liver disease in EtOH binge rats.
+PRKAA2	addiction	intoxication	25703252	Our present observations demonstrate that the impaired Adip SIRT1 <strong>AMPK</strong> signaling pathway contributes, at least in part, to the development of alcoholic fatty liver disease in EtOH <b>binge</b> rats.
+PRKAA2	drug	alcohol	24283421	<b>Ethanol</b> intoxication altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (<strong>AMPK</strong>), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (TNF α) expression.
+PRKAA2	addiction	intoxication	24283421	Ethanol <b>intoxication</b> altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (<strong>AMPK</strong>), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (TNF α) expression.
+PRKAA2	drug	alcohol	22563259	These results demonstrated that cilostazol effectively decrease the <b>ethanol</b> mediated TNFα production both in murine macrophage and in liver from binge drinking mice and <strong>AMPK</strong> may be responsible for the inhibition of TNFα production by cilostazol.
+PRKAA2	addiction	intoxication	22563259	These results demonstrated that cilostazol effectively decrease the ethanol mediated TNFα production both in murine macrophage and in liver from <b>binge</b> drinking mice and <strong>AMPK</strong> may be responsible for the inhibition of TNFα production by cilostazol.
+PRKAA2	drug	alcohol	22451512	Deficiency in <strong>AMPK</strong> attenuates <b>ethanol</b> induced cardiac contractile dysfunction through inhibition of autophagosome formation.
+PRKAA2	addiction	intoxication	22451512	<b>Binge</b> drinking often triggers compromised myocardial contractile function while activating AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAA2	drug	alcohol	22451512	Given the role of <strong>AMPK</strong> in the initiation of autophagy through the mammalian target of rapamycin complex 1 (mTORC1) and Unc51 like kinase (ULK1), this study was designed to examine the impact of <strong>AMPK</strong> deficiency on cardiac function and the mechanism involved with a focus on autophagy following an acute <b>ethanol</b> challenge.
+PRKAA2	drug	alcohol	22451512	Wild type (WT) and transgenic mice overexpressing a kinase dead (KD) α2 isoform (K45R mutation) of <strong>AMPK</strong> were challenged with <b>ethanol</b>.
+PRKAA2	drug	alcohol	22451512	<b>Ethanol</b> exposure triggered glucose intolerance and compromised cardiac contraction accompanied by increased phosphorylation of <strong>AMPK</strong> and ACC as well as autophagosome accumulation (increased LC3II and p62), the effects of which were attenuated or mitigated by <strong>AMPK</strong> deficiency or inhibition.
+PRKAA2	drug	alcohol	22451512	<b>Ethanol</b> dampened and stimulated, respectively, the phosphorylation of mTOR and Raptor, the effects of which were abolished by <strong>AMPK</strong> deficiency.
+PRKAA2	drug	alcohol	22451512	ULK1 phosphorylation at Ser(757) and Ser(777) was down regulated and up regulated, respectively, by <b>ethanol</b>, the effect of which was nullified by <strong>AMPK</strong> deficiency or inhibition.
+PRKAA2	drug	alcohol	22451512	Moreover, the <b>ethanol</b> challenge enhanced LC3 puncta in H9c2 cells and promoted cardiac contractile dysfunction, and these effects were ablated by the inhibition of autophagy or <strong>AMPK</strong>.
+PRKAA2	drug	alcohol	22451512	In summary, these data suggest that <b>ethanol</b> exposure may trigger myocardial dysfunction through a mechanism associated with <strong>AMPK</strong> mTORC1 ULK1 mediated autophagy.
+PRKAA2	drug	nicotine	22315316	The aim of this study was to investigate the effect of <b>nicotine</b> on hypothalamic AMP activated protein kinase (<strong>AMPK</strong>) and its effect on energy balance.
+PRKAA2	drug	nicotine	22315316	Here we demonstrate that <b>nicotine</b> induced weight loss is associated with inactivation of hypothalamic <strong>AMPK</strong>, decreased orexigenic signaling in the hypothalamus, increased energy expenditure as a result of increased locomotor activity, increased thermogenesis in brown adipose tissue (BAT), and alterations in fuel substrate utilization.
+PRKAA2	drug	nicotine	22315316	Conversely, <b>nicotine</b> withdrawal or genetic activation of hypothalamic <strong>AMPK</strong> in the ventromedial nucleus of the hypothalamus reversed <b>nicotine</b> induced negative energy balance.
+PRKAA2	addiction	withdrawal	22315316	Conversely, nicotine <b>withdrawal</b> or genetic activation of hypothalamic <strong>AMPK</strong> in the ventromedial nucleus of the hypothalamus reversed nicotine induced negative energy balance.
+PRKAA2	drug	nicotine	22315316	Overall these data demonstrate that the effects of <b>nicotine</b> on energy balance involve specific modulation of the hypothalamic <strong>AMPK</strong> BAT axis.
+PRKAA2	drug	alcohol	22272351	In primary rat alveolar type II cells <b>alcohol</b> and adenosine decreased the abundance of the Na,K ATPase at the basolateral membrane via a mechanism that required activation of the <strong>AMPK</strong>.
+PRKAA2	drug	alcohol	21062897	Moreover, activation of <strong>AMPK</strong>, a known positive modulator of sirtuin activity, prevented the <b>ethanol</b> induced suppression of sirtuin 3 activity and the attendant increase of cyclophilin D acetylation, activity and association with ANT 1.
+PRKAA2	drug	alcohol	21062897	Additionally, <strong>AMPK</strong> reactivation of sirtuin 3 prevented the sensitization to the MPT and the enhancement of cell killing by TNF in cells exposed to <b>ethanol</b>.
+PRKAA2	addiction	sensitization	21062897	Additionally, <strong>AMPK</strong> reactivation of sirtuin 3 prevented the <b>sensitization</b> to the MPT and the enhancement of cell killing by TNF in cells exposed to ethanol.
+PRKAA2	drug	alcohol	20585647	Involvement of <strong>AMPK</strong> in <b>alcohol</b> dehydrogenase accentuated myocardial dysfunction following acute <b>ethanol</b> challenge in mice.
+PRKAA2	drug	alcohol	20585647	This study was designed to examine the impact of cardiac specific overexpression of <b>alcohol</b> dehydrogenase (ADH) on <b>ethanol</b> induced change in cardiac contractile function, intracellular Ca(2+) homeostasis, insulin and AMP dependent kinase (<strong>AMPK</strong>) signaling.
+PRKAA2	drug	alcohol	20585647	<b>Ethanol</b> exposure led to glucose intolerance, elevated plasma insulin, compromised cardiac contractile and intracellular Ca(2+) properties, downregulated protein phosphatase PP2A subunit and PPAR gamma, as well as phosphorylation of <strong>AMPK</strong>, ACC and LKB1, all of which except plasma insulin were overtly accentuated by ADH transgene.
+PRKAA2	drug	alcohol	20585647	In addition, the <strong>AMPK</strong> inhibitor compound C (10 microM) abrogated acute <b>ethanol</b> exposure elicited cardiomyocyte mechanical dysfunction.
+PRKAA2	drug	alcohol	20585647	In summary, these data suggest that the ADH transgene exacerbated acute <b>ethanol</b> toxicity induced myocardial contractile dysfunction, intracellular Ca(2+) mishandling and glucose intolerance, indicating a role of ADH in acute <b>ethanol</b> toxicity induced cardiac dysfunction possibly related to altered cellular fuel <strong>AMPK</strong> signaling cascade.
+PRKAA2	drug	alcohol	19942091	<b>Ethanol</b> treatment dampened phosphorylation of Akt and <strong>AMPK</strong> associated with up regulated PP2A and PP2C, which was abrogated by ALDH2.
+PRKAA2	drug	alcohol	19942091	ALDH2 significantly attenuated <b>ethanol</b> induced decrease in Akt  and <strong>AMPK</strong> stimulated phosphorylation of Foxo3 at Thr32 and Ser413, respectively.
+PRKAA2	drug	alcohol	19942091	Our results suggest that ALDH2 is cardioprotective against acute <b>ethanol</b> toxicity, possibly through inhibition of protein phosphatases, leading to enhanced Akt and <strong>AMPK</strong> activation, and subsequently, inhibition of Foxo3, apoptosis, and mitochondrial dysfunction.
+PRKAA1	drug	alcohol	32113062	Longer periods of <b>ethanol</b> exposure and associated chronic suppression of <strong>AMPK</strong> activity activates regulatory mechanisms, including gene expression, that operate over longer time scales, both in onset and reversal.
+PRKAA1	drug	opioid	31756370	Activation of the <strong>AMPK</strong> pathway inhibits mTOR and p38 MAPK ameliorating neuroinflammation and tolerance induced by <b>morphine</b>.
+PRKAA1	drug	alcohol	31734306	Repeated <b>ethanol</b> exposure influences key enzymes in cholesterol and lipid homeostasis via the <strong>AMPK</strong> pathway in the rat prefrontal cortex.
+PRKAA1	drug	alcohol	31734306	Similarly, the phosphorylation of <strong>AMPK</strong> and the upstream regulators, LKB1 and CaMK4, were transiently increased only in chronically <b>ethanol</b> treated animals.
+PRKAA1	drug	alcohol	31734306	The phosphorylation of TAK1, another upstream kinase of <strong>AMPK</strong>, was increased only from 30 min to 24 h after the chronic treatment with <b>ethanol</b>.
+PRKAA1	drug	alcohol	31734306	This effect seems to be mediated by the <strong>AMPK</strong> system, and may contribute to the long lasting neuroadaptation involved in the development of <b>alcohol</b> dependence.
+PRKAA1	addiction	dependence	31734306	This effect seems to be mediated by the <strong>AMPK</strong> system, and may contribute to the long lasting neuroadaptation involved in the development of alcohol <b>dependence</b>.
+PRKAA1	drug	alcohol	31199934	Behavioral cross sensitization between cocaine and <b>ethanol</b> is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAA1	drug	cocaine	31199934	Behavioral cross sensitization between <b>cocaine</b> and ethanol is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAA1	addiction	sensitization	31199934	Behavioral cross <b>sensitization</b> between cocaine and ethanol is accompanied by parallel changes in the activity of <strong>AMPK</strong> system.
+PRKAA1	drug	alcohol	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross sensitization between cocaine and <b>ethanol</b> in the rat prefrontal cortex and dorsal striatum.
+PRKAA1	drug	cocaine	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross sensitization between <b>cocaine</b> and ethanol in the rat prefrontal cortex and dorsal striatum.
+PRKAA1	addiction	sensitization	31199934	Thus, the present study examined <strong>AMPK</strong> signaling following reciprocal cross <b>sensitization</b> between cocaine and ethanol in the rat prefrontal cortex and dorsal striatum.
+PRKAA1	drug	alcohol	31199934	Although the same changes were found for two upstream kinases of <strong>AMPK</strong> (LKB1 and CaMK4), TAK1 responded differently and was not affected by acute challenges from either cocaine or <b>ethanol</b>.
+PRKAA1	drug	cocaine	31199934	Although the same changes were found for two upstream kinases of <strong>AMPK</strong> (LKB1 and CaMK4), TAK1 responded differently and was not affected by acute challenges from either <b>cocaine</b> or ethanol.
+PRKAA1	drug	alcohol	31195351	In addition, PLE obviously suppressed the expression of SREBP1 and enhanced phosphorylation of <strong>AMPK</strong> compared with chronic <b>ethanol</b> administration.
+PRKAA1	drug	alcohol	31195351	AML12 cells were pretreated with different concentrations of PLE for 2 h and then exposed to <b>ethanol</b> for 48 h. PLE suppressed the expression of SREBP1 and enhanced phosphorylation of <strong>AMPK</strong> in AML12 cells exposed to <b>ethanol</b>.
+PRKAA1	drug	alcohol	31195351	<strong>AMPK</strong> interference confirms that PLE downregulation SREBP1 and F4/80 depending on <strong>AMPK</strong> activation in <b>ethanol</b> treated AML12 cells.
+PRKAA1	drug	alcohol	31167126	CD74 knockout attenuates <b>alcohol</b> intake induced cardiac dysfunction through <strong>AMPK</strong> Skp2 mediated regulation of autophagy.
+PRKAA1	drug	alcohol	31167126	<b>Ethanol</b> challenge upregulated autophagy (p < 0.001), promoted <strong>AMPK</strong> phosphorylation and Sirt1 levels (p < 0.003) while suppressing mTOR phosphorylation and Skp2 levels (p < 0.02).
+PRKAA1	drug	alcohol	31167126	Moreover, the CD74 ablation offered beneficial effects against <b>ethanol</b> induced cardiomyocyte dysfunction, and GFP Puncta formation were nullified by the <strong>AMPK</strong> activator AICAR, the Skp2 inhibitor C1 or the Sirt1 activator SRT1720 (p < 0.0001).
+PRKAA1	drug	alcohol	31167126	Taken together, our data revealed that CD74 ablation counteracts acute <b>ethanol</b> challenge induced myocardial dysfunction, inflammation and apoptosis possibly through an <strong>AMPK</strong> mTOR Skp2 mediated regulation of autophagy.
+PRKAA1	drug	alcohol	30836218	While, the PUE+SIL treatment showed the most effective protection, which was associated with reducing <b>alcohol</b> induced hepatic steatosis via upregulating LKB1/<strong>AMPK</strong>/ACC signaling, and inhibiting hepatic inflammation via LPS triggered TLR4 mediated NF κB signaling pathway.
+PRKAA1	drug	cocaine	30788886	Activation of <strong>AMPK</strong> dependent autophagy in the nucleus accumbens opposes <b>cocaine</b> induced behaviors of mice.
+PRKAA1	drug	cocaine	30788886	Here, we reported that D1 receptor  CaMKII <strong>AMPK</strong> FoxO3a signaling pathway was involved in acute <b>cocaine</b> application induced autophagy in the nucleus accumbens (NAc) both in vitro and in vivo.
+PRKAA1	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase <strong>AMPK</strong> AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+PRKAA1	drug	alcohol	30200508	Finally, GN administration promoted hepatic sirtuin1 (SIRT1) AMP activated protein kinase (<strong>AMPK</strong>) signaling in <b>ethanol</b> fed mice.
+PRKAA1	drug	alcohol	30200508	Moreover, GN prevented <b>ethanol</b> mediated reduction in SIRT1 and phosphorylated <strong>AMPK</strong>.
+PRKAA1	drug	opioid	30146703	We examined the effects of chronic treatment of <b>morphine</b> and/or <b>methadone</b> in the presence or absence of metformin with or without <strong>AMPK</strong> inhibitor (dorsomorphin hydrochloride) on levels of nitric oxide and cyclic adenosine monophosphate (cAMP), phosphorylated and dephosphorylated ribosomal protein S6 kinase β 1 (S6K1) and 4E binding protein 1 (4E BP1) in T98G cells.
+PRKAA1	drug	opioid	30146703	Pretreatment of cells with metformin (40 µM) with or without <strong>AMPK</strong> inhibitor (dorsomorphin hydrochloride; 1 µM) before adding of <b>morphine</b> (2.5 µM) or <b>methadone</b> (1 µM) revealed a protective effects on the development of <b>opioid</b> tolerance.
+PRKAA1	drug	alcohol	29906537	Phenolic acid and flavonoid rich fraction of Sasa quelpaertensis Nakai leaves prevent <b>alcohol</b> induced fatty liver through <strong>AMPK</strong> activation.
+PRKAA1	drug	nicotine	29610348	Activation of <strong>AMPK</strong> by metformin improves withdrawal signs precipitated by <b>nicotine</b> withdrawal.
+PRKAA1	addiction	withdrawal	29610348	Activation of <strong>AMPK</strong> by metformin improves <b>withdrawal</b> signs precipitated by nicotine <b>withdrawal</b>.
+PRKAA1	drug	nicotine	29610348	Here we show that the AMP activated protein kinase (<strong>AMPK</strong>) pathway in the hippocampus is activated following chronic <b>nicotine</b> use, an effect that is rapidly reversed by <b>nicotine</b> withdrawal.
+PRKAA1	addiction	withdrawal	29610348	Here we show that the AMP activated protein kinase (<strong>AMPK</strong>) pathway in the hippocampus is activated following chronic nicotine use, an effect that is rapidly reversed by nicotine <b>withdrawal</b>.
+PRKAA1	drug	nicotine	29610348	Increasing pAMPK levels and, consequently, downstream <strong>AMPK</strong> signaling pharmacologically attenuate anxiety like behavior following <b>nicotine</b> withdrawal.
+PRKAA1	addiction	withdrawal	29610348	Increasing pAMPK levels and, consequently, downstream <strong>AMPK</strong> signaling pharmacologically attenuate anxiety like behavior following nicotine <b>withdrawal</b>.
+PRKAA1	addiction	withdrawal	29610348	We show that metformin, a known <strong>AMPK</strong> activator in the periphery, reduces <b>withdrawal</b> symptoms through a mechanism dependent on the presence of the AMPKα subunits within the hippocampus.
+PRKAA1	drug	nicotine	29610348	This study provides evidence of a direct effect of <strong>AMPK</strong> modulation on <b>nicotine</b> withdrawal symptoms and suggests central <strong>AMPK</strong> activation as a therapeutic target for <b>smoking</b> cessation.
+PRKAA1	addiction	withdrawal	29610348	This study provides evidence of a direct effect of <strong>AMPK</strong> modulation on nicotine <b>withdrawal</b> symptoms and suggests central <strong>AMPK</strong> activation as a therapeutic target for smoking cessation.
+PRKAA1	drug	amphetamine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, neuropeptide Y, pro opiomelanocortin, and cocaine  and <b>amphetamine</b> related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (<strong>AMPK</strong>), mechanistic target of rapamycin and cAMP response element binding protein (CREB).
+PRKAA1	drug	cocaine	29427522	We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti related protein, neuropeptide Y, pro opiomelanocortin, and <b>cocaine</b>  and amphetamine related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP activated protein kinase (<strong>AMPK</strong>), mechanistic target of rapamycin and cAMP response element binding protein (CREB).
+PRKAA1	drug	alcohol	29338075	Up regulated SREBP1, down regulated PPARα and phosphorylated acetyl CoA carboxylase caused by acute and chronic <b>alcohol</b> feeding were modulated by gentiopicroside, through the elevation of LKB1 and <strong>AMPK</strong>.
+PRKAA1	drug	alcohol	29338075	Genetic or pharmacological blockade of P2X7 receptors enhanced <strong>AMPK</strong> activity and reduced SREBP1 expression in <b>ethanol</b> treated HepG2 cells.
+PRKAA1	drug	alcohol	29338075	Activation of LKB1/<strong>AMPK</strong> signalling by gentiopicroside was mediated by the P2X7 receptor NLRP3 inflammasome, suggesting the therapeutic value of blocking P2X7 receptors in the treatment of <b>alcoholic</b> hepatosteatosis.
+PRKAA1	drug	alcohol	29091708	Chronic <b>alcohol</b> consumption causes <b>alcohol</b> induced lipogenesis and promotes hepatic injury by preventing the oxidation of hepatocellular fatty acids through the suppression of the activation of AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAA1	drug	alcohol	28847514	Our results demonstrated that endogenous and exogenous n 3 PUFA enrichment ameliorates <b>ethanol</b> stimulated adipose lipolysis by increasing PDE3B activity and reducing cAMP accumulation in adipocyte, which was associated with activation of GPR120 and regulation of Ca2+/CaMKKβ/<strong>AMPK</strong> signaling, resultantly blocking fatty acid trafficking from adipose tissue to the liver, which contributing to ameliorating <b>ethanol</b> induced adipose dysfunction and liver injury.
+PRKAA1	drug	cocaine	28432301	<strong>AMPK</strong> signaling in the nucleus accumbens core mediates cue induced reinstatement of <b>cocaine</b> seeking.
+PRKAA1	addiction	relapse	28432301	<strong>AMPK</strong> signaling in the nucleus accumbens core mediates cue induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+PRKAA1	drug	cocaine	28432301	Here, we investigated the role of <strong>AMPK</strong> activity in the nucleus accumbens (NAc) in relapse to <b>cocaine</b> seeking.
+PRKAA1	addiction	relapse	28432301	Here, we investigated the role of <strong>AMPK</strong> activity in the nucleus accumbens (NAc) in <b>relapse</b> to cocaine <b>seeking</b>.
+PRKAA1	drug	cocaine	28432301	We found that exposure to drug related cues reinstated <b>cocaine</b> seeking behavior and increased <strong>AMPK</strong> and p70s6k phosphorylation in the NAc core but not shell.
+PRKAA1	addiction	relapse	28432301	We found that exposure to drug related cues reinstated cocaine <b>seeking</b> behavior and increased <strong>AMPK</strong> and p70s6k phosphorylation in the NAc core but not shell.
+PRKAA1	drug	cocaine	28432301	Augmenting <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> activator 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide (AICAR) or adenovirus expressing constitutively active subunits of <strong>AMPK</strong> decreased cue induced reinstatement of <b>cocaine</b> seeking and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal regulated kinase 1/2 (ERK1/2) pathways.
+PRKAA1	addiction	relapse	28432301	Augmenting <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> activator 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide (AICAR) or adenovirus expressing constitutively active subunits of <strong>AMPK</strong> decreased cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal regulated kinase 1/2 (ERK1/2) pathways.
+PRKAA1	drug	cocaine	28432301	In contrast, inhibition of <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> inhibitor compound C or adenovirus expressing dominant negative subunits of <strong>AMPK</strong> increased cue induced reinstatement of <b>cocaine</b> seeking and enhanced mTORC1 and ERK1/2 activity.
+PRKAA1	addiction	relapse	28432301	In contrast, inhibition of <strong>AMPK</strong> activity by intra NAc core infusions of the <strong>AMPK</strong> inhibitor compound C or adenovirus expressing dominant negative subunits of <strong>AMPK</strong> increased cue induced <b>reinstatement</b> of cocaine <b>seeking</b> and enhanced mTORC1 and ERK1/2 activity.
+PRKAA1	drug	cocaine	28432301	The regulation of <strong>AMPK</strong> activity in the NAc shell had no effect on cue induced <b>cocaine</b> seeking.
+PRKAA1	addiction	relapse	28432301	The regulation of <strong>AMPK</strong> activity in the NAc shell had no effect on cue induced cocaine <b>seeking</b>.
+PRKAA1	drug	cocaine	28432301	Altogether, these results indicate that <strong>AMPK</strong> activity in the NAc core is critical for the cue induced reinstatement of <b>cocaine</b> seeking, which may be mediated by mTORC1 and ERK1/2 signaling.
+PRKAA1	addiction	relapse	28432301	Altogether, these results indicate that <strong>AMPK</strong> activity in the NAc core is critical for the cue induced <b>reinstatement</b> of cocaine <b>seeking</b>, which may be mediated by mTORC1 and ERK1/2 signaling.
+PRKAA1	drug	alcohol	27901267	Binge <b>Alcohol</b> Intake After Hypergravity Stress Sustainably Decreases <strong>AMPK</strong> and Transcription Factors Necessary for Hepatocyte Survival.
+PRKAA1	addiction	intoxication	27901267	<b>Binge</b> Alcohol Intake After Hypergravity Stress Sustainably Decreases <strong>AMPK</strong> and Transcription Factors Necessary for Hepatocyte Survival.
+PRKAA1	drug	alcohol	27901267	This study investigated whether a combination of hypergravity stress and binge <b>alcohol</b> intake has a detrimental effect on AMP activated protein kinase (<strong>AMPK</strong>) and other molecules necessary for hepatocyte survival.
+PRKAA1	addiction	intoxication	27901267	This study investigated whether a combination of hypergravity stress and <b>binge</b> alcohol intake has a detrimental effect on AMP activated protein kinase (<strong>AMPK</strong>) and other molecules necessary for hepatocyte survival.
+PRKAA1	drug	cocaine	27132751	Region specific activation of the <strong>AMPK</strong> system by <b>cocaine</b>: The role of D1 and D2 receptors.
+PRKAA1	drug	cocaine	27132751	Thus, the present study examined whether the sensitizing effects of <b>cocaine</b> could be observed in the <strong>AMPK</strong> system and aimed to determine whether these effects were mediated by dopamine (DA) D1 or D2 receptors.
+PRKAA1	drug	cocaine	27132751	In the drug naïve state, acute treatment with <b>cocaine</b> produced an increase in locomotor activity and increased <strong>AMPK</strong> phosphorylation in the frontal cortex but decreased it in the dorsal striatum.
+PRKAA1	drug	cocaine	27132751	In the drug sensitized state (following repeated treatment), the behavioral responsiveness to <b>cocaine</b> was augmented and accompanied by alterations in <strong>AMPK</strong> activity.
+PRKAA1	drug	cocaine	27132751	The opposite effects induced by <b>cocaine</b> in the <strong>AMPK</strong> system in the dorsal striatum and frontal cortex may be explained by the differential activations of DA D1 and D2 receptors in these brain regions.
+PRKAA1	drug	alcohol	26776965	Betulin alleviated <b>ethanol</b> induced <b>alcoholic</b> liver injury via SIRT1/<strong>AMPK</strong> signaling pathway.
+PRKAA1	drug	alcohol	26776965	Betulin suppressed the expression of sterol regulatory element binding protein 1 (SREBP 1), and genetic deletion of <strong>AMPK</strong> blocked the effect of betulin on SREBP 1 in <b>ethanol</b> treated LX 2 cells.
+PRKAA1	drug	alcohol	26776965	In vivo, betulin attenuated the increases in serum aminotransferase and triglyceride levels in the mice fed with chronic binge <b>ethanol</b>, while significantly inhibited SREBP 1 expression and activated LKB1 <strong>AMPK</strong> phosphorylation.
+PRKAA1	addiction	intoxication	26776965	In vivo, betulin attenuated the increases in serum aminotransferase and triglyceride levels in the mice fed with chronic <b>binge</b> ethanol, while significantly inhibited SREBP 1 expression and activated LKB1 <strong>AMPK</strong> phosphorylation.
+PRKAA1	drug	alcohol	26776965	Taken together, betulin alleviates <b>alcoholic</b> liver injury possibly through blocking the regulation of SREBP 1 on fatty acid synthesis and activating SIRT1 LKB1 <strong>AMPK</strong> signaling pathway.
+PRKAA1	drug	opioid	26378398	Activation of adenosine monophosphate activated kinase (<strong>AMPK</strong>) has been associated with the inhibition of inflammatory nociception and the attenuation of <b>morphine</b> antinociceptive tolerance.
+PRKAA1	addiction	withdrawal	26378398	Resveratrol and 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide, the <strong>AMPK</strong> activators, significantly attenuated bone cancer pain in rats with tumor cell implantation (TCI; threshold of mechanical <b>withdrawal</b>, resveratrol vs. vehicle: 10.1 ± 0.56 vs. 4.1 ± 0.37; 5 amino 1 β D ribofuranosyl imidazole 4 carboxamide vs. vehicle: 8.2 ± 0.17 vs. 4.1 ± 0.37, mean ± SEM); these effects were reversed by the <strong>AMPK</strong> inhibitor compound C (compound C vs. resveratrol: 6.2 ± 1.35 vs. 10.1 ± 0.56, mean ± SEM).
+PRKAA1	drug	alcohol	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates <b>ethanol</b> induced liver injury through modulation of <strong>AMPK</strong> and Nrf2 related signals in a binge drinking mouse model.
+PRKAA1	addiction	intoxication	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates ethanol induced liver injury through modulation of <strong>AMPK</strong> and Nrf2 related signals in a <b>binge</b> drinking mouse model.
+PRKAA1	drug	alcohol	25703252	The adiponectin SIRT1 <strong>AMPK</strong> pathway in <b>alcoholic</b> fatty liver disease in the rat.
+PRKAA1	addiction	intoxication	25703252	Our previous work showed that <b>binge</b> drinking in the rat induced hepatic steatosis which correlated with reduced expression of AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAA1	drug	alcohol	25703252	The serum Adip and tumor necrosis factor alpha (TNF α) as well as liver Adip receptors (AdipoR1 and AdipoR2) SIRT1, <strong>AMPK</strong>, phosphorylated <strong>AMPK</strong> (p <strong>AMPK</strong>), sterol regulatory element binding proteins (SREBPs), acetyl CoA carboxylase (ACC), LIP 1, lipocalin 2 (LCN2), and serum amyloid A1 were assessed in the rat model where 16 weeks of gavaged <b>alcohol</b> were administered.
+PRKAA1	drug	alcohol	25703252	Our present observations demonstrate that the impaired Adip SIRT1 <strong>AMPK</strong> signaling pathway contributes, at least in part, to the development of <b>alcoholic</b> fatty liver disease in EtOH binge rats.
+PRKAA1	addiction	intoxication	25703252	Our present observations demonstrate that the impaired Adip SIRT1 <strong>AMPK</strong> signaling pathway contributes, at least in part, to the development of alcoholic fatty liver disease in EtOH <b>binge</b> rats.
+PRKAA1	drug	alcohol	24283421	<b>Ethanol</b> intoxication altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (<strong>AMPK</strong>), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (TNF α) expression.
+PRKAA1	addiction	intoxication	24283421	Ethanol <b>intoxication</b> altered liver metabolism as evidenced by a decrease in peroxisome proliferator activated receptor (PPARα), AMP dependent protein kinase (<strong>AMPK</strong>), and nuclear factor kappa B cells (NFκB) and by an increase in tumor necrosis factor (TNF α) expression.
+PRKAA1	drug	alcohol	22563259	These results demonstrated that cilostazol effectively decrease the <b>ethanol</b> mediated TNFα production both in murine macrophage and in liver from binge drinking mice and <strong>AMPK</strong> may be responsible for the inhibition of TNFα production by cilostazol.
+PRKAA1	addiction	intoxication	22563259	These results demonstrated that cilostazol effectively decrease the ethanol mediated TNFα production both in murine macrophage and in liver from <b>binge</b> drinking mice and <strong>AMPK</strong> may be responsible for the inhibition of TNFα production by cilostazol.
+PRKAA1	drug	alcohol	22451512	Deficiency in <strong>AMPK</strong> attenuates <b>ethanol</b> induced cardiac contractile dysfunction through inhibition of autophagosome formation.
+PRKAA1	addiction	intoxication	22451512	<b>Binge</b> drinking often triggers compromised myocardial contractile function while activating AMP activated protein kinase (<strong>AMPK</strong>).
+PRKAA1	drug	alcohol	22451512	Given the role of <strong>AMPK</strong> in the initiation of autophagy through the mammalian target of rapamycin complex 1 (mTORC1) and Unc51 like kinase (ULK1), this study was designed to examine the impact of <strong>AMPK</strong> deficiency on cardiac function and the mechanism involved with a focus on autophagy following an acute <b>ethanol</b> challenge.
+PRKAA1	drug	alcohol	22451512	Wild type (WT) and transgenic mice overexpressing a kinase dead (KD) α2 isoform (K45R mutation) of <strong>AMPK</strong> were challenged with <b>ethanol</b>.
+PRKAA1	drug	alcohol	22451512	<b>Ethanol</b> exposure triggered glucose intolerance and compromised cardiac contraction accompanied by increased phosphorylation of <strong>AMPK</strong> and ACC as well as autophagosome accumulation (increased LC3II and p62), the effects of which were attenuated or mitigated by <strong>AMPK</strong> deficiency or inhibition.
+PRKAA1	drug	alcohol	22451512	<b>Ethanol</b> dampened and stimulated, respectively, the phosphorylation of mTOR and Raptor, the effects of which were abolished by <strong>AMPK</strong> deficiency.
+PRKAA1	drug	alcohol	22451512	ULK1 phosphorylation at Ser(757) and Ser(777) was down regulated and up regulated, respectively, by <b>ethanol</b>, the effect of which was nullified by <strong>AMPK</strong> deficiency or inhibition.
+PRKAA1	drug	alcohol	22451512	Moreover, the <b>ethanol</b> challenge enhanced LC3 puncta in H9c2 cells and promoted cardiac contractile dysfunction, and these effects were ablated by the inhibition of autophagy or <strong>AMPK</strong>.
+PRKAA1	drug	alcohol	22451512	In summary, these data suggest that <b>ethanol</b> exposure may trigger myocardial dysfunction through a mechanism associated with <strong>AMPK</strong> mTORC1 ULK1 mediated autophagy.
+PRKAA1	drug	nicotine	22315316	The aim of this study was to investigate the effect of <b>nicotine</b> on hypothalamic AMP activated protein kinase (<strong>AMPK</strong>) and its effect on energy balance.
+PRKAA1	drug	nicotine	22315316	Here we demonstrate that <b>nicotine</b> induced weight loss is associated with inactivation of hypothalamic <strong>AMPK</strong>, decreased orexigenic signaling in the hypothalamus, increased energy expenditure as a result of increased locomotor activity, increased thermogenesis in brown adipose tissue (BAT), and alterations in fuel substrate utilization.
+PRKAA1	drug	nicotine	22315316	Conversely, <b>nicotine</b> withdrawal or genetic activation of hypothalamic <strong>AMPK</strong> in the ventromedial nucleus of the hypothalamus reversed <b>nicotine</b> induced negative energy balance.
+PRKAA1	addiction	withdrawal	22315316	Conversely, nicotine <b>withdrawal</b> or genetic activation of hypothalamic <strong>AMPK</strong> in the ventromedial nucleus of the hypothalamus reversed nicotine induced negative energy balance.
+PRKAA1	drug	nicotine	22315316	Overall these data demonstrate that the effects of <b>nicotine</b> on energy balance involve specific modulation of the hypothalamic <strong>AMPK</strong> BAT axis.
+PRKAA1	drug	alcohol	22272351	In primary rat alveolar type II cells <b>alcohol</b> and adenosine decreased the abundance of the Na,K ATPase at the basolateral membrane via a mechanism that required activation of the <strong>AMPK</strong>.
+PRKAA1	drug	alcohol	21062897	Moreover, activation of <strong>AMPK</strong>, a known positive modulator of sirtuin activity, prevented the <b>ethanol</b> induced suppression of sirtuin 3 activity and the attendant increase of cyclophilin D acetylation, activity and association with ANT 1.
+PRKAA1	drug	alcohol	21062897	Additionally, <strong>AMPK</strong> reactivation of sirtuin 3 prevented the sensitization to the MPT and the enhancement of cell killing by TNF in cells exposed to <b>ethanol</b>.
+PRKAA1	addiction	sensitization	21062897	Additionally, <strong>AMPK</strong> reactivation of sirtuin 3 prevented the <b>sensitization</b> to the MPT and the enhancement of cell killing by TNF in cells exposed to ethanol.
+PRKAA1	drug	alcohol	20585647	Involvement of <strong>AMPK</strong> in <b>alcohol</b> dehydrogenase accentuated myocardial dysfunction following acute <b>ethanol</b> challenge in mice.
+PRKAA1	drug	alcohol	20585647	This study was designed to examine the impact of cardiac specific overexpression of <b>alcohol</b> dehydrogenase (ADH) on <b>ethanol</b> induced change in cardiac contractile function, intracellular Ca(2+) homeostasis, insulin and AMP dependent kinase (<strong>AMPK</strong>) signaling.
+PRKAA1	drug	alcohol	20585647	<b>Ethanol</b> exposure led to glucose intolerance, elevated plasma insulin, compromised cardiac contractile and intracellular Ca(2+) properties, downregulated protein phosphatase PP2A subunit and PPAR gamma, as well as phosphorylation of <strong>AMPK</strong>, ACC and LKB1, all of which except plasma insulin were overtly accentuated by ADH transgene.
+PRKAA1	drug	alcohol	20585647	In addition, the <strong>AMPK</strong> inhibitor compound C (10 microM) abrogated acute <b>ethanol</b> exposure elicited cardiomyocyte mechanical dysfunction.
+PRKAA1	drug	alcohol	20585647	In summary, these data suggest that the ADH transgene exacerbated acute <b>ethanol</b> toxicity induced myocardial contractile dysfunction, intracellular Ca(2+) mishandling and glucose intolerance, indicating a role of ADH in acute <b>ethanol</b> toxicity induced cardiac dysfunction possibly related to altered cellular fuel <strong>AMPK</strong> signaling cascade.
+PRKAA1	drug	alcohol	19942091	<b>Ethanol</b> treatment dampened phosphorylation of Akt and <strong>AMPK</strong> associated with up regulated PP2A and PP2C, which was abrogated by ALDH2.
+PRKAA1	drug	alcohol	19942091	ALDH2 significantly attenuated <b>ethanol</b> induced decrease in Akt  and <strong>AMPK</strong> stimulated phosphorylation of Foxo3 at Thr32 and Ser413, respectively.
+PRKAA1	drug	alcohol	19942091	Our results suggest that ALDH2 is cardioprotective against acute <b>ethanol</b> toxicity, possibly through inhibition of protein phosphatases, leading to enhanced Akt and <strong>AMPK</strong> activation, and subsequently, inhibition of Foxo3, apoptosis, and mitochondrial dysfunction.
+PUM3	addiction	sensitization	31437488	We observed protective associations for vitamin D (odds ratio [OR], 0.69 [95% CI, 0.53 0.89] for allergic rhinitis), the sum of the n 3 PUFAs eicosapentaenoic acid and docosahexaenoic acid (OR, 0.81 [95% CI, 0.66 0.99] for current asthma), and the n 3 <strong>PUFA</strong> α linolenic acid (OR, 0.78 [95% CI, 0.64 0.95] for allergen <b>sensitization</b> and OR, 0.80 [95% CI 0.65 0.99] for current asthma).
+PUM3	drug	opioid	31416242	Using the self directed intake model, we characterize the observed profile of <b>opioid</b> use and demonstrate that an n 3 <strong>PUFA</strong> enriched diet ameliorates <b>oxycodone</b> seeking behaviors in the absence of drug availability and reduces anxiety.
+PUM3	addiction	relapse	31416242	Using the self directed intake model, we characterize the observed profile of opioid use and demonstrate that an n 3 <strong>PUFA</strong> enriched diet ameliorates oxycodone <b>seeking</b> behaviors in the absence of drug availability and reduces anxiety.
+PUM3	drug	opioid	31416242	Guided by the major role gut microbiota have on brain function, neuropathology, and anxiety, we profile the microbiome composition and the effects of chronic <b>opioid</b> exposure and n 3 <strong>PUFA</strong> supplementation.
+PUM3	drug	opioid	31416242	We demonstrate that the withdrawal of <b>opioids</b> led to a significant depletion in specific microbiota genera, whereas n 3 <strong>PUFA</strong> supplementation increased microbial richness, phylogenetic diversity, and evenness.
+PUM3	addiction	withdrawal	31416242	We demonstrate that the <b>withdrawal</b> of opioids led to a significant depletion in specific microbiota genera, whereas n 3 <strong>PUFA</strong> supplementation increased microbial richness, phylogenetic diversity, and evenness.
+PUM3	drug	amphetamine	30951972	Here, we assessed the influence of fish oil (FO), which is rich in n 3 <strong>PUFA</strong>, on withdrawal and relapse symptoms following re exposure to <b>AMPH</b>.
+PUM3	addiction	relapse	30951972	Here, we assessed the influence of fish oil (FO), which is rich in n 3 <strong>PUFA</strong>, on withdrawal and <b>relapse</b> symptoms following re exposure to AMPH.
+PUM3	addiction	withdrawal	30951972	Here, we assessed the influence of fish oil (FO), which is rich in n 3 <strong>PUFA</strong>, on <b>withdrawal</b> and relapse symptoms following re exposure to AMPH.
+PUM3	drug	opioid	30898663	Rats fed with MBD (chow plus 20% soybean  and fish oil  n 6/n 3 <strong>PUFA</strong> 1:1) or WBD (WBD  PO or WBD IF: chow plus 20% of palm oil or interesterified fat, respectively; high n 6/n 3 <strong>PUFA</strong> ratio) were exposed to <b>morphine</b> in conditioned place preference (CPP) paradigm.
+PUM3	addiction	reward	30898663	Rats fed with MBD (chow plus 20% soybean  and fish oil  n 6/n 3 <strong>PUFA</strong> 1:1) or WBD (WBD  PO or WBD IF: chow plus 20% of palm oil or interesterified fat, respectively; high n 6/n 3 <strong>PUFA</strong> ratio) were exposed to morphine in conditioned place preference (<b>CPP</b>) paradigm.
+PUM3	drug	alcohol	28847514	The impacts of omega 3 polyunsaturated fatty acids (n 3 <strong>PUFA</strong>) on <b>ethanol</b> induced fatty liver are well documented.
+PUM3	drug	alcohol	28847514	However, the role of n 3 <strong>PUFA</strong> in <b>ethanol</b> induced adipose lipolysis has not been sufficiently addressed.
+PUM3	drug	alcohol	28847514	In this study, the fat 1 transgenic mice that synthesizes endogenous n 3 from n 6 <strong>PUFA</strong> and their wild type littermates with an exogenous n 3 <strong>PUFA</strong> enriched diet were subjected to a chronic <b>ethanol</b> feeding plus a single binge as model to induce liver injury with adipose lipolysis.
+PUM3	addiction	intoxication	28847514	In this study, the fat 1 transgenic mice that synthesizes endogenous n 3 from n 6 <strong>PUFA</strong> and their wild type littermates with an exogenous n 3 <strong>PUFA</strong> enriched diet were subjected to a chronic ethanol feeding plus a single <b>binge</b> as model to induce liver injury with adipose lipolysis.
+PUM3	drug	alcohol	28847514	Our results demonstrated that endogenous and exogenous n 3 <strong>PUFA</strong> enrichment ameliorates <b>ethanol</b> stimulated adipose lipolysis by increasing PDE3B activity and reducing cAMP accumulation in adipocyte, which was associated with activation of GPR120 and regulation of Ca2+/CaMKKβ/AMPK signaling, resultantly blocking fatty acid trafficking from adipose tissue to the liver, which contributing to ameliorating <b>ethanol</b> induced adipose dysfunction and liver injury.
+PUM3	drug	alcohol	28847514	Our findings identify that endogenous and exogenous n 3 <strong>PUFA</strong> enrichment ameliorated <b>alcoholic</b> liver injury by activation of GPR120 to suppress <b>ethanol</b> stimulated adipose lipolysis, which provides the new insight to the hepatoprotective effect of n 3 <strong>PUFA</strong> against <b>alcoholic</b> liver disease.
+PUM3	drug	opioid	28380057	We used an 8 week regimen of n 3 <strong>PUFA</strong> supplementation followed by 8 days of <b>morphine</b> in the presence of this diet.
+PUM3	drug	opioid	28380057	Analysis of the D2 striatal connectome by a retrogradely transported pseudorabies virus showed that n 3 <strong>PUFA</strong> supplementation reversed the effect of chronic <b>morphine</b> on the innervation of D2 neurons by the dorsomedial prefontal and piriform cortices.
+PUM3	drug	nicotine	28126360	IL 6 was weakly inverse associated with omega 6 <strong>PUFA</strong>, and highly increased in <b>nicotine</b> users.
+PUM3	drug	nicotine	27004534	The aim of this study was to evaluate the relationship between omega 3 intake and <b>tobacco</b> <b>smoking</b>, taking into account the qualitative differences in dietary intake between <b>smokers</b> and non <b>smokers</b>, the amount of the ingested <strong>PUFA</strong> and their red blood (RBC) contents.
+PUM3	addiction	sensitization	26937141	Furthermore, a high fat diet increased but <strong>PUFA</strong> enriched diet decreased <b>sensitization</b> to LPS induced hepatic NLRP3 inflammasome activation in vivo.
+PUM3	drug	amphetamine	25290576	Cortical PC was positively correlated with n 6/n 3 <strong>PUFA</strong> ratio, locomotion and anxiety like behavior, and hippocampal PC was positively correlated with <b>AMPH</b> preference, reinforcing connections between oxidative damage and <b>AMPH</b> induced preference/abstinence behaviors.
+PUM3	addiction	reward	25290576	Cortical PC was positively correlated with n 6/n 3 <strong>PUFA</strong> ratio, locomotion and anxiety like behavior, and hippocampal PC was positively correlated with AMPH preference, <b>reinforcing</b> connections between oxidative damage and AMPH induced preference/abstinence behaviors.
+PUM3	addiction	addiction	25290576	As brain incorporation of trans and n 6 <strong>PUFA</strong> modifies its physiological functions, it may facilitate drug <b>addiction</b>.
+PUM3	drug	nicotine	24899596	Although stress is well linked to <b>smoking</b> urges and behavior, no research to date has examined the effects of <strong>PUFA</strong> supplementation on <b>tobacco</b> craving.
+PUM3	addiction	relapse	24899596	Although stress is well linked to smoking urges and behavior, no research to date has examined the effects of <strong>PUFA</strong> supplementation on tobacco <b>craving</b>.
+PUM3	drug	nicotine	24899596	This is the first study demonstrating that omega 3 <strong>PUFA</strong> supplementation reduces <b>tobacco</b> craving in regular <b>smokers</b>, compared to placebo treatment.
+PUM3	addiction	relapse	24899596	This is the first study demonstrating that omega 3 <strong>PUFA</strong> supplementation reduces tobacco <b>craving</b> in regular smokers, compared to placebo treatment.
+PUM3	drug	alcohol	24706101	Effect of wheatgrass on membrane fatty acid composition during hepatotoxicity induced by <b>alcohol</b> and heated <strong>PUFA</strong>.
+PUM3	drug	alcohol	24706101	Fried food items prepared with repeatedly heated polyunsaturated fatty acid (<strong>PUFA</strong>) exacerbate the disturbances induced by <b>alcohol</b>.
+PUM3	drug	alcohol	24706101	The present study was undertaken to evaluate the efficacy of WG on preserving membrane integrity in liver damage induced by <b>alcohol</b> and heated <strong>PUFA</strong> (ΔPUFA).The rats were divided into four groups.
+PUM3	drug	opioid	23684444	We found that omega 3 <strong>PUFA</strong> treatment significantly decreased acetic acid induced abdominal contortions as well as the first and second phases of the formalin test, which were reversed by <b>naloxone</b>.
+PUM3	drug	alcohol	19878718	<b>Ethanol</b> withdrawal increases lipid peroxidation of the polyunsaturated fatty acid (<strong>PUFA</strong>) docosahexaenoate (22:6; n 3) in the CNS.
+PUM3	addiction	withdrawal	19878718	Ethanol <b>withdrawal</b> increases lipid peroxidation of the polyunsaturated fatty acid (<strong>PUFA</strong>) docosahexaenoate (22:6; n 3) in the CNS.
+PUM3	drug	alcohol	19406265	Long chain n 3 <strong>PUFA</strong> intake was inversely associated with plasma concentrations of interleukin 6 (p = 0.01) and matrix metalloproteinase 3 (p = 0.03) independent of age, body mass index, physical activity, smoking, <b>alcohol</b> consumption, and dietary variables.
+PUM3	drug	nicotine	19406265	Long chain n 3 <strong>PUFA</strong> intake was inversely associated with plasma concentrations of interleukin 6 (p = 0.01) and matrix metalloproteinase 3 (p = 0.03) independent of age, body mass index, physical activity, <b>smoking</b>, alcohol consumption, and dietary variables.
+PUM3	drug	alcohol	20021087	Protective Role of a Novel Curcuminoid on <b>Alcohol</b> and <strong>PUFA</strong> Induced Hyperlipidemia.
+PUM3	drug	alcohol	20021087	The results showed that the levels of cholesterol, TGs, and FFAs were increased significantly in <b>alcohol</b>, thermally oxidized sunflower oil (Delta <strong>PUFA</strong>), and <b>alcohol</b> + Delta PUFAs treated groups.
+PUM3	drug	alcohol	20021087	The phospholipid (PL) levels, which were decreased in the liver and kidney and increased in the heart in the <b>alcohol</b>, Delta <strong>PUFA</strong>, and <b>alcohol</b> + Delta <strong>PUFA</strong> groups, were positively modulated by treatment with synthetic curcuminoid (CA).
+PUM3	drug	alcohol	20021087	From the results obtained, we could conclude that the synthetic curcuminoid effectively protects the system against <b>alcohol</b> and Delta <strong>PUFA</strong> induced hyperlipidemia and may become an effective therapeutic agent for the treatment of hyperlipidemia.
+PUM3	drug	alcohol	15548339	Cluster 3 (<b>Alcohol</b> & Convenience Foods) had the highest intakes of <b>alcohol</b>, protein, cholesterol, vitamin B(12), vitamin B(6), folate, iron, phosphorus, selenium and zinc, and the lowest intakes of <strong>PUFA</strong>, vitamin A and antioxidant vitamins (vitamins C and E).
+PUM3	drug	alcohol	15381826	Influence of ferulic acid on circulatory prooxidant antioxidant status during <b>alcohol</b> and <strong>PUFA</strong> induced toxicity.
+PUM3	drug	alcohol	15381826	<b>Alcohol</b> related disabilities are more pronounced when taken along with diet rich in polyunsaturated fatty acid (<strong>PUFA</strong>).
+PUM3	drug	alcohol	15381826	The present work aims at analysing the protective role of ferulic acid (FA), a naturally occurring nutritional component on <b>alcohol</b> and <strong>PUFA</strong> induced oxidative stress.
+PUM3	drug	alcohol	15381826	The results showed that the levels of oxidative markers; thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP) and levels of copper (Cu) and ferritin were increased significantly in plasma of <b>alcohol</b>, thermally oxidised <strong>PUFA</strong> (DeltaPUFA) and <b>alcohol</b> + DeltaPUFA groups, which were decreased significantly on treatment with both the doses of ferulic acid.
+PUM3	drug	alcohol	15381826	Thus from the results obtained, we conclude that FA effectively protects the system against <b>alcohol</b> and <strong>PUFA</strong> induced oxidative stress.
+PUM3	drug	cocaine	14500111	In this study, we explored the possibility that the relapse rates of <b>cocaine</b> addicts discharged after a period of detoxification on an inpatient unit would be associated with their <strong>PUFA</strong> status.
+PUM3	addiction	relapse	14500111	In this study, we explored the possibility that the <b>relapse</b> rates of cocaine addicts discharged after a period of detoxification on an inpatient unit would be associated with their <strong>PUFA</strong> status.
+PUM3	drug	cocaine	14500111	In conclusion, low <strong>PUFA</strong> status at baseline was a better predictor of relapse than <b>cocaine</b> use, sociodemographic or clinical parameters.
+PUM3	addiction	relapse	14500111	In conclusion, low <strong>PUFA</strong> status at baseline was a better predictor of <b>relapse</b> than cocaine use, sociodemographic or clinical parameters.
+PUM3	drug	cocaine	14500111	These data suggest, but do not prove, the existence of a causal relationship between n 6 or n 3 status and relapse vulnerability in <b>cocaine</b> addicts, and provide a rationale for the exploration of possible relationships between relapse to addictive disorders and <strong>PUFA</strong> status in observational and interventional trials.
+PUM3	addiction	addiction	14500111	These data suggest, but do not prove, the existence of a causal relationship between n 6 or n 3 status and relapse vulnerability in cocaine addicts, and provide a rationale for the exploration of possible relationships between relapse to <b>addictive</b> disorders and <strong>PUFA</strong> status in observational and interventional trials.
+PUM3	addiction	relapse	14500111	These data suggest, but do not prove, the existence of a causal relationship between n 6 or n 3 status and <b>relapse</b> vulnerability in cocaine addicts, and provide a rationale for the exploration of possible relationships between <b>relapse</b> to addictive disorders and <strong>PUFA</strong> status in observational and interventional trials.
+PUM3	drug	alcohol	11744800	A significance of <b>alcohol</b> drinking, use of vitamin supplements, consumption of raw eggs and intake of nutrients other than n 6 <strong>PUFA</strong> and calcium, though previously suggested, was not shown in the present study.
+PUM3	drug	alcohol	11505055	Polyunsaturated fatty acids (<strong>PUFA</strong>) play a major role in membrane structures that are modified during <b>alcoholism</b>.
+PUM3	drug	alcohol	11505055	<b>Alcohol</b> has been related to hypertension and to alterations in liver <strong>PUFA</strong> metabolism.
+PUM3	drug	alcohol	11505055	We investigated the effects of <b>ethanol</b> on <strong>PUFA</strong> biogenesis in hepatocytes of Wistar Kyoto (WKY) rats and Spontaneously Hypertensive Rats (SHR).
+PUM3	drug	alcohol	11505055	Isolated hepatocytes from male normotensive Wistar Kyoto (WKY) rats and SHR were incubated for 60 min in the presence of labeled linoleic acid and DGLA, which are precursors of the limiting desaturation steps of <strong>PUFA</strong> biosynthesis, into a medium containing different concentrations of <b>ethanol</b>.
+PUM3	drug	alcohol	11505055	First, the hepatic biogenesis of <strong>PUFA</strong> is dependent on the level of <b>ethanol</b> in the incubation medium.
+PUM3	drug	alcohol	11505055	Fourth, in the presence of <b>ethanol</b>, the biogenesis of <strong>PUFA</strong> was altered in isolated hepatocytes from SHR that were fed the diet supplemented with n 3 <strong>PUFA</strong>, particularly via an inhibition of Delta5 desaturation.
+PUM3	drug	alcohol	11505055	Our study showed that hepatocyte <strong>PUFA</strong> biogenesis is dependent on <b>ethanol</b> concentration.
+PUM3	drug	alcohol	11505055	<b>Ethanol</b> strongly inhibits the synthesis of <strong>PUFA</strong> in hepatocytes from SHR, which can explain the deficit of prostaglandin precursors observed in cardiovascular diseases linked to <b>ethanol</b> intoxication.
+PUM3	addiction	intoxication	11505055	Ethanol strongly inhibits the synthesis of <strong>PUFA</strong> in hepatocytes from SHR, which can explain the deficit of prostaglandin precursors observed in cardiovascular diseases linked to ethanol <b>intoxication</b>.
+PUM3	drug	alcohol	11303463	For absolute nutrient values, intakes of protein, CHO, total fat, <strong>PUFA</strong>, thiamin, iron, dietary fibre and <b>alcohol</b> were not significantly different between the FAQ and FR, and Pearson's correlation coefficients ranged from 0.28 for protein to 0.88 for total fat.
+PUM3	drug	alcohol	27406018	Animals on <b>ethanol</b> (EtOH) containing diets (BASE EtOH and <strong>PUFA</strong> EtOH) experienced eight intermittent <b>ethanol</b> withdrawal periods during the three month exposure period.
+PUM3	addiction	withdrawal	27406018	Animals on ethanol (EtOH) containing diets (BASE EtOH and <strong>PUFA</strong> EtOH) experienced eight intermittent ethanol <b>withdrawal</b> periods during the three month exposure period.
+PUM3	drug	alcohol	27406018	Long chain <strong>PUFA</strong>, at 1.0 en%, could generally not prevent the neurotransmitter lowering effect of <b>alcohol</b>, but it led to an elevation of these levels in <strong>PUFA</strong> animals compared with BASE.
+PUM3	drug	alcohol	8512244	After adjustment for age, sex, and occupational group, smokers had a substantially higher saturated fat (SFA) intake and much lower polyunsaturated fat (<strong>PUFA</strong>), principally due to a lower linoleic acid (LA) intake, resulting in a lower P:S ratio compared with never smokers, and these dietary differences remained after adjustment for <b>alcohol</b> consumption, BMI, and energy intake.
+PUM3	drug	nicotine	8512244	After adjustment for age, sex, and occupational group, <b>smokers</b> had a substantially higher saturated fat (SFA) intake and much lower polyunsaturated fat (<strong>PUFA</strong>), principally due to a lower linoleic acid (LA) intake, resulting in a lower P:S ratio compared with never <b>smokers</b>, and these dietary differences remained after adjustment for alcohol consumption, BMI, and energy intake.
+PUM3	drug	nicotine	8512244	<b>Smokers</b> also had different food choices obtaining more <strong>PUFA</strong> from saturated fat products such as dairy foods, lard, and ordinary margarine, and less from concentrated sources such as <strong>PUFA</strong> margarines and vegetable oils than nonsmokers.
+PUM3	drug	nicotine	8512244	The food choices of cigarette <b>smokers</b> leading to a higher SFA and lower <strong>PUFA</strong> intakes may partly explain their increased risk of coronary heart disease.
+PUM3	drug	alcohol	1449561	The present study addresses the possible interacting effects of dietary n 6/n 3 polyunsaturated fatty acid (<strong>PUFA</strong>) balance and chronic <b>ethanol</b> intoxication on the synaptic membrane responses to <b>ethanol</b> and the development of tolerance in rats.
+PUM3	addiction	intoxication	1449561	The present study addresses the possible interacting effects of dietary n 6/n 3 polyunsaturated fatty acid (<strong>PUFA</strong>) balance and chronic ethanol <b>intoxication</b> on the synaptic membrane responses to ethanol and the development of tolerance in rats.
+PUM3	drug	alcohol	1449561	Furthermore, the n 6/n 3 <strong>PUFA</strong> balance in the synaptic membrane needs to be kept within very narrow limits to allow normal development of the adaptive response to <b>ethanol</b>.
+ITGAM	drug	amphetamine	31775383	RNAseq was utilized to determine expression changes in Fluorescence activated cell sorted (FACS) <strong>CD11b</strong>/c+ cells from the striatum (STR) and prefrontal cortex (PFC) of male Sprague Dawley rats after a <b>methamphetamine</b> (<b>METH</b>) binge dosing regimen.
+ITGAM	addiction	intoxication	31775383	RNAseq was utilized to determine expression changes in Fluorescence activated cell sorted (FACS) <strong>CD11b</strong>/c+ cells from the striatum (STR) and prefrontal cortex (PFC) of male Sprague Dawley rats after a methamphetamine (METH) <b>binge</b> dosing regimen.
+ITGAM	drug	amphetamine	31282647	Systemically administered <b>METH</b> (1 mg/kg) was found to specifically up regulate expression of both <strong>CD11b</strong> (microglial activation marker) and the proinflammatory cytokine interleukin 6 (IL 6) mRNAs in the ventral tegmental area (VTA), but not in either the nucleus accumbens shell (NAc) or prefrontal cortex (PFC).
+ITGAM	drug	alcohol	29274031	Expression of pro inflammatory marker <strong>CD11b</strong> was higher on PD5 in <b>alcohol</b> exposed (AE) females compared to AE males.
+ITGAM	drug	alcohol	28973966	We found that adult rats exposed to an acute binge like level of <b>alcohol</b>, regardless of gestational <b>alcohol</b> exposure, have a robust increase in the expression of Interleukin (IL) 6 within the brain, and a significant decrease in the expression of IL 1β and <strong>CD11b</strong>.
+ITGAM	addiction	intoxication	28973966	We found that adult rats exposed to an acute <b>binge</b> like level of alcohol, regardless of gestational alcohol exposure, have a robust increase in the expression of Interleukin (IL) 6 within the brain, and a significant decrease in the expression of IL 1β and <strong>CD11b</strong>.
+ITGAM	addiction	sensitization	28941277	Chronic EtOH also caused a lasting <b>sensitization</b> of stress induced microglial <strong>CD11b</strong>, but not neuronal c Fos.
+ITGAM	addiction	sensitization	28941277	Chronic EtOH followed by acute stress also increased plasma endotoxin and microglial <strong>CD11b</strong>, suggesting a lasting <b>sensitization</b> to acute stress.
+ITGAM	drug	alcohol	27647531	Adolescent intermittent <b>ethanol</b> treatment increased expression of phosphorylated (activated) NF κB p65 as well as markers of microglial activation (i.e., Iba 1 and <strong>CD11b</strong>) in the adult DRN.
+ITGAM	drug	alcohol	26996510	Furthermore, both <b>alcohol</b> exposed and SI animals had increased levels of pro inflammatory cytokines IL 1β, TNF α, <strong>CD11b</strong>, and CCL4; in addition, CCL4 was significantly increased in <b>alcohol</b> exposed animals compared to SI as well.
+ITGAM	drug	amphetamine	25678251	<b>Methamphetamine</b> using rats had a higher frequency of CD8(+) T cells, but fewer of them produced TNF α. <strong>CD11b</strong>/c and CD200 expression were unchanged.
+ITGAM	addiction	intoxication	25477000	We found that after chronic plus <b>binge</b> feeding of Lieber DeCarli liquid diet in male C57BL/6 mice, type I, but not type II, NKT cells are activated, leading to recruitment of inflammatory Gr 1(high) <strong>CD11b</strong>(+) cells into the liver.
+ITGAM	drug	opioid	23793269	We used fluorescence activated cell sorting of neurons (Thy1+), astrocytes (GLT1+), and microglia (<strong>CD11b</strong>+) from the NAcc for the analysis of cell type specific gene expression following <b>morphine</b> or saline treatment.
+ITGAM	drug	amphetamine	23026442	In allergic rats, the treatment with <b>AMPH</b> exacerbated the lung cell recruitment due increased expression of ICAM 1, PECAM 1 and <strong>Mac 1</strong> in granulocytes and macrophages recovered from bronchoalveolar lavage.
+ITGAM	drug	amphetamine	23026442	Our data strongly indicate that <b>AMPH</b> positively modulates allergic lung inflammation via the increase of ICAM 1, PECAM 1, <strong>Mac 1</strong> and IL 4.
+ITGAM	addiction	withdrawal	22037228	Bilateral paw pressure threshold and paw <b>withdrawal</b> latencies were measured, and the extent of glial activation was dertermined by measuring macrophage antigen complex 1 (<strong>Mac 1</strong>) and glial fibrillary acidic protein (GFAP).
+ITGAM	drug	alcohol	18212642	<b>Alcohol</b> exhibited differing effects on the inflammatory potential of neutrophils in regards to <strong>CD11b</strong> expression, elastase production, and superoxide production.
+ITGAM	drug	alcohol	18090004	<b>Ethanol</b> inhibited this LPS induced upregulation of <strong>CD11b</strong> (p < 0.001).
+ITGAM	drug	alcohol	18090004	Stimulation with IL 8 significantly upregulated <strong>CD11b</strong> expression (5.3 +/  1.7 to 7.5 +/  2.7, p < 0.01) and this IL 8 induced upregulation of <strong>CD11b</strong> was also inhibited by <b>ethanol</b> pretreatment (p < 0.001).
+ITGAM	drug	alcohol	18090004	The impairment of <strong>CD11b</strong> expression on leukocytes suggests that <b>alcohol</b> intake interferes with the migration of leukocytes to sites of inflammation, which may explain, in part, why <b>alcohol</b> intoxication increases susceptibility to infection.
+ITGAM	addiction	intoxication	18090004	The impairment of <strong>CD11b</strong> expression on leukocytes suggests that alcohol intake interferes with the migration of leukocytes to sites of inflammation, which may explain, in part, why alcohol <b>intoxication</b> increases susceptibility to infection.
+ITGAM	drug	alcohol	12488491	Previous studies have shown that T cells from human <b>alcoholics</b> overexpress activation or memory markers such as human leukocyte antigen DR, CD45RO, CD57, and <strong>CD11b</strong> and may have reduced levels of CD62L.
+ITGAM	drug	alcohol	10455517	In LPS plus <b>ethanol</b> treated rats gender differences were noted in terms of adhesion molecule (<strong>CD11b</strong>/c) expression on circulating neutrophils, and cytoskeletal reorganization in blood recruited neutrophils and Kupffer cells.
+ITGAM	drug	alcohol	10371409	In vitro 100 mM <b>ethanol</b> suppressed phagocytosis and <strong>CD11b</strong> adhesion molecule expression by PMNs, regardless of the stage of SIV infection.
+ITGAM	drug	alcohol	10228066	<b>Ethanol</b> also inhibited <strong>CD11b</strong>/c expression on recruited neutrophils and suppressed the phagocytic activity of circulating neutrophils.
+ITGAM	drug	alcohol	10228066	G CSF pretreatment up regulated <strong>CD11b</strong>/c expression on circulating polymorphonuclear leukocytes, augmented the recruitment of neutrophils into the lung, and enhanced the phagocytic activity of circulating and recruited neutrophils in both the absence and presence of acute <b>ethanol</b> intoxication.
+ITGAM	addiction	intoxication	10228066	G CSF pretreatment up regulated <strong>CD11b</strong>/c expression on circulating polymorphonuclear leukocytes, augmented the recruitment of neutrophils into the lung, and enhanced the phagocytic activity of circulating and recruited neutrophils in both the absence and presence of acute ethanol <b>intoxication</b>.
+ITGAM	drug	alcohol	9884149	In order to test this possibility, endotoxin induced neutrophil beta2 integrins <strong>CD11b</strong> and CD18 expression, phagocytosis, and hydrogen peroxide generation were examined in normal and HIV 1 Tat transgenic mice in the absence and presence of <b>ethanol</b> intoxication.
+ITGAM	addiction	intoxication	9884149	In order to test this possibility, endotoxin induced neutrophil beta2 integrins <strong>CD11b</strong> and CD18 expression, phagocytosis, and hydrogen peroxide generation were examined in normal and HIV 1 Tat transgenic mice in the absence and presence of ethanol <b>intoxication</b>.
+ITGAM	drug	alcohol	9884149	<b>Ethanol</b> intoxication inhibited endotoxin induced <strong>CD11b</strong> and CD18 expression in normal mice and totally abolished endotoxin induced <strong>CD11b</strong> and CD18 expression in Tat transgenic mice.
+ITGAM	addiction	intoxication	9884149	Ethanol <b>intoxication</b> inhibited endotoxin induced <strong>CD11b</strong> and CD18 expression in normal mice and totally abolished endotoxin induced <strong>CD11b</strong> and CD18 expression in Tat transgenic mice.
+ITGAM	drug	alcohol	9514298	Acute <b>ethanol</b> intoxication inhibited this endotoxin induced upregulation of <strong>CD11b</strong>/c and CD18 expression on PMNs.
+ITGAM	addiction	intoxication	9514298	Acute ethanol <b>intoxication</b> inhibited this endotoxin induced upregulation of <strong>CD11b</strong>/c and CD18 expression on PMNs.
+ITGAM	drug	alcohol	9514298	G CSF pretreatment enhanced neutrophil phagocytosis, <strong>CD11b</strong>/c and CD18 expression in endotoxin infused rats, and prevented the <b>ethanol</b> induced inhibition of neutrophil CD18 expression and phagocytosis.
+ITGAM	drug	alcohol	9267524	This upregulation of <strong>CD11b</strong>/c expression was abolished by <b>ethanol</b> intoxication.
+ITGAM	addiction	intoxication	9267524	This upregulation of <strong>CD11b</strong>/c expression was abolished by ethanol <b>intoxication</b>.
+ITGAM	drug	alcohol	8865968	Significant gender differences exist in the extent of hepatic PMN infiltration in <b>ethanol</b> plus LPS treated rats, which is paralleled by very similar differences in <strong>CD11b</strong>/c adhesion molecule expression in circulating PMNs and cytokine induced neutrophil chemoattractant generation by hepatocytes and Kupffer cells.
+ITGAM	drug	alcohol	7515214	In other results, the percentage of CD8hi lymphocytes epxressing <strong>CD11b</strong> (beta integrin) is shown to be reciprocal with the percentage expressing L selectin both in normals and <b>alcoholics</b>.
+ITGAM	drug	alcohol	7515214	However, the regression function of <strong>CD11b</strong> vs. L selectin on CD8hi cells is different for the <b>alcoholics</b> than for the normals, indicating an abnormality in the regulation of the expression of these two adhesion markers.
+ITGAM	drug	cocaine	1943440	<b>Cocaine</b> as well as saline injected mice showed a decrease in the percentage of CD4+ CD8+ and <strong>Mac 1</strong>+ cells and an increase in B cells in the spleens of well nourished mice.
+ITGAM	drug	alcohol	3279136	Similarly, resting surface expression of the adhesive glycoprotein <strong>Mac 1</strong> was unaffected by <b>ethanol</b>, but its up regulation induced by fMLP was inhibited by 25.5% at 250 mg of <b>ethanol</b>/dL and by 52.3% at 1000 mg/dL.
+CNR2	drug	cannabinoid	32471216	High Expression of <strong><b>Cannabinoid</b> Receptor 2</strong> on Cytokine Induced Killer Cells and Multiple Myeloma Cells.
+CNR2	drug	cannabinoid	32471216	CBD is known to exert immunomodulatory effects through the activation of <strong><b>cannabinoid</b> receptor 2</strong> (CB2), which is expressed in high levels in the hematopoietic system.
+CNR2	drug	cannabinoid	32093166	Targeting Peripherally Restricted <b>Cannabinoid</b> Receptor 1, <strong><b>Cannabinoid</b> Receptor 2</strong>, and <b>Endocannabinoid</b> Degrading Enzymes for the Treatment of Neuropathic Pain Including Neuropathic Orofacial Pain.
+CNR2	drug	cannabinoid	32057593	In the mPFC and hippocampus, EtOH rats had significantly higher mRNA expression of <b>endocannabinoid</b> signaling (mPFC: Ppara, Dagla, Daglb and Napepld; and hippocampus: <strong>Cnr2</strong>, Dagla and Mgll) and neuroinflammation associated genes (mPFC: Gfap; and hippocampus: Aif1) than in controls.
+CNR2	drug	cannabinoid	31940843	<strong><b>Cannabinoid</b> Receptor 2</strong> Modulates Maturation of Dendritic Cells and Their Capacity to Induce Hapten Induced Contact Hypersensitivity.
+CNR2	drug	alcohol	31245644	We then determined whether there are any pharmacokinetic or pharmacodynamic interactions between BCPO and <b>ethanol</b>, using blood <b>ethanol</b> analysis and pretreatments with the selective <strong>cannabinoid receptor 2</strong> (CB2) antagonist AM630, respectively.
+CNR2	drug	cannabinoid	31245644	We then determined whether there are any pharmacokinetic or pharmacodynamic interactions between BCPO and ethanol, using blood ethanol analysis and pretreatments with the selective <strong><b>cannabinoid</b> receptor 2</strong> (CB2) antagonist AM630, respectively.
+CNR2	drug	cannabinoid	31159897	We highlight the putative role of selective <strong><b>cannabinoid</b> receptor 2</strong> (CB2) agonists in BD and briefly discuss findings which provide a rationale for targeting the ECS to assuage the symptoms of BD.
+CNR2	drug	cannabinoid	30508607	Here we report on the behavioral effects of psychostimulants in DAT <strong>Cnr2</strong> conditional knockout (cKO) mice with selective deletion of type 2 <b>cannabinoid</b> receptors in dopamine neurons.
+CNR2	addiction	sensitization	30508607	There was enhanced psychostimulant induced hyperactivity in DAT <strong>Cnr2</strong> cKO mice, but the psychostimulant induced <b>sensitization</b> was absent in DAT <strong>Cnr2</strong> cKO compared to the WT mice.
+CNR2	drug	amphetamine	30508607	Intriguingly, lower doses of <b>amphetamine</b> reduced locomotor activity of the DAT <strong>Cnr2</strong> cKO mice.
+CNR2	drug	amphetamine	30508607	While cocaine, <b>amphetamine</b> and <b>methamphetamine</b> produced robust conditioned place preference (CPP) in both DAT <strong>Cnr2</strong> cKO and WT mice, nicotine at the dose used induced CPP only in the WT but not in the DAT Cn2 cKO mice.
+CNR2	drug	cocaine	30508607	While <b>cocaine</b>, amphetamine and methamphetamine produced robust conditioned place preference (CPP) in both DAT <strong>Cnr2</strong> cKO and WT mice, nicotine at the dose used induced CPP only in the WT but not in the DAT Cn2 cKO mice.
+CNR2	drug	nicotine	30508607	While cocaine, amphetamine and methamphetamine produced robust conditioned place preference (CPP) in both DAT <strong>Cnr2</strong> cKO and WT mice, <b>nicotine</b> at the dose used induced CPP only in the WT but not in the DAT Cn2 cKO mice.
+CNR2	addiction	reward	30508607	While cocaine, amphetamine and methamphetamine produced robust conditioned place preference (<b>CPP</b>) in both DAT <strong>Cnr2</strong> cKO and WT mice, nicotine at the dose used induced <b>CPP</b> only in the WT but not in the DAT Cn2 cKO mice.
+CNR2	drug	alcohol	30505884	The <b>alcohol</b> preference model was combined with the conditioned place preference paradigm to determine <b>alcohol</b> conditioning and preference following the deletion of CB2 cannabinoid receptors in dopaminergic neurons in the DAT <strong>Cnr2</strong> Cre recombinant conditional knockout (cKO) mice in comparison with the wild type control mice.
+CNR2	drug	cannabinoid	30505884	The alcohol preference model was combined with the conditioned place preference paradigm to determine alcohol conditioning and preference following the deletion of CB2 <b>cannabinoid</b> receptors in dopaminergic neurons in the DAT <strong>Cnr2</strong> Cre recombinant conditional knockout (cKO) mice in comparison with the wild type control mice.
+CNR2	drug	cannabinoid	30504240	AM1710 (3 (1,1 dimethyl heptyl) 1 hydroxy 9 methoxy benzo(c) chromen 6 one), a cannabilactone <strong><b>cannabinoid</b> receptor 2</strong> (CB2) agonist, suppresses chemotherapy induced neuropathic pain in rodents without producing tolerance or unwanted side effects associated with CB1 receptors; however, the signaling profile of AM1710 remains incompletely characterized.
+CNR2	drug	cannabinoid	30500557	A pharmacoinformatic approach on <strong><b>Cannabinoid</b> receptor 2</strong> (CB2) and different small molecules: Homology modelling, molecular docking, MD simulations, drug designing and ADME analysis.
+CNR2	drug	opioid	30063884	By means of real time polymerase chain reaction (PCR), we also analysed relative gene expression of tyrosine hydroxylase (TH) in the ventral tegmental area (VTA), and of mu <b>opioid</b> receptor (OPRM1), CNR1 and <strong>CNR2</strong> in the nucleus accumbens (NAcc).
+CNR2	drug	cannabinoid	29778010	In addition, <strong><b>cannabinoid</b> receptor 2</strong> has been found expressed also in the central nervous system at postsynaptic level.
+CNR2	drug	cannabinoid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the opioid μ receptor (Oprm1), <b>cannabinoid</b> CB1 receptor (Cnr1) and CB2 receptor (<strong>Cnr2</strong>) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+CNR2	drug	opioid	29624642	Furthermore, gene expression changes in TH in the ventral tegmental area, and in the <b>opioid</b> μ receptor (Oprm1), cannabinoid CB1 receptor (Cnr1) and CB2 receptor (<strong>Cnr2</strong>) in the nucleus accumbens, were also evaluated using the real time PCR technique.
+CNR2	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (Cnr1, <strong>Cnr2</strong>, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and TRPV1 sensitizing kinases (Mapk3, Mapk14, Prkcg, and Prkaca).
+CNR2	drug	cannabinoid	28879802	Anti nociceptive interactions between opioids and a <strong><b>cannabinoid</b> receptor 2</strong> agonist in inflammatory pain.
+CNR2	drug	opioid	28879802	Anti nociceptive interactions between <b>opioids</b> and a <strong>cannabinoid receptor 2</strong> agonist in inflammatory pain.
+CNR2	drug	cannabinoid	28592614	GW405833, widely accepted as a <strong><b>cannabinoid</b> receptor 2</strong> (CB2) agonist, suppresses pathologic pain in preclinical models without the unwanted central side effects of <b>cannabinoid</b> receptor 1 (CB1) agonists; however, recent in vitro studies have suggested that GW405833 may also behave as a noncompetitive CB1 antagonist, suggesting that its pharmacology is more complex than initially appreciated.
+CNR2	drug	cannabinoid	28065934	Brain <strong><b>cannabinoid</b> receptor 2</strong>: expression, function and modulation.
+CNR2	drug	cannabinoid	28007501	Synergistic attenuation of chronic pain using mu opioid and <strong><b>cannabinoid</b> receptor 2</strong> agonists.
+CNR2	drug	opioid	28007501	Synergistic attenuation of chronic pain using mu <b>opioid</b> and <strong>cannabinoid receptor 2</strong> agonists.
+CNR2	drug	cannabinoid	27875353	<strong><b>Cannabinoid</b> Receptor 2</strong> Functional Variant Contributes to the Risk for Pediatric Inflammatory Bowel Disease.
+CNR2	drug	cannabinoid	27810775	With the help of HTDocking program, we predicted four novel targets for salvinorin A, including muscarinic acetylcholine receptor 2, <b>cannabinoid</b> receptor 1, <strong><b>cannabinoid</b> receptor 2</strong> and dopamine receptor 2.
+CNR2	drug	alcohol	27346657	The <strong>Cannabinoid Receptor 2</strong> Protects Against <b>Alcoholic</b> Liver Disease Via a Macrophage Autophagy Dependent Pathway.
+CNR2	drug	cannabinoid	27346657	The <strong><b>Cannabinoid</b> Receptor 2</strong> Protects Against Alcoholic Liver Disease Via a Macrophage Autophagy Dependent Pathway.
+CNR2	drug	cannabinoid	27186994	<strong><b>Cannabinoid</b> receptor 2</strong> (CB2), a G protein coupled receptor (GPCR), is a promising target for the treatment of neuropathic pain, osteoporosis, immune system, cancer, and drug abuse.
+CNR2	drug	alcohol	26756798	Recently, the <strong>cannabinoid receptor 2</strong> (CB2R) was shown to be expressed in brain reward circuitry and is implicated in modulating the rewarding effects of <b>alcohol</b>.
+CNR2	drug	cannabinoid	26756798	Recently, the <strong><b>cannabinoid</b> receptor 2</strong> (CB2R) was shown to be expressed in brain reward circuitry and is implicated in modulating the rewarding effects of alcohol.
+CNR2	addiction	reward	26756798	Recently, the <strong>cannabinoid receptor 2</strong> (CB2R) was shown to be expressed in brain <b>reward</b> circuitry and is implicated in modulating the rewarding effects of alcohol.
+CNR2	drug	alcohol	25827923	Interaction of <strong>cannabinoid receptor 2</strong> and social environment modulates chronic <b>alcohol</b> consumption.
+CNR2	drug	cannabinoid	25827923	Interaction of <strong><b>cannabinoid</b> receptor 2</strong> and social environment modulates chronic alcohol consumption.
+CNR2	drug	alcohol	25403433	<strong>Cannabinoid receptor 2</strong> agonist attenuates pain related behavior in rats with chronic <b>alcohol</b>/high fat diet induced pancreatitis.
+CNR2	drug	cannabinoid	25403433	<strong><b>Cannabinoid</b> receptor 2</strong> agonist attenuates pain related behavior in rats with chronic alcohol/high fat diet induced pancreatitis.
+CNR2	drug	cannabinoid	25403433	In particular, <strong><b>cannabinoid</b> receptor 2</strong> (CB2) has emerged as an attractive target for management of chronic pain, as demonstrated in several studies with inflammatory and neuropathic preclinical pain models.
+CNR2	drug	cannabinoid	25374096	Species differences in <strong><b>cannabinoid</b> receptor 2</strong> and receptor responses to cocaine self administration in mice and rats.
+CNR2	drug	cocaine	25374096	Species differences in <strong>cannabinoid receptor 2</strong> and receptor responses to <b>cocaine</b> self administration in mice and rats.
+CNR2	drug	cannabinoid	25015040	<strong><b>Cannabinoid</b> receptor 2</strong> and HIV associated neurocognitive disorders.
+CNR2	drug	cannabinoid	25015040	In this regard, <strong><b>cannabinoid</b> receptor 2</strong>(CB2) activation is a promising means to attenuate HAND by inhibiting HIV replication, down regulating inflammation, and suppressing chemokine like activity of viral neurotoxic proteins (for example, Tat and HIV 1gp120), and thereby prevent neuronal and synaptic loss.
+CNR2	drug	alcohol	24999220	The <strong>cannabinoid receptor 2</strong> agonist, β caryophyllene, reduced voluntary <b>alcohol</b> intake and attenuated <b>ethanol</b> induced place preference and sensitivity in mice.
+CNR2	drug	cannabinoid	24999220	The <strong><b>cannabinoid</b> receptor 2</strong> agonist, β caryophyllene, reduced voluntary alcohol intake and attenuated ethanol induced place preference and sensitivity in mice.
+CNR2	drug	cannabinoid	24853387	Chronic <strong><b>cannabinoid</b> receptor 2</strong> activation reverses paclitaxel neuropathy without tolerance or <b>cannabinoid</b> receptor 1 dependent withdrawal.
+CNR2	addiction	withdrawal	24853387	Chronic <strong>cannabinoid receptor 2</strong> activation reverses paclitaxel neuropathy without tolerance or cannabinoid receptor 1 dependent <b>withdrawal</b>.
+CNR2	drug	alcohol	24060590	Therefore, we studied the expression of CNR1 and <strong>CNR2</strong>, and the novel cannabinoid G protein coupled receptor (GPCR) 55 (GPR55) in human monocyte derived dendritic cells (MDDCs) from <b>alcohol</b> users.
+CNR2	drug	cannabinoid	24060590	Therefore, we studied the expression of CNR1 and <strong>CNR2</strong>, and the novel <b>cannabinoid</b> G protein coupled receptor (GPCR) 55 (GPR55) in human monocyte derived dendritic cells (MDDCs) from alcohol users.
+CNR2	drug	alcohol	24060590	MDDCs from <b>alcohol</b> users show significantly higher levels of <strong>CNR2</strong> and GPR55 compared to MDDCs from non users.
+CNR2	drug	alcohol	24060590	Our results provide insights into <b>alcohol</b> mechanisms of DC regulation and show, for the first time, that <b>alcohol</b> is inducing <strong>CNR2</strong> and GPR55 in human DCs.
+CNR2	drug	cannabinoid	23471521	<strong><b>Cannabinoid</b> receptor 2</strong>: potential role in immunomodulation and neuroinflammation.
+CNR2	drug	amphetamine	21886587	Association Study of Two Cannabinoid Receptor Genes, CNR1 and <strong>CNR2</strong>, with <b>Methamphetamine</b> Dependence.
+CNR2	drug	cannabinoid	21886587	Association Study of Two <b>Cannabinoid</b> Receptor Genes, CNR1 and <strong>CNR2</strong>, with Methamphetamine Dependence.
+CNR2	addiction	dependence	21886587	Association Study of Two Cannabinoid Receptor Genes, CNR1 and <strong>CNR2</strong>, with Methamphetamine <b>Dependence</b>.
+CNR2	drug	amphetamine	21886587	To examine the possible association of the CNR1 and <strong>CNR2</strong> genes, which encode cannabinoid receptors CB1 and CB2, with <b>methamphetamine</b> dependence, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the CNR1 gene and a nonsynonymous SNP, Q63R, in the <strong>CNR2</strong> gene.
+CNR2	drug	cannabinoid	21886587	To examine the possible association of the CNR1 and <strong>CNR2</strong> genes, which encode <b>cannabinoid</b> receptors CB1 and CB2, with methamphetamine dependence, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the CNR1 gene and a nonsynonymous SNP, Q63R, in the <strong>CNR2</strong> gene.
+CNR2	addiction	dependence	21886587	To examine the possible association of the CNR1 and <strong>CNR2</strong> genes, which encode cannabinoid receptors CB1 and CB2, with methamphetamine <b>dependence</b>, we investigated three single nucleotide polymorphisms (SNPs) (rs806379, rs1535255, rs2023239) in intron 2 of the CNR1 gene and a nonsynonymous SNP, Q63R, in the <strong>CNR2</strong> gene.
+CNR2	drug	cocaine	21785434	We found that systemic, intranasal or intra accumbens local administration of JWH133, a selective CB(2) receptor agonist, dose dependently inhibited intravenous <b>cocaine</b> self administration, <b>cocaine</b> enhanced locomotion, and <b>cocaine</b> enhanced accumbens extracellular dopamine in wild type and CB(1) receptor knockout (CB(1)( / ), also known as Cnr1( / )) mice, but not in CB(2)( / ) (<strong>Cnr2</strong>( / )) mice.
+CNR2	drug	cannabinoid	21463073	Chronic Δ⁹ <b>THC</b> also significantly reduced CB 1 and <strong>CB 2</strong> receptor levels in the hippocampus, attenuated the expression of a proinflammatory cytokine (MCP 1), and did not increase viral load in plasma, cerebrospinal fluid, or brain tissue compared to vehicle treated subjects with SIV.
+CNR2	drug	cannabinoid	21397004	Agonists of <strong><b>cannabinoid</b> receptor 2</strong> (CB₂) possess potent anti inflammatory and neuroprotective properties.
+CNR2	drug	cannabinoid	21341382	In M. mulatta, the <b>cannabinoid</b> receptor 1 (CNR1) mRNA was expressed in the all tissues; in contrast, the <b>cannabinoid</b> receptor 2 (<strong>CNR2</strong>) mRNA was only present in the spleen.
+CNR2	drug	cannabinoid	19886064	It is composed of <b>cannabinoid</b> receptors CB1 and CB2, and their genes (CNR1 and <strong>CNR2</strong>), their endogenous ligands and the enzymes which mediate endogenous ligands' biosynthesis and degradation.
+CNR2	drug	cannabinoid	19768813	We investigated the association between <strong>CNR2</strong> gene, which encodes <b>cannabinoid</b> CB2 receptor (CB2 R) and eating disorders in 204 subjects with eating disorders and 1876 healthy volunteers in Japanese population.
+CNR2	drug	cannabinoid	19276557	Focusing on the two genes with the smallest p value, H3 histone and <strong><b>cannabinoid</b> receptor 2</strong>, notable increases in these genes were found in peripheral blood mRNA in subjects with lower MMSE scores.
+CNR2	drug	alcohol	18991890	There was a reduction in <strong>CNR2</strong> gene expression in the ventral mid brain region of mice that developed <b>alcohol</b> preference, but not in those that did not develop <b>alcohol</b> preference.
+CCKAR	drug	opioid	30147637	Therefore, <strong>CCK1R</strong> and CCK2R function differently in chronic <b>morphine</b> dependence, but the mechanism is still unclear.
+CCKAR	addiction	dependence	30147637	Therefore, <strong>CCK1R</strong> and CCK2R function differently in chronic morphine <b>dependence</b>, but the mechanism is still unclear.
+CCKAR	drug	opioid	30147637	In this study, HEK 293 cells co transfected with µ <b>opioid</b> receptors (HEK293 hMOR) and <strong>CCK1R</strong> or CCK2R were established.
+CCKAR	drug	opioid	30147637	Over expression of <strong>CCK1R</strong> reversed CREB and ERK1/2 activation in HEK293 hMOR cells exposed to <b>morphine</b>.
+CCKAR	drug	opioid	30147637	Our study identifies over expression of <strong>CCK1R</strong> significantly blocked <b>morphine</b> dependence, which was related with phosphorylation of CREB, and ERK1/2 signaling activation.
+CCKAR	addiction	dependence	30147637	Our study identifies over expression of <strong>CCK1R</strong> significantly blocked morphine <b>dependence</b>, which was related with phosphorylation of CREB, and ERK1/2 signaling activation.
+CCKAR	drug	alcohol	20662806	Chronic <b>ethanol</b> intake or abstinence did not induce any change in the expression of <strong>CCK A</strong> receptors.
+CCKAR	drug	opioid	19944533	In the same animals we show that spinal blockade of <strong>CCK A</strong> receptors prevents cross tolerance at spinal delta <b>opioid</b> receptors that normally occurs with high frequency TENS; and blockade of CCK B receptors prevents cross tolerance at spinal mu <b>opioid</b> receptors that normally occurs with low frequency TENS.
+CCKAR	drug	alcohol	15767271	Differences in <b>ethanol</b> ingestion between <strong>cholecystokinin A receptor</strong> deficient and  B receptor deficient mice.
+CCKAR	drug	nicotine	15740988	Cholecystokinin (CCK) and the <strong>CCKA</strong> receptor gene polymorphism, and <b>smoking</b> behavior.
+CCKAR	drug	nicotine	15740988	We analyzed genetic variants of the promoter region of the cholecystokinin (CCK; which modulates the release of dopamine) gene, and intron 1 and exon 5 of the <strong>CCKA</strong> receptor gene, and performed association analyses of <b>nicotine</b> dependence using an allele specific amplification (ASA) method and PCR RFLP methods.
+CCKAR	addiction	dependence	15740988	We analyzed genetic variants of the promoter region of the cholecystokinin (CCK; which modulates the release of dopamine) gene, and intron 1 and exon 5 of the <strong>CCKA</strong> receptor gene, and performed association analyses of nicotine <b>dependence</b> using an allele specific amplification (ASA) method and PCR RFLP methods.
+CCKAR	drug	amphetamine	14972658	We have previously shown that while <strong>CCKA</strong> receptor antagonists generally do not affect locomotor behaviors, systemic administration of a <strong>CCKA</strong> receptor antagonist attenuates <b>amphetamine</b> (<b>AMPH</b>) induced locomotion in animals previously treated chronically with <b>AMPH</b>, suggesting that chronic stimulant pretreatment may sensitize CCK systems.
+CCKAR	drug	amphetamine	14972658	The present studies examined this issue by testing the effects of <strong>CCKA</strong> antagonists on <b>AMPH</b>  and novel environment induced locomotor activity following two manipulations which are known to alter mesolimbic system function: Chronic <b>AMPH</b> administration and chronic restraint stress (RS).
+CCKAR	drug	amphetamine	14972658	Results indicated that intra NAcc microinjections of the selective <strong>CCKA</strong> receptor antagonist PD 140548 attenuated <b>AMPH</b> induced and novel environment induced locomotion only in animals which had previously been exposed to chronic <b>AMPH</b> or chronic RS pretreatment.
+CCKAR	drug	alcohol	14691070	Association of <strong>cholecystokinin A receptor</strong> gene polymorphism with <b>alcohol</b> dependence in a Japanese population.
+CCKAR	addiction	dependence	14691070	Association of <strong>cholecystokinin A receptor</strong> gene polymorphism with alcohol <b>dependence</b> in a Japanese population.
+CCKAR	drug	cocaine	12393241	In another experiment, <strong>CCK A</strong> or B receptor antagonists were infused into nucleus accumbens or amygdala to determine which brain area are involved in the role of different CCK receptors in stress or drug induced relapse to <b>cocaine</b> seeking.
+CCKAR	addiction	relapse	12393241	In another experiment, <strong>CCK A</strong> or B receptor antagonists were infused into nucleus accumbens or amygdala to determine which brain area are involved in the role of different CCK receptors in stress or drug induced <b>relapse</b> to cocaine <b>seeking</b>.
+CCKAR	addiction	relapse	12393241	These findings demonstrate that <strong>CCK A</strong> and B receptor have different roles in <b>relapse</b> to drug <b>craving</b> and further suggest that the brain areas involved in the CCK receptors on <b>reinstatement</b> of drug <b>seeking</b> are not identical.
+CCKAR	drug	alcohol	12198366	Investigation of quantitative trait loci in the <strong>CCKAR</strong> gene with susceptibility to <b>alcoholism</b>.
+CCKAR	drug	alcohol	12198366	We previously reported genetic variations in the promoter and coding regions of the CCKA receptor (<strong>CCKAR</strong>), CCKBR, and CCK genes and a possible association between polymorphisms of the <strong>CCKAR</strong> gene and <b>alcoholism</b>.
+CCKAR	drug	alcohol	12198366	We previously reported genetic variations in the promoter and coding regions of the <strong>CCKA</strong> receptor (<strong>CCKAR</strong>), CCKBR, and CCK genes and a possible association between polymorphisms of the <strong>CCKAR</strong> gene and <b>alcoholism</b>.
+CCKAR	drug	alcohol	12198366	In this study, association analyses were re examined between the polymorphisms of the promoter region of the <strong>CCKAR</strong> gene and patients with <b>alcohol</b> withdrawal symptoms, in addition to patients with <b>alcoholic</b> liver injury.
+CCKAR	addiction	withdrawal	12198366	In this study, association analyses were re examined between the polymorphisms of the promoter region of the <strong>CCKAR</strong> gene and patients with alcohol <b>withdrawal</b> symptoms, in addition to patients with alcoholic liver injury.
+CCKAR	drug	alcohol	12198366	The data from the case control suggest that polymorphisms of the promoter region of the <strong>CCKAR</strong> gene do not play a major role in the pathogenesis of <b>alcohol</b> withdrawal symptoms or <b>alcoholic</b> liver injury.
+CCKAR	addiction	withdrawal	12198366	The data from the case control suggest that polymorphisms of the promoter region of the <strong>CCKAR</strong> gene do not play a major role in the pathogenesis of alcohol <b>withdrawal</b> symptoms or alcoholic liver injury.
+CCKAR	drug	alcohol	11513220	Polymorphisms of the CCK, <strong>CCKAR</strong> and CCKBR genes: an association with <b>alcoholism</b> study.
+CCKAR	drug	alcohol	11513220	We analyzed genetic variations in the promoter and coding regions of the CCK, CCKA receptor (<strong>CCKAR</strong>) and CCKB receptor (CCKBR) genes, and performed association analyses with <b>alcoholism</b>.
+CCKAR	drug	alcohol	11513220	We analyzed genetic variations in the promoter and coding regions of the CCK, <strong>CCKA</strong> receptor (<strong>CCKAR</strong>) and CCKB receptor (CCKBR) genes, and performed association analyses with <b>alcoholism</b>.
+CCKAR	drug	alcohol	11513220	Nominally significant differences between <b>alcoholics</b> and controls were found at the  85 locus of the <strong>CCKAR</strong> gene (p = .035).
+CCKAR	drug	alcohol	11513220	Our data suggest that polymorphisms of the CCK, <strong>CCKAR</strong> and CCKBR genes do not play a major role in <b>alcohol</b> withdrawal symptoms (even though significant associations were found among polymorphisms at the  388 and  333 loci of the <strong>CCKAR</strong> gene and hallucinations, the rate was nonsignificant after Bonferroni correction).
+CCKAR	addiction	withdrawal	11513220	Our data suggest that polymorphisms of the CCK, <strong>CCKAR</strong> and CCKBR genes do not play a major role in alcohol <b>withdrawal</b> symptoms (even though significant associations were found among polymorphisms at the  388 and  333 loci of the <strong>CCKAR</strong> gene and hallucinations, the rate was nonsignificant after Bonferroni correction).
+CCKAR	drug	cocaine	11457511	The research articles document features of cardiovascular regulation, reduced <b>cocaine</b> sensitization and decreased satiety in rats that lack the <strong>CCK A</strong> receptor.
+CCKAR	addiction	sensitization	11457511	The research articles document features of cardiovascular regulation, reduced cocaine <b>sensitization</b> and decreased satiety in rats that lack the <strong>CCK A</strong> receptor.
+CCKAR	drug	benzodiazepine	11420071	To further examine the relationship between cholecystokinin (CCK) and GABA, the present study assessed the ability of the <strong>CCK A</strong> antagonist devazepide and the CCK B antagonist L 365,260 to substitute for the stimulus effects of <b>chlordiazepoxide</b> (CDP), as well as the ability of CCK 8s to block these effects, in female Long Evans rats within the conditioned taste aversion baseline of drug discrimination learning.
+CCKAR	addiction	aversion	11420071	To further examine the relationship between cholecystokinin (CCK) and GABA, the present study assessed the ability of the <strong>CCK A</strong> antagonist devazepide and the CCK B antagonist L 365,260 to substitute for the stimulus effects of chlordiazepoxide (CDP), as well as the ability of CCK 8s to block these effects, in female Long Evans rats within the conditioned taste <b>aversion</b> baseline of drug discrimination learning.
+CCKAR	drug	alcohol	11384782	For this reason, the aim of the present study was to compare the density of <strong>CCK A</strong> and  B receptors and the mRNA encoding preproCCK throughout the brains of an <b>alcohol</b> preferring (Fawn Hooded) rat strain with that of a non <b>alcohol</b> preferring (Wistar Kyoto) strain of rat.
+CCKAR	drug	opioid	11173090	The present study demonstrated that CCK B receptor but not <strong>CCK A</strong> receptor is involved in the maintenance and reactivation of <b>morphine</b> CPP.
+CCKAR	addiction	reward	11173090	The present study demonstrated that CCK B receptor but not <strong>CCK A</strong> receptor is involved in the maintenance and reactivation of morphine <b>CPP</b>.
+CCKAR	drug	alcohol	9922984	The role of cholecystokinin (CCK), <strong>CCK A</strong> or CCK B receptor antagonists in the spontaneous preference for drugs of abuse (<b>alcohol</b> or cocaine) in naive rats.
+CCKAR	drug	cocaine	9922984	The role of cholecystokinin (CCK), <strong>CCK A</strong> or CCK B receptor antagonists in the spontaneous preference for drugs of abuse (alcohol or <b>cocaine</b>) in naive rats.
+CCKAR	drug	alcohol	9922984	These results indicate that the <strong>CCK A</strong> or B receptors are selectively involved in the modulation of <b>alcohol</b> or cocaine intake, respectively, and suggest an involvement of the CCKergic system in the drug seeking behavior.
+CCKAR	drug	cocaine	9922984	These results indicate that the <strong>CCK A</strong> or B receptors are selectively involved in the modulation of alcohol or <b>cocaine</b> intake, respectively, and suggest an involvement of the CCKergic system in the drug seeking behavior.
+CCKAR	addiction	relapse	9922984	These results indicate that the <strong>CCK A</strong> or B receptors are selectively involved in the modulation of alcohol or cocaine intake, respectively, and suggest an involvement of the CCKergic system in the drug <b>seeking</b> behavior.
+CCKAR	drug	alcohol	9922984	In particular, the data imply a <strong>CCK A</strong> receptor mechanism in the regulation of individual sensitivity towards <b>ethanol</b> and a CCK B receptor mechanism in the regulation of individual sensitivity towards cocaine.
+CCKAR	drug	cocaine	9922984	In particular, the data imply a <strong>CCK A</strong> receptor mechanism in the regulation of individual sensitivity towards ethanol and a CCK B receptor mechanism in the regulation of individual sensitivity towards <b>cocaine</b>.
+CCKAR	drug	alcohol	9922984	Thus, a potential therapeutic role for <strong>CCK A</strong> antagonists in the treatment of <b>ethanol</b> abuse and for CCK B antagonists in the treatment of cocaine abuse is proposed.
+CCKAR	drug	cocaine	9922984	Thus, a potential therapeutic role for <strong>CCK A</strong> antagonists in the treatment of ethanol abuse and for CCK B antagonists in the treatment of <b>cocaine</b> abuse is proposed.
+CCKAR	drug	benzodiazepine	9832933	The effects of CR 2945, an antranilic acid derivative member of a novel family of non peptide CCKB receptor antagonists, have been compared with those of CAM 1028, an analogue of the CCKB receptor antagonist CI 988, L 365,260 a <b>benzodiazepine</b> derivative CCKB antagonist, CR 1795, an analogue of the <strong>CCKA</strong> receptor antagonist lorglumide and <b>diazepam</b>, a <b>benzodiazepine</b> receptor agonist, in several rodent screens sensitive to conventional anxiolytics.
+CCKAR	drug	opioid	9578139	Several cholecystokinin ligands were chronically administered during the development of <b>morphine</b> dependence: the <strong>CCKA</strong> antagonist devazepide, the CCKB antagonists PD 134,308 and L 365,260, and the CCKB agonist BC 264.
+CCKAR	addiction	dependence	9578139	Several cholecystokinin ligands were chronically administered during the development of morphine <b>dependence</b>: the <strong>CCKA</strong> antagonist devazepide, the CCKB antagonists PD 134,308 and L 365,260, and the CCKB agonist BC 264.
+CCKAR	drug	benzodiazepine	9276016	We previously described a series of 3 (1H indazol 3 ylmethyl) 1,5 <b>benzodiazepine</b> <strong>CCK A</strong> agonists exemplified by compound 1 (GW 5823), which is the first reported binding selective <strong>CCK A</strong> full agonist demonstrating oral efficacy in a rat feeding model.
+CCKAR	addiction	dependence	9276016	Binding affinity for the <strong>CCK A</strong> vs CCK B receptor showed little <b>dependence</b> on the structure of the C3 moiety but was affected by the nature of the second substituent at C3.
+CCKAR	drug	alcohol	9022085	The <b>ethanol</b> induced increase in amylase output can be completely inhibited by the <strong>CCK A</strong> receptor antagonist L 364,718 and partially inhibited by the muscarinic cholinergic antagonist atropine.
+CCKAR	drug	opioid	8947930	The overlapping distribution of <b>opioid</b> and cholecystokinin (CCK) peptides and their receptors (mu and delta <b>opioid</b> receptors; <strong>CCK A</strong> and CCK B receptors) in the central nervous system have led to a large number of studies aimed at clarifying the functional relationships between these two neuropeptides.
+CCKAR	drug	opioid	8836616	Modulation of the in vivo actions of <b>morphine</b> by the mixed <strong>CCKA</strong>/B receptor antagonist PD 142898.
+CCKAR	drug	opioid	8836616	The ability of a mixed <strong>CCKA</strong>/B receptor antagonist PD 142898 (benzenebutanic acid, beta [[3 (1 H indol 3 yl) 2 methyl 2 [[[(2 methyl  cyclohexyl)oxy]carbonyl]amino] 1 oxopropyl]amino] [1 S [1 alpha [S*(R*)] 2 beta]]) to modulate the antinociceptive, positive reinforcing and gastrointestinal actions of <b>morphine</b> was investigated in the rat.
+CCKAR	addiction	reward	8836616	The ability of a mixed <strong>CCKA</strong>/B receptor antagonist PD 142898 (benzenebutanic acid, beta [[3 (1 H indol 3 yl) 2 methyl 2 [[[(2 methyl  cyclohexyl)oxy]carbonyl]amino] 1 oxopropyl]amino] [1 S [1 alpha [S*(R*)] 2 beta]]) to modulate the antinociceptive, positive <b>reinforcing</b> and gastrointestinal actions of morphine was investigated in the rat.
+CCKAR	drug	opioid	8836616	It is argued that the effect of PD 142898 in the conditioned place preference test involves antagonism of <strong>CCKA</strong> receptors, whilst the potentiation of the antinociceptive action of <b>morphine</b> is mediated via blockade of CCKB receptors.
+CCKAR	drug	opioid	8836616	These results suggest that the mixed <strong>CCKA</strong>/B receptor antagonist may potentiate the analgesic action of <b>morphine</b>, block the development of tolerance without a concomitant increase in constipation and may also reduce the abuse potential of the opiate.
+CCKAR	drug	opioid	8818359	The ability of a selective <strong>CCKA</strong> receptor antagonist PD 140548 and a selective CCKB receptor antagonist CI 988 (formerly PD 134308) to modulate the various in vivo properties of <b>morphine</b> was investigated in the rat.
+CCKAR	drug	opioid	8818359	In conclusion, the results of the present study indicate that <strong>CCKA</strong> and CCKB receptors modulate different properties of <b>morphine</b>.
+CCKAR	drug	opioid	8818359	Thus, whilst a selective <strong>CCKA</strong> receptor antagonist blocked the rewarding properties of <b>morphine</b>, a selective CCKB receptor antagonist potentiated the antinociceptive action.
+CCKAR	addiction	reward	8741936	Devazepide, a <strong>CCKA</strong> receptor antagonist, impairs the acquisition of conditioned <b>reward</b> and conditioned activity.
+CCKAR	addiction	reward	8741936	Experiment 1 examined the effects of systemic administration of the <strong>CCKA</strong> receptor selective antagonist, devazepide (0, 0.001, 0.01, 0.1 mg/kg), on the acquisition of conditioned <b>reward</b>.
+CCKAR	addiction	reward	8741936	Together, these results provide converging evidence that intact <strong>CCKA</strong> function may be necessary for the development of conditioned <b>incentive</b> learning.
+CCKAR	addiction	aversion	8735976	Several roles of <strong>CCKA</strong> and CCKB receptor subtypes in CCK 8 induced and LiCl induced taste <b>aversion</b> conditioning.
+CCKAR	drug	benzodiazepine	8735976	Because the CCK antagonists affected TAC like <b>chlordiazepoxide</b>, blockade of <strong>CCKA</strong> and CCKB mechanisms may produce a mild anxiolytic effect.
+CCKAR	drug	opioid	8617406	For example, CCK appears to exert its anti <b>opioid</b> actions mainly through the activation of CCK B receptors, whereas its <b>opioid</b> like effects seem to result from the stimulation of <strong>CCK A</strong> receptors.
+CCKAR	drug	opioid	8004452	The <strong>CCKA</strong> receptor antagonist devazepide does not modify <b>opioid</b> self administration or drug discrimination: comparison with the dopamine antagonist haloperidol.
+CCKAR	drug	opioid	8004452	We previously reported that the selective cholecystokininA (<strong>CCKA</strong>) receptor antagonist, devazepide, blocked the acquisition of a <b>morphine</b> conditioned place preference (ref 28).
+CCKAR	drug	opioid	8004452	The present results therefore cast doubt on the potential utility of selective <strong>CCKA</strong> antagonists as treatments for <b>opioid</b> abuse, and further suggest that CCKB antagonists may not potentiate the subjective effects of <b>opioids</b>, an important finding considering that such drugs have been proposed as adjuncts to <b>opioid</b> therapy for the treatment of pain relief.
+CCKAR	drug	benzodiazepine	1356807	It is concluded that the reduction in aversive responding caused by pharmacological manipulation at the <b>benzodiazepine</b>, 5 HT receptor subtypes 5 HT1A, 5 HT1C/5 HT2 and 5 HT3 (but not at the cholecystokin <strong>CCKA</strong> or angiotensin receptors or inhibition of angiotensin converting enzyme) can be inhibited by R(+) and S( ) zacopride.
+CCKAR	addiction	aversion	1356807	It is concluded that the reduction in <b>aversive</b> responding caused by pharmacological manipulation at the benzodiazepine, 5 HT receptor subtypes 5 HT1A, 5 HT1C/5 HT2 and 5 HT3 (but not at the cholecystokin <strong>CCKA</strong> or angiotensin receptors or inhibition of angiotensin converting enzyme) can be inhibited by R(+) and S( ) zacopride.
+CCKAR	drug	opioid	1611514	<b>Morphine</b> place conditioning is differentially affected by <strong>CCKA</strong> and CCKB receptor antagonists.
+CCKAR	drug	opioid	2311658	The effects of the selective <strong>CCK A</strong> antagonist L 365,031 and the selective CCK B antagonist L 365,260 on <b>morphine</b> analgesia and opiate tolerance and dependence in rats were examined.
+CCKAR	addiction	dependence	2311658	The effects of the selective <strong>CCK A</strong> antagonist L 365,031 and the selective CCK B antagonist L 365,260 on morphine analgesia and opiate tolerance and <b>dependence</b> in rats were examined.
+CAMK2A	drug	opioid	30260900	Association of <strong>CamK2A</strong> genetic variants with transition time from occasional to regular <b>heroin</b> use in a sample of <b>heroin</b> dependent individuals.
+CAMK2A	drug	opioid	30260900	We hypothesized, that <strong>CamK2A</strong> genetic variation may play a role in the transition from occasional to regular <b>heroin</b> use.
+CAMK2A	drug	opioid	30260900	Using quantitative trait association analysis, we addressed this hypothesis by correlating the self reported time interval between occasional and regular <b>heroin</b> use with the frequency of 12 single nucleotide polymorphisms located within the genomic region of the <strong>CamK2A</strong> gene.
+CAMK2A	drug	opioid	30260900	Our results propose that genetic variants located in the genomic region of the <strong>CamK2A</strong> gene may be involved in transition time from occasional to regular <b>heroin</b> use.
+CAMK2A	drug	alcohol	28714806	These different transcription patterns have been associated to the presence of <b>alcohol</b>, in the Camk2n1 and Gja1 genes; to the amount of <b>ethanol</b> consumed, in the <strong>Camk2a</strong> gene; and to the loss of control in the <b>alcohol</b> consumption, in the Pkp2 gene.
+CAMK2A	drug	alcohol	25579851	<b>Alcohol</b> sensitive proteins included <strong>calcium/calmodulin dependent protein kinase II alpha</strong> (CaMKIIα) and a network of functionally linked proteins that regulate neural plasticity and glutamate mediated synaptic activity.
+CAMK2A	drug	cocaine	25290264	To translate the rodent findings to human conditions, several <strong>CAMK2A</strong> gene polymorphisms were tested regarding their risk for a fast establishment of <b>cocaine</b> dependence in two independent samples of regular <b>cocaine</b> users from Brazil (n=688) and Switzerland (n=141).
+CAMK2A	addiction	dependence	25290264	To translate the rodent findings to human conditions, several <strong>CAMK2A</strong> gene polymorphisms were tested regarding their risk for a fast establishment of cocaine <b>dependence</b> in two independent samples of regular cocaine users from Brazil (n=688) and Switzerland (n=141).
+CAMK2A	drug	cocaine	25290264	A meta analysis across both samples confirmed that <strong>CAMK2A</strong> rs3776823 TT allele carriers display a faster transition to severe <b>cocaine</b> use than C allele carriers.
+CAMK2A	drug	alcohol	23459588	In order to compare findings in mice with the human condition, we tested 23 single nucleotide polymorphisms (SNPs) in the <strong>CAMK2A</strong> gene for their association with <b>alcohol</b> dependence in a population of 1333 male patients with severe <b>alcohol</b> dependence and 939 controls.
+CAMK2A	addiction	dependence	23459588	In order to compare findings in mice with the human condition, we tested 23 single nucleotide polymorphisms (SNPs) in the <strong>CAMK2A</strong> gene for their association with alcohol <b>dependence</b> in a population of 1333 male patients with severe alcohol <b>dependence</b> and 939 controls.
+CAMK2A	drug	alcohol	23459588	We found seven significant associations between <strong>CAMK2A</strong> SNPs and <b>alcohol</b> dependence, one of which in an autophosphorylation related area of the gene.
+CAMK2A	addiction	dependence	23459588	We found seven significant associations between <strong>CAMK2A</strong> SNPs and alcohol <b>dependence</b>, one of which in an autophosphorylation related area of the gene.
+CAMK2A	drug	opioid	20053885	Furthermore, <b>morphine</b> failed to induce OIH in <strong>CaMKIIalpha</strong>(T286A) point mutant mice, although wild type littermate mice developed robust OIH after repeated treatments with <b>morphine</b>.
+CAMK2A	drug	opioid	20053885	These data implicate, for the first time, an essential role of <strong>CaMKIIalpha</strong> as a cellular mechanism leading to and maintaining <b>opioid</b> induced hyperalgesia.
+CAMK2A	drug	cocaine	20010550	Chronic <b>cocaine</b> induced H3 acetylation and transcriptional activation of <strong>CaMKIIalpha</strong> in the nucleus accumbens is critical for motivation for drug reinforcement.
+CAMK2A	addiction	reward	20010550	Chronic cocaine induced H3 acetylation and transcriptional activation of <strong>CaMKIIalpha</strong> in the nucleus accumbens is critical for motivation for drug <b>reinforcement</b>.
+CAMK2A	drug	cocaine	20010550	Among the genes activated by chronic <b>cocaine</b> experiences, the expression of <strong>CaMKIIalpha</strong>, but not CaMKIIbeta, correlated positively with motivation for the drug.
+CAMK2A	drug	cocaine	20010550	Lentivirus mediated shRNA knockdown experiments showed that <strong>CaMKIIalpha</strong>, but not CaMKIIbeta, in the NAc shell is essential for the maintenance of motivation to self administered <b>cocaine</b>.
+CAMK2A	addiction	reward	20010550	These findings suggest that chronic drug use induced transcriptional activation of genes, such as <strong>CaMKIIalpha</strong>, modulated by H3 acetylation in the NAc is a critical regulatory mechanism underlying motivation for drug <b>reinforcement</b>.
+CAMK2A	addiction	withdrawal	19909283	Since L VGCC (L type voltage gated calcium channel) current density was doubled on drug <b>withdrawal</b> and up to 2 days, Ca(2+) entry through L VGCCs and perhaps subsequently through Ca(2+) permeable AMPARs are proposed to be responsible for enhanced <strong>CaMKIIalpha</strong> levels and AMPAR potentiation.
+CAMK2A	drug	amphetamine	17603807	Because the levels of both CaMKIIbeta and <strong>CaMKIIalpha</strong> play a role in neuronal function and synapse formation, the present finding of an elevated level of CaMKII beta and alpha subunit mRNA in the <b>amphetamine</b> sensitized model of psychosis points to the possibility of dysregulated levels of CaMKII subunits in human psychosis.
+CAMK2A	addiction	withdrawal	16616767	Opiate <b>withdrawal</b> induces dynamic expressions of AMPA receptors and its regulatory molecule <strong>CaMKIIalpha</strong> in hippocampal synapses.
+CAMK2A	drug	benzodiazepine	15009662	Most transcript changes were transient except for the decrease of the <strong>CaMKIIalpha</strong> transcript which persisted even 40 h after the single dose of <b>diazepam</b>.
+CAMK2A	drug	opioid	14706789	To clarify this issue we explored mRNA and protein expression of <strong>CaMKIIalpha</strong> in spinal cord tissue from control and <b>morphine</b> treated mice using real time polymerase chain reaction, Western blot analysis and confocal microscopy.
+CAMK2A	drug	opioid	14706789	The results indicate that the levels of <strong>CaMKIIalpha</strong> mRNA and protein were robustly increased in spinal cord tissue from <b>morphine</b> treated mice.
+CAMK2A	drug	opioid	14706789	In addition, the abundance of phosphorylated <strong>CaMKIIalpha</strong> was increased in spinal cord tissue from <b>morphine</b> treated mice.
+CAMK2A	drug	opioid	14706789	We conclude that enhanced <strong>CaMKIIalpha</strong> expression and activity in spinal cord tissue may contribute to the development of <b>morphine</b> tolerance in mice.
+ADORA1	drug	cannabinoid	32199997	<strong>Adenosine A1 receptor</strong> agonist induces visceral antinociception via 5 HT1A, 5 HT2A, dopamine D1 or <b>cannabinoid</b> CB1 receptors, and the opioid system in the central nervous system.
+ADORA1	drug	opioid	32199997	<strong>Adenosine A1 receptor</strong> agonist induces visceral antinociception via 5 HT1A, 5 HT2A, dopamine D1 or cannabinoid CB1 receptors, and the <b>opioid</b> system in the central nervous system.
+ADORA1	drug	cannabinoid	32070652	preadministration of naloxone (a non selective opioid receptor antagonist; 5 µg/5 µl), (2); AM281 (a selective <b>cannabinoid</b> receptor type 1 [CB1] antagonist; 2 µg/5 µl), (3); and 1,3 dipropyl 8 cyclopentylxanthine (DPCPX; a selective <strong>adenosine A1 receptor</strong> antagonist; 10 nmol/5 µl), on the antihyperalgesic (pain relieving) effect of WWIT against CFA induced hyperalgesia.
+ADORA1	drug	opioid	32070652	preadministration of <b>naloxone</b> (a non selective <b>opioid</b> receptor antagonist; 5 µg/5 µl), (2); AM281 (a selective cannabinoid receptor type 1 [CB1] antagonist; 2 µg/5 µl), (3); and 1,3 dipropyl 8 cyclopentylxanthine (DPCPX; a selective <strong>adenosine A1 receptor</strong> antagonist; 10 nmol/5 µl), on the antihyperalgesic (pain relieving) effect of WWIT against CFA induced hyperalgesia.
+ADORA1	addiction	relapse	30470862	These results demonstrate the sufficiency of dopamine D3 receptors to reinstate MA <b>seeking</b> that is inhibited when combined with <strong>adenosine A1 receptor</strong> stimulation.
+ADORA1	drug	cannabinoid	30342057	Pretreatment with subcutaneous injection of naloxone hydrochloride, a peripheral and central opioid antagonist, blocked the oxytocin induced visceral antinociception while neither subcutaneous injection of naloxone methiodide, a peripheral selective opioid antagonist, sulpiride, a dopamine D2 receptor antagonist, DPCPX, an <strong>adenosine A1 receptor</strong> antagonist, AM251, a <b>cannabinoid</b> 1 receptor antagonist nor AM630, a <b>cannabinoid</b> 2 receptor antagonist blocked the antinociception.
+ADORA1	drug	opioid	30342057	Pretreatment with subcutaneous injection of <b>naloxone</b> hydrochloride, a peripheral and central <b>opioid</b> antagonist, blocked the oxytocin induced visceral antinociception while neither subcutaneous injection of <b>naloxone</b> methiodide, a peripheral selective <b>opioid</b> antagonist, sulpiride, a dopamine D2 receptor antagonist, DPCPX, an <strong>adenosine A1 receptor</strong> antagonist, AM251, a cannabinoid 1 receptor antagonist nor AM630, a cannabinoid 2 receptor antagonist blocked the antinociception.
+ADORA1	drug	opioid	29476749	Pretreatment with subcutaneous injection of either <b>naloxone</b> hydrochloride or sulpiride, a dopamine D2 receptor antagonist, significantly blocked ghrelin induced visceral antinociception; furthermore, neither subcutaneous injection of <b>naloxone</b> methiodide, a peripheral selective <b>opioid</b> antagonist, SCH23390, a dopamine D1 receptor antagonist, nor DPCPX, an <strong>adenosine A1 receptor</strong> antagonist, blocked antinociception.
+ADORA1	drug	opioid	28440280	These EA based effects were abolished by the <b>opioid</b> receptor antagonist <b>naloxone</b> and the <strong>adenosine A1 receptor</strong> antagonist rolofylline.
+ADORA1	drug	opioid	28440280	Administration of <b>opioid</b> receptor agonist endomorphin (EM) or <strong>adenosine A1 receptor</strong> agonist N6 cyclopentyladenosine (CPA) has similar results to EA.
+ADORA1	drug	alcohol	28196272	Two variant sets were significant at the q value <0.10 level: a genic enhancer for ADHFE1 (p = 1.47 × 10 5 ; q = 0.019), an <b>alcohol</b> dehydrogenase, and <strong>ADORA1</strong> (p = 5.29 × 10 5 ; q = 0.035), an adenosine receptor that belongs to a G protein coupled receptor gene family.
+ADORA1	drug	psychedelics	25702084	The anti immobility effect of creatine (1 mg/kg, po) or <b>ketamine</b> (a fast acting antidepressant, 1 mg/kg, ip) in the TST was prevented by pretreatment of mice with caffeine (3 mg/kg, ip, nonselective adenosine receptor antagonist), 8 cyclopentyl 1,3 dipropylxanthine (DPCPX) (2 mg/kg, ip, selective <strong>adenosine A1 receptor</strong> antagonist), and 4 (2 [7 amino 2 {2 furyl}{1,2,4}triazolo {2,3 a}{1,3,5}triazin 5 yl amino]ethyl) phenol (ZM241385) (1 mg/kg, ip, selective adenosine A2A receptor antagonist).
+ADORA1	drug	psychedelics	25702084	Moreover, the administration of subeffective doses of creatine or <b>ketamine</b> combined with N 6 cyclohexyladenosine (CHA) (0.05 mg/kg, ip, selective <strong>adenosine A1 receptor</strong> agonist), N 6 [2 (3,5 dimethoxyphenyl) 2 (methylphenyl)ethyl]adenosine (DPMA) (0.1 mg/kg, ip, selective adenosine A2A receptor agonist), or dipyridamole (0.1 μg/mouse, icv, adenosine transporter inhibitor) produced a synergistic antidepressant like effect in the TST.
+ADORA1	drug	cannabinoid	25079058	preadministration of naloxone (a nonselective opioid receptor antagonist; 5 µg/paw), caffeine (a nonselective adenosine receptor antagonist; 150 nmol/paw), 1,3 dipropyl 8 cyclopentylxanthine (DPCPX; a selective <strong>adenosine A1 receptor</strong> antagonist; 10 nmol/paw), and AM630 (a selective <b>cannabinoid</b> receptor type 2 antagonist; 4 µg/paw) on the antiallodynic effect of WWIT against CFA induced allodynia.
+ADORA1	drug	opioid	25079058	preadministration of <b>naloxone</b> (a nonselective <b>opioid</b> receptor antagonist; 5 µg/paw), caffeine (a nonselective adenosine receptor antagonist; 150 nmol/paw), 1,3 dipropyl 8 cyclopentylxanthine (DPCPX; a selective <strong>adenosine A1 receptor</strong> antagonist; 10 nmol/paw), and AM630 (a selective cannabinoid receptor type 2 antagonist; 4 µg/paw) on the antiallodynic effect of WWIT against CFA induced allodynia.
+ADORA1	addiction	withdrawal	24562064	Following a 1 week <b>withdrawal</b>, the direct effects of adenosine receptor modulation were tested by administering the <strong>adenosine A1 receptor</strong> agonist, N(6) cyclopentyladenosine (CPA, 0.03 and 0.1 mg/kg), the adenosine A2A agonist, CGS 21680 (0.03 and 0.1 mg/kg), the presynaptic adenosine A2A receptor antagonist, SCH 442416 (0.3, 1, and 3 mg/kg), or vehicle prior to each of six daily extinction sessions.
+ADORA1	addiction	relapse	24562064	Interestingly, <strong>adenosine A1 receptor</strong> stimulation or presynaptic adenosine A2A receptor blockade during extinction produces lasting changes in <b>relapse</b> susceptibility.
+ADORA1	drug	opioid	23810661	Interaction of the <strong>adenosine A1 receptor</strong> agonist N6 cyclopentyladenosine (CPA) and <b>opioid</b> receptors in spinal cord nociceptive reflexes.
+ADORA1	drug	opioid	23810661	CPA mediated antinociception was challenged by the selective <strong>adenosine A1 receptor</strong> antagonist 8 cyclopentyl 1, 3 dimethylxanthine (CPT) and by the <b>opioid</b> receptor antagonist <b>naloxone</b> on male adult Wistar rats with carrageenan induced inflammation.
+ADORA1	drug	opioid	23810661	The present study provides strong in vivo evidence of an antinociceptive activity mediated by the <strong>adenosine A1 receptor</strong> system in the spinal cord, linked to an activation of <b>opioid</b> receptors in adult animals with inflammation.
+ADORA1	drug	alcohol	22272351	<b>Alcohol</b> worsens acute lung injury by inhibiting alveolar sodium transport through the <strong>adenosine A1 receptor</strong>.
+ADORA1	drug	amphetamine	21886579	Association analysis of the <strong>adenosine A1 receptor</strong> gene polymorphisms in patients with <b>methamphetamine</b> dependence/psychosis.
+ADORA1	addiction	dependence	21886579	Association analysis of the <strong>adenosine A1 receptor</strong> gene polymorphisms in patients with methamphetamine <b>dependence</b>/psychosis.
+ADORA1	drug	amphetamine	21886579	We therefore hypothesized that variations in the A1 adenosine receptor (<strong>ADORA1</strong>) gene modify genetic susceptibility to <b>METH</b> dependence/psychosis.
+ADORA1	addiction	dependence	21886579	We therefore hypothesized that variations in the A1 adenosine receptor (<strong>ADORA1</strong>) gene modify genetic susceptibility to METH <b>dependence</b>/psychosis.
+ADORA1	drug	amphetamine	21886579	These results suggest that the <strong>ADORA1</strong> gene variants may make little or no contribution to vulnerability to <b>METH</b> dependence/psychosis.
+ADORA1	addiction	dependence	21886579	These results suggest that the <strong>ADORA1</strong> gene variants may make little or no contribution to vulnerability to METH <b>dependence</b>/psychosis.
+ADORA1	drug	opioid	19442100	Also, the <strong>adenosine A1 receptor</strong> agonist, N6 Cyclopentyladenosine (CPA) was able to reduce dose dependently <b>naloxone</b> precipitated withdrawal whereas the selective adenosine A(2A) receptor agonist CGS 21680 increased the <b>naloxone</b> precipitated withdrawal phenomenon.
+ADORA1	addiction	withdrawal	19442100	Also, the <strong>adenosine A1 receptor</strong> agonist, N6 Cyclopentyladenosine (CPA) was able to reduce dose dependently naloxone precipitated <b>withdrawal</b> whereas the selective adenosine A(2A) receptor agonist CGS 21680 increased the naloxone precipitated <b>withdrawal</b> phenomenon.
+ADORA1	drug	alcohol	18482156	Sex differences in the neurotoxic effects of <strong>adenosine A1 receptor</strong> antagonism during <b>ethanol</b> withdrawal: reversal with an A1 receptor agonist or an NMDA receptor antagonist.
+ADORA1	addiction	withdrawal	18482156	Sex differences in the neurotoxic effects of <strong>adenosine A1 receptor</strong> antagonism during ethanol <b>withdrawal</b>: reversal with an A1 receptor agonist or an NMDA receptor antagonist.
+ADORA1	drug	alcohol	17517168	In contrast, combinations of the selective <strong>adenosine A1 receptor</strong> antagonist, DPCPX, with either SCH 58261 or MTEP had no effect on <b>alcohol</b> responding.
+ADORA1	addiction	withdrawal	17085856	The non selective adenosine receptor antagonist (caffeine), and the selective <strong>adenosine A1 receptor</strong> antagonist (DPCPX), injected 15 min before the application of pentetrazole and flumazenil, were able to intensify BDZ <b>withdrawal</b> signs in mice.
+ADORA1	addiction	withdrawal	17085856	The obtained data demonstrate that the adenosinergic system is involved in BDZ <b>withdrawal</b> signs in mice, and <strong>adenosine A1 receptor</strong> plays an important role in this process.
+ADORA1	addiction	withdrawal	16407902	The acute administration of 'nonanxiolytic' doses of adenosine and the selective <strong>adenosine A1 receptor</strong> agonist 2 chloro N6 cyclopentyladenosine (CCPA), but not the adenosine A2A receptor agonist N6 [2 (3,5 dimethoxyphenyl) 2 (2 methylphenyl)ethyl]adenosine (DPMA), at the onset of peak <b>withdrawal</b> (18 h), reduced this anxiogenic like response.
+ADORA1	drug	alcohol	16407902	In addition, the effect of CCPA on the anxiety like behavior of <b>ethanol</b> hangover was reversed by pretreatment with the selective <strong>adenosine A1 receptor</strong> antagonist 8 cyclopentyl 1,3 dipropylxanthine (DPCPX).
+ADORA1	drug	alcohol	16407902	These results reinforce the notion of the involvement of adenosine receptors in the anxiety like responses and indicate the potential of <strong>adenosine A1 receptor</strong> agonists to reduce the anxiogenic effects during <b>ethanol</b> withdrawal.
+ADORA1	addiction	withdrawal	16407902	These results reinforce the notion of the involvement of adenosine receptors in the anxiety like responses and indicate the potential of <strong>adenosine A1 receptor</strong> agonists to reduce the anxiogenic effects during ethanol <b>withdrawal</b>.
+ADORA1	drug	benzodiazepine	16226742	The results confirm that adenosine A1 and A2A receptors are involved in <b>benzodiazepine</b> withdrawal signs, and <strong>adenosine A1 receptor</strong> plays a predominant role in this phenomenon.
+ADORA1	addiction	withdrawal	16226742	The results confirm that adenosine A1 and A2A receptors are involved in benzodiazepine <b>withdrawal</b> signs, and <strong>adenosine A1 receptor</strong> plays a predominant role in this phenomenon.
+ADORA1	drug	alcohol	15983797	In connection with the rota rod apparatus, the effects of acute administration of the adenosine receptor antagonists caffeine (non selective), 8 cyclopentyl 1,3 dipropylxanthine (DPCPX, <strong>adenosine A1 receptor</strong> antagonist) and 4 (2 [7 amino 2 {2 furyl}{1,2,4}triazolo {2,3 a}{1,3,5}triazin 5 yl amino]ethyl)phenol (ZM241385, adenosine A2A receptor antagonist), together with R(+) 7 chloro 8 hydroxy 3 methyl 1 phenyl 2,3,4,5 tetrahydro 1H 3 benzazepine (SCH23390, dopamine D1 receptor antagonist) and sulpiride (dopamine D2 receptor antagonist), alone or in combination with <b>ethanol</b> (2.25 g/kg, i.p.
+ADORA1	drug	opioid	15673876	In this study, we examined the effect of intrathecal <b>morphine</b> on the antiallodynic state induced by the <strong>adenosine A1 receptor</strong> agonist, N(6) (2 phenylisopropyl) adenosine R ( )isomer (R PIA), in a rat model of nerve ligation injury.
+ADORA1	drug	alcohol	15363961	The effects of acute administration of the adenosine receptor antagonists caffeine (nonselective), 8 cyclopentyl 1,3 dipropylxanthine (DPCPX, <strong>adenosine A1 receptor</strong> antagonist) and 4 (2 [7 amino 2 [2 furyl][1,2,4]triazolo [2,3 a][1,3,5]triazin 5 yl amino]ethyl)phenol (ZM241385, adenosine A(2A) receptor antagonist), together with the <strong>adenosine A1 receptor</strong> agonist 2 chloro N6 cyclopentyladenosine (CCPA), and their interaction with <b>ethanol</b> in the elevated plus maze test in mice were studied.
+ADORA1	drug	amphetamine	14506310	Selective <strong>adenosine A1 receptor</strong> agonist, CPA, significantly reduced the acquisition of CPP induced by <b>amphetamine</b>.
+ADORA1	addiction	reward	14506310	Selective <strong>adenosine A1 receptor</strong> agonist, CPA, significantly reduced the acquisition of <b>CPP</b> induced by amphetamine.
+ADORA1	drug	amphetamine	14506310	It suggests that <strong>adenosine A1 receptor</strong> is involved in rewarding effects of <b>amphetamine</b>.
+ADORA1	drug	amphetamine	14506310	Therefore, it seems that selective <strong>adenosine A1 receptor</strong> agonists may have some attenuating influence on the development of <b>amphetamine</b> dependence.
+ADORA1	addiction	dependence	14506310	Therefore, it seems that selective <strong>adenosine A1 receptor</strong> agonists may have some attenuating influence on the development of amphetamine <b>dependence</b>.
+ADORA1	drug	cocaine	12139108	Selective <strong>adenosine A1 receptor</strong> antagonist, 8 cyclopentyltheophylline (CPT), A2 receptor antagonist, 3,7 dimethyl 1 propargylxanthine, DMPX, and caffeine (non selective A1/A2 receptor antagonist) markedly and significantly decreased the expression of CPP induced by <b>cocaine</b>, and caffeine (20 mg/kg) decreased also the acquisition of this reaction.
+ADORA1	addiction	reward	12139108	Selective <strong>adenosine A1 receptor</strong> antagonist, 8 cyclopentyltheophylline (CPT), A2 receptor antagonist, 3,7 dimethyl 1 propargylxanthine, DMPX, and caffeine (non selective A1/A2 receptor antagonist) markedly and significantly decreased the expression of <b>CPP</b> induced by cocaine, and caffeine (20 mg/kg) decreased also the acquisition of this reaction.
+ADORA1	drug	opioid	11166287	The spontaneous activity of paragigantocellularis neurons was significantly decreased by microinjection of both adenosine (10 nM) and an <strong>adenosine A1 receptor</strong> selective agonist, cyclohexyladenosine (200 microM), into the paragigantocellularis nucleus of both control and <b>morphine</b> dependent rats, but the decrease in firing rate of paragigantocellularis neurons of <b>morphine</b> dependent rats was greater than that of control ones.
+ADORA1	drug	opioid	10714888	The same effect was induced by the <strong>adenosine A1 receptor</strong> agonist, N6 Cyclopentyladenosine (CPA) whereas the selective adenosine A2A receptor agonist CGS 21680 increased the <b>naloxone</b> precipitated withdrawal phenomenon.
+ADORA1	addiction	withdrawal	10714888	The same effect was induced by the <strong>adenosine A1 receptor</strong> agonist, N6 Cyclopentyladenosine (CPA) whereas the selective adenosine A2A receptor agonist CGS 21680 increased the naloxone precipitated <b>withdrawal</b> phenomenon.
+ADORA1	addiction	withdrawal	10548160	<strong>Adenosine A1 receptor</strong> agonist R N6(phenylisopropyl)adenosine (0.15 and 0.3 mg/ kg) reduced <b>withdrawal</b> signs 0.5 and 1.5 h after drug administration in a dose dependent fashion.
+ADORA1	drug	opioid	10204676	The <strong>adenosine A1 receptor</strong> agonists, N6 cyclohexyladenosine (CHA: 0.1, 0.25 and 0.5 mg kg( 1)) and R isomer of N6 phenylisopropyladenosine (R PIA: 0.1, 0.3 and 1 mg kg( 1)), decreased jumping and diarrhea induced by <b>naloxone</b> in <b>morphine</b> dependent mice.
+ADORA1	drug	opioid	8788434	The <strong>adenosine A1 receptor</strong> agonist cyclohexyladenosine induced decreases in diastolic blood pressure which were significantly reduced in <b>morphine</b> dependent rats when compared to opiate naive rats.
+ADORA1	drug	opioid	7820640	Increased concentrations of cortical <strong>adenosine A1 receptor</strong> sites, but not striatal adenosine A2a sites, were found in saturation binding studies from <b>morphine</b> dependent mice.
+ADORA1	drug	alcohol	7945566	2 Chloro N6 cyclopentyladenosine (CCPA), an <strong>adenosine A1 receptor</strong> agonist, suppresses <b>ethanol</b> withdrawal syndrome in rats.
+ADORA1	addiction	withdrawal	7945566	2 Chloro N6 cyclopentyladenosine (CCPA), an <strong>adenosine A1 receptor</strong> agonist, suppresses ethanol <b>withdrawal</b> syndrome in rats.
+ADORA1	drug	opioid	1631178	The <strong>adenosine A1 receptor</strong> agonist N6 [(R) 1 methyl 2 phenylethyl]adenosine (R PIA), the A2 agonist 2 (phenylamino)adenosine (CV 1808), the nonselective A1, A2 agonist (adenosine 5' ethylcarboxamide (NECA), and the alpha 2 adrenoceptor agonist clonidine were screened (each at 30, 100, and 300 micrograms/kg, SC) for their ability to alter naloxine precipitated withdrawal signs in <b>morphine</b> dependent rats.
+ADORA1	addiction	withdrawal	1631178	The <strong>adenosine A1 receptor</strong> agonist N6 [(R) 1 methyl 2 phenylethyl]adenosine (R PIA), the A2 agonist 2 (phenylamino)adenosine (CV 1808), the nonselective A1, A2 agonist (adenosine 5' ethylcarboxamide (NECA), and the alpha 2 adrenoceptor agonist clonidine were screened (each at 30, 100, and 300 micrograms/kg, SC) for their ability to alter naloxine precipitated <b>withdrawal</b> signs in morphine dependent rats.
+GPT	addiction	reward	29352865	In addition, the histopathological observations of mice livers and the <strong>GPT</strong> activities indicated that <b>CPP</b> 2 could attenuate liver cell injury.
+GPT	drug	benzodiazepine	25667858	This is the first report regarding possible compulsive gambling, provoked by AEMs in a patient with idiopathic generalized epilepsy, who presented with nonconvulsive status epilepticus, having previously not achieved seizure control with carbamazepine, valproate, (VPA), topiramate, gabapentin (<strong>GPT</strong>), lamotrigine (LTG), and <b>clobazam</b>.
+GPT	addiction	addiction	25667858	This is the first report regarding possible <b>compulsive</b> gambling, provoked by AEMs in a patient with idiopathic generalized epilepsy, who presented with nonconvulsive status epilepticus, having previously not achieved seizure control with carbamazepine, valproate, (VPA), topiramate, gabapentin (<strong>GPT</strong>), lamotrigine (LTG), and clobazam.
+GPT	drug	alcohol	24163503	Biochemical parameters, including hemoglobin, <b>ethanol</b>, glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (<strong>GPT</strong>), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), and creatine phosphokinase (CPK), were measured at 30 min before induction of HS and 0, 1, 3, 6, 9, 12, 18, 24, and 48 h after HS.
+GPT	drug	alcohol	24163503	Acute <b>ethanol</b> intoxication further increased serum levels of GOT, <strong>GPT</strong>, BUN, Cre, LDH, CPK, TNF  α and IL 6 elevation following HS.
+GPT	addiction	intoxication	24163503	Acute ethanol <b>intoxication</b> further increased serum levels of GOT, <strong>GPT</strong>, BUN, Cre, LDH, CPK, TNF  α and IL 6 elevation following HS.
+GPT	addiction	intoxication	15688776	The biological effects of lead <b>intoxication</b> consist in the occurrence of stippled basophilic erythrocytes (2 cases with 46,000/1 mil erythrocytes), the anemia (only 4 cases with haematocrit L 40%) and the liver cytolytic syndrome (the increase of <strong>GPT</strong>, GOT and of g GT).
+GPT	drug	alcohol	12748988	The <b>ethanol</b> extracts of Ricinus communis did not cause any hepatotoxicity since the hepatic GOT and <strong>GPT</strong> levels were unaltered.
+GPT	drug	alcohol	9289524	At the end of a year follow up there were statistically significant differences in: percentage of risk drinkers who decreased <b>alcohol</b> intake below 280 g weekly (82% intervention group; 47% control group); percentage of reduction in <strong>GPT</strong>, GGT, triglycerides, systolic blood pressure and the MALT questionnaire.
+GPT	drug	alcohol	8587701	In contrast to the currently used parameters GOT, <strong>GPT</strong>, gammaGT, LDH and MCV, CDT measures chronic <b>alcoholism</b> exclusively.
+GPT	drug	alcohol	8404476	Jaundice developed 13 days after onset of treatment and acute liver failure was diagnosed on the 18th day after a total <b>disulfiram</b> dose of 4.5 g (Quick value < 10%; bilirubin 460 mumol/l; <strong>GPT</strong> 5099 U/l; GOT 4142 U/l), as well as early renal failure (creatinine 300 mumol/l).
+GPT	addiction	dependence	16666927	The <b>dependence</b> of <strong>GPT</strong> induction on high levels of nitrate in the media was tested by comparing activity levels in Hoagland solution and a nitrate free nutrient solution.
+GPT	drug	alcohol	2529084	Compared with a control group of patients undergoing traditional therapy (sedative and multi vitamin drugs), metadoxine showed a significant improvement of the values of gamma GT, <strong>GPT</strong>, blood ammonia, blood <b>alcohol</b> and of neuropsychic and behavioural parameters such as agitation, tremor, asterixis, sopor and depression.
+GPT	drug	alcohol	2706096	The liver enzymes GGT, GOT and <strong>GPT</strong>, as well as MCV, of 40 <b>alcoholics</b> were examined.
+GPT	addiction	intoxication	3613606	Aqueous extracts of young sprouts show a significant hepatoprotective effect on plasma <strong>GPT</strong> levels when given as pretreatment before carbon tetrachloride <b>intoxication</b> while the whole plant extract was inactive.
+GPT	drug	alcohol	3814348	There were no differences between the two groups in levels of blood <b>ethanol</b>, serum GOT, <strong>GPT</strong> and gamma GTP.
+GPT	drug	alcohol	3747559	Ethanolic extracts of these plants were investigated for their ability to reduce mortality of mice after <b>ethanol</b> intoxication and to lower the activities of plasma glutamic pyruvic transaminase (<strong>GPT</strong>) after carbon tetrachloride induced hepatitis in rats.
+GPT	addiction	intoxication	3747559	Ethanolic extracts of these plants were investigated for their ability to reduce mortality of mice after ethanol <b>intoxication</b> and to lower the activities of plasma glutamic pyruvic transaminase (<strong>GPT</strong>) after carbon tetrachloride induced hepatitis in rats.
+GPT	drug	alcohol	6892238	An increase of the <strong>GPT</strong>, GOT and LDH enzymatic activities was demonstrated in the rats of both groups but it was higher in the rats treated with HgCl2 and <b>alcohol</b> combined.
+GPT	drug	alcohol	7169302	In particular, four administrations of allyl <b>alcohol</b>, given every other day, increased glutamate oxaloacetate transaminase (GOT) for at least 48 hours from the last dose; ethionine reduced the bromsulphthalein (BSP) clearance even after 48 hours from the 1st, 2nd, or 3rd administration given on the 1st, 5th, or 12th day; ANIT, administered daily for seven days, increased glutamate pyruvate transaminase (<strong>GPT</strong>), alkaline phosphatase (AP), bilirubin, triglycerides (TG) and cholesterol (CH) while it decreased the body weight and retarded growth for at least six to seven days after intoxication.
+GPT	addiction	intoxication	7169302	In particular, four administrations of allyl alcohol, given every other day, increased glutamate oxaloacetate transaminase (GOT) for at least 48 hours from the last dose; ethionine reduced the bromsulphthalein (BSP) clearance even after 48 hours from the 1st, 2nd, or 3rd administration given on the 1st, 5th, or 12th day; ANIT, administered daily for seven days, increased glutamate pyruvate transaminase (<strong>GPT</strong>), alkaline phosphatase (AP), bilirubin, triglycerides (TG) and cholesterol (CH) while it decreased the body weight and retarded growth for at least six to seven days after <b>intoxication</b>.
+GPT	drug	alcohol	7169302	In fact, DHBE reduced the plasma GOT levels increased by allyl <b>alcohol</b>, improved the BSP clearance impaired by ethionine and tended to normalize the parameters modified by ANIT by lowering <strong>GPT</strong>, AP, CH, TG and bilirubin plasma levels and by enhancing body growth.
+GPT	drug	alcohol	6104856	When studied in connexion with the behaviour of serum triglyceride and alanineaminotransferase (<strong>GPT</strong>) levels, gammaGT activity was found to be particularly high in hypertriglyceridemic <b>alcoholics</b> and in those presenting a moderate increase of serum transaminases.
+CYP2C19	drug	alcohol	31957548	Effects of <strong>CYP2C19</strong>*2 polymorphisms on the efficacy and safety of phenazepam in patients with anxiety disorder and comorbid <b>alcohol</b> use disorder.
+CYP2C19	drug	alcohol	31957548	The purpose of this research was to study the effect of the <strong>CYP2C19</strong>*2 (681G>A, rs4244285) in patients with anxiety disorders and <b>alcohol</b> dependence taking phenazepam therapy.
+CYP2C19	addiction	dependence	31957548	The purpose of this research was to study the effect of the <strong>CYP2C19</strong>*2 (681G>A, rs4244285) in patients with anxiety disorders and alcohol <b>dependence</b> taking phenazepam therapy.
+CYP2C19	drug	nicotine	30734152	<b>Smoking</b> status (p = 0.07) and the <strong>CYP2C19</strong> phenotype (p = 0.07), but not the CYP2D6 genotype (p = 0.61), showed marginally significant effects on TOR activity.
+CYP2C19	drug	benzodiazepine	30696292	Clinical consequences related to a defective elimination of <b>clobazam</b> caused by homozygous mutated <strong>CYP2C19</strong> allele.
+CYP2C19	drug	benzodiazepine	30696292	We report an interesting case of voluntary drug intoxication with <b>clobazam</b> (CLB) in a patient with a homozygous mutated <strong>CYP2C19</strong> genotype.
+CYP2C19	addiction	intoxication	30696292	We report an interesting case of voluntary drug <b>intoxication</b> with clobazam (CLB) in a patient with a homozygous mutated <strong>CYP2C19</strong> genotype.
+CYP2C19	addiction	dependence	30696292	The half life elimination of CLB is 18 h that of NCLB is between 40 and 50 h. However, there is considerable inter individual variation in the metabolism of CLB and of the report NCLB/CLB under the <b>dependence</b> of genotype of <strong>CYP2C19</strong>.
+CYP2C19	drug	alcohol	30325732	Effects of <strong>CYP2C19</strong>*17 polymorphisms on the efficacy and safety of bromodigyrochlorophenylbenzodiazepine in patients with anxiety disorder and comorbid <b>alcohol</b> use disorder.
+CYP2C19	drug	alcohol	30325732	Conclusions Thus, it has been shown that the polymorphism of the <strong>CYP2C19</strong> gene may influence the effectiveness indices of Phenazepam therapy in patients with anxiety disorders comorbid with <b>alcohol</b> dependence.
+CYP2C19	addiction	dependence	30325732	Conclusions Thus, it has been shown that the polymorphism of the <strong>CYP2C19</strong> gene may influence the effectiveness indices of Phenazepam therapy in patients with anxiety disorders comorbid with alcohol <b>dependence</b>.
+CYP2C19	drug	opioid	30205091	<b>Methadone</b> undergoes N demethylation by multiple cytochrome P450 (CYP) enzymes including CYP3A4, CYP2B6, <strong>CYP2C19</strong>, CYP2D6, CYP2C9, and CYP2C8.
+CYP2C19	drug	opioid	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, <strong>CYP2C19</strong>, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+CYP2C19	addiction	dependence	29333880	Variants in six pharmacokinetic genes (CYP1A2, CYP2B6, <strong>CYP2C19</strong>, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+CYP2C19	drug	benzodiazepine	28958437	Given that <b>clobazam</b> is primarily demethylated to N CLB by cytochrome P450 (CYP) enzyme, CYP3A4, the mean plasma time concentration profile of <b>clobazam</b> was unchanged with the exclusion of <strong>CYP2C19</strong> poor metabolizers.
+CYP2C19	drug	opioid	27386066	It seems that <b>methadone</b> as <strong>CYP2C19</strong> inhibitor affects ticlopidine activity in vivo.
+CYP2C19	drug	alcohol	27099220	Role of <strong>CYP2C19</strong> gene polymorphism in acute <b>alcohol</b> withdrawal treatment with loading dose of diazepam in a South Indian population.
+CYP2C19	drug	benzodiazepine	27099220	Role of <strong>CYP2C19</strong> gene polymorphism in acute alcohol withdrawal treatment with loading dose of <b>diazepam</b> in a South Indian population.
+CYP2C19	addiction	withdrawal	27099220	Role of <strong>CYP2C19</strong> gene polymorphism in acute alcohol <b>withdrawal</b> treatment with loading dose of diazepam in a South Indian population.
+CYP2C19	drug	alcohol	27099220	We studied the effect of <strong>CYP2C19</strong> gene polymorphisms on diazepam loading dose requirement and time to reversal of acute <b>alcohol</b> withdrawal symptoms.
+CYP2C19	drug	benzodiazepine	27099220	We studied the effect of <strong>CYP2C19</strong> gene polymorphisms on <b>diazepam</b> loading dose requirement and time to reversal of acute alcohol withdrawal symptoms.
+CYP2C19	addiction	withdrawal	27099220	We studied the effect of <strong>CYP2C19</strong> gene polymorphisms on diazepam loading dose requirement and time to reversal of acute alcohol <b>withdrawal</b> symptoms.
+CYP2C19	drug	benzodiazepine	27099220	We found that <strong>CYP2C19</strong> polymorphism did not have any significant effect on the <b>diazepam</b> dose requirement, time duration needed for successful treatment or on the persistent symptoms after loading dose of <b>diazepam</b> in South Indian population.
+CYP2C19	drug	opioid	27061230	To examine whether certain genotypes were associated with this, we examined the frequencies of 29 SNPs located in candidate genes related to <b>opioid</b> pharmacology: ABCB1, OPRM1, UGT2B7, CYP3A5, CYP2B6, <strong>CYP2C19</strong>, CYP2D6, COMT, KCNJ6 and SCN9A in 274 deceased patients with OA (DOA), 309 living patients with OA (LOA) and in 394 healthy volunteers (HV).
+CYP2C19	drug	alcohol	26020462	Extreme Duration of Diazepam Associated Sedation in a Patient With <b>Alcohol</b> Delirium and <strong>CYP2C19</strong> Polymorphisms.
+CYP2C19	drug	benzodiazepine	26020462	Extreme Duration of <b>Diazepam</b> Associated Sedation in a Patient With Alcohol Delirium and <strong>CYP2C19</strong> Polymorphisms.
+CYP2C19	drug	benzodiazepine	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) methadone), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the <b>midazolam</b> test, R,S methadone trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, ABCB1, CYP2B6, CYP3A5, <strong>CYP2C19</strong> and CYP2D6 genes.
+CYP2C19	drug	opioid	25556837	Eighty one stable patients (60 men and 21 women, 43.7 ± 8.1 years old, 63.1 ± 50.9 mg day( 1) <b>methadone</b>), divided into quartiles with respect to the median daily dose, were enrolled and underwent clinical examination, treatment history and determination of liver/intestinal cytochrome P450 (CYP) 3A4 activity measured by the midazolam test, R,S <b>methadone</b> trough concentration and clinically significant polymorphisms of the OPRM1, DRD2, COMT, ABCB1, CYP2B6, CYP3A5, <strong>CYP2C19</strong> and CYP2D6 genes.
+CYP2C19	drug	opioid	25278738	We found that the SNPs on CYP2B6 were associated with plasma S <b>methadone</b> concentration; SNPs on CYP3A4 were associated with withdrawal symptoms and side effects; and SNPs on <strong>CYP2C19</strong> were associated with <b>methadone</b> dose.
+CYP2C19	addiction	withdrawal	25278738	We found that the SNPs on CYP2B6 were associated with plasma S methadone concentration; SNPs on CYP3A4 were associated with <b>withdrawal</b> symptoms and side effects; and SNPs on <strong>CYP2C19</strong> were associated with methadone dose.
+CYP2C19	drug	opioid	24016178	Functional genetic polymorphisms in <strong>CYP2C19</strong> gene in relation to cardiac side effects and treatment dose in a <b>methadone</b> maintenance cohort.
+CYP2C19	drug	opioid	24016178	This study tested the influence of functional genetic polymorphisms in <strong>CYP2C19</strong> gene encoding a CYP450 enzyme that contributes to <b>methadone</b> metabolism on treatment dose, plasma concentration, and side effects of <b>methadone</b>.
+CYP2C19	drug	opioid	24016178	Using the gene dose (GD) models where the <strong>CYP2C19</strong> SNPs were clustered into poor (0 GD) versus intermediate (1 GD) and extensive (2 GD) metabolizers, we found that the extensive metabolizers required a higher dose of <b>methadone</b> (p=0.035), and showed a lower plasma R <b>methadone</b>/<b>methadone</b> dose ratio (p=0.007) in urine opiate test negative patients, as well as a greater QTc change (p=0.008) and higher total scores of TESS (p=0.018) in urine opiate test positive patients, than poor metabolizers.
+CYP2C19	drug	opioid	24016178	These results in a large study sample from Taiwan suggest that the gene dose of <strong>CYP2C19</strong> may potentially serve as an indicator for the plasma R <b>methadone</b>/<b>methadone</b> dose ratio and cardiac side effect in patients receiving <b>methadone</b> maintenance therapy.
+CYP2C19	drug	opioid	22926004	Study goals were to (1) characterize changes in <b>methadone</b> dose across childbearing, (2) determine enantiomer specific <b>methadone</b> withdrawal kinetics from steady state during late pregnancy, (3) assess enantiomer specific changes in <b>methadone</b> level/dose (L/D) ratios across childbearing, and (4) explore relationships between CYP2B6, <strong>CYP2C19</strong>, and CYP3A4 single nucleotide polymorphisms and maternal dose, plasma concentration, and L/D.
+CYP2C19	addiction	withdrawal	22926004	Study goals were to (1) characterize changes in methadone dose across childbearing, (2) determine enantiomer specific methadone <b>withdrawal</b> kinetics from steady state during late pregnancy, (3) assess enantiomer specific changes in methadone level/dose (L/D) ratios across childbearing, and (4) explore relationships between CYP2B6, <strong>CYP2C19</strong>, and CYP3A4 single nucleotide polymorphisms and maternal dose, plasma concentration, and L/D.
+CYP2C19	drug	cocaine	21766908	Development of <b>cocaine</b> induced interstitial lung damage in two <strong>CYP2C</strong> and VKORC1 variant allele carriers.
+CYP2C19	drug	cocaine	21766908	The described drug abuse cases suggest that an association between the presence of <strong>CYP2C</strong> and VKORC1 allelic variants and <b>cocaine</b> induced interstitial lung damage is highly likely.
+CYP2C19	drug	opioid	21589866	Patients were clinically assessed and blood samples were obtained to determine plasma concentrations of (R,S) , (R) and (S) <b>methadone</b> and to study allelic variants of genes encoding CYP3A5, CYP2D6, CYP2B6, CYP2C9, <strong>CYP2C19</strong>, and P glycoprotein.
+CYP2C19	drug	opioid	20394193	It was shown that molecular genetic studies at postmortem <b>morphine</b> concentrations of up to 0.5 mg/l as a rule identify mutant alleles (CYP2D6*3*4; <strong>CYP2C19</strong>*2*3).
+CYP2C19	drug	opioid	20394193	Mutant alleles CYP2D6* and <strong>CYP2C19</strong>* are most frequently detected at postmortem blood <b>morphine</b> levels ranging from 1 to 4 mg/I.
+CYP2C19	drug	opioid	20394193	The remaining subjects lacking mutations in CYP2D6 and <strong>CYP2C19</strong> genes are considered to be ordinary metabolizers dying at toxic concentrations of <b>morphine</b> in their blood (from 1 to 4 mg/I); such cases need no genetic studies to be carried out to identify CYP2D6 and <strong>CYP2C19</strong> polymorphism.
+CYP2C19	drug	benzodiazepine	14586385	A marginally significant dependence of <b>alprazolam</b> concentrations from the <strong>CYP2C19</strong> allele *2 was found (P =.04).
+CYP2C19	addiction	dependence	14586385	A marginally significant <b>dependence</b> of alprazolam concentrations from the <strong>CYP2C19</strong> allele *2 was found (P =.04).
+CYP2C19	drug	psychedelics	12019193	Metabolism of 18 methoxycoronaridine, an <b>ibogaine</b> analog, to 18 hydroxycoronaridine by genetically variable <strong>CYP2C19</strong>.
+CYP2C19	drug	benzodiazepine	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes CYP2D6 (codeine, amphetamines, dextromethorphan), CYP2A6 (nicotine) and <strong>CYP2C19</strong> (<b>flunitrazepam</b>).
+CYP2C19	drug	nicotine	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes CYP2D6 (codeine, amphetamines, dextromethorphan), CYP2A6 (<b>nicotine</b>) and <strong>CYP2C19</strong> (flunitrazepam).
+CYP2C19	drug	opioid	10911933	Using in vitro studies, we have identified drugs of abuse that are substrates of the polymorphic enzymes CYP2D6 (<b>codeine</b>, amphetamines, dextromethorphan), CYP2A6 (nicotine) and <strong>CYP2C19</strong> (flunitrazepam).
+TST	drug	cocaine	31998090	Mice that showed less submission during defeat episodes, a lower percentage of time in the open arms of the EPM, low novelty seeking, high social interaction, greater immobility in the <strong>TST</strong> and a higher frequency of grooming were those that were resilient to the long term effects of social defeat on <b>cocaine</b> reward since they behaved like controls and did not develop CPP.
+TST	addiction	relapse	31998090	Mice that showed less submission during defeat episodes, a lower percentage of time in the open arms of the EPM, low novelty <b>seeking</b>, high social interaction, greater immobility in the <strong>TST</strong> and a higher frequency of grooming were those that were resilient to the long term effects of social defeat on cocaine reward since they behaved like controls and did not develop CPP.
+TST	addiction	reward	31998090	Mice that showed less submission during defeat episodes, a lower percentage of time in the open arms of the EPM, low novelty seeking, high social interaction, greater immobility in the <strong>TST</strong> and a higher frequency of grooming were those that were resilient to the long term effects of social defeat on cocaine <b>reward</b> since they behaved like controls and did not develop <b>CPP</b>.
+TST	addiction	intoxication	31494454	The aim of the current study was to test the predictive utility of temporal self regulation theory (<strong>TST</strong>), and the additional construct of 'sensitivity to reward', in accounting for variance in <b>binge</b> drinking behavior amongst Australian university students.
+TST	addiction	reward	31494454	The aim of the current study was to test the predictive utility of temporal self regulation theory (<strong>TST</strong>), and the additional construct of 'sensitivity to <b>reward</b>', in accounting for variance in binge drinking behavior amongst Australian university students.
+TST	addiction	reward	31494454	At time one, participants completed self report measures assessing <strong>TST</strong> constructs (intention, behavior prepotency, self regulation), as well as 'sensitivity to <b>reward</b>'.
+TST	addiction	intoxication	31494454	Using hierarchical multiple regression analyses, <strong>TST</strong> significantly predicted <b>binge</b> drinking behaviors (<b>binge</b> drinking episodes: R2 = 0.41, p < .001; peak consumption: R2 = 0.41, p < .001), with equally large effect sizes for both, f2 = 0.69.
+TST	addiction	withdrawal	30993081	In experiment 1, elevated plus maze (EPM), open field test (OFT), forced swim test (FST), and tail suspension test (<strong>TST</strong>) were used to examine anxiety and depression in animals during <b>withdrawal</b> period.
+TST	drug	amphetamine	30993081	In the first experiment, duloxetine at all doses attenuated <b>methamphetamine</b> withdrawal induced depression, anxiety, and motor disturbances in FST, OFT, EPM, and <strong>TST</strong>.
+TST	addiction	withdrawal	30993081	In the first experiment, duloxetine at all doses attenuated methamphetamine <b>withdrawal</b> induced depression, anxiety, and motor disturbances in FST, OFT, EPM, and <strong>TST</strong>.
+TST	drug	alcohol	29704590	The behavioral studies were conducted employing forced swim test (FST), and tail suspension test (<strong>TST</strong>) on day 18 to determine the effects of N acetylcysteine and fluoxetine in the <b>ethanol</b> withdrawal induced depression.
+TST	addiction	withdrawal	29704590	The behavioral studies were conducted employing forced swim test (FST), and tail suspension test (<strong>TST</strong>) on day 18 to determine the effects of N acetylcysteine and fluoxetine in the ethanol <b>withdrawal</b> induced depression.
+TST	drug	alcohol	29704590	The results revealed that <b>alcohol</b> abstinence group depicted increased immobility time in FST and <strong>TST</strong>.
+TST	drug	opioid	28028518	Chronic <b>morphine</b> administration caused depression and anxiety as observed by FST, EPM, and <strong>TST</strong> and decreased motor activity in OFT and caused impairment in learning and memory performance in MWM.
+TST	drug	nicotine	26512426	<b>Nicotine</b> dependent animals indicated a reflective depression and anxiety in a dose dependent manner in FST, EPM, and <strong>TST</strong>, which were significantly different from the control group and also can significantly attenuate the motor activity and anxiety in OFT.
+TST	drug	psychedelics	25702084	The anti immobility effect of creatine (1 mg/kg, po) or <b>ketamine</b> (a fast acting antidepressant, 1 mg/kg, ip) in the <strong>TST</strong> was prevented by pretreatment of mice with caffeine (3 mg/kg, ip, nonselective adenosine receptor antagonist), 8 cyclopentyl 1,3 dipropylxanthine (DPCPX) (2 mg/kg, ip, selective adenosine A1 receptor antagonist), and 4 (2 [7 amino 2 {2 furyl}{1,2,4}triazolo {2,3 a}{1,3,5}triazin 5 yl amino]ethyl) phenol (ZM241385) (1 mg/kg, ip, selective adenosine A2A receptor antagonist).
+TST	drug	psychedelics	25702084	Moreover, the administration of subeffective doses of creatine or <b>ketamine</b> combined with N 6 cyclohexyladenosine (CHA) (0.05 mg/kg, ip, selective adenosine A1 receptor agonist), N 6 [2 (3,5 dimethoxyphenyl) 2 (methylphenyl)ethyl]adenosine (DPMA) (0.1 mg/kg, ip, selective adenosine A2A receptor agonist), or dipyridamole (0.1 μg/mouse, icv, adenosine transporter inhibitor) produced a synergistic antidepressant like effect in the <strong>TST</strong>.
+TST	drug	psychedelics	25702084	These results indicate that creatine, similarly to <b>ketamine</b>, exhibits antidepressant like effect in the <strong>TST</strong> probably mediated by the activation of both adenosine A1 and A2A receptors, further reinforcing the potential of targeting the purinergic system to the management of mood disorders.
+TST	addiction	reward	25702084	These results indicate that creatine, similarly to ketamine, exhibits antidepressant like effect in the <strong>TST</strong> probably mediated by the activation of both adenosine A1 and A2A receptors, further <b>reinforcing</b> the potential of targeting the purinergic system to the management of mood disorders.
+TST	drug	alcohol	22651960	We have found potential antidepressant like effect of <b>acamprosate</b> at doses of 100 400 mg/kg in the <strong>TST</strong> in C57BL/6J mice.
+TST	drug	alcohol	22651960	Furthermore we have shown that the antidepressant like effect of <b>acamprosate</b> used at a dose of 200 mg/kg was dependent on NMDA and mGlu5 receptor blockade, since NMDA (25 mg/kg) and mGlu5 receptor positive allosteric modulator, CDPPB (3 mg/kg), antagonized its activity in the <strong>TST</strong>.
+TST	drug	opioid	20014914	Currently, tuberculin skin testing (<strong>TST</strong>) is recommended for patients enrolling in <b>methadone</b> maintenance treatment (MMT), but not for those enrolling in <b>buprenorphine</b> maintenance treatment (BMT).
+TST	drug	opioid	20014914	These results confirm a similar high prevalence of <strong>TST</strong> positivity in <b>opioid</b> dependent patients enrolling in MMT and BMT programs.
+TST	drug	opioid	20014914	These data suggest the importance of incorporating <strong>TST</strong> screening in emerging BMT programs as a mechanism to provide increased detection and treatment of tuberculosis infection in <b>opioid</b> dependent patient populations.
+TST	drug	psychedelics	18458881	One week after a single administration of <b>ketamine</b> (50 160 mg/kg), otherwise experimentally naive rats and mice were tested either in the forced swim test (FST) or the tail suspension test (<strong>TST</strong>).
+TST	drug	opioid	17122073	The first relies on <b>naloxone</b> induced withdrawal in <b>morphine</b> dependent (MD) OVX rats, resulting in an acute rise in <strong>TST</strong>.
+TST	addiction	withdrawal	17122073	The first relies on naloxone induced <b>withdrawal</b> in morphine dependent (MD) OVX rats, resulting in an acute rise in <strong>TST</strong>.
+TST	drug	opioid	17122073	Further evaluation showed that orally administered DVS acutely and dose dependently (10 100 mg/kg) abated a <b>naloxone</b> induced rise in <strong>TST</strong> of MD rats and alleviated OVX induced temperature dysfunction in the telemetry model.
+TST	drug	opioid	15527744	The first model is based on measurement of the tail skin temperature (<strong>TST</strong>) increase following <b>naloxone</b> induced withdrawal in <b>morphine</b> dependent ovariectomized (OVX) rats (MD model), while the second model relies on telemetric assessment of diurnal <strong>TST</strong> changes in ovariectomized rats (telemetry model).
+TST	addiction	withdrawal	15527744	The first model is based on measurement of the tail skin temperature (<strong>TST</strong>) increase following naloxone induced <b>withdrawal</b> in morphine dependent ovariectomized (OVX) rats (MD model), while the second model relies on telemetric assessment of diurnal <strong>TST</strong> changes in ovariectomized rats (telemetry model).
+TST	drug	opioid	15527744	Treatment with a 5 HT(2A/2C) receptor agonist, ( ) 2,5 dimethoxy 4 iodoamphetamine hydrochloride (DOI), prevented the <b>naloxone</b> induced <strong>TST</strong> increase in the MD model and restored normal active phase <strong>TST</strong> in the telemetry model.
+TST	drug	opioid	15527744	Interestingly, MDL 100907 increased <strong>TST</strong> in both models when given alone, with the <strong>TST</strong> increase occurring prior to the <b>naloxone</b> induced flush in the MD model.
+TST	drug	opioid	15002736	In addition, the total serum testosterone (<strong>TST</strong>) concentrations in male rats at different times of <b>morphine</b> administration and abstinence were measured.
+TST	drug	opioid	15002736	Acute and chronic administration of <b>morphine</b> severely inhibited the sexual behavior of the rats and lowered their <strong>TST</strong> concentrations.
+TST	drug	opioid	15002736	<strong>TST</strong> concentrations recovered to normal within 24 h after the last <b>morphine</b> injection, while sexual behavior remained suppressed for at least 7 days.
+TST	drug	opioid	15002736	Electroacupuncture (2/100 Hz alternately) administered once daily for 7 days during <b>morphine</b> withdrawal facilitated the recovery of male sexual behavior and increased <strong>TST</strong> concentrations to above normal.
+TST	addiction	withdrawal	15002736	Electroacupuncture (2/100 Hz alternately) administered once daily for 7 days during morphine <b>withdrawal</b> facilitated the recovery of male sexual behavior and increased <strong>TST</strong> concentrations to above normal.
+TST	addiction	reward	11420067	Successive conditioning phases were: free shaping (FS), continuous <b>reinforcement</b> (CRF), <b>operant</b> extinction (EXT), successive discrimination (DIS) and two stimuli test (<strong>TST</strong>).
+TST	drug	alcohol	11420067	Finally, <b>alcohol</b> deteriorated behavioral inhibition (DIS and <strong>TST</strong>) tested immediately after drinking.
+TST	drug	alcohol	8750043	Two statistically significant interactions were found: consistent with our hypothesis, stimulant abusers showed greater total sleep (<strong>TST</strong>) and REM sleep during acute withdrawal than subacute withdrawal, compared with <b>alcoholics</b>.
+TST	addiction	withdrawal	8750043	Two statistically significant interactions were found: consistent with our hypothesis, stimulant abusers showed greater total sleep (<strong>TST</strong>) and REM sleep during acute <b>withdrawal</b> than subacute <b>withdrawal</b>, compared with alcoholics.
+TST	drug	alcohol	8750043	In contrast, <b>alcoholics</b> showed less <strong>TST</strong> and REM sleep during acute withdrawal than during subacute withdrawal.
+TST	addiction	withdrawal	8750043	In contrast, alcoholics showed less <strong>TST</strong> and REM sleep during acute <b>withdrawal</b> than during subacute <b>withdrawal</b>.
+TST	drug	opioid	8187842	Following addiction to <b>morphine</b>, young and aged rats were evaluated for tail skin temperature (<strong>TST</strong>), rectal temperature (Tr), behavior, rhinorrhea, lacrimation, salivation, and diarrhea in response to <b>naloxone</b> administration.
+TST	addiction	addiction	8187842	Following <b>addiction</b> to morphine, young and aged rats were evaluated for tail skin temperature (<strong>TST</strong>), rectal temperature (Tr), behavior, rhinorrhea, lacrimation, salivation, and diarrhea in response to naloxone administration.
+TST	addiction	withdrawal	8187842	Young rats showed the expected <strong>TST</strong> increase and Tr decline in response to <b>withdrawal</b>.
+TST	drug	opioid	8187842	The majority of aged rats showed an exaggerated <strong>TST</strong> response to <b>naloxone</b>, while some aged rats failed to exhibit any <strong>TST</strong> response to withdrawal.
+TST	addiction	withdrawal	8187842	The majority of aged rats showed an exaggerated <strong>TST</strong> response to naloxone, while some aged rats failed to exhibit any <strong>TST</strong> response to <b>withdrawal</b>.
+TST	drug	opioid	1907349	The present study was designed to evaluate the effects of E2 CDS vs. E2, on the tail skin temperature (<strong>TST</strong>) surge associated with administration of <b>naloxone</b> to <b>morphine</b> dependent rats, an animal model for menopausal hot flush.
+TST	drug	opioid	1907349	The mean maximal elevation in <strong>TST</strong> of the control animals was 6.4 +/  0.2 degrees C. A single injection of E2 CDS attenuated the <b>naloxone</b> induced rise in <strong>TST</strong> by 25%, while multiple injections resulted in significant attenuation of the rise in <strong>TST</strong> (3.4 +/  0.6).
+TST	drug	opioid	1967837	Adrenalectomy and peripheral administration of propranolol (10 mg/kg sc) both resulted in a significant attenuation of the surge in <strong>TST</strong> and the fall in core temperature in the <b>morphine</b> dependent rat which suggest some peripherally mediated event is necessary to produce the full skin temperature surge.
+TST	drug	opioid	1967837	Collectively, the data suggest a role for the adrenal gland and adrenergic receptors in producing the surge in <strong>TST</strong> in <b>morphine</b> dependent rats.
+TST	drug	opioid	2388522	<b>Naloxone</b> caused a tail skin temperature (<strong>TST</strong>) response of 5.7 +/  0.5 degrees C in <b>morphine</b> dependent rats.
+TST	drug	opioid	2388522	Intraperitoneal administration 2 deoxyglucose (2DG) caused <strong>TST</strong> responses in placebo treated and <b>morphine</b> dependent rats of 4.8 +/  0.6 and 6.2 +/  0.5 degrees C, respectively.
+TST	drug	opioid	2388522	These data indicate that the activation of the sympathetic nervous system by cellular glucoprivation causes a <strong>TST</strong> response which is equivalent in magnitude to that induced by precipitating withdrawal with <b>naloxone</b>.
+TST	addiction	withdrawal	2388522	These data indicate that the activation of the sympathetic nervous system by cellular glucoprivation causes a <strong>TST</strong> response which is equivalent in magnitude to that induced by precipitating <b>withdrawal</b> with naloxone.
+TST	drug	opioid	2388522	This effect of 2DG appears to be mediated by the brain, since icy administration of 2DG caused a <strong>TST</strong> response, similar to that induced by <b>naloxone</b> treatment of <b>morphine</b> dependent rats.
+TST	drug	opioid	2274603	Studies were undertaken to determine the effects of acute alterations in plasma glucose levels on the tail skin temperature (<strong>TST</strong>) response of <b>morphine</b> dependent rats to <b>naloxone</b> precipitated withdrawal.
+TST	addiction	withdrawal	2274603	Studies were undertaken to determine the effects of acute alterations in plasma glucose levels on the tail skin temperature (<strong>TST</strong>) response of morphine dependent rats to naloxone precipitated <b>withdrawal</b>.
+TST	drug	opioid	2274603	In <b>morphine</b> dependent rats, treatment with dextrose at doses of 0.5 or 2.5 g/kg did not alter the normal 6.0 +/  0.3 degrees C <strong>TST</strong> response to <b>naloxone</b>.
+TST	drug	opioid	2274603	However, treatment with 5, 10 or 20 g dextrose/kg, which increased plasma glucose to 250 mg/dl or greater, blocked the <strong>TST</strong> response during <b>morphine</b> withdrawal.
+TST	addiction	withdrawal	2274603	However, treatment with 5, 10 or 20 g dextrose/kg, which increased plasma glucose to 250 mg/dl or greater, blocked the <strong>TST</strong> response during morphine <b>withdrawal</b>.
+TST	drug	opioid	2274603	In contrast, an IV injection of 2.5 IU insulin (Na porcine)/kg, which reduced plasma glucose for 2 h, caused a delayed <strong>TST</strong> response of 4.7 +/  0.4 degrees C in control rats and exaggerated the <strong>TST</strong> response normally observed in <b>morphine</b> dependent rats treated with <b>naloxone</b>.
+TST	drug	opioid	2670064	Administration of <b>naloxone</b> to these animals results in a surge in LH secretion which precedes the elevation in tail skin temperature (<strong>TST</strong>).
+TST	drug	opioid	2670064	Central administration of <b>naloxone</b> was without effect in controls but produced a 5 6 degree C rise of <strong>TST</strong> in the <b>morphine</b> dependent rat while central administration of 10 microliters of the saline vehicle produced no changes in <strong>TST</strong> in either group.
+TST	drug	opioid	2670064	Administration of 5 or 10 micrograms of the LH RH agonist (Des Gly10, [im Bzl D His6]LH RH ethylamide) into the LV produced a significantly greater elevation in <strong>TST</strong> (4 degrees C) in the <b>morphine</b> dependent rats compared to a negligible rise in <strong>TST</strong> in the control rats; however, administration of a larger dose of 20 micrograms of the LH RH agonist produced similar <strong>TST</strong> responses of about 4 degrees C in both groups.
+TST	drug	opioid	2670064	In a subsequent study central administration of the LH RH agonist (5 micrograms/10 microliters) resulted in a similar rise in serum LH in both control and <b>morphine</b> dependent rats, suggesting that the elevation in <strong>TST</strong> is not closely associated with LH secretion.
+TST	drug	opioid	2670064	Further support for a role of LH RH in our animal model was obtained following central administration of an LH RH antagonist [(D Phe2.6, Pro3]LH RH) which blocked the rise in <strong>TST</strong> associated with systemic administration of <b>naloxone</b> (1 mg/kg, s.c.) in <b>morphine</b> dependent rats.
+TST	drug	opioid	2825916	Studies were undertaken to evaluate the role of central noradrenergic neurons in the tail skin temperature (<strong>TST</strong>) surge that accompanies <b>morphine</b> withdrawal in the rat.
+TST	addiction	withdrawal	2825916	Studies were undertaken to evaluate the role of central noradrenergic neurons in the tail skin temperature (<strong>TST</strong>) surge that accompanies morphine <b>withdrawal</b> in the rat.
+TST	drug	opioid	2825916	A 5 degrees C increase in <strong>TST</strong> and a 1 2 degrees C decrease in rectal temperature (Tr) was observed following administration of a dose of <b>naloxone</b> HCl (NAL, 1 mg/kg, s.c.) which precipitated withdrawal in <b>morphine</b> dependent rats.
+TST	addiction	withdrawal	2825916	A 5 degrees C increase in <strong>TST</strong> and a 1 2 degrees C decrease in rectal temperature (Tr) was observed following administration of a dose of naloxone HCl (NAL, 1 mg/kg, s.c.) which precipitated <b>withdrawal</b> in morphine dependent rats.
+TST	drug	opioid	2825916	injection of clonidine HCl, a partial alpha 2 adrenergic agonist did not alter <strong>TST</strong> in <b>morphine</b> dependent animals.
+TST	drug	opioid	2825916	given 10 min prior to the administration of NAL completely blocked the <strong>TST</strong> response to the opiate antagonist in the <b>morphine</b> dependent animals.
+TST	drug	opioid	2825916	failed to alter <strong>TST</strong> when administered alone, but the highest dose significantly reduced the <strong>TST</strong> response to <b>naloxone</b> in the <b>morphine</b> dependent rat.
+TST	drug	opioid	2825916	Collectively, these data indicate that brain noradrenergic neurons play a role in the <strong>TST</strong> surge which accompanies NAL precipitated <b>morphine</b> withdrawal, and that the <strong>TST</strong> and Tr responses can be dissociated in the <b>morphine</b> dependent rat.
+TST	addiction	withdrawal	2825916	Collectively, these data indicate that brain noradrenergic neurons play a role in the <strong>TST</strong> surge which accompanies NAL precipitated morphine <b>withdrawal</b>, and that the <strong>TST</strong> and Tr responses can be dissociated in the morphine dependent rat.
+TST	drug	opioid	6092986	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal caused a prompt increase (4.9 +/  0.76 degrees C) in tail skin temperature (<strong>TST</strong>) and a subsequent decline in Tr ( 2.8 degrees C).
+TST	addiction	withdrawal	6092986	Naloxone precipitated morphine <b>withdrawal</b> caused a prompt increase (4.9 +/  0.76 degrees C) in tail skin temperature (<strong>TST</strong>) and a subsequent decline in Tr ( 2.8 degrees C).
+TST	drug	opioid	6092986	Similarly, <b>naloxone</b> administration to HYP rats caused a dramatic <strong>TST</strong> response which was coincident with the onset of severe HYP.
+TST	drug	opioid	6092986	This effect of <b>naloxone</b> was maximal at 7 weeks of tumor growth when a <strong>TST</strong> response of 4.8 +/  0.3 degrees C was observed but was not evident prior to or 1 week following tumor inoculation, when serum prolactin levels were low.
+TST	drug	opioid	6092986	The <strong>TST</strong> response to <b>naloxone</b> in chronic HYP exhibited distinct pulses with an amplitude of 3.4 +/  0.4 degrees C and a frequency of 2.2 +/  0.5 pulses per 120 min.
+TST	drug	opioid	6092986	These effects of chronic HYP on the <strong>TST</strong> response to <b>naloxone</b> were not influenced by ovariectomy, suggesting that changes in ovarian secretions were not involved in the response.
+TST	drug	opioid	6835016	In response to precipitous, <b>naloxone</b> induced withdrawal, rats showed surges in tail skin temperature (<strong>TST</strong>) which were similar in magnitude (4.8 to 7.2 degrees C) and duration (60 to 90 min.)
+TST	addiction	withdrawal	6835016	In response to precipitous, naloxone induced <b>withdrawal</b>, rats showed surges in tail skin temperature (<strong>TST</strong>) which were similar in magnitude (4.8 to 7.2 degrees C) and duration (60 to 90 min.)
+TST	drug	opioid	6835016	Additionally, a brief period of accelerated heart rate (59%) and a 9 fold hypersecretion of luteinizing hormone (LH) preceded the <strong>TST</strong> response to <b>morphine</b> withdrawal.
+TST	addiction	withdrawal	6835016	Additionally, a brief period of accelerated heart rate (59%) and a 9 fold hypersecretion of luteinizing hormone (LH) preceded the <strong>TST</strong> response to morphine <b>withdrawal</b>.
+TST	drug	opioid	6835016	Additionally, protracted <b>morphine</b> withdrawal subsequent to abstention, resulted in <strong>TST</strong> instability characterized by spontaneous, high amplitude <strong>TST</strong> fluctuations.
+TST	addiction	withdrawal	6835016	Additionally, protracted morphine <b>withdrawal</b> subsequent to abstention, resulted in <strong>TST</strong> instability characterized by spontaneous, high amplitude <strong>TST</strong> fluctuations.
+TST	drug	alcohol	710268	Twenty four hospitalized "<b>alcoholics</b>" were allocated to one of the following three group: (i) SST, (ii) CR, and (iii) traditional supportive therapy (<strong>TST</strong>).
+MAPK1	drug	cocaine	31116258	A gene network approach showed that the EHMT1, EHMT2, <strong>MAPK1</strong>, MAPK3, MAP2K1, and HDAC5 genes, which are involved in transcription and chromatin regulation cellular signaling pathways, were also associated with <b>cocaine</b> dependence.
+MAPK1	addiction	dependence	31116258	A gene network approach showed that the EHMT1, EHMT2, <strong>MAPK1</strong>, MAPK3, MAP2K1, and HDAC5 genes, which are involved in transcription and chromatin regulation cellular signaling pathways, were also associated with cocaine <b>dependence</b>.
+MAPK1	drug	opioid	31071414	<b>Oxycodone</b> CPP males have: a) increases in Bdnf (brain derived neurotrophic factor) expression, which is known to be produced in granule cells, relative to females; b) elevated <strong>Mapk1</strong> expression and pMAPK ir in the dentate hilus which harbors newly generated granule cells; and c) increases in CRHR1 ir in CA3 pyramidal cell soma.
+MAPK1	addiction	reward	31071414	Oxycodone <b>CPP</b> males have: a) increases in Bdnf (brain derived neurotrophic factor) expression, which is known to be produced in granule cells, relative to females; b) elevated <strong>Mapk1</strong> expression and pMAPK ir in the dentate hilus which harbors newly generated granule cells; and c) increases in CRHR1 ir in CA3 pyramidal cell soma.
+MAPK1	addiction	sensitization	30024967	The spinal NR2BR/<strong>ERK2</strong> pathway as a target for the central <b>sensitization</b> of collagen induced arthritis pain.
+MAPK1	drug	opioid	30024967	Extracellular signal regulated protein kinases 2 (<strong>ERK2</strong>) activity synchronized with the synaptic expression of NR2BR, which was downregulated by the action of <b>tramadol</b>.
+MAPK1	drug	psychedelics	28948570	Since GluN2B, via inhibition of ERK, regulates the membrane expression of GluA1, we measured ERK2 phosphorylation in the crude synaptosomal fraction of these brain regions, which was significantly reduced suggesting that <b>ketamine</b> induced phosphorylation of αCaMKII promotes GluN2B (S1303) phosphorylation that, in turn, inhibits <strong>ERK 2</strong> signaling, an effect that results in reduced membrane expression and phosphorylation of GluA1.
+MAPK1	drug	psychedelics	28948570	Since GluN2B, via inhibition of ERK, regulates the membrane expression of GluA1, we measured <strong>ERK2</strong> phosphorylation in the crude synaptosomal fraction of these brain regions, which was significantly reduced suggesting that <b>ketamine</b> induced phosphorylation of αCaMKII promotes GluN2B (S1303) phosphorylation that, in turn, inhibits <strong>ERK 2</strong> signaling, an effect that results in reduced membrane expression and phosphorylation of GluA1.
+MAPK1	drug	cocaine	26398380	In <b>cocaine</b> pretreated caged rats no changes in p CREB/CREB levels were observed, while <strong>ERK2</strong> levels either decreased (frontal cortex) or increased (nucleus accumbens).
+MAPK1	drug	opioid	26349634	In mice pretreated with all <b>opioids</b>, baseline <strong>ERK2</strong> activation levels were unchanged and increased in response to quinpirole.
+MAPK1	drug	opioid	26349634	However, quinpirole induced <strong>ERK2</strong> activation was significantly higher than drug naïve animals only in the <b>morphine</b> pretreated mice.
+MAPK1	drug	opioid	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for GluR1 AMPA receptor (AMPAR), phosphorylated <strong>ERK2</strong> (pERK2), CREB (pCREB), TrKB (pTrkB) were performed in brain areas relevant for sensitization from KO and WT and/or <b>naloxone</b>  and vehicle pre treated animals.
+MAPK1	addiction	sensitization	25431310	On day 21, microdialysis measures of accumbal extracellular dopamine, Western blotting for GluR1 AMPA receptor (AMPAR), phosphorylated <strong>ERK2</strong> (pERK2), CREB (pCREB), TrKB (pTrkB) were performed in brain areas relevant for <b>sensitization</b> from KO and WT and/or naloxone  and vehicle pre treated animals.
+MAPK1	drug	opioid	24950452	Ultra low dose <b>morphine</b> intensively increased pERK1 contents in the PAG and cortex and, to a lesser extent, increased cortical <strong>ERK2</strong> and JNK phosphorylation.
+MAPK1	drug	cocaine	24452697	MPH + FLX, or <b>cocaine</b> exposure in juvenile mice increased mRNA expression of <strong>ERK2</strong> and its downstream targets (CREB, cFos, and Zif268), and increased protein phosphorylation of <strong>ERK2</strong> and CREB 2 months after drug exposure.
+MAPK1	drug	opioid	24296091	During three phases of <b>morphine</b> induced CPP, the expression levels of ERK1 and <strong>ERK2</strong> mRNA were altered in various brain regions.
+MAPK1	addiction	reward	24296091	During three phases of morphine induced <b>CPP</b>, the expression levels of ERK1 and <strong>ERK2</strong> mRNA were altered in various brain regions.
+MAPK1	drug	opioid	24296091	In the PFC, the expression levels of ERK1 and <strong>ERK2</strong> mRNA were increased after chronic <b>morphine</b> injection (p=0.003, p=0.000), and did not return to the basal level after extinction training (p=0.025, p=0.000), but decreased after a priming injection (p=0.000, p=0.000).
+MAPK1	drug	opioid	24296091	Different from other brain regions, the expression levels of ERK1 and <strong>ERK2</strong> mRNA were decreased in three phases of <b>morphine</b> induced CPP in the hippocampus (ERK1: p=0.000, p=0.040, p=0.000; <strong>ERK2</strong>: p=0.000, p=0.000, p=0.000, respectively).
+MAPK1	addiction	reward	24296091	Different from other brain regions, the expression levels of ERK1 and <strong>ERK2</strong> mRNA were decreased in three phases of morphine induced <b>CPP</b> in the hippocampus (ERK1: p=0.000, p=0.040, p=0.000; <strong>ERK2</strong>: p=0.000, p=0.000, p=0.000, respectively).
+MAPK1	drug	opioid	24296091	These results suggest region specific changes of ERK1 and <strong>ERK2</strong> mRNA expression during <b>morphine</b> induced CPP.
+MAPK1	addiction	reward	24296091	These results suggest region specific changes of ERK1 and <strong>ERK2</strong> mRNA expression during morphine induced <b>CPP</b>.
+MAPK1	drug	cocaine	23970867	The abundance of surrogate markers of dopamine signaling and plasticity in the dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC) were examined: glycosylated and non glycosylated forms of the dopamine transporter (efficiency of dopamine transport), tyrosine hydroxylase (TH; marker of dopamine synthesis) and phosphorylated TH at Serine 30 and 40 (markers of enzyme activity), extracellular signal regulated kinase 1 and 2 (ERK1 and <strong>ERK 2</strong>), and phosphorylated ERK1 and ERK2 (phosphorylates TH Serine 31; markers of synaptic plasticity), and markers of synaptic integrity, spinophilin and post synaptic density protein 95 (roles in dopamine signaling and response to <b>cocaine</b>).
+MAPK1	drug	cocaine	23970867	The abundance of surrogate markers of dopamine signaling and plasticity in the dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC) were examined: glycosylated and non glycosylated forms of the dopamine transporter (efficiency of dopamine transport), tyrosine hydroxylase (TH; marker of dopamine synthesis) and phosphorylated TH at Serine 30 and 40 (markers of enzyme activity), extracellular signal regulated kinase 1 and 2 (ERK1 and <strong>ERK 2</strong>), and phosphorylated ERK1 and <strong>ERK2</strong> (phosphorylates TH Serine 31; markers of synaptic plasticity), and markers of synaptic integrity, spinophilin and post synaptic density protein 95 (roles in dopamine signaling and response to <b>cocaine</b>).
+MAPK1	drug	cocaine	23266327	Considering that activation of the extracellular signal regulated protein kinase (ERK) is suggested to be involved in <b>cocaine</b> induced behavioral sensitization, we study the effects of perinatal protein deprivation on phosphorylated <strong>ERK2</strong> (pERK2) protein levels in the NAc (core and shell) during different drug free withdrawal periods.
+MAPK1	addiction	sensitization	23266327	Considering that activation of the extracellular signal regulated protein kinase (ERK) is suggested to be involved in cocaine induced behavioral <b>sensitization</b>, we study the effects of perinatal protein deprivation on phosphorylated <strong>ERK2</strong> (pERK2) protein levels in the NAc (core and shell) during different drug free withdrawal periods.
+MAPK1	addiction	withdrawal	23266327	Considering that activation of the extracellular signal regulated protein kinase (ERK) is suggested to be involved in cocaine induced behavioral sensitization, we study the effects of perinatal protein deprivation on phosphorylated <strong>ERK2</strong> (pERK2) protein levels in the NAc (core and shell) during different drug free <b>withdrawal</b> periods.
+MAPK1	drug	cocaine	23266327	In contrast, in the NAc shell, only sensitized D rats with <b>cocaine</b> 10 mg/kg showed <strong>ERK2</strong> activation on WD21.
+MAPK1	drug	cocaine	21940447	Intra NAc pharmacological manipulations indicate that the Ca(v)1.2 activated CaM kinase II (CaMKII) mediates <b>cocaine</b> induced increase in S831 P GluA1 and that both Ca(v)1.2 activated CaMKII and extracellular signal regulated kinase 2 (<strong>ERK2</strong>) mediate the increase in GluA1 cell surface levels specific to the sensitized response.
+MAPK1	drug	alcohol	21790671	Elevated activation of ERK1 and <strong>ERK2</strong> accompany enhanced liver injury following <b>alcohol</b> binge in chronically <b>ethanol</b> fed rats.
+MAPK1	addiction	intoxication	21790671	Elevated activation of ERK1 and <strong>ERK2</strong> accompany enhanced liver injury following alcohol <b>binge</b> in chronically ethanol fed rats.
+MAPK1	drug	alcohol	21790671	Chronic binge group also showed significant increase (compared with chronic <b>ethanol</b> alone) in the phosphorylation of extracellular regulated kinase 1 (ERK1), <strong>ERK2</strong>, and RSK.
+MAPK1	addiction	intoxication	21790671	Chronic <b>binge</b> group also showed significant increase (compared with chronic ethanol alone) in the phosphorylation of extracellular regulated kinase 1 (ERK1), <strong>ERK2</strong>, and RSK.
+MAPK1	addiction	intoxication	21790671	Among other alterations, the activated levels of ERK1, and more so <strong>ERK2</strong>, were remarkably amplified by <b>binge</b> suggesting a role of these isotypes in the <b>binge</b> amplification of the injury.
+MAPK1	drug	alcohol	21790671	This study offers chronic followed by repeat binge as a model for the study of progression of liver injury by <b>ethanol</b> and highlights the involvement of ERK1 and <strong>ERK2</strong> isotypes in the amplification of liver injury by binge <b>ethanol</b>.
+MAPK1	addiction	intoxication	21790671	This study offers chronic followed by repeat <b>binge</b> as a model for the study of progression of liver injury by ethanol and highlights the involvement of ERK1 and <strong>ERK2</strong> isotypes in the amplification of liver injury by <b>binge</b> ethanol.
+MAPK1	drug	nicotine	21420997	In the <b>nicotine</b> treated groups, the levels of phosphorylated CREB and <strong>ERK2</strong> in the PFC were increased in HIV 1Tg rats, but decreased in F344 animals.
+MAPK1	drug	nicotine	21420997	Moreover, repeated <b>nicotine</b> administration reduced phosphorylated <strong>ERK2</strong> in the VTA of HIV 1Tg rats and in the NAc of F344 rats, but had no effect on phosphorylated CREB, indicating a region specific change of intracellular signaling.
+MAPK1	drug	opioid	21392541	Mitosis activated protein kinase1 (<strong>MAPK1</strong>) was increased in the stages of extinction and reinstatement of <b>morphine</b> induced CPP, while glial fibrillary acidic protein (GFAP) was decreased in the stage of extinction.
+MAPK1	addiction	relapse	21392541	Mitosis activated protein kinase1 (<strong>MAPK1</strong>) was increased in the stages of extinction and <b>reinstatement</b> of morphine induced CPP, while glial fibrillary acidic protein (GFAP) was decreased in the stage of extinction.
+MAPK1	addiction	reward	21392541	Mitosis activated protein kinase1 (<strong>MAPK1</strong>) was increased in the stages of extinction and reinstatement of morphine induced <b>CPP</b>, while glial fibrillary acidic protein (GFAP) was decreased in the stage of extinction.
+MAPK1	drug	amphetamine	21372109	Absence of the GPR37/PAEL receptor impairs striatal Akt and <strong>ERK2</strong> phosphorylation, DeltaFosB expression, and conditioned place preference to <b>amphetamine</b> and cocaine.
+MAPK1	drug	cocaine	21372109	Absence of the GPR37/PAEL receptor impairs striatal Akt and <strong>ERK2</strong> phosphorylation, DeltaFosB expression, and conditioned place preference to amphetamine and <b>cocaine</b>.
+MAPK1	drug	amphetamine	21372109	The basal phosphorylation of the D1 activated <strong>ERK2</strong> kinase was not altered, but acute treatments with <b>amphetamine</b> or cocaine failed to produce its specific increase, as detected in samples from wild type littermates.
+MAPK1	drug	cocaine	21372109	The basal phosphorylation of the D1 activated <strong>ERK2</strong> kinase was not altered, but acute treatments with amphetamine or <b>cocaine</b> failed to produce its specific increase, as detected in samples from wild type littermates.
+MAPK1	addiction	withdrawal	21276808	The maintenance of CP AMPARs in NAc synapses during <b>withdrawal</b> is accompanied by activation of CaMKII and <strong>ERK2</strong> but not CaMKI.
+MAPK1	drug	nicotine	21172385	Since activation of extracellular signal related kinase (<strong>ERK2</strong>) is involved in the rewarding effects of several classes of drugs of abuse, we then measured the level of <strong>ERK2</strong> phosphorylation in the nucleus accumbens shell (NACsh) and core (NACco) of GAL /  and GAL+/+ mice following re exposure to the CPP chamber previously paired with <b>nicotine</b> as a marker of mesolimbic system activation.
+MAPK1	addiction	reward	21172385	Since activation of extracellular signal related kinase (<strong>ERK2</strong>) is involved in the rewarding effects of several classes of drugs of abuse, we then measured the level of <strong>ERK2</strong> phosphorylation in the nucleus accumbens shell (NACsh) and core (NACco) of GAL /  and GAL+/+ mice following re exposure to the <b>CPP</b> chamber previously paired with nicotine as a marker of mesolimbic system activation.
+MAPK1	drug	nicotine	21172385	Finally, we examined whether acute <b>nicotine</b> administration affects <strong>ERK2</strong> activity in GAL /  and GAL+/+ mice.
+MAPK1	drug	nicotine	21172385	In the conditioning groups showing significant expression of <b>nicotine</b> CPP, only GAL+/+ mice showed <strong>ERK2</strong> activation in the NACsh.
+MAPK1	addiction	reward	21172385	In the conditioning groups showing significant expression of nicotine <b>CPP</b>, only GAL+/+ mice showed <strong>ERK2</strong> activation in the NACsh.
+MAPK1	drug	nicotine	21172385	In addition, no activation of <strong>ERK2</strong> was observed following acute <b>nicotine</b> administration in either genotype.
+MAPK1	drug	opioid	20359526	These observations suggest that spinal <strong>ERK2</strong>, P38 and PKCgamma are likely involved in multiple adaptive responses following systemic <b>morphine</b> administration, whereas DYN and CGRP may contribute selectively to the development of antinociceptive tolerance.
+MAPK1	drug	cannabinoid	19004548	Expression of FCA was associated with increased relative phospho <strong>ERK2</strong> expression in the amygdala, an effect blocked by naloxone, SR141716A, and <b>SR144528</b>.
+MAPK1	drug	opioid	19004548	Expression of FCA was associated with increased relative phospho <strong>ERK2</strong> expression in the amygdala, an effect blocked by <b>naloxone</b>, SR141716A, and SR144528.
+MAPK1	drug	opioid	18940233	In the present study, we found that compared to the <b>morphine</b> unpaired and saline paired and saline unpaired groups, <b>morphine</b> paired mice showed depressed <strong>ERK2</strong> activity in the Frontal Association Cortex (FrA), whereas ERK1 activity was not changed in the same region.
+MAPK1	drug	cocaine	18940233	In the Accumbens Nucleus (Acb) and Caudate Putamen (CPu) that are associated with <b>cocaine</b> addiction, the activities of ERK1 and <strong>ERK2</strong> among four groups showed no difference.
+MAPK1	addiction	addiction	18940233	In the Accumbens Nucleus (Acb) and Caudate Putamen (CPu) that are associated with cocaine <b>addiction</b>, the activities of ERK1 and <strong>ERK2</strong> among four groups showed no difference.
+MAPK1	drug	opioid	18940233	These results suggest that the FrA plays an important role in <b>morphine</b> craving and that <strong>ERK2</strong> is involved in eliciting the environment related <b>morphine</b> craving, which is totally different from those induced by <b>morphine</b> itself.
+MAPK1	addiction	relapse	18940233	These results suggest that the FrA plays an important role in morphine <b>craving</b> and that <strong>ERK2</strong> is involved in eliciting the environment related morphine <b>craving</b>, which is totally different from those induced by morphine itself.
+MAPK1	addiction	reward	17085074	We suggest that the <strong>ERK2</strong> pathway acts as a logical AND gate, permissive for plasticity, in neurons on which dopamine mediated <b>reward</b> signals and glutamate mediated contextual information converge.
+MAPK1	drug	cocaine	16407894	We report here that deletion of the ERK1 isoform, which leads to increased <strong>ERK2</strong> stimulus dependent signaling, facilitates the development of <b>cocaine</b> induced psychomotor sensitization and the acquisition of a <b>cocaine</b> conditioned place preference.
+MAPK1	addiction	sensitization	16407894	We report here that deletion of the ERK1 isoform, which leads to increased <strong>ERK2</strong> stimulus dependent signaling, facilitates the development of cocaine induced psychomotor <b>sensitization</b> and the acquisition of a cocaine conditioned place preference.
+MAPK1	drug	cocaine	16407894	Our results suggest that enhanced <strong>ERK2</strong> signaling following repeated drug exposure may facilitate the development of forms of <b>cocaine</b> induced plasticity that contribute to addiction.
+MAPK1	addiction	addiction	16407894	Our results suggest that enhanced <strong>ERK2</strong> signaling following repeated drug exposure may facilitate the development of forms of cocaine induced plasticity that contribute to <b>addiction</b>.
+MAPK1	addiction	sensitization	16176357	Kv 4.3(+) neurons also expressed <strong>ERK 2</strong> and mGluR 5, which are molecules related to the induction of central <b>sensitization</b>, a mechanism mediating nociceptive plasticity.
+MAPK1	drug	alcohol	12676135	<b>Ethanol</b> significantly reduced carbachol stimulated Ca(2+) signaling, as well as Erk1/<strong>Erk2</strong>, Akt and cyclic AMP response element binding phosphorylations in a dose dependent manner.
+MAPK1	drug	nicotine	9600337	The present study provides evidence that <b>nicotine</b> (a) activates the mitogen activated protein (MAP) kinase signalling pathway in lung cancer cells, specifically extracellular signal regulated kinase (<strong>ERK2</strong>), resulting in increased expression of the bcl 2 protein and inhibition of apoptosis in these cells; and (b) blocks the inhibition of protein kinase C (PKC) and <strong>ERK2</strong> activity in lung cancer cells by anti cancer agents, such as therapeutic opioid drugs, and thus can adversely affect cancer therapy.
+MAPK1	drug	opioid	9600337	The present study provides evidence that nicotine (a) activates the mitogen activated protein (MAP) kinase signalling pathway in lung cancer cells, specifically extracellular signal regulated kinase (<strong>ERK2</strong>), resulting in increased expression of the bcl 2 protein and inhibition of apoptosis in these cells; and (b) blocks the inhibition of protein kinase C (PKC) and <strong>ERK2</strong> activity in lung cancer cells by anti cancer agents, such as therapeutic <b>opioid</b> drugs, and thus can adversely affect cancer therapy.
+MAPK1	drug	nicotine	9600337	While exposure to <b>nicotine</b> can result in the activation of the two major signalling pathways (MAP kinase and PKC) that are known to inhibit apoptosis, <b>nicotine</b> regulation of MAP (<strong>ERK2</strong>) kinase activity is not dependent on PKC.
+GARS1	drug	cannabinoid	32608538	<b>Cannabinoids</b> exert therapeutic effects on several diseases such as chronic pain and startle disease by targeting glycine receptors (<strong>GlyRs</strong>).
+GARS1	drug	cannabinoid	32608538	Membrane cholesterol reduction significantly inhibits <b>cannabinoid</b> potentiation of glycine activated currents in cultured spinal neurons and in HEK 293T cells expressing α1/α3 <strong>GlyRs</strong>.
+GARS1	drug	alcohol	32436225	It has been shown that glycine receptors (<strong>GlyRs</strong>) present in the nAc are potentiated by clinically relevant concentrations of <b>ethanol</b>, where α1 and α2 are the predominant subunits expressed.
+GARS1	drug	alcohol	32436225	The differences in <b>ethanol</b> consumption between WT and KO mice provide additional evidence supporting the conclusion that <strong>GlyRs</strong> are biologically relevant targets for the sedative and rewarding properties of <b>ethanol</b>.
+GARS1	addiction	addiction	32432025	To outline the process used to select risk alleles of reward genes for the Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>) test.
+GARS1	addiction	reward	32432025	To outline the process used to select risk alleles of <b>reward</b> genes for the Genetic Addiction Risk Score (<strong>GARS</strong>) test.
+GARS1	addiction	addiction	32432025	Review of the literature related to the function of risk alleles of reward genes associated with hypodopaminergia relevant case control association studies for the selection of alleles to be measured by the Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>) test.
+GARS1	addiction	reward	32432025	Review of the literature related to the function of risk alleles of <b>reward</b> genes associated with hypodopaminergia relevant case control association studies for the selection of alleles to be measured by the Genetic Addiction Risk Score (<strong>GARS</strong>) test.
+GARS1	drug	alcohol	32357359	Using this mouse model denoted knock in α2 (KI α2), our electrophysiological studies showed that neurons in the adult nAc expressed functional KI <strong>GlyRs</strong> that were rather insensitive to <b>ethanol</b> when compared with WT <strong>GlyRs</strong>.
+GARS1	drug	alcohol	32357359	These results show that the α2 subunit is important for the potentiation of <strong>GlyRs</strong> in the adult brain and this might result in reduced sedation and increased <b>ethanol</b> consumption.
+GARS1	addiction	addiction	31824737	So, to be clear, there may be other promising modalities other than MAT such as repetitive transcranial magnetic stimulation (rTMS), exercise and even new medications with positive allosteric modulators of GABA A receptors, as well as the highly researched Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>) coupled with precision KB220Z.
+GARS1	addiction	addiction	31820688	This case series presents the novel Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>®) coupled with a customized pro dopamine regulator matched to polymorphic reward genes having a hypodopaminergic risk.
+GARS1	addiction	reward	31820688	This case series presents the novel Genetic Addiction Risk Score (<strong>GARS</strong>®) coupled with a customized pro dopamine regulator matched to polymorphic <b>reward</b> genes having a hypodopaminergic risk.
+GARS1	addiction	addiction	31660252	The benefits of genetic <b>addiction</b> risk score (<strong>GARS</strong>™) and pro dopamine regulation in combating suicide in the American Indian population.
+GARS1	addiction	addiction	31660252	It seems reasonable that early identification, especially in children, be tested with the Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>) and concomitantly be offered the precision pro dopamine regulator (KB220PAM), one that matches their unique brain polymorphisms involving serotonergic, endorphinergic, glutaminergic, gabaergic and dopaminergic pathways among others.
+GARS1	drug	alcohol	31521620	Here, using electrophysiological recordings, we report that <strong>GlyRs</strong> in D1(+) MSNs are highly sensitive to <b>ethanol</b>, with potentiation starting at 5 mM (26 ± 5%).
+GARS1	drug	alcohol	31521620	These results indicate that <strong>GlyRs</strong> present in D1(+) MSNs are sensitive to low concentrations of <b>ethanol</b>, and that potentiation of this inhibitory current regulates the activation of nAc, acting as a homeostatic signal that would prevent over activation of the reward system when drugs like <b>ethanol</b> are consumed.
+GARS1	addiction	reward	31521620	These results indicate that <strong>GlyRs</strong> present in D1(+) MSNs are sensitive to low concentrations of ethanol, and that potentiation of this inhibitory current regulates the activation of nAc, acting as a homeostatic signal that would prevent over activation of the <b>reward</b> system when drugs like ethanol are consumed.
+GARS1	drug	alcohol	31254534	The lateral habenula (LHb) is activated by a range of aversive states including those related to <b>alcohol</b> withdrawal and has glycine receptors (<strong>GlyRs</strong>), a sensitive target of <b>alcohol</b>.
+GARS1	addiction	aversion	31254534	The lateral habenula (LHb) is activated by a range of <b>aversive</b> states including those related to alcohol withdrawal and has glycine receptors (<strong>GlyRs</strong>), a sensitive target of alcohol.
+GARS1	addiction	withdrawal	31254534	The lateral habenula (LHb) is activated by a range of aversive states including those related to alcohol <b>withdrawal</b> and has glycine receptors (<strong>GlyRs</strong>), a sensitive target of alcohol.
+GARS1	drug	alcohol	31254534	However, whether <strong>GlyRs</strong> in the LHb contribute to <b>alcohol</b> related behaviors is unknown.
+GARS1	drug	alcohol	31254534	Activation of <strong>GlyRs</strong> reverses LHb hyperactivity, alleviates aberrant behaviors, and reduces <b>alcohol</b> intake, thus highlighting the <strong>GlyRs</strong> in the LHb as a potential therapeutic target for <b>alcohol</b> use disorders.
+GARS1	drug	alcohol	30884072	Here, we used knock in (KI) mice that have <b>ethanol</b> insensitive alpha 1 glycine receptors (<strong>GlyRs</strong>) (KK385/386AA) to examine how alpha 1 <strong>GlyRs</strong> might affect binge drinking and conditioned place preference.
+GARS1	addiction	intoxication	30884072	Here, we used knock in (KI) mice that have ethanol insensitive alpha 1 glycine receptors (<strong>GlyRs</strong>) (KK385/386AA) to examine how alpha 1 <strong>GlyRs</strong> might affect <b>binge</b> drinking and conditioned place preference.
+GARS1	drug	alcohol	30884072	This study suggests that nonsynaptic alpha 1 containing <strong>GlyRs</strong> have a role in motivational and early reinforcing effects of <b>ethanol</b>.
+GARS1	addiction	reward	30884072	This study suggests that nonsynaptic alpha 1 containing <strong>GlyRs</strong> have a role in motivational and early <b>reinforcing</b> effects of ethanol.
+GARS1	drug	alcohol	30884072	Little is known about the role that ligand gated ion channels (LGICs), such as glycine receptors (<strong>GlyRs</strong>), have in regulating levels of <b>ethanol</b> intake and place preference.
+GARS1	drug	alcohol	30884072	In this study, we used knock in (KI) mice that have <b>ethanol</b> insensitive α1 <strong>GlyRs</strong> (KK385/386AA) and a combination of electrophysiological and behavioral approaches to examine how expression of <b>ethanol</b> resistant α1 <strong>GlyRs</strong> in brain neurons might affect binge drinking and conditioned place preference.
+GARS1	addiction	intoxication	30884072	In this study, we used knock in (KI) mice that have ethanol insensitive α1 <strong>GlyRs</strong> (KK385/386AA) and a combination of electrophysiological and behavioral approaches to examine how expression of ethanol resistant α1 <strong>GlyRs</strong> in brain neurons might affect <b>binge</b> drinking and conditioned place preference.
+GARS1	drug	alcohol	30884072	Behavioral studies showed that the KI mice have a higher intake of <b>ethanol</b> upon first exposure to drinking and greater conditioned place preference to <b>ethanol</b>, suggesting that α1 <strong>GlyRs</strong> in the brain have a protective role against abuse.
+GARS1	drug	alcohol	30884072	This study suggests that nonsynaptic α1 containing <strong>GlyRs</strong> have a role in motivational and early reinforcing effects of <b>ethanol</b> and open a novel opportunity for pharmacotherapy development to treat <b>alcohol</b> use disorders.
+GARS1	addiction	reward	30884072	This study suggests that nonsynaptic α1 containing <strong>GlyRs</strong> have a role in motivational and early <b>reinforcing</b> effects of ethanol and open a novel opportunity for pharmacotherapy development to treat alcohol use disorders.
+GARS1	addiction	addiction	30370423	It is also agreed by most that there is a need to provide early genetic identification possibly through a novel researched technology referred to Genetic <b>Addiction</b> Risk Score(<strong>GARS</strong>).™ The existing FDA approved medications promote blocking dopamine, however, we argue that a more prudent paradigm shift should be biphasic short term blockade and long term upregulation, enhancing functional connectivity of brain reward.
+GARS1	addiction	reward	30370423	It is also agreed by most that there is a need to provide early genetic identification possibly through a novel researched technology referred to Genetic Addiction Risk Score(<strong>GARS</strong>).™ The existing FDA approved medications promote blocking dopamine, however, we argue that a more prudent paradigm shift should be biphasic short term blockade and long term upregulation, enhancing functional connectivity of brain <b>reward</b>.
+GARS1	drug	cocaine	30158054	SMURF1 protein expression was decreased, while SMURF1 substrates RhoA and <strong>SMAD1</strong>/5 were increased, in the nucleus accumbens on withdrawal day 7, but not on withdrawal day 1, following <b>cocaine</b> self administration.
+GARS1	addiction	withdrawal	30158054	SMURF1 protein expression was decreased, while SMURF1 substrates RhoA and <strong>SMAD1</strong>/5 were increased, in the nucleus accumbens on <b>withdrawal</b> day 7, but not on <b>withdrawal</b> day 1, following cocaine self administration.
+GARS1	drug	cocaine	30158054	Furthermore, SMURF1 regulated, <strong>SMAD1</strong>/5 associated transcription factor Runt related transcript factor 2 displayed increased binding at promoter regions of genes previously associated with <b>cocaine</b> induced plasticity.
+GARS1	drug	benzodiazepine	31750006	Would induction of dopamine homeostasis via coupling genetic addiction risk score (<strong>GARS</strong>®) and pro dopamine regulation benefit <b>benzodiazepine</b> use disorder (BUD)?
+GARS1	addiction	addiction	31750006	Would induction of dopamine homeostasis via coupling genetic <b>addiction</b> risk score (<strong>GARS</strong>®) and pro dopamine regulation benefit benzodiazepine use disorder (BUD)?
+GARS1	addiction	addiction	31750006	This proposition involves coupling the Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>) with a subsequent polymorphic matched genetic customized Pro Dopamine Regulator known as KB220ZPBM (Precision Behavioral Management).
+GARS1	drug	alcohol	29372187	In a large multi addiction centre study involving seven diverse treatment programs, the genetic addiction risk score (<strong>GARS</strong>™) was shown to have a predictive relationship with ASI MV derived <b>alcohol</b> (≥ seven alleles), and other drugs (≥ 4 alleles) severity risk scores.
+GARS1	addiction	addiction	29372187	In a large multi <b>addiction</b> centre study involving seven diverse treatment programs, the genetic <b>addiction</b> risk score (<strong>GARS</strong>™) was shown to have a predictive relationship with ASI MV derived alcohol (≥ seven alleles), and other drugs (≥ 4 alleles) severity risk scores.
+GARS1	drug	opioid	30957097	We are continuing research especially as it relates to genetic risk, including the now patented Genetic Addiction Risk Score (<strong>GARS</strong>®) and the development of "Precision Addiction Management (PAM)" to potentially combat the <b>opioid</b>/psychostimulant epidemic.
+GARS1	addiction	addiction	30957097	We are continuing research especially as it relates to genetic risk, including the now patented Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>®) and the development of "Precision <b>Addiction</b> Management (PAM)" to potentially combat the opioid/psychostimulant epidemic.
+GARS1	drug	opioid	28930612	Genetic addiction risk score (<strong>GARS</strong>) ™, a predictor of vulnerability to <b>opioid</b> dependence.
+GARS1	addiction	addiction	28930612	Genetic <b>addiction</b> risk score (<strong>GARS</strong>) ™, a predictor of vulnerability to opioid dependence.
+GARS1	addiction	dependence	28930612	Genetic addiction risk score (<strong>GARS</strong>) ™, a predictor of vulnerability to opioid <b>dependence</b>.
+GARS1	addiction	addiction	28930612	This discussion authored by a group of concerned scientists and clinicians examines the Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>), the first test to accurately predict vulnerability to pain, <b>addiction</b>, and other <b>compulsive</b> behaviors, defined as Reward Deficiency Syndrome (RDS).
+GARS1	addiction	reward	28930612	This discussion authored by a group of concerned scientists and clinicians examines the Genetic Addiction Risk Score (<strong>GARS</strong>), the first test to accurately predict vulnerability to pain, addiction, and other compulsive behaviors, defined as <b>Reward</b> Deficiency Syndrome (RDS).
+GARS1	drug	alcohol	28833225	It is suggested that <strong>GlyRs</strong> are involved in (i) the dopamine activating effect of EtOH, (ii) regulating EtOH intake, and (iii) the relapse preventing effect of <b>acamprosate</b>.
+GARS1	addiction	relapse	28833225	It is suggested that <strong>GlyRs</strong> are involved in (i) the dopamine activating effect of EtOH, (ii) regulating EtOH intake, and (iii) the <b>relapse</b> preventing effect of acamprosate.
+GARS1	drug	alcohol	28524260	Glycine receptors (<strong>GlyRs</strong>) are potentiated by <b>ethanol</b> and they have been implicated in the regulation of accumbal dopamine levels.
+GARS1	drug	alcohol	28524260	Here, we investigated the presence of <strong>GlyRs</strong> in accumbal dopamine receptor medium spiny neurons (MSNs) of C57BL/6J mice, analysing mRNA expression levels and immunoreactivity of GlyR subunits, as well as <b>ethanol</b> sensitivity.
+GARS1	drug	alcohol	28066828	In the forefront is the development of the Genetic Addiction Risk Score (<strong>GARS</strong>™), which unlike 23andMe, has predictive value for the severity of drug and <b>alcohol</b> abuse as well as other non substance related addictive behaviors.
+GARS1	addiction	addiction	28066828	In the forefront is the development of the Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>™), which unlike 23andMe, has predictive value for the severity of drug and alcohol abuse as well as other non substance related <b>addictive</b> behaviors.
+GARS1	addiction	addiction	30198022	The Benefits of Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>™) Testing in Substance Use Disorder (SUD).
+GARS1	addiction	addiction	30198022	Following 25 years of extensive research by many scientists worldwide, a panel of ten reward gene risk variants, called the Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>), has been developed.
+GARS1	addiction	reward	30198022	Following 25 years of extensive research by many scientists worldwide, a panel of ten <b>reward</b> gene risk variants, called the Genetic Addiction Risk Score (<strong>GARS</strong>), has been developed.
+GARS1	drug	alcohol	30198022	In unpublished work, when <strong>GARS</strong> was compared to the Addiction Severity Index (ASI), which has been used in many clinical settings, <strong>GARS</strong> significantly predicted the severity of both <b>alcohol</b> and drug dependency.
+GARS1	addiction	addiction	30198022	In unpublished work, when <strong>GARS</strong> was compared to the <b>Addiction</b> Severity Index (ASI), which has been used in many clinical settings, <strong>GARS</strong> significantly predicted the severity of both alcohol and drug dependency.
+GARS1	drug	alcohol	30198022	To our knowledge, <strong>GARS</strong> is the only panel of genes with established polymorphisms reflecting the Brain Reward Cascade (BRC), which has been correlated with the ASI MV <b>alcohol</b> and drug risk severity score.
+GARS1	addiction	reward	30198022	To our knowledge, <strong>GARS</strong> is the only panel of genes with established polymorphisms reflecting the Brain <b>Reward</b> Cascade (BRC), which has been correlated with the ASI MV alcohol and drug risk severity score.
+GARS1	addiction	addiction	28033474	Conclusions/Importance: We are proposing a Reward Deficiency Solution System (RDSS) that includes: Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>); Comprehensive Analysis of Reported Drugs (CARD); and a glutaminergic dopaminergic optimization complex (Kb220Z).
+GARS1	addiction	reward	28033474	Conclusions/Importance: We are proposing a <b>Reward</b> Deficiency Solution System (RDSS) that includes: Genetic Addiction Risk Score (<strong>GARS</strong>); Comprehensive Analysis of Reported Drugs (CARD); and a glutaminergic dopaminergic optimization complex (Kb220Z).
+GARS1	drug	alcohol	26158502	<strong>GlyRs</strong> are relevant for the effects of <b>ethanol</b> because they are found in the spinal cord and brain stem where they primarily express the α1 subunit.
+GARS1	drug	alcohol	26158502	Here, we review data on the following aspects of <b>ethanol</b> effects on <strong>GlyRs</strong>: (1) direct interaction of <b>ethanol</b> with amino acids in the extracellular or transmembrane domains, and indirect mechanisms through the activation of signal transduction pathways; (2) analysis of α2 and α3 subunits having different sensitivities to <b>ethanol</b> which allows the identification of structural requirements for <b>ethanol</b> modulation present in the intracellular domain and C terminal region; (3) Genetically modified knock in mice for α1 <strong>GlyRs</strong> that have an impaired interaction with G protein and demonstrate reduced <b>ethanol</b> sensitivity without changes in glycinergic transmission; and (4) <strong>GlyRs</strong> as potential therapeutic targets.
+GARS1	drug	alcohol	25678534	<b>Ethanol</b> enhances the function of brain <strong>GlyRs</strong>, and the GlyRα1 subunit is associated with some of the behavioral actions of <b>ethanol</b>, such as loss of righting reflex.
+GARS1	drug	alcohol	25589412	Previous studies have shown that the effect of <b>ethanol</b> onglycine receptors (<strong>GlyRs</strong>) containing the a1 subunit is affected by interaction with heterotrimeric G proteins (Gβγ).
+GARS1	addiction	sensitization	25589412	<strong>GlyRs</strong> containing the α3 subunit are involved in inflammatory pain <b>sensitization</b> and rhythmic breathing and have received much recent attention.
+GARS1	drug	alcohol	25589412	Residue A254 in TM2, the α3L splice cassette, and the C terminal domain of α3GlyRs are determinants for low <b>ethanol</b> sensitivity and form the molecular basis of subtype selective modulation of <strong>GlyRs</strong> by <b>alcohol</b>.
+GARS1	drug	alcohol	24686030	Our previous work in rats has demonstrated that accumbal glycine receptors (<strong>GlyRs</strong>) are involved in mediating the dopamine activating effects of <b>ethanol</b>, and in modulating <b>ethanol</b> intake.
+GARS1	drug	alcohol	24686030	The dopamine increasing effect of systemic <b>ethanol</b> and the drug induced change in neurotransmission in vitro, as measured by microdialysis and field potential recordings, were dependent on <strong>GlyRs</strong> in nAc.
+GARS1	drug	cannabinoid	24686030	Accumbal <strong>GlyRs</strong> were also involved in the actions of <b>tetrahydrocannabinol</b> and nicotine, but not in those of cocaine or morphine.
+GARS1	drug	cocaine	24686030	Accumbal <strong>GlyRs</strong> were also involved in the actions of tetrahydrocannabinol and nicotine, but not in those of <b>cocaine</b> or morphine.
+GARS1	drug	nicotine	24686030	Accumbal <strong>GlyRs</strong> were also involved in the actions of tetrahydrocannabinol and <b>nicotine</b>, but not in those of cocaine or morphine.
+GARS1	drug	opioid	24686030	Accumbal <strong>GlyRs</strong> were also involved in the actions of tetrahydrocannabinol and nicotine, but not in those of cocaine or <b>morphine</b>.
+GARS1	drug	alcohol	24686030	These data indicate that accumbal <strong>GlyRs</strong> play a key role in <b>ethanol</b> induced dopamine activation and contribute also to that of cannabinoids and nicotine.
+GARS1	drug	cannabinoid	24686030	These data indicate that accumbal <strong>GlyRs</strong> play a key role in ethanol induced dopamine activation and contribute also to that of <b>cannabinoids</b> and nicotine.
+GARS1	drug	nicotine	24686030	These data indicate that accumbal <strong>GlyRs</strong> play a key role in ethanol induced dopamine activation and contribute also to that of cannabinoids and <b>nicotine</b>.
+GARS1	drug	opioid	24616834	Coupling Genetic Addiction Risk Score (<strong>GARS</strong>) with Electrotherapy: Fighting Iatrogenic <b>Opioid</b> Dependence.
+GARS1	addiction	addiction	24616834	Coupling Genetic <b>Addiction</b> Risk Score (<strong>GARS</strong>) with Electrotherapy: Fighting Iatrogenic Opioid Dependence.
+GARS1	addiction	dependence	24616834	Coupling Genetic Addiction Risk Score (<strong>GARS</strong>) with Electrotherapy: Fighting Iatrogenic Opioid <b>Dependence</b>.
+GARS1	drug	alcohol	24264816	These findings identify extrasynaptic <strong>GlyRs</strong> as critical regulators of DR excitability and a novel molecular target for <b>ethanol</b>.
+GARS1	drug	alcohol	22238211	In the current study, we tested the hypothesis that the activation of the presynaptic <strong>GlyRs</strong> in the VTA might interfere with <b>ethanol</b> self administration.
+GARS1	drug	alcohol	22238211	The effects of glycine probably were mediated by strychnine sensitive <strong>GlyRs</strong>, because the coinjection of glycine and strychnine reduced neither <b>ethanol</b> intake in the home cages nor lever press responding for <b>ethanol</b> in the operant chambers.
+GARS1	addiction	reward	22238211	The effects of glycine probably were mediated by strychnine sensitive <strong>GlyRs</strong>, because the coinjection of glycine and strychnine reduced neither ethanol intake in the home cages nor lever press responding for ethanol in the <b>operant</b> chambers.
+GARS1	drug	alcohol	22238211	Thus, <strong>GlyRs</strong> in the VTA may play a critical role in <b>ethanol</b> self administration in animals chronically exposed to <b>ethanol</b>.
+GARS1	drug	alcohol	22238211	Therefore, drugs targeting <strong>GlyRs</strong> may be beneficial for <b>alcoholics</b>.
+GARS1	drug	alcohol	22037202	Thus, in addition to reducing <b>ethanol</b> action on the <strong>GlyRs</strong>, these mutations reduced glycinergic inhibition, which may also alter sensitivity to GABAergic drugs.
+GARS1	drug	alcohol	21790901	Our previous research suggested that glycine receptors (<strong>GlyRs</strong>) in the nucleus accumbens (nAc) play a major part in mediating the dopamine elevating properties of <b>ethanol</b> and are highly involved in the <b>ethanol</b> intake reducing effect of <b>acamprosate</b>.
+GARS1	drug	alcohol	21790901	Taken together with our previous data demonstrating the importance of accumbal <strong>GlyRs</strong> both in <b>ethanol</b> induced elevation of nAc dopamine and in <b>ethanol</b> consumption, it is plausible that the effects of MPEP treatment, on dopamine output and on <b>ethanol</b> intake, may be mediated via interaction with the same neuronal circuitry that previously has been demonstrated for <b>ethanol</b>, taurine and <b>acamprosate</b>.
+GARS1	drug	alcohol	19860810	Glycine receptors (<strong>GlyRs</strong>) in the nucleus accumbens (nAc) and nicotinic acetylcholine receptors (nAChRs) in the ventral tegmental area (VTA) have been suggested to be involved in the positive reinforcing and dopamine elevating effects of <b>ethanol</b>.
+GARS1	addiction	reward	19860810	Glycine receptors (<strong>GlyRs</strong>) in the nucleus accumbens (nAc) and nicotinic acetylcholine receptors (nAChRs) in the ventral tegmental area (VTA) have been suggested to be involved in the positive <b>reinforcing</b> and dopamine elevating effects of ethanol.
+GARS1	drug	alcohol	19860810	These results suggest that both systemic and local application of <b>acamprosate</b> elevate extracellular dopamine levels in the nAc by activating accumbal <strong>GlyRs</strong>, and, secondarily, tegmental nAChRs.
+GARS1	drug	alcohol	19860809	We have previously demonstrated that strychnine sensitive glycine receptors (<strong>GlyRs</strong>) in the nucleus accumbens (nAc) and nicotinic acetylcholine receptors (nAChRs) in the ventral tegmental area are involved in mediating <b>ethanol</b> (EtOH) induced elevation of dopamine in the rat mesolimbic dopamine system.
+GARS1	drug	alcohol	19860809	This neuronal circuitry was also demonstrated to mediate dopamine elevation in the nAc after both taurine, an endogenous agonist of <strong>GlyRs</strong>, and <b>acamprosate</b>, a synthetic derivate of homotaurine.
+GARS1	drug	alcohol	19860809	The aim of this study was to investigate whether the EtOH intake reducing effect of <b>acamprosate</b> involves accumbal <strong>GlyRs</strong>.
+GARS1	drug	alcohol	19860809	Based on current and previous results, we suggest that <b>acamprosate</b> primarily interacts with accumbal <strong>GlyRs</strong> and secondarily with ventral tegmental nAChRs, in a similar manner to that previously observed with EtOH and taurine.
+GARS1	drug	alcohol	19860809	The interaction between <b>acamprosate</b> and <strong>GlyRs</strong> does not only influence dopamine output in the nAc but also EtOH consumption, giving further support for our hypothesis that <strong>GlyRs</strong> are of importance in EtOH reinforcement.
+GARS1	addiction	reward	19860809	The interaction between acamprosate and <strong>GlyRs</strong> does not only influence dopamine output in the nAc but also EtOH consumption, giving further support for our hypothesis that <strong>GlyRs</strong> are of importance in EtOH <b>reinforcement</b>.
+GARS1	drug	alcohol	19781529	Previous studies by our group have suggested a role for <strong>GlyRs</strong> and its endogenous ligands glycine and taurine in the mesolimbic dopamine activating and reinforcing effects of <b>ethanol</b>.
+GARS1	addiction	reward	19781529	Previous studies by our group have suggested a role for <strong>GlyRs</strong> and its endogenous ligands glycine and taurine in the mesolimbic dopamine activating and <b>reinforcing</b> effects of ethanol.
+GARS1	drug	alcohol	19781529	However, correlations found between <b>alcohol</b> consumption and/or preference and GlyR expression support a role for <strong>GlyRs</strong> in <b>alcohol</b> consumption.
+GARS1	drug	alcohol	19543795	Glycine receptors (<strong>GlyRs</strong>) in the nucleus accumbens (nAc) have recently been suggested to be involved in the reinforcing and dopamine elevating properties of <b>ethanol</b> via a neuronal circuitry involving the VTA.
+GARS1	addiction	reward	19543795	Glycine receptors (<strong>GlyRs</strong>) in the nucleus accumbens (nAc) have recently been suggested to be involved in the <b>reinforcing</b> and dopamine elevating properties of ethanol via a neuronal circuitry involving the VTA.
+GARS1	drug	alcohol	19543795	Apart from <b>ethanol</b>, both glycine and taurine have the ability to modulate dopamine output via <strong>GlyRs</strong> in the same brain region.
+GARS1	drug	alcohol	19389199	The results are in line with previous findings and it is suggested that the effects observed involve interference with accumbal <strong>GlyRs</strong> and are related to the <b>alcohol</b> consumption modulating effect of Org 25935.
+GARS1	drug	alcohol	17098748	Previous findings from our group indicate that accumbal glycine receptors (<strong>GlyRs</strong>) are involved in mediating the dopamine (DA) activating effects of <b>ethanol</b> (EtOH), and that administration of glycine locally into the nucleus accumbens (nAc) reduces EtOH consumption in EtOH high preferring rats.
+GARS1	drug	alcohol	16820013	The present results suggest that taurine may be an endogenous ligand for <strong>GlyRs</strong> in the nAcc and that the taurine induced elevation of DA levels in this area, similarly to that observed after local <b>ethanol</b>, is mediated via a neuronal loop involving endogenous activation of nAChRs in the VTA.
+GARS1	addiction	reward	15654289	The mechanisms underlying this DA activation and how they relate to EtOH <b>reinforcement</b> remain to be elucidated, but recent data indicate that glycine receptors (<strong>GlyRs</strong>) in the nAc may be involved.
+GARS1	drug	alcohol	15654287	The possibility of pharmacologically interfering with <strong>GlyRs</strong> to combat psychiatric disorders, in which the mesolimbic DA system is implicated, such as <b>alcoholism</b>, drug addiction, and psychosis, should be explored.
+GARS1	addiction	addiction	15654287	The possibility of pharmacologically interfering with <strong>GlyRs</strong> to combat psychiatric disorders, in which the mesolimbic DA system is implicated, such as alcoholism, drug <b>addiction</b>, and psychosis, should be explored.
+PRKCG	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (Cnr1, Cnr2, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and TRPV1 sensitizing kinases (Mapk3, Mapk14, <strong>Prkcg</strong>, and Prkaca).
+PRKCG	drug	opioid	27329776	As <strong>PKCg</strong> activity related to N methyl D aspartate receptor activation is critical in <b>opioid</b> tolerance, these results help to understand the mechanisms of BMSC produced long term antihyperalgesia, which requires <b>opioid</b> receptors in rostral ventromedial medulla and apparently lacks the development of tolerance.
+PRKCG	drug	alcohol	27063791	Candidate genes for mediating the behavioral interaction between <b>ethanol</b> consumption and wheel running include multiple potassium channel genes, Oprm1, <strong>Prkcg</strong>, Stxbp1, Crhr1, Gabra3, Slc6a13, Stx1b, Pomc, Rassf5 and Camta2.
+PRKCG	drug	cocaine	24506432	Group I metabotropic glutamate receptor mediated activation of <strong>PKC gamma</strong> in the nucleus accumbens core promotes the reinstatement of <b>cocaine</b> seeking.
+PRKCG	addiction	relapse	24506432	Group I metabotropic glutamate receptor mediated activation of <strong>PKC gamma</strong> in the nucleus accumbens core promotes the <b>reinstatement</b> of cocaine <b>seeking</b>.
+PRKCG	drug	cocaine	23986250	Stimulation of mGluR5 in the accumbens shell promotes <b>cocaine</b> seeking by activating <strong>PKC gamma</strong>.
+PRKCG	addiction	relapse	23986250	Stimulation of mGluR5 in the accumbens shell promotes cocaine <b>seeking</b> by activating <strong>PKC gamma</strong>.
+PRKCG	drug	opioid	21105149	Gene knockdown with lentiviral vector mediated intrathecal RNA interference of <strong>protein kinase C gamma</strong> reverses chronic <b>morphine</b> tolerance in rats.
+PRKCG	drug	opioid	20359526	These observations suggest that spinal ERK2, P38 and <strong>PKCgamma</strong> are likely involved in multiple adaptive responses following systemic <b>morphine</b> administration, whereas DYN and CGRP may contribute selectively to the development of antinociceptive tolerance.
+PRKCG	addiction	sensitization	19607847	Several mechanisms have been suggested to be responsible for OIH such as <b>sensitization</b> of peripheral nociceptors, enhanced production/release of glutamate and neuropeptides in the spinal cord, <strong>protein kinase C gamma</strong> induced signaling, and/or enhanced descending facilitation of nociceptive pathways from the rostral ventromedial medulla; however signaling pathways known to lead to directly to OIH remain undiscovered.
+PRKCG	drug	alcohol	17566760	More recent studies using transgenic mice have identified two isozymes, <strong>PKCgamma</strong> and PKCepsilon, that have opposing roles in mediating the behavioral effects of <b>ethanol</b>.
+PRKCG	drug	alcohol	17566760	Genetic deletion of <strong>PKCgamma</strong> produces mice with a high <b>ethanol</b> drinking phenotype which are impulsive and require high levels of <b>ethanol</b> to reach intoxication, perhaps modeling the human condition of individuals who are at risk for developing <b>alcoholism</b>.
+PRKCG	addiction	intoxication	17566760	Genetic deletion of <strong>PKCgamma</strong> produces mice with a high ethanol drinking phenotype which are impulsive and require high levels of ethanol to reach <b>intoxication</b>, perhaps modeling the human condition of individuals who are at risk for developing alcoholism.
+PRKCG	drug	alcohol	17566760	These findings suggest that drugs targeting <strong>PKCgamma</strong> and PKCepsilon may be useful to curb excessive drinking, the key symptom of <b>alcohol</b> use disorders.
+PRKCG	drug	alcohol	17508994	The rationale for this study was based on the impulsive behavior and increased <b>ethanol</b> consumption observed in the protein kinase C gamma (<strong>PKC gamma</strong>) deficient mouse model.
+PRKCG	drug	alcohol	17508994	The rationale for this study was based on the impulsive behavior and increased <b>ethanol</b> consumption observed in the <strong>protein kinase C gamma</strong> (<strong>PKC gamma</strong>) deficient mouse model.
+PRKCG	addiction	relapse	17508994	Two composite behavioral disinhibition phenotypes and their component behavioral scores [conduct disorder, attention deficit hyperactivity disorder (ADHD), substance experimentation (SUB) and novelty <b>seeking</b>] were examined for association with five independent <strong>PRKCG</strong> single nucleotide polymorphisms (SNPs).
+PRKCG	drug	opioid	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and <strong>PKCgamma</strong> immunoreactivity, and whether pharmacological inhibition of PKC would attenuate <b>morphine</b> withdrawal induced c Fos expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+PRKCG	addiction	withdrawal	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and <strong>PKCgamma</strong> immunoreactivity, and whether pharmacological inhibition of PKC would attenuate morphine <b>withdrawal</b> induced c Fos expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+PRKCG	drug	opioid	16176357	Kv 4.3(+) neurons were a subset of excitatory inerneurons with calretinin(+)/calbindin( )/<strong>PKCgamma</strong>( ) markers, and a fraction of them expressed micro <b>opioid</b> receptors.
+PRKCG	drug	opioid	15830100	During <b>morphine</b> dependence, but not <b>naloxone</b> precipitated withdrawal, <strong>PKC gamma</strong> in the spinal cord translocated from cytosol to membrane fraction, and intrathecal administration of CHE did not change the expression of <strong>PKC gamma</strong> in the spinal cord of <b>naloxone</b> precipitated withdrawal rats.
+PRKCG	addiction	dependence	15830100	During morphine <b>dependence</b>, but not naloxone precipitated withdrawal, <strong>PKC gamma</strong> in the spinal cord translocated from cytosol to membrane fraction, and intrathecal administration of CHE did not change the expression of <strong>PKC gamma</strong> in the spinal cord of naloxone precipitated withdrawal rats.
+PRKCG	addiction	withdrawal	15830100	During morphine dependence, but not naloxone precipitated <b>withdrawal</b>, <strong>PKC gamma</strong> in the spinal cord translocated from cytosol to membrane fraction, and intrathecal administration of CHE did not change the expression of <strong>PKC gamma</strong> in the spinal cord of naloxone precipitated <b>withdrawal</b> rats.
+PRKCG	drug	alcohol	15655532	The present studies were designed to test the hypothesis that neuronal specific protein kinase Cgamma (<strong>PKCgamma</strong>) plays a critical role in acute <b>ethanol</b> withdrawal hyper responsiveness in spinal cord.
+PRKCG	addiction	withdrawal	15655532	The present studies were designed to test the hypothesis that neuronal specific protein kinase Cgamma (<strong>PKCgamma</strong>) plays a critical role in acute ethanol <b>withdrawal</b> hyper responsiveness in spinal cord.
+PRKCG	drug	alcohol	15655532	Exposure to <b>ethanol</b> (100 mM) induced <strong>PKCgamma</strong> translocation from the nucleus to cytoplasm in motor neurons.
+PRKCG	drug	alcohol	15655532	The results show that <strong>PKCgamma</strong> mediates <b>ethanol</b> withdrawal hyper responsiveness in spinal motor neurons; the results may be relevant to some symptoms of <b>ethanol</b> withdrawal in vivo.
+PRKCG	addiction	withdrawal	15655532	The results show that <strong>PKCgamma</strong> mediates ethanol <b>withdrawal</b> hyper responsiveness in spinal motor neurons; the results may be relevant to some symptoms of ethanol <b>withdrawal</b> in vivo.
+PRKCG	drug	opioid	15379885	Additionally, acute as well as chronic intraperitoneal <b>morphine</b> administration changed the abundance of <strong>PKC gamma</strong>, gamma1 subunit of GABAA and hsp70 genes.
+PRKCG	drug	opioid	15355330	Using immunoblot analysis, we confirmed that the increased level of protein kinase Cgamma (<strong>PKCgamma</strong>) isoform was observed in the limbic forebrain of ICR mice conditioned with <b>morphine</b>.
+PRKCG	drug	opioid	15355330	The present data provide direct evidence that the activation of mGlu5 receptor linked to the increased <strong>PKCgamma</strong> isoform in the mouse limbic forebrain is implicated in the development of rewarding effect of <b>morphine</b>.
+PRKCG	addiction	withdrawal	15275778	Consistent with this finding, a specific peptide inhibitor of calcium independent PKC, but not an inhibitor of calcium dependent <strong>PKC gamma</strong>, blocked <b>withdrawal</b> hyperresponsiveness of the sVRP.
+PRKCG	drug	opioid	15275778	Similarly, in vivo in 7 day old rat pups, inhibition of PKC, but not <strong>PKC gamma</strong>, prevented thermal hyperalgesia precipitated by <b>naloxone</b> at 30 min post <b>morphine</b>.
+PRKCG	drug	opioid	15275778	In addition the difference between <b>naloxone</b> precipitated and spontaneous withdrawal in vivo suggests that in postnatal day 7 rats, <b>morphine</b> exposure produces an early phase of primary afferent sensitization dependent upon PKC translocation, followed by a later phase involving spinal sensitization mediated by <strong>PKC gamma</strong>.
+PRKCG	addiction	sensitization	15275778	In addition the difference between naloxone precipitated and spontaneous withdrawal in vivo suggests that in postnatal day 7 rats, morphine exposure produces an early phase of primary afferent <b>sensitization</b> dependent upon PKC translocation, followed by a later phase involving spinal <b>sensitization</b> mediated by <strong>PKC gamma</strong>.
+PRKCG	addiction	withdrawal	15275778	In addition the difference between naloxone precipitated and spontaneous <b>withdrawal</b> in vivo suggests that in postnatal day 7 rats, morphine exposure produces an early phase of primary afferent sensitization dependent upon PKC translocation, followed by a later phase involving spinal sensitization mediated by <strong>PKC gamma</strong>.
+PRKCG	drug	alcohol	12649378	<b>Ethanol</b> differentially enhances hippocampal GABA A receptor mediated responses in protein kinase C gamma (<strong>PKC gamma</strong>) and PKC epsilon null mice.
+PRKCG	drug	alcohol	12649378	<b>Ethanol</b> differentially enhances hippocampal GABA A receptor mediated responses in <strong>protein kinase C gamma</strong> (<strong>PKC gamma</strong>) and PKC epsilon null mice.
+PRKCG	drug	alcohol	12649378	We examined acute effects of <b>ethanol</b> on GABA(A) receptor mediated inhibitory postsynaptic currents (IPSCs) in mice lacking either <strong>PKCgamma</strong> (<strong>PKCgamma</strong>( / )) or PKCepsilon (PKCepsilon( / )) isozymes and compared the results to those from corresponding wild type littermates (<strong>PKCgamma</strong>(+/+) and PKCepsilon(+/+)).
+PRKCG	drug	alcohol	12649378	<b>Ethanol</b> (80 mM) enhanced the IPSC response amplitude and area in <strong>PKCgamma</strong>(+/+) mice, but not in the <strong>PKCgamma</strong>( / ) mice.
+PRKCG	drug	alcohol	12649378	These results suggest that <strong>PKCgamma</strong> and PKCepsilon signaling pathways reciprocally modulate both <b>ethanol</b> enhancement of GABA(A) receptor function and hypnotic sensitivity to <b>ethanol</b>.
+PRKCG	drug	opioid	11731061	Reduced development of tolerance to the analgesic effects of <b>morphine</b> and clonidine in <strong>PKC gamma</strong> mutant mice.
+PRKCG	drug	opioid	11731061	These results indicate that <strong>PKC gamma</strong> contributes to the development of tolerance to the analgesic effects of both <b>morphine</b> and clonidine.
+PRKCG	drug	opioid	11731061	To assess the contribution of <strong>PKC gamma</strong> to this process, we studied the responses of wild type and mutant mice to an intraplantar injection of formalin (a model of persistent pain) following chronic <b>morphine</b> treatment.
+PRKCG	drug	opioid	11731061	Although <b>morphine</b> tolerance increased formalin evoked persistent pain behavior and Fos LI in wild type mice, there was no difference between placebo  and <b>morphine</b> treated mutant mice, suggesting that <strong>PKC gamma</strong> also contributes to chronic <b>morphine</b> induced changes in nociceptive processing.
+PRKCG	drug	alcohol	11427306	The protein level of membrane bound PKCalpha and <strong>PKCgamma</strong> isoforms, which are defined as Ca2+ dependent PKC isoforms (cPKC), in the limbic forebrain during chronic <b>ethanol</b> treatment was significantly increased, whereas the levels of both were significantly decreased in the frontal cortex.
+PRKCG	drug	opioid	11246146	The protein level of <strong>PKCgamma</strong> was significantly up regulated in membrane preparations of the limbic forebrain obtained from the <b>morphine</b> conditioned mice compared to that from the saline conditioned mice.
+PRKCG	drug	opioid	11246146	Furthermore, we investigated the rewarding properties of <b>morphine</b> in mice lacking <strong>PKCgamma</strong> gene.
+PRKCG	drug	opioid	11246146	A significant place preference was observed following treatment with <b>morphine</b> in wild type mice, whereas such an effect of <b>morphine</b> was not found in <strong>PKCgamma</strong> knockout mice.
+PRKCG	drug	opioid	11246146	These findings suggest that activated <strong>PKCgamma</strong> in the limbic forebrain following the treatment with <b>morphine</b> may be critical for the development and/or maintenance of reinforcing effects induced by <b>morphine</b> in mice.
+PRKCG	addiction	reward	11246146	These findings suggest that activated <strong>PKCgamma</strong> in the limbic forebrain following the treatment with morphine may be critical for the development and/or maintenance of <b>reinforcing</b> effects induced by morphine in mice.
+PRKCG	drug	opioid	11144149	We therefore propose that <strong>PKC gamma</strong> may play a critical role in the development of <b>morphine</b> tolerance.
+PRKCG	addiction	sensitization	10375678	Protein kinase C (PKC) is thought to have a role in <b>sensitization</b> of dorsal horn neurons in certain pain states, and a recent study has reported that mice which lack the gamma isoform (<strong>PKCgamma</strong>) show reduced neuropathic pain after peripheral nerve injury.
+PRKCG	drug	opioid	10375678	Dual immunofluorescence labelling showed that <strong>PKCgamma</strong> was not randomly distributed amongst non GABAergic neurons, since it was present in 76% of cells with neurotensin and 45% of those with somatostatin, but only 5% of those with the mu <b>opioid</b> receptor (MOR 1).
+GAD2	drug	alcohol	32329567	Finally, we found that in mice pretreated with sazetidine A, <b>alcohol</b> induced Fos transcript in Th , but not <strong>Gad2</strong> expressing neurons in the VTA as measured by increased Fos transcript expression.
+GAD2	drug	opioid	31866536	GAD1 but not <strong>GAD2</strong> polymorphisms are associated with <b>heroin</b> addiction phenotypes.
+GAD2	addiction	addiction	31866536	GAD1 but not <strong>GAD2</strong> polymorphisms are associated with heroin <b>addiction</b> phenotypes.
+GAD2	drug	opioid	31866536	The results of association analyses of <strong>GAD2</strong> with phenotypes of <b>heroin</b> addiction showed no significant differences.
+GAD2	addiction	addiction	31866536	The results of association analyses of <strong>GAD2</strong> with phenotypes of heroin <b>addiction</b> showed no significant differences.
+GAD2	drug	nicotine	31744841	This, coupled with expression data demonstrating coexpression of vesicular glutamate transporter 2 (VGluT2) and glutamate decarboxylase 2 (<strong>Gad2</strong>) in mVTA neurons, suggests that <b>nicotine</b> is able to stimulate GABA corelease from mVTA VGluT2+ neurons.
+GAD2	drug	nicotine	31744841	This, coupled with expression data demonstrating coexpression of vesicular glutamate transporter 2 (VGluT2) and <strong>glutamate decarboxylase 2</strong> (<strong>Gad2</strong>) in mVTA neurons, suggests that <b>nicotine</b> is able to stimulate GABA corelease from mVTA VGluT2+ neurons.
+GAD2	drug	nicotine	31744841	<b>Nicotine</b> had an altogether different effect on mVTA to latVTA GABA release from <strong>Gad2</strong>+ cells; <b>nicotine</b> suppressed GABA release from mVTA <strong>Gad2</strong>+ terminals in nearly all cells tested.
+GAD2	drug	nicotine	31733321	During short term <b>nicotine</b> exposure, glutamate decarboxylase 67 (GAD67), <strong>GAD65</strong>, and μ opioid receptors (MOR) up regulated.
+GAD2	drug	opioid	31733321	During short term nicotine exposure, glutamate decarboxylase 67 (GAD67), <strong>GAD65</strong>, and μ <b>opioid</b> receptors (MOR) up regulated.
+GAD2	drug	nicotine	31733321	<b>Nicotine</b> appears to alter pain sensitivity by affecting the expression of <strong>GAD65</strong>, GAD67, MOR, endorphins, and GABA.
+GAD2	drug	opioid	30682345	Pharmacological activation of dopamine D4 receptor modulates <b>morphine</b> induced changes in the expression of <strong>GAD65</strong>/67 and GABAB receptors in the basal ganglia.
+GAD2	drug	opioid	30682345	It has been demonstrated that the co administration of a D4R agonist together with <b>morphine</b> leads to a restoration of GABA signaling by preventing drug induced changes in <strong>GAD65</strong>/67 expression in the caudate putamen, globus palidus and substantia nigra.
+GAD2	drug	cocaine	30294670	In the prelimbic PFC, both 1 and 5 d of <b>cocaine</b> exposure increased <strong>GAD65</strong>/67 puncta near PNN surrounded PV cells, with an increase in the <strong>GAD65</strong>/67 to VGluT1 puncta ratio after 5 d of <b>cocaine</b> exposure.
+GAD2	drug	nicotine	30170085	Our results showed that in the group that received acute <b>nicotine</b>, both <strong>GAD65</strong> and GAD67 protein levels were downregulated in the vHPC, but not in dHPC.
+GAD2	drug	nicotine	30170085	Finally, using c fos/<strong>GAD65</strong>/67 double immunofluorescence, we showed that <b>nicotine</b> mainly increased c fos expression in non GABAergic ventral hippocampal cells, indicating that acute <b>nicotine</b> increases vHPC excitability.
+GAD2	drug	cocaine	29139213	In addition, we found increased <strong>GAD65</strong> expression after 10 but not 60 days of <b>cocaine</b> self administration in the rostral mesencephalic tegmental nucleus.
+GAD2	drug	amphetamine	28351548	Based on our previous findings, we also found significant correlations between GAD67, GAT1 and parvalbumin while GAD67, <strong>GAD65</strong> and GAT1 were positively correlated with cholecystokinin in the PRL of <b>METH</b> sensitized rats.
+GAD2	drug	amphetamine	27967329	Association of polymorphisms in GAD1 and <strong>GAD2</strong> genes with <b>methamphetamine</b> dependence.
+GAD2	addiction	dependence	27967329	Association of polymorphisms in GAD1 and <strong>GAD2</strong> genes with methamphetamine <b>dependence</b>.
+GAD2	drug	amphetamine	27967329	Genotypes of rs769404 and rs701492 in GAD1 and rs2236418 in <strong>GAD2</strong> polymorphisms were determined in 100 <b>METH</b> dependent male subjects and 102 matched controls.
+GAD2	drug	amphetamine	27967329	The genotype and allele frequencies of rs2236418 (<strong>GAD2</strong>) were associated with <b>METH</b> dependence and <b>METH</b> with psychosis, in which the G allele was related to increased risk.
+GAD2	addiction	dependence	27967329	The genotype and allele frequencies of rs2236418 (<strong>GAD2</strong>) were associated with METH <b>dependence</b> and METH with psychosis, in which the G allele was related to increased risk.
+GAD2	drug	amphetamine	27967329	This study indicates that genetic variability in GAD1 and <strong>GAD2</strong> contributes to risk of <b>METH</b> dependence and <b>METH</b> psychosis in the Thai population and indicates the role of the GABAergic system in these disorders.
+GAD2	addiction	dependence	27967329	This study indicates that genetic variability in GAD1 and <strong>GAD2</strong> contributes to risk of METH <b>dependence</b> and METH psychosis in the Thai population and indicates the role of the GABAergic system in these disorders.
+GAD2	drug	opioid	27862708	In the present study, we found that reexposure to <b>morphine</b> paired environment significantly increased the activity of hippocampal CA3 neurons, increased the excitability of GABAergic neurons and expression of glutamic acid decarboxylase 65/67 in the caudal lateral septum (LSc) and decreased the activity of GABAergic neurons and <strong>GAD65</strong>/67 expression in ventral tegmental area (VTA), leading to activation (disinhibition) of dopaminergic neurons.
+GAD2	drug	opioid	27862708	Inactivation of CA3 neurons attenuated GABAergic neurons activity and decreased the upregulation of <strong>GAD65</strong>/67 in LSc, prevented the dopaminergic neurons activation,and <strong>GAD65</strong>/67 downregulation in VTA and ameliorated the CPP behavior following exposure to <b>morphine</b> paired context.
+GAD2	addiction	reward	27862708	Inactivation of CA3 neurons attenuated GABAergic neurons activity and decreased the upregulation of <strong>GAD65</strong>/67 in LSc, prevented the dopaminergic neurons activation,and <strong>GAD65</strong>/67 downregulation in VTA and ameliorated the <b>CPP</b> behavior following exposure to morphine paired context.
+GAD2	drug	opioid	27862708	Blockade of NMDA receptor in LSc also prevented the upregulation of <strong>GAD65</strong>/67 in LSc and formation of CPP induced by stimulus of <b>morphine</b> paired environment.
+GAD2	addiction	reward	27862708	Blockade of NMDA receptor in LSc also prevented the upregulation of <strong>GAD65</strong>/67 in LSc and formation of <b>CPP</b> induced by stimulus of morphine paired environment.
+GAD2	drug	opioid	27862708	Suppression of GAD activity in LSc also remarkably attenuated the dopaminergic neurons activation and the <strong>GAD65</strong>/67 downregulation in VTA and prevented the formation of CPP induced by reexposure to <b>morphine</b> associated context.
+GAD2	addiction	reward	27862708	Suppression of GAD activity in LSc also remarkably attenuated the dopaminergic neurons activation and the <strong>GAD65</strong>/67 downregulation in VTA and prevented the formation of <b>CPP</b> induced by reexposure to morphine associated context.
+GAD2	drug	psychedelics	26068050	The results showed that chronic <b>MDMA</b> caused hippocampal protein deficits in adolescent and young adult rats at different levels: (1) impaired serotonergic (5 HT2A and 5 HT2C post synaptic receptors) and GABAergic (<strong>GAD2</strong> enzyme) signaling, and (2) decreased structural cytoskeletal neurofilament proteins (NF H, NF M and NF L).
+GAD2	drug	nicotine	26041923	In mice expressing Leu9'Ser α4 nAChR subunits in VTA GABAergic neurons (<strong>Gad2</strong>(VTA):Leu9'Ser mice), subreward threshold doses of <b>nicotine</b> were sufficient to selectively activate VTA GABAergic neurons and elicit acute hypolocomotion, with subsequent <b>nicotine</b> exposures eliciting tolerance to this effect, compared to control animals.
+GAD2	drug	nicotine	26041923	In the conditioned place preference procedure, <b>nicotine</b> was sufficient to condition a significant place preference in <strong>Gad2</strong>(VTA):Leu9'Ser mice at low <b>nicotine</b> doses that failed to condition control animals.
+GAD2	drug	opioid	23745257	Chronic administration of <b>morphine</b> downregulated the expression of <strong>GAD65</strong> in the spinal cord dorsal horn of young rats.
+GAD2	drug	opioid	23745257	Chronic <b>morphine</b> administration could induce mechanical hyperalgesia in young rats, and the downregulation of <strong>GAD65</strong> in the spinal cord dorsal horn might play a critical role in the molecular mechanisms of <b>morphine</b> induced hyperalgesia.
+GAD2	drug	alcohol	22253714	There were also expression changes specific to cocaine addicts (GAD1, <strong>GAD2</strong>), <b>alcoholics</b> (GABRA2) and P rats (ABAT, GABRG3).
+GAD2	drug	cocaine	22253714	There were also expression changes specific to <b>cocaine</b> addicts (GAD1, <strong>GAD2</strong>), alcoholics (GABRA2) and P rats (ABAT, GABRG3).
+GAD2	drug	benzodiazepine	21497611	<strong>GAD65</strong> /  mice showed a significant reduction in the duration of LORR and LTWR produced by propofol and <b>midazolam</b>, but not sevoflurane.
+GAD2	drug	cocaine	20581658	<b>Cocaine</b> self administration attenuated the effects of 6 OHDA lesions on the mRNA expression of alpha2 GABAA and beta2 GABAA subunits in the prefrontal cortex, reversed the mRNA expression of alpha2 GABAA subunits in the striatum and of alpha4 GABAA subunits in the prefrontal cortex and in the hippocampus, and reversed the mRNA expression of <strong>GAD65</strong> and GAD67 in the brain areas studied.
+GAD2	drug	alcohol	20002022	Mice lacking <strong>Gad2</strong> show altered behavioral effects of <b>ethanol</b>, flurazepam and gabaxadol.
+GAD2	drug	benzodiazepine	20002022	Mice lacking <strong>Gad2</strong> show altered behavioral effects of ethanol, <b>flurazepam</b> and gabaxadol.
+GAD2	drug	alcohol	20002022	Deletion of <strong>Gad2</strong> increased <b>ethanol</b> palatability and intake and slightly reduced the severity of <b>ethanol</b> induced withdrawal, but these effects depended strongly on genetic background.
+GAD2	addiction	withdrawal	20002022	Deletion of <strong>Gad2</strong> increased ethanol palatability and intake and slightly reduced the severity of ethanol induced <b>withdrawal</b>, but these effects depended strongly on genetic background.
+GAD2	drug	benzodiazepine	20002022	Deletion of <strong>Gad2</strong> reduced the effect of <b>flurazepam</b> on motor incoordination and increased the effect of extrasynaptic GABAA receptor agonist gabaxadol without changing the duration of loss of righting reflex produced by these drugs.
+GAD2	drug	cocaine	19855903	Influence of progesterone on <strong>GAD65</strong> and GAD67 mRNA expression in the dorsolateral striatum and prefrontal cortex of female rats repeatedly treated with <b>cocaine</b>.
+GAD2	drug	alcohol	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as <b>alcohol</b> dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and <strong>GAD2</strong>), the nucleoside transporter (SLC29A1) and diazepam binding inhibitor (DBI).
+GAD2	drug	benzodiazepine	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as alcohol dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and <strong>GAD2</strong>), the nucleoside transporter (SLC29A1) and <b>diazepam</b> binding inhibitor (DBI).
+GAD2	addiction	withdrawal	19233937	The open field test, loss of righting reflex (LORR), loss of tail pinch <b>withdrawal</b> response (LTWR), and locomotor activity were compared between wild type (WT) mice and <strong>GAD65</strong>( / ) mice.
+GAD2	drug	psychedelics	19233937	In conclusion, <strong>GAD65</strong>( / ) mice show a diminished response to propofol, but not <b>ketamine</b>, indicating that <strong>GAD65</strong> mediated GABA synthesis plays an important role in hypnotic and immobilizing actions of propofol.
+GAD2	drug	alcohol	17067345	This study examined the possible roles of the genes that code for 2 forms of GAD (GAD1 and <strong>GAD2</strong>) in the development of <b>alcoholism</b>.
+GAD2	drug	alcohol	17067345	Three valid SNPs at the <strong>GAD2</strong> gene demonstrated no associations with <b>alcoholism</b>.
+GAD2	drug	alcohol	17034009	Mutation screen of the <strong>GAD2</strong> gene and association study of <b>alcoholism</b> in three populations.
+GAD2	drug	alcohol	17034009	We examined whether variation in glutamate decarboxylase 2 (<strong>GAD2</strong>), a gene encoding for a major enzyme in the synthesis of GABA, contributes to risk of <b>alcohol</b> dependence (AD).
+GAD2	addiction	dependence	17034009	We examined whether variation in glutamate decarboxylase 2 (<strong>GAD2</strong>), a gene encoding for a major enzyme in the synthesis of GABA, contributes to risk of alcohol <b>dependence</b> (AD).
+GAD2	drug	alcohol	17034009	We examined whether variation in <strong>glutamate decarboxylase 2</strong> (<strong>GAD2</strong>), a gene encoding for a major enzyme in the synthesis of GABA, contributes to risk of <b>alcohol</b> dependence (AD).
+GAD2	addiction	dependence	17034009	We examined whether variation in <strong>glutamate decarboxylase 2</strong> (<strong>GAD2</strong>), a gene encoding for a major enzyme in the synthesis of GABA, contributes to risk of alcohol <b>dependence</b> (AD).
+GAD2	drug	alcohol	17034009	Analyses in these populations did not support a role for <strong>GAD2</strong> in <b>alcoholism</b>.
+GAD2	addiction	aversion	15036622	Preference/<b>aversion</b> responses to four basic tastes were not different between <strong>GAD65</strong>( / ) and wild type mice during a 48 h two bottle choice test.
+GAD2	drug	alcohol	12691782	Evaluation of the glutamate decarboxylase genes Gad1 and <strong>Gad2</strong> as candidate genes for acute <b>ethanol</b> withdrawal severity in mice.
+GAD2	addiction	withdrawal	12691782	Evaluation of the glutamate decarboxylase genes Gad1 and <strong>Gad2</strong> as candidate genes for acute ethanol <b>withdrawal</b> severity in mice.
+GAD2	drug	alcohol	12691782	Previous studies in crosses between the C57BL/6J (B6) and the DBA/2J (D2) mice have implicated a role of the genes encoding for the 67  and 65 kDa isoforms of the glutamate decarboxylase (Gad1 and <strong>Gad2</strong>) in the manifestation and severity of multiple <b>ethanol</b> related traits such as acute <b>ethanol</b> withdrawal severity [Buck, K.J., Metten, P., Belknap, J.K., Crabbe, J.C., 1997.
+GAD2	addiction	withdrawal	12691782	Previous studies in crosses between the C57BL/6J (B6) and the DBA/2J (D2) mice have implicated a role of the genes encoding for the 67  and 65 kDa isoforms of the glutamate decarboxylase (Gad1 and <strong>Gad2</strong>) in the manifestation and severity of multiple ethanol related traits such as acute ethanol <b>withdrawal</b> severity [Buck, K.J., Metten, P., Belknap, J.K., Crabbe, J.C., 1997.
+GAD2	drug	alcohol	12691782	In addition, no significant <strong>GAD65</strong> or GAD67 expression differences were detected in either drug nai;ve or acute <b>ethanol</b> withdrawn animals by Western blot experiments.
+GAD2	drug	alcohol	12691782	Therefore, these results do not support the hypothesis of an involvement of Gad1 or <strong>Gad2</strong> in the pathophysiology of acute <b>ethanol</b> withdrawal severity and the other <b>ethanol</b> related traits.
+GAD2	addiction	withdrawal	12691782	Therefore, these results do not support the hypothesis of an involvement of Gad1 or <strong>Gad2</strong> in the pathophysiology of acute ethanol <b>withdrawal</b> severity and the other ethanol related traits.
+SOAT1	drug	alcohol	30472309	In the first experiments, rats were infused with 25, 50, 100, or 200 ng of IL 6; or 0.3, 3.0, or 9.0 μg of the JAK/<strong>STAT</strong> inhibitor AG490 30 min prior to a high dose <b>ethanol</b> challenge.
+SOAT1	addiction	addiction	28550509	Seven genes were picked out (Acss2, Acss3, <strong>Acat1</strong>, Acsl1, Acaa2, Hadh, and Hadhb) and the mRNA level of the Acss2 gene was increased only in the "<b>compulsive</b> like" group (p = 0.004).
+SOAT1	addiction	intoxication	26327308	<strong>STAT</strong> toxicology screening may be necessary, when sexual assault under GHB <b>intoxication</b> is suspected.
+SOAT1	drug	nicotine	25548313	A personal or family history of stroke, <b>smoking</b> status, and time of event (in hours/out of hours) were not significantly associated with adapted <strong>STAT</strong> scores.
+SOAT1	drug	nicotine	24398389	A variety of signaling cascades are induced by <b>nicotine</b> through nAChRs, including the mitogen activated protein kinase/extracellular signal regulated kinase pathway, phosphoinositide 3 kinase/AKT pathway, and janus activated kinase/<strong>STAT</strong> signaling.
+SOAT1	drug	benzodiazepine	23853649	<strong>stat</strong> dose of 0.1 mg/kg <b>diazepam</b> and 0.1 mg/kg <strong>stat</strong> dose of <b>midazolam</b> and a 0.1 mg/kg/h infusion of these drugs were administered for different groups of patients, respectively.
+SOAT1	drug	alcohol	22141444	Pathway analyses implicated nuclear factor κ light chain enhancer of activated B cells (NF κB) and Janus kinase (JAK)/signal transducer and activator of transcription (<strong>STAT</strong>) as possible mediators of <b>ethanol</b> induced effects on immune related proteins in primates.
+SOAT1	drug	alcohol	22141444	Chronic <b>ethanol</b> consumption in primates leads to an allostatic state of physiological compromise with respect to circulating immune  and stress related proteins in NF κB  and <strong>STAT</strong>/JAK related pathways in correlation with altered endocrine activity.
+SOAT1	drug	alcohol	20388501	Pathway analysis showed that <b>alcohol</b> differentially affected various pathways in a K ras dependent manner   some of which previously shown to be regulated by <b>alcohol</b>   including the insulin/PI3K pathway, the NF kappaB, the phosphodiesterases (PDEs) pathway, the Jak/<strong>Stat</strong> and the adipokine signaling pathways.
+SOAT1	drug	nicotine	18364498	<strong>Stat</strong> bite: Medicaid coverage of <b>tobacco</b> dependence treatments.
+SOAT1	addiction	dependence	18364498	<strong>Stat</strong> bite: Medicaid coverage of tobacco <b>dependence</b> treatments.
+SOAT1	drug	opioid	16081842	In addition, Western blot and EMSA experiments revealed that <b>morphine</b> withdrawal induced Th2 differentiation was mediated through the classical Th2 transcription factors <strong>Stat</strong> 6 and GATA 3.
+SOAT1	addiction	withdrawal	16081842	In addition, Western blot and EMSA experiments revealed that morphine <b>withdrawal</b> induced Th2 differentiation was mediated through the classical Th2 transcription factors <strong>Stat</strong> 6 and GATA 3.
+SOAT1	drug	opioid	12535947	Under the present conditions <b>fentanyl</b> did not affect extracellular signal regulated protein kinase 1 and 2, <strong>Stat</strong> and cyclic AMP response element binding protein activity.
+SOAT1	drug	nicotine	12036789	<b>Tobacco</b> industry surveillance of public health groups: the case of <strong>STAT</strong> (Stop Teenage Addiction to <b>Tobacco</b>) and INFACT (Infant Formula Action Coalition).
+SOAT1	addiction	addiction	12036789	Tobacco industry surveillance of public health groups: the case of <strong>STAT</strong> (Stop Teenage <b>Addiction</b> to Tobacco) and INFACT (Infant Formula Action Coalition).
+SOAT1	drug	cocaine	8987828	Influence of <b>cocaine</b> on the JAK <strong>STAT</strong> pathway in the mesolimbic dopamine system.
+SOAT1	drug	cocaine	8987828	These findings suggest a scheme whereby some of the effects of chronic <b>cocaine</b> on VTA dopaminergic neurons are mediated directly by regulation of the JAK <strong>STAT</strong> pathway in these cells, as well as perhaps indirectly by regulation of this pathway in nondopaminergic cells.
+SOAT1	addiction	dependence	1473845	Static compliance (C <strong>stat</strong>), static pressure volume (<strong>Stat</strong> P V) hysteresis, vital capacity (VC), frequency <b>dependence</b> of dynamic compliance (C dyn) and collateral ventilation (Coll V) of the lung were studied in six mongrel dogs.
+SOAT1	drug	alcohol	2213933	In contrast, only 16% received a <strong>stat</strong> on site psychiatric consultation (although dangerous behaviors are common in <b>alcoholics</b>).
+SOAT1	drug	alcohol	2806666	The disordered functional <strong>stat</strong> of the spinal cord's segmental apparatus seems to be due to depolarizing effect of <b>alcohol</b> and may be one of the causes of the motor breakdown in <b>alcohol</b> intoxication.
+SOAT1	addiction	intoxication	2806666	The disordered functional <strong>stat</strong> of the spinal cord's segmental apparatus seems to be due to depolarizing effect of alcohol and may be one of the causes of the motor breakdown in alcohol <b>intoxication</b>.
+SLC1A3	drug	alcohol	32329706	Actions of <b>alcohol</b> in brain: Genetics, Metabolomics, GABA receptors, Proteomics and Glutamate Transporter GLAST/<strong>EAAT1</strong>.
+SLC1A3	drug	alcohol	32329706	Actions of <b>alcohol</b> in brain: Genetics, Metabolomics, GABA receptors, Proteomics and Glutamate Transporter <strong>GLAST</strong>/<strong>EAAT1</strong>.
+SLC1A3	drug	alcohol	32329706	Neurochemical studies found the increased expression of glutamate transporter GLAST/<strong>EAAT1</strong> in brain as one of the largest changes caused by <b>alcoholism</b>.
+SLC1A3	drug	alcohol	32329706	Neurochemical studies found the increased expression of glutamate transporter <strong>GLAST</strong>/<strong>EAAT1</strong> in brain as one of the largest changes caused by <b>alcoholism</b>.
+SLC1A3	drug	alcohol	32329706	Given that GLAST/<strong>EAAT1</strong> is one of the most abundant proteins in the nervous tissue and is intimately associated with the function of the excitatory (glutamatergic) synapses, this may be among the most important effects of chronic <b>alcohol</b> on brain function.
+SLC1A3	drug	alcohol	32329706	Given that <strong>GLAST</strong>/<strong>EAAT1</strong> is one of the most abundant proteins in the nervous tissue and is intimately associated with the function of the excitatory (glutamatergic) synapses, this may be among the most important effects of chronic <b>alcohol</b> on brain function.
+SLC1A3	drug	alcohol	32329706	It has so far been observed mainly in the prefrontal cortex We show several experiments suggesting that acute <b>alcohol</b> can translocate GLAST/<strong>EAAT1</strong> in astrocytes towards the plasma membrane (and this effect is inhibited by the GABA(B) agonist baclofen) but neither the mechanism nor the specificity (to <b>alcohol</b>) of this phenomenon have been established.
+SLC1A3	drug	alcohol	32329706	It has so far been observed mainly in the prefrontal cortex We show several experiments suggesting that acute <b>alcohol</b> can translocate <strong>GLAST</strong>/<strong>EAAT1</strong> in astrocytes towards the plasma membrane (and this effect is inhibited by the GABA(B) agonist baclofen) but neither the mechanism nor the specificity (to <b>alcohol</b>) of this phenomenon have been established.
+SLC1A3	drug	alcohol	32329706	Furthermore, as GLAST/<strong>EAAT1</strong> is also expressed in testes and sperm (and could also be affected there by chronic <b>alcohol</b>), the levels of GLAST/<strong>EAAT1</strong> in sperm could be used as a diagnostic tool in testing the severity of <b>alcoholism</b> in human males.
+SLC1A3	drug	alcohol	32329706	Furthermore, as <strong>GLAST</strong>/<strong>EAAT1</strong> is also expressed in testes and sperm (and could also be affected there by chronic <b>alcohol</b>), the levels of <strong>GLAST</strong>/<strong>EAAT1</strong> in sperm could be used as a diagnostic tool in testing the severity of <b>alcoholism</b> in human males.
+SLC1A3	drug	alcohol	28826758	In this study, we tested clavulanic acid, which is another β lactam compound with negligible antimicrobial activity, on <b>ethanol</b> consumption and expression of GLT 1, xCT and glutamate aspartate transporter (<strong>GLAST</strong>) in male <b>alcohol</b> preferring (P) rats.
+SLC1A3	drug	nicotine	28347687	In the present study, for the first time, we investigated the effect of chronic exposure to electronic (e) cigarette vapor containing <b>nicotine</b>, for one hour daily for six months, on GLT 1, xCT, and <strong>GLAST</strong> expression in frontal cortex (FC), striatum (STR), and hippocampus (HIP) in outbred female CD1 mice.
+SLC1A3	drug	alcohol	27993695	Therefore, we examined the effects of orally administered Augmentin on <b>ethanol</b> intake as well as GLT 1, xCT and <strong>GLAST</strong> expression in male <b>alcohol</b> preferring (P) rats.
+SLC1A3	drug	opioid	27461080	By expression of a dominant negative TNF peptide via lentiviral vector injection in rat PAG to sequester soluble TNF (solTNF), we demonstrate that solTNF mediates <b>morphine</b> tolerance induced by TLR4 signaling, stimulates neuroinflammation (increased IL 1β and TLR4 mRNA), and disrupts glutamate reuptake (decreased GLT 1 and <strong>GLAST</strong> mRNA).
+SLC1A3	drug	alcohol	27199635	In this study, we examined the effects of amoxicillin and Augmentin on GLT 1 isoforms (GLT 1a and GLT 1b), xCT, and glutamate/aspartate transporter (<strong>GLAST</strong>) expression in NAc and PFC as well as <b>ethanol</b> intake in male P rats.
+SLC1A3	drug	alcohol	26821293	The expression of <strong>GLAST</strong> and xCT were unchanged in the <b>ethanol</b> withdrawal (EW) group compared to control group.
+SLC1A3	addiction	withdrawal	26821293	The expression of <strong>GLAST</strong> and xCT were unchanged in the ethanol <b>withdrawal</b> (EW) group compared to control group.
+SLC1A3	drug	alcohol	25972039	Finally, we review evidence of <strong>EAAT1</strong>/GLAST involvement in mechanisms of brain response to <b>alcoholism</b> and present some preliminary data showing that <b>ethanol</b>, at concentrations which may be reached following heavy drinking, can have an effect on the distribution of <strong>EAAT1</strong>/GLAST in cultured astrocytes; the effect is blocked by baclofen, a GABA B receptor agonist and a drug potentially useful in the treatment of <b>alcoholism</b>.
+SLC1A3	drug	alcohol	25972039	Finally, we review evidence of <strong>EAAT1</strong>/<strong>GLAST</strong> involvement in mechanisms of brain response to <b>alcoholism</b> and present some preliminary data showing that <b>ethanol</b>, at concentrations which may be reached following heavy drinking, can have an effect on the distribution of <strong>EAAT1</strong>/<strong>GLAST</strong> in cultured astrocytes; the effect is blocked by baclofen, a GABA B receptor agonist and a drug potentially useful in the treatment of <b>alcoholism</b>.
+SLC1A3	drug	alcohol	25972039	We argue that more research effort should be focused on <strong>EAAT1</strong>/GLAST, particularly in relation to <b>alcoholism</b> and drug addiction.
+SLC1A3	addiction	addiction	25972039	We argue that more research effort should be focused on <strong>EAAT1</strong>/GLAST, particularly in relation to alcoholism and drug <b>addiction</b>.
+SLC1A3	drug	alcohol	25972039	We argue that more research effort should be focused on <strong>EAAT1</strong>/<strong>GLAST</strong>, particularly in relation to <b>alcoholism</b> and drug addiction.
+SLC1A3	addiction	addiction	25972039	We argue that more research effort should be focused on <strong>EAAT1</strong>/<strong>GLAST</strong>, particularly in relation to alcoholism and drug <b>addiction</b>.
+SLC1A3	drug	alcohol	25619881	We focus in this study to determine the effects of ceftriaxone, β lactam antibiotic, on glial proteins such as GLT1 isoforms, xCT, glutamate aspartate transporter (<strong>GLAST</strong>), and several associated signaling pathways as well as <b>ethanol</b> intake in P rats.
+SLC1A3	drug	alcohol	24687412	In this study, we investigated the effects of ceftriaxone on the levels of xCT in both continuous and relapse like <b>ethanol</b> drinking, as well as GLT 1 isoforms, and glutamate aspartate transporter (<strong>GLAST</strong>) in relapse like <b>ethanol</b> intake.
+SLC1A3	addiction	relapse	24687412	In this study, we investigated the effects of ceftriaxone on the levels of xCT in both continuous and <b>relapse</b> like ethanol drinking, as well as GLT 1 isoforms, and glutamate aspartate transporter (<strong>GLAST</strong>) in <b>relapse</b> like ethanol intake.
+SLC1A3	drug	opioid	23359982	To investigate the effects of intrathecal injection of ginsenoside Rg1 at different doses on the changes of the behavior and the expressions of excitatory amino acid transporter 1 (<strong>EAAT1</strong>), i. e., glutamate aspartate transporter (GLAST) in the spinal dorsal horn of the arthritis rats with chronic <b>morphine</b> tolerance, and further to explore its mechanisms for <b>morphine</b> tolerance.
+SLC1A3	drug	opioid	23359982	To investigate the effects of intrathecal injection of ginsenoside Rg1 at different doses on the changes of the behavior and the expressions of excitatory amino acid transporter 1 (<strong>EAAT1</strong>), i. e., glutamate aspartate transporter (<strong>GLAST</strong>) in the spinal dorsal horn of the arthritis rats with chronic <b>morphine</b> tolerance, and further to explore its mechanisms for <b>morphine</b> tolerance.
+SLC1A3	drug	alcohol	22342743	Reduced <b>alcohol</b> intake and reward associated with impaired endocannabinoid signaling in mice with a deletion of the glutamate transporter <strong>GLAST</strong>.
+SLC1A3	drug	cannabinoid	22342743	Reduced alcohol intake and reward associated with impaired <b>endocannabinoid</b> signaling in mice with a deletion of the glutamate transporter <strong>GLAST</strong>.
+SLC1A3	addiction	reward	22342743	Reduced alcohol intake and <b>reward</b> associated with impaired endocannabinoid signaling in mice with a deletion of the glutamate transporter <strong>GLAST</strong>.
+SLC1A3	drug	alcohol	22342743	This hypothesis predicts that an impairment of glutamate clearance through inactivation of the astrocytic glutamate transporter, GLAST (<strong>EAAT1</strong>), will result in escalation of <b>alcohol</b> consumption.
+SLC1A3	addiction	addiction	22342743	This hypothesis predicts that an impairment of glutamate clearance through inactivation of the astrocytic glutamate transporter, GLAST (<strong>EAAT1</strong>), will result in <b>escalation</b> of alcohol consumption.
+SLC1A3	drug	alcohol	22342743	This hypothesis predicts that an impairment of glutamate clearance through inactivation of the astrocytic glutamate transporter, <strong>GLAST</strong> (<strong>EAAT1</strong>), will result in escalation of <b>alcohol</b> consumption.
+SLC1A3	addiction	addiction	22342743	This hypothesis predicts that an impairment of glutamate clearance through inactivation of the astrocytic glutamate transporter, <strong>GLAST</strong> (<strong>EAAT1</strong>), will result in <b>escalation</b> of alcohol consumption.
+SLC1A3	drug	alcohol	22342743	WT and <strong>GLAST</strong> KO mice were tested for <b>alcohol</b> consumption using two bottle free choice drinking.
+SLC1A3	drug	alcohol	22342743	Contrary to our hypothesis, <strong>GLAST</strong> KO mice showed markedly decreased <b>alcohol</b> consumption, and lacked CPP for <b>alcohol</b>, despite a higher locomotor response to this drug.
+SLC1A3	addiction	reward	22342743	Contrary to our hypothesis, <strong>GLAST</strong> KO mice showed markedly decreased alcohol consumption, and lacked <b>CPP</b> for alcohol, despite a higher locomotor response to this drug.
+SLC1A3	drug	alcohol	22342743	Constitutive deletion of <strong>GLAST</strong> unexpectedly results in markedly reduced <b>alcohol</b> consumption and preference, associated with markedly reduced <b>alcohol</b> reward.
+SLC1A3	addiction	reward	22342743	Constitutive deletion of <strong>GLAST</strong> unexpectedly results in markedly reduced alcohol consumption and preference, associated with markedly reduced alcohol <b>reward</b>.
+SLC1A3	drug	alcohol	22342743	Endocannabinoid signaling appears to be down regulated upstream of the CB1 receptor as a result of the <strong>GLAST</strong> deletion, and is a candidate mechanism behind the reduction of <b>alcohol</b> reward observed.
+SLC1A3	drug	cannabinoid	22342743	<b>Endocannabinoid</b> signaling appears to be down regulated upstream of the CB1 receptor as a result of the <strong>GLAST</strong> deletion, and is a candidate mechanism behind the reduction of alcohol reward observed.
+SLC1A3	addiction	reward	22342743	Endocannabinoid signaling appears to be down regulated upstream of the CB1 receptor as a result of the <strong>GLAST</strong> deletion, and is a candidate mechanism behind the reduction of alcohol <b>reward</b> observed.
+SLC1A3	drug	opioid	21865493	In contrast, ultra low dose (15 ng) <b>naloxone</b> enhanced the antinociceptive effect of <b>morphine</b> (10 μg), with an increase in the paw withdrawal threshold to thermal stimulus (from 19% to 35%) and to tactile stimulus (from 33% to 55%) compared with <b>morphine</b> treatment alone, and this was associated with restoration of <strong>GLAST</strong> and GLT 1 expression to control levels (102% and 114%, respectively) in the astrocytes of laminae I and II in the spinal cord dorsal horn ipsilateral to the PST hindlimb and a decrease in EAA levels in the CSF dialysate (glutamate: 10.0 μM; aspartate: 1.1 μM).
+SLC1A3	addiction	withdrawal	21865493	In contrast, ultra low dose (15 ng) naloxone enhanced the antinociceptive effect of morphine (10 μg), with an increase in the paw <b>withdrawal</b> threshold to thermal stimulus (from 19% to 35%) and to tactile stimulus (from 33% to 55%) compared with morphine treatment alone, and this was associated with restoration of <strong>GLAST</strong> and GLT 1 expression to control levels (102% and 114%, respectively) in the astrocytes of laminae I and II in the spinal cord dorsal horn ipsilateral to the PST hindlimb and a decrease in EAA levels in the CSF dialysate (glutamate: 10.0 μM; aspartate: 1.1 μM).
+SLC1A3	drug	opioid	21865493	Ultra low dose <b>naloxone</b> enhanced the antinociceptive effect of <b>morphine</b> in PST rats, possibly by restoration of <strong>GLAST</strong> and GLT 1 expression in astrocytes, which inhibited the accumulation of EAAs in the synapses, resulting in a neuroprotective effect.
+SLC1A3	drug	alcohol	20153402	The decreased expression of <strong>GLAST</strong>, GLT 1 and GluR2 in the <b>alcoholic</b> patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug seeking and chronic relapse.
+SLC1A3	addiction	relapse	20153402	The decreased expression of <strong>GLAST</strong>, GLT 1 and GluR2 in the alcoholic patients may increase glutamate tone and activity in the basolateral amygdala and this may contribute to neurodegeneration as well as the expression of associative memories and anxiety which underlie continued drug <b>seeking</b> and chronic <b>relapse</b>.
+SLC1A3	drug	alcohol	18657127	A recent study investigated the mRNA expression of selected genes in the prefrontal cortex and found that the levels of mRNA encoding the neurotrophic factor, midkine (MDK), and the excitatory amino acid transporter 1 (<strong>EAAT1</strong>) were significantly higher in <b>alcoholics</b> compared with nonalcoholic controls.
+SLC1A3	drug	alcohol	18657127	Quantitative changes in protein levels of MDK and <strong>EAAT1</strong> were investigated in <b>alcoholic</b> and control cases using Western blots.
+SLC1A3	drug	alcohol	18657127	Immunolabeling of the <strong>EAAT1</strong> was densest in cortical layer II in control cases and induced in deeper layers in <b>alcoholic</b> cases.
+SLC1A3	drug	alcohol	18606955	Genotype profiles for <strong>GLAST</strong>; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with <b>alcohol</b> dependence using multivariate statistical analysis.
+SLC1A3	addiction	dependence	18606955	Genotype profiles for <strong>GLAST</strong>; N methyl d aspartate receptor subunits NR1, NR2A, and NR2B; MGLUR5; NNOS; PRKG2; CAMK4; the regulatory subunit of PI3K; and CREB were analyzed for association with alcohol <b>dependence</b> using multivariate statistical analysis.
+SLC1A3	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (<strong>EAAT1</strong>, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, GluR3), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+SLC1A3	drug	alcohol	15770106	The <b>ethanol</b> induced deficit in glutamate uptake was not associated with decreased total tissue levels of the transporters <strong>GLAST</strong> or GLT1.
+SLC1A3	drug	opioid	15542740	By Northern blot analysis, the expression of glial glutamate transporter GLT 1, but not <strong>GLAST</strong>, mRNA was decreased in the striatum/nucleus accumbens (NAc) and thalamus of <b>morphine</b> dependent rats.
+SLC1A3	drug	cannabinoid	15509898	Prenatal <b>cannabinoid</b> exposure down  regulates glutamate transporter expressions (<strong>GLAST</strong> and EAAC1) in the rat cerebellum.
+SLC1A3	drug	cannabinoid	15509898	This study analyzed the expression of the glial (<strong>GLAST</strong>) and neuronal (EAAC1) subtypes of glutamate transporter in the cerebellum of male and female offspring exposed pre  and postnatally to Delta9 <b>tetrahydrocannabinol</b> (<b>THC</b>, the main component of <b>marijuana</b>).
+SLC1A3	drug	cannabinoid	15509898	The expression of the glutamate transporter <strong>GLAST</strong> in astroglial cells and EAAC1 in Purkinje neurons decreased in <b>THC</b> exposed offspring compared to controls.
+SLC1A3	drug	opioid	11423104	The expression of mRNAs for the glial glutamate transporters, GLT 1 and <strong>GLAST</strong>, in the rat brain accompanied with <b>morphine</b> dependence and <b>naloxone</b> precipitated withdrawal was investigated by Northern blot analysis.
+SLC1A3	addiction	dependence	11423104	The expression of mRNAs for the glial glutamate transporters, GLT 1 and <strong>GLAST</strong>, in the rat brain accompanied with morphine <b>dependence</b> and naloxone precipitated withdrawal was investigated by Northern blot analysis.
+SLC1A3	addiction	withdrawal	11423104	The expression of mRNAs for the glial glutamate transporters, GLT 1 and <strong>GLAST</strong>, in the rat brain accompanied with morphine dependence and naloxone precipitated <b>withdrawal</b> was investigated by Northern blot analysis.
+SLC1A3	drug	alcohol	9416769	In addition, the <b>ethanol</b> induced increase in Vmax for glutamate was reversed by the protein kinase C inhibitors, calphostin C and bisindolylmaleimide, and was not associated with an increase in the expression of either of the major glutamate transporter proteins, GLT 1 or <strong>GLAST</strong>.
+RBFOX3	drug	cannabinoid	31162770	Our results show that a 6 day repeated temozolomide treatment (25 mg/kg/day), a chemotherapy drug that blocks hippocampal neurogenesis, prevented <b>cannabidiol</b> induced increment in the early stages of neuronal maturation and differentiation, without altering the basal levels of BrdU/<strong>NeuN</strong> and doublecortin immunostaining.
+RBFOX3	drug	alcohol	29449568	<b>Alcohol</b> exposure reduced the number of both <strong>NeuN</strong> positive and doublecortin positive cells in the hippocampus.
+RBFOX3	drug	amphetamine	29174638	We found that CCL7 mRNA level was upregulated in the prefrontal cortex (PFC) after <b>Meth</b> administration (3mg/kg, subcutaneous), and increased CCL7 immunoreactivity was localized to the PFC <strong>NeuN</strong> positive neurons.
+RBFOX3	drug	alcohol	28965654	Broad spectrum protein kinase inhibition by the staurosporine analog KT 5720 reverses <b>ethanol</b> withdrawal associated loss of NeuN/<strong>Fox 3</strong>.
+RBFOX3	addiction	withdrawal	28965654	Broad spectrum protein kinase inhibition by the staurosporine analog KT 5720 reverses ethanol <b>withdrawal</b> associated loss of NeuN/<strong>Fox 3</strong>.
+RBFOX3	drug	alcohol	28965654	Broad spectrum protein kinase inhibition by the staurosporine analog KT 5720 reverses <b>ethanol</b> withdrawal associated loss of <strong>NeuN</strong>/<strong>Fox 3</strong>.
+RBFOX3	addiction	withdrawal	28965654	Broad spectrum protein kinase inhibition by the staurosporine analog KT 5720 reverses ethanol <b>withdrawal</b> associated loss of <strong>NeuN</strong>/<strong>Fox 3</strong>.
+RBFOX3	drug	alcohol	28965654	Concomitant application of <b>ethanol</b> and KT 5720 restored the loss of NeuN/<strong>Fox 3</strong> IF in pyramidal CA1 and granule DG cell layers produced by CIE, but there was no restoration in CA3.
+RBFOX3	drug	alcohol	28965654	Concomitant application of <b>ethanol</b> and KT 5720 restored the loss of <strong>NeuN</strong>/<strong>Fox 3</strong> IF in pyramidal CA1 and granule DG cell layers produced by CIE, but there was no restoration in CA3.
+RBFOX3	drug	alcohol	28965654	Application of KT 5720 during EWD failed to significantly alter levels of <strong>NeuN</strong> IF, implying that <b>ethanol</b> exposure activates protein kinases that, in part, mediate the effects of EWD.
+RBFOX3	drug	alcohol	28965654	These data demonstrate that CIE exposure alters protein kinase activity to promote <b>ethanol</b> withdrawal associated loss of NeuN/<strong>Fox 3</strong> and highlight the influence of kinase signaling on distinct cell types in the developing hippocampus.
+RBFOX3	addiction	withdrawal	28965654	These data demonstrate that CIE exposure alters protein kinase activity to promote ethanol <b>withdrawal</b> associated loss of NeuN/<strong>Fox 3</strong> and highlight the influence of kinase signaling on distinct cell types in the developing hippocampus.
+RBFOX3	drug	alcohol	28965654	These data demonstrate that CIE exposure alters protein kinase activity to promote <b>ethanol</b> withdrawal associated loss of <strong>NeuN</strong>/<strong>Fox 3</strong> and highlight the influence of kinase signaling on distinct cell types in the developing hippocampus.
+RBFOX3	addiction	withdrawal	28965654	These data demonstrate that CIE exposure alters protein kinase activity to promote ethanol <b>withdrawal</b> associated loss of <strong>NeuN</strong>/<strong>Fox 3</strong> and highlight the influence of kinase signaling on distinct cell types in the developing hippocampus.
+RBFOX3	drug	amphetamine	27931227	Moreover, SPION miD2861 identified enhanced HDAC5 expression in the lateral septum and the striatum after <b>amphetamine</b>, where we found neurprogenitor cells coexpressing <strong>NeuN</strong> and GFAP.
+RBFOX3	drug	alcohol	27177604	<b>Ethanol</b> Stimulates Endoplasmic Reticulum Inositol Triphosphate and Sigma Receptors to Promote Withdrawal Associated Loss of Neuron Specific Nuclear Protein/<strong>Fox 3</strong>.
+RBFOX3	addiction	withdrawal	27177604	Ethanol Stimulates Endoplasmic Reticulum Inositol Triphosphate and Sigma Receptors to Promote <b>Withdrawal</b> Associated Loss of Neuron Specific Nuclear Protein/<strong>Fox 3</strong>.
+RBFOX3	drug	opioid	25988842	Alterations of the corticotropin releasing factor (CRF), glucocorticoid receptor (NR3C1), tyrosine hydroxylase (TH), mu <b>opioid</b> receptor (MOr), brain derived neurotrophic factor (BDNF), neuronal nuclei (<strong>NeuN</strong>), microtubule associated protein 2 (MAP2) and neurofilament heavy (NF200) immunoreactive fibers were studied in the paraventricular nucleus of the hypothalamus (PVN), ventral tegmental area (VTA), nucleus accumbens (NAc) or hippocampus (HIP).
+RBFOX3	drug	amphetamine	23895375	Fos and <strong>NeuN</strong> (a neuronal marker) immunohistochemistry indicate that 5 6% of dorsal striatum neurons were activated 90 min after acute <b>methamphetamine</b> injections (5 mg/kg, i.p.)
+RBFOX3	drug	alcohol	23844726	The majority of newborn cells in <b>ethanol</b> and control groups co localized with <strong>NeuN</strong>, indicating a neuronal phenotype and therefore a 1.6 fold increase in hippocampal neurogenesis during abstinence.
+RBFOX3	addiction	withdrawal	22626265	Confocal IHC of samples taken 48 hours into <b>withdrawal</b> demonstrate the presence of TNF α staining surrounding cells expressing the neural marker <strong>NeuN</strong> and endothelial cells colabeled with ICAM 1 (CD54) and RECA 1, markers associated with an inflammatory response.
+RBFOX3	addiction	reward	22340086	Similarly, in another experiment, in that the perfusion was done 28 days after <b>CPP</b> test, most BrdU+ cells were co localized with <strong>NeuN</strong>.
+RBFOX3	drug	alcohol	19076732	Confocal analyses indicated that approximately 75% of co localization of BrdU(+) cells with <strong>NeuN</strong> in the hippocampal dentate gyrus (DG) resulting a net increase in neurogenesis in the <b>alcohol</b> abstinent group compared to controls.
+RBFOX3	drug	alcohol	18828802	<strong>NeuN</strong> staining showed no evidence of neuronal loss in either prefrontal cortex or hippocampus after withdrawal from chronic <b>alcohol</b> treatment.
+RBFOX3	addiction	withdrawal	18828802	<strong>NeuN</strong> staining showed no evidence of neuronal loss in either prefrontal cortex or hippocampus after <b>withdrawal</b> from chronic alcohol treatment.
+NCAM1	drug	cocaine	32124535	Hyperfunction of the stress response system and novelty induced hyperactivity correlate with enhanced <b>cocaine</b> induced conditioned place preference in <strong>NCAM</strong> deficient mice.
+NCAM1	drug	cocaine	32124535	Here we hypothesize that <strong>NCAM</strong> deficiency causes an altered response to <b>cocaine</b>.
+NCAM1	drug	cocaine	32124535	<b>Cocaine</b> induced behaviors of <strong>NCAM</strong> /  mice and wild type (+/+) littermates were analyzed in the conditioned place preference (CPP) test.
+NCAM1	addiction	reward	32124535	Cocaine induced behaviors of <strong>NCAM</strong> /  mice and wild type (+/+) littermates were analyzed in the conditioned place preference (<b>CPP</b>) test.
+NCAM1	drug	cocaine	32124535	<strong>NCAM</strong> /  mice showed an elevated <b>cocaine</b> induced sensitization, enhanced CPP, impaired extinction, and potentiated <b>cocaine</b> induced hyperlocomotion and CPP after extinction.
+NCAM1	addiction	reward	32124535	<strong>NCAM</strong> /  mice showed an elevated cocaine induced sensitization, enhanced <b>CPP</b>, impaired extinction, and potentiated cocaine induced hyperlocomotion and <b>CPP</b> after extinction.
+NCAM1	addiction	sensitization	32124535	<strong>NCAM</strong> /  mice showed an elevated cocaine induced <b>sensitization</b>, enhanced CPP, impaired extinction, and potentiated cocaine induced hyperlocomotion and CPP after extinction.
+NCAM1	drug	cocaine	32124535	<strong>NCAM</strong> /  showed no potentiated CPP as compared with <strong>NCAM</strong>+/+ littermates when a natural rewarding stimulus (ie, an unfamiliar female) was used, suggesting that the behavioral alterations of <strong>NCAM</strong> /  mice observed in the CPP test are specific to the effects of <b>cocaine</b>.
+NCAM1	addiction	reward	32124535	<strong>NCAM</strong> /  showed no potentiated <b>CPP</b> as compared with <strong>NCAM</strong>+/+ littermates when a natural rewarding stimulus (ie, an unfamiliar female) was used, suggesting that the behavioral alterations of <strong>NCAM</strong> /  mice observed in the <b>CPP</b> test are specific to the effects of cocaine.
+NCAM1	drug	cocaine	32124535	Activation of the prefrontal cortex and nucleus accumbens induced by the <b>cocaine</b> associated context was enhanced in <strong>NCAM</strong> /  compared with <strong>NCAM</strong>+/+ mice.
+NCAM1	drug	cocaine	32124535	Finally, <b>cocaine</b> induced behavior correlated positively with novelty induced behavior and plasma corticosterone levels in <strong>NCAM</strong> /  mice and negatively with <strong>NCAM</strong> mRNA levels in the hippocampus and nucleus accumbens in wild type mice.
+NCAM1	drug	cocaine	32124535	Our findings indicate that <strong>NCAM</strong> deficiency affects <b>cocaine</b> induced CPP in mice and support the view that hyperfunction of the stress response system and reactivity to novelty predict the behavioral responses to <b>cocaine</b>.
+NCAM1	addiction	reward	32124535	Our findings indicate that <strong>NCAM</strong> deficiency affects cocaine induced <b>CPP</b> in mice and support the view that hyperfunction of the stress response system and reactivity to novelty predict the behavioral responses to cocaine.
+NCAM1	drug	opioid	31951160	Neural cell adhesion molecule (<strong>NCAM</strong>) in the central nervous system may regulate <b>opioid</b> withdrawal and analgesic responses.
+NCAM1	addiction	withdrawal	31951160	Neural cell adhesion molecule (<strong>NCAM</strong>) in the central nervous system may regulate opioid <b>withdrawal</b> and analgesic responses.
+NCAM1	drug	nicotine	31867628	Genetic and Epigenetic Analysis Revealing Variants in the <strong>NCAM1</strong> TTC12 ANKK1 DRD2 Cluster Associated Significantly With <b>Nicotine</b> Dependence in Chinese Han <b>Smokers</b>.
+NCAM1	addiction	dependence	31867628	Genetic and Epigenetic Analysis Revealing Variants in the <strong>NCAM1</strong> TTC12 ANKK1 DRD2 Cluster Associated Significantly With Nicotine <b>Dependence</b> in Chinese Han Smokers.
+NCAM1	drug	psychedelics	31812709	This review seeks to delineate the relationship between PCP/<b>ketamine</b> induced loss of cortical neurons and the reduced level of polysialic acid neural cell adhesion molecule (PSA <strong>NCAM</strong>) in the striatum, and the likely changes in striatal synaptogenesis during development.
+NCAM1	drug	alcohol	30277635	The <b>ethanol</b> exposed rat hippocampus showed a decrease in the mRNA levels of neurotrophic (Bdnf and Ntf 3) and neurogenic (Mki67, Sox2, Dcx, <strong>Ncam1</strong> and Calb1) factors, associated to a deactivation of the neurogenic regulator mitogen activated protein kinase extracellular signal regulated kinase.
+NCAM1	drug	cannabinoid	27023175	Nonetheless, gene based tests identified four genes significantly associated with lifetime <b>cannabis</b> use: <strong>NCAM1</strong>, CADM2, SCOC and KCNT2.
+NCAM1	drug	cannabinoid	27023175	Previous studies reported associations of <strong>NCAM1</strong> with cigarette smoking and other substance use, and those of CADM2 with body mass index, processing speed and autism disorders, which are phenotypes previously reported to be associated with <b>cannabis</b> use.
+NCAM1	drug	nicotine	27023175	Previous studies reported associations of <strong>NCAM1</strong> with cigarette <b>smoking</b> and other substance use, and those of CADM2 with body mass index, processing speed and autism disorders, which are phenotypes previously reported to be associated with cannabis use.
+NCAM1	drug	opioid	26821693	The effects of <b>morphine</b> treatment on the <strong>NCAM</strong> and its signaling in the MLDS of rats.
+NCAM1	drug	alcohol	26821693	Moreover, it has been shown that <strong>NCAM</strong> were related to risk of <b>alcoholism</b> in human populations.
+NCAM1	drug	opioid	26821693	Here, coimmunoprecipitation and western blotting were used to investigate whether <b>morphine</b> treatment induced alteration of the expression of <strong>NCAM</strong> or its signaling level in MLDS.
+NCAM1	drug	opioid	26821693	The results showed that <b>morphine</b> treatment had no significant effect on the expression of <strong>NCAM</strong>, but downregulated the phosphorylation of <strong>NCAM</strong> associated focal adhesion kinase (FAK) in the VTA and PFC of rats.
+NCAM1	drug	opioid	26821693	In the NAc of rats, however, the expression of <strong>NCAM</strong> and its signaling were not altered significantly by <b>morphine</b> treatment.
+NCAM1	drug	opioid	26821693	These results indicated that the downregulation of <strong>NCAM</strong> signaling in the VTA and PFC might be involved in the formation of <b>morphine</b> addiction.
+NCAM1	addiction	addiction	26821693	These results indicated that the downregulation of <strong>NCAM</strong> signaling in the VTA and PFC might be involved in the formation of morphine <b>addiction</b>.
+NCAM1	drug	nicotine	26423011	We also discovered five new genome wide significant signals for <b>smoking</b> behaviour, including a variant in <strong>NCAM1</strong> (chromosome 11) and a variant on chromosome 2 (between TEX41 and PABPC1P2) that has a trans effect on expression of <strong>NCAM1</strong> in brain tissue.
+NCAM1	drug	nicotine	25273375	<strong>NCAM1</strong> TTC12 ANKK1 DRD2 variants and <b>smoking</b> motives as intermediate phenotypes for <b>nicotine</b> dependence.
+NCAM1	addiction	dependence	25273375	<strong>NCAM1</strong> TTC12 ANKK1 DRD2 variants and smoking motives as intermediate phenotypes for nicotine <b>dependence</b>.
+NCAM1	drug	nicotine	25273375	Based on prior evidence of the role of genetic variation in the <strong>NCAM1</strong> TTC12 ANKK1 DRD2 region on chromosome 11q23 in <b>smoking</b> behavior, associations among 12 region loci with <b>nicotine</b> dependence and PDM phenotypes were examined using haplotype and individual loci approaches.
+NCAM1	addiction	dependence	25273375	Based on prior evidence of the role of genetic variation in the <strong>NCAM1</strong> TTC12 ANKK1 DRD2 region on chromosome 11q23 in smoking behavior, associations among 12 region loci with nicotine <b>dependence</b> and PDM phenotypes were examined using haplotype and individual loci approaches.
+NCAM1	drug	nicotine	25273375	<strong>NCAM1</strong> TTC12 ANKK1 DRD2 region loci and haplotypes were significantly associated with the motive of Automaticity and, further, Automaticity significantly mediated associations among <strong>NCAM1</strong> TTC12 ANKK1 DRD2 cluster variants and <b>nicotine</b> dependence.
+NCAM1	addiction	dependence	25273375	<strong>NCAM1</strong> TTC12 ANKK1 DRD2 region loci and haplotypes were significantly associated with the motive of Automaticity and, further, Automaticity significantly mediated associations among <strong>NCAM1</strong> TTC12 ANKK1 DRD2 cluster variants and nicotine <b>dependence</b>.
+NCAM1	drug	nicotine	25273375	Further, <strong>NCAM1</strong> TTC12 ANKK1 DRD2 variants may increase the likelihood that a person will become dependent via a highly automatic <b>smoking</b> ritual that can be elicited with little awareness.
+NCAM1	drug	opioid	24399412	<strong>NCAM</strong> signaling mediates the effects of GDNF on chronic <b>morphine</b> induced neuroadaptations.
+NCAM1	drug	opioid	24399412	The purpose of this study was to investigate whether <strong>NCAM</strong> was involved in the effects of GDNF on the neuroadaptations induced by chronic <b>morphine</b> exposure.
+NCAM1	drug	opioid	24399412	These results suggest that <strong>NCAM</strong> signaling is involved in the negative regulatory effects of GDNF on chronic <b>morphine</b> induced neuroadaptations.
+NCAM1	drug	opioid	23303482	ANKK1, TTC12, and <strong>NCAM1</strong> polymorphisms and <b>heroin</b> dependence: importance of considering drug exposure.
+NCAM1	addiction	dependence	23303482	ANKK1, TTC12, and <strong>NCAM1</strong> polymorphisms and heroin <b>dependence</b>: importance of considering drug exposure.
+NCAM1	drug	opioid	23303482	To examine association of 1430 candidate gene single nucleotide polymorphisms (SNPs) with <b>heroin</b> dependence, reporting here only the 71 SNPs in the chromosome 11 gene cluster (<strong>NCAM1</strong>, TTC12, ANKK1, DRD2) that include the strongest observed associations.
+NCAM1	addiction	dependence	23303482	To examine association of 1430 candidate gene single nucleotide polymorphisms (SNPs) with heroin <b>dependence</b>, reporting here only the 71 SNPs in the chromosome 11 gene cluster (<strong>NCAM1</strong>, TTC12, ANKK1, DRD2) that include the strongest observed associations.
+NCAM1	drug	opioid	23303482	Aggregate <b>heroin</b> dependence risk associated with 2 SNPs, rs877138 and rs4492854 (located in <strong>NCAM1</strong>), varied more than 4 fold (P = 2.7 × 10( 9) for the risk associated linear trend).
+NCAM1	addiction	dependence	23303482	Aggregate heroin <b>dependence</b> risk associated with 2 SNPs, rs877138 and rs4492854 (located in <strong>NCAM1</strong>), varied more than 4 fold (P = 2.7 × 10( 9) for the risk associated linear trend).
+NCAM1	drug	alcohol	22922785	Low prefrontal PSA <strong>NCAM</strong> confers risk for <b>alcoholism</b> related behavior.
+NCAM1	drug	alcohol	22922785	We identified in rodents an innate endophenotype predicting individual risk for <b>alcohol</b> related behaviors that was associated with decreased expression of the neuroplasticity related polysialylated neural cell adhesion molecule (PSA <strong>NCAM</strong>).
+NCAM1	drug	alcohol	22922785	Depletion of PSA <strong>NCAM</strong> in the ventromedial prefrontal cortex was sufficient to render mice unable to extinguish <b>alcohol</b> seeking, indicating a causal role of naturally occurring variation.
+NCAM1	addiction	relapse	22922785	Depletion of PSA <strong>NCAM</strong> in the ventromedial prefrontal cortex was sufficient to render mice unable to extinguish alcohol <b>seeking</b>, indicating a causal role of naturally occurring variation.
+NCAM1	drug	alcohol	19796663	Apomorphine challenge tests measuring GH responses on 5 time points were performed on day 1 of <b>alcohol</b> detoxification in 43 patients with <b>alcohol</b> dependence; patients were genotyped for 11 polymorphisms including DRD2, ANKK1, <strong>NCAM1</strong> and TTC12.
+NCAM1	addiction	dependence	19796663	Apomorphine challenge tests measuring GH responses on 5 time points were performed on day 1 of alcohol detoxification in 43 patients with alcohol <b>dependence</b>; patients were genotyped for 11 polymorphisms including DRD2, ANKK1, <strong>NCAM1</strong> and TTC12.
+NCAM1	drug	alcohol	18828801	Haplotypic variants in DRD2, ANKK1, TTC12, and <strong>NCAM1</strong> are associated with comorbid <b>alcohol</b> and drug dependence.
+NCAM1	addiction	dependence	18828801	Haplotypic variants in DRD2, ANKK1, TTC12, and <strong>NCAM1</strong> are associated with comorbid alcohol and drug <b>dependence</b>.
+NCAM1	drug	alcohol	17761687	Association of haplotypic variants in DRD2, ANKK1, TTC12 and <strong>NCAM1</strong> to <b>alcohol</b> dependence in independent case control and family samples.
+NCAM1	addiction	dependence	17761687	Association of haplotypic variants in DRD2, ANKK1, TTC12 and <strong>NCAM1</strong> to alcohol <b>dependence</b> in independent case control and family samples.
+NCAM1	addiction	sensitization	17658493	Here, we investigated the expression levels of a neural cell adhesion molecule (<strong>NCAM</strong>) and a polysialylated form of the neuronal cell adhesion molecule (PSA <strong>NCAM</strong>) as markers of synaptic plasticity, in the associative learning mechanisms related to behavioral <b>sensitization</b>.
+NCAM1	drug	amphetamine	17658493	To achieve our goal we examined the effects of <b>amphetamine</b> treatment on the expression levels of PSA <strong>NCAM</strong> and <strong>NCAM</strong> in mouse hippocampus, cortex and striatum in a context specific behavioral sensitization model.
+NCAM1	addiction	sensitization	17658493	To achieve our goal we examined the effects of amphetamine treatment on the expression levels of PSA <strong>NCAM</strong> and <strong>NCAM</strong> in mouse hippocampus, cortex and striatum in a context specific behavioral <b>sensitization</b> model.
+NCAM1	drug	amphetamine	17658493	Immunoblotting analysis demonstrated that acute administration of <b>amphetamine</b> selectively and time dependently decreases the expression of 180 200 kDa isoform of PSA <strong>NCAM</strong> in hippocampus in both context associated (the Paired) as well as context non associated (the Unpaired) groups.
+NCAM1	drug	amphetamine	17658493	Thus, our results suggest that acute <b>amphetamine</b> administration time dependently decreases the expression of 180 200 kDa isoform of PSA <strong>NCAM</strong> in mouse hippocampus and PSA <strong>NCAM</strong> is not involved in <b>amphetamine</b> induced associated learning mechanism.
+NCAM1	drug	nicotine	17085484	Haplotype spanning TTC12 and ANKK1, flanked by the DRD2 and <strong>NCAM1</strong> loci, is strongly associated to <b>nicotine</b> dependence in two distinct American populations.
+NCAM1	addiction	dependence	17085484	Haplotype spanning TTC12 and ANKK1, flanked by the DRD2 and <strong>NCAM1</strong> loci, is strongly associated to nicotine <b>dependence</b> in two distinct American populations.
+NCAM1	addiction	dependence	17085484	DRD2 and <strong>NCAM1</strong> are functional candidate genes for substance <b>dependence</b>; the TTC12 and ANKK1 loci are not well characterized.
+NCAM1	drug	cocaine	16081054	Acute and repeated administration of <b>cocaine</b> differentially regulates expression of PSA <strong>NCAM</strong> positive neurons in the rat hippocampus.
+NCAM1	drug	cocaine	16081054	Recent data indicating that addictive substances are able to alter brain plasticity and its morphology inclined us to determine whether acute and chronic <b>cocaine</b> administration could modify the expression of a polysialylated form of the neuronal cell adhesion molecule (PSA <strong>NCAM</strong>) in the dentate gyrus of the rat hippocampus.
+NCAM1	addiction	addiction	16081054	Recent data indicating that <b>addictive</b> substances are able to alter brain plasticity and its morphology inclined us to determine whether acute and chronic cocaine administration could modify the expression of a polysialylated form of the neuronal cell adhesion molecule (PSA <strong>NCAM</strong>) in the dentate gyrus of the rat hippocampus.
+NCAM1	drug	cocaine	16081054	The number of PSA <strong>NCAM</strong> immunopositive cells was determined at six time points after <b>cocaine</b> treatment: 6 h and 1, 2, 4, 6, and 10 days (both in acute and repeated treatment).
+NCAM1	drug	cocaine	16081054	It was found that a single injection of <b>cocaine</b> induced a time dependent decrease in the number of PSA <strong>NCAM</strong> cells in the dentate gyrus.
+NCAM1	drug	cocaine	16081054	In contrast, an increase in the number of PSA <strong>NCAM</strong> positive cells in the dentate gyrus was observed 2 and 4 days after the last dose of repeated <b>cocaine</b>.
+NCAM1	drug	cocaine	16081054	It is concluded that <b>cocaine</b> can evoke long lasting changes in the PSA <strong>NCAM</strong> protein expression in the dentate gyrus and that the direction of <b>cocaine</b> induced PSA <strong>NCAM</strong> changes depends on the regimen of <b>cocaine</b> administration.
+NCAM1	drug	alcohol	16039825	Controlling for MD, age, gender, racial background, and medical status, <b>alcohol</b> dependence was associated with decreased circulating B lymphocytes (p<.02), possibly decreased <strong>CD56</strong>+ (NK) cells (p<.06), and increased monocytes (p<.04).
+NCAM1	addiction	dependence	16039825	Controlling for MD, age, gender, racial background, and medical status, alcohol <b>dependence</b> was associated with decreased circulating B lymphocytes (p<.02), possibly decreased <strong>CD56</strong>+ (NK) cells (p<.06), and increased monocytes (p<.04).
+NCAM1	drug	alcohol	12543998	No significant correlations were detected between <b>ethanol</b> preference and either receptor binding or Drd2 expression; however, a significant correlation was found between preference and <strong>Ncam</strong> expression.
+NCAM1	drug	nicotine	11978841	It was found that <b>nicotine</b> self administration profoundly decreased, in a dose dependent manner, the expression of PSA <strong>NCAM</strong> in the DG; a significant effect was observed at all the doses tested (0.02, 0.04, and 0.08 mg/kg per infusion).
+NCAM1	drug	alcohol	10443986	CONTROLLING for age and gender, ANCOVA revealed no differences (p > 0.1) between <b>alcohol</b> dependent and control subjects in leukocyte and lymphocyte subsets or in circulating <strong>CD56</strong>+ (natural killer) cells.
+NCAM1	addiction	withdrawal	9141423	After 3 months of EtOH <b>withdrawal</b>, PB mononuclear cells (PBMC) from the AWLD group patients still displayed an increased NK cytolytic activity; in addition, the number of PB NK cells (CD3 /<strong>CD56</strong>+ and CD8 /CD57+) and CD3+/<strong>CD56</strong>+ PB T cells continued to be increased.
+NCAM1	drug	alcohol	8979026	During the <b>alcohol</b> intake period, the most striking findings were a significant (P < 0.05) expansion of the CD8+ T lymphocyte subset, which coexpresses the activation associated antigens HLA DR and CD11c, as well as a significant increase in both NK cells (CD3 /<strong>CD56</strong>+) and the T cell subset with NK activity coexpressing CD3 and <strong>CD56</strong> (P < 0.05 and P < 0.01, respectively).
+NCAM1	drug	alcohol	8986204	Regarding the <b>alcohol</b> intake period, the most relevant findings were a significant activation of the PB T cell compartment, and specifically of the TCR alpha beta + subset, as reflected by an increased expression of both the HLA DR and CD11c antigens as well as a significant increase of both the PB NK cells (CD3 /<strong>CD56</strong>+) and the cytotoxic T cells coexpressing the CD3 and <strong>CD56</strong> molecules.
+MIP	drug	nicotine	32691297	The aim of this study was to test the effects of casein phosphopeptide amorphous calcium phosphate (CPP ACP) crème, or MI Paste™ (<strong>MIP</strong>), on <b>nicotine</b> induced Streptococcus mutans biofilm.
+MIP	addiction	reward	32691297	The aim of this study was to test the effects of casein phosphopeptide amorphous calcium phosphate (<b>CPP</b> ACP) crème, or MI Paste™ (<strong>MIP</strong>), on nicotine induced Streptococcus mutans biofilm.
+MIP	drug	nicotine	32691297	The experiment utilized S. mutans biofilm assays with varying concentrations of <b>nicotine</b> and <strong>MIP</strong> aqueous concentrate levels.
+MIP	drug	nicotine	32691297	First hand exposure to <b>nicotine</b> has been demonstrated to significantly increase S. mutans biofilm formation, while the active component, CPP ACP, in <strong>MIP</strong> has been shown to reduce S. mutans biofilm formation.
+MIP	addiction	reward	32691297	First hand exposure to nicotine has been demonstrated to significantly increase S. mutans biofilm formation, while the active component, <b>CPP</b> ACP, in <strong>MIP</strong> has been shown to reduce S. mutans biofilm formation.
+MIP	drug	nicotine	32691297	A 24 h culture of S. mutans UA159 in microtiter plates were treated with varying <b>nicotine</b> concentrations (0 32 mg/ml) in Tryptic Soy Broth supplemented with 1% sucrose (TSBS) with or without <strong>MIP</strong> aqueous concentrate.
+MIP	drug	nicotine	32691297	The presence of <strong>MIP</strong> aqueous concentrate inhibits <b>nicotine</b> induced S. mutans biofilm formation at different concentrations of <b>nicotine</b> (0 32 mg/ml).
+MIP	drug	nicotine	32691297	The results demonstrated <b>nicotine</b> induced S. mutans biofilm formation is decreased in the presence of <strong>MIP</strong>.
+MIP	drug	nicotine	32691297	This provides further evidence about the cariostatic properties of CPP ACP, the active soluble ingredient in the <strong>MIP</strong>, and reconfirms the harmful effects of <b>nicotine</b>.
+MIP	addiction	reward	32691297	This provides further evidence about the cariostatic properties of <b>CPP</b> ACP, the active soluble ingredient in the <strong>MIP</strong>, and reconfirms the harmful effects of nicotine.
+MIP	drug	nicotine	32691297	<b>Smokers</b> may gain dual benefits from the use of <strong>MIP</strong>, as a remineralization agent and as a cariostatic agent, by inhibiting <b>nicotine</b> induced S. mutans biofilm formation.
+MIP	drug	alcohol	31838202	Pre treatment of mice with P Esbp prior to <b>alcohol</b> binge attenuated <b>alcohol</b> induced serum transaminase (ALT, AST) elevation, reduced pro inflammatory cytokines (TNFα and IL 1ẞ) and chemokines (<strong>MIP</strong> 2/CXCL2 and MCP 1/CCL2) in National Institute on <b>Alcohol</b> Abuse and <b>Alcoholism</b> (NIAAA) model.
+MIP	addiction	intoxication	31838202	Pre treatment of mice with P Esbp prior to alcohol <b>binge</b> attenuated alcohol induced serum transaminase (ALT, AST) elevation, reduced pro inflammatory cytokines (TNFα and IL 1ẞ) and chemokines (<strong>MIP</strong> 2/CXCL2 and MCP 1/CCL2) in National Institute on Alcohol Abuse and Alcoholism (NIAAA) model.
+MIP	addiction	withdrawal	30774343	The dietary supplement had negligible effect on depressed mood, but sad <strong>MIP</strong> is a very reliable method that can be applied in future studies to assess other interventions for preventing dysphoric mood during early cigarette <b>withdrawal</b>.
+MIP	drug	alcohol	30459651	There were significant differences in age, marital status, age of drug use onset, MA use years, Average MA use dose, interval of MA use, maximum dose, concurrent use of <b>alcohol</b>, and other drugs, VAS score, MA dependence, BDI 13 scores, HAMA 14 scores, verbal learning memory, and visual learning memory between the <strong>MIP</strong> group and the none <strong>MIP</strong> group (P < 0.05).
+MIP	addiction	dependence	30459651	There were significant differences in age, marital status, age of drug use onset, MA use years, Average MA use dose, interval of MA use, maximum dose, concurrent use of alcohol, and other drugs, VAS score, MA <b>dependence</b>, BDI 13 scores, HAMA 14 scores, verbal learning memory, and visual learning memory between the <strong>MIP</strong> group and the none <strong>MIP</strong> group (P < 0.05).
+MIP	addiction	dependence	30459651	The age of drug use onset (OR = 0.978, p = 0.011), average drug use dose (OR = 1.800, p = 0.015), craving score (OR = 1.069, p = 0.031), MA <b>dependence</b> (OR = 2.214, p < 0.001), and HAMA scores (OR = 1.028, p < 0.001) were associated to <strong>MIP</strong>.
+MIP	addiction	relapse	30459651	The age of drug use onset (OR = 0.978, p = 0.011), average drug use dose (OR = 1.800, p = 0.015), <b>craving</b> score (OR = 1.069, p = 0.031), MA dependence (OR = 2.214, p < 0.001), and HAMA scores (OR = 1.028, p < 0.001) were associated to <strong>MIP</strong>.
+MIP	addiction	relapse	30459651	Earlier onset of drug use, higher quantity of drug use, higher <b>craving</b>, middle or severe drug use disorder and more anxiety symptoms may be related risk factors of <strong>MIP</strong>.
+MIP	drug	cocaine	29038767	Regarding inflammatory factors, we observed significantly lower plasma levels of IL 17α (p < 0.001), <strong>MIP</strong> 1α (p < 0.001) and TGFα (p < 0.05) in the <b>cocaine</b> group compared with the levels in the control group.
+MIP	drug	cocaine	29038767	IL 17α, <strong>MIP</strong> 1α and TGFα levels are different between the <b>cocaine</b> and control groups, and TGFα levels facilitate the identification of patients with dual diagnosis.
+MIP	drug	alcohol	28951767	Baicalin attenuated <b>ethanol</b> induced proinflammatory molecules such as TNF α, IL 1β, <strong>MIP</strong> 2, and MCP 1 and reversed redox sensitive transcription factor NF κB activation.
+MIP	drug	alcohol	27699959	The results showed that <b>alcohol</b> intoxication increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (<strong>MIP</strong> 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+MIP	addiction	intoxication	27699959	The results showed that alcohol <b>intoxication</b> increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, IL 17A, IL 1β, IL 2, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (<strong>MIP</strong> 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+MIP	drug	alcohol	27699959	In wild type female adolescent mice, intermittent <b>ethanol</b> treatment increased the levels of several cytokines (IL 17A and IL 1β) and chemokines (MCP 1, <strong>MIP</strong> 1α and fractalkine) in PFC and in serum (IL 17A, MCP 1 and <strong>MIP</strong> 1α), but significant differences in the fractalkine levels in PFC were observed only in male mice.
+MIP	drug	alcohol	25661730	Importantly, several cytokines and chemokines (e.g., <strong>MIP</strong> 2, <strong>MIP</strong> 1, IL 4, IL 6 and osteopontin) involved in neutrophil infiltration were upregulated in hepatic NKT cells isolated from chronic plus binge <b>ethanol</b> fed mice compared to pair fed mice.
+MIP	addiction	intoxication	25661730	Importantly, several cytokines and chemokines (e.g., <strong>MIP</strong> 2, <strong>MIP</strong> 1, IL 4, IL 6 and osteopontin) involved in neutrophil infiltration were upregulated in hepatic NKT cells isolated from chronic plus <b>binge</b> ethanol fed mice compared to pair fed mice.
+MIP	drug	amphetamine	25530901	<b>Methamphetamine</b> induced psychosis (<strong>MIP</strong>) in Iran has turned into a serious issue in terms of health and treatment, lacking any obvious treatment methods for its resistant cases.
+MIP	drug	amphetamine	24521142	To explore the clinical features of <b>methamphetamine</b> induced paranoia (<strong>MIP</strong>) and associations between <strong>MIP</strong> and a genetic polymorphism in dopamine β hydroxylase (DBH 1021C→T).
+MIP	addiction	intoxication	24521142	Within <b>binge</b> latency to <strong>MIP</strong> onset occurred more rapidly in the most recent compared with initial <strong>MIP</strong> episode (P = 0.02), despite unchanging intake (P = 0.89).
+MIP	drug	opioid	23031399	Incision after saline or escalating <b>morphine</b> treatment upregulated skin IL 1β, IL 6, G CSF and <strong>MIP</strong> 1α levels in ppt A( / ) and wt mice similarly.
+MIP	drug	alcohol	19968830	The IQ of 34 methamphetamine induced psychosis (<strong>MIP</strong>) patients (age, 28.7 +/  6.1 years) and 34 <b>alcohol</b> dependent (AD) patients (age, 40.7 +/  7.3 years) was compared using the Chinese version of the Wechsler Adult Intelligence Scale Third Edition (WAIS III).
+MIP	drug	amphetamine	19968830	The IQ of 34 <b>methamphetamine</b> induced psychosis (<strong>MIP</strong>) patients (age, 28.7 +/  6.1 years) and 34 alcohol dependent (AD) patients (age, 40.7 +/  7.3 years) was compared using the Chinese version of the Wechsler Adult Intelligence Scale Third Edition (WAIS III).
+MIP	drug	alcohol	16046875	Macrophage inflammatory protein 2 (<strong>MIP</strong> 2), a rat ELR+ CXC chemokine, or live Klebsiella pneumoniae (K. pneumoniae) was administered it to induce alveolar neutrophil migration in the absence or presence of acute <b>ethanol</b> intoxication.
+MIP	addiction	intoxication	16046875	Macrophage inflammatory protein 2 (<strong>MIP</strong> 2), a rat ELR+ CXC chemokine, or live Klebsiella pneumoniae (K. pneumoniae) was administered it to induce alveolar neutrophil migration in the absence or presence of acute ethanol <b>intoxication</b>.
+MIP	drug	alcohol	16046875	Neutrophil counts were significantly elevated in bronchoalveolar lavage fluid (BALF) of rats receiving IT <strong>MIP</strong> 2 compared with vehicle treated rats, and this response was significantly decreased in animals pretreated with <b>ethanol</b>.
+MIP	drug	alcohol	16046875	CINC IV enhanced the neutrophil response to IT <strong>MIP</strong> 2 in both the absence and presence of acute <b>ethanol</b> intoxication.
+MIP	addiction	intoxication	16046875	CINC IV enhanced the neutrophil response to IT <strong>MIP</strong> 2 in both the absence and presence of acute ethanol <b>intoxication</b>.
+MIP	drug	alcohol	16046875	In rats challenged with K. pneumoniae, <b>ethanol</b> pretreatment significantly reduced BALF levels of CINC and <strong>MIP</strong> 2, suppressed alveolar neutrophil recruitment, and decreased whole lung myeloperoxidase activity.
+MIP	drug	alcohol	16046875	<b>Ethanol</b> significantly inhibits the pulmonary inflammatory responses to both <strong>MIP</strong> 2 and K. pneumoniae.
+MIP	drug	alcohol	14634502	BALF <strong>MIP</strong> 2 and cytokine induced neutrophil chemoattractant were decreased by <b>alcohol</b>, and BALF from <b>alcohol</b> intoxicated animals had decreased chemotactic activity for neutrophils, as well as a decreased ability to up regulate neutrophil adhesion molecule expression, compared with controls.
+MIP	drug	alcohol	14634502	<b>Alcohol</b> also suppressed neutrophil recruitment after intrapulmonary challenge with <strong>MIP</strong> 2, suggesting that mechanisms other than chemokine suppression contribute to the <b>alcohol</b> induced effect.
+MIP	drug	alcohol	12470499	However, <b>ethanol</b> withdrawal + I/R did not significantly alter CINC and <strong>MIP</strong> 2 production at 3 h of reperfusion.
+MIP	addiction	withdrawal	12470499	However, ethanol <b>withdrawal</b> + I/R did not significantly alter CINC and <strong>MIP</strong> 2 production at 3 h of reperfusion.
+MIP	drug	alcohol	12062632	This model correlates closely with <b>alcoholic</b> hepatitis in human beings, characterized by increased IL 8, RANTES (regulated upon activation, normal T cell expressed and secreted), and macrophage inflammatory protein 1 (<strong>MIP</strong> 1) and profound increases in neutrophils and lymphocytes in the liver.
+MIP	drug	alcohol	12045006	Serum ALT, endotoxin, <strong>MIP</strong> 1alpha, MCP 1 and RANTES, (but not CINC and <strong>MIP</strong> 2) were also increased in the <b>ethanol</b> fed rats than in the pair fed group.
+MIP	drug	alcohol	12045006	Isolated Kupffer cells from <b>ethanol</b> fed rats were primed for enhanced <strong>MIP</strong> 1alpha, MCP 1, and RANTES production in vitro, while the endothelial cells were primed for enhanced <strong>MIP</strong> 1alpha release only.
+MIP	drug	alcohol	11821656	This study investigated the effects of <b>alcohol</b> on CXC chemokine macrophage inflammatory protein 2 (<strong>MIP</strong> 2) and cytokine induced neutrophil chemoattractant (CINC) responses in rats challenged with intravenous lipopolysaccharide (LPS).
+MIP	drug	alcohol	11821656	<b>Alcohol</b> intoxication suppressed the <strong>MIP</strong> 2, CINC, and TNFalpha responses in the bloodstream during endotoxemia.
+MIP	addiction	intoxication	11821656	Alcohol <b>intoxication</b> suppressed the <strong>MIP</strong> 2, CINC, and TNFalpha responses in the bloodstream during endotoxemia.
+MIP	drug	alcohol	11821656	<b>Alcohol</b> suppressed the up regulation of <strong>MIP</strong> 2 mRNA expression in all of these organs and CINC mRNA expression in the lungs of rats with endotoxemia.
+MIP	drug	alcohol	11598836	Before neutrophil recruitment, bronchoalveolar lavage (BAL) macrophage inflammatory protein 2 (<strong>MIP</strong> 2) and cytokine induced neutrophil chemoattractant (CINC) were decreased by <b>alcohol</b>.
+MIP	drug	alcohol	11598836	<strong>MIP</strong> 2 and CINC mRNA contents also were suppressed by <b>alcohol</b> 4 and 6 h after infection.
+MIP	drug	alcohol	11524180	Thus, this work examined the regulation of chemokines   i.e., cytokine induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein 2 (<strong>MIP</strong> 2)  produced by hepatocytes after HIV 1 glycoprotein 120 (gp120) vaccination in Wistar rats fed with <b>ethanol</b> for 30 weeks.
+MIP	drug	alcohol	11524180	However, serum CINC and <strong>MIP</strong> 2 levels were more elevated in the <b>ethanol</b> fed rats than in the pair fed group.
+MIP	drug	alcohol	11524180	After HIV 1 gp120 treatment, isolated hepatocytes obtained from the <b>ethanol</b> fed group produced more CINC and <strong>MIP</strong> 2 than did those of pair fed rats.
+MIP	drug	alcohol	11388697	Results show that in vivo <b>ethanol</b> was associated with downregulation of <strong>MIP</strong> 1alpha and MCP 1 mRNA expression and protein release in primary cultures of Kupffer cells.
+MIP	addiction	relapse	11293664	The mRNA for cytokines IL 1beta, IL 6, IL 10 and the chemokines CINC, <strong>MIP</strong> 1alpha, MCP 1 were significantly (P < 0.05) elevated and persisted for 2 weeks, decreased in 6 weeks and increased again during <b>relapse</b>.
+MIP	drug	alcohol	10719799	This work tests the hypotheses that Kupffer cells are a major source of CC chemokines (<strong>MIP</strong> 1alpha, MCP 1, RANTES) during acute endotoxemia and that acute <b>ethanol</b> intoxication modulates Escherichia coli lipopolysaccharide (LPS, 1 mg/Kg, i.v.)
+MIP	addiction	intoxication	10719799	This work tests the hypotheses that Kupffer cells are a major source of CC chemokines (<strong>MIP</strong> 1alpha, MCP 1, RANTES) during acute endotoxemia and that acute ethanol <b>intoxication</b> modulates Escherichia coli lipopolysaccharide (LPS, 1 mg/Kg, i.v.)
+MIP	drug	opioid	10654191	In this study, chemotaxis of monkey leukocytes was evaluated using human chemokines IL 8 (interleukin 8), <strong>MIP</strong> 1 beta and RANTES as the chemoattractants, and the effects of micro <b>opioid</b> receptor agonists, <b>morphine</b>, DAMGO, <b>methadone</b> and endomorphine, on the efficiency of chemotaxis were examined.
+MIP	drug	alcohol	10228066	Acute <b>ethanol</b> intoxication inhibited tumor necrosis factor (TNF) alpha and macrophage inflammatory protein (<strong>MIP</strong>) 2 production in the lung and suppressed the recruitment of neutrophils into the lung.
+MIP	addiction	intoxication	10228066	Acute ethanol <b>intoxication</b> inhibited tumor necrosis factor (TNF) alpha and macrophage inflammatory protein (<strong>MIP</strong>) 2 production in the lung and suppressed the recruitment of neutrophils into the lung.
+MIP	drug	alcohol	9347081	In this study, we assessed the effect of <b>alcohol</b> ingestion on the expression of tumor necrosis factor alpha (TNF alpha), and the chemokines macrophage inflammatory protein 2 (<strong>MIP</strong> 2) and macrophage inflammatory protein 1 alpha (<strong>MIP</strong> 1 alpha) from murine alveolar macrophages (AMs) cultured ex vivo.
+MIP	drug	alcohol	9347081	Two week <b>ethanol</b> feeding resulted in substantial impairment in the lipopolysaccharide (LPS) induced expression of TNF alpha, <strong>MIP</strong> 2, and <strong>MIP</strong> 1 alpha mRNA, and protein from LPS stimulated AMs, compared with cytokine production from AMs obtained from CD 1 mice receiving an isocaloric control diet.
+LY86	addiction	relapse	31829430	CBT + MI versus standard care At 12 months, there was no clear difference between treatment groups for numbers lost to treatment (RR 0.99, 95% CI 0.62 to 1.59; participants = 327; studies = 1; low quality evidence), number of deaths (RR 0.60, 95% CI 0.20 to 1.76; participants = 603; studies = 4; low quality evidence), <b>relapse</b> (RR 0.50, 95% CI 0.24 to 1.04; participants = 36; studies = 1; very low quality evidence), or GAF scores (<strong>MD 1</strong>.24, 95% CI  1.86 to 4.34; participants = 445; studies = 4; very low quality evidence).
+LY86	drug	nicotine	31790979	In experiment 2 go/no go performance was improved (<strong>MD 1</strong>.12, 95% CI: 0.16 2.08) and craving was lower (RC  18.59, 95% CI:  24.63 to  12.55) <b>smokers</b> abstinent overnight receiving NRT compared with placebo.
+LY86	addiction	relapse	31790979	In experiment 2 go/no go performance was improved (<strong>MD 1</strong>.12, 95% CI: 0.16 2.08) and <b>craving</b> was lower (RC  18.59, 95% CI:  24.63 to  12.55) smokers abstinent overnight receiving NRT compared with placebo.
+LY86	addiction	relapse	30484285	In all but one of the studies, participants in both the baclofen and placebo groups received psychosocial treatment or counselling of various intensity.We judged most of the studies at low risk of selection, performance, detection (subjective outcome), attrition and reporting bias.We did not find any difference between baclofen and placebo for the primary outcomes: <b>relapse</b> return to any drinking (RR 0.88, 95% CI 0.74 to 1.04; 5 studies, 781 participants, moderate certainty evidence); frequency of use by percentage of days abstinent (MD 0.39, 95% CI  11.51 to 12.29; 6 studies, 465 participants, low certainty evidence) and frequency of use by percentage of heavy drinking days at the end of treatment (MD 0.25, 95% CI  1.25 to 1.76; 3 studies, 186 participants, moderate certainty evidence); number of participants with at least one adverse event (RR 1.04, 95% CI 0.99 to 1.10; 4 studies, 430 participants, high certainty evidence); the dropout rate at the end of treatment (RR 0.98, 95% CI 0.77 to 1.26, 8 studies, 977 participants, high certainty evidence) and dropout due to adverse events (RR 1.11, 95% CI 0.59 to 2.07; 7 studies, 913 participants, high certainty evidence).We found evidence that baclofen increases amount of use (drink per drinking days), (<strong>MD 1</strong>.55, 95% CI 1.32 to 1.77; 2 studies, 72 participants, low certainty evidence).Among secondary outcomes, there was no difference on <b>craving</b> (<strong>MD 1</strong>.38, 95% CI  1.28 to 4.03, 5 studies, 469 participants), and anxiety (SMD 0.07, 95% CI  0.14 to 0.28; 5 trials, 509 participants).
+LY86	drug	cannabinoid	30406638	The mean CRP in the <b>cannabidiol</b> group was 9.428 mg/L compared to 7.638 mg/L in the placebo group (<strong>MD 1</strong>.79, 95% CI  5.67 to 9.25; moderate certainty evidence).
+LY86	addiction	withdrawal	29688573	However, other outcomes such as the rate of abstinent days did not differ between antidepressants and placebo (9 studies, 821 participants, <strong>MD 1</strong>.34, 95% Cl  1.66 to 4.34; low quality evidence).Low quality evidence suggested no differences between antidepressants and placebo in the number of dropouts (17 studies, 1159 participants, RR 0.98, 95% Cl 0.79 to 1.22) and adverse events as <b>withdrawal</b> for medical reasons (10 studies, 947 participants, RR 1.15, 95% Cl 0.65 to 2.04).There were few studies comparing one antidepressant versus another antidepressant or antidepressants versus other interventions, and these had a small sample size and were heterogeneous in terms of the types of interventions that were compared, yielding results that were not informative.
+LY86	drug	opioid	27140500	IA <b>morphine</b> was not better than local anaesthetic agents at early phase (<strong>MD 1</strong>.43, 95% CI 0.49 to 2.37; participants = 248; studies = 5; low quality evidence), NSAIDs at early phase (MD 0.95, 95% CI  0.95 to 2.85; participants = 80; studies = 2; very low quality evidence), sufentanil, <b>fentanyl</b> or pethidine for pain intensity.
+LY86	drug	alcohol	24092525	We found no significant differences on loss to treatment (n = 603, 3 RCTs, RR 1.09 CI 0.82 to 1.45, low quality of evidence), death by 3 years (n = 421, 2 RCTs, RR 1.18 CI 0.39 to 3.57, low quality of evidence), <b>alcohol</b> use (not in remission at 36 months) (n = 143, 1 RCT, RR 1.15 CI 0.84 to 1.56,low quality of evidence), substance use (n = 85, 1 RCT, RR 0.89 CI 0.63 to 1.25, low quality of evidence), global assessment of functioning (n = 171, 1 RCT, MD 0.7 CI 2.07 to 3.47, low quality of evidence), or general life satisfaction (n = 372, 2 RCTs, MD 0.02 higher CI 0.28 to 0.32, moderate quality of evidence).For evaluation of non integrated intensive case management with usual treatment (4 RCTs, n = 163) we found no statistically significant difference for loss to treatment at 12 months (n = 134, 3 RCTs, RR 1.21 CI 0.73 to 1.99, very low quality of evidence).Motivational interviewing plus cognitive behavioural therapy compared to usual treatment (7 RCTs, total n = 878) did not reveal any advantage for retaining participants at 12 months (n = 327, 1 RCT, RR 0.99 CI 0.62 to 1.59, low quality of evidence) or for death (n = 493, 3 RCTs, RR 0.72 CI 0.22 to 2.41, low quality of evidence), and no benefit for reducing substance use (n = 119, 1 RCT, MD 0.19 CI  0.22 to 0.6, low quality of evidence), relapse (n = 36, 1 RCT, RR 0.5 CI 0.24 to 1.04, very low quality of evidence) or global functioning (n = 445, 4 RCTs, <strong>MD 1</strong>.24 CI 1.86 to 4.34, very low quality of evidence).Cognitive behavioural therapy alone compared with usual treatment (2 RCTs, n = 152) showed no significant difference for losses from treatment at 3 months (n = 152, 2 RCTs, RR 1.12 CI 0.44 to 2.86, low quality of evidence).
+LY86	addiction	relapse	24092525	We found no significant differences on loss to treatment (n = 603, 3 RCTs, RR 1.09 CI 0.82 to 1.45, low quality of evidence), death by 3 years (n = 421, 2 RCTs, RR 1.18 CI 0.39 to 3.57, low quality of evidence), alcohol use (not in remission at 36 months) (n = 143, 1 RCT, RR 1.15 CI 0.84 to 1.56,low quality of evidence), substance use (n = 85, 1 RCT, RR 0.89 CI 0.63 to 1.25, low quality of evidence), global assessment of functioning (n = 171, 1 RCT, MD 0.7 CI 2.07 to 3.47, low quality of evidence), or general life satisfaction (n = 372, 2 RCTs, MD 0.02 higher CI 0.28 to 0.32, moderate quality of evidence).For evaluation of non integrated intensive case management with usual treatment (4 RCTs, n = 163) we found no statistically significant difference for loss to treatment at 12 months (n = 134, 3 RCTs, RR 1.21 CI 0.73 to 1.99, very low quality of evidence).Motivational interviewing plus cognitive behavioural therapy compared to usual treatment (7 RCTs, total n = 878) did not reveal any advantage for retaining participants at 12 months (n = 327, 1 RCT, RR 0.99 CI 0.62 to 1.59, low quality of evidence) or for death (n = 493, 3 RCTs, RR 0.72 CI 0.22 to 2.41, low quality of evidence), and no benefit for reducing substance use (n = 119, 1 RCT, MD 0.19 CI  0.22 to 0.6, low quality of evidence), <b>relapse</b> (n = 36, 1 RCT, RR 0.5 CI 0.24 to 1.04, very low quality of evidence) or global functioning (n = 445, 4 RCTs, <strong>MD 1</strong>.24 CI 1.86 to 4.34, very low quality of evidence).Cognitive behavioural therapy alone compared with usual treatment (2 RCTs, n = 152) showed no significant difference for losses from treatment at 3 months (n = 152, 2 RCTs, RR 1.12 CI 0.44 to 2.86, low quality of evidence).
+APOE	drug	nicotine	31771811	Varenicline aggravates atherosclerotic plaque formation in <b>nicotine</b> pretreated <strong>ApoE</strong> knockout mice due to enhanced oxLDL uptake by macrophages through downregulation of ABCA1 and ABCG1 expression.
+APOE	drug	nicotine	31771811	Here, we examined the effect of varenicline on atherosclerotic plaque formation in <b>nicotine</b> pretreated <strong>ApoE</strong> KO mice and oxidized low density lipoprotein (oxLDL) uptake in <b>nicotine</b> treated peritoneal macrophages.
+APOE	drug	nicotine	31771811	Varenicline caused significant progression of plaque formation in the whole aorta and aortic root and further accelerated the increased formation of a macrophage rich plaque area in the aortic root in <b>nicotine</b> pretreated <strong>ApoE</strong> KO mice.
+APOE	drug	alcohol	30513887	RCT was measured with a standardized, radioisotope based technique in three groups of atherosclerosis prone <strong>apolipoprotein E</strong> knock out mice: Placebo group, receiving water, which would mimic the abstainers; moderate group, receiving 0.8 g/kg <b>alcohol</b>/day for 28 days, which would mimic a moderate intake; binge group, receiving 0.8 g/kg <b>alcohol</b>/day for 5 days/week, followed by the administration of 2.8 g/kg <b>alcohol</b>/day for 2 days/week, which would mimic a heavy intake in a short period.
+APOE	addiction	intoxication	30513887	RCT was measured with a standardized, radioisotope based technique in three groups of atherosclerosis prone <strong>apolipoprotein E</strong> knock out mice: Placebo group, receiving water, which would mimic the abstainers; moderate group, receiving 0.8 g/kg alcohol/day for 28 days, which would mimic a moderate intake; <b>binge</b> group, receiving 0.8 g/kg alcohol/day for 5 days/week, followed by the administration of 2.8 g/kg alcohol/day for 2 days/week, which would mimic a heavy intake in a short period.
+APOE	drug	nicotine	27834689	<b>Nicotine</b> Accelerates Atherosclerosis in <strong>Apolipoprotein E</strong> Deficient Mice by Activating α7 Nicotinic Acetylcholine Receptor on Mast Cells.
+APOE	drug	nicotine	27834689	<b>Nicotine</b> administration increased the size of atherosclerotic lesions in apolipoprotein E deficient (<strong>Apoe</strong> / ) mice fed a fat enriched diet.
+APOE	drug	nicotine	27834689	<b>Nicotine</b> administration increased the size of atherosclerotic lesions in <strong>apolipoprotein E</strong> deficient (<strong>Apoe</strong> / ) mice fed a fat enriched diet.
+APOE	drug	nicotine	27834689	MC deficiency in <strong>Apoe</strong> /  mice (<strong>Apoe</strong> / KitW sh/W sh) diminished <b>nicotine</b> induced atherosclerosis.
+APOE	drug	nicotine	27834689	<b>Nicotine</b> did not change atherosclerotic lesion size of <strong>Apoe</strong> / KitW sh/W sh mice reconstituted with MCs from <strong>Apoe</strong> / α7nAChR /  animals.
+APOE	drug	alcohol	27396498	The present study examined the association between self reported concussion history and genetics (apolipoprotein E [<strong>APOE</strong>], brain derived neurotrophic factor [BDNF], and D2 dopamine receptor genes [DRD2]), trait personality measures (impulsive sensation seeking and trait aggression hostility), and current <b>alcohol</b> use.
+APOE	addiction	relapse	27396498	The present study examined the association between self reported concussion history and genetics (apolipoprotein E [<strong>APOE</strong>], brain derived neurotrophic factor [BDNF], and D2 dopamine receptor genes [DRD2]), trait personality measures (impulsive sensation <b>seeking</b> and trait aggression hostility), and current alcohol use.
+APOE	drug	alcohol	27396498	The present study examined the association between self reported concussion history and genetics (<strong>apolipoprotein E</strong> [<strong>APOE</strong>], brain derived neurotrophic factor [BDNF], and D2 dopamine receptor genes [DRD2]), trait personality measures (impulsive sensation seeking and trait aggression hostility), and current <b>alcohol</b> use.
+APOE	addiction	relapse	27396498	The present study examined the association between self reported concussion history and genetics (<strong>apolipoprotein E</strong> [<strong>APOE</strong>], brain derived neurotrophic factor [BDNF], and D2 dopamine receptor genes [DRD2]), trait personality measures (impulsive sensation <b>seeking</b> and trait aggression hostility), and current alcohol use.
+APOE	drug	alcohol	25800888	The analyses were performed by stratifying <b>alcohol</b> consumption and the <strong>APOE</strong> status.
+APOE	drug	alcohol	25491588	The aim of this case control study (398 cases and 149 controls) was to investigate whether Val158Met polymorphism influences the onset of AD stratified according to <b>alcohol</b> consumption and apolipoprotein E (<strong>APOE</strong>) status.
+APOE	drug	alcohol	25491588	The aim of this case control study (398 cases and 149 controls) was to investigate whether Val158Met polymorphism influences the onset of AD stratified according to <b>alcohol</b> consumption and <strong>apolipoprotein E</strong> (<strong>APOE</strong>) status.
+APOE	addiction	withdrawal	25085446	All participants provided written informed consent, and underwent additional venous blood <b>withdrawal</b> for DNA extraction for genetic study of the <strong>ApoE</strong> gene polymorphism.
+APOE	drug	cocaine	23840704	Furthermore, treatment with high dose hdAD <strong>ApoE</strong> mCocH vector (1.7 × 10(12) particles) prevented locomotor abnormalities, other behavioral signs, and release of hepatic alanine amino transferase after a <b>cocaine</b> dose fatal to most control mice (120 mg/kg).
+APOE	drug	alcohol	23739027	The gene coding for <strong>apolipoprotein E</strong> receptor 2 (APOER2) and the gene coding for ubiquitin associated protein 2 (UBAP2) are among the most appropriate for follow up in human and nonhuman species as contributors to risk for <b>alcohol</b> dependence.
+APOE	addiction	dependence	23739027	The gene coding for <strong>apolipoprotein E</strong> receptor 2 (APOER2) and the gene coding for ubiquitin associated protein 2 (UBAP2) are among the most appropriate for follow up in human and nonhuman species as contributors to risk for alcohol <b>dependence</b>.
+APOE	drug	nicotine	23247396	<strong>APOE</strong> ɛ4, an Alzheimer's disease susceptibility allele, and <b>smoking</b> cessation.
+APOE	drug	nicotine	23247396	Possessing an apolipoprotein E (<strong>APOE</strong>) ɛ4 allele, advanced age and <b>smoking</b> are risk factors for Alzheimer's disease and cognitive decline.
+APOE	drug	nicotine	23247396	Possessing an <strong>apolipoprotein E</strong> (<strong>APOE</strong>) ɛ4 allele, advanced age and <b>smoking</b> are risk factors for Alzheimer's disease and cognitive decline.
+APOE	drug	amphetamine	22426312	<strong>Apolipoprotein E</strong> controls adenosine triphosphate binding cassette transporters ABCB1 and ABCC1 on cerebral microvessels after <b>methamphetamine</b> intoxication.
+APOE	addiction	intoxication	22426312	<strong>Apolipoprotein E</strong> controls adenosine triphosphate binding cassette transporters ABCB1 and ABCC1 on cerebral microvessels after methamphetamine <b>intoxication</b>.
+APOE	drug	amphetamine	22426312	Whether and how <b>methamphetamine</b> influences the expression of tight junctions and adenosine triphosphate binding cassette transporters, which have previously been shown to be regulated by apolipoprotein E (<strong>ApoE</strong>) under conditions of brain ischemia, was unknown.
+APOE	drug	amphetamine	22426312	Whether and how <b>methamphetamine</b> influences the expression of tight junctions and adenosine triphosphate binding cassette transporters, which have previously been shown to be regulated by <strong>apolipoprotein E</strong> (<strong>ApoE</strong>) under conditions of brain ischemia, was unknown.
+APOE	drug	amphetamine	22426312	C57BL/6J mice received intraperitoneal injections of <b>methamphetamine</b> (3 times 4 mg/kg separated by 3 hours) either alone or in combination with the <strong>ApoE</strong> receptor 2 inhibitor receptor associated protein (40 μg/kg) or the inducible nitric oxide synthase inhibitor 1400W (5 mg/kg).
+APOE	drug	amphetamine	22426312	Elevated expression of <strong>ApoE</strong> was noted in the brain parenchyma by <b>methamphetamine</b>, activating <strong>ApoE</strong> receptor 2 on brain capillaries, deactivating c Jun N terminal kinase 1/2 and c Jun, and regulating ABCB1 and ABCC1 expression.
+APOE	drug	amphetamine	22426312	Acute exposure to <b>methamphetamine</b> at doses comparable to those consumed in drug addiction does not induce tight junction breakdown but differentially regulates adenosine triphosphate binding cassette transporters through the <strong>ApoE</strong>/<strong>ApoE</strong> receptor 2/c Jun N terminal kinase 1/2 pathway.
+APOE	addiction	addiction	22426312	Acute exposure to methamphetamine at doses comparable to those consumed in drug <b>addiction</b> does not induce tight junction breakdown but differentially regulates adenosine triphosphate binding cassette transporters through the <strong>ApoE</strong>/<strong>ApoE</strong> receptor 2/c Jun N terminal kinase 1/2 pathway.
+APOE	drug	alcohol	21930274	<strong>ApoE</strong> k/o mouse were fed (1) 'daily moderate' (blood <b>alcohol</b> content: 0.07%) or (2) 'weekend binge' (blood <b>alcohol</b> content: 0.23%), or (3) an isocaloric cornstarch mix.
+APOE	addiction	intoxication	21930274	<strong>ApoE</strong> k/o mouse were fed (1) 'daily moderate' (blood alcohol content: 0.07%) or (2) 'weekend <b>binge</b>' (blood alcohol content: 0.23%), or (3) an isocaloric cornstarch mix.
+APOE	drug	nicotine	19473356	<strong>Apolipoprotein E</strong> polymorphism interacts with cigarette <b>smoking</b> in progression of multiple sclerosis.
+APOE	drug	nicotine	19473356	In this study, we aimed to investigate whether an interaction of <b>smoking</b> with the <strong>ApoE</strong> polymorphism influences the progression of disability in MS patients.
+APOE	drug	nicotine	19473356	<strong>ApoE</strong> polymorphism was examined in all patients and stratified according to <b>smoking</b> status and associations with the clinical data investigated.
+APOE	drug	nicotine	19473356	In women carrying the <strong>ApoE</strong> E4 isoform, <b>smokers</b> had a lower EDSS (P = 0.033) and MSSS (P = 0.023) in comparison with non <b>smokers</b>.
+APOE	drug	nicotine	19473356	Our data suggest that in women with MS carrying the <strong>ApoE</strong> E4 isoform, cigarette <b>smoking</b> may have a protective influence on disease progression and accumulation of disability.
+APOE	drug	alcohol	19219710	Of 33 identified articles, six investigated non <b>alcohol</b> withdrawal delirium, and from those six, five evaluated an association with apolipoprotein E (<strong>APOE</strong>).
+APOE	addiction	withdrawal	19219710	Of 33 identified articles, six investigated non alcohol <b>withdrawal</b> delirium, and from those six, five evaluated an association with apolipoprotein E (<strong>APOE</strong>).
+APOE	drug	alcohol	19219710	Of 33 identified articles, six investigated non <b>alcohol</b> withdrawal delirium, and from those six, five evaluated an association with <strong>apolipoprotein E</strong> (<strong>APOE</strong>).
+APOE	addiction	withdrawal	19219710	Of 33 identified articles, six investigated non alcohol <b>withdrawal</b> delirium, and from those six, five evaluated an association with <strong>apolipoprotein E</strong> (<strong>APOE</strong>).
+APOE	drug	alcohol	17708369	Evaluation of apolipoprotein E (<strong>apoE</strong>) and lipoprotein profile in severe <b>alcohol</b> dependent individuals.
+APOE	drug	alcohol	17708369	Evaluation of <strong>apolipoprotein E</strong> (<strong>apoE</strong>) and lipoprotein profile in severe <b>alcohol</b> dependent individuals.
+APOE	drug	alcohol	17708369	Chronic <b>alcohol</b> consumption down regulates the expression of sialytransferase genes resulting in impaired sialylation of apolipoprotein E (<strong>apoE</strong>) and decreased association with HDL.
+APOE	drug	alcohol	17708369	Chronic <b>alcohol</b> consumption down regulates the expression of sialytransferase genes resulting in impaired sialylation of <strong>apolipoprotein E</strong> (<strong>apoE</strong>) and decreased association with HDL.
+APOE	drug	alcohol	17708369	There are a limited number of studies with contradictory data on the effect of <b>alcohol</b> dependence on human plasma <strong>apoE</strong>.
+APOE	addiction	dependence	17708369	There are a limited number of studies with contradictory data on the effect of alcohol <b>dependence</b> on human plasma <strong>apoE</strong>.
+APOE	drug	alcohol	17708369	The aim of the present work is to determine and compare the levels of <strong>apoE</strong> in relation to the other lipoproteins in <b>alcohol</b> dependent individuals in order to evaluate the possible role of <strong>apoE</strong> in lipoprotein metabolism in conditions of severe <b>alcohol</b> dependence.
+APOE	addiction	dependence	17708369	The aim of the present work is to determine and compare the levels of <strong>apoE</strong> in relation to the other lipoproteins in alcohol dependent individuals in order to evaluate the possible role of <strong>apoE</strong> in lipoprotein metabolism in conditions of severe alcohol <b>dependence</b>.
+APOE	drug	alcohol	17708369	Upon admission, all <b>alcohol</b> dependent individuals had significantly higher hepatic enzyme levels, <strong>apoE</strong> and HDL values compared to controls.
+APOE	drug	alcohol	17708369	Additionally, a significant correlation was observed between <b>alcohol</b> consumption during the previous year of <b>alcohol</b> abuse and the <strong>apoE</strong> values both upon admission to and on discharge from the detoxification program.
+APOE	drug	alcohol	17708369	The statistical correlation between <strong>apoE</strong> on admission and discharge with <b>alcohol</b> consumption during the previous year suggests that <strong>apoE</strong> is dependent on <b>alcohol</b> consumption and can serve as a sensitive marker of severe <b>alcohol</b> abuse.
+APOE	drug	alcohol	17420762	<strong>Apolipoprotein E</strong> polymorphism, homocysteine serum levels and hippocampal volume in patients with <b>alcoholism</b>: an investigation of a gene environment interaction.
+APOE	drug	alcohol	17420762	The <strong>ApoE4</strong> allele constitutes a risk factor for hippocampal volume loss in patients with <b>alcohol</b> dependence under the conditions of hyperhomocysteinemia.
+APOE	addiction	dependence	17420762	The <strong>ApoE4</strong> allele constitutes a risk factor for hippocampal volume loss in patients with alcohol <b>dependence</b> under the conditions of hyperhomocysteinemia.
+APOE	drug	alcohol	17106421	Obsessive compulsive <b>alcohol</b> craving is not associated with <strong>Apolipoprotein E</strong> genotype.
+APOE	addiction	addiction	17106421	Obsessive <b>compulsive</b> alcohol craving is not associated with <strong>Apolipoprotein E</strong> genotype.
+APOE	addiction	relapse	17106421	Obsessive compulsive alcohol <b>craving</b> is not associated with <strong>Apolipoprotein E</strong> genotype.
+APOE	drug	alcohol	17106421	Statistical analysis revealed no significant association between <strong>Apolipoprotein E</strong> polymorphism and obsessive compulsive <b>alcohol</b> craving (analysis of variance: F=1.11, P=0.358).
+APOE	addiction	addiction	17106421	Statistical analysis revealed no significant association between <strong>Apolipoprotein E</strong> polymorphism and obsessive <b>compulsive</b> alcohol craving (analysis of variance: F=1.11, P=0.358).
+APOE	addiction	relapse	17106421	Statistical analysis revealed no significant association between <strong>Apolipoprotein E</strong> polymorphism and obsessive compulsive alcohol <b>craving</b> (analysis of variance: F=1.11, P=0.358).
+APOE	drug	alcohol	16959267	<strong>Apolipoprotein E</strong> gene polymorphism and previous <b>alcohol</b> withdrawal seizures.
+APOE	addiction	withdrawal	16959267	<strong>Apolipoprotein E</strong> gene polymorphism and previous alcohol <b>withdrawal</b> seizures.
+APOE	drug	alcohol	16959267	Aim of this study was to investigate the possible association of apolipoprotein E (<strong>ApoE</strong>) gene polymorphism with a history of <b>alcohol</b> withdrawal seizures.
+APOE	addiction	withdrawal	16959267	Aim of this study was to investigate the possible association of apolipoprotein E (<strong>ApoE</strong>) gene polymorphism with a history of alcohol <b>withdrawal</b> seizures.
+APOE	drug	alcohol	16959267	Aim of this study was to investigate the possible association of <strong>apolipoprotein E</strong> (<strong>ApoE</strong>) gene polymorphism with a history of <b>alcohol</b> withdrawal seizures.
+APOE	addiction	withdrawal	16959267	Aim of this study was to investigate the possible association of <strong>apolipoprotein E</strong> (<strong>ApoE</strong>) gene polymorphism with a history of alcohol <b>withdrawal</b> seizures.
+APOE	addiction	withdrawal	16959267	For the <strong>ApoE4</strong> allele group no significant differences were found regarding a history of <b>withdrawal</b> seizures.
+APOE	drug	alcohol	16713503	Aim of this prospective study was to investigate a possible association between the apolipoprotein E4 (<strong>ApoE4</strong>) genotype and clinically well known cognition deficits during <b>alcohol</b> withdrawal.
+APOE	addiction	withdrawal	16713503	Aim of this prospective study was to investigate a possible association between the apolipoprotein E4 (<strong>ApoE4</strong>) genotype and clinically well known cognition deficits during alcohol <b>withdrawal</b>.
+APOE	drug	alcohol	16713503	Even though <strong>ApoE4</strong> plays an important role in <b>alcoholism</b> related brain atrophy and cognition deficits in demented as well as in nondemented healthy elderly people, this study provides no evidence for an association with short term cognition deficits during <b>alcohol</b> withdrawal.
+APOE	addiction	withdrawal	16713503	Even though <strong>ApoE4</strong> plays an important role in alcoholism related brain atrophy and cognition deficits in demented as well as in nondemented healthy elderly people, this study provides no evidence for an association with short term cognition deficits during alcohol <b>withdrawal</b>.
+APOE	drug	opioid	16697650	In vitro studies showed that HIV proteins, gp120 and Tat, Tat + <b>morphine</b> but not tumor necrosis factor alpha (TNF alpha), caused increased neurotoxicity in human neuronal cultures with <strong>ApoE4</strong> allele.
+APOE	drug	alcohol	15099924	Enhanced <b>ethanol</b> , but not cocaine induced, conditioned place preference in <strong>Apoe</strong>( / ) mice.
+APOE	drug	cocaine	15099924	Enhanced ethanol , but not <b>cocaine</b> induced, conditioned place preference in <strong>Apoe</strong>( / ) mice.
+APOE	drug	alcohol	15099924	Recent data showing that <strong>apoE</strong> mRNA expression is reduced in the frontal cortex of <b>alcoholics</b> raise the possibility that <strong>apoE</strong> may also be related to the rewarding properties of <b>ethanol</b>.
+APOE	drug	alcohol	15099924	In this study, we examined whether <strong>Apoe</strong> deletion affects the rewarding properties of <b>ethanol</b> in mice.
+APOE	drug	alcohol	15099924	Male and female wild type (WT; C57BL/6J) and <strong>apoE</strong> knockout (<strong>Apoe</strong>( / ); C57BL/6J <strong>Apoe</strong>(tm1Unc)) mice underwent an unbiased place conditioning procedure with <b>ethanol</b> (2 g/kg) or cocaine (5 mg/kg).
+APOE	drug	cocaine	15099924	Male and female wild type (WT; C57BL/6J) and <strong>apoE</strong> knockout (<strong>Apoe</strong>( / ); C57BL/6J <strong>Apoe</strong>(tm1Unc)) mice underwent an unbiased place conditioning procedure with ethanol (2 g/kg) or <b>cocaine</b> (5 mg/kg).
+APOE	drug	alcohol	15099924	<strong>Apoe</strong>( / ) mice showed greater <b>ethanol</b> induced conditioned place preference (CPP).
+APOE	addiction	reward	15099924	<strong>Apoe</strong>( / ) mice showed greater ethanol induced conditioned place preference (<b>CPP</b>).
+APOE	drug	alcohol	15099924	These findings suggest that <strong>apoE</strong> normally reduces the conditioned rewarding properties of <b>ethanol</b> but not of cocaine.
+APOE	drug	cocaine	15099924	These findings suggest that <strong>apoE</strong> normally reduces the conditioned rewarding properties of ethanol but not of <b>cocaine</b>.
+APOE	drug	alcohol	15099924	While the exact mechanisms underlying these effects of <strong>apoE</strong> are unknown, these data support a possible role for <strong>apoE</strong> in modulating the conditioned rewarding properties of <b>ethanol</b>.
+APOE	drug	alcohol	11981126	Changes in serum apolipoprotein and lipoprotein profile after <b>alcohol</b> withdrawal: effect of <strong>apolipoprotein E</strong> polymorphism.
+APOE	addiction	withdrawal	11981126	Changes in serum apolipoprotein and lipoprotein profile after alcohol <b>withdrawal</b>: effect of <strong>apolipoprotein E</strong> polymorphism.
+APOE	drug	alcohol	11981126	The aim of this study was to investigate this gene/environment interaction by analyzing the effect of the <strong>apoE</strong> genotype on the <b>alcohol</b> withdrawal induced alterations in the serum Apo and Lp profile.
+APOE	addiction	withdrawal	11981126	The aim of this study was to investigate this gene/environment interaction by analyzing the effect of the <strong>apoE</strong> genotype on the alcohol <b>withdrawal</b> induced alterations in the serum Apo and Lp profile.
+APOE	drug	alcohol	11981126	<strong>ApoE</strong> genotypes and concentrations of serum cholesterol, triglyceride, and Lps containing apoA I, A II, B, E, and C III were determined in 84 male <b>alcohol</b> abusers before and after 3 weeks of abstinence.
+APOE	addiction	withdrawal	11981126	After <b>withdrawal</b>, concentrations of serum apoA I, LpA I, LpA I/A II, apoC III, LpC III non B, <strong>apoE</strong>, and LpE non B significantly decreased, whereas those of triglycerides and apoB increased; levels of cholesterol, LpC III:B, and LpB:E were not affected.
+APOE	drug	alcohol	11981126	ANOVA shows that <strong>apoE</strong> polymorphism effects were quite similar before and after <b>alcohol</b> withdrawal on all serum Apos and Lps (the interaction term between withdrawal and <strong>apoE</strong> genotype was not significant).
+APOE	addiction	withdrawal	11981126	ANOVA shows that <strong>apoE</strong> polymorphism effects were quite similar before and after alcohol <b>withdrawal</b> on all serum Apos and Lps (the interaction term between <b>withdrawal</b> and <strong>apoE</strong> genotype was not significant).
+APOE	addiction	withdrawal	11981126	Before <b>withdrawal</b>, no association between apoB level and <strong>apoE</strong> polymorphism was observed, whereas after abstinence, a borderline significant (p < or = 0.10) gradient of concentration across the three groups of subjects (epsilon2 carriers < epsilon3/epsilon3 < epsilon4 carriers) was noticed.
+APOE	drug	alcohol	11981126	Heavy <b>alcohol</b> consumption seems to alter the effect of <strong>apoE</strong> polymorphism on apoB levels, and further investigations are needed to clarify the mechanisms involved in this phenomenon: a defect in sialylation of <strong>apoE</strong>, formation of acetaldehyde adducts on apoB, or both.
+APOE	addiction	reward	11714857	In conclusion, this work, in addition to the <b>reinforcement</b> of the already known associations between APOB, <strong>APOE</strong>, and APOC3 genes and lipids, leads to new perspectives in the complex relationships among genes and environmental factors.
+APOE	drug	opioid	9790747	Population studies of polymorphisms at loci of neuropsychiatric interest (tryptophan hydroxylase (TPH), dopamine transporter protein (SLC6A3), D3 dopamine receptor (DRD3), apolipoprotein E (<strong>APOE</strong>), mu <b>opioid</b> receptor (OPRM1), and ciliary neurotrophic factor (CNTF)).
+APOE	drug	opioid	9790747	Population studies of polymorphisms at loci of neuropsychiatric interest (tryptophan hydroxylase (TPH), dopamine transporter protein (SLC6A3), D3 dopamine receptor (DRD3), <strong>apolipoprotein E</strong> (<strong>APOE</strong>), mu <b>opioid</b> receptor (OPRM1), and ciliary neurotrophic factor (CNTF)).
+APOE	drug	opioid	9790747	We determined allele frequencies for polymorphisms at several loci of interest in neuropsychiatry tryptophan hydroxylase (TPH), dopamine transporter protein (SLC6A3), D3 dopamine receptor (DRD3), apolipoprotein E (<strong>APOE</strong>), ciliary neurotrophic factor (CNTF), and the mu <b>opioid</b> receptor (OPRM1) in samples of individuals from populations in several different parts of the world.
+APOE	drug	opioid	9790747	We determined allele frequencies for polymorphisms at several loci of interest in neuropsychiatry tryptophan hydroxylase (TPH), dopamine transporter protein (SLC6A3), D3 dopamine receptor (DRD3), <strong>apolipoprotein E</strong> (<strong>APOE</strong>), ciliary neurotrophic factor (CNTF), and the mu <b>opioid</b> receptor (OPRM1) in samples of individuals from populations in several different parts of the world.
+APOE	drug	alcohol	8855152	No significant difference between these four types of <b>alcohol</b> consumption was noticed for cholesterol, triglycerides, <strong>apo E</strong>, and Lp(a).
+APOE	addiction	withdrawal	8855152	After <b>withdrawal</b>, the concentrations of serum apo A I, apo C III, LpA I, LpA I:A II, and LpC III decreased significantly (P </= 0.01), reaching values comparable with those in low drinkers; concentrations of triglycerides, apo B, <strong>apo E</strong>, and Lp(a) rose; and cholesterol concentration was unaffected.
+ALK	drug	alcohol	32154588	MY10 prevented the <b>alcohol</b> induced down regulation of Ptprz1 (p = 0.004) and anaplastic lymphoma kinase (<strong>Alk</strong>; p = 0.013) expression.
+ALK	drug	alcohol	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), RET proto oncogene (RET), anaplastic lymphoma kinase (<strong>ALK</strong>), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate <b>alcohol</b> drinking and other behaviors related to <b>alcohol</b> addiction.
+ALK	addiction	addiction	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), RET proto oncogene (RET), anaplastic lymphoma kinase (<strong>ALK</strong>), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate alcohol drinking and other behaviors related to alcohol <b>addiction</b>.
+ALK	drug	alcohol	31617071	This review will examine the preclinical evidence describing TrkB, RET, <strong>ALK</strong>, FGFR, and EGFR modulation of <b>alcohol</b> drinking and other behaviors relevant to <b>alcohol</b> abuse.
+ALK	drug	alcohol	29753117	We found that <b>ethanol</b> treatment of neuroblastoma cells increased phosphorylation of anaplastic lymphoma kinase (<strong>ALK</strong>) and TrkA, known substrates of RPTPβ/ζ.
+ALK	drug	alcohol	28860990	Anaplastic lymphoma kinase (<strong>ALK</strong>) is a receptor tyrosine kinase recently implicated in biochemical, physiological, and behavioral responses to <b>ethanol</b>.
+ALK	drug	alcohol	28860990	Thus, manipulation of <strong>ALK</strong> signaling may represent a novel approach to treating <b>alcohol</b> use disorder (AUD).
+ALK	drug	alcohol	28860990	Here, we report that <strong>Alk</strong> knockout (AlkKO) mice consumed greater doses of <b>ethanol</b>, relative to wild type (AlkWT) mice, in an operant self administration model.
+ALK	addiction	reward	28860990	Here, we report that <strong>Alk</strong> knockout (AlkKO) mice consumed greater doses of ethanol, relative to wild type (AlkWT) mice, in an <b>operant</b> self administration model.
+ALK	drug	alcohol	28860990	Thus, loss of <strong>ALK</strong> activity in mice is associated with elevated <b>ethanol</b> consumption and enhanced excitatory transmission in NAcSh D1MSNs.
+ALK	drug	alcohol	28860990	These findings add to the mounting evidence of a relationship between excitatory synaptic transmission onto NAcSh D1MSNs and <b>ethanol</b> consumption, point toward <strong>ALK</strong> as one important molecular mediator of this interaction, and further validate <strong>ALK</strong> as a target for therapeutic intervention in the treatment of AUD.
+ALK	drug	alcohol	26946429	Dependence induced <b>ethanol</b> drinking and GABA neurotransmission are altered in <strong>Alk</strong> deficient mice.
+ALK	addiction	dependence	26946429	<b>Dependence</b> induced ethanol drinking and GABA neurotransmission are altered in <strong>Alk</strong> deficient mice.
+ALK	drug	alcohol	26946429	Anaplastic lymphoma kinase (<strong>ALK</strong>) is a receptor tyrosine kinase that is expressed in the brain and implicated in <b>alcohol</b> abuse in humans and behavioral responses to <b>ethanol</b> in mice.
+ALK	drug	alcohol	26946429	Previous studies have shown an association of human <strong>ALK</strong> with acute responses to <b>alcohol</b> and <b>alcohol</b> dependence.
+ALK	addiction	dependence	26946429	Previous studies have shown an association of human <strong>ALK</strong> with acute responses to alcohol and alcohol <b>dependence</b>.
+ALK	drug	alcohol	26946429	In addition, <strong>Alk</strong> knockout (<strong>Alk</strong>  / ) mice consume more <b>ethanol</b> in a binge drinking test and show increased sensitivity to <b>ethanol</b> sedation.
+ALK	addiction	intoxication	26946429	In addition, <strong>Alk</strong> knockout (<strong>Alk</strong>  / ) mice consume more ethanol in a <b>binge</b> drinking test and show increased sensitivity to ethanol sedation.
+ALK	drug	alcohol	26946429	However, the function of <strong>ALK</strong> in excessive drinking following the establishment of <b>ethanol</b> dependence has not been examined.
+ALK	addiction	dependence	26946429	However, the function of <strong>ALK</strong> in excessive drinking following the establishment of ethanol <b>dependence</b> has not been examined.
+ALK	drug	alcohol	26946429	In this study, we tested <strong>Alk</strong>  /  mice for dependence induced drinking using the chronic intermittent <b>ethanol</b> two bottle choice drinking (CIE 2BC) protocol.
+ALK	addiction	dependence	26946429	In this study, we tested <strong>Alk</strong>  /  mice for <b>dependence</b> induced drinking using the chronic intermittent ethanol two bottle choice drinking (CIE 2BC) protocol.
+ALK	drug	alcohol	26946429	We found that <strong>Alk</strong>  /  mice initially consume more <b>ethanol</b> prior to CIE exposure, but do not escalate <b>ethanol</b> consumption after exposure, suggesting that <strong>ALK</strong> may promote the escalation of drinking after <b>ethanol</b> dependence.
+ALK	addiction	addiction	26946429	We found that <strong>Alk</strong>  /  mice initially consume more ethanol prior to CIE exposure, but do not escalate ethanol consumption after exposure, suggesting that <strong>ALK</strong> may promote the <b>escalation</b> of drinking after ethanol dependence.
+ALK	addiction	dependence	26946429	We found that <strong>Alk</strong>  /  mice initially consume more ethanol prior to CIE exposure, but do not escalate ethanol consumption after exposure, suggesting that <strong>ALK</strong> may promote the escalation of drinking after ethanol <b>dependence</b>.
+ALK	drug	alcohol	26946429	GABA transmission in <b>ethanol</b> naïve <strong>Alk</strong>  /  mice was enhanced at baseline and potentiated in response to acute <b>ethanol</b> application when compared to wild type (<strong>Alk</strong> +/+) mice.
+ALK	addiction	dependence	26946429	These data suggest that <strong>ALK</strong> plays a role in <b>dependence</b> induced drinking and the regulation of presynaptic GABA release in the CeA.
+ALK	drug	alcohol	26752591	Anaplastic lymphoma kinase (<strong>ALK</strong>) is a receptor tyrosine kinase associated with <b>alcohol</b> dependence in humans and behavioral responses to <b>ethanol</b> in mice.
+ALK	addiction	dependence	26752591	Anaplastic lymphoma kinase (<strong>ALK</strong>) is a receptor tyrosine kinase associated with alcohol <b>dependence</b> in humans and behavioral responses to ethanol in mice.
+ALK	drug	alcohol	26752591	To characterize the ability of <strong>ALK</strong> to control <b>ethanol</b> consumption, we treated mice with the <strong>ALK</strong> inhibitors TAE684 or alectinib before testing them for binge like drinking using the drinking in the dark protocol.
+ALK	addiction	intoxication	26752591	To characterize the ability of <strong>ALK</strong> to control ethanol consumption, we treated mice with the <strong>ALK</strong> inhibitors TAE684 or alectinib before testing them for <b>binge</b> like drinking using the drinking in the dark protocol.
+ALK	drug	alcohol	26752591	Mice treated with <strong>ALK</strong> inhibitors drank less <b>ethanol</b> than controls.
+ALK	drug	alcohol	26752591	In addition, TAE684 treatment abolished <b>ethanol</b> conditioned place preference, indicating that <strong>ALK</strong> regulates the rewarding properties of <b>ethanol</b>.
+ALK	drug	alcohol	26752591	Because the ventral tegmental area (VTA) is a key brain region involved in the rewarding effects of <b>ethanol</b>, we determined if <strong>Alk</strong> expression in the VTA is important for binge like <b>ethanol</b> consumption.
+ALK	addiction	intoxication	26752591	Because the ventral tegmental area (VTA) is a key brain region involved in the rewarding effects of ethanol, we determined if <strong>Alk</strong> expression in the VTA is important for <b>binge</b> like ethanol consumption.
+ALK	drug	alcohol	26752591	Mice expressing a short hairpin ribonucleic acid targeting <strong>Alk</strong> in the VTA drank less <b>ethanol</b> compared with controls.
+ALK	drug	alcohol	26752591	Extracellular recordings of putative DA neurons in VTA slices demonstrated that <strong>ALK</strong> inhibition did not affect the ability of <b>ethanol</b> to stimulate, or DA to inhibit, the firing of DA neurons.
+ALK	drug	alcohol	26752591	These data support the possibility that <strong>ALK</strong> might be a novel target of pharmacotherapy for reducing excessive <b>alcohol</b> consumption.
+ALK	addiction	relapse	26646246	<strong>ALK</strong> fusion was neither a risk factor nor protective factor in <b>relapse</b> free survival and overall survival.
+ALK	drug	nicotine	26646246	Male, current <b>smoker</b>, and EML4 <strong>ALK</strong> variant 3 indicated poor prognosis among <strong>ALK</strong> fusion positive lung adenocarcinomas.
+ALK	drug	alcohol	26206265	MDK and one of its receptors, anaplastic lymphoma kinase (<strong>ALK</strong>), also regulate behavioral responses to <b>ethanol</b> in mice.
+ALK	drug	alcohol	26206265	The goal of this study was to determine whether MDK and <strong>ALK</strong> expression and signaling are activated by <b>ethanol</b>.
+ALK	drug	alcohol	26206265	We found that <b>ethanol</b> treatment of neuroblastoma cells increased MDK and <strong>ALK</strong> expression.
+ALK	drug	alcohol	26206265	We also assessed activation of <strong>ALK</strong> by <b>ethanol</b> in cells and found that <strong>ALK</strong> and <strong>ALK</strong> dependent extracellular signal regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3) phosphorylation increased rapidly with <b>ethanol</b> exposure.
+ALK	drug	alcohol	26206265	Similarly, treatment of cells with recombinant MDK protein increased <strong>ALK</strong>, ERK and STAT3 phosphorylation, suggesting that <b>ethanol</b> may utilize MDK to activate <strong>ALK</strong> signaling.
+ALK	drug	alcohol	26206265	In support of this, transfection of cells with MDK siRNAs attenuated <strong>ALK</strong> signaling in response to <b>ethanol</b>.
+ALK	drug	alcohol	26206265	We found that inhibition of <strong>ALK</strong> or knockout of MDK attenuated <b>ethanol</b> induced ERK phosphorylation in mouse amygdala.
+ALK	drug	alcohol	26206265	These results demonstrate that <b>ethanol</b> engages MDK and <strong>ALK</strong> signaling, which has important consequences for <b>alcohol</b> induced neurotoxicity and the regulation of behaviors related to <b>alcohol</b> abuse.
+ALK	addiction	addiction	25929953	With therapeutic approaches based on oncogene <b>addiction</b> offering significant anticancer benefit, the identification of anaplastic lymphoma kinase (<strong>ALK</strong>) rearrangements is a key aspect of the management of lung cancers.
+ALK	drug	nicotine	25929953	The EML4 <strong>ALK</strong> gene fusion is detected in 4 8% of all lung cancers, predominantly in light <b>smokers</b> or nonsmokers.
+ALK	addiction	dependence	25855381	In conclusion, our findings indicate that LADCs with <strong>ALK</strong>, RET, and ROS1 fusions develop exclusively via their <b>dependence</b> on these oncogene fusions.
+ALK	drug	nicotine	25152623	The <strong>ALK</strong> rearrangements were more frequently observed in tumors with a minor mucinous component, while the KRAS mutations were more prevalent in <b>smokers</b>.
+ALK	addiction	relapse	23775406	ANCCA expression was evaluated by immunohistochemistry in 143 surgically resected lung adenocarcinomas and was correlated with clinicopathologic and molecular variables including adenocarcinoma histologic subtypes, tumor, node, metastasis status, <b>relapse</b> free survival, overall survival, EGFR mutations, KRAS mutations, HER2 mutations and <strong>ALK</strong> fusions.
+ALK	drug	nicotine	23150706	Patients with lung adenocarcinomas with RET fusion gene had more poorly differentiated tumors (63.6%; P = .029 for RET v <strong>ALK</strong>, P = .007 for RET v EGFR), with a tendency to be younger (≤ 60 years; 72.7%) and never <b>smokers</b> (81.8%) and to have solid subtype (63.6%) and a smaller tumor (≤ 3 cm) with N2 disease (54.4%).
+ALK	drug	nicotine	22464348	EGFR mutations are more frequent in never <b>smokers</b>, as are EML4 <strong>ALK</strong> fusions.
+ALK	drug	cocaine	21976498	<strong>Alk</strong> is a transcriptional target of LMO4 and ERα that promotes <b>cocaine</b> sensitization and reward.
+ALK	addiction	reward	21976498	<strong>Alk</strong> is a transcriptional target of LMO4 and ERα that promotes cocaine sensitization and <b>reward</b>.
+ALK	addiction	sensitization	21976498	<strong>Alk</strong> is a transcriptional target of LMO4 and ERα that promotes cocaine <b>sensitization</b> and reward.
+ALK	drug	cocaine	21976498	Here we show that transcription of anaplastic lymphoma kinase (<strong>Alk</strong>) is repressed by LMO4 in the striatum and that <strong>Alk</strong> promotes the development of <b>cocaine</b> sensitization and conditioned place preference, a measure of <b>cocaine</b> reward.
+ALK	addiction	reward	21976498	Here we show that transcription of anaplastic lymphoma kinase (<strong>Alk</strong>) is repressed by LMO4 in the striatum and that <strong>Alk</strong> promotes the development of cocaine sensitization and conditioned place preference, a measure of cocaine <b>reward</b>.
+ALK	addiction	sensitization	21976498	Here we show that transcription of anaplastic lymphoma kinase (<strong>Alk</strong>) is repressed by LMO4 in the striatum and that <strong>Alk</strong> promotes the development of cocaine <b>sensitization</b> and conditioned place preference, a measure of cocaine reward.
+ALK	drug	cocaine	21976498	Moreover, we show that ERα knock out mice exhibit enhanced <b>cocaine</b> sensitization and conditioned place preference and an increase in <strong>Alk</strong> expression in the nucleus accumbens.
+ALK	addiction	sensitization	21976498	Moreover, we show that ERα knock out mice exhibit enhanced cocaine <b>sensitization</b> and conditioned place preference and an increase in <strong>Alk</strong> expression in the nucleus accumbens.
+ALK	drug	cocaine	21976498	Our data suggest that estrogen regulation of <strong>Alk</strong> may be one mechanism responsible for sexually dimorphic responses to <b>cocaine</b>.
+ALK	drug	alcohol	21703634	In addition, <strong>ALK</strong>, CASC4, and SEMA5A were strongly associated with <b>alcohol</b> dependence (p<2 × 10( 5)) in the meta analysis.
+ALK	addiction	dependence	21703634	In addition, <strong>ALK</strong>, CASC4, and SEMA5A were strongly associated with alcohol <b>dependence</b> (p<2 × 10( 5)) in the meta analysis.
+ALK	drug	nicotine	21655907	In addition, most adenocarcinomas in never <b>smokers</b> harbor one of the proto oncogene aberrations that occur in a mutually exclusive manner (EGFR mutation, KRAS mutation, HER2 mutations, or <strong>ALK</strong> translocation).
+ALK	drug	nicotine	20979469	Patients with <strong>ALK</strong> rearrangements tended to be younger than those without the rearrangements, and most of the patients had little or no exposure to <b>tobacco</b> and had adenocarcinomas.
+ALK	drug	cocaine	11931612	This work describes the application of chemometric methods to a data set of 54 N(1) benzhydryl oxy alkyl N(4) phenyl <strong>alk</strong>(en)yl piperazines (GBR compounds) and chemically related mepyramines as putative candidates in <b>cocaine</b> abuse therapy.
+ALK	drug	alcohol	11103363	A questionnaire for self assessment of disturbances in several cognitive and perceptual areas (the Eppendorf Schizophrenia Inventory, or ESI) was constructed and administered to first episode schizophrenics (SCHe, n = 45), negative syndrome schizophrenics (SCHn, n = 45), remitted schizophrenics (SCHr, n = 24), depressives (DEP, n = 43), <b>alcoholics</b> (<strong>ALK</strong>, n = 48), obsessive compulsive patients (ZWA, n = 46), and healthy controls (KON, n = 57).
+ALK	addiction	addiction	11103363	A questionnaire for self assessment of disturbances in several cognitive and perceptual areas (the Eppendorf Schizophrenia Inventory, or ESI) was constructed and administered to first episode schizophrenics (SCHe, n = 45), negative syndrome schizophrenics (SCHn, n = 45), remitted schizophrenics (SCHr, n = 24), depressives (DEP, n = 43), alcoholics (<strong>ALK</strong>, n = 48), obsessive <b>compulsive</b> patients (ZWA, n = 46), and healthy controls (KON, n = 57).
+ADH7	drug	alcohol	29084628	We evaluated the presence of SNPs in the ADH (ADH1B, ADH1C, and <strong>ADH4</strong>) and ALDH (ALDH2) genes in <b>alcohol</b> users of Goiânia, State of Goiás   Brazil, and then we established a possible relationship with AUD by allelic and genotypic study.
+ADH7	drug	alcohol	28805974	Effect of single nucleotide polymorphisms in ADH1B, <strong>ADH4</strong>, ADH1C, OPRM1, DRD2, BDNF, and ALDH2 genes on <b>alcohol</b> dependence in a Caucasian population.
+ADH7	addiction	dependence	28805974	Effect of single nucleotide polymorphisms in ADH1B, <strong>ADH4</strong>, ADH1C, OPRM1, DRD2, BDNF, and ALDH2 genes on alcohol <b>dependence</b> in a Caucasian population.
+ADH7	drug	alcohol	27172571	The interactions of religious involvement with ADH1B rs2066702, ADH1C rs698, and <strong>ADH4</strong> rs1042364 were significantly associated with maximum drinks and <b>alcohol</b> dependence symptoms.
+ADH7	addiction	dependence	27172571	The interactions of religious involvement with ADH1B rs2066702, ADH1C rs698, and <strong>ADH4</strong> rs1042364 were significantly associated with maximum drinks and alcohol <b>dependence</b> symptoms.
+ADH7	drug	alcohol	28453170	Single nucleotide polymorphism (SNP) of the gene encoding ADH class IV (<strong>ADH7</strong>) affects its <b>ethanol</b> oxidizing activity in the gastric lumen, thereby influencing the first pass metabolism (FPM) of the substance.
+ADH7	drug	alcohol	28453170	The findings published by various research centres have demonstrated that specific SNP changes in the <strong>ADH7</strong> gene are of different significance for the risk of <b>alcohol</b> dependence according to the population studied.
+ADH7	addiction	dependence	28453170	The findings published by various research centres have demonstrated that specific SNP changes in the <strong>ADH7</strong> gene are of different significance for the risk of alcohol <b>dependence</b> according to the population studied.
+ADH7	drug	alcohol	26230553	Alleles involved in inefficient (ADH1B2*2 and ALDH2*2) or efficient (SNP6, <strong>ADH4</strong> gene) <b>alcohol</b> metabolism may influence the risk of <b>alcoholism</b>.
+ADH7	drug	alcohol	25527893	A protective variant (rs991316) located downstream from the <strong>ADH7</strong> (<b>alcohol</b> dehydrogenase 7) gene showed suggestive significance in association with <b>alcohol</b> dependence symptom counts derived from DSM III R and DSM IV criteria, as well as to clustered <b>alcohol</b> dependence symptoms.
+ADH7	addiction	dependence	25527893	A protective variant (rs991316) located downstream from the <strong>ADH7</strong> (alcohol dehydrogenase 7) gene showed suggestive significance in association with alcohol <b>dependence</b> symptom counts derived from DSM III R and DSM IV criteria, as well as to clustered alcohol <b>dependence</b> symptoms.
+ADH7	drug	alcohol	25527893	<strong>ADH7</strong> has been shown to have a protective role against <b>alcohol</b> dependence in previous studies involving other ethnicities, but has not been reported for Mexican Americans.
+ADH7	addiction	dependence	25527893	<strong>ADH7</strong> has been shown to have a protective role against alcohol <b>dependence</b> in previous studies involving other ethnicities, but has not been reported for Mexican Americans.
+ADH7	drug	alcohol	25527893	These results suggest that variants near <strong>ADH7</strong> may play a role in protection from <b>alcohol</b> dependence in this Mexican American cohort.
+ADH7	addiction	dependence	25527893	These results suggest that variants near <strong>ADH7</strong> may play a role in protection from alcohol <b>dependence</b> in this Mexican American cohort.
+ADH7	drug	alcohol	25270064	Variants in or near <strong>ADH7</strong> were significantly negatively associated with <b>alcohol</b> related phenotypes, suggesting a potential protective effect of this gene.
+ADH7	drug	alcohol	24889829	Rs1800759 (previously known to be associated to AD) and CpG cg12011299 (distance: 37 bp) are both located in <b>alcohol</b> dehydrogenase (ADH) 4 gene (<strong>ADH4</strong>) promoter region.
+ADH7	drug	alcohol	24692236	Linkage studies of <b>alcoholism</b> have implicated several chromosome regions, leading to the successful identification of susceptibility genes, including <strong>ADH4</strong> and GABRA2 on chromosome 4.
+ADH7	drug	alcohol	24505444	We investigated six variants known to influence nicotine addiction or <b>alcohol</b> metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (<strong>ADH7</strong>), and rs4767364 (ALDH2).
+ADH7	drug	nicotine	24505444	We investigated six variants known to influence <b>nicotine</b> addiction or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (<strong>ADH7</strong>), and rs4767364 (ALDH2).
+ADH7	addiction	addiction	24505444	We investigated six variants known to influence nicotine <b>addiction</b> or alcohol metabolism, including rs16969968 (CHRNA5), rs578776 (CHRNA3), rs1229984 (ADH1B), rs698 (ADH1C), rs1573496 (<strong>ADH7</strong>), and rs4767364 (ALDH2).
+ADH7	drug	alcohol	23468174	Humans express at least seven <b>alcohol</b> dehydrogenase (ADH) isoforms that are encoded by ADH gene cluster (<strong>ADH7</strong> ADH1C ADH1B ADH1A ADH6 ADH4 ADH5) at chromosome 4.
+ADH7	drug	alcohol	23468174	Humans express at least seven <b>alcohol</b> dehydrogenase (ADH) isoforms that are encoded by ADH gene cluster (<strong>ADH7</strong> ADH1C ADH1B ADH1A ADH6 <strong>ADH4</strong> ADH5) at chromosome 4.
+ADH7	drug	alcohol	22232963	[Research on associations between selected polymorphisms of genes DRD2, 5HTT, GRIK3, <strong>ADH4</strong> and <b>alcohol</b> dependence syndrome].
+ADH7	addiction	dependence	22232963	[Research on associations between selected polymorphisms of genes DRD2, 5HTT, GRIK3, <strong>ADH4</strong> and alcohol <b>dependence</b> syndrome].
+ADH7	drug	alcohol	22232963	The aim of this study was to assess the relation between the <b>alcohol</b> dependence syndrome (ADS) and the polymorphism of the selected genes (GRIK3, 5HTT, ANKK1, <strong>ADH4</strong>).
+ADH7	addiction	dependence	22232963	The aim of this study was to assess the relation between the alcohol <b>dependence</b> syndrome (ADS) and the polymorphism of the selected genes (GRIK3, 5HTT, ANKK1, <strong>ADH4</strong>).
+ADH7	drug	alcohol	22232963	Comparison between the patients with ADS and the patients from the control group demonstrated statistically significant association of <strong>ADH4</strong> (rs1800759) with the <b>alcohol</b> dependence syndrome.
+ADH7	addiction	dependence	22232963	Comparison between the patients with ADS and the patients from the control group demonstrated statistically significant association of <strong>ADH4</strong> (rs1800759) with the alcohol <b>dependence</b> syndrome.
+ADH7	drug	alcohol	22232963	Our results suggest that the analysed polymorphisms ofANKK1 and <strong>ADH4</strong> can play an important part in the pathogenesis of <b>alcohol</b> abuse.
+ADH7	drug	alcohol	22044940	<strong>ADH4</strong> intronic variations are associated with <b>alcohol</b> dependence: results from an Italian case control association study.
+ADH7	addiction	dependence	22044940	<strong>ADH4</strong> intronic variations are associated with alcohol <b>dependence</b>: results from an Italian case control association study.
+ADH7	drug	alcohol	22044940	This study investigated the involvement of <strong>ADH4</strong> gene polymorphisms in the susceptibility to <b>alcohol</b> use disorders.
+ADH7	drug	alcohol	22044940	Thirty eight single nucleotide polymorphisms (SNPs) in and around the <strong>ADH4</strong> gene were investigated in 136 Italian <b>alcoholics</b> and 276 healthy controls.
+ADH7	drug	alcohol	22044940	Case control comparisons for allele and genotype frequencies showed that <strong>ADH4</strong> SNPs were associated with <b>alcohol</b> dependence but not with <b>alcohol</b> abuse.
+ADH7	addiction	dependence	22044940	Case control comparisons for allele and genotype frequencies showed that <strong>ADH4</strong> SNPs were associated with alcohol <b>dependence</b> but not with alcohol abuse.
+ADH7	drug	alcohol	22044940	A logistic regression analysis confirmed the association between <strong>ADH4</strong> variants and <b>alcohol</b> dependence when sex, age, years of education, marital status and the allele genotype, haplotype and diplotype data of the six haplotype tag SNP were considered.
+ADH7	addiction	dependence	22044940	A logistic regression analysis confirmed the association between <strong>ADH4</strong> variants and alcohol <b>dependence</b> when sex, age, years of education, marital status and the allele genotype, haplotype and diplotype data of the six haplotype tag SNP were considered.
+ADH7	drug	alcohol	22044940	These data suggest that <strong>ADH4</strong> intronic variants play a role in <b>alcohol</b> dependence susceptibility in Italian populations.
+ADH7	addiction	dependence	22044940	These data suggest that <strong>ADH4</strong> intronic variants play a role in alcohol <b>dependence</b> susceptibility in Italian populations.
+ADH7	drug	alcohol	21635275	No evidence for association with the <b>alcohol</b> dependence diagnosis was observed, but an SNP in exon 9 of ADH1B (rs2066702; ADH1B*3) and an SNP at the 5' end of <strong>ADH4</strong> (rs3762894) showed significant evidence of association with the presence of withdrawal symptoms (p = 0.0018 and 0.0012, respectively).
+ADH7	addiction	dependence	21635275	No evidence for association with the alcohol <b>dependence</b> diagnosis was observed, but an SNP in exon 9 of ADH1B (rs2066702; ADH1B*3) and an SNP at the 5' end of <strong>ADH4</strong> (rs3762894) showed significant evidence of association with the presence of withdrawal symptoms (p = 0.0018 and 0.0012, respectively).
+ADH7	addiction	withdrawal	21635275	No evidence for association with the alcohol dependence diagnosis was observed, but an SNP in exon 9 of ADH1B (rs2066702; ADH1B*3) and an SNP at the 5' end of <strong>ADH4</strong> (rs3762894) showed significant evidence of association with the presence of <b>withdrawal</b> symptoms (p = 0.0018 and 0.0012, respectively).
+ADH7	drug	alcohol	21635275	These results suggest that variants in the ADH1B and <strong>ADH4</strong> genes may be protective against the development of some symptoms associated with <b>alcohol</b> dependence.
+ADH7	addiction	dependence	21635275	These results suggest that variants in the ADH1B and <strong>ADH4</strong> genes may be protective against the development of some symptoms associated with alcohol <b>dependence</b>.
+ADH7	drug	alcohol	21083667	The systematic evaluation of <b>alcohol</b> metabolizing genes in four non East Asian populations has shown only modest associations with AD, largely for ALDH1A1 and <strong>ADH4</strong>.
+ADH7	drug	alcohol	20714161	We develop a pharmacokinetic model describing how genetic variations in ADH1B, ADH1C, <strong>ADH7</strong>, ALDH2, and TAS2R38 affect consumption behavior, and <b>alcohol</b> and acetaldehyde levels over time in various tissues of individuals with a particular genotype to predict their susceptibility to <b>alcohol</b> dependence.
+ADH7	addiction	dependence	20714161	We develop a pharmacokinetic model describing how genetic variations in ADH1B, ADH1C, <strong>ADH7</strong>, ALDH2, and TAS2R38 affect consumption behavior, and alcohol and acetaldehyde levels over time in various tissues of individuals with a particular genotype to predict their susceptibility to alcohol <b>dependence</b>.
+ADH7	drug	alcohol	20626721	Association of <strong>ADH4</strong> genetic variants with <b>alcohol</b> dependence risk and related phenotypes: results from a larger multicenter association study.
+ADH7	addiction	dependence	20626721	Association of <strong>ADH4</strong> genetic variants with alcohol <b>dependence</b> risk and related phenotypes: results from a larger multicenter association study.
+ADH7	drug	alcohol	20626721	Genetic variants of the <b>alcohol</b> metabolizing enzyme <strong>ADH4</strong>, located on chromosome 4q22 4q23, have been related to <b>alcohol</b> dependence (AD) risk in previous research.
+ADH7	addiction	dependence	20626721	Genetic variants of the alcohol metabolizing enzyme <strong>ADH4</strong>, located on chromosome 4q22 4q23, have been related to alcohol <b>dependence</b> (AD) risk in previous research.
+ADH7	drug	alcohol	20626721	The aim of this association study in a large multicenter sample of <b>alcohol</b> dependent individuals and controls is to confirm <strong>ADH4</strong> single nucleotide polymorphism (SNP) and haplotype association with AD and relevant related phenotypes.
+ADH7	drug	alcohol	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as <b>alcohol</b> dehydrogenase (<strong>ADH7</strong>), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and diazepam binding inhibitor (DBI).
+ADH7	drug	benzodiazepine	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as alcohol dehydrogenase (<strong>ADH7</strong>), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and <b>diazepam</b> binding inhibitor (DBI).
+ADH7	drug	alcohol	19193628	Alleles of <strong>ADH7</strong> SNPs were associated with the early stages of <b>alcohol</b> metabolism, with additional effects in the ADH1A, ADH1B and ADH4 regions.
+ADH7	drug	alcohol	19193628	Alleles of <strong>ADH7</strong> SNPs were associated with the early stages of <b>alcohol</b> metabolism, with additional effects in the ADH1A, ADH1B and <strong>ADH4</strong> regions.
+ADH7	drug	alcohol	19182438	Polymorphisms in the promoter region of the human class II <b>alcohol</b> dehydrogenase (<strong>ADH4</strong>) gene affect both transcriptional activity and <b>ethanol</b> metabolism in Japanese subjects.
+ADH7	drug	alcohol	19182438	Class II <b>alcohol</b> dehydrogenase (pi ADH), encoded by <b>alcohol</b> dehydrogenase (<strong>ADH4</strong>), is considered to contribute to <b>ethanol</b> (EtOH) oxidation in the liver at high concentration.
+ADH7	drug	alcohol	19182438	These results suggested that the SNP at  136bp in the <strong>ADH4</strong> promoter had an effect on transcriptional regulation, and that the higher activity of the  136A allele compared with the  136C allele caused a lower level of blood EtOH after <b>alcohol</b> ingestion; that is, individuals with the  136A allele may consume more EtOH and might have a higher risk for development of <b>alcohol</b> dependence than those without the  136A allele.
+ADH7	addiction	dependence	19182438	These results suggested that the SNP at  136bp in the <strong>ADH4</strong> promoter had an effect on transcriptional regulation, and that the higher activity of the  136A allele compared with the  136C allele caused a lower level of blood EtOH after alcohol ingestion; that is, individuals with the  136A allele may consume more EtOH and might have a higher risk for development of alcohol <b>dependence</b> than those without the  136A allele.
+ADH7	drug	alcohol	18996923	After controlling for rs1229984, an independent association was observed between rs1042026 (ADH1B) and <b>alcohol</b> intake (P=4.7 x 10( 5)) and suggestive associations (P<0.001) between <b>alcohol</b> consumption phenotypes and rs1693482 (ADH1C), rs1230165 (ADH5) and rs3762894 (<strong>ADH4</strong>).
+ADH7	addiction	dependence	18801187	Recessive genetic mode of an <strong>ADH4</strong> variant in substance <b>dependence</b> in African Americans: A model of utility of the HWD test.
+ADH7	drug	alcohol	18801187	In our previous studies, we reported positive associations between seven <strong>ADH4</strong> polymorphisms and substance dependence [i.e., <b>alcohol</b> dependence (AD) and/or drug dependence (DD)] in European Americans (EAs).
+ADH7	addiction	dependence	18801187	In our previous studies, we reported positive associations between seven <strong>ADH4</strong> polymorphisms and substance <b>dependence</b> [i.e., alcohol <b>dependence</b> (AD) and/or drug <b>dependence</b> (DD)] in European Americans (EAs).
+ADH7	addiction	dependence	18801187	In the present study, we address the relationship between <strong>ADH4</strong> variation and substance <b>dependence</b> in an African American (AA) population, and report evidence that supports an association between a different <strong>ADH4</strong> polymorphism (rs2226896) and these phenotypes in AAs.
+ADH7	addiction	dependence	18801187	Two family based association study methods, i.e., TDT and FBAT, were applied to test the relationship between <strong>ADH4</strong> variation and substance <b>dependence</b> in Sample 3 (112 small nuclear families) and in Sample 4 (632 pedigrees), respectively.
+ADH7	addiction	dependence	18801187	<strong>ADH4</strong> variation might play a role in risk for substance <b>dependence</b> in AAs, potentially via a recessive mechanism.
+ADH7	drug	alcohol	17918242	Recently, associations between <b>alcohol</b> dehydrogenase 7 (<strong>ADH7</strong>) and SD have been reported, which led us to investigate the relationship between <strong>ADH7</strong> variation and personality traits.
+ADH7	drug	alcohol	16571603	There was strong evidence that variations in <strong>ADH4</strong> are associated with <b>alcoholism</b>: 12 SNPs were significantly associated.
+ADH7	drug	alcohol	16571603	Haplotype tag SNPs were selected for the block in the <strong>ADH4</strong> gene that provided evidence of association and subsequently used in association analysis; the haplotype was significantly associated with <b>alcoholism</b> (P=0.01) There was weaker evidence that variations in ADH1A and ADH1B might also play a role in modifying risk.
+ADH7	drug	alcohol	16237392	<strong>ADH4</strong> gene variation is associated with <b>alcohol</b> dependence and drug dependence in European Americans: results from HWD tests and case control association studies.
+ADH7	addiction	dependence	16237392	<strong>ADH4</strong> gene variation is associated with alcohol <b>dependence</b> and drug <b>dependence</b> in European Americans: results from HWD tests and case control association studies.
+ADH7	drug	alcohol	16237392	The <strong>ADH4</strong> gene, an important member of this family, is a functional and positional candidate for <b>alcohol</b> dependence.
+ADH7	addiction	dependence	16237392	The <strong>ADH4</strong> gene, an important member of this family, is a functional and positional candidate for alcohol <b>dependence</b>.
+ADH7	drug	alcohol	16237392	The present study aimed to investigate the relationship between <strong>ADH4</strong> gene variation and <b>alcohol</b> dependence and drug dependence in European Americans (EAs) and African Americans (AAs).
+ADH7	addiction	dependence	16237392	The present study aimed to investigate the relationship between <strong>ADH4</strong> gene variation and alcohol <b>dependence</b> and drug <b>dependence</b> in European Americans (EAs) and African Americans (AAs).
+ADH7	drug	alcohol	16237392	Seven single nucleotide polymorphisms (SNPs) spanning the <strong>ADH4</strong> gene were genotyped in 365 healthy controls (317 EAs and 48 AAs) and 561 subjects (400 EAs and 161 AAs) affected with <b>alcohol</b> dependence and/or drug dependence (436 with <b>alcohol</b> dependence; 356 with drug dependence).
+ADH7	addiction	dependence	16237392	Seven single nucleotide polymorphisms (SNPs) spanning the <strong>ADH4</strong> gene were genotyped in 365 healthy controls (317 EAs and 48 AAs) and 561 subjects (400 EAs and 161 AAs) affected with alcohol <b>dependence</b> and/or drug <b>dependence</b> (436 with alcohol <b>dependence</b>; 356 with drug <b>dependence</b>).
+ADH7	drug	alcohol	16237392	These findings suggest that <strong>ADH4</strong> genotypes predispose to <b>alcohol</b> dependence and drug dependence in a recessive manner, a predisposition that is population specific.
+ADH7	addiction	dependence	16237392	These findings suggest that <strong>ADH4</strong> genotypes predispose to alcohol <b>dependence</b> and drug <b>dependence</b> in a recessive manner, a predisposition that is population specific.
+ADH7	drug	alcohol	16220108	<strong>ADH4</strong> gene variation is associated with <b>alcohol</b> and drug dependence: results from family controlled and population structured association studies.
+ADH7	addiction	dependence	16220108	<strong>ADH4</strong> gene variation is associated with alcohol and drug <b>dependence</b>: results from family controlled and population structured association studies.
+ADH7	drug	alcohol	16220108	We found strong associations between <strong>ADH4</strong> gene variation and <b>alcohol</b> and drug dependence by the Hardy Weinberg Disequilibrium (HWD) test and case control association analysis in an initial study.
+ADH7	addiction	dependence	16220108	We found strong associations between <strong>ADH4</strong> gene variation and alcohol and drug <b>dependence</b> by the Hardy Weinberg Disequilibrium (HWD) test and case control association analysis in an initial study.
+ADH7	drug	alcohol	16220108	Structured association analysis demonstrated that the genotypes of six <strong>ADH4</strong> markers were associated with <b>alcohol</b> dependence, and all seven <strong>ADH4</strong> markers were associated with drug dependence (P=10 0.047).
+ADH7	addiction	dependence	16220108	Structured association analysis demonstrated that the genotypes of six <strong>ADH4</strong> markers were associated with alcohol <b>dependence</b>, and all seven <strong>ADH4</strong> markers were associated with drug <b>dependence</b> (P=10 0.047).
+ADH7	drug	alcohol	16220108	Transmission disequilibrium test, haplotype based haplotype relative risk and genotype based haplotype relative risk analyses all confirmed the association of the <strong>ADH4</strong> markers with <b>alcohol</b> dependence and drug dependence.
+ADH7	addiction	dependence	16220108	Transmission disequilibrium test, haplotype based haplotype relative risk and genotype based haplotype relative risk analyses all confirmed the association of the <strong>ADH4</strong> markers with alcohol <b>dependence</b> and drug <b>dependence</b>.
+ADH7	drug	alcohol	16220108	Using rigorous study designs that account for possible population stratification, these findings confirm and extend our original observations indicating that variation at <strong>ADH4</strong> predisposes to <b>alcohol</b> and drug dependence.
+ADH7	addiction	dependence	16220108	Using rigorous study designs that account for possible population stratification, these findings confirm and extend our original observations indicating that variation at <strong>ADH4</strong> predisposes to alcohol and drug <b>dependence</b>.
+ADH7	drug	alcohol	15863808	The authors evaluated the association of three functional promoter polymorphisms of the <strong>ADH4</strong> gene with <b>alcohol</b> dependence.
+ADH7	addiction	dependence	15863808	The authors evaluated the association of three functional promoter polymorphisms of the <strong>ADH4</strong> gene with alcohol <b>dependence</b>.
+ADH7	drug	alcohol	15863808	These preliminary results suggest that <strong>ADH4</strong> may play a role in the etiology of <b>alcohol</b> dependence.
+ADH7	addiction	dependence	15863808	These preliminary results suggest that <strong>ADH4</strong> may play a role in the etiology of alcohol <b>dependence</b>.
+TGFB1	drug	alcohol	25710054	Assessment of the frequency of the <strong>transforming growth factor beta 1</strong> sequence polymorphisms in patients with <b>alcohol</b> dependence syndrome.
+TGFB1	addiction	dependence	25710054	Assessment of the frequency of the <strong>transforming growth factor beta 1</strong> sequence polymorphisms in patients with alcohol <b>dependence</b> syndrome.
+TGFB1	drug	alcohol	22295116	LTBP1, by interacting <strong>TGFB1</strong>, may down regulate enzymes directly participating in <b>alcohol</b> metabolism.
+TGFB1	drug	alcohol	19794996	<b>Ethanol</b> and its metabolite acetaldehyde increase transforming growth factor beta1 (<strong>TGF beta1</strong>) expression in animal studies.
+TGFB1	drug	alcohol	19794996	Blood samples were collected from 41 patients with <b>alcohol</b> dependence, <strong>TGF beta1</strong> levels measured by ELISA were compared with 41 normal subjects.
+TGFB1	addiction	dependence	19794996	Blood samples were collected from 41 patients with alcohol <b>dependence</b>, <strong>TGF beta1</strong> levels measured by ELISA were compared with 41 normal subjects.
+TGFB1	drug	alcohol	19794996	Plasma <strong>TGF beta1</strong> levels in the patients with <b>alcohol</b> dependence (1,653.11+/ 532.45 pg/mL) were significantly higher than those of healthy subjects (669.87+/ 366.53 pg/mL) (P=0.000).
+TGFB1	addiction	dependence	19794996	Plasma <strong>TGF beta1</strong> levels in the patients with alcohol <b>dependence</b> (1,653.11+/ 532.45 pg/mL) were significantly higher than those of healthy subjects (669.87+/ 366.53 pg/mL) (P=0.000).
+TGFB1	drug	alcohol	19794996	Increased <strong>TGF beta1</strong> may mediate deleterious effect of <b>alcohol</b> such as hepatic fibrosis and suppressed neuronal developments in <b>alcohol</b> dependence patients.
+TGFB1	addiction	dependence	19794996	Increased <strong>TGF beta1</strong> may mediate deleterious effect of alcohol such as hepatic fibrosis and suppressed neuronal developments in alcohol <b>dependence</b> patients.
+TGFB1	drug	nicotine	18060582	Potentiation of HIV 1 expression in microglial cells by <b>nicotine</b>: involvement of <strong>transforming growth factor beta 1</strong>.
+TGFB1	drug	alcohol	17347308	We also found that immediately after <b>ethanol</b> treatments there was a significant reduction in the expression of proopiomelanocortin and adenylyl cyclases mRNA and an increased expression of several <strong>TGF beta1</strong> linked apoptotic genes in beta EP neurons isolated by laser captured microdissection from arcuate nuclei of young rats.
+TGFB1	drug	alcohol	17347308	These data suggest that <b>ethanol</b> exposure during the developmental period causes beta EP neuronal death by cellular mechanisms involving the suppression of cyclic AMP production and activation of <strong>TGF beta1</strong> linked apoptotic signaling and produces long term structural and functional deficiency of beta EP neurons in the hypothalamus.
+TGFB1	drug	opioid	17048692	Intraperitoneal injection of <b>morphine</b> (6 mg/kg) induced significant inhibition of salivary flow rate, total protein, calcium, and <strong>TGF beta1</strong> concentrations.
+TGFB1	drug	opioid	17048692	In combination treatment, ACBD prevented <b>morphine</b> induced reduction of flow rate, total protein, calcium, and <strong>TGF beta1</strong> and reached control levels.
+TGFB1	drug	nicotine	15710343	The present study aimed at investigating the effect of <b>nicotine</b> on <strong>TGF beta1</strong>, IL 10, IL 12, and TNF alpha production in Cpn infected human peripheral blood mononuclear cells (PBMCs).
+TGFB1	drug	nicotine	15710343	<b>Nicotine</b> treatment of the Cpn infected cells up regulated IL 10, but not TNF alpha and IL 12, and also resulted in significant down regulation of <strong>TGF beta1</strong> production which was marked in the Cpn infected control cells.
+TGFB1	addiction	addiction	15205914	A phase I study of POH for 14 days out of every 28 days in subjects with advanced malignancies was performed to evaluate dose <b>escalation</b>, toxicity, pharmacokinetics, and effects on <strong>TGFbeta</strong> and Ras.
+TGFB1	drug	alcohol	9719112	<strong>TGFbeta1</strong> was extracted using an acid/<b>ethanol</b> method.
+TGFB1	addiction	addiction	9719112	Thus, monitoring of plasma <strong>TGFbeta1</strong> levels may identify candidates for dose <b>escalation</b> studies in the treatment of lung cancer.
+TGFB1	drug	alcohol	2307396	These results demonstrate (a) that lipocytes isolated from the rats given the high fat diet and <b>ethanol</b> are markedly proliferative and produce more collagen; and (b) that the Kupffer cells derived from these animals release factors that stimulate proliferation and collagen formation of lipocytes and (c) that the high fat diet sensitizes lipocytes for stimulatory effects of the Kupffer cell derived factors and <strong>transforming growth factor beta 1</strong>.
+STAT3	drug	alcohol	32116692	TSG 6 Inhibits Oxidative Stress and Induces M2 Polarization of Hepatic Macrophages in Mice With <b>Alcoholic</b> Hepatitis via Suppression of <strong>STAT3</strong> Activation.
+STAT3	drug	alcohol	31931878	Mesenchymal stem cells alleviate liver injury induced by chronic binge <b>ethanol</b> feeding in mice via release of TSG6 and suppression of <strong>STAT3</strong> activation.
+STAT3	addiction	intoxication	31931878	Mesenchymal stem cells alleviate liver injury induced by chronic <b>binge</b> ethanol feeding in mice via release of TSG6 and suppression of <strong>STAT3</strong> activation.
+STAT3	drug	opioid	31751616	Additionally, repeated context exposure with <b>morphine</b> conditioning increased the phosphorylation of <strong>STAT3</strong> and the acetylation of histone H4 in CXCL12 expressing neurons in CA1.
+STAT3	drug	opioid	31751616	Immunoprecipitation and chromatin immunoprecipitation assays demonstrated that repeated context exposure with <b>morphine</b> conditioning increased the binding of <strong>STAT3</strong> to the CXCL12 gene promoter and the interaction between <strong>STAT3</strong> and p300, which contributed to the enhanced transcription of CXCL12 by increasing the acetylation of histone H4 in the CXCL12 gene promoter.
+STAT3	drug	alcohol	31334440	Deficient IL 6/<strong>Stat3</strong> Signaling, High TLR7, and Type I Interferons in Early Human <b>Alcoholic</b> Liver Disease: A Triad for Liver Damage and Fibrosis.
+STAT3	drug	alcohol	31334440	Conclusion: In humans, inflammation, activation of the TLR7 IFN axis, and inhibition of <strong>Stat3</strong> dependent repair mechanisms in early <b>alcoholic</b> liver disease pave the way for fibrosis development and ultimately disease progression.
+STAT3	drug	alcohol	31321478	S100A4 promotes inflammation but suppresses lipid accumulation via the <strong>STAT3</strong> pathway in chronic <b>ethanol</b> induced fatty liver.
+STAT3	drug	alcohol	31321478	Further mechanistic studies have found that S100A4 promotes early <b>alcoholic</b> hepatitis mainly by activating the <strong>STAT3</strong> pathway and its downstream proinflammatory gene expression.
+STAT3	drug	alcohol	31321478	Further mechanistic studies have found that S100A4 promotes early <b>alcoholic</b> hepatitis mainly by activating the <strong>STAT3</strong> pathway and its downstream proinflammatory gene expression.
+STAT3	addiction	reward	30634502	We found that LDOC1 deficiency led to <b>reinforcing</b> a reciprocal loop of IL 6/JAK2/<strong>STAT3</strong>, through which LDOC1 mediates the cancer progression.
+STAT3	drug	nicotine	30634502	Overall, our results elucidated a crucial role of LDOC1 in lung cancer and revealed how LDOC1 acts as a bridge between <b>tobacco</b> exposure and the IL 6/JAK2/<strong>STAT3</strong> loop in this human malignancy.
+STAT3	drug	alcohol	30237578	Astaxanthin alleviated <b>ethanol</b> induced liver injury by inhibition of oxidative stress and inflammatory responses via blocking of <strong>STAT3</strong> activity.
+STAT3	drug	alcohol	30237578	Therefore, these results suggest that AXT could prevent <b>ethanol</b> induced hepatic injury via inhibition of oxidant and inflammatory responses via blocking of <strong>STAT3</strong> activity.
+STAT3	drug	opioid	29715476	In addition, molecular analysis revealed that <b>morphine</b> conditioning increased the occupancy of p <strong>STAT3</strong> in the specific binding site ( 1667/ 1685) of CXCL12 promoter regions, and enhanced the interaction between acetyltransferase p300 and <strong>STAT3</strong>, and, hence, induced the histone H4 hyperacetylation in the promoter region and facilitated the transcription and expression of CXCL12 in VTA.
+STAT3	drug	opioid	28827130	Activation of TLR4/<strong>STAT3</strong> signaling in VTA contributes to the acquisition and maintenance of <b>morphine</b> induced conditioned place preference.
+STAT3	drug	opioid	28827130	In addition, chronic <b>morphine</b> treatment significantly activated <strong>STAT3</strong> on day 6 and 11 in VTA, and bilateral microinjection of <strong>STAT3</strong> inhibitor S3I 201 into the VTA suppressed the acquisition and maintenance of <b>morphine</b> induced CPP in rats.
+STAT3	addiction	reward	28827130	In addition, chronic morphine treatment significantly activated <strong>STAT3</strong> on day 6 and 11 in VTA, and bilateral microinjection of <strong>STAT3</strong> inhibitor S3I 201 into the VTA suppressed the acquisition and maintenance of morphine induced <b>CPP</b> in rats.
+STAT3	drug	opioid	28827130	Furthermore, local knockout of <strong>STAT3</strong> by injection of the AAV Cre GFP into the VTA area of STAT3flox/flox mice also significantly impaired the acquisition of <b>morphine</b> CPP.
+STAT3	addiction	reward	28827130	Furthermore, local knockout of <strong>STAT3</strong> by injection of the AAV Cre GFP into the VTA area of STAT3flox/flox mice also significantly impaired the acquisition of morphine <b>CPP</b>.
+STAT3	drug	opioid	28827130	Importantly, the TLR4 expression is colocalized with p <strong>STAT3</strong> positive cell in VTA, and repeated injection of LPS RS significantly attenuated the <strong>STAT3</strong> activation in VTA induced by chronic <b>morphine</b> treatment.
+STAT3	drug	opioid	28827130	Collectively, these data suggest that TLR4/<strong>STAT3</strong> signaling pathway in VTA might play a critical role in the acquisition and maintenance of <b>morphine</b> CPP, and provides new evidence that TLR4/<strong>STAT3</strong> signaling pathway might be a potential target for treatment of <b>morphine</b> addiction.
+STAT3	addiction	addiction	28827130	Collectively, these data suggest that TLR4/<strong>STAT3</strong> signaling pathway in VTA might play a critical role in the acquisition and maintenance of morphine CPP, and provides new evidence that TLR4/<strong>STAT3</strong> signaling pathway might be a potential target for treatment of morphine <b>addiction</b>.
+STAT3	addiction	reward	28827130	Collectively, these data suggest that TLR4/<strong>STAT3</strong> signaling pathway in VTA might play a critical role in the acquisition and maintenance of morphine <b>CPP</b>, and provides new evidence that TLR4/<strong>STAT3</strong> signaling pathway might be a potential target for treatment of morphine addiction.
+STAT3	drug	nicotine	28750889	Reciprocal activation of α5 nAChR and <strong>STAT3</strong> in <b>nicotine</b> induced human lung cancer cell proliferation.
+STAT3	drug	nicotine	28750889	In the present study, we demonstrate that the expression of α5 nAChR is correlated with phosphorylated <strong>STAT3</strong> (pSTAT3) expression, <b>smoking</b> history and lower survival of non small cell lung cancer (NSCLC) samples.
+STAT3	drug	nicotine	28750889	<b>Nicotine</b> increased the levels of α5 nAChR mRNA and protein in NSCLC cell lines and activated the JAK2/<strong>STAT3</strong> signaling cascade.
+STAT3	drug	nicotine	28750889	<b>Nicotine</b> induced activation of JAK2/<strong>STAT3</strong> signaling was inhibited by the silencing of α5 nAChR.
+STAT3	drug	nicotine	28750889	By silencing <strong>STAT3</strong> expression, <b>nicotine</b> induced upregulation of α5 nAChR was suppressed.
+STAT3	drug	nicotine	28750889	Downregulation of α5 nAChR and/or <strong>STAT3</strong> expression inhibited <b>nicotine</b> induced lung cancer cell proliferation.
+STAT3	drug	nicotine	28750889	These results suggest that there is a feedback loop between α5 nAChR and <strong>STAT3</strong> that contributes to the <b>nicotine</b> induced tumor cell proliferation, which indicates that α5 nAChR is an important therapeutic target involved in <b>tobacco</b> associated lung carcinogenesis.
+STAT3	drug	alcohol	28498296	Knockout of signal transducer and activator of transcription factor 3 (<strong>STAT3</strong>) in intestine epithelial cells resulted in complete loss of IL 22 protection, demonstrating that <strong>STAT3</strong> is required for intestine barrier protection following <b>ethanol</b> combined with injury.
+STAT3	drug	cocaine	27922639	In addition, prior exposure to saccharin increased LepR mRNA and <strong>STAT3</strong> phosphorylation in the NAc and VTA and impaired <b>cocaine</b> CPP.
+STAT3	addiction	reward	27922639	In addition, prior exposure to saccharin increased LepR mRNA and <strong>STAT3</strong> phosphorylation in the NAc and VTA and impaired cocaine <b>CPP</b>.
+STAT3	drug	alcohol	27901267	Similarly, the combination of <b>alcohol</b> and hypergravity suppressed the levels of <strong>STAT3</strong>, FOXO1/3, C/EBPβ, and CREB, transcription factors necessary for cell survival.
+STAT3	drug	alcohol	26206265	We also assessed activation of ALK by <b>ethanol</b> in cells and found that ALK and ALK dependent extracellular signal regulated kinase (ERK) and signal transducer and activator of transcription 3 (<strong>STAT3</strong>) phosphorylation increased rapidly with <b>ethanol</b> exposure.
+STAT3	drug	alcohol	26206265	We also assessed activation of ALK by <b>ethanol</b> in cells and found that ALK and ALK dependent extracellular signal regulated kinase (ERK) and <strong>signal transducer and activator of transcription 3</strong> (<strong>STAT3</strong>) phosphorylation increased rapidly with <b>ethanol</b> exposure.
+STAT3	drug	alcohol	26206265	Similarly, treatment of cells with recombinant MDK protein increased ALK, ERK and <strong>STAT3</strong> phosphorylation, suggesting that <b>ethanol</b> may utilize MDK to activate ALK signaling.
+STAT3	drug	alcohol	24710718	We hypothesized that Cav 1 could attenuate <b>ethanol</b> mediated nitrosative stress and liver damage through regulating epidermal growth factor receptor/signal transducer and activator of transcription 3/inducible nitric oxide synthase (EGFR/<strong>STAT3</strong>/iNOS) signaling cascades.
+STAT3	drug	alcohol	24710718	We hypothesized that Cav 1 could attenuate <b>ethanol</b> mediated nitrosative stress and liver damage through regulating epidermal growth factor receptor/<strong>signal transducer and activator of transcription 3</strong>/inducible nitric oxide synthase (EGFR/<strong>STAT3</strong>/iNOS) signaling cascades.
+STAT3	drug	alcohol	24710718	Furthermore, the results revealed that the <b>ethanol</b> mediated Cav 1 increase was in an extracellular signal regulated kinase dependent manner, and Cav 1 protected hepatocytes from <b>ethanol</b> mediated apoptosis by inhibiting iNOS activity and regulating EGFR  and <strong>STAT3</strong> signaling cascades.
+STAT3	drug	alcohol	24710718	Cav 1 could be a cellular defense protein against <b>alcoholic</b> hepatic injury through inhibiting reactive nitrogen species and regulating EGFR/<strong>STAT3</strong>/iNOS signaling cascades.
+STAT3	drug	nicotine	24668500	<b>Nicotine</b> promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell like properties via a signaling cascade involving galectin 3, α9 nicotinic acetylcholine receptor and <strong>STAT3</strong>.
+STAT3	drug	nicotine	24668500	<b>Nicotine</b> induced up regulation of galectin 3 is due to an increased expression of α9 isoform of nicotinic acetylcholine receptor (α9nAChR), which activates transcription factor <strong>STAT3</strong> that in turn, physically binds to galectin 3 (LGALS3) promoter and induces transcription of galectin 3.
+STAT3	drug	nicotine	24668500	Moreover, <b>nicotine</b> induced enrichment of side population cells with cancer stem cell like properties was modulated by galectin 3 expression and could be significantly reduced by transient knock down of LGALS3 and its upstream signaling molecules <strong>STAT3</strong> and α9nAChR.
+STAT3	drug	nicotine	24668500	Thus, galectin 3 or its upstream signaling molecule <strong>STAT3</strong> or α9nAChR could be a potential target to prevent <b>nicotine</b> induced chemoresistance in breast cancer.
+STAT3	drug	alcohol	24421048	Therefore, acute <b>alcohol</b> intoxication leads to decreased MRSA clearance in part by inhibiting IL 6/<strong>STAT3</strong> induction of the antimicrobial protein Reg3γ in the pulmonary epithelium.
+STAT3	addiction	intoxication	24421048	Therefore, acute alcohol <b>intoxication</b> leads to decreased MRSA clearance in part by inhibiting IL 6/<strong>STAT3</strong> induction of the antimicrobial protein Reg3γ in the pulmonary epithelium.
+STAT3	drug	nicotine	22300039	The nonneuronal α7 nicotinic cholinergic receptors are a primary target for <b>nicotine</b> through the JAK2 and <strong>STAT3</strong>/NF κB pathways, ultimately mediating the inhibition of pro inflammatory gene transcription.
+STAT3	drug	alcohol	21357267	<b>Alcohol</b> suppresses the granulopoietic response to pulmonary Streptococcus pneumoniae infection with enhancement of <strong>STAT3</strong> signaling.
+STAT3	drug	alcohol	21357267	<b>Alcohol</b> treatment significantly enhanced <strong>STAT3</strong> phosphorylation in bone marrow cells of animals challenged with S. pneumoniae.
+STAT3	drug	alcohol	21357267	In vitro experiments showed that G CSF induced activation of <strong>STAT3</strong> p27(Kip1) pathway in murine myeloid progenitor cell line 32D G CSFR cells was markedly enhanced by <b>alcohol</b> exposure.
+STAT3	drug	alcohol	21357267	These data suggest that <b>alcohol</b> enhances G CSF associated <strong>STAT3</strong> p27(Kip1) signaling, which impairs granulopoietic progenitor cell proliferation by inducing cell cycling arrest and facilitating their terminal differentiation during the granulopoietic response to pulmonary infection.
+STAT3	drug	alcohol	20842630	Interleukin 22 treatment ameliorates <b>alcoholic</b> liver injury in a murine model of chronic binge <b>ethanol</b> feeding: role of <strong>signal transducer and activator of transcription 3</strong>.
+STAT3	addiction	intoxication	20842630	Interleukin 22 treatment ameliorates alcoholic liver injury in a murine model of chronic <b>binge</b> ethanol feeding: role of <strong>signal transducer and activator of transcription 3</strong>.
+STAT3	drug	alcohol	20842630	Using this model, we demonstrate that treatment with IL 22 recombinant protein activates hepatic signal transducer and activator of transcription 3 (<strong>STAT3</strong>) and ameliorates <b>alcoholic</b> fatty liver, liver injury, and hepatic oxidative stress.
+STAT3	drug	alcohol	20842630	Using this model, we demonstrate that treatment with IL 22 recombinant protein activates hepatic <strong>signal transducer and activator of transcription 3</strong> (<strong>STAT3</strong>) and ameliorates <b>alcoholic</b> fatty liver, liver injury, and hepatic oxidative stress.
+STAT3	drug	alcohol	20842630	Deletion of <strong>STAT3</strong> in hepatocytes abolishes the hepatoprotection provided by IL 22 in <b>alcoholic</b> liver injury.
+STAT3	drug	nicotine	20106947	Long term <b>nicotine</b> exposure induced chemoresistance is mediated by activation of <strong>Stat3</strong> and downregulation of ERK1/2 via nAChR and beta adrenoceptors in human bladder cancer cells.
+STAT3	drug	nicotine	20106947	The objective of this study was to identify the role of <strong>Stat3</strong> in chemoresistance induced by <b>nicotine</b> in human bladder cancer cell line, T24 cells.
+STAT3	drug	nicotine	20106947	We provide evidence for the first time that <b>nicotine</b> strongly activated <strong>Stat3</strong>, leading to Cyclin D1 overexpression, cell cycle perturbations, and chemoresistance.
+STAT3	drug	nicotine	20106947	Furthermore, <b>nicotine</b> mobilized <strong>Stat3</strong> signaling, resulting in the loss of extracellular signal regulated protein kinase 1/2 (ERK 1/2) activation and reduced chemosensitivity via nicotinic acetylcholine receptors and beta adrenoceptors.
+STAT3	drug	nicotine	20106947	<strong>Stat3</strong> could be the major target for increasing chemosensitivity in patients who develop chemoresistance during chemotherapy, and avoidance of cigarette <b>smoking</b> or <b>nicotine</b> based treatments may increase the efficacy of chemotherapy.
+STAT3	drug	alcohol	20052772	Although IL 10 receptor surface expression on Kupffer cells was not affected by <b>ethanol</b> feeding, IL 10 mediated phosphorylation of <strong>STAT3</strong> and expression of HO 1 was higher in Kupffer cells after <b>ethanol</b> feeding.
+STAT3	drug	alcohol	12130710	Also using immunohistochemistry to identify potential intracellular mechanisms associated with <b>alcohol</b> induced c Fos expression in Edinger Westphal, we show time dependent increases in serine 727 phospho signal transducer and activator of transcription 3 (<strong>Stat3</strong>) but no changes in phospho cAMP response element binding protein and phospho Elk1.
+STAT3	drug	alcohol	12130710	Also using immunohistochemistry to identify potential intracellular mechanisms associated with <b>alcohol</b> induced c Fos expression in Edinger Westphal, we show time dependent increases in serine 727 phospho <strong>signal transducer and activator of transcription 3</strong> (<strong>Stat3</strong>) but no changes in phospho cAMP response element binding protein and phospho Elk1.
+STAT3	drug	alcohol	12130710	Finally, blockade of ERK 1/2 phosphorylation with the mitogen activated protein kinase (MEK) 1/2 inhibitor SL327 blocked <b>alcohol</b> induced c Fos expression, suggesting that <b>alcohol</b> induces c Fos in Edinger Westphal neurons through activation of the MEK1/2 ERK1/2 <strong>Stat3</strong> pathway.
+SIRT1	drug	cocaine	31993108	Nicotinamide phosphoribosyltransferase contributes to <b>cocaine</b> addiction through <strong>sirtuin 1</strong>.
+SIRT1	addiction	addiction	31993108	Nicotinamide phosphoribosyltransferase contributes to cocaine <b>addiction</b> through <strong>sirtuin 1</strong>.
+SIRT1	drug	cocaine	31993108	A recent study published in Experimental Neurology by Cen group demonstrated that NAMPT contributes to <b>cocaine</b> reward through sirtuin 1 (<strong>SIRT1</strong>) signaling in the brain ventral tegmental area.
+SIRT1	addiction	reward	31993108	A recent study published in Experimental Neurology by Cen group demonstrated that NAMPT contributes to cocaine <b>reward</b> through sirtuin 1 (<strong>SIRT1</strong>) signaling in the brain ventral tegmental area.
+SIRT1	drug	cocaine	31993108	A recent study published in Experimental Neurology by Cen group demonstrated that NAMPT contributes to <b>cocaine</b> reward through <strong>sirtuin 1</strong> (<strong>SIRT1</strong>) signaling in the brain ventral tegmental area.
+SIRT1	addiction	reward	31993108	A recent study published in Experimental Neurology by Cen group demonstrated that NAMPT contributes to cocaine <b>reward</b> through <strong>sirtuin 1</strong> (<strong>SIRT1</strong>) signaling in the brain ventral tegmental area.
+SIRT1	drug	cocaine	31993108	Thus, targeting NAMPT/<strong>SIRT1</strong> signaling pathway may provide a promising therapeutic strategy against <b>cocaine</b> addiction.
+SIRT1	addiction	addiction	31993108	Thus, targeting NAMPT/<strong>SIRT1</strong> signaling pathway may provide a promising therapeutic strategy against cocaine <b>addiction</b>.
+SIRT1	drug	alcohol	31610175	Intestinal <strong>SIRT1</strong> Deficiency Protects Mice from <b>Ethanol</b> Induced Liver Injury by Mitigating Ferroptosis.
+SIRT1	drug	alcohol	31610175	Aberrant liver sirtuin 1 (<strong>SIRT1</strong>), a mammalian NAD+ dependent protein deacetylase, is implicated in the pathogenesis of <b>alcoholic</b> liver disease (ALD).
+SIRT1	drug	alcohol	31610175	Aberrant liver <strong>sirtuin 1</strong> (<strong>SIRT1</strong>), a mammalian NAD+ dependent protein deacetylase, is implicated in the pathogenesis of <b>alcoholic</b> liver disease (ALD).
+SIRT1	drug	alcohol	31610175	This study investigated the involvement of intestine specific <strong>SIRT1</strong> in <b>ethanol</b> induced liver dysfunction in mice.
+SIRT1	drug	alcohol	31610175	<b>Ethanol</b> feeding studies were performed on knockout mice with intestinal specific <strong>SIRT1</strong> deletion [SIRT1i knockout (KO)] and flox control [wild type (WT)] mice with a chronic plus binge <b>ethanol</b> feeding protocol.
+SIRT1	addiction	intoxication	31610175	Ethanol feeding studies were performed on knockout mice with intestinal specific <strong>SIRT1</strong> deletion [SIRT1i knockout (KO)] and flox control [wild type (WT)] mice with a chronic plus <b>binge</b> ethanol feeding protocol.
+SIRT1	drug	alcohol	31610175	After <b>ethanol</b> administration, hepatic inflammation and liver injury were substantially attenuated in the SIRT1iKO mice compared with the WT mice, suggesting that intestinal <strong>SIRT1</strong> played a detrimental role in the <b>ethanol</b> induced liver injury.
+SIRT1	drug	alcohol	31610175	Mechanistically, the hepatic protective effect of intestinal <strong>SIRT1</strong> deficiency was attributable to ameliorated dysfunctional iron metabolism, increased hepatic glutathione contents, and attenuated lipid peroxidation, along with inhibition of a panel of genes implicated in the ferroptosis process in the livers of <b>ethanol</b> fed mice.
+SIRT1	drug	alcohol	31610175	This study demonstrates that ablation of intestinal <strong>SIRT1</strong> protected mice from the <b>ethanol</b> induced inflammation and liver damage.
+SIRT1	drug	alcohol	31167126	<b>Ethanol</b> challenge upregulated autophagy (p < 0.001), promoted AMPK phosphorylation and <strong>Sirt1</strong> levels (p < 0.003) while suppressing mTOR phosphorylation and Skp2 levels (p < 0.02).
+SIRT1	drug	alcohol	31167126	Moreover, the CD74 ablation offered beneficial effects against <b>ethanol</b> induced cardiomyocyte dysfunction, and GFP Puncta formation were nullified by the AMPK activator AICAR, the Skp2 inhibitor C1 or the <strong>Sirt1</strong> activator SRT1720 (p < 0.0001).
+SIRT1	drug	alcohol	31141180	These results demonstrated that 5 ALA/SFC treatment ameliorated binge <b>alcohol</b> exposure liver injury in a rat model of HIV infected patients by reducing macrophage activation and expression of inflammatory cytokines/chemokines, and by inducing HO 1, HO 2, and <strong>Sirt1</strong> expression.
+SIRT1	addiction	intoxication	31141180	These results demonstrated that 5 ALA/SFC treatment ameliorated <b>binge</b> alcohol exposure liver injury in a rat model of HIV infected patients by reducing macrophage activation and expression of inflammatory cytokines/chemokines, and by inducing HO 1, HO 2, and <strong>Sirt1</strong> expression.
+SIRT1	addiction	sensitization	30721374	L Serine induced mitochondrial gene expression, fatty acid oxidation, and insulin <b>sensitization</b> were mediated by enhanced <strong>SIRT1</strong> activity, which was verified by selective <strong>SIRT1</strong> inhibitor (Ex 527) and siRNA directed to <strong>SIRT1</strong>.
+SIRT1	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids <strong>SIRT1</strong> sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+SIRT1	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 heme oxygenase 1; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids <strong>SIRT1</strong> <strong>sirtuin 1</strong> SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+SIRT1	drug	nicotine	30504847	Using western blot, we confirmed downregulation of <strong>SIRT1</strong> and increased cleaved caspase 3 expression in the brains of <b>nicotine</b> exposed female rats and no change in expression levels in the other groups.
+SIRT1	drug	nicotine	30504847	Collectively, our findings highlight a miR 199/214 regulatory network that, through <strong>SIRT1</strong>, may be associated with <b>nicotine</b> seeking in females which may serve as a potential therapeutic target for sex specific treatment approaches.
+SIRT1	addiction	relapse	30504847	Collectively, our findings highlight a miR 199/214 regulatory network that, through <strong>SIRT1</strong>, may be associated with nicotine <b>seeking</b> in females which may serve as a potential therapeutic target for sex specific treatment approaches.
+SIRT1	drug	alcohol	30200508	Finally, GN administration promoted hepatic sirtuin1 (<strong>SIRT1</strong>) AMP activated protein kinase (AMPK) signaling in <b>ethanol</b> fed mice.
+SIRT1	drug	alcohol	30200508	Finally, GN administration promoted hepatic <strong>sirtuin1</strong> (<strong>SIRT1</strong>) AMP activated protein kinase (AMPK) signaling in <b>ethanol</b> fed mice.
+SIRT1	drug	alcohol	30200508	Moreover, GN prevented <b>ethanol</b> mediated reduction in <strong>SIRT1</strong> and phosphorylated AMPK.
+SIRT1	drug	opioid	29870523	Effect of <strong>Sirtuin 1</strong> on Synaptic Plasticity in Nucleus Accumbens in a Rat Model of <b>Heroin</b> Addiction.
+SIRT1	addiction	addiction	29870523	Effect of <strong>Sirtuin 1</strong> on Synaptic Plasticity in Nucleus Accumbens in a Rat Model of Heroin <b>Addiction</b>.
+SIRT1	drug	opioid	29870523	MATERIAL AND METHODS <b>Heroin</b> addiction, <strong>SIRT1</strong> overexpression, and <strong>SIRT1</strong> silenced rat models were established.
+SIRT1	addiction	addiction	29870523	MATERIAL AND METHODS Heroin <b>addiction</b>, <strong>SIRT1</strong> overexpression, and <strong>SIRT1</strong> silenced rat models were established.
+SIRT1	drug	opioid	29870523	RESULTS <b>Naloxone</b> withdrawal symptoms appeared in the <strong>SIRT1</strong> overexpression group.
+SIRT1	addiction	withdrawal	29870523	RESULTS Naloxone <b>withdrawal</b> symptoms appeared in the <strong>SIRT1</strong> overexpression group.
+SIRT1	drug	opioid	29870523	Immunohistochemistry and Western blotting results showed that FOXO1 expression decreased in the <b>heroin</b> addiction (HA) group but increased in the <strong>SIRT1</strong> silenced group (p<0.05).
+SIRT1	addiction	addiction	29870523	Immunohistochemistry and Western blotting results showed that FOXO1 expression decreased in the heroin <b>addiction</b> (HA) group but increased in the <strong>SIRT1</strong> silenced group (p<0.05).
+SIRT1	drug	opioid	29870523	CONCLUSIONS <strong>SIRT1</strong> and other synaptic plasticity related genes in NAc are involved in the regulation of <b>heroin</b> addiction.
+SIRT1	addiction	addiction	29870523	CONCLUSIONS <strong>SIRT1</strong> and other synaptic plasticity related genes in NAc are involved in the regulation of heroin <b>addiction</b>.
+SIRT1	addiction	sensitization	29870523	<strong>SIRT1</strong> overexpression can increase behavioral <b>sensitization</b> in the NAc of rats, and <strong>SIRT1</strong> silencing might ease withdrawal symptoms and reduce conditioned place preferences.
+SIRT1	addiction	withdrawal	29870523	<strong>SIRT1</strong> overexpression can increase behavioral sensitization in the NAc of rats, and <strong>SIRT1</strong> silencing might ease <b>withdrawal</b> symptoms and reduce conditioned place preferences.
+SIRT1	drug	cocaine	29753648	Nicotinamide phosphoribosyltransferase regulates <b>cocaine</b> reward through <strong>Sirtuin 1</strong>.
+SIRT1	addiction	reward	29753648	Nicotinamide phosphoribosyltransferase regulates cocaine <b>reward</b> through <strong>Sirtuin 1</strong>.
+SIRT1	drug	cocaine	29753648	Using 1H nuclear magnetic resonance metabolomic analysis, we found that the content of NAD and NMN were increased in the VTA of <b>cocaine</b> conditioned mice; moreover, the expression of <strong>SIRT1</strong> was also upregulated.
+SIRT1	drug	cocaine	29753648	Interestingly, the inhibitory effect of FK866 on <b>cocaine</b> reward was significantly weakened in <strong>Sirt1</strong> midbrain conditional knockout mice.
+SIRT1	addiction	reward	29753648	Interestingly, the inhibitory effect of FK866 on cocaine <b>reward</b> was significantly weakened in <strong>Sirt1</strong> midbrain conditional knockout mice.
+SIRT1	drug	cocaine	29753648	Our results suggest that NAMPT mediated NAD biosynthesis may modify <b>cocaine</b> behavioral effects through <strong>SIRT1</strong>.
+SIRT1	drug	cocaine	29753648	Moreover, our findings reveal that the interplay between NAD biosynthesis and <strong>SIRT1</strong> regulation may comprise a novel regulatory pathway that responds to chronic <b>cocaine</b> stimuli.
+SIRT1	drug	cocaine	29728703	NAD+ cellular redox and <strong>SIRT1</strong> regulate the diurnal rhythms of tyrosine hydroxylase and conditioned <b>cocaine</b> reward.
+SIRT1	addiction	reward	29728703	NAD+ cellular redox and <strong>SIRT1</strong> regulate the diurnal rhythms of tyrosine hydroxylase and conditioned cocaine <b>reward</b>.
+SIRT1	drug	cocaine	29728703	Furthermore, CLOCK and <strong>SIRT1</strong> are important for regulating <b>cocaine</b> reward and dopaminergic (DAergic) activity, with interesting differences depending on whether DAergic activity is in a heightened state and if there is a functional CLOCK protein.
+SIRT1	addiction	reward	29728703	Furthermore, CLOCK and <strong>SIRT1</strong> are important for regulating cocaine <b>reward</b> and dopaminergic (DAergic) activity, with interesting differences depending on whether DAergic activity is in a heightened state and if there is a functional CLOCK protein.
+SIRT1	drug	alcohol	29457836	Aberrant activation of mTORC1 was likely attributed to the defects of the DEP domain containing mTOR interacting protein (DEPTOR) and the nicotinamide adenine dinucleotide dependent deacetylase sirtuin 1 (<strong>SIRT1</strong>) in the liver of chronic plus binge <b>ethanol</b> fed mice and in the liver of patients with ALD.
+SIRT1	addiction	intoxication	29457836	Aberrant activation of mTORC1 was likely attributed to the defects of the DEP domain containing mTOR interacting protein (DEPTOR) and the nicotinamide adenine dinucleotide dependent deacetylase sirtuin 1 (<strong>SIRT1</strong>) in the liver of chronic plus <b>binge</b> ethanol fed mice and in the liver of patients with ALD.
+SIRT1	drug	alcohol	29457836	Aberrant activation of mTORC1 was likely attributed to the defects of the DEP domain containing mTOR interacting protein (DEPTOR) and the nicotinamide adenine dinucleotide dependent deacetylase <strong>sirtuin 1</strong> (<strong>SIRT1</strong>) in the liver of chronic plus binge <b>ethanol</b> fed mice and in the liver of patients with ALD.
+SIRT1	addiction	intoxication	29457836	Aberrant activation of mTORC1 was likely attributed to the defects of the DEP domain containing mTOR interacting protein (DEPTOR) and the nicotinamide adenine dinucleotide dependent deacetylase <strong>sirtuin 1</strong> (<strong>SIRT1</strong>) in the liver of chronic plus <b>binge</b> ethanol fed mice and in the liver of patients with ALD.
+SIRT1	drug	alcohol	29457836	Furthermore, hepatocyte specific deletion of <strong>SIRT1</strong> disrupted DEPTOR function, enhanced mTORC1 activity, and exacerbated <b>alcoholic</b> fatty liver, inflammation, and liver injury in mice.
+SIRT1	drug	alcohol	28466267	17β Estradiol via <strong>SIRT1</strong>/Acetyl p53/NF kB Signaling Pathway Rescued Postnatal Rat Brain Against Acute <b>Ethanol</b> Intoxication.
+SIRT1	addiction	intoxication	28466267	17β Estradiol via <strong>SIRT1</strong>/Acetyl p53/NF kB Signaling Pathway Rescued Postnatal Rat Brain Against Acute Ethanol <b>Intoxication</b>.
+SIRT1	drug	alcohol	28466267	Whether it can stimulate <strong>SIRT1</strong> signaling against <b>ethanol</b> intoxicity in developing brain remain elusive.
+SIRT1	drug	alcohol	28466267	Here, we report for the first time that 17β estradiol activated <strong>SIRT1</strong> to deacetylate p53 proteins against acute <b>ethanol</b> induced oxidative stress, neuroinflammation, and neurodegeneration.
+SIRT1	drug	alcohol	28466267	Interestingly, <strong>SIRT1</strong> inhibition with its inhibitor, i.e., EX527 further enhanced <b>ethanol</b> intoxication and also abolished the beneficial effects of 17β estradiol against <b>ethanol</b> in the young rat's brain.
+SIRT1	addiction	intoxication	28466267	Interestingly, <strong>SIRT1</strong> inhibition with its inhibitor, i.e., EX527 further enhanced ethanol <b>intoxication</b> and also abolished the beneficial effects of 17β estradiol against ethanol in the young rat's brain.
+SIRT1	drug	alcohol	27871879	Aging aggravates <b>alcoholic</b> liver injury and fibrosis in mice by downregulating <strong>sirtuin 1</strong> expression.
+SIRT1	drug	alcohol	27871879	Restoration of <strong>SIRT1</strong> expression via the administration of adenovirus <strong>SIRT1</strong> vector ameliorated short term plus binge <b>ethanol</b> induced liver injury and fibrosis in middle aged mice.
+SIRT1	addiction	intoxication	27871879	Restoration of <strong>SIRT1</strong> expression via the administration of adenovirus <strong>SIRT1</strong> vector ameliorated short term plus <b>binge</b> ethanol induced liver injury and fibrosis in middle aged mice.
+SIRT1	drug	alcohol	27871879	Finally, HSC specific <strong>SIRT1</strong> knockout mice were more susceptible to long term chronic plus multiple binges of <b>ethanol</b> induced liver fibrosis with upregulation of PDGFR α expression.
+SIRT1	drug	alcohol	27871879	Aged mice are more susceptible to <b>alcohol</b> induced liver injury and fibrosis, which is, at least in part, due to lower levels of <strong>sirtuin 1</strong> protein in hepatocytes and hepatic stellate cells.
+SIRT1	drug	alcohol	27871879	Our findings suggest that <strong>sirtuin 1</strong> activators may have beneficial effects for the treatment of <b>alcoholic</b> liver disease in aged patients.
+SIRT1	drug	alcohol	27170122	Sir2/<strong>Sirt1</strong> Links Acute Inebriation to Presynaptic Changes and the Development of <b>Alcohol</b> Tolerance, Preference, and Reward.
+SIRT1	addiction	reward	27170122	Sir2/<strong>Sirt1</strong> Links Acute Inebriation to Presynaptic Changes and the Development of Alcohol Tolerance, Preference, and <b>Reward</b>.
+SIRT1	drug	alcohol	27170122	<strong>Sir2</strong>/<strong>Sirt1</strong> Links Acute Inebriation to Presynaptic Changes and the Development of <b>Alcohol</b> Tolerance, Preference, and Reward.
+SIRT1	addiction	reward	27170122	<strong>Sir2</strong>/<strong>Sirt1</strong> Links Acute Inebriation to Presynaptic Changes and the Development of Alcohol Tolerance, Preference, and <b>Reward</b>.
+SIRT1	drug	alcohol	27170122	<b>Ethanol</b> markedly changes histone acetylation, and the sirtuin Sir2/<strong>SIRT1</strong> that deacetylates histones and transcription factors is essential for the rewarding effects of long term drug use.
+SIRT1	drug	alcohol	27170122	<b>Ethanol</b> markedly changes histone acetylation, and the sirtuin <strong>Sir2</strong>/<strong>SIRT1</strong> that deacetylates histones and transcription factors is essential for the rewarding effects of long term drug use.
+SIRT1	drug	alcohol	27170122	We find that <strong>Sir2</strong> in the mushroom bodies of the fruit fly Drosophila promotes short term <b>ethanol</b> induced behavioral plasticity by allowing changes in the expression of presynaptic molecules.
+SIRT1	drug	alcohol	27170122	Flies lacking <strong>Sir2</strong> globally, in the adult nervous system, or specifically in the mushroom body α/β lobes show reduced <b>ethanol</b> sensitivity and tolerance.
+SIRT1	drug	alcohol	27170122	<strong>Sir2</strong> dependent <b>ethanol</b> reward is also localized to the mushroom bodies, and <strong>Sir2</strong> mutants prefer <b>ethanol</b> even without a priming <b>ethanol</b> pre exposure.
+SIRT1	addiction	reward	27170122	<strong>Sir2</strong> dependent ethanol <b>reward</b> is also localized to the mushroom bodies, and <strong>Sir2</strong> mutants prefer ethanol even without a priming ethanol pre exposure.
+SIRT1	drug	alcohol	27170122	Transcriptomic analysis reveals that specific presynaptic molecules, including the synaptic vesicle pool regulator Synapsin, depend on <strong>Sir2</strong> to be regulated by <b>ethanol</b>.
+SIRT1	drug	alcohol	27170122	We propose that the regulation of Sir2/<strong>SIRT1</strong> by acute inebriation forms part of a transcriptional program in mushroom body neurons to alter presynaptic properties and neural responses to favor the development of <b>ethanol</b> tolerance, preference, and reward.
+SIRT1	addiction	reward	27170122	We propose that the regulation of Sir2/<strong>SIRT1</strong> by acute inebriation forms part of a transcriptional program in mushroom body neurons to alter presynaptic properties and neural responses to favor the development of ethanol tolerance, preference, and <b>reward</b>.
+SIRT1	drug	alcohol	27170122	We propose that the regulation of <strong>Sir2</strong>/<strong>SIRT1</strong> by acute inebriation forms part of a transcriptional program in mushroom body neurons to alter presynaptic properties and neural responses to favor the development of <b>ethanol</b> tolerance, preference, and reward.
+SIRT1	addiction	reward	27170122	We propose that the regulation of <strong>Sir2</strong>/<strong>SIRT1</strong> by acute inebriation forms part of a transcriptional program in mushroom body neurons to alter presynaptic properties and neural responses to favor the development of ethanol tolerance, preference, and <b>reward</b>.
+SIRT1	drug	cocaine	26790673	Levels of MDA and TNFα in PFC, and levels of MDA, SOD, GSH, IL 6, IL 1β, TNFα, caspase 3 and BAX in HP, but not <strong>SIRT1</strong> expression in both regions were significantly changed during <b>cocaine</b> withdrawal period.
+SIRT1	addiction	withdrawal	26790673	Levels of MDA and TNFα in PFC, and levels of MDA, SOD, GSH, IL 6, IL 1β, TNFα, caspase 3 and BAX in HP, but not <strong>SIRT1</strong> expression in both regions were significantly changed during cocaine <b>withdrawal</b> period.
+SIRT1	drug	cocaine	26790673	Furthermore, RSV induced a greater upregulation of <strong>SIRT1</strong> expression in PFC in <b>cocaine</b> withdrawn rats than that in saline controls.
+SIRT1	drug	cocaine	26790673	Oxidative stress, inflammation, apoptosis, and <strong>SIRT1</strong> signaling pathway in HP or PFC might be involved in mediating effects of RSV on behaviors in <b>cocaine</b> withdrawn rats.
+SIRT1	drug	alcohol	26776965	Betulin alleviated <b>ethanol</b> induced <b>alcoholic</b> liver injury via <strong>SIRT1</strong>/AMPK signaling pathway.
+SIRT1	drug	alcohol	26776965	Additionally, betulin enhanced the sirtuin 1 (<strong>SIRT1</strong>) expression mediated by <b>ethanol</b>.
+SIRT1	drug	alcohol	26776965	Additionally, betulin enhanced the <strong>sirtuin 1</strong> (<strong>SIRT1</strong>) expression mediated by <b>ethanol</b>.
+SIRT1	drug	alcohol	26776965	Taken together, betulin alleviates <b>alcoholic</b> liver injury possibly through blocking the regulation of SREBP 1 on fatty acid synthesis and activating <strong>SIRT1</strong> LKB1 AMPK signaling pathway.
+SIRT1	drug	alcohol	25761756	While the expression and activity of the NAD(+) dependent deacetylase <strong>sirtuin 1</strong>, a ChREBP negative target, were down regulated in the liver of <b>alcohol</b> fed mice, they were restored to control levels upon ChREBP silencing.
+SIRT1	drug	alcohol	25703252	The adiponectin <strong>SIRT1</strong> AMPK pathway in <b>alcoholic</b> fatty liver disease in the rat.
+SIRT1	drug	alcohol	25703252	The serum Adip and tumor necrosis factor alpha (TNF α) as well as liver Adip receptors (AdipoR1 and AdipoR2) <strong>SIRT1</strong>, AMPK, phosphorylated AMPK (p AMPK), sterol regulatory element binding proteins (SREBPs), acetyl CoA carboxylase (ACC), LIP 1, lipocalin 2 (LCN2), and serum amyloid A1 were assessed in the rat model where 16 weeks of gavaged <b>alcohol</b> were administered.
+SIRT1	drug	alcohol	25703252	Our present observations demonstrate that the impaired Adip <strong>SIRT1</strong> AMPK signaling pathway contributes, at least in part, to the development of <b>alcoholic</b> fatty liver disease in EtOH binge rats.
+SIRT1	addiction	intoxication	25703252	Our present observations demonstrate that the impaired Adip <strong>SIRT1</strong> AMPK signaling pathway contributes, at least in part, to the development of alcoholic fatty liver disease in EtOH <b>binge</b> rats.
+SIRT1	drug	cocaine	25698746	<strong>SIRT1</strong> FOXO3a regulate <b>cocaine</b> actions in the nucleus accumbens.
+SIRT1	drug	cocaine	25698746	Previous studies have shown that chronic <b>cocaine</b> administration induces <strong>SIRT1</strong>, a Class III histone deacetylase, in the nucleus accumbens (NAc), a key brain reward region, and that such induction influences the gene regulation and place conditioning effects of <b>cocaine</b>.
+SIRT1	addiction	reward	25698746	Previous studies have shown that chronic cocaine administration induces <strong>SIRT1</strong>, a Class III histone deacetylase, in the nucleus accumbens (NAc), a key brain <b>reward</b> region, and that such induction influences the gene regulation and place conditioning effects of cocaine.
+SIRT1	drug	cocaine	25698746	To determine the mechanisms by which <strong>SIRT1</strong> mediates <b>cocaine</b> induced plasticity in NAc, we used chromatin immunoprecipitation followed by massively parallel sequencing (ChIP seq), 1 d after 7 daily <b>cocaine</b> (20 mg/kg) or saline injections, to map <strong>SIRT1</strong> binding genome wide in mouse NAc.
+SIRT1	drug	cocaine	25698746	First, despite its induction in NAc, chronic <b>cocaine</b> causes depletion of <strong>SIRT1</strong> from most affected gene promoters in concert with enrichment of H4K16ac (itself a deacetylation target of <strong>SIRT1</strong>), which is associated with increased expression of these genes.
+SIRT1	drug	cocaine	25698746	Second, we deduced the forkhead transcription factor (FOXO) family to be a downstream mechanism through which <strong>SIRT1</strong> regulates <b>cocaine</b> action.
+SIRT1	drug	cocaine	25698746	The discovery of these two actions of <strong>SIRT1</strong> in NAc in the context of behavioral adaptations to <b>cocaine</b> represents an important step forward in advancing our understanding of the molecular adaptations underlying <b>cocaine</b> action.
+SIRT1	drug	opioid	24561089	Resveratrol attenuates <b>morphine</b> antinociceptive tolerance via <strong>SIRT1</strong> regulation in the rat spinal cord.
+SIRT1	drug	opioid	24561089	However, little research has been conducted examining the involvement of <strong>SIRT1</strong> in chronic <b>morphine</b> tolerance.
+SIRT1	drug	opioid	24561089	The aim of this study was to investigate the role of spinal <strong>SIRT1</strong> and acetyl histone H3(Ac H3) in chronic <b>morphine</b> tolerance in rats.
+SIRT1	drug	opioid	24561089	Administration of <b>morphine</b> for 6 days induced a stabilized antinociceptive tolerance, down regulated <strong>SIRT1</strong> expression and up regulated Ac H3 expression in the spinal dorsal horn.
+SIRT1	drug	opioid	24561089	Resveratrol treatment from day 7 to 13 increased <strong>SIRT1</strong> expression, suppressed global Ac H3 expression compared to the <b>morphine</b> tolerance (MT) group, and significantly reversed <b>morphine</b> antinociceptive tolerance.
+SIRT1	drug	opioid	24561089	These results suggest that resveratrol reversed <b>morphine</b> tolerance by upregulating the expression of <strong>SIRT1</strong> in the spinal dorsal horn.
+SIRT1	drug	opioid	24561089	<strong>SIRT1</strong> and global Ac H3 in the spinal cord may play an important role in the mechanisms of chronic <b>morphine</b> tolerance.
+SIRT1	addiction	intoxication	24416161	In addition, we measured the effects of <b>binge</b> EtOH exposure on hippocampal Drosha and Dicer mRNA levels, as well as the putative miR target genes, BDNF and <strong>SIRT1</strong>.
+SIRT1	drug	amphetamine	24239129	<b>Methamphetamine</b> exposure also increased repressor element 1 silencing transcription factor (REST) corepressor 1, methylated CpG binding protein 2, and histone deacetylase 2 enrichment, but not of <strong>sirtuin 1</strong> or sirtuin 2, onto GluA1 and GluA2 gene sequences.
+SIRT1	drug	cocaine	24107942	Essential role of <strong>SIRT1</strong> signaling in the nucleus accumbens in <b>cocaine</b> and morphine action.
+SIRT1	drug	opioid	24107942	Essential role of <strong>SIRT1</strong> signaling in the nucleus accumbens in cocaine and <b>morphine</b> action.
+SIRT1	drug	cocaine	24107942	Here, we establish an essential role for <strong>SIRT1</strong> and SIRT2 in regulating behavioral responses to <b>cocaine</b> and morphine through actions in the nucleus accumbens (NAc), a key brain reward region.
+SIRT1	drug	opioid	24107942	Here, we establish an essential role for <strong>SIRT1</strong> and SIRT2 in regulating behavioral responses to cocaine and <b>morphine</b> through actions in the nucleus accumbens (NAc), a key brain reward region.
+SIRT1	addiction	reward	24107942	Here, we establish an essential role for <strong>SIRT1</strong> and SIRT2 in regulating behavioral responses to cocaine and morphine through actions in the nucleus accumbens (NAc), a key brain <b>reward</b> region.
+SIRT1	drug	cocaine	24107942	We show that chronic <b>cocaine</b> administration increases <strong>SIRT1</strong> and SIRT2 expression in the mouse NAc, while chronic morphine administration induces <strong>SIRT1</strong> expression alone, with no regulation of all other sirtuin family members observed.
+SIRT1	drug	opioid	24107942	We show that chronic cocaine administration increases <strong>SIRT1</strong> and SIRT2 expression in the mouse NAc, while chronic <b>morphine</b> administration induces <strong>SIRT1</strong> expression alone, with no regulation of all other sirtuin family members observed.
+SIRT1	drug	cocaine	24107942	Viral mediated overexpression of <strong>SIRT1</strong> or SIRT2 in the NAc enhances the rewarding effects of both <b>cocaine</b> and morphine.
+SIRT1	drug	opioid	24107942	Viral mediated overexpression of <strong>SIRT1</strong> or SIRT2 in the NAc enhances the rewarding effects of both cocaine and <b>morphine</b>.
+SIRT1	addiction	reward	24107942	In contrast, the local knockdown of <strong>SIRT1</strong> from the NAc of floxed <strong>Sirt1</strong> mice decreases drug <b>reward</b>.
+SIRT1	drug	cocaine	23499958	Resveratrol is known as an activator of <strong>SIRT1</strong>, which leads to the deacetylation of histone and non histone protein substrates, but also has other pharmacological profiles such as the inhibition of monoamine oxidase (MAO) A and MAO B. Resveratrol was previously demonstrated to potentiate the rewarding effects of chronic <b>cocaine</b> via activation of <strong>SIRT1</strong>.
+SIRT1	drug	cocaine	22729177	We found that impairment of Agouti related protein (AgRP) circuitry by either <strong>Sirt1</strong> knockdown in AgRP expressing neurons or early postnatal ablation of these neurons increased exploratory behavior and enhanced responses to <b>cocaine</b>.
+SIRT1	drug	alcohol	19951294	Flies harboring deletions of the genes encoding the olfactory co receptor Or83b or the sirtuin <strong>Sir2</strong> showed marked changes in the development of <b>ethanol</b> tolerance.
+SIRT1	drug	cocaine	19447090	The findings also provide comprehensive insight into the molecular pathways regulated by <b>cocaine</b> including a new role for sirtuins (<strong>Sirt1</strong> and Sirt2) which are induced in the nucleus accumbens by <b>cocaine</b> and, in turn, dramatically enhance the behavioral effects of the drug.
+CHRNB2	drug	nicotine	29666375	Association and cis mQTL analysis of variants in CHRNA3 A5, CHRNA7, <strong>CHRNB2</strong>, and CHRNB4 in relation to <b>nicotine</b> dependence in a Chinese Han population.
+CHRNB2	addiction	dependence	29666375	Association and cis mQTL analysis of variants in CHRNA3 A5, CHRNA7, <strong>CHRNB2</strong>, and CHRNB4 in relation to nicotine <b>dependence</b> in a Chinese Han population.
+CHRNB2	drug	nicotine	29411706	Our results confirmed the genetic effect of CHRNA4 and <strong>CHRNB2</strong> on <b>smoking</b> related depression.
+CHRNB2	drug	nicotine	27428758	<b>Nicotine</b> intake is correlated negatively with <strong>Chrnb2</strong>, Chrna7 and positively with Drd1 expression.
+CHRNB2	drug	nicotine	27327258	Besides the CHRNA4, <strong>CHRNB2</strong> and CHRNA5/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the CHRNB3 CHRNA6 gene cluster on chromosome 8 in <b>nicotine</b> dependence (ND).
+CHRNB2	addiction	dependence	27327258	Besides the CHRNA4, <strong>CHRNB2</strong> and CHRNA5/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the CHRNB3 CHRNA6 gene cluster on chromosome 8 in nicotine <b>dependence</b> (ND).
+CHRNB2	drug	nicotine	26416825	Three hundred sixty four Mexican Mestizo Mexico City residents from 87 families with at least one <b>smoker</b> were assessed for association of 12 gene variants of six candidate genes (CHRNA4, <strong>CHRNB2</strong>, DRD2, ANKK1, SLC6A3, and CYP2A6) with cigarette consumption, age of initiation and <b>smoking</b> duration.
+CHRNB2	drug	nicotine	26416825	The Family Based Association Test showed statistically significant association between the rs2072658 polymorphism of the <strong>CHRNB2</strong> gene and <b>smoking</b> related phenotypes such as: <b>smoking</b> status (SS), age of onset (AO), years of <b>smoking</b>, and psychological dependence (PD) evaluated by the Glover Nilsson <b>Smoking</b> Behavior Questionnaire.
+CHRNB2	addiction	dependence	26416825	The Family Based Association Test showed statistically significant association between the rs2072658 polymorphism of the <strong>CHRNB2</strong> gene and smoking related phenotypes such as: smoking status (SS), age of onset (AO), years of smoking, and psychological <b>dependence</b> (PD) evaluated by the Glover Nilsson Smoking Behavior Questionnaire.
+CHRNB2	drug	nicotine	26416825	Our results indicate effects of the rs2072658 <strong>CHRNB2</strong> and rs28399433 CYP2A6 gene variants on AO, SS and PD in Mexican Mestizo <b>smokers</b>.
+CHRNB2	drug	nicotine	25774163	In the context of personalized medicine, the main aim of the present study was to evaluate whether the CHRNA4 and <strong>CHRNB2</strong> polymorphisms are associated with response to <b>smoking</b> cessation therapies in patients from a <b>smoker</b> assistance program.
+CHRNB2	drug	nicotine	25640319	The possible role of maternal bonding style and <strong>CHRNB2</strong> gene polymorphisms in <b>nicotine</b> dependence and related depressive phenotype.
+CHRNB2	addiction	dependence	25640319	The possible role of maternal bonding style and <strong>CHRNB2</strong> gene polymorphisms in nicotine <b>dependence</b> and related depressive phenotype.
+CHRNB2	drug	nicotine	25640319	Since both <b>nicotine</b> dependence (ND) and depressive phenotype are complex disorders, we investigated the effects of a significant early life experience, maternal bonding style (MB) and <strong>CHRNB2</strong> gene SNPs on <b>smoking</b> related depression.
+CHRNB2	addiction	dependence	25640319	Since both nicotine <b>dependence</b> (ND) and depressive phenotype are complex disorders, we investigated the effects of a significant early life experience, maternal bonding style (MB) and <strong>CHRNB2</strong> gene SNPs on smoking related depression.
+CHRNB2	drug	nicotine	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, <strong>CHRNB2</strong>, BDNF, and NTRK2 associated with <b>nicotine</b> dependence in the Study of Addiction: Genetics and Environment sample, suggesting the biological role of these genes in <b>nicotine</b> dependence development.
+CHRNB2	addiction	addiction	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, <strong>CHRNB2</strong>, BDNF, and NTRK2 associated with nicotine dependence in the Study of <b>Addiction</b>: Genetics and Environment sample, suggesting the biological role of these genes in nicotine dependence development.
+CHRNB2	addiction	dependence	24057800	In application to a real dataset, we detected one significant tetragenic interaction among CHRNA4, <strong>CHRNB2</strong>, BDNF, and NTRK2 associated with nicotine <b>dependence</b> in the Study of Addiction: Genetics and Environment sample, suggesting the biological role of these genes in nicotine <b>dependence</b> development.
+CHRNB2	drug	nicotine	23553665	We investigated whether <b>nicotine</b> dependence affects these endophenotypes in Japanese schizophrenia patients and whether alpha4 and beta2 subunits of neuronal nicotinic acetylcholine receptor genes (alpha4 subunit of the nAChR gene (CHRNA4)/beta2 subunit of the nAChR gene (<strong>CHRNB2</strong>)) were associated with <b>nicotine</b> dependence in patients (n = 100) and healthy controls (n = 107).
+CHRNB2	addiction	dependence	23553665	We investigated whether nicotine <b>dependence</b> affects these endophenotypes in Japanese schizophrenia patients and whether alpha4 and beta2 subunits of neuronal nicotinic acetylcholine receptor genes (alpha4 subunit of the nAChR gene (CHRNA4)/beta2 subunit of the nAChR gene (<strong>CHRNB2</strong>)) were associated with nicotine <b>dependence</b> in patients (n = 100) and healthy controls (n = 107).
+CHRNB2	drug	nicotine	23553665	Finally, using 12 tagging single nucleotide polymorphisms in each the CHRNA4/<strong>CHRNB2</strong>, we used multiple linear regression analysis to examine the association between <b>nicotine</b> dependence measures and each selected single nucleotide polymorphism.
+CHRNB2	addiction	dependence	23553665	Finally, using 12 tagging single nucleotide polymorphisms in each the CHRNA4/<strong>CHRNB2</strong>, we used multiple linear regression analysis to examine the association between nicotine <b>dependence</b> measures and each selected single nucleotide polymorphism.
+CHRNB2	drug	alcohol	23419392	We conducted a battery of tests in mice lacking the β2* coding gene (<strong>Chrnb2</strong>) or pretreated with a selective β2* nAChR antagonist for a range of <b>ethanol</b> induced behaviors including locomotor depression, hypothermia, hypnosis, and anxiolysis.
+CHRNB2	drug	alcohol	23419392	<strong>Chrnb2</strong> deletion had no effect on <b>ethanol</b> drinking behavior, however.
+CHRNB2	drug	nicotine	23037950	Possible association of nicotinic acetylcholine receptor gene (CHRNA4 and <strong>CHRNB2</strong>) polymorphisms with <b>nicotine</b> dependence in Japanese males: an exploratory study.
+CHRNB2	addiction	dependence	23037950	Possible association of nicotinic acetylcholine receptor gene (CHRNA4 and <strong>CHRNB2</strong>) polymorphisms with nicotine <b>dependence</b> in Japanese males: an exploratory study.
+CHRNB2	drug	nicotine	23037950	It has been reported that the nicotinic acetylcholine receptor (CHRNA4 and <strong>CHRNB2</strong>) genes might be associated with <b>smoking</b> behavior in several ethnic populations.
+CHRNB2	drug	nicotine	23037950	We found <strong>CHRNB2</strong> rs4845652 genotypes to be associated with FTND scores under an additive genetic model: rs4845652 T allele carriers had lower ND levels (p=0.038; when adjusted for <b>smoking</b> duration: p=0.052).
+CHRNB2	drug	nicotine	23037950	Furthermore, we demonstrated a possible gene gene interaction of CHRNA4 and <strong>CHRNB2</strong> on ND in a dose dependent manner: those <b>smokers</b> with CHRNA4 rs1044397 GG or GA genotypes along with <strong>CHRNB2</strong> rs4845652 CC genotype are likely to demonstrate higher ND scores.
+CHRNB2	drug	nicotine	20854418	<strong>CHRNB2</strong> promoter region: association with subjective effects to <b>nicotine</b> and gene expression differences.
+CHRNB2	drug	nicotine	20854418	The human genetic study and functional assays suggest that variation in the promoter region of <strong>CHRNB2</strong> gene may be important in mediating levels of expression of the β2 nicotinic receptor subunit, which may be associated with variation in subjective response to <b>nicotine</b>.
+CHRNB2	drug	nicotine	20736995	Exons of 10 genes were resequenced with next generation sequencing technology in 448 European American participants of a <b>smoking</b> cessation trial, and <strong>CHRNB2</strong> and CHRNA4 were resequenced by Sanger technology to improve sequence coverage.
+CHRNB2	drug	alcohol	20496163	This report explores the association between six nAChR subunit genes (Chrna3, Chrna4, Chrnb4, <strong>Chrnb2</strong>, Chrna5, and Chrna7) with <b>alcohol</b> preference (AP) using co segregation of AP with nAChR subunit genotypes in a F(2) population produced from reciprocal crosses of <b>alcohol</b> preferring C57BL/6J (B6) and <b>alcohol</b> avoiding DBA/2J (D2) strains of mice.
+CHRNB2	drug	nicotine	19755656	Nicotinic acetylcholine receptor beta2 subunit (<strong>CHRNB2</strong>) gene and short term ability to quit <b>smoking</b> in response to <b>nicotine</b> patch.
+CHRNB2	drug	nicotine	19755656	We examined the association of a 3' untranslated region polymorphism (rs2072661) in the nicotinic acetylcholine receptor beta2 subunit (<strong>CHRNB2</strong>) gene with quitting success in response to <b>nicotine</b> versus placebo patch during a short term test of patch effects.
+CHRNB2	drug	nicotine	19755656	<b>Smokers</b> with the <strong>CHRNB2</strong> GG genotype had more days of abstinence during the <b>nicotine</b> versus placebo patch week compared with those with the AG or AA genotypes (P < 0.01).
+CHRNB2	drug	nicotine	19698703	20 tag SNPs in five <b>nicotine</b> receptor subunit genes (CHRNA3, 4, and 6; <strong>CHRNB2</strong> and 3) were genotyped and analysed for single marker and haplotype associations.
+CHRNB2	addiction	relapse	19482438	There were possible associations between the temperament trait novelty <b>seeking</b> and CHRNA4 rs1044396, CHRNA5 rs16969968 and <strong>CHRNB2</strong> rs4845378, but these associations were not robust to correction for multiple testing.
+CHRNB2	drug	nicotine	19482438	We conclude that the analysis of polymorphisms in genes coding for four nicotinic acetylcholine receptor subunits (CHRNA4, CHRNA5, <strong>CHRNB2</strong> and CHRNB3) and several <b>smoking</b> related phenotypes revealed no statistically significant association.
+CHRNB2	drug	amphetamine	18991851	Therefore, we conducted a genetic association analysis of the alpha4 gene (CHRNA4) and beta2 gene (<strong>CHRNB2</strong>) with <b>methamphetamine</b> (<b>METH</b>) use disorder (191 cases and 753 controls).
+CHRNB2	drug	amphetamine	18991851	In conclusion, our results suggest that neither CHRNA4 nor <strong>CHRNB2</strong> plays a major role in Japanese <b>METH</b> use disorder.
+CHRNB2	drug	nicotine	18593715	Overall, while our results indicate strong evidence for <strong>CHRNB2</strong> in ability to quit <b>smoking</b>, these results require replication in an independent sample.
+CHRNB2	drug	nicotine	18534558	Gene gene interactions among CHRNA4, <strong>CHRNB2</strong>, BDNF, and NTRK2 in <b>nicotine</b> dependence.
+CHRNB2	addiction	dependence	18534558	Gene gene interactions among CHRNA4, <strong>CHRNB2</strong>, BDNF, and NTRK2 in nicotine <b>dependence</b>.
+CHRNB2	drug	nicotine	18534558	To determine if gene gene interactions exist among the four genes, we genotyped six single nucleotide polymorphisms (SNPs) for CHRNA4 and BDNF, nine SNPs for NTRK2, and four SNPs for <strong>CHRNB2</strong> in a case control sample containing 275 unrelated <b>smokers</b> with a Fagerström Test for <b>Nicotine</b> Dependence score of 4.0 or more and 348 unrelated nonsmokers.
+CHRNB2	addiction	dependence	18534558	To determine if gene gene interactions exist among the four genes, we genotyped six single nucleotide polymorphisms (SNPs) for CHRNA4 and BDNF, nine SNPs for NTRK2, and four SNPs for <strong>CHRNB2</strong> in a case control sample containing 275 unrelated smokers with a Fagerström Test for Nicotine <b>Dependence</b> score of 4.0 or more and 348 unrelated nonsmokers.
+CHRNB2	drug	alcohol	17226798	Association of the neuronal nicotinic receptor beta2 subunit gene (<strong>CHRNB2</strong>) with subjective responses to <b>alcohol</b> and nicotine.
+CHRNB2	drug	nicotine	17226798	Association of the neuronal nicotinic receptor beta2 subunit gene (<strong>CHRNB2</strong>) with subjective responses to alcohol and <b>nicotine</b>.
+CHRNB2	drug	alcohol	17226798	We have examined two neuronal nicotinic receptor subunit genes (CHRNA4 and <strong>CHRNB2</strong>) for possible associations with nicotine and <b>alcohol</b> phenotypes, including measures of frequency of use and measures of initial subjective response in the period shortly after first using the drugs.
+CHRNB2	drug	nicotine	17226798	We have examined two neuronal nicotinic receptor subunit genes (CHRNA4 and <strong>CHRNB2</strong>) for possible associations with <b>nicotine</b> and alcohol phenotypes, including measures of frequency of use and measures of initial subjective response in the period shortly after first using the drugs.
+CHRNB2	drug	alcohol	17226798	However, a SNP (rs2072658) located immediately upstream of <strong>CHRNB2</strong> was associated with the initial subjective response to both <b>alcohol</b> and tobacco.
+CHRNB2	drug	nicotine	17226798	However, a SNP (rs2072658) located immediately upstream of <strong>CHRNB2</strong> was associated with the initial subjective response to both alcohol and <b>tobacco</b>.
+CHRNB2	drug	alcohol	17226798	This study provides the first evidence for association between the <strong>CHRNB2</strong> gene and nicotine  and <b>alcohol</b> related phenotypes, and suggests that polymorphisms in <strong>CHRNB2</strong> may be important in mediating early responses to nicotine and <b>alcohol</b>.
+CHRNB2	drug	nicotine	17226798	This study provides the first evidence for association between the <strong>CHRNB2</strong> gene and <b>nicotine</b>  and alcohol related phenotypes, and suggests that polymorphisms in <strong>CHRNB2</strong> may be important in mediating early responses to <b>nicotine</b> and alcohol.
+CHRNB2	drug	nicotine	16314871	We found nominally significant (P<0.05) allelic and genotypic association with <b>smoking</b> initiation of SNP rs2072660 and multilocus haplotypes (P<0.007 0.05) in <strong>CHRNB2</strong> and nominal (P<0.05) allelic or genotypic association of SNPs in CHRNA7 (rs1909884), CHRNA9 (rs4861065) and CHRNB3 (rs9298629) with <b>nicotine</b> dependence.
+CHRNB2	addiction	dependence	16314871	We found nominally significant (P<0.05) allelic and genotypic association with smoking initiation of SNP rs2072660 and multilocus haplotypes (P<0.007 0.05) in <strong>CHRNB2</strong> and nominal (P<0.05) allelic or genotypic association of SNPs in CHRNA7 (rs1909884), CHRNA9 (rs4861065) and CHRNB3 (rs9298629) with nicotine <b>dependence</b>.
+CHRNB2	drug	nicotine	16314871	Employing logistic regression and controlling for known risk factors, the best fitting model for <b>smoking</b> initiation encompassed a 5 SNP haplotype in <strong>CHRNB2</strong>, neuroticism and novelty seeking (P=5.9 x 10( 14), Nagelkerke r(2)=0.30).
+CHRNB2	addiction	relapse	16314871	Employing logistic regression and controlling for known risk factors, the best fitting model for smoking initiation encompassed a 5 SNP haplotype in <strong>CHRNB2</strong>, neuroticism and novelty <b>seeking</b> (P=5.9 x 10( 14), Nagelkerke r(2)=0.30).
+CHRNB2	drug	nicotine	15790597	We tested six single nucleotide polymorphisms (SNPs) in the alpha4 subunit gene (CHRNA4) and four SNPs in the beta2 subunit gene (<strong>CHRNB2</strong>) of nicotinic acetylcholine receptors (nAChRs) for association with <b>nicotine</b> dependence (ND), which was assessed by <b>smoking</b> quantity (SQ), the heaviness of <b>smoking</b> index (HSI) and the Fagerstrom test for ND (FTND) in 2037 subjects from 602 nuclear families of either European American (EA) or African American (AA) ancestry.
+CHRNB2	addiction	dependence	15790597	We tested six single nucleotide polymorphisms (SNPs) in the alpha4 subunit gene (CHRNA4) and four SNPs in the beta2 subunit gene (<strong>CHRNB2</strong>) of nicotinic acetylcholine receptors (nAChRs) for association with nicotine <b>dependence</b> (ND), which was assessed by smoking quantity (SQ), the heaviness of smoking index (HSI) and the Fagerstrom test for ND (FTND) in 2037 subjects from 602 nuclear families of either European American (EA) or African American (AA) ancestry.
+CHRNB2	drug	nicotine	15154117	We studied six single nucleotide polymorphisms (SNPs) in the CHRNA4 gene and four SNPs in the <strong>CHRNB2</strong> gene with respect to <b>nicotine</b> dependence in a collection of 901 subjects (815 siblings and 86 parents) from 222 nuclear families with multiple <b>nicotine</b> addicted siblings.
+CHRNB2	addiction	dependence	15154117	We studied six single nucleotide polymorphisms (SNPs) in the CHRNA4 gene and four SNPs in the <strong>CHRNB2</strong> gene with respect to nicotine <b>dependence</b> in a collection of 901 subjects (815 siblings and 86 parents) from 222 nuclear families with multiple nicotine addicted siblings.
+CHRNB2	drug	nicotine	11906688	The beta2 neuronal nicotinic acetylcholine receptor gene (<strong>CHRNB2</strong>) is a logical candidate for influencing <b>smoking</b> behavior and <b>nicotine</b> dependence.
+CHRNB2	addiction	dependence	11906688	The beta2 neuronal nicotinic acetylcholine receptor gene (<strong>CHRNB2</strong>) is a logical candidate for influencing smoking behavior and nicotine <b>dependence</b>.
+CHRNB2	drug	nicotine	11054772	Haplotypes of four novel single nucleotide polymorphisms in the nicotinic acetylcholine receptor beta2 subunit (<strong>CHRNB2</strong>) gene show no association with <b>smoking</b> initiation or <b>nicotine</b> dependence.
+CHRNB2	addiction	dependence	11054772	Haplotypes of four novel single nucleotide polymorphisms in the nicotinic acetylcholine receptor beta2 subunit (<strong>CHRNB2</strong>) gene show no association with smoking initiation or nicotine <b>dependence</b>.
+CHRNB2	drug	nicotine	11054772	Several types of evidence, including experiments with mice that lack the nicotinic acetylcholine receptor beta2 subunit gene (<strong>CHRNB2</strong>), have suggested that a beta2 containing nicotinic receptor is necessary for at least some of the reinforcing properties of <b>nicotine</b>.
+CHRNB2	addiction	reward	11054772	Several types of evidence, including experiments with mice that lack the nicotinic acetylcholine receptor beta2 subunit gene (<strong>CHRNB2</strong>), have suggested that a beta2 containing nicotinic receptor is necessary for at least some of the <b>reinforcing</b> properties of nicotine.
+CHRNB2	drug	nicotine	11054772	However, sequence variations in <strong>CHRNB2</strong> have not been reported, and its role in influencing human <b>smoking</b> behavior and <b>nicotine</b> dependence is not known.
+CHRNB2	addiction	dependence	11054772	However, sequence variations in <strong>CHRNB2</strong> have not been reported, and its role in influencing human smoking behavior and nicotine <b>dependence</b> is not known.
+SHBG	drug	nicotine	32707117	Adjusting for age, BMI, cycle stage, <b>smoking</b>, parity, partner status, and psychoactive medication, sexual desire was positively associated with serum dehydroepiandrosterone (β coefficient 3·39, 95% CI 0·65 to 6·03) and androstenedione (4·81, 0·16 to 9·12), and negatively with <strong>SHBG</strong> ( 5.74,  9.54 to  1·90), each model explaining less than 4% of the variation in desire.
+SHBG	drug	nicotine	26680482	There was a drop in <strong>SHBG</strong> already in the first week of non <b>smoking</b>, and levels continued to remain low.
+SHBG	drug	alcohol	25567620	When CS were compared with the rest of the sample (non smokers, NS + PS), in a multivariate model (analysis of covariance, ANCOVA) adjusted for age, lifestyle (including <b>alcohol</b>, cannabis and physical activity), BMI and <strong>sex hormone binding globulin</strong>, significantly higher androgen (total testosterone, P = 0.001; calculated free testosterone, P < 0.005) and lower FSH (P < 0.05) levels were observed in CS.
+SHBG	drug	cannabinoid	25567620	When CS were compared with the rest of the sample (non smokers, NS + PS), in a multivariate model (analysis of covariance, ANCOVA) adjusted for age, lifestyle (including alcohol, <b>cannabis</b> and physical activity), BMI and <strong>sex hormone binding globulin</strong>, significantly higher androgen (total testosterone, P = 0.001; calculated free testosterone, P < 0.005) and lower FSH (P < 0.05) levels were observed in CS.
+SHBG	drug	nicotine	25567620	When CS were compared with the rest of the sample (non <b>smokers</b>, NS + PS), in a multivariate model (analysis of covariance, ANCOVA) adjusted for age, lifestyle (including alcohol, cannabis and physical activity), BMI and <strong>sex hormone binding globulin</strong>, significantly higher androgen (total testosterone, P = 0.001; calculated free testosterone, P < 0.005) and lower FSH (P < 0.05) levels were observed in CS.
+SHBG	drug	alcohol	25277121	<b>Alcohol</b> consumption was also linked to changes in testosterone and <strong>SHBG</strong> levels.
+SHBG	drug	nicotine	24457405	Our objectives were to examine the association of cigarette <b>smoking</b> and serum levels of sex hormone binding globulin (<strong>SHBG</strong>), total testosterone (TT) and free testosterone (FT) in a large male population.
+SHBG	drug	nicotine	24457405	Our objectives were to examine the association of cigarette <b>smoking</b> and serum levels of <strong>sex hormone binding globulin</strong> (<strong>SHBG</strong>), total testosterone (TT) and free testosterone (FT) in a large male population.
+SHBG	drug	nicotine	24457405	(d) <b>Smoking</b> was not found to be an independent predictor of <strong>SHBG</strong> level after adjustment for confounders in multivariate regression model (P >0.05), although a positive association between increasing pack years and <strong>SHBG</strong> level was observed (r = 0.174, P <0.001).
+SHBG	addiction	relapse	15627810	Positive relationships between total testosterone and the Disinhibition scale of the Sensation <b>Seeking</b> Scale Form V were replicated, although they were affected by <strong>SHBG</strong>.
+SHBG	drug	alcohol	15627810	It was suggested that relationships between <strong>SHBG</strong> and sensation seeking in inmates could be mediated by items referring to <b>alcohol</b> and drugs.
+SHBG	addiction	relapse	15627810	It was suggested that relationships between <strong>SHBG</strong> and sensation <b>seeking</b> in inmates could be mediated by items referring to alcohol and drugs.
+SHBG	drug	opioid	15483091	We therefore assayed testosterone, free testosterone, estradiol, <strong>SHBG</strong>, LH, FSH, and prolactin in 17 men treated with <b>buprenorphine</b>.
+SHBG	drug	alcohol	11320584	Our results suggest: 1) decreased testicular reserve of free testosterone and normal level of total testosterone, 2) decreased initial level and functional reserve of 17 OH progesterone, 3) mild hyperoestrogenism, 4) no significant difference of LH, FSH, <strong>SHBG</strong> levels between <b>alcoholics</b> and controls, 5) these results were not changed after 6 months observation.
+SHBG	drug	alcohol	10659727	<strong>Sex hormone binding globulin</strong> in non cirrhotic <b>alcoholic</b> patients during early withdrawal and after longer abstinence.
+SHBG	addiction	withdrawal	10659727	<strong>Sex hormone binding globulin</strong> in non cirrhotic alcoholic patients during early <b>withdrawal</b> and after longer abstinence.
+SHBG	drug	alcohol	10659727	In recently intoxicated non cirrhotic male <b>alcohol</b> misusing and  dependent patients, we studied, during early withdrawal and more prolonged abstinence, the rate of changes of sex hormones and their binding globulin (<strong>SHBG</strong>), the prevalence of hypo androgenism and possible determinant factors of <strong>SHBG</strong> increase.
+SHBG	addiction	withdrawal	10659727	In recently intoxicated non cirrhotic male alcohol misusing and  dependent patients, we studied, during early <b>withdrawal</b> and more prolonged abstinence, the rate of changes of sex hormones and their binding globulin (<strong>SHBG</strong>), the prevalence of hypo androgenism and possible determinant factors of <strong>SHBG</strong> increase.
+SHBG	drug	alcohol	10659727	We conclude that excessive <b>alcohol</b> ingestion is associated with marked increases of <strong>SHBG</strong> which slowly revert during abstinence.
+SHBG	drug	alcohol	10659727	High <strong>SHBG</strong> does not fully explain the low Tf values or the presence of clinical hypo androgenism in <b>alcoholics</b>.
+SHBG	drug	alcohol	10659727	This <strong>SHBG</strong> response to <b>ethanol</b> makes it a potential marker of excessive <b>alcohol</b> intake.
+SHBG	drug	nicotine	9673113	It is concluded that levels of testosterone and <strong>SHBG</strong> are not the proper markers of individual susceptibility to genotoxicity of <b>tobacco</b> smoke carcinogens.
+SHBG	drug	alcohol	9541143	High concentrations of TT and <strong>SHBG</strong> were consistently related to type II <b>alcoholism</b>, but not pure <b>alcohol</b> dependence.
+SHBG	addiction	dependence	9541143	High concentrations of TT and <strong>SHBG</strong> were consistently related to type II alcoholism, but not pure alcohol <b>dependence</b>.
+SHBG	drug	alcohol	8814647	Further, high levels of <strong>SHBG</strong> were related to a history of seizures and younger <b>alcoholics</b> received higher ratings on the paranoid aggressive subscale.
+SHBG	drug	alcohol	8590623	To investigate the androgen, weak androgen, estrogen, and gonadotrophin response to clomiphene in <b>alcoholics</b>, we determined in 63 male patients (25 with and 38 without liver cirrhosis) serum testosterone, sexual hormone binding protein (<strong>SHBG</strong>), dehidroepiandrosterone, androstenedione, LH, FSH, prolactin, and estradiol levels, on the first and the sixth day after admission, and after a course of 8 days of clomiphene 200 mg/day.
+SHBG	drug	alcohol	8590623	<strong>SHBG</strong> levels were higher in both groups of <b>alcoholics</b> than in controls, pointing to a worse degree of hypogonadism, because only the free hormone is active.
+SHBG	drug	alcohol	8655923	It is concluded that <b>alcoholic</b> patients without clinical signs of liver failure have normal plasma testosterone levels, irrespective of their histologic liver alterations and high plasma <strong>SHBG</strong> levels that decreased significantly after a short abstinence.
+SHBG	drug	alcohol	8655923	Fast changes in <strong>SHBG</strong> levels rise the possibility that this protein is candidate marker of <b>alcoholism</b>.
+SHBG	drug	alcohol	7792345	Serum concentrations of luteinizing hormone, follicle stimulating hormone, testosterone, androstenedione, estradiol, <strong>sex hormone binding globulin</strong>, cortisol, and prolactin were measured in 12 male chronic <b>alcoholics</b> once during withdrawal and once after 21 days of abstinence.
+SHBG	addiction	withdrawal	7792345	Serum concentrations of luteinizing hormone, follicle stimulating hormone, testosterone, androstenedione, estradiol, <strong>sex hormone binding globulin</strong>, cortisol, and prolactin were measured in 12 male chronic alcoholics once during <b>withdrawal</b> and once after 21 days of abstinence.
+SHBG	drug	alcohol	8222764	In postmenopausal women with <b>alcoholic</b> and non <b>alcoholic</b> liver disease, the main disturbances of sex hormone metabolism consist of elevated oestrone and sex hormone binding globulin (<strong>SHBG</strong>) concentrations, while serum concentrations of steroid sulphates and 5 alpha dihydrotestosterone (DHT) are reduced, and the degree of liver dysfunction is a major determinant for the observed disturbances.
+SHBG	drug	alcohol	8222764	In postmenopausal women with <b>alcoholic</b> and non <b>alcoholic</b> liver disease, the main disturbances of sex hormone metabolism consist of elevated oestrone and <strong>sex hormone binding globulin</strong> (<strong>SHBG</strong>) concentrations, while serum concentrations of steroid sulphates and 5 alpha dihydrotestosterone (DHT) are reduced, and the degree of liver dysfunction is a major determinant for the observed disturbances.
+SHBG	drug	opioid	569031	The mean <strong>sex hormone binding globulin</strong> binding capacity was higher in <b>heroin</b> addicts (60.1 +/  5.2 mM) than in healthy controls (35.5 +/  2.1 mM).
+SHBG	drug	opioid	569031	The finding of significantly lower total and free T together with higher <strong>SHBG</strong> indicates an abnormal testicular function in <b>heroin</b> addiction.
+SHBG	addiction	addiction	569031	The finding of significantly lower total and free T together with higher <strong>SHBG</strong> indicates an abnormal testicular function in heroin <b>addiction</b>.
+PER2	drug	alcohol	31329297	We have recently shown that binge or heavy levels of <b>alcohol</b> drinking increase deoxyribonucleic acid (DNA) methylation and reduce gene expression of proopiomelanocortin (POMC) and period 2 (<strong>PER2</strong>) in adult human subjects (Gangisetty et al., <b>Alcohol</b> Clin Exp Res, 43, 2019, 212).
+PER2	addiction	intoxication	31329297	We have recently shown that <b>binge</b> or heavy levels of alcohol drinking increase deoxyribonucleic acid (DNA) methylation and reduce gene expression of proopiomelanocortin (POMC) and period 2 (<strong>PER2</strong>) in adult human subjects (Gangisetty et al., Alcohol Clin Exp Res, 43, 2019, 212).
+PER2	drug	alcohol	31329297	We conducted a series of studies to determine DNA methylation changes in stress regulatory genes proopiomelanocortin (POMC) and period 2 (<strong>PER2</strong>) using biological samples from 3 separate cohorts of patients: (i) pregnant women who consumed moderate to high levels of <b>alcohol</b> or low/unexposed controls, (ii) children with PAE and non <b>alcohol</b> exposed controls, and (iii) children with PAE treated with or without choline.
+PER2	drug	alcohol	31329297	We found pregnant women who consumed moderate to high levels of <b>alcohol</b> and gave birth to PAE children had higher DNA methylation of POMC and <strong>PER2</strong>.
+PER2	drug	nicotine	31329297	The differences in the gene methylation of <strong>PER2</strong> and POMC between PAE and controls did not differ by maternal <b>smoking</b> status.
+PER2	drug	alcohol	30597578	Methylation specific polymerase chain reaction (PCR) assays were used to measure changes in gene methylation of period 2 (<strong>PER2</strong>) and proopiomelanocortin (POMC) genes in peripheral blood samples collected from nonsmoking moderate, nonbinging, binge, and heavy social drinkers who participated in a 3 day behavioral <b>alcohol</b> motivation experiment of imagery exposure to either stress, neutral, or <b>alcohol</b> related cues, 1 per day, presented on consecutive days in counterbalanced order.
+PER2	addiction	intoxication	30597578	Methylation specific polymerase chain reaction (PCR) assays were used to measure changes in gene methylation of period 2 (<strong>PER2</strong>) and proopiomelanocortin (POMC) genes in peripheral blood samples collected from nonsmoking moderate, nonbinging, <b>binge</b>, and heavy social drinkers who participated in a 3 day behavioral alcohol motivation experiment of imagery exposure to either stress, neutral, or alcohol related cues, 1 per day, presented on consecutive days in counterbalanced order.
+PER2	addiction	intoxication	30597578	In the sample of moderate, <b>binge</b>, and heavy drinkers, we found increased methylation of the <strong>PER2</strong> and POMC DNA, reduced expression of these genes in the blood samples of the <b>binge</b> and heavy drinkers relative to the moderate, nonbinge drinkers.
+PER2	drug	alcohol	30597578	Increased <strong>PER2</strong> and POMC DNA methylation was also significantly predictive of both increased levels of subjective <b>alcohol</b> craving immediately following imagery (p < 0.0001), and with presentation of the <b>alcohol</b> (2 beers) (p < 0.0001) prior to the ATT, as well as with <b>alcohol</b> amount consumed during the ATT (p < 0.003).
+PER2	addiction	relapse	30597578	Increased <strong>PER2</strong> and POMC DNA methylation was also significantly predictive of both increased levels of subjective alcohol <b>craving</b> immediately following imagery (p < 0.0001), and with presentation of the alcohol (2 beers) (p < 0.0001) prior to the ATT, as well as with alcohol amount consumed during the ATT (p < 0.003).
+PER2	drug	alcohol	30597578	These data establish significant association between binge or heavy levels of <b>alcohol</b> drinking and elevated levels of methylation and reduced levels of expression of POMC and <strong>PER2</strong> genes.
+PER2	addiction	intoxication	30597578	These data establish significant association between <b>binge</b> or heavy levels of alcohol drinking and elevated levels of methylation and reduced levels of expression of POMC and <strong>PER2</strong> genes.
+PER2	drug	alcohol	30597578	Furthermore, elevated methylation of POMC and <strong>PER2</strong> genes is associated with greater subjective and behavioral motivation for <b>alcohol</b>.
+PER2	drug	amphetamine	30091820	The circadian gene, <strong>Per2</strong>, influences <b>methamphetamine</b> sensitization and reward through the dopaminergic system in the striatum of mice.
+PER2	addiction	reward	30091820	The circadian gene, <strong>Per2</strong>, influences methamphetamine sensitization and <b>reward</b> through the dopaminergic system in the striatum of mice.
+PER2	addiction	sensitization	30091820	The circadian gene, <strong>Per2</strong>, influences methamphetamine <b>sensitization</b> and reward through the dopaminergic system in the striatum of mice.
+PER2	addiction	addiction	30091820	<strong>Per2</strong>, a circadian gene, plays a role in drug <b>addiction</b>.
+PER2	drug	alcohol	30091820	Previous studies using <strong>Per2</strong> knockout mice have shown a role for <strong>Per2</strong> in cocaine, morphine and <b>alcohol</b> addiction.
+PER2	drug	cocaine	30091820	Previous studies using <strong>Per2</strong> knockout mice have shown a role for <strong>Per2</strong> in <b>cocaine</b>, morphine and alcohol addiction.
+PER2	drug	opioid	30091820	Previous studies using <strong>Per2</strong> knockout mice have shown a role for <strong>Per2</strong> in cocaine, <b>morphine</b> and alcohol addiction.
+PER2	addiction	addiction	30091820	Previous studies using <strong>Per2</strong> knockout mice have shown a role for <strong>Per2</strong> in cocaine, morphine and alcohol <b>addiction</b>.
+PER2	drug	amphetamine	30091820	In the present study, we investigated the role of <strong>Per2</strong> in <b>methamphetamine</b> (<b>METH</b>) addiction using <strong>Per2</strong> overexpression and knockout mice.
+PER2	addiction	addiction	30091820	In the present study, we investigated the role of <strong>Per2</strong> in methamphetamine (METH) <b>addiction</b> using <strong>Per2</strong> overexpression and knockout mice.
+PER2	drug	amphetamine	30091820	<strong>Per2</strong> overexpressed mice showed decreased locomotor sensitization and rewarding effects of <b>METH</b> compared to the wildtype mice, whereas the opposite was observed in <strong>Per2</strong> knockout mice.
+PER2	addiction	sensitization	30091820	<strong>Per2</strong> overexpressed mice showed decreased locomotor <b>sensitization</b> and rewarding effects of METH compared to the wildtype mice, whereas the opposite was observed in <strong>Per2</strong> knockout mice.
+PER2	drug	amphetamine	30091820	Taken together, <strong>Per2</strong> expression levels may influence the addictive effects of <b>METH</b> through the dopaminergic system in the striatum of mice.
+PER2	addiction	addiction	30091820	Taken together, <strong>Per2</strong> expression levels may influence the <b>addictive</b> effects of METH through the dopaminergic system in the striatum of mice.
+PER2	drug	alcohol	28776866	RNA Seq analysis confirmed a prenatal AR mediated control of adult expression of <b>alcohol</b> drinking related genes like Bdnf and <strong>Per2</strong>.
+PER2	drug	amphetamine	27581301	Furthermore, <strong>PER2</strong> bioluminescence rhythms in two extra SCN brain oscillators, the dorsomedial hypothalamus and the habenula, were altered by <b>METH</b> in wild type but not in KO mice.
+PER2	drug	opioid	27070740	Here we compared the effects of repeated daily treatment of rats with <b>morphine</b> or <b>methadone</b> and subsequent <b>naloxone</b> precipitated withdrawal on the expression of the Per1, <strong>Per2</strong>, and Avp mRNAs in the suprachiasmatic nucleus and on arylalkylamine N acetyltransferase activity in the pineal gland.
+PER2	addiction	withdrawal	27070740	Here we compared the effects of repeated daily treatment of rats with morphine or methadone and subsequent naloxone precipitated <b>withdrawal</b> on the expression of the Per1, <strong>Per2</strong>, and Avp mRNAs in the suprachiasmatic nucleus and on arylalkylamine N acetyltransferase activity in the pineal gland.
+PER2	drug	opioid	26892296	Here we have studied the effect of constant light on <b>morphine</b> voluntary consumption and withdrawal symptoms and also investigated the involvement of Per1, <strong>Per2</strong> and dopamine D1 receptor in these processes.
+PER2	addiction	withdrawal	26892296	Here we have studied the effect of constant light on morphine voluntary consumption and <b>withdrawal</b> symptoms and also investigated the involvement of Per1, <strong>Per2</strong> and dopamine D1 receptor in these processes.
+PER2	drug	opioid	26892296	It is concluded that exposure to constant light by up regulation of <strong>Per2</strong> and dopamine D1 receptor in the striatum and prefrontal cortex and up regulation of Per1 in the striatum and the possible involvement of melatonin makes animals vulnerable to <b>morphine</b> preference and addiction.
+PER2	addiction	addiction	26892296	It is concluded that exposure to constant light by up regulation of <strong>Per2</strong> and dopamine D1 receptor in the striatum and prefrontal cortex and up regulation of Per1 in the striatum and the possible involvement of melatonin makes animals vulnerable to morphine preference and <b>addiction</b>.
+PER2	drug	alcohol	25677407	Concerning <b>alcohol</b> use, the current findings give support, but are preliminary to, the associations of ARNTL (BMAL1) rs6486120 with <b>alcohol</b> consumption, ARNTL2 rs7958822 and ARNTL2 rs4964057 with <b>alcohol</b> abuse, and PER1 rs3027172 and <strong>PER2</strong> rs56013859 with <b>alcohol</b> dependence.
+PER2	addiction	dependence	25677407	Concerning alcohol use, the current findings give support, but are preliminary to, the associations of ARNTL (BMAL1) rs6486120 with alcohol consumption, ARNTL2 rs7958822 and ARNTL2 rs4964057 with alcohol abuse, and PER1 rs3027172 and <strong>PER2</strong> rs56013859 with alcohol <b>dependence</b>.
+PER2	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, <strong>Per2</strong>, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+PER2	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, <strong>Per2</strong>, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+PER2	drug	alcohol	23608482	The circadian Per1 and <strong>Per2</strong> genes influence <b>alcohol</b> intake, reinforcement, and blood <b>alcohol</b> levels.
+PER2	addiction	reward	23608482	The circadian Per1 and <strong>Per2</strong> genes influence alcohol intake, <b>reinforcement</b>, and blood alcohol levels.
+PER2	drug	alcohol	23608482	This study tested <b>ethanol</b> consumption, reinforcement, and metabolism in mice containing functional mutations in Per1 and/or <strong>Per2</strong> genes on an <b>ethanol</b> preferring background, C57BL/6J mice.
+PER2	addiction	reward	23608482	This study tested ethanol consumption, <b>reinforcement</b>, and metabolism in mice containing functional mutations in Per1 and/or <strong>Per2</strong> genes on an ethanol preferring background, C57BL/6J mice.
+PER2	drug	alcohol	23608482	Mutation of either Per1 or <strong>Per2</strong>, as well as mutations of both genes, increases <b>ethanol</b> intake and reinforcement in an <b>ethanol</b> preferring mouse model.
+PER2	addiction	reward	23608482	Mutation of either Per1 or <strong>Per2</strong>, as well as mutations of both genes, increases ethanol intake and <b>reinforcement</b> in an ethanol preferring mouse model.
+PER2	drug	alcohol	23550834	In particular, the <strong>Per2</strong> gene regulates <b>alcohol</b> consumption in mutant animals, and in humans with AUD, the 10870 variant in <strong>PER2</strong> has been associated with <b>alcohol</b> consumption.
+PER2	drug	amphetamine	23518151	In the striatum, acute injection of d <b>amphetamine</b> did not alter Period (Per)1, <strong>Per2</strong> and Reverse erythroblastosis virus α (Rev erbα) expressions.
+PER2	drug	amphetamine	23518151	Chronic administration shifted the phase of Per1 and <strong>Per2</strong> expressions from a nocturnal to diurnal pattern and advance shifted the peak of Rev erbα in d <b>amphetamine</b> treated animals.
+PER2	drug	cocaine	22832851	Repeat variation in the human <strong>PER2</strong> gene as a new genetic marker associated with <b>cocaine</b> addiction and brain dopamine D2 receptor availability.
+PER2	addiction	addiction	22832851	Repeat variation in the human <strong>PER2</strong> gene as a new genetic marker associated with cocaine <b>addiction</b> and brain dopamine D2 receptor availability.
+PER2	addiction	addiction	22832851	Aberrant periodicity of <strong>PER2</strong> contributes to the incidence and severity of various brain disorders, including drug <b>addiction</b>.
+PER2	drug	cocaine	22832851	We also detected a biased <strong>PER2</strong> genotype distribution among healthy controls and <b>cocaine</b> addicted individuals.
+PER2	drug	cocaine	22832851	Taken together, these results provide preliminary evidence for the role of the <strong>PER2</strong> gene in regulating striatal D2R availability in the human brain and in vulnerability for <b>cocaine</b> addiction.
+PER2	addiction	addiction	22832851	Taken together, these results provide preliminary evidence for the role of the <strong>PER2</strong> gene in regulating striatal D2R availability in the human brain and in vulnerability for cocaine <b>addiction</b>.
+PER2	drug	alcohol	22286266	Chronic administration of <b>ethanol</b> significantly augmented mean expression of pituitary nitric oxide synthase (NOS) 2, heme oxygenase (HO) 1, Per1 and <strong>Per2</strong> genes and disrupted their diurnal rhythmicity.
+PER2	drug	alcohol	22286266	Decreased NOS 1 and NOS 2 expression during scotophase, together with suppression of the rhythm in Per1 and <strong>Per2</strong> expression, were found in the discontinuous <b>ethanol</b> group.
+PER2	drug	alcohol	21929298	The <strong>PER2</strong> clock gene modulates <b>ethanol</b> consumption, such that mutant mice not expressing functional mPer2 have altered circadian behavior that promotes higher <b>ethanol</b> intake and preference.
+PER2	addiction	withdrawal	21536108	and its <b>withdrawal</b> on 24 h wheel running activity and on the expression of the clock protein, PERIOD2 (<strong>PER2</strong>), in the suprachiasmatic nucleus (SCN), oval nucleus of the bed nucleus of the stria terminalis (BNSTov), central amygdala (CEA), and dorsal striatum.
+PER2	drug	opioid	21536108	Neither <b>morphine</b> injection nor its withdrawal affected <strong>PER2</strong> expression in the SCN, whereas the normal daily peaks of <strong>PER2</strong> in the BNSTov, CEA, and dorsal striatum were blunted both during <b>morphine</b> administration and its withdrawal.
+PER2	addiction	withdrawal	21536108	Neither morphine injection nor its <b>withdrawal</b> affected <strong>PER2</strong> expression in the SCN, whereas the normal daily peaks of <strong>PER2</strong> in the BNSTov, CEA, and dorsal striatum were blunted both during morphine administration and its <b>withdrawal</b>.
+PER2	drug	opioid	21536108	Treatment with a dopaminergic agonist (the D2/3 agonist, quinpirole, 1.0 mg/kg) or a noradrenergic agonist (alpha2 agonist, clonidine, 0.1 mg/kg) in <b>morphine</b> withdrawal did not restore normal <strong>PER2</strong> patterns in each affected region; however, both quinpirole and clonidine themselves altered normal daily <strong>PER2</strong> expression patterns in <b>morphine</b> naive rats.
+PER2	addiction	withdrawal	21536108	Treatment with a dopaminergic agonist (the D2/3 agonist, quinpirole, 1.0 mg/kg) or a noradrenergic agonist (alpha2 agonist, clonidine, 0.1 mg/kg) in morphine <b>withdrawal</b> did not restore normal <strong>PER2</strong> patterns in each affected region; however, both quinpirole and clonidine themselves altered normal daily <strong>PER2</strong> expression patterns in morphine naive rats.
+PER2	drug	opioid	21536108	Furthermore, catecholaminergic drugs, which have been previously found to alleviate symptoms of opiate withdrawal, do not alleviate the effects of <b>morphine</b> withdrawal on <strong>PER2</strong>, but do modulate daily patterns of <strong>PER2</strong> expression in saline controls.
+PER2	addiction	withdrawal	21536108	Furthermore, catecholaminergic drugs, which have been previously found to alleviate symptoms of opiate <b>withdrawal</b>, do not alleviate the effects of morphine <b>withdrawal</b> on <strong>PER2</strong>, but do modulate daily patterns of <strong>PER2</strong> expression in saline controls.
+PER2	drug	opioid	20434889	At first, we checked the absence of initial differences in the expression of several gene transcripts involved in the development of <b>morphine</b> dependence in <strong>Per2</strong>(Brdm1) mutant mice and in their respective wild type (WT) control littermates.
+PER2	addiction	dependence	20434889	At first, we checked the absence of initial differences in the expression of several gene transcripts involved in the development of morphine <b>dependence</b> in <strong>Per2</strong>(Brdm1) mutant mice and in their respective wild type (WT) control littermates.
+PER2	addiction	withdrawal	20434889	The <strong>Per2</strong>(Brdm1) mutant mice clearly developed less tolerance and showed attenuated <b>withdrawal</b> signs compared to WT.
+PER2	drug	opioid	19786507	Many genes were significantly regulated by <b>oxycodone</b> (e.g., Fkbp5, <strong>Per2</strong>, Rt1.Dalpha, Slc16a1, and Abcg2).
+PER2	drug	cocaine	17360649	Recent studies have suggested that components of the circadian pacemaker, such as the Clock and <strong>Per2</strong> gene products, regulate a wide variety of processes, including obesity, sensitization to <b>cocaine</b>, cancer susceptibility, and morbidity to chemotherapeutic agents.
+PER2	addiction	sensitization	17360649	Recent studies have suggested that components of the circadian pacemaker, such as the Clock and <strong>Per2</strong> gene products, regulate a wide variety of processes, including obesity, <b>sensitization</b> to cocaine, cancer susceptibility, and morbidity to chemotherapeutic agents.
+PER2	drug	cocaine	17106427	Human clock, PER1 and <strong>PER2</strong> polymorphisms: lack of association with <b>cocaine</b> dependence susceptibility and <b>cocaine</b> induced paranoia.
+PER2	addiction	dependence	17106427	Human clock, PER1 and <strong>PER2</strong> polymorphisms: lack of association with cocaine <b>dependence</b> susceptibility and cocaine induced paranoia.
+PER2	drug	cocaine	17051414	Previously, our lab demonstrated the involvement of mouse Per1 (mPer1) and <strong>Per2</strong> (mPer2) in modulating <b>cocaine</b> sensitization and reward.
+PER2	addiction	reward	17051414	Previously, our lab demonstrated the involvement of mouse Per1 (mPer1) and <strong>Per2</strong> (mPer2) in modulating cocaine sensitization and <b>reward</b>.
+PER2	addiction	sensitization	17051414	Previously, our lab demonstrated the involvement of mouse Per1 (mPer1) and <strong>Per2</strong> (mPer2) in modulating cocaine <b>sensitization</b> and reward.
+PER2	drug	alcohol	17051414	What is more, we investigated voluntary <b>alcohol</b> consumption in <strong>Per2</strong> (Brdm1) mice with the results suggesting a relationship between this circadian clock gene and <b>ethanol</b> consumption.
+PER2	drug	alcohol	16156052	In turn, <strong>per2</strong> gene activity regulates <b>alcohol</b> intake through its effects on the glutamatergic system through glutamate reuptake mechanisms and thereby may affect a variety of physiological processes that are governed by our internal clock.
+PER2	drug	alcohol	15608650	The clock gene <strong>Per2</strong> influences the glutamatergic system and modulates <b>alcohol</b> consumption.
+PER2	drug	alcohol	15608650	In humans, variations of the <strong>PER2</strong> gene are associated with regulation of <b>alcohol</b> consumption.
+PER2	drug	alcohol	15608650	This drug reduced augmented glutamate levels and normalized increased <b>alcohol</b> consumption in <strong>Per2</strong>(Brdm1) mutant mice.
+PER2	drug	alcohol	15608650	Collectively, these data establish glutamate as a link between dysfunction of the circadian clock gene <strong>Per2</strong> and enhanced <b>alcohol</b> intake.
+PER2	drug	amphetamine	15542705	Several clones were chosen as positive candidates for <b>methamphetamine</b> induced changes; however, only <strong>Per2</strong> and mKIAA0099 genes showed a significantly increased expression (P < .05).
+PER2	drug	amphetamine	15542705	Chronic administration of <b>methamphetamine</b> (8 mg/kg, i.p., for 10 days) caused increased <strong>Per2</strong> protein expression in the hippocampus.
+PER2	drug	cocaine	12687634	A differential expression of somatostatin receptor SSTR2, not known to be a <b>cocaine</b> responsive gene, as well as the clock gene <strong>Per2</strong>, were found by microarrays and confirmed by RNase protection assay.
+NFE2L2	drug	alcohol	32710977	Sulforaphane alleviates <b>ethanol</b> mediated central inhibition and reverses chronic stress induced aggravation of acute <b>alcoholism</b> via targeting <strong>Nrf2</strong> regulated catalase expression.
+NFE2L2	drug	alcohol	32710977	Sulforaphane alleviates <b>ethanol</b> mediated central inhibition and reverses chronic stress induced aggravation of acute <b>alcoholism</b> via targeting <strong><strong>Nrf2</strong></strong> regulated catalase expression.
+NFE2L2	drug	alcohol	32710977	Here, we reported that chronic unpredictable stress increased the sensitivity to the acute <b>ethanol</b> intoxication in mice via impairing nuclear factor (erythroid derived 2) like 2 (<strong>Nrf2</strong>) catalase signaling.
+NFE2L2	addiction	intoxication	32710977	Here, we reported that chronic unpredictable stress increased the sensitivity to the acute ethanol <b>intoxication</b> in mice via impairing nuclear factor (erythroid derived 2) like 2 (<strong>Nrf2</strong>) catalase signaling.
+NFE2L2	drug	alcohol	32710977	Here, we reported that chronic unpredictable stress increased the sensitivity to the acute <b>ethanol</b> intoxication in mice via impairing nuclear factor (erythroid derived 2) like 2 (<strong><strong>Nrf2</strong></strong>) catalase signaling.
+NFE2L2	addiction	intoxication	32710977	Here, we reported that chronic unpredictable stress increased the sensitivity to the acute ethanol <b>intoxication</b> in mice via impairing nuclear factor (erythroid derived 2) like 2 (<strong><strong>Nrf2</strong></strong>) catalase signaling.
+NFE2L2	drug	alcohol	32710977	<strong>Nrf2</strong> activity regulates the expression of catalase, a key antioxidant enzyme that mediates <b>ethanol</b> oxidation in the brain.
+NFE2L2	drug	alcohol	32710977	<strong><strong>Nrf2</strong></strong> activity regulates the expression of catalase, a key antioxidant enzyme that mediates <b>ethanol</b> oxidation in the brain.
+NFE2L2	drug	alcohol	32710977	Pharmacological blockade of catalase or <strong>Nrf2</strong> activity significantly aggravated acute <b>ethanol</b> intoxication.
+NFE2L2	addiction	intoxication	32710977	Pharmacological blockade of catalase or <strong>Nrf2</strong> activity significantly aggravated acute ethanol <b>intoxication</b>.
+NFE2L2	drug	alcohol	32710977	Pharmacological blockade of catalase or <strong><strong>Nrf2</strong></strong> activity significantly aggravated acute <b>ethanol</b> intoxication.
+NFE2L2	addiction	intoxication	32710977	Pharmacological blockade of catalase or <strong><strong>Nrf2</strong></strong> activity significantly aggravated acute ethanol <b>intoxication</b>.
+NFE2L2	drug	alcohol	32710977	Sulforaphane, a cruciferous vegetable derived activator of <strong>Nrf2</strong>, significantly attenuated acute <b>ethanol</b> intoxication.
+NFE2L2	addiction	intoxication	32710977	Sulforaphane, a cruciferous vegetable derived activator of <strong>Nrf2</strong>, significantly attenuated acute ethanol <b>intoxication</b>.
+NFE2L2	drug	alcohol	32710977	Sulforaphane, a cruciferous vegetable derived activator of <strong><strong>Nrf2</strong></strong>, significantly attenuated acute <b>ethanol</b> intoxication.
+NFE2L2	addiction	intoxication	32710977	Sulforaphane, a cruciferous vegetable derived activator of <strong><strong>Nrf2</strong></strong>, significantly attenuated acute ethanol <b>intoxication</b>.
+NFE2L2	drug	alcohol	32710977	Our findings suggest that <strong>Nrf2</strong> may function as a novel drug target for the prevention of acute <b>alcoholism</b>, especially in psychiatric patients, by controlling catalase mediated <b>ethanol</b> oxidation.
+NFE2L2	drug	alcohol	32710977	Our findings suggest that <strong><strong>Nrf2</strong></strong> may function as a novel drug target for the prevention of acute <b>alcoholism</b>, especially in psychiatric patients, by controlling catalase mediated <b>ethanol</b> oxidation.
+NFE2L2	addiction	intoxication	32416118	Our results indicate that MC4R agonist reduces hippocampal oxidative damage promoting antioxidant (<strong>Nrf 2</strong>) and mitochondrial biogenesis (PGC1 alpha) pathways in animals subjected to the <b>binge</b> like protocol.
+NFE2L2	drug	alcohol	32378055	These results suggest that the stimulation of MC4R prevents oxidative damage and mitochondrial stress induced by <b>ethanol</b> through the activation of the <strong>Nrf 2</strong> pathway in cultured hippocampal neurons.
+NFE2L2	drug	amphetamine	31775383	Additionally, Ingenuity® Pathway Analysis along with details of RNA expression changes revealed cyclo oxygenase 2 (COX2) driven prostaglandin (PG) E2 synthesis, glutamine uptake, and the Nuclear factor erythroid2 related factor 2 (<strong>NRF2</strong>) canonical pathway in microglia were associated with the binge administration regimen of <b>METH</b>.
+NFE2L2	addiction	intoxication	31775383	Additionally, Ingenuity® Pathway Analysis along with details of RNA expression changes revealed cyclo oxygenase 2 (COX2) driven prostaglandin (PG) E2 synthesis, glutamine uptake, and the Nuclear factor erythroid2 related factor 2 (<strong>NRF2</strong>) canonical pathway in microglia were associated with the <b>binge</b> administration regimen of METH.
+NFE2L2	drug	amphetamine	31775383	Additionally, Ingenuity® Pathway Analysis along with details of RNA expression changes revealed cyclo oxygenase 2 (COX2) driven prostaglandin (PG) E2 synthesis, glutamine uptake, and the Nuclear factor erythroid2 related factor 2 (<strong><strong>NRF2</strong></strong>) canonical pathway in microglia were associated with the binge administration regimen of <b>METH</b>.
+NFE2L2	addiction	intoxication	31775383	Additionally, Ingenuity® Pathway Analysis along with details of RNA expression changes revealed cyclo oxygenase 2 (COX2) driven prostaglandin (PG) E2 synthesis, glutamine uptake, and the Nuclear factor erythroid2 related factor 2 (<strong><strong>NRF2</strong></strong>) canonical pathway in microglia were associated with the <b>binge</b> administration regimen of METH.
+NFE2L2	drug	cocaine	31100299	We also analyzed the ability of the β lactam antibiotic, ceftriaxone, to attenuate the persistence of CPP after a <b>cocaine</b> free period in animals showing vulnerability to <b>cocaine</b> rewarding effects, and furthermore we determined GLT 1, xCT, NF κB and <strong>Nrf2</strong> protein expression.
+NFE2L2	addiction	reward	31100299	We also analyzed the ability of the β lactam antibiotic, ceftriaxone, to attenuate the persistence of <b>CPP</b> after a cocaine free period in animals showing vulnerability to cocaine rewarding effects, and furthermore we determined GLT 1, xCT, NF κB and <strong>Nrf2</strong> protein expression.
+NFE2L2	drug	cocaine	31100299	We also analyzed the ability of the β lactam antibiotic, ceftriaxone, to attenuate the persistence of CPP after a <b>cocaine</b> free period in animals showing vulnerability to <b>cocaine</b> rewarding effects, and furthermore we determined GLT 1, xCT, NF κB and <strong><strong>Nrf2</strong></strong> protein expression.
+NFE2L2	addiction	reward	31100299	We also analyzed the ability of the β lactam antibiotic, ceftriaxone, to attenuate the persistence of <b>CPP</b> after a cocaine free period in animals showing vulnerability to cocaine rewarding effects, and furthermore we determined GLT 1, xCT, NF κB and <strong><strong>Nrf2</strong></strong> protein expression.
+NFE2L2	drug	alcohol	31096703	Natural Dietary Supplementation of Curcumin Protects Mice Brains against <b>Ethanol</b> Induced Oxidative Stress Mediated Neurodegeneration and Memory Impairment via <strong>Nrf2</strong>/TLR4/RAGE Signaling.
+NFE2L2	drug	alcohol	31096703	Natural Dietary Supplementation of Curcumin Protects Mice Brains against <b>Ethanol</b> Induced Oxidative Stress Mediated Neurodegeneration and Memory Impairment via <strong><strong>Nrf2</strong></strong>/TLR4/RAGE Signaling.
+NFE2L2	drug	alcohol	31096703	According to our findings, <b>ethanol</b> triggered reactive oxygen species (ROS), apoptosis, neuroinflammation, and memory impairment, which were significantly inhibited with the administration of curcumin, as assessed by ROS, lipid peroxidation (LPO), and <strong>Nrf2</strong>/HO 1 (nuclear factor erythroid 2 related factor 2/Heme oxygenase 1) expression in the experimental mice brains.
+NFE2L2	drug	alcohol	31096703	According to our findings, <b>ethanol</b> triggered reactive oxygen species (ROS), apoptosis, neuroinflammation, and memory impairment, which were significantly inhibited with the administration of curcumin, as assessed by ROS, lipid peroxidation (LPO), and <strong><strong>Nrf2</strong></strong>/HO 1 (nuclear factor erythroid 2 related factor 2/Heme oxygenase 1) expression in the experimental mice brains.
+NFE2L2	drug	nicotine	30533170	Coincubation with N acetylcysteine or L ascorbate improves impaired osteogenesis caused by cigarette smoke exposure by both activation of nuclear factor erythroid 2 related factor 2 (<strong>Nrf2</strong>) signaling and scavenging of ROS, which thus might represent therapeutic targets to support fracture healing in <b>smokers</b>.
+NFE2L2	drug	nicotine	30533170	Coincubation with N acetylcysteine or L ascorbate improves impaired osteogenesis caused by cigarette smoke exposure by both activation of nuclear factor erythroid 2 related factor 2 (<strong><strong>Nrf2</strong></strong>) signaling and scavenging of ROS, which thus might represent therapeutic targets to support fracture healing in <b>smokers</b>.
+NFE2L2	drug	amphetamine	30500461	Exposure to FIR protects from <b>methamphetamine</b> (MA) induced memory impairments via phosphorylation of ERK 1/2 signaling by positive modulation of protein kinase C δ (PKCδ), M1 muscarinic acetylcholine receptor (M1 mAChR), and nuclear factor E2 related factor 2 (<strong>Nrf2</strong>) transcription factor.
+NFE2L2	drug	amphetamine	30500461	Exposure to FIR protects from <b>methamphetamine</b> (MA) induced memory impairments via phosphorylation of ERK 1/2 signaling by positive modulation of protein kinase C δ (PKCδ), M1 muscarinic acetylcholine receptor (M1 mAChR), and nuclear factor E2 related factor 2 (<strong><strong>Nrf2</strong></strong>) transcription factor.
+NFE2L2	drug	alcohol	30248482	<strong>NRF2</strong> mitigates acute <b>alcohol</b> induced hepatic and pancreatic injury in mice.
+NFE2L2	drug	alcohol	30248482	<strong><strong>NRF2</strong></strong> mitigates acute <b>alcohol</b> induced hepatic and pancreatic injury in mice.
+NFE2L2	drug	alcohol	30248482	However, the role of <strong>NRF2</strong> in acute <b>alcoholism</b> and associated pathologies remains unclear.
+NFE2L2	drug	alcohol	30248482	However, the role of <strong><strong>NRF2</strong></strong> in acute <b>alcoholism</b> and associated pathologies remains unclear.
+NFE2L2	drug	alcohol	30248482	We found that <strong>Nrf2</strong> knockout (<strong>Nrf2</strong> KO) mice had exaggerated hypoglycemia and hypothermia and increased mortality compared to wildtype mice after binge <b>ethanol</b> exposure.
+NFE2L2	addiction	intoxication	30248482	We found that <strong>Nrf2</strong> knockout (<strong>Nrf2</strong> KO) mice had exaggerated hypoglycemia and hypothermia and increased mortality compared to wildtype mice after <b>binge</b> ethanol exposure.
+NFE2L2	drug	alcohol	30248482	We found that <strong><strong>Nrf2</strong></strong> knockout (<strong><strong>Nrf2</strong></strong> KO) mice had exaggerated hypoglycemia and hypothermia and increased mortality compared to wildtype mice after binge <b>ethanol</b> exposure.
+NFE2L2	addiction	intoxication	30248482	We found that <strong><strong>Nrf2</strong></strong> knockout (<strong><strong>Nrf2</strong></strong> KO) mice had exaggerated hypoglycemia and hypothermia and increased mortality compared to wildtype mice after <b>binge</b> ethanol exposure.
+NFE2L2	drug	alcohol	30248482	Acute high dose of <b>alcohol</b> exposure resulted in substantially worsened liver and pancreatic injuries in <strong>Nrf2</strong> KO mice.
+NFE2L2	drug	alcohol	30248482	Acute high dose of <b>alcohol</b> exposure resulted in substantially worsened liver and pancreatic injuries in <strong><strong>Nrf2</strong></strong> KO mice.
+NFE2L2	drug	alcohol	30248482	Importantly, deficiency of <strong>Nrf2</strong> allowed severe pancreatitis and pancreatic β cell injury with increased insulin secretion and/or leaking during binge <b>ethanol</b> exposure, which contributed to hypoglycemia.
+NFE2L2	addiction	intoxication	30248482	Importantly, deficiency of <strong>Nrf2</strong> allowed severe pancreatitis and pancreatic β cell injury with increased insulin secretion and/or leaking during <b>binge</b> ethanol exposure, which contributed to hypoglycemia.
+NFE2L2	drug	alcohol	30248482	Importantly, deficiency of <strong><strong>Nrf2</strong></strong> allowed severe pancreatitis and pancreatic β cell injury with increased insulin secretion and/or leaking during binge <b>ethanol</b> exposure, which contributed to hypoglycemia.
+NFE2L2	addiction	intoxication	30248482	Importantly, deficiency of <strong><strong>Nrf2</strong></strong> allowed severe pancreatitis and pancreatic β cell injury with increased insulin secretion and/or leaking during <b>binge</b> ethanol exposure, which contributed to hypoglycemia.
+NFE2L2	drug	alcohol	30248482	In contrast, a clinically used <strong>NRF2</strong> activator dimethyl fumarate (DMF) protected against hypoglycemia and lethality induced by acute <b>ethanol</b> exposure.
+NFE2L2	drug	alcohol	30248482	In contrast, a clinically used <strong><strong>NRF2</strong></strong> activator dimethyl fumarate (DMF) protected against hypoglycemia and lethality induced by acute <b>ethanol</b> exposure.
+NFE2L2	drug	alcohol	30248482	Taken together, <strong>NRF2</strong> plays an important protective role against acute binge <b>alcohol</b> induced hepatic and pancreatic damage, which may be partially attributable to its primary regulating role in antioxidant response and impact on <b>ethanol</b> metabolism.
+NFE2L2	addiction	intoxication	30248482	Taken together, <strong>NRF2</strong> plays an important protective role against acute <b>binge</b> alcohol induced hepatic and pancreatic damage, which may be partially attributable to its primary regulating role in antioxidant response and impact on ethanol metabolism.
+NFE2L2	drug	alcohol	30248482	Taken together, <strong><strong>NRF2</strong></strong> plays an important protective role against acute binge <b>alcohol</b> induced hepatic and pancreatic damage, which may be partially attributable to its primary regulating role in antioxidant response and impact on <b>ethanol</b> metabolism.
+NFE2L2	addiction	intoxication	30248482	Taken together, <strong><strong>NRF2</strong></strong> plays an important protective role against acute <b>binge</b> alcohol induced hepatic and pancreatic damage, which may be partially attributable to its primary regulating role in antioxidant response and impact on ethanol metabolism.
+NFE2L2	drug	alcohol	28951767	Baicalin Ameliorates Liver Injury Induced by Chronic plus Binge <b>Ethanol</b> Feeding by Modulating Oxidative Stress and Inflammation via CYP2E1 and <strong>NRF2</strong> in Mice.
+NFE2L2	addiction	intoxication	28951767	Baicalin Ameliorates Liver Injury Induced by Chronic plus <b>Binge</b> Ethanol Feeding by Modulating Oxidative Stress and Inflammation via CYP2E1 and <strong>NRF2</strong> in Mice.
+NFE2L2	drug	alcohol	28951767	Baicalin Ameliorates Liver Injury Induced by Chronic plus Binge <b>Ethanol</b> Feeding by Modulating Oxidative Stress and Inflammation via CYP2E1 and <strong><strong>NRF2</strong></strong> in Mice.
+NFE2L2	addiction	intoxication	28951767	Baicalin Ameliorates Liver Injury Induced by Chronic plus <b>Binge</b> Ethanol Feeding by Modulating Oxidative Stress and Inflammation via CYP2E1 and <strong><strong>NRF2</strong></strong> in Mice.
+NFE2L2	drug	alcohol	28951767	Baicalin also enhanced <b>ethanol</b> induced <strong>NRF2</strong> nuclear translocation and increased downstream target gene HO 1 as antioxidant defense.
+NFE2L2	drug	alcohol	28951767	Baicalin also enhanced <b>ethanol</b> induced <strong><strong>NRF2</strong></strong> nuclear translocation and increased downstream target gene HO 1 as antioxidant defense.
+NFE2L2	drug	alcohol	28924552	Schisandra sphenanthera extract (Wuzhi Tablet) protects against chronic binge and acute <b>alcohol</b> induced liver injury by regulating the <strong>NRF2</strong> ARE pathway in mice.
+NFE2L2	addiction	intoxication	28924552	Schisandra sphenanthera extract (Wuzhi Tablet) protects against chronic <b>binge</b> and acute alcohol induced liver injury by regulating the <strong>NRF2</strong> ARE pathway in mice.
+NFE2L2	drug	alcohol	28924552	Schisandra sphenanthera extract (Wuzhi Tablet) protects against chronic binge and acute <b>alcohol</b> induced liver injury by regulating the <strong><strong>NRF2</strong></strong> ARE pathway in mice.
+NFE2L2	addiction	intoxication	28924552	Schisandra sphenanthera extract (Wuzhi Tablet) protects against chronic <b>binge</b> and acute alcohol induced liver injury by regulating the <strong><strong>NRF2</strong></strong> ARE pathway in mice.
+NFE2L2	drug	alcohol	28924552	Collectively, our study demonstrates that WZ protected against <b>alcohol</b> induced liver injury by reducing oxidative stress and improving antioxidant defense, possibly by activating the <strong>NRF2</strong> ARE pathway.
+NFE2L2	drug	alcohol	28924552	Collectively, our study demonstrates that WZ protected against <b>alcohol</b> induced liver injury by reducing oxidative stress and improving antioxidant defense, possibly by activating the <strong><strong>NRF2</strong></strong> ARE pathway.
+NFE2L2	addiction	intoxication	28776218	Molecular pathology of cerebral TNF α, IL 1β, iNOS and <strong>Nrf2</strong> in forensic autopsy cases with special regard to deaths due to environmental hazards and <b>intoxication</b>.
+NFE2L2	addiction	intoxication	28776218	Molecular pathology of cerebral TNF α, IL 1β, iNOS and <strong><strong>Nrf2</strong></strong> in forensic autopsy cases with special regard to deaths due to environmental hazards and <b>intoxication</b>.
+NFE2L2	drug	amphetamine	28776218	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of IL 1β, TNF α and iNOS, and lower expression of <strong>Nrf2</strong> in <b>methamphetamine</b> intoxication and hyperthermia cases, higher expression of iNOS in phenobarbital intoxication cases, and higher expression of <strong>Nrf2</strong> in phenobarbital intoxication and hypothermia cases.
+NFE2L2	addiction	intoxication	28776218	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of IL 1β, TNF α and iNOS, and lower expression of <strong>Nrf2</strong> in methamphetamine <b>intoxication</b> and hyperthermia cases, higher expression of iNOS in phenobarbital <b>intoxication</b> cases, and higher expression of <strong>Nrf2</strong> in phenobarbital <b>intoxication</b> and hypothermia cases.
+NFE2L2	drug	amphetamine	28776218	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of IL 1β, TNF α and iNOS, and lower expression of <strong><strong>Nrf2</strong></strong> in <b>methamphetamine</b> intoxication and hyperthermia cases, higher expression of iNOS in phenobarbital intoxication cases, and higher expression of <strong><strong>Nrf2</strong></strong> in phenobarbital intoxication and hypothermia cases.
+NFE2L2	addiction	intoxication	28776218	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of IL 1β, TNF α and iNOS, and lower expression of <strong><strong>Nrf2</strong></strong> in methamphetamine <b>intoxication</b> and hyperthermia cases, higher expression of iNOS in phenobarbital <b>intoxication</b> cases, and higher expression of <strong><strong>Nrf2</strong></strong> in phenobarbital <b>intoxication</b> and hypothermia cases.
+NFE2L2	drug	nicotine	28641491	<b>Nicotine</b> and cigarette smoke modulate <strong>Nrf2</strong> BDNF dopaminergic signal and neurobehavioral disorders in adult rat cerebral cortex.
+NFE2L2	drug	nicotine	28641491	<b>Nicotine</b> and cigarette smoke modulate <strong><strong>Nrf2</strong></strong> BDNF dopaminergic signal and neurobehavioral disorders in adult rat cerebral cortex.
+NFE2L2	drug	alcohol	28501008	<b>Ethanol</b> extract and its dichloromethane fraction of Alpinia oxyphylla Miquel exhibited hepatoprotective effects against CCl4 induced oxidative damage in vitro and in vivo with the involvement of <strong>Nrf2</strong>.
+NFE2L2	drug	alcohol	28501008	<b>Ethanol</b> extract and its dichloromethane fraction of Alpinia oxyphylla Miquel exhibited hepatoprotective effects against CCl4 induced oxidative damage in vitro and in vivo with the involvement of <strong><strong>Nrf2</strong></strong>.
+NFE2L2	drug	amphetamine	26427884	We investigated whether <strong>Nrf2</strong> is activated by <b>methamphetamine</b> (<b>METH</b>) thereby altering neurotoxicity in <strong>Nrf2</strong> +/+ and  /  adult mouse brain.
+NFE2L2	drug	amphetamine	26427884	We investigated whether <strong><strong>Nrf2</strong></strong> is activated by <b>methamphetamine</b> (<b>METH</b>) thereby altering neurotoxicity in <strong><strong>Nrf2</strong></strong> +/+ and  /  adult mouse brain.
+NFE2L2	drug	amphetamine	26427884	A single dose of <b>METH</b> can induce the mRNA levels of <strong>Nrf2</strong> regulated antioxidant and cytoprotective proteins in mouse brain.
+NFE2L2	drug	amphetamine	26427884	A single dose of <b>METH</b> can induce the mRNA levels of <strong><strong>Nrf2</strong></strong> regulated antioxidant and cytoprotective proteins in mouse brain.
+NFE2L2	drug	amphetamine	26427884	These <strong>Nrf2</strong> dependent effects were independent of changes in <b>METH</b> metabolism or the induction of hyperthermia.
+NFE2L2	drug	amphetamine	26427884	These <strong><strong>Nrf2</strong></strong> dependent effects were independent of changes in <b>METH</b> metabolism or the induction of hyperthermia.
+NFE2L2	drug	amphetamine	26427884	<strong>Nrf2</strong> mediated pathways accordingly may protect against the neurodegenerative effects and functional deficits initiated by <b>METH</b> and perhaps other reactive oxygen species enhancing neurotoxicants, when there is time for transcriptional activation and protein induction.
+NFE2L2	drug	amphetamine	26427884	<strong><strong>Nrf2</strong></strong> mediated pathways accordingly may protect against the neurodegenerative effects and functional deficits initiated by <b>METH</b> and perhaps other reactive oxygen species enhancing neurotoxicants, when there is time for transcriptional activation and protein induction.
+NFE2L2	drug	amphetamine	26427884	In human users of <b>METH</b>, this mechanism may be essential when differences in drug abuse patterns may alter the induction and duration of <strong>Nrf2</strong> activation thereby modulating susceptibility to the neurotoxic effects of <b>METH</b>.
+NFE2L2	drug	amphetamine	26427884	In human users of <b>METH</b>, this mechanism may be essential when differences in drug abuse patterns may alter the induction and duration of <strong><strong>Nrf2</strong></strong> activation thereby modulating susceptibility to the neurotoxic effects of <b>METH</b>.
+NFE2L2	drug	alcohol	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates <b>ethanol</b> induced liver injury through modulation of AMPK and <strong>Nrf2</strong> related signals in a binge drinking mouse model.
+NFE2L2	addiction	intoxication	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates ethanol induced liver injury through modulation of AMPK and <strong>Nrf2</strong> related signals in a <b>binge</b> drinking mouse model.
+NFE2L2	drug	alcohol	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates <b>ethanol</b> induced liver injury through modulation of AMPK and <strong><strong>Nrf2</strong></strong> related signals in a binge drinking mouse model.
+NFE2L2	addiction	intoxication	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates ethanol induced liver injury through modulation of AMPK and <strong><strong>Nrf2</strong></strong> related signals in a <b>binge</b> drinking mouse model.
+NFE2L2	drug	opioid	25542428	However, the <b>morphine</b> induced increase in <strong>nrf2</strong> nuclear translocation in the frontal cortex and striatum was inhibited by bergenin treatment.
+NFE2L2	drug	opioid	25542428	However, the <b>morphine</b> induced increase in <strong><strong>nrf2</strong></strong> nuclear translocation in the frontal cortex and striatum was inhibited by bergenin treatment.
+NFE2L2	drug	alcohol	24060752	Sulforaphane induces <strong>Nrf2</strong> and protects against CYP2E1 dependent binge <b>alcohol</b> induced liver steatosis.
+NFE2L2	addiction	intoxication	24060752	Sulforaphane induces <strong>Nrf2</strong> and protects against CYP2E1 dependent <b>binge</b> alcohol induced liver steatosis.
+NFE2L2	drug	alcohol	24060752	Sulforaphane induces <strong><strong>Nrf2</strong></strong> and protects against CYP2E1 dependent binge <b>alcohol</b> induced liver steatosis.
+NFE2L2	addiction	intoxication	24060752	Sulforaphane induces <strong><strong>Nrf2</strong></strong> and protects against CYP2E1 dependent <b>binge</b> alcohol induced liver steatosis.
+NFE2L2	drug	alcohol	24060752	The current study was designed to evaluate the ability of sulforaphane, an activator of <strong>Nrf2</strong>, to blunt CYP2E1 dependent, <b>ethanol</b> induced steatosis in vivo and in vitro.
+NFE2L2	drug	alcohol	24060752	The current study was designed to evaluate the ability of sulforaphane, an activator of <strong><strong>Nrf2</strong></strong>, to blunt CYP2E1 dependent, <b>ethanol</b> induced steatosis in vivo and in vitro.
+NFE2L2	drug	alcohol	24060752	The sulforaphane treatment activated <strong>Nrf2</strong>, increased levels of the <strong>Nrf2</strong> target heme oxygenase 1 and subsequently lowered oxidant stress as shown by the decline in lipid peroxidation and 3 nitrotyrosine protein adducts and an increase in GSH levels after the acute <b>ethanol</b> treatment.
+NFE2L2	drug	alcohol	24060752	The sulforaphane treatment activated <strong><strong>Nrf2</strong></strong>, increased levels of the <strong><strong>Nrf2</strong></strong> target heme oxygenase 1 and subsequently lowered oxidant stress as shown by the decline in lipid peroxidation and 3 nitrotyrosine protein adducts and an increase in GSH levels after the acute <b>ethanol</b> treatment.
+NFE2L2	drug	alcohol	24060752	Similar results were found in vitro as addition of sulforaphane to HepG2 E47 cells, which express CYP2E1, elevated <strong>Nrf2</strong> levels and decreased the accumulation of lipid in cells cultured with <b>ethanol</b>.
+NFE2L2	drug	alcohol	24060752	Similar results were found in vitro as addition of sulforaphane to HepG2 E47 cells, which express CYP2E1, elevated <strong><strong>Nrf2</strong></strong> levels and decreased the accumulation of lipid in cells cultured with <b>ethanol</b>.
+NFE2L2	addiction	addiction	24024172	In this study we show that activation of <strong>Nrf2</strong>, either by the small molecule sulforaphane or knockout of the <strong>Nrf2</strong> inhibitor Keap1, leads to increased cellular glucose uptake and increased glucose <b>addiction</b> in fibroblasts.
+NFE2L2	addiction	addiction	24024172	In this study we show that activation of <strong><strong>Nrf2</strong></strong>, either by the small molecule sulforaphane or knockout of the <strong><strong>Nrf2</strong></strong> inhibitor Keap1, leads to increased cellular glucose uptake and increased glucose <b>addiction</b> in fibroblasts.
+NFE2L2	drug	amphetamine	22903344	Moreover, our results also show that <b>METH</b> downregulated another transcription factor, the nuclear factor erythroid 2 related factor (<strong>Nrf2</strong>), a transcription factor implicated in the expression of several antioxidant/detoxificant enzymes.
+NFE2L2	drug	amphetamine	22903344	Moreover, our results also show that <b>METH</b> downregulated another transcription factor, the nuclear factor erythroid 2 related factor (<strong><strong>Nrf2</strong></strong>), a transcription factor implicated in the expression of several antioxidant/detoxificant enzymes.
+NFE2L2	drug	amphetamine	22903344	These results demonstrate, for the first time, that <b>METH</b> directly induces inflammation in neurons via an NF κB dependent pathway and that the anti neuroinflammatory effects of melatonin result from the inhibition of activated NF κB in parallel with potentiated antioxidant/detoxificant defense by activated <strong>Nrf2</strong> pathway.
+NFE2L2	drug	amphetamine	22903344	These results demonstrate, for the first time, that <b>METH</b> directly induces inflammation in neurons via an NF κB dependent pathway and that the anti neuroinflammatory effects of melatonin result from the inhibition of activated NF κB in parallel with potentiated antioxidant/detoxificant defense by activated <strong><strong>Nrf2</strong></strong> pathway.
+NFE2L2	drug	nicotine	22686525	<strong>Nrf2</strong>: friend and foe in preventing cigarette <b>smoking</b> dependent lung disease.
+NFE2L2	drug	nicotine	22686525	<strong><strong>Nrf2</strong></strong>: friend and foe in preventing cigarette <b>smoking</b> dependent lung disease.
+NFE2L2	addiction	dependence	22686525	This chemical trait is virtually predestined to be sensitized by the major route leading to <strong>Nrf2</strong> activation, characterized by its <b>dependence</b> on the interaction of electrophiles with specific cysteine residues inherited by <strong>Nrf2</strong>'s negative cytosolic regulator Keap1 (Kelch like ECH associated protein 1).
+NFE2L2	addiction	dependence	22686525	This chemical trait is virtually predestined to be sensitized by the major route leading to <strong><strong>Nrf2</strong></strong> activation, characterized by its <b>dependence</b> on the interaction of electrophiles with specific cysteine residues inherited by <strong><strong>Nrf2</strong></strong>'s negative cytosolic regulator Keap1 (Kelch like ECH associated protein 1).
+NFE2L2	drug	nicotine	22686525	In terms of the two major <b>smoking</b> related diseases of the lung, that is, emphysema and lung cancer, a fully functional <strong>Nrf2</strong> genotype seems to be necessary, although not sufficient by itself, to protect the <b>smoker</b> from acquiring emphysema.
+NFE2L2	drug	nicotine	22686525	In terms of the two major <b>smoking</b> related diseases of the lung, that is, emphysema and lung cancer, a fully functional <strong><strong>Nrf2</strong></strong> genotype seems to be necessary, although not sufficient by itself, to protect the <b>smoker</b> from acquiring emphysema.
+NFE2L2	drug	nicotine	22686525	Contrasting with this protective role, however, <strong>Nrf2</strong> function may be potentially fatal in <b>smoking</b> related lung tumorigenesis: as concluded from recent clinical investigations, lung tumor tissues harbor increased mutation or, alternatively, aberrant expression rates in either the KEAP1 or the <strong>NRF2</strong> gene, generally resulting in constitutive <strong>Nrf2</strong> activation, suggesting that "abuse" of <strong>Nrf2</strong> function is an advantageous strategy of the (developing) tumor to protect itself against oxidative stress in general.
+NFE2L2	drug	nicotine	22686525	Contrasting with this protective role, however, <strong><strong>Nrf2</strong></strong> function may be potentially fatal in <b>smoking</b> related lung tumorigenesis: as concluded from recent clinical investigations, lung tumor tissues harbor increased mutation or, alternatively, aberrant expression rates in either the KEAP1 or the <strong><strong>NRF2</strong></strong> gene, generally resulting in constitutive <strong><strong>Nrf2</strong></strong> activation, suggesting that "abuse" of <strong><strong>Nrf2</strong></strong> function is an advantageous strategy of the (developing) tumor to protect itself against oxidative stress in general.
+NFE2L2	drug	nicotine	22686525	On the basis of the fundamental significance of the <strong>Nrf2</strong> pathway in <b>smoking</b> dependent disease development, several attempts have been described for dietary and pharmacological intervention, the majority of which are intended to activate <strong>Nrf2</strong> aiming at emphysema prevention.
+NFE2L2	drug	nicotine	22686525	On the basis of the fundamental significance of the <strong><strong>Nrf2</strong></strong> pathway in <b>smoking</b> dependent disease development, several attempts have been described for dietary and pharmacological intervention, the majority of which are intended to activate <strong><strong>Nrf2</strong></strong> aiming at emphysema prevention.
+NFE2L2	drug	alcohol	22552773	<b>Ethanol</b> induction of CYP2A5: role of CYP2E1 ROS <strong>Nrf2</strong> pathway.
+NFE2L2	drug	alcohol	22552773	<b>Ethanol</b> induction of CYP2A5: role of CYP2E1 ROS <strong><strong>Nrf2</strong></strong> pathway.
+NFE2L2	drug	alcohol	22552773	The redox sensitive transcription factor nuclear factor erythroid 2 related factor 2 (<strong>Nrf2</strong>) was also induced by acute <b>ethanol</b> in Cyp2e1 ( / ) KI mice but not in Cyp2e1 ( / ) mice.
+NFE2L2	drug	alcohol	22552773	The redox sensitive transcription factor nuclear factor erythroid 2 related factor 2 (<strong><strong>Nrf2</strong></strong>) was also induced by acute <b>ethanol</b> in Cyp2e1 ( / ) KI mice but not in Cyp2e1 ( / ) mice.
+NFE2L2	drug	alcohol	22552773	<b>Ethanol</b> induction of CYP2A5 in <strong>Nrf2</strong> knockout (<strong>Nrf2</strong> ( / )) mice was lower compared with that in WT mice, whereas CYP2E1 induction by <b>ethanol</b> was comparable in WT and <strong>Nrf2</strong> ( / ) mice.
+NFE2L2	drug	alcohol	22552773	<b>Ethanol</b> induction of CYP2A5 in <strong><strong>Nrf2</strong></strong> knockout (<strong><strong>Nrf2</strong></strong> ( / )) mice was lower compared with that in WT mice, whereas CYP2E1 induction by <b>ethanol</b> was comparable in WT and <strong><strong>Nrf2</strong></strong> ( / ) mice.
+NFE2L2	drug	alcohol	22552773	Antioxidants (N acetyl cysteine and vitamin C), which blocked oxidative stress induced by chronic <b>ethanol</b> in WT mice and acute <b>ethanol</b> in Cyp2e1 ( / ) KI mice, also blunted the induction of CYP2A5 and <strong>Nrf2</strong> by <b>ethanol</b> but not the induction of CYP2E1 by <b>ethanol</b>.
+NFE2L2	drug	alcohol	22552773	Antioxidants (N acetyl cysteine and vitamin C), which blocked oxidative stress induced by chronic <b>ethanol</b> in WT mice and acute <b>ethanol</b> in Cyp2e1 ( / ) KI mice, also blunted the induction of CYP2A5 and <strong><strong>Nrf2</strong></strong> by <b>ethanol</b> but not the induction of CYP2E1 by <b>ethanol</b>.
+NFE2L2	drug	alcohol	22552773	These results suggest that oxidative stress induced by <b>ethanol</b> via induction of CYP2E1 upregulates <strong>Nrf2</strong> activity, which in turn regulates <b>ethanol</b> induction of CYP2A5.
+NFE2L2	drug	alcohol	22552773	These results suggest that oxidative stress induced by <b>ethanol</b> via induction of CYP2E1 upregulates <strong><strong>Nrf2</strong></strong> activity, which in turn regulates <b>ethanol</b> induction of CYP2A5.
+NFE2L2	drug	alcohol	22552773	Results obtained from primary hepatocytes, mice gavaged with binge <b>ethanol</b> or fed chronic <b>ethanol</b>, show that <strong>Nrf2</strong> regulated <b>ethanol</b> induction of CYP2A5 protects against <b>ethanol</b> induced steatosis.
+NFE2L2	addiction	intoxication	22552773	Results obtained from primary hepatocytes, mice gavaged with <b>binge</b> ethanol or fed chronic ethanol, show that <strong>Nrf2</strong> regulated ethanol induction of CYP2A5 protects against ethanol induced steatosis.
+NFE2L2	drug	alcohol	22552773	Results obtained from primary hepatocytes, mice gavaged with binge <b>ethanol</b> or fed chronic <b>ethanol</b>, show that <strong><strong>Nrf2</strong></strong> regulated <b>ethanol</b> induction of CYP2A5 protects against <b>ethanol</b> induced steatosis.
+NFE2L2	addiction	intoxication	22552773	Results obtained from primary hepatocytes, mice gavaged with <b>binge</b> ethanol or fed chronic ethanol, show that <strong><strong>Nrf2</strong></strong> regulated ethanol induction of CYP2A5 protects against ethanol induced steatosis.
+IL17A	drug	alcohol	32051339	Blockade of <strong>IL 17</strong> signaling reverses <b>alcohol</b> induced liver injury and excessive <b>alcohol</b> drinking in mice.
+IL17A	drug	alcohol	32051339	We compared experimental models of <b>alcoholic</b> liver disease (ALD) and <b>alcohol</b> dependence in mice and demonstrated that genetic ablation of <strong>IL 17</strong> receptor A (IL 17ra / ) or pharmacological blockade of <strong>IL 17</strong> signaling effectively suppressed the increased voluntary <b>alcohol</b> drinking in <b>alcohol</b> dependent mice and blocked <b>alcohol</b> induced hepatocellular and neurological damage.
+IL17A	addiction	dependence	32051339	We compared experimental models of alcoholic liver disease (ALD) and alcohol <b>dependence</b> in mice and demonstrated that genetic ablation of <strong>IL 17</strong> receptor A (IL 17ra / ) or pharmacological blockade of <strong>IL 17</strong> signaling effectively suppressed the increased voluntary alcohol drinking in alcohol dependent mice and blocked alcohol induced hepatocellular and neurological damage.
+IL17A	drug	alcohol	32051339	The level of circulating <strong>IL 17A</strong> positively correlated with the <b>alcohol</b> use in excessive drinkers and was further increased in patients with ALD as compared with healthy individuals.
+IL17A	drug	alcohol	32051339	Our data suggest that <strong>IL 17A</strong> is a common mediator of excessive <b>alcohol</b> consumption and <b>alcohol</b> induced liver/brain injury, and targeting <strong>IL 17A</strong> may provide a novel strategy for treatment of <b>alcohol</b> induced pathology.
+IL17A	drug	alcohol	31849082	Following binge <b>ethanol</b> drinking, <strong>IL 17A</strong> production primarily increased in γδ T cells of wild type (WT) mice, whereas the production of <strong>IL 17A</strong> was mainly facilitated by CD4+ T cells in acute on chronic <b>ethanol</b> consumption.
+IL17A	addiction	intoxication	31849082	Following <b>binge</b> ethanol drinking, <strong>IL 17A</strong> production primarily increased in γδ T cells of wild type (WT) mice, whereas the production of <strong>IL 17A</strong> was mainly facilitated by CD4+ T cells in acute on chronic ethanol consumption.
+IL17A	addiction	dependence	31439682	Elevated serum IgE, oral corticosteroid <b>dependence</b> and <strong>IL 17</strong>/22 expression in highly neutrophilic asthma.
+IL17A	drug	nicotine	31439682	Excluding <b>smokers</b> revealed increased IL 17A+ and IL 22+ cells in highly neutrophilic patients.We provide new evidence linking the presence of high bronchial neutrophilia in asthma to an adaptive immune response associated with allergy (IgE) and <strong>IL 17</strong>/22 cytokine expression.
+IL17A	drug	nicotine	31439682	Excluding <b>smokers</b> revealed increased <strong>IL 17A</strong>+ and IL 22+ cells in highly neutrophilic patients.We provide new evidence linking the presence of high bronchial neutrophilia in asthma to an adaptive immune response associated with allergy (IgE) and <strong>IL 17</strong>/22 cytokine expression.
+IL17A	drug	opioid	31379246	<b>Morphine</b> treatment resulted in 1) the promotion of C. rodentium systemic dissemination, 2) an increase in the expression of the virulence factors of C. rodentium colonization in intestinal contents, 3) altered gut microbiome, 4) damaged integrity of gut epithelial barrier function, 5) inhibition of the C. rodentium induced increase in goblet cells, and 6) dysregulated <strong>IL 17A</strong> immune response.
+IL17A	drug	alcohol	31105269	<b>Alcohol</b> induced <strong>IL 17A</strong> production in Paneth cells amplifies endoplasmic reticulum stress, apoptosis, and inflammasome IL 18 activation in the proximal small intestine in mice.
+IL17A	drug	alcohol	31105269	Using a mouse model of <b>alcoholic</b> hepatitis, we investigated the effects of chronic <b>alcohol</b> plus binge and found increased abundance of Paneth cells and <strong>IL 17A</strong> in the proximal small intestine (PSI).
+IL17A	addiction	intoxication	31105269	Using a mouse model of alcoholic hepatitis, we investigated the effects of chronic alcohol plus <b>binge</b> and found increased abundance of Paneth cells and <strong>IL 17A</strong> in the proximal small intestine (PSI).
+IL17A	drug	alcohol	31105269	<b>Alcohol</b> increased <strong>IL 17A</strong> production and pro apoptotic signaling evidenced by Bax, Bim, caspase 3, and caspase 8 increases via endoplasmic reticulum (ER) stress indicated by C/EBP homologous protein (CHOP) upregulation; this was prevented by the ER stress inhibitor, 4 PBA, in isolated crypts in vitro and in vivo.
+IL17A	drug	alcohol	31105269	Mechanistically, <strong>IL 17</strong> augmented <b>alcohol</b> induced ER stress in isolated crypts.
+IL17A	drug	alcohol	31105269	In vivo <strong>IL 17A</strong> blocking antibody administration in <b>alcohol</b> treated mice attenuated ER stress mediated apoptosis and IL 18 induction and prevented <b>alcohol</b> induced impairment of tight junctions in the PSI and LPS translocation to the liver.
+IL17A	drug	alcohol	31105269	Our data suggest that <b>alcohol</b> upregulates innate immune mechanisms by increasing Paneth cell numbers and <strong>IL 17A</strong> release contributing to apoptosis amplification, inflammasome activation, and gut leakiness in the PSI.
+IL17A	drug	alcohol	30368255	<b>Alcohol</b> feeding significantly increased the expression of proinflammatory cytokines such as Tnfα, Mcp1, Hmgb1, <strong>Il 17</strong>, and Il 23 in the brain and intestine.
+IL17A	drug	alcohol	27699959	The results showed that <b>alcohol</b> intoxication increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, <strong>IL 17A</strong>, IL 1β, IL 2, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+IL17A	addiction	intoxication	27699959	The results showed that alcohol <b>intoxication</b> increased the plasma levels of several cytokine and chemokine [interferon γ, interleukin (IL) 10, <strong>IL 17A</strong>, IL 1β, IL 2, IL 4, IL 6, IL 8, fractalkine, monocyte chemoattractant protein 1 (MCP 1) and macrophage inflammatory protein 1α (MIP 1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony stimulating factor was only observed in the plasma of males.
+IL17A	drug	alcohol	27699959	In wild type female adolescent mice, intermittent <b>ethanol</b> treatment increased the levels of several cytokines (<strong>IL 17A</strong> and IL 1β) and chemokines (MCP 1, MIP 1α and fractalkine) in PFC and in serum (<strong>IL 17A</strong>, MCP 1 and MIP 1α), but significant differences in the fractalkine levels in PFC were observed only in male mice.
+IL17A	drug	opioid	27622168	This study aimed to investigate the changes in serum levels of interferon gamma (IFN γ) and interleukin 17 (<strong>IL 17</strong>) during the <b>morphine</b> withdrawal syndrome induced by 8 weeks of moderate exercise and their effects on the immune system function.
+IL17A	addiction	withdrawal	27622168	This study aimed to investigate the changes in serum levels of interferon gamma (IFN γ) and interleukin 17 (<strong>IL 17</strong>) during the morphine <b>withdrawal</b> syndrome induced by 8 weeks of moderate exercise and their effects on the immune system function.
+IL17A	drug	opioid	27622168	Moderate exercise for 8 weeks increased the IFN γ and decreased the <strong>IL 17</strong> serum levels in the <b>morphine</b> dependent rats.
+IL17A	drug	alcohol	27239399	The role of <strong>IL 17</strong> signaling in regulation of the liver brain axis and intestinal permeability in <b>Alcoholic</b> Liver Disease.
+IL17A	drug	alcohol	26617183	Importantly, flow cytometry analysis showed that <b>alcohol</b> reduced Treg cell population while increased TH17 cell population as well as <strong>IL 17</strong> secretion, which was reversed by LGG s administration.
+IL17A	drug	alcohol	25754201	As interleukin 17 (<strong>IL 17</strong>) is a critical cytokine in host defense against extracellular pathogens, including S. pneumoniae, we hypothesized that <b>ethanol</b> impairs mucosal immunity against this pathogen by disrupting <strong>IL 17</strong> production or <strong>IL 17</strong> receptor (IL 17R) signaling.
+IL17A	drug	alcohol	25754201	Transcriptome analysis of bronchial brushes in the nonhuman primate model showed downregulation of the expression of <strong>IL 17</strong> regulated chemokines in <b>ethanol</b> fed animals, a finding also replicated in the murine model.
+IL17A	drug	alcohol	25754201	Surprisingly, recombinant CXCL1 and CXCL5 but not <strong>IL 17</strong> or IL 23 plus IL 1β rescued bacterial burden in the <b>ethanol</b> group to control levels.
+IL17A	drug	alcohol	25754201	Taken together, the results of this study suggest that <b>ethanol</b> impairs <strong>IL 17</strong> mediated chemokine production in the lung.
+IL17A	addiction	relapse	25615631	Four <strong>IL 17A</strong> gene polymorphisms (rs8193036, rs3819024, rs2275913 and rs8193037) were genotyped by 5' exonuclease TaqMan assays in a group of 900 patients with premature CAD and 667 healthy controls (with negative calcium score by computed tomography), <b>seeking</b> associations with CAD and other metabolic and cardiovascular risk factors using logistic regression analyses.
+IL17A	drug	opioid	24721689	Therefore, we investigated nociceptive sensitization, immune cell infiltration, myeloperoxidase (MPO) activity, and expression of multiple cytokines and <b>opioid</b> peptides in damaged nerves of wild type (<strong>IL 17</strong>(+/+)) and <strong>IL 17</strong> knock out (<strong>IL 17</strong>( / )) mice after partial sciatic nerve ligation.
+IL17A	addiction	sensitization	24721689	Therefore, we investigated nociceptive <b>sensitization</b>, immune cell infiltration, myeloperoxidase (MPO) activity, and expression of multiple cytokines and opioid peptides in damaged nerves of wild type (<strong>IL 17</strong>(+/+)) and <strong>IL 17</strong> knock out (<strong>IL 17</strong>( / )) mice after partial sciatic nerve ligation.
+IL17A	drug	cannabinoid	25812351	These effects of morphine and <b>cannabinoids</b> T cell suppression were accompanied by elevation of IL 10 level and concomitant reduction in <strong>IL 17</strong> secretion from cultured CD4+ T cells.
+IL17A	drug	opioid	25812351	These effects of <b>morphine</b> and cannabinoids T cell suppression were accompanied by elevation of IL 10 level and concomitant reduction in <strong>IL 17</strong> secretion from cultured CD4+ T cells.
+IL17A	addiction	relapse	24050582	Mizadj, clinically EDSS and <b>relapse</b> rate as well as immunological factors (IL 4, IFN γ and <strong>IL 17</strong>) were assessed at baseline and after 6 months.
+IL17A	addiction	intoxication	23989051	When combined with EtOH <b>intoxication</b>, burn injury significantly decreased <strong>IL 17</strong> and IL 22, as compared with sham injury.
+IL17A	drug	alcohol	21143255	Furthermore, <b>ethanol</b> treated cells alone or in combination with LPS had significantly fewer <strong>IL 17</strong>  and IFN γ secreting CD4+ T cells but constant proportion of Treg cells when compared to control cells.
+IL17A	drug	opioid	19995896	<b>Morphine</b> disrupts interleukin 23 (IL 23)/<strong>IL 17</strong> mediated pulmonary mucosal host defense against Streptococcus pneumoniae infection.
+IL17A	drug	opioid	19995896	Using a well established murine model of opiate abuse and S. pneumoniae lung infection, we explored the influence of <b>morphine</b> treatment on the interleukin 23 (IL 23)/<strong>IL 17</strong> axis and related innate immunity.
+IL17A	drug	opioid	19995896	Impairment of early IL 23/<strong>IL 17</strong> production caused by <b>morphine</b> treatment was associated with delayed neutrophil migration and decreased pneumococcal clearance.
+IL17A	drug	opioid	19995896	In conclusion, <b>morphine</b> treatment causes a dysfunction in IL 23 producing dendritic cells and macrophages and <strong>IL 17</strong> producing gammadeltaT lymphocytes in response to S. pneumoniae lung infection.
+IL17A	drug	alcohol	16792568	Interleukin 23 (IL 23) is a recently described cytokine critical for <strong>IL 17</strong> induction and host survival during Klebsiella pneumoniae infection, a pulmonary pathogen commonly seen in <b>alcoholics</b>.
+IL17A	drug	alcohol	16792568	Alveolar macrophages (AM) were cultured with bacteria in <b>ethanol</b> (0, 50, and 100 mM) to determine <b>alcohol</b>'s effect on AM IL 23 expression, the bioactivity of which was determined by splenocyte <strong>IL 17</strong> inducing activity.
+IL17A	addiction	intoxication	16792568	Interferon gamma priming antagonizes IL 23 and is, therefore, not likely to be a useful adjuvant therapy in restoring IL 23/<strong>IL 17</strong> responses during infection and <b>intoxication</b>.
+CHRNB3	drug	nicotine	31164900	However, results from our analysis suggest heterogeneous effects of CHRNA6 and <strong>CHRNB3</strong> on <b>nicotine</b> dependence in males and females.
+CHRNB3	addiction	dependence	31164900	However, results from our analysis suggest heterogeneous effects of CHRNA6 and <strong>CHRNB3</strong> on nicotine <b>dependence</b> in males and females.
+CHRNB3	drug	nicotine	29621993	In the context of personalized medicine, the aims of this study were to evaluate whether cholinergic receptor nicotinic alpha 2 (CHRNA2), cholinergic receptor nicotinic alpha 3 (CHRNA3), cholinergic receptor nicotinic alpha 5 (CHRNA5) and cholinergic receptor nicotinic beta 3 (<strong>CHRNB3</strong>) polymorphisms were associated with <b>nicotine</b> dependence severity, and to investigate possible pharmacogenetics markers of <b>smoking</b> cessation treatment.
+CHRNB3	addiction	dependence	29621993	In the context of personalized medicine, the aims of this study were to evaluate whether cholinergic receptor nicotinic alpha 2 (CHRNA2), cholinergic receptor nicotinic alpha 3 (CHRNA3), cholinergic receptor nicotinic alpha 5 (CHRNA5) and cholinergic receptor nicotinic beta 3 (<strong>CHRNB3</strong>) polymorphisms were associated with nicotine <b>dependence</b> severity, and to investigate possible pharmacogenetics markers of smoking cessation treatment.
+CHRNB3	drug	nicotine	28851948	Significant association of the <strong>CHRNB3</strong> CHRNA6 gene cluster with <b>nicotine</b> dependence in the Chinese Han population.
+CHRNB3	addiction	dependence	28851948	Significant association of the <strong>CHRNB3</strong> CHRNA6 gene cluster with nicotine <b>dependence</b> in the Chinese Han population.
+CHRNB3	drug	alcohol	28850771	In a real data application, we apply our method to the sequencing data from Minnesota Twin Study (MTS) and found potential associations of several nicotine receptor subunit (CHRN) genes, including <strong>CHRNB3</strong>, associated with nicotine dependence and/or <b>alcohol</b> dependence.
+CHRNB3	drug	nicotine	28850771	In a real data application, we apply our method to the sequencing data from Minnesota Twin Study (MTS) and found potential associations of several <b>nicotine</b> receptor subunit (CHRN) genes, including <strong>CHRNB3</strong>, associated with <b>nicotine</b> dependence and/or alcohol dependence.
+CHRNB3	addiction	dependence	28850771	In a real data application, we apply our method to the sequencing data from Minnesota Twin Study (MTS) and found potential associations of several nicotine receptor subunit (CHRN) genes, including <strong>CHRNB3</strong>, associated with nicotine <b>dependence</b> and/or alcohol <b>dependence</b>.
+CHRNB3	drug	nicotine	27327258	Crucial roles of the <strong>CHRNB3</strong> CHRNA6 gene cluster on chromosome 8 in <b>nicotine</b> dependence: update and subjects for future research.
+CHRNB3	addiction	dependence	27327258	Crucial roles of the <strong>CHRNB3</strong> CHRNA6 gene cluster on chromosome 8 in nicotine <b>dependence</b>: update and subjects for future research.
+CHRNB3	drug	nicotine	27327258	Besides the CHRNA4, CHRNB2 and CHRNA5/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the <strong>CHRNB3</strong> CHRNA6 gene cluster on chromosome 8 in <b>nicotine</b> dependence (ND).
+CHRNB3	addiction	dependence	27327258	Besides the CHRNA4, CHRNB2 and CHRNA5/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the <strong>CHRNB3</strong> CHRNA6 gene cluster on chromosome 8 in nicotine <b>dependence</b> (ND).
+CHRNB3	drug	nicotine	27327258	To gain a better understanding of the pathological processes underlying ND and ND related behaviors and to promote the development of effective <b>smoking</b> cessation therapies, we here present the most recent studies concerning the genetic effects of the <strong>CHRNB3</strong> CHRNA6 gene cluster in ND.
+CHRNB3	drug	alcohol	25399692	More recent studies in family based samples have implicated GABRA2, nicotinic receptor genes such as <strong>CHRNB3</strong>, and a number of other specific single genes as associated with <b>alcohol</b> use disorders.
+CHRNB3	drug	nicotine	25233467	We evaluated 23 single nucleotide polymorphisms (SNPs) in the five nicotinic receptor related genes (<strong>CHRNB3</strong>, CHRNA6, and CHRNA5/A3/B4) previously reported to be associated with lung cancer risk and <b>smoking</b> behavior and 14 SNPs in the four 'control' genes (TERT, CLPTM1L, CYP1A1, and TP53), which were not reported in the <b>smoking</b> GWA studies.
+CHRNB3	drug	nicotine	25110504	Genetic Association of <strong>CHRNB3</strong> and CHRNA6 Gene Polymorphisms with <b>Nicotine</b> Dependence Syndrome Scale in Korean Population.
+CHRNB3	addiction	dependence	25110504	Genetic Association of <strong>CHRNB3</strong> and CHRNA6 Gene Polymorphisms with Nicotine <b>Dependence</b> Syndrome Scale in Korean Population.
+CHRNB3	drug	nicotine	25110504	Previous studies have found that CHRNA6 <strong>CHRNB3</strong> cluster polymorphisms were significantly associated with the risk of ND and various <b>tobacco</b> behaviors.
+CHRNB3	drug	nicotine	25110504	The aim of study was to evaluate the genetic association of <strong>CHRNB3</strong> and CHRNA6 polymorphisms with the risk of ND based on the Fagerstrom Test for <b>Nicotine</b> Dependence (FTND) score and five subscales of <b>nicotine</b> dependence syndrome scale (NDSS) in Korean population.
+CHRNB3	addiction	dependence	25110504	The aim of study was to evaluate the genetic association of <strong>CHRNB3</strong> and CHRNA6 polymorphisms with the risk of ND based on the Fagerstrom Test for Nicotine <b>Dependence</b> (FTND) score and five subscales of nicotine <b>dependence</b> syndrome scale (NDSS) in Korean population.
+CHRNB3	drug	nicotine	25110504	<strong>CHRNB3</strong> rs4954 and CHRNA6 rs16891604 showed significant associations with NDSSF1 (drive) in dominant models among moderate to severe ND among <b>smokers</b> after correction (p(corr) =0.02 and 0.001, respectively), whereas other four SNPs showed significant associations among mild ND after correction (p(corr) =0.03 0.02 in dominant model).
+CHRNB3	drug	nicotine	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, CHRNB4, CHRNA6 and <strong>CHRNB3</strong> genes and found that rare missense variants at conserved residues in CHRNB4 are associated with reduced risk of <b>nicotine</b> dependence among African Americans.
+CHRNB3	addiction	dependence	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, CHRNB4, CHRNA6 and <strong>CHRNB3</strong> genes and found that rare missense variants at conserved residues in CHRNB4 are associated with reduced risk of nicotine <b>dependence</b> among African Americans.
+CHRNB3	drug	nicotine	24731518	<strong>CHRNB3</strong> c. 57A>G functional promoter change affects Parkinson's disease and <b>smoking</b>.
+CHRNB3	drug	nicotine	24731518	The β3 nicotinic acetylcholine receptor subunit (encoded by <strong>CHRNB3</strong>) is depleted in the striatum of PD patients and associated with <b>nicotine</b> dependence.
+CHRNB3	addiction	dependence	24731518	The β3 nicotinic acetylcholine receptor subunit (encoded by <strong>CHRNB3</strong>) is depleted in the striatum of PD patients and associated with nicotine <b>dependence</b>.
+CHRNB3	drug	nicotine	24731518	These findings suggest that the <strong>CHRNB3</strong> c. 57A>G alteration affects the promoter activity and is associated with PD and <b>smoking</b> in PD patients.
+CHRNB3	drug	cocaine	24675634	Variants near <strong>CHRNB3</strong> CHRNA6 are associated with DSM 5 <b>cocaine</b> use disorder: evidence for pleiotropy.
+CHRNB3	drug	cocaine	24675634	Using genotypic data from a GWAS of the Study of Addiction: Genetics and Environment (SAGE) dataset, we tested for association of <strong>CHRNB3</strong> A6 SNPs with DSM 5 <b>cocaine</b> use disorder.
+CHRNB3	addiction	addiction	24675634	Using genotypic data from a GWAS of the Study of <b>Addiction</b>: Genetics and Environment (SAGE) dataset, we tested for association of <strong>CHRNB3</strong> A6 SNPs with DSM 5 cocaine use disorder.
+CHRNB3	drug	cocaine	24675634	These results suggest that the <strong>CHRNB3</strong> A6 locus contains multiple variants affecting risk for vulnerability to <b>cocaine</b> and nicotine dependence as well as bipolar disorder, suggesting that they have pleiotropic effects.
+CHRNB3	drug	nicotine	24675634	These results suggest that the <strong>CHRNB3</strong> A6 locus contains multiple variants affecting risk for vulnerability to cocaine and <b>nicotine</b> dependence as well as bipolar disorder, suggesting that they have pleiotropic effects.
+CHRNB3	addiction	dependence	24675634	These results suggest that the <strong>CHRNB3</strong> A6 locus contains multiple variants affecting risk for vulnerability to cocaine and nicotine <b>dependence</b> as well as bipolar disorder, suggesting that they have pleiotropic effects.
+CHRNB3	drug	nicotine	24401102	Multiple distinct <strong>CHRNB3</strong> CHRNA6 variants are genetic risk factors for <b>nicotine</b> dependence in African Americans and European Americans.
+CHRNB3	addiction	dependence	24401102	Multiple distinct <strong>CHRNB3</strong> CHRNA6 variants are genetic risk factors for nicotine <b>dependence</b> in African Americans and European Americans.
+CHRNB3	drug	alcohol	24401102	The common variant rs13273442 in the <strong>CHRNB3</strong> CHNRA6 region is associated significantly with nicotine dependence in European Americans and African Americans across studies recruited for nicotine, <b>alcohol</b> and cocaine dependence.
+CHRNB3	drug	cocaine	24401102	The common variant rs13273442 in the <strong>CHRNB3</strong> CHNRA6 region is associated significantly with nicotine dependence in European Americans and African Americans across studies recruited for nicotine, alcohol and <b>cocaine</b> dependence.
+CHRNB3	drug	nicotine	24401102	The common variant rs13273442 in the <strong>CHRNB3</strong> CHNRA6 region is associated significantly with <b>nicotine</b> dependence in European Americans and African Americans across studies recruited for <b>nicotine</b>, alcohol and cocaine dependence.
+CHRNB3	addiction	dependence	24401102	The common variant rs13273442 in the <strong>CHRNB3</strong> CHNRA6 region is associated significantly with nicotine <b>dependence</b> in European Americans and African Americans across studies recruited for nicotine, alcohol and cocaine <b>dependence</b>.
+CHRNB3	drug	alcohol	24057674	Rare missense variants in <strong>CHRNB3</strong> and CHRNA3 are associated with risk of <b>alcohol</b> and cocaine dependence.
+CHRNB3	drug	cocaine	24057674	Rare missense variants in <strong>CHRNB3</strong> and CHRNA3 are associated with risk of alcohol and <b>cocaine</b> dependence.
+CHRNB3	addiction	dependence	24057674	Rare missense variants in <strong>CHRNB3</strong> and CHRNA3 are associated with risk of alcohol and cocaine <b>dependence</b>.
+CHRNB3	drug	alcohol	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically <b>alcohol</b> and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, CHRNB4, CHRNA6 and <strong>CHRNB3</strong> in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of <b>Alcoholism</b> (COGA).
+CHRNB3	drug	cocaine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically alcohol and <b>cocaine</b> dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, CHRNB4, CHRNA6 and <strong>CHRNB3</strong> in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNB3	drug	nicotine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than <b>nicotine</b> dependence, specifically alcohol and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, CHRNB4, CHRNA6 and <strong>CHRNB3</strong> in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNB3	addiction	dependence	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine <b>dependence</b>, specifically alcohol and cocaine <b>dependence</b>, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, CHRNB4, CHRNA6 and <strong>CHRNB3</strong> in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNB3	drug	alcohol	24057674	For European Americans, we find increased DSM IV cocaine dependence symptoms (FamSKAT P = 2 × 10( 4)) and increased DSM IV <b>alcohol</b> dependence symptoms (FamSKAT P = 5 × 10( 4)) among carriers of missense variants in <strong>CHRNB3</strong>.
+CHRNB3	drug	cocaine	24057674	For European Americans, we find increased DSM IV <b>cocaine</b> dependence symptoms (FamSKAT P = 2 × 10( 4)) and increased DSM IV alcohol dependence symptoms (FamSKAT P = 5 × 10( 4)) among carriers of missense variants in <strong>CHRNB3</strong>.
+CHRNB3	addiction	dependence	24057674	For European Americans, we find increased DSM IV cocaine <b>dependence</b> symptoms (FamSKAT P = 2 × 10( 4)) and increased DSM IV alcohol <b>dependence</b> symptoms (FamSKAT P = 5 × 10( 4)) among carriers of missense variants in <strong>CHRNB3</strong>.
+CHRNB3	drug	alcohol	24057674	Replication in an independent sample supports the role of rare variants in <strong>CHRNB3</strong> and <b>alcohol</b> dependence (P = 0.006).
+CHRNB3	addiction	dependence	24057674	Replication in an independent sample supports the role of rare variants in <strong>CHRNB3</strong> and alcohol <b>dependence</b> (P = 0.006).
+CHRNB3	drug	alcohol	24057674	These are the first results to implicate rare variants in <strong>CHRNB3</strong> or CHRNA3 in risk for <b>alcohol</b> dependence or cocaine dependence.
+CHRNB3	drug	cocaine	24057674	These are the first results to implicate rare variants in <strong>CHRNB3</strong> or CHRNA3 in risk for alcohol dependence or <b>cocaine</b> dependence.
+CHRNB3	addiction	dependence	24057674	These are the first results to implicate rare variants in <strong>CHRNB3</strong> or CHRNA3 in risk for alcohol <b>dependence</b> or cocaine <b>dependence</b>.
+CHRNB3	drug	nicotine	23319001	Significant association of <strong>CHRNB3</strong> variants with <b>nicotine</b> dependence in multiple ethnic populations.
+CHRNB3	addiction	dependence	23319001	Significant association of <strong>CHRNB3</strong> variants with nicotine <b>dependence</b> in multiple ethnic populations.
+CHRNB3	drug	nicotine	22524403	<strong>CHRNB3</strong> is more strongly associated with Fagerström test for cigarette dependence based <b>nicotine</b> dependence than cigarettes per day: phenotype definition changes genome wide association studies results.
+CHRNB3	addiction	dependence	22524403	<strong>CHRNB3</strong> is more strongly associated with Fagerström test for cigarette <b>dependence</b> based nicotine <b>dependence</b> than cigarettes per day: phenotype definition changes genome wide association studies results.
+CHRNB3	drug	nicotine	22524403	The genetic locus most strongly associated with <b>nicotine</b> dependence was rs1451240 on chromosome 8 in the region of <strong>CHRNB3</strong> [odds ratio (OR) = 0.65, P = 2.4 × 10( 8) ].
+CHRNB3	addiction	dependence	22524403	The genetic locus most strongly associated with nicotine <b>dependence</b> was rs1451240 on chromosome 8 in the region of <strong>CHRNB3</strong> [odds ratio (OR) = 0.65, P = 2.4 × 10( 8) ].
+CHRNB3	drug	nicotine	22309839	Our results provided confirmation of the previous findings that DRD2, DRD3, DDC, <strong>CHRNB3</strong>, GABBR2 and CHRNA4 are associated with <b>nicotine</b> dependence.
+CHRNB3	addiction	dependence	22309839	Our results provided confirmation of the previous findings that DRD2, DRD3, DDC, <strong>CHRNB3</strong>, GABBR2 and CHRNA4 are associated with nicotine <b>dependence</b>.
+CHRNB3	drug	nicotine	22042774	Genome wide association studies have identified common variation in the CHRNA5 CHRNA3 CHRNB4 and CHRNA6 <strong>CHRNB3</strong> gene clusters that contribute to <b>nicotine</b> dependence.
+CHRNB3	addiction	dependence	22042774	Genome wide association studies have identified common variation in the CHRNA5 CHRNA3 CHRNB4 and CHRNA6 <strong>CHRNB3</strong> gene clusters that contribute to nicotine <b>dependence</b>.
+CHRNB3	drug	nicotine	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, CHRNB4, CHRNA6 and <strong>CHRNB3</strong> genes in African American and European American <b>nicotine</b> dependent <b>smokers</b> and <b>smokers</b> without symptoms of dependence.
+CHRNB3	addiction	dependence	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, CHRNB4, CHRNA6 and <strong>CHRNB3</strong> genes in African American and European American nicotine dependent smokers and smokers without symptoms of <b>dependence</b>.
+CHRNB3	addiction	relapse	21606657	The GG genotype of SNP rs13261190 in the <strong>CHRNB3</strong> was associated with increased novelty <b>seeking</b>, while SNPs of the ghrelin signaling system were associated with decreased self directedness (AA of rs495225, GHSR) and alterations in self transcendence (AA of both rs42451 and rs35680, GHRL).
+CHRNB3	drug	nicotine	21191315	On the basis of known associations with <b>nicotine</b> dependence, we genotyped eight single nucleotide polymorphisms (SNPs) on chromosome 8 (three bins) in the regions of <strong>CHRNB3</strong> and CHRNA6, and six SNPs on chromosome 15 (three bins) in the regions of CHRNA5 and CHRNA3.
+CHRNB3	addiction	dependence	21191315	On the basis of known associations with nicotine <b>dependence</b>, we genotyped eight single nucleotide polymorphisms (SNPs) on chromosome 8 (three bins) in the regions of <strong>CHRNB3</strong> and CHRNA6, and six SNPs on chromosome 15 (three bins) in the regions of CHRNA5 and CHRNA3.
+CHRNB3	drug	nicotine	21191315	Our results suggest that (i) bipolar disorder does not modify the association between <b>nicotine</b> dependence and nicotinic receptor subunit genes, and (ii) variants in <strong>CHRNB3</strong>/CHRNA6 are independently associated with bipolar disorder.
+CHRNB3	addiction	dependence	21191315	Our results suggest that (i) bipolar disorder does not modify the association between nicotine <b>dependence</b> and nicotinic receptor subunit genes, and (ii) variants in <strong>CHRNB3</strong>/CHRNA6 are independently associated with bipolar disorder.
+CHRNB3	drug	nicotine	20840187	Here we test the hypothesis that the nicotinic receptor genes CHRNA5 (rs16969968), CHRNA3 (rs578776), <strong>CHRNB3</strong> (rs13277254) and CHRND (rs12466358) modify the risk for <b>nicotine</b> dependence associated with peer <b>smoking</b>.
+CHRNB3	addiction	dependence	20840187	Here we test the hypothesis that the nicotinic receptor genes CHRNA5 (rs16969968), CHRNA3 (rs578776), <strong>CHRNB3</strong> (rs13277254) and CHRND (rs12466358) modify the risk for nicotine <b>dependence</b> associated with peer smoking.
+CHRNB3	drug	nicotine	20418888	Sequence variants at <strong>CHRNB3</strong> CHRNA6 and CYP2A6 affect <b>smoking</b> behavior.
+CHRNB3	drug	nicotine	20418888	Among the genes at the two newly associated loci are genes encoding <b>nicotine</b> metabolizing enzymes (CYP2A6 and CYP2B6) and nicotinic acetylcholine receptor subunits (<strong>CHRNB3</strong> and CHRNA6), all of which have been highlighted in previous studies of <b>smoking</b> and <b>nicotine</b> dependence.
+CHRNB3	addiction	dependence	20418888	Among the genes at the two newly associated loci are genes encoding nicotine metabolizing enzymes (CYP2A6 and CYP2B6) and nicotinic acetylcholine receptor subunits (<strong>CHRNB3</strong> and CHRNA6), all of which have been highlighted in previous studies of smoking and nicotine <b>dependence</b>.
+CHRNB3	drug	alcohol	19500157	SNPs in CHRNA6 and <strong>CHRNB3</strong> are associated with <b>alcohol</b> consumption in a nationally representative sample.
+CHRNB3	drug	nicotine	19500157	The CHRNA6 and <strong>CHRNB3</strong> genes have been associated with <b>nicotine</b> dependence and early subjective response to <b>nicotine</b>.
+CHRNB3	addiction	dependence	19500157	The CHRNA6 and <strong>CHRNB3</strong> genes have been associated with nicotine <b>dependence</b> and early subjective response to nicotine.
+CHRNB3	drug	alcohol	19500157	Three SNPs in CHRNA6 (rs1072003, P = 0.015; rs892413, P = 0.0033 and rs2304297, P = 0.012) and one SNP in <strong>CHRNB3</strong> (rs13280604, P = 0.0053) were associated with a composite of the <b>alcohol</b> phenotypes.
+CHRNB3	drug	nicotine	19482438	We conclude that the analysis of polymorphisms in genes coding for four nicotinic acetylcholine receptor subunits (CHRNA4, CHRNA5, CHRNB2 and <strong>CHRNB3</strong>) and several <b>smoking</b> related phenotypes revealed no statistically significant association.
+CHRNB3	drug	nicotine	18704094	Genetic association of the CHRNA6 and <strong>CHRNB3</strong> genes with <b>tobacco</b> dependence in a nationally representative sample.
+CHRNB3	addiction	dependence	18704094	Genetic association of the CHRNA6 and <strong>CHRNB3</strong> genes with tobacco <b>dependence</b> in a nationally representative sample.
+CHRNB3	drug	nicotine	18704094	Previous studies have found evidence for significant association between single nucleotide polymorphisms (SNPs) in the genomic region containing the CHRNA6 and <strong>CHRNB3</strong> genes and <b>tobacco</b> behaviors.
+CHRNB3	drug	nicotine	18704094	Together these results further implicate the region downstream of CHRNA6 and the region upstream of <strong>CHRNB3</strong> in risk of <b>nicotine</b> dependence.
+CHRNB3	addiction	dependence	18704094	Together these results further implicate the region downstream of CHRNA6 and the region upstream of <strong>CHRNB3</strong> in risk of nicotine <b>dependence</b>.
+CHRNB3	drug	nicotine	18055561	The neuronal nicotinic receptor subunit genes (CHRNA6 and <strong>CHRNB3</strong>) are associated with subjective responses to <b>tobacco</b>.
+CHRNB3	drug	alcohol	18055561	In this paper, we present findings from an exploratory study of single nucleotide polymorphisms (SNPs) in the <strong>CHRNB3</strong> and CHRNA6 genes with tobacco and <b>alcohol</b> phenotypes, including frequency of use and three subjective response factors occurring shortly after initiation of use.
+CHRNB3	drug	nicotine	18055561	In this paper, we present findings from an exploratory study of single nucleotide polymorphisms (SNPs) in the <strong>CHRNB3</strong> and CHRNA6 genes with <b>tobacco</b> and alcohol phenotypes, including frequency of use and three subjective response factors occurring shortly after initiation of use.
+CHRNB3	drug	nicotine	18055561	The most significant associations were found between two <strong>CHRNB3</strong> SNPs (rs4950 and rs13280604) and the three subjective response factors to initial <b>tobacco</b> use.
+CHRNB3	drug	nicotine	18055561	Both <strong>CHRNB3</strong> SNPs were found to be associated with similar measures of subjective response to <b>tobacco</b>.
+CHRNB3	drug	nicotine	16314871	We found nominally significant (P<0.05) allelic and genotypic association with <b>smoking</b> initiation of SNP rs2072660 and multilocus haplotypes (P<0.007 0.05) in CHRNB2 and nominal (P<0.05) allelic or genotypic association of SNPs in CHRNA7 (rs1909884), CHRNA9 (rs4861065) and <strong>CHRNB3</strong> (rs9298629) with <b>nicotine</b> dependence.
+CHRNB3	addiction	dependence	16314871	We found nominally significant (P<0.05) allelic and genotypic association with smoking initiation of SNP rs2072660 and multilocus haplotypes (P<0.007 0.05) in CHRNB2 and nominal (P<0.05) allelic or genotypic association of SNPs in CHRNA7 (rs1909884), CHRNA9 (rs4861065) and <strong>CHRNB3</strong> (rs9298629) with nicotine <b>dependence</b>.
+VIP	drug	alcohol	32424821	Evaluation of Very Integrated Program (<strong>VIP</strong>): Health promotion for patients with <b>alcohol</b> and drug addiction   A Randomized Trial.
+VIP	addiction	addiction	32424821	Evaluation of Very Integrated Program (<strong>VIP</strong>): Health promotion for patients with alcohol and drug <b>addiction</b>   A Randomized Trial.
+VIP	drug	alcohol	32424821	The objective of this study was to test the efficacy of the Very Integrated Program (<strong>VIP</strong>) on treatment and health outcomes for patients diagnosed with <b>alcohol</b> and drug addiction.
+VIP	addiction	addiction	32424821	The objective of this study was to test the efficacy of the Very Integrated Program (<strong>VIP</strong>) on treatment and health outcomes for patients diagnosed with alcohol and drug <b>addiction</b>.
+VIP	drug	alcohol	32424821	Overall, adding <strong>VIP</strong> intervention did not improve outcome of the <b>alcohol</b> or drug addiction care or the lifestyle compared to the addiction care alone.
+VIP	addiction	addiction	32424821	Overall, adding <strong>VIP</strong> intervention did not improve outcome of the alcohol or drug <b>addiction</b> care or the lifestyle compared to the <b>addiction</b> care alone.
+VIP	drug	amphetamine	31288386	Additionally, the proportion of GAL expressing cell bodies simultaneously immunoreactive to vasoactive intestinal peptide (<strong>VIP</strong>), neuronal nitric oxide synthase (nNOS) and cocaine  and <b>amphetamine</b>  regulated transcript peptide (CART) also increased.
+VIP	drug	cocaine	31288386	Additionally, the proportion of GAL expressing cell bodies simultaneously immunoreactive to vasoactive intestinal peptide (<strong>VIP</strong>), neuronal nitric oxide synthase (nNOS) and <b>cocaine</b>  and amphetamine  regulated transcript peptide (CART) also increased.
+VIP	drug	amphetamine	31288386	Additionally, the proportion of GAL expressing cell bodies simultaneously immunoreactive to <strong>vasoactive intestinal peptide</strong> (<strong>VIP</strong>), neuronal nitric oxide synthase (nNOS) and cocaine  and <b>amphetamine</b>  regulated transcript peptide (CART) also increased.
+VIP	drug	cocaine	31288386	Additionally, the proportion of GAL expressing cell bodies simultaneously immunoreactive to <strong>vasoactive intestinal peptide</strong> (<strong>VIP</strong>), neuronal nitric oxide synthase (nNOS) and <b>cocaine</b>  and amphetamine  regulated transcript peptide (CART) also increased.
+VIP	addiction	intoxication	31288386	The results suggest neurotrophic or/and neuroprotective properties of GAL and possible co operation of GAL with <strong>VIP</strong>, nNOS, CART in the recovery processes in the stomach enteric nervous system (ENS) neurons following acrylamide <b>intoxication</b>.
+VIP	drug	alcohol	31261620	Compliance with the Very Integrated Program (<strong>VIP</strong>) for Smoking Cessation, Nutrition, Physical Activity and Comorbidity Education Among Patients in Treatment for <b>Alcohol</b> and Drug Addiction.
+VIP	drug	nicotine	31261620	Compliance with the Very Integrated Program (<strong>VIP</strong>) for <b>Smoking</b> Cessation, Nutrition, Physical Activity and Comorbidity Education Among Patients in Treatment for Alcohol and Drug Addiction.
+VIP	addiction	addiction	31261620	Compliance with the Very Integrated Program (<strong>VIP</strong>) for Smoking Cessation, Nutrition, Physical Activity and Comorbidity Education Among Patients in Treatment for Alcohol and Drug <b>Addiction</b>.
+VIP	drug	amphetamine	30838766	The commercial antibodies against substance P (SP), vasoactive intestinal polypeptide (<strong>VIP</strong>), galanin (GAL), vesicular acetylcholine transporter (VAChT), and cocaine  and <b>amphetamine</b> regulated transcript peptide (CART) were used.
+VIP	drug	cocaine	30838766	The commercial antibodies against substance P (SP), vasoactive intestinal polypeptide (<strong>VIP</strong>), galanin (GAL), vesicular acetylcholine transporter (VAChT), and <b>cocaine</b>  and amphetamine regulated transcript peptide (CART) were used.
+VIP	drug	amphetamine	28351548	<b>METH</b> sensitization increased the transcriptional expression of calbindin, calretinin, somatostatin, cholecyctokinin and <strong>vasoactive intestinal peptide</strong> in the PRL while parvalbumin, calbindin, cholectokinin and <strong>vasoactive intestinal peptide</strong> were upregulated in the OFC.
+VIP	addiction	sensitization	28351548	METH <b>sensitization</b> increased the transcriptional expression of calbindin, calretinin, somatostatin, cholecyctokinin and <strong>vasoactive intestinal peptide</strong> in the PRL while parvalbumin, calbindin, cholectokinin and <strong>vasoactive intestinal peptide</strong> were upregulated in the OFC.
+VIP	drug	nicotine	26081405	All eligible studies published up to 2014 were searched out from PubMed, China National Knowledge Internet (CNKI), ISI Web of knowledge (ISI), <strong>vip</strong> citation databases (<strong>VIP</strong>), Chinese BioMedical Literature (CBM) and Elsevier Science Direct, searching words were "smok*","<b>nicotine</b> dependence","CYP2A6","cytochrome P450 2A6","polymorphism","mut*"and"varia*", while 436 articles were concluded.
+VIP	addiction	dependence	26081405	All eligible studies published up to 2014 were searched out from PubMed, China National Knowledge Internet (CNKI), ISI Web of knowledge (ISI), <strong>vip</strong> citation databases (<strong>VIP</strong>), Chinese BioMedical Literature (CBM) and Elsevier Science Direct, searching words were "smok*","nicotine <b>dependence</b>","CYP2A6","cytochrome P450 2A6","polymorphism","mut*"and"varia*", while 436 articles were concluded.
+VIP	drug	cocaine	23840704	The advanced AAV <strong>VIP</strong> mCocH vector generated a dose dependent rise in plasma <b>cocaine</b> hydrolase activity from 20 fold (10(10) particles) to 20,000 fold (10(13) particles), while the hdAD vector (1.7 × 10(12) particles) yielded a 300,000 fold increase.
+VIP	drug	nicotine	23713328	Up to December of 2011, the domestic and overseas literatures of acupuncture for <b>smoking</b> cessation are searched and collected through Pubmed, CNKI, Wanfang and Chongqing <strong>VIP</strong> databases, which are analyzed from treatment method, action mechanism, influencing factors of efficacy and efficacy evaluation research and so on.
+VIP	drug	cannabinoid	21631400	The present review discusses these therapeutic targets including noradrenaline and 5 HT reuptake inhibitors; sodium, calcium and potassium channels; inhibitory and excitatory neurotransmitters; neuropeptides including bradykinin, tachykinin, cholecystokinin, neuropeptide Y, <strong>vasoactive intestinal peptide</strong>, and CGRP; pro inflammatory cytokines; MAP kinases; PPAR γ; Na(+)/Ca(2+) exchanger; nitric oxide; purinergic receptors; neuronal nicotinic receptors; cation dependent chloride transporters; oxidative stress; matrix metalloproteinase and plasminogen activators; growth factors; transient receptor potential (TRP) channels; <b>endocannabinoids</b>; histamine receptors; dopamine; sigma receptors, beta adrenergic receptors, endothelins, and D amino acid oxidase.
+VIP	drug	nicotine	21249644	We searched the Cochrane <b>Tobacco</b> Addiction Group specialized register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, BIOSIS Previews, PsycINFO, Science Citation Index, AMED, Acubriefs in November 2010; and four Chinese databases: Chinese Biomedical Database, China National Knowledge Infrastructure, Wanfang Data and <strong>VIP</strong> in November 2010.
+VIP	addiction	addiction	21249644	We searched the Cochrane Tobacco <b>Addiction</b> Group specialized register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, BIOSIS Previews, PsycINFO, Science Citation Index, AMED, Acubriefs in November 2010; and four Chinese databases: Chinese Biomedical Database, China National Knowledge Infrastructure, Wanfang Data and <strong>VIP</strong> in November 2010.
+VIP	drug	alcohol	20554694	ARNTL rs6486120 T(+) allelic status (P = 0.0007, q = 0.17), ADCYAP1 rs2856966 GG genotype (P = 0.0006, q = 0.17) and <strong>VIP</strong> CC haplotype (rs3823082 rs688136) (P = 0.0006) were suggestively associated with <b>alcohol</b> consumption in socially drinking controls.
+VIP	drug	alcohol	20554694	ARNTL, ARNTL2, <strong>VIP</strong> and ADCYAP1 were indicated as having influence on <b>alcohol</b> use or abuse.
+VIP	drug	alcohol	17960055	The effect of binge fetal <b>alcohol</b> exposure on the number of <strong>vasoactive intestinal peptide</strong> producing neurons in fetal sheep brain.
+VIP	addiction	intoxication	17960055	The effect of <b>binge</b> fetal alcohol exposure on the number of <strong>vasoactive intestinal peptide</strong> producing neurons in fetal sheep brain.
+VIP	drug	alcohol	17960055	We hypothesized that early fetal <b>alcohol</b> exposure alters the number of fetal neurons expressing vasoactive intestinal peptide (<strong>VIP</strong>), a potent cerebral vasodilator.
+VIP	drug	alcohol	17960055	We hypothesized that early fetal <b>alcohol</b> exposure alters the number of fetal neurons expressing <strong>vasoactive intestinal peptide</strong> (<strong>VIP</strong>), a potent cerebral vasodilator.
+VIP	drug	alcohol	17960055	<b>Alcohol</b> exposed fetal sheep brains had fewer <strong>VIP</strong> immunopositive neurons per hemisphere, 14.6 x 10(6), compared to saline controls, 19.8 x 10(6).
+VIP	drug	alcohol	17960055	The total neuron number was not different, 1.19 x 10(9) versus 1.23 x 10(9) respectively, indicating a selective decrease in <strong>VIP</strong> neurons as a result of <b>alcohol</b> exposure.
+VIP	drug	alcohol	17960055	In sheep, <b>alcohol</b> exposure early in gestation is associated with fewer <strong>VIP</strong> producing neurons later in gestation compared to saline controls; therefore, <b>alcohol</b> related changes in the number of <strong>VIP</strong> expressing neurons may be responsible in part for the attenuated hypoxic cerebral vasodilation described in fetal and neonatal sheep exposed to <b>alcohol</b> earlier in gestation.
+VIP	drug	alcohol	15834231	<strong>Vasoactive intestinal peptide</strong> and corticotropin releasing hormone increase beta endorphin release and proopiomelanocortin messenger RNA levels in primary cultures of hypothalamic cells: effects of acute and chronic <b>ethanol</b> treatment.
+VIP	drug	alcohol	15834231	Furthermore, the authors studied the effects of acute and chronic treatment with <b>ethanol</b> on the response of beta EP neurons to <strong>VIP</strong> and CRH.
+VIP	drug	alcohol	15834231	Acute treatment with <b>ethanol</b> increased beta EP neuronal gene expression and the secretory response to CRH and <strong>VIP</strong>.
+VIP	drug	alcohol	15834231	However, previous exposure to chronic <b>ethanol</b> reduced the CRH and <strong>VIP</strong> responses of these neurons.
+VIP	drug	alcohol	15834231	These results indicate that <strong>VIP</strong> and CRH stimulate beta EP release from hypothalamic cells in primary cultures and that the stimulatory and adaptive responses of beta EP neurons to <b>ethanol</b> may involve alteration in the responsiveness of beta EP secreting neurons to CRH and <strong>VIP</strong>.
+VIP	drug	alcohol	15520530	It has been previously shown that withdrawal from <b>alcohol</b> decreases the synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (<strong>VIP</strong>) in the suprachiasmatic nucleus (SCN), and that the infusion of NGF over 1 month completely restores these changes.
+VIP	addiction	withdrawal	15520530	It has been previously shown that <b>withdrawal</b> from alcohol decreases the synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (<strong>VIP</strong>) in the suprachiasmatic nucleus (SCN), and that the infusion of NGF over 1 month completely restores these changes.
+VIP	drug	alcohol	12914967	It was also recently shown that NGF, infused over 1 month, offsets the decreased synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (<strong>VIP</strong>) in the suprachiasmatic nucleus (SCN) of rats submitted to chronic <b>ethanol</b> treatment and withdrawal.
+VIP	addiction	withdrawal	12914967	It was also recently shown that NGF, infused over 1 month, offsets the decreased synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (<strong>VIP</strong>) in the suprachiasmatic nucleus (SCN) of rats submitted to chronic ethanol treatment and <b>withdrawal</b>.
+VIP	drug	opioid	12480163	However, <strong>VIP</strong> (1 microM) and the delta <b>opioid</b> selective agonist, [D Pen(2,5)] enkephalin (DPDPE; 1 microM), in combination, manifest a striking facilitative interaction to augment spinal levels of cAMP.
+VIP	drug	opioid	12480163	Facilitative interactions between <strong>VIP</strong> and kappa  or mu <b>opioids</b> were of a reduced magnitude or not observed, respectively.
+VIP	drug	opioid	12480163	Blockade of delta <b>opioid</b> or <strong>VIP</strong> receptors using naltrindole or VIP6 28, respectively antagonized the <strong>VIP</strong> DPDPE facilitative interaction, as did pertussis toxin treatment.
+VIP	drug	opioid	12480163	This suggests that modulation of Ca(2+) trafficking by <strong>VIP</strong> and delta <b>opioid</b> agonists is a point of convergence of their respective signal transduction cascades, the concomitant action at which achieves cytosolic Ca(2+) concentrations that are now sufficient for the activation of signaling molecules, e.g.
+VIP	drug	opioid	12409215	On the grounds of our previous studies with vasoactive intestinal polypeptide (<strong>VIP</strong>), it appears that different receptors are involved in the effects of PACAP in acute and chronic <b>morphine</b> actions.
+VIP	drug	alcohol	11709626	In <b>ethanol</b> treated and withdrawn rats, NGF produced increases in the number of AVP  and <strong>VIP</strong> immunostained neurons to values identical to those of controls.
+VIP	addiction	dependence	9920454	The present study related to the effects of centrally (intracerebroventricularly) administered <strong>VIP</strong> on pain sensitivity and on opiate tolerance and <b>dependence</b> in intact male CFLP mice.
+VIP	drug	opioid	9920454	<strong>VIP</strong> decreased the analgesic effect of a single subcutaneous <b>morphine</b> injection and the development of chronic tolerance to <b>morphine</b>.
+VIP	drug	opioid	9920454	<b>Morphine</b> withdrawal signs were not significantly affected after <strong>VIP</strong> pretreatment.
+VIP	addiction	withdrawal	9920454	Morphine <b>withdrawal</b> signs were not significantly affected after <strong>VIP</strong> pretreatment.
+VIP	drug	alcohol	9006974	Withdrawal from <b>alcohol</b> did not reduce but rather augmented the loss of <strong>VIP</strong>  and GRP immunoreactive neurons.
+VIP	addiction	withdrawal	9006974	<b>Withdrawal</b> from alcohol did not reduce but rather augmented the loss of <strong>VIP</strong>  and GRP immunoreactive neurons.
+VIP	drug	alcohol	1327722	It has previously been shown that the K+ potentiation of <strong>vasoactive intestinal peptide</strong> stimulated cAMP and cGMP responses was inhibited by <b>ethanol</b> in rat pinealocytes, suggesting an inhibitory action of <b>ethanol</b> on the voltage dependent Ca2+ channels (VDCC).
+VIP	drug	opioid	1697894	We tested here the inhibition of cyclic AMP (cAMP) accumulation by <b>morphine</b> under a variety of conditions: after stimulation with prostaglandin E1 (PGE1), forskolin, and vasoactive intestinal peptide (<strong>VIP</strong>), both in the presence and in the absence of the phosphodiesterase inhibitor 3 isobutyl 1 methylxanthine (IBMX).
+VIP	drug	opioid	1697894	We tested here the inhibition of cyclic AMP (cAMP) accumulation by <b>morphine</b> under a variety of conditions: after stimulation with prostaglandin E1 (PGE1), forskolin, and <strong>vasoactive intestinal peptide</strong> (<strong>VIP</strong>), both in the presence and in the absence of the phosphodiesterase inhibitor 3 isobutyl 1 methylxanthine (IBMX).
+VIP	drug	opioid	1697894	In contrast, deletion of IBMX enhanced <b>morphine</b>'s inhibition of the PGE1 and <strong>VIP</strong> cAMP response from approximately 50 to approximately 80%.
+TDO2	drug	opioid	30059533	Impacts of GRIN3A, GRM6 and <strong>TPH2</strong> genetic polymorphisms on quality of life in <b>methadone</b> maintenance therapy population.
+TDO2	drug	alcohol	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and binge drinking at first follow up, two genetic variants on tryptophan hydroxylase 2 (<strong>TPH2</strong>; rs17110451, rs7963717), sensation seeking and impulsivity, and having a greater fraction of peers who drink or encourage drinking <b>alcohol</b> were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for binge drinking at second follow up.
+TDO2	addiction	intoxication	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and <b>binge</b> drinking at first follow up, two genetic variants on tryptophan hydroxylase 2 (<strong>TPH2</strong>; rs17110451, rs7963717), sensation seeking and impulsivity, and having a greater fraction of peers who drink or encourage drinking alcohol were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for <b>binge</b> drinking at second follow up.
+TDO2	addiction	relapse	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and binge drinking at first follow up, two genetic variants on tryptophan hydroxylase 2 (<strong>TPH2</strong>; rs17110451, rs7963717), sensation <b>seeking</b> and impulsivity, and having a greater fraction of peers who drink or encourage drinking alcohol were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for binge drinking at second follow up.
+TDO2	addiction	relapse	29697747	Genetic variants in TPH1 (rs591556) were associated with sensation <b>seeking</b> and impulsivity, while genetic variants in <strong>TPH2</strong> (rs17110451) were associated with the fraction of drinkers in family.
+TDO2	drug	cocaine	28590957	Genetic moderation of <b>cocaine</b> subjective effects by variation in the TPH1, <strong>TPH2</strong>, and SLC6A4 serotonin genes.
+TDO2	drug	cocaine	28590957	This study investigated variants of tryptophan hydroxylase (TPH)1, <strong>TPH2</strong>, and SLC6A4 in the moderation of the subjective effects of <b>cocaine</b>.
+TDO2	drug	cocaine	28590957	These findings indicate that TPH1, <strong>TPH2</strong>, and SLC6A4 variants moderate the subjective effects of <b>cocaine</b> in non treatment seeking <b>cocaine</b> dependent participants.
+TDO2	addiction	relapse	28590957	These findings indicate that TPH1, <strong>TPH2</strong>, and SLC6A4 variants moderate the subjective effects of cocaine in non treatment <b>seeking</b> cocaine dependent participants.
+TDO2	addiction	addiction	26497913	However, little is known about the impact of <strong>Tph2</strong> gene variants on <b>addiction</b>.
+TDO2	drug	alcohol	26497913	Mice expressing a human <strong>Tph2</strong> loss of function variant were used to investigate consequences of aversive conditions on <b>ethanol</b> intake.
+TDO2	addiction	aversion	26497913	Mice expressing a human <strong>Tph2</strong> loss of function variant were used to investigate consequences of <b>aversive</b> conditions on ethanol intake.
+TDO2	drug	alcohol	26497913	Effect of familiarization to <b>ethanol</b> or an <b>ethanol</b> quinine solution was then evaluated using a two bottles preference test in <strong>Tph2</strong> KI and control littermates.
+TDO2	drug	alcohol	26497913	These results indicate that loss of function mutation in <strong>Tph2</strong> results in greater motivation for <b>ethanol</b> consumption under aversive conditions and may confer enhanced sensitivity to <b>alcohol</b> use disorder.
+TDO2	addiction	aversion	26497913	These results indicate that loss of function mutation in <strong>Tph2</strong> results in greater motivation for ethanol consumption under <b>aversive</b> conditions and may confer enhanced sensitivity to alcohol use disorder.
+TDO2	drug	alcohol	26265436	Current evidence suggests that genetic variability of the serotonergic biosynthesis enzyme tryptophan hydroxylase 2 (<strong>TPH2</strong>) and the serotonin transporter (SLC6A4) genes mediates the efficacy of several addiction treatments, such as ondansetron and <b>disulfiram</b>, and the antidepressants bupropion, nortriptyline and sertraline.
+TDO2	addiction	addiction	26265436	Current evidence suggests that genetic variability of the serotonergic biosynthesis enzyme tryptophan hydroxylase 2 (<strong>TPH2</strong>) and the serotonin transporter (SLC6A4) genes mediates the efficacy of several <b>addiction</b> treatments, such as ondansetron and disulfiram, and the antidepressants bupropion, nortriptyline and sertraline.
+TDO2	drug	amphetamine	26259827	<strong>Tph2</strong> gene deletion enhances <b>amphetamine</b> induced hypermotility: effect of 5 HT restoration and role of striatal noradrenaline release.
+TDO2	addiction	addiction	26259827	Variants of tryptophan hydroxylase 2 (<strong>Tph2</strong>), the gene encoding enzyme responsible for the synthesis of brain serotonin (5 HT), have been associated with neuropsychiatric disorders, substance abuse and <b>addiction</b>.
+TDO2	drug	amphetamine	26259827	This study assessed the effect of <strong>Tph2</strong> gene deletion on motor behavior and found that motor activity induced by 2.5 and 5 mg/kg <b>amphetamine</b> was enhanced in <strong>Tph2</strong>( / ) mice.
+TDO2	drug	amphetamine	26259827	Using the in vivo microdialysis technique we found that the ability of <b>amphetamine</b> to stimulate noradrenaline (NA) release in the striatum was reduced by about 50% in <strong>Tph2</strong>( / ) mice while the release of dopamine (DA) was not affected.
+TDO2	drug	amphetamine	26259827	The role of endogenous 5 HT in enhancing the effect of <b>amphetamine</b> was confirmed showing that treatment with the 5 HT precursor 5 hydroxytryptophan (10 mg/kg) restored tissue and extracellular levels of brain 5 HT and the effects of <b>amphetamine</b> on striatal NA release and motor activity in <strong>Tph2</strong>( / ) mice.
+TDO2	drug	amphetamine	26259827	Treatment with the NA precursor dihydroxyphenylserine (400 mg/kg) was sufficient to restore the effect of <b>amphetamine</b> on striatal NA release and motor activity in <strong>Tph2</strong>( / ) mice.
+TDO2	drug	amphetamine	26259827	Here, we show that deletion of <strong>Tph2</strong>, the gene responsible for brain 5 HT synthesis, enhances the motor effect of <b>amphetamine</b> in mice through the inhibition of striatal NA release.
+TDO2	drug	alcohol	26232682	The present genetic association study explored the role of <strong>TPH2</strong> polymorphisms and their haplotypes to investigate its role in <b>alcohol</b> dependence and comorbid psychopathological symptoms.
+TDO2	addiction	dependence	26232682	The present genetic association study explored the role of <strong>TPH2</strong> polymorphisms and their haplotypes to investigate its role in alcohol <b>dependence</b> and comorbid psychopathological symptoms.
+TDO2	drug	alcohol	26232682	<strong>TPH2</strong> genotypes were not associated with <b>alcohol</b> dependence, but GGAA haplotype was less common (p=0.038) and GTAA and GGGT were more common (p=0.011 and p=0.021, respectively), in currently dependent patients compared to controls.
+TDO2	addiction	dependence	26232682	<strong>TPH2</strong> genotypes were not associated with alcohol <b>dependence</b>, but GGAA haplotype was less common (p=0.038) and GTAA and GGGT were more common (p=0.011 and p=0.021, respectively), in currently dependent patients compared to controls.
+TDO2	drug	alcohol	26232682	Our findings support a potential role of <strong>TPH2</strong> in <b>alcohol</b> dependence.
+TDO2	addiction	dependence	26232682	Our findings support a potential role of <strong>TPH2</strong> in alcohol <b>dependence</b>.
+TDO2	drug	alcohol	26232682	<strong>TPH2</strong> genetic variability may be also associated with anxiety and aggression traits in <b>alcohol</b> dependent subjects.
+TDO2	drug	cocaine	26013962	Two hundred twenty participants (126 <b>cocaine</b> users, 94 controls) were assessed with visuospatial, spatial, and verbal WM tasks, genotyped for the length polymorphism in the promoter region of the 5 HTT (5 HTTLPR), the variable number of tandem repeats in the second intron of the 5 HTT (VNTR In2), two single nucleotide polymorphisms (rs4570625 and rs1386497) in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene and quantified for peripheral 5 HTT mRNA expression in whole blood samples.
+TDO2	drug	cocaine	26013962	Several significant gene × environment interactions between 5 HT genotypes and <b>cocaine</b> use on WM emerged: in <b>cocaine</b> users, the long/long (5 HTTLPR), 9+10/9+10 (VNTR In2) and C/C (<strong>TPH2</strong> rs1386497) genotypes were risk alleles for WM impairments, whereas in healthy controls these polymorphisms were associated with improved WM performance.
+TDO2	drug	alcohol	23995203	Studies investigating suicide, <b>alcohol</b> related suicide and the rate limiting enzyme of serotonin synthesis, tryptophan hydroxylase 2 (<strong>TPH2</strong>), remain to date rather limited.
+TDO2	drug	alcohol	23995203	Recent studies of <strong>TPH2</strong> showed a range of strong, mild or no association with suicide and <b>alcohol</b> related suicide, depending on a study group and genetic variants tested.
+TDO2	drug	alcohol	23995203	However, based on current results we cannot draw any conclusions, but further research to clarify the interplay between serotonergic system dysfunction, suicide, <b>alcohol</b> dependence, impulsivity and the role of <strong>TPH2</strong> enzyme is needed.
+TDO2	addiction	dependence	23995203	However, based on current results we cannot draw any conclusions, but further research to clarify the interplay between serotonergic system dysfunction, suicide, alcohol <b>dependence</b>, impulsivity and the role of <strong>TPH2</strong> enzyme is needed.
+TDO2	drug	opioid	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ <b>opioid</b> receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (<strong>TPH2</strong>) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of <b>morphine</b> exposure, withdrawal and post withdrawal stress.
+TDO2	addiction	withdrawal	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ opioid receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (<strong>TPH2</strong>) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of morphine exposure, <b>withdrawal</b> and post <b>withdrawal</b> stress.
+TDO2	drug	opioid	24055683	5 HT1A receptor mRNA expression was decreased following 3h of <b>morphine</b> exposure, while <strong>TPH2</strong> mRNA expression was decreased after 7days of withdrawal with swim stress.
+TDO2	addiction	withdrawal	24055683	5 HT1A receptor mRNA expression was decreased following 3h of morphine exposure, while <strong>TPH2</strong> mRNA expression was decreased after 7days of <b>withdrawal</b> with swim stress.
+TDO2	drug	alcohol	23558111	Characterization of functional polymorphisms and glucocorticoid responsive elements in the promoter of <strong>TDO2</strong>, a candidate gene for <b>ethanol</b> induced behavioural disorders.
+TDO2	drug	alcohol	23558111	In response to acute <b>ethanol</b> consumption, <strong>tryptophan 2,3 dioxygenase</strong> (TDO) induces the kynurenine pathway (KP) through a glucocorticoid mediated mechanism, which could lead to a dramatic accumulation of neurotoxic metabolites in association with serotonin depletion.
+TDO2	addiction	relapse	23190435	In a multivariable model, being male, having higher sensation <b>seeking</b> tendencies and at least one copy of the minor allele for SNPs in angiotensin I converting enzyme gene [ACE; rs8066276 odds ratio (OR) = 1.44; P = 0.012] and tryptophan hydroxylase 2 gene (<strong>TPH2</strong>; rs11615016 OR = 1.73; P = 0.021) were associated with increased likelihood of meeting PA recommendations.
+TDO2	drug	alcohol	22925276	Modifying the role of serotonergic 5 HTTLPR and <strong>TPH2</strong> variants on <b>disulfiram</b> treatment of cocaine addiction: a preliminary study.
+TDO2	drug	cocaine	22925276	Modifying the role of serotonergic 5 HTTLPR and <strong>TPH2</strong> variants on disulfiram treatment of <b>cocaine</b> addiction: a preliminary study.
+TDO2	addiction	addiction	22925276	Modifying the role of serotonergic 5 HTTLPR and <strong>TPH2</strong> variants on disulfiram treatment of cocaine <b>addiction</b>: a preliminary study.
+TDO2	drug	alcohol	22925276	<b>Disulfiram</b> is a cocaine pharmacotherapy that may act through increasing serotonin, benefiting patients with genetically low serotonin transporter levels (5 HTTLPR, S' allele carriers) and low serotonin synthesis (<strong>TPH2</strong>, A allele carriers).
+TDO2	drug	cocaine	22925276	Disulfiram is a <b>cocaine</b> pharmacotherapy that may act through increasing serotonin, benefiting patients with genetically low serotonin transporter levels (5 HTTLPR, S' allele carriers) and low serotonin synthesis (<strong>TPH2</strong>, A allele carriers).
+TDO2	drug	alcohol	22925276	We genotyped the SLC6A4 5 HTTLPR (rs4795541, rs25531) and <strong>TPH2</strong> 1125A>T (rs4290270) variants and evaluated their role in moderating <b>disulfiram</b> treatment for cocaine dependence.
+TDO2	drug	cocaine	22925276	We genotyped the SLC6A4 5 HTTLPR (rs4795541, rs25531) and <strong>TPH2</strong> 1125A>T (rs4290270) variants and evaluated their role in moderating disulfiram treatment for <b>cocaine</b> dependence.
+TDO2	addiction	dependence	22925276	We genotyped the SLC6A4 5 HTTLPR (rs4795541, rs25531) and <strong>TPH2</strong> 1125A>T (rs4290270) variants and evaluated their role in moderating disulfiram treatment for cocaine <b>dependence</b>.
+TDO2	drug	alcohol	22925276	<strong>TPH2</strong> A allele carriers responded better to <b>disulfiram</b> than placebo (F = 16.0; df = 1,223; P < 0.0001).
+TDO2	drug	alcohol	22925276	Patients with both an S' allele and a <strong>TPH2</strong> A allele reduced cocaine urines from 71% to 53% on <b>disulfiram</b> and had no change on placebo (F = 21.6; df = 1,185; P < 0.00001).
+TDO2	drug	cocaine	22925276	Patients with both an S' allele and a <strong>TPH2</strong> A allele reduced <b>cocaine</b> urines from 71% to 53% on disulfiram and had no change on placebo (F = 21.6; df = 1,185; P < 0.00001).
+TDO2	drug	amphetamine	21886586	We analyzed the association between the variations in the brain tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene, a rate limiting enzyme for serotonin biosynthesis, and <b>methamphetamine</b> (<b>METH</b>) dependence/psychosis in a Japanese population.
+TDO2	addiction	dependence	21886586	We analyzed the association between the variations in the brain tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene, a rate limiting enzyme for serotonin biosynthesis, and methamphetamine (METH) <b>dependence</b>/psychosis in a Japanese population.
+TDO2	drug	amphetamine	21886586	These results suggest that the <strong>TPH2</strong> gene variants may not be a factor in vulnerability to <b>METH</b> dependence/psychosis.
+TDO2	addiction	dependence	21886586	These results suggest that the <strong>TPH2</strong> gene variants may not be a factor in vulnerability to METH <b>dependence</b>/psychosis.
+TDO2	drug	alcohol	21797889	This study investigated whether drinking motives mediate the associations between <b>alcohol</b> consumption and 2 single nucleotide polymorphisms (SNPs) from genes involved in serotonin (<strong>TPH2</strong>; rs1386496) and dopamine synthesis (DDC; rs3779084).
+TDO2	drug	alcohol	21621273	Association of polymorphisms in HTR2A, HTR1A and <strong>TPH2</strong> genes with suicide attempts in <b>alcohol</b> dependence: a preliminary report.
+TDO2	addiction	dependence	21621273	Association of polymorphisms in HTR2A, HTR1A and <strong>TPH2</strong> genes with suicide attempts in alcohol <b>dependence</b>: a preliminary report.
+TDO2	drug	alcohol	21621273	We investigated a relationship between selected polymorphisms: rs6313 in HTR2A, rs6295 in HTR1A and rs1386494 in <strong>TPH2</strong>, and suicidal behaviour in 150 <b>alcohol</b> dependent patients.
+TDO2	drug	alcohol	21182896	<strong>TPH2</strong> polymorphisms and <b>alcohol</b> related suicide.
+TDO2	drug	alcohol	21182896	In conclusion, our results suggest implication of polymorphisms in suicide and <b>alcohol</b> related suicide, but further studies are needed to clarify the interplay among serotonergic system disfunction, suicide, <b>alcohol</b> dependence, impulsivity and the role of <strong>TPH2</strong> enzyme.
+TDO2	addiction	dependence	21182896	In conclusion, our results suggest implication of polymorphisms in suicide and alcohol related suicide, but further studies are needed to clarify the interplay among serotonergic system disfunction, suicide, alcohol <b>dependence</b>, impulsivity and the role of <strong>TPH2</strong> enzyme.
+TDO2	drug	alcohol	21143251	While no results survive the burden of multiple testing, nominal findings in <strong>TPH2</strong> and DDC suggest the potential role of the serotonin synthesis pathway in <b>alcohol</b> consumption.
+TDO2	drug	alcohol	19759277	We examined (1) the association of SLC6A4 genotypes and <b>alcohol</b> dependence (AD) in a sample of <b>alcoholics</b>; (2) the validity of lifetime occurrence of blacked out violent impulsive behaviour (BOVIB) during binge drinking bouts as a criterion for subtyping AD patients and (3) a mechanistic hypothesis for BOVIB involving <strong>tryptophan 2,3 dioxygenase</strong> (TDO) activity.
+TDO2	addiction	dependence	19759277	We examined (1) the association of SLC6A4 genotypes and alcohol <b>dependence</b> (AD) in a sample of alcoholics; (2) the validity of lifetime occurrence of blacked out violent impulsive behaviour (BOVIB) during binge drinking bouts as a criterion for subtyping AD patients and (3) a mechanistic hypothesis for BOVIB involving <strong>tryptophan 2,3 dioxygenase</strong> (TDO) activity.
+TDO2	addiction	intoxication	19759277	We examined (1) the association of SLC6A4 genotypes and alcohol dependence (AD) in a sample of alcoholics; (2) the validity of lifetime occurrence of blacked out violent impulsive behaviour (BOVIB) during <b>binge</b> drinking bouts as a criterion for subtyping AD patients and (3) a mechanistic hypothesis for BOVIB involving <strong>tryptophan 2,3 dioxygenase</strong> (TDO) activity.
+TDO2	drug	alcohol	19742166	Epistasis between IL1A, IL1B, TNF, HTR2A, 5 HTTLPR and <strong>TPH2</strong> variations does not impact <b>alcohol</b> dependence disorder features.
+TDO2	addiction	dependence	19742166	Epistasis between IL1A, IL1B, TNF, HTR2A, 5 HTTLPR and <strong>TPH2</strong> variations does not impact alcohol <b>dependence</b> disorder features.
+TDO2	drug	alcohol	19742166	In both groups we genotyped 11 genetic variations (rs1800587; rs3087258; rs1799724; 5 HTTLPR; rs1386493; rs1386494; rs1487275; rs1843809; rs4570625; rs2129575; rs6313) located in genes whose impact on <b>alcohol</b> related behaviors and disorders has been hypothesized (IL1A, IL1B, TNF, 5 HTTLPR, <strong>TPH2</strong> and HTR2A).
+TDO2	drug	alcohol	19734157	The <strong>TPH2</strong> gene may play an important role in suicide vulnerability especially in individuals who did not drink <b>alcohol</b> before suicide.
+TDO2	drug	alcohol	19361870	<strong>TPH2</strong> gene variants and anxiety during <b>alcohol</b> detoxification outcome.
+TDO2	drug	alcohol	19361870	<strong>TPH2</strong> variants have been consistently associated with anxiety related traits; since anxiety is critical for <b>alcohol</b> dependence treatment, in the present paper we investigated 9 SNPs within the THP2 gene in anxiety symptoms during the detoxification procedure.
+TDO2	addiction	dependence	19361870	<strong>TPH2</strong> variants have been consistently associated with anxiety related traits; since anxiety is critical for alcohol <b>dependence</b> treatment, in the present paper we investigated 9 SNPs within the THP2 gene in anxiety symptoms during the detoxification procedure.
+TDO2	addiction	relapse	19170664	Genetic polymorphisms in several genes (<strong>TPH2</strong>, SLC6A4, HTR1A, HTR2A, COMT, and BDNF) were tested as predictors of <b>relapse</b> (defined as any drinking during follow up) while controlling for baseline measures.
+TDO2	drug	alcohol	18405071	A case group of males with type 2 <b>alcoholism</b> (N=59) and a control group of healthy males (N=282), both of Croatian origin, were analyzed for the frequency distribution of polymorphisms in 5HT transporter (5HTT VNTR2, 5HTT LPR), monoamine oxidase A (MAOA uVNTR) and B (MAOB A/G) and tryptophan hydroxylase 1 (TPH1 A218C) and 2 (<strong>TPH2</strong> G 703T) genes.
+TDO2	drug	opioid	18181017	<strong>TPH2</strong> and TPH1: association of variants and interactions with <b>heroin</b> addiction.
+TDO2	addiction	addiction	18181017	<strong>TPH2</strong> and TPH1: association of variants and interactions with heroin <b>addiction</b>.
+TDO2	addiction	addiction	18181017	In a cohort of 583 consecutively ascertained subjects, including normal volunteers and those with specific <b>addictive</b> diseases, six common <strong>TPH2</strong> and one TPH1 variant were genotyped.
+TDO2	drug	opioid	18181017	At the two locus genotype level in Hispanics, the TPH1 rs1799913 variant was found to significantly interact with the <strong>TPH2</strong> rs7963720 variant and <b>heroin</b> addiction (P=0.022), and with the <strong>TPH2</strong> rs4290270 variant and <b>heroin</b> addiction (P=0.011).
+TDO2	addiction	addiction	18181017	At the two locus genotype level in Hispanics, the TPH1 rs1799913 variant was found to significantly interact with the <strong>TPH2</strong> rs7963720 variant and heroin <b>addiction</b> (P=0.022), and with the <strong>TPH2</strong> rs4290270 variant and heroin <b>addiction</b> (P=0.011).
+TDO2	drug	opioid	18181017	In the African American group, a significant association of a specific <strong>TPH2</strong> haplotype with <b>heroin</b> addiction also was found (SNPHAP, P=0.004; PHASE P=0.036).
+TDO2	addiction	addiction	18181017	In the African American group, a significant association of a specific <strong>TPH2</strong> haplotype with heroin <b>addiction</b> also was found (SNPHAP, P=0.004; PHASE P=0.036).
+TDO2	drug	nicotine	17986837	The role of the TPH1 and <strong>TPH2</strong> genes for <b>nicotine</b> dependence: a genetic association study in two different age cohorts.
+TDO2	addiction	dependence	17986837	The role of the TPH1 and <strong>TPH2</strong> genes for nicotine <b>dependence</b>: a genetic association study in two different age cohorts.
+TDO2	drug	nicotine	17986837	Based on pharmacological and genetic studies suggesting a role of the serotonergic system for <b>nicotine</b> dependence, two genetic variants, one on the tryptophan hydroxylase 1 (TPH1) and one on the <strong>TPH2</strong> gene, were investigated.
+TDO2	addiction	dependence	17986837	Based on pharmacological and genetic studies suggesting a role of the serotonergic system for nicotine <b>dependence</b>, two genetic variants, one on the tryptophan hydroxylase 1 (TPH1) and one on the <strong>TPH2</strong> gene, were investigated.
+TDO2	drug	nicotine	17986837	The <strong>TPH2</strong>  703G/T promoter polymorphism was associated with <b>smoking</b> status and age of <b>smoking</b> onset in two independent Caucasian samples of different age cohorts.
+TDO2	drug	nicotine	17986837	The <strong>TPH2</strong>  703G/T was significantly associated with age of <b>smoking</b> onset in both samples.
+TDO2	drug	alcohol	17251907	We performed single SNP (single nucleotide polymorphism), linkage disequilibrium and haplotype studies on 353 <b>alcohol</b> dependent patients of whom 102 individuals had a history of at least one suicide attempt and 305 healthy controls with 20 SNPs covering the entire gene region of <strong>TPH2</strong>.
+TDO2	drug	alcohol	17251907	One major haplotype block of strong linkage disequilibrium between introns 5 and 8 of the <strong>TPH2</strong> gene has been found in <b>alcoholics</b> and controls, which is in concordance with recent reports.
+TDO2	drug	alcohol	17251907	In conclusion, our results suggest that single SNPs, respectively, haplotypes of the <strong>TPH2</strong> gene are unlikely to play a major role in the pathophysiology of <b>alcohol</b> dependence or the <b>alcoholism</b> related phenotype suicidal behavior.
+TDO2	addiction	dependence	17251907	In conclusion, our results suggest that single SNPs, respectively, haplotypes of the <strong>TPH2</strong> gene are unlikely to play a major role in the pathophysiology of alcohol <b>dependence</b> or the alcoholism related phenotype suicidal behavior.
+TDO2	drug	cocaine	16759340	Analysis of variations in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene in <b>cocaine</b> dependence.
+TDO2	addiction	dependence	16759340	Analysis of variations in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene in cocaine <b>dependence</b>.
+TDO2	drug	cocaine	16759340	The focus of the present study is to determine whether genetic variation in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene, which encodes the enzyme responsible for synthesis of the majority of the serotonin contained in neurons of the central nervous system, contributes to the pathophysiology of <b>cocaine</b> dependence.
+TDO2	addiction	dependence	16759340	The focus of the present study is to determine whether genetic variation in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene, which encodes the enzyme responsible for synthesis of the majority of the serotonin contained in neurons of the central nervous system, contributes to the pathophysiology of cocaine <b>dependence</b>.
+TDO2	drug	cocaine	16759340	To examine this hypothesis, we used a case control study design in which the genotype and allele distributions for six single nucleotide polymorphisms (SNPs) in the <strong>TPH2</strong> gene were compared between <b>cocaine</b> dependent (n = 299) and control individuals (n = 208) of African descent.
+TDO2	drug	cocaine	16759340	The results indicate that none of the SNPs in the <strong>TPH2</strong> gene examined in this study associate with the <b>cocaine</b> dependent phenotype.
+TDO2	drug	cocaine	16759340	This work suggests that variations in the <strong>TPH2</strong> gene are not a risk factor for the development of <b>cocaine</b> dependence, but these findings require confirmation in larger, independent samples of <b>cocaine</b> dependent and control subjects.
+TDO2	addiction	dependence	16759340	This work suggests that variations in the <strong>TPH2</strong> gene are not a risk factor for the development of cocaine <b>dependence</b>, but these findings require confirmation in larger, independent samples of cocaine dependent and control subjects.
+TDO2	drug	opioid	15048644	We found correspondence between linkage and microarray/candidate gene studies for genes involved with the mitogen activated protein kinase (MAPK) signaling system, nuclear factor kappa B (NFKB) complex, neuropeptide Y (NPY) neurotransmission, a nicotinic receptor subunit (CHRNA2), the vesicular monoamine transporter (SLC18A2), genes in pathways implicated in human anxiety (HTR7, <strong>TDO2</strong>, and the endozepine related protein precursor, DKFZP434A2417), and the micro 1 <b>opioid</b> receptor (OPRM1).
+SNAP25	addiction	relapse	32524927	National concerns over food insecurity and obesity have prompted legislation <b>seeking</b> to further restrict Supplemental Nutrition Assistance Program (<strong>SNAP</strong>) purchases.
+SNAP25	drug	alcohol	32524927	The objective of this study is to provide insight on the potential impact of proposed purchase restrictions by comparing <strong>SNAP</strong> participant and income eligible non participants' expenditures on current <strong>SNAP</strong> restricted foods, that is, hot foods, prepared foods, <b>alcohol</b>, vitamins and meal supplements.
+SNAP25	drug	opioid	32278265	This paper includes the voices of people who are members of a peer led drug user group (<strong>SNAP</strong>) in Canada who are receiving <b>heroin</b> assisted treatment (HAT) outside of a clinical trial.
+SNAP25	drug	opioid	32278265	Drawing from critical drug studies, we problematize the criteria for severe <b>opioid</b> use disorder (OUD) from the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, by exploring <strong>SNAP</strong> members' experiences in relation to <b>heroin</b> assisted treatment, and examining how <strong>SNAP</strong> participants' narratives challenge conventional notions of what constitutes severe <b>opioid</b> use disorder.
+SNAP25	drug	opioid	32278265	Although <strong>SNAP</strong> participants were diagnosed as suffering from OUD, the DSM 5 criteria for OUD fails to encompass their diverse experiences of <b>opioid</b> use.
+SNAP25	drug	opioid	32278265	<strong>SNAP</strong>, and their allies, are rupturing conventional ideas about <b>heroin</b> and taken for granted assumptions about people who use <b>heroin</b>.
+SNAP25	drug	alcohol	30341114	Brief intervention on Smoking, Nutrition, <b>Alcohol</b> and Physical (<strong>SNAP</strong>) inactivity for smoking relapse prevention after release from smoke free prisons: a study protocol for a multicentre, investigator blinded, randomised controlled trial.
+SNAP25	drug	nicotine	30341114	Brief intervention on <b>Smoking</b>, Nutrition, Alcohol and Physical (<strong>SNAP</strong>) inactivity for <b>smoking</b> relapse prevention after release from smoke free prisons: a study protocol for a multicentre, investigator blinded, randomised controlled trial.
+SNAP25	addiction	relapse	30341114	Brief intervention on Smoking, Nutrition, Alcohol and Physical (<strong>SNAP</strong>) inactivity for smoking <b>relapse</b> prevention after release from smoke free prisons: a study protocol for a multicentre, investigator blinded, randomised controlled trial.
+SNAP25	drug	alcohol	30341114	Heavy Smoking is often associated with poor Nutrition, <b>Alcohol</b> abuse and Physical inactivity (known as '<strong>SNAP</strong>').
+SNAP25	drug	nicotine	30341114	Heavy <b>Smoking</b> is often associated with poor Nutrition, Alcohol abuse and Physical inactivity (known as '<strong>SNAP</strong>').
+SNAP25	drug	nicotine	30341114	This multicentre, investigator blinded, randomised parallel superiority trial will evaluate the effectiveness of a brief intervention on <strong>SNAP</strong> versus usual care in preventing <b>smoking</b> relapse among people released from smoke free prisons in the Northern Territory, Australia.
+SNAP25	addiction	relapse	30341114	This multicentre, investigator blinded, randomised parallel superiority trial will evaluate the effectiveness of a brief intervention on <strong>SNAP</strong> versus usual care in preventing smoking <b>relapse</b> among people released from smoke free prisons in the Northern Territory, Australia.
+SNAP25	drug	alcohol	29926762	The galanin receptor 3 antagonist, <strong>SNAP</strong> 37889, inhibits cue induced reinstatement of <b>alcohol</b> seeking and increases c Fos expression in the nucleus accumbens shell of <b>alcohol</b> preferring rats.
+SNAP25	addiction	relapse	29926762	The galanin receptor 3 antagonist, <strong>SNAP</strong> 37889, inhibits cue induced <b>reinstatement</b> of alcohol <b>seeking</b> and increases c Fos expression in the nucleus accumbens shell of alcohol preferring rats.
+SNAP25	drug	alcohol	29926762	This study aimed to investigate the effects of the galanin 3 receptor antagonist, <strong>SNAP</strong> 37889, on c Fos protein expression after cue induced reinstatement of <b>alcohol</b> seeking in the brains of <b>alcohol</b> preferring rats.
+SNAP25	addiction	relapse	29926762	This study aimed to investigate the effects of the galanin 3 receptor antagonist, <strong>SNAP</strong> 37889, on c Fos protein expression after cue induced <b>reinstatement</b> of alcohol <b>seeking</b> in the brains of alcohol preferring rats.
+SNAP25	drug	alcohol	29926762	Administration of <strong>SNAP</strong> 37889 reduced cue induced reinstatement of <b>ethanol</b> seeking behaviour.
+SNAP25	addiction	relapse	29926762	Administration of <strong>SNAP</strong> 37889 reduced cue induced <b>reinstatement</b> of ethanol <b>seeking</b> behaviour.
+SNAP25	addiction	relapse	29926762	To examine the effect of <strong>SNAP</strong> 37889 and cue induced <b>reinstatement</b> on neuronal activation, c Fos expression was measured in subregions of the medial prefrontal cortex and nucleus accumbens.
+SNAP25	drug	opioid	28884870	Phosphorylated <strong>SNAP25</strong> in the CA1 regulates <b>morphine</b> associated contextual memory retrieval via increasing GluN2B NMDAR surface localization.
+SNAP25	drug	opioid	28884870	Interestingly, we also found that phosphorylation of <strong>SNAP25</strong> at Ser187 (pSer187 <strong>SNAP25</strong>), a PKC activated target, was significantly increased following <b>morphine</b> CPP expression.
+SNAP25	addiction	reward	28884870	Interestingly, we also found that phosphorylation of <strong>SNAP25</strong> at Ser187 (pSer187 <strong>SNAP25</strong>), a PKC activated target, was significantly increased following morphine <b>CPP</b> expression.
+SNAP25	drug	opioid	28884870	Blocking the pSer187 <strong>SNAP25</strong> by intra CA1 injection of an interfering peptide impaired <b>morphine</b> CPP expression and accompanied by the reduced ratio of GluN2B membrane/total in the CA1.
+SNAP25	addiction	reward	28884870	Blocking the pSer187 <strong>SNAP25</strong> by intra CA1 injection of an interfering peptide impaired morphine <b>CPP</b> expression and accompanied by the reduced ratio of GluN2B membrane/total in the CA1.
+SNAP25	addiction	reward	28884870	In addition, intra CA1 blockade of pSer187 <strong>SNAP25</strong> did not affect natural learning and memory process as evidenced by intact sucrose induced <b>CPP</b> expression and normal locomotor activity in rats.
+SNAP25	addiction	addiction	28884870	Therefore, our results reveal that enhanced pSer187 <strong>SNAP25</strong> by PKC recruits GluN2B NMDAR to the membrane surface in the hippocampal CA1 and mediates context induced <b>addiction</b> memory retrieval.
+SNAP25	drug	alcohol	28274821	The galanin 3 receptor antagonist, <strong>SNAP</strong> 37889, suppresses <b>alcohol</b> drinking and morphine self administration in mice.
+SNAP25	drug	opioid	28274821	The galanin 3 receptor antagonist, <strong>SNAP</strong> 37889, suppresses alcohol drinking and <b>morphine</b> self administration in mice.
+SNAP25	drug	alcohol	28274821	We have previously shown that the GAL3 antagonist, <strong>SNAP</strong> 37889, reduces <b>ethanol</b> self administration and cue induced re instatement in <b>alcohol</b> preferring (iP) rats with no alterations in locomotor activity or anxiety like behaviour.
+SNAP25	drug	opioid	28274821	The aim of this study was to investigate whether <strong>SNAP</strong> 37889 reduces binge drinking and/or self administration of <b>morphine</b> in mice.
+SNAP25	addiction	intoxication	28274821	The aim of this study was to investigate whether <strong>SNAP</strong> 37889 reduces <b>binge</b> drinking and/or self administration of morphine in mice.
+SNAP25	drug	alcohol	28274821	Using the Scheduled High <b>Alcohol</b> Consumption (SHAC) procedure, <strong>SNAP</strong> 37889 (30 mg/kg) treated mice drank significantly less <b>ethanol</b>, sucrose and saccharin than vehicle treated mice.
+SNAP25	drug	opioid	28274821	Using an operant paradigm, <strong>SNAP</strong> 37889 reduced <b>morphine</b> self administration but failed to impact cue induced relapse like behaviour.
+SNAP25	addiction	relapse	28274821	Using an operant paradigm, <strong>SNAP</strong> 37889 reduced morphine self administration but failed to impact cue induced <b>relapse</b> like behaviour.
+SNAP25	addiction	reward	28274821	Using an <b>operant</b> paradigm, <strong>SNAP</strong> 37889 reduced morphine self administration but failed to impact cue induced relapse like behaviour.
+SNAP25	addiction	reward	28274821	<strong>SNAP</strong> 37889 had no significant effect on locomotor activity, motor co ordination, anxiety, nor was <strong>SNAP</strong> 37889 itself positively <b>reinforcing</b>.
+SNAP25	drug	alcohol	28274821	Liver assays showed that there was no alteration in the rate of hepatic <b>ethanol</b> metabolism between <strong>SNAP</strong> 37889 and vehicle treated mice suggesting that the reduction in <b>ethanol</b> intake via <strong>SNAP</strong> 37889 is due to a central effect of GAL3 signalling.
+SNAP25	drug	alcohol	27606314	We found affected subjects with a diagnosis of <b>alcohol</b> use disorder (AUD) had a lower level of <strong>SNAP</strong> 25b BA24 protein compared to those without AUD.
+SNAP25	drug	amphetamine	27582038	In addition, <strong>SNAP25</strong>, RAB18, FABP5, ARF5 and LDHA, which are related genes to schizophrenia and <b>methamphetamine</b> sensitization, are also decreased in crmp2 /  mice.
+SNAP25	addiction	sensitization	27582038	In addition, <strong>SNAP25</strong>, RAB18, FABP5, ARF5 and LDHA, which are related genes to schizophrenia and methamphetamine <b>sensitization</b>, are also decreased in crmp2 /  mice.
+SNAP25	drug	nicotine	27559543	We observed significant effects of <b>nicotine</b> exposure on the β2* nAChR associated proteome in human and mouse cortex, particularly in the abundance of the nAChR subunits themselves, as well as putative interacting proteins that make up core components of neuronal excitability (Na/K ATPase subunits), presynaptic neurotransmitter release (syntaxins, <strong>SNAP25</strong>, synaptotagmin), and a member of a known nAChR protein chaperone family (14 3 3ζ).
+SNAP25	drug	alcohol	24881957	Galanin 3 receptor antagonism by <strong>SNAP</strong> 37889 reduces motivation to self administer <b>alcohol</b> and attenuates cue induced reinstatement of <b>alcohol</b> seeking in iP rats.
+SNAP25	addiction	relapse	24881957	Galanin 3 receptor antagonism by <strong>SNAP</strong> 37889 reduces motivation to self administer alcohol and attenuates cue induced <b>reinstatement</b> of alcohol <b>seeking</b> in iP rats.
+SNAP25	drug	alcohol	24881957	We have previously shown that the selective GALR3 antagonist <strong>SNAP</strong> 37889 reduced voluntary <b>alcohol</b> consumption in iP (<b>alcohol</b> preferring) rats.
+SNAP25	drug	alcohol	24881957	<strong>SNAP</strong> 37889 also significantly reduced reinstatement of <b>alcohol</b> seeking in response to re exposure to conditioned cues that were previously associated with the availability of <b>alcohol</b>.
+SNAP25	addiction	relapse	24881957	<strong>SNAP</strong> 37889 also significantly reduced <b>reinstatement</b> of alcohol <b>seeking</b> in response to re exposure to conditioned cues that were previously associated with the availability of alcohol.
+SNAP25	drug	alcohol	24881957	These findings validate further research in to the potential use of <strong>SNAP</strong> 37889 and other GALR3 antagonists to treat <b>alcohol</b> abuse disorders in humans.
+SNAP25	addiction	sensitization	24599450	Similarly, treatment with the nitric oxide donor, S Nitroso N acetyl DL penicillamine (<strong>SNAP</strong>), attenuated the expression of locomotor <b>sensitization</b> by promoting GluR2 surface expression.
+SNAP25	drug	cocaine	24599450	Noticeably, exogenous injection of <strong>SNAP</strong> into NAc also attenuated the expression of <b>cocaine</b> induced conditioned place preference.
+SNAP25	drug	amphetamine	23449013	Infusion of the MCH receptor 1 (MCHR1) antagonist <strong>SNAP</strong> 94847 into the NAc shell but not core augmented the initiation of locomotor sensitization and amplitude of elevated phosphorylated ERK levels induced by <b>Meth</b>.
+SNAP25	addiction	sensitization	23449013	Infusion of the MCH receptor 1 (MCHR1) antagonist <strong>SNAP</strong> 94847 into the NAc shell but not core augmented the initiation of locomotor <b>sensitization</b> and amplitude of elevated phosphorylated ERK levels induced by Meth.
+SNAP25	drug	amphetamine	23449013	The expression of <b>Meth</b> induced locomotor sensitization and ERK alterations after 1 wk withdrawal were not affected by either MCH or <strong>SNAP</strong> 94847 infused into the NAc shell or core.
+SNAP25	addiction	sensitization	23449013	The expression of Meth induced locomotor <b>sensitization</b> and ERK alterations after 1 wk withdrawal were not affected by either MCH or <strong>SNAP</strong> 94847 infused into the NAc shell or core.
+SNAP25	addiction	withdrawal	23449013	The expression of Meth induced locomotor sensitization and ERK alterations after 1 wk <b>withdrawal</b> were not affected by either MCH or <strong>SNAP</strong> 94847 infused into the NAc shell or core.
+SNAP25	drug	cannabinoid	23190435	Participants with at least one copy of the minor allele for SNPs in synaptosomal associated protein 25 gene (<strong>SNAP25</strong>; rs363035 OR = 0.53; P = 0.005) and <b>cannabinoid</b> receptor 1 gene (CNR1; rs6454672 OR = 0.62; P = 0.022) have decreased likelihood of meeting PA recommendations.
+SNAP25	drug	nicotine	22028400	Among committed never <b>smokers</b> (N = 872), three genes (OPRM1, <strong>SNAP25</strong>, HTR1B) were associated with experimentation as were all psychosocial factors.
+SNAP25	drug	cocaine	21426264	We examined the possible contribution to <b>cocaine</b> dependence of 16 genes involved in the cellular machinery that controls neurotransmitter release: genes encoding proteins of the SNARE complex (STX1A, <strong>SNAP25</strong>, VAMP1 and VAMP2), fusion control elements (SYT1, SYT2, CPLX1, CPLX2, CPLX3 and CPLX4) and regulatory elements (STXBP1, SYP, SNPH, NSF, NAPA and RAB3A).
+SNAP25	addiction	dependence	21426264	We examined the possible contribution to cocaine <b>dependence</b> of 16 genes involved in the cellular machinery that controls neurotransmitter release: genes encoding proteins of the SNARE complex (STX1A, <strong>SNAP25</strong>, VAMP1 and VAMP2), fusion control elements (SYT1, SYT2, CPLX1, CPLX2, CPLX3 and CPLX4) and regulatory elements (STXBP1, SYP, SNPH, NSF, NAPA and RAB3A).
+SNAP25	drug	alcohol	20736033	The galanin 3 receptor antagonist, <strong>SNAP</strong> 37889, reduces operant responding for <b>ethanol</b> in <b>alcohol</b> preferring rats.
+SNAP25	addiction	reward	20736033	The galanin 3 receptor antagonist, <strong>SNAP</strong> 37889, reduces <b>operant</b> responding for ethanol in alcohol preferring rats.
+SNAP25	drug	alcohol	20736033	The present study investigated the potential of the novel selective GALR3 antagonist, <strong>SNAP</strong> 37889, to reduce anxiety like behaviour and voluntary <b>ethanol</b> consumption in the iP (<b>alcohol</b> preferring) rat.
+SNAP25	drug	alcohol	18720419	To address this hypothesis in the context of <b>ethanol</b> dependence in humans, we used semiquantitative immunoblotting to compare the immunoreactivities of synaptophysin I, syntaxin 1A, <strong>synaptosome associated protein 25</strong>, and vesicle associated membrane protein in the prefrontal and motor cortices between chronic <b>alcoholics</b> and control subjects.
+SNAP25	addiction	dependence	18720419	To address this hypothesis in the context of ethanol <b>dependence</b> in humans, we used semiquantitative immunoblotting to compare the immunoreactivities of synaptophysin I, syntaxin 1A, <strong>synaptosome associated protein 25</strong>, and vesicle associated membrane protein in the prefrontal and motor cortices between chronic alcoholics and control subjects.
+SNAP25	drug	benzodiazepine	10940605	There were many empty <strong>snap</strong> out sheets for <b>flunitrazepam</b> tablets in the trash at his bedside.
+SNAP25	drug	opioid	8912014	Ipsilateral intraplantar injections of <b>morphine</b> (0.5 8 micrograms/paw) or <strong>SNAP</strong> (S nitroso N acetyl D,L penicillamine, 50 200) micrograms/paw) dose dependently antagonized spinally induced PGE2 hyperalgesia (ANOVA, p < 0.001).
+SNAP25	drug	opioid	7532832	In these experiments, the rat paw hyperalgesia pressure test in which inflammatory hyperalgesia is blocked by the intraplantar administration of <b>morphine</b> (MPH) or <strong>SNAP</strong>, a NO donor was used.
+LPP	drug	alcohol	32765317	The review also shows the usefulness of other components, implicated in affective and substance related processing (P1, N1, or the late positive potential <strong>LPP</strong>), as well as event related oscillations, such as theta power, with a possible use as vulnerability or clinical marker in <b>alcohol</b> dependence.
+LPP	addiction	dependence	32765317	The review also shows the usefulness of other components, implicated in affective and substance related processing (P1, N1, or the late positive potential <strong>LPP</strong>), as well as event related oscillations, such as theta power, with a possible use as vulnerability or clinical marker in alcohol <b>dependence</b>.
+LPP	drug	nicotine	32608084	The present study tested the associations between ETS exposure and ERPs reflecting cue reactivity (P3, <strong>LPP</strong>), inhibitory control (N2, P3), and reward processing (anticipation P3 (P3), feedback related negativity (FRN)) among never <b>smoking</b> adolescents.
+LPP	addiction	reward	32608084	The present study tested the associations between ETS exposure and ERPs reflecting cue reactivity (P3, <strong>LPP</strong>), inhibitory control (N2, P3), and <b>reward</b> processing (anticipation P3 (P3), feedback related negativity (FRN)) among never smoking adolescents.
+LPP	addiction	addiction	32592733	Regulation of craving (ROC) is a promising method of intervention in <b>addiction</b> and has received attention in event related potential (ERP) research investigating the late positive potential (<strong>LPP</strong>).
+LPP	addiction	relapse	32592733	Regulation of <b>craving</b> (ROC) is a promising method of intervention in addiction and has received attention in event related potential (ERP) research investigating the late positive potential (<strong>LPP</strong>).
+LPP	addiction	relapse	32592733	This replicates the mismatch between self reported <b>craving</b> and <strong>LPP</strong>.
+LPP	addiction	addiction	31945829	We found that the MI group alone presented heightened late positive potential (<strong>LPP</strong>) responses while processing cigarette (<b>addictive</b>) stimuli compared to neutral images (t value = 3.11 at Cz, 3.92 at Pz).
+LPP	drug	nicotine	31945829	Our study illustrates the significance of the <strong>LPP</strong> as a promising biomarker to assess <b>tobacco</b> addiction in individuals facing mental illness.
+LPP	addiction	addiction	31945829	Our study illustrates the significance of the <strong>LPP</strong> as a promising biomarker to assess tobacco <b>addiction</b> in individuals facing mental illness.
+LPP	drug	alcohol	31825472	We found that both craving ratings and the <strong>LPP</strong> significantly decreased in response to <b>alcohol</b> cues from pre  to post treatment, but not for other image cues.
+LPP	addiction	relapse	31825472	We found that both <b>craving</b> ratings and the <strong>LPP</strong> significantly decreased in response to alcohol cues from pre  to post treatment, but not for other image cues.
+LPP	addiction	relapse	31825472	Active tDCS was not associated with <b>craving</b> ratings, but it was associated with greater <strong>LPP</strong> amplitudes across image types.
+LPP	drug	opioid	31692007	The overlap genes of top 10 hub genes in significant modules (PRR11, SLC35E1, <strong>LPP</strong>, ZNF721, ZNF611, LRRFIP1) were selected to identify as candidate genes in the regulation mechanism of NAc in <b>heroin</b> dependence.
+LPP	addiction	dependence	31692007	The overlap genes of top 10 hub genes in significant modules (PRR11, SLC35E1, <strong>LPP</strong>, ZNF721, ZNF611, LRRFIP1) were selected to identify as candidate genes in the regulation mechanism of NAc in heroin <b>dependence</b>.
+LPP	drug	alcohol	31547662	To further validate the <strong>LPP</strong> model, umbrella sampling was used to calculate <b>ethanol</b> permeability in comparison with experiment (log(P) values obtained from modeling the SC's multiple <strong>LPP</strong> layers are  7.6 and  6.6 cm/s, and that from experiment on cadaver skin is  6.65 cm/s).
+LPP	drug	nicotine	30824792	Unlike previous studies, there were no differences between male and female <b>smokers</b> with regard to <strong>LPP</strong> responses to cigarette related images.
+LPP	drug	cannabinoid	29737034	<b>Cannabis</b> cue elicited modulation of the 1000  to 3000 milliseconds <strong>LPP</strong> was larger in high DI users at post stressor only, although the effect was only robust in the 1000  to 2000 milliseconds window.
+LPP	drug	cannabinoid	29737034	Negative and <b>cannabis</b> stimuli elicited <strong>LPP</strong> modulation appear to index distinct, CUD relevant neural processes in high DI <b>cannabis</b> users.
+LPP	drug	alcohol	29227243	In heavy social drinkers, <b>alcoholic</b> content <strong>LPP</strong> was increased and P100 latency was shorter compared with nonalcoholic cues.
+LPP	drug	alcohol	29227243	Linear regression for <b>alcohol</b> content condition in the overall sample revealed shorter P100 latency and increased <strong>LPP</strong> amplitude predicting AUDIT scores.
+LPP	drug	nicotine	29220524	At both sessions, we measured the amplitude of the late positive potential (<strong>LPP</strong>), an ERP component reliably associated with motivational relevance, and self reported tonic craving using the brief version of the Questionnaire of <b>Smoking</b> Urges (QSU Brief).
+LPP	addiction	relapse	29220524	At both sessions, we measured the amplitude of the late positive potential (<strong>LPP</strong>), an ERP component reliably associated with motivational relevance, and self reported tonic <b>craving</b> using the brief version of the Questionnaire of Smoking Urges (QSU Brief).
+LPP	drug	nicotine	29220524	While both varenicline and bupropion reduced self reported tonic craving, neither medication altered the amplitude of the <strong>LPP</strong> to cigarette related or emotional pictures in <b>smokers</b> attempting to quit.
+LPP	addiction	relapse	29220524	While both varenicline and bupropion reduced self reported tonic <b>craving</b>, neither medication altered the amplitude of the <strong>LPP</strong> to cigarette related or emotional pictures in smokers attempting to quit.
+LPP	drug	nicotine	29065198	Analyses of P300 and <strong>LPP</strong> responses to GHWLs suggest that disgust focused images interfere with the EEG indexed attentional processing of <b>smoking</b> cues and do so better than health anxiety focused messages.
+LPP	drug	nicotine	28275830	Prior to treatment randomization, <b>smokers</b> (N = 180) in a placebo controlled trial using bupropion and varenicline completed event related potential recording (late positive potential, <strong>LPP</strong>) while viewing pleasant (P), cigarette (C) related, and other pictures.
+LPP	drug	cocaine	28245173	In this study we used the late positive potential (<strong>LPP</strong>) to investigate whether such increased attention bias toward drug related relative to non drug related cues changes over a protracted period of reduced drug use in treatment seeking individuals with a <b>cocaine</b> use disorder (CUD).
+LPP	addiction	relapse	28245173	In this study we used the late positive potential (<strong>LPP</strong>) to investigate whether such increased attention bias toward drug related relative to non drug related cues changes over a protracted period of reduced drug use in treatment <b>seeking</b> individuals with a cocaine use disorder (CUD).
+LPP	drug	cocaine	28245173	The results showed a reversal in attention bias (i.e., <strong>LPP</strong> amplitude) from baseline (i.e., drug > pleasant) to follow up (i.e., pleasant > drug) driven by an increased attentional engagement with pleasant pictures; this <strong>LPP</strong> reversal was paralleled by a concomitant reduction in self reported wanting and craving for <b>cocaine</b> in the CUD group.
+LPP	addiction	relapse	28245173	The results showed a reversal in attention bias (i.e., <strong>LPP</strong> amplitude) from baseline (i.e., drug > pleasant) to follow up (i.e., pleasant > drug) driven by an increased attentional engagement with pleasant pictures; this <strong>LPP</strong> reversal was paralleled by a concomitant reduction in self reported wanting and <b>craving</b> for cocaine in the CUD group.
+LPP	addiction	relapse	28245173	Results collectively indicate that, by tracking with drug abstinence, <strong>LPP</strong> in response to drug related relative to pleasant cues may serve as an indicator of clinical progress in treatment <b>seeking</b> individuals with CUD.
+LPP	drug	cocaine	27434467	In this study we used the late positive potential (<strong>LPP</strong>) to investigate whether such increased attention bias toward drug related relative to non drug related cues changes over a protracted period of reduced drug use in treatment seeking individuals with a <b>cocaine</b> use disorder (CUD).
+LPP	addiction	relapse	27434467	In this study we used the late positive potential (<strong>LPP</strong>) to investigate whether such increased attention bias toward drug related relative to non drug related cues changes over a protracted period of reduced drug use in treatment <b>seeking</b> individuals with a cocaine use disorder (CUD).
+LPP	drug	cocaine	27434467	The results showed a reversal in attention bias (i.e., <strong>LPP</strong> amplitude) from baseline (i.e., drug > pleasant) to follow up (i.e., pleasant > drug) driven by an increased attentional engagement with pleasant pictures; this <strong>LPP</strong> reversal was paralleled by a concomitant reduction in self reported wanting and craving for <b>cocaine</b> in the CUD group.
+LPP	addiction	relapse	27434467	The results showed a reversal in attention bias (i.e., <strong>LPP</strong> amplitude) from baseline (i.e., drug > pleasant) to follow up (i.e., pleasant > drug) driven by an increased attentional engagement with pleasant pictures; this <strong>LPP</strong> reversal was paralleled by a concomitant reduction in self reported wanting and <b>craving</b> for cocaine in the CUD group.
+LPP	addiction	relapse	27434467	Results collectively indicate that, by tracking with drug abstinence, <strong>LPP</strong> in response to drug related relative to pleasant cues may serve as an indicator of clinical progress in treatment <b>seeking</b> individuals with CUD.
+LPP	drug	nicotine	27277662	The objective of the present study is to investigate the association between <b>smoking</b> relapse and resumption and ERPs reflecting <b>smoking</b> cue reactivity (i.e., P300, <strong>LPP</strong>), inhibitory control (i.e., N2, P3), and error processing (i.e., error related negativity (ERN), Pe).
+LPP	addiction	relapse	27277662	The objective of the present study is to investigate the association between smoking <b>relapse</b> and resumption and ERPs reflecting smoking cue reactivity (i.e., P300, <strong>LPP</strong>), inhibitory control (i.e., N2, P3), and error processing (i.e., error related negativity (ERN), Pe).
+LPP	drug	nicotine	27141838	We tested whether individual differences in brain responses to cigarette related and pleasant stimuli require a long history of <b>smoking</b> to develop by measuring the late positive potential (<strong>LPP</strong>) to cigarette cues, emotional, and neutral stimuli in 45 young, light <b>smokers</b> (ages 18 25).
+LPP	addiction	intoxication	25915691	The current study examines the relation between symptoms of depression, <b>binge</b> drinking, and the magnitude of early (early posterior negativity, EPN) and later (P3 and late positive potential, <strong>LPP</strong>) visual processing components of affectively negative, positive, and neutral visual stimuli.
+LPP	drug	alcohol	25915691	Results of repeated measures analyses of variance (ANOVAs; Depression × Binge × Emotion × Laterality) showed that binge drinkers exhibited lower <strong>LPP</strong> amplitudes for negative images, compared with nonbinge drinkers, regardless of depression, consistent with motivational models of <b>alcohol</b> abuse.
+LPP	addiction	intoxication	25915691	Results of repeated measures analyses of variance (ANOVAs; Depression × <b>Binge</b> × Emotion × Laterality) showed that <b>binge</b> drinkers exhibited lower <strong>LPP</strong> amplitudes for negative images, compared with nonbinge drinkers, regardless of depression, consistent with motivational models of alcohol abuse.
+LPP	addiction	intoxication	25915691	Otherwise, differences across depressed and nondepressed groups were largest among <b>binge</b> drinkers, including a pattern of stronger early attentional engagement (EPN) to negative and neutral images, but decreased later processing (P3 and <strong>LPP</strong>) across all emotional categories, consistent with a vigilance avoidance response pattern.
+LPP	drug	opioid	25867962	Previous research has suggested that the late positive potential (<strong>LPP</strong>) of <b>heroin</b> users is increased by <b>heroin</b> related stimuli because of the attention grabbing nature of such stimuli.
+LPP	drug	opioid	25385024	Treatment with MORE was associated with significant increases in <strong>LPP</strong> response to natural reward stimuli relative to neutral stimuli which were correlated with enhanced positive affective cue responses and reductions in <b>opioid</b> craving from pre  to post treatment.
+LPP	addiction	relapse	25385024	Treatment with MORE was associated with significant increases in <strong>LPP</strong> response to natural reward stimuli relative to neutral stimuli which were correlated with enhanced positive affective cue responses and reductions in opioid <b>craving</b> from pre  to post treatment.
+LPP	addiction	reward	25385024	Treatment with MORE was associated with significant increases in <strong>LPP</strong> response to natural <b>reward</b> stimuli relative to neutral stimuli which were correlated with enhanced positive affective cue responses and reductions in opioid craving from pre  to post treatment.
+LPP	drug	cannabinoid	24913137	Response to emotional and <b>cannabis</b> associated visual stimuli was assessed using self report, event related potentials (using the late positive potential [<strong>LPP</strong>]), facial electromyography and skin conductance response.
+LPP	drug	cannabinoid	24913137	Reduced <strong>LPP</strong> response to pleasant stimuli was predictive of more frequent subsequent <b>cannabis</b> use (β =  0.24, p = 0.034).
+LPP	drug	cannabinoid	24913137	The <strong>LPP</strong> captures a reward processing deficit in patients with SSD and shows potential as a biomarker for identifying patients at risk of heavy <b>cannabis</b> use.
+LPP	addiction	reward	24913137	The <strong>LPP</strong> captures a <b>reward</b> processing deficit in patients with SSD and shows potential as a biomarker for identifying patients at risk of heavy cannabis use.
+LPP	drug	nicotine	24065931	<b>Smokers</b> were assigned to two groups (IRS+/IRS ) based on the amplitude of the late positive potential (<strong>LPP</strong>) component to the pictures, a neural marker of motivational salience.
+LPP	drug	nicotine	24065931	<b>Smokers</b> (n = 42) with blunted brain responses to intrinsically rewarding (pleasant) pictures and enhanced responses to cigarette pictures were assigned to the IRS  group, while <b>smokers</b> (n = 62) with the opposite pattern of <strong>LPP</strong> responding were assigned to the IRS+ group.
+LPP	drug	opioid	23723052	In this study, we compared the effect of thienorphine with <b>morphine</b> on long term potentiation (LTP) in the lateral perforant path (<strong>LPP</strong>) granule cell synapse of the rat dentate gyrus (DG).
+LPP	drug	opioid	23723052	Chronic thienorphine treatment facilitated LTP in the <strong>LPP</strong> DG cell synapses more than chronic <b>morphine</b> treatment.
+LPP	drug	nicotine	23643564	The late positive potential (<strong>LPP</strong>) in response to varying types of emotional and cigarette stimuli in <b>smokers</b>: a content comparison.
+LPP	drug	nicotine	23643564	We recorded ERPs from 180 <b>smokers</b> prior to their participation in a <b>smoking</b> cessation clinical trial and assessed emotional salience by measuring the amplitude of the late positive potential (<strong>LPP</strong>; 400 to 600 ms after picture onset).
+LPP	drug	nicotine	23643564	However, unlike emotional pictures, no difference was noted for the <strong>LPP</strong> between cigarette stimuli containing people versus those containing only objects, suggesting that in contrast to emotional objects, cigarette related objects are highly relevant for <b>smokers</b>.
+LPP	drug	nicotine	22087333	Early and late <strong>LPP</strong> components in response to passively viewed neutral and <b>smoking</b> pictures were compared with LPPs in response to <b>smoking</b> pictures that were reappraised with three different reappraisal strategies.
+LPP	drug	nicotine	22087333	Results show that when <b>smokers</b> actively imagine how pleasant it would be to smoke (pleasant condition), their early <strong>LPP</strong> in response to <b>smoking</b> cues increases, but when <b>smokers</b> actively focus on an alternative stimulus (distraction condition) or think of a rational, uninvolved interpretation of the situation (rational condition), <b>smoking</b> related late <strong>LPP</strong> amplitude decreases to the processing level of neutral stimuli.
+LPP	drug	nicotine	22087333	Present results are the first to indicate that <b>smoking</b> cue elicited <strong>LPP</strong> amplitudes can be modulated by cognitive strategies, suggesting that attentive processing of <b>smoking</b> cues can be intentionally regulated by <b>smokers</b> with various levels of dependence.
+LPP	addiction	dependence	22087333	Present results are the first to indicate that smoking cue elicited <strong>LPP</strong> amplitudes can be modulated by cognitive strategies, suggesting that attentive processing of smoking cues can be intentionally regulated by smokers with various levels of <b>dependence</b>.
+LPP	drug	nicotine	21967530	Cluster analysis was used to assign <b>smokers</b> to two groups based on the amplitude of the late positive potential (<strong>LPP</strong>) to the experimental stimuli.
+LPP	drug	cocaine	21450043	In particular, the late positive potential (<strong>LPP</strong>) appears to be enhanced following <b>cocaine</b> related compared with neutral stimuli in human participants with <b>cocaine</b> use disorders (CUD).
+LPP	drug	cocaine	21450043	<b>Cocaine</b> pictures elicited increased electrocortical measures of motivated attention in ways similar to affectively pleasant and unpleasant pictures in all CUD, an effect that was no longer discernible during the late <strong>LPP</strong> window for the current users.
+LPP	drug	cocaine	18331370	In abstinent <b>cocaine</b> dependent patients and a healthy control group, we studied the late positive potential (<strong>LPP</strong>) amplitudes elicited by neutral and <b>cocaine</b> related stimuli.
+LPP	drug	cocaine	18331370	The results show that <b>cocaine</b> dependent patients have an enhanced electrophysiological response in the late <strong>LPP</strong> time window to <b>cocaine</b> related stimuli as compared to controls, suggesting an enhanced processing of these stimuli.
+LPP	drug	cocaine	18331370	Most importantly, a robust association was observed between <b>cocaine</b> craving and <strong>LPP</strong> amplitude.
+LPP	addiction	relapse	18331370	Most importantly, a robust association was observed between cocaine <b>craving</b> and <strong>LPP</strong> amplitude.
+LPP	addiction	relapse	18331370	High <b>craving</b> levels were associated with larger <strong>LPP</strong> amplitudes at central electrode sites in the right hemisphere.
+LPP	drug	alcohol	14561117	For those in the <b>alcohol</b> groups, negative targets behaving positively elicited the largest <strong>LPP</strong> and recall responses.
+LPP	drug	opioid	11701207	Experiments were performed to investigate the effects of acute and chronic intracerebroventricular (icv) <b>morphine</b> infusions via osmotic minipumps on long term potentiation (LTP) in the lateral perforant path (<strong>LPP</strong>) granule cell synapse of the rat dentate gyrus.
+LPP	drug	opioid	11701207	LTP induction was significantly attenuated after acute <b>morphine</b> infusion (1 h) in <strong>LPP</strong> granule cell synapses of the dentate gyrus.
+LPP	drug	opioid	11701207	These results suggest a difference between the effects of acute and chronic intracerebroventricular <b>morphine</b> infusions on synaptic plasticity in the <strong>LPP</strong> granule cell synapses of the dentate gyrus.
+IL1RN	drug	cannabinoid	32714224	ii) Nominally significant differences were observed in the levels of <strong>IL 1RA</strong> (p = 0.0059), YKL40 (p = 0.0069), CatS (p = 0.013), sTNFR1 (p = 0.031), and BDNF (p = 0.020), where these factors exhibited higher plasma levels in <b>Cannabis</b> user SCZ patients than in non users.
+IL1RN	drug	alcohol	31854009	C57BL/6J male and female mice were provided a 2 bottle choice of <b>alcohol</b> at increasing concentrations (3, 6, 9, and 12%, 4 days each) or water, and some were treated with daily injections of an NLRP3 inhibitor (MCC950), a caspase 1 inhibitor (VX765), IL 1 receptor antagonist (<strong>IL 1ra</strong>; anakinra), or vehicle injection.
+IL1RN	drug	alcohol	31854009	Treatment with VX765, MCC950, and <strong>IL 1ra</strong> significantly reduced <b>alcohol</b> consumption and preference in female mice (p < 0.05).
+IL1RN	drug	alcohol	31854009	Treatment with MCC950 and <strong>IL 1ra</strong> reduced <b>alcohol</b> consumption, while <strong>IL 1ra</strong> reduced <b>alcohol</b> preference in male mice (p < 0.05).
+IL1RN	drug	alcohol	31736187	<b>Alcohol</b> craving and serum measures of tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1 (TNFR1), interleukin 6 (IL 6), and interleukin 1 receptor antagonist (<strong>IL 1ra</strong>) were collected prior to and following imagery exposure.
+IL1RN	addiction	relapse	31736187	Alcohol <b>craving</b> and serum measures of tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1 (TNFR1), interleukin 6 (IL 6), and interleukin 1 receptor antagonist (<strong>IL 1ra</strong>) were collected prior to and following imagery exposure.
+IL1RN	drug	alcohol	31736187	<b>Alcohol</b> craving and serum measures of tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1 (TNFR1), interleukin 6 (IL 6), and <strong>interleukin 1 receptor antagonist</strong> (<strong>IL 1ra</strong>) were collected prior to and following imagery exposure.
+IL1RN	addiction	relapse	31736187	Alcohol <b>craving</b> and serum measures of tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1 (TNFR1), interleukin 6 (IL 6), and <strong>interleukin 1 receptor antagonist</strong> (<strong>IL 1ra</strong>) were collected prior to and following imagery exposure.
+IL1RN	drug	alcohol	31736187	Dampened <strong>IL 1ra</strong> and IL 6 in response to stress was observed as a function of <b>alcohol</b> dependence and not moderated by depressive symptoms.
+IL1RN	addiction	dependence	31736187	Dampened <strong>IL 1ra</strong> and IL 6 in response to stress was observed as a function of alcohol <b>dependence</b> and not moderated by depressive symptoms.
+IL1RN	drug	alcohol	30791967	Overall, we found that IL 1β expression is significantly increased in microglia and neurons of Dep compared to Non Dep and naïve mice, IL 1β and <strong>IL 1ra</strong> bi directionally modulate GABA transmission through both pre  and postsynaptic mechanisms in all three groups, and IL 1β and <strong>IL 1ra</strong> do not alter the facilitation of GABA release induced by acute <b>ethanol</b>.
+IL1RN	drug	alcohol	28427424	Acute <b>ethanol</b> withdrawal dose dependently increased neuroimmune gene (e.g., TNFα, Ccl2, <strong>IL 1ra</strong>, IL 4) expression beginning at high doses.
+IL1RN	addiction	withdrawal	28427424	Acute ethanol <b>withdrawal</b> dose dependently increased neuroimmune gene (e.g., TNFα, Ccl2, <strong>IL 1ra</strong>, IL 4) expression beginning at high doses.
+IL1RN	drug	alcohol	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, Ccl2) gene expression and enhanced anti inflammatory (e.g., <strong>IL 1ra</strong>, IL 4) gene expression during acute binge <b>ethanol</b> withdrawal.
+IL1RN	addiction	intoxication	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, Ccl2) gene expression and enhanced anti inflammatory (e.g., <strong>IL 1ra</strong>, IL 4) gene expression during acute <b>binge</b> ethanol withdrawal.
+IL1RN	addiction	withdrawal	28427424	Microglial depletion blunted pro inflammatory (e.g., TNFα, Ccl2) gene expression and enhanced anti inflammatory (e.g., <strong>IL 1ra</strong>, IL 4) gene expression during acute binge ethanol <b>withdrawal</b>.
+IL1RN	drug	alcohol	28147432	Measures of tumor necrosis factor alpha (TNFα), interleukin 6 (IL 6), interleukin 1 receptor antagonist (<strong>IL 1ra</strong>), <b>alcohol</b> craving, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+IL1RN	addiction	relapse	28147432	Measures of tumor necrosis factor alpha (TNFα), interleukin 6 (IL 6), interleukin 1 receptor antagonist (<strong>IL 1ra</strong>), alcohol <b>craving</b>, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+IL1RN	drug	alcohol	28147432	Measures of tumor necrosis factor alpha (TNFα), interleukin 6 (IL 6), <strong>interleukin 1 receptor antagonist</strong> (<strong>IL 1ra</strong>), <b>alcohol</b> craving, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+IL1RN	addiction	relapse	28147432	Measures of tumor necrosis factor alpha (TNFα), interleukin 6 (IL 6), <strong>interleukin 1 receptor antagonist</strong> (<strong>IL 1ra</strong>), alcohol <b>craving</b>, and anxiety were assessed at baseline, immediately following imagery exposure and at discreet beer cue presentation in the ATT.
+IL1RN	drug	alcohol	28090151	Within 2 hours of <b>alcohol</b> intake, levels of <strong>IL 1Ra</strong> were elevated and remained so throughout the assessment period (p for trend = 0.015).
+IL1RN	drug	alcohol	26365025	Bilateral infusions of IL 1 receptor antagonist (<strong>IL 1Ra</strong>) reduced <b>ethanol</b> consumption when infused into the BLA but not the CeA.
+IL1RN	drug	alcohol	26365025	These observations were specific to <b>ethanol</b> drinking as the <strong>IL 1Ra</strong> did not alter either sucrose drinking or open field locomotor activity.
+IL1RN	drug	alcohol	25839897	Gene expression studies identified the interleukin 1 receptor type I (IL 1R1) as part of a pathway associated with a genetic predisposition to high <b>alcohol</b> consumption, and lack of the endogenous IL 1 receptor antagonist (<strong>IL 1ra</strong>) strongly reduced <b>ethanol</b> intake in mice.
+IL1RN	drug	alcohol	25839897	Here, we compared <b>ethanol</b> mediated behaviors in mice lacking <strong>Il1rn</strong> or Il1r1.
+IL1RN	drug	alcohol	25839897	Deletion of <strong>Il1rn</strong> (the gene encoding IL 1ra) increases sensitivity to the sedative/hypnotic effects of <b>ethanol</b> and flurazepam and reduces severity of acute <b>ethanol</b> withdrawal.
+IL1RN	drug	benzodiazepine	25839897	Deletion of <strong>Il1rn</strong> (the gene encoding IL 1ra) increases sensitivity to the sedative/hypnotic effects of ethanol and <b>flurazepam</b> and reduces severity of acute ethanol withdrawal.
+IL1RN	addiction	withdrawal	25839897	Deletion of <strong>Il1rn</strong> (the gene encoding IL 1ra) increases sensitivity to the sedative/hypnotic effects of ethanol and flurazepam and reduces severity of acute ethanol <b>withdrawal</b>.
+IL1RN	drug	alcohol	25839897	Deletion of <strong>Il1rn</strong> (the gene encoding <strong>IL 1ra</strong>) increases sensitivity to the sedative/hypnotic effects of <b>ethanol</b> and flurazepam and reduces severity of acute <b>ethanol</b> withdrawal.
+IL1RN	drug	benzodiazepine	25839897	Deletion of <strong>Il1rn</strong> (the gene encoding <strong>IL 1ra</strong>) increases sensitivity to the sedative/hypnotic effects of ethanol and <b>flurazepam</b> and reduces severity of acute ethanol withdrawal.
+IL1RN	addiction	withdrawal	25839897	Deletion of <strong>Il1rn</strong> (the gene encoding <strong>IL 1ra</strong>) increases sensitivity to the sedative/hypnotic effects of ethanol and flurazepam and reduces severity of acute ethanol <b>withdrawal</b>.
+IL1RN	drug	alcohol	25839897	Mice lacking <strong>Il1rn</strong> (but not Il1r1) showed increased <b>ethanol</b> clearance and decreased <b>ethanol</b> induced conditioned taste aversion.
+IL1RN	addiction	aversion	25839897	Mice lacking <strong>Il1rn</strong> (but not Il1r1) showed increased ethanol clearance and decreased ethanol induced conditioned taste <b>aversion</b>.
+IL1RN	drug	alcohol	25839897	The increased <b>ethanol</b>  and flurazepam induced sedation in <strong>Il1rn</strong> KO mice was decreased by administration of IL 1ra (Kineret), and pre treatment with Kineret also restored the severity of acute <b>ethanol</b> withdrawal.
+IL1RN	drug	benzodiazepine	25839897	The increased ethanol  and <b>flurazepam</b> induced sedation in <strong>Il1rn</strong> KO mice was decreased by administration of IL 1ra (Kineret), and pre treatment with Kineret also restored the severity of acute ethanol withdrawal.
+IL1RN	addiction	withdrawal	25839897	The increased ethanol  and flurazepam induced sedation in <strong>Il1rn</strong> KO mice was decreased by administration of IL 1ra (Kineret), and pre treatment with Kineret also restored the severity of acute ethanol <b>withdrawal</b>.
+IL1RN	drug	alcohol	25839897	The increased <b>ethanol</b>  and flurazepam induced sedation in <strong>Il1rn</strong> KO mice was decreased by administration of <strong>IL 1ra</strong> (Kineret), and pre treatment with Kineret also restored the severity of acute <b>ethanol</b> withdrawal.
+IL1RN	drug	benzodiazepine	25839897	The increased ethanol  and <b>flurazepam</b> induced sedation in <strong>Il1rn</strong> KO mice was decreased by administration of <strong>IL 1ra</strong> (Kineret), and pre treatment with Kineret also restored the severity of acute ethanol withdrawal.
+IL1RN	addiction	withdrawal	25839897	The increased ethanol  and flurazepam induced sedation in <strong>Il1rn</strong> KO mice was decreased by administration of <strong>IL 1ra</strong> (Kineret), and pre treatment with Kineret also restored the severity of acute ethanol <b>withdrawal</b>.
+IL1RN	drug	alcohol	25582105	Kupffer cells and IL 1β were required for the hepatic iNKT accumulation, as either blocking IL 1β signaling with a recombinant IL 1 receptor antagonist (<strong>IL 1Ra</strong>), depleting Kupffer cells by clodronate liposomes, or specifically silencing IL 1β in Kupffer cells by nanoparticle encapsulated siRNA, resulted in inhibited hepatic iNKT cell accumulation and activation, as well as amelioration of <b>alcoholic</b> fatty liver.
+IL1RN	drug	alcohol	25175870	Pharmacotherapies covered in this review include ibudilast, minocycline, doxycycline, topiramate, indomethacin, rolipram, anakinra (<strong>IL 1Ra</strong>), peroxisome proliferator activated receptor agonists, <b>naltrexone</b>, and naloxone.
+IL1RN	drug	opioid	25175870	Pharmacotherapies covered in this review include ibudilast, minocycline, doxycycline, topiramate, indomethacin, rolipram, anakinra (<strong>IL 1Ra</strong>), peroxisome proliferator activated receptor agonists, naltrexone, and <b>naloxone</b>.
+IL1RN	drug	alcohol	22921768	In follow up studies, neither indomethacin (Experiment 5) nor <strong>interleukin 1 receptor antagonist</strong> (Experiment 6) pre exposure reversed the <b>ethanol</b> withdrawal induced behavioral changes observed in this social investigation test.
+IL1RN	addiction	withdrawal	22921768	In follow up studies, neither indomethacin (Experiment 5) nor <strong>interleukin 1 receptor antagonist</strong> (Experiment 6) pre exposure reversed the ethanol <b>withdrawal</b> induced behavioral changes observed in this social investigation test.
+IL1RN	drug	nicotine	22327782	This study evaluated polymorphisms <strong>IL 1RN</strong> VNTR and TNFB+252A/G in a population from Southeast Brazil with regard to the risk of chronic gastritis and gastric cancer and the presence of an association of gastric lesions with risk factors such as gender, age, <b>smoking</b>, drinking and Helicobacter pylori infection.
+IL1RN	addiction	reward	22327782	So, our results indicated that the <strong>IL 1RN</strong>*2 allele may increase the risk of gastric cancer and precancerous lesions in the Southeast Brazilian population, <b>reinforcing</b> the importance of host genetic factors in the susceptibility to gastric cancer and the participation of cytokines in both the inflammation and the carcinogenic process.
+IL1RN	drug	cocaine	22220556	All participants were asked to complete two implicit assessment procedures, a Drug Stroop protocol and an Implicit Relational Assessment Procedure (<strong>IRAP</strong>), as well as explicit measures of <b>cocaine</b> craving and the consequences of <b>cocaine</b> use, prior to beginning treatment.
+IL1RN	addiction	relapse	22220556	All participants were asked to complete two implicit assessment procedures, a Drug Stroop protocol and an Implicit Relational Assessment Procedure (<strong>IRAP</strong>), as well as explicit measures of cocaine <b>craving</b> and the consequences of cocaine use, prior to beginning treatment.
+IL1RN	drug	alcohol	19764937	<b>Alcohol</b> dependent patients showed an excess of IL 1alpha 889 C/T [50.8% vs. 39.3%, chi(2) (df) = 7.30 (2), uncorrected p = 0.026, corrected p = 0.104] and <strong>IL 1RA</strong> (86 bp)(n) A1/A1 genotypes [64.8% vs. 50.8%, chi(2) (df) = 12.65 (3), corrected p = 0.020].
+IL1RN	drug	alcohol	16548517	Temperature dependence of benzyl <b>alcohol</b>  and 8 anilinonaphthalene 1 sulfonate induced aggregation of recombinant human <strong>interleukin 1 receptor antagonist</strong>.
+IL1RN	addiction	dependence	16548517	Temperature <b>dependence</b> of benzyl alcohol  and 8 anilinonaphthalene 1 sulfonate induced aggregation of recombinant human <strong>interleukin 1 receptor antagonist</strong>.
+IL1RN	drug	alcohol	16548517	Recombinant human <strong>interleukin 1 receptor antagonist</strong> (rhIL 1ra) and the ligands benzyl <b>alcohol</b> and 8 anilinonaphthalene 1 sulfonate (ANS) were used.
+IL1RN	drug	alcohol	15289211	In 36 <b>alcoholics</b> without liver disease, at the point of commencing withdrawal from <b>alcohol</b>, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, <strong>IL1RA</strong>, IL4, IL6, IL8, IL10 and IL12).
+IL1RN	addiction	withdrawal	15289211	In 36 alcoholics without liver disease, at the point of commencing <b>withdrawal</b> from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, <strong>IL1RA</strong>, IL4, IL6, IL8, IL10 and IL12).
+IL1RN	drug	alcohol	15289211	In 36 <b>alcoholics</b> without liver disease, at the point of commencing withdrawal from <b>alcohol</b>, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, <strong><strong>IL1RA</strong></strong>, IL4, IL6, IL8, IL10 and IL12).
+IL1RN	addiction	withdrawal	15289211	In 36 alcoholics without liver disease, at the point of commencing <b>withdrawal</b> from alcohol, the following measures of immune competence were measured: the immunophenotypes of cells, acute phase proteins, the endotoxin neutralizing capacity (ENC) of the serum, titers of anti lipopolysaccharide (LPS) antibodies, and ex vivo cytokine inducibility in T cells and monocytes (TNFalpha, IL1beta, <strong><strong>IL1RA</strong></strong>, IL4, IL6, IL8, IL10 and IL12).
+IL1RN	addiction	withdrawal	14597094	Spleen cells from mice undergoing <b>withdrawal</b> also had decreased splenic mRNA and/or protein levels of IL 1beta, <strong>IL 1Ra</strong>, TNF alpha, IL 12, and IFN gamma.
+IL1RN	drug	nicotine	10792346	Soluble <strong>interleukin 1 receptor antagonist</strong> concentration in patients with Graves' ophthalmopathy is neither related to cigarette <b>smoking</b> nor predictive of subsequent response to glucocorticoids.
+IL1RN	drug	nicotine	10792346	The aim of the present study was to evaluate serum soluble <strong>interleukin 1 receptor antagonist</strong> (sIL 1RA) concentration and its relationship with the degree of cigarette <b>smoking</b> in patients with Graves' ophthalmopathy (GO).
+IL1RN	drug	nicotine	10792346	Our study suggests that circulating soluble <strong>interleukin 1 receptor antagonist</strong> levels, both at baseline and during glucocorticoid treatment, are neither influenced by cigarette <b>smoking</b> nor predictive of subsequent response to glucocorticoid treatment.
+IL1RN	drug	alcohol	9895030	This study examines i) the activity of serum prolyl endopeptidase (PEP) and dipeptidlyl peptidase IV (DPP IV) in detoxified <b>alcohol</b> dependent patients without liver disease versus normal controls, and ii) the relationships between serum DPP IV and PEP activity and the production of cytokines or cytokine receptors, such as interleukin 6 (IL 6), tumor necrosis factor alpha (TNF alpha), interferon y (IFN y), IL 1 receptor antagonist (<strong>IL 1RA</strong>), and IL 10, and granulocyte macrophage colony stimulatory factor (GM CSF).
+HMGB1	drug	opioid	32733481	(d) <b>Opioid</b> receptor agonists induce the production of high mobility group box 1 (<strong>HMGB1</strong>), an endogenous TLR4 agonist, supporting intercellular (neuron to glia or glia to neuron) interactions.
+HMGB1	drug	opioid	32733481	(d) <b>Opioid</b> receptor agonists induce the production of <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>), an endogenous TLR4 agonist, supporting intercellular (neuron to glia or glia to neuron) interactions.
+HMGB1	drug	alcohol	32588826	<b>Ethanol</b> consumption leads to activation of neuroimmune signaling in the central nervous system through many types of Toll like receptors (TLRs), as well as the release of their endogenous agonists (<strong>HMGB1</strong> protein, S100 protein, heat shock proteins, extracellular matrix breakdown proteins).
+HMGB1	drug	opioid	31879851	Chronic <b>morphine</b> mediated upregulation of <strong>high mobility group box 1</strong> in the spinal cord contributes to analgesic tolerance and hyperalgesia in rats.
+HMGB1	drug	opioid	31879851	We examined whether spinal high mobility group box 1 (<strong>HMGB1</strong>) is involved in <b>morphine</b> tolerance and its underlying mechanisms by using a model of repeated intrathecal (i.t.)
+HMGB1	drug	opioid	31879851	We examined whether spinal <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) is involved in <b>morphine</b> tolerance and its underlying mechanisms by using a model of repeated intrathecal (i.t.)
+HMGB1	drug	opioid	31879851	<b>morphine</b> exposure led to increased expression of <strong>HMGB1</strong>, Toll like receptor 4 (TLR4), and receptor for advanced glycation end products (RAGE) and their mRNAs in the dorsal horn.
+HMGB1	drug	opioid	31879851	<b>Morphine</b> challenge also promoted <strong>HMGB1</strong> expression and release in cultured spinal neurons, but these effects were inhibited by TAK 242, <b>naloxone</b> (antagonists of TLR4), and TLR4 siRNA.
+HMGB1	drug	opioid	31879851	Intrathecal coadministration of <b>morphine</b> with TAK 242 or PDTC (inhibitor of NF κB activation) also reduced <strong>HMGB1</strong> expression in the spinal cord.
+HMGB1	drug	opioid	31879851	coinjections of <b>morphine</b> with glycyrrhizin (GL, an <strong>HMGB1</strong> inhibitor) or <strong>HMGB1</strong> siRNA prevented reduction of the maximal possible analgesic effect (MPAE) of <b>morphine</b> and alleviated <b>morphine</b> withdrawal induced hyperalgesia.
+HMGB1	addiction	withdrawal	31879851	coinjections of morphine with glycyrrhizin (GL, an <strong>HMGB1</strong> inhibitor) or <strong>HMGB1</strong> siRNA prevented reduction of the maximal possible analgesic effect (MPAE) of morphine and alleviated morphine <b>withdrawal</b> induced hyperalgesia.
+HMGB1	drug	opioid	31879851	injections of GL or <strong>HMGB1</strong> antibody started at day 7 of <b>morphine</b> injection.
+HMGB1	drug	opioid	31879851	injections of <b>morphine</b> with <strong>HMGB1</strong> siRNA inhibited the activation of NF κB, but not that of JNK and p38.
+HMGB1	drug	opioid	31879851	Together, these results suggest that <b>morphine</b> mediated upregulation of spinal <strong>HMGB1</strong> contributes to analgesic tolerance and hyperalgesia via activation of TLR4/NF κB signaling, and the <strong>HMGB1</strong> inhibitor might be a promising adjuvant to <b>morphine</b> in the treatment of intractable pain in the clinic.
+HMGB1	drug	alcohol	31666409	The effects of acute (single) and chronic <b>ethanol</b> administration on the level of pro inflammatory cytokines (IL 1β and TNF α), as well as on the level of mRNA NF κB, TLR4 and its endogenous agonist, <strong>HMGB1</strong> protein, were investigated in rats.
+HMGB1	drug	alcohol	31666409	The <b>ethanol</b> withdrawal after prolonged administration resulted in dysregulation of cytokine levels, TLR4 and <strong>HMGB1</strong>.
+HMGB1	addiction	withdrawal	31666409	The ethanol <b>withdrawal</b> after prolonged administration resulted in dysregulation of cytokine levels, TLR4 and <strong>HMGB1</strong>.
+HMGB1	drug	alcohol	31510019	Co culture blunted <b>ethanol</b> induced high mobility group box protein 1 (<strong>HMGB1</strong>) TLR responses, corresponding with reduced <b>ethanol</b> induction of several proinflammatory NFκB target genes.
+HMGB1	drug	cocaine	31056833	Neuronal <strong>HMGB1</strong> in nucleus accumbens regulates <b>cocaine</b> reward memory.
+HMGB1	addiction	reward	31056833	Neuronal <strong>HMGB1</strong> in nucleus accumbens regulates cocaine <b>reward</b> memory.
+HMGB1	drug	cocaine	31056833	Previous studies of <strong>HMGB1</strong> in the CNS have largely focused on immune function, and the role of <strong>HMGB1</strong> in neurons and <b>cocaine</b> addiction remains unknown.
+HMGB1	addiction	addiction	31056833	Previous studies of <strong>HMGB1</strong> in the CNS have largely focused on immune function, and the role of <strong>HMGB1</strong> in neurons and cocaine <b>addiction</b> remains unknown.
+HMGB1	drug	cocaine	31056833	Here, we show that <b>cocaine</b> exposure induced the translocation and release of <strong>HMGB1</strong> in the nucleus accumbens (NAc) neurons.
+HMGB1	drug	cocaine	31056833	Gain and loss of <strong>HMGB1</strong> in the NAc bidirectionally regulate <b>cocaine</b> induced conditioned place preference.
+HMGB1	drug	cocaine	31056833	From the nucleus to the cytosol, <strong>HMGB1</strong> binds to glutamate receptor subunits (GluA2/GluN2B) on the membrane, which regulates <b>cocaine</b> induced synaptic adaptation and the formation of <b>cocaine</b> related memory.
+HMGB1	addiction	addiction	31056833	These data unveil the role of <strong>HMGB1</strong> in neurons and provide the evidence for the <strong>HMGB1</strong> involvement in drug <b>addiction</b>.
+HMGB1	addiction	withdrawal	30554034	Little or no changes in these molecules were seen in the frontal cortex except for <strong>HMG1</strong> and fractalkine that were reduced and elevated, respectively, at day 28 following <b>withdrawal</b>.
+HMGB1	drug	alcohol	30368255	<b>Alcohol</b> feeding significantly increased the expression of proinflammatory cytokines such as Tnfα, Mcp1, <strong>Hmgb1</strong>, Il 17, and Il 23 in the brain and intestine.
+HMGB1	drug	nicotine	30358437	Acute <b>nicotine</b> inhalation caused increased pulmonary edema and lung injury as measured by enhanced bronchoalveolar lavage fluid protein, IgM, lung wet to dry weight ratio, and high mobility group box 1 (<strong>HMGB1</strong>) protein and decreased lung E cadherin protein.
+HMGB1	drug	nicotine	30358437	Acute <b>nicotine</b> inhalation caused increased pulmonary edema and lung injury as measured by enhanced bronchoalveolar lavage fluid protein, IgM, lung wet to dry weight ratio, and <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) protein and decreased lung E cadherin protein.
+HMGB1	drug	nicotine	30358437	In in vitro air liquid interface cultures of airway epithelial cells, there was a dose dependent increase in <strong>HMGB1</strong> release with <b>nicotine</b> treatment.
+HMGB1	drug	alcohol	29339456	We now find in 4 day binged HEC slice cultures (100 mM <b>ethanol</b>) that PARP1 elevations after two overnight binges precede PAR, cPLA2, and sPLA2 enhancements by 1 day and high mobility group box 1 (<strong>HMGB1</strong>), an <b>ethanol</b> responsive alarmin that augments proinflammatory cytokines via toll like receptor 4 (TLR4), by 2 days.
+HMGB1	drug	alcohol	29339456	We now find in 4 day binged HEC slice cultures (100 mM <b>ethanol</b>) that PARP1 elevations after two overnight binges precede PAR, cPLA2, and sPLA2 enhancements by 1 day and <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>), an <b>ethanol</b> responsive alarmin that augments proinflammatory cytokines via toll like receptor 4 (TLR4), by 2 days.
+HMGB1	drug	alcohol	29339456	Also, PJ34 and olaparib blocked <b>ethanol</b> induced <strong>HMGB1</strong> elevations, linking brain PARP induction to TLR4 activation.
+HMGB1	drug	alcohol	29339456	The results provide evidence in adult brains that induction of PARP1 may mediate dual neuroinflammatory pathways (PLA2→phospholipid→ARA and <strong>HMGB1</strong>→TLR4→proinflammatory cytokines) that are complicit in binge <b>ethanol</b> induced neurodegeneration.
+HMGB1	addiction	intoxication	29339456	The results provide evidence in adult brains that induction of PARP1 may mediate dual neuroinflammatory pathways (PLA2→phospholipid→ARA and <strong>HMGB1</strong>→TLR4→proinflammatory cytokines) that are complicit in <b>binge</b> ethanol induced neurodegeneration.
+HMGB1	drug	alcohol	29178411	Increased plasma oleoylethanolamide and palmitoleoylethanolamide levels correlate with inflammatory changes in <b>alcohol</b> binge drinkers: the case of <strong>HMGB1</strong> in women.
+HMGB1	drug	cannabinoid	29178411	Increased plasma <b>oleoylethanolamide</b> and palmitoleoylethanolamide levels correlate with inflammatory changes in alcohol binge drinkers: the case of <strong>HMGB1</strong> in women.
+HMGB1	addiction	intoxication	29178411	Increased plasma oleoylethanolamide and palmitoleoylethanolamide levels correlate with inflammatory changes in alcohol <b>binge</b> drinkers: the case of <strong>HMGB1</strong> in women.
+HMGB1	drug	alcohol	29178411	Additionally, plasma oleoylethanolamide positively correlated with plasma levels of <strong>high mobility group box 1</strong>, which is a danger associated molecular pattern and an endogenous TLR4 agonist, specifically in female <b>alcohol</b> binge drinkers.
+HMGB1	drug	cannabinoid	29178411	Additionally, plasma <b>oleoylethanolamide</b> positively correlated with plasma levels of <strong>high mobility group box 1</strong>, which is a danger associated molecular pattern and an endogenous TLR4 agonist, specifically in female alcohol binge drinkers.
+HMGB1	addiction	intoxication	29178411	Additionally, plasma oleoylethanolamide positively correlated with plasma levels of <strong>high mobility group box 1</strong>, which is a danger associated molecular pattern and an endogenous TLR4 agonist, specifically in female alcohol <b>binge</b> drinkers.
+HMGB1	drug	alcohol	29102800	<strong>HMGB1</strong>/IL 1β complexes regulate neuroimmune responses in <b>alcoholism</b>.
+HMGB1	drug	alcohol	29102800	Previous studies find <strong>HMGB1</strong> andIL 1β form heterocomplexes in vitro with enhanced immune responses, lead to our hypothesis that <strong>HMGB1</strong> and IL 1β heterocomplexes formed in vivo to contribute to the pathology of <b>alcoholism</b>.
+HMGB1	drug	alcohol	29102800	These <strong>HMGB1</strong>/IL 1β complexes were found to be increased in post mortem human <b>alcoholic</b> hippocampus by co immunoprecipiation.
+HMGB1	drug	alcohol	29102800	In mice, acute binge <b>ethanol</b> induced both <strong>HMGB1</strong> and IL 1β in the brain and plasma.
+HMGB1	addiction	intoxication	29102800	In mice, acute <b>binge</b> ethanol induced both <strong>HMGB1</strong> and IL 1β in the brain and plasma.
+HMGB1	drug	alcohol	29102800	<strong>HMGB1</strong> and IL 1β complexes were found only in mouse brain, with confocal microscopy revealing an <b>ethanol</b> induced <strong>HMGB1</strong> and IL 1β cytoplasmic co localization.
+HMGB1	drug	alcohol	29102800	Studies in hippocampal brain slice culture found <b>ethanol</b> increased <strong>HMGB1</strong>/IL 1β complexes in the media.
+HMGB1	drug	alcohol	29102800	Immunogenic <strong>HMGB1</strong>/IL 1β complexes represent a novel target for immune modulatory therapy in <b>alcohol</b> use disorders, and should be investigated in other psychiatric diseases that involve a neuroimmune component.
+HMGB1	drug	opioid	28860068	Here, we demonstrate that spinal levels of the damage associated molecular patterns (DAMPs) high mobility group box 1 (<strong>HMGB1</strong>) and biglycan are elevated during <b>morphine</b> induced persistent sensitization in male rats; that is, 5weeks after cessation of <b>morphine</b> dosing.
+HMGB1	addiction	sensitization	28860068	Here, we demonstrate that spinal levels of the damage associated molecular patterns (DAMPs) high mobility group box 1 (<strong>HMGB1</strong>) and biglycan are elevated during morphine induced persistent <b>sensitization</b> in male rats; that is, 5weeks after cessation of morphine dosing.
+HMGB1	drug	opioid	28860068	Here, we demonstrate that spinal levels of the damage associated molecular patterns (DAMPs) <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) and biglycan are elevated during <b>morphine</b> induced persistent sensitization in male rats; that is, 5weeks after cessation of <b>morphine</b> dosing.
+HMGB1	addiction	sensitization	28860068	Here, we demonstrate that spinal levels of the damage associated molecular patterns (DAMPs) <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) and biglycan are elevated during morphine induced persistent <b>sensitization</b> in male rats; that is, 5weeks after cessation of morphine dosing.
+HMGB1	drug	opioid	28860068	Finally, pharmacological attenuation of the DAMPs <strong>HMGB1</strong>, biglycan, heat shock protein 90 and fibronectin persistently reversed <b>morphine</b> prolonged allodynia.
+HMGB1	drug	alcohol	28840951	The immune/inflammatory changes were more prominent in female drinkers, who showed elevated levels of <b>alcohol</b> danger associated molecules, such as <strong>high mobility group box 1</strong>, indicating that there are sex related differences in the peripheral inflammatory response to <b>alcohol</b>.
+HMGB1	addiction	intoxication	28840951	Finally, higher levels of inflammatory markers, mainly monocyte chemoattractant protein 1, as well as LPS, <strong>high mobility group box 1</strong>, toll like receptor 4, IL 6 and ciclooxygenase 2, correlated with worse scores on episodic memory and executive functioning tasks in female <b>binge</b> drinkers but not in male <b>binge</b> drinkers.
+HMGB1	addiction	addiction	28210782	This study aims to illuminate the critical interrelationship of the innate immune system (e.g., toll like receptors [TLRs], high mobility group box 1 [<strong>HMGB1</strong>]) in the neurobiology of <b>addiction</b>.
+HMGB1	addiction	addiction	28210782	This study aims to illuminate the critical interrelationship of the innate immune system (e.g., toll like receptors [TLRs], <strong>high mobility group box 1</strong> [<strong>HMGB1</strong>]) in the neurobiology of <b>addiction</b>.
+HMGB1	drug	alcohol	28210782	Multiple TLRs, <strong>HMGB1</strong>, and miRNAs are induced in the brain by stress, <b>alcohol</b>, and other drugs of abuse and are increased in the postmortem human <b>alcoholic</b> brain.
+HMGB1	drug	alcohol	28159648	Microglia, the innate immune cells of the brain, and neurons respond to <b>alcohol</b>, signaling through Toll like receptors (TLRs), high mobility group box 1 (<strong>HMGB1</strong>), miRNAs, pro inflammatory cytokines and their associated receptors involved in signaling between microglia, other glia and neurons.
+HMGB1	drug	alcohol	28159648	Microglia, the innate immune cells of the brain, and neurons respond to <b>alcohol</b>, signaling through Toll like receptors (TLRs), <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>), miRNAs, pro inflammatory cytokines and their associated receptors involved in signaling between microglia, other glia and neurons.
+HMGB1	drug	alcohol	28159648	Repeated cycles of <b>alcohol</b> and stress cause a progressive, persistent induction of <strong>HMGB1</strong>, miRNA and TLR receptors in brain that appear to underlie the progressive and persistent loss of behavioral control, increased impulsivity and anxiety, as well as craving, coupled with increasing ventral striatal responses that promote reward seeking behavior and increase risk of developing <b>alcohol</b> use disorders.
+HMGB1	addiction	relapse	28159648	Repeated cycles of alcohol and stress cause a progressive, persistent induction of <strong>HMGB1</strong>, miRNA and TLR receptors in brain that appear to underlie the progressive and persistent loss of behavioral control, increased impulsivity and anxiety, as well as <b>craving</b>, coupled with increasing ventral striatal responses that promote reward <b>seeking</b> behavior and increase risk of developing alcohol use disorders.
+HMGB1	addiction	reward	28159648	Repeated cycles of alcohol and stress cause a progressive, persistent induction of <strong>HMGB1</strong>, miRNA and TLR receptors in brain that appear to underlie the progressive and persistent loss of behavioral control, increased impulsivity and anxiety, as well as craving, coupled with increasing ventral striatal responses that promote <b>reward</b> seeking behavior and increase risk of developing alcohol use disorders.
+HMGB1	drug	alcohol	27527870	<b>Ethanol</b> caused both apoptotic and necrotic cell death which was demonstrated by the increase in active caspase 3, caspase 8, cleaved PARP, cleaved CK 18 and the secretion of high mobility group protein B1 (<strong>HMGB1</strong>).
+HMGB1	drug	alcohol	26857094	Oleoylethanolamide prevents neuroimmune <strong>HMGB1</strong>/TLR4/NF kB danger signaling in rat frontal cortex and depressive like behavior induced by <b>ethanol</b> binge administration.
+HMGB1	drug	cannabinoid	26857094	<b>Oleoylethanolamide</b> prevents neuroimmune <strong>HMGB1</strong>/TLR4/NF kB danger signaling in rat frontal cortex and depressive like behavior induced by ethanol binge administration.
+HMGB1	addiction	intoxication	26857094	Oleoylethanolamide prevents neuroimmune <strong>HMGB1</strong>/TLR4/NF kB danger signaling in rat frontal cortex and depressive like behavior induced by ethanol <b>binge</b> administration.
+HMGB1	drug	alcohol	26857094	previous each <b>alcohol</b> gavage blocked the expression of high mobility group box 1 (<strong>HMGB1</strong>) danger signal and the innate immunity Toll like receptors 4 (TLR4) in frontal cortex, and inhibited the nuclear factor kappa B (NF kB) proinflammatory cascade induced by <b>alcohol</b> binge administration.
+HMGB1	addiction	intoxication	26857094	previous each alcohol gavage blocked the expression of high mobility group box 1 (<strong>HMGB1</strong>) danger signal and the innate immunity Toll like receptors 4 (TLR4) in frontal cortex, and inhibited the nuclear factor kappa B (NF kB) proinflammatory cascade induced by alcohol <b>binge</b> administration.
+HMGB1	drug	alcohol	26857094	previous each <b>alcohol</b> gavage blocked the expression of <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) danger signal and the innate immunity Toll like receptors 4 (TLR4) in frontal cortex, and inhibited the nuclear factor kappa B (NF kB) proinflammatory cascade induced by <b>alcohol</b> binge administration.
+HMGB1	addiction	intoxication	26857094	previous each alcohol gavage blocked the expression of <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) danger signal and the innate immunity Toll like receptors 4 (TLR4) in frontal cortex, and inhibited the nuclear factor kappa B (NF kB) proinflammatory cascade induced by alcohol <b>binge</b> administration.
+HMGB1	drug	alcohol	26695754	<b>Ethanol</b> exposure activates signaling pathways featuring <strong>high mobility group box 1</strong> and Toll like receptor 4 (TLR4), resulting in induction of the transcription factor nuclear factor kappa light chain enhancer of activated B cells, which regulates expression of several cytokine genes involved in innate immunity, and its target genes.
+HMGB1	drug	alcohol	25816800	<strong>HMGB1</strong> has been implicated in the pathophysiology of several neuroinflammatory conditions including ischemia, traumatic brain injury, seizure and chronic <b>ethanol</b> use.
+HMGB1	addiction	sensitization	25816800	In light of recent evidence suggesting that <strong>HMGB1</strong> may also mediate stress induced <b>sensitization</b> of neuroinflammatory responses, mechanisms of <strong>HMGB1</strong> action in neuroinflammatory priming are explored.
+HMGB1	drug	alcohol	25787746	Studies from our laboratory employing reverse transcription polymerase chain reaction (RT PCR) to assess mRNA, immunohistochemistry and Western blot analysis to assess protein expression, and others suggest that <b>ethanol</b> increases brain neuroimmune gene and protein expression through two distinct mechanisms involving (1) systemic induction of innate immune molecules that are transported from blood to the brain and (2) the direct release of high mobility group box 1 (<strong>HMGB1</strong>) from neurons in the brain.
+HMGB1	drug	alcohol	25787746	Studies from our laboratory employing reverse transcription polymerase chain reaction (RT PCR) to assess mRNA, immunohistochemistry and Western blot analysis to assess protein expression, and others suggest that <b>ethanol</b> increases brain neuroimmune gene and protein expression through two distinct mechanisms involving (1) systemic induction of innate immune molecules that are transported from blood to the brain and (2) the direct release of <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) from neurons in the brain.
+HMGB1	drug	alcohol	25787746	Expression of <strong>HMGB1</strong>, TLRs, and other ISMs is increased several fold in the human orbital frontal cortex, and expression of these molecules is highly correlated with each other as well as lifetime <b>alcohol</b> consumption and age of drinking onset.
+HMGB1	drug	alcohol	25787746	The persistent and cumulative nature of <b>alcohol</b> on <strong>HMGB1</strong> and TLR gene induction support their involvement in <b>alcohol</b> induced long term changes in brain function and neurodegeneration.
+HMGB1	drug	alcohol	25486089	Using wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with <b>ethanol</b> (3.0g/kg) for 2weeks, we show that binge like <b>ethanol</b> treatment activates TLR4 signaling pathways (MAPK, NFκB) leading to the up regulation of cytokines and pro inflammatory mediators (COX 2, iNOS, <strong>HMGB1</strong>), impairing synaptic and myelin protein levels and causing ultrastructural alterations.
+HMGB1	addiction	intoxication	25486089	Using wild type (WT) and TLR4 deficient (TLR4 KO) adolescent mice treated intermittently with ethanol (3.0g/kg) for 2weeks, we show that <b>binge</b> like ethanol treatment activates TLR4 signaling pathways (MAPK, NFκB) leading to the up regulation of cytokines and pro inflammatory mediators (COX 2, iNOS, <strong>HMGB1</strong>), impairing synaptic and myelin protein levels and causing ultrastructural alterations.
+HMGB1	drug	alcohol	25175868	In addition, <strong>HMGB1</strong> TLR4 and innate immune NF κB target genes are increased leading to persistent and sensitized neuroimmune responses to <b>ethanol</b> and other agents that release <strong>HMGB1</strong> or directly stimulate TLR receptors and/or NMDA receptors.
+HMGB1	drug	alcohol	24551070	Release of neuronal <strong>HMGB1</strong> by <b>ethanol</b> through decreased HDAC activity activates brain neuroimmune signaling.
+HMGB1	drug	alcohol	24551070	We previously found increased <strong>HMGB1</strong> in post mortem <b>alcoholic</b> human brain as well as in <b>ethanol</b> treated mice and rat brain slice cultures.
+HMGB1	drug	alcohol	24551070	The present study investigated the mechanisms for <b>ethanol</b> induced release of <strong>HMGB1</strong> and neuroimmune activation in a model of rat hippocampal entorhinal cortex (HEC) brain slice cultures.
+HMGB1	drug	alcohol	24551070	<b>Ethanol</b> exposure triggered dose dependent <strong>HMGB1</strong> release, predominantly from neuronal cells.
+HMGB1	drug	alcohol	24551070	Similarly, <b>ethanol</b> treatment was found to induce the translocation of HDAC1/4 and <strong>HMGB1</strong> proteins from nuclear to cytosolic fractions.
+HMGB1	drug	alcohol	24551070	Furthermore, <b>ethanol</b> treatment reduced HDAC1/4 mRNA and increased acetylated <strong>HMGB1</strong> release into the media.
+HMGB1	drug	alcohol	24551070	These results suggest decreased HDAC activity may be critical in regulating acetylated <strong>HMGB1</strong> release from neurons in response to <b>ethanol</b>.
+HMGB1	drug	alcohol	24551070	<b>Ethanol</b> and <strong>HMGB1</strong> treatment increased mRNA expression of proinflammatory cytokines TNFα and IL 1β as well as toll like receptor 4 (TLR4).
+HMGB1	drug	alcohol	24551070	Targeting <strong>HMGB1</strong> or microglial TLR4 by using siRNAs to <strong>HMGB1</strong> and TLR4, <strong>HMGB1</strong> neutralizing antibody, <strong>HMGB1</strong> inhibitor glycyrrhizin and TLR4 antagonist as well as inhibitor of microglial activation all blocked <b>ethanol</b> induced expression of proinflammatory cytokines TNFα and IL 1β.
+HMGB1	drug	alcohol	24551070	These results support the hypothesis that <b>ethanol</b> alters HDACs that regulate <strong>HMGB1</strong> release and that danger signal <strong>HMGB1</strong> as endogenous ligand for TLR4 mediates <b>ethanol</b> induced brain neuroimmune signaling through activation of microglial TLR4.
+HMGB1	drug	alcohol	23895427	The cytokine mRNA increase induced by withdrawal from chronic <b>ethanol</b> in the sterile environment of brain is mediated by CRF and <strong>HMGB1</strong> release.
+HMGB1	addiction	withdrawal	23895427	The cytokine mRNA increase induced by <b>withdrawal</b> from chronic ethanol in the sterile environment of brain is mediated by CRF and <strong>HMGB1</strong> release.
+HMGB1	addiction	withdrawal	23895427	Therefore, the hypothesis is tested that release of an endogenous TLR4 agonist, high mobility group box 1 (<strong>HMGB1</strong>) and/or corticotropin releasing factor (CRF) during CE <b>withdrawal</b> are responsible for CE protocols increasing cytokine mRNAs.
+HMGB1	addiction	withdrawal	23895427	Therefore, the hypothesis is tested that release of an endogenous TLR4 agonist, <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) and/or corticotropin releasing factor (CRF) during CE <b>withdrawal</b> are responsible for CE protocols increasing cytokine mRNAs.
+HMGB1	addiction	withdrawal	23895427	To test whether <strong>HMGB1</strong> and/or CRF support the CE <b>withdrawal</b> increase in cytokine mRNAs, the <strong>HMGB1</strong> antagonists, glycyrrhizin and ethyl pyruvate, and a CRF1 receptor antagonist (CRF1RA) are administered during 24 hours of CE <b>withdrawal</b>.
+HMGB1	addiction	withdrawal	23895427	While chronic LPS had no effect on <strong>HMGB1</strong> mRNA, <b>withdrawal</b> from CE protocols significantly elevated <strong>HMGB1</strong> mRNA.
+HMGB1	addiction	withdrawal	23895427	Systemic administration of <strong>HMGB1</strong> antagonists or a CRF1RA significantly reduced the cytokine mRNA increase following CE <b>withdrawal</b>.
+HMGB1	addiction	withdrawal	23895427	The CRF1RA and the <strong>HMGB1</strong> antagonist, ethyl pyruvate, also reduced the <strong>HMGB1</strong> mRNA increase that followed CE <b>withdrawal</b>.
+HMGB1	addiction	withdrawal	23895427	By blocking <strong>HMGB1</strong> or CRF action during CE <b>withdrawal</b>, evidence is provided that <strong>HMGB1</strong> and CRF release are critical for the CE <b>withdrawal</b> induction of selected brain cytokine mRNAs.
+HMGB1	addiction	intoxication	23867237	This manuscript tested the hypothesis that adolescent <b>binge</b> drinking upregulates RAGE and Toll like receptor (TLR) 4 as well as their endogenous agonist, high mobility group box 1 (<strong>HMGB1</strong>).
+HMGB1	addiction	intoxication	23867237	This manuscript tested the hypothesis that adolescent <b>binge</b> drinking upregulates RAGE and Toll like receptor (TLR) 4 as well as their endogenous agonist, <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>).
+HMGB1	drug	alcohol	23867237	Adolescent intermittent <b>ethanol</b> exposure also increased TLR4 and <strong>HMGB1</strong> expression at P56 that persisted into young adulthood (P80).
+HMGB1	drug	alcohol	23867237	Together, these human and animal data support the hypothesis that an early age of drinking onset upregulates RAGE/TLR4 <strong>HMGB1</strong> and other neuroimmune genes that persist into young adulthood and could contribute to risk of <b>alcoholism</b> or other brain diseases associated with neuroinflammation.
+HMGB1	drug	alcohol	23206318	<strong>High mobility group box 1</strong>/Toll like receptor danger signaling increases brain neuroimmune activation in <b>alcohol</b> dependence.
+HMGB1	addiction	dependence	23206318	<strong>High mobility group box 1</strong>/Toll like receptor danger signaling increases brain neuroimmune activation in alcohol <b>dependence</b>.
+HMGB1	drug	alcohol	23206318	We investigated expression of <strong>HMGB1</strong>, TLR2, TLR3, and TLR4 in chronic <b>ethanol</b> treated mouse brain, postmortem human <b>alcoholic</b> brain, and rat brain slice culture to test the hypothesis that neuroimmune activation in <b>alcoholic</b> brain involves <b>ethanol</b> activation of <strong>HMGB1</strong>/TLR danger signaling.
+HMGB1	drug	alcohol	23206318	<b>Ethanol</b> treatment of mice increased brain mRNA and +IR protein expression of <strong>HMGB1</strong>, TLR2, TLR3, and TLR4.
+HMGB1	drug	alcohol	23206318	Postmortem human <b>alcoholic</b> brain also showed increased <strong>HMGB1</strong>, TLR2, TLR3, and TLR4 +IR cells that correlated with lifetime <b>alcohol</b> consumption, as well as each other.
+HMGB1	drug	alcohol	23206318	<b>Ethanol</b> treatment of brain slice culture released <strong>HMGB1</strong> into the media and induced the proinflammatory cytokine, interleukin 1 beta (IL 1β).
+HMGB1	drug	alcohol	23206318	Neutralizing antibodies to <strong>HMGB1</strong> and small inhibitory mRNA to <strong>HMGB1</strong> or TLR4 blunted <b>ethanol</b> induction of IL 1β.
+HMGB1	drug	alcohol	23206318	<b>Ethanol</b> induced <strong>HMGB1</strong>/TLR signaling contributes to induction of the proinflammatory cytokine, IL 1β.
+HMGB1	drug	alcohol	23206318	Increased expression of <strong>HMGB1</strong>, TLR2, TLR3, and TLR4 in <b>alcoholic</b> brain and in mice treated with <b>ethanol</b> suggests that chronic <b>alcohol</b> induced brain neuroimmune activation occurs through <strong>HMGB1</strong>/TLR signaling.
+HMGB1	addiction	intoxication	22986167	Adolescent <b>binge</b> drinking increases expression of the danger signal receptor agonist <strong>HMGB1</strong> and Toll like receptors in the adult prefrontal cortex.
+HMGB1	drug	alcohol	22986167	Recent studies have found that <b>ethanol</b> increases neuroinflammation via upregulated high mobility group box 1 (<strong>HMGB1</strong>) signaling through Toll like receptors (TLRs).
+HMGB1	drug	alcohol	22986167	Recent studies have found that <b>ethanol</b> increases neuroinflammation via upregulated <strong>high mobility group box 1</strong> (<strong>HMGB1</strong>) signaling through Toll like receptors (TLRs).
+HMGB1	drug	alcohol	22709825	<b>Ethanol</b> potentiation of poly I:C was associated with <b>ethanol</b> increased expression of TLR3 and endogenous agonist <strong>HMGB1</strong> in the brain.
+HMGB1	drug	alcohol	22709825	<b>Ethanol</b> potentiation of TLR3 agonist responses is consistent with priming microglia monocytes and increased NOX, ROS, <strong>HMGB1</strong> TLR3 and markers of neurodegeneration.
+F10	drug	alcohol	32621471	The examination included 74 men admitted in the clinic at Mental Health Research Institute NRMC diagnosed as having «Mental and behavioral disorders due to use of <b>alcohol</b>» (dependence syndrome <strong>F10</strong>.21 and withdrawal state   <strong>F10</strong>.30) according to ICD 10.
+F10	addiction	dependence	32621471	The examination included 74 men admitted in the clinic at Mental Health Research Institute NRMC diagnosed as having «Mental and behavioral disorders due to use of alcohol» (<b>dependence</b> syndrome <strong>F10</strong>.21 and withdrawal state   <strong>F10</strong>.30) according to ICD 10.
+F10	addiction	withdrawal	32621471	The examination included 74 men admitted in the clinic at Mental Health Research Institute NRMC diagnosed as having «Mental and behavioral disorders due to use of alcohol» (dependence syndrome <strong>F10</strong>.21 and <b>withdrawal</b> state   <strong>F10</strong>.30) according to ICD 10.
+F10	drug	alcohol	31980380	The outcomes were ICD 10 of Diseases and Related Health Problems diagnoses relating to <b>alcohol</b> (<strong>F10</strong>) and other substances (F11 F19).
+F10	drug	alcohol	31925836	Proportions of monthly hospital admissions for <b>alcohol</b> intoxication (ICD 10 diagnoses <strong>F10</strong>.0/<strong>F10</strong>.1, T51.0) per 1000 monthly overall admissions.
+F10	addiction	intoxication	31925836	Proportions of monthly hospital admissions for alcohol <b>intoxication</b> (ICD 10 diagnoses <strong>F10</strong>.0/<strong>F10</strong>.1, T51.0) per 1000 monthly overall admissions.
+F10	drug	alcohol	31901192	The Trnava region corresponds to <strong>F10</strong>   Acute <b>alcohol</b> intoxication.
+F10	addiction	intoxication	31901192	The Trnava region corresponds to <strong>F10</strong>   Acute alcohol <b>intoxication</b>.
+F10	drug	alcohol	31603459	The rate of hospital discharges due to any condition from the <strong>F10</strong> diagnostic category (mental and behavioural disorders due to <b>alcohol</b>) was moderately correlated with AD prevalence (r = 0.56), while the rate due to any condition from the K70 diagnostic category (<b>alcoholic</b> liver disease) was weakly correlated with AD prevalence (r = 0.21).
+F10	drug	alcohol	31161915	Objective: The objective of the study was to examine the correlates, phenomenology, and short term treatment response to benzodiazepines and antipsychotics in an inpatient sample with <b>alcohol</b> induced psychotic disorder, predominant hallucinations i.e., <strong>F10</strong>.52.
+F10	drug	alcohol	31089097	Thirty patients, aged from 18 to 40 years, with the diagnosis of '<b>alcohol</b> withdrawal, uncomplicated' (<strong>F10</strong>.302) or '<b>alcohol</b> withdrawal complicated by delirium' (<strong>F10</strong>.40) were examined in the acute state and after 2 weeks of therapy.
+F10	addiction	withdrawal	31089097	Thirty patients, aged from 18 to 40 years, with the diagnosis of 'alcohol <b>withdrawal</b>, uncomplicated' (<strong>F10</strong>.302) or 'alcohol <b>withdrawal</b> complicated by delirium' (<strong>F10</strong>.40) were examined in the acute state and after 2 weeks of therapy.
+F10	drug	alcohol	31081924	The present study investigated the degree to which combining CBM and tDCS (2.0 mA anodal current over <strong>F10</strong>) could reduce <b>alcohol</b> approach biases and <b>alcohol</b> consumption.
+F10	drug	alcohol	30784955	Randomized, double blind, placebo controlled trial with 40 patients fulfilling criteria for ICD 10 diagnosis of <b>alcohol</b> dependence (<strong>F10</strong>.2), admitted for <b>alcohol</b> detoxification and withdrawal treatment.
+F10	addiction	dependence	30784955	Randomized, double blind, placebo controlled trial with 40 patients fulfilling criteria for ICD 10 diagnosis of alcohol <b>dependence</b> (<strong>F10</strong>.2), admitted for alcohol detoxification and withdrawal treatment.
+F10	addiction	withdrawal	30784955	Randomized, double blind, placebo controlled trial with 40 patients fulfilling criteria for ICD 10 diagnosis of alcohol dependence (<strong>F10</strong>.2), admitted for alcohol detoxification and <b>withdrawal</b> treatment.
+F10	drug	alcohol	28784393	To understand the predictors of coping behaviour and perceived expressed emotion in persons with <b>alcohol</b> dependence, 60 adults who approached an institutional setting for treatment and satisfied the ICD 10 <strong>F10</strong> criteria without other psychotic disorder were administered the Socio Demographic Interview Schedule, <b>Alcohol</b> Use Disorders Identification Test (AUDIT), Coping Behaviour Inventory (CBI) and Level of Expressed Emotion Scale (LEE).
+F10	addiction	dependence	28784393	To understand the predictors of coping behaviour and perceived expressed emotion in persons with alcohol <b>dependence</b>, 60 adults who approached an institutional setting for treatment and satisfied the ICD 10 <strong>F10</strong> criteria without other psychotic disorder were administered the Socio Demographic Interview Schedule, Alcohol Use Disorders Identification Test (AUDIT), Coping Behaviour Inventory (CBI) and Level of Expressed Emotion Scale (LEE).
+F10	drug	alcohol	25350241	[Secondary data analysis of the prevalence of <b>alcohol</b> dependence (<strong>F10</strong>.2) in Germany].
+F10	addiction	dependence	25350241	[Secondary data analysis of the prevalence of alcohol <b>dependence</b> (<strong>F10</strong>.2) in Germany].
+F10	drug	alcohol	25350241	Within this study, the coding of <b>alcohol</b> abuse (<strong>F10</strong>.2 diagnosis) was analyzed separately for outpatient and inpatient sector in the insured population ≥ 18 years and presented over time.
+F10	drug	alcohol	25350241	For insured persons with at least one inpatient or outpatient <strong>F10</strong>.2 diagnosis, the prevalence continuously rises from 1,04% in 2006 to 1.14% in 2010; the prevalence of insured persons who received an <b>alcohol</b> dependence diagnosis only in the outpatient sector, increased from 0,67% to 0,79% in that time scale.
+F10	addiction	dependence	25350241	For insured persons with at least one inpatient or outpatient <strong>F10</strong>.2 diagnosis, the prevalence continuously rises from 1,04% in 2006 to 1.14% in 2010; the prevalence of insured persons who received an alcohol <b>dependence</b> diagnosis only in the outpatient sector, increased from 0,67% to 0,79% in that time scale.
+F10	drug	alcohol	25343650	A total of 907 patients admitted for acute <b>alcohol</b> intoxication (<strong>F10</strong>.0) were included, of whom 592 were male.
+F10	addiction	intoxication	25343650	A total of 907 patients admitted for acute alcohol <b>intoxication</b> (<strong>F10</strong>.0) were included, of whom 592 were male.
+F10	drug	alcohol	24988979	One hundred and seven patients, mean age 64.4±8.5 years, with transition (II III) stage of <b>alcoholism</b> (<strong>F10</strong>.2 in CD 10) were examined.
+F10	drug	alcohol	24818357	We determined the DBI genotypes using a novel method involving PCR RFLP in healthy controls and <b>alcoholics</b> with a diagnosis of <b>alcohol</b> dependence by ICD 10 (<strong>F10</strong>.20).
+F10	addiction	dependence	24818357	We determined the DBI genotypes using a novel method involving PCR RFLP in healthy controls and alcoholics with a diagnosis of alcohol <b>dependence</b> by ICD 10 (<strong>F10</strong>.20).
+F10	drug	alcohol	23374162	Cases which had a measurement of BAC (Y90) coded, or only a subjective assessment of <b>alcohol</b> intoxication (<strong>F10</strong>.0).
+F10	addiction	intoxication	23374162	Cases which had a measurement of BAC (Y90) coded, or only a subjective assessment of alcohol <b>intoxication</b> (<strong>F10</strong>.0).
+F10	drug	alcohol	22611694	The questionnaire was tested in 106 inpatients diagnosed with <b>alcohol</b> dependence (ICD 10, item <strong>F10</strong>.2).
+F10	addiction	dependence	22611694	The questionnaire was tested in 106 inpatients diagnosed with alcohol <b>dependence</b> (ICD 10, item <strong>F10</strong>.2).
+F10	drug	alcohol	19823613	The case notes of all in patients with a primary diagnosis of <b>alcohol</b> and/or opioid dependence syndrome (<strong>F10</strong>.24 and F11.24) in the calendar year 2006 were examined.
+F10	drug	opioid	19823613	The case notes of all in patients with a primary diagnosis of alcohol and/or <b>opioid</b> dependence syndrome (<strong>F10</strong>.24 and F11.24) in the calendar year 2006 were examined.
+F10	addiction	dependence	19823613	The case notes of all in patients with a primary diagnosis of alcohol and/or opioid <b>dependence</b> syndrome (<strong>F10</strong>.24 and F11.24) in the calendar year 2006 were examined.
+F10	drug	alcohol	18927971	The study of 85 patients with <b>alcohol</b> dependence appointed to forensic psychiatric expertise in the Serbsky research center of social and forensic psychiatry revealed the manifestation of polymorphic psychiatric and behavioral disorders (ICD 10 diagnosis <strong>F10</strong>.7  residual and late onset psychotic disorders) after stopping the intoxication, withdrawal and post withdralwal disorders.
+F10	addiction	dependence	18927971	The study of 85 patients with alcohol <b>dependence</b> appointed to forensic psychiatric expertise in the Serbsky research center of social and forensic psychiatry revealed the manifestation of polymorphic psychiatric and behavioral disorders (ICD 10 diagnosis <strong>F10</strong>.7  residual and late onset psychotic disorders) after stopping the intoxication, withdrawal and post withdralwal disorders.
+F10	addiction	intoxication	18927971	The study of 85 patients with alcohol dependence appointed to forensic psychiatric expertise in the Serbsky research center of social and forensic psychiatry revealed the manifestation of polymorphic psychiatric and behavioral disorders (ICD 10 diagnosis <strong>F10</strong>.7  residual and late onset psychotic disorders) after stopping the <b>intoxication</b>, withdrawal and post withdralwal disorders.
+F10	addiction	withdrawal	18927971	The study of 85 patients with alcohol dependence appointed to forensic psychiatric expertise in the Serbsky research center of social and forensic psychiatry revealed the manifestation of polymorphic psychiatric and behavioral disorders (ICD 10 diagnosis <strong>F10</strong>.7  residual and late onset psychotic disorders) after stopping the intoxication, <b>withdrawal</b> and post withdralwal disorders.
+F10	drug	alcohol	18534165	We examined the medical records of patients who were treated as inpatients in 1998 2006 and discharged with the ICD 10 diagnoses <strong>F10</strong>.4 (<b>alcohol</b> withdrawal delirium) or <strong>F10</strong>.5 (<b>alcohol</b> induced psychotic disorder).
+F10	addiction	withdrawal	18534165	We examined the medical records of patients who were treated as inpatients in 1998 2006 and discharged with the ICD 10 diagnoses <strong>F10</strong>.4 (alcohol <b>withdrawal</b> delirium) or <strong>F10</strong>.5 (alcohol induced psychotic disorder).
+F10	drug	alcohol	20711392	One hundred male subjects admitted to a deaddiction centre with a diagnosis of <b>alcohol</b> dependence syndrome with simple withdrawal symptoms (<strong>F10</strong>.30, ICD 10 criteria) were assessed for sexual dysfunction using a sexual dysfunction checklist, constructed using items from the Diagnostic Criteria for Research [ICD 10] for sexual dysfunction.
+F10	addiction	dependence	20711392	One hundred male subjects admitted to a deaddiction centre with a diagnosis of alcohol <b>dependence</b> syndrome with simple withdrawal symptoms (<strong>F10</strong>.30, ICD 10 criteria) were assessed for sexual dysfunction using a sexual dysfunction checklist, constructed using items from the Diagnostic Criteria for Research [ICD 10] for sexual dysfunction.
+F10	addiction	withdrawal	20711392	One hundred male subjects admitted to a deaddiction centre with a diagnosis of alcohol dependence syndrome with simple <b>withdrawal</b> symptoms (<strong>F10</strong>.30, ICD 10 criteria) were assessed for sexual dysfunction using a sexual dysfunction checklist, constructed using items from the Diagnostic Criteria for Research [ICD 10] for sexual dysfunction.
+F10	drug	alcohol	17076934	A total of 299 detoxified <b>alcohol</b> dependent patients (ICD 10: <strong>F10</strong>.2) received either tiapride (300 mg/d) or placebo over a 24 wk study period.
+F10	drug	alcohol	16930855	In a sample of 103 individuals diagnosed with <b>alcohol</b> dependence (ICD 10 <strong>F10</strong>.2), we compared the EQ 5D against a quality of life measure (WHOQoL BREF), a utility scale (TTO), measures of psychopathology (SCL 90R, CGI S) and measures of social functioning (GAF, GARF, SOFAS, HoNOS).
+F10	addiction	dependence	16930855	In a sample of 103 individuals diagnosed with alcohol <b>dependence</b> (ICD 10 <strong>F10</strong>.2), we compared the EQ 5D against a quality of life measure (WHOQoL BREF), a utility scale (TTO), measures of psychopathology (SCL 90R, CGI S) and measures of social functioning (GAF, GARF, SOFAS, HoNOS).
+F10	drug	alcohol	16633972	We performed a retrospective analysis of clinical data and ECG's from patients discharged between 1995 and 2005 with the diagnosis of DT (ICD Code <strong>F10</strong>.4) or <b>alcohol</b> withdrawal seizures (<strong>F10</strong>.3).
+F10	addiction	withdrawal	16633972	We performed a retrospective analysis of clinical data and ECG's from patients discharged between 1995 and 2005 with the diagnosis of DT (ICD Code <strong>F10</strong>.4) or alcohol <b>withdrawal</b> seizures (<strong>F10</strong>.3).
+F10	drug	alcohol	15082461	22 drug free, detoxified patients (15 men, seven women) aged between 27 and 58 (mean 41.5 +/  8.1) years, diagnosed as <b>alcohol</b> dependent (ICD 10: <strong>F10</strong>.23) were included in the study.
+F10	drug	alcohol	14505267	A disproportionately large number of those in somatic wards, mainly internal medicine wards, were in the diagnostic categories F13 (medication dependency), <strong>F10</strong> (<b>alcohol</b> related), F0 09 (cerebral organic disorders) and F40 48 (neurotic disorders).
+F10	drug	alcohol	14505267	On the internal medicine wards the second most common diagnostic group in the age group 16 64 years, after ischaemic heart disease (I25), was <b>alcohol</b> related disorders (<strong>F10</strong>).
+F10	drug	alcohol	11042866	To study the influence of <b>alcohol</b> and psychosocial variables on delinquent behavior, we coded data from the psychiatric evaluation of 254 defendants using a standardized score sheet, analyzing correlations between acute intoxication at the time of the crime (ICD 10:<strong>F10</strong>.0), diagnosis of <b>alcohol</b> dependency according to ICD 10 (<strong>F10</strong>.2), psycho biographical variables, criminal history, and parameters relating to the index offence.
+F10	addiction	intoxication	11042866	To study the influence of alcohol and psychosocial variables on delinquent behavior, we coded data from the psychiatric evaluation of 254 defendants using a standardized score sheet, analyzing correlations between acute <b>intoxication</b> at the time of the crime (ICD 10:<strong>F10</strong>.0), diagnosis of alcohol dependency according to ICD 10 (<strong>F10</strong>.2), psycho biographical variables, criminal history, and parameters relating to the index offence.
+F10	drug	alcohol	10619208	According to the diagnoses of the primary care physicians, 7.4% of the residents had mental and behavioural disorders due to <b>alcohol</b> (ICD 10: <strong>F10</strong>).
+F10	drug	alcohol	9340658	The main substance was <b>alcohol</b> (<strong>F10</strong>.1 or <strong>F10</strong>.2; 52.2%), followed by cannabis (F12; 25%), opiates (F11; 4.1%), sedatives or hypnotics (F13; 2.7%) and cocaine (F16; 0.5%).
+F10	drug	cannabinoid	9340658	The main substance was alcohol (<strong>F10</strong>.1 or <strong>F10</strong>.2; 52.2%), followed by <b>cannabis</b> (F12; 25%), opiates (F11; 4.1%), sedatives or hypnotics (F13; 2.7%) and cocaine (F16; 0.5%).
+F10	drug	cocaine	9340658	The main substance was alcohol (<strong>F10</strong>.1 or <strong>F10</strong>.2; 52.2%), followed by cannabis (F12; 25%), opiates (F11; 4.1%), sedatives or hypnotics (F13; 2.7%) and <b>cocaine</b> (F16; 0.5%).
+DBCN	drug	nicotine	31316930	The numbers of the <strong>doublecortin</strong> (DCX) positive cells and 5 bromo 2' deoxyuridine (BrdU) positive cells in the dentate gyrus were suppressed in the <b>nicotine</b> withdrawal rats, in contrast, treadmill running enhanced the numbers of DCX positive cells and BrdU positive cells.
+DBCN	addiction	withdrawal	31316930	The numbers of the <strong>doublecortin</strong> (DCX) positive cells and 5 bromo 2' deoxyuridine (BrdU) positive cells in the dentate gyrus were suppressed in the nicotine <b>withdrawal</b> rats, in contrast, treadmill running enhanced the numbers of DCX positive cells and BrdU positive cells.
+DBCN	drug	cannabinoid	31162770	Our results show that a 6 day repeated temozolomide treatment (25 mg/kg/day), a chemotherapy drug that blocks hippocampal neurogenesis, prevented <b>cannabidiol</b> induced increment in the early stages of neuronal maturation and differentiation, without altering the basal levels of BrdU/NeuN and <strong>doublecortin</strong> immunostaining.
+DBCN	drug	opioid	30728362	Further, we demonstrate that the μ <b>opioid</b> receptor (MOR) is expressed on DG NSCs and that MSA leads to a two fold elevation of endogenous MOR levels in <strong>doublecortin</strong> expressing (DCX+) NSC progenies in the rat DG.
+DBCN	drug	opioid	30447281	Removal of microglial specific MyD88 signaling alters dentate gyrus <strong>doublecortin</strong> and enhances <b>opioid</b> addiction like behaviors.
+DBCN	addiction	addiction	30447281	Removal of microglial specific MyD88 signaling alters dentate gyrus <strong>doublecortin</strong> and enhances opioid <b>addiction</b> like behaviors.
+DBCN	drug	opioid	30447281	Furthermore, <b>morphine</b> treated Cretg/0 mice showed increased <strong>doublecortin</strong> (DCX) signal relative to Cre0/0 control mice in the hippocampus, indicative of increased number of immature neurons.
+DBCN	drug	nicotine	30391635	Impaired neurogenesis, as shown by reduction in the expression of the endogenous cell proliferation marker Ki67 and the early neuron marker <strong>doublecortin</strong>, was also associated with <b>nicotine</b> abstinence.
+DBCN	drug	alcohol	29449568	<b>Alcohol</b> exposure reduced the number of both NeuN positive and <strong>doublecortin</strong> positive cells in the hippocampus.
+DBCN	drug	opioid	27078155	Using cell type selective markers, we observed that <b>morphine</b> reduced the number of late stage progenitors and immature neurons such as <strong>Doublecortin</strong> (DCX) and βIII Tubulin (TuJ1) positive cells in the SGZ but did not reduce the number of early progenitors such as Nestin, SOX2, or neurogenic differentiation 1 (NeuroD1) positive cells.
+DBCN	drug	amphetamine	26366944	The results showed that <b>METH</b> caused a decrease in neuronal phenotypes as determined by the expressions of nestin, <strong>doublecortin</strong> (DCX) and beta III tubulin while causing an increase in glial fibrillary acidic protein (GFAP) expression.
+DBCN	drug	cannabinoid	25944409	These changes included proteins involved in impulsivity like behavior, synaptic plasticity, and <b>cannabinoid</b> signaling modulation, such as alpha synuclein, phosphatase 1 alpha, <strong>doublecortin</strong> like kinase 2, and diacylglycerol kinase zeta, and were validated by immunoblotting.
+DBCN	drug	alcohol	25729346	Using a rodent model of adolescent intermittent <b>ethanol</b> (AIE; 5.0 g/kg, i.g., 20% EtOH w/v; 2 days on/2 days off from postnatal day [P]25 to P55), we discovered that AIE treatment reduced neurogenesis (i.e., <strong>doublecortin</strong> immunoreactive [DCX + IR] cells) in both the dorsal and ventral hippocampal dentate gyrus of late adolescent (P56) male Wistar rats that persisted during abstinence into adulthood (P220).
+DBCN	drug	cocaine	25294309	Overall level of neurogenesis, as detected by the S phase marker 5' bromo 2' deoxyuridine (BrdU) and the immature neuron marker <strong>doublecortin</strong> (DCX), was unaltered by <b>cocaine</b> conditioning.
+DBCN	drug	amphetamine	25201326	Moreover, <b>METH</b> (10nM) increased <strong>doublecortin</strong> (DCX) protein levels consistent with neuronal differentiation.
+DBCN	drug	alcohol	23844726	Increased proliferation was followed by a 75% increase in <strong>doublecortin</strong> expression and a 56% increase in surviving bromodeoxyuridine labeled cells 14 and 35 days post <b>ethanol</b> exposure, respectively.
+DBCN	addiction	withdrawal	23844726	Although these results mirror the magnitude of reactive neurogenesis described in adult rat studies, ectopic bromodeoxyuridine and <strong>doublecortin</strong> positive cells were detected in the molecular layer and hilus of adolescent rats displaying severe <b>withdrawal</b> symptoms, an effect that has not been described in adults.
+DBCN	drug	alcohol	23567812	Quantitative analyses of immunoreactivity revealed a significant reduction in measures of neurogenesis, progenitor proliferation, as indexed by <strong>doublecortin</strong> (DCX), Ki67, and increased markers of cell death as indexed by cleaved caspase 3, and Fluoro Jade at 72 days, and decreases in DCX, and increases in cleaved caspase 3 at 114 days in the <b>ethanol</b> vapor exposed rats.
+DBCN	drug	opioid	23213573	Increases in <strong>doublecortin</strong> immunoreactivity in the dentate gyrus following extinction of <b>heroin</b> seeking behavior.
+DBCN	addiction	relapse	23213573	Increases in <strong>doublecortin</strong> immunoreactivity in the dentate gyrus following extinction of heroin <b>seeking</b> behavior.
+DBCN	addiction	relapse	23213573	We investigated the effects of extinction of drug <b>seeking</b> behavior on the formation of immature neurons in the DG as assessed by quantification of <strong>doublecortin</strong> (DCX) immunoreactivity.
+DBCN	drug	opioid	22487733	Surprisingly, <b>methadone</b> did not alter any of three quantified parameters relevant to adult hippocampal neurogenesis (number of Ki67 , <strong>doublecortin</strong> , or BrdU immunoreactive cells [BrdU given prior to saline/<b>methadone</b> exposure]).
+DBCN	addiction	reward	22340086	When measured 24 hours following the <b>CPP</b> test, there was no effect of EtOH on <strong>doublecortin</strong> (DCX) expression or Fluoro Jade B staining.
+DBCN	drug	opioid	22079577	Here, we show that two commonly used post operative <b>buprenorphine</b> dosing regimes significantly inhibit the proliferation of <strong>doublecortin</strong> positive neuroblasts but not other hippocampal stem and progenitor cell populations in adult mice.
+DBCN	drug	opioid	22079577	<b>Buprenorphine</b>, administered in schedules of three 0.05 mg/kg subcutaneous injections over a single day or seven 0.05 mg/kg injections over a 3 day period decreased the number of actively proliferating 5 iodo 2' deoxyuridine labeled <strong>doublecortin</strong> positive cells for up to 6 days after opiate withdrawal.
+DBCN	addiction	withdrawal	22079577	Buprenorphine, administered in schedules of three 0.05 mg/kg subcutaneous injections over a single day or seven 0.05 mg/kg injections over a 3 day period decreased the number of actively proliferating 5 iodo 2' deoxyuridine labeled <strong>doublecortin</strong> positive cells for up to 6 days after opiate <b>withdrawal</b>.
+DBCN	drug	alcohol	19554644	After 4 days of binge <b>alcohol</b> exposure, neurogenesis was decreased by 33 and 28% at 0 and 2 days after the last dose according to <strong>doublecortin</strong> expression.
+DBCN	addiction	intoxication	19554644	After 4 days of <b>binge</b> alcohol exposure, neurogenesis was decreased by 33 and 28% at 0 and 2 days after the last dose according to <strong>doublecortin</strong> expression.
+DBCN	drug	benzodiazepine	19437554	Phenobarbital and <b>clonazepam</b> significantly inhibited cell proliferation by 63% and 59%, respectively, and <strong>doublecortin</strong> immunoreactivity (indicator of neurogenesis) in the dorsal hippocampus was also significantly decreased by 26% and 24%, respectively.
+DBCN	drug	cocaine	18322096	Unexpectedly, CSA WD and CSA CONT resulted in more immature <strong>doublecortin</strong> immunopositive (+) neurons in the posterior SGZ and a normal number of adult generated BrdU+ neurons in the SGZ, suggesting an enduring impact of CSA regardless of whether <b>cocaine</b> intake was stopped or continued.
+DBCN	drug	psychedelics	16949621	We used 5' bromo 2 deoxyuridine (BrdU) and Ki 67 as mitotic markers, and <strong>doublecortin</strong> (DCX) as a marker of immature neurons, to study proliferation, survival and maturation of adult generated cells in the dentate gyrus (DG) of the hippocampus following binge administration of <b>MDMA</b> (8 injections of 5 mg/kg at 6 h intervals).
+DBCN	addiction	intoxication	16949621	We used 5' bromo 2 deoxyuridine (BrdU) and Ki 67 as mitotic markers, and <strong>doublecortin</strong> (DCX) as a marker of immature neurons, to study proliferation, survival and maturation of adult generated cells in the dentate gyrus (DG) of the hippocampus following <b>binge</b> administration of MDMA (8 injections of 5 mg/kg at 6 h intervals).
+RPS6KB1	drug	alcohol	32333810	Phosphorylation levels of 4E BP1 and <strong>p70 S6K</strong> were also increased following <b>alcohol</b> exposure.
+RPS6KB1	drug	alcohol	31733664	Results also showed that <b>alcohol</b> use was associated with a general reduction in Akt/mTOR signaling via several phosphoproteins (IR, IRS1, IGF1R, PTEN, ERK, mTOR, <strong>p70S6K</strong>, RPS6) in multiple brain regions including hippocampus and entorhinal cortex.
+RPS6KB1	drug	psychedelics	31128500	However, no changes in the <strong>p70S6K</strong>, PSD 95, GluA1, and synapsin immunocontents were found in the hippocampus of <b>ketamine</b> plus guanosine treated mice.
+RPS6KB1	drug	opioid	30146703	We examined the effects of chronic treatment of <b>morphine</b> and/or <b>methadone</b> in the presence or absence of metformin with or without AMPK inhibitor (dorsomorphin hydrochloride) on levels of nitric oxide and cyclic adenosine monophosphate (cAMP), phosphorylated and dephosphorylated ribosomal protein S6 kinase β 1 (<strong>S6K1</strong>) and 4E binding protein 1 (4E BP1) in T98G cells.
+RPS6KB1	drug	amphetamine	29574227	Behaviorally, <b>METH</b> sensitized mice possessed increased levels of phosphorylated mTOR/S2448 and its down stream regulator <strong>p70S6K</strong> and pS6 in the ventral striatum.
+RPS6KB1	drug	alcohol	29457836	Chronic plus binge <b>ethanol</b> feeding led to hyperactivation of mTORC1, as evidenced by increased phosphorylation of mTOR and its downstream kinase S6 kinase 1 (<strong>S6K1</strong>) in hepatocytes.
+RPS6KB1	addiction	intoxication	29457836	Chronic plus <b>binge</b> ethanol feeding led to hyperactivation of mTORC1, as evidenced by increased phosphorylation of mTOR and its downstream kinase S6 kinase 1 (<strong>S6K1</strong>) in hepatocytes.
+RPS6KB1	drug	alcohol	29457836	Chronic plus binge <b>ethanol</b> feeding led to activation of SREBP 1 and lipin 1 through <strong>S6K1</strong> dependent and independent mechanisms.
+RPS6KB1	addiction	intoxication	29457836	Chronic plus <b>binge</b> ethanol feeding led to activation of SREBP 1 and lipin 1 through <strong>S6K1</strong> dependent and independent mechanisms.
+RPS6KB1	drug	cocaine	28432301	We found that exposure to drug related cues reinstated <b>cocaine</b> seeking behavior and increased AMPK and <strong>p70s6k</strong> phosphorylation in the NAc core but not shell.
+RPS6KB1	addiction	relapse	28432301	We found that exposure to drug related cues reinstated cocaine <b>seeking</b> behavior and increased AMPK and <strong>p70s6k</strong> phosphorylation in the NAc core but not shell.
+RPS6KB1	drug	alcohol	26373814	<b>Ethanol</b> + NNK had synergistic stimulatory effects on 8 iso PGF 2α, inhibitory effects on p <strong>p70S6K</strong>, tau and p tau and trend effects on insulin like growth factor type 1 (IGF 1) receptor expression and phosphorylation.
+RPS6KB1	addiction	intoxication	25257868	The stimulation induced increase in the phosphorylation of <strong>S6K1</strong> Thr(421)/Ser(424) (20 52%), <strong>S6K1</strong> Thr(389) (45 57%), and its substrate rpS6 Ser(240/244) (37 72%) was blunted by EtOH at 30 min, 4 h, and 12 h. Phosphorylation of 4E BP1 Ser(65) was also attenuated by EtOH (61%) at 4 h. Conversely, phosphorylation of extracellular signal regulated kinase Thr(202)/Tyr(204) was increased by stimulation in Control and EtOH mice at 30 min but only in Control at 4 h. Our data indicate that acute EtOH <b>intoxication</b> suppresses muscle protein synthesis for at least 12 h and greatly impairs contraction induced changes in synthesis and mTOR signaling.
+RPS6KB1	drug	nicotine	24916432	The initiation of <b>nicotine</b> induced locomotor sensitization was accompanied by the increased phosphorylated level of mTORC1 downstream target proteins including p <strong>p70s6k</strong> and p 4EBP in the BLA, but not CeA.
+RPS6KB1	addiction	sensitization	24916432	The initiation of nicotine induced locomotor <b>sensitization</b> was accompanied by the increased phosphorylated level of mTORC1 downstream target proteins including p <strong>p70s6k</strong> and p 4EBP in the BLA, but not CeA.
+RPS6KB1	drug	nicotine	24916432	Increased p <strong>p70s6k</strong> and p 4EBP were also observed in the expression of <b>nicotine</b> sensitization, which was demonstrated to be inhibited by systemic rapamycin administration.
+RPS6KB1	addiction	sensitization	24916432	Increased p <strong>p70s6k</strong> and p 4EBP were also observed in the expression of nicotine <b>sensitization</b>, which was demonstrated to be inhibited by systemic rapamycin administration.
+RPS6KB1	drug	cocaine	24595501	Using a mouse model of conditioned place preference, regulation of the activity of glycogen synthase kinase 3 (GSK3), mammalian target of Rapamycin complex 1 (mTORC1), <strong>P70S6K</strong>, β catenin, and the upstream signaling molecule Akt, was studied in cortico limbic striatal circuitry after re exposure to an environment previously paired with <b>cocaine</b>.
+RPS6KB1	drug	cocaine	24595501	Levels of phosporylated Akt Thr308, GSK3α Ser21, GSK3β Ser9, mTORC1, and <strong>P70S6K</strong> were reduced in the nucleus accumbens and hippocampus 10 min after the reactivation of <b>cocaine</b> cue memories.
+RPS6KB1	drug	cannabinoid	23727505	This study evaluated the status of <b>cannabinoid</b> (CB) CB1 and CB2 receptors, the endocytic cycle of CB1 receptors, G protein coupled receptor regulatory kinases (GRK), and associated signaling (mammalian target of rapamicin (mTOR) and 70kDa ribosomal protein S6 kinase (<strong>p70S6K</strong>)) in brain cortices of drug abusers and cocaine  and <b>cannabinoid</b> treated rodents.
+RPS6KB1	drug	cocaine	23727505	This study evaluated the status of cannabinoid (CB) CB1 and CB2 receptors, the endocytic cycle of CB1 receptors, G protein coupled receptor regulatory kinases (GRK), and associated signaling (mammalian target of rapamicin (mTOR) and 70kDa ribosomal protein S6 kinase (<strong>p70S6K</strong>)) in brain cortices of drug abusers and <b>cocaine</b>  and cannabinoid treated rodents.
+RPS6KB1	drug	cannabinoid	23727505	<b>Rimonabant</b> and AM281 also behaved as inverse agonists on the activation of mTOR and its target <strong>p70S6K</strong>.
+RPS6KB1	drug	cocaine	23727505	Chronic <b>cocaine</b> in mice was associated with tolerance to the acute activation of mTOR and <strong>p70S6K</strong>.
+RPS6KB1	drug	cocaine	23727505	In long term <b>cocaine</b> addicts, mTOR and <strong>p70S6K</strong> activations were not altered when compared with controls, indicating that CB1 receptor signaling was dampened.
+RPS6KB1	drug	cocaine	23727505	The dysregulation of CB1 receptor, GRK2/3/5, and mTOR/<strong>p70S6K</strong> signaling by <b>cocaine</b> may contribute to alterations of neuroplasticity and/or neurotoxicity in brains of <b>cocaine</b> addicts.
+RPS6KB1	drug	cocaine	20861369	We found that exposure to a <b>cocaine</b> related cue induced reinstatement to <b>cocaine</b> seeking and increased phosphorylation of p70s6 kinase (<strong>p70s6k</strong>) and ribosomal protein s6 (rps6), measures of mTOR activity, in the nucleus accumbens (NAc) core but not shell.
+RPS6KB1	addiction	relapse	20861369	We found that exposure to a cocaine related cue induced <b>reinstatement</b> to cocaine <b>seeking</b> and increased phosphorylation of p70s6 kinase (<strong>p70s6k</strong>) and ribosomal protein s6 (rps6), measures of mTOR activity, in the nucleus accumbens (NAc) core but not shell.
+RPS6KB1	drug	cocaine	20861369	Furthermore, inhibition of NAc core but not shell <strong>p70s6k</strong> and rps6 phosphorylation by rapamycin decreased cue induced reinstatement of <b>cocaine</b> seeking.
+RPS6KB1	addiction	relapse	20861369	Furthermore, inhibition of NAc core but not shell <strong>p70s6k</strong> and rps6 phosphorylation by rapamycin decreased cue induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+RPS6KB1	addiction	relapse	20861369	Finally, stimulation of NAc core <strong>p70s6k</strong> and rps6 phosphorylation by NMDA enhanced cue induced <b>reinstatement</b>, an effect reversed by rapamycin pretreatment.
+RPS6KB1	drug	opioid	20826199	Here, we tested the role of PI3K/Akt mTOR <strong>p70S6K</strong> signaling pathway in <b>morphine</b> induced CPP in the hippocampus.
+RPS6KB1	addiction	reward	20826199	Here, we tested the role of PI3K/Akt mTOR <strong>p70S6K</strong> signaling pathway in morphine induced <b>CPP</b> in the hippocampus.
+RPS6KB1	drug	opioid	20826199	Likewise, levels of phosphorylated mTOR and <strong>p70S6K</strong> were significantly enhanced in the CA3 following <b>morphine</b> CPP.
+RPS6KB1	addiction	reward	20826199	Likewise, levels of phosphorylated mTOR and <strong>p70S6K</strong> were significantly enhanced in the CA3 following morphine <b>CPP</b>.
+RPS6KB1	drug	alcohol	18317950	Differential phosphorylation of translation initiation regulators 4EBP1, <strong>S6k1</strong>, and Erk 1/2 following inhibition of <b>alcohol</b> metabolism in mouse heart.
+RPS6KB1	drug	alcohol	18317950	The purpose of the present set of experiments was designed to examine the effects of inhibitors of <b>ethanol</b> metabolism on the phosphorylation of 4E binding protein (4EBP1) and <strong>S6k1</strong>(Thr(389)), two factors regulating mRNA translation initiation.
+RPS6KB1	drug	alcohol	18317950	Phosphorylation of 4E BP1, <strong>S6k1</strong>(Thr(389)), and Erk 1/2 was reduced 2 h following IP injection of <b>alcohol</b>.
+RPS6KB1	drug	alcohol	18317950	Pretreatment with 4 methylpyrazole (4 MP), an inhibitor of <b>alcohol</b> dehydrogenase (ADH), did not attenuate the <b>ethanol</b> induced decrease in phosphorylation of 4EBP1 and <strong>S6k1</strong>(Thr(389)).
+RPS6KB1	drug	alcohol	18317950	Pretreatment with cyanamide, an inhibitor of aldehyde dehydrogenase, did not attenuate the <b>ethanol</b> induced decrease in phosphorylation <strong>S6k1</strong>(Thr(389)), but partially prevented the <b>ethanol</b> induced lowering of 4EBP1 phosphorylation.
+RPS6KB1	drug	amphetamine	15837117	The aim of the present study was to investigate the role of p70 S6 kinase (<strong>p70 S6K</strong>) phosphorylation, which contributes to the selective translation of a unique family of mRNA, in mediating both the <b>METH</b> induced rewarding effect and its sensitization.
+RPS6KB1	addiction	sensitization	15837117	The aim of the present study was to investigate the role of p70 S6 kinase (<strong>p70 S6K</strong>) phosphorylation, which contributes to the selective translation of a unique family of mRNA, in mediating both the METH induced rewarding effect and its <b>sensitization</b>.
+RPS6KB1	drug	amphetamine	15837117	pre injection with 0.025 pmol/rat of a selective <strong>p70 S6K</strong> inhibitor rapamycin failed to affect the <b>METH</b> induced conditioned place preference.
+RPS6KB1	drug	alcohol	15547464	<b>Alcohol</b> intoxication impairs phosphorylation of <strong>S6K1</strong> and S6 in skeletal muscle independently of <b>ethanol</b> metabolism.
+RPS6KB1	addiction	intoxication	15547464	Alcohol <b>intoxication</b> impairs phosphorylation of <strong>S6K1</strong> and S6 in skeletal muscle independently of ethanol metabolism.
+RPS6KB1	drug	alcohol	15547464	The purpose of this study was to characterize the ability of <b>alcohol</b> to suppress insulin like growth factor (IGF) I stimulation of ribosomal S6 kinase 1 (<strong>S6K1</strong>) and 4E BP1 phosphorylation, which are central elements in the signal transduction pathway used to coordinate the protein synthetic response and may contribute to the development of <b>alcoholic</b> myopathy.
+RPS6KB1	drug	alcohol	15547464	In contrast, IGF I failed to stimulate <strong>S6K1</strong> or S6 phosphorylation 2.5 hr after intraperitoneal administration of <b>alcohol</b> when the blood <b>alcohol</b> concentration was increased between approximately 165 and 300 mg/dl.
+RPS6KB1	drug	alcohol	15547464	With a maximal suppressive dose of <b>alcohol</b>, the inhibitory effect on <strong>S6K1</strong>/S6 phosphorylation was observed as early as 1 hr and for up to 8 hr.
+RPS6KB1	drug	alcohol	15547464	The ability of <b>alcohol</b> to impair phosphorylation of <strong>S6K1</strong> and S6 was independent of gender (male versus female), nutritional status (fed versus fasted), and route of <b>alcohol</b> administration (intraperitoneal versus oral).
+RPS6KB1	drug	alcohol	15547464	The direct effect of <b>alcohol</b> on IGF stimulated <strong>S6K1</strong>/S6 phosphorylation was also present when the isolated hindlimb was perfused in situ with buffer containing <b>alcohol</b>.
+RPS6KB1	drug	alcohol	15547464	In contrast to <strong>S6K1</strong>, acute <b>alcohol</b> intoxication did not consistently impair the ability of IGF I to stimulate 4E BP1 phosphorylation under any of the experimental conditions.
+RPS6KB1	addiction	intoxication	15547464	In contrast to <strong>S6K1</strong>, acute alcohol <b>intoxication</b> did not consistently impair the ability of IGF I to stimulate 4E BP1 phosphorylation under any of the experimental conditions.
+RPS6KB1	drug	alcohol	15547464	These data indicate that acute <b>alcohol</b> intoxication selectively impairs IGF I signaling via <strong>S6K1</strong>, but not 4E BP1, and that this defect is independent of gender, nutritional state, route of administration, and <b>alcohol</b> metabolism.
+RPS6KB1	addiction	intoxication	15547464	These data indicate that acute alcohol <b>intoxication</b> selectively impairs IGF I signaling via <strong>S6K1</strong>, but not 4E BP1, and that this defect is independent of gender, nutritional state, route of administration, and alcohol metabolism.
+RPS6KB1	drug	alcohol	12944322	<b>Alcohol</b> impairs leucine mediated phosphorylation of 4E BP1, <strong>S6K1</strong>, eIF4G, and mTOR in skeletal muscle.
+RPS6KB1	drug	alcohol	12944322	Hence, <b>ethanol</b> produces a leucine resistance in skeletal muscle, as evidenced by the impaired phosphorylation of 4E BP1, eIF4G, <strong>S6K1</strong>, and mTOR, that is independent of elevations in endogenous glucocorticoids.
+RPS6KB1	drug	alcohol	12658115	IGF I induced phosphorylation of <strong>S6K1</strong> and 4E BP1 in heart is impaired by acute <b>alcohol</b> intoxication.
+RPS6KB1	addiction	intoxication	12658115	IGF I induced phosphorylation of <strong>S6K1</strong> and 4E BP1 in heart is impaired by acute alcohol <b>intoxication</b>.
+RPS6KB1	drug	alcohol	12376318	<b>Alcohol</b> impairs insulin and IGF I stimulation of <strong>S6K1</strong> but not 4E BP1 in skeletal muscle.
+PROC	drug	nicotine	30978583	We evaluated cross lagged panel models for negative affect and <b>smoking</b> using <strong>PROC</strong> CALIS in SAS.
+PROC	drug	cocaine	23770647	In a generalized linear mixed model (SAS <strong>Proc</strong> Glimmix), <b>cocaine</b> use varied by time of day relative to business hours (p<0.0001) and there was a significant interaction between Day of the Week and Time Relative to Business Hours (p<0.002) regardless of current work status.
+PROC	drug	alcohol	22547331	The nAChR α4β2 subunit partial agonist varenicline (Chantix™), which is approved by the Food and Drug Administration for smoking cessation, also decreases <b>ethanol</b> consumption in rodents (Steensland et al., <strong>Proc</strong> Natl Acad Sci U S A 104:12518 12523, 2007) and in human laboratory and open label studies (Fucito et al., Psychopharmacology (Berl) 215:655 663, 2011; McKee et al., Biol Psychiatry 66:185 190 2009).
+PROC	drug	nicotine	22547331	The nAChR α4β2 subunit partial agonist varenicline (Chantix™), which is approved by the Food and Drug Administration for <b>smoking</b> cessation, also decreases ethanol consumption in rodents (Steensland et al., <strong>Proc</strong> Natl Acad Sci U S A 104:12518 12523, 2007) and in human laboratory and open label studies (Fucito et al., Psychopharmacology (Berl) 215:655 663, 2011; McKee et al., Biol Psychiatry 66:185 190 2009).
+PROC	drug	nicotine	20177882	These data confirm a previous report (Hollander et al., <strong>Proc</strong> Natl Acad Sci U S A 105:19480 19485, 2008) that the hypocretin receptor hcrtR1 is activated in <b>nicotine</b> reinforcement and in addition show that both the arcuate nucleus and lateral hypothalamus are sites at which hcrt receptor mechanisms may influence reinforcement.
+PROC	addiction	reward	20177882	These data confirm a previous report (Hollander et al., <strong>Proc</strong> Natl Acad Sci U S A 105:19480 19485, 2008) that the hypocretin receptor hcrtR1 is activated in nicotine <b>reinforcement</b> and in addition show that both the arcuate nucleus and lateral hypothalamus are sites at which hcrt receptor mechanisms may influence <b>reinforcement</b>.
+PROC	addiction	relapse	18686188	Using a series of multilevel models (SAS <strong>Proc</strong> Mixed Procedure), significant impulsivity x time analyses revealed differences in <b>craving</b>, F(2, 96) = 3.74, p<.05, and anxiety, F(2, 96) = 3.23, p<.05.
+PROC	addiction	relapse	17521748	High novelty <b>seeking</b> rats (high responders, HR) self administered corticosterone at a much higher rate than low novelty <b>seeking</b> rats (low responders, LR) do [Piazza PV, Deroche V, Deminiere JM, Maccari S, Le Moal M, Simon H, Corticosterone in the range of stress induced levels possesses reinforcing properties: implications for sensation <b>seeking</b> behaviors, <strong>Proc</strong> Natl Acad Sci USA 1993;90:11738 42].
+PROC	addiction	reward	17521748	High novelty seeking rats (high responders, HR) self administered corticosterone at a much higher rate than low novelty seeking rats (low responders, LR) do [Piazza PV, Deroche V, Deminiere JM, Maccari S, Le Moal M, Simon H, Corticosterone in the range of stress induced levels possesses <b>reinforcing</b> properties: implications for sensation seeking behaviors, <strong>Proc</strong> Natl Acad Sci USA 1993;90:11738 42].
+PROC	drug	nicotine	16085524	SAS <strong>Proc</strong> Traj, a group based mixture modeling procedure, was used to determine cigarette use trajectories over time (i.e., patterns of <b>smoking</b> resumption).
+PROC	drug	alcohol	2294963	Phosphatidylinositol (PI) has previously been reported to be responsible for conferring membrane tolerance to liver microsomes in <b>ethanol</b> fed rats (Taraschi, T.F., Ellingson, J.S., Wu, A., Zimmerman, R. and Rubin, E. (1986) <strong>Proc</strong>.
+PAL	drug	alcohol	32630729	Full models of tobacco and <b>alcohol</b> use were differently predicted by variables, so <strong>PAL</strong> (Physical Activity Level) could predict tobacco consumption but not <b>alcohol</b>.
+PAL	drug	nicotine	32630729	Full models of <b>tobacco</b> and alcohol use were differently predicted by variables, so <strong>PAL</strong> (Physical Activity Level) could predict <b>tobacco</b> consumption but not alcohol.
+PAL	drug	alcohol	31998950	In total, 37 inpatient patients with an <b>alcohol</b> use disorder (AUD) and 37 matched healthy controls completed the behavioral activation system scale (BAS scale), the Pleasant Activities List (<strong>PAL</strong>), the Snaith Hamilton Pleasure Scale (SHAPS) and the Delay Discounting Task (DDT).
+PAL	addiction	addiction	31855782	We analyzed data from the Peer ALternatives for <b>Addiction</b> (<strong>PAL</strong>) Study, a longitudinal study comparing the nature and effectiveness of 12 step groups, WFS, LifeRing, and SMART (N = 647).
+PAL	drug	opioid	30129820	<b>Morphine</b> for Refractory Dyspnea in Interstitial Lung Disease: A Phase I Study (JORTC <strong>PAL</strong> 05).
+PAL	addiction	addiction	29606223	The current study addresses this need, offering outcome data from the first longitudinal, comparative study of 12 step groups and their alternatives: The Peer ALlternatives for <b>Addiction</b> (<strong>PAL</strong>) Study.
+PAL	drug	amphetamine	28889212	NE preferring releasers were approximately 13 fold more potent for NE compared to dopamine release and ranged in potency for serotonin release (<strong>PAL</strong> 329 < l <b>methamphetamine</b> < <strong>PAL</strong> 169).
+PAL	drug	amphetamine	28889212	Among the "NE preferring" releasers, <strong>PAL</strong> 329 and l <b>methamphetamine</b> also dose dependently substituted for cocaine but differed in potency.
+PAL	drug	cocaine	28889212	Among the "NE preferring" releasers, <strong>PAL</strong> 329 and l methamphetamine also dose dependently substituted for <b>cocaine</b> but differed in potency.
+PAL	drug	cocaine	28889212	<strong>PAL</strong> 169 failed to substitute for <b>cocaine</b> up to a dose that disrupted responding.
+PAL	drug	amphetamine	28889212	When administered prior to cocaine, only d <b>amphetamine</b> and <strong>PAL</strong> 329 significantly shifted the cocaine dose effect function leftward indicating enhancement of cocaine's discriminative stimulus effects.
+PAL	drug	cocaine	28889212	When administered prior to <b>cocaine</b>, only d amphetamine and <strong>PAL</strong> 329 significantly shifted the <b>cocaine</b> dose effect function leftward indicating enhancement of <b>cocaine</b>'s discriminative stimulus effects.
+PAL	drug	psychedelics	26041338	The aim of this study is to investigate whether 5 HT2C receptor activation is necessary for rate decreasing effects produced in an ICSS procedure in rats by the 5 HT selective monoamine releaser fenfluramine and the non selective releasers napthylisopropylamine (<strong>PAL</strong> 287) and (+) 3,4 <b>methylenedioxymethamphetamine</b> ((+) <b>MDMA</b>).
+PAL	addiction	reward	26041338	The aim of this study is to investigate whether 5 HT2C receptor activation is necessary for rate decreasing effects produced in an <b>ICSS</b> procedure in rats by the 5 HT selective monoamine releaser fenfluramine and the non selective releasers napthylisopropylamine (<strong>PAL</strong> 287) and (+) 3,4 methylenedioxymethamphetamine ((+) MDMA).
+PAL	drug	psychedelics	26041338	Effectiveness of the 5 HT2C antagonist SB 242,084 was evaluated to block rate decreasing effects produced by (1) the 5 HT2C agonist Ro 60 0175, (2) the 5 HT selective releaser fenfluramine, and (3) the mixed action dopamine (DA)/norepinephrine (NE)/5 HT releasers <strong>PAL</strong> 287 (1.0 5.6 mg/kg) and (+) <b>MDMA</b> (1.0 3.2 mg/kg).
+PAL	drug	psychedelics	26041338	SB 242,084 blunted the rate decreasing effects and enhanced expression of rate increasing effects of <strong>PAL</strong> 287 and (+) <b>MDMA</b>.
+PAL	drug	amphetamine	25902874	The purpose of this study was to determine if <b>amphetamine</b>  and MK 801 induced impairment represent distinct models of cognitive impairment by testing their sensitivity to common antipsychotics and determine the relative contributions of D1 versus D2 receptors on performance of <strong>PAL</strong>.
+PAL	drug	amphetamine	25902874	These data suggest that <b>amphetamine</b> and MK 801 represent dissociable models of impairment in <strong>PAL</strong>, dependent on different underlying neurobiology.
+PAL	drug	nicotine	25897655	Initial daily text/telephone support, a quitting <strong>pal</strong>, vouchers for > £20.00 per month and values up to £80.00 increase the likelihood of <b>smoking</b> cessation.
+PAL	addiction	reward	25897655	<b>Incentive</b> interventions provide opportunity 'rungs' to help, including regular skilled flexible support, a <strong>pal</strong>, setting goals, monitoring and outcome verification.
+PAL	drug	cocaine	24796848	Anticocaine effects of the compound with highest selectivity to release DA/5HT versus NE (<strong>PAL</strong> 542) were tested in an assay of <b>cocaine</b> versus food choice in rhesus monkeys, and <strong>PAL</strong> 542 failed to reduce <b>cocaine</b> choice.
+PAL	drug	amphetamine	24662914	The effects of PCP, ketamine, <b>amphetamine</b>, LSD, scopolamine, and biperiden (recently proposed as an alternative to scopolamine) were then tested on animals performing the <strong>PAL</strong> task.
+PAL	drug	psychedelics	24662914	The effects of PCP, <b>ketamine</b>, amphetamine, <b>LSD</b>, scopolamine, and biperiden (recently proposed as an alternative to scopolamine) were then tested on animals performing the <strong>PAL</strong> task.
+PAL	drug	amphetamine	24662914	While all compounds influenced responding during <strong>PAL</strong>, only PCP and <b>amphetamine</b> impaired performance with minimal changes in secondary measures (response latencies, trials completed).
+PAL	drug	nicotine	24033763	The following covariates were evaluated: demographic data (age, body weight, height, sex), biological data (creatinine, urea, AST, ALT, albumin, PR, VGM, <strong>PAL</strong>, CDT, GGT), and <b>tobacco</b> consumption (number of cigarettes and Fagerstrom test).
+PAL	drug	cocaine	23768644	Effects of methcathinone and 3 Cl methcathinone (<strong>PAL</strong> 434) in <b>cocaine</b> discrimination or self administration in rhesus monkeys.
+PAL	drug	cocaine	23768644	was administered chronically (one injection every 20 min for 23 h/d) for 7–10 d. In discrimination studies, both compounds dose dependently increased <b>cocaine</b> like responding but with different potencies (<b>cocaine</b>=methcathinone ><strong>PAL</strong> 434).
+PAL	drug	cocaine	23768644	Chronic treatment with methcathinone or <strong>PAL</strong> 434 dose dependently and selectively reduced <b>cocaine</b> self administration.
+PAL	drug	cocaine	23768644	<strong>PAL</strong> 434 was about 4 fold and methcathinone about 1.6 fold more potent at decreasing <b>cocaine</b>  over food maintained responding.
+PAL	drug	nicotine	22805627	Logistic regression analysis showed that NS use was significantly associated with moderate or high physical activity level (<strong>PAL</strong>), <b>smoking</b>, gender, eating attitude, and age.
+PAL	drug	nicotine	22805627	In conclusion, NS users were more likely to be female, younger, and <b>smokers</b>; to have moderate or high <strong>PAL</strong>; and to be more prone to eating disorders than nonusers.
+PAL	drug	cocaine	21256854	The subsensitivity of lead rats to <strong>PAL</strong> 353 is consistent with a lead induced diminution of dopamine function, an effect noted earlier for the reuptake inhibitor <b>cocaine</b> (Nation et al.
+PAL	drug	alcohol	24061673	The complexation of 2 aminobenzothiazole (2abt) [A] with Ni(II) in presence of amino acids viz., glycine (gly), L alanine (ala), L valine (val) and L phenylalanine (<strong>pal</strong>) [B] in 50% (v/v) water <b>ethanol</b> mixture containing NaClO4 (0.15 M) has been studied by pH metrically at various temperatures (300, 310, 320 and 330 ± 0.1 K).
+PAL	drug	amphetamine	19766133	<b>Amphetamine</b> and <strong>PAL</strong> 353, which have relatively high selectivity for releasing dopamine vs. serotonin, increased accumbens dopamine levels and induced stimulant effects on behavior maintained by a fixed interval schedule of reinforcement.
+PAL	addiction	reward	19766133	Amphetamine and <strong>PAL</strong> 353, which have relatively high selectivity for releasing dopamine vs. serotonin, increased accumbens dopamine levels and induced stimulant effects on behavior maintained by a fixed interval schedule of <b>reinforcement</b>.
+PAL	addiction	intoxication	19497334	<b>Binge</b> drinkers recorded a significantly shorter movement time to target in the RTI, and completed fewer stages on first trial in the <strong>PAL</strong>, compared with non bingers.
+PAL	drug	cocaine	19086767	Finally, the authors discuss recently published data with <strong>PAL</strong> 287, a novel nonamphetamine DA/5 HT releasing agent that suppresses <b>cocaine</b> self administration but lacks positive reinforcing properties.
+PAL	addiction	reward	19086767	Finally, the authors discuss recently published data with <strong>PAL</strong> 287, a novel nonamphetamine DA/5 HT releasing agent that suppresses cocaine self administration but lacks positive <b>reinforcing</b> properties.
+PAL	drug	amphetamine	18772043	Finally, we discuss recently published data with <strong>PAL</strong> 287, a novel non <b>amphetamine</b> DA/5 HT releasing agent that suppresses cocaine self administration but lacks positive reinforcing properties.
+PAL	drug	cocaine	18772043	Finally, we discuss recently published data with <strong>PAL</strong> 287, a novel non amphetamine DA/5 HT releasing agent that suppresses <b>cocaine</b> self administration but lacks positive reinforcing properties.
+PAL	addiction	reward	18772043	Finally, we discuss recently published data with <strong>PAL</strong> 287, a novel non amphetamine DA/5 HT releasing agent that suppresses cocaine self administration but lacks positive <b>reinforcing</b> properties.
+PAL	drug	amphetamine	17408232	Finally, we discuss our recently published data about <strong>PAL</strong> 287 (naphthylisopropylamine), a novel non <b>amphetamine</b> DA /5 HT releasing agent that suppresses cocaine self administration but lacks positive reinforcing properties.
+PAL	drug	cocaine	17408232	Finally, we discuss our recently published data about <strong>PAL</strong> 287 (naphthylisopropylamine), a novel non amphetamine DA /5 HT releasing agent that suppresses <b>cocaine</b> self administration but lacks positive reinforcing properties.
+PAL	addiction	reward	17408232	Finally, we discuss our recently published data about <strong>PAL</strong> 287 (naphthylisopropylamine), a novel non amphetamine DA /5 HT releasing agent that suppresses cocaine self administration but lacks positive <b>reinforcing</b> properties.
+PAL	drug	amphetamine	17071819	The releasers varied along a continuum from dopamine/norepinephrine selective to serotonin selective [m fluoroamphetamine (<strong>PAL</strong> 353), <b>methamphetamine</b>, m methylamphetamine (<strong>PAL</strong> 314), 1 napthyl 2 aminopropane (<strong>PAL</strong> 287), fenfluramine].
+PAL	drug	amphetamine	17017961	As a specific example, we describe the development of <strong>PAL</strong> 287 (alpha methylnapthylethylamine), a dual DA/5 HT releasing agent that suppresses cocaine self administration in rhesus monkeys, without the adverse effects associated with older phenylethylamine 5 HT releasers (e.g., fenfluramine) and DA releasers (e.g., <b>amphetamine</b>).
+PAL	drug	cocaine	17017961	As a specific example, we describe the development of <strong>PAL</strong> 287 (alpha methylnapthylethylamine), a dual DA/5 HT releasing agent that suppresses <b>cocaine</b> self administration in rhesus monkeys, without the adverse effects associated with older phenylethylamine 5 HT releasers (e.g., fenfluramine) and DA releasers (e.g., amphetamine).
+PAL	drug	alcohol	16292660	Elicitors induced a rapid stimulation of the monolignol pathway, as confirmed by the increase in <strong>PAL</strong> (phenylalanine ammonia lyase, EC 4.1.3.5), CCR (cinnamoyl CoA reductase EC 1.2.1.44) and CAD (cinnamyl <b>alcohol</b> dehydrogenase EC 1.1.1.195) gene expression and <strong>PAL</strong> activity.
+PAL	drug	amphetamine	15761112	<strong>PAL</strong> 287 induced substantially less locomotor stimulation than (+) <b>amphetamine</b>, a drug that increases only extracellular DA.
+PAL	drug	amphetamine	15761112	Administration of high dose (+) <b>methamphetamine</b> or (+/ ) 3,4 methylenedioxymethamphetamine to rats produced long lasting depletion of cortical 5 HT, whereas <strong>PAL</strong> 287 (18 mg/kg i.p.
+PAL	drug	psychedelics	15761112	Administration of high dose (+) methamphetamine or (+/ ) 3,4 <b>methylenedioxymethamphetamine</b> to rats produced long lasting depletion of cortical 5 HT, whereas <strong>PAL</strong> 287 (18 mg/kg i.p.
+PAL	drug	cocaine	15761112	<strong>PAL</strong> 287 displayed little or no reinforcing properties in rhesus monkeys trained to self administer <b>cocaine</b>, yet <strong>PAL</strong> 287 produced a dose dependent decrease in responding for <b>cocaine</b> when infused at a dose of 1.0 mg/kg/h.
+PAL	addiction	reward	15761112	<strong>PAL</strong> 287 displayed little or no <b>reinforcing</b> properties in rhesus monkeys trained to self administer cocaine, yet <strong>PAL</strong> 287 produced a dose dependent decrease in responding for cocaine when infused at a dose of 1.0 mg/kg/h.
+PAL	addiction	dependence	15761112	Collectively, the findings reported here demonstrate that nonamphetamine monoamine releasing agents such as <strong>PAL</strong> 287 might be promising candidate medications for the treatment of stimulant <b>dependence</b>.
+P4HTM	drug	alcohol	30263368	The emulsion comprised tocopherol stripped soybean oil (40 g), citrate buffer (60 g, <strong>pH 4</strong>.0), xanthan gum (35mg), and FeSO4 (0.5mg) with 80% <b>ethanol</b> extracts of rosemary (Rosmarinus officinalis), basil (Ocimum basilicum), peppermint (Mentha piperita), thyme (Thymus vulgaris), or oregano (Origanum vulgare).
+P4HTM	drug	alcohol	26318575	Silanization was carried out using an experimental silane blend (0.5 vol% bis 1,2 (triethoxysilyl)ethane+1.0 vol% 3 acryloxypropyltrimethoxysilane in <b>ethanol</b>, at <strong>pH 4</strong>.0).
+P4HTM	drug	alcohol	25656650	The second order rate constants (k2) for the reaction of CAP toward 2,2 diphenyl 1 picrylhydrazyl (DPPH) and galvinoxyl have been measured in methanol, <b>ethanol</b>, 2 propanol/water (5:1, v/v), and aqueous micellar suspensions containing 5% Triton X 100 (<strong>pH 4</strong>.0 to 10.0), respectively.
+P4HTM	drug	alcohol	24780565	Both proteins showed qualitatively different aggregation behavior and structure changes by <b>ethanol</b> at <strong>pH 4</strong>.0 and 7.0, at which BSA has opposite charges and RNase A has different degree of net positive charges.
+P4HTM	drug	alcohol	16471837	The voltammograms recorded in water <b>alcohol</b> media show, in comparison to water, the following effects: an increase of the dissolution currents measured at pH>2 and an opposite effect at pH<2; a distortion of the curve, with a relative increase of the characteristic currents in the region of low applied potentials, indicating easier dissolution of the "wet" oxide forming under those conditions; a shift of the maximum of the current pH curves from about pH 3 in water to about <strong>pH 4</strong> in 50% <b>ethanol</b> v/v.
+P4HTM	drug	alcohol	14718651	In the presence of 90% (v/v) <b>ethanol</b>, the fully reduced HEWL adopts beta sheet secondary structure at <strong>pH 4</strong>.5 and 5.0, and an alpha to beta transition is observed at <strong>pH 4</strong>.0.
+P4HTM	drug	opioid	11516497	<b>Buprenorphine</b> HCl (1 mg/ml) in citrate buffer (<strong>pH 4</strong>.0) was delivered in vitro across human epidermis via iontophoresis using a current density of 0.5 mA/cm(2) and silver silver chloride electrodes.
+P4HTM	drug	alcohol	9542117	Urine (0.1 ml) was diluted 10 fold with phosphate buffered saline, pH 7.4 (PBS), loaded onto a solid phase immunoextraction column and washed with 15 ml PBS followed by elution with 2 ml of elution buffer (40% <b>ethanol</b> in PBS, <strong>pH 4</strong>).
+P4HTM	drug	alcohol	7548012	Furthermore, at <strong>pH 4</strong>.5, the physiological pH of Phanerochaete chrysosporium, LiPH2 oxidizes Mn2+ at a much faster rate (25 times) than veratryl <b>alcohol</b> (VA).
+P4HTM	drug	alcohol	18623138	Sodium caseinate (10% w/v) was hydrolyzed by Novo trypsin (commercial grade) at 50 degrees C for 2 h and CPP were purified from the acid clarified hydrolysate by a single step selective precipitation procedure involving Ca(2+) (20 mol/mol casein) and <b>ethanol</b> (50% v/v) at <strong>pH 4</strong>.6 or 8.0.
+P4HTM	addiction	reward	18623138	Sodium caseinate (10% w/v) was hydrolyzed by Novo trypsin (commercial grade) at 50 degrees C for 2 h and <b>CPP</b> were purified from the acid clarified hydrolysate by a single step selective precipitation procedure involving Ca(2+) (20 mol/mol casein) and ethanol (50% v/v) at <strong>pH 4</strong>.6 or 8.0.
+P4HTM	drug	alcohol	18623138	However, in order to prepare casein phosphopeptides predominantly containing the cluster sequence  Ser(P) Ser(P) Ser(P) Glu Glu , the single step selective precipitation with Ca(2+)/<b>ethanol</b> should be performed at <strong>pH 4</strong>.6 rather than pH 8.0.
+P4HTM	drug	alcohol	8180177	In the presence of 100 microM H2O2, veratryl <b>alcohol</b> (VA) significantly enhanced cytochrome c oxidation at pH 3.0 but had little effect above <strong>pH 4</strong>.5.
+OXT	drug	benzodiazepine	32385158	Therefore, the rationale of this ultra high field functional MRI (fMRI) study was to test <strong>OXT</strong> against the clinical comparator <b>lorazepam</b> (LZP) with regard to their neuromodulatory effects on local and network responses to fear related stimuli.
+OXT	addiction	reward	32142721	The neuropeptide oxytocin (<strong>OXT</strong>) plays a key role in adaptive processes associated with <b>reward</b>, tolerance, memory and stress responses.
+OXT	drug	alcohol	32142721	Through interactions with brain reward and stress systems, <strong>OXT</strong> is known to play a role in several neuropsychiatric disorders, particularly those that involve altered social integration, such as <b>alcohol</b> and drug addiction (Heilig et al., 2016).
+OXT	addiction	addiction	32142721	Through interactions with brain reward and stress systems, <strong>OXT</strong> is known to play a role in several neuropsychiatric disorders, particularly those that involve altered social integration, such as alcohol and drug <b>addiction</b> (Heilig et al., 2016).
+OXT	addiction	reward	32142721	Through interactions with brain <b>reward</b> and stress systems, <strong>OXT</strong> is known to play a role in several neuropsychiatric disorders, particularly those that involve altered social integration, such as alcohol and drug addiction (Heilig et al., 2016).
+OXT	drug	alcohol	32142721	Accumulating preclinical evidence suggests that administration of <strong>OXT</strong> influences the development of tolerance, sensitization and withdrawal symptoms, and modulates numerous <b>alcohol</b>/drug seeking and <b>alcohol</b>/drug taking behaviors.
+OXT	addiction	relapse	32142721	Accumulating preclinical evidence suggests that administration of <strong>OXT</strong> influences the development of tolerance, sensitization and withdrawal symptoms, and modulates numerous alcohol/drug <b>seeking</b> and alcohol/drug taking behaviors.
+OXT	addiction	sensitization	32142721	Accumulating preclinical evidence suggests that administration of <strong>OXT</strong> influences the development of tolerance, <b>sensitization</b> and withdrawal symptoms, and modulates numerous alcohol/drug seeking and alcohol/drug taking behaviors.
+OXT	addiction	withdrawal	32142721	Accumulating preclinical evidence suggests that administration of <strong>OXT</strong> influences the development of tolerance, sensitization and <b>withdrawal</b> symptoms, and modulates numerous alcohol/drug seeking and alcohol/drug taking behaviors.
+OXT	drug	alcohol	32142721	Further, there is some evidence to suggest that <strong>OXT</strong> may help to reverse neuroadaptations that occur as a result of chronic <b>alcohol</b> or drug exposure.
+OXT	drug	alcohol	32142721	This review summarizes the preclinical and clinical literature on the effects of <strong>OXT</strong> administration on <b>alcohol</b>  and drug related behaviors.
+OXT	addiction	addiction	32142721	In addition, we discuss <strong>OXT</strong> interactions with the hypothalamic pituitaryadrenal axis and multiple neurotransmitter systems within <b>addiction</b> circuitry.
+OXT	drug	opioid	31609135	Conclusion: We propose the inclusion of <strong>OXT</strong> and OXTR alterations in the enhancement of <b>morphine</b> induced CPP and addiction vulnerability following FR.
+OXT	addiction	addiction	31609135	Conclusion: We propose the inclusion of <strong>OXT</strong> and OXTR alterations in the enhancement of morphine induced CPP and <b>addiction</b> vulnerability following FR.
+OXT	addiction	reward	31609135	Conclusion: We propose the inclusion of <strong>OXT</strong> and OXTR alterations in the enhancement of morphine induced <b>CPP</b> and addiction vulnerability following FR.
+OXT	drug	alcohol	31339663	For stress genes, nPE1 /  had lowered basal <strong>Oxt</strong> (oxytocin) and Avp (arginine vasopressin) that were restored by low <b>alcohol</b> intake to basal levels of nPE1+/+ .
+OXT	drug	alcohol	31339663	In nPE1+/+ , excessive <b>alcohol</b> intake decreased <strong>Oxt</strong> and Avpi1 (AVP induced protein1).
+OXT	drug	alcohol	30923836	The neuropeptide oxytocin (<strong>OXT</strong>) has emerged as a potential therapeutic intervention in the treatment of both <b>alcohol</b> use disorder (AUD) and stress related psychiatric illnesses.
+OXT	drug	alcohol	30923836	<strong>OXT</strong> treatment on <b>alcohol</b> relapse like behavior in male and female mice.
+OXT	addiction	relapse	30923836	<strong>OXT</strong> treatment on alcohol <b>relapse</b> like behavior in male and female mice.
+OXT	drug	alcohol	30923836	<strong>OXT</strong> attenuated <b>alcohol</b> seeking behavior in a dose related manner in male and female mice in response to acute challenge with a predator odor.
+OXT	addiction	relapse	30923836	<strong>OXT</strong> attenuated alcohol <b>seeking</b> behavior in a dose related manner in male and female mice in response to acute challenge with a predator odor.
+OXT	drug	alcohol	30923836	Additionally, <strong>OXT</strong> administration produced a similar decrease in <b>alcohol</b> relapse like behavior triggered by the pharmacological stressor yohimbine in both sexes.
+OXT	addiction	relapse	30923836	Additionally, <strong>OXT</strong> administration produced a similar decrease in alcohol <b>relapse</b> like behavior triggered by the pharmacological stressor yohimbine in both sexes.
+OXT	drug	cannabinoid	30521833	The hormone oxytocin (<strong>OXT</strong>) modulates stress and may have therapeutic efficacy for substance use disorders, but few studies have examined <strong>OXT</strong> in <b>cannabis</b> users.
+OXT	drug	cannabinoid	30521833	oxytocin (<strong>OXT</strong>; 40 IU) administration on stress reactivity (using the Trier Social Stress Test; TSST) and <b>cannabis</b> (5.6% <b>THC</b>) self administration was assessed in recreational <b>cannabis</b> using men (n = 31) and women (n = 32) relative to i.n.
+OXT	drug	cannabinoid	30521833	These results suggest that <strong>OXT</strong> administration may lead to greater stress reactivity in recreational <b>cannabis</b> users, particularly women, and support growing evidence that sex differences should be carefully considered when examining the therapeutic potential of <strong>OXT</strong>.
+OXT	drug	cocaine	30448423	<strong>OXT</strong> plays a role in stress response and in drug reward, but to date no studies have evaluated its implication in the long lasting increase of the motivational effects of <b>cocaine</b> induced by repeated social defeat (RSD).
+OXT	addiction	reward	30448423	<strong>OXT</strong> plays a role in stress response and in drug <b>reward</b>, but to date no studies have evaluated its implication in the long lasting increase of the motivational effects of cocaine induced by repeated social defeat (RSD).
+OXT	drug	cocaine	30448423	Moreover, <strong>OXT</strong> prevents RSD induced increases in the motivational effects of <b>cocaine</b>.
+OXT	drug	cocaine	30448423	Administration of <strong>OXT</strong> before each social defeat blocked the social defeat induced increment in the conditioned rewarding effects of <b>cocaine</b> in the CPP, favored the extinction of <b>cocaine</b> associated memories in both the CPP and SA, and decreased reinstatement of <b>cocaine</b> seeking behavior in the SA.
+OXT	addiction	relapse	30448423	Administration of <strong>OXT</strong> before each social defeat blocked the social defeat induced increment in the conditioned rewarding effects of cocaine in the CPP, favored the extinction of cocaine associated memories in both the CPP and SA, and decreased <b>reinstatement</b> of cocaine <b>seeking</b> behavior in the SA.
+OXT	addiction	reward	30448423	Administration of <strong>OXT</strong> before each social defeat blocked the social defeat induced increment in the conditioned rewarding effects of cocaine in the <b>CPP</b>, favored the extinction of cocaine associated memories in both the <b>CPP</b> and SA, and decreased reinstatement of cocaine seeking behavior in the SA.
+OXT	drug	opioid	29899398	Touch activates <b>opioids</b> (OP) and oxytocin (<strong>OXT</strong>), two neuromodulators involved in affiliative behaviors and social bonding.
+OXT	addiction	reward	29899398	We examined whether touch serves as an unconditioned <b>reward</b> in affective conditioning of human faces, a basic process in social bonding, and whether this process is mediated by variation in mu OP (OPRM1) and <strong>OXT</strong> (rs53576) receptor genes.
+OXT	drug	cocaine	29671014	To investigate a relationship between <strong>OXT</strong>, sex, and <b>cocaine</b> seeking, we examined Fos on ED1 in <strong>OXT</strong> neurons of paraventricular (PVN) and supraoptic nuclei (SON) compared to homecage (<b>cocaine</b> experienced) or naïve male and female rats.
+OXT	addiction	relapse	29671014	To investigate a relationship between <strong>OXT</strong>, sex, and cocaine <b>seeking</b>, we examined Fos on ED1 in <strong>OXT</strong> neurons of paraventricular (PVN) and supraoptic nuclei (SON) compared to homecage (cocaine experienced) or naïve male and female rats.
+OXT	addiction	relapse	29671014	We also administered <strong>OXT</strong> 30 min prior to ED1 testing or cued <b>reinstatement</b> testing.
+OXT	addiction	withdrawal	29671014	<strong>OXT</strong> neurons had decreased activity (as reflected by Fos protein) in PVN and SON on <b>withdrawal</b> day 1 (homecage) compared to naïve rats.
+OXT	drug	cocaine	29671014	Fos in <strong>OXT</strong> neurons was further decreased on ED1, compared to homecage controls, in both males and females even though in SON, <b>cocaine</b> exposure increased the number of <strong>OXT</strong> expressing neurons.
+OXT	drug	cocaine	29671014	In addition, systemically administered <strong>OXT</strong> reduced <b>cocaine</b> seeking during ED1 and cue induced reinstatement of <b>cocaine</b> seeking but delayed extinction, similarly among male and female rats.
+OXT	addiction	relapse	29671014	In addition, systemically administered <strong>OXT</strong> reduced cocaine <b>seeking</b> during ED1 and cue induced <b>reinstatement</b> of cocaine <b>seeking</b> but delayed extinction, similarly among male and female rats.
+OXT	drug	cocaine	29671014	These data indicate that <strong>OXT</strong> neurons in PVN and SON may be involved in <b>cocaine</b> seeking during ED1 and support <strong>OXT</strong> as a possible therapeutic to decrease <b>cocaine</b> seeking during initial abstinence and in response to <b>cocaine</b> associated cues.
+OXT	addiction	relapse	29671014	These data indicate that <strong>OXT</strong> neurons in PVN and SON may be involved in cocaine <b>seeking</b> during ED1 and support <strong>OXT</strong> as a possible therapeutic to decrease cocaine <b>seeking</b> during initial abstinence and in response to cocaine associated cues.
+OXT	drug	alcohol	29040351	The associations between <strong>OXT</strong> genotype, social support and psychological health were analyzed in data from 269 adults diagnosed with DSM IV <b>alcohol</b> dependence (25% female) admitted into residential treatment programs and outpatient centers in Warsaw, Poland.
+OXT	addiction	dependence	29040351	The associations between <strong>OXT</strong> genotype, social support and psychological health were analyzed in data from 269 adults diagnosed with DSM IV alcohol <b>dependence</b> (25% female) admitted into residential treatment programs and outpatient centers in Warsaw, Poland.
+OXT	drug	alcohol	26810371	In this context, the neuropeptide oxytocin (<strong>OXT</strong>) has emerged as a promising potential treatment option for a number of substance use disorders, including <b>alcoholism</b>.
+OXT	addiction	relapse	26810371	The utility of <strong>OXT</strong> in reducing consumption of and <b>craving</b> for a wide range of substances may lie in its ability to modulate drug induced neurochemical effects within the mesolimbic dopamine pathway.
+OXT	addiction	relapse	26700240	After extinction training, rats were injected with 1 mg/kg, ip oxytocin (<strong>OXT</strong>) or saline 30 min before a cue induced <b>reinstatement</b> test followed by re extinction and a TMT induced <b>reinstatement</b> test.
+OXT	drug	amphetamine	26700240	In Experiment 2, TMT pre exposure was followed by 10 days of 1 mg/kg <strong>OXT</strong> or saline injections before <b>METH</b> self administration, extinction, and a TMT induced reinstatement test.
+OXT	addiction	relapse	26700240	In Experiment 2, TMT pre exposure was followed by 10 days of 1 mg/kg <strong>OXT</strong> or saline injections before METH self administration, extinction, and a TMT induced <b>reinstatement</b> test.
+OXT	drug	amphetamine	26700240	A single injection of <strong>OXT</strong> 30 min before reinstatement suppressed <b>METH</b> seeking in both saline  and TMT pre exposed rats.
+OXT	addiction	relapse	26700240	A single injection of <strong>OXT</strong> 30 min before <b>reinstatement</b> suppressed METH <b>seeking</b> in both saline  and TMT pre exposed rats.
+OXT	drug	amphetamine	26700240	<strong>OXT</strong> injections for 10 days prior to <b>METH</b> self administration blocked only the stress induced exacerbation of drug seeking in TMT pre exposed rats.
+OXT	addiction	relapse	26700240	<strong>OXT</strong> injections for 10 days prior to METH self administration blocked only the stress induced exacerbation of drug <b>seeking</b> in TMT pre exposed rats.
+OXT	drug	alcohol	26282397	Because oxytocin (<strong>OXT</strong>) and vasopressin (AVP) contribute to rewarding social behavior, the present study utilized a genetic strategy to determine whether <strong>OXT</strong> and AVP receptors (OXTR, AVPR1a) are essential for female mice to demonstrate a conditioned social preference for <b>ethanol</b>.
+OXT	drug	opioid	25225634	To better understand the <b>opioid</b> <strong>OXT</strong> interplay in the central nervous system, we first determined the expression of the oxytocin receptor (OXTR) in the brain of WT C57BL6/J mice by quantitative autoradiography; we then evaluated OXTR regional alterations in Oprm1 ( / ) mice.
+OXT	drug	opioid	25225634	Taken together, our results provide evidence of an interaction between <strong>OXT</strong> and <b>opioids</b> in socially relevant brain areas and in the modulation of social behavior.
+OXT	drug	cocaine	23880214	Oxytocin (<strong>Oxt</strong>) is critical in regulating social behaviors and central levels are disrupted following acute and chronic <b>cocaine</b> (CC) treatment in postpartum rat dams, coincident with deficits in maternal care.
+OXT	addiction	addiction	23880214	The relevance of disrupted <strong>Oxt</strong> to intergenerational transmission of <b>addiction</b> is briefly discussed.
+OXT	drug	cannabinoid	22917880	Recently, it has been also hypothesize that <strong>OXT</strong>, increasing intracellular concentration of calcium, could regulate the production of mediators, like <b>endocannabinoids</b> (eCB).
+OXT	addiction	withdrawal	22917880	Intracerebroventricular (icv) administration of <strong>OXT</strong>, but neither intraperitoneal nor intraplantar route, induces an antihyperalgesic effect increasing paw <b>withdrawal</b> latency to mechanical or thermal stimuli.
+OXT	drug	cannabinoid	22917880	In conclusion, our experiments suggest that central administration of <strong>OXT</strong> reduces hyperalgesia induced by intraplantar injection of carrageenan, and this effect may work via <b>cannabinoid</b> and opioid systems.
+OXT	drug	opioid	22917880	In conclusion, our experiments suggest that central administration of <strong>OXT</strong> reduces hyperalgesia induced by intraplantar injection of carrageenan, and this effect may work via cannabinoid and <b>opioid</b> systems.
+OXT	drug	alcohol	11755902	Using conventional histological techniques, immunohistochemistry and in situ hybridization, the structural organization and the synthesis and expression of vasopressin (VP) and oxytocin (<strong>OXT</strong>) in the magnocellular component of the PVN were studied under normal conditions and following chronic <b>ethanol</b> treatment (6 or 10 months) and withdrawal (4 months after 6 months of <b>alcohol</b> intake).
+OXT	addiction	withdrawal	11755902	Using conventional histological techniques, immunohistochemistry and in situ hybridization, the structural organization and the synthesis and expression of vasopressin (VP) and oxytocin (<strong>OXT</strong>) in the magnocellular component of the PVN were studied under normal conditions and following chronic ethanol treatment (6 or 10 months) and <b>withdrawal</b> (4 months after 6 months of alcohol intake).
+OXT	drug	alcohol	11755902	After <b>ethanol</b> treatment, there was a marked decrease in the number of VP  and <strong>OXT</strong> immunoreactive magnocellular neurons that was attributable to cell death.
+OXT	addiction	withdrawal	11755902	<b>Withdrawal</b> did not alter the number of VP  and <strong>OXT</strong> producing neurons or the gene expression of these peptides.
+OXT	drug	alcohol	11755902	These results substantiate the view that after prolonged <b>ethanol</b> exposure numerous neurons of the hypothalamic magnocellular system degenerate, but the mRNA levels of VP and <strong>OXT</strong> are not decreased due to compensatory changes undergone by the surviving neurons.
+OXT	drug	opioid	9924746	<strong>OXT</strong> acts within the CNS and has been shown to inhibit the development of tolerance to <b>morphine</b>, and to attenuate various symptoms of <b>morphine</b> withdrawal in mice.
+OXT	addiction	withdrawal	9924746	<strong>OXT</strong> acts within the CNS and has been shown to inhibit the development of tolerance to morphine, and to attenuate various symptoms of morphine <b>withdrawal</b> in mice.
+OXT	drug	opioid	9924746	In rats, intravenous self administration of <b>heroin</b> was potently decreased by <strong>OXT</strong> treatment.
+OXT	drug	cocaine	9924746	In relation to <b>cocaine</b> abuse, <strong>OXT</strong> dose dependently decreased <b>cocaine</b> induced hyperlocomotion and stereotyped grooming behavior.
+OXT	drug	cocaine	9924746	Following chronic <b>cocaine</b> treatment, the behavioral tolerance to the sniffing inducing effect of <b>cocaine</b> was markedly inhibited by <strong>OXT</strong>.
+OXT	drug	cocaine	9924746	Behavioral sensitization to <b>cocaine</b>, on the other hand, was facilitated by <strong>OXT</strong>.
+OXT	addiction	sensitization	9924746	Behavioral <b>sensitization</b> to cocaine, on the other hand, was facilitated by <strong>OXT</strong>.
+OXT	drug	cocaine	9924746	<strong>OXT</strong> receptors in the CNS  mainly those located in limbic and basal forebrain structures  are responsible for mediating various effects of <strong>OXT</strong> in the opiate  and <b>cocaine</b> addicted organism.
+OXT	drug	alcohol	9924746	hypothermia inducing effect of <b>ethanol</b>) also was inhibited by <strong>OXT</strong>.
+OXT	drug	opioid	7700499	The secretion of oxytocin (<strong>OXT</strong>) from the neurohypophysis is modulated by the actions of <b>opioids</b> acting via kappa receptors.
+OXT	drug	opioid	7700499	The vasopressin (AVP) containing nerve terminals in the neurohypophysis contain the kappa <b>opioid</b> agonist dynorphin, but endogenous <b>opioid</b> restraint of <strong>OXT</strong> secretion is observed even when AVP release is not activated, suggesting that another source of <b>opioids</b> is responsible for modulating <strong>OXT</strong> secretion.
+OXT	drug	opioid	7700499	However, depletion of Met Enk was also observed following <b>naloxone</b> precipitated <b>opioid</b> withdrawal accompanying selective hypersecretion of <strong>OXT</strong>, suggesting co secretion of <strong>OXT</strong> and Met Enk.
+OXT	addiction	withdrawal	7700499	However, depletion of Met Enk was also observed following naloxone precipitated opioid <b>withdrawal</b> accompanying selective hypersecretion of <strong>OXT</strong>, suggesting co secretion of <strong>OXT</strong> and Met Enk.
+OXT	addiction	dependence	9210215	Because adaptation and learning are likely to be involved in the neural events leading to drug tolerance and <b>dependence</b>, the question logically arose whether <strong>OXT</strong> is able to influence the development of tolerance of and <b>dependence</b> on abused drugs.
+OXT	drug	opioid	9210215	In this review, we summarize our results on the effects of <strong>OXT</strong> on opiate (including <b>morphine</b>, <b>heroin</b>, and the endogenous opiates beta endorphin and enkephalin) tolerance and dependence, <b>heroin</b> self administration, psychostimulant induced behavioral changes, and behavioral tolerance and sensitization.
+OXT	addiction	dependence	9210215	In this review, we summarize our results on the effects of <strong>OXT</strong> on opiate (including morphine, heroin, and the endogenous opiates beta endorphin and enkephalin) tolerance and <b>dependence</b>, heroin self administration, psychostimulant induced behavioral changes, and behavioral tolerance and sensitization.
+OXT	addiction	sensitization	9210215	In this review, we summarize our results on the effects of <strong>OXT</strong> on opiate (including morphine, heroin, and the endogenous opiates beta endorphin and enkephalin) tolerance and dependence, heroin self administration, psychostimulant induced behavioral changes, and behavioral tolerance and <b>sensitization</b>.
+OXT	drug	opioid	9210215	<strong>OXT</strong> inhibited the development of tolerance to <b>morphine</b>, <b>heroin</b>, beta endorphin, and enkephalin, <strong>OXT</strong> also inhibited the development of cross tolerance between the predominantly mu agonist <b>heroin</b> and the predominantly delta agonist enkephalin in mice.
+OXT	drug	opioid	9210215	<b>Naloxone</b> precipitated <b>morphine</b> withdrawal syndrome was also attenuated by <strong>OXT</strong>.
+OXT	addiction	withdrawal	9210215	Naloxone precipitated morphine <b>withdrawal</b> syndrome was also attenuated by <strong>OXT</strong>.
+OXT	drug	opioid	9210215	<b>Heroin</b> self administration was decreased by <strong>OXT</strong> administration in <b>heroin</b> tolerant rats.
+OXT	drug	cocaine	9210215	<strong>OXT</strong> inhibited <b>cocaine</b> induced exploratory activity, locomotor hyperactivity, and stereotyped behavior in rats and in mice.
+OXT	drug	cocaine	9210215	Behavioral tolerance to <b>cocaine</b> was also attenuated by <strong>OXT</strong>.
+OXT	drug	cocaine	9210215	On the contrary, <strong>OXT</strong> stimulated the development of behavioral sensitization to <b>cocaine</b>.
+OXT	addiction	sensitization	9210215	On the contrary, <strong>OXT</strong> stimulated the development of behavioral <b>sensitization</b> to cocaine.
+OXT	drug	amphetamine	9210215	<strong>OXT</strong> did not alter the stereotyped behavior induced by <b>amphetamine</b>.
+OXT	drug	cocaine	9210215	Intracerebro ventricular (ICV) and intracerebral (IC) administration of an <strong>OXT</strong> receptor antagonist inhibited the effects of peripherally administered <strong>OXT</strong> on morphine tolerance, heroin self administration, and <b>cocaine</b> induced sniffing behavior.
+OXT	drug	opioid	9210215	Intracerebro ventricular (ICV) and intracerebral (IC) administration of an <strong>OXT</strong> receptor antagonist inhibited the effects of peripherally administered <strong>OXT</strong> on <b>morphine</b> tolerance, <b>heroin</b> self administration, and cocaine induced sniffing behavior.
+OXT	drug	cocaine	9210215	Local IC microinjection of <strong>OXT</strong> in physiological doses into the posterior olfactory nucleus, tuberculum olfactorium, nucleus accumbens, central amygdaloid nucleus, and the hippocampus inhibited the development of tolerance to and dependence on morphine as well as <b>cocaine</b> induced sniffing behavior and tolerance to <b>cocaine</b>.
+OXT	drug	opioid	9210215	Local IC microinjection of <strong>OXT</strong> in physiological doses into the posterior olfactory nucleus, tuberculum olfactorium, nucleus accumbens, central amygdaloid nucleus, and the hippocampus inhibited the development of tolerance to and dependence on <b>morphine</b> as well as cocaine induced sniffing behavior and tolerance to cocaine.
+OXT	addiction	dependence	9210215	Local IC microinjection of <strong>OXT</strong> in physiological doses into the posterior olfactory nucleus, tuberculum olfactorium, nucleus accumbens, central amygdaloid nucleus, and the hippocampus inhibited the development of tolerance to and <b>dependence</b> on morphine as well as cocaine induced sniffing behavior and tolerance to cocaine.
+OXT	drug	opioid	9210215	The physiological role of endogenous <strong>OXT</strong> in acute <b>morphine</b> tolerance has also been demonstrated, since <strong>OXT</strong> antiserum (ICV) and <strong>OXT</strong> receptor antagonist (injected into the basal forebrain structures) potentiated the development of <b>morphine</b> tolerance.
+OXT	drug	cocaine	9210215	In light of this information, it appears that <strong>OXT</strong> inhibits the development of opiate tolerance, dependence, and self administration as well as the acute behavioral actions of and chronic tolerance to <b>cocaine</b>.
+OXT	addiction	dependence	9210215	In light of this information, it appears that <strong>OXT</strong> inhibits the development of opiate tolerance, <b>dependence</b>, and self administration as well as the acute behavioral actions of and chronic tolerance to cocaine.
+OXT	addiction	addiction	9210215	Therefore, <strong>OXT</strong> may act as a neuromodulator on dopaminergic neurotransmission in limbic basal forebrain structures to regulate adaptive CNS processes leading to drug <b>addiction</b>.
+OXT	drug	cocaine	1438486	The effects of repeated administration of the neurohypophyseal hormones oxytocin (<strong>OXT</strong>) and arginine8 vasopressin (AVP) on the development of behavioral sensitization induced by subchronic treatment with <b>cocaine</b> were investigated in mice.
+OXT	addiction	sensitization	1438486	The effects of repeated administration of the neurohypophyseal hormones oxytocin (<strong>OXT</strong>) and arginine8 vasopressin (AVP) on the development of behavioral <b>sensitization</b> induced by subchronic treatment with cocaine were investigated in mice.
+OXT	drug	cocaine	1438486	Repeated treatment of <strong>OXT</strong> and AVP did not modify the locomotor stimulatory effect of the challenge dose of <b>cocaine</b> in <b>cocaine</b> naive control animals.
+OXT	drug	cocaine	1438486	<strong>OXT</strong> in a dose of 0.5 microgram (sc) augmented the <b>cocaine</b> induced behavioral sensitization.
+OXT	addiction	sensitization	1438486	<strong>OXT</strong> in a dose of 0.5 microgram (sc) augmented the cocaine induced behavioral <b>sensitization</b>.
+OXT	addiction	dependence	2806642	The effect of oxytocin (<strong>OXT</strong>) administration into the brain ventricles on the process of narcotic <b>dependence</b> formation was studied before and following hippocampal lesion.
+OXT	addiction	dependence	2806642	<strong>OXT</strong> was found to inhibit the process of narcotic <b>dependence</b> formation.
+OXT	drug	opioid	3376556	The paper deals with the effect of oxytocin (<strong>OXT</strong>) and its antagonist  oxytocin antiserum (ANT) microinjected in the ventral hippocampus  on learning of <b>heroin</b> intravenous self administration in rats.
+OXT	drug	opioid	3376556	<strong>OXT</strong> weakened the processes of <b>heroin</b> self administration, while ANT in contrast improved the learning.
+OXT	drug	opioid	3041139	The systemic injection of oxytocin (<strong>OXT</strong>) decreases the self administration of <b>heroin</b> in <b>heroin</b> tolerant rats.
+OXT	drug	opioid	3041139	In <b>heroin</b> tolerant rats, the microinjection of <strong>OXT</strong> (2 ng) into the anterodorsal part of the nucleus accumbens or into the ventral hippocampus disrupted the self administration of <b>heroin</b>.
+OXT	drug	opioid	3041139	The administration of N alpha acetyl (2 0 methyltyrosine) oxytocin (ACME <strong>OXT</strong>), an inhibitor of oxytocin receptors, prevented the disruptive effect of intrahippocampal <strong>OXT</strong> injections on <b>heroin</b> self administration.
+OXT	drug	opioid	3041139	It is concluded that limbic mesolimbic brain structures have an essential role in the expression of the disruptive action of <strong>OXT</strong> on <b>heroin</b> self administration.
+OXT	drug	alcohol	3593487	The effect of oxytocin (<strong>OXT</strong>) and vasopressin (VP) on <b>alcohol</b> withdrawal was investigated.
+OXT	addiction	withdrawal	3593487	The effect of oxytocin (<strong>OXT</strong>) and vasopressin (VP) on alcohol <b>withdrawal</b> was investigated.
+OXT	addiction	withdrawal	3593487	<strong>OXT</strong> treated mice displayed milder <b>withdrawal</b> symptoms in response to increasing doses of peptide (0.2 2.0 IU).
+OXT	drug	opioid	3556459	Acute <b>morphine</b> treatment caused a <b>naloxone</b> reversible increase in <strong>OXT</strong> content in all three brain regions.
+OXT	drug	opioid	3556459	In mice rendered tolerant to/dependent on <b>morphine</b> with subcutaneous <b>morphine</b> pellets, the <strong>OXT</strong> levels in the limbic brain structures were in the control range (basal forebrain and amygdala) or even decreased (hippocampus).
+OXT	drug	opioid	3556459	<b>Naloxone</b> precipitated withdrawal syndrome in the tolerant/dependent animals resulted in abrupt increases in the <strong>OXT</strong> and AVP levels of the hippocampus and in the <strong>OXT</strong> content of the basal forebrain structures.
+OXT	addiction	withdrawal	3556459	Naloxone precipitated <b>withdrawal</b> syndrome in the tolerant/dependent animals resulted in abrupt increases in the <strong>OXT</strong> and AVP levels of the hippocampus and in the <strong>OXT</strong> content of the basal forebrain structures.
+OXT	drug	opioid	4058258	Subcutaneous injection of oxytocin (<strong>OXT</strong> (1 9)) and of its behaviorally active fragments desglycinamide9 oxytocin (<strong>OXT</strong> (1 8)) and [pGlu4,Cyt6] oxytocin (4 8) (<strong>OXT</strong> (4 8)) decreased the amount of <b>heroin</b> self injected.
+OXT	drug	opioid	2991800	The effects of oxytocin (<strong>OXT</strong>) and of dipeptides derived from the C terminal portion of oxytocin (Z prolyl leucine and Z prolyl D leucine) on the development of acute and chronic tolerance to, and dependence on <b>morphine</b> were tested in the mouse.
+OXT	addiction	dependence	2991800	The effects of oxytocin (<strong>OXT</strong>) and of dipeptides derived from the C terminal portion of oxytocin (Z prolyl leucine and Z prolyl D leucine) on the development of acute and chronic tolerance to, and <b>dependence</b> on morphine were tested in the mouse.
+OXT	drug	opioid	4038622	Acute <b>morphine</b> treatment increased h <strong>OXT</strong>, which effect was reversed by <b>naloxone</b>.
+OXT	drug	opioid	4038622	In mice rendered tolerant to and dependent on <b>morphine</b> h <strong>OXT</strong> was lower than in placebo pellet implanted control mice.
+OXT	drug	opioid	4038622	In the tolerant/dependent animals <b>naloxone</b> resulted in precipitated withdrawal syndrome which was associated with a slight increase in h <strong>OXT</strong>.
+OXT	addiction	withdrawal	4038622	In the tolerant/dependent animals naloxone resulted in precipitated <b>withdrawal</b> syndrome which was associated with a slight increase in h <strong>OXT</strong>.
+OXT	drug	opioid	4038622	The data indicate that h <strong>OXT</strong> is affected by acute <b>morphine</b> treatment and by <b>morphine</b> tolerance/dependence and raises the possibility that h <strong>OXT</strong> participates in the adaptive response of the organism towards narcotic drugs.
+OXT	addiction	dependence	4038622	The data indicate that h <strong>OXT</strong> is affected by acute morphine treatment and by morphine tolerance/<b>dependence</b> and raises the possibility that h <strong>OXT</strong> participates in the adaptive response of the organism towards narcotic drugs.
+OXT	drug	opioid	6542796	Recent data indicate that the neurohypophyseal hormone oxytocin (<strong>OXT</strong>) and Z prolyl D leucine (Z Pro D Leu), a synthetic dipeptide derived from the C terminal part of <strong>OXT</strong>, attenuate the development of tolerance to and dependence on <b>morphine</b> in the mouse.
+OXT	addiction	dependence	6542796	Recent data indicate that the neurohypophyseal hormone oxytocin (<strong>OXT</strong>) and Z prolyl D leucine (Z Pro D Leu), a synthetic dipeptide derived from the C terminal part of <strong>OXT</strong>, attenuate the development of tolerance to and <b>dependence</b> on morphine in the mouse.
+OXT	drug	opioid	6542796	The present results confirm this hypothesis, since intracerebroventricular (i.c.v., 50 ng) and local (0.5 ng) injections of <strong>OXT</strong> and Z Pro D Leu into the dorsal hippocampus and the mesolimbic nucleus accumbens attenuate <b>morphine</b> tolerance/dependence, similarly to systemic injections of these peptides in higher amounts (5 50 micrograms).
+OXT	addiction	dependence	6542796	The present results confirm this hypothesis, since intracerebroventricular (i.c.v., 50 ng) and local (0.5 ng) injections of <strong>OXT</strong> and Z Pro D Leu into the dorsal hippocampus and the mesolimbic nucleus accumbens attenuate morphine tolerance/<b>dependence</b>, similarly to systemic injections of these peptides in higher amounts (5 50 micrograms).
+OXT	drug	opioid	6542796	Lesion of the nucleus accumbens by the catecholaminergic neurotoxin 6 hydroxydopamine (6 OHDA) completely prevents the effects of Z Pro D Leu and partially those of <strong>OXT</strong> on <b>morphine</b> tolerance/dependence.
+OXT	addiction	dependence	6542796	Lesion of the nucleus accumbens by the catecholaminergic neurotoxin 6 hydroxydopamine (6 OHDA) completely prevents the effects of Z Pro D Leu and partially those of <strong>OXT</strong> on morphine tolerance/<b>dependence</b>.
+NR4A2	drug	amphetamine	32569805	Then, we evaluated changes in nuclear receptor related 1 protein (<strong>Nurr1</strong>) expression and the levels of inflammatory cytokines in primary cultured astrocytes exposed to <b>METH</b> or α syn.
+NR4A2	drug	amphetamine	32569805	We found that <b>METH</b> or α syn exposure decreased <strong>Nurr1</strong> expression and increased proinflammatory cytokine expression in astrocytes.
+NR4A2	drug	amphetamine	32569805	<strong>Nurr1</strong> may play a crucial role in this process and could be a therapeutic target for inflammatory damage caused by <b>METH</b>.
+NR4A2	drug	cocaine	32457073	We identified 133 genes differentially expressed between CUD case patients and <b>cocaine</b> free control subjects, including previously implicated candidates for <b>cocaine</b> use/addiction (FOSB, ARC, KCNJ9/GIRK3, <strong>NR4A2</strong>, JUNB, and MECP2).
+NR4A2	addiction	addiction	32457073	We identified 133 genes differentially expressed between CUD case patients and cocaine free control subjects, including previously implicated candidates for cocaine use/<b>addiction</b> (FOSB, ARC, KCNJ9/GIRK3, <strong>NR4A2</strong>, JUNB, and MECP2).
+NR4A2	drug	nicotine	31202491	Specifically, glutamatergic neurons are first primed to express transcription factor <strong>Nurr1</strong>, then acquire the dopaminergic phenotype following <b>nicotine</b> re exposure in adulthood.
+NR4A2	drug	nicotine	31202491	Enhanced neuronal activity combined with <strong>Nurr1</strong> expression is both necessary and sufficient for the <b>nicotine</b> mediated neurotransmitter plasticity to occur.
+NR4A2	drug	cocaine	30998946	Epigenetic regulation of immediate early gene <strong>Nr4a2</strong>/Nurr1 in the medial habenula during reinstatement of <b>cocaine</b> associated behavior.
+NR4A2	addiction	relapse	30998946	Epigenetic regulation of immediate early gene <strong>Nr4a2</strong>/Nurr1 in the medial habenula during <b>reinstatement</b> of cocaine associated behavior.
+NR4A2	drug	cocaine	30998946	Epigenetic regulation of immediate early gene <strong>Nr4a2</strong>/<strong>Nurr1</strong> in the medial habenula during reinstatement of <b>cocaine</b> associated behavior.
+NR4A2	addiction	relapse	30998946	Epigenetic regulation of immediate early gene <strong>Nr4a2</strong>/<strong>Nurr1</strong> in the medial habenula during <b>reinstatement</b> of cocaine associated behavior.
+NR4A2	drug	cocaine	30998946	To better understand the effect of drug induced changes on epigenetic function and behavior, we investigated HDAC3 mediated regulation of <strong>Nr4a2</strong>/Nurr1 in the medial habenula, an understudied pathway in <b>cocaine</b> associated behaviors.
+NR4A2	drug	cocaine	30998946	To better understand the effect of drug induced changes on epigenetic function and behavior, we investigated HDAC3 mediated regulation of <strong>Nr4a2</strong>/<strong>Nurr1</strong> in the medial habenula, an understudied pathway in <b>cocaine</b> associated behaviors.
+NR4A2	drug	cocaine	30998946	<strong>Nr4a2</strong>, a transcription factor critical in <b>cocaine</b> associated behaviors and necessary for MHb development, is enriched in the cholinergic cell population of the MHb; yet, the role of <strong>NR4A2</strong> within the MHb in the adult brain remains elusive.
+NR4A2	drug	cocaine	30998946	Here, we evaluated whether epigenetic regulation of <strong>Nr4a2</strong> in the MHb has a role in reinstatement of <b>cocaine</b> associated behaviors.
+NR4A2	addiction	relapse	30998946	Here, we evaluated whether epigenetic regulation of <strong>Nr4a2</strong> in the MHb has a role in <b>reinstatement</b> of cocaine associated behaviors.
+NR4A2	drug	cocaine	30998946	We found that HDAC3 disengages from <strong>Nr4a2</strong> in the MHb in response to <b>cocaine</b> primed reinstatement.
+NR4A2	addiction	relapse	30998946	We found that HDAC3 disengages from <strong>Nr4a2</strong> in the MHb in response to cocaine primed <b>reinstatement</b>.
+NR4A2	addiction	relapse	30998946	Whereas enhancing HDAC3 function in the MHb had no effect on <b>reinstatement</b>, we found, using a dominant negative splice variant (NURR2C), that loss of <strong>NR4A2</strong> function in the MHb blocked <b>reinstatement</b> behaviors.
+NR4A2	addiction	relapse	30998946	These results show for the first time that regulation of <strong>NR4A2</strong> function in the MHb is critical in <b>relapse</b> like behaviors.
+NR4A2	drug	opioid	30634592	Dysregulation of Dopaminergic Regulatory Factors TH, <strong>Nurr1</strong>, and Pitx3 in the Ventral Tegmental Area Associated with Neuronal Injury Induced by Chronic <b>Morphine</b> Dependence.
+NR4A2	addiction	dependence	30634592	Dysregulation of Dopaminergic Regulatory Factors TH, <strong>Nurr1</strong>, and Pitx3 in the Ventral Tegmental Area Associated with Neuronal Injury Induced by Chronic Morphine <b>Dependence</b>.
+NR4A2	drug	opioid	30634592	Immunohistochemistry showed that the number of TH⁺, <strong>Nurr1</strong>⁺, and Pitx3⁺ cells, and the number of TH⁺ cells expressing <strong>Nurr1</strong> or Pitx3, significantly decreased in the VTA after a long period of <b>morphine</b> dependence.
+NR4A2	addiction	dependence	30634592	Immunohistochemistry showed that the number of TH⁺, <strong>Nurr1</strong>⁺, and Pitx3⁺ cells, and the number of TH⁺ cells expressing <strong>Nurr1</strong> or Pitx3, significantly decreased in the VTA after a long period of morphine <b>dependence</b>.
+NR4A2	addiction	addiction	29576706	Increasing evidence supports the contributions of cAMP response element binding protein (CREB), nuclear receptor related 1 (<strong>Nurr1</strong>), and brain derived neurotrophic factor (BDNF) in modulating neural and behavioral plasticity which was induced by <b>addictive</b> drugs.
+NR4A2	drug	psychedelics	29576706	To investigate the effects of Rhy on the behavior and the levels of phosphorylated CREB (p CREB), <strong>Nurr1</strong>, and BDNF in the hippocampus of <b>ketamine</b> induced conditioned place preference (CPP) rats.
+NR4A2	addiction	reward	29576706	To investigate the effects of Rhy on the behavior and the levels of phosphorylated CREB (p CREB), <strong>Nurr1</strong>, and BDNF in the hippocampus of ketamine induced conditioned place preference (<b>CPP</b>) rats.
+NR4A2	drug	psychedelics	29576706	At the same time, expression of p CREB, <strong>Nurr1</strong>, and BDNF, which was significantly increased by <b>ketamine</b>, was restored in the Rhy  treated group.
+NR4A2	drug	psychedelics	29576706	This study indicates that Rhy can reverse the reward effect induced by <b>ketamine</b> in rats and the mechanism can probably be related to regulate the hippocampal protein expression of p CREB, <strong>Nurr1</strong>, and BDNF.
+NR4A2	addiction	reward	29576706	This study indicates that Rhy can reverse the <b>reward</b> effect induced by ketamine in rats and the mechanism can probably be related to regulate the hippocampal protein expression of p CREB, <strong>Nurr1</strong>, and BDNF.
+NR4A2	drug	psychedelics	29576706	P CREB, <strong>Nurr1</strong> and BDNF play an important role in the formation of <b>ketamine</b> induced place preference in ratsRhynchophylline reversed the expression of p CREB, <strong>Nurr1</strong> and BDNF which was activated by <b>ketamine</b> in the hippocampusRhynchophylline demonstrates the potential effect of mediates <b>ketamine</b> induced rewarding effect.
+NR4A2	drug	amphetamine	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; <strong>Nurr1</strong>: Nuclear receptor related 1; BDNF: Brain derived neurotrophic factor; CPP: Conditioned place preference; NMDA: N methyl D aspartic acid; <b>METH</b>: <b>Methamphetamine</b>; CNS: Central nervous system; PFA: Paraformaldehyde; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+NR4A2	addiction	reward	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; <strong>Nurr1</strong>: Nuclear receptor related 1; BDNF: Brain derived neurotrophic factor; <b>CPP</b>: Conditioned place preference; NMDA: N methyl D aspartic acid; METH: Methamphetamine; CNS: Central nervous system; PFA: Paraformaldehyde; GAPDH: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+NR4A2	drug	psychedelics	29476799	However, the transcription of the protein upstream of <strong>Nurr1</strong>, cyclic adenosine monophosphate response element binding protein (CREB), did not show any significant differences between the <b>ketamine</b> group and the <b>ketamine</b> + rhynchophylline group.
+NR4A2	drug	psychedelics	29476799	In summary, miR 331 5p is a key regulatory factor of <strong>Nurr1</strong>, and rhynchophylline can participate in the process of resistance to <b>ketamine</b> addiction through the miR 331 5p/<strong>Nurr1</strong>/BDNF pathway or inhibition of CREB phosphorylation.
+NR4A2	addiction	addiction	29476799	In summary, miR 331 5p is a key regulatory factor of <strong>Nurr1</strong>, and rhynchophylline can participate in the process of resistance to ketamine <b>addiction</b> through the miR 331 5p/<strong>Nurr1</strong>/BDNF pathway or inhibition of CREB phosphorylation.
+NR4A2	drug	cocaine	28466092	The aim of the present study was to compare the long term effects of RSD on the conditioned rewarding effects of <b>cocaine</b> and levels of the transcription factors Pitx3 and <strong>Nurr1</strong> in the ventral tegmental area (VTA), the dopamine transporter (DAT), the D2 dopamine receptor (D2DR) and precursor of brain derived neurotrophic factor (proBDNF) signaling pathways, and the tropomyosin related kinase B (TrkB) receptor in the nucleus accumbens (NAc) in adult and adolescent mice.
+NR4A2	drug	cocaine	27936186	Furthermore, animals exposed to maternal separation and treated with <b>cocaine</b> exhibited increased DA turnover and protein expression levels of DAT and D2R, while decreased <strong>Nurr1</strong> and Pitx3 protein expression levels were observed when compared with saline treated mice.
+NR4A2	drug	amphetamine	27687740	Opposite effects of acute and chronic <b>amphetamine</b> on <strong>Nurr1</strong> and NF κB p65 in the rat ventral tegmental area.
+NR4A2	drug	amphetamine	27687740	In this study we evaluated the effects of single and repeated <b>amphetamine</b> administration in the expression of <strong>Nurr1</strong> and the NF κB p65 subunit in the rat ventral tegmental area (VTA).
+NR4A2	drug	amphetamine	27687740	We found that acute <b>amphetamine</b> treatment increased <strong>Nurr1</strong>, p65 and TH protein levels in the VTA.
+NR4A2	drug	amphetamine	27687740	On the other hand, chronic <b>amphetamine</b> treatment decreased <strong>Nurr1</strong> and p65 protein levels, but TH was unchanged.
+NR4A2	addiction	addiction	27547496	In human DA neurons, which provide an appropriate cellular milieu, VPA treatment alters the expression of several genes important for dopaminergic neuron function including DAT, <strong>Nurr1</strong>, and TH; this might partly explain its action in regulating <b>addictive</b> behaviors.
+NR4A2	drug	alcohol	26621272	The results indicate that <b>alcohol</b> dependence is associated with high expression of SNCA and DRD4 (signifi cantly higher than in the control group) and is not associated with changes in the work of <strong>NR4A2</strong> and DRD3 genes.
+NR4A2	addiction	dependence	26621272	The results indicate that alcohol <b>dependence</b> is associated with high expression of SNCA and DRD4 (signifi cantly higher than in the control group) and is not associated with changes in the work of <strong>NR4A2</strong> and DRD3 genes.
+NR4A2	addiction	addiction	25522207	Previously, it has been proposed that the transcription factors <strong>Nurr1</strong> and Pitx3, which are critical for transcription of a set of genes involved in DA metabolism in the mesolimbic pathway, are associated with <b>addiction</b> pathology.
+NR4A2	drug	opioid	25522207	We found that the increased <strong>Nurr1</strong> and/or Pitx3 levels during <b>morphine</b> dependence and in <b>morphine</b> withdrawn rats were associated to an increase of DAT, VMAT2 and DRD2.
+NR4A2	addiction	dependence	25522207	We found that the increased <strong>Nurr1</strong> and/or Pitx3 levels during morphine <b>dependence</b> and in morphine withdrawn rats were associated to an increase of DAT, VMAT2 and DRD2.
+NR4A2	drug	opioid	25522207	Altogether, present data indicate that <b>morphine</b> dependence and withdrawal induced consistent alterations of most of the DA markers, which was correlated with transcription factors involved in the maintenance of DA neurons in drug reward pathways, suggesting that <strong>Nurr1</strong> and Pitx3 regulation might be associated with controlling adaptation to chronic <b>morphine</b> and to <b>morphine</b> withdrawal induced alterations of DA neurons activity in the mesolimbic pathway.
+NR4A2	addiction	dependence	25522207	Altogether, present data indicate that morphine <b>dependence</b> and withdrawal induced consistent alterations of most of the DA markers, which was correlated with transcription factors involved in the maintenance of DA neurons in drug reward pathways, suggesting that <strong>Nurr1</strong> and Pitx3 regulation might be associated with controlling adaptation to chronic morphine and to morphine withdrawal induced alterations of DA neurons activity in the mesolimbic pathway.
+NR4A2	addiction	reward	25522207	Altogether, present data indicate that morphine dependence and withdrawal induced consistent alterations of most of the DA markers, which was correlated with transcription factors involved in the maintenance of DA neurons in drug <b>reward</b> pathways, suggesting that <strong>Nurr1</strong> and Pitx3 regulation might be associated with controlling adaptation to chronic morphine and to morphine withdrawal induced alterations of DA neurons activity in the mesolimbic pathway.
+NR4A2	addiction	withdrawal	25522207	Altogether, present data indicate that morphine dependence and <b>withdrawal</b> induced consistent alterations of most of the DA markers, which was correlated with transcription factors involved in the maintenance of DA neurons in drug reward pathways, suggesting that <strong>Nurr1</strong> and Pitx3 regulation might be associated with controlling adaptation to chronic morphine and to morphine <b>withdrawal</b> induced alterations of DA neurons activity in the mesolimbic pathway.
+NR4A2	addiction	addiction	24706046	Previously, it has been proposed that the transcription factors <strong>Nurr1</strong> and Pitx3, which are critical for transcription of a set of genes involved in DA metabolism in the mesolimbic pathway, are associated with <b>addiction</b> pathology.
+NR4A2	drug	opioid	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single <b>morphine</b> administration, <b>morphine</b> dependence and <b>morphine</b> withdrawal on <strong>Nurr1</strong> and Pitx3 expression as well as on the DA marker tyrosine hydroxylase (TH) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+NR4A2	addiction	dependence	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single morphine administration, morphine <b>dependence</b> and morphine withdrawal on <strong>Nurr1</strong> and Pitx3 expression as well as on the DA marker tyrosine hydroxylase (TH) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+NR4A2	addiction	withdrawal	24706046	Using quantitative real time PCR, immunofluorescence, HPLC and Western blotting, here we studied the effects of single morphine administration, morphine dependence and morphine <b>withdrawal</b> on <strong>Nurr1</strong> and Pitx3 expression as well as on the DA marker tyrosine hydroxylase (TH) and the turnover of DA in the ventral tegmental area (VTA) and/or nucleus accumbens.
+NR4A2	drug	opioid	24706046	We showed that the three experimental conditions caused induction of <strong>Nurr1</strong> and Pitx3 in the VTA, which correlated with changes in TH expression during chronic <b>morphine</b> administration.
+NR4A2	drug	opioid	24706046	Furthermore, during <b>morphine</b> dependence, <strong>Nurr1</strong> was detected in the nucleus compartment of VTA TH positive neurons, whereas Pitx3 was strongly detected in the nucleus of TH positive neurons after single <b>morphine</b> administration and during <b>morphine</b> withdrawal.
+NR4A2	addiction	dependence	24706046	Furthermore, during morphine <b>dependence</b>, <strong>Nurr1</strong> was detected in the nucleus compartment of VTA TH positive neurons, whereas Pitx3 was strongly detected in the nucleus of TH positive neurons after single morphine administration and during morphine withdrawal.
+NR4A2	addiction	withdrawal	24706046	Furthermore, during morphine dependence, <strong>Nurr1</strong> was detected in the nucleus compartment of VTA TH positive neurons, whereas Pitx3 was strongly detected in the nucleus of TH positive neurons after single morphine administration and during morphine <b>withdrawal</b>.
+NR4A2	addiction	addiction	24706046	Present data provide novel insight into the potential correlation between <strong>Nurr1</strong> and Pitx3 and DA neurons plasticity during opiate <b>addiction</b> in the mesolimbic pathway.
+NR4A2	drug	opioid	23783774	Furthermore, a meta analysis of the common striatal DEGs in this study along with <b>morphine</b> regulated striatal transcriptomes in mice (National Center for Biotechnology Information Gene Expression Omnibus Database Accession Code GSE7762) suggested similar expression profiles of genes involved in neuronal development (e.g., Bhlhe22, <strong>Nr4a2</strong>).
+NR4A2	drug	nicotine	23562942	The Nr4a family member, <strong>nr4a2</strong>/nurr1, showed increased striatal expression after all three drug treatments, while striatal nr4a3/nor 1 expression was increased by the drug combination whereas NAc nr4a1/nurr77 was decreased by <b>nicotine</b> and the drug combination.
+NR4A2	drug	nicotine	23562942	The Nr4a family member, <strong>nr4a2</strong>/<strong>nurr1</strong>, showed increased striatal expression after all three drug treatments, while striatal nr4a3/nor 1 expression was increased by the drug combination whereas NAc nr4a1/nurr77 was decreased by <b>nicotine</b> and the drug combination.
+NR4A2	addiction	addiction	23215787	Alterations in transcription factors that regulate the development and maintenance of dopamine (DA) neurons (such as <strong>Nurr1</strong> and Pitx3) play an important role in the pathogenesis of <b>addiction</b> diseases.
+NR4A2	drug	opioid	23215787	We have examined the effects of acute and chronic <b>morphine</b> and <b>morphine</b> withdrawal on TH expression and activity as well as expression of <strong>Nurr1</strong>, Pitx3 and Ago2 in the ventral tegmental area (VTA) and nucleus accumbens (NAc) of the rat.
+NR4A2	addiction	withdrawal	23215787	We have examined the effects of acute and chronic morphine and morphine <b>withdrawal</b> on TH expression and activity as well as expression of <strong>Nurr1</strong>, Pitx3 and Ago2 in the ventral tegmental area (VTA) and nucleus accumbens (NAc) of the rat.
+NR4A2	drug	opioid	23215787	Acute <b>morphine</b> produced a marked increase in TH activity and DA turnover in the NAc, concomitantly with increased <strong>Nurr1</strong> and Pitx3 expression in the VTA.
+NR4A2	drug	opioid	23215787	The combined decrease in Ago2 and increases in <strong>Nurr1</strong> and Pitx3 might represent some of the mechanisms that served to protect against accumbal TH regulation observed in <b>morphine</b> withdrawn rats, which may be critical for DA bioavailability to influence behaviour.
+NR4A2	drug	alcohol	23066323	To investigate the association of polymorphisms of nur related receptor 1 (<strong>Nurr1</strong>) and development of <b>alcohol</b> dependence in Mexican Americans.
+NR4A2	addiction	dependence	23066323	To investigate the association of polymorphisms of nur related receptor 1 (<strong>Nurr1</strong>) and development of alcohol <b>dependence</b> in Mexican Americans.
+NR4A2	drug	alcohol	23066323	Polymorphisms in the regulatory region of <strong>Nurr1</strong> are implicated in pathogenesis of <b>alcohol</b> dependence and the <strong>Nurr1</strong>/dopamine signaling pathway might be important for this dependence development in Mexican Americans.
+NR4A2	addiction	dependence	23066323	Polymorphisms in the regulatory region of <strong>Nurr1</strong> are implicated in pathogenesis of alcohol <b>dependence</b> and the <strong>Nurr1</strong>/dopamine signaling pathway might be important for this <b>dependence</b> development in Mexican Americans.
+NR4A2	drug	amphetamine	21547080	Moreover, toxic <b>METH</b> doses caused decreases in the expression of the dopamine developmental factors, Shh, Lmx1b, and <strong>Nurr1</strong>, but not in the levels of Otx2 and Pitx3, in saline pretreated rats.
+NR4A2	drug	amphetamine	21547080	<b>METH</b> pretreatment followed by <b>METH</b> challenges also decreased <strong>Nurr1</strong> but increased Otx2 and Pitx3 expression in the midbrain.
+NR4A2	drug	amphetamine	21229349	Unexpectedly, acute <b>METH</b> challenge to <b>METH</b> pretreated animals caused further decreases in <strong>Nr4a2</strong> (Nurr1) mRNA levels.
+NR4A2	drug	amphetamine	21229349	Unexpectedly, acute <b>METH</b> challenge to <b>METH</b> pretreated animals caused further decreases in <strong>Nr4a2</strong> (<strong>Nurr1</strong>) mRNA levels.
+NR4A2	drug	amphetamine	21151937	Decreased level of <strong>Nurr1</strong> in heterozygous young adult mice leads to exacerbated acute and long term toxicity after repeated <b>methamphetamine</b> exposure.
+NR4A2	drug	amphetamine	21151937	In this study, we examined the synergistic effects of repeated early exposure to <b>methamphetamine</b> in adolescence and reduction in <strong>Nurr1</strong> gene levels.
+NR4A2	drug	nicotine	20659174	We have, therefore, analysed the association of six single nucleotide polymorphisms (SNPs) within the three genes belonging to the NR4A orphan nuclear receptor family, NR4A1 (rs2603751, rs2701124), <strong>NR4A2</strong> (rs12803, rs834835) and NR4A3 (rs1131339, rs1405209), with the degree of <b>smoking</b> in a sample of 204 unrelated schizophrenia patients, which included 126 <b>smokers</b> and 78 non <b>smokers</b>.
+NR4A2	drug	opioid	20560679	This study aimed to investigate the associations between response to <b>methadone</b> maintenance treatment (MMT) and polymorphisms in genes coding for the OPRM1 <b>opioid</b> receptor, the metabotropic glutamate receptors GRM6 and GRM8, the nuclear receptor <strong>NR4A2</strong>, the photolyase enzyme cryptochrome 1 (CRY1), and the transcription factor myocardin (MYOCD), which have previously been associated with the risk of <b>opioid</b> dependence disorder.
+NR4A2	addiction	dependence	20560679	This study aimed to investigate the associations between response to methadone maintenance treatment (MMT) and polymorphisms in genes coding for the OPRM1 opioid receptor, the metabotropic glutamate receptors GRM6 and GRM8, the nuclear receptor <strong>NR4A2</strong>, the photolyase enzyme cryptochrome 1 (CRY1), and the transcription factor myocardin (MYOCD), which have previously been associated with the risk of opioid <b>dependence</b> disorder.
+NR4A2	drug	amphetamine	18930103	mRNA expression of the <strong>Nurr1</strong> and NGFI B nuclear receptor families following acute and chronic administration of <b>methamphetamine</b>.
+NR4A2	drug	amphetamine	18930103	One to three hours after 4 mg/kg acute <b>methamphetamine</b> (<b>METH</b>) administration, the levels of <strong>Nurr1</strong> mRNA were significantly higher in the prelimbic (PrL), primary motor (M1) and primary somatosensory (S1) cortices and ventral tegmental area (VTA), as compared with the basal level.
+NR4A2	drug	amphetamine	18930103	Pretreatment with 0.5 mg/kg of SCH23390 prevented the acute <b>METH</b> induced increase in <strong>Nurr1</strong> mRNA levels in these brain regions.
+NR4A2	drug	amphetamine	18930103	After the saline challenge, the group chronically exposed to <b>METH</b> displayed significantly higher levels of <strong>Nurr1</strong> mRNA in the PrL, S1 and VTA, and of NGFI B mRNA in the PrL, M1, S1, striatum and AcbC than did the group chronically treated with saline.
+NR4A2	drug	amphetamine	18930103	The groups chronically exposed to <b>METH</b> failed to increase <strong>Nurr1</strong> mRNA in the VTA, and NGFI B mRNA in the AcbC, when challenged with 4 mg/kg <b>METH</b>.
+NR4A2	drug	amphetamine	18930103	These results suggest that <strong>Nurr1</strong> and NGFI B mRNA play differential roles upon exposure to <b>METH</b>.
+NR4A2	drug	opioid	18195715	Evidence was found for involvement of five genes in <b>heroin</b> addiction, the genes coding for the mu <b>opioid</b> receptor, the metabotropic receptors mGluR6 and mGluR8, nuclear receptor <strong>NR4A2</strong> and cryptochrome 1 (photolyase like).
+NR4A2	addiction	addiction	18195715	Evidence was found for involvement of five genes in heroin <b>addiction</b>, the genes coding for the mu opioid receptor, the metabotropic receptors mGluR6 and mGluR8, nuclear receptor <strong>NR4A2</strong> and cryptochrome 1 (photolyase like).
+NR4A2	drug	opioid	18057194	We examined mRNA expression levels of DA transporter (DAT), tyrosine hydroxylase (TH), dopamine D2 receptor, alpha synuclein, and nuclear receptor related 1 (<strong>Nurr1</strong>) in discrete mesocorticolimbic and nigrostriatal subpopulations of <b>heroin</b> users and control subjects.
+NR4A2	drug	opioid	18057194	Moreover, the results revealed an exaggerated reduction of <strong>Nurr1</strong> expression with age in <b>heroin</b> users (r =  0.8268, p < 0.001 vs controls, r =  0.6204, p = 0.0746).
+NR4A2	drug	opioid	18057194	Altogether the current findings provide direct neurobiological evidence that midbrain reward circuits have the most prominent DA and <b>opioid</b> impairments in human <b>heroin</b> abusers and that abnormal <strong>Nurr1</strong> transcription with opiate use may exacerbate limbic dysfunction with age.
+NR4A2	addiction	reward	18057194	Altogether the current findings provide direct neurobiological evidence that midbrain <b>reward</b> circuits have the most prominent DA and opioid impairments in human heroin abusers and that abnormal <strong>Nurr1</strong> transcription with opiate use may exacerbate limbic dysfunction with age.
+NR4A2	drug	cocaine	17070804	We show that chronic, but not acute or subchronic, <b>cocaine</b> administration downregulates <strong>Nurr1</strong> and Pitx3 transcripts whereas En1 transcripts are upregulated.
+NR4A2	drug	alcohol	12814373	Decreased <b>ethanol</b> preference and wheel running in <strong>Nurr1</strong> deficient mice.
+NR4A2	drug	alcohol	12814373	We have investigated the impact of heterozygous deletion of <strong>Nurr1</strong> on <b>ethanol</b> consumption in adult mice as a model for drug induced reward and on wheel running as a model for natural reward.
+NR4A2	addiction	reward	12814373	We have investigated the impact of heterozygous deletion of <strong>Nurr1</strong> on ethanol consumption in adult mice as a model for drug induced <b>reward</b> and on wheel running as a model for natural <b>reward</b>.
+NR4A2	drug	alcohol	12814373	Interestingly, <strong>Nurr1</strong> heterozygous mice never developed high <b>ethanol</b> consumption nor did they develop as much running behaviour as did the wild type animals.
+NR4A2	drug	alcohol	12814373	Thus, <strong>Nurr1</strong> appears to have a key role for the reinforcing properties of <b>ethanol</b> and running that underlies the development of excessive reward seeking behaviours characteristic for addiction.
+NR4A2	addiction	addiction	12814373	Thus, <strong>Nurr1</strong> appears to have a key role for the reinforcing properties of ethanol and running that underlies the development of excessive reward seeking behaviours characteristic for <b>addiction</b>.
+NR4A2	addiction	relapse	12814373	Thus, <strong>Nurr1</strong> appears to have a key role for the reinforcing properties of ethanol and running that underlies the development of excessive reward <b>seeking</b> behaviours characteristic for addiction.
+NR4A2	addiction	reward	12814373	Thus, <strong>Nurr1</strong> appears to have a key role for the <b>reinforcing</b> properties of ethanol and running that underlies the development of excessive <b>reward</b> seeking behaviours characteristic for addiction.
+NR4A2	drug	alcohol	12814373	Quantitative trait loci mapping using C57Bl/6 and DBA/2 mice describe a locus for <b>ethanol</b> preference on chromosome 2, wherein <strong>Nurr1</strong> is located.
+NR4A2	drug	alcohol	12814373	We found two dinucleotide repeats in the <strong>Nurr1</strong> promoter that were longer in mice with low preference for <b>ethanol</b> (DBA/2 and 129/Sv) than in mice with high preference for <b>ethanol</b> (C57Bl/6J and C57Bl/6NIH).
+NR4A2	drug	alcohol	12814373	These sequential data are compatible with <strong>Nurr1</strong> as a candidate gene responsible for the quantitative trait loci for <b>ethanol</b> preference on mouse chromosome 2.
+NR4A2	drug	alcohol	12814373	Together, our data thus imply involvement of <strong>Nurr1</strong> in the transition to a state of high <b>ethanol</b> consumption as well as in the development of a high amount of wheel running in mice.
+NR4A2	drug	alcohol	11840500	We examined 48 Japanese patients with schizophrenia and 32 patients with <b>alcohol</b> dependence to detect mutations in the retinoid X receptor beta gene (RXRB) on chromosome 6p21.3, the NURR1 gene (<strong>NR4A2</strong>) on chromosome 2q22 q23, and the PPAR alpha gene (PPARA) on chromosome 22q12.2 13.1.
+NR4A2	addiction	dependence	11840500	We examined 48 Japanese patients with schizophrenia and 32 patients with alcohol <b>dependence</b> to detect mutations in the retinoid X receptor beta gene (RXRB) on chromosome 6p21.3, the NURR1 gene (<strong>NR4A2</strong>) on chromosome 2q22 q23, and the PPAR alpha gene (PPARA) on chromosome 22q12.2 13.1.
+NR4A2	drug	alcohol	11840500	We examined 48 Japanese patients with schizophrenia and 32 patients with <b>alcohol</b> dependence to detect mutations in the retinoid X receptor beta gene (RXRB) on chromosome 6p21.3, the <strong>NURR1</strong> gene (<strong>NR4A2</strong>) on chromosome 2q22 q23, and the PPAR alpha gene (PPARA) on chromosome 22q12.2 13.1.
+NR4A2	addiction	dependence	11840500	We examined 48 Japanese patients with schizophrenia and 32 patients with alcohol <b>dependence</b> to detect mutations in the retinoid X receptor beta gene (RXRB) on chromosome 6p21.3, the <strong>NURR1</strong> gene (<strong>NR4A2</strong>) on chromosome 2q22 q23, and the PPAR alpha gene (PPARA) on chromosome 22q12.2 13.1.
+NR4A2	drug	alcohol	11840500	However, they revealed a significant association between the <strong>NR4A2</strong> gene haplotype and <b>alcohol</b> dependence, indicating that 2q22 q23 including the <strong>NR4A2</strong> gene locus is a possible genomic region contributing to genetic susceptibility to <b>alcohol</b> dependence.
+NR4A2	addiction	dependence	11840500	However, they revealed a significant association between the <strong>NR4A2</strong> gene haplotype and alcohol <b>dependence</b>, indicating that 2q22 q23 including the <strong>NR4A2</strong> gene locus is a possible genomic region contributing to genetic susceptibility to alcohol <b>dependence</b>.
+NLRP5	addiction	sensitization	25903913	Surgical trauma, adherence of the musculature to the dura <strong>mater</strong>, peripheral nerve injury, development of neurinomas in the surgical scar, and central <b>sensitization</b> may be involved in the genesis of such headaches.
+NLRP5	drug	opioid	11454653	Electrical stimulation of the dura <strong>mater</strong> evoked neurogenic dural vasodilation which was significantly inhibited by <b>morphine</b> (1 mg kg( 1)) the selective mu <b>opioid</b> agonist DAGO (10 microg kg( 1)) and the mixed agonist/antagonist butorphanol (1 mg kg( 1)) but not by the kappa  and delta <b>opioid</b> agonists (+/ ) U50488H (100 microg kg( 1)) and DPDPE (1 mg kg( 1)).
+NLRP5	drug	nicotine	9599854	Using data from the <strong>Mater</strong> Hospital  University of Queensland Study of Pregnancy, we report family income related to rates of <b>smoking</b> before, during and after a pregnancy.
+IL5	drug	alcohol	29733875	We measured the acute concentrations and dynamics of lipoxins LxA4 and LxB4 and the interleukins IL 4, <strong>IL 5</strong>, IL 9, IL 10, and IL 13 in the serum of patients treated with methyl <b>alcohol</b> poisoning and the follow up concentrations in survivors two years after discharge from the hospital.
+IL5	addiction	intoxication	29317484	Repeated pairings of adolescent rats to <b>binge</b> concentrations of toluene vapor previously shown to enhance dopamine release in reward sensitive areas of the brain produced CPP that persisted for 7 but not 30 d. Toluene induced CPP was associated with increased excitability of <strong>IL5</strong>/6 mPFC neurons projecting to the core of the NAc and reduced excitability of those projecting to the NAc shell.
+IL5	addiction	reward	29317484	Repeated pairings of adolescent rats to binge concentrations of toluene vapor previously shown to enhance dopamine release in <b>reward</b> sensitive areas of the brain produced <b>CPP</b> that persisted for 7 but not 30 d. Toluene induced <b>CPP</b> was associated with increased excitability of <strong>IL5</strong>/6 mPFC neurons projecting to the core of the NAc and reduced excitability of those projecting to the NAc shell.
+IL5	addiction	reward	29317484	Chemogenetic reversal of the toluene induced decrease in <strong>IL5</strong>/6 NAc shell neurons blocked the expression of toluene induced <b>CPP</b> while manipulating <strong>IL5</strong>/6 NAc core neuron activity had no effect.
+IL5	drug	alcohol	27951519	However, the levels of cytokine expression were significantly lower after 4 weeks of abstinence from <b>alcohol</b> (P≤0.001, except for IL 1β and <strong>IL 5</strong>).
+IL5	addiction	sensitization	24389455	TH1 cytokines (IL 2, IFN γ) and TH2 cytokines (IL 4, <strong>IL 5</strong>) releases from lymph node cell culture were also investigated as contact <b>sensitization</b> endpoints.
+IL5	drug	alcohol	22003193	Pulmonary exposure to 2% furfuryl <b>alcohol</b> resulted in enhanced airway hyperreactivity, eosinophilic infiltration into the lungs, and enhanced cytokine production (IL 4, <strong>IL 5</strong>, and interferon γ) by ex vivo stimulated lung associated draining lymphoid cells.
+IL5	addiction	withdrawal	21802933	Sputum was also analysed for mRNA levels of haemoxygenase 1, tumour necrosis factor α, RANTES, interleukin 5(<strong>IL 5</strong>), IL 10, IL 12, IL 13, transforming growth factor β, and interferon γ. Cox regression analyses were performed using time to exacerbation as outcome variable to identify significant hazards for a COPD exacerbation after ICS <b>withdrawal</b>.
+IL5	addiction	withdrawal	21802933	Sputum was also analysed for mRNA levels of haemoxygenase 1, tumour necrosis factor α, RANTES, <strong>interleukin 5</strong>(<strong>IL 5</strong>), IL 10, IL 12, IL 13, transforming growth factor β, and interferon γ. Cox regression analyses were performed using time to exacerbation as outcome variable to identify significant hazards for a COPD exacerbation after ICS <b>withdrawal</b>.
+IL5	addiction	sensitization	21602845	After <b>sensitization</b> and challenge with rDer p2, mice that were fed with total protein extracted from transgenic plants showed decreases in serum Der p2 specific IgE and IgG1 titers, decreased <strong>IL 5</strong> and eotaxin levels in bronchial alveolar lavage fluid, and eosinophil infiltration in the airway.
+IL5	drug	alcohol	21421450	Serum <strong>IL 5</strong> levels were decreased in both <b>alcoholic</b> groups.
+IL5	drug	opioid	17974159	In contrast, <strong>IL 5</strong> levels stimulated by PHA showed a significant increase in both groups, while no significant effect of <b>naloxone</b> could be observed.
+IL5	drug	opioid	14741432	We had previously shown that chronic <b>morphine</b> treatment in vivo and in vitro decreases IL 2 and IFNgamma (Th1) protein levels and increases IL 4 and <strong>IL 5</strong> (Th2) protein levels in a time dependent manner.
+IL5	drug	opioid	14741432	In addition in this paper, we show that chronic <b>morphine</b> treatment resulted in a decrease in IFNgamma and IL 2 mRNA and an increase in IL 4 and <strong>IL 5</strong> mRNA accumulation in murine splenocytes.
+IL5	drug	cannabinoid	12668119	<b>Cannabinol</b> (CBN) or Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>; 50 mg/kg, ip), administered daily for 3 consecutive days before sensitization and then before challenge, significantly attenuated the elevation of IL 2, IL 4, <strong>IL 5</strong>, and IL 13 steady state mRNA expression elicited by Ova challenge in the lungs.
+IL5	addiction	sensitization	12668119	Cannabinol (CBN) or Delta(9) tetrahydrocannabinol (Delta(9) THC; 50 mg/kg, ip), administered daily for 3 consecutive days before <b>sensitization</b> and then before challenge, significantly attenuated the elevation of IL 2, IL 4, <strong>IL 5</strong>, and IL 13 steady state mRNA expression elicited by Ova challenge in the lungs.
+IL5	addiction	sensitization	26368638	In addition, analysis of mediator expression and release over the <b>sensitization</b> phase has revealed that PM exposure can enhance production of Th2 cytokines such as interleukin 5 (<strong>IL 5</strong>) and the proinflammatory cytokine tumor necrosis factor alpha (TNF α).
+IL5	addiction	sensitization	26368638	In addition, analysis of mediator expression and release over the <b>sensitization</b> phase has revealed that PM exposure can enhance production of Th2 cytokines such as <strong>interleukin 5</strong> (<strong>IL 5</strong>) and the proinflammatory cytokine tumor necrosis factor alpha (TNF α).
+HAL	drug	psychedelics	31749223	Pretreatment with SCH23390 (SCH), Haloperidol (<strong>HAL</strong>), and ketanserin (KS), antagonists of dopamine D1 (DRD1), dopamine D2 (DRD2), and serotonin 2A (5 HT2A receptor) receptors, respectively, was utilized during a CPP test to investigate the involvement of the dopaminergic and serotonergic systems in 25B <b>NBOMe</b> mediated effects.
+HAL	addiction	reward	31749223	Pretreatment with SCH23390 (SCH), Haloperidol (<strong>HAL</strong>), and ketanserin (KS), antagonists of dopamine D1 (DRD1), dopamine D2 (DRD2), and serotonin 2A (5 HT2A receptor) receptors, respectively, was utilized during a <b>CPP</b> test to investigate the involvement of the dopaminergic and serotonergic systems in 25B NBOMe mediated effects.
+HAL	drug	psychedelics	31749223	SCH and <strong>HAL</strong> blocked 25B <b>NBOMe</b> induced CPP, whereas KS did not.
+HAL	addiction	reward	31749223	SCH and <strong>HAL</strong> blocked 25B NBOMe induced <b>CPP</b>, whereas KS did not.
+HAL	drug	psychedelics	31749223	Furthermore, 25B <b>NBOMe</b> altered delta and gamma wave activity, which was normalized by SCH and <strong>HAL</strong>.
+HAL	drug	amphetamine	31219367	Thirty (nine female) non comorbid GD subjects with low (LI), moderate (MI), or high impulsivity (HI) received the preferential D2 antagonist haloperidol (<strong>HAL</strong>; 3 mg) or the mixed D1 D2 antagonist fluphenazine (FLU; 3 mg), on separate sessions before a 15 minute slot machine game or <b>amphetamine</b> (<b>AMPH</b>; 20 mg), in a placebo controlled, double blind, counterbalanced design.
+HAL	drug	amphetamine	30243682	We found that, continuous infusion of a clinically relevant dose of <strong>HAL</strong> (0.5 mg/kg/day) effectively ameliorated <b>AMPH</b> sensitization induced sensorimotor gating disruptions after seven days of treatment.
+HAL	addiction	sensitization	30243682	We found that, continuous infusion of a clinically relevant dose of <strong>HAL</strong> (0.5 mg/kg/day) effectively ameliorated AMPH <b>sensitization</b> induced sensorimotor gating disruptions after seven days of treatment.
+HAL	drug	amphetamine	28522313	Only CONT <strong>HAL</strong> rats showed potentiated <b>amphetamine</b> induced locomotion, indicating dopamine supersensitivity.
+HAL	drug	amphetamine	28522313	Compared to intra NAc saline, intra NAc neurotensin suppressed <b>amphetamine</b> induced locomotion in CONT <strong>HAL</strong> rats, but not in INT <strong>HAL</strong> or control rats.
+HAL	drug	amphetamine	27624149	To isolate D1R, half the subjects were pretreated with the preferential D2 receptor antagonist haloperidol (<strong>HAL</strong>; 3 mg), and the other half with the mixed D1 D2 antagonist fluphenazine (FLU; 3 mg) before the game (Phase I) and <b>AMPH</b> (Phase II).
+HAL	drug	amphetamine	27624149	<strong>HAL</strong> decreased and FLU increased the post game desire to gamble and post <b>AMPH</b> desire to take <b>AMPH</b> again, as well as <b>amphetamine</b> scale ratings on the Addiction Research Center Inventory after gambling and <b>AMPH</b>.
+HAL	addiction	addiction	27624149	<strong>HAL</strong> decreased and FLU increased the post game desire to gamble and post AMPH desire to take AMPH again, as well as amphetamine scale ratings on the <b>Addiction</b> Research Center Inventory after gambling and AMPH.
+HAL	drug	amphetamine	27624149	<strong>HAL</strong> also decreased the salience of gambling words after <b>AMPH</b>.
+HAL	drug	amphetamine	26032742	We have previously shown that chronic haloperidol (<strong>HAL</strong>) treatment reduces <b>amphetamine</b> (<b>AMPH</b>) induced locomotor activity in <b>AMPH</b> sensitized rats, but only when paired with high levels of the estrogen, 17 β estradiol.
+HAL	drug	amphetamine	26032742	The aim of the current study was to assess this interaction by investigating the effects of estradiol, <b>AMPH</b> and <strong>HAL</strong> on brain volume changes in awake female rats.
+HAL	drug	amphetamine	25823912	<strong>HAL</strong> treated rats were dopamine supersensitive, as indicated by sensitization to systemic <b>AMPH</b> induced potentiation of both locomotor activity and operant responding for a conditioned reward (CR).
+HAL	addiction	reward	25823912	<strong>HAL</strong> treated rats were dopamine supersensitive, as indicated by sensitization to systemic AMPH induced potentiation of both locomotor activity and <b>operant</b> responding for a conditioned <b>reward</b> (CR).
+HAL	addiction	sensitization	25823912	<strong>HAL</strong> treated rats were dopamine supersensitive, as indicated by <b>sensitization</b> to systemic AMPH induced potentiation of both locomotor activity and operant responding for a conditioned reward (CR).
+HAL	drug	amphetamine	25823912	Intra NAc injections of <b>AMPH</b> enhanced operant responding for CR in OLZ treated and control rats, but not in <strong>HAL</strong> treated rats.
+HAL	addiction	reward	25823912	Intra NAc injections of AMPH enhanced <b>operant</b> responding for CR in OLZ treated and control rats, but not in <strong>HAL</strong> treated rats.
+HAL	drug	amphetamine	25823912	In <strong>HAL</strong> treated rats, inhibition of the NAc also failed to disrupt systemic <b>AMPH</b> induced potentiation of operant responding for CR.
+HAL	addiction	reward	25823912	In <strong>HAL</strong> treated rats, inhibition of the NAc also failed to disrupt systemic AMPH induced potentiation of <b>operant</b> responding for CR.
+HAL	drug	amphetamine	25823912	Furthermore, while intra NAc <b>AMPH</b> enhanced locomotion in both <strong>HAL</strong> treated and control animals, inhibition of the NAc disrupted systemic <b>AMPH</b> induced locomotion only in control rats.
+HAL	addiction	withdrawal	24464874	The present study explored the impact of <b>withdrawal</b> from repeated haloperidol (<strong>HAL</strong>) treatment, as well as the response to a novel α5 gamma aminobutyric acid (GABA(A)) receptor positive allosteric modulator (α5PAM), on the activity of the DA system in the methylazoxymethanol acetate (MAM) neurodevelopmental model of schizophrenia.
+HAL	addiction	withdrawal	24464874	Electrophysiological recordings were conducted from DA neurons in the ventral tegmental area of MAM and saline (SAL) rats following 7 day <b>withdrawal</b> from repeated <strong>HAL</strong> (21 d, 0.6 mg/kg, orally).
+HAL	drug	amphetamine	24464874	SAL rats withdrawn from <strong>HAL</strong> demonstrated reduced spontaneous DA neuron activity along with an enhanced locomotor response to <b>amphetamine</b>, indicative of the development of DA supersensitivity.
+HAL	addiction	withdrawal	24464874	Both α5PAM treatment and ventral hippocampal (vHPC) inactivation reversed the DA neuron depolarization block following <strong>HAL</strong> <b>withdrawal</b> in SAL rats.
+HAL	drug	amphetamine	24464874	In contrast, MAM rats withdrawn from <strong>HAL</strong> exhibited reduced spontaneous DA activity and enhanced locomotor response to <b>amphetamine</b> compared with untreated SAL rats; however, this condition was unresponsive to α5PAM treatment or vHPC inactivation.
+HAL	addiction	withdrawal	24464874	<b>Withdrawal</b> from prior <strong>HAL</strong> treatment interferes with the therapeutic actions of this novel treatment in the MAM model of schizophrenia.
+HAL	drug	amphetamine	22927669	We have shown previously that rats withdrawn from continuous haloperidol (<strong>HAL</strong>) treatment (via subcutaneous minipump) develop dopamine supersensitivity and pursue reward cues more vigorously than <strong>HAL</strong> naive rats following an <b>amphetamine</b> (<b>AMPH</b>) challenge.
+HAL	addiction	reward	22927669	We have shown previously that rats withdrawn from continuous haloperidol (<strong>HAL</strong>) treatment (via subcutaneous minipump) develop dopamine supersensitivity and pursue <b>reward</b> cues more vigorously than <strong>HAL</strong> naive rats following an amphetamine (AMPH) challenge.
+HAL	addiction	reward	22927669	Thus, we compared the effects of <strong>HAL</strong> and the atypical antipsychotic olanzapine (OLZ) on the pursuit of <b>reward</b> cues.
+HAL	addiction	withdrawal	22927669	<b>Withdrawal</b> from <strong>HAL</strong>, but not from OLZ, enhanced this effect.
+HAL	drug	amphetamine	22927669	<strong>HAL</strong>, but not OLZ, also enhanced <b>AMPH</b> induced psychomotor activation and c fos mRNA expression in the caudate putamen.
+HAL	drug	amphetamine	22927669	Thus, prior <strong>HAL</strong>, but not OLZ, enhanced conditioned reward following an <b>AMPH</b> challenge, and this was potentially linked to enhanced behavioral sensitivity to <b>AMPH</b> and <b>AMPH</b> induced engagement of the caudate putamen.
+HAL	addiction	reward	22927669	Thus, prior <strong>HAL</strong>, but not OLZ, enhanced conditioned <b>reward</b> following an AMPH challenge, and this was potentially linked to enhanced behavioral sensitivity to AMPH and AMPH induced engagement of the caudate putamen.
+HAL	addiction	reward	22927669	These findings suggest that <strong>HAL</strong>, but not an atypical like OLZ, modifies <b>reward</b> circuitry in ways that increase responsiveness to <b>reward</b> cues.
+HAL	drug	amphetamine	20557320	Three experiments were designed to evaluate the roles of DAD2 receptor antagonist haloperidol (<strong>HAL</strong>) and glutamatergic N methyl d aspartate receptor antagonist MK 801 on both the induction and the expression stage of <b>AMPH</b> sensitization in SIP rats.
+HAL	addiction	sensitization	20557320	Three experiments were designed to evaluate the roles of DAD2 receptor antagonist haloperidol (<strong>HAL</strong>) and glutamatergic N methyl d aspartate receptor antagonist MK 801 on both the induction and the expression stage of AMPH <b>sensitization</b> in SIP rats.
+HAL	drug	amphetamine	20557320	Second, <strong>HAL</strong> or MK 801 was co administered with <b>AMPH</b> on five consecutive days and their effect on induction was examined 14 days after withdrawal.
+HAL	addiction	withdrawal	20557320	Second, <strong>HAL</strong> or MK 801 was co administered with AMPH on five consecutive days and their effect on induction was examined 14 days after <b>withdrawal</b>.
+HAL	drug	amphetamine	20557320	Finally, <strong>HAL</strong> or MK 801 was co administered with <b>AMPH</b> on the final day of testing in SIP rats in which <b>AMPH</b> sensitization had been established previously.
+HAL	addiction	sensitization	20557320	Finally, <strong>HAL</strong> or MK 801 was co administered with AMPH on the final day of testing in SIP rats in which AMPH <b>sensitization</b> had been established previously.
+HAL	drug	amphetamine	20557320	The present results showed that <strong>HAL</strong> and MK 801 affected the effect of <b>AMPH</b> differently during the process of sensitization.
+HAL	addiction	sensitization	20557320	The present results showed that <strong>HAL</strong> and MK 801 affected the effect of AMPH differently during the process of <b>sensitization</b>.
+HAL	addiction	sensitization	20557320	Whereas <strong>HAL</strong> influenced the <b>sensitization</b> during both the induction and the expression phases, MK 801 affected only the induction phase; thus, once the <b>sensitization</b> had been established, MK 801 had no further influence.
+HAL	drug	amphetamine	20034231	However pretreatment with DAD2 antagonist haloperidol (<strong>HAL</strong>) prevented the sensitization to <b>AMPH</b> in the long term rather than short term withdrawal conditions.
+HAL	addiction	sensitization	20034231	However pretreatment with DAD2 antagonist haloperidol (<strong>HAL</strong>) prevented the <b>sensitization</b> to AMPH in the long term rather than short term withdrawal conditions.
+HAL	addiction	withdrawal	20034231	However pretreatment with DAD2 antagonist haloperidol (<strong>HAL</strong>) prevented the sensitization to AMPH in the long term rather than short term <b>withdrawal</b> conditions.
+HAL	drug	amphetamine	19298320	We compared the effects of withdrawal from long term administration of the typical neuroleptic haloperidol (<strong>Hal</strong>) and/or the atypical agent risperidone (Ris) on MDS and NDS, behaviorally evaluated by <b>amphetamine</b> induced locomotor stimulation (AILS) and apomorphine induced stereotypy (AIS) in mice, respectively.
+HAL	addiction	withdrawal	19298320	We compared the effects of <b>withdrawal</b> from long term administration of the typical neuroleptic haloperidol (<strong>Hal</strong>) and/or the atypical agent risperidone (Ris) on MDS and NDS, behaviorally evaluated by amphetamine induced locomotor stimulation (AILS) and apomorphine induced stereotypy (AIS) in mice, respectively.
+HAL	addiction	withdrawal	19298320	<b>Withdrawal</b> (48 hours) from long term (20 days) <strong>Hal</strong> (0.5 mg/kg i.p.)
+HAL	addiction	withdrawal	19298320	Ten days after <b>withdrawal</b> from long term treatment with <strong>Hal</strong> (but not with Ris or Ris + <strong>Hal</strong>), a potentiation in AILS was still observed.
+HAL	drug	alcohol	17005368	Haloperidol (<strong>HAL</strong>) evoked DA release was suppressed in groups exposed prenatally to <b>ethanol</b>, while <strong>HAL</strong> evoked DOPAC and HVA release was greatest after co exposure to prenatal cadmium and <b>ethanol</b>.
+HAL	drug	alcohol	17005368	These in vivo microdialysis results indicate that ontogenetic co exposure to cadmium, and <b>ethanol</b> produces a long lived suppressive effect on <strong>HAL</strong> evoked DA release and a long lived enhancing effect on AMPH evoked DA release in rat striatum.
+HAL	drug	amphetamine	17005368	These in vivo microdialysis results indicate that ontogenetic co exposure to cadmium, and ethanol produces a long lived suppressive effect on <strong>HAL</strong> evoked DA release and a long lived enhancing effect on <b>AMPH</b> evoked DA release in rat striatum.
+HAL	drug	amphetamine	16768607	Either <b>amphetamine</b> (<b>AMPH</b>; 0.5 or 1.0 mg/kg) or haloperidol (<strong>HAL</strong>; 0.1 mg/kg) were injected before 1 or all of the 3 PE sessions.
+HAL	drug	amphetamine	16768607	<b>AMPH</b> blocked the acquisition of LI if it was injected before each or before only the last PE session and <strong>HAL</strong> potentiated LI.
+HAL	drug	amphetamine	15894057	In the present experiment rats were trained on a three lever, drug discrimination task to discriminate the cues associated with 0.30 mg/kg of the indirect dopamine (DA) agonist, <b>amphetamine</b> (<b>AMPH</b>), saline (SAL), and 0.03 mg/kg of the DA, D2 receptor antagonist, haloperidol (<strong>HAL</strong>).
+HAL	drug	amphetamine	15894057	Choice behavior determined from tests on 0.30 and 0.15 mg/kg <b>AMPH</b>, SAL 0.03 and 0.015 mg/kg <strong>HAL</strong> provided a behavioral baseline presumed to represent changes along a continuum of DA mediated, interoceptive cues.
+HAL	drug	amphetamine	15894057	Results from separate groups tested on 0.30 and 0.15 mg/kg <b>AMPH</b>, SAL, 0.03 and 0.015 mg/kg <strong>HAL</strong>, 24 h post treatment with an acute 7.5 mg/kg dose of <b>AMPH</b>, showed rapid tolerance and withdrawal to the <b>AMPH</b> cue and sensitization to the <strong>HAL</strong> cue.
+HAL	addiction	sensitization	15894057	Results from separate groups tested on 0.30 and 0.15 mg/kg AMPH, SAL, 0.03 and 0.015 mg/kg <strong>HAL</strong>, 24 h post treatment with an acute 7.5 mg/kg dose of AMPH, showed rapid tolerance and withdrawal to the AMPH cue and <b>sensitization</b> to the <strong>HAL</strong> cue.
+HAL	addiction	withdrawal	15894057	Results from separate groups tested on 0.30 and 0.15 mg/kg AMPH, SAL, 0.03 and 0.015 mg/kg <strong>HAL</strong>, 24 h post treatment with an acute 7.5 mg/kg dose of AMPH, showed rapid tolerance and <b>withdrawal</b> to the AMPH cue and sensitization to the <strong>HAL</strong> cue.
+HAL	drug	amphetamine	15894057	The same tests 24 h following treatment with 1.0 mg/kg <strong>HAL</strong> showed rapid tolerance to the <strong>HAL</strong> cue, sensitization to the <b>AMPH</b> cue, but not <b>AMPH</b> like withdrawal cues.
+HAL	addiction	sensitization	15894057	The same tests 24 h following treatment with 1.0 mg/kg <strong>HAL</strong> showed rapid tolerance to the <strong>HAL</strong> cue, <b>sensitization</b> to the AMPH cue, but not AMPH like withdrawal cues.
+HAL	addiction	withdrawal	15894057	The same tests 24 h following treatment with 1.0 mg/kg <strong>HAL</strong> showed rapid tolerance to the <strong>HAL</strong> cue, sensitization to the AMPH cue, but not AMPH like <b>withdrawal</b> cues.
+HAL	drug	amphetamine	15894057	Analysis of the results showed that tolerance to the <b>AMPH</b> and <strong>HAL</strong> cues reflected neuroadaptive baseline shifts and not weaker cue properties.
+HAL	drug	amphetamine	15582685	Since dopamine (DA) has been implicated in mediating the <b>AMPH</b> cue, rats were trained to discriminate between 0.25 mg/kg <b>AMPH</b>, an indirect DA agonist, and 0.033 mg/kg haloperidol (<strong>HAL</strong>), a DA antagonist at the D2 receptor site.
+HAL	drug	amphetamine	15582685	Following acquisition of the discrimination, rats were tested for choice of responding on the <b>AMPH</b> and <strong>HAL</strong> levers at intervals from 6 to 72 h following treatment with a single dose of 3.0 mg/<b>AMPH</b>.
+HAL	drug	amphetamine	15582685	At short intervals after treatment with 3.0 mg/kg <b>AMPH</b>, rats responded primarily on the <b>AMPH</b> lever followed by a shift to predominant responding on the <strong>HAL</strong> lever 16 30 h post treatment, before returning to predrug levels.
+HAL	drug	amphetamine	12898122	It is well established that LI is impaired in rats and in humans by injections of the indirect dopamine agonist <b>amphetamine</b> (<b>AMPH</b>), and that this disruption can be prevented by co administration of either the typical neuroleptic haloperidol (<strong>HAL</strong>) or the atypical neuroleptic clozapine (CLZ).
+HAL	drug	amphetamine	12898122	We tested whether <b>AMPH</b> (0.5 mg/kg) pretreatment would disrupt LI of a conditioned aversion to sucrose, and if so, which stage of the procedure is critical for mediating the disruption; in addition, we tested whether <strong>HAL</strong> (0.2 mg/kg) or CLZ (5.0 mg/kg) could restore such an expected LI disruption.
+HAL	addiction	aversion	12898122	We tested whether AMPH (0.5 mg/kg) pretreatment would disrupt LI of a conditioned <b>aversion</b> to sucrose, and if so, which stage of the procedure is critical for mediating the disruption; in addition, we tested whether <strong>HAL</strong> (0.2 mg/kg) or CLZ (5.0 mg/kg) could restore such an expected LI disruption.
+HAL	drug	amphetamine	12898122	When <strong>HAL</strong> or CLZ was given 40 min before <b>AMPH</b> (before both pre exposure and conditioning), it blocked LI disruption.
+HAL	drug	amphetamine	9972698	Both of those stress induced immunosuppressive responses were no longer evident when <b>AMPH</b> pretreated rats were injected with haloperidol (<strong>HAL</strong>, 1 mg/kg i.p.)
+HAL	drug	amphetamine	8808141	Apomorphine (APO), <b>amphetamine</b> (AMP), and haloperidol (<strong>HAL</strong>) were administered systemically.
+HAL	addiction	reward	8201803	Our paper compares the effect of homopantothenic acid (HOPA) and haloperidol (<strong>HAL</strong>), i.e., representative neuroleptics, on intracranial self stimulation (<b>ICSS</b>) and locomotor activity.
+HAL	addiction	reward	8201803	On the other hand, haloperidol (<strong>HAL</strong>) markedly inhibited both <b>ICSS</b> and abnormal hyperactivity induced by MAP.
+HAL	addiction	withdrawal	8216693	The release and metabolism of dopamine (DA) in the striatum of these animals was then assessed using intracranial microdialysis during week 32 of <strong>HAL</strong> administration and 3 days after <b>withdrawal</b> of <strong>HAL</strong>.
+HAL	addiction	withdrawal	8216693	Three days after <b>withdrawal</b> from <strong>HAL</strong>, no difference was seen in basal extracellular concentrations of any of the analytes.
+HAL	drug	amphetamine	8216693	No difference in the magnitude of DA release was seen between groups following local application of <b>amphetamine</b> (10 microM) through the dialysis probe during or after chronic <strong>HAL</strong> administration.
+HAL	addiction	withdrawal	8216693	These results confirm previous findings that long term <strong>HAL</strong> administration produces increased DA turnover during <strong>HAL</strong> administration, but that this increase does not persist following <strong>HAL</strong> <b>withdrawal</b>.
+HAL	addiction	sensitization	1615128	The results indicated that injections of <strong>HAL</strong> given at IDIs of 1 or 2 days produced neither tolerance nor <b>sensitization</b>, whereas injections given at intervals of 7 or 14 days produced <b>sensitization</b>.
+HAL	addiction	sensitization	1615128	<b>Sensitization</b> was also observed in the control groups, perhaps as a result of the intermittent schedule of <strong>HAL</strong> injections given during the dose response tests.
+HAL	drug	amphetamine	1615128	Sensitization to <strong>HAL</strong> was not accompanied by changes in sensitivity to <b>amphetamine</b>.
+HAL	addiction	sensitization	1615128	<b>Sensitization</b> to <strong>HAL</strong> was not accompanied by changes in sensitivity to amphetamine.
+HAL	addiction	sensitization	1615128	In addition, evidence is presented that <b>sensitization</b> to <strong>HAL</strong> induced hypophagia is contingent on behavioral experience under the drug.
+HAL	drug	alcohol	1480736	The Halikas Crosby Drug Impairment Rating Scale for Cocaine (<strong>HAL</strong> DIRS C) is designed to measure improvement in drug treatment through interval assessment of impact of cocaine use on daily functioning, relationships with other people, other <b>alcohol</b> and drug use, cocaine withdrawal symptoms, adverse effects associated with cocaine use, and personal outlook over the previous week.
+HAL	drug	cocaine	1480736	The Halikas Crosby Drug Impairment Rating Scale for <b>Cocaine</b> (<strong>HAL</strong> DIRS C) is designed to measure improvement in drug treatment through interval assessment of impact of <b>cocaine</b> use on daily functioning, relationships with other people, other alcohol and drug use, <b>cocaine</b> withdrawal symptoms, adverse effects associated with <b>cocaine</b> use, and personal outlook over the previous week.
+HAL	addiction	withdrawal	1480736	The Halikas Crosby Drug Impairment Rating Scale for Cocaine (<strong>HAL</strong> DIRS C) is designed to measure improvement in drug treatment through interval assessment of impact of cocaine use on daily functioning, relationships with other people, other alcohol and drug use, cocaine <b>withdrawal</b> symptoms, adverse effects associated with cocaine use, and personal outlook over the previous week.
+HAL	drug	cocaine	1480736	The results support the validity of the <strong>HAL</strong> DIRS C as a standardized measure of improvement or outcome in clinical research involving the treatment of <b>cocaine</b> abuse.
+HAL	drug	amphetamine	1365673	Rats were trained to discriminate between 0.25 mg/kg <b>amphetamine</b> (<b>AMPH</b>) and 0.03 mg/kg haloperidol (<strong>HAL</strong>) in a two lever drug discrimination task.
+HAL	drug	amphetamine	1365673	In order to test for a drug induced withdrawal state, animals were assigned to one of three chronic treatment groups and given injections of <b>AMPH</b>, <strong>HAL</strong>, or distilled water (DW) for 10 consecutive days.
+HAL	addiction	withdrawal	1365673	In order to test for a drug induced <b>withdrawal</b> state, animals were assigned to one of three chronic treatment groups and given injections of AMPH, <strong>HAL</strong>, or distilled water (DW) for 10 consecutive days.
+HAL	drug	amphetamine	1365673	At the 24 h retest interval, subjects injected with <b>AMPH</b> responded as though administered an acute dose of <strong>HAL</strong> (0.028 mg/kg) and subjects injected with chronic <strong>HAL</strong> responded as though administered an acute dose of <b>AMPH</b> (0.15 mg/kg).
+HAL	drug	amphetamine	1365673	To determine whether the rebound observed after 10 days of drug treatment was present after a single injection, independent groups of subjects were injected with single doses of either 10 mg/kg <b>AMPH</b> or 1.0 mg/kg <strong>HAL</strong> and then retested from 4 h to 48 h later.
+HAL	drug	amphetamine	1365673	Single doses of both <b>AMPH</b> and <strong>HAL</strong> produced significant rebounds that peaked between 20 h (<b>AMPH</b>) and 24 h (<strong>HAL</strong>) following administration.
+HAL	drug	amphetamine	1365673	In a third experiment, animals were tested with or without acute doses of drug following pretreatment with either <strong>HAL</strong> or <b>AMPH</b>.
+HAL	drug	amphetamine	1365673	Receptor supersensitivity accounts for the tolerance observed to <strong>HAL</strong> 24 h after treatment with 1.0 mg/kg <strong>HAL</strong>, whereas receptor subsensitivity accounts for the tolerance observed 20 h after treatment with 10 mg/kg <b>AMPH</b>.
+HAL	drug	amphetamine	1646666	Haloperidol (<strong>HAL</strong>) treatment failed to block the stimulant induced increase in kindling acquisition indicating that changes in dopamine (DA) are not necessary for the <b>AMPH</b>/kindling synergism to develop.
+HAL	drug	cocaine	1811758	The Halikas Crosby Drug Impairment Rating Scale for <b>Cocaine</b> (<strong>HAL</strong> DIRS C) is designed to measure the adverse impact of <b>cocaine</b> use upon life functioning over the previous week.
+HAL	drug	cocaine	1811758	The <strong>HAL</strong> DIRS C correlated significantly with self reported <b>cocaine</b> use, craving for <b>cocaine</b>, and independent ratings of the severity of addiction.
+HAL	addiction	addiction	1811758	The <strong>HAL</strong> DIRS C correlated significantly with self reported cocaine use, craving for cocaine, and independent ratings of the severity of <b>addiction</b>.
+HAL	addiction	relapse	1811758	The <strong>HAL</strong> DIRS C correlated significantly with self reported cocaine use, <b>craving</b> for cocaine, and independent ratings of the severity of addiction.
+HAL	drug	cocaine	1811758	Our results suggest that the <strong>HAL</strong> DIRS C may be useful as a standardized measure of improvement or outcome in clinical research involving the treatment of <b>cocaine</b> abuse.
+HAL	drug	amphetamine	1982903	The effects of the following drugs on the duration of footshock induced freezing were studied: diazepam (DZP); 2 amino 4,5 (1,2 cyclohexyl) 7 phosphonoheptonic acid (NPC 12626); 3 ((+/ ) 2 carboxypiperazine 4 yl) propyl l phosphonic acid (CPP); [(+) 5 methyl 10 11,dihydroxy 5H dibenzo(a,d)cyclohepten 5,10  imine (MK 801); buspirone hydrochloride (BUS); DL <b>amphetamine</b> sulfate (AMP); haloperidol (<strong>HAL</strong>); ethyl beta carboline 3 carboxylate (beta CCE).
+HAL	drug	benzodiazepine	1982903	The effects of the following drugs on the duration of footshock induced freezing were studied: <b>diazepam</b> (DZP); 2 amino 4,5 (1,2 cyclohexyl) 7 phosphonoheptonic acid (NPC 12626); 3 ((+/ ) 2 carboxypiperazine 4 yl) propyl l phosphonic acid (CPP); [(+) 5 methyl 10 11,dihydroxy 5H dibenzo(a,d)cyclohepten 5,10  imine (MK 801); buspirone hydrochloride (BUS); DL amphetamine sulfate (AMP); haloperidol (<strong>HAL</strong>); ethyl beta carboline 3 carboxylate (beta CCE).
+HAL	addiction	reward	1982903	The effects of the following drugs on the duration of footshock induced freezing were studied: diazepam (DZP); 2 amino 4,5 (1,2 cyclohexyl) 7 phosphonoheptonic acid (NPC 12626); 3 ((+/ ) 2 carboxypiperazine 4 yl) propyl l phosphonic acid (<b>CPP</b>); [(+) 5 methyl 10 11,dihydroxy 5H dibenzo(a,d)cyclohepten 5,10  imine (MK 801); buspirone hydrochloride (BUS); DL amphetamine sulfate (AMP); haloperidol (<strong>HAL</strong>); ethyl beta carboline 3 carboxylate (beta CCE).
+HAL	addiction	withdrawal	4080767	This study was designed to assess whether phencyclidine (PCP) produces dopamine (DA) dependent behaviors such as licking, biting and gnawing at low doses after <b>withdrawal</b> from chronic haloperidol (<strong>HAL</strong>) treatment in rats.
+HAL	addiction	withdrawal	4080767	Low doses of PCP (2.5 and 5 mg/kg) produced licking, gnawing, biting and self biting in rats after <b>withdrawal</b> from chronic <strong>HAL</strong> treatment, which were not observed in the vehicle pretreated rats given PCP at the same dose range.
+HAL	drug	amphetamine	4080767	These behaviors were similar to DA dependent behaviors produced by <b>methamphetamine</b> and apomorphine in rats after withdrawal from chronic <strong>HAL</strong> treatment.
+HAL	addiction	withdrawal	4080767	These behaviors were similar to DA dependent behaviors produced by methamphetamine and apomorphine in rats after <b>withdrawal</b> from chronic <strong>HAL</strong> treatment.
+HAL	addiction	withdrawal	4080767	Furthermore, at doses of 5 or 7.5 mg/kg, PCP induced head weaving and backpedalling, which were mediated by both DA and serotonin (5 HT) neurons, significantly increased in rats after <b>withdrawal</b> from chronic <strong>HAL</strong> treatment.
+HAL	drug	benzodiazepine	6151209	Acute drug effects on the three dependent variables were assessed for dose ranges of haloperidol (<strong>HAL</strong>), chlorpromazine (CPZ), clozapine (CLZ), and <b>chlordiazepoxide</b> (CDP).
+TSPO	drug	benzodiazepine	32698131	Despite being a highly conserved protein, the precise role of the mitochondrial translocator protein (<strong>TSPO</strong>), previously known as the peripheral <b>benzodiazepine</b> receptor (PBR), remains elusive.
+TSPO	drug	benzodiazepine	32698131	Despite being a highly conserved protein, the precise role of the mitochondrial <strong>translocator protein</strong> (<strong>TSPO</strong>), previously known as the peripheral <b>benzodiazepine</b> receptor (PBR), remains elusive.
+TSPO	addiction	reward	32698131	These findings provide further <b>reinforcement</b> that the much sought after mechanism of <strong>TSPO</strong>/PBR function remains correlated with the extent of cellular triglyceride metabolism.
+TSPO	drug	amphetamine	32570138	No significant elevation of <strong>translocator protein</strong> binding in the brains of recently abstinent <b>methamphetamine</b> users.
+TSPO	drug	amphetamine	32570138	One study using this approach showed substantial <strong>TSPO</strong> elevation throughout the brain in chronic <b>methamphetamine</b> users following long term abstinence (0.5 4 years), but clients typically present for treatment earlier in abstinence.
+TSPO	drug	amphetamine	32570138	We used PET with [11C]DAA1106 to compare standardized uptake values (SUVs) as an index of <strong>TSPO</strong> binding in the brains of <b>methamphetamine</b> dependent participants who were abstinent for < 6 months (n = 11) and healthy controls (n = 12).
+TSPO	drug	amphetamine	32570138	The discrepancy between the lack of significant difference in <strong>TSPO</strong> binding in early abstinent <b>methamphetamine</b> users vs. controls in this study and a previous report of elevated binding in longer abstinent <b>methamphetamine</b> users may reflect methodological differences or limitations of <strong>TSPO</strong> binding as an index of neuroinflammation.
+TSPO	drug	amphetamine	32017280	Microglia imaging in <b>methamphetamine</b> use disorder: a positron emission tomography study with the 18 kDa <strong>translocator protein</strong> radioligand [F 18]FEPPA.
+TSPO	drug	alcohol	31713961	<strong>TSPO</strong> polymorphism in individuals with <b>alcohol</b> use disorder: Association with cholesterol levels and withdrawal severity.
+TSPO	addiction	withdrawal	31713961	<strong>TSPO</strong> polymorphism in individuals with alcohol use disorder: Association with cholesterol levels and <b>withdrawal</b> severity.
+TSPO	drug	alcohol	31713961	Although it is recognized that <b>alcohol</b> increases plasma high density lipoproteins (HDLs), its effects on total cholesterol and triglycerides along with its relationship to <strong>TSPO</strong> genotype have not been assessed.
+TSPO	drug	alcohol	31713961	Additionally, we showed a significant effect of <strong>TSPO</strong> rs6971 on withdrawal scores (Clinical Institute Withdrawal Assessment for <b>Alcohol</b> [CIWA]), with higher scores in AA (n = 50) compared with AG (n = 238) and GG (n = 428).
+TSPO	addiction	withdrawal	31713961	Additionally, we showed a significant effect of <strong>TSPO</strong> rs6971 on <b>withdrawal</b> scores (Clinical Institute <b>Withdrawal</b> Assessment for Alcohol [CIWA]), with higher scores in AA (n = 50) compared with AG (n = 238) and GG (n = 428).
+TSPO	addiction	withdrawal	31713961	We also reveal for the first time an association in AUD participants between <strong>TSPO</strong> rs6971 genotype and plasma cholesterol, LDL, and triglyceride levels (not for HDL) and with <b>withdrawal</b> severity.
+TSPO	drug	alcohol	31713961	Mediation analyses revealed that LDL (but not HDL) influenced the association between <strong>TSPO</strong> and <b>alcohol</b> withdrawal severity.
+TSPO	addiction	withdrawal	31713961	Mediation analyses revealed that LDL (but not HDL) influenced the association between <strong>TSPO</strong> and alcohol <b>withdrawal</b> severity.
+TSPO	drug	alcohol	31176599	Corrigendum to "Evaluation of <strong>TSPO</strong> PET imaging, a marker of glial activation, to study the neuroimmune footprints of morphine exposure and withdrawal" [Drug <b>Alcohol</b> Depend.
+TSPO	drug	opioid	31176599	Corrigendum to "Evaluation of <strong>TSPO</strong> PET imaging, a marker of glial activation, to study the neuroimmune footprints of <b>morphine</b> exposure and withdrawal" [Drug Alcohol Depend.
+TSPO	addiction	withdrawal	31176599	Corrigendum to "Evaluation of <strong>TSPO</strong> PET imaging, a marker of glial activation, to study the neuroimmune footprints of morphine exposure and <b>withdrawal</b>" [Drug Alcohol Depend.
+TSPO	drug	alcohol	30803059	Detecting neuroinflammation in the brain following chronic <b>alcohol</b> exposure in rats: A comparison between in vivo and in vitro <strong>TSPO</strong> radioligand binding.
+TSPO	drug	alcohol	30803059	However, positron emission tomography (PET) studies using radioligands for the 18 kDa translocator protein (<strong>TSPO</strong>), which is considered a biomarker of neuroinflammation, reported decreased binding in <b>alcohol</b> use disorder (AUD) participants compared to controls.
+TSPO	drug	alcohol	30803059	However, positron emission tomography (PET) studies using radioligands for the 18 kDa <strong>translocator protein</strong> (<strong>TSPO</strong>), which is considered a biomarker of neuroinflammation, reported decreased binding in <b>alcohol</b> use disorder (AUD) participants compared to controls.
+TSPO	drug	alcohol	30803059	In contrast, autoradiographic findings in <b>alcohol</b> exposed rats reported increases in <strong>TSPO</strong> radioligand binding.
+TSPO	drug	alcohol	30803059	Failure to observe similar increases in [11 C]PBR28 binding in vivo suggests the possibility that a mechanism mediated by chronic <b>alcohol</b> exposure interferes with [11 C]PBR28 binding to <strong>TSPO</strong> in vivo.
+TSPO	addiction	addiction	30695700	With an emphasis on neuroimaging techniques, this review examines human studies of <b>addiction</b> using positron emission tomography to identify binding of translocator protein (<strong>TSPO</strong>), which is upregulated in reactive glial cells and activated microglia during pathological states.
+TSPO	addiction	addiction	30695700	With an emphasis on neuroimaging techniques, this review examines human studies of <b>addiction</b> using positron emission tomography to identify binding of <strong>translocator protein</strong> (<strong>TSPO</strong>), which is upregulated in reactive glial cells and activated microglia during pathological states.
+TSPO	drug	amphetamine	30695700	High <strong>TSPO</strong> levels have been shown in <b>methamphetamine</b> use but exhibits variable patterns in cocaine use.
+TSPO	drug	cocaine	30695700	High <strong>TSPO</strong> levels have been shown in methamphetamine use but exhibits variable patterns in <b>cocaine</b> use.
+TSPO	drug	alcohol	30695700	<b>Alcohol</b> and nicotine use, however, are associated with lower <strong>TSPO</strong> levels.
+TSPO	drug	nicotine	30695700	Alcohol and <b>nicotine</b> use, however, are associated with lower <strong>TSPO</strong> levels.
+TSPO	drug	nicotine	30343364	Using positron emission tomography (PET) scanning, our group recently demonstrated that <b>smokers</b> in the satiated state had 16.8% less binding of the radiotracer [11C]DAA1106 (a radioligand for <strong>TSPO</strong>) in the brain than nonsmokers.
+TSPO	drug	nicotine	30343364	Forty participants (22 <b>smokers</b> and 18 nonsmokers) completed the study (at one of two sites) and had usable data, which included images from a dynamic [11C]DAA1106 PET scanning session (with <b>smokers</b> having been abstinent for 17.9 ± 2.3 h) and a blood sample for <strong>TSPO</strong> genotyping.
+TSPO	drug	nicotine	30343364	Whole brain standardized uptake values (SUVs) were determined, and analysis of variance was performed, with group (overnight abstinent <b>smoker</b> vs. nonsmoker), site, and <strong>TSPO</strong> genotype as factors, thereby controlling for site and genotype.
+TSPO	drug	alcohol	28944558	Imaging the neuroimmune response to <b>alcohol</b> exposure in adolescent baboons: a <strong>TSPO</strong> PET study using 18 F DPA 714.
+TSPO	drug	alcohol	28944558	The neuroimmune response to an initial and acute <b>alcohol</b> exposure was investigated using translocator protein 18 kDa (<strong>TSPO</strong>) PET imaging, a non invasive marker of glial activation, in adolescent baboons.
+TSPO	drug	alcohol	28944558	The neuroimmune response to an initial and acute <b>alcohol</b> exposure was investigated using <strong>translocator protein</strong> 18 kDa (<strong>TSPO</strong>) PET imaging, a non invasive marker of glial activation, in adolescent baboons.
+TSPO	drug	benzodiazepine	28405935	The translocator protein (<strong>TSPO</strong>), formerly known as the peripheral type <b>benzodiazepine</b> receptor (PBR), is considered an important regulator of steroidogenesis and a potential therapeutic target in neurological disorders.
+TSPO	drug	benzodiazepine	28405935	The <strong>translocator protein</strong> (<strong>TSPO</strong>), formerly known as the peripheral type <b>benzodiazepine</b> receptor (PBR), is considered an important regulator of steroidogenesis and a potential therapeutic target in neurological disorders.
+TSPO	addiction	withdrawal	28405935	Finally, our findings suggest that <strong>TSPO</strong> might be involved in reducing oxidative stress by preserving mitochondrial functions in astrocytic cells exposed to glucose <b>withdrawal</b>.
+TSPO	drug	alcohol	28242869	In vivo imaging of <strong>translocator protein</strong>, a marker of activated microglia, in <b>alcohol</b> dependence.
+TSPO	addiction	dependence	28242869	In vivo imaging of <strong>translocator protein</strong>, a marker of activated microglia, in alcohol <b>dependence</b>.
+TSPO	drug	alcohol	28242869	Brain levels of 18 kDa translocator protein (<strong>TSPO</strong>), a marker of microglial activation and neuroinflammation, were measured with [11C]PBR28 positron emission tomography imaging in 15 healthy controls and 15 <b>alcohol</b> dependent subjects.
+TSPO	drug	alcohol	28242869	Brain levels of 18 kDa <strong>translocator protein</strong> (<strong>TSPO</strong>), a marker of microglial activation and neuroinflammation, were measured with [11C]PBR28 positron emission tomography imaging in 15 healthy controls and 15 <b>alcohol</b> dependent subjects.
+TSPO	drug	alcohol	28242869	Linear mixed modeling of partial volume corrected [11C]PBR28 data revealed a main effect of <b>alcohol</b> dependence (P=0.034), corresponding to 10% lower <strong>TSPO</strong> levels in <b>alcohol</b> dependent subjects.
+TSPO	addiction	dependence	28242869	Linear mixed modeling of partial volume corrected [11C]PBR28 data revealed a main effect of alcohol <b>dependence</b> (P=0.034), corresponding to 10% lower <strong>TSPO</strong> levels in alcohol dependent subjects.
+TSPO	drug	alcohol	28242869	Within this group, exploratory analyses found a negative association of <strong>TSPO</strong> levels in the hippocampus and striatum with <b>alcohol</b> dependence severity (P<0.035).
+TSPO	addiction	dependence	28242869	Within this group, exploratory analyses found a negative association of <strong>TSPO</strong> levels in the hippocampus and striatum with alcohol <b>dependence</b> severity (P<0.035).
+TSPO	drug	alcohol	28072413	Decreased hippocampal <strong>translocator protein</strong> (18 kDa) expression in <b>alcohol</b> dependence: a [11C]PBR28 PET study.
+TSPO	addiction	dependence	28072413	Decreased hippocampal <strong>translocator protein</strong> (18 kDa) expression in alcohol <b>dependence</b>: a [11C]PBR28 PET study.
+TSPO	drug	alcohol	28072413	We investigated whether there was microglial activation in recently detoxified <b>alcohol</b> dependent patients (ADP), using [11C]PBR28 positron emission tomography (PET), selective for the 18kDa translocator protein (<strong>TSPO</strong>) highly expressed in activated microglia and astrocytes.
+TSPO	drug	alcohol	28072413	We investigated whether there was microglial activation in recently detoxified <b>alcohol</b> dependent patients (ADP), using [11C]PBR28 positron emission tomography (PET), selective for the 18kDa <strong>translocator protein</strong> (<strong>TSPO</strong>) highly expressed in activated microglia and astrocytes.
+TSPO	drug	opioid	27875800	Evaluation of <strong>TSPO</strong> PET imaging, a marker of glial activation, to study the neuroimmune footprints of <b>morphine</b> exposure and withdrawal.
+TSPO	addiction	withdrawal	27875800	Evaluation of <strong>TSPO</strong> PET imaging, a marker of glial activation, to study the neuroimmune footprints of morphine exposure and <b>withdrawal</b>.
+TSPO	drug	opioid	27875800	We hypothesized that <strong>TSPO</strong> PET imaging may be used to study the neuroimmune component of <b>opioid</b> tolerance and withdrawal.
+TSPO	addiction	withdrawal	27875800	We hypothesized that <strong>TSPO</strong> PET imaging may be used to study the neuroimmune component of opioid tolerance and <b>withdrawal</b>.
+TSPO	drug	opioid	27875800	The baseline binding of [18F]DPA 714 to the brain (VT=0.086±0.009mLcm 3) was not increased by <b>morphine</b> exposure and withdrawal (VT=0.079±0.010mLcm 3) indicating the absence of <strong>TSPO</strong> overexpression, even at the regional level.
+TSPO	addiction	withdrawal	27875800	The baseline binding of [18F]DPA 714 to the brain (VT=0.086±0.009mLcm 3) was not increased by morphine exposure and <b>withdrawal</b> (VT=0.079±0.010mLcm 3) indicating the absence of <strong>TSPO</strong> overexpression, even at the regional level.
+TSPO	addiction	dependence	27599516	<b>Dependence</b> of anxiolytic effects of the dipeptide <strong>TSPO</strong> ligand GD 23 on neurosteroid biosynthesis.
+TSPO	drug	benzodiazepine	27485488	To determine if the effects of these drugs were due to the GABAA receptor and/or translocator protein (<strong>TSPO</strong>), we also pretreated rats with an antagonist for the <b>benzodiazepine</b> binding site on the GABAA receptor (i.e., flumazenil) and a <strong>TSPO</strong> antagonist (i.e., PK11195) prior to <b>alprazolam</b> or <b>oxazepam</b> administration.
+TSPO	drug	benzodiazepine	27485488	To determine if the effects of these drugs were due to the GABAA receptor and/or <strong>translocator protein</strong> (<strong>TSPO</strong>), we also pretreated rats with an antagonist for the <b>benzodiazepine</b> binding site on the GABAA receptor (i.e., flumazenil) and a <strong>TSPO</strong> antagonist (i.e., PK11195) prior to <b>alprazolam</b> or <b>oxazepam</b> administration.
+TSPO	drug	amphetamine	27485488	The GABAA receptor is responsible for the alprazolam induced enhancement of <b>methamphetamine</b> self administration, while the activation of both the GABAA receptor and <strong>TSPO</strong> are responsible for the oxazepam induced reduction of <b>methamphetamine</b> self administration.
+TSPO	drug	benzodiazepine	27485488	The GABAA receptor is responsible for the <b>alprazolam</b> induced enhancement of methamphetamine self administration, while the activation of both the GABAA receptor and <strong>TSPO</strong> are responsible for the <b>oxazepam</b> induced reduction of methamphetamine self administration.
+TSPO	drug	benzodiazepine	25589941	It also modulates GABAA receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa translocator protein (<strong>TSPO</strong>) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral <b>benzodiazepine</b> receptor (PBR).
+TSPO	drug	benzodiazepine	25589941	It also modulates GABAA receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa <strong>translocator protein</strong> (<strong>TSPO</strong>) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral <b>benzodiazepine</b> receptor (PBR).
+TSPO	drug	benzodiazepine	25589941	It seems promising that non <b>benzodiazepine</b> anxiolytics including etifoxine will replenish shortcomings of benzodiazepines and selective serotonin reuptake inhibitors according to animated studies related to <strong>TSPO</strong>.
+TSPO	drug	cocaine	25057196	<b>Cocaine</b> abuse in humans is not associated with increased microglial activation: an 18 kDa <strong>translocator protein</strong> positron emission tomography imaging study with [11C]PBR28.
+TSPO	drug	cocaine	25057196	To test this hypothesis, we used positron emission tomography imaging to measure the binding of [(11)C]PBR28 to the 18 kDa translocator protein (<strong>TSPO</strong>), a marker for microglial activation in a group of 15 recently abstinent <b>cocaine</b> abusers and 17 matched healthy controls.
+TSPO	drug	cocaine	25057196	To test this hypothesis, we used positron emission tomography imaging to measure the binding of [(11)C]PBR28 to the 18 kDa <strong>translocator protein</strong> (<strong>TSPO</strong>), a marker for microglial activation in a group of 15 recently abstinent <b>cocaine</b> abusers and 17 matched healthy controls.
+TSPO	drug	cocaine	25057196	The results of this in vivo study do not support increased <strong>TSPO</strong> expression and, by extension, microglial activation in chronic <b>cocaine</b> abusing humans.
+TSPO	drug	benzodiazepine	24763106	Recently, the translocator protein (18 kDa) (<strong>TSPO</strong>), previously called peripheral <b>benzodiazepine</b> receptor (PBR) and both the starting point and an important rate limiting step in neurosteroidogenesis, has received increased attention in the pathophysiology of post traumatic stress disorder (PTSD) because it affects the production of neurosteroids, reinforcing the hypothesis that selective <strong>TSPO</strong> ligands could potentially be used as anti PTSD drugs.
+TSPO	addiction	reward	24763106	Recently, the translocator protein (18 kDa) (<strong>TSPO</strong>), previously called peripheral benzodiazepine receptor (PBR) and both the starting point and an important rate limiting step in neurosteroidogenesis, has received increased attention in the pathophysiology of post traumatic stress disorder (PTSD) because it affects the production of neurosteroids, <b>reinforcing</b> the hypothesis that selective <strong>TSPO</strong> ligands could potentially be used as anti PTSD drugs.
+TSPO	drug	benzodiazepine	24763106	Recently, the <strong>translocator protein</strong> (18 kDa) (<strong>TSPO</strong>), previously called peripheral <b>benzodiazepine</b> receptor (PBR) and both the starting point and an important rate limiting step in neurosteroidogenesis, has received increased attention in the pathophysiology of post traumatic stress disorder (PTSD) because it affects the production of neurosteroids, reinforcing the hypothesis that selective <strong>TSPO</strong> ligands could potentially be used as anti PTSD drugs.
+TSPO	addiction	reward	24763106	Recently, the <strong>translocator protein</strong> (18 kDa) (<strong>TSPO</strong>), previously called peripheral benzodiazepine receptor (PBR) and both the starting point and an important rate limiting step in neurosteroidogenesis, has received increased attention in the pathophysiology of post traumatic stress disorder (PTSD) because it affects the production of neurosteroids, <b>reinforcing</b> the hypothesis that selective <strong>TSPO</strong> ligands could potentially be used as anti PTSD drugs.
+TSPO	addiction	sensitization	24763106	As expected, we showed that chronic treatment with YL IPA08 [N ethyl N (2 pyridinylmethyl) 2 (3,4 ichlorophenyl) 7 methylimidazo [1,2 a] pyridine 3 acetamide hydrochloride], a potent and selective <strong>TSPO</strong> ligand synthesized by our institute, caused significant suppression of enhanced anxiety and contextual fear induced in the inescapable electric foot shock induced mouse model of PTSD and the time dependent <b>sensitization</b> (TDS) procedure.
+TSPO	drug	alcohol	24566803	Using double immunofluorescent labeling we determined that adrenal dependence of 3α,5α THP induction by <b>ethanol</b> is not due to a lack of colocalization of 3α,5α THP with the cholesterol transporters steroidogenic acute regulatory protein (StAR) or translocator protein (<strong>TSPO</strong>).
+TSPO	addiction	dependence	24566803	Using double immunofluorescent labeling we determined that adrenal <b>dependence</b> of 3α,5α THP induction by ethanol is not due to a lack of colocalization of 3α,5α THP with the cholesterol transporters steroidogenic acute regulatory protein (StAR) or translocator protein (<strong>TSPO</strong>).
+TSPO	drug	alcohol	24566803	Using double immunofluorescent labeling we determined that adrenal dependence of 3α,5α THP induction by <b>ethanol</b> is not due to a lack of colocalization of 3α,5α THP with the cholesterol transporters steroidogenic acute regulatory protein (StAR) or <strong>translocator protein</strong> (<strong>TSPO</strong>).
+TSPO	addiction	dependence	24566803	Using double immunofluorescent labeling we determined that adrenal <b>dependence</b> of 3α,5α THP induction by ethanol is not due to a lack of colocalization of 3α,5α THP with the cholesterol transporters steroidogenic acute regulatory protein (StAR) or <strong>translocator protein</strong> (<strong>TSPO</strong>).
+TSPO	drug	amphetamine	23739178	<b>METH</b>, but not MMC, self administration elevated <strong>TSPO</strong> receptor density in the nucleus accumbens and hippocampus, while MMC, but not <b>METH</b>, self administration decreased striatal 5 hydroxyindolacetic acid (5 HIAA) concentrations.
+TSPO	drug	benzodiazepine	19541954	<strong>Translocator protein</strong> (18 kD) as target for anxiolytics without <b>benzodiazepine</b> like side effects.
+TSPO	addiction	withdrawal	19497344	Lack of tolerance to anxiolysis and <b>withdrawal</b> symptoms in mice repeatedly treated with AC 5216, a selective <strong>TSPO</strong> ligand.
+TSPO	drug	benzodiazepine	18333964	The translocator protein (18 kDa; <strong>TSPO</strong>), formerly known as the peripheral <b>benzodiazepine</b> receptor, is an outer mitochondrial membrane protein that associates with the mitochondrial permeability transition pore to regulate both steroidogenesis and apoptosis.
+TSPO	drug	benzodiazepine	18333964	The <strong>translocator protein</strong> (18 kDa; <strong>TSPO</strong>), formerly known as the peripheral <b>benzodiazepine</b> receptor, is an outer mitochondrial membrane protein that associates with the mitochondrial permeability transition pore to regulate both steroidogenesis and apoptosis.
+TSPO	addiction	withdrawal	18333964	The <strong>TSPO</strong> ligand Ro5 4864 rescued cultured neonatal DRG neurons from nerve growth factor <b>withdrawal</b> induced apoptosis and protected neonatal spinal cord motor neurons from death due to sciatic nerve axotomy.
+TSPO	drug	benzodiazepine	17561380	The influence of clozapine treatment and other antipsychotics on the 18 kDa <strong>translocator protein</strong>, formerly named the peripheral type <b>benzodiazepine</b> receptor, and steroid production.
+TSPO	drug	benzodiazepine	17561380	The 18 kDa translocator protein (<strong>TSPO</strong>), formerly known as the peripheral type <b>benzodiazepine</b> receptor, has been demonstrated to be involved in the process of steroid biosynthesis, in peripheral steroidogenic tissues as well as in glia cells in the brain.
+TSPO	drug	benzodiazepine	17561380	The 18 kDa <strong>translocator protein</strong> (<strong>TSPO</strong>), formerly known as the peripheral type <b>benzodiazepine</b> receptor, has been demonstrated to be involved in the process of steroid biosynthesis, in peripheral steroidogenic tissues as well as in glia cells in the brain.
+TPH2	drug	opioid	30059533	Impacts of GRIN3A, GRM6 and <strong>TPH2</strong> genetic polymorphisms on quality of life in <b>methadone</b> maintenance therapy population.
+TPH2	drug	alcohol	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and binge drinking at first follow up, two genetic variants on tryptophan hydroxylase 2 (<strong>TPH2</strong>; rs17110451, rs7963717), sensation seeking and impulsivity, and having a greater fraction of peers who drink or encourage drinking <b>alcohol</b> were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for binge drinking at second follow up.
+TPH2	addiction	intoxication	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and <b>binge</b> drinking at first follow up, two genetic variants on tryptophan hydroxylase 2 (<strong>TPH2</strong>; rs17110451, rs7963717), sensation seeking and impulsivity, and having a greater fraction of peers who drink or encourage drinking alcohol were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for <b>binge</b> drinking at second follow up.
+TPH2	addiction	relapse	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and binge drinking at first follow up, two genetic variants on tryptophan hydroxylase 2 (<strong>TPH2</strong>; rs17110451, rs7963717), sensation <b>seeking</b> and impulsivity, and having a greater fraction of peers who drink or encourage drinking alcohol were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for binge drinking at second follow up.
+TPH2	drug	alcohol	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and binge drinking at first follow up, two genetic variants on <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>; rs17110451, rs7963717), sensation seeking and impulsivity, and having a greater fraction of peers who drink or encourage drinking <b>alcohol</b> were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for binge drinking at second follow up.
+TPH2	addiction	intoxication	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and <b>binge</b> drinking at first follow up, two genetic variants on <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>; rs17110451, rs7963717), sensation seeking and impulsivity, and having a greater fraction of peers who drink or encourage drinking alcohol were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for <b>binge</b> drinking at second follow up.
+TPH2	addiction	relapse	29697747	After adjusting for demographic characteristics, underlying genetic clustering, and binge drinking at first follow up, two genetic variants on <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>; rs17110451, rs7963717), sensation <b>seeking</b> and impulsivity, and having a greater fraction of peers who drink or encourage drinking alcohol were associated with greater risk whereas another genetic variant on <strong>TPH2</strong> (rs11178999) and having a greater fraction of close family relationships were associated with reduced risk for binge drinking at second follow up.
+TPH2	addiction	relapse	29697747	Genetic variants in TPH1 (rs591556) were associated with sensation <b>seeking</b> and impulsivity, while genetic variants in <strong>TPH2</strong> (rs17110451) were associated with the fraction of drinkers in family.
+TPH2	drug	nicotine	29310005	Rs4570625 of <strong>tryptophan hydroxylase 2</strong> was significantly associated with <b>smoking</b> cessation in dominant model (p=0.03).
+TPH2	drug	cocaine	28590957	Genetic moderation of <b>cocaine</b> subjective effects by variation in the TPH1, <strong>TPH2</strong>, and SLC6A4 serotonin genes.
+TPH2	drug	cocaine	28590957	This study investigated variants of tryptophan hydroxylase (TPH)1, <strong>TPH2</strong>, and SLC6A4 in the moderation of the subjective effects of <b>cocaine</b>.
+TPH2	drug	cocaine	28590957	These findings indicate that TPH1, <strong>TPH2</strong>, and SLC6A4 variants moderate the subjective effects of <b>cocaine</b> in non treatment seeking <b>cocaine</b> dependent participants.
+TPH2	addiction	relapse	28590957	These findings indicate that TPH1, <strong>TPH2</strong>, and SLC6A4 variants moderate the subjective effects of cocaine in non treatment <b>seeking</b> cocaine dependent participants.
+TPH2	drug	alcohol	26497913	Increased <b>ethanol</b> consumption despite taste aversion in mice with a human <strong>tryptophan hydroxylase 2</strong> loss of function mutation.
+TPH2	addiction	aversion	26497913	Increased ethanol consumption despite taste <b>aversion</b> in mice with a human <strong>tryptophan hydroxylase 2</strong> loss of function mutation.
+TPH2	addiction	addiction	26497913	However, little is known about the impact of <strong>Tph2</strong> gene variants on <b>addiction</b>.
+TPH2	drug	alcohol	26497913	Mice expressing a human <strong>Tph2</strong> loss of function variant were used to investigate consequences of aversive conditions on <b>ethanol</b> intake.
+TPH2	addiction	aversion	26497913	Mice expressing a human <strong>Tph2</strong> loss of function variant were used to investigate consequences of <b>aversive</b> conditions on ethanol intake.
+TPH2	drug	alcohol	26497913	Effect of familiarization to <b>ethanol</b> or an <b>ethanol</b> quinine solution was then evaluated using a two bottles preference test in <strong>Tph2</strong> KI and control littermates.
+TPH2	drug	alcohol	26497913	These results indicate that loss of function mutation in <strong>Tph2</strong> results in greater motivation for <b>ethanol</b> consumption under aversive conditions and may confer enhanced sensitivity to <b>alcohol</b> use disorder.
+TPH2	addiction	aversion	26497913	These results indicate that loss of function mutation in <strong>Tph2</strong> results in greater motivation for ethanol consumption under <b>aversive</b> conditions and may confer enhanced sensitivity to alcohol use disorder.
+TPH2	drug	alcohol	26265436	Current evidence suggests that genetic variability of the serotonergic biosynthesis enzyme tryptophan hydroxylase 2 (<strong>TPH2</strong>) and the serotonin transporter (SLC6A4) genes mediates the efficacy of several addiction treatments, such as ondansetron and <b>disulfiram</b>, and the antidepressants bupropion, nortriptyline and sertraline.
+TPH2	addiction	addiction	26265436	Current evidence suggests that genetic variability of the serotonergic biosynthesis enzyme tryptophan hydroxylase 2 (<strong>TPH2</strong>) and the serotonin transporter (SLC6A4) genes mediates the efficacy of several <b>addiction</b> treatments, such as ondansetron and disulfiram, and the antidepressants bupropion, nortriptyline and sertraline.
+TPH2	drug	alcohol	26265436	Current evidence suggests that genetic variability of the serotonergic biosynthesis enzyme <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) and the serotonin transporter (SLC6A4) genes mediates the efficacy of several addiction treatments, such as ondansetron and <b>disulfiram</b>, and the antidepressants bupropion, nortriptyline and sertraline.
+TPH2	addiction	addiction	26265436	Current evidence suggests that genetic variability of the serotonergic biosynthesis enzyme <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) and the serotonin transporter (SLC6A4) genes mediates the efficacy of several <b>addiction</b> treatments, such as ondansetron and disulfiram, and the antidepressants bupropion, nortriptyline and sertraline.
+TPH2	drug	amphetamine	26259827	<strong>Tph2</strong> gene deletion enhances <b>amphetamine</b> induced hypermotility: effect of 5 HT restoration and role of striatal noradrenaline release.
+TPH2	addiction	addiction	26259827	Variants of tryptophan hydroxylase 2 (<strong>Tph2</strong>), the gene encoding enzyme responsible for the synthesis of brain serotonin (5 HT), have been associated with neuropsychiatric disorders, substance abuse and <b>addiction</b>.
+TPH2	addiction	addiction	26259827	Variants of <strong>tryptophan hydroxylase 2</strong> (<strong>Tph2</strong>), the gene encoding enzyme responsible for the synthesis of brain serotonin (5 HT), have been associated with neuropsychiatric disorders, substance abuse and <b>addiction</b>.
+TPH2	drug	amphetamine	26259827	This study assessed the effect of <strong>Tph2</strong> gene deletion on motor behavior and found that motor activity induced by 2.5 and 5 mg/kg <b>amphetamine</b> was enhanced in <strong>Tph2</strong>( / ) mice.
+TPH2	drug	amphetamine	26259827	Using the in vivo microdialysis technique we found that the ability of <b>amphetamine</b> to stimulate noradrenaline (NA) release in the striatum was reduced by about 50% in <strong>Tph2</strong>( / ) mice while the release of dopamine (DA) was not affected.
+TPH2	drug	amphetamine	26259827	The role of endogenous 5 HT in enhancing the effect of <b>amphetamine</b> was confirmed showing that treatment with the 5 HT precursor 5 hydroxytryptophan (10 mg/kg) restored tissue and extracellular levels of brain 5 HT and the effects of <b>amphetamine</b> on striatal NA release and motor activity in <strong>Tph2</strong>( / ) mice.
+TPH2	drug	amphetamine	26259827	Treatment with the NA precursor dihydroxyphenylserine (400 mg/kg) was sufficient to restore the effect of <b>amphetamine</b> on striatal NA release and motor activity in <strong>Tph2</strong>( / ) mice.
+TPH2	drug	amphetamine	26259827	Here, we show that deletion of <strong>Tph2</strong>, the gene responsible for brain 5 HT synthesis, enhances the motor effect of <b>amphetamine</b> in mice through the inhibition of striatal NA release.
+TPH2	drug	alcohol	26232682	Genetic variability in <strong>tryptophan hydroxylase 2</strong> gene in <b>alcohol</b> dependence and <b>alcohol</b> related psychopathological symptoms.
+TPH2	addiction	dependence	26232682	Genetic variability in <strong>tryptophan hydroxylase 2</strong> gene in alcohol <b>dependence</b> and alcohol related psychopathological symptoms.
+TPH2	drug	alcohol	26232682	The present genetic association study explored the role of <strong>TPH2</strong> polymorphisms and their haplotypes to investigate its role in <b>alcohol</b> dependence and comorbid psychopathological symptoms.
+TPH2	addiction	dependence	26232682	The present genetic association study explored the role of <strong>TPH2</strong> polymorphisms and their haplotypes to investigate its role in alcohol <b>dependence</b> and comorbid psychopathological symptoms.
+TPH2	drug	alcohol	26232682	<strong>TPH2</strong> genotypes were not associated with <b>alcohol</b> dependence, but GGAA haplotype was less common (p=0.038) and GTAA and GGGT were more common (p=0.011 and p=0.021, respectively), in currently dependent patients compared to controls.
+TPH2	addiction	dependence	26232682	<strong>TPH2</strong> genotypes were not associated with alcohol <b>dependence</b>, but GGAA haplotype was less common (p=0.038) and GTAA and GGGT were more common (p=0.011 and p=0.021, respectively), in currently dependent patients compared to controls.
+TPH2	drug	alcohol	26232682	Our findings support a potential role of <strong>TPH2</strong> in <b>alcohol</b> dependence.
+TPH2	addiction	dependence	26232682	Our findings support a potential role of <strong>TPH2</strong> in alcohol <b>dependence</b>.
+TPH2	drug	alcohol	26232682	<strong>TPH2</strong> genetic variability may be also associated with anxiety and aggression traits in <b>alcohol</b> dependent subjects.
+TPH2	drug	cocaine	26013962	Two hundred twenty participants (126 <b>cocaine</b> users, 94 controls) were assessed with visuospatial, spatial, and verbal WM tasks, genotyped for the length polymorphism in the promoter region of the 5 HTT (5 HTTLPR), the variable number of tandem repeats in the second intron of the 5 HTT (VNTR In2), two single nucleotide polymorphisms (rs4570625 and rs1386497) in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene and quantified for peripheral 5 HTT mRNA expression in whole blood samples.
+TPH2	drug	cocaine	26013962	Two hundred twenty participants (126 <b>cocaine</b> users, 94 controls) were assessed with visuospatial, spatial, and verbal WM tasks, genotyped for the length polymorphism in the promoter region of the 5 HTT (5 HTTLPR), the variable number of tandem repeats in the second intron of the 5 HTT (VNTR In2), two single nucleotide polymorphisms (rs4570625 and rs1386497) in the <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) gene and quantified for peripheral 5 HTT mRNA expression in whole blood samples.
+TPH2	drug	cocaine	26013962	Several significant gene × environment interactions between 5 HT genotypes and <b>cocaine</b> use on WM emerged: in <b>cocaine</b> users, the long/long (5 HTTLPR), 9+10/9+10 (VNTR In2) and C/C (<strong>TPH2</strong> rs1386497) genotypes were risk alleles for WM impairments, whereas in healthy controls these polymorphisms were associated with improved WM performance.
+TPH2	drug	alcohol	23995203	<strong>Tryptophan hydroxylase 2</strong> (TPH 2) single nucleotide polymorphisms, suicide, and <b>alcohol</b> related suicide.
+TPH2	drug	alcohol	23995203	Studies investigating suicide, <b>alcohol</b> related suicide and the rate limiting enzyme of serotonin synthesis, tryptophan hydroxylase 2 (<strong>TPH2</strong>), remain to date rather limited.
+TPH2	drug	alcohol	23995203	Studies investigating suicide, <b>alcohol</b> related suicide and the rate limiting enzyme of serotonin synthesis, <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>), remain to date rather limited.
+TPH2	drug	alcohol	23995203	Recent studies of <strong>TPH2</strong> showed a range of strong, mild or no association with suicide and <b>alcohol</b> related suicide, depending on a study group and genetic variants tested.
+TPH2	drug	alcohol	23995203	However, based on current results we cannot draw any conclusions, but further research to clarify the interplay between serotonergic system dysfunction, suicide, <b>alcohol</b> dependence, impulsivity and the role of <strong>TPH2</strong> enzyme is needed.
+TPH2	addiction	dependence	23995203	However, based on current results we cannot draw any conclusions, but further research to clarify the interplay between serotonergic system dysfunction, suicide, alcohol <b>dependence</b>, impulsivity and the role of <strong>TPH2</strong> enzyme is needed.
+TPH2	drug	opioid	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ <b>opioid</b> receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (<strong>TPH2</strong>) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of <b>morphine</b> exposure, withdrawal and post withdrawal stress.
+TPH2	addiction	withdrawal	24055683	Gene expression for brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), corticotrophin releasing factor (CRF) R1, CRF R2, alpha 1 subunit of the GABAA receptor (GABAA α1), μ opioid receptor (MOR), 5 HT1A receptor, tryptophan hydroxylase2 (<strong>TPH2</strong>) and the 5 HT transporter was then measured using quantitative real time polymerase chain reaction at multiple time points across the model of morphine exposure, <b>withdrawal</b> and post <b>withdrawal</b> stress.
+TPH2	drug	opioid	24055683	5 HT1A receptor mRNA expression was decreased following 3h of <b>morphine</b> exposure, while <strong>TPH2</strong> mRNA expression was decreased after 7days of withdrawal with swim stress.
+TPH2	addiction	withdrawal	24055683	5 HT1A receptor mRNA expression was decreased following 3h of morphine exposure, while <strong>TPH2</strong> mRNA expression was decreased after 7days of <b>withdrawal</b> with swim stress.
+TPH2	addiction	relapse	23190435	In a multivariable model, being male, having higher sensation <b>seeking</b> tendencies and at least one copy of the minor allele for SNPs in angiotensin I converting enzyme gene [ACE; rs8066276 odds ratio (OR) = 1.44; P = 0.012] and tryptophan hydroxylase 2 gene (<strong>TPH2</strong>; rs11615016 OR = 1.73; P = 0.021) were associated with increased likelihood of meeting PA recommendations.
+TPH2	addiction	relapse	23190435	In a multivariable model, being male, having higher sensation <b>seeking</b> tendencies and at least one copy of the minor allele for SNPs in angiotensin I converting enzyme gene [ACE; rs8066276 odds ratio (OR) = 1.44; P = 0.012] and <strong>tryptophan hydroxylase 2</strong> gene (<strong>TPH2</strong>; rs11615016 OR = 1.73; P = 0.021) were associated with increased likelihood of meeting PA recommendations.
+TPH2	drug	alcohol	22925276	Modifying the role of serotonergic 5 HTTLPR and <strong>TPH2</strong> variants on <b>disulfiram</b> treatment of cocaine addiction: a preliminary study.
+TPH2	drug	cocaine	22925276	Modifying the role of serotonergic 5 HTTLPR and <strong>TPH2</strong> variants on disulfiram treatment of <b>cocaine</b> addiction: a preliminary study.
+TPH2	addiction	addiction	22925276	Modifying the role of serotonergic 5 HTTLPR and <strong>TPH2</strong> variants on disulfiram treatment of cocaine <b>addiction</b>: a preliminary study.
+TPH2	drug	alcohol	22925276	<b>Disulfiram</b> is a cocaine pharmacotherapy that may act through increasing serotonin, benefiting patients with genetically low serotonin transporter levels (5 HTTLPR, S' allele carriers) and low serotonin synthesis (<strong>TPH2</strong>, A allele carriers).
+TPH2	drug	cocaine	22925276	Disulfiram is a <b>cocaine</b> pharmacotherapy that may act through increasing serotonin, benefiting patients with genetically low serotonin transporter levels (5 HTTLPR, S' allele carriers) and low serotonin synthesis (<strong>TPH2</strong>, A allele carriers).
+TPH2	drug	alcohol	22925276	We genotyped the SLC6A4 5 HTTLPR (rs4795541, rs25531) and <strong>TPH2</strong> 1125A>T (rs4290270) variants and evaluated their role in moderating <b>disulfiram</b> treatment for cocaine dependence.
+TPH2	drug	cocaine	22925276	We genotyped the SLC6A4 5 HTTLPR (rs4795541, rs25531) and <strong>TPH2</strong> 1125A>T (rs4290270) variants and evaluated their role in moderating disulfiram treatment for <b>cocaine</b> dependence.
+TPH2	addiction	dependence	22925276	We genotyped the SLC6A4 5 HTTLPR (rs4795541, rs25531) and <strong>TPH2</strong> 1125A>T (rs4290270) variants and evaluated their role in moderating disulfiram treatment for cocaine <b>dependence</b>.
+TPH2	drug	alcohol	22925276	<strong>TPH2</strong> A allele carriers responded better to <b>disulfiram</b> than placebo (F = 16.0; df = 1,223; P < 0.0001).
+TPH2	drug	alcohol	22925276	Patients with both an S' allele and a <strong>TPH2</strong> A allele reduced cocaine urines from 71% to 53% on <b>disulfiram</b> and had no change on placebo (F = 21.6; df = 1,185; P < 0.00001).
+TPH2	drug	cocaine	22925276	Patients with both an S' allele and a <strong>TPH2</strong> A allele reduced <b>cocaine</b> urines from 71% to 53% on disulfiram and had no change on placebo (F = 21.6; df = 1,185; P < 0.00001).
+TPH2	drug	amphetamine	21886586	Association analysis of the <strong>tryptophan hydroxylase 2</strong> gene polymorphisms in patients with <b>methamphetamine</b> dependence/psychosis.
+TPH2	addiction	dependence	21886586	Association analysis of the <strong>tryptophan hydroxylase 2</strong> gene polymorphisms in patients with methamphetamine <b>dependence</b>/psychosis.
+TPH2	drug	amphetamine	21886586	We analyzed the association between the variations in the brain tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene, a rate limiting enzyme for serotonin biosynthesis, and <b>methamphetamine</b> (<b>METH</b>) dependence/psychosis in a Japanese population.
+TPH2	addiction	dependence	21886586	We analyzed the association between the variations in the brain tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene, a rate limiting enzyme for serotonin biosynthesis, and methamphetamine (METH) <b>dependence</b>/psychosis in a Japanese population.
+TPH2	drug	amphetamine	21886586	We analyzed the association between the variations in the brain <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) gene, a rate limiting enzyme for serotonin biosynthesis, and <b>methamphetamine</b> (<b>METH</b>) dependence/psychosis in a Japanese population.
+TPH2	addiction	dependence	21886586	We analyzed the association between the variations in the brain <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) gene, a rate limiting enzyme for serotonin biosynthesis, and methamphetamine (METH) <b>dependence</b>/psychosis in a Japanese population.
+TPH2	drug	amphetamine	21886586	These results suggest that the <strong>TPH2</strong> gene variants may not be a factor in vulnerability to <b>METH</b> dependence/psychosis.
+TPH2	addiction	dependence	21886586	These results suggest that the <strong>TPH2</strong> gene variants may not be a factor in vulnerability to METH <b>dependence</b>/psychosis.
+TPH2	drug	alcohol	21797889	This study investigated whether drinking motives mediate the associations between <b>alcohol</b> consumption and 2 single nucleotide polymorphisms (SNPs) from genes involved in serotonin (<strong>TPH2</strong>; rs1386496) and dopamine synthesis (DDC; rs3779084).
+TPH2	drug	alcohol	21621273	Association of polymorphisms in HTR2A, HTR1A and <strong>TPH2</strong> genes with suicide attempts in <b>alcohol</b> dependence: a preliminary report.
+TPH2	addiction	dependence	21621273	Association of polymorphisms in HTR2A, HTR1A and <strong>TPH2</strong> genes with suicide attempts in alcohol <b>dependence</b>: a preliminary report.
+TPH2	drug	alcohol	21621273	We investigated a relationship between selected polymorphisms: rs6313 in HTR2A, rs6295 in HTR1A and rs1386494 in <strong>TPH2</strong>, and suicidal behaviour in 150 <b>alcohol</b> dependent patients.
+TPH2	drug	alcohol	21182896	<strong>TPH2</strong> polymorphisms and <b>alcohol</b> related suicide.
+TPH2	drug	alcohol	21182896	Recent studies of the <strong>tryptophan hydroxylase 2</strong> showed mild or no association with suicide and <b>alcohol</b> related suicide.
+TPH2	drug	alcohol	21182896	In conclusion, our results suggest implication of polymorphisms in suicide and <b>alcohol</b> related suicide, but further studies are needed to clarify the interplay among serotonergic system disfunction, suicide, <b>alcohol</b> dependence, impulsivity and the role of <strong>TPH2</strong> enzyme.
+TPH2	addiction	dependence	21182896	In conclusion, our results suggest implication of polymorphisms in suicide and alcohol related suicide, but further studies are needed to clarify the interplay among serotonergic system disfunction, suicide, alcohol <b>dependence</b>, impulsivity and the role of <strong>TPH2</strong> enzyme.
+TPH2	drug	alcohol	21143251	While no results survive the burden of multiple testing, nominal findings in <strong>TPH2</strong> and DDC suggest the potential role of the serotonin synthesis pathway in <b>alcohol</b> consumption.
+TPH2	drug	alcohol	19742166	Epistasis between IL1A, IL1B, TNF, HTR2A, 5 HTTLPR and <strong>TPH2</strong> variations does not impact <b>alcohol</b> dependence disorder features.
+TPH2	addiction	dependence	19742166	Epistasis between IL1A, IL1B, TNF, HTR2A, 5 HTTLPR and <strong>TPH2</strong> variations does not impact alcohol <b>dependence</b> disorder features.
+TPH2	drug	alcohol	19742166	In both groups we genotyped 11 genetic variations (rs1800587; rs3087258; rs1799724; 5 HTTLPR; rs1386493; rs1386494; rs1487275; rs1843809; rs4570625; rs2129575; rs6313) located in genes whose impact on <b>alcohol</b> related behaviors and disorders has been hypothesized (IL1A, IL1B, TNF, 5 HTTLPR, <strong>TPH2</strong> and HTR2A).
+TPH2	drug	alcohol	19734157	Those who did not drink <b>alcohol</b> before suicide were more likely to have a diagnosis of major depressive disorder in their medical record and more often had the TT genotype of the <strong>tryptophan hydroxylase 2</strong> gene.
+TPH2	drug	alcohol	19734157	The <strong>TPH2</strong> gene may play an important role in suicide vulnerability especially in individuals who did not drink <b>alcohol</b> before suicide.
+TPH2	drug	alcohol	19361870	<strong>TPH2</strong> gene variants and anxiety during <b>alcohol</b> detoxification outcome.
+TPH2	drug	alcohol	19361870	<strong>TPH2</strong> variants have been consistently associated with anxiety related traits; since anxiety is critical for <b>alcohol</b> dependence treatment, in the present paper we investigated 9 SNPs within the THP2 gene in anxiety symptoms during the detoxification procedure.
+TPH2	addiction	dependence	19361870	<strong>TPH2</strong> variants have been consistently associated with anxiety related traits; since anxiety is critical for alcohol <b>dependence</b> treatment, in the present paper we investigated 9 SNPs within the THP2 gene in anxiety symptoms during the detoxification procedure.
+TPH2	addiction	relapse	19170664	Genetic polymorphisms in several genes (<strong>TPH2</strong>, SLC6A4, HTR1A, HTR2A, COMT, and BDNF) were tested as predictors of <b>relapse</b> (defined as any drinking during follow up) while controlling for baseline measures.
+TPH2	drug	alcohol	18405071	A case group of males with type 2 <b>alcoholism</b> (N=59) and a control group of healthy males (N=282), both of Croatian origin, were analyzed for the frequency distribution of polymorphisms in 5HT transporter (5HTT VNTR2, 5HTT LPR), monoamine oxidase A (MAOA uVNTR) and B (MAOB A/G) and tryptophan hydroxylase 1 (TPH1 A218C) and 2 (<strong>TPH2</strong> G 703T) genes.
+TPH2	drug	opioid	18181017	<strong>TPH2</strong> and TPH1: association of variants and interactions with <b>heroin</b> addiction.
+TPH2	addiction	addiction	18181017	<strong>TPH2</strong> and TPH1: association of variants and interactions with heroin <b>addiction</b>.
+TPH2	addiction	addiction	18181017	In a cohort of 583 consecutively ascertained subjects, including normal volunteers and those with specific <b>addictive</b> diseases, six common <strong>TPH2</strong> and one TPH1 variant were genotyped.
+TPH2	drug	opioid	18181017	At the two locus genotype level in Hispanics, the TPH1 rs1799913 variant was found to significantly interact with the <strong>TPH2</strong> rs7963720 variant and <b>heroin</b> addiction (P=0.022), and with the <strong>TPH2</strong> rs4290270 variant and <b>heroin</b> addiction (P=0.011).
+TPH2	addiction	addiction	18181017	At the two locus genotype level in Hispanics, the TPH1 rs1799913 variant was found to significantly interact with the <strong>TPH2</strong> rs7963720 variant and heroin <b>addiction</b> (P=0.022), and with the <strong>TPH2</strong> rs4290270 variant and heroin <b>addiction</b> (P=0.011).
+TPH2	drug	opioid	18181017	In the African American group, a significant association of a specific <strong>TPH2</strong> haplotype with <b>heroin</b> addiction also was found (SNPHAP, P=0.004; PHASE P=0.036).
+TPH2	addiction	addiction	18181017	In the African American group, a significant association of a specific <strong>TPH2</strong> haplotype with heroin <b>addiction</b> also was found (SNPHAP, P=0.004; PHASE P=0.036).
+TPH2	drug	nicotine	17986837	The role of the TPH1 and <strong>TPH2</strong> genes for <b>nicotine</b> dependence: a genetic association study in two different age cohorts.
+TPH2	addiction	dependence	17986837	The role of the TPH1 and <strong>TPH2</strong> genes for nicotine <b>dependence</b>: a genetic association study in two different age cohorts.
+TPH2	drug	nicotine	17986837	Based on pharmacological and genetic studies suggesting a role of the serotonergic system for <b>nicotine</b> dependence, two genetic variants, one on the tryptophan hydroxylase 1 (TPH1) and one on the <strong>TPH2</strong> gene, were investigated.
+TPH2	addiction	dependence	17986837	Based on pharmacological and genetic studies suggesting a role of the serotonergic system for nicotine <b>dependence</b>, two genetic variants, one on the tryptophan hydroxylase 1 (TPH1) and one on the <strong>TPH2</strong> gene, were investigated.
+TPH2	drug	nicotine	17986837	The <strong>TPH2</strong>  703G/T promoter polymorphism was associated with <b>smoking</b> status and age of <b>smoking</b> onset in two independent Caucasian samples of different age cohorts.
+TPH2	drug	nicotine	17986837	The <strong>TPH2</strong>  703G/T was significantly associated with age of <b>smoking</b> onset in both samples.
+TPH2	drug	alcohol	17251907	SNP  and haplotype analysis of the <strong>tryptophan hydroxylase 2</strong> gene in <b>alcohol</b> dependent patients and <b>alcohol</b> related suicide.
+TPH2	drug	alcohol	17251907	We performed single SNP (single nucleotide polymorphism), linkage disequilibrium and haplotype studies on 353 <b>alcohol</b> dependent patients of whom 102 individuals had a history of at least one suicide attempt and 305 healthy controls with 20 SNPs covering the entire gene region of <strong>TPH2</strong>.
+TPH2	drug	alcohol	17251907	One major haplotype block of strong linkage disequilibrium between introns 5 and 8 of the <strong>TPH2</strong> gene has been found in <b>alcoholics</b> and controls, which is in concordance with recent reports.
+TPH2	drug	alcohol	17251907	In conclusion, our results suggest that single SNPs, respectively, haplotypes of the <strong>TPH2</strong> gene are unlikely to play a major role in the pathophysiology of <b>alcohol</b> dependence or the <b>alcoholism</b> related phenotype suicidal behavior.
+TPH2	addiction	dependence	17251907	In conclusion, our results suggest that single SNPs, respectively, haplotypes of the <strong>TPH2</strong> gene are unlikely to play a major role in the pathophysiology of alcohol <b>dependence</b> or the alcoholism related phenotype suicidal behavior.
+TPH2	drug	cocaine	16759340	Analysis of variations in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene in <b>cocaine</b> dependence.
+TPH2	addiction	dependence	16759340	Analysis of variations in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene in cocaine <b>dependence</b>.
+TPH2	drug	cocaine	16759340	Analysis of variations in the <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) gene in <b>cocaine</b> dependence.
+TPH2	addiction	dependence	16759340	Analysis of variations in the <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) gene in cocaine <b>dependence</b>.
+TPH2	drug	cocaine	16759340	The focus of the present study is to determine whether genetic variation in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene, which encodes the enzyme responsible for synthesis of the majority of the serotonin contained in neurons of the central nervous system, contributes to the pathophysiology of <b>cocaine</b> dependence.
+TPH2	addiction	dependence	16759340	The focus of the present study is to determine whether genetic variation in the tryptophan hydroxylase 2 (<strong>TPH2</strong>) gene, which encodes the enzyme responsible for synthesis of the majority of the serotonin contained in neurons of the central nervous system, contributes to the pathophysiology of cocaine <b>dependence</b>.
+TPH2	drug	cocaine	16759340	The focus of the present study is to determine whether genetic variation in the <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) gene, which encodes the enzyme responsible for synthesis of the majority of the serotonin contained in neurons of the central nervous system, contributes to the pathophysiology of <b>cocaine</b> dependence.
+TPH2	addiction	dependence	16759340	The focus of the present study is to determine whether genetic variation in the <strong>tryptophan hydroxylase 2</strong> (<strong>TPH2</strong>) gene, which encodes the enzyme responsible for synthesis of the majority of the serotonin contained in neurons of the central nervous system, contributes to the pathophysiology of cocaine <b>dependence</b>.
+TPH2	drug	cocaine	16759340	To examine this hypothesis, we used a case control study design in which the genotype and allele distributions for six single nucleotide polymorphisms (SNPs) in the <strong>TPH2</strong> gene were compared between <b>cocaine</b> dependent (n = 299) and control individuals (n = 208) of African descent.
+TPH2	drug	cocaine	16759340	The results indicate that none of the SNPs in the <strong>TPH2</strong> gene examined in this study associate with the <b>cocaine</b> dependent phenotype.
+TPH2	drug	cocaine	16759340	This work suggests that variations in the <strong>TPH2</strong> gene are not a risk factor for the development of <b>cocaine</b> dependence, but these findings require confirmation in larger, independent samples of <b>cocaine</b> dependent and control subjects.
+TPH2	addiction	dependence	16759340	This work suggests that variations in the <strong>TPH2</strong> gene are not a risk factor for the development of cocaine <b>dependence</b>, but these findings require confirmation in larger, independent samples of cocaine dependent and control subjects.
+IL18	addiction	withdrawal	31589333	After 1 day of <b>withdrawal</b>, <strong>IL 18</strong> was reduced, and IP 10 was elevated, whereas both IP 10 and IL 10 were elevated at 28 days following <b>withdrawal</b>.
+IL18	drug	alcohol	31105269	<b>Alcohol</b> induced IL 17A production in Paneth cells amplifies endoplasmic reticulum stress, apoptosis, and inflammasome <strong>IL 18</strong> activation in the proximal small intestine in mice.
+IL18	drug	alcohol	31105269	In vivo IL 17A blocking antibody administration in <b>alcohol</b> treated mice attenuated ER stress mediated apoptosis and <strong>IL 18</strong> induction and prevented <b>alcohol</b> induced impairment of tight junctions in the PSI and LPS translocation to the liver.
+IL18	drug	alcohol	31105269	Acute on chronic <b>alcohol</b> resulted in inflammasome activation, caspase 1 cleavage, and <strong>IL 18</strong> production in the PSI.
+IL18	drug	alcohol	30870678	Moreover, <b>alcohol</b> increased the expression of intestinal HIF 2α, the proportion of NKB cells and the level of serum <strong>IL 18</strong>, while BMMSCs or P BMMSCs reduced these factors.
+IL18	drug	alcohol	30576537	Concentrations of LH, FSH and inhibin B (inhB) in serum were measured by immunoassay and total testosterone by liquid chromatography mass spectrometry.At 17 years of age, a liver ultrasound examination was performed to determine the presence of non <b>alcoholic</b> fatty liver disease (NAFLD), and serum analysed for the cytokines <strong>interleukin 18</strong> and soluble tumour necrosis factor receptor 1 and 2 (sTNFR1, sTNFR2).At 17 and 20 years of age, fasting blood samples were analysed for serum liver enzymes, insulin, glucose, triglycerides (TG), total cholesterol, high density lipoprotein and low density lipoprotein cholesterol, high sensitivity C reactive protein and uric acid.
+IL18	drug	opioid	28580822	Compared with chronic constriction injury, normal saline and <b>morphine</b> groups, the mRNA and protein expressions of NLRP3, apoptosis associated speck like protein, Caspase 1, IL 1β, and <strong>IL 18</strong> were significantly decreased in the miR 223 and miR 223 + <b>morphine</b> groups, while mRNA and protein expressions of NLRP3, apoptosis associated speck like protein, Caspase 1, IL 1β, and <strong>IL 18</strong> were significantly increased in the NLRP3 and NLRP3 + <b>morphine</b> group.
+IL18	addiction	sensitization	28189648	This current study aimed to extend tested chemicals, and to provide a simple in vitro method for estimation of the expected <b>sensitization</b> induction level interpolating in vitro EC50 and <strong>IL 18</strong> SI2 values to predict LLNA EC3 and/or human NOEL from standards curves generated using reference contact allergens.
+IL18	drug	psychedelics	26589393	Relationship of serum levels of TNF α, IL 6 and <strong>IL 18</strong> and schizophrenia like symptoms in chronic <b>ketamine</b> abusers.
+IL18	drug	psychedelics	26589393	This study aims to examine the serum TNF α, IL 6 and <strong>IL 18</strong> levels in chronic human <b>ketamine</b> users as compared to healthy subjects.
+IL18	drug	psychedelics	26589393	Serum IL 6 and <strong>IL 18</strong> levels were significantly higher, while serum TNF α level was significantly lower among <b>ketamine</b> users than among healthy controls (p<0.05).
+IL18	drug	psychedelics	26589393	Serum levels of TNF α, IL 6 and <strong>IL 18</strong> were altered in chronic <b>ketamine</b> abusers which may play a role in schizophrenia like symptoms in chronic <b>ketamine</b> abusers.
+IL18	drug	alcohol	24766056	In patients with mild ALD, 1 week of <b>alcohol</b> withdrawal was sufficient to decrease expression level of total macrophage markers in the adipose tissue, to orient adipose tissue macrophages (ATM) towards an anti inflammatory M2 phenotype and to decrease the mRNA expression of cytokines/chemokines (<strong>IL18</strong>, CCL2, osteopontin, semaphorin 7A).
+IL18	addiction	withdrawal	24766056	In patients with mild ALD, 1 week of alcohol <b>withdrawal</b> was sufficient to decrease expression level of total macrophage markers in the adipose tissue, to orient adipose tissue macrophages (ATM) towards an anti inflammatory M2 phenotype and to decrease the mRNA expression of cytokines/chemokines (<strong>IL18</strong>, CCL2, osteopontin, semaphorin 7A).
+IL18	drug	opioid	24379262	A significant increase of <strong>IL 18</strong>, NGAL and β2M activity in <b>heroin</b> addicts compared to the control group was noted as well as the influence of HIV infection on NGAL and β2M excretion.
+IL18	addiction	sensitization	23063874	We have recently identified interleukin 18 (<strong>IL 18</strong>) production in keratinocyte as a potentially useful endpoint for determination of contact <b>sensitization</b> potential of low molecular weight chemicals.
+IL18	addiction	sensitization	23063874	We have recently identified <strong>interleukin 18</strong> (<strong>IL 18</strong>) production in keratinocyte as a potentially useful endpoint for determination of contact <b>sensitization</b> potential of low molecular weight chemicals.
+IL18	drug	alcohol	22001439	Alteration in intestine tight junction protein phosphorylation and apoptosis is associated with increase in <strong>IL 18</strong> levels following <b>alcohol</b> intoxication and burn injury.
+IL18	addiction	intoxication	22001439	Alteration in intestine tight junction protein phosphorylation and apoptosis is associated with increase in <strong>IL 18</strong> levels following alcohol <b>intoxication</b> and burn injury.
+IL18	drug	alcohol	22001439	We have shown a role for <strong>IL 18</strong> in impaired gut barrier function following acute <b>alcohol</b> (EtOH) intoxication combined with burn injury.
+IL18	addiction	intoxication	22001439	We have shown a role for <strong>IL 18</strong> in impaired gut barrier function following acute alcohol (EtOH) <b>intoxication</b> combined with burn injury.
+IL18	addiction	intoxication	22001439	Altogether, these findings suggest that <strong>IL 18</strong> modulates tight junction proteins and cause apoptosis leading to impaired intestinal mucosal integrity following EtOH <b>intoxication</b> combined with burn injury.
+IL18	drug	opioid	21145535	Association of plasma <strong>interleukin 18</strong> levels with emotion regulation and μ <b>opioid</b> neurotransmitter function in major depression and healthy volunteers.
+IL18	drug	opioid	21145535	In MDDs, <strong>IL 18</strong> was positively correlated with baseline regional μ OR BP(ND) and with sadness induced μ <b>opioid</b> system activation in the subgenual anterior cingulate, ventral basal ganglia, and amygdala.
+IL18	drug	opioid	21145535	This study links plasma <strong>IL 18</strong> with sadness induced emotional responses in healthy subjects, the diagnosis of MDD, and μ <b>opioid</b> functioning, itself involved in stress adaptation, emotion regulation, and reward.
+IL18	addiction	reward	21145535	This study links plasma <strong>IL 18</strong> with sadness induced emotional responses in healthy subjects, the diagnosis of MDD, and μ opioid functioning, itself involved in stress adaptation, emotion regulation, and <b>reward</b>.
+IL18	drug	opioid	21145535	This suggests that <strong>IL 18</strong> represents a marker associated with emotion regulation/dysregulation at least in part through central <b>opioid</b> mechanisms.
+IL18	drug	alcohol	20844839	<strong>Interleukin 18</strong> delays neutrophil apoptosis following <b>alcohol</b> intoxication and burn injury.
+IL18	addiction	intoxication	20844839	<strong>Interleukin 18</strong> delays neutrophil apoptosis following alcohol <b>intoxication</b> and burn injury.
+IL18	addiction	intoxication	20844839	The purpose of this study was to examine whether EtOH <b>intoxication</b> combined with burn injury influences neutrophil apoptosis and whether <strong>IL 18</strong> plays any role in this setting.
+IL18	drug	alcohol	19497959	Neutrophil chemokines and their role in <strong>IL 18</strong> mediated increase in neutrophil O2  production and intestinal edema following <b>alcohol</b> intoxication and burn injury.
+IL18	addiction	intoxication	19497959	Neutrophil chemokines and their role in <strong>IL 18</strong> mediated increase in neutrophil O2  production and intestinal edema following alcohol <b>intoxication</b> and burn injury.
+IL18	addiction	intoxication	19497959	However, the finding that the treatment of rats with anti <strong>IL 18</strong> antibodies inhibits CINC 1 and CINC 3 supports the notion that <strong>IL 18</strong> plays a critical role in increased neutrophil tissue damaging action following a combined insult of EtOH <b>intoxication</b> and burn injury.
+IL18	addiction	sensitization	19397996	The aim of the present study was to evaluate the possibility to use intracellular interleukin 18 (<strong>IL 18</strong>) production to assess in vitro the contact <b>sensitization</b> potential of low molecular weight chemicals.
+IL18	addiction	sensitization	19397996	The aim of the present study was to evaluate the possibility to use intracellular <strong>interleukin 18</strong> (<strong>IL 18</strong>) production to assess in vitro the contact <b>sensitization</b> potential of low molecular weight chemicals.
+IL18	drug	alcohol	17220368	Acute <b>alcohol</b> intoxication increases <strong>interleukin 18</strong> mediated neutrophil infiltration and lung inflammation following burn injury in rats.
+IL18	addiction	intoxication	17220368	Acute alcohol <b>intoxication</b> increases <strong>interleukin 18</strong> mediated neutrophil infiltration and lung inflammation following burn injury in rats.
+IL18	drug	alcohol	17220368	In this study, we examined whether <strong>IL 18</strong> plays a role in lung inflammation following <b>alcohol</b> (EtOH) and burn injury.
+IL18	addiction	intoxication	17220368	On day 1 after injury, lung tissue <strong>IL 18</strong>, neutrophil chemokines (CINC 1/CINC 3), ICAM 1, neutrophil infiltration, MPO activity, and water content (i.e., edema) were significantly increased in rats receiving a combined insult of EtOH and burn injury compared with rats receiving either EtOH <b>intoxication</b> or burn injury alone.
+IL18	addiction	intoxication	17220368	These findings suggest that acute EtOH <b>intoxication</b> before burn injury upregulates <strong>IL 18</strong>, which in turn contributes to increased neutrophil infiltration.
+IL18	drug	alcohol	16707557	A novel role for <strong>IL 18</strong> in corticosterone mediated intestinal damage in a two hit rodent model of <b>alcohol</b> intoxication and injury.
+IL18	addiction	intoxication	16707557	A novel role for <strong>IL 18</strong> in corticosterone mediated intestinal damage in a two hit rodent model of alcohol <b>intoxication</b> and injury.
+IL18	addiction	intoxication	16707557	To further delineate the mechanism of impaired intestinal barrier function, the present study examined the role of corticosterone (CORT) and interleukin (IL) 18, as CORT and <strong>IL 18</strong> are elevated following a combined insult of EtOH <b>intoxication</b> and burn injury.
+IL18	addiction	intoxication	16707557	These findings suggest that a combined insult of EtOH and burn injury results in increased CORT levels, which in turn up regulates intestinal <strong>IL 18</strong> levels and thereby causes altered intestinal barrier function following a combined insult of EtOH <b>intoxication</b> and burn injury.
+AGRP	drug	alcohol	32045262	Acute <b>alcohol</b> exposure also increases both the activity of agouti related protein (<strong>AgRP</strong>) expressing neurons and <strong>AgRP</strong> immunoreactivity.
+AGRP	drug	alcohol	32045262	Here, we show that adenosine receptor A2B signaling in the brain modulates the extent of <b>alcohol</b> induced fatty liver in mice and that both the <strong>AgRP</strong> neuropeptide and the sympathetic nervous system are indispensable for hepatic steatosis induced by bingelike <b>alcohol</b> consumption.
+AGRP	drug	alcohol	32045262	Together, these results indicate that the brain plays an integral role in <b>alcohol</b> induced hepatic lipid accumulation and that central adenosine signaling, hypothalamic <strong>AgRP</strong>, and the sympathetic nervous system are crucial mediators of this process.
+AGRP	drug	amphetamine	30929417	Lorcaserin stimulates proopiomelanocortin (POMC)/cocaine  and <b>amphetamine</b> regulated transcript (CART) neurons and inhibits neuropeptide Y (NPY)/agouti related peptide (<strong>AgRP</strong>) neurons, which results in the activation of melanocortin 3/4 receptors.
+AGRP	drug	cocaine	30929417	Lorcaserin stimulates proopiomelanocortin (POMC)/<b>cocaine</b>  and amphetamine regulated transcript (CART) neurons and inhibits neuropeptide Y (NPY)/agouti related peptide (<strong>AgRP</strong>) neurons, which results in the activation of melanocortin 3/4 receptors.
+AGRP	addiction	reward	30929417	The hypophagic effect of liraglutide is mediated through the direct activation of POMC/CART neurons and the indirect suppression of NPY/<strong>AgRP</strong> neurons through γ aminobutyric acid dependent signaling, with adjunctive suppression of the mesolimbic dopamine <b>reward</b> system.
+AGRP	drug	amphetamine	30396596	Finally, rats were sacrificed and agouti related peptide (<strong>AgRP</strong>), neuropeptide Y (NPY), pro opiomelanocortin (POMC) and cocaine  and <b>amphetamine</b> regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+AGRP	drug	cocaine	30396596	Finally, rats were sacrificed and agouti related peptide (<strong>AgRP</strong>), neuropeptide Y (NPY), pro opiomelanocortin (POMC) and <b>cocaine</b>  and amphetamine regulated transcript (CART) and fatty acid amide hydrolase (FAAH) gene expression in the hypothalamus was measured by real time reverse transcription polymerase chain reaction.
+AGRP	drug	cannabinoid	29231147	Inclusion criteria were: 1) full text available in English; 2) published in a peerreviewed journal and using the following keywords: neurotransmitters (<strong>AgRP</strong>, BDNF, αMSH, NP Y, <b>endocannabinoids</b>, adiponectin, CCK, ghrelin, GLP 1, insulin, leptin, PP, PYY), hormones (FSH, LH, estrogen, progesterone, testosterone) and bulimia nervosa, eating disorders.
+AGRP	drug	alcohol	29056149	There is a large body of research showing the role of the MC and <strong>AgRP</strong> systems in neurobiological responses to drugs of abuse, in particular, neurobiological responses to <b>ethanol</b>.
+AGRP	drug	alcohol	29056149	In this chapter, we discuss the most recent evidence that supports the role of the MC/<strong>AgRP</strong> systems in modulating neurobiological responses to drugs of abuse, with a focus on <b>ethanol</b> consumption.
+AGRP	drug	amphetamine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [proopiomelanocortin (POMC), cocaine  and <b>amphetamine</b> related transcript (CART), neuropeptide Y (NPY), and agouti related peptide (<strong>AgRP</strong>)].
+AGRP	drug	cocaine	29046316	The decreased food intake observed in fish treated intracerebroventricularly with leucine could relate to changes in mRNA abundance of hypothalamic neuropeptides [proopiomelanocortin (POMC), <b>cocaine</b>  and amphetamine related transcript (CART), neuropeptide Y (NPY), and agouti related peptide (<strong>AgRP</strong>)].
+AGRP	drug	alcohol	28936166	In this regard, binge like <b>ethanol</b> exposure during adolescence reduces basal alpha melanocyte stimulating hormone (α MSH) and alters the levels of agouti related peptide (<strong>AgRP</strong>) in hypothalamic and limbic areas.
+AGRP	addiction	intoxication	28936166	In this regard, <b>binge</b> like ethanol exposure during adolescence reduces basal alpha melanocyte stimulating hormone (α MSH) and alters the levels of agouti related peptide (<strong>AgRP</strong>) in hypothalamic and limbic areas.
+AGRP	drug	amphetamine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, <strong>AgRP</strong>, cocaine  and <b>amphetamine</b> related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+AGRP	drug	cocaine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, <strong>AgRP</strong>, <b>cocaine</b>  and amphetamine related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (HCRT), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+AGRP	drug	alcohol	25975524	Male C57BL/6J mice were exposed to one, three or six cycles of binge like <b>ethanol</b>, sucrose or water drinking, after which brain tissue was processed via immunohistochemistry (IHC) for analysis of key MC peptides, including alpha melanocyte stimulating hormone (α MSH) and agouti related protein (<strong>AgRP</strong>).
+AGRP	addiction	intoxication	25975524	Male C57BL/6J mice were exposed to one, three or six cycles of <b>binge</b> like ethanol, sucrose or water drinking, after which brain tissue was processed via immunohistochemistry (IHC) for analysis of key MC peptides, including alpha melanocyte stimulating hormone (α MSH) and agouti related protein (<strong>AgRP</strong>).
+AGRP	drug	alcohol	25975524	Results indicated that α MSH expression was selectively decreased, while <strong>AgRP</strong> expression was selectively increased, within specific hypothalamic subregions following repeated binge like <b>ethanol</b> drinking.
+AGRP	addiction	intoxication	25975524	Results indicated that α MSH expression was selectively decreased, while <strong>AgRP</strong> expression was selectively increased, within specific hypothalamic subregions following repeated <b>binge</b> like ethanol drinking.
+AGRP	drug	alcohol	25975524	We found that the nonselective MCR agonist melanotan II (MTII) blunted, while the nonselective MCR antagonist <strong>AgRP</strong> augmented, binge like <b>ethanol</b> consumption when delivered into the LH.
+AGRP	addiction	intoxication	25975524	We found that the nonselective MCR agonist melanotan II (MTII) blunted, while the nonselective MCR antagonist <strong>AgRP</strong> augmented, <b>binge</b> like ethanol consumption when delivered into the LH.
+AGRP	drug	alcohol	24917782	This review highlights recent genetic and pharmacological findings that have implicated roles for the MC and <strong>AgRP</strong> systems in modulating <b>ethanol</b> consumption.
+AGRP	drug	alcohol	24917782	<b>Ethanol</b> consumption is associated with significant alterations in the expression levels of various MC peptides/protein, which suggests that <b>ethanol</b> induced perturbations of MC/<strong>AgRP</strong> signaling may modulate excessive <b>ethanol</b> intake.
+AGRP	drug	alcohol	24917782	Consistently, MCR agonists decrease, and <strong>AgRP</strong> increases, <b>ethanol</b> consumption in mice.
+AGRP	drug	alcohol	24917782	Finally, mutant mice lacking <strong>AgRP</strong> exhibit blunted voluntary and binge like <b>ethanol</b> drinking, consistent with pharmacological studies.
+AGRP	addiction	intoxication	24917782	Finally, mutant mice lacking <strong>AgRP</strong> exhibit blunted voluntary and <b>binge</b> like ethanol drinking, consistent with pharmacological studies.
+AGRP	drug	cocaine	23872279	or intra nucleus accumbens injection with <strong>AgRP</strong>(83 132) or saline, to determine whether we could inhibit <b>cocaine</b> induced locomotor sensitisation.
+AGRP	drug	cocaine	23872279	injections of <strong>AgRP</strong>(83 132) inhibit <b>cocaine</b> induced locomotor sensitisation.
+AGRP	drug	cocaine	23872279	This effect is not regulated via the nucleus accumbens, since injecting the melanocortin receptor inverse agonist <strong>AgRP</strong>(83 132) directly into the nucleus accumbens was unable to inhibit the <b>cocaine</b> induced locomotor sensitisation.
+AGRP	drug	alcohol	23792540	Given the involvement of MC and the endogenous inverse agonist <strong>AgRP</strong> in <b>ethanol</b> drinking, here we evaluate whether a binge like pattern of <b>ethanol</b> treatment during adolescence has a relevant impact on basal and/or <b>ethanol</b> stimulated α MSH and <strong>AgRP</strong> activities during adulthood.
+AGRP	addiction	intoxication	23792540	Given the involvement of MC and the endogenous inverse agonist <strong>AgRP</strong> in ethanol drinking, here we evaluate whether a <b>binge</b> like pattern of ethanol treatment during adolescence has a relevant impact on basal and/or ethanol stimulated α MSH and <strong>AgRP</strong> activities during adulthood.
+AGRP	drug	alcohol	23792540	Following 25 <b>ethanol</b> free days, we evaluated α MSH and <strong>AgRP</strong> immunoreactivity (IR) in the limbic and hypothalamic nuclei of adult rats (PND63) in response to <b>ethanol</b> (1.5 or 3.0 g/kgi.p.)
+AGRP	drug	alcohol	23792540	Additionally, acute <b>ethanol</b> elicited <strong>AgRP</strong> IR in the Arc.
+AGRP	drug	alcohol	23792540	Rats given the adolescent <b>ethanol</b> treatment required higher doses of <b>ethanol</b> than saline treated rats to express <strong>AgRP</strong>.
+AGRP	drug	alcohol	23792540	In light of previous evidence that endogenous MC and <strong>AgRP</strong> regulate <b>ethanol</b> intake through MC receptor signaling, we speculate that the α MSH and <strong>AgRP</strong> disturbances induced by binge like <b>ethanol</b> exposure during adolescence may contribute to excessive <b>ethanol</b> consumption during adulthood.
+AGRP	addiction	intoxication	23792540	In light of previous evidence that endogenous MC and <strong>AgRP</strong> regulate ethanol intake through MC receptor signaling, we speculate that the α MSH and <strong>AgRP</strong> disturbances induced by <b>binge</b> like ethanol exposure during adolescence may contribute to excessive ethanol consumption during adulthood.
+AGRP	drug	cocaine	22729177	We found that impairment of Agouti related protein (<strong>AgRP</strong>) circuitry by either Sirt1 knockdown in <strong>AgRP</strong> expressing neurons or early postnatal ablation of these neurons increased exploratory behavior and enhanced responses to <b>cocaine</b>.
+AGRP	addiction	reward	22729177	Thus, <strong>AgRP</strong> neurons determine the set point of the <b>reward</b> circuitry and associated behaviors.
+AGRP	drug	alcohol	22245775	Finally, recent evidence shows that corticotropin releasing factor (CRF), agouti related protein (<strong>AgRP</strong>), neuropeptide Y (NPY), and ghrelin are also implicated as impacting this pattern of <b>ethanol</b> consumption.
+AGRP	drug	cannabinoid	21243475	serotonergic, opioid, <b>cannabinoid</b> and dopaminergic receptors, and brain derived neurotrophic factor (BDNF)], appetite regulatory peptides and their receptors [leptin, ghrelin, agouti related protein (<strong>AgRP</strong>), melanocortin receptors, neuropeptide Y], energy balance systems (e.g.
+AGRP	drug	opioid	21243475	serotonergic, <b>opioid</b>, cannabinoid and dopaminergic receptors, and brain derived neurotrophic factor (BDNF)], appetite regulatory peptides and their receptors [leptin, ghrelin, agouti related protein (<strong>AgRP</strong>), melanocortin receptors, neuropeptide Y], energy balance systems (e.g.
+AGRP	drug	opioid	21243475	Candidate gene association has implicated BDNF, delta 1 <b>opioid</b> receptor (OPDR1) and <strong>AgRP</strong>.
+AGRP	drug	nicotine	20803089	Hypothalamic <strong>AgRP</strong> might play a role for maintaining energy balance under the <b>nicotine</b> induced negative energy status.
+AGRP	drug	alcohol	20102560	<b>Ethanol</b> induced increase of agouti related protein (<strong>AgRP</strong>) immunoreactivity in the arcuate nucleus of the hypothalamus of C57BL/6J, but not 129/SvJ, inbred mice.
+AGRP	drug	alcohol	20102560	Consistently, genetic deletion of the endogenous MCR antagonist, agouti related protein (<strong>AgRP</strong>), causes reductions of <b>ethanol</b> reinforced lever pressing and binge like <b>ethanol</b> drinking in C57BL/6J mice.
+AGRP	addiction	intoxication	20102560	Consistently, genetic deletion of the endogenous MCR antagonist, agouti related protein (<strong>AgRP</strong>), causes reductions of ethanol reinforced lever pressing and <b>binge</b> like ethanol drinking in C57BL/6J mice.
+AGRP	drug	alcohol	20102560	To further characterize the role of the MC system in responses to <b>ethanol</b>, here we compared <strong>AgRP</strong> and alpha MSH immunoreactivity in response to an acute injection of saline or <b>ethanol</b> between high <b>ethanol</b> drinking C57BL/6J mice and moderate <b>ethanol</b> drinking 129/SvJ mice.
+AGRP	drug	alcohol	20102560	Results indicated that acute <b>ethanol</b> administration triggered a dose dependent increase in <strong>AgRP</strong> immunoreactivity in the arcuate (ARC) of C57BL/6J mice, an effect that was not evident in the 129/SvJ strain.
+AGRP	drug	alcohol	20102560	The results show that acute <b>ethanol</b> exposure has direct effects on endogenous <strong>AgRP</strong> activity in <b>ethanol</b> preferring C57BL/6J mice.
+AGRP	drug	alcohol	20102560	It is suggested that <b>ethanol</b> induced increases in <strong>AgRP</strong> may be part of a positive feedback system that stimulates excessive binge like <b>ethanol</b> drinking in C57BL/6J mice.
+AGRP	addiction	intoxication	20102560	It is suggested that ethanol induced increases in <strong>AgRP</strong> may be part of a positive feedback system that stimulates excessive <b>binge</b> like ethanol drinking in C57BL/6J mice.
+AGRP	drug	alcohol	19566712	Because central administration of the functionally active <strong>AgRP</strong> fragment <strong>AgRP</strong> (83 132) increases <b>ethanol</b> intake by C57BL/6 J mice, we determined if mutant mice lacking normal production of <strong>AgRP</strong> (<strong>AgRP</strong>( / )) and maintained on a C57BL/6 J genetic background would show reduced self administration of <b>ethanol</b> relative to littermate wild type (<strong>AgRP</strong>(+/+)) mice.
+AGRP	drug	alcohol	19566712	<strong>AgRP</strong>( / ) mice showed reduced 8% (v/v) <b>ethanol</b> reinforced lever pressing behavior relative to <strong>AgRP</strong>(+/+) mice in daily 2 h sessions, but normal sucrose , saccharin  and water reinforced lever pressing.
+AGRP	drug	alcohol	19566712	Similarly, <strong>AgRP</strong>( / ) mice showed reduced consumption of 8% <b>ethanol</b> in a two bottle limited access test (2 h/day), although this effect was largely sex dependent.
+AGRP	drug	alcohol	19566712	Using drinking in the dark (DID) procedures, <strong>AgRP</strong>( / ) mice showed blunted binge like drinking of 20% (v/v) <b>ethanol</b> which was associated with lower blood <b>ethanol</b> levels (85 mg/dl) relative to <strong>AgRP</strong>(+/+) mice (133 mg/dl) after 4 h of intake.
+AGRP	addiction	intoxication	19566712	Using drinking in the dark (DID) procedures, <strong>AgRP</strong>( / ) mice showed blunted <b>binge</b> like drinking of 20% (v/v) ethanol which was associated with lower blood ethanol levels (85 mg/dl) relative to <strong>AgRP</strong>(+/+) mice (133 mg/dl) after 4 h of intake.
+AGRP	drug	alcohol	19566712	<strong>AgRP</strong>( / ) mice showed normal <b>ethanol</b> metabolism and did not show altered sensitivity to the sedative effects of <b>ethanol</b>.
+AGRP	drug	alcohol	19566712	These observations with genetically altered mice are consistent with previous pharmacological data and suggest that endogenous <strong>AgRP</strong> signaling modulates the reinforcing properties of <b>ethanol</b> and binge like <b>ethanol</b> drinking.
+AGRP	addiction	intoxication	19566712	These observations with genetically altered mice are consistent with previous pharmacological data and suggest that endogenous <strong>AgRP</strong> signaling modulates the reinforcing properties of ethanol and <b>binge</b> like ethanol drinking.
+AGRP	addiction	reward	19566712	These observations with genetically altered mice are consistent with previous pharmacological data and suggest that endogenous <strong>AgRP</strong> signaling modulates the <b>reinforcing</b> properties of ethanol and binge like ethanol drinking.
+AGRP	drug	alcohol	18162070	We also determined if <b>ethanol</b> exposure would alter the immunoreactivity of agouti related protein (<strong>AgRP</strong>), an endogenous MCR antagonist.
+AGRP	drug	alcohol	18162070	No significant <b>ethanol</b> induced alterations in hypothalamic <strong>AgRP</strong> immunoreactivity were detected.
+AGRP	drug	alcohol	16198024	To better understand the role of the MC system in the control of <b>ethanol</b> intake, we tested the acute and chronic effects of lateral ventricular (LV) injections of 0.01 1 nmol MTII, of 0.1 1 nmol of the MC3/4R receptor antagonist agouti related peptide (<strong>AgRP</strong>), and 0.1 0.5 nmol of the MC3/4R receptor antagonist SHU9119 on food, water, and 10% <b>ethanol</b> intake in Marchigian Sardinian <b>alcohol</b> preferring (msP) rats, which spontaneously ingest pharmacologically relevant quantities of <b>ethanol</b> both under short and long term access conditions.
+AGRP	drug	alcohol	16198024	Finally, acute LV injection of neither <strong>AgRP</strong> nor SHU9119 affected <b>ethanol</b> intake under ad libitum conditions, although both antagonists significantly increased food and water intake.
+AGRP	drug	opioid	12851315	Given these observations, we wished to examine whether the effects of <strong>AgRP</strong> on ingestive behavior resemble those of <b>opioids</b>.
+AGRP	drug	opioid	12851315	As a result of <strong>AgRP</strong> injection, animals increased intake of chow but not sucrose relative to controls, in contrast to what has been seen with <b>opioid</b> agonists.
+AGRP	drug	opioid	12851315	These results together with prior findings suggest that the primary effect of <strong>AgRP</strong> is to cause an increase in food intake to satisfy energy needs, though <strong>AgRP</strong> also has <b>opioid</b> like effects, possibly due to melanocortin <b>opioid</b> interactions.
+AGRP	drug	opioid	12151802	Initial studies suggest similarities between the effects of <strong>Agrp</strong> and <b>opioid</b> peptides on ingestive behavior.
+AGRP	drug	opioid	12151802	Given these observations, we examined whether <strong>Agrp</strong>, similarly to <b>opioids</b>, alleviates conditioned taste aversion (CTA) generated by peripheral injection of LiCl.
+AGRP	addiction	aversion	12151802	Given these observations, we examined whether <strong>Agrp</strong>, similarly to opioids, alleviates conditioned taste <b>aversion</b> (<b>CTA</b>) generated by peripheral injection of LiCl.
+AGRP	addiction	aversion	12151802	<strong>Agrp</strong> (1 nmol) delivered to the lateral cerebral ventricle, a dose known to cause orexigenic effects, was shown to partially block acquisition of LiCl induced <b>CTA</b>.
+AGRP	drug	opioid	12151802	Inhibitory effects of <strong>Agrp</strong> on acquisition of CTA and aversion associated activation of oxytocin neurons parallel what has previously been shown with <b>opioid</b> receptor agonists.
+AGRP	addiction	aversion	12151802	Inhibitory effects of <strong>Agrp</strong> on acquisition of <b>CTA</b> and <b>aversion</b> associated activation of oxytocin neurons parallel what has previously been shown with opioid receptor agonists.
+TACR1	drug	alcohol	32067964	<strong>NK1R</strong> activity has been shown to influence reward and reinforcement for opiate drugs, stimulatory and neurochemical responses to cocaine, and escalated and stress induced <b>alcohol</b> seeking.
+TACR1	drug	cocaine	32067964	<strong>NK1R</strong> activity has been shown to influence reward and reinforcement for opiate drugs, stimulatory and neurochemical responses to <b>cocaine</b>, and escalated and stress induced alcohol seeking.
+TACR1	addiction	relapse	32067964	<strong>NK1R</strong> activity has been shown to influence reward and reinforcement for opiate drugs, stimulatory and neurochemical responses to cocaine, and escalated and stress induced alcohol <b>seeking</b>.
+TACR1	addiction	reward	32067964	<strong>NK1R</strong> activity has been shown to influence <b>reward</b> and <b>reinforcement</b> for opiate drugs, stimulatory and neurochemical responses to cocaine, and escalated and stress induced alcohol seeking.
+TACR1	addiction	relapse	32067964	In <b>reinstatement</b> models of <b>relapse</b> like behavior, <strong>NK1R</strong> antagonism attenuates stress induced <b>reinstatement</b> for all classes of drugs tested to date.
+TACR1	drug	alcohol	31242442	Our previous work has demonstrated that P rats show increased expression of the neurokinin 1 receptor (<strong>NK1R</strong>) in the central nucleus of the amygdala (CeA), and this functionally contributes to escalated <b>alcohol</b> consumption in this strain.
+TACR1	addiction	relapse	31242442	We hypothesized that P rats would show increased sensitivity to yohimbine induced <b>reinstatement</b> that is also mediated by <strong>NK1R</strong> in the CeA.
+TACR1	drug	alcohol	31242442	Using Fos staining, site specific infusion of <strong>NK1R</strong> antagonist, and viral vector overexpression, we examined the influence of <strong>NK1R</strong> on the sensitivity to yohimbine induced reinstatement of <b>alcohol</b> seeking.
+TACR1	addiction	relapse	31242442	Using Fos staining, site specific infusion of <strong>NK1R</strong> antagonist, and viral vector overexpression, we examined the influence of <strong>NK1R</strong> on the sensitivity to yohimbine induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+TACR1	addiction	relapse	31242442	Intra CeA infusion of <strong>NK1R</strong> antagonist attenuates yohimbine induced <b>reinstatement</b> in P rats.
+TACR1	drug	alcohol	31242442	Conversely, upregulation of <strong>NK1R</strong> within the CeA of Wistar rats increases <b>alcohol</b> consumption and sensitivity to yohimbine induced reinstatement.
+TACR1	addiction	relapse	31242442	Conversely, upregulation of <strong>NK1R</strong> within the CeA of Wistar rats increases alcohol consumption and sensitivity to yohimbine induced <b>reinstatement</b>.
+TACR1	drug	alcohol	31242442	These findings suggest that <strong>NK1R</strong> upregulation in the CeA contributes to multiple <b>alcohol</b> related phenotypes in the P rat, including <b>alcohol</b> consumption and sensitivity to relapse.
+TACR1	addiction	relapse	31242442	These findings suggest that <strong>NK1R</strong> upregulation in the CeA contributes to multiple alcohol related phenotypes in the P rat, including alcohol consumption and sensitivity to <b>relapse</b>.
+TACR1	drug	alcohol	30054674	Although <b>alcohol</b> use disorder and anxiety disorders are highly comorbid in humans, controversy remains regarding whether anxiety predisposes individuals to <b>alcohol</b> reward, and the relationship with neurokinin 1 receptor (<strong>NK1R</strong>) is unclear.
+TACR1	addiction	reward	30054674	Although alcohol use disorder and anxiety disorders are highly comorbid in humans, controversy remains regarding whether anxiety predisposes individuals to alcohol <b>reward</b>, and the relationship with neurokinin 1 receptor (<strong>NK1R</strong>) is unclear.
+TACR1	drug	alcohol	30054674	The objectives of the study are to investigate the association between anxiety like behavior and <b>alcohol</b> induced conditioned place preference (CPP) and to examine the effect of <strong>NK1R</strong> antagonist L 703,606 on this preference and levels of <strong>NK1R</strong> protein in different brain regions in adolescent mice.
+TACR1	addiction	reward	30054674	The objectives of the study are to investigate the association between anxiety like behavior and alcohol induced conditioned place preference (<b>CPP</b>) and to examine the effect of <strong>NK1R</strong> antagonist L 703,606 on this preference and levels of <strong>NK1R</strong> protein in different brain regions in adolescent mice.
+TACR1	drug	alcohol	30054674	After the reinforcement of <b>ethanol</b> was established by <b>alcohol</b> induced CPP (2 g/kg), <strong>NK1R</strong> expression was quantified in the hippocampus, prefrontal cortex, and amygdala.
+TACR1	addiction	reward	30054674	After the <b>reinforcement</b> of ethanol was established by alcohol induced <b>CPP</b> (2 g/kg), <strong>NK1R</strong> expression was quantified in the hippocampus, prefrontal cortex, and amygdala.
+TACR1	drug	alcohol	30054674	LAM showed a greater <b>ethanol</b> preference (P = 0.004) and a higher level of <strong>NK1R</strong> protein in the hippocampus (P = 0.026) than HAM group.
+TACR1	addiction	reward	30054674	Interestingly, the <b>CPP</b> score positively correlated with OT% (r = 0.520, P = 0.016) and the level of <strong>NK1R</strong> protein (r = 0.476, P = 0.029) in the hippocampus.
+TACR1	drug	alcohol	30054674	The present results highlight the negative correlation between anxiety like behavior and the propensity for <b>alcohol</b> and the critical role for <strong>NK1R</strong> in <b>alcohol</b> reward in adolescent mice.
+TACR1	addiction	reward	30054674	The present results highlight the negative correlation between anxiety like behavior and the propensity for alcohol and the critical role for <strong>NK1R</strong> in alcohol <b>reward</b> in adolescent mice.
+TACR1	drug	alcohol	30054674	Importantly, the <strong>NK1R</strong> antagonist L 703,606 might be a promising therapeutic target for <b>alcohol</b> use disorder.
+TACR1	drug	alcohol	29758386	We have previously demonstrated that the neurokinin 1 receptor (<strong>NK1R</strong>) is upregulated in the central nucleus of the amygdala of <b>alcohol</b> preferring (P) rats and that this receptor mediates escalated <b>alcohol</b> consumption in this strain.
+TACR1	drug	alcohol	29758386	We found that escalated <b>alcohol</b> consumption induced by both yohimbine injection and intermittent access is attenuated by systemic administration of the <strong>NK1R</strong> antagonist L822429.
+TACR1	drug	alcohol	29758386	Also, when compared to continuous <b>alcohol</b> access or access to water alone, <strong>NK1R</strong> expression was increased in the nucleus accumbens (NAC) and dorsal striatum, but not the amygdala.
+TACR1	drug	alcohol	29758386	Taken together, these results suggest that <strong>NK1R</strong> upregulation contributes to escalated <b>alcohol</b> consumption that is induced by genetic selection, yohimbine injection, and intermittent access.
+TACR1	addiction	relapse	29056150	Several preclinical studies have also demonstrated a role of the <strong>NK1R</strong> in drug taking and drug <b>seeking</b>, especially as it relates to escalated consumption and stress elicited <b>seeking</b>.
+TACR1	drug	alcohol	29056150	Given promising clinical findings for the efficacy of <strong>NK1R</strong> antagonists on craving in <b>alcoholics</b>, along with recent data suggesting that a number of negative results from <strong>NK1R</strong> trials were likely due to insufficient receptor occupancy, the <strong>NK1R</strong> merits being revisited as a target for the development of novel pharmacotherapeutics for addiction.
+TACR1	addiction	addiction	29056150	Given promising clinical findings for the efficacy of <strong>NK1R</strong> antagonists on craving in alcoholics, along with recent data suggesting that a number of negative results from <strong>NK1R</strong> trials were likely due to insufficient receptor occupancy, the <strong>NK1R</strong> merits being revisited as a target for the development of novel pharmacotherapeutics for <b>addiction</b>.
+TACR1	addiction	relapse	29056150	Given promising clinical findings for the efficacy of <strong>NK1R</strong> antagonists on <b>craving</b> in alcoholics, along with recent data suggesting that a number of negative results from <strong>NK1R</strong> trials were likely due to insufficient receptor occupancy, the <strong>NK1R</strong> merits being revisited as a target for the development of novel pharmacotherapeutics for addiction.
+TACR1	drug	opioid	28485408	Genome editing of the neurokinin 1 receptor (<strong>NK1R</strong>) in the VTA renders <b>morphine</b> non rewarding.
+TACR1	drug	opioid	28485408	Complementing our genetic approach, we demonstrate utility of a bivalent pharmacophore with dual activity as a μ/δ <b>opioid</b> agonist and <strong>NK1R</strong> antagonist in inhibiting nociception in an animal model of acute pain while lacking any positive reinforcement.
+TACR1	addiction	reward	28485408	Complementing our genetic approach, we demonstrate utility of a bivalent pharmacophore with dual activity as a μ/δ opioid agonist and <strong>NK1R</strong> antagonist in inhibiting nociception in an animal model of acute pain while lacking any positive <b>reinforcement</b>.
+TACR1	drug	opioid	28485408	These data indicate that dual targeting of the dopaminergic reward circuitry and pain pathways with a multifunctional <b>opioid</b> agonist <strong>NK1R</strong> antagonist may be an efficacious strategy in developing future analgesics that lack abuse potential.
+TACR1	addiction	reward	28485408	These data indicate that dual targeting of the dopaminergic <b>reward</b> circuitry and pain pathways with a multifunctional opioid agonist <strong>NK1R</strong> antagonist may be an efficacious strategy in developing future analgesics that lack abuse potential.
+TACR1	drug	alcohol	28150369	Bidirectional relationship between <b>alcohol</b> intake and sensitivity to social defeat: association with <strong>Tacr1</strong> and Avp expression.
+TACR1	addiction	addiction	28150369	We quantified <strong>Tacr1</strong> (neurokinin 1 receptor gene) and Avp (vasopressin peptide gene) mRNA in brain regions involved in depression, <b>addiction</b> and social behavior.
+TACR1	drug	alcohol	28150369	Quantification of mRNA revealed that increased expression of <strong>Tacr1</strong> and Avp generally associated with decreased SI and increased <b>alcohol</b> intake.
+TACR1	drug	opioid	28013351	Neurokinin 1 receptor (<strong>NK1R</strong>) signaling modulates behaviors associated with psychostimulants and <b>opioids</b>.
+TACR1	drug	amphetamine	28013351	Attenuation of <b>AMPH</b> or cocaine induced CPP and locomotor activation by aprepitant suggests a role for <strong>NK1R</strong> signaling in psychostimulant mediated behaviors.
+TACR1	drug	cocaine	28013351	Attenuation of AMPH or <b>cocaine</b> induced CPP and locomotor activation by aprepitant suggests a role for <strong>NK1R</strong> signaling in psychostimulant mediated behaviors.
+TACR1	addiction	reward	28013351	Attenuation of AMPH or cocaine induced <b>CPP</b> and locomotor activation by aprepitant suggests a role for <strong>NK1R</strong> signaling in psychostimulant mediated behaviors.
+TACR1	drug	opioid	28013351	Stimulation of <b>morphine</b> induced CPP expression and suppression of locomotor activity of <b>morphine</b> conditioned mice suggest differential effects of <strong>NK1R</strong> antagonism on conditioned psychostimulant versus <b>opioid</b> reward.
+TACR1	addiction	reward	28013351	Stimulation of morphine induced <b>CPP</b> expression and suppression of locomotor activity of morphine conditioned mice suggest differential effects of <strong>NK1R</strong> antagonism on conditioned psychostimulant versus opioid <b>reward</b>.
+TACR1	drug	opioid	28409174	<b>Opioid</b> receptors and neurokinin 1 receptor (<strong>NK1R</strong>) are found highly expressed in the central nervous system.
+TACR1	drug	opioid	28409174	In this review, we explore the relationships between <b>opioid</b> receptors and <strong>NK1R</strong>.
+TACR1	drug	opioid	28409174	<strong>NK1R</strong> is found participating in the mechanisms of the side effects of the <b>opioids</b>, including <b>opioid</b> analgesic tolerance, hyperalgesia, anxiety behaviors of <b>morphine</b> reward and <b>opioids</b> related respiratory depression.
+TACR1	addiction	reward	28409174	<strong>NK1R</strong> is found participating in the mechanisms of the side effects of the opioids, including opioid analgesic tolerance, hyperalgesia, anxiety behaviors of morphine <b>reward</b> and opioids related respiratory depression.
+TACR1	drug	opioid	28409174	A series of compounds such as <strong>NK1R</strong> antagonists and ligands works on both mu/delta <b>opioid</b> receptor (MOR/DOR) and <strong>NK1R</strong> were synthesized as novel analgesics that enhance the clinical pain management efficacy and reduce the dosage and side effects.
+TACR1	drug	alcohol	26223289	We discovered that substance P (SP) in the aPVT can stimulate intermittent access <b>ethanol</b> drinking, similar to OX, and that SP receptor [neurokinin 1 receptor/tachykinin receptor 1 (<strong>NK1R</strong>)] antagonists in this subregion reduce <b>ethanol</b> drinking.
+TACR1	drug	alcohol	26223289	We discovered that substance P (SP) in the aPVT can stimulate intermittent access <b>ethanol</b> drinking, similar to OX, and that SP receptor [neurokinin 1 receptor/<strong>tachykinin receptor 1</strong> (<strong>NK1R</strong>)] antagonists in this subregion reduce <b>ethanol</b> drinking.
+TACR1	drug	alcohol	26223289	A functional relationship between OX and SP in the aPVT is suggested by our additional finding that <b>ethanol</b> drinking induced by OX is blocked by a local <strong>NK1R</strong> antagonist administered at a sub threshold dose.
+TACR1	drug	alcohol	26188146	Substance P (SP) and its cognate neurokinin 1 receptor (<strong>NK1R</strong>) are involved in <b>alcohol</b> related behaviors.
+TACR1	drug	alcohol	26188146	We have previously reported that <strong>NK1R</strong> antagonism attenuates stress induced reinstatement of <b>alcohol</b> seeking and suppresses escalated <b>alcohol</b> self administration, but does not affect primary reinforcement or cue induced reinstatement.
+TACR1	addiction	relapse	26188146	We have previously reported that <strong>NK1R</strong> antagonism attenuates stress induced <b>reinstatement</b> of alcohol <b>seeking</b> and suppresses escalated alcohol self administration, but does not affect primary reinforcement or cue induced <b>reinstatement</b>.
+TACR1	addiction	reward	26188146	We have previously reported that <strong>NK1R</strong> antagonism attenuates stress induced reinstatement of alcohol seeking and suppresses escalated alcohol self administration, but does not affect primary <b>reinforcement</b> or cue induced reinstatement.
+TACR1	drug	alcohol	26188146	Here, we administered an <strong>NK1R</strong> antagonist or vehicle prior to footshock induced reinstatement of <b>alcohol</b> seeking, and mapped the resulting neuronal activation using Fos immunohistochemistry.
+TACR1	addiction	relapse	26188146	Here, we administered an <strong>NK1R</strong> antagonist or vehicle prior to footshock induced <b>reinstatement</b> of alcohol <b>seeking</b>, and mapped the resulting neuronal activation using Fos immunohistochemistry.
+TACR1	drug	alcohol	26188146	Infusion of the <strong>NK1R</strong> antagonist L822429 into the NAC shell blocked stress induced reinstatement of <b>alcohol</b> seeking.
+TACR1	addiction	relapse	26188146	Infusion of the <strong>NK1R</strong> antagonist L822429 into the NAC shell blocked stress induced <b>reinstatement</b> of alcohol <b>seeking</b>.
+TACR1	drug	alcohol	26188146	Taken together, our results outline a potential pathway through which endogenous <strong>NK1R</strong> activation mediates stress induced <b>alcohol</b> seeking.
+TACR1	addiction	relapse	26188146	Taken together, our results outline a potential pathway through which endogenous <strong>NK1R</strong> activation mediates stress induced alcohol <b>seeking</b>.
+TACR1	addiction	relapse	25038175	The SP/<strong>NK1R</strong> system is a major mediator of stress and anxiety, and over the last several years, it has been demonstrated that the SP/<strong>NK1R</strong> system can have effects similar to those of CRH on drug taking and drug <b>seeking</b>.
+TACR1	drug	alcohol	25038175	Specifically, <strong>NK1R</strong> inhibition attenuates escalated self administration of <b>alcohol</b> as well as stress induced reinstatement of <b>alcohol</b> and cocaine seeking; however, in contrast to other stress systems, the <strong>NK1R</strong> also appears to have a role in primary reward and reinforcement for opiates.
+TACR1	drug	cocaine	25038175	Specifically, <strong>NK1R</strong> inhibition attenuates escalated self administration of alcohol as well as stress induced reinstatement of alcohol and <b>cocaine</b> seeking; however, in contrast to other stress systems, the <strong>NK1R</strong> also appears to have a role in primary reward and reinforcement for opiates.
+TACR1	addiction	relapse	25038175	Specifically, <strong>NK1R</strong> inhibition attenuates escalated self administration of alcohol as well as stress induced <b>reinstatement</b> of alcohol and cocaine <b>seeking</b>; however, in contrast to other stress systems, the <strong>NK1R</strong> also appears to have a role in primary reward and reinforcement for opiates.
+TACR1	addiction	reward	25038175	Specifically, <strong>NK1R</strong> inhibition attenuates escalated self administration of alcohol as well as stress induced reinstatement of alcohol and cocaine seeking; however, in contrast to other stress systems, the <strong>NK1R</strong> also appears to have a role in primary <b>reward</b> and <b>reinforcement</b> for opiates.
+TACR1	addiction	relapse	25038175	This review outlines the role of <strong>NK1R</strong> in drug <b>seeking</b> behaviors and highlights recent results from clinical studies that suggest that the <strong>NK1R</strong> may be a promising drug target going forward.
+TACR1	drug	alcohol	24817687	Genetic association of the tachykinin receptor 1 <strong>TACR1</strong> gene in bipolar disorder, attention deficit hyperactivity disorder, and the <b>alcohol</b> dependence syndrome.
+TACR1	addiction	dependence	24817687	Genetic association of the tachykinin receptor 1 <strong>TACR1</strong> gene in bipolar disorder, attention deficit hyperactivity disorder, and the alcohol <b>dependence</b> syndrome.
+TACR1	drug	alcohol	24817687	Genetic association of the <strong>tachykinin receptor 1</strong> <strong>TACR1</strong> gene in bipolar disorder, attention deficit hyperactivity disorder, and the <b>alcohol</b> dependence syndrome.
+TACR1	addiction	dependence	24817687	Genetic association of the <strong>tachykinin receptor 1</strong> <strong>TACR1</strong> gene in bipolar disorder, attention deficit hyperactivity disorder, and the alcohol <b>dependence</b> syndrome.
+TACR1	drug	alcohol	24817687	Single nucleotide polymorphisms (SNPs) in the tachykinin receptor 1 gene (<strong>TACR1</strong>) are nominally associated with bipolar affective disorder (BPAD) in a genome wide association study and in several case control samples of BPAD, <b>alcohol</b> dependence syndrome (ADS) and attention deficit hyperactivity disorder (ADHD).
+TACR1	addiction	dependence	24817687	Single nucleotide polymorphisms (SNPs) in the tachykinin receptor 1 gene (<strong>TACR1</strong>) are nominally associated with bipolar affective disorder (BPAD) in a genome wide association study and in several case control samples of BPAD, alcohol <b>dependence</b> syndrome (ADS) and attention deficit hyperactivity disorder (ADHD).
+TACR1	drug	alcohol	24817687	Single nucleotide polymorphisms (SNPs) in the <strong>tachykinin receptor 1</strong> gene (<strong>TACR1</strong>) are nominally associated with bipolar affective disorder (BPAD) in a genome wide association study and in several case control samples of BPAD, <b>alcohol</b> dependence syndrome (ADS) and attention deficit hyperactivity disorder (ADHD).
+TACR1	addiction	dependence	24817687	Single nucleotide polymorphisms (SNPs) in the <strong>tachykinin receptor 1</strong> gene (<strong>TACR1</strong>) are nominally associated with bipolar affective disorder (BPAD) in a genome wide association study and in several case control samples of BPAD, alcohol <b>dependence</b> syndrome (ADS) and attention deficit hyperactivity disorder (ADHD).
+TACR1	drug	alcohol	24817687	To further elucidate the role of <strong>TACR1</strong> in affective disorders, rs3771829 was genotyped in a second BPAD sample of 593 subjects (UCL2), in 997 subjects with ADS, and a subsample of 143 individuals diagnosed with BPAD and comorbid <b>alcohol</b> dependence (BPALC).
+TACR1	addiction	dependence	24817687	To further elucidate the role of <strong>TACR1</strong> in affective disorders, rs3771829 was genotyped in a second BPAD sample of 593 subjects (UCL2), in 997 subjects with ADS, and a subsample of 143 individuals diagnosed with BPAD and comorbid alcohol <b>dependence</b> (BPALC).
+TACR1	drug	alcohol	24173499	We recently reported that <strong>NK1R</strong> antagonism also blocks stress induced reinstatement of <b>alcohol</b> seeking in rats, but it is presently unknown whether these antirelapse properties extend to other drug classes.
+TACR1	addiction	relapse	24173499	We recently reported that <strong>NK1R</strong> antagonism also blocks stress induced <b>reinstatement</b> of alcohol <b>seeking</b> in rats, but it is presently unknown whether these antirelapse properties extend to other drug classes.
+TACR1	drug	cocaine	24173499	Although some work has suggested that intracranial substance P (SP) infusion reinstates <b>cocaine</b> seeking following extinction, no studies have indicated a direct role for the <strong>NK1R</strong> in reinstatement of <b>cocaine</b> seeking.
+TACR1	addiction	relapse	24173499	Although some work has suggested that intracranial substance P (SP) infusion reinstates cocaine <b>seeking</b> following extinction, no studies have indicated a direct role for the <strong>NK1R</strong> in <b>reinstatement</b> of cocaine <b>seeking</b>.
+TACR1	drug	alcohol	24173499	Here, we explored the effect of the <strong>NK1R</strong> antagonist L822429 on yohimbine induced reinstatement of <b>alcohol</b> or cocaine seeking in Long Evans rats.
+TACR1	drug	cocaine	24173499	Here, we explored the effect of the <strong>NK1R</strong> antagonist L822429 on yohimbine induced reinstatement of alcohol or <b>cocaine</b> seeking in Long Evans rats.
+TACR1	addiction	relapse	24173499	Here, we explored the effect of the <strong>NK1R</strong> antagonist L822429 on yohimbine induced <b>reinstatement</b> of alcohol or cocaine <b>seeking</b> in Long Evans rats.
+TACR1	drug	cocaine	24173499	We observed a similar suppression of yohimbine induced reinstatement of <b>cocaine</b> seeking by L822429, and found that Long Evans rats exhibit greater sensitivity to <strong>NK1R</strong> antagonism than Wistar rats.
+TACR1	addiction	relapse	24173499	We observed a similar suppression of yohimbine induced <b>reinstatement</b> of cocaine <b>seeking</b> by L822429, and found that Long Evans rats exhibit greater sensitivity to <strong>NK1R</strong> antagonism than Wistar rats.
+TACR1	drug	alcohol	24173499	Combined, our findings suggest that while <strong>NK1R</strong> antagonism differentially influences <b>alcohol</b>  and cocaine related behavior, this receptor mediates stress induced seeking of both drugs.
+TACR1	drug	cocaine	24173499	Combined, our findings suggest that while <strong>NK1R</strong> antagonism differentially influences alcohol  and <b>cocaine</b> related behavior, this receptor mediates stress induced seeking of both drugs.
+TACR1	addiction	relapse	24173499	Combined, our findings suggest that while <strong>NK1R</strong> antagonism differentially influences alcohol  and cocaine related behavior, this receptor mediates stress induced <b>seeking</b> of both drugs.
+TACR1	drug	alcohol	23419547	<strong>Tacr1</strong> gene variation and neurokinin 1 receptor expression is associated with antagonist efficacy in genetically selected <b>alcohol</b> preferring rats.
+TACR1	drug	alcohol	23419547	Genetic deletion or antagonism of the neurokinin 1 receptor (NK1R) decreases <b>alcohol</b> intake, <b>alcohol</b> reward, and stress induced <b>alcohol</b> relapse in rodents, while <strong>TACR1</strong> variation is associated with <b>alcoholism</b> in humans.
+TACR1	addiction	relapse	23419547	Genetic deletion or antagonism of the neurokinin 1 receptor (NK1R) decreases alcohol intake, alcohol reward, and stress induced alcohol <b>relapse</b> in rodents, while <strong>TACR1</strong> variation is associated with alcoholism in humans.
+TACR1	addiction	reward	23419547	Genetic deletion or antagonism of the neurokinin 1 receptor (NK1R) decreases alcohol intake, alcohol <b>reward</b>, and stress induced alcohol relapse in rodents, while <strong>TACR1</strong> variation is associated with alcoholism in humans.
+TACR1	drug	alcohol	23419547	Genetic deletion or antagonism of the neurokinin 1 receptor (<strong>NK1R</strong>) decreases <b>alcohol</b> intake, <b>alcohol</b> reward, and stress induced <b>alcohol</b> relapse in rodents, while <strong>TACR1</strong> variation is associated with <b>alcoholism</b> in humans.
+TACR1	addiction	relapse	23419547	Genetic deletion or antagonism of the neurokinin 1 receptor (<strong>NK1R</strong>) decreases alcohol intake, alcohol reward, and stress induced alcohol <b>relapse</b> in rodents, while <strong>TACR1</strong> variation is associated with alcoholism in humans.
+TACR1	addiction	reward	23419547	Genetic deletion or antagonism of the neurokinin 1 receptor (<strong>NK1R</strong>) decreases alcohol intake, alcohol <b>reward</b>, and stress induced alcohol relapse in rodents, while <strong>TACR1</strong> variation is associated with alcoholism in humans.
+TACR1	drug	alcohol	23419547	We used L822429, a specific antagonist with high affinity for the rat <strong>NK1R</strong>, and examined whether sensitivity to <strong>NK1R</strong> blockade is altered in <b>alcohol</b> preferring (P) rats.
+TACR1	drug	alcohol	23419547	Genetic variation at the <strong>Tacr1</strong> locus may contribute to elevated rates of <b>alcohol</b> self administration, while at the same time increasing sensitivity to NK1R antagonist treatment.
+TACR1	drug	alcohol	23419547	Genetic variation at the <strong>Tacr1</strong> locus may contribute to elevated rates of <b>alcohol</b> self administration, while at the same time increasing sensitivity to <strong>NK1R</strong> antagonist treatment.
+TACR1	drug	opioid	23303056	Genetic deletion of the neurokinin 1 receptor (<strong>NK1R</strong>) has been shown to decrease the reinforcing properties of <b>opioids</b>, but it is unknown whether pharmacological <strong>NK1R</strong> blockade has the same effect.
+TACR1	addiction	reward	23303056	Genetic deletion of the neurokinin 1 receptor (<strong>NK1R</strong>) has been shown to decrease the <b>reinforcing</b> properties of opioids, but it is unknown whether pharmacological <strong>NK1R</strong> blockade has the same effect.
+TACR1	drug	opioid	23303056	Here, we examined the effect of L822429, a rat specific <strong>NK1R</strong> antagonist, on the reinforcing properties of <b>heroin</b> in rats on short (1 h: ShA) or long (12 h: LgA) access to intravenous <b>heroin</b> self administration.
+TACR1	addiction	reward	23303056	Here, we examined the effect of L822429, a rat specific <strong>NK1R</strong> antagonist, on the <b>reinforcing</b> properties of heroin in rats on short (1 h: ShA) or long (12 h: LgA) access to intravenous heroin self administration.
+TACR1	drug	opioid	23303056	Expression of <strong>TacR1</strong> (the gene encoding NK1R) was decreased in reward  and stress related brain areas both in ShA and LgA rats compared with <b>heroin</b> naïve rats, but did not differ between the two <b>heroin</b> experienced groups.
+TACR1	addiction	reward	23303056	Expression of <strong>TacR1</strong> (the gene encoding NK1R) was decreased in <b>reward</b>  and stress related brain areas both in ShA and LgA rats compared with heroin naïve rats, but did not differ between the two heroin experienced groups.
+TACR1	drug	opioid	23303056	Expression of <strong>TacR1</strong> (the gene encoding <strong>NK1R</strong>) was decreased in reward  and stress related brain areas both in ShA and LgA rats compared with <b>heroin</b> naïve rats, but did not differ between the two <b>heroin</b> experienced groups.
+TACR1	addiction	reward	23303056	Expression of <strong>TacR1</strong> (the gene encoding <strong>NK1R</strong>) was decreased in <b>reward</b>  and stress related brain areas both in ShA and LgA rats compared with heroin naïve rats, but did not differ between the two heroin experienced groups.
+TACR1	drug	opioid	23303056	In contrast, passive exposure to <b>heroin</b> produced increases in <strong>TacR1</strong> expression in the prefrontal cortex and nucleus accumbens.
+TACR1	drug	opioid	23303056	Taken together, these results show that pharmacological <strong>NK1R</strong> blockade attenuates <b>heroin</b> reinforcement.
+TACR1	addiction	reward	23303056	Taken together, these results show that pharmacological <strong>NK1R</strong> blockade attenuates heroin <b>reinforcement</b>.
+TACR1	drug	opioid	23303056	The observation that animals with ShA and LgA to <b>heroin</b> were similarly affected by L822429 indicates that the SP/<strong>NK1R</strong> system is not specifically involved in neuroadaptations that underlie escalation resulting from LgA self administration.
+TACR1	addiction	addiction	23303056	The observation that animals with ShA and LgA to heroin were similarly affected by L822429 indicates that the SP/<strong>NK1R</strong> system is not specifically involved in neuroadaptations that underlie <b>escalation</b> resulting from LgA self administration.
+TACR1	drug	opioid	23303056	Instead, the <strong>NK1R</strong> antagonist appears to attenuate acute, positively reinforcing properties of <b>heroin</b> and may be useful as an adjunct to relapse prevention in detoxified <b>opioid</b> dependent subjects.
+TACR1	addiction	relapse	23303056	Instead, the <strong>NK1R</strong> antagonist appears to attenuate acute, positively reinforcing properties of heroin and may be useful as an adjunct to <b>relapse</b> prevention in detoxified opioid dependent subjects.
+TACR1	addiction	reward	23303056	Instead, the <strong>NK1R</strong> antagonist appears to attenuate acute, positively <b>reinforcing</b> properties of heroin and may be useful as an adjunct to relapse prevention in detoxified opioid dependent subjects.
+TACR1	drug	cocaine	23256992	The aim of this research was to identify the <strong>tacr1</strong> gene, study the effects of <b>cocaine</b> on <strong>tacr1</strong>, and analyze the interaction between <strong>tacr1</strong> and opioid receptors.
+TACR1	drug	opioid	23256992	The aim of this research was to identify the <strong>tacr1</strong> gene, study the effects of cocaine on <strong>tacr1</strong>, and analyze the interaction between <strong>tacr1</strong> and <b>opioid</b> receptors.
+TACR1	drug	alcohol	23078527	<strong>TACR1</strong> genotypes predict fMRI response to <b>alcohol</b> cues and level of <b>alcohol</b> dependence.
+TACR1	addiction	dependence	23078527	<strong>TACR1</strong> genotypes predict fMRI response to alcohol cues and level of alcohol <b>dependence</b>.
+TACR1	drug	alcohol	23078527	The tachykinin receptor 1 (<strong>TACR1</strong>) gene is a promising candidate gene in the search for the genetic basis of <b>alcohol</b> dependence (AD); <strong>TACR1</strong> antagonists improve symptomology not only in preclinical models of AD but also in a clinical sample of detoxified <b>alcoholics</b> (George et al., Science 319:1536, 2008).
+TACR1	addiction	dependence	23078527	The tachykinin receptor 1 (<strong>TACR1</strong>) gene is a promising candidate gene in the search for the genetic basis of alcohol <b>dependence</b> (AD); <strong>TACR1</strong> antagonists improve symptomology not only in preclinical models of AD but also in a clinical sample of detoxified alcoholics (George et al., Science 319:1536, 2008).
+TACR1	drug	alcohol	23078527	The <strong>tachykinin receptor 1</strong> (<strong>TACR1</strong>) gene is a promising candidate gene in the search for the genetic basis of <b>alcohol</b> dependence (AD); <strong>TACR1</strong> antagonists improve symptomology not only in preclinical models of AD but also in a clinical sample of detoxified <b>alcoholics</b> (George et al., Science 319:1536, 2008).
+TACR1	addiction	dependence	23078527	The <strong>tachykinin receptor 1</strong> (<strong>TACR1</strong>) gene is a promising candidate gene in the search for the genetic basis of alcohol <b>dependence</b> (AD); <strong>TACR1</strong> antagonists improve symptomology not only in preclinical models of AD but also in a clinical sample of detoxified alcoholics (George et al., Science 319:1536, 2008).
+TACR1	drug	alcohol	23078527	The purpose of the current study was to determine whether <strong>TACR1</strong> single nucleotide polymorphisms (SNPs) were associated with (i) blood oxygen level dependent (BOLD) activation in response to gustatory <b>alcohol</b> cues in a sample of heavy drinkers and (ii) Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision (DSM IV TR) AD symptom count in a large, publicly available data set the Study of Addictions: Genetics and Environment Genome Wide Association study (SAGE GWAS) (Bierut et al., 2010).
+TACR1	drug	alcohol	23078527	First, we examined relationships between <strong>TACR1</strong> genotypes and neural responses during a craving task in 326 individuals with <b>alcohol</b> use disorders.
+TACR1	addiction	relapse	23078527	First, we examined relationships between <strong>TACR1</strong> genotypes and neural responses during a <b>craving</b> task in 326 individuals with alcohol use disorders.
+TACR1	addiction	relapse	23078527	Each of the 5 SNPs in the <strong>TACR1</strong> gene that was significantly related to AD severity in the SAGE data set and/or the BOLD response to the <b>craving</b> task is near the 3' or 5' areas of the gene and may therefore be near mutations with potential functional significance.
+TACR1	drug	opioid	21909635	The abuse potential of <b>opioids</b> may be due to their reinforcing and rewarding effects, which may be attenuated by neurokinin 1 receptor (<strong>NK1R</strong>) antagonists.
+TACR1	addiction	reward	21909635	The abuse potential of opioids may be due to their <b>reinforcing</b> and rewarding effects, which may be attenuated by neurokinin 1 receptor (<strong>NK1R</strong>) antagonists.
+TACR1	drug	opioid	21909635	This study was conducted to measure the effects of <b>opioid</b> and <strong>NK1R</strong> blockade on the potentiation of brain stimulation reward (BSR) by <b>morphine</b> using the intracranial self stimulation method.
+TACR1	addiction	reward	21909635	This study was conducted to measure the effects of opioid and <strong>NK1R</strong> blockade on the potentiation of brain stimulation <b>reward</b> (BSR) by morphine using the intracranial self stimulation method.
+TACR1	drug	opioid	21909635	The BSR threshold (θ(0)) and maximum response rate (MAX) were determined before and after intraperitoneal administration of saline, <b>morphine</b> (1.0 17.0 mg/kg), or the <strong>NK1R</strong> antagonists L 733,060 (1.0 17.0 mg/kg) and L 703,606 (1.0 17.0 mg/kg).
+TACR1	drug	opioid	21909635	The decrease in θ(0) by <b>morphine</b> reflects its rewarding effects, which were attenuated by <strong>NK1R</strong> and <b>opioid</b> receptor blockade.
+TACR1	addiction	reward	20347940	The neuropeptide substance P and the neurokinin 1 receptor (<strong>NK1R</strong>) are involved in the stress response and drug <b>reward</b> systems.
+TACR1	drug	alcohol	20112009	Neurokinin 1 receptors (<strong>NK1R</strong>:s), <b>alcohol</b> consumption, and <b>alcohol</b> reward in mice.
+TACR1	addiction	reward	20112009	Neurokinin 1 receptors (<strong>NK1R</strong>:s), alcohol consumption, and alcohol <b>reward</b> in mice.
+TACR1	drug	alcohol	20112009	Reduced voluntary <b>alcohol</b> consumption was recently found in neurokinin 1 receptor (<strong>NK1R</strong>) deficient (KO) mice.
+TACR1	drug	alcohol	20112009	It remains unknown whether this reflects developmental effects or direct regulation of <b>alcohol</b> consumption by <strong>NK1R</strong>:s, and whether the reduced consumption reflects motivational effects.
+TACR1	drug	alcohol	20112009	The objective of this study is to obtain an expanded preclinical validation of <strong>NK1R</strong> antagonism as a candidate therapeutic mechanism in <b>alcohol</b> use disorders.
+TACR1	drug	alcohol	20112009	The <strong>NK1R</strong> antagonist L 703,606 and <strong>NK1R</strong> KO mice were used in models that assess <b>alcohol</b> related behaviors.
+TACR1	drug	alcohol	20112009	dose dependently suppressed <b>alcohol</b> intake in WT C57BL/6 mice under two bottle free choice conditions but was ineffective in <strong>NK1R</strong> KO:s, demonstrating the receptor specificity of the effect.
+TACR1	drug	alcohol	20112009	<b>Alcohol</b> reward, measured as conditioned place preference for <b>alcohol</b>, was reduced by <strong>NK1R</strong> receptor deletion in a gene dose dependent manner.
+TACR1	addiction	reward	20112009	Alcohol <b>reward</b>, measured as conditioned place preference for alcohol, was reduced by <strong>NK1R</strong> receptor deletion in a gene dose dependent manner.
+TACR1	drug	alcohol	20112009	Acute blockade of <strong>NK1R</strong>:s mimics the effects of NKR1 gene deletion on <b>alcohol</b> consumption, supporting a direct rather than developmental role of the receptor in regulation of <b>alcohol</b> intake.
+TACR1	drug	alcohol	20112009	Inactivation of <strong>NK1R</strong>:s critically modulates <b>alcohol</b> reward and escalation, two key characteristics of addiction.
+TACR1	addiction	addiction	20112009	Inactivation of <strong>NK1R</strong>:s critically modulates alcohol reward and <b>escalation</b>, two key characteristics of <b>addiction</b>.
+TACR1	addiction	reward	20112009	Inactivation of <strong>NK1R</strong>:s critically modulates alcohol <b>reward</b> and escalation, two key characteristics of addiction.
+TACR1	drug	alcohol	20112009	These data provide critical support for <strong>NK1R</strong> antagonism as a candidate mechanism for treatment of <b>alcoholism</b>.
+TACR1	drug	amphetamine	19748515	In the course of this work, we discovered that <strong>NK1R</strong> /  mice express locomotor hyperactivity that is prevented by psychostimulants (d <b>amphetamine</b> or methylphenidate).
+TACR1	drug	amphetamine	19748515	Moreover, hyperactivity is induced in wildtypes by treating them with an <strong>NK1R</strong> antagonist (at doses that have no effect on the behaviour of <strong>NK1R</strong> /  mice): this hyperactivity is prevented by d <b>amphetamine</b>, as in <strong>NK1R</strong> /  mice.
+TACR1	drug	alcohol	19553914	Genetic and pharmacological studies show that binding of ligands to <strong>NK1R</strong> decreases anxiety related behaviors, and therefore, self administration of <b>alcohol</b> in mice and craving for <b>alcohol</b> in humans.
+TACR1	addiction	relapse	19553914	Genetic and pharmacological studies show that binding of ligands to <strong>NK1R</strong> decreases anxiety related behaviors, and therefore, self administration of alcohol in mice and <b>craving</b> for alcohol in humans.
+TACR1	drug	alcohol	19553914	As genetic variants may result in differential expression of the receptor through various molecular mechanisms, we examined whether allelic variations in the <strong>NK1R</strong> gene are associated with <b>alcohol</b> dependence (AD) by genotyping 11 single nucleotide polymorphisms (SNPs) across <strong>NK1R</strong> in <b>alcoholic</b> (n=271) and healthy control (n=337) participants of Caucasian descent.
+TACR1	addiction	dependence	19553914	As genetic variants may result in differential expression of the receptor through various molecular mechanisms, we examined whether allelic variations in the <strong>NK1R</strong> gene are associated with alcohol <b>dependence</b> (AD) by genotyping 11 single nucleotide polymorphisms (SNPs) across <strong>NK1R</strong> in alcoholic (n=271) and healthy control (n=337) participants of Caucasian descent.
+TACR1	drug	opioid	19129399	<strong>NK1R</strong> activation affects <b>opioid</b> reward specifically, however, and the cellular basis for this specificity is unknown.
+TACR1	addiction	reward	19129399	<strong>NK1R</strong> activation affects opioid <b>reward</b> specifically, however, and the cellular basis for this specificity is unknown.
+TACR1	drug	opioid	19129399	<strong>NK1R</strong> mediated regulation of MOR trafficking was associated with reduced <b>opioid</b> induced desensitization of adenylyl cyclase signaling in striatal neurons.
+TACR1	drug	opioid	19129399	These results identify a cell autonomous mechanism that may underlie the highly specific effects of <strong>NK1R</strong> on <b>opioid</b> signaling and suggest, more generally, that receptor specific trafficking of arrestins may represent a fundamental mechanism for coordinating distinct GPCR mediated signals at the level of individual CNS neurons.
+TACR1	drug	alcohol	19081000	In a preclinical and experimental clinical study George and colleagues first investigated the role of Substance P and its receptor (<strong>NK1R</strong>) in the context of <b>alcoholism</b>.
+TACR1	drug	alcohol	18276852	We investigated the role of the neurokinin 1 receptor (<strong>NK1R</strong>), a mediator of behavioral stress responses, in <b>alcohol</b> dependence and treatment.
+TACR1	addiction	dependence	18276852	We investigated the role of the neurokinin 1 receptor (<strong>NK1R</strong>), a mediator of behavioral stress responses, in alcohol <b>dependence</b> and treatment.
+TACR1	drug	alcohol	18276852	In preclinical studies, mice genetically deficient in <strong>NK1R</strong> showed a marked decrease in voluntary <b>alcohol</b> consumption and had an increased sensitivity to the sedative effects of <b>alcohol</b>.
+TACR1	drug	alcohol	18276852	In a randomized controlled experimental study, we treated recently detoxified <b>alcoholic</b> inpatients with an <strong>NK1R</strong> antagonist (LY686017; n = 25) or placebo (n = 25).
+TACR1	drug	alcohol	18276852	Thus, as assessed by these surrogate markers of efficacy, <strong>NK1R</strong> antagonism warrants further investigation as a treatment in <b>alcoholism</b>.
+TACR1	drug	opioid	15908510	Intrathecal <b>morphine</b> infusion (40 nmol/microl/h) for 1 day possessed similar analgesic efficacy as acute <b>morphine</b> and blocked compression induced spinal <strong>NK1r</strong> internalization.
+TACR1	drug	opioid	15908510	After 5 days of <b>morphine</b> infusion, thermal escape latencies were the same as in preinfusion animals or saline infused controls, and compression evoked <strong>NK1r</strong> internalization was no longer suppressed.
+TACR1	drug	opioid	15908510	Systemic administration of <b>naloxone</b> to rats on day 6 of <b>morphine</b> infusion resulted in prominent withdrawal behaviors and a concomitant increase in <strong>NK1r</strong> internalization in dorsal horn.
+TACR1	addiction	withdrawal	15908510	Systemic administration of naloxone to rats on day 6 of morphine infusion resulted in prominent <b>withdrawal</b> behaviors and a concomitant increase in <strong>NK1r</strong> internalization in dorsal horn.
+TACR1	drug	opioid	15908510	The <b>naloxone</b> induced internalization was blocked by <strong>NK1r</strong> antagonist L 703,606 [cis 2 (diphenylmethyl) N [(2 iodophenyl)methyl] 1 azabicyclo[2.2.2]octan 3 amine] or pretreatment with capsaicin, confirming that the internalization is due to the endogenous SP release from the primary afferents.
+PARP1	drug	cocaine	32641757	Interestingly, acute or chronic <b>cocaine</b> exposure downregulated miR 124 levels concomitant with upregulation of <strong>PARP</strong> 1 protein in dopaminergic like neuronal cells in culture.
+PARP1	drug	cocaine	32641757	Collectively, these studies identify <strong>Parp</strong> 1 as a direct target of miR 124 in neuronal cells, establish miR 124 as a <b>cocaine</b> regulated miRNA in the mouse NAc, and highlight a novel pathway underlying the molecular effects of <b>cocaine</b>.
+PARP1	drug	amphetamine	32086884	In addition, to explore <b>METH</b> induced neurotoxicity, we measured the level of Parkin and the phosphorylation levels of α syn, Polo like kinase 2 (PLK2), the proteasome activity marker CD3δ, and the apoptosis related proteins Caspase 3 and <strong>PARP</strong>.
+PARP1	drug	alcohol	31251945	<strong>PARP</strong> inhibition in vivo blocks <b>alcohol</b> induced brain neurodegeneration and neuroinflammatory cytosolic phospholipase A2 elevations.
+PARP1	drug	alcohol	31251945	Concurrent with neurodegeneration, <b>alcohol</b> elevates poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1) and cytosolic phospholipase A2 (cPLA2) levels.
+PARP1	drug	alcohol	31251945	Inhibitors of <strong>PARP</strong> exert in vitro neuroprotection while suppressing cPLA2 elevations in <b>alcohol</b> treated HC ECX slice cultures.
+PARP1	drug	alcohol	31251945	Here, we examined in vivo neuroprotection and cPLA2 suppression by the <strong>PARP</strong> inhibitor, veliparib, in a recognized adult rat model of <b>alcohol</b> binging.
+PARP1	drug	alcohol	31251945	These in vivo results support an emerging key role for <strong>PARP</strong> in binge <b>alcohol</b> induced neurodegeneration and cPLA2 related neuroinflammation.
+PARP1	addiction	intoxication	31251945	These in vivo results support an emerging key role for <strong>PARP</strong> in <b>binge</b> alcohol induced neurodegeneration and cPLA2 related neuroinflammation.
+PARP1	addiction	aversion	30648291	Furthermore, Nth AD+ was engaged in cholera toxin A (<b>CTA</b>) catalyzed mono(th ADP ribosyl)ation, but was found incapable in promoting <strong>PARP1</strong> mediated poly(th ADP ribosyl)ation.
+PARP1	drug	alcohol	29339456	<strong>PARP</strong> Inhibition Prevents <b>Ethanol</b> Induced Neuroinflammatory Signaling and Neurodegeneration in Rat Adult Age Brain Slice Cultures.
+PARP1	drug	alcohol	29339456	Using rat adult age hippocampal entorhinal cortical (HEC) slice cultures, we examined the role of poly [ADP ribose] polymerase (<strong>PARP</strong>) in binge <b>ethanol</b>'s brain inflammatory and neurodegenerative mechanisms.
+PARP1	addiction	intoxication	29339456	Using rat adult age hippocampal entorhinal cortical (HEC) slice cultures, we examined the role of poly [ADP ribose] polymerase (<strong>PARP</strong>) in <b>binge</b> ethanol's brain inflammatory and neurodegenerative mechanisms.
+PARP1	drug	alcohol	29339456	Previously, we found that brain <strong>PARP1</strong> levels were upregulated by neurotoxic <b>ethanol</b> binges in adult rats and HEC slices, and PARP inhibitor PJ34 abrogated slice neurodegeneration.
+PARP1	drug	alcohol	29339456	Previously, we found that brain <strong>PARP1</strong> levels were upregulated by neurotoxic <b>ethanol</b> binges in adult rats and HEC slices, and <strong>PARP</strong> inhibitor PJ34 abrogated slice neurodegeneration.
+PARP1	drug	alcohol	29339456	We now find in 4 day binged HEC slice cultures (100 mM <b>ethanol</b>) that <strong>PARP1</strong> elevations after two overnight binges precede PAR, cPLA2, and sPLA2 enhancements by 1 day and high mobility group box 1 (HMGB1), an <b>ethanol</b> responsive alarmin that augments proinflammatory cytokines via toll like receptor 4 (TLR4), by 2 days.
+PARP1	drug	alcohol	29339456	After verifying that PJ34 effectively blocks <strong>PARP</strong> activity (↑PAR), we demonstrated that, like PJ34, three other <strong>PARP</strong> inhibitors olaparib, veliparib, and 4 aminobenzamide provided neuroprotection from <b>ethanol</b>.
+PARP1	drug	alcohol	29339456	Importantly, PJ34 and olaparib also prevented <b>ethanol</b>'s amplification of the PLA2 isoenzymes, and two PLA2 inhibitors were neuroprotective thus coupling <strong>PARP</strong> to PLA2, with PLA2 activity promoting neurodegeneration.
+PARP1	drug	alcohol	29339456	Also, PJ34 and olaparib blocked <b>ethanol</b> induced HMGB1 elevations, linking brain <strong>PARP</strong> induction to TLR4 activation.
+PARP1	drug	alcohol	29339456	The results provide evidence in adult brains that induction of <strong>PARP1</strong> may mediate dual neuroinflammatory pathways (PLA2→phospholipid→ARA and HMGB1→TLR4→proinflammatory cytokines) that are complicit in binge <b>ethanol</b> induced neurodegeneration.
+PARP1	addiction	intoxication	29339456	The results provide evidence in adult brains that induction of <strong>PARP1</strong> may mediate dual neuroinflammatory pathways (PLA2→phospholipid→ARA and HMGB1→TLR4→proinflammatory cytokines) that are complicit in <b>binge</b> ethanol induced neurodegeneration.
+PARP1	drug	alcohol	27901267	Binge <b>alcohol</b> intake in mice immediately after a 1 hour exposure to a +9 Gz hypergravity load repressed hepatic Akt and <strong>PARP</strong> 1 levels at 24 hours posttreatment.
+PARP1	addiction	intoxication	27901267	<b>Binge</b> alcohol intake in mice immediately after a 1 hour exposure to a +9 Gz hypergravity load repressed hepatic Akt and <strong>PARP</strong> 1 levels at 24 hours posttreatment.
+PARP1	drug	cocaine	27595592	<strong>PARP</strong> 1 is required for retrieval of <b>cocaine</b> associated memory by binding to the promoter of a novel gene encoding a putative transposase inhibitor.
+PARP1	drug	cocaine	27595592	We demonstrate herein that auto poly(ADP ribosyl)ation of activated <strong>PARP</strong> 1 was significantly pronounced during retrieval of <b>cocaine</b> associated contextual memory, in the central amygdala (CeA) of rats expressing <b>cocaine</b> conditioned place preference (CPP).
+PARP1	addiction	reward	27595592	We demonstrate herein that auto poly(ADP ribosyl)ation of activated <strong>PARP</strong> 1 was significantly pronounced during retrieval of cocaine associated contextual memory, in the central amygdala (CeA) of rats expressing cocaine conditioned place preference (<b>CPP</b>).
+PARP1	drug	cocaine	27595592	Intra CeA pharmacological and short hairpin RNA depletion of <strong>PARP</strong> 1 activity during <b>cocaine</b> associated memory retrieval abolished CPP.
+PARP1	addiction	reward	27595592	Intra CeA pharmacological and short hairpin RNA depletion of <strong>PARP</strong> 1 activity during cocaine associated memory retrieval abolished <b>CPP</b>.
+PARP1	addiction	reward	27595592	In contrast, <strong>PARP</strong> 1 inhibition after memory retrieval did not affect <b>CPP</b> reconsolidation process and subsequent retrievals.
+PARP1	drug	cocaine	27595592	We identified among <strong>PARP</strong> targets in CeA a single gene, yet uncharacterized and encoding a putative transposase inhibitor, at which <strong>PARP</strong> 1 enrichment markedly increases during <b>cocaine</b> associated memory retrieval and positively correlates with CPP.
+PARP1	addiction	reward	27595592	We identified among <strong>PARP</strong> targets in CeA a single gene, yet uncharacterized and encoding a putative transposase inhibitor, at which <strong>PARP</strong> 1 enrichment markedly increases during cocaine associated memory retrieval and positively correlates with <b>CPP</b>.
+PARP1	drug	alcohol	27527870	<b>Ethanol</b> caused both apoptotic and necrotic cell death which was demonstrated by the increase in active caspase 3, caspase 8, cleaved <strong>PARP</strong>, cleaved CK 18 and the secretion of high mobility group protein B1 (HMGB1).
+PARP1	drug	psychedelics	26068050	In fact, chronic <b>MDMA</b> inhibited proteins of the apoptotic pathway (i.e., pro apoptotic FADD, Bax and cytochrome c) leading to an inhibition of cell death markers (i.e., p JNK1/2, cleavage of <strong>PARP</strong> 1) and suggesting regulatory mechanisms in response to the neurochemical changes caused by the drug.
+PARP1	drug	amphetamine	25631491	In addition, blocking caspase 11 expression inhibited <b>METH</b> induced activation of caspase 3 and <strong>PARP</strong> in vitro and in vivo, suggesting that caspase 11/caspase 3 signal pathway is involved in <b>METH</b> induced neurotoxicity.
+PARP1	drug	alcohol	25029343	We report here that neurotoxic binge <b>ethanol</b> exposure produces comparable significant effects in vivo and in vitro on adult rat brain levels of AQP4 as well as neuroinflammation linked enzymes: key phospholipase A2 (PLA2) family members and poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1).
+PARP1	addiction	intoxication	25029343	We report here that neurotoxic <b>binge</b> ethanol exposure produces comparable significant effects in vivo and in vitro on adult rat brain levels of AQP4 as well as neuroinflammation linked enzymes: key phospholipase A2 (PLA2) family members and poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1).
+PARP1	drug	alcohol	25029343	In adult male rats, repetitive <b>ethanol</b> intoxication (3 gavages/d for 4 d, ∼ 9 g/kg/d, achieving blood <b>ethanol</b> levels ∼ 375 mg/dl; "Majchrowicz" model) significantly increased AQP4, Ca+2 dependent PLA2 GIVA (cPLA2), phospho cPLA2 GIVA (p cPLA2), secretory PLA2 GIIA (sPLA2) and <strong>PARP</strong> 1 in regions incurring extensive neurodegeneration in this model  hippocampus, entorhinal cortex, and olfactory bulb  but not in two regions typically lacking neurodamage, frontal cortex and cerebellum.
+PARP1	addiction	intoxication	25029343	In adult male rats, repetitive ethanol <b>intoxication</b> (3 gavages/d for 4 d, ∼ 9 g/kg/d, achieving blood ethanol levels ∼ 375 mg/dl; "Majchrowicz" model) significantly increased AQP4, Ca+2 dependent PLA2 GIVA (cPLA2), phospho cPLA2 GIVA (p cPLA2), secretory PLA2 GIIA (sPLA2) and <strong>PARP</strong> 1 in regions incurring extensive neurodegeneration in this model  hippocampus, entorhinal cortex, and olfactory bulb  but not in two regions typically lacking neurodamage, frontal cortex and cerebellum.
+PARP1	drug	alcohol	25029343	Furthermore, supplementation with docosahexaenoic acid (DHA; 22:6n 3), known to quell AQP4 and neurodegeneration in <b>ethanol</b> treated slices, blocked <strong>PARP</strong> 1 and PLA2 changes while counteracting endogenous DHA reduction and increases in oxidative stress footprints (3 nitrotyrosinated proteins).
+PARP1	drug	alcohol	25029343	Notably, the <strong>PARP</strong> 1 inhibitor PJ 34 suppressed binge <b>ethanol</b> dependent neurodegeneration, indicating <strong>PARP</strong> upstream involvement.
+PARP1	addiction	intoxication	25029343	Notably, the <strong>PARP</strong> 1 inhibitor PJ 34 suppressed <b>binge</b> ethanol dependent neurodegeneration, indicating <strong>PARP</strong> upstream involvement.
+PARP1	drug	opioid	24959978	In this study, we investigated the effects of <b>morphine</b> induced conditioned place preference (CPP) in the presence and absence of stress on the changes of apoptotic factors (Bax/Bcl 2 ratio, caspase 3 activation and <strong>PARP</strong> degradation) in the MCL system.
+PARP1	addiction	reward	24959978	In this study, we investigated the effects of morphine induced conditioned place preference (<b>CPP</b>) in the presence and absence of stress on the changes of apoptotic factors (Bax/Bcl 2 ratio, caspase 3 activation and <strong>PARP</strong> degradation) in the MCL system.
+PARP1	drug	alcohol	24705861	Concomitant with PLA(2) activation, the results have further implicated binge <b>alcohol</b> elevated poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1), an oxidative stress responsive DNA repair enzyme linked to parthanatos, a necrotic like neuronal death process.
+PARP1	addiction	intoxication	24705861	Concomitant with PLA(2) activation, the results have further implicated <b>binge</b> alcohol elevated poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1), an oxidative stress responsive DNA repair enzyme linked to parthanatos, a necrotic like neuronal death process.
+PARP1	drug	alcohol	24705861	Importantly, supplementation of the brain slice cultures with docosahexaenoic acid (22:6 ω3) exerted potent suppression of the induced changes in PLA(2) isoforms, AQP4, <strong>PARP</strong> 1 and oxidative stress footprints, and prevention of the binge <b>alcohol</b> neurotoxicity, by as yet unknown mechanisms.
+PARP1	addiction	intoxication	24705861	Importantly, supplementation of the brain slice cultures with docosahexaenoic acid (22:6 ω3) exerted potent suppression of the induced changes in PLA(2) isoforms, AQP4, <strong>PARP</strong> 1 and oxidative stress footprints, and prevention of the <b>binge</b> alcohol neurotoxicity, by as yet unknown mechanisms.
+PARP1	drug	cocaine	24449909	Here, we identify an essential role for <strong>PARP</strong> 1 in <b>cocaine</b> induced molecular, neural, and behavioral plasticity.
+PARP1	drug	cocaine	24449909	Repeated <b>cocaine</b> administration, including self administration, increased global levels of <strong>PARP</strong> 1 and its mark PAR in mouse nucleus accumbens (NAc), a key brain reward region.
+PARP1	addiction	reward	24449909	Repeated cocaine administration, including self administration, increased global levels of <strong>PARP</strong> 1 and its mark PAR in mouse nucleus accumbens (NAc), a key brain <b>reward</b> region.
+PARP1	drug	cocaine	24449909	Using <strong>PARP</strong> 1 inhibitors and viral mediated gene transfer, we established that <strong>PARP</strong> 1 induction in NAc mediates enhanced behavioral responses to <b>cocaine</b>, including increased self administration of the drug.
+PARP1	drug	cocaine	24449909	Using chromatin immunoprecipitation sequencing, we demonstrated a global, genome wide enrichment of <strong>PARP</strong> 1 in NAc of <b>cocaine</b> exposed mice and identified several <strong>PARP</strong> 1 target genes that could contribute to the lasting effects of <b>cocaine</b>.
+PARP1	drug	cocaine	24449909	Specifically, we identified sidekick 1  important for synaptic connections during development  as a critical <strong>PARP</strong> 1 target gene involved in <b>cocaine</b>'s behavioral effects as well as in its ability to induce dendritic spines on NAc neurons.
+PARP1	drug	cocaine	24449909	These findings establish the involvement of <strong>PARP</strong> 1 and PARylation in the long term actions of <b>cocaine</b>.
+PARP1	drug	opioid	24281942	In the HPC, <b>morphine</b> significantly increased the ratio of Bax/Bcl 2, caspases 3, and <strong>PARP</strong> by the lowest dose (0.5 mg/kg), but, in the VTA, a considerable increase was seen in the dose of 5 mg/kg; promotion of apoptotic factors in the HPC and VTA insinuates that <b>morphine</b> can affect the molecular mechanisms that interfere with apoptosis through different receptors.
+PARP1	drug	opioid	24096212	In the NAc, <b>morphine</b> significantly increased the Bax/Bcl 2 ratio, caspase3 and <strong>PARP</strong> in the lowest dose (0.5mg/kg) but in the PFC considerable increase was seen in dose of 5mg/kg.
+PARP1	addiction	reward	27385959	In this study, the effects of acute and subchronic stress on the changes in apoptotic factors (Bax/Bcl 2 ratio, caspase 3 activation and <strong>PARP</strong> degradation) in the HYP and HIP during conditioned place preference (<b>CPP</b>) paradigm were evaluated.
+PARP1	drug	opioid	27385959	Caspase 3 and <strong>PARP</strong> increased during AS and SS in saline  or <b>morphine</b> treated animals.
+PARP1	drug	opioid	27385959	For example, caspase 3 increased during AS and SS in <b>morphine</b> treated animals by 2.4 folds and <strong>PARP</strong> (89 KDa) increased by 3.1 and 3.5 folds, respectively.
+PARP1	drug	alcohol	23102656	Effect of repetitive daily <b>ethanol</b> intoxication on adult rat brain: significant changes in phospholipase A2 enzyme levels in association with increased <strong>PARP</strong> 1 indicate neuroinflammatory pathway activation.
+PARP1	addiction	intoxication	23102656	Effect of repetitive daily ethanol <b>intoxication</b> on adult rat brain: significant changes in phospholipase A2 enzyme levels in association with increased <strong>PARP</strong> 1 indicate neuroinflammatory pathway activation.
+PARP1	drug	alcohol	23102656	Collaborating on studies of subchronic daily intoxication in juvenile and adult rats, we examined whether the repetitive <b>ethanol</b> treatments at these two life stages altered levels of key neuroinflammation associated proteins aquaporin 4 (AQP4), certain phospholipase A2 (PLA2) enzymes, <strong>PARP</strong> 1 and caspase 3 in hippocampus (HC) and entorhinal cortex (EC).
+PARP1	addiction	intoxication	23102656	Collaborating on studies of subchronic daily <b>intoxication</b> in juvenile and adult rats, we examined whether the repetitive ethanol treatments at these two life stages altered levels of key neuroinflammation associated proteins aquaporin 4 (AQP4), certain phospholipase A2 (PLA2) enzymes, <strong>PARP</strong> 1 and caspase 3 in hippocampus (HC) and entorhinal cortex (EC).
+PARP1	drug	alcohol	23102656	Furthermore, the robust <strong>PARP</strong> 1 elevations accompanied by negligible caspase 3 activation indicate that repetitive <b>ethanol</b> intoxication may be potentiating non apoptotic neurodegenerative processes such as parthanatos.
+PARP1	addiction	intoxication	23102656	Furthermore, the robust <strong>PARP</strong> 1 elevations accompanied by negligible caspase 3 activation indicate that repetitive ethanol <b>intoxication</b> may be potentiating non apoptotic neurodegenerative processes such as parthanatos.
+PARP1	drug	cocaine	21925237	This postmortem human brain study examined the status of canonical apoptotic pathways, signaling partners, and the cleavage of poly(ADP ribose) polymerase 1 (<strong>PARP</strong> 1), a sensor of DNA damage, in prefrontal cortex (PFC) of a small but well characterized cohort of <b>cocaine</b> abusers (n=10).
+PARP1	drug	cocaine	21925237	In the same brain samples of <b>cocaine</b> abusers, the proteolytic cleavage of <strong>PARP</strong> 1 was increased (+39%).
+PARP1	drug	cocaine	21925237	Chronic exposure to <b>cocaine</b> in rats, including withdrawal for 3 days, did not alter Fas FADD receptor complex, cytochrome c, caspase 3/fragments, AIF, <strong>PARP</strong> 1 cleavage, and associated signaling in the cerebral cortex.
+PARP1	addiction	withdrawal	21925237	Chronic exposure to cocaine in rats, including <b>withdrawal</b> for 3 days, did not alter Fas FADD receptor complex, cytochrome c, caspase 3/fragments, AIF, <strong>PARP</strong> 1 cleavage, and associated signaling in the cerebral cortex.
+PARP1	drug	alcohol	21803053	After 4h, a single dose of <b>ethanol</b> induced upregulation of Bax, release of mitochondrial cytochrome c into the cytosol, activation of caspase 3 and cleavage of poly (ADP ribose) polymerase (<strong>PARP</strong> 1), all of which promote apoptosis.
+PARP1	drug	opioid	19447888	In this study, our data suggest that <strong>PARP</strong> 1 positively regulates MOR gene transcription via G( 172)   > T, which might influence individual specificity in therapeutic <b>opioid</b> effects.
+PARP1	drug	amphetamine	16210775	Pretreatment with NMDA receptor antagonists, such as MK 801 and 3 ((R) 2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (CPP), and benzamide [poly(ADP ribose) polymerase (<strong>PARP</strong>) inhibitor] significantly attenuated the increased lethality induced by <b>methamphetamine</b> and morphine.
+PARP1	drug	opioid	16210775	Pretreatment with NMDA receptor antagonists, such as MK 801 and 3 ((R) 2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (CPP), and benzamide [poly(ADP ribose) polymerase (<strong>PARP</strong>) inhibitor] significantly attenuated the increased lethality induced by methamphetamine and <b>morphine</b>.
+PARP1	addiction	reward	16210775	Pretreatment with NMDA receptor antagonists, such as MK 801 and 3 ((R) 2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (<b>CPP</b>), and benzamide [poly(ADP ribose) polymerase (<strong>PARP</strong>) inhibitor] significantly attenuated the increased lethality induced by methamphetamine and morphine.
+PARP1	drug	amphetamine	16210775	These results suggest that activation of NMDA receptors and <strong>PARP</strong> play an important role in the increased lethality induced by <b>methamphetamine</b> and morphine.
+PARP1	drug	opioid	16210775	These results suggest that activation of NMDA receptors and <strong>PARP</strong> play an important role in the increased lethality induced by methamphetamine and <b>morphine</b>.
+PARP1	drug	amphetamine	15113847	The oxidative stress induced by <b>METH</b> putatively activates nuclear enzyme poly(ADP ribose) polymerase (<strong>PARP</strong>), with excessive <strong>PARP</strong> activation eventually leading to cell death.
+PARP1	drug	amphetamine	15113847	In this study, we show that prevention of <strong>PARP</strong> activation by treatment with FR261529 [2 (4 chlorophenyl) 5 quinoxalinecarboxamide], the compound that was recently identified as a novel <strong>PARP</strong> inhibitor (IC50 for <strong>PARP</strong> 1 = 33 nM, IC50 for <strong>PARP</strong> 2 = 7 nM), protects against both ROS induced cells injury in vitro and <b>METH</b> induced dopaminergic neuronal damage in an in vivo Parkinson's disease (PD) model.
+PARP1	drug	amphetamine	15113847	In PC12 cells, exposure of hydrogen peroxide or <b>METH</b> markedly induced <strong>PARP</strong> activation, and treatment with FR261529 (1 microM) significantly reduced <strong>PARP</strong> activation and attenuated cell death.
+PARP1	drug	amphetamine	15113847	These findings indicate that the neuroprotective effects of a novel <strong>PARP</strong> inhibitor, FR261529, were accompanied by inhibition of <b>METH</b> induced <strong>PARP</strong> activation, suggesting that <b>METH</b> induces nigrostriatal dopaminergic neurodegeneration involving <strong>PARP</strong> activation and also orally active and brain penetrable <strong>PARP</strong> inhibitor FR261529 could be a novel attractive therapeutic candidate for neurodegenerative disorders such as PD.
+NTRK1	drug	alcohol	30779268	Adolescent intermittent <b>ethanol</b> caused a persistent increase in adult H3K9me2 and DNA methylation at promoter regions of Chat and H3K9me2 of <strong>Trka</strong>, which was restored by wheel running.
+NTRK1	drug	alcohol	30779268	Adolescent intermittent <b>ethanol</b> caused a persistent increase in adult H3K9me2 and DNA methylation at promoter regions of Chat and H3K9me2 of <strong><strong>Trka</strong></strong>, which was restored by wheel running.
+NTRK1	drug	alcohol	29753117	We found that <b>ethanol</b> treatment of neuroblastoma cells increased phosphorylation of anaplastic lymphoma kinase (ALK) and <strong>TrkA</strong>, known substrates of RPTPβ/ζ.
+NTRK1	drug	alcohol	29753117	We found that <b>ethanol</b> treatment of neuroblastoma cells increased phosphorylation of anaplastic lymphoma kinase (ALK) and <strong><strong>TrkA</strong></strong>, known substrates of RPTPβ/ζ.
+NTRK1	drug	alcohol	29753117	These results demonstrate for the first time that <b>ethanol</b> engages <strong>TrkA</strong> signaling and that RPTPβ/ζ modulates signaling pathways activated by <b>alcohol</b> and behavioral responses to this drug.
+NTRK1	drug	alcohol	29753117	These results demonstrate for the first time that <b>ethanol</b> engages <strong><strong>TrkA</strong></strong> signaling and that RPTPβ/ζ modulates signaling pathways activated by <b>alcohol</b> and behavioral responses to this drug.
+NTRK1	drug	amphetamine	29165617	Selective Activation of Striatal NGF <strong>TrkA</strong>/p75NTR/MAPK Intracellular Signaling in Rats That Show Suppression of <b>Methamphetamine</b> Intake 30 Days following Drug Abstinence.
+NTRK1	drug	amphetamine	29165617	Selective Activation of Striatal NGF <strong><strong>TrkA</strong></strong>/p75NTR/MAPK Intracellular Signaling in Rats That Show Suppression of <b>Methamphetamine</b> Intake 30 Days following Drug Abstinence.
+NTRK1	drug	amphetamine	29165617	These findings support the notion that animals with distinct phenotypes for <b>methamphetamine</b> intake in the presence of adverse consequences also display differential changes in an intracellular signaling cascade activated by nerve growth factor <strong>TrkA</strong>/p75NTR interactions.
+NTRK1	drug	amphetamine	29165617	These findings support the notion that animals with distinct phenotypes for <b>methamphetamine</b> intake in the presence of adverse consequences also display differential changes in an intracellular signaling cascade activated by nerve growth factor <strong><strong>TrkA</strong></strong>/p75NTR interactions.
+NTRK1	drug	cocaine	26538265	Results suggested that the BDNF <strong>TrkA</strong>/p75(NTR) ILK Akt signaling pathway may be active in <b>cocaine</b> sensitization and associated neural plasticity in the mPFC and NAc core.
+NTRK1	addiction	sensitization	26538265	Results suggested that the BDNF <strong>TrkA</strong>/p75(NTR) ILK Akt signaling pathway may be active in cocaine <b>sensitization</b> and associated neural plasticity in the mPFC and NAc core.
+NTRK1	drug	cocaine	26538265	Results suggested that the BDNF <strong><strong>TrkA</strong></strong>/p75(NTR) ILK Akt signaling pathway may be active in <b>cocaine</b> sensitization and associated neural plasticity in the mPFC and NAc core.
+NTRK1	addiction	sensitization	26538265	Results suggested that the BDNF <strong><strong>TrkA</strong></strong>/p75(NTR) ILK Akt signaling pathway may be active in cocaine <b>sensitization</b> and associated neural plasticity in the mPFC and NAc core.
+NTRK1	drug	alcohol	24061482	Our primary interest is the examination of how regions that receive BF cholinergic projections are influenced by short term <b>ethanol</b> exposure through alterations in the mRNA levels of neurotrophic factors [nerve growth factor/<strong>TrkA</strong>, brain derived neurotrophic factor/TrkB, and glial derived neurotrophic factor (GDNF)/GDNF family receptor α1].
+NTRK1	drug	alcohol	24061482	Our primary interest is the examination of how regions that receive BF cholinergic projections are influenced by short term <b>ethanol</b> exposure through alterations in the mRNA levels of neurotrophic factors [nerve growth factor/<strong><strong>TrkA</strong></strong>, brain derived neurotrophic factor/TrkB, and glial derived neurotrophic factor (GDNF)/GDNF family receptor α1].
+NTRK1	drug	cocaine	22832183	Intra ventricular infusion with K252a, a mixed <strong>TrkA</strong> and TrkB antagonist, did not affect the protective effects of companions on local NGF, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and <b>cocaine</b> induced CPP.
+NTRK1	addiction	reward	22832183	Intra ventricular infusion with K252a, a mixed <strong>TrkA</strong> and TrkB antagonist, did not affect the protective effects of companions on local NGF, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and cocaine induced <b>CPP</b>.
+NTRK1	drug	cocaine	22832183	Intra ventricular infusion with K252a, a mixed <strong><strong>TrkA</strong></strong> and TrkB antagonist, did not affect the protective effects of companions on local NGF, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and <b>cocaine</b> induced CPP.
+NTRK1	addiction	reward	22832183	Intra ventricular infusion with K252a, a mixed <strong><strong>TrkA</strong></strong> and TrkB antagonist, did not affect the protective effects of companions on local NGF, BDNF levels in DG, but abolished the companions' protective effects against the stressor decreased DG neurogenesis and cocaine induced <b>CPP</b>.
+NTRK1	drug	alcohol	22497026	Functional nerve growth factor and <strong>trkA</strong> autocrine/paracrine circuits in adult rat cortex are revealed by episodic <b>ethanol</b> exposure and withdrawal.
+NTRK1	addiction	withdrawal	22497026	Functional nerve growth factor and <strong>trkA</strong> autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and <b>withdrawal</b>.
+NTRK1	drug	alcohol	22497026	Functional nerve growth factor and <strong><strong>trkA</strong></strong> autocrine/paracrine circuits in adult rat cortex are revealed by episodic <b>ethanol</b> exposure and withdrawal.
+NTRK1	addiction	withdrawal	22497026	Functional nerve growth factor and <strong><strong>trkA</strong></strong> autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and <b>withdrawal</b>.
+NTRK1	drug	amphetamine	21704677	The data clearly suggest that endogenous MK limits <b>amphetamine</b> induced astrocytosis through Fyn , <strong>TrkA</strong>  and ERK1/2 independent mechanisms and identify previously unexpected functional differences between MK and pleiotrophin, the only other member of the MK family of growth factors, in the modulation of effects of drugs of abuse.
+NTRK1	drug	amphetamine	21704677	The data clearly suggest that endogenous MK limits <b>amphetamine</b> induced astrocytosis through Fyn , <strong><strong>TrkA</strong></strong>  and ERK1/2 independent mechanisms and identify previously unexpected functional differences between MK and pleiotrophin, the only other member of the MK family of growth factors, in the modulation of effects of drugs of abuse.
+NTRK1	drug	alcohol	19861148	We found that exposure to <b>ethanol</b> resulted in elevated levels of nerve growth factor (NGF) and <strong>TrkA</strong> mRNA expression but a decreased level of brain derived neurotrophic factor (BDNF) mRNA expression.
+NTRK1	drug	alcohol	19861148	We found that exposure to <b>ethanol</b> resulted in elevated levels of nerve growth factor (NGF) and <strong><strong>TrkA</strong></strong> mRNA expression but a decreased level of brain derived neurotrophic factor (BDNF) mRNA expression.
+NTRK1	drug	psychedelics	19579000	From the respective receptors, only <strong>TrkA</strong> was enhanced when <b>ketamine</b> withdrawal was combined with risperidone or haloperidol.
+NTRK1	addiction	withdrawal	19579000	From the respective receptors, only <strong>TrkA</strong> was enhanced when ketamine <b>withdrawal</b> was combined with risperidone or haloperidol.
+NTRK1	drug	psychedelics	19579000	From the respective receptors, only <strong><strong>TrkA</strong></strong> was enhanced when <b>ketamine</b> withdrawal was combined with risperidone or haloperidol.
+NTRK1	addiction	withdrawal	19579000	From the respective receptors, only <strong><strong>TrkA</strong></strong> was enhanced when ketamine <b>withdrawal</b> was combined with risperidone or haloperidol.
+NTRK1	addiction	sensitization	17693023	As the anti NGF antibody does not appreciably cross the blood brain barrier, the present data suggest that the anti hyperalgesic action of anti NGF therapy results from blockade of activation and/or <b>sensitization</b> of the CGRP/<strong>trkA</strong> positive fibers that normally constitute the majority of sensory fibers that innervate the bone.
+NTRK1	addiction	sensitization	17693023	As the anti NGF antibody does not appreciably cross the blood brain barrier, the present data suggest that the anti hyperalgesic action of anti NGF therapy results from blockade of activation and/or <b>sensitization</b> of the CGRP/<strong><strong>trkA</strong></strong> positive fibers that normally constitute the majority of sensory fibers that innervate the bone.
+NTRK1	drug	alcohol	17316397	Functional nerve growth factor and <strong>trkA</strong> autocrine/paracrine circuits in adult rat cortex are revealed by episodic <b>ethanol</b> exposure and withdrawal.
+NTRK1	addiction	withdrawal	17316397	Functional nerve growth factor and <strong>trkA</strong> autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and <b>withdrawal</b>.
+NTRK1	drug	alcohol	17316397	Functional nerve growth factor and <strong><strong>trkA</strong></strong> autocrine/paracrine circuits in adult rat cortex are revealed by episodic <b>ethanol</b> exposure and withdrawal.
+NTRK1	addiction	withdrawal	17316397	Functional nerve growth factor and <strong><strong>trkA</strong></strong> autocrine/paracrine circuits in adult rat cortex are revealed by episodic ethanol exposure and <b>withdrawal</b>.
+NTRK1	addiction	sensitization	15836976	Mechanistically, the great majority of sensory fibers that innervate the bone are CGRP/<strong>TrkA</strong> expressing fibers, and if the <b>sensitization</b> and activation of these fibers is blocked by anti NGF therapy there would not be another population of nociceptors, such as the non peptidergic IB4/RET IR nerve fibers, to take their place in signaling nociceptive events.
+NTRK1	addiction	sensitization	15836976	Mechanistically, the great majority of sensory fibers that innervate the bone are CGRP/<strong><strong>TrkA</strong></strong> expressing fibers, and if the <b>sensitization</b> and activation of these fibers is blocked by anti NGF therapy there would not be another population of nociceptors, such as the non peptidergic IB4/RET IR nerve fibers, to take their place in signaling nociceptive events.
+MYH14	drug	psychedelics	32685891	<strong>Myosin</strong> activated coagulation seems a potential cause of <b>MDMA</b> related coagulopathy in the setting of rhabdomyolysis and serotonin syndrome.
+MYH14	drug	amphetamine	32066582	<b>Methamphetamine</b> learning induces persistent and selective nonmuscle <strong>myosin</strong> II dependent spine motility in the basolateral amygdala.
+MYH14	drug	amphetamine	32066582	Nonmuscle <strong>myosin</strong> II inhibition (NMIIi) in the basolateral amygdala (BLA), but not dorsal hippocampus (CA1), selectively disrupts memories associated with <b>methamphetamine</b> (<b>METH</b>) days after learning, without retrieval.
+MYH14	drug	amphetamine	32066582	We employed time lapse two photon imaging of dendritic spine motility in acutely prepared brain slices from female and male mice following <b>METH</b> associated learning as a readout of actin <strong>myosin</strong> dynamics.
+MYH14	drug	cocaine	31596232	The release of EVs occurs when <b>cocaine</b> causes dissociation of the Sig 1R from ADP ribosylation factor (ARF6), a G protein regulating EV trafficking, leading to activation of <strong>myosin</strong> light chain kinase (MLCK).
+MYH14	drug	alcohol	31411733	While <b>alcohol</b> did not alter the content of high energy phosphates or oxidative phosphorylation complexes I V, it did reduce <strong>myosin</strong> heavy chain and troponin T content.
+MYH14	drug	amphetamine	30115760	Using pharmacologic and genetic approaches targeting actin or the actin driving molecular motor, nonmuscle <strong>myosin</strong> II (NMII), we previously discovered an immediate, retrieval independent, and long lasting disruption of <b>methamphetamine</b>  (<b>METH</b> ) and <b>amphetamine</b> associated memories.
+MYH14	drug	psychedelics	28890736	Treatment of the larvae with 25B <b>NBOMe</b> decreased their survival rate, locomotion, altered birefringence of the skeletal muscle and immunostainings for dystroglycan (a myoseptal protein) and <strong>myosin</strong> heavy chain (a myofibril protein), which were consistent with rhabdomyolysis.
+MYH14	drug	amphetamine	28082169	Nonmuscle <strong>myosin</strong> II inhibition disrupts <b>methamphetamine</b> associated memory in females and adolescents.
+MYH14	drug	alcohol	26859989	It has been shown that chronic <b>alcoholic</b> myopathy develops after 10 years of <b>alcohol</b> abuse; proximal paresis is observed only in patients with atrophy of muscle fibers, thus there is a transformation of <strong>myosin</strong> phenotype from slow to fast.
+MYH14	drug	amphetamine	26239291	Nonmuscle <strong>myosin</strong> IIB as a therapeutic target for the prevention of relapse to <b>methamphetamine</b> use.
+MYH14	addiction	relapse	26239291	Nonmuscle <strong>myosin</strong> IIB as a therapeutic target for the prevention of <b>relapse</b> to methamphetamine use.
+MYH14	addiction	relapse	26239291	A single intra BLC treatment with Blebbistatin (Blebb), a small molecule inhibitor of class II <strong>myosin</strong> isoforms, including NMIIB, produced a long lasting disruption of context induced drug <b>seeking</b> (at least 30 days).
+MYH14	addiction	relapse	26022262	Similar to an actin depolymerizing compound, pre test inhibition of <strong>myosin</strong> II ATPase activity in the AMY produced a rapid and lasting disruption of drug <b>seeking</b> behavior.
+MYH14	addiction	relapse	26022262	While many questions remain, these findings indicate that <strong>myosin</strong> II represents a potential therapeutic avenue to target the actin cytoskeleton and disrupt the powerful, extinction resistant memories capable of triggering <b>relapse</b>.
+MYH14	drug	alcohol	25257290	Pharmacologic agents were used to test the roles of <b>alcohol</b> metabolism, oxidative stress, p38 mitogen activated protein kinase (MAPK), <strong>myosin</strong> light chain kinase (MLCK), rho kinase (ROCK), and exchange protein activated by cAMP (Epac).
+MYH14	drug	amphetamine	24012327	Conditioned place preference (n = 112) and context induced reinstatement of self administration (n = 19) were used to assess the role of F actin polymerization and <strong>myosin</strong> II, a molecular motor that drives memory promoting dendritic spine actin polymerization, in the maintenance of <b>METH</b> associated memories and related structural plasticity.
+MYH14	addiction	relapse	24012327	Conditioned place preference (n = 112) and context induced <b>reinstatement</b> of self administration (n = 19) were used to assess the role of F actin polymerization and <strong>myosin</strong> II, a molecular motor that drives memory promoting dendritic spine actin polymerization, in the maintenance of METH associated memories and related structural plasticity.
+MYH14	drug	amphetamine	24012327	Inhibition of non muscle <strong>myosin</strong> II also resulted in a disruption of <b>METH</b> associated memory.
+MYH14	drug	alcohol	23376955	As this combined insult causes elevated intestinal morphological damage, tight junction protein localization alterations, and phosphorylated <strong>myosin</strong> light chain levels, we sought to determine the role of IL 6 in these intestinal responses using a model of binge <b>ethanol</b> exposure and burn injury.
+MYH14	addiction	intoxication	23376955	As this combined insult causes elevated intestinal morphological damage, tight junction protein localization alterations, and phosphorylated <strong>myosin</strong> light chain levels, we sought to determine the role of IL 6 in these intestinal responses using a model of <b>binge</b> ethanol exposure and burn injury.
+MYH14	drug	alcohol	22790598	Inhibition of long <strong>myosin</strong> light chain kinase activation alleviates intestinal damage after binge <b>ethanol</b> exposure and burn injury.
+MYH14	addiction	intoxication	22790598	Inhibition of long <strong>myosin</strong> light chain kinase activation alleviates intestinal damage after <b>binge</b> ethanol exposure and burn injury.
+MYH14	drug	alcohol	22790598	Knowing that long <strong>myosin</strong> light chain kinase (MLCK) is important for epithelial barrier maintenance and can be activated by proinflammatory cytokines, we examined whether inhibition of MLCK alleviated detrimental intestinal responses seen after <b>ethanol</b> exposure and burn injury.
+MYH14	drug	amphetamine	20139112	Treatment with <b>methamphetamine</b> also resulted in the tyrosine nitration of myofilament (desmin, <strong>myosin</strong> light chain) and mitochondrial (ATP synthase, NADH dehydrogenase, cytochrome c oxidase, prohibitin) proteins.
+MYH14	addiction	dependence	19805075	The <b>dependence</b> of TMV, PVX, and TBSV on intact microfilaments for intercellular movement led us to investigate the role of <strong>myosin</strong> motors in this process.
+MYH14	addiction	sensitization	16472257	Sustained smooth muscle contraction or its experimental counterpart, Ca2+ <b>sensitization</b>, by G(q/13) coupled receptor agonists is mediated via RhoA dependent inhibition of MLC (<strong>myosin</strong> light chain) phosphatase and MLC20 (20 kDa regulatory light chain of <strong>myosin</strong> II) phosphorylation by a Ca2+ independent MLCK (MLC kinase).
+MYH14	drug	alcohol	15976526	<b>Ethanol</b> induced activation of <strong>myosin</strong> light chain kinase leads to dysfunction of tight junctions and blood brain barrier compromise.
+MYH14	drug	alcohol	15690316	The cellular content of actin and alpha  <strong>myosin</strong> heavy chain isoform was significantly reduced and there was an increase in the beta  <strong>myosin</strong> heavy chain isoform after feeding rats a diet containing <b>alcohol</b>.
+MYH14	drug	alcohol	15690316	These results suggest that (1) the reduced protein content observed in the heart after feeding a diet containing <b>alcohol</b> is a consequence of reduced synthesis of both myofibrillar and sarcoplasmic proteins, and (2) the expression of both actin and alpha <strong>myosin</strong> heavy chain isoform is affected independently of the messenger RNA content of the proteins.
+MYH14	drug	alcohol	11226116	Although <b>ethanol</b> did not affect regulatory <strong>myosin</strong> light chain (rMLC) phosphorylation during stimulation with Ca(2+) alone, it decreased rMLC phosphorylation by Ca(2+) during muscarinic receptor stimulation.
+MYH14	drug	alcohol	1591620	Electrophoretic analysis or these <b>ethanol</b> exposed fibroblast and myocyte cultures revealed specific reduction in the cellular contents of alpha actinin, <strong>myosin</strong>, and actin.
+MPO	drug	nicotine	30358437	Lung <strong>myeloperoxidase</strong> mRNA and protein increased in the <b>nicotine</b> exposed rats.
+MPO	drug	alcohol	30030149	Moreover, indicators of NET formation including citrullinated histone H3, neutrophil elastase, and neutrophil <strong>myeloperoxidase</strong> were decreased at an early time point after LPS challenge in mice receiving binge <b>alcohol</b>, suggesting decreased NET formation.
+MPO	addiction	intoxication	30030149	Moreover, indicators of NET formation including citrullinated histone H3, neutrophil elastase, and neutrophil <strong>myeloperoxidase</strong> were decreased at an early time point after LPS challenge in mice receiving <b>binge</b> alcohol, suggesting decreased NET formation.
+MPO	drug	opioid	28595532	The harmane β carboline alkaloid has shown several pharmacological activities such as antianxiety, antidepressant, antiplatelet, antidiabetic, acetylcholinesterase and <strong>myeloperoxidase</strong> inhibition, antioxidant, antiparasitic, hypotensive, <b>morphine</b> withdrawal syndrome alleviation, and antinociceptive effects.
+MPO	addiction	withdrawal	28595532	The harmane β carboline alkaloid has shown several pharmacological activities such as antianxiety, antidepressant, antiplatelet, antidiabetic, acetylcholinesterase and <strong>myeloperoxidase</strong> inhibition, antioxidant, antiparasitic, hypotensive, morphine <b>withdrawal</b> syndrome alleviation, and antinociceptive effects.
+MPO	drug	nicotine	28427334	Estimates of daily <b>smoking</b> rates for the mobile phone only (<strong>MPO</strong>) population have been found to be substantially higher than the rest of the population and telephone surveys that use a dual sampling frame (landline and mobile phones) are now considered best practice.
+MPO	drug	nicotine	28427334	Both the PHS and NDSHS gave the same estimates for daily <b>smoking</b> (12%) and similar estimates for <strong>MPO</strong> users (20% and 18% respectively).
+MPO	drug	nicotine	28427334	Pooled data showed that daily <b>smoking</b> was 19% for <strong>MPO</strong> users, compared to 10% for dual phone owners, and 12% for landline phone only users.
+MPO	drug	alcohol	28350851	We found that bacterial load suppression prevented <b>alcohol</b> related increases in the number of myeloperoxidase  (<strong>MPO</strong>) positive infiltrating neutrophils in the liver.
+MPO	drug	alcohol	28350851	We found that bacterial load suppression prevented <b>alcohol</b> related increases in the number of <strong>myeloperoxidase</strong>  (<strong>MPO</strong>) positive infiltrating neutrophils in the liver.
+MPO	drug	opioid	28214183	Occasionally, this may also lead to misuse of prescription <b>opioids</b> (<strong>MPO</strong>).
+MPO	addiction	addiction	28214183	<strong>MPO</strong> preferentially occurs in vulnerable individuals, i.e., those with a young age, history of other <b>addictive</b> or psychiatric disorders, especially anxious and depressive disorders.
+MPO	drug	opioid	28214183	Prevention of <strong>MPO</strong> begins before the <b>opioid</b> prescription, with the identification of potential vulnerability factors.
+MPO	addiction	addiction	28214183	Patients with suspected <strong>MPO</strong> should be referred early to pain or <b>addiction</b> centers.
+MPO	drug	opioid	28214183	The treatment of <strong>MPO</strong> should be based on multidisciplinary strategies, involving both the addiction and pain aspects: progressive <b>opioid</b> withdrawal, non pharmacological measures against pain, or switching to medication assisted treatment of addiction (i.e., <b>buprenorphine</b> or <b>methadone</b>).
+MPO	addiction	addiction	28214183	The treatment of <strong>MPO</strong> should be based on multidisciplinary strategies, involving both the <b>addiction</b> and pain aspects: progressive opioid withdrawal, non pharmacological measures against pain, or switching to medication assisted treatment of <b>addiction</b> (i.e., buprenorphine or methadone).
+MPO	addiction	withdrawal	28214183	The treatment of <strong>MPO</strong> should be based on multidisciplinary strategies, involving both the addiction and pain aspects: progressive opioid <b>withdrawal</b>, non pharmacological measures against pain, or switching to medication assisted treatment of addiction (i.e., buprenorphine or methadone).
+MPO	drug	nicotine	27613897	Chronic <b>nicotine</b> administration or its withdrawal reduced lipid peroxidation and <strong>MPO</strong> activity and prevented GSH depletion with some varying results in different target tissues.
+MPO	addiction	withdrawal	27613897	Chronic nicotine administration or its <b>withdrawal</b> reduced lipid peroxidation and <strong>MPO</strong> activity and prevented GSH depletion with some varying results in different target tissues.
+MPO	drug	nicotine	27613897	<b>Nicotine</b> injection prior to sepsis depressed <strong>MPO</strong> activity in all tissues and reduced MDA levels except for the lung, while GSH levels were elevated only in the hepatic and ileal tissues.
+MPO	drug	nicotine	27613897	When <b>nicotine</b> was withdrawn for 5 days, its inhibitory effect on <strong>MPO</strong> activity was still present in all the tissues except for the liver.
+MPO	drug	opioid	27435374	on nociception (thermal hyperalgesia, mechanical allodynia and arthritis score), inflammation (edema, <strong>myeloperoxidase</strong> activity), immobility (forced swimming test), locomotor activity (open field), gastrointestinal transit, hyperalgesia and <b>naloxone</b> precipitated <b>morphine</b> withdrawal syndrome was evaluated.
+MPO	addiction	withdrawal	27435374	on nociception (thermal hyperalgesia, mechanical allodynia and arthritis score), inflammation (edema, <strong>myeloperoxidase</strong> activity), immobility (forced swimming test), locomotor activity (open field), gastrointestinal transit, hyperalgesia and naloxone precipitated morphine <b>withdrawal</b> syndrome was evaluated.
+MPO	addiction	relapse	26311010	Importantly, at time of the <b>relapse</b>, the patient became positive for both <strong>myeloperoxidase</strong> antineutrophil cytoplasmic antibody (ANCA) and proteinase 3 ANCA.
+MPO	drug	opioid	24721689	Therefore, we investigated nociceptive sensitization, immune cell infiltration, myeloperoxidase (<strong>MPO</strong>) activity, and expression of multiple cytokines and <b>opioid</b> peptides in damaged nerves of wild type (IL 17(+/+)) and IL 17 knock out (IL 17( / )) mice after partial sciatic nerve ligation.
+MPO	addiction	sensitization	24721689	Therefore, we investigated nociceptive <b>sensitization</b>, immune cell infiltration, myeloperoxidase (<strong>MPO</strong>) activity, and expression of multiple cytokines and opioid peptides in damaged nerves of wild type (IL 17(+/+)) and IL 17 knock out (IL 17( / )) mice after partial sciatic nerve ligation.
+MPO	drug	opioid	24721689	Therefore, we investigated nociceptive sensitization, immune cell infiltration, <strong>myeloperoxidase</strong> (<strong>MPO</strong>) activity, and expression of multiple cytokines and <b>opioid</b> peptides in damaged nerves of wild type (IL 17(+/+)) and IL 17 knock out (IL 17( / )) mice after partial sciatic nerve ligation.
+MPO	addiction	sensitization	24721689	Therefore, we investigated nociceptive <b>sensitization</b>, immune cell infiltration, <strong>myeloperoxidase</strong> (<strong>MPO</strong>) activity, and expression of multiple cytokines and opioid peptides in damaged nerves of wild type (IL 17(+/+)) and IL 17 knock out (IL 17( / )) mice after partial sciatic nerve ligation.
+MPO	drug	nicotine	24287136	Biosynthesis of <b>nicotine</b> in <b>tobacco</b> requires N methylputrescine oxidase (<strong>MPO</strong>), which belongs to the copper containing amine oxidase superfamily.
+MPO	drug	opioid	23831400	Variables measured included myeloperoxidase (<strong>MPO</strong>) activity, several inflammatory cell infiltration profiles, cytokines, and endogenous <b>opioid</b> peptide expression in damaged nerves.
+MPO	drug	opioid	23831400	Variables measured included <strong>myeloperoxidase</strong> (<strong>MPO</strong>) activity, several inflammatory cell infiltration profiles, cytokines, and endogenous <b>opioid</b> peptide expression in damaged nerves.
+MPO	drug	alcohol	22654445	In TNBS 25% <b>ethanol</b> treated group, the pathological score and <strong>MPO</strong> activity were significantly lowered compared to that of the TNBS 50% <b>ethanol</b> treated group, while AWR threshold pressure were significantly elevated (36.33 ± 0.61 mmHg vs 23.33 ± 1.33 mmHg, P < 0.05); and (4) TNBS (5 mg/0.8 mL per rat, in 50% <b>ethanol</b>, 8 cm from anus) treated rats recovered completely from the inflammation with acquired visceral hyperalgesia and EC cell hyperplasia at 4 wk after TNBS administration.
+MPO	drug	nicotine	21802933	Higher sputum % eosinophils, higher sputum <strong>MPO</strong>/neutrophil level, longer duration of COPD symptoms, <40 packyears <b>smoking</b>, and ICS withdrawal in November, December or January were significant hazards (all p<0.05) for experiencing a COPD exacerbation after ICS withdrawal in a monovariate model.
+MPO	addiction	withdrawal	21802933	Higher sputum % eosinophils, higher sputum <strong>MPO</strong>/neutrophil level, longer duration of COPD symptoms, <40 packyears smoking, and ICS <b>withdrawal</b> in November, December or January were significant hazards (all p<0.05) for experiencing a COPD exacerbation after ICS <b>withdrawal</b> in a monovariate model.
+MPO	drug	alcohol	20624996	Lack of MyD88 or <strong>MPO</strong> did not significantly alter survival in the presence or absence of <b>ethanol</b>.
+MPO	drug	opioid	20600830	<b>Morphine</b> decreased plasma NO (p<0.05 vs IR), serum creatinine and BUN (p<0.01), FE(Na), <strong>MPO</strong> activity, MDA level, iNOS expression, and tissue damage (p<0.05), but increased creatinine clearance (p<0.05).
+MPO	drug	nicotine	21783940	Chronic administration of <b>nicotine</b> did not have a potentiating effect on acetic acid induced gastric ulcer, since the gastric injury, as assessed by both macroscopic and microscopic evaluation and increased gastric <strong>myeloperoxidase</strong> activity indicating neutrophil recruitment, was not exaggerated or attenuated by <b>nicotine</b> intake.
+MPO	drug	opioid	17908329	Separate analyses measuring myeloperoxidase (<strong>MPO</strong>) and using immunohistochemistry demonstrated that <b>morphine</b> dose dependently reduced the infiltration of neutrophils into the peri incisional tissue.
+MPO	drug	opioid	17908329	Separate analyses measuring <strong>myeloperoxidase</strong> (<strong>MPO</strong>) and using immunohistochemistry demonstrated that <b>morphine</b> dose dependently reduced the infiltration of neutrophils into the peri incisional tissue.
+MPO	drug	cocaine	17420087	The activity of tissue <strong>MPO</strong> was significantly increased in the <b>cocaine</b> group compared with control rats.
+MPO	addiction	intoxication	17220368	On day 1 after injury, lung tissue IL 18, neutrophil chemokines (CINC 1/CINC 3), ICAM 1, neutrophil infiltration, <strong>MPO</strong> activity, and water content (i.e., edema) were significantly increased in rats receiving a combined insult of EtOH and burn injury compared with rats receiving either EtOH <b>intoxication</b> or burn injury alone.
+MPO	drug	alcohol	16046875	In rats challenged with K. pneumoniae, <b>ethanol</b> pretreatment significantly reduced BALF levels of CINC and MIP 2, suppressed alveolar neutrophil recruitment, and decreased whole lung <strong>myeloperoxidase</strong> activity.
+MPO	drug	alcohol	16046875	Alternatively, IT chemokine instillation partially restored BALF neutrophil recruitment but not whole lung <strong>myeloperoxidase</strong> activity in <b>ethanol</b> treated rats.
+MPO	drug	alcohol	9835289	Despite an increased bacterial burden in both the lung and liver at 24 hr after initiating E. coli infection in <b>alcohol</b> intoxicated animals, PMN tissue recruitment, indexed as <strong>myeloperoxidase</strong> activity, did not differ between control and <b>alcohol</b> treated rats.
+MAP2	drug	alcohol	30208635	Protein levels of histone deacetylase 6 (HDAC6), and the microtubule associated proteins <strong>MAP 2</strong> and MAP tau were reduced in <b>alcoholic</b> cohorts, although for MAPs this was not significant.
+MAP2	drug	opioid	29154860	The present study explored the effects of Cav 1 on the expression levels of 2 markers of neurite outgrowth, growth association protein 43 (GAP 43) and microtubule associated protein 2 (<strong>MAP 2</strong>), during the process of <b>morphine</b> induced changes in the structural plasticity.
+MAP2	drug	opioid	29154860	The present study explored the effects of Cav 1 on the expression levels of 2 markers of neurite outgrowth, growth association protein 43 (GAP 43) and <strong>microtubule associated protein 2</strong> (<strong>MAP 2</strong>), during the process of <b>morphine</b> induced changes in the structural plasticity.
+MAP2	drug	opioid	29154860	The results showed that <b>morphine</b> at a concentration of 10.0μmol/L had no adverse effect on neuronal viability, but enhanced the Cav 1 and GAP 43 levels and induced the outgrowth of <strong>MAP 2</strong> labeled neurites.
+MAP2	drug	opioid	29154860	Moreover, Cav 1 knockdown inhibited the <b>morphine</b> induced upregulation of GAP 43 expression and the prolongation of <strong>MAP 2</strong> labeled neurites.
+MAP2	drug	opioid	29154860	Inhibition of Cav 1 expression reduced the <b>morphine</b> induced increase in the neuronal growth markers GAP 43 and <strong>MAP 2</strong>.
+MAP2	drug	amphetamine	28089854	Effects of adolescent <b>methamphetamine</b> and nicotine exposure on behavioral performance and <strong>MAP 2</strong> immunoreactivity in the nucleus accumbens of adolescent mice.
+MAP2	drug	nicotine	28089854	Effects of adolescent methamphetamine and <b>nicotine</b> exposure on behavioral performance and <strong>MAP 2</strong> immunoreactivity in the nucleus accumbens of adolescent mice.
+MAP2	drug	amphetamine	27098516	Using logistic regression models, we analyzed associations of <b>Meth</b> with cerebral gliosis (immunohistochemistry for ionized calcium binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) in frontal, temporo parietal, and putamen internal capsule regions), synaptodendritic loss (confocal microscopy for synaptophysin (SYP) and microtubule associated protein 2 (<strong>MAP2</strong>) in frontal cortex), β amyloid plaque deposition (immunohistochemistry in frontal and temporo parietal cortex and putamen), and arteriolosclerosis (histopathology in forebrain white matter).
+MAP2	drug	amphetamine	27098516	Using logistic regression models, we analyzed associations of <b>Meth</b> with cerebral gliosis (immunohistochemistry for ionized calcium binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) in frontal, temporo parietal, and putamen internal capsule regions), synaptodendritic loss (confocal microscopy for synaptophysin (SYP) and <strong>microtubule associated protein 2</strong> (<strong>MAP2</strong>) in frontal cortex), β amyloid plaque deposition (immunohistochemistry in frontal and temporo parietal cortex and putamen), and arteriolosclerosis (histopathology in forebrain white matter).
+MAP2	drug	amphetamine	27098516	There was no significant association of <b>Meth</b> with GFAP gliosis, SYP or <strong>MAP2</strong> loss, β amyloid plaque deposition, or arteriolosclerosis.
+MAP2	drug	opioid	25988842	Alterations of the corticotropin releasing factor (CRF), glucocorticoid receptor (NR3C1), tyrosine hydroxylase (TH), mu <b>opioid</b> receptor (MOr), brain derived neurotrophic factor (BDNF), neuronal nuclei (NeuN), microtubule associated protein 2 (<strong>MAP2</strong>) and neurofilament heavy (NF200) immunoreactive fibers were studied in the paraventricular nucleus of the hypothalamus (PVN), ventral tegmental area (VTA), nucleus accumbens (NAc) or hippocampus (HIP).
+MAP2	drug	opioid	25988842	Alterations of the corticotropin releasing factor (CRF), glucocorticoid receptor (NR3C1), tyrosine hydroxylase (TH), mu <b>opioid</b> receptor (MOr), brain derived neurotrophic factor (BDNF), neuronal nuclei (NeuN), <strong>microtubule associated protein 2</strong> (<strong>MAP2</strong>) and neurofilament heavy (NF200) immunoreactive fibers were studied in the paraventricular nucleus of the hypothalamus (PVN), ventral tegmental area (VTA), nucleus accumbens (NAc) or hippocampus (HIP).
+MAP2	addiction	aversion	23796670	The lack of CB₂r impaired <b>aversive</b> memory consolidation, reduced <strong>MAP2</strong>, NF200 and SYN immunoreactive fibers and also reduced the number of synapses in DG of CB2KO mice.
+MAP2	drug	amphetamine	19663261	Furthermore, high concentration of <b>METH</b>, but not MPH, reduced <strong>MAP2a</strong>/b positive cells and activated the immunoreactivity of the cleaved caspase 3 in primary cultured limbic neurons, whereas MPH had no such effect.
+MAP2	drug	alcohol	15948156	Chronic <b>ethanol</b> exposure did not markedly alter rNP22 colocalization with F actin, alpha tubulin, or <strong>MAP2</strong>, although colocalization at the periphery of the neuronal soma with F actin was observed only after chronic <b>ethanol</b> exposure and withdrawal.
+MAP2	addiction	withdrawal	15948156	Chronic ethanol exposure did not markedly alter rNP22 colocalization with F actin, alpha tubulin, or <strong>MAP2</strong>, although colocalization at the periphery of the neuronal soma with F actin was observed only after chronic ethanol exposure and <b>withdrawal</b>.
+MAP2	addiction	withdrawal	15948156	Rat NP22 colocalization with <strong>MAP2</strong> was reduced during <b>withdrawal</b>, whereas association with alpha tubulin and actin was maintained.
+MAP2	drug	opioid	15183518	In the core, neuronal apoptotic inhibitory protein (NAIP), GABA A alpha1 subunit, GRIN2C, GRIA1, mGluR1, D4 dopamine receptor and PSD 95 were upregulated by <b>morphine</b> administration whereas bax, bcl x, cox 1 and <strong>MAP2</strong> were decreased.
+MAP2	drug	alcohol	9813323	Long term <b>alcohol</b> self administration and <b>alcohol</b> withdrawal differentially modulate microtubule associated protein 2 (<strong>MAP2</strong>) gene expression in the rat brain.
+MAP2	addiction	withdrawal	9813323	Long term alcohol self administration and alcohol <b>withdrawal</b> differentially modulate microtubule associated protein 2 (<strong>MAP2</strong>) gene expression in the rat brain.
+MAP2	drug	alcohol	9813323	Long term <b>alcohol</b> self administration and <b>alcohol</b> withdrawal differentially modulate <strong>microtubule associated protein 2</strong> (<strong>MAP2</strong>) gene expression in the rat brain.
+MAP2	addiction	withdrawal	9813323	Long term alcohol self administration and alcohol <b>withdrawal</b> differentially modulate <strong>microtubule associated protein 2</strong> (<strong>MAP2</strong>) gene expression in the rat brain.
+MAP2	drug	alcohol	9813323	Here we studied the expression of the neuronal cytoskeletal microtubule associated protein 2 (<strong>MAP2</strong>) following long term <b>alcohol</b> consumption and subsequent <b>alcohol</b> withdrawal.
+MAP2	addiction	withdrawal	9813323	Here we studied the expression of the neuronal cytoskeletal microtubule associated protein 2 (<strong>MAP2</strong>) following long term alcohol consumption and subsequent alcohol <b>withdrawal</b>.
+MAP2	drug	alcohol	9813323	Here we studied the expression of the neuronal cytoskeletal <strong>microtubule associated protein 2</strong> (<strong>MAP2</strong>) following long term <b>alcohol</b> consumption and subsequent <b>alcohol</b> withdrawal.
+MAP2	addiction	withdrawal	9813323	Here we studied the expression of the neuronal cytoskeletal <strong>microtubule associated protein 2</strong> (<strong>MAP2</strong>) following long term alcohol consumption and subsequent alcohol <b>withdrawal</b>.
+MAP2	drug	alcohol	9813323	Other areas such as the hippocampus, frontoparietal cortex and cerebellum were less affected by chronic <b>alcohol</b> intake, however, in these regions the <strong>MAP2</strong> mRNA levels were increased during <b>alcohol</b> withdrawal.
+MAP2	addiction	withdrawal	9813323	Other areas such as the hippocampus, frontoparietal cortex and cerebellum were less affected by chronic alcohol intake, however, in these regions the <strong>MAP2</strong> mRNA levels were increased during alcohol <b>withdrawal</b>.
+MAP2	drug	alcohol	2088116	Immunocytochemical studies using a monoclonal antibody against microtubule associated protein 2 (<strong>MAP2</strong>) indicated that cerebellar lobules containing Purkinje cells that are in the process of extending dendrites are ones that are more vulnerable to <b>alcohol</b> than lobules containing Purkinje cells that mature later.
+MAP2	drug	alcohol	2088116	Immunocytochemical studies using a monoclonal antibody against <strong>microtubule associated protein 2</strong> (<strong>MAP2</strong>) indicated that cerebellar lobules containing Purkinje cells that are in the process of extending dendrites are ones that are more vulnerable to <b>alcohol</b> than lobules containing Purkinje cells that mature later.
+HTR2B	drug	benzodiazepine	31196061	A hydroalcoholic, thujone free extract from freshly harvested Salvia officinalis leaves (A.Vogel Menosan®) was investigated in an acetylcholinesterase enzyme assay and several receptor binding assays (adrenergic alpha 2A, GABA (<b>benzodiazepine</b> site), GABAB; muscarinic M3, μ opioid, serotonin 5 HT1A, serotonin <strong>5 HT2B</strong>, serotonin 5 HT2C and serotonin transporter).
+HTR2B	drug	opioid	31196061	A hydroalcoholic, thujone free extract from freshly harvested Salvia officinalis leaves (A.Vogel Menosan®) was investigated in an acetylcholinesterase enzyme assay and several receptor binding assays (adrenergic alpha 2A, GABA (benzodiazepine site), GABAB; muscarinic M3, μ <b>opioid</b>, serotonin 5 HT1A, serotonin <strong>5 HT2B</strong>, serotonin 5 HT2C and serotonin transporter).
+HTR2B	drug	cocaine	30608182	A positive association between a polymorphism in the <strong>HTR2B</strong> gene and <b>cocaine</b> crack in a French Afro Caribbean population.
+HTR2B	drug	cocaine	28935766	To answer these questions, we investigated the contribution of <strong>5 HT2B</strong> receptors to <b>cocaine</b> dependent behavioral responses.
+HTR2B	drug	cocaine	28935766	Male mice permanently lacking <strong>5 HT2B</strong> receptors, even restricted to dopamine neurons, developed heightened <b>cocaine</b> induced locomotor responses.
+HTR2B	drug	cocaine	28935766	These data identify the <strong>5 HT2B</strong> receptor as a pharmacological intermediate and provide mechanistic insight into attenuated dopamine tone following exposure to drugs of abuse.SIGNIFICANCE STATEMENT Here we report that mice lacking <strong>5 HT2B</strong> receptors totally or exclusively in dopamine neurons exhibit heightened <b>cocaine</b> induced locomotor responses.
+HTR2B	drug	cocaine	28935766	These data support the idea that the chronic <strong>5 HT2B</strong> receptor inhibition makes mice behave like animals already exposed to <b>cocaine</b> with higher <b>cocaine</b> induced locomotion associated with changes in dopamine neuron reactivity.
+HTR2B	drug	psychedelics	19956756	Role of serotonin via <strong>5 HT2B</strong> receptors in the reinforcing effects of <b>MDMA</b> in mice.
+HTR2B	addiction	reward	19956756	Role of serotonin via <strong>5 HT2B</strong> receptors in the <b>reinforcing</b> effects of MDMA in mice.
+HTR2B	drug	psychedelics	18337424	Serotonin <strong>5 HT2B</strong> receptors are required for 3,4 <b>methylenedioxymethamphetamine</b> induced hyperlocomotion and 5 HT release in vivo and in vitro.
+HTR2B	drug	cocaine	17899022	We investigated whether Ro 60 0175, a nonselective <strong>5 HT2B</strong> 2C agonist, influences cue elicited reinstatement of <b>cocaine</b> seeking behavior.
+HTR2B	addiction	relapse	17899022	We investigated whether Ro 60 0175, a nonselective <strong>5 HT2B</strong> 2C agonist, influences cue elicited <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+HTR2B	addiction	addiction	9886683	Thus, the anti <b>punishment</b> action of BW 723C86 is likely to be <strong>5 HT2B</strong> receptor mediated.
+DNMT1	addiction	reward	31735530	via its receptor specifically blocked Oxy <b>CPP</b>, normalized synaptic density, and regulated <strong>DNMT1</strong> and TET2 3 causing reverse of DNA demethylation of Syn and Psd95.
+DNMT1	drug	opioid	31526808	Following restraint stress induced reinstatement of <b>oxycodone</b> CPP, OT significantly increased mRNA levels of <strong>Dnmt1</strong>, decreased Tet1 mRNA, synaptic proteins and synaptic density in the hippocampus.
+DNMT1	addiction	relapse	31526808	Following restraint stress induced <b>reinstatement</b> of oxycodone CPP, OT significantly increased mRNA levels of <strong>Dnmt1</strong>, decreased Tet1 mRNA, synaptic proteins and synaptic density in the hippocampus.
+DNMT1	addiction	reward	31526808	Following restraint stress induced reinstatement of oxycodone <b>CPP</b>, OT significantly increased mRNA levels of <strong>Dnmt1</strong>, decreased Tet1 mRNA, synaptic proteins and synaptic density in the hippocampus.
+DNMT1	drug	alcohol	31229451	One hour after last adolescent intermittent <b>ethanol</b> (AIE), growth arrest and DNA damage inducible protein 45 (Gadd45a, Gadd45b, and Gadd45g) mRNA expression was increased and DNA methyltransferase (<strong>DNMT</strong>) activity and Dnmt3b expression was decreased in the amygdala as compared to adolescent intermittent saline (AIS) rats.
+DNMT1	drug	alcohol	31229451	Treatment with the <strong>DNMT</strong> inhibitor 5 azacytidine (5 azaC) at adulthood normalizes the AIE induced DNA hypermethylation of Npy and Bdnf exon IV with concomitant reversal of AIE induced anxiety like and <b>alcohol</b> drinking behaviors.
+DNMT1	drug	opioid	30950138	<strong>DNMT</strong> inhibitor 5 aza 2 deoxycytidine (5 aza) microinjected into the hippocampal CA1 significantly attenuated the acquisition of <b>morphine</b> SA.
+DNMT1	drug	cocaine	30730091	Our results showed that after silencing Dnmt3a in the NAc during the induction phase of <b>cocaine</b> induced sensitization, overall <strong>DNMT</strong> activity decreases, correlating negatively with behavioral sensitization.
+DNMT1	addiction	sensitization	30730091	Our results showed that after silencing Dnmt3a in the NAc during the induction phase of cocaine induced <b>sensitization</b>, overall <strong>DNMT</strong> activity decreases, correlating negatively with behavioral <b>sensitization</b>.
+DNMT1	drug	cocaine	30730091	<b>Cocaine</b> withdrawal and a challenge dose increased <strong>DNMT</strong> activity in the NAc, which was associated with the expression of behavioral sensitization.
+DNMT1	addiction	sensitization	30730091	Cocaine withdrawal and a challenge dose increased <strong>DNMT</strong> activity in the NAc, which was associated with the expression of behavioral <b>sensitization</b>.
+DNMT1	addiction	withdrawal	30730091	Cocaine <b>withdrawal</b> and a challenge dose increased <strong>DNMT</strong> activity in the NAc, which was associated with the expression of behavioral sensitization.
+DNMT1	drug	cocaine	30730091	Long term selective Dnmt3a transcription silencing in the NAc did not alter <strong>DNMT</strong> activity or the expression of <b>cocaine</b> induced behavioral sensitization.
+DNMT1	addiction	sensitization	30730091	Long term selective Dnmt3a transcription silencing in the NAc did not alter <strong>DNMT</strong> activity or the expression of cocaine induced behavioral <b>sensitization</b>.
+DNMT1	drug	cocaine	30730091	However, bilateral intra NAc injection of a non specific inhibitor of <strong>DNMT</strong> (RG108) during withdrawal from <b>cocaine</b> decreased <strong>DNMT</strong> activity in the NAc and had a small effect on the expression of <b>cocaine</b> induced behavioral sensitization.
+DNMT1	addiction	sensitization	30730091	However, bilateral intra NAc injection of a non specific inhibitor of <strong>DNMT</strong> (RG108) during withdrawal from cocaine decreased <strong>DNMT</strong> activity in the NAc and had a small effect on the expression of cocaine induced behavioral <b>sensitization</b>.
+DNMT1	addiction	withdrawal	30730091	However, bilateral intra NAc injection of a non specific inhibitor of <strong>DNMT</strong> (RG108) during <b>withdrawal</b> from cocaine decreased <strong>DNMT</strong> activity in the NAc and had a small effect on the expression of cocaine induced behavioral sensitization.
+DNMT1	drug	cocaine	30730091	Thus, <b>cocaine</b> treatment and withdrawal is associated with biphasic changes in <strong>DNMT</strong> activity in the NAc, and the expression of behavioral sensitization decreases with non selective inhibition of <strong>DNMT</strong> but not with selective silencing of Dnmt3a.
+DNMT1	addiction	sensitization	30730091	Thus, cocaine treatment and withdrawal is associated with biphasic changes in <strong>DNMT</strong> activity in the NAc, and the expression of behavioral <b>sensitization</b> decreases with non selective inhibition of <strong>DNMT</strong> but not with selective silencing of Dnmt3a.
+DNMT1	addiction	withdrawal	30730091	Thus, cocaine treatment and <b>withdrawal</b> is associated with biphasic changes in <strong>DNMT</strong> activity in the NAc, and the expression of behavioral sensitization decreases with non selective inhibition of <strong>DNMT</strong> but not with selective silencing of Dnmt3a.
+DNMT1	drug	cocaine	30030395	Here we examined the role of the <strong>Dnmt</strong> isoforms, Dnmt3a1 and Dnmt3a2, within the nucleus accumbens (NAc) on transcriptional activity of immediate early genes (IEGs) and acute and long lasting responsiveness to <b>cocaine</b> and <b>cocaine</b> conditioned cues.
+DNMT1	drug	cocaine	29964092	Using a mouse behavioral sensitization model, we demonstrated that acute <b>cocaine</b> (AC; 0.5 h) treatment significantly decreased <strong>Dnmt1</strong>, Dnmt3a, Tet1, and Tet2 mRNA levels in the NAc and PBC, whereas at 24 h after AC treatment, Dnmt mRNA expression and enzyme activity levels were significantly increased.
+DNMT1	addiction	sensitization	29964092	Using a mouse behavioral <b>sensitization</b> model, we demonstrated that acute cocaine (AC; 0.5 h) treatment significantly decreased <strong>Dnmt1</strong>, Dnmt3a, Tet1, and Tet2 mRNA levels in the NAc and PBC, whereas at 24 h after AC treatment, Dnmt mRNA expression and enzyme activity levels were significantly increased.
+DNMT1	drug	cocaine	29964092	Using a mouse behavioral sensitization model, we demonstrated that acute <b>cocaine</b> (AC; 0.5 h) treatment significantly decreased <strong>Dnmt1</strong>, Dnmt3a, Tet1, and Tet2 mRNA levels in the NAc and PBC, whereas at 24 h after AC treatment, <strong>Dnmt</strong> mRNA expression and enzyme activity levels were significantly increased.
+DNMT1	addiction	sensitization	29964092	Using a mouse behavioral <b>sensitization</b> model, we demonstrated that acute cocaine (AC; 0.5 h) treatment significantly decreased <strong>Dnmt1</strong>, Dnmt3a, Tet1, and Tet2 mRNA levels in the NAc and PBC, whereas at 24 h after AC treatment, <strong>Dnmt</strong> mRNA expression and enzyme activity levels were significantly increased.
+DNMT1	drug	cocaine	29964092	Additionally, <b>cocaine</b> withdrawal increased <strong>DNMT</strong> but decreased TET activity levels, and these changes were associated with enhanced global and selected candidate gene promoter region DNA methylation and hydroxymethylation levels in the NAc and PBCs.
+DNMT1	addiction	withdrawal	29964092	Additionally, cocaine <b>withdrawal</b> increased <strong>DNMT</strong> but decreased TET activity levels, and these changes were associated with enhanced global and selected candidate gene promoter region DNA methylation and hydroxymethylation levels in the NAc and PBCs.
+DNMT1	drug	alcohol	28433417	There is growing evidence that small molecule inhibitors of epigenetic modulators, such as histone deacetylases (HDAC) and DNA methyltransferases (<strong>DNMT</strong>), can reduce voluntary <b>ethanol</b> consumption in animal models, but molecular and cellular processes underlying this behavioral effect are poorly understood.
+DNMT1	drug	alcohol	28433417	We used C57BL/6J male mice to investigate the effects of two FDA approved drugs, decitabine (a <strong>DNMT</strong> inhibitor) and SAHA (an HDAC inhibitor), on <b>ethanol</b> consumption using two tests: binge like drinking in the dark (DID) and chronic intermittent every other day (EOD) drinking.
+DNMT1	addiction	intoxication	28433417	We used C57BL/6J male mice to investigate the effects of two FDA approved drugs, decitabine (a <strong>DNMT</strong> inhibitor) and SAHA (an HDAC inhibitor), on ethanol consumption using two tests: <b>binge</b> like drinking in the dark (DID) and chronic intermittent every other day (EOD) drinking.
+DNMT1	drug	opioid	27618384	Moreover, chronic <b>morphine</b> induced hypermethylation of GR 17 promoter may be at least partially due to the increase in hippocampal <strong>DNMT</strong> 1 expression and its binding at GR 17 promoter in the rat hippocampus.
+DNMT1	drug	alcohol	26610727	Rats exposed to ELS were more sensitive to <b>ethanol</b> induced changes in Vglut expression in the VTA, Acb, and dStr and in <strong>Dnmt1</strong> and Mecp2 expression in the striatal regions.
+DNMT1	drug	opioid	26535894	The expression of proopiomelanocortin Pomc encoding β endorphin and Oprm1 encoding the mu <b>opioid</b> receptor were upregulated peripherally after incision; moreover, Oprm1 expression was further increased under <strong>DNMT</strong> inhibitor treatment.
+DNMT1	drug	cocaine	26289919	Here, we investigated the role of <strong>DNMT</strong> activity in the reconsolidation of <b>cocaine</b> associated memories.
+DNMT1	drug	cocaine	26289919	Bilateral intra basolateral amygdala (BLA) infusion of the <strong>DNMT</strong> inhibitor5 azacytidine (5 AZA, 1 μg per side) immediately following reactivation decreased subsequent reinstatement induced by cues or <b>cocaine</b> priming as well as cue maintained <b>cocaine</b> seeking behaviour.
+DNMT1	addiction	relapse	26289919	Bilateral intra basolateral amygdala (BLA) infusion of the <strong>DNMT</strong> inhibitor5 azacytidine (5 AZA, 1 μg per side) immediately following reactivation decreased subsequent <b>reinstatement</b> induced by cues or cocaine priming as well as cue maintained cocaine <b>seeking</b> behaviour.
+DNMT1	drug	cocaine	26289919	These findings indicate that memory reconsolidation for a <b>cocaine</b> paired stimulus depends critically on <strong>DNMT</strong> activity in the BLA.
+DNMT1	drug	cannabinoid	25418810	The overexpression of four genes, DNA methyltransferase 1 (<strong>DNMT1</strong>), δ opioid receptor (OPRD1), <b>cannabinoid</b> receptor 1 (CNR1), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+DNMT1	drug	opioid	25418810	The overexpression of four genes, DNA methyltransferase 1 (<strong>DNMT1</strong>), δ <b>opioid</b> receptor (OPRD1), cannabinoid receptor 1 (CNR1), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+DNMT1	drug	cannabinoid	25418810	The overexpression of four genes, <strong>DNA methyltransferase 1</strong> (<strong>DNMT1</strong>), δ opioid receptor (OPRD1), <b>cannabinoid</b> receptor 1 (CNR1), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+DNMT1	drug	opioid	25418810	The overexpression of four genes, <strong>DNA methyltransferase 1</strong> (<strong>DNMT1</strong>), δ <b>opioid</b> receptor (OPRD1), cannabinoid receptor 1 (CNR1), and catechol o methyltransferase (COMT), was strongly associated with overall poor performance.
+DNMT1	drug	alcohol	24968059	We investigated the effects of acute <b>ethanol</b> exposure on anxiety measures and function of histone deacetylases (HDAC) and DNA methyltransferases (<strong>DNMT</strong>) in the amygdala and bed nucleus of stria terminalis (BNST) of adolescent rats.
+DNMT1	drug	alcohol	24968059	The lower dose of <b>ethanol</b> (1 g/kg) produced neither anxiolysis, nor inhibited the HDAC and <strong>DNMT</strong> activities in the amygdala and BNST, except <strong>DNMT</strong> activity in BNST was attenuated.
+DNMT1	drug	alcohol	24968059	<strong>DNMT</strong> activity in the amygdala and BNST, and nuclear HDAC activity in the amygdala, but not in the BNST were also inhibited by these doses of <b>ethanol</b>.
+DNMT1	drug	alcohol	24968059	A lack of tolerance was observed on <b>ethanol</b> induced inhibition of <strong>DNMT</strong> activity in the amygdala and BNST, and nuclear HDAC activity in the amygdala, as well to anxiolysis produced by <b>ethanol</b> (2 g/kg).
+DNMT1	drug	alcohol	24968059	However, <strong>DNMT1</strong> and DNMT3a expression in the BNST was increased, whereas DNMT3l mRNA was decreased in the amygdala, after 2 doses of 2 g/kg <b>ethanol</b>.
+DNMT1	drug	alcohol	24968059	These results suggest that reduced sensitivity to anxiolysis and the lack of rapid tolerance to the anxiolytic effects of <b>ethanol</b> and inhibition of HDAC and <strong>DNMT</strong> functions may play a role in engaging adolescents in binge drinking patterns.
+DNMT1	addiction	intoxication	24968059	These results suggest that reduced sensitivity to anxiolysis and the lack of rapid tolerance to the anxiolytic effects of ethanol and inhibition of HDAC and <strong>DNMT</strong> functions may play a role in engaging adolescents in <b>binge</b> drinking patterns.
+DNMT1	drug	alcohol	24527678	<b>Ethanol</b> increased the gene expression of DNA methyltransferases (<strong>Dnmt1</strong> and Dnmt3a), the corepressor <strong>Dnmt1</strong> associated protein 1 (Dmap1), and the RNA methyltransferase Trdmt1.
+DNMT1	drug	cocaine	23688924	<b>Cocaine</b> also increased DNMT3 expression, resulting in PP1Cβ repression that did not occur in the presence of <strong>DNMT</strong> inhibitor.
+DNMT1	drug	alcohol	23423140	Specifically, we show that decreasing DNA methylation by inhibiting the activity of DNA methyltransferase (<strong>DNMT</strong>) with systemic administration of the FDA approved drug, 5 azacitidine (5 AzaC) prevents excessive <b>alcohol</b> use in mice.
+DNMT1	drug	alcohol	23423140	Importantly, the actions of both <strong>DNMT</strong> and HDAC inhibitors are specific for <b>alcohol</b>, as no changes in saccharin or sucrose intake were observed.
+DNMT1	drug	alcohol	23423140	In line with these behavioral findings, we demonstrate that excessive <b>alcohol</b> drinking increases <strong>DNMT1</strong> levels and reduces histone H4 acetylation in the nucleus accumbens (NAc) of rodents.
+DNMT1	drug	alcohol	23423140	Our study therefore highlights the possibility that <strong>DNMT</strong> and HDAC inhibitors can be used to treat harmful <b>alcohol</b> abuse.
+DNMT1	drug	alcohol	23110077	Brains were then removed 30 min after a saline or 2 g/kg <b>ethanol</b> challenge to assess i) gene expression using PCR array targeting 84 epigenetic related genes and ii) histone deacetylases (HDAC), histone acetylases (HAT) and DNA methyltransferases (<strong>DNMT</strong>) activities as well as H4K12 acetylation.
+DNMT1	drug	alcohol	23110077	Acute <b>ethanol</b> administration decreased <strong>dnmt1</strong>, esco2 and rps6ka5 genes expression.
+DNMT1	drug	alcohol	23110077	Whereas global HAT or <strong>DNMT</strong> activity was not affected, global HDAC activity was reduced after an acute <b>ethanol</b> injection.
+DNMT1	drug	cocaine	22438930	We also found that both mRNA and protein level of <strong>DNMT</strong> (DNA methytransferase) 3b in the PFC were downregulated following the establishment of <b>cocaine</b> CPP, and the downregulation could be reversed by repeated administration of methionine.
+DNMT1	addiction	reward	22438930	We also found that both mRNA and protein level of <strong>DNMT</strong> (DNA methytransferase) 3b in the PFC were downregulated following the establishment of cocaine <b>CPP</b>, and the downregulation could be reversed by repeated administration of methionine.
+DNMT1	drug	cocaine	20720536	We also found that pharmacological inhibition of <strong>DNMT</strong> by zebularine treatment decreased <b>cocaine</b> induced DNA hypermethylation at the PP1c promoter and attenuated PP1c mRNA downregulation in NAc.
+DNMT1	drug	amphetamine	17254711	<b>Methamphetamine</b> alters expression of <strong>DNA methyltransferase 1</strong> mRNA in rat brain.
+DNMT1	drug	amphetamine	17254711	In the present study, we found subchronic <b>methamphetamine</b> treatment (4 mg/kg, i.p., once daily for 21 days) to induce different patterns of <strong>Dnmt1</strong> mRNA expression in the nucleus caudatus and nucleus accumbens of two inbred rat strains, Fischer 344/N (increased <strong>Dnmt1</strong>) and Lewis/N (decreased <strong>Dnmt1</strong>).
+CCS	drug	opioid	32124022	<b>Codeine</b> containing cough syrup (<strong>CCS</strong>) is considered as one of the most popular drug of dependence among adolescents because of its inexpensiveness and easy availability.
+CCS	addiction	dependence	32124022	Codeine containing cough syrup (<strong>CCS</strong>) is considered as one of the most popular drug of <b>dependence</b> among adolescents because of its inexpensiveness and easy availability.
+CCS	addiction	addiction	32124022	These findings suggest that the high impulse behavioural expression in <strong>CCS</strong> <b>addiction</b> is associated with widespread brain regions, particularly within those in the frontal cortex.
+CCS	drug	nicotine	31711874	Switching to electronic cigarettes (ECs) may be a viable option to reduce the negative health effects for <b>smokers</b> who are unable or unwilling to quit <b>smoking</b> combustible cigarettes (<strong>CCs</strong>).
+CCS	drug	nicotine	31711874	Switching from <strong>CCs</strong> to ECs in HIV positive <b>smokers</b> who are not ready to quit <b>smoking</b> in the next 30 days appears to be feasible.
+CCS	drug	opioid	31677934	The higher a country's <strong>CCS</strong>, the better it was at managing <b>opioid</b> related health care issues.
+CCS	drug	nicotine	31582950	Positive perceptions of electronic cigarettes (e cigarettes) relative to combustible cigarettes (<strong>CCs</strong>) may erode support for endgame policies on <strong>CCs</strong> through <b>smoking</b> renormalization (increasing public acceptance of <b>smoking</b>).
+CCS	drug	nicotine	31582950	Multivariable regressions yielded adjusted odds ratios (AORs) of supporting endgame policies (individual policy items, all 5 policy items, at least 1 policy item, banning the sale/use of <strong>CCs</strong>) in relation to perceptions of e cigarettes relative to <strong>CCs</strong>, adjusting for age, education attainment, marital status, CC <b>smoking</b> status and ever e cigarette use.
+CCS	addiction	addiction	31582950	Few respondents perceived e cigarettes as more harmful (16.6%) or more <b>addictive</b> (9.3%) than <strong>CCs</strong>.
+CCS	drug	nicotine	31582950	Positive perceptions of e cigarettes (24.0%) were associated with less support for 'ban CC sales in 10 years if there is a product providing <b>nicotine</b> not made from <b>tobacco</b>' (AOR=0.62, 95% CI: 0.40 0.97), 'ban CC use when it's prevalence falls below 5%' (AOR=0.66, 95% CI: 0.44 0.98) and 'banning the sale of <strong>CCs</strong>' (AOR=0.63, 95% CI: 0.42 0.94).
+CCS	drug	alcohol	31443663	Clinics randomized to the intervention group received a prompt when a patient reported consuming <b>alcohol</b> above the Canadian Cancer Society (<strong>CCS</strong>) guidelines; the control group did not receive computer alerts.
+CCS	drug	alcohol	31443663	The primary outcome was an offer of an appropriate educational <b>alcohol</b> resource, an <b>alcohol</b> reduction workbook for patients drinking above the <strong>CCS</strong> guidelines, and an abstinence workbook to patients scoring above 20 points in the AUDIT screening tool; the secondary outcome was patient acceptance of the resource.
+CCS	drug	alcohol	31443663	The tertiary outcome was patient abstinence from smoking, and <b>alcohol</b> consumption within <strong>CCS</strong> guidelines, at 6 month follow up.
+CCS	drug	nicotine	31443663	The tertiary outcome was patient abstinence from <b>smoking</b>, and alcohol consumption within <strong>CCS</strong> guidelines, at 6 month follow up.
+CCS	drug	alcohol	31443663	From the 15,222 patients that enrolled in the smoking cessation program, 15,150 (99.6% of patients) were screened for <b>alcohol</b> use and 5715 patients were identified as drinking above the <strong>CCS</strong> guidelines.
+CCS	drug	nicotine	31443663	From the 15,222 patients that enrolled in the <b>smoking</b> cessation program, 15,150 (99.6% of patients) were screened for alcohol use and 5715 patients were identified as drinking above the <strong>CCS</strong> guidelines.
+CCS	drug	alcohol	31443663	No statistically significant difference between groups was seen in practitioner offer of an educational <b>alcohol</b> resource to appropriate patients (OR = 1.19, 95% CI 0.88 1.64, p = 0.261) or in patient abstinence from smoking and drinking within the <strong>CCS</strong> guidelines at 6 month follow up (OR = 0.93, 95% CI 0.71 1.22, p = 0.594).
+CCS	drug	nicotine	31443663	No statistically significant difference between groups was seen in practitioner offer of an educational alcohol resource to appropriate patients (OR = 1.19, 95% CI 0.88 1.64, p = 0.261) or in patient abstinence from <b>smoking</b> and drinking within the <strong>CCS</strong> guidelines at 6 month follow up (OR = 0.93, 95% CI 0.71 1.22, p = 0.594).
+CCS	drug	alcohol	31261813	In this research program, polyvinyl <b>alcohol</b> (PVA) and copper coated steel (<strong>CCS</strong>) fibers were used in concrete for improving the EZ performance of PT beams.
+CCS	drug	opioid	30980125	The study aimed to explore the effects of <b>codeine</b> containing cough syrup (<strong>CCS</strong>) exposure on cortical morphology and the relationship between cortical characteristics and <strong>CCS</strong> dependence.
+CCS	addiction	dependence	30980125	The study aimed to explore the effects of codeine containing cough syrup (<strong>CCS</strong>) exposure on cortical morphology and the relationship between cortical characteristics and <strong>CCS</strong> <b>dependence</b>.
+CCS	drug	nicotine	30476301	ROS, carbonyl compounds (<strong>CCs</strong>), and total <b>nicotine</b> and its partitioning between free base and protonated forms were quantified in the IQOS aerosol by fluorescence, high performance liquid chromatography, and gas chromatography, respectively.
+CCS	drug	nicotine	30476301	For a given <b>nicotine</b> intake, inhalation exposure to ROS and <strong>CCs</strong> from IQOS is likely to be significantly less than that for combustible cigarettes.
+CCS	drug	nicotine	30416951	Participants in the present study were categorized as having 0, 1 2, or ≥3 <b>smoking</b> related chronic health conditions (i.e., chronic condition severity, <strong>CCS</strong>).
+CCS	drug	nicotine	30416951	Repeated measures analysis of variance was used to examine whether <strong>CCS</strong> moderated response to cigarettes across measures of addiction potential (i.e., concurrent choice testing between <b>nicotine</b> dose pairs, Cigarette Purchase Task (CPT) performance, positive subjective effects), <b>tobacco</b> withdrawal, cigarette craving, and <b>smoking</b> topography.
+CCS	addiction	addiction	30416951	Repeated measures analysis of variance was used to examine whether <strong>CCS</strong> moderated response to cigarettes across measures of <b>addiction</b> potential (i.e., concurrent choice testing between nicotine dose pairs, Cigarette Purchase Task (CPT) performance, positive subjective effects), tobacco withdrawal, cigarette craving, and smoking topography.
+CCS	addiction	relapse	30416951	Repeated measures analysis of variance was used to examine whether <strong>CCS</strong> moderated response to cigarettes across measures of addiction potential (i.e., concurrent choice testing between nicotine dose pairs, Cigarette Purchase Task (CPT) performance, positive subjective effects), tobacco withdrawal, cigarette <b>craving</b>, and smoking topography.
+CCS	addiction	withdrawal	30416951	Repeated measures analysis of variance was used to examine whether <strong>CCS</strong> moderated response to cigarettes across measures of addiction potential (i.e., concurrent choice testing between nicotine dose pairs, Cigarette Purchase Task (CPT) performance, positive subjective effects), tobacco <b>withdrawal</b>, cigarette craving, and smoking topography.
+CCS	drug	nicotine	30416951	No main effects of <strong>CCS</strong> or interactions of <strong>CCS</strong> and <b>nicotine</b> dose were observed for concurrent choice testing, positive subjective effects, <b>tobacco</b> withdrawal, or <b>smoking</b> topography.
+CCS	addiction	withdrawal	30416951	No main effects of <strong>CCS</strong> or interactions of <strong>CCS</strong> and nicotine dose were observed for concurrent choice testing, positive subjective effects, tobacco <b>withdrawal</b>, or smoking topography.
+CCS	drug	nicotine	30416951	There was an interaction of <strong>CCS</strong> and <b>nicotine</b> dose on Factor 1 of the Questionnaire on <b>Smoking</b> Urges with the effects of dose significant only among those with 1 2 chronic conditions.
+CCS	drug	nicotine	30126382	We aimed to investigate <b>nicotine</b> cessation for both ECs and <strong>CCs</strong>.
+CCS	drug	nicotine	30126382	Only 3.3% of observed users quit both ECs and <strong>CCs</strong>, whereas 20.5% quit <b>smoking</b> <strong>CCs</strong>.
+CCS	drug	nicotine	30126382	Quitting ECs and <strong>CCs</strong> was significantly higher among sole EC users (5 vs 2, respectively; OR: 5.62; P = 0.036) than it was among dual users, a result that was similar for <strong>CCs</strong> <b>smoking</b> (29 vs. 15; OR: 6.33; P ≤ 0.001).
+CCS	drug	opioid	29988765	<b>Codeine</b> containing cough syrups (<strong>CCS</strong>) have become one of the most popular drugs of abuse in young population worldwide.
+CCS	addiction	dependence	29988765	However, the neurobiological mechanisms underlying <strong>CCS</strong> <b>dependence</b> are yet ill defined.
+CCS	addiction	reward	29988765	The rs fMRI study suggested that the abnormal intrinsic dysconnectivity pattern of whole brain functional networks may provide an insight into the neural substrates of abnormalities in the cognitive control circuit, the <b>reward</b> circuit, and the learning and memory circuit in <strong>CCS</strong> dependent individuals.
+CCS	drug	nicotine	29248487	The safety profile of Puritane™, a closed system electronic vapour product (EVP), was evaluated when used by <b>smokers</b> of conventional cigarettes (<strong>CCs</strong>) for 24 months in a real life setting.
+CCS	drug	cocaine	28076644	The research database "Between rocks and shots: user profiles, consumption strategies, and social impact of crack <b>cocaine</b>" (CEP/<strong>CCS</strong>/UFPE no.
+CCS	drug	cannabinoid	26315824	Older <strong>CCS</strong> were at higher risk of substance use, and depression was associated with greater <b>marijuana</b> use.
+CCS	drug	nicotine	27769828	A randomised, parallel group clinical study was performed to evaluate the safety profile of an e vapour product (EVP; 2.0% <b>nicotine</b>) in <b>smokers</b> of conventional cigarettes (<strong>CCs</strong>) switching to use the EVP for 12 weeks.
+CCS	drug	nicotine	27769828	The data presented here shows the potential EVPs may offer <b>smokers</b> looking for an alternative to <strong>CCs</strong>.
+CCS	drug	nicotine	27613951	Exposure measurements are required to determine whether it may be possible to reduce the individual health risk compared to <b>smoking</b> combustible cigarettes (<strong>CCs</strong>).
+CCS	drug	nicotine	27613951	THS 2.1 is a promising alternative to <b>smoking</b> <strong>CCs</strong>.
+CCS	drug	nicotine	27613951	Heating <b>tobacco</b> instead of burning can offer a potentially lower risk of delivering <b>nicotine</b> compared to <strong>CCs</strong>.
+CCS	drug	opioid	27341655	To identify <b>codeine</b> containing cough syrups (<strong>CCS</strong>) related modulations of intrinsic connectivity network (ICN) and to investigate whether these changes of ICN can be related to duration of <strong>CCS</strong> use and to impulsivity behavior in <strong>CCS</strong> dependent individuals.
+CCS	drug	opioid	27329520	To characterize interhemispheric functional and anatomical connectivity and their relationships with impulsive behaviour in <b>codeine</b> containing cough syrup (<strong>CCS</strong>) dependent male adolescents and young adults.
+CCS	drug	nicotine	27329520	We compared volumes of corpus callosum (CC) and its five subregion and voxel mirrored homotopic functional connectivity (VMHC) in 33 <strong>CCS</strong> dependent male adolescents and young adults and 38 healthy controls, group matched for age, education and <b>smoking</b> status.
+CCS	addiction	addiction	27329520	These findings reveal CC abnormalities and disruption of interhemispheric homotopic connectivity in <strong>CCS</strong> dependent male adolescents and young adults, which provide a novel insight into the impact of interhemispheric disconnectivity on impulsive behaviour in substance <b>addiction</b> pathophysiology.
+CCS	drug	alcohol	26863292	The proportion of respondents who had any signs of <b>alcohol</b> abuse symptoms was 72.2% of <strong>CCS</strong> compared with 81.1% of matched controls (p = 0.16), while <strong>CCS</strong> with severe <b>alcohol</b> abuse was 51.1% compared with 59.1% of matched controls (p = 0.28).
+CCS	addiction	intoxication	26863292	Whether they engaged in <b>binge</b> drinking in the past 12 months was 43.3% for <strong>CCS</strong> and 46.4% for healthy respondents.
+CCS	drug	alcohol	26863292	Logistic regression analyses were performed to examine predictors of smoking, <b>alcohol</b> use, and binge drinking among <strong>CCS</strong>.
+CCS	drug	nicotine	26863292	Logistic regression analyses were performed to examine predictors of <b>smoking</b>, alcohol use, and binge drinking among <strong>CCS</strong>.
+CCS	addiction	intoxication	26863292	Logistic regression analyses were performed to examine predictors of smoking, alcohol use, and <b>binge</b> drinking among <strong>CCS</strong>.
+CCS	addiction	intoxication	26863292	<strong>CCS</strong> in good health were more likely to <b>binge</b> drink (OR = 3.67, p < 0.05).
+CCS	drug	nicotine	26752454	The onset of conventional cigarette (CC) use among nonsmokers, and <b>smoking</b> cessation, quit attempts, changes in the number of <strong>CCs</strong> smoked among <b>smokers</b> at baseline were compared between vapers and nonvapers at follow up, adjusted for <b>nicotine</b> dependence.
+CCS	addiction	dependence	26752454	The onset of conventional cigarette (CC) use among nonsmokers, and smoking cessation, quit attempts, changes in the number of <strong>CCs</strong> smoked among smokers at baseline were compared between vapers and nonvapers at follow up, adjusted for nicotine <b>dependence</b>.
+CCS	drug	nicotine	26752454	The number of <strong>CCs</strong> smoked increased between baseline and follow up among occasional <b>smokers</b> (b = 6.06, 95% CI 4.44, 7.68) and decreased among daily <b>smokers</b> (b =  5.03, 95% CI  8.69,  1.38), but there were no differential changes between vapers and nonvapers.
+CCS	drug	alcohol	26662031	To investigate alterations of resting brain function in codeine containing cough syrups (<strong>CCS</strong>) dependent individuals before and after ultra rapid opioid detoxification under general anaesthesia (UROD) combined with <b>naltrexone</b> treatment (NMT).
+CCS	drug	opioid	26662031	To investigate alterations of resting brain function in <b>codeine</b> containing cough syrups (<strong>CCS</strong>) dependent individuals before and after ultra rapid <b>opioid</b> detoxification under general anaesthesia (UROD) combined with naltrexone treatment (NMT).
+CCS	addiction	withdrawal	26662031	Decreased ALFFs in the left PoCG and left MOC were associated with decreased <b>withdrawal</b> syndrome severity in <strong>CCS</strong> dependent individuals.
+CCS	addiction	relapse	26618795	We hypothesized that within subject variation in EC use (yes/no each day) would be inversely associated with within subject variation in number of <strong>CCs</strong> consumed and <b>craving</b> during that same day.
+CCS	addiction	relapse	26618795	Participants completed EMA surveys throughout the day, which assessed CC <b>craving</b>, and end of day surveys, which assessed EC use and the number of <strong>CCs</strong> smoked that day.
+CCS	drug	nicotine	26618795	Generalized linear mixed models were used to predict day level EC use, with number of <strong>CCs</strong> smoked and craving during that same day, gender, and <b>nicotine</b> dependence as predictors (n = 501).
+CCS	addiction	dependence	26618795	Generalized linear mixed models were used to predict day level EC use, with number of <strong>CCs</strong> smoked and craving during that same day, gender, and nicotine <b>dependence</b> as predictors (n = 501).
+CCS	addiction	relapse	26618795	Generalized linear mixed models were used to predict day level EC use, with number of <strong>CCs</strong> smoked and <b>craving</b> during that same day, gender, and nicotine dependence as predictors (n = 501).
+CCS	drug	nicotine	26502572	By using the techniques of drug self administration and conditioned place preference, <b>nicotine</b>'s specific property of forming seeking/taking behavior is well characterized, and the mechanisms of seeking/taking could be partly explained by discrete and/or contextual conditioned stimuli (dCS and <strong>cCS</strong>).
+CCS	addiction	relapse	26502572	By using the techniques of drug self administration and conditioned place preference, nicotine's specific property of forming <b>seeking</b>/taking behavior is well characterized, and the mechanisms of <b>seeking</b>/taking could be partly explained by discrete and/or contextual conditioned stimuli (dCS and <strong>cCS</strong>).
+CCS	drug	nicotine	26502572	The <b>nicotine</b> associated <strong>cCS</strong> also activated this neural system, which resulted in decreasing the ICSS threshold approximately 20% in the testing session under the <strong>cCS</strong> presentation.
+CCS	addiction	reward	26502572	The nicotine associated <strong>cCS</strong> also activated this neural system, which resulted in decreasing the <b>ICSS</b> threshold approximately 20% in the testing session under the <strong>cCS</strong> presentation.
+CCS	drug	opioid	24223847	In the past twenty years, <b>codeine</b> containing cough syrups (<strong>CCS</strong>) was recognized as a new type of addictive drugs.
+CCS	addiction	addiction	24223847	In the past twenty years, codeine containing cough syrups (<strong>CCS</strong>) was recognized as a new type of <b>addictive</b> drugs.
+CCS	addiction	dependence	24223847	However, the exact neurobiologic mechanisms underlying <strong>CCS</strong> <b>dependence</b> are still ill defined.
+CCS	drug	cannabinoid	22855882	In this study, we focused on a sample of 142 participants (mean age 19.54) that reported either smoking only tobacco cigarettes (CIG group, n = 70) or smoking both tobacco cigarettes and <b>cannabis</b> (<strong>CCS</strong> group, n = 72).
+CCS	drug	nicotine	22855882	In this study, we focused on a sample of 142 participants (mean age 19.54) that reported either <b>smoking</b> only <b>tobacco</b> cigarettes (CIG group, n = 70) or <b>smoking</b> both <b>tobacco</b> cigarettes and cannabis (<strong>CCS</strong> group, n = 72).
+CCS	drug	opioid	21477952	In recent years, <b>codeine</b> containing cough syrups (<strong>CCS</strong>) have been reported as substances of abuse, especially in adolescents.
+CCS	addiction	dependence	21477952	Chronic <strong>CCS</strong> abuse can induce physical and psychological <b>dependence</b>.
+CCS	addiction	dependence	21477952	Taken together, these results suggest that chronic <strong>CCS</strong> abuse may cause serious damage to the brain and the neuroimaging findings further illustrate the mechanism of <strong>CCS</strong> <b>dependence</b>.
+CCS	drug	cocaine	19718490	Participants completed an assessment battery that included the extended, 45 item version of the <b>Cocaine</b> Craving Questionnaire (CCQ N 45)   in which the CCQ N 10 is embedded  , the <b>Cocaine</b> Craving Scale (<strong>CCS</strong>), a Visual Analog Craving Scale (VAS), the Severity of Dependence Scale (SDS), and the Clinical Psychiatric Impression (CPI).
+CCS	addiction	dependence	19718490	Participants completed an assessment battery that included the extended, 45 item version of the Cocaine Craving Questionnaire (CCQ N 45)   in which the CCQ N 10 is embedded  , the Cocaine Craving Scale (<strong>CCS</strong>), a Visual Analog Craving Scale (VAS), the Severity of <b>Dependence</b> Scale (SDS), and the Clinical Psychiatric Impression (CPI).
+CCS	addiction	relapse	19718490	Participants completed an assessment battery that included the extended, 45 item version of the Cocaine <b>Craving</b> Questionnaire (CCQ N 45)   in which the CCQ N 10 is embedded  , the Cocaine <b>Craving</b> Scale (<strong>CCS</strong>), a Visual Analog <b>Craving</b> Scale (VAS), the Severity of Dependence Scale (SDS), and the Clinical Psychiatric Impression (CPI).
+CCS	drug	alcohol	11967466	We use the Clinical Classification Software (<strong>CCS</strong>) to distinguish between affective disorders, schizophrenia and related disorders, other psychoses, anxiety and related disorders, pre adult disorders, and <b>alcohol</b> , substance  related mental disorders and other mental disorders.
+CCS	drug	opioid	9581010	To study the socio demographic and clinical profile of patients seeking treatment for abuse of <b>codeine</b> containing cough syrups (<strong>CCS</strong>).
+CCS	addiction	relapse	9581010	To study the socio demographic and clinical profile of patients <b>seeking</b> treatment for abuse of codeine containing cough syrups (<strong>CCS</strong>).
+CCS	addiction	dependence	9581010	Forty six consecutive treatment seeking patients of DSM III R diagnosed <b>dependence</b> on <strong>CCS</strong>, from January 1994 to June 1995.
+CCS	addiction	relapse	9581010	Forty six consecutive treatment <b>seeking</b> patients of DSM III R diagnosed dependence on <strong>CCS</strong>, from January 1994 to June 1995.
+CCS	drug	opioid	9581010	The combination of an <b>opioid</b> and a sympathomimetic agent in the <strong>CCS</strong> may cause a special, distinct euphoretic effect.
+CCS	drug	amphetamine	8369955	The role of corticosterone (<strong>CCS</strong>) in regulating sensitization to <b>amphetamine</b>'s locomotor activating effects was measured in female DBA/2 mice that had been sham operated or adrenalectomized and implanted with <strong>CCS</strong> containing or cholesterol pellets.
+CCS	addiction	sensitization	8369955	The role of corticosterone (<strong>CCS</strong>) in regulating <b>sensitization</b> to amphetamine's locomotor activating effects was measured in female DBA/2 mice that had been sham operated or adrenalectomized and implanted with <strong>CCS</strong> containing or cholesterol pellets.
+CCS	drug	amphetamine	8369955	Chronic <strong>CCS</strong> treatment did not significantly alter initial responsiveness to <b>amphetamine</b> in either sham operated or ADX animals, but it did alter the dose dependent sensitization to <b>amphetamine</b>.
+CCS	addiction	sensitization	8369955	Chronic <strong>CCS</strong> treatment did not significantly alter initial responsiveness to amphetamine in either sham operated or ADX animals, but it did alter the dose dependent <b>sensitization</b> to amphetamine.
+CCS	drug	amphetamine	8369955	<strong>CCS</strong> treated sham operated animals exhibited sensitization to the locomotor activating effects of <b>amphetamine</b> at the lowest dose used (1.0 mg/kg) and increased stereotype following treatment with the higher doses.
+CCS	addiction	sensitization	8369955	<strong>CCS</strong> treated sham operated animals exhibited <b>sensitization</b> to the locomotor activating effects of amphetamine at the lowest dose used (1.0 mg/kg) and increased stereotype following treatment with the higher doses.
+CCS	drug	amphetamine	8369955	ADX/<strong>CCS</strong> animals developed sensitization to the locomotor activating effects of <b>amphetamine</b> following chronic injection with the 2.5 mg/kg dose, and showed sensitization to <b>amphetamine</b> induced stereotypy at higher doses.
+CCS	addiction	sensitization	8369955	ADX/<strong>CCS</strong> animals developed <b>sensitization</b> to the locomotor activating effects of amphetamine following chronic injection with the 2.5 mg/kg dose, and showed <b>sensitization</b> to amphetamine induced stereotypy at higher doses.
+CCS	drug	cocaine	1609038	The response to gepirone at a mean dose of 16.25 mg/day did not differ from placebo by measures of time in study, positive urine <b>cocaine</b> screens (greater than 6 weeks), Clinical Global Impressions (CGI) Global Improvements Scale, <b>Cocaine</b> Craving Scale (<strong>CCS</strong>), Quantitative <b>Cocaine</b> Inventory (QCI), Addiction Severity Index (ASI), Global Assessment Scale (GAS), Hamilton Rating Scale for Depression (HAM D), and Hamilton Anxiety Scale (HAM A).
+CCS	addiction	addiction	1609038	The response to gepirone at a mean dose of 16.25 mg/day did not differ from placebo by measures of time in study, positive urine cocaine screens (greater than 6 weeks), Clinical Global Impressions (CGI) Global Improvements Scale, Cocaine Craving Scale (<strong>CCS</strong>), Quantitative Cocaine Inventory (QCI), <b>Addiction</b> Severity Index (ASI), Global Assessment Scale (GAS), Hamilton Rating Scale for Depression (HAM D), and Hamilton Anxiety Scale (HAM A).
+CCS	addiction	relapse	1609038	The response to gepirone at a mean dose of 16.25 mg/day did not differ from placebo by measures of time in study, positive urine cocaine screens (greater than 6 weeks), Clinical Global Impressions (CGI) Global Improvements Scale, Cocaine <b>Craving</b> Scale (<strong>CCS</strong>), Quantitative Cocaine Inventory (QCI), Addiction Severity Index (ASI), Global Assessment Scale (GAS), Hamilton Rating Scale for Depression (HAM D), and Hamilton Anxiety Scale (HAM A).
+CCS	drug	cocaine	1609038	The following demographic and study measures suggested favorable trends for study outcomes: older age, divorced status, higher pre treatment <b>cocaine</b> use, lower <strong>CCS</strong> scores, and lower self reports of <b>cocaine</b> use according to QCI.
+AIF1	drug	cocaine	32278944	Consistently, we found elevated protein levels of <strong>Iba1</strong>, CCL2, TLR4 and mature IL1β in the striatum, not in the mPFc of <b>cocaine</b> receiving mice.
+AIF1	drug	cannabinoid	32057593	In the mPFC and hippocampus, EtOH rats had significantly higher mRNA expression of <b>endocannabinoid</b> signaling (mPFC: Ppara, Dagla, Daglb and Napepld; and hippocampus: Cnr2, Dagla and Mgll) and neuroinflammation associated genes (mPFC: Gfap; and hippocampus: <strong>Aif1</strong>) than in controls.
+AIF1	drug	cocaine	31998080	In parallel, <b>cocaine</b> self administration alone specifically and differentially affects activation of glial cells by decreasing GFAP expression in astrocytes but increasing <strong>Iba1</strong> expression in microglia.
+AIF1	drug	alcohol	31733666	<strong>Allograft Inflammatory Factor 1</strong> mRNA was increased in both young and aged mice by <b>alcohol</b> exposure; however, only in the aged mice did the <b>alcohol</b> effect persist.
+AIF1	drug	opioid	29729431	Pretreatment with 3mg/kg AM1241 decreased the chronic <b>morphine</b> induced <strong>Iba1</strong> expression in spinal cord.
+AIF1	addiction	withdrawal	28654797	Changes in brain gene expression levels of induced nitric oxide synthase (iNOS), astroglia marker, glial fibrillary acidic protein (GFAP), ionized calcium binding protein (<strong>Iba1</strong>) a microglia activation marker, a pro inflammatory mediator and tumor necrosis alpha (TNF α) were measured after <b>withdrawal</b> by real time polymerase chain reaction (RT PCR).
+AIF1	drug	opioid	28654797	Administration of <b>naloxone</b> was associated with the increased expression of TNF α, GFAP, <strong>Iba1</strong> and iNOS in the brain samples of <b>morphine</b> dependent mice, while the nine days treatment with both 5 and 10mg/kg simvastatin reduced such changes.
+AIF1	drug	alcohol	28427424	Acute binge <b>ethanol</b> biphasically changed microglial (e.g., <strong>Iba1</strong>, CD68) gene expression, with initial decreases during intoxication and subsequent increases during withdrawal.
+AIF1	addiction	intoxication	28427424	Acute <b>binge</b> ethanol biphasically changed microglial (e.g., <strong>Iba1</strong>, CD68) gene expression, with initial decreases during <b>intoxication</b> and subsequent increases during withdrawal.
+AIF1	addiction	withdrawal	28427424	Acute binge ethanol biphasically changed microglial (e.g., <strong>Iba1</strong>, CD68) gene expression, with initial decreases during intoxication and subsequent increases during <b>withdrawal</b>.
+AIF1	addiction	withdrawal	28062186	We attempted to verify <b>withdrawal</b> regulation of induced nitric oxide synthase (iNOS), astroglia marker, glial fibrillary acidic protein (GFAP), ionized calcium binding protein (<strong>Iba1</strong>), a microglia activation marker, a pro inflammatory mediator, tumor necrosis alpha (TNF α) and immune receptor, toll like receptor 4 (TLR 4) genes by real time polymerase chain reaction (RT PCR).
+AIF1	drug	opioid	28062186	Brain expression levels of TNF α, GFAP, <strong>Iba1</strong> and iNOS increased in <b>morphine</b> withdrawn animals which were attenuated by nine days treatment with atorvastatin.
+AIF1	drug	opioid	27875800	Immunohistochemistry (IHC) experiments on striatal brain slices were performed to assess the expression of glial markers (<strong>Iba1</strong>, GFAP and CD68) during 14days after <b>morphine</b> discontinuation.
+AIF1	drug	amphetamine	27098516	Using logistic regression models, we analyzed associations of <b>Meth</b> with cerebral gliosis (immunohistochemistry for ionized calcium binding adapter molecule 1 (<strong>Iba1</strong>) and glial fibrillary acidic protein (GFAP) in frontal, temporo parietal, and putamen internal capsule regions), synaptodendritic loss (confocal microscopy for synaptophysin (SYP) and microtubule associated protein 2 (MAP2) in frontal cortex), β amyloid plaque deposition (immunohistochemistry in frontal and temporo parietal cortex and putamen), and arteriolosclerosis (histopathology in forebrain white matter).
+AIF1	drug	alcohol	27098516	We found that Meth was associated with marked <strong>Iba1</strong> gliosis in the temporo parietal region (odds ratio, 4.42 (95 % confidence interval, 1.36, 14.39), p = 0.014, n = 62), which remained statistically significant after adjusting for HIV encephalitis, white matter lesions, and opportunistic diseases (n = 61); hepatitis C virus seropositivity (n = 54); and lifetime dependence on <b>alcohol</b>, opiates, and cannabis (n = 62).
+AIF1	drug	amphetamine	27098516	We found that <b>Meth</b> was associated with marked <strong>Iba1</strong> gliosis in the temporo parietal region (odds ratio, 4.42 (95 % confidence interval, 1.36, 14.39), p = 0.014, n = 62), which remained statistically significant after adjusting for HIV encephalitis, white matter lesions, and opportunistic diseases (n = 61); hepatitis C virus seropositivity (n = 54); and lifetime dependence on alcohol, opiates, and cannabis (n = 62).
+AIF1	drug	cannabinoid	27098516	We found that Meth was associated with marked <strong>Iba1</strong> gliosis in the temporo parietal region (odds ratio, 4.42 (95 % confidence interval, 1.36, 14.39), p = 0.014, n = 62), which remained statistically significant after adjusting for HIV encephalitis, white matter lesions, and opportunistic diseases (n = 61); hepatitis C virus seropositivity (n = 54); and lifetime dependence on alcohol, opiates, and <b>cannabis</b> (n = 62).
+AIF1	addiction	dependence	27098516	We found that Meth was associated with marked <strong>Iba1</strong> gliosis in the temporo parietal region (odds ratio, 4.42 (95 % confidence interval, 1.36, 14.39), p = 0.014, n = 62), which remained statistically significant after adjusting for HIV encephalitis, white matter lesions, and opportunistic diseases (n = 61); hepatitis C virus seropositivity (n = 54); and lifetime <b>dependence</b> on alcohol, opiates, and cannabis (n = 62).
+AIF1	drug	opioid	26478469	The aim of the present study was to investigate the molecular effects of perinatal exposure to lead (Pb) on protein and mRNA expression of purine receptors: P2X4, P2X7, adenosine receptor A1; and astrocytes (GFAP mRNA expression) and on microglia activation (<strong>Iba1</strong> mRNA expression) in several structures of the mesolimbic system (striatum, hippocampus, prefrontal cortex) in rats expressing tolerance to the antinociceptive effect of <b>morphine</b>.
+AIF1	drug	nicotine	25637801	<b>Nicotine</b> also promoted elevations in the expression of glial fibrillary acidic protein (GFAP), a biomarker of activated astrocytes, and the microglia biomarker ionized calcium binding adapter molecule 1 (<strong>Iba1</strong>).
+AIF1	drug	cannabinoid	24409127	Both acute and repeated cocaine exposure increased the number of cleaved caspase 3 , GFAP  and <strong>Iba1</strong> ir cells in the hippocampus, and this effect was counteracted by AM630 or <b>Rimonabant</b>, which increased the number of BrdU , GFAP , and <strong>Iba1</strong> ir cells in the hippocampus.
+AIF1	drug	cocaine	24409127	Both acute and repeated <b>cocaine</b> exposure increased the number of cleaved caspase 3 , GFAP  and <strong>Iba1</strong> ir cells in the hippocampus, and this effect was counteracted by AM630 or Rimonabant, which increased the number of BrdU , GFAP , and <strong>Iba1</strong> ir cells in the hippocampus.
+AIF1	drug	opioid	22362187	In the present study, by combining the techniques of in situ hybridization of MOR mRNA with immunohistochemistry of glial fibrillary acidic protein (GFAP; an astrocyte marker) and <strong>Iba1</strong> (a microglial marker), we examined expression and distribution of GFAP, <strong>Iba1</strong>, and MOR mRNA in the spinal cord of rats under chronic <b>morphine</b> tolerance conditions.
+AIF1	drug	opioid	22362187	Intrathecal injections of <b>morphine</b> twice daily for 7 days reduced <b>morphine</b> analgesic effect and increased both GFAP and <strong>Iba1</strong> immunostaining densities in the spinal cord.
+AIF1	addiction	sensitization	20035859	We also show that MA <b>sensitization</b> decreased LPS  or acute MA induced microglial <strong>Iba1</strong> expression compared to non sensitized mice.
+ADH1A	drug	alcohol	31870920	To answer these questions, we measured the expression and activity of <b>alcohol</b> dehydrogenase 1 (<strong>ADH1</strong>) and acetaldehyde dehydrogenase 2 (ALDH2) enzymes, <b>ethanol</b> and acetaldehyde levels in vivo, and binge like and preferential drinking behaviors with drinking in the dark and two bottle choice in animal models with liver injury.
+ADH1A	addiction	intoxication	31870920	To answer these questions, we measured the expression and activity of alcohol dehydrogenase 1 (<strong>ADH1</strong>) and acetaldehyde dehydrogenase 2 (ALDH2) enzymes, ethanol and acetaldehyde levels in vivo, and <b>binge</b> like and preferential drinking behaviors with drinking in the dark and two bottle choice in animal models with liver injury.
+ADH1A	drug	alcohol	31870920	In addition, chronic CCl4 and acute LPS treatment inhibited hepatic <strong>ADH1</strong> expression and activity, leading to increases in blood and liver <b>ethanol</b> concentrations.
+ADH1A	drug	alcohol	31648290	In this paper, we demonstrate the efficient recruitment of pyruvate decarboxylase (Pdc1) and <b>alcohol</b> dehydrogenase (<strong>Adh1</strong>) fermentation enzymes into the viral replication compartment.
+ADH1A	drug	alcohol	31018006	Then, <b>alcohol</b> dehydrogenase (<strong>ADH1</strong>) and aldehyde dehydrogenase (ALDH2) protein levels and enzymatic activities in the livers were quantified.
+ADH1A	drug	alcohol	31018006	The studies show that treatment with fenofibrate not only increased the activity of catalase in the liver of <b>alcohol</b> drinking rats, as reported earlier, but also increased the levels and enzymatic activity of <strong>ADH1</strong>, while ALDH2 remained unchanged.
+ADH1A	drug	alcohol	31018006	The increases in <strong>ADH1</strong> contribute to explaining the remarkable effect of fenofibrate in raising blood levels of acetaldehyde in <b>ethanol</b> consuming animals, in which a marked reduction of <b>alcohol</b> intake is recorded.
+ADH1A	drug	alcohol	31018006	Tras eso, se midieron los niveles hepáticos y actividades enzimáticas de <b>alcohol</b> deshidrogenasa (<strong>ADH1</strong>) y de aldehído deshidrogenasa (ALDH2).
+ADH1A	drug	alcohol	31018006	Los resultados muestran que el tratamiento con fenofibrato no solo aumenta la actividad de catalasa en el hígado de ratas bebedoras de <b>alcohol</b>, sino que también incrementa los niveles y la actividad de <strong>ADH1</strong>, sin alterar ALDH2.
+ADH1A	drug	alcohol	31002879	The association between <b>alcohol</b> metabolism and genetic variants of <strong>ADH1A</strong>, SRPRB, and PGM1 in Korea.
+ADH1A	drug	alcohol	31002879	We identified variations in the <strong>ADH1A</strong>, SRPRB, and PGM1 genes, which are directly associated with blood <b>alcohol</b> or acetaldehyde concentrations.
+ADH1A	drug	alcohol	31002879	Namely, the T allele of SRPRB rs17376019 and the C allele of PGM1 rs4643 were associated with lower blood <b>alcohol</b> levels, while the <strong>ADH1</strong> rs1229976 C allele group exhibited markedly higher blood acetaldehyde levels than those of the <strong>ADH1</strong> rs1229976 T allele group.
+ADH1A	drug	alcohol	31002879	This study demonstrates that genetic variations in <strong>ADH1A</strong>, SRPRB, and PGM1 are associated with variations in blood <b>alcohol</b> and acetaldehyde concentration after <b>alcohol</b> intake.
+ADH1A	drug	alcohol	30470859	Gene expression of enzymes involved in the metabolism of <b>ethanol</b>, i.e., <strong>Adh1</strong> and Aldh2, were altered by hypothyroidism and T4/T3 supplementation.
+ADH1A	drug	alcohol	29431616	Pxr null mice displayed higher basal mRNA levels of hepatic lipogenic transcription factor sterol regulatory element binding protein 1c (Srebp 1c) and its target stearoyl CoA desaturase 1 (Scd1) and the lipid peroxide detoxifying aldo keto reductase 1b7 (Akr1b7) and higher protein levels of EtOH metabolizing <b>alcohol</b> dehydrogenase 1 (<strong>ADH1</strong>).
+ADH1A	addiction	intoxication	29431616	In contrast, Pxr null mice displayed increased Akr1b7 gene and <strong>ADH1</strong> protein expression and hypertriglyceridemia following <b>binge</b> EtOH exposure.
+ADH1A	drug	alcohol	28815635	In this study, we assessed sequencing variants in the ADH genomic region (<strong>ADH1</strong> 7) and tested for their associations with AUD phenotypes in 2 independent populations: an American Indian (AI) community sample and an EA cohort from the San Francisco Family <b>Alcohol</b> Study.
+ADH1A	drug	alcohol	28810607	Intriguingly, 1% <b>ethanol</b> intake remarkably elevated (10 fold, P<0.05) mRNA of brain <b>alcohol</b> dehydrogenase 1 (<strong>Adh1</strong>), which metabolizes lipid peroxidation products and is involved in the synthesis of retinoic acid, a neuroprotective factor.
+ADH1A	drug	alcohol	27538709	Chronic plus binge <b>ethanol</b> exposure increased the expression of <strong>ADH1</strong> and CYP2E1.
+ADH1A	addiction	intoxication	27538709	Chronic plus <b>binge</b> ethanol exposure increased the expression of <strong>ADH1</strong> and CYP2E1.
+ADH1A	drug	alcohol	25270064	We assessed ancestry admixture and tested for associations between <b>alcohol</b> related phenotypes in the genomic regions around the <strong>ADH1</strong> 7 and ALDH2 and ALDH1A1 genes.
+ADH1A	drug	alcohol	23847486	Gene specific modifications reviewed here show that an increased liver generation of acetaldehyde (by transduction of a gene coding for a high activity liver <b>alcohol</b> dehydrogenase <strong>ADH1</strong>(*)B2) leads to increased blood acetaldehyde levels and aversion to <b>ethanol</b> in animals.
+ADH1A	addiction	aversion	23847486	Gene specific modifications reviewed here show that an increased liver generation of acetaldehyde (by transduction of a gene coding for a high activity liver alcohol dehydrogenase <strong>ADH1</strong>(*)B2) leads to increased blood acetaldehyde levels and <b>aversion</b> to ethanol in animals.
+ADH1A	drug	alcohol	23468174	Humans express at least seven <b>alcohol</b> dehydrogenase (ADH) isoforms that are encoded by ADH gene cluster (ADH7 ADH1C ADH1B <strong>ADH1A</strong> ADH6 ADH4 ADH5) at chromosome 4.
+ADH1A	drug	alcohol	20828554	The <b>ethanol</b> elimination rate is regulated by <b>alcohol</b> metabolizing enzymes, primarily <b>alcohol</b> dehydrogenase (<strong>ADH1</strong>), acetaldehyde dehydrogenase (ALDH), and cytochrome P450 (CYP2E1).
+ADH1A	drug	alcohol	20617019	The conventional view is that <b>alcohol</b> metabolism is carried out by <strong>ADH1</strong> (Class I) in the liver.
+ADH1A	drug	alcohol	20617019	Over the past three decades, vigorous attempts to identify the enzyme responsible for the non <strong>ADH1</strong> pathway have focused on the microsomal <b>ethanol</b> oxidizing system (MEOS) and catalase, but have failed to clarify their roles in systemic <b>alcohol</b> metabolism.
+ADH1A	drug	alcohol	20617019	When various doses of <b>ethanol</b> are administered to mice, liver ADH3 activity is dynamically regulated through induction or kinetic activation, while <strong>ADH1</strong> activity is markedly lower at high doses (3 5 g/kg).
+ADH1A	drug	alcohol	20617019	These data suggest that ADH3 plays a dynamic role in <b>alcohol</b> metabolism, either collaborating with <strong>ADH1</strong> or compensating for the reduced role of <strong>ADH1</strong>.
+ADH1A	drug	alcohol	20617019	A complex two ADH model that ascribes total liver ADH activity to both <strong>ADH1</strong> and ADH3 explains the dose dependent changes in the pharmacokinetic parameters (beta, CL(T), AUC) of blood <b>ethanol</b> very well, suggesting that <b>alcohol</b> metabolism in mice is primarily governed by these two ADHs.
+ADH1A	drug	alcohol	20617019	In patients with <b>alcoholic</b> liver disease, liver ADH3 activity increases, while <strong>ADH1</strong> activity decreases, as <b>alcohol</b> intake increases.
+ADH1A	drug	alcohol	20617019	These data suggest that chronic binge drinking and the resulting liver disease shifts the key enzyme in <b>alcohol</b> metabolism from low K(m) <strong>ADH1</strong> to high K(m) ADH3, thereby reducing the rate of <b>alcohol</b> metabolism.
+ADH1A	addiction	intoxication	20617019	These data suggest that chronic <b>binge</b> drinking and the resulting liver disease shifts the key enzyme in alcohol metabolism from low K(m) <strong>ADH1</strong> to high K(m) ADH3, thereby reducing the rate of alcohol metabolism.
+ADH1A	drug	alcohol	20617019	The interdependent increase in the ADH3/<strong>ADH1</strong> activity ratio and AUC may be a factor in the development of <b>alcoholic</b> liver disease.
+ADH1A	addiction	dependence	19526455	<strong>ADH1A</strong> variation predisposes to personality traits and substance <b>dependence</b>.
+ADH1A	drug	alcohol	19526455	Recently, significant associations between <b>alcohol</b> dehydrogenase type 1A gene (<strong>ADH1A</strong>) and SD have been reported, which led us to investigate the impact of <strong>ADH1A</strong> variation on personality traits and risk of SD.
+ADH1A	drug	alcohol	19489444	<b>Alcohol</b> metabolism is known to be mainly carried out by the classic <strong>ADH1</strong> (Class I) of the liver.
+ADH1A	drug	alcohol	19489444	Over the past three decades, vigorous attempts to identify the enzyme responsible for the non <strong>ADH1</strong> pathway have focused on the microsomal oxidizing system (MEOS) and catalase, but have failed to clarify their roles in systemic <b>alcohol</b> metabolism.
+ADH1A	drug	alcohol	19489444	By acute administrations of <b>ethanol</b> to mice at various doses, liver ADH3 activity was dynamically regulated through induction or kinetic activation, though <strong>ADH1</strong> activity was markedly decreased at higher doses (3   5 g/kg).
+ADH1A	drug	alcohol	19489444	These data suggest that ADH3 plays a dynamical share in <b>alcohol</b> metabolism with <strong>ADH1</strong>, collaborating with it or supplementing the decreased role of <strong>ADH1</strong>.
+ADH1A	drug	alcohol	19489444	The two ADH complex model, which ascribes total liver ADH activity to both <strong>ADH1</strong> and ADH3, explained well the dose dependent changes in pharmacokinetic parameters (beta, CL(T), AUC) of blood <b>ethanol</b>, suggesting that <b>alcohol</b> metabolism in mice is primarily governed by the two ADHs.
+ADH1A	drug	alcohol	19489444	In patients with <b>alcoholic</b> liver diseases, the liver ADH3 activity increased but the <strong>ADH1</strong> activity decreased with an increase in <b>alcohol</b> intake.
+ADH1A	drug	alcohol	19489444	These data suggest that heavy and chronic drinking shifts the main enzyme in <b>alcohol</b> metabolism from low Km <strong>ADH1</strong> to high Km ADH3 to develop <b>alcoholic</b> liver diseases by the nonlinear increase in AUC due to the decrease of the metabolic rate.
+ADH1A	drug	alcohol	19193628	Alleles of ADH7 SNPs were associated with the early stages of <b>alcohol</b> metabolism, with additional effects in the <strong>ADH1A</strong>, ADH1B and ADH4 regions.
+ADH1A	drug	alcohol	16571603	Haplotype tag SNPs were selected for the block in the ADH4 gene that provided evidence of association and subsequently used in association analysis; the haplotype was significantly associated with <b>alcoholism</b> (P=0.01) There was weaker evidence that variations in <strong>ADH1A</strong> and ADH1B might also play a role in modifying risk.
+ADH1A	drug	alcohol	16431092	<b>Alcohol</b> metabolism in vivo cannot be explained solely by the action of the classical <b>alcohol</b> dehydrogenase, Class I ADH (<strong>ADH1</strong>).
+ADH1A	drug	alcohol	16431092	Over the past three decades, attempts to identify the metabolizing enzymes responsible for the <strong>ADH1</strong> independent pathway have focused on the microsomal <b>ethanol</b> oxidizing system (MEOS) and catalase, but have failed to clarify their roles in systemic <b>alcohol</b> metabolism.
+ADH1A	drug	alcohol	12095699	Distal and proximal cis linked sequences are needed for the total expression phenotype of the mouse <b>alcohol</b> dehydrogenase 1 (<strong>Adh1</strong>) gene.
+ADH1A	drug	alcohol	12095699	Mouse <b>alcohol</b> dehydrogenase 1 (<strong>Adh1</strong>) gene expression occurs at high levels in liver and adrenal, moderate levels in kidney and intestine, low levels in a number of other tissues, and is undetectable in thymus, spleen and brain by Northern analysis.
+ADH1A	drug	alcohol	11960985	Here we have examined mice for the effect of either acute <b>ethanol</b> intoxication or <strong>Adh1</strong> gene disruption on RA synthesis and degradation.
+ADH1A	addiction	intoxication	11960985	Here we have examined mice for the effect of either acute ethanol <b>intoxication</b> or <strong>Adh1</strong> gene disruption on RA synthesis and degradation.
+ADH1A	drug	alcohol	11960985	RA produced in <strong>Adh1</strong> null mutant mice following a 50 mg/kg dose of retinol was reduced 82% relative to wild type mice, thus similar to wild type mice pretreated with <b>ethanol</b>.
+ADH1A	drug	alcohol	11960985	Reduced RA production was associated with increased retinol levels in both <b>ethanol</b> treated wild type mice and <strong>Adh1</strong> null mutant mice, indicating reduced clearance of the retinol dose.
+ADH1A	drug	alcohol	11960985	RA degradation following a dose of RA (10 mg/kg) was increased only 42% by <b>ethanol</b> pretreatment (3.5 g/kg) and only 26% in <strong>Adh1</strong> null mutant mice relative to wild type mice.
+ADH1A	drug	alcohol	11253427	Repetitive gametic selection for a higher frequency of the <strong>Adh1</strong> S semilethal mutant allele of the <b>alcohol</b> dehydrogenase (ADH) gene yielded viable homozygotes <strong>Adh1</strong> SS.
+TUBB4A	drug	alcohol	7515684	Four of thes are the same types of double helices as previously found in <b>ethanol</b> (i.e., a symmetric left handed parallel <strong>beta 5</strong>.6 double helix, an unsymmetric left handed parallel <strong>beta 5</strong>.6 double helix, a symmetric left handed antiparallel <strong>beta 5</strong>.6 double helix, a symmetric right handed parallel <strong>beta 5</strong>.6 double helix); the fifth is possibly a symmetric right handed antiparallel <strong>beta 5</strong>.6 double helix.
+PPARG	drug	alcohol	32445052	Proinflammatory processes have been implicated in <b>alcohol</b> addiction, craving, and relapse, while studies in experimental animals have suggested that activation of <strong>peroxisome proliferator activated receptor gamma</strong> (PPARγ) inhibits proinflammatory signaling.
+PPARG	addiction	addiction	32445052	Proinflammatory processes have been implicated in alcohol <b>addiction</b>, craving, and relapse, while studies in experimental animals have suggested that activation of <strong>peroxisome proliferator activated receptor gamma</strong> (PPARγ) inhibits proinflammatory signaling.
+PPARG	addiction	relapse	32445052	Proinflammatory processes have been implicated in alcohol addiction, <b>craving</b>, and <b>relapse</b>, while studies in experimental animals have suggested that activation of <strong>peroxisome proliferator activated receptor gamma</strong> (PPARγ) inhibits proinflammatory signaling.
+PPARG	drug	alcohol	30195735	Among them, drugs interacting with acylethanolamide receptors including cannabinoid CB1 receptor antagonists/inverse agonists, peroxisome proliferator activated receptor alpha (PPARα) agonists or <strong>peroxisome proliferator activated receptor gamma</strong> (PPARγ) agonists have demonstrated utility in the reduction of <b>alcohol</b> intake in animal models.
+PPARG	drug	cannabinoid	30195735	Among them, drugs interacting with acylethanolamide receptors including <b>cannabinoid</b> CB1 receptor antagonists/inverse agonists, peroxisome proliferator activated receptor alpha (PPARα) agonists or <strong>peroxisome proliferator activated receptor gamma</strong> (PPARγ) agonists have demonstrated utility in the reduction of alcohol intake in animal models.
+PPARG	drug	alcohol	28220523	<strong>Peroxisome proliferator activated receptor gamma</strong> (PPARγ) plays a complex role in lipid metabolism and inflammation; therefore, the purpose of this study was to dissect its role in regulating steatosis and neutrophil infiltration in a clinically relevant mouse steatohepatitis model of 3 month high fat diet (HFD) feeding plus a binge of <b>ethanol</b> (HFD plus binge <b>ethanol</b>).
+PPARG	addiction	intoxication	28220523	<strong>Peroxisome proliferator activated receptor gamma</strong> (PPARγ) plays a complex role in lipid metabolism and inflammation; therefore, the purpose of this study was to dissect its role in regulating steatosis and neutrophil infiltration in a clinically relevant mouse steatohepatitis model of 3 month high fat diet (HFD) feeding plus a <b>binge</b> of ethanol (HFD plus <b>binge</b> ethanol).
+PPARG	drug	alcohol	28220523	Hepatocyte specific <strong>Pparg</strong> disruption reduced liver steatosis but surprisingly increased hepatic neutrophil infiltration after HFD plus binge <b>ethanol</b>.
+PPARG	addiction	intoxication	28220523	Hepatocyte specific <strong>Pparg</strong> disruption reduced liver steatosis but surprisingly increased hepatic neutrophil infiltration after HFD plus <b>binge</b> ethanol.
+PPARG	drug	alcohol	28220523	Moreover, hepatocyte specific deletion of the <strong>Pparg</strong> gene, but not the fat specific protein 27 gene, markedly up regulated hepatic levels of the gene for chemokine (C X C motif) ligand 1 (Cxcl1, a chemokine for neutrophil infiltration) in HFD plus binge <b>ethanol</b> fed mice.
+PPARG	addiction	intoxication	28220523	Moreover, hepatocyte specific deletion of the <strong>Pparg</strong> gene, but not the fat specific protein 27 gene, markedly up regulated hepatic levels of the gene for chemokine (C X C motif) ligand 1 (Cxcl1, a chemokine for neutrophil infiltration) in HFD plus <b>binge</b> ethanol fed mice.
+PPARG	drug	cocaine	27939396	A Role for <strong>Peroxisome Proliferator Activated Receptor Gamma</strong> Coactivator 1α in Nucleus Accumbens Neuron Subtypes in <b>Cocaine</b> Action.
+PPARG	drug	cocaine	27939396	Molecules critically involved in <b>cocaine</b> behavioral plasticity are known to regulate and interact with <strong>peroxisome proliferator activated receptor gamma</strong> coactivator 1α (PGC 1α).
+PPARG	drug	opioid	27714428	We recently demonstrated that activation of <strong>peroxisome proliferator activated receptor gamma</strong> (PPARγ) by pioglitazone reduces the motivation for <b>heroin</b> and attenuates its rewarding properties.
+PPARG	drug	alcohol	26968209	The <b>ethanol</b> feeding induced liver fat accumulation and mRNA expression of hepatic <strong>Pparg2</strong> in WT mice, which suggests that a high level of PPARγ2 is a common driving force for fat accumulation induced by <b>ethanol</b> or a high fat diet.
+PPARG	drug	alcohol	26968209	Interestingly, <b>ethanol</b> fed SHP( / ) mice displayed hepatic fat accumulation similar to that of <b>ethanol</b> fed WT mice, even though their <strong>Pparg2</strong> expression level remained lower.
+PPARG	drug	alcohol	26099526	Inhibition of <strong>PPARG</strong> and cyclic AMP responsive element binding protein H (CREBH) prevented the increases in Fsp27α and FSP27β mRNAs, respectively, and reduced liver injury in this chronic plus binge <b>ethanol</b> feeding model.
+PPARG	addiction	intoxication	26099526	Inhibition of <strong>PPARG</strong> and cyclic AMP responsive element binding protein H (CREBH) prevented the increases in Fsp27α and FSP27β mRNAs, respectively, and reduced liver injury in this chronic plus <b>binge</b> ethanol feeding model.
+PPARG	drug	alcohol	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different PPAR genes (PPARA, PPARD, <strong>PPARG</strong>, and PPARGC1A) with 2 phenotypes: DSM IV <b>alcohol</b> dependence (AD) and the DSM IV criterion of withdrawal.
+PPARG	addiction	dependence	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of Alcoholism (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different PPAR genes (PPARA, PPARD, <strong>PPARG</strong>, and PPARGC1A) with 2 phenotypes: DSM IV alcohol <b>dependence</b> (AD) and the DSM IV criterion of withdrawal.
+PPARG	addiction	withdrawal	25516156	Data from a human genome wide association study (GWAS) completed in the Collaborative Study on the Genetics of Alcoholism (COGA) were then used to analyze the association of single nucleotide polymorphisms (SNPs) in different PPAR genes (PPARA, PPARD, <strong>PPARG</strong>, and PPARGC1A) with 2 phenotypes: DSM IV alcohol dependence (AD) and the DSM IV criterion of <b>withdrawal</b>.
+PPARG	drug	alcohol	25516156	The GWAS from COGA supported an association of SNPs in PPARA and <strong>PPARG</strong> with <b>alcohol</b> withdrawal and PPARGC1A with AD but found no association for PPARD with either phenotype.
+PPARG	addiction	withdrawal	25516156	The GWAS from COGA supported an association of SNPs in PPARA and <strong>PPARG</strong> with alcohol <b>withdrawal</b> and PPARGC1A with AD but found no association for PPARD with either phenotype.
+PPARG	drug	alcohol	25455889	On the other hand, berberine significantly blunted the lipid accumulation in liver due to chronic <b>alcohol</b> consumption, at least partially, through restoring peroxisome proliferator activated receptor α/<strong>peroxisome proliferator activated receptor gamma</strong> Co activator 1α and hepatocyte nuclear factor 4α/microsomal triglyceride transfer protein pathways.
+PPARG	drug	alcohol	19673747	A total of 258 male <b>alcoholics</b> (161 without liver disease and 97 with ALC) and 101 healthy controls were genotyped for the  94ins/delATTG NFKB1, 3' UTR+126G>A NFKBIA, and 34C>G <strong>PPARG2</strong> polymorphisms.
+PPARG	drug	cannabinoid	19457281	These include numerous G protein coupled receptors (mu  and delta opioid, alpha(2) adrenergic, purinergic A1, neuropeptide Y1 and Y2, <b>cannabinoid</b> CB1 and CB2, muscarinic M2, gamma amino butyric acid type B, metabotropic glutamate type II III, somatostatin) and perhaps nuclear receptors (<strong>peroxisome proliferator activated receptor gamma</strong>).
+PPARG	drug	opioid	19457281	These include numerous G protein coupled receptors (mu  and delta <b>opioid</b>, alpha(2) adrenergic, purinergic A1, neuropeptide Y1 and Y2, cannabinoid CB1 and CB2, muscarinic M2, gamma amino butyric acid type B, metabotropic glutamate type II III, somatostatin) and perhaps nuclear receptors (<strong>peroxisome proliferator activated receptor gamma</strong>).
+PPARG	addiction	sensitization	17710237	These results suggest that the PPARpan compounds may be expected to maintain the beneficial insulin <b>sensitization</b> effects of a <strong>PPARgamma</strong> agonist while either maintaining weight or producing weight loss.
+PPARG	drug	amphetamine	17019405	<strong>Peroxisome proliferator activated receptor gamma</strong> activation relieves expression of behavioral sensitization to <b>methamphetamine</b> in mice.
+PPARG	addiction	sensitization	17019405	<strong>Peroxisome proliferator activated receptor gamma</strong> activation relieves expression of behavioral <b>sensitization</b> to methamphetamine in mice.
+PPARG	drug	amphetamine	17019405	We examined the involvement of <strong>PPARgamma</strong>, one of the isotypes of PPAR, in development of behavioral sensitization to the stimulant effect of <b>methamphetamine</b> (<b>METH</b>) (1 mg/kg, subcutaneously) in mice.
+PPARG	addiction	sensitization	17019405	We examined the involvement of <strong>PPARgamma</strong>, one of the isotypes of PPAR, in development of behavioral <b>sensitization</b> to the stimulant effect of methamphetamine (METH) (1 mg/kg, subcutaneously) in mice.
+PPARG	drug	amphetamine	17019405	The protein level and the activity of <strong>PPARgamma</strong> were significantly increased in the nuclear fraction of whole brain after 5 days of <b>METH</b> administration (test day 5) and on withdrawal day 7 (test day 12).
+PPARG	addiction	withdrawal	17019405	The protein level and the activity of <strong>PPARgamma</strong> were significantly increased in the nuclear fraction of whole brain after 5 days of METH administration (test day 5) and on <b>withdrawal</b> day 7 (test day 12).
+PPARG	addiction	sensitization	17019405	In addition, the magnitude of expression of behavioral <b>sensitization</b> was augmented by treatments with GW9662 (a <strong>PPARgamma</strong> antagonist; 0.5 5.0 microg i.c.v., once daily) during the withdrawal period.
+PPARG	addiction	withdrawal	17019405	In addition, the magnitude of expression of behavioral sensitization was augmented by treatments with GW9662 (a <strong>PPARgamma</strong> antagonist; 0.5 5.0 microg i.c.v., once daily) during the <b>withdrawal</b> period.
+PPARG	drug	amphetamine	17019405	These results suggest that <strong>PPARgamma</strong> has a significant role in the expression of behavioral sensitization to <b>METH</b> in mice.
+PPARG	addiction	sensitization	17019405	These results suggest that <strong>PPARgamma</strong> has a significant role in the expression of behavioral <b>sensitization</b> to METH in mice.
+PPARG	addiction	sensitization	15318101	<strong>Peroxisome proliferator activated receptor gamma</strong> (PPAR gamma), which is a ligand dependent transcriptional factor, forms a heterodimer with retinoid X receptor (RXR) and controls many genes that are relevant to the regulation of lipid metabolism and insulin <b>sensitization</b>.
+PPARG	drug	alcohol	12805475	Prevention of <b>ethanol</b> induced liver injury in rats by an agonist of <strong>peroxisome proliferator activated receptor gamma</strong>, pioglitazone.
+LPO	drug	alcohol	32651817	We studied <strong>LPO</strong> intensity and respiration of mitochondria in brain and heart cells of rats receiving 5% <b>ethanol</b> for 20 weeks and treated with derivatives of neuroactive amino acids.
+LPO	drug	alcohol	32651817	Chronic semicompulsory <b>alcohol</b> intoxication increased the concentration of <strong>LPO</strong> products in cardiac and cerebral mitochondria by 46 and 45% (diene conjugates), by 97 and 8% (diketones), and by 28 and 81% (malondialdehyde), respectively, reduced activity of antioxidant enzymes in cardiac and cerebral mitochondria by 24 and 45% (glutathione peroxidase) and by 22 and 26% (superoxide dismutase), respectively, and uncoupled the process of respiration and ATP synthesis, which manifested in a decrease in respiratory control (V3/V4 ratio according to Chance).
+LPO	addiction	intoxication	32651817	Chronic semicompulsory alcohol <b>intoxication</b> increased the concentration of <strong>LPO</strong> products in cardiac and cerebral mitochondria by 46 and 45% (diene conjugates), by 97 and 8% (diketones), and by 28 and 81% (malondialdehyde), respectively, reduced activity of antioxidant enzymes in cardiac and cerebral mitochondria by 24 and 45% (glutathione peroxidase) and by 22 and 26% (superoxide dismutase), respectively, and uncoupled the process of respiration and ATP synthesis, which manifested in a decrease in respiratory control (V3/V4 ratio according to Chance).
+LPO	addiction	reward	32009893	Its direct and indirect projections to the ventral tegmental area (VTA) suggest that the <strong>LPO</strong> could modulate the activity of the VTA and the <b>reward</b> related behaviors that the VTA underlies.
+LPO	drug	cocaine	32009893	We examined the role of the <strong>LPO</strong> on reward taking and seeking using operant self administration of <b>cocaine</b> or sucrose.
+LPO	addiction	relapse	32009893	We examined the role of the <strong>LPO</strong> on reward taking and <b>seeking</b> using operant self administration of cocaine or sucrose.
+LPO	addiction	reward	32009893	We examined the role of the <strong>LPO</strong> on <b>reward</b> taking and seeking using <b>operant</b> self administration of cocaine or sucrose.
+LPO	addiction	relapse	32009893	We tested if stimulating the <strong>LPO</strong> pharmacologically with bicuculline or chemogenetically with Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) modifies self administration and/or <b>seeking</b>.
+LPO	drug	cocaine	32009893	In another set of experiments, we tested if manipulating the <strong>LPO</strong> influences <b>cocaine</b> self administration during and after punishment.
+LPO	addiction	addiction	32009893	In another set of experiments, we tested if manipulating the <strong>LPO</strong> influences cocaine self administration during and after <b>punishment</b>.
+LPO	drug	cocaine	32009893	We found that stimulating the <strong>LPO</strong> reinstated <b>cocaine</b> and sucrose seeking behavior but had no effect on reward intake.
+LPO	addiction	relapse	32009893	We found that stimulating the <strong>LPO</strong> reinstated cocaine and sucrose <b>seeking</b> behavior but had no effect on reward intake.
+LPO	addiction	reward	32009893	We found that stimulating the <strong>LPO</strong> reinstated cocaine and sucrose seeking behavior but had no effect on <b>reward</b> intake.
+LPO	drug	cocaine	32009893	Furthermore, both stimulating and inhibiting the <strong>LPO</strong> prevented the sustained reduction in <b>cocaine</b> intake seen after punishment.
+LPO	addiction	addiction	32009893	Furthermore, both stimulating and inhibiting the <strong>LPO</strong> prevented the sustained reduction in cocaine intake seen after <b>punishment</b>.
+LPO	addiction	addiction	32009893	These findings indicate that the <strong>LPO</strong> has the capacity to drive reward seeking, modulate sustained reductions in self administration following <b>punishment</b>, and regulate the activity of VTA neurons.
+LPO	addiction	relapse	32009893	These findings indicate that the <strong>LPO</strong> has the capacity to drive reward <b>seeking</b>, modulate sustained reductions in self administration following punishment, and regulate the activity of VTA neurons.
+LPO	addiction	reward	32009893	These findings indicate that the <strong>LPO</strong> has the capacity to drive <b>reward</b> seeking, modulate sustained reductions in self administration following punishment, and regulate the activity of VTA neurons.
+LPO	addiction	reward	32009893	Taken together, these findings implicate the <strong>LPO</strong> as a previously overlooked member of the <b>reward</b> circuit.
+LPO	drug	alcohol	31096703	According to our findings, <b>ethanol</b> triggered reactive oxygen species (ROS), apoptosis, neuroinflammation, and memory impairment, which were significantly inhibited with the administration of curcumin, as assessed by ROS, lipid peroxidation (<strong>LPO</strong>), and Nrf2/HO 1 (nuclear factor erythroid 2 related factor 2/Heme oxygenase 1) expression in the experimental mice brains.
+LPO	drug	psychedelics	31001375	The present findings demonstrate that the early hours of <b>ketamine</b> withdrawal induced oxidative biochemistry unbalance in the blood samples, with elevated levels of nitrite and <strong>LPO</strong>.
+LPO	addiction	withdrawal	31001375	The present findings demonstrate that the early hours of ketamine <b>withdrawal</b> induced oxidative biochemistry unbalance in the blood samples, with elevated levels of nitrite and <strong>LPO</strong>.
+LPO	addiction	intoxication	30911348	The present findings demonstrate that the <b>binge</b> drinking protocol induced oxidative biochemistry misbalance, from the decrease of TEAC levels and higher <strong>LPO</strong> related to tissue damage and motor impairment.
+LPO	drug	alcohol	30584872	Chronic <b>alcohol</b> intoxication aggravates the neurodegeneration, significantly reducing the indices of the neuroglial index, the number of functioning vessels and activating the <strong>LPO</strong> processes.
+LPO	addiction	intoxication	30584872	Chronic alcohol <b>intoxication</b> aggravates the neurodegeneration, significantly reducing the indices of the neuroglial index, the number of functioning vessels and activating the <strong>LPO</strong> processes.
+LPO	addiction	addiction	29700637	It was recently shown that unilateral infusion of the GABAA receptor antagonist, bicuculline, into the <strong>LPO</strong> strongly invigorates exploratory locomotion, whereas bicuculline infused unilaterally into the VP has a negligible locomotor effect, but when infused bilaterally, produces vigorous, abnormal pivoting and gnawing movements and <b>compulsive</b> ingestion.
+LPO	drug	amphetamine	29700637	We observed that bilateral <strong>LPO</strong> infusions of bicuculline activate exploratory locomotion only slightly more potently than unilateral infusions and that unilateral and bilateral <strong>LPO</strong> injections of the GABAA receptor agonist muscimol potently suppress basal locomotion, but only modestly inhibit locomotion invigorated by <b>amphetamine</b>.
+LPO	addiction	reward	29352865	The results showed that treatment with <b>CPP</b> 2 could improve blood lipid levels (TC, TG, HDL C and LDL C), liver lipid levels (TC and TG) and antioxidant status (SOD, T AOC, GSH PX, MDA and <strong>LPO</strong>).
+LPO	addiction	intoxication	28706418	NAR administration prevented increases in ALT, AP, γ GTP, and GPx enzymatic activity; depletion of GSH and glycogen; and increases in <strong>LPO</strong> and collagen produced by chronic CCl4 <b>intoxication</b> (P < 0.05).
+LPO	drug	opioid	26288306	To evaluate gender effects on the correlation between cortisol, molecular products of lipid peroxidation (<strong>LPO</strong>) and carbonylation of proteins in patients with <b>heroin</b> addiction.
+LPO	addiction	addiction	26288306	To evaluate gender effects on the correlation between cortisol, molecular products of lipid peroxidation (<strong>LPO</strong>) and carbonylation of proteins in patients with heroin <b>addiction</b>.
+LPO	drug	alcohol	23955400	In addition, <b>ethanol</b> administration enhanced lipid peroxidation (<strong>LPO</strong>) process assessed by the accumulation of malondialdehyde (MDA) in the testis.
+LPO	drug	alcohol	23955400	Interestingly, co administration of KV with <b>ethanol</b> led to almost complete inhibition of testicular <strong>LPO</strong> thereby enhancing antioxidant status of the testis.
+LPO	addiction	intoxication	18703112	The <b>intoxication</b> of Cd(II) lead to the enhanced production of <strong>LPO</strong> and PCO, treatment with EM1 can effectively ameliorate the increase of <strong>LPO</strong> and PCO compared to the Cd(II) group.
+LPO	drug	opioid	17639720	The state of an enzymatic component of the antioxidant system, intencity of lipid peroxidation (<strong>LPO</strong>) in the liver, nitric oxide level in blood plasma were investigated in rats subjected to chronic <b>morphine</b> intoxication.
+LPO	addiction	intoxication	17639720	The state of an enzymatic component of the antioxidant system, intencity of lipid peroxidation (<strong>LPO</strong>) in the liver, nitric oxide level in blood plasma were investigated in rats subjected to chronic morphine <b>intoxication</b>.
+LPO	drug	alcohol	17585507	<b>Ethanol</b> consumption significantly lowered the SOD and CAT activities in both the age groups, whereas a significant increase was observed in the XOD and <strong>LPO</strong> levels.
+LPO	drug	alcohol	17585507	In contrast, the combination of exercise training plus <b>ethanol</b> lowered XOD and <strong>LPO</strong> levels in both the age groups of rats compared to <b>ethanol</b> treated rats.
+LPO	drug	alcohol	12660848	<strong>LPO</strong> and <b>ethanol</b> biotransformation systems in the liver as markers of predisposition to <b>ethanol</b> hepatotoxicity.
+LPO	drug	alcohol	12660848	A relationship between congenital activity of <strong>LPO</strong> processes in rat liver (before <b>ethanol</b> intoxication) and the type and severity of <b>ethanol</b> induced damage to the liver was demonstrated using methods of mathematical modeling.
+LPO	addiction	intoxication	12660848	A relationship between congenital activity of <strong>LPO</strong> processes in rat liver (before ethanol <b>intoxication</b>) and the type and severity of ethanol induced damage to the liver was demonstrated using methods of mathematical modeling.
+LPO	drug	opioid	11780318	Determined and compared plasma levels of nitric oxide (P NO), vitamin C (P VC), vitamin E (P VE), beta carotene (P beta CAR), lipoperoxides (P <strong>LPO</strong>) and erythrocyte activities of superoxide dismutase (E SOD), catalase (E CAT), glutathione peroxidase (E GSH Px) and erythrocyte level of lipoperoxides (E <strong>LPO</strong>) in 137 cases of <b>heroin</b> abusers (HAs) and 100 cases of healthy volunteers (HVs), used linear regression and correlation, stepwise regression and correlation to analyze correlation among <b>heroin</b> abusing duration (HAD), daily <b>heroin</b> abusing quantity (DHAQ) with above determination values in the HAs.
+LPO	drug	opioid	11055015	To further reveal the risks of <b>heroin</b> abuse to human body, and to determine the injuries of oxidation, peroxidation and lipoperoxidation induced by nitric oxide and other free radicals to <b>heroin</b> abusers, we determined and compared plasma values of lipoperoxides (<strong>LPO</strong>), nitric oxide (NO), vitamin C (VC), vitamin E (VE), beta carotene (beta CAR) and erythrocyte values of <strong>LPO</strong>, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH Px) in 114 <b>heroin</b> abusers and 100 healthy volunteers.
+LPO	drug	opioid	11055015	The results showed that, compared with the healthy volunteer groups, the average plasma values of <strong>LPO</strong>, and NO, and the average erythrocyte value of <strong>LPO</strong> in the <b>heroin</b> abuser group were significantly increased (P < 0.0001), and the average plasma values of VC, VE, and beta CAR and the average erythrocyte values of SOD, CAT, and GSH Px were significantly decreased (P < 0.0001).
+LPO	drug	opioid	11055015	Analysis of linear regression and correlation showed that with prolonged <b>heroin</b> abusing and with increased daily quantity in the <b>heroin</b> abusers, the plasma values of <strong>LPO</strong>, and NO, and the erythrocyte value of <strong>LPO</strong> were gradually increased (P < 0.001), whereas the plasma values of VC, VE, and beta CAR and the erythrocyte values of SOD, CAT, and GSH Px were gradually decreased (P < 0.001).
+LPO	drug	alcohol	8058388	The effect of antibodies to serotonin on lipid peroxidation (<strong>LPO</strong>) in acute <b>alcoholic</b> intoxication was studied in rabbit experiments.
+LPO	addiction	intoxication	8058388	The effect of antibodies to serotonin on lipid peroxidation (<strong>LPO</strong>) in acute alcoholic <b>intoxication</b> was studied in rabbit experiments.
+LPO	drug	alcohol	1305455	<b>Ethanol</b>, 1 g/kg, increased <strong>LPO</strong> levels in the 14 day embryonic brain, whereas its dose of 3 g/kg decreased them.
+LPO	drug	opioid	1363943	Diverse behavioral disorders and the intensity of lipid peroxidation (<strong>LPO</strong>) of biological membranes were estimated in different rat tissues after the 7 day administration and subsequent withdrawal of <b>morphine</b> or promedol.
+LPO	addiction	withdrawal	1363943	Diverse behavioral disorders and the intensity of lipid peroxidation (<strong>LPO</strong>) of biological membranes were estimated in different rat tissues after the 7 day administration and subsequent <b>withdrawal</b> of morphine or promedol.
+KCNJ6	drug	cocaine	30837265	Overexpression of GIRK3 decreased somatodendritic GABABR  and D2R dependent signaling and increased <b>cocaine</b> induced locomotor activity, whereas overexpression of <strong>GIRK2</strong> increased GABABR dependent signaling and decreased <b>cocaine</b> induced locomotion.
+KCNJ6	drug	cocaine	30837265	Together, these data show that behavioral sensitivity to <b>cocaine</b> in mice is inversely proportional to the strength of GIRK channel activity in VTA DA neurons and suggest that direct activators of the unique VTA DA neuron GIRK channel subtype (<strong>GIRK2</strong>/GIRK3 heteromer) could represent a promising therapeutic target for treatment of addiction.SIGNIFICANCE STATEMENT Inhibitory G protein signaling in dopamine (DA) neurons, including that mediated by G protein gated inwardly rectifying K+ (GIRK) channels, has been implicated in behavioral sensitivity to <b>cocaine</b>.
+KCNJ6	addiction	addiction	30837265	Together, these data show that behavioral sensitivity to cocaine in mice is inversely proportional to the strength of GIRK channel activity in VTA DA neurons and suggest that direct activators of the unique VTA DA neuron GIRK channel subtype (<strong>GIRK2</strong>/GIRK3 heteromer) could represent a promising therapeutic target for treatment of <b>addiction</b>.SIGNIFICANCE STATEMENT Inhibitory G protein signaling in dopamine (DA) neurons, including that mediated by G protein gated inwardly rectifying K+ (GIRK) channels, has been implicated in behavioral sensitivity to cocaine.
+KCNJ6	addiction	reward	27993610	A <strong>KCNJ6</strong> gene polymorphism modulates theta oscillations during <b>reward</b> processing.
+KCNJ6	drug	alcohol	27993610	A recent family genome wide association study (GWAS) by the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) found that theta EROs during visual target detection were associated at genome wide levels with several single nucleotide polymorphisms (SNPs), including a synonymous SNP, rs702859, in the <strong>KCNJ6</strong> gene that encodes GIRK2, a G protein inward rectifying potassium channel that regulates excitability of neuronal networks.
+KCNJ6	drug	alcohol	27993610	A recent family genome wide association study (GWAS) by the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) found that theta EROs during visual target detection were associated at genome wide levels with several single nucleotide polymorphisms (SNPs), including a synonymous SNP, rs702859, in the <strong>KCNJ6</strong> gene that encodes <strong>GIRK2</strong>, a G protein inward rectifying potassium channel that regulates excitability of neuronal networks.
+KCNJ6	addiction	reward	27993610	The present study examined the effect of the <strong>KCNJ6</strong> SNP (rs702859), previously associated with theta ERO to targets in a visual oddball task, on theta EROs during <b>reward</b> processing in a monetary gambling task.
+KCNJ6	addiction	reward	27993610	These findings indicate that variations in the <strong>KCNJ6</strong> SNP influence magnitude of theta oscillations at posterior loci during the evaluation of loss and gain, reflecting a genetic influence on neuronal circuits involved in <b>reward</b> processing.
+KCNJ6	drug	opioid	27061230	To examine whether certain genotypes were associated with this, we examined the frequencies of 29 SNPs located in candidate genes related to <b>opioid</b> pharmacology: ABCB1, OPRM1, UGT2B7, CYP3A5, CYP2B6, CYP2C19, CYP2D6, COMT, <strong>KCNJ6</strong> and SCN9A in 274 deceased patients with OA (DOA), 309 living patients with OA (LOA) and in 394 healthy volunteers (HV).
+KCNJ6	drug	alcohol	26490875	The <strong>Kir3.2</strong> channel, a member of the Kir3 subfamily of G protein activated potassium channels (GIRKs), plays several roles in the nervous system, including key responsibility in the GABAB pathway of inhibition, in pain perception pathways via opioid receptors, and is also involved in <b>alcoholism</b>.
+KCNJ6	drug	opioid	26490875	The <strong>Kir3.2</strong> channel, a member of the Kir3 subfamily of G protein activated potassium channels (GIRKs), plays several roles in the nervous system, including key responsibility in the GABAB pathway of inhibition, in pain perception pathways via <b>opioid</b> receptors, and is also involved in alcoholism.
+KCNJ6	drug	alcohol	26490875	The inwardly rectifying potassium 3.2 (<strong>Kir3.2</strong>) channel is found principally in neurons that regulate diverse brain functions, including pain perception, <b>alcoholism</b>, and substance addiction.
+KCNJ6	addiction	addiction	26490875	The inwardly rectifying potassium 3.2 (<strong>Kir3.2</strong>) channel is found principally in neurons that regulate diverse brain functions, including pain perception, alcoholism, and substance <b>addiction</b>.
+KCNJ6	drug	alcohol	26490875	The <strong>Kir3.2</strong> channel is subject to regulation by intracellular signals including sodium, G proteins, <b>ethanol</b>, the phospholipid phosphatidylinositol bis phosphate, and phosphorylation by protein kinases.
+KCNJ6	drug	opioid	25948263	Nevertheless, neither constitutive genetic ablation of Girk1 or <strong>Girk2</strong>, nor the selective ablation of GIRK channels in GABA neurons, diminished <b>morphine</b> induced motor activity in mice.
+KCNJ6	addiction	addiction	25948263	Collectively, these data support the contention that the unique GIRK channel subtype in VTA DA neurons, the <strong>GIRK2</strong>/GIRK3 heteromer, regulates the sensitivity of the mouse mesolimbic DA system to drugs with <b>addictive</b> potential.
+KCNJ6	drug	nicotine	25346042	Association between <strong>KCNJ6</strong> (GIRK2) gene polymorphism rs2835859 and post operative analgesia, pain sensitivity, and <b>nicotine</b> dependence.
+KCNJ6	addiction	dependence	25346042	Association between <strong>KCNJ6</strong> (GIRK2) gene polymorphism rs2835859 and post operative analgesia, pain sensitivity, and nicotine <b>dependence</b>.
+KCNJ6	drug	nicotine	25346042	Association between <strong>KCNJ6</strong> (<strong>GIRK2</strong>) gene polymorphism rs2835859 and post operative analgesia, pain sensitivity, and <b>nicotine</b> dependence.
+KCNJ6	addiction	dependence	25346042	Association between <strong>KCNJ6</strong> (<strong>GIRK2</strong>) gene polymorphism rs2835859 and post operative analgesia, pain sensitivity, and nicotine <b>dependence</b>.
+KCNJ6	drug	opioid	25346042	We focused on a GIRK channel subunit that plays a pivotal role in the brain, GIRK2, and investigated the contribution of genetic variations of the GIRK2 (<strong>KCNJ6</strong>) gene to individual differences in the sensitivity to <b>opioid</b> analgesia.
+KCNJ6	drug	opioid	25346042	We focused on a GIRK channel subunit that plays a pivotal role in the brain, <strong>GIRK2</strong>, and investigated the contribution of genetic variations of the <strong>GIRK2</strong> (<strong>KCNJ6</strong>) gene to individual differences in the sensitivity to <b>opioid</b> analgesia.
+KCNJ6	drug	amphetamine	25069259	The authors have focused on G protein activated inwardly rectifying potassium (GIRK) channel subunits, <strong>GIRK2</strong> and GIRK3, which are important molecules in opioid transmission, and found that the SNPs within the <strong>GIRK2</strong> and GIRK3 gene region were significantly associated with postoperative analgesic requirements, one of which was also associated with vulnerability to <b>methamphetamine</b> (<b>METH</b>) dependence.
+KCNJ6	drug	opioid	25069259	The authors have focused on G protein activated inwardly rectifying potassium (GIRK) channel subunits, <strong>GIRK2</strong> and GIRK3, which are important molecules in <b>opioid</b> transmission, and found that the SNPs within the <strong>GIRK2</strong> and GIRK3 gene region were significantly associated with postoperative analgesic requirements, one of which was also associated with vulnerability to methamphetamine (METH) dependence.
+KCNJ6	addiction	dependence	25069259	The authors have focused on G protein activated inwardly rectifying potassium (GIRK) channel subunits, <strong>GIRK2</strong> and GIRK3, which are important molecules in opioid transmission, and found that the SNPs within the <strong>GIRK2</strong> and GIRK3 gene region were significantly associated with postoperative analgesic requirements, one of which was also associated with vulnerability to methamphetamine (METH) <b>dependence</b>.
+KCNJ6	drug	opioid	24956254	Nevertheless many genetic factors have been investigated including those affecting its metabolism (CYP2B6 consistent results), efflux transport (P gp inconsistent results), target μ <b>opioid</b> receptor (μ <b>opioid</b> receptor inconsistent results) and a host of other receptors (DRD2) and signaling elements (<strong>GIRK2</strong> and ARRB2; not replicated).
+KCNJ6	drug	amphetamine	24946391	The authors have focused on G protein activated inwardly rectifying potassium (GIRK) channel subunits, <strong>GIRK2</strong> and GIRK3, that are important molecules in opioid transmission, and found that the single nucleotide polymorphisms (SNPs) within the <strong>GIRK2</strong> and GIRK3 gene regions were significantly associated with postoperative requirements of analgesics including opioids in patients who underwent abdominal surgery and mRNA expression of these genes in postmortem specimens, one of which was also associated with vulnerability to <b>methamphetamine</b> (<b>METH</b>) dependence.
+KCNJ6	drug	opioid	24946391	The authors have focused on G protein activated inwardly rectifying potassium (GIRK) channel subunits, <strong>GIRK2</strong> and GIRK3, that are important molecules in <b>opioid</b> transmission, and found that the single nucleotide polymorphisms (SNPs) within the <strong>GIRK2</strong> and GIRK3 gene regions were significantly associated with postoperative requirements of analgesics including <b>opioids</b> in patients who underwent abdominal surgery and mRNA expression of these genes in postmortem specimens, one of which was also associated with vulnerability to methamphetamine (METH) dependence.
+KCNJ6	addiction	dependence	24946391	The authors have focused on G protein activated inwardly rectifying potassium (GIRK) channel subunits, <strong>GIRK2</strong> and GIRK3, that are important molecules in opioid transmission, and found that the single nucleotide polymorphisms (SNPs) within the <strong>GIRK2</strong> and GIRK3 gene regions were significantly associated with postoperative requirements of analgesics including opioids in patients who underwent abdominal surgery and mRNA expression of these genes in postmortem specimens, one of which was also associated with vulnerability to methamphetamine (METH) <b>dependence</b>.
+KCNJ6	drug	opioid	23818182	The K(+) channel <strong>GIRK2</strong> is both necessary and sufficient for peripheral <b>opioid</b> mediated analgesia.
+KCNJ6	drug	alcohol	23712313	Studies continue to reveal other genes in which variants affect the risk of <b>alcoholism</b> or related traits, including GABRA2, CHRM2, <strong>KCNJ6</strong> and AUTS2.
+KCNJ6	drug	cocaine	21865468	While total <strong>Girk2</strong> and GABA(B)R1 mRNA and protein levels were unaltered by <b>cocaine</b> exposure in VTA DA neurons, the <b>cocaine</b> induced decrease in GABA(B)R Girk signaling correlated with a reduction in <strong>Girk2</strong> containing channels at the plasma membrane in VTA DA neurons.
+KCNJ6	drug	alcohol	21307845	<strong>KCNJ6</strong> is associated with adult <b>alcohol</b> dependence and involved in gene × early life stress interactions in adolescent <b>alcohol</b> drinking.
+KCNJ6	addiction	dependence	21307845	<strong>KCNJ6</strong> is associated with adult alcohol <b>dependence</b> and involved in gene × early life stress interactions in adolescent alcohol drinking.
+KCNJ6	drug	alcohol	21307845	Therefore, we sought to examine the role of <strong>KCNJ6</strong> polymorphisms in adult <b>alcohol</b> dependence and stress related <b>alcohol</b> abuse in adolescents.
+KCNJ6	addiction	dependence	21307845	Therefore, we sought to examine the role of <strong>KCNJ6</strong> polymorphisms in adult alcohol <b>dependence</b> and stress related alcohol abuse in adolescents.
+KCNJ6	drug	alcohol	21307845	We selected 11 SNPs in the promoter region of <strong>KCNJ6</strong>, which were genotyped in 1152 adult <b>alcohol</b> dependents and 1203 controls.
+KCNJ6	drug	alcohol	21307845	Our findings show that <strong>KCNJ6</strong> is associated with <b>alcohol</b> dependence and may moderate the effect of early psychosocial stress on risky <b>alcohol</b> drinking in adolescents.
+KCNJ6	addiction	dependence	21307845	Our findings show that <strong>KCNJ6</strong> is associated with alcohol <b>dependence</b> and may moderate the effect of early psychosocial stress on risky alcohol drinking in adolescents.
+KCNJ6	drug	cocaine	20557431	Despite differences in the contribution of Girk1 and <strong>Girk2</strong> subunits to Girk signaling in midbrain dopamine neurons, Girk1( / ) and <strong>Girk2</strong>( / ) mice exhibited comparable baseline hyperactivities and enhanced responses to <b>cocaine</b>.
+KCNJ6	addiction	reward	20557431	We conclude that dopamine dependent phenotypes in <strong>Girk2</strong>( / ) mice are not solely attributable to a loss of Girk signaling in dopamine neurons, and likely involve secondary adaptations facilitating glutamatergic signaling in the mesolimbic <b>reward</b> system.
+KCNJ6	drug	opioid	20220551	A <strong>KCNJ6</strong> (Kir3.2, GIRK2) gene polymorphism modulates <b>opioid</b> effects on analgesia and addiction but not on pupil size.
+KCNJ6	addiction	addiction	20220551	A <strong>KCNJ6</strong> (Kir3.2, GIRK2) gene polymorphism modulates opioid effects on analgesia and <b>addiction</b> but not on pupil size.
+KCNJ6	drug	opioid	20220551	A <strong>KCNJ6</strong> (Kir3.2, <strong>GIRK2</strong>) gene polymorphism modulates <b>opioid</b> effects on analgesia and addiction but not on pupil size.
+KCNJ6	addiction	addiction	20220551	A <strong>KCNJ6</strong> (Kir3.2, <strong>GIRK2</strong>) gene polymorphism modulates opioid effects on analgesia and <b>addiction</b> but not on pupil size.
+KCNJ6	drug	opioid	20220551	A <strong>KCNJ6</strong> (<strong>Kir3.2</strong>, <strong>GIRK2</strong>) gene polymorphism modulates <b>opioid</b> effects on analgesia and addiction but not on pupil size.
+KCNJ6	addiction	addiction	20220551	A <strong>KCNJ6</strong> (<strong>Kir3.2</strong>, <strong>GIRK2</strong>) gene polymorphism modulates opioid effects on analgesia and <b>addiction</b> but not on pupil size.
+KCNJ6	drug	opioid	20220551	<strong>KCNJ6</strong> coding for potassium inwardly rectifying channels (Kir3.2, GIRK2) is important for <b>opioid</b> receptor transmission.
+KCNJ6	drug	opioid	20220551	<strong>KCNJ6</strong> coding for potassium inwardly rectifying channels (Kir3.2, <strong>GIRK2</strong>) is important for <b>opioid</b> receptor transmission.
+KCNJ6	drug	opioid	20220551	<strong>KCNJ6</strong> coding for potassium inwardly rectifying channels (<strong>Kir3.2</strong>, <strong>GIRK2</strong>) is important for <b>opioid</b> receptor transmission.
+KCNJ6	drug	opioid	20220551	The <strong>KCNJ6</strong> rs2070995 AA genotype has been associated with increased <b>opioid</b> analgesic requirements in Japanese.
+KCNJ6	drug	opioid	20220551	The association of the <strong>KCNJ6</strong> rs2070995 AA genotype with increased <b>opioid</b> requirements extends from analgesia to opiate substitution therapy.
+KCNJ6	drug	opioid	18400906	The <b>morphine</b> withdrawal syndrome was strongly attenuated, whereas <b>morphine</b> analgesia was mostly preserved in mice lacking both <strong>GIRK2</strong> and GIRK3 (<strong>GIRK2</strong>/3( / ) mice).
+KCNJ6	addiction	withdrawal	18400906	The morphine <b>withdrawal</b> syndrome was strongly attenuated, whereas morphine analgesia was mostly preserved in mice lacking both <strong>GIRK2</strong> and GIRK3 (<strong>GIRK2</strong>/3( / ) mice).
+KCNJ6	drug	opioid	18400906	In acute slices containing the locus ceruleus (LC) from <strong>GIRK2</strong>/3( / ) mice, the increase in spontaneous firing typically associated with <b>morphine</b> withdrawal was absent.
+KCNJ6	addiction	withdrawal	18400906	In acute slices containing the locus ceruleus (LC) from <strong>GIRK2</strong>/3( / ) mice, the increase in spontaneous firing typically associated with morphine <b>withdrawal</b> was absent.
+KCNJ6	drug	opioid	18400906	Moreover, although <b>morphine</b> elicited normal presynaptic inhibition in the LC, postsynaptic GIRK currents were completely abolished in <strong>GIRK2</strong>/3( / ) mice.
+KCNJ6	drug	opioid	18400906	Consistent with this hypothesis, <b>morphine</b> withdrawal behavior was rescued in <strong>GIRK2</strong>/3( / ) mice by ablation of adrenergic fibers using the neurotoxin N (2 chloroethyl) N ethyl 2 bromobenzylamine.
+KCNJ6	addiction	withdrawal	18400906	Consistent with this hypothesis, morphine <b>withdrawal</b> behavior was rescued in <strong>GIRK2</strong>/3( / ) mice by ablation of adrenergic fibers using the neurotoxin N (2 chloroethyl) N ethyl 2 bromobenzylamine.
+KCNJ6	addiction	dependence	18400906	Our data suggest that inhibition of adrenergic tone is required for the induction of <b>dependence</b>, and that channels containing <strong>GIRK2</strong> and GIRK3 serve as an inhibitory gate.
+KCNJ6	drug	opioid	17368966	In a functional assay system comprised of MOR 1 mu <b>opioid</b> receptors and <strong>GIRK2</strong> potassium channels expressed in Xenopus oocytes, lobeline had no effect on the resting current, but maximally inhibited (IC(50)=1.1 microM) <b>morphine</b>  and DAMGO activated potassium current in a concentration dependent manner.
+KCNJ6	drug	alcohol	15544578	Mice lacking a functional copy of G protein gated potassium channel subunit 2 (<strong>Girk2</strong>) show a decrease in the aversive effects of <b>ethanol</b>, whereas preproenkephalin (Penk) null mutant mice show the opposite response.
+KCNJ6	addiction	aversion	15544578	Mice lacking a functional copy of G protein gated potassium channel subunit 2 (<strong>Girk2</strong>) show a decrease in the <b>aversive</b> effects of ethanol, whereas preproenkephalin (Penk) null mutant mice show the opposite response.
+KCNJ6	drug	alcohol	15542767	It has been shown that the function of GIRK channels is involved in seizure susceptibility, antinociception by opioids, cannabinoids, or <b>ethanol</b>, and cocaine reinforcement in studies using GIRK knockout mice and weaver mutant mice that have mutant <strong>GIRK2</strong> channels insensitive to G proteins and <b>ethanol</b>.
+KCNJ6	drug	cannabinoid	15542767	It has been shown that the function of GIRK channels is involved in seizure susceptibility, antinociception by opioids, <b>cannabinoids</b>, or ethanol, and cocaine reinforcement in studies using GIRK knockout mice and weaver mutant mice that have mutant <strong>GIRK2</strong> channels insensitive to G proteins and ethanol.
+KCNJ6	drug	cocaine	15542767	It has been shown that the function of GIRK channels is involved in seizure susceptibility, antinociception by opioids, cannabinoids, or ethanol, and <b>cocaine</b> reinforcement in studies using GIRK knockout mice and weaver mutant mice that have mutant <strong>GIRK2</strong> channels insensitive to G proteins and ethanol.
+KCNJ6	drug	opioid	15542767	It has been shown that the function of GIRK channels is involved in seizure susceptibility, antinociception by <b>opioids</b>, cannabinoids, or ethanol, and cocaine reinforcement in studies using GIRK knockout mice and weaver mutant mice that have mutant <strong>GIRK2</strong> channels insensitive to G proteins and ethanol.
+KCNJ6	addiction	reward	15542767	It has been shown that the function of GIRK channels is involved in seizure susceptibility, antinociception by opioids, cannabinoids, or ethanol, and cocaine <b>reinforcement</b> in studies using GIRK knockout mice and weaver mutant mice that have mutant <strong>GIRK2</strong> channels insensitive to G proteins and ethanol.
+KCNJ6	drug	alcohol	12721779	Reduced <b>ethanol</b> induced conditioned taste aversion and conditioned place preference in <strong>GIRK2</strong> null mutant mice.
+KCNJ6	addiction	aversion	12721779	Reduced ethanol induced conditioned taste <b>aversion</b> and conditioned place preference in <strong>GIRK2</strong> null mutant mice.
+KCNJ6	drug	alcohol	12721779	Previous studies have shown that <strong>GIRK2</strong> channel function is enhanced by <b>ethanol</b> and that <strong>GIRK2</strong> null mutant mice are less sensitive to some of <b>ethanol</b>'s effects, including anxiolysis, habituated locomotor stimulation, and acute handling induced convulsions than wild types.
+KCNJ6	drug	alcohol	12721779	Under some conditions, <strong>GIRK2</strong> knockout mice consume more <b>ethanol</b> than wild types, but it is unclear whether they do so because they are more sensitive to <b>ethanol</b>'s rewarding effects or less sensitive to its aversive effects.
+KCNJ6	addiction	aversion	12721779	Under some conditions, <strong>GIRK2</strong> knockout mice consume more ethanol than wild types, but it is unclear whether they do so because they are more sensitive to ethanol's rewarding effects or less sensitive to its <b>aversive</b> effects.
+KCNJ6	drug	alcohol	12721779	To further assess the role of <strong>GIRK2</strong> in <b>ethanol</b> action, <strong>GIRK2</strong> null mutant and wild type mice were tested in conditioning models that measure the motivational effects of <b>ethanol</b>.
+KCNJ6	drug	alcohol	12721779	These studies show that <strong>GIRK2</strong> deletion reduced <b>ethanol</b>'s impact in tasks that are commonly used to index the drug's rewarding and aversive effects.
+KCNJ6	addiction	aversion	12721779	These studies show that <strong>GIRK2</strong> deletion reduced ethanol's impact in tasks that are commonly used to index the drug's rewarding and <b>aversive</b> effects.
+KCNJ6	drug	cocaine	12637950	Here, we assessed the contribution of G protein gated, inwardly rectifying potassium (Kir3/GIRK) channels to the locomotor stimulatory and reinforcing effects of <b>cocaine</b> using knockout mice lacking one or both of the key neuronal channel subunits, <strong>Kir3.2</strong> and Kir3.3.
+KCNJ6	addiction	reward	12637950	Here, we assessed the contribution of G protein gated, inwardly rectifying potassium (Kir3/GIRK) channels to the locomotor stimulatory and <b>reinforcing</b> effects of cocaine using knockout mice lacking one or both of the key neuronal channel subunits, <strong>Kir3.2</strong> and Kir3.3.
+KCNJ6	drug	cocaine	12637950	<b>Cocaine</b> stimulated increases in horizontal locomotor activity in wild type, <strong>Kir3.2</strong> knockout, Kir3.3 knockout, and <strong>Kir3.2</strong>/3.3 double knockout mice, with only minor differences observed between the mouse lines.
+KCNJ6	drug	cocaine	12637950	In contrast, <strong>Kir3.2</strong> and Kir3.3 knockout mice exhibited dramatically reduced intravenous self administration of <b>cocaine</b> relative to wild type mice over a range of <b>cocaine</b> doses.
+KCNJ6	drug	cocaine	12637950	Paradoxically, <strong>Kir3.2</strong>/3.3 double knockout mice self administered <b>cocaine</b> at levels significantly higher than either single knockout alone.
+KCNJ6	drug	alcohol	11454913	Potassium channels as targets for <b>ethanol</b>: studies of G protein coupled inwardly rectifying potassium channel 2 (<strong>GIRK2</strong>) null mutant mice.
+KCNJ6	drug	alcohol	11454913	Selective enhancement of <strong>GIRK2</strong> function by intoxicating concentrations of <b>ethanol</b> was recently shown for recombinant homomeric and heteromeric channels.
+KCNJ6	drug	alcohol	11454913	We proposed that specific behavioral actions of <b>ethanol</b> are due to activation of GIRK channels and that these behaviors would be reduced or eliminated in <strong>GIRK2</strong> null mutant ("knockout") mice.
+KCNJ6	drug	alcohol	11454913	In the absence of <b>ethanol</b>, <strong>GIRK2</strong> knockout mice showed more motor activity, less anxiety, and higher HIC.
+KCNJ6	drug	alcohol	11454913	These results provide evidence that <strong>GIRK2</strong> channels mediate specific behaviors, including anxiety and convulsions, and may influence effects of <b>ethanol</b> on these behaviors.
+HSPA4	addiction	reward	32446966	Significantly upregulated expression of immune related genes (anti lipopolysaccharide factors (alf), peroxiredoxin (prx5), cathepsin B (ctsb), mitochondrial manganese superoxide dismutase (mtMnsod), cyclophilin A (cypa), glutathione peroxidase (gpx), Toll like receptor 3 (tlr3), and heat shock protein 70 (<strong>hsp70</strong>)) was detected in the crayfish fed the diets supplemented with 0.15% and 0.20% <b>CPP</b> diet compared with the levels observed in the control crayfish.
+HSPA4	drug	opioid	30497790	Recombinant Mycobacterium tuberculosis <strong>Hsp70</strong> was appended with <b>heroin</b> haptens and the resulting immunoconjugate granted anti <b>heroin</b> antibody production and blunted <b>heroin</b> induced antinociception.
+HSPA4	drug	opioid	30497790	Moreover, <strong>Hsp70</strong> as a carrier protein surpassed our benchmark Her KLH cocktail through antibody mediated blockade of 6 acetylmorphine, the main mediator of <b>heroin</b>'s psychoactivity.
+HSPA4	drug	opioid	26907924	Protein expression of <strong>HSP70</strong>, HSP105, and Vcp in the <b>Heroin</b>+acupuncture and <b>Heroin</b>+<b>methadone</b> groups was significantly higher than the <b>Heroin</b> group (p<0.01).
+HSPA4	drug	opioid	26907924	The positive effects of acupuncture on brain damage caused by <b>heroin</b> may be closely related to up regulation of <strong>HSP70</strong>, HSP105, and Vcp, and reduced apoptosis.
+HSPA4	drug	opioid	26728895	Our previous studies have identified the significance of heat shock protein 70 (<strong>Hsp70</strong>) in the development of a single <b>morphine</b> exposure induced behavioral sensitization.
+HSPA4	addiction	sensitization	26728895	Our previous studies have identified the significance of heat shock protein 70 (<strong>Hsp70</strong>) in the development of a single morphine exposure induced behavioral <b>sensitization</b>.
+HSPA4	drug	opioid	26728895	The present study expands upon these findings by investigating the effect of environment on the expression of behavioral sensitization induced by a single <b>morphine</b> exposure, and the potential involvement of <strong>Hsp70</strong> protein levels in these effects.
+HSPA4	addiction	sensitization	26728895	The present study expands upon these findings by investigating the effect of environment on the expression of behavioral <b>sensitization</b> induced by a single morphine exposure, and the potential involvement of <strong>Hsp70</strong> protein levels in these effects.
+HSPA4	drug	opioid	26728895	The expression of single <b>morphine</b> exposure induced behavioral sensitization was accompanied by a significant increase in <strong>Hsp70</strong> expression in NAc.
+HSPA4	addiction	sensitization	26728895	The expression of single morphine exposure induced behavioral <b>sensitization</b> was accompanied by a significant increase in <strong>Hsp70</strong> expression in NAc.
+HSPA4	drug	opioid	26728895	In contrast, the unpaired <b>morphine</b> treated group failed to exhibit behavioral sensitization or higher <strong>Hsp70</strong> expression.
+HSPA4	addiction	sensitization	26728895	In contrast, the unpaired morphine treated group failed to exhibit behavioral <b>sensitization</b> or higher <strong>Hsp70</strong> expression.
+HSPA4	addiction	sensitization	26728895	Additionally, by adding a habituation process prior to the challenge, we demonstrated that conditioned hyperactivity, which was not accompanied by an increased expression of <strong>Hsp70</strong>, is not essential for behavioral <b>sensitization</b>.
+HSPA4	addiction	sensitization	26728895	Furthermore, alterations in <strong>Hsp70</strong> expression in the NAc may represent a neurobiological <b>sensitization</b> mechanism mediating context  and time dependent behavioral <b>sensitization</b>.
+HSPA4	drug	opioid	26377394	We demonstrated increased levels of <strong>hsp70</strong> and BiP expression as well as phosphorylation of eIF2α in various rat brain areas after <b>oxycodone</b> administration.
+HSPA4	drug	alcohol	25024384	Moderate <b>alcohol</b> induces stress proteins HSF1 and <strong>hsp70</strong> and inhibits proinflammatory cytokines resulting in endotoxin tolerance.
+HSPA4	drug	alcohol	25024384	In this study, we show that cellular stress proteins HSF1 and <strong>hsp70</strong> play a mechanistic role in <b>alcohol</b> mediated inhibition of the TLR4/MyD88 pathway.
+HSPA4	drug	alcohol	25024384	Furthermore, HSF1 target gene <strong>hsp70</strong> mRNA and protein are upregulated by <b>alcohol</b> in monocytes.
+HSPA4	drug	alcohol	25024384	Furthermore, association of <strong>hsp70</strong> with NF κB subunit p50 in <b>alcohol</b> treated macrophages correlates with reduced NF κB activation at later time points.
+HSPA4	drug	alcohol	25024384	<strong>Hsp70</strong> overexpression in macrophages was sufficient to block LPS induced NF κB promoter activity, suggesting <b>alcohol</b> mediated immunosuppression by <strong>hsp70</strong>.
+HSPA4	drug	alcohol	25024384	The direct crosstalk of <strong>hsp70</strong> and HSF1 was further confirmed by the loss of <b>alcohol</b> mediated endotoxin tolerance in <strong>hsp70</strong>  and HSF1 silenced macrophages.
+HSPA4	drug	alcohol	25024384	Our data suggest that <b>alcohol</b> mediated activation of HSF1 and induction of <strong>hsp70</strong> inhibit TLR4 MyD88 signaling and are required for <b>alcohol</b> induced endotoxin tolerance.
+HSPA4	drug	opioid	24685564	Chronic <b>morphine</b> treatment induces over expression of <strong>HSP70</strong> in mice striatum related with abnormal ubiquitin proteasome degradation.
+HSPA4	drug	opioid	24685564	These data strongly suggest <b>morphine</b> induced <strong>HSP70</strong> overexpression in the striatum is closely related with its abnormal degradation by UPS and it seems to be an important mechanism associated with <b>morphine</b> dependence.
+HSPA4	addiction	dependence	24685564	These data strongly suggest morphine induced <strong>HSP70</strong> overexpression in the striatum is closely related with its abnormal degradation by UPS and it seems to be an important mechanism associated with morphine <b>dependence</b>.
+HSPA4	drug	opioid	24280010	Focusing on the NAc core and shell, the present study aims to provide further findings for our understanding of the relation between behavioural sensitization to <b>morphine</b> and <strong>Hsp70</strong> at transcriptional and functional levels in rats.
+HSPA4	addiction	sensitization	24280010	Focusing on the NAc core and shell, the present study aims to provide further findings for our understanding of the relation between behavioural <b>sensitization</b> to morphine and <strong>Hsp70</strong> at transcriptional and functional levels in rats.
+HSPA4	drug	opioid	24280010	Secondly, <strong>Hsp70</strong> protein expression in the NAc core was time  and dose relatedly induced during the development of behavioural sensitization to a single <b>morphine</b> exposure in rats, and Pearson analysis indicated a positive correlation between behavioural sensitization and <strong>Hsp70</strong> expression in NAc core.
+HSPA4	addiction	sensitization	24280010	Secondly, <strong>Hsp70</strong> protein expression in the NAc core was time  and dose relatedly induced during the development of behavioural <b>sensitization</b> to a single morphine exposure in rats, and Pearson analysis indicated a positive correlation between behavioural <b>sensitization</b> and <strong>Hsp70</strong> expression in NAc core.
+HSPA4	addiction	sensitization	24280010	Thirdly, at the transcriptional level, intra NAc core injection of the specific heat shock factor I (HSF I) inhibitor N Formyl 3,4 methylenedioxy benzylidine γ butyrolactam (KNK437) suppressed <strong>Hsp70</strong> expression and the development of behavioural <b>sensitization</b>, while the HSF I specific inducer geranylgeranylacetone (GGA) promoted both of them.
+HSPA4	addiction	sensitization	24280010	Finally, both the functional inhibition of <strong>Hsp70</strong> ATPase activity by methylene blue (MB), and the antagonism of <strong>Hsp70</strong> substrate binding site (SBD) activity by pifithrin μ (PES) impaired the development of behavioural <b>sensitization</b> when they were microinjected into the NAc core.
+HSPA4	drug	opioid	24280010	Taken together, the critical involvement of chaperone <strong>Hsp70</strong> in behavioural sensitization to <b>morphine</b> identifies a biological target for long lasting adaptations with relevance to addiction.
+HSPA4	addiction	addiction	24280010	Taken together, the critical involvement of chaperone <strong>Hsp70</strong> in behavioural sensitization to morphine identifies a biological target for long lasting adaptations with relevance to <b>addiction</b>.
+HSPA4	addiction	sensitization	24280010	Taken together, the critical involvement of chaperone <strong>Hsp70</strong> in behavioural <b>sensitization</b> to morphine identifies a biological target for long lasting adaptations with relevance to addiction.
+HSPA4	drug	opioid	23056601	Significant alterations were found in the expression of heat shock proteins (HSP27, α B crystallin, <strong>HSP70</strong>, HSP10 and HSP60), whose levels were markedly up regulated after <b>morphine</b> treatment or withdrawal.
+HSPA4	addiction	withdrawal	23056601	Significant alterations were found in the expression of heat shock proteins (HSP27, α B crystallin, <strong>HSP70</strong>, HSP10 and HSP60), whose levels were markedly up regulated after morphine treatment or <b>withdrawal</b>.
+HSPA4	drug	opioid	22647551	Thus, this study was designed to extend our understanding of the role of <strong>Hsp70</strong> in the development of behavioural sensitization induced by a single <b>morphine</b> exposure in mice.
+HSPA4	addiction	sensitization	22647551	Thus, this study was designed to extend our understanding of the role of <strong>Hsp70</strong> in the development of behavioural <b>sensitization</b> induced by a single morphine exposure in mice.
+HSPA4	drug	opioid	22647551	Second, <strong>Hsp70</strong> protein expression in the nucleus accumbens correlated positively with locomotor responses of sensitized mice and, more importantly, the expression of <strong>Hsp70</strong> increased within 1 h after the first <b>morphine</b> injection.
+HSPA4	drug	opioid	22647551	Third, AD and CHX both prevented expression of <strong>Hsp70</strong> and disrupted the development of the single <b>morphine</b> induced behavioural sensitization, which further implied <strong>Hsp70</strong> was highly associated with behavioural sensitization.
+HSPA4	addiction	sensitization	22647551	Third, AD and CHX both prevented expression of <strong>Hsp70</strong> and disrupted the development of the single morphine induced behavioural <b>sensitization</b>, which further implied <strong>Hsp70</strong> was highly associated with behavioural <b>sensitization</b>.
+HSPA4	drug	opioid	22647551	Taken together, we draw the conclusion that <strong>Hsp70</strong> is crucially involved in the labile phase of the development of behavioural sensitization induced by a single <b>morphine</b> exposure, probably functioning as a molecular chaperone.
+HSPA4	addiction	sensitization	22647551	Taken together, we draw the conclusion that <strong>Hsp70</strong> is crucially involved in the labile phase of the development of behavioural <b>sensitization</b> induced by a single morphine exposure, probably functioning as a molecular chaperone.
+HSPA4	drug	opioid	22285390	This study was designed to investigate the effects of geranylgeranylacetone (GGA), a pharmacological inducer of Trx 1 and <strong>Hsp70</strong>, on <b>morphine</b> induced hyperlocomotion, rewarding effect, and withdrawal syndrome.
+HSPA4	addiction	withdrawal	22285390	This study was designed to investigate the effects of geranylgeranylacetone (GGA), a pharmacological inducer of Trx 1 and <strong>Hsp70</strong>, on morphine induced hyperlocomotion, rewarding effect, and <b>withdrawal</b> syndrome.
+HSPA4	drug	opioid	22285390	In the nucleus accumbens, GGA enhanced <b>morphine</b> induced expression of Trx 1 and <strong>Hsp70</strong> after <b>morphine</b> withdrawal.
+HSPA4	addiction	withdrawal	22285390	In the nucleus accumbens, GGA enhanced morphine induced expression of Trx 1 and <strong>Hsp70</strong> after morphine <b>withdrawal</b>.
+HSPA4	drug	opioid	22285390	These results suggest that strengthening the expression of Trx 1 and <strong>Hsp70</strong> in the brain by using noncytotoxic pharmacological inducers may provide a novel therapeutic strategy for <b>morphine</b> dependence.
+HSPA4	addiction	dependence	22285390	These results suggest that strengthening the expression of Trx 1 and <strong>Hsp70</strong> in the brain by using noncytotoxic pharmacological inducers may provide a novel therapeutic strategy for morphine <b>dependence</b>.
+HSPA4	drug	opioid	21763353	<strong>Hsp70</strong> 1A, 84, 86 and 105 genes were similarly regulated by an acute injection of <b>morphine</b> in two subpopulations of Sprague Dawley (SD) rats showing different rates of extinction of <b>morphine</b> conditioned preference.
+HSPA4	drug	opioid	20519062	Transcription and protein synthesis inhibitors reduce the induction of behavioural sensitization to a single <b>morphine</b> exposure and regulate <strong>Hsp70</strong> expression in the mouse nucleus accumbens.
+HSPA4	addiction	sensitization	20519062	Transcription and protein synthesis inhibitors reduce the induction of behavioural <b>sensitization</b> to a single morphine exposure and regulate <strong>Hsp70</strong> expression in the mouse nucleus accumbens.
+HSPA4	drug	opioid	20519062	The results from RT PCR array and Western blot indicated that the changes of <strong>Hsp70</strong> expression in the NAc of mice were associated with behavioural sensitization induced by a single <b>morphine</b> exposure.
+HSPA4	addiction	sensitization	20519062	The results from RT PCR array and Western blot indicated that the changes of <strong>Hsp70</strong> expression in the NAc of mice were associated with behavioural <b>sensitization</b> induced by a single morphine exposure.
+HSPA4	drug	opioid	20519062	Together, these findings suggest that induction of behavioural sensitization to a single <b>morphine</b> exposure requires new protein synthesis, potentially involving <strong>Hsp70</strong> expression in the NAc of mice.
+HSPA4	addiction	sensitization	20519062	Together, these findings suggest that induction of behavioural <b>sensitization</b> to a single morphine exposure requires new protein synthesis, potentially involving <strong>Hsp70</strong> expression in the NAc of mice.
+HSPA4	drug	alcohol	20488642	<b>Ethanol</b> increases <strong>HSP70</strong> concentrations in honeybee (Apis mellifera L.) brain tissue.
+HSPA4	drug	alcohol	20488642	The purpose of this study was to evaluate whether <b>ethanol</b> doses that affect honeybee behavior also induce a significant stress response, measured by heat shock protein 70 (<strong>HSP70</strong>) concentrations, in honeybee brain tissues.
+HSPA4	drug	alcohol	20488642	Experiment 2 investigated the relationship between <b>ethanol</b> dose and brain <strong>HSP70</strong> concentrations.
+HSPA4	drug	alcohol	20488642	Bees in <b>ethanol</b> treatments were fed 1.5M sucrose (control) and 1.5M sucrose <b>ethanol</b> solutions containing 2.5, 5, and 10% <b>ethanol</b>, allowed to sit for 4h, and dissected brains were assayed for <strong>HSP70</strong>.
+HSPA4	drug	alcohol	20488642	We observed <b>ethanol</b> induced increases in honeybee brain <strong>HSP70</strong> concentrations from the control group through the 5% <b>ethanol</b> group.
+HSPA4	drug	alcohol	20488642	Only bees in the 5% <b>ethanol</b> group had <strong>HSP70</strong> concentrations significantly higher than the control group.
+HSPA4	drug	alcohol	20488642	The inverted U shaped <b>ethanol</b> dose <strong>HSP70</strong> concentration response curve indicated that ingestion of 2.5% <b>ethanol</b> and 5% <b>ethanol</b> stimulated the stress response, whereas ingestion of 10% <b>ethanol</b> inhibited the stress response.
+HSPA4	drug	alcohol	20488642	Doses that show maximum <strong>HSP70</strong> concentration (5% <b>ethanol</b>) or <strong>HSP70</strong> inhibition (10% <b>ethanol</b>) correspond to those (> or =5% <b>ethanol</b>) that also impaired honeybees in previous studies.
+HSPA4	drug	alcohol	16410189	<strong>Hsp70</strong> accumulation and ultrastructural features of lung and liver induced by <b>ethanol</b> treatment with and without L carnitine protection in rats.
+HSPA4	drug	alcohol	16410189	This study examined <strong>Hsp70</strong> accumulation and the subcellular characteristics of liver and lung when exposed to <b>ethanol</b> (EtOH), with and without L carnitine protection.
+HSPA4	drug	alcohol	16317704	<b>Alcohol</b> administration to ob/ob mice did not increase oxidative stress despite increased CYP2E1, but increased plasma TNF alpha, further increased <strong>Hsp70</strong>, and profoundly decreased p65 nuclear factor kappaB (NF kappaB) protein and DNA binding activity in nuclear extracts.
+HSPA4	drug	alcohol	15976529	At three days of <b>ethanol</b> withdrawal, we found region specific and sex selective alterations in levels of GAD (glutamic acid decarboxylase, GABA synthetic enzyme), GABA and glutamate transporters, and the synapse associated proteins <strong>HSP70</strong>, PSD 95, and synaptophysin.
+HSPA4	addiction	withdrawal	15976529	At three days of ethanol <b>withdrawal</b>, we found region specific and sex selective alterations in levels of GAD (glutamic acid decarboxylase, GABA synthetic enzyme), GABA and glutamate transporters, and the synapse associated proteins <strong>HSP70</strong>, PSD 95, and synaptophysin.
+HSPA4	drug	opioid	15379885	After 30 days of forced abstinence from <b>morphine</b> self administration, abundance of <strong>hsp70</strong> and lysozyme returned to basal levels.
+HSPA4	drug	opioid	15379885	Additionally, acute as well as chronic intraperitoneal <b>morphine</b> administration changed the abundance of PKC gamma, gamma1 subunit of GABAA and <strong>hsp70</strong> genes.
+HSPA4	drug	alcohol	11917132	Here we show that the aerobic growth ability on <b>ethanol</b> depends also on protection of the mutant AdhE against metal catalyzed oxidation by the chaperone DnaK (a member of the <strong>Hsp70</strong> family).
+HSPA4	drug	alcohol	9626570	In the present study we measured in various brain areas and in liver the intracellular levels of <strong>HSP70</strong> proteins, sulfhydryl groups and the antioxidant enzyme status after chronic administration of mild intoxicating doses of <b>ethanol</b> to rats.
+HSPA4	drug	alcohol	9626570	Expression of <strong>HSP70</strong> in response to <b>alcohol</b> administration was particularly high in the hippocampus and striatum.
+HSPA4	drug	alcohol	9626570	This study agrees with our previous results performed on acute <b>alcohol</b> intoxication and supports the hypothesis that <strong>HSP70</strong> induction protects the different brain areas against oxidative stress.
+HSPA4	addiction	intoxication	9626570	This study agrees with our previous results performed on acute alcohol <b>intoxication</b> and supports the hypothesis that <strong>HSP70</strong> induction protects the different brain areas against oxidative stress.
+HSPA4	drug	alcohol	1989992	Regulation of Hsc70 by 50 200 mM <b>ethanol</b> appeared to be a specific change in expression of an <b>ethanol</b> responsive gene rather than a typical stress protein response since no induction of the highly inducible stress protein, <strong>Hsp70</strong>, was seen at these <b>ethanol</b> concentrations.
+HCRT	drug	alcohol	31840823	Possible Role of CRF <strong>Hcrt</strong> Interaction in the Infralimbic Cortex in the Emergence and Maintenance of Compulsive <b>Alcohol</b> Seeking Behavior.
+HCRT	addiction	addiction	31840823	Possible Role of CRF <strong>Hcrt</strong> Interaction in the Infralimbic Cortex in the Emergence and Maintenance of <b>Compulsive</b> Alcohol Seeking Behavior.
+HCRT	addiction	relapse	31840823	Possible Role of CRF <strong>Hcrt</strong> Interaction in the Infralimbic Cortex in the Emergence and Maintenance of Compulsive Alcohol <b>Seeking</b> Behavior.
+HCRT	drug	alcohol	31840823	This transition from positive reinforcement  to negative reinforcement driven consumption involves the corticotropin releasing factor (CRF) system, although mounting evidence now suggests that the CRF system interacts with other neural systems to ultimately produce behaviors that are symptomatic of compulsive <b>alcohol</b> use, such as the hypocretin (<strong>Hcrt</strong>) system.
+HCRT	addiction	addiction	31840823	This transition from positive reinforcement  to negative reinforcement driven consumption involves the corticotropin releasing factor (CRF) system, although mounting evidence now suggests that the CRF system interacts with other neural systems to ultimately produce behaviors that are symptomatic of <b>compulsive</b> alcohol use, such as the hypocretin (<strong>Hcrt</strong>) system.
+HCRT	addiction	reward	31840823	This transition from positive <b>reinforcement</b>  to negative <b>reinforcement</b> driven consumption involves the corticotropin releasing factor (CRF) system, although mounting evidence now suggests that the CRF system interacts with other neural systems to ultimately produce behaviors that are symptomatic of compulsive alcohol use, such as the hypocretin (<strong>Hcrt</strong>) system.
+HCRT	drug	alcohol	31840823	Furthermore, the manner in which CRF interacts with <strong>Hcrt</strong> in this region as it pertains to <b>alcohol</b> seeking behavior is largely unknown, although immunohistochemical and electrophysiological experiments have shown that CRF and <strong>Hcrt</strong> directly interact in the mPFC, suggesting that the interaction between CRF and <strong>Hcrt</strong> in the IL may be critically important for the development and subsequent maintenance of compulsive <b>alcohol</b> seeking.
+HCRT	addiction	addiction	31840823	Furthermore, the manner in which CRF interacts with <strong>Hcrt</strong> in this region as it pertains to alcohol seeking behavior is largely unknown, although immunohistochemical and electrophysiological experiments have shown that CRF and <strong>Hcrt</strong> directly interact in the mPFC, suggesting that the interaction between CRF and <strong>Hcrt</strong> in the IL may be critically important for the development and subsequent maintenance of <b>compulsive</b> alcohol seeking.
+HCRT	addiction	relapse	31840823	Furthermore, the manner in which CRF interacts with <strong>Hcrt</strong> in this region as it pertains to alcohol <b>seeking</b> behavior is largely unknown, although immunohistochemical and electrophysiological experiments have shown that CRF and <strong>Hcrt</strong> directly interact in the mPFC, suggesting that the interaction between CRF and <strong>Hcrt</strong> in the IL may be critically important for the development and subsequent maintenance of compulsive alcohol <b>seeking</b>.
+HCRT	drug	alcohol	31840823	This review aims to consolidate recent literature regarding the role of the IL in <b>alcohol</b> seeking behavior and to discuss evidence that supports a functional interaction between <strong>Hcrt</strong> and CRF in the IL.
+HCRT	addiction	relapse	31840823	This review aims to consolidate recent literature regarding the role of the IL in alcohol <b>seeking</b> behavior and to discuss evidence that supports a functional interaction between <strong>Hcrt</strong> and CRF in the IL.
+HCRT	drug	alcohol	31394141	In rodents and zebrafish, our studies show that embryonic exposure to low dose <b>ethanol</b>, in addition to increasing voluntary <b>ethanol</b> intake during adolescence, increases the density of hypothalamic hypocretin (<strong>hcrt</strong>) neurons, a neuropeptide known to regulate reward related behaviors.
+HCRT	addiction	reward	31394141	In rodents and zebrafish, our studies show that embryonic exposure to low dose ethanol, in addition to increasing voluntary ethanol intake during adolescence, increases the density of hypothalamic hypocretin (<strong>hcrt</strong>) neurons, a neuropeptide known to regulate <b>reward</b> related behaviors.
+HCRT	drug	alcohol	31394141	To determine if preconception maternal <b>ethanol</b> consumption also affects these <strong>hcrt</strong> neurons and behavior in the offspring, we first standardized a method of measuring voluntary <b>ethanol</b> consumption in AB strain adult and larval zebrafish given gelatin meals containing 10% or 0.1% <b>ethanol</b>, respectively.
+HCRT	drug	alcohol	31394141	Whereas <b>ethanol</b> consumption by adult female HuC:GFP transgenic zebrafish had no impact on the number of differentiated HuC+ neurons at 28 h post fertilization (hpf), preconception <b>ethanol</b> consumption by adult female <strong>hcrt</strong>:EGFP zebrafish significantly increased the number of <strong>hcrt</strong> neurons in the offspring, an effect observed at 28 hpf and confirmed at 6 and 12 days post fertilization (dpf).
+HCRT	drug	alcohol	31394141	This increase in <strong>hcrt</strong> neurons was primarily present on the left side of the brain, indicating asymmetry in <b>ethanol</b>'s actions, and it was accompanied by behavioral changes in the offspring, including a significant increase in novelty induced locomotor activity but not thigmotaxis measured at 6 dpf and also in voluntary consumption of 0.1% <b>ethanol</b> gelatin at 12 dpf.
+HCRT	drug	alcohol	31394141	Notably, these measures of <b>ethanol</b> intake and locomotor activity stimulated by preconception <b>ethanol</b> were strongly, positively correlated with the number of <strong>hcrt</strong> neurons.
+HCRT	drug	alcohol	31394141	These findings demonstrate that preconception maternal <b>ethanol</b> consumption affects the brain and behavior of the offspring, producing effects similar to those caused by embryonic <b>ethanol</b> exposure, and they provide further evidence that the <b>ethanol</b> induced increase in <strong>hcrt</strong> neurogenesis contributes to the behavioral disturbances caused by <b>ethanol</b>.
+HCRT	addiction	reward	31206717	With zebrafish having marked advantages for elucidating neural mechanisms underlying brain disorders, we recently tested and showed in these fish, similar to rodents, that low dose embryonic EtOH stimulates voluntary consumption of EtOH while increasing expression of hypocretin/orexin (<strong>hcrt</strong>) neurons, a neuropeptide that promotes consummatory and <b>reward</b> related behaviors.
+HCRT	addiction	relapse	30796894	In the early 2000s, <strong>hcrt</strong>/ox transmission was shown to underlie mating behavior in male rats suggesting a novel role in reward <b>seeking</b>.
+HCRT	addiction	reward	30796894	In the early 2000s, <strong>hcrt</strong>/ox transmission was shown to underlie mating behavior in male rats suggesting a novel role in <b>reward</b> seeking.
+HCRT	drug	cocaine	30796894	Soon thereafter, <strong>hcrt</strong>/ox neurons were shown to respond to drug associated stimuli, and <strong>hcrt</strong>/ox transmission was found to facilitate motivated responding for intravenous <b>cocaine</b>.
+HCRT	addiction	relapse	30796894	Notably, blocking <strong>hcrt</strong>/ox transmission using systemic or site directed pharmacological antagonists markedly reduced motivated drug taking as well as drug <b>seeking</b> in tests of <b>relapse</b>.
+HCRT	drug	cocaine	30796894	This review will unfold the current state of knowledge implicating <strong>hcrt</strong>/ox receptor transmission in the context of <b>cocaine</b> abuse and provide detailed background on animal models and underlying midbrain circuits.
+HCRT	drug	cocaine	30796894	The review will conclude with discussion of recent preclinical studies assessing utility of suvorexant   the first and only FDA approved <strong>hcrt</strong>/ox receptor antagonist   against <b>cocaine</b> associated behaviors.
+HCRT	drug	alcohol	30293056	The current study used an animal model that combined an intermittent pattern of <b>alcohol</b> vapor exposure with voluntary drinking of 20% unsweetened <b>alcohol</b> in adolescent male and female Wistar rats (postnatal day [PD] 22 62), in order to test for potential differences in behavioral changes, <b>ethanol</b> drinking, and hypocretin/orexin (<strong>Hcrt</strong>/OX) signaling associated with exposure status.
+HCRT	drug	alcohol	30293056	Histological results indicated that adolescent <b>alcohol</b> did not alter <strong>Hcrt</strong>/OX 1 or <strong>Hcrt</strong>/OX 2 receptor mRNA expression levels in adult rats compared to control adults.
+HCRT	drug	alcohol	30293056	These data suggest that our current model of intermittent <b>ethanol</b> exposure in adolescence can modestly affect both behavior and future consumption of <b>alcohol</b> and that <strong>Hcrt</strong>/OX receptor signaling differs between males and females.
+HCRT	addiction	reward	29703996	The hypocretin/orexin (<strong>HCRT</strong>) neuropeptide system regulates feeding, arousal state, stress responses, and <b>reward</b>, especially under conditions of enhanced motivational relevance.
+HCRT	addiction	relapse	29703996	In particular, <strong>HCRT</strong> neurotransmission facilitates drug <b>seeking</b> behavior in circumstances that demand increased effort and/or motivation to take the drug.
+HCRT	drug	cocaine	29703996	The present study used a shRNA encoding adeno associated viral vector to knockdown <strong>Hcrt</strong> expression throughout the dorsal hypothalamus in adult rats and determine the role of <strong>HCRT</strong> in <b>cocaine</b> self administration.
+HCRT	drug	cocaine	29703996	Chronic <strong>Hcrt</strong> silencing did not impact <b>cocaine</b> self administration under short access conditions, but robustly attenuated <b>cocaine</b> intake under extended access conditions, a model that mimics key features of compulsive <b>cocaine</b> taking.
+HCRT	addiction	addiction	29703996	Chronic <strong>Hcrt</strong> silencing did not impact cocaine self administration under short access conditions, but robustly attenuated cocaine intake under extended access conditions, a model that mimics key features of <b>compulsive</b> cocaine taking.
+HCRT	drug	cocaine	29703996	In addition, <strong>Hcrt</strong> silencing decreased motivation for both <b>cocaine</b> and a highly palatable food reward (i.e., sweetened condensed milk; SCM) under a progressive ratio schedule of reinforcement, but did not alter responding for SCM under a fixed ratio schedule.
+HCRT	addiction	reward	29703996	In addition, <strong>Hcrt</strong> silencing decreased motivation for both cocaine and a highly palatable food <b>reward</b> (i.e., sweetened condensed milk; SCM) under a progressive ratio schedule of <b>reinforcement</b>, but did not alter responding for SCM under a fixed ratio schedule.
+HCRT	addiction	reward	29703996	These original findings support the hypothesis that <strong>HCRT</strong> neurotransmission promotes <b>operant</b> responding for both drug and non drug rewards, preferentially under conditions requiring a high degree of motivation.
+HCRT	drug	cocaine	29703996	Furthermore, the current study provides compelling evidence for the involvement of the <strong>HCRT</strong> system in <b>cocaine</b> self administration also under low effort conditions in rats allowed extended access, possibly via functional interactions with DYN and MCH signaling.
+HCRT	drug	cocaine	29454841	Our observations show that whereas all mice exhibited quite similar responses to acute administration of <b>cocaine</b>, only <strong>Hcrt</strong> KO mice exhibited reduced <b>cocaine</b> seeking behaviors following a period of abstinence or extinction, and reduced <b>cocaine</b> incubation craving.
+HCRT	addiction	relapse	29454841	Our observations show that whereas all mice exhibited quite similar responses to acute administration of cocaine, only <strong>Hcrt</strong> KO mice exhibited reduced cocaine <b>seeking</b> behaviors following a period of abstinence or extinction, and reduced cocaine incubation <b>craving</b>.
+HCRT	drug	cocaine	29454841	We thus report that innate disruption of hypocretin/orexin signaling moderately alters <b>cocaine</b> reward but significantly reduces long term affective dependence that may explain the lack of relapse for <b>cocaine</b> seeking seen in <strong>Hcrt</strong> KO mice.
+HCRT	addiction	dependence	29454841	We thus report that innate disruption of hypocretin/orexin signaling moderately alters cocaine reward but significantly reduces long term affective <b>dependence</b> that may explain the lack of relapse for cocaine seeking seen in <strong>Hcrt</strong> KO mice.
+HCRT	addiction	relapse	29454841	We thus report that innate disruption of hypocretin/orexin signaling moderately alters cocaine reward but significantly reduces long term affective dependence that may explain the lack of <b>relapse</b> for cocaine <b>seeking</b> seen in <strong>Hcrt</strong> KO mice.
+HCRT	addiction	reward	29454841	We thus report that innate disruption of hypocretin/orexin signaling moderately alters cocaine <b>reward</b> but significantly reduces long term affective dependence that may explain the lack of relapse for cocaine seeking seen in <strong>Hcrt</strong> KO mice.
+HCRT	addiction	reward	28786030	Pharmacological agents that disrupt excitatory transmission onto midbrain DA producing neurons, including hypothalamic hypocretin/orexin (<strong>hcrt</strong>/ox) receptor antagonists, present attractive targets to aide abstinence maintenance by reducing psychostimulant associated <b>reward</b> and <b>reinforcement</b>.
+HCRT	drug	amphetamine	28729827	It is also home to a heterogeneous population of neurons that express and co express multiple neuropeptides including hypocretin (<strong>Hcrt</strong>), melanin concentrating hormone (MCH), cocaine  and <b>amphetamine</b> regulated transcript (CART) and neurotensin (NT).
+HCRT	drug	cocaine	28729827	It is also home to a heterogeneous population of neurons that express and co express multiple neuropeptides including hypocretin (<strong>Hcrt</strong>), melanin concentrating hormone (MCH), <b>cocaine</b>  and amphetamine regulated transcript (CART) and neurotensin (NT).
+HCRT	drug	amphetamine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, AgRP, cocaine  and <b>amphetamine</b> related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (<strong>HCRT</strong>), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+HCRT	drug	cocaine	28085909	Modulation of the expression of brain neuropeptides and receptors including NPY, POMC, AgRP, <b>cocaine</b>  and amphetamine related transcript (CART), corticotropin releasing hormone (CRH) and prepro orexin (<strong>HCRT</strong>), and Y2 and Y5 neuropeptide Y, MC4 (melanocortin), OX1 and OX2 orexin receptors (Y2R, Y5R, MC4R, OX1R and OX2R, respectively) was also explored.
+HCRT	addiction	relapse	27567312	The lateral hypothalamic hypocretin/orexin (<strong>HCRT</strong>) system has been implicated in drug taking and the <b>reinstatement</b> of drug <b>seeking</b>.
+HCRT	addiction	relapse	27567312	Evidence suggests that <strong>HCRT</strong> may drive drug <b>seeking</b> through activation of specific brain regions implicated in stress system dysfunction, including the central amygdala (CeA).
+HCRT	drug	cocaine	27567312	The role of <strong>HCRT</strong> in the persistence of compulsive like <b>cocaine</b> taking has yet to be fully elucidated.
+HCRT	addiction	addiction	27567312	The role of <strong>HCRT</strong> in the persistence of <b>compulsive</b> like cocaine taking has yet to be fully elucidated.
+HCRT	drug	cocaine	27567312	Systemic and intra CeA microinfusions of the <strong>HCRT</strong> receptor 1 antagonist, SB 334867, were administered to rats allowed either short (1 hour; ShA) or long (6 hours; LgA) access to <b>cocaine</b> self administration.
+HCRT	drug	cocaine	27567312	These findings suggest that <strong>HCRT</strong> neurotransmission within the CeA is implicated in compulsive like <b>cocaine</b> seeking.
+HCRT	addiction	addiction	27567312	These findings suggest that <strong>HCRT</strong> neurotransmission within the CeA is implicated in <b>compulsive</b> like cocaine seeking.
+HCRT	addiction	relapse	27567312	These findings suggest that <strong>HCRT</strong> neurotransmission within the CeA is implicated in compulsive like cocaine <b>seeking</b>.
+HCRT	drug	cocaine	27558790	This investigation addressed this question by contrasting hypothalamic Orx/<strong>Hcrt</strong> neuronal activation associated with reinstatement of reward seeking induced by stimuli conditioned to <b>cocaine</b> (COC) versus highly palatable food reward, sweetened condensed milk (SCM).
+HCRT	addiction	relapse	27558790	This investigation addressed this question by contrasting hypothalamic Orx/<strong>Hcrt</strong> neuronal activation associated with <b>reinstatement</b> of reward <b>seeking</b> induced by stimuli conditioned to cocaine (COC) versus highly palatable food reward, sweetened condensed milk (SCM).
+HCRT	addiction	reward	27558790	This investigation addressed this question by contrasting hypothalamic Orx/<strong>Hcrt</strong> neuronal activation associated with reinstatement of <b>reward</b> seeking induced by stimuli conditioned to cocaine (COC) versus highly palatable food <b>reward</b>, sweetened condensed milk (SCM).
+HCRT	addiction	relapse	27558790	Orx/<strong>Hcrt</strong> neuronal activation in the lateral hypothalamus, dorsomedial hypothalamus and perifornical area, determined by dual c fos/orx immunocytochemistry, was quantified in rat brains, following <b>reinstatement</b> of reward <b>seeking</b> induced by a discriminative stimulus (S+) conditioned to COC or SCM.
+HCRT	addiction	reward	27558790	Orx/<strong>Hcrt</strong> neuronal activation in the lateral hypothalamus, dorsomedial hypothalamus and perifornical area, determined by dual c fos/orx immunocytochemistry, was quantified in rat brains, following reinstatement of <b>reward</b> seeking induced by a discriminative stimulus (S+) conditioned to COC or SCM.
+HCRT	addiction	addiction	27558790	These findings point toward a role for the Orx/<strong>Hcrt</strong> system in perseverating, <b>compulsive</b> like COC seeking but not behavior motivated by palatable food.
+HCRT	addiction	relapse	27558790	These findings point toward a role for the Orx/<strong>Hcrt</strong> system in perseverating, compulsive like COC <b>seeking</b> but not behavior motivated by palatable food.
+HCRT	addiction	relapse	27558790	Moreover, analysis of the Orx/<strong>Hcrt</strong> recruitment patterns suggests that failure of Orx/<strong>Hcrt</strong> neurons in the lateral hypothalamus to respond to inhibitory inputs from Orx/<strong>Hcrt</strong> neurons in the dorsomedial hypothalamus/perifornical area may contribute to the perseverating nature of COC <b>seeking</b>.
+HCRT	addiction	addiction	27540003	Orexin/hypocretin (Orx/<strong>Hcrt</strong>) projections from the lateral hypothalamus to the paraventricular nucleus of the thalamus (PVT) are implicated in drug <b>addiction</b>.
+HCRT	drug	cocaine	27540003	This study investigated the role of pPVT Orx/<strong>Hcrt</strong> transmission in <b>cocaine</b> seeking behavior.
+HCRT	addiction	relapse	27540003	This study investigated the role of pPVT Orx/<strong>Hcrt</strong> transmission in cocaine <b>seeking</b> behavior.
+HCRT	drug	cocaine	27540003	Because the effects of Orx/<strong>Hcrt</strong> are mediated by two Orx/<strong>Hcrt</strong> receptors (<strong>Hcrt</strong> r1 and <strong>Hcrt</strong> r2), we examined the extent to which <strong>Hcrt</strong> r1 and <strong>Hcrt</strong> r2 are involved in Orx/<strong>Hcrt</strong> induced <b>cocaine</b> seeking.
+HCRT	addiction	relapse	27540003	Because the effects of Orx/<strong>Hcrt</strong> are mediated by two Orx/<strong>Hcrt</strong> receptors (<strong>Hcrt</strong> r1 and <strong>Hcrt</strong> r2), we examined the extent to which <strong>Hcrt</strong> r1 and <strong>Hcrt</strong> r2 are involved in Orx/<strong>Hcrt</strong> induced cocaine <b>seeking</b>.
+HCRT	drug	cocaine	27540003	Orx A/<strong>Hcrt</strong> 1 alone reinstated (primed) <b>cocaine</b> seeking.
+HCRT	addiction	relapse	27540003	Orx A/<strong>Hcrt</strong> 1 alone reinstated (primed) cocaine <b>seeking</b>.
+HCRT	drug	cocaine	27540003	Unexpectedly, coadministration of Orx A/<strong>Hcrt</strong> 1 with SB334867 did not have any effects on Orx A/<strong>Hcrt</strong> 1 induced reinstatement, whereas when coadministered with Orx A/<strong>Hcrt</strong> 1, TCSOX229 prevented <b>cocaine</b> seeking behavior.
+HCRT	addiction	relapse	27540003	Unexpectedly, coadministration of Orx A/<strong>Hcrt</strong> 1 with SB334867 did not have any effects on Orx A/<strong>Hcrt</strong> 1 induced <b>reinstatement</b>, whereas when coadministered with Orx A/<strong>Hcrt</strong> 1, TCSOX229 prevented cocaine <b>seeking</b> behavior.
+HCRT	drug	cocaine	27540003	These results indicate that <strong>Hcrt</strong> r2 in the pPVT mediates the reinstating effect of Orx A/<strong>Hcrt</strong> 1 in animals with a history of <b>cocaine</b> dependence and further identify <strong>Hcrt</strong> r2 as a possible molecular target that can guide future therapeutic approaches for the prevention of drug seeking behavior.
+HCRT	addiction	dependence	27540003	These results indicate that <strong>Hcrt</strong> r2 in the pPVT mediates the reinstating effect of Orx A/<strong>Hcrt</strong> 1 in animals with a history of cocaine <b>dependence</b> and further identify <strong>Hcrt</strong> r2 as a possible molecular target that can guide future therapeutic approaches for the prevention of drug seeking behavior.
+HCRT	addiction	relapse	27540003	These results indicate that <strong>Hcrt</strong> r2 in the pPVT mediates the reinstating effect of Orx A/<strong>Hcrt</strong> 1 in animals with a history of cocaine dependence and further identify <strong>Hcrt</strong> r2 as a possible molecular target that can guide future therapeutic approaches for the prevention of drug <b>seeking</b> behavior.
+HCRT	addiction	reward	27480648	The hypocretin/orexin (<strong>HCRT</strong>) system is implicated in <b>reward</b> and <b>reinforcement</b> processes through actions on the mesolimbic dopamine (DA) system.
+HCRT	drug	cocaine	27480648	The ability of <b>cocaine</b> to elicit reward related behaviors in mice lacking the <strong>HCRT</strong> prepro peptide (<strong>HCRT</strong> knock out; KO) and wild type controls was determined using conditioned place preference.
+HCRT	addiction	reward	27480648	The ability of cocaine to elicit <b>reward</b> related behaviors in mice lacking the <strong>HCRT</strong> prepro peptide (<strong>HCRT</strong> knock out; KO) and wild type controls was determined using conditioned place preference.
+HCRT	drug	cocaine	27480648	We show that, unlike wild type mice, <strong>HCRT</strong> KO mice fail to develop characteristic conditioned place preference for <b>cocaine</b>.
+HCRT	drug	cocaine	27480648	Further, diminished DA signaling in <strong>HCRT</strong> KO mice persists following administration of <b>cocaine</b>.
+HCRT	drug	cocaine	27480648	These findings indicate that <strong>HCRT</strong> is essential for the expression of behaviors associated with the rewarding effects of <b>cocaine</b>, and suggest that <strong>HCRT</strong> regulation of reward and reinforcement may be related to disruptions to DA neurotransmission.
+HCRT	addiction	reward	27480648	These findings indicate that <strong>HCRT</strong> is essential for the expression of behaviors associated with the rewarding effects of cocaine, and suggest that <strong>HCRT</strong> regulation of <b>reward</b> and <b>reinforcement</b> may be related to disruptions to DA neurotransmission.
+HCRT	addiction	dependence	26564129	We first described a low frequency of illicit drug use, <b>dependence</b>, or abuse in patients with central hypersomnia, whether <strong>Hcrt</strong> deficient or not, and whether drug free or medicated, in the same range as in controls.
+HCRT	drug	alcohol	26055195	We showed that activation of the neuropeptide S (NPS) system exacerbates reinstatement vulnerability to cocaine and <b>alcohol</b> via stimulation of the hypocretin 1/orexin A (<strong>Hcrt</strong> 1/Ox A) system.
+HCRT	drug	cocaine	26055195	We showed that activation of the neuropeptide S (NPS) system exacerbates reinstatement vulnerability to <b>cocaine</b> and alcohol via stimulation of the hypocretin 1/orexin A (<strong>Hcrt</strong> 1/Ox A) system.
+HCRT	addiction	relapse	26055195	We showed that activation of the neuropeptide S (NPS) system exacerbates <b>reinstatement</b> vulnerability to cocaine and alcohol via stimulation of the hypocretin 1/orexin A (<strong>Hcrt</strong> 1/Ox A) system.
+HCRT	drug	alcohol	26055195	Combining pharmacologic manipulations with immunohistochemistry techniques, we sought to determine how NPS and <strong>Hcrt</strong> 1/Ox A systems interact to modulate reinstatement of <b>alcohol</b> seeking in rats.
+HCRT	addiction	relapse	26055195	Combining pharmacologic manipulations with immunohistochemistry techniques, we sought to determine how NPS and <strong>Hcrt</strong> 1/Ox A systems interact to modulate <b>reinstatement</b> of alcohol <b>seeking</b> in rats.
+HCRT	drug	alcohol	26055195	Confirming this assumption, intra BNST or PVN <strong>Hcrt</strong> 1/Ox A injection enhanced <b>alcohol</b> seeking similarly to hypothalamic NPS injection but to a lesser degree.
+HCRT	addiction	relapse	26055195	Confirming this assumption, intra BNST or PVN <strong>Hcrt</strong> 1/Ox A injection enhanced alcohol <b>seeking</b> similarly to hypothalamic NPS injection but to a lesser degree.
+HCRT	addiction	relapse	26055195	Results suggest that the <strong>Hcrt</strong> 1/Ox A neurocircuitry mediating the facilitation of cue induced <b>reinstatement</b> by NPS involves structures critically involved in stress regulation such as the PVN and the BNST.
+HCRT	drug	opioid	25367502	The hypocretin/orexin (<strong>HCRT</strong>) system has been associated with both positive and negative drug reinforcement, implicating <strong>HCRT</strong> receptor 1 (<strong>HCRT</strong> R1) signaling in drug related behaviors for all major drug classes, including <b>opioids</b>.
+HCRT	addiction	reward	25367502	The hypocretin/orexin (<strong>HCRT</strong>) system has been associated with both positive and negative drug <b>reinforcement</b>, implicating <strong>HCRT</strong> receptor 1 (<strong>HCRT</strong> R1) signaling in drug related behaviors for all major drug classes, including opioids.
+HCRT	addiction	addiction	25367502	However, to date there are limited studies investigating the role of <strong>HCRT</strong> receptor 2 (<strong>HCRT</strong> R2) signaling in <b>compulsive</b> like drug seeking.
+HCRT	addiction	relapse	25367502	However, to date there are limited studies investigating the role of <strong>HCRT</strong> receptor 2 (<strong>HCRT</strong> R2) signaling in compulsive like drug <b>seeking</b>.
+HCRT	drug	opioid	25367502	The current study examined the effects of a <strong>HCRT</strong> R2 antagonist, NBI 80713, on <b>heroin</b> self administration in rats allowed short  (1 h; ShA) or long  (12 h; LgA) access to intravenous <b>heroin</b> self administration.
+HCRT	drug	opioid	25367502	These observations suggest a functional role for <strong>HCRT</strong> R2 signaling in compulsive like <b>heroin</b> self administration associated with extended access and indicate <strong>HCRT</strong> R2 antagonism as a potential pharmacological target for the treatment of <b>heroin</b> dependence.
+HCRT	addiction	addiction	25367502	These observations suggest a functional role for <strong>HCRT</strong> R2 signaling in <b>compulsive</b> like heroin self administration associated with extended access and indicate <strong>HCRT</strong> R2 antagonism as a potential pharmacological target for the treatment of heroin dependence.
+HCRT	addiction	dependence	25367502	These observations suggest a functional role for <strong>HCRT</strong> R2 signaling in compulsive like heroin self administration associated with extended access and indicate <strong>HCRT</strong> R2 antagonism as a potential pharmacological target for the treatment of heroin <b>dependence</b>.
+HCRT	drug	cocaine	24407199	To advance our understanding of the potential of the Orx/<strong>Hcrt</strong> receptor 1 (<strong>Hcrt</strong> r1) as a treatment target for <b>cocaine</b> addiction, the effect of SB334867 [N (2 methyl 6 benzoxazolyl) N' 1,5 n aphthyridin 4 yl urea], a specific <strong>Hcrt</strong> r1 antagonist, on reinstatement elicited by <b>cocaine</b> associated stimuli versus stimuli associated with a highly palatable conventional reinforcer [sweetened condensed milk (SCM)] was tested.
+HCRT	addiction	addiction	24407199	To advance our understanding of the potential of the Orx/<strong>Hcrt</strong> receptor 1 (<strong>Hcrt</strong> r1) as a treatment target for cocaine <b>addiction</b>, the effect of SB334867 [N (2 methyl 6 benzoxazolyl) N' 1,5 n aphthyridin 4 yl urea], a specific <strong>Hcrt</strong> r1 antagonist, on reinstatement elicited by cocaine associated stimuli versus stimuli associated with a highly palatable conventional reinforcer [sweetened condensed milk (SCM)] was tested.
+HCRT	addiction	relapse	24407199	To advance our understanding of the potential of the Orx/<strong>Hcrt</strong> receptor 1 (<strong>Hcrt</strong> r1) as a treatment target for cocaine addiction, the effect of SB334867 [N (2 methyl 6 benzoxazolyl) N' 1,5 n aphthyridin 4 yl urea], a specific <strong>Hcrt</strong> r1 antagonist, on <b>reinstatement</b> elicited by cocaine associated stimuli versus stimuli associated with a highly palatable conventional reinforcer [sweetened condensed milk (SCM)] was tested.
+HCRT	drug	cocaine	24407199	<strong>Hcrt</strong> r1 blockade by SB334867 (1 10 mg/kg, intraperitoneal) dose dependently and selectively reversed conditioned reinstatement induced by <b>cocaine</b> related stimuli, without interfering with reward seeking produced by the same stimulus when conditioned to SCM.
+HCRT	addiction	relapse	24407199	<strong>Hcrt</strong> r1 blockade by SB334867 (1 10 mg/kg, intraperitoneal) dose dependently and selectively reversed conditioned <b>reinstatement</b> induced by cocaine related stimuli, without interfering with reward <b>seeking</b> produced by the same stimulus when conditioned to SCM.
+HCRT	addiction	reward	24407199	<strong>Hcrt</strong> r1 blockade by SB334867 (1 10 mg/kg, intraperitoneal) dose dependently and selectively reversed conditioned reinstatement induced by cocaine related stimuli, without interfering with <b>reward</b> seeking produced by the same stimulus when conditioned to SCM.
+HCRT	drug	cocaine	24407199	The findings suggest an important role for <strong>Hcrt</strong> r1 in appetitive behavior controlled by reward related stimuli with selectivity for <b>cocaine</b> seeking and identify <strong>Hcrt</strong> r1 as a potential treatment target for <b>cocaine</b> relapse prevention.
+HCRT	addiction	relapse	24407199	The findings suggest an important role for <strong>Hcrt</strong> r1 in appetitive behavior controlled by reward related stimuli with selectivity for cocaine <b>seeking</b> and identify <strong>Hcrt</strong> r1 as a potential treatment target for cocaine <b>relapse</b> prevention.
+HCRT	addiction	reward	24407199	The findings suggest an important role for <strong>Hcrt</strong> r1 in appetitive behavior controlled by <b>reward</b> related stimuli with selectivity for cocaine seeking and identify <strong>Hcrt</strong> r1 as a potential treatment target for cocaine relapse prevention.
+HCRT	drug	cocaine	22837742	Considerable evidence suggests that transmission at hypocretin 1 (orexin 1) receptors (<strong>Hcrt</strong> R1) plays an important role in the reinstatement of extinguished <b>cocaine</b> seeking behaviors in rodents.
+HCRT	addiction	relapse	22837742	Considerable evidence suggests that transmission at hypocretin 1 (orexin 1) receptors (<strong>Hcrt</strong> R1) plays an important role in the <b>reinstatement</b> of extinguished cocaine <b>seeking</b> behaviors in rodents.
+HCRT	drug	cocaine	22837742	Here, we investigated the effects of the selective <strong>Hcrt</strong> R1 antagonist SB 334867 on <b>cocaine</b> intake, as measured by intravenous (IV) <b>cocaine</b> self administration in rats.
+HCRT	drug	cocaine	22837742	Finally, to definitively establish a role for <strong>Hcrt</strong> R1 in regulating <b>cocaine</b> intake, we assessed IV <b>cocaine</b> self administration in <strong>Hcrt</strong> R1 knockout mice.
+HCRT	drug	cocaine	22837742	Finally, we found that <strong>Hcrt</strong> R1 knockout mice self administered far less <b>cocaine</b> than wildtype mice across the entire dose response function.
+HCRT	drug	cocaine	22837742	These data demonstrate that <strong>Hcrt</strong> R1 play an important role in regulating the reinforcing and reward enhancing properties of <b>cocaine</b> and suggest that hypocretin transmission is likely essential for establishing and maintaining the <b>cocaine</b> habit in human addicts.
+HCRT	addiction	reward	22837742	These data demonstrate that <strong>Hcrt</strong> R1 play an important role in regulating the <b>reinforcing</b> and <b>reward</b> enhancing properties of cocaine and suggest that hypocretin transmission is likely essential for establishing and maintaining the cocaine habit in human addicts.
+HCRT	drug	alcohol	22830647	This study was designed to test the effect of the specific Orx/<strong>Hcrt</strong> receptor 1 (<strong>Hcrt</strong> r1) antagonist, N (2 methyl 6 benzoxazolyl) N' 1,5 naphthyridin 4 yl urea (SB334867), on reinstatement elicited by <b>ethanol</b> (EtOH) associated stimuli versus stimuli associated with a conventional reinforcer [i.e.
+HCRT	addiction	relapse	22830647	This study was designed to test the effect of the specific Orx/<strong>Hcrt</strong> receptor 1 (<strong>Hcrt</strong> r1) antagonist, N (2 methyl 6 benzoxazolyl) N' 1,5 naphthyridin 4 yl urea (SB334867), on <b>reinstatement</b> elicited by ethanol (EtOH) associated stimuli versus stimuli associated with a conventional reinforcer [i.e.
+HCRT	addiction	relapse	22830647	These findings support a differential role of <strong>Hcrt</strong> r1 in mediating EtOH <b>seeking</b> versus natural reward <b>seeking</b>.
+HCRT	addiction	reward	22830647	These findings support a differential role of <strong>Hcrt</strong> r1 in mediating EtOH seeking versus natural <b>reward</b> seeking.
+HCRT	drug	cocaine	20974945	Of note, intra LH and intra PeF administration of NPS increased conditioned reinstatement of <b>cocaine</b> responding, an effect that was selectively blocked with the <strong>Hcrt</strong> 1/Ox A receptor selective antagonist SB334867.
+HCRT	addiction	relapse	20974945	Of note, intra LH and intra PeF administration of NPS increased conditioned <b>reinstatement</b> of cocaine responding, an effect that was selectively blocked with the <strong>Hcrt</strong> 1/Ox A receptor selective antagonist SB334867.
+HCRT	drug	nicotine	20177882	The hypocretin (<strong>hcrt</strong>) system has been implicated in addiction relevant effects of several drugs, but its role in <b>nicotine</b> dependence has been little studied.
+HCRT	addiction	addiction	20177882	The hypocretin (<strong>hcrt</strong>) system has been implicated in <b>addiction</b> relevant effects of several drugs, but its role in nicotine dependence has been little studied.
+HCRT	addiction	dependence	20177882	The hypocretin (<strong>hcrt</strong>) system has been implicated in addiction relevant effects of several drugs, but its role in nicotine <b>dependence</b> has been little studied.
+HCRT	drug	nicotine	20177882	These experiments examined the role of the <strong>hcrt</strong> system in <b>nicotine</b> reinforcement.
+HCRT	addiction	reward	20177882	These experiments examined the role of the <strong>hcrt</strong> system in nicotine <b>reinforcement</b>.
+HCRT	drug	nicotine	20177882	These data confirm a previous report (Hollander et al., Proc Natl Acad Sci U S A 105:19480 19485, 2008) that the hypocretin receptor hcrtR1 is activated in <b>nicotine</b> reinforcement and in addition show that both the arcuate nucleus and lateral hypothalamus are sites at which <strong>hcrt</strong> receptor mechanisms may influence reinforcement.
+HCRT	addiction	reward	20177882	These data confirm a previous report (Hollander et al., Proc Natl Acad Sci U S A 105:19480 19485, 2008) that the hypocretin receptor hcrtR1 is activated in nicotine <b>reinforcement</b> and in addition show that both the arcuate nucleus and lateral hypothalamus are sites at which <strong>hcrt</strong> receptor mechanisms may influence <b>reinforcement</b>.
+HCRT	drug	nicotine	20147556	Intracerebroventricular infusion of hypocretin 1 (<strong>Hcrt</strong> 1) (0.75 nmol/1 mul) or footshock stress reinstated a previously extinguished <b>nicotine</b> seeking behavior.
+HCRT	addiction	relapse	20147556	Intracerebroventricular infusion of hypocretin 1 (<strong>Hcrt</strong> 1) (0.75 nmol/1 mul) or footshock stress reinstated a previously extinguished nicotine <b>seeking</b> behavior.
+HCRT	drug	nicotine	20147556	Therefore, the <strong>Hcrt</strong> system interacts with CRF and AVP neurons in the PVN and modulates the anxiogenic like effects of <b>nicotine</b> whereas <strong>Hcrt</strong> and CRF play a different role in the reinstatement of <b>nicotine</b> seeking.
+HCRT	addiction	relapse	20147556	Therefore, the <strong>Hcrt</strong> system interacts with CRF and AVP neurons in the PVN and modulates the anxiogenic like effects of nicotine whereas <strong>Hcrt</strong> and CRF play a different role in the <b>reinstatement</b> of nicotine <b>seeking</b>.
+HCRT	drug	nicotine	20147556	Indeed, <strong>Hcrt</strong> 1 reinstates <b>nicotine</b> seeking through a mechanism independent of CRF activation whereas CRF mediates the reinstatement induced by stress.
+HCRT	addiction	relapse	20147556	Indeed, <strong>Hcrt</strong> 1 reinstates nicotine <b>seeking</b> through a mechanism independent of CRF activation whereas CRF mediates the <b>reinstatement</b> induced by stress.
+HCRT	addiction	addiction	20026088	Recent evidence demonstrated that interactions between CRF N/OFQ and CRF Orx/<strong>Hcrt</strong> systems may be functionally relevant for the control of stress related <b>addictive</b> behavior.
+HCRT	addiction	reward	19741128	Here, we show that orexin/hypocretin receptor 1 (ox/<strong>hcrt</strong> 1R) signaling is important for motivation for highly salient, positive <b>reinforcement</b>.
+HCRT	drug	cocaine	19741128	Blockade of ox/<strong>hcrt</strong> 1R selectively reduced work to self administer <b>cocaine</b> or high fat food pellets.
+HCRT	drug	cocaine	19741128	Moreover, oxA/<strong>hcrt</strong> 1 strengthened presynaptic glutamatergic inputs to the ventral tegmental area (VTA) only in <b>cocaine</b> or high fat self administering rats.
+HCRT	addiction	aversion	19741128	Finally, oxA/<strong>hcrt</strong> 1 mediated excitatory synaptic transmission onto VTA neurons was not potentiated following an arousing, <b>aversive</b> stimulus, suggesting that oxA/<strong>hcrt</strong> 1 mediated glutamatergic synaptic transmission was potentiated selectively with highly salient positive reinforcers.
+HCRT	drug	nicotine	19529922	Theoretically, hypocretin (<strong>hcrt</strong>) mechanisms appear to be potential substrates for <b>nicotine</b> addiction: arousal and attentional mechanisms influence use and withdrawal symptoms, and <strong>hcrt</strong> systems overlap anatomically with a number of brain regions associated with <b>nicotine</b> addiction.
+HCRT	addiction	addiction	19529922	Theoretically, hypocretin (<strong>hcrt</strong>) mechanisms appear to be potential substrates for nicotine <b>addiction</b>: arousal and attentional mechanisms influence use and withdrawal symptoms, and <strong>hcrt</strong> systems overlap anatomically with a number of brain regions associated with nicotine <b>addiction</b>.
+HCRT	addiction	withdrawal	19529922	Theoretically, hypocretin (<strong>hcrt</strong>) mechanisms appear to be potential substrates for nicotine addiction: arousal and attentional mechanisms influence use and <b>withdrawal</b> symptoms, and <strong>hcrt</strong> systems overlap anatomically with a number of brain regions associated with nicotine addiction.
+HCRT	drug	nicotine	19529922	This review summarizes the studies that have examined <strong>hcrt</strong> mechanisms in the effects of <b>nicotine</b> and describes <strong>hcrt</strong> innervation of, and effects in, several brain regions implicated in <b>nicotine</b> addiction.
+HCRT	addiction	addiction	19529922	This review summarizes the studies that have examined <strong>hcrt</strong> mechanisms in the effects of nicotine and describes <strong>hcrt</strong> innervation of, and effects in, several brain regions implicated in nicotine <b>addiction</b>.
+HCRT	drug	nicotine	19529922	The review speculates on the possible mechanisms by which <strong>hcrt</strong> may contribute to <b>nicotine</b> addiction in these regions, with the objective of encouraging research in this area.
+HCRT	addiction	addiction	19529922	The review speculates on the possible mechanisms by which <strong>hcrt</strong> may contribute to nicotine <b>addiction</b> in these regions, with the objective of encouraging research in this area.
+HCRT	drug	nicotine	19529922	In a small literature, both experimenter administered and self administered <b>nicotine</b> have been shown to elicit or depend on <strong>hcrt</strong> signaling.
+HCRT	drug	nicotine	19529922	However, although untested in experimental designs, there is compelling evidence that <strong>hcrt</strong> mechanisms in the ventral tegmental area, the pontine region, thalamocortical circuits, the prefrontal cortex, and the amygdala could have a broad influence on <b>nicotine</b> addiction.
+HCRT	addiction	addiction	19529922	However, although untested in experimental designs, there is compelling evidence that <strong>hcrt</strong> mechanisms in the ventral tegmental area, the pontine region, thalamocortical circuits, the prefrontal cortex, and the amygdala could have a broad influence on nicotine <b>addiction</b>.
+HCRT	drug	nicotine	19529922	Evidence reviewed leads to the conclusion that <strong>hcrt</strong> mechanisms could mediate several dimensions of <b>nicotine</b> addiction, including a multi faceted regulation of mesocorticolimbic dopaminergic function, but beyond dopaminergic mechanisms, <strong>hcrt</strong> could influence <b>nicotine</b> use and relapse during abstinence through broadly based arousal/attentional effects.
+HCRT	addiction	addiction	19529922	Evidence reviewed leads to the conclusion that <strong>hcrt</strong> mechanisms could mediate several dimensions of nicotine <b>addiction</b>, including a multi faceted regulation of mesocorticolimbic dopaminergic function, but beyond dopaminergic mechanisms, <strong>hcrt</strong> could influence nicotine use and relapse during abstinence through broadly based arousal/attentional effects.
+HCRT	addiction	relapse	19529922	Evidence reviewed leads to the conclusion that <strong>hcrt</strong> mechanisms could mediate several dimensions of nicotine addiction, including a multi faceted regulation of mesocorticolimbic dopaminergic function, but beyond dopaminergic mechanisms, <strong>hcrt</strong> could influence nicotine use and <b>relapse</b> during abstinence through broadly based arousal/attentional effects.
+HCRT	drug	cocaine	19251246	Intra VTA <strong>Hcrt</strong> reinstates morphine conditioned place preferences, and intracerebroventricular and intra VTA corticotropin releasing factor (CRF) reinstate <b>cocaine</b> seeking.
+HCRT	drug	opioid	19251246	Intra VTA <strong>Hcrt</strong> reinstates <b>morphine</b> conditioned place preferences, and intracerebroventricular and intra VTA corticotropin releasing factor (CRF) reinstate cocaine seeking.
+HCRT	addiction	relapse	19251246	Intra VTA <strong>Hcrt</strong> reinstates morphine conditioned place preferences, and intracerebroventricular and intra VTA corticotropin releasing factor (CRF) reinstate cocaine <b>seeking</b>.
+HCRT	drug	cocaine	19251246	Here, we examined the possibility that VTA perfusion of <strong>Hcrt</strong> reinstates <b>cocaine</b> seeking and, if so, whether it does so through the VTA mechanism that is implicated in reinstatement by CRF.
+HCRT	addiction	relapse	19251246	Here, we examined the possibility that VTA perfusion of <strong>Hcrt</strong> reinstates cocaine <b>seeking</b> and, if so, whether it does so through the VTA mechanism that is implicated in <b>reinstatement</b> by CRF.
+HCRT	addiction	relapse	19251246	<b>Reinstatement</b> behavior was tested and VTA dialysates were collected and assayed for glutamate or dopamine following footshock or perfusion of <strong>Hcrt</strong> or CRF, with or without <strong>Hcrt</strong> or CRF antagonists, into the VTA.
+HCRT	drug	cocaine	19251246	Ventral tegmental area perfusion of <strong>Hcrt</strong> 1 or footshock stress reinstated <b>cocaine</b> seeking and caused release of VTA glutamate and dopamine.
+HCRT	addiction	relapse	19251246	Ventral tegmental area perfusion of <strong>Hcrt</strong> 1 or footshock stress reinstated cocaine <b>seeking</b> and caused release of VTA glutamate and dopamine.
+HCRT	addiction	relapse	19251246	The <strong>Hcrt</strong> 1 antagonist did not block CRF dependent footshock induced <b>reinstatement</b> or glutamate or dopamine release.
+HCRT	addiction	relapse	19251246	The behavioral and neurochemical effects of <strong>Hcrt</strong> 1 were attenuated but not blocked by kynurenic acid, an ionotropic glutamate antagonist that blocks footshock induced <b>reinstatement</b> and glutamate release.
+HCRT	drug	cocaine	19251246	While <strong>Hcrt</strong> and CRF are known to interact in some area of the brain, in the VTA proper they appear to have largely independent actions on the mesolimbic dopamine mechanisms of <b>cocaine</b> seeking.
+HCRT	addiction	relapse	19251246	While <strong>Hcrt</strong> and CRF are known to interact in some area of the brain, in the VTA proper they appear to have largely independent actions on the mesolimbic dopamine mechanisms of cocaine <b>seeking</b>.
+HCRT	drug	nicotine	19033203	Blockade of <strong>Hcrt</strong> 1 receptors also abolished the stimulatory effects of <b>nicotine</b> on brain reward circuitries, as measured by reversal of <b>nicotine</b> induced lowering of intracranial self stimulation thresholds.
+HCRT	addiction	reward	19033203	Blockade of <strong>Hcrt</strong> 1 receptors also abolished the stimulatory effects of nicotine on brain <b>reward</b> circuitries, as measured by reversal of nicotine induced lowering of intracranial self stimulation thresholds.
+HCRT	drug	nicotine	19033203	In addition, we show that hypocretin containing fibers innervate the insula, <strong>Hcrt</strong> 1 receptors are located on insular cells, and blockade of <strong>Hcrt</strong> 1 receptors in the insula but not in the adjacent somatosensory cortex decreases <b>nicotine</b> self administration.
+HCRT	drug	alcohol	18470506	The results suggest that inhibition of OX 1/<strong>Hcrt</strong> 1 receptors modulates operant <b>ethanol</b> self administration and also plays a significant role in yohimbine induced reinstatement of both <b>ethanol</b> and sucrose seeking in rats.
+HCRT	addiction	relapse	18470506	The results suggest that inhibition of OX 1/<strong>Hcrt</strong> 1 receptors modulates operant ethanol self administration and also plays a significant role in yohimbine induced <b>reinstatement</b> of both ethanol and sucrose <b>seeking</b> in rats.
+HCRT	addiction	reward	18470506	The results suggest that inhibition of OX 1/<strong>Hcrt</strong> 1 receptors modulates <b>operant</b> ethanol self administration and also plays a significant role in yohimbine induced reinstatement of both ethanol and sucrose seeking in rats.
+HCRT	drug	cocaine	16357203	Here we show that intracerebroventricular infusions of <strong>Hcrt</strong> 1 lead to a dose related reinstatement of <b>cocaine</b> seeking without altering <b>cocaine</b> intake in rats.
+HCRT	addiction	relapse	16357203	Here we show that intracerebroventricular infusions of <strong>Hcrt</strong> 1 lead to a dose related <b>reinstatement</b> of cocaine <b>seeking</b> without altering cocaine intake in rats.
+HCRT	drug	cocaine	16357203	<strong>Hcrt</strong> 1 also dramatically elevates intracranial self stimulation thresholds, indicating that, unlike treatments with reinforcing properties such as <b>cocaine</b>, <strong>Hcrt</strong> 1 negatively regulates the activity of brain reward circuitries.
+HCRT	addiction	reward	16357203	<strong>Hcrt</strong> 1 also dramatically elevates intracranial self stimulation thresholds, indicating that, unlike treatments with <b>reinforcing</b> properties such as cocaine, <strong>Hcrt</strong> 1 negatively regulates the activity of brain <b>reward</b> circuitries.
+HCRT	drug	cocaine	16357203	Hypocretin induced reinstatement of <b>cocaine</b> seeking was prevented by blockade of noradrenergic and corticotropin releasing factor systems, suggesting that <strong>Hcrt</strong> 1 reinstated drug seeking through induction of a stress like state.
+HCRT	addiction	relapse	16357203	Hypocretin induced <b>reinstatement</b> of cocaine <b>seeking</b> was prevented by blockade of noradrenergic and corticotropin releasing factor systems, suggesting that <strong>Hcrt</strong> 1 reinstated drug <b>seeking</b> through induction of a stress like state.
+HCRT	drug	cocaine	16357203	Consistent with this interpretation, the selective <strong>Hcrt</strong> 1 receptor antagonist SB 334867 blocked footshock induced reinstatement of previously extinguished <b>cocaine</b> seeking behavior.
+HCRT	addiction	relapse	16357203	Consistent with this interpretation, the selective <strong>Hcrt</strong> 1 receptor antagonist SB 334867 blocked footshock induced <b>reinstatement</b> of previously extinguished cocaine <b>seeking</b> behavior.
+GRM7	drug	alcohol	31260653	The present study was conducted to evaluate the influence of AMN082, the metabotropic glutamate receptor subtype 7 (<strong>mGlu7</strong>) allosteric agonist on different stages of memory processes connected with fear conditioning in the passive avoidance (PA) learning task in mice and negative emotional state (anxiety like) induced by <b>ethanol</b>  and morphine withdrawal in the elevated plus maze (EPM) test in rats.
+GRM7	drug	opioid	31260653	The present study was conducted to evaluate the influence of AMN082, the metabotropic glutamate receptor subtype 7 (<strong>mGlu7</strong>) allosteric agonist on different stages of memory processes connected with fear conditioning in the passive avoidance (PA) learning task in mice and negative emotional state (anxiety like) induced by ethanol  and <b>morphine</b> withdrawal in the elevated plus maze (EPM) test in rats.
+GRM7	addiction	withdrawal	31260653	The present study was conducted to evaluate the influence of AMN082, the metabotropic glutamate receptor subtype 7 (<strong>mGlu7</strong>) allosteric agonist on different stages of memory processes connected with fear conditioning in the passive avoidance (PA) learning task in mice and negative emotional state (anxiety like) induced by ethanol  and morphine <b>withdrawal</b> in the elevated plus maze (EPM) test in rats.
+GRM7	drug	alcohol	31260653	Taken together, the results show that <strong>mGlu7</strong> is involved in fear learning to the context and anxiety like state connected with unpleasant experiences after <b>ethanol</b>  and morphine withdrawal in rodents.
+GRM7	drug	opioid	31260653	Taken together, the results show that <strong>mGlu7</strong> is involved in fear learning to the context and anxiety like state connected with unpleasant experiences after ethanol  and <b>morphine</b> withdrawal in rodents.
+GRM7	addiction	withdrawal	31260653	Taken together, the results show that <strong>mGlu7</strong> is involved in fear learning to the context and anxiety like state connected with unpleasant experiences after ethanol  and morphine <b>withdrawal</b> in rodents.
+GRM7	drug	opioid	29800675	Previous documents have shown the extensive distributions of the different types of mGluRs, including <strong>mGluR7</strong>, in regions that are involved in <b>opioid</b> reward, such as the NAc.
+GRM7	addiction	reward	29800675	Previous documents have shown the extensive distributions of the different types of mGluRs, including <strong>mGluR7</strong>, in regions that are involved in opioid <b>reward</b>, such as the NAc.
+GRM7	drug	opioid	29800675	In this study, seventy male Wistar rats were used to investigate the role of <strong>mGluR7</strong> receptors in the NAc on the acquisition and expression of <b>morphine</b> induced conditioned place preference (CPP).
+GRM7	addiction	reward	29800675	In this study, seventy male Wistar rats were used to investigate the role of <strong>mGluR7</strong> receptors in the NAc on the acquisition and expression of morphine induced conditioned place preference (<b>CPP</b>).
+GRM7	drug	opioid	29800675	In Experiment 1, to determine the effect of AMN082, a selective <strong>mGluR7</strong> allosteric agonist, on the acquisition of <b>morphine</b> induced conditioned place preference (CPP), the rats bilaterally received AMN082 (1, 3 and 5 μg/0.5 μL DMSO) during three day conditioning by <b>morphine</b> (5 mg/kg).
+GRM7	addiction	reward	29800675	In Experiment 1, to determine the effect of AMN082, a selective <strong>mGluR7</strong> allosteric agonist, on the acquisition of morphine induced conditioned place preference (<b>CPP</b>), the rats bilaterally received AMN082 (1, 3 and 5 μg/0.5 μL DMSO) during three day conditioning by morphine (5 mg/kg).
+GRM7	drug	opioid	29800675	The findings propose that the <strong>mGluR7</strong> in the NAc inhibits the acquisition of <b>morphine</b> induced CPP that could be mediated by inhibition of NMDA receptors in the NAc.
+GRM7	addiction	reward	29800675	The findings propose that the <strong>mGluR7</strong> in the NAc inhibits the acquisition of morphine induced <b>CPP</b> that could be mediated by inhibition of NMDA receptors in the NAc.
+GRM7	drug	opioid	29605484	Previous studies have shown the extensive distributions of the different types of mGluRs, including <strong>mGluR7</strong>, in regions that are involved in <b>opioid</b> reward, such as NAc.
+GRM7	addiction	reward	29605484	Previous studies have shown the extensive distributions of the different types of mGluRs, including <strong>mGluR7</strong>, in regions that are involved in opioid <b>reward</b>, such as NAc.
+GRM7	drug	opioid	29605484	In this study, CPP was used to investigate the effect of <strong>mGluR7</strong> on the extinction period, and the reinstatement of <b>morphine</b>.
+GRM7	addiction	relapse	29605484	In this study, CPP was used to investigate the effect of <strong>mGluR7</strong> on the extinction period, and the <b>reinstatement</b> of morphine.
+GRM7	addiction	reward	29605484	In this study, <b>CPP</b> was used to investigate the effect of <strong>mGluR7</strong> on the extinction period, and the reinstatement of morphine.
+GRM7	drug	opioid	29605484	The findings suggested that the <strong>mGluR7</strong> in the NAc facilitates the extinction and inhibits the reinstatement of the <b>morphine</b> induced CPP that could have been mediated by an increase in the release of extracellular glutamate.
+GRM7	addiction	relapse	29605484	The findings suggested that the <strong>mGluR7</strong> in the NAc facilitates the extinction and inhibits the <b>reinstatement</b> of the morphine induced CPP that could have been mediated by an increase in the release of extracellular glutamate.
+GRM7	addiction	reward	29605484	The findings suggested that the <strong>mGluR7</strong> in the NAc facilitates the extinction and inhibits the reinstatement of the morphine induced <b>CPP</b> that could have been mediated by an increase in the release of extracellular glutamate.
+GRM7	drug	alcohol	29378211	Pharmacological activation of mGlu4 and <strong>mGlu7</strong> receptors, by LSP2 9166, reduces <b>ethanol</b> consumption and relapse in rat.
+GRM7	addiction	relapse	29378211	Pharmacological activation of mGlu4 and <strong>mGlu7</strong> receptors, by LSP2 9166, reduces ethanol consumption and <b>relapse</b> in rat.
+GRM7	drug	alcohol	29378211	Thus, the aim of the present study is to determine whether LSP2 9166, a mixed mGlu4/<strong>mGlu7</strong> orthosteric agonist, could reduce <b>ethanol</b> self administration, <b>ethanol</b> motivation and reacquisition after protracted abstinence in a preclinical model of excessive <b>ethanol</b> intake.
+GRM7	drug	opioid	29307544	Role of <strong>mGlu7</strong> receptor in <b>morphine</b> rewarding effects is uncovered by a novel orthosteric agonist.
+GRM7	drug	opioid	29307544	So we investigated the role of group III mGlu receptors in <b>morphine</b> rewarding effects through the expression and the reinstatement of conditioned place preference (CPP) using a newly synthesized mGlu4/<strong>mGlu7</strong> receptor orthosteric agonist, LSP2 9166.
+GRM7	addiction	relapse	29307544	So we investigated the role of group III mGlu receptors in morphine rewarding effects through the expression and the <b>reinstatement</b> of conditioned place preference (CPP) using a newly synthesized mGlu4/<strong>mGlu7</strong> receptor orthosteric agonist, LSP2 9166.
+GRM7	addiction	reward	29307544	So we investigated the role of group III mGlu receptors in morphine rewarding effects through the expression and the reinstatement of conditioned place preference (<b>CPP</b>) using a newly synthesized mGlu4/<strong>mGlu7</strong> receptor orthosteric agonist, LSP2 9166.
+GRM7	addiction	reward	29307544	Blockade of <b>CPP</b> expression with LSP2 9166 was abolished when using XAP044, a <strong>mGlu7</strong> antagonist.
+GRM7	addiction	addiction	29307544	Altogether our data demonstrated that group III mGlu receptors, and more specifically <strong>mGlu7</strong>, might be a valuable target in opiate <b>addiction</b>.
+GRM7	drug	alcohol	28242339	Among the glutamate receptors involved in <b>alcohol</b> drinking behavior are the metabotropic receptors such as mGluR1/5, mGluR2/3, and <strong>mGluR7</strong>, as well as the ionotropic receptors, NMDA and AMPA.
+GRM7	drug	alcohol	27788777	Test for association of common variants in <strong>GRM7</strong> with <b>alcohol</b> consumption.
+GRM7	drug	alcohol	27788777	Recent work using a mouse model has identified the glutamate metabotropic receptor 7 (<strong>Grm7</strong>) gene as a strong candidate gene for <b>alcohol</b> consumption.
+GRM7	drug	alcohol	27788777	Recent work using a mouse model has identified the <strong>glutamate metabotropic receptor 7</strong> (<strong>Grm7</strong>) gene as a strong candidate gene for <b>alcohol</b> consumption.
+GRM7	drug	alcohol	27788777	The current study aimed to evaluate evidence for association between <strong>GRM7</strong> and <b>alcohol</b> behaviors in humans using a single nucleotide polymorphism (SNP) approach, as well as a gene based approach.
+GRM7	drug	alcohol	27788777	Using 1803 non Hispanic European Americans (EAs) (source: the Colorado Center on Antisocial Drug Dependence [CADD]) and 1049 EA subjects from an independent replication sample (source: the Genetics of Antisocial Drug Dependence [GADD]), two SNPs in <strong>GRM7</strong> were examined for possible association with <b>alcohol</b> consumption using two family based association tests implemented in FBAT and QTDT.
+GRM7	addiction	dependence	27788777	Using 1803 non Hispanic European Americans (EAs) (source: the Colorado Center on Antisocial Drug <b>Dependence</b> [CADD]) and 1049 EA subjects from an independent replication sample (source: the Genetics of Antisocial Drug <b>Dependence</b> [GADD]), two SNPs in <strong>GRM7</strong> were examined for possible association with alcohol consumption using two family based association tests implemented in FBAT and QTDT.
+GRM7	drug	alcohol	27788777	A gene based test using four Genome Wide Association Studies (GWAS) revealed no association between variation in <strong>GRM7</strong> and <b>alcohol</b> consumption.
+GRM7	drug	alcohol	27788777	This study had several limitations: the SNPs chosen likely do not tag expression quantitative trait loci; a human <b>alcohol</b> consumption phenotype was used, complicating the interpretation with respect to rodent studies that found evidence for a cis regulatory link between <b>alcohol</b> preference and <strong>Grm7</strong>; and only common SNPs imputed in all four datasets were included in the gene based test.
+GRM7	drug	nicotine	27711239	However, a few linkage studies have reported suggestive linkage to the 3p26.1 region, and a few genome wide association studies (GWAS) have reported markers in the gene (<strong>GRM7</strong>) nearest to this 3p26.1 area of polymorphic deletions are associated with measures of <b>nicotine</b> dependence among subjects of European ancestry.
+GRM7	addiction	dependence	27711239	However, a few linkage studies have reported suggestive linkage to the 3p26.1 region, and a few genome wide association studies (GWAS) have reported markers in the gene (<strong>GRM7</strong>) nearest to this 3p26.1 area of polymorphic deletions are associated with measures of nicotine <b>dependence</b> among subjects of European ancestry.
+GRM7	addiction	dependence	26022263	Metabotropic Glutamate Receptor 7 (<strong>mGluR7</strong>) as a Target for the Treatment of Psychostimulant <b>Dependence</b>.
+GRM7	drug	cocaine	26022263	This review summarizes nonhuman experimental animal data that indicate a critical role for <strong>mGluR7</strong> in drug taking and drug seeking behaviors for the psychostimulants <b>cocaine</b> and nicotine.
+GRM7	drug	nicotine	26022263	This review summarizes nonhuman experimental animal data that indicate a critical role for <strong>mGluR7</strong> in drug taking and drug seeking behaviors for the psychostimulants cocaine and <b>nicotine</b>.
+GRM7	addiction	relapse	26022263	This review summarizes nonhuman experimental animal data that indicate a critical role for <strong>mGluR7</strong> in drug taking and drug <b>seeking</b> behaviors for the psychostimulants cocaine and nicotine.
+GRM7	addiction	dependence	26022263	AMN082, the only commercially available allosteric receptor agonist, has been used to investigate the role of <strong>mGluR7</strong> in psychostimulant <b>dependence</b>.
+GRM7	drug	cocaine	26022263	These findings indicate an important role for <strong>mGluR7</strong> in mesolimbic areas in modulating the reinforcing effects of psychostimulant drugs, such as nicotine and <b>cocaine</b>, and the conditioned behaviors associated with drugs of abuse.
+GRM7	drug	nicotine	26022263	These findings indicate an important role for <strong>mGluR7</strong> in mesolimbic areas in modulating the reinforcing effects of psychostimulant drugs, such as <b>nicotine</b> and cocaine, and the conditioned behaviors associated with drugs of abuse.
+GRM7	addiction	reward	26022263	These findings indicate an important role for <strong>mGluR7</strong> in mesolimbic areas in modulating the <b>reinforcing</b> effects of psychostimulant drugs, such as nicotine and cocaine, and the conditioned behaviors associated with drugs of abuse.
+GRM7	addiction	dependence	26022263	Thus, selective <strong>mGluR7</strong> agonists or positive allosteric modulators may have the potential to treat psychostimulant <b>dependence</b>.
+GRM7	drug	cocaine	25448778	The aim of the present study was to determine whether systemic injection of AMN082, a selective <strong>mGluR7</strong> allosteric agonist, reduces the <b>cocaine</b>  and morphine induced hyperactivity and the development and expression of locomotor sensitization, and also affects the reciprocal cross sensitization to the stimulant effect of <b>cocaine</b> and morphine in mice.
+GRM7	drug	opioid	25448778	The aim of the present study was to determine whether systemic injection of AMN082, a selective <strong>mGluR7</strong> allosteric agonist, reduces the cocaine  and <b>morphine</b> induced hyperactivity and the development and expression of locomotor sensitization, and also affects the reciprocal cross sensitization to the stimulant effect of cocaine and <b>morphine</b> in mice.
+GRM7	addiction	sensitization	25448778	The aim of the present study was to determine whether systemic injection of AMN082, a selective <strong>mGluR7</strong> allosteric agonist, reduces the cocaine  and morphine induced hyperactivity and the development and expression of locomotor <b>sensitization</b>, and also affects the reciprocal cross <b>sensitization</b> to the stimulant effect of cocaine and morphine in mice.
+GRM7	drug	cocaine	25448778	), a selective <strong>mGluR7</strong> antagonist reversed the inhibitory effect of AMN082 on the development or expression of <b>cocaine</b> or morphine sensitization.
+GRM7	drug	opioid	25448778	), a selective <strong>mGluR7</strong> antagonist reversed the inhibitory effect of AMN082 on the development or expression of cocaine or <b>morphine</b> sensitization.
+GRM7	addiction	sensitization	25448778	), a selective <strong>mGluR7</strong> antagonist reversed the inhibitory effect of AMN082 on the development or expression of cocaine or morphine <b>sensitization</b>.
+GRM7	drug	alcohol	25262781	<b>Alcoholics</b> showed up regulation of three genes relative to controls and cocaine addicts: GRIA4 (encoding GluA4), GRIK3 (<strong>GluR7</strong>) and GRM4 (mGluR4).
+GRM7	drug	cocaine	25262781	Alcoholics showed up regulation of three genes relative to controls and <b>cocaine</b> addicts: GRIA4 (encoding GluA4), GRIK3 (<strong>GluR7</strong>) and GRM4 (mGluR4).
+GRM7	drug	alcohol	23006490	The aim of this study was to evaluate the role of the glutamate receptor subunit 7 (<strong>GluR7</strong>, GRIK 3) rs6691840 (Ser310Ala, T928G) in the pathogenesis of <b>alcohol</b> dependence (AD).
+GRM7	addiction	dependence	23006490	The aim of this study was to evaluate the role of the glutamate receptor subunit 7 (<strong>GluR7</strong>, GRIK 3) rs6691840 (Ser310Ala, T928G) in the pathogenesis of alcohol <b>dependence</b> (AD).
+GRM7	drug	alcohol	22781839	Viral mediated knockdown of <strong>mGluR7</strong> in the nucleus accumbens mediates excessive <b>alcohol</b> drinking and increased <b>ethanol</b> elicited conditioned place preference in rats.
+GRM7	addiction	reward	22781839	Whether metabotropic glutamate 7 (<strong>mGluR7</strong>)  activation enhances or diminishes the <b>reinforcing</b> properties of psychostimulants remains unclear.
+GRM7	drug	alcohol	22781839	We have previously shown that systemic <strong>mGluR7</strong> activation reduced <b>alcohol</b> consumption and preference as well as locomotor stimulating and rewarding properties of <b>ethanol</b>.
+GRM7	drug	alcohol	22781839	In this study, we further examined the contribution of <strong>mGluR7</strong> on the effect of <b>ethanol</b> within the nucleus accumbens (NAcc), a neural target for many drugs of abuse.
+GRM7	drug	alcohol	22781839	Using short hairpin RNA (shRNA) expressing lentiviral vectors (LV) to alter locally the activity of <strong>mGluR7</strong> in male rats, we have shown that blocking <strong>mGluR7</strong> expression increased <b>ethanol</b> consumption and preference in a two bottle choice drinking paradigm with no effect either on saccharin or on quinine used for taste discrimination.
+GRM7	drug	alcohol	22781839	In addition, <strong>mGluR7</strong> knockdown increases preference for environments previously paired with low doses of <b>ethanol</b> in the conditioned place preference (CPP) test, as it shifted the dose response curve for <b>ethanol</b> CPP to the left, indicating alterations in the rewarding effects of <b>alcohol</b>.
+GRM7	addiction	reward	22781839	In addition, <strong>mGluR7</strong> knockdown increases preference for environments previously paired with low doses of ethanol in the conditioned place preference (<b>CPP</b>) test, as it shifted the dose response curve for ethanol <b>CPP</b> to the left, indicating alterations in the rewarding effects of alcohol.
+GRM7	drug	alcohol	22781839	More importantly, <strong>mGluR7</strong> blockade in the dorsal striatum (DS) neither affected <b>ethanol</b> consumption nor <b>ethanol</b> elicited CPP.
+GRM7	addiction	reward	22781839	More importantly, <strong>mGluR7</strong> blockade in the dorsal striatum (DS) neither affected ethanol consumption nor ethanol elicited <b>CPP</b>.
+GRM7	drug	alcohol	22781839	These results show that levels of <strong>mGluR7</strong> in the NAcc regulate responsiveness to <b>alcohol</b>.
+GRM7	drug	alcohol	22781839	Taken together, these findings clearly demonstrate that <strong>mGluR7</strong> signaling within the NAcc is a key modulator of functional responses to <b>ethanol</b> and offer an important target for regulating the addictive effects of <b>alcohol</b>.
+GRM7	addiction	addiction	22781839	Taken together, these findings clearly demonstrate that <strong>mGluR7</strong> signaling within the NAcc is a key modulator of functional responses to ethanol and offer an important target for regulating the <b>addictive</b> effects of alcohol.
+GRM7	drug	cocaine	22546614	Metabotropic glutamate 7 (<strong>mGlu7</strong>) receptor: a target for medication development for the treatment of <b>cocaine</b> dependence.
+GRM7	addiction	dependence	22546614	Metabotropic glutamate 7 (<strong>mGlu7</strong>) receptor: a target for medication development for the treatment of cocaine <b>dependence</b>.
+GRM7	addiction	dependence	22546614	In this review article, we focus on the <strong>mGlu7</strong> receptor subtype, and discuss recent findings with AMN082, a selective <strong>mGlu7</strong> receptor allosteric agonist, in animal models with relevance to drug <b>dependence</b>.
+GRM7	addiction	dependence	22546614	Taken together, these findings suggest that the <strong>mGlu7</strong> receptor is an important target for medication development for the treatment of drug <b>dependence</b>.
+GRM7	drug	cocaine	22546614	AMN082 or other <strong>mGlu7</strong> receptor allosteric agonists may have potential as novel pharmacotherapies for <b>cocaine</b> addiction.
+GRM7	addiction	addiction	22546614	AMN082 or other <strong>mGlu7</strong> receptor allosteric agonists may have potential as novel pharmacotherapies for cocaine <b>addiction</b>.
+GRM7	drug	amphetamine	22479593	Extinction dependent alterations in corticostriatal mGluR2/3 and <strong>mGluR7</strong> receptors following chronic <b>methamphetamine</b> self administration in rats.
+GRM7	drug	amphetamine	22479593	Extended access to <b>meth</b> self administration followed by abstinence decreased surface and total levels of mGluR2/3 receptors in the NAc and dSTR, while in the PFC, only a loss of surface mGluR2/3 and <strong>mGluR7</strong> receptors was detected.
+GRM7	drug	amphetamine	22479593	Daily extinction trials reversed the downregulation of mGluR2/3 receptors in the NAc and dSTR and <strong>mGluR7</strong> in the PFC, but downregulation of surface mGluR2/3 receptors in the PFC was present regardless of post <b>meth</b> experience.
+GRM7	drug	alcohol	22269296	Our previous findings have shown that in rats, the <strong>mGluR7</strong> positive allosteric agonist AMN082, but not its allosteric antagonist MMPIP, prevented <b>ethanol</b> consumption and preference in the two bottle choice paradigm.
+GRM7	drug	alcohol	22269296	AMN082 and MMPIP were administered during extinction of <b>ethanol</b> CPP to determine whether <strong>mGluR7</strong> signaling is required.
+GRM7	addiction	reward	22269296	AMN082 and MMPIP were administered during extinction of ethanol <b>CPP</b> to determine whether <strong>mGluR7</strong> signaling is required.
+GRM7	drug	alcohol	22269296	Our results indicate that <strong>mGluR7</strong> pharmacological modulation had no effect on <b>ethanol</b> elicited CPP extinction.
+GRM7	addiction	reward	22269296	Our results indicate that <strong>mGluR7</strong> pharmacological modulation had no effect on ethanol elicited <b>CPP</b> extinction.
+GRM7	drug	alcohol	22269296	In contrast, <strong>mGluR7</strong> activation using AMN082 reduced <b>ethanol</b> induced CPP reinstatement, an effect reversed by co administration of MMPIP.
+GRM7	addiction	relapse	22269296	In contrast, <strong>mGluR7</strong> activation using AMN082 reduced ethanol induced CPP <b>reinstatement</b>, an effect reversed by co administration of MMPIP.
+GRM7	addiction	reward	22269296	In contrast, <strong>mGluR7</strong> activation using AMN082 reduced ethanol induced <b>CPP</b> reinstatement, an effect reversed by co administration of MMPIP.
+GRM7	drug	alcohol	22269296	Collectively, these results indicate, for the first time, that activation of the <strong>mGluR7</strong> receptor is effective in reducing the reinstatement of conditioned rewarding effects of <b>ethanol</b>.
+GRM7	addiction	relapse	22269296	Collectively, these results indicate, for the first time, that activation of the <strong>mGluR7</strong> receptor is effective in reducing the <b>reinstatement</b> of conditioned rewarding effects of ethanol.
+GRM7	drug	alcohol	22056957	The pre synaptic metabotropic glutamate receptor 7 "<strong>mGluR7</strong>" is a critical modulator of <b>ethanol</b> sensitivity in mice.
+GRM7	drug	alcohol	22056957	Recent studies demonstrated that the metabotropic glutamate receptor subtype 7 "<strong>mGluR7</strong>" activation may reduce motivational aspects of <b>ethanol</b> dependence.
+GRM7	addiction	dependence	22056957	Recent studies demonstrated that the metabotropic glutamate receptor subtype 7 "<strong>mGluR7</strong>" activation may reduce motivational aspects of ethanol <b>dependence</b>.
+GRM7	drug	alcohol	22056957	We investigated the role of <strong>mGlu7</strong> receptor in <b>ethanol</b> related behaviors using the allosteric agonist AMN082 in mice.
+GRM7	drug	alcohol	22056957	Results have shown that <strong>mGluR7</strong> activation increased the sedative effect of <b>ethanol</b> as measured by the duration of loss of righting reflex (LORR) and reduced the severity of <b>ethanol</b> induced withdrawal.
+GRM7	addiction	withdrawal	22056957	Results have shown that <strong>mGluR7</strong> activation increased the sedative effect of ethanol as measured by the duration of loss of righting reflex (LORR) and reduced the severity of ethanol induced <b>withdrawal</b>.
+GRM7	drug	alcohol	22056957	Importantly, the protective effect of the drug on <b>alcohol</b> induced withdrawal was found when the AMN082 was injected before, but not after, injection of <b>ethanol</b> suggesting that <strong>mGluR7</strong> activation prevented development of dependence rather than producing an anti convulsant effect.
+GRM7	addiction	dependence	22056957	Importantly, the protective effect of the drug on alcohol induced withdrawal was found when the AMN082 was injected before, but not after, injection of ethanol suggesting that <strong>mGluR7</strong> activation prevented development of <b>dependence</b> rather than producing an anti convulsant effect.
+GRM7	addiction	withdrawal	22056957	Importantly, the protective effect of the drug on alcohol induced <b>withdrawal</b> was found when the AMN082 was injected before, but not after, injection of ethanol suggesting that <strong>mGluR7</strong> activation prevented development of dependence rather than producing an anti convulsant effect.
+GRM7	drug	alcohol	22056957	In addition, <b>ethanol</b> induced locomotor stimulation was blocked by following <strong>mGluR7</strong> activation.
+GRM7	drug	alcohol	22056957	Taken together, these findings provide evidence for the crucial role of <strong>mGluR7</strong> in <b>ethanol</b> related behaviors, especially in voluntary <b>alcohol</b> drinking and <b>alcohol</b> reward.
+GRM7	addiction	reward	22056957	Taken together, these findings provide evidence for the crucial role of <strong>mGluR7</strong> in ethanol related behaviors, especially in voluntary alcohol drinking and alcohol <b>reward</b>.
+GRM7	drug	alcohol	22056957	Thus, pharmacological targeting <strong>mGluR7</strong> with AMN082 like compounds might be a potential means to tackle <b>ethanol</b> abuse and <b>alcoholism</b> in the future.
+GRM7	drug	alcohol	21706135	Retracted article: Selective activation of the metabotropic glutamate receptor subtype 7 "<strong>mGluR7</strong>" attenuates acquisition, expression, and reinstatement of <b>ethanol</b> place preference.
+GRM7	addiction	relapse	21706135	Retracted article: Selective activation of the metabotropic glutamate receptor subtype 7 "<strong>mGluR7</strong>" attenuates acquisition, expression, and <b>reinstatement</b> of ethanol place preference.
+GRM7	drug	alcohol	21448595	<strong>mGluR7</strong> genetics and <b>alcohol</b>: intersection yields clues for addiction.
+GRM7	addiction	addiction	21448595	<strong>mGluR7</strong> genetics and alcohol: intersection yields clues for <b>addiction</b>.
+GRM7	drug	alcohol	21448595	Quantitative genetic analysis of voluntary <b>alcohol</b> drinking, and mapping of the involved genes in the quasi congenic Recombinant QTL Introgression strain system, identified Eac2 as a Quantitative Trait Locus (QTL) on mouse chromosome 6 which explained 18% of the variance with an effect size of 2.09 g/kg/day <b>alcohol</b> consumption, and <strong>Grm7</strong> as a quantitative trait gene underlying Eac2 [Vadasz et al.
+GRM7	drug	alcohol	21448595	Here, in experiments with mice, we show that (1) <strong>Grm7</strong> knockout mice express increased <b>alcohol</b> consumption, (2) sub congenic, and congenic mice carrying a <strong>Grm7</strong> variant characterized by higher <strong>Grm7</strong> mRNA drink less <b>alcohol</b>, and show a tendency for higher circadian dark phase motor activity in a wheel running paradigm, respectively, and (3) there are significant genetic differences in <strong>Grm7</strong> mRNA abundance in the mouse brain between congenic and background mice identifying brain areas whose function is implicated in addiction related processes.
+GRM7	addiction	addiction	21448595	Here, in experiments with mice, we show that (1) <strong>Grm7</strong> knockout mice express increased alcohol consumption, (2) sub congenic, and congenic mice carrying a <strong>Grm7</strong> variant characterized by higher <strong>Grm7</strong> mRNA drink less alcohol, and show a tendency for higher circadian dark phase motor activity in a wheel running paradigm, respectively, and (3) there are significant genetic differences in <strong>Grm7</strong> mRNA abundance in the mouse brain between congenic and background mice identifying brain areas whose function is implicated in <b>addiction</b> related processes.
+GRM7	addiction	reward	21448595	We hypothesize that metabotropic glutamate receptors may function as regulators of homeostasis, and <strong>Grm7</strong> (mGluR7) is involved in multiple processes (including stress, circadian activity, <b>reward</b> control, memory, etc.)
+GRM7	addiction	reward	21448595	We hypothesize that metabotropic glutamate receptors may function as regulators of homeostasis, and <strong>Grm7</strong> (<strong>mGluR7</strong>) is involved in multiple processes (including stress, circadian activity, <b>reward</b> control, memory, etc.)
+GRM7	addiction	addiction	21448595	In conclusion, we suggest that <strong>mGluR7</strong> is a significant new therapeutic target in <b>addiction</b> and related neurobehavioral disorders.
+GRM7	drug	alcohol	21392179	Pharmacological modulation of <strong>mGluR7</strong> with AMN082 and MMPIP exerts specific influences on <b>alcohol</b> consumption and preference in rats.
+GRM7	drug	alcohol	21392179	<b>Alcohol</b> dependence, for instance, has a genetic component, and the recent discovery that variations in the gene coding for <strong>mGluR7</strong> modulate <b>alcohol</b> consumption further validates involvement of the L glutamate system.
+GRM7	addiction	dependence	21392179	Alcohol <b>dependence</b>, for instance, has a genetic component, and the recent discovery that variations in the gene coding for <strong>mGluR7</strong> modulate alcohol consumption further validates involvement of the L glutamate system.
+GRM7	drug	alcohol	21392179	To this end, we performed a detailed behavioral pharmacology study to investigate the regulation of <b>alcohol</b> consumption and preference following administration of the <strong>mGluR7</strong> selective drugs N,N' dibenzyhydryl ethane 1,2 diamine dihydrochloride (AMN082) and 6 (4 Methoxyphenyl) 5 methyl 3 (4 pyridinyl) isoxazolo[4,5 c]pyridin 4(5H) one hydrochloride (MMPIP).
+GRM7	drug	alcohol	21392179	In conclusion, these findings support a specific regulatory role for <strong>mGluR7</strong> on <b>alcohol</b> drinking and preference and provide evidence for the use of AMN082 type drugs as potential new treatments for <b>alcohol</b> use disorders in man.
+GRM7	drug	alcohol	20534005	The metabotropic glutamate receptor 7 (<strong>mGluR7</strong>) has been reported to be involved in cocaine and <b>alcohol</b> self administration.
+GRM7	drug	cocaine	20534005	The metabotropic glutamate receptor 7 (<strong>mGluR7</strong>) has been reported to be involved in <b>cocaine</b> and alcohol self administration.
+GRM7	addiction	relapse	20534005	However, the role of <strong>mGluR7</strong> in <b>relapse</b> to drug <b>seeking</b> is unknown.
+GRM7	drug	cocaine	20534005	Using a rat relapse model, we found that systemic administration of AMN082, a selective <strong>mGluR7</strong> allosteric agonist, dose dependently inhibits <b>cocaine</b> induced reinstatement of drug seeking behavior.
+GRM7	addiction	relapse	20534005	Using a rat <b>relapse</b> model, we found that systemic administration of AMN082, a selective <strong>mGluR7</strong> allosteric agonist, dose dependently inhibits cocaine induced <b>reinstatement</b> of drug <b>seeking</b> behavior.
+GRM7	drug	cocaine	20534005	Intracranial microinjections of AMN082 into the nucleus accumbens (NAc) or ventral pallidum, but not the dorsal striatum, also inhibited <b>cocaine</b> primed reinstatement, an effect that was blocked by local co administration of MMPIP, a selective <strong>mGluR7</strong> antagonist.
+GRM7	addiction	relapse	20534005	Intracranial microinjections of AMN082 into the nucleus accumbens (NAc) or ventral pallidum, but not the dorsal striatum, also inhibited cocaine primed <b>reinstatement</b>, an effect that was blocked by local co administration of MMPIP, a selective <strong>mGluR7</strong> antagonist.
+GRM7	drug	cocaine	20534005	These data suggest that <strong>mGluR7</strong> activation inhibits <b>cocaine</b> induced reinstatement of drug seeking behavior by a glutamate mGluR2/3 mechanism in the NAc.
+GRM7	addiction	relapse	20534005	These data suggest that <strong>mGluR7</strong> activation inhibits cocaine induced <b>reinstatement</b> of drug <b>seeking</b> behavior by a glutamate mGluR2/3 mechanism in the NAc.
+GRM7	drug	cocaine	20534005	The present findings support the potential use of <strong>mGluR7</strong> agonists for the treatment of <b>cocaine</b> addiction.
+GRM7	addiction	addiction	20534005	The present findings support the potential use of <strong>mGluR7</strong> agonists for the treatment of cocaine <b>addiction</b>.
+GRM7	drug	cocaine	19158667	In this study, we investigated the possible involvement of <strong>mGluR7</strong> in <b>cocaine</b> reward in animal models of drug addiction.
+GRM7	addiction	addiction	19158667	In this study, we investigated the possible involvement of <strong>mGluR7</strong> in cocaine reward in animal models of drug <b>addiction</b>.
+GRM7	addiction	reward	19158667	In this study, we investigated the possible involvement of <strong>mGluR7</strong> in cocaine <b>reward</b> in animal models of drug addiction.
+GRM7	drug	cocaine	19158667	These data suggest: (1) <strong>mGluR7</strong> is critically involved in <b>cocaine</b>'s acute reinforcement; (2) GABA , but not DA , dependent mechanisms in the ventral striatopallidal pathway appear to underlie AMN082's actions; and (3) AMN082 or other <strong>mGluR7</strong> selective agonists may be useful in the treatment of <b>cocaine</b> addiction.
+GRM7	addiction	addiction	19158667	These data suggest: (1) <strong>mGluR7</strong> is critically involved in cocaine's acute reinforcement; (2) GABA , but not DA , dependent mechanisms in the ventral striatopallidal pathway appear to underlie AMN082's actions; and (3) AMN082 or other <strong>mGluR7</strong> selective agonists may be useful in the treatment of cocaine <b>addiction</b>.
+GRM7	addiction	reward	19158667	These data suggest: (1) <strong>mGluR7</strong> is critically involved in cocaine's acute <b>reinforcement</b>; (2) GABA , but not DA , dependent mechanisms in the ventral striatopallidal pathway appear to underlie AMN082's actions; and (3) AMN082 or other <strong>mGluR7</strong> selective agonists may be useful in the treatment of cocaine addiction.
+GRM7	drug	alcohol	18593591	Nonselective suppression of operant <b>ethanol</b> and sucrose self administration by the <strong>mGluR7</strong> positive allosteric modulator AMN082.
+GRM7	addiction	reward	18593591	Nonselective suppression of <b>operant</b> ethanol and sucrose self administration by the <strong>mGluR7</strong> positive allosteric modulator AMN082.
+GRM7	drug	alcohol	18593591	The goal of this preclinical study was to further characterize mGluR regulation of <b>ethanol</b> self administration by examining effects of AMN082, an allosteric positive modulator of presynaptic <strong>mGluR7</strong> activity.
+GRM7	drug	alcohol	17936574	Here, using near isogenic advanced animal models with reduced genetic background interactions, we integrate gene mapping and gene mRNA expression data in segregating and congenic mice and identify glutamate receptor metabotropic 7 (<strong>Grm7</strong>) as a cis regulated gene for <b>alcohol</b> consumption.
+GRM7	drug	alcohol	17936574	These data suggest for the first time that <strong>Grm7</strong> is a risk factor for <b>alcohol</b> drinking and a new target in addiction therapy.
+GRM7	addiction	addiction	17936574	These data suggest for the first time that <strong>Grm7</strong> is a risk factor for alcohol drinking and a new target in <b>addiction</b> therapy.
+GRM7	drug	alcohol	15365315	In the CA3 region, the mRNA expression of mGlu1, mGlu5, and <strong>mGlu7</strong> receptors showed substantial decreases after <b>ethanol</b> exposure.
+GRM7	drug	alcohol	11912074	No association between metabotropic glutamate receptors 7 and 8 (<strong>mGlur7</strong> and mGlur8) gene polymorphisms and withdrawal seizures and delirium tremens in <b>alcohol</b> dependent individuals.
+GRM7	addiction	withdrawal	11912074	No association between metabotropic glutamate receptors 7 and 8 (<strong>mGlur7</strong> and mGlur8) gene polymorphisms and <b>withdrawal</b> seizures and delirium tremens in alcohol dependent individuals.
+GABPA	drug	alcohol	32710977	Sulforaphane alleviates <b>ethanol</b> mediated central inhibition and reverses chronic stress induced aggravation of acute <b>alcoholism</b> via targeting <strong>Nrf2</strong> regulated catalase expression.
+GABPA	drug	alcohol	32710977	Here, we reported that chronic unpredictable stress increased the sensitivity to the acute <b>ethanol</b> intoxication in mice via impairing nuclear factor (erythroid derived 2) like 2 (<strong>Nrf2</strong>) catalase signaling.
+GABPA	addiction	intoxication	32710977	Here, we reported that chronic unpredictable stress increased the sensitivity to the acute ethanol <b>intoxication</b> in mice via impairing nuclear factor (erythroid derived 2) like 2 (<strong>Nrf2</strong>) catalase signaling.
+GABPA	drug	alcohol	32710977	<strong>Nrf2</strong> activity regulates the expression of catalase, a key antioxidant enzyme that mediates <b>ethanol</b> oxidation in the brain.
+GABPA	drug	alcohol	32710977	Pharmacological blockade of catalase or <strong>Nrf2</strong> activity significantly aggravated acute <b>ethanol</b> intoxication.
+GABPA	addiction	intoxication	32710977	Pharmacological blockade of catalase or <strong>Nrf2</strong> activity significantly aggravated acute ethanol <b>intoxication</b>.
+GABPA	drug	alcohol	32710977	Sulforaphane, a cruciferous vegetable derived activator of <strong>Nrf2</strong>, significantly attenuated acute <b>ethanol</b> intoxication.
+GABPA	addiction	intoxication	32710977	Sulforaphane, a cruciferous vegetable derived activator of <strong>Nrf2</strong>, significantly attenuated acute ethanol <b>intoxication</b>.
+GABPA	drug	alcohol	32710977	Our findings suggest that <strong>Nrf2</strong> may function as a novel drug target for the prevention of acute <b>alcoholism</b>, especially in psychiatric patients, by controlling catalase mediated <b>ethanol</b> oxidation.
+GABPA	drug	amphetamine	31775383	Additionally, Ingenuity® Pathway Analysis along with details of RNA expression changes revealed cyclo oxygenase 2 (COX2) driven prostaglandin (PG) E2 synthesis, glutamine uptake, and the Nuclear factor erythroid2 related factor 2 (<strong>NRF2</strong>) canonical pathway in microglia were associated with the binge administration regimen of <b>METH</b>.
+GABPA	addiction	intoxication	31775383	Additionally, Ingenuity® Pathway Analysis along with details of RNA expression changes revealed cyclo oxygenase 2 (COX2) driven prostaglandin (PG) E2 synthesis, glutamine uptake, and the Nuclear factor erythroid2 related factor 2 (<strong>NRF2</strong>) canonical pathway in microglia were associated with the <b>binge</b> administration regimen of METH.
+GABPA	drug	cocaine	31100299	We also analyzed the ability of the β lactam antibiotic, ceftriaxone, to attenuate the persistence of CPP after a <b>cocaine</b> free period in animals showing vulnerability to <b>cocaine</b> rewarding effects, and furthermore we determined GLT 1, xCT, NF κB and <strong>Nrf2</strong> protein expression.
+GABPA	addiction	reward	31100299	We also analyzed the ability of the β lactam antibiotic, ceftriaxone, to attenuate the persistence of <b>CPP</b> after a cocaine free period in animals showing vulnerability to cocaine rewarding effects, and furthermore we determined GLT 1, xCT, NF κB and <strong>Nrf2</strong> protein expression.
+GABPA	drug	alcohol	31096703	Natural Dietary Supplementation of Curcumin Protects Mice Brains against <b>Ethanol</b> Induced Oxidative Stress Mediated Neurodegeneration and Memory Impairment via <strong>Nrf2</strong>/TLR4/RAGE Signaling.
+GABPA	drug	alcohol	31096703	According to our findings, <b>ethanol</b> triggered reactive oxygen species (ROS), apoptosis, neuroinflammation, and memory impairment, which were significantly inhibited with the administration of curcumin, as assessed by ROS, lipid peroxidation (LPO), and <strong>Nrf2</strong>/HO 1 (nuclear factor erythroid 2 related factor 2/Heme oxygenase 1) expression in the experimental mice brains.
+GABPA	drug	nicotine	30533170	Coincubation with N acetylcysteine or L ascorbate improves impaired osteogenesis caused by cigarette smoke exposure by both activation of nuclear factor erythroid 2 related factor 2 (<strong>Nrf2</strong>) signaling and scavenging of ROS, which thus might represent therapeutic targets to support fracture healing in <b>smokers</b>.
+GABPA	drug	amphetamine	30500461	Exposure to FIR protects from <b>methamphetamine</b> (MA) induced memory impairments via phosphorylation of ERK 1/2 signaling by positive modulation of protein kinase C δ (PKCδ), M1 muscarinic acetylcholine receptor (M1 mAChR), and nuclear factor E2 related factor 2 (<strong>Nrf2</strong>) transcription factor.
+GABPA	drug	alcohol	30248482	<strong>NRF2</strong> mitigates acute <b>alcohol</b> induced hepatic and pancreatic injury in mice.
+GABPA	drug	alcohol	30248482	However, the role of <strong>NRF2</strong> in acute <b>alcoholism</b> and associated pathologies remains unclear.
+GABPA	drug	alcohol	30248482	We found that <strong>Nrf2</strong> knockout (<strong>Nrf2</strong> KO) mice had exaggerated hypoglycemia and hypothermia and increased mortality compared to wildtype mice after binge <b>ethanol</b> exposure.
+GABPA	addiction	intoxication	30248482	We found that <strong>Nrf2</strong> knockout (<strong>Nrf2</strong> KO) mice had exaggerated hypoglycemia and hypothermia and increased mortality compared to wildtype mice after <b>binge</b> ethanol exposure.
+GABPA	drug	alcohol	30248482	Acute high dose of <b>alcohol</b> exposure resulted in substantially worsened liver and pancreatic injuries in <strong>Nrf2</strong> KO mice.
+GABPA	drug	alcohol	30248482	Importantly, deficiency of <strong>Nrf2</strong> allowed severe pancreatitis and pancreatic β cell injury with increased insulin secretion and/or leaking during binge <b>ethanol</b> exposure, which contributed to hypoglycemia.
+GABPA	addiction	intoxication	30248482	Importantly, deficiency of <strong>Nrf2</strong> allowed severe pancreatitis and pancreatic β cell injury with increased insulin secretion and/or leaking during <b>binge</b> ethanol exposure, which contributed to hypoglycemia.
+GABPA	drug	alcohol	30248482	In contrast, a clinically used <strong>NRF2</strong> activator dimethyl fumarate (DMF) protected against hypoglycemia and lethality induced by acute <b>ethanol</b> exposure.
+GABPA	drug	alcohol	30248482	Taken together, <strong>NRF2</strong> plays an important protective role against acute binge <b>alcohol</b> induced hepatic and pancreatic damage, which may be partially attributable to its primary regulating role in antioxidant response and impact on <b>ethanol</b> metabolism.
+GABPA	addiction	intoxication	30248482	Taken together, <strong>NRF2</strong> plays an important protective role against acute <b>binge</b> alcohol induced hepatic and pancreatic damage, which may be partially attributable to its primary regulating role in antioxidant response and impact on ethanol metabolism.
+GABPA	drug	alcohol	28951767	Baicalin Ameliorates Liver Injury Induced by Chronic plus Binge <b>Ethanol</b> Feeding by Modulating Oxidative Stress and Inflammation via CYP2E1 and <strong>NRF2</strong> in Mice.
+GABPA	addiction	intoxication	28951767	Baicalin Ameliorates Liver Injury Induced by Chronic plus <b>Binge</b> Ethanol Feeding by Modulating Oxidative Stress and Inflammation via CYP2E1 and <strong>NRF2</strong> in Mice.
+GABPA	drug	alcohol	28951767	Baicalin also enhanced <b>ethanol</b> induced <strong>NRF2</strong> nuclear translocation and increased downstream target gene HO 1 as antioxidant defense.
+GABPA	drug	alcohol	28924552	Schisandra sphenanthera extract (Wuzhi Tablet) protects against chronic binge and acute <b>alcohol</b> induced liver injury by regulating the <strong>NRF2</strong> ARE pathway in mice.
+GABPA	addiction	intoxication	28924552	Schisandra sphenanthera extract (Wuzhi Tablet) protects against chronic <b>binge</b> and acute alcohol induced liver injury by regulating the <strong>NRF2</strong> ARE pathway in mice.
+GABPA	drug	alcohol	28924552	Collectively, our study demonstrates that WZ protected against <b>alcohol</b> induced liver injury by reducing oxidative stress and improving antioxidant defense, possibly by activating the <strong>NRF2</strong> ARE pathway.
+GABPA	addiction	intoxication	28776218	Molecular pathology of cerebral TNF α, IL 1β, iNOS and <strong>Nrf2</strong> in forensic autopsy cases with special regard to deaths due to environmental hazards and <b>intoxication</b>.
+GABPA	drug	amphetamine	28776218	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of IL 1β, TNF α and iNOS, and lower expression of <strong>Nrf2</strong> in <b>methamphetamine</b> intoxication and hyperthermia cases, higher expression of iNOS in phenobarbital intoxication cases, and higher expression of <strong>Nrf2</strong> in phenobarbital intoxication and hypothermia cases.
+GABPA	addiction	intoxication	28776218	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of IL 1β, TNF α and iNOS, and lower expression of <strong>Nrf2</strong> in methamphetamine <b>intoxication</b> and hyperthermia cases, higher expression of iNOS in phenobarbital <b>intoxication</b> cases, and higher expression of <strong>Nrf2</strong> in phenobarbital <b>intoxication</b> and hypothermia cases.
+GABPA	drug	nicotine	28641491	<b>Nicotine</b> and cigarette smoke modulate <strong>Nrf2</strong> BDNF dopaminergic signal and neurobehavioral disorders in adult rat cerebral cortex.
+GABPA	drug	alcohol	28501008	<b>Ethanol</b> extract and its dichloromethane fraction of Alpinia oxyphylla Miquel exhibited hepatoprotective effects against CCl4 induced oxidative damage in vitro and in vivo with the involvement of <strong>Nrf2</strong>.
+GABPA	drug	amphetamine	26427884	We investigated whether <strong>Nrf2</strong> is activated by <b>methamphetamine</b> (<b>METH</b>) thereby altering neurotoxicity in <strong>Nrf2</strong> +/+ and  /  adult mouse brain.
+GABPA	drug	amphetamine	26427884	A single dose of <b>METH</b> can induce the mRNA levels of <strong>Nrf2</strong> regulated antioxidant and cytoprotective proteins in mouse brain.
+GABPA	drug	amphetamine	26427884	These <strong>Nrf2</strong> dependent effects were independent of changes in <b>METH</b> metabolism or the induction of hyperthermia.
+GABPA	drug	amphetamine	26427884	<strong>Nrf2</strong> mediated pathways accordingly may protect against the neurodegenerative effects and functional deficits initiated by <b>METH</b> and perhaps other reactive oxygen species enhancing neurotoxicants, when there is time for transcriptional activation and protein induction.
+GABPA	drug	amphetamine	26427884	In human users of <b>METH</b>, this mechanism may be essential when differences in drug abuse patterns may alter the induction and duration of <strong>Nrf2</strong> activation thereby modulating susceptibility to the neurotoxic effects of <b>METH</b>.
+GABPA	drug	alcohol	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates <b>ethanol</b> induced liver injury through modulation of AMPK and <strong>Nrf2</strong> related signals in a binge drinking mouse model.
+GABPA	addiction	intoxication	26178909	A polymethoxy flavonoids rich Citrus aurantium extract ameliorates ethanol induced liver injury through modulation of AMPK and <strong>Nrf2</strong> related signals in a <b>binge</b> drinking mouse model.
+GABPA	drug	opioid	25542428	However, the <b>morphine</b> induced increase in <strong>nrf2</strong> nuclear translocation in the frontal cortex and striatum was inhibited by bergenin treatment.
+GABPA	drug	alcohol	24060752	Sulforaphane induces <strong>Nrf2</strong> and protects against CYP2E1 dependent binge <b>alcohol</b> induced liver steatosis.
+GABPA	addiction	intoxication	24060752	Sulforaphane induces <strong>Nrf2</strong> and protects against CYP2E1 dependent <b>binge</b> alcohol induced liver steatosis.
+GABPA	drug	alcohol	24060752	The current study was designed to evaluate the ability of sulforaphane, an activator of <strong>Nrf2</strong>, to blunt CYP2E1 dependent, <b>ethanol</b> induced steatosis in vivo and in vitro.
+GABPA	drug	alcohol	24060752	The sulforaphane treatment activated <strong>Nrf2</strong>, increased levels of the <strong>Nrf2</strong> target heme oxygenase 1 and subsequently lowered oxidant stress as shown by the decline in lipid peroxidation and 3 nitrotyrosine protein adducts and an increase in GSH levels after the acute <b>ethanol</b> treatment.
+GABPA	drug	alcohol	24060752	Similar results were found in vitro as addition of sulforaphane to HepG2 E47 cells, which express CYP2E1, elevated <strong>Nrf2</strong> levels and decreased the accumulation of lipid in cells cultured with <b>ethanol</b>.
+GABPA	addiction	addiction	24024172	In this study we show that activation of <strong>Nrf2</strong>, either by the small molecule sulforaphane or knockout of the <strong>Nrf2</strong> inhibitor Keap1, leads to increased cellular glucose uptake and increased glucose <b>addiction</b> in fibroblasts.
+GABPA	drug	amphetamine	22903344	Moreover, our results also show that <b>METH</b> downregulated another transcription factor, the nuclear factor erythroid 2 related factor (<strong>Nrf2</strong>), a transcription factor implicated in the expression of several antioxidant/detoxificant enzymes.
+GABPA	drug	amphetamine	22903344	These results demonstrate, for the first time, that <b>METH</b> directly induces inflammation in neurons via an NF κB dependent pathway and that the anti neuroinflammatory effects of melatonin result from the inhibition of activated NF κB in parallel with potentiated antioxidant/detoxificant defense by activated <strong>Nrf2</strong> pathway.
+GABPA	drug	nicotine	22686525	<strong>Nrf2</strong>: friend and foe in preventing cigarette <b>smoking</b> dependent lung disease.
+GABPA	addiction	dependence	22686525	This chemical trait is virtually predestined to be sensitized by the major route leading to <strong>Nrf2</strong> activation, characterized by its <b>dependence</b> on the interaction of electrophiles with specific cysteine residues inherited by <strong>Nrf2</strong>'s negative cytosolic regulator Keap1 (Kelch like ECH associated protein 1).
+GABPA	drug	nicotine	22686525	In terms of the two major <b>smoking</b> related diseases of the lung, that is, emphysema and lung cancer, a fully functional <strong>Nrf2</strong> genotype seems to be necessary, although not sufficient by itself, to protect the <b>smoker</b> from acquiring emphysema.
+GABPA	drug	nicotine	22686525	Contrasting with this protective role, however, <strong>Nrf2</strong> function may be potentially fatal in <b>smoking</b> related lung tumorigenesis: as concluded from recent clinical investigations, lung tumor tissues harbor increased mutation or, alternatively, aberrant expression rates in either the KEAP1 or the <strong>NRF2</strong> gene, generally resulting in constitutive <strong>Nrf2</strong> activation, suggesting that "abuse" of <strong>Nrf2</strong> function is an advantageous strategy of the (developing) tumor to protect itself against oxidative stress in general.
+GABPA	drug	nicotine	22686525	On the basis of the fundamental significance of the <strong>Nrf2</strong> pathway in <b>smoking</b> dependent disease development, several attempts have been described for dietary and pharmacological intervention, the majority of which are intended to activate <strong>Nrf2</strong> aiming at emphysema prevention.
+GABPA	drug	alcohol	22552773	<b>Ethanol</b> induction of CYP2A5: role of CYP2E1 ROS <strong>Nrf2</strong> pathway.
+GABPA	drug	alcohol	22552773	The redox sensitive transcription factor nuclear factor erythroid 2 related factor 2 (<strong>Nrf2</strong>) was also induced by acute <b>ethanol</b> in Cyp2e1 ( / ) KI mice but not in Cyp2e1 ( / ) mice.
+GABPA	drug	alcohol	22552773	<b>Ethanol</b> induction of CYP2A5 in <strong>Nrf2</strong> knockout (<strong>Nrf2</strong> ( / )) mice was lower compared with that in WT mice, whereas CYP2E1 induction by <b>ethanol</b> was comparable in WT and <strong>Nrf2</strong> ( / ) mice.
+GABPA	drug	alcohol	22552773	Antioxidants (N acetyl cysteine and vitamin C), which blocked oxidative stress induced by chronic <b>ethanol</b> in WT mice and acute <b>ethanol</b> in Cyp2e1 ( / ) KI mice, also blunted the induction of CYP2A5 and <strong>Nrf2</strong> by <b>ethanol</b> but not the induction of CYP2E1 by <b>ethanol</b>.
+GABPA	drug	alcohol	22552773	These results suggest that oxidative stress induced by <b>ethanol</b> via induction of CYP2E1 upregulates <strong>Nrf2</strong> activity, which in turn regulates <b>ethanol</b> induction of CYP2A5.
+GABPA	drug	alcohol	22552773	Results obtained from primary hepatocytes, mice gavaged with binge <b>ethanol</b> or fed chronic <b>ethanol</b>, show that <strong>Nrf2</strong> regulated <b>ethanol</b> induction of CYP2A5 protects against <b>ethanol</b> induced steatosis.
+GABPA	addiction	intoxication	22552773	Results obtained from primary hepatocytes, mice gavaged with <b>binge</b> ethanol or fed chronic ethanol, show that <strong>Nrf2</strong> regulated ethanol induction of CYP2A5 protects against ethanol induced steatosis.
+FYN	addiction	sensitization	32579948	We concluded that an SFK, likely <strong>Fyn</strong>, maintains latent <b>sensitization</b> induced by inflammation or nerve injury.
+FYN	drug	alcohol	30536923	The <strong>Fyn</strong> kinase inhibitor, AZD0530, suppresses mouse <b>alcohol</b> self administration and seeking.
+FYN	addiction	relapse	30536923	The <strong>Fyn</strong> kinase inhibitor, AZD0530, suppresses mouse alcohol self administration and <b>seeking</b>.
+FYN	drug	alcohol	30536923	<strong>Fyn</strong> is a member of the Src family of protein tyrosine kinases (PTKs) that plays an important role not only in normal synaptic functions but also in brain pathologies including <b>alcohol</b> use disorder.
+FYN	drug	alcohol	30536923	We previously reported that repeated cycles of binge drinking and withdrawal activate <strong>Fyn</strong> in the dorsomedial striatum (DMS) of rodents, and that <strong>Fyn</strong> signaling in the DMS contributes to rat <b>alcohol</b> intake and relapse.
+FYN	addiction	intoxication	30536923	We previously reported that repeated cycles of <b>binge</b> drinking and withdrawal activate <strong>Fyn</strong> in the dorsomedial striatum (DMS) of rodents, and that <strong>Fyn</strong> signaling in the DMS contributes to rat alcohol intake and relapse.
+FYN	addiction	relapse	30536923	We previously reported that repeated cycles of binge drinking and withdrawal activate <strong>Fyn</strong> in the dorsomedial striatum (DMS) of rodents, and that <strong>Fyn</strong> signaling in the DMS contributes to rat alcohol intake and <b>relapse</b>.
+FYN	addiction	withdrawal	30536923	We previously reported that repeated cycles of binge drinking and <b>withdrawal</b> activate <strong>Fyn</strong> in the dorsomedial striatum (DMS) of rodents, and that <strong>Fyn</strong> signaling in the DMS contributes to rat alcohol intake and relapse.
+FYN	drug	alcohol	30536923	We show that systemic administration of AZD0530 prevents <b>alcohol</b> induced <strong>Fyn</strong> activation and GluN2B phosphorylation in the DMS of mice.
+FYN	drug	alcohol	30536923	Together, our findings suggest that AZD0530, through its inhibitory actions on <strong>Fyn</strong> kinase, dampens <b>alcohol</b> seeking and drinking.
+FYN	addiction	relapse	30536923	Together, our findings suggest that AZD0530, through its inhibitory actions on <strong>Fyn</strong> kinase, dampens alcohol <b>seeking</b> and drinking.
+FYN	drug	cocaine	29520592	Thus, by triggering the activation and degranulation of mast cells dependent on the tyrosine kinase c kit and <strong>Fyn</strong>, the latter being also involved in NMDA dependent synaptic plasticity, <b>cocaine</b> and heroin may indirectly influence the neural mechanisms that mediate their reinforcing properties.
+FYN	drug	opioid	29520592	Thus, by triggering the activation and degranulation of mast cells dependent on the tyrosine kinase c kit and <strong>Fyn</strong>, the latter being also involved in NMDA dependent synaptic plasticity, cocaine and <b>heroin</b> may indirectly influence the neural mechanisms that mediate their reinforcing properties.
+FYN	addiction	reward	29520592	Thus, by triggering the activation and degranulation of mast cells dependent on the tyrosine kinase c kit and <strong>Fyn</strong>, the latter being also involved in NMDA dependent synaptic plasticity, cocaine and heroin may indirectly influence the neural mechanisms that mediate their <b>reinforcing</b> properties.
+FYN	drug	cocaine	29520592	Masitinib, a novel tyrosine kinase inhibitor with high selectivity for c Kit, <strong>Fyn</strong> and Lyn, may alter the aberrant consequences of the activation of these tyrosine kinases by <b>cocaine</b> and heroin.
+FYN	drug	opioid	29520592	Masitinib, a novel tyrosine kinase inhibitor with high selectivity for c Kit, <strong>Fyn</strong> and Lyn, may alter the aberrant consequences of the activation of these tyrosine kinases by cocaine and <b>heroin</b>.
+FYN	drug	alcohol	27906494	Specifically, we show that enzymes that participate in the regulation of NMDAR function including <strong>Fyn</strong> kinase as well as signaling cascades downstream of NMDAR including calcium/calmodulin dependent protein kinase II (CamKII), the α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid receptor (AMPAR) and the mammalian target of rapamycin complex 1 (mTORC1) play a major role in mechanisms underlying <b>alcohol</b> drinking behaviors.
+FYN	drug	alcohol	24588427	Previously, we found that <b>ethanol</b> activates <strong>Fyn</strong> in the dorsomedial striatum (DMS) leading to GluN2B phosphorylation, which, in turn, underlies the development of <b>ethanol</b> intake (J.
+FYN	drug	alcohol	24588427	Here, we tested the hypothesis that inhibition of STEP61 by <b>ethanol</b> is upstream of <strong>Fyn</strong>/GluN2B.
+FYN	drug	alcohol	24588427	Specific knockdown of STEP61 in the DMS of mice enhanced <b>ethanol</b> mediated <strong>Fyn</strong> activation and GluN2B phosphorylation, and increased <b>ethanol</b> intake without altering the level of water, saccharine, quinine consumption or spontaneous locomotor activity.
+FYN	drug	alcohol	24588427	Together, our data suggest that blockade of STEP61 activity in response to <b>ethanol</b> is sufficient for the activation of the <strong>Fyn</strong>/GluN2B pathway in the DMS.
+FYN	drug	alcohol	24588427	Being upstream of <strong>Fyn</strong> and GluN2B, inactive STEP61 in the DMS primes the induction of <b>ethanol</b> intake.
+FYN	drug	alcohol	24588427	We show that <b>ethanol</b> mediated inhibition of STEP61 in the DMS leads to <strong>Fyn</strong> activation and GluN2B phosphorylation.
+FYN	drug	alcohol	24588427	The inhibition of STEP61 activity contributes to the activation of <strong>Fyn</strong> in response to <b>ethanol</b>, which, in turn, phosphorylates GluN2B.
+FYN	drug	alcohol	24005290	We previously found that excessive <b>ethanol</b> drinking activates <strong>Fyn</strong> in the dorsomedial striatum (DMS) (Wang et al., 2010; Gibb et al., 2011).
+FYN	drug	alcohol	24005290	<b>Ethanol</b> mediated <strong>Fyn</strong> activation in the DMS leads to the phosphorylation of the GluN2B subunit of the NMDA receptor, to the enhancement of the channel's activity, and to the development and/or maintenance of <b>ethanol</b> drinking behaviors (Wang et al., 2007, 2010).
+FYN	drug	alcohol	24005290	Protein tyrosine phosphatase α (PTPα) is essential for <strong>Fyn</strong> kinase activation (Bhandari et al., 1998), and we showed that <b>ethanol</b> mediated <strong>Fyn</strong> activation is facilitated by the recruitment of PTPα to synaptic membranes, the compartment where <strong>Fyn</strong> resides (Gibb et al., 2011).
+FYN	drug	alcohol	24005290	Here we tested the hypothesis that PTPα in the DMS is part of the <strong>Fyn</strong>/GluN2B pathway and is thus a major contributor to the neuroadaptations underlying excessive <b>ethanol</b> intake behaviors.
+FYN	drug	alcohol	24005290	Furthermore, downregulation of PTPα in the DMS of mice significantly reduces <b>ethanol</b> mediated <strong>Fyn</strong> activation, GluN2B phosphorylation, and <b>ethanol</b> withdrawal induced long term facilitation of NMDAR activity without altering the intrinsic features of DMS neurons.
+FYN	addiction	withdrawal	24005290	Furthermore, downregulation of PTPα in the DMS of mice significantly reduces ethanol mediated <strong>Fyn</strong> activation, GluN2B phosphorylation, and ethanol <b>withdrawal</b> induced long term facilitation of NMDAR activity without altering the intrinsic features of DMS neurons.
+FYN	drug	alcohol	24005290	Together, these results position PTPα upstream of <strong>Fyn</strong> within the DMS and demonstrate the important contribution of the phosphatase to the maladaptive synaptic changes that lead to excessive <b>ethanol</b> intake.
+FYN	drug	alcohol	21985328	The NMDA receptor is a major target of <b>ethanol</b> in the brain, and accumulating evidence suggests that <strong>Fyn</strong> mediates the effects of <b>ethanol</b> by regulating the phosphorylation of GluN2B NMDA receptor subunits.
+FYN	drug	alcohol	21985328	Furthermore, <strong>Fyn</strong> has been shown to regulate <b>alcohol</b> withdrawal and acute tolerance to <b>ethanol</b> through a GluN2B dependent mechanism.
+FYN	addiction	withdrawal	21985328	Furthermore, <strong>Fyn</strong> has been shown to regulate alcohol <b>withdrawal</b> and acute tolerance to ethanol through a GluN2B dependent mechanism.
+FYN	drug	alcohol	21919909	<b>Ethanol</b> induced increase in <strong>Fyn</strong> kinase activity in the dorsomedial striatum is associated with subcellular redistribution of protein tyrosine phosphatase α.
+FYN	drug	alcohol	21919909	In vivo exposure of rodents to <b>ethanol</b> leads to a long lasting increase in <strong>Fyn</strong> kinase activity in the dorsomedial striatum (DMS).
+FYN	drug	alcohol	21919909	In this study, we set out to identify a molecular mechanism that contributes to the enhancement of <strong>Fyn</strong> activity in response to <b>ethanol</b> in the DMS.
+FYN	drug	alcohol	21919909	Protein tyrosine phosphatase α (PTPα) positively regulates the activity of <strong>Fyn</strong>, and we found that repeated systemic administration or binge drinking of <b>ethanol</b> results in an increase in the synaptic localization of PTPα in the DMS, the same site where <strong>Fyn</strong> resides.
+FYN	addiction	intoxication	21919909	Protein tyrosine phosphatase α (PTPα) positively regulates the activity of <strong>Fyn</strong>, and we found that repeated systemic administration or <b>binge</b> drinking of ethanol results in an increase in the synaptic localization of PTPα in the DMS, the same site where <strong>Fyn</strong> resides.
+FYN	drug	alcohol	21919909	We also demonstrate that binge drinking of <b>ethanol</b> leads to an increase in <strong>Fyn</strong> activity and to the co localization of <strong>Fyn</strong> and PTPα in lipid rafts in the DMS.
+FYN	addiction	intoxication	21919909	We also demonstrate that <b>binge</b> drinking of ethanol leads to an increase in <strong>Fyn</strong> activity and to the co localization of <strong>Fyn</strong> and PTPα in lipid rafts in the DMS.
+FYN	drug	alcohol	21919909	Together, our results suggest that the redistribution of PTPα in the DMS into compartments where <strong>Fyn</strong> resides is a potential mechanism by which the activity of the kinase is increased upon <b>ethanol</b> exposure.
+FYN	drug	amphetamine	21704677	The data clearly suggest that endogenous MK limits <b>amphetamine</b> induced astrocytosis through <strong>Fyn</strong> , TrkA  and ERK1/2 independent mechanisms and identify previously unexpected functional differences between MK and pleiotrophin, the only other member of the MK family of growth factors, in the modulation of effects of drugs of abuse.
+FYN	drug	alcohol	20668202	We previously observed that ex vivo acute exposure of the dorsal striatum to, and withdrawal from, <b>alcohol</b> induces long term facilitation (LTF) of the activity of NR2B containing NMDA receptors (NR2B NMDARs) in a mechanism that requires the Src family protein tyrosine kinase (PTK), <strong>Fyn</strong> (Wang et al., 2007).
+FYN	addiction	withdrawal	20668202	We previously observed that ex vivo acute exposure of the dorsal striatum to, and <b>withdrawal</b> from, alcohol induces long term facilitation (LTF) of the activity of NR2B containing NMDA receptors (NR2B NMDARs) in a mechanism that requires the Src family protein tyrosine kinase (PTK), <strong>Fyn</strong> (Wang et al., 2007).
+FYN	drug	alcohol	19119613	Studies in neuropsychopharmacology and molecular neurobiology indicate that neurotransmitters and its receptors play important roles in <b>alcohol</b> abuse and addiction, and post receptor signal transduction pathways, including cyclic adenosine 3', 5' monophosphate (cAMP) protein kinase A (PKA), phosphoinositide (PI), Ca2+  calmodulin (CAM), phospholipase D (PLD) and tyrosine kinase <strong>Fyn</strong> signaling cascade.
+FYN	addiction	addiction	19119613	Studies in neuropsychopharmacology and molecular neurobiology indicate that neurotransmitters and its receptors play important roles in alcohol abuse and <b>addiction</b>, and post receptor signal transduction pathways, including cyclic adenosine 3', 5' monophosphate (cAMP) protein kinase A (PKA), phosphoinositide (PI), Ca2+  calmodulin (CAM), phospholipase D (PLD) and tyrosine kinase <strong>Fyn</strong> signaling cascade.
+FYN	drug	cocaine	19046409	<b>Cocaine</b> induced an increase in the activity of both <strong>Fyn</strong> and Src kinases, and the Src protein tyrosine kinase (Src PTKs) inhibitor, 4 amino 5 (4 chlorophenyl) 7 (t butyl)pyrazolo[3,4 d]pyrimidine (PP2), abolished both <b>cocaine</b> induced increase in tyrosine phosphorylation of the NR2A subunit and the increase in the expression of NR1, NR2A, and NR2B in the VTA.
+FYN	drug	alcohol	18849153	Genetic association between  93A/G polymorphism in the <strong>Fyn</strong> kinase gene and <b>alcohol</b> dependence in Spanish men.
+FYN	addiction	dependence	18849153	Genetic association between  93A/G polymorphism in the <strong>Fyn</strong> kinase gene and alcohol <b>dependence</b> in Spanish men.
+FYN	drug	alcohol	18849153	<strong>Fyn</strong> tyrosine kinase is a member of the Scr family that phosphorylates the NR2A and NR2B subunits of the NMDA receptors reducing the inhibitory effects of <b>ethanol</b> and therefore may regulate the individual sensitivity to <b>ethanol</b>.
+FYN	drug	alcohol	18849153	To investigate whether there is any relationship between the polymorphism at position  93 of the <strong>Fyn</strong> kinase gene and the susceptibility to develop <b>alcoholism</b>.
+FYN	drug	alcohol	18849153	We studied the distribution of genotypes and alleles of the polymorphism  93A/G (137346 T/C) in the 5' UTR region of the <strong>fyn</strong> gene in 207 male heavy drinkers (119 with <b>alcohol</b> dependence and 88 with <b>alcohol</b> abuse) and 100 control subjects from Castilla y León (Spain).
+FYN	addiction	dependence	18849153	We studied the distribution of genotypes and alleles of the polymorphism  93A/G (137346 T/C) in the 5' UTR region of the <strong>fyn</strong> gene in 207 male heavy drinkers (119 with alcohol <b>dependence</b> and 88 with alcohol abuse) and 100 control subjects from Castilla y León (Spain).
+FYN	drug	alcohol	18849153	Our results show that the  93G allele of <strong>Fyn</strong> kinase gene is associated with higher risk to develop <b>alcohol</b> dependence in Spanish men.
+FYN	addiction	dependence	18849153	Our results show that the  93G allele of <strong>Fyn</strong> kinase gene is associated with higher risk to develop alcohol <b>dependence</b> in Spanish men.
+FYN	drug	alcohol	17392475	We found that, in the dorsal striatum, <b>alcohol</b> (<b>ethanol</b>) exposure produced an increase in the phosphorylation of the NR2B subunit of the NMDAR, and a corresponding increase in the activity of <strong>Fyn</strong> kinase, which phosphorylates NR2B.
+FYN	drug	alcohol	17392475	Finally, dorsal but not ventral striatum infusion of a <strong>Fyn</strong> or NR2B NMDAR inhibitor reduced rat operant self administration of <b>ethanol</b>.
+FYN	addiction	reward	17392475	Finally, dorsal but not ventral striatum infusion of a <strong>Fyn</strong> or NR2B NMDAR inhibitor reduced rat <b>operant</b> self administration of ethanol.
+FYN	drug	alcohol	17392475	Our results suggest that the <strong>Fyn</strong> mediated phosphorylation and LTF of NR2B NMDAR activity in the dorsal striatum after exposure to <b>ethanol</b> may underlie aberrant plasticity that contributes to mechanisms underlying <b>alcohol</b> drinking behavior.
+FYN	drug	alcohol	15902902	<strong>Fyn</strong> kinase does not reduce <b>ethanol</b> inhibition of zinc insensitive NR2A containing N methyl D aspartate receptors.
+FYN	drug	alcohol	15902902	Results of studies also support the suggestion that the <b>ethanol</b> inhibition on NR1/2A receptors is reduced by <strong>Fyn</strong> kinase mediated tyrosine phosphorylation.
+FYN	drug	alcohol	15902902	In the current study, the effect of <strong>Fyn</strong> kinase on the <b>ethanol</b> inhibition of NR1/2A receptors was determined under conditions in which zinc sensitivity is eliminated.
+FYN	drug	alcohol	15902902	Under these conditions, <strong>Fyn</strong> kinase did not reduce <b>ethanol</b> inhibition of wild type receptors.
+FYN	drug	alcohol	15902902	<strong>Fyn</strong> kinase also had no effect on the magnitude of <b>ethanol</b> inhibition of zinc insensitive NR1/2A(H128S) receptors.
+FYN	drug	alcohol	15902902	Together, results of the current study indicate that <strong>Fyn</strong> kinase does not directly affect the <b>ethanol</b> sensitivity of NR1/2A receptors.
+FYN	addiction	dependence	14764659	Deletion of the <strong>fyn</strong> kinase gene alters sensitivity to GABAergic drugs: <b>dependence</b> on beta2/beta3 GABAA receptor subunits.
+FYN	drug	alcohol	14675807	Analysis of genetic variations of protein tyrosine kinase <strong>fyn</strong> and their association with <b>alcohol</b> dependence in two independent cohorts.
+FYN	addiction	dependence	14675807	Analysis of genetic variations of protein tyrosine kinase <strong>fyn</strong> and their association with alcohol <b>dependence</b> in two independent cohorts.
+FYN	drug	alcohol	14675807	Decreased sensitivity to and increased tolerance for the effects of <b>alcohol</b> is a phenotype, which was shown to be associated with an increased risk for <b>alcoholism</b> in humans and was observed in protein tyrosine kinase (PTK) <strong>fyn</strong> knockout mice.
+FYN	drug	alcohol	14675807	We performed an association study of genetic variations of PTK <strong>fyn</strong> in 430 <b>alcohol</b> dependent patients and 365 unrelated control subjects from two independent samples.
+FYN	drug	alcohol	14675807	Our results indicate a possible association of <b>alcohol</b> dependence with a genotype of the SNP T137346C of the PTK <strong>fyn</strong>, with C being the risk allele.
+FYN	addiction	dependence	14675807	Our results indicate a possible association of alcohol <b>dependence</b> with a genotype of the SNP T137346C of the PTK <strong>fyn</strong>, with C being the risk allele.
+FYN	drug	alcohol	14634488	<strong>Fyn</strong> kinase and NR2B containing NMDA receptors regulate acute <b>ethanol</b> sensitivity but not <b>ethanol</b> intake or conditioned reward.
+FYN	addiction	reward	14634488	<strong>Fyn</strong> kinase and NR2B containing NMDA receptors regulate acute ethanol sensitivity but not ethanol intake or conditioned <b>reward</b>.
+FYN	drug	alcohol	14634488	The tyrosine kinase <strong>Fyn</strong> previously has been shown to play a key role in mediating acute tolerance to <b>ethanol</b>.
+FYN	drug	alcohol	14634488	Recently, we found that the compartmentalization of <strong>Fyn</strong> to the NR2B subunit of the NMDA receptor (NMDAR) in the hippocampus regulates <strong>Fyn</strong> phosphorylation of NR2B in response to <b>ethanol</b>, which mediates the acute tolerance of NMDAR to <b>ethanol</b> inhibition in hippocampal slices.
+FYN	drug	alcohol	14634488	In this study we determined, first, whether acute tolerance to <b>ethanol</b> inhibition is mediated via NR2B containing NMDARs in vivo and, second, whether the increase in acute sensitivity to <b>ethanol</b> in the <strong>Fyn</strong> /  mice influences <b>ethanol</b> consumption or <b>ethanol</b>'s conditioned rewarding effects.
+FYN	drug	alcohol	14634488	We found that systemic injection of the NR2B containing NMDAR selective antagonist, ifenprodil, abolished the differences between <strong>Fyn</strong>+/+ and <strong>Fyn</strong> /  mice in sensitivity to the acute sedative effects of <b>ethanol</b>.
+FYN	drug	alcohol	14634488	Moreover, we found that <strong>Fyn</strong> /  and <strong>Fyn</strong>+/+ mice did not differ in their voluntary <b>ethanol</b> consumption or in the rewarding properties of <b>ethanol</b>.
+FYN	drug	alcohol	14634488	Our results suggest that the interaction between <strong>Fyn</strong> and NR2B mediates the acute sedative effects of <b>ethanol</b>, and that alteration in acute <b>ethanol</b> sensitivity does not necessarily correlate with levels of <b>ethanol</b> consumption or the rewarding properties of <b>ethanol</b>.
+FYN	drug	alcohol	12966312	Role of <strong>Fyn</strong> tyrosine kinase in <b>ethanol</b> consumption by mice.
+FYN	drug	alcohol	12966312	Mice deficient for the intracellular protein <strong>Fyn</strong> tyrosine kinase (fynZ/fynZ mice) have been reported to show increased <b>alcohol</b> sensitivity and lack of tolerance to the effects of <b>ethanol</b>.
+FYN	drug	alcohol	12966312	To further study the involvement of <strong>Fyn</strong> in neurobehavioral effects of <b>alcohol</b>, we examined <b>ethanol</b> consumption and relapse drinking behavior in fynZ/fynZ mice.
+FYN	addiction	relapse	12966312	To further study the involvement of <strong>Fyn</strong> in neurobehavioral effects of alcohol, we examined ethanol consumption and <b>relapse</b> drinking behavior in fynZ/fynZ mice.
+FYN	drug	alcohol	12966312	Deletion of the <strong>Fyn</strong> tyrosine kinase gene may be involved in <b>ethanol</b> sensitivity but this effect may depend on a gene environment interaction.
+FYN	drug	alcohol	12966312	<strong>Fyn</strong> does not influence <b>ethanol</b> consumption, neither under basal conditions nor following a deprivation period or stress.
+FYN	drug	alcohol	12966312	This finding indicates that phosphorylation and activation of N methyl D aspartate (NMDA) receptors through <strong>Fyn</strong> is not a critical mechanism in <b>alcohol</b> drinking or relapse behavior.
+FYN	addiction	relapse	12966312	This finding indicates that phosphorylation and activation of N methyl D aspartate (NMDA) receptors through <strong>Fyn</strong> is not a critical mechanism in alcohol drinking or <b>relapse</b> behavior.
+FYN	drug	alcohol	12878908	Deletion of the <strong>fyn</strong> kinase gene alters behavioral sensitivity to <b>ethanol</b>.
+FYN	drug	alcohol	12878908	An earlier study showed that deletion of the <strong>fyn</strong> kinase gene enhanced sensitivity to <b>ethanol</b>'s sedative hypnotic effects and suggested that this was associated with diminished <strong>fyn</strong> kinase phosphorylation of NMDA receptors.
+FYN	drug	alcohol	12878908	To address the role of <strong>fyn</strong> kinase in mediating acute tolerance, as well as sensitivity to several other behavioral effects of <b>ethanol</b>, we studied an independently generated population of <strong>fyn</strong> null mutant and wild type mice.
+FYN	drug	alcohol	12878908	<strong>Fyn</strong> kinase null mutants were more sensitive to the anxiolytic effects of <b>ethanol</b> when tested using the elevated plus maze, and males displayed a lower preference for <b>ethanol</b> in a two bottle choice paradigm.
+FYN	drug	alcohol	12878908	These results show that <strong>fyn</strong> kinase modulates acute tolerance to <b>ethanol</b> and suggest a role for <strong>fyn</strong> in mediating <b>ethanol</b>'s anxiolytic and reinforcing properties.
+FYN	addiction	reward	12878908	These results show that <strong>fyn</strong> kinase modulates acute tolerance to ethanol and suggest a role for <strong>fyn</strong> in mediating ethanol's anxiolytic and <b>reinforcing</b> properties.
+FYN	drug	alcohol	12736333	Scaffolding of <strong>Fyn</strong> kinase to the NMDA receptor determines brain region sensitivity to <b>ethanol</b>.
+FYN	drug	alcohol	12736333	We report here that the brain region specific compartmentalization of <strong>Fyn</strong> kinase determines NMDA receptor sensitivity to <b>ethanol</b>.
+FYN	drug	alcohol	12736333	During acute exposure to <b>ethanol</b>, RACK1 is dissociated from the complex, thereby facilitating <strong>Fyn</strong> mediated phosphorylation of NR2B, which enhances channel activity, counteracting the inhibitory actions of <b>ethanol</b>.
+FYN	drug	cannabinoid	12657697	The <b>endocannabinoid</b> induced stimulation of ERK was lost in <strong>Fyn</strong> knock out mice, in slices and in vivo, although it was insensitive to inhibitors of Src family tyrosine kinases in vitro, suggesting a noncatalytic role of <strong>Fyn</strong>.
+FYN	drug	alcohol	12399115	Resistance to <b>alcohol</b> withdrawal induced behaviour in <strong>Fyn</strong> transgenic mice and its reversal by ifenprodil.
+FYN	addiction	withdrawal	12399115	Resistance to alcohol <b>withdrawal</b> induced behaviour in <strong>Fyn</strong> transgenic mice and its reversal by ifenprodil.
+FYN	drug	alcohol	12399115	Recent studies suggest that the protein tyrosine kinase <strong>Fyn</strong> constitutes a determinant of fear and anxiety as well as <b>alcohol</b> sensitivity in mice.
+FYN	drug	alcohol	12399115	This apparent lack of <b>alcohol</b> withdrawal induced behavioural effects was associated with increased <strong>Fyn</strong> activity and tyrosine phosphorylation of several proteins including the NMDA receptor subunit NR2B in the different mutant lines.
+FYN	addiction	withdrawal	12399115	This apparent lack of alcohol <b>withdrawal</b> induced behavioural effects was associated with increased <strong>Fyn</strong> activity and tyrosine phosphorylation of several proteins including the NMDA receptor subunit NR2B in the different mutant lines.
+FYN	drug	alcohol	12399115	NR2B phosphorylation itself remained unaffected by the chronic <b>alcohol</b> ingestion and subsequent withdrawal, but challenge with an NR2B antagonist, ifenprodil, restored a normal behavioural response in <b>alcohol</b> withdrawn <strong>fyn</strong> mutants.
+FYN	addiction	withdrawal	12399115	NR2B phosphorylation itself remained unaffected by the chronic alcohol ingestion and subsequent <b>withdrawal</b>, but challenge with an NR2B antagonist, ifenprodil, restored a normal behavioural response in alcohol withdrawn <strong>fyn</strong> mutants.
+FYN	drug	alcohol	12399115	Together, these results suggest that <strong>Fyn</strong> can modulate <b>alcohol</b> consumption and prevent behavioural changes during <b>alcohol</b> withdrawal, possibly via phosphorylation of NR2B.
+FYN	addiction	withdrawal	12399115	Together, these results suggest that <strong>Fyn</strong> can modulate alcohol consumption and prevent behavioural changes during alcohol <b>withdrawal</b>, possibly via phosphorylation of NR2B.
+FYN	drug	alcohol	11391051	The presentations were (1) cAMP signaling in <b>ethanol</b> sensitivity and tolerance, by Boris Tabakoff; (2) Synaptic signaling pathways of <strong>Fyn</strong> tyrosine kinase, by Takeshi Yagi; (3) <b>Ethanol</b> drinking and sensitization in dopaminergic and serotonergic receptor knockouts, by Tamara J. Phillips; (4) ICAM 1 is involved in early <b>alcohol</b> induced liver injury in the mouse given enteral <b>alcohol</b>, by Hiroshi Kono; and (5) Strategies for targeted and regulated knockouts, by Robert O. Messing and Doo Sup Choi.
+FYN	addiction	sensitization	11391051	The presentations were (1) cAMP signaling in ethanol sensitivity and tolerance, by Boris Tabakoff; (2) Synaptic signaling pathways of <strong>Fyn</strong> tyrosine kinase, by Takeshi Yagi; (3) Ethanol drinking and <b>sensitization</b> in dopaminergic and serotonergic receptor knockouts, by Tamara J. Phillips; (4) ICAM 1 is involved in early alcohol induced liver injury in the mouse given enteral alcohol, by Hiroshi Kono; and (5) Strategies for targeted and regulated knockouts, by Robert O. Messing and Doo Sup Choi.
+FGF2	drug	alcohol	31375540	We recently found in rodents that <b>alcohol</b> increases fibroblast growth factor 2 (<strong>FGF2</strong>) expression in the dorsomedial striatum (DMS), which promotes <b>alcohol</b> consumption.
+FGF2	drug	alcohol	31375540	We recently found in rodents that <b>alcohol</b> increases <strong>fibroblast growth factor 2</strong> (<strong>FGF2</strong>) expression in the dorsomedial striatum (DMS), which promotes <b>alcohol</b> consumption.
+FGF2	drug	alcohol	31375540	Here, we show that systemic or intra DMS blockade of the <strong>FGF2</strong> receptor, FGF receptor 1 (FGFR1), suppresses <b>alcohol</b> consumption, and that the effects of <strong>FGF2</strong> FGFR1 on <b>alcohol</b> drinking are mediated via the phosphoinositide 3 kinase (PI3K) signaling pathway.
+FGF2	drug	alcohol	31375540	Finally, inhibition of the PI3K, but not of the mitogen activated protein kinase (MAPK) signaling pathway, blocked the effects of <strong>FGF2</strong> on <b>alcohol</b> intake and preference.
+FGF2	drug	alcohol	31375540	Our results suggest that activation of FGFR1 by <strong>FGF2</strong> in the DMS leads to activation of the PI3K signaling pathway, which promotes excessive <b>alcohol</b> consumption, and that inhibition of FGFR1 may provide a novel therapeutic target for <b>alcohol</b> use disorder.SIGNIFICANCE STATEMENT Long term <b>alcohol</b> consumption causes neuroadaptations in the mesostriatal reward system, leading to addiction related behaviors.
+FGF2	addiction	addiction	31375540	Our results suggest that activation of FGFR1 by <strong>FGF2</strong> in the DMS leads to activation of the PI3K signaling pathway, which promotes excessive alcohol consumption, and that inhibition of FGFR1 may provide a novel therapeutic target for alcohol use disorder.SIGNIFICANCE STATEMENT Long term alcohol consumption causes neuroadaptations in the mesostriatal reward system, leading to <b>addiction</b> related behaviors.
+FGF2	addiction	reward	31375540	Our results suggest that activation of FGFR1 by <strong>FGF2</strong> in the DMS leads to activation of the PI3K signaling pathway, which promotes excessive alcohol consumption, and that inhibition of FGFR1 may provide a novel therapeutic target for alcohol use disorder.SIGNIFICANCE STATEMENT Long term alcohol consumption causes neuroadaptations in the mesostriatal <b>reward</b> system, leading to addiction related behaviors.
+FGF2	drug	alcohol	31375540	We recently showed that <b>alcohol</b> upregulates the expression of fibroblast growth factor 2 (<strong>FGF2</strong>) in dorsomedial striatum (DMS) or rats and mice, and in turn, <strong>FGF2</strong> increases <b>alcohol</b> consumption.
+FGF2	drug	alcohol	31375540	We recently showed that <b>alcohol</b> upregulates the expression of <strong>fibroblast growth factor 2</strong> (<strong>FGF2</strong>) in dorsomedial striatum (DMS) or rats and mice, and in turn, <strong>FGF2</strong> increases <b>alcohol</b> consumption.
+FGF2	drug	alcohol	31375540	Here, we show that long term <b>alcohol</b> intake also increases the expression of the <strong>FGF2</strong> receptor, FGFR1 in the DMS.
+FGF2	drug	alcohol	31375540	We further show that the effects of <strong>FGF2</strong> FGFR1 on <b>alcohol</b> drinking are mediated via activation of the PI3K intracellular signaling pathway, providing an insight on the mechanism for this effect.
+FGF2	addiction	addiction	30144335	The role of <strong>fibroblast growth factor 2</strong> in drug <b>addiction</b>.
+FGF2	addiction	addiction	30144335	Over the past decade, <strong>FGF2</strong> has been implicated in learning and memory, as well as in several neuropsychiatric disorders, including anxiety, stress, depression and drug <b>addiction</b>.
+FGF2	drug	alcohol	30144335	In this review, we present accumulating evidence indicating the involvement of <strong>FGF2</strong> in neuroadaptations caused by drugs of abuse, namely, amphetamine, cocaine, nicotine and <b>alcohol</b>.
+FGF2	drug	amphetamine	30144335	In this review, we present accumulating evidence indicating the involvement of <strong>FGF2</strong> in neuroadaptations caused by drugs of abuse, namely, <b>amphetamine</b>, cocaine, nicotine and alcohol.
+FGF2	drug	cocaine	30144335	In this review, we present accumulating evidence indicating the involvement of <strong>FGF2</strong> in neuroadaptations caused by drugs of abuse, namely, amphetamine, <b>cocaine</b>, nicotine and alcohol.
+FGF2	drug	nicotine	30144335	In this review, we present accumulating evidence indicating the involvement of <strong>FGF2</strong> in neuroadaptations caused by drugs of abuse, namely, amphetamine, cocaine, <b>nicotine</b> and alcohol.
+FGF2	drug	alcohol	30144335	Moreover, evidence suggests that <strong>FGF2</strong> is a positive regulator of <b>alcohol</b> and drug related behaviors.
+FGF2	drug	cocaine	30012881	<strong>bFGF</strong> expression is differentially regulated by <b>cocaine</b> seeking versus extinction in learning related brain regions.
+FGF2	addiction	relapse	30012881	<strong>bFGF</strong> expression is differentially regulated by cocaine <b>seeking</b> versus extinction in learning related brain regions.
+FGF2	addiction	relapse	30012881	The persistence of drug associated cues in eliciting drug <b>seeking</b> suggests enduring changes in structural and functional plasticity, which may be mediated by basic fibroblast growth factor (bFGF, <strong>FGF2</strong>).
+FGF2	addiction	relapse	30012881	The persistence of drug associated cues in eliciting drug <b>seeking</b> suggests enduring changes in structural and functional plasticity, which may be mediated by basic fibroblast growth factor (<strong>bFGF</strong>, <strong>FGF2</strong>).
+FGF2	addiction	reward	30012881	Stimulant drug use increases <strong>bFGF</strong> expression in <b>reward</b>  and learning related brain regions, such as the infralimbic medial prefrontal cortex (IL mPFC), and we previously found that this increase was reversed by extinction.
+FGF2	drug	cocaine	30012881	Therefore, we used the conditioned place preference (CPP) paradigm to assess <strong>bFGF</strong> expression following <b>cocaine</b> associated CPP or extinction of that CPP within the mPFC, nucleus accumbens (NAc), hippocampus (Hipp), and basolateral amygdala (BLA).
+FGF2	addiction	reward	30012881	Therefore, we used the conditioned place preference (<b>CPP</b>) paradigm to assess <strong>bFGF</strong> expression following cocaine associated <b>CPP</b> or extinction of that <b>CPP</b> within the mPFC, nucleus accumbens (NAc), hippocampus (Hipp), and basolateral amygdala (BLA).
+FGF2	drug	cocaine	30012881	<strong>bFGF</strong> expression was increased in IL mPFC and NAc Core and  Shell following a <b>cocaine</b> associated CPP, an effect reversed by extinction.
+FGF2	addiction	reward	30012881	<strong>bFGF</strong> expression was increased in IL mPFC and NAc Core and  Shell following a cocaine associated <b>CPP</b>, an effect reversed by extinction.
+FGF2	drug	cocaine	30012881	These results demonstrate differential regulation of <strong>bFGF</strong> following <b>cocaine</b> associated CPP or extinction of that CPP in discrete brain regions.
+FGF2	addiction	reward	30012881	These results demonstrate differential regulation of <strong>bFGF</strong> following cocaine associated <b>CPP</b> or extinction of that <b>CPP</b> in discrete brain regions.
+FGF2	drug	nicotine	29222992	Patients 45 years of age or older had significantly higher plasma levels of CCL11, fibroblast growth factor 2 (<strong>FGF 2</strong>), <b>nicotine</b> metabolite cotinine, and a longer duration of addiction.
+FGF2	addiction	addiction	29222992	Patients 45 years of age or older had significantly higher plasma levels of CCL11, fibroblast growth factor 2 (<strong>FGF 2</strong>), nicotine metabolite cotinine, and a longer duration of <b>addiction</b>.
+FGF2	drug	nicotine	29222992	Patients 45 years of age or older had significantly higher plasma levels of CCL11, <strong>fibroblast growth factor 2</strong> (<strong>FGF 2</strong>), <b>nicotine</b> metabolite cotinine, and a longer duration of addiction.
+FGF2	addiction	addiction	29222992	Patients 45 years of age or older had significantly higher plasma levels of CCL11, <strong>fibroblast growth factor 2</strong> (<strong>FGF 2</strong>), nicotine metabolite cotinine, and a longer duration of <b>addiction</b>.
+FGF2	drug	alcohol	28821667	<strong>Fibroblast Growth Factor 2</strong> in the Dorsomedial Striatum Is a Novel Positive Regulator of <b>Alcohol</b> Consumption.
+FGF2	drug	alcohol	28821667	Here, we report on a positive regulatory feedback loop of <b>alcohol</b> and <strong>FGF2</strong> in rodent models.
+FGF2	drug	alcohol	28821667	Voluntary prolonged and excessive <b>alcohol</b> consumption in a 2 bottle choice procedure increased <strong>Fgf2</strong> expression selectively in dorsomedial striatum (DMS) of both mice and rats.
+FGF2	drug	alcohol	28821667	Importantly, we found that systemic administration of recombinant <strong>FGF2</strong> (rFGF2) in mice, or rFGF2 infusion into the dorsal striatum or DMS of rats, increased <b>alcohol</b> consumption and preference, with no similar effects on saccharin or sucrose consumption.
+FGF2	drug	alcohol	28821667	Finally, we found that inhibition of the endogenous <strong>FGF2</strong> function in the DMS, by an anti <strong>FGF2</strong> neutralizing antibody, suppressed <b>alcohol</b> consumption and preference.
+FGF2	drug	alcohol	28821667	Together, our results suggest that <b>alcohol</b> consumption increases the expression of <strong>Fgf2</strong> in the DMS, and that striatal <strong>FGF2</strong> promotes <b>alcohol</b> consumption, suggesting that <strong>FGF2</strong> in the DMS is a positive regulator of <b>alcohol</b> drinking.SIGNIFICANCE STATEMENT Long term <b>alcohol</b> intake may lead to neuroadaptations in the mesostriatal reward system, resulting in addiction phenotypes.
+FGF2	addiction	addiction	28821667	Together, our results suggest that alcohol consumption increases the expression of <strong>Fgf2</strong> in the DMS, and that striatal <strong>FGF2</strong> promotes alcohol consumption, suggesting that <strong>FGF2</strong> in the DMS is a positive regulator of alcohol drinking.SIGNIFICANCE STATEMENT Long term alcohol intake may lead to neuroadaptations in the mesostriatal reward system, resulting in <b>addiction</b> phenotypes.
+FGF2	addiction	reward	28821667	Together, our results suggest that alcohol consumption increases the expression of <strong>Fgf2</strong> in the DMS, and that striatal <strong>FGF2</strong> promotes alcohol consumption, suggesting that <strong>FGF2</strong> in the DMS is a positive regulator of alcohol drinking.SIGNIFICANCE STATEMENT Long term alcohol intake may lead to neuroadaptations in the mesostriatal <b>reward</b> system, resulting in addiction phenotypes.
+FGF2	drug	alcohol	28821667	Here, we provide evidence for the involvement of <strong>FGF2</strong> in <b>alcohol</b> drinking behaviors.
+FGF2	drug	alcohol	28821667	We show that <b>alcohol</b> increases <strong>Fgf2</strong> expression in the dorsal striatum, an effect mediated via dopamine D2 like receptors.
+FGF2	drug	alcohol	28821667	Importantly, we show that infusion of recombinant <strong>FGF2</strong> into the dorsomedial striatum increases <b>alcohol</b> consumption, whereas inhibiting the endogenous <strong>FGF2</strong> function suppresses consumption.
+FGF2	drug	alcohol	28821667	Thus, <strong>FGF2</strong> is an <b>alcohol</b> responsive gene constituting a positive regulatory feedback loop with <b>alcohol</b>.
+FGF2	drug	alcohol	28821667	This loop leads to facilitation of <b>alcohol</b> consumption, marking <strong>FGF2</strong> as a potential new therapeutic target for <b>alcohol</b> addiction.
+FGF2	addiction	addiction	28821667	This loop leads to facilitation of alcohol consumption, marking <strong>FGF2</strong> as a potential new therapeutic target for alcohol <b>addiction</b>.
+FGF2	drug	cocaine	27129861	Region specific effects of developmental exposure to <b>cocaine</b> on <strong>fibroblast growth factor 2</strong> expression in the rat brain.
+FGF2	drug	cocaine	27129861	By microdissection of brain areas via punching, we investigated whether repeated exposure to <b>cocaine</b> during adolescence (from postnatal day 28 [PND28] to PND42) has altered fibroblast growth factor 2 (<strong>FGF 2</strong>) messenger RNA (mRNA) levels in selected brain subregions critical for the action of <b>cocaine</b>.
+FGF2	drug	cocaine	27129861	By microdissection of brain areas via punching, we investigated whether repeated exposure to <b>cocaine</b> during adolescence (from postnatal day 28 [PND28] to PND42) has altered <strong>fibroblast growth factor 2</strong> (<strong>FGF 2</strong>) messenger RNA (mRNA) levels in selected brain subregions critical for the action of <b>cocaine</b>.
+FGF2	addiction	reward	27129861	Last, we found reduced <strong>FGF 2</strong> mRNA levels also in brain regions which, although in a different manner, contribute to the <b>reward</b> system, i.e., the central nucleus of amygdala (cAmy) and the ventral portion of hippocampus (vHip).
+FGF2	drug	cocaine	27129861	The widespread and coordinated reduction of <strong>FGF 2</strong> mRNA levels across the brain's reward neurocircuitry might represent a defensive strategy set in motion to oppose to the psychostimulant properties of <b>cocaine</b>.
+FGF2	addiction	reward	27129861	The widespread and coordinated reduction of <strong>FGF 2</strong> mRNA levels across the brain's <b>reward</b> neurocircuitry might represent a defensive strategy set in motion to oppose to the psychostimulant properties of cocaine.
+FGF2	drug	cocaine	27129861	Moreover, given the role of <strong>FGF 2</strong> in modulating mood disorders, the reduced trophic support here observed might sustain the negative emotional state set in motion by repeated exposure to <b>cocaine</b>.
+FGF2	drug	cocaine	27114539	In contrast, low <strong>FGF2</strong> levels, which appear immutable even following prolonged <b>cocaine</b> exposure, may serve as a protective factor.
+FGF2	drug	cocaine	25994078	Blocking Infralimbic Basic Fibroblast Growth Factor (bFGF or <strong>FGF2</strong>) Facilitates Extinction of Drug Seeking After <b>Cocaine</b> Self Administration.
+FGF2	addiction	relapse	25994078	Blocking Infralimbic Basic Fibroblast Growth Factor (bFGF or <strong>FGF2</strong>) Facilitates Extinction of Drug <b>Seeking</b> After Cocaine Self Administration.
+FGF2	drug	cocaine	25994078	Blocking Infralimbic Basic Fibroblast Growth Factor (<strong>bFGF</strong> or <strong>FGF2</strong>) Facilitates Extinction of Drug Seeking After <b>Cocaine</b> Self Administration.
+FGF2	addiction	relapse	25994078	Blocking Infralimbic Basic Fibroblast Growth Factor (<strong>bFGF</strong> or <strong>FGF2</strong>) Facilitates Extinction of Drug <b>Seeking</b> After Cocaine Self Administration.
+FGF2	drug	cocaine	25994078	Following <b>cocaine</b> exposure, <strong>bFGF</strong> is increased in addiction related brain regions, including the infralimbic medial prefrontal cortex (IL mPFC).
+FGF2	addiction	addiction	25994078	Following cocaine exposure, <strong>bFGF</strong> is increased in <b>addiction</b> related brain regions, including the infralimbic medial prefrontal cortex (IL mPFC).
+FGF2	addiction	relapse	25994078	The IL mPFC is necessary for extinction, but whether drug induced overexpression of <strong>bFGF</strong> in this region affects extinction of drug <b>seeking</b> is unknown.
+FGF2	drug	cocaine	25994078	Thus, we determined whether blocking <strong>bFGF</strong> in IL mPFC would facilitate extinction following <b>cocaine</b> self administration.
+FGF2	drug	cocaine	25994078	Furthermore, <strong>bFGF</strong> protein expression increased in IL mPFC following <b>cocaine</b> self administration, an effect reversed by extinction.
+FGF2	drug	cocaine	25994078	These results suggest that <b>cocaine</b> induced overexpression of <strong>bFGF</strong> inhibits extinction, as blocking <strong>bFGF</strong> during extinction permits rapid extinction.
+FGF2	addiction	addiction	25994078	Therefore, targeted reductions in <strong>bFGF</strong> during therapeutic interventions could enhance treatment outcomes for <b>addiction</b>.
+FGF2	drug	cannabinoid	25550231	The purpose of this review is to outline the literature showing how pharmacological interventions targeting neurotransmitter systems including serotonin, dopamine, noradrenaline, histamine, glutamate, GABA, <b>cannabinoids</b>, neuropeptides (oxytocin, neuropeptides Y and S, opioids) and other targets (neurotrophins BDNF and <strong>FGF2</strong>, glucocorticoids, L type calcium channels, epigenetic modifications) as well as their downstream signaling pathways, can augment fear extinction and strengthen extinction memory persistently in preclinical models.
+FGF2	drug	opioid	25550231	The purpose of this review is to outline the literature showing how pharmacological interventions targeting neurotransmitter systems including serotonin, dopamine, noradrenaline, histamine, glutamate, GABA, cannabinoids, neuropeptides (oxytocin, neuropeptides Y and S, <b>opioids</b>) and other targets (neurotrophins BDNF and <strong>FGF2</strong>, glucocorticoids, L type calcium channels, epigenetic modifications) as well as their downstream signaling pathways, can augment fear extinction and strengthen extinction memory persistently in preclinical models.
+FGF2	drug	cocaine	25124315	A single exposure to <b>cocaine</b> during development elicits regionally selective changes in basal basic Fibroblast Growth Factor (<strong>FGF 2</strong>) gene expression and alters the trophic response to a second injection.
+FGF2	drug	cocaine	25124315	Recently, attention has been focused on basic fibroblast growth factor (<strong>FGF 2</strong>) given that its administration early in life enhances the acquisition of <b>cocaine</b> self administration and sensitization at adulthood (Turner et al.
+FGF2	addiction	sensitization	25124315	Recently, attention has been focused on basic fibroblast growth factor (<strong>FGF 2</strong>) given that its administration early in life enhances the acquisition of cocaine self administration and <b>sensitization</b> at adulthood (Turner et al.
+FGF2	drug	cocaine	25124315	Additionally, we found that abstinence from adolescent <b>cocaine</b> exposure long lastingly dysregulates <strong>FGF 2</strong> transcription (Giannotti et al.
+FGF2	drug	cocaine	25124315	The objectives of the study are to evaluate if (1) a single injection of <b>cocaine</b> (20 mg/kg) at postnatal day 35 alters <strong>FGF 2</strong> messenger RNA (mRNA) levels and (2) the first injection influences the trophic response to a second injection (10 mg/kg) provided 24 h or 7 days later.
+FGF2	drug	cocaine	25124315	We found regional differences in the <strong>FGF 2</strong> expression pattern as either the first or the second injection of <b>cocaine</b> by themselves upregulated <strong>FGF 2</strong> mRNA in the medial prefrontal cortex and nucleus accumbens while downregulating it in the hippocampus.
+FGF2	drug	cocaine	25124315	Of note, 24 h after the first injection, accumbal and hippocampal <strong>FGF 2</strong> changes produced by <b>cocaine</b> in saline pretreated rats were prevented in <b>cocaine</b> pretreated rats.
+FGF2	drug	cocaine	25124315	Conversely, in the medial prefrontal cortex and hippocampus 7 days after the first injection, the <b>cocaine</b> induced <strong>FGF 2</strong> changes were modified by the subsequent exposure to the psychostimulant.
+FGF2	drug	cocaine	22895673	Dynamic modulation of basic Fibroblast Growth Factor (<strong>FGF 2</strong>) expression in the rat brain following repeated exposure to <b>cocaine</b> during adolescence.
+FGF2	drug	cocaine	22895673	Our study stems from four related lines of evidence: (1) <strong>FGF 2</strong> is expressed in the developing brain; (2) psychostimulants modulate <strong>FGF 2</strong> expression; (3) stress alters <strong>FGF 2</strong> expression; and (4) exogenous administration of <strong>FGF 2</strong> long lastingly alters <b>cocaine</b> acquisition of self administration.
+FGF2	drug	cocaine	22895673	This research aims to study the effects of adolescent <b>cocaine</b> exposure on <strong>FGF 2</strong> mRNA levels and its influence on the response to stress.
+FGF2	drug	cocaine	22895673	In the prefrontal cortex, repeated <b>cocaine</b> treatment during adolescence increased <strong>FGF 2</strong> mRNA levels in PND 90 rats and altered its response to an acute stress in both PND 45 and PND 90 rats.
+FGF2	drug	cocaine	22895673	In the hippocampus of PND 45 rats, we found an increase of <strong>FGF 2</strong> mRNA levels following repeated <b>cocaine</b> administration.
+FGF2	drug	cocaine	22895673	Our data show that <b>cocaine</b> exposure during adolescence alters <strong>FGF 2</strong> mRNA levels throughout life in rat prefrontal cortex and modulates its response to an adverse event.
+FGF2	drug	cocaine	22895673	These results point to <strong>FGF 2</strong> as a potential molecular target through which exposure to <b>cocaine</b> early in life may dynamically and persistently alter brain homeostasis.
+FGF2	addiction	relapse	22819969	We previously reported increased levels of basic fibroblast growth factor (<strong>FGF2</strong>) in high novelty/drug <b>seeking</b> rats (bred high responders, bHR) compared to low novelty/drug <b>seeking</b> rats(bred low responders, bLRs).
+FGF2	drug	cocaine	22819969	The present study asked whether an early life manipulation of the FGF system(a single <strong>FGF2</strong> injection on postnatal day 2) can impact <b>cocaine</b> sensitization and associated neurobiological markers in adult bHR/bLR animals.
+FGF2	addiction	sensitization	22819969	The present study asked whether an early life manipulation of the FGF system(a single <strong>FGF2</strong> injection on postnatal day 2) can impact cocaine <b>sensitization</b> and associated neurobiological markers in adult bHR/bLR animals.
+FGF2	drug	cocaine	22819969	Neonatal <strong>FGF2</strong>  and vehicle treated bHR/bLR rats were sensitized to <b>cocaine</b>(7 daily injections, 15 mg/kg/day, i.p.)
+FGF2	drug	cocaine	22819969	Neonatal <strong>FGF2</strong> markedly increased bLRs' typically low psychomotor sensitization to <b>cocaine</b> (day 7 locomotor response to <b>cocaine</b>), but had little effect on bHRs' <b>cocaine</b> sensitization.
+FGF2	addiction	sensitization	22819969	Neonatal <strong>FGF2</strong> markedly increased bLRs' typically low psychomotor <b>sensitization</b> to cocaine (day 7 locomotor response to cocaine), but had little effect on bHRs' cocaine <b>sensitization</b>.
+FGF2	drug	cocaine	22819969	Gene expression studies examined dopaminergic molecules as well as <strong>FGF2</strong> and the FGFR1 receptor in <b>cocaine</b> naïve animals, to investigate possible neurobiological alterations induced by neonatal <strong>FGF2</strong> exposure that may influence behavioral response to <b>cocaine</b>.
+FGF2	drug	cocaine	22819969	Neonatal <strong>FGF2</strong> selectively increased D1 receptor and <strong>FGF2</strong> mRNA in the accumbens core of bLRs, which may contribute to their heightened <b>cocaine</b> sensitization.
+FGF2	addiction	sensitization	22819969	Neonatal <strong>FGF2</strong> selectively increased D1 receptor and <strong>FGF2</strong> mRNA in the accumbens core of bLRs, which may contribute to their heightened cocaine <b>sensitization</b>.
+FGF2	drug	cocaine	22819969	Our results suggest increased <strong>FGF2</strong> in the mesodopaminergic circuit (as in baseline bHRs and neonatal <strong>FGF2</strong> exposed bLRs vs. baseline bLRs) enhances an individual's susceptibility to <b>cocaine</b> sensitization and may increase vulnerability to drug seeking and addiction.
+FGF2	addiction	addiction	22819969	Our results suggest increased <strong>FGF2</strong> in the mesodopaminergic circuit (as in baseline bHRs and neonatal <strong>FGF2</strong> exposed bLRs vs. baseline bLRs) enhances an individual's susceptibility to cocaine sensitization and may increase vulnerability to drug seeking and <b>addiction</b>.
+FGF2	addiction	relapse	22819969	Our results suggest increased <strong>FGF2</strong> in the mesodopaminergic circuit (as in baseline bHRs and neonatal <strong>FGF2</strong> exposed bLRs vs. baseline bLRs) enhances an individual's susceptibility to cocaine sensitization and may increase vulnerability to drug <b>seeking</b> and addiction.
+FGF2	addiction	sensitization	22819969	Our results suggest increased <strong>FGF2</strong> in the mesodopaminergic circuit (as in baseline bHRs and neonatal <strong>FGF2</strong> exposed bLRs vs. baseline bLRs) enhances an individual's susceptibility to cocaine <b>sensitization</b> and may increase vulnerability to drug seeking and addiction.
+FGF2	drug	nicotine	22198237	The anti angiogenic activity of MG624 was mediated via the suppression of <b>nicotine</b> induced <strong>FGF2</strong> levels in HMEC Ls.
+FGF2	drug	nicotine	22198237	MG624 decreased <b>nicotine</b> induced early growth response gene 1 (Egr 1) levels in HMEC Ls, and reduced the levels of Egr 1 on the <strong>FGF2</strong> promoter.
+FGF2	addiction	dependence	21673064	<b>Dependence</b> on secreted <strong>FGF2</strong> for cell growth was tested with FP 1039, an FGFR1 Fc fusion protein.
+FGF2	drug	cocaine	19014962	Neonatal <strong>FGF2</strong> alters <b>cocaine</b> self administration in the adult rat.
+FGF2	addiction	relapse	19014962	We report here that rats that were selectively bred for greater drug <b>seeking</b> behavior exhibited higher levels of <strong>FGF2</strong> gene expression.
+FGF2	drug	cocaine	19014962	Indeed, early life <strong>FGF2</strong> enhanced the acquisition of <b>cocaine</b> self administration in adulthood.
+FGF2	addiction	reward	19014962	However, early life <strong>FGF2</strong> did not alter spatial or <b>operant</b> learning in adulthood.
+FGF2	addiction	addiction	19014962	Thus, <strong>FGF2</strong> may be an antecedent of vulnerability for drug taking behavior and may provide clues to novel therapeutic approaches for the treatment of <b>addiction</b>.
+FGF2	drug	amphetamine	18513704	<b>Amphetamine</b> induced rotations performed 3, 6 and 9 weeks postgrafting revealed that grafts of <strong>FGF2</strong> expanded cells induced a significantly faster and better functional recovery than grafts of FGF8 expanded cells or control cells (P<0.05 for both).
+FGF2	drug	cocaine	17914648	Stress and <b>cocaine</b> interact to modulate basic fibroblast growth factor (<strong>FGF 2</strong>) expression in rat brain.
+FGF2	drug	cocaine	17914648	Our laboratory has previously demonstrated that the expression of basic fibroblast growth factor (<strong>FGF 2</strong>), a protein involved in survival and maintenance of several cell phenotypes as well as in synaptic plasticity, is modulated by stress (Molteni et al., Brain Res Rev 37:249 258, 2001; Fumagalli et al., Neurobiol Dis 20:731 737, 2005) and <b>cocaine</b> (Fumagalli et al., J Neurochem 96:996 1004, 2006).
+FGF2	drug	cocaine	17914648	Since it is widely recognized that stress influences drug seeking, we decided to investigate whether stress, acute or repeated, could influence the changes in <strong>FGF 2</strong> gene expression brought about by <b>cocaine</b>.
+FGF2	addiction	relapse	17914648	Since it is widely recognized that stress influences drug <b>seeking</b>, we decided to investigate whether stress, acute or repeated, could influence the changes in <strong>FGF 2</strong> gene expression brought about by cocaine.
+FGF2	drug	cocaine	17914648	Our data demonstrate that stress and <b>cocaine</b> interact to produce significant changes on <strong>FGF 2</strong> expression in rat prefrontal cortex and striatum.
+FGF2	drug	cocaine	17914648	In prefrontal cortex, our experiments demonstrated that a single exposure to stress potentiated <b>cocaine</b> induced <strong>FGF 2</strong> elevation, whereas prolonged stress prevented the modulation of the trophic factor in response to <b>cocaine</b>.
+FGF2	drug	cocaine	17914648	In striatum, the magnitude of <b>cocaine</b> induced <strong>FGF 2</strong> response is enhanced by repeated stress, whereas no interaction was observed when acute stress and single exposure to <b>cocaine</b> were combined.
+FGF2	drug	cocaine	17914648	Our findings demonstrate that stress interacts with <b>cocaine</b> to alter the pattern of <strong>FGF 2</strong> expression in a way that depends on whether stress is acute or chronic and in a regionally selective fashion.
+FGF2	addiction	withdrawal	17406596	Hepatic differentiation and maturation of cells is accomplished by <b>withdrawal</b> of Activin A and <strong>FGF 2</strong> and by exposure to liver nonparenchymal cell derived growth factors, a deleted variant of hepatocyte growth factor (dHGF) and dexamethasone.
+FGF2	drug	amphetamine	16487142	In vivo studies suggest that <b>AMPH</b> sensitization requires enhanced expression of basic fibroblast growth factor (<strong>bFGF</strong>) in the nucleus of midbrain astrocytes.
+FGF2	addiction	sensitization	16487142	In vivo studies suggest that AMPH <b>sensitization</b> requires enhanced expression of basic fibroblast growth factor (<strong>bFGF</strong>) in the nucleus of midbrain astrocytes.
+FGF2	drug	amphetamine	16487142	One idea is that the <b>AMPH</b> induced increase in <strong>bFGF</strong> expression in astrocytes leads to enhanced secretion of this peptide and to long term plasticity in DA neurons.
+FGF2	drug	amphetamine	16487142	Together these data demonstrate that under basal conditions (in the absence of a pharmacological stimulus such as <b>amphetamine</b>) <strong>bFGF</strong> is not secreted even though there is abundant nuclear expression in astrocytes.
+FGF2	drug	alcohol	12676135	We have expanded neuroepithelial cells dissociated from the embryonic rat telencephalon in serum free defined medium containing basic fibroblast growth factor (<strong>bFGF</strong>) in order to generate a model neuroepithelium to study the interaction of <b>ethanol</b> with both growth factor  and transmitter stimulated proliferation.
+FGF2	drug	alcohol	12676135	<b>Ethanol</b> blocked proliferation stimulated by <strong>bFGF</strong> and by carbachol, an agonist at muscarinic acetylcholine receptors, in a dose dependent manner.
+FGF2	drug	alcohol	12676135	In addition, <b>ethanol</b> attenuated autonomous expansion of neuroepithelial cells occurring following withdrawal of <strong>bFGF</strong>.
+FGF2	addiction	withdrawal	12676135	In addition, ethanol attenuated autonomous expansion of neuroepithelial cells occurring following <b>withdrawal</b> of <strong>bFGF</strong>.
+FGF2	addiction	sensitization	10972461	Possible mechanisms whereby <strong>bFGF</strong> participates in the development of <b>sensitization</b>, including interactions with other neurotrophic factors, are discussed.
+FGF2	drug	amphetamine	10632621	We reported previously that repeated <b>amphetamine</b> treatment results in increased astrocytic expression of basic fibroblast growth factor (<strong>bFGF</strong>) in the ventral tegmental area (VTA) and substantia nigra compacta (SNc) and that this effect is prevented by coadministration of a nonspecific glutamate receptor antagonist.
+FGF2	drug	amphetamine	10632621	Here we show that the development of sensitization to <b>amphetamine</b> is prevented when <b>amphetamine</b> injections are preceded by infusions of a neutralizing antibody to <strong>bFGF</strong> into the VTA.
+FGF2	addiction	sensitization	10632621	Here we show that the development of <b>sensitization</b> to amphetamine is prevented when amphetamine injections are preceded by infusions of a neutralizing antibody to <strong>bFGF</strong> into the VTA.
+FGF2	addiction	sensitization	10632621	In addition, we show that astrocytic <strong>bFGF</strong> expression is increased in the VTA and SNc of animals that exhibit behavioral <b>sensitization</b> and that the number of <strong>bFGF</strong> immunoreactive astrocytes in these regions is strongly and positively correlated with the magnitude of <b>sensitization</b>.
+FGF2	addiction	sensitization	10632621	Cotreatment with an NMDA glutamate receptor antagonist blocks both the development of behavioral <b>sensitization</b> and <strong>bFGF</strong> induction.
+FGF2	drug	amphetamine	10632621	These results show that endogenous <strong>bFGF</strong> is necessary for the development of sensitization to <b>amphetamine</b> and suggest that <strong>bFGF</strong> mediates the glutamatergic dopaminergic interaction that initiates the long term consequences of repeated drug use.
+FGF2	addiction	sensitization	10632621	These results show that endogenous <strong>bFGF</strong> is necessary for the development of <b>sensitization</b> to amphetamine and suggest that <strong>bFGF</strong> mediates the glutamatergic dopaminergic interaction that initiates the long term consequences of repeated drug use.
+FGF2	drug	amphetamine	9801391	Because glutamate participates in the development of sensitization to stimulant drugs, we assessed the effect of the glutamate antagonist, kynurenic acid (KYN), on <b>amphetamine</b> induced <strong>bFGF</strong> IR.
+FGF2	addiction	sensitization	9801391	Because glutamate participates in the development of <b>sensitization</b> to stimulant drugs, we assessed the effect of the glutamate antagonist, kynurenic acid (KYN), on amphetamine induced <strong>bFGF</strong> IR.
+FGF2	drug	amphetamine	9801391	Coadministration of KYN prevented the increases in <strong>bFGF</strong> IR in both VTA and SNc assessed 1 week after the <b>amphetamine</b> treatment.
+DLG4	addiction	withdrawal	32450347	At hippocampal level, the <b>withdrawal</b> induced changes in the levels of AMPA receptor GluA1 and GluA2/3 subunits, PSD 95 protein, corticotropin releasing factor (Crf) and Crf receptor 1 (CrfR1) mRNA were biphasic: AMPA receptor subunit and <strong>PSD95</strong> protein levels initially remained unchanged and decreased after 60 90 days, whereas Crf/CrfR1 mRNA levels initially increased and then markedly decreased after 60 days.
+DLG4	drug	opioid	31735530	Methylation in Syn and <strong>Psd95</strong> genes underlie the inhibitory effect of oxytocin on <b>oxycodone</b> induced conditioned place preference.
+DLG4	addiction	reward	31735530	via its receptor specifically blocked Oxy <b>CPP</b>, normalized synaptic density, and regulated DNMT1 and TET2 3 causing reverse of DNA demethylation of Syn and <strong>Psd95</strong>.
+DLG4	drug	opioid	31454827	D <b>methadone</b> administration also increased levels of the synaptic proteins, <strong>PSD95</strong>, GluA1, and Synapsin 1 and enhanced synaptic function in the mPFC.
+DLG4	addiction	withdrawal	30733663	We then analyzed the expression levels of presynaptic (vGlut1, vGlut2, CB1 receptor, synaptophysin) and postsynaptic (<strong>PSD95</strong>, GluN1, GluN2A, GluN2B, GluA1, GluA2, mGluR1 and mGluR5) proteins after 7 days EtOH incubation or after EtOH <b>withdrawal</b>.
+DLG4	drug	cannabinoid	30623520	We analyzed <strong>PSD95</strong> and gephyrin protein levels, gene expression of glutamatergic, GABAergic and <b>endocannabinoid</b> elements, and amino acid transmitter levels.
+DLG4	drug	cocaine	30144237	In <b>cocaine</b> naïve animals, SERT removal led to reduced baseline Hb mRNA levels of critical determinants of glutamate transmission, such as SLC1A2, the main glutamate transporter and N methyl D aspartate (Grin1, Grin2A and Grin2B) as well as α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid (Gria1 and Gria2) receptor subunits, with no changes in the scaffolding protein <strong>Dlg4</strong>.
+DLG4	drug	amphetamine	29441405	In rats that reinstated <b>methamphetamine</b> seeking, these altered electrophysiological properties of GCNs were associated with enhanced expression of Fos, GluN2A subunits and <strong>PSD95</strong> and reduced expression of GABAA subunits in the DG and enhanced expression of synaptic PSD in the molecular layer.
+DLG4	addiction	relapse	29441405	In rats that reinstated methamphetamine <b>seeking</b>, these altered electrophysiological properties of GCNs were associated with enhanced expression of Fos, GluN2A subunits and <strong>PSD95</strong> and reduced expression of GABAA subunits in the DG and enhanced expression of synaptic PSD in the molecular layer.
+DLG4	addiction	addiction	29234834	One day after the final self administration session, the rats were euthanized and the dmPFC was removed for quantification of mRNA expression of critical glutamatergic signaling genes, Homer2, Grin1, and <strong>Dlg4</strong>, as these genes and brain region have been previously implicated in <b>addiction</b>, learning, and memory.
+DLG4	drug	cocaine	29234834	Lastly, Homer2, Grin1, and <strong>Dlg4</strong> mRNA were impacted by both duration and mode of <b>cocaine</b> exposure.
+DLG4	drug	opioid	26442368	[Effect of <b>Heroin</b> on <strong>DLG4</strong> Expression in Hippocampus, Amygdala and Frontal Cortex of Rats].
+DLG4	drug	opioid	26442368	To observe the expression of discs large homolog 4 (<strong>DLG4</strong>) protein in hippocampus, amygdala and frontal cortex of rats and evaluate postsynaptic density in <b>heroin</b> dependence.
+DLG4	addiction	dependence	26442368	To observe the expression of discs large homolog 4 (<strong>DLG4</strong>) protein in hippocampus, amygdala and frontal cortex of rats and evaluate postsynaptic density in heroin <b>dependence</b>.
+DLG4	drug	opioid	26442368	<strong>DLG4</strong> proteins in hippocampus, amygdala and frontal cortex of <b>heroin</b> dependent 9, 18, 36 days rats were detected with immunohistochemical staining and compared with that in the control group.
+DLG4	drug	opioid	26442368	<strong>DLG4</strong> proteins in hippocampus, amygdala and frontal cortex were gradually reduced with extension of <b>heroin</b> dependent time.
+DLG4	drug	alcohol	25755642	Western blot analysis of tissue samples from the NAc enriched for PSD proteins revealed a main effect of <b>ethanol</b> treatment on the expression of GluN2B, but there was no effect of genotype or treatment on the expression other glutamate receptor subunits or <strong>PSD95</strong>.
+DLG4	drug	opioid	24704371	An upregulation of expression of phosphorylated cAMP response element binding protein (pCREB) and the occupancy of pCREB in the <strong>Dlg4</strong> promoter region were shown in the VTA of the <b>morphine</b> conditioned rats.
+DLG4	drug	opioid	24704371	Inhibition of pCREB activity significantly decreased the histone H3 acetylation in <strong>Dlg4</strong> promoter region, PSD 95 upregulation, enhancement of glutamatergic strength and the preference to <b>morphine</b> paired chamber in the rats with <b>morphine</b> conditioning.
+DLG4	drug	cocaine	20600170	In the ventral tegmental area, <b>cocaine</b> self administration elevated glutamatergic receptor subunits NR1 and GluR1 and scaffolding protein <strong>PSD95</strong>, but not GABA(A)β, protein levels.
+DLG4	drug	cannabinoid	19384563	A significant decrease in synaptophysin and <strong>PSD95</strong> proteins was found in the prefrontal cortex of <b>THC</b> pre treated rats, with no alterations in the hippocampus.
+DLG4	drug	nicotine	17164261	Fine mapping of a linkage region on chromosome 17p13 reveals that GABARAP and <strong>DLG4</strong> are associated with vulnerability to <b>nicotine</b> dependence in European Americans.
+DLG4	addiction	dependence	17164261	Fine mapping of a linkage region on chromosome 17p13 reveals that GABARAP and <strong>DLG4</strong> are associated with vulnerability to nicotine <b>dependence</b> in European Americans.
+DLG4	drug	nicotine	17164261	Taken together, our two stage association analysis and linkage analysis results indicate that the GABARAP and <strong>DLG4</strong> genes are involved in the etiology of ND in EA <b>smokers</b>.
+DLG4	drug	cocaine	14684468	<b>Cocaine</b> induced expression differences in PSD 95/<strong>SAP 90</strong> associated protein 4 and in Ca2+/calmodulin dependent protein kinase subunits in amygdalae of taste aversion prone and taste aversion resistant rats.
+DLG4	addiction	aversion	14684468	Cocaine induced expression differences in PSD 95/<strong>SAP 90</strong> associated protein 4 and in Ca2+/calmodulin dependent protein kinase subunits in amygdalae of taste <b>aversion</b> prone and taste <b>aversion</b> resistant rats.
+CYP1A2	drug	nicotine	32376004	<b>Tobacco</b> is well identified for its effects as an inducer of <strong>CYP1A2</strong> enzyme.
+CYP1A2	drug	nicotine	32376004	In a COVID+ patient, the consequences of an abrupt cessation of <b>smoking</b>, particularly related with the appearance of respiratory symptoms (cough, dyspnea), must therefore be anticipated for patients receiving psychotropics metabolized by <strong>CYP1A2</strong>.
+CYP1A2	drug	nicotine	29871580	<strong>CYP1A2</strong> is induced by cigarette <b>smoking</b>, which may change the plasma level of clozapine, especially if consuming habits change.
+CYP1A2	drug	opioid	29333880	Variants in six pharmacokinetic genes (<strong>CYP1A2</strong>, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of <b>methadone</b> and <b>buprenorphine</b>/<b>naloxone</b> for the treatment of <b>opioid</b> dependence (n = 764; 68.7% male).
+CYP1A2	addiction	dependence	29333880	Variants in six pharmacokinetic genes (<strong>CYP1A2</strong>, CYP2B6, CYP2C19, CYP2C9, CYP2D6, CYP3A4) and five pharmacodynamic genes (HTR2A, OPRM1, ADRA2A, COMT, SLC6A4) were genotyped in samples from a 24 week, randomized, open label trial of methadone and buprenorphine/naloxone for the treatment of opioid <b>dependence</b> (n = 764; 68.7% male).
+CYP1A2	drug	nicotine	27106177	On the basis of the estimated half life of <strong>CYP1A2</strong>, dose reduction of CYP1A drugs may be necessary as early as the first few days after <b>smoking</b> cessation to prevent toxicity, especially for drugs with a narrow therapeutic index.
+CYP1A2	addiction	dependence	27067104	Emphasis was placed on 3 hydroxymethylantipyrine (3HMAP), the metabolite with the greatest <b>dependence</b> on dioxin inducible cytochrome P4501A2 (<strong>CYP1A2</strong>) activity.
+CYP1A2	drug	nicotine	27067104	Multiple regression models were constructed using the three major AP metabolites as a dependent variable to assess the influence of age, <b>smoking</b> as urinary cotinine concentration, dioxin exposure (as either WHO TEQ or body burden), group, and <strong>CYP1A2</strong>*F ( 163C>A) genotypes.
+CYP1A2	addiction	addiction	26626327	Although depressive or obsessive <b>compulsive</b> symptoms may improve, a SSRI with no <strong>CYP1A2</strong> inhibition should rather be used (C).
+CYP1A2	drug	nicotine	25052559	Several statistically significant interactions were observed between <b>smoking</b> and genetic variants (<strong>CYP1A2</strong> 1548C>T, CYP1A1 3801T>C, CYP1B1 4326G>C, NAT1 c. 85 1014T>A, UGT1A7 W208R 622T>C, SOD2 c.47T>C, GSTT1 deletion).
+CYP1A2	drug	nicotine	24170642	<b>Smoking</b> is very common among psychiatric patients and can induce <strong>CYP1A2</strong> enzymes, thereby lowering expected plasma levels of certain SGAs.
+CYP1A2	drug	opioid	19133059	Contribution of the activities of CYP3A, CYP2D6, <strong>CYP1A2</strong> and other potential covariates to the disposition of <b>methadone</b> in patients undergoing <b>methadone</b> maintenance treatment.
+CYP1A2	drug	benzodiazepine	19133059	CYP2D6 activity [3 h plasma metabolic ratio of dextromethorphan (DEX) to dextrorphan (DOR)] was determined in 44 patients (29 male; 24 55 years), <strong>CYP1A2</strong> activity (salivary caffeine elimination half life) in 44 patients (21 male; 24 55 years) and CYP3A activity (oral clearance of <b>midazolam</b>) in 49 patients (33 male; 23 55 years).
+CYP1A2	drug	opioid	19133059	Neither CYP2D6 nor <strong>CYP1A2</strong> activity was related to <b>methadone</b> disposition.
+CYP1A2	drug	opioid	15501692	CYP2D6 and probably <strong>CYP1A2</strong> are also involved in <b>methadone</b> metabolism.
+CYP1A2	drug	nicotine	12618594	The effect of <b>smoking</b> and cytochrome P450 <strong>CYP1A2</strong> genetic polymorphism on clozapine clearance and dose requirement.
+CYP1A2	drug	nicotine	12618594	<b>Smoking</b> is a potent inducer of <strong>CYP1A2</strong> enzyme activity, resulting in significant lower clozapine serum concentrations in <b>smokers</b> compared with non <b>smokers</b>, upon a given dose.
+CYP1A2	drug	nicotine	12618594	Because this polymorphism in relation to <b>smoking</b> behaviour may be relevant in treatment with clozapine, we studied the effect of <strong>CYP1A2</strong> genotype on clozapine clearance and dose requirement in a group of 80 <b>smoking</b> and non <b>smoking</b> schizophrenic patients on long term clozapine therapy.
+CYP1A2	drug	nicotine	12618594	Neither among <b>smokers</b>, nor among non <b>smokers</b> mean C/D ratios and daily doses did vary significantly between patients with the different <strong>CYP1A2</strong> genotypes.
+CYP1A2	drug	nicotine	12618594	The results show that clozapine clearance and daily dose requirement are strongly associated with <b>smoking</b> behaviour, while the <strong>CYP1A2</strong> genetic polymorphism seems to have no significant clinical effect.
+CYP1A2	drug	nicotine	12189363	<strong>CYP1A2</strong> activity was measured in 2 women highly exposed to 2,3,7,8 tetrachlorodibenzo p dioxin (TCDD), in 1 man moderately exposed, and in 50 control subjects (30 nonsmokers and 20 heavy <b>smokers</b>).
+CYP1A2	drug	nicotine	11981356	Plasma levels of clozapine and olanzapine are lower in <b>smokers</b> than in nonsmokers, which is mainly due to induction of cytochrome P4501A2 (<strong>CYP1A2</strong>) by some smoke constituents.
+CYP1A2	drug	nicotine	11981356	<b>Smoking</b> cessation in patients treated with antipsychotic drugs that are <strong>CYP1A2</strong> substrates may result in increased plasma levels of the drug and, consequently, in adverse drug effects.
+CYP1A2	drug	nicotine	11981356	The clinical implication of these observations is that <b>smoking</b> patients treated with <strong>CYP1A2</strong> substrate antipsychotics should regularly be monitored with regard to their <b>smoking</b> consumption in order to adjust doses in cases of a reduction or increase in <b>smoking</b>.
+CYP1A2	drug	alcohol	9390106	Impact of long term <b>ethanol</b> consumption on <strong>CYP1A2</strong> activity.
+CYP1A2	drug	alcohol	9390106	The aim of our study was to evaluate the impact of <b>ethanol</b> consumption on the activity of <strong>CYP1A2</strong>, which has been shown to be influenced by drugs (inhibited or induced).
+CYP1A2	drug	alcohol	9390106	Our results confirm the well known induction of <strong>CYP1A2</strong> activity by tobacco smoking and show that this induction is masked by long term <b>ethanol</b> consumption.
+CYP1A2	drug	nicotine	9390106	Our results confirm the well known induction of <strong>CYP1A2</strong> activity by <b>tobacco</b> <b>smoking</b> and show that this induction is masked by long term ethanol consumption.
+CYP1A2	drug	alcohol	7786308	In contrast, immunoreactive <strong>CYP1A2</strong> was found to decrease significantly (by 30 40%) during <b>ethanol</b> withdrawal (24, 48, 72, 168 hr).
+CYP1A2	addiction	withdrawal	7786308	In contrast, immunoreactive <strong>CYP1A2</strong> was found to decrease significantly (by 30 40%) during ethanol <b>withdrawal</b> (24, 48, 72, 168 hr).
+CPM	drug	opioid	31719641	<strong>CPM</strong> identified an <b>opioid</b> abstinence network (p = 0.018), characterized by stronger within network motor/sensory connectivity, and reduced connectivity between the motor/sensory network and medial frontal, default mode, and frontoparietal networks.
+CPM	drug	cocaine	30606049	The authors sought to identify a brain based predictor of <b>cocaine</b> abstinence by using connectome based predictive modeling (<strong>CPM</strong>), a recently developed machine learning approach.
+CPM	drug	cocaine	30606049	<strong>CPM</strong> with leave one out cross validation was conducted to identify pretreatment networks that predicted abstinence (percent <b>cocaine</b> negative urine samples during treatment).
+CPM	drug	opioid	29288475	Nurses' knowledge was better in regard of <strong>CPM</strong> guidelines, while they had poor knowledge about pharmacological pain management and <b>opioid</b> addiction.
+CPM	addiction	addiction	29288475	Nurses' knowledge was better in regard of <strong>CPM</strong> guidelines, while they had poor knowledge about pharmacological pain management and opioid <b>addiction</b>.
+CPM	drug	opioid	29288475	Physicians and nurses perceived knowledge deficit, lack of pain assessment, <b>opioid</b> unavailability, and lack of psychological interventions as the most common barriers to <strong>CPM</strong>.
+CPM	addiction	withdrawal	29047208	At approximately day 10 following the 3rd injection, <strong>CPM</strong> treated rats exhibited colorectal hyperalgesia as they showed significantly greater abdominal <b>withdrawal</b> responses (AWR) to graded colorectal distension (CRD, 0 100 mm Hg) than the saline group.
+CPM	drug	opioid	29047208	Immunofluorescent staining and Western blot assay revealed that <strong>CPM</strong> induced colorectal hyperalgesia was associated with significantly increased expression of aromatase and phosphorylated μ type <b>opioid</b> receptor (pMOR) and decreased expression of total MOR in the RVM.
+CPM	drug	opioid	28944405	Nurses appeared knowledgeable about <strong>CPM</strong> guidelines but were unfamiliar regarding pharmacological management and had negative attitudes toward <b>opioids</b> addiction and pain assessment.
+CPM	addiction	addiction	28944405	Nurses appeared knowledgeable about <strong>CPM</strong> guidelines but were unfamiliar regarding pharmacological management and had negative attitudes toward opioids <b>addiction</b> and pain assessment.
+CPM	drug	opioid	28722815	There were no significant effects of <b>naloxone</b> nor nocebo on PPT, deep tissue pain, temporal summation or <strong>CPM</strong> in the control group.
+CPM	drug	opioid	28722815	Besides, neither <b>morphine</b> nor <b>naloxone</b> influenced deep tissue pain, temporal summation or <strong>CPM</strong>.
+CPM	drug	opioid	28722815	Therefore, these results suggest that the <b>opioid</b> system is not dominant in (enhanced) bottom up sensitization (temporal summation) or (impaired) endogenous pain inhibition (<strong>CPM</strong>) in patients with CFS/FM or RA.
+CPM	addiction	sensitization	28722815	Therefore, these results suggest that the opioid system is not dominant in (enhanced) bottom up <b>sensitization</b> (temporal summation) or (impaired) endogenous pain inhibition (<strong>CPM</strong>) in patients with CFS/FM or RA.
+CPM	drug	alcohol	28289647	We report the case of a young woman who presented with gait disturbance and <b>alcohol</b> withdrawal, and who was eventually diagnosed with <strong>CPM</strong>.
+CPM	addiction	withdrawal	28289647	We report the case of a young woman who presented with gait disturbance and alcohol <b>withdrawal</b>, and who was eventually diagnosed with <strong>CPM</strong>.
+CPM	drug	alcohol	28289647	Generally, the cause and pathogenesis of <strong>CPM</strong> in chronic <b>alcoholics</b> remain unclear.
+CPM	drug	alcohol	27610136	Central pontine myelinolysis (<strong>CPM</strong>), a potentially fatal and debilitating neurological condition, was first described in 1959 in a study on <b>alcoholic</b> and malnourished patients.
+CPM	drug	alcohol	27610136	Chronic <b>alcoholism</b> associated <strong>CPM</strong> tends to be benign with a favorable prognosis compared to <strong>CPM</strong> secondary to rapid correction of hyponatremia.
+CPM	drug	alcohol	27610136	We describe a normonatremic, <b>alcoholic</b> patient who presented with <strong>CPM</strong> after a rapid rise in his sodium levels.
+CPM	drug	alcohol	27610136	Furthermore, clinical evolution of <strong>CPM</strong> can be difficult to discern from the natural course of <b>alcohol</b> withdrawal delirium, requiring astuteness and maintenance of a high degree of clinical suspicion on the part of the physician.
+CPM	addiction	withdrawal	27610136	Furthermore, clinical evolution of <strong>CPM</strong> can be difficult to discern from the natural course of alcohol <b>withdrawal</b> delirium, requiring astuteness and maintenance of a high degree of clinical suspicion on the part of the physician.
+CPM	drug	alcohol	25102585	<b>Alcohol</b> withdrawal represents an additional vulnerability factor, being responsible for electrolyte imbalances which are not always demonstrable but are certainly involved in the development of <strong>CPM</strong> and/or EPM.
+CPM	addiction	withdrawal	25102585	Alcohol <b>withdrawal</b> represents an additional vulnerability factor, being responsible for electrolyte imbalances which are not always demonstrable but are certainly involved in the development of <strong>CPM</strong> and/or EPM.
+CPM	drug	opioid	24640176	Identification of barriers to <b>opioid</b> use by the physicians and policy makers/regulators, and their level of knowledge and attitudes concerning its use are influential factors for cancer pain management (<strong>CPM</strong>).
+CPM	drug	opioid	24640176	This study was performed to assess the knowledge and attitudes physicians and policy makers/regulators have regarding use of <b>opioids</b> for <strong>CPM</strong>.
+CPM	drug	opioid	24640176	The strengthening of ongoing educational programs regarding <b>opioid</b> use for <strong>CPM</strong>, and cooperation among key groups are needed.
+CPM	drug	nicotine	24162926	Study 1 results revealed that 90% of videos illustrated a four step <strong>CPM</strong> technique: 'Loosening the <b>tobacco</b>'; 'Dumping the <b>tobacco</b>'; 'Removing the cigar binder' and 'Repacking the <b>tobacco</b>'.
+CPM	drug	nicotine	24162926	These findings highlight a novel means for youth to access information concerning <strong>CPM</strong> that may have important implications for <b>tobacco</b> control policy and prevention.
+CPM	drug	alcohol	24069831	Until now, brain magnetic resonance imaging (MRI) follow up in <b>alcoholic</b> <strong>CPM</strong> cases after <b>alcohol</b> withdrawal has been rarely described.
+CPM	addiction	withdrawal	24069831	Until now, brain magnetic resonance imaging (MRI) follow up in alcoholic <strong>CPM</strong> cases after alcohol <b>withdrawal</b> has been rarely described.
+CPM	drug	alcohol	24069831	The presented case demonstrates that <strong>CPM</strong> in chronic <b>alcoholics</b> may have a benign clinical course after <b>alcohol</b> withdrawal, which is not necessarily associated with the reduction of lesions on brain MRI.
+CPM	addiction	withdrawal	24069831	The presented case demonstrates that <strong>CPM</strong> in chronic alcoholics may have a benign clinical course after alcohol <b>withdrawal</b>, which is not necessarily associated with the reduction of lesions on brain MRI.
+CPM	drug	alcohol	22347796	Thus, it is clinically relevant to differentiate between <strong>CPM</strong>, schizophrenia, and <b>alcohol</b> withdrawal as the treatment and prognostic outcomes for each diagnosis are distinct.
+CPM	addiction	withdrawal	22347796	Thus, it is clinically relevant to differentiate between <strong>CPM</strong>, schizophrenia, and alcohol <b>withdrawal</b> as the treatment and prognostic outcomes for each diagnosis are distinct.
+CPM	drug	alcohol	22347796	We present a series of events that led to a misdiagnosis of a patient admitted to the medical emergency center presenting with confusion, psychomotor agitation, and delirium who was first diagnosed with schizophrenia and <b>alcohol</b> withdrawal by emergency medical physicians and later discovered by the psychiatric consult team to have <strong>CPM</strong>.
+CPM	addiction	withdrawal	22347796	We present a series of events that led to a misdiagnosis of a patient admitted to the medical emergency center presenting with confusion, psychomotor agitation, and delirium who was first diagnosed with schizophrenia and alcohol <b>withdrawal</b> by emergency medical physicians and later discovered by the psychiatric consult team to have <strong>CPM</strong>.
+CPM	drug	alcohol	22347796	Differentiating between <strong>CPM</strong>, schizophrenia, and <b>alcohol</b> withdrawal using neuroimaging techniques and preventing the risks for <strong>CPM</strong> using slow sodium correction are paramount.
+CPM	addiction	withdrawal	22347796	Differentiating between <strong>CPM</strong>, schizophrenia, and alcohol <b>withdrawal</b> using neuroimaging techniques and preventing the risks for <strong>CPM</strong> using slow sodium correction are paramount.
+CPM	drug	alcohol	20228603	These findings suggest that cytotoxic edema is central to the pathogenesis of <strong>CPM</strong>, but vasogenic edema plays an important role in the pathogenesis of EPM occurring during <b>alcohol</b> withdrawal.
+CPM	addiction	withdrawal	20228603	These findings suggest that cytotoxic edema is central to the pathogenesis of <strong>CPM</strong>, but vasogenic edema plays an important role in the pathogenesis of EPM occurring during alcohol <b>withdrawal</b>.
+CPM	drug	alcohol	19940203	Central pontine myelinolysis (<strong>CPM</strong>) has been described in <b>alcoholic</b> patients and in the aftermath of rapid correction of chronic hyponatraemia.
+CPM	drug	alcohol	19940203	This is the first reported case of nephrogenic DI resulting in the development of <strong>CPM</strong>, despite a relatively slow rise in plasma sodium of less than 12 mmol/L/24 h. Coexisting <b>alcohol</b> abuse, hypoxaemia and hypokalaemia may have contributed significantly to the development of <strong>CPM</strong> in this patient.
+CPM	drug	alcohol	18678596	Central pontine myelinolysis (<strong>CPM</strong>) and extrapontine myelinolysis (EPM) are well recognized syndromes that are related to various conditions such as rapid correction of hyponatremia and chronic <b>alcoholism</b>.
+CPM	drug	alcohol	18678596	We report a very case of a patient with dysarthria, dysphagia and psychiatric symptoms including abnormal behavior starting after <b>alcohol</b> withdrawal, with radiological evidence of <strong>CPM</strong> and EPM.
+CPM	addiction	withdrawal	18678596	We report a very case of a patient with dysarthria, dysphagia and psychiatric symptoms including abnormal behavior starting after alcohol <b>withdrawal</b>, with radiological evidence of <strong>CPM</strong> and EPM.
+CPM	addiction	relapse	16173886	This was largely a result of changes in self reported <b>craving</b> and was interpreted as consistent with the <strong>CPM</strong>.
+CPM	drug	opioid	15827729	The effectiveness of cancer pain management (<strong>CPM</strong>) is influenced by nurses' willingness to maximize <b>opioid</b> analgesia for severe cancer pain.
+CPM	drug	opioid	15827729	The purposes of this study were to identify the willingness of nurses to provide maximum dose <b>opioids</b> whenever needed for <strong>CPM</strong> and to determine its associated predictors.
+CPM	drug	opioid	15827729	The respondents who were more likely to recommend <b>morphine</b> showed the following characteristics: older nurses (odds ratio, OR, 1.57; confidence interval, CI, 1.13 2.19); they knew the effectiveness of <b>opioids</b> for <strong>CPM</strong> (OR 1.53; CI 1.06 2.20); rarely concerned about a patient's addiction to <b>opioids</b> (OR 2.16; CI 1.48 3.15), or to a family member's addiction (OR 1.81; CI 1.20 2.73); prior experience with pain assessment tools (OR 1.62; CI 1.11 2.37); practical experience caring for cancer patients with pain over 51% (OR 1.55; CI 1.09 2.19).
+CPM	addiction	addiction	15827729	The respondents who were more likely to recommend morphine showed the following characteristics: older nurses (odds ratio, OR, 1.57; confidence interval, CI, 1.13 2.19); they knew the effectiveness of opioids for <strong>CPM</strong> (OR 1.53; CI 1.06 2.20); rarely concerned about a patient's <b>addiction</b> to opioids (OR 2.16; CI 1.48 3.15), or to a family member's <b>addiction</b> (OR 1.81; CI 1.20 2.73); prior experience with pain assessment tools (OR 1.62; CI 1.11 2.37); practical experience caring for cancer patients with pain over 51% (OR 1.55; CI 1.09 2.19).
+CPM	drug	opioid	15827729	Our multicenter study suggested that in order to improve nurses' willingness to recommend <b>opioids</b> liberally in <strong>CPM</strong>: (1) attitudes about fear of <b>opioid</b> addiction must be changed; (2) the efficiency of <b>opioids</b> in <strong>CPM</strong> must be taught; and (3) implementation of pain assessment tools must be undertaken.
+CPM	addiction	addiction	15827729	Our multicenter study suggested that in order to improve nurses' willingness to recommend opioids liberally in <strong>CPM</strong>: (1) attitudes about fear of opioid <b>addiction</b> must be changed; (2) the efficiency of opioids in <strong>CPM</strong> must be taught; and (3) implementation of pain assessment tools must be undertaken.
+CPM	drug	alcohol	14504969	Nine <b>alcoholic</b> patients with central pontine myelinolysis (<strong>CPM</strong>),who showed a favorable prognosis, are reported.
+CPM	drug	opioid	16967581	To determine the prevalence of 12 proposed myths or misconceptions about <b>morphine</b> use in cancer pain management (<strong>CPM</strong>), we surveyed all physicians engaged in direct patient care in Duluth, Minnesota (N = 243).
+CPM	drug	opioid	16967581	Many were unaware of the use of adjuvant analgesics (29%), efficacy of oral <b>morphine</b> (27%), and nonexistent risk of addiction in <strong>CPM</strong> (20%).
+CPM	addiction	addiction	16967581	Many were unaware of the use of adjuvant analgesics (29%), efficacy of oral morphine (27%), and nonexistent risk of <b>addiction</b> in <strong>CPM</strong> (20%).
+CPM	drug	opioid	16967581	Strategies to change physician attitudes and beliefs regarding <b>morphine</b> in <strong>CPM</strong> should focus on tolerance concepts, dosing schemes, safety, efficacy, lack of addictive risk, use of drug combinations, and the fact that cancer pain can be relieved.
+CPM	addiction	addiction	16967581	Strategies to change physician attitudes and beliefs regarding morphine in <strong>CPM</strong> should focus on tolerance concepts, dosing schemes, safety, efficacy, lack of <b>addictive</b> risk, use of drug combinations, and the fact that cancer pain can be relieved.
+CPM	drug	alcohol	2723450	However, the strong sensitizer, oxazolone (OXAZ), has no water soluble analogue and lymphocytes from mice sensitized to OXAZ responded poorly in vitro (less than 2000 <strong>CPM</strong>) to an <b>ethanol</b> solubilized OXAZ preparation in spite of very strong in vivo sensitization (ear swelling assay).
+CPM	addiction	sensitization	2723450	However, the strong sensitizer, oxazolone (OXAZ), has no water soluble analogue and lymphocytes from mice sensitized to OXAZ responded poorly in vitro (less than 2000 <strong>CPM</strong>) to an ethanol solubilized OXAZ preparation in spite of very strong in vivo <b>sensitization</b> (ear swelling assay).
+ALDH1A1	drug	alcohol	29665144	<b>Disulfiram</b>/copper targets stem cell like ALDH+ population of multiple myeloma by inhibition of <strong>ALDH1A1</strong> and Hedgehog pathway.
+ALDH1A1	drug	alcohol	29190005	Associations between <strong>ALDH1A1</strong> polymorphisms, <b>alcohol</b> consumption, and mortality among Hispanic and non Hispanic white women diagnosed with breast cancer: the Breast Cancer Health Disparities Study.
+ALDH1A1	drug	alcohol	29190005	<strong>ALDH1A1</strong>, one of the main isotopes of aldehyde dehydrogenase 1 is involved in the differentiation and protection of normal hematopoietic stem cells and functions in <b>alcohol</b> sensitivity and dependence.
+ALDH1A1	addiction	dependence	29190005	<strong>ALDH1A1</strong>, one of the main isotopes of aldehyde dehydrogenase 1 is involved in the differentiation and protection of normal hematopoietic stem cells and functions in alcohol sensitivity and <b>dependence</b>.
+ALDH1A1	drug	alcohol	29190005	We evaluated the associations between <strong>ALDH1A1</strong> polymorphisms, <b>alcohol</b> consumption, and mortality among Hispanic and non Hispanic white (NHW) breast cancer (BC) cases from the Breast Cancer Health Disparities Study.
+ALDH1A1	drug	alcohol	29190005	Future BC studies examining the relationship between <strong>ALDH1A1</strong> and mortality should consider the modifying effects of <b>alcohol</b> consumption and NA ancestry.
+ALDH1A1	addiction	relapse	26944893	<strong>ALDH1A1</strong> expression improved <b>relapse</b> free survival in young patients.
+ALDH1A1	drug	alcohol	26458734	Three of the GWS loci identified (rs200889048, rs12490016 and rs1630623) were not previously reported by GWAS of BMI in the general population, and two of them raise interesting hypotheses: rs12490016 a regulatory variant located within LINC00880, where there are other GWAS identified variants associated with birth size, adiposity in newborns and bulimia symptoms, which also interact with social stress in relation to birth size; rs1630623 a regulatory variant related to <strong>ALDH1A1</strong>, a gene involved in <b>alcohol</b> metabolism and adipocyte plasticity.
+ALDH1A1	drug	alcohol	26430123	Moreover, GABA co release is modulated by <b>ethanol</b> (EtOH) at concentrations seen in blood <b>alcohol</b> after binge drinking, and diminished <strong>ALDH1a1</strong> leads to enhanced <b>alcohol</b> consumption and preference.
+ALDH1A1	addiction	intoxication	26430123	Moreover, GABA co release is modulated by ethanol (EtOH) at concentrations seen in blood alcohol after <b>binge</b> drinking, and diminished <strong>ALDH1a1</strong> leads to enhanced alcohol consumption and preference.
+ALDH1A1	drug	alcohol	25270064	We assessed ancestry admixture and tested for associations between <b>alcohol</b> related phenotypes in the genomic regions around the ADH1 7 and ALDH2 and <strong>ALDH1A1</strong> genes.
+ALDH1A1	drug	alcohol	22591209	Association of the <strong>ALDH1A1</strong>*2 promoter polymorphism with <b>alcohol</b> phenotypes in young adults with or without ALDH2*2.
+ALDH1A1	drug	alcohol	22591209	Prior studies suggest a possible association of a promoter polymorphism in the <strong>ALDH1A1</strong> gene (<strong>ALDH1A1</strong>*2) with <b>alcohol</b> use or dependence.
+ALDH1A1	addiction	dependence	22591209	Prior studies suggest a possible association of a promoter polymorphism in the <strong>ALDH1A1</strong> gene (<strong>ALDH1A1</strong>*2) with alcohol use or <b>dependence</b>.
+ALDH1A1	drug	alcohol	22577853	Nine hundred fifty single nucleotide polymorphisms (SNPs) spanning 14 genes (ACN9, ACSS1, ACSS2, <strong>ALDH1A1</strong>, CAT, CYP2E1, GOT1, GOT2, MDH1, MDH2, SLC25A10, SLC25A11, SLC25A12, SLC25A13) were genotyped in 352 young adults who participated in an <b>alcohol</b> challenge study.
+ALDH1A1	drug	alcohol	22577853	We also observed suggestive patterns of association with variants in <strong>ALDH1A1</strong> and on chromosome 17 near SLC25A11 for aspects of blood and breath <b>alcohol</b> metabolism.
+ALDH1A1	drug	alcohol	21083667	The systematic evaluation of <b>alcohol</b> metabolizing genes in four non East Asian populations has shown only modest associations with AD, largely for <strong>ALDH1A1</strong> and ADH4.
+ALDH1A1	drug	alcohol	19129088	The role of aldehyde dehydrogenase 1 (<strong>ALDH1A1</strong>) polymorphisms in harmful <b>alcohol</b> consumption in a Finnish population.
+ALDH1A1	drug	alcohol	19129088	Liver cystolic aldehyde dehydrogenase 1 (<strong>ALDH1A1</strong>) has been previously associated with both <b>alcohol</b> dependence and <b>alcohol</b> consumption behaviour, and has been implicated in <b>alcohol</b> induced flushing and <b>alcohol</b> sensitivity in Caucasians.
+ALDH1A1	addiction	dependence	19129088	Liver cystolic aldehyde dehydrogenase 1 (<strong>ALDH1A1</strong>) has been previously associated with both alcohol <b>dependence</b> and alcohol consumption behaviour, and has been implicated in alcohol induced flushing and alcohol sensitivity in Caucasians.
+ALDH1A1	drug	alcohol	19129088	The present study tested for association between <strong>ALDH1A1</strong> and <b>alcohol</b> consumption behaviour and susceptibility to problem drinking or <b>alcohol</b> dependence in Finnish cohorts of unrelated male subjects recruited from <b>alcoholism</b> clinical treatment facilities (n = 104) and from the general population (n = 201).
+ALDH1A1	addiction	dependence	19129088	The present study tested for association between <strong>ALDH1A1</strong> and alcohol consumption behaviour and susceptibility to problem drinking or alcohol <b>dependence</b> in Finnish cohorts of unrelated male subjects recruited from alcoholism clinical treatment facilities (n = 104) and from the general population (n = 201).
+ALDH1A1	drug	alcohol	19129088	All participants completed the <b>Alcohol</b> Use Disorder Identification Test (AUDIT) and were genotyped for eight single nucleotide polymorphisms (SNPs) within or flanking <strong>ALDH1A1</strong> .
+ALDH1A1	drug	alcohol	19129088	This study provides further evidence for a role for <strong>ALDH1A1</strong> in <b>alcohol</b> consumption behaviour, including problem drinking and possibly <b>alcohol</b> dependence, in our Finnish population.
+ALDH1A1	addiction	dependence	19129088	This study provides further evidence for a role for <strong>ALDH1A1</strong> in alcohol consumption behaviour, including problem drinking and possibly alcohol <b>dependence</b>, in our Finnish population.
+ALDH1A1	drug	alcohol	17718398	<strong>ALDH1A1</strong>*1/*2) was found to be associated with an increase in <b>alcohol</b> dependence in Indo Trinidadians.
+ALDH1A1	addiction	dependence	17718398	<strong>ALDH1A1</strong>*1/*2) was found to be associated with an increase in alcohol <b>dependence</b> in Indo Trinidadians.
+ALDH1A1	drug	alcohol	17673211	This study was aimed at investigating whether cytosolic <strong>ALDH1</strong>, with a relatively low Km value (11 18 microM) for acetaldehyde, could be also inhibited in <b>ethanol</b> exposed rats.
+ALDH1A1	drug	alcohol	17673211	Chronic or binge <b>ethanol</b> exposure significantly decreased <strong>ALDH1</strong> activity, which was restored by addition of dithiothreitol.
+ALDH1A1	addiction	intoxication	17673211	Chronic or <b>binge</b> ethanol exposure significantly decreased <strong>ALDH1</strong> activity, which was restored by addition of dithiothreitol.
+ALDH1A1	drug	alcohol	17673211	Immunoblot analysis with the anti S nitroso Cys antibody showed one immunoreactive band in the immunoprecipitated <strong>ALDH1</strong> only from <b>ethanol</b> exposed rats, but not from pair fed controls, suggesting S nitrosylation of <strong>ALDH1</strong>.
+ALDH1A1	drug	alcohol	17673211	Therefore inactivation of <strong>ALDH1</strong> via S nitrosylation can result in accumulation of acetaldehyde upon <b>ethanol</b> exposure.
+ALDH1A1	drug	alcohol	17286337	Association of <strong>ALDH1</strong> promoter polymorphisms with <b>alcohol</b> related phenotypes in Trinidad and Tobago.
+ALDH1A1	drug	alcohol	17286337	The present study sought to determine whether an association exists between <strong>ALDH1A1</strong> genotypes, <b>alcohol</b> dependence, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ALDH1A1	addiction	dependence	17286337	The present study sought to determine whether an association exists between <strong>ALDH1A1</strong> genotypes, alcohol <b>dependence</b>, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT).
+ALDH1A1	drug	alcohol	17286337	Twenty four participants (10%) possessed the <strong>ALDH1A1</strong>*1/*2 genotype (frequency = .05), 4 were Afro TT (2 <b>alcohol</b> dependents, 2 controls), and 20 were Indo TT (18 <b>alcohol</b> dependents, 2 controls).
+ALDH1A1	drug	alcohol	17286337	Two participants (1 Indo TT <b>alcohol</b> dependent, 1 Afro TT <b>alcohol</b> dependent) had the <strong>ALDH1A1</strong>*2/*2 genotype.
+ALDH1A1	drug	alcohol	17286337	Indo TT participants with at least one <strong>ALDH1A1</strong>*2 allele were more likely to have a lifetime diagnosis of Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, <b>alcohol</b> dependence (p < .002).
+ALDH1A1	addiction	dependence	17286337	Indo TT participants with at least one <strong>ALDH1A1</strong>*2 allele were more likely to have a lifetime diagnosis of Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, alcohol <b>dependence</b> (p < .002).
+ALDH1A1	drug	alcohol	17286337	Indo TT participants with <strong>ALDH1A1</strong>*2 also reported significantly higher levels of current <b>alcohol</b> consumption (p < .05).
+ALDH1A1	drug	alcohol	17286337	Results from this study suggest that <strong>ALDH1A1</strong>*2 may be associated with increased risk for the development of <b>alcohol</b> dependence in Indo Trinidadians.
+ALDH1A1	addiction	dependence	17286337	Results from this study suggest that <strong>ALDH1A1</strong>*2 may be associated with increased risk for the development of alcohol <b>dependence</b> in Indo Trinidadians.
+ALDH1A1	drug	alcohol	15967764	Aldehyde dehydrogenase 1 (<strong>ALDH1</strong>) has been advocated as a marker of <b>alcohol</b> intake.
+ALDH1A1	drug	alcohol	15967764	The absence or low levels of <strong>ALDH1</strong> may be associated with <b>alcohol</b> induced flushing or other reactions to <b>alcohol</b> in Europeans and therefore, with reduced <b>alcohol</b> use.
+ALDH1A1	drug	alcohol	15967764	This study tested whether variation in erythrocyte <strong>ALDH1</strong> activity was associated with <b>alcohol</b> use, <b>alcohol</b> dependence or reactions to <b>alcohol</b> in unselected subjects of European descent, and whether variation in <strong>ALDH1</strong> activity was subject to genetic influences.
+ALDH1A1	addiction	dependence	15967764	This study tested whether variation in erythrocyte <strong>ALDH1</strong> activity was associated with alcohol use, alcohol <b>dependence</b> or reactions to alcohol in unselected subjects of European descent, and whether variation in <strong>ALDH1</strong> activity was subject to genetic influences.
+ALDH1A1	drug	alcohol	15597079	Association of <strong>ALDH1</strong> promoter polymorphisms with <b>alcohol</b> related phenotypes in southwest California Indians.
+ALDH1A1	drug	alcohol	15597079	Individuals with an <strong>ALDH1A1</strong>*2 allele had lower rates of <b>alcohol</b> dependence and regular tobacco use than those without this allele.
+ALDH1A1	drug	nicotine	15597079	Individuals with an <strong>ALDH1A1</strong>*2 allele had lower rates of alcohol dependence and regular <b>tobacco</b> use than those without this allele.
+ALDH1A1	addiction	dependence	15597079	Individuals with an <strong>ALDH1A1</strong>*2 allele had lower rates of alcohol <b>dependence</b> and regular tobacco use than those without this allele.
+ALDH1A1	drug	alcohol	15597079	Individuals with <strong>ALDH1A1</strong>*2 also reported a significantly lower maximum number of drinks ever consumed in a 24 hr period, reported drinking fewer drinks per occasion when they first started drinking regularly, and reported lower expectations of <b>alcohol</b>'s effects compared with individuals without this allele.
+ALDH1A1	drug	alcohol	15597079	Results from this study suggest that <strong>ALDH1A1</strong>*2 may be associated with protection from the development of <b>alcohol</b> and other substance use disorders.
+ALDH1A1	drug	alcohol	14506398	Cytosolic aldehyde dehydrogenase, or <strong>ALDH1A1</strong>, functions in <b>ethanol</b> detoxification, metabolism of neurotransmitters, and synthesis of retinoic acid.
+ALDH1A1	drug	alcohol	14506398	Because the promoter region of a gene can influence gene expression, the <strong>ALDH1A1</strong> promoter regions were studied to identify polymorphism, to assess their functional significance, and to determine whether they were associated with a risk for developing <b>alcoholism</b>.
+ALDH1A1	drug	alcohol	14506398	In an African American population, a trend for higher frequencies of the <strong>ALDH1A1</strong>*2 and <strong>ALDH1A1</strong>*3 alleles was observed in a population of <b>alcoholics</b> (p = 0.03 and f = 0.12, respectively) compared with the control population.
+ALDH1A1	drug	alcohol	14506398	Both <strong>ALDH1A1</strong>*2 and <strong>ALDH1A1</strong>*3 produce a trend in an African American population that may be indicative of an association with <b>alcoholism</b>; however, more samples are required to validate this observation.
+ALDH1A1	drug	alcohol	9862807	The relative sizes of the tunnels also suggest why the bulky <b>alcohol</b> aversive drug <b>disulfiram</b> reacts more rapidly with <strong>ALDH1</strong> than ALDH2.
+ALDH1A1	addiction	aversion	9862807	The relative sizes of the tunnels also suggest why the bulky alcohol <b>aversive</b> drug disulfiram reacts more rapidly with <strong>ALDH1</strong> than ALDH2.
+ALDH1A1	drug	alcohol	3189338	Genotypes of <b>alcohol</b> metabolizing enzymes in Japanese with <b>alcohol</b> liver diseases: a strong association of the usual Caucasian type aldehyde dehydrogenase gene (<strong>ALDH1</strong>(2)) with the disease.
+ALDH1A1	drug	alcohol	3189338	The results indicate that Japanese with the atypical ALDH2(2) allele are at a much lower risk in developing the <b>alcoholic</b> liver diseases than are those with homozygous, usual (Caucasian type) <strong>ALDH1</strong>(2)/<strong>ALDH1</strong>(2), presumably owing to their sensitivity to <b>alcohol</b> intoxication.
+ALDH1A1	addiction	intoxication	3189338	The results indicate that Japanese with the atypical ALDH2(2) allele are at a much lower risk in developing the alcoholic liver diseases than are those with homozygous, usual (Caucasian type) <strong>ALDH1</strong>(2)/<strong>ALDH1</strong>(2), presumably owing to their sensitivity to alcohol <b>intoxication</b>.
+PRKCA	drug	cannabinoid	29364174	Following MIA administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (Cnr1, Cnr2, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and TRPV1 sensitizing kinases (Mapk3, Mapk14, Prkcg, and <strong>Prkaca</strong>).
+PRKCA	drug	cocaine	21210085	Our results show that the combination of repeated exposure to <b>cocaine</b> and acute stress significantly enhances nELAV expression and phosphorylation in the hippocampus with a concomitant increase of GAP43 expression (a specific nELAV target), an effect that seems to involve, upstream, <strong>protein kinase C alpha</strong> (PKCα).
+PRKCA	drug	opioid	19719778	Native MORs are differentially desensitized through separate, agonist dependent signalling pathways; desensitization of the <b>morphine</b> occupied receptor occurs via a <strong>protein kinase C alpha</strong> dependent pathway while [D Ala(2), N MePhe(4), Gly ol]enkephalin mediated desensitization is via a G protein receptor kinase subtype 2 dependent mechanism.
+PRKCA	drug	opioid	16202991	The present study was designed to investigate the possible changes of protein kinase A (PKA) and different isoforms of protein kinase C (PKC): <strong>PKC alpha</strong>, PKC delta and PKC zeta after <b>naloxone</b> induced <b>morphine</b> withdrawal in the heart.
+PRKCA	addiction	withdrawal	16202991	The present study was designed to investigate the possible changes of protein kinase A (PKA) and different isoforms of protein kinase C (PKC): <strong>PKC alpha</strong>, PKC delta and PKC zeta after naloxone induced morphine <b>withdrawal</b> in the heart.
+PRKCA	drug	opioid	16202991	By contrast, <b>morphine</b> withdrawal induced down regulation of <strong>PKC alpha</strong>.
+PRKCA	addiction	withdrawal	16202991	By contrast, morphine <b>withdrawal</b> induced down regulation of <strong>PKC alpha</strong>.
+PRKCA	drug	opioid	16190878	Role of <strong>PKC alpha</strong>,gamma isoforms in regulation of c Fos and TH expression after <b>naloxone</b> induced <b>morphine</b> withdrawal in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups.
+PRKCA	addiction	withdrawal	16190878	Role of <strong>PKC alpha</strong>,gamma isoforms in regulation of c Fos and TH expression after naloxone induced morphine <b>withdrawal</b> in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups.
+PRKCA	drug	opioid	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in <strong>PKCalpha</strong> and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate <b>morphine</b> withdrawal induced c Fos expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+PRKCA	addiction	withdrawal	16190878	The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in <strong>PKCalpha</strong> and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate morphine <b>withdrawal</b> induced c Fos expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
+PRKCA	drug	opioid	16190878	The protein levels of <strong>PKCalpha</strong> and gamma were significantly down regulated in the PVN and NTS/VLM from the <b>morphine</b> withdrawn rats.
+PRKCA	drug	opioid	15830100	[Different roles of the spinal <strong>protein kinase C alpha</strong> and gamma in <b>morphine</b> dependence and <b>naloxone</b> precipitated withdrawal].
+PRKCA	addiction	dependence	15830100	[Different roles of the spinal <strong>protein kinase C alpha</strong> and gamma in morphine <b>dependence</b> and naloxone precipitated withdrawal].
+PRKCA	addiction	withdrawal	15830100	[Different roles of the spinal <strong>protein kinase C alpha</strong> and gamma in morphine dependence and naloxone precipitated <b>withdrawal</b>].
+PRKCA	drug	opioid	15830100	One hour after <b>naloxone</b> precipitated withdrawal, Fos protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of cytosol and membrane fraction of <strong>PKC alpha</strong> and gamma in the rat spinal cord.
+PRKCA	addiction	withdrawal	15830100	One hour after naloxone precipitated <b>withdrawal</b>, Fos protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of cytosol and membrane fraction of <strong>PKC alpha</strong> and gamma in the rat spinal cord.
+PRKCA	drug	opioid	15830100	The expression of cytosol and membrane fraction of <strong>PKC alpha</strong> was significantly increased in the spinal cord of rats with <b>morphine</b> dependence.
+PRKCA	addiction	dependence	15830100	The expression of cytosol and membrane fraction of <strong>PKC alpha</strong> was significantly increased in the spinal cord of rats with morphine <b>dependence</b>.
+PRKCA	drug	opioid	15830100	<b>Naloxone</b> precipitated withdrawal induced <strong>PKC alpha</strong> translocation from cytosol to membrane fraction, which was prevented by intrathecal administration of CHE.
+PRKCA	addiction	withdrawal	15830100	Naloxone precipitated <b>withdrawal</b> induced <strong>PKC alpha</strong> translocation from cytosol to membrane fraction, which was prevented by intrathecal administration of CHE.
+PRKCA	drug	opioid	15830100	It is suggested that up regulation and translocation of PKC in the spinal cord contribute to <b>morphine</b> dependence and <b>naloxone</b> precipitated withdrawal in rats and that <strong>PKC alpha</strong> and gamma play different roles in the above mentioned effect.
+PRKCA	addiction	dependence	15830100	It is suggested that up regulation and translocation of PKC in the spinal cord contribute to morphine <b>dependence</b> and naloxone precipitated withdrawal in rats and that <strong>PKC alpha</strong> and gamma play different roles in the above mentioned effect.
+PRKCA	addiction	withdrawal	15830100	It is suggested that up regulation and translocation of PKC in the spinal cord contribute to morphine dependence and naloxone precipitated <b>withdrawal</b> in rats and that <strong>PKC alpha</strong> and gamma play different roles in the above mentioned effect.
+PRKCA	drug	alcohol	11427306	The protein level of membrane bound <strong>PKCalpha</strong> and PKCgamma isoforms, which are defined as Ca2+ dependent PKC isoforms (cPKC), in the limbic forebrain during chronic <b>ethanol</b> treatment was significantly increased, whereas the levels of both were significantly decreased in the frontal cortex.
+PRKCA	drug	opioid	10385232	Parallel modulation of receptor for activated C kinase 1 and <strong>protein kinase C alpha</strong> and beta isoforms in brains of <b>morphine</b> treated rats.
+PRKCA	drug	opioid	10385232	Because opiate drugs modulate the levels of brain PKC (Ventayol et al., 1997), the aim of this study was to assess in parallel the effects of <b>morphine</b> on RACK1 and <strong>PKC alpha</strong> and beta isozymes densities in rat brain frontal cortex by immunoblot assays.
+PRKCA	drug	opioid	10385232	Acute <b>morphine</b> (30 mg kg( 1), i.p., 2 h) induced significant increases in the densities of RACK1 (33%), <strong>PKC alpha</strong> (35%) and PKC beta (23%).
+PRKCA	drug	opioid	10385232	In contrast, chronic <b>morphine</b> (10 100 mg kg( 1), i.p., 5 days) induced a decrease in RACK1 levels (22%), paralleled by decreases in the levels of <strong>PKC alpha</strong> (16%) and PKC beta (16%).
+PRKCA	drug	opioid	10385232	Spontaneous (48 h) and <b>naloxone</b> (2 mg kg( 1), i.p., 2 h) precipitated <b>morphine</b> withdrawal after chronic <b>morphine</b> induced marked up regulations in the levels of RACK1 (38 41%), <strong>PKC alpha</strong> (51 52%) and PKC beta (48 62%).
+PRKCA	addiction	withdrawal	10385232	Spontaneous (48 h) and naloxone (2 mg kg( 1), i.p., 2 h) precipitated morphine <b>withdrawal</b> after chronic morphine induced marked up regulations in the levels of RACK1 (38 41%), <strong>PKC alpha</strong> (51 52%) and PKC beta (48 62%).
+PRKCA	drug	opioid	10385232	These data indicate that RACK1 is involved in the short  and long term effects of <b>morphine</b> and in opiate withdrawal, and that RACK1 modulation by <b>morphine</b> or its withdrawal is parallel to those of <strong>PKC alpha</strong> and beta isozymes.
+PRKCA	addiction	withdrawal	10385232	These data indicate that RACK1 is involved in the short  and long term effects of morphine and in opiate <b>withdrawal</b>, and that RACK1 modulation by morphine or its <b>withdrawal</b> is parallel to those of <strong>PKC alpha</strong> and beta isozymes.
+PRKCA	drug	opioid	9153634	Regulation of immunolabelled mu <b>opioid</b> receptors and <strong>protein kinase C alpha</strong> and zeta isoforms in the frontal cortex of human opiate addicts.
+PRKCA	drug	opioid	9153634	The sustained down regulation of <strong>PKC alpha</strong> in the brain of opiate addicts would allow the up regulation of G alpha(i1/2) proteins aimed at compensating the postulated desensitization of the mu <b>opioid</b> receptor system.
+PRKCA	drug	opioid	9109366	Modulation of immunoreactive <strong>protein kinase C alpha</strong> and beta isoforms and G proteins by acute and chronic treatments with <b>morphine</b> and other opiate drugs in rat brain.
+PRKCA	drug	opioid	9109366	After the chronic treatments, spontaneous (48 h) or <b>naloxone</b> (2 mg/kg) precipitated opiate withdrawal (2 h) resulted in up regulation of PKC alphabeta above control levels (30 38%), and in the case of <b>morphine</b> withdrawal in a concomitant marked increase in the expression of <strong>PKC alpha</strong> mRNA levels (2.3 fold).
+PRKCA	addiction	withdrawal	9109366	After the chronic treatments, spontaneous (48 h) or naloxone (2 mg/kg) precipitated opiate <b>withdrawal</b> (2 h) resulted in up regulation of PKC alphabeta above control levels (30 38%), and in the case of morphine <b>withdrawal</b> in a concomitant marked increase in the expression of <strong>PKC alpha</strong> mRNA levels (2.3 fold).
+PRKCA	drug	opioid	8813382	Moreover, the longitudinal muscle myenteric plexus content of <strong>PKC alpha</strong> and PKC beta is substantially elevated following chronic <b>morphine</b> treatment.
+PRKCA	drug	opioid	7798919	Loss of <strong>protein kinase C alpha</strong> beta in brain of <b>heroin</b> addicts and <b>morphine</b> dependent rats.
+PRKCA	drug	opioid	7798919	In the frontal cortex, a marked decrease (53%, p < 0.05) in the immunoreactivity of <strong>PKC alpha</strong> beta was found in <b>heroin</b> addicts compared with matched controls.
+PRKCA	drug	opioid	7798919	The loss of <strong>PKC alpha</strong> beta in the brain of human addicts paralleled that observed in the frontal cortex of rats after chronic treatment with <b>morphine</b> (10 100 mg/kg i.p.
+PRKCA	drug	opioid	7798919	However, in <b>morphine</b> dependent rats, <b>naloxone</b> precipitated withdrawal induced a rapid and strong behavioral reaction with a concomitant up regulation of <strong>PKC alpha</strong> beta immunoreactivity to control values.
+PRKCA	addiction	withdrawal	7798919	However, in morphine dependent rats, naloxone precipitated <b>withdrawal</b> induced a rapid and strong behavioral reaction with a concomitant up regulation of <strong>PKC alpha</strong> beta immunoreactivity to control values.
+PRKCA	drug	opioid	7798919	These results indicated that the decrease of brain <strong>PKC alpha</strong> beta induced by <b>heroin</b>/<b>morphine</b> is a mu <b>opioid</b> receptor mediated effect.
+MBP	drug	alcohol	32070690	Then immunohistochemistry, western blot, quantitative real time PCR and transmission electron microscopy were performed to determine the effects of quetiapine on alterations of brain white matter markers (myelin basic protein, <strong>MBP</strong>; proteolipid protein, PLP) and morphology caused by chronic <b>ethanol</b> exposure.
+MBP	drug	alcohol	32070690	Then immunohistochemistry, western blot, quantitative real time PCR and transmission electron microscopy were performed to determine the effects of quetiapine on alterations of brain white matter markers (<strong>myelin basic protein</strong>, <strong>MBP</strong>; proteolipid protein, PLP) and morphology caused by chronic <b>ethanol</b> exposure.
+MBP	drug	alcohol	32070690	Chronic <b>ethanol</b> exposure reduced Y type electric maze scores and the protein/mRNA expression levels of <strong>MBP</strong> and PLP in the prefrontal cortex and hippocampus, and these effects were reversed by quetiapine treatment.
+MBP	drug	cocaine	31550894	Several proteoform changes occurred in the ventral tegmental area after combined <b>cocaine</b> and E2 treatments, with the most numerous proteoform alterations on <strong>myelin basic protein</strong>, indicating possible changes in white matter structure.
+MBP	drug	cocaine	30411050	Following a CPP test and final exposure to either a <b>cocaine</b>  or saline associated context, peptides were measured in brain tissue extracts using label free matrix assisted laser desorption/ionization mass spectrometry (MS) and stable isotopic labeling with liquid chromatography and electrospray ionization MS. CPP in mice was significantly reduced with running, which correlated to decreased <strong>myelin basic protein</strong> derivatives in the dentate gyrus extracts, possibly reflecting increased unmyelinated granule neuron density.
+MBP	addiction	reward	30411050	Following a <b>CPP</b> test and final exposure to either a cocaine  or saline associated context, peptides were measured in brain tissue extracts using label free matrix assisted laser desorption/ionization mass spectrometry (MS) and stable isotopic labeling with liquid chromatography and electrospray ionization MS. <b>CPP</b> in mice was significantly reduced with running, which correlated to decreased <strong>myelin basic protein</strong> derivatives in the dentate gyrus extracts, possibly reflecting increased unmyelinated granule neuron density.
+MBP	addiction	withdrawal	30306515	However, intrafascicular lidocaine brought about macrophage migration into the damaged fascicle, Schwann cell proliferation, increased intensity of <strong>myelin basic protein</strong>, and shorten <b>withdrawal</b> time to mechanical stimuli.
+MBP	drug	alcohol	28669901	Behavioural effects were associated with an upregulation of pro inflammatory signalling (Toll like receptor 4, nuclear factor kappa B p65, NOD like receptor protein 3, caspase 1, and interleukin 1β), gliosis, neuronal cell death and a reduction in several structural myelin proteins (myelin associated glycoprotein, <strong>myelin basic protein</strong>, myelin proteolipid protein and myelin regulatory factor) in both the prefrontal cortex and hippocampus of adult mice exposed to <b>alcohol</b>.
+MBP	drug	alcohol	25655461	Gene level disturbances in cellular and molecular networks impacted by <b>alcohol</b> and <b>alcoholism</b> pathology include transketolase (TKT), transferrin (TF), and myelin (e.g., <strong>MBP</strong>, MOBP, and MOG).
+MBP	addiction	intoxication	25355229	Degraded <strong>myelin basic protein</strong> in the gray matter medial to the CCFM of <b>binge</b> rats indicated myelin was damaged on axons in the mPFC.
+MBP	addiction	sensitization	24814827	Moreover, in the subjects with allergic <b>sensitization</b>, the expression levels of <strong>MBP</strong> and EPO mRNAs were significantly higher in those with airway hyperresponsiveness (13 subjects) than in those without airway hyperresponsiveness (32 subjects) (P = 0.004 and 0.010, respectively).
+MBP	drug	cocaine	24529965	Both <strong>MBP</strong> and PLP immunoreactivities in white matter at the level of the precommissural striatum were significantly lower in tissue from monkeys self administering <b>cocaine</b> as compared to controls.
+MBP	drug	alcohol	23084028	After oral administration of <b>alcohol</b> and then hemorrhage, the recovery of mean blood pressure (<strong>MBP</strong>); increase in plasma level of norepinephrine, epinephrine, and vasopressin; and survival interval decreased in a dose dependent manner as the blood <b>alcohol</b> level increased.
+MBP	drug	opioid	30625688	So we investigated the effect of <b>fentanyl</b> on tourniquet induced changes of mean arterial blood pressure (<strong>MBP</strong>), heart rate (HR), and cardiac index (CI).
+MBP	drug	opioid	30625688	At 60 min, <strong>MBP</strong> was lower in the <b>fentanyl</b> than the control group.
+MBP	drug	opioid	18381654	Analysis of their pups at different postnatal ages indicated that exposure to 0.3 mg/kg/day <b>buprenorphine</b> caused an accelerated and significant increase in the brain expression of all myelin basic protein (<strong>MBP</strong>) splicing isoforms.
+MBP	drug	opioid	18381654	Analysis of their pups at different postnatal ages indicated that exposure to 0.3 mg/kg/day <b>buprenorphine</b> caused an accelerated and significant increase in the brain expression of all <strong>myelin basic protein</strong> (<strong>MBP</strong>) splicing isoforms.
+MBP	drug	cocaine	15849025	A striking exception is a group of myelin related genes, consisting of multiple transcripts representing myelin basic protein (<strong>MBP</strong>), proteolipid protein (PLP) and myelin associated oligodendrocyte basic protein (MOBP), which as a group are substantially decreased in <b>cocaine</b> abusers compared to controls.
+MBP	drug	cocaine	15849025	A striking exception is a group of myelin related genes, consisting of multiple transcripts representing <strong>myelin basic protein</strong> (<strong>MBP</strong>), proteolipid protein (PLP) and myelin associated oligodendrocyte basic protein (MOBP), which as a group are substantially decreased in <b>cocaine</b> abusers compared to controls.
+MBP	drug	opioid	11749769	<b>Morphine</b> withdrawal syndrome in rats was precipitated by iv <b>naloxone</b> following daily injection of increasing dose of <b>morphine</b> for 2 weeks, the changes in mean arterial blood pressure (<strong>MBP</strong>) caused by acetylcholine (ACh) were recorded.
+MBP	addiction	withdrawal	11749769	Morphine <b>withdrawal</b> syndrome in rats was precipitated by iv naloxone following daily injection of increasing dose of morphine for 2 weeks, the changes in mean arterial blood pressure (<strong>MBP</strong>) caused by acetylcholine (ACh) were recorded.
+MBP	addiction	reward	11452859	Heart rate (HR), mean arterial blood pressure (<strong>MBP</strong>), ICP, <b>CPP</b> and respiratory frequency (f) were registered before and in the 1st, 3rd, 8th, and 15th minute after T. Analgetic effect was evaluated in 22 conscious pts by comparing the pain intensity before and 30 minutes after T using a five point verbal response scale.
+MBP	addiction	reward	11452859	There were no statistically significant changes in HR, <strong>MBP</strong>, ICP, and <b>CPP</b> after T in any particular group, nor were there changes in ICP in subgroups with normal and elevated ICP.
+MBP	addiction	addiction	11268408	They are relatively resistant to CIA, AIA, <strong>MBP</strong> EAE, SAG EAU, and IRBP EAU, and they are relatively resistant to <b>addiction</b>.
+MBP	drug	benzodiazepine	10456288	Pretreatment with <b>diazepam</b> prevented the convulsions, assessed by electroencephalogram (EEG) recording, but modified neither the magnitude nor the kinetics of the pressor and tachycardic effects of soman (delta <strong>MBP</strong> = 74 +/  2 and 73 +/  5 mmHg, delta HR = 69 +/  10 and 79 +/  7 bpm, maximum <strong>MBP</strong> = 186 +/  3 and 182 +/  6 mmHg, maximum HR = 545 +/  9 and 522 +/  16 bpm in solvent  (n = 8) and <b>diazepam</b>  (n = 8) pre treated rats, respectively).
+MBP	drug	cocaine	9676719	Initially, the mean blood pressure (<strong>MBP</strong>) increased followed by a precipitate decrease at a mean dose of 2.03 +/  0.5 mg/kg of <b>cocaine</b>.
+MBP	addiction	aversion	2287487	Both <b>aversive</b> brain stimulation or foot shocks applied at threshold intensities caused running or jumps concomitant with increases in mean arterial blood pressure (<strong>MBP</strong>) and heart rate (HR).
+IL13	drug	alcohol	31510019	<b>Ethanol</b> Induction of Innate Immune Signals Across BV2 Microglia and SH SY5Y Neuroblastoma Involves Induction of IL 4 and <strong>IL 13</strong>.
+IL13	drug	alcohol	31510019	In contrast, co culture resulted in <b>ethanol</b> upregulation of cytokines IL 4 and <strong>IL 13</strong> in BV2 and corresponding receptors, that is, IL 4 and <strong>IL 13</strong> receptors, in SH SY5Y, suggesting induction of a novel signaling pathway.
+IL13	drug	alcohol	29733875	We measured the acute concentrations and dynamics of lipoxins LxA4 and LxB4 and the interleukins IL 4, IL 5, IL 9, IL 10, and <strong>IL 13</strong> in the serum of patients treated with methyl <b>alcohol</b> poisoning and the follow up concentrations in survivors two years after discharge from the hospital.
+IL13	drug	opioid	27862172	Electroencephalographic spectral power as well as amplitudes and latencies of mismatch negativity (MMN), P300, and <strong>P600</strong> components were evaluated among 19 male <b>heroin</b> addicts and 19 healthy nonsmoker subjects using a paradigm consisting of three subparadigms, namely (1) digit span Wechsler test, (2) auditory oddball, and (3) visual cue reactivity oddball paradigms.
+IL13	addiction	intoxication	27455577	It was established in experiments on noninbred albino rats that the acute <b>intoxication</b> with methanol (1.0 LD50) decreased cellular and humoral immune responses, Th2 lymphocyte activity (to a greater extent as compared to the function of Th1 cells), reduced the blood concentration of immunoregulatory (IFN g, IL 2, IL 4) and proinflammatory (TNF, IL 1b, IL 6) cytokines on the average by 36.5% (p < 0.05), and did not affect the content of anti inflammatory cytokines (IL 10, <strong>IL 13</strong>).
+IL13	drug	opioid	26748947	Chronic <b>heroin</b> addiction causes increased β and α2 power activity, latency of P300 and <strong>P600</strong>, and diminished P300 and <strong>P600</strong> amplitude.
+IL13	addiction	addiction	26748947	Chronic heroin <b>addiction</b> causes increased β and α2 power activity, latency of P300 and <strong>P600</strong>, and diminished P300 and <strong>P600</strong> amplitude.
+IL13	drug	nicotine	22187950	Maternal cytokines (<strong>IL 13</strong>, IL 17E and IFN γ) and maternal <b>smoking</b>/exposure to <b>tobacco</b> smoke during pregnancy were also associated with decreased cord blood Treg numbers (adj.
+IL13	addiction	withdrawal	21802933	Sputum was also analysed for mRNA levels of haemoxygenase 1, tumour necrosis factor α, RANTES, interleukin 5(IL 5), IL 10, IL 12, <strong>IL 13</strong>, transforming growth factor β, and interferon γ. Cox regression analyses were performed using time to exacerbation as outcome variable to identify significant hazards for a COPD exacerbation after ICS <b>withdrawal</b>.
+IL13	drug	nicotine	18410779	To determine whether infants exposed to environmental <b>tobacco</b> smoke (ETS) having the interleukin 4 (IL 4) or interleukin 13 (<strong>IL 13</strong>) gene polymorphisms were at increased risk of wheezing.
+IL13	drug	nicotine	18410779	To determine whether infants exposed to environmental <b>tobacco</b> smoke (ETS) having the interleukin 4 (IL 4) or <strong>interleukin 13</strong> (<strong>IL 13</strong>) gene polymorphisms were at increased risk of wheezing.
+IL13	addiction	sensitization	15007352	These findings not only suggested that variants in the IL4, <strong>IL13</strong>, and IL4RA genes play an important role in controlling specific IgE response but also strengthened our understanding of gene gene and gene environment interaction on the development of specific <b>sensitization</b> in this study population.
+IL13	drug	cannabinoid	12668119	<b>Cannabinol</b> (CBN) or Delta(9) <b>tetrahydrocannabinol</b> (Delta(9) <b>THC</b>; 50 mg/kg, ip), administered daily for 3 consecutive days before sensitization and then before challenge, significantly attenuated the elevation of IL 2, IL 4, IL 5, and <strong>IL 13</strong> steady state mRNA expression elicited by Ova challenge in the lungs.
+IL13	addiction	sensitization	12668119	Cannabinol (CBN) or Delta(9) tetrahydrocannabinol (Delta(9) THC; 50 mg/kg, ip), administered daily for 3 consecutive days before <b>sensitization</b> and then before challenge, significantly attenuated the elevation of IL 2, IL 4, IL 5, and <strong>IL 13</strong> steady state mRNA expression elicited by Ova challenge in the lungs.
+IL13	drug	alcohol	11505051	No difference was observed regarding IL 10, IL 12, and <strong>IL 13</strong> production between <b>alcoholics</b> and controls.
+IL13	drug	opioid	11409757	Abnormal <strong>P600</strong> in <b>heroin</b> addicts with prolonged abstinence elicited during a working memory test.
+IL13	drug	opioid	11409757	The present study is focused on <strong>P600</strong> elicited during a WM test in twenty <b>heroin</b> addicts with prolonged abstinence compared with an equal number of healthy controls.
+IL13	drug	opioid	11409757	These findings may indicate that abstinent <b>heroin</b> addicts manifest abnormal aspects of second pass parsing processes as are reflected by the <strong>P600</strong> latencies, elicited during a WM test.
+IFI30	drug	opioid	17142651	Magnesium sulphate (100 mg x kg( 1)) was injected <strong>ip 30</strong> min prior to the first sc <b>fentanyl</b> injection.
+IFI30	drug	amphetamine	15985714	Moreover, <b>AMPH</b> injected 8 days after the last dose of repeated <b>AMPH</b> administration did not change NPY LI up to 72 h. The minimal dose of haloperidol, the strong mixed dopaminergic D2/D1 receptor antagonist, (0.75 mg/kg injected <strong>ip 30</strong> min before each of the multiple <b>AMPH</b> administrations) that was sufficient to completely block stereotypy and hyperlocomotion elicited by multiple <b>AMPH</b> administrations enhanced the <b>AMPH</b> induced decrease in the striatal and accumbens NPY LI.
+IFI30	drug	cannabinoid	11498713	Another group of rats was initially trained to discriminate between 3 mg/kg Delta9 <b>THC</b> and vehicle given <strong>IP 30</strong> min prior to session onset; for anandamide testing, the animals were retrained with 1.8 and 5.6 mg/kg Delta9 <b>THC</b>.
+IFI30	addiction	withdrawal	11063315	Three barrows and three gilts, housed in metabolism crates, were fed 1 ppm [14C]clenbuterol HCl for seven consecutive days in three separate trials; a single barrow and <strong>gilt</strong> from each trial was slaughtered after 0 , 3 , or 7 d preslaughter <b>withdrawal</b> periods.
+IFI30	addiction	withdrawal	2838131	The partial inverse agonist, FG 7142 (5 mg/kg <strong>IP 30</strong> min before test) had no significant effect on the <b>withdrawal</b> anxiety.
+FKBP5	addiction	intoxication	32154593	GR antagonism (with both mifepristone and CORT113176) selectively reduced <b>binge</b> like EtOH intake and BECs in the HDID 1 mice, while inhibition of <strong>FKBP51</strong> did not alter intake or BECs.
+FKBP5	drug	alcohol	31173432	The selective <strong>FKBP51</strong> inhibitor SAFit2 reduces <b>alcohol</b> consumption and reinstatement of conditioned <b>alcohol</b> effects in mice.
+FKBP5	addiction	relapse	31173432	The selective <strong>FKBP51</strong> inhibitor SAFit2 reduces alcohol consumption and <b>reinstatement</b> of conditioned alcohol effects in mice.
+FKBP5	drug	alcohol	31173432	Here we asked whether selective inhibitors of <strong>FKBP51</strong>, exemplified by SAFit2, may serve as a new pharmacological strategy to reduce <b>alcohol</b> consumption and conditioned <b>alcohol</b> effects in a mouse model.
+FKBP5	drug	alcohol	31173432	Altogether, these data may suggest pharmacological inhibition of <strong>FKBP51</strong> as a viable strategy to reduce <b>alcohol</b> seeking and consumption.
+FKBP5	addiction	relapse	31173432	Altogether, these data may suggest pharmacological inhibition of <strong>FKBP51</strong> as a viable strategy to reduce alcohol <b>seeking</b> and consumption.
+FKBP5	drug	cocaine	31029877	Chronic <b>cocaine</b> administration upregulates <strong>FKBP5</strong> in the extended amygdala of male and female rats.
+FKBP5	drug	cocaine	31029877	While <strong>FKBP5</strong> is known to be involved in mood  and stress related disorders, less is known regarding <strong>FKBP5</strong> and <b>cocaine</b> abuse.
+FKBP5	drug	cocaine	31029877	This study investigated the regulation of <strong>FKBP5</strong> expression in the extended amygdala and paraventricular nucleus of the hypothalamus, regions important in the control of stress responses and HPA axis function, following chronic and acute <b>cocaine</b> administration.
+FKBP5	drug	cocaine	31029877	<strong>FKBP5</strong> mRNA levels were significantly elevated as a result of chronic <b>cocaine</b> administration in both males and females in the PVN and BNST 30 min and 24 h after the final injection.
+FKBP5	drug	cocaine	31029877	Following acute <b>cocaine</b>, <strong>FKBP5</strong> gene expression was unaltered except for elevated levels in the BNST of females 24 h later.
+FKBP5	drug	cocaine	31029877	These results demonstrate that <strong>FKBP5</strong> mRNA is regulated by <b>cocaine</b> administration.
+FKBP5	drug	cocaine	31029877	Increased <strong>FKBP5</strong> expression may play a role in the dysregulation of the stress axis following chronic <b>cocaine</b> exposure, contributing to the negative affective symptoms of <b>cocaine</b> withdrawal.
+FKBP5	addiction	withdrawal	31029877	Increased <strong>FKBP5</strong> expression may play a role in the dysregulation of the stress axis following chronic cocaine exposure, contributing to the negative affective symptoms of cocaine <b>withdrawal</b>.
+FKBP5	drug	alcohol	30349266	Positive metacognitions about <b>alcohol</b> mediate the relationship between <strong>FKBP5</strong> variability and problematic drinking in a sample of young women.
+FKBP5	drug	alcohol	30349266	Previous research has shown that polymorphisms in the <strong>FKBP5</strong> gene are related to some psychiatric conditions, including <b>alcohol</b> dependence.
+FKBP5	addiction	dependence	30349266	Previous research has shown that polymorphisms in the <strong>FKBP5</strong> gene are related to some psychiatric conditions, including alcohol <b>dependence</b>.
+FKBP5	drug	alcohol	30349266	This study attempted to identify relationships between <strong>FKBP5</strong> polymorphisms and metacognitions about the positive effects of <b>alcohol</b> use and problematic drinking in a group differing in levels of childhood trauma.
+FKBP5	drug	cannabinoid	28822116	Almost consistently, these studies revealed that polymorphisms in COMT, BDNF, and <strong>FKBP5</strong> genes might interact with early life stress and <b>cannabis</b> abuse or dependence, influencing various outcomes of schizophrenia spectrum disorders and BD.
+FKBP5	addiction	dependence	28822116	Almost consistently, these studies revealed that polymorphisms in COMT, BDNF, and <strong>FKBP5</strong> genes might interact with early life stress and cannabis abuse or <b>dependence</b>, influencing various outcomes of schizophrenia spectrum disorders and BD.
+FKBP5	drug	alcohol	27709495	Evidence for a Link Between <strong>Fkbp5</strong>/<strong>FKBP5</strong>, Early Life Social Relations and <b>Alcohol</b> Drinking in Young Adult Rats and Humans.
+FKBP5	drug	alcohol	27709495	The aim of the present study was to further understand the <strong>Fkbp5</strong>/<strong>FKBP5</strong> related genetic underpinnings underlying the relationship between early life social relations and <b>alcohol</b> drinking.
+FKBP5	drug	alcohol	27709495	The effect of maternal separation and voluntary <b>alcohol</b> drinking on <strong>Fkbp5</strong> expression was investigated in the brain of young adult rats, whereas the interaction effect of the functional <strong>FKBP5</strong> single nucleotide polymorphism rs1360780 genotype and parent child relationship on problematic drinking was examined in young adult humans.
+FKBP5	drug	alcohol	27709495	In rats, <strong>Fkbp5</strong> expression in the nucleus accumbens and ventral tegmental area, core regions of the reward system, was affected in a region dependent manner and in opposite direction by maternal separation and <b>alcohol</b> drinking.
+FKBP5	addiction	reward	27709495	In rats, <strong>Fkbp5</strong> expression in the nucleus accumbens and ventral tegmental area, core regions of the <b>reward</b> system, was affected in a region dependent manner and in opposite direction by maternal separation and alcohol drinking.
+FKBP5	drug	alcohol	27709495	<strong>Fkbp5</strong> expression in the cingulate cortex was affected by the combined effect of maternal separation and <b>alcohol</b> drinking.
+FKBP5	drug	alcohol	27709495	The present findings suggest that <strong>Fkbp5</strong> expression in mesocorticolimbic dopaminergic regions associates with early life stress mediated sensitivity to <b>alcohol</b> drinking and that <strong>FKBP5</strong> genotype interacts with parent child relationship to influence <b>alcohol</b> drinking.
+FKBP5	drug	alcohol	27709495	These findings are the first to point to a role of <strong>FKBP5</strong> in propensity to <b>alcohol</b> misuse and call for studies of the underlying molecular mechanisms to identify potential drug targets.
+FKBP5	drug	alcohol	27527158	The <strong>FKBP5</strong> Gene Affects <b>Alcohol</b> Drinking in Knockout Mice and Is Implicated in <b>Alcohol</b> Drinking in Humans.
+FKBP5	drug	alcohol	27527158	<strong>FKBP5</strong> encodes FK506 binding protein 5, a glucocorticoid receptor (GR) binding protein implicated in various psychiatric disorders and <b>alcohol</b> withdrawal severity.
+FKBP5	addiction	withdrawal	27527158	<strong>FKBP5</strong> encodes FK506 binding protein 5, a glucocorticoid receptor (GR) binding protein implicated in various psychiatric disorders and alcohol <b>withdrawal</b> severity.
+FKBP5	drug	alcohol	27527158	The purpose of this study is to characterize <b>alcohol</b> preference and related phenotypes in <strong>Fkbp5</strong> knockout (KO) mice and to examine the role of <strong>FKBP5</strong> in human <b>alcohol</b> consumption.
+FKBP5	drug	alcohol	27527158	(1) <strong>Fkbp5</strong> KO and wild type (WT) EtOH consumption was tested using a two bottle choice paradigm; (2) The EtOH elimination rate was measured after intraperitoneal (IP) injection of 2.0 g/kg EtOH; (3) Blood <b>alcohol</b> concentration (BAC) was measured after 3 h limited access of <b>alcohol</b>; (4) Brain region expression of <strong>Fkbp5</strong> was identified using LacZ staining; (5) Baseline corticosterone (CORT) was assessed.
+FKBP5	drug	alcohol	27527158	Additionally, two SNPs, rs1360780 (C/T) and rs3800373 (T/G), were selected to study the association of <strong>FKBP5</strong> with <b>alcohol</b> consumption in humans.
+FKBP5	drug	alcohol	27527158	Finally, single nucleotide polymorphisms (SNPs) in <strong>FKBP5</strong> were found to be associated with <b>alcohol</b> drinking in humans.
+FKBP5	drug	alcohol	27527158	These results suggest that the association between <strong>FKBP5</strong> and <b>alcohol</b> consumption is conserved in both mice and humans.
+FKBP5	drug	nicotine	27062383	The Effect of <b>Nicotine</b> on HPA Axis Activity in Females is Modulated by the <strong>FKBP5</strong> Genotype.
+FKBP5	drug	nicotine	27062383	Our results suggest that <b>nicotine</b> is an important confounder in the modulation of HPA axis activity by <strong>FKBP5</strong>.
+FKBP5	drug	nicotine	27062383	In light of these findings, future studies on <strong>FKBP5</strong> should seek to include data on <b>nicotine</b> consumption as a covariate.
+FKBP5	drug	cannabinoid	26535939	Developmental pathways from child maltreatment to adolescent <b>marijuana</b> dependence: Examining moderation by FK506 binding protein 5 gene (<strong>FKBP5</strong>).
+FKBP5	addiction	dependence	26535939	Developmental pathways from child maltreatment to adolescent marijuana <b>dependence</b>: Examining moderation by FK506 binding protein 5 gene (<strong>FKBP5</strong>).
+FKBP5	drug	cannabinoid	26535939	Results indicated that higher levels of child externalizing symptoms significantly mediated the effect of child maltreatment on adolescent <b>marijuana</b> dependence symptoms for individuals with one or two copies of the <strong>FKBP5</strong> CATT haplotype only.
+FKBP5	addiction	dependence	26535939	Results indicated that higher levels of child externalizing symptoms significantly mediated the effect of child maltreatment on adolescent marijuana <b>dependence</b> symptoms for individuals with one or two copies of the <strong>FKBP5</strong> CATT haplotype only.
+FKBP5	drug	cannabinoid	26535939	We did not find support for an internalizing pathway from child maltreatment to adolescent <b>marijuana</b> dependence, nor did we find evidence of moderation of the internalizing pathway by <strong>FKBP5</strong> haplotype variation.
+FKBP5	addiction	dependence	26535939	We did not find support for an internalizing pathway from child maltreatment to adolescent marijuana <b>dependence</b>, nor did we find evidence of moderation of the internalizing pathway by <strong>FKBP5</strong> haplotype variation.
+FKBP5	addiction	withdrawal	26004981	We also showed reduced expression of the GR co chaperone <strong>FKBP51</strong>, that normally keeps the receptor in the cytoplasm, and increased expression of Src1, which cooperates in the activation of GR transcriptional activity, revealing that short <b>withdrawal</b> alters the finely tuned mechanisms regulating GR action.
+FKBP5	drug	nicotine	25532758	<strong>FKBP5</strong> variation is associated with the acute and chronic effects of <b>nicotine</b>.
+FKBP5	drug	nicotine	25532758	Here, we systematically examine the contribution of a stress response gene, <strong>FKBP5</strong>, to the acute and chronic behavioral effects of <b>nicotine</b> in <b>smokers</b>.
+FKBP5	drug	nicotine	25532758	<strong>FKBP5</strong> rs3800373 genotype was analyzed for association to several outcomes, including <b>nicotine</b> withdrawal and the acute subjective, heart rate (HR), blood pressure and plasma cortisol responses to IV <b>nicotine</b>.
+FKBP5	addiction	withdrawal	25532758	<strong>FKBP5</strong> rs3800373 genotype was analyzed for association to several outcomes, including nicotine <b>withdrawal</b> and the acute subjective, heart rate (HR), blood pressure and plasma cortisol responses to IV nicotine.
+FKBP5	drug	nicotine	25532758	Low <strong>FKBP5</strong> mRNA expression was associated lower cortisol levels, lower subjective ratings of negative drug effects and a blunted HR response to <b>nicotine</b>.
+FKBP5	drug	nicotine	25532758	Stress hormone regulation via <strong>FKBP5</strong> warrants further investigation as a potential contributor to the effects of <b>nicotine</b> withdrawal, which occurs commonly, and has an important role in the maintenance of <b>smoking</b> behavior and relapse following a quit attempt.
+FKBP5	addiction	relapse	25532758	Stress hormone regulation via <strong>FKBP5</strong> warrants further investigation as a potential contributor to the effects of nicotine withdrawal, which occurs commonly, and has an important role in the maintenance of smoking behavior and <b>relapse</b> following a quit attempt.
+FKBP5	addiction	withdrawal	25532758	Stress hormone regulation via <strong>FKBP5</strong> warrants further investigation as a potential contributor to the effects of nicotine <b>withdrawal</b>, which occurs commonly, and has an important role in the maintenance of smoking behavior and relapse following a quit attempt.
+FKBP5	drug	opioid	24845178	Stress related genes and <b>heroin</b> addiction: a role for a functional <strong>FKBP5</strong> haplotype.
+FKBP5	addiction	addiction	24845178	Stress related genes and heroin <b>addiction</b>: a role for a functional <strong>FKBP5</strong> haplotype.
+FKBP5	drug	opioid	24845178	Nineteen single nucleotide polymorphisms (SNPs) in 9 genes (AVP, AVPR1A, CRHR1, CRHR2, <strong>FKBP5</strong>, GAL, GLRA1, NPY1R and NR3C2) showed nominally significant association with <b>heroin</b> addiction.
+FKBP5	addiction	addiction	24845178	Nineteen single nucleotide polymorphisms (SNPs) in 9 genes (AVP, AVPR1A, CRHR1, CRHR2, <strong>FKBP5</strong>, GAL, GLRA1, NPY1R and NR3C2) showed nominally significant association with heroin <b>addiction</b>.
+FKBP5	addiction	addiction	24845178	This study suggests that variations in the <strong>FKBP5</strong> gene contribute to the development of opiate <b>addiction</b> by modulating the stress response.
+FKBP5	drug	opioid	24766650	Fourteen SNPs showed nominally significant association with <b>heroin</b> addiction (p < 0.05), including the African specific, missense SNP rs5376 (Asn334Ser) in the galanin receptor type 1 gene (GALR1) and the functional <strong>FKBP5</strong> intronic SNP rs1360780.
+FKBP5	addiction	addiction	24766650	Fourteen SNPs showed nominally significant association with heroin <b>addiction</b> (p < 0.05), including the African specific, missense SNP rs5376 (Asn334Ser) in the galanin receptor type 1 gene (GALR1) and the functional <strong>FKBP5</strong> intronic SNP rs1360780.
+FKBP5	drug	alcohol	24603855	<strong>FKBP5</strong> moderates <b>alcohol</b> withdrawal severity: human genetic association and functional validation in knockout mice.
+FKBP5	addiction	withdrawal	24603855	<strong>FKBP5</strong> moderates alcohol <b>withdrawal</b> severity: human genetic association and functional validation in knockout mice.
+FKBP5	drug	alcohol	24603855	This study aimed to examine the effects of single nucleotide polymorphisms (SNPs) of the <strong>FKBP5</strong> gene in humans and the effect of <strong>Fkbp5</strong> gene deletion in mice on <b>alcohol</b> withdrawal severity.
+FKBP5	addiction	withdrawal	24603855	This study aimed to examine the effects of single nucleotide polymorphisms (SNPs) of the <strong>FKBP5</strong> gene in humans and the effect of <strong>Fkbp5</strong> gene deletion in mice on alcohol <b>withdrawal</b> severity.
+FKBP5	drug	alcohol	24603855	We genotyped six <strong>FKBP5</strong> SNPs (rs3800373, rs9296158, rs3777747, rs9380524, rs1360780, and rs9470080) in 399 <b>alcohol</b> dependent inpatients with <b>alcohol</b> consumption 48 h before admission and recorded scores from the Clinical Institute Withdrawal Assessment <b>Alcohol</b> revised (CIWA Ar).
+FKBP5	addiction	withdrawal	24603855	We genotyped six <strong>FKBP5</strong> SNPs (rs3800373, rs9296158, rs3777747, rs9380524, rs1360780, and rs9470080) in 399 alcohol dependent inpatients with alcohol consumption 48 h before admission and recorded scores from the Clinical Institute <b>Withdrawal</b> Assessment Alcohol revised (CIWA Ar).
+FKBP5	drug	alcohol	24603855	<strong>Fkbp5</strong> gene knockout (KO) and wild type (WT) mice were assessed for <b>alcohol</b> withdrawal using handling induced convulsions (HICs) following both acute and chronic <b>alcohol</b> exposure.
+FKBP5	addiction	withdrawal	24603855	<strong>Fkbp5</strong> gene knockout (KO) and wild type (WT) mice were assessed for alcohol <b>withdrawal</b> using handling induced convulsions (HICs) following both acute and chronic alcohol exposure.
+FKBP5	drug	alcohol	24603855	<strong>Fkbp5</strong> KO mice showed significantly greater HICs during withdrawal from chronic <b>alcohol</b> exposure compared with WT controls.
+FKBP5	addiction	withdrawal	24603855	<strong>Fkbp5</strong> KO mice showed significantly greater HICs during <b>withdrawal</b> from chronic alcohol exposure compared with WT controls.
+FKBP5	drug	alcohol	24603855	This study is the first to show a genetic effect of <strong>FKBP5</strong> on the severity of <b>alcohol</b> withdrawal syndrome.
+FKBP5	addiction	withdrawal	24603855	This study is the first to show a genetic effect of <strong>FKBP5</strong> on the severity of alcohol <b>withdrawal</b> syndrome.
+FKBP5	drug	alcohol	24603855	In mice, the absence of the <strong>Fkbp5</strong> gene enhances sensitivity to <b>alcohol</b> withdrawal.
+FKBP5	addiction	withdrawal	24603855	In mice, the absence of the <strong>Fkbp5</strong> gene enhances sensitivity to alcohol <b>withdrawal</b>.
+FKBP5	drug	alcohol	24603855	We suggest that <strong>FKBP5</strong> variants may trigger different adaptive changes in HPA axis regulation during <b>alcohol</b> withdrawal with concomitant effects on withdrawal severity.
+FKBP5	addiction	withdrawal	24603855	We suggest that <strong>FKBP5</strong> variants may trigger different adaptive changes in HPA axis regulation during alcohol <b>withdrawal</b> with concomitant effects on <b>withdrawal</b> severity.
+FKBP5	addiction	withdrawal	22974489	Traumatic stress induced expression of Tsc22d3, Nfkbia, Plat and <strong>Fkbp5</strong> genes and developed social <b>withdrawal</b> in DBA/2J mice.
+FKBP5	drug	alcohol	20459597	The second group of genes (including <strong>Fkbp5</strong> and S3 12), which are controlled, in part, by the release of steroid hormones, was strongly activated by <b>ethanol</b> and opioids.
+FKBP5	drug	opioid	20459597	The second group of genes (including <strong>Fkbp5</strong> and S3 12), which are controlled, in part, by the release of steroid hormones, was strongly activated by ethanol and <b>opioids</b>.
+FKBP5	drug	alcohol	20393453	In addition, in EAs, <b>alcohol</b> dependence was observed to interact with childhood adverse experiences, and also <strong>FKBP5</strong> polymorphisms, to increase the risk for PTSD.
+FKBP5	addiction	dependence	20393453	In addition, in EAs, alcohol <b>dependence</b> was observed to interact with childhood adverse experiences, and also <strong>FKBP5</strong> polymorphisms, to increase the risk for PTSD.
+FKBP5	drug	opioid	19786507	Many genes were significantly regulated by <b>oxycodone</b> (e.g., <strong>Fkbp5</strong>, Per2, Rt1.Dalpha, Slc16a1, and Abcg2).
+CCL5	drug	cocaine	31557508	In rats treated repeatedly with <b>cocaine</b> (10 mg/kg × 4 days, IP), CCR5 gene expression was upregulated in the nucleus accumbens and ventral tegmental area but mRNA levels of CCR5 ligands (i.e., CCL3, CCL4 and <strong>CCL5</strong>) were not affected.
+CCL5	drug	alcohol	30447270	There was a profound downregulation in PNPLA3 and <strong>RANTES</strong> levels after <b>ethanol</b> exposure.
+CCL5	drug	alcohol	29445009	In vivo and in vitro binge <b>alcohol</b> exposure significantly inhibited the TLR4 MyD88 cytokines TNF α and IL 6, as well as the TLR4 TRIF cytokines/chemokines IFN β, IP 10, and <strong>RANTES</strong>, in human monocytes, but not TLR3 TRIF induced cytokines/chemokines, as detected by quantitative PCR and ELISA.
+CCL5	addiction	intoxication	29445009	In vivo and in vitro <b>binge</b> alcohol exposure significantly inhibited the TLR4 MyD88 cytokines TNF α and IL 6, as well as the TLR4 TRIF cytokines/chemokines IFN β, IP 10, and <strong>RANTES</strong>, in human monocytes, but not TLR3 TRIF induced cytokines/chemokines, as detected by quantitative PCR and ELISA.
+CCL5	drug	opioid	29146238	Protein array analyses revealed only minor changes to cytokine profiles when <b>morphine</b> was administered acutely or repeatedly; however, 24 h post <b>morphine</b> administration, the expression of several cytokines was greatly increased, including endogenous CCR5 chemokine ligands (CCL3, CCL4, and <strong>CCL5</strong>), as well as CCL2.
+CCL5	drug	alcohol	28806641	On the other hand, in the case of traumatic intracerebral hemorrhage, the cytokine profile was dominated by KC, <strong>CCL5</strong>, M CSF and several interleukins and <b>ethanol</b> pretreatment did not produce any modification.
+CCL5	addiction	sensitization	28126501	The prevention of this hyperalgesia by diclofenac (1 10μg), the inhibitors of COX 1 SC 560 (0.1 1μg) or COX 2 celecoxib (1 5μg), the TRPV1 antagonist capsazepine (0.03 0.3μg) or the TRPA1 antagonist HC030031 (10 50μg) demonstrates the involvement of prostaglandin synthesis and TRP <b>sensitization</b> in <strong>CCL5</strong> evoked hyperalgesia.
+CCL5	drug	opioid	28126501	Finally, the expression of the endogenous <b>opioid</b> peptide dynorphin A was demonstrated by double immunofluorescence assays in these neutrophils attracted by <strong>CCL5</strong>.
+CCL5	drug	alcohol	27043532	Inflammatory cytokines (interferon γ induced protein 10 (IP 10); monocyte chemoattractant protein 1 (MCP1); regulated on activation, normal T cell expressed and secreted (<strong>RANTES</strong>)) were significantly elevated in <b>alcoholism</b> compared to controls while bone marrow derived hematopoietic cytokines and chemokines (granulocyte colony stimulating factor (GCSF); soluble CD40 ligand (sCD40L); growth related oncogene (GRO)) were significantly reduced.
+CCL5	drug	alcohol	27043532	The novel association between <strong>RANTES</strong> and GRO and impulsivity phenotype in <b>alcoholism</b> should be further investigated in <b>alcoholism</b> and psychiatric conditions with core impulsivity and anxiety phenotypes lending support for therapeutic intervention.
+CCL5	drug	opioid	25760046	<b>Methadone</b> and <b>buprenorphine</b> alone had no effect, but <b>methadone</b> interacted with Tat to further increase production of <strong>CCL5</strong>/RANTES.
+CCL5	drug	opioid	25760046	<b>Methadone</b> and <b>buprenorphine</b> alone had no effect, but <b>methadone</b> interacted with Tat to further increase production of <strong>CCL5</strong>/<strong>RANTES</strong>.
+CCL5	drug	opioid	25623966	<strong>CCL5</strong> expression can be up regulated by chronic <b>morphine</b>.
+CCL5	drug	opioid	25623966	The neuroprotective effect of <b>morphine</b> was significantly attenuated by expressing <strong>CCL5</strong> shRNA.
+CCL5	drug	opioid	23968971	<strong>CCL5</strong> and cytokine expression in the rat brain: differential modulation by chronic <b>morphine</b> and <b>morphine</b> withdrawal.
+CCL5	addiction	withdrawal	23968971	<strong>CCL5</strong> and cytokine expression in the rat brain: differential modulation by chronic morphine and morphine <b>withdrawal</b>.
+CCL5	drug	opioid	23968971	However, recent data have shown that activation of <b>opioid</b> receptors increases the expression and release of the neuroprotective chemokine <strong>CCL5</strong> from astrocytes in vitro.
+CCL5	drug	opioid	23968971	To further define the interaction between <strong>CCL5</strong> and inflammation in response to <b>opioids</b>, we have examined the effect of chronic <b>morphine</b> and <b>morphine</b> withdrawal on the in vivo expression of <strong>CCL5</strong> as well as of pro inflammatory cytokines interleukin 1β (IL 1β) and tumor necrosis factor α (TNF α).
+CCL5	addiction	withdrawal	23968971	To further define the interaction between <strong>CCL5</strong> and inflammation in response to opioids, we have examined the effect of chronic morphine and morphine <b>withdrawal</b> on the in vivo expression of <strong>CCL5</strong> as well as of pro inflammatory cytokines interleukin 1β (IL 1β) and tumor necrosis factor α (TNF α).
+CCL5	drug	opioid	23968971	Rats undergoing a chronic <b>morphine</b> paradigm (10 mg/kg increasing to 30 mg/kg, twice a day for 5 days) showed a twofold increase of <strong>CCL5</strong> protein and mRNA within the cortex and striatum.
+CCL5	drug	opioid	23968971	A chronic <b>morphine</b> paradigm with no escalating doses (10 mg/kg, twice a day) did not alter <strong>CCL5</strong> levels compared to saline treated animals.
+CCL5	drug	opioid	23968971	On the contrary, rats undergoing spontaneous <b>morphine</b> withdrawal exhibited lower levels of <strong>CCL5</strong> within the cortex as well as increased levels of pro inflammatory cytokines and Iba 1 positive cells than saline treated rats.
+CCL5	addiction	withdrawal	23968971	On the contrary, rats undergoing spontaneous morphine <b>withdrawal</b> exhibited lower levels of <strong>CCL5</strong> within the cortex as well as increased levels of pro inflammatory cytokines and Iba 1 positive cells than saline treated rats.
+CCL5	drug	alcohol	23605000	A positive relationship between regulated and normal T cell expressed and secreted (<strong>RANTES</strong>) with increasing severity of <b>alcohol</b> dependence was observed, independent of cigarette smoking (P = 0.0001).
+CCL5	drug	nicotine	23605000	A positive relationship between regulated and normal T cell expressed and secreted (<strong>RANTES</strong>) with increasing severity of alcohol dependence was observed, independent of cigarette <b>smoking</b> (P = 0.0001).
+CCL5	addiction	dependence	23605000	A positive relationship between regulated and normal T cell expressed and secreted (<strong>RANTES</strong>) with increasing severity of alcohol <b>dependence</b> was observed, independent of cigarette smoking (P = 0.0001).
+CCL5	drug	nicotine	23605000	Collectively, our work suggests that AUDs and cigarette <b>smoking</b> each contribute to a proinflammatory pulmonary milieu in human subjects through independent effects on BAL <strong>RANTES</strong> and IL 1β.
+CCL5	drug	opioid	22494919	Nociceptive sensitization, immune cell infiltration, multiple cytokine expression, and <b>opioid</b> peptide expression in damaged nerves were studied in wild type (<strong>CCL5</strong> +/+) and <strong>CCL5</strong> deficient (<strong>CCL5</strong>  / ) mice after partial sciatic nerve ligation (PSNL).
+CCL5	addiction	sensitization	22494919	Nociceptive <b>sensitization</b>, immune cell infiltration, multiple cytokine expression, and opioid peptide expression in damaged nerves were studied in wild type (<strong>CCL5</strong> +/+) and <strong>CCL5</strong> deficient (<strong>CCL5</strong>  / ) mice after partial sciatic nerve ligation (PSNL).
+CCL5	drug	cocaine	21806491	Levels of MPA, sCD40L, NAP 2 and <strong>RANTES</strong> were significantly higher (all p < 0.05) in <b>cocaine</b> addicts compared to controls at baseline.
+CCL5	addiction	withdrawal	21802933	Sputum was also analysed for mRNA levels of haemoxygenase 1, tumour necrosis factor α, <strong>RANTES</strong>, interleukin 5(IL 5), IL 10, IL 12, IL 13, transforming growth factor β, and interferon γ. Cox regression analyses were performed using time to exacerbation as outcome variable to identify significant hazards for a COPD exacerbation after ICS <b>withdrawal</b>.
+CCL5	drug	opioid	18815890	<strong>CCL5</strong>/RANTES gene deletion attenuates <b>opioid</b> induced increases in glial CCL2/MCP 1 immunoreactivity and activation in HIV 1 Tat exposed mice.
+CCL5	drug	opioid	18815890	<strong>CCL5</strong>/<strong>RANTES</strong> gene deletion attenuates <b>opioid</b> induced increases in glial CCL2/MCP 1 immunoreactivity and activation in HIV 1 Tat exposed mice.
+CCL5	drug	opioid	18815890	To assess the role of CC chemokine ligand 5 (<strong>CCL5</strong>)/RANTES in opiate drug abuse and human immunodeficiency virus type 1 (HIV 1) comorbidity, the effects of systemic <b>morphine</b> and intrastriatal HIV 1 Tat on macrophage/microglial and astroglial activation were assessed in wild type and <strong>CCL5</strong> knockout mice.
+CCL5	drug	opioid	18815890	To assess the role of CC chemokine ligand 5 (<strong>CCL5</strong>)/<strong>RANTES</strong> in opiate drug abuse and human immunodeficiency virus type 1 (HIV 1) comorbidity, the effects of systemic <b>morphine</b> and intrastriatal HIV 1 Tat on macrophage/microglial and astroglial activation were assessed in wild type and <strong>CCL5</strong> knockout mice.
+CCL5	drug	opioid	18815890	Glial activation was significantly reduced in <strong>CCL5</strong>( / ) compared to wild type mice at 7 days following combined Tat and <b>morphine</b> exposure.
+CCL5	drug	opioid	18815890	Moreover, the percentage of 3 nitrotyrosine immunopositive macrophages/microglia was markedly reduced in <strong>CCL5</strong>( / ) mice injected with Tat +/  <b>morphine</b> compared to wild type counterparts, suggesting that <strong>CCL5</strong> contributes to nitrosative stress in HIV 1 encephalitis.
+CCL5	drug	opioid	18815890	In <strong>CCL5</strong>( / ) mice, the reductions in Tat +/  <b>morphine</b> induced gliosis coincided with significant declines in the proportion of CCL2/MCP 1 immunoreactive astrocytes and macrophages/microglia compared to wild type counterparts.
+CCL5	drug	opioid	18815890	Macrophages/microglia differed showing modest, albeit significant, increases in the proportion of CCL2 positive cells with combined Tat and <b>morphine</b> exposure, suggesting that <strong>CCL5</strong> preferentially affects CCL2 expression by astroglia.
+CCL5	drug	opioid	18815890	Thus, <strong>CCL5</strong> mediates glial activation caused by Tat and <b>morphine</b>, thereby aggravating HIV 1 neuropathogenesis in opiate abusers and non abusers.
+CCL5	drug	alcohol	12062632	This model correlates closely with <b>alcoholic</b> hepatitis in human beings, characterized by increased IL 8, <strong>RANTES</strong> (regulated upon activation, normal T cell expressed and secreted), and macrophage inflammatory protein 1 (MIP 1) and profound increases in neutrophils and lymphocytes in the liver.
+CCL5	drug	alcohol	12045006	Serum ALT, endotoxin, MIP 1alpha, MCP 1 and <strong>RANTES</strong>, (but not CINC and MIP 2) were also increased in the <b>ethanol</b> fed rats than in the pair fed group.
+CCL5	drug	alcohol	12045006	Isolated Kupffer cells from <b>ethanol</b> fed rats were primed for enhanced MIP 1alpha, MCP 1, and <strong>RANTES</strong> production in vitro, while the endothelial cells were primed for enhanced MIP 1alpha release only.
+CCL5	drug	alcohol	12044837	Acute <b>ethanol</b> administration downregulates human immunodeficiency virus 1 glycoprotein 120 induced KC and <strong>RANTES</strong> production by murine Kupffer cells and splenocytes.
+CCL5	drug	alcohol	12044837	Oral administration of <b>ethanol</b> significantly suppressed HIV 1gp120 induced KC and <strong>RANTES</strong> release.
+CCL5	drug	alcohol	11388697	However, <b>ethanol</b> alone primed isolated Kupffer cells for enhanced <strong>RANTES</strong> mRNA and protein release in the presence or absence of HIV 1 gp120.
+CCL5	drug	alcohol	10719799	This work tests the hypotheses that Kupffer cells are a major source of CC chemokines (MIP 1alpha, MCP 1, <strong>RANTES</strong>) during acute endotoxemia and that acute <b>ethanol</b> intoxication modulates Escherichia coli lipopolysaccharide (LPS, 1 mg/Kg, i.v.)
+CCL5	addiction	intoxication	10719799	This work tests the hypotheses that Kupffer cells are a major source of CC chemokines (MIP 1alpha, MCP 1, <strong>RANTES</strong>) during acute endotoxemia and that acute ethanol <b>intoxication</b> modulates Escherichia coli lipopolysaccharide (LPS, 1 mg/Kg, i.v.)
+CCL5	drug	alcohol	10719799	<b>Ethanol</b> alone significantly upregulated the expression of CC chemokine mRNA, and primed the Kupffer cells for enhanced <strong>RANTES</strong> release.
+CCL5	drug	opioid	10708810	In this study, chemotaxis of monkey leukocytes was evaluated using the chemokines interleukin 8 (IL 8) and regulated upon activation, normal T cell expressed (<strong>RANTES</strong>) as the chemoattractants, and the effects of various <b>opioid</b> agonists and antagonists on the efficiency of chemotaxis were examined.
+CCL5	drug	opioid	10708810	<b>Opioids</b> were either incubated with monkey leukocytes or added directly to chemokines, and the number of cells migrating toward IL 8 (for neutrophils) or <strong>RANTES</strong> (for monocytes) was scored.
+CCL5	drug	opioid	10654191	In this study, chemotaxis of monkey leukocytes was evaluated using human chemokines IL 8 (interleukin 8), MIP 1 beta and <strong>RANTES</strong> as the chemoattractants, and the effects of micro <b>opioid</b> receptor agonists, <b>morphine</b>, DAMGO, <b>methadone</b> and endomorphine, on the efficiency of chemotaxis were examined.
+CCL5	drug	cocaine	7732307	Deaths by acute reaction from drugs consumption (RAD) particularly heroine or <b>cocaine</b>, collected in routine morality statistics, have not changed substantially during the last ten years, whereas an specific collection system (State Information System on Drug Abuse <strong>SISD</strong>) presented a great increase.
+APOA1	addiction	dependence	24376512	The present study identified a multiplier effect from a polymorphism in CETP with ABCA1, <strong>APOA1</strong>, and SR B1, as well as a dose <b>dependence</b> according to the number of alleles present.
+APOA1	drug	alcohol	24051266	WHR, HOMA ir, systolic blood pressure, and ApoB/<strong>ApoA1</strong> loaded significantly on the principal "metabolic factor", leisure time physical activity and self rated health loaded significantly on the "vitality factor", and smoking and <b>alcohol</b> consumption loaded significantly on the "addiction factor".
+APOA1	drug	nicotine	24051266	WHR, HOMA ir, systolic blood pressure, and ApoB/<strong>ApoA1</strong> loaded significantly on the principal "metabolic factor", leisure time physical activity and self rated health loaded significantly on the "vitality factor", and <b>smoking</b> and alcohol consumption loaded significantly on the "addiction factor".
+APOA1	addiction	addiction	24051266	WHR, HOMA ir, systolic blood pressure, and ApoB/<strong>ApoA1</strong> loaded significantly on the principal "metabolic factor", leisure time physical activity and self rated health loaded significantly on the "vitality factor", and smoking and alcohol consumption loaded significantly on the "<b>addiction</b> factor".
+APOA1	drug	opioid	21453194	The aim was to evaluate the frequency in serum lipid disturbances of hepatitis C virus (HCV) seronegative <b>heroin</b> addicts; the capacity of high density lipoprotein (HDL) C and apolipoprotein B (apoB)/apolipoprotein A I (<strong>apoA</strong> I) for predicting hypertriglyceridemia/low HDL C profile; correlation of HDL C with the apoB/<strong>apoA</strong> I and their correlation to plasma apo/lipoproteins.
+APOA1	drug	opioid	21453194	ApoB/<strong>apoA</strong> I showed stronger correlation with the observed apo/lipoproteins than the HDL C. The logistic regression model showed that apoB/<strong>apoA</strong> I index (OR 89.1, 95% CI 1.3 5971.2) is more significant predictor in developing hypertriglyceridemia/low HDL profile than HDL C. <b>Heroin</b> addiction is associated with decreased plasma concentrations of HDL C, <strong>apoA</strong> I, apoB, and increased TGL concentrations.
+APOA1	addiction	addiction	21453194	ApoB/<strong>apoA</strong> I showed stronger correlation with the observed apo/lipoproteins than the HDL C. The logistic regression model showed that apoB/<strong>apoA</strong> I index (OR 89.1, 95% CI 1.3 5971.2) is more significant predictor in developing hypertriglyceridemia/low HDL profile than HDL C. Heroin <b>addiction</b> is associated with decreased plasma concentrations of HDL C, <strong>apoA</strong> I, apoB, and increased TGL concentrations.
+APOA1	drug	opioid	21453194	In <b>heroin</b> addicts, HDL C concentrations are significantly associated with the apoB/<strong>apoA</strong> I index, which correlates to all lipid fractions and is a stronger predictor of metabolic syndrome lipid profile in <b>heroin</b> addicts.
+APOA1	drug	alcohol	16739925	<b>Ethanol</b> inhibited LCAT and LPL activities, and increased <strong>apoA</strong> containing LP in blood serum.
+APOA1	drug	nicotine	16372134	Plasma APOB and LDL C, but not <strong>APOA1</strong> and HDL C, were shown to be markedly elevated in <b>smokers</b> versus non <b>smokers</b>, affirming that <b>smoking</b> may selectively impact the former pathway.
+APOA1	drug	alcohol	12916168	The 14th day after <b>alcohol</b> abolition was characterized by tendency to normalization of these disturbances, but at the 30th day of soberness a recurrence growing the changes of <strong>apoA</strong> containing lipoproteins transformation was observed.
+APOA1	drug	alcohol	12916168	In the patients under intoxication period and first 3 days after <b>alcohol</b> abolition a significant increase of quantity of all the <strong>apoA</strong> containing lipoprotein populations took place which was restored completely in remission.
+APOA1	addiction	intoxication	12916168	In the patients under <b>intoxication</b> period and first 3 days after alcohol abolition a significant increase of quantity of all the <strong>apoA</strong> containing lipoprotein populations took place which was restored completely in remission.
+APOA1	addiction	sensitization	12486210	It is concluded that troglitazone doses known to achieve insulin <b>sensitization</b> did not enhance rat <strong>apoA</strong> I promoter activity sufficiently to result in an increased <strong>apoA</strong> I mRNA or protein expression in the intact rat.
+APOA1	drug	alcohol	11981126	ApoE genotypes and concentrations of serum cholesterol, triglyceride, and Lps containing <strong>apoA</strong> I, A II, B, E, and C III were determined in 84 male <b>alcohol</b> abusers before and after 3 weeks of abstinence.
+APOA1	addiction	withdrawal	11981126	After <b>withdrawal</b>, concentrations of serum <strong>apoA</strong> I, LpA I, LpA I/A II, apoC III, LpC III non B, apoE, and LpE non B significantly decreased, whereas those of triglycerides and apoB increased; levels of cholesterol, LpC III:B, and LpB:E were not affected.
+APOA1	drug	alcohol	8855152	Serum concentrations of <strong>apo A</strong> I, LpA I, LpA I:A II, apo C III, and LpC III significantly (P </= 0.01) increased with <b>alcohol</b> intake (mean +/  SE in low drinkers vs in <b>alcoholics</b>)  1.45 +/  0.03 vs 1.78 +/  0.05 g/L; 0.45 +/  0.02 vs 0.56 +/  0.02 g/L; 0.99 +/  0.02 vs 1.22 +/  0.04 g/L; 27.6 +/  1.5 vs 39.7 +/  1.7 mg/L; and 8.4 +/  0.9 vs 24.7 +/  1.7 mg/L, respectively whereas apo B and LpC III:B concentrations tended to decrease  1.20 +/  0.04 vs 1.06 +/  0.04 g/L and 19.3 +/  1.2 vs 14.9 +/  1.0 mg/L, respectively.
+APOA1	addiction	withdrawal	8855152	After <b>withdrawal</b>, the concentrations of serum <strong>apo A</strong> I, apo C III, LpA I, LpA I:A II, and LpC III decreased significantly (P </= 0.01), reaching values comparable with those in low drinkers; concentrations of triglycerides, apo B, apo E, and Lp(a) rose; and cholesterol concentration was unaffected.
+APOA1	drug	alcohol	8855152	In multiple regression analysis, after adjustment for serum concentrations of albumin, aspartate aminotransferase, and gamma glutamyltransferase and for the Quetelet index, <b>alcohol</b> consumption remained positively correlated to <strong>apo A</strong> I, LpA I:A II, apo C III, and LpC III concentrations.
+APOA1	drug	alcohol	8855152	Study of other determinants of serum apo and lipoprotein concentrations suggests that <b>alcohol</b> related variations in some of them, especially <strong>apo A</strong> I, might depend on the metabolic ability of the liver to synthesize proteins and on induction phenomena.
+APOA1	drug	alcohol	8003113	<strong>Apo A</strong> I levels decreased ( 39%, P = 0.0002) and the magnitude of the decrease after <b>alcohol</b> withdrawal was positively related to the duration of hospitalization.
+APOA1	addiction	withdrawal	8003113	<strong>Apo A</strong> I levels decreased ( 39%, P = 0.0002) and the magnitude of the decrease after alcohol <b>withdrawal</b> was positively related to the duration of hospitalization.
+APOA1	drug	alcohol	8003113	It is concluded that the modifications of HDL cholesterol, HDL3 cholesterol, HDL2 cholesterol <strong>Apo A</strong> I and Apo B values were induced by <b>alcohol</b> withdrawal in this population of chronic french <b>alcoholics</b>.
+APOA1	addiction	withdrawal	8003113	It is concluded that the modifications of HDL cholesterol, HDL3 cholesterol, HDL2 cholesterol <strong>Apo A</strong> I and Apo B values were induced by alcohol <b>withdrawal</b> in this population of chronic french alcoholics.
+APOA1	drug	alcohol	8375458	Among <strong>apo A</strong> I containing lipoproteins the most prominent change occurred in Lp A I:A II, which fell by 32% (P < 0.01) during 1 week's <b>alcohol</b> withdrawal.
+APOA1	addiction	withdrawal	8375458	Among <strong>apo A</strong> I containing lipoproteins the most prominent change occurred in Lp A I:A II, which fell by 32% (P < 0.01) during 1 week's alcohol <b>withdrawal</b>.
+APOA1	drug	alcohol	8375458	In contrast to <b>alcoholic</b> men, studied previously by us using the same study design and methods, there was no significant elevation of HDL3 cholesterol and <strong>apo A</strong> I.
+APOA1	drug	alcohol	1521980	Adjustment for age, body mass index, smoking, <b>alcohol</b> consumption, stress and tension at work, shift work, noise exposure and educational level in multiple linear regression analysis showed significant effects of the CS2 index on systolic BP, diastolic BP, cholesterol, HDL cholesterol, LDL cholesterol, <strong>apolipoprotein A1</strong>, apolipoprotein B, the LDL cholesterol/apolipoprotein B and HDL cholesterol/<strong>apolipoprotein A1</strong> ratios; there were no significant effects on the triglycerides.
+APOA1	drug	nicotine	1521980	Adjustment for age, body mass index, <b>smoking</b>, alcohol consumption, stress and tension at work, shift work, noise exposure and educational level in multiple linear regression analysis showed significant effects of the CS2 index on systolic BP, diastolic BP, cholesterol, HDL cholesterol, LDL cholesterol, <strong>apolipoprotein A1</strong>, apolipoprotein B, the LDL cholesterol/apolipoprotein B and HDL cholesterol/<strong>apolipoprotein A1</strong> ratios; there were no significant effects on the triglycerides.
+APOA1	addiction	withdrawal	1410896	HDL cholesterol, <strong>apo A</strong> I and apo B showed a biphasic variation with significant post <b>withdrawal</b> changes which became less pronounced after 6 months of abstinence.
+APOA1	drug	alcohol	3517775	STA, <strong>apoA</strong> lipoprotein, HDL cholesterol, total cholesterol and triglycerides were tested in 44 men dealt in 4 groups (subjects with normal or elevated STA, <b>alcoholic</b> or withdrawn).
+ABAT	addiction	reward	29381352	We previously designed the mechanism based inactivator (1S,3S) 3 amino 4 difluoromethylenyl 1 cyclopentanoic acid (2), now called <b>CPP</b> 115, that is 186 times more efficient in inactivating <strong>GABA AT</strong> than vigabatrin, the only FDA approved drug that is an inactivator of <strong>GABA AT</strong>.
+ABAT	addiction	reward	29381352	Herein we report the design, using molecular dynamics simulations, synthesis, and biological evaluation of a new mechanism based inactivator, (S) 3 amino 4 (difluoromethylenyl)cyclopent 1 ene 1 carboxylic acid (5), which was found to be almost 10 times more efficient as an inactivator of <strong>GABA AT</strong> than <b>CPP</b> 115.
+ABAT	drug	alcohol	22253714	There were also expression changes specific to cocaine addicts (GAD1, GAD2), <b>alcoholics</b> (GABRA2) and P rats (<strong>ABAT</strong>, GABRG3).
+ABAT	drug	cocaine	22253714	There were also expression changes specific to <b>cocaine</b> addicts (GAD1, GAD2), alcoholics (GABRA2) and P rats (<strong>ABAT</strong>, GABRG3).
+ABAT	addiction	addiction	22128851	Vigabatrin, a GABA aminotransferase (<strong>GABA AT</strong>) inactivator, is used to treat infantile spasms and refractory complex partial seizures and is in clinical trials to treat <b>addiction</b>.
+ABAT	addiction	reward	22128851	We evaluated a novel <strong>GABA AT</strong> inactivator (1S, 3S) 3 amino 4 difluoromethylenyl 1 cyclopentanoic acid (<b>CPP</b> 115, compound 1) and observed that it does not exhibit other GABAergic or off target activities and is rapidly and completely orally absorbed and eliminated.
+ABAT	drug	alcohol	16834758	Consistent with their ability to enhance the action of <strong>GABA at</strong> GABA(A) receptors, these steroid derivatives (termed neuroactive steroids) possess anticonvulsant, antidepressant and anxiolytic effects in addition to altering aspects of sexual  and <b>alcohol</b> related behaviors.
+ABAT	drug	benzodiazepine	15926867	Non selective <b>benzodiazepine</b> (BZ) binding site full agonists, exemplified by <b>diazepam</b>, act by enhancing the inhibitory effects of <strong>GABA at</strong> GABA(A) receptors containing either an alpha1,  2,  3 or  5 subunit.
+ABAT	drug	benzodiazepine	15864560	In contrast, other BZ binding site ligands, such as 6 (2bromophenyl) 8 fluoro 4H imidazo [1,5 a][1,4] <b>benzodiazepine</b> 3 carboxamide (imidazenil), which fail to allosterically and positively modulate the action of <strong>GABA at</strong> GABA(A) receptors with alpha(1) subunits but that selectively allosterically modulate cortical GABA(A) receptors containing alpha(5) subunits, contribute to the anxiolytic, antipanic, and anticonvulsant actions of these ligands without producing sedation, amnesia, or tolerance.
+ABAT	drug	benzodiazepine	12434260	The behavioral effects of racemic zopiclone are similar to those of benzodiazepines that positively modulate <strong>GABA at</strong> the GABA(A) receptor complex; however, it is not clear how enantiomers or metabolites of zopiclone contribute to the <b>benzodiazepine</b> like behavioral effects of racemic zopiclone.
+ABAT	drug	alcohol	12108574	We propose that the N methyl D aspartate (NMDA) antagonist and gamma aminobutyric (GABA)mimetic properties of <b>ethanol</b> are responsible for its apoptogenic action, in that we have found that other drugs that block NMDA glutamate receptors or mimic <strong>GABA at</strong> GABA(A) receptors also trigger apoptotic neurodegeneration in the developing brain.
+ABAT	addiction	reward	11280926	"The <b>reward</b> cascade" involves the release of serotonin, which in turn at the hypothalmus stimulates enkephalin, which in turn inhibits <strong>GABA at</strong> the substania nigra, which in turn fine tunes the amount of DA released at the nucleus accumbens or "<b>reward</b> site."
+ABAT	drug	alcohol	10604976	Although it is well documented that chronic <b>ethanol</b> (EtOH) administration produces cross tolerance to the positive modulatory effect of benzodiazepines and <strong>GABA at</strong> GABA(A) receptors, recent findings suggest that sensitivity to 3alpha,5alpha P is enhanced during EtOH withdrawal.
+ABAT	addiction	withdrawal	10604976	Although it is well documented that chronic ethanol (EtOH) administration produces cross tolerance to the positive modulatory effect of benzodiazepines and <strong>GABA at</strong> GABA(A) receptors, recent findings suggest that sensitivity to 3alpha,5alpha P is enhanced during EtOH <b>withdrawal</b>.
+ABAT	drug	opioid	10066284	This report describes an acute presynaptic inhibition of GABAB mediated IPSPs by mu  and kappa <b>opioid</b> receptors and the effects of withdrawal from chronic <b>morphine</b> treatment on the release of <strong>GABA at</strong> this synapse.
+ABAT	addiction	withdrawal	10066284	This report describes an acute presynaptic inhibition of GABAB mediated IPSPs by mu  and kappa opioid receptors and the effects of <b>withdrawal</b> from chronic morphine treatment on the release of <strong>GABA at</strong> this synapse.
+ABAT	drug	alcohol	9361331	The results of the present study provide further evidence of the similarities between the effects of <b>ethanol</b> and benzodiazepine receptor agonists on learning and memory, and are consistent with the hypothesis that <b>ethanol</b>'s potentiation of <strong>GABA at</strong> GABAA receptors contributes to the learning and memory impairments produced by <b>ethanol</b>.
+ABAT	drug	benzodiazepine	9361331	The results of the present study provide further evidence of the similarities between the effects of ethanol and <b>benzodiazepine</b> receptor agonists on learning and memory, and are consistent with the hypothesis that ethanol's potentiation of <strong>GABA at</strong> GABAA receptors contributes to the learning and memory impairments produced by ethanol.
+ABAT	drug	alcohol	26735441	We have studied the activities of the GABA metabolizing enzymes GABA aminotransferase (<strong>GABA AT</strong>), succinic semialdehyde dehydrogenase (SSA DH) and SSA reductase (SSA R) and the levels of GABA, glutamine and glutamate in rats preferring water (WP) or <b>ethanol</b> (EP) after 6 months of <b>ethanol</b> consumption and 12 hours to 7 days after withdrawal.
+ABAT	addiction	withdrawal	26735441	We have studied the activities of the GABA metabolizing enzymes GABA aminotransferase (<strong>GABA AT</strong>), succinic semialdehyde dehydrogenase (SSA DH) and SSA reductase (SSA R) and the levels of GABA, glutamine and glutamate in rats preferring water (WP) or ethanol (EP) after 6 months of ethanol consumption and 12 hours to 7 days after <b>withdrawal</b>.
+ABAT	drug	alcohol	26735441	We showed decreased GABA levels in the brain stem, decreased <strong>GABA AT</strong> activity in the hemispheres and brain stem, and enhanced <strong>GABA AT</strong> activity in the striatum of EP rats compared with the control or WP animals following chronic consumption of <b>ethanol</b>.
+ABAT	drug	alcohol	8730228	These results suggest that neither low plasma <strong>GABA at</strong> baseline nor altered plasma GABA response to diazepam is associated with increased genetic risk for <b>alcoholism</b>.
+ABAT	drug	benzodiazepine	8730228	These results suggest that neither low plasma <strong>GABA at</strong> baseline nor altered plasma GABA response to <b>diazepam</b> is associated with increased genetic risk for alcoholism.
+ABAT	drug	alcohol	7841849	The neurochemical basis for the rewarding effects of <b>alcohol</b> may be the potentiation of <strong>GABA at</strong> GABAA receptors (causing relaxation) and release of dopamine from mesolimbic neurones (causing euphoria).
+ABAT	drug	benzodiazepine	3016590	The effect of drugs which down regulate the function of <strong>GABA at</strong> the level of the GABA/<b>benzodiazepine</b> receptor complex was studied on the conflict test in the rat.
+ABAT	drug	alcohol	6152602	The increase in striatal <strong>GABA at</strong> day 7 of withdrawal after 30 days of <b>ethanol</b> may be a rebound phenomenon and may reflect the presence of a hypogabaergic state which has been shown to occur during <b>ethanol</b> withdrawal.
+ABAT	addiction	withdrawal	6152602	The increase in striatal <strong>GABA at</strong> day 7 of <b>withdrawal</b> after 30 days of ethanol may be a rebound phenomenon and may reflect the presence of a hypogabaergic state which has been shown to occur during ethanol <b>withdrawal</b>.
+PHOX2B	drug	alcohol	31909580	Additional subject level behavioral covariates (fruit and vegetable consumption, leisure exercise frequency, <b>alcohol</b> consumption, smoking, and body mass index [BMI]) were included in the <strong>CCHS</strong> analysis.
+PHOX2B	drug	nicotine	31909580	Additional subject level behavioral covariates (fruit and vegetable consumption, leisure exercise frequency, alcohol consumption, <b>smoking</b>, and body mass index [BMI]) were included in the <strong>CCHS</strong> analysis.
+PHOX2B	drug	alcohol	30086425	Cigarette smoking, frequency of <b>alcohol</b> consumption, last month non prescribed cannabis use (vs. last year use), and last 3 months regular (≥once/week) and occasional (<once/week) use of crack/cocaine, speed (amphetamine), and heroin (vs. last year use) were examined in WLWH from the 2013 2015 Canadian HIV Women's Sexual and Reproductive Health Cohort Study (CHIWOS; N = 1422) and compared with general population women from the 2013 2014 Canadian Community Health Survey (<strong>CCHS</strong>; N = 46,831).
+PHOX2B	drug	amphetamine	30086425	Cigarette smoking, frequency of alcohol consumption, last month non prescribed cannabis use (vs. last year use), and last 3 months regular (≥once/week) and occasional (<once/week) use of crack/cocaine, speed (<b>amphetamine</b>), and heroin (vs. last year use) were examined in WLWH from the 2013 2015 Canadian HIV Women's Sexual and Reproductive Health Cohort Study (CHIWOS; N = 1422) and compared with general population women from the 2013 2014 Canadian Community Health Survey (<strong>CCHS</strong>; N = 46,831).
+PHOX2B	drug	cannabinoid	30086425	Cigarette smoking, frequency of alcohol consumption, last month non prescribed <b>cannabis</b> use (vs. last year use), and last 3 months regular (≥once/week) and occasional (<once/week) use of crack/cocaine, speed (amphetamine), and heroin (vs. last year use) were examined in WLWH from the 2013 2015 Canadian HIV Women's Sexual and Reproductive Health Cohort Study (CHIWOS; N = 1422) and compared with general population women from the 2013 2014 Canadian Community Health Survey (<strong>CCHS</strong>; N = 46,831).
+PHOX2B	drug	cocaine	30086425	Cigarette smoking, frequency of alcohol consumption, last month non prescribed cannabis use (vs. last year use), and last 3 months regular (≥once/week) and occasional (<once/week) use of crack/<b>cocaine</b>, speed (amphetamine), and heroin (vs. last year use) were examined in WLWH from the 2013 2015 Canadian HIV Women's Sexual and Reproductive Health Cohort Study (CHIWOS; N = 1422) and compared with general population women from the 2013 2014 Canadian Community Health Survey (<strong>CCHS</strong>; N = 46,831).
+PHOX2B	drug	nicotine	30086425	Cigarette <b>smoking</b>, frequency of alcohol consumption, last month non prescribed cannabis use (vs. last year use), and last 3 months regular (≥once/week) and occasional (<once/week) use of crack/cocaine, speed (amphetamine), and heroin (vs. last year use) were examined in WLWH from the 2013 2015 Canadian HIV Women's Sexual and Reproductive Health Cohort Study (CHIWOS; N = 1422) and compared with general population women from the 2013 2014 Canadian Community Health Survey (<strong>CCHS</strong>; N = 46,831).
+PHOX2B	drug	opioid	30086425	Cigarette smoking, frequency of alcohol consumption, last month non prescribed cannabis use (vs. last year use), and last 3 months regular (≥once/week) and occasional (<once/week) use of crack/cocaine, speed (amphetamine), and <b>heroin</b> (vs. last year use) were examined in WLWH from the 2013 2015 Canadian HIV Women's Sexual and Reproductive Health Cohort Study (CHIWOS; N = 1422) and compared with general population women from the 2013 2014 Canadian Community Health Survey (<strong>CCHS</strong>; N = 46,831).
+PHOX2B	drug	opioid	28459825	We used data from the 2003 Canadian Community Health Survey (<strong>CCHS</strong>), which asked respondents about their use of specific analgesic medications, including <b>opioids</b>, and their history of tooth pain in the past month.
+PHOX2B	drug	nicotine	15971513	Trends in <b>smoking</b> rates were calculated using cross sectional data from the NPHS and the <strong>CCHS</strong>.
+KRAS	drug	nicotine	32649943	<b>Nicotine</b> inhibited the proliferation of SKOV3 and TOV112D OC cells, which have TP53 mutation and wild type <strong>KRAS</strong>, but did not inhibit the proliferation of TOV21G or HEY OC cells, which have <strong>KRAS</strong> mutation and wild type TP53.
+KRAS	drug	nicotine	32649943	<b>Nicotine</b> inhibited the proliferation of SKOV3 and TOV112D OC cells, which have TP53 mutation and wild type <strong><strong>KRAS</strong></strong>, but did not inhibit the proliferation of TOV21G or HEY OC cells, which have <strong><strong>KRAS</strong></strong> mutation and wild type TP53.
+KRAS	drug	alcohol	31985512	Cluster analysis was used to discern <strong>RALD</strong> patterns, which were examined as predictors of <b>alcohol</b> use using multivariate regression.
+KRAS	drug	alcohol	31985512	Concerns about impacts on medications, school, and disease status were the most frequently endorsed <strong>RALD</strong>; prior negative experiences with <b>alcohol</b> and family history were the least frequently endorsed.
+KRAS	drug	alcohol	31985512	Compared to the cluster with high endorsement of multiple general and health related <strong>RALD</strong>, those predominantly citing concerns about addiction and those not strongly endorsing any <strong>RALD</strong> consistently reported greater <b>alcohol</b> use.
+KRAS	addiction	addiction	31985512	Compared to the cluster with high endorsement of multiple general and health related <strong>RALD</strong>, those predominantly citing concerns about <b>addiction</b> and those not strongly endorsing any <strong>RALD</strong> consistently reported greater alcohol use.
+KRAS	drug	alcohol	31985512	Among recent drinkers, the cluster characterized by low concern across multiple <strong>RALD</strong> also consistently reported greater <b>alcohol</b> use compared to their counterparts expressing moderate concern.
+KRAS	drug	nicotine	31125062	In certain subgroups, PFS was positively associated with PD L1 expression (<strong>KRAS</strong>, EGFR) and with <b>smoking</b> status (BRAF, HER2).
+KRAS	drug	nicotine	31125062	In certain subgroups, PFS was positively associated with PD L1 expression (<strong><strong>KRAS</strong></strong>, EGFR) and with <b>smoking</b> status (BRAF, HER2).
+KRAS	drug	nicotine	30230541	Comparing with <strong>KRAS</strong> mutations, NF1 mutations were found more common in female and never <b>smokers</b> (p = 0.003 and p = 0.004, respectively).
+KRAS	drug	nicotine	30230541	Comparing with <strong><strong>KRAS</strong></strong> mutations, NF1 mutations were found more common in female and never <b>smokers</b> (p = 0.003 and p = 0.004, respectively).
+KRAS	drug	nicotine	29186353	EGFR mutations were found predominantly in never <b>smokers</b>; <strong>KRAS</strong> in current/former <b>smokers</b>.
+KRAS	drug	nicotine	29186353	EGFR mutations were found predominantly in never <b>smokers</b>; <strong><strong>KRAS</strong></strong> in current/former <b>smokers</b>.
+KRAS	addiction	sensitization	28898697	Chronic Cigarette Smoke Induced Epigenomic Changes Precede <b>Sensitization</b> of Bronchial Epithelial Cells to Single Step Transformation by <strong>KRAS</strong> Mutations.
+KRAS	addiction	sensitization	28898697	Chronic Cigarette Smoke Induced Epigenomic Changes Precede <b>Sensitization</b> of Bronchial Epithelial Cells to Single Step Transformation by <strong><strong>KRAS</strong></strong> Mutations.
+KRAS	drug	alcohol	27992614	Additionally, the rs61764370 polymorphism in the <strong>KRAS</strong> gene is located in a binding site for the let 7 micro RNA family, which is potentially involved in <b>alcohol</b> induced inflammation.
+KRAS	drug	alcohol	27992614	Additionally, the rs61764370 polymorphism in the <strong><strong>KRAS</strong></strong> gene is located in a binding site for the let 7 micro RNA family, which is potentially involved in <b>alcohol</b> induced inflammation.
+KRAS	drug	nicotine	26955281	<strong>KRAS</strong> mutation was more frequently found in male patients and former/current <b>smoker</b> patients.
+KRAS	drug	nicotine	26955281	<strong><strong>KRAS</strong></strong> mutation was more frequently found in male patients and former/current <b>smoker</b> patients.
+KRAS	addiction	relapse	26955281	No statistical significance was found in <b>relapse</b> free survival or overall survival between patients with <strong>KRAS</strong> mutation and patients with other mutations.
+KRAS	addiction	relapse	26955281	No statistical significance was found in <b>relapse</b> free survival or overall survival between patients with <strong><strong>KRAS</strong></strong> mutation and patients with other mutations.
+KRAS	drug	nicotine	25152623	The ALK rearrangements were more frequently observed in tumors with a minor mucinous component, while the <strong>KRAS</strong> mutations were more prevalent in <b>smokers</b>.
+KRAS	drug	nicotine	25152623	The ALK rearrangements were more frequently observed in tumors with a minor mucinous component, while the <strong><strong>KRAS</strong></strong> mutations were more prevalent in <b>smokers</b>.
+KRAS	addiction	relapse	23775406	ANCCA expression was evaluated by immunohistochemistry in 143 surgically resected lung adenocarcinomas and was correlated with clinicopathologic and molecular variables including adenocarcinoma histologic subtypes, tumor, node, metastasis status, <b>relapse</b> free survival, overall survival, EGFR mutations, <strong>KRAS</strong> mutations, HER2 mutations and ALK fusions.
+KRAS	addiction	relapse	23775406	ANCCA expression was evaluated by immunohistochemistry in 143 surgically resected lung adenocarcinomas and was correlated with clinicopathologic and molecular variables including adenocarcinoma histologic subtypes, tumor, node, metastasis status, <b>relapse</b> free survival, overall survival, EGFR mutations, <strong><strong>KRAS</strong></strong> mutations, HER2 mutations and ALK fusions.
+KRAS	drug	nicotine	22464348	The type of molecular mutation in p53 or <strong>KRAS</strong> varies with <b>smoking</b> status.
+KRAS	drug	nicotine	22464348	The type of molecular mutation in p53 or <strong><strong>KRAS</strong></strong> varies with <b>smoking</b> status.
+KRAS	drug	nicotine	21655907	In addition, most adenocarcinomas in never <b>smokers</b> harbor one of the proto oncogene aberrations that occur in a mutually exclusive manner (EGFR mutation, <strong>KRAS</strong> mutation, HER2 mutations, or ALK translocation).
+KRAS	drug	nicotine	21655907	In addition, most adenocarcinomas in never <b>smokers</b> harbor one of the proto oncogene aberrations that occur in a mutually exclusive manner (EGFR mutation, <strong><strong>KRAS</strong></strong> mutation, HER2 mutations, or ALK translocation).
+KRAS	drug	alcohol	20388501	Genome wide gene expression analysis identifies <strong>K ras</strong> as a regulator of <b>alcohol</b> intake.
+KRAS	drug	alcohol	20388501	Expression of the small G protein <strong>K ras</strong> was differentially regulated following both single and repeated <b>alcohol</b> administration.
+KRAS	drug	alcohol	20388501	We also observed that voluntary <b>alcohol</b> intake in <strong>K ras</strong> heterozygous null mice (<strong>K ras</strong>(+/ )) did not increase after withdrawal from repeated cycles of intermittent <b>ethanol</b> vapor exposure, unlike in their wild type littermates.
+KRAS	addiction	withdrawal	20388501	We also observed that voluntary alcohol intake in <strong>K ras</strong> heterozygous null mice (<strong>K ras</strong>(+/ )) did not increase after <b>withdrawal</b> from repeated cycles of intermittent ethanol vapor exposure, unlike in their wild type littermates.
+KRAS	drug	alcohol	20388501	To identify <strong>K ras</strong> regulated pathways, we then profiled gene expression in the ACC of <strong>K ras</strong>(+/ ), heterozygous null mice for the <strong>K ras</strong> negative regulator Nf1 (Nf1(+/ )) and wild type mice following repeated administration of an intoxicating dose of <b>alcohol</b>.
+KRAS	drug	alcohol	20388501	Pathway analysis showed that <b>alcohol</b> differentially affected various pathways in a <strong>K ras</strong> dependent manner   some of which previously shown to be regulated by <b>alcohol</b>   including the insulin/PI3K pathway, the NF kappaB, the phosphodiesterases (PDEs) pathway, the Jak/Stat and the adipokine signaling pathways.
+KRAS	drug	alcohol	20388501	Altogether, the data implicate <strong>K ras</strong> regulated pathways in the regulation of excessive <b>alcohol</b> drinking after a history of dependence.
+KRAS	addiction	dependence	20388501	Altogether, the data implicate <strong>K ras</strong> regulated pathways in the regulation of excessive alcohol drinking after a history of <b>dependence</b>.
+KRAS	drug	alcohol	20380822	We recently identified the small G protein <strong>K ras</strong> as an <b>alcohol</b> regulated gene in the ACC by gene expression analysis.
+KRAS	drug	alcohol	20380822	We show here that the adiponectin receptor 2 (AdipoR2) was differentially regulated by <b>alcohol</b> in the ACC in a <strong>K ras</strong> dependent manner.
+KRAS	drug	alcohol	20380822	Altogether, the data implicate <strong>K ras</strong> regulated pathways involving AdipoR2 in the cellular and behavioral actions of <b>alcohol</b> that may contribute to overactivity of the ACC during withdrawal and excessive <b>alcohol</b> drinking.
+KRAS	addiction	withdrawal	20380822	Altogether, the data implicate <strong>K ras</strong> regulated pathways involving AdipoR2 in the cellular and behavioral actions of alcohol that may contribute to overactivity of the ACC during <b>withdrawal</b> and excessive alcohol drinking.
+KRAS	drug	nicotine	19787214	<strong>KRAS</strong> mutation was significantly associated to gender (p=0.027) and pathology types (p=0.000), but not to <b>smoking</b>.
+KRAS	drug	nicotine	19787214	<strong><strong>KRAS</strong></strong> mutation was significantly associated to gender (p=0.027) and pathology types (p=0.000), but not to <b>smoking</b>.
+KRAS	addiction	dependence	19787214	The results also exhibit <b>dependence</b> of <strong>KRAS</strong> mutation in China on ethnicity.
+KRAS	addiction	dependence	19787214	The results also exhibit <b>dependence</b> of <strong><strong>KRAS</strong></strong> mutation in China on ethnicity.
+KRAS	drug	benzodiazepine	10353384	For example: (1) ozone induced lung neoplasms had two unique mutations, one (codon 61 <strong>K ras</strong> CTA mutation) consistent with a direct genotoxic event and a second (codon 12 <strong>K ras</strong> G   > T transversion) consistent with an indirect genotoxic effect; (2) isoprene induced Harderian gland neoplasms had a unique <strong>K ras</strong> A   > T transversion at codon 61 which provided evidence that formation of an epoxide intermediate was involved; (3) 1,3 butadiene induced neoplasms had a characteristic <strong>K ras</strong> G   > C transversion mutation at codon 13 which was also consistent with a chemical specific effect; (4) methylene chloride induced liver neoplasms had an H ras mutation profile at codon 61 similar to that of spontaneous tumours, suggesting that methylene chloride promotes cells with 'spontaneously initiated' ras mutations and (5) <b>oxazepam</b> induced liver neoplasms had a low frequency of ras mutations, suggesting a nonmutagenic pathway of carcinogenesis.
+KRAS	addiction	aversion	10353384	For example: (1) ozone induced lung neoplasms had two unique mutations, one (codon 61 <strong>K ras</strong> <b>CTA</b> mutation) consistent with a direct genotoxic event and a second (codon 12 <strong>K ras</strong> G   > T transversion) consistent with an indirect genotoxic effect; (2) isoprene induced Harderian gland neoplasms had a unique <strong>K ras</strong> A   > T transversion at codon 61 which provided evidence that formation of an epoxide intermediate was involved; (3) 1,3 butadiene induced neoplasms had a characteristic <strong>K ras</strong> G   > C transversion mutation at codon 13 which was also consistent with a chemical specific effect; (4) methylene chloride induced liver neoplasms had an H ras mutation profile at codon 61 similar to that of spontaneous tumours, suggesting that methylene chloride promotes cells with 'spontaneously initiated' ras mutations and (5) oxazepam induced liver neoplasms had a low frequency of ras mutations, suggesting a nonmutagenic pathway of carcinogenesis.
+KRAS	drug	nicotine	8208681	Point mutations of the oncogene <strong>K ras</strong> is found in 15 to 30% of adenoma carcinomas, especially in <b>smokers</b>.
+GSTM1	drug	opioid	32344532	Our aim was to update the knowledge on this issue, particularly on the influence of an <b>Opioid</b> Receptor <strong>Mu 1</strong> (OPRM1) genetic polymorphism.
+GSTM1	drug	opioid	32014377	Stressed mice also showed significant increase in TLR4, Nuclear Factor Kappa B (NF kB), inducible nitric oxide synthase (iNOS), dopamine receptor D2 (DRD2), cyclic adenosine monophosphate (cAMP) response element binding protein 1 (CREB 1) and <b>opioid</b> receptor <strong>MU 1</strong> (OPRM 1) genes expression compared with control and LPS RS treated stressed mice.
+GSTM1	drug	opioid	30552906	In a functional imaging study, we investigated the influence of the single nucleotide polymorphism of the <strong>mu 1</strong> subtype <b>opioid</b> receptor gene (OPRM1), implicated in sociability, on correlates of trait and state aggression to delineate the function of these influences in aggression.
+GSTM1	drug	opioid	30508992	Clinically actionable polymorphisms in CYP2D6 (cytochrome p450 2D6) and OPRM1 (<strong>mu 1</strong> <b>opioid</b> receptor), the most important gene coding, respectively, for a metabolizing enzyme and receptor for <b>opioids</b> are reviewed, and functional effects described.
+GSTM1	drug	opioid	29649967	Among ALSPAC children, the rs29132 SNP in the Vesicle associated membrane protein associated protein A (VAPA) gene was associated with five sun exposure variables whilst the rs650662 SNP in the <b>Opioid</b> Receptor <strong>Mu 1</strong> (OPRM1) gene was associated with three.
+GSTM1	drug	alcohol	29582627	ADH1B, ALDH2, <strong>GSTM1</strong> and GSTT1 Gene Polymorphic Frequencies among <b>Alcoholics</b> and Controls in the Arcadian Population of Central India Background: Epidemiological research has highlighted the global burden of primary liver cancer cases due to <b>alcohol</b> consumption, even in a low consumption country like India.
+GSTM1	drug	alcohol	29582627	<b>Alcohol</b> detoxification is governed by ADH1B, ALDH2, <strong>GSTM1</strong> and GSTT1 genes that encode functional enzymes which are coordinated with each other to remove highly toxic metabolites i.e.
+GSTM1	drug	alcohol	29582627	Methods: The aim of this study was to screen the arcadian population of central India in order to investigate and compare the genotype distribution and allele frequencies of <b>alcohol</b> metabolizing genes (ADH1B, ALDH2, <strong>GSTM1</strong> and GSTT1) in both <b>alcoholic</b> (N=121) and control (N=145) healthy subjects.
+GSTM1	drug	nicotine	29137427	Association of opioid receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with <b>nicotine</b> dependence.
+GSTM1	drug	opioid	29137427	Association of <b>opioid</b> receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with nicotine dependence.
+GSTM1	addiction	dependence	29137427	Association of opioid receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with nicotine <b>dependence</b>.
+GSTM1	drug	nicotine	29137427	Whether opioid receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) is associated with <b>nicotine</b> dependence is controversial.
+GSTM1	drug	opioid	29137427	Whether <b>opioid</b> receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) is associated with nicotine dependence is controversial.
+GSTM1	addiction	dependence	29137427	Whether opioid receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) is associated with nicotine <b>dependence</b> is controversial.
+GSTM1	drug	alcohol	29070014	Lack of associations of the opioid receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with <b>alcohol</b> dependence: review and meta analysis of retrospective controlled studies.
+GSTM1	drug	opioid	29070014	Lack of associations of the <b>opioid</b> receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with alcohol dependence: review and meta analysis of retrospective controlled studies.
+GSTM1	addiction	dependence	29070014	Lack of associations of the opioid receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with alcohol <b>dependence</b>: review and meta analysis of retrospective controlled studies.
+GSTM1	drug	alcohol	29070014	Studies have sought associations of the opioid receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with <b>alcohol</b> dependence, but findings are inconsistent.
+GSTM1	drug	opioid	29070014	Studies have sought associations of the <b>opioid</b> receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with alcohol dependence, but findings are inconsistent.
+GSTM1	addiction	dependence	29070014	Studies have sought associations of the opioid receptor <strong>mu 1</strong> (OPRM1) A118G polymorphism (rs1799971) with alcohol <b>dependence</b>, but findings are inconsistent.
+GSTM1	addiction	relapse	28696839	<b>Relapse</b> free times were shorter for NAT2 slow and ultra slow, GSTT1 positive and <strong>GSTM1</strong> negative cases.
+GSTM1	drug	opioid	28650467	By unbiased genome wide RNAi screening, we found that among 10 resistant ALL clones, six hits were for <b>opioid</b> receptor <strong>mu 1</strong> (oprm1), two hits were for carbonic anhydrase 1 (ca1) and another two hits were for ubiquitin conjugating enzyme E2C (ube2c).
+GSTM1	drug	nicotine	26812289	There were no significant associations between GSTT1, <strong>GSTM1</strong> and GSTT1/M1 genetic variants and the Fagerström test for ND, age at onset, <b>smoking</b> cessation or a family history of ND.
+GSTM1	drug	opioid	26792136	<b>Methadone</b> is a full agonist of the <b>opioid</b> receptor <strong>mu 1</strong> which is encoded by the OPRM1 gene.
+GSTM1	drug	nicotine	26406947	Association of epidemiological factors like gender, active/passive <b>smoking</b>, naswar addiction, residential area and family history were associated neither with <strong>GSTM1</strong> deletion nor to GSTT1 deletion in both cancers (P ≥ 0.05).
+GSTM1	addiction	addiction	26406947	Association of epidemiological factors like gender, active/passive smoking, naswar <b>addiction</b>, residential area and family history were associated neither with <strong>GSTM1</strong> deletion nor to GSTT1 deletion in both cancers (P ≥ 0.05).
+GSTM1	drug	opioid	26339899	In an exploratory analysis, emotional well being increased in a subgroup of participants with AA genotype of <b>opioid</b> receptor, <strong>mu 1</strong> (OPRM1) A118G polymorphism (p = 0.02).
+GSTM1	drug	alcohol	26042510	Association between Opioid Receptor <strong>mu 1</strong> (OPRM1) Gene Polymorphisms and Tobacco and <b>Alcohol</b> Consumption in a Spanish Population.
+GSTM1	drug	nicotine	26042510	Association between Opioid Receptor <strong>mu 1</strong> (OPRM1) Gene Polymorphisms and <b>Tobacco</b> and Alcohol Consumption in a Spanish Population.
+GSTM1	drug	opioid	26042510	Association between <b>Opioid</b> Receptor <strong>mu 1</strong> (OPRM1) Gene Polymorphisms and Tobacco and Alcohol Consumption in a Spanish Population.
+GSTM1	drug	alcohol	26042510	Our aim is to assess the influence of genetic variations in the opioid receptor <strong>mu 1</strong> on <b>alcohol</b> and tobacco consumption in a Spanish population.
+GSTM1	drug	nicotine	26042510	Our aim is to assess the influence of genetic variations in the opioid receptor <strong>mu 1</strong> on alcohol and <b>tobacco</b> consumption in a Spanish population.
+GSTM1	drug	opioid	26042510	Our aim is to assess the influence of genetic variations in the <b>opioid</b> receptor <strong>mu 1</strong> on alcohol and tobacco consumption in a Spanish population.
+GSTM1	drug	opioid	26042510	Individuals were genotyped for three polymorphisms in the <b>opioid</b> receptor <strong>mu 1</strong> (OPRM1) gene, using a TaqMan protocol.
+GSTM1	drug	opioid	26003511	Association between null alleles of <strong>GSTM1</strong> and GSTT1 and dependence to <b>heroin</b> and opium.
+GSTM1	addiction	dependence	26003511	Association between null alleles of <strong>GSTM1</strong> and GSTT1 and <b>dependence</b> to heroin and opium.
+GSTM1	drug	opioid	25744370	No <b>opioid</b> receptor, <strong>mu 1</strong> (OPRM1) gene polymorphisms, including the functional single nucleotide polymorphism (SNP) rs1799971, have been conclusively associated with <b>heroin</b>/other <b>opioid</b> addiction, despite their biological plausibility.
+GSTM1	addiction	addiction	25744370	No opioid receptor, <strong>mu 1</strong> (OPRM1) gene polymorphisms, including the functional single nucleotide polymorphism (SNP) rs1799971, have been conclusively associated with heroin/other opioid <b>addiction</b>, despite their biological plausibility.
+GSTM1	drug	amphetamine	27843993	Association between <strong>GSTM1</strong> and GSTT1 polymorphisms and susceptibility to <b>methamphetamine</b> dependence.
+GSTM1	addiction	dependence	27843993	Association between <strong>GSTM1</strong> and GSTT1 polymorphisms and susceptibility to methamphetamine <b>dependence</b>.
+GSTM1	drug	amphetamine	27843993	The aim of the present study is to investigate the association between <strong>GSTM1</strong> and GSTT1 polymorphisms and <b>methamphetamine</b> dependence.
+GSTM1	addiction	dependence	27843993	The aim of the present study is to investigate the association between <strong>GSTM1</strong> and GSTT1 polymorphisms and methamphetamine <b>dependence</b>.
+GSTM1	drug	amphetamine	27843993	Neither <strong>GSTM1</strong> (OR=0.92, 95% CI: 0.52 1.61, P=0.771) nor GSTT1 (OR=0.71, 95% CI: 0.33 1.54, P=0.381) null genotypes were significantly associated with risk of <b>methamphetamine</b> dependence.
+GSTM1	addiction	dependence	27843993	Neither <strong>GSTM1</strong> (OR=0.92, 95% CI: 0.52 1.61, P=0.771) nor GSTT1 (OR=0.71, 95% CI: 0.33 1.54, P=0.381) null genotypes were significantly associated with risk of methamphetamine <b>dependence</b>.
+GSTM1	drug	amphetamine	27843993	It should be noted that although there was no association between the <strong>GSTM1</strong> null genotype and risk of <b>methamphetamine</b> dependence, in both genders, there was significant interaction between gender and <strong>GSTM1</strong> polymorphism (P=0.029).
+GSTM1	addiction	dependence	27843993	It should be noted that although there was no association between the <strong>GSTM1</strong> null genotype and risk of methamphetamine <b>dependence</b>, in both genders, there was significant interaction between gender and <strong>GSTM1</strong> polymorphism (P=0.029).
+GSTM1	drug	amphetamine	27843993	The combination genotypes of the <strong>GSTM1</strong> and GSTT1 polymorphisms revealed that the genotypes of these two polymorphisms had no additive effect in relation to the susceptibility to <b>methamphetamine</b> dependence.
+GSTM1	addiction	dependence	27843993	The combination genotypes of the <strong>GSTM1</strong> and GSTT1 polymorphisms revealed that the genotypes of these two polymorphisms had no additive effect in relation to the susceptibility to methamphetamine <b>dependence</b>.
+GSTM1	drug	amphetamine	27843993	The present study revealed that genetic polymorphisms of GSTT1 and <strong>GSTM1</strong> are not risk factors for <b>methamphetamine</b> dependence.
+GSTM1	addiction	dependence	27843993	The present study revealed that genetic polymorphisms of GSTT1 and <strong>GSTM1</strong> are not risk factors for methamphetamine <b>dependence</b>.
+GSTM1	drug	nicotine	25266401	It is a complex behaviour that involves the brain reward system and is regulated by genetic and environmental factors, such as the opioid receptor <strong>mu 1</strong> gene (OPRM1) and prenatal exposure to maternal cigarette <b>smoking</b> (PEMCS).
+GSTM1	drug	opioid	25266401	It is a complex behaviour that involves the brain reward system and is regulated by genetic and environmental factors, such as the <b>opioid</b> receptor <strong>mu 1</strong> gene (OPRM1) and prenatal exposure to maternal cigarette smoking (PEMCS).
+GSTM1	addiction	reward	25266401	It is a complex behaviour that involves the brain <b>reward</b> system and is regulated by genetic and environmental factors, such as the opioid receptor <strong>mu 1</strong> gene (OPRM1) and prenatal exposure to maternal cigarette smoking (PEMCS).
+GSTM1	drug	nicotine	24637631	The primary hypothesis of this study was to identify whether the polymorphisms of two glutathione S transferase enzymes (<strong>GSTM1</strong> and GSTT1 genes) predict an increased risk of mood and anxiety disorders in <b>smokers</b> with <b>nicotine</b> dependence.
+GSTM1	addiction	dependence	24637631	The primary hypothesis of this study was to identify whether the polymorphisms of two glutathione S transferase enzymes (<strong>GSTM1</strong> and GSTT1 genes) predict an increased risk of mood and anxiety disorders in smokers with nicotine <b>dependence</b>.
+GSTM1	drug	nicotine	24637631	Compared with individuals who had both <strong>GSTM1</strong> and GSTT1 genes, a higher frequency of at least one deletion of the <strong>GSTM1</strong> and GSTT1 genes was identified in anxious <b>smokers</b> [odds ratio (OR)=2.21, 95% confidence interval (CI)=1.05 4.65, P=0.034], but there was no association with bipolar and unipolar depression (P=0.943).
+GSTM1	drug	nicotine	24637631	This study suggests that at least one deletion of the <strong>GSTM1</strong> and GSTT1 genes represents a risk factor for anxious <b>smokers</b>.
+GSTM1	drug	opioid	23337944	<b>Opioid</b> receptor <strong>mu 1</strong> gene, fat intake and obesity in adolescence.
+GSTM1	drug	alcohol	22545783	The level of gluathione S transferase mu isoform (<strong>GSTM1</strong>) increased after chronic <b>ethanol</b> but was lower after chronic <b>ethanol</b> binge compared to chronic <b>ethanol</b> treatment.
+GSTM1	addiction	intoxication	22545783	The level of gluathione S transferase mu isoform (<strong>GSTM1</strong>) increased after chronic ethanol but was lower after chronic ethanol <b>binge</b> compared to chronic ethanol treatment.
+GSTM1	drug	alcohol	22143634	The opioid receptor <strong>mu 1</strong> (OPRM1) gene may play a role in both PTSD and <b>alcohol</b> use.
+GSTM1	drug	opioid	22143634	The <b>opioid</b> receptor <strong>mu 1</strong> (OPRM1) gene may play a role in both PTSD and alcohol use.
+GSTM1	drug	alcohol	21507127	The polymorphism of opioid receptor <strong>mu 1</strong> gene is of interest because it alters the treatment effects of <b>naltrexone</b>.
+GSTM1	drug	opioid	21507127	The polymorphism of <b>opioid</b> receptor <strong>mu 1</strong> gene is of interest because it alters the treatment effects of naltrexone.
+GSTM1	drug	alcohol	21223303	An integrative analysis including other <b>alcohol</b> studies suggested several top candidates for functional validation, including Mt2, <strong>Gstm1</strong>, Scn4b, Prkcz, and Park7.
+GSTM1	drug	amphetamine	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, <strong>GSTM1</strong>, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with <b>METH</b> psychosis.
+GSTM1	addiction	dependence	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, <strong>GSTM1</strong>, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.
+GSTM1	drug	opioid	18181266	The opioidergic hypothesis suggests an association between genetic variations at the <b>opioid</b> receptor <strong>mu 1</strong> (OPRM1) gene locus and opiate addiction.
+GSTM1	addiction	addiction	18181266	The opioidergic hypothesis suggests an association between genetic variations at the opioid receptor <strong>mu 1</strong> (OPRM1) gene locus and opiate <b>addiction</b>.
+GSTM1	drug	alcohol	16940154	Microarray analysis from medial prefrontal cortex (mPFC), a key brain region for drug reward, indicated increased expression of glutathione S transferases of the alpha (Gsta4) and mu (<strong>Gstm1</strong> 5) classes in <b>ethanol</b> preferring AA rats compared with nonpreferring ANA rats.
+GSTM1	addiction	reward	16940154	Microarray analysis from medial prefrontal cortex (mPFC), a key brain region for drug <b>reward</b>, indicated increased expression of glutathione S transferases of the alpha (Gsta4) and mu (<strong>Gstm1</strong> 5) classes in ethanol preferring AA rats compared with nonpreferring ANA rats.
+GSTM1	drug	nicotine	16030123	Risks were decreased in subjects with > or =1 inactive <strong>GSTM1</strong> alleles (OR, 0.6; 95% CI, 0.4 0.9); and the association was independent of <b>smoking</b> status (P interaction = 0.59).
+GSTM1	drug	nicotine	16030123	In summary, this is the first study to report associations between colorectal adenomas and <strong>GSTM1</strong> wild type and GSTT1 null allele among <b>smokers</b>.
+GSTM1	drug	alcohol	12960511	Association analyses between polymorphisms of the phase II detoxification enzymes (<strong>GSTM1</strong>, NQO1, NQO2) and <b>alcohol</b> withdrawal symptoms.
+GSTM1	addiction	withdrawal	12960511	Association analyses between polymorphisms of the phase II detoxification enzymes (<strong>GSTM1</strong>, NQO1, NQO2) and alcohol <b>withdrawal</b> symptoms.
+GSTM1	drug	alcohol	12960511	In this study, we investigated a possible association between polymorphisms of the <strong>GSTM1</strong>, NQO1, and NQO2 genes and <b>alcohol</b> withdrawal symptoms such as delirium tremens, hallucination, and seizure.
+GSTM1	addiction	withdrawal	12960511	In this study, we investigated a possible association between polymorphisms of the <strong>GSTM1</strong>, NQO1, and NQO2 genes and alcohol <b>withdrawal</b> symptoms such as delirium tremens, hallucination, and seizure.
+GSTM1	drug	alcohol	12960511	Moreover, <strong>GSTM1</strong> gene deletion and missense mutation (Pro187Ser) of the NQO1 gene showed no significant association with <b>alcohol</b> withdrawal symptoms.
+GSTM1	addiction	withdrawal	12960511	Moreover, <strong>GSTM1</strong> gene deletion and missense mutation (Pro187Ser) of the NQO1 gene showed no significant association with alcohol <b>withdrawal</b> symptoms.
+GSTM1	drug	nicotine	12507920	CYP1A1 and <strong>GSTM1</strong> genotypes affect benzo[a]pyrene DNA adducts in <b>smokers</b>' lung: comparison with aromatic/hydrophobic adduct formation.
+GSTM1	drug	nicotine	12507920	In this review, we summarize the published data on modulation of (+) anti BPDE DNA adduct levels in <b>smokers</b>' lungs by CYP1A1*2 genotypes alone or in combination with <strong>GSTM1</strong> polymorphism and compare these results with those reported for aromatic/hydrophobic (bulky) DNA adducts.
+GSTM1	addiction	dependence	12507920	In contrast, a clear <b>dependence</b> of (+) anti BPDE DNA adduct levels was found as a function of the CYP1A1 and <strong>GSTM1</strong> genotypes: In lung parenchyma, this adduct was more pronounced in persons with the <strong>GSTM1</strong>*0 genotype, and CYP1A1*2 <strong>GSTM1</strong>*0 carriers had higher (+) anti BPDE DNA adduct levels than those with CYP1A1*1/*1 <strong>GSTM1</strong>*0.
+GSTM1	drug	nicotine	11815259	<b>Smoking</b> and <strong>GSTM1</strong> genotype were significant predictors for log transformed 1 OHPG by multiple regression analysis (overall model R(2)=0.565, P<0.001), whereas <b>smoking</b> was the only significant predictor for log transformed aromatic DNA adducts (overall model R(2)=0.249, P=0.201).
+GSTM1	drug	nicotine	11815259	Our results suggest that the significant increase in urinary 1 OHPG in the exposed workers is due to higher prevalence of <b>smokers</b> among them, and that the association between urinary PAH metabolites and aromatic DNA adducts in workers of industrial waste handling may be modulated by <strong>GSTM1</strong> genotype.
+GSTM1	drug	opioid	11733709	<b>Opioid</b> <strong>mu 1</strong> receptor binding increased significantly in the cingulate cortex, hippocampus, locus coeruleus and accumbens shell.
+GSTM1	drug	nicotine	23889309	<b>Smoking</b> increased adduct levels only in occupationally exposed workers with the <strong>GSTM1</strong> deletion (<strong>GSTM1</strong> null) (p = 0:034).
+GSTM1	drug	nicotine	23889309	The dependence of BPDE SA adduct levels and frequency on the CYP1A1 *1/*1 genotype was most pronounced in <strong>GSTM1</strong> deficient <b>smokers</b>.
+GSTM1	addiction	dependence	23889309	The <b>dependence</b> of BPDE SA adduct levels and frequency on the CYP1A1 *1/*1 genotype was most pronounced in <strong>GSTM1</strong> deficient smokers.
+GSTM1	drug	nicotine	10667460	Some CYP1A1/<strong>GSTM1</strong> 0/0 genotype combinations seem to predispose the lung, esophagus, and oral cavity of <b>smokers</b> to an even higher risk for cancer or DNA damage, requiring, however, confirmation.
+GSTM1	drug	nicotine	10026994	BPDE DNA adduct levels in bronchial tissue of <b>smokers</b> with high pulmonary CYP1A1 inducibility (by immunohistochemistry) and <strong>GSTM1</strong> inactive were approximately 100 fold higher than in subjects with an active <strong>GSTM1</strong> at similar <b>smoking</b> dose.
+GSTM1	drug	nicotine	10026994	Further genetic analyses confirmed that the combination of CYP1A1 homozygous mutants and <strong>GSTM1</strong> inactive leads to high levels of BPDE DNA adducts in human lung of <b>smokers</b> and white blood cells of PAH exposed coke oven workers.
+GSTM1	drug	nicotine	9921921	After grouping by the <b>smoking</b> status, among <b>smokers</b> in both cancer groups (62.1% in lung cancer and 71.4% in the bladder cancer group, respectively) there were statistically significantly (p < 0.05) increased frequencies of the <strong>GSTM1</strong> deletion genotype as compared to the control group (49.6%).
+GSTM1	drug	nicotine	9921921	<b>Smokers</b> with absence of the <strong>GSTM1</strong> gene were at an approximately 1.7 fold higher risk for lung cancer (odds ratio  OR = 1.67, 95% confidence interval  CI 95% = 1.0 2.7, p = 0.04) and an approximately 2.5 fold higher risk for bladder cancer (OR = 2.54, CI 95% = 1.2 5.5, p = 0.02).
+GSTM1	addiction	dependence	9921921	The findings suggest that the <strong>GSTM1</strong> null genotype may be associated with susceptibility to lung and urinary bladder cancer in <b>dependence</b> on the exposure to carcinogens in cigarette smoke and that the GSTT1 null genotype is not a critical factor in mediating the risk of lung cancer, but may be associated with an increased susceptibility to bladder cancer.
+GSTM1	drug	alcohol	9394782	administration of the opioid antagonist <b>naltrexone</b> or the <strong>mu 1</strong> selective antagonist naloxonazine blocked conditioned alterations of immune status, indicating that activity at mu opioid receptors is involved in conditioned immunomodulation.
+GSTM1	drug	opioid	9394782	administration of the <b>opioid</b> antagonist naltrexone or the <strong>mu 1</strong> selective antagonist naloxonazine blocked conditioned alterations of immune status, indicating that activity at mu <b>opioid</b> receptors is involved in conditioned immunomodulation.
+GSTM1	drug	opioid	9394782	Collectively, the results of this study indicate that the alterations of immune status produced by an aversive conditioned stimulus require activity at mu <b>opioid</b> receptors, possibly <strong>mu 1</strong>, within the central nervous system.
+GSTM1	addiction	aversion	9394782	Collectively, the results of this study indicate that the alterations of immune status produced by an <b>aversive</b> conditioned stimulus require activity at mu opioid receptors, possibly <strong>mu 1</strong>, within the central nervous system.
+GSTM1	drug	opioid	9264103	Involvement of <b>opioid</b> <strong>mu 1</strong> receptors in <b>morphine</b> induced conditioned place preference in rats.
+GSTM1	drug	opioid	9264103	The main purpose of this study was to evaluate the role of <strong>mu 1</strong> <b>opioid</b> receptors in <b>morphine</b> reward.
+GSTM1	addiction	reward	9264103	The main purpose of this study was to evaluate the role of <strong>mu 1</strong> opioid receptors in morphine <b>reward</b>.
+GSTM1	drug	opioid	9264103	Therefore, we studied the ability of a <strong>mu 1</strong> selective antagonist, naloxonazine [15 mg/kg intraperitoneally (IP)], to antagonize the conditioned place preference (CPP) induced by <b>morphine</b> [3 mg/kg subcutaneously (SC)].
+GSTM1	addiction	reward	9264103	Therefore, we studied the ability of a <strong>mu 1</strong> selective antagonist, naloxonazine [15 mg/kg intraperitoneally (IP)], to antagonize the conditioned place preference (<b>CPP</b>) induced by morphine [3 mg/kg subcutaneously (SC)].
+GSTM1	drug	opioid	9264103	These results suggest an active role for <strong>mu 1</strong> <b>opioid</b> receptors in <b>morphine</b> reward, whereas <b>morphine</b> induced hyperthermia does not appear to be mediated by <strong>mu 1</strong> <b>opioid</b> receptors.
+GSTM1	addiction	reward	9264103	These results suggest an active role for <strong>mu 1</strong> opioid receptors in morphine <b>reward</b>, whereas morphine induced hyperthermia does not appear to be mediated by <strong>mu 1</strong> opioid receptors.
+GSTM1	drug	opioid	9160346	From behavioral, biochemical and molecular biological studies, it is suggested so far that development of physical dependence on <b>morphine</b> results predominantly from an activation of <strong>mu 1</strong> and mu 2 <b>opioid</b> receptors which causes functional changes in Gi/o, adenylate cyclase, protein kinases A and C, beta adrenoceptor and NMDA receptor in the locus coeruleus.
+GSTM1	addiction	dependence	9160346	From behavioral, biochemical and molecular biological studies, it is suggested so far that development of physical <b>dependence</b> on morphine results predominantly from an activation of <strong>mu 1</strong> and mu 2 opioid receptors which causes functional changes in Gi/o, adenylate cyclase, protein kinases A and C, beta adrenoceptor and NMDA receptor in the locus coeruleus.
+GSTM1	drug	opioid	8981054	The dermorphin family also includes <strong>mu 1</strong> <b>opioid</b> receptor selective agonists that produce intense <b>opioid</b> analgesia, but stimulate pulmonary ventilation.
+GSTM1	addiction	dependence	7543377	The age <b>dependence</b> was higher in the <strong>GSTM1</strong> negative slow acetylators (3.1%/year) as compared to the three other genotype combinations (2.4 2.5%/year).
+GSTM1	drug	opioid	7712029	The dose response curves of [Lys7]dermorphin antinociception were shifted to the right by the pretreatment with <b>naloxone</b> (0.1 mg kg 1, s.c.) or with the <strong>mu 1</strong> selective antagonist, naloxonazine (10 mg kg 1, i.v.
+GSTM1	drug	opioid	7861658	Effects of highly selective delta <b>opioid</b> receptor antagonists on the <b>morphine</b> induced place preference in ddY and <strong>mu 1</strong> <b>opioid</b> receptor deficient CXBK mice were investigated.
+GSTM1	drug	opioid	7861658	On the other hand, in <strong>mu 1</strong> <b>opioid</b> receptor deficient CXBK mice, pretreatment with these selective delta <b>opioid</b> receptor antagonists did not affect the <b>morphine</b> induced place preference, although pretreatment with beta funaltrexamine (beta FNA: a selective mu <b>opioid</b> receptor antagonist) significantly inhibited the <b>morphine</b> induced place preference.
+GSTM1	drug	opioid	8069669	At the <b>opioid</b> receptor subtype, laudanosine lowered radiolabeled <b>opioid</b> binding at the <strong>mu 1</strong>, mu 2, delta, kappa 1, and kappa 3 receptors with Ki values of 2.7, 13, 5.5, 21, and 24 microM, respectively, concentrations seen clinically in blood and approaching those measured in cerebrospinal fluid.
+GSTM1	drug	opioid	8069669	These results suggest an interaction between laudanosine and the low affinity GABA receptor, as well as <b>opioid</b> <strong>mu 1</strong> and mu 2 receptors.
+GSTM1	drug	opioid	8289581	<b>Opioid</b> mu receptor subtypes (possibly <strong>mu 1</strong> and mu 2) revealed by <b>morphine</b> induced antinociception vs endothelin 1 in recombinant inbred CXBK mice.
+GSTM1	drug	opioid	8383571	The role of mu <b>opioid</b> receptor subtypes, <strong>mu 1</strong> and mu 2, in <b>morphine</b> conditioned place preference was examined using ddY and <strong>mu 1</strong> <b>opioid</b> receptor deficient CXBK mice.
+GSTM1	drug	opioid	8383571	Under this condition, the influence of pretreatment with the selective <strong>mu 1</strong> <b>opioid</b> receptor antagonist naloxonazine on <b>morphine</b> induced place preference was investigated in ddY mice.
+GSTM1	drug	opioid	8383571	Although pretreatment with the selective <strong>mu 1</strong> antagonist naloxonazine (35 mg/kg, s.c.) did not modify the <b>morphine</b> induced place preference, pretreatment with the selective mu antagonist beta funaltrexamine (beta FNA 10 mg/kg, s.c.) eliminated the appetitive effect of <b>morphine</b>.
+CYP1A1	drug	nicotine	31616461	Results: We identified 23 CpGs (genome wide p level: 1.06 × 10 7) that were associated with maternal <b>smoking</b> during pregnancy, including associated genes AHRR (cancer development), FTO (obesity), CNTNAP2 (developmental processes), <strong>CYP1A1</strong> (detoxification), MYO1G (cell signalling), and FRMD4A (<b>nicotine</b> dependence).
+CYP1A1	addiction	dependence	31616461	Results: We identified 23 CpGs (genome wide p level: 1.06 × 10 7) that were associated with maternal smoking during pregnancy, including associated genes AHRR (cancer development), FTO (obesity), CNTNAP2 (developmental processes), <strong>CYP1A1</strong> (detoxification), MYO1G (cell signalling), and FRMD4A (nicotine <b>dependence</b>).
+CYP1A1	drug	nicotine	31616461	Results: We identified 23 CpGs (genome wide p level: 1.06 × 10 7) that were associated with maternal <b>smoking</b> during pregnancy, including associated genes <strong>AHRR</strong> (cancer development), FTO (obesity), CNTNAP2 (developmental processes), <strong>CYP1A1</strong> (detoxification), MYO1G (cell signalling), and FRMD4A (<b>nicotine</b> dependence).
+CYP1A1	addiction	dependence	31616461	Results: We identified 23 CpGs (genome wide p level: 1.06 × 10 7) that were associated with maternal smoking during pregnancy, including associated genes <strong>AHRR</strong> (cancer development), FTO (obesity), CNTNAP2 (developmental processes), <strong>CYP1A1</strong> (detoxification), MYO1G (cell signalling), and FRMD4A (nicotine <b>dependence</b>).
+CYP1A1	drug	alcohol	29886839	<b>Ethanol</b> decreased <strong>CYP1A1</strong> mRNA expression relative to control (P=0.02), and combined <b>ethanol</b>+NNK exposures decreased the expression of <strong>CYP1A1</strong> (P=0.01) and CYP2C6 (P=0.03).
+CYP1A1	drug	alcohol	29404485	The number of EVs and the amounts of EV CYP2E1, CYP2A, <strong>CYP1A1</strong>/2, and CYP4B proteins were markedly elevated in both patients with <b>alcoholism</b> and <b>alcohol</b> exposed rats and mice.
+CYP1A1	drug	nicotine	28816414	Prior epigenome wide association studies indicate that methylation status at cg05575921, a CpG residue located in the aryl hydrocarbon receptor repressor (<strong>AHRR</strong>) gene, may be a robust indicator of <b>smoking</b> status in individuals with as little as half of a pack year of <b>smoking</b>.
+CYP1A1	drug	nicotine	26356606	<b>Smoking</b>, Methylation at <strong>AHRR</strong>, and Recidivism Risk in a Community Correction Sample of Individuals at High Risk for Recidivism.
+CYP1A1	drug	nicotine	25233467	We evaluated 23 single nucleotide polymorphisms (SNPs) in the five nicotinic receptor related genes (CHRNB3, CHRNA6, and CHRNA5/A3/B4) previously reported to be associated with lung cancer risk and <b>smoking</b> behavior and 14 SNPs in the four 'control' genes (TERT, CLPTM1L, <strong>CYP1A1</strong>, and TP53), which were not reported in the <b>smoking</b> GWA studies.
+CYP1A1	drug	nicotine	25052559	Several statistically significant interactions were observed between <b>smoking</b> and genetic variants (CYP1A2 1548C>T, <strong>CYP1A1</strong> 3801T>C, CYP1B1 4326G>C, NAT1 c. 85 1014T>A, UGT1A7 W208R 622T>C, SOD2 c.47T>C, GSTT1 deletion).
+CYP1A1	drug	alcohol	24663500	The expression and activity of <strong>CYP1A1</strong>, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3 methylcholanthrene (3 MC), cyclophosphamide (CPA), <b>ethanol</b> and known neurotoxicant  monocrotophos (MCP), a widely used organophosphorous pesticide.
+CYP1A1	drug	nicotine	23840148	Combination of the <strong>CYP1A1</strong> 2C and NQO1 609CC genotypes was associated with a decreased risk of colorectal adenomas regardless of <b>smoking</b> status.
+CYP1A1	addiction	sensitization	19789301	Treatment with 17 AAG, an Hsp90 inhibitor, caused a marked decrease in levels of AhR; inhibited UVR , aTRP , and FICZ mediated induction of <strong>CYP1A1</strong> and CYP1B1; and blocked the <b>sensitization</b> of HaCaT cells to B[a]P induced DNA adduct formation.
+CYP1A1	drug	nicotine	19563927	Cytochrome P450 1A1 (<strong>CYP1A1</strong>) is a key enzyme that metabolizes the cigarette toxin relevant to <b>smoking</b> induced atherogenesis.
+CYP1A1	drug	nicotine	19563927	This case control study examined the role of <strong>CYP1A1</strong> polymorphisms, <strong>CYP1A1</strong> 2A (T6235C) and <strong>CYP1A1</strong> 2C (A4889G), in susceptibility to <b>smoking</b> related CAD.
+CYP1A1	drug	nicotine	19563927	The beneficial effect of the <strong>CYP1A1</strong> 2C G/G genotype was even greater for never <b>smokers</b> than those carrying the A/A genotype (OR=0.23, 95% CI=0.08 0.71).
+CYP1A1	drug	nicotine	19563927	Our findings suggest that the <strong>CYP1A1</strong> 2C G/G genotype may reduce the risk for CAD in the Taiwanese population and this effect appeared to be more pronounced among never <b>smokers</b>.
+CYP1A1	addiction	dependence	18569604	Evaluation of time <b>dependence</b> and interindividual differences in benzo[a]pyrene mediated <strong>CYP1A1</strong> induction and genotoxicity in porcine urinary bladder cell cultures.
+CYP1A1	drug	alcohol	17513011	The aims of this study were to compare the antibacterial efficacy of handrubbing with an <b>alcoholic</b> rinse (<strong>AHRR</strong>) and two different <b>alcoholic</b> gels (AHRG) in reducing hand contamination under practical use conditions.
+CYP1A1	drug	nicotine	17053541	Interaction between <strong>CYP1A1</strong> T3801C and AHR G1661A polymorphisms according to <b>smoking</b> status on blood pressure in the Stanislas cohort.
+CYP1A1	drug	nicotine	17053541	<strong>CYP1A1</strong>, one of the key enzymes in detoxifying toxic components produced during cigarette <b>smoking</b>, is regulated by aromatic hydrocarbon receptor (AHR).
+CYP1A1	drug	nicotine	17053541	To investigate the genetic influence of <strong>CYP1A1</strong> T3801C and AHR G1661A polymorphisms on BP in relation to <b>tobacco</b> consumption.
+CYP1A1	drug	nicotine	17053541	However, systolic and diastolic blood pressures differed significantly according to <strong>CYP1A1</strong> T3801C genotype between ex <b>smokers</b> and <b>smokers</b>.
+CYP1A1	drug	nicotine	12507920	<strong>CYP1A1</strong> and GSTM1 genotypes affect benzo[a]pyrene DNA adducts in <b>smokers</b>' lung: comparison with aromatic/hydrophobic adduct formation.
+CYP1A1	drug	nicotine	12507920	In this review, we summarize the published data on modulation of (+) anti BPDE DNA adduct levels in <b>smokers</b>' lungs by <strong>CYP1A1</strong>*2 genotypes alone or in combination with GSTM1 polymorphism and compare these results with those reported for aromatic/hydrophobic (bulky) DNA adducts.
+CYP1A1	addiction	dependence	12507920	In contrast, a clear <b>dependence</b> of (+) anti BPDE DNA adduct levels was found as a function of the <strong>CYP1A1</strong> and GSTM1 genotypes: In lung parenchyma, this adduct was more pronounced in persons with the GSTM1*0 genotype, and <strong>CYP1A1</strong>*2 GSTM1*0 carriers had higher (+) anti BPDE DNA adduct levels than those with <strong>CYP1A1</strong>*1/*1 GSTM1*0.
+CYP1A1	drug	nicotine	23889309	<b>Smokers</b> from the exposed group had higher adduct levels when they were <strong>CYP1A1</strong> *1/*1 wild type rather than heterozygous and homozygous for the variant alleles (<strong>CYP1A1</strong> *1/*2 plus *2/*2) (p = 0:01).
+CYP1A1	drug	nicotine	23889309	The dependence of BPDE SA adduct levels and frequency on the <strong>CYP1A1</strong> *1/*1 genotype was most pronounced in GSTM1 deficient <b>smokers</b>.
+CYP1A1	addiction	dependence	23889309	The <b>dependence</b> of BPDE SA adduct levels and frequency on the <strong>CYP1A1</strong> *1/*1 genotype was most pronounced in GSTM1 deficient smokers.
+CYP1A1	drug	nicotine	10667460	We summarize here the results of case control studies published since 1990 on the effects of genetic variants of <strong>CYP1A1</strong>, 1A2, 1B1, 2A6, 2D6, 2E1, 2C9, 2C19, 17, and 19 alone or in combination with detoxifying enzymes as modifiers of the risk for <b>tobacco</b> related cancers.
+CYP1A1	drug	nicotine	10667460	Some <strong>CYP1A1</strong>/GSTM1 0/0 genotype combinations seem to predispose the lung, esophagus, and oral cavity of <b>smokers</b> to an even higher risk for cancer or DNA damage, requiring, however, confirmation.
+CYP1A1	drug	nicotine	10026994	BPDE DNA adduct levels in bronchial tissue of <b>smokers</b> with high pulmonary <strong>CYP1A1</strong> inducibility (by immunohistochemistry) and GSTM1 inactive were approximately 100 fold higher than in subjects with an active GSTM1 at similar <b>smoking</b> dose.
+CYP1A1	drug	nicotine	10026994	Further genetic analyses confirmed that the combination of <strong>CYP1A1</strong> homozygous mutants and GSTM1 inactive leads to high levels of BPDE DNA adducts in human lung of <b>smokers</b> and white blood cells of PAH exposed coke oven workers.
+CYP1A1	drug	alcohol	7786308	Both proteins were induced significantly by chronic <b>ethanol</b> administration (<strong>CYP1A1</strong>, 1.9 fold; CYP2B1, 4 fold).
+COMETT	drug	nicotine	31127298	Each of the fourteen TCORS, and two other NIH funded research programs, the Center for the Evaluation of <b>Nicotine</b> in Cigarettes (CENIC) and the Consortium on Methods Evaluating <b>Tobacco</b> (<strong>COMET</strong>), pursued specific research themes relevant to FDA's priorities.
+COMETT	drug	nicotine	31127298	The <b>Tobacco</b> Centers of Regulatory Science, CENIC, and <strong>COMET</strong> have had a high output of scientific articles since 2013.
+COMETT	drug	amphetamine	28138562	Pulmonary artery endothelial cells (PAECs) from <b>AMPH</b> associated PAH patients show DNA damage as judged by γH2AX foci and DNA <strong>comet</strong> tails.
+COMETT	drug	amphetamine	25867833	In this study, we examined the effect of <b>METH</b> on DNA damage in vivo using the single cell gel electrophoresis assay (<strong>comet</strong> assay) under two different conditions.
+COMETT	drug	cocaine	25264678	We assessed genome instability by means of the <strong>comet</strong> assay and the cytokinesis block micronucleus technique in crack <b>cocaine</b> users at the time of admission to a rehabilitation clinic and at two times after the beginning of withdrawal.
+COMETT	addiction	withdrawal	25264678	We assessed genome instability by means of the <strong>comet</strong> assay and the cytokinesis block micronucleus technique in crack cocaine users at the time of admission to a rehabilitation clinic and at two times after the beginning of <b>withdrawal</b>.
+COMETT	addiction	aversion	23271343	<b>CTA</b>, MN, and <strong>comet</strong> assay frequency were significantly greater in polyvinyl chloride (PVC) factory workers (p < 0.05) with long duration work.
+COMETT	addiction	aversion	23271343	<b>CTA</b>, MN, and <strong>comet</strong> assay values were found to be increased with age in exposed subjects as well as in controls, with exposed subjects showing a statistically greater degree.
+COMETT	drug	cocaine	21071548	The purpose of the present study was to characterize the genetic damage induced by paradoxical sleep deprivation (PSD) in combination with <b>cocaine</b> or ecstasy (3,4 methylenedioxymethamphetamine; MDMA) in multiple organs of male mice using the single cell gel (<strong>comet</strong>) assay.
+COMETT	drug	psychedelics	21071548	The purpose of the present study was to characterize the genetic damage induced by paradoxical sleep deprivation (PSD) in combination with cocaine or <b>ecstasy</b> (3,4 <b>methylenedioxymethamphetamine</b>; <b>MDMA</b>) in multiple organs of male mice using the single cell gel (<strong>comet</strong>) assay.
+COMETT	drug	alcohol	20958327	Oxidative DNA damage, possible metabolic pathways of <b>ethanol</b> in human peripheral lymphocytes, and the repair system involved in the DNA auto repair process were examined by <strong>comet</strong> assay, flow cytometry, time of flight mass spectrometry (TOF MS), reverse transcription polymerase chain reaction (RT PCR), and western blotting.
+COMETT	drug	alcohol	18684230	The present study, by the use of single cell gel electrophoresis (<strong>comet</strong> assay), investigated the potential genotoxicity of acute and long term <b>ethanol</b> administration in mouse peripheral leucocytes.
+COMETT	drug	psychedelics	17762515	In particular, we examined whether administration of <b>MDMA</b>, at doses producing hippocampal hyperexcitability also produces rearrangements of DNA strands measured by the <strong>comet</strong> assay.
+COMETT	drug	nicotine	17610937	<strong>Comet</strong> assay was performed for 18 <b>smokers</b>, 143 ETS exposed subjects and 130 non <b>smokers</b> to measure DNA damage.
+COMETT	drug	nicotine	17610937	The results of this study suggest that <strong>comet</strong> assay are reliable biomarkers for monitoring pregnant women exposed to <b>tobacco</b> smoke and indicate fetal growth effects from environmental exposure to <b>tobacco</b> smoke.
+COMETT	drug	alcohol	17567031	By using the single cell gel electrophoresis (<strong>comet</strong> assay), a simple and sensitive technique for genotoxicity studies, the potential genotoxicity of acute and chronic <b>ethanol</b> administration in the different brain regions was investigated.
+COMETT	drug	alcohol	16705883	Limitations and critical features presently linked to <strong>comet</strong> test applications, with particular regard to the biomonitoring of individuals exposed to genotoxic agents, include: lack of sensitivity with respect to aneugens (agents inducing numerical chromosomal aberrations), possible underestimation of genotoxic potency of agents with mixed action mechanisms, sensitivity depending on the genotoxic agent itself, dependence an biological substrate with regard to the influence of cytotoxicity on the assay results, influence of age, tobacco smoke, <b>alcohol</b> and drug consumption, diet, kinetics of DNA adducts and DNA repair mechanisms.
+COMETT	drug	nicotine	16705883	Limitations and critical features presently linked to <strong>comet</strong> test applications, with particular regard to the biomonitoring of individuals exposed to genotoxic agents, include: lack of sensitivity with respect to aneugens (agents inducing numerical chromosomal aberrations), possible underestimation of genotoxic potency of agents with mixed action mechanisms, sensitivity depending on the genotoxic agent itself, dependence an biological substrate with regard to the influence of cytotoxicity on the assay results, influence of age, <b>tobacco</b> smoke, alcohol and drug consumption, diet, kinetics of DNA adducts and DNA repair mechanisms.
+COMETT	addiction	dependence	16705883	Limitations and critical features presently linked to <strong>comet</strong> test applications, with particular regard to the biomonitoring of individuals exposed to genotoxic agents, include: lack of sensitivity with respect to aneugens (agents inducing numerical chromosomal aberrations), possible underestimation of genotoxic potency of agents with mixed action mechanisms, sensitivity depending on the genotoxic agent itself, <b>dependence</b> an biological substrate with regard to the influence of cytotoxicity on the assay results, influence of age, tobacco smoke, alcohol and drug consumption, diet, kinetics of DNA adducts and DNA repair mechanisms.
+COMETT	drug	nicotine	15858221	To assess the genotoxicity of <b>nicotine</b>, the DNA damaging effect on human lymphocytes and target cells from lymphatic tissue of the palatine tonsils from 10 healthy patients was tested with the alkaline single cell microgel electrophoresis (<strong>Comet</strong>) assay.
+COMETT	drug	alcohol	14700736	Exposure of canine cerebral vascular smooth muscle cells (VSMCs) to <b>ethanol</b> (10, 25 and 100 mM) for 1, 3 and 5 days induced apoptosis with its typical characteristics of nuclear shrinkage, condensation, and DNA breakage as well as formation of apoptotic bodies observed by fluorescence staining, terminal deoxyribonucleotidyl transferase mediated dUTP nick end labeling and <strong>comet</strong> assays.
+COL11A2	drug	cocaine	32641757	Interestingly, acute or chronic <b>cocaine</b> exposure downregulated miR 124 levels concomitant with upregulation of <strong>PARP</strong> 1 protein in dopaminergic like neuronal cells in culture.
+COL11A2	drug	cocaine	32641757	Collectively, these studies identify <strong>Parp</strong> 1 as a direct target of miR 124 in neuronal cells, establish miR 124 as a <b>cocaine</b> regulated miRNA in the mouse NAc, and highlight a novel pathway underlying the molecular effects of <b>cocaine</b>.
+COL11A2	drug	amphetamine	32086884	In addition, to explore <b>METH</b> induced neurotoxicity, we measured the level of Parkin and the phosphorylation levels of α syn, Polo like kinase 2 (PLK2), the proteasome activity marker CD3δ, and the apoptosis related proteins Caspase 3 and <strong>PARP</strong>.
+COL11A2	drug	alcohol	31251945	<strong>PARP</strong> inhibition in vivo blocks <b>alcohol</b> induced brain neurodegeneration and neuroinflammatory cytosolic phospholipase A2 elevations.
+COL11A2	drug	alcohol	31251945	Concurrent with neurodegeneration, <b>alcohol</b> elevates poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1) and cytosolic phospholipase A2 (cPLA2) levels.
+COL11A2	drug	alcohol	31251945	Inhibitors of <strong>PARP</strong> exert in vitro neuroprotection while suppressing cPLA2 elevations in <b>alcohol</b> treated HC ECX slice cultures.
+COL11A2	drug	alcohol	31251945	Here, we examined in vivo neuroprotection and cPLA2 suppression by the <strong>PARP</strong> inhibitor, veliparib, in a recognized adult rat model of <b>alcohol</b> binging.
+COL11A2	drug	alcohol	31251945	These in vivo results support an emerging key role for <strong>PARP</strong> in binge <b>alcohol</b> induced neurodegeneration and cPLA2 related neuroinflammation.
+COL11A2	addiction	intoxication	31251945	These in vivo results support an emerging key role for <strong>PARP</strong> in <b>binge</b> alcohol induced neurodegeneration and cPLA2 related neuroinflammation.
+COL11A2	drug	alcohol	29339456	<strong>PARP</strong> Inhibition Prevents <b>Ethanol</b> Induced Neuroinflammatory Signaling and Neurodegeneration in Rat Adult Age Brain Slice Cultures.
+COL11A2	drug	alcohol	29339456	Using rat adult age hippocampal entorhinal cortical (HEC) slice cultures, we examined the role of poly [ADP ribose] polymerase (<strong>PARP</strong>) in binge <b>ethanol</b>'s brain inflammatory and neurodegenerative mechanisms.
+COL11A2	addiction	intoxication	29339456	Using rat adult age hippocampal entorhinal cortical (HEC) slice cultures, we examined the role of poly [ADP ribose] polymerase (<strong>PARP</strong>) in <b>binge</b> ethanol's brain inflammatory and neurodegenerative mechanisms.
+COL11A2	drug	alcohol	29339456	Previously, we found that brain PARP1 levels were upregulated by neurotoxic <b>ethanol</b> binges in adult rats and HEC slices, and <strong>PARP</strong> inhibitor PJ34 abrogated slice neurodegeneration.
+COL11A2	drug	alcohol	29339456	After verifying that PJ34 effectively blocks <strong>PARP</strong> activity (↑PAR), we demonstrated that, like PJ34, three other <strong>PARP</strong> inhibitors olaparib, veliparib, and 4 aminobenzamide provided neuroprotection from <b>ethanol</b>.
+COL11A2	drug	alcohol	29339456	Importantly, PJ34 and olaparib also prevented <b>ethanol</b>'s amplification of the PLA2 isoenzymes, and two PLA2 inhibitors were neuroprotective thus coupling <strong>PARP</strong> to PLA2, with PLA2 activity promoting neurodegeneration.
+COL11A2	drug	alcohol	29339456	Also, PJ34 and olaparib blocked <b>ethanol</b> induced HMGB1 elevations, linking brain <strong>PARP</strong> induction to TLR4 activation.
+COL11A2	drug	alcohol	27901267	Binge <b>alcohol</b> intake in mice immediately after a 1 hour exposure to a +9 Gz hypergravity load repressed hepatic Akt and <strong>PARP</strong> 1 levels at 24 hours posttreatment.
+COL11A2	addiction	intoxication	27901267	<b>Binge</b> alcohol intake in mice immediately after a 1 hour exposure to a +9 Gz hypergravity load repressed hepatic Akt and <strong>PARP</strong> 1 levels at 24 hours posttreatment.
+COL11A2	drug	cocaine	27595592	<strong>PARP</strong> 1 is required for retrieval of <b>cocaine</b> associated memory by binding to the promoter of a novel gene encoding a putative transposase inhibitor.
+COL11A2	drug	cocaine	27595592	We demonstrate herein that auto poly(ADP ribosyl)ation of activated <strong>PARP</strong> 1 was significantly pronounced during retrieval of <b>cocaine</b> associated contextual memory, in the central amygdala (CeA) of rats expressing <b>cocaine</b> conditioned place preference (CPP).
+COL11A2	addiction	reward	27595592	We demonstrate herein that auto poly(ADP ribosyl)ation of activated <strong>PARP</strong> 1 was significantly pronounced during retrieval of cocaine associated contextual memory, in the central amygdala (CeA) of rats expressing cocaine conditioned place preference (<b>CPP</b>).
+COL11A2	drug	cocaine	27595592	Intra CeA pharmacological and short hairpin RNA depletion of <strong>PARP</strong> 1 activity during <b>cocaine</b> associated memory retrieval abolished CPP.
+COL11A2	addiction	reward	27595592	Intra CeA pharmacological and short hairpin RNA depletion of <strong>PARP</strong> 1 activity during cocaine associated memory retrieval abolished <b>CPP</b>.
+COL11A2	addiction	reward	27595592	In contrast, <strong>PARP</strong> 1 inhibition after memory retrieval did not affect <b>CPP</b> reconsolidation process and subsequent retrievals.
+COL11A2	drug	cocaine	27595592	We identified among <strong>PARP</strong> targets in CeA a single gene, yet uncharacterized and encoding a putative transposase inhibitor, at which <strong>PARP</strong> 1 enrichment markedly increases during <b>cocaine</b> associated memory retrieval and positively correlates with CPP.
+COL11A2	addiction	reward	27595592	We identified among <strong>PARP</strong> targets in CeA a single gene, yet uncharacterized and encoding a putative transposase inhibitor, at which <strong>PARP</strong> 1 enrichment markedly increases during cocaine associated memory retrieval and positively correlates with <b>CPP</b>.
+COL11A2	drug	alcohol	27527870	<b>Ethanol</b> caused both apoptotic and necrotic cell death which was demonstrated by the increase in active caspase 3, caspase 8, cleaved <strong>PARP</strong>, cleaved CK 18 and the secretion of high mobility group protein B1 (HMGB1).
+COL11A2	drug	psychedelics	26068050	In fact, chronic <b>MDMA</b> inhibited proteins of the apoptotic pathway (i.e., pro apoptotic FADD, Bax and cytochrome c) leading to an inhibition of cell death markers (i.e., p JNK1/2, cleavage of <strong>PARP</strong> 1) and suggesting regulatory mechanisms in response to the neurochemical changes caused by the drug.
+COL11A2	drug	amphetamine	25631491	In addition, blocking caspase 11 expression inhibited <b>METH</b> induced activation of caspase 3 and <strong>PARP</strong> in vitro and in vivo, suggesting that caspase 11/caspase 3 signal pathway is involved in <b>METH</b> induced neurotoxicity.
+COL11A2	drug	alcohol	25029343	We report here that neurotoxic binge <b>ethanol</b> exposure produces comparable significant effects in vivo and in vitro on adult rat brain levels of AQP4 as well as neuroinflammation linked enzymes: key phospholipase A2 (PLA2) family members and poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1).
+COL11A2	addiction	intoxication	25029343	We report here that neurotoxic <b>binge</b> ethanol exposure produces comparable significant effects in vivo and in vitro on adult rat brain levels of AQP4 as well as neuroinflammation linked enzymes: key phospholipase A2 (PLA2) family members and poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1).
+COL11A2	drug	alcohol	25029343	In adult male rats, repetitive <b>ethanol</b> intoxication (3 gavages/d for 4 d, ∼ 9 g/kg/d, achieving blood <b>ethanol</b> levels ∼ 375 mg/dl; "Majchrowicz" model) significantly increased AQP4, Ca+2 dependent PLA2 GIVA (cPLA2), phospho cPLA2 GIVA (p cPLA2), secretory PLA2 GIIA (sPLA2) and <strong>PARP</strong> 1 in regions incurring extensive neurodegeneration in this model  hippocampus, entorhinal cortex, and olfactory bulb  but not in two regions typically lacking neurodamage, frontal cortex and cerebellum.
+COL11A2	addiction	intoxication	25029343	In adult male rats, repetitive ethanol <b>intoxication</b> (3 gavages/d for 4 d, ∼ 9 g/kg/d, achieving blood ethanol levels ∼ 375 mg/dl; "Majchrowicz" model) significantly increased AQP4, Ca+2 dependent PLA2 GIVA (cPLA2), phospho cPLA2 GIVA (p cPLA2), secretory PLA2 GIIA (sPLA2) and <strong>PARP</strong> 1 in regions incurring extensive neurodegeneration in this model  hippocampus, entorhinal cortex, and olfactory bulb  but not in two regions typically lacking neurodamage, frontal cortex and cerebellum.
+COL11A2	drug	alcohol	25029343	Furthermore, supplementation with docosahexaenoic acid (DHA; 22:6n 3), known to quell AQP4 and neurodegeneration in <b>ethanol</b> treated slices, blocked <strong>PARP</strong> 1 and PLA2 changes while counteracting endogenous DHA reduction and increases in oxidative stress footprints (3 nitrotyrosinated proteins).
+COL11A2	drug	alcohol	25029343	Notably, the <strong>PARP</strong> 1 inhibitor PJ 34 suppressed binge <b>ethanol</b> dependent neurodegeneration, indicating <strong>PARP</strong> upstream involvement.
+COL11A2	addiction	intoxication	25029343	Notably, the <strong>PARP</strong> 1 inhibitor PJ 34 suppressed <b>binge</b> ethanol dependent neurodegeneration, indicating <strong>PARP</strong> upstream involvement.
+COL11A2	drug	opioid	24959978	In this study, we investigated the effects of <b>morphine</b> induced conditioned place preference (CPP) in the presence and absence of stress on the changes of apoptotic factors (Bax/Bcl 2 ratio, caspase 3 activation and <strong>PARP</strong> degradation) in the MCL system.
+COL11A2	addiction	reward	24959978	In this study, we investigated the effects of morphine induced conditioned place preference (<b>CPP</b>) in the presence and absence of stress on the changes of apoptotic factors (Bax/Bcl 2 ratio, caspase 3 activation and <strong>PARP</strong> degradation) in the MCL system.
+COL11A2	drug	alcohol	24705861	Concomitant with PLA(2) activation, the results have further implicated binge <b>alcohol</b> elevated poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1), an oxidative stress responsive DNA repair enzyme linked to parthanatos, a necrotic like neuronal death process.
+COL11A2	addiction	intoxication	24705861	Concomitant with PLA(2) activation, the results have further implicated <b>binge</b> alcohol elevated poly (ADP ribose) polymerase 1 (<strong>PARP</strong> 1), an oxidative stress responsive DNA repair enzyme linked to parthanatos, a necrotic like neuronal death process.
+COL11A2	drug	alcohol	24705861	Importantly, supplementation of the brain slice cultures with docosahexaenoic acid (22:6 ω3) exerted potent suppression of the induced changes in PLA(2) isoforms, AQP4, <strong>PARP</strong> 1 and oxidative stress footprints, and prevention of the binge <b>alcohol</b> neurotoxicity, by as yet unknown mechanisms.
+COL11A2	addiction	intoxication	24705861	Importantly, supplementation of the brain slice cultures with docosahexaenoic acid (22:6 ω3) exerted potent suppression of the induced changes in PLA(2) isoforms, AQP4, <strong>PARP</strong> 1 and oxidative stress footprints, and prevention of the <b>binge</b> alcohol neurotoxicity, by as yet unknown mechanisms.
+COL11A2	drug	cocaine	24449909	Here, we identify an essential role for <strong>PARP</strong> 1 in <b>cocaine</b> induced molecular, neural, and behavioral plasticity.
+COL11A2	drug	cocaine	24449909	Repeated <b>cocaine</b> administration, including self administration, increased global levels of <strong>PARP</strong> 1 and its mark PAR in mouse nucleus accumbens (NAc), a key brain reward region.
+COL11A2	addiction	reward	24449909	Repeated cocaine administration, including self administration, increased global levels of <strong>PARP</strong> 1 and its mark PAR in mouse nucleus accumbens (NAc), a key brain <b>reward</b> region.
+COL11A2	drug	cocaine	24449909	Using <strong>PARP</strong> 1 inhibitors and viral mediated gene transfer, we established that <strong>PARP</strong> 1 induction in NAc mediates enhanced behavioral responses to <b>cocaine</b>, including increased self administration of the drug.
+COL11A2	drug	cocaine	24449909	Using chromatin immunoprecipitation sequencing, we demonstrated a global, genome wide enrichment of <strong>PARP</strong> 1 in NAc of <b>cocaine</b> exposed mice and identified several <strong>PARP</strong> 1 target genes that could contribute to the lasting effects of <b>cocaine</b>.
+COL11A2	drug	cocaine	24449909	Specifically, we identified sidekick 1  important for synaptic connections during development  as a critical <strong>PARP</strong> 1 target gene involved in <b>cocaine</b>'s behavioral effects as well as in its ability to induce dendritic spines on NAc neurons.
+COL11A2	drug	cocaine	24449909	These findings establish the involvement of <strong>PARP</strong> 1 and PARylation in the long term actions of <b>cocaine</b>.
+COL11A2	drug	opioid	24281942	In the HPC, <b>morphine</b> significantly increased the ratio of Bax/Bcl 2, caspases 3, and <strong>PARP</strong> by the lowest dose (0.5 mg/kg), but, in the VTA, a considerable increase was seen in the dose of 5 mg/kg; promotion of apoptotic factors in the HPC and VTA insinuates that <b>morphine</b> can affect the molecular mechanisms that interfere with apoptosis through different receptors.
+COL11A2	drug	opioid	24096212	In the NAc, <b>morphine</b> significantly increased the Bax/Bcl 2 ratio, caspase3 and <strong>PARP</strong> in the lowest dose (0.5mg/kg) but in the PFC considerable increase was seen in dose of 5mg/kg.
+COL11A2	addiction	reward	27385959	In this study, the effects of acute and subchronic stress on the changes in apoptotic factors (Bax/Bcl 2 ratio, caspase 3 activation and <strong>PARP</strong> degradation) in the HYP and HIP during conditioned place preference (<b>CPP</b>) paradigm were evaluated.
+COL11A2	drug	opioid	27385959	Caspase 3 and <strong>PARP</strong> increased during AS and SS in saline  or <b>morphine</b> treated animals.
+COL11A2	drug	opioid	27385959	For example, caspase 3 increased during AS and SS in <b>morphine</b> treated animals by 2.4 folds and <strong>PARP</strong> (89 KDa) increased by 3.1 and 3.5 folds, respectively.
+COL11A2	drug	alcohol	23102656	Effect of repetitive daily <b>ethanol</b> intoxication on adult rat brain: significant changes in phospholipase A2 enzyme levels in association with increased <strong>PARP</strong> 1 indicate neuroinflammatory pathway activation.
+COL11A2	addiction	intoxication	23102656	Effect of repetitive daily ethanol <b>intoxication</b> on adult rat brain: significant changes in phospholipase A2 enzyme levels in association with increased <strong>PARP</strong> 1 indicate neuroinflammatory pathway activation.
+COL11A2	drug	alcohol	23102656	Collaborating on studies of subchronic daily intoxication in juvenile and adult rats, we examined whether the repetitive <b>ethanol</b> treatments at these two life stages altered levels of key neuroinflammation associated proteins aquaporin 4 (AQP4), certain phospholipase A2 (PLA2) enzymes, <strong>PARP</strong> 1 and caspase 3 in hippocampus (HC) and entorhinal cortex (EC).
+COL11A2	addiction	intoxication	23102656	Collaborating on studies of subchronic daily <b>intoxication</b> in juvenile and adult rats, we examined whether the repetitive ethanol treatments at these two life stages altered levels of key neuroinflammation associated proteins aquaporin 4 (AQP4), certain phospholipase A2 (PLA2) enzymes, <strong>PARP</strong> 1 and caspase 3 in hippocampus (HC) and entorhinal cortex (EC).
+COL11A2	drug	alcohol	23102656	Furthermore, the robust <strong>PARP</strong> 1 elevations accompanied by negligible caspase 3 activation indicate that repetitive <b>ethanol</b> intoxication may be potentiating non apoptotic neurodegenerative processes such as parthanatos.
+COL11A2	addiction	intoxication	23102656	Furthermore, the robust <strong>PARP</strong> 1 elevations accompanied by negligible caspase 3 activation indicate that repetitive ethanol <b>intoxication</b> may be potentiating non apoptotic neurodegenerative processes such as parthanatos.
+COL11A2	drug	cocaine	21925237	This postmortem human brain study examined the status of canonical apoptotic pathways, signaling partners, and the cleavage of poly(ADP ribose) polymerase 1 (<strong>PARP</strong> 1), a sensor of DNA damage, in prefrontal cortex (PFC) of a small but well characterized cohort of <b>cocaine</b> abusers (n=10).
+COL11A2	drug	cocaine	21925237	In the same brain samples of <b>cocaine</b> abusers, the proteolytic cleavage of <strong>PARP</strong> 1 was increased (+39%).
+COL11A2	drug	cocaine	21925237	Chronic exposure to <b>cocaine</b> in rats, including withdrawal for 3 days, did not alter Fas FADD receptor complex, cytochrome c, caspase 3/fragments, AIF, <strong>PARP</strong> 1 cleavage, and associated signaling in the cerebral cortex.
+COL11A2	addiction	withdrawal	21925237	Chronic exposure to cocaine in rats, including <b>withdrawal</b> for 3 days, did not alter Fas FADD receptor complex, cytochrome c, caspase 3/fragments, AIF, <strong>PARP</strong> 1 cleavage, and associated signaling in the cerebral cortex.
+COL11A2	drug	alcohol	21803053	After 4h, a single dose of <b>ethanol</b> induced upregulation of Bax, release of mitochondrial cytochrome c into the cytosol, activation of caspase 3 and cleavage of poly (ADP ribose) polymerase (<strong>PARP</strong> 1), all of which promote apoptosis.
+COL11A2	drug	opioid	19447888	In this study, our data suggest that <strong>PARP</strong> 1 positively regulates MOR gene transcription via G( 172)   > T, which might influence individual specificity in therapeutic <b>opioid</b> effects.
+COL11A2	drug	amphetamine	16210775	Pretreatment with NMDA receptor antagonists, such as MK 801 and 3 ((R) 2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (CPP), and benzamide [poly(ADP ribose) polymerase (<strong>PARP</strong>) inhibitor] significantly attenuated the increased lethality induced by <b>methamphetamine</b> and morphine.
+COL11A2	drug	opioid	16210775	Pretreatment with NMDA receptor antagonists, such as MK 801 and 3 ((R) 2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (CPP), and benzamide [poly(ADP ribose) polymerase (<strong>PARP</strong>) inhibitor] significantly attenuated the increased lethality induced by methamphetamine and <b>morphine</b>.
+COL11A2	addiction	reward	16210775	Pretreatment with NMDA receptor antagonists, such as MK 801 and 3 ((R) 2 carboxypiperazin 4 yl) propyl 1 phosphonic acid (<b>CPP</b>), and benzamide [poly(ADP ribose) polymerase (<strong>PARP</strong>) inhibitor] significantly attenuated the increased lethality induced by methamphetamine and morphine.
+COL11A2	drug	amphetamine	16210775	These results suggest that activation of NMDA receptors and <strong>PARP</strong> play an important role in the increased lethality induced by <b>methamphetamine</b> and morphine.
+COL11A2	drug	opioid	16210775	These results suggest that activation of NMDA receptors and <strong>PARP</strong> play an important role in the increased lethality induced by methamphetamine and <b>morphine</b>.
+COL11A2	drug	amphetamine	15113847	The oxidative stress induced by <b>METH</b> putatively activates nuclear enzyme poly(ADP ribose) polymerase (<strong>PARP</strong>), with excessive <strong>PARP</strong> activation eventually leading to cell death.
+COL11A2	drug	amphetamine	15113847	In this study, we show that prevention of <strong>PARP</strong> activation by treatment with FR261529 [2 (4 chlorophenyl) 5 quinoxalinecarboxamide], the compound that was recently identified as a novel <strong>PARP</strong> inhibitor (IC50 for <strong>PARP</strong> 1 = 33 nM, IC50 for <strong>PARP</strong> 2 = 7 nM), protects against both ROS induced cells injury in vitro and <b>METH</b> induced dopaminergic neuronal damage in an in vivo Parkinson's disease (PD) model.
+COL11A2	drug	amphetamine	15113847	In PC12 cells, exposure of hydrogen peroxide or <b>METH</b> markedly induced <strong>PARP</strong> activation, and treatment with FR261529 (1 microM) significantly reduced <strong>PARP</strong> activation and attenuated cell death.
+COL11A2	drug	amphetamine	15113847	These findings indicate that the neuroprotective effects of a novel <strong>PARP</strong> inhibitor, FR261529, were accompanied by inhibition of <b>METH</b> induced <strong>PARP</strong> activation, suggesting that <b>METH</b> induces nigrostriatal dopaminergic neurodegeneration involving <strong>PARP</strong> activation and also orally active and brain penetrable <strong>PARP</strong> inhibitor FR261529 could be a novel attractive therapeutic candidate for neurodegenerative disorders such as PD.
+CAV1	drug	cocaine	31905369	Contribution of D1R expressing neurons of the dorsal dentate gyrus and <strong>Cav1</strong>.2 channels in extinction of <b>cocaine</b> conditioned place preference.
+CAV1	drug	cocaine	31905369	Here, we extend our previous findings for a role of <strong>Cav1</strong>.2 L type Ca2+ channels in dopamine 1 receptor (D1R) expressing cells in extinction of <b>cocaine</b> conditioned place preference (CPP) in adult male mice.
+CAV1	addiction	reward	31905369	Here, we extend our previous findings for a role of <strong>Cav1</strong>.2 L type Ca2+ channels in dopamine 1 receptor (D1R) expressing cells in extinction of cocaine conditioned place preference (<b>CPP</b>) in adult male mice.
+CAV1	drug	cocaine	31905369	We report that attenuated <b>cocaine</b> CPP extinction in mice lacking <strong>Cav1</strong>.2 channels in D1R expressing cells (D1cre, <strong>Cav1</strong>.2fl/fl) can be rescued through chemogenetic activation of D1R expressing cells within the dorsal dentate gyrus (dDG), but not the dorsal CA1 (dCA1).
+CAV1	addiction	reward	31905369	We report that attenuated cocaine <b>CPP</b> extinction in mice lacking <strong>Cav1</strong>.2 channels in D1R expressing cells (D1cre, <strong>Cav1</strong>.2fl/fl) can be rescued through chemogenetic activation of D1R expressing cells within the dorsal dentate gyrus (dDG), but not the dorsal CA1 (dCA1).
+CAV1	drug	cocaine	31905369	This is supported by the finding that <strong>Cav1</strong>.2 channels are required in excitatory cells of the dDG, but not in the dCA1, for <b>cocaine</b> CPP extinction.
+CAV1	addiction	reward	31905369	This is supported by the finding that <strong>Cav1</strong>.2 channels are required in excitatory cells of the dDG, but not in the dCA1, for cocaine <b>CPP</b> extinction.
+CAV1	drug	cocaine	31905369	These findings outline an essential role for the interaction between D1R, <strong>Cav1</strong>.2, and GluA1 signaling in the dDG for extinction of <b>cocaine</b> associated contextual memories.
+CAV1	addiction	relapse	31501511	Importantly, both forms of <b>reinstatement</b> require <strong>Cav1</strong>.2 L type Ca2+ channels (LTCCs) in cells of the prelimbic cortex that project to the nucleus accumbens core (PrL→NAcC).
+CAV1	drug	cocaine	31501511	Using projection specific chemogenetic manipulations, we show that PrL→NAcC activity is required for both <b>cocaine</b>  and stress primed reinstatement, and that activation of this projection in <strong>Cav1</strong>.2 deficient mice restores reinstatement.
+CAV1	addiction	relapse	31501511	Using projection specific chemogenetic manipulations, we show that PrL→NAcC activity is required for both cocaine  and stress primed <b>reinstatement</b>, and that activation of this projection in <strong>Cav1</strong>.2 deficient mice restores <b>reinstatement</b>.
+CAV1	drug	opioid	30550947	Results also showed up regulation of the <strong>Cav1</strong>.3 and <strong>Cav1</strong>.2 expression in the cerebral cortex and mesolimbic regions through the development of <b>morphine</b> dependence.
+CAV1	addiction	dependence	30550947	Results also showed up regulation of the <strong>Cav1</strong>.3 and <strong>Cav1</strong>.2 expression in the cerebral cortex and mesolimbic regions through the development of morphine <b>dependence</b>.
+CAV1	drug	opioid	30550947	Moreover, chronic administration of fluoxetine with <b>morphine</b> reduced the observed up regulation of <strong>Cav1</strong>.3 and <strong>Cav1</strong>.2 expression in cortex and mesolimbic tissues.
+CAV1	drug	opioid	29154860	The role of <strong>caveolin 1</strong> in <b>morphine</b> induced structural plasticity in primary cultured mouse cerebral cortical neurons.
+CAV1	drug	cocaine	29089442	Extinction of Contextual <b>Cocaine</b> Memories Requires <strong>Cav1</strong>.2 within D1R Expressing Cells and Recruits Hippocampal <strong>Cav1</strong>.2 Dependent Signaling Mechanisms.
+CAV1	drug	cocaine	29089442	We report that extinction, but not acquisition, of <b>cocaine</b> conditioned place preference (CPP) in male mice increased <strong>Cav1</strong>.2 L type Ca2+ channel mRNA and protein in postsynaptic density (PSD) fractions of the hippocampus, a brain region involved in drug context associations.
+CAV1	addiction	reward	29089442	We report that extinction, but not acquisition, of cocaine conditioned place preference (<b>CPP</b>) in male mice increased <strong>Cav1</strong>.2 L type Ca2+ channel mRNA and protein in postsynaptic density (PSD) fractions of the hippocampus, a brain region involved in drug context associations.
+CAV1	drug	cocaine	29089442	Moreover, viral mediated deletion of <strong>Cav1</strong>.2 in the dorsal hippocampus attenuated extinction of <b>cocaine</b> CPP.
+CAV1	addiction	reward	29089442	Moreover, viral mediated deletion of <strong>Cav1</strong>.2 in the dorsal hippocampus attenuated extinction of cocaine <b>CPP</b>.
+CAV1	drug	cocaine	29089442	Finally, conditional knock out of <strong>Cav1</strong>.2 in dopamine D1 receptor (D1R) expressing cells resulted in attenuation of <b>cocaine</b> CPP extinction and lack of extinction dependent changes in hippocampal PSD CaMKII expression and S831 GluA1 phosphorylation.
+CAV1	addiction	reward	29089442	Finally, conditional knock out of <strong>Cav1</strong>.2 in dopamine D1 receptor (D1R) expressing cells resulted in attenuation of cocaine <b>CPP</b> extinction and lack of extinction dependent changes in hippocampal PSD CaMKII expression and S831 GluA1 phosphorylation.
+CAV1	drug	cocaine	29089442	In summary, we demonstrate an essential role for the hippocampal <strong>Cav1</strong>.2/CaMKII/S831 GluA1 pathway in <b>cocaine</b> CPP extinction, with data supporting contribution of hippocampal D1R expressing cells in this process.
+CAV1	addiction	reward	29089442	In summary, we demonstrate an essential role for the hippocampal <strong>Cav1</strong>.2/CaMKII/S831 GluA1 pathway in cocaine <b>CPP</b> extinction, with data supporting contribution of hippocampal D1R expressing cells in this process.
+CAV1	drug	cocaine	29089442	These findings demonstrate a novel role for <strong>Cav1</strong>.2 channels in extinction of contextual <b>cocaine</b> associated memories.SIGNIFICANCE STATEMENT Continued drug seeking behavior, a defining characteristic of <b>cocaine</b> addiction, can be precipitated by contextual cues, yet the molecular mechanisms required for extinction of these context specific memories remain poorly understood.
+CAV1	addiction	addiction	29089442	These findings demonstrate a novel role for <strong>Cav1</strong>.2 channels in extinction of contextual cocaine associated memories.SIGNIFICANCE STATEMENT Continued drug seeking behavior, a defining characteristic of cocaine <b>addiction</b>, can be precipitated by contextual cues, yet the molecular mechanisms required for extinction of these context specific memories remain poorly understood.
+CAV1	addiction	relapse	29089442	These findings demonstrate a novel role for <strong>Cav1</strong>.2 channels in extinction of contextual cocaine associated memories.SIGNIFICANCE STATEMENT Continued drug <b>seeking</b> behavior, a defining characteristic of cocaine addiction, can be precipitated by contextual cues, yet the molecular mechanisms required for extinction of these context specific memories remain poorly understood.
+CAV1	drug	cocaine	29089442	Here, we have uncovered a novel and selective role of the <strong>Cav1</strong>.2 L type Ca2+ channel and its downstream signaling pathway in the hippocampus that mediate extinction of <b>cocaine</b> conditioned place preference (CPP).
+CAV1	addiction	reward	29089442	Here, we have uncovered a novel and selective role of the <strong>Cav1</strong>.2 L type Ca2+ channel and its downstream signaling pathway in the hippocampus that mediate extinction of cocaine conditioned place preference (<b>CPP</b>).
+CAV1	drug	cocaine	29089442	We additionally provide evidence that supports a role of <strong>Cav1</strong>.2 within dopamine D1 receptor expressing cells of the hippocampus for extinction of <b>cocaine</b> CPP.
+CAV1	addiction	reward	29089442	We additionally provide evidence that supports a role of <strong>Cav1</strong>.2 within dopamine D1 receptor expressing cells of the hippocampus for extinction of cocaine <b>CPP</b>.
+CAV1	drug	cocaine	29089442	Therefore, these findings reveal a previously unknown role of <strong>Cav1</strong>.2 channels within the hippocampus and in D1 receptor expressing cells in extinction of <b>cocaine</b> associated memories, providing a framework for further exploration of mechanisms underlying extinction of <b>cocaine</b> seeking behavior.
+CAV1	addiction	relapse	29089442	Therefore, these findings reveal a previously unknown role of <strong>Cav1</strong>.2 channels within the hippocampus and in D1 receptor expressing cells in extinction of cocaine associated memories, providing a framework for further exploration of mechanisms underlying extinction of cocaine <b>seeking</b> behavior.
+CAV1	drug	opioid	29053731	The reversible increases of <strong>caveolin 1</strong> and cholesterol levels suggest participation of membrane domains in compensatory responses during <b>opioid</b> withdrawal.
+CAV1	addiction	withdrawal	29053731	The reversible increases of <strong>caveolin 1</strong> and cholesterol levels suggest participation of membrane domains in compensatory responses during opioid <b>withdrawal</b>.
+CAV1	addiction	relapse	28764937	Moreover, the effects of L type calcium channels (LTCCs) and the subtypes <strong>Cav1</strong>.2 and <strong>Cav1</strong>.3, which are downstream of D1R and D2R, respectively, on habitual drug <b>seeking</b> behavior have yet to be revealed.
+CAV1	drug	cocaine	28764937	Therefore, based on the establishment of habitual <b>cocaine</b> seeking behavior with changeable fixed interval (FI) self administration (SA) training in rats, we compared the distinctive changes in D1R vs. D2R and <strong>Cav1</strong>.2 vs. <strong>Cav1</strong>.3 in the expression of habitual <b>cocaine</b> seeking behavior in the dorsomedial striatum (DMS) and dorsolateral striatum (DLS).
+CAV1	addiction	relapse	28764937	Therefore, based on the establishment of habitual cocaine <b>seeking</b> behavior with changeable fixed interval (FI) self administration (SA) training in rats, we compared the distinctive changes in D1R vs. D2R and <strong>Cav1</strong>.2 vs. <strong>Cav1</strong>.3 in the expression of habitual cocaine <b>seeking</b> behavior in the dorsomedial striatum (DMS) and dorsolateral striatum (DLS).
+CAV1	drug	cocaine	28764937	In addition, the total and membrane <strong>Cav1</strong>.2 and D1R in the DLS demonstrated higher expression, but the total and membrane <strong>Cav1</strong>.3 and D2R in the DMS demonstrated lower expression in well established <b>cocaine</b> habitual behavior animals compared with non established habitual behavior animals.
+CAV1	drug	cocaine	28764937	These results suggested that upregulation of D1R <strong>Cav1</strong>.2 signaling may enhance the function of the DLS and that inactivation of D2R <strong>Cav1</strong>.3 caused depressed activity in the DMS during expression of habitual <b>cocaine</b> seeking behavior.
+CAV1	addiction	relapse	28764937	These results suggested that upregulation of D1R <strong>Cav1</strong>.2 signaling may enhance the function of the DLS and that inactivation of D2R <strong>Cav1</strong>.3 caused depressed activity in the DMS during expression of habitual cocaine <b>seeking</b> behavior.
+CAV1	addiction	dependence	28497380	Clinical studies with LTCC blockers testing their efficacy to alleviate symptoms associated with BD, SCZ, and drug <b>dependence</b> have provided mixed results, underscoring the importance of further exploring the neurobiological consequences of dysregulated <strong>Cav1</strong>.2 and <strong>Cav1</strong>.3.
+CAV1	addiction	addiction	28497380	Here, we provide a review of clinical studies that have evaluated LTCC blockers for BD, SCZ, and drug dependence associated symptoms, as well as rodent studies that have identified <strong>Cav1</strong>.2  and <strong>Cav1</strong>.3 specific molecular and cellular cascades that underlie mood (anxiety, depression), social behavior, cognition, and <b>addiction</b>.
+CAV1	addiction	dependence	28497380	Here, we provide a review of clinical studies that have evaluated LTCC blockers for BD, SCZ, and drug <b>dependence</b> associated symptoms, as well as rodent studies that have identified <strong>Cav1</strong>.2  and <strong>Cav1</strong>.3 specific molecular and cellular cascades that underlie mood (anxiety, depression), social behavior, cognition, and addiction.
+CAV1	drug	cocaine	28194001	Enhancing VTA <strong>Cav1</strong>.3 L type Ca2+ channel activity promotes <b>cocaine</b> and mood related behaviors via overlapping AMPA receptor mechanisms in the nucleus accumbens.
+CAV1	addiction	addiction	28194001	Rodent studies have begun to elucidate a role of <strong>Cav1</strong>.3 L type Ca2+ channels in neuropsychiatric related behaviors, such as <b>addictive</b> and depressive like behaviors.
+CAV1	drug	cocaine	28194001	In the present study, we directly manipulated <strong>Cav1</strong>.3 channels in <strong>Cav1</strong>.2 dihydropyridine insensitive mutant mice and found that ventral tegmental area (VTA) <strong>Cav1</strong>.3 channels mediate <b>cocaine</b> related and depressive like behavior through a common nucleus accumbens (NAc) shell calcium permeable α amino 3 hydroxy 5 methyl 4 isoxazolepropionic acid receptor (CP AMPAR) mechanism that requires GluA1 phosphorylation at S831.
+CAV1	drug	cocaine	28194001	Selective activation of VTA <strong>Cav1</strong>.3 with (±) BayK 8644 (BayK) enhanced <b>cocaine</b> conditioned place preference and <b>cocaine</b> psychomotor activity while inducing depressive like behavior, an effect not observed in S831A phospho mutant mice.
+CAV1	drug	cocaine	28194001	Together, our findings reveal novel, overlapping mechanisms through which VTA <strong>Cav1</strong>.3 mediates <b>cocaine</b> related, depressive like and social phenotypes, suggesting that <strong>Cav1</strong>.3 may serve as a target for the treatment of neuropsychiatric symptoms.
+CAV1	drug	nicotine	28185965	<strong>Cav1</strong>.2, but not <strong>Cav1</strong>.3, L type calcium channel subtype mediates <b>nicotine</b> induced conditioned place preference in mice.
+CAV1	drug	nicotine	28185965	Although L type calcium channels (LTCCs) are involved in <b>nicotine</b> addiction, the contribution of the two primary LTCC subtypes (<strong>Cav1</strong>.2 and 1.3) is unknown.
+CAV1	addiction	addiction	28185965	Although L type calcium channels (LTCCs) are involved in nicotine <b>addiction</b>, the contribution of the two primary LTCC subtypes (<strong>Cav1</strong>.2 and 1.3) is unknown.
+CAV1	drug	nicotine	28185965	This study aims to determine the contribution of these two LTCC subtypes to <b>nicotine</b> induced conditioned place preference (CPP) responses by using transgenic mouse models that do not express <strong>Cav1</strong>.3 (<strong>Cav1</strong>.3 / ) or contain a mutation in the dihydropyridine (DHP) site of the <strong>Cav1</strong>.2 (<strong>Cav1</strong>.2DHP / ).
+CAV1	addiction	reward	28185965	This study aims to determine the contribution of these two LTCC subtypes to nicotine induced conditioned place preference (<b>CPP</b>) responses by using transgenic mouse models that do not express <strong>Cav1</strong>.3 (<strong>Cav1</strong>.3 / ) or contain a mutation in the dihydropyridine (DHP) site of the <strong>Cav1</strong>.2 (<strong>Cav1</strong>.2DHP / ).
+CAV1	drug	nicotine	28185965	Similarly, <strong>Cav1</strong>.3 /  mice showed <b>nicotine</b> induced place preference which was antagonized by nifedipine.
+CAV1	drug	nicotine	28185965	In contrast, nifedipine pretreatment of <strong>Cav1</strong>.2DHP /  mice had no effect on <b>nicotine</b> induced CPP responses, suggesting an involvement of <strong>Cav1</strong>.2 subtype in the <b>nicotine</b> induced CPP response.
+CAV1	addiction	reward	28185965	In contrast, nifedipine pretreatment of <strong>Cav1</strong>.2DHP /  mice had no effect on nicotine induced <b>CPP</b> responses, suggesting an involvement of <strong>Cav1</strong>.2 subtype in the nicotine induced <b>CPP</b> response.
+CAV1	drug	nicotine	28185965	These results collectively indicate <strong>Cav1</strong>.2, but not <strong>Cav1</strong>.3 LTCC subtype regulates, at least in part, the reinforcing effects of <b>nicotine</b> use.
+CAV1	addiction	reward	28185965	These results collectively indicate <strong>Cav1</strong>.2, but not <strong>Cav1</strong>.3 LTCC subtype regulates, at least in part, the <b>reinforcing</b> effects of nicotine use.
+CAV1	drug	alcohol	27905406	It has previously been shown that the inhibition of L type calcium channels (LTCCs) decreases <b>alcohol</b> consumption, although the contribution of the central LTCC subtypes <strong>Cav1</strong>.2 and <strong>Cav1</strong>.3 remains unknown.
+CAV1	drug	alcohol	27905406	Here, we determined changes in <strong>Cav1</strong>.2 (Cacna1c) and <strong>Cav1</strong>.3 (Cacna1d) mRNA and protein expression in <b>alcohol</b> dependent rats during protracted abstinence and naive controls using in situ hybridization and western blot analysis.
+CAV1	drug	alcohol	27905406	Further studies in conditional <strong>Cav1</strong>.2 KO mice showed a lack of dependence induced increase of <b>alcohol</b> seeking behavior.
+CAV1	addiction	dependence	27905406	Further studies in conditional <strong>Cav1</strong>.2 KO mice showed a lack of <b>dependence</b> induced increase of alcohol seeking behavior.
+CAV1	addiction	relapse	27905406	Further studies in conditional <strong>Cav1</strong>.2 KO mice showed a lack of dependence induced increase of alcohol <b>seeking</b> behavior.
+CAV1	drug	alcohol	27905406	Together, our data indicate that central <strong>Cav1</strong>.2 channels, rather than <strong>Cav1</strong>.3, mediate <b>alcohol</b> seeking behavior.
+CAV1	addiction	relapse	27905406	Together, our data indicate that central <strong>Cav1</strong>.2 channels, rather than <strong>Cav1</strong>.3, mediate alcohol <b>seeking</b> behavior.
+CAV1	drug	opioid	27726130	Chronic <b>opioid</b> treatment augments <strong>caveolin 1</strong> scaffolding: relevance to stimulatory μ <b>opioid</b> receptor adenylyl cyclase signaling.
+CAV1	drug	opioid	27726130	This study reveals that chronic <b>opioid</b> exposure of μ <b>opioid</b> receptor (MOR) expressing Chinese hamster ovary cells (MOR CHO) and chronic in vivo <b>morphine</b> exposure of rat spinal cord augmented recruitment of multiple components of MOR adenylyl cyclase (AC) stimulatory signaling by <strong>caveolin 1</strong>.
+CAV1	drug	opioid	27726130	Strikingly, in MOR CHO and spinal cord, blocking the <strong>caveolin 1</strong> scaffolding domain substantially attenuated the chronic <b>morphine</b> induced increased interaction of <strong>caveolin 1</strong> with MOR, Gsα, protein phosphatase 2A (PP2A), and AC.
+CAV1	drug	opioid	27726130	In the aggregate, our data strongly suggest that augmented <strong>caveolin 1</strong> scaffolding undergirds the ability of chronic <b>opioids</b> to recruit an ancillary signaling pathway by acting as an organizing template for MOR Gs α AC signaling and delimiting the membrane compartment(s) in which it occurs.
+CAV1	drug	opioid	27726130	Since <strong>caveolin 1</strong> binds to a wide spectrum of signaling molecules, altered <strong>caveolin 1</strong> scaffolding following chronic <b>opioid</b> treatment is likely to pertain to most, if not all, MOR signaling partners.
+CAV1	drug	opioid	27726130	The chronic <b>morphine</b> induced trigger that augments <strong>caveolin 1</strong> scaffolding could represent a seminal perturbation that initiates the wide spectrum of adaptations thought to contribute to <b>opioid</b> tolerance and dependence.
+CAV1	addiction	dependence	27726130	The chronic morphine induced trigger that augments <strong>caveolin 1</strong> scaffolding could represent a seminal perturbation that initiates the wide spectrum of adaptations thought to contribute to opioid tolerance and <b>dependence</b>.
+CAV1	drug	amphetamine	27138644	<b>Methamphetamine</b> reduces expression of <strong>caveolin 1</strong> in the dorsal striatum: Implication for dysregulation of neuronal function.
+CAV1	addiction	reward	26677947	We determined that: (i) the two genotypes acquired the <b>operant</b> task and maintained similar levels of COC SA, (ii) forced abstinence from COC SA enhanced mPFC PN excitability in both genotypes, and neurons from Tg rats exhibited the greatest pathophysiology, (iii) neurons from SAL Yoked Tg rats were more excitable than those from SAL Yoked non Tg rats, and in Tg rats (iv) blockade of L type Ca(2+) channels reduced the enhanced excitability, and (v) <strong>Cav1</strong>.2 immunoreactivity was increased.
+CAV1	drug	alcohol	26100537	Furthermore, administration of isradipine or a <strong>CaV1</strong>.3 subtype selective LTCC antagonist (systemic or intra VTA) before a single extinction or reinstatement session, while having no immediate effect at the time of administration, abolished previously acquired cocaine and <b>alcohol</b> (<b>ethanol</b>) CPP on subsequent days.
+CAV1	drug	cocaine	26100537	Furthermore, administration of isradipine or a <strong>CaV1</strong>.3 subtype selective LTCC antagonist (systemic or intra VTA) before a single extinction or reinstatement session, while having no immediate effect at the time of administration, abolished previously acquired <b>cocaine</b> and alcohol (ethanol) CPP on subsequent days.
+CAV1	addiction	relapse	26100537	Furthermore, administration of isradipine or a <strong>CaV1</strong>.3 subtype selective LTCC antagonist (systemic or intra VTA) before a single extinction or <b>reinstatement</b> session, while having no immediate effect at the time of administration, abolished previously acquired cocaine and alcohol (ethanol) CPP on subsequent days.
+CAV1	addiction	reward	26100537	Furthermore, administration of isradipine or a <strong>CaV1</strong>.3 subtype selective LTCC antagonist (systemic or intra VTA) before a single extinction or reinstatement session, while having no immediate effect at the time of administration, abolished previously acquired cocaine and alcohol (ethanol) <b>CPP</b> on subsequent days.
+CAV1	drug	alcohol	25556199	<b>Alcohol</b> Withdrawal Induced Seizure Susceptibility is Associated with an Upregulation of <strong>CaV1</strong>.3 Channels in the Rat Inferior Colliculus.
+CAV1	addiction	withdrawal	25556199	Alcohol <b>Withdrawal</b> Induced Seizure Susceptibility is Associated with an Upregulation of <strong>CaV1</strong>.3 Channels in the Rat Inferior Colliculus.
+CAV1	drug	alcohol	25556199	We previously reported increased current density through L type voltage gated Ca(2+) (<strong>CaV1</strong>) channels in inferior colliculus (IC) neurons during <b>alcohol</b> withdrawal.
+CAV1	addiction	withdrawal	25556199	We previously reported increased current density through L type voltage gated Ca(2+) (<strong>CaV1</strong>) channels in inferior colliculus (IC) neurons during alcohol <b>withdrawal</b>.
+CAV1	drug	alcohol	25556199	The IC was dissected at various time intervals following <b>alcohol</b> withdrawal, and the mRNA and protein levels of the <strong>CaV1</strong>.3 and <strong>CaV1</strong>.2 α1 subunits were measured.
+CAV1	addiction	withdrawal	25556199	The IC was dissected at various time intervals following alcohol <b>withdrawal</b>, and the mRNA and protein levels of the <strong>CaV1</strong>.3 and <strong>CaV1</strong>.2 α1 subunits were measured.
+CAV1	drug	alcohol	25556199	At 24 hours, Western blot analyses revealed that the levels of the <strong>CaV1</strong>.3 and <strong>CaV1</strong>.2 α1 subunits increased by 52% and 32%, respectively, 24 hours after <b>alcohol</b> withdrawal.
+CAV1	addiction	withdrawal	25556199	At 24 hours, Western blot analyses revealed that the levels of the <strong>CaV1</strong>.3 and <strong>CaV1</strong>.2 α1 subunits increased by 52% and 32%, respectively, 24 hours after alcohol <b>withdrawal</b>.
+CAV1	drug	alcohol	25556199	In contrast, the <strong>CaV1</strong>.2 and <strong>CaV1</strong>.3 α1 subunits were not altered at either 3 or 48 hours during <b>alcohol</b> withdrawal.
+CAV1	addiction	withdrawal	25556199	In contrast, the <strong>CaV1</strong>.2 and <strong>CaV1</strong>.3 α1 subunits were not altered at either 3 or 48 hours during alcohol <b>withdrawal</b>.
+CAV1	drug	amphetamine	24996399	With regard to the molecular mechanisms underlying drug addiction, <strong>Cav1</strong>.3 channels are necessary for the development and <strong>Cav1</strong>.2 channels for the expression of cocaine and <b>amphetamine</b> behavioural sensitisation.
+CAV1	drug	cocaine	24996399	With regard to the molecular mechanisms underlying drug addiction, <strong>Cav1</strong>.3 channels are necessary for the development and <strong>Cav1</strong>.2 channels for the expression of <b>cocaine</b> and amphetamine behavioural sensitisation.
+CAV1	addiction	addiction	24996399	With regard to the molecular mechanisms underlying drug <b>addiction</b>, <strong>Cav1</strong>.3 channels are necessary for the development and <strong>Cav1</strong>.2 channels for the expression of cocaine and amphetamine behavioural sensitisation.
+CAV1	addiction	intoxication	24710718	<strong>Caveolin 1</strong> is essential for protecting against <b>binge</b> drinking induced liver damage through inhibiting reactive nitrogen species.
+CAV1	drug	alcohol	24710718	<strong>Caveolin 1</strong> (Cav 1) is known to participate in many diseases, but its roles in <b>alcoholic</b> liver injury remain unknown.
+CAV1	drug	nicotine	24470632	Transcriptional regulation of L type calcium channel subtypes <strong>Cav1</strong>.2 and <strong>Cav1</strong>.3 by <b>nicotine</b> and their potential role in <b>nicotine</b> sensitization.
+CAV1	addiction	sensitization	24470632	Transcriptional regulation of L type calcium channel subtypes <strong>Cav1</strong>.2 and <strong>Cav1</strong>.3 by nicotine and their potential role in nicotine <b>sensitization</b>.
+CAV1	drug	cocaine	21940447	<strong>Cav1</strong>.2 L type Ca²⁺ channels mediate <b>cocaine</b> induced GluA1 trafficking in the nucleus accumbens, a long term adaptation dependent on ventral tegmental area Ca(v)1.3 channels.
+CAV1	addiction	dependence	17949410	These results indicate that BZDs examined here have the potential to increase L type HVCC functions mediated via the enhanced expression of not only <strong>Cav1</strong>.2 and <strong>Cav1</strong>.3 but also alpha2/delta1 subunit after their sustained exposure, which may participate in the development of physical <b>dependence</b> by these BZDs.
+CAV1	drug	amphetamine	17689567	In addition, chronic <b>amphetamine</b> upregulates subtype <strong>Cav1</strong>.2 containing L type calcium channels.
+CASP8	drug	amphetamine	32120831	Moreover, diminished expression of anti apoptotic proteins, including Bcl 2, Caspase3, Caspase7, and <strong>Caspase8</strong> in <b>METH</b> exposed SH SY5y cells, was significantly recovered by treatment with lupenone.
+CASP8	drug	opioid	31680075	Significant alterations in expression level of apoptosis related proteins in <b>methadone</b> hydrochloride treated CCRF CEM cells were found involving upregulation of <strong>caspase 8</strong> expression and downregulation of survivin expression.
+CASP8	drug	opioid	31680075	<b>Methadone</b> hydrochloride induced apoptosis in HL 60 cells involved upregulation of Bid and <strong>caspase 8</strong> expression and downregulation of Bcl 2, p21 and survivin expression.
+CASP8	drug	alcohol	31105269	<b>Alcohol</b> increased IL 17A production and pro apoptotic signaling evidenced by Bax, Bim, caspase 3, and <strong>caspase 8</strong> increases via endoplasmic reticulum (ER) stress indicated by C/EBP homologous protein (CHOP) upregulation; this was prevented by the ER stress inhibitor, 4 PBA, in isolated crypts in vitro and in vivo.
+CASP8	drug	cocaine	28253291	In the frame of the longitudinal Zurich <b>Cocaine</b> Cognition Study, the Machiavellianism Questionnaire (<strong>MACH</strong> IV) was assessed in 68 recreational and 30 dependent <b>cocaine</b> users as well as in 68 psychostimulant naïve controls at baseline.
+CASP8	drug	cocaine	28253291	At the one year follow up, 57 <b>cocaine</b> users and 48 controls were reassessed with the <strong>MACH</strong> IV.
+CASP8	drug	cocaine	28253291	During the one year interval, <strong>MACH</strong> IV scores showed high test retest reliability and also the significant gap between <b>cocaine</b> users and controls remained.
+CASP8	drug	alcohol	27527870	<b>Ethanol</b> caused both apoptotic and necrotic cell death which was demonstrated by the increase in active caspase 3, <strong>caspase 8</strong>, cleaved PARP, cleaved CK 18 and the secretion of high mobility group protein B1 (HMGB1).
+CASP8	drug	alcohol	26857094	OEA also prevented <b>ethanol</b> induced lipid peroxidation, <strong>caspase 8</strong> and pro apoptotic caspase 3 activation in frontal cortex.
+CASP8	drug	alcohol	25421516	Levels of pro apoptotic <strong>caspase 8</strong> (C8), X linked inhibitor of apoptosis protein (XIAP), direct IAP binding protein with low pI (DIABLO), proliferating cell nuclear antigen (PCNA), and density of cells immunoreactive for proliferation marker Ki 67 (Ki 67 IR) were measured postmortem in the left orbitofrontal cortex (OFC) of 29 subjects with <b>alcohol</b> dependence and 23 nonpsychiatric comparison subjects.
+CASP8	addiction	dependence	25421516	Levels of pro apoptotic <strong>caspase 8</strong> (C8), X linked inhibitor of apoptosis protein (XIAP), direct IAP binding protein with low pI (DIABLO), proliferating cell nuclear antigen (PCNA), and density of cells immunoreactive for proliferation marker Ki 67 (Ki 67 IR) were measured postmortem in the left orbitofrontal cortex (OFC) of 29 subjects with alcohol <b>dependence</b> and 23 nonpsychiatric comparison subjects.
+CASP8	drug	alcohol	24625836	Several fold increases for cytochrome P450 2E1, <strong>caspase 8</strong> and caspase 3 found in the lungs of <b>ethanol</b> fed mice as compared to pair fed controls suggest role of oxidative stress in <b>ethanol</b> induced lung injury.
+CASP8	addiction	reward	22469627	The present study investigated the effects of biperiden, a muscarinic cholinergic (<strong>mACh</strong>) antagonist in two animal models: conditioned place preference (<b>CPP</b>) and behavioral sensitization.
+CASP8	addiction	sensitization	22469627	The present study investigated the effects of biperiden, a muscarinic cholinergic (<strong>mACh</strong>) antagonist in two animal models: conditioned place preference (CPP) and behavioral <b>sensitization</b>.
+CASP8	drug	cocaine	22469627	Biperiden, as other <strong>mACh</strong> antagonists, may be a promising drug for the pharmacologic treatment of <b>cocaine</b> addiction.
+CASP8	addiction	addiction	22469627	Biperiden, as other <strong>mACh</strong> antagonists, may be a promising drug for the pharmacologic treatment of cocaine <b>addiction</b>.
+CASP8	drug	alcohol	21664448	These structures showed activation of caspase 3 and 9 but not of <strong>caspase 8</strong> suggesting that <b>alcohol</b> induced apoptosis could occur by the intrinsic pathway.
+CASP8	drug	alcohol	20090911	Neither <b>ethanol</b> nor ADH affected the expression of ANP, total pro caspase 9, cytosolic and total pro <strong>caspase 8</strong>, TNF alpha, Fas receptor, Fas L and cytosolic AIF.
+CASP8	drug	opioid	17384938	This study analyzes the effects of prolonged administration of <b>methadone</b> and withdrawal on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and <strong>caspase 8</strong>) and the mitochondrial (Bcl 2, Bcl x(L), Bad, and Bax) apoptotic pathways.
+CASP8	addiction	withdrawal	17384938	This study analyzes the effects of prolonged administration of methadone and <b>withdrawal</b> on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and <strong>caspase 8</strong>) and the mitochondrial (Bcl 2, Bcl x(L), Bad, and Bax) apoptotic pathways.
+CASP8	drug	opioid	17384938	Both the chronic <b>methadone</b> and repeated withdrawal groups showed up regulation of several pro apoptotic proteins (FasL, the active fragment of <strong>caspase 8</strong>, and Bad) in the cortex and hippocampus, indicating activation of both the death receptor and mitochondrial apoptotic pathways.
+CASP8	addiction	withdrawal	17384938	Both the chronic methadone and repeated <b>withdrawal</b> groups showed up regulation of several pro apoptotic proteins (FasL, the active fragment of <strong>caspase 8</strong>, and Bad) in the cortex and hippocampus, indicating activation of both the death receptor and mitochondrial apoptotic pathways.
+CASP8	addiction	addiction	16909207	In <b>addiction</b>, release of cytochrome c and caspase 9 and <strong>caspase 8</strong> activation were detected.
+CASP8	drug	alcohol	14724834	<b>Ethanol</b> binge increased caspase 3 and <strong>caspase 8</strong> activity, the expression of Fas ligand, and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling in fa/fa rats.
+CASP8	addiction	intoxication	14724834	Ethanol <b>binge</b> increased caspase 3 and <strong>caspase 8</strong> activity, the expression of Fas ligand, and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling in fa/fa rats.
+CASP8	drug	nicotine	14622092	The mechanism of TNFalpha mediated neuroprotection and antagonism by <b>nicotine</b> was independent of <strong>caspase 8</strong> activation or nuclear factor kappa B translocation in neurons but C6 ceramide addition to neuronal cultures subsequently exposed to NMDA mimicked the neuroprotective effect of TNFalpha and, like TNFalpha, it was antagonized by cotreatment with <b>nicotine</b>.
+CASP8	drug	alcohol	14502238	In the present study, following <b>ethanol</b> administration to infant mice, we found no change in activated <strong>caspase 8</strong>, which suggests that the extrinsic pathway is not involved in <b>ethanol</b> induced apoptosis.
+CASP8	drug	nicotine	11353030	The intrinsic burst facilitation and PDS depression provoked by Ach or Cch were mimicked by methyl acetylcholine (<strong>mAch</strong>, 100 400 microM, n = 11), were reversed by atropine application (1 50 microM, n = 3), and were not mimicked by <b>nicotine</b> (50 100 microM, n = 4), indicating the involvement of muscarinic receptors.
+CASP8	drug	benzodiazepine	2985852	On the other hand, radiolabeled ligand binding to CNS receptors in the <b>benzodiazepine</b> (BDZ) , muscarinic cholinergic (<strong>mACh</strong>) , methionine enkephalin (ENK)  and thyrotropin releasing hormone (TRH) RRA systems was not inhibited even by the addition of HOPA up to 100 microM.
+SNCA	drug	alcohol	32432761	The mutation of <strong>SNCA</strong> can influence the formation of nerve fibers and the function of dopaminergic neurons, and that may be related to addictive behavior, such as <b>alcohol</b> dependence.
+SNCA	addiction	addiction	32432761	The mutation of <strong>SNCA</strong> can influence the formation of nerve fibers and the function of dopaminergic neurons, and that may be related to <b>addictive</b> behavior, such as alcohol dependence.
+SNCA	addiction	dependence	32432761	The mutation of <strong>SNCA</strong> can influence the formation of nerve fibers and the function of dopaminergic neurons, and that may be related to addictive behavior, such as alcohol <b>dependence</b>.
+SNCA	drug	alcohol	32432761	<strong>SNCA</strong> may overlap with the pathogenesis of schizophrenia and Parkinson's disease or <b>alcohol</b> dependence associated with the dopamine pathway.
+SNCA	addiction	dependence	32432761	<strong>SNCA</strong> may overlap with the pathogenesis of schizophrenia and Parkinson's disease or alcohol <b>dependence</b> associated with the dopamine pathway.
+SNCA	drug	amphetamine	31150652	At the same time, <b>Meth</b> induced alterations, specifically within alpha synuclein gene (<strong>SNCA</strong>) or its promoter, were evaluated.
+SNCA	drug	alcohol	30120834	<b>Ethanol</b> (EtOH) Related Behaviors in α Synuclein Mutant Mice and Association of <strong>SNCA</strong> SNPs with Anxiety in EtOH Dependent Patients.
+SNCA	addiction	withdrawal	30120834	We used the C57BL/6JOlaHsd <strong>Snca</strong> mutant mice to assess EtOH intake; sensitivity to the anxiolytic effects of EtOH in a test battery comprising the open field, the light dark box, and the elevated plus maze; and both anxiety and convulsions induced by EtOH <b>withdrawal</b>.
+SNCA	drug	alcohol	29502276	DAVID functional annotation analysis identified 9 proteins (<strong>SNCA</strong>, GSTP1, PRDX3, PPP3R1, EIF5A, PHB, PEBP1/RKIP, GAPDH, AND SOD1) that were significantly overrepresented in a functional cluster that included the Gene Ontology categories "response to <b>alcohol</b>" and "aging."
+SNCA	drug	alcohol	28833174	Interestingly, independent genome wide association studies also identified <strong>SNCA</strong> as the most important candidate gene for <b>alcoholism</b>.
+SNCA	drug	alcohol	28833174	These results provide experimental confirmation of <strong>SNCA</strong> as a candidate gene for <b>alcoholism</b> in addition to its known link to PD.
+SNCA	drug	alcohol	26621272	The results indicate that <b>alcohol</b> dependence is associated with high expression of <strong>SNCA</strong> and DRD4 (signifi cantly higher than in the control group) and is not associated with changes in the work of NR4A2 and DRD3 genes.
+SNCA	addiction	dependence	26621272	The results indicate that alcohol <b>dependence</b> is associated with high expression of <strong>SNCA</strong> and DRD4 (signifi cantly higher than in the control group) and is not associated with changes in the work of NR4A2 and DRD3 genes.
+SNCA	drug	alcohol	26621272	The expression of <strong>SNCA</strong> and DRD4 genes can serve as an important peripheral marker of <b>alcohol</b> dependence development, which is essential for antipsychotic therapy.
+SNCA	addiction	dependence	26621272	The expression of <strong>SNCA</strong> and DRD4 genes can serve as an important peripheral marker of alcohol <b>dependence</b> development, which is essential for antipsychotic therapy.
+SNCA	drug	alcohol	26297298	Previous studies have found that the gene for α synuclein, <strong>SNCA</strong>, is differentially expressed in <b>alcohol</b> misusers.
+SNCA	drug	alcohol	26297298	The present study measured the expression of three α synuclein variants, <strong>SNCA</strong> 140, <strong>SNCA</strong> 112, and <strong>SNCA</strong> 115 in the prefrontal cortex of controls and <b>alcohol</b> misusers with and without cirrhosis of the liver.
+SNCA	drug	alcohol	26297298	The expression of <strong>SNCA</strong> 140 and <strong>SNCA</strong> 112 was significantly lower in <b>alcohol</b> misusers with cirrhosis than in controls.
+SNCA	drug	alcohol	26297298	However, <strong>SNCA</strong> 115 expression was significantly greater in <b>alcohol</b> misusers with cirrhosis than in controls.
+SNCA	drug	alcohol	24844177	The top CFG scoring gene for <b>alcoholism</b> from the initial discovery step, synuclein alpha (<strong>SNCA</strong>) remained the top gene after the stress reactive animal model cross validation.
+SNCA	drug	alcohol	24844177	The top CFG scoring gene for <b>alcoholism</b> from the initial discovery step, <strong>synuclein alpha</strong> (<strong>SNCA</strong>) remained the top gene after the stress reactive animal model cross validation.
+SNCA	drug	alcohol	24844177	<strong>SNCA</strong> by itself was able to separate <b>alcoholics</b> from controls in the <b>alcohol</b> dependent cohort (P=0.000013) and the <b>alcohol</b> abuse cohort (P=0.023).
+SNCA	drug	alcohol	23384371	Genetic variation in the alpha synuclein gene (<strong>SNCA</strong>) is associated with BOLD response to <b>alcohol</b> cues.
+SNCA	drug	alcohol	23384371	Preclinical studies implicate the gene encoding the alpha synuclein protein (<strong>SNCA</strong>) in the pathophysiology of <b>alcohol</b> dependence and dopamine neuron function.
+SNCA	addiction	dependence	23384371	Preclinical studies implicate the gene encoding the alpha synuclein protein (<strong>SNCA</strong>) in the pathophysiology of alcohol <b>dependence</b> and dopamine neuron function.
+SNCA	drug	alcohol	23384371	This study aimed to examine whether polymorphisms in the <strong>SNCA</strong> gene were associated with <b>alcohol</b> taste cue elicited responses in the brain, one such intermediate phenotype.
+SNCA	drug	alcohol	23384371	<strong>SNCA</strong> genotype was found to be associated with the degree of fMRI BOLD response during exposure to the taste of <b>alcohol</b> versus a control taste.
+SNCA	drug	alcohol	23345080	Furthermore, C57BL/6(<strong>Snca</strong> / ) mice showed an increase in <b>alcohol</b> consumption when offered a 10% <b>alcohol</b> solution.
+SNCA	drug	alcohol	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, DRD2, DRD3, DRD4) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of craving, as well as alpha synuclein (<strong>SNCA</strong>), which has been previously found to be associated with craving, were associated with <b>alcohol</b> craving in this sample.
+SNCA	addiction	relapse	22481050	For genetic analyses, we first examined whether genes in the dopamine pathway, including dopamine receptor genes (DRD1, DRD2, DRD3, DRD4) and the dopamine transporter gene (SLC6A3), which have been implicated in neurobiological studies of <b>craving</b>, as well as alpha synuclein (<strong>SNCA</strong>), which has been previously found to be associated with <b>craving</b>, were associated with alcohol <b>craving</b> in this sample.
+SNCA	addiction	relapse	22481050	When examining genes in the dopamine pathway, single nucleotide polymorphisms (SNPs) in DRD3 and <strong>SNCA</strong> were associated with <b>craving</b> (p<0.05).
+SNCA	drug	alcohol	21513161	[Inheritance mechnisam of gene <strong>SNCA</strong> for <b>alcohol</b> dependence].
+SNCA	addiction	dependence	21513161	[Inheritance mechnisam of gene <strong>SNCA</strong> for alcohol <b>dependence</b>].
+SNCA	drug	alcohol	21513161	<strong>SNCA</strong> gene is located in a quantitative trait locus for <b>alcohol</b> preference.
+SNCA	drug	alcohol	21513161	Alpha synuclein coded by <strong>SNCA</strong> gene can regulate the function of dopamine in multiple levels, and dopamine is an important neurotransmitter in <b>alcohol</b> preference.
+SNCA	drug	alcohol	21513161	Variation has been found in <strong>SNCA</strong> gene carried by <b>alcohol</b> dependent patients.
+SNCA	drug	alcohol	21513161	Meanwhile, significant increase of <strong>SNCA</strong> gene expression also occurs in <b>alcohol</b> dependent patients, which is closely associated with the level of <b>alcohol</b> dependence.
+SNCA	addiction	dependence	21513161	Meanwhile, significant increase of <strong>SNCA</strong> gene expression also occurs in alcohol dependent patients, which is closely associated with the level of alcohol <b>dependence</b>.
+SNCA	drug	alcohol	21513161	Therefore, <strong>SNCA</strong> gene is believed to contribute to genetic mechanism of <b>alcohol</b> dependence.
+SNCA	addiction	dependence	21513161	Therefore, <strong>SNCA</strong> gene is believed to contribute to genetic mechanism of alcohol <b>dependence</b>.
+SNCA	drug	alcohol	21513161	Here, the relationship between <strong>SNCA</strong> gene and dopamine, the variation and expression of <strong>SNCA</strong> gene in <b>alcohol</b> dependent patients were reviewed.
+SNCA	addiction	relapse	21309955	Research suggests that alpha synuclein (<strong>SNCA</strong>) and NACP Rep1, a polymorphic complex microsatellite repeat ~10 kb upstream of the <strong>SNCA</strong> gene translational start, may be involved in substance use behaviors and <b>craving</b>.
+SNCA	addiction	relapse	21309955	This study was the first to examine the effects of diacetylmorphine (DAM) on peripheral <strong>SNCA</strong> protein expression along with <b>craving</b> in opiate dependent patients and to compare their NACP Rep1 allele lengths with those of healthy controls.
+SNCA	addiction	relapse	21309955	One way repeated measures ANOVAs provided significant overall effects for <strong>SNCA</strong> protein content (P = 0.028), <b>craving</b> (P < 0.001), withdrawal symptomatology (P < 0.001) and mood (P < 0.001), indicating that DAM injections may not only reduce <b>craving</b> but also <strong>SNCA</strong> protein expression.
+SNCA	addiction	withdrawal	21309955	One way repeated measures ANOVAs provided significant overall effects for <strong>SNCA</strong> protein content (P = 0.028), craving (P < 0.001), <b>withdrawal</b> symptomatology (P < 0.001) and mood (P < 0.001), indicating that DAM injections may not only reduce craving but also <strong>SNCA</strong> protein expression.
+SNCA	addiction	dependence	21309955	The findings provide evidence of a contributory role of <strong>SNCA</strong> and NACP Rep1 for opiate <b>dependence</b>.
+SNCA	drug	alcohol	21271299	Alpha synuclein (<strong>SNCA</strong>) is associated with a range of psychiatric diseases including neurodegeneration, <b>alcohol</b> craving, and depression.
+SNCA	addiction	relapse	21271299	Alpha synuclein (<strong>SNCA</strong>) is associated with a range of psychiatric diseases including neurodegeneration, alcohol <b>craving</b>, and depression.
+SNCA	drug	amphetamine	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, <strong>SNCA</strong>, and SOD2) with <b>METH</b> psychosis.
+SNCA	addiction	dependence	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, <strong>SNCA</strong>, and SOD2) with METH psychosis.
+SNCA	addiction	addiction	17374033	Despite modest support for association between multiple <strong>SNCA</strong> SNPs and several of the <b>addictive</b> disorders tested in this study, statistical significance disappeared after correction for multiple testing.
+SNCA	drug	alcohol	17374033	Thus, our data do not support a role for a variant in the <strong>SNCA</strong> gene that contributes to <b>alcohol</b> or drug addiction in the 2 studied American Indian populations.
+SNCA	addiction	addiction	17374033	Thus, our data do not support a role for a variant in the <strong>SNCA</strong> gene that contributes to alcohol or drug <b>addiction</b> in the 2 studied American Indian populations.
+SNCA	drug	alcohol	17374032	Association of <b>alcohol</b> craving with alpha synuclein (<strong>SNCA</strong>).
+SNCA	addiction	relapse	17374032	Association of alcohol <b>craving</b> with alpha synuclein (<strong>SNCA</strong>).
+SNCA	drug	alcohol	17374032	Studies have found that genomic variation in the gene <strong>SNCA</strong>, which encodes the protein alpha synuclein, may contribute to the variation in <b>alcohol</b> consumption in an inbred rat model of <b>alcohol</b> preference.
+SNCA	drug	alcohol	17374032	Studies in humans have provided support for an association between <strong>SNCA</strong> and craving for <b>alcohol</b>.
+SNCA	addiction	relapse	17374032	Studies in humans have provided support for an association between <strong>SNCA</strong> and <b>craving</b> for alcohol.
+SNCA	drug	alcohol	17374032	To examine the role of this gene in <b>alcohol</b> dependence and related phenotypes, 30 single nucleotide polymorphisms (SNPs) were genotyped across the <strong>SNCA</strong> gene in a sample of 219 multiplex <b>alcoholic</b> families of European American descent.
+SNCA	addiction	dependence	17374032	To examine the role of this gene in alcohol <b>dependence</b> and related phenotypes, 30 single nucleotide polymorphisms (SNPs) were genotyped across the <strong>SNCA</strong> gene in a sample of 219 multiplex alcoholic families of European American descent.
+SNCA	drug	alcohol	17374032	There was no evidence of association between any of the <strong>SNCA</strong> SNPs and <b>alcohol</b> dependence (p>or=0.13).
+SNCA	addiction	dependence	17374032	There was no evidence of association between any of the <strong>SNCA</strong> SNPs and alcohol <b>dependence</b> (p>or=0.13).
+SNCA	drug	alcohol	17374032	These results suggest that variation in <strong>SNCA</strong> contributes to <b>alcohol</b> craving, a common, although not uniform, feature of <b>alcohol</b> dependence.
+SNCA	addiction	dependence	17374032	These results suggest that variation in <strong>SNCA</strong> contributes to alcohol craving, a common, although not uniform, feature of alcohol <b>dependence</b>.
+SNCA	addiction	relapse	17374032	These results suggest that variation in <strong>SNCA</strong> contributes to alcohol <b>craving</b>, a common, although not uniform, feature of alcohol dependence.
+SNCA	drug	alcohol	16762686	The gene <strong>SNCA</strong> (or NACP), which codes for alpha synuclein, a small synaptic protein involved in dopaminergic neurotransmission, maps to a quantitative trait locus for <b>alcohol</b> preference and is differentially expressed in specific brain regions in <b>alcohol</b> preferring versus  nonpreferring rats.
+SNCA	drug	alcohol	16459936	Using Latent Growth Mixture Modeling, a four class model was identified: Severe Chronic <b>Alcoholics</b>; Severe Non Chronic <b>Alcoholics</b> (<strong>SNCA</strong>); Late Onset <b>Alcoholics</b>; and Young Adult <b>Alcoholics</b>.
+SNCA	drug	alcohol	16459936	Counterparts for three trajectories could be found in the larger <b>alcoholism</b> literature, whereas the fourth type (<strong>SNCA</strong>) has not been described, notwithstanding its seeming importance and prevalence.
+RGS4	addiction	reward	30036561	Regulator of G protein signaling (RGS) proteins such as RGS2 and <strong>RGS4</strong> are widely distributed in brain regions that play a role in drug <b>reward</b>.
+RGS4	drug	cocaine	30036561	Importantly, RGS2 and <strong>RGS4</strong> negatively regulate G protein coupled receptor signaling pathways of monoaminergic neurotransmitters that play a role in the rewarding effects of <b>cocaine</b> by enhancing the rate of hydrolysis of Gα bound guanine nucleotide triphosphate.
+RGS4	drug	cocaine	30036561	Thus, the objective of this study was to investigate the effects of <b>cocaine</b> on conditioned place preference (CPP) and locomotor activity in mice that lacked either RGS2 or <strong>RGS4</strong> (i.e.
+RGS4	addiction	reward	30036561	Thus, the objective of this study was to investigate the effects of cocaine on conditioned place preference (<b>CPP</b>) and locomotor activity in mice that lacked either RGS2 or <strong>RGS4</strong> (i.e.
+RGS4	drug	cocaine	30036561	<b>Cocaine</b> induced CPP was attenuated in male, but not female <strong>RGS4</strong> KO mice compared to respective <strong>RGS4</strong> WT mice.
+RGS4	addiction	reward	30036561	Cocaine induced <b>CPP</b> was attenuated in male, but not female <strong>RGS4</strong> KO mice compared to respective <strong>RGS4</strong> WT mice.
+RGS4	drug	cocaine	30036561	Similarly, <b>cocaine</b> induced locomotor activity was not influenced by deletion of either RGS2 or <strong>RGS4</strong> irrespective of sex.
+RGS4	drug	cocaine	30036561	Together, the data indicate that the rewarding effects of <b>cocaine</b> were attenuated in the absence of <strong>RGS4</strong> expression, but not in the absence of RGS2 expression in a sex dependent manner.
+RGS4	drug	cocaine	30036561	Importantly, these data suggest that <strong>RGS4</strong> can serve as a potential target for medications that can be used to treat <b>cocaine</b> addiction.
+RGS4	addiction	addiction	30036561	Importantly, these data suggest that <strong>RGS4</strong> can serve as a potential target for medications that can be used to treat cocaine <b>addiction</b>.
+RGS4	drug	opioid	29754475	Regulator of G Protein Signaling 4 (<strong>RGS4</strong>) Controls <b>Morphine</b> Reward by Glutamate Receptor Activation in the Nucleus Accumbens of Mouse Brain.
+RGS4	addiction	reward	29754475	Regulator of G Protein Signaling 4 (<strong>RGS4</strong>) Controls Morphine <b>Reward</b> by Glutamate Receptor Activation in the Nucleus Accumbens of Mouse Brain.
+RGS4	drug	opioid	29754475	<strong>Regulator of G Protein Signaling 4</strong> (<strong>RGS4</strong>) Controls <b>Morphine</b> Reward by Glutamate Receptor Activation in the Nucleus Accumbens of Mouse Brain.
+RGS4	addiction	reward	29754475	<strong>Regulator of G Protein Signaling 4</strong> (<strong>RGS4</strong>) Controls Morphine <b>Reward</b> by Glutamate Receptor Activation in the Nucleus Accumbens of Mouse Brain.
+RGS4	drug	opioid	29754475	The present study used a short hairpin RNA (shRNA) mediated knock down of <strong>RGS4</strong> in the NAc of the mouse brain to investigate the relationship between the activation of ionotropic glutamate receptors and <strong>RGS4</strong> in the NAc during <b>morphine</b> reward.
+RGS4	addiction	reward	29754475	The present study used a short hairpin RNA (shRNA) mediated knock down of <strong>RGS4</strong> in the NAc of the mouse brain to investigate the relationship between the activation of ionotropic glutamate receptors and <strong>RGS4</strong> in the NAc during morphine <b>reward</b>.
+RGS4	drug	opioid	29754475	Additionally, the shRNA mediated <strong>RGS4</strong> knock down was implemented in NAc/striatal primary cultured neurons to investigate the role that striatal neurons have in the <b>morphine</b> induced activation of ionotropic glutamate receptors.
+RGS4	drug	opioid	29754475	The results of this study show that the NAc specific knockdown of <strong>RGS4</strong> significantly increased the behaviors associated with <b>morphine</b> and did so by phosphorylation of the GluR1 (Ser831) and NR2A (Tyr1325) glutamate receptors in the NAc.
+RGS4	drug	opioid	29754475	Furthermore, the knock down of <strong>RGS4</strong> enhanced the phosphorylation of the GluR1 and NR2A glutamate receptors in the primary NAc/striatal neurons during spontaneous <b>morphine</b> withdrawal.
+RGS4	addiction	withdrawal	29754475	Furthermore, the knock down of <strong>RGS4</strong> enhanced the phosphorylation of the GluR1 and NR2A glutamate receptors in the primary NAc/striatal neurons during spontaneous morphine <b>withdrawal</b>.
+RGS4	drug	opioid	29754475	These findings show a novel molecular mechanism of <strong>RGS4</strong> in glutamatergic transmission that underlies the negative symptoms associated with <b>morphine</b> administration.
+RGS4	drug	cocaine	27261631	Animals abstinent from chronic <b>cocaine</b> showed decreased expression of regulator of G protein signaling 2 (RGS2) and <strong>RGS4</strong>, as well as upregulation of RGS9.
+RGS4	drug	cannabinoid	26478461	Inhibition of the regulator of G protein signalling <strong>RGS4</strong> in the spinal cord decreases neuropathic hyperalgesia and restores <b>cannabinoid</b> CB1 receptor signalling.
+RGS4	drug	cannabinoid	26478461	Because the reduced potency of analgesic agents in neuropathic pain may reflect alterations in RGS, we assessed the effects of CCG 63802, a specific <strong>RGS4</strong> inhibitor, on pain hypersensitivity and signalling through <b>cannabinoid</b> receptors, in a model of neuropathic pain.
+RGS4	drug	amphetamine	26321241	The mRNA levels of RGS2 and <strong>RGS4</strong> in both the VTA and NAc were positively correlated with the rate of <b>AMPH</b> intake.
+RGS4	drug	amphetamine	24513972	<b>AMPH</b> had no effects on the midbrain expression and trafficking of other RGS proteins such as <strong>RGS4</strong> and RGS8.
+RGS4	addiction	addiction	23630294	<strong>Rgs4</strong> is expressed in several brain regions involved in mood, movement, cognition, and <b>addiction</b> and is regulated by psychotropic drugs, stress, and corticosteroids.
+RGS4	drug	opioid	23630294	Interestingly, in prefrontal cortex, <strong>Rgs4</strong> acts as a negative modulator of the actions of nonmonoamine directed drugs that are purported to act as antidepressants: the N methyl D aspartate glutamate receptor antagonist ketamine and the delta <b>opioid</b> agonist (+) 4 [(αR) α ((2S,5R) 4 Allyl 2,5 dimethyl 1 piperazinyl) 3 methoxybenzyl] N,N diethylbenzamide.
+RGS4	drug	psychedelics	23630294	Interestingly, in prefrontal cortex, <strong>Rgs4</strong> acts as a negative modulator of the actions of nonmonoamine directed drugs that are purported to act as antidepressants: the N methyl D aspartate glutamate receptor antagonist <b>ketamine</b> and the delta opioid agonist (+) 4 [(αR) α ((2S,5R) 4 Allyl 2,5 dimethyl 1 piperazinyl) 3 methoxybenzyl] N,N diethylbenzamide.
+RGS4	drug	amphetamine	22193724	<strong>RGS4</strong> overexpression in the rat dorsal striatum modulates mGluR5  and <b>amphetamine</b> mediated behavior and signaling.
+RGS4	addiction	addiction	22193724	Decreased availability of <strong>RGS4</strong> in the frontal cortex and striatum has been described in animal models of schizophrenia and drug <b>addiction</b>.
+RGS4	drug	amphetamine	22193724	This study aims to investigate whether <strong>RGS4</strong>, through inhibiting the function of mGluR5 receptors in the dorsal striatum (dSTR), regulates cellular and behavioral responses to acute <b>amphetamine</b>.
+RGS4	drug	amphetamine	22193724	The effect of <strong>RGS4</strong> overexpression on behavioral activity induced by the intrastriatal mGluR5 agonist, DHPG, or <b>amphetamine</b> was recorded.
+RGS4	drug	amphetamine	22193724	<strong>RGS4</strong> overexpression or the mGluR5 antagonist, 3 ((2 methyl 4 thiazolyl)ethynyl)pyridine (MTEP), attenuated <b>amphetamine</b> induced phospho ERK (but not phospho Akt) levels.
+RGS4	drug	amphetamine	22193724	<strong>RGS4</strong> suppressed <b>amphetamine</b> induced vertical activity and augmented horizontal activity over 90 min.
+RGS4	drug	amphetamine	22193724	The present data demonstrate that <strong>RGS4</strong> in the dSTR attenuates <b>amphetamine</b> induced ERK signaling and decreases the behavioral efficacy of acute <b>amphetamine</b> likely by limiting mGluR5 function.
+RGS4	drug	opioid	22129844	Several members of this family, in particular <strong>RGS4</strong> and RGS9 2 have been demonstrated to influence MOR signaling and <b>morphine</b> induced behaviors, including reward.
+RGS4	addiction	reward	22129844	Several members of this family, in particular <strong>RGS4</strong> and RGS9 2 have been demonstrated to influence MOR signaling and morphine induced behaviors, including <b>reward</b>.
+RGS4	drug	opioid	22129844	Moreover, this interaction is not unidirectional since <b>morphine</b> has been demonstrated to modulate expression levels of RGS proteins, especially <strong>RGS4</strong> and RGS9 2, in a tissue and time dependent manner.
+RGS4	drug	amphetamine	22074218	Neurochemical assays indicated that there is a decrease in dopamine D1 receptor ligand binding and an increase in the expression of <strong>RGS4</strong> mRNA in the striatum of <b>METH</b> treated μ opioid receptor knockout mice but not of <b>METH</b> treated wild type mice.
+RGS4	drug	opioid	22074218	Neurochemical assays indicated that there is a decrease in dopamine D1 receptor ligand binding and an increase in the expression of <strong>RGS4</strong> mRNA in the striatum of METH treated μ <b>opioid</b> receptor knockout mice but not of METH treated wild type mice.
+RGS4	drug	amphetamine	22074218	These results indicate that down regulation of the expression of the dopamine D1 receptor and up regulation of <strong>RGS4</strong> mRNA expression in the striatum may contribute to the reduced response to <b>METH</b> induced stereotypy behavior in μ opioid receptor knockout mice.
+RGS4	drug	opioid	22074218	These results indicate that down regulation of the expression of the dopamine D1 receptor and up regulation of <strong>RGS4</strong> mRNA expression in the striatum may contribute to the reduced response to METH induced stereotypy behavior in μ <b>opioid</b> receptor knockout mice.
+RGS4	drug	opioid	22056472	<strong>RGS4</strong>, RGS9 and RGS10 levels were also studied in brains (frontal cortex) of rats submitted to acute and chronic <b>morphine</b> treatment and to spontaneous and <b>naloxone</b> precipitated opiate withdrawal.
+RGS4	addiction	withdrawal	22056472	<strong>RGS4</strong>, RGS9 and RGS10 levels were also studied in brains (frontal cortex) of rats submitted to acute and chronic morphine treatment and to spontaneous and naloxone precipitated opiate <b>withdrawal</b>.
+RGS4	drug	opioid	22056472	Chronic <b>morphine</b> treatment in rats was associated with an increase in <strong>RGS4</strong> protein immunoreactivity (Δ = 28 ± 7%), which persisted in spontaneous (Δ = 35 ± 8%) and <b>naloxone</b> precipitated withdrawal (Δ = 30 ± 9%) without significant changes in RGS9 and RGS10 proteins.
+RGS4	addiction	withdrawal	22056472	Chronic morphine treatment in rats was associated with an increase in <strong>RGS4</strong> protein immunoreactivity (Δ = 28 ± 7%), which persisted in spontaneous (Δ = 35 ± 8%) and naloxone precipitated <b>withdrawal</b> (Δ = 30 ± 9%) without significant changes in RGS9 and RGS10 proteins.
+RGS4	addiction	dependence	22056472	The specific modulation of <strong>RGS4</strong> and RGS10 protein expression observed in the prefrontal cortex of opiate abusers might be relevant in the neurobiology of opiate tolerance, <b>dependence</b> and withdrawal.
+RGS4	addiction	withdrawal	22056472	The specific modulation of <strong>RGS4</strong> and RGS10 protein expression observed in the prefrontal cortex of opiate abusers might be relevant in the neurobiology of opiate tolerance, dependence and <b>withdrawal</b>.
+RGS4	drug	alcohol	20430014	Association of polymorphisms in <strong>RGS4</strong> and expression of RGS transcripts in the brains of human <b>alcoholics</b>.
+RGS4	drug	alcohol	20430014	We used Real Time PCR to measure the expression of two members of the RGS family, <strong>RGS4</strong> and RGS7, in the superior frontal gyrus and primary motor cortex from <b>alcoholic</b> and non <b>alcoholic</b> cases.
+RGS4	drug	alcohol	20430014	Overall, cirrhotic <b>alcoholics</b> had lower expression levels of <strong>RGS4</strong> mRNA than controls and non cirrhotic <b>alcoholics</b>.
+RGS4	drug	alcohol	20430014	We also report that the four <strong>RGS4</strong> SNPs (SNP1, 4, 7 and 18) may be associated with <b>alcoholism</b> in European Caucasians at the haplotype level.
+RGS4	drug	opioid	19914603	Brain region specific actions of <strong>regulator of G protein signaling 4</strong> oppose <b>morphine</b> reward and dependence but promote analgesia.
+RGS4	addiction	dependence	19914603	Brain region specific actions of <strong>regulator of G protein signaling 4</strong> oppose morphine reward and <b>dependence</b> but promote analgesia.
+RGS4	addiction	reward	19914603	Brain region specific actions of <strong>regulator of G protein signaling 4</strong> oppose morphine <b>reward</b> and dependence but promote analgesia.
+RGS4	drug	opioid	19914603	Inducible knockout or selective overexpression of <strong>RGS4</strong> in the nucleus accumbens reveals that, in this brain region, <strong>RGS4</strong> acts as a negative regulator of <b>morphine</b> reward, whereas in the locus coeruleus <strong>RGS4</strong> opposes <b>morphine</b> physical dependence.
+RGS4	addiction	dependence	19914603	Inducible knockout or selective overexpression of <strong>RGS4</strong> in the nucleus accumbens reveals that, in this brain region, <strong>RGS4</strong> acts as a negative regulator of morphine reward, whereas in the locus coeruleus <strong>RGS4</strong> opposes morphine physical <b>dependence</b>.
+RGS4	addiction	reward	19914603	Inducible knockout or selective overexpression of <strong>RGS4</strong> in the nucleus accumbens reveals that, in this brain region, <strong>RGS4</strong> acts as a negative regulator of morphine <b>reward</b>, whereas in the locus coeruleus <strong>RGS4</strong> opposes morphine physical dependence.
+RGS4	drug	opioid	19914603	In contrast, we show that <strong>RGS4</strong> does not affect <b>morphine</b> analgesia or tolerance but is a positive modulator of certain opiate analgesics, such as <b>methadone</b> and <b>fentanyl</b>.
+RGS4	drug	amphetamine	18221378	Chronic <b>AMPH</b> or cocaine also alters the regulation of inhibitory G protein coupled receptors in the striatum, as evident by a prolonged decrease in the level of <strong>regulator of G protein signaling 4</strong> after non contingent or contingent (self administered) drug exposure.
+RGS4	drug	cocaine	18221378	Chronic AMPH or <b>cocaine</b> also alters the regulation of inhibitory G protein coupled receptors in the striatum, as evident by a prolonged decrease in the level of <strong>regulator of G protein signaling 4</strong> after non contingent or contingent (self administered) drug exposure.
+RGS4	drug	amphetamine	17693584	<strong>Regulator of G protein signaling 4</strong> interacts with metabotropic glutamate receptor subtype 5 in rat striatum: relevance to <b>amphetamine</b> behavioral sensitization.
+RGS4	addiction	sensitization	17693584	<strong>Regulator of G protein signaling 4</strong> interacts with metabotropic glutamate receptor subtype 5 in rat striatum: relevance to amphetamine behavioral <b>sensitization</b>.
+RGS4	drug	amphetamine	17693584	However, it is not known whether <strong>RGS4</strong> and mGluR5 interactions occur in rat striatum and whether chronic <b>amphetamine</b> (<b>AMPH</b>) treatment produces changes in <strong>RGS4</strong> levels that are correlated with mGluR5 receptor activity.
+RGS4	drug	amphetamine	17693584	At this time point, animals pretreated with <b>AMPH</b> displayed sensitized behavioral responses to <b>AMPH</b> challenge and decreased <strong>RGS4</strong> protein in dorsal striatum and nucleus accumbens.
+RGS4	drug	amphetamine	17693584	This study further suggests that <b>AMPH</b> induced changes in mGluR5 associated protein levels (<strong>RGS4</strong>, Galpha(q/11), and PLCbeta1) may be related to altered coupling of striatal mGluR5 receptors in animals sensitized to <b>AMPH</b>.
+RGS4	drug	cocaine	17632279	Chronic <b>cocaine</b> reduces <strong>RGS4</strong> mRNA in rat prefrontal cortex and dorsal striatum.
+RGS4	drug	cocaine	17632279	In this report, chronic noncontingent (<b>cocaine</b> binge) or response contingent (self administration) delivery of <b>cocaine</b> followed by 2 3 weeks of abstinence resulted in a decrease of <strong>RGS4</strong> mRNA in the dorsal striatum and prefrontal cortex.
+RGS4	addiction	intoxication	17632279	In this report, chronic noncontingent (cocaine <b>binge</b>) or response contingent (self administration) delivery of cocaine followed by 2 3 weeks of abstinence resulted in a decrease of <strong>RGS4</strong> mRNA in the dorsal striatum and prefrontal cortex.
+RGS4	drug	cocaine	17632279	Furthermore, re exposure to the <b>cocaine</b> associated context after abstinence renewed the drug seeking and restored the levels of <strong>RGS4</strong> mRNA to control values.
+RGS4	addiction	relapse	17632279	Furthermore, re exposure to the cocaine associated context after abstinence renewed the drug <b>seeking</b> and restored the levels of <strong>RGS4</strong> mRNA to control values.
+RGS4	drug	cocaine	17632279	Changes in <strong>RGS4</strong> mRNA levels might signal abnormal receptor G protein coupling that impacts <b>cocaine</b> seeking.
+RGS4	addiction	relapse	17632279	Changes in <strong>RGS4</strong> mRNA levels might signal abnormal receptor G protein coupling that impacts cocaine <b>seeking</b>.
+RGS4	drug	opioid	15870291	Behavioral testing on mutant adults revealed subtle sensorimotor deficits but, so far, supported neither the proposed status of <strong>Rgs4</strong> as a schizophrenia susceptibility gene (by showing intact prepulse inhibition in the mutants) nor (unlike another member of the Rgs family, Rgs9) a role of <strong>Rgs4</strong> in the acute or chronic response to <b>opioids</b>.
+RGS4	drug	cocaine	14534355	The protein levels of the 5 HT2A receptor, Galphaz protein, and <strong>RGS4</strong> or RGS7 proteins were not altered by <b>cocaine</b> withdrawal in any of the above mentioned brain regions.
+RGS4	addiction	withdrawal	14534355	The protein levels of the 5 HT2A receptor, Galphaz protein, and <strong>RGS4</strong> or RGS7 proteins were not altered by cocaine <b>withdrawal</b> in any of the above mentioned brain regions.
+RGS4	drug	cocaine	12687634	Genes downregulated by <b>cocaine</b> include several genes associated with energy metabolism in mitochondria, as well as the phosphatydylinositol 4 kinase and the regulator of G protein signaling protein 4 (<strong>RGS4</strong>).
+RGS4	drug	opioid	12653973	The increases in RGS2 and  4 mRNA peak after 6 h of withdrawal and return to control levels by 24 h. Immunoblot analysis of <strong>RGS4</strong> revealed a striking divergence between mRNA and protein responses in LC: protein levels are elevated twofold following chronic <b>morphine</b> and decrease to control values by 6 h of withdrawal.
+RGS4	addiction	withdrawal	12653973	The increases in RGS2 and  4 mRNA peak after 6 h of <b>withdrawal</b> and return to control levels by 24 h. Immunoblot analysis of <strong>RGS4</strong> revealed a striking divergence between mRNA and protein responses in LC: protein levels are elevated twofold following chronic morphine and decrease to control values by 6 h of <b>withdrawal</b>.
+RGS4	drug	opioid	12653973	Intracellular application of wild type <strong>RGS4</strong>, but not a GTPase accelerating deficient mutant of <strong>RGS4</strong>, into LC neurons diminished electrophysiological responses to <b>morphine</b>.
+RGS4	drug	opioid	12653973	The observed subtype  and time specific regulation of <strong>RGS4</strong> protein and mRNA, and the diminished <b>morphine</b> induced currents in the presence of elevated <strong>RGS4</strong> protein levels, indicate that <b>morphine</b> induction of <strong>RGS4</strong> could contribute to aspects of opiate tolerance and dependence displayed by LC neurons.
+RGS4	addiction	dependence	12653973	The observed subtype  and time specific regulation of <strong>RGS4</strong> protein and mRNA, and the diminished morphine induced currents in the presence of elevated <strong>RGS4</strong> protein levels, indicate that morphine induction of <strong>RGS4</strong> could contribute to aspects of opiate tolerance and <b>dependence</b> displayed by LC neurons.
+RGS4	drug	amphetamine	12638131	Novel genes, RL/IF 1 (coding for I kappa B alpha chain) and serum/glucocorticoid regulated serine/threonine protein kinase (SGK) also were increased throughout the striatum, at 1 but not 3 h. Conversely, <b>amphetamine</b> increased the mRNA coding for the secretogranin II precursor (chromogranin C) only at the 3 h time point when a specific decrease in regulator of G protein signaling 4 (<strong>RGS4</strong>) mRNA was also observed.
+RGS4	drug	amphetamine	12638131	Novel genes, RL/IF 1 (coding for I kappa B alpha chain) and serum/glucocorticoid regulated serine/threonine protein kinase (SGK) also were increased throughout the striatum, at 1 but not 3 h. Conversely, <b>amphetamine</b> increased the mRNA coding for the secretogranin II precursor (chromogranin C) only at the 3 h time point when a specific decrease in <strong>regulator of G protein signaling 4</strong> (<strong>RGS4</strong>) mRNA was also observed.
+RGS4	drug	amphetamine	12270694	This study was undertaken to determine whether morphine, cocaine, or <b>amphetamine</b> would modulate <strong>RGS4</strong> mRNA levels in relevant brain regions.
+RGS4	drug	cocaine	12270694	This study was undertaken to determine whether morphine, <b>cocaine</b>, or amphetamine would modulate <strong>RGS4</strong> mRNA levels in relevant brain regions.
+RGS4	drug	opioid	12270694	This study was undertaken to determine whether <b>morphine</b>, cocaine, or amphetamine would modulate <strong>RGS4</strong> mRNA levels in relevant brain regions.
+RGS4	drug	cocaine	12270694	Acute administration of morphine and <b>cocaine</b> decreased levels of <strong>RGS4</strong> mRNA in the reticulotegmental pontine nucleus (RtTg) and locus coeruleus (LC).
+RGS4	drug	opioid	12270694	Acute administration of <b>morphine</b> and cocaine decreased levels of <strong>RGS4</strong> mRNA in the reticulotegmental pontine nucleus (RtTg) and locus coeruleus (LC).
+RGS4	drug	opioid	11955717	We also found the lack of changes in the level of the <strong>regulator of G protein signaling 4</strong>, which is a specific G(q/11alpha) dependent GTPase activating protein, in the limbic forebrain obtained from <b>morphine</b> sensitized mice.
+HDAC2	addiction	intoxication	31056842	Memory and plasticity impairment after <b>binge</b> drinking in adolescent rat hippocampus: GluN2A/GluN2B NMDA receptor subunits imbalance through <strong>HDAC2</strong>.
+HDAC2	addiction	intoxication	31056842	In conclusion, the memory impairing effects of two <b>binge</b> like EtOH exposure involve NMDA receptor dependent LTD deficits due to a GluN2A/GluN2B imbalance resulting from changes in GluN2B expression induced by <strong>HDAC2</strong>.
+HDAC2	drug	alcohol	30851364	The goal of this study was to examine depression like behavior during <b>alcohol</b> withdrawal and associated changes in histone acetylation and expression of histone deacetylase 2 (<strong>HDAC2</strong>) in the hippocampus, a brain region critical for mood regulation and depression.
+HDAC2	addiction	withdrawal	30851364	The goal of this study was to examine depression like behavior during alcohol <b>withdrawal</b> and associated changes in histone acetylation and expression of histone deacetylase 2 (<strong>HDAC2</strong>) in the hippocampus, a brain region critical for mood regulation and depression.
+HDAC2	drug	alcohol	30851364	The goal of this study was to examine depression like behavior during <b>alcohol</b> withdrawal and associated changes in histone acetylation and expression of <strong>histone deacetylase 2</strong> (<strong>HDAC2</strong>) in the hippocampus, a brain region critical for mood regulation and depression.
+HDAC2	addiction	withdrawal	30851364	The goal of this study was to examine depression like behavior during alcohol <b>withdrawal</b> and associated changes in histone acetylation and expression of <strong>histone deacetylase 2</strong> (<strong>HDAC2</strong>) in the hippocampus, a brain region critical for mood regulation and depression.
+HDAC2	drug	alcohol	30851364	In a separate group of rats, the hippocampus was analyzed for mRNA and protein expression of <strong>HDAC2</strong> and levels of histone H3 lysine 9 acetylation (H3K9ac) during chronic <b>ethanol</b> exposure and withdrawal.
+HDAC2	addiction	withdrawal	30851364	In a separate group of rats, the hippocampus was analyzed for mRNA and protein expression of <strong>HDAC2</strong> and levels of histone H3 lysine 9 acetylation (H3K9ac) during chronic ethanol exposure and <b>withdrawal</b>.
+HDAC2	drug	alcohol	30851364	Rats undergoing <b>ethanol</b> withdrawal exhibited depression like behavior and had increased <strong>HDAC2</strong> and decreased H3K9ac levels in specific structures of the hippocampus.
+HDAC2	addiction	withdrawal	30851364	Rats undergoing ethanol <b>withdrawal</b> exhibited depression like behavior and had increased <strong>HDAC2</strong> and decreased H3K9ac levels in specific structures of the hippocampus.
+HDAC2	addiction	withdrawal	30851364	Treatment with SAHA during <b>withdrawal</b> ameliorated depression like behavior and normalized changes in hippocampal <strong>HDAC2</strong> and H3K9ac levels.
+HDAC2	drug	amphetamine	30811820	We found that <b>METH</b> increased H4ac in class IIa Hdac4 and Hdac5 and decreased H3/H4ac at class I Hdac1, <strong>Hdac2</strong>, and Hdac8.
+HDAC2	drug	amphetamine	30811820	At the mRNA level, repeated <b>METH</b> increased Hdac4 and decreased <strong>Hdac2</strong>.
+HDAC2	addiction	withdrawal	30103280	EtOH <b>withdrawal</b> was associated with increased <strong>HDAC2</strong> and decreased acH3K9 protein levels; SAHA treatment normalized acH3K9 levels.
+HDAC2	drug	amphetamine	30056065	In this study, we measured the effects of single dose injections of modafinil and <b>METH</b> on the protein levels of acetylated histone H3 (H3ac) and H4ac, deacetylases HDAC1 and <strong>HDAC2</strong>, and of the NMDA subunit GluN1 in the medial PFC (mPFC) of mice euthanized 1 h after drug administration.
+HDAC2	drug	amphetamine	30056065	Acute modafinil and <b>METH</b> injections caused similar effects on total histone acetylation, increasing H3ac and decreasing H4ac, and they also increased HDAC1, <strong>HDAC2</strong> and GluN1 protein levels in the mouse mPFC.
+HDAC2	drug	alcohol	29520058	We found that chronic <b>ethanol</b> exposure using either <b>ethanol</b> gavage or two bottle choice voluntary access paradigms decreased Gabra1 expression and increased <strong>Hdac2</strong> and Hdac3 expression.
+HDAC2	drug	alcohol	29520058	Administration of the HDAC inhibitor trichostatin A (TSA) after chronic <b>ethanol</b> exposure prevents the decrease in Gabra1 expression and function as well as the increase in <strong>Hdac2</strong> and Hdac3 expression in both the cortex and the medial prefrontal cortex (mPFC).
+HDAC2	drug	alcohol	29520058	Chronic <b>ethanol</b> exposure and withdrawal, but not acute <b>ethanol</b> exposure or acute withdrawal, cause a selective upregulation of <strong>HDAC2</strong> and HDAC3 associated with the Gabra1 promoter that accompanies a decrease in H3 acetylation of the Gabra1 promoter and the reduction in GABAAR α1 subunit expression.
+HDAC2	addiction	withdrawal	29520058	Chronic ethanol exposure and <b>withdrawal</b>, but not acute ethanol exposure or acute <b>withdrawal</b>, cause a selective upregulation of <strong>HDAC2</strong> and HDAC3 associated with the Gabra1 promoter that accompanies a decrease in H3 acetylation of the Gabra1 promoter and the reduction in GABAAR α1 subunit expression.
+HDAC2	drug	alcohol	28174112	Additionally, innately higher expression of the <strong>HDAC2</strong> isoform leads to a deficit in global and gene specific histone acetylation in the amygdala that is associated with a decrease in the expression of several synaptic plasticity associated genes and maintaining heightened anxiety like behavior and excessive <b>alcohol</b> intake.
+HDAC2	drug	alcohol	28174112	Adolescent <b>alcohol</b> exposure also leads to higher expression of <strong>HDAC2</strong> and a deficit in histone acetylation leading to decreased expression of synaptic plasticity associated genes and high anxiety and drinking behavior in adulthood.
+HDAC2	drug	opioid	27306674	Using a combination of immunohistochemistry, Western blot, and whole cell patch clamp recording in rat midbrain slices, we show that <b>morphine</b> increased <strong>HDAC2</strong> activity in VTA DA neurons and reduced histone H3 acetylation at lysine 9 (Ac H3K9) in the VTA 24 h after the injection.
+HDAC2	drug	opioid	27306674	Our results suggest that acute <b>morphine</b> induced changes in VTA DA activity and synaptic transmission engage <strong>HDAC2</strong> activity locally in the VTA to maintain synaptic modifications through histone hypoacetylation.
+HDAC2	drug	nicotine	25981209	Expression of <b>nicotine</b> induced CPP was accompanied by an increase of phospho CREB (cyclic AMP responsive element binding protein) and <strong>HDAC2</strong> (histone deacetylase 2) expression in the nucleus accumbens.
+HDAC2	addiction	reward	25981209	Expression of nicotine induced <b>CPP</b> was accompanied by an increase of phospho CREB (cyclic AMP responsive element binding protein) and <strong>HDAC2</strong> (histone deacetylase 2) expression in the nucleus accumbens.
+HDAC2	drug	nicotine	25981209	Expression of <b>nicotine</b> induced CPP was accompanied by an increase of phospho CREB (cyclic AMP responsive element binding protein) and <strong>HDAC2</strong> (<strong>histone deacetylase 2</strong>) expression in the nucleus accumbens.
+HDAC2	addiction	reward	25981209	Expression of nicotine induced <b>CPP</b> was accompanied by an increase of phospho CREB (cyclic AMP responsive element binding protein) and <strong>HDAC2</strong> (<strong>histone deacetylase 2</strong>) expression in the nucleus accumbens.
+HDAC2	drug	nicotine	25859479	COPD patients, commonly <b>smokers</b> develop resistance to inhaled steroids attributed to deficiency of histone deacetylase 2 (<strong>HDAC2</strong>).
+HDAC2	drug	nicotine	25859479	COPD patients, commonly <b>smokers</b> develop resistance to inhaled steroids attributed to deficiency of <strong>histone deacetylase 2</strong> (<strong>HDAC2</strong>).
+HDAC2	drug	cocaine	24527678	Gene expression of <strong>histone deacetylase 2</strong> and glutamate receptor kainate 1 were only increased by <b>cocaine</b> treatment.
+HDAC2	drug	amphetamine	24239129	<b>Methamphetamine</b> exposure also increased repressor element 1 silencing transcription factor (REST) corepressor 1, methylated CpG binding protein 2, and <strong>histone deacetylase 2</strong> enrichment, but not of sirtuin 1 or sirtuin 2, onto GluA1 and GluA2 gene sequences.
+HDAC2	drug	amphetamine	24239129	Moreover, <b>METH</b> caused interactions of REST corepressor 1 and methylated CpG binding protein 2 with <strong>histone deacetylase 2</strong> and of REST with histone deacetylase 1.
+HDAC2	drug	alcohol	23485013	We employed <strong>HDAC2</strong> small interfering RNA infusion into the central nucleus of amygdala (CeA) of P rats to determine the causal role of <strong>HDAC2</strong> in anxiety like and <b>alcohol</b> drinking behaviors.
+HDAC2	drug	alcohol	23485013	Acute <b>ethanol</b> exposure decreased amygdaloid HDAC activity and <strong>HDAC2</strong> protein levels, increased global and gene (Bdnf and Arc) specific histone acetylation, and attenuated anxiety like behaviors in P rats but had no effects in NP rats.
+HDAC2	drug	alcohol	23485013	The <strong>HDAC2</strong> knockdown in the CeA attenuated anxiety like behaviors and voluntary <b>alcohol</b> but not sucrose consumption in P rats and increased histone acetylation of Bdnf and Arc with a resultant increase in protein levels that correlated with increased dendritic spine density.
+HDAC2	drug	alcohol	23485013	These novel data demonstrate the role of <strong>HDAC2</strong> mediated epigenetic mechanisms in anxiety and <b>alcoholism</b>.
+HDAC2	drug	alcohol	23474591	Here, we investigated modulation of withdrawal induced changes in GABA sensitivity of pDAergic VTA neurons by HDAC inhibitors (HDACi), and also measured the levels of <strong>HDAC2</strong>, histone (H3 K9) acetylation, and GABA Aα1 receptor (GABA (A α1) R) subunit in VTA during <b>ethanol</b> withdrawal.
+HDAC2	addiction	withdrawal	23474591	Here, we investigated modulation of <b>withdrawal</b> induced changes in GABA sensitivity of pDAergic VTA neurons by HDAC inhibitors (HDACi), and also measured the levels of <strong>HDAC2</strong>, histone (H3 K9) acetylation, and GABA Aα1 receptor (GABA (A α1) R) subunit in VTA during ethanol <b>withdrawal</b>.
+HDAC2	drug	alcohol	23474591	In addition, <b>ethanol</b> withdrawal was associated with an increase in levels of <strong>HDAC2</strong> and a decrease in histone (H3 K9) acetylation and levels of GABA (A α1) R subunits in the VTA.
+HDAC2	addiction	withdrawal	23474591	In addition, ethanol <b>withdrawal</b> was associated with an increase in levels of <strong>HDAC2</strong> and a decrease in histone (H3 K9) acetylation and levels of GABA (A α1) R subunits in the VTA.
+HDAC2	drug	alcohol	23474591	Therefore, blockade of upregulation of <strong>HDAC2</strong> by HDACi normalizes GABA hyposensitivity of pDAergic neurons developed during withdrawal after chronic <b>ethanol</b> treatment, which suggests the possibility that inhibition of HDACs can reverse <b>ethanol</b> induced neuroadaptational changes in reward circuitry.
+HDAC2	addiction	reward	23474591	Therefore, blockade of upregulation of <strong>HDAC2</strong> by HDACi normalizes GABA hyposensitivity of pDAergic neurons developed during withdrawal after chronic ethanol treatment, which suggests the possibility that inhibition of HDACs can reverse ethanol induced neuroadaptational changes in <b>reward</b> circuitry.
+HDAC2	addiction	withdrawal	23474591	Therefore, blockade of upregulation of <strong>HDAC2</strong> by HDACi normalizes GABA hyposensitivity of pDAergic neurons developed during <b>withdrawal</b> after chronic ethanol treatment, which suggests the possibility that inhibition of HDACs can reverse ethanol induced neuroadaptational changes in reward circuitry.
+HDAC2	drug	cocaine	23375146	Decrease in <b>cocaine</b> self administration was accompanied with reduced expression of the epigenetic markers methyl CpG binding protein 2 (MeCP2) and histone deacetylase 2 (<strong>HDAC2</strong>) in dopaminergic projection areas.
+HDAC2	drug	cocaine	23375146	Decrease in <b>cocaine</b> self administration was accompanied with reduced expression of the epigenetic markers methyl CpG binding protein 2 (MeCP2) and <strong>histone deacetylase 2</strong> (<strong>HDAC2</strong>) in dopaminergic projection areas.
+HDAC2	drug	cocaine	23375146	Since MeCP2 and <strong>HDAC2</strong> are known to modulate dynamic functions in the adult brain, such as synaptic plasticity, our results showing that activation of the cGMP signal transduction pathway decreased both <b>cocaine</b> intake and expression of the epigenetic markers strongly suggest that the MeCP2/<strong>HDAC2</strong> complex is involved in the analysis of the reinforcing properties of <b>cocaine</b> in the prefrontal cortex.
+HDAC2	addiction	reward	23375146	Since MeCP2 and <strong>HDAC2</strong> are known to modulate dynamic functions in the adult brain, such as synaptic plasticity, our results showing that activation of the cGMP signal transduction pathway decreased both cocaine intake and expression of the epigenetic markers strongly suggest that the MeCP2/<strong>HDAC2</strong> complex is involved in the analysis of the <b>reinforcing</b> properties of cocaine in the prefrontal cortex.
+HDAC2	drug	amphetamine	22470541	Our study investigated the effects of a non toxic <b>METH</b> injection (20 mg/kg) on gene expression, histone acetylation, and the expression of the histone acetyltransferase (HAT), ATF2, and of the histone deacetylases (HDACs), HDAC1 and <strong>HDAC2</strong>, in that structure.
+HDAC2	drug	alcohol	21447001	Effects of <b>alcohol</b> on histone deacetylase 2 (<strong>HDAC2</strong>) and the neuroprotective role of trichostatin A (TSA).
+HDAC2	drug	alcohol	21447001	Effects of <b>alcohol</b> on <strong>histone deacetylase 2</strong> (<strong>HDAC2</strong>) and the neuroprotective role of trichostatin A (TSA).
+HDAC2	drug	alcohol	21447001	Although HDACs and HDIs have been associated with drug addiction, there is no evidence of the neurodegenerative role of <strong>HDAC2</strong> and neuroprotective role of TSA in <b>alcohol</b> addiction.
+HDAC2	addiction	addiction	21447001	Although HDACs and HDIs have been associated with drug <b>addiction</b>, there is no evidence of the neurodegenerative role of <strong>HDAC2</strong> and neuroprotective role of TSA in alcohol <b>addiction</b>.
+HDAC2	drug	alcohol	21447001	Therefore, we hypothesize that <b>alcohol</b> modulates <strong>HDAC2</strong> through mechanisms involving oxidative stress.
+HDAC2	drug	alcohol	21447001	To test our hypothesis, the human neuronal cell line, SK N MC, was treated with different concentrations of <b>ethanol</b> (EtOH); <strong>HDAC2</strong> gene and protein expression were assessed at different time points.
+HDAC2	drug	alcohol	21447001	Additionally, <b>alcohol</b> significantly induced ROS, and pharmacological inhibition of <strong>HDAC2</strong> with TSA was shown to be neuroprotective by significantly inhibiting <strong>HDAC2</strong> and ROS.
+HDAC2	drug	alcohol	21447001	These results suggest that EtOH can upregulate <strong>HDAC2</strong> through mechanisms involving oxidative stress and HDACs may play an important role in <b>alcohol</b> use disorders (AUDs).
+HDAC2	drug	nicotine	21166804	We measured immunohistochemically the acetylation of lysine 9 of histone H3, and the expression of phosphorylated cAMP response element binding protein, <strong>HDAC2</strong> and methyl CpG binding protein 2 in the striatum and prefrontal cortex of rats displaying <b>nicotine</b> preference or aversion and treated with phenylbutyrate.
+HDAC2	addiction	aversion	21166804	We measured immunohistochemically the acetylation of lysine 9 of histone H3, and the expression of phosphorylated cAMP response element binding protein, <strong>HDAC2</strong> and methyl CpG binding protein 2 in the striatum and prefrontal cortex of rats displaying nicotine preference or <b>aversion</b> and treated with phenylbutyrate.
+HDAC2	drug	nicotine	21166804	Moreover, striatal expression of <strong>HDAC2</strong> in response to phenylbutyrate mirrored the behavioral effects of the inhibitor, suggesting that <strong>HDAC2</strong> is involved in promoting synaptic plasticity underlying the preference for <b>nicotine</b>.
+HDAC2	drug	cocaine	19939859	<b>Cocaine</b> self administration was accompanied by an increased synthesis of Mecp2, <strong>HDAC2</strong> and HDAC11 and by a decreased nuclear localization of HDAC5 and of the phospho form of HDAC5, suggesting a nuclear export of this protein in response to the drug.
+GRM3	drug	alcohol	31339221	The increase in <b>ethanol</b> self administration was associated with (a) reductions in levels of the endocannabinoids N arachidonoylethanolomine and 2 arachidonoylglycerol in the CeA, (b) increased amygdalar gene expression of cannabinoid type 1 receptor (CB1), N acyl phosphatidylethanolamine phospholipase D (Nape pld), fatty acid amid hydrolase (Faah), (c) decreased amygdalar gene expression of ionotropic AMPA (GluA2 and GluA4) and metabotropic (<strong>mGlu3</strong>) glutamate receptors, and (d) increased glutamatergic receptor function.
+GRM3	drug	cannabinoid	31339221	The increase in ethanol self administration was associated with (a) reductions in levels of the <b>endocannabinoids</b> N arachidonoylethanolomine and 2 arachidonoylglycerol in the CeA, (b) increased amygdalar gene expression of <b>cannabinoid</b> type 1 receptor (CB1), N acyl phosphatidylethanolamine phospholipase D (Nape pld), fatty acid amid hydrolase (Faah), (c) decreased amygdalar gene expression of ionotropic AMPA (GluA2 and GluA4) and metabotropic (<strong>mGlu3</strong>) glutamate receptors, and (d) increased glutamatergic receptor function.
+GRM3	drug	alcohol	31070489	The lack of conditioned place preference, but unaltered stimulatory and ataxic effects of <b>alcohol</b> in <strong>mGluR3</strong> KO mice.
+GRM3	drug	alcohol	31070489	The metabotropic glutamate receptor subtype 3 knockout (<strong>mGluR3</strong> KO) mouse line was used to study <b>alcohol</b> induced place preference, locomotor activating and ataxic effects, limited access <b>alcohol</b> drinking, and preference for sucrose and saccharin.
+GRM3	drug	alcohol	31070489	<b>Alcohol</b> induced horizontal locomotor stimulation and reduced rearing behaviour remained unchanged in the <strong>mGluR3</strong> KO mice.
+GRM3	drug	alcohol	31070489	However, <b>alcohol</b> induced place conditioning in an unbiased paradigm setup was lacking in the <strong>mGluR3</strong> KO mice, but clearly present in wildtype mice.
+GRM3	drug	alcohol	31070489	<b>Alcohol</b> consumption, studied through the 'drinking in the dark' model, remained unchanged in the <strong>mGluR3</strong> KO mice, although low consumption in both wildtype and knockout mice hampers interpretation.
+GRM3	drug	amphetamine	30950164	Shati/Nat8l overexpression in the nucleus accumbens (NAc) attenuates the pharmacological response to <b>METH</b> via <strong>mGluR3</strong>.
+GRM3	drug	alcohol	29220747	The mGluR2/3 agonist LY379268 (LY37) and selective mGluR2 positive allosteric modulator biphenyl‑indanone A (BINA) were used to investigate the relative contribution of mGlu2 and <strong>mGlu3</strong> receptors on <b>ethanol</b>  and sucrose seeking and consumption.
+GRM3	addiction	relapse	29220747	The mGluR2/3 agonist LY379268 (LY37) and selective mGluR2 positive allosteric modulator biphenyl‑indanone A (BINA) were used to investigate the relative contribution of mGlu2 and <strong>mGlu3</strong> receptors on ethanol  and sucrose <b>seeking</b> and consumption.
+GRM3	drug	alcohol	28285415	NAAG Peptidase Inhibitors Act via <strong>mGluR3</strong>: Animal Models of Memory, Alzheimer's, and <b>Ethanol</b> Intoxication.
+GRM3	addiction	intoxication	28285415	NAAG Peptidase Inhibitors Act via <strong>mGluR3</strong>: Animal Models of Memory, Alzheimer's, and Ethanol <b>Intoxication</b>.
+GRM3	drug	alcohol	28285415	2 PMPA also moderated the effect of <b>ethanol</b> on short term memory in mGluR2 ko mice but failed to do so in <strong>mGluR3</strong> ko mice.
+GRM3	drug	alcohol	27339394	Group II metabotropic glutamate receptors (mGluR2 and <strong>mGluR3</strong>) may control relapse of <b>alcohol</b> seeking, but previously available Group II agonists were unable to discriminate between mGluR2 and <strong>mGluR3</strong>.
+GRM3	addiction	relapse	27339394	Group II metabotropic glutamate receptors (mGluR2 and <strong>mGluR3</strong>) may control <b>relapse</b> of alcohol <b>seeking</b>, but previously available Group II agonists were unable to discriminate between mGluR2 and <strong>mGluR3</strong>.
+GRM3	addiction	relapse	26149611	Group II metabotropic glutamate receptors (mGluR2 and <strong>mGluR3</strong>) have been suggested to play an important role in mediation of drug reinforced behaviors, as well as in the mechanisms underlying <b>relapse</b> in abstinent subjects.
+GRM3	addiction	addiction	25802079	Based on rodent studies, group II metabotropic glutamate receptors (mGluR2 and <strong>mGluR3</strong>) were suggested as targets for <b>addiction</b> treatment.
+GRM3	drug	cocaine	25539508	An overall decrease was observed in the mRNA expression of the glutamate synthesizing gene kidney type glutaminase (KGA), the metabotropic glutamate receptors (<strong>mGluR3</strong> and GluR), and subunits of NMDA ionotropic receptors (NR1, NR2A, NR2B and NR2C) after acute <b>cocaine</b> administration, while mice repeatedly exposed to <b>cocaine</b> only displayed an increase in NR2C.
+GRM3	drug	cocaine	25539508	However, in <b>cocaine</b> sensitized mice primed with <b>cocaine</b>, this inhibition was reversed and a strong increase was detected in the mGluR5, NR2 subunits, and both GluR1 and <strong>GluR3</strong>.
+GRM3	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, <strong>Grm3</strong>, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+GRM3	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: Per1, Per2, Arc, Homer2, Creb1, <strong>Grm3</strong>, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+GRM3	drug	alcohol	25262781	Expression of both <strong>GRM3</strong> (mGluR3) and GRIN2D (GluN2D) was up regulated in <b>alcoholics</b> and down regulated in cocaine addicts relative to controls.
+GRM3	drug	cocaine	25262781	Expression of both <strong>GRM3</strong> (mGluR3) and GRIN2D (GluN2D) was up regulated in alcoholics and down regulated in <b>cocaine</b> addicts relative to controls.
+GRM3	drug	alcohol	25262781	Expression of both <strong>GRM3</strong> (<strong>mGluR3</strong>) and GRIN2D (GluN2D) was up regulated in <b>alcoholics</b> and down regulated in cocaine addicts relative to controls.
+GRM3	drug	cocaine	25262781	Expression of both <strong>GRM3</strong> (<strong>mGluR3</strong>) and GRIN2D (GluN2D) was up regulated in alcoholics and down regulated in <b>cocaine</b> addicts relative to controls.
+GRM3	drug	alcohol	25046171	The functional <strong>GRM3</strong> Kozak sequence variant rs148754219 affects the risk of schizophrenia and <b>alcohol</b> dependence as well as bipolar disorder.
+GRM3	addiction	dependence	25046171	The functional <strong>GRM3</strong> Kozak sequence variant rs148754219 affects the risk of schizophrenia and alcohol <b>dependence</b> as well as bipolar disorder.
+GRM3	drug	cocaine	24634647	Results indicated that acute <b>cocaine</b> exposure decreased DAGLα expression, suggesting a down regulation of 2 arachidonylglycerol (2 AG) production, as well as gene expression of TH, KGA, <strong>mGluR3</strong> and all ionotropic receptor subunits analyzed in the cerebellum.
+GRM3	drug	alcohol	24585043	Association of single nucleotide polymorphisms in a metabotropic glutamate receptor <strong>GRM3</strong> gene subunit to <b>alcohol</b> dependent male subjects.
+GRM3	drug	alcohol	24585043	The purpose of this study was to investigate the association between the metabotropic glutamate receptor 3 (<strong>GRM3</strong>) subunit gene and <b>alcohol</b> dependence by the single nucleotide polymorphisms (SNPs).
+GRM3	addiction	dependence	24585043	The purpose of this study was to investigate the association between the metabotropic glutamate receptor 3 (<strong>GRM3</strong>) subunit gene and alcohol <b>dependence</b> by the single nucleotide polymorphisms (SNPs).
+GRM3	drug	alcohol	24585043	Our results supplied the first evidence that the polymorphism of <strong>GRM3</strong> gene associates with the morbidity of <b>alcohol</b> dependence in human being, which may support a new potential target for <b>alcoholism</b> treatment.
+GRM3	addiction	dependence	24585043	Our results supplied the first evidence that the polymorphism of <strong>GRM3</strong> gene associates with the morbidity of alcohol <b>dependence</b> in human being, which may support a new potential target for alcoholism treatment.
+GRM3	addiction	dependence	24498053	Metabotropic glutamate receptor subtype 3 (mGluR3, encoded by <strong>GRM3</strong>) plays important roles in the pathophysiology of schizophrenia, depression, and drug <b>dependence</b>.
+GRM3	addiction	dependence	24498053	Metabotropic glutamate receptor subtype 3 (<strong>mGluR3</strong>, encoded by <strong>GRM3</strong>) plays important roles in the pathophysiology of schizophrenia, depression, and drug <b>dependence</b>.
+GRM3	drug	opioid	24498053	The goal of this study was to replicate the association of <strong>GRM3</strong> with schizophrenia and depression and to explore <strong>GRM3</strong>'s potential association with <b>heroin</b> dependence (HD) in a Chinese population.
+GRM3	addiction	dependence	24498053	The goal of this study was to replicate the association of <strong>GRM3</strong> with schizophrenia and depression and to explore <strong>GRM3</strong>'s potential association with heroin <b>dependence</b> (HD) in a Chinese population.
+GRM3	drug	cocaine	23624743	In an attempt to dissect the role played by mGluR2 and <strong>mGluR3</strong> in cue induced reinstatement, we analyzed the mRNA expression patterns in several relevant brain areas but did not find any significant differences between <b>cocaine</b> addict like and non addict like rats, suggesting that the behavioral differences observed are due to translational rather than transcriptional regulation.
+GRM3	addiction	relapse	23624743	In an attempt to dissect the role played by mGluR2 and <strong>mGluR3</strong> in cue induced <b>reinstatement</b>, we analyzed the mRNA expression patterns in several relevant brain areas but did not find any significant differences between cocaine addict like and non addict like rats, suggesting that the behavioral differences observed are due to translational rather than transcriptional regulation.
+GRM3	addiction	addiction	23624743	Another possibility to study the contributions of mGluR2 and <strong>mGluR3</strong> in mediating <b>addictive</b> like behavior is the use of knockout models.
+GRM3	addiction	reward	23624743	Because mGluR2 knockouts cannot be used in <b>operant</b> procedures due to motoric impairment, we only tested <strong>mGluR3</strong> knockouts.
+GRM3	drug	benzodiazepine	23392308	The mRNA expression levels of mGluR2 and <strong>mGluR3</strong> were lowered in the cerebral cortex of mice pretreated with <b>diazepam</b> or <b>alprazolam</b>.
+GRM3	drug	alcohol	22909248	We studied the effects of single nucleotide polymorphisms (SNPs) in the metabotropic glutamate receptor 3 (<strong>GRM3</strong>) gene on brain N acetylaspartate (NAA) concentrations and executive function (EF) skills in non smoking, active <b>alcoholics</b>, and evaluated associations between these variables.
+GRM3	drug	nicotine	22909248	We studied the effects of single nucleotide polymorphisms (SNPs) in the metabotropic glutamate receptor 3 (<strong>GRM3</strong>) gene on brain N acetylaspartate (NAA) concentrations and executive function (EF) skills in non <b>smoking</b>, active alcoholics, and evaluated associations between these variables.
+GRM3	drug	alcohol	22909248	SNPs (rs6465084, rs1468412, and rs2299225) in <strong>GRM3</strong> were genotyped in 49 male, non smoking, <b>alcohol</b> dependent patients and 45 healthy control subjects using ligase detection reactions.
+GRM3	drug	nicotine	22909248	SNPs (rs6465084, rs1468412, and rs2299225) in <strong>GRM3</strong> were genotyped in 49 male, non <b>smoking</b>, alcohol dependent patients and 45 healthy control subjects using ligase detection reactions.
+GRM3	drug	alcohol	22909248	It is possible that certain <strong>GRM3</strong> SNP genotypes (the A/A genotype of rs6465084 and the T allele of rs1468412) may further lower NAA/Cr levels and EF skills in addition to the effect of <b>alcohol</b>.
+GRM3	drug	alcohol	22511924	Other major hub genes like <strong>Grm3</strong>, Pten and Nrg3 represent novel targets of <b>ethanol</b> effects.
+GRM3	drug	cocaine	21887497	These behavioural changes were associated to alterations on the expression of metabotropic <strong>mGLUR3</strong> glutamate receptors and on the actions of <b>cocaine</b> on the GLUR1 subunit of AMPA glutamate receptors in the hippocampus of maLPA(1) animals.
+GRM3	drug	amphetamine	21886583	No Association Between <strong>GRM3</strong> and Japanese <b>Methamphetamine</b> Induced Psychosis.
+GRM3	drug	amphetamine	21886583	The metabotropic glutamate 3 receptor (<strong>mGluR3</strong>) gene was reported to be associated with schizophrenia, and paranoid type schizophrenia has symptoms that are similar to those of <b>methamphetamine</b> induced psychosis.
+GRM3	drug	amphetamine	21886583	This suggests that mGluR3 gene (<strong>GRM3</strong>) is a good candidate gene for the pathogenesis of <b>methamphetamine</b> induced psychosis.
+GRM3	drug	amphetamine	21886583	This suggests that <strong>mGluR3</strong> gene (<strong>GRM3</strong>) is a good candidate gene for the pathogenesis of <b>methamphetamine</b> induced psychosis.
+GRM3	drug	amphetamine	21886583	To evaluate the association between <strong>GRM3</strong> and <b>methamphetamine</b> induced psychosis, we conducted a case control study of Japanese samples (181 <b>methamphetamine</b> induced psychosis and 232 controls).
+GRM3	drug	amphetamine	21886583	We did not detect an association between rs6465084 in <strong>GRM3</strong> and Japanese <b>methamphetamine</b> induced psychosis.
+GRM3	drug	amphetamine	21886583	Our findings suggest that rs6465084 in <strong>GRM3</strong> does not play a major role in the pathophysiology of <b>methamphetamine</b> induced psychosis in the Japanese population.
+GRM3	drug	cocaine	20868701	Under basal conditions and in response to a single <b>cocaine</b> injection the levels of GluR1, GluR2, and <strong>GluR3</strong> AMPA receptor subunits did not differ between WT and 5 LOX deficient mice, but the response of GluR1 phosphorylation to a single <b>cocaine</b> injection was greater under the 5 LOX deficiency.
+GRM3	drug	opioid	20159947	Immunoblotting studies show that 12 h after <b>morphine</b> treatment, GluR1 subunits are increased at the postsynaptic density (PSD) and at extrasynaptic sites, whereas <strong>GluR3</strong> subunits are only increased at the PSD, and they show how this alters receptor subunit composition.
+GRM3	drug	cocaine	19703487	Recent evidence indicates that group II metabotropic glutamate receptors (mGluR2 and <strong>mGluR3</strong>) may play a role in the pathology of <b>cocaine</b> addiction.
+GRM3	addiction	addiction	19703487	Recent evidence indicates that group II metabotropic glutamate receptors (mGluR2 and <strong>mGluR3</strong>) may play a role in the pathology of cocaine <b>addiction</b>.
+GRM3	drug	cocaine	19559037	Pharmacological activation of group II metabotropic glutamate (mGlu2 and <strong>mGlu3</strong>) receptors inhibits reward seeking behavior and/or rewarding efficacy induced by drugs (<b>cocaine</b>, nicotine) or natural rewards (food, sucrose).
+GRM3	drug	nicotine	19559037	Pharmacological activation of group II metabotropic glutamate (mGlu2 and <strong>mGlu3</strong>) receptors inhibits reward seeking behavior and/or rewarding efficacy induced by drugs (cocaine, <b>nicotine</b>) or natural rewards (food, sucrose).
+GRM3	addiction	relapse	19559037	Pharmacological activation of group II metabotropic glutamate (mGlu2 and <strong>mGlu3</strong>) receptors inhibits reward <b>seeking</b> behavior and/or rewarding efficacy induced by drugs (cocaine, nicotine) or natural rewards (food, sucrose).
+GRM3	addiction	reward	19559037	Pharmacological activation of group II metabotropic glutamate (mGlu2 and <strong>mGlu3</strong>) receptors inhibits <b>reward</b> seeking behavior and/or rewarding efficacy induced by drugs (cocaine, nicotine) or natural rewards (food, sucrose).
+GRM3	drug	opioid	18671727	Decreased AMPA GluR2, but not <strong>GluR3</strong>, mRNA expression in rat amygdala and dorsal hippocampus following <b>morphine</b> induced behavioural sensitization.
+GRM3	addiction	sensitization	18671727	Decreased AMPA GluR2, but not <strong>GluR3</strong>, mRNA expression in rat amygdala and dorsal hippocampus following morphine induced behavioural <b>sensitization</b>.
+GRM3	drug	opioid	18671727	In order to evaluate the mechanism underlying the behavioural responses, quantitative real time reverse transcription polymerase chain reaction was used to evaluate mRNA expression of the AMPA receptor subunits GluR2 and <strong>GluR3</strong> in the striatum, prefrontal cortex, hippocampus, hypothalamus and amygdala of animals treated repeatedly with <b>morphine</b>.
+GRM3	drug	opioid	18671727	Repeated <b>morphine</b> treatment did not alter <strong>GluR3</strong> mRNA expression in any brain area assessed.
+GRM3	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, <strong>GluR3</strong>), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRM3	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, <strong>GluR3</strong>), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, <strong>mGluR3</strong>, mGluR5) in six different brain regions.
+GRM3	drug	alcohol	15846778	Bioinformatic analysis of these molecular targets showed that <strong>mGluR3</strong> and cacna2d1 fall within chromosomal locations reported to be <b>alcohol</b> related by the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) as well as quantitative trait loci (QTL) studies.
+GRM3	drug	alcohol	15365315	In the dentate gyrus, <strong>mGlu3</strong> and mGlu5 receptor mRNA levels were significantly lower in the <b>ethanol</b> treated rats than in the control rats.
+GRM3	drug	amphetamine	9183816	Repeated <b>amphetamine</b> administration decreased levels of GluR1 and GluR2 but not <strong>GluR3</strong> mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal.
+GRM3	addiction	withdrawal	9183816	Repeated amphetamine administration decreased levels of GluR1 and GluR2 but not <strong>GluR3</strong> mRNAs in both core and shell subregions of the NAc at the 14 day <b>withdrawal</b> time; no changes were observed after 3 days of <b>withdrawal</b>.
+EIF4EBP1	drug	alcohol	32333810	<b>Alcohol</b> exposure resulted in dysregulation of fetal hippocampal mTORC1 signaling, as evidenced by an increase in total <strong>4E BP1</strong> expression.
+EIF4EBP1	drug	alcohol	32333810	Phosphorylation levels of <strong>4E BP1</strong> and p70 S6K were also increased following <b>alcohol</b> exposure.
+EIF4EBP1	drug	opioid	30547365	Co intraperitoneal injection of rapamycin also attenuated the <b>morphine</b> induced increases in the levels of phosphorylated mTOR and its downstream target phosphorylated <strong>4E BP1</strong> in the spinal cord dorsal horn.
+EIF4EBP1	drug	opioid	30146703	We examined the effects of chronic treatment of <b>morphine</b> and/or <b>methadone</b> in the presence or absence of metformin with or without AMPK inhibitor (dorsomorphin hydrochloride) on levels of nitric oxide and cyclic adenosine monophosphate (cAMP), phosphorylated and dephosphorylated ribosomal protein S6 kinase β 1 (S6K1) and 4E binding protein 1 (<strong>4E BP1</strong>) in T98G cells.
+EIF4EBP1	drug	nicotine	25307796	In SBP, <b>smoking</b> status at baseline was predictive of persistence of <strong>BP 1</strong> year from symptom onset (differentiating SBPp and SBPr with 0.62 accuracy).
+EIF4EBP1	addiction	intoxication	25257868	The stimulation induced increase in the phosphorylation of S6K1 Thr(421)/Ser(424) (20 52%), S6K1 Thr(389) (45 57%), and its substrate rpS6 Ser(240/244) (37 72%) was blunted by EtOH at 30 min, 4 h, and 12 h. Phosphorylation of <strong>4E BP1</strong> Ser(65) was also attenuated by EtOH (61%) at 4 h. Conversely, phosphorylation of extracellular signal regulated kinase Thr(202)/Tyr(204) was increased by stimulation in Control and EtOH mice at 30 min but only in Control at 4 h. Our data indicate that acute EtOH <b>intoxication</b> suppresses muscle protein synthesis for at least 12 h and greatly impairs contraction induced changes in synthesis and mTOR signaling.
+EIF4EBP1	drug	alcohol	23747720	Cancer cells treated with the plant derived perillyl <b>alcohol</b> (POH) or the mechanistic target of rapamycin (mTOR) inhibitor rapamycin dephosphorylate eIF4E binding protein (<strong>4E BP1</strong>) and attenuate cap dependent translation.
+EIF4EBP1	drug	alcohol	20237068	<b>Alcohol</b> decreased protein synthesis in WT mice, a change associated with less <strong>4EBP1</strong> phosphorylation, eIF4E eIF4G binding, and raptor <strong>4EBP1</strong> binding, but greater mTOR raptor complex formation.
+EIF4EBP1	drug	alcohol	20237068	<b>Alcohol</b> impaired the ability of IGF I to increase muscle protein synthesis, <strong>4EBP1</strong> and 70 kilodalton ribosomal protein S6 kinase 1 phosphorylation, eIF4E eIF4G binding, and <strong>4EBP1</strong> raptor binding in WT mice.
+EIF4EBP1	drug	alcohol	19549760	Increased assembly of the active eIF4G.eIF4E complex was associated with a 130% rise in phosphorylation of eIF4G(Ser(1108)) and a decreased assembly (approximately 30%) of inactive eIF4E binding protein1 (<strong>4EBP1</strong>).eIF4E complex in rats administered <b>ethanol</b>.
+EIF4EBP1	drug	alcohol	19549760	Leu gavage accelerates myocardial protein synthesis following acute <b>ethanol</b> intoxication by enhancing eIF4G.eIF4E complex assembly through increased phosphorylation of eIF4G and decreased association of <strong>4EBP1</strong> with eIF4E.
+EIF4EBP1	addiction	intoxication	19549760	Leu gavage accelerates myocardial protein synthesis following acute ethanol <b>intoxication</b> by enhancing eIF4G.eIF4E complex assembly through increased phosphorylation of eIF4G and decreased association of <strong>4EBP1</strong> with eIF4E.
+EIF4EBP1	drug	alcohol	18336631	In contradistinction to the changes observed with acute EtOH intoxication, REDD1 mRNA/protein was not changed in gastrocnemius from chronic <b>alcohol</b> fed rats despite the reduction in <strong>4E BP1</strong> phosphorylation.
+EIF4EBP1	addiction	intoxication	18336631	In contradistinction to the changes observed with acute EtOH <b>intoxication</b>, REDD1 mRNA/protein was not changed in gastrocnemius from chronic alcohol fed rats despite the reduction in <strong>4E BP1</strong> phosphorylation.
+EIF4EBP1	drug	alcohol	18317950	Differential phosphorylation of translation initiation regulators <strong>4EBP1</strong>, S6k1, and Erk 1/2 following inhibition of <b>alcohol</b> metabolism in mouse heart.
+EIF4EBP1	drug	alcohol	18317950	The purpose of the present set of experiments was designed to examine the effects of inhibitors of <b>ethanol</b> metabolism on the phosphorylation of 4E binding protein (<strong>4EBP1</strong>) and S6k1(Thr(389)), two factors regulating mRNA translation initiation.
+EIF4EBP1	drug	alcohol	18317950	Phosphorylation of <strong>4E BP1</strong>, S6k1(Thr(389)), and Erk 1/2 was reduced 2 h following IP injection of <b>alcohol</b>.
+EIF4EBP1	drug	alcohol	18317950	Pretreatment with 4 methylpyrazole (4 MP), an inhibitor of <b>alcohol</b> dehydrogenase (ADH), did not attenuate the <b>ethanol</b> induced decrease in phosphorylation of <strong>4EBP1</strong> and S6k1(Thr(389)).
+EIF4EBP1	drug	alcohol	18317950	Pretreatment with cyanamide, an inhibitor of aldehyde dehydrogenase, did not attenuate the <b>ethanol</b> induced decrease in phosphorylation S6k1(Thr(389)), but partially prevented the <b>ethanol</b> induced lowering of <strong>4EBP1</strong> phosphorylation.
+EIF4EBP1	drug	alcohol	15547464	The purpose of this study was to characterize the ability of <b>alcohol</b> to suppress insulin like growth factor (IGF) I stimulation of ribosomal S6 kinase 1 (S6K1) and <strong>4E BP1</strong> phosphorylation, which are central elements in the signal transduction pathway used to coordinate the protein synthetic response and may contribute to the development of <b>alcoholic</b> myopathy.
+EIF4EBP1	drug	alcohol	15547464	In contrast to S6K1, acute <b>alcohol</b> intoxication did not consistently impair the ability of IGF I to stimulate <strong>4E BP1</strong> phosphorylation under any of the experimental conditions.
+EIF4EBP1	addiction	intoxication	15547464	In contrast to S6K1, acute alcohol <b>intoxication</b> did not consistently impair the ability of IGF I to stimulate <strong>4E BP1</strong> phosphorylation under any of the experimental conditions.
+EIF4EBP1	drug	alcohol	15547464	These data indicate that acute <b>alcohol</b> intoxication selectively impairs IGF I signaling via S6K1, but not <strong>4E BP1</strong>, and that this defect is independent of gender, nutritional state, route of administration, and <b>alcohol</b> metabolism.
+EIF4EBP1	addiction	intoxication	15547464	These data indicate that acute alcohol <b>intoxication</b> selectively impairs IGF I signaling via S6K1, but not <strong>4E BP1</strong>, and that this defect is independent of gender, nutritional state, route of administration, and alcohol metabolism.
+EIF4EBP1	drug	alcohol	15388509	<b>Alcohol</b> administration lowered formation of the active eIF4G.eIF4E complex by >90%, whereas it increased the abundance of the inactive 4E binding protein 1 (<strong>4E BP1</strong>).eIF4E complex by approximately 160%.
+EIF4EBP1	drug	alcohol	15388509	Phosphorylation of <strong>4E BP1</strong> and S6 kinase 1 (Thr(389)), downstream targets of mTOR, were also reduced after acute <b>alcohol</b> administration.
+EIF4EBP1	drug	alcohol	12944322	<b>Alcohol</b> impairs leucine mediated phosphorylation of <strong>4E BP1</strong>, S6K1, eIF4G, and mTOR in skeletal muscle.
+EIF4EBP1	drug	alcohol	12944322	Hence, <b>ethanol</b> produces a leucine resistance in skeletal muscle, as evidenced by the impaired phosphorylation of <strong>4E BP1</strong>, eIF4G, S6K1, and mTOR, that is independent of elevations in endogenous glucocorticoids.
+EIF4EBP1	drug	alcohol	12658115	IGF I induced phosphorylation of S6K1 and <strong>4E BP1</strong> in heart is impaired by acute <b>alcohol</b> intoxication.
+EIF4EBP1	addiction	intoxication	12658115	IGF I induced phosphorylation of S6K1 and <strong>4E BP1</strong> in heart is impaired by acute alcohol <b>intoxication</b>.
+EIF4EBP1	drug	alcohol	12376318	<b>Alcohol</b> impairs insulin and IGF I stimulation of S6K1 but not <strong>4E BP1</strong> in skeletal muscle.
+EIF4EBP1	drug	alcohol	11331201	Moreover, this <b>alcohol</b> induced impairment in initiation is associated with a decreased availability of eukaryotic initiation factor (eIF) 4E in striated muscle, as evidenced by an increase in the amount of the inactive eIF4E.<strong>4E BP1</strong> complex and decrease in the active eIF4E.eIF4G complex.
+EIF4EBP1	drug	alcohol	11052957	Acute <b>alcohol</b> exposure increased the binding of 4E binding protein 1 (<strong>4E BP1</strong>) to eIF4E (55%), diminished the amount of eIF4E bound to eIF4G (70%), reduced the amount of <strong>4E BP1</strong> in the phosphorylated gamma form (40%), and decreased the phosphorylation of p70S6 kinase and the ribosomal protein S6.
+EIF4EBP1	drug	alcohol	10776669	However, <b>alcohol</b> did not alter the amount of 4E binding protein 1 (<strong>4E BP1</strong>) bound to eIF4E, cIF4E bound to eIF4G, or the phosphorylation state of either <strong>4E BP1</strong> or eIF4E.
+EIF4EBP1	drug	alcohol	10776669	However, acute <b>alcohol</b> intoxication increased binding of <strong>4E BP1</strong> to eIF4E (113%), decreased the amount of cIF4E bound to cIF4G (81%), and decreased the amount of <strong>4E BP1</strong> in the phosphorylated gamma form (77%).
+EIF4EBP1	addiction	intoxication	10776669	However, acute alcohol <b>intoxication</b> increased binding of <strong>4E BP1</strong> to eIF4E (113%), decreased the amount of cIF4E bound to cIF4G (81%), and decreased the amount of <strong>4E BP1</strong> in the phosphorylated gamma form (77%).
+CHRNA6	drug	nicotine	31164900	However, results from our analysis suggest heterogeneous effects of <strong>CHRNA6</strong> and CHRNB3 on <b>nicotine</b> dependence in males and females.
+CHRNA6	addiction	dependence	31164900	However, results from our analysis suggest heterogeneous effects of <strong>CHRNA6</strong> and CHRNB3 on nicotine <b>dependence</b> in males and females.
+CHRNA6	drug	nicotine	28851948	Significant association of the CHRNB3 <strong>CHRNA6</strong> gene cluster with <b>nicotine</b> dependence in the Chinese Han population.
+CHRNA6	addiction	dependence	28851948	Significant association of the CHRNB3 <strong>CHRNA6</strong> gene cluster with nicotine <b>dependence</b> in the Chinese Han population.
+CHRNA6	drug	alcohol	27793544	We compared binge like <b>ethanol</b> consumption and <b>ethanol</b> reward sensitivity between knockout (KO) mice that do not express <strong>chrna6</strong> (the gene encoding the α6 nAChR subunit, the α6 KO line) and wild type (WT) littermates using the Drinking in the Dark (DID) and Conditioned Place Preference (CPP) assay, respectively.
+CHRNA6	addiction	intoxication	27793544	We compared <b>binge</b> like ethanol consumption and ethanol reward sensitivity between knockout (KO) mice that do not express <strong>chrna6</strong> (the gene encoding the α6 nAChR subunit, the α6 KO line) and wild type (WT) littermates using the Drinking in the Dark (DID) and Conditioned Place Preference (CPP) assay, respectively.
+CHRNA6	addiction	reward	27793544	We compared binge like ethanol consumption and ethanol <b>reward</b> sensitivity between knockout (KO) mice that do not express <strong>chrna6</strong> (the gene encoding the α6 nAChR subunit, the α6 KO line) and wild type (WT) littermates using the Drinking in the Dark (DID) and Conditioned Place Preference (<b>CPP</b>) assay, respectively.
+CHRNA6	drug	nicotine	27327258	Crucial roles of the CHRNB3 <strong>CHRNA6</strong> gene cluster on chromosome 8 in <b>nicotine</b> dependence: update and subjects for future research.
+CHRNA6	addiction	dependence	27327258	Crucial roles of the CHRNB3 <strong>CHRNA6</strong> gene cluster on chromosome 8 in nicotine <b>dependence</b>: update and subjects for future research.
+CHRNA6	drug	nicotine	27327258	Besides the CHRNA4, CHRNB2 and CHRNA5/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the CHRNB3 <strong>CHRNA6</strong> gene cluster on chromosome 8 in <b>nicotine</b> dependence (ND).
+CHRNA6	addiction	dependence	27327258	Besides the CHRNA4, CHRNB2 and CHRNA5/A3/B4 cluster on chromosome 15, which has been investigated intensively, recent evidence from both genome wide association studies and candidate gene based association studies has revealed the crucial roles of the CHRNB3 <strong>CHRNA6</strong> gene cluster on chromosome 8 in nicotine <b>dependence</b> (ND).
+CHRNA6	drug	nicotine	27327258	To gain a better understanding of the pathological processes underlying ND and ND related behaviors and to promote the development of effective <b>smoking</b> cessation therapies, we here present the most recent studies concerning the genetic effects of the CHRNB3 <strong>CHRNA6</strong> gene cluster in ND.
+CHRNA6	drug	nicotine	25233467	We evaluated 23 single nucleotide polymorphisms (SNPs) in the five nicotinic receptor related genes (CHRNB3, <strong>CHRNA6</strong>, and CHRNA5/A3/B4) previously reported to be associated with lung cancer risk and <b>smoking</b> behavior and 14 SNPs in the four 'control' genes (TERT, CLPTM1L, CYP1A1, and TP53), which were not reported in the <b>smoking</b> GWA studies.
+CHRNA6	drug	nicotine	25110504	Genetic Association of CHRNB3 and <strong>CHRNA6</strong> Gene Polymorphisms with <b>Nicotine</b> Dependence Syndrome Scale in Korean Population.
+CHRNA6	addiction	dependence	25110504	Genetic Association of CHRNB3 and <strong>CHRNA6</strong> Gene Polymorphisms with Nicotine <b>Dependence</b> Syndrome Scale in Korean Population.
+CHRNA6	drug	nicotine	25110504	Previous studies have found that <strong>CHRNA6</strong> CHRNB3 cluster polymorphisms were significantly associated with the risk of ND and various <b>tobacco</b> behaviors.
+CHRNA6	drug	nicotine	25110504	The aim of study was to evaluate the genetic association of CHRNB3 and <strong>CHRNA6</strong> polymorphisms with the risk of ND based on the Fagerstrom Test for <b>Nicotine</b> Dependence (FTND) score and five subscales of <b>nicotine</b> dependence syndrome scale (NDSS) in Korean population.
+CHRNA6	addiction	dependence	25110504	The aim of study was to evaluate the genetic association of CHRNB3 and <strong>CHRNA6</strong> polymorphisms with the risk of ND based on the Fagerstrom Test for Nicotine <b>Dependence</b> (FTND) score and five subscales of nicotine <b>dependence</b> syndrome scale (NDSS) in Korean population.
+CHRNA6	drug	nicotine	25110504	CHRNB3 rs4954 and <strong>CHRNA6</strong> rs16891604 showed significant associations with NDSSF1 (drive) in dominant models among moderate to severe ND among <b>smokers</b> after correction (p(corr) =0.02 and 0.001, respectively), whereas other four SNPs showed significant associations among mild ND after correction (p(corr) =0.03 0.02 in dominant model).
+CHRNA6	drug	nicotine	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, CHRNB4, <strong>CHRNA6</strong> and CHRNB3 genes and found that rare missense variants at conserved residues in CHRNB4 are associated with reduced risk of <b>nicotine</b> dependence among African Americans.
+CHRNA6	addiction	dependence	24804708	We previously undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, CHRNB4, <strong>CHRNA6</strong> and CHRNB3 genes and found that rare missense variants at conserved residues in CHRNB4 are associated with reduced risk of nicotine <b>dependence</b> among African Americans.
+CHRNA6	drug	cocaine	24675634	Variants near CHRNB3 <strong>CHRNA6</strong> are associated with DSM 5 <b>cocaine</b> use disorder: evidence for pleiotropy.
+CHRNA6	drug	nicotine	24401102	Multiple distinct CHRNB3 <strong>CHRNA6</strong> variants are genetic risk factors for <b>nicotine</b> dependence in African Americans and European Americans.
+CHRNA6	addiction	dependence	24401102	Multiple distinct CHRNB3 <strong>CHRNA6</strong> variants are genetic risk factors for nicotine <b>dependence</b> in African Americans and European Americans.
+CHRNA6	drug	alcohol	24401102	The common variant rs13273442 in the CHRNB3 <strong>CHNRA6</strong> region is associated significantly with nicotine dependence in European Americans and African Americans across studies recruited for nicotine, <b>alcohol</b> and cocaine dependence.
+CHRNA6	drug	cocaine	24401102	The common variant rs13273442 in the CHRNB3 <strong>CHNRA6</strong> region is associated significantly with nicotine dependence in European Americans and African Americans across studies recruited for nicotine, alcohol and <b>cocaine</b> dependence.
+CHRNA6	drug	nicotine	24401102	The common variant rs13273442 in the CHRNB3 <strong>CHNRA6</strong> region is associated significantly with <b>nicotine</b> dependence in European Americans and African Americans across studies recruited for <b>nicotine</b>, alcohol and cocaine dependence.
+CHRNA6	addiction	dependence	24401102	The common variant rs13273442 in the CHRNB3 <strong>CHNRA6</strong> region is associated significantly with nicotine <b>dependence</b> in European Americans and African Americans across studies recruited for nicotine, alcohol and cocaine <b>dependence</b>.
+CHRNA6	drug	nicotine	24253422	Significant associations of CHRNA2 and <strong>CHRNA6</strong> with <b>nicotine</b> dependence in European American and African American populations.
+CHRNA6	addiction	dependence	24253422	Significant associations of CHRNA2 and <strong>CHRNA6</strong> with nicotine <b>dependence</b> in European American and African American populations.
+CHRNA6	drug	nicotine	24253422	Together, these findings indicate that both CHRNA2 and <strong>CHRNA6</strong> play a significant role in the etiology of ND in AA and EA <b>smokers</b>.
+CHRNA6	drug	alcohol	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically <b>alcohol</b> and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, CHRNB4, <strong>CHRNA6</strong> and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of <b>Alcoholism</b> (COGA).
+CHRNA6	drug	cocaine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine dependence, specifically alcohol and <b>cocaine</b> dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, CHRNB4, <strong>CHRNA6</strong> and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA6	drug	nicotine	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than <b>nicotine</b> dependence, specifically alcohol and cocaine dependence, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, CHRNB4, <strong>CHRNA6</strong> and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA6	addiction	dependence	24057674	To investigate the possible contribution of rare variants to the development of substance dependencies other than nicotine <b>dependence</b>, specifically alcohol and cocaine <b>dependence</b>, we undertook pooled sequencing of the coding regions and flanking sequence of CHRNA5, CHRNA3, CHRNB4, <strong>CHRNA6</strong> and CHRNB3 in 287 African American and 1028 European American individuals from the Collaborative Study of the Genetics of Alcoholism (COGA).
+CHRNA6	drug	alcohol	23811312	In contrast, <b>ethanol</b> did not significantly increase activity of VTA DAergic neurons in mice that do not express <strong>CHRNA6</strong>, the gene encoding the α6 nAChR subunit (α6 knock out (KO) mice).
+CHRNA6	drug	nicotine	22042774	Genome wide association studies have identified common variation in the CHRNA5 CHRNA3 CHRNB4 and <strong>CHRNA6</strong> CHRNB3 gene clusters that contribute to <b>nicotine</b> dependence.
+CHRNA6	addiction	dependence	22042774	Genome wide association studies have identified common variation in the CHRNA5 CHRNA3 CHRNB4 and <strong>CHRNA6</strong> CHRNB3 gene clusters that contribute to nicotine <b>dependence</b>.
+CHRNA6	drug	nicotine	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, CHRNB4, <strong>CHRNA6</strong> and CHRNB3 genes in African American and European American <b>nicotine</b> dependent <b>smokers</b> and <b>smokers</b> without symptoms of dependence.
+CHRNA6	addiction	dependence	22042774	We undertook pooled sequencing of the coding regions and flanking sequence of the CHRNA5, CHRNA3, CHRNB4, <strong>CHRNA6</strong> and CHRNB3 genes in African American and European American nicotine dependent smokers and smokers without symptoms of <b>dependence</b>.
+CHRNA6	drug	nicotine	21191315	On the basis of known associations with <b>nicotine</b> dependence, we genotyped eight single nucleotide polymorphisms (SNPs) on chromosome 8 (three bins) in the regions of CHRNB3 and <strong>CHRNA6</strong>, and six SNPs on chromosome 15 (three bins) in the regions of CHRNA5 and CHRNA3.
+CHRNA6	addiction	dependence	21191315	On the basis of known associations with nicotine <b>dependence</b>, we genotyped eight single nucleotide polymorphisms (SNPs) on chromosome 8 (three bins) in the regions of CHRNB3 and <strong>CHRNA6</strong>, and six SNPs on chromosome 15 (three bins) in the regions of CHRNA5 and CHRNA3.
+CHRNA6	drug	nicotine	21191315	Our results suggest that (i) bipolar disorder does not modify the association between <b>nicotine</b> dependence and nicotinic receptor subunit genes, and (ii) variants in CHRNB3/<strong>CHRNA6</strong> are independently associated with bipolar disorder.
+CHRNA6	addiction	dependence	21191315	Our results suggest that (i) bipolar disorder does not modify the association between nicotine <b>dependence</b> and nicotinic receptor subunit genes, and (ii) variants in CHRNB3/<strong>CHRNA6</strong> are independently associated with bipolar disorder.
+CHRNA6	drug	nicotine	20418888	Sequence variants at CHRNB3 <strong>CHRNA6</strong> and CYP2A6 affect <b>smoking</b> behavior.
+CHRNA6	drug	nicotine	20418888	Among the genes at the two newly associated loci are genes encoding <b>nicotine</b> metabolizing enzymes (CYP2A6 and CYP2B6) and nicotinic acetylcholine receptor subunits (CHRNB3 and <strong>CHRNA6</strong>), all of which have been highlighted in previous studies of <b>smoking</b> and <b>nicotine</b> dependence.
+CHRNA6	addiction	dependence	20418888	Among the genes at the two newly associated loci are genes encoding nicotine metabolizing enzymes (CYP2A6 and CYP2B6) and nicotinic acetylcholine receptor subunits (CHRNB3 and <strong>CHRNA6</strong>), all of which have been highlighted in previous studies of smoking and nicotine <b>dependence</b>.
+CHRNA6	drug	alcohol	19698703	Two haplotypes of the <strong>CHRNA6</strong> (CCCC and TCGA) were associated with heavy <b>alcohol</b> consumption (p=0.004 and p=0.035 respectively) and with increased <b>alcohol</b> intake (p=0.004) for the CCCC haplotype compared to non carriers of these haplotypes.
+CHRNA6	drug	alcohol	19698703	Moreover, one haplotype of the CHRNA4 (GGTG) was associated with increased body weight as compared to non carriers of this haplotype, especially in the heavy consumers of <b>alcohol</b> (p=0.004).The present findings are the first to disclose a haplotype association between the <strong>CHRNA6</strong> gene and heavy <b>alcohol</b> use as well as an association of the CHRNA4 gene with increased body mass in heavy consumers of <b>alcohol</b>.
+CHRNA6	drug	alcohol	19500157	SNPs in <strong>CHRNA6</strong> and CHRNB3 are associated with <b>alcohol</b> consumption in a nationally representative sample.
+CHRNA6	drug	nicotine	19500157	The <strong>CHRNA6</strong> and CHRNB3 genes have been associated with <b>nicotine</b> dependence and early subjective response to <b>nicotine</b>.
+CHRNA6	addiction	dependence	19500157	The <strong>CHRNA6</strong> and CHRNB3 genes have been associated with nicotine <b>dependence</b> and early subjective response to nicotine.
+CHRNA6	drug	alcohol	19500157	Three SNPs in <strong>CHRNA6</strong> (rs1072003, P = 0.015; rs892413, P = 0.0033 and rs2304297, P = 0.012) and one SNP in CHRNB3 (rs13280604, P = 0.0053) were associated with a composite of the <b>alcohol</b> phenotypes.
+CHRNA6	drug	nicotine	18704094	Genetic association of the <strong>CHRNA6</strong> and CHRNB3 genes with <b>tobacco</b> dependence in a nationally representative sample.
+CHRNA6	addiction	dependence	18704094	Genetic association of the <strong>CHRNA6</strong> and CHRNB3 genes with tobacco <b>dependence</b> in a nationally representative sample.
+CHRNA6	drug	nicotine	18704094	Previous studies have found evidence for significant association between single nucleotide polymorphisms (SNPs) in the genomic region containing the <strong>CHRNA6</strong> and CHRNB3 genes and <b>tobacco</b> behaviors.
+CHRNA6	drug	nicotine	18704094	Variation in <strong>CHRNA6</strong> was found to be associated with <b>tobacco</b> dependence (p=0.007 in Caucasians).
+CHRNA6	addiction	dependence	18704094	Variation in <strong>CHRNA6</strong> was found to be associated with tobacco <b>dependence</b> (p=0.007 in Caucasians).
+CHRNA6	drug	nicotine	18704094	Together these results further implicate the region downstream of <strong>CHRNA6</strong> and the region upstream of CHRNB3 in risk of <b>nicotine</b> dependence.
+CHRNA6	addiction	dependence	18704094	Together these results further implicate the region downstream of <strong>CHRNA6</strong> and the region upstream of CHRNB3 in risk of nicotine <b>dependence</b>.
+CHRNA6	drug	nicotine	18055561	The neuronal nicotinic receptor subunit genes (<strong>CHRNA6</strong> and CHRNB3) are associated with subjective responses to <b>tobacco</b>.
+CHRNA6	drug	alcohol	18055561	In this paper, we present findings from an exploratory study of single nucleotide polymorphisms (SNPs) in the CHRNB3 and <strong>CHRNA6</strong> genes with tobacco and <b>alcohol</b> phenotypes, including frequency of use and three subjective response factors occurring shortly after initiation of use.
+CHRNA6	drug	nicotine	18055561	In this paper, we present findings from an exploratory study of single nucleotide polymorphisms (SNPs) in the CHRNB3 and <strong>CHRNA6</strong> genes with <b>tobacco</b> and alcohol phenotypes, including frequency of use and three subjective response factors occurring shortly after initiation of use.
+AURKA	drug	nicotine	28283957	However, a woman with migraine with <strong>aura</strong> should be encouraged to cease <b>smoking</b> and avoid taking oral contraceptives with high estrogen doses.
+AURKA	drug	cocaine	27110213	This <strong>aura</strong> of innovative brilliance in turn communicated itself to the medical professionals who employed <b>cocaine</b> in their work, so that many patients and practitioners alike depicted <b>cocaine</b> as a most fitting emblem for the idealized selfhood of the modern medical man.
+AURKA	drug	nicotine	24246525	Potential medical contraindications were defined as self reported history of hypertension, myocardial infarction, cerebral vascular accidents, migraines with <strong>aura</strong>, any migraine and age 35 years or older, <b>smoking</b> in women older than 35 years, venous thromboembolism, or liver disease.
+AURKA	drug	nicotine	24246525	After chart review, only 24 of 1010 participants desiring CHC (2.38%; 95% CI, 1.53 3.52%) were found to have true medical contraindications to CHC including 17 with hypertension, 2 with migraines with <strong>aura</strong>, 2 with a history of venous thromboembolism, and 3 <b>smokers</b> aged 35 years or older.
+AURKA	drug	alcohol	21787169	Furthermore, the TT genotype has been previously linked with migraine with <strong>aura</strong> a comorbid condition and with <b>alcohol</b> withdrawal seizures.
+AURKA	addiction	withdrawal	21787169	Furthermore, the TT genotype has been previously linked with migraine with <strong>aura</strong> a comorbid condition and with alcohol <b>withdrawal</b> seizures.
+AURKA	drug	nicotine	20423277	Distribution of initiated contraceptive methods and of examinations and tests included, application of limits and contraindications in relation to age, <b>smoking</b>, body mass index or weight, blood pressure (BP) and migraine with <strong>aura</strong> when prescribing CHC (combined oral contraceptives (COCs), vaginal ring and contraceptive patch).
+AURKA	drug	nicotine	19788473	Symptoms of CA were associated with female gender, body mass index, current <b>smoking</b>, presence of <strong>aura</strong>, chronic headaches, transformed headaches, severe headache related disability, and duration of migraine illness from onset.
+AURKA	addiction	withdrawal	19271947	The newest combined oral contraceptive formulations are generally well tolerated in migraine without <strong>aura</strong>, and the majority of migraine without <strong>aura</strong> sufferers do not show any problems with their use; nevertheless, the last International Classification of Headache Disorders identifies at least two entities evidently related to the use of combined oral contraceptives: exogenous hormone induced headache and estrogen <b>withdrawal</b> headache.
+AURKA	drug	nicotine	19271947	Other risk factors (<b>tobacco</b> use, hypertension, hyperlipidemia, obesity and diabetes) must be carefully considered when prescribing combined oral contraceptives in migraine without <strong>aura</strong> patients, in particular in women aged over 35 years.
+AURKA	drug	nicotine	19200688	The toxicity is higher among female <b>smokers</b>, especially when they have several risk factors such as oral contraceptiveS and migraine with <strong>aura</strong>.
+SP1	drug	amphetamine	29158267	In the present study, we hypothesized that <b>METH</b> impacts HIV infection of neural progenitor cells (NPCs) by a mechanism encompassing NFκB/<strong>SP1</strong> mediated HIV LTR activation.
+SP1	drug	amphetamine	29158267	<b>METH</b> treatment induced transcriptional activity of the HIV LTR promotor, an effect that required both NFκB and <strong>SP1</strong> signaling.
+SP1	drug	amphetamine	29158267	This study indicates that <b>METH</b> increases HIV infectivity of NPCs, through the NFκB/<strong>SP1</strong> dependent activation of the HIV LTR and with the subsequent alterations of NPC neurogenesis.
+SP1	drug	opioid	29067285	The pharmacologic protocol (<strong>SP1</strong>) for infants treated between 2005 and March 2014 (n = 146) dosed oral <b>morphine</b> every 4 h and utilized phenobarbital as adjuvant therapy.
+SP1	drug	opioid	29067285	The length of <b>morphine</b> therapy was decreased by 8.5 days from 35 to 26.5 days (95% CI 4.5 12 days) for infants treated with SP2 vs. <strong>SP1</strong> (p < 0.001).
+SP1	drug	nicotine	24089524	<b>Nicotine</b> induces the up regulation of the α7 nicotinic receptor (α7 nAChR) in human squamous cell lung cancer cells via the <strong>Sp1</strong>/GATA protein pathway.
+SP1	drug	nicotine	24089524	ChIP assays showed that <b>nicotine</b> induced the binding of GATA4 or GATA6 to <strong>Sp1</strong> on the α7 nAChR promoter, thereby inducing its transcription and increasing its levels in human SCC L. Our data are clinically relevant because SCC L patients smoked for decades before being diagnosed with cancer.
+SP1	drug	opioid	15501527	The substance P (SP) heptapeptide fragment <strong>SP1</strong> 7 alters the density of dopamine receptors in rat brain mesocorticolimbic structures during <b>morphine</b> withdrawal.
+SP1	addiction	withdrawal	15501527	The substance P (SP) heptapeptide fragment <strong>SP1</strong> 7 alters the density of dopamine receptors in rat brain mesocorticolimbic structures during morphine <b>withdrawal</b>.
+SP1	drug	nicotine	11509018	To test this hypothesis we examined the association of the C 45T promoter polymorphism in the <strong>Sp1</strong> binding region of the CCK gene with <b>smoking</b> and BMI in two independent groups of subjects.
+SP1	drug	alcohol	10889557	Recently, a number of studies have indicated that a C 36 to T transition in the CCK gene promoter <strong>Sp1</strong> element4 (Figure 1) is associated with <b>alcoholism</b> and withdrawal symptoms as well as panic disorder.5 7 Moreover, it has been proposed that the polymorphism plays a direct role in the pathogenesis of the disorders by decreasing the expression and synthesis of CCK peptides.
+SP1	addiction	withdrawal	10889557	Recently, a number of studies have indicated that a C 36 to T transition in the CCK gene promoter <strong>Sp1</strong> element4 (Figure 1) is associated with alcoholism and <b>withdrawal</b> symptoms as well as panic disorder.5 7 Moreover, it has been proposed that the polymorphism plays a direct role in the pathogenesis of the disorders by decreasing the expression and synthesis of CCK peptides.
+SP1	drug	alcohol	10871699	Finally, an acute bolus dose of <b>ethanol</b> did not affect Egr DNA binding activity and <b>ethanol</b> treatment did not alter the DNA binding activity or protein levels of the transcription factor <strong>Sp1</strong>.
+SP1	drug	alcohol	10803770	We investigated the relationship between the C to T substitution in the <strong>Sp1</strong> binding cis element of the CCK gene promoter region (at position  45 numbered from initiation codon) and <b>alcohol</b> withdrawal symptoms.
+SP1	addiction	withdrawal	10803770	We investigated the relationship between the C to T substitution in the <strong>Sp1</strong> binding cis element of the CCK gene promoter region (at position  45 numbered from initiation codon) and alcohol <b>withdrawal</b> symptoms.
+SP1	drug	alcohol	10611471	To define the molecular basis of <b>ethanol</b> dependence, the changes in gene transcription factor stimulatory protein 1 (<strong>SP1</strong>) and nuclear factor kB (NF kB) DNA binding activities were investigated in the rat cortex and hippocampus during <b>ethanol</b> treatment (15 days) and its withdrawal.
+SP1	addiction	dependence	10611471	To define the molecular basis of ethanol <b>dependence</b>, the changes in gene transcription factor stimulatory protein 1 (<strong>SP1</strong>) and nuclear factor kB (NF kB) DNA binding activities were investigated in the rat cortex and hippocampus during ethanol treatment (15 days) and its withdrawal.
+SP1	addiction	withdrawal	10611471	To define the molecular basis of ethanol dependence, the changes in gene transcription factor stimulatory protein 1 (<strong>SP1</strong>) and nuclear factor kB (NF kB) DNA binding activities were investigated in the rat cortex and hippocampus during ethanol treatment (15 days) and its <b>withdrawal</b>.
+SP1	drug	alcohol	10611471	Time course studies of the changes in <strong>SP1</strong> DNA binding activity during <b>ethanol</b> withdrawal (0, 12, 24, and 72 h) after protracted <b>ethanol</b> exposure indicated that <strong>SP1</strong> DNA binding in the rat cortex was significantly decreased at 0 h, and that it remained decreased at 12, 24, and 72 h of withdrawal.
+SP1	addiction	withdrawal	10611471	Time course studies of the changes in <strong>SP1</strong> DNA binding activity during ethanol <b>withdrawal</b> (0, 12, 24, and 72 h) after protracted ethanol exposure indicated that <strong>SP1</strong> DNA binding in the rat cortex was significantly decreased at 0 h, and that it remained decreased at 12, 24, and 72 h of <b>withdrawal</b>.
+SP1	drug	alcohol	10611471	On the other hand, <strong>SP1</strong> DNA binding activity did not change in the rat hippocampus during <b>ethanol</b> treatment but was significantly decreased at 12, 24, and 72 h of withdrawal.
+SP1	addiction	withdrawal	10611471	On the other hand, <strong>SP1</strong> DNA binding activity did not change in the rat hippocampus during ethanol treatment but was significantly decreased at 12, 24, and 72 h of <b>withdrawal</b>.
+SP1	drug	alcohol	10611471	These results suggest the possibility that decreased <strong>SP1</strong> dependent gene transcription in the rat cortex and hippocampus may be associated with the molecular mechanisms of <b>ethanol</b> dependence.
+SP1	addiction	dependence	10611471	These results suggest the possibility that decreased <strong>SP1</strong> dependent gene transcription in the rat cortex and hippocampus may be associated with the molecular mechanisms of ethanol <b>dependence</b>.
+SP1	drug	alcohol	10604945	Hsc70 promoter constructs with diminished <b>ethanol</b> responsiveness in NG108 15 cells similarly had decreased transcriptional activation by exogenous <strong>Sp1</strong> in Drosophila SL2 cells.
+SP1	drug	alcohol	10604945	Some artificial promoter constructs containing multiple <strong>Sp1</strong> sites were highly responsive to <b>ethanol</b>, but others were not, suggesting that the organization of the proximal promoter region was an additional factor that affected the <b>ethanol</b> response.
+SP1	drug	alcohol	10604945	However <b>ethanol</b> exposure did not alter <strong>Sp1</strong> DNA binding activity.
+SP1	drug	alcohol	10604945	Together, our findings show that <b>ethanol</b> induction of Hsc70 requires a functional <strong>Sp1</strong> binding site.
+SP1	drug	alcohol	10604945	Additional proximal promoter elements may also play a role in determining whether an <strong>Sp1</strong> containing promoter will respond to <b>ethanol</b>.
+SP1	drug	opioid	9886677	Its N terminal fragment <strong>SP1</strong> 7 may inhibit the intensity of the withdrawal reactions in <b>morphine</b> dependent mice.
+SP1	addiction	withdrawal	9886677	Its N terminal fragment <strong>SP1</strong> 7 may inhibit the intensity of the <b>withdrawal</b> reactions in morphine dependent mice.
+SP1	drug	opioid	9886677	This study was designed to determine whether the endogenous concentrations of the <strong>SP1</strong> 7 fragment in the brain are affected during <b>naloxone</b> precipitated withdrawal in the male rat.
+SP1	addiction	withdrawal	9886677	This study was designed to determine whether the endogenous concentrations of the <strong>SP1</strong> 7 fragment in the brain are affected during naloxone precipitated <b>withdrawal</b> in the male rat.
+SP1	drug	opioid	9886677	The results indicated that the concentrations of <strong>SP1</strong> 7 were significantly elevated in the ventral tegmental area both in <b>morphine</b> tolerant rats and during <b>naloxone</b> precipitated withdrawal.
+SP1	addiction	withdrawal	9886677	The results indicated that the concentrations of <strong>SP1</strong> 7 were significantly elevated in the ventral tegmental area both in morphine tolerant rats and during naloxone precipitated <b>withdrawal</b>.
+SP1	drug	opioid	9886677	It was concluded that the enhanced content of <strong>SP1</strong> 7 may also indicate the involvement of the SP system during <b>opioid</b> withdrawal in the rat.
+SP1	addiction	withdrawal	9886677	It was concluded that the enhanced content of <strong>SP1</strong> 7 may also indicate the involvement of the SP system during opioid <b>withdrawal</b> in the rat.
+SP1	addiction	withdrawal	9886677	The enhanced production of <strong>SP1</strong> 7 may reflect an increased release and/or metabolism of SP, which, in turn, counteracts the <b>withdrawal</b>.
+SP1	addiction	sensitization	7682611	Behavioral <b>sensitization</b> to kainic acid (KA) in the mouse spinal cord appears to be mediated by the amino (N) terminus of substance P (SP), as potentiation of KA is sensitive to capsaicin, mimicked by <strong>SP1</strong> 7 but not SP5 11, and blocked by <strong>SP1</strong> 7 antagonists but not by neurokinin antagonists.
+SP1	drug	opioid	7682611	As <b>naloxone</b> inhibits some effects of <strong>SP1</strong> 7, this study examines the role of <b>opioid</b> receptors in the mediation of KA induced sensitization by the N terminus of SP.
+SP1	addiction	sensitization	7682611	As naloxone inhibits some effects of <strong>SP1</strong> 7, this study examines the role of opioid receptors in the mediation of KA induced <b>sensitization</b> by the N terminus of SP.
+SP1	drug	opioid	7682611	The ability of 22.5 pmol of <strong>SP1</strong> 7 to enhance subsequent KA responses was blocked when coadministered with 0.1 micrograms of <b>naloxone</b>.
+SP1	drug	opioid	7682611	When administered with KA, <b>naloxone</b> not only failed to reverse the potentiative effect of <strong>SP1</strong> 7, but further enhanced responses to KA for 2 hr after <strong>SP1</strong> 7.
+SP1	drug	opioid	6180443	Substance P undecapeptide (<strong>SP1</strong> 11) produces a tonic contraction of the ileum in <b>morphine</b> independent rats and also in <b>morphine</b> dependent rats.
+SP1	drug	opioid	6180443	When <b>morphine</b> dependent rats with <b>naloxone</b> induced "gut dependence" are given <strong>SP1</strong> 11, they show an additional increase in tonus followed by a rapid tonus inhibition.
+SP1	addiction	dependence	6180443	When morphine dependent rats with naloxone induced "gut <b>dependence</b>" are given <strong>SP1</strong> 11, they show an additional increase in tonus followed by a rapid tonus inhibition.
+SP1	drug	opioid	6180443	In contrast to <strong>SP1</strong> 11, SP5 11 produces neither a tonus superposition nor a tonus inhibition in <b>morphine</b> dependent rats with <b>naloxone</b> induced "gut dependence".
+SP1	addiction	dependence	6180443	In contrast to <strong>SP1</strong> 11, SP5 11 produces neither a tonus superposition nor a tonus inhibition in morphine dependent rats with naloxone induced "gut <b>dependence</b>".
+SOD2	drug	opioid	28368370	<strong>MnSOD</strong> mediated by HSV vectors in the periaqueductal gray suppresses <b>morphine</b> withdrawal in rats.
+SOD2	addiction	withdrawal	28368370	<strong>MnSOD</strong> mediated by HSV vectors in the periaqueductal gray suppresses morphine <b>withdrawal</b> in rats.
+SOD2	drug	opioid	28368370	<strong><strong>MnSOD</strong></strong> mediated by HSV vectors in the periaqueductal gray suppresses <b>morphine</b> withdrawal in rats.
+SOD2	addiction	withdrawal	28368370	<strong><strong>MnSOD</strong></strong> mediated by HSV vectors in the periaqueductal gray suppresses morphine <b>withdrawal</b> in rats.
+SOD2	drug	opioid	28368370	These results suggest that overexpression of <strong>MnSOD</strong> by HSV vectors may relieve <b>opioid</b> dependence.
+SOD2	addiction	dependence	28368370	These results suggest that overexpression of <strong>MnSOD</strong> by HSV vectors may relieve opioid <b>dependence</b>.
+SOD2	drug	opioid	28368370	These results suggest that overexpression of <strong><strong>MnSOD</strong></strong> by HSV vectors may relieve <b>opioid</b> dependence.
+SOD2	addiction	dependence	28368370	These results suggest that overexpression of <strong><strong>MnSOD</strong></strong> by HSV vectors may relieve opioid <b>dependence</b>.
+SOD2	drug	alcohol	27207918	Association of Superoxide Dismutase 2 (<strong>SOD2</strong>) Genotype with Gray Matter Volume Shrinkage in Chronic <b>Alcohol</b> Users: Replication and Further Evaluation of an Addiction Gene Panel.
+SOD2	addiction	addiction	27207918	Association of Superoxide Dismutase 2 (<strong>SOD2</strong>) Genotype with Gray Matter Volume Shrinkage in Chronic Alcohol Users: Replication and Further Evaluation of an <b>Addiction</b> Gene Panel.
+SOD2	drug	alcohol	27207918	Association of <strong>Superoxide Dismutase 2</strong> (<strong>SOD2</strong>) Genotype with Gray Matter Volume Shrinkage in Chronic <b>Alcohol</b> Users: Replication and Further Evaluation of an Addiction Gene Panel.
+SOD2	addiction	addiction	27207918	Association of <strong>Superoxide Dismutase 2</strong> (<strong>SOD2</strong>) Genotype with Gray Matter Volume Shrinkage in Chronic Alcohol Users: Replication and Further Evaluation of an <b>Addiction</b> Gene Panel.
+SOD2	drug	alcohol	27207918	High variance in the degree of gray matter tissue shrinkage among <b>alcohol</b> dependent individuals and a previous neuroimaging genetics report suggest the involvement of environmental and/or genetic factors, such as superoxide dismutase 2 (<strong>SOD2</strong>).
+SOD2	drug	alcohol	27207918	High variance in the degree of gray matter tissue shrinkage among <b>alcohol</b> dependent individuals and a previous neuroimaging genetics report suggest the involvement of environmental and/or genetic factors, such as <strong>superoxide dismutase 2</strong> (<strong>SOD2</strong>).
+SOD2	drug	alcohol	27207918	We replicated a significant association of a functional <strong>SOD2</strong> single nucleotide polymorphism with normalized gray matter volume, which had been reported previously in an independent smaller sample of <b>alcohol</b> dependent individuals.
+SOD2	drug	alcohol	27207918	Converging independent evidence for a <strong>SOD2</strong> gene association with gray matter volume shrinkage in chronic <b>alcohol</b> users suggests that <strong>SOD2</strong> genetic variants predict differential brain volume loss mediated by free radicals.
+SOD2	addiction	sensitization	27095683	Further, m(PEA/PLD) treatment increased spinal <strong>MnSOD</strong> expression, prevented IkB α degradation and nuclear factor κB translocation, suggesting a possible role on central <b>sensitization</b>.
+SOD2	addiction	sensitization	27095683	Further, m(PEA/PLD) treatment increased spinal <strong><strong>MnSOD</strong></strong> expression, prevented IkB α degradation and nuclear factor κB translocation, suggesting a possible role on central <b>sensitization</b>.
+SOD2	drug	alcohol	26805422	Neither binge <b>ethanol</b> nor MAOI treatment significantly affected protein expression levels of the oxidative stress enzymes, <strong>SOD2</strong> or catalase.
+SOD2	addiction	intoxication	26805422	Neither <b>binge</b> ethanol nor MAOI treatment significantly affected protein expression levels of the oxidative stress enzymes, <strong>SOD2</strong> or catalase.
+SOD2	drug	nicotine	26544677	In this study, we hypothesized that the functional polymorphism of <strong>MnSOD</strong> Ala 9Val was associated with <b>smoking</b> in patients with schizophrenia.
+SOD2	drug	nicotine	26544677	In this study, we hypothesized that the functional polymorphism of <strong><strong>MnSOD</strong></strong> Ala 9Val was associated with <b>smoking</b> in patients with schizophrenia.
+SOD2	drug	nicotine	26544677	The results showed no significant differences in <strong>MnSOD</strong> Ala 9Val genotype and allele distributions between the patients and healthy controls or between <b>smokers</b> and never <b>smokers</b> in either patients or healthy controls alone.
+SOD2	drug	nicotine	26544677	The results showed no significant differences in <strong><strong>MnSOD</strong></strong> Ala 9Val genotype and allele distributions between the patients and healthy controls or between <b>smokers</b> and never <b>smokers</b> in either patients or healthy controls alone.
+SOD2	drug	nicotine	26544677	These results suggest that the <strong>MnSOD</strong> Ala 9Val polymorphism may not influence <b>smoking</b> status in a Chinese male schizophrenia population, but may influence the age at which <b>smoking</b> is started among schizophrenia <b>smokers</b>.
+SOD2	drug	nicotine	26544677	These results suggest that the <strong><strong>MnSOD</strong></strong> Ala 9Val polymorphism may not influence <b>smoking</b> status in a Chinese male schizophrenia population, but may influence the age at which <b>smoking</b> is started among schizophrenia <b>smokers</b>.
+SOD2	drug	nicotine	25052559	Several statistically significant interactions were observed between <b>smoking</b> and genetic variants (CYP1A2 1548C>T, CYP1A1 3801T>C, CYP1B1 4326G>C, NAT1 c. 85 1014T>A, UGT1A7 W208R 622T>C, <strong>SOD2</strong> c.47T>C, GSTT1 deletion).
+SOD2	drug	opioid	20637262	We have recently reported that nitration and inactivation of spinal mitochondrial superoxide dismutase (<strong>MnSOD</strong>) provides a critical source of these reactive oxygen and nitrogen species during central sensitization associated with the development of <b>morphine</b> induced hyperalgesia and antinociceptive tolerance.
+SOD2	addiction	sensitization	20637262	We have recently reported that nitration and inactivation of spinal mitochondrial superoxide dismutase (<strong>MnSOD</strong>) provides a critical source of these reactive oxygen and nitrogen species during central <b>sensitization</b> associated with the development of morphine induced hyperalgesia and antinociceptive tolerance.
+SOD2	drug	opioid	20637262	We have recently reported that nitration and inactivation of spinal mitochondrial superoxide dismutase (<strong><strong>MnSOD</strong></strong>) provides a critical source of these reactive oxygen and nitrogen species during central sensitization associated with the development of <b>morphine</b> induced hyperalgesia and antinociceptive tolerance.
+SOD2	addiction	sensitization	20637262	We have recently reported that nitration and inactivation of spinal mitochondrial superoxide dismutase (<strong><strong>MnSOD</strong></strong>) provides a critical source of these reactive oxygen and nitrogen species during central <b>sensitization</b> associated with the development of morphine induced hyperalgesia and antinociceptive tolerance.
+SOD2	drug	alcohol	20043000	Association of <strong>SOD2</strong>, a mitochondrial antioxidant enzyme, with gray matter volume shrinkage in <b>alcoholics</b>.
+SOD2	drug	alcohol	20043000	In this exploratory analysis, a putative functional missense variant of <strong>SOD2</strong> appears to influence gray matter loss in <b>alcoholics</b>.
+SOD2	drug	alcohol	21525761	<strong>MnSOD</strong> overexpression prevents liver mitochondrial DNA depletion after an <b>alcohol</b> binge but worsens this effect after prolonged <b>alcohol</b> consumption in mice.
+SOD2	addiction	intoxication	21525761	<strong>MnSOD</strong> overexpression prevents liver mitochondrial DNA depletion after an alcohol <b>binge</b> but worsens this effect after prolonged alcohol consumption in mice.
+SOD2	drug	alcohol	21525761	<strong><strong>MnSOD</strong></strong> overexpression prevents liver mitochondrial DNA depletion after an <b>alcohol</b> binge but worsens this effect after prolonged <b>alcohol</b> consumption in mice.
+SOD2	addiction	intoxication	21525761	<strong><strong>MnSOD</strong></strong> overexpression prevents liver mitochondrial DNA depletion after an alcohol <b>binge</b> but worsens this effect after prolonged alcohol consumption in mice.
+SOD2	drug	alcohol	21525761	To test whether manganese superoxide dismutase (<strong>MnSOD</strong>) overexpression modulates acute and chronic <b>alcohol</b> induced mtDNA lesions, transgenic <strong>MnSOD</strong> overexpressing (TgMnSOD(+++)) mice and wild type (WT) mice were treated by <b>alcohol</b>, either chronically (7 weeks in drinking water) or acutely (single intragastric dose of 5 g/kg).
+SOD2	drug	alcohol	21525761	To test whether manganese superoxide dismutase (<strong><strong>MnSOD</strong></strong>) overexpression modulates acute and chronic <b>alcohol</b> induced mtDNA lesions, transgenic <strong><strong>MnSOD</strong></strong> overexpressing (TgMnSOD(+++)) mice and wild type (WT) mice were treated by <b>alcohol</b>, either chronically (7 weeks in drinking water) or acutely (single intragastric dose of 5 g/kg).
+SOD2	drug	alcohol	21525761	In conclusion, <strong>MnSOD</strong> overexpression prevents mtDNA depletion after an acute <b>alcohol</b> binge but aggravates this effect after prolonged <b>alcohol</b> consumption, which selectively triggers iron accumulation in TgMnSOD(+++) mice but not in WT mice.
+SOD2	addiction	intoxication	21525761	In conclusion, <strong>MnSOD</strong> overexpression prevents mtDNA depletion after an acute alcohol <b>binge</b> but aggravates this effect after prolonged alcohol consumption, which selectively triggers iron accumulation in TgMnSOD(+++) mice but not in WT mice.
+SOD2	drug	alcohol	21525761	In conclusion, <strong><strong>MnSOD</strong></strong> overexpression prevents mtDNA depletion after an acute <b>alcohol</b> binge but aggravates this effect after prolonged <b>alcohol</b> consumption, which selectively triggers iron accumulation in TgMnSOD(+++) mice but not in WT mice.
+SOD2	addiction	intoxication	21525761	In conclusion, <strong><strong>MnSOD</strong></strong> overexpression prevents mtDNA depletion after an acute alcohol <b>binge</b> but aggravates this effect after prolonged alcohol consumption, which selectively triggers iron accumulation in TgMnSOD(+++) mice but not in WT mice.
+SOD2	drug	alcohol	21525761	In the model of acute <b>alcohol</b> binge, the protective effects of <strong>MnSOD</strong>, tempol, NOS inhibitors and uric acid suggested a role of the superoxide anion reacting with NO to form mtDNA damaging peroxynitrite.
+SOD2	addiction	intoxication	21525761	In the model of acute alcohol <b>binge</b>, the protective effects of <strong>MnSOD</strong>, tempol, NOS inhibitors and uric acid suggested a role of the superoxide anion reacting with NO to form mtDNA damaging peroxynitrite.
+SOD2	drug	alcohol	21525761	In the model of acute <b>alcohol</b> binge, the protective effects of <strong><strong>MnSOD</strong></strong>, tempol, NOS inhibitors and uric acid suggested a role of the superoxide anion reacting with NO to form mtDNA damaging peroxynitrite.
+SOD2	addiction	intoxication	21525761	In the model of acute alcohol <b>binge</b>, the protective effects of <strong><strong>MnSOD</strong></strong>, tempol, NOS inhibitors and uric acid suggested a role of the superoxide anion reacting with NO to form mtDNA damaging peroxynitrite.
+SOD2	drug	alcohol	20016022	To test whether manganese superoxide dismutase (<strong>MnSOD</strong>) modulates acute <b>alcohol</b> induced mitochondrial alterations, transgenic <strong>MnSOD</strong> overexpressing (<strong>MnSOD</strong>(+++)) mice, heterozygous knockout (<strong>MnSOD</strong>(+/ )) mice, and wild type (WT) littermates were sacrificed 2 or 24 h after intragastric <b>ethanol</b> administration (5 g/kg).
+SOD2	drug	alcohol	20016022	To test whether manganese superoxide dismutase (<strong><strong>MnSOD</strong></strong>) modulates acute <b>alcohol</b> induced mitochondrial alterations, transgenic <strong><strong>MnSOD</strong></strong> overexpressing (<strong><strong>MnSOD</strong></strong>(+++)) mice, heterozygous knockout (<strong><strong>MnSOD</strong></strong>(+/ )) mice, and wild type (WT) littermates were sacrificed 2 or 24 h after intragastric <b>ethanol</b> administration (5 g/kg).
+SOD2	drug	alcohol	20016022	<b>Alcohol</b> administration further increased <strong>MnSOD</strong> activity in <strong>MnSOD</strong>(+++) mice, but further decreased it in <strong>MnSOD</strong>(+/ ) mice.
+SOD2	drug	alcohol	20016022	<b>Alcohol</b> administration further increased <strong><strong>MnSOD</strong></strong> activity in <strong><strong>MnSOD</strong></strong>(+++) mice, but further decreased it in <strong><strong>MnSOD</strong></strong>(+/ ) mice.
+SOD2	drug	alcohol	20016022	In conclusion, <strong>MnSOD</strong> overexpression prevents, and <strong>MnSOD</strong> deficiency prolongs, mtDNA depletion after an acute <b>alcohol</b> binge in mice.
+SOD2	addiction	intoxication	20016022	In conclusion, <strong>MnSOD</strong> overexpression prevents, and <strong>MnSOD</strong> deficiency prolongs, mtDNA depletion after an acute alcohol <b>binge</b> in mice.
+SOD2	drug	alcohol	20016022	In conclusion, <strong><strong>MnSOD</strong></strong> overexpression prevents, and <strong><strong>MnSOD</strong></strong> deficiency prolongs, mtDNA depletion after an acute <b>alcohol</b> binge in mice.
+SOD2	addiction	intoxication	20016022	In conclusion, <strong><strong>MnSOD</strong></strong> overexpression prevents, and <strong><strong>MnSOD</strong></strong> deficiency prolongs, mtDNA depletion after an acute alcohol <b>binge</b> in mice.
+SOD2	drug	opioid	19607887	We have recently reported that formation of peroxynitrite (ONOO( ), PN) in the dorsal horn of the spinal cord plays a critical role in the development of <b>morphine</b> antinociceptive tolerance and have further documented that nitration and enzymatic inactivation of mitochondrial superoxide dismutase (<strong>MnSOD</strong>) at that site provides a source for this nitroxidative species.
+SOD2	drug	opioid	19607887	We have recently reported that formation of peroxynitrite (ONOO( ), PN) in the dorsal horn of the spinal cord plays a critical role in the development of <b>morphine</b> antinociceptive tolerance and have further documented that nitration and enzymatic inactivation of mitochondrial superoxide dismutase (<strong><strong>MnSOD</strong></strong>) at that site provides a source for this nitroxidative species.
+SOD2	drug	opioid	19607887	Co administration of <b>morphine</b> with potent Mn porphyrin based peroxynitrite scavengers, Mn(III) 5,10,15,20 tetrakis(N ethylpyridinium 2 yl)porphyrin (MnTE 2 PyP5+) and Mn(III) 5,10,15,20 tetrakis(N n hexylpyridinium 2 yl)porphyrin (MnTnHex 2 PyP5+) (1) restored the enzymatic activity of <strong>MnSOD</strong>, (2) attenuated PN derived nitroxidative stress, and (3) blocked the development of <b>morphine</b> induced antinociceptive tolerance.
+SOD2	drug	opioid	19607887	Co administration of <b>morphine</b> with potent Mn porphyrin based peroxynitrite scavengers, Mn(III) 5,10,15,20 tetrakis(N ethylpyridinium 2 yl)porphyrin (MnTE 2 PyP5+) and Mn(III) 5,10,15,20 tetrakis(N n hexylpyridinium 2 yl)porphyrin (MnTnHex 2 PyP5+) (1) restored the enzymatic activity of <strong><strong>MnSOD</strong></strong>, (2) attenuated PN derived nitroxidative stress, and (3) blocked the development of <b>morphine</b> induced antinociceptive tolerance.
+SOD2	drug	opioid	19607887	Collectively, these data suggest that PN mediated enzymatic inactivation of supraspinal <strong>MnSOD</strong> provides a source of nitroxidative stress, which in turn contributes to central sensitization associated with the development of <b>morphine</b> antinociceptive tolerance.
+SOD2	addiction	sensitization	19607887	Collectively, these data suggest that PN mediated enzymatic inactivation of supraspinal <strong>MnSOD</strong> provides a source of nitroxidative stress, which in turn contributes to central <b>sensitization</b> associated with the development of morphine antinociceptive tolerance.
+SOD2	drug	opioid	19607887	Collectively, these data suggest that PN mediated enzymatic inactivation of supraspinal <strong><strong>MnSOD</strong></strong> provides a source of nitroxidative stress, which in turn contributes to central sensitization associated with the development of <b>morphine</b> antinociceptive tolerance.
+SOD2	addiction	sensitization	19607887	Collectively, these data suggest that PN mediated enzymatic inactivation of supraspinal <strong><strong>MnSOD</strong></strong> provides a source of nitroxidative stress, which in turn contributes to central <b>sensitization</b> associated with the development of morphine antinociceptive tolerance.
+SOD2	drug	amphetamine	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and <strong>SOD2</strong>) with <b>METH</b> psychosis.
+SOD2	addiction	dependence	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and <strong>SOD2</strong>) with METH psychosis.
+SOD2	drug	amphetamine	18411704	As to risks of rapid onset of <b>methamphetamine</b> psychosis, worse prognosis or complication of spontaneous relapse, the dopamine D2 receptors, dopamine transporter, monoamine oxidase A, catechol O methyltransferese, <strong>SOD2</strong>, NQO2, PICK1 gene were identified.
+SOD2	addiction	relapse	18411704	As to risks of rapid onset of methamphetamine psychosis, worse prognosis or complication of spontaneous <b>relapse</b>, the dopamine D2 receptors, dopamine transporter, monoamine oxidase A, catechol O methyltransferese, <strong>SOD2</strong>, NQO2, PICK1 gene were identified.
+SOD2	drug	alcohol	15522206	In normal mice exposed to a subacute (3 weeks) <b>ethanol</b> intoxication, a significant increase in the number of apoptotic hepatocytes was observed in concomitance with the up regulation of the mitochondrial superoxide scavenger <strong>MnSOD</strong>, a reliable indicator of oxidative stress.
+SOD2	addiction	intoxication	15522206	In normal mice exposed to a subacute (3 weeks) ethanol <b>intoxication</b>, a significant increase in the number of apoptotic hepatocytes was observed in concomitance with the up regulation of the mitochondrial superoxide scavenger <strong>MnSOD</strong>, a reliable indicator of oxidative stress.
+SOD2	drug	alcohol	15522206	In normal mice exposed to a subacute (3 weeks) <b>ethanol</b> intoxication, a significant increase in the number of apoptotic hepatocytes was observed in concomitance with the up regulation of the mitochondrial superoxide scavenger <strong><strong>MnSOD</strong></strong>, a reliable indicator of oxidative stress.
+SOD2	addiction	intoxication	15522206	In normal mice exposed to a subacute (3 weeks) ethanol <b>intoxication</b>, a significant increase in the number of apoptotic hepatocytes was observed in concomitance with the up regulation of the mitochondrial superoxide scavenger <strong><strong>MnSOD</strong></strong>, a reliable indicator of oxidative stress.
+SOD2	drug	alcohol	9088787	Mean manganese superoxide dismutase (<strong>Mn SOD</strong>) concentrations in the serum of patients suffering from <b>alcohol</b> dependence is almost twice as high as in serum of non dependent controls.
+SOD2	addiction	dependence	9088787	Mean manganese superoxide dismutase (<strong>Mn SOD</strong>) concentrations in the serum of patients suffering from alcohol <b>dependence</b> is almost twice as high as in serum of non dependent controls.
+SOD2	drug	alcohol	9131893	Oxidative stress associated parameters [concentrations of lactoferrin, Cu,Zn superoxide dismutase (SOD) and <strong>Mn SOD</strong>] were determined in sera of 20 patients suffering from <b>alcohol</b> dependence immediately after detoxification and in 15 non dependent healthy subjects as controls.
+SOD2	addiction	dependence	9131893	Oxidative stress associated parameters [concentrations of lactoferrin, Cu,Zn superoxide dismutase (SOD) and <strong>Mn SOD</strong>] were determined in sera of 20 patients suffering from alcohol <b>dependence</b> immediately after detoxification and in 15 non dependent healthy subjects as controls.
+SOD2	drug	alcohol	1417973	The activities of Cu,Zn superoxide dismutase (SOD) and glutathione S transferase were higher in <b>ethanol</b> fed rats than in controls, whereas <strong>Mn SOD</strong>, catalase and glutathione peroxidase activities were not altered by <b>ethanol</b> treatment.
+SOD2	drug	alcohol	6685298	Manganese superoxide dismutase (<strong>Mn SOD</strong>) studied during <b>ethanol</b> vapor inhalation shows no changes during the inhalation period (4 days) and a transient increase 12 hours after <b>ethanol</b> withdrawal.
+SOD2	addiction	withdrawal	6685298	Manganese superoxide dismutase (<strong>Mn SOD</strong>) studied during ethanol vapor inhalation shows no changes during the inhalation period (4 days) and a transient increase 12 hours after ethanol <b>withdrawal</b>.
+SARS2	drug	nicotine	32650305	The associations between symptoms potentially related to <strong>SARS</strong> CoV 2 infection and NPS results were calculated as adjusted odds ratios with 95% confidence intervals (aOR, 95%CI) by means of multiple logistic regression analysis controlling for age, sex, education, <b>smoking</b> habits, and the number of co morbidities.
+SARS2	drug	nicotine	32582324	<b>Smoking</b> <b>tobacco</b> (cigarette, e cigarettes or waterpipe) produces exhaled smoke, coughing or sneezing, aerosols containing <strong>SARS</strong> CoV 2 in the surroundings and contaminating surfaces.
+SARS2	drug	alcohol	32540735	Pubmed and Google Scholar are searched with the following key terms  "COVID 19", "<strong>SARS</strong> CoV2", "Pandemic", "Addiction", "Opioid", "<b>Alcohol</b>", "Smoking", "Addiction Psychiatry", "Deaddiction", "Substance use disorders", "Behavioral addiction".
+SARS2	drug	nicotine	32540735	Pubmed and Google Scholar are searched with the following key terms  "COVID 19", "<strong>SARS</strong> CoV2", "Pandemic", "Addiction", "Opioid", "Alcohol", "<b>Smoking</b>", "Addiction Psychiatry", "Deaddiction", "Substance use disorders", "Behavioral addiction".
+SARS2	drug	opioid	32540735	Pubmed and Google Scholar are searched with the following key terms  "COVID 19", "<strong>SARS</strong> CoV2", "Pandemic", "Addiction", "<b>Opioid</b>", "Alcohol", "Smoking", "Addiction Psychiatry", "Deaddiction", "Substance use disorders", "Behavioral addiction".
+SARS2	addiction	addiction	32540735	Pubmed and Google Scholar are searched with the following key terms  "COVID 19", "<strong>SARS</strong> CoV2", "Pandemic", "<b>Addiction</b>", "Opioid", "Alcohol", "Smoking", "<b>Addiction</b> Psychiatry", "Deaddiction", "Substance use disorders", "Behavioral <b>addiction</b>".
+SARS2	drug	alcohol	32505493	Secondary to misinformation about the potential for <b>alcohol</b> to neutralize <strong>SARS</strong> CoV 2, there has also been a significant escalation in methanol related morbidity and mortality, with over 5000 people poisoned and over 500 confirmed deaths for the same period from February through April 2020.
+SARS2	addiction	addiction	32505493	Secondary to misinformation about the potential for alcohol to neutralize <strong>SARS</strong> CoV 2, there has also been a significant <b>escalation</b> in methanol related morbidity and mortality, with over 5000 people poisoned and over 500 confirmed deaths for the same period from February through April 2020.
+SARS2	drug	nicotine	32455539	<b>Smoking</b> Mediated Upregulation of the Androgen Pathway Leads to Increased <strong>SARS</strong> CoV 2 Susceptibility.
+SARS2	drug	nicotine	32455539	In this study, we aim to analyze how <b>smoking</b> may affect the <strong>SARS</strong> CoV 2 infection rate.
+SARS2	drug	nicotine	32455539	We found that the receptor and transmembrane protease necessary for <strong>SARS</strong> CoV 2 entry into host cells, ACE2 and TMPRSS2, respectively, were upregulated in <b>smoking</b> samples from both lung and oral epithelial tissue.
+SARS2	drug	opioid	32375887	Opiate users may misinterpret <strong>SARS</strong> CoV2 symptoms as opiate withdrawal and manage this by using <b>opioids</b>.
+SARS2	addiction	withdrawal	32375887	Opiate users may misinterpret <strong>SARS</strong> CoV2 symptoms as opiate <b>withdrawal</b> and manage this by using opioids.
+SARS2	drug	nicotine	31250643	In this work, a portable device is fabricated for sensitive on site evaluation of <b>nicotine</b> in <b>tobacco</b> and environmental <b>tobacco</b> smoke based on surface enhanced Raman scattering (<strong>SERS</strong>).
+SARS2	drug	cannabinoid	30907578	Surface enhanced Raman scattering (<strong>SERS</strong>) sensing has been increasingly used to detect illicit drugs; however, only limited <strong>SERS</strong> sensing results of <b>THC</b> in methanol solution have been reported, while its presence in body fluids, such as saliva or plasma, has yet to be investigated.
+SARS2	drug	cannabinoid	30907578	In this article, we demonstrate the trace detection of <b>THC</b> in human plasma and saliva solution using a <strong>SERS</strong> active substrate formed by in situ growth of silver nanoparticles (Ag NPs) on diatom frustules.
+SARS2	drug	cannabinoid	30907578	The <strong>SERS</strong> peak at 1603 cm 1 with standard deviation of 3.4 cm 1 was used for the evaluation of <b>THC</b> concentration in a methanol solution.
+SARS2	drug	cannabinoid	30907578	Additionally, we observed that <b>THC</b> in plasma or saliva samples produces a strong <strong>SERS</strong> peak at 1621 cm 1 due to the stretching mode of O C═O, which is related to the metabolic change of <b>THC</b> structures in body fluid.
+SARS2	drug	cannabinoid	30907578	To conduct a quantitative analysis, principal component analysis (PCA) was applied to analyze the <strong>SERS</strong> spectra of 1 pM <b>THC</b> in methanol solution, plasma, and purified saliva samples.
+SARS2	drug	cannabinoid	30907578	Similarly, the <strong>SERS</strong> spectra of <b>THC</b> in raw saliva solution under various metabolic times were studied using PCA and 98% of the variability is accounted for in the first three principal components.
+SARS2	drug	cannabinoid	30907578	In summary, the hybrid plasmonic biosilica <strong>SERS</strong> substrate can achieve ultrasensitive, near quantitative detection of trace levels of <b>THC</b> in complex body fluids, which can potentially transform forensic sensing techniques to detect <b>marijuana</b> abuse.
+SARS2	drug	alcohol	29289665	<b>Disulfiram</b> can inhibit MERS and <strong>SARS</strong> coronavirus papain like proteases via different modes.
+SARS2	drug	alcohol	29289665	Here we show that a clinically available <b>alcohol</b> aversive drug, <b>disulfiram</b>, can inhibit the papain like proteases (PLpros) of MERS CoV and <strong>SARS</strong> CoV.
+SARS2	addiction	aversion	29289665	Here we show that a clinically available alcohol <b>aversive</b> drug, disulfiram, can inhibit the papain like proteases (PLpros) of MERS CoV and <strong>SARS</strong> CoV.
+SARS2	drug	alcohol	29289665	Our findings suggest that <b>disulfiram</b> acts as an allosteric inhibitor of MERS CoV PLpro but as a competitive (or mixed) inhibitor of <strong>SARS</strong> CoV PLpro.
+SARS2	drug	alcohol	29289665	The phenomenon of slow binding inhibition and the irrecoverability of enzyme activity after removing unbound <b>disulfiram</b> indicate covalent inactivation of <strong>SARS</strong> CoV PLpro by <b>disulfiram</b>, while synergistic inhibition of MERS CoV PLpro by <b>disulfiram</b> and 6 thioguanine or mycophenolic acid implies the potential for combination treatments using these three clinically available drugs.
+SARS2	drug	opioid	28944090	The <strong>SERS</strong> based POC analyzer was used to identify <b>buprenorphine</b> and <b>opioids</b> in saliva samples by matching library spectra to samples collected from 7 veterans.
+SARS2	drug	cocaine	27698368	Caffeine and <b>cocaine</b> were utilized as molecular probes to test the combined <strong>SERS</strong>/SALDI response of RaMassays, showing excellent sensitivity and reproducibility.
+SARS2	drug	amphetamine	27698368	The differentiation between <b>amphetamine</b>/ephedrine and theophylline/theobromine couples demonstrated the synergistic reciprocal reinforcement of <strong>SERS</strong> and SALDI.
+SARS2	addiction	reward	27698368	The differentiation between amphetamine/ephedrine and theophylline/theobromine couples demonstrated the synergistic reciprocal <b>reinforcement</b> of <strong>SERS</strong> and SALDI.
+SARS2	drug	nicotine	23807309	This TLC <strong>SERS</strong> method allows the direct detection of cotinine in the urine samples of both active and passive <b>smokers</b> and the detection of 3HC in <b>smokers</b>.
+SARS2	drug	alcohol	18790829	<b>Alcohol</b> abuse/dependence symptoms among hospital employees exposed to a <strong>SARS</strong> outbreak.
+SARS2	addiction	dependence	18790829	Alcohol abuse/<b>dependence</b> symptoms among hospital employees exposed to a <strong>SARS</strong> outbreak.
+SARS2	drug	alcohol	18790829	The aim of this study was to examine <b>alcohol</b> abuse/dependence symptoms among hospital employees exposed to a severe acute respiratory syndrome (<strong>SARS</strong>) outbreak, and the relationship between types of exposure to the <strong>SARS</strong> outbreak and subsequent <b>alcohol</b> abuse/dependence symptoms.
+SARS2	addiction	dependence	18790829	The aim of this study was to examine alcohol abuse/<b>dependence</b> symptoms among hospital employees exposed to a severe acute respiratory syndrome (<strong>SARS</strong>) outbreak, and the relationship between types of exposure to the <strong>SARS</strong> outbreak and subsequent alcohol abuse/<b>dependence</b> symptoms.
+SARS2	drug	alcohol	18790829	Current <b>alcohol</b> abuse/dependence symptom counts 3 years after the outbreak were positively associated with having been quarantined, or worked in high risk locations such as <strong>SARS</strong> wards, during the outbreak.
+SARS2	addiction	dependence	18790829	Current alcohol abuse/<b>dependence</b> symptom counts 3 years after the outbreak were positively associated with having been quarantined, or worked in high risk locations such as <strong>SARS</strong> wards, during the outbreak.
+SARS2	drug	alcohol	18790829	However, having had family members or friends contract, <strong>SARS</strong> was not related to <b>alcohol</b> abuse/dependence symptom count.
+SARS2	addiction	dependence	18790829	However, having had family members or friends contract, <strong>SARS</strong> was not related to alcohol abuse/<b>dependence</b> symptom count.
+SARS2	drug	cocaine	11170654	Structure activity relationships (<strong>SARs</strong>) have been developed that contrast with those described for <b>cocaine</b>, despite significant structural similarity.
+SARS1	drug	nicotine	32650305	The associations between symptoms potentially related to <strong>SARS</strong> CoV 2 infection and NPS results were calculated as adjusted odds ratios with 95% confidence intervals (aOR, 95%CI) by means of multiple logistic regression analysis controlling for age, sex, education, <b>smoking</b> habits, and the number of co morbidities.
+SARS1	drug	nicotine	32582324	<b>Smoking</b> <b>tobacco</b> (cigarette, e cigarettes or waterpipe) produces exhaled smoke, coughing or sneezing, aerosols containing <strong>SARS</strong> CoV 2 in the surroundings and contaminating surfaces.
+SARS1	drug	alcohol	32540735	Pubmed and Google Scholar are searched with the following key terms  "COVID 19", "<strong>SARS</strong> CoV2", "Pandemic", "Addiction", "Opioid", "<b>Alcohol</b>", "Smoking", "Addiction Psychiatry", "Deaddiction", "Substance use disorders", "Behavioral addiction".
+SARS1	drug	nicotine	32540735	Pubmed and Google Scholar are searched with the following key terms  "COVID 19", "<strong>SARS</strong> CoV2", "Pandemic", "Addiction", "Opioid", "Alcohol", "<b>Smoking</b>", "Addiction Psychiatry", "Deaddiction", "Substance use disorders", "Behavioral addiction".
+SARS1	drug	opioid	32540735	Pubmed and Google Scholar are searched with the following key terms  "COVID 19", "<strong>SARS</strong> CoV2", "Pandemic", "Addiction", "<b>Opioid</b>", "Alcohol", "Smoking", "Addiction Psychiatry", "Deaddiction", "Substance use disorders", "Behavioral addiction".
+SARS1	addiction	addiction	32540735	Pubmed and Google Scholar are searched with the following key terms  "COVID 19", "<strong>SARS</strong> CoV2", "Pandemic", "<b>Addiction</b>", "Opioid", "Alcohol", "Smoking", "<b>Addiction</b> Psychiatry", "Deaddiction", "Substance use disorders", "Behavioral <b>addiction</b>".
+SARS1	drug	alcohol	32505493	Secondary to misinformation about the potential for <b>alcohol</b> to neutralize <strong>SARS</strong> CoV 2, there has also been a significant escalation in methanol related morbidity and mortality, with over 5000 people poisoned and over 500 confirmed deaths for the same period from February through April 2020.
+SARS1	addiction	addiction	32505493	Secondary to misinformation about the potential for alcohol to neutralize <strong>SARS</strong> CoV 2, there has also been a significant <b>escalation</b> in methanol related morbidity and mortality, with over 5000 people poisoned and over 500 confirmed deaths for the same period from February through April 2020.
+SARS1	drug	nicotine	32455539	<b>Smoking</b> Mediated Upregulation of the Androgen Pathway Leads to Increased <strong>SARS</strong> CoV 2 Susceptibility.
+SARS1	drug	nicotine	32455539	In this study, we aim to analyze how <b>smoking</b> may affect the <strong>SARS</strong> CoV 2 infection rate.
+SARS1	drug	nicotine	32455539	We found that the receptor and transmembrane protease necessary for <strong>SARS</strong> CoV 2 entry into host cells, ACE2 and TMPRSS2, respectively, were upregulated in <b>smoking</b> samples from both lung and oral epithelial tissue.
+SARS1	drug	opioid	32375887	Opiate users may misinterpret <strong>SARS</strong> CoV2 symptoms as opiate withdrawal and manage this by using <b>opioids</b>.
+SARS1	addiction	withdrawal	32375887	Opiate users may misinterpret <strong>SARS</strong> CoV2 symptoms as opiate <b>withdrawal</b> and manage this by using opioids.
+SARS1	drug	nicotine	31250643	In this work, a portable device is fabricated for sensitive on site evaluation of <b>nicotine</b> in <b>tobacco</b> and environmental <b>tobacco</b> smoke based on surface enhanced Raman scattering (<strong>SERS</strong>).
+SARS1	drug	cannabinoid	30907578	Surface enhanced Raman scattering (<strong>SERS</strong>) sensing has been increasingly used to detect illicit drugs; however, only limited <strong>SERS</strong> sensing results of <b>THC</b> in methanol solution have been reported, while its presence in body fluids, such as saliva or plasma, has yet to be investigated.
+SARS1	drug	cannabinoid	30907578	In this article, we demonstrate the trace detection of <b>THC</b> in human plasma and saliva solution using a <strong>SERS</strong> active substrate formed by in situ growth of silver nanoparticles (Ag NPs) on diatom frustules.
+SARS1	drug	cannabinoid	30907578	The <strong>SERS</strong> peak at 1603 cm 1 with standard deviation of 3.4 cm 1 was used for the evaluation of <b>THC</b> concentration in a methanol solution.
+SARS1	drug	cannabinoid	30907578	Additionally, we observed that <b>THC</b> in plasma or saliva samples produces a strong <strong>SERS</strong> peak at 1621 cm 1 due to the stretching mode of O C═O, which is related to the metabolic change of <b>THC</b> structures in body fluid.
+SARS1	drug	cannabinoid	30907578	To conduct a quantitative analysis, principal component analysis (PCA) was applied to analyze the <strong>SERS</strong> spectra of 1 pM <b>THC</b> in methanol solution, plasma, and purified saliva samples.
+SARS1	drug	cannabinoid	30907578	Similarly, the <strong>SERS</strong> spectra of <b>THC</b> in raw saliva solution under various metabolic times were studied using PCA and 98% of the variability is accounted for in the first three principal components.
+SARS1	drug	cannabinoid	30907578	In summary, the hybrid plasmonic biosilica <strong>SERS</strong> substrate can achieve ultrasensitive, near quantitative detection of trace levels of <b>THC</b> in complex body fluids, which can potentially transform forensic sensing techniques to detect <b>marijuana</b> abuse.
+SARS1	drug	alcohol	29289665	<b>Disulfiram</b> can inhibit MERS and <strong>SARS</strong> coronavirus papain like proteases via different modes.
+SARS1	drug	alcohol	29289665	Here we show that a clinically available <b>alcohol</b> aversive drug, <b>disulfiram</b>, can inhibit the papain like proteases (PLpros) of MERS CoV and <strong>SARS</strong> CoV.
+SARS1	addiction	aversion	29289665	Here we show that a clinically available alcohol <b>aversive</b> drug, disulfiram, can inhibit the papain like proteases (PLpros) of MERS CoV and <strong>SARS</strong> CoV.
+SARS1	drug	alcohol	29289665	Our findings suggest that <b>disulfiram</b> acts as an allosteric inhibitor of MERS CoV PLpro but as a competitive (or mixed) inhibitor of <strong>SARS</strong> CoV PLpro.
+SARS1	drug	alcohol	29289665	The phenomenon of slow binding inhibition and the irrecoverability of enzyme activity after removing unbound <b>disulfiram</b> indicate covalent inactivation of <strong>SARS</strong> CoV PLpro by <b>disulfiram</b>, while synergistic inhibition of MERS CoV PLpro by <b>disulfiram</b> and 6 thioguanine or mycophenolic acid implies the potential for combination treatments using these three clinically available drugs.
+SARS1	drug	opioid	28944090	The <strong>SERS</strong> based POC analyzer was used to identify <b>buprenorphine</b> and <b>opioids</b> in saliva samples by matching library spectra to samples collected from 7 veterans.
+SARS1	drug	cocaine	27698368	Caffeine and <b>cocaine</b> were utilized as molecular probes to test the combined <strong>SERS</strong>/SALDI response of RaMassays, showing excellent sensitivity and reproducibility.
+SARS1	drug	amphetamine	27698368	The differentiation between <b>amphetamine</b>/ephedrine and theophylline/theobromine couples demonstrated the synergistic reciprocal reinforcement of <strong>SERS</strong> and SALDI.
+SARS1	addiction	reward	27698368	The differentiation between amphetamine/ephedrine and theophylline/theobromine couples demonstrated the synergistic reciprocal <b>reinforcement</b> of <strong>SERS</strong> and SALDI.
+SARS1	drug	nicotine	23807309	This TLC <strong>SERS</strong> method allows the direct detection of cotinine in the urine samples of both active and passive <b>smokers</b> and the detection of 3HC in <b>smokers</b>.
+SARS1	drug	alcohol	18790829	<b>Alcohol</b> abuse/dependence symptoms among hospital employees exposed to a <strong>SARS</strong> outbreak.
+SARS1	addiction	dependence	18790829	Alcohol abuse/<b>dependence</b> symptoms among hospital employees exposed to a <strong>SARS</strong> outbreak.
+SARS1	drug	alcohol	18790829	The aim of this study was to examine <b>alcohol</b> abuse/dependence symptoms among hospital employees exposed to a severe acute respiratory syndrome (<strong>SARS</strong>) outbreak, and the relationship between types of exposure to the <strong>SARS</strong> outbreak and subsequent <b>alcohol</b> abuse/dependence symptoms.
+SARS1	addiction	dependence	18790829	The aim of this study was to examine alcohol abuse/<b>dependence</b> symptoms among hospital employees exposed to a severe acute respiratory syndrome (<strong>SARS</strong>) outbreak, and the relationship between types of exposure to the <strong>SARS</strong> outbreak and subsequent alcohol abuse/<b>dependence</b> symptoms.
+SARS1	drug	alcohol	18790829	Current <b>alcohol</b> abuse/dependence symptom counts 3 years after the outbreak were positively associated with having been quarantined, or worked in high risk locations such as <strong>SARS</strong> wards, during the outbreak.
+SARS1	addiction	dependence	18790829	Current alcohol abuse/<b>dependence</b> symptom counts 3 years after the outbreak were positively associated with having been quarantined, or worked in high risk locations such as <strong>SARS</strong> wards, during the outbreak.
+SARS1	drug	alcohol	18790829	However, having had family members or friends contract, <strong>SARS</strong> was not related to <b>alcohol</b> abuse/dependence symptom count.
+SARS1	addiction	dependence	18790829	However, having had family members or friends contract, <strong>SARS</strong> was not related to alcohol abuse/<b>dependence</b> symptom count.
+SARS1	drug	cocaine	11170654	Structure activity relationships (<strong>SARs</strong>) have been developed that contrast with those described for <b>cocaine</b>, despite significant structural similarity.
+RAC1	drug	opioid	32641997	Decreased Neuronal Excitability in Medial Prefrontal Cortex during <b>Morphine</b> Withdrawal is associated with enhanced SK channel activity and upregulation of small GTPase <strong>Rac1</strong>.
+RAC1	addiction	withdrawal	32641997	Decreased Neuronal Excitability in Medial Prefrontal Cortex during Morphine <b>Withdrawal</b> is associated with enhanced SK channel activity and upregulation of small GTPase <strong>Rac1</strong>.
+RAC1	drug	opioid	32641997	Decreased Neuronal Excitability in Medial Prefrontal Cortex during <b>Morphine</b> Withdrawal is associated with enhanced SK channel activity and upregulation of small GTPase <strong><strong>Rac1</strong></strong>.
+RAC1	addiction	withdrawal	32641997	Decreased Neuronal Excitability in Medial Prefrontal Cortex during Morphine <b>Withdrawal</b> is associated with enhanced SK channel activity and upregulation of small GTPase <strong><strong>Rac1</strong></strong>.
+RAC1	addiction	withdrawal	32641997	We verified the hypothesis that <strong>Rac1</strong>, a member of Rho family of small GTPases, implicated in SK channel regulation, modulate SK channel neuroadaptations during opiate <b>withdrawal</b>.
+RAC1	addiction	withdrawal	32641997	We verified the hypothesis that <strong><strong>Rac1</strong></strong>, a member of Rho family of small GTPases, implicated in SK channel regulation, modulate SK channel neuroadaptations during opiate <b>withdrawal</b>.
+RAC1	addiction	withdrawal	32641997	In the IL, <strong>Rac1</strong> signaling was increased during <b>withdrawal</b>, and the <strong>Rac1</strong> inhibitor NSC23766 disrupted SK current, which increased neuronal firing.
+RAC1	addiction	withdrawal	32641997	In the IL, <strong><strong>Rac1</strong></strong> signaling was increased during <b>withdrawal</b>, and the <strong><strong>Rac1</strong></strong> inhibitor NSC23766 disrupted SK current, which increased neuronal firing.
+RAC1	drug	opioid	32641997	Suppression of <strong>Rac1</strong> inhibited <b>morphine</b> induced CPP and expression of SK channels in IL.
+RAC1	addiction	reward	32641997	Suppression of <strong>Rac1</strong> inhibited morphine induced <b>CPP</b> and expression of SK channels in IL.
+RAC1	drug	opioid	32641997	Suppression of <strong><strong>Rac1</strong></strong> inhibited <b>morphine</b> induced CPP and expression of SK channels in IL.
+RAC1	addiction	reward	32641997	Suppression of <strong><strong>Rac1</strong></strong> inhibited morphine induced <b>CPP</b> and expression of SK channels in IL.
+RAC1	drug	opioid	32641997	Conclusions: These findings highlight the potential value of SK channels and the upstream molecule <strong>Rac1</strong>, which may throw light on the therapeutic mechanism of neuromodulation treatment for <b>opioid</b> dependence.
+RAC1	addiction	dependence	32641997	Conclusions: These findings highlight the potential value of SK channels and the upstream molecule <strong>Rac1</strong>, which may throw light on the therapeutic mechanism of neuromodulation treatment for opioid <b>dependence</b>.
+RAC1	drug	opioid	32641997	Conclusions: These findings highlight the potential value of SK channels and the upstream molecule <strong><strong>Rac1</strong></strong>, which may throw light on the therapeutic mechanism of neuromodulation treatment for <b>opioid</b> dependence.
+RAC1	addiction	dependence	32641997	Conclusions: These findings highlight the potential value of SK channels and the upstream molecule <strong><strong>Rac1</strong></strong>, which may throw light on the therapeutic mechanism of neuromodulation treatment for opioid <b>dependence</b>.
+RAC1	drug	amphetamine	31660086	Different roles of <strong>Rac1</strong> in the acquisition and extinction of <b>methamphetamine</b> associated contextual memory in the nucleus accumbens.
+RAC1	drug	amphetamine	31660086	Different roles of <strong><strong>Rac1</strong></strong> in the acquisition and extinction of <b>methamphetamine</b> associated contextual memory in the nucleus accumbens.
+RAC1	drug	amphetamine	31660086	Here, we explored whether <strong>Rac1</strong> in the NAc mediates <b>METH</b> associated contextual memory and spine remodelling.
+RAC1	drug	amphetamine	31660086	Here, we explored whether <strong><strong>Rac1</strong></strong> in the NAc mediates <b>METH</b> associated contextual memory and spine remodelling.
+RAC1	drug	amphetamine	31660086	Methods: Pharmacological and genetic manipulations of <strong>Rac1</strong> were used to investigate its role during the acquisition, reconsolidation and extinction of <b>METH</b> associated contextual memory.
+RAC1	drug	amphetamine	31660086	Methods: Pharmacological and genetic manipulations of <strong><strong>Rac1</strong></strong> were used to investigate its role during the acquisition, reconsolidation and extinction of <b>METH</b> associated contextual memory.
+RAC1	drug	amphetamine	31660086	Results: Using viral mediated gene transfer, we demonstrated that decreased <strong>Rac1</strong> activity was required for the acquisition of <b>METH</b> associated contextual memory and the <b>METH</b> induced increase in thin spine density, whereas increased <strong>Rac1</strong> signalling was important for the extinction of <b>METH</b> associated contextual memory and the related elimination of thin spines.
+RAC1	drug	amphetamine	31660086	Results: Using viral mediated gene transfer, we demonstrated that decreased <strong><strong>Rac1</strong></strong> activity was required for the acquisition of <b>METH</b> associated contextual memory and the <b>METH</b> induced increase in thin spine density, whereas increased <strong><strong>Rac1</strong></strong> signalling was important for the extinction of <b>METH</b> associated contextual memory and the related elimination of thin spines.
+RAC1	drug	amphetamine	31660086	Interestingly, <strong>Rac1</strong> was responsible for <b>METH</b> induced spine plasticity in D1 MSNs but not in D2 MSNs.
+RAC1	drug	amphetamine	31660086	Interestingly, <strong><strong>Rac1</strong></strong> was responsible for <b>METH</b> induced spine plasticity in D1 MSNs but not in D2 MSNs.
+RAC1	drug	amphetamine	31660086	Additionally, we found that microinjection of a <strong>Rac1</strong> inhibitor or activator into the NAc was not sufficient to disrupt reconsolidation, and the pharmacological activation of <strong>Rac1</strong> in the NAc facilitated the extinction of <b>METH</b> associated contextual memory.
+RAC1	drug	amphetamine	31660086	Additionally, we found that microinjection of a <strong><strong>Rac1</strong></strong> inhibitor or activator into the NAc was not sufficient to disrupt reconsolidation, and the pharmacological activation of <strong><strong>Rac1</strong></strong> in the NAc facilitated the extinction of <b>METH</b> associated contextual memory.
+RAC1	drug	amphetamine	31660086	Regarding cognitive memory, decreased <strong>Rac1</strong> activity improved the <b>METH</b> induced impairment in object recognition memory.
+RAC1	drug	amphetamine	31660086	Regarding cognitive memory, decreased <strong><strong>Rac1</strong></strong> activity improved the <b>METH</b> induced impairment in object recognition memory.
+RAC1	drug	amphetamine	31660086	Conclusion: Our findings indicate that <strong>Rac1</strong> plays opposing roles in the acquisition and extinction of <b>METH</b> associated contextual memory and reveal the cell specific role of <strong>Rac1</strong> in <b>METH</b> associated spine remodelling, suggesting that <strong>Rac1</strong> is a potential therapeutic target for reducing relapse in <b>METH</b> addiction and remediating <b>METH</b> induced recognition memory impairment.
+RAC1	addiction	addiction	31660086	Conclusion: Our findings indicate that <strong>Rac1</strong> plays opposing roles in the acquisition and extinction of METH associated contextual memory and reveal the cell specific role of <strong>Rac1</strong> in METH associated spine remodelling, suggesting that <strong>Rac1</strong> is a potential therapeutic target for reducing relapse in METH <b>addiction</b> and remediating METH induced recognition memory impairment.
+RAC1	addiction	relapse	31660086	Conclusion: Our findings indicate that <strong>Rac1</strong> plays opposing roles in the acquisition and extinction of METH associated contextual memory and reveal the cell specific role of <strong>Rac1</strong> in METH associated spine remodelling, suggesting that <strong>Rac1</strong> is a potential therapeutic target for reducing <b>relapse</b> in METH addiction and remediating METH induced recognition memory impairment.
+RAC1	drug	amphetamine	31660086	Conclusion: Our findings indicate that <strong><strong>Rac1</strong></strong> plays opposing roles in the acquisition and extinction of <b>METH</b> associated contextual memory and reveal the cell specific role of <strong><strong>Rac1</strong></strong> in <b>METH</b> associated spine remodelling, suggesting that <strong><strong>Rac1</strong></strong> is a potential therapeutic target for reducing relapse in <b>METH</b> addiction and remediating <b>METH</b> induced recognition memory impairment.
+RAC1	addiction	addiction	31660086	Conclusion: Our findings indicate that <strong><strong>Rac1</strong></strong> plays opposing roles in the acquisition and extinction of METH associated contextual memory and reveal the cell specific role of <strong><strong>Rac1</strong></strong> in METH associated spine remodelling, suggesting that <strong><strong>Rac1</strong></strong> is a potential therapeutic target for reducing relapse in METH <b>addiction</b> and remediating METH induced recognition memory impairment.
+RAC1	addiction	relapse	31660086	Conclusion: Our findings indicate that <strong><strong>Rac1</strong></strong> plays opposing roles in the acquisition and extinction of METH associated contextual memory and reveal the cell specific role of <strong><strong>Rac1</strong></strong> in METH associated spine remodelling, suggesting that <strong><strong>Rac1</strong></strong> is a potential therapeutic target for reducing <b>relapse</b> in METH addiction and remediating METH induced recognition memory impairment.
+RAC1	drug	alcohol	31558618	Here we investigate the role of <strong>Rac1</strong> and its downstream target, the actin severing protein cofilin, in <b>alcohol</b> consumption preference.
+RAC1	drug	alcohol	31558618	Here we investigate the role of <strong><strong>Rac1</strong></strong> and its downstream target, the actin severing protein cofilin, in <b>alcohol</b> consumption preference.
+RAC1	drug	alcohol	31558618	We show that these two regulators of actin dynamics can alter male experience dependent <b>alcohol</b> preference in a bidirectional manner: expressing either activated <strong>Rac1</strong> or dominant negative cofilin in the mushroom bodies (MBs) abolishes experience dependent <b>alcohol</b> preference.
+RAC1	drug	alcohol	31558618	We show that these two regulators of actin dynamics can alter male experience dependent <b>alcohol</b> preference in a bidirectional manner: expressing either activated <strong><strong>Rac1</strong></strong> or dominant negative cofilin in the mushroom bodies (MBs) abolishes experience dependent <b>alcohol</b> preference.
+RAC1	drug	alcohol	31558618	Conversely, dominant negative <strong>Rac1</strong> or activated cofilin MB expression lead to faster acquisition of <b>alcohol</b> preference.
+RAC1	drug	alcohol	31558618	Conversely, dominant negative <strong><strong>Rac1</strong></strong> or activated cofilin MB expression lead to faster acquisition of <b>alcohol</b> preference.
+RAC1	drug	alcohol	31558618	Our data show that <strong>Rac1</strong> and cofilin activity are key to determining the rate of acquisition of <b>alcohol</b> preference, revealing a critical role of actin dynamics regulation in the development of voluntary self administration in Drosophila SIGNIFICANCE STATEMENT The risks for developing an <b>alcohol</b> use disorder (AUD) are strongly determined by genetic factors.
+RAC1	drug	alcohol	31558618	Our data show that <strong><strong>Rac1</strong></strong> and cofilin activity are key to determining the rate of acquisition of <b>alcohol</b> preference, revealing a critical role of actin dynamics regulation in the development of voluntary self administration in Drosophila SIGNIFICANCE STATEMENT The risks for developing an <b>alcohol</b> use disorder (AUD) are strongly determined by genetic factors.
+RAC1	drug	opioid	31515267	We found that DAMGO, but not <b>morphine</b>, activates Ras related C3 botulinum toxin substrate 1 (<strong>Rac1</strong>).
+RAC1	drug	opioid	31515267	We found that DAMGO, but not <b>morphine</b>, activates Ras related C3 botulinum toxin substrate 1 (<strong><strong>Rac1</strong></strong>).
+RAC1	drug	opioid	31413370	Meanwhile, <b>morphine</b> enhances the inhibitory inputs from somatostatin+ (SST) INs onto PV INs, and thus disinhibits pyramidal neurons via δ <b>opioid</b> receptor (DOR) dependent <strong>Rac1</strong> upregulation in SST INs.
+RAC1	drug	opioid	31413370	Meanwhile, <b>morphine</b> enhances the inhibitory inputs from somatostatin+ (SST) INs onto PV INs, and thus disinhibits pyramidal neurons via δ <b>opioid</b> receptor (DOR) dependent <strong><strong>Rac1</strong></strong> upregulation in SST INs.
+RAC1	drug	opioid	31413370	We show that MOR in PV INs is required for <b>morphine</b> induced behavioral sensitization, while DOR as well as <strong>Rac1</strong> activity in SST INs is required for <b>morphine</b> induced conditioned place preference and hyper locomotion.
+RAC1	addiction	sensitization	31413370	We show that MOR in PV INs is required for morphine induced behavioral <b>sensitization</b>, while DOR as well as <strong>Rac1</strong> activity in SST INs is required for morphine induced conditioned place preference and hyper locomotion.
+RAC1	drug	opioid	31413370	We show that MOR in PV INs is required for <b>morphine</b> induced behavioral sensitization, while DOR as well as <strong><strong>Rac1</strong></strong> activity in SST INs is required for <b>morphine</b> induced conditioned place preference and hyper locomotion.
+RAC1	addiction	sensitization	31413370	We show that MOR in PV INs is required for morphine induced behavioral <b>sensitization</b>, while DOR as well as <strong><strong>Rac1</strong></strong> activity in SST INs is required for morphine induced conditioned place preference and hyper locomotion.
+RAC1	drug	amphetamine	31153969	Four putative targets (Sema3A, Plxna4, <strong>Rac1</strong>, and Pak3) enriched in axon guidance also exhibited significant changes in the NAc after <b>METH</b> challenge injection.
+RAC1	drug	amphetamine	31153969	Four putative targets (Sema3A, Plxna4, <strong><strong>Rac1</strong></strong>, and Pak3) enriched in axon guidance also exhibited significant changes in the NAc after <b>METH</b> challenge injection.
+RAC1	drug	amphetamine	31060803	Dopamine D1 and D2 Receptors Differentially Regulate <strong>Rac1</strong> and Cdc42 Signaling in the Nucleus Accumbens to Modulate Behavioral and Structural Plasticity After Repeated <b>Methamphetamine</b> Treatment.
+RAC1	drug	amphetamine	31060803	Dopamine D1 and D2 Receptors Differentially Regulate <strong><strong>Rac1</strong></strong> and Cdc42 Signaling in the Nucleus Accumbens to Modulate Behavioral and Structural Plasticity After Repeated <b>Methamphetamine</b> Treatment.
+RAC1	drug	amphetamine	31060803	However, how dopamine D1 and D2 receptors (D1Rs and D2Rs, respectively) as well as downstream signaling pathways, such as those involving <strong>Rac1</strong> and Cdc42, modulate <b>METH</b> induced behavioral and structural plasticity is largely unknown.
+RAC1	drug	amphetamine	31060803	However, how dopamine D1 and D2 receptors (D1Rs and D2Rs, respectively) as well as downstream signaling pathways, such as those involving <strong><strong>Rac1</strong></strong> and Cdc42, modulate <b>METH</b> induced behavioral and structural plasticity is largely unknown.
+RAC1	drug	amphetamine	31060803	Using NAc conditional D1R and D2R deletion mice, <strong>Rac1</strong> and Cdc42 mutant viruses, and a series of behavioral and morphological methods, we assessed the effects of D1Rs and D2Rs on <strong>Rac1</strong> and Cdc42 in modulating <b>METH</b> induced behavioral and structural plasticity in the NAc.
+RAC1	drug	amphetamine	31060803	Using NAc conditional D1R and D2R deletion mice, <strong><strong>Rac1</strong></strong> and Cdc42 mutant viruses, and a series of behavioral and morphological methods, we assessed the effects of D1Rs and D2Rs on <strong><strong>Rac1</strong></strong> and Cdc42 in modulating <b>METH</b> induced behavioral and structural plasticity in the NAc.
+RAC1	drug	amphetamine	31060803	Interestingly, <strong>Rac1</strong> and Cdc42 signaling were oppositely modulated by <b>METH</b>, and suppression of <strong>Rac1</strong> signaling and activation of Cdc42 signaling were crucial to <b>METH</b> induced conditioned place preference and structural plasticity but not to locomotor activation.
+RAC1	drug	amphetamine	31060803	Interestingly, <strong><strong>Rac1</strong></strong> and Cdc42 signaling were oppositely modulated by <b>METH</b>, and suppression of <strong><strong>Rac1</strong></strong> signaling and activation of Cdc42 signaling were crucial to <b>METH</b> induced conditioned place preference and structural plasticity but not to locomotor activation.
+RAC1	drug	amphetamine	31060803	D1Rs activated <strong>Rac1</strong> and Cdc42 signaling, while D2Rs inhibited <strong>Rac1</strong> signaling but activated Cdc42 signaling to mediate <b>METH</b> induced conditioned place preference and structural plasticity but not locomotor activation.
+RAC1	drug	amphetamine	31060803	D1Rs activated <strong><strong>Rac1</strong></strong> and Cdc42 signaling, while D2Rs inhibited <strong><strong>Rac1</strong></strong> signaling but activated Cdc42 signaling to mediate <b>METH</b> induced conditioned place preference and structural plasticity but not locomotor activation.
+RAC1	drug	amphetamine	31060803	In addition, NAc D1R deletion aggravated <b>METH</b> withdrawal induced spatial learning and memory impairment by suppressing <strong>Rac1</strong> signaling but not Cdc42 signaling, while NAc D2R deletion aggravated <b>METH</b> withdrawal induced anxiety without affecting <strong>Rac1</strong> or Cdc42 signaling.
+RAC1	addiction	withdrawal	31060803	In addition, NAc D1R deletion aggravated METH <b>withdrawal</b> induced spatial learning and memory impairment by suppressing <strong>Rac1</strong> signaling but not Cdc42 signaling, while NAc D2R deletion aggravated METH <b>withdrawal</b> induced anxiety without affecting <strong>Rac1</strong> or Cdc42 signaling.
+RAC1	drug	amphetamine	31060803	In addition, NAc D1R deletion aggravated <b>METH</b> withdrawal induced spatial learning and memory impairment by suppressing <strong><strong>Rac1</strong></strong> signaling but not Cdc42 signaling, while NAc D2R deletion aggravated <b>METH</b> withdrawal induced anxiety without affecting <strong><strong>Rac1</strong></strong> or Cdc42 signaling.
+RAC1	addiction	withdrawal	31060803	In addition, NAc D1R deletion aggravated METH <b>withdrawal</b> induced spatial learning and memory impairment by suppressing <strong><strong>Rac1</strong></strong> signaling but not Cdc42 signaling, while NAc D2R deletion aggravated METH <b>withdrawal</b> induced anxiety without affecting <strong><strong>Rac1</strong></strong> or Cdc42 signaling.
+RAC1	drug	amphetamine	31060803	D1Rs and D2Rs differentially regulate <strong>Rac1</strong> and Cdc42 signaling to modulate <b>METH</b> induced behavioral plasticity and the structural remodeling of medium spiny neurons in the NAc.
+RAC1	drug	amphetamine	31060803	D1Rs and D2Rs differentially regulate <strong><strong>Rac1</strong></strong> and Cdc42 signaling to modulate <b>METH</b> induced behavioral plasticity and the structural remodeling of medium spiny neurons in the NAc.
+RAC1	drug	cocaine	28726800	<b>Cocaine</b> significantly decreased SAM/SAH ratio levels in the DS, which was accompanied with the decreased activities of <strong>Rac1</strong> and RhoA.
+RAC1	drug	cocaine	28726800	<b>Cocaine</b> significantly decreased SAM/SAH ratio levels in the DS, which was accompanied with the decreased activities of <strong><strong>Rac1</strong></strong> and RhoA.
+RAC1	drug	cocaine	28726800	Lentivirus mediated knockdown of Nnmt in the dorsomedial striatum (DMS) attenuated <b>cocaine</b> conditioned place preference (CPP) reward, but increased striatal SAM/SAH ratio levels as well as <strong>Rac1</strong> and RhoA activities.
+RAC1	addiction	reward	28726800	Lentivirus mediated knockdown of Nnmt in the dorsomedial striatum (DMS) attenuated cocaine conditioned place preference (<b>CPP</b>) <b>reward</b>, but increased striatal SAM/SAH ratio levels as well as <strong>Rac1</strong> and RhoA activities.
+RAC1	drug	cocaine	28726800	Lentivirus mediated knockdown of Nnmt in the dorsomedial striatum (DMS) attenuated <b>cocaine</b> conditioned place preference (CPP) reward, but increased striatal SAM/SAH ratio levels as well as <strong><strong>Rac1</strong></strong> and RhoA activities.
+RAC1	addiction	reward	28726800	Lentivirus mediated knockdown of Nnmt in the dorsomedial striatum (DMS) attenuated cocaine conditioned place preference (<b>CPP</b>) <b>reward</b>, but increased striatal SAM/SAH ratio levels as well as <strong><strong>Rac1</strong></strong> and RhoA activities.
+RAC1	drug	cocaine	28726800	In addition, pharmacological inhibition of NNMT through intra DMS infusion of MeN attenuated <b>cocaine</b> CPP and the activities of <strong>Rac1</strong> and RhoA, but increased SAM/SAH ratio.
+RAC1	addiction	reward	28726800	In addition, pharmacological inhibition of NNMT through intra DMS infusion of MeN attenuated cocaine <b>CPP</b> and the activities of <strong>Rac1</strong> and RhoA, but increased SAM/SAH ratio.
+RAC1	drug	cocaine	28726800	In addition, pharmacological inhibition of NNMT through intra DMS infusion of MeN attenuated <b>cocaine</b> CPP and the activities of <strong><strong>Rac1</strong></strong> and RhoA, but increased SAM/SAH ratio.
+RAC1	addiction	reward	28726800	In addition, pharmacological inhibition of NNMT through intra DMS infusion of MeN attenuated cocaine <b>CPP</b> and the activities of <strong><strong>Rac1</strong></strong> and RhoA, but increased SAM/SAH ratio.
+RAC1	drug	cocaine	28726800	The results showed that <b>cocaine</b> increased the association of RhoGDIα with <strong>Rac1</strong> or RhoA, whereas such effect was inhibited by Nnmt knockdown.
+RAC1	drug	cocaine	28726800	The results showed that <b>cocaine</b> increased the association of RhoGDIα with <strong><strong>Rac1</strong></strong> or RhoA, whereas such effect was inhibited by Nnmt knockdown.
+RAC1	drug	cocaine	28726800	Collectively, our findings show that NNMT regulates <b>cocaine</b> CPP through SAM mediated modification of <strong>Rac1</strong> and RhoA.
+RAC1	addiction	reward	28726800	Collectively, our findings show that NNMT regulates cocaine <b>CPP</b> through SAM mediated modification of <strong>Rac1</strong> and RhoA.
+RAC1	drug	cocaine	28726800	Collectively, our findings show that NNMT regulates <b>cocaine</b> CPP through SAM mediated modification of <strong><strong>Rac1</strong></strong> and RhoA.
+RAC1	addiction	reward	28726800	Collectively, our findings show that NNMT regulates cocaine <b>CPP</b> through SAM mediated modification of <strong><strong>Rac1</strong></strong> and RhoA.
+RAC1	addiction	aversion	28630256	The Small GTPase <strong>Rac1</strong> Contributes to Extinction of <b>Aversive</b> Memories of Drug Withdrawal by Facilitating GABAA Receptor Endocytosis in the vmPFC.
+RAC1	addiction	withdrawal	28630256	The Small GTPase <strong>Rac1</strong> Contributes to Extinction of Aversive Memories of Drug <b>Withdrawal</b> by Facilitating GABAA Receptor Endocytosis in the vmPFC.
+RAC1	addiction	aversion	28630256	The Small GTPase <strong><strong>Rac1</strong></strong> Contributes to Extinction of <b>Aversive</b> Memories of Drug Withdrawal by Facilitating GABAA Receptor Endocytosis in the vmPFC.
+RAC1	addiction	withdrawal	28630256	The Small GTPase <strong><strong>Rac1</strong></strong> Contributes to Extinction of Aversive Memories of Drug <b>Withdrawal</b> by Facilitating GABAA Receptor Endocytosis in the vmPFC.
+RAC1	drug	opioid	28630256	Here, we report that extinction of conditioned place aversion (CPA) to <b>naloxone</b> precipitated opiate withdrawal in male rats activates Rho GTPase <strong>Rac1</strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RAC1	addiction	aversion	28630256	Here, we report that extinction of conditioned place <b>aversion</b> (CPA) to naloxone precipitated opiate withdrawal in male rats activates Rho GTPase <strong>Rac1</strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RAC1	addiction	withdrawal	28630256	Here, we report that extinction of conditioned place aversion (CPA) to naloxone precipitated opiate <b>withdrawal</b> in male rats activates Rho GTPase <strong>Rac1</strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RAC1	drug	opioid	28630256	Here, we report that extinction of conditioned place aversion (CPA) to <b>naloxone</b> precipitated opiate withdrawal in male rats activates Rho GTPase <strong><strong>Rac1</strong></strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RAC1	addiction	aversion	28630256	Here, we report that extinction of conditioned place <b>aversion</b> (CPA) to naloxone precipitated opiate withdrawal in male rats activates Rho GTPase <strong><strong>Rac1</strong></strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RAC1	addiction	withdrawal	28630256	Here, we report that extinction of conditioned place aversion (CPA) to naloxone precipitated opiate <b>withdrawal</b> in male rats activates Rho GTPase <strong><strong>Rac1</strong></strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RAC1	addiction	aversion	28630256	Thus, the present study provides first evidence that <strong>Rac1</strong> dependent GABAAR endocytosis plays a crucial role in extinction of <b>aversive</b> memories and reveals the sequence of molecular events that contribute to learning experience modulation of synaptic GABAAR endocytosis.SIGNIFICANCE STATEMENT This study reveals that <strong>Rac1</strong> dependent GABAAR endocytosis plays a crucial role in extinction of <b>aversive</b> memories associated with drug withdrawal and identifies Arc as a downstream effector of <strong>Rac1</strong> regulations of synaptic plasticity as well as learning and memory, thereby suggesting therapeutic targets to promote extinction of the unwanted memories.
+RAC1	addiction	withdrawal	28630256	Thus, the present study provides first evidence that <strong>Rac1</strong> dependent GABAAR endocytosis plays a crucial role in extinction of aversive memories and reveals the sequence of molecular events that contribute to learning experience modulation of synaptic GABAAR endocytosis.SIGNIFICANCE STATEMENT This study reveals that <strong>Rac1</strong> dependent GABAAR endocytosis plays a crucial role in extinction of aversive memories associated with drug <b>withdrawal</b> and identifies Arc as a downstream effector of <strong>Rac1</strong> regulations of synaptic plasticity as well as learning and memory, thereby suggesting therapeutic targets to promote extinction of the unwanted memories.
+RAC1	addiction	aversion	28630256	Thus, the present study provides first evidence that <strong><strong>Rac1</strong></strong> dependent GABAAR endocytosis plays a crucial role in extinction of <b>aversive</b> memories and reveals the sequence of molecular events that contribute to learning experience modulation of synaptic GABAAR endocytosis.SIGNIFICANCE STATEMENT This study reveals that <strong><strong>Rac1</strong></strong> dependent GABAAR endocytosis plays a crucial role in extinction of <b>aversive</b> memories associated with drug withdrawal and identifies Arc as a downstream effector of <strong><strong>Rac1</strong></strong> regulations of synaptic plasticity as well as learning and memory, thereby suggesting therapeutic targets to promote extinction of the unwanted memories.
+RAC1	addiction	withdrawal	28630256	Thus, the present study provides first evidence that <strong><strong>Rac1</strong></strong> dependent GABAAR endocytosis plays a crucial role in extinction of aversive memories and reveals the sequence of molecular events that contribute to learning experience modulation of synaptic GABAAR endocytosis.SIGNIFICANCE STATEMENT This study reveals that <strong><strong>Rac1</strong></strong> dependent GABAAR endocytosis plays a crucial role in extinction of aversive memories associated with drug <b>withdrawal</b> and identifies Arc as a downstream effector of <strong><strong>Rac1</strong></strong> regulations of synaptic plasticity as well as learning and memory, thereby suggesting therapeutic targets to promote extinction of the unwanted memories.
+RAC1	drug	alcohol	26366560	Previously, we described that regulators of actin dynamics, such as the Rho family GTPases <strong>Rac1</strong>, Rho1, and Cdc42, alter Drosophila's sensitivity to <b>ethanol</b> induced sedation.
+RAC1	drug	alcohol	26366560	Previously, we described that regulators of actin dynamics, such as the Rho family GTPases <strong><strong>Rac1</strong></strong>, Rho1, and Cdc42, alter Drosophila's sensitivity to <b>ethanol</b> induced sedation.
+RAC1	drug	alcohol	26170296	Together, these data suggest a conserved role for integrin/Rsu1/<strong>Rac1</strong>/actin signaling in modulating reward related phenotypes, including <b>ethanol</b> consumption, across phyla.
+RAC1	addiction	reward	26170296	Together, these data suggest a conserved role for integrin/Rsu1/<strong>Rac1</strong>/actin signaling in modulating <b>reward</b> related phenotypes, including ethanol consumption, across phyla.
+RAC1	drug	alcohol	26170296	Together, these data suggest a conserved role for integrin/Rsu1/<strong><strong>Rac1</strong></strong>/actin signaling in modulating reward related phenotypes, including <b>ethanol</b> consumption, across phyla.
+RAC1	addiction	reward	26170296	Together, these data suggest a conserved role for integrin/Rsu1/<strong><strong>Rac1</strong></strong>/actin signaling in modulating <b>reward</b> related phenotypes, including ethanol consumption, across phyla.
+RAC1	drug	cocaine	25957559	Dishevelled 2 regulates <b>cocaine</b> induced structural plasticity and <strong>Rac1</strong> activity in the nucleus accumbens.
+RAC1	drug	cocaine	25957559	Dishevelled 2 regulates <b>cocaine</b> induced structural plasticity and <strong><strong>Rac1</strong></strong> activity in the nucleus accumbens.
+RAC1	drug	cocaine	25957559	In this study we examined whether isoforms of Dishevelled, a key hub protein of multiple branches of Wnt signaling, including <strong>Rac1</strong>, are regulated in the NAc by chronic <b>cocaine</b>, and whether these Dishevelled isoforms control <strong>Rac1</strong> activity in this brain region in vivo.
+RAC1	drug	cocaine	25957559	In this study we examined whether isoforms of Dishevelled, a key hub protein of multiple branches of Wnt signaling, including <strong><strong>Rac1</strong></strong>, are regulated in the NAc by chronic <b>cocaine</b>, and whether these Dishevelled isoforms control <strong><strong>Rac1</strong></strong> activity in this brain region in vivo.
+RAC1	drug	cocaine	25957559	We found that chronic <b>cocaine</b> administration decreased expression of Dishevelled 2, and several other Wnt signaling components, in the NAc, and that overexpression of Dishevelled 2, but not Dishevelled 1, conversely upregulated <strong>Rac1</strong> activity and prevented the <b>cocaine</b> induction of dendritic spines on NAc MSNs.
+RAC1	drug	cocaine	25957559	We found that chronic <b>cocaine</b> administration decreased expression of Dishevelled 2, and several other Wnt signaling components, in the NAc, and that overexpression of Dishevelled 2, but not Dishevelled 1, conversely upregulated <strong><strong>Rac1</strong></strong> activity and prevented the <b>cocaine</b> induction of dendritic spines on NAc MSNs.
+RAC1	drug	cocaine	25957559	We posit that the <b>cocaine</b> induced downregulation of Dishevelled 2 in the NAc is an upstream regulator of <strong>Rac1</strong> activity and plays an important role in the dynamic structural plasticity of NAc MSNs seen in response to chronic <b>cocaine</b> exposure.
+RAC1	drug	cocaine	25957559	We posit that the <b>cocaine</b> induced downregulation of Dishevelled 2 in the NAc is an upstream regulator of <strong><strong>Rac1</strong></strong> activity and plays an important role in the dynamic structural plasticity of NAc MSNs seen in response to chronic <b>cocaine</b> exposure.
+RAC1	drug	cocaine	25595128	<b>Cocaine</b> activates <strong>Rac1</strong> to control structural and behavioral plasticity in caudate putamen.
+RAC1	drug	cocaine	25595128	<b>Cocaine</b> activates <strong><strong>Rac1</strong></strong> to control structural and behavioral plasticity in caudate putamen.
+RAC1	drug	cocaine	25595128	In this study, we investigated the role of <strong>Rac1</strong> in <b>cocaine</b> induced dendritic and behavioral plasticity in the CPu.
+RAC1	drug	cocaine	25595128	In this study, we investigated the role of <strong><strong>Rac1</strong></strong> in <b>cocaine</b> induced dendritic and behavioral plasticity in the CPu.
+RAC1	drug	cocaine	25595128	We found that <strong>Rac1</strong> activation was reduced in the NAc but increased in the CPu following repeated <b>cocaine</b> treatment.
+RAC1	drug	cocaine	25595128	We found that <strong><strong>Rac1</strong></strong> activation was reduced in the NAc but increased in the CPu following repeated <b>cocaine</b> treatment.
+RAC1	drug	cocaine	25595128	Inhibition of <strong>Rac1</strong> activity by a <strong>Rac1</strong> specific inhibitor NSC23766, overexpression of a dominant negative mutant of <strong>Rac1</strong> (T17N <strong>Rac1</strong>) or local knockout of <strong>Rac1</strong> attenuated the <b>cocaine</b> induced increase in dendrites and spine density in the CPu, whereas overexpression of a constitutively active <strong>Rac1</strong> exert the opposite effect.
+RAC1	drug	cocaine	25595128	Inhibition of <strong><strong>Rac1</strong></strong> activity by a <strong><strong>Rac1</strong></strong> specific inhibitor NSC23766, overexpression of a dominant negative mutant of <strong><strong>Rac1</strong></strong> (T17N <strong><strong>Rac1</strong></strong>) or local knockout of <strong><strong>Rac1</strong></strong> attenuated the <b>cocaine</b> induced increase in dendrites and spine density in the CPu, whereas overexpression of a constitutively active <strong><strong>Rac1</strong></strong> exert the opposite effect.
+RAC1	drug	cocaine	25595128	Downregulation of <strong>Rac1</strong> activity likewise attenuates behavioral reward responses to <b>cocaine</b> exposure, with activation of <strong>Rac1</strong> producing the opposite effect.
+RAC1	addiction	reward	25595128	Downregulation of <strong>Rac1</strong> activity likewise attenuates behavioral <b>reward</b> responses to cocaine exposure, with activation of <strong>Rac1</strong> producing the opposite effect.
+RAC1	drug	cocaine	25595128	Downregulation of <strong><strong>Rac1</strong></strong> activity likewise attenuates behavioral reward responses to <b>cocaine</b> exposure, with activation of <strong><strong>Rac1</strong></strong> producing the opposite effect.
+RAC1	addiction	reward	25595128	Downregulation of <strong><strong>Rac1</strong></strong> activity likewise attenuates behavioral <b>reward</b> responses to cocaine exposure, with activation of <strong><strong>Rac1</strong></strong> producing the opposite effect.
+RAC1	drug	cocaine	25595128	Thus, <strong>Rac1</strong> signaling is differentially regulated in the NAc and CPu after repeated <b>cocaine</b> treatment, and induction of <strong>Rac1</strong> activation in the CPu is important for <b>cocaine</b> exposure induced dendritic remodeling and behavioral plasticity.
+RAC1	drug	cocaine	25595128	Thus, <strong><strong>Rac1</strong></strong> signaling is differentially regulated in the NAc and CPu after repeated <b>cocaine</b> treatment, and induction of <strong><strong>Rac1</strong></strong> activation in the CPu is important for <b>cocaine</b> exposure induced dendritic remodeling and behavioral plasticity.
+RAC1	drug	alcohol	25257290	<b>Alcohol</b> rapidly decreased GTP bound <strong>Rac1</strong> but not RhoA during the drop in TER.
+RAC1	drug	alcohol	25257290	<b>Alcohol</b> rapidly decreased GTP bound <strong><strong>Rac1</strong></strong> but not RhoA during the drop in TER.
+RAC1	drug	cocaine	23825406	On withdrawal day 14, we found that Kal 7 levels and activation of its downstream effectors <strong>Rac 1</strong> and PAK were increased in the NAc of <b>cocaine</b> sensitized rats.
+RAC1	addiction	withdrawal	23825406	On <b>withdrawal</b> day 14, we found that Kal 7 levels and activation of its downstream effectors <strong>Rac 1</strong> and PAK were increased in the NAc of cocaine sensitized rats.
+RAC1	drug	cocaine	23628212	These studies confirmed the classical hypothesis of movement control and reward seeking behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in <b>cocaine</b> reward; dissected the roles of glutamatergic and dopaminergic inputs to striatum in reward; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in reward and the rho GTPase <strong>Rac1</strong> in <b>cocaine</b> reward and <b>cocaine</b> induced structural plasticity.
+RAC1	addiction	relapse	23628212	These studies confirmed the classical hypothesis of movement control and reward <b>seeking</b> behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in cocaine reward; dissected the roles of glutamatergic and dopaminergic inputs to striatum in reward; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in reward and the rho GTPase <strong>Rac1</strong> in cocaine reward and cocaine induced structural plasticity.
+RAC1	addiction	reward	23628212	These studies confirmed the classical hypothesis of movement control and <b>reward</b> seeking behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in cocaine <b>reward</b>; dissected the roles of glutamatergic and dopaminergic inputs to striatum in <b>reward</b>; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in <b>reward</b> and the rho GTPase <strong>Rac1</strong> in cocaine <b>reward</b> and cocaine induced structural plasticity.
+RAC1	drug	cocaine	23628212	These studies confirmed the classical hypothesis of movement control and reward seeking behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in <b>cocaine</b> reward; dissected the roles of glutamatergic and dopaminergic inputs to striatum in reward; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in reward and the rho GTPase <strong><strong>Rac1</strong></strong> in <b>cocaine</b> reward and <b>cocaine</b> induced structural plasticity.
+RAC1	addiction	relapse	23628212	These studies confirmed the classical hypothesis of movement control and reward <b>seeking</b> behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in cocaine reward; dissected the roles of glutamatergic and dopaminergic inputs to striatum in reward; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in reward and the rho GTPase <strong><strong>Rac1</strong></strong> in cocaine reward and cocaine induced structural plasticity.
+RAC1	addiction	reward	23628212	These studies confirmed the classical hypothesis of movement control and <b>reward</b> seeking behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in cocaine <b>reward</b>; dissected the roles of glutamatergic and dopaminergic inputs to striatum in <b>reward</b>; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in <b>reward</b> and the rho GTPase <strong><strong>Rac1</strong></strong> in cocaine <b>reward</b> and cocaine induced structural plasticity.
+RAC1	addiction	aversion	23564082	The small GTPase RhoA, but not <strong>Rac1</strong>, is essential for conditioned <b>aversive</b> memory formation through regulation of actin rearrangements in rat dorsal hippocampus.
+RAC1	addiction	aversion	23564082	The small GTPase RhoA, but not <strong><strong>Rac1</strong></strong>, is essential for conditioned <b>aversive</b> memory formation through regulation of actin rearrangements in rat dorsal hippocampus.
+RAC1	drug	alcohol	23223291	Adult neuronal Arf6 controls <b>ethanol</b> induced behavior with Arfaptin downstream of <strong>Rac1</strong> and RhoGAP18B.
+RAC1	drug	alcohol	23223291	Adult neuronal Arf6 controls <b>ethanol</b> induced behavior with Arfaptin downstream of <strong><strong>Rac1</strong></strong> and RhoGAP18B.
+RAC1	drug	alcohol	23223291	We also find that the Drosophila Arfaptin protein directly binds to the activated forms of Arf6 and <strong>Rac1</strong> GTPases, and mutants in Arfaptin also display <b>ethanol</b> sensitivity.
+RAC1	drug	alcohol	23223291	We also find that the Drosophila Arfaptin protein directly binds to the activated forms of Arf6 and <strong><strong>Rac1</strong></strong> GTPases, and mutants in Arfaptin also display <b>ethanol</b> sensitivity.
+RAC1	drug	alcohol	23223291	Arf6 acts downstream of <strong>Rac1</strong> and Arfaptin to regulate <b>ethanol</b> induced behaviors, and we thus demonstrate that this conserved <strong>Rac1</strong>/Arfaptin/Arf6 pathway is a major mediator of <b>ethanol</b> induced behavioral responses.
+RAC1	drug	alcohol	23223291	Arf6 acts downstream of <strong><strong>Rac1</strong></strong> and Arfaptin to regulate <b>ethanol</b> induced behaviors, and we thus demonstrate that this conserved <strong><strong>Rac1</strong></strong>/Arfaptin/Arf6 pathway is a major mediator of <b>ethanol</b> induced behavioral responses.
+RAC1	drug	cocaine	18952886	<b>Cocaine</b> induced reactive oxygen species (ROS) production was associated with significant increases (approximately 2 fold) in the protein expressions of Nox2 (an isoform of NADPH oxidase) and its regulatory subunits: p22(phox), p67(phox), p47(phox), p40(phox), and <strong>Rac1</strong>, and in p47(phox) phosphorylation as detected by immunoblotting (all p < 0.03).
+RAC1	drug	cocaine	18952886	<b>Cocaine</b> induced reactive oxygen species (ROS) production was associated with significant increases (approximately 2 fold) in the protein expressions of Nox2 (an isoform of NADPH oxidase) and its regulatory subunits: p22(phox), p67(phox), p47(phox), p40(phox), and <strong><strong>Rac1</strong></strong>, and in p47(phox) phosphorylation as detected by immunoblotting (all p < 0.03).
+RAC1	drug	alcohol	17018286	Indeed, expression of constitutively active forms of Rho1 or <strong>Rac1</strong> in adult flies results in <b>ethanol</b> resistance similar to that observed in whir mutants.
+RAC1	drug	alcohol	17018286	Indeed, expression of constitutively active forms of Rho1 or <strong><strong>Rac1</strong></strong> in adult flies results in <b>ethanol</b> resistance similar to that observed in whir mutants.
+RAC1	drug	opioid	16472257	Somatostatin acting via G(i)1 coupled sstr3 receptor, DPDPE ([D Pen2,D Pen5]enkephalin; where Pen is penicillamine) acting via G(i)2 coupled delta <b>opioid</b> receptors, and cyclopentyl adenosine acting via G(i)3 coupled adenosine A1 receptors preferentially activated PI3K (phosphoinositide 3 kinase) and ILK (integrin linked kinase), whereas ACh (acetylcholine) acting via G(i)3 coupled M2 receptors preferentially activated PI3K, Cdc42 (cell division cycle 42)/<strong>Rac1</strong>, PAK1 (p21 activated kinase 1) and p38 MAPK (mitogen activated protein kinase).
+RAC1	drug	opioid	16472257	Somatostatin acting via G(i)1 coupled sstr3 receptor, DPDPE ([D Pen2,D Pen5]enkephalin; where Pen is penicillamine) acting via G(i)2 coupled delta <b>opioid</b> receptors, and cyclopentyl adenosine acting via G(i)3 coupled adenosine A1 receptors preferentially activated PI3K (phosphoinositide 3 kinase) and ILK (integrin linked kinase), whereas ACh (acetylcholine) acting via G(i)3 coupled M2 receptors preferentially activated PI3K, Cdc42 (cell division cycle 42)/<strong><strong>Rac1</strong></strong>, PAK1 (p21 activated kinase 1) and p38 MAPK (mitogen activated protein kinase).
+RAC1	addiction	withdrawal	15785859	In contrast, that of <strong>Rac1</strong> did not change after the <b>withdrawal</b>.
+RAC1	addiction	withdrawal	15785859	In contrast, that of <strong><strong>Rac1</strong></strong> did not change after the <b>withdrawal</b>.
+NOS3	drug	opioid	31873938	This action increases shear stress (friction) to vascular endothelium that stimulates endothelial nitric oxide synthase (<strong>eNOS</strong>) to increase NO that decreases oxidative stress and inflammation, and, slows accelerated vascular ageing associated with <b>opioids</b>.
+NOS3	drug	opioid	31873938	These pharmacotherapy aids to withdrawal and tapering <b>opioid</b> dosagadrenoceptor agonists that act through <strong>eNOS</strong> to inhibit norepinephrine.
+NOS3	addiction	withdrawal	31873938	These pharmacotherapy aids to <b>withdrawal</b> and tapering opioid dosagadrenoceptor agonists that act through <strong>eNOS</strong> to inhibit norepinephrine.
+NOS3	drug	alcohol	29363778	Immunoblotting indicated that <b>alcohol</b> decreased the level of endothelial excitatory P Ser1177 endothelial NO synthase (<strong>eNOS</strong>) (p < 0.05) and total <strong>eNOS</strong> expression (p < 0.05) compared to both the normal and pair fed controls.
+NOS3	drug	alcohol	29363778	This is the first study to demonstrate maternal binge <b>alcohol</b> consumption during pregnancy disrupts uterine artery vascular function via impairment of the <strong>eNOS</strong> vasodilatory system.
+NOS3	addiction	intoxication	29363778	This is the first study to demonstrate maternal <b>binge</b> alcohol consumption during pregnancy disrupts uterine artery vascular function via impairment of the <strong>eNOS</strong> vasodilatory system.
+NOS3	drug	nicotine	29050484	<strong>eNOS</strong> and XRCC4 VNTR variants contribute to formation of <b>nicotine</b> dependence and/or schizophrenia.
+NOS3	addiction	dependence	29050484	<strong>eNOS</strong> and XRCC4 VNTR variants contribute to formation of nicotine <b>dependence</b> and/or schizophrenia.
+NOS3	drug	nicotine	29050484	This study aimed to evaluate whether VNTR variants in the Endothelial Nitric Oxide Synthase (<strong>eNOS</strong>) and the XRCC4 gene play any role in <b>nicotine</b> dependence (ND) and/or Schizophrenia+ND (Sch+ND) ethiopathogenesis.
+NOS3	addiction	dependence	29050484	This study aimed to evaluate whether VNTR variants in the Endothelial Nitric Oxide Synthase (<strong>eNOS</strong>) and the XRCC4 gene play any role in nicotine <b>dependence</b> (ND) and/or Schizophrenia+ND (Sch+ND) ethiopathogenesis.
+NOS3	drug	alcohol	27207918	Additional associations between normalized gray matter volume and other candidate genes such as <b>alcohol</b> dehydrogenase gene cluster (ADH), GCLC, <strong>NOS3</strong>, and SYT1 were observed across the entire sample but did not survive corrections for multiple comparisons.
+NOS3	drug	alcohol	26555891	Moreover, caffeine protection against <b>alcohol</b> increased nitric oxide (NO•) levels over those found in the presence of <b>ethanol</b> alone, disappeared upon blocking NO• synthase, and could not be detected in pressurized cerebral arteries from endothelial nitric oxide synthase knockout (<strong>eNOS</strong>( / )) mice.
+NOS3	drug	nicotine	25262772	Cigarette <b>smoking</b> had been recorded as the main cause of impaired endothelium  dependent vasodilation in <b>smokers</b> by reducing nitric oxide (NO), a production of endothelial nitric oxide synthase (<strong>eNOS</strong>).
+NOS3	drug	nicotine	25262772	In this study, cell passage is suggested to be a relevant factor to <strong>eNOS</strong> expression under cigarette <b>smoking</b> stress.
+NOS3	drug	nicotine	25262772	After exposure of cigarette <b>smoking</b> extract (CSE) solution, MTT assay and Western blot method were performed to check the cell viability as well as <strong>eNOS</strong> protein concentration.
+NOS3	drug	alcohol	24300283	We herein investigated chronic in vitro binge like <b>alcohol</b> effects on umbilical endothelial nitric oxide synthase (<strong>eNOS</strong>) multi site phosphorylation and related redox switches under basal (unstimulated) and stimulated (with ATP) states.
+NOS3	addiction	intoxication	24300283	We herein investigated chronic in vitro <b>binge</b> like alcohol effects on umbilical endothelial nitric oxide synthase (<strong>eNOS</strong>) multi site phosphorylation and related redox switches under basal (unstimulated) and stimulated (with ATP) states.
+NOS3	drug	alcohol	24300283	<b>Alcohol</b> decreased endothelial excitatory (Pser1177)<strong>eNOS</strong> (P<0.001), whereas excitatory (Pser635)<strong>eNOS</strong> exhibited a main effect of <b>alcohol</b> (↓P=0.016) and ATP (↑P<0.001).
+NOS3	drug	alcohol	24300283	<b>Alcohol</b> decreased (Pthr495)<strong>eNOS</strong> (P=0.004) levels, whereas inhibitory (Pser116)<strong>eNOS</strong> exhibited an <b>alcohol</b> main effect in both basal and stimulated states (↑P=0.005).
+NOS3	drug	alcohol	24300283	Total <strong>eNOS</strong> was reduced by <b>alcohol</b> (P=0.038).
+NOS3	drug	alcohol	24300283	Thus, <b>alcohol</b> effects on multi site post translational modifications and redox switches related to vasodilatory <strong>eNOS</strong> underscore the necessity for investigating <b>alcohol</b> induced gestational vascular dysfunction.
+NOS3	drug	alcohol	21599719	In this study, we hypothesized that in vitro chronic binge like <b>alcohol</b> will decrease uterine arterial endothelial <strong>eNOS</strong> expression and alter its multisite phosphorylation activity state via disruption of AKT signaling.
+NOS3	addiction	intoxication	21599719	In this study, we hypothesized that in vitro chronic <b>binge</b> like alcohol will decrease uterine arterial endothelial <strong>eNOS</strong> expression and alter its multisite phosphorylation activity state via disruption of AKT signaling.
+NOS3	drug	alcohol	21599719	LD and HD binge like <b>alcohol</b> decreased uterine arterial <strong>eNOS</strong> expression (p = 0.009).
+NOS3	addiction	intoxication	21599719	LD and HD <b>binge</b> like alcohol decreased uterine arterial <strong>eNOS</strong> expression (p = 0.009).
+NOS3	drug	alcohol	21599719	<strong>eNOS</strong> multisite phosphorylation activation state was altered: P(635) <strong>eNOS</strong> was decreased (p = 0.017), P(1177) <strong>eNOS</strong> was not altered, and P(495) <strong>eNOS</strong> exhibited an inverse U shaped dose dependent relationship with <b>alcohol</b>.
+NOS3	drug	alcohol	21599719	LD and HD <b>alcohol</b> decreased the major <strong>eNOS</strong> associated protein cav 1 (p < 0.001).
+NOS3	drug	alcohol	21599719	Altered <strong>eNOS</strong> multisite phosphorylation also suggests that <b>alcohol</b> produces specific effects at the level of posttranslational modifications critical for pregnancy induced uterine vascular adaptations.
+NOS3	drug	nicotine	21092740	Estrogen dependence of the renal vasodilatory effect of <b>nicotine</b> in rats: role of α7 nicotinic cholinergic receptor/<strong>eNOS</strong> signaling.
+NOS3	addiction	dependence	21092740	Estrogen <b>dependence</b> of the renal vasodilatory effect of nicotine in rats: role of α7 nicotinic cholinergic receptor/<strong>eNOS</strong> signaling.
+NOS3	drug	nicotine	21092740	We recently reported that acute exposure to <b>nicotine</b> vasodilates the renal vasculature of male rats via facilitation of endothelial nitric oxide synthase (<strong>eNOS</strong>).
+NOS3	drug	psychedelics	17521446	Intrathecal administration of CPP and <b>ketamine</b> reduced nNOS expression in monoarthritic rats but increased the expression of iNOS and <strong>eNOS</strong>.
+NOS3	addiction	reward	17521446	Intrathecal administration of <b>CPP</b> and ketamine reduced nNOS expression in monoarthritic rats but increased the expression of iNOS and <strong>eNOS</strong>.
+NOS3	drug	cocaine	17420087	<b>Cocaine</b> treated rats had significantly decreased <strong>eNOS</strong> expression and NO production.
+NOS3	drug	opioid	11354793	Intrathecal injection of <strong>eNOS</strong> antisense oligonucleotides inhibited the expression of NMDA1AR mRNA in the spinal cord of <b>morphine</b> withdrawal rats, but did not in the brainstem.
+NOS3	addiction	withdrawal	11354793	Intrathecal injection of <strong>eNOS</strong> antisense oligonucleotides inhibited the expression of NMDA1AR mRNA in the spinal cord of morphine <b>withdrawal</b> rats, but did not in the brainstem.
+NMS	drug	cannabinoid	31129719	<b>Nabilone</b> for non motor symptoms of Parkinson's disease: a randomized placebo controlled, double blind, parallel group, enriched enrolment randomized withdrawal study (The <strong>NMS</strong> Nab Study).
+NMS	addiction	withdrawal	31129719	Nabilone for non motor symptoms of Parkinson's disease: a randomized placebo controlled, double blind, parallel group, enriched enrolment randomized <b>withdrawal</b> study (The <strong>NMS</strong> Nab Study).
+NMS	drug	cannabinoid	31129719	Although open label observations report a positive effect of <b>cannabinoids</b> on non motor symptoms (<strong>NMS</strong>) in Parkinson's disease (PD) patients, these effects remain to be investigated in a controlled trial for a broader use in <strong>NMS</strong> in PD patients.
+NMS	drug	cannabinoid	31129719	Therefore, we decided to design a proof of concept study to assess the synthetic <b>cannabinoid</b> <b>nabilone</b> for the treatment of <strong>NMS</strong>.
+NMS	drug	cannabinoid	31129719	We hypothesize that <b>nabilone</b> will improve <strong>NMS</strong> in patients with PD and have a favorable safety profile.
+NMS	addiction	withdrawal	31129719	The <strong>NMS</strong> Nab Study is as a mono centric phase II, randomized, placebo controlled, double blind, parallel group, enriched enrollment <b>withdrawal</b> study.
+NMS	addiction	relapse	30946882	Next, rats were tested in delayed match to sample (DMS) and (non)match to sample (<strong>NMS</strong>) tasks, and finally in a single context + cue <b>relapse</b> test on day 90 of abstinence.
+NMS	drug	psychedelics	30698723	The GC MS method was used for the reanalysis of 12 blood samples (eight cases) where 25I <b>NBOMe</b>, 25C <b>NBOMe</b>, methoxetamine and methylone had previously been detected by <strong>NMS</strong> laboratories.
+NMS	drug	cocaine	30634141	The purpose of this work was to quantify <b>cocaine</b> and cutting agents in 116 illicit samples from <strong>NMS</strong> Labs, Willow Grove, PA, U.S. Gas chromatography   mass spectrometry (GC MS) and handle portable gas chromatography toroidal ion trap mass spectrometry (GC TMS) were used as screening methods A liquid chromatography tandem mass spectrometry (LC MS/MS) method was developed and validated for the quantification of <b>cocaine</b>, levamisole, benzocaine, phenacetin, hydroxyzine, theophylline, diltiazem, acetaminophen and caffeine.
+NMS	drug	cocaine	28660166	We herein report a case of a 54 year old trauma patient with <strong>NMS</strong> precipitated by a combination of <b>cocaine</b> withdrawal and neuroleptic medications.
+NMS	addiction	withdrawal	28660166	We herein report a case of a 54 year old trauma patient with <strong>NMS</strong> precipitated by a combination of cocaine <b>withdrawal</b> and neuroleptic medications.
+NMS	addiction	dependence	27130114	The <b>dependence</b> of the degree of <strong>NMs</strong> sorption on the average degree of polymer network crosslinking and pore diameters was investigated.
+NMS	drug	cannabinoid	26539755	In this study, we seek to evaluate potential morphological changes in neurons of the frontal cortex (FCx) and nucleus accumbens (NAcc), in the expression of receptors and enzymes of the <b>endocannabinoid</b> and dopamine systems and in second messengers, such as Akt, in adult rats subjected to MS and early stress (MS + ES; 2 × 180 min daily) vs. nonseparated rats (<strong>NMS</strong>).
+NMS	drug	psychedelics	26378143	On the basis of the case history, the hospital blood and urine were sent to <strong>NMS</strong> Labs for <b>NBOMe</b> and psilocin confirmation.
+NMS	drug	alcohol	22230486	Treatment with a 70% <b>ethanol</b> extract of S. chinensis (0.3g/kg and 1.5g/kg/day) for 7 days resulted in an increase in the pain threshold (<strong>NMS</strong> control: 19.1±1.0mmHg vs low dose: 24.8±1.3mmHg and high dose: 25.2±1.8mmHg, p<0.01), and abolished the elevated AWR and EMG responses to CRD in <strong>NMS</strong> rats (AUC values of EMG response curve were: 1952±202 in <strong>NMS</strong> control group vs 1074±90 in low dose group and 1145±92 in high dose group, p<0.001), indicating that S. chinensis could reverse the visceral hypersensitivity induced by early life stress event.
+NMS	drug	benzodiazepine	20581793	CPK was markedly elevated despite the absence of neuroleptic malignant syndrome (<strong>NMS</strong>) and responded to <b>lorazepam</b>, as did the catatonia.
+NMS	drug	benzodiazepine	20581793	This appears to be the first case report of catatonia without <strong>NMS</strong> associated with each of the following: neurosyphilis, aripiprazole, and <b>temazepam</b> withdrawal.
+NMS	addiction	withdrawal	20581793	This appears to be the first case report of catatonia without <strong>NMS</strong> associated with each of the following: neurosyphilis, aripiprazole, and temazepam <b>withdrawal</b>.
+NMS	drug	opioid	16294079	The experimental group (<strong>NMS</strong>) received nebulized <b>morphine</b> every 4 hours and normal saline by PCA.
+NMS	drug	opioid	16294079	The mean 4 hour dose of <b>morphine</b> was 11.96 +/  3.4 mg for <strong>NMS</strong> and 6.22 +/  4.7 mg for PCA (p < 0.001).
+NMS	drug	cocaine	9972840	The preferential effects of <b>cocaine</b> on muscarinic and D2 like receptors were also demonstrated in vitro where decreases in [3H] <strong>NMS</strong> and [3H] spiroperidol binding were observed.
+NMS	drug	opioid	17589122	We report four cases of <strong>NMS</strong>; one following levodopa/bromocriptine withdrawal, two related to neuroleptic administration and one following <b>heroin</b> use.
+NMS	addiction	withdrawal	17589122	We report four cases of <strong>NMS</strong>; one following levodopa/bromocriptine <b>withdrawal</b>, two related to neuroleptic administration and one following heroin use.
+NMS	drug	opioid	17589122	There are no previous reports linking <b>heroin</b> to <strong>NMS</strong>.
+NMS	drug	cocaine	3055940	A mechanism for rapid death in <b>cocaine</b> abusers is proposed based on the neuroleptic malignant syndrome (<strong>NMS</strong>).
+NMS	drug	cocaine	3055940	The mechanism involves decreased postsynaptic availability of dopamine either through direct receptor blockade, as postulated in classical <strong>NMS</strong>, or through relative dopamine depletion, as postulated in <b>cocaine</b> withdrawal.
+NMS	addiction	withdrawal	3055940	The mechanism involves decreased postsynaptic availability of dopamine either through direct receptor blockade, as postulated in classical <strong>NMS</strong>, or through relative dopamine depletion, as postulated in cocaine <b>withdrawal</b>.
+NMS	drug	cocaine	3055940	The hallmark symptoms of <strong>NMS</strong> include hyperpyrexia and muscular rigidity, but the <b>cocaine</b> associated syndrome is atypical in having minimal rigidity.
+NDUFS3	drug	nicotine	24042971	Men are more likely to use manufactured cigarettes (31.8% [95% <strong>CI 30</strong>.6 33.1]) than shisha (6.2% [95% CI 5.6 6.9]) or smokeless <b>tobacco</b> (4.1% [95% CI 3.4 4.8]).
+NDUFS3	drug	nicotine	23850306	The crude population attributable risk percentage (PAR%) due to higher pocket money (≥200 RMB/month) for current <b>smoking</b> was 50.4% (95% CI 42.2 57.4), and adjusted PAR% was 43.3% (95% <strong>CI 30</strong>.7 53.1).
+NDUFS3	drug	alcohol	20561675	In the first 3000 cases (n=2337, 78%, with ischaemic stroke; n=663, 22%, with intracerebral haemorrhagic stroke) and 3000 controls, significant risk factors for all stroke were: history of hypertension (OR 2.64, 99% CI 2.26 3.08; PAR 34.6%, 99% <strong>CI 30</strong>.4 39.1); current smoking (2.09, 1.75 2.51; 18.9%, 15.3 23.1); waist to hip ratio (1.65, 1.36 1.99 for highest vs lowest tertile; 26.5%, 18.8 36.0); diet risk score (1.35, 1.11 1.64 for highest vs lowest tertile; 18.8%, 11.2 29.7); regular physical activity (0.69, 0.53 0.90; 28.5%, 14.5 48.5); diabetes mellitus (1.36, 1.10 1.68; 5.0%, 2.6 9.5); <b>alcohol</b> intake (1.51, 1.18 1.92 for more than 30 drinks per month or binge drinking; 3.8%, 0.9 14.4); psychosocial stress (1.30, 1.06 1.60; 4.6%, 2.1 9.6) and depression (1.35, 1.10 1.66; 5.2%, 2.7 9.8); cardiac causes (2.38, 1.77 3.20; 6.7%, 4.8 9.1); and ratio of apolipoproteins B to A1 (1.89, 1.49 2.40 for highest vs lowest tertile; 24.9%, 15.7 37.1).
+NDUFS3	drug	nicotine	20561675	In the first 3000 cases (n=2337, 78%, with ischaemic stroke; n=663, 22%, with intracerebral haemorrhagic stroke) and 3000 controls, significant risk factors for all stroke were: history of hypertension (OR 2.64, 99% CI 2.26 3.08; PAR 34.6%, 99% <strong>CI 30</strong>.4 39.1); current <b>smoking</b> (2.09, 1.75 2.51; 18.9%, 15.3 23.1); waist to hip ratio (1.65, 1.36 1.99 for highest vs lowest tertile; 26.5%, 18.8 36.0); diet risk score (1.35, 1.11 1.64 for highest vs lowest tertile; 18.8%, 11.2 29.7); regular physical activity (0.69, 0.53 0.90; 28.5%, 14.5 48.5); diabetes mellitus (1.36, 1.10 1.68; 5.0%, 2.6 9.5); alcohol intake (1.51, 1.18 1.92 for more than 30 drinks per month or binge drinking; 3.8%, 0.9 14.4); psychosocial stress (1.30, 1.06 1.60; 4.6%, 2.1 9.6) and depression (1.35, 1.10 1.66; 5.2%, 2.7 9.8); cardiac causes (2.38, 1.77 3.20; 6.7%, 4.8 9.1); and ratio of apolipoproteins B to A1 (1.89, 1.49 2.40 for highest vs lowest tertile; 24.9%, 15.7 37.1).
+NDUFS3	addiction	intoxication	20561675	In the first 3000 cases (n=2337, 78%, with ischaemic stroke; n=663, 22%, with intracerebral haemorrhagic stroke) and 3000 controls, significant risk factors for all stroke were: history of hypertension (OR 2.64, 99% CI 2.26 3.08; PAR 34.6%, 99% <strong>CI 30</strong>.4 39.1); current smoking (2.09, 1.75 2.51; 18.9%, 15.3 23.1); waist to hip ratio (1.65, 1.36 1.99 for highest vs lowest tertile; 26.5%, 18.8 36.0); diet risk score (1.35, 1.11 1.64 for highest vs lowest tertile; 18.8%, 11.2 29.7); regular physical activity (0.69, 0.53 0.90; 28.5%, 14.5 48.5); diabetes mellitus (1.36, 1.10 1.68; 5.0%, 2.6 9.5); alcohol intake (1.51, 1.18 1.92 for more than 30 drinks per month or <b>binge</b> drinking; 3.8%, 0.9 14.4); psychosocial stress (1.30, 1.06 1.60; 4.6%, 2.1 9.6) and depression (1.35, 1.10 1.66; 5.2%, 2.7 9.8); cardiac causes (2.38, 1.77 3.20; 6.7%, 4.8 9.1); and ratio of apolipoproteins B to A1 (1.89, 1.49 2.40 for highest vs lowest tertile; 24.9%, 15.7 37.1).
+MTHFR	drug	alcohol	29953924	Lack of association between <strong>MTHFR</strong> C677T Gene polymorphism with <b>alcohol</b> dependence: A meta analysis of case control studies.
+MTHFR	addiction	dependence	29953924	Lack of association between <strong>MTHFR</strong> C677T Gene polymorphism with alcohol <b>dependence</b>: A meta analysis of case control studies.
+MTHFR	drug	alcohol	29953924	Many studies have reported that <strong>MTHFR</strong> C677T (rs 1801133) polymorphism is associated with the risk of <b>alcohol</b> dependence(AD).
+MTHFR	addiction	dependence	29953924	Many studies have reported that <strong>MTHFR</strong> C677T (rs 1801133) polymorphism is associated with the risk of alcohol <b>dependence</b>(AD).
+MTHFR	drug	alcohol	25188266	We also found that one carbon metabolism (OCM) impairment plays a significant role in <b>alcohol</b> toxicity to the PFC seen from the difference in the effects of acute and chronic <b>alcohol</b> exposure on DNA repair and from exaggeration of the damaging effects upon additional OCM impairment in mice deficient in a key OCM enzyme, methylenetetrahydrofolate reductase (<strong>MTHFR</strong>).
+MTHFR	drug	alcohol	25188266	We also found that one carbon metabolism (OCM) impairment plays a significant role in <b>alcohol</b> toxicity to the PFC seen from the difference in the effects of acute and chronic <b>alcohol</b> exposure on DNA repair and from exaggeration of the damaging effects upon additional OCM impairment in mice deficient in a key OCM enzyme, <strong>methylenetetrahydrofolate reductase</strong> (<strong>MTHFR</strong>).
+MTHFR	drug	alcohol	26317030	A Study on <strong>MTHFR</strong> C677T Gene Polymorphism and <b>Alcohol</b> Dependence among Meiteis of Manipur, India.
+MTHFR	addiction	dependence	26317030	A Study on <strong>MTHFR</strong> C677T Gene Polymorphism and Alcohol <b>Dependence</b> among Meiteis of Manipur, India.
+MTHFR	drug	alcohol	26317030	Chronic <b>alcohol</b> consumption is reported to be associated with increase in plasma homocysteine levels which is further influenced by the polymorphism in methylenetetrahydrofolate reductase (<strong>MTHFR</strong>) gene.
+MTHFR	drug	alcohol	26317030	Chronic <b>alcohol</b> consumption is reported to be associated with increase in plasma homocysteine levels which is further influenced by the polymorphism in <strong>methylenetetrahydrofolate reductase</strong> (<strong>MTHFR</strong>) gene.
+MTHFR	drug	alcohol	26317030	The present study aims to understand the extent of the <strong>MTHFR</strong> C677T polymorphism in <b>alcohol</b> dependent (AD) cases of Meiteis of Manipur, a Mendelian population of India.
+MTHFR	drug	alcohol	26317030	<strong>MTHFR</strong> C677T polymorphism was screened in 313 controls and 139 <b>alcohol</b> dependent (AD) cases who all met DSM IV criteria for <b>alcohol</b> dependence.
+MTHFR	addiction	dependence	26317030	<strong>MTHFR</strong> C677T polymorphism was screened in 313 controls and 139 alcohol dependent (AD) cases who all met DSM IV criteria for alcohol <b>dependence</b>.
+MTHFR	drug	alcohol	23335901	The <strong>MTHFR</strong> C677T Variant is Associated with Responsiveness to <b>Disulfiram</b> Treatment for Cocaine Dependency.
+MTHFR	drug	cocaine	23335901	The <strong>MTHFR</strong> C677T Variant is Associated with Responsiveness to Disulfiram Treatment for <b>Cocaine</b> Dependency.
+MTHFR	drug	alcohol	23335901	Since <b>disulfiram</b> and cocaine both affect levels of global methylation we hypothesized the <strong>MTHFR</strong> gene, whose product is involved in supplying methyl groups for DNA and protein methylation, may be associated with responsiveness to <b>disulfiram</b> in cocaine dependent individuals.
+MTHFR	drug	cocaine	23335901	Since disulfiram and <b>cocaine</b> both affect levels of global methylation we hypothesized the <strong>MTHFR</strong> gene, whose product is involved in supplying methyl groups for DNA and protein methylation, may be associated with responsiveness to disulfiram in <b>cocaine</b> dependent individuals.
+MTHFR	drug	alcohol	23335901	Patients were genotyped for the <strong>MTHFR</strong> (rs1801133, also known as C677T) polymorphism and the data was evaluated for association with cocaine free urines in the <b>disulfiram</b> or placebo groups.
+MTHFR	drug	cocaine	23335901	Patients were genotyped for the <strong>MTHFR</strong> (rs1801133, also known as C677T) polymorphism and the data was evaluated for association with <b>cocaine</b> free urines in the disulfiram or placebo groups.
+MTHFR	drug	alcohol	23335901	The CT or TT <strong>MTHFR</strong> genotype group (N = 32) dropped from 73 to 52% cocaine positive urines on <b>disulfiram</b> (p = 0.0001), while the placebo group showed no treatment effect.
+MTHFR	drug	cocaine	23335901	The CT or TT <strong>MTHFR</strong> genotype group (N = 32) dropped from 73 to 52% <b>cocaine</b> positive urines on disulfiram (p = 0.0001), while the placebo group showed no treatment effect.
+MTHFR	drug	alcohol	23335901	The CC <strong>MTHFR</strong> genotype group (N = 24) showed a smaller, but still significant, reduction in cocaine positive urines on <b>disulfiram</b> compared to placebo; 81 69% (p = 0.007).
+MTHFR	drug	cocaine	23335901	The CC <strong>MTHFR</strong> genotype group (N = 24) showed a smaller, but still significant, reduction in <b>cocaine</b> positive urines on disulfiram compared to placebo; 81 69% (p = 0.007).
+MTHFR	drug	alcohol	23335901	This study indicates that a patient's <strong>MTHFR</strong> genotype may be used to identify individuals who might show improved response to <b>disulfiram</b> treatment for cocaine dependence.
+MTHFR	drug	cocaine	23335901	This study indicates that a patient's <strong>MTHFR</strong> genotype may be used to identify individuals who might show improved response to disulfiram treatment for <b>cocaine</b> dependence.
+MTHFR	addiction	dependence	23335901	This study indicates that a patient's <strong>MTHFR</strong> genotype may be used to identify individuals who might show improved response to disulfiram treatment for cocaine <b>dependence</b>.
+MTHFR	drug	alcohol	19650814	Association between <strong>MTHFR</strong> 677C T polymorphism and <b>alcohol</b> dependence according to Lesch and Babor typology.
+MTHFR	addiction	dependence	19650814	Association between <strong>MTHFR</strong> 677C T polymorphism and alcohol <b>dependence</b> according to Lesch and Babor typology.
+MTHFR	drug	alcohol	19650814	This study determines and compares <strong>MTHFR</strong> 677C T distribution and examines its consequences on homocysteine metabolism and <b>alcohol</b> dependence in <b>alcoholic</b> patients classified according to the Babor and Lesch typologies.
+MTHFR	addiction	dependence	19650814	This study determines and compares <strong>MTHFR</strong> 677C T distribution and examines its consequences on homocysteine metabolism and alcohol <b>dependence</b> in alcoholic patients classified according to the Babor and Lesch typologies.
+MTHFR	drug	alcohol	19650814	<strong>MTHFR</strong> TT genotype was more prevalent in AD patients with milder <b>alcohol</b> dependence (Babor type A) and with Lesch type 3, associated with depression.
+MTHFR	addiction	dependence	19650814	<strong>MTHFR</strong> TT genotype was more prevalent in AD patients with milder alcohol <b>dependence</b> (Babor type A) and with Lesch type 3, associated with depression.
+MTHFR	drug	alcohol	18328637	Protective effect against <b>alcohol</b> dependence of the thermolabile variant of <strong>MTHFR</strong>.
+MTHFR	addiction	dependence	18328637	Protective effect against alcohol <b>dependence</b> of the thermolabile variant of <strong>MTHFR</strong>.
+MTHFR	drug	alcohol	18328637	Our objective was to study the prevalence of the <strong>MTHFR</strong> C677T polymorphism in <b>alcohol</b> dependent subjects and the influence of this polymorphism on symptoms associated with <b>alcoholism</b>.
+MTHFR	drug	alcohol	18328637	<strong>MTHFR</strong> C677T polymorphism was determined in 93 control subjects and 242 <b>alcohol</b> dependent subjects.
+MTHFR	drug	alcohol	18328637	<b>Alcohol</b> dependent subjects showed a significant decrease in <strong>MTHFR</strong> 677TT prevalence (9%, 21/242) compared to controls (18%, 17/93) (p<0.02).
+MTHFR	drug	alcohol	18328637	<strong>MTHFR</strong> 677TT genotype could play a protective role against <b>alcohol</b> dependence.
+MTHFR	addiction	dependence	18328637	<strong>MTHFR</strong> 677TT genotype could play a protective role against alcohol <b>dependence</b>.
+MTHFR	drug	alcohol	18328637	Moreover, when subjects with <strong>MTHFR</strong> 677TT genotype become dependent to <b>alcohol</b>, they seem to constitute a subgroup of <b>alcoholic</b> patients with a decreased risk for developing neurotoxic withdrawal symptoms and hepatic toxicity.
+MTHFR	addiction	withdrawal	18328637	Moreover, when subjects with <strong>MTHFR</strong> 677TT genotype become dependent to alcohol, they seem to constitute a subgroup of alcoholic patients with a decreased risk for developing neurotoxic <b>withdrawal</b> symptoms and hepatic toxicity.
+MTHFR	drug	nicotine	18080853	Clinical (sex, age, type of MS, relapse, disease duration, coexisting disease, <b>smoking</b> habit, and physical disability) and laboratory variables (HHcy, low serum levels of folate and vit.B12, <strong>MTHFR</strong> genotype) were evaluated for their ability to predict cognitive impairment.
+MTHFR	addiction	relapse	18080853	Clinical (sex, age, type of MS, <b>relapse</b>, disease duration, coexisting disease, smoking habit, and physical disability) and laboratory variables (HHcy, low serum levels of folate and vit.B12, <strong>MTHFR</strong> genotype) were evaluated for their ability to predict cognitive impairment.
+MTHFR	addiction	sensitization	18070159	A recent study suggested a link between folate metabolism and atopy, based on a positive association between a common polymorphism of the methylenetetrahydrofolate reductase (<strong>MTHFR</strong>) gene and allergic <b>sensitization</b> in Danish adults.
+MTHFR	addiction	sensitization	18070159	A recent study suggested a link between folate metabolism and atopy, based on a positive association between a common polymorphism of the <strong>methylenetetrahydrofolate reductase</strong> (<strong>MTHFR</strong>) gene and allergic <b>sensitization</b> in Danish adults.
+MTHFR	drug	alcohol	17117960	<strong>Methylenetetrahydrofolate reductase</strong> C677T polymorphism and its association with <b>alcohol</b> withdrawal seizure.
+MTHFR	addiction	withdrawal	17117960	<strong>Methylenetetrahydrofolate reductase</strong> C677T polymorphism and its association with alcohol <b>withdrawal</b> seizure.
+MTHFR	drug	alcohol	17117960	It was investigated whether the T allele of the <strong>MTHFR</strong> C677T polymorphism is associated with <b>alcohol</b> dependence, <b>alcohol</b> withdrawal seizure (WS), or the daily amount of <b>alcohol</b> consumption.
+MTHFR	addiction	dependence	17117960	It was investigated whether the T allele of the <strong>MTHFR</strong> C677T polymorphism is associated with alcohol <b>dependence</b>, alcohol withdrawal seizure (WS), or the daily amount of alcohol consumption.
+MTHFR	addiction	withdrawal	17117960	It was investigated whether the T allele of the <strong>MTHFR</strong> C677T polymorphism is associated with alcohol dependence, alcohol <b>withdrawal</b> seizure (WS), or the daily amount of alcohol consumption.
+MTHFR	drug	alcohol	17117960	The present study suggests an influence of the <strong>MTHFR</strong> C677T polymorphism on the etiology of <b>alcohol</b> WS and <b>alcohol</b> dependence in men in a western European population.
+MTHFR	addiction	dependence	17117960	The present study suggests an influence of the <strong>MTHFR</strong> C677T polymorphism on the etiology of alcohol WS and alcohol <b>dependence</b> in men in a western European population.
+MTHFR	drug	alcohol	17117960	An influence of <strong>MTHFR</strong> C677T on the daily amount of <b>alcohol</b> intake before admission among <b>alcohol</b> dependent patients could not be shown.
+MTHFR	addiction	aversion	16997330	We have studied the effect of genetic polymorphisms in the DNA repair genes hOGG1, XRCC1, XRCC3, ERCC2 and the <strong>MTHFR</strong> gene in the folate metabolism on the frequencies of cells with chromosomal aberrations (CA), chromosome type aberrations (CSA), chromatid type aberrations (<b>CTA</b>), chromatid breaks (CTB) and chromatid gaps (CTG) scored in peripheral blood lymphocytes from 651 Norwegian subjects of Caucasian descendant.
+MTHFR	drug	nicotine	16997330	Carrying the <strong>MTHFR</strong> 222Val allele gave an increased risk for chromosome and chromatid type aberrations for both non <b>smokers</b> and <b>smokers</b>, especially for individuals in the older age group, and with variable results in the youngest age group.
+MTHFR	drug	alcohol	16627623	Taking into account that <b>alcohol</b> dependence is associated with elevated homocysteine levels, this study was undertaken to investigate different <strong>MTHFR</strong> (methylenetetrahydrofolate reductase) genotypes related to homocysteine metabolism in patients with <b>alcohol</b> dependence who were classified according to Lesch's typology (LT).
+MTHFR	addiction	dependence	16627623	Taking into account that alcohol <b>dependence</b> is associated with elevated homocysteine levels, this study was undertaken to investigate different <strong>MTHFR</strong> (methylenetetrahydrofolate reductase) genotypes related to homocysteine metabolism in patients with alcohol <b>dependence</b> who were classified according to Lesch's typology (LT).
+MTHFR	drug	alcohol	16627623	Taking into account that <b>alcohol</b> dependence is associated with elevated homocysteine levels, this study was undertaken to investigate different <strong>MTHFR</strong> (<strong>methylenetetrahydrofolate reductase</strong>) genotypes related to homocysteine metabolism in patients with <b>alcohol</b> dependence who were classified according to Lesch's typology (LT).
+MTHFR	addiction	dependence	16627623	Taking into account that alcohol <b>dependence</b> is associated with elevated homocysteine levels, this study was undertaken to investigate different <strong>MTHFR</strong> (<strong>methylenetetrahydrofolate reductase</strong>) genotypes related to homocysteine metabolism in patients with alcohol <b>dependence</b> who were classified according to Lesch's typology (LT).
+MTHFR	drug	alcohol	15054427	To examine the associations between various lifestyle factors  smoking habits, physical activity, dietary habits, coffee, tea, and <b>alcohol</b> consumption  and homocysteine (tHcy) in relation to <strong>MTHFR</strong>(C677T) genotype.
+MTHFR	drug	nicotine	15054427	To examine the associations between various lifestyle factors  <b>smoking</b> habits, physical activity, dietary habits, coffee, tea, and alcohol consumption  and homocysteine (tHcy) in relation to <strong>MTHFR</strong>(C677T) genotype.
+MTHFR	drug	nicotine	15054427	Interaction was observed between <b>smoking</b> status and <strong>MTHFR</strong> genotype, <b>smoking</b> status and sex, and beer consumption and age.
+MTHFR	drug	alcohol	11747974	High prevalence of hyperhomocysteinemia in chronic <b>alcoholism</b>: the importance of the thermolabile form of the enzyme methylenetetrahydrofolate reductase (<strong>MTHFR</strong>).
+MTHFR	drug	alcohol	11747974	High prevalence of hyperhomocysteinemia in chronic <b>alcoholism</b>: the importance of the thermolabile form of the enzyme <strong>methylenetetrahydrofolate reductase</strong> (<strong>MTHFR</strong>).
+MTHFR	drug	alcohol	11319182	However, we found no evidence for an association between the <strong>MTHFR</strong> C677T and A1298C polymorphisms and risk of lung cancer in either all of the subjects or the low folate intake subgroup; nor did we find evidence for an interaction between these two <strong>MTHFR</strong> polymorphisms and dietary folate intake or <b>alcohol</b> use.
+MMP2	drug	amphetamine	32044305	Moreover, a regulator of the extracellular matrix, matrix metalloproteinase 14 (MMP 14) in the retina, and <strong>MMP 2</strong> and MMP 9 in plasma, were increased by <b>METH</b> treatment.
+MMP2	addiction	relapse	31062493	Unlike t SP observed in NAcore during reinstated drug <b>seeking</b>, neither dendrite spine head enlargement nor activation of matrix metalloproteases (<strong>MMP2</strong>/9) accompanied the increased AMPA:NMDA in NAshell during refraining.
+MMP2	drug	alcohol	30648329	Subsequently, rat brains were extracted after initial or stable escalated <b>alcohol</b> self administration phases of acute withdrawal and analyzed by immunoblot to detect <strong>MMP 2</strong>,  3, and  9 levels in the anterior cingulate cortex (ACC), bed nucleus of the stria terminalis, central amygdala (CeA), hippocampus, and nucleus accumbens (NAc).
+MMP2	addiction	withdrawal	30648329	Subsequently, rat brains were extracted after initial or stable escalated alcohol self administration phases of acute <b>withdrawal</b> and analyzed by immunoblot to detect <strong>MMP 2</strong>,  3, and  9 levels in the anterior cingulate cortex (ACC), bed nucleus of the stria terminalis, central amygdala (CeA), hippocampus, and nucleus accumbens (NAc).
+MMP2	addiction	addiction	28969088	From the result, rs243849 which located in <strong>MMP2</strong> were 1.355 (1.014 1.811), 1.34 (1.01 1.78) in allele model and log <b>addictive</b> model, respectively.
+MMP2	drug	cocaine	28123012	Manipulating the interaction between mGluR5, NO production, or <strong>MMP 2</strong> and MMP 9 pharmacologically or genetically is sufficient to recapitulate transient synaptic potentiation and reinstate <b>cocaine</b> seeking.
+MMP2	addiction	relapse	28123012	Manipulating the interaction between mGluR5, NO production, or <strong>MMP 2</strong> and MMP 9 pharmacologically or genetically is sufficient to recapitulate transient synaptic potentiation and reinstate cocaine <b>seeking</b>.
+MMP2	drug	amphetamine	26507236	Using a murine model of <b>METH</b> administration and wound infection, we demonstrated that <b>METH</b> reduces wound healing and facilitates host mediated collagen degradation by increased expression and production of matrix metalloproteinase 2 (<strong>MMP 2</strong>).
+MMP2	drug	cocaine	25326689	We found enduring increases in <strong>MMP 2</strong> activity in rats after withdrawal from self administered <b>cocaine</b> and transient increases in MMP 9 during cue induced <b>cocaine</b> relapse.
+MMP2	addiction	relapse	25326689	We found enduring increases in <strong>MMP 2</strong> activity in rats after withdrawal from self administered cocaine and transient increases in MMP 9 during cue induced cocaine <b>relapse</b>.
+MMP2	addiction	withdrawal	25326689	We found enduring increases in <strong>MMP 2</strong> activity in rats after <b>withdrawal</b> from self administered cocaine and transient increases in MMP 9 during cue induced cocaine relapse.
+MMP2	drug	nicotine	25260978	In vitro exposure of cells to single doses or seven days of <b>nicotine</b> induced the protein expression of <strong>MMP 2</strong>, MMP 9 and EGR 1 and these responses were blocked by GABA.
+MMP2	drug	amphetamine	24522335	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of AQP4 and MMP9, lower expression of CLDN5 in <b>METH</b> intoxication cases and lower expression of <strong>MMP2</strong> in phenobarbital intoxication cases.
+MMP2	addiction	intoxication	24522335	Relative mRNA quantification using Taqman real time PCR assay demonstrated higher expression of AQP4 and MMP9, lower expression of CLDN5 in METH <b>intoxication</b> cases and lower expression of <strong>MMP2</strong> in phenobarbital <b>intoxication</b> cases.
+MMP2	addiction	sensitization	24282543	Hallmarks of central <b>sensitization</b>, significant spinal astrogliosis and increases in activity of metalloproteases <strong>MMP 2</strong> and MMP 9 in the spinal cord were evident in the model of OA pain.
+MMP2	drug	nicotine	25157203	Present results indicate transient changes in hippocampal <strong>MMP 2</strong>,  3, and  9 expression following context dependent learning of <b>nicotine</b> induced conditioned place preference (CPP).
+MMP2	addiction	reward	25157203	Present results indicate transient changes in hippocampal <strong>MMP 2</strong>,  3, and  9 expression following context dependent learning of nicotine induced conditioned place preference (<b>CPP</b>).
+MMP2	drug	opioid	20519536	The other gelatinase, <strong>MMP 2</strong>, is not involved in <b>morphine</b> dependence.
+MMP2	addiction	dependence	20519536	The other gelatinase, <strong>MMP 2</strong>, is not involved in morphine <b>dependence</b>.
+MMP2	drug	opioid	20519536	Inhibiting spinal MMP 9 or <strong>MMP 2</strong> reduces chronic and/or acute <b>morphine</b> tolerance.
+MMP2	drug	psychedelics	19579000	<b>Ketamine</b> withdrawal has no effect on the expression of VEGF, <strong>MMP2</strong>, or BCL 2.
+MMP2	addiction	withdrawal	19579000	Ketamine <b>withdrawal</b> has no effect on the expression of VEGF, <strong>MMP2</strong>, or BCL 2.
+MMP2	drug	psychedelics	19579000	The findings indicate a promoting effect of risperidone and haloperidol on survival of young neurons in the hippocampus by enhancing the expression of the anti apoptotic protein BCL 2 and by activation of VEGF/<strong>MMP2</strong>, whereby an interference with <b>ketamine</b> and thus a priority role of the NMDA system was not evident.
+MMP2	drug	cocaine	18792988	Here we explored whether <b>cocaine</b> primed reinstatement was associated with increased activity of the gelatinases, <strong>MMP 2</strong> or MMP 9, in the medial prefrontal cortex (mPFC) or dorsal hippocampus.
+MMP2	addiction	relapse	18792988	Here we explored whether cocaine primed <b>reinstatement</b> was associated with increased activity of the gelatinases, <strong>MMP 2</strong> or MMP 9, in the medial prefrontal cortex (mPFC) or dorsal hippocampus.
+MMP2	drug	amphetamine	18198472	Repeated <b>METH</b> treatment induced behavioral sensitization, which was accompanied by an increase in <strong>MMP 2</strong>/ 9/TIMP 2 activity in the brain.
+MMP2	addiction	sensitization	18198472	Repeated METH treatment induced behavioral <b>sensitization</b>, which was accompanied by an increase in <strong>MMP 2</strong>/ 9/TIMP 2 activity in the brain.
+MMP2	drug	amphetamine	18198472	<strong>MMP 2</strong>/ 9 inhibitors blocked the <b>METH</b> induced behavioral sensitization and conditioned place preference (CPP), a measure of the rewarding effect of a drug, and reduced the <b>METH</b> increased dopamine release in the NAc.
+MMP2	addiction	reward	18198472	<strong>MMP 2</strong>/ 9 inhibitors blocked the METH induced behavioral sensitization and conditioned place preference (<b>CPP</b>), a measure of the rewarding effect of a drug, and reduced the METH increased dopamine release in the NAc.
+MMP2	addiction	sensitization	18198472	<strong>MMP 2</strong>/ 9 inhibitors blocked the METH induced behavioral <b>sensitization</b> and conditioned place preference (CPP), a measure of the rewarding effect of a drug, and reduced the METH increased dopamine release in the NAc.
+MMP2	drug	amphetamine	18198472	In <strong>MMP 2</strong>  and MMP 9 deficient mice, <b>METH</b> induced behavioral sensitization and CPP as well as dopamine release were attenuated.
+MMP2	addiction	reward	18198472	In <strong>MMP 2</strong>  and MMP 9 deficient mice, METH induced behavioral sensitization and <b>CPP</b> as well as dopamine release were attenuated.
+MMP2	addiction	sensitization	18198472	In <strong>MMP 2</strong>  and MMP 9 deficient mice, METH induced behavioral <b>sensitization</b> and CPP as well as dopamine release were attenuated.
+MMP2	drug	alcohol	18047805	<b>Disulfiram</b> suppresses invasive ability of osteosarcoma cells via the inhibition of <strong>MMP 2</strong> and MMP 9 expression.
+MMP2	drug	alcohol	18047805	In this study, we reported the effects of <b>disulfiram</b>, a clinically used anti <b>alcoholism</b> drug, on tumor invasion suppression, as well as its effects on the activity of <strong>MMP 2</strong> and MMP 9 in human osteosarcoma cells (U2OS).
+MMP2	drug	alcohol	18047805	In conclusion, <b>disulfiram</b> inhibited expression of <strong>MMP 2</strong> and MMP 9 and it regulated the invasion of human osteosarcoma cells.
+MMP2	drug	amphetamine	17472698	We have demonstrated that <b>methamphetamine</b> (<b>METH</b>) induced behavioral sensitization and reward were markedly attenuated in <strong>MMP 2</strong>  and MMP 9 deficient [<strong>MMP 2</strong> ( / ) and MMP 9 ( / )] mice compared with those in wild type mice, suggesting that <b>METH</b> induced expression of <strong>MMP 2</strong> and MMP 9 in the brain plays a role in the development of <b>METH</b> induced sensitization and reward.
+MMP2	addiction	reward	17472698	We have demonstrated that methamphetamine (METH) induced behavioral sensitization and <b>reward</b> were markedly attenuated in <strong>MMP 2</strong>  and MMP 9 deficient [<strong>MMP 2</strong> ( / ) and MMP 9 ( / )] mice compared with those in wild type mice, suggesting that METH induced expression of <strong>MMP 2</strong> and MMP 9 in the brain plays a role in the development of METH induced sensitization and <b>reward</b>.
+MMP2	addiction	sensitization	17472698	We have demonstrated that methamphetamine (METH) induced behavioral <b>sensitization</b> and reward were markedly attenuated in <strong>MMP 2</strong>  and MMP 9 deficient [<strong>MMP 2</strong> ( / ) and MMP 9 ( / )] mice compared with those in wild type mice, suggesting that METH induced expression of <strong>MMP 2</strong> and MMP 9 in the brain plays a role in the development of METH induced <b>sensitization</b> and reward.
+MMP2	drug	amphetamine	17472698	On the other hand, <strong>MMP 2</strong>/ 9 inhibitors blocked the <b>METH</b> induced behavioral sensitization and conditioned place preference, a measure of the rewarding effect, and reduced the <b>METH</b> increased dopamine release in the NAc.
+MMP2	addiction	sensitization	17472698	On the other hand, <strong>MMP 2</strong>/ 9 inhibitors blocked the METH induced behavioral <b>sensitization</b> and conditioned place preference, a measure of the rewarding effect, and reduced the METH increased dopamine release in the NAc.
+MMP2	drug	amphetamine	17472698	Repeated <b>METH</b> treatment also reduced dopamine D2 receptor agonist stimulated [(35)S]GTPgammaS binding in wild type mice, but such changes were significantly attenuated in <strong>MMP 2</strong> ( / ) and MMP 9 ( / ) mice.
+MMP2	drug	amphetamine	17348864	Here, we investigated whether <strong>MMP 2</strong> and MMP 9 are involved in the rewarding effects of and sensitization to <b>methamphetamine</b> (<b>METH</b>) in animals, in which the remodelling of neural circuits may play a crucial role.
+MMP2	addiction	sensitization	17348864	Here, we investigated whether <strong>MMP 2</strong> and MMP 9 are involved in the rewarding effects of and <b>sensitization</b> to methamphetamine (METH) in animals, in which the remodelling of neural circuits may play a crucial role.
+MMP2	drug	amphetamine	17348864	Repeated <b>METH</b> treatment induced behavioural sensitization, which was accompanied by an increase in <strong>MMP 2</strong> and MMP 9 activity in the brain.
+MMP2	addiction	sensitization	17348864	Repeated METH treatment induced behavioural <b>sensitization</b>, which was accompanied by an increase in <strong>MMP 2</strong> and MMP 9 activity in the brain.
+MMP2	drug	amphetamine	17348864	In <strong>MMP 2</strong>  and MMP 9 deficient mice [<strong>MMP 2</strong> ( / ) and MMP 9 ( / )], <b>METH</b> induced behavioural sensitization and conditioned place preference, a measure of the rewarding effect, as well as <b>METH</b> increased dopamine release in the nucleus accumbens (NAc) were attenuated compared with those in wild type mice.
+MMP2	addiction	sensitization	17348864	In <strong>MMP 2</strong>  and MMP 9 deficient mice [<strong>MMP 2</strong> ( / ) and MMP 9 ( / )], METH induced behavioural <b>sensitization</b> and conditioned place preference, a measure of the rewarding effect, as well as METH increased dopamine release in the nucleus accumbens (NAc) were attenuated compared with those in wild type mice.
+MMP2	drug	amphetamine	17348864	In contrast, infusion of purified human <strong>MMP 2</strong> into the NAc significantly potentiated the <b>METH</b> increased dopamine release.
+MMP2	drug	amphetamine	17348864	The [(3)H]dopamine uptake into striatal synaptosomes was reduced in wild type mice after repeated <b>METH</b> treatment, but <b>METH</b> induced changes in [(3)H]dopamine uptake were significantly attenuated in <strong>MMP 2</strong> ( / ) and MMP 9 ( / ) mice.
+MMP2	drug	amphetamine	17348864	These results suggest that both <strong>MMP 2</strong> and MMP 9 play a crucial role in <b>METH</b> induced behavioural sensitization and reward by regulating <b>METH</b> induced dopamine release and uptake in the NAc.
+MMP2	addiction	reward	17348864	These results suggest that both <strong>MMP 2</strong> and MMP 9 play a crucial role in METH induced behavioural sensitization and <b>reward</b> by regulating METH induced dopamine release and uptake in the NAc.
+MMP2	addiction	sensitization	17348864	These results suggest that both <strong>MMP 2</strong> and MMP 9 play a crucial role in METH induced behavioural <b>sensitization</b> and reward by regulating METH induced dopamine release and uptake in the NAc.
+MMP2	addiction	intoxication	15233026	In the <b>intoxication</b> with stimulants we usually demonstrated <strong>MMP 2</strong> in the myocardium interstitium, MMP 9 being observed in two cases and MMP 1 in one case.
+CBS	drug	cannabinoid	32437941	Also, do the sexes respond similarly to exogenous <b>cannabinoids</b> (<strong>CBs</strong>) following stress?
+CBS	drug	cannabinoid	32437941	Certainly this review should draw the attention of clinicians working with children, adolescents and adults exposed to early trauma and provide some perspective on the dysregulation of the <b>endocannabinoid</b> system in the response to trauma, the complex actions of exogenous <strong>CBs</strong> based on stress history and the unique effects of these factors in men and women.
+CBS	drug	alcohol	31690747	We tested whether cannabinoids (<strong>CBs</strong>) potentiate <b>alcohol</b> induced birth defects in mice and zebrafish, and explored the underlying pathogenic mechanisms on Sonic Hedgehog (Shh) signaling.
+CBS	drug	cannabinoid	31690747	We tested whether <b>cannabinoids</b> (<strong>CBs</strong>) potentiate alcohol induced birth defects in mice and zebrafish, and explored the underlying pathogenic mechanisms on Sonic Hedgehog (Shh) signaling.
+CBS	drug	alcohol	31690747	The <strong>CBs</strong>, Δ9 THC, cannabidiol, HU 210, and CP 55,940 caused <b>alcohol</b> like effects on craniofacial and brain development, phenocopying Shh mutations.
+CBS	drug	cannabinoid	31690747	The <strong>CBs</strong>, Δ9 <b>THC</b>, <b>cannabidiol</b>, HU 210, and CP 55,940 caused alcohol like effects on craniofacial and brain development, phenocopying Shh mutations.
+CBS	drug	cannabinoid	31559334	In their natural form, <strong>CBs</strong> such as Δ9 tetrahydrocannabinolic acid and cannabidiolic acid are inactive at these receptors, while their decarboxylated forms (Δ9 <b>tetrahydrocannabinol</b> and <b>cannabidiol</b>, respectively) are potent ligands at CB receptors.
+CBS	drug	cannabinoid	31559334	Factors such as temperature and exposure time play important roles in the decarboxylation of phytocannabinoids, thereby generating pharmacologically active <strong>CBs</strong>, and these conditions may differ for each <b>cannabis</b> cultivar.
+CBS	drug	cannabinoid	31159897	Further, data encourage basic and clinical studies to determine how <b>cannabis</b> and <b>cannabinoids</b> (<strong>CBs</strong>) can affect mood and to investigate emerging CB based options as probable treatment approaches.
+CBS	drug	alcohol	28918416	Use patterns of smoking, <b>alcohol</b> use and other psychoactive substances were measured as well as that of certain behavioural addictions (problematic gambling   PGSI, DSM V, eating disorders   SCOFF, problematic internet use   PIUQ, problematic on line gaming   POGO, problematic social media use   FAS, exercise addictions   EAI HU, work addiction   BWAS, compulsive buying   <strong>CBS</strong>).
+CBS	drug	nicotine	28918416	Use patterns of <b>smoking</b>, alcohol use and other psychoactive substances were measured as well as that of certain behavioural addictions (problematic gambling   PGSI, DSM V, eating disorders   SCOFF, problematic internet use   PIUQ, problematic on line gaming   POGO, problematic social media use   FAS, exercise addictions   EAI HU, work addiction   BWAS, compulsive buying   <strong>CBS</strong>).
+CBS	addiction	addiction	28918416	Use patterns of smoking, alcohol use and other psychoactive substances were measured as well as that of certain behavioural addictions (problematic gambling   PGSI, DSM V, eating disorders   SCOFF, problematic internet use   PIUQ, problematic on line gaming   POGO, problematic social media use   FAS, exercise addictions   EAI HU, work <b>addiction</b>   BWAS, <b>compulsive</b> buying   <strong>CBS</strong>).
+CBS	drug	cannabinoid	28583800	The organized, tightly regulated signaling relays engaged by the <b>cannabinoid</b> receptors (<strong>CBs</strong>) and their ligands, G proteins and other effectors, together constitute the <b>endocannabinoid</b> system (ECS).
+CBS	addiction	sensitization	26512068	On the other hand, we have found that AEA modulates the NTG induced changes, thus it influences the activation and central <b>sensitization</b> process in the trigeminal system, probably via <strong>CBs</strong>.
+CBS	addiction	addiction	25630963	In AUD subjects, direct correlations between BIS 11 and <b>Compulsive</b> Buying Scale (<strong>CBS</strong>), Internet <b>Addiction</b> Disorder test (IAD), Exercise <b>Addiction</b> Inventory Short Form (EAI SF) scores (p<.01), between OCDS obsessive and <strong>CBS</strong> and VASc and <strong>CBS</strong>, IAD scores (p<.003), were found.
+CBS	drug	cannabinoid	25143817	Synthetic <b>cannabinoids</b> (<strong>CBs</strong>) such as the JWH series have caused social problems concerning their abuse liability.
+CBS	drug	cannabinoid	25143817	In this study, three synthetic <strong>CBs</strong> with different binding affinities to the CB1 receptor (JWH 073, 081, and 210) and Δ(9) <b>tetrahydrocannabinol</b> (Δ(9) <b>THC</b>) were evaluated for their potential for psychological dependence.
+CBS	addiction	dependence	25143817	In this study, three synthetic <strong>CBs</strong> with different binding affinities to the CB1 receptor (JWH 073, 081, and 210) and Δ(9) tetrahydrocannabinol (Δ(9) THC) were evaluated for their potential for psychological <b>dependence</b>.
+CBS	addiction	dependence	25143817	These findings suggest the possibility to predict <b>dependence</b> potential of synthetic <strong>CBs</strong> through a receptor binding assay at the screening level.
+CBS	drug	cannabinoid	22991092	We argue that a review of neuroscience research suggests that synthetic <strong>CBs</strong> that act like Δ⁹ <b>tetrahydrocannabinol</b> (<b>THC</b>) by directly binding to and stimulating CB receptors (i.e.
+CBS	addiction	reward	22991092	Specifically, neurochemical research into how <strong>CBs</strong> influence mesolimbic dopamine release, a reliable and consistent marker of drugs' rewarding/<b>reinforcing</b> effects, provides the most useful indication of CB abuse liability, and may have implications for the generation of rational drug policy.
+CBS	drug	cannabinoid	22718500	Synthetic <b>cannabinoids</b> (<strong>CBs</strong>) [naphthalen 1 yl (1 pentylindol 3 yl) methanone (JWH 018) and naphthalen 1 yl (1 butylindol 3 yl) methanone (JWH 073)] are marketed, sold, and used as alternatives to <b>cannabis</b>.
+CBS	drug	cannabinoid	22718500	Synthetic <strong>CBs</strong> appear to have effects similar to those of Δ⁹ <b>tetrahydrocannabinol</b> (Δ⁹ <b>THC</b>), the drug primarily responsible for the behavioral effects of <b>cannabis</b>.
+CBS	drug	cannabinoid	22718500	The greater loss of sensitivity to Δ⁹ <b>THC</b> relative to CP 55,940 and JWH 018 suggests that differences in CB₁ receptor agonist efficacy are important in vivo and might underlie differences in the dependence liability and adverse effects of synthetic <strong>CBs</strong> versus <b>cannabis</b>.
+CBS	addiction	dependence	22718500	The greater loss of sensitivity to Δ⁹ THC relative to CP 55,940 and JWH 018 suggests that differences in CB₁ receptor agonist efficacy are important in vivo and might underlie differences in the <b>dependence</b> liability and adverse effects of synthetic <strong>CBs</strong> versus cannabis.
+CBS	drug	alcohol	20537734	Addictive drugs (opiates, <b>ethanol</b>, cannabinoids (<strong>CBs</strong>), nicotine, cocaine, amphetamines) induce activation of the hypothalamic pituitary adrenal (HPA) axis, with the subsequent release of adrenocorticotropic hormone and glucocorticoids.
+CBS	drug	cannabinoid	20537734	Addictive drugs (opiates, ethanol, <b>cannabinoids</b> (<strong>CBs</strong>), nicotine, cocaine, amphetamines) induce activation of the hypothalamic pituitary adrenal (HPA) axis, with the subsequent release of adrenocorticotropic hormone and glucocorticoids.
+CBS	drug	cocaine	20537734	Addictive drugs (opiates, ethanol, cannabinoids (<strong>CBs</strong>), nicotine, <b>cocaine</b>, amphetamines) induce activation of the hypothalamic pituitary adrenal (HPA) axis, with the subsequent release of adrenocorticotropic hormone and glucocorticoids.
+CBS	drug	nicotine	20537734	Addictive drugs (opiates, ethanol, cannabinoids (<strong>CBs</strong>), <b>nicotine</b>, cocaine, amphetamines) induce activation of the hypothalamic pituitary adrenal (HPA) axis, with the subsequent release of adrenocorticotropic hormone and glucocorticoids.
+CBS	addiction	addiction	20537734	<b>Addictive</b> drugs (opiates, ethanol, cannabinoids (<strong>CBs</strong>), nicotine, cocaine, amphetamines) induce activation of the hypothalamic pituitary adrenal (HPA) axis, with the subsequent release of adrenocorticotropic hormone and glucocorticoids.
+CBS	drug	cocaine	20537734	<strong>CBs</strong>, nicotine, <b>cocaine</b>).
+CBS	drug	nicotine	20537734	<strong>CBs</strong>, <b>nicotine</b>, cocaine).
+CBS	addiction	dependence	20528011	The presented BSIE versus BSSE <b>dependence</b> can greatly aid in obtaining <strong>CBS</strong> results for large molecular systems of chemical or biological interest.
+CBS	drug	cannabinoid	19480992	<b>Cannabinoids</b> (<strong>CBs</strong>) inhibit tumor growth by inducing apoptosis of tumor cells and impairing tumor angiogenesis.
+CBS	drug	cannabinoid	17877812	Furthermore, based on the reported similarity in the mechanisms responsible for NC induced anxiety  and depression related symptoms, as well as the contribution of brain <b>cannabinoid</b> (CB) receptors to these behavioral symptoms, the effects of anxiolytics and CB receptor ligands (<strong>CBs</strong>) against these behavioral symptoms were investigated.
+CBS	drug	alcohol	16332761	Crude cell extracts of a hydrolysate tolerant strain (TMB3000) converted both furfural and 5 hydroxymethyl furfural to the corresponding <b>alcohol</b> at a rate that was severalfold higher than the rate observed for cell extracts of a less tolerant strain (<strong>CBS</strong> 8066), thereby confirming that there is a correlation between the fermentation rate in a lignocellulosic hydrolysate and the bioconversion capacity of a strain.
+CBS	addiction	relapse	1957121	Duodenal ulcer <b>relapse</b> at 12 months after initial healing with <strong>CBS</strong> is significantly less than with H2 antagonist therapy.
+CBS	drug	nicotine	1957121	Ulcer healing with <strong>CBS</strong> is not influenced by <b>smoking</b>.
+CBS	addiction	relapse	1957121	H. pylori eradication with <strong>CBS</strong> appears to have little effect in ulcer healing but is of major importance in preventing ulcer <b>relapse</b>.
+CBS	drug	alcohol	2665050	<strong>CBS</strong> exhibits gastric protection (cytoprotection) against, for example, <b>ethanol</b> lesions.
+CBS	addiction	relapse	2665050	The favourable <b>relapse</b> rates with <strong>CBS</strong> might be explained by the permanent eradication of C. pylori.
+APOB	drug	alcohol	24051266	WHR, HOMA ir, systolic blood pressure, and <strong>ApoB</strong>/ApoA1 loaded significantly on the principal "metabolic factor", leisure time physical activity and self rated health loaded significantly on the "vitality factor", and smoking and <b>alcohol</b> consumption loaded significantly on the "addiction factor".
+APOB	drug	nicotine	24051266	WHR, HOMA ir, systolic blood pressure, and <strong>ApoB</strong>/ApoA1 loaded significantly on the principal "metabolic factor", leisure time physical activity and self rated health loaded significantly on the "vitality factor", and <b>smoking</b> and alcohol consumption loaded significantly on the "addiction factor".
+APOB	addiction	addiction	24051266	WHR, HOMA ir, systolic blood pressure, and <strong>ApoB</strong>/ApoA1 loaded significantly on the principal "metabolic factor", leisure time physical activity and self rated health loaded significantly on the "vitality factor", and smoking and alcohol consumption loaded significantly on the "<b>addiction</b> factor".
+APOB	drug	nicotine	23541965	Levels of OxPL/<strong>apoB</strong> were positively associated with risk of PAD in men and women: pooled relative risk: 1.37, 95% confidence interval: 1.19 to 1.58 for each 1 SD increase after adjusting age, <b>smoking</b>, fasting status, month of blood draw, lipids, body mass index, and other cardiovascular disease risk factors.
+APOB	drug	opioid	21453194	The aim was to evaluate the frequency in serum lipid disturbances of hepatitis C virus (HCV) seronegative <b>heroin</b> addicts; the capacity of high density lipoprotein (HDL) C and apolipoprotein B (<strong>apoB</strong>)/apolipoprotein A I (apoA I) for predicting hypertriglyceridemia/low HDL C profile; correlation of HDL C with the <strong>apoB</strong>/apoA I and their correlation to plasma apo/lipoproteins.
+APOB	drug	opioid	21453194	The aim was to evaluate the frequency in serum lipid disturbances of hepatitis C virus (HCV) seronegative <b>heroin</b> addicts; the capacity of high density lipoprotein (HDL) C and <strong>apolipoprotein B</strong> (<strong>apoB</strong>)/apolipoprotein A I (apoA I) for predicting hypertriglyceridemia/low HDL C profile; correlation of HDL C with the <strong>apoB</strong>/apoA I and their correlation to plasma apo/lipoproteins.
+APOB	drug	opioid	21453194	<strong>ApoB</strong>/apoA I showed stronger correlation with the observed apo/lipoproteins than the HDL C. The logistic regression model showed that <strong>apoB</strong>/apoA I index (OR 89.1, 95% CI 1.3 5971.2) is more significant predictor in developing hypertriglyceridemia/low HDL profile than HDL C. <b>Heroin</b> addiction is associated with decreased plasma concentrations of HDL C, apoA I, <strong>apoB</strong>, and increased TGL concentrations.
+APOB	addiction	addiction	21453194	<strong>ApoB</strong>/apoA I showed stronger correlation with the observed apo/lipoproteins than the HDL C. The logistic regression model showed that <strong>apoB</strong>/apoA I index (OR 89.1, 95% CI 1.3 5971.2) is more significant predictor in developing hypertriglyceridemia/low HDL profile than HDL C. Heroin <b>addiction</b> is associated with decreased plasma concentrations of HDL C, apoA I, <strong>apoB</strong>, and increased TGL concentrations.
+APOB	drug	opioid	21453194	In <b>heroin</b> addicts, HDL C concentrations are significantly associated with the <strong>apoB</strong>/apoA I index, which correlates to all lipid fractions and is a stronger predictor of metabolic syndrome lipid profile in <b>heroin</b> addicts.
+APOB	addiction	intoxication	16805392	During remission a general pattern of <strong>apoB</strong> containing LP was similar to the period of <b>intoxication</b>.
+APOB	drug	nicotine	16372134	These analyses revealed that R219K has a strong effect on apolipoprotein B (<strong>APOB</strong>) and LDL cholesterol (LDL C) among <b>smokers</b> (P = 0.000055 and P = 0.00059, respectively), but not among non <b>smokers</b>.
+APOB	drug	nicotine	16372134	These analyses revealed that R219K has a strong effect on <strong>apolipoprotein B</strong> (<strong>APOB</strong>) and LDL cholesterol (LDL C) among <b>smokers</b> (P = 0.000055 and P = 0.00059, respectively), but not among non <b>smokers</b>.
+APOB	drug	nicotine	16372134	Plasma <strong>APOB</strong> and LDL C, but not APOA1 and HDL C, were shown to be markedly elevated in <b>smokers</b> versus non <b>smokers</b>, affirming that <b>smoking</b> may selectively impact the former pathway.
+APOB	drug	alcohol	16272676	This study demonstrates the ability of TC, <strong>ApoB</strong> and LDL/HDL c (among lipid measures) and AST and GGT (among liver measures) in discriminating <b>alcohol</b> dependents from non dependent subjects.
+APOB	drug	alcohol	12963008	<b>Alcohol</b> ingestion along with a fat load increases the number (increased net <strong>apoB48</strong> secretion) and reduces the size (reduced TAG/<strong>apoB48</strong> ratio) of CM secreted into the mesenteric lymph duct.
+APOB	drug	alcohol	12916168	Under intoxication disturbances the individual <strong>apoB</strong> containing fractions were minimal as compared with the control, while at the initial stages of <b>alcohol</b> abolition their redistribution was noticed as reflecting the growth of the processes of cholesterol transportation from liver to peripheral tissues.
+APOB	addiction	intoxication	12916168	Under <b>intoxication</b> disturbances the individual <strong>apoB</strong> containing fractions were minimal as compared with the control, while at the initial stages of alcohol abolition their redistribution was noticed as reflecting the growth of the processes of cholesterol transportation from liver to peripheral tissues.
+APOB	addiction	withdrawal	11981126	After <b>withdrawal</b>, concentrations of serum apoA I, LpA I, LpA I/A II, apoC III, LpC III non B, apoE, and LpE non B significantly decreased, whereas those of triglycerides and <strong>apoB</strong> increased; levels of cholesterol, LpC III:B, and LpB:E were not affected.
+APOB	addiction	withdrawal	11981126	Before <b>withdrawal</b>, no association between <strong>apoB</strong> level and apoE polymorphism was observed, whereas after abstinence, a borderline significant (p < or = 0.10) gradient of concentration across the three groups of subjects (epsilon2 carriers < epsilon3/epsilon3 < epsilon4 carriers) was noticed.
+APOB	drug	alcohol	11981126	Heavy <b>alcohol</b> consumption seems to alter the effect of apoE polymorphism on <strong>apoB</strong> levels, and further investigations are needed to clarify the mechanisms involved in this phenomenon: a defect in sialylation of apoE, formation of acetaldehyde adducts on <strong>apoB</strong>, or both.
+APOB	addiction	reward	11714857	In conclusion, this work, in addition to the <b>reinforcement</b> of the already known associations between <strong>APOB</strong>, APOE, and APOC3 genes and lipids, leads to new perspectives in the complex relationships among genes and environmental factors.
+APOB	drug	alcohol	1332524	To assess the effect of <b>alcohol</b> on these analytes, we determined the concentration of Lp(a), apolipoprotein A I, <strong>apolipoprotein B</strong>, total cholesterol, and high density lipoprotein cholesterol, and calculated low density lipoprotein cholesterol in serum of 12 patients meeting DSM III R criteria for <b>alcohol</b> dependence at the time of admission for treatment of <b>alcohol</b> withdrawal (before).
+APOB	addiction	dependence	1332524	To assess the effect of alcohol on these analytes, we determined the concentration of Lp(a), apolipoprotein A I, <strong>apolipoprotein B</strong>, total cholesterol, and high density lipoprotein cholesterol, and calculated low density lipoprotein cholesterol in serum of 12 patients meeting DSM III R criteria for alcohol <b>dependence</b> at the time of admission for treatment of alcohol withdrawal (before).
+APOB	addiction	withdrawal	1332524	To assess the effect of alcohol on these analytes, we determined the concentration of Lp(a), apolipoprotein A I, <strong>apolipoprotein B</strong>, total cholesterol, and high density lipoprotein cholesterol, and calculated low density lipoprotein cholesterol in serum of 12 patients meeting DSM III R criteria for alcohol dependence at the time of admission for treatment of alcohol <b>withdrawal</b> (before).
+APOB	drug	alcohol	1332524	<strong>Apolipoprotein B</strong> and low density lipoprotein cholesterol showed no significant changes before and after <b>alcohol</b> abstinence.
+APOB	drug	alcohol	1521980	Adjustment for age, body mass index, smoking, <b>alcohol</b> consumption, stress and tension at work, shift work, noise exposure and educational level in multiple linear regression analysis showed significant effects of the CS2 index on systolic BP, diastolic BP, cholesterol, HDL cholesterol, LDL cholesterol, apolipoprotein A1, <strong>apolipoprotein B</strong>, the LDL cholesterol/<strong>apolipoprotein B</strong> and HDL cholesterol/apolipoprotein A1 ratios; there were no significant effects on the triglycerides.
+APOB	drug	nicotine	1521980	Adjustment for age, body mass index, <b>smoking</b>, alcohol consumption, stress and tension at work, shift work, noise exposure and educational level in multiple linear regression analysis showed significant effects of the CS2 index on systolic BP, diastolic BP, cholesterol, HDL cholesterol, LDL cholesterol, apolipoprotein A1, <strong>apolipoprotein B</strong>, the LDL cholesterol/<strong>apolipoprotein B</strong> and HDL cholesterol/apolipoprotein A1 ratios; there were no significant effects on the triglycerides.
+APOB	drug	alcohol	1930937	The plasma concentrations and chemical compositions of the <strong>apolipoprotein B</strong> containing lipoproteins (VLDL, IDL and LDL) were studied in 29 male <b>alcoholic</b> subjects at the end of a drinking period and in 17 healthy controls.
+APOB	drug	alcohol	1930937	These studies suggest that the alterations in all the <strong>apoB</strong> containing lipoproteins may contribute to the delayed progression of atherosclerosis observed in <b>alcohol</b> users.
+APOB	addiction	intoxication	1878009	<b>Binge</b> drinking produced a selective increase in low density lipoprotein (LDL) cholesterol and <strong>apolipoprotein B</strong>, and a depression in the fractional LCAT rate (% esterified/min).
+APOB	addiction	intoxication	1878009	By contrast, when this same average weekly dose is concentrated in a <b>binge</b> cycle, unfavorable alterations in lipoprotein composition (increases LDL cholesterol, increases <strong>apolipoprotein B</strong>) and metabolism (decreases LCAT activity) occur along with weight loss and depletion of body fat.
+APOB	drug	alcohol	3607081	<strong>Apolipoprotein B</strong> was isolated from human plasma low density lipoprotein without precipitation by diethyl ether/<b>ethanol</b> extraction of the protein in 6 M guanidine hydrochloride.
+APOB	addiction	dependence	3607081	Furthermore, an irreversible temperature <b>dependence</b> of <strong>apolipoprotein B</strong> reduced viscosity indicated that residual structure remained in solutions of 6 M guanidine hydrochloride/20 mM dithiothreitol.
+SULT2A1	drug	opioid	30630161	The current study was designed to evaluate the effect of OT on withdrawal, craving and anxiety scores, cortisol and dehydroepiandrosterone sulphate (<strong>DHEAS</strong>) blood level in <b>heroin</b> dependent male patients.
+SULT2A1	addiction	relapse	30630161	The current study was designed to evaluate the effect of OT on withdrawal, <b>craving</b> and anxiety scores, cortisol and dehydroepiandrosterone sulphate (<strong>DHEAS</strong>) blood level in heroin dependent male patients.
+SULT2A1	addiction	withdrawal	30630161	The current study was designed to evaluate the effect of OT on <b>withdrawal</b>, craving and anxiety scores, cortisol and dehydroepiandrosterone sulphate (<strong>DHEAS</strong>) blood level in heroin dependent male patients.
+SULT2A1	drug	opioid	30630161	Single dose of OT decreased the level of cortisol and improved the cortisol/<strong>DHEAS</strong> ratio in the <b>heroin</b> users during abstinence (p < 0.01).
+SULT2A1	drug	opioid	29279713	<b>Tramadol</b> decreased the levels of serum cortisol and <strong>DHEAS</strong> hormones.
+SULT2A1	addiction	dependence	28807679	pH <b>Dependence</b> and kinetics experiments indicated that the catalytic properties of zebrafish Sult2 family members in mediating the sulfation of 5α cyprinol were different from those of either zebrafish Sult3st4 or human <strong>SULT2A1</strong>.
+SULT2A1	drug	alcohol	28807679	Collectively, these results imply that both Sult2st2 and Sult2st3 have evolved to sulfate specifically C27 bile <b>alcohol</b>, 5α cyprinol, in Cypriniform fish, whereas the enzymatic characteristics of zebrafish Sult3 members, particularly Sult3st4, correlated with those of human <strong>SULT2A1</strong>.
+SULT2A1	drug	nicotine	23771199	Dehydroepiandrosterone (DHEA) and DHEA sulfate (<strong>DHEAS</strong>) are neurosteroids that have been associated with mood measures as well as <b>smoking</b> status, and <b>nicotine</b> is associated with increased DHEA and <strong>DHEAS</strong> levels.
+SULT2A1	drug	nicotine	23771199	Given the difficulties with mood experienced by <b>smokers</b> with PTSD, the purpose of the current study was to evaluate the association between negative affect and anxiety sensitivity with DHEA and <strong>DHEAS</strong> levels.
+SULT2A1	drug	nicotine	23771199	Given that <b>nicotine</b> is known to elevate DHEA(S) levels, these results suggest that <strong>DHEAS</strong> may serve as a biomarker of the association between mood and <b>nicotine</b> among <b>smokers</b>.
+SULT2A1	drug	nicotine	23771199	Implications for the results include (1) the use of <strong>DHEAS</strong> measurement across time and across quit attempts and (2) the potential for careful use of DHEA supplementation to facilitate abstinence during <b>smoking</b> cessation.
+SULT2A1	drug	opioid	22946908	A systematic analysis using eleven known human SULTs revealed SULT1A3 and <strong>SULT2A1</strong> as the major responsible SULTs for the sulfation of, respectively, pentazocine and <b>buprenorphine</b>; whereas three other SULTs, SULT1A1, SULT1A2, and SULT1C4, were capable of sulfating <b>naloxone</b>.
+SULT2A1	addiction	dependence	22433179	To investigate whether long term exposure to the neurosteroid dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) induces adaptive changes of GABA(A) receptors related to the development of tolerance and <b>dependence</b>.
+SULT2A1	drug	benzodiazepine	22433179	We compared the parameters of [(3)H]<strong>DHEAS</strong> binding and the effects of <strong>DHEAS</strong> on [(3)H]<b>flunitrazepam</b> binding in the membranes of HEK 293 cells, nontransfected or stably transfected with recombinant α(1)β(2)γ(2S) GABA(A) receptors.
+SULT2A1	drug	benzodiazepine	22433179	In HEK 293 cells expressing α(1)β(2)γ(2S) GABA(A) receptors, we investigated the effects of long term <strong>DHEAS</strong> treatment on the [(3)H]<b>flunitrazepam</b> and [(3)H]t butylbicycloorthobenzoate ([(3)H]TBOB) binding and on their modulation with GABA.
+SULT2A1	drug	benzodiazepine	22433179	Exposure of cells to 100 μmol/l <strong>DHEAS</strong> for 48 h did not change the number or affinity of <b>benzodiazepine</b> and convulsive binding sites.
+SULT2A1	drug	benzodiazepine	22433179	Long term <strong>DHEAS</strong> treatment failed to affect functional allosteric interactions between GABA(A) receptor binding sites, as evidenced by an unchanged ability of GABA to stimulate or to inhibit [(3)H]<b>flunitrazepam</b> and [(3)H]TBOB binding, respectively.
+SULT2A1	addiction	dependence	22433179	The findings that prolonged <strong>DHEAS</strong> treatment does not produce changes in GABA(A) receptor expression and functional coupling, assumed to underlie the development of tolerance and <b>dependence</b>, might have importance in the long term therapy necessary for the observed beneficial effects of <strong>DHEAS</strong>.
+SULT2A1	addiction	dependence	21839837	To further investigate the sulfation of bile acids and bile alcohols by the two Zebra danio SULT3 STs and the human <strong>SULT2A1</strong>, pH <b>dependence</b> and kinetics of the sulfation of bile acids/alcohols were analyzed.
+SULT2A1	drug	alcohol	21839837	pH dependence experiments showed that the mechanisms underlying substrate recognition for the sulfation of lithocholic acid (a bile acid) and 5α petromyzonol (a bile <b>alcohol</b>) differed between the human <strong>SULT2A1</strong> and the Zebra danio SULT3 ST2 and ST3.
+SULT2A1	addiction	dependence	21839837	pH <b>dependence</b> experiments showed that the mechanisms underlying substrate recognition for the sulfation of lithocholic acid (a bile acid) and 5α petromyzonol (a bile alcohol) differed between the human <strong>SULT2A1</strong> and the Zebra danio SULT3 ST2 and ST3.
+SULT2A1	addiction	dependence	21598681	It had been shown that the blockade with dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) affects enhanced aldosterone level in doses 1, 5 and 30 mg/kg without the dose <b>dependence</b> under multi repeated cold exposure.
+SULT2A1	drug	opioid	21598681	These <strong>DHEAS</strong> effects are realized through micro <b>opioid</b> receptors.
+SULT2A1	drug	opioid	21598681	The <strong>DHEAS</strong> (30 mg/kg) blocking effect was manifested too, but not through micro <b>opioid</b> receptors under acute cold exposure.
+SULT2A1	drug	alcohol	17913324	Serum levels of basal cortisol and dehydroepiandrosterone sulphate (<strong>DHEAS</strong>) were measured three times, and cortisol and <strong>DHEAS</strong> response to dexamethasone twice during the early and late withdrawal periods in <b>alcohol</b> dependent males (n=30) and once in healthy control males (n=20).
+SULT2A1	addiction	withdrawal	17913324	Serum levels of basal cortisol and dehydroepiandrosterone sulphate (<strong>DHEAS</strong>) were measured three times, and cortisol and <strong>DHEAS</strong> response to dexamethasone twice during the early and late <b>withdrawal</b> periods in alcohol dependent males (n=30) and once in healthy control males (n=20).
+SULT2A1	addiction	withdrawal	17913324	The study revealed reduced basal <strong>DHEAS</strong> levels and reduced <strong>DHEAS</strong> response to dexamethasone in late <b>withdrawal</b>.
+SULT2A1	addiction	withdrawal	17913324	While basal <strong>DHEAS</strong> levels were low in the high aggression group only in early <b>withdrawal</b>, it was reduced in the low aggression group during late <b>withdrawal</b> period.
+SULT2A1	drug	alcohol	17511983	In the present report, we attempted to examine whether neurosteroids progesterone and dehydroepiandrosterone sulphate (<strong>DHEAS</strong>), which modulate gamma aminobutyric acid (GABA(A)) receptor function, affects development of tolerance to <b>ethanol</b> anxiolysis and withdrawal anxiety.
+SULT2A1	addiction	withdrawal	17511983	In the present report, we attempted to examine whether neurosteroids progesterone and dehydroepiandrosterone sulphate (<strong>DHEAS</strong>), which modulate gamma aminobutyric acid (GABA(A)) receptor function, affects development of tolerance to ethanol anxiolysis and <b>withdrawal</b> anxiety.
+SULT2A1	drug	alcohol	17511983	Rats on <b>ethanol</b> (6% v/v in nutritionally balanced liquid diet) for prolong period (10 days) were injected twice daily either with vehicle, progesterone (a precursor of allopregnanolone, positive GABA(A) receptor modulator), finasteride (5alpha reductase inhibitor) or <strong>DHEAS</strong> (negative GABA(A) receptor modulator).
+SULT2A1	drug	alcohol	17511983	While progesterone significantly advanced the development of tolerance to <b>ethanol</b> anxiolysis and enhanced withdrawal anxiety, <strong>DHEAS</strong> and finasteride prevented such behavioral alterations.
+SULT2A1	addiction	withdrawal	17511983	While progesterone significantly advanced the development of tolerance to ethanol anxiolysis and enhanced <b>withdrawal</b> anxiety, <strong>DHEAS</strong> and finasteride prevented such behavioral alterations.
+SULT2A1	drug	alcohol	17511983	These data highlight the important role played by GABAergic neurosteroids progesterone and <strong>DHEAS</strong> in the development of tolerance to <b>ethanol</b> anxiolysis and withdrawal anxiety in rats.
+SULT2A1	addiction	withdrawal	17511983	These data highlight the important role played by GABAergic neurosteroids progesterone and <strong>DHEAS</strong> in the development of tolerance to ethanol anxiolysis and <b>withdrawal</b> anxiety in rats.
+SULT2A1	drug	cocaine	16908055	It has been hypothesized that increased baseline dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) levels may act as a natural antidepressant to attenuate negative affect during <b>cocaine</b> withdrawal and abstinence, decreasing the probability of relapse.
+SULT2A1	addiction	relapse	16908055	It has been hypothesized that increased baseline dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) levels may act as a natural antidepressant to attenuate negative affect during cocaine withdrawal and abstinence, decreasing the probability of <b>relapse</b>.
+SULT2A1	addiction	withdrawal	16908055	It has been hypothesized that increased baseline dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) levels may act as a natural antidepressant to attenuate negative affect during cocaine <b>withdrawal</b> and abstinence, decreasing the probability of relapse.
+SULT2A1	addiction	withdrawal	16908055	These findings suggest that, although <strong>DHEAS</strong> related enhancement of resiliency to <b>withdrawal</b> may occur, the extent of this protective effect may be modulated by additional factors that warrant further research.
+SULT2A1	drug	nicotine	16609903	To determine whether changes in plasma cortisol, DHEA, or <strong>DHEAS</strong> levels and emergence of depressive symptoms during <b>smoking</b> cessation are associated with <b>smoking</b> relapse.
+SULT2A1	addiction	relapse	16609903	To determine whether changes in plasma cortisol, DHEA, or <strong>DHEAS</strong> levels and emergence of depressive symptoms during smoking cessation are associated with smoking <b>relapse</b>.
+SULT2A1	drug	nicotine	16402195	<b>Nicotine</b> administration alters neuroactive steroids in rodent models, and serum levels of the neuroactive steroid <strong>DHEAS</strong> (dehydroepiandrosterone sulfate) appear to be higher in <b>smokers</b>.
+SULT2A1	drug	nicotine	16402195	This study aims to investigate <strong>DHEAS</strong>, allopregnanolone, pregnenolone, and other steroids in male <b>smokers</b> to determine potential associations with <b>nicotine</b> dependence severity and negative affect.
+SULT2A1	addiction	dependence	16402195	This study aims to investigate <strong>DHEAS</strong>, allopregnanolone, pregnenolone, and other steroids in male smokers to determine potential associations with nicotine <b>dependence</b> severity and negative affect.
+SULT2A1	drug	nicotine	16402195	Allopregnanolone and pregnenolone serum levels were determined by gas chromatography/mass spectrometry, while <strong>DHEAS</strong> and other steroid levels were determined by radioimmunoassay in 28 male <b>smokers</b>.
+SULT2A1	addiction	addiction	16402195	<strong>DHEAS</strong> levels were inversely correlated with the negative affect subscale of the Shiffman Jarvik Withdrawal Questionnaire (r= 0.60, p=0.002) and the RTS craving item (r= 0.43, p=0.03), and tended to be inversely correlated with the FTND scores (r= 0.38, p=0.067) and the ISMQ <b>addiction</b> subscale (r= 0.38, p=0.059), adjusting for age.
+SULT2A1	addiction	relapse	16402195	<strong>DHEAS</strong> levels were inversely correlated with the negative affect subscale of the Shiffman Jarvik Withdrawal Questionnaire (r= 0.60, p=0.002) and the RTS <b>craving</b> item (r= 0.43, p=0.03), and tended to be inversely correlated with the FTND scores (r= 0.38, p=0.067) and the ISMQ addiction subscale (r= 0.38, p=0.059), adjusting for age.
+SULT2A1	addiction	withdrawal	16402195	<strong>DHEAS</strong> levels were inversely correlated with the negative affect subscale of the Shiffman Jarvik <b>Withdrawal</b> Questionnaire (r= 0.60, p=0.002) and the RTS craving item (r= 0.43, p=0.03), and tended to be inversely correlated with the FTND scores (r= 0.38, p=0.067) and the ISMQ addiction subscale (r= 0.38, p=0.059), adjusting for age.
+SULT2A1	drug	nicotine	16402195	<strong>DHEAS</strong> levels were inversely correlated with negative affect and craving measures, and may predict <b>nicotine</b> dependence severity.
+SULT2A1	addiction	dependence	16402195	<strong>DHEAS</strong> levels were inversely correlated with negative affect and craving measures, and may predict nicotine <b>dependence</b> severity.
+SULT2A1	addiction	relapse	16402195	<strong>DHEAS</strong> levels were inversely correlated with negative affect and <b>craving</b> measures, and may predict nicotine dependence severity.
+SULT2A1	drug	cocaine	16309898	Chronic <b>cocaine</b> self administration induced elevation in brain DHEA, its sulfate ester, <strong>DHEAS</strong>, and pregnenolone.
+SULT2A1	drug	alcohol	15894035	Some progesterone metabolites, including three pregnanolone isomers (PI), abate, while pregnenolone sulfate (PregS) and dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) increase, <b>alcohol</b> tolerance.
+SULT2A1	drug	opioid	15456529	In contrast, there were no significant effects of <b>morphine</b> dependence on the brain concentrations of allopregnanolone (AP), dihydroepiandrosterone (DHEA), and dihydroepiandrosterone sulfate (<strong>DHEAS</strong>).
+SULT2A1	addiction	dependence	15456529	In contrast, there were no significant effects of morphine <b>dependence</b> on the brain concentrations of allopregnanolone (AP), dihydroepiandrosterone (DHEA), and dihydroepiandrosterone sulfate (<strong>DHEAS</strong>).
+SULT2A1	drug	opioid	15456529	<b>Naloxone</b> induced withdrawal produced a significant increase in the concentrations of PREG, PROG, AP, DHEA, PREGS, and <strong>DHEAS</strong> as compared with the control group.
+SULT2A1	addiction	withdrawal	15456529	Naloxone induced <b>withdrawal</b> produced a significant increase in the concentrations of PREG, PROG, AP, DHEA, PREGS, and <strong>DHEAS</strong> as compared with the control group.
+SULT2A1	drug	cocaine	15358439	<strong>DHEAS</strong> and POMS measures identify <b>cocaine</b> dependence treatment outcome.
+SULT2A1	addiction	dependence	15358439	<strong>DHEAS</strong> and POMS measures identify cocaine <b>dependence</b> treatment outcome.
+SULT2A1	drug	cocaine	15358439	Quantitative urine levels of the <b>cocaine</b> metabolite benzoylecgonine (BE) and other substance of abuse analytes, plasma levels of <strong>DHEAS</strong>, DHEA, cortisol, and prolactin, and the profile of mood states (POMS) were serially measured in 38 male <b>cocaine</b> dependent (DSM IV) patients and in 28 controls of similar gender and age over a six month study.
+SULT2A1	drug	cocaine	15358439	When treatment outcome was collapsed into whether patients completed (ABST) or did not complete 90 days of treatment (90N), ABST plasma <strong>DHEAS</strong> and cortisol were significantly elevated compared to the 90N patients and controls across the first 3 weeks of <b>cocaine</b> withdrawal.
+SULT2A1	addiction	withdrawal	15358439	When treatment outcome was collapsed into whether patients completed (ABST) or did not complete 90 days of treatment (90N), ABST plasma <strong>DHEAS</strong> and cortisol were significantly elevated compared to the 90N patients and controls across the first 3 weeks of cocaine <b>withdrawal</b>.
+SULT2A1	addiction	withdrawal	15358439	In the ABST patients, distressed mood during <b>withdrawal</b> may have been mitigated through antidepressant like actions of enhanced endogenous <strong>DHEAS</strong> activity, thus contributing to improved abstinence and treatment retention.
+SULT2A1	drug	opioid	15196791	In the present study, we investigated how the neurosteroid, dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) affects the development of <b>morphine</b> dependence and tolerance in mice.
+SULT2A1	addiction	dependence	15196791	In the present study, we investigated how the neurosteroid, dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) affects the development of morphine <b>dependence</b> and tolerance in mice.
+SULT2A1	drug	opioid	15196791	Co administration of <strong>DHEAS</strong> (10 mg/kg) with <b>morphine</b> significantly inhibited the development, but not the expression, of tolerance to <b>morphine</b> induced analgesia and the <b>naloxone</b> precipitated withdrawal.
+SULT2A1	addiction	withdrawal	15196791	Co administration of <strong>DHEAS</strong> (10 mg/kg) with morphine significantly inhibited the development, but not the expression, of tolerance to morphine induced analgesia and the naloxone precipitated <b>withdrawal</b>.
+SULT2A1	drug	opioid	15196791	The expression of c fos mRNA was observed in the frontal cortex and thalamus of mice showing signs of <b>naloxone</b> precipitated withdrawal, while the expression of c fos mRNA was significantly diminished by co administration of <strong>DHEAS</strong> with <b>morphine</b>.
+SULT2A1	addiction	withdrawal	15196791	The expression of c fos mRNA was observed in the frontal cortex and thalamus of mice showing signs of naloxone precipitated <b>withdrawal</b>, while the expression of c fos mRNA was significantly diminished by co administration of <strong>DHEAS</strong> with morphine.
+SULT2A1	drug	opioid	15196791	On the <b>naloxone</b> precipitated withdrawal, mice showed a significant elevation of cyclic AMP (cAMP) levels in the thalamus, whereas chronic administration of <strong>DHEAS</strong> with <b>morphine</b> did not affect the increase in cAMP.
+SULT2A1	addiction	withdrawal	15196791	On the naloxone precipitated <b>withdrawal</b>, mice showed a significant elevation of cyclic AMP (cAMP) levels in the thalamus, whereas chronic administration of <strong>DHEAS</strong> with morphine did not affect the increase in cAMP.
+SULT2A1	drug	opioid	15196791	Interestingly, repeated co administration of <strong>DHEAS</strong> with <b>morphine</b> prevented the withdrawal induced phosphorylation of extracellular signal regulated protein kinase (ERK) 2 in the frontal cortex.
+SULT2A1	addiction	withdrawal	15196791	Interestingly, repeated co administration of <strong>DHEAS</strong> with morphine prevented the <b>withdrawal</b> induced phosphorylation of extracellular signal regulated protein kinase (ERK) 2 in the frontal cortex.
+SULT2A1	drug	opioid	15196791	These results showed that <strong>DHEAS</strong> prevented the development of <b>morphine</b> tolerance and dependence and suggested that the attenuating effects of <strong>DHEAS</strong> might result from the regulation of c fos mRNA expression, which is possibly involved the signaling activation of ERK, but not of cAMP pathway.
+SULT2A1	addiction	dependence	15196791	These results showed that <strong>DHEAS</strong> prevented the development of morphine tolerance and <b>dependence</b> and suggested that the attenuating effects of <strong>DHEAS</strong> might result from the regulation of c fos mRNA expression, which is possibly involved the signaling activation of ERK, but not of cAMP pathway.
+SULT2A1	drug	benzodiazepine	11311894	Dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (<strong>DHEAS</strong>) inhibited the binding of [(3)H]<b>flunitrazepam</b> (2 nM), [(3)H]muscimol (5 nM) and 4 nM [(35)S]t butylbicyclophosphorothionate [(35)S]TBPS in the rat cerebellum as well as cerebral cortex.
+SULT2A1	drug	alcohol	11311894	<strong>DHEAS</strong>, unlike DHEA, inhibited [(3)H]flunitrazepam binding significantly to a lesser extent in the cerebellum of <b>ethanol</b> dependent rats as compared to the control group (I(max):82+/ 1vs.92+/ 2%, p<0.005).
+SULT2A1	drug	benzodiazepine	11311894	<strong>DHEAS</strong>, unlike DHEA, inhibited [(3)H]<b>flunitrazepam</b> binding significantly to a lesser extent in the cerebellum of ethanol dependent rats as compared to the control group (I(max):82+/ 1vs.92+/ 2%, p<0.005).
+SULT2A1	drug	alcohol	11311894	However, DHEA, unlike <strong>DHEAS</strong>, inhibited [(35)S]TBPS binding to a greater extent in the <b>ethanol</b> dependent rat cerebellum as compared to the control group (I(max):31+/ 2vs.19+/ 2%, p<0.005).
+SULT2A1	drug	alcohol	9266103	Trend for increasing <strong>DHEAS</strong> with <b>alcohol</b> consumption was also statistically significant after controlling for age and history of hysterectomy (p for trend = 0.01).
+RGS9	addiction	addiction	30006367	In this study, we examined the cellular and molecular mechanisms underlying the action of <strong>RGS9</strong> 2, a key GPCR regulator in MSNs implicated in both movement control and actions of <b>addictive</b> drugs.
+RGS9	drug	psychedelics	30006367	Accordingly, male mice lacking <strong>RGS9</strong> 2 displayed behavioral hypersensitivity to NMDAR blockade by MK 801 or <b>ketamine</b>.
+RGS9	drug	opioid	28074831	<strong>RGS9</strong> 2 Modulates Responses to <b>Oxycodone</b> in Pain Free and Chronic Pain States.
+RGS9	drug	opioid	28074831	Regulator of G protein signaling 9 2 (<strong>RGS9</strong> 2) is a striatal enriched signal transduction modulator known to have a critical role in the development of addiction related behaviors following exposure to psychostimulants or <b>opioids</b>.
+RGS9	addiction	addiction	28074831	Regulator of G protein signaling 9 2 (<strong>RGS9</strong> 2) is a striatal enriched signal transduction modulator known to have a critical role in the development of <b>addiction</b> related behaviors following exposure to psychostimulants or opioids.
+RGS9	drug	opioid	28074831	<strong>Regulator of G protein signaling 9</strong> 2 (<strong>RGS9</strong> 2) is a striatal enriched signal transduction modulator known to have a critical role in the development of addiction related behaviors following exposure to psychostimulants or <b>opioids</b>.
+RGS9	addiction	addiction	28074831	<strong>Regulator of G protein signaling 9</strong> 2 (<strong>RGS9</strong> 2) is a striatal enriched signal transduction modulator known to have a critical role in the development of <b>addiction</b> related behaviors following exposure to psychostimulants or opioids.
+RGS9	drug	opioid	28074831	<strong>RGS9</strong> 2 controls the function of several G protein coupled receptors, including dopamine receptor and mu <b>opioid</b> receptor (MOR).
+RGS9	drug	opioid	28074831	We previously showed that <strong>RGS9</strong> 2 complexes negatively control <b>morphine</b> analgesia, and promote the development of <b>morphine</b> tolerance.
+RGS9	drug	opioid	28074831	In contrast, <strong>RGS9</strong> 2 positively modulates the actions of other <b>opioid</b> analgesics, such as <b>fentanyl</b> and <b>methadone</b>.
+RGS9	drug	opioid	28074831	Here we investigate the role of <strong>RGS9</strong> 2 in regulating responses to <b>oxycodone</b>, an MOR agonist prescribed for the treatment of severe pain conditions that has addictive properties.
+RGS9	addiction	addiction	28074831	Here we investigate the role of <strong>RGS9</strong> 2 in regulating responses to oxycodone, an MOR agonist prescribed for the treatment of severe pain conditions that has <b>addictive</b> properties.
+RGS9	drug	opioid	28074831	Using mice lacking the <strong>Rgs9</strong> gene (RGS9KO), we demonstrate that <strong>RGS9</strong> 2 positively regulates the rewarding effects of <b>oxycodone</b> in pain free states, and in a model of neuropathic pain.
+RGS9	drug	opioid	28074831	Furthermore, although <strong>RGS9</strong> 2 does not affect the analgesic efficacy of <b>oxycodone</b> or the expression of physical withdrawal, it opposes the development of <b>oxycodone</b> tolerance, in both acute pain and chronic neuropathic pain models.
+RGS9	addiction	withdrawal	28074831	Furthermore, although <strong>RGS9</strong> 2 does not affect the analgesic efficacy of oxycodone or the expression of physical <b>withdrawal</b>, it opposes the development of oxycodone tolerance, in both acute pain and chronic neuropathic pain models.
+RGS9	drug	cocaine	27261631	Animals abstinent from chronic <b>cocaine</b> showed decreased expression of regulator of G protein signaling 2 (RGS2) and RGS4, as well as upregulation of <strong>RGS9</strong>.
+RGS9	addiction	reward	26811338	In the nervous system, RGS7 and <strong>RGS9</strong> 2 play essential role in vision, <b>reward</b> processing, and movement control.
+RGS9	drug	opioid	26305935	The striatal protein Regulator of G protein signaling 9 2 (<strong>RGS9</strong> 2) plays a key modulatory role in <b>opioid</b>, monoamine, and other G protein coupled receptor responses.
+RGS9	drug	opioid	26305935	The striatal protein <strong>Regulator of G protein signaling 9</strong> 2 (<strong>RGS9</strong> 2) plays a key modulatory role in <b>opioid</b>, monoamine, and other G protein coupled receptor responses.
+RGS9	addiction	reward	26305935	Here, we use the murine spared nerve injury model of neuropathic pain to investigate the mechanism by which <strong>RGS9</strong> 2 in the nucleus accumbens (NAc), a brain region involved in mood, <b>reward</b>, and motivation, modulates the actions of tricyclic antidepressants (TCAs).
+RGS9	drug	opioid	25591550	Evidence for the contribution of genetic variations in <strong>regulator of G protein signaling 9</strong> to the genetic susceptibility of <b>heroin</b> dependence.
+RGS9	addiction	dependence	25591550	Evidence for the contribution of genetic variations in <strong>regulator of G protein signaling 9</strong> to the genetic susceptibility of heroin <b>dependence</b>.
+RGS9	drug	opioid	25591550	<strong>RGS9</strong>‑2, a brain‑specific splice variant of the <strong>RGS9</strong> gene, is highly expressed in the striatum but lowly expressed in the periaqueductal gray and spinal cord, which mediate various actions of <b>morphine</b> and other opiates.
+RGS9	drug	opioid	25591550	In order to identify the markers that contribute to the genetic susceptibility of <b>heroin</b> dependence, the potential association between <b>heroin</b> dependence and 10 single nucleotide polymorphisms (SNPs), including rs8077696, rs8070231, rs2292593, rs2292592, rs9916525, rs1122079, rs4790953, rs1530351, rs4791230 and rs2869577 of the <strong>RGS9</strong> gene was evaluated using the MassARRAY system.
+RGS9	addiction	dependence	25591550	In order to identify the markers that contribute to the genetic susceptibility of heroin <b>dependence</b>, the potential association between heroin <b>dependence</b> and 10 single nucleotide polymorphisms (SNPs), including rs8077696, rs8070231, rs2292593, rs2292592, rs9916525, rs1122079, rs4790953, rs1530351, rs4791230 and rs2869577 of the <strong>RGS9</strong> gene was evaluated using the MassARRAY system.
+RGS9	drug	opioid	25591550	The results revealed that two SNPs (rs1530351 and rs4791230) located in the promoter region of the <strong>RGS9</strong> gene, were significantly associated with <b>heroin</b> dependence (P<0.05).
+RGS9	addiction	dependence	25591550	The results revealed that two SNPs (rs1530351 and rs4791230) located in the promoter region of the <strong>RGS9</strong> gene, were significantly associated with heroin <b>dependence</b> (P<0.05).
+RGS9	drug	opioid	25591550	These findings indicate a role for <strong>RGS9</strong> gene polymorphisms in <b>heroin</b> dependence and may be informative for future genetic or biological studies on <b>heroin</b> dependence.
+RGS9	addiction	dependence	25591550	These findings indicate a role for <strong>RGS9</strong> gene polymorphisms in heroin <b>dependence</b> and may be informative for future genetic or biological studies on heroin <b>dependence</b>.
+RGS9	drug	amphetamine	25455864	Effects of gender on locomotor sensitivity to <b>amphetamine</b>, body weight, and fat mass in regulator of G protein signaling 9 (<strong>RGS9</strong>) knockout mice.
+RGS9	drug	amphetamine	25455864	Effects of gender on locomotor sensitivity to <b>amphetamine</b>, body weight, and fat mass in <strong>regulator of G protein signaling 9</strong> (<strong>RGS9</strong>) knockout mice.
+RGS9	addiction	sensitization	25455864	<strong>RGS9</strong> knockout (KO) mice show increased psychostimulant induced behavioral <b>sensitization</b>, as well as exhibit higher body weights and greater fat accumulation compared to wild type (WT) littermates.
+RGS9	drug	amphetamine	25455864	Female <strong>RGS9</strong> KO mice exhibited greater locomotor sensitization to <b>amphetamine</b> (1.0mg/kg) treatment as compared to male <strong>RGS9</strong> KO mice.
+RGS9	addiction	sensitization	25455864	Female <strong>RGS9</strong> KO mice exhibited greater locomotor <b>sensitization</b> to amphetamine (1.0mg/kg) treatment as compared to male <strong>RGS9</strong> KO mice.
+RGS9	drug	opioid	24561386	Nucleus accumbens specific interventions in <strong>RGS9</strong> 2 activity modulate responses to <b>morphine</b>.
+RGS9	drug	opioid	24561386	Our recent work identified <strong>Rgs9</strong> 2 complexes in the striatum associated with acute or chronic exposures to mu <b>opioid</b> receptor (MOR) agonists.
+RGS9	addiction	addiction	24561386	In this study we use several new genetic tools that allow manipulations of <strong>Rgs9</strong> 2 activity in particular brain regions of adult mice in order to better understand the mechanism via which this protein modulates opiate <b>addiction</b> and analgesia.
+RGS9	drug	opioid	24561386	We used adeno associated viruses (AAVs) to express forms of <strong>Rgs9</strong> 2 in the dorsal and ventral striatum (nucleus accumbens, NAc) in order to examine the influence of this protein in <b>morphine</b> actions.
+RGS9	drug	opioid	24561386	Consistent with earlier behavioural findings from constitutive <strong>Rgs9</strong> knockout mice, we show that <strong>Rgs9</strong> 2 actions in the NAc modulate <b>morphine</b> reward and dependence.
+RGS9	addiction	dependence	24561386	Consistent with earlier behavioural findings from constitutive <strong>Rgs9</strong> knockout mice, we show that <strong>Rgs9</strong> 2 actions in the NAc modulate morphine reward and <b>dependence</b>.
+RGS9	addiction	reward	24561386	Consistent with earlier behavioural findings from constitutive <strong>Rgs9</strong> knockout mice, we show that <strong>Rgs9</strong> 2 actions in the NAc modulate morphine <b>reward</b> and dependence.
+RGS9	drug	opioid	24561386	Notably, <strong>Rgs9</strong> 2 in the NAc affects the analgesic actions of <b>morphine</b> as well as the development of analgesic tolerance.
+RGS9	drug	opioid	24561386	Using optogenetics we demonstrate that activation of Channelrhodopsin2 in <strong>Rgs9</strong> 2 expressing neurons, or in D1 dopamine receptor (Drd1) enriched medium spiny neurons, accelerates the development of <b>morphine</b> tolerance, whereas activation of D2 dopamine receptor (Drd2) enriched neurons does not significantly affect the development of tolerance.
+RGS9	drug	opioid	23857581	In neurons of the striatum, two RGS proteins, RGS7 and <strong>RGS9</strong> 2, regulate signaling by μ <b>opioid</b> receptor (MOR) and dopamine D2 receptor (D2R) and are implicated in drug addiction, movement disorders, and nociception.
+RGS9	addiction	addiction	23857581	In neurons of the striatum, two RGS proteins, RGS7 and <strong>RGS9</strong> 2, regulate signaling by μ opioid receptor (MOR) and dopamine D2 receptor (D2R) and are implicated in drug <b>addiction</b>, movement disorders, and nociception.
+RGS9	addiction	sensitization	22932702	The complex of G protein regulator <strong>RGS9</strong> 2 and Gβ(5) controls <b>sensitization</b> and signaling kinetics of type 5 adenylyl cyclase in the striatum.
+RGS9	drug	opioid	22932702	We showed that the complex of the ninth regulator of G protein signaling (<strong>RGS9</strong> 2) with the G protein β subunit (Gβ(5)) critically controlled signaling from dopamine and <b>opioid</b> GPCRs to AC5 in the striatum.
+RGS9	drug	opioid	22932702	Mice lacking <strong>RGS9</strong> showed increased cAMP production and, upon withdrawal from <b>opioid</b> administration, enhanced sensitization of AC5.
+RGS9	addiction	sensitization	22932702	Mice lacking <strong>RGS9</strong> showed increased cAMP production and, upon withdrawal from opioid administration, enhanced <b>sensitization</b> of AC5.
+RGS9	addiction	withdrawal	22932702	Mice lacking <strong>RGS9</strong> showed increased cAMP production and, upon <b>withdrawal</b> from opioid administration, enhanced sensitization of AC5.
+RGS9	addiction	sensitization	22932702	Our findings establish <strong>RGS9</strong> 2/Gβ(5) complexes as regulators of three key aspects of cAMP signaling: basal activity, <b>sensitization</b>, and temporal kinetics of AC5, thus highlighting the role of this complex in regulating both inhibitory and stimulatory GPCRs that shape cAMP signaling in the striatum.
+RGS9	drug	opioid	22129844	Several members of this family, in particular RGS4 and <strong>RGS9</strong> 2 have been demonstrated to influence MOR signaling and <b>morphine</b> induced behaviors, including reward.
+RGS9	addiction	reward	22129844	Several members of this family, in particular RGS4 and <strong>RGS9</strong> 2 have been demonstrated to influence MOR signaling and morphine induced behaviors, including <b>reward</b>.
+RGS9	drug	opioid	22129844	Moreover, this interaction is not unidirectional since <b>morphine</b> has been demonstrated to modulate expression levels of RGS proteins, especially RGS4 and <strong>RGS9</strong> 2, in a tissue and time dependent manner.
+RGS9	drug	opioid	22089315	<strong>RGS9</strong> 2 is a potent negative modulator of opiate and psychostimulant addiction and promotes the development of analgesic tolerance to <b>morphine</b>, whereas the role of RGS6 and RGS7 in addiction remains unknown.
+RGS9	addiction	addiction	22089315	<strong>RGS9</strong> 2 is a potent negative modulator of opiate and psychostimulant <b>addiction</b> and promotes the development of analgesic tolerance to morphine, whereas the role of RGS6 and RGS7 in <b>addiction</b> remains unknown.
+RGS9	drug	opioid	22056472	RGS4, <strong>RGS9</strong> and RGS10 levels were also studied in brains (frontal cortex) of rats submitted to acute and chronic <b>morphine</b> treatment and to spontaneous and <b>naloxone</b> precipitated opiate withdrawal.
+RGS9	addiction	withdrawal	22056472	RGS4, <strong>RGS9</strong> and RGS10 levels were also studied in brains (frontal cortex) of rats submitted to acute and chronic morphine treatment and to spontaneous and naloxone precipitated opiate <b>withdrawal</b>.
+RGS9	drug	opioid	22056472	Chronic <b>morphine</b> treatment in rats was associated with an increase in RGS4 protein immunoreactivity (Δ = 28 ± 7%), which persisted in spontaneous (Δ = 35 ± 8%) and <b>naloxone</b> precipitated withdrawal (Δ = 30 ± 9%) without significant changes in <strong>RGS9</strong> and RGS10 proteins.
+RGS9	addiction	withdrawal	22056472	Chronic morphine treatment in rats was associated with an increase in RGS4 protein immunoreactivity (Δ = 28 ± 7%), which persisted in spontaneous (Δ = 35 ± 8%) and naloxone precipitated <b>withdrawal</b> (Δ = 30 ± 9%) without significant changes in <strong>RGS9</strong> and RGS10 proteins.
+RGS9	drug	amphetamine	21886588	Association between the <strong>Regulator of G protein Signaling 9</strong> Gene and Patients with <b>Methamphetamine</b> Use Disorder and Schizophrenia.
+RGS9	drug	amphetamine	21886588	Therefore, we investigated the association between the <strong>RGS9</strong> gene and two related dopamine psychoses, schizophrenia and <b>methamphetamine</b> use disorders.
+RGS9	drug	amphetamine	21886588	The present study suggested that the <strong>RGS9</strong> gene is unlikely to play a major role in schizophrenia and <b>methamphetamine</b> dependence liability and/or the development of <b>methamphetamine</b> induced psychosis, at least in a Japanese population.
+RGS9	addiction	dependence	21886588	The present study suggested that the <strong>RGS9</strong> gene is unlikely to play a major role in schizophrenia and methamphetamine <b>dependence</b> liability and/or the development of methamphetamine induced psychosis, at least in a Japanese population.
+RGS9	drug	opioid	21741448	<strong>RGS9</strong> 2 modulates nociceptive behaviour and <b>opioid</b> mediated synaptic transmission in the spinal dorsal horn.
+RGS9	addiction	withdrawal	21741448	In the present study, we monitored tail <b>withdrawal</b> latencies to noxious thermal stimuli and performed in vitro whole cell patch clamp electrophysiological recordings from neurons in lamina II of the spinal dorsal horn to examine the role of <strong>RGS9</strong> 2 in the dorsal horn of the spinal cord in nociceptive behaviours and opiate mediated modulation of synaptic transmission.
+RGS9	drug	opioid	21741448	Our findings obtained from <strong>RGS9</strong> knockout mice indicate that the lack of <strong>RGS9</strong> 2 protein decreases sensitivity to thermal stimuli and to the analgesic actions of <b>morphine</b> in the tail immersion paradigm.
+RGS9	drug	opioid	21741448	This modulatory role of <strong>RGS9</strong> 2 on opiate mediated responses was further supported by electrophysiological studies showing that hyperpolarization of neurons in lamina II of the spinal dorsal horn evoked by application of DAMGO ([d Ala2, N MePhe4, Gly ol] enkephalin, a mu <b>opioid</b> receptor agonist) was diminished in <strong>RGS9</strong> knockout mice.
+RGS9	drug	opioid	21741448	The results indicate that <strong>RGS9</strong> 2 enhances the effect of <b>morphine</b> and may play a crucial role in opiate mediated analgesic mechanisms at the level of the spinal cord.
+RGS9	addiction	addiction	20477943	Regulator of G protein signaling 9 2 (<strong>RGS9</strong> 2), a member of the RGS family of GTPase accelerating proteins, is expressed specifically in the striatum, a brain region involved in controlling movement, motivation, mood and <b>addiction</b>.
+RGS9	addiction	addiction	20477943	<strong>Regulator of G protein signaling 9</strong> 2 (<strong>RGS9</strong> 2), a member of the RGS family of GTPase accelerating proteins, is expressed specifically in the striatum, a brain region involved in controlling movement, motivation, mood and <b>addiction</b>.
+RGS9	addiction	reward	20477943	<strong>RGS9</strong> 2 can be found co localized with D(2) class dopamine receptors in medium spiny striatal neurons and altered functioning of both <strong>RGS9</strong> 2 and D(2) like dopamine receptors have been implicated in schizophrenia, movement disorders and <b>reward</b> responses.
+RGS9	drug	opioid	20477943	In addition, the agonist mediated internalization of the G protein coupled delta <b>opioid</b> receptor was unaffected by <strong>RGS9</strong> 2 expression.
+RGS9	drug	opioid	20095651	In the mammalian nervous system, a member of the Regulator of G protein Signaling family, <strong>RGS9</strong> 2 (Regulator of G protein Signaling, type 9), is a key regulator of dopamine and <b>opioid</b> signaling pathways that mediate motor control and reward behavior.
+RGS9	addiction	reward	20095651	In the mammalian nervous system, a member of the Regulator of G protein Signaling family, <strong>RGS9</strong> 2 (Regulator of G protein Signaling, type 9), is a key regulator of dopamine and opioid signaling pathways that mediate motor control and <b>reward</b> behavior.
+RGS9	drug	cocaine	20043004	R7BP complexes with <strong>RGS9</strong> 2 and RGS7 in the striatum differentially control motor learning and locomotor responses to <b>cocaine</b>.
+RGS9	drug	opioid	20043004	In this study, we report that elimination of R7BP in mice results in motor coordination deficits and greater locomotor response to <b>morphine</b> administration, consistent with the essential role of R7BP in maintaining <strong>RGS9</strong> 2 expression in the striatum.
+RGS9	drug	cocaine	20043004	However, in contrast to previously reported observations with <strong>RGS9</strong> 2 knockouts, mice lacking R7BP do not show higher sensitivity to locomotor stimulating effects of <b>cocaine</b>.
+RGS9	drug	cocaine	20043004	Using a striatum specific knockdown approach, we show that the sensitivity of motor stimulation to <b>cocaine</b> is instead dependent on RGS7, whose complex formation with R7BP is dictated by <strong>RGS9</strong> 2 expression.
+RGS9	addiction	addiction	19211160	Among the RGS proteins expressed in the brain, <strong>RGS9</strong> 2 is very abundant in the striatum, a brain region involved in movement, motivation, mood and <b>addiction</b>.
+RGS9	drug	opioid	18094251	A member of regulator of G protein signaling family, <strong>RGS9</strong> 2, is an essential modulator of signaling through neuronal dopamine and <b>opioid</b> G protein coupled receptors.
+RGS9	addiction	reward	18094251	Recent findings indicate that the abundance of <strong>RGS9</strong> 2 determines sensitivity of signaling in the locomotor and <b>reward</b> systems in the striatum.
+RGS9	drug	amphetamine	17493623	Evidence for the involvement of ERbeta and <strong>RGS9</strong> 2 in 17 beta estradiol enhancement of <b>amphetamine</b> induced place preference behavior.
+RGS9	drug	amphetamine	17493623	How cocaine and <b>amphetamine</b> elicit more robust behavioral responses in females remains unclear, but studies have shown that the Regulator of G protein Signaling 9 2 (<strong>RGS9</strong> 2) protein is an important modulator of the behavioral responses to these drugs.
+RGS9	drug	cocaine	17493623	How <b>cocaine</b> and amphetamine elicit more robust behavioral responses in females remains unclear, but studies have shown that the Regulator of G protein Signaling 9 2 (<strong>RGS9</strong> 2) protein is an important modulator of the behavioral responses to these drugs.
+RGS9	drug	amphetamine	17493623	How cocaine and <b>amphetamine</b> elicit more robust behavioral responses in females remains unclear, but studies have shown that the <strong>Regulator of G protein Signaling 9</strong> 2 (<strong>RGS9</strong> 2) protein is an important modulator of the behavioral responses to these drugs.
+RGS9	drug	cocaine	17493623	How <b>cocaine</b> and amphetamine elicit more robust behavioral responses in females remains unclear, but studies have shown that the <strong>Regulator of G protein Signaling 9</strong> 2 (<strong>RGS9</strong> 2) protein is an important modulator of the behavioral responses to these drugs.
+RGS9	drug	amphetamine	17493623	The present studies were designed to further evaluate the involvement of <strong>RGS9</strong> 2 in estradiol enhancement of <b>amphetamine</b> induced place preference behavior and to examine which estrogen receptor subtype mediates the effect of estradiol.
+RGS9	drug	amphetamine	17493623	In situ hybridization histochemistry and Western blotting identified an inverse relationship between <strong>RGS9</strong> 2 protein expression in the nucleus accumbens shell and the hormonal enhancement of <b>amphetamine</b> induced place preference behavior.
+RGS9	drug	amphetamine	17493623	Moreover, treatment of ovariectomized female rats with the selective estrogen receptor beta agonist, diarylpropionitrile (1 mg/kg), for 2 weeks also facilitated <b>amphetamine</b> induced place preference behavior and selectively reduced nucleus accumbens shell <strong>RGS9</strong> 2 protein expression.
+RGS9	drug	opioid	15870291	Behavioral testing on mutant adults revealed subtle sensorimotor deficits but, so far, supported neither the proposed status of Rgs4 as a schizophrenia susceptibility gene (by showing intact prepulse inhibition in the mutants) nor (unlike another member of the Rgs family, <strong>Rgs9</strong>) a role of Rgs4 in the acute or chronic response to <b>opioids</b>.
+RGS9	drug	opioid	15199376	At 2 h after administering the acute <b>opioid</b>, RGS7 mRNA levels in the striatum plus those of <strong>RGS9</strong> 2 in the striatum and thalamus were increased, whereas <strong>RGS9</strong> 2 and RGS11 mRNA were reduced in the cortex.
+RGS9	drug	opioid	15199376	At 2 days after commencing sustained <b>morphine</b> treatment, the levels of mRNA for RGS7, <strong>RGS9</strong> 2, RGS11, and Gbeta5 increased in most of the brain structures studied (striatum, thalamus, periaqueductal gray matter (PAG), and cortex).
+RGS9	drug	opioid	15199376	In these <b>morphine</b> tolerant dependent mice, the greater changes were found for <strong>RGS9</strong> 2 in the thalamus (>500%) and PAG (>200%).
+RGS9	drug	opioid	15065220	Attenuation of chronic <b>morphine</b> effects after antisense oligodeoxynucleotide knock down of <strong>RGS9</strong> protein in cells expressing the cloned Mu <b>opioid</b> receptor.
+RGS9	drug	opioid	15065220	In the present study, we examined the effects of <b>morphine</b> treatment (1 microM, 20 h) on DAMGO stimulated high affinity [35S]GTP gamma S binding and DAMGO mediated inhibition of forskolin stimulated cAMP accumulation in HN9.10 cells stably expressing the cloned rat mu <b>opioid</b> receptor, in the absence and presence of the <strong>RGS9</strong> protein knock down condition (confirmed by Western blot analysis).
+RGS9	drug	opioid	15065220	<b>Morphine</b> treatment increased the EC50 (6.2 fold) for DAMGO mediated inhibition of forskolin stimulated cAMP activity in control cells but not in cells treated with AS 114 to knock down <strong>RGS9</strong>.
+RGS9	drug	opioid	15065220	These results provide additional evidence for involvement of <strong>RGS9</strong> protein in modulating <b>opioid</b> signaling, which may contribute to the development of <b>morphine</b> tolerance and dependence.
+RGS9	addiction	dependence	15065220	These results provide additional evidence for involvement of <strong>RGS9</strong> protein in modulating opioid signaling, which may contribute to the development of morphine tolerance and <b>dependence</b>.
+RGS9	drug	opioid	14595021	<strong>RGS9</strong> 2, a brain specific splice variant of the <strong>RGS9</strong> gene, is highly enriched in striatum and also expressed at much lower levels in periaqueductal gray and spinal cord, structures known to mediate various actions of <b>morphine</b> and other opiates.
+RGS9	drug	opioid	14595021	We show here that acute <b>morphine</b> administration increases expression of <strong>RGS9</strong> 2 in NAc and the other CNS regions, whereas chronic exposure decreases <strong>RGS9</strong> 2 levels.
+RGS9	drug	opioid	14595021	Mice lacking <strong>RGS9</strong> show enhanced behavioral responses to acute and chronic <b>morphine</b>, including a dramatic increase in <b>morphine</b> reward, increased <b>morphine</b> analgesia with delayed tolerance, and exacerbated <b>morphine</b> physical dependence and withdrawal.
+RGS9	addiction	dependence	14595021	Mice lacking <strong>RGS9</strong> show enhanced behavioral responses to acute and chronic morphine, including a dramatic increase in morphine reward, increased morphine analgesia with delayed tolerance, and exacerbated morphine physical <b>dependence</b> and withdrawal.
+RGS9	addiction	reward	14595021	Mice lacking <strong>RGS9</strong> show enhanced behavioral responses to acute and chronic morphine, including a dramatic increase in morphine <b>reward</b>, increased morphine analgesia with delayed tolerance, and exacerbated morphine physical dependence and withdrawal.
+RGS9	addiction	withdrawal	14595021	Mice lacking <strong>RGS9</strong> show enhanced behavioral responses to acute and chronic morphine, including a dramatic increase in morphine reward, increased morphine analgesia with delayed tolerance, and exacerbated morphine physical dependence and <b>withdrawal</b>.
+PRTN3	drug	cocaine	27579207	In this paper we report the case of a 23 year old female <b>cocaine</b> user that presented with purpuric rash and skin necrosis, found to have positive <strong>c ANCA</strong> and anti proteinase 3 antibodies.
+PRTN3	drug	cocaine	27579207	In this paper we report the case of a 23 year old female <b>cocaine</b> user that presented with purpuric rash and skin necrosis, found to have positive <strong>c ANCA</strong> and anti <strong>proteinase 3</strong> antibodies.
+PRTN3	addiction	relapse	26311010	Importantly, at time of the <b>relapse</b>, the patient became positive for both myeloperoxidase antineutrophil cytoplasmic antibody (ANCA) and <strong>proteinase 3</strong> ANCA.
+PRTN3	drug	cannabinoid	22425597	During the second phase of the study, doses of <b>THC</b> and <b>rimonabant</b> that did not affect the responses/total reinforced responses were chosen for further evaluation in a series of PR schedules with step sizes of <strong>PR 3</strong>, PR 5, PR 10, and PR exponential.
+PRTN3	addiction	reward	14665979	Opiate <b>reinforcement</b> was evaluated under a progressive ratio (PR) schedule often used for psychostimulant self administration (termed '<strong>PR 3</strong> 4' because the third response requirement was four lever presses) and three additional schedules that were modified to provide successively lower levels of difficulty by decreasing the steepness of response requirement progression (termed 'PR 9 4', 'PR 14 4', and 'PR 26 4' because a response requirement of four was reached with step numbers of 9, 14 and 26, respectively).
+PRTN3	drug	opioid	14665979	With the exception of the <strong>PR 3</strong> 4 schedule, all of the schedules supported <b>morphine</b> self administration, and <b>morphine</b> self administration during initial exposure and reacquisition did not differ by more than 10%.
+PRTN3	drug	cocaine	14665979	In contrast to morphine, <b>cocaine</b> was self administered under the <strong>PR 3</strong> 4 schedule, with responding clearly exceeding levels during extinction.
+PRTN3	drug	opioid	14665979	In contrast to <b>morphine</b>, cocaine was self administered under the <strong>PR 3</strong> 4 schedule, with responding clearly exceeding levels during extinction.
+PRTN3	drug	cocaine	14665979	This compares with a value of 21.0% for <b>cocaine</b> self administration under the <strong>PR 3</strong> 4 schedule compared to an FR 1 schedule.
+PRTN3	drug	alcohol	7892640	For women, factors linked to drug use were: <b>alcohol</b> consumption (PR6.5, CI:1.5 28.3); father drug user (<strong>PR 3</strong>.2, CI:1.1 9.5).
+PRTN3	drug	cocaine	7892640	For men, factors linked to drug use were: age (<strong>PR 3</strong>.2; CI: 1.5 7.4); non religious practice (PR 2.7, CI: 1.2 6.4); acquaintances who are users of marihuana, <b>cocaine</b> or heroine opium (PR 12.2, 6.6 and 7.0 respectively); and if the father, a brother or another relative are drug users (PR 4.1, 7.1 and 3.5 respectively).
+PER1	drug	cannabinoid	30526093	We report an association between several Single Nucleotide Polymorphism (SNP)s in main circadian genes SNPs, especially the gene locus HES7/<strong>PER1</strong> on chromosome 17 and <b>cannabis</b> consumption as well as the development of neuropsychiatric and social disorders.
+PER1	drug	opioid	28243713	In <strong>Per1</strong> Brdm1 null mutant mice and wild type (WT) littermates, we examined whether there were any differences in the development of <b>morphine</b> antinociception, tolerance to antinociception, withdrawal, sensitization to locomotion, and conditioned place preference (CPP).
+PER1	addiction	reward	28243713	In <strong>Per1</strong> Brdm1 null mutant mice and wild type (WT) littermates, we examined whether there were any differences in the development of morphine antinociception, tolerance to antinociception, withdrawal, sensitization to locomotion, and conditioned place preference (<b>CPP</b>).
+PER1	addiction	sensitization	28243713	In <strong>Per1</strong> Brdm1 null mutant mice and wild type (WT) littermates, we examined whether there were any differences in the development of morphine antinociception, tolerance to antinociception, withdrawal, <b>sensitization</b> to locomotion, and conditioned place preference (CPP).
+PER1	addiction	withdrawal	28243713	In <strong>Per1</strong> Brdm1 null mutant mice and wild type (WT) littermates, we examined whether there were any differences in the development of morphine antinociception, tolerance to antinociception, <b>withdrawal</b>, sensitization to locomotion, and conditioned place preference (CPP).
+PER1	drug	opioid	28243713	<strong>Per1</strong> Brdm1 mutant mice did not show any difference in <b>morphine</b> antinociception, tolerance development, nor in physical withdrawal signs precipitated by <b>naloxone</b> administration compared to WT.
+PER1	addiction	withdrawal	28243713	<strong>Per1</strong> Brdm1 mutant mice did not show any difference in morphine antinociception, tolerance development, nor in physical <b>withdrawal</b> signs precipitated by naloxone administration compared to WT.
+PER1	drug	opioid	28243713	However, <b>morphine</b> induced locomotor sensitization and CPP were significantly impaired in <strong>Per1</strong> Brdm1 mutant mice.
+PER1	addiction	reward	28243713	However, morphine induced locomotor sensitization and <b>CPP</b> were significantly impaired in <strong>Per1</strong> Brdm1 mutant mice.
+PER1	addiction	sensitization	28243713	However, morphine induced locomotor <b>sensitization</b> and CPP were significantly impaired in <strong>Per1</strong> Brdm1 mutant mice.
+PER1	drug	opioid	28243713	As opposed to WT controls, <strong>Per1</strong> Brdm1 mutant mice showed significantly enhanced striatal global HDAC activity within the striatum when exposed to a locomotor sensitizing <b>morphine</b> administration regimen.
+PER1	drug	opioid	28243713	Furthermore, the administration of the HDAC inhibitor NaBut restored the ability of <b>morphine</b> to promote locomotor sensitization and reward in <strong>Per1</strong> Brdm1 mutant mice.
+PER1	addiction	reward	28243713	Furthermore, the administration of the HDAC inhibitor NaBut restored the ability of morphine to promote locomotor sensitization and <b>reward</b> in <strong>Per1</strong> Brdm1 mutant mice.
+PER1	addiction	sensitization	28243713	Furthermore, the administration of the HDAC inhibitor NaBut restored the ability of morphine to promote locomotor <b>sensitization</b> and reward in <strong>Per1</strong> Brdm1 mutant mice.
+PER1	drug	opioid	27070740	Here we compared the effects of repeated daily treatment of rats with <b>morphine</b> or <b>methadone</b> and subsequent <b>naloxone</b> precipitated withdrawal on the expression of the <strong>Per1</strong>, Per2, and Avp mRNAs in the suprachiasmatic nucleus and on arylalkylamine N acetyltransferase activity in the pineal gland.
+PER1	addiction	withdrawal	27070740	Here we compared the effects of repeated daily treatment of rats with morphine or methadone and subsequent naloxone precipitated <b>withdrawal</b> on the expression of the <strong>Per1</strong>, Per2, and Avp mRNAs in the suprachiasmatic nucleus and on arylalkylamine N acetyltransferase activity in the pineal gland.
+PER1	drug	alcohol	27065929	<strong>PER1</strong> rs3027172 Genotype Interacts with Early Life Stress to Predict Problematic <b>Alcohol</b> Use, but Not Reward Related Ventral Striatum Activity.
+PER1	addiction	reward	27065929	<strong>PER1</strong> rs3027172 Genotype Interacts with Early Life Stress to Predict Problematic Alcohol Use, but Not <b>Reward</b> Related Ventral Striatum Activity.
+PER1	addiction	reward	27065929	Initial analyses found that <strong>PER1</strong> rs3027172 genotype interacted with ELS to predict both problematic drinking and VS reactivity; minor C allele carriers, who were also exposed to elevated ELS reported greater problematic drinking and exhibited greater ventral striatum reactivity to <b>reward</b> related stimuli.
+PER1	drug	alcohol	27065929	These results extend our understanding of relationships between <strong>PER1</strong> genotype, ELS, and problematic <b>alcohol</b> use, and serve as a cautionary tale on the importance of controlling for potential confounders in studies of moderation including gene × environment interactions.
+PER1	drug	opioid	26892296	Here we have studied the effect of constant light on <b>morphine</b> voluntary consumption and withdrawal symptoms and also investigated the involvement of <strong>Per1</strong>, Per2 and dopamine D1 receptor in these processes.
+PER1	addiction	withdrawal	26892296	Here we have studied the effect of constant light on morphine voluntary consumption and <b>withdrawal</b> symptoms and also investigated the involvement of <strong>Per1</strong>, Per2 and dopamine D1 receptor in these processes.
+PER1	drug	opioid	26892296	It is concluded that exposure to constant light by up regulation of Per2 and dopamine D1 receptor in the striatum and prefrontal cortex and up regulation of <strong>Per1</strong> in the striatum and the possible involvement of melatonin makes animals vulnerable to <b>morphine</b> preference and addiction.
+PER1	addiction	addiction	26892296	It is concluded that exposure to constant light by up regulation of Per2 and dopamine D1 receptor in the striatum and prefrontal cortex and up regulation of <strong>Per1</strong> in the striatum and the possible involvement of melatonin makes animals vulnerable to morphine preference and <b>addiction</b>.
+PER1	drug	alcohol	25677407	Concerning <b>alcohol</b> use, the current findings give support, but are preliminary to, the associations of ARNTL (BMAL1) rs6486120 with <b>alcohol</b> consumption, ARNTL2 rs7958822 and ARNTL2 rs4964057 with <b>alcohol</b> abuse, and <strong>PER1</strong> rs3027172 and PER2 rs56013859 with <b>alcohol</b> dependence.
+PER1	addiction	dependence	25677407	Concerning alcohol use, the current findings give support, but are preliminary to, the associations of ARNTL (BMAL1) rs6486120 with alcohol consumption, ARNTL2 rs7958822 and ARNTL2 rs4964057 with alcohol abuse, and <strong>PER1</strong> rs3027172 and PER2 rs56013859 with alcohol <b>dependence</b>.
+PER1	addiction	addiction	25414651	Over 100 <b>addiction</b>/reward related genes were identified and these included: <strong>Per1</strong>, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+PER1	addiction	reward	25414651	Over 100 addiction/<b>reward</b> related genes were identified and these included: <strong>Per1</strong>, Per2, Arc, Homer2, Creb1, Grm3, Fosb, Gabrb3, Adra2a, Ntrk2, Cry1, Penk, Cartpt, Adcy1, Npy1r, Htr1a, Drd1a, Gria1, and Pdyn.
+PER1	drug	alcohol	23608482	The circadian <strong>Per1</strong> and Per2 genes influence <b>alcohol</b> intake, reinforcement, and blood <b>alcohol</b> levels.
+PER1	addiction	reward	23608482	The circadian <strong>Per1</strong> and Per2 genes influence alcohol intake, <b>reinforcement</b>, and blood alcohol levels.
+PER1	drug	alcohol	23608482	This study tested <b>ethanol</b> consumption, reinforcement, and metabolism in mice containing functional mutations in <strong>Per1</strong> and/or Per2 genes on an <b>ethanol</b> preferring background, C57BL/6J mice.
+PER1	addiction	reward	23608482	This study tested ethanol consumption, <b>reinforcement</b>, and metabolism in mice containing functional mutations in <strong>Per1</strong> and/or Per2 genes on an ethanol preferring background, C57BL/6J mice.
+PER1	drug	alcohol	23608482	Mutation of either <strong>Per1</strong> or Per2, as well as mutations of both genes, increases <b>ethanol</b> intake and reinforcement in an <b>ethanol</b> preferring mouse model.
+PER1	addiction	reward	23608482	Mutation of either <strong>Per1</strong> or Per2, as well as mutations of both genes, increases ethanol intake and <b>reinforcement</b> in an ethanol preferring mouse model.
+PER1	drug	amphetamine	23518151	Chronic administration shifted the phase of <strong>Per1</strong> and Per2 expressions from a nocturnal to diurnal pattern and advance shifted the peak of Rev erbα in d <b>amphetamine</b> treated animals.
+PER1	drug	alcohol	22286266	Chronic administration of <b>ethanol</b> significantly augmented mean expression of pituitary nitric oxide synthase (NOS) 2, heme oxygenase (HO) 1, <strong>Per1</strong> and Per2 genes and disrupted their diurnal rhythmicity.
+PER1	drug	alcohol	22286266	Decreased NOS 1 and NOS 2 expression during scotophase, together with suppression of the rhythm in <strong>Per1</strong> and Per2 expression, were found in the discontinuous <b>ethanol</b> group.
+PER1	drug	alcohol	21828288	Effects of the circadian rhythm gene period 1 (<strong>per1</strong>) on psychosocial stress induced <b>alcohol</b> drinking.
+PER1	drug	alcohol	21828288	The authors hypothesized that <strong>Per1</strong> is involved in integrating stress response and circadian rhythmicity and explored its relevance to <b>alcohol</b> drinking.
+PER1	drug	cocaine	21127416	<strong>Per1</strong>(Brdm1) mice self administer <b>cocaine</b> and reinstate <b>cocaine</b> seeking behaviour following extinction.
+PER1	addiction	relapse	21127416	<strong>Per1</strong>(Brdm1) mice self administer cocaine and reinstate cocaine <b>seeking</b> behaviour following extinction.
+PER1	drug	cocaine	21127416	For instance, Period 1 (<strong>Per1</strong>(Brdm1)) mutant mice do not display behavioural sensitization in response to repeated <b>cocaine</b> administration and do not express <b>cocaine</b> conditioned place preference, in contrast to control littermates.
+PER1	addiction	sensitization	21127416	For instance, Period 1 (<strong>Per1</strong>(Brdm1)) mutant mice do not display behavioural <b>sensitization</b> in response to repeated cocaine administration and do not express cocaine conditioned place preference, in contrast to control littermates.
+PER1	drug	cocaine	21127416	To assess the involvement of the mPer1 gene in a robust model of <b>cocaine</b> reinforcement and relapse like behaviour, we tested <strong>Per1</strong>(Brdm1) mutant mice and their littermates for self administration of several doses (0.06 0.75 mg/kg/infusion) of <b>cocaine</b>, and for reinstatement of an extinguished <b>cocaine</b> seeking response.
+PER1	addiction	relapse	21127416	To assess the involvement of the mPer1 gene in a robust model of cocaine reinforcement and <b>relapse</b> like behaviour, we tested <strong>Per1</strong>(Brdm1) mutant mice and their littermates for self administration of several doses (0.06 0.75 mg/kg/infusion) of cocaine, and for <b>reinstatement</b> of an extinguished cocaine <b>seeking</b> response.
+PER1	addiction	reward	21127416	To assess the involvement of the mPer1 gene in a robust model of cocaine <b>reinforcement</b> and relapse like behaviour, we tested <strong>Per1</strong>(Brdm1) mutant mice and their littermates for self administration of several doses (0.06 0.75 mg/kg/infusion) of cocaine, and for reinstatement of an extinguished cocaine seeking response.
+PER1	drug	cocaine	21127416	<strong>Per1</strong>(Brdm1) mutant mice did not differ from control littermates in their propensity to self administer <b>cocaine</b> or to reinstate an extinguished <b>cocaine</b> seeking behaviour in response to drug associated cues or <b>cocaine</b> priming.
+PER1	addiction	relapse	21127416	<strong>Per1</strong>(Brdm1) mutant mice did not differ from control littermates in their propensity to self administer cocaine or to reinstate an extinguished cocaine <b>seeking</b> behaviour in response to drug associated cues or cocaine priming.
+PER1	drug	cocaine	21127416	In contrast to our earlier data on <strong>Per1</strong>(Brdm1) mutant mice in <b>cocaine</b> sensitization and conditioned place preference, this finding does not suggest a relationship between the circadian clock gene mPer1 in <b>cocaine</b> self administration and reinstatement of <b>cocaine</b> seeking behaviour.
+PER1	addiction	relapse	21127416	In contrast to our earlier data on <strong>Per1</strong>(Brdm1) mutant mice in cocaine sensitization and conditioned place preference, this finding does not suggest a relationship between the circadian clock gene mPer1 in cocaine self administration and <b>reinstatement</b> of cocaine <b>seeking</b> behaviour.
+PER1	addiction	sensitization	21127416	In contrast to our earlier data on <strong>Per1</strong>(Brdm1) mutant mice in cocaine <b>sensitization</b> and conditioned place preference, this finding does not suggest a relationship between the circadian clock gene mPer1 in cocaine self administration and reinstatement of cocaine seeking behaviour.
+PER1	addiction	addiction	18850497	Recent studies demonstrated that the Period1 gene (<strong>Per1</strong>) is involved in behavioral alterations induced by <b>addictive</b> drugs.
+PER1	drug	opioid	18850497	We explored the effects of inhibiting expression in brain of <strong>Per1</strong> on <b>morphine</b> conditioned place preference (CPP) and <b>morphine</b> induced phosphorylation of extracellular signal regulated kinase (ERK) and cAMP response element binding protein (CREB) in mice.
+PER1	addiction	reward	18850497	We explored the effects of inhibiting expression in brain of <strong>Per1</strong> on morphine conditioned place preference (<b>CPP</b>) and morphine induced phosphorylation of extracellular signal regulated kinase (ERK) and cAMP response element binding protein (CREB) in mice.
+PER1	drug	opioid	18850497	injected with vehicle or deoxyribozyme 164 (DRz164) which cleaves <strong>per1</strong> mRNA before subcutaneous (s.c.) injection <b>morphine</b>.
+PER1	drug	opioid	18850497	Our results indicated that <strong>per1</strong> plays an important role in <b>morphine</b> reward, and ERK CREB pathway was involved in the effects of <strong>per1</strong>.
+PER1	addiction	reward	18850497	Our results indicated that <strong>per1</strong> plays an important role in morphine <b>reward</b>, and ERK CREB pathway was involved in the effects of <strong>per1</strong>.
+PER1	drug	cocaine	17106427	Human clock, <strong>PER1</strong> and PER2 polymorphisms: lack of association with <b>cocaine</b> dependence susceptibility and <b>cocaine</b> induced paranoia.
+PER1	addiction	dependence	17106427	Human clock, <strong>PER1</strong> and PER2 polymorphisms: lack of association with cocaine <b>dependence</b> susceptibility and cocaine induced paranoia.
+PER1	drug	alcohol	17051414	<b>Ethanol</b> self administration and reinstatement of <b>ethanol</b> seeking behavior in <strong>Per1</strong>(Brdm1) mutant mice.
+PER1	addiction	relapse	17051414	Ethanol self administration and <b>reinstatement</b> of ethanol <b>seeking</b> behavior in <strong>Per1</strong>(Brdm1) mutant mice.
+PER1	drug	cocaine	17051414	Previously, our lab demonstrated the involvement of mouse <strong>Per1</strong> (mPer1) and Per2 (mPer2) in modulating <b>cocaine</b> sensitization and reward.
+PER1	addiction	reward	17051414	Previously, our lab demonstrated the involvement of mouse <strong>Per1</strong> (mPer1) and Per2 (mPer2) in modulating cocaine sensitization and <b>reward</b>.
+PER1	addiction	sensitization	17051414	Previously, our lab demonstrated the involvement of mouse <strong>Per1</strong> (mPer1) and Per2 (mPer2) in modulating cocaine <b>sensitization</b> and reward.
+PER1	drug	alcohol	17051414	Using operant conditions, <strong>Per1</strong> (Brdm1) and wild type mice were trained to self administer <b>ethanol</b> (10%) under a fixed ratio 1 (FR1) paradigm.
+PER1	addiction	reward	17051414	Using <b>operant</b> conditions, <strong>Per1</strong> (Brdm1) and wild type mice were trained to self administer ethanol (10%) under a fixed ratio 1 (FR1) paradigm.
+PER1	addiction	reward	16161281	To study the cleavage of the deoxyribozyme targeting Period1 (<strong>Per1</strong>) mRNA in vitro and its effect on the opiate induced <b>reward</b> in mice.
+PER1	drug	opioid	15977398	[The effect of ribozyme specially cleaving <strong>per1</strong> mRNA on c fos mRNA and its expression in hippocampus of <b>morphine</b> addicted mice].
+PER1	drug	opioid	15977398	To study the change of c fos mRNA and protein in hippocampus of <b>morphine</b> addicted mice after injected with ribozyme specially cleaving <strong>per1</strong> mRNA.
+PER1	drug	opioid	15977398	The recombined plasmid pcDNA 3.1 per1RZ DNA was injected into the ventricles of <b>morphine</b> addicted mice to transcript the corresponding ribozyme which cleaves <strong>per1</strong> mRNA particularly.
+PER1	drug	opioid	15977398	The ribozyme specially cleaving <strong>per1</strong> mRNA has potential function in inhibiting the transcription and expression of c fos and blocking the <b>morphine</b> addiction.
+PER1	addiction	addiction	15977398	The ribozyme specially cleaving <strong>per1</strong> mRNA has potential function in inhibiting the transcription and expression of c fos and blocking the morphine <b>addiction</b>.
+PER1	drug	cocaine	15388282	Using inbred mice, we recently reported that both <b>cocaine</b> sensitization and striatal "clock" gene Period1 (<strong>PER1</strong> for protein) levels demonstrate a diurnal pattern that is maintained by the rhythm of pineal products N acetylserotonin (NAS) and melatonin.
+PER1	addiction	sensitization	15388282	Using inbred mice, we recently reported that both cocaine <b>sensitization</b> and striatal "clock" gene Period1 (<strong>PER1</strong> for protein) levels demonstrate a diurnal pattern that is maintained by the rhythm of pineal products N acetylserotonin (NAS) and melatonin.
+PER1	drug	cocaine	15388282	We found that regardless of the species/strains, subjects with regular NAS and melatonin rhythms present diurnal <b>cocaine</b> sensitization and striatal <strong>PER1</strong> rhythm.
+PER1	addiction	sensitization	15388282	We found that regardless of the species/strains, subjects with regular NAS and melatonin rhythms present diurnal cocaine <b>sensitization</b> and striatal <strong>PER1</strong> rhythm.
+PER1	drug	cocaine	12865893	Clock genes such as Period1 (<strong>Per1</strong>) show rhythmic region  and strain dependent expression in the mouse brain, and mice mutant for the <strong>Per1</strong> gene lack <b>cocaine</b> sensitization.
+PER1	addiction	sensitization	12865893	Clock genes such as Period1 (<strong>Per1</strong>) show rhythmic region  and strain dependent expression in the mouse brain, and mice mutant for the <strong>Per1</strong> gene lack cocaine <b>sensitization</b>.
+PER1	drug	cocaine	12865893	Here, for the first time we show circadian changes of <strong>PER1</strong> protein levels in the mouse striatum, a brain region crucial for the development of locomotor sensitization to <b>cocaine</b>.
+PER1	addiction	sensitization	12865893	Here, for the first time we show circadian changes of <strong>PER1</strong> protein levels in the mouse striatum, a brain region crucial for the development of locomotor <b>sensitization</b> to cocaine.
+PER1	drug	cocaine	12865893	We analyzed circadian <b>cocaine</b> sensitization at times when striatal <strong>PER1</strong> protein levels in control mice (naive and sham pinealectomized) were high and low, respectively.
+PER1	addiction	sensitization	12865893	We analyzed circadian cocaine <b>sensitization</b> at times when striatal <strong>PER1</strong> protein levels in control mice (naive and sham pinealectomized) were high and low, respectively.
+PER1	drug	cocaine	12865893	Only mice with circadian changes in striatal <strong>Per1</strong> expression showed the night time absence of <b>cocaine</b> sensitization, whereas pinealectomized mice were without circadian changes in striatal <strong>Per1</strong> and were sensitized to <b>cocaine</b> regardless of diurnal rhythm.
+PER1	addiction	sensitization	12865893	Only mice with circadian changes in striatal <strong>Per1</strong> expression showed the night time absence of cocaine <b>sensitization</b>, whereas pinealectomized mice were without circadian changes in striatal <strong>Per1</strong> and were sensitized to cocaine regardless of diurnal rhythm.
+PER1	drug	cocaine	12865893	Our results indicate that both the striatal circadian <strong>Per1</strong> expression and diurnal locomotor <b>cocaine</b> sensitization are strongly influenced by pineal products.
+PER1	addiction	sensitization	12865893	Our results indicate that both the striatal circadian <strong>Per1</strong> expression and diurnal locomotor cocaine <b>sensitization</b> are strongly influenced by pineal products.
+NLRP3	drug	alcohol	31854009	Here, we targeted components of the NOD like receptor family pyrin domain containing 3 (<strong>NLRP3</strong>) inflammasome cascade, which senses and responds to immunologic stimuli, to determine whether <strong>NLRP3</strong> inhibition modulates <b>alcohol</b> consumption.
+NLRP3	drug	alcohol	31854009	C57BL/6J male and female mice were provided a 2 bottle choice of <b>alcohol</b> at increasing concentrations (3, 6, 9, and 12%, 4 days each) or water, and some were treated with daily injections of an <strong>NLRP3</strong> inhibitor (MCC950), a caspase 1 inhibitor (VX765), IL 1 receptor antagonist (IL 1ra; anakinra), or vehicle injection.
+NLRP3	drug	alcohol	31854009	Inhibition of <strong>NLRP3</strong> inflammasome activation and the inflammasome IL 1β cascade opens novel insights into the development of new therapies to address <b>alcohol</b> use disorder in an era of targeted and precision medicine.
+NLRP3	drug	alcohol	31646907	This knowledge, enriched by a focus on the immunomodulatory effects of <b>ethanol</b> and its metabolites, in particular on the <strong>NLRP3</strong> inflammasome pathway, might facilitate the development of treatments that can reduce <b>ethanol</b>'s harmful effects or accentuate its beneficial effects.
+NLRP3	drug	alcohol	30411084	Treatment with BA receptor agonists in both models of <b>ethanol</b> administration modulated lipogenic gene expression, and decreased liver interleukin 1β mRNA expression associated with increased ubiquitination of <strong>NLRP3</strong> inflammasome through cyclic adenosine monophosphate induced activation of protein kinase A.
+NLRP3	drug	amphetamine	30394308	Involvement of <strong>NLRP3</strong> inflammasome in <b>methamphetamine</b> induced microglial activation through miR 143/PUMA axis.
+NLRP3	drug	amphetamine	30394308	However, whether <strong>NLRP3</strong> inflammasome activation contributes to the microglial activation induced by <b>methamphetamine</b> remains elusive.
+NLRP3	drug	amphetamine	30394308	<b>Methamphetamine</b> treatment induced <strong>NLRP3</strong> inflammasome activation as well microglial activation in animal model.
+NLRP3	drug	nicotine	30146678	Rosmarinic acid inhibits <b>nicotine</b> induced C reactive protein generation by inhibiting <strong>NLRP3</strong> inflammasome activation in smooth muscle cells.
+NLRP3	drug	nicotine	30146678	In addition, RA also inhibited the activation of NLR family pyrin domain containing 3 (<strong>NLRP3</strong>) inflammasome and reactive oxygen species (ROS) production resulting from <b>nicotine</b> treatment in VSMCs.
+NLRP3	drug	nicotine	30146678	In addition, RA also inhibited the activation of <strong>NLR family pyrin domain containing 3</strong> (<strong>NLRP3</strong>) inflammasome and reactive oxygen species (ROS) production resulting from <b>nicotine</b> treatment in VSMCs.
+NLRP3	drug	nicotine	30146678	RA also led to diminished <b>nicotine</b> induced activation of <strong>NLRP3</strong> inflammasome and elevation in the CRP level in the aortic tissue of the model rats.
+NLRP3	drug	nicotine	30146678	The results of this study suggested a protective role of RA in <b>nicotine</b> induced atherosclerosis by inhibiting the ROS <strong>NLRP3</strong> inflammasome CRP axial, and RA therefore represented a potential effective therapeutic approach to atherosclerosis, in particular for those who smoke.
+NLRP3	drug	amphetamine	29492824	It is our hypothesis that <b>Meth</b> activates <strong>NLRP3</strong> inflammasome in microglia and promotes the processing and release of interleukin (IL) 1β, resulting in neurotoxic activity.
+NLRP3	drug	alcohol	29475852	Consequently, treatment of hepatocytes with <b>ethanol</b> resulted in TXNIP overexpression, activating <strong>NLRP3</strong> inflammasome and caspase 1 mediated pyroptosis.
+NLRP3	drug	alcohol	29475852	<b>Alcohol</b> decreases miR 148a expression in hepatocytes through FoxO1, facilitating TXNIP overexpression and <strong>NLRP3</strong> inflammasome activation, which induces hepatocyte pyroptosis.
+NLRP3	drug	alcohol	29355515	Spliceosome Associated Protein 130 Exacerbates <b>Alcohol</b> Induced Liver Injury by Inducing <strong>NLRP3</strong> Inflammasome Mediated IL 1β in Mice.
+NLRP3	drug	alcohol	29338075	Regulating P2X7 receptor mediated activation of <strong>NLRP3</strong> inflammasomes could be a therapeutic strategy to treat <b>alcoholic</b> hepatosteatosis.
+NLRP3	drug	alcohol	29338075	In <b>ethanol</b> exposed HepG2 cells, gentiopicroside reduced lipogenesis and promoted lipid oxidation via activation of P2X7 receptor <strong>NLRP3</strong> inflammasomes.
+NLRP3	drug	alcohol	29338075	Activation of LKB1/AMPK signalling by gentiopicroside was mediated by the P2X7 receptor <strong>NLRP3</strong> inflammasome, suggesting the therapeutic value of blocking P2X7 receptors in the treatment of <b>alcoholic</b> hepatosteatosis.
+NLRP3	drug	opioid	28860068	Maintenance of this <b>morphine</b> induced persistent sensitization was dependent on spinal NOD like receptor protein 3 (<strong>NLRP3</strong>) inflammasomes protein complexes that proteolytically activate interleukin 1β (IL 1β) via caspase 1.
+NLRP3	addiction	sensitization	28860068	Maintenance of this morphine induced persistent <b>sensitization</b> was dependent on spinal NOD like receptor protein 3 (<strong>NLRP3</strong>) inflammasomes protein complexes that proteolytically activate interleukin 1β (IL 1β) via caspase 1.
+NLRP3	drug	opioid	28860068	However, it is still unclear how <strong>NLRP3</strong> inflammasome signaling is maintained long after <b>morphine</b> is cleared.
+NLRP3	drug	opioid	28860068	We conclude that after peripheral nerve injury, <b>morphine</b> treatment results in persistent DAMP release via TLR4, P2X7R and caspase 1, which are involved in formation/activation of <strong>NLRP3</strong> inflammasomes.
+NLRP3	drug	opioid	28580822	Effects of microRNA 223 on <b>morphine</b> analgesic tolerance by targeting <strong>NLRP3</strong> in a rat model of neuropathic pain.
+NLRP3	drug	opioid	28580822	Objective To investigate the effects of microRNA 223 on <b>morphine</b> analgesic tolerance by targeting <strong>NLRP3</strong> in a rat model of neuropathic pain.
+NLRP3	drug	opioid	28580822	Methods Our study selected 100 clean grade healthy Sprague Dawley adult male rats weighing 200 to 250 g. After establishment of a rat model of chronic constriction injury, these rats were divided into 10 groups (10 rats in each group): the normal control, sham operation, chronic constriction injury, normal saline, <b>morphine</b>, miR 223, <strong>NLRP3</strong>, miR 223 + <b>morphine</b>, <strong>NLRP3</strong> + <b>morphine</b>, and miR 223 + <strong>NLRP3</strong> + <b>morphine</b> groups.
+NLRP3	drug	opioid	28580822	Expressions of miR 223 in the miR 223, miR 223 + <b>morphine</b>, and miR 223 + <strong>NLRP3</strong> + <b>morphine</b> were significantly higher than those in the chronic constriction injury, normal saline, and <b>morphine</b> groups.
+NLRP3	drug	opioid	28580822	Compared with chronic constriction injury, normal saline and <b>morphine</b> groups, the mRNA and protein expressions of <strong>NLRP3</strong>, apoptosis associated speck like protein, Caspase 1, IL 1β, and IL 18 were significantly decreased in the miR 223 and miR 223 + <b>morphine</b> groups, while mRNA and protein expressions of <strong>NLRP3</strong>, apoptosis associated speck like protein, Caspase 1, IL 1β, and IL 18 were significantly increased in the <strong>NLRP3</strong> and <strong>NLRP3</strong> + <b>morphine</b> group.
+NLRP3	drug	opioid	28580822	Conclusion Our study provides strong evidence that miR 223 could suppress the activities of <strong>NLRP3</strong> inflammasomes (<strong>NLRP3</strong>, apoptosis associated speck like protein, and Caspase 1) to relieve <b>morphine</b> analgesic tolerance in rats by down regulating <strong>NLRP3</strong>.
+NLRP3	drug	cocaine	28057531	To empirically test these assumptions, we evaluated the (neuro)psychological trait and the functional organization of the resting state brain networks associated with the NAcs in 18 former <b>cocaine</b> abusers (<strong>FCAs</strong>), while being in drug abstinence since 5 months.
+NLRP3	drug	cocaine	28057531	In the 8 <strong>FCAs</strong> who relapsed into <b>cocaine</b> use after 3 months, the level of functional connectivity between the NAcs and dPFC was lower than the functional connectivity estimated in the group of patients that did not relapsed.
+NLRP3	drug	opioid	27247388	<b>Morphine</b> paradoxically prolongs neuropathic pain in rats by amplifying spinal <strong>NLRP3</strong> inflammasome activation.
+NLRP3	drug	opioid	27247388	Using pharmacologic and genetic approaches, we discovered that the initiation and maintenance of this multimonth prolongation of neuropathic pain was mediated by a previously unidentified mechanism for spinal cord and pain namely, <b>morphine</b> induced spinal NOD like receptor protein 3 (<strong>NLRP3</strong>) inflammasomes and associated release of interleukin 1β (IL 1β).
+NLRP3	addiction	sensitization	26937141	SFA palmitic acid (PA) directly activated <strong>NLRP3</strong> inflammasome and increased <b>sensitization</b> to LPS induced inflammasome activation in hepatocytes.
+NLRP3	addiction	sensitization	26937141	Furthermore, a high fat diet increased but PUFA enriched diet decreased <b>sensitization</b> to LPS induced hepatic <strong>NLRP3</strong> inflammasome activation in vivo.
+NLRP3	drug	alcohol	26937141	Hepatic <strong>NLRP3</strong> inflammasome activation played an important role in the development of non <b>alcoholic</b> fatty liver disease.
+NLRP3	drug	alcohol	25582105	It was reported that <b>alcohol</b> consumption activated the <strong>NLRP3</strong> inflammasome in Kupffer cells, leading to mature interleukin (IL) 1β release in <b>alcoholic</b> liver injury; however, how IL 1β promotes liver injury remains unclear.
+NLRP3	drug	alcohol	25582105	Increased gene and protein expression of mature IL 1β correlated with elevated expression of the <strong>NLRP3</strong> inflammasome components <strong>NLRP3</strong>, ASC, and cleaved caspase 1 in Kupffer cells from <b>ethanol</b> exposed wild type mice.
+NLRP3	drug	alcohol	25582105	<strong>NLRP3</strong> deficiency led to the attenuation of <b>alcoholic</b> steatosis, similarly as Kupffer cell depletion, almost without hepatic NKT cells.
+NLRP3	drug	alcohol	25582105	After <b>alcohol</b> exposure Kupffer cell derived IL 1β triggered by <strong>NLRP3</strong> activation, recruits and activates hepatic iNKT cells, subsequently promoting liver inflammation and neutrophil infiltration, and inducing <b>alcoholic</b> liver injury.
+NLRP3	drug	opioid	23352192	Involvement of the <strong>NLRP3</strong> inflammasome in the modulation of an LPS induced inflammatory response during <b>morphine</b> tolerance.
+NLRP3	drug	opioid	23352192	We have explored the effects of lipopolysaccharide (LPS) during <b>morphine</b> tolerance on expression of the <strong>NLRP3</strong> inflammasome and related inflammatory genes.
+NLRP3	drug	opioid	23352192	In response to LPS, expression of 27 genes, including <strong>NLRP3</strong>, TNF α, IL 1β, and IL 6, was significantly increased, and expression of 3 genes was significantly decreased in both the <b>morphine</b> tolerant and placebo control groups compared to the saline treated animals.
+NLRP3	drug	opioid	23352192	However, there was only a 2.7 fold increase in <strong>NLRP3</strong> expression in response to LPS in the <b>morphine</b> tolerant rats compared to a 4.5 fold increase in the placebo control animals.
+NLRP3	drug	opioid	23352192	Our data indicate that, in the <b>morphine</b> tolerant state, LPS induced expression of <strong>NLRP3</strong> is suppressed and cytokine/chemokine expression is inhibited, which may be one of the mechanisms involved in <b>morphine</b> induced immunosuppression.
+NGFR	addiction	intoxication	31693929	This study investigated the effect of <b>binge</b> like MA dosing (4 x 4 mg/kg, s.c., 2 h (h) apart) at a range of different time points (from 2 h to 7 days after treatment) on brain derived neurotrophic factor (BDNF) levels and its receptors, TrkB and <strong>p75NTR</strong>.
+NGFR	drug	opioid	31173919	Conversely, the lack of extinction training (sham extinction) upregulated genes associated with kinases (Camk2g), neurotrophins (<strong>Ngfr</strong>), synaptic connectivity factors (Ephb2), glutamate neurotransmission (Grm8) and <b>opioid</b> receptors (μ1, Δ1).
+NGFR	drug	alcohol	31156431	The BDNF signaling mechanism is complex and depends on two receptor systems, TrkB and <strong>p75NTR</strong>, which appear to have opposite effects on <b>alcohol</b> seeking behavior in animal models.
+NGFR	addiction	relapse	31156431	The BDNF signaling mechanism is complex and depends on two receptor systems, TrkB and <strong>p75NTR</strong>, which appear to have opposite effects on alcohol <b>seeking</b> behavior in animal models.
+NGFR	drug	cannabinoid	30339727	Treatment of <strong>CD271</strong> expressing melanoma subpopulations with RNA interference and small molecule inhibitors to <strong>CD271</strong> reduced the development of MEKi resistance, while clinically applicable autophagy modulatory agents   including Δ9 <b>tetrahydrocannabinol</b> and Vps34   reduced survival of MEKi resistant melanoma cells.
+NGFR	drug	alcohol	29520063	ProBDNF/<strong>p75NTR</strong>/sortilin pathway is activated in peripheral blood of patients with <b>alcohol</b> dependence.
+NGFR	addiction	dependence	29520063	ProBDNF/<strong>p75NTR</strong>/sortilin pathway is activated in peripheral blood of patients with alcohol <b>dependence</b>.
+NGFR	drug	alcohol	29520063	We found that the protein levels of proBDNF and <strong>p75NTR</strong> were increased, but not the sortilin protein level; while the TrkB protein level was decreased in the <b>alcohol</b> dependence patients compared with healthy controls.
+NGFR	addiction	dependence	29520063	We found that the protein levels of proBDNF and <strong>p75NTR</strong> were increased, but not the sortilin protein level; while the TrkB protein level was decreased in the alcohol <b>dependence</b> patients compared with healthy controls.
+NGFR	drug	alcohol	29520063	The levels of mBDNF and TrkB were negatively correlated with the average amount of daily <b>ethanol</b> consumption, and the levels of proBDNF, <strong>p75NTR</strong> and sortilin were positively correlated with the average amount of <b>ethanol</b> consumption per day.
+NGFR	drug	alcohol	29520063	The balance between the proBDNF/<strong>p75NTR</strong> and mBDNF/TrkB signalling pathways appeared dysregulated in <b>alcohol</b> dependence.
+NGFR	addiction	dependence	29520063	The balance between the proBDNF/<strong>p75NTR</strong> and mBDNF/TrkB signalling pathways appeared dysregulated in alcohol <b>dependence</b>.
+NGFR	drug	amphetamine	29165617	Selective Activation of Striatal NGF TrkA/<strong>p75NTR</strong>/MAPK Intracellular Signaling in Rats That Show Suppression of <b>Methamphetamine</b> Intake 30 Days following Drug Abstinence.
+NGFR	drug	amphetamine	29165617	These findings support the notion that animals with distinct phenotypes for <b>methamphetamine</b> intake in the presence of adverse consequences also display differential changes in an intracellular signaling cascade activated by nerve growth factor TrkA/<strong>p75NTR</strong> interactions.
+NGFR	drug	alcohol	28032807	Reverse transcription PCR (RT PCR) was performed to measure mRNA levels for BDNF, TrkB, <strong>P75NTR</strong>, and sortilin in the prefrontal cortex, hippocampus, and dorsal striatum of Kunming mice after chronic <b>alcohol</b> exposure.
+NGFR	drug	alcohol	27683907	We report that intermittent access to 20% <b>alcohol</b> in a two bottle choice paradigm that models excessive <b>alcohol</b> drinking produces a mobilization of DLS p75 neurotrophin receptor (<strong>p75NTR</strong>), whose activities oppose those of the Trk receptors, including TrkB.
+NGFR	drug	alcohol	27683907	Furthermore, short hairpin RNA (shRNA) mediated knockdown of the <strong>p75NTR</strong> gene in the DLS, as well as intra DLS infusion or systemic administration of the <strong>p75NTR</strong> modulator, LM11A 31, significantly reduced binge drinking of <b>alcohol</b>.
+NGFR	addiction	intoxication	27683907	Furthermore, short hairpin RNA (shRNA) mediated knockdown of the <strong>p75NTR</strong> gene in the DLS, as well as intra DLS infusion or systemic administration of the <strong>p75NTR</strong> modulator, LM11A 31, significantly reduced <b>binge</b> drinking of alcohol.
+NGFR	drug	alcohol	27683907	Together, our results suggest that excessive <b>alcohol</b> consumption produces a change in BDNF signaling in the DLS, which is mediated by the recruitment of <strong>p75NTR</strong>.
+NGFR	drug	alcohol	27683907	Our data also imply that modulators of <strong>p75NTR</strong> signaling could be developed as medications for <b>alcohol</b> abuse disorders.
+NGFR	drug	alcohol	27683907	Here, we show that a history of excessive <b>alcohol</b> intake produces neuroadaptations in the DLS that preclude BDNF's ability to gate <b>alcohol</b> self administration in rats by the recruitment of the low affinity neurotrophin receptor, <strong>p75NTR</strong>, whose activities opposes those of the Trk receptors.
+NGFR	drug	alcohol	27683907	Finally, we show that the administration of the <strong>p75NTR</strong> modulator, LM11A 31, significantly reduces excessive <b>alcohol</b> intake suggesting that the drug may be developed as a new treatment for <b>alcohol</b> abuse disorders.
+NGFR	drug	opioid	19114089	Because neurotrophins universally bind the p75 neurotrophin receptor (<strong>p75NTR</strong>), we investigated whether the activity of this receptor is involved in the development of <b>opioid</b> analgesic tolerance and physical dependence.
+NGFR	addiction	dependence	19114089	Because neurotrophins universally bind the p75 neurotrophin receptor (<strong>p75NTR</strong>), we investigated whether the activity of this receptor is involved in the development of opioid analgesic tolerance and physical <b>dependence</b>.
+NGFR	drug	opioid	19114089	However, the loss of <b>morphine</b> analgesia was not observed in <strong>p75NTR</strong> /  mice.
+NGFR	addiction	withdrawal	19114089	This challenge precipitated a robust <b>withdrawal</b> syndrome that was comparable in wild type mice and <strong>p75NTR</strong> /  mice.
+NGFR	drug	opioid	19114089	The findings suggest that <strong>p75NTR</strong> activity plays a critical role in the development of <b>opioid</b> analgesic tolerance but not in the induction or the expression of <b>opioid</b> physical dependence.
+NGFR	addiction	dependence	19114089	The findings suggest that <strong>p75NTR</strong> activity plays a critical role in the development of opioid analgesic tolerance but not in the induction or the expression of opioid physical <b>dependence</b>.
+NGFR	drug	alcohol	15246696	Alterations of cerebellar mRNA specific for BDNF, <strong>p75NTR</strong>, and TrkB receptor isoforms occur within hours of <b>ethanol</b> administration to 4 day old rat pups.
+IFITM1	drug	nicotine	23901338	The multivariate model showed that anemia (AOR: 19.8, 95% CI: 5.6 35.5), positive sputum smear (AOR: 13.4, 95% CI: 6.8 33.6), <b>smoking</b> (AOR: 12.9, 95% CI: 3.<strong>9 27</strong>.3), drug hepatitis (AOR: 12.3, 95% CI: 6.7 24.7), diabetes mellitus (AOR: 9.7, 95% CI: 2.9 32.0), drug use (AOR: 7.8, 95% CI: 2.4 25.5), and history of previous TB (AOR: 6.8, 95% CI: 2.2 21.3) were major risk factors for death in TB patients.
+IFITM1	drug	nicotine	22189160	Youths were 18 times more likely to be current <b>smokers</b> (95% CI = 11.<strong>9 27</strong>.2, p < 0.001) if they endorsed any AUTOS item.
+IFITM1	drug	nicotine	19360537	Compared with youth of European background (11.4%; 95% CI 6.7 15.1), Indigenous (23.0%; 95% CI 21.0 25.0), and Mixed ethnicity (23%; 95% CI 18.<strong>9 27</strong>.1) youth had higher prevalence of current <b>smoking</b>.
+GPR55	drug	cannabinoid	31437433	Strikingly, this reduction in both cocaine self administration and BSR was blocked by AM630 (a <b>cannabinoid</b> CB2 receptor antagonist), WAY100135 (a 5 HT1A receptor antagonist), or capsazepine (a TRPV1 channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a <strong>GPR55</strong> antagonist), or naloxone (an opioid receptor antagonist), suggesting the involvement of CB2, 5 HT1A, and TRPV1 receptors in CBD action.
+GPR55	drug	cocaine	31437433	Strikingly, this reduction in both <b>cocaine</b> self administration and BSR was blocked by AM630 (a cannabinoid CB2 receptor antagonist), WAY100135 (a 5 HT1A receptor antagonist), or capsazepine (a TRPV1 channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a <strong>GPR55</strong> antagonist), or naloxone (an opioid receptor antagonist), suggesting the involvement of CB2, 5 HT1A, and TRPV1 receptors in CBD action.
+GPR55	drug	opioid	31437433	Strikingly, this reduction in both cocaine self administration and BSR was blocked by AM630 (a cannabinoid CB2 receptor antagonist), WAY100135 (a 5 HT1A receptor antagonist), or capsazepine (a TRPV1 channel blocker), but not by AM251 (a CB1 receptor antagonist), CID16020046 (a <strong>GPR55</strong> antagonist), or <b>naloxone</b> (an <b>opioid</b> receptor antagonist), suggesting the involvement of CB2, 5 HT1A, and TRPV1 receptors in CBD action.
+GPR55	drug	cannabinoid	30767756	Recent studies have suggested that in addition to CB1 and CB2, there are non CB1 and non CB2 <b>cannabinoid</b> related orphan GPCRs including GPR18, <strong>GPR55</strong>, and GPR119.
+GPR55	drug	cannabinoid	30391203	PEA targets not only the peroxisome proliferator activated receptor alpha (PPAR α), but also the <b>endocannabinoid</b> system, binding the <strong>G protein coupled receptor 55</strong>, a non CB1/CB2 <b>cannabinoid</b> receptor, and also the CB1/CB2 receptors, although with a weak affinity.
+GPR55	drug	alcohol	29957399	<b>Ethanol</b> induced modulation of <strong>GPR55</strong> expression in human monocyte derived dendritic cells is accompanied by H4K12 acetylation.
+GPR55	drug	alcohol	29957399	Our lab has shown that the G protein coupled receptor (<strong>GPR55</strong>), a novel cannabinoid receptor, is upregulated in binge drinkers and in cells treated acutely with <b>ethanol</b>.
+GPR55	drug	cannabinoid	29957399	Our lab has shown that the G protein coupled receptor (<strong>GPR55</strong>), a novel <b>cannabinoid</b> receptor, is upregulated in binge drinkers and in cells treated acutely with ethanol.
+GPR55	addiction	intoxication	29957399	Our lab has shown that the G protein coupled receptor (<strong>GPR55</strong>), a novel cannabinoid receptor, is upregulated in <b>binge</b> drinkers and in cells treated acutely with ethanol.
+GPR55	drug	alcohol	29957399	However, the regulatory mechanism of <strong>GPR55</strong> within the immune system under the influence of <b>ethanol</b> is poorly understood.
+GPR55	drug	alcohol	29957399	Since changes in histone modifications might lead to changes in gene expression, we hypothesize that the mechanism of <b>ethanol</b> induced upregulation of <strong>GPR55</strong> is linked to epigenetic changes on histone proteins.
+GPR55	drug	alcohol	29957399	Taking into account previous findings from our lab, the goal of the present study was to determine whether there is any relevant association between histone hyperacetylation and the regulation of the novel cannabinoid receptor <strong>GPR55</strong> in monocyte derived dendritic cells (MDDCs) of human origin treated acutely with <b>ethanol</b>.
+GPR55	drug	cannabinoid	29957399	Taking into account previous findings from our lab, the goal of the present study was to determine whether there is any relevant association between histone hyperacetylation and the regulation of the novel <b>cannabinoid</b> receptor <strong>GPR55</strong> in monocyte derived dendritic cells (MDDCs) of human origin treated acutely with ethanol.
+GPR55	drug	alcohol	29957399	The cells were treated with <b>ethanol</b> for 24 h, harvested, fixed, and stained with antibodies against <strong>GPR55</strong>.
+GPR55	drug	alcohol	29957399	As expected, based on previous findings, confocal microscopy showed that <b>ethanol</b> exposure increases <strong>GPR55</strong> expression.
+GPR55	drug	alcohol	29957399	In order to demonstrate the correlation between histone acetylation and <strong>GPR55</strong> expression regulation, the cells were treated with <b>ethanol</b>, harvested, and then the chromatin was extracted and fractionated for chromatin immunoprecipitation (ChIP) assay, followed by real time qPCR for the analysis of DNA fragments.
+GPR55	drug	alcohol	29957399	The results showed an enrichment of the histone modification H4K12ac in the <strong>GPR55</strong> gene of MDDCs treated with <b>ethanol</b>.
+GPR55	drug	alcohol	29957399	In conjunction, these results indicate that in the presence of <b>ethanol</b>, the upregulation of <strong>GPR55</strong> expression is accompanied by H4K12 acetylation, which might have a significant effect in the ability of this innate immune system's cells to cope with cellular stress induced by <b>ethanol</b>.
+GPR55	drug	alcohol	29957399	However, the causality of <b>ethanol</b> regulation of H4K12ac in <strong>GPR55</strong> expression changes still lacks further elucidation; therefore, additional experimental approaches to confirm a significant causality between H4K12 acetylation and <b>ethanol</b> regulation of <strong>GPR55</strong> are currently undergoing in our lab.
+GPR55	drug	cannabinoid	29773016	It has wide spectrum of action because it acts through <b>endocannabinoid</b> receptors; CB1 and CB2 and it also acts on other receptors, such as GPR18, <strong>GPR55</strong>, GPR 119, 5HT1A, and TRPV2.
+GPR55	drug	cannabinoid	28861501	<b>Palmitoylethanolamide</b> Modulates <strong>GPR55</strong> Receptor Signaling in the Ventral Hippocampus to Regulate Mesolimbic Dopamine Activity, Social Interaction, and Memory Processing.
+GPR55	drug	cannabinoid	28861501	Introduction: The <strong>GPR55</strong> receptor has been identified as an atypical <b>cannabinoid</b> receptor and is implicated in various physiological processes.
+GPR55	drug	cannabinoid	28861501	Materials and Methods: Using a combination of in vivo electrophysiology and behavioral pharmacological assays in rats, we tested whether intra vHipp activation of <strong>GPR55</strong> receptor transmission with the fatty acid amide, <b>palmitoylethanolamide</b> (PEA), a lipid neuromodulator with agonist actions at the <strong>GPR55</strong> receptor, may modulate mesolimbic dopaminergic activity states.
+GPR55	addiction	reward	28861501	Furthermore, while PEA induced activation of <strong>GPR55</strong> transmission had no effects on opiate related <b>reward</b> related memory formation, we observed strong disruptions in social interaction and recognition memory, spatial location memory, and context independent associative fear memory formation.
+GPR55	drug	cannabinoid	28861501	Conclusions: The present results add to a growing body of evidence demonstrating important functional roles for <strong>GPR55</strong> signaling in <b>cannabinoid</b> related neuronal and behavioral phenomena and underscore the potential for <strong>GPR55</strong> signaling in the mediation of <b>cannabinoid</b> related effects independently of the CB1/CB2 receptor systems.
+GPR55	drug	cannabinoid	28428628	The G protein coupled receptor <strong>GPR55</strong> has been postulated to serve as a novel <b>cannabinoid</b> receptor.
+GPR55	drug	cannabinoid	28194850	Gene expression analyses of tyrosine hydroxylase in ventral tegmental area and μ opioid (Oprm1), <b>cannabinoid</b> (CB1 r and CB2 r) and <strong>GPR55</strong> receptors in nucleus accumbens (NAcc) were carried out by real time polymerase chain reaction.
+GPR55	drug	opioid	28194850	Gene expression analyses of tyrosine hydroxylase in ventral tegmental area and μ <b>opioid</b> (Oprm1), cannabinoid (CB1 r and CB2 r) and <strong>GPR55</strong> receptors in nucleus accumbens (NAcc) were carried out by real time polymerase chain reaction.
+GPR55	drug	cannabinoid	26971034	Previous studies show that some non CB1/non CB2 effects of <b>cannabinoids</b> are mediated through G protein coupled receptor 55 (<strong>GPR55</strong>).
+GPR55	drug	cannabinoid	26971034	Previous studies show that some non CB1/non CB2 effects of <b>cannabinoids</b> are mediated through <strong>G protein coupled receptor 55</strong> (<strong>GPR55</strong>).
+GPR55	drug	cannabinoid	26971034	This study examined the effect of atypical <b>cannabinoid</b> O 1602 as a <strong>GPR55</strong> agonist on morphine induced conditioned place preference (CPP) and physical dependence.
+GPR55	drug	opioid	26971034	This study examined the effect of atypical cannabinoid O 1602 as a <strong>GPR55</strong> agonist on <b>morphine</b> induced conditioned place preference (CPP) and physical dependence.
+GPR55	addiction	dependence	26971034	This study examined the effect of atypical cannabinoid O 1602 as a <strong>GPR55</strong> agonist on morphine induced conditioned place preference (CPP) and physical <b>dependence</b>.
+GPR55	addiction	reward	26971034	This study examined the effect of atypical cannabinoid O 1602 as a <strong>GPR55</strong> agonist on morphine induced conditioned place preference (<b>CPP</b>) and physical dependence.
+GPR55	drug	alcohol	24060590	Therefore, we studied the expression of CNR1 and CNR2, and the novel cannabinoid G protein coupled receptor (GPCR) 55 (<strong>GPR55</strong>) in human monocyte derived dendritic cells (MDDCs) from <b>alcohol</b> users.
+GPR55	drug	cannabinoid	24060590	Therefore, we studied the expression of CNR1 and CNR2, and the novel <b>cannabinoid</b> G protein coupled receptor (GPCR) 55 (<strong>GPR55</strong>) in human monocyte derived dendritic cells (MDDCs) from alcohol users.
+GPR55	drug	alcohol	24060590	MDDCs from <b>alcohol</b> users show significantly higher levels of CNR2 and <strong>GPR55</strong> compared to MDDCs from non users.
+GPR55	drug	alcohol	24060590	Our results provide insights into <b>alcohol</b> mechanisms of DC regulation and show, for the first time, that <b>alcohol</b> is inducing CNR2 and <strong>GPR55</strong> in human DCs.
+GPR55	drug	cannabinoid	23643692	CB1 or CB2 receptor expression was not altered in any of the regions examined, however VPA exposed rats exhibited reduced PPARα and <strong>GPR55</strong> expression in the frontal cortex and PPARγ and <strong>GPR55</strong> expression in the hippocampus, additional receptor targets of the <b>endocannabinoids</b>.
+GPR55	drug	cannabinoid	22820167	<strong>GPR55</strong> and GPR35 and their relationship to <b>cannabinoid</b> and lysophospholipid receptors.
+GPR55	drug	cannabinoid	22820167	This review presents a summary of what is known about the G protein coupled receptors GPR35 and <strong>GPR55</strong> and their potential characterization as lysophospholipid or <b>cannabinoid</b> receptors, respectively.
+GPR55	drug	cannabinoid	22820167	Similarly, <strong>GPR55</strong> has been suggested to be a <b>cannabinoid</b> receptor, but is quite clearly also a receptor for lysophosphatidylinositol.
+GPR55	drug	cannabinoid	22141465	Although similar alterations in FAAH mRNA were evident following either continuous or intermittent EtOH exposure, alterations in MAGL and <b>cannabinoid</b> receptor related mRNA (e.g., CB(1) , CB(2) , <strong>GPR55</strong>) were more pronounced following intermittent exposure.
+GPR55	drug	cannabinoid	21907912	The G protein coupled receptor 55 (<strong>GPR55</strong>) was recently proposed as a novel component of this system; however, its classification as a <b>cannabinoid</b> receptor has been significantly hampered by its complex pharmacology, signaling, and cellular function.
+GPR55	drug	cannabinoid	21907912	The <strong>G protein coupled receptor 55</strong> (<strong>GPR55</strong>) was recently proposed as a novel component of this system; however, its classification as a <b>cannabinoid</b> receptor has been significantly hampered by its complex pharmacology, signaling, and cellular function.
+GPR55	drug	cannabinoid	21907912	<strong>GPR55</strong> is phylogenetically distinct from the traditional <b>cannabinoid</b> receptors, but in some experimental paradigms, it is activated by <b>endocannabinoids</b>, phytocannabinoids, and synthetic <b>cannabinoid</b> ligands.
+GPR55	drug	cannabinoid	19723626	Atypical responsiveness of the orphan receptor <strong>GPR55</strong> to <b>cannabinoid</b> ligands.
+GPR55	drug	cannabinoid	19723626	Whether the orphan G protein coupled receptor <strong>GPR55</strong> is also a <b>cannabinoid</b> receptor remains unclear as a result of conflicting pharmacological studies.
+GPR55	drug	cannabinoid	19723626	<strong>GPR55</strong> has been reported to be activated by exogenous and endogenous <b>cannabinoid</b> compounds but surprisingly also by the endogenous non <b>cannabinoid</b> mediator lysophosphatidylinositol (LPI).
+GPR55	drug	cannabinoid	19723626	We examined the effects of a representative panel of <b>cannabinoid</b> ligands and LPI on <strong>GPR55</strong> using a beta arrestin green fluorescent protein biosensor as a direct readout of agonist mediated receptor activation.
+GPR55	drug	cannabinoid	19723626	Our data demonstrate that AM251 and SR141716A (<b>rimonabant</b>), which are <b>cannabinoid</b> antagonists, and the lipid LPI, which is not a <b>cannabinoid</b> receptor ligand, are <strong>GPR55</strong> agonists.
+GPR55	drug	cannabinoid	19723626	Conversely, the potent synthetic <b>cannabinoid</b> agonist CP55,940 acts as a <strong>GPR55</strong> antagonist/partial agonist.
+GPR55	drug	cannabinoid	19723626	CP55,940 blocks <strong>GPR55</strong> internalization, the formation of beta arrestin <strong>GPR55</strong> complexes, and the phosphorylation of ERK1/2; CP55,940 produces only a slight amount of protein kinase CbetaII membrane recruitment but does not stimulate membrane remodeling like LPI, AM251, or <b>rimonabant</b>.
+GPR55	drug	cannabinoid	19723626	Our studies provide a paradigm for measuring the responsiveness of <strong>GPR55</strong> to a variety of ligand scaffolds comprising <b>cannabinoid</b> and novel compounds and suggest that at best <strong>GPR55</strong> is an atypical <b>cannabinoid</b> responder.
+GPR55	drug	cannabinoid	19723626	The activation of <strong>GPR55</strong> by <b>rimonabant</b> may be responsible for some of the off target effects that led to its removal as a potential obesity therapy.
+GPR55	drug	cannabinoid	19335651	Gene association studies are presented for (a) genes posited to have specific influences on <b>cannabis</b> use disorders: CNR1, CB2, FAAH, MGLL, TRPV1 and <strong>GPR55</strong> and (b) genes from various neurotransmitter systems that are likely to exert a non specific influence on risk of <b>cannabis</b> use disorders, e.g.
+GPR55	drug	cannabinoid	19306092	The <b>cannabinoid</b> receptor family currently includes two cloned metabotropic receptors: CB1, CB2 and possibly <strong>GPR55</strong> which are distributed widely across many key loci in pain modulating pathways, including the peripheral terminals of primary afferents.
+GPR55	drug	cannabinoid	17704827	The novel <b>endocannabinoid</b> receptor <strong>GPR55</strong> is activated by atypical <b>cannabinoids</b> but does not mediate their vasodilator effects.
+GPR55	drug	cannabinoid	17704827	Recent reports suggest <strong>GPR55</strong> is an atypical <b>cannabinoid</b> receptor, making it a candidate for the vasodilator 'CBx' receptor.
+GPR55	drug	cannabinoid	17704827	The purpose of the present study was to test the hypothesis that human recombinant <strong>GPR55</strong> is activated by atypical <b>cannabinoids</b> and mediates vasodilator responses to these agents.
+GPR55	drug	cannabinoid	17704827	In <strong>GPR55</strong> deficient and wild type littermate control mice, in vivo blood pressure measurement and isolated resistance artery myography were used to determine <strong>GPR55</strong> dependence of atypical <b>cannabinoid</b> induced haemodynamic and vasodilator responses.
+GPR55	addiction	dependence	17704827	In <strong>GPR55</strong> deficient and wild type littermate control mice, in vivo blood pressure measurement and isolated resistance artery myography were used to determine <strong>GPR55</strong> <b>dependence</b> of atypical cannabinoid induced haemodynamic and vasodilator responses.
+GPR55	drug	cannabinoid	17704827	Atypical <b>cannabinoids</b> O 1602 and abnormal <b>cannabidiol</b> both stimulated <strong>GPR55</strong> dependent GTPgammaS activity (EC50 approximately 2 nM), whereas the CB1 and CB2 selective agonist WIN 55,212 2 showed no effect in <strong>GPR55</strong> expressing HEK293T cell membranes.
+GPR55	drug	cannabinoid	17704827	These results demonstrate that while <strong>GPR55</strong> is activated by atypical <b>cannabinoids</b>, it does not appear to mediate the vasodilator effects of these agents.
+ECD	addiction	dependence	25650831	Cell death caused by the amphipathic helix had features similar to HR, such as <strong>SGT1</strong> <b>dependence</b>.
+ECD	drug	psychedelics	23775255	After behavioral testing was complete, monoamine and associated metabolite levels in discrete brain regions were quantified using high performance liquid chromatography coupled to electrochemical detection (HPLC <strong>ECD</strong>) to determine if adolescent animals displayed a different neurochemical profile than did adult animals after being exposed to subcutaneous low doses of <b>MDMA</b>.
+ECD	drug	nicotine	20640803	For comparison, we also built the <strong>ECD</strong> models of alpha4beta2, and alpha7 subunits of human nACHRs which are neurochemical targets for cessation of <b>smoking</b>.
+ECD	drug	amphetamine	20370784	<b>Methamphetamine</b> has been present in arrest related death cases in which an electronic control device (<strong>ECD</strong>) was used.
+ECD	drug	amphetamine	20370784	The primary purpose of this study was to determine the cardiac effects of an <strong>ECD</strong> in a <b>methamphetamine</b> intoxication model.
+ECD	addiction	intoxication	20370784	The primary purpose of this study was to determine the cardiac effects of an <strong>ECD</strong> in a methamphetamine <b>intoxication</b> model.
+ECD	drug	amphetamine	20370784	In smaller animals (32 kg or less), <strong>ECD</strong> exposure exacerbated atrial and ventricular irritability induced by <b>methamphetamine</b> intoxication, but this effect was not seen in larger, adult sized animals.
+ECD	addiction	intoxication	20370784	In smaller animals (32 kg or less), <strong>ECD</strong> exposure exacerbated atrial and ventricular irritability induced by methamphetamine <b>intoxication</b>, but this effect was not seen in larger, adult sized animals.
+ECD	drug	amphetamine	20370784	There were no episodes of ventricular fibrillation after exposure associated with <strong>ECD</strong> exposure in <b>methamphetamine</b> intoxicated sheep.
+ECD	drug	alcohol	17724867	[Evaluation of regional cerebral blood flow using 99mTc <strong>ECD</strong> SPECT in <b>ethanol</b> dependent patients: pilot study].
+ECD	drug	alcohol	17724867	The aim of the study is to evaluate morphologic and functional status of CNS using 99mTc <strong>ECD</strong> SPECT in chronic <b>alcoholics</b>.
+ECD	addiction	dependence	16752921	Besides becoming resistant to detergent inhibition, the soluble human E NTPDase 8 <strong>ECD</strong> displays greater activity with Ca nucleotide substrates, an increased affinity for ATP, different pH <b>dependence</b>, and a decreased sensitivity to azide inhibition when compared to the membrane bound enzyme.
+ECD	drug	alcohol	16480820	In order to further characterize the different effects of drugs induced AA release in the striatum and NAc, in the present study, we investigated the effect of <b>ethanol</b>, morphine, methamphetamine, nicotine induced AA release in these two nuclei using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC <strong>ECD</strong>).
+ECD	drug	amphetamine	16480820	In order to further characterize the different effects of drugs induced AA release in the striatum and NAc, in the present study, we investigated the effect of ethanol, morphine, <b>methamphetamine</b>, nicotine induced AA release in these two nuclei using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC <strong>ECD</strong>).
+ECD	drug	nicotine	16480820	In order to further characterize the different effects of drugs induced AA release in the striatum and NAc, in the present study, we investigated the effect of ethanol, morphine, methamphetamine, <b>nicotine</b> induced AA release in these two nuclei using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC <strong>ECD</strong>).
+ECD	drug	opioid	16480820	In order to further characterize the different effects of drugs induced AA release in the striatum and NAc, in the present study, we investigated the effect of ethanol, <b>morphine</b>, methamphetamine, nicotine induced AA release in these two nuclei using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC <strong>ECD</strong>).
+ECD	drug	cocaine	15846468	Extracellular fluid (ECF) DA levels were measured after intravenous administration of the BZT analogues AHN 1055 and AHN 2005, as well as <b>cocaine</b> using high performance liquid chromatography electrochemical detection (HPLC <strong>ECD</strong>).
+ECD	drug	amphetamine	15820231	Regional postmortem concentrations of dopamine and its metabolites were examined in tissue from age matched <b>AMPH</b> naive and <b>AMPH</b> sensitized monkeys using high performance liquid chromatography with electrochemical detection (HPLC <strong>ECD</strong>).
+ECD	drug	alcohol	12425888	[Behavior of brain perfusion with SPECT tomography 99mTc ethylene dicysteine (<strong>ECD</strong>) in <b>alcohol</b> and cocaine dependents during abstinence].
+ECD	drug	cocaine	12425888	[Behavior of brain perfusion with SPECT tomography 99mTc ethylene dicysteine (<strong>ECD</strong>) in alcohol and <b>cocaine</b> dependents during abstinence].
+ECD	drug	alcohol	12425888	In conclusion, after 28 days of <b>alcohol</b> and / or cocaine abstinence there is significant presence of brain perfusion abnormalities with 99mTc <strong>ECD</strong>.
+ECD	drug	cocaine	12425888	In conclusion, after 28 days of alcohol and / or <b>cocaine</b> abstinence there is significant presence of brain perfusion abnormalities with 99mTc <strong>ECD</strong>.
+ECD	drug	alcohol	10397294	Fourteen adults meeting DSM IV criteria for <b>alcohol</b> dependence (mean age 35, 8 SD; 10 men) and participating in a double blind detoxification medication study underwent a brain perfusion Tc99 m <strong>ECD</strong> (Neurolite) single photon emission computed tomography scan on days 7 through 9 (mean 7.6, .5 SD) after their last drink and 2 to 3 days since their last detoxification medication.
+ECD	addiction	dependence	10397294	Fourteen adults meeting DSM IV criteria for alcohol <b>dependence</b> (mean age 35, 8 SD; 10 men) and participating in a double blind detoxification medication study underwent a brain perfusion Tc99 m <strong>ECD</strong> (Neurolite) single photon emission computed tomography scan on days 7 through 9 (mean 7.6, .5 SD) after their last drink and 2 to 3 days since their last detoxification medication.
+ECD	addiction	aversion	9329072	The neurochemical consequences of <b>aversive</b> behavior based on novelty, rat social interaction, have been assessed in various rat brain regions utilizing high performance liquid chromatography coupled with an electrochemical detector (HPLC <strong>ECD</strong>) technique.
+ECD	drug	opioid	1754029	The animals were decapitated at 0.5 h or 1 h after <b>naloxone</b> injections and their brains analysed for monoamine concentrations by HPLC <strong>ECD</strong>.
+CTRL	drug	alcohol	31257463	At 12 h (sub‑acute) or 2 h (acute) before the experiment, female Lewis rats received a single oral dose of <b>alcohol</b> (<b>ethanol</b>, EtOH) or saline (NaCl, <strong>ctrl</strong>), followed by TxT, hemorrhagic shock (35±3 mm Hg) and resuscitation (H/R).
+CTRL	drug	alcohol	31161472	In pursuit of identifying brain structural substrates of impairment in <b>alcoholism</b>, we assessed executive functions (EF), episodic memory (MEM), and static postural balance (BAL) and measured regional brain gray matter volumes of cortical, subcortical, and cerebellar structures commonly affected in individuals with <b>alcohol</b> dependence (ALC) compared with healthy controls (<strong>CTRL</strong>).
+CTRL	addiction	dependence	31161472	In pursuit of identifying brain structural substrates of impairment in alcoholism, we assessed executive functions (EF), episodic memory (MEM), and static postural balance (BAL) and measured regional brain gray matter volumes of cortical, subcortical, and cerebellar structures commonly affected in individuals with alcohol <b>dependence</b> (ALC) compared with healthy controls (<strong>CTRL</strong>).
+CTRL	drug	cannabinoid	29882015	To determine differential associations of concomitant use of <b>cannabis</b> and nicotine, isolated <b>cannabis</b> use and isolated nicotine use on brain network connectivity, we examined systems level neural functioning via independent components analysis (ICA) on resting state networks (RSNs) in <b>cannabis</b> users (CAN, n = 53), nicotine users (NIC, n = 28), concomitant nicotine and <b>cannabis</b> users (NIC + CAN, n = 26), and non users (<strong>CTRL</strong>, n = 30).
+CTRL	drug	nicotine	29882015	To determine differential associations of concomitant use of cannabis and <b>nicotine</b>, isolated cannabis use and isolated <b>nicotine</b> use on brain network connectivity, we examined systems level neural functioning via independent components analysis (ICA) on resting state networks (RSNs) in cannabis users (CAN, n = 53), <b>nicotine</b> users (NIC, n = 28), concomitant <b>nicotine</b> and cannabis users (NIC + CAN, n = 26), and non users (<strong>CTRL</strong>, n = 30).
+CTRL	drug	amphetamine	29224181	The aim of this study was to assess the magnitude of social cognition impairment and its association with aggression in individuals with <b>methamphetamine</b> (MA) dependence, <b>methamphetamine</b> associated psychosis (MAP), and healthy controls (<strong>CTRL</strong>).
+CTRL	addiction	dependence	29224181	The aim of this study was to assess the magnitude of social cognition impairment and its association with aggression in individuals with methamphetamine (MA) <b>dependence</b>, methamphetamine associated psychosis (MAP), and healthy controls (<strong>CTRL</strong>).
+CTRL	drug	alcohol	28887129	In this study we show that <b>disulfiram</b> potently inhibits the <strong>chymotrypsin like</strong> activity of purified human 20S proteasome at low micromolar pharmacological concentrations.
+CTRL	drug	cocaine	27181613	UE rats (n = 10) self administered more <b>cocaine</b> on Day 1 of LgA than control rats (<strong>Ctrl</strong> + Coc; n = 8).
+CTRL	drug	alcohol	26922280	<strong>Chymotrypsin like</strong> activity was measured after 2 h, 24 h, and 48 h exposure to 5 μM cocaine or 40 mM <b>ethanol</b>.
+CTRL	drug	cocaine	26922280	<strong>Chymotrypsin like</strong> activity was measured after 2 h, 24 h, and 48 h exposure to 5 μM <b>cocaine</b> or 40 mM ethanol.
+CTRL	drug	alcohol	26922280	Treatments modified proteasome function in opposite directions, since cocaine increased and <b>ethanol</b> reduced <strong>chymotrypsin like</strong> activity.
+CTRL	drug	cocaine	26922280	Treatments modified proteasome function in opposite directions, since <b>cocaine</b> increased and ethanol reduced <strong>chymotrypsin like</strong> activity.
+CTRL	drug	psychedelics	25894683	For this, 48 Wistar rats were divided into four groups: control + saline (<strong>CTRL</strong> + SAL), control + <b>ketamine</b> (<strong>CTRL</strong> + KET), CUS + saline (CUS + SAL), CUS + <b>ketamine</b> (CUS + KET).
+CTRL	drug	alcohol	24481563	The effects produced by binge <b>ethanol</b> consumption in the liver of male Wistar rats fed a standard (<strong>Ctrl</strong>) or a high fat diet HFD were compared.
+CTRL	addiction	intoxication	24481563	The effects produced by <b>binge</b> ethanol consumption in the liver of male Wistar rats fed a standard (<strong>Ctrl</strong>) or a high fat diet HFD were compared.
+CTRL	drug	alcohol	23451104	We demonstrate that <b>ethanol</b> impairs proteasome function in peritoneal macrophages through suppression of <strong>chymotrypsin like</strong> (Cht L) proteasome activity as well as composition of the immunoproteasome subunit LMP7.
+CTRL	drug	alcohol	22550557	14 h before H/R, rats were gavaged with single dose of <b>ethanol</b> or saline (5 g/kg, EtOH and <strong>ctrl</strong>; H/R_EtOH or H/R_ctrl, resp.).
+CTRL	drug	alcohol	21881571	Following <b>ethanol</b> self administration training and conditioning procedures, rats were made <b>ethanol</b> dependent, using <b>ethanol</b> vapor inhalation, under three conditions: a single intoxication and withdrawal episode (SW), repeated cycles of intoxication and withdrawal (RW), or no intoxication (<strong>CTRL</strong>).
+CTRL	addiction	intoxication	21881571	Following ethanol self administration training and conditioning procedures, rats were made ethanol dependent, using ethanol vapor inhalation, under three conditions: a single <b>intoxication</b> and withdrawal episode (SW), repeated cycles of <b>intoxication</b> and withdrawal (RW), or no <b>intoxication</b> (<strong>CTRL</strong>).
+CTRL	addiction	withdrawal	21881571	Following ethanol self administration training and conditioning procedures, rats were made ethanol dependent, using ethanol vapor inhalation, under three conditions: a single intoxication and <b>withdrawal</b> episode (SW), repeated cycles of intoxication and <b>withdrawal</b> (RW), or no intoxication (<strong>CTRL</strong>).
+CTRL	drug	cocaine	17895914	Experiment 1 Rats trained to self administer <b>cocaine</b>, under short (ShA, 1 h) or long (LgA, 6 h) access conditions, or noncaloric food pellets (<strong>Ctrl</strong>, 1 h), were tested for stress reactivity in the shock probe defensive burying test following 1, 14, 42, or 84 days of abstinence.
+CTRL	drug	alcohol	12664190	Subsequently, rats were divided into three groups and exposed to control vapor (<strong>CTRL</strong>), to 12 day <b>ethanol</b> vapor prior to withdrawal (SW), or to three cycles of 3 day intoxication experiences (MW), respectively.
+CTRL	addiction	intoxication	12664190	Subsequently, rats were divided into three groups and exposed to control vapor (<strong>CTRL</strong>), to 12 day ethanol vapor prior to withdrawal (SW), or to three cycles of 3 day <b>intoxication</b> experiences (MW), respectively.
+CTRL	addiction	withdrawal	12664190	Subsequently, rats were divided into three groups and exposed to control vapor (<strong>CTRL</strong>), to 12 day ethanol vapor prior to <b>withdrawal</b> (SW), or to three cycles of 3 day intoxication experiences (MW), respectively.
+CTRL	drug	alcohol	11755313	The liver proteasomal <strong>chymotrypsin like</strong> activity (ChT L) in rats fed <b>ethanol</b> was inhibited.
+CTRL	addiction	aversion	8255921	A subsequent test for passive avoidance confirmed that the 75 dB SIGNAL was <b>aversive</b> for mice that had received noise conditioning but not for <strong>Ctrl</strong> mice.
+AIFM2	drug	opioid	32732685	Cases of surgical injection drug use associated infective endocarditis (IDU IE) are on the rise, <strong>amid</strong> the US <b>opioid</b> epidemic.
+AIFM2	drug	opioid	31795056	Bouncing back: Brain rehabilitation <strong>amid</strong> <b>opioid</b> and stimulant epidemics.
+AIFM2	drug	alcohol	31766530	: <strong>Amid</strong> concerns about increasing <b>alcohol</b> related violence in licensed premises, Queensland introduced a system of risk based licensing (RBL) in 2009, the first of five Australian jurisdictions to do so.
+AIFM2	drug	alcohol	31339221	The increase in <b>ethanol</b> self administration was associated with (a) reductions in levels of the endocannabinoids N arachidonoylethanolomine and 2 arachidonoylglycerol in the CeA, (b) increased amygdalar gene expression of cannabinoid type 1 receptor (CB1), N acyl phosphatidylethanolamine phospholipase D (Nape pld), fatty acid <strong>amid</strong> hydrolase (Faah), (c) decreased amygdalar gene expression of ionotropic AMPA (GluA2 and GluA4) and metabotropic (mGlu3) glutamate receptors, and (d) increased glutamatergic receptor function.
+AIFM2	drug	cannabinoid	31339221	The increase in ethanol self administration was associated with (a) reductions in levels of the <b>endocannabinoids</b> N arachidonoylethanolomine and 2 arachidonoylglycerol in the CeA, (b) increased amygdalar gene expression of <b>cannabinoid</b> type 1 receptor (CB1), N acyl phosphatidylethanolamine phospholipase D (Nape pld), fatty acid <strong>amid</strong> hydrolase (Faah), (c) decreased amygdalar gene expression of ionotropic AMPA (GluA2 and GluA4) and metabotropic (mGlu3) glutamate receptors, and (d) increased glutamatergic receptor function.
+AIFM2	drug	opioid	30933576	News Media Reporting On Medication Treatment For <b>Opioid</b> Use Disorder <strong>Amid</strong> The <b>Opioid</b> Epidemic.
+AIFM2	drug	opioid	30933576	Given the importance of the news media as a source of health information for the public and its role in shaping knowledge about these medications, we examined reporting on OUD medication treatment <strong>amid</strong> the <b>opioid</b> crisis.
+AIFM2	drug	opioid	30791718	Drug Induced Liver Injury Caused by <b>Kratom</b> Use as an Alternative Pain Treatment <strong>Amid</strong> an Ongoing <b>Opioid</b> Epidemic.
+AIFM2	drug	opioid	30675818	<strong>Amid</strong> worsening <b>opioid</b> overdose death rates, the nation continues to face a persistent addiction treatment gap limiting access to quality care for <b>opioid</b> use disorder (OUD).
+AIFM2	addiction	addiction	30675818	<strong>Amid</strong> worsening opioid overdose death rates, the nation continues to face a persistent <b>addiction</b> treatment gap limiting access to quality care for opioid use disorder (OUD).
+AIFM2	drug	opioid	30082370	North America is <strong>amid</strong> an <b>opioid</b> use epidemic.
+AIFM2	drug	opioid	29911684	The United States are <strong>amid</strong> an <b>opioid</b> overdose epidemic; we are challenged to provide non addicting/non pharmacological alternatives to assist in pain attenuation.
+AIFM2	drug	nicotine	29432572	Integration of these literatures suggests that CC contributes to both self regulation (ie, brake pedal) and <b>nicotine</b> related reinforcement (ie, gas pedal) <strong>amid</strong> the catastrophic effects of long term <b>smoking</b>, which may reduce self regulatory control over <b>smoking</b> while also enhancing indirect reinforcement.
+AIFM2	addiction	reward	29432572	Integration of these literatures suggests that CC contributes to both self regulation (ie, brake pedal) and nicotine related <b>reinforcement</b> (ie, gas pedal) <strong>amid</strong> the catastrophic effects of long term smoking, which may reduce self regulatory control over smoking while also enhancing indirect <b>reinforcement</b>.
+AIFM2	drug	nicotine	28802179	<strong>Amid</strong> decreasing rates of cigarette <b>smoking</b> and a rise in e cigarette use, there is a need to understand population patterns of use to inform <b>tobacco</b> control efforts and evaluate whether e cigarettes may play a role in <b>tobacco</b> harm reduction.
+AIFM2	drug	nicotine	28610966	The aim of the present study was to investigate university students’ <b>smoking</b> habits and exposure to secondary smoke <strong>amid</strong> a financial crisis.
+AIFM2	addiction	relapse	28446040	Our data may illustrate more accurately the situation of youth social withdrawal <strong>amid</strong> the general population than data from help <b>seeking</b> patients or online questionnaires.
+AIFM2	addiction	withdrawal	28446040	Our data may illustrate more accurately the situation of youth social <b>withdrawal</b> <strong>amid</strong> the general population than data from help seeking patients or online questionnaires.
+AIFM2	drug	opioid	27898133	The United States is <strong>amid</strong> an epidemic of prescription <b>opioid</b> drug abuse, bringing with it not only high rates of overdose, but growing rates of <b>heroin</b> abuse and addiction.
+AIFM2	addiction	addiction	27898133	The United States is <strong>amid</strong> an epidemic of prescription opioid drug abuse, bringing with it not only high rates of overdose, but growing rates of heroin abuse and <b>addiction</b>.
+AIFM2	drug	opioid	24857185	<strong>Amid</strong> the global transition to treat <b>opioid</b> addiction as an illness, many people who inject drugs (PWID) face heterogeneous legal environments that include both punitive and harm reduction measures.
+AIFM2	addiction	addiction	24857185	<strong>Amid</strong> the global transition to treat opioid <b>addiction</b> as an illness, many people who inject drugs (PWID) face heterogeneous legal environments that include both punitive and harm reduction measures.
+AIFM2	addiction	reward	23829366	Further, the involvement of CB1 and CB2 receptors, as well the fatty acid <strong>amid</strong> hydrolase (FAAH) enzyme in <b>reward</b> processes is investigated through presentation of respective genetic ablation studies in mice.
+AIFM2	addiction	reward	22047719	It is possible that the lower FA and higher RD in the RHU group reflect microstructural injury to frontal circuitries, and these may underlie the reduced cognitive control <strong>amid</strong> heightened <b>reward</b> sensitivity associated with resumption of heavy drinking.
+AIFM2	drug	alcohol	17207119	The history of the Journal of Inebriety mirrors efforts in America to forge a legitimized field of addiction medicine <strong>amid</strong> conflicting conceptualizations of the nature of severe <b>alcohol</b> and other drug problems.
+AIFM2	addiction	addiction	17207119	The history of the Journal of Inebriety mirrors efforts in America to forge a legitimized field of <b>addiction</b> medicine <strong>amid</strong> conflicting conceptualizations of the nature of severe alcohol and other drug problems.
+AIFM2	addiction	dependence	16426261	Only a few years later, <strong>amid</strong> widespread reports of abuse and <b>dependence</b>, primarily in migraine patients, its manufacturer voluntarily requested the Food and Drug Administration to reschedule the drug as a Schedule IV narcotic.
+SUCLA2	drug	opioid	31168735	Among injectors, female gender, racial minority status, suspicion of drugs containing <b>fentanyl</b>, and drug use in public/semi public settings were associated with higher willingness to use <strong>a SCS</strong>; prior arrest was associated with lower willingness.
+SUCLA2	drug	psychedelics	28266890	This study adds to the literature by using the 5d ASC, a psychometrically sound measure of altered states of consciousness (<strong>ASCs</strong>), to examine the <strong>ASCs</strong> induced by <b>ibogaine</b> and discusses the demographic characteristics of those who seek <b>ibogaine</b> treatment (N = 27).
+SUCLA2	drug	psychedelics	28266890	Results indicated a positive correlation between the various dimensions of the <strong>ASCs</strong> and the outcome (ability to make changes in one's life, cravings, and how changed the person was as a result of <b>ibogaine</b> treatment).
+SUCLA2	drug	opioid	18521004	<b>Morphine</b> inhibits herpetic allodynia through mu <b>opioid</b> receptors induced in <strong>Abeta</strong> fiber neurons.
+SUCLA2	drug	opioid	18521004	Mechanical allodynia is mainly mediated by <strong>Abeta</strong> fibers, whereas mu <b>opioid</b> receptors are present in C and Adelta fibers.
+SUCLA2	drug	opioid	18521004	Viral propagation in the sensory ganglion may induce mu <b>opioid</b> receptor expression in <strong>Abeta</strong> fibers, which may be responsible for the inhibitory action of local <b>opioids</b> on mechanical allodynia in mice with herpetic pain.
+SUCLA2	addiction	withdrawal	18088441	Furthermore, in a novel electrical stimulation induced paw <b>withdrawal</b> (EPW) test, the thresholds for stimulation through C , Adelta  and <strong>Abeta</strong> fibers were all decreased by AS ODN pretreatments.
+SUCLA2	drug	alcohol	17253767	<strong>Abeta</strong> binding <b>alcohol</b> dehydrogenase (ABAD) is an NAD dependent mitochondrial dehydrogenase.
+SUCLA2	addiction	dependence	17253767	In this study, surface plasmon resonance (SPR) was employed to determine the temperature <b>dependence</b> of the affinity of the ABAD <strong>Abeta</strong> interaction.
+SUCLA2	addiction	reward	16372134	Here, genetic association of the common R219K variant of ABCA1 is shown with cerebrospinal fluid (CSF) <strong>Abeta</strong> 1 42 levels, <b>reinforcing</b> emerging evidence of a connection between lipid and <strong>Abeta</strong> metabolism.
+SUCLA2	drug	alcohol	16340465	Therefore, the current studies aimed to investigate the effects of exposure to 50 or 100 mM <b>ethanol</b> (EtOH) and withdrawal on hippocampal injury induced by <strong>Abeta</strong> peptide treatment.
+SUCLA2	addiction	withdrawal	16340465	Therefore, the current studies aimed to investigate the effects of exposure to 50 or 100 mM ethanol (EtOH) and <b>withdrawal</b> on hippocampal injury induced by <strong>Abeta</strong> peptide treatment.
+SUCLA2	drug	alcohol	16340465	The present studies exposed organotypic hippocampal slice cultures to 50 or 100 mM <b>ethanol</b> (EtOH) for 10 days, after which the slices underwent <b>ethanol</b> withdrawal (EWD) in the presence of varying concentrations of <strong>Abeta</strong> 25 35 (0.1, 1, 10 microM), or 35 25 (200 microM), a negative control reverse sequence peptide.
+SUCLA2	addiction	withdrawal	16340465	The present studies exposed organotypic hippocampal slice cultures to 50 or 100 mM ethanol (EtOH) for 10 days, after which the slices underwent ethanol <b>withdrawal</b> (EWD) in the presence of varying concentrations of <strong>Abeta</strong> 25 35 (0.1, 1, 10 microM), or 35 25 (200 microM), a negative control reverse sequence peptide.
+SUCLA2	drug	alcohol	16340465	Exposure to <strong>Abeta</strong> in <b>ethanol</b> naïve cultures did not produce significant cytotoxicity.
+SUCLA2	addiction	withdrawal	16340465	Further, this EtOH exposure and <b>withdrawal</b> regimen sensitizes the hippocampus to the toxic effects of <strong>Abeta</strong> treatment in a manner reflecting over activity of NMDA receptor function.
+SUCLA2	drug	nicotine	12970390	Using these cells as a model system, we designed experiments to more directly determine whether <strong>Abeta</strong> peptides (Abeta1 42 and Abeta1 40) interfere with a potential nicotinic cytoprotective action and with the ability of <b>nicotine</b> to increase intracellular Ca2+.
+RNASE1	drug	opioid	32641997	Decreased Neuronal Excitability in Medial Prefrontal Cortex during <b>Morphine</b> Withdrawal is associated with enhanced SK channel activity and upregulation of small GTPase <strong>Rac1</strong>.
+RNASE1	addiction	withdrawal	32641997	Decreased Neuronal Excitability in Medial Prefrontal Cortex during Morphine <b>Withdrawal</b> is associated with enhanced SK channel activity and upregulation of small GTPase <strong>Rac1</strong>.
+RNASE1	addiction	withdrawal	32641997	We verified the hypothesis that <strong>Rac1</strong>, a member of Rho family of small GTPases, implicated in SK channel regulation, modulate SK channel neuroadaptations during opiate <b>withdrawal</b>.
+RNASE1	addiction	withdrawal	32641997	In the IL, <strong>Rac1</strong> signaling was increased during <b>withdrawal</b>, and the <strong>Rac1</strong> inhibitor NSC23766 disrupted SK current, which increased neuronal firing.
+RNASE1	drug	opioid	32641997	Suppression of <strong>Rac1</strong> inhibited <b>morphine</b> induced CPP and expression of SK channels in IL.
+RNASE1	addiction	reward	32641997	Suppression of <strong>Rac1</strong> inhibited morphine induced <b>CPP</b> and expression of SK channels in IL.
+RNASE1	drug	opioid	32641997	Conclusions: These findings highlight the potential value of SK channels and the upstream molecule <strong>Rac1</strong>, which may throw light on the therapeutic mechanism of neuromodulation treatment for <b>opioid</b> dependence.
+RNASE1	addiction	dependence	32641997	Conclusions: These findings highlight the potential value of SK channels and the upstream molecule <strong>Rac1</strong>, which may throw light on the therapeutic mechanism of neuromodulation treatment for opioid <b>dependence</b>.
+RNASE1	drug	amphetamine	31660086	Different roles of <strong>Rac1</strong> in the acquisition and extinction of <b>methamphetamine</b> associated contextual memory in the nucleus accumbens.
+RNASE1	drug	amphetamine	31660086	Here, we explored whether <strong>Rac1</strong> in the NAc mediates <b>METH</b> associated contextual memory and spine remodelling.
+RNASE1	drug	amphetamine	31660086	Methods: Pharmacological and genetic manipulations of <strong>Rac1</strong> were used to investigate its role during the acquisition, reconsolidation and extinction of <b>METH</b> associated contextual memory.
+RNASE1	drug	amphetamine	31660086	Results: Using viral mediated gene transfer, we demonstrated that decreased <strong>Rac1</strong> activity was required for the acquisition of <b>METH</b> associated contextual memory and the <b>METH</b> induced increase in thin spine density, whereas increased <strong>Rac1</strong> signalling was important for the extinction of <b>METH</b> associated contextual memory and the related elimination of thin spines.
+RNASE1	drug	amphetamine	31660086	Interestingly, <strong>Rac1</strong> was responsible for <b>METH</b> induced spine plasticity in D1 MSNs but not in D2 MSNs.
+RNASE1	drug	amphetamine	31660086	Additionally, we found that microinjection of a <strong>Rac1</strong> inhibitor or activator into the NAc was not sufficient to disrupt reconsolidation, and the pharmacological activation of <strong>Rac1</strong> in the NAc facilitated the extinction of <b>METH</b> associated contextual memory.
+RNASE1	drug	amphetamine	31660086	Regarding cognitive memory, decreased <strong>Rac1</strong> activity improved the <b>METH</b> induced impairment in object recognition memory.
+RNASE1	drug	amphetamine	31660086	Conclusion: Our findings indicate that <strong>Rac1</strong> plays opposing roles in the acquisition and extinction of <b>METH</b> associated contextual memory and reveal the cell specific role of <strong>Rac1</strong> in <b>METH</b> associated spine remodelling, suggesting that <strong>Rac1</strong> is a potential therapeutic target for reducing relapse in <b>METH</b> addiction and remediating <b>METH</b> induced recognition memory impairment.
+RNASE1	addiction	addiction	31660086	Conclusion: Our findings indicate that <strong>Rac1</strong> plays opposing roles in the acquisition and extinction of METH associated contextual memory and reveal the cell specific role of <strong>Rac1</strong> in METH associated spine remodelling, suggesting that <strong>Rac1</strong> is a potential therapeutic target for reducing relapse in METH <b>addiction</b> and remediating METH induced recognition memory impairment.
+RNASE1	addiction	relapse	31660086	Conclusion: Our findings indicate that <strong>Rac1</strong> plays opposing roles in the acquisition and extinction of METH associated contextual memory and reveal the cell specific role of <strong>Rac1</strong> in METH associated spine remodelling, suggesting that <strong>Rac1</strong> is a potential therapeutic target for reducing <b>relapse</b> in METH addiction and remediating METH induced recognition memory impairment.
+RNASE1	drug	alcohol	31558618	Here we investigate the role of <strong>Rac1</strong> and its downstream target, the actin severing protein cofilin, in <b>alcohol</b> consumption preference.
+RNASE1	drug	alcohol	31558618	We show that these two regulators of actin dynamics can alter male experience dependent <b>alcohol</b> preference in a bidirectional manner: expressing either activated <strong>Rac1</strong> or dominant negative cofilin in the mushroom bodies (MBs) abolishes experience dependent <b>alcohol</b> preference.
+RNASE1	drug	alcohol	31558618	Conversely, dominant negative <strong>Rac1</strong> or activated cofilin MB expression lead to faster acquisition of <b>alcohol</b> preference.
+RNASE1	drug	alcohol	31558618	Our data show that <strong>Rac1</strong> and cofilin activity are key to determining the rate of acquisition of <b>alcohol</b> preference, revealing a critical role of actin dynamics regulation in the development of voluntary self administration in Drosophila SIGNIFICANCE STATEMENT The risks for developing an <b>alcohol</b> use disorder (AUD) are strongly determined by genetic factors.
+RNASE1	drug	opioid	31515267	We found that DAMGO, but not <b>morphine</b>, activates Ras related C3 botulinum toxin substrate 1 (<strong>Rac1</strong>).
+RNASE1	drug	opioid	31413370	Meanwhile, <b>morphine</b> enhances the inhibitory inputs from somatostatin+ (SST) INs onto PV INs, and thus disinhibits pyramidal neurons via δ <b>opioid</b> receptor (DOR) dependent <strong>Rac1</strong> upregulation in SST INs.
+RNASE1	drug	opioid	31413370	We show that MOR in PV INs is required for <b>morphine</b> induced behavioral sensitization, while DOR as well as <strong>Rac1</strong> activity in SST INs is required for <b>morphine</b> induced conditioned place preference and hyper locomotion.
+RNASE1	addiction	sensitization	31413370	We show that MOR in PV INs is required for morphine induced behavioral <b>sensitization</b>, while DOR as well as <strong>Rac1</strong> activity in SST INs is required for morphine induced conditioned place preference and hyper locomotion.
+RNASE1	drug	amphetamine	31153969	Four putative targets (Sema3A, Plxna4, <strong>Rac1</strong>, and Pak3) enriched in axon guidance also exhibited significant changes in the NAc after <b>METH</b> challenge injection.
+RNASE1	drug	amphetamine	31060803	Dopamine D1 and D2 Receptors Differentially Regulate <strong>Rac1</strong> and Cdc42 Signaling in the Nucleus Accumbens to Modulate Behavioral and Structural Plasticity After Repeated <b>Methamphetamine</b> Treatment.
+RNASE1	drug	amphetamine	31060803	However, how dopamine D1 and D2 receptors (D1Rs and D2Rs, respectively) as well as downstream signaling pathways, such as those involving <strong>Rac1</strong> and Cdc42, modulate <b>METH</b> induced behavioral and structural plasticity is largely unknown.
+RNASE1	drug	amphetamine	31060803	Using NAc conditional D1R and D2R deletion mice, <strong>Rac1</strong> and Cdc42 mutant viruses, and a series of behavioral and morphological methods, we assessed the effects of D1Rs and D2Rs on <strong>Rac1</strong> and Cdc42 in modulating <b>METH</b> induced behavioral and structural plasticity in the NAc.
+RNASE1	drug	amphetamine	31060803	Interestingly, <strong>Rac1</strong> and Cdc42 signaling were oppositely modulated by <b>METH</b>, and suppression of <strong>Rac1</strong> signaling and activation of Cdc42 signaling were crucial to <b>METH</b> induced conditioned place preference and structural plasticity but not to locomotor activation.
+RNASE1	drug	amphetamine	31060803	D1Rs activated <strong>Rac1</strong> and Cdc42 signaling, while D2Rs inhibited <strong>Rac1</strong> signaling but activated Cdc42 signaling to mediate <b>METH</b> induced conditioned place preference and structural plasticity but not locomotor activation.
+RNASE1	drug	amphetamine	31060803	In addition, NAc D1R deletion aggravated <b>METH</b> withdrawal induced spatial learning and memory impairment by suppressing <strong>Rac1</strong> signaling but not Cdc42 signaling, while NAc D2R deletion aggravated <b>METH</b> withdrawal induced anxiety without affecting <strong>Rac1</strong> or Cdc42 signaling.
+RNASE1	addiction	withdrawal	31060803	In addition, NAc D1R deletion aggravated METH <b>withdrawal</b> induced spatial learning and memory impairment by suppressing <strong>Rac1</strong> signaling but not Cdc42 signaling, while NAc D2R deletion aggravated METH <b>withdrawal</b> induced anxiety without affecting <strong>Rac1</strong> or Cdc42 signaling.
+RNASE1	drug	amphetamine	31060803	D1Rs and D2Rs differentially regulate <strong>Rac1</strong> and Cdc42 signaling to modulate <b>METH</b> induced behavioral plasticity and the structural remodeling of medium spiny neurons in the NAc.
+RNASE1	drug	cocaine	28726800	<b>Cocaine</b> significantly decreased SAM/SAH ratio levels in the DS, which was accompanied with the decreased activities of <strong>Rac1</strong> and RhoA.
+RNASE1	drug	cocaine	28726800	Lentivirus mediated knockdown of Nnmt in the dorsomedial striatum (DMS) attenuated <b>cocaine</b> conditioned place preference (CPP) reward, but increased striatal SAM/SAH ratio levels as well as <strong>Rac1</strong> and RhoA activities.
+RNASE1	addiction	reward	28726800	Lentivirus mediated knockdown of Nnmt in the dorsomedial striatum (DMS) attenuated cocaine conditioned place preference (<b>CPP</b>) <b>reward</b>, but increased striatal SAM/SAH ratio levels as well as <strong>Rac1</strong> and RhoA activities.
+RNASE1	drug	cocaine	28726800	In addition, pharmacological inhibition of NNMT through intra DMS infusion of MeN attenuated <b>cocaine</b> CPP and the activities of <strong>Rac1</strong> and RhoA, but increased SAM/SAH ratio.
+RNASE1	addiction	reward	28726800	In addition, pharmacological inhibition of NNMT through intra DMS infusion of MeN attenuated cocaine <b>CPP</b> and the activities of <strong>Rac1</strong> and RhoA, but increased SAM/SAH ratio.
+RNASE1	drug	cocaine	28726800	The results showed that <b>cocaine</b> increased the association of RhoGDIα with <strong>Rac1</strong> or RhoA, whereas such effect was inhibited by Nnmt knockdown.
+RNASE1	drug	cocaine	28726800	Collectively, our findings show that NNMT regulates <b>cocaine</b> CPP through SAM mediated modification of <strong>Rac1</strong> and RhoA.
+RNASE1	addiction	reward	28726800	Collectively, our findings show that NNMT regulates cocaine <b>CPP</b> through SAM mediated modification of <strong>Rac1</strong> and RhoA.
+RNASE1	addiction	aversion	28630256	The Small GTPase <strong>Rac1</strong> Contributes to Extinction of <b>Aversive</b> Memories of Drug Withdrawal by Facilitating GABAA Receptor Endocytosis in the vmPFC.
+RNASE1	addiction	withdrawal	28630256	The Small GTPase <strong>Rac1</strong> Contributes to Extinction of Aversive Memories of Drug <b>Withdrawal</b> by Facilitating GABAA Receptor Endocytosis in the vmPFC.
+RNASE1	drug	opioid	28630256	Here, we report that extinction of conditioned place aversion (CPA) to <b>naloxone</b> precipitated opiate withdrawal in male rats activates Rho GTPase <strong>Rac1</strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RNASE1	addiction	aversion	28630256	Here, we report that extinction of conditioned place <b>aversion</b> (CPA) to naloxone precipitated opiate withdrawal in male rats activates Rho GTPase <strong>Rac1</strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RNASE1	addiction	withdrawal	28630256	Here, we report that extinction of conditioned place aversion (CPA) to naloxone precipitated opiate <b>withdrawal</b> in male rats activates Rho GTPase <strong>Rac1</strong> in the ventromedial prefrontal cortex (vmPFC) in a BDNF dependent manner, which determines GABAA receptor (GABAAR) endocytosis via triggering synaptic translocation of activity regulated cytoskeleton associated protein (Arc) through facilitating actin polymerization.
+RNASE1	addiction	aversion	28630256	Thus, the present study provides first evidence that <strong>Rac1</strong> dependent GABAAR endocytosis plays a crucial role in extinction of <b>aversive</b> memories and reveals the sequence of molecular events that contribute to learning experience modulation of synaptic GABAAR endocytosis.SIGNIFICANCE STATEMENT This study reveals that <strong>Rac1</strong> dependent GABAAR endocytosis plays a crucial role in extinction of <b>aversive</b> memories associated with drug withdrawal and identifies Arc as a downstream effector of <strong>Rac1</strong> regulations of synaptic plasticity as well as learning and memory, thereby suggesting therapeutic targets to promote extinction of the unwanted memories.
+RNASE1	addiction	withdrawal	28630256	Thus, the present study provides first evidence that <strong>Rac1</strong> dependent GABAAR endocytosis plays a crucial role in extinction of aversive memories and reveals the sequence of molecular events that contribute to learning experience modulation of synaptic GABAAR endocytosis.SIGNIFICANCE STATEMENT This study reveals that <strong>Rac1</strong> dependent GABAAR endocytosis plays a crucial role in extinction of aversive memories associated with drug <b>withdrawal</b> and identifies Arc as a downstream effector of <strong>Rac1</strong> regulations of synaptic plasticity as well as learning and memory, thereby suggesting therapeutic targets to promote extinction of the unwanted memories.
+RNASE1	drug	alcohol	26366560	Previously, we described that regulators of actin dynamics, such as the Rho family GTPases <strong>Rac1</strong>, Rho1, and Cdc42, alter Drosophila's sensitivity to <b>ethanol</b> induced sedation.
+RNASE1	drug	alcohol	26170296	Together, these data suggest a conserved role for integrin/Rsu1/<strong>Rac1</strong>/actin signaling in modulating reward related phenotypes, including <b>ethanol</b> consumption, across phyla.
+RNASE1	addiction	reward	26170296	Together, these data suggest a conserved role for integrin/Rsu1/<strong>Rac1</strong>/actin signaling in modulating <b>reward</b> related phenotypes, including ethanol consumption, across phyla.
+RNASE1	drug	cocaine	25957559	Dishevelled 2 regulates <b>cocaine</b> induced structural plasticity and <strong>Rac1</strong> activity in the nucleus accumbens.
+RNASE1	drug	cocaine	25957559	In this study we examined whether isoforms of Dishevelled, a key hub protein of multiple branches of Wnt signaling, including <strong>Rac1</strong>, are regulated in the NAc by chronic <b>cocaine</b>, and whether these Dishevelled isoforms control <strong>Rac1</strong> activity in this brain region in vivo.
+RNASE1	drug	cocaine	25957559	We found that chronic <b>cocaine</b> administration decreased expression of Dishevelled 2, and several other Wnt signaling components, in the NAc, and that overexpression of Dishevelled 2, but not Dishevelled 1, conversely upregulated <strong>Rac1</strong> activity and prevented the <b>cocaine</b> induction of dendritic spines on NAc MSNs.
+RNASE1	drug	cocaine	25957559	We posit that the <b>cocaine</b> induced downregulation of Dishevelled 2 in the NAc is an upstream regulator of <strong>Rac1</strong> activity and plays an important role in the dynamic structural plasticity of NAc MSNs seen in response to chronic <b>cocaine</b> exposure.
+RNASE1	drug	cocaine	25595128	<b>Cocaine</b> activates <strong>Rac1</strong> to control structural and behavioral plasticity in caudate putamen.
+RNASE1	drug	cocaine	25595128	In this study, we investigated the role of <strong>Rac1</strong> in <b>cocaine</b> induced dendritic and behavioral plasticity in the CPu.
+RNASE1	drug	cocaine	25595128	We found that <strong>Rac1</strong> activation was reduced in the NAc but increased in the CPu following repeated <b>cocaine</b> treatment.
+RNASE1	drug	cocaine	25595128	Inhibition of <strong>Rac1</strong> activity by a <strong>Rac1</strong> specific inhibitor NSC23766, overexpression of a dominant negative mutant of <strong>Rac1</strong> (T17N <strong>Rac1</strong>) or local knockout of <strong>Rac1</strong> attenuated the <b>cocaine</b> induced increase in dendrites and spine density in the CPu, whereas overexpression of a constitutively active <strong>Rac1</strong> exert the opposite effect.
+RNASE1	drug	cocaine	25595128	Downregulation of <strong>Rac1</strong> activity likewise attenuates behavioral reward responses to <b>cocaine</b> exposure, with activation of <strong>Rac1</strong> producing the opposite effect.
+RNASE1	addiction	reward	25595128	Downregulation of <strong>Rac1</strong> activity likewise attenuates behavioral <b>reward</b> responses to cocaine exposure, with activation of <strong>Rac1</strong> producing the opposite effect.
+RNASE1	drug	cocaine	25595128	Thus, <strong>Rac1</strong> signaling is differentially regulated in the NAc and CPu after repeated <b>cocaine</b> treatment, and induction of <strong>Rac1</strong> activation in the CPu is important for <b>cocaine</b> exposure induced dendritic remodeling and behavioral plasticity.
+RNASE1	drug	alcohol	25257290	<b>Alcohol</b> rapidly decreased GTP bound <strong>Rac1</strong> but not RhoA during the drop in TER.
+RNASE1	drug	cocaine	23628212	These studies confirmed the classical hypothesis of movement control and reward seeking behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in <b>cocaine</b> reward; dissected the roles of glutamatergic and dopaminergic inputs to striatum in reward; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in reward and the rho GTPase <strong>Rac1</strong> in <b>cocaine</b> reward and <b>cocaine</b> induced structural plasticity.
+RNASE1	addiction	relapse	23628212	These studies confirmed the classical hypothesis of movement control and reward <b>seeking</b> behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in cocaine reward; dissected the roles of glutamatergic and dopaminergic inputs to striatum in reward; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in reward and the rho GTPase <strong>Rac1</strong> in cocaine reward and cocaine induced structural plasticity.
+RNASE1	addiction	reward	23628212	These studies confirmed the classical hypothesis of movement control and <b>reward</b> seeking behavior through direct versus indirect pathway MSNs; illuminated a selective role for TANs in cocaine <b>reward</b>; dissected the roles of glutamatergic and dopaminergic inputs to striatum in <b>reward</b>; and highlighted a role for striatal signaling molecules including an adrenergic G protein coupled receptor in <b>reward</b> and the rho GTPase <strong>Rac1</strong> in cocaine <b>reward</b> and cocaine induced structural plasticity.
+RNASE1	addiction	aversion	23564082	The small GTPase RhoA, but not <strong>Rac1</strong>, is essential for conditioned <b>aversive</b> memory formation through regulation of actin rearrangements in rat dorsal hippocampus.
+RNASE1	drug	alcohol	23223291	Adult neuronal Arf6 controls <b>ethanol</b> induced behavior with Arfaptin downstream of <strong>Rac1</strong> and RhoGAP18B.
+RNASE1	drug	alcohol	23223291	We also find that the Drosophila Arfaptin protein directly binds to the activated forms of Arf6 and <strong>Rac1</strong> GTPases, and mutants in Arfaptin also display <b>ethanol</b> sensitivity.
+RNASE1	drug	alcohol	23223291	Arf6 acts downstream of <strong>Rac1</strong> and Arfaptin to regulate <b>ethanol</b> induced behaviors, and we thus demonstrate that this conserved <strong>Rac1</strong>/Arfaptin/Arf6 pathway is a major mediator of <b>ethanol</b> induced behavioral responses.
+RNASE1	drug	cocaine	18952886	<b>Cocaine</b> induced reactive oxygen species (ROS) production was associated with significant increases (approximately 2 fold) in the protein expressions of Nox2 (an isoform of NADPH oxidase) and its regulatory subunits: p22(phox), p67(phox), p47(phox), p40(phox), and <strong>Rac1</strong>, and in p47(phox) phosphorylation as detected by immunoblotting (all p < 0.03).
+RNASE1	drug	alcohol	17018286	Indeed, expression of constitutively active forms of Rho1 or <strong>Rac1</strong> in adult flies results in <b>ethanol</b> resistance similar to that observed in whir mutants.
+RNASE1	drug	opioid	16472257	Somatostatin acting via G(i)1 coupled sstr3 receptor, DPDPE ([D Pen2,D Pen5]enkephalin; where Pen is penicillamine) acting via G(i)2 coupled delta <b>opioid</b> receptors, and cyclopentyl adenosine acting via G(i)3 coupled adenosine A1 receptors preferentially activated PI3K (phosphoinositide 3 kinase) and ILK (integrin linked kinase), whereas ACh (acetylcholine) acting via G(i)3 coupled M2 receptors preferentially activated PI3K, Cdc42 (cell division cycle 42)/<strong>Rac1</strong>, PAK1 (p21 activated kinase 1) and p38 MAPK (mitogen activated protein kinase).
+RNASE1	addiction	withdrawal	15785859	In contrast, that of <strong>Rac1</strong> did not change after the <b>withdrawal</b>.
+PROS1	drug	cocaine	21796101	Among the daily <b>cocaine</b> induced changes in redox homeostasis were an increase in <strong>protein S</strong> glutathionylation and a decrease in expression of GSH S transferase pi (GSTpi).
+PROS1	drug	cannabinoid	17432216	<b>Marijuana</b> may have accelerated stroke onset, but essential cause of stroke in this case must be <strong>protein S</strong> mutation.
+PROS1	drug	alcohol	6539134	The content of the neurospecific <strong>protein S</strong> 100 in the cerebellum measured by rocket immunoelectrophoresis was demonstrated to be the same in animals preferring water and <b>ethanol</b>.
+OTP	drug	nicotine	32222562	We described past year <strong>OTP</strong> (i.e., cigars/cigarillos, waterpipe, sundry <b>tobacco</b> products (i.e., pipe, bidis, chewing <b>tobacco</b>, snuff)) use and ND over 4 years in these groups.
+OTP	drug	nicotine	32222562	At age 20, sustained <b>smokers</b> reported using a mean(SD) of 1.1(0.9) <strong>OTP</strong> in the past year; relapsers reported 0.5(0.6); shorter term quitters reported 0.9(0.7); longer term quitters reported 0.3(0.6); and never <b>smokers</b> reported 0.2(0.4).
+OTP	drug	nicotine	32222562	There was no change in <strong>OTP</strong> use or ND in never <b>smokers</b> and longer term quitters.
+OTP	drug	nicotine	32222562	<strong>OTP</strong> use and ND were stable in early adulthood among never <b>smokers</b>, sustained <b>smokers</b> and longer term quitters, but fluctuated in parallel with stopping and starting to smoke.
+OTP	addiction	addiction	28961545	Baseline <b>Addiction</b> Severity Index data were examined along with publicly available dates of arrest and arrest charges from the year before and after <strong>OTP</strong> entry.
+OTP	drug	cannabinoid	28952897	Participants who reported <b>cannabis</b> use on ≥5 days per week were recruited from an urban, outpatient opioid treatment program (<strong>OTP</strong>).
+OTP	drug	opioid	28952897	Participants who reported cannabis use on ≥5 days per week were recruited from an urban, outpatient <b>opioid</b> treatment program (<strong>OTP</strong>).
+OTP	drug	opioid	28952897	Participants were randomized to either four weeks of standard <strong>OTP</strong> clinical care (SCC; medication assisted treatment for <b>opioid</b> use disorder and individual behavioral counseling), followed by four weeks of SCC plus varenicline (SCC+VT), or to four weeks of SCC+VT followed by four weeks of SCC.
+OTP	drug	opioid	28854060	In a nationwide prevalence study, 69,140 patients newly admitted to an <b>opioid</b> treatment program (<strong>OTP</strong>) completed a brief self administered survey of past month <b>heroin</b> use and PO misuse from January 2005 through September 2016.
+OTP	drug	opioid	28854060	We calculated <b>heroin</b> use and PO misuse prevalence rates, and prevalence rate ratios of Black and Latino <strong>OTP</strong> entrants compared to White entrants over time.
+OTP	drug	opioid	28854060	Among <strong>OTP</strong> entrants, racially/ethnically disparate rates of <b>heroin</b> use, and to a lesser extent, of PO misuse have become more similar over time.
+OTP	drug	nicotine	28711748	The goal of this study was to test the hypothesis that personality traits related to affect regulation would be associated with greater frequency of other <b>tobacco</b> product (<strong>OTP</strong>) use in a sample of young adult non daily <b>smokers</b>.
+OTP	addiction	relapse	28711748	Longitudinal negative binomial regression models indicated that greater sensation <b>seeking</b> and lack of premeditation were associated with more frequent <strong>OTP</strong> use (ps<0.05).
+OTP	drug	nicotine	28711748	Young, non daily cigarette <b>smokers</b> with high levels of sensation seeking and/or lack of premeditation may be at increased risk for harms related to <strong>OTP</strong> use and may benefit from prevention and cessation strategies that specifically address affect.
+OTP	addiction	relapse	28711748	Young, non daily cigarette smokers with high levels of sensation <b>seeking</b> and/or lack of premeditation may be at increased risk for harms related to <strong>OTP</strong> use and may benefit from prevention and cessation strategies that specifically address affect.
+OTP	drug	nicotine	28633484	Weighted regression analyses for <b>smoking</b> status, time to first cigarette, cigarettes per day and non cigarette other <b>tobacco</b> products (<strong>OTP</strong>) were conducted across education levels.
+OTP	addiction	addiction	28543418	An <strong>OTP</strong> can be ethically justified as a tool to prevent and treat iatrogenic <b>addiction</b> under a specific paradigm one that adopts a default position of professional epistemic humility and holds all collaborative parties accountable in chronic pain management.
+OTP	addiction	intoxication	28495220	<strong>OTP</strong> use among young adult LGB bar patrons and the relationship among past quit attempts, intention to quit, and <b>binge</b> drinking with <strong>OTP</strong> use was examined.
+OTP	drug	opioid	28107680	Study design was a 2 (In Prison Treatment: Condition: <b>Buprenorphine</b> Treatment: vs. Counseling Only)×2 [Post Release Service Setting Condition: <b>Opioid</b> Treatment: Program (<strong>OTP</strong>) vs. Community Health Center (CHC)]×2 (Gender) factorial design.
+OTP	drug	nicotine	27664553	Little is known about types of <strong>OTP</strong> used and the reasons for use, and how <strong>OTP</strong> use and reasons for use correlate with <b>smoking</b> patterns and <b>nicotine</b> dependence in daily and nondaily <b>smokers</b>.
+OTP	addiction	dependence	27664553	Little is known about types of <strong>OTP</strong> used and the reasons for use, and how <strong>OTP</strong> use and reasons for use correlate with smoking patterns and nicotine <b>dependence</b> in daily and nondaily smokers.
+OTP	drug	nicotine	27664553	Logistic regression models assessed the association of <b>smoking</b> status with <strong>OTP</strong> use (ever and current) and reasons for use.
+OTP	drug	nicotine	27664553	Within each <b>smoking</b> group, separate logistic regression models examined the associations of <strong>OTP</strong> use and reasons for use with cigarette consumption and <b>nicotine</b> dependence.
+OTP	addiction	dependence	27664553	Within each smoking group, separate logistic regression models examined the associations of <strong>OTP</strong> use and reasons for use with cigarette consumption and nicotine <b>dependence</b>.
+OTP	drug	nicotine	27664553	Among non daily <b>smokers</b>, <b>nicotine</b> dependence was associated with a higher likelihood of current <strong>OTP</strong> use (OR=1.04 [95% CI 1.01 1.07]; p<0.05), whereas cigarette consumption was not.
+OTP	addiction	dependence	27664553	Among non daily smokers, nicotine <b>dependence</b> was associated with a higher likelihood of current <strong>OTP</strong> use (OR=1.04 [95% CI 1.01 1.07]; p<0.05), whereas cigarette consumption was not.
+OTP	drug	nicotine	27664553	Results suggest <strong>OTP</strong> use in nondaily <b>smokers</b> does not correlate with less frequent <b>smoking</b>, but may correlate with higher <b>nicotine</b> dependence.
+OTP	addiction	dependence	27664553	Results suggest <strong>OTP</strong> use in nondaily smokers does not correlate with less frequent smoking, but may correlate with higher nicotine <b>dependence</b>.
+OTP	drug	opioid	27745534	This report identifies the institutional barriers to, and benefits of, <b>buprenorphine</b> maintenance treatment (BMT) integration in an established hospital based <b>opioid</b> treatment program (<strong>OTP</strong>).
+OTP	drug	opioid	27745534	This case study presents the authors' experiences at the clinic, hospital, and corporation levels during efforts to integrate BMT into a hospital based <strong>OTP</strong> in New York City and a descriptive quantitative analysis of the characteristics of hospital outpatients treated with <b>buprenorphine</b> from 2006 to 2013 (N=735).
+OTP	drug	nicotine	27707516	We examined the associations between <b>tobacco</b> marketing receptivity and other <b>tobacco</b> product (<strong>OTP</strong>) use among young adult bar patrons (aged 18 26 years).
+OTP	drug	nicotine	27707516	Multivariable logistic regression analyses in 2015 examined if <b>tobacco</b> marketing receptivity was associated (1) with current (past 30 day) <strong>OTP</strong> use controlling for demographic factors and (2) with dual/poly use among current cigarette <b>smokers</b> (n = 3,045), controlling for demographics and <b>nicotine</b> dependence.
+OTP	addiction	dependence	27707516	Multivariable logistic regression analyses in 2015 examined if tobacco marketing receptivity was associated (1) with current (past 30 day) <strong>OTP</strong> use controlling for demographic factors and (2) with dual/poly use among current cigarette smokers (n = 3,045), controlling for demographics and nicotine <b>dependence</b>.
+OTP	drug	nicotine	27707516	Among the entire sample of young adult bar patrons (Meanage = 23.7, standard deviation = 1.8; 48.1% female), marketing receptivity was consistently associated with current use of all <strong>OTP</strong> including smokeless <b>tobacco</b> (adjusted odds ratio [AOR]= 2.56, 95% confidence interval [CI] 2.08 3.16, p < .001), hookah (AOR = 1.97, 95% CI 1.58 2.43, p < .001), cigarillos (AOR = 3.00, 95% CI 2.21 4.08, p < .001), electronic cigarettes (AOR = 2.43, 95% CI 1.93 3.04, p < .001), and multiple <b>tobacco</b> products (AOR = 2.93, 95% CI 2.45 3.51, p < .001).
+OTP	drug	nicotine	27707516	<strong>OTP</strong> use is common among young adult bar patrons, and it is associated with <b>tobacco</b> marketing receptivity.
+OTP	drug	nicotine	27707516	Efforts to limit <b>tobacco</b> marketing should address <strong>OTP</strong> in addition to cigarettes.
+OTP	drug	opioid	24680219	Data were obtained from the Researched Abuse, Diversion, and Addiction Related Surveillance (RADARS) System Poison Center, Drug Diversion, <b>Opioid</b> Treatment (<strong>OTP</strong>), Survey of Key Informants' Patients (SKIP), and College Survey Programs through December 2012.
+OTP	addiction	addiction	24680219	Data were obtained from the Researched Abuse, Diversion, and <b>Addiction</b> Related Surveillance (RADARS) System Poison Center, Drug Diversion, Opioid Treatment (<strong>OTP</strong>), Survey of Key Informants' Patients (SKIP), and College Survey Programs through December 2012.
+OTP	drug	opioid	24035556	This randomized clinical trial evaluates the feasibility and acceptability of Web based videoconferencing in community <b>opioid</b> treatment program (<strong>OTP</strong>) participants.
+OTP	drug	opioid	22105061	This study compared <b>buprenorphine</b> therapy delivered in 3 distinct treatment settings: an <b>opioid</b> treatment program (<strong>OTP</strong>) offering individual counseling, a group counseling program utilizing the manualized Matrix Model (MMM) of cognitive behavioral treatment, and a private clinic setting mirroring standard medical management for <b>buprenorphine</b> treatment provided specifically at a psychiatrist's private practice (primary care setting).
+OTP	drug	opioid	21170143	To explore HIV infected patients' attitudes about <b>buprenorphine</b> treatment in office based and <b>opioid</b> treatment program (<strong>OTP</strong>) settings.
+OTP	drug	opioid	21170143	We conducted in depth qualitative interviews with 29 patients with co existing HIV infection and <b>opioid</b> dependence seeking <b>buprenorphine</b> maintenance therapy in office based and <strong>OTP</strong> settings.
+OTP	addiction	dependence	21170143	We conducted in depth qualitative interviews with 29 patients with co existing HIV infection and opioid <b>dependence</b> seeking buprenorphine maintenance therapy in office based and <strong>OTP</strong> settings.
+OTP	addiction	relapse	21170143	We conducted in depth qualitative interviews with 29 patients with co existing HIV infection and opioid dependence <b>seeking</b> buprenorphine maintenance therapy in office based and <strong>OTP</strong> settings.
+OTP	drug	opioid	21170143	HIV infected patients with <b>opioid</b> dependence preferred office based <b>buprenorphine</b> because they perceived it as offering a more patient centered approach to care compared with <strong>OTP</strong> referral.
+OTP	addiction	dependence	21170143	HIV infected patients with opioid <b>dependence</b> preferred office based buprenorphine because they perceived it as offering a more patient centered approach to care compared with <strong>OTP</strong> referral.
+OTP	addiction	addiction	18615321	In a randomized controlled trial the effectiveness of an outreach treatment program (<strong>OTP</strong>) was compared with standard <b>addiction</b> care services for hard drug addicts in Rotterdam (The Netherlands).
+OTP	drug	opioid	15943950	In a cross sectional and longitudinal analysis, we compared patients entering a clinical trial of <b>buprenorphine</b> in a Primary Care Clinic (PCC) and those entering a local <b>Opioid</b> Treatment Program (<strong>OTP</strong>) and we compared the clinical characteristics and treatment outcomes of PCC patients with no history of <b>methadone</b> treatment (new to treatment) to those with prior <b>methadone</b> treatment.
+OTP	drug	opioid	15943950	<strong>OTP</strong> subjects (N=94) were enrolled in <b>methadone</b> maintenance during the same time period.
+OTP	drug	opioid	15943950	PCC subjects compared with <strong>OTP</strong> subjects were more likely to be male (77% versus 55%, p<0.01), full time employed (46% versus 15%, p<0.001), have no history of <b>methadone</b> treatment (46% versus 61%, p<0.05), have fewer years of <b>opioid</b> dependence (10 versus 15, p<0.001), and lower rates of injection drug use (IDU) (44% versus 60%, p=0.03).
+OTP	addiction	dependence	15943950	PCC subjects compared with <strong>OTP</strong> subjects were more likely to be male (77% versus 55%, p<0.01), full time employed (46% versus 15%, p<0.001), have no history of methadone treatment (46% versus 61%, p<0.05), have fewer years of opioid <b>dependence</b> (10 versus 15, p<0.001), and lower rates of injection drug use (IDU) (44% versus 60%, p=0.03).
+MYOGLOBIN	drug	psychedelics	32542550	Use of the adsorber device was associated with a decline in <b>MDMA</b> concentrations in serum from 540 to 140 ng/ml within the first 24 h, a decrease of interleukin 6 and <strong>myoglobin</strong> levels, and subsequent clinical improvement.
+MYOGLOBIN	drug	cannabinoid	31673506	For 6 of the assays (buprenorphine, cotinine, oxycodone, and <b>tetrahydrocannabinol</b> qualitative drug screens; microalbumin and urine <strong>myoglobin</strong> quantitative assays), hydroxychloroquine produced significant bias and/or instrument alarms.
+MYOGLOBIN	drug	opioid	31673506	For 6 of the assays (<b>buprenorphine</b>, cotinine, <b>oxycodone</b>, and tetrahydrocannabinol qualitative drug screens; microalbumin and urine <strong>myoglobin</strong> quantitative assays), hydroxychloroquine produced significant bias and/or instrument alarms.
+MYOGLOBIN	drug	amphetamine	29566034	A relevant <strong>myoglobin</strong> decoration of renal tubules was only shown for <b>methamphetamine</b> abuse in the study presented.
+MYOGLOBIN	drug	amphetamine	28835159	We investigated whether <b>METH</b> dependence and <b>METH</b> induced psychosis may involve an effect on DNA methylation of the <strong>PVALB</strong> promoter.
+MYOGLOBIN	addiction	dependence	28835159	We investigated whether METH <b>dependence</b> and METH induced psychosis may involve an effect on DNA methylation of the <strong>PVALB</strong> promoter.
+MYOGLOBIN	drug	amphetamine	28835159	The methylation of a <strong>PVALB</strong> promoter sequence was determined in 100 <b>METH</b> dependent and 102 control subjects using pyrosequencing.
+MYOGLOBIN	drug	amphetamine	28835159	A significant increase in <strong>PVALB</strong> methylation was observed in <b>METH</b> dependence and <b>METH</b> induced psychosis.
+MYOGLOBIN	addiction	dependence	28835159	A significant increase in <strong>PVALB</strong> methylation was observed in METH <b>dependence</b> and METH induced psychosis.
+MYOGLOBIN	drug	amphetamine	28835159	These results demonstrate a specific association between elevated <strong>PVALB</strong> methylation and <b>METH</b> induced psychosis.
+MYOGLOBIN	drug	cannabinoid	28487743	Delirium and High Creatine Kinase and <strong>Myoglobin</strong> Levels Related to Synthetic <b>Cannabinoid</b> Withdrawal.
+MYOGLOBIN	addiction	withdrawal	28487743	Delirium and High Creatine Kinase and <strong>Myoglobin</strong> Levels Related to Synthetic Cannabinoid <b>Withdrawal</b>.
+MYOGLOBIN	drug	alcohol	26156494	Composition dependent multiple structural transformations of <strong>myoglobin</strong> in aqueous <b>ethanol</b> solution: a combined experimental and theoretical study.
+MYOGLOBIN	drug	alcohol	26156494	Experimental studies (circular dichroism and ultra violet (UV) absorption spectra) and large scale atomistic molecular dynamics simulations (accompanied by order parameter analyses) are combined to establish a number of remarkable (and unforeseen) structural transformations of protein <strong>myoglobin</strong> in aqueous <b>ethanol</b> mixture at various <b>ethanol</b> concentrations.
+MYOGLOBIN	addiction	relapse	25623945	Behavioral characterization of our transgenic (Tg) mice uncovered that the <strong>Pvalb</strong>/Gad1 Tg mice have pronounced sensorimotor gating deficits, increased novelty <b>seeking</b> and reduced fear extinction.
+MYOGLOBIN	addiction	relapse	25623945	Our results suggest that reduction of GABAergic transmission from <strong>PVALB</strong>+ interneurons primarily impacts behavioral domains related to fear and novelty <b>seeking</b> and that these alterations might be related to the behavioral phenotype observed in schizophrenia.
+MYOGLOBIN	drug	psychedelics	12835872	We report the case of a 21 year old male who took a suicidal overdose of <b>MDMA</b> and subsequently developed severe hyperpyrexia (>43 degrees C/109.4 degrees F), rhabdomyolysis with an initial <strong>myoglobin</strong> level of 88,000 microg/l, disseminated intravascular coagulation (DIC) and beginning renal and liver failure.
+MYOGLOBIN	drug	alcohol	9046374	Binge drinking of <b>alcohol</b>, cocaine overdose, or overexertion can lead to rhabdomyolysis characterized by elevated creatine kinase (CK) and <strong>myoglobin</strong> in the serum, myoglobinuria, and muscle tenderness.
+MYOGLOBIN	drug	cocaine	9046374	Binge drinking of alcohol, <b>cocaine</b> overdose, or overexertion can lead to rhabdomyolysis characterized by elevated creatine kinase (CK) and <strong>myoglobin</strong> in the serum, myoglobinuria, and muscle tenderness.
+MYOGLOBIN	addiction	intoxication	9046374	<b>Binge</b> drinking of alcohol, cocaine overdose, or overexertion can lead to rhabdomyolysis characterized by elevated creatine kinase (CK) and <strong>myoglobin</strong> in the serum, myoglobinuria, and muscle tenderness.
+MYOGLOBIN	drug	alcohol	3716884	<b>Ethanol</b> reduces <strong>myoglobin</strong> release during isokinetic muscle exercise.
+MYOGLOBIN	drug	alcohol	3716884	Although the performed muscle work, maximal heart rate, and blood lactate levels did not differ between the three test occasions, the serum <strong>myoglobin</strong> increments after exercise were significantly reduced (p less than 0.05) in the <b>ethanol</b> intoxicated state and also 10 15 hours after <b>ethanol</b> intake.
+MYOGLOBIN	drug	alcohol	3716884	The mechanism, therefore, is likely to be a reduction of <strong>myoglobin</strong> release from skeletal muscle due to an <b>ethanol</b> induced alteration of the muscle cell membrane, possibly by means of adenylate cyclase activation.
+MYOGLOBIN	drug	alcohol	6872872	Non infarct associated increases of <strong>myoglobin</strong> in serum were seen in patients with terminal renal failure, severe shock, muscle trauma, muscle diseases, <b>alcohol</b> intoxication and after reanimation.
+MYOGLOBIN	addiction	intoxication	6872872	Non infarct associated increases of <strong>myoglobin</strong> in serum were seen in patients with terminal renal failure, severe shock, muscle trauma, muscle diseases, alcohol <b>intoxication</b> and after reanimation.
+MYOGLOBIN	drug	alcohol	6255983	Considered in conjunction with related parameters from ferrihemoglobin and ferrimyoglobin, the spectral and thermodynamic data are consistent with models in which methanol is bound directly to the ferric ion of cytochrome c, methanol and <b>ethanol</b> are bound directly to the ferric ions of hemoglobin and <strong>myoglobin</strong>, and 1 propanol is bound to a hydrophobic region of cytochrome c. Both the absolute and <b>alcohol</b> induced optical difference spectra of these proteins have been simulated, the former through summation of Gaussian bands and the latter as the difference between two such summations, one with parameters slightly altered from the other.
+GRIA3	drug	amphetamine	31146278	Here, for <b>methamphetamine</b>, we observed no significant change in surface or total GluA1 (GluA2 and <strong>GluA3</strong> were also unchanged).
+GRIA3	drug	amphetamine	29338492	Genetic variation of <strong>GRIA3</strong> gene is associated with vulnerability to <b>methamphetamine</b> dependence and its associated psychosis.
+GRIA3	addiction	dependence	29338492	Genetic variation of <strong>GRIA3</strong> gene is associated with vulnerability to methamphetamine <b>dependence</b> and its associated psychosis.
+GRIA3	drug	amphetamine	29338492	Genotyping of GRIA1 rs1428920, GRIA2 rs3813296, <strong>GRIA3</strong> rs3761554, rs502434 and rs989638 was performed in 102 male Thai controls and 100 <b>METH</b> dependent subjects (53 with <b>METH</b> dependent psychosis).
+GRIA3	drug	amphetamine	29338492	We observed no evidence of association with <b>METH</b> dependence and <b>METH</b> dependent psychosis in the GRIA1 and GRIA2 polymorphisms, nor with single polymorphisms rs3761554 and rs989638 in <strong>GRIA3</strong>.
+GRIA3	addiction	dependence	29338492	We observed no evidence of association with METH <b>dependence</b> and METH dependent psychosis in the GRIA1 and GRIA2 polymorphisms, nor with single polymorphisms rs3761554 and rs989638 in <strong>GRIA3</strong>.
+GRIA3	drug	amphetamine	29338492	An association of <strong>GRIA3</strong> rs502434 was identified with both <b>METH</b> dependence and <b>METH</b> dependent psychosis, although this did not withstand correction for multiple testing.
+GRIA3	addiction	dependence	29338492	An association of <strong>GRIA3</strong> rs502434 was identified with both METH <b>dependence</b> and METH dependent psychosis, although this did not withstand correction for multiple testing.
+GRIA3	drug	amphetamine	29338492	These preliminary findings indicate that genetic variability in <strong>GRIA3</strong> may interact with a functional BDNF polymorphism to provide a strong risk factor for the development of <b>METH</b> dependence in the Thai population.
+GRIA3	addiction	dependence	29338492	These preliminary findings indicate that genetic variability in <strong>GRIA3</strong> may interact with a functional BDNF polymorphism to provide a strong risk factor for the development of METH <b>dependence</b> in the Thai population.
+GRIA3	drug	cocaine	25539508	However, in <b>cocaine</b> sensitized mice primed with <b>cocaine</b>, this inhibition was reversed and a strong increase was detected in the mGluR5, NR2 subunits, and both GluR1 and <strong>GluR3</strong>.
+GRIA3	drug	amphetamine	24535653	FR increased GluA1 in the PSD, and D <b>amphetamine</b> increased p Ser845 GluA1, GluA1, GluA2, but not <strong>GluA3</strong>, with a greater effect in FR than AL rats.
+GRIA3	drug	alcohol	24523671	Out of the 16 glutamate receptor subunits, mRNAs encoding two AMPA [2 amino 3 (3 hydroxy 5 methyl isoxazol 4 yl)propanoic acid] receptor subunits GluA2 and <strong>GluA3</strong>; three kainate receptor subunits GluK2, GluK3 and GluK5 and five NMDA (N methyl D aspartate) receptor subunits GluN1, GluN2A, GluN2C, GluN2D, and GluN3A were significantly increased in the HP DG region in <b>alcoholics</b>.
+GRIA3	drug	alcohol	22291662	Expression levels of <strong>GRIA3</strong> flip and flop and GRIA4 flop mRNAs in this region were positively correlated with daily <b>ethanol</b> intake and blood <b>ethanol</b> concentrations (BEC) averaged over the 6 months prior to necropsy.
+GRIA3	drug	cocaine	21216391	Among them, GluA1 and <strong>GluA3</strong> are preferentially upregulated in their palmitoylation levels by a systemic injection of <b>cocaine</b>.
+GRIA3	drug	cocaine	20868701	Under basal conditions and in response to a single <b>cocaine</b> injection the levels of GluR1, GluR2, and <strong>GluR3</strong> AMPA receptor subunits did not differ between WT and 5 LOX deficient mice, but the response of GluR1 phosphorylation to a single <b>cocaine</b> injection was greater under the 5 LOX deficiency.
+GRIA3	drug	opioid	20159947	Immunoblotting studies show that 12 h after <b>morphine</b> treatment, GluR1 subunits are increased at the postsynaptic density (PSD) and at extrasynaptic sites, whereas <strong>GluR3</strong> subunits are only increased at the PSD, and they show how this alters receptor subunit composition.
+GRIA3	drug	opioid	18671727	Decreased AMPA GluR2, but not <strong>GluR3</strong>, mRNA expression in rat amygdala and dorsal hippocampus following <b>morphine</b> induced behavioural sensitization.
+GRIA3	addiction	sensitization	18671727	Decreased AMPA GluR2, but not <strong>GluR3</strong>, mRNA expression in rat amygdala and dorsal hippocampus following morphine induced behavioural <b>sensitization</b>.
+GRIA3	drug	opioid	18671727	In order to evaluate the mechanism underlying the behavioural responses, quantitative real time reverse transcription polymerase chain reaction was used to evaluate mRNA expression of the AMPA receptor subunits GluR2 and <strong>GluR3</strong> in the striatum, prefrontal cortex, hippocampus, hypothalamus and amygdala of animals treated repeatedly with <b>morphine</b>.
+GRIA3	drug	opioid	18671727	Repeated <b>morphine</b> treatment did not alter <strong>GluR3</strong> mRNA expression in any brain area assessed.
+GRIA3	drug	psychedelics	18419818	The aim of the present study was to investigate the effect of repeated intermittent <b>MDMA</b> administration upon gene transcript expression of the glutamate transporters (EAAT1, EAAT2 1, EAAT2 2), the glutamate receptor subunits of AMPA (GluR1, GluR2, <strong>GluR3</strong>), the glutamate receptor subunits of NMDA (NR1, NR2A and NR2B), as well as metabotropic glutamate receptors (mGluR1, mGluR2, mGluR3, mGluR5) in six different brain regions.
+GRIA3	drug	alcohol	16436610	Involvement of the AMPA receptor <strong>GluR C</strong> subunit in <b>alcohol</b> seeking behavior and relapse.
+GRIA3	addiction	relapse	16436610	Involvement of the AMPA receptor <strong>GluR C</strong> subunit in alcohol <b>seeking</b> behavior and <b>relapse</b>.
+GRIA3	drug	alcohol	16436610	<strong>GluR C</strong> KOs displayed a blunted, cue induced reinstatement response and <b>alcohol</b> deprivation effect, when compared with wild type controls; however, no differences between genotypes could be observed regarding <b>ethanol</b> self administration under operant or home cage drinking conditions.
+GRIA3	addiction	relapse	16436610	<strong>GluR C</strong> KOs displayed a blunted, cue induced <b>reinstatement</b> response and alcohol deprivation effect, when compared with wild type controls; however, no differences between genotypes could be observed regarding ethanol self administration under operant or home cage drinking conditions.
+GRIA3	addiction	reward	16436610	<strong>GluR C</strong> KOs displayed a blunted, cue induced reinstatement response and alcohol deprivation effect, when compared with wild type controls; however, no differences between genotypes could be observed regarding ethanol self administration under <b>operant</b> or home cage drinking conditions.
+GRIA3	drug	alcohol	16436610	These results imply a role for <strong>GluR C</strong> in <b>alcohol</b> relapse, although this phenotype could also be attributable to a reduction in the total number of AMPA receptors in specific brain areas.
+GRIA3	addiction	relapse	16436610	These results imply a role for <strong>GluR C</strong> in alcohol <b>relapse</b>, although this phenotype could also be attributable to a reduction in the total number of AMPA receptors in specific brain areas.
+GRIA3	drug	amphetamine	9183816	Repeated <b>amphetamine</b> administration decreased levels of GluR1 and GluR2 but not <strong>GluR3</strong> mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal.
+GRIA3	addiction	withdrawal	9183816	Repeated amphetamine administration decreased levels of GluR1 and GluR2 but not <strong>GluR3</strong> mRNAs in both core and shell subregions of the NAc at the 14 day <b>withdrawal</b> time; no changes were observed after 3 days of <b>withdrawal</b>.
+DDIT3	drug	amphetamine	32203791	We further examined ER stress related proteins and mitochondrial apoptosis pathway in the VTA and NAc, and found that <b>METH</b> increased the expressions of glucose regulated protein 78 (GRP78), C/EBP homologous protein (<strong>CHOP</strong>), and Bax, as same time decreased the expressions of procaspase12, Bcl 2, and procaspase3, while Trx 1 overexpression blocked these changes.
+DDIT3	drug	amphetamine	31396089	Ad libitum HRW consumption also had an inhibitory effect on the <b>METH</b> induced increase in the expression of Bax/Bcl 2, cleaved caspase 3, glucose related protein 78 (GRP 78), CCAAT/enhancer binding protein homologous protein (<strong>CHOP</strong>), and p NF kB p65 expression and elevation of interleukin (IL) 6 and tumor necrosis factor (TNF) α levels in the hippocampus.
+DDIT3	drug	alcohol	31105269	<b>Alcohol</b> increased IL 17A production and pro apoptotic signaling evidenced by Bax, Bim, caspase 3, and caspase 8 increases via endoplasmic reticulum (ER) stress indicated by C/EBP homologous protein (<strong>CHOP</strong>) upregulation; this was prevented by the ER stress inhibitor, 4 PBA, in isolated crypts in vitro and in vivo.
+DDIT3	addiction	intoxication	31009094	Interestingly, the UPR signature in AH patients and in mice following Gao <b>Binge</b> feeding was biased toward cell death with increased expression of pro cell death CCAAT enhancer binding protein homologous protein (<strong>CHOP</strong>) and decreased prosurvival GRP78.
+DDIT3	drug	alcohol	30908665	Antivirals and <b>alcohol</b> synergistically increased expression of organelle stress markers of <strong>CHOP</strong>, sXBP 1, ATF6, and GCP60.
+DDIT3	addiction	intoxication	30748014	Administration of PBA also suppressed chronic plus <b>binge</b> EtOH induced up regulation of ER stress related genes including binding immunoglobulin protein (Bip), unspliced and spliced forms of X box binding protein 1 (uXBP1 and sXBP1, respectively), inositol trisphosphate receptor (IP3R), and C/EBP homologous protein (<strong>CHOP</strong>).
+DDIT3	addiction	intoxication	30748014	Chronic EtOH alone (without <b>binge</b>) increased Bip and uXBP1, but it did not affect those of sXBP1, IP3R, <strong>CHOP</strong>, or HO 1.
+DDIT3	drug	alcohol	29523156	Further the effect of <b>Naltrexone</b> on wound healing (scratch assay), cytokine production and endoplasmic reticulum (ER) stress (GRP78 and <strong>CHOP</strong> western blot analysis, immunohistochemistry) were investigated in HCT116 and CACO2 intestinal epithelial cells, human IBD intestinal organoids and patient samples.
+DDIT3	drug	opioid	28546432	Compared with the <b>Heroin</b> group, mRNA and protein expression of PERK, eIF2a, <strong>CHOP</strong>, IRE1 and JNK in the hippocampus and VTA were significantly downregulated in the <b>Heroin</b>+acupuncture group (p<0.05).
+DDIT3	drug	opioid	28546432	Inhibition of <strong>CHOP</strong> and JNK upregulation and reduction of nerve cell apoptosis may be the main mechanisms underlying the effects of acupuncture on <b>heroin</b> addiction induced brain injury.
+DDIT3	addiction	addiction	28546432	Inhibition of <strong>CHOP</strong> and JNK upregulation and reduction of nerve cell apoptosis may be the main mechanisms underlying the effects of acupuncture on heroin <b>addiction</b> induced brain injury.
+DDIT3	addiction	intoxication	27664470	On the contrary, the control diet plus maltose <b>binge</b> caused lipid accumulation in Shp /  mice, which was accompanied by a sharp elevation of <strong>CHOP</strong>, SREBP 1c, and REV ERBα proteins but a diminished ATF4.
+DDIT3	drug	alcohol	27664470	Our study revealed a critical role of SHP and REV ERBα in controlling rhythmic <strong>CHOP</strong> expression in <b>alcoholic</b> fatty liver.
+DDIT3	drug	alcohol	27527870	<b>Ethanol</b> induced endoplasmic reticulum stress was demonstrated by a significant increase in ATF6, <strong>CHOP</strong>, and the phosphorylation of PERK and eiF 2alpha.
+DDIT3	drug	cocaine	23644055	Restraint stress and <b>cocaine</b> induced transcription of the classic ER stress induced genes (BIP, <strong>CHOP</strong>, ATF3 and GADD34) and of two other ER stress components x box binding protein 1 (XBP1) and ATF6.
+DDIT3	addiction	intoxication	22868979	A descriptive retrospective study of acute <b>intoxication</b> cases registered at the Complexo Hospitalario de Pontevedra (<strong>CHOP</strong>) between January 2005 and December 2008 was performed to find out the number and types of poisoning cases treated, their distribution according to patient's sex and age, chronology, type of toxic agents involved, intentionality, history, symptoms, clinical development, treatment and toxicological analysis used for diagnosis.
+DDIT3	drug	amphetamine	22174933	<b>METH</b> also caused up regulation of ER stress genes, Atf2, Atf3, Atf4, <strong>CHOP</strong>/Gadd153 and Gadd34.
+DDIT3	drug	amphetamine	22174933	<b>METH</b> also caused up regulation of ER stress genes, Atf2, Atf3, Atf4, <strong>CHOP</strong>/<strong>Gadd153</strong> and Gadd34.
+DDIT3	drug	amphetamine	21789578	<b>Methamphetamine</b> induces endoplasmic reticulum stress related gene CHOP/Gadd153/<strong>ddit3</strong> in dopaminergic cells.
+DDIT3	drug	amphetamine	21789578	<b>Methamphetamine</b> induces endoplasmic reticulum stress related gene <strong>CHOP</strong>/Gadd153/<strong>ddit3</strong> in dopaminergic cells.
+DDIT3	drug	amphetamine	21789578	<b>Methamphetamine</b> induces endoplasmic reticulum stress related gene <strong>CHOP</strong>/<strong>Gadd153</strong>/<strong>ddit3</strong> in dopaminergic cells.
+DDIT3	drug	amphetamine	21789578	Use of the quantitative real time polymerase chain reaction revealed that transcripts of the endoplasmic reticulum stress related gene (CHOP/Gadd153/<strong>ddit3</strong>) were considerably induced at 24 48 h after <b>methamphetamine</b> administration (but only under apoptotic conditions), whereas dopamine slightly induced CHOP/Gadd153/<strong>ddit3</strong> transcripts at an early stage.
+DDIT3	drug	amphetamine	21789578	Use of the quantitative real time polymerase chain reaction revealed that transcripts of the endoplasmic reticulum stress related gene (<strong>CHOP</strong>/Gadd153/<strong>ddit3</strong>) were considerably induced at 24 48 h after <b>methamphetamine</b> administration (but only under apoptotic conditions), whereas dopamine slightly induced <strong>CHOP</strong>/Gadd153/<strong>ddit3</strong> transcripts at an early stage.
+DDIT3	drug	amphetamine	21789578	Use of the quantitative real time polymerase chain reaction revealed that transcripts of the endoplasmic reticulum stress related gene (<strong>CHOP</strong>/<strong>Gadd153</strong>/<strong>ddit3</strong>) were considerably induced at 24 48 h after <b>methamphetamine</b> administration (but only under apoptotic conditions), whereas dopamine slightly induced <strong>CHOP</strong>/<strong>Gadd153</strong>/<strong>ddit3</strong> transcripts at an early stage.
+DDIT3	drug	amphetamine	21789578	Analysis by immunofluorescence microscopy demonstrated an increase of CHOP/Gadd153/<strong>ddit3</strong> and Grp78/Bip proteins at 24 h after <b>methamphetamine</b> administration.
+DDIT3	drug	amphetamine	21789578	Analysis by immunofluorescence microscopy demonstrated an increase of <strong>CHOP</strong>/Gadd153/<strong>ddit3</strong> and Grp78/Bip proteins at 24 h after <b>methamphetamine</b> administration.
+DDIT3	drug	amphetamine	21789578	Analysis by immunofluorescence microscopy demonstrated an increase of <strong>CHOP</strong>/<strong>Gadd153</strong>/<strong>ddit3</strong> and Grp78/Bip proteins at 24 h after <b>methamphetamine</b> administration.
+DDIT3	drug	amphetamine	17105900	Analysis of the expression of genes downstream of <strong>CHOP</strong> (DOCs) revealed significant <b>METH</b> induced increases in their expression.
+DCR	drug	alcohol	32335597	Cases of <b>alcohol</b> dependence syndrome were diagnosed based on ICD 10 <strong>DCR</strong> presenting to psychiatry department of Tribhuvan University Teaching Hospital, over the period of 6 months.
+DCR	addiction	dependence	32335597	Cases of alcohol <b>dependence</b> syndrome were diagnosed based on ICD 10 <strong>DCR</strong> presenting to psychiatry department of Tribhuvan University Teaching Hospital, over the period of 6 months.
+DCR	addiction	addiction	30796121	Secondary objectives are to assess how <strong>DCR</strong> (a) influence other drug related practices, such as the transition from intravenous to less risky modes of use, (b) reduce drug use frequency/quantity, (c) increase access to treatment for <b>addiction</b> and comorbidities (infectious, psychiatric and other), (d) improve social conditions and (e) reduce levels of violence experienced and drug related offences.
+DCR	drug	opioid	25316933	In a cross sectional design, 60 ICD 10 <strong>DCR</strong> diagnosed <b>opioid</b> dependent male subjects (30 with AOOD≤20 years and 30 with AOOD≥22 years) comprised the two index groups (EO and LO, respectively), with their respective age matched control groups (EOC and LOC).
+DCR	addiction	dependence	23709302	Consenting male subjects between 20 and 45 years of age who fulfilled the ICD 10 <strong>DCR</strong> criteria for opiate <b>dependence</b> syndrome were randomly assigned in a double blind, double dummy placebo controlled trial for detoxification.
+DCR	drug	opioid	22263714	Medication assisted treatment (MAT) with opiate agonists, such as <b>methadone</b> or <b>buprenorphine</b>, constitutes standard of care; to guide planning for an expansion of drug treatment services in correctional facilities, a needs assessment was conducted at the Department of Correction and Rehabilitation (<strong>DCR</strong>) of Puerto Rico (PR).
+DCR	addiction	dependence	21660873	The objective of this work is to study the age wise and order wise chronologies of International Classification of Diseases Tenth Revision Diagnostic Criteria for Research (ICD 10 <strong>DCR</strong>) <b>dependence</b> criteria in individuals with ADS.
+DCR	drug	alcohol	21660873	Consecutively admitted and consenting inpatients with ICD 10 <strong>DCR</strong> diagnosis of ADS were evaluated in a structured interview after detoxification using Semi Structured Assessment for the Genetics of <b>Alcoholism</b> (SSAGA) II.
+DCR	drug	alcohol	20606941	Consecutively admitted patients during the period August 2005 to May 2006, in the Center for Addiction Psychiatry, Central Institute of Psychiatry, Ranchi, India, with ICD 10 (<strong>DCR</strong>) diagnosis of <b>alcohol</b> dependence syndrome or opioid dependence syndrome were recruited for the study and administered the <b>alcohol</b> or other drug (opioid) section of SSAGA II, respectively, and the data was entered in the corresponding tally sheet.
+DCR	drug	opioid	20606941	Consecutively admitted patients during the period August 2005 to May 2006, in the Center for Addiction Psychiatry, Central Institute of Psychiatry, Ranchi, India, with ICD 10 (<strong>DCR</strong>) diagnosis of alcohol dependence syndrome or <b>opioid</b> dependence syndrome were recruited for the study and administered the alcohol or other drug (<b>opioid</b>) section of SSAGA II, respectively, and the data was entered in the corresponding tally sheet.
+DCR	addiction	addiction	20606941	Consecutively admitted patients during the period August 2005 to May 2006, in the Center for <b>Addiction</b> Psychiatry, Central Institute of Psychiatry, Ranchi, India, with ICD 10 (<strong>DCR</strong>) diagnosis of alcohol dependence syndrome or opioid dependence syndrome were recruited for the study and administered the alcohol or other drug (opioid) section of SSAGA II, respectively, and the data was entered in the corresponding tally sheet.
+DCR	addiction	dependence	20606941	Consecutively admitted patients during the period August 2005 to May 2006, in the Center for Addiction Psychiatry, Central Institute of Psychiatry, Ranchi, India, with ICD 10 (<strong>DCR</strong>) diagnosis of alcohol <b>dependence</b> syndrome or opioid <b>dependence</b> syndrome were recruited for the study and administered the alcohol or other drug (opioid) section of SSAGA II, respectively, and the data was entered in the corresponding tally sheet.
+DCR	drug	alcohol	20078462	We performed a prospective, single blind, sham controlled study involving 45 patients with <b>alcohol</b> dependence syndrome (according to ICD 10 <strong>DCR</strong>), with Clinical Institute of Withdrawal Assessment in <b>Alcohol</b> Withdrawal (CIWA Ar) scores <or=10.
+DCR	addiction	dependence	20078462	We performed a prospective, single blind, sham controlled study involving 45 patients with alcohol <b>dependence</b> syndrome (according to ICD 10 <strong>DCR</strong>), with Clinical Institute of Withdrawal Assessment in Alcohol Withdrawal (CIWA Ar) scores <or=10.
+DCR	addiction	withdrawal	20078462	We performed a prospective, single blind, sham controlled study involving 45 patients with alcohol dependence syndrome (according to ICD 10 <strong>DCR</strong>), with Clinical Institute of <b>Withdrawal</b> Assessment in Alcohol <b>Withdrawal</b> (CIWA Ar) scores <or=10.
+DCR	addiction	dependence	19876496	To study the age wise and order wise chronologies of ICD 10 (<strong>DCR</strong>) <b>dependence</b> criteria in individuals with ADS.
+DCR	drug	alcohol	19876496	Consecutively admitted and consenting inpatients with ICD 10 (<strong>DCR</strong>) diagnosis of ADS were evaluated in a structured interview after detoxification using Semi Structured Assessment for the Genetics of <b>Alcoholism</b> (SSAGA) II.
+DCR	drug	opioid	18831352	Twenty three male <b>opioid</b> dependent (ICD 10 <strong>DCR</strong>) subjects, were assigned to double blind randomized controlled trial of 2 and 4 mg/day doses of <b>buprenorphine</b> in an inpatient setting.
+DCR	addiction	addiction	18314853	Seventy subjects with ICD 10 <strong>DCR</strong> diagnosis of substance dependence admitted consecutively in Center for <b>Addiction</b> Psychiatry, Central Institute of Psychiatry (CIP), Ranchi, were taken up for the study after taking written informed consent.
+DCR	addiction	dependence	18314853	Seventy subjects with ICD 10 <strong>DCR</strong> diagnosis of substance <b>dependence</b> admitted consecutively in Center for Addiction Psychiatry, Central Institute of Psychiatry (CIP), Ranchi, were taken up for the study after taking written informed consent.
+DCR	addiction	dependence	11827628	The prevalence of potential <b>dependence</b> amongst long term users was assessed by a semi structured questionnaire applying the Diagnostic Criteria for Research (<strong>DCR</strong> 10) criteria for <b>Dependence</b> Syndrome.
+DCR	drug	opioid	11827628	The study found that an estimated 40% of patients on low potency <b>opioids</b> fulfilled the <strong>DCR</strong> 10 criteria for Dependence Syndrome.
+DCR	addiction	dependence	11827628	The study found that an estimated 40% of patients on low potency opioids fulfilled the <strong>DCR</strong> 10 criteria for <b>Dependence</b> Syndrome.
+DCR	addiction	dependence	24931787	The prevalence of potential <b>dependence</b> amongst long term users was assessed by a semi structured questionnaire applying the <strong>DCR</strong> 10 criteria for <b>Dependence</b> Syndrome.
+DCR	drug	opioid	24931787	An estimated 31% and 40% of patients on NSAIDs and low potency <b>opioids</b> respectively fulfilled the <strong>DCR</strong> 10 criteria for Dependence Syndrome.
+DCR	addiction	dependence	24931787	An estimated 31% and 40% of patients on NSAIDs and low potency opioids respectively fulfilled the <strong>DCR</strong> 10 criteria for <b>Dependence</b> Syndrome.
+DCR	drug	alcohol	21494439	One hundred wives of <b>alcoholics</b> with a confirmed diagnosis of <b>alcohol</b> dependence syndrome according to <strong>DCR</strong> 10 were studied with a "coping with drinking questionnaire".
+DCR	addiction	dependence	21494439	One hundred wives of alcoholics with a confirmed diagnosis of alcohol <b>dependence</b> syndrome according to <strong>DCR</strong> 10 were studied with a "coping with drinking questionnaire".
+CHRM2	drug	alcohol	29478862	When compared to the general population, this genetic polymorphism was not found to be more common in <b>alcohol</b> dependence per se, which excludes the possibility of spurious association between <strong>CHRM2</strong> and DT.
+CHRM2	addiction	dependence	29478862	When compared to the general population, this genetic polymorphism was not found to be more common in alcohol <b>dependence</b> per se, which excludes the possibility of spurious association between <strong>CHRM2</strong> and DT.
+CHRM2	drug	alcohol	28361821	With respect to the 5 hydroxytryptamine (5HT) transporter long promoter region (5HTTLPR), cholinergic receptor muscarinic (<strong>CHRM2</strong>) and <b>alcohol</b> dehydrogenase 1B (ADH1B) genes, there was no significant difference between the cases and the controls.
+CHRM2	drug	opioid	24755993	SNPs in the genes for brain derived neurotrophic factor (BDNF), the muscarinic acetylcholine receptor M2 (<strong>CHRM2</strong>), the dopamine receptor D4 (DRD4) and the μ1 <b>opioid</b> receptor (OPRM1) significantly moderated the impact of treatment condition over time on PA. Genetic variation in the genes for <strong>CHRM2</strong> and OPRM1 specifically had an impact on the level of PA following MBCT.
+CHRM2	addiction	dependence	24530440	This group also showed a greater prevalence of a <strong>CHRM2</strong> genotype previously associated with substance <b>dependence</b> and Major Depressive Disorder as well as a modest elevation on a non planning impulsiveness scale.
+CHRM2	drug	alcohol	23963516	Discrete time survival analysis was used to assess the age specific association of event related oscillations (EROs) and <strong>CHRM2</strong> gene variants on the onset of regular <b>alcohol</b> use and <b>alcohol</b> dependence.
+CHRM2	addiction	dependence	23963516	Discrete time survival analysis was used to assess the age specific association of event related oscillations (EROs) and <strong>CHRM2</strong> gene variants on the onset of regular alcohol use and alcohol <b>dependence</b>.
+CHRM2	drug	alcohol	23747232	Cholinergic receptor gene (<strong>CHRM2</strong>) variation and familial loading for <b>alcohol</b> dependence predict childhood developmental trajectories of P300.
+CHRM2	addiction	dependence	23747232	Cholinergic receptor gene (<strong>CHRM2</strong>) variation and familial loading for alcohol <b>dependence</b> predict childhood developmental trajectories of P300.
+CHRM2	drug	alcohol	23712313	Studies continue to reveal other genes in which variants affect the risk of <b>alcoholism</b> or related traits, including GABRA2, <strong>CHRM2</strong>, KCNJ6 and AUTS2.
+CHRM2	drug	alcohol	22129841	The analysis used logistic and Cox regression methods to evaluate the contributions of age; sex; number of intake <b>alcohol</b>, drug use, and depression symptoms; and either GABRA2, <strong>CHRM2</strong>, ANKK1, BDNF, or KIBRA SNP genotypes to outcome.
+CHRM2	drug	alcohol	21441226	We report one such effort with respect to <strong>CHRM2</strong>, which codes for the cholinergic muscarinic 2 receptor and was of interest originally for its association with <b>alcohol</b> dependence.
+CHRM2	addiction	dependence	21441226	We report one such effort with respect to <strong>CHRM2</strong>, which codes for the cholinergic muscarinic 2 receptor and was of interest originally for its association with alcohol <b>dependence</b>.
+CHRM2	drug	alcohol	21176104	Association of <strong>CHRM2</strong> polymorphisms with severity of <b>alcohol</b> dependence.
+CHRM2	addiction	dependence	21176104	Association of <strong>CHRM2</strong> polymorphisms with severity of alcohol <b>dependence</b>.
+CHRM2	drug	alcohol	21176104	The cholinergic muscarinic 2 receptor (<strong>CHRM2</strong>) gene has been considered a candidate gene for the <b>alcohol</b> dependence in that it might underpin certain risk factors for this condition.
+CHRM2	addiction	dependence	21176104	The cholinergic muscarinic 2 receptor (<strong>CHRM2</strong>) gene has been considered a candidate gene for the alcohol <b>dependence</b> in that it might underpin certain risk factors for this condition.
+CHRM2	drug	alcohol	21176104	This study examined variations in the <strong>CHRM2</strong> between the patients with <b>alcohol</b> dependence and population controls in Korean and explored the associations between <strong>CHRM2</strong> polymorphisms and severity of symptoms in the patients with <b>alcohol</b> dependence.
+CHRM2	addiction	dependence	21176104	This study examined variations in the <strong>CHRM2</strong> between the patients with alcohol <b>dependence</b> and population controls in Korean and explored the associations between <strong>CHRM2</strong> polymorphisms and severity of symptoms in the patients with alcohol <b>dependence</b>.
+CHRM2	drug	alcohol	21176104	Three single nucleotide polymorphisms (SNPs) of <strong>CHRM2</strong> were genotyped using the TaqMan assay and analyzed with the severity of symptoms of <b>alcohol</b> dependence.
+CHRM2	addiction	dependence	21176104	Three single nucleotide polymorphisms (SNPs) of <strong>CHRM2</strong> were genotyped using the TaqMan assay and analyzed with the severity of symptoms of alcohol <b>dependence</b>.
+CHRM2	drug	nicotine	19644963	Association of a variant in the muscarinic acetylcholine receptor 2 gene (<strong>CHRM2</strong>) with <b>nicotine</b> addiction.
+CHRM2	addiction	addiction	19644963	Association of a variant in the muscarinic acetylcholine receptor 2 gene (<strong>CHRM2</strong>) with nicotine <b>addiction</b>.
+CHRM2	drug	nicotine	19644963	In the present study we provide evidence that a common single nucleotide polymorphism (SNP) in the 5' untranslated region of <strong>CHRM2</strong>, the gene coding for the muscarinic acetylcholine receptor 2 is associated with <b>nicotine</b> addiction.
+CHRM2	addiction	addiction	19644963	In the present study we provide evidence that a common single nucleotide polymorphism (SNP) in the 5' untranslated region of <strong>CHRM2</strong>, the gene coding for the muscarinic acetylcholine receptor 2 is associated with nicotine <b>addiction</b>.
+CHRM2	drug	alcohol	19644963	<strong>CHRM2</strong> was defined as a candidate gene for nicotine addiction based on previous evidence that linked variations in <strong>CHRM2</strong> to <b>alcohol</b> and drug dependence.
+CHRM2	drug	nicotine	19644963	<strong>CHRM2</strong> was defined as a candidate gene for <b>nicotine</b> addiction based on previous evidence that linked variations in <strong>CHRM2</strong> to alcohol and drug dependence.
+CHRM2	addiction	addiction	19644963	<strong>CHRM2</strong> was defined as a candidate gene for nicotine <b>addiction</b> based on previous evidence that linked variations in <strong>CHRM2</strong> to alcohol and drug dependence.
+CHRM2	addiction	dependence	19644963	<strong>CHRM2</strong> was defined as a candidate gene for nicotine addiction based on previous evidence that linked variations in <strong>CHRM2</strong> to alcohol and drug <b>dependence</b>.
+CHRM2	drug	nicotine	19644963	The impact of three SNPs in <strong>CHRM2</strong> on <b>smoking</b> behavior/<b>nicotine</b> addiction was investigated using logistic regression models or a quasi Poisson regression model, respectively.
+CHRM2	addiction	addiction	19644963	The impact of three SNPs in <strong>CHRM2</strong> on smoking behavior/nicotine <b>addiction</b> was investigated using logistic regression models or a quasi Poisson regression model, respectively.
+CHRM2	addiction	addiction	19644963	Our data provide further evidence that variations in <strong>CHRM2</strong> may be associated with the genetic risk of <b>addiction</b> in general or with certain personality traits that predispose to the development of <b>addiction</b>.
+CHRM2	drug	nicotine	19644963	Alternatively, variations in <strong>CHRM2</strong> could modulate presynaptic auto regulation in cholinergic systems and may thereby affect an individual's response to <b>nicotine</b> more specifically.
+CHRM2	drug	alcohol	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (<strong>CHRM2</strong>), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as <b>alcohol</b> dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and diazepam binding inhibitor (DBI).
+CHRM2	drug	benzodiazepine	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (<strong>CHRM2</strong>), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as alcohol dehydrogenase (ADH7), glutamic acid decarboxylase (GAD1 and GAD2), the nucleoside transporter (SLC29A1) and <b>diazepam</b> binding inhibitor (DBI).
+CHRM2	drug	alcohol	18316677	Association analyses of a candidate gene, <strong>CHRM2</strong>, previously of interest in the Collaborative Study on the Genetics of <b>Alcoholism</b>, suggest that it is involved in a general externalizing phenotype.
+CHRM2	drug	alcohol	17982586	We found significant linkage and association between brain oscillations and genes involved with inhibitory neural networks (e.g., GABRA2, <strong>CHRM2</strong>), including frontal networks that are deficient in individuals with <b>alcohol</b> dependence, impulsivity, and related disinhibitory disorders.
+CHRM2	addiction	dependence	17982586	We found significant linkage and association between brain oscillations and genes involved with inhibitory neural networks (e.g., GABRA2, <strong>CHRM2</strong>), including frontal networks that are deficient in individuals with alcohol <b>dependence</b>, impulsivity, and related disinhibitory disorders.
+CHRM2	drug	alcohol	17982586	We also reported significant linkage and linkage disequilibrium between the theta and delta event related oscillations underlying P3 to target stimuli and <strong>CHRM2</strong>, a cholinergic muscarinic receptor gene on chromosome 7, which we found is also associated with diagnosis of <b>alcohol</b> dependence and related disorders.
+CHRM2	addiction	dependence	17982586	We also reported significant linkage and linkage disequilibrium between the theta and delta event related oscillations underlying P3 to target stimuli and <strong>CHRM2</strong>, a cholinergic muscarinic receptor gene on chromosome 7, which we found is also associated with diagnosis of alcohol <b>dependence</b> and related disorders.
+CHRM2	drug	alcohol	17567401	In this study, we tested for heterogeneity in the association between the muscarinic acetylcholine M2 receptor gene (<strong>CHRM2</strong>) and <b>alcohol</b> dependence, reported previously in the full sample, among the subgroups of <b>alcohol</b> dependent individuals with and without comorbid drug dependence.
+CHRM2	addiction	dependence	17567401	In this study, we tested for heterogeneity in the association between the muscarinic acetylcholine M2 receptor gene (<strong>CHRM2</strong>) and alcohol <b>dependence</b>, reported previously in the full sample, among the subgroups of alcohol dependent individuals with and without comorbid drug <b>dependence</b>.
+CHRM2	drug	alcohol	17567401	The evidence for association between <strong>CHRM2</strong> and <b>alcohol</b> dependence came entirely from the subgroup of individuals with comorbid drug dependence.
+CHRM2	addiction	dependence	17567401	The evidence for association between <strong>CHRM2</strong> and alcohol <b>dependence</b> came entirely from the subgroup of individuals with comorbid drug <b>dependence</b>.
+CHRM2	drug	alcohol	17567401	There was no evidence of association with <strong>CHRM2</strong> among the <b>alcohol</b> dependent individuals without drug dependence.
+CHRM2	addiction	dependence	17567401	There was no evidence of association with <strong>CHRM2</strong> among the alcohol dependent individuals without drug <b>dependence</b>.
+CHRM2	drug	alcohol	17160701	In the Collaborative Study on the Genetics of <b>Alcoholism</b> (COGA) sample, we have previously reported linkage and association to the cholinergic muscarinic 2 receptor gene (<strong>CHRM2</strong>) on chromosome 7 with evoked EEG oscillations (Jones et al.
+CHRM2	drug	alcohol	16612210	(d) Examination of family based samples has identified several genes including GABRA2 and <strong>CHRM2</strong> thought to be associated with <b>alcohol</b> dependence.
+CHRM2	addiction	dependence	16612210	(d) Examination of family based samples has identified several genes including GABRA2 and <strong>CHRM2</strong> thought to be associated with alcohol <b>dependence</b>.
+CHRM2	drug	alcohol	16000316	<strong>CHRM2</strong> gene predisposes to <b>alcohol</b> dependence, drug dependence and affective disorders: results from an extended case control structured association study.
+CHRM2	addiction	dependence	16000316	<strong>CHRM2</strong> gene predisposes to alcohol <b>dependence</b>, drug <b>dependence</b> and affective disorders: results from an extended case control structured association study.
+CHRM2	drug	alcohol	16000316	(2004) Evidence of common and specific genetic effects: association of the muscarinic acetylcholine receptor M2 (<strong>CHRM2</strong>) gene with <b>alcohol</b> dependence and major depressive syndrome.
+CHRM2	addiction	dependence	16000316	(2004) Evidence of common and specific genetic effects: association of the muscarinic acetylcholine receptor M2 (<strong>CHRM2</strong>) gene with alcohol <b>dependence</b> and major depressive syndrome.
+CHRM2	drug	alcohol	16000316	Genet., 13, 1903 1911] reported that variation in <strong>CHRM2</strong> gene predisposed to <b>alcohol</b> dependence (AD) and major depressive syndrome.
+CHRM2	addiction	dependence	16000316	Genet., 13, 1903 1911] reported that variation in <strong>CHRM2</strong> gene predisposed to alcohol <b>dependence</b> (AD) and major depressive syndrome.
+CHRM2	addiction	dependence	16000316	We examined the relationships between variation in <strong>CHRM2</strong> and AD, drug <b>dependence</b> (DD) and affective disorders, using a novel extended case control structured association (SA) method.
+CHRM2	drug	alcohol	15229186	Evidence of common and specific genetic effects: association of the muscarinic acetylcholine receptor M2 (<strong>CHRM2</strong>) gene with <b>alcohol</b> dependence and major depressive syndrome.
+CHRM2	addiction	dependence	15229186	Evidence of common and specific genetic effects: association of the muscarinic acetylcholine receptor M2 (<strong>CHRM2</strong>) gene with alcohol <b>dependence</b> and major depressive syndrome.
+CHRM2	drug	alcohol	15229186	In this study, we evaluated whether genetic variation in the <strong>CHRM2</strong> gene is also a risk factor for the correlated clinical characteristics of <b>alcoholism</b> and depression.
+ANG	drug	amphetamine	30867225	A total of 17 miRNAs targeting <strong>Ang</strong> II in NAc were found to be associated with the voluntary intake of <b>METH</b>.
+ANG	drug	nicotine	30088946	The literature presented in this review strongly suggests that <b>nicotine</b> alters the homeostasis of the RAS by upregulating the detrimental angiotensin converting enzyme (ACE)/angiotensin (<strong>ANG</strong>) II/<strong>ANG</strong> II type 1 receptor axis and downregulating the compensatory ACE2/<strong>ANG</strong> (1 7)/Mas receptor axis, contributing to the development of CVPD.
+ANG	addiction	sensitization	29976627	Using behavioral readouts of pain hypersensitivity induced by angiotensin II (<strong>Ang</strong> II) injection into mouse hindpaws, our study shows that activation of the type 2 <strong>Ang</strong> II receptor (AT2R) and the cell damage sensing ion channel TRPA1 are required for peripheral mechanical pain <b>sensitization</b> induced by <strong>Ang</strong> II in male and female mice.
+ANG	drug	opioid	27494747	<strong>Ang</strong> iH rats never responded to <b>morphine</b>.
+ANG	drug	opioid	27494747	No MAP response to biphalin or <b>morphine</b> in <strong>Ang</strong> iH could depend on angiotensin induced alterations of the vascular wall morphology and function.
+ANG	drug	amphetamine	26211645	Angiotensin II (<strong>Ang</strong> II) increased the DA release in mPFC and striatum and this effect was enhanced in <b>AMPH</b> + IH group.
+ANG	drug	alcohol	25557835	<b>Ethanol</b> withdrawal significantly increased systolic blood pressure and plasma angiotensin II (<strong>ANG</strong> II) levels without an effect on plasma renin activity (PRA), angiotensin converting enzyme (ACE) activity, or plasma angiotensin I (<strong>ANG</strong> I) levels.
+ANG	addiction	withdrawal	25557835	Ethanol <b>withdrawal</b> significantly increased systolic blood pressure and plasma angiotensin II (<strong>ANG</strong> II) levels without an effect on plasma renin activity (PRA), angiotensin converting enzyme (ACE) activity, or plasma angiotensin I (<strong>ANG</strong> I) levels.
+ANG	drug	alcohol	25557835	Additionally, our study provides novel evidence that <b>ethanol</b> withdrawal does not affect the vascular <strong>ANG</strong> II generating system while stimulating systemic RAS.
+ANG	addiction	withdrawal	25557835	Additionally, our study provides novel evidence that ethanol <b>withdrawal</b> does not affect the vascular <strong>ANG</strong> II generating system while stimulating systemic RAS.
+ANG	addiction	sensitization	25046593	A second group of animals was used to explore the possible role of <strong>Ang</strong> II AT1 receptors in the expression of behavioral <b>sensitization</b>.
+ANG	drug	amphetamine	24089683	It was already found that <strong>Ang</strong> II AT₁ receptors are involved in the neuroadaptative changes induced by a single exposure to <b>amphetamine</b>, and such changes are related to the development of behavioral and neurochemical sensitization.
+ANG	addiction	sensitization	24089683	It was already found that <strong>Ang</strong> II AT₁ receptors are involved in the neuroadaptative changes induced by a single exposure to amphetamine, and such changes are related to the development of behavioral and neurochemical <b>sensitization</b>.
+ANG	drug	amphetamine	24089683	Our results indicate an important role for brain <strong>Ang</strong> II in the behavioral and neuronal sensitization induced by <b>amphetamine</b>.
+ANG	addiction	sensitization	24089683	Our results indicate an important role for brain <strong>Ang</strong> II in the behavioral and neuronal <b>sensitization</b> induced by amphetamine.
+ANG	drug	amphetamine	20936684	The hypothesis was tested that <strong>Ang</strong> II AT₁ receptors are involved in the neuroadaptative changes induced by a single exposure to <b>amphetamine</b> and that such changes are related to the development of behavioral and neurochemical sensitization.
+ANG	addiction	sensitization	20936684	The hypothesis was tested that <strong>Ang</strong> II AT₁ receptors are involved in the neuroadaptative changes induced by a single exposure to amphetamine and that such changes are related to the development of behavioral and neurochemical <b>sensitization</b>.
+ANG	drug	amphetamine	20936684	The results support the idea that the development of neuroadaptive changes induced by <b>amphetamine</b> involves brain AT₁ <strong>Ang</strong> II receptor activation.
+ANG	drug	opioid	19700383	The present study was undertaken to investigate the effects of <strong>Ang</strong> II and captopril injection into VTA on <b>morphine</b> self administration.
+ANG	drug	opioid	19700383	The animals were divided into 4 groups (saline, <b>morphine</b>, captopril and <strong>Ang</strong> II) and were placed in self administration apparatus and allowed to self administer <b>morphine</b> (0.5 mg per infusion all test groups) or saline (saline group) during consecutive days, for 2 h/sessions.
+ANG	drug	opioid	19700383	In <strong>Ang</strong> II group, the number of active lever pressing was significantly lower than <b>morphine</b> group (p < 0.01).
+ANG	drug	opioid	19700383	This study suggests the probable interaction between <strong>Ang</strong> II and <b>opioid</b> system in the VTA.
+ANG	drug	opioid	19579802	With an aim to investigate the effects of injection of angiotensin II (<strong>Ang</strong> II) and captopril into the nucleus accumbens (NAC) on <b>morphine</b> self administration, male Wistar rats were first trained to receive small pellets of food by pressing the active lever in self administration apparatus.
+ANG	drug	opioid	19579802	The animals, divided into 4 groups (saline, <b>morphine</b>, captopril and <strong>Ang</strong> II) were placed in self administration apparatus and were allowed to self administer <b>morphine</b> (0.5 mg per infusion all test groups) or saline (saline group) during consecutive days, for 2 h/sessions.
+ANG	drug	opioid	17907742	The effects of captopril and <strong>Ang</strong> II on <b>morphine</b> induced conditioned place preference (CPP) and <b>morphine</b> self administration in male Wistar rat were investigated.
+ANG	addiction	reward	17907742	The effects of captopril and <strong>Ang</strong> II on morphine induced conditioned place preference (<b>CPP</b>) and morphine self administration in male Wistar rat were investigated.
+ANG	drug	opioid	17907742	The results showed that captopril significantly decreased <b>morphine</b> induced conditional place preference and <b>morphine</b> self administration but the effect of <strong>Ang</strong> II was not significant.
+ANG	drug	opioid	17408935	Rats were allowed to recover from the surgery and conditioned place preference was induced by <b>morphine</b>, and the time spent in <b>morphine</b> compartment was compared in saline, <b>morphine</b>, captopril and <strong>Ang</strong> II groups.
+ANG	drug	opioid	17408935	<b>Morphine</b> withdrawal signs were compared in three other groups of rats: <b>morphine</b> alone, captopril+<b>morphine</b> and <strong>Ang</strong> II+<b>morphine</b> 4 days after <b>morphine</b> injections (three times in each day) with <b>naloxone</b> injection on 4th day.
+ANG	addiction	withdrawal	17408935	Morphine <b>withdrawal</b> signs were compared in three other groups of rats: morphine alone, captopril+morphine and <strong>Ang</strong> II+morphine 4 days after morphine injections (three times in each day) with naloxone injection on 4th day.
+ANG	drug	opioid	17408935	Results with rats conditioned place preference induced by <b>morphine</b> showed that icv captopril decreased significantly the time in <b>morphine</b> compartment (P<0.01) while <strong>Ang</strong> II had no effect.
+ANG	drug	opioid	17408935	<strong>Ang</strong> II administration augmented some of withdrawal signs than in the <b>morphine</b> group (P<0.01 and P<0.001).
+ANG	addiction	withdrawal	17408935	<strong>Ang</strong> II administration augmented some of <b>withdrawal</b> signs than in the morphine group (P<0.01 and P<0.001).
+ANG	drug	alcohol	9305468	<strong>Ang</strong> II impairment of retention and <b>ethanol</b> inhibition of LTP can both be blocked by pretreatment with losartan.
+ANG	drug	alcohol	9305468	Results confirmed the general hypothesis that <b>ethanol</b> induced cognitive deficits are mediated by <strong>Ang</strong> II and the AT1 receptor and that the impairment can be reduced by pretreatment with losartan.
+ANG	drug	alcohol	8840909	Mice that were habituated to drinking <b>ethanol</b> solution and mice that had drunk water only (naive mice) were given an ICV infusion of angiotensin II (<strong>Ang</strong> II) at 2.9 ng/h for 8 days to determine the effect of chronic <b>ethanol</b> intake on the ingestive response to this potent dipsogen.
+ANG	drug	alcohol	8840909	<strong>Ang</strong> II infusion in <b>alcohol</b> naive mice increased daily water intake from 3.7 +/  0.2 ml (mean +/  SE, n = 6) to 11.0 +/  1.5 ml on day 4 (p < 0.001) and to 18.3 +/  2.6 ml on day 8 (p < 0.001).
+ANG	drug	alcohol	8840909	In subsequent experiments, mice had access to 4% <b>ethanol</b> solution up to day 4 and then to water for 4 days during the <strong>Ang</strong> II infusion.
+ANG	drug	alcohol	8840909	Taste aversion, plus previous experience from ingestion of <b>ethanol</b> in habituated mice, may explain the rejection of <b>ethanol</b> to quench <strong>Ang</strong> II induced thirst.
+ANG	addiction	aversion	8840909	Taste <b>aversion</b>, plus previous experience from ingestion of ethanol in habituated mice, may explain the rejection of ethanol to quench <strong>Ang</strong> II induced thirst.
+ANG	drug	alcohol	8724449	Neurotensin enhances some of the behavioral effects of <b>alcohol</b> including motor impairment, narcosis, hypothermia and also interacts with some of the physiological actions of angiotensin (<strong>ANG</strong>) II including aldosterone release and increased blood pressure.
+ANG	drug	alcohol	8724449	<strong>ANG</strong> II injections also produce a dose dependent antagonist reversible reduction in <b>alcohol</b> drinking.
+ANG	drug	alcohol	8724449	When intake stabilized <strong>ANG</strong> II (400 micrograms/kg per day) or vehicle were administered subcutaneously (SC) just prior to <b>alcohol</b> availability but only the group receiving <strong>ANG</strong> II showed a marked reduction in <b>alcohol</b> intake.
+ANG	drug	alcohol	8724449	Neurotensin alone did not affect <b>alcohol</b> intake at any of the doses tested but did attenuate, in a dose dependent fashion, the reduction in <b>alcohol</b> intake produced by <strong>ANG</strong> II.
+ANG	drug	alcohol	8724449	These results demonstrate neurotensin's ability to alter the behavioral effect of <strong>ANG</strong> II on <b>alcohol</b> intake.
+ANG	drug	alcohol	7748510	Because weight reduction alters angiotensin (<strong>ANG</strong>) II activity, and <strong>ANG</strong> II is known to modulate <b>alcohol</b> intake, <strong>ANG</strong> II may play a role in the enhanced <b>alcohol</b> consumption of food deprived weight reduced rats and in the drop in <b>alcohol</b> intake when these rats are refed.
+ANG	drug	alcohol	7748510	These findings suggest that the increase in <b>alcohol</b> intake with food restriction and its decline following refeeding are, in part, related to changes in <strong>ANG</strong> II activity.
+ANG	drug	alcohol	3149773	Angiotensin II (<strong>ANG</strong> II) administered (ICV, 2.0 micrograms) 12 h after the withdrawal of the <b>alcohol</b> not only neutralized the toxic effect of <b>ethanol</b> but also improved learning.
+ANG	addiction	withdrawal	3149773	Angiotensin II (<strong>ANG</strong> II) administered (ICV, 2.0 micrograms) 12 h after the <b>withdrawal</b> of the alcohol not only neutralized the toxic effect of ethanol but also improved learning.
+ANG	drug	alcohol	3149773	When administered on the 5th day after <b>ethanol</b> withdrawal, the effect of <strong>ANG</strong> II was weaker.
+ANG	addiction	withdrawal	3149773	When administered on the 5th day after ethanol <b>withdrawal</b>, the effect of <strong>ANG</strong> II was weaker.
+ANG	drug	alcohol	3149773	It was shown that both chronic <b>alcohol</b> treatment and <strong>ANG</strong> II alone increased apomorphine (1 mg/kg) and amphetamine (7.5 mg/kg) stereotypy but the effects of <strong>ANG</strong> II were greater.
+ANG	drug	amphetamine	3149773	It was shown that both chronic alcohol treatment and <strong>ANG</strong> II alone increased apomorphine (1 mg/kg) and <b>amphetamine</b> (7.5 mg/kg) stereotypy but the effects of <strong>ANG</strong> II were greater.
+ANG	drug	alcohol	3149773	<strong>ANG</strong> II did not change the stereotypy induced by amphetamine but increased the stereotypy induced by apomorphine in the group of animals chronically treated with <b>alcohol</b>.
+ANG	drug	amphetamine	3149773	<strong>ANG</strong> II did not change the stereotypy induced by <b>amphetamine</b> but increased the stereotypy induced by apomorphine in the group of animals chronically treated with alcohol.
+ANG	drug	alcohol	3149773	<strong>ANG</strong> II alone intensified catalepsy and eliminated the effect of <b>ethanol</b>.
+ANG	drug	alcohol	3149773	Both <strong>ANG</strong> II and <b>alcohol</b> increased striatal dopamine (DA) concentration.
+ANG	drug	alcohol	3149773	This effect of <strong>ANG</strong> II was significantly greater in the animals chronically treated with <b>alcohol</b>.
+ANG	drug	alcohol	3149773	The results suggest involvement of the central dopaminergic system in the effect of <strong>ANG</strong> II on the <b>ethanol</b> induced impairment of acquisition of active avoidance but, however, the results of the biochemical determinations of DA turnover do not provide an explanation of these changes.
+AFP	drug	alcohol	20844957	The predictors of surveillance intent for <strong>AFP</strong> were absence of <b>alcoholism</b>, abdominal pain, ascites, diabetes and high AST levels.
+AFP	addiction	dependence	20844957	For US, the predictors of surveillance were prior <strong>AFP</strong> testing and HIV status and absence of abdominal pain, ascites, or drug <b>dependence</b>.
+AFP	drug	nicotine	19458807	General practice is suited to implement interventions for <b>smoking</b> prevention and cessation at every patient encounter, particularly in younger individuals.royal, australian, college, general, practitioner, gp, doctor, medical, practice, racgp, health, care, medication, information, practitioners, family, physician, 2009, <strong>AFP</strong>, May, sleep, rural, <b>smokers</b>, prevention
+AFP	drug	nicotine	15962361	<strong>Alpha fetoprotein</strong>, <b>smoking</b>, transfusions, stage and resectability did not differ between groups.
+AFP	drug	alcohol	15962361	Asians were more likely to have hepatitis B, while non Asians were more likely to have hepatitis C. Factors that decreased survival included hepatitis B, <b>alcohol</b>, elevated <strong>alpha fetoprotein</strong>, CLIP>2 and increased Child's class.
+AFP	drug	alcohol	15962361	Hepatitis B, <b>alcohol</b>, and <strong>alpha fetoprotein</strong> are more important factors for survival than ethnicity.
+AFP	drug	nicotine	11987570	At each woman the anamnestic (age, parity, pregravid BMI, weight gain until 20th week, significant risk from patient's history, cigarette <b>smoking</b>, risk pregnancy symptoms until 20th week), laboratory (maternal serum concentration of <strong>AFP</strong>, hCG, and uE3/triple test/at 16th week, the blood count and ferritin concentration at 18th 20th week, bacteriological cultivation of the smear from the cervix at 34th 36th week), and USG (transvaginal cervicometry and doppler flowmetry of the uterine arteries at 18th 20th week) data were established.
+AFP	drug	nicotine	11803210	To evaluate the impact of <b>smoking</b> and number of previous births on maternal serum levels of <strong>alpha fetoprotein</strong> and free beta subunit of human chorionic gonadotropin (free beta hCG).
+AFP	drug	nicotine	11803210	The median maternal serum <strong>alpha fetoprotein</strong> MoM values did not show any significant dependence, neither with regard to <b>smoking</b> (p = 0.65) nor with regard to parity (p = 0.07).
+AFP	addiction	dependence	11803210	The median maternal serum <strong>alpha fetoprotein</strong> MoM values did not show any significant <b>dependence</b>, neither with regard to smoking (p = 0.65) nor with regard to parity (p = 0.07).
+AFP	addiction	intoxication	6178134	The occurrence of <strong>AFP</strong> was studied in normal and diseased livers of mice and rats: (a) fetal and neonatal livers; (b) liver regeneration after CCl4 <b>intoxication</b>; (c) chemical hepatocarcinogenesis.
+AFP	addiction	intoxication	6178134	After CCl4 <b>intoxication</b> of low and high <strong>AFP</strong> producing mouse strains, cellular <strong>AFP</strong> is found in hepatocytes of portal, periportal and intermediate zones.
+ABETA	drug	alcohol	31733664	Bioinformatics identified the AD associated proteins MAPT (Tau), <strong>amyloid beta precursor protein</strong> (APP), and presenilin 1 (PSEN 1) as the main modulators of <b>alcohol</b> sensitive protein networks that included AD related proteins that regulate energy metabolism (ATP5D, HK1, AK1, PGAM1, CKB), cytoskeletal development (BASP1, CAP1, DPYSL2 [CRMP2], ALDOA, TUBA1A, CFL2, ACTG1), cellular/oxidative stress (HSPA5, HSPA8, ENO1, ENO2), and DNA regulation (PURA, YWHAZ).
+ABETA	drug	opioid	18521004	<b>Morphine</b> inhibits herpetic allodynia through mu <b>opioid</b> receptors induced in <strong>Abeta</strong> fiber neurons.
+ABETA	drug	opioid	18521004	Mechanical allodynia is mainly mediated by <strong>Abeta</strong> fibers, whereas mu <b>opioid</b> receptors are present in C and Adelta fibers.
+ABETA	drug	opioid	18521004	Viral propagation in the sensory ganglion may induce mu <b>opioid</b> receptor expression in <strong>Abeta</strong> fibers, which may be responsible for the inhibitory action of local <b>opioids</b> on mechanical allodynia in mice with herpetic pain.
+ABETA	addiction	withdrawal	18088441	Furthermore, in a novel electrical stimulation induced paw <b>withdrawal</b> (EPW) test, the thresholds for stimulation through C , Adelta  and <strong>Abeta</strong> fibers were all decreased by AS ODN pretreatments.
+ABETA	drug	alcohol	17253767	<strong>Abeta</strong> binding <b>alcohol</b> dehydrogenase (ABAD) is an NAD dependent mitochondrial dehydrogenase.
+ABETA	addiction	dependence	17253767	In this study, surface plasmon resonance (SPR) was employed to determine the temperature <b>dependence</b> of the affinity of the ABAD <strong>Abeta</strong> interaction.
+ABETA	addiction	reward	16372134	Here, genetic association of the common R219K variant of ABCA1 is shown with cerebrospinal fluid (CSF) <strong>Abeta</strong> 1 42 levels, <b>reinforcing</b> emerging evidence of a connection between lipid and <strong>Abeta</strong> metabolism.
+ABETA	drug	alcohol	16340465	Therefore, the current studies aimed to investigate the effects of exposure to 50 or 100 mM <b>ethanol</b> (EtOH) and withdrawal on hippocampal injury induced by <strong>Abeta</strong> peptide treatment.
+ABETA	addiction	withdrawal	16340465	Therefore, the current studies aimed to investigate the effects of exposure to 50 or 100 mM ethanol (EtOH) and <b>withdrawal</b> on hippocampal injury induced by <strong>Abeta</strong> peptide treatment.
+ABETA	drug	alcohol	16340465	The present studies exposed organotypic hippocampal slice cultures to 50 or 100 mM <b>ethanol</b> (EtOH) for 10 days, after which the slices underwent <b>ethanol</b> withdrawal (EWD) in the presence of varying concentrations of <strong>Abeta</strong> 25 35 (0.1, 1, 10 microM), or 35 25 (200 microM), a negative control reverse sequence peptide.
+ABETA	addiction	withdrawal	16340465	The present studies exposed organotypic hippocampal slice cultures to 50 or 100 mM ethanol (EtOH) for 10 days, after which the slices underwent ethanol <b>withdrawal</b> (EWD) in the presence of varying concentrations of <strong>Abeta</strong> 25 35 (0.1, 1, 10 microM), or 35 25 (200 microM), a negative control reverse sequence peptide.
+ABETA	drug	alcohol	16340465	Exposure to <strong>Abeta</strong> in <b>ethanol</b> naïve cultures did not produce significant cytotoxicity.
+ABETA	addiction	withdrawal	16340465	Further, this EtOH exposure and <b>withdrawal</b> regimen sensitizes the hippocampus to the toxic effects of <strong>Abeta</strong> treatment in a manner reflecting over activity of NMDA receptor function.
+ABETA	drug	nicotine	12970390	Using these cells as a model system, we designed experiments to more directly determine whether <strong>Abeta</strong> peptides (Abeta1 42 and Abeta1 40) interfere with a potential nicotinic cytoprotective action and with the ability of <b>nicotine</b> to increase intracellular Ca2+.
+TRPA1	drug	alcohol	31412038	Mice avoided water sources surrounded by both volatile TRPV1 (cyclohexanone) and <strong>TRPA1</strong> (allyl isothiocyanate) irritants and the aversion to cyclohexanone was mitigated when combined with a pure odorant (rose fragrance, phenylethyl <b>alcohol</b>, PEA).
+TRPA1	addiction	aversion	31412038	Mice avoided water sources surrounded by both volatile TRPV1 (cyclohexanone) and <strong>TRPA1</strong> (allyl isothiocyanate) irritants and the <b>aversion</b> to cyclohexanone was mitigated when combined with a pure odorant (rose fragrance, phenylethyl alcohol, PEA).
+TRPA1	drug	cannabinoid	31096838	Finally, we analyzed <b>cannabinoid</b> responses at nociceptive channels other than TRPV1 (TRPV2, TRPM8, and <strong>TRPA1</strong>), and report that <b>cannabinoids</b> differentially activate these channels.
+TRPA1	addiction	sensitization	29976627	Using behavioral readouts of pain hypersensitivity induced by angiotensin II (Ang II) injection into mouse hindpaws, our study shows that activation of the type 2 Ang II receptor (AT2R) and the cell damage sensing ion channel <strong>TRPA1</strong> are required for peripheral mechanical pain <b>sensitization</b> induced by Ang II in male and female mice.
+TRPA1	addiction	sensitization	29430557	It has been shown in rat models that repeated exposure to acrolein induces trigeminovascular <b>sensitization</b> to both <strong>TRPA1</strong> and TRP vanilloid 1 (TRPV1) agonists, a phenomenon linked to headache.
+TRPA1	addiction	sensitization	29430557	These data support the hypothesis that lipid signaling may represent a mechanism by which repeated exposure to the <strong>TRPA1</strong> agonist and environmental toxin, acrolein, drives trigeminovascular <b>sensitization</b>.
+TRPA1	drug	nicotine	29247491	The hydrophilic <b>nicotine</b> was ineffective unless applied unprotonated in alkaline (pH9) solution, activating <strong>TRPA1</strong> and TRPV1.
+TRPA1	addiction	sensitization	28126501	The prevention of this hyperalgesia by diclofenac (1 10μg), the inhibitors of COX 1 SC 560 (0.1 1μg) or COX 2 celecoxib (1 5μg), the TRPV1 antagonist capsazepine (0.03 0.3μg) or the <strong>TRPA1</strong> antagonist HC030031 (10 50μg) demonstrates the involvement of prostaglandin synthesis and TRP <b>sensitization</b> in CCL5 evoked hyperalgesia.
+TRPA1	addiction	sensitization	26480812	Human and animal studies indicate a critical role for oxidative stress and activation of transient receptor potential (TRP) cation channel subfamily members TRPV1 and <strong>TRPA1</strong> on pancreatic nociceptors in <b>sensitization</b> mechanisms that result in pain.
+TRPA1	drug	nicotine	26142526	Effects of <b>nicotine</b>, a known chemical irritant and agonist of <strong>TRPA1</strong> are also inhibited by borneol in both systems.
+TRPA1	drug	nicotine	26142526	It is concluded that borneol, being an inhibitor of <strong>TRPA1</strong>, could be a safer therapeutic combination in clinical situations where <strong>TRPA1</strong> channelopathies like neuropathic pain, trigeminal neuralgia or <b>nicotine</b> withdrawal treatments are involved.
+TRPA1	addiction	withdrawal	26142526	It is concluded that borneol, being an inhibitor of <strong>TRPA1</strong>, could be a safer therapeutic combination in clinical situations where <strong>TRPA1</strong> channelopathies like neuropathic pain, trigeminal neuralgia or nicotine <b>withdrawal</b> treatments are involved.
+TRPA1	drug	cannabinoid	23956775	Selective ionotropic <b>cannabinoids</b> may also produce cross desensitization of the <strong>TRPA1</strong> TRPV1 heteromeric nociceptor channels by being negative allosteric modulators of these channels leading to antinociception and antihyperalgesia.
+TRPA1	drug	alcohol	23446826	[Dimensions of parental rearing styles in <b>alcohol</b> dependent patients: first results of the questionnaire on parental attitudes and rearing practices (<strong>FEPS</strong>)].
+TRPA1	drug	alcohol	23446826	Therefore the aim of this study was the confirmatory evaluation of the factor structure of the Questionnaire on Parental Attitudes and Rearing Practices (<strong>FEPS</strong>) in 186 <b>alcohol</b> dependent patients.
+TRPA1	drug	alcohol	23446826	These results indicate the factorial validity of the <strong>FEPS</strong> in patients with <b>alcohol</b> dependence.
+TRPA1	addiction	dependence	23446826	These results indicate the factorial validity of the <strong>FEPS</strong> in patients with alcohol <b>dependence</b>.
+TRPA1	drug	cannabinoid	23337417	The mechanism of analgesic action of topical propofol is not clear, but may involve desensitization of TRPV1 or <strong>TRPA1</strong> receptors expressed in peripheral nociceptive nerve endings, engagement of <b>endocannabinoids</b>, or activation of peripheral γ aminobutyric acid A receptors.
+TRPA1	drug	nicotine	22618163	It also showed strain specificity, generalizing to hydrogen peroxide (an activator of <strong>TRPA1</strong>) in C57BL/6J mice and to the olfactory cue of <b>nicotine</b> in DBA/2J mice.
+TRPA1	drug	alcohol	22378825	Fetal <b>ethanol</b> exposure attenuates aversive oral effects of TrpV1, but not <strong>TrpA1</strong> agonists in rats.
+TRPA1	addiction	aversion	22378825	Fetal ethanol exposure attenuates <b>aversive</b> oral effects of TrpV1, but not <strong>TrpA1</strong> agonists in rats.
+TRPA1	addiction	aversion	22378825	We focused on two excitatory ligand gated ion channels, TrpV1 and <strong>TrpA1</strong>, which are expressed in oral trigeminal neurons and mediate the <b>aversive</b> orosensory response to many chemical irritants.
+TRPA1	addiction	sensitization	22171045	Transient receptor potential subtype vanilloid 1 (TRPV1) and TRP ankyryn 1 (<strong>TRPA1</strong>) contribute importantly to the genesis of inflammatory pain via both peripheral mechanisms (peripheral <b>sensitization</b>) and spinal cord mechanisms (central <b>sensitization</b>).
+TRPA1	drug	opioid	21395865	In these neurons, Ret is a critical regulator of several ion channels and receptors, including Nav1.8, Nav1.9, ASIC2a, P2X3, TrpC3, TrpM8, <strong>TrpA1</strong>, delta <b>opioid</b> receptor, MrgD, MrgA1 and MrgB4.
+TRPA1	drug	opioid	19371406	High concentrations of <b>morphine</b> sensitize and activate mouse dorsal root ganglia via TRPV1 and <strong>TRPA1</strong> receptors.
+TRPA1	drug	opioid	19371406	To study a possible involvement of TRP receptors in the pro nociceptive effects of <b>morphine</b> (0.3   10 mM), two models of nociception were employed using C57BL/6 mice and genetically related TRPV1 and <strong>TRPA1</strong> knockout animals, which were crossed and generated double knockouts.
+TRPA1	drug	opioid	19371406	<b>Morphine</b> induced release of calcitonin gene related peptide and sensitized the release evoked by heat or the <strong>TRPA1</strong> agonist acrolein.
+TRPA1	drug	opioid	19371406	<b>Morphine</b> activated HEK293t cells transfected with TRPV1 or <strong>TRPA1</strong>.
+TRPA1	drug	opioid	19371406	In neurons from TRPV1 and <strong>TRPA1</strong> knockout animals activation by <b>morphine</b> was markedly reduced, in the TRPV1/A1 double knockout animals this <b>morphine</b> effect was abrogated.
+TRPA1	drug	opioid	19371406	Nociceptor activation and sensitization by <b>morphine</b> is conveyed by TRPV1 and <strong>TRPA1</strong>.
+TRPA1	addiction	sensitization	19371406	Nociceptor activation and <b>sensitization</b> by morphine is conveyed by TRPV1 and <strong>TRPA1</strong>.
+TRPA1	drug	opioid	16945367	activation of transient receptor potential channels, TRPM8 and <strong>TRPA1</strong>) of icilin rather than its unusual and pronounced behavioral effects, often classified as quasi <b>morphine</b> withdrawal.
+TRPA1	addiction	withdrawal	16945367	activation of transient receptor potential channels, TRPM8 and <strong>TRPA1</strong>) of icilin rather than its unusual and pronounced behavioral effects, often classified as quasi morphine <b>withdrawal</b>.
+RET	drug	alcohol	32539883	Hazardous/harmful beer drinking volunteers (N = 120) were factorially randomised to retrieve (<strong>RET</strong>) or not retrieve (No <strong>RET</strong>) <b>alcohol</b> reward memories with (PE) or without (No PE) <b>alcohol</b> reward prediction error.
+RET	addiction	reward	32539883	Hazardous/harmful beer drinking volunteers (N = 120) were factorially randomised to retrieve (<strong>RET</strong>) or not retrieve (No <strong>RET</strong>) alcohol <b>reward</b> memories with (PE) or without (No PE) alcohol <b>reward</b> prediction error.
+RET	drug	alcohol	32539883	'Responsiveness' to counterconditioning predicted subsequent responses to acute <b>alcohol</b> in <strong>RET</strong> + PE only, consistent with reconsolidation update mechanisms.
+RET	drug	alcohol	31772157	MRM retrieval + ketamine (<strong>RET</strong> + KET) effectively reduced the reinforcing effects of <b>alcohol</b> and long term drinking levels, compared to ketamine or retrieval alone.
+RET	drug	psychedelics	31772157	MRM retrieval + <b>ketamine</b> (<strong>RET</strong> + KET) effectively reduced the reinforcing effects of alcohol and long term drinking levels, compared to <b>ketamine</b> or retrieval alone.
+RET	addiction	reward	31772157	MRM retrieval + ketamine (<strong>RET</strong> + KET) effectively reduced the <b>reinforcing</b> effects of alcohol and long term drinking levels, compared to ketamine or retrieval alone.
+RET	drug	alcohol	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), <strong>RET</strong> proto oncogene (<strong>RET</strong>), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate <b>alcohol</b> drinking and other behaviors related to <b>alcohol</b> addiction.
+RET	addiction	addiction	31617071	Evidence has emerged that 5 RTKs (tropomyosin related kinase B (TrkB), <strong>RET</strong> proto oncogene (<strong>RET</strong>), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate alcohol drinking and other behaviors related to alcohol <b>addiction</b>.
+RET	drug	alcohol	31617071	This review will examine the preclinical evidence describing TrkB, <strong>RET</strong>, ALK, FGFR, and EGFR modulation of <b>alcohol</b> drinking and other behaviors relevant to <b>alcohol</b> abuse.
+RET	drug	nicotine	29128428	In large retrospective studies, <strong>RET</strong> rearrangements correlate with adenocarcinoma histologic subtype, never <b>smoking</b> status, younger age, more advanced disease stage, potentially higher chemosensitivity (in particular, to pemetrexed based regimens), and coexistence of other genomic alterations.
+RET	drug	amphetamine	29031851	Constitutive <strong>Ret</strong> signaling leads to long lasting expression of <b>amphetamine</b> induced place conditioning via elevation of mesolimbic dopamine.
+RET	drug	amphetamine	29031851	The duration of <b>amphetamine</b> induced CPP was greatly enhanced in <strong>MEN2B</strong> mice, but not in the GDNF hypermorphic mice.
+RET	addiction	reward	29031851	The duration of amphetamine induced <b>CPP</b> was greatly enhanced in <strong>MEN2B</strong> mice, but not in the GDNF hypermorphic mice.
+RET	addiction	relapse	29031851	Together, our results suggest that downstream components of GDNF signaling, in this case <strong>Ret</strong>, may mediate persistent drug <b>seeking</b> behavior through increased TH expression and dopamine levels in the mesolimbic dopamine neurons.
+RET	addiction	addiction	26188473	We identified 78 miRNA and 150 mRNA transcripts that were differentially expressed (fdr adjusted p < 0.05, absolute log2 fold change >0.5); these included genes not previously associated with <b>addiction</b> (miR 125a 5p, miR 145 and Foxa1), loci encoding receptors related to drug <b>addiction</b> behaviors and genes with previously recognized roles in <b>addiction</b> such as miR 124, miR 181a, DAT and <strong>Ret</strong>.
+RET	addiction	dependence	25855381	In conclusion, our findings indicate that LADCs with ALK, <strong>RET</strong>, and ROS1 fusions develop exclusively via their <b>dependence</b> on these oncogene fusions.
+RET	drug	benzodiazepine	23195112	Given that the defensive factor was sensitive to drugs known to attenuate (<b>alprazolam</b> and chronic fluoxetine) and induce (caffeine) panic attack, we suggest the <strong>RET</strong> as a useful test to assess the effects of panicolytic and panicogenic drugs.
+RET	drug	nicotine	23150706	Patients with lung adenocarcinomas with <strong>RET</strong> fusion gene had more poorly differentiated tumors (63.6%; P = .029 for <strong>RET</strong> v ALK, P = .007 for <strong>RET</strong> v EGFR), with a tendency to be younger (≤ 60 years; 72.7%) and never <b>smokers</b> (81.8%) and to have solid subtype (63.6%) and a smaller tumor (≤ 3 cm) with N2 disease (54.4%).
+RET	drug	opioid	21395865	In these neurons, <strong>Ret</strong> is a critical regulator of several ion channels and receptors, including Nav1.8, Nav1.9, ASIC2a, P2X3, TrpC3, TrpM8, TrpA1, delta <b>opioid</b> receptor, MrgD, MrgA1 and MrgB4.
+RET	addiction	sensitization	21395865	<strong>Ret</strong> deficient mice fail to respond to mustard oil induced neurogenic inflammation, have elevated basal responses and a failure to terminate injury induced <b>sensitization</b> to cold stimuli, hypersensitivity to basal but not injury induced mechanical stimuli, while heat sensation is largely intact.
+RET	drug	amphetamine	19422887	Importantly, 10 of the regulated genes have been previously related with learning and memory or neural plasticity, including the cocaine and <b>amphetamine</b> regulated transcript (Cart), adenylate cyclase activating polypeptide 1 (Adcyap1), serum/glucocorticoid regulated kinase (Sgk), <strong>Ret</strong> proto oncogene (<strong>Ret</strong>), and Fos.
+RET	drug	cocaine	19422887	Importantly, 10 of the regulated genes have been previously related with learning and memory or neural plasticity, including the <b>cocaine</b> and amphetamine regulated transcript (Cart), adenylate cyclase activating polypeptide 1 (Adcyap1), serum/glucocorticoid regulated kinase (Sgk), <strong>Ret</strong> proto oncogene (<strong>Ret</strong>), and Fos.
+RET	addiction	sensitization	15836976	Mechanistically, the great majority of sensory fibers that innervate the bone are CGRP/TrkA expressing fibers, and if the <b>sensitization</b> and activation of these fibers is blocked by anti NGF therapy there would not be another population of nociceptors, such as the non peptidergic IB4/<strong>RET</strong> IR nerve fibers, to take their place in signaling nociceptive events.
+RET	drug	psychedelics	15659598	In dopaminergic neuron like SHSY5Y cells, <b>ibogaine</b> treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, <strong>Ret</strong>, and the downstream kinase, ERK1 (extracellular signal regulated kinase 1).
+RET	drug	opioid	11798749	To investigate the expression of glial cell derived neurotrophic factor (GDNF) and its receptor GDNFR alpha (GFRalpha 1) and GDNFR beta (<strong>Ret</strong>) genes and the effects of muscarinic receptor antagonists, NMDA receptor antagonist, inhibitor of nitric oxide synthase on the expression of these genes in the spinal cord, brainstem and frontal cortex during <b>morphine</b> withdrawal, and to observe the effects of GDNF antisense oligoneucleotide (i.c.v) on the <b>morphine</b> withdrawal symptoms in rats.
+RET	addiction	withdrawal	11798749	To investigate the expression of glial cell derived neurotrophic factor (GDNF) and its receptor GDNFR alpha (GFRalpha 1) and GDNFR beta (<strong>Ret</strong>) genes and the effects of muscarinic receptor antagonists, NMDA receptor antagonist, inhibitor of nitric oxide synthase on the expression of these genes in the spinal cord, brainstem and frontal cortex during morphine <b>withdrawal</b>, and to observe the effects of GDNF antisense oligoneucleotide (i.c.v) on the morphine <b>withdrawal</b> symptoms in rats.
+KCNH2	drug	opioid	31748404	These results confirm that OREX 1019 has little or no efficacy at μ <b>opioid</b> receptorsand has low abuse potential, and, combined with promising safety (clean profile vs. other off target proteins including the <strong>hERG</strong> (human ether a go go related gene) K+ channel) and pharmacokinetic data (supporting administration by subcutaneous or sublingual routes, but with low oral bioavailability), suggest it could be a safe and effective alternative to current treatments for <b>opioid</b> use disorders particularly as applied to relapse prevention.
+KCNH2	addiction	relapse	31748404	These results confirm that OREX 1019 has little or no efficacy at μ opioid receptorsand has low abuse potential, and, combined with promising safety (clean profile vs. other off target proteins including the <strong>hERG</strong> (human ether a go go related gene) K+ channel) and pharmacokinetic data (supporting administration by subcutaneous or sublingual routes, but with low oral bioavailability), suggest it could be a safe and effective alternative to current treatments for opioid use disorders particularly as applied to <b>relapse</b> prevention.
+KCNH2	drug	nicotine	29723392	Results were compared to data collected in non human primates and beagle dogs during pharmacological challenges and torsadogenic <strong>hERG</strong> blockers exposure, in 127 genotyped LQT1 patients on/off β blocker treatment and in subgroups of <b>smoking</b> and non <b>smoking</b> subjects.
+KCNH2	drug	nicotine	29723392	S2 oscillations were proportionally increased by torsadogenic <strong>hERG</strong> blocking drugs, whereas <b>smoking</b> caused an increase in S3 oscillations.
+KCNH2	addiction	dependence	28830713	Loperamide also altered the voltage <b>dependence</b> of steady state <strong>hERG</strong> current properties.
+KCNH2	drug	psychedelics	26807959	CARDIOTOXICITY: Ether a go go related gene (<strong>hERG</strong>) potassium channels in the heart might play a crucial role in <b>ibogaine</b>'s cardiotoxicity, as <strong>hERG</strong> channels are vital in the repolarization phase of cardiac action potentials and blockade by <b>ibogaine</b> delays this repolarization, resulting in QT (time interval between the start of the Q wave and the end of the T wave in the electrical cycle of the heart) interval prolongation and, subsequently, in arrhythmias and sudden cardiac arrest.
+KCNH2	drug	benzodiazepine	25733807	So far, the effects of <b>midazolam</b> on cardiac human ether à go go related gene (<strong>hERG</strong>) channels have not been analyzed.
+KCNH2	drug	benzodiazepine	25733807	The inhibitory effects of <b>midazolam</b> on heterologously expressed <strong>hERG</strong> channels were analyzed in Xenopus oocytes using the double electrode voltage clamp technique.
+KCNH2	drug	benzodiazepine	25733807	We found that <b>midazolam</b> inhibits <strong>hERG</strong> channels in a concentration dependent manner, yielding an IC50 of 170 μM in Xenopus oocytes.
+KCNH2	drug	benzodiazepine	25733807	<b>Midazolam</b> resulted in a small negative shift of the activation curve of <strong>hERG</strong> channels.
+KCNH2	drug	benzodiazepine	25733807	Using the <strong>hERG</strong> pore mutants F656A and Y652A we provide evidence that <b>midazolam</b> uses a classical binding site within the channel pore.
+KCNH2	drug	benzodiazepine	25733807	Analyzing the subacute effects of <b>midazolam</b> on <strong>hERG</strong> channel trafficking, we further found that <b>midazolam</b> does not affect channel surface expression.
+KCNH2	drug	benzodiazepine	25733807	Taken together, we show that the anesthetic <b>midazolam</b> is a low affinity inhibitor of cardiac <strong>hERG</strong> channels without additional effects on channel surface expression.
+KCNH2	drug	psychedelics	23707769	We have recently reported that <b>ibogaine</b> inhibits human ERG (<strong>hERG</strong>) potassium channels at concentrations similar to the drugs affinity for several of its known brain targets.
+KCNH2	drug	psychedelics	23707769	We confirmed that heterologously expressed <strong>hERG</strong> currents are reduced by <b>ibogaine</b> in low micromolar concentrations.
+KCNH2	drug	psychedelics	23707769	Unexpectedly, although blocking <strong>hERG</strong> channels, <b>ibogaine</b> did not prolong the action potential (AP) in guinea pig cardiomyocytes at low micromolar concentrations.
+KCNH2	drug	opioid	23537174	Using both human and experimental animal studies it then presents the pharmacodynamic activity of parent drug and metabolites at the mu <b>opioid</b> receptor, as P glycoprotein substrates and plasma/brain concentration ratios, and activity at the <strong>hERG</strong> K(+) channel.
+KCNH2	drug	psychedelics	22458604	Anti addiction drug <b>ibogaine</b> inhibits <strong>hERG</strong> channels: a cardiac arrhythmia risk.
+KCNH2	addiction	addiction	22458604	Anti <b>addiction</b> drug ibogaine inhibits <strong>hERG</strong> channels: a cardiac arrhythmia risk.
+KCNH2	drug	opioid	22381725	Many explorations have helped in understanding the physiopathology by showing that <b>opioids</b>, including <b>methadone</b>, cause a blockage of the potassium channels of the gene <strong>HERG</strong> K+P.
+KCNH2	drug	amphetamine	21229349	Chronic <b>METH</b> treatment alone reduced the expression of AP1, <strong>Erg1</strong> 3, and Nr4a1 transcription factors below control levels.
+KCNH2	drug	opioid	20930594	Using patch clamp recording in human stem cell derived cardiomyocytes and stably transfected mammalian cells, we found that <b>methadone</b> produced concentration dependent AP prolongation and ion channel block at low micromolar concentrations: <strong>hERG</strong> (IC50 = 1.7 μM), hNav1.5 (11.2 μM tonic block; 5.5 μM phasic block), and hCav1.2 (26.7 μM tonic block; 7.7 μM phasic block).
+KCNH2	drug	benzodiazepine	20930594	However, coadministration of 1 μM <b>diazepam</b> with methadone caused a statistically significant increase in AP duration and a 4 fold attenuation of hNav1.5 block (IC50 values were 44.2 μM and 26.6 μM, respectively, for tonic and phasic block), with no significant effect on methadone induced block of <strong>hERG</strong>, hCav1.2, hKv4.3/hKChIP2.2, and hKvLQT1/hminK channels.
+KCNH2	drug	opioid	20930594	However, coadministration of 1 μM diazepam with <b>methadone</b> caused a statistically significant increase in AP duration and a 4 fold attenuation of hNav1.5 block (IC50 values were 44.2 μM and 26.6 μM, respectively, for tonic and phasic block), with no significant effect on <b>methadone</b> induced block of <strong>hERG</strong>, hCav1.2, hKv4.3/hKChIP2.2, and hKvLQT1/hminK channels.
+KCNH2	drug	benzodiazepine	20930594	Thus, although <b>diazepam</b> alone does not prolong the QT interval, the relief of methadone induced Na channel block may leave <strong>hERG</strong> K channel block uncompensated, thereby increasing cardiac risk.
+KCNH2	drug	opioid	20930594	Thus, although diazepam alone does not prolong the QT interval, the relief of <b>methadone</b> induced Na channel block may leave <strong>hERG</strong> K channel block uncompensated, thereby increasing cardiac risk.
+KCNH2	drug	opioid	18071169	To compare the effects of 3 known <strong>hERG</strong> associated channel blockers on the corrected QT (QTc), we conducted a randomized, controlled trial of <b>opioid</b> addicted subjects.
+IGF1	drug	cocaine	30414405	During <b>cocaine</b> taking, growth hormone and acetylated ghrelin increased 10 fold; glucagon like peptide 1 (GLP 1) doubled; non acetylated ghrelin, <strong>insulin like growth factor 1</strong> (IGF 1), and corticosterone increased by 50% and adiponectin increased by 17%.
+IGF1	drug	alcohol	29108028	In order to further clarify the impact of chronic <b>alcohol</b> consumption on circulating growth factors, a cross sectional study was performed in abstinent AUD patients (<b>alcohol</b> group, N = 91) and healthy control subjects (control group, N = 55) to examine plasma concentrations of brain derived neurotrophic factor (BDNF), <strong>insulin like growth factor 1</strong> (IGF 1) and IGF 1 binding protein 3 (IGFBP 3).
+IGF1	drug	alcohol	26792039	This study aims to reveal the relationship of depression with growth factors such as brain derived neurotrophic factor (BDNF), nerve growth factor (NGF), and <strong>insulin like growth factor 1</strong> (IGF 1) in inpatients diagnosed with <b>alcohol</b> dependence, and to identify candidate growth factors as biological markers to indicate the comorbid of <b>alcohol</b> dependence and depression.
+IGF1	addiction	dependence	26792039	This study aims to reveal the relationship of depression with growth factors such as brain derived neurotrophic factor (BDNF), nerve growth factor (NGF), and <strong>insulin like growth factor 1</strong> (IGF 1) in inpatients diagnosed with alcohol <b>dependence</b>, and to identify candidate growth factors as biological markers to indicate the comorbid of alcohol <b>dependence</b> and depression.
+IGF1	drug	opioid	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of <b>morphine</b> dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (<strong>IGF1</strong>) as well as their receptors in rat brain regions after spontaneous <b>morphine</b> withdrawal in dependent animals.
+IGF1	addiction	dependence	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine <b>dependence</b> on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (<strong>IGF1</strong>) as well as their receptors in rat brain regions after spontaneous morphine withdrawal in dependent animals.
+IGF1	addiction	withdrawal	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin like growth factor 1 (<strong>IGF1</strong>) as well as their receptors in rat brain regions after spontaneous morphine <b>withdrawal</b> in dependent animals.
+IGF1	drug	opioid	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of <b>morphine</b> dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and <strong>insulin like growth factor 1</strong> (<strong>IGF1</strong>) as well as their receptors in rat brain regions after spontaneous <b>morphine</b> withdrawal in dependent animals.
+IGF1	addiction	dependence	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine <b>dependence</b> on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and <strong>insulin like growth factor 1</strong> (<strong>IGF1</strong>) as well as their receptors in rat brain regions after spontaneous morphine withdrawal in dependent animals.
+IGF1	addiction	withdrawal	26346883	Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine dependence on the expression of brain derived neurotrophic factor (BDNF), glial derived neurotrophic factor (GDNF), nerve growth factor (NGF), and <strong>insulin like growth factor 1</strong> (<strong>IGF1</strong>) as well as their receptors in rat brain regions after spontaneous morphine <b>withdrawal</b> in dependent animals.
+IGF1	drug	opioid	26346883	The expression of the BDNF, GDNF, NGF, <strong>IGF1</strong>, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after <b>morphine</b> withdrawal.
+IGF1	addiction	withdrawal	26346883	The expression of the BDNF, GDNF, NGF, <strong>IGF1</strong>, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after morphine <b>withdrawal</b>.
+IGF1	drug	opioid	26346883	<b>Morphine</b> withdrawal was accompanied by upregulation of BDNF, <strong>IGF1</strong>, and their receptors TrkB and IGF1R, respectively, on the mRNA level in the frontal cortex, and only BDNF in hippocampus and midbrain.
+IGF1	addiction	withdrawal	26346883	Morphine <b>withdrawal</b> was accompanied by upregulation of BDNF, <strong>IGF1</strong>, and their receptors TrkB and IGF1R, respectively, on the mRNA level in the frontal cortex, and only BDNF in hippocampus and midbrain.
+IGF1	drug	cocaine	25734326	Because the neurotrophic factors are involved in neural plasticity, neurogenesis and neuronal survival, we have determined plasma concentrations of brain derived neurotrophic factor (BDNF), <strong>insulin like growth factor 1</strong> (IGF 1) and IGF 1 binding protein 3 (IGFBP 3) in a cross sectional study with abstinent <b>cocaine</b> users who sought outpatient treatment for <b>cocaine</b> (n = 100) and age/body mass matched controls (n = 85).
+IGF1	drug	alcohol	25283991	Association between <strong>insulin like growth factor 1</strong> and cognitive functions in <b>alcohol</b> dependent patients.
+IGF1	drug	alcohol	21959607	<strong>IGF I</strong> and IGFBP 3 before and after inpatient <b>alcohol</b> detoxification in <b>alcohol</b> dependent subjects.
+IGF1	drug	alcohol	21959607	<b>Alcohol</b> abuse is associated with low <strong>IGF I</strong> levels that tend to rise after <b>alcohol</b> withdrawal.
+IGF1	addiction	withdrawal	21959607	Alcohol abuse is associated with low <strong>IGF I</strong> levels that tend to rise after alcohol <b>withdrawal</b>.
+IGF1	drug	alcohol	21959607	There is a paucity of studies on the course of IGFBP 3 (the main binding protein for <strong>IGF I</strong>) after <b>alcohol</b> detoxification.
+IGF1	drug	alcohol	21959607	We prospectively assessed <strong>IGF I</strong> and IGFBP 3 changes at the time of admission and after 4 to 6 weeks of detoxification in an inpatient <b>alcohol</b> detoxification facility in 118 <b>alcohol</b> dependent subjects given a regular hospital diet.
+IGF1	drug	alcohol	21959607	Changes in <strong>IGF I</strong> after <b>alcohol</b> detoxification showed a marked dimorphism in altered hepatic biochemistry upon admission, with a rise in those with normal liver enzymes upon admission (p = 0.016, Kruskall Wallis) and a drop in those with elevated liver enzymes upon admission (p = 0.05); the latter was noted in subjects that had consumed <b>alcohol</b> close to the time of admission.
+IGF1	drug	alcohol	21959607	Overall, however, <strong>IGF I</strong> and IGFBP 3 were within normal limits for most subjects both upon admission and after <b>alcohol</b> detoxification; no significant differences were detected among the examined parameters in men vs. women, and there were no significant correlations of <strong>IGF I</strong>, IGFBP 3 or the <strong>IGF I</strong>/IGFBP 3 molar ratio with BMI or age.
+IGF1	drug	alcohol	21959607	Regardless of hepatic enzymes' elevation, <b>alcohol</b> detoxification had overall slight effects on <strong>IGF I</strong> and IGFBP 3.
+IGF1	drug	alcohol	21223309	Validation of specific genes by Sequenom analysis demonstrated that <b>alcohol</b> exposure prevented methylation of specific genes associated with neural development [cut like 2 (cutl2), insulin like growth factor 1 (<strong>Igf1</strong>), epidermal growth factor containing fibulin like extracellular matrix protein 1 (Efemp1), and SRY box containing gene 7 (Sox 7)]; eye development, lens intrinsic membrane protein 2 (Lim 2); the epigenetic mark Smarca2 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2); and developmental disorder [DiGeorge syndrome critical region gene 2 (Dgcr2)].
+IGF1	drug	alcohol	21223309	Validation of specific genes by Sequenom analysis demonstrated that <b>alcohol</b> exposure prevented methylation of specific genes associated with neural development [cut like 2 (cutl2), <strong>insulin like growth factor 1</strong> (<strong>Igf1</strong>), epidermal growth factor containing fibulin like extracellular matrix protein 1 (Efemp1), and SRY box containing gene 7 (Sox 7)]; eye development, lens intrinsic membrane protein 2 (Lim 2); the epigenetic mark Smarca2 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2); and developmental disorder [DiGeorge syndrome critical region gene 2 (Dgcr2)].
+IGF1	drug	alcohol	20237068	<b>Alcohol</b> induced <strong>IGF I</strong> resistance is ameliorated in mice deficient for mitochondrial branched chain aminotransferase.
+IGF1	drug	alcohol	20237068	<b>Alcohol</b> impaired the ability of <strong>IGF I</strong> to increase muscle protein synthesis, 4EBP1 and 70 kilodalton ribosomal protein S6 kinase 1 phosphorylation, eIF4E eIF4G binding, and 4EBP1 raptor binding in WT mice.
+IGF1	drug	alcohol	20237068	However, in <b>alcohol</b> treated BCATm KO mice, this <strong>IGF I</strong> resistance was not manifested.
+IGF1	drug	alcohol	20237068	These data suggest that whereas the sustained elevation in plasma BCAA is not sufficient to ameliorate the catabolic effect of acute <b>alcohol</b> intoxication on muscle protein synthesis, it does improve the anabolic effect of <strong>IGF I</strong>.
+IGF1	addiction	intoxication	20237068	These data suggest that whereas the sustained elevation in plasma BCAA is not sufficient to ameliorate the catabolic effect of acute alcohol <b>intoxication</b> on muscle protein synthesis, it does improve the anabolic effect of <strong>IGF I</strong>.
+IGF1	drug	alcohol	20034543	<strong>Insulin like growth factor 1</strong> stimulation of hypothalamic KiSS 1 gene expression is mediated by Akt: effect of <b>alcohol</b>.
+IGF1	addiction	addiction	19897085	This article reviews current knowledge of the somatotrophic axis, including GH and <strong>insulin like growth factor 1</strong> (IGF 1), in the brain and also discusses the potential use of GH/IGF 1 as agents for treatment of brain pathology in <b>addictive</b> diseases.
+IGF1	drug	alcohol	17855333	Serum <strong>insulin like growth factor 1</strong> (IGF 1), interleukin (IL) 6, IL 8, IL 10, TNF alpha, PTH, estradiol, free testosterone, and corticosterone were measured in 36 <b>alcoholics</b>, ten of them cirrhotics, who also underwent brain CT, which recorded the presence of cortical atrophy or cerebellar atrophy, Evan's, Huckmann's, cella media, bicaudate, cortical atrophy, bifrontal, and ventricular indices, and diameter of the third ventricle; subjective nutritional assessment, midarm anthropometry, and evaluation of liver function.
+IGF1	drug	alcohol	17003241	Compared with controls, <b>ethanol</b> exposure reduced fetal weight at day 120 by 19%, transiently reduced maternal plasma <strong>IGF I</strong> ( 35%) at 30 h, and decreased fetal plasma IGF II ( 28%) from 24 to 54 h after the first infusion.
+IGF1	drug	alcohol	16024131	We conducted a randomized double blind placebo controlled clinical trial to evaluate the effect of subcutaneous administration of <strong>IGF I</strong> (20 microg/kg/day with dose escalation to 50 100 microg/kg/day) for 4 months in patients with <b>alcoholic</b> or primary biliary cirrhosis (PBC) and subnormal <strong>IGF I</strong> levels.
+IGF1	addiction	addiction	16024131	We conducted a randomized double blind placebo controlled clinical trial to evaluate the effect of subcutaneous administration of <strong>IGF I</strong> (20 microg/kg/day with dose <b>escalation</b> to 50 100 microg/kg/day) for 4 months in patients with alcoholic or primary biliary cirrhosis (PBC) and subnormal <strong>IGF I</strong> levels.
+IGF1	drug	alcohol	16024131	<strong>IGF I</strong> treatment also tended to increase REE (P = 0.085); this difference was significant (P = 0.049) in the subgroup of <b>alcoholic</b> patients.
+IGF1	drug	alcohol	15547464	In vivo studies examined the dose and time dependency of the ability of <b>alcohol</b> to impair signal transduction under basal and <strong>IGF I</strong> stimulated conditions.
+IGF1	drug	alcohol	15547464	In contrast, <strong>IGF I</strong> failed to stimulate S6K1 or S6 phosphorylation 2.5 hr after intraperitoneal administration of <b>alcohol</b> when the blood <b>alcohol</b> concentration was increased between approximately 165 and 300 mg/dl.
+IGF1	drug	alcohol	15547464	In contrast to S6K1, acute <b>alcohol</b> intoxication did not consistently impair the ability of <strong>IGF I</strong> to stimulate 4E BP1 phosphorylation under any of the experimental conditions.
+IGF1	addiction	intoxication	15547464	In contrast to S6K1, acute alcohol <b>intoxication</b> did not consistently impair the ability of <strong>IGF I</strong> to stimulate 4E BP1 phosphorylation under any of the experimental conditions.
+IGF1	drug	alcohol	15547464	These data indicate that acute <b>alcohol</b> intoxication selectively impairs <strong>IGF I</strong> signaling via S6K1, but not 4E BP1, and that this defect is independent of gender, nutritional state, route of administration, and <b>alcohol</b> metabolism.
+IGF1	addiction	intoxication	15547464	These data indicate that acute alcohol <b>intoxication</b> selectively impairs <strong>IGF I</strong> signaling via S6K1, but not 4E BP1, and that this defect is independent of gender, nutritional state, route of administration, and alcohol metabolism.
+IGF1	drug	alcohol	15547464	The <strong>IGF I</strong> resistance may represent a participating mechanism by which <b>alcohol</b> directly limits the translation of selected messenger RNAs and, ultimately, protein synthesis in skeletal muscle.
+IGF1	addiction	dependence	14502603	However, we did not detect <strong>IGF I</strong> expression, both in <b>dependence</b> on or in the absence of 9 cis RA acting on cumulus granulosa cells.
+IGF1	drug	alcohol	12658115	<strong>IGF I</strong> induced phosphorylation of S6K1 and 4E BP1 in heart is impaired by acute <b>alcohol</b> intoxication.
+IGF1	addiction	intoxication	12658115	<strong>IGF I</strong> induced phosphorylation of S6K1 and 4E BP1 in heart is impaired by acute alcohol <b>intoxication</b>.
+IGF1	drug	alcohol	12658115	This <strong>IGF I</strong> resistance may represent a participating mechanism by which <b>alcohol</b> limits protein synthesis in heart.
+IGF1	drug	alcohol	12376318	<b>Alcohol</b> impairs insulin and <strong>IGF I</strong> stimulation of S6K1 but not 4E BP1 in skeletal muscle.
+IGF1	drug	alcohol	12376318	The present study determined whether acute <b>alcohol</b> (<b>ethanol</b>; EtOH) intoxication in rats impaired components of the insulin  and <strong>IGF I</strong> signaling pathway in skeletal muscle.
+IGF1	addiction	intoxication	12376318	The present study determined whether acute alcohol (ethanol; EtOH) <b>intoxication</b> in rats impaired components of the insulin  and <strong>IGF I</strong> signaling pathway in skeletal muscle.
+IGF1	drug	alcohol	10195820	Changes in other glucoregulators, such as insulin like growth factor I (<strong>IGF I</strong>) and IGF binding protein 1 (IGFBP 1) may also be related to <b>alcohol</b> abuse.
+IGF1	drug	alcohol	10195820	We studied the effects of <b>alcohol</b> withdrawal on blood glucose, serum insulin and C peptide, and plasma <strong>IGF I</strong> and IGFBP 1 levels in 27 noncirrhotic male <b>alcoholics</b> aged 43 +/  9.0 (mean +/  SD) years on four consecutive days immediately after withdrawal.
+IGF1	addiction	withdrawal	10195820	We studied the effects of alcohol <b>withdrawal</b> on blood glucose, serum insulin and C peptide, and plasma <strong>IGF I</strong> and IGFBP 1 levels in 27 noncirrhotic male alcoholics aged 43 +/  9.0 (mean +/  SD) years on four consecutive days immediately after <b>withdrawal</b>.
+IGF1	drug	alcohol	10195820	Glucose, insulin, <strong>IGF I</strong>, and IGFBP 1 did not differ significantly between the groups at the baseline, but C peptide was higher in <b>alcoholics</b> (p < 0.01).
+IGF1	drug	alcohol	10195820	During the 4 day observation period in <b>alcoholics</b>, IGFBP 1 levels declined by 59%, whereas <strong>IGF I</strong> increased by 41% (p < 0.001 for both comparisons).
+IGF1	addiction	withdrawal	9691979	Food <b>withdrawal</b> evoked an increase in circulating IGF II, while <strong>IGF I</strong> levels were reduced.
+IGF1	drug	alcohol	9555872	<b>Alcohol</b> withdrawal induced change in lipoprotein(a): association with the growth hormone/insulin like growth factor I (<strong>IGF I</strong>)/IGF binding protein 1 (IGFBP 1) axis.
+IGF1	addiction	withdrawal	9555872	Alcohol <b>withdrawal</b> induced change in lipoprotein(a): association with the growth hormone/insulin like growth factor I (<strong>IGF I</strong>)/IGF binding protein 1 (IGFBP 1) axis.
+IGF1	drug	alcohol	9555872	<b>Alcohol</b> inhibits the growth hormone (GH)/insulin like growth factor I (<strong>IGF I</strong>) axis.
+IGF1	drug	alcohol	9555872	<b>Alcohol</b> might also affect IGF binding protein 1 (IGFBP 1), which is an acute inhibitor of <strong>IGF I</strong>.
+IGF1	drug	alcohol	9555872	We studied how <b>alcohol</b> withdrawal affects Lp(a) levels and the GH/<strong>IGF I</strong>/IGFBP 1 axis.
+IGF1	addiction	withdrawal	9555872	We studied how alcohol <b>withdrawal</b> affects Lp(a) levels and the GH/<strong>IGF I</strong>/IGFBP 1 axis.
+IGF1	drug	alcohol	9555872	Lp(a), GH, and <strong>IGF I</strong> tended to be lower and IGFBP 1 higher in the <b>alcoholics</b> immediately after <b>alcohol</b> withdrawal than in the control subjects.
+IGF1	addiction	withdrawal	9555872	Lp(a), GH, and <strong>IGF I</strong> tended to be lower and IGFBP 1 higher in the alcoholics immediately after alcohol <b>withdrawal</b> than in the control subjects.
+IGF1	drug	alcohol	9555872	During the 4 day observation in <b>alcoholics</b>, Lp(a) levels increased by 64% and <strong>IGF I</strong> levels by 41%, whereas IGFBP 1 levels decreased by 59% (P<.001 after ANOVA for all comparisons).
+IGF1	addiction	withdrawal	9249006	The effect of serum <b>withdrawal</b> could be partially reversed by the addition of albumin to the culture medium, whereas insulin and the insulin like growth factor <strong>IGF I</strong> had no additional effect.
+IGF1	drug	alcohol	8679009	Effects of <b>alcohol</b> and liver cirrhosis on the GH <strong>IGF I</strong> axis.
+IGF1	drug	alcohol	8679009	To analyse which of them is the main cause of GH <strong>IGF I</strong> axis alterations, serum levels of growth hormone (GH), growth hormone releasing factor (GHRH), <strong>IGF I</strong> and its binding protein IGFBP 3 were measured in 85 hospitalized <b>alcoholics</b> (51 without cirrhosis, 15 with compensated cirrhosis and 19 with cirrhosis with ascites) and in 25 healthy controls.
+IGF1	drug	alcohol	8679009	Serum <strong>IGF I</strong> and IGFBP 3 levels were lower in <b>alcoholics</b>, particularly in those with liver cirrhosis.
+HMOX1	drug	nicotine	31813548	Low dose <b>nicotine</b> promotes autophagy of cardiomyocytes by upregulating <strong>HO 1</strong> expression.
+HMOX1	drug	nicotine	31813548	Moreover, low dose <b>nicotine</b> upregulated <strong>heme oxygenase 1</strong> (HO 1) expression and knocking down HO 1 abolished the effects of <b>nicotine</b> on the autophagy and apoptosis of NMCMs.
+HMOX1	drug	nicotine	31813548	Moreover, low dose <b>nicotine</b> upregulated <strong>heme oxygenase 1</strong> (<strong>HO 1</strong>) expression and knocking down <strong>HO 1</strong> abolished the effects of <b>nicotine</b> on the autophagy and apoptosis of NMCMs.
+HMOX1	drug	nicotine	31813548	Methyllycaconitine citrate (α7 nAChR blocker, MLA) inhibited <strong>HO 1</strong> expression and the effects of <b>nicotine</b> on autophagy and apoptosis of NMCMs.
+HMOX1	drug	nicotine	31813548	Furthermore, low dose <b>nicotine</b> improved the inhibited autophagy and increased apoptosis induced by palmitic acid (PA) in NMCMs and these effects were reversed by knocking down <strong>HO 1</strong>.
+HMOX1	drug	nicotine	31813548	In conclusion, our data suggested that low dose <b>nicotine</b> promoted autophagy and inhibited apoptosis of cardiomyocytes by upregulating <strong>HO 1</strong>.
+HMOX1	drug	alcohol	31141180	These results demonstrated that 5 ALA/SFC treatment ameliorated binge <b>alcohol</b> exposure liver injury in a rat model of HIV infected patients by reducing macrophage activation and expression of inflammatory cytokines/chemokines, and by inducing <strong>HO 1</strong>, HO 2, and Sirt1 expression.
+HMOX1	addiction	intoxication	31141180	These results demonstrated that 5 ALA/SFC treatment ameliorated <b>binge</b> alcohol exposure liver injury in a rat model of HIV infected patients by reducing macrophage activation and expression of inflammatory cytokines/chemokines, and by inducing <strong>HO 1</strong>, HO 2, and Sirt1 expression.
+HMOX1	drug	alcohol	31096703	According to our findings, <b>ethanol</b> triggered reactive oxygen species (ROS), apoptosis, neuroinflammation, and memory impairment, which were significantly inhibited with the administration of curcumin, as assessed by ROS, lipid peroxidation (LPO), and Nrf2/HO 1 (nuclear factor erythroid 2 related factor 2/<strong>Heme oxygenase 1</strong>) expression in the experimental mice brains.
+HMOX1	drug	alcohol	31096703	According to our findings, <b>ethanol</b> triggered reactive oxygen species (ROS), apoptosis, neuroinflammation, and memory impairment, which were significantly inhibited with the administration of curcumin, as assessed by ROS, lipid peroxidation (LPO), and Nrf2/<strong>HO 1</strong> (nuclear factor erythroid 2 related factor 2/<strong>Heme oxygenase 1</strong>) expression in the experimental mice brains.
+HMOX1	addiction	intoxication	30748014	Further, it blocked chronic plus <b>binge</b> EtOH induced expression of the oxidative stress marker <strong>heme oxygenase 1</strong> (HO 1) and 4 hydroxynonenal.
+HMOX1	addiction	intoxication	30748014	Further, it blocked chronic plus <b>binge</b> EtOH induced expression of the oxidative stress marker <strong>heme oxygenase 1</strong> (<strong>HO 1</strong>) and 4 hydroxynonenal.
+HMOX1	addiction	intoxication	30748014	Chronic EtOH alone (without <b>binge</b>) increased Bip and uXBP1, but it did not affect those of sXBP1, IP3R, CHOP, or <strong>HO 1</strong>.
+HMOX1	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; HO 1 <strong>heme oxygenase 1</strong>; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+HMOX1	drug	alcohol	30580553	ABBREVIATION AA arachidonic acid ACC acetyl CoA carboxylase ACLY ATP citrate lyase ACO acyl CoA oxidase ALA α linolenic acid ALD <b>alcoholic</b> liver disease ALP alkaline phosphatase ALT alanine aminotransferase AMPK AMP activated protein kinase AST aspartate aminotransferase ATGL adipose triglyceride lipase cAMP cyclic adenosine 3',5' monophosphate COX cyclooxygenases CPT1 carnitine palmitoyltransferase 1 CYP2E1 cytochrome P450 2E1 DGAT2 diacylglycerol acyltransferase 2 DGLA dihomo γ linolenic acid DHA docosahexaenoic acid DPA docosapentaenoic acid DTA docosatetraenoic acid EPA eicosapentaenoic acid ER endoplasmic reticulum ETA eicosatetraenoic acid FAS fatty acid synthase FATPs fatty acid transporter proteins GLA,γ linolenic acid GPR120 G protein coupled receptor 120 GSH glutathione; H&E haematoxylin eosin; <strong>HO 1</strong> <strong>heme oxygenase 1</strong>; HSL hormone sensitive lipase; IL 6 interleukin 6 iNOS nitric oxide synthase LA linoleic acid LBP lipopolysaccharide binding protein LOX lipoxygenases LXR liver X receptor LXREs LXR response elements MCP 1 monocyte chemotactic protein 1 MTP microsomal triglyceride transfer protein MUFA monounsaturated fatty acids MyD88 myeloid differentiation factor 88 n 3 PUFAs omega 3 polyunsaturated fatty acid NAFLD nonalcoholic fatty liver disease NASH nonalcoholic steatohepatitis NF κB transcription factor nuclear factor κB PDE3B phosphodiesterase 3B PPAR peroxisome proliferator activated receptor ROS reactive oxygen species RXR retinoid X receptor SCD 1 stearyl CoA desaturase 1 SDA stearidonic acid SFA saturated fatty acids SIRT1 sirtuin 1 SOD superoxide dismutase SREBP sterol regulatory element binding protein TB total bilirubin TC total cholesterol TG triacylglycerol TLR4 Toll like receptor 4 TNF α tumor necrosis factor α VLDLR very low density lipoprotein receptor WT wild type; ZO 1 zonula occludens 1.
+HMOX1	drug	opioid	30039753	Since heme oxygenase, via its products bilirubin and carbon monoxide, functions as a physiological inhibitor of various isoforms of NADPH oxidase, phase 2 inducing nutraceuticals with blood brain barrier permeability such as lipoic acid, an effective inducer of <strong>heme oxygenase 1</strong>, may have potential for prevention of <b>morphine</b> tolerance; indeed, this has been demonstrated in a mouse study.
+HMOX1	drug	nicotine	29145840	Moreover, 180 mg/kg/d MEGR reversed increases in malondialdehyde production, decreases in superoxide dismutase and catalase activities, and the reduced expression of nuclear factor erythroid 2 related factor 2 and <strong>heme oxygenase 1</strong> in the <b>nicotine</b> sensitized Nacc.
+HMOX1	drug	alcohol	28951767	Baicalin also enhanced <b>ethanol</b> induced NRF2 nuclear translocation and increased downstream target gene <strong>HO 1</strong> as antioxidant defense.
+HMOX1	drug	alcohol	24060752	The sulforaphane treatment activated Nrf2, increased levels of the Nrf2 target <strong>heme oxygenase 1</strong> and subsequently lowered oxidant stress as shown by the decline in lipid peroxidation and 3 nitrotyrosine protein adducts and an increase in GSH levels after the acute <b>ethanol</b> treatment.
+HMOX1	drug	alcohol	20238399	Anti inflammatory pathways and <b>alcoholic</b> liver disease: role of an adiponectin/interleukin 10/<strong>heme oxygenase 1</strong> pathway.
+HMOX1	drug	alcohol	20238399	Recent studies have identified an adiponectin/interleukin 10/<strong>heme oxygenase 1</strong> (HO 1) pathway that is profoundly effective in dampening the enhanced activation of innate immune responses in primary cultures of Kupffer cells, as well as in an in vivo mouse model of chronic <b>ethanol</b> feeding.
+HMOX1	drug	alcohol	20238399	Recent studies have identified an adiponectin/interleukin 10/<strong>heme oxygenase 1</strong> (<strong>HO 1</strong>) pathway that is profoundly effective in dampening the enhanced activation of innate immune responses in primary cultures of Kupffer cells, as well as in an in vivo mouse model of chronic <b>ethanol</b> feeding.
+HMOX1	drug	alcohol	20238399	Importantly, induction of <strong>HO 1</strong> also reduces <b>ethanol</b> induced hepatocellular apoptosis in this in vivo model.
+HMOX1	drug	alcohol	20052772	Here we tested the hypothesis that adiponectin mediated suppression of LPS signaling in Kupffer cells is mediated via an interleukin 10 (IL 10)/<strong>heme oxygenase 1</strong> (HO 1) pathway after chronic <b>ethanol</b> feeding.
+HMOX1	drug	alcohol	20052772	Here we tested the hypothesis that adiponectin mediated suppression of LPS signaling in Kupffer cells is mediated via an interleukin 10 (IL 10)/<strong>heme oxygenase 1</strong> (<strong>HO 1</strong>) pathway after chronic <b>ethanol</b> feeding.
+HMOX1	drug	alcohol	20052772	gAcrp increased IL 10 mRNA and protein expression, as well as expression of the IL 10 inducible gene, <strong>HO 1</strong>; expression was higher in Kupffer cells from <b>ethanol</b> fed rats compared with pair fed controls.
+HMOX1	drug	alcohol	20052772	Although IL 10 receptor surface expression on Kupffer cells was not affected by <b>ethanol</b> feeding, IL 10 mediated phosphorylation of STAT3 and expression of <strong>HO 1</strong> was higher in Kupffer cells after <b>ethanol</b> feeding.
+HMOX1	drug	alcohol	20052772	When mice were treated with cobalt protoporphyrin to induce <strong>HO 1</strong> expression, <b>ethanol</b> induced sensitivity to LPS was ameliorated.
+HMOX1	drug	alcohol	18453614	<strong>Heme oxygenase 1</strong> protects against neutrophil mediated intestinal damage by down regulation of neutrophil p47phox and p67phox activity and O2  production in a two hit model of <b>alcohol</b> intoxication and burn injury.
+HMOX1	addiction	intoxication	18453614	<strong>Heme oxygenase 1</strong> protects against neutrophil mediated intestinal damage by down regulation of neutrophil p47phox and p67phox activity and O2  production in a two hit model of alcohol <b>intoxication</b> and burn injury.
+HMOX1	drug	alcohol	17221286	<strong>Heme oxygenase 1</strong> expression in rat liver during ageing and <b>ethanol</b> intoxication.
+HMOX1	addiction	intoxication	17221286	<strong>Heme oxygenase 1</strong> expression in rat liver during ageing and ethanol <b>intoxication</b>.
+HMOX1	drug	alcohol	17221286	However, while 2.5 month old rats responded to acute <b>ethanol</b> intoxication by displaying increased expression of liver <strong>HO 1</strong> mRNA, and 6 month old rats exhibited a mild response, 18 month old rats did not show any response; this phenomenon suggests that during development and ageing the transcriptional response to oxidative stress decreases.
+HMOX1	addiction	intoxication	17221286	However, while 2.5 month old rats responded to acute ethanol <b>intoxication</b> by displaying increased expression of liver <strong>HO 1</strong> mRNA, and 6 month old rats exhibited a mild response, 18 month old rats did not show any response; this phenomenon suggests that during development and ageing the transcriptional response to oxidative stress decreases.
+GAP43	drug	opioid	29154860	The present study explored the effects of Cav 1 on the expression levels of 2 markers of neurite outgrowth, growth association protein 43 (<strong>GAP 43</strong>) and microtubule associated protein 2 (MAP 2), during the process of <b>morphine</b> induced changes in the structural plasticity.
+GAP43	drug	opioid	29154860	The results showed that <b>morphine</b> at a concentration of 10.0μmol/L had no adverse effect on neuronal viability, but enhanced the Cav 1 and <strong>GAP 43</strong> levels and induced the outgrowth of MAP 2 labeled neurites.
+GAP43	drug	opioid	29154860	Moreover, Cav 1 knockdown inhibited the <b>morphine</b> induced upregulation of <strong>GAP 43</strong> expression and the prolongation of MAP 2 labeled neurites.
+GAP43	drug	opioid	29154860	Inhibition of Cav 1 expression reduced the <b>morphine</b> induced increase in the neuronal growth markers <strong>GAP 43</strong> and MAP 2.
+GAP43	drug	cocaine	26850084	We previously demonstrated that nELAV/<strong>GAP 43</strong> pathway is pivotal for learning and its hippocampal expression is up regulated by acute stress following repeated <b>cocaine</b> administration.
+GAP43	drug	cocaine	26850084	We therefore hypothesized that abstinence induced stress may sustain nELAV/<strong>GAP 43</strong> pathway during early abstinence following 2 weeks of <b>cocaine</b> self administration.
+GAP43	drug	cocaine	26850084	We found that contingent, but not non contingent, <b>cocaine</b> exposure selectively increases hippocampal nELAV, but not <strong>GAP 43</strong>, expression immediately after the last self administration session, an effect that wanes after 24 h and that comes back 7 days later when nELAV activation becomes associated with increased expression of <strong>GAP 43</strong>, an effect again observed only in animals self administering the psychostimulant.
+GAP43	drug	cocaine	26850084	This nELAV profile suggests that its initial transient alteration is perhaps related to the daily administration of <b>cocaine</b>, while the increase in the nELAV/<strong>GAP 43</strong> pathway following a week of abstinence may reflect the activation of this cascade as a target of stressful conditions associated with drug related memories.
+GAP43	drug	opioid	24466769	[Expression of <strong>GAP 43</strong> in midbrain ventral tegmental area of <b>morphine</b> withdrawal rats].
+GAP43	addiction	withdrawal	24466769	[Expression of <strong>GAP 43</strong> in midbrain ventral tegmental area of morphine <b>withdrawal</b> rats].
+GAP43	drug	opioid	24466769	To observe the protein expression of growth associated protein 43 (<strong>GAP 43</strong>) in midbrain ventral tegmental area in <b>morphine</b> withdrawal rats at different time, and to evaluate the effect of <strong>GAP 43</strong> on <b>morphine</b> withdrawal memory.
+GAP43	addiction	withdrawal	24466769	To observe the protein expression of growth associated protein 43 (<strong>GAP 43</strong>) in midbrain ventral tegmental area in morphine <b>withdrawal</b> rats at different time, and to evaluate the effect of <strong>GAP 43</strong> on morphine <b>withdrawal</b> memory.
+GAP43	drug	opioid	24466769	To observe the protein expression of <strong>growth associated protein 43</strong> (<strong>GAP 43</strong>) in midbrain ventral tegmental area in <b>morphine</b> withdrawal rats at different time, and to evaluate the effect of <strong>GAP 43</strong> on <b>morphine</b> withdrawal memory.
+GAP43	addiction	withdrawal	24466769	To observe the protein expression of <strong>growth associated protein 43</strong> (<strong>GAP 43</strong>) in midbrain ventral tegmental area in morphine <b>withdrawal</b> rats at different time, and to evaluate the effect of <strong>GAP 43</strong> on morphine <b>withdrawal</b> memory.
+GAP43	drug	opioid	24466769	<strong>GAP 43</strong> could play a role in <b>morphine</b> withdrawal memory in midbrain ventral tegmental area.
+GAP43	addiction	withdrawal	24466769	<strong>GAP 43</strong> could play a role in morphine <b>withdrawal</b> memory in midbrain ventral tegmental area.
+GAP43	drug	alcohol	21367572	Opposite effects of acute <b>ethanol</b> exposure on <strong>GAP 43</strong> and BDNF expression in the hippocampus versus the cerebellum of juvenile rats.
+GAP43	drug	alcohol	21367572	The present study addresses the effects of a single acute <b>ethanol</b> exposure on growth associated protein 43 (<strong>GAP 43</strong>) and brain derived neurotrophic factor (BDNF) gene expression in neurons in the cerebellum and hippocampus of adolescent rats.
+GAP43	drug	alcohol	21367572	The present study addresses the effects of a single acute <b>ethanol</b> exposure on <strong>growth associated protein 43</strong> (<strong>GAP 43</strong>) and brain derived neurotrophic factor (BDNF) gene expression in neurons in the cerebellum and hippocampus of adolescent rats.
+GAP43	drug	alcohol	21367572	Analyses of total RNA and protein by quantitative reverse transcription PCR and western blotting, respectively, revealed that this single <b>ethanol</b> exposure significantly decreased the levels of <strong>GAP 43</strong> mRNA and protein in the cerebellum but increased the levels of mRNA and protein in the hippocampus.
+GAP43	drug	alcohol	21367572	In situ hybridizations revealed that <strong>GAP 43</strong> and BDNF mRNA levels were primarily increased by <b>alcohol</b> exposure in hippocampal dentate granule cells and CA3 neurons.
+GAP43	addiction	intoxication	21367572	Overall, the reported alterations in the expression of the plasticity associated genes <strong>GAP 43</strong> and BDNF in juvenile rats are consistent with the known deleterious effects of <b>binge</b> drinking on motor coordination and cognitive function.
+GAP43	drug	cocaine	21210085	ELAV <strong>GAP43</strong> pathway activation following combined exposure to <b>cocaine</b> and stress.
+GAP43	drug	cocaine	21210085	Our results show that the combination of repeated exposure to <b>cocaine</b> and acute stress significantly enhances nELAV expression and phosphorylation in the hippocampus with a concomitant increase of <strong>GAP43</strong> expression (a specific nELAV target), an effect that seems to involve, upstream, protein kinase C alpha (PKCα).
+GAP43	drug	alcohol	16219774	We further demonstrated the advantage of our test by revealing a significant association (P = 0.00067) between <b>alcohol</b> dependence and a SNP in the <strong>growth associated protein 43</strong>.
+GAP43	addiction	dependence	16219774	We further demonstrated the advantage of our test by revealing a significant association (P = 0.00067) between alcohol <b>dependence</b> and a SNP in the <strong>growth associated protein 43</strong>.
+GAP43	drug	cocaine	15548228	A single high dose of <b>cocaine</b> induces behavioural sensitization and modifies mRNA encoding GluR1 and <strong>GAP 43</strong> in rats.
+GAP43	addiction	sensitization	15548228	A single high dose of cocaine induces behavioural <b>sensitization</b> and modifies mRNA encoding GluR1 and <strong>GAP 43</strong> in rats.
+GAP43	drug	cocaine	15548228	The present study investigated whether in Sprague Dawley rats a single, behavioural sensitizing dose of <b>cocaine</b> is sufficient to induce changes in the mRNA levels of growth associated protein 43 (<strong>GAP 43</strong>), an important protein in mediating experience dependent plasticity and synaptic reorganization, and of glutamate receptor 1 (GluR1), a subunit of AMPA glutamate receptors, a protein that is up regulated with repeated <b>cocaine</b>.
+GAP43	drug	cocaine	15548228	The present study investigated whether in Sprague Dawley rats a single, behavioural sensitizing dose of <b>cocaine</b> is sufficient to induce changes in the mRNA levels of <strong>growth associated protein 43</strong> (<strong>GAP 43</strong>), an important protein in mediating experience dependent plasticity and synaptic reorganization, and of glutamate receptor 1 (GluR1), a subunit of AMPA glutamate receptors, a protein that is up regulated with repeated <b>cocaine</b>.
+GAP43	drug	cocaine	15548228	Single dose of 20 but not 10 mg/kg <b>cocaine</b> 48 h before scheduled death significantly enhanced GluR1 and <strong>GAP 43</strong> mRNA expression in the nucleus accumbens (NAc), both shell and core subregions, and ventral tegmental area (VTA).
+GAP43	drug	cocaine	15548228	No changes were found in the levels of mRNA for GluR1 and <strong>GAP 43</strong> in the frontal cortex, caudate putamen, dentate gyrus of hippocampus and basolateral nucleus of the amygdala after the single dose of 20 mg/kg <b>cocaine</b>.
+GAP43	addiction	sensitization	15548228	These results further strengthen the involvement of NAc and VTA in the behavioural <b>sensitization</b> and suggest a role of <strong>GAP 43</strong> in the synaptic reorganization associated to drug abuse.
+GAP43	addiction	withdrawal	12231455	After 10 days of <b>withdrawal</b>, there was an increase in the percentage of cells with neurites (approximately 30%) and the length of neurites as well as an increase in the level of <strong>GAP 43</strong> and neurofilament M. Neurite outgrowth was enhanced as <b>withdrawal</b> time was increased.
+GAD1	drug	opioid	31866536	<strong>GAD1</strong> but not GAD2 polymorphisms are associated with <b>heroin</b> addiction phenotypes.
+GAD1	addiction	addiction	31866536	<strong>GAD1</strong> but not GAD2 polymorphisms are associated with heroin <b>addiction</b> phenotypes.
+GAD1	drug	opioid	31866536	We found that the frequencies of G allele of <strong>GAD1</strong> rs3749034 and rs3762555 were associated with daily dose of <b>methadone</b> use and memory change after <b>heroin</b> addiction.
+GAD1	addiction	addiction	31866536	We found that the frequencies of G allele of <strong>GAD1</strong> rs3749034 and rs3762555 were associated with daily dose of methadone use and memory change after heroin <b>addiction</b>.
+GAD1	drug	opioid	31866536	The C allele frequency of <strong>GAD1</strong> rs3762556 was associated with lower daily dose of <b>methadone</b> use.
+GAD1	drug	opioid	31866536	In <strong>GAD1</strong>, SNPs rs3762556, rs3762555, rs3791878 and rs3749034 had strong linkage, and the frequency of the C G C A haplotype was higher in the lower dose of <b>methadone</b> group.
+GAD1	drug	opioid	31866536	<strong>GAD1</strong> polymorphisms were associated with phenotypes of <b>heroin</b> addiction, especially the daily dose of <b>methadone</b> use and memory change in the Han Chinese population.
+GAD1	addiction	addiction	31866536	<strong>GAD1</strong> polymorphisms were associated with phenotypes of heroin <b>addiction</b>, especially the daily dose of methadone use and memory change in the Han Chinese population.
+GAD1	drug	alcohol	31818977	Using RNAScope in situ hybridization to characterize activity of different VP cell types during relapse to <b>alcohol</b> seeking provoked by renewal (context induced reinstatement), we found that VP <strong>Gad1</strong> and parvalbumin (PV), but not vGlut2, neurons show relapse associated changes in c Fos expression.
+GAD1	addiction	relapse	31818977	Using RNAScope in situ hybridization to characterize activity of different VP cell types during <b>relapse</b> to alcohol <b>seeking</b> provoked by renewal (context induced <b>reinstatement</b>), we found that VP <strong>Gad1</strong> and parvalbumin (PV), but not vGlut2, neurons show <b>relapse</b> associated changes in c Fos expression.
+GAD1	drug	amphetamine	30275762	In addition, significant increases of GABA A α1 receptor and <strong>GAD1</strong> genes expression were found in the ED binge <b>METH</b> group.
+GAD1	addiction	intoxication	30275762	In addition, significant increases of GABA A α1 receptor and <strong>GAD1</strong> genes expression were found in the ED <b>binge</b> METH group.
+GAD1	addiction	relapse	29656870	The AcbSh→ventral tegmental area (VTA) pathway promotes <b>relapse</b> via projections to VTA <strong>Gad1</strong> neurons.
+GAD1	drug	amphetamine	27967329	Association of polymorphisms in <strong>GAD1</strong> and GAD2 genes with <b>methamphetamine</b> dependence.
+GAD1	addiction	dependence	27967329	Association of polymorphisms in <strong>GAD1</strong> and GAD2 genes with methamphetamine <b>dependence</b>.
+GAD1	drug	amphetamine	27967329	Genotypes of rs769404 and rs701492 in <strong>GAD1</strong> and rs2236418 in GAD2 polymorphisms were determined in 100 <b>METH</b> dependent male subjects and 102 matched controls.
+GAD1	drug	amphetamine	27967329	The presence of the rs769404 rs701492 (<strong>GAD1</strong>) C C haplotype was associated with <b>METH</b> psychosis.
+GAD1	drug	amphetamine	27967329	This study indicates that genetic variability in <strong>GAD1</strong> and GAD2 contributes to risk of <b>METH</b> dependence and <b>METH</b> psychosis in the Thai population and indicates the role of the GABAergic system in these disorders.
+GAD1	addiction	dependence	27967329	This study indicates that genetic variability in <strong>GAD1</strong> and GAD2 contributes to risk of METH <b>dependence</b> and METH psychosis in the Thai population and indicates the role of the GABAergic system in these disorders.
+GAD1	addiction	addiction	26277529	In addition, SNPs GABRB3 rs7165224; DBI rs12613135; <strong>GAD1</strong> SNPs rs2058725, rs1978340, rs2241164; and GRIN2A rs1650420 were previously reported in associations with drug <b>addiction</b> or related phenotypes.
+GAD1	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (<strong>GAD1</strong>, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+GAD1	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (<strong>GAD1</strong>, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+GAD1	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., GABRA1, GABRA2, and GABRG1), glutaminergic (<strong>GAD1</strong>, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+GAD1	addiction	relapse	25623945	Behavioral characterization of our transgenic (Tg) mice uncovered that the Pvalb/<strong>Gad1</strong> Tg mice have pronounced sensorimotor gating deficits, increased novelty <b>seeking</b> and reduced fear extinction.
+GAD1	drug	opioid	25252306	[Association study of CNR1, <strong>GAD1</strong> and BDNF polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan].
+GAD1	addiction	dependence	25252306	[Association study of CNR1, <strong>GAD1</strong> and BDNF polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan].
+GAD1	drug	cannabinoid	25252306	In order to analyze the association of CNR1(<b>Cannabinoid</b> receptor 1), <strong>GAD1</strong>(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+GAD1	drug	opioid	25252306	In order to analyze the association of CNR1(Cannabinoid receptor 1), <strong>GAD1</strong>(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+GAD1	addiction	dependence	25252306	In order to analyze the association of CNR1(Cannabinoid receptor 1), <strong>GAD1</strong>(Glutamate decarboxylase 1), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+GAD1	drug	cannabinoid	25252306	In order to analyze the association of CNR1(<b>Cannabinoid</b> receptor 1), <strong>GAD1</strong>(<strong>Glutamate decarboxylase 1</strong>), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+GAD1	drug	opioid	25252306	In order to analyze the association of CNR1(Cannabinoid receptor 1), <strong>GAD1</strong>(<strong>Glutamate decarboxylase 1</strong>), and BDNF(Brain derived neurotrophic factor) polymorphisms with male <b>heroin</b> dependence in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+GAD1	addiction	dependence	25252306	In order to analyze the association of CNR1(Cannabinoid receptor 1), <strong>GAD1</strong>(<strong>Glutamate decarboxylase 1</strong>), and BDNF(Brain derived neurotrophic factor) polymorphisms with male heroin <b>dependence</b> in the Dai population in Yunnan Province, an eight SNP co amplification protocol was established to genotype on the SNaPshot platform.
+GAD1	drug	opioid	25252306	A case control study was performed with 8 SNPs from CNR1, <strong>GAD1</strong>, and BDNF genes in 165 <b>heroin</b> dependent males and 170 healthy males of the Dai population.
+GAD1	drug	opioid	25252306	These results indicate that the linkage between rs1978340 and rs3791878 in <strong>GAD1</strong> has a strong association with <b>heroin</b> dependence.
+GAD1	addiction	dependence	25252306	These results indicate that the linkage between rs1978340 and rs3791878 in <strong>GAD1</strong> has a strong association with heroin <b>dependence</b>.
+GAD1	drug	opioid	25252306	Furthermore, polymorphisms in CNR1 (rs1049353), <strong>GAD1</strong> (rs1978340 and rs11542313), and BDNF (rs6265 and rs13306221) were associated with <b>heroin</b> dependence in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be <b>heroin</b> dependent.
+GAD1	addiction	dependence	25252306	Furthermore, polymorphisms in CNR1 (rs1049353), <strong>GAD1</strong> (rs1978340 and rs11542313), and BDNF (rs6265 and rs13306221) were associated with heroin <b>dependence</b> in the Yunnan Dai population, and individuals with the rs6265 A allele were more likely to be heroin dependent.
+GAD1	drug	alcohol	24929233	The severity of fetal <b>alcohol</b> syndrome (FAS) morphological phenotypes, such as microphthalmia, depends on the embryonic stage and concentration of <b>alcohol</b> exposure, as does diminution of retinal Pax6a or forebrain and hindbrain <strong>GAD1</strong> gene expression.
+GAD1	drug	alcohol	23857790	Genes SSTR4, ALDH1L2, <strong>GAD1</strong>, DBH and GABRP may participate in the biological process of <b>alcohol</b> dependence.
+GAD1	addiction	dependence	23857790	Genes SSTR4, ALDH1L2, <strong>GAD1</strong>, DBH and GABRP may participate in the biological process of alcohol <b>dependence</b>.
+GAD1	drug	opioid	22564729	Polymorphisms in the <strong>glutamate decarboxylase 1</strong> gene associated with <b>heroin</b> dependence.
+GAD1	addiction	dependence	22564729	Polymorphisms in the <strong>glutamate decarboxylase 1</strong> gene associated with heroin <b>dependence</b>.
+GAD1	addiction	dependence	22564729	The <strong>GAD1</strong> gene encodes the 67 kDa glutamic acid decarboxylase isoform (GAD67), the rate limiting enzyme responsible for γ aminobutyric acid (GABA) biosynthesis from glutamic acid, and may be involved in the development of drug <b>dependence</b>.
+GAD1	drug	opioid	22564729	To identify markers contributing to the genetic susceptibility to <b>heroin</b> dependence, this study examined the potential association between <b>heroin</b> dependence and 15 single nucleotide polymorphisms (SNPs, rs1978340, rs3762556, rs3791878, rs3749034, rs11542313, rs2241165, rs2241164, rs769407, rs3749033, rs16858977, rs701492, rs16858988, rs4668331, rs7578661, rs769395) of <strong>GAD1</strong> gene using the MassARRAY system.
+GAD1	addiction	dependence	22564729	To identify markers contributing to the genetic susceptibility to heroin <b>dependence</b>, this study examined the potential association between heroin <b>dependence</b> and 15 single nucleotide polymorphisms (SNPs, rs1978340, rs3762556, rs3791878, rs3749034, rs11542313, rs2241165, rs2241164, rs769407, rs3749033, rs16858977, rs701492, rs16858988, rs4668331, rs7578661, rs769395) of <strong>GAD1</strong> gene using the MassARRAY system.
+GAD1	drug	opioid	22564729	These findings point to a role for <strong>GAD1</strong> polymorphism in <b>heroin</b> dependence among Han Chinese, and may be informative for future genetic or neurobiological studies on <b>heroin</b> dependence.
+GAD1	addiction	dependence	22564729	These findings point to a role for <strong>GAD1</strong> polymorphism in heroin <b>dependence</b> among Han Chinese, and may be informative for future genetic or neurobiological studies on heroin <b>dependence</b>.
+GAD1	drug	alcohol	22253714	There were also expression changes specific to cocaine addicts (<strong>GAD1</strong>, GAD2), <b>alcoholics</b> (GABRA2) and P rats (ABAT, GABRG3).
+GAD1	drug	cocaine	22253714	There were also expression changes specific to <b>cocaine</b> addicts (<strong>GAD1</strong>, GAD2), alcoholics (GABRA2) and P rats (ABAT, GABRG3).
+GAD1	drug	alcohol	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as <b>alcohol</b> dehydrogenase (ADH7), glutamic acid decarboxylase (<strong>GAD1</strong> and GAD2), the nucleoside transporter (SLC29A1) and diazepam binding inhibitor (DBI).
+GAD1	drug	benzodiazepine	19500151	These SNPs are from genes encoding several receptors: adrenergic (ADRA1A), arginine vasopressin (AVPR1A), cholinergic (CHRM2), dopamine (DRD1), GABA A (GABRB3), glutamate (GRIN2A) and serotonin (HTR3A) as well as alcohol dehydrogenase (ADH7), glutamic acid decarboxylase (<strong>GAD1</strong> and GAD2), the nucleoside transporter (SLC29A1) and <b>diazepam</b> binding inhibitor (DBI).
+GAD1	drug	alcohol	19111404	Three markers in the intronic regions of <strong>GAD1</strong> were associated with initial sensitivity to <b>alcohol</b> (P=0.002); the associations remained significant after a FDR based correction for multiple testing.
+GAD1	drug	alcohol	17067345	This study examined the possible roles of the genes that code for 2 forms of GAD (<strong>GAD1</strong> and GAD2) in the development of <b>alcoholism</b>.
+GAD1	drug	alcohol	17067345	This is the first report indicating a possible significant role of the <strong>GAD1</strong> gene in the development of <b>alcohol</b> dependence and/or the course of <b>alcohol</b> withdrawal and outcome of <b>alcoholism</b>.
+GAD1	addiction	dependence	17067345	This is the first report indicating a possible significant role of the <strong>GAD1</strong> gene in the development of alcohol <b>dependence</b> and/or the course of alcohol withdrawal and outcome of alcoholism.
+GAD1	addiction	withdrawal	17067345	This is the first report indicating a possible significant role of the <strong>GAD1</strong> gene in the development of alcohol dependence and/or the course of alcohol <b>withdrawal</b> and outcome of alcoholism.
+GAD1	drug	alcohol	12691782	Evaluation of the glutamate decarboxylase genes <strong>Gad1</strong> and Gad2 as candidate genes for acute <b>ethanol</b> withdrawal severity in mice.
+GAD1	addiction	withdrawal	12691782	Evaluation of the glutamate decarboxylase genes <strong>Gad1</strong> and Gad2 as candidate genes for acute ethanol <b>withdrawal</b> severity in mice.
+GAD1	drug	alcohol	12691782	Previous studies in crosses between the C57BL/6J (B6) and the DBA/2J (D2) mice have implicated a role of the genes encoding for the 67  and 65 kDa isoforms of the glutamate decarboxylase (<strong>Gad1</strong> and Gad2) in the manifestation and severity of multiple <b>ethanol</b> related traits such as acute <b>ethanol</b> withdrawal severity [Buck, K.J., Metten, P., Belknap, J.K., Crabbe, J.C., 1997.
+GAD1	addiction	withdrawal	12691782	Previous studies in crosses between the C57BL/6J (B6) and the DBA/2J (D2) mice have implicated a role of the genes encoding for the 67  and 65 kDa isoforms of the glutamate decarboxylase (<strong>Gad1</strong> and Gad2) in the manifestation and severity of multiple ethanol related traits such as acute ethanol <b>withdrawal</b> severity [Buck, K.J., Metten, P., Belknap, J.K., Crabbe, J.C., 1997.
+GAD1	drug	alcohol	12691782	Therefore, these results do not support the hypothesis of an involvement of <strong>Gad1</strong> or Gad2 in the pathophysiology of acute <b>ethanol</b> withdrawal severity and the other <b>ethanol</b> related traits.
+GAD1	addiction	withdrawal	12691782	Therefore, these results do not support the hypothesis of an involvement of <strong>Gad1</strong> or Gad2 in the pathophysiology of acute ethanol <b>withdrawal</b> severity and the other ethanol related traits.
+FTCD	drug	nicotine	32247097	Regarding the evaluation of <b>tobacco</b> addiction, the most commonly used questionnaires are the Fagerström tests (<strong>FTCD</strong>, HSI…), which are well correlated with cotinine concentration.
+FTCD	addiction	addiction	32247097	Regarding the evaluation of tobacco <b>addiction</b>, the most commonly used questionnaires are the Fagerström tests (<strong>FTCD</strong>, HSI…), which are well correlated with cotinine concentration.
+FTCD	drug	nicotine	31519135	Objective: The purpose of this study was to evaluate the degree of agreement between the Fagerström Test for Cigarette Dependence (<strong>FTCD</strong>) and the Heaviness of <b>Smoking</b> Index (HSI) in daily <b>smokers</b> admitted to <b>smoking</b> cessation clinics from National Healthcare System in Spain and Argentine Republic.
+FTCD	addiction	dependence	31519135	Objective: The purpose of this study was to evaluate the degree of agreement between the Fagerström Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>) and the Heaviness of Smoking Index (HSI) in daily smokers admitted to smoking cessation clinics from National Healthcare System in Spain and Argentine Republic.
+FTCD	drug	nicotine	31412892	Early abstainers were older with more comorbidities, presenting longer <b>smoking</b> duration, higher exhaled carbon monoxide (CO) concentration and Fagerstrom Test of Cigarette Dependence (<strong>FTCD</strong>) scores.
+FTCD	addiction	dependence	31412892	Early abstainers were older with more comorbidities, presenting longer smoking duration, higher exhaled carbon monoxide (CO) concentration and Fagerstrom Test of Cigarette <b>Dependence</b> (<strong>FTCD</strong>) scores.
+FTCD	drug	nicotine	30874804	At baseline, participants completed the e cigarette Fagerström Test of Cigarette Dependence (e <strong>FTCD</strong>), the e cigarette Wisconsin Inventory of <b>Smoking</b> Dependence Motives (e WISDM), and the Penn State Electronic Cigarette Dependence Index (PS ECDI).
+FTCD	addiction	dependence	30874804	At baseline, participants completed the e cigarette Fagerström Test of Cigarette <b>Dependence</b> (e <strong>FTCD</strong>), the e cigarette Wisconsin Inventory of Smoking <b>Dependence</b> Motives (e WISDM), and the Penn State Electronic Cigarette <b>Dependence</b> Index (PS ECDI).
+FTCD	addiction	addiction	30874804	The e WISDM and PS ECDI had stronger internal consistency than did the e <strong>FTCD</strong>, despite the e <strong>FTCD</strong>'s single factor structure, but all 3 measures appear to be valid measures of e cigarette dependence as suggested by their significant relations with self perceived <b>addiction</b>, heavy use, early use after overnight deprivation, and continued use over time.
+FTCD	addiction	dependence	30874804	The e WISDM and PS ECDI had stronger internal consistency than did the e <strong>FTCD</strong>, despite the e <strong>FTCD</strong>'s single factor structure, but all 3 measures appear to be valid measures of e cigarette <b>dependence</b> as suggested by their significant relations with self perceived addiction, heavy use, early use after overnight deprivation, and continued use over time.
+FTCD	addiction	dependence	30874804	This research provides empirical support for three e cigarette <b>dependence</b> measures: the e <strong>FTCD</strong>, the PS ECDI, and the e WISDM among dual users of e cigarettes and combustible cigarettes.
+FTCD	drug	nicotine	30831339	Participants answered a four part survey: i) demographics; ii) current <b>smoking</b> behaviour and dependence (including the Fagerström Test of Cigarette Dependence [<strong>FTCD</strong>]); iii) previous quit attempts; and iv) e cigarettes perceptions.
+FTCD	addiction	dependence	30831339	Participants answered a four part survey: i) demographics; ii) current smoking behaviour and <b>dependence</b> (including the Fagerström Test of Cigarette <b>Dependence</b> [<strong>FTCD</strong>]); iii) previous quit attempts; and iv) e cigarettes perceptions.
+FTCD	addiction	dependence	30831339	High levels of cigarette <b>dependence</b> were observed (<strong>FTCD</strong>: M = 7.78, sd ± 0.98).
+FTCD	drug	nicotine	30316531	To evaluate the association between degrees of <b>nicotine</b> dependence measured by the Fagerström test (<strong>FTCD</strong>) and different tests of motivation to stop <b>smoking</b>.
+FTCD	addiction	dependence	30316531	To evaluate the association between degrees of nicotine <b>dependence</b> measured by the Fagerström test (<strong>FTCD</strong>) and different tests of motivation to stop smoking.
+FTCD	drug	nicotine	30316531	Demographics, <b>smoking</b> status, <strong>FTCD</strong> scores, and motivation test results were collected: Richmond test (TR), Henri Mondor Paris motivation test (HMP), Khimji Watts test (KW), and the visual analog scale of motivation to stop <b>smoking</b>.
+FTCD	drug	nicotine	30316531	We found no association between <strong>FTCD</strong> and the motivation tests to stop <b>smoking</b> used in this study.
+FTCD	drug	nicotine	30265063	The breakpoint measures were administered along with the Cigarette Purchase Task (CPT), Fagerström Test for Cigarette Dependence (<strong>FTCD</strong>), and The Questionnaire of <b>Smoking</b> Urges (QSU brief).
+FTCD	addiction	dependence	30265063	The breakpoint measures were administered along with the Cigarette Purchase Task (CPT), Fagerström Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>), and The Questionnaire of Smoking Urges (QSU brief).
+FTCD	drug	nicotine	30265063	In addition, both single item measures were associated with metrics of <b>tobacco</b> dependence (e.g., <strong>FTCD</strong>, QSU) with effect sizes that are similar to the ones found between CPT derived breakpoint and those same metrics.
+FTCD	addiction	dependence	30265063	In addition, both single item measures were associated with metrics of tobacco <b>dependence</b> (e.g., <strong>FTCD</strong>, QSU) with effect sizes that are similar to the ones found between CPT derived breakpoint and those same metrics.
+FTCD	drug	nicotine	29890766	By the multivariate logistic regression model, the predictive factors of abstinence were <b>smokers</b> who had a lower Fagerstr&ouml;m test for cigarette dependence (<strong>FTCD</strong>), lower exhaled carbon monoxide (CO) concentration, or who smoked less than 20 cigarettes per day at the first visit.
+FTCD	addiction	dependence	29890766	By the multivariate logistic regression model, the predictive factors of abstinence were smokers who had a lower Fagerstr&ouml;m test for cigarette <b>dependence</b> (<strong>FTCD</strong>), lower exhaled carbon monoxide (CO) concentration, or who smoked less than 20 cigarettes per day at the first visit.
+FTCD	drug	alcohol	29508470	Smoker characteristics measured at baseline were country, psychiatric history, sex, age, body mass index (BMI), ethnic group, life time suicidal ideation/behaviour, anxiety, depression, aggression, psychotropic medication, history of <b>alcohol</b>/substance use disorder, age of starting smoking, cigarette dependence [Fagerström Test for Cigarette Dependence (<strong>FTCD</strong>)] and prior use of study medicines.
+FTCD	drug	nicotine	29508470	<b>Smoker</b> characteristics measured at baseline were country, psychiatric history, sex, age, body mass index (BMI), ethnic group, life time suicidal ideation/behaviour, anxiety, depression, aggression, psychotropic medication, history of alcohol/substance use disorder, age of starting <b>smoking</b>, cigarette dependence [Fagerström Test for Cigarette Dependence (<strong>FTCD</strong>)] and prior use of study medicines.
+FTCD	addiction	dependence	29508470	Smoker characteristics measured at baseline were country, psychiatric history, sex, age, body mass index (BMI), ethnic group, life time suicidal ideation/behaviour, anxiety, depression, aggression, psychotropic medication, history of alcohol/substance use disorder, age of starting smoking, cigarette <b>dependence</b> [Fagerström Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>)] and prior use of study medicines.
+FTCD	drug	nicotine	28950117	The Fagerström Test for Cigarette Dependence (<strong>FTCD</strong>) and the Heaviness of <b>Smoking</b> Index (HSI) are the gold standard measures to assess cigarette dependence.
+FTCD	addiction	dependence	28950117	The Fagerström Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>) and the Heaviness of Smoking Index (HSI) are the gold standard measures to assess cigarette <b>dependence</b>.
+FTCD	drug	nicotine	28950117	HSI seems highly recommended in clinical settings addressed to heavy <b>smokers</b> while <strong>FTCD</strong> would be better used in <b>smokers</b> with a level of cigarette dependence ranging between low and high.
+FTCD	addiction	dependence	28950117	HSI seems highly recommended in clinical settings addressed to heavy smokers while <strong>FTCD</strong> would be better used in smokers with a level of cigarette <b>dependence</b> ranging between low and high.
+FTCD	drug	nicotine	28431293	This study aims to evaluate long term effects of a worksite <b>smoking</b> cessation intervention based on cognitive behavioral cessation groups combined with first line medications, and determine to what extent cigarette dependence (<strong>FTCD</strong>) and depressive symptoms may influence results at five year follow up.
+FTCD	addiction	dependence	28431293	This study aims to evaluate long term effects of a worksite smoking cessation intervention based on cognitive behavioral cessation groups combined with first line medications, and determine to what extent cigarette <b>dependence</b> (<strong>FTCD</strong>) and depressive symptoms may influence results at five year follow up.
+FTCD	drug	nicotine	27698094	The objective of our study was to investigate the validity of the Fagerstrom Test for Cigarette Dependence (<strong>FTCD</strong>) and Heaviness of <b>Smoking</b> Index (HSI) as measures of cigarette dependence in the second and third trimesters of pregnancy by comparing them to serum cotinine levels.
+FTCD	addiction	dependence	27698094	The objective of our study was to investigate the validity of the Fagerstrom Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>) and Heaviness of Smoking Index (HSI) as measures of cigarette <b>dependence</b> in the second and third trimesters of pregnancy by comparing them to serum cotinine levels.
+FTCD	addiction	dependence	27698094	Both the <strong>FTCD</strong> and HSI can be used to assess cigarette <b>dependence</b> in the second and third trimester of pregnancy.
+FTCD	addiction	dependence	27698094	There is lack of data on the validity of the <strong>FTCD</strong> and the HSI as markers of cigarette <b>dependence</b> during the second and third trimester of pregnancy.
+FTCD	drug	nicotine	27698094	Our study suggests that both the <strong>FTCD</strong> and HSI perform well in assessing cigarette dependence in the second and third trimester of pregnancy and can be used to plan <b>smoking</b> cessation programs.
+FTCD	addiction	dependence	27698094	Our study suggests that both the <strong>FTCD</strong> and HSI perform well in assessing cigarette <b>dependence</b> in the second and third trimester of pregnancy and can be used to plan smoking cessation programs.
+FTCD	drug	nicotine	27192133	Though this study confirms that regret for <b>smoking</b> is associated with perceived future risks as well as supports previous findings between <strong>FTCD</strong> and DD, it shows little association between DD and perceived future risks.
+FTCD	drug	nicotine	26997495	Using random effect logistic regression models, we analysed the effects of baseline measures of cigarette dependence, including numbers of cigarettes smoked daily, Fagerström Test of Cigarette Dependence (<strong>FTCD</strong>) score, the two <strong>FTCD</strong> subscales of Heaviness of <b>Smoking</b> Index (HSI) and non Heaviness of <b>Smoking</b> Index (non HSI), expired carbon monoxide (CO) level and urges to smoke (strength and frequency) on <b>smoking</b> cessation.
+FTCD	addiction	dependence	26997495	Using random effect logistic regression models, we analysed the effects of baseline measures of cigarette <b>dependence</b>, including numbers of cigarettes smoked daily, Fagerström Test of Cigarette <b>Dependence</b> (<strong>FTCD</strong>) score, the two <strong>FTCD</strong> subscales of Heaviness of Smoking Index (HSI) and non Heaviness of Smoking Index (non HSI), expired carbon monoxide (CO) level and urges to smoke (strength and frequency) on smoking cessation.
+FTCD	drug	nicotine	26547043	Fagerström Test of Cigarette Dependence (<strong>FTCD</strong>), Heaviness of <b>Smoking</b> Index (HSI), and motivation to stop <b>smoking</b> (composite of determination to quit and importance of quitting) were measured at baseline.
+FTCD	addiction	dependence	26547043	Fagerström Test of Cigarette <b>Dependence</b> (<strong>FTCD</strong>), Heaviness of Smoking Index (HSI), and motivation to stop smoking (composite of determination to quit and importance of quitting) were measured at baseline.
+FTCD	drug	nicotine	26547043	Cigarette dependence, measured by the <strong>FTCD</strong>, or by its HSI or non HSI components, predicts both short term and medium term outcomes of attempts to stop <b>smoking</b> in treatment seeking <b>smokers</b> involved in a clinical trial, whereas strength of motivation to stop predicts neither.
+FTCD	addiction	dependence	26547043	Cigarette <b>dependence</b>, measured by the <strong>FTCD</strong>, or by its HSI or non HSI components, predicts both short term and medium term outcomes of attempts to stop smoking in treatment seeking smokers involved in a clinical trial, whereas strength of motivation to stop predicts neither.
+FTCD	addiction	relapse	26547043	Cigarette dependence, measured by the <strong>FTCD</strong>, or by its HSI or non HSI components, predicts both short term and medium term outcomes of attempts to stop smoking in treatment <b>seeking</b> smokers involved in a clinical trial, whereas strength of motivation to stop predicts neither.
+FTCD	addiction	dependence	25995159	Two widely used brief measures of cigarette <b>dependence</b> are the six item Fagerström Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>) and five item Cigarette <b>Dependence</b> Scale (CDS 5).
+FTCD	drug	nicotine	25995159	The <strong>FTCD</strong>, CDS 5, craving to smoke, and withdrawal symptoms failed to predict <b>smoking</b> status 2 weeks following the quit date.
+FTCD	addiction	relapse	25995159	The <strong>FTCD</strong>, CDS 5, <b>craving</b> to smoke, and withdrawal symptoms failed to predict smoking status 2 weeks following the quit date.
+FTCD	addiction	withdrawal	25995159	The <strong>FTCD</strong>, CDS 5, craving to smoke, and <b>withdrawal</b> symptoms failed to predict smoking status 2 weeks following the quit date.
+FTCD	drug	nicotine	25795690	<b>Nicotine</b> dependence level assessed by Fagerström Test for Cigarette Dependence (<strong>FTCD</strong>), <b>smoking</b> cessation attempts during the previous 12 months and motivators for <b>smoking</b> cessation.
+FTCD	addiction	dependence	25795690	Nicotine <b>dependence</b> level assessed by Fagerström Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>), smoking cessation attempts during the previous 12 months and motivators for smoking cessation.
+FTCD	drug	nicotine	25555385	The objective of this study was to test whether individual differences in the level of <b>nicotine</b> dependence (as measured by the Fagerstrom Test of Cigarette Dependence [<strong>FTCD</strong>]) and/or the rate of <b>nicotine</b> metabolism influence <b>smoking</b> behavior and exposure to <b>tobacco</b> toxicants when <b>smokers</b> are switched to reduced <b>nicotine</b> content cigarettes (RNC).
+FTCD	addiction	dependence	25555385	The objective of this study was to test whether individual differences in the level of nicotine <b>dependence</b> (as measured by the Fagerstrom Test of Cigarette <b>Dependence</b> [<strong>FTCD</strong>]) and/or the rate of nicotine metabolism influence smoking behavior and exposure to tobacco toxicants when smokers are switched to reduced nicotine content cigarettes (RNC).
+FTCD	drug	nicotine	25555385	Higher baseline <strong>FTCD</strong> predicted <b>smoking</b> more cigarettes per day (CPD), higher cotinine and smoke toxicant levels while <b>smoking</b> RNC throughout the study, with no interaction by RNC level.
+FTCD	drug	nicotine	25555385	<strong>FTCD</strong> is associated with overall exposure to <b>nicotine</b> and other constituents of <b>tobacco</b> smoke, while a short TFC is associated with an increased compensatory response after switching to RNC.
+FTCD	drug	alcohol	25052789	All participants completed the following measures online: Depression Anxiety Stress Scales (DASS 21), the Negative Mood Regulation (NMR) scale, the Frontal Systems Behavior Scale (FrSBe), the Fagerström Test for Cigarette Dependence (<strong>FTCD</strong>), and the <b>Alcohol</b> Use Disorders Identification Test (AUDIT).
+FTCD	addiction	dependence	25052789	All participants completed the following measures online: Depression Anxiety Stress Scales (DASS 21), the Negative Mood Regulation (NMR) scale, the Frontal Systems Behavior Scale (FrSBe), the Fagerström Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>), and the Alcohol Use Disorders Identification Test (AUDIT).
+FTCD	drug	nicotine	22799320	The Fagerstrom Test for Cigarette Dependence (<strong>FTCD</strong>) (formally FTND) is widely used for measuring physical dependence on <b>nicotine</b>.
+FTCD	addiction	dependence	22799320	The Fagerstrom Test for Cigarette <b>Dependence</b> (<strong>FTCD</strong>) (formally FTND) is widely used for measuring physical <b>dependence</b> on nicotine.
+FTCD	drug	nicotine	22799320	The psychometric properties of the <strong>FTCD</strong> were assessed in a subsample (91 regular cigarette <b>smokers</b>) of purposively selected 204 UK resident Yemeni khat chewers recruited during random visits to khat sale outlets.
+FTCD	drug	nicotine	22524403	The aim of this paper is to evaluate the importance of phenotype definition (i.e., CPD versus Fagerström test for cigarette dependence (<strong>FTCD</strong>) score as a measure of <b>nicotine</b> dependence) on genome wide association studies of <b>nicotine</b> dependence.
+FTCD	addiction	dependence	22524403	The aim of this paper is to evaluate the importance of phenotype definition (i.e., CPD versus Fagerström test for cigarette <b>dependence</b> (<strong>FTCD</strong>) score as a measure of nicotine <b>dependence</b>) on genome wide association studies of nicotine <b>dependence</b>.
+FTCD	drug	nicotine	22524403	<b>Nicotine</b> dependence defined by <strong>FTCD</strong> score ≥4, CPD.
+FTCD	addiction	dependence	22524403	Nicotine <b>dependence</b> defined by <strong>FTCD</strong> score ≥4, CPD.
+F11R	drug	opioid	26939351	New research reported in <strong>JAMA</strong> Internal Medicine suggests that the over prescribing of <b>opioids</b> is a problem shared by a broad cross section of health professionals, not a small subset, as some have suggested.
+F11R	drug	alcohol	25346505	<strong>JAMA</strong> 2006; 295:2003), the largest study of pharmacotherapy for <b>alcoholism</b> in the United States to date, and to validate these results in PREDICT (Mann et al.
+F11R	drug	alcohol	15288384	This work further suggests that high levels of DRD2 may be protective against <b>alcohol</b> abuse [<strong>JAMA</strong> 263 (1990) 2055; Arch, Gen. Psychiatr.
+DAGLA	drug	cannabinoid	32057593	In the mPFC and hippocampus, EtOH rats had significantly higher mRNA expression of <b>endocannabinoid</b> signaling (mPFC: Ppara, <strong>Dagla</strong>, Daglb and Napepld; and hippocampus: Cnr2, <strong>Dagla</strong> and Mgll) and neuroinflammation associated genes (mPFC: Gfap; and hippocampus: Aif1) than in controls.
+DAGLA	drug	cannabinoid	30987110	Immunohistochemical staining further confirmed the presence of <strong>diacylglycerol lipase alpha</strong>, an <b>endocannabinoid</b> synthesizing enzyme, in oriens interneurons.
+DAGLA	drug	cannabinoid	27394933	Five genes known to play a role in the <b>endocannabinoid</b> system and CUDs were examined in a community sample of young adult Mexican Americans (MAs): CNR1, MGLL, FAAH, <strong>DAGLA</strong>, and DAGLB.
+DAGLA	drug	cannabinoid	26811312	Regarding the <b>endocannabinoid</b> system, acute and repeated cocaine administration were associated with an increased gene/protein expression of CB1 receptors and a decreased gene/protein expression of the <b>endocannabinoid</b> synthesis enzymes N acyl phosphatidylethanolamine D (NAPE PLD) and <strong>diacylglycerol lipase alpha</strong> (DAGLα).
+DAGLA	drug	cocaine	26811312	Regarding the endocannabinoid system, acute and repeated <b>cocaine</b> administration were associated with an increased gene/protein expression of CB1 receptors and a decreased gene/protein expression of the endocannabinoid synthesis enzymes N acyl phosphatidylethanolamine D (NAPE PLD) and <strong>diacylglycerol lipase alpha</strong> (DAGLα).
+DAGLA	drug	cannabinoid	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: <strong>DAGLA</strong>, DAGLB, NAPEPLD; catabolism: MGLL, FAAH; binding: CNR1; SNPs N = 65) and childhood sexual abuse (CSA) predict <b>cannabis</b> dependence symptoms.
+DAGLA	addiction	dependence	26595473	We employed a system level gene based analysis of data from the Comorbidity and Trauma Study (N = 1,558) to examine whether genetic variation in six eCB genes (anabolism: <strong>DAGLA</strong>, DAGLB, NAPEPLD; catabolism: MGLL, FAAH; binding: CNR1; SNPs N = 65) and childhood sexual abuse (CSA) predict cannabis <b>dependence</b> symptoms.
+DAGLA	drug	cannabinoid	25539508	These protein changes were accompanied by an overall decrease in the ratios of <b>endocannabinoid</b> synthesis/degradation, especially the N acyl phosphatidylethanolamine phospholipase D/FAAH and <strong>diacylglycerol lipase alpha</strong>/MAGL ratios.
+DAGLA	drug	cannabinoid	24634647	To this end, we investigated whether eCB signaling related gene and protein expression {<b>cannabinoid</b> receptor type 1 receptors and enzymes that produce [<strong>diacylglycerol lipase alpha</strong>/beta (DAGLα/β) and N acyl phosphatidylethanolamine phospholipase D (NAPE PLD)] and degrade [monoacylglycerol lipase (MAGL) and fatty acid amino hydrolase (FAAH)] eCB} were altered.
+DAGLA	drug	cannabinoid	17655884	In situ hybridization for sn 1 <strong>diacylglycerol lipase alpha</strong> (DGL alpha), the biosynthetic enzyme of the most abundant <b>endocannabinoid</b>, 2 arachidonoylglycerol (2 AG), revealed that DGL alpha was expressed at moderate to high levels by most neurons of the VTA.
+DAGLA	drug	cannabinoid	17451066	It is synthesized by <strong>diacylglycerol lipase alpha</strong> (DGL alpha), and exerts its action via type 1 <b>cannabinoid</b> receptors (CB1).
+ARRB2	drug	opioid	28855588	The tyrosine kinase, c Src, participates in mu <b>opioid</b> receptor (MOP) mediated inhibition in sensory neurons in which β arrestin2 (β <strong>arr2</strong>) is implicated in its recruitment.
+ARRB2	drug	opioid	28855588	Mice lacking β <strong>arr2</strong> exhibit increased sensitivity to <b>morphine</b> reinforcement; however, whether β <strong>arr2</strong> and/or c Src participate in the actions of <b>opioids</b> in neurons within the reward pathway is unknown.
+ARRB2	addiction	reward	28855588	Mice lacking β <strong>arr2</strong> exhibit increased sensitivity to morphine <b>reinforcement</b>; however, whether β <strong>arr2</strong> and/or c Src participate in the actions of opioids in neurons within the <b>reward</b> pathway is unknown.
+ARRB2	drug	opioid	28855588	We examined the involvement of MOPs, DOPs, β <strong>arr2</strong> and c Src in the inhibition by <b>morphine</b> of GABAergic inhibitory postsynaptic currents (IPSCs) recorded from neurons in the mouse ventral tegmental area.
+ARRB2	drug	opioid	28855588	Inhibition of IPSC frequency by <b>morphine</b> was also reduced in β <strong>arr2</strong> /  neurons in which PP2 caused no further reduction.
+ARRB2	drug	opioid	28855588	These data suggest that inhibition of IPSCs by <b>morphine</b> involves a β <strong>arr2</strong>/c Src mediated mechanism.
+ARRB2	drug	nicotine	25450229	Rare variants in NRXN1, CHRNA9, CHRNA2, NTRK2, GABBR2, GRIN3A, DNM1, NRXN2, NRXN3 and <strong>ARRB2</strong> were significantly associated with <b>smoking</b> status in the MSTCC AA sample, with weighted sum statistic (WSS) P values ranging from 2.42 × 10( 3) to 1.31 × 10( 4) after 10(6) phenotype rearrangements.
+ARRB2	drug	opioid	24956254	Nevertheless many genetic factors have been investigated including those affecting its metabolism (CYP2B6 consistent results), efflux transport (P gp inconsistent results), target μ <b>opioid</b> receptor (μ <b>opioid</b> receptor inconsistent results) and a host of other receptors (DRD2) and signaling elements (GIRK2 and <strong>ARRB2</strong>; not replicated).
+ARRB2	drug	opioid	26574964	Blood samples were taken for the determination of serum levels of racemic <b>methadone</b> and its R and S enantiomers, and for typing of candidate alleles of POR, CYP2B6, ABCB1, GRIN1, OPRM1, SLC6A3, DßH and <strong>ARRB2</strong> genes, all associated with the metabolism, tissue distribution and mechanism of action of <b>methadone</b>.
+ARRB2	drug	nicotine	24447405	The purpose of the present study was to examine the associations of single nucleotide polymorphisms (SNPs) in the genes encoding mu opioid receptor (MOR) and the MOR interacting proteins (including OPRM1, <strong>ARRB2</strong>, and HINT1) with <b>smoking</b> behaviors in Chinese men.
+ARRB2	drug	opioid	24447405	The purpose of the present study was to examine the associations of single nucleotide polymorphisms (SNPs) in the genes encoding mu <b>opioid</b> receptor (MOR) and the MOR interacting proteins (including OPRM1, <strong>ARRB2</strong>, and HINT1) with smoking behaviors in Chinese men.
+ARRB2	drug	opioid	24447405	Participant samples were genotyped for six SNPs in the <b>opioid</b> pathway genes: rs1799971 in OPRM1, rs1045280, rs2036657 and rs3786047 in <strong>ARRB2</strong>, rs3852209 and rs2278060 in HINT1.
+ARRB2	drug	nicotine	24447405	No haplotypes in <strong>ARRB2</strong> or HINT1 were related to <b>smoking</b> status.
+ARRB2	drug	opioid	24223972	Sub acute <b>morphine</b> administration resulted in a decrease of NMDAR1 and <strong>Arrb2</strong> whereas during longer <b>opioid</b> treatment the expression NMDAR1 and <strong>Arrb2</strong> mRNA increased again to baseline values.
+ARRB2	drug	psychedelics	24223972	Coadministration of s <b>ketamine</b> or clonidine resulted in a reversal of the mechanical hyperalgesia and inhibited the normalization of NMDAR1 mRNA expression but had no effect on the expression of <strong>Arrb2</strong> mRNA.
+ARRB2	drug	alcohol	23779257	We have previously shown that ablation of β arrestin 2 (<strong>Arrb2</strong>), a crucial regulator of μ opioid receptor function, attenuates <b>alcohol</b> induced hyperlocomotion and c fos activation in the nucleus accumbens.
+ARRB2	drug	opioid	23779257	We have previously shown that ablation of β arrestin 2 (<strong>Arrb2</strong>), a crucial regulator of μ <b>opioid</b> receptor function, attenuates alcohol induced hyperlocomotion and c fos activation in the nucleus accumbens.
+ARRB2	drug	alcohol	23779257	Here, we further investigated the role of <strong>Arrb2</strong> in modulating <b>alcohol</b> induced dopamine (DA) release and conditioned place preference (CPP).
+ARRB2	addiction	reward	23779257	Here, we further investigated the role of <strong>Arrb2</strong> in modulating alcohol induced dopamine (DA) release and conditioned place preference (<b>CPP</b>).
+ARRB2	drug	alcohol	23779257	We also assessed the functional importance of <strong>Arrb2</strong> for μ opioid receptor surface expression and signaling following an acute <b>alcohol</b> challenge.
+ARRB2	drug	opioid	23779257	We also assessed the functional importance of <strong>Arrb2</strong> for μ <b>opioid</b> receptor surface expression and signaling following an acute alcohol challenge.
+ARRB2	drug	alcohol	23779257	In line with these results, <strong>Arrb2</strong> knockout mice display increased CPP for <b>alcohol</b> as compared to wt mice.
+ARRB2	addiction	reward	23779257	In line with these results, <strong>Arrb2</strong> knockout mice display increased <b>CPP</b> for alcohol as compared to wt mice.
+ARRB2	drug	alcohol	23779257	Finally, <strong>Arrb2</strong> mutant mice display increased μ opioid receptor signaling in the ventral and dorsal striatum and amygdala in response to a low dose of <b>alcohol</b>, indicating impaired desensitization mechanisms in these mice.
+ARRB2	drug	opioid	23779257	Finally, <strong>Arrb2</strong> mutant mice display increased μ <b>opioid</b> receptor signaling in the ventral and dorsal striatum and amygdala in response to a low dose of alcohol, indicating impaired desensitization mechanisms in these mice.
+ARRB2	drug	alcohol	23779257	Our results show that <strong>Arrb2</strong> modulates the response to low doses of <b>alcohol</b> on various levels including μ opioid receptor signaling, DA release, and reward.
+ARRB2	drug	opioid	23779257	Our results show that <strong>Arrb2</strong> modulates the response to low doses of alcohol on various levels including μ <b>opioid</b> receptor signaling, DA release, and reward.
+ARRB2	addiction	reward	23779257	Our results show that <strong>Arrb2</strong> modulates the response to low doses of alcohol on various levels including μ opioid receptor signaling, DA release, and <b>reward</b>.
+ARRB2	addiction	reward	23779257	They also reveal a clear dissociation between the effects of <strong>Arrb2</strong> on psychomotor and <b>reward</b> behaviors.
+ARRB2	drug	cocaine	23598874	We assessed the conditioned place preference (CPP) induced by low (10 mg/kg), moderate (20 mg/kg) and high (30 mg/kg) doses of <b>cocaine</b> in <strong>Arrb2</strong>( / ) mice and <strong>Arrb2</strong>(+/+) controls.
+ARRB2	addiction	reward	23598874	We assessed the conditioned place preference (<b>CPP</b>) induced by low (10 mg/kg), moderate (20 mg/kg) and high (30 mg/kg) doses of cocaine in <strong>Arrb2</strong>( / ) mice and <strong>Arrb2</strong>(+/+) controls.
+ARRB2	drug	cocaine	23598874	In the <strong>Arrb2</strong>( / ) mice, moderate and high, but not low, dose of <b>cocaine</b> induced pronounced increases of CPP scores, which were higher than those in the <strong>Arrb2</strong>(+/+) mice.
+ARRB2	addiction	reward	23598874	In the <strong>Arrb2</strong>( / ) mice, moderate and high, but not low, dose of cocaine induced pronounced increases of <b>CPP</b> scores, which were higher than those in the <strong>Arrb2</strong>(+/+) mice.
+ARRB2	drug	cocaine	23598874	Moreover, <b>cocaine</b> induced locomotor activity was significantly lower in <strong>Arrb2</strong>( / ) mice than that of <strong>Arrb2</strong>(+/+) littermate controls.
+ARRB2	drug	opioid	22491351	Evidence that behavioral phenotypes of <b>morphine</b> in β <strong>arr2</strong> /  mice are due to the unmasking of JNK signaling.
+ARRB2	drug	opioid	22491351	Using neurons lacking β arrestin 2 (β <strong>arr2</strong> / ) to examine this interaction, we found that β <strong>arr2</strong> /  neurons show altered intracellular distribution of JNK and cJun, and that <b>morphine</b>, but not <b>fentanyl</b>, increased the nuclear localization of the phosphorylated, therefore activated, form of cJun, a JNK target in dorsal root ganglia neurons.
+ARRB2	drug	opioid	22491351	Indeed, two different JNK inhibitors reversed the enhanced analgesic effect of <b>morphine</b>, a known phenotype of β <strong>arr2</strong> /  mice, to +/+ levels.
+ARRB2	drug	opioid	22491351	Both the reduced locomotor effect of <b>morphine</b> and the psychomotor sensitization to repeated <b>morphine</b> administration in β <strong>arr2</strong> /  mice were also returned to +/+ levels by inhibiting JNK.
+ARRB2	addiction	sensitization	22491351	Both the reduced locomotor effect of morphine and the psychomotor <b>sensitization</b> to repeated morphine administration in β <strong>arr2</strong> /  mice were also returned to +/+ levels by inhibiting JNK.
+ARRB2	drug	opioid	22491351	Furthermore, a PKC inhibitor had a similar effect as inhibiting JNK in reducing the enhanced analgesic effect of <b>morphine</b> in β <strong>arr2</strong> /  mice to +/+ levels.
+ARRB2	drug	cocaine	22472784	Association study of the β arrestin 2 gene (<strong>ARRB2</strong>) with opioid and <b>cocaine</b> dependence in a European American population.
+ARRB2	drug	opioid	22472784	Association study of the β arrestin 2 gene (<strong>ARRB2</strong>) with <b>opioid</b> and cocaine dependence in a European American population.
+ARRB2	addiction	dependence	22472784	Association study of the β arrestin 2 gene (<strong>ARRB2</strong>) with opioid and cocaine <b>dependence</b> in a European American population.
+ARRB2	drug	cocaine	22472784	In this case control association study, DNA samples from <b>cocaine</b> dependent (n=336) and opioid dependent (n=335) patients and controls (n=656) were genotyped for seven single nucleotide polymorphisms (rs11868227, rs3786047, rs4522461, rs1045280, rs2271167, rs2036657, and rs4790694) across <strong>ARRB2</strong>, the gene encoding the β arrestin 2 protein.
+ARRB2	drug	opioid	22472784	In this case control association study, DNA samples from cocaine dependent (n=336) and <b>opioid</b> dependent (n=335) patients and controls (n=656) were genotyped for seven single nucleotide polymorphisms (rs11868227, rs3786047, rs4522461, rs1045280, rs2271167, rs2036657, and rs4790694) across <strong>ARRB2</strong>, the gene encoding the β arrestin 2 protein.
+ARRB2	drug	cocaine	22472784	Further studies are needed to determine whether variations in <strong>ARRB2</strong> (or other MORIPs) are relevant to <b>cocaine</b> or opioid dependence in different ethnic populations or whether they confer a risk that is specific to dependence on other drugs of abuse.
+ARRB2	drug	opioid	22472784	Further studies are needed to determine whether variations in <strong>ARRB2</strong> (or other MORIPs) are relevant to cocaine or <b>opioid</b> dependence in different ethnic populations or whether they confer a risk that is specific to dependence on other drugs of abuse.
+ARRB2	addiction	dependence	22472784	Further studies are needed to determine whether variations in <strong>ARRB2</strong> (or other MORIPs) are relevant to cocaine or opioid <b>dependence</b> in different ethnic populations or whether they confer a risk that is specific to <b>dependence</b> on other drugs of abuse.
+ARRB2	addiction	reward	21486473	We administered these agents to β <strong>arr2</strong>⁻/⁻ mice to explore the role of constitutive μ receptor activity in nociception and <b>hedonic</b> tone.
+ARRB2	addiction	withdrawal	21486473	This study demonstrates that the induction of constitutive μ receptor activity in vivo in β <strong>arr2</strong>⁻/⁻ mice prolongs tail <b>withdrawal</b> from noxious heat, a phenomenon that was reversed by inverse agonists, but not by antagonists that lack negative efficacy.
+ARRB2	addiction	aversion	21486473	By contrast, the <b>aversive</b> effects of inverse agonists were similar in β <strong>arr2</strong>⁻/⁻ and β <strong>arr2</strong>+/+ mice, suggesting that hedonic tone was unaffected.
+ARRB2	addiction	reward	21486473	By contrast, the aversive effects of inverse agonists were similar in β <strong>arr2</strong>⁻/⁻ and β <strong>arr2</strong>+/+ mice, suggesting that <b>hedonic</b> tone was unaffected.
+ARRB2	drug	alcohol	20864483	Lack of association between genetic polymorphisms of <strong>ARRB2</strong> and <b>alcohol</b> dependence in a Caucasian population.
+ARRB2	addiction	dependence	20864483	Lack of association between genetic polymorphisms of <strong>ARRB2</strong> and alcohol <b>dependence</b> in a Caucasian population.
+ARRB2	drug	amphetamine	20478633	A total of 193 non psychotic males (117 <b>methamphetamine</b> dependent and 76 controls) were genotyped for variants located in six genes (AKT1, <strong>ARRB2</strong>, BDNF, COMT, GSTP1, OPRM1).
+ARRB2	drug	amphetamine	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with <b>METH</b> abuse, nine (<strong>ARRB2</strong>, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with <b>METH</b> psychosis.
+ARRB2	addiction	dependence	19219857	Three genes (COMT, DRD4, and GABRA1) were associated with METH abuse, nine (<strong>ARRB2</strong>, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.
+ARRB2	drug	alcohol	18367649	We identified elevated expression of the beta arrestin 2 gene (<strong>Arrb2</strong>) in the striatum and the hippocampus of <b>ethanol</b> preferring AA rats compared to their nonpreferring counterpart ANA line.
+ARRB2	drug	alcohol	18367649	These findings were functionally validated using mice lacking <strong>Arrb2</strong>, which displayed both reduced voluntary <b>ethanol</b> consumption and <b>ethanol</b> induced psychomotor stimulation.
+ARRB2	drug	nicotine	17978999	Extending a previous finding of an association between functional genetic variation in the mu opioid receptor gene and response to <b>nicotine</b> replacement therapy, we explored the role of genetic variants in two genes encoding mu opioid receptor interacting proteins, namely <strong>ARRB2</strong> and HINT1.
+ARRB2	drug	opioid	17978999	Extending a previous finding of an association between functional genetic variation in the mu <b>opioid</b> receptor gene and response to nicotine replacement therapy, we explored the role of genetic variants in two genes encoding mu <b>opioid</b> receptor interacting proteins, namely <strong>ARRB2</strong> and HINT1.
+ARRB2	drug	nicotine	17579607	On the basis of our previous identified linkage regions for <b>nicotine</b> dependence (ND), we selected seven and four single nucleotide polymorphisms (SNPs) in the beta arrestins 1 (ARRB1) and 2 (<strong>ARRB2</strong>), respectively, to determine the associations of the two genes with ND in a total of 2037 subjects from 602 nuclear families of European American (EA) and African American (AA) origin.
+ARRB2	addiction	dependence	17579607	On the basis of our previous identified linkage regions for nicotine <b>dependence</b> (ND), we selected seven and four single nucleotide polymorphisms (SNPs) in the beta arrestins 1 (ARRB1) and 2 (<strong>ARRB2</strong>), respectively, to determine the associations of the two genes with ND in a total of 2037 subjects from 602 nuclear families of European American (EA) and African American (AA) origin.
+ARRB2	drug	nicotine	17579607	Further, the strength of these associations increased after removing the SQ component from HSI and FTND scores in both the EA and AA samples, suggesting that ARRB1 and <strong>ARRB2</strong> play an important role in biological processes involved in the regulation of <b>smoking</b> urgency (that is time to smoke first cigarette).
+ARRB2	drug	opioid	14614085	Mice lacking beta(arrestin) 2 (beta(<strong>arr2</strong>)) display enhanced sensitivity to <b>morphine</b> in tests of pain perception attributable to impaired desensitization of muOR.
+ARRB2	drug	cocaine	14614085	In the present study, we examined this question by assessing the effects of morphine and <b>cocaine</b> on locomotor activity, behavioral sensitization, conditioned place preference, and striatal dopamine release in beta(<strong>arr2</strong>) knock out (beta(<strong>arr2</strong>) KO) mice and their wild type (WT) controls.
+ARRB2	drug	opioid	14614085	In the present study, we examined this question by assessing the effects of <b>morphine</b> and cocaine on locomotor activity, behavioral sensitization, conditioned place preference, and striatal dopamine release in beta(<strong>arr2</strong>) knock out (beta(<strong>arr2</strong>) KO) mice and their wild type (WT) controls.
+ARRB2	addiction	sensitization	14614085	In the present study, we examined this question by assessing the effects of morphine and cocaine on locomotor activity, behavioral <b>sensitization</b>, conditioned place preference, and striatal dopamine release in beta(<strong>arr2</strong>) knock out (beta(<strong>arr2</strong>) KO) mice and their wild type (WT) controls.
+ARRB2	drug	opioid	14614085	However, in the beta(<strong>arr2</strong>) KO mice, <b>morphine</b> induced more pronounced increases in striatal extracellular dopamine than in WT mice.
+ARRB2	drug	opioid	14614085	Moreover, the rewarding properties of <b>morphine</b> in the conditioned place preference test were greater in the beta(<strong>arr2</strong>) KO mice when compared with the WT mice.
+ARRB2	drug	cocaine	14614085	Thus, beta(<strong>arr2</strong>) appears to play a more important role in the dopaminergic effects mediated by morphine than those induced by <b>cocaine</b>.
+ARRB2	drug	opioid	14614085	Thus, beta(<strong>arr2</strong>) appears to play a more important role in the dopaminergic effects mediated by <b>morphine</b> than those induced by cocaine.
+ARRB2	drug	opioid	11130073	Using a knockout mouse lacking beta arrestin 2 (beta <strong>arr2</strong> / ), we have assessed the contribution of desensitization of the mu <b>opioid</b> receptor to the development of <b>morphine</b> antinociceptive tolerance and the subsequent onset of physical dependence.
+ARRB2	addiction	dependence	11130073	Using a knockout mouse lacking beta arrestin 2 (beta <strong>arr2</strong> / ), we have assessed the contribution of desensitization of the mu opioid receptor to the development of morphine antinociceptive tolerance and the subsequent onset of physical <b>dependence</b>.
+APEX1	addiction	relapse	32167932	High <strong>APEX1</strong> expression correlated with resistance to sorafenib and anti programmed death 1 (PD 1) therapies in HCC patients, and it associated with poorer overall survival, disease specific survival, progression free survival, and <b>relapse</b> free survival in early  and advanced stage HCC patients.
+APEX1	drug	alcohol	32167932	High <strong>APEX1</strong> expression also associated with poor prognosis in non <b>alcoholic</b>, vascular invasion negative, and hepatitis virus negative HCC patients.
+APEX1	drug	alcohol	25557834	The second was a two bottle choice procedure that utilized selectively bred High <b>Alcohol</b> Preferring 1 (<strong>HAP1</strong>) mice to model chronic <b>ethanol</b> access.
+APEX1	drug	alcohol	25557834	<strong>HAP1</strong> mice are selectively bred to consume pharmacologically relevant amounts of <b>ethanol</b> in a 24 h two bottle choice paradigm.
+APEX1	drug	cocaine	25050821	Extinction attenuated <b>cocaine</b> induced cFos activation in NA neurons of the caudal ventrolateral medulla (A1/C1 cell groups), and attenuated cFos within the paraventricular nucleus of the hypothalamus, the <strong>apex</strong> of the central neuroendocrine stress axis.
+APEX1	drug	nicotine	24920473	Our results have shown that the local field potentials corresponding to the neurons located in the PIF region of the VTA have <strong>ApEn</strong> values significantly higher (p = 2x10 4) in the maternal <b>nicotine</b> cases when compared to the saline.
+APEX1	drug	alcohol	23909817	Crossed high <b>alcohol</b> preferring (cHAP) mice were selectively bred from a cross of the <strong>HAP1</strong> × HAP2 replicate lines and demonstrate blood <b>ethanol</b> concentrations (BECs) during free choice drinking reminiscent of those observed in <b>alcohol</b> dependent humans.
+APEX1	drug	alcohol	22126215	All HAP lines reached and maintained a rate of <b>alcohol</b> intake above the rate at which <strong>HAP1</strong> mice metabolize <b>alcohol</b>, and BECs were consistent with this finding.
+APEX1	drug	alcohol	22126215	Free choice drinking demonstrated by the <strong>HAP1</strong> and cHAP lines may provide a unique opportunity for modeling the excessive intake that often occurs in <b>alcohol</b> dependent individuals, and allow for exploration of predisposing factors for excessive consumption, as well as the development of physiological, behavioral and toxicological outcomes following <b>alcohol</b> exposure.
+APEX1	addiction	dependence	21992190	The concentration <b>dependence</b> of ABCB4 appears to be a direct effect on transporter activity, as ABCB4 expression and ABCB4 plasma membrane (PM) localisation at the root <strong>apex</strong> are relatively insensitive to changes in auxin concentration.
+APEX1	drug	alcohol	19120064	The high and low <b>alcohol</b> preferring (<strong>HAP1</strong> and LAP1) mouse lines were selectively bred for differences in <b>alcohol</b> intake.
+APEX1	addiction	reward	18214604	The present study examined Drd2 mRNA expression differences between the <strong>HAP1</strong> and LAP1 mice in brain regions important in the dopaminergic <b>reward</b> pathway, including the nucleus accumbens, hippocampus, amygdala, and septum.
+APEX1	drug	alcohol	18214604	Results show that <b>alcohol</b> naïve <strong>HAP1</strong> mice exhibited lower levels of Drd2 mRNA expression in the nucleus accumbens and the hippocampus compared to LAP1 mice.
+APEX1	drug	alcohol	17850641	The purpose of the present study was to examine whether acute <b>alcohol</b> withdrawal responses, as measured by acoustic startle and prepulse inhibition (PPI) of acoustic startle, may be genetically related to innate differences in <b>alcohol</b> preference in 2 mouse lines selectively bred for high (<strong>HAP1</strong> and HAP2) or low (LAP1 and LAP2) <b>alcohol</b> preference.
+APEX1	addiction	withdrawal	17850641	The purpose of the present study was to examine whether acute alcohol <b>withdrawal</b> responses, as measured by acoustic startle and prepulse inhibition (PPI) of acoustic startle, may be genetically related to innate differences in alcohol preference in 2 mouse lines selectively bred for high (<strong>HAP1</strong> and HAP2) or low (LAP1 and LAP2) alcohol preference.
+APEX1	drug	alcohol	17850641	<b>Alcohol</b> naive, male and female <strong>HAP1</strong> (n = 35) and LAP1 (n = 32) and HAP2 (n = 43) and LAP2 (n = 40) mice were tested under baseline conditions and during withdrawal from a single injection of 4.0 g/kg <b>alcohol</b> or equal volume of saline at 4, 8, and 12 hours post injection.
+APEX1	addiction	withdrawal	17850641	Alcohol naive, male and female <strong>HAP1</strong> (n = 35) and LAP1 (n = 32) and HAP2 (n = 43) and LAP2 (n = 40) mice were tested under baseline conditions and during <b>withdrawal</b> from a single injection of 4.0 g/kg alcohol or equal volume of saline at 4, 8, and 12 hours post injection.
+APEX1	addiction	withdrawal	17850641	In contrast, both <strong>HAP1</strong> males and females showed a trend toward enhanced startle at 4 hours in <b>withdrawal</b>.
+ADM	drug	opioid	31960799	Initiation of glia neuron signaling networks in the peripheral and central nervous system by <strong>adrenomedullin</strong> is involved in the formation and maintenance of <b>morphine</b> tolerance.
+ADM	addiction	reward	29981631	The purpose of this review was to investigate outcomes in patients with abdominal wall hernia undergoing primary closure with component separation (CS) versus CS with acellular dermal matrix (<strong>ADM</strong>) <b>reinforcement</b> (CS + mesh).
+ADM	addiction	reward	29981631	Medical records of consecutive patients who underwent abdominal wall reconstruction using CS with or without <strong>ADM</strong> <b>reinforcement</b> were retrospectively reviewed.
+ADM	addiction	reward	29981631	<strong>ADM</strong> <b>reinforcement</b> when used was performed using the underlay technique.
+ADM	addiction	reward	29981631	<strong>ADM</strong> <b>reinforcement</b> at the time of components separation is often selected in more complex, higher risk patients.
+ADM	addiction	addiction	26597980	<b>Addiction</b> medicine (<strong>ADM</strong>) is an emerging medical field.
+ADM	addiction	addiction	26597980	Certification and maintenance of certification in <strong>ADM</strong> are available currently through the American Board of <b>Addiction</b> Medicine (ABAM).
+ADM	drug	alcohol	25814498	Tobacco cessation therapy is not consistently provided for <b>alcohol</b>, drug abuse and mental health (<strong>ADM</strong>) populations, despite the enormous health consequences of tobacco addiction in these groups and research supporting the effectiveness of treatment.
+ADM	drug	nicotine	25814498	<b>Tobacco</b> cessation therapy is not consistently provided for alcohol, drug abuse and mental health (<strong>ADM</strong>) populations, despite the enormous health consequences of <b>tobacco</b> addiction in these groups and research supporting the effectiveness of treatment.
+ADM	addiction	addiction	25814498	Tobacco cessation therapy is not consistently provided for alcohol, drug abuse and mental health (<strong>ADM</strong>) populations, despite the enormous health consequences of tobacco <b>addiction</b> in these groups and research supporting the effectiveness of treatment.
+ADM	drug	nicotine	25814498	Our goal was to determine whether popular reporting accurately reflects findings from the scientific literature on <b>tobacco</b> cessation treatment for <strong>ADM</strong> populations in treatment.
+ADM	drug	nicotine	25814498	Our results suggest that the failure to consistently provide <b>tobacco</b> cessation therapy to <strong>ADM</strong> populations in treatment is not due to poor research translation.
+ADM	drug	opioid	24132052	Half of the patients were scanned after/before daily <b>methadone</b> intake (<strong>ADM</strong>/BDM patient groups).
+ADM	drug	alcohol	21731413	PURPOSE: Stigma related feelings, including degree of enthusiasm and willingness to work with <b>alcohol</b>, drug, and mental disorder (<strong>ADM</strong>) patients, as well as anticipated success in such work, will be required for the United States to be successful in its new initiatives for <strong>ADM</strong> screening, brief intervention, and effective referral to treatment and rehabilitation services (SBIRT).
+ADM	addiction	addiction	21534129	In the United States accredited residency programs in <b>addiction</b> exist only for psychiatrists specializing in <b>addiction</b> psychiatry (ADP); nonpsychiatrists seeking training in <b>addiction</b> medicine (<strong>ADM</strong>) can train in nonaccredited "fellowships," or can receive training in some ADP programs, only to not be granted a certificate of completion of accredited training.
+ADM	addiction	relapse	21534129	In the United States accredited residency programs in addiction exist only for psychiatrists specializing in addiction psychiatry (ADP); nonpsychiatrists <b>seeking</b> training in addiction medicine (<strong>ADM</strong>) can train in nonaccredited "fellowships," or can receive training in some ADP programs, only to not be granted a certificate of completion of accredited training.
+ADM	drug	alcohol	12236383	To compare adults with different insurance coverage in care for <b>alcohol</b>, drug abuse, and mental health (<strong>ADM</strong>) problems.
+ADM	drug	alcohol	11971152	BACKGROUND: In the United States, insurance benefits for treating <b>alcohol</b>, drug abuse and mental health (<strong>ADM</strong>) problems have been much more limited than medical care benefits.
+ADM	drug	alcohol	11810776	Transcatheter arterial chemo embolization (TACE, THP 30 60 mg, E <strong>ADM</strong> 20 40 mg, CDDP 40 80 mg, MMC 10 20 mg, iodine oil 5 30 ml), percutaneous <b>ethanol</b> injection (PEI), bioimmunotherapy and the traditional Chinese medicine were used pre  and post operatively.
+ADM	drug	alcohol	11330001	This study estimates unmet need and barriers to <b>alcohol</b>, drug, and mental health (<strong>ADM</strong>) services in 1997 to 1998 using data from a national household survey (n = 9,585).
+ADM	drug	alcohol	11327191	We tested the hypothesis, stemming from the appraisal disruption model (<strong>ADM</strong>), that <b>alcohol</b> would be more likely to reduce stress when consumed prior to exposure to a stressor than when consumed following exposure.
+ADM	drug	alcohol	11327191	Findings were consistent with predictions stemming from the <strong>ADM</strong>. <b>Alcohol</b> appears to be more likely to reduce stress when initial stress appraisal occurs during intoxication.
+ADM	addiction	intoxication	11327191	Findings were consistent with predictions stemming from the <strong>ADM</strong>. Alcohol appears to be more likely to reduce stress when initial stress appraisal occurs during <b>intoxication</b>.
+ADM	drug	alcohol	10778825	We found that going to an EAP substantially increases both the probability of an <b>alcohol</b>, drug abuse, or mental health (<strong>ADM</strong>) claim and the number of <strong>ADM</strong> claims in the same quarter as EAP contact.
+ADM	drug	alcohol	10178432	What is the cost of <strong>ADM</strong> (<b>alcohol</b> and drug abuse and mental health) in the U.S.?
+ADM	drug	alcohol	7811346	The purpose of this microiontophoretic study was to explore GABAergic and cholinergic central mechanisms in adult rats exposed to <b>alcohol</b> in the third phase of prenatal life (<strong>ADM</strong>), when their mothers were subjected to <b>alcohol</b> physical dependence induction (9.6 g/kg/day).
+ADM	addiction	dependence	7811346	The purpose of this microiontophoretic study was to explore GABAergic and cholinergic central mechanisms in adult rats exposed to alcohol in the third phase of prenatal life (<strong>ADM</strong>), when their mothers were subjected to alcohol physical <b>dependence</b> induction (9.6 g/kg/day).
+ADM	drug	alcohol	7811346	<b>alcohol</b> injection (1.6 g/kg) spontaneous firing was depressed in <strong>ADM</strong> animals to a lesser extent than in C rats.
+ADM	drug	alcohol	10170864	Medicaid expenditures for <b>alcohol</b>, drug abuse, and mental health (<strong>ADM</strong>) services in 1984 were examined for the States of California and Michigan.
+ADM	drug	alcohol	2526093	This paper measures the cost of short stay hospitalization in 1985 for <b>alcohol</b> and drug abuse and mental illness (<strong>ADM</strong>).
+ADM	drug	alcohol	3533719	The question of psychiatry's role in medicine, and in particular its role in the training of primary care physicians (PCPs), is heightened by the knowledge that 60% of the 15% of patients who have DSM III diagnosable <b>alcohol</b>, drug abuse, and mental health (<strong>ADM</strong>) disorders are seen exclusively in the general health sector.
+ADM	drug	alcohol	390264	Although many of the studies suggested that <b>alcohol</b>, drug abuse or mental health (<strong>ADM</strong>) treatment was a cause of the subsequent reduction in medical care utilization, such causality was not definitively established, due to frequent methodological limitations, such as inadequate comparison groups, short time spans, small samples and lack of trend analysis.
+UROD	drug	alcohol	30683557	Porphyria cutanea tarda (PCT) is the most common human porphyria, due to hepatic deficiency of uroporphyrinogen decarboxylase (<strong>UROD</strong>), which is acquired in the presence of iron overload and various susceptibility factors, such as <b>alcohol</b> abuse, smoking, hepatitis C virus (HCV) infection, HIV infection, iron overload with HFE gene mutations, use of estrogens, and <strong>UROD</strong> mutation.
+UROD	drug	nicotine	30683557	Porphyria cutanea tarda (PCT) is the most common human porphyria, due to hepatic deficiency of uroporphyrinogen decarboxylase (<strong>UROD</strong>), which is acquired in the presence of iron overload and various susceptibility factors, such as alcohol abuse, <b>smoking</b>, hepatitis C virus (HCV) infection, HIV infection, iron overload with HFE gene mutations, use of estrogens, and <strong>UROD</strong> mutation.
+UROD	drug	alcohol	30683557	Porphyria cutanea tarda (PCT) is the most common human porphyria, due to hepatic deficiency of <strong>uroporphyrinogen decarboxylase</strong> (<strong>UROD</strong>), which is acquired in the presence of iron overload and various susceptibility factors, such as <b>alcohol</b> abuse, smoking, hepatitis C virus (HCV) infection, HIV infection, iron overload with HFE gene mutations, use of estrogens, and <strong>UROD</strong> mutation.
+UROD	drug	nicotine	30683557	Porphyria cutanea tarda (PCT) is the most common human porphyria, due to hepatic deficiency of <strong>uroporphyrinogen decarboxylase</strong> (<strong>UROD</strong>), which is acquired in the presence of iron overload and various susceptibility factors, such as alcohol abuse, <b>smoking</b>, hepatitis C virus (HCV) infection, HIV infection, iron overload with HFE gene mutations, use of estrogens, and <strong>UROD</strong> mutation.
+UROD	drug	opioid	26662031	Short term <strong>UROD</strong> treatment on cerebral function in <b>codeine</b> containing cough syrups dependent male individuals.
+UROD	drug	alcohol	26662031	To investigate alterations of resting brain function in codeine containing cough syrups (CCS) dependent individuals before and after ultra rapid opioid detoxification under general anaesthesia (<strong>UROD</strong>) combined with <b>naltrexone</b> treatment (NMT).
+UROD	drug	opioid	26662031	To investigate alterations of resting brain function in <b>codeine</b> containing cough syrups (CCS) dependent individuals before and after ultra rapid <b>opioid</b> detoxification under general anaesthesia (<strong>UROD</strong>) combined with naltrexone treatment (NMT).
+UROD	addiction	withdrawal	26662031	We offer the first report describing how regional and integral synchronous neural activity occurs after <strong>UROD</strong> and short term NMT, accompanied by decreased <b>withdrawal</b> syndrome severity.
+UROD	addiction	relapse	25741479	One month after <strong>UROD</strong>, 48 patients (75%) reported <b>relapse</b> and 16 (25%) reported abstinence; however, four patients of the non relapsed group reported one episode of opiate use.
+UROD	drug	opioid	25741479	Although <strong>UROD</strong> by <b>naloxone</b> is a safe and effective method of detoxification, if used alone, it has a very high relapse rate in long term.
+UROD	addiction	relapse	25741479	Although <strong>UROD</strong> by naloxone is a safe and effective method of detoxification, if used alone, it has a very high <b>relapse</b> rate in long term.
+UROD	drug	alcohol	24471478	Ultra rapid opioid detoxification (<strong>UROD</strong>) and subsequently induction of <b>naltrexone</b> maintenance therapy can be regarded as a safe and effective detoxification method for use in patients with opiate addiction.
+UROD	drug	opioid	24471478	Ultra rapid <b>opioid</b> detoxification (<strong>UROD</strong>) and subsequently induction of naltrexone maintenance therapy can be regarded as a safe and effective detoxification method for use in patients with opiate addiction.
+UROD	addiction	addiction	24471478	Ultra rapid opioid detoxification (<strong>UROD</strong>) and subsequently induction of naltrexone maintenance therapy can be regarded as a safe and effective detoxification method for use in patients with opiate <b>addiction</b>.
+UROD	addiction	relapse	24471478	The aim of this article was to assess <strong>UROD</strong> efficacy and estimate the <b>relapse</b> rate in the 2 year follow up period.
+UROD	addiction	relapse	24471478	<strong>UROD</strong> could be an effective method of detoxification in addicted patients, but case selection, sticking to the guidelines, and maintenance therapy accompanied with social support is necessary to minimize <b>relapse</b> and withdrawal symptoms.
+UROD	addiction	withdrawal	24471478	<strong>UROD</strong> could be an effective method of detoxification in addicted patients, but case selection, sticking to the guidelines, and maintenance therapy accompanied with social support is necessary to minimize relapse and <b>withdrawal</b> symptoms.
+UROD	drug	opioid	21137665	Ultra rapid <b>opioid</b> detoxification (<strong>UROD</strong>) is one of the new methods of detoxification.
+UROD	addiction	withdrawal	21137665	The objective of this study was to evaluate effects of anesthesia duration in <strong>UROD</strong> on severity of <b>withdrawal</b> syndrome.
+UROD	addiction	relapse	21137665	Sixty addicted patients <b>seeking</b> <strong>UROD</strong> procedure assigned randomly to one of the 2 hr, 4 hr or 6 hr anesthesia duration groups.
+UROD	addiction	withdrawal	20924880	The aim of study was determine the effect of ultra rapid opiate detoxification (<strong>UROD</strong>) on the presence or absence of <b>withdrawal</b> syndrome in a group of patients with opiate dependency.
+UROD	drug	opioid	20924880	In this study, withdrawal syndrome of 173 patients with opiate addiction was evaluated before and after <strong>UROD</strong> using the Objective <b>Opioid</b> Withdrawal Scale.
+UROD	addiction	addiction	20924880	In this study, withdrawal syndrome of 173 patients with opiate <b>addiction</b> was evaluated before and after <strong>UROD</strong> using the Objective Opioid Withdrawal Scale.
+UROD	addiction	withdrawal	20924880	In this study, <b>withdrawal</b> syndrome of 173 patients with opiate addiction was evaluated before and after <strong>UROD</strong> using the Objective Opioid <b>Withdrawal</b> Scale.
+UROD	addiction	withdrawal	20924880	Hence, each patient was observed for 5 minutes before <strong>UROD</strong> and at different hours afterward to observe any <b>withdrawal</b> sign.
+UROD	addiction	withdrawal	20924880	The most prevalent <b>withdrawal</b> sign before <strong>UROD</strong> was anxiety.
+UROD	drug	opioid	20924880	Patients with <b>opioid</b> dependency who underwent <strong>UROD</strong> showed the highest rate of withdrawal symptoms at one hour after anesthesia.
+UROD	addiction	withdrawal	20924880	Patients with opioid dependency who underwent <strong>UROD</strong> showed the highest rate of <b>withdrawal</b> symptoms at one hour after anesthesia.
+UROD	drug	opioid	20924880	<strong>UROD</strong> can be applied for detoxification of patients with <b>opioid</b> dependency with safety.
+UROD	drug	alcohol	20101570	The aim of this retrospective study was to assess ultra rapid opiate detoxification (<strong>UROD</strong>) and to estimate the retention rate in <b>naltrexone</b> maintenance treatment.
+UROD	drug	alcohol	20101570	After <strong>UROD</strong>, <b>naltrexone</b> 50 mg/day was prescribed for 9 months with assessments in 4 week intervals.
+UROD	drug	alcohol	20101570	<strong>UROD</strong> and subsequently induction of <b>naltrexone</b> maintenance therapy can be regarded as safe and effective in patients with pure opiate addiction.
+UROD	addiction	addiction	20101570	<strong>UROD</strong> and subsequently induction of naltrexone maintenance therapy can be regarded as safe and effective in patients with pure opiate <b>addiction</b>.
+UROD	drug	opioid	19453966	To perform an <b>opioid</b> free, balanced anesthetic for an Active Duty soldier undergoing cervical ganglionectomy for intractable occipital neuralgia 7 days after ultra rapid <b>opioid</b> detoxification (<strong>UROD</strong>) under general anesthesia.
+UROD	drug	opioid	19453966	We report a case of successful non <b>opioid</b> analgesia in a patient that presented for a cervical ganglionectomy 7 days after <strong>UROD</strong>.
+UROD	addiction	withdrawal	17156115	<strong>UROD</strong> has been modified over 3 decades resulting in a safe and an effective general anesthetic that results in hemodynamically stable <b>withdrawal</b> without manifestation of central nervous system hyperarousal.
+UROD	addiction	withdrawal	17156115	Psychosocial issues should be evaluated by a trained addictionalist and most people will succeed from the <strong>UROD</strong> procedure without experiencing the horrible <b>withdrawal</b> syndrome.
+UROD	drug	opioid	12189623	Ultra rapid <b>opioid</b> detoxification (<strong>UROD</strong>) is a new technique with the use of mu <b>opioid</b> receptor antagonists to precipitate withdrawal.
+UROD	addiction	withdrawal	12189623	Ultra rapid opioid detoxification (<strong>UROD</strong>) is a new technique with the use of mu opioid receptor antagonists to precipitate <b>withdrawal</b>.
+UROD	drug	alcohol	12189623	It is discussed that exposure to naloxone ore <b>naltrexone</b> during <strong>UROD</strong> is associated with development of increasing in opioidergic neurotransmission.
+UROD	drug	opioid	12189623	It is discussed that exposure to <b>naloxone</b> ore naltrexone during <strong>UROD</strong> is associated with development of increasing in opioidergic neurotransmission.
+UROD	drug	opioid	11772672	Rapid and ultrarapid <b>opioid</b> detoxification (ROD and <strong>UROD</strong>) centers promise quick, painless, same day detoxification treatment for patients with <b>opioid</b> addiction.
+UROD	addiction	addiction	11772672	Rapid and ultrarapid opioid detoxification (ROD and <strong>UROD</strong>) centers promise quick, painless, same day detoxification treatment for patients with opioid <b>addiction</b>.
+UROD	drug	alcohol	11772672	The goal of ROD and <strong>UROD</strong> is to provide a rapid transition from opioid dependency to oral <b>naltrexone</b> therapy.
+UROD	drug	opioid	11772672	The goal of ROD and <strong>UROD</strong> is to provide a rapid transition from <b>opioid</b> dependency to oral naltrexone therapy.
+UROD	drug	alcohol	11772672	This article reports six cases of complications from the same detoxification center that performed <strong>UROD</strong> with <b>naltrexone</b> pellet implantation, including pulmonary edema, prolonged withdrawal, drug toxicity, withdrawal from cross addiction to <b>alcohol</b> and benzodiazepines, variceal rupture, aspiration pneumonia, and death.
+UROD	addiction	addiction	11772672	This article reports six cases of complications from the same detoxification center that performed <strong>UROD</strong> with naltrexone pellet implantation, including pulmonary edema, prolonged withdrawal, drug toxicity, withdrawal from cross <b>addiction</b> to alcohol and benzodiazepines, variceal rupture, aspiration pneumonia, and death.
+UROD	addiction	withdrawal	11772672	This article reports six cases of complications from the same detoxification center that performed <strong>UROD</strong> with naltrexone pellet implantation, including pulmonary edema, prolonged <b>withdrawal</b>, drug toxicity, <b>withdrawal</b> from cross addiction to alcohol and benzodiazepines, variceal rupture, aspiration pneumonia, and death.
+UROD	drug	opioid	11407272	Ultra rapid <b>opioid</b> detoxification (<strong>UROD</strong>) is an increasingly popular technique for detoxifying patients addicted to opiates.
+UROD	drug	alcohol	10809517	<strong>UROD</strong> followed by <b>naltrexone</b> maintenance and an aftercare program.
+UROD	drug	alcohol	10809517	(1) Completion of <strong>UROD</strong> as determined by a non reactive response to a naloxone challenge test under anesthesia and non reactive response to <b>naltrexone</b> administration before discharge.
+UROD	drug	opioid	10809517	(1) Completion of <strong>UROD</strong> as determined by a non reactive response to a <b>naloxone</b> challenge test under anesthesia and non reactive response to naltrexone administration before discharge.
+UROD	addiction	relapse	10809517	(2) Patient outcome as determined at six month follow up of <strong>UROD</strong> patients' self reported <b>relapse</b> free status confirmed by urine drug screen, significant other reports, and/or therapist reports.
+UROD	drug	alcohol	10605854	Ultra rapid opiate detoxification (<strong>UROD</strong>) methods attempt to obtain this goal by administering <b>naltrexone</b> under deep sedation or anaesthesia.
+UROD	drug	alcohol	10605854	We present a case study on accidental ingestion of <b>naltrexone</b> in a methadone maintenance patient, which shows close methodological similarities with <strong>UROD</strong> procedures.
+UROD	drug	opioid	10605854	We present a case study on accidental ingestion of naltrexone in a <b>methadone</b> maintenance patient, which shows close methodological similarities with <strong>UROD</strong> procedures.
+UROD	drug	alcohol	10605854	<b>Naltrexone</b> was effective in reducing withdrawal duration, but not as much as <strong>UROD</strong> studies report.
+UROD	addiction	withdrawal	10605854	Naltrexone was effective in reducing <b>withdrawal</b> duration, but not as much as <strong>UROD</strong> studies report.
+UROD	drug	alcohol	1295774	In the genetic type of porphyria cutanea tarda triggered by <b>alcohol</b>, oral contraceptives, and liver damage the <strong>uroporphyrinogen decarboxylase</strong> is decreased to about 50%.
+UROD	drug	alcohol	6800821	Compared with control subjects the activity of the initial and rate controlling enzyme of the pathway, ALA synthase, was increased (P less than 0.01) and the activities of ALA dehydratase and <strong>uroporphyrinogen decarboxylase</strong> depressed (P less than 0.01, P less than 0.02 respectively) on the day after admission but all returned to normal by the tenth to twentieth days after <b>alcohol</b> withdrawal.
+UROD	addiction	withdrawal	6800821	Compared with control subjects the activity of the initial and rate controlling enzyme of the pathway, ALA synthase, was increased (P less than 0.01) and the activities of ALA dehydratase and <strong>uroporphyrinogen decarboxylase</strong> depressed (P less than 0.01, P less than 0.02 respectively) on the day after admission but all returned to normal by the tenth to twentieth days after alcohol <b>withdrawal</b>.
+UROD	drug	alcohol	6800821	This stimulation of ALA synthase and inhibition of <strong>uroporphyrinogen decarboxylase</strong> explains the mechanism by which chronic <b>alcohol</b> ingestion may precipitate cutaneous hepatic porphyria.
+TBC1D24	drug	psychedelics	29753748	This article is part of the Special Issue entitled '<b>Psychedelics</b>: New <strong>Doors</strong>, Altered Perceptions'.
+TBC1D24	drug	psychedelics	29476779	This article is part of the Special Issue entitled '<b>Psychedelics</b>: New <strong>Doors</strong>, Altered Perceptions'.
+TBC1D24	drug	psychedelics	29427652	This article is part of the Special Issue entitled '<b>Psychedelics</b>: New <strong>Doors</strong>, Altered Perceptions'.
+TBC1D24	drug	psychedelics	29339294	This article is part of the Special Issue entitled '<b>Psychedelics</b>: New <strong>Doors</strong>, Altered Perceptions'.
+TBC1D24	drug	psychedelics	29309770	This article is part of the Special Issue entitled '<b>Psychedelics</b>: New <strong>Doors</strong>, Altered Perceptions'.
+TBC1D24	drug	psychedelics	29246856	This article is part of the Special Issue entitled '<b>Psychedelics</b>: New <strong>Doors</strong>, Altered Perceptions'.
+TBC1D24	drug	psychedelics	29196183	This article is part of the Special Issue entitled '<b>Psychedelics</b>: New <strong>Doors</strong>, Altered Perceptions'.
+TBC1D24	drug	psychedelics	29126911	This article is part of the Special Issue entitled '<b>Psychedelics</b>: New <strong>Doors</strong>, Altered Perceptions'.
+TBC1D24	addiction	reward	29016710	Healthy BD (N = 27) and NBD (N = 23) none meeting AUD criteria completed a <b>reward</b> guessing game, the '<strong>Doors</strong>' task, during functional magnetic resonance imaging.
+TBC1D24	drug	opioid	28863059	This past year, a new law called the Comprehensive Addictions Recovery Act has helped to open <strong>doors</strong> for nurse practitioners and physician assistants to prescribe <b>buprenorphine</b>.
+TBC1D24	addiction	relapse	28066828	Findings by both, Kenneth Blum, Ph.D. and Ernest Noble, Ph.D. concerning the role of genes in shaping cravings and pleasure  <b>seeking</b>, opened the <strong>doors</strong> to comprehension of how genetics control our actions and effect our mental and physical health.
+TBC1D24	drug	alcohol	28055143	No Wrong <strong>Doors</strong>: Findings from a Critical Review of Behavioral Randomized Clinical Trials for Individuals with Co Occurring <b>Alcohol</b>/Drug Problems and Posttraumatic Stress Disorder.
+TBC1D24	drug	opioid	19801178	Recent legislation permits the treatment of <b>opioid</b> dependent patients with <b>buprenorphine</b> in the primary care setting, opening <strong>doors</strong> for the development of new treatment models for <b>opioid</b> dependence.
+TBC1D24	addiction	dependence	19801178	Recent legislation permits the treatment of opioid dependent patients with buprenorphine in the primary care setting, opening <strong>doors</strong> for the development of new treatment models for opioid <b>dependence</b>.
+TBC1D24	drug	opioid	16018736	Endogenous <b>morphine</b>: opening new <strong>doors</strong> for the treatment of pain and addiction.
+TBC1D24	addiction	addiction	16018736	Endogenous morphine: opening new <strong>doors</strong> for the treatment of pain and <b>addiction</b>.
+TBC1D24	drug	cannabinoid	15792943	Furthermore, the role of <b>cannabinoid</b> CB1 receptor activation for milk suckling in newborns may open new <strong>doors</strong> toward understanding nonorganic failure to thrive in infants, who display growth failure without known organic cause.
+TBC1D24	drug	nicotine	10911934	The global opportunities to serve public health via medication development are growing even more rapidly as country after country recognizes the impending economic and health care problems posed by <b>tobacco</b> dependence and are opening their <strong>doors</strong> to treatment.
+TBC1D24	addiction	dependence	10911934	The global opportunities to serve public health via medication development are growing even more rapidly as country after country recognizes the impending economic and health care problems posed by tobacco <b>dependence</b> and are opening their <strong>doors</strong> to treatment.
+SPINK5	drug	alcohol	31433552	Perineuronal <strong>nets</strong> in the insula regulate aversion resistant <b>alcohol</b> drinking.
+SPINK5	addiction	aversion	31433552	Perineuronal <strong>nets</strong> in the insula regulate <b>aversion</b> resistant alcohol drinking.
+SPINK5	drug	cocaine	30867569	Break the net, break the cycle: removal of perineuronal <strong>nets</strong> in the lateral hypothalamus decreases <b>cocaine</b> relapse.
+SPINK5	addiction	relapse	30867569	Break the net, break the cycle: removal of perineuronal <strong>nets</strong> in the lateral hypothalamus decreases cocaine <b>relapse</b>.
+SPINK5	drug	cocaine	30294670	<b>Cocaine</b> Exposure Modulates Perineuronal <strong>Nets</strong> and Synaptic Excitability of Fast Spiking Interneurons in the Medial Prefrontal Cortex.
+SPINK5	drug	cocaine	30294670	We previously reported that perineuronal <strong>nets</strong> (PNNs) are required for <b>cocaine</b> associated memories.
+SPINK5	drug	cocaine	30258113	Perineuronal <strong>nets</strong> in the lateral hypothalamus area regulate cue induced reinstatement of <b>cocaine</b> seeking behavior.
+SPINK5	addiction	relapse	30258113	Perineuronal <strong>nets</strong> in the lateral hypothalamus area regulate cue induced <b>reinstatement</b> of cocaine <b>seeking</b> behavior.
+SPINK5	addiction	intoxication	30030149	Herein, we studied NET formation and the process of neutrophil cell death (NETosis), as well as the clearance of <strong>NETs</strong> by macrophages (MΦ) (efferocytosis) in acute sepsis following <b>binge</b> drinking.
+SPINK5	drug	alcohol	30030149	Inducers of <strong>NETs</strong> (endotoxin and bacterial DNA) significantly increased in the circulation after binge <b>alcohol</b> drinking in humans.
+SPINK5	addiction	intoxication	30030149	Inducers of <strong>NETs</strong> (endotoxin and bacterial DNA) significantly increased in the circulation after <b>binge</b> alcohol drinking in humans.
+SPINK5	drug	alcohol	30030149	However, in the efferocytosis phase (15 h after LPS) citrullinated histone H3 was increased in the liver in <b>alcohol</b> binge mice, suggesting decreased clearance of <strong>NETs</strong>.
+SPINK5	addiction	intoxication	30030149	However, in the efferocytosis phase (15 h after LPS) citrullinated histone H3 was increased in the liver in alcohol <b>binge</b> mice, suggesting decreased clearance of <strong>NETs</strong>.
+SPINK5	addiction	addiction	29289347	Releasing <b>Addiction</b> Memories Trapped in Perineuronal <strong>Nets</strong>.
+SPINK5	addiction	addiction	29289347	Recently, perineuronal <strong>nets</strong> (PNNs), extracellular matrix (ECM) structures surrounding neurons, have emerged as regulators of learning, memory, and <b>addiction</b> behaviors.
+SPINK5	drug	cannabinoid	29031852	Interestingly, we did not observe an alteration of perineuronal <strong>nets</strong> of extracellular matrix, but a reinstatement of the capability to evoke long term depression at inhibitory synapses (iLTD), which depended on presynaptic <b>endocannabinoid</b> receptors and was a sign of the rejuvenated GABAergic synapses.
+SPINK5	addiction	relapse	29031852	Interestingly, we did not observe an alteration of perineuronal <strong>nets</strong> of extracellular matrix, but a <b>reinstatement</b> of the capability to evoke long term depression at inhibitory synapses (iLTD), which depended on presynaptic endocannabinoid receptors and was a sign of the rejuvenated GABAergic synapses.
+SPINK5	drug	cocaine	28322980	Role of perineuronal <strong>nets</strong> in the anterior dorsal lateral hypothalamic area in the acquisition of <b>cocaine</b> induced conditioned place preference and self administration.
+SPINK5	drug	nicotine	27312847	We report that <b>nicotine</b> induces neutrophils to release <strong>NETs</strong> in a dose dependent manner.
+SPINK5	drug	nicotine	27312847	These findings demonstrate that <b>nicotine</b> induces <strong>NETs</strong>, which may in turn contribute to <b>smoking</b> related diseases.
+SPINK5	drug	nicotine	27549591	<b>Nicotine</b> self administration remodels perineuronal <strong>nets</strong> in ventral tegmental area and orbitofrontal cortex in adult male rats.
+SPINK5	addiction	intoxication	26332441	Repeated <b>Binge</b> Drinking Increases Perineuronal <strong>Nets</strong> in the Insular Cortex.
+SPINK5	drug	cocaine	25762666	Removal of perineuronal <strong>nets</strong> in the medial prefrontal cortex impairs the acquisition and reconsolidation of a <b>cocaine</b> induced conditioned place preference memory.
+SPINK5	drug	cocaine	25619460	In the present study, we investigated the effects of a chronic <b>cocaine</b> treatment on molecular and structural plasticity in the cerebellum, including BDNF, D3 dopamine receptors, ΔFosB, the Glu2 AMPA receptor subunit, structural modifications in Purkinje neurons and, finally, the evaluation of perineuronal <strong>nets</strong> (PNNs) in the projection neurons of the medial nucleus, the output of the cerebellar vermis.
+SPINK5	drug	nicotine	22579738	Many of the differences between carcinoids and high grade lung <strong>NETs</strong> can be ascribed to <b>tobacco</b> consumption, which is strongly linked to the occurrence of high grade NE carcinomas.
+SPINK5	drug	cocaine	10411589	There were small but significant differences between the rat NET and the human or bovine <strong>NETs</strong> with respect to the affinities of sodium ions (greater for rat than for bovine) of the substrates norepinephrine, epinephrine, and 1 methyl 4 phenylpyridinium (greater for human than for rat), and of the inhibitor <b>cocaine</b> (greater for human and bovine than for rat), whereas the affinities of dopamine and of most inhibitors, including tricyclic antidepressants, showed no species differences.
+SPINK5	drug	cocaine	10411589	The fact that the affinities for some substrates, <b>cocaine</b> and sodium ions exhibited small but significant interspecies differences among the rat, human, and bovine <strong>NETs</strong> suggests that ligand recognition, the translocation process, and sodium ion dependence are influenced differentially by just a few amino acid exchanges in the primary sequences of the transporters.
+SPINK5	addiction	dependence	10411589	The fact that the affinities for some substrates, cocaine and sodium ions exhibited small but significant interspecies differences among the rat, human, and bovine <strong>NETs</strong> suggests that ligand recognition, the translocation process, and sodium ion <b>dependence</b> are influenced differentially by just a few amino acid exchanges in the primary sequences of the transporters.
+RAF1	drug	opioid	32690613	Depolarization dependent <strong>C Raf</strong> signaling promotes hyperexcitability and reduces <b>opioid</b> sensitivity of isolated nociceptors after spinal cord injury.
+RAF1	drug	opioid	32690613	Expression of an activated <strong>C Raf</strong> reduces sensitivity of adenylyl cyclase to <b>opioids</b> in non excitable HEK293 cells, while inhibition of <strong>C Raf</strong> or treatment with the hyperpolarizing drug retigabine restores <b>opioid</b> responsiveness and blocks spontaneous activity of nociceptors after SCI.
+RAF1	drug	opioid	32690613	Inhibition of ERK downstream of <strong>C Raf</strong> also blocks SCI induced hyperexcitability and depolarization, without direct effects on <b>opioid</b> responsiveness.
+RAF1	drug	opioid	32690613	Thus, depolarization dependent <strong>C Raf</strong> and downstream ERK activity maintain a depolarized resting membrane potential and nociceptor hyperactivity after SCI, providing a self reinforcing mechanism to persistently promote nociceptor hyperexcitability and limit the therapeutic effectiveness of <b>opioids</b>.Significance StatementChronic pain induced by spinal cord injury (SCI) is often permanent and debilitating, and usually refractory to treatment with analgesics, including <b>opioids</b>.
+RAF1	addiction	reward	32690613	Thus, depolarization dependent <strong>C Raf</strong> and downstream ERK activity maintain a depolarized resting membrane potential and nociceptor hyperactivity after SCI, providing a self <b>reinforcing</b> mechanism to persistently promote nociceptor hyperexcitability and limit the therapeutic effectiveness of opioids.Significance StatementChronic pain induced by spinal cord injury (SCI) is often permanent and debilitating, and usually refractory to treatment with analgesics, including opioids.
+RAF1	drug	opioid	32690613	This study shows that SCI and one consequence of SCI    chronic depolarization of resting membrane potential    decrease sensitivity to <b>opioid</b> mediated inhibition of cAMP and promote hyperactivity of nociceptors by enhancing <strong>C Raf</strong> activity.
+RAF1	drug	nicotine	27228072	Treatment of cells with <b>nicotine</b> induced the mRNA and protein levels of α7 nAChR; this could be abrogated by treatment with inhibitors targeting Src, PI3K, MEK, α7 nAChR, CDK4/6 or a disruptor of the Rb <strong>Raf 1</strong> interaction.
+RAF1	drug	opioid	24824948	Moreover, NaHS pre treatment suppressed <b>naloxone</b> stimulated activation of protein kinase C (PKC) α, <strong>Raf 1</strong>, and extracellular signal regulated kinase (ERK) 1/2 in rat spinal cord.
+RAF1	drug	opioid	24824948	Our data suggest that H2S prevents the development of <b>opioid</b> withdrawal induced hyperalgesia via suppression of synthesis of CGRP in spine through inhibition of AC/cAMP and PKC/<strong>Raf 1</strong>/ERK pathways.
+RAF1	addiction	withdrawal	24824948	Our data suggest that H2S prevents the development of opioid <b>withdrawal</b> induced hyperalgesia via suppression of synthesis of CGRP in spine through inhibition of AC/cAMP and PKC/<strong>Raf 1</strong>/ERK pathways.
+RAF1	drug	alcohol	22859298	<strong>Raf 1</strong> kinase inhibitory protein (RKIP) mediates <b>ethanol</b> induced sensitization of secretagogue signaling in pancreatic acinar cells.
+RAF1	addiction	sensitization	22859298	<strong>Raf 1</strong> kinase inhibitory protein (RKIP) mediates ethanol induced <b>sensitization</b> of secretagogue signaling in pancreatic acinar cells.
+RAF1	drug	alcohol	22859298	In this study we identify <strong>Raf 1</strong> kinase inhibitory protein as an essential mediator of <b>ethanol</b> induced sensitization of cholecystokinin  and carbachol regulated Ca(2+) signaling in pancreatic acinar cells.
+RAF1	addiction	sensitization	22859298	In this study we identify <strong>Raf 1</strong> kinase inhibitory protein as an essential mediator of ethanol induced <b>sensitization</b> of cholecystokinin  and carbachol regulated Ca(2+) signaling in pancreatic acinar cells.
+RAF1	drug	alcohol	22859298	We show that exposure of rodent acinar cells to <b>ethanol</b> induces protein kinase C dependent <strong>Raf 1</strong> kinase inhibitory protein phosphorylation, sensitization of cholecystokinin stimulated Ca(2+) signaling, and potentiation of both basal and cholecystokinin stimulated extracellular signal regulated kinase activation.
+RAF1	addiction	sensitization	22859298	We show that exposure of rodent acinar cells to ethanol induces protein kinase C dependent <strong>Raf 1</strong> kinase inhibitory protein phosphorylation, <b>sensitization</b> of cholecystokinin stimulated Ca(2+) signaling, and potentiation of both basal and cholecystokinin stimulated extracellular signal regulated kinase activation.
+RAF1	drug	alcohol	22859298	Furthermore, we show that either suppression of <strong>Raf 1</strong> kinase inhibitory protein expression using short hairpin RNA or gene ablation prevented the sensitizing effects of <b>ethanol</b> on cholecystokinin  and carbachol stimulated Ca(2+) signaling and intracellular chymotrypsin activation in pancreatic acinar cells, suggesting that the modulation of <strong>Raf 1</strong> inhibitory protein expression may have future therapeutic utility in the prevention or treatment of <b>alcohol</b> associated pancreatitis.
+RAF1	drug	nicotine	22240023	Inhibiting E2F1 activity using RRD 251, a disruptor of the Rb <strong>Raf 1</strong> kinase interaction, could significantly inhibit the <b>nicotine</b> induced recruitment of E2F1 to the E selectin promoter as well as E selectin expression.
+RAF1	drug	opioid	20718739	Sustained <b>morphine</b> mediated pain sensitization and antinociceptive tolerance are blocked by intrathecal treatment with <strong>Raf 1</strong> selective siRNA.
+RAF1	addiction	sensitization	20718739	Sustained morphine mediated pain <b>sensitization</b> and antinociceptive tolerance are blocked by intrathecal treatment with <strong>Raf 1</strong> selective siRNA.
+RAF1	drug	opioid	20718739	Previous in vitro studies from our group indicated that <strong>Raf 1</strong> kinase mediated adenylyl cyclase superactivation played a crucial role in sustained <b>morphine</b> mediated augmentation of basal and evoked CGRP release from cultured primary sensory neurons.
+RAF1	drug	opioid	20718739	Rats were intrathecally (i.th) injected with a <strong>Raf 1</strong> selective small interfering RNA (siRNA) mixture for 3 days and were subsequently infused with saline or <b>morphine</b>, s.c. for 7 days.
+RAF1	drug	opioid	20718739	Selective knockdown of spinal <strong>Raf 1</strong> protein levels by i.th <strong>Raf 1</strong> selective siRNA pretreatment significantly attenuated sustained <b>morphine</b> mediated up regulation of CGRP immunoreactivity in the spinal cord of rats and prevented the development of thermal hyperalgesia, mechanical allodynia and antinociceptive tolerance.
+RAF1	drug	opioid	20718739	<strong>Raf 1</strong> played a significant role in sustained <b>morphine</b> mediated paradoxical pain sensitization and antinociceptive tolerance in vivo.
+RAF1	addiction	sensitization	20718739	<strong>Raf 1</strong> played a significant role in sustained morphine mediated paradoxical pain <b>sensitization</b> and antinociceptive tolerance in vivo.
+RAF1	addiction	sensitization	20613834	This action occurs through miR 212 enhanced <strong>Raf1</strong> activity, resulting in adenylyl cyclase <b>sensitization</b> and increased expression of the essential CREB co activator TORC (transducer of regulated CREB; also known as CRTC).
+RAF1	addiction	sensitization	20613834	This action occurs through miR 212 enhanced <strong><strong>Raf1</strong></strong> activity, resulting in adenylyl cyclase <b>sensitization</b> and increased expression of the essential CREB co activator TORC (transducer of regulated CREB; also known as CRTC).
+RAF1	drug	opioid	19491327	Sustained <b>morphine</b> treatment augments capsaicin evoked calcitonin gene related peptide release from primary sensory neurons in a protein kinase A  and <strong>Raf 1</strong> dependent manner.
+RAF1	drug	opioid	19491327	In the present study, we demonstrate that sustained <b>morphine</b> mediated augmentation of CGRP release from isolated primary sensory dorsal root ganglion neurons is dependent on protein kinase A and <strong>Raf 1</strong> kinase.
+RAF1	drug	opioid	18976650	Intrathecal <strong>Raf 1</strong> selective siRNA attenuates sustained <b>morphine</b> mediated thermal hyperalgesia.
+RAF1	drug	opioid	18976650	Recently we have demonstrated that inhibition of <strong>Raf 1</strong> attenuates sustained <b>morphine</b> treatment mediated augmentation of CGRP release in vitro, in cultured primary sensory neurons.
+RAF1	drug	opioid	18976650	In the present study, we show that knockdown of spinal <strong>Raf 1</strong> levels in vivo by intrathecal administration of <strong>Raf 1</strong> specific siRNA attenuates sustained <b>morphine</b> mediated thermal hyperalgesia in rats.
+RAF1	drug	opioid	18328477	Sustained <b>morphine</b> treatment augments basal CGRP release from cultured primary sensory neurons in a <strong>Raf 1</strong> dependent manner.
+RAF1	drug	opioid	18328477	Moreover, we have shown earlier that sustained <b>opioid</b> agonist treatment leads to a <strong>Raf 1</strong> dependent sensitization of adenylyl cyclase(s) (AC superactivation), augmenting forskolin stimulated cAMP formation upon <b>opioid</b> withdrawal (cAMP overshoot).
+RAF1	addiction	sensitization	18328477	Moreover, we have shown earlier that sustained opioid agonist treatment leads to a <strong>Raf 1</strong> dependent <b>sensitization</b> of adenylyl cyclase(s) (AC superactivation), augmenting forskolin stimulated cAMP formation upon opioid withdrawal (cAMP overshoot).
+RAF1	addiction	withdrawal	18328477	Moreover, we have shown earlier that sustained opioid agonist treatment leads to a <strong>Raf 1</strong> dependent sensitization of adenylyl cyclase(s) (AC superactivation), augmenting forskolin stimulated cAMP formation upon opioid <b>withdrawal</b> (cAMP overshoot).
+RAF1	drug	opioid	18328477	Therefore, in the present study we examined the role of <strong>Raf 1</strong> in sustained <b>morphine</b> mediated regulation of cAMP formation and basal CGRP release in vitro, in cultured neonatal rat dorsal root ganglion (DRG) neurons.
+RAF1	drug	opioid	18328477	Since our present data also demonstrated that selective <strong>Raf 1</strong> inhibitor, GW 5074, attenuated both the cAMP overshoot and the augmentation of CGRP release mediated by sustained <b>morphine</b> in neonatal rat DRG neurons, we suggest that <strong>Raf 1</strong> mediated sensitization of the intracellular cAMP formation may play an important role in sustained <b>morphine</b> mediated augmentation of spinal pain neurotransmitter release.
+RAF1	addiction	sensitization	18328477	Since our present data also demonstrated that selective <strong>Raf 1</strong> inhibitor, GW 5074, attenuated both the cAMP overshoot and the augmentation of CGRP release mediated by sustained morphine in neonatal rat DRG neurons, we suggest that <strong>Raf 1</strong> mediated <b>sensitization</b> of the intracellular cAMP formation may play an important role in sustained morphine mediated augmentation of spinal pain neurotransmitter release.
+RAF1	drug	cannabinoid	17139682	Treatment with SR141716A after chronic WIN55212 2 resulted in the expected <b>cannabinoid</b> withdrawal syndrome, without concomitant alterations in the phosphorylation state of <strong>c Raf</strong> 1, MEK1/2, or ERK1/2.
+RAF1	addiction	withdrawal	17139682	Treatment with SR141716A after chronic WIN55212 2 resulted in the expected cannabinoid <b>withdrawal</b> syndrome, without concomitant alterations in the phosphorylation state of <strong>c Raf</strong> 1, MEK1/2, or ERK1/2.
+RAF1	addiction	sensitization	15683739	Inhibition of <strong>Raf1</strong> modestly inhibited the magnitude of D2L receptor induced <b>sensitization</b> of AC6; however, activation of PKC robustly enhanced D2L receptor mediated AC6 <b>sensitization</b> in a <strong>Raf1</strong> dependent manner.
+RAF1	addiction	sensitization	15683739	Inhibition of <strong><strong>Raf1</strong></strong> modestly inhibited the magnitude of D2L receptor induced <b>sensitization</b> of AC6; however, activation of PKC robustly enhanced D2L receptor mediated AC6 <b>sensitization</b> in a <strong><strong>Raf1</strong></strong> dependent manner.
+RAF1	addiction	sensitization	15683739	These data indicate that, although PKC and <strong>Raf1</strong> are not required for <b>sensitization</b>, activation of the PKC <strong>Raf1</strong> pathway robustly potentiated D2L receptor mediated <b>sensitization</b> of AC6.
+RAF1	addiction	sensitization	15683739	These data indicate that, although PKC and <strong><strong>Raf1</strong></strong> are not required for <b>sensitization</b>, activation of the PKC <strong><strong>Raf1</strong></strong> pathway robustly potentiated D2L receptor mediated <b>sensitization</b> of AC6.
+RAF1	addiction	withdrawal	14607258	<strong>Raf 1</strong> in turn phosphorylates and sensitizes the native adenylyl cyclase VI isoenzyme in hDOR/CHO cells, causing a rebound increase in forskolin stimulated cAMP formation upon agonist <b>withdrawal</b>.
+RAF1	addiction	dependence	8626548	The interaction of RafC with PA displayed a pH <b>dependence</b> distinct from the interaction between the cysteine rich domain of <strong>Raf 1</strong> and PA. Also, the RafC PA interaction was unaffected at high ionic strength.
+RAF1	drug	alcohol	8626548	RafC did not bind phosphatidyl alcohols; also, inhibition of PA formation in Madin Darby canine kidney cells by treatment with 1% <b>ethanol</b> significantly reduced the translocation of <strong>Raf 1</strong> from the cytosol to the membrane following stimulation with 12 O tetradecanoylphorbol 13 acetate.
+PDE4A	drug	cocaine	30831136	These results indicate that GXE enhances sensitivity to repeated <b>cocaine</b> exposure via an increase in <strong>PDE4</strong> activity in NAc D2 recptor expressing neurons, leading to the development of <b>cocaine</b> addictive behaviors.
+PDE4A	addiction	addiction	30831136	These results indicate that GXE enhances sensitivity to repeated cocaine exposure via an increase in <strong>PDE4</strong> activity in NAc D2 recptor expressing neurons, leading to the development of cocaine <b>addictive</b> behaviors.
+PDE4A	addiction	addiction	28974957	Here, we review the current knowledge about central nervous system (CNS) distribution of <strong>PDE4</strong> isoforms and the effects of systemic and brain region specific inhibition of <strong>PDE4</strong> on behavioral models of drug <b>addiction</b>.
+PDE4A	drug	alcohol	28974957	Using behavioral sensitization, conditioned place preference and drug self administration as behavioral models, a large number of studies have shown that local or systemic administration of <strong>PDE4</strong> inhibitors reduce drug intake and/or drug seeking for psychostimulants, <b>alcohol</b>, and opioids in rats or mice.
+PDE4A	drug	opioid	28974957	Using behavioral sensitization, conditioned place preference and drug self administration as behavioral models, a large number of studies have shown that local or systemic administration of <strong>PDE4</strong> inhibitors reduce drug intake and/or drug seeking for psychostimulants, alcohol, and <b>opioids</b> in rats or mice.
+PDE4A	addiction	relapse	28974957	Using behavioral sensitization, conditioned place preference and drug self administration as behavioral models, a large number of studies have shown that local or systemic administration of <strong>PDE4</strong> inhibitors reduce drug intake and/or drug <b>seeking</b> for psychostimulants, alcohol, and opioids in rats or mice.
+PDE4A	addiction	sensitization	28974957	Using behavioral <b>sensitization</b>, conditioned place preference and drug self administration as behavioral models, a large number of studies have shown that local or systemic administration of <strong>PDE4</strong> inhibitors reduce drug intake and/or drug seeking for psychostimulants, alcohol, and opioids in rats or mice.
+PDE4A	addiction	addiction	28974957	We conclude by identifying opportunities for the development of subtype selective <strong>PDE4</strong> inhibitors that may reduce <b>addiction</b> liability and minimize the side effects that limit the clinical potential of non selective <strong>PDE4</strong> inhibitors.
+PDE4A	addiction	addiction	28974957	There is a promising possibility to repurpose these <strong>PDE4</strong> inhibitors for the treatment of drug <b>addiction</b> as they are safe and well tolerated in patients.
+PDE4A	drug	alcohol	28748375	Our previous results have shown that inhibition of phosphodiesterase 4 (<strong>PDE4</strong>) decreased <b>ethanol</b> seeking and drinking in <b>alcohol</b> preferring rodents.
+PDE4A	addiction	relapse	28748375	Our previous results have shown that inhibition of phosphodiesterase 4 (<strong>PDE4</strong>) decreased ethanol <b>seeking</b> and drinking in alcohol preferring rodents.
+PDE4A	drug	alcohol	28748375	However, little is known about whether <strong>PDE4</strong> is involved in <b>ethanol</b> abstinence related behavior.
+PDE4A	drug	alcohol	28748375	The objective of this study was to characterize the role of <strong>PDE4</strong> in the development of anxiety  and depressive like behavior induced by abstinence from <b>ethanol</b> exposure in different animal models.
+PDE4A	drug	alcohol	28748375	Using three rodent models of <b>ethanol</b> abstinence, we examined the effects of rolipram, a prototypical, selective <strong>PDE4</strong> inhibitor, on (1) anxiety like behavior induced by repeated <b>ethanol</b> abstinence in the elevated plus maze test in fawn hooded (FH/Wjd) rats, (2) anxiety like behavior in the open field test and light dark transition test following acute <b>ethanol</b> abstinence in C57BL/6J mice, and (3) anxiety  and depressive like behavior induced by protracted <b>ethanol</b> abstinence in the elevated plus maze, forced swim, and tail suspension tests in C57BL/6J mice.
+PDE4A	drug	alcohol	28748375	These results provide the first demonstration for that <strong>PDE4</strong> plays a role in modulating the development of negative emotional reactions associated with <b>ethanol</b> abstinence, including anxiety and depression.
+PDE4A	drug	alcohol	28748375	<strong>PDE4</strong> inhibitors may be a novel class of drugs for treatment of <b>alcoholism</b>.
+PDE4A	drug	psychedelics	28558784	<strong>PDE4</strong> inhibitors were reported to reverse xylazine/<b>ketamine</b> induced anesthesia in rats and triggered vomiting in ferrets.
+PDE4A	drug	cocaine	28497801	<strong>PDE4</strong> Inhibition Restores the Balance Between Excitation and Inhibition in VTA Dopamine Neurons Disrupted by Repeated In Vivo <b>Cocaine</b> Exposure.
+PDE4A	drug	cocaine	28497801	<strong>PDE4</strong> inhibitors have been shown to regulate the rewarding and reinforcing effects of <b>cocaine</b>, but the underlying mechanisms remain poorly understood.
+PDE4A	addiction	reward	28497801	<strong>PDE4</strong> inhibitors have been shown to regulate the rewarding and <b>reinforcing</b> effects of cocaine, but the underlying mechanisms remain poorly understood.
+PDE4A	drug	cocaine	28497801	Here we show that pretreatments with the <strong>PDE4</strong> inhibitor rolipram attenuated <b>cocaine</b> induced locomotor sensitization in mice.
+PDE4A	addiction	sensitization	28497801	Here we show that pretreatments with the <strong>PDE4</strong> inhibitor rolipram attenuated cocaine induced locomotor <b>sensitization</b> in mice.
+PDE4A	drug	cocaine	28497801	These results suggest that repeated <b>cocaine</b> exposure in vivo disrupts the balance between excitation and inhibition in VTA dopamine neurons, while <strong>PDE4</strong> inhibition reestablishes the balance between excitation and inhibition through distinct mechanisms.
+PDE4A	drug	alcohol	28477089	Phosphodiesterase 4 (<strong>PDE4</strong>), an enzyme that specifically hydrolyzes intracellular cyclic AMP (cAMP), has been involved in <b>alcohol</b> use disorders.
+PDE4A	addiction	aversion	28477089	Intake of sucrose or quinine was also tested to determine whether natural reward preference and <b>aversive</b> stimuli were involved in the effect of <strong>PDE4</strong> inhibitors.
+PDE4A	addiction	reward	28477089	Intake of sucrose or quinine was also tested to determine whether natural <b>reward</b> preference and aversive stimuli were involved in the effect of <strong>PDE4</strong> inhibitors.
+PDE4A	drug	opioid	25744400	Therefore, we examined the effects of caffeine, a methylxanthine non selective phosphodiesterase (PDE) inhibitor with adenosine antagonistic activity, and rolipram, a racetam selective <strong>PDE4</strong> inhibitor, on ventilatory depression induced by <b>morphine</b>.
+PDE4A	drug	opioid	25744400	Inhibition of <strong>PDE4</strong> may be a possible approach for overcoming <b>morphine</b> induced ventilatory depression without loss of analgesia.
+PDE4A	drug	alcohol	24904269	Rolipram, an inhibitor of <strong>PDE4</strong>, markedly reduced <b>ethanol</b> intake and preference in mice and reduced <b>ethanol</b> seeking and consumption in <b>alcohol</b> preferring fawn hooded rats (Hu et al., 2011; Wen et al., 2012).
+PDE4A	addiction	relapse	24904269	Rolipram, an inhibitor of <strong>PDE4</strong>, markedly reduced ethanol intake and preference in mice and reduced ethanol <b>seeking</b> and consumption in alcohol preferring fawn hooded rats (Hu et al., 2011; Wen et al., 2012).
+PDE4A	drug	alcohol	24904269	Only the selective <strong>PDE4</strong> inhibitors reduced <b>ethanol</b> intake and preference in the 24 h two bottle choice test.
+PDE4A	drug	alcohol	24904269	Our results provide novel evidence for a selective role of <strong>PDE4</strong> in regulating <b>ethanol</b> drinking in mice.
+PDE4A	drug	alcohol	24904269	We suggest that inhibition of <strong>PDE4</strong> may be an unexplored target for medication development to reduce excessive <b>alcohol</b> consumption.
+PDE4A	drug	opioid	24832929	However, it is not known whether <strong>PDE4</strong> is involved in <b>heroin</b> seeking.
+PDE4A	addiction	relapse	24832929	However, it is not known whether <strong>PDE4</strong> is involved in heroin <b>seeking</b>.
+PDE4A	drug	opioid	24832929	with rolipram (0.03 0.3 mg/kg), a prototypical, selective <strong>PDE4</strong> inhibitor, failed to inhibit <b>heroin</b> self administration under the FR1 schedule, but decreased the reward values under the progressive ratio schedule in a dose dependent manner.
+PDE4A	addiction	reward	24832929	with rolipram (0.03 0.3 mg/kg), a prototypical, selective <strong>PDE4</strong> inhibitor, failed to inhibit heroin self administration under the FR1 schedule, but decreased the <b>reward</b> values under the progressive ratio schedule in a dose dependent manner.
+PDE4A	drug	opioid	24832929	The results suggest that <strong>PDE4</strong> plays an essential role in mediating <b>heroin</b> seeking and that <strong>PDE4</strong> inhibitors may be used as a potential pharmacotherapeutic approach for <b>heroin</b> addiction.
+PDE4A	addiction	addiction	24832929	The results suggest that <strong>PDE4</strong> plays an essential role in mediating heroin seeking and that <strong>PDE4</strong> inhibitors may be used as a potential pharmacotherapeutic approach for heroin <b>addiction</b>.
+PDE4A	addiction	relapse	24832929	The results suggest that <strong>PDE4</strong> plays an essential role in mediating heroin <b>seeking</b> and that <strong>PDE4</strong> inhibitors may be used as a potential pharmacotherapeutic approach for heroin addiction.
+PDE4A	drug	cannabinoid	22713909	Here, we report that selective <strong>PDE4</strong> inhibitors rolipram and Ro 20 1724 blocked I LTD and acute depression of inhibitory postsynaptic currents (IPSCs) induced by D₂ dopamine receptor and <b>cannabinoid</b> CB₁ receptor agonists in VTA dopamine neurons.
+PDE4A	drug	cocaine	22713909	We also show that intra VTA microinjections of <strong>PDE4</strong> inhibitor rolipram impaired the acquisition, but not the expression, of conditioned place preference (CPP) to <b>cocaine</b>.
+PDE4A	addiction	reward	22713909	We also show that intra VTA microinjections of <strong>PDE4</strong> inhibitor rolipram impaired the acquisition, but not the expression, of conditioned place preference (<b>CPP</b>) to cocaine.
+PDE4A	drug	cocaine	22713909	Together, our results suggest that blockade of <b>cocaine</b> induced inhibitory synaptic plasticity (I LTD) and enhancement of CREB activation are two putative cellular mechanisms by which <strong>PDE4</strong> inhibition impairs the acquisition of <b>cocaine</b> CPP.
+PDE4A	addiction	reward	22713909	Together, our results suggest that blockade of cocaine induced inhibitory synaptic plasticity (I LTD) and enhancement of CREB activation are two putative cellular mechanisms by which <strong>PDE4</strong> inhibition impairs the acquisition of cocaine <b>CPP</b>.
+PDE4A	drug	alcohol	22671516	The phosphodiesterase 4 (<strong>PDE4</strong>) inhibitor rolipram decreases <b>ethanol</b> seeking and consumption in <b>alcohol</b> preferring Fawn Hooded rats.
+PDE4A	addiction	relapse	22671516	The phosphodiesterase 4 (<strong>PDE4</strong>) inhibitor rolipram decreases ethanol <b>seeking</b> and consumption in alcohol preferring Fawn Hooded rats.
+PDE4A	drug	alcohol	22671516	Thus, it was of interest to determine whether <strong>PDE4</strong> was involved in the regulation of <b>alcohol</b> use and abuse.
+PDE4A	drug	alcohol	22671516	Male Fawn Hooded (FH/Wjd) rats were tested for 5% (v/v) <b>ethanol</b> (EtOH) and 10% (w/v) sucrose operant oral self administration following treatment with the selective <strong>PDE4</strong> inhibitor rolipram (0.0125, 0.025, or 0.05 mg/kg, subcutaneous [s.c.]); rolipram at higher doses (0.05, 0.1, and 0.2 mg/kg, s.c.) was tested to determine its impact on the intake of EtOH, sucrose, or water using the 2 bottle choice drinking paradigm.
+PDE4A	addiction	reward	22671516	Male Fawn Hooded (FH/Wjd) rats were tested for 5% (v/v) ethanol (EtOH) and 10% (w/v) sucrose <b>operant</b> oral self administration following treatment with the selective <strong>PDE4</strong> inhibitor rolipram (0.0125, 0.025, or 0.05 mg/kg, subcutaneous [s.c.]); rolipram at higher doses (0.05, 0.1, and 0.2 mg/kg, s.c.) was tested to determine its impact on the intake of EtOH, sucrose, or water using the 2 bottle choice drinking paradigm.
+PDE4A	drug	alcohol	22671516	These results suggest that <strong>PDE4</strong> plays a role in <b>alcohol</b> seeking and consumption behavior.
+PDE4A	addiction	relapse	22671516	These results suggest that <strong>PDE4</strong> plays a role in alcohol <b>seeking</b> and consumption behavior.
+PDE4A	drug	alcohol	22671516	Drugs interfering with <strong>PDE4</strong> may be a potential pharmacotherapy for <b>alcohol</b> dependence.
+PDE4A	addiction	dependence	22671516	Drugs interfering with <strong>PDE4</strong> may be a potential pharmacotherapy for alcohol <b>dependence</b>.
+PDE4A	drug	alcohol	21509503	However, the role of <strong>PDE4</strong> in <b>ethanol</b> consumption remains unknown.
+PDE4A	drug	alcohol	21509503	The objective of this study is to examine whether <strong>PDE4</strong> was involved in regulating <b>ethanol</b> intake.
+PDE4A	drug	alcohol	21509503	The two bottle choice paradigm was used to assess intake of <b>ethanol</b>, sucrose, and quinine in C57BL/6J mice treated with the selective <strong>PDE4</strong> inhibitor rolipram or Ro 20 1724; locomotor activity was also monitored using the open field test in mice treated with rolipram.
+PDE4A	drug	alcohol	21509503	These results suggest that <strong>PDE4</strong> is a novel target for drugs that reduce <b>ethanol</b> intake; <strong>PDE4</strong> inhibitors may be used for treatment of <b>alcohol</b> dependence.
+PDE4A	addiction	dependence	21509503	These results suggest that <strong>PDE4</strong> is a novel target for drugs that reduce ethanol intake; <strong>PDE4</strong> inhibitors may be used for treatment of alcohol <b>dependence</b>.
+PDE4A	drug	cocaine	19588125	Whether <strong>PDE4</strong> disruption attenuates induction of behavioral sensitization to <b>cocaine</b> and subsequent NAc expression of phosphorylated extracellular signal regulated kinase (ERK), which is involved in <b>cocaine</b> induced sensitization, is unknown.
+PDE4A	addiction	sensitization	19588125	Whether <strong>PDE4</strong> disruption attenuates induction of behavioral <b>sensitization</b> to cocaine and subsequent NAc expression of phosphorylated extracellular signal regulated kinase (ERK), which is involved in cocaine induced <b>sensitization</b>, is unknown.
+PDE4A	drug	cocaine	19588125	Mice were administered the <strong>PDE4</strong> inhibitor, rolipram, or vehicle before or after five daily injections of <b>cocaine</b> or saline, and activity was monitored on days 1 and 5.
+PDE4A	drug	cocaine	19588125	<strong>PDE4</strong> inhibition, during the induction of sensitization, reduced behavioral sensitization only if rolipram (1.0 mg/kg) was administered before <b>cocaine</b>.
+PDE4A	addiction	sensitization	19588125	<strong>PDE4</strong> inhibition, during the induction of <b>sensitization</b>, reduced behavioral <b>sensitization</b> only if rolipram (1.0 mg/kg) was administered before cocaine.
+PDE4A	drug	cocaine	19588125	Although <strong>PDE4</strong> inhibition during the induction of sensitization blocks the locomotor component of sensitization, other long term changes induced by repeated <b>cocaine</b> treatment remain.
+PDE4A	addiction	sensitization	19588125	Although <strong>PDE4</strong> inhibition during the induction of <b>sensitization</b> blocks the locomotor component of <b>sensitization</b>, other long term changes induced by repeated cocaine treatment remain.
+PDE4A	drug	nicotine	16814262	Chronic <b>nicotine</b> doses down regulate <strong>PDE4</strong> isoforms that are targets of antidepressants in adolescent female rats.
+PDE4A	drug	opioid	16753260	In the present study, to clarify the involvement of phosphodiesterase (PDE) 4, degradation enzyme of cyclic AMP in <b>morphine</b> dependence and withdrawal we investigated the activities of <strong>PDE4</strong> after <b>naloxone</b> precipitation in single <b>morphine</b> treatment and repeated <b>morphine</b> treatment (<b>morphine</b> dependence) rats.
+PDE4A	addiction	dependence	16753260	In the present study, to clarify the involvement of phosphodiesterase (PDE) 4, degradation enzyme of cyclic AMP in morphine <b>dependence</b> and withdrawal we investigated the activities of <strong>PDE4</strong> after naloxone precipitation in single morphine treatment and repeated morphine treatment (morphine <b>dependence</b>) rats.
+PDE4A	addiction	withdrawal	16753260	In the present study, to clarify the involvement of phosphodiesterase (PDE) 4, degradation enzyme of cyclic AMP in morphine dependence and <b>withdrawal</b> we investigated the activities of <strong>PDE4</strong> after naloxone precipitation in single morphine treatment and repeated morphine treatment (morphine dependence) rats.
+PDE4A	drug	opioid	16753260	<b>Naloxone</b> challenge caused an increase in <strong>PDE4</strong> activities in the brain of rats treated with single <b>morphine</b> in connection with the elevation of brain cyclic AMP.
+PDE4A	drug	opioid	16753260	In contrast, increase in the <strong>PDE4</strong> activities was not caused by <b>naloxone</b> challenge in all brain regions of <b>morphine</b> dependent rats, although brain cyclic AMP was significantly increased.
+PDE4A	drug	opioid	16753260	These results suggest that the lack of <strong>PDE4</strong> activation leading to remarkable elevation of cyclic AMP is involved in <b>naloxone</b> precipitated <b>morphine</b> withdrawal symptoms.
+PDE4A	addiction	withdrawal	16753260	These results suggest that the lack of <strong>PDE4</strong> activation leading to remarkable elevation of cyclic AMP is involved in naloxone precipitated morphine <b>withdrawal</b> symptoms.
+PDE4A	drug	cocaine	15128409	To examine the potential role of <strong>PDE4</strong> in reward mediated behaviour, we measured the effects of rolipram, a <strong>PDE4</strong> selective inhibitor, on <b>cocaine</b> (18 mg/kg i.p.)
+PDE4A	addiction	reward	15128409	To examine the potential role of <strong>PDE4</strong> in <b>reward</b> mediated behaviour, we measured the effects of rolipram, a <strong>PDE4</strong> selective inhibitor, on cocaine (18 mg/kg i.p.)
+PDE4A	addiction	reward	15128409	Thus, <strong>PDE4</strong> mediated regulation of cAMP levels could underlie the establishment of <b>reward</b> valence to abused drugs.
+PDE4A	drug	cocaine	9880581	In contrast, expression of <strong>PDE4A</strong> and PDE4B were not influenced by short term treatment (1 or 7 d) and were not influenced by chronic administration of nonantidepressant psychotropic drugs (<b>cocaine</b> or haloperidol), demonstrating the time dependence and pharmacological specificity of these effects.
+PDE4A	addiction	dependence	9880581	In contrast, expression of <strong>PDE4A</strong> and PDE4B were not influenced by short term treatment (1 or 7 d) and were not influenced by chronic administration of nonantidepressant psychotropic drugs (cocaine or haloperidol), demonstrating the time <b>dependence</b> and pharmacological specificity of these effects.
+NMU	addiction	addiction	31424512	The Researched, Abuse, Diversion and <b>Addiction</b> Related Surveillance (RADARS®) Survey of Nonmedical Use of Prescription Drugs (NMURx) was utilized to study <strong>NMU</strong> of loperamide among the adult population in the UK and US in 2017.
+NMU	drug	opioid	31424512	In the current international environment of <b>opioid</b> addiction involving both therapeutic and illicit <b>opioids</b>, awareness of the <strong>NMU</strong> of loperamide is important.
+NMU	addiction	addiction	31424512	In the current international environment of opioid <b>addiction</b> involving both therapeutic and illicit opioids, awareness of the <strong>NMU</strong> of loperamide is important.
+NMU	drug	alcohol	31193512	When individuals with <strong>NMU</strong> were compared to those without <strong>NMU</strong> (Non <strong>NMU</strong>) and those with MUO, respectively, some correlates consistently identified, including young adulthood, tobacco smoking, <b>alcohol</b> drinking, and greater AUDIT's scores for analgesics, as well as hard drug use and greater DAST's scores for sedatives/hypnotics.
+NMU	drug	nicotine	31193512	When individuals with <strong>NMU</strong> were compared to those without <strong>NMU</strong> (Non <strong>NMU</strong>) and those with MUO, respectively, some correlates consistently identified, including young adulthood, <b>tobacco</b> <b>smoking</b>, alcohol drinking, and greater AUDIT's scores for analgesics, as well as hard drug use and greater DAST's scores for sedatives/hypnotics.
+NMU	drug	benzodiazepine	31165490	There is concern in the UK about nonmedical use (<strong>NMU</strong>) of <b>alprazolam</b> (<b>Xanax</b>).
+NMU	drug	benzodiazepine	31165490	We investigated the epidemiology of <b>alprazolam</b> <strong>NMU</strong> compared with <b>diazepam</b> using data from the Survey of Non Medical Use of Prescription Drugs (NMURx) programme (collected 28 September 1 December 2017).
+NMU	drug	benzodiazepine	31165490	The estimated national prevalence of lifetime <strong>NMU</strong> of <b>alprazolam</b> was 0.32% (95% confidence interval: 0.19 0.46), and 1.30% (1.06 1.54) for <b>diazepam</b>.
+NMU	drug	benzodiazepine	31165490	The prevalence of <strong>NMU</strong> in the last 90 days was significantly different when split by age category for <b>alprazolam</b> (P < .001), but not for <b>diazepam</b> (P = .262) with <b>alprazolam</b> <strong>NMU</strong> being more common among younger adults (age 16 24 years: 0.37%; age 25 34 years: 0.14%; 35 years or older: 0.01%).
+NMU	drug	benzodiazepine	31165490	Further research is needed to fully understand the motivations of <b>alprazolam</b> <strong>NMU</strong> and to monitor whether the popularity of <b>alprazolam</b> will rise.
+NMU	drug	alcohol	31069918	Brain region specific <strong>neuromedin U</strong> signalling regulates <b>alcohol</b> related behaviours and food intake in rodents.
+NMU	drug	alcohol	31069918	Albeit neuromedin U (<strong>NMU</strong>) attenuates <b>alcohol</b> mediated behaviours, its mechanisms of action are poorly defined.
+NMU	drug	alcohol	31069918	Albeit <strong>neuromedin U</strong> (<strong>NMU</strong>) attenuates <b>alcohol</b> mediated behaviours, its mechanisms of action are poorly defined.
+NMU	drug	alcohol	31069918	Providing that the behavioural effects of <b>alcohol</b> are processed within the nucleus accumbens (NAc) shell, anterior ventral tegmental area (aVTA), and laterodorsal tegmental area (LDTg), we assessed the involvement of <strong>NMU</strong> signalling in the aforementioned areas on <b>alcohol</b> mediated behaviours in rodents.
+NMU	drug	alcohol	31069918	We further examined the expression of <strong>NMU</strong> and <strong>NMU</strong> receptor 2 (NMUR2) in NAc and the dorsal striatum of high compared with low <b>alcohol</b> consuming rats, as this area is of importance in the maintenance of <b>alcohol</b> use disorder (AUD).
+NMU	addiction	reward	31069918	Finally, we investigated the involvement of NAc shell, aVTA and LDTg in the consumption of chow and palatable peanut butter, to expand the link between <strong>NMU</strong> and <b>reward</b> related behaviours.
+NMU	drug	alcohol	31069918	We demonstrated here, that <strong>NMU</strong> into the NAc shell, but not aVTA or LDTg, blocked the ability of acute <b>alcohol</b> to cause locomotor stimulation and to induce memory retrieval of <b>alcohol</b> reward, as well as reduced peanut butter in mice.
+NMU	addiction	reward	31069918	We demonstrated here, that <strong>NMU</strong> into the NAc shell, but not aVTA or LDTg, blocked the ability of acute alcohol to cause locomotor stimulation and to induce memory retrieval of alcohol <b>reward</b>, as well as reduced peanut butter in mice.
+NMU	drug	alcohol	31069918	In addition, <strong>NMU</strong> into NAc shell decreased <b>alcohol</b> intake in rats.
+NMU	drug	alcohol	31069918	On a molecular level, we found increased <strong>NMU</strong> and decreased NMUR2 expression in the dorsal striatum in high compared with low <b>alcohol</b> consuming rats.
+NMU	drug	amphetamine	30592231	Of 198,411 respondents, 4,185 reported prescription stimulant <strong>NMU</strong>, prevalence ranged from 0.33% for methylphenidate IR to 1.61% for <b>amphetamine</b> mixed salts.
+NMU	drug	amphetamine	30592231	Prescription adjusted prevalence of <strong>NMU</strong> was highest for methylphenidate IR (0.51%) and lowest for <b>amphetamine</b> ER (0.28%).
+NMU	drug	cocaine	30483076	<b>Cocaine</b> Evoked Locomotor Activity Negatively Correlates With the Expression of <strong>Neuromedin U</strong> Receptor 2 in the Nucleus Accumbens.
+NMU	drug	cocaine	30483076	Immediately following locomotor assay, tissue was taken and we demonstrate that accumbal NMUR2 mRNA expression, but not <strong>NMU</strong> mRNA expression, is negatively correlated with non sensitized <b>cocaine</b> evoked locomotor activity, but the correlation is lost following <b>cocaine</b> sensitization.
+NMU	addiction	sensitization	30483076	Immediately following locomotor assay, tissue was taken and we demonstrate that accumbal NMUR2 mRNA expression, but not <strong>NMU</strong> mRNA expression, is negatively correlated with non sensitized cocaine evoked locomotor activity, but the correlation is lost following cocaine <b>sensitization</b>.
+NMU	drug	alcohol	30439457	The present review therefore summarizes the current studies investigating the ability of the gut brain peptides ghrelin, glucagon like peptide 1 (GLP 1), amylin and neuromedin U (<strong>NMU</strong>) to modulate <b>alcohol</b>  and drug related behaviors in rodents and humans.
+NMU	drug	alcohol	30439457	The present review therefore summarizes the current studies investigating the ability of the gut brain peptides ghrelin, glucagon like peptide 1 (GLP 1), amylin and <strong>neuromedin U</strong> (<strong>NMU</strong>) to modulate <b>alcohol</b>  and drug related behaviors in rodents and humans.
+NMU	drug	alcohol	30439457	On the other hand, the anorexigenic peptides GLP 1, amylin and <strong>NMU</strong> independently inhibits reward from <b>alcohol</b> and drugs of abuse in rodents.
+NMU	addiction	reward	30439457	On the other hand, the anorexigenic peptides GLP 1, amylin and <strong>NMU</strong> independently inhibits <b>reward</b> from alcohol and drugs of abuse in rodents.
+NMU	addiction	addiction	30439457	Collectively, these rodent and human studies imply that central ghrelin, GLP 1, amylin and <strong>NMU</strong> signaling may contribute to <b>addiction</b> processes.
+NMU	drug	opioid	28377810	Aims and method We examined non medical use (<strong>NMU</strong>) of olanzapine among adults on <b>methadone</b> treatment.
+NMU	addiction	reward	28377810	Clinical implications Self medication is the dominant motivator for <strong>NMU</strong> of olanzapine, but <b>hedonic</b> motivations also occur.
+NMU	addiction	addiction	28377810	All doctors should be aware of the potential <strong>NMU</strong> of olanzapine, especially among patients with history of <b>addiction</b>.
+NMU	drug	amphetamine	27139195	The Anorexigenic Peptide Neuromedin U (<strong>NMU</strong>) Attenuates <b>Amphetamine</b> Induced Locomotor Stimulation, Accumbal Dopamine Release and Expression of Conditioned Place Preference in Mice.
+NMU	drug	amphetamine	27139195	The Anorexigenic Peptide <strong>Neuromedin U</strong> (<strong>NMU</strong>) Attenuates <b>Amphetamine</b> Induced Locomotor Stimulation, Accumbal Dopamine Release and Expression of Conditioned Place Preference in Mice.
+NMU	addiction	reward	27139195	A novel candidate for <b>reward</b> regulation is the anorexigenic peptide neuromedin U (<strong>NMU</strong>).
+NMU	addiction	reward	27139195	A novel candidate for <b>reward</b> regulation is the anorexigenic peptide <strong>neuromedin U</strong> (<strong>NMU</strong>).
+NMU	drug	amphetamine	27139195	We therefore investigated the effects of intracerebroventricular (icv) administration of <strong>NMU</strong> on <b>amphetamine</b>'s well documented effects on the mesoaccumbal dopamine system, i.e.
+NMU	addiction	reward	27139195	The effect of <strong>NMU</strong>, icv or intra NAc, on the expression of conditioned place preference (<b>CPP</b>) was elucidated.
+NMU	drug	amphetamine	27139195	Firstly, we showed that icv administration of <strong>NMU</strong> attenuate the <b>amphetamine</b> induced locomotor stimulation, accumbal dopamine release and expression of CPP in mice.
+NMU	addiction	reward	27139195	Firstly, we showed that icv administration of <strong>NMU</strong> attenuate the amphetamine induced locomotor stimulation, accumbal dopamine release and expression of <b>CPP</b> in mice.
+NMU	drug	amphetamine	27139195	Secondly, we found that a lower dose of <strong>NMU</strong> (icv) reduce the <b>amphetamine</b> induced locomotor stimulation in mice.
+NMU	drug	amphetamine	27139195	Thirdly, we demonstrated that <strong>NMU</strong> administration into the NAc block the ability of <b>amphetamine</b> to cause a locomotor stimulation in mice.
+NMU	drug	amphetamine	27139195	However, accumbal <strong>NMU</strong> administration did not attenuate the <b>amphetamine</b> induced expression of CPP in mice.
+NMU	addiction	reward	27139195	However, accumbal <strong>NMU</strong> administration did not attenuate the amphetamine induced expression of <b>CPP</b> in mice.
+NMU	drug	amphetamine	27139195	Our novel data suggest that central <strong>NMU</strong> signalling is involved in development of <b>amphetamine</b> dependence.
+NMU	addiction	dependence	27139195	Our novel data suggest that central <strong>NMU</strong> signalling is involved in development of amphetamine <b>dependence</b>.
+NMU	addiction	reward	27105831	Gamma Aminobutyric Acidergic Projections From the Dorsal Raphe to the Nucleus Accumbens Are Regulated by Neuromedin U. Neuromedin U (<strong>NMU</strong>) is a neuropeptide enriched in the nucleus accumbens shell (NAcSh), a brain region associated with <b>reward</b>.
+NMU	addiction	reward	27105831	Gamma Aminobutyric Acidergic Projections From the Dorsal Raphe to the Nucleus Accumbens Are Regulated by <strong>Neuromedin U</strong>. <strong>Neuromedin U</strong> (<strong>NMU</strong>) is a neuropeptide enriched in the nucleus accumbens shell (NAcSh), a brain region associated with <b>reward</b>.
+NMU	drug	cocaine	27105831	While <strong>NMU</strong> and its receptor, <strong>NMU</strong> receptor 2 (NMUR2), have been studied for the ability to regulate food reward, <strong>NMU</strong> has not been studied in the context of drugs of abuse (e.g., <b>cocaine</b>).
+NMU	addiction	reward	27105831	While <strong>NMU</strong> and its receptor, <strong>NMU</strong> receptor 2 (NMUR2), have been studied for the ability to regulate food <b>reward</b>, <strong>NMU</strong> has not been studied in the context of drugs of abuse (e.g., cocaine).
+NMU	drug	cocaine	27105831	The behavioral effects of <strong>NMU</strong> microinjection directly to the NAcSh were investigated using <b>cocaine</b> evoked locomotion (n = 93).
+NMU	drug	cocaine	27105831	Next, we evaluated the effects of <strong>NMU</strong> microinjection on behavioral sensitization to <b>cocaine</b>.
+NMU	addiction	sensitization	27105831	Next, we evaluated the effects of <strong>NMU</strong> microinjection on behavioral <b>sensitization</b> to cocaine.
+NMU	drug	cocaine	27105831	When repeatedly administered throughout the sensitization regimen, <strong>NMU</strong> attenuated <b>cocaine</b> evoked hyperactivity.
+NMU	addiction	sensitization	27105831	When repeatedly administered throughout the <b>sensitization</b> regimen, <strong>NMU</strong> attenuated cocaine evoked hyperactivity.
+NMU	drug	alcohol	26769653	Central administration of the anorexigenic peptide <strong>neuromedin U</strong> decreases <b>alcohol</b> intake and attenuates <b>alcohol</b> induced reward in rodents.
+NMU	addiction	reward	26769653	Central administration of the anorexigenic peptide <strong>neuromedin U</strong> decreases alcohol intake and attenuates alcohol induced <b>reward</b> in rodents.
+NMU	addiction	reward	26769653	In contrast to the common view of the function of gut brain peptides, such as neuromedin U (<strong>NMU</strong>), to regulate food intake and appetite, a novel role in <b>reinforcement</b> mediation has been implied.
+NMU	addiction	reward	26769653	In contrast to the common view of the function of gut brain peptides, such as <strong>neuromedin U</strong> (<strong>NMU</strong>), to regulate food intake and appetite, a novel role in <b>reinforcement</b> mediation has been implied.
+NMU	drug	alcohol	26769653	The present experiments were therefore set up to investigate the effect of intracerebroventricular administration of <strong>NMU</strong> on <b>alcohol</b> mediated behaviors in rodents.
+NMU	drug	alcohol	26769653	We found that central administration of <strong>NMU</strong> attenuated <b>alcohol</b> induced locomotor stimulation, accumbal dopamine release and the expression of conditioned place preference in mice.
+NMU	drug	alcohol	26769653	In addition, <strong>NMU</strong> dose dependently decreased <b>alcohol</b> intake in high, but not in low, <b>alcohol</b> consuming rats.
+NMU	drug	alcohol	26769653	Central <strong>NMU</strong> administration did not alter the blood <b>alcohol</b> concentrations nor change the corticosterone levels in rodents.
+NMU	drug	alcohol	26518254	Medical Users Only and MU+<strong>NMU</strong> youth did not differ from Non Users in cigarette, <b>alcohol</b>, and illicit drug use.
+NMU	addiction	intoxication	26518254	Compared to MU+<strong>NMU</strong> youth, Nonmedical Users Only were more likely to have close friends who tried Adderall (p=0.0123), endorse <b>binge</b> drinking (p=0.0118) and illicit drug use (p<0.0015).
+NMU	drug	amphetamine	25295651	The review covers nonmedical use (<strong>NMU</strong>) of both stimulant (methylphenidate and <b>amphetamine</b>) and nonstimulant (α adrenergic agonists and atomoxetine) prescription medications, and provides a discussion on the relevance for ADHD treatment today.
+NMU	drug	alcohol	21876473	The genes implicated, which replicated genes previously shown to be associated with <b>alcoholism</b> were: cadherin 11, collagen type 11 α2, <strong>neuromedin U</strong> receptor 2, exportin7, and semaphorin associated protein 5A.
+NMU	drug	opioid	21354703	Few studies have systematically evaluated nonmedical use of prescription <b>opioids</b> (<strong>NMU</strong>) among U.S. military veterans, those who report pain, and those with human immunodeficiency virus (HIV).
+NMU	drug	opioid	21354703	An increased understanding of the factors associated with <strong>NMU</strong> may help providers to balance maintaining patient access to prescription <b>opioids</b> for legitimate medical reasons and reducing the risks of addiction.
+NMU	addiction	addiction	21354703	An increased understanding of the factors associated with <strong>NMU</strong> may help providers to balance maintaining patient access to prescription opioids for legitimate medical reasons and reducing the risks of <b>addiction</b>.
+NMU	drug	alcohol	21354703	In multivariable analysis, <strong>NMU</strong> was associated with: being Hispanic (adjusted odds ratio [AOR] 1.8); aged 40 44 years (AOR 1.6); <b>Alcohol</b> Use Disorders Identification Test score ≥20 (AOR 2.0); drug use disorder (AOR 1.9); opioid use disorder (AOR 2.7); past month cigarette use (AOR 1.3); receiving a past year Veterans Health Administration opioid prescription (AOR 1.9); hepatitis C (AOR 1.5); and pain interference (AOR 1.1).
+NMU	drug	opioid	21354703	In multivariable analysis, <strong>NMU</strong> was associated with: being Hispanic (adjusted odds ratio [AOR] 1.8); aged 40 44 years (AOR 1.6); Alcohol Use Disorders Identification Test score ≥20 (AOR 2.0); drug use disorder (AOR 1.9); <b>opioid</b> use disorder (AOR 2.7); past month cigarette use (AOR 1.3); receiving a past year Veterans Health Administration <b>opioid</b> prescription (AOR 1.9); hepatitis C (AOR 1.5); and pain interference (AOR 1.1).
+NMU	drug	opioid	12927633	Intrathecal administration of <strong>NMU</strong> 23 (0.4, 1.1, and 3.8 nmol/10 microl) dose dependently decreased thermal withdrawal latencies and produced a <b>morphine</b> sensitive behavioral response.
+NMU	addiction	withdrawal	12927633	Intrathecal administration of <strong>NMU</strong> 23 (0.4, 1.1, and 3.8 nmol/10 microl) dose dependently decreased thermal <b>withdrawal</b> latencies and produced a morphine sensitive behavioral response.
+NMU	drug	cocaine	1503220	This technique is compared and contrasted with conventional single frequency collisional activation for the molecular ion of N,N dimethylaniline, protonated <b>cocaine</b>, the molecular anion of 2,4,6 trinitrotoluene, and doubly pronated <strong>neuromedin U</strong> 8.
+MZB1	drug	nicotine	32476165	Recent evidence implicates endogenous pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) in the aversive effect of <b>nicotine</b>.
+MZB1	addiction	aversion	32476165	Recent evidence implicates endogenous pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) in the <b>aversive</b> effect of nicotine.
+MZB1	drug	nicotine	32476165	In the present study, we assessed if <b>nicotine</b> induced conditioned place preference (CPP) or affective signs of <b>nicotine</b> withdrawal would be altered in the absence of <strong>PACAP</strong> and if there were any sex related differences in these responses.
+MZB1	addiction	reward	32476165	In the present study, we assessed if nicotine induced conditioned place preference (<b>CPP</b>) or affective signs of nicotine withdrawal would be altered in the absence of <strong>PACAP</strong> and if there were any sex related differences in these responses.
+MZB1	addiction	withdrawal	32476165	In the present study, we assessed if nicotine induced conditioned place preference (CPP) or affective signs of nicotine <b>withdrawal</b> would be altered in the absence of <strong>PACAP</strong> and if there were any sex related differences in these responses.
+MZB1	drug	nicotine	32476165	Male and female mice lacking <strong>PACAP</strong> and their wild type controls were tested for baseline place preference on day 1, received conditioning with saline or <b>nicotine</b> (1 mg/kg) on alternate days for 6 days and were then tested for CPP the next day.
+MZB1	addiction	reward	32476165	Male and female mice lacking <strong>PACAP</strong> and their wild type controls were tested for baseline place preference on day 1, received conditioning with saline or nicotine (1 mg/kg) on alternate days for 6 days and were then tested for <b>CPP</b> the next day.
+MZB1	addiction	reward	32476165	Our results showed that male but not female mice lacking <strong>PACAP</strong> expressed a significant <b>CPP</b> that was comparable to their wild type controls.
+MZB1	drug	nicotine	32476165	These results suggest that endogenous <strong>PACAP</strong> is involved in affective signs of <b>nicotine</b> withdrawal, but there is a sex related difference in this response.
+MZB1	addiction	withdrawal	32476165	These results suggest that endogenous <strong>PACAP</strong> is involved in affective signs of nicotine <b>withdrawal</b>, but there is a sex related difference in this response.
+MZB1	addiction	addiction	32325064	A review of the literature on PubMed revealed that <strong>PACAP</strong> and its receptors also play a significant role in the actions of <b>addictive</b> drugs.
+MZB1	addiction	addiction	32325064	The goal of this review is to discuss the literature regarding the involvements of <strong>PACAP</strong> and its receptors in the motivational effects of <b>addictive</b> drugs.
+MZB1	drug	cocaine	32312805	PFC NAcc gene network topological analyses, following <b>cocaine</b> exposure, reveal distinct top nodes in the WIN preexposed group, which include <strong>PACAP</strong>/ADCYAP1.
+MZB1	addiction	dependence	31883848	The present review develops the hypothesis that, although <strong>PACAP</strong> normally functions to tightly regulate intake, inhibiting it through negative feedback, this relationship can become dysregulated with the development of <b>dependence</b>, such that <strong>PACAP</strong> instead acts through positive feedback to promote excessive intake.
+MZB1	addiction	addiction	31883848	We propose that repeated exposure to palatable food and drugs of abuse can alter the downstream responses of specific populations of neurons to stimulation by <strong>PACAP</strong>, leading to the perpetuation of the <b>addiction</b> cycle.
+MZB1	drug	alcohol	31883848	Next, it will present literature on palatable food, cocaine, <b>alcohol</b>, and nicotine, which overall demonstrates that <strong>PACAP</strong> in specific limbic brain regions can promote their seeking and intake and itself is stimulated by their intake.
+MZB1	drug	cocaine	31883848	Next, it will present literature on palatable food, <b>cocaine</b>, alcohol, and nicotine, which overall demonstrates that <strong>PACAP</strong> in specific limbic brain regions can promote their seeking and intake and itself is stimulated by their intake.
+MZB1	drug	nicotine	31883848	Next, it will present literature on palatable food, cocaine, alcohol, and <b>nicotine</b>, which overall demonstrates that <strong>PACAP</strong> in specific limbic brain regions can promote their seeking and intake and itself is stimulated by their intake.
+MZB1	addiction	relapse	31883848	Next, it will present literature on palatable food, cocaine, alcohol, and nicotine, which overall demonstrates that <strong>PACAP</strong> in specific limbic brain regions can promote their <b>seeking</b> and intake and itself is stimulated by their intake.
+MZB1	addiction	relapse	31883848	Then, it will present literature on affective behavior, which shows that chronic stress increases levels of <strong>PACAP</strong>, which then promotes anxiety and depression, factors that can trigger substance <b>seeking</b>.
+MZB1	drug	alcohol	31883848	While many questions remain to be addressed, the current evidence suggests that <strong>PACAP</strong> could be a viable medication target for the treatment of binge eating and drug and <b>alcohol</b> use disorders.
+MZB1	addiction	intoxication	31883848	While many questions remain to be addressed, the current evidence suggests that <strong>PACAP</strong> could be a viable medication target for the treatment of <b>binge</b> eating and drug and alcohol use disorders.
+MZB1	drug	nicotine	31028757	The role of endogenous pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) in <b>nicotine</b> self administration, reward and aversion.
+MZB1	addiction	aversion	31028757	The role of endogenous pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) in nicotine self administration, reward and <b>aversion</b>.
+MZB1	addiction	reward	31028757	The role of endogenous pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) in nicotine self administration, <b>reward</b> and aversion.
+MZB1	drug	nicotine	31028757	Pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) and its receptors (PAC1, VPAC1, and VPAC2) are localized in brain regions implicated in stress response, reward seeking and aversive responses, raising the possibility that <strong>PACAP</strong> may be involved in motivational effects of <b>nicotine</b>.
+MZB1	addiction	aversion	31028757	Pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) and its receptors (PAC1, VPAC1, and VPAC2) are localized in brain regions implicated in stress response, reward seeking and <b>aversive</b> responses, raising the possibility that <strong>PACAP</strong> may be involved in motivational effects of nicotine.
+MZB1	addiction	relapse	31028757	Pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) and its receptors (PAC1, VPAC1, and VPAC2) are localized in brain regions implicated in stress response, reward <b>seeking</b> and aversive responses, raising the possibility that <strong>PACAP</strong> may be involved in motivational effects of nicotine.
+MZB1	addiction	reward	31028757	Pituitary adenylyl cyclase activating polypeptide (<strong>PACAP</strong>) and its receptors (PAC1, VPAC1, and VPAC2) are localized in brain regions implicated in stress response, <b>reward</b> seeking and aversive responses, raising the possibility that <strong>PACAP</strong> may be involved in motivational effects of nicotine.
+MZB1	drug	nicotine	31028757	To test this hypothesis, we used two bottle choice (TBC) and place conditioning paradigms and assessed if <b>nicotine</b> preference or conditioned place preference (CPP) or aversion (CPA) induced by <b>nicotine</b> would be altered in mice lacking <strong>PACAP</strong> compared to their wild type controls.
+MZB1	addiction	aversion	31028757	To test this hypothesis, we used two bottle choice (TBC) and place conditioning paradigms and assessed if nicotine preference or conditioned place preference (CPP) or <b>aversion</b> (CPA) induced by nicotine would be altered in mice lacking <strong>PACAP</strong> compared to their wild type controls.
+MZB1	addiction	reward	31028757	To test this hypothesis, we used two bottle choice (TBC) and place conditioning paradigms and assessed if nicotine preference or conditioned place preference (<b>CPP</b>) or aversion (CPA) induced by nicotine would be altered in mice lacking <strong>PACAP</strong> compared to their wild type controls.
+MZB1	drug	nicotine	31028757	We discovered that mice lacking <strong>PACAP</strong> compared to their wild type controls exhibited more preference for <b>nicotine</b> over water in the TBC paradigm, particularly at the two higher concentrations of <b>nicotine</b>.
+MZB1	drug	nicotine	31028757	While the rewarding action of the low dose <b>nicotine</b> was not altered in mice lacking <strong>PACAP</strong>, the aversive effect of the high dose <b>nicotine</b> was blunted in these mice compared to their wild type controls.
+MZB1	addiction	aversion	31028757	While the rewarding action of the low dose nicotine was not altered in mice lacking <strong>PACAP</strong>, the <b>aversive</b> effect of the high dose nicotine was blunted in these mice compared to their wild type controls.
+MZB1	drug	nicotine	31028757	The present results suggest that endogenous <strong>PACAP</strong> may play a functional role in <b>nicotine</b> preference and its aversive effect.
+MZB1	addiction	aversion	31028757	The present results suggest that endogenous <strong>PACAP</strong> may play a functional role in nicotine preference and its <b>aversive</b> effect.
+MZB1	drug	alcohol	30682380	Therapeutic potential of <strong>PACAP</strong> in <b>alcohol</b> toxicity.
+MZB1	drug	alcohol	30682380	Pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) is an endogenous 38 amino acid neuropeptide with demonstrated protection against neuronal injury, trauma as well as various endogenous and exogenous toxic agents including <b>alcohol</b>.
+MZB1	drug	alcohol	30682380	In this mini review, following a brief presentation of <b>alcohol</b> addiction and its neurotoxicity, the potential of <strong>PACAP</strong> as a therapeutic intervention in toxicological consequences of this devastating disorder is discussed.
+MZB1	addiction	addiction	30682380	In this mini review, following a brief presentation of alcohol <b>addiction</b> and its neurotoxicity, the potential of <strong>PACAP</strong> as a therapeutic intervention in toxicological consequences of this devastating disorder is discussed.
+MZB1	addiction	addiction	30074172	Pituitary Adenylate Cyclase Activating Peptide (<strong>PACAP</strong>) Signaling and the Dark Side of <b>Addiction</b>.
+MZB1	drug	cocaine	30074172	Similar to footshock stress, the BNST administration of <strong>PACAP</strong> or the PAC1 receptor specific agonist maxadilan can facilitate relapse following extinction of <b>cocaine</b> seeking behavior.
+MZB1	addiction	relapse	30074172	Similar to footshock stress, the BNST administration of <strong>PACAP</strong> or the PAC1 receptor specific agonist maxadilan can facilitate <b>relapse</b> following extinction of cocaine <b>seeking</b> behavior.
+MZB1	addiction	relapse	30074172	Further, in the same paradigm, the footshock induced <b>relapse</b> could be attenuated following BNST pretreatment with PAC1 receptor antagonist PACAP6 38, implicating <strong>PACAP</strong> systems as critical components underlying stress induced <b>reinstatement</b>.
+MZB1	addiction	relapse	28656976	Here we ask whether <strong>PACAP</strong> is also involved in producing <b>reinstatement</b> in a model of stress induced <b>relapse</b> to drug taking.
+MZB1	drug	cocaine	28656976	Reinstatement of <b>cocaine</b> seeking was then tested after footshock exposure in different groups of rats that were pretreated with vehicle solution, a PAC1 receptor antagonist (experiment 2), or a <strong>PACAP</strong> agonist (experiment 3) without footshock.
+MZB1	addiction	relapse	28656976	<b>Reinstatement</b> of cocaine <b>seeking</b> was then tested after footshock exposure in different groups of rats that were pretreated with vehicle solution, a PAC1 receptor antagonist (experiment 2), or a <strong>PACAP</strong> agonist (experiment 3) without footshock.
+MZB1	drug	cocaine	28656976	In experiment 1, <b>cocaine</b> self administration increased BNST <strong>PACAP</strong> transcript levels similar to what we have previously reported with chronic stress.
+MZB1	drug	cocaine	28656976	In experiment 2, intra BNST infusions of the PAC1/VPAC2 antagonist, <strong>PACAP</strong> 6 38, prevented footshock induced reinstatement of extinguished <b>cocaine</b> seeking.
+MZB1	addiction	relapse	28656976	In experiment 2, intra BNST infusions of the PAC1/VPAC2 antagonist, <strong>PACAP</strong> 6 38, prevented footshock induced <b>reinstatement</b> of extinguished cocaine <b>seeking</b>.
+MZB1	drug	cocaine	28656976	In experiment 3, intra BNST <strong>PACAP</strong> infusion reinstated previously extinguished <b>cocaine</b> seeking behavior in the absence of footshock.
+MZB1	addiction	relapse	28656976	In experiment 3, intra BNST <strong>PACAP</strong> infusion reinstated previously extinguished cocaine <b>seeking</b> behavior in the absence of footshock.
+MZB1	drug	cocaine	28656976	<b>Cocaine</b> self administration elevated BNST <strong>PACAP</strong>, and BNST <strong>PACAP</strong> receptor activation was necessary and sufficient for stress induced reinstatement of <b>cocaine</b> seeking.
+MZB1	addiction	relapse	28656976	Cocaine self administration elevated BNST <strong>PACAP</strong>, and BNST <strong>PACAP</strong> receptor activation was necessary and sufficient for stress induced <b>reinstatement</b> of cocaine <b>seeking</b>.
+MZB1	addiction	relapse	28656976	These data suggest that BNST <strong>PACAP</strong> systems may be viable targets for <b>relapse</b> prevention.
+MZB1	drug	nicotine	28506824	Hypoxia and <b>nicotine</b> effects on Pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) and its receptor 1 (PAC1) in the developing piglet brainstem.
+MZB1	drug	nicotine	28506824	Using piglet models of these risk factors, intermittent hypercapnic hypoxia (IHH mimicking rebreathing in prone position) and <b>nicotine</b> (main reinforcing element of cigarettes), this study aimed to determine their effects on <strong>PACAP</strong> and PAC1 protein expression in the medulla.
+MZB1	addiction	reward	28506824	Using piglet models of these risk factors, intermittent hypercapnic hypoxia (IHH mimicking rebreathing in prone position) and nicotine (main <b>reinforcing</b> element of cigarettes), this study aimed to determine their effects on <strong>PACAP</strong> and PAC1 protein expression in the medulla.
+MZB1	drug	nicotine	28506824	No <strong>PACAP</strong> change was noted in the <b>nicotine</b> exposed piglets, however, a decrease in PAC1 was found in the DMNV (p=0.02).
+MZB1	drug	nicotine	28506824	IHH exposure in piglets with pre exposure to <b>nicotine</b> led to a significant decrease in <strong>PACAP</strong> in the Grac (p=0.04) but had no effect on PAC1.
+MZB1	drug	nicotine	28506824	These findings show for the first time, the vulnerability of <strong>PACAP</strong> in the brainstem during early development to an acute hypercapnic hypoxic exposure and that those effects are greater than from <b>nicotine</b> exposure.
+MZB1	drug	alcohol	27826748	<strong>PACAP</strong> Protects the Adolescent and Adult Mice Brain from <b>Ethanol</b> Toxicity and Modulates Distinct Sets of Genes Regulating Similar Networks.
+MZB1	drug	alcohol	27826748	To explore the capacity of endogenous <strong>PACAP</strong> to prevent <b>ethanol</b> toxicity, adolescent and adult <strong>PACAP</strong> knockout (KO) mice were injected with <b>ethanol</b> in a binge drinking like manner.
+MZB1	addiction	intoxication	27826748	To explore the capacity of endogenous <strong>PACAP</strong> to prevent ethanol toxicity, adolescent and adult <strong>PACAP</strong> knockout (KO) mice were injected with ethanol in a <b>binge</b> drinking like manner.
+MZB1	drug	alcohol	27826748	Biochemical analyses revealed that <b>ethanol</b> administration induced an increase in the production of reactive oxygen species and the activity of caspase 3 in <strong>PACAP</strong> KO mice in an age independent manner.
+MZB1	drug	alcohol	27826748	In order to characterize the mechanisms underlying the sensitivity of <strong>PACAP</strong> KO mice, a whole genome microarray analysis was performed to compare gene regulations induced by <b>ethanol</b> in adolescent and adult wild type and <strong>PACAP</strong> KO mice.
+MZB1	drug	alcohol	27826748	These data imply that <b>ethanol</b> induces serious DNA damages and cell cycle alteration in <strong>PACAP</strong> KO mice.
+MZB1	drug	alcohol	27826748	This hypothesis, based on the transcriptomic data, could be confirmed by functional studies which showed that cell proliferation decreased in adolescent and adult <strong>PACAP</strong> KO mice treated with <b>ethanol</b> but recovered after a 30 day withdrawal period.
+MZB1	addiction	withdrawal	27826748	This hypothesis, based on the transcriptomic data, could be confirmed by functional studies which showed that cell proliferation decreased in adolescent and adult <strong>PACAP</strong> KO mice treated with ethanol but recovered after a 30 day <b>withdrawal</b> period.
+MZB1	drug	alcohol	27826748	These data, obtained with <strong>PACAP</strong> KO animals, demonstrate that endogenous <strong>PACAP</strong> protects the brain of adolescent and adult mice from <b>alcohol</b> toxicity and modulates distinct sets of genes according to the maturation status of the brain.
+MZB1	addiction	reward	26229039	Dose dependent disruptions in motivation, social interaction, and attention were produced by <strong>PACAP</strong>, as reflected by increases in <b>reward</b> thresholds, decreases in social behaviors, and decreases in correct responses and alterations in posterror accuracy.
+MZB1	drug	amphetamine	23868736	<b>Methamphetamine</b> withdrawal stress activates <strong>PACAP</strong> DBI pathway in rat salivary gland, resulting in inhibition of salivary secretion.
+MZB1	addiction	withdrawal	23868736	Methamphetamine <b>withdrawal</b> stress activates <strong>PACAP</strong> DBI pathway in rat salivary gland, resulting in inhibition of salivary secretion.
+MZB1	drug	amphetamine	23868736	In addition, <b>METH</b> withdrawal stress also elicited an increase in pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) and PBR mRNA, which is associated with DBI activity.
+MZB1	addiction	withdrawal	23868736	In addition, METH <b>withdrawal</b> stress also elicited an increase in pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) and PBR mRNA, which is associated with DBI activity.
+MZB1	drug	amphetamine	23868736	These results suggest that <b>METH</b> withdrawal stress activates a <strong>PACAP</strong> DBI pathway in salivary gland, enhancing steroid genesis and inhibiting secretion.
+MZB1	addiction	withdrawal	23868736	These results suggest that METH <b>withdrawal</b> stress activates a <strong>PACAP</strong> DBI pathway in salivary gland, enhancing steroid genesis and inhibiting secretion.
+MZB1	drug	opioid	22226680	The aim of the present investigation was to study the effects of pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) on <b>morphine</b> withdrawal induced behavioral changes and hypothermia in male CFLP mice.
+MZB1	addiction	withdrawal	22226680	The aim of the present investigation was to study the effects of pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) on morphine <b>withdrawal</b> induced behavioral changes and hypothermia in male CFLP mice.
+MZB1	addiction	withdrawal	22226680	administration of <strong>PACAP</strong> alone had no significant effect on <b>withdrawal</b> induced anxiolysis and total activity at doses of 500 ng and 1 μg.
+MZB1	drug	opioid	22226680	At dose of 500 ng, however, <strong>PACAP</strong> significantly counteracted the reduced motor activity in the EPM test in mice treated with <b>morphine</b> and diminished the hypothermia and shortened jump latency induced by <b>naloxone</b> in mice treated with <b>morphine</b>.
+MZB1	drug	opioid	22226680	These findings indicate that anxiolytic like behavior may be mediated via a <strong>PACAP</strong> involved pathway and <strong>PACAP</strong> may play an important role in chronic <b>morphine</b> withdrawal induced hypothermia as well.
+MZB1	addiction	withdrawal	22226680	These findings indicate that anxiolytic like behavior may be mediated via a <strong>PACAP</strong> involved pathway and <strong>PACAP</strong> may play an important role in chronic morphine <b>withdrawal</b> induced hypothermia as well.
+MZB1	drug	alcohol	19944672	Increased <b>ethanol</b> preference and serotonin 1A receptor dependent attenuation of <b>ethanol</b> induced hypothermia in <strong>PACAP</strong> deficient mice.
+MZB1	drug	alcohol	19944672	Pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) deficient mice display remarkable behavioral changes including increased novelty seeking behavior and reduced hypothermia induced by either serotonin (5 HT)(1A) receptor agonists or <b>ethanol</b>.
+MZB1	addiction	relapse	19944672	Pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) deficient mice display remarkable behavioral changes including increased novelty <b>seeking</b> behavior and reduced hypothermia induced by either serotonin (5 HT)(1A) receptor agonists or ethanol.
+MZB1	drug	alcohol	19944672	Because 5 HT(1A) receptors have been implicated in the development of <b>alcohol</b> dependence, we have examined <b>ethanol</b> preference in <strong>PACAP</strong> deficient mice using a two bottle choice and a conditioned place preference test, as well as additive effects of <b>ethanol</b> and 5 HT(1A) receptor agents on hypothermia.
+MZB1	addiction	dependence	19944672	Because 5 HT(1A) receptors have been implicated in the development of alcohol <b>dependence</b>, we have examined ethanol preference in <strong>PACAP</strong> deficient mice using a two bottle choice and a conditioned place preference test, as well as additive effects of ethanol and 5 HT(1A) receptor agents on hypothermia.
+MZB1	drug	alcohol	19944672	<strong>PACAP</strong> deficient mice showed an increased preference towards <b>ethanol</b> compared with wild type mice.
+MZB1	drug	alcohol	19944672	These results demonstrate increased <b>ethanol</b> preference in <strong>PACAP</strong> deficient mice that may be mediated by 5 HT(1A) receptor dependent attenuation of <b>ethanol</b> induced central inhibition.
+MZB1	drug	opioid	19199096	The role of endogenous <strong>PACAP</strong> in motor stimulation and conditioned place preference induced by <b>morphine</b> in mice.
+MZB1	drug	opioid	19199096	The present study was designed to determine if <strong>PACAP</strong> plays a role in acute motor stimulatory and rewarding actions of <b>morphine</b>.
+MZB1	drug	opioid	19199096	The effect of intracerebroventricular <strong>PACAP</strong> administration (0, 0.03, 0.3, 1.0, or 3.0 microg/3 microL) was studied on basal motor activity as well as on <b>morphine</b> (5 mg/kg) stimulated motor activity.
+MZB1	drug	opioid	19199096	Motor stimulation and conditioned place preference (CPP) induced by <b>morphine</b> (5 or 10 mg/kg) were also determined in mice lacking <strong>PACAP</strong> and their wild type controls.
+MZB1	addiction	reward	19199096	Motor stimulation and conditioned place preference (<b>CPP</b>) induced by morphine (5 or 10 mg/kg) were also determined in mice lacking <strong>PACAP</strong> and their wild type controls.
+MZB1	drug	opioid	19199096	Paradoxically, low doses of <strong>PACAP</strong> which did not alter basal motor activity were found to enhance the motor stimulatory action of <b>morphine</b>.
+MZB1	drug	opioid	19199096	Furthermore, <b>morphine</b> induced motor stimulation was blunted in <strong>PACAP</strong> deficient mice.
+MZB1	drug	opioid	19199096	Additionally, <b>morphine</b> induced CPP following a single, but not repeated, alternate day saline/<b>morphine</b> (10 mg/kg) conditioning was blunted in <strong>PACAP</strong> deficient mice compared to their wild type littermates/controls.
+MZB1	addiction	reward	19199096	Additionally, morphine induced <b>CPP</b> following a single, but not repeated, alternate day saline/morphine (10 mg/kg) conditioning was blunted in <strong>PACAP</strong> deficient mice compared to their wild type littermates/controls.
+MZB1	drug	opioid	19199096	The present results suggest that endogenous <strong>PACAP</strong>, at low doses, positively modulates the acute motor stimulatory and rewarding actions of <b>morphine</b>.
+MZB1	drug	benzodiazepine	21318965	We examined the effect of chronic administration of MAP on the mRNA expression of DBI and DBI related proteins, such as alpha 2 subunit of GABAA receptor (GABA α2), peripheral type <b>benzodiazepine</b> receptor (PBR), and pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) in seven regions (diencephalon, cerebral cortex, cerebellum, striatum, hippocampus, midbrain, and pons medulla) of the rat brain.
+MZB1	drug	amphetamine	17658665	<b>Methamphetamine</b> induced hyperactivity and behavioral sensitization in <strong>PACAP</strong> deficient mice.
+MZB1	addiction	sensitization	17658665	Methamphetamine induced hyperactivity and behavioral <b>sensitization</b> in <strong>PACAP</strong> deficient mice.
+MZB1	drug	amphetamine	17658665	Mice lacking the <strong>PACAP</strong> gene (<strong>PACAP</strong>( / )) display psychomotor abnormalities such as novelty induced hyperactivity and jumping behavior, and they show different responses to <b>amphetamine</b>, a typical psychostimulant.
+MZB1	drug	amphetamine	17658665	The present study examined the possible role of endogenous <strong>PACAP</strong> in <b>methamphetamine</b> (<b>METH</b>) induced hyperactivity and behavioral sensitization.
+MZB1	addiction	sensitization	17658665	The present study examined the possible role of endogenous <strong>PACAP</strong> in methamphetamine (METH) induced hyperactivity and behavioral <b>sensitization</b>.
+MZB1	drug	amphetamine	17658665	Single administration of <b>METH</b> (1 and 2mg/kg) caused a robust increase in locomotor activity of mice, but this effect did not differ between wild type and <strong>PACAP</strong>( / ) mice.
+MZB1	drug	amphetamine	17658665	There was no difference in the degree of development and expression of <b>METH</b> induced behavioral sensitization between wild type and <strong>PACAP</strong>( / ) mice.
+MZB1	addiction	sensitization	17658665	There was no difference in the degree of development and expression of METH induced behavioral <b>sensitization</b> between wild type and <strong>PACAP</strong>( / ) mice.
+MZB1	drug	amphetamine	17658665	These results suggest that endogenous <strong>PACAP</strong> is not involved in the locomotor stimulant activity of acute <b>METH</b> and repeated <b>METH</b> induced behavioral and neurochemical sensitization.
+MZB1	addiction	sensitization	17658665	These results suggest that endogenous <strong>PACAP</strong> is not involved in the locomotor stimulant activity of acute METH and repeated METH induced behavioral and neurochemical <b>sensitization</b>.
+MZB1	drug	opioid	12409215	The effects of pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) on pain sensitivity, on <b>morphine</b> analgesia, on <b>morphine</b> tolerance and withdrawal were investigated in mice.
+MZB1	addiction	withdrawal	12409215	The effects of pituitary adenylate cyclase activating polypeptide (<strong>PACAP</strong>) on pain sensitivity, on morphine analgesia, on morphine tolerance and <b>withdrawal</b> were investigated in mice.
+MZB1	drug	opioid	12409215	administration of <strong>PACAP</strong> alone had no effect on pain sensitivity but in a dose of 500 ng, it significantly diminished the analgesic effect of a single dose of <b>morphine</b> (2.25 mg/kg, s.c.).
+MZB1	drug	opioid	12409215	pretreatment significantly enhanced the effect of <strong>PACAP</strong> on <b>morphine</b> analgesia but the effects of <strong>PACAP</strong> on tolerance and withdrawal were unaffected upon theophylline administration.
+MZB1	addiction	withdrawal	12409215	pretreatment significantly enhanced the effect of <strong>PACAP</strong> on morphine analgesia but the effects of <strong>PACAP</strong> on tolerance and <b>withdrawal</b> were unaffected upon theophylline administration.
+MZB1	drug	opioid	12409215	On the grounds of our previous studies with vasoactive intestinal polypeptide (VIP), it appears that different receptors are involved in the effects of <strong>PACAP</strong> in acute and chronic <b>morphine</b> actions.
+MZB1	drug	opioid	12409215	Our results indicate that <strong>PACAP</strong> induced actions likely participate in acute and chronic effects of <b>morphine</b> and suggest a potential role of <strong>PACAP</strong> in <b>opioid</b> analgesia, tolerance and withdrawal.
+MZB1	addiction	withdrawal	12409215	Our results indicate that <strong>PACAP</strong> induced actions likely participate in acute and chronic effects of morphine and suggest a potential role of <strong>PACAP</strong> in opioid analgesia, tolerance and <b>withdrawal</b>.
+MZB1	drug	alcohol	12270109	In Drosophila, loss of function mutations in a <strong>PACAP</strong> like neuropeptide gene, amnesiac (amn), affect both memory retention and <b>ethanol</b> sensitivity.
+MZB1	addiction	relapse	12270109	Meanwhile, <strong>PACAP</strong> deficient mice display a high early mortality rate and additional CNS phenotypes including behavioral and psychological phenotypes (e.g., hyperlocomotion, intense novelty <b>seeking</b> behavior, and explosive jumping).
+MZB1	drug	alcohol	20575839	Peptides of the <strong>PACAP</strong> family provide intracellular signaling that involves kinases, scaffolding interactions, Ca2 + mobilization, and gene expression to facilitate development of tolerance to <b>alcohol</b> and development of associative memories.
+MIA	drug	cannabinoid	31937359	Local injection of KML29 (700 μg) reduced joint pain at day 14 post <strong>MIA</strong> induction, and this analgesic effect was blocked by the <b>cannabinoid</b> receptor antagonists AM281 and AM630 (P < 0.0001; n = 6).
+MIA	addiction	withdrawal	31937359	During the acute inflammatory phase of the <strong>MIA</strong> model (day 1), a significant reduction in <b>withdrawal</b> threshold (P < 0.0001; n = 6 8) and leukocyte trafficking was seen after treatment with KML29 + CXB (P < 0.0001; n = 6 8).
+MIA	addiction	withdrawal	31752825	The paw <b>withdrawal</b> threshold (PWT) in <strong>MIA</strong> injected rats was measured by the von Frey test using the up down method.
+MIA	drug	cannabinoid	31551729	Here, we hypothesized that adolescent Δ9 <b>tetrahydrocannabinol</b> (<b>THC</b>) worsens the impact of prenatal maternal immune activation (<strong>MIA</strong>) on ventral tegmental area (VTA) dopamine cells in rat offspring.
+MIA	drug	cocaine	31551729	Additionally, since substance abuse disorder is particularly prevalent among schizophrenia patients, we also tested how VTA dopamine neurons in <strong>MIA</strong> offspring respond to acute nicotine and <b>cocaine</b> administration.
+MIA	drug	nicotine	31551729	Additionally, since substance abuse disorder is particularly prevalent among schizophrenia patients, we also tested how VTA dopamine neurons in <strong>MIA</strong> offspring respond to acute <b>nicotine</b> and cocaine administration.
+MIA	drug	cannabinoid	31551729	Adolescent <b>THC</b> attenuated several <strong>MIA</strong> induced effects.
+MIA	drug	cannabinoid	31551729	Contrary to our expectations, adolescent <b>THC</b> did not worsen <strong>MIA</strong> induced deficits.
+MIA	drug	cannabinoid	31202911	We have recently shown that treatment with the non intoxicating <b>phytocannabinoid</b>, <b>cannabidiol</b> (CBD), can improve cognition and social interaction deficits in a maternal immune activation (<strong>MIA</strong>) model relevant to the aetiology of schizophrenia, however, the mechanisms underlying this effect are unknown.
+MIA	addiction	withdrawal	30945071	HU210, WIN55, 212, and PEA in a dose dependent manner restored the paw <b>withdrawal</b> threshold (PWT) and the weight bearing difference induced by <strong>MIA</strong> injection.
+MIA	drug	cannabinoid	29364174	Following <strong>MIA</strong> administration, we observed 2 4 fold increase in mRNA expression of targeted receptors (Cnr1, Cnr2, and Trpv1), <b>endocannabinoid</b> degradation enzymes (Faah, Ptgs2, and Alox12), and TRPV1 sensitizing kinases (Mapk3, Mapk14, Prkcg, and Prkaca).
+MIA	drug	amphetamine	29116368	The objective of this study is to investigate N acetyl cysteine (NAC) as a therapeutic antioxidant to reverse schizophrenia like bio behavioural changes in rats exposed to maternal immune activation (<strong>MIA</strong>), adolescent <b>methamphetamine</b> (MA) or a combination thereof.
+MIA	drug	nicotine	28497655	However, <b>nicotine</b>, but not saline self administration, significantly ameliorated the cognitive deficits induced by <strong>MIA</strong>.
+MIA	drug	nicotine	28497655	While the male offspring of mothers prenatally exposed to lipopolysaccharide was only slightly more sensitive to the reinforcing effects of <b>nicotine</b>, after self administration, the <strong>MIA</strong> induced cognitive deficits significantly improved.
+MIA	addiction	reward	28497655	While the male offspring of mothers prenatally exposed to lipopolysaccharide was only slightly more sensitive to the <b>reinforcing</b> effects of nicotine, after self administration, the <strong>MIA</strong> induced cognitive deficits significantly improved.
+MIA	addiction	reward	28320059	Both IA and RVM lidocaine D35, administered post <strong>MIA</strong>, induced <b>CPP</b> in sedentary but not exercised <strong>MIA</strong> treated rats, indicating that exercise blocks <strong>MIA</strong> induced ongoing pain.
+MIA	drug	opioid	28320059	<b>Naloxone</b> reestablished weight asymmetry in <strong>MIA</strong> treated rats undergoing exercise and induced conditioned place aversion, indicating that exercise induced pain relief is dependent on endogenous <b>opioids</b>.
+MIA	addiction	aversion	28320059	Naloxone reestablished weight asymmetry in <strong>MIA</strong> treated rats undergoing exercise and induced conditioned place <b>aversion</b>, indicating that exercise induced pain relief is dependent on endogenous opioids.
+MIA	drug	cannabinoid	27955699	The aim of this study was to evaluate the effect of adelmidrol, a synthetic <b>palmitoylethanolamide</b> analogue, combined with hyaluronic acid on pain severity and modulation of the inflammatory response in a rat model of monosodium iodoacetate (<strong>MIA</strong>) induced osteoarthritis.
+MIA	addiction	withdrawal	27501482	Effects of MJN110 on <strong>MIA</strong> induced weight bearing asymmetry and lowered paw <b>withdrawal</b> thresholds (PWTs), changes in spinal gene expression and brain levels of relevant lipids were determined.
+MIA	drug	cannabinoid	20722027	The functional role of <b>endocannabinoids</b> in the spinal cords of <strong>MIA</strong> treated rats was increased via activation of <b>cannabinoid</b> 1 (CB(1)) and CB(2) receptors, and blockade of the catabolism of anandamide had significantly greater inhibitory effects in <strong>MIA</strong> treated rats compared with control rats.
+MIA	drug	nicotine	20301944	Minimal anti <b>tobacco</b> intervention (<strong>MIA</strong>) is an efficient and inexpensive method of <b>smoking</b> cessation intervention.
+MIA	drug	alcohol	9443546	In the present study, we examined the development of environment independent and environment dependent tolerance to <b>ethanol</b> induced analgesia (EIA) and cross tolerance with morphine induced analgesia (<strong>MIA</strong>).
+MIA	drug	opioid	9443546	In the present study, we examined the development of environment independent and environment dependent tolerance to ethanol induced analgesia (EIA) and cross tolerance with <b>morphine</b> induced analgesia (<strong>MIA</strong>).
+MIA	drug	opioid	1672380	The selective 5 HT1A agonist, (+ ) 8 hydroxy diprolaminotetralin HBr (8 OH DPAT), dose dependently antagonized <b>morphine</b> induced antinociception (<strong>MIA</strong>) without affecting the latency to respond when applied alone.
+GRK2	drug	alcohol	30322021	Phosphoproteomic Analysis of the Amygdala Response to Adolescent Glucocorticoid Exposure Reveals <strong>G Protein Coupled Receptor Kinase 2</strong> as a Target for Reducing Motivation for <b>Alcohol</b>.
+GRK2	drug	alcohol	30322021	We found that intra amygdala infusion of a peptidergic <strong>GRK2</strong> inhibitor reduced <b>alcohol</b> seeking, as measured by progressive ratio and stress reinstatement tests, and induced by the α2AAR antagonist yohimbine.
+GRK2	addiction	relapse	30322021	We found that intra amygdala infusion of a peptidergic <strong>GRK2</strong> inhibitor reduced alcohol <b>seeking</b>, as measured by progressive ratio and stress <b>reinstatement</b> tests, and induced by the α2AAR antagonist yohimbine.
+GRK2	drug	alcohol	30322021	These results suggest that <strong>GRK2</strong> represents a novel target for treating stress induced motivation for <b>alcohol</b> which may counteract alterations in brain function induced by adolescent stress exposure.
+GRK2	drug	opioid	30076211	Estrogen Regulation of <strong>GRK2</strong> Inactivates Kappa <b>Opioid</b> Receptor Signaling Mediating Analgesia, But Not Aversion.
+GRK2	addiction	aversion	30076211	Estrogen Regulation of <strong>GRK2</strong> Inactivates Kappa Opioid Receptor Signaling Mediating Analgesia, But Not <b>Aversion</b>.
+GRK2	drug	opioid	30076211	<strong>GRK2</strong>/3 inhibition by CMPD101 increased KOR stimulation of phospho ERK in females, decreased sex differences in KOR mediated inhibition of dopamine release, and enhanced mu <b>opioid</b> receptor and KOR mediated analgesia in females.
+GRK2	drug	opioid	30076211	These studies suggest that estradiol, through increased phosphorylation of <strong>GRK2</strong> and possible sequestration of Gβγ by <strong>GRK2</strong>, blunts G protein mediated signals.SIGNIFICANCE STATEMENT Chronic pain disorders are more prevalent in females than males, but <b>opioid</b> receptor agonists show inconsistent analgesic efficacy in females.
+GRK2	drug	opioid	30076211	Our studies identify an intracellular mechanism involving estradiol regulation of <strong>G protein coupled receptor kinase 2</strong> that is responsible for sexually dimorphic analgesic responses following <b>opioid</b> receptor activation.
+GRK2	drug	opioid	30018083	We have previously shown that high efficacy <b>opioids</b> such as DAMGO stimulate a <strong>GRK2</strong>/3 mediated multisite phosphorylation of conserved C terminal tail serine and threonine residues, which facilitates internalization of the receptor.
+GRK2	drug	opioid	24517854	In fact, <b>morphine</b> induces a selective S375 phosphorylation that is predominantly catalysed by GPCR kinase 5 (GRK5), whereas multisite phosphorylation induced by high efficacy <b>opioids</b> specifically requires <strong>GRK2</strong>/3.
+GRK2	drug	cocaine	23727505	In <b>cocaine</b> addicts, the reductions of CB1 receptors and <strong>GRK2</strong>/3/5 ( 26% to  30%) indicated receptor desensitization.
+GRK2	drug	cocaine	23727505	The dysregulation of CB1 receptor, <strong>GRK2</strong>/3/5, and mTOR/p70S6K signaling by <b>cocaine</b> may contribute to alterations of neuroplasticity and/or neurotoxicity in brains of <b>cocaine</b> addicts.
+GRK2	drug	alcohol	23430162	Furthermore, the <strong>GRK2</strong> protein level was significantly increased by treatment with <b>ethanol</b>.
+GRK2	drug	alcohol	23430162	On the other hand, this enhancement of the rewarding effects of morphine by <b>ethanol</b> treatment was significantly inhibited by the <strong>GRK2</strong> inhibitor β adrenergic receptor kinase 1 inhibitor.
+GRK2	drug	opioid	23430162	On the other hand, this enhancement of the rewarding effects of <b>morphine</b> by ethanol treatment was significantly inhibited by the <strong>GRK2</strong> inhibitor β adrenergic receptor kinase 1 inhibitor.
+GRK2	drug	alcohol	23430162	The present study demonstrated that chronic treatment with <b>ethanol</b> enhanced the rewarding effects of morphine by up regulating functional changes in μ opioid receptor, mediated by <strong>GRK2</strong>.
+GRK2	drug	opioid	23430162	The present study demonstrated that chronic treatment with ethanol enhanced the rewarding effects of <b>morphine</b> by up regulating functional changes in μ <b>opioid</b> receptor, mediated by <strong>GRK2</strong>.
+GRK2	drug	opioid	23239825	Higher order phosphorylation involving T370, T376, and T379 specifically requires <strong>GRK2</strong>/3 isoforms, and the same sequence controls <b>opioid</b> receptor internalization in neurons.
+GRK2	drug	cocaine	22895728	In contrast, we found that <strong>GRK2</strong> deficiency in cholinergic neurons does not alter <b>cocaine</b> induced psychomotor activation, behavioral sensitization, or conditioned place preference.
+GRK2	addiction	sensitization	22895728	In contrast, we found that <strong>GRK2</strong> deficiency in cholinergic neurons does not alter cocaine induced psychomotor activation, behavioral <b>sensitization</b>, or conditioned place preference.
+GRK2	drug	cocaine	19562697	Regulation of dynamin 2 and <strong>G protein coupled receptor kinase 2</strong> in rat nucleus accumbens during acute and repeated <b>cocaine</b> administration.
+GRK2	drug	cocaine	19562697	This study investigated potential mechanisms of <b>cocaine</b> induced receptor and transporter regulation by measuring levels of two proteins involved in receptor and transporter trafficking, dynamin 2 and G protein coupled receptor kinase 2 (<strong>GRK2</strong>).
+GRK2	drug	cocaine	19562697	This study investigated potential mechanisms of <b>cocaine</b> induced receptor and transporter regulation by measuring levels of two proteins involved in receptor and transporter trafficking, dynamin 2 and <strong>G protein coupled receptor kinase 2</strong> (<strong>GRK2</strong>).
+GRK2	drug	cocaine	19562697	Acute binge pattern <b>cocaine</b> administration produced a significant increase in both dynamin 2  and <strong>GRK2</strong> immunoreactivity (227% and 358% of control) in the nucleus accumbens and GKR2 (150% of control) in the caudate putamen.
+GRK2	addiction	intoxication	19562697	Acute <b>binge</b> pattern cocaine administration produced a significant increase in both dynamin 2  and <strong>GRK2</strong> immunoreactivity (227% and 358% of control) in the nucleus accumbens and GKR2 (150% of control) in the caudate putamen.
+GRK2	drug	cocaine	19562697	In contrast, dynamin 2 and <strong>GRK2</strong> were significantly decreased in the nucleus accumbens after chronic <b>cocaine</b>.
+GRK2	drug	cocaine	19562697	Pretreatment with either the dopamine (DA) D1 receptor antagonist SCH 23390 or D2 receptor antagonist eticlopride prior to acute <b>cocaine</b> blocked the upregulation of dynamin 2 and <strong>GRK2</strong> in the nucleus accumbens.
+GRK2	drug	alcohol	17156932	Under these conditions, immunoblotting showed a robust increase in phosphorylated cPKC immunoreactivity (p cPKC IR) in the spinal cord from chronic <b>ethanol</b> fed rats, whereas phosphorylated protein kinase A (PKA), dynamin II and G protein coupled receptor kinase 2 (<strong>GRK2</strong>) were not affected in the spinal cord of <b>ethanol</b> fed rats.
+GRK2	drug	alcohol	17156932	Under these conditions, immunoblotting showed a robust increase in phosphorylated cPKC immunoreactivity (p cPKC IR) in the spinal cord from chronic <b>ethanol</b> fed rats, whereas phosphorylated protein kinase A (PKA), dynamin II and <strong>G protein coupled receptor kinase 2</strong> (<strong>GRK2</strong>) were not affected in the spinal cord of <b>ethanol</b> fed rats.
+GRK2	drug	opioid	15849022	Whereas <b>morphine</b> treatment does not lead to major alterations in the expression of mu <b>opioid</b> receptors (MOR), there is transcriptional regulation of proteins involved in MOR trafficking such as <strong>GRK2</strong> or beta arrestin 2 as well as altered expression of other receptors such as dopamine receptors, NMDA receptors, GABA(A) receptor and alpha(2A) adrenoceptor.
+GRK2	drug	opioid	12384166	Acute and chronic <b>morphine</b> treatments and <b>morphine</b> withdrawal differentially regulate <strong>GRK2</strong> and GRK5 gene expression in rat brain.
+GRK2	addiction	withdrawal	12384166	Acute and chronic morphine treatments and morphine <b>withdrawal</b> differentially regulate <strong>GRK2</strong> and GRK5 gene expression in rat brain.
+GRK2	drug	opioid	12384166	The current study investigated the potential regulatory effects of acute and chronic <b>morphine</b> administration and withdrawal on <strong>GRK2</strong> and GRK5 gene expression in rat brain.
+GRK2	addiction	withdrawal	12384166	The current study investigated the potential regulatory effects of acute and chronic morphine administration and <b>withdrawal</b> on <strong>GRK2</strong> and GRK5 gene expression in rat brain.
+GRK2	drug	opioid	12384166	Chronic <b>morphine</b> treatment resulted in 30 70% down regulation of <strong>GRK2</strong> expression in cerebral cortex, hippocampus, thalamus, and locus coeruleus, opposite to what observed with the single <b>morphine</b> administration.
+GRK2	drug	opioid	12384166	Moreover, spontaneous and <b>naloxone</b> precipitated <b>morphine</b> withdrawal resulted in aberrant increases in <strong>GRK2</strong> and GRK5 mRNA levels in these brain regions.
+GRK2	addiction	withdrawal	12384166	Moreover, spontaneous and naloxone precipitated morphine <b>withdrawal</b> resulted in aberrant increases in <strong>GRK2</strong> and GRK5 mRNA levels in these brain regions.
+GRK2	drug	opioid	11040053	Identification of <strong>G protein coupled receptor kinase 2</strong> phosphorylation sites responsible for agonist stimulated delta <b>opioid</b> receptor phosphorylation.
+GRK2	drug	opioid	11040053	Taken together, we have demonstrated that agonist induced <b>opioid</b> receptor phosphorylation occurs exclusively at two phosphate acceptor sites (T358 and S363) of <strong>GRK2</strong> at the DOR carboxyl terminus.
+GRK2	drug	opioid	9489748	The effects of opiate drugs (<b>heroin</b>, <b>morphine</b>, and <b>methadone</b>) on the levels of G protein coupled receptor kinase 2 (<strong>GRK2</strong>) were studied in rat and human brain frontal cortices.
+GRK2	drug	opioid	9489748	The effects of opiate drugs (<b>heroin</b>, <b>morphine</b>, and <b>methadone</b>) on the levels of <strong>G protein coupled receptor kinase 2</strong> (<strong>GRK2</strong>) were studied in rat and human brain frontal cortices.
+GRK2	drug	opioid	9489748	The density of brain <strong>GRK2</strong> was measured by immunoblot assays in acute and chronic opiate treated rats as well as in opiate dependent rats after spontaneous or <b>naloxone</b> precipitated withdrawal and in human opiate addicts who had died of an opiate overdose.
+GRK2	addiction	withdrawal	9489748	The density of brain <strong>GRK2</strong> was measured by immunoblot assays in acute and chronic opiate treated rats as well as in opiate dependent rats after spontaneous or naloxone precipitated <b>withdrawal</b> and in human opiate addicts who had died of an opiate overdose.
+GRK2	drug	opioid	9489748	Acute treatments with <b>morphine</b> and <b>methadone</b> induced dose  and time dependent increases (8 22%) in total <strong>GRK2</strong> concentrations [higher increases were observed for the membrane associated enzyme (46%)].
+GRK2	drug	opioid	9489748	Spontaneous and <b>naloxone</b> precipitated withdrawal after chronic <b>morphine</b> or <b>methadone</b> induced a marked up regulation in the levels of total <strong>GRK2</strong> in the rat frontal cortex (18 25%).
+GRK2	addiction	withdrawal	9489748	Spontaneous and naloxone precipitated <b>withdrawal</b> after chronic morphine or methadone induced a marked up regulation in the levels of total <strong>GRK2</strong> in the rat frontal cortex (18 25%).
+GRK2	drug	opioid	9489748	These results suggest that <strong>GRK2</strong> is involved in the short term regulation of mu <b>opioid</b> receptors in vivo and that the activity of this regulatory kinase in brain could have a relevant role in opiate tolerance, dependence, and withdrawal.
+GRK2	addiction	dependence	9489748	These results suggest that <strong>GRK2</strong> is involved in the short term regulation of mu opioid receptors in vivo and that the activity of this regulatory kinase in brain could have a relevant role in opiate tolerance, <b>dependence</b>, and withdrawal.
+GRK2	addiction	withdrawal	9489748	These results suggest that <strong>GRK2</strong> is involved in the short term regulation of mu opioid receptors in vivo and that the activity of this regulatory kinase in brain could have a relevant role in opiate tolerance, dependence, and <b>withdrawal</b>.
+GRK2	drug	opioid	9413931	Finally, highly purified recombinant <strong>betaARK1</strong> proved active to phosphorylate enriched delta <b>opioid</b> receptor preparations in an <b>opioid</b> agonist dependent manner.
+GABRA1	drug	alcohol	30417952	Chronic <b>alcohol</b> exposure induced gut microbiota dysbiosis and its correlations with neuropsychic behaviors and brain BDNF/<strong>Gabra1</strong> changes in mice.
+GABRA1	drug	alcohol	30417952	was positively correlated with <b>alcohol</b> preference and negatively correlated with anxiety like behavior and BDNF/<strong>Gabra1</strong> changes in PFC.
+GABRA1	drug	alcohol	30417952	Taken together, our study showed that gut microbiota dysbiosis during chronic <b>alcohol</b> exposure was closely correlated with <b>alcohol</b> induced neuropsychic behaviors and BDNF/<strong>Gabra1</strong> expression, which provides a new perspective for understanding underlying mechanisms in <b>alcohol</b> addiction.
+GABRA1	addiction	addiction	30417952	Taken together, our study showed that gut microbiota dysbiosis during chronic alcohol exposure was closely correlated with alcohol induced neuropsychic behaviors and BDNF/<strong>Gabra1</strong> expression, which provides a new perspective for understanding underlying mechanisms in alcohol <b>addiction</b>.
+GABRA1	drug	alcohol	29520058	In rodents, GABAAR hypofunction results from decreases in <strong>Gabra1</strong> expression, although the underlying mechanism controlling <strong>Gabra1</strong> expression after chronic <b>ethanol</b> exposure is still unknown.
+GABRA1	drug	alcohol	29520058	We found that chronic <b>ethanol</b> exposure using either <b>ethanol</b> gavage or two bottle choice voluntary access paradigms decreased <strong>Gabra1</strong> expression and increased Hdac2 and Hdac3 expression.
+GABRA1	drug	alcohol	29520058	Administration of the HDAC inhibitor trichostatin A (TSA) after chronic <b>ethanol</b> exposure prevents the decrease in <strong>Gabra1</strong> expression and function as well as the increase in Hdac2 and Hdac3 expression in both the cortex and the medial prefrontal cortex (mPFC).
+GABRA1	drug	alcohol	29520058	Chronic <b>ethanol</b> exposure and withdrawal, but not acute <b>ethanol</b> exposure or acute withdrawal, cause a selective upregulation of HDAC2 and HDAC3 associated with the <strong>Gabra1</strong> promoter that accompanies a decrease in H3 acetylation of the <strong>Gabra1</strong> promoter and the reduction in GABAAR α1 subunit expression.
+GABRA1	addiction	withdrawal	29520058	Chronic ethanol exposure and <b>withdrawal</b>, but not acute ethanol exposure or acute <b>withdrawal</b>, cause a selective upregulation of HDAC2 and HDAC3 associated with the <strong>Gabra1</strong> promoter that accompanies a decrease in H3 acetylation of the <strong>Gabra1</strong> promoter and the reduction in GABAAR α1 subunit expression.
+GABRA1	drug	benzodiazepine	29163035	Additionally, we identified Gabra genes as transcriptional targets of NPAS2, found that Npas2 null mutant mice exhibit reduced sensitivity to the GABAa positive allosteric modulator, <b>diazepam</b> and that knockdown of Npas2 reduced <strong>Gabra1</strong> expression and response to <b>diazepam</b> in the ventral striatum.
+GABRA1	drug	alcohol	29156239	In this report, we utilized induced pluripotent stem cell (iPSCs) derived neural cell cultures obtained from healthy individuals (CTLs) and those with <b>alcohol</b> dependence (ADs) to 1) examine the effect of 21 day <b>alcohol</b> exposure on mRNA expression of three genes encoding GABAA receptor subunits (<strong>GABRA1</strong>, GABRG2, and GABRD) using quantitative PCR, and 2) examine the effect of acute and chronic <b>alcohol</b> exposure on GABA evoked currents using whole cell patch clamp electrophysiology.
+GABRA1	addiction	dependence	29156239	In this report, we utilized induced pluripotent stem cell (iPSCs) derived neural cell cultures obtained from healthy individuals (CTLs) and those with alcohol <b>dependence</b> (ADs) to 1) examine the effect of 21 day alcohol exposure on mRNA expression of three genes encoding GABAA receptor subunits (<strong>GABRA1</strong>, GABRG2, and GABRD) using quantitative PCR, and 2) examine the effect of acute and chronic alcohol exposure on GABA evoked currents using whole cell patch clamp electrophysiology.
+GABRA1	drug	alcohol	29156239	Following 21 day <b>alcohol</b> exposure, significant treatment effects were observed in <strong>GABRA1</strong>, GABRG2, and GABRD mRNA expression.
+GABRA1	drug	alcohol	28798030	<b>Ethanol</b> Exposure Regulates <strong>Gabra1</strong> Expression via Histone Deacetylation at the Promoter in Cultured Cortical Neurons.
+GABRA1	drug	alcohol	28798030	Overall our results indicate that <b>ethanol</b> deacetylates histones associated with the <strong>Gabra1</strong> promoter through class I HDACs and that pharmacologic, genetic, or epigenetic intervention prevents decreases in α1 expression in cultured cortical neurons.
+GABRA1	drug	alcohol	26902358	Acute exposure to <b>ethanol</b> elevated expression of genes Gabrb1 (by 1.7 times), <strong>Gabra1</strong> (by 3.8 times), and Gabra4 (by 6.5 times), although it diminished expression of Gabra2 gene by 1.4 times.
+GABRA1	drug	alcohol	26357588	Eleven hours after removal of <b>alcohol</b>, Gabra4 was downregulated, with a modest increase in the expression of Gabrg2, but no change in the expression of <strong>Gabra1</strong>, Gabrd, or Gabrb2.
+GABRA1	drug	cocaine	26096050	Adolescent onset <strong>Gabra1</strong> knockdown delayed the acquisition of a <b>cocaine</b> reinforced instrumental response but spared <b>cocaine</b> seeking in extinction and in a cue induced reinstatement procedure.
+GABRA1	addiction	relapse	26096050	Adolescent onset <strong>Gabra1</strong> knockdown delayed the acquisition of a cocaine reinforced instrumental response but spared cocaine <b>seeking</b> in extinction and in a cue induced <b>reinstatement</b> procedure.
+GABRA1	drug	alcohol	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., <strong>GABRA1</strong>, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of <b>alcohol</b>.
+GABRA1	drug	opioid	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain reward processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., <strong>GABRA1</strong>, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and <b>opioid</b> (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact reinforcing properties of alcohol.
+GABRA1	addiction	reward	25655461	Genetic biomarkers included neurotransmitter pathways associated with brain <b>reward</b> processes for dopaminergic (e.g., DRD2, MAOA, and COMT), serotoninergic (e.g., HTR3A, HTR1B, HTR3B, and SLC6A4), GABAergic (e.g., <strong>GABRA1</strong>, GABRA2, and GABRG1), glutaminergic (GAD1, GRIK3, and GRIN2C) and opioid (e.g., OPRM1, OPRD1, and OPRK1) pathways which presumably impact <b>reinforcing</b> properties of alcohol.
+GABRA1	drug	alcohol	25191505	A total of 186 <b>alcohol</b> dependent subjects (in the first phase 139, then 47 more samples) and 182 controls were genotyped for 25 single nucleotide polymorphisms (SNPs) of genes encoding the alpha 1 subunit of GABA A receptor (<strong>GABRA1</strong>) and subunits 1 and 2 of GABA B receptor (GABBR1 and GABBR2).
+GABRA1	drug	alcohol	24136292	To reconcile the conflicting associations with substance dependence traits, we performed a meta analysis of variants in the GABAA receptor genes (GABRB2, GABRA6, <strong>GABRA1</strong>, and GABRG2 on chromosome 5q and GABRA2 on chromosome 4p12) using genotype data from 4739 cases of <b>alcohol</b>, opioid, or methamphetamine dependence and 4924 controls.
+GABRA1	drug	amphetamine	24136292	To reconcile the conflicting associations with substance dependence traits, we performed a meta analysis of variants in the GABAA receptor genes (GABRB2, GABRA6, <strong>GABRA1</strong>, and GABRG2 on chromosome 5q and GABRA2 on chromosome 4p12) using genotype data from 4739 cases of alcohol, opioid, or <b>methamphetamine</b> dependence and 4924 controls.
+GABRA1	drug	opioid	24136292	To reconcile the conflicting associations with substance dependence traits, we performed a meta analysis of variants in the GABAA receptor genes (GABRB2, GABRA6, <strong>GABRA1</strong>, and GABRG2 on chromosome 5q and GABRA2 on chromosome 4p12) using genotype data from 4739 cases of alcohol, <b>opioid</b>, or methamphetamine dependence and 4924 controls.
+GABRA1	addiction	dependence	24136292	To reconcile the conflicting associations with substance <b>dependence</b> traits, we performed a meta analysis of variants in the GABAA receptor genes (GABRB2, GABRA6, <strong>GABRA1</strong>, and GABRG2 on chromosome 5q and GABRA2 on chromosome 4p12) using genotype data from 4739 cases of alcohol, opioid, or methamphetamine <b>dependence</b> and 4924 controls.
+GABRA1	drug	amphetamine	19219857	Three genes (COMT, DRD4, and <strong>GABRA1</strong>) were associated with <b>METH</b> abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with <b>METH</b> dependence, two (AKT1 and GABRG2) with <b>METH</b> abuse/dependence, and four (DTNBP1, OPRM1, SNCA, and SOD2) with <b>METH</b> psychosis.
+GABRA1	addiction	dependence	19219857	Three genes (COMT, DRD4, and <strong>GABRA1</strong>) were associated with METH abuse, nine (ARRB2, BDNF, CYP2D6, GLYT1, GSTM1, GSTP1, PDYN, PICK1, and SLC22A3) with METH <b>dependence</b>, two (AKT1 and GABRG2) with METH abuse/<b>dependence</b>, and four (DTNBP1, OPRM1, SNCA, and SOD2) with METH psychosis.
+GABRA1	drug	alcohol	18180303	Changes in GABA(A) receptor alpha1 subunit gene (<strong>GABRA1</strong>) expression have been reported in animal models of epilepsy, <b>alcohol</b> abuse, withdrawal, and stress.
+GABRA1	addiction	withdrawal	18180303	Changes in GABA(A) receptor alpha1 subunit gene (<strong>GABRA1</strong>) expression have been reported in animal models of epilepsy, alcohol abuse, <b>withdrawal</b>, and stress.
+GABRA1	drug	opioid	17440936	Single nucleotide polymorphisms (SNPs) of the GABAA receptor subunits GABRB2, GABRA6, <strong>GABRA1</strong>, and GABRG2 were examined in 178 male Han Chinese <b>heroin</b> dependent and 170 male control subjects.
+GABRA1	drug	alcohol	16792556	Association between <strong>GABRA1</strong> and drinking behaviors in the collaborative study on the genetics of <b>alcoholism</b> sample.
+GABRA1	drug	alcohol	16792556	In <strong>GABRA1</strong>, we found evidence of association with several of the drinking behavior phenotypes, including COGA <b>alcohol</b> dependence, history of blackouts, age at first drunkenness, and level of response to <b>alcohol</b>.
+GABRA1	addiction	dependence	16792556	In <strong>GABRA1</strong>, we found evidence of association with several of the drinking behavior phenotypes, including COGA alcohol <b>dependence</b>, history of blackouts, age at first drunkenness, and level of response to alcohol.
+GABRA1	drug	alcohol	16792556	We found evidence for association between <strong>GABRA1</strong> and COGA <b>alcohol</b> dependence, history of blackouts, age at first drunkenness, and level of response to <b>alcohol</b>.
+GABRA1	addiction	dependence	16792556	We found evidence for association between <strong>GABRA1</strong> and COGA alcohol <b>dependence</b>, history of blackouts, age at first drunkenness, and level of response to alcohol.
+GABRA1	drug	alcohol	15690551	Chromosome 5 contains a cluster of GABA(A) receptor genes, <strong>GABRA1</strong>, GABRA6, GABRB2, and GABRG2, which have been among the most extensively studied in relation to <b>alcohol</b> use.
+GABRA1	drug	alcohol	12555233	Genes encoding <strong>GABRA1</strong> and GABRA6, on chromosome 5, did not provide evidence for association with <b>alcoholism</b>.
+ERBB2	drug	nicotine	31125062	In certain subgroups, PFS was positively associated with PD L1 expression (KRAS, EGFR) and with <b>smoking</b> status (BRAF, <strong>HER2</strong>).
+ERBB2	drug	alcohol	30611309	Normally, 35% of breast cancer is Erb B2 Receptor Tyrosine Kinase 2 (<strong>ERBB2</strong>) positive that predisposes to poor prognosis and relapse, while <b>ethanol</b> drinking leads to invasion of their <strong>ERBB2</strong> positive cells triggering the phosphorylation status of mitogen activated protein kinase.
+ERBB2	addiction	relapse	30611309	Normally, 35% of breast cancer is Erb B2 Receptor Tyrosine Kinase 2 (<strong>ERBB2</strong>) positive that predisposes to poor prognosis and <b>relapse</b>, while ethanol drinking leads to invasion of their <strong>ERBB2</strong> positive cells triggering the phosphorylation status of mitogen activated protein kinase.
+ERBB2	drug	alcohol	30611309	Normally, 35% of breast cancer is <strong>Erb B2 Receptor Tyrosine Kinase 2</strong> (<strong>ERBB2</strong>) positive that predisposes to poor prognosis and relapse, while <b>ethanol</b> drinking leads to invasion of their <strong>ERBB2</strong> positive cells triggering the phosphorylation status of mitogen activated protein kinase.
+ERBB2	addiction	relapse	30611309	Normally, 35% of breast cancer is <strong>Erb B2 Receptor Tyrosine Kinase 2</strong> (<strong>ERBB2</strong>) positive that predisposes to poor prognosis and <b>relapse</b>, while ethanol drinking leads to invasion of their <strong>ERBB2</strong> positive cells triggering the phosphorylation status of mitogen activated protein kinase.
+ERBB2	drug	alcohol	30611309	In this study, we demonstrate that <b>ethanol</b> administration promotes STARD10 and <strong>ERBB2</strong> expression that is significantly associated with increased cell malignancy and aggressiveness.
+ERBB2	drug	alcohol	30611309	We investigated the effect of <b>ethanol</b> on STARD10 <strong>ERBB2</strong> cross talk in breast cancer cells, MMTV neu transgenic mice and in clinical <strong>ERBB2</strong> positive breast cancer specimens with Western Blotting and Real time PCR.
+ERBB2	drug	alcohol	30611309	<b>Ethanol</b> administration induces STARD10 and <strong>ERBB2</strong> expression in vitro and in vivo.
+ERBB2	drug	alcohol	30611309	<b>Ethanol</b> and STARD10 mediated cellular membrane fluidity and intracellular calcium concentration impact <strong>ERBB2</strong> signaling pathway as evaluated by enhanced p65 nuclear translocation and binding to both <strong>ERBB2</strong> and STARD10 promoters.
+ERBB2	drug	alcohol	30611309	Taken together, our data demonstrate that <b>ethanol</b> can modulate <strong>ERBB2</strong>'s function in breast cancer via a novel interplay with STARD10.
+ERBB2	drug	alcohol	29774782	We have used phospho receptor tyrosine kinase (RTK) arrays to screen the impact of <b>ethanol</b> on TBI induced activation of RTK in somatosensory cortex, identifying <strong>ErbB2</strong>/ErbB3 among the RTKs activated by TBI and suppressed by <b>ethanol</b>.
+ERBB2	drug	nicotine	28974261	Why are mutation rates in epidermal growth factor receptor (EGFR) and erb b2 receptor tyrosine kinase 2 (<strong>ERBB2</strong>) higher in lung cancer from never <b>smokers</b> than that from <b>smokers</b>?
+ERBB2	drug	nicotine	28974261	Why are mutation rates in epidermal growth factor receptor (EGFR) and <strong>erb b2 receptor tyrosine kinase 2</strong> (<strong>ERBB2</strong>) higher in lung cancer from never <b>smokers</b> than that from <b>smokers</b>?
+ERBB2	drug	nicotine	27008586	Compared with the <strong>HER2</strong> insertion negative group, patients with <strong>HER2</strong> insertions were more likely to be never <b>smokers</b> (97.1 %, 34/35 patients, P < 0.001), significantly associated with female (91.4 %, 32/35 patients, P < 0.001), adenocarcinoma (91.4 %, 32/35 patients, P = 0.01), and with a tendency to be no more than 60 years of age (71.4 %, 25/35 patients, P = 0.051).
+ERBB2	drug	opioid	25734987	<b>Morphine</b> does not facilitate breast cancer progression in two preclinical mouse models for human invasive lobular and <strong>HER2</strong>⁺ breast cancer.
+ERBB2	drug	opioid	25734987	Using preclinical mouse models for metastatic invasive lobular and <strong>HER2</strong> breast cancer, we show that analgesic doses of <b>morphine</b> do not affect mammary tumor growth, angiogenesis, and the composition of tumor infiltrating immune cells.
+ERBB2	addiction	relapse	23775406	ANCCA expression was evaluated by immunohistochemistry in 143 surgically resected lung adenocarcinomas and was correlated with clinicopathologic and molecular variables including adenocarcinoma histologic subtypes, tumor, node, metastasis status, <b>relapse</b> free survival, overall survival, EGFR mutations, KRAS mutations, <strong>HER2</strong> mutations and ALK fusions.
+ERBB2	drug	nicotine	21655907	In addition, most adenocarcinomas in never <b>smokers</b> harbor one of the proto oncogene aberrations that occur in a mutually exclusive manner (EGFR mutation, KRAS mutation, <strong>HER2</strong> mutations, or ALK translocation).
+ERBB2	drug	cannabinoid	20649976	<b>Cannabinoids</b> reduce <strong>ErbB2</strong> driven breast cancer progression through Akt inhibition.
+ERBB2	addiction	relapse	20649976	Although specific <strong>ErbB2</strong> targeted therapies have been designed, only a small percentage of patients respond to these treatments and most of them eventually <b>relapse</b>.
+ERBB2	drug	cannabinoid	20649976	The purpose of this study was to determine whether <b>cannabinoids</b> might constitute a new therapeutic tool for the treatment of <strong>ErbB2</strong> positive breast tumors.
+ERBB2	drug	cannabinoid	20649976	We also found that 91% of <strong>ErbB2</strong> positive tumors express the non psychotropic <b>cannabinoid</b> receptor CB2.
+ERBB2	drug	cannabinoid	20649976	Taken together, these results provide a strong preclinical evidence for the use of <b>cannabinoid</b> based therapies for the management of <strong>ErbB2</strong> positive breast cancer.
+ERBB2	drug	nicotine	18705409	Statistically significant associations between high Ki67 and poorly differentiated tumors (P = 0.016) and a <b>smoking</b> history (P = 0.053); p53 positivity and high Ki67 (P = 0.002); <strong>HER 2</strong> positivity and adenocarcinoma subtype (P = 0.015) and presence of lymph node involvement (P = 0.006); and Bcl 2 positivity and squamous cell carcinoma subtype (P = 0.058) were observed.
+DUSP26	addiction	withdrawal	27618597	Similarly, in the paw <b>withdrawal</b> test, this substance generated a strong analgesic effect (with over 200% of analgesia) in the control group, whereas its action in the rats with <strong>DSP 4</strong> lesions was statistically significant.
+DUSP26	drug	alcohol	26549324	While degeneration [N (2 chloroethyl) N ethyl 2 bromobenzylamine hydrochloride, <strong>DSP 4</strong>, intraperitoneal route] or silencing (lidocaine or muscimol, both via intra LC route) of the LC noradrenergic neurons decreased, phenylephrine via the intra LC route reinstated <b>ethanol</b> self administration.
+DUSP26	drug	alcohol	26549324	<b>Ethanol</b> self administration significantly increased tyrosine hydroxylase immunoreactivity in pVTA and LC; the response was blocked by <strong>DSP 4</strong> pre treatment.
+DUSP26	addiction	dependence	25601230	<strong>DSP 4</strong> treated SD rats demonstrated a <b>dependence</b> like phenotype, whereas WKY rats were unchanged.
+DUSP26	drug	cocaine	20678524	The effect of denervation of the locus coeruleus projections with N (2 chloroethyl) N ethyl 2 bromobenzylamine (<strong>DSP 4</strong>) on <b>cocaine</b> induced locomotion and place preference in rats.
+DUSP26	drug	cocaine	20678524	The potential contribution of locus coeruleus (LC) derived noradrenaline (NA) in the motor activating and rewarding effects of <b>cocaine</b> (15 mg/kg) were assessed following administration of the neurotoxin N (2 chloroethyl) N ethyl 2 bromobenzylamine (<strong>DSP 4</strong>).
+DUSP26	drug	cocaine	20678524	In Experiment 1, administration of 10 mg/kg of <strong>DSP 4</strong> similarly to substantial denervation with 50 mg/kg of <strong>DSP 4</strong> significantly attenuated the activating effects of <b>cocaine</b> during the first <b>cocaine</b> paired training session (30 min) in the conditioned place preference (CPP) apparatus.
+DUSP26	addiction	reward	20678524	In Experiment 1, administration of 10 mg/kg of <strong>DSP 4</strong> similarly to substantial denervation with 50 mg/kg of <strong>DSP 4</strong> significantly attenuated the activating effects of cocaine during the first cocaine paired training session (30 min) in the conditioned place preference (<b>CPP</b>) apparatus.
+DUSP26	drug	cocaine	20678524	<b>Cocaine</b> CPP as measured by increment of time spent in the previously <b>cocaine</b> paired chamber during drug free conditions before and after <b>cocaine</b> paired trainings was clearly revealed only in animals with intact projections from the LC, and was entirely absent after a large lesion of LC projections by <strong>DSP 4</strong> (50 mg/kg).
+DUSP26	addiction	reward	20678524	Cocaine <b>CPP</b> as measured by increment of time spent in the previously cocaine paired chamber during drug free conditions before and after cocaine paired trainings was clearly revealed only in animals with intact projections from the LC, and was entirely absent after a large lesion of LC projections by <strong>DSP 4</strong> (50 mg/kg).
+DUSP26	drug	cocaine	20678524	Because recovery of noradrenaline levels by the end of experiment did not allow assessment of the efficacy of the neurotoxin, the effect of <strong>DSP 4</strong> pre treatment on the acute psychomotor effect of <b>cocaine</b> was re examined in an independent experiment (Experiment 2).
+DUSP26	drug	cocaine	20678524	Near complete denervation of the LC projections again reduced the effect of <b>cocaine</b>, but the lower dose of <strong>DSP 4</strong> had no effect, suggesting that small lesions of the LC do not have a robust impact.
+DUSP26	drug	psychedelics	20002520	Experiment 1 investigated <b>MDMA</b> induced changes in levels of the serotonin transporter (SERT) and the vesicular monoamine transporter 2 (VMAT 2) in the hippocampus, a region with sparse dopaminergic innervation, after lesioning noradrenergic input with N (2 chloroethyl) N ethyl 2 bromobenzylamine (<strong>DSP 4</strong>).
+DUSP26	drug	psychedelics	20002520	Adult male Sprague Dawley rats were administered 100 mg/kg <strong>DSP 4</strong> or saline 1 week prior to either an <b>MDMA</b> (10 mg/kg x 4) or saline binge.
+DUSP26	addiction	intoxication	20002520	Adult male Sprague Dawley rats were administered 100 mg/kg <strong>DSP 4</strong> or saline 1 week prior to either an MDMA (10 mg/kg x 4) or saline <b>binge</b>.
+DUSP26	drug	psychedelics	20002520	Two weeks following the binge treatment, the <strong>DSP 4</strong>/<b>MDMA</b> group unexpectedly showed little change in hippocampal VMAT 2 protein expression compared with <strong>DSP 4</strong>/Saline controls, despite large reductions in SERT levels in all regions examined in the <b>MDMA</b> treated animals.
+DUSP26	addiction	intoxication	20002520	Two weeks following the <b>binge</b> treatment, the <strong>DSP 4</strong>/MDMA group unexpectedly showed little change in hippocampal VMAT 2 protein expression compared with <strong>DSP 4</strong>/Saline controls, despite large reductions in SERT levels in all regions examined in the MDMA treated animals.
+DUSP26	drug	amphetamine	17156751	In the present study the <b>amphetamine</b> induced locomotor activity and behavioral sensitization to <b>amphetamine</b> (0.5 mg/kg) was investigated in rats with high or low spontaneous exploratory activity (HE  and LE rats, respectively) after partial denervation of the locus coeruleus (LC) projections with a low dose of the selective neurotoxin <strong>DSP 4</strong> (N (2 chloroethyl) N ethyl 2 bromobenzylamine; 10 mg/kg).
+DUSP26	addiction	sensitization	17156751	In the present study the amphetamine induced locomotor activity and behavioral <b>sensitization</b> to amphetamine (0.5 mg/kg) was investigated in rats with high or low spontaneous exploratory activity (HE  and LE rats, respectively) after partial denervation of the locus coeruleus (LC) projections with a low dose of the selective neurotoxin <strong>DSP 4</strong> (N (2 chloroethyl) N ethyl 2 bromobenzylamine; 10 mg/kg).
+DUSP26	drug	amphetamine	17156751	<b>Amphetamine</b> stimulated locomotor activity was attenuated by the <strong>DSP 4</strong> pretreatment only in the HE rats and this effect persisted over repeated testing.
+DUSP26	addiction	withdrawal	15781512	Depletion of systemic norepinephrine with the neurotoxin <strong>DSP 4</strong> caused a reduction in baseline <b>withdrawal</b> latencies and prevented isoflurane pronociception.
+DUSP26	drug	opioid	14715456	Effects of alpha adrenoceptor agonists in chronic <b>morphine</b> administered <strong>DSP4</strong> treated rats: evidence for functional cross sensitization.
+DUSP26	addiction	sensitization	14715456	Effects of alpha adrenoceptor agonists in chronic morphine administered <strong>DSP4</strong> treated rats: evidence for functional cross <b>sensitization</b>.
+DUSP26	drug	opioid	14715456	Five experiments were performed to study the effects of the Alpha adrenoceptor agonists, clonidine and guanfacine, upon spontaneous motor activity in chronically <b>morphine</b> administered <strong>DSP4</strong> treated and control rats.
+DUSP26	drug	opioid	14715456	<strong>DSP4</strong> pretreatment and chronic <b>morphine</b> injections each reduced motor activity during the first 30 min of testing; combined <strong>DSP4</strong> and <b>morphine</b> treatment potentiated the hypoactivity.
+DUSP26	drug	opioid	14715456	Habituation quotients indicated deficits in habituation to the novel test environment by the Vehicle <b>morphine</b> (Quoteint2 only) and <strong>DSP4</strong> <b>morphine</b> groups.
+DUSP26	drug	opioid	14715456	Acute clonidine treatment (0.04 mg/kg s.c.) reduced motor activity during the first 30 min of testing but attenuated or blocked the <b>morphine</b> induced hypoactivity in <strong>DSP4</strong> treated and control rats.
+DUSP26	drug	opioid	14715456	During the 60 90 min test period, clonidine, but not guanfacine (0.08 mg/kg), potentiated <b>morphine</b> induced hyperactivity in control rats; acute clonidine enhanced this effect, whereas acute guanfacine reduced it, in the <strong>DSP4</strong> treated rats.
+DUSP26	drug	opioid	14715456	<b>Naloxone</b> (0.1 mg/kg s.c.), injected after the 1st 30 min of testing, potentiated markely the clonidine induced elevations of motor activity in <b>morphine</b> administered control rats; in the <strong>DSP4</strong> treated rats, these effects were dramatically potentiated, underlining the cross sensitivity effect.
+DUSP26	drug	opioid	14715456	Acute guanfacine treatment reduced motor activity during the first 30 min of testing but did not attenuate reliably <b>morphine</b> induced hypoactivity in control or <strong>DSP4</strong> rats.
+DUSP26	drug	opioid	14715456	<b>Naloxone</b> did not potentiate the guanfacine induced hyperactivity of <b>morphine</b> administered control rats but induced a marked enhancement in the <strong>DSP4</strong> treated rats, a specific case of cross reactivity.
+DUSP26	drug	opioid	14715456	The major findings pertain to a cross sensitization effect of <b>morphine</b> upon clonidine induced motor activity in both <strong>DSP4</strong> treated and control rats, and to a lesser extent between <b>morphine</b> and guanfacine in NA denervated rats only.
+DUSP26	addiction	sensitization	14715456	The major findings pertain to a cross <b>sensitization</b> effect of morphine upon clonidine induced motor activity in both <strong>DSP4</strong> treated and control rats, and to a lesser extent between morphine and guanfacine in NA denervated rats only.
+DUSP26	drug	opioid	12963158	), an <b>opioid</b> antagonist, and <strong>DSP 4</strong> (50 mg/kg, i.p.
+DUSP26	drug	opioid	8858297	The ability of N (2 chloroethyl) N ethyl 2 bromobenzylamine (<strong>DSP 4</strong>), a potent and selective noradrenergic neurotoxic compound, to modify <b>morphine</b> tolerance and dependence was investigated in mice <strong>DSP 4</strong> pretreatment, either 50 or 100 mg/kg i.p., had no effect on the development of tolerance to the analgesic effect of <b>morphine</b> evaluated by the tail flick test.
+DUSP26	addiction	dependence	8858297	The ability of N (2 chloroethyl) N ethyl 2 bromobenzylamine (<strong>DSP 4</strong>), a potent and selective noradrenergic neurotoxic compound, to modify morphine tolerance and <b>dependence</b> was investigated in mice <strong>DSP 4</strong> pretreatment, either 50 or 100 mg/kg i.p., had no effect on the development of tolerance to the analgesic effect of morphine evaluated by the tail flick test.
+DUSP26	drug	opioid	8858297	On the contrary, the higher dose of <strong>DSP 4</strong> prevented repetitive vertical jumping, a major <b>naloxone</b> precipitated withdrawal symptom in mice.
+DUSP26	addiction	withdrawal	8858297	On the contrary, the higher dose of <strong>DSP 4</strong> prevented repetitive vertical jumping, a major naloxone precipitated <b>withdrawal</b> symptom in mice.
+DUSP26	drug	opioid	8786160	In the interaction studies, pretreatment with the <b>opioid</b> antagonist, <b>naloxone</b> (1 mg/kg) and the central noradrenaline depleter, <strong>DSP 4</strong> (50 mg/kg) attenuated AI analgesia by differential degrees in both experimental models, whereas, the serotonin synthesis inhibitor, PCPA (300 mg/kg) potentiated the same.
+DUSP26	drug	opioid	7540267	The involvement of neurones of the locus coeruleus (LC) in expression of opiate withdrawal behaviour was tested in <b>morphine</b> dependent rats using N 2 chloroethyl N ethyl 2 bromobenzylamine (<strong>DSP4</strong>), a neurotoxin selective for noradrenergic terminals arising from LC.
+DUSP26	addiction	withdrawal	7540267	The involvement of neurones of the locus coeruleus (LC) in expression of opiate <b>withdrawal</b> behaviour was tested in morphine dependent rats using N 2 chloroethyl N ethyl 2 bromobenzylamine (<strong>DSP4</strong>), a neurotoxin selective for noradrenergic terminals arising from LC.
+DUSP26	drug	opioid	7509021	pretreatment with the noradrenergic neurotoxin <strong>DSP 4</strong> and beta 1  and beta 2 adrenoceptor antagonists on the expression of <b>morphine</b> withdrawal signs were investigated in mice.
+DUSP26	addiction	withdrawal	7509021	pretreatment with the noradrenergic neurotoxin <strong>DSP 4</strong> and beta 1  and beta 2 adrenoceptor antagonists on the expression of morphine <b>withdrawal</b> signs were investigated in mice.
+DUSP26	drug	opioid	7509021	Treatment with <strong>DSP 4</strong> before the <b>naloxone</b> challenge suppressed the expression of <b>morphine</b> withdrawal signs, including jumping and "wet dog" shakes.
+DUSP26	addiction	withdrawal	7509021	Treatment with <strong>DSP 4</strong> before the naloxone challenge suppressed the expression of morphine <b>withdrawal</b> signs, including jumping and "wet dog" shakes.
+DUSP26	drug	cocaine	2070264	Such potentiating effects of <b>cocaine</b> on GABA mediated inhibition were not evident in animals pretreated with the selective noradrenergic toxins <strong>DSP 4</strong>.
+DUSP26	drug	benzodiazepine	3126522	Depletion of central noradrenaline produced by systemic injections of <strong>DSP4</strong> did not affect <b>diazepam</b> induced place preference conditioning.
+DUSP26	drug	amphetamine	3110849	<strong>DSP4</strong> alters the effect of d <b>amphetamine</b> on variable interval performance: analysis in terms of Herrnstein's equation.
+DUSP26	drug	amphetamine	3110849	The effect of d <b>amphetamine</b> (0.1 3.2 mg/kg) on performance in variable interval 1 min and variable interval 12 min schedules of positive reinforcement was examined in ten rats treated with the selective noradrenaline neurotoxin <strong>DSP4</strong> and 12 control rats.
+DUSP26	addiction	reward	3110849	The effect of d amphetamine (0.1 3.2 mg/kg) on performance in variable interval 1 min and variable interval 12 min schedules of positive <b>reinforcement</b> was examined in ten rats treated with the selective noradrenaline neurotoxin <strong>DSP4</strong> and 12 control rats.
+DUSP26	drug	amphetamine	3110849	In the case of both schedules, lower doses of d <b>amphetamine</b> were more suppressant and higher doses less suppressant in the <strong>DSP4</strong> treated group than in the control group.
+DUSP26	drug	amphetamine	3110849	The results indicate that treatment with <strong>DSP4</strong> attenuated both the facilitatory and the suppressant effects of d <b>amphetamine</b> on variable interval performance.
+DUSP26	drug	alcohol	3816531	Suppression of <b>ethanol</b> tolerance and dependence in rats treated with <strong>DSP 4</strong>, a noradrenergic neurotoxin.
+DUSP26	addiction	dependence	3816531	Suppression of ethanol tolerance and <b>dependence</b> in rats treated with <strong>DSP 4</strong>, a noradrenergic neurotoxin.
+DUSP26	drug	alcohol	3816531	The formation of tolerance to the hypothermic effect of <b>ethanol</b> was inhibited in rats after intraperitoneal injection of the neurotoxin <strong>DSP 4</strong> 50 mg/kg.
+DUSP26	drug	amphetamine	3011984	alpha methyltyrosine, N 2 chloroethyl N ethyl 2 bromobenzylamine (<strong>DSP 4</strong>), pimozide, remoxipride and prazosin did not antagonize the effect of PCA nor did (+) <b>amphetamine</b> inhibit the cage leaving response.
+DUSP26	addiction	reward	3837857	p Chloroamphetamine caused a dose dependent ejaculatory response that was inhibited by the inhibitor of the synthesis of 5 hydroxytryptamine (5 HT), p chlorophenylalanine (PCPA), neurotoxic doses of PCA, reserpine, <strong>DSP 4</strong> a selective noradrenergic neurotoxin given 48 hr before PCA, the inhibitor of synthesis of noradrenaline (NA) FLA 63, the specific inhibitors of uptake of 5 HT, alaproclate, fluoxetine and norzimeldine and the selective inhibitor of the uptake of NA, <b>CPP</b> 199, the E form of norzimeldine.
+DAP	addiction	addiction	32080764	This is a secondary analysis of the baseline survey of the European Drug <b>Addiction</b> Prevention (EU <strong>Dap</strong>) trial which took place in seven European countries and involved 7079 students.
+DAP	addiction	addiction	29453006	The <strong>DAP</strong> is a novel source of information for healthcare decisions and can empirically inform law enforcement about drug misuse and <b>addiction</b>.
+DAP	drug	opioid	27340958	A county level analysis of <b>opioid</b> prescriptions (N = 1.22 million) reported to the Maine Prescription Monitoring Program (M PMP) in 2014 and the agents implicated in arrests as reported to the Maine Diversion Alert Program (<strong>DAP</strong>, N = 2,700) in 2014/15 also was completed.
+DAP	drug	opioid	27340958	Continued vigilance and use of tools like the PMP and <strong>DAP</strong> are necessary to minimize nonmedical use of <b>opioids</b> in Maine.
+DAP	drug	alcohol	26894657	This study aimed to describe the process of cultural adaptation and evaluation of the Brazilian Portuguese language of the European Drug Addiction Prevention Trial (EU <strong>Dap</strong>) questionnaire to identify <b>alcohol</b>, tobacco, and other drug use among adolescents.
+DAP	drug	nicotine	26894657	This study aimed to describe the process of cultural adaptation and evaluation of the Brazilian Portuguese language of the European Drug Addiction Prevention Trial (EU <strong>Dap</strong>) questionnaire to identify alcohol, <b>tobacco</b>, and other drug use among adolescents.
+DAP	addiction	addiction	26894657	This study aimed to describe the process of cultural adaptation and evaluation of the Brazilian Portuguese language of the European Drug <b>Addiction</b> Prevention Trial (EU <strong>Dap</strong>) questionnaire to identify alcohol, tobacco, and other drug use among adolescents.
+DAP	drug	alcohol	27933317	This study examined the effects of maternal <b>alcohol</b> consumption and binge drinking during pregnancy on children's Draw A Person (<strong>DAP</strong>) scores.
+DAP	addiction	intoxication	27933317	This study examined the effects of maternal alcohol consumption and <b>binge</b> drinking during pregnancy on children's Draw A Person (<strong>DAP</strong>) scores.
+DAP	drug	alcohol	27933317	Findings suggest that prenatal exposure to moderate weekly doses of <b>alcohol</b> and binge drinking episodes are associated with lowered scores on the <strong>DAP</strong>.
+DAP	addiction	intoxication	27933317	Findings suggest that prenatal exposure to moderate weekly doses of alcohol and <b>binge</b> drinking episodes are associated with lowered scores on the <strong>DAP</strong>.
+DAP	drug	alcohol	25817357	The influence of the new enkephalin derivative, cyclo[N(ε),N(β) carbonyl d Lys(2),<strong>Dap</strong>(5)] enkephalinamide (cUENK6), on reinstatement of <b>ethanol</b> induced conditioned place preference in rats.
+DAP	addiction	relapse	25817357	The influence of the new enkephalin derivative, cyclo[N(ε),N(β) carbonyl d Lys(2),<strong>Dap</strong>(5)] enkephalinamide (cUENK6), on <b>reinstatement</b> of ethanol induced conditioned place preference in rats.
+DAP	drug	alcohol	25817357	The aim of the present study was to determine whether a new cyclic analog of enkephalin, cyclo[N(ε),N(β) carbonyl d Lys(2),<strong>Dap</strong>(5)] enkephalinamide (cUENK6), a preferential μ (MORs), and, to a lower extent, a δ opioid receptor (DORs) agonist in vitro, could reinstate <b>ethanol</b> induced conditioned place preference (CPP).
+DAP	drug	opioid	25817357	The aim of the present study was to determine whether a new cyclic analog of enkephalin, cyclo[N(ε),N(β) carbonyl d Lys(2),<strong>Dap</strong>(5)] enkephalinamide (cUENK6), a preferential μ (MORs), and, to a lower extent, a δ <b>opioid</b> receptor (DORs) agonist in vitro, could reinstate ethanol induced conditioned place preference (CPP).
+DAP	addiction	reward	25817357	The aim of the present study was to determine whether a new cyclic analog of enkephalin, cyclo[N(ε),N(β) carbonyl d Lys(2),<strong>Dap</strong>(5)] enkephalinamide (cUENK6), a preferential μ (MORs), and, to a lower extent, a δ opioid receptor (DORs) agonist in vitro, could reinstate ethanol induced conditioned place preference (<b>CPP</b>).
+DAP	drug	alcohol	25716198	Enkephalin analog, cyclo[N(ε),N(β) carbonyl D Lys(2),<strong>Dap</strong>(5)] enkephalinamide (cUENK6), inhibits the <b>ethanol</b> withdrawal induced anxiety like behavior in rats.
+DAP	addiction	withdrawal	25716198	Enkephalin analog, cyclo[N(ε),N(β) carbonyl D Lys(2),<strong>Dap</strong>(5)] enkephalinamide (cUENK6), inhibits the ethanol <b>withdrawal</b> induced anxiety like behavior in rats.
+DAP	drug	opioid	25716198	An analog of enkephalin, cyclo[N(ε),N(β) carbonyl D Lys(2),<strong>Dap</strong>(5)] enkephalinamide (cUENK6), is predominantly a functional agonist of μ <b>opioid</b> receptors (MOPr) and, to a lesser extent, of δ <b>opioid</b> receptors (DOPr) in vitro.
+DAP	addiction	addiction	20080363	To evaluate the effectiveness of a school based substance abuse prevention program developed in the EU <strong>Dap</strong> study (EUropean Drug <b>Addiction</b> Prevention trial).
+DAP	drug	alcohol	18657569	To evaluate the effectiveness of the school based drug abuse prevention program developed in the EU <strong>Dap</strong> study (EUropean Drug Abuse Prevention trial) in preventing the use of tobacco, <b>alcohol</b> and drugs at the post test.
+DAP	drug	nicotine	18657569	To evaluate the effectiveness of the school based drug abuse prevention program developed in the EU <strong>Dap</strong> study (EUropean Drug Abuse Prevention trial) in preventing the use of <b>tobacco</b>, alcohol and drugs at the post test.
+DAP	addiction	reward	17658111	HW 80 questionnaire includes 80 items on demographic characteristics, self reported health, job related stress, work organization, pattern of abuse, physical activity and others, and several of these items have been taken or derived from repeatedly validated questionnaires (SF 12, CAGE, Job Strain, Effort <b>Reward</b>, EU <strong>DAP</strong>, etc.).
+DAP	drug	alcohol	10742352	To determine the internal consistency and 1 week test retest reliability of the Simple Screening Instrument for <b>Alcohol</b> and Other Drug Abuse (SSI AOD), the CAGE AA (CAGE questions adapted for adolescents), and 4 modified items from the Drug and <b>Alcohol</b> Problem QuickScreen (<strong>DAP</strong> 4) among adolescents.
+DAP	addiction	dependence	1395767	The coefficients of determination (r2) indicated that the radial aortic <b>dependence</b> was 0.44 for the SAP, 0.90 for the <strong>DAP</strong>, and 0.98 for the MAP relationship.
+DAP	drug	alcohol	2403500	Using the Drug and <b>Alcohol</b> Problem (<strong>DAP</strong>) Quick Screen, a 30 item questionnaire.
+CD48	drug	cannabinoid	31518568	We have found that treatment with the <b>cannabinoid</b> type 2 receptor (CB2) inverse agonist SMM 189 for 2 weeks after closed head <strong>blast</strong> TBI greatly attenuates the visual deficits and retinal pathology this otherwise produces in mice, by modulating the deleterious role of microglia in the injury process after trauma.
+CD48	addiction	aversion	31518568	In the current studies, we found that a high pressure air <strong>blast</strong> in the absence of raloxifene treatment yields deficits in visual acuity and contrast sensitivity, reductions in the A wave and B wave of the scotopic electroretinogram (ERG), light <b>aversion</b>, and increased pupil constriction to light.
+CD48	drug	opioid	30456793	Repeated <strong>blast</strong> model of mild traumatic brain injury alters <b>oxycodone</b> self administration and drug seeking.
+CD48	addiction	relapse	30456793	Repeated <strong>blast</strong> model of mild traumatic brain injury alters oxycodone self administration and drug <b>seeking</b>.
+CD48	addiction	addiction	30456793	A single <strong>blast</strong> exposure, inducing mTBI alters the medial prefrontal cortex, an area implicated in <b>addiction</b>, for at least 30 days post injury in rats.
+CD48	addiction	addiction	30456793	Repeated <strong>blast</strong> exposures result in greater physiological and behavioral dysfunction than single exposure; however, the impact of repeated mTBI on <b>addiction</b> is unknown.
+CD48	drug	nicotine	30395620	The impact of e liquid on TPM concentration is illustrated by comparing emissions from an NJOY Vape Pen filled with AVAIL Arctic <strong>Blast</strong>, <b>Tobacco</b> Row, and Mardi Gras e liquids.
+CD48	addiction	addiction	29967344	Effects of Mild <strong>Blast</strong> Traumatic Brain Injury on Cognitive  and <b>Addiction</b> Related Behaviors.
+CD48	addiction	addiction	29967344	Therefore, we used a previously characterized <strong>blast</strong> model of mTBI (bTBI) to examine cognitive  and <b>addiction</b> related outcomes.
+CD48	addiction	addiction	27447979	The cognitive concepts and neural substrates noted for <b>addictive</b> disorders may also be relevant for problems in self identification of functional impairment resulting from injury following war related <strong>blast</strong>, sport related concussion, and insidiously occurring dementia.
+CD48	drug	alcohol	25910266	Voluntary <b>Alcohol</b> Intake following <strong>Blast</strong> Exposure in a Rat Model of Mild Traumatic Brain Injury.
+CD48	drug	alcohol	25910266	In this study, we used a rodent <strong>blast</strong> exposure model to investigate the relationship between mTBI and voluntary <b>alcohol</b> drinking in <b>alcohol</b> naïve rats.
+CD48	drug	alcohol	25910266	<b>Alcohol</b> naïve Sprague Dawley rats were subjected to a <strong>blast</strong> model of mTBI (or sham conditions) and then tested in several common measures of voluntary <b>alcohol</b> intake.
+CD48	drug	alcohol	25910266	In a seven week intermittent two bottle choice <b>alcohol</b> drinking test, sham and <strong>blast</strong> exposed rats had comparable levels of <b>alcohol</b> intake.
+CD48	drug	alcohol	25910266	We found no effect of <strong>blast</strong> when rats were tested for an <b>alcohol</b> deprivation effect or compulsive drinking in a quinine adulteration test.
+CD48	addiction	addiction	25910266	We found no effect of <strong>blast</strong> when rats were tested for an alcohol deprivation effect or <b>compulsive</b> drinking in a quinine adulteration test.
+CD48	drug	alcohol	25910266	In conclusion, <strong>blast</strong> exposure had a minimal impact on overall <b>alcohol</b> intake in Sprague Dawley rats, although intake was increased in a subpopulation of <strong>blast</strong> animals in a short access session following intermittent access exposure.
+CD48	drug	alcohol	25796167	Furthermore, the observation of factors that are uniquely associated with <strong>Blast</strong> mTBI (number of deployments) or with PTSD (Lifetime <b>Alcohol</b> Dependence and low Social Closeness), as well as a factor (region of abnormal MD) that had opposite effects on the likelihood of each diagnosis, indicates that the complex relationships between personality, psychopathology, and nature of mTBI need to be considered when interpreting chronic post concussive symptoms.
+CD48	addiction	dependence	25796167	Furthermore, the observation of factors that are uniquely associated with <strong>Blast</strong> mTBI (number of deployments) or with PTSD (Lifetime Alcohol <b>Dependence</b> and low Social Closeness), as well as a factor (region of abnormal MD) that had opposite effects on the likelihood of each diagnosis, indicates that the complex relationships between personality, psychopathology, and nature of mTBI need to be considered when interpreting chronic post concussive symptoms.
+CD48	drug	alcohol	25705183	Reduction of cavitation by exposing worms to shock waves in polyvinyl <b>alcohol</b> resulted in reduced effect, implicating primary <strong>blast</strong> effects as damaging components in shock wave induced trauma.
+CD48	drug	benzodiazepine	16730332	Juvenile monkeys that were trained to associate a visual stimulus with a fear inducing air <strong>blast</strong> to the face were tested after acute administration of different doses of buspirone <b>diazepam</b>, morphine, or vehicle.
+CD48	drug	opioid	16730332	Juvenile monkeys that were trained to associate a visual stimulus with a fear inducing air <strong>blast</strong> to the face were tested after acute administration of different doses of buspirone diazepam, <b>morphine</b>, or vehicle.
+CD48	addiction	aversion	10194966	To determine if the inability to take advantage of the predictability of an <b>aversive</b> stimulus to diminish its psychological impact reflects a deficit in inhibitory control related to the development of substance dependence, we recorded skin conductance responses (SCRs), heart rate (HR), and anticipatory electrodermal nonspecific fluctuations (NSFs) from 175 16 18 year old boys when a white noise <strong>blast</strong> was either unpredictable or temporally predictable.
+CD48	addiction	dependence	10194966	To determine if the inability to take advantage of the predictability of an aversive stimulus to diminish its psychological impact reflects a deficit in inhibitory control related to the development of substance <b>dependence</b>, we recorded skin conductance responses (SCRs), heart rate (HR), and anticipatory electrodermal nonspecific fluctuations (NSFs) from 175 16 18 year old boys when a white noise <strong>blast</strong> was either unpredictable or temporally predictable.
+CD48	addiction	relapse	9796190	Fuungemia frequently occurred in patients with following factors: 1) advanced disease, such as <b>relapse</b> of acute leukemia or malignant lymphoma or <strong>blast</strong> crisis of chronic myelogenous leukemia; 2) neutrophil count less than 100/microliter; 3) administration of antibiotics; 4) focal infection, gastrointestinal hemorrhage or urinary catheterization; and 5) isolation of causative organisms from surveillance cultures obtained just before the onset of fungemia.
+CD48	addiction	reward	3061831	<b>CPP</b> at doses of 5 10 mg/kg did not reduce seizure severity in gerbils in which generalized tonic clonic seizures were induced by air <strong>blast</strong> stimulation, but, as in mice and rats, it caused motor impairment.
+CD48	drug	alcohol	3668280	When solubilized in <b>ethanol</b>, there was a marked effect on thymidine uptake but not on <strong>blast</strong> transformation when compared to parallel controls.
+CD48	drug	benzodiazepine	3703887	Air <strong>blast</strong> stress induced a significant elevation in hypothalamic HA levels and HD activity in vehicle treated controls, <b>diazepam</b> treated and <b>diazepam</b> withdrawn rats, but the change in HD activity was significantly greater in the last group.
+CD48	addiction	reward	6890211	Cats trained in 4 6 weeks to obtain a <b>reward</b> (food pellet) were made 'neurotic' by a randomly occurring air <strong>blast</strong> at the <b>reward</b> box.
+AAAS	drug	alcohol	22036976	The common structural element for the AAA fragrance ingredients is an <b>alcohol</b> group  C (R1)(R2)OH and generically the <strong>AAAs</strong> fragrances can be represented as an Ar C (R1)(R2)OH or Ar Alkyl C (R1)(R2)OH group.
+AAAS	drug	alcohol	19297380	The measurements included: a content analysis of sponsors' responses; Severity of <b>Alcohol</b> Dependence Questionnaire Community version (SADQ C) and <b>Alcoholics</b> Anonymous Affiliation Scale (<strong>AAAS</strong>).
+AAAS	addiction	dependence	19297380	The measurements included: a content analysis of sponsors' responses; Severity of Alcohol <b>Dependence</b> Questionnaire Community version (SADQ C) and Alcoholics Anonymous Affiliation Scale (<strong>AAAS</strong>).
+TXN	drug	amphetamine	32203791	<strong>Thioredoxin</strong> 1 blocks <b>methamphetamine</b> induced injury in brain through inhibiting endoplasmic reticulum and mitochondria mediated apoptosis in mice.
+TXN	drug	alcohol	30708098	The aim of the present work was to evaluate cardiac sympathetic activity and the expression and activation of two antioxidant proteins: heat shock protein27 (HSP27) and <strong>thioredoxin</strong> 1 (Trx 1) after voluntary binge <b>ethanol</b> consumption, alone and in combination with MDMA.
+TXN	drug	psychedelics	30708098	The aim of the present work was to evaluate cardiac sympathetic activity and the expression and activation of two antioxidant proteins: heat shock protein27 (HSP27) and <strong>thioredoxin</strong> 1 (Trx 1) after voluntary binge ethanol consumption, alone and in combination with <b>MDMA</b>.
+TXN	addiction	intoxication	30708098	The aim of the present work was to evaluate cardiac sympathetic activity and the expression and activation of two antioxidant proteins: heat shock protein27 (HSP27) and <strong>thioredoxin</strong> 1 (Trx 1) after voluntary <b>binge</b> ethanol consumption, alone and in combination with MDMA.
+TXN	drug	amphetamine	30136629	Downregulation of <strong>thioredoxin</strong> 1 in the ventral tegmental area delays extinction of <b>methamphetamine</b> induced conditioned place preference.
+TXN	drug	amphetamine	30136629	Previous study has reported that <strong>thioredoxin</strong> 1 overexpression prevents the acquisition of <b>methamphetamine</b> conditioned place preference.
+TXN	drug	amphetamine	30136629	Here, we aimed to investigate the effect of <strong>thioredoxin</strong> 1 on <b>methamphetamine</b> conditioned place preference extinction and the possible mechanism.
+TXN	drug	amphetamine	30136629	(a) An extinction procedure in mice was employed to investigate the effect of <strong>thioredoxin</strong> 1 on the extinction of <b>methamphetamine</b> conditioned place preference.
+TXN	drug	amphetamine	30136629	After the acquisition of <b>methamphetamine</b> conditioned place preference, mice underwent the following procedures: the injection of <strong>thioredoxin</strong> 1 small interfering RNA in the ventral tegmental area followed by the post conditioned place preference test, four days of extinction training followed by four days of recovery after surgery.
+TXN	drug	amphetamine	30136629	<strong>Thioredoxin</strong> 1 downregulation in the ventral tegmental area delayed <b>methamphetamine</b> conditioned place preference extinction.
+TXN	drug	amphetamine	30136629	The expression of <strong>thioredoxin</strong> 1 was decreased in the ventral tegmental area of mice in control and negative groups after <b>methamphetamine</b> conditioned place preference extinction, but not in the <strong>thioredoxin</strong> 1 siRNA group.
+TXN	drug	amphetamine	30136629	The levels of dopamine D1 receptor, tyrosine hydroxylase, phosphorylated extracellular regulated kinase, and phosphorylated cyclic adenosine monophosphate response element binding protein were decreased in the ventral tegmental area, nucleus accumbens, and prefrontal cortex of mice in the control and negative groups after <b>methamphetamine</b> conditioned place preference extinction, but were inversely increased in <strong>thioredoxin</strong> 1 siRNA group.
+TXN	drug	amphetamine	30136629	The results suggest that downregulation of <strong>thioredoxin</strong> 1 in the ventral tegmental area may delay <b>methamphetamine</b> conditioned place preference extinction by regulating the mesocorticolimbic dopaminergic signaling pathway.
+TXN	drug	amphetamine	29981334	<strong>Thioredoxin</strong> 1 downregulation in the nucleus accumbens promotes <b>methamphetamine</b> primed reinstatement in mice.
+TXN	addiction	relapse	29981334	<strong>Thioredoxin</strong> 1 downregulation in the nucleus accumbens promotes methamphetamine primed <b>reinstatement</b> in mice.
+TXN	drug	amphetamine	29981334	<strong>Thioredoxin</strong> 1 (Trx 1) is an important regulator of neuroprotection, and inhibits morphine induced hyperlocomotion, reward and withdrawal signs, as well as blocks <b>methamphetamine</b> (<b>METH</b>) induced conditioned place preference (CPP).
+TXN	drug	opioid	29981334	<strong>Thioredoxin</strong> 1 (Trx 1) is an important regulator of neuroprotection, and inhibits <b>morphine</b> induced hyperlocomotion, reward and withdrawal signs, as well as blocks methamphetamine (METH) induced conditioned place preference (CPP).
+TXN	addiction	reward	29981334	<strong>Thioredoxin</strong> 1 (Trx 1) is an important regulator of neuroprotection, and inhibits morphine induced hyperlocomotion, <b>reward</b> and withdrawal signs, as well as blocks methamphetamine (METH) induced conditioned place preference (<b>CPP</b>).
+TXN	addiction	withdrawal	29981334	<strong>Thioredoxin</strong> 1 (Trx 1) is an important regulator of neuroprotection, and inhibits morphine induced hyperlocomotion, reward and <b>withdrawal</b> signs, as well as blocks methamphetamine (METH) induced conditioned place preference (CPP).
+TXN	drug	opioid	29770121	Overexpression of <strong>Thioredoxin</strong> 1 Blocks <b>Morphine</b> Induced Conditioned Place Preference Through Regulating the Interaction of γ Aminobutyric Acid and Dopamine Systems.
+TXN	drug	amphetamine	28782589	The role of <strong>thioredoxin</strong> 1 in resisting <b>methamphetamine</b> induced rewarding effect.
+TXN	drug	amphetamine	26684867	The overexpression of <strong>Thioredoxin</strong> 1 suppressing inflammation induced by <b>methamphetamine</b> in spleen.
+TXN	drug	opioid	26313266	CP 154,526 Modifies CREB Phosphorylation and <strong>Thioredoxin</strong> 1 Expression in the Dentate Gyrus following <b>Morphine</b> Induced Conditioned Place Preference.
+TXN	addiction	addiction	26313266	<strong>Thioredoxin</strong> 1 (Trx 1) is a functional protein controlling the redox status of several proteins, which is involved in <b>addictive</b> processes.
+TXN	drug	alcohol	20374208	In the current study, we examine sensation seeking in middle aged long term abstinent <b>alcoholics</b> (LTAA) and in younger actively drinking treatment naïve <b>alcoholics</b> (<strong>TxN</strong>).
+TXN	addiction	relapse	20374208	In the current study, we examine sensation <b>seeking</b> in middle aged long term abstinent alcoholics (LTAA) and in younger actively drinking treatment naïve alcoholics (<strong>TxN</strong>).
+TXN	addiction	relapse	20374208	A modified version of the Sensation <b>Seeking</b> Scale (SSS) was administered to 52 middle aged LTAA (average age = 46.6 years) and 86 younger <strong>TxN</strong> (average age = 31.2 years), each study with its own age and gender comparable nonalcoholic controls (NAC).
+TXN	drug	alcohol	19860794	We previously demonstrated, in a small sample, steeper age related gray matter shrinkage in treatment naïve <b>alcohol</b> dependent (<strong>TxN</strong>) men compared to nonalcoholic controls, but could not separate out the contributions of age and lifetime duration of <b>alcohol</b> use (which were highly correlated) to this effect.
+TXN	drug	amphetamine	17210125	During <b>METH</b> intoxication, we found that peroxiredoxins and thioredoxins/<strong>thioredoxin</strong> reductases (peroxiredoxin reducing systems) which are known to prevent oxidative stress and apoptosis were differentially downregulated and upregulated, respectively.
+TXN	addiction	intoxication	17210125	During METH <b>intoxication</b>, we found that peroxiredoxins and thioredoxins/<strong>thioredoxin</strong> reductases (peroxiredoxin reducing systems) which are known to prevent oxidative stress and apoptosis were differentially downregulated and upregulated, respectively.
+TXN	drug	amphetamine	17210125	Thus, <b>METH</b> induced differential regulation and oxidation of peroxiredoxins and <strong>thioredoxin</strong> may be an important mechanism for apoptosis.
+TXN	drug	alcohol	16737453	This study examines decision making on the SGT in young adults with <b>alcohol</b> dependence who are treatment naive (<strong>TxN</strong>).
+TXN	addiction	dependence	16737453	This study examines decision making on the SGT in young adults with alcohol <b>dependence</b> who are treatment naive (<strong>TxN</strong>).
+TXN	drug	alcohol	16737453	The results suggest that our sample of young adult <strong>TxN</strong> adults with <b>alcohol</b> dependence do not have global deficits in decision making as measured by the SGT, and that their poor decisions regarding their <b>alcohol</b> consumption are more specific to drinking.
+TXN	addiction	dependence	16737453	The results suggest that our sample of young adult <strong>TxN</strong> adults with alcohol <b>dependence</b> do not have global deficits in decision making as measured by the SGT, and that their poor decisions regarding their alcohol consumption are more specific to drinking.
+S100A10	drug	cannabinoid	28418321	<strong>S100A10</strong> identified in a genome wide gene × <b>cannabis</b> dependence interaction analysis of risky sexual behaviours.
+S100A10	addiction	dependence	28418321	<strong>S100A10</strong> identified in a genome wide gene × cannabis <b>dependence</b> interaction analysis of risky sexual behaviours.
+S100A10	addiction	addiction	26059306	P11 (<strong>S100A10</strong>) is a promising target for manipulating depression and <b>addiction</b> in mice.
+S100A10	addiction	addiction	24725970	Downregulation of p11 (<strong>S100A10</strong>), specifically in the NAc, elicits depressive like behaviors in mice, but its role in drug <b>addiction</b> is unknown.
+S100A10	drug	psychedelics	21585054	[Effects of electroacupuncture on expression of tyrosine hydroxylase and c fos in hippocampal <strong>CA 1</strong> area in <b>ketamine</b> addiction rats].
+S100A10	addiction	addiction	21585054	[Effects of electroacupuncture on expression of tyrosine hydroxylase and c fos in hippocampal <strong>CA 1</strong> area in ketamine <b>addiction</b> rats].
+S100A10	drug	psychedelics	21585054	EA of "Zusanli"(ST 36) "Sanyinjiao" (SP 6) can downregulate <b>ketamine</b> addiction induced increase of expression of tyrosine hydroxylase and c fos in the hippocampal <strong>CA 1</strong> region in <b>ketamine</b> addiction rats, which may contribute to its effect in relieving <b>ketamine</b> addiction symptoms in clinic.
+S100A10	addiction	addiction	21585054	EA of "Zusanli"(ST 36) "Sanyinjiao" (SP 6) can downregulate ketamine <b>addiction</b> induced increase of expression of tyrosine hydroxylase and c fos in the hippocampal <strong>CA 1</strong> region in ketamine <b>addiction</b> rats, which may contribute to its effect in relieving ketamine <b>addiction</b> symptoms in clinic.
+RPS4X	drug	opioid	31105913	Further, a significant relationship was reported between the increased duration of <b>morphine</b> use and the number of created <strong>scar</strong> glial cells.
+RPS4X	drug	opioid	31105913	After long term use, <b>opioids</b> can result in increased number of astrocytes and creating glial <strong>scar</strong> centers in the affected areas in response to the inflammation.
+RPS4X	addiction	sensitization	25903913	Surgical trauma, adherence of the musculature to the dura mater, peripheral nerve injury, development of neurinomas in the surgical <strong>scar</strong>, and central <b>sensitization</b> may be involved in the genesis of such headaches.
+RPS4X	addiction	reward	23566343	The incidences of <b>CPP</b> in the pelvic and <strong>scar</strong> areas were evaluated in all patients three months after surgery.
+RPS4X	drug	nicotine	22158818	<strong>RPS4</strong> EDS1 and AvrRps4 EDS1 complexes are detected inside nuclei of living <b>tobacco</b> cells after transient coexpression and in Arabidopsis soluble leaf extracts after resistance activation.
+RPS4X	addiction	relapse	17399662	We recommend this technique as a safe alternative in patients <b>seeking</b> autologous breast reconstruction in the presence of a midline abdominal <strong>scar</strong>.
+RPS4X	addiction	sensitization	11439794	In 43 women the area of allodynia around the <strong>scar</strong> was mapped as a measure of the degree of central <b>sensitization</b>.
+RHOA	drug	amphetamine	31912366	We previously found that the biochemical cascade leading to this cellular process involves entry of <b>AMPH</b> into the cell through the DAT, stimulation of an intracellular trace amine associated receptor, TAAR1, and activation of the small GTPase, <strong>RhoA</strong>.
+RHOA	drug	amphetamine	31912366	<strong>RhoA</strong> activation is dependent on calcium, but not CaMKII, explaining a divergence in <b>AMPH</b> mediated endocytosis of DAT and NET from that of EAAT3.
+RHOA	drug	nicotine	30227235	Our data suggest that response similar to <b>nicotine</b> withdrawal or/and hypoxia induced by childhood chronic asthma enhances the BDNF Cdc42/<strong>RhoA</strong> signaling pathway and activates cofilin1, leading to the remodeling of actin, causing the loss of dendritic spines and atrophy of dendrites, eventually resulting in behavioral alterations.
+RHOA	addiction	withdrawal	30227235	Our data suggest that response similar to nicotine <b>withdrawal</b> or/and hypoxia induced by childhood chronic asthma enhances the BDNF Cdc42/<strong>RhoA</strong> signaling pathway and activates cofilin1, leading to the remodeling of actin, causing the loss of dendritic spines and atrophy of dendrites, eventually resulting in behavioral alterations.
+RHOA	drug	cocaine	30158054	Viral mediated gene transfer (n = 7 12/group) and intra accumbal microinjections (n = 9 10/group) were used to examine causal roles of SMURF1 and substrate <strong>RhoA</strong>, respectively, in cue induced <b>cocaine</b> seeking.
+RHOA	addiction	relapse	30158054	Viral mediated gene transfer (n = 7 12/group) and intra accumbal microinjections (n = 9 10/group) were used to examine causal roles of SMURF1 and substrate <strong>RhoA</strong>, respectively, in cue induced cocaine <b>seeking</b>.
+RHOA	drug	cocaine	30158054	SMURF1 protein expression was decreased, while SMURF1 substrates <strong>RhoA</strong> and SMAD1/5 were increased, in the nucleus accumbens on withdrawal day 7, but not on withdrawal day 1, following <b>cocaine</b> self administration.
+RHOA	addiction	withdrawal	30158054	SMURF1 protein expression was decreased, while SMURF1 substrates <strong>RhoA</strong> and SMAD1/5 were increased, in the nucleus accumbens on <b>withdrawal</b> day 7, but not on <b>withdrawal</b> day 1, following cocaine self administration.
+RHOA	drug	cocaine	30158054	Viral mediated gene transfer of Smurf1 or constitutive activation of <strong>RhoA</strong> attenuated cue induced <b>cocaine</b> seeking, while catalytically inactive Smurf1 enhanced <b>cocaine</b> seeking.
+RHOA	addiction	relapse	30158054	Viral mediated gene transfer of Smurf1 or constitutive activation of <strong>RhoA</strong> attenuated cue induced cocaine <b>seeking</b>, while catalytically inactive Smurf1 enhanced cocaine <b>seeking</b>.
+RHOA	drug	opioid	30071134	Withdrawal from repeated <b>morphine</b> administration augments expression of the <strong>RhoA</strong> network in the nucleus accumbens to control synaptic structure.
+RHOA	addiction	withdrawal	30071134	<b>Withdrawal</b> from repeated morphine administration augments expression of the <strong>RhoA</strong> network in the nucleus accumbens to control synaptic structure.
+RHOA	drug	opioid	30071134	The <strong>RhoA</strong> small GTPase is among the most well characterized members of the Ras superfamily of small GTPases, and recent work highlights an important role for hippocampal <strong>RhoA</strong> in <b>morphine</b> facilitated reward behavior.
+RHOA	addiction	reward	30071134	The <strong>RhoA</strong> small GTPase is among the most well characterized members of the Ras superfamily of small GTPases, and recent work highlights an important role for hippocampal <strong>RhoA</strong> in morphine facilitated <b>reward</b> behavior.
+RHOA	drug	opioid	30071134	Despite this, it remains unclear how <strong>RhoA</strong> pathway signaling in the NAc is affected by withdrawal from <b>morphine</b>.
+RHOA	addiction	withdrawal	30071134	Despite this, it remains unclear how <strong>RhoA</strong> pathway signaling in the NAc is affected by <b>withdrawal</b> from morphine.
+RHOA	drug	opioid	30071134	To investigate this question, using subcellular fractionation and subsequent protein profiling we examined the expression of key components of the <strong>RhoA</strong> pathway in NAc nuclear, cytoplasmic, and synaptosomal compartments during multiple withdrawal periods from repeated <b>morphine</b> administration.
+RHOA	addiction	withdrawal	30071134	To investigate this question, using subcellular fractionation and subsequent protein profiling we examined the expression of key components of the <strong>RhoA</strong> pathway in NAc nuclear, cytoplasmic, and synaptosomal compartments during multiple <b>withdrawal</b> periods from repeated morphine administration.
+RHOA	drug	opioid	30071134	Our findings reveal an important role for <strong>RhoA</strong> signaling cascades in mediating the effects of long term <b>morphine</b> withdrawal on NAc MSN dendritic spine elimination.
+RHOA	addiction	withdrawal	30071134	Our findings reveal an important role for <strong>RhoA</strong> signaling cascades in mediating the effects of long term morphine <b>withdrawal</b> on NAc MSN dendritic spine elimination.
+RHOA	drug	cocaine	28726800	<b>Cocaine</b> significantly decreased SAM/SAH ratio levels in the DS, which was accompanied with the decreased activities of Rac1 and <strong>RhoA</strong>.
+RHOA	drug	cocaine	28726800	Lentivirus mediated knockdown of Nnmt in the dorsomedial striatum (DMS) attenuated <b>cocaine</b> conditioned place preference (CPP) reward, but increased striatal SAM/SAH ratio levels as well as Rac1 and <strong>RhoA</strong> activities.
+RHOA	addiction	reward	28726800	Lentivirus mediated knockdown of Nnmt in the dorsomedial striatum (DMS) attenuated cocaine conditioned place preference (<b>CPP</b>) <b>reward</b>, but increased striatal SAM/SAH ratio levels as well as Rac1 and <strong>RhoA</strong> activities.
+RHOA	drug	cocaine	28726800	In addition, pharmacological inhibition of NNMT through intra DMS infusion of MeN attenuated <b>cocaine</b> CPP and the activities of Rac1 and <strong>RhoA</strong>, but increased SAM/SAH ratio.
+RHOA	addiction	reward	28726800	In addition, pharmacological inhibition of NNMT through intra DMS infusion of MeN attenuated cocaine <b>CPP</b> and the activities of Rac1 and <strong>RhoA</strong>, but increased SAM/SAH ratio.
+RHOA	drug	cocaine	28726800	The results showed that <b>cocaine</b> increased the association of RhoGDIα with Rac1 or <strong>RhoA</strong>, whereas such effect was inhibited by Nnmt knockdown.
+RHOA	drug	cocaine	28726800	Collectively, our findings show that NNMT regulates <b>cocaine</b> CPP through SAM mediated modification of Rac1 and <strong>RhoA</strong>.
+RHOA	addiction	reward	28726800	Collectively, our findings show that NNMT regulates cocaine <b>CPP</b> through SAM mediated modification of Rac1 and <strong>RhoA</strong>.
+RHOA	drug	opioid	27170097	We found that synaptic expression of <strong>RhoA</strong> increased with <b>morphine</b> conditioning and blocking <strong>RhoA</strong> signaling prevented the expression of <b>morphine</b> induced CPP.
+RHOA	addiction	reward	27170097	We found that synaptic expression of <strong>RhoA</strong> increased with morphine conditioning and blocking <strong>RhoA</strong> signaling prevented the expression of morphine induced <b>CPP</b>.
+RHOA	drug	alcohol	26728616	The effect of sub chronic systemic <b>ethanol</b> treatment on corpus cavernosal smooth muscle contraction: the contribution of <strong>RhoA</strong>/Rho kinase.
+RHOA	drug	alcohol	26728616	The aim of this study was to evaluate whether the sub chronic systemic <b>ethanol</b> exposure has direct effect on cavernosal smooth muscle contractions induced by KCl (depolarizing) and phenylephrine (α1 receptor agonist), and the possible involvement of <strong>RhoA</strong>/Rho kinase pathway.
+RHOA	drug	alcohol	26728616	In <b>ethanol</b> treated group, the expression of <strong>RhoA</strong> decreased compared to sham treated group.
+RHOA	addiction	sensitization	26728616	From these findings, it seems that phenylephrine and KCl induced contractions depends on <strong>RhoA</strong>/Rho kinase mediated Ca(2+) <b>sensitization</b>.
+RHOA	drug	alcohol	26728616	Also, these results suggest that the <b>ethanol</b> treatment decreased the expression of <strong>RhoA</strong>, and the inhibitory effect of <b>ethanol</b> on KCl induced contractions may be due to, at least in part, the inhibition of a <strong>RhoA</strong>/Rho kinase in mouse corpus cavernosum.
+RHOA	drug	alcohol	26169563	Effects of <b>ethanol</b> on <strong>RhoA</strong>/Rho kinase mediated calcium sensitization in mouse lung parenchymal tissue.
+RHOA	addiction	sensitization	26169563	Effects of ethanol on <strong>RhoA</strong>/Rho kinase mediated calcium <b>sensitization</b> in mouse lung parenchymal tissue.
+RHOA	addiction	sensitization	26169563	Calcium <b>sensitization</b> by the <strong>RhoA</strong>/Rho kinase (ROCK) pathway contributes to the contraction in smooth muscle.
+RHOA	drug	alcohol	26169563	Also, we investigated the effect of <b>ethanol</b> on <strong>RhoA</strong>/Rho kinase pathway.
+RHOA	drug	alcohol	26169563	In <b>ethanol</b> treated group, expression of <strong>RhoA</strong> and ROCK1 but not ROCK2 decreased compared to control.
+RHOA	addiction	sensitization	26169563	These results suggest that <strong>RhoA</strong>/Rho kinase signaling pathway plays an important role in phenylephrine  and KCl induced Ca(2)(+) <b>sensitization</b> in mouse lung parenchymal tissue.
+RHOA	drug	alcohol	26169563	Also, <b>ethanol</b> may be decrease phenylephrine  and KCl induced contraction due to lowering the <strong>RhoA</strong>/Rho kinase mediated Ca(2+) sensitizing by inhibiting <strong>RhoA</strong>/Rho kinase pathway in parenchymal tissue.
+RHOA	drug	alcohol	25257290	<b>Alcohol</b> rapidly decreased GTP bound Rac1 but not <strong>RhoA</strong> during the drop in TER.
+RHOA	drug	cocaine	25100957	Results of complementary Ingenuity Pathways Analyses (IPA) and gene set enrichment analyses (GSEA), both performed using protein quantitative data, demonstrate that <b>cocaine</b> increases vesicular transporters for dopamine and glutamate as well as increasing proteins in the <strong>RhoA</strong> pathway.
+RHOA	addiction	aversion	23564082	The small GTPase <strong>RhoA</strong>, but not Rac1, is essential for conditioned <b>aversive</b> memory formation through regulation of actin rearrangements in rat dorsal hippocampus.
+RHOA	drug	alcohol	23237297	Reduced <strong>RhoA</strong> activity mediates acute <b>alcohol</b> intoxication induced inhibition of lymphatic myogenic constriction despite increased cytosolic [Ca(2+) ].
+RHOA	addiction	intoxication	23237297	Reduced <strong>RhoA</strong> activity mediates acute alcohol <b>intoxication</b> induced inhibition of lymphatic myogenic constriction despite increased cytosolic [Ca(2+) ].
+RHOA	drug	alcohol	23237297	Because of the known role of Ca(2+) in smooth muscle contractile responses, we investigated how <b>alcohol</b> impacts cyclic Ca(2+) and whether changes in <strong>RhoA</strong>/ROCK mediated Ca(2+) sensitivity underlie the <b>alcohol</b> induced reduction of myogenic responsiveness.
+RHOA	drug	alcohol	23237297	The data strongly suggest that the <b>alcohol</b> induced inhibition of mesenteric lymphatic myogenic constriction is mediated by reduced <strong>RhoA</strong>/ROCK mediated Ca(2+) sensitivity.
+RHOA	drug	nicotine	21757850	It has been suggested that an augmented agonist induced, <strong>RhoA</strong> mediated Ca²⁺ sensitization is responsible for the enhanced bronchial smooth muscle contraction induced by cigarette <b>smoking</b>.
+RHOA	addiction	sensitization	21757850	It has been suggested that an augmented agonist induced, <strong>RhoA</strong> mediated Ca²⁺ <b>sensitization</b> is responsible for the enhanced bronchial smooth muscle contraction induced by cigarette smoking.
+RHOA	drug	nicotine	21757850	On the other hand, inhalation of <b>nicotine</b> had no effect on either the ACh  and high K⁺ depolarization induced contractions or the expression of <strong>RhoA</strong> protein.
+RHOA	drug	alcohol	20837132	Here we report that acute <b>ethanol</b> exposure profoundly disrupts the actin cytoskeleton in C6 cells decreasing stress fiber formation and downregulating <strong>RhoA</strong> and vinculin immunocontent.
+RHOA	drug	cocaine	19580848	<b>Cocaine</b> regulates ezrin radixin moesin proteins and <strong>RhoA</strong> signaling in the nucleus accumbens.
+RHOA	drug	cocaine	19580848	Further, we show that the amount of active <strong>RhoA</strong>, a small GTPase protein, is significantly reduced in the NAcc by <b>cocaine</b>, while the phosphorylation levels of ERM protein are also decreased by bilateral microinjections in this site of the Rho kinase inhibitors.
+RHOA	drug	cocaine	19580848	Together, these results suggest that <b>cocaine</b> reduces phosphorylated ERM levels in the NAcc by making downregulation of <strong>RhoA</strong> Rho kinase signaling, which may importantly contribute to initiate synaptic changes in this site leading to drug addiction.
+RHOA	addiction	addiction	19580848	Together, these results suggest that cocaine reduces phosphorylated ERM levels in the NAcc by making downregulation of <strong>RhoA</strong> Rho kinase signaling, which may importantly contribute to initiate synaptic changes in this site leading to drug <b>addiction</b>.
+RHOA	drug	nicotine	17284169	<strong>RhoA</strong>, encoding a Rho GTPase, is associated with <b>smoking</b> initiation.
+RHOA	drug	nicotine	17284169	For the <strong>RhoA</strong> gene, rs2878298 showed highly significant genotypic association with both <b>smoking</b> initiation (SI) and ND (P = 0.00005 for SI and P = 0.0007 for ND).
+RHOA	drug	nicotine	17284169	Our results indicated that the <strong>RhoA</strong> gene is likely involved in initiation of <b>tobacco</b> <b>smoking</b> and ND.
+RHOA	addiction	sensitization	16472257	Sustained smooth muscle contraction or its experimental counterpart, Ca2+ <b>sensitization</b>, by G(q/13) coupled receptor agonists is mediated via <strong>RhoA</strong> dependent inhibition of MLC (myosin light chain) phosphatase and MLC20 (20 kDa regulatory light chain of myosin II) phosphorylation by a Ca2+ independent MLCK (MLC kinase).
+RHOA	drug	nicotine	16166743	Taken together, these findings suggest that the augmented agonist induced, <strong>RhoA</strong> mediated Ca2+ sensitization may be responsible for the enhanced bronchial smooth muscle contraction induced by cigarette <b>smoking</b>, which has relevance to airway hyperresponsiveness in patients with chronic obstructive pulmonary disease.
+RHOA	addiction	sensitization	16166743	Taken together, these findings suggest that the augmented agonist induced, <strong>RhoA</strong> mediated Ca2+ <b>sensitization</b> may be responsible for the enhanced bronchial smooth muscle contraction induced by cigarette smoking, which has relevance to airway hyperresponsiveness in patients with chronic obstructive pulmonary disease.
+RHOA	drug	opioid	15987828	In the present study, we hypothesized that chronic <b>morphine</b> alters the expression and functional effects of G alpha12, a G protein that regulates downstream cytoskeletal proteins via its control of <strong>RhoA</strong>.
+RHOA	drug	opioid	15987828	Chronic <b>morphine</b> treatment significantly enhanced thrombin stimulated <strong>RhoA</strong> activity and thrombin stimulated expression of alpha actinin, a cytoskeletal anchoring protein, in hMOR CHO cells.
+POU5F1	drug	opioid	31857840	Herein, we describe the application of Theravance's multivalent approach to drug discovery coupled with a physicochemical property design strategy by which the N substituted endo 3 (8 aza bicyclo[3.2.1]<strong>oct 3</strong> yl) phenyl carboxamide series of μ <b>opioid</b> receptor antagonists was optimized to afford the orally absorbed, non CNS penetrant, Phase 3 ready clinical compound axelopran (TD 1211) 19i as a potential treatment for <b>opioid</b> induced constipation.
+POU5F1	drug	amphetamine	29915156	This study determined the pharmacokinetics, tissue exposure, and partition ratios of <b>methamphetamine</b> and major metabolites in various mouse tissues and investigated the impact of organic cation transporter 3 (<strong>Oct3</strong>) following i.v.
+POU5F1	drug	amphetamine	29915156	This study determined the pharmacokinetics, tissue exposure, and partition ratios of <b>methamphetamine</b> and major metabolites in various mouse tissues and investigated the impact of organic cation transporter 3 (<strong><strong>Oct3</strong></strong>) following i.v.
+POU5F1	drug	amphetamine	29915156	injection of <b>methamphetamine</b> to male <strong>Oct3</strong>+/+ and <strong>Oct3</strong> /  mice.
+POU5F1	drug	amphetamine	29915156	injection of <b>methamphetamine</b> to male <strong><strong>Oct3</strong></strong>+/+ and <strong><strong>Oct3</strong></strong> /  mice.
+POU5F1	drug	amphetamine	29915156	<b>Methamphetamine</b>, <b>amphetamine</b>, and p OHMA were readily detectable in plasma with <strong>Oct3</strong>+/+ and <strong>Oct3</strong> /  mice displaying similar plasma pharmacokinetic profiles for all three analytes.
+POU5F1	drug	amphetamine	29915156	<b>Methamphetamine</b>, <b>amphetamine</b>, and p OHMA were readily detectable in plasma with <strong><strong>Oct3</strong></strong>+/+ and <strong><strong>Oct3</strong></strong> /  mice displaying similar plasma pharmacokinetic profiles for all three analytes.
+POU5F1	drug	amphetamine	29915156	Our findings suggest that local tissue accumulation of <b>methamphetamine</b> and/or its metabolites may play a role in several of the reported peripheral toxicities of <b>methamphetamine</b>, and <strong>Oct3</strong> can significantly impact tissue exposure to its substrates without affecting systemic elimination.
+POU5F1	drug	amphetamine	29915156	Our findings suggest that local tissue accumulation of <b>methamphetamine</b> and/or its metabolites may play a role in several of the reported peripheral toxicities of <b>methamphetamine</b>, and <strong><strong>Oct3</strong></strong> can significantly impact tissue exposure to its substrates without affecting systemic elimination.
+POU5F1	drug	cocaine	27604564	We previously reported that stress, via elevated corticosterone, potentiates <b>cocaine</b> primed reinstatement of <b>cocaine</b> seeking following self administration in rats and that this potentiation appears to involve corticosterone induced blockade of dopamine clearance via the organic cation transporter 3 (<strong>OCT3</strong>).
+POU5F1	addiction	relapse	27604564	We previously reported that stress, via elevated corticosterone, potentiates cocaine primed <b>reinstatement</b> of cocaine <b>seeking</b> following self administration in rats and that this potentiation appears to involve corticosterone induced blockade of dopamine clearance via the organic cation transporter 3 (<strong>OCT3</strong>).
+POU5F1	drug	cocaine	27604564	We previously reported that stress, via elevated corticosterone, potentiates <b>cocaine</b> primed reinstatement of <b>cocaine</b> seeking following self administration in rats and that this potentiation appears to involve corticosterone induced blockade of dopamine clearance via the organic cation transporter 3 (<strong><strong>OCT3</strong></strong>).
+POU5F1	addiction	relapse	27604564	We previously reported that stress, via elevated corticosterone, potentiates cocaine primed <b>reinstatement</b> of cocaine <b>seeking</b> following self administration in rats and that this potentiation appears to involve corticosterone induced blockade of dopamine clearance via the organic cation transporter 3 (<strong><strong>OCT3</strong></strong>).
+POU5F1	drug	cocaine	27604564	In the present study, we use a conditioned place preference/reinstatement paradigm in mice to directly test the hypothesis that corticosterone potentiates <b>cocaine</b> primed reinstatement by blockade of <strong>OCT3</strong>.
+POU5F1	addiction	relapse	27604564	In the present study, we use a conditioned place preference/<b>reinstatement</b> paradigm in mice to directly test the hypothesis that corticosterone potentiates cocaine primed <b>reinstatement</b> by blockade of <strong>OCT3</strong>.
+POU5F1	drug	cocaine	27604564	In the present study, we use a conditioned place preference/reinstatement paradigm in mice to directly test the hypothesis that corticosterone potentiates <b>cocaine</b> primed reinstatement by blockade of <strong><strong>OCT3</strong></strong>.
+POU5F1	addiction	relapse	27604564	In the present study, we use a conditioned place preference/<b>reinstatement</b> paradigm in mice to directly test the hypothesis that corticosterone potentiates cocaine primed <b>reinstatement</b> by blockade of <strong><strong>OCT3</strong></strong>.
+POU5F1	drug	cocaine	27604564	To determine the role of <strong>OCT3</strong> blockade in these effects, we examined the abilities of corticosterone and normetanephrine to potentiate <b>cocaine</b> primed reinstatement in <strong>OCT3</strong> deficient and wild type mice.
+POU5F1	addiction	relapse	27604564	To determine the role of <strong>OCT3</strong> blockade in these effects, we examined the abilities of corticosterone and normetanephrine to potentiate cocaine primed <b>reinstatement</b> in <strong>OCT3</strong> deficient and wild type mice.
+POU5F1	drug	cocaine	27604564	To determine the role of <strong><strong>OCT3</strong></strong> blockade in these effects, we examined the abilities of corticosterone and normetanephrine to potentiate <b>cocaine</b> primed reinstatement in <strong><strong>OCT3</strong></strong> deficient and wild type mice.
+POU5F1	addiction	relapse	27604564	To determine the role of <strong><strong>OCT3</strong></strong> blockade in these effects, we examined the abilities of corticosterone and normetanephrine to potentiate cocaine primed <b>reinstatement</b> in <strong><strong>OCT3</strong></strong> deficient and wild type mice.
+POU5F1	drug	cocaine	27604564	However, corticosterone and normetanephrine failed to potentiate <b>cocaine</b> primed reinstatement in <strong>OCT3</strong> deficient mice.
+POU5F1	addiction	relapse	27604564	However, corticosterone and normetanephrine failed to potentiate cocaine primed <b>reinstatement</b> in <strong>OCT3</strong> deficient mice.
+POU5F1	drug	cocaine	27604564	However, corticosterone and normetanephrine failed to potentiate <b>cocaine</b> primed reinstatement in <strong><strong>OCT3</strong></strong> deficient mice.
+POU5F1	addiction	relapse	27604564	However, corticosterone and normetanephrine failed to potentiate cocaine primed <b>reinstatement</b> in <strong><strong>OCT3</strong></strong> deficient mice.
+POU5F1	drug	cocaine	27604564	Together, these data provide the first direct evidence that the interaction of corticosterone with <strong>OCT3</strong> mediates corticosterone effects on drug seeking behavior and establish <strong>OCT3</strong> function as an important determinant of susceptibility to <b>cocaine</b> use.
+POU5F1	addiction	relapse	27604564	Together, these data provide the first direct evidence that the interaction of corticosterone with <strong>OCT3</strong> mediates corticosterone effects on drug <b>seeking</b> behavior and establish <strong>OCT3</strong> function as an important determinant of susceptibility to cocaine use.
+POU5F1	drug	cocaine	27604564	Together, these data provide the first direct evidence that the interaction of corticosterone with <strong><strong>OCT3</strong></strong> mediates corticosterone effects on drug seeking behavior and establish <strong><strong>OCT3</strong></strong> function as an important determinant of susceptibility to <b>cocaine</b> use.
+POU5F1	addiction	relapse	27604564	Together, these data provide the first direct evidence that the interaction of corticosterone with <strong><strong>OCT3</strong></strong> mediates corticosterone effects on drug <b>seeking</b> behavior and establish <strong><strong>OCT3</strong></strong> function as an important determinant of susceptibility to cocaine use.
+POU5F1	drug	amphetamine	27478387	Extracellular serotonin levels are regulated by the serotonin transporter (SERT) and organic cation transporter 3 (<strong>OCT3</strong>), and vHipp <strong>OCT3</strong> expression is enhanced during 24 hours of <b>amphetamine</b> withdrawal, while SERT expression is unaltered.
+POU5F1	addiction	withdrawal	27478387	Extracellular serotonin levels are regulated by the serotonin transporter (SERT) and organic cation transporter 3 (<strong>OCT3</strong>), and vHipp <strong>OCT3</strong> expression is enhanced during 24 hours of amphetamine <b>withdrawal</b>, while SERT expression is unaltered.
+POU5F1	drug	amphetamine	27478387	Extracellular serotonin levels are regulated by the serotonin transporter (SERT) and organic cation transporter 3 (<strong><strong>OCT3</strong></strong>), and vHipp <strong><strong>OCT3</strong></strong> expression is enhanced during 24 hours of <b>amphetamine</b> withdrawal, while SERT expression is unaltered.
+POU5F1	addiction	withdrawal	27478387	Extracellular serotonin levels are regulated by the serotonin transporter (SERT) and organic cation transporter 3 (<strong><strong>OCT3</strong></strong>), and vHipp <strong><strong>OCT3</strong></strong> expression is enhanced during 24 hours of amphetamine <b>withdrawal</b>, while SERT expression is unaltered.
+POU5F1	addiction	withdrawal	27478387	Here, we tested whether <strong>OCT3</strong> and SERT expression in the CeA is also affected during acute <b>withdrawal</b> to explain opposing regional alterations in limbic serotonergic neurotransmission and if respective changes continued with two weeks of <b>withdrawal</b>.
+POU5F1	addiction	withdrawal	27478387	Here, we tested whether <strong><strong>OCT3</strong></strong> and SERT expression in the CeA is also affected during acute <b>withdrawal</b> to explain opposing regional alterations in limbic serotonergic neurotransmission and if respective changes continued with two weeks of <b>withdrawal</b>.
+POU5F1	addiction	withdrawal	27478387	<strong>OCT3</strong> and SERT expression increased in the CeA at both <b>withdrawal</b> timepoints.
+POU5F1	addiction	withdrawal	27478387	<strong><strong>OCT3</strong></strong> and SERT expression increased in the CeA at both <b>withdrawal</b> timepoints.
+POU5F1	addiction	withdrawal	27478387	In the vHipp, <strong>OCT3</strong> expression increased only at 24 hours of <b>withdrawal</b>, with an equivalent pattern seen in the dorsomedial hypothalamus.
+POU5F1	addiction	withdrawal	27478387	In the vHipp, <strong><strong>OCT3</strong></strong> expression increased only at 24 hours of <b>withdrawal</b>, with an equivalent pattern seen in the dorsomedial hypothalamus.
+POU5F1	drug	amphetamine	27478387	These regionally specific changes in limbic <strong>OCT3</strong> and SERT expression may partially contribute to the serotonergic imbalance and negative affect during <b>amphetamine</b> withdrawal.
+POU5F1	addiction	withdrawal	27478387	These regionally specific changes in limbic <strong>OCT3</strong> and SERT expression may partially contribute to the serotonergic imbalance and negative affect during amphetamine <b>withdrawal</b>.
+POU5F1	drug	amphetamine	27478387	These regionally specific changes in limbic <strong><strong>OCT3</strong></strong> and SERT expression may partially contribute to the serotonergic imbalance and negative affect during <b>amphetamine</b> withdrawal.
+POU5F1	addiction	withdrawal	27478387	These regionally specific changes in limbic <strong><strong>OCT3</strong></strong> and SERT expression may partially contribute to the serotonergic imbalance and negative affect during amphetamine <b>withdrawal</b>.
+POU5F1	drug	nicotine	26359313	Accordingly, this study compared the effects of <b>nicotine</b>, the selective α4/6β2 agonist 5 (123I)iodo 3 [2(S) 2 azetidinylmethoxy]pyridine (5 I A 85380), and the selective α7 agonist N (3R) 1 azabicyclo(2.2.2)<strong>oct 3</strong> yl 4 chlorobenzamide in assays of pain stimulated and pain depressed behavior in male Sprague Dawley rats.
+POU5F1	addiction	reward	26359313	5 I A 85380 also blocked both acid stimulated stretching and acid induced depression of <b>ICSS</b>, whereas N (3R) 1 azabicyclo(2.2.2)<strong>oct 3</strong> yl 4 chlorobenzamide produced no effect in either procedure.
+POU5F1	drug	nicotine	24627467	It is noteworthy that the selective partial agonists for α4β2, ABT 089 [2 methyl 3 [2(S) pyrrolidinylmethoxy]pyridine], and α7, ABT 107 [5 (6 [(3R) 1 azabicyclo[2.2.2]<strong>oct 3</strong> yloxy] pyridazin 3 yl) 1H indole] (AbbVie, North Chicago, IL), have not been evaluated as possible therapeutics for <b>nicotine</b> cessation.
+POU5F1	drug	amphetamine	22084709	<strong>OCT3</strong> single nucleotide polymorphisms (SNPs) have been investigated for their association with psychiatric disorders such as <b>methamphetamine</b> use disorder and obsessive compulsive disorder in children and adolescents, but not depression.
+POU5F1	addiction	addiction	22084709	<strong>OCT3</strong> single nucleotide polymorphisms (SNPs) have been investigated for their association with psychiatric disorders such as methamphetamine use disorder and obsessive <b>compulsive</b> disorder in children and adolescents, but not depression.
+POU5F1	drug	amphetamine	22084709	<strong><strong>OCT3</strong></strong> single nucleotide polymorphisms (SNPs) have been investigated for their association with psychiatric disorders such as <b>methamphetamine</b> use disorder and obsessive compulsive disorder in children and adolescents, but not depression.
+POU5F1	addiction	addiction	22084709	<strong><strong>OCT3</strong></strong> single nucleotide polymorphisms (SNPs) have been investigated for their association with psychiatric disorders such as methamphetamine use disorder and obsessive <b>compulsive</b> disorder in children and adolescents, but not depression.
+POU5F1	drug	opioid	19151246	JNJ 20788560 [9 (8 azabicyclo[3.2.1]<strong>oct 3</strong> ylidene) 9H xanthene 3 carboxylic acid diethylamide], a selective delta <b>opioid</b> receptor agonist, is a potent and efficacious antihyperalgesic agent that does not produce respiratory depression, pharmacologic tolerance, or physical dependence.
+POU5F1	addiction	dependence	19151246	JNJ 20788560 [9 (8 azabicyclo[3.2.1]<strong>oct 3</strong> ylidene) 9H xanthene 3 carboxylic acid diethylamide], a selective delta opioid receptor agonist, is a potent and efficacious antihyperalgesic agent that does not produce respiratory depression, pharmacologic tolerance, or physical <b>dependence</b>.
+POU5F1	drug	amphetamine	17988657	We have previously demonstrated that rats with behavioral sensitization to <b>methamphetamine</b> (<b>METH</b>) increased the brain penetration of <b>METH</b> with decreased expression of <strong>OCT3</strong> in brain.
+POU5F1	addiction	sensitization	17988657	We have previously demonstrated that rats with behavioral <b>sensitization</b> to methamphetamine (METH) increased the brain penetration of METH with decreased expression of <strong>OCT3</strong> in brain.
+POU5F1	drug	amphetamine	17988657	We have previously demonstrated that rats with behavioral sensitization to <b>methamphetamine</b> (<b>METH</b>) increased the brain penetration of <b>METH</b> with decreased expression of <strong><strong>OCT3</strong></strong> in brain.
+POU5F1	addiction	sensitization	17988657	We have previously demonstrated that rats with behavioral <b>sensitization</b> to methamphetamine (METH) increased the brain penetration of METH with decreased expression of <strong><strong>OCT3</strong></strong> in brain.
+POU5F1	drug	amphetamine	17988657	Considering the earlier in vitro studies demonstrating that 1) <strong>OCT3</strong> could transport dopamine (DA) and 2) the specific transport via <strong>OCT3</strong> could be inhibited by <b>METH</b>, these results suggest that decreased <strong>OCT3</strong> might decrease the efflux of <b>METH</b> and/or DA from brain, subsequently causing the development of behavioral sensitization.
+POU5F1	addiction	sensitization	17988657	Considering the earlier in vitro studies demonstrating that 1) <strong>OCT3</strong> could transport dopamine (DA) and 2) the specific transport via <strong>OCT3</strong> could be inhibited by METH, these results suggest that decreased <strong>OCT3</strong> might decrease the efflux of METH and/or DA from brain, subsequently causing the development of behavioral <b>sensitization</b>.
+POU5F1	drug	amphetamine	17988657	Considering the earlier in vitro studies demonstrating that 1) <strong><strong>OCT3</strong></strong> could transport dopamine (DA) and 2) the specific transport via <strong><strong>OCT3</strong></strong> could be inhibited by <b>METH</b>, these results suggest that decreased <strong><strong>OCT3</strong></strong> might decrease the efflux of <b>METH</b> and/or DA from brain, subsequently causing the development of behavioral sensitization.
+POU5F1	addiction	sensitization	17988657	Considering the earlier in vitro studies demonstrating that 1) <strong><strong>OCT3</strong></strong> could transport dopamine (DA) and 2) the specific transport via <strong><strong>OCT3</strong></strong> could be inhibited by METH, these results suggest that decreased <strong><strong>OCT3</strong></strong> might decrease the efflux of METH and/or DA from brain, subsequently causing the development of behavioral <b>sensitization</b>.
+POU5F1	drug	amphetamine	17988657	Both <b>METH</b> induced hyperlocomotion and <b>METH</b> induced extracellular DA levels in nucleus accumbens and prefrontal cortex were significantly increased in <strong>OCT3</strong> AS treated rats.
+POU5F1	drug	amphetamine	17988657	Both <b>METH</b> induced hyperlocomotion and <b>METH</b> induced extracellular DA levels in nucleus accumbens and prefrontal cortex were significantly increased in <strong><strong>OCT3</strong></strong> AS treated rats.
+POU5F1	drug	amphetamine	17988657	Moreover, the concentrations of <b>METH</b> were significantly increased in cerebrospinal fluid as well as extracellular areas at the nucleus accumbens in <strong>OCT3</strong> AS treated rats.
+POU5F1	drug	amphetamine	17988657	Moreover, the concentrations of <b>METH</b> were significantly increased in cerebrospinal fluid as well as extracellular areas at the nucleus accumbens in <strong><strong>OCT3</strong></strong> AS treated rats.
+POU5F1	drug	amphetamine	17988657	These results suggested that decreased <strong>OCT3</strong> elevated the concentration of <b>METH</b> and/or DA in brain, subsequently enhancing dopaminergic neuronal transmission and increasing <b>METH</b> induced hyperlocomotion.
+POU5F1	drug	amphetamine	17988657	These results suggested that decreased <strong><strong>OCT3</strong></strong> elevated the concentration of <b>METH</b> and/or DA in brain, subsequently enhancing dopaminergic neuronal transmission and increasing <b>METH</b> induced hyperlocomotion.
+POU5F1	drug	amphetamine	17988657	In summary, <strong>OCT3</strong> at the CP could regulate the effect of <b>METH</b> by controlling the levels of <b>METH</b> and/or DA in brain.
+POU5F1	drug	amphetamine	17988657	In summary, <strong><strong>OCT3</strong></strong> at the CP could regulate the effect of <b>METH</b> by controlling the levels of <b>METH</b> and/or DA in brain.
+POU5F1	drug	amphetamine	17988657	Thus, these results suggest that <strong>OCT3</strong> may be a new molecular target to treat <b>METH</b> related disorders such as drug abuse and schizophrenia.
+POU5F1	drug	amphetamine	17988657	Thus, these results suggest that <strong><strong>OCT3</strong></strong> may be a new molecular target to treat <b>METH</b> related disorders such as drug abuse and schizophrenia.
+POU5F1	drug	amphetamine	17460357	Repeated <b>METH</b> treatment decreased the expression of <b>METH</b> transposable and CORT sensitive transporter, organic cation transporter 3 (<strong>OCT3</strong>), in the brain of WIS rats.
+POU5F1	drug	amphetamine	17460357	Repeated <b>METH</b> treatment decreased the expression of <b>METH</b> transposable and CORT sensitive transporter, organic cation transporter 3 (<strong><strong>OCT3</strong></strong>), in the brain of WIS rats.
+POU5F1	drug	amphetamine	17460357	However, the intensity of the decrement of <strong>OCT3</strong> with repeated <b>METH</b> treatment was similar between both strains.
+POU5F1	drug	amphetamine	17460357	However, the intensity of the decrement of <strong><strong>OCT3</strong></strong> with repeated <b>METH</b> treatment was similar between both strains.
+POU5F1	addiction	dependence	17010131	Moreover, SLC22A3 (which encodes <strong>OCT3</strong>) is a candidate gene for MAP <b>dependence</b> because it is located within a chromosomal region associated with substance <b>dependence</b>.
+POU5F1	addiction	dependence	17010131	Moreover, SLC22A3 (which encodes <strong><strong>OCT3</strong></strong>) is a candidate gene for MAP <b>dependence</b> because it is located within a chromosomal region associated with substance <b>dependence</b>.
+POU5F1	drug	cannabinoid	15629265	The effect of the most effective dose (10 ng/rat) was prevented by pre treatment with the CB1 <b>cannabinoid</b> (SR 141716A) [N piperidino 5 (4 chlorophenyl) 1 (2, 4 dichloro phenyl) 4 methyl pyrazole 3 carboxamide hydrochloride] (0.5 mg kg( 1)), the opioid (naloxone) (2 mg kg( 1)), and the serotonin 5 HT3, tropisetron [endo 8 methyl 8 azabicyclo [3.2.1] <strong>oct 3</strong> olindol 3 yl carboxylate hydrochloride] (1 mg kg( 1)), receptor antagonists, which did not induce place conditioning on their own.
+POU5F1	drug	opioid	15629265	The effect of the most effective dose (10 ng/rat) was prevented by pre treatment with the CB1 cannabinoid (SR 141716A) [N piperidino 5 (4 chlorophenyl) 1 (2, 4 dichloro phenyl) 4 methyl pyrazole 3 carboxamide hydrochloride] (0.5 mg kg( 1)), the <b>opioid</b> (<b>naloxone</b>) (2 mg kg( 1)), and the serotonin 5 HT3, tropisetron [endo 8 methyl 8 azabicyclo [3.2.1] <strong>oct 3</strong> olindol 3 yl carboxylate hydrochloride] (1 mg kg( 1)), receptor antagonists, which did not induce place conditioning on their own.
+POU5F1	addiction	aversion	8097165	The S isomer of the novel 5 HT3 receptor antagonist RS 42358 ((S) N (1 azabicyclo[2.2.2]<strong>oct 3</strong> yl) 2,4,5,6 tetrahydro 1 H  benzo[de]isoquinolin 1 one, RS 42358 197) disinhibited behaviour in the mouse suppressed by the <b>aversive</b> situation of the light/dark test box.
+GAPDH	drug	amphetamine	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; BDNF: Brain derived neurotrophic factor; CPP: Conditioned place preference; NMDA: N methyl D aspartic acid; <b>METH</b>: <b>Methamphetamine</b>; CNS: Central nervous system; PFA: Paraformaldehyde; <strong>GAPDH</strong>: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+GAPDH	addiction	reward	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; BDNF: Brain derived neurotrophic factor; <b>CPP</b>: Conditioned place preference; NMDA: N methyl D aspartic acid; METH: Methamphetamine; CNS: Central nervous system; PFA: Paraformaldehyde; <strong>GAPDH</strong>: Glyceraldehyde 3 phosphate dehydrogenase; LTP: long term potentiation.
+GAPDH	drug	amphetamine	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; BDNF: Brain derived neurotrophic factor; CPP: Conditioned place preference; NMDA: N methyl D aspartic acid; <b>METH</b>: <b>Methamphetamine</b>; CNS: Central nervous system; PFA: Paraformaldehyde; <strong>GAPDH</strong>: <strong>Glyceraldehyde 3 phosphate dehydrogenase</strong>; LTP: long term potentiation.
+GAPDH	addiction	reward	29576706	Abbreviations used: Rhy: Rhynchophylline; CREB: cAMP response element binding protein; Nurr1: Nuclear receptor related 1; BDNF: Brain derived neurotrophic factor; <b>CPP</b>: Conditioned place preference; NMDA: N methyl D aspartic acid; METH: Methamphetamine; CNS: Central nervous system; PFA: Paraformaldehyde; <strong>GAPDH</strong>: <strong>Glyceraldehyde 3 phosphate dehydrogenase</strong>; LTP: long term potentiation.
+GAPDH	drug	alcohol	29502276	DAVID functional annotation analysis identified 9 proteins (SNCA, GSTP1, PRDX3, PPP3R1, EIF5A, PHB, PEBP1/RKIP, <strong>GAPDH</strong>, AND SOD1) that were significantly overrepresented in a functional cluster that included the Gene Ontology categories "response to <b>alcohol</b>" and "aging."
+GAPDH	drug	opioid	29053731	Plasma membrane marker Na, K ATPase, actin and <strong>GAPDH</strong> were unaffected by <b>morphine</b> in both types of PNS.
+GAPDH	drug	alcohol	22890201	Furthermore, KLF11 may influence MAO B expression and augment glyceraldehyde 3 phosphate dehydrogenase (<strong>GAPDH</strong>) to upregulate MAO B transcription upon exposure to <b>ethanol</b>.
+GAPDH	drug	alcohol	22890201	Furthermore, KLF11 may influence MAO B expression and augment <strong>glyceraldehyde 3 phosphate dehydrogenase</strong> (<strong>GAPDH</strong>) to upregulate MAO B transcription upon exposure to <b>ethanol</b>.
+GAPDH	drug	alcohol	20022592	A novel role for <strong>glyceraldehyde 3 phosphate dehydrogenase</strong> and monoamine oxidase B cascade in <b>ethanol</b> induced cellular damage.
+GAPDH	drug	alcohol	20022592	<b>Ethanol</b> significantly increases levels of <strong>GAPDH</strong>, especially nuclear <strong>GAPDH</strong>, and MAO B in neuronal cells as well as in human and rat brains.
+GAPDH	drug	alcohol	20022592	<b>Ethanol</b> elicited nuclear <strong>GAPDH</strong> augments TIEG2 mediated MAO B, which might play a role in brain damage in subjects with <b>alcoholism</b>.
+GAPDH	drug	alcohol	19853595	Energy metabolism cluster enzymes <strong>glyceraldehyde 3 phosphate dehydrogenase</strong>, phosphoglycerate kinase, enolase and <b>alcohol</b> dehydrogenase were induced after 5h of exposure.
+GAPDH	drug	amphetamine	17581970	<b>METH</b> also increases glyceraldehyde 3 phosphate dehydrogenase (<strong>GAPDH</strong>) protein in the crude vesicle fraction.
+GAPDH	drug	amphetamine	17581970	<b>METH</b> also increases <strong>glyceraldehyde 3 phosphate dehydrogenase</strong> (<strong>GAPDH</strong>) protein in the crude vesicle fraction.
+GAPDH	drug	amphetamine	17581970	<b>METH</b> induced increases in cortical VGLUT1 mRNA, as well as striatal VGLUT1 and <strong>GAPDH</strong>, are GABA(A) receptor dependent because they are blocked by GABA(A) receptor antagonism in the substantia nigra.
+GAPDH	drug	benzodiazepine	11923223	Among the proteins, which are tyrosine  nitrated by ammonia, <strong>glyceraldehyde 3 phosphate dehydrogenase</strong>, the peripheral type <b>benzodiazepine</b> receptor, Erk 1, and glutamine synthetase are identified.
+GAPDH	drug	alcohol	10871698	To verify that the differences observed were not due to an <b>ethanol</b> induced global alteration in gene transcription, mRNA levels of the housekeeping gene <strong>glyceraldehyde 3 phosphate dehydrogenase</strong> were measured.
+GAPDH	drug	alcohol	10871698	<strong>Glyceraldehyde 3 phosphate dehydrogenase</strong> expression was unchanged following both chronic exposure to <b>ethanol</b> and chronic exposure followed by withdrawal.
+GAPDH	addiction	withdrawal	10871698	<strong>Glyceraldehyde 3 phosphate dehydrogenase</strong> expression was unchanged following both chronic exposure to ethanol and chronic exposure followed by <b>withdrawal</b>.
+GAPDH	drug	alcohol	10036312	The steady state levels of messenger RNA (mRNA) of the glucose transporters 1 and 3 and the glycolytic enzymes hexokinase, phosphofructokinase, <strong>glyceraldehyde 3 phosphate dehydrogenase</strong> and pyruvate dehydrogenase were measured in up to seven brain regions of the rat in a recently developed animal model of 'behavioral dependence' on <b>ethanol</b>.
+GAPDH	addiction	dependence	10036312	The steady state levels of messenger RNA (mRNA) of the glucose transporters 1 and 3 and the glycolytic enzymes hexokinase, phosphofructokinase, <strong>glyceraldehyde 3 phosphate dehydrogenase</strong> and pyruvate dehydrogenase were measured in up to seven brain regions of the rat in a recently developed animal model of 'behavioral <b>dependence</b>' on ethanol.
+GAPDH	drug	alcohol	6388629	Direct transfer of reduced nicotinamide adenine dinucleotide from <strong>glyceraldehyde 3 phosphate dehydrogenase</strong> to liver <b>alcohol</b> dehydrogenase.
+GAPDH	drug	alcohol	6388629	The reduction of benzaldehyde and p nitrobenzaldehyde by NADH, catalyzed by horse liver <b>alcohol</b> dehydrogenase (LADH), has been found to be faster when NADH is bound to <strong>glyceraldehyde 3 phosphate dehydrogenase</strong> (GPDH) than with free NADH.
+EDN1	drug	cannabinoid	31505241	This review focused on how transient receptor potential vanilloid 1, <strong>endothelin 1</strong>/endothelin type A receptor, and <b>cannabinoid</b> receptors contributed to the pathophysiology of SCD associated pain.
+EDN1	drug	alcohol	30053411	Mild stimulation, which was defined as 5 20% of 60 mM KCl induced contraction, with thromboxane A2 mimetic U46619, <strong>endothelin 1</strong> or KCl tremendously increased contractive response of RCAs to <b>ethanol</b> (0.8 8.0 mg/ml).
+EDN1	drug	cocaine	26164164	Between March and June 2014, a total of 57 African American <b>cocaine</b> users with contrast enhanced CT angiography confirmed less than 50% coronary stenosis in Baltimore, Maryland, were enrolled in a 6 month follow up study to investigate whether <b>cocaine</b> abstinence or reduction in <b>cocaine</b> use is associated with decreased <strong>endothelin 1</strong> (ET 1) levels and coronary plaque progression at the 6 month follow up.
+EDN1	drug	alcohol	24173596	We found that chronic <b>alcohol</b> consumption induced a variety of behavioral abnormalities, accompanied by severe pathological changes in cerebral arterioles, prefrontal cortex and cerebellar tissue, as well as an upregulation of vascular endothelial growth factor (VEGF), leptin receptor (ob R) and <strong>endothelin 1</strong> (ET 1).
+EDN1	drug	cocaine	21601240	We determined circulating endothelial cells (CECs) and plasma levels of stromal cell derived factor 1 (SDF 1), monocyte chemotactic protein 1(MCP 1), soluble intracellular adhesion molecule (sICAM), high sensitivity C reactive protein (hsCRP) and <strong>endothelin 1</strong>(ET 1), in DSM IV <b>cocaine</b> addicts at baseline and after one month of <b>cocaine</b> abstinence.
+EDN1	addiction	sensitization	20559459	Injection of <strong>endothelin 1</strong> (ET 1) into the plantar rat hindpaw causes acute pain at high concentrations and tactile <b>sensitization</b> at low concentrations.
+EDN1	drug	alcohol	17980786	<b>Alcohol</b> induced endothelial damage or protection may be related to the synthesis or action of several markers, such as nitric oxide, cortisol, <strong>endothelin 1</strong>, adhesion molecules, tumor necrosis factor alpha, interleukin 6, C reactive protein, and haemostatic factors.
+EDN1	drug	alcohol	17211243	The maximal percentage of flow mediated dilatation was reduced in detoxified <b>alcoholics</b> (10.1 +/  4.6 versus 14.9 +/  7.4, P < 0.001) who also showed significantly higher blood pressure (systolic 127.5 +/  12.9 versus 118.2 +/  10.7 mmHg, P < 0.001; diastolic 79.4 +/  7.1 versus 74.6 +/  6.4 mmHg, P < 0.01; mean 95.4 +/  8.2 versus 89.1 +/  7.3 mmHg, P < 0.001), uric acid (5.0 +/  1.1 versus 4.4 +/  0.8 mg/dl, P < 0.05), high sensitivity C reactive protein (2.1 +/  2.0 versus 1.0 +/  0.9 mg/l, P < 0.01), <strong>endothelin 1</strong> (0.38 +/  0.11 versus 0.17 +/  0.10 pg/ml, P < 0.001) and fasting insulin (10.4 +/  4.5 versus 5.6 +/  1.6 muU/ml, P < 0.001) with abnormal homeostasis model assessment index of insulin resistance (2.3 +/  1.1 versus 1.2 +/  0.4, P < 0.001).
+EDN1	drug	alcohol	16269920	We tested the effects of <b>alcohol</b> withdrawal in heavy <b>alcohol</b> consumers and compared the plasma levels of <strong>endothelin 1</strong>, nitric oxide, plasminogen activator inhibitor 1, von Willebrand factor, malondialdehyde, and intracellular glutathione with those of <b>alcoholics</b> that did not modify their <b>alcohol</b> intake and teetotalers.
+EDN1	addiction	withdrawal	16269920	We tested the effects of alcohol <b>withdrawal</b> in heavy alcohol consumers and compared the plasma levels of <strong>endothelin 1</strong>, nitric oxide, plasminogen activator inhibitor 1, von Willebrand factor, malondialdehyde, and intracellular glutathione with those of alcoholics that did not modify their alcohol intake and teetotalers.
+EDN1	drug	alcohol	16269920	<b>Alcohol</b> increased the levels of <strong>endothelin 1</strong>, nitric oxide, and plasminogen activator inhibitor 1 and decreased the levels of von Willebrand factor both in vivo and in vitro.
+EDN1	addiction	sensitization	15351928	Moreover, short pretreatment of bronchi with capsaicin (10 microM) or capsazepine (1 microM) after <b>sensitization</b> by fenoterol decreased the rise in smooth muscle contraction to <strong>endothelin 1</strong>.
+EDN1	addiction	sensitization	15351928	In conclusion, fenoterol induces <b>sensitization</b> of human isolated bronchi to <strong>endothelin 1</strong> in part through the stimulation of the vanilloid TRPV 1 receptor on tachykininergic sensory nerves.
+EDN1	drug	nicotine	8587374	Effect of cigarette <b>smoking</b> and <b>nicotine</b> on plasma <strong>endothelin 1</strong> levels.
+EDN1	drug	opioid	8289581	<b>Opioid</b> mu receptor subtypes (possibly mu 1 and mu 2) revealed by <b>morphine</b> induced antinociception vs <strong>endothelin 1</strong> in recombinant inbred CXBK mice.
+EDN1	drug	opioid	8289581	<b>Morphine</b> induced antinociception against acetylcholine was strain dependent, whereas against <strong>endothelin 1</strong> it was not.
+EDN1	drug	cocaine	8438922	Plasma concentration of <strong>endothelin 1</strong> in women with <b>cocaine</b> associated pregnancy complications.
+EDN1	drug	cocaine	8438922	The purpose of this study was to determine if the plasma concentration of <strong>endothelin 1</strong> is elevated in pregnant women abusing <b>cocaine</b> and to determine how these levels differ from those in patients with preeclampsia and in women with uncomplicated pregnancies.
+EDN1	drug	cocaine	8438922	Plasma <strong>endothelin 1</strong> levels were measured in 30 women with acute <b>cocaine</b> intoxication, 32 women with preeclampsia, 14 pregnant women with chronic hypertension, 26 women with uncomplicated pregnancies, and 16 nonpregnant individuals.
+EDN1	addiction	intoxication	8438922	Plasma <strong>endothelin 1</strong> levels were measured in 30 women with acute cocaine <b>intoxication</b>, 32 women with preeclampsia, 14 pregnant women with chronic hypertension, 26 women with uncomplicated pregnancies, and 16 nonpregnant individuals.
+EDN1	drug	cocaine	8438922	The mean <strong>endothelin 1</strong> concentration in those with <b>cocaine</b> abuse was 18.2 +/  8.1 pg/ml (95% confidence interval 15.2 to 21.2).
+EDN1	drug	cocaine	8438922	<strong>Endothelin 1</strong> levels in women abusing <b>cocaine</b> are comparable to those in women with preeclampsia and are significantly higher than those in gravid women with chronic hypertension and women with uncomplicated pregnancies.
+EDN1	drug	cocaine	8438922	Elevated levels of <strong>endothelin 1</strong> may contribute to some of the pregnancy related complications in women abusing <b>cocaine</b>.
+CPZ	addiction	reward	29343767	In the present study, we performed conditioned place preference (<b>CPP</b>) and self administration tests to examine the effects of capsazepine (<strong>CPZ</strong>) and SB366791 (SB) on MAP <b>reward</b>.
+CPZ	addiction	reward	29343767	We found that both <strong>CPZ</strong> and SB significantly inhibited MAP induced <b>CPP</b> and self administration; in contrast, TRPV1 knock out (KO) mice did not develop MAP induced <b>CPP</b>.
+CPZ	addiction	reward	29343767	Furthermore, attenuated dopamine transporter (DAT) binding levels in the NAc and DSt regions of MAP induced <b>CPP</b> mice were reversed by <strong>CPZ</strong>.
+CPZ	drug	opioid	25118895	Based on the general role of TRPV1 antagonist in blocking neural over excitability by both pre  and post synaptic mechanisms, TRPV1 antagonist capsazepine (<strong>CPZ</strong>) was tested for its ability to prohibit persistent <b>opioid</b> craving in rats.
+CPZ	addiction	relapse	25118895	Based on the general role of TRPV1 antagonist in blocking neural over excitability by both pre  and post synaptic mechanisms, TRPV1 antagonist capsazepine (<strong>CPZ</strong>) was tested for its ability to prohibit persistent opioid <b>craving</b> in rats.
+CPZ	drug	opioid	25118895	In the present study, we assessed the expression of TRPV1 in nucleus accumbens and investigated the effect of <strong>CPZ</strong> in bilateral nucleus accumbens on persistent <b>morphine</b> conditioned place preference (mCPP) in rats.
+CPZ	drug	opioid	25118895	We found that <b>morphine</b> conditioned place preference increased the TRPV1 expression and <strong>CPZ</strong> attenuated <b>morphine</b> conditioned place preference in a dose dependent and target specific manner after both short  and long term spontaneous withdrawal, reflected by the reduction of the increased time in <b>morphine</b> paired side.
+CPZ	addiction	withdrawal	25118895	We found that morphine conditioned place preference increased the TRPV1 expression and <strong>CPZ</strong> attenuated morphine conditioned place preference in a dose dependent and target specific manner after both short  and long term spontaneous <b>withdrawal</b>, reflected by the reduction of the increased time in morphine paired side.
+CPZ	drug	opioid	25118895	<strong>CPZ</strong> (10 nM) could induce prolonged and stable inhibition of <b>morphine</b> conditioned place preference expression.
+CPZ	drug	amphetamine	20709144	<b>Methamphetamine</b> induced withdrawal was not affected by the 5 HT(2B/2C) receptor agonist meta chlorophenylpiperazine (m <strong>CPZ</strong>) (0.1 20 μM).
+CPZ	addiction	withdrawal	20709144	Methamphetamine induced <b>withdrawal</b> was not affected by the 5 HT(2B/2C) receptor agonist meta chlorophenylpiperazine (m <strong>CPZ</strong>) (0.1 20 μM).
+CPZ	drug	amphetamine	11071394	of d <b>amphetamine</b> (<b>AMPH</b>) or chlorpromazine (<strong>CPZ</strong>) at 1 2 week intervals.
+CPZ	drug	benzodiazepine	7711985	Two to three hours after abrupt withdrawal, the outpatients were given 15 mg DM every hour, 25 or 50 mg chlorpromazine (<strong>CPZ</strong>) + 4 mg TIZ every six hours and 10 mg <b>diazepam</b> + 10 mg hyoscine N butyl Br + 250 mg dipyrone every six hours three hours following <strong>CPZ</strong>.
+CPZ	addiction	withdrawal	7711985	Two to three hours after abrupt <b>withdrawal</b>, the outpatients were given 15 mg DM every hour, 25 or 50 mg chlorpromazine (<strong>CPZ</strong>) + 4 mg TIZ every six hours and 10 mg diazepam + 10 mg hyoscine N butyl Br + 250 mg dipyrone every six hours three hours following <strong>CPZ</strong>.
+CPZ	drug	amphetamine	7933709	When chlorpromazine (<strong>CPZ</strong>) and lithium chloride (LiCl) are compared, the former suppresses both rat's intracranial self stimulation (ICSS) and <b>methamphetamine</b> (MAP) induced hyperactivity.
+CPZ	addiction	reward	7933709	When chlorpromazine (<strong>CPZ</strong>) and lithium chloride (LiCl) are compared, the former suppresses both rat's intracranial self stimulation (<b>ICSS</b>) and methamphetamine (MAP) induced hyperactivity.
+CPZ	drug	amphetamine	1505855	Effects of mosapramine (Y 516), a new dopamine D2 antagonist, on reverse tolerance (sensitization) after repeated administration of <b>methamphetamine</b> (MAP; 2 mg/kg, s.c.) were investigated by means of ambulatory activity in mice; and they were compared with those of clocapramine (CCP), bromperidol (BPD) and chlorpromazine (<strong>CPZ</strong>).
+CPZ	addiction	sensitization	1505855	Effects of mosapramine (Y 516), a new dopamine D2 antagonist, on reverse tolerance (<b>sensitization</b>) after repeated administration of methamphetamine (MAP; 2 mg/kg, s.c.) were investigated by means of ambulatory activity in mice; and they were compared with those of clocapramine (CCP), bromperidol (BPD) and chlorpromazine (<strong>CPZ</strong>).
+CPZ	drug	benzodiazepine	2187002	Four mg chlorpromazine (<strong>CPZ</strong>) was administered every hour and 10 mg <b>diazepam</b> (DIA) every 6 hours to a group consisting of two female and nineteen male inpatients.
+CPZ	drug	opioid	2187002	The remaining subjects received 15 mg non <b>opioid</b> antitussive dextromethorphan (DM) instead of <strong>CPZ</strong>.
+CPZ	drug	benzodiazepine	2540276	Daily intraperitoneal administration to rats of 5 mg/kg of chlorpromazine (<strong>CPZ</strong>) for 21 days induced a significant up regulation (51%) of peripheral <b>benzodiazepine</b> binding sites (PBSs) in cerebral cortex and a down regulation of PBSs in the heart (25%) and kidney (14%), whereas no alteration in [3H]<b>flunitrazepam</b> binding in cerebral cortex was observed.
+CPZ	addiction	withdrawal	2540276	[3H]PK 11195 binding to cerebral cortex returned to normal following 5 days of <strong>CPZ</strong> <b>withdrawal</b>, whereas the density of PBSs in the heart and kidney remained reduced.
+CPZ	drug	amphetamine	2496967	In addition, provocative pharmacologic challenges were employed to assess the interaction between A23187 and the centrally active drugs <b>amphetamine</b> (<b>AMPH</b>), scopolamine (SCOP), or chlorpromazine (<strong>CPZ</strong>).
+CPZ	drug	amphetamine	2496967	In the pharmacological challenge studies, <b>AMPH</b> and SCOP both attenuated and <strong>CPZ</strong> enhanced the acute hypomotility induced by 0.5 mg A23187/kg.
+CPZ	drug	benzodiazepine	6151209	Acute drug effects on the three dependent variables were assessed for dose ranges of haloperidol (HAL), chlorpromazine (<strong>CPZ</strong>), clozapine (CLZ), and <b>chlordiazepoxide</b> (CDP).
+CPZ	drug	benzodiazepine	6415749	Food presentation or cocaine injection occurred only at the end of each daily session, thereby allowing assessment of the effects of presession administration of cocaine, chlorpromazine (<strong>CPZ</strong>), and <b>chlordiazepoxide</b> (CDP) on responding at times when the direct effects of consequent cocaine injections were minimal or absent.
+CPZ	drug	cocaine	6415749	Food presentation or <b>cocaine</b> injection occurred only at the end of each daily session, thereby allowing assessment of the effects of presession administration of <b>cocaine</b>, chlorpromazine (<strong>CPZ</strong>), and chlordiazepoxide (CDP) on responding at times when the direct effects of consequent <b>cocaine</b> injections were minimal or absent.
+CPZ	drug	cocaine	6415749	Presession treatment with suitable doses of <b>cocaine</b> increased low rates of food  or <b>cocaine</b> maintained responding under both types of second order schedules, whereas <strong>CPZ</strong> only decreased responding.
+CPZ	drug	cocaine	6415749	Thus, the behavioral effects of <b>cocaine</b>, CDP, and <strong>CPZ</strong> were largely independent of whether responding was maintained by food or by <b>cocaine</b>.
+CPZ	drug	benzodiazepine	6177889	The B dependent rats were grouped according to the following 5 states: G I, B dependent state; G II, B withdrawn state; G III, cross administration of <b>nitrazepam</b> (NZP) following B withdrawal; G IV, cross administration of chlorpromazine (<strong>CPZ</strong>) following B withdrawal; and G V, cross administration of phenytoin following B withdrawal.
+CPZ	addiction	withdrawal	6177889	The B dependent rats were grouped according to the following 5 states: G I, B dependent state; G II, B withdrawn state; G III, cross administration of nitrazepam (NZP) following B <b>withdrawal</b>; G IV, cross administration of chlorpromazine (<strong>CPZ</strong>) following B <b>withdrawal</b>; and G V, cross administration of phenytoin following B <b>withdrawal</b>.
+CPZ	addiction	withdrawal	6177889	On the other hand, <strong>CPZ</strong> and phenytoin, which inhibit B <b>withdrawal</b> convulsion slightly, failed to recover completely the 5 HT turnover rate during B <b>withdrawal</b>.
+CPZ	drug	benzodiazepine	6118452	In the crossphysical dependence study, two drug combinations, i.e., phenobarbital (PhB) chloropromazine (<strong>CPZ</strong>), PhB diphenhydramine (DPH) and <b>nitrazepam</b> chlorprothixene, and 3 drug combinations (i.e., PhB <strong>CPZ</strong> promethazine and PhB <strong>CPZ</strong> DPH were evaluated.
+CPZ	addiction	dependence	6118452	In the crossphysical <b>dependence</b> study, two drug combinations, i.e., phenobarbital (PhB) chloropromazine (<strong>CPZ</strong>), PhB diphenhydramine (DPH) and nitrazepam chlorprothixene, and 3 drug combinations (i.e., PhB <strong>CPZ</strong> promethazine and PhB <strong>CPZ</strong> DPH were evaluated.
+CPZ	addiction	reward	7297414	Chlorpromazine (<strong>CPZ</strong>) and haloperidol (H) have been suggested as possible antagonists of the <b>reinforcing</b> effects of psychomotor stimulant drugs.
+CPZ	drug	cocaine	7297414	Continuous infusions of low or intermediate doses of <strong>CPZ</strong> or H either did not affect or increased the frequency of <b>cocaine</b> choice.
+CPZ	drug	cocaine	7297414	Although ther appears to be a mutual antagonism of some of the effects of <b>cocaine</b> and these antipsychotic compounds, the results of the present experiment fail to support the hypothesis that the reinforcing effects of <b>cocaine</b> can be antagonized with <strong>CPZ</strong> or H.
+CPZ	addiction	reward	7297414	Although ther appears to be a mutual antagonism of some of the effects of cocaine and these antipsychotic compounds, the results of the present experiment fail to support the hypothesis that the <b>reinforcing</b> effects of cocaine can be antagonized with <strong>CPZ</strong> or H.
+CPZ	drug	amphetamine	7443736	Effects of d <b>amphetamine</b> (AM), chlorpromazine (<strong>CPZ</strong>) and diazepam (DZ) on schedule controlled responding (lever pressing) and adjunctive drinking under a fixed interval (FI) 1.5 min schedule of food reinforcement in rats were investigated.
+CPZ	drug	benzodiazepine	7443736	Effects of d amphetamine (AM), chlorpromazine (<strong>CPZ</strong>) and <b>diazepam</b> (DZ) on schedule controlled responding (lever pressing) and adjunctive drinking under a fixed interval (FI) 1.5 min schedule of food reinforcement in rats were investigated.
+CPZ	addiction	reward	7443736	Effects of d amphetamine (AM), chlorpromazine (<strong>CPZ</strong>) and diazepam (DZ) on schedule controlled responding (lever pressing) and adjunctive drinking under a fixed interval (FI) 1.5 min schedule of food <b>reinforcement</b> in rats were investigated.
+CPZ	drug	benzodiazepine	32386	After 72 hr, chlorpromazine (<strong>CPZ</strong> 1,2 and 4 mg/kg), haloperidol (0.2, 0.4 and 0.8 mg/kg), thioridazine (10, 20 and 40 mg/kg), <b>chlordiazepoxide</b> (2,4 and 8 mg/kg), <b>diazepam</b> (DPM, 1, 2 and 4 mg/kg) or vehicle was injected s.c. 55 min before precipitation of abstinence with naloxone (1 mg/kg s.c.).
+CPZ	drug	opioid	32386	After 72 hr, chlorpromazine (<strong>CPZ</strong> 1,2 and 4 mg/kg), haloperidol (0.2, 0.4 and 0.8 mg/kg), thioridazine (10, 20 and 40 mg/kg), chlordiazepoxide (2,4 and 8 mg/kg), diazepam (DPM, 1, 2 and 4 mg/kg) or vehicle was injected s.c. 55 min before precipitation of abstinence with <b>naloxone</b> (1 mg/kg s.c.).
+CPZ	drug	benzodiazepine	32386	Jumping was exacerbated by <strong>CPZ</strong> (4 mg/kg), <b>chlordiazepoxide</b> (4 and 8 mg/kg) and DPM (1, 2 and 4 mg/kg); haloperidol and thioridazine had no significant effect on this sign.
+CPZ	addiction	reward	825884	Chlorpromazine (<strong>CPZ</strong>) doses of 0.5 and 1.0 mg/kg decreased caudate <b>ICSS</b> significantly more than lateral hypothalamic <b>ICSS</b>.
+CPZ	drug	amphetamine	825884	These findings, using ICSS as a behavioral measure, suggest that the effects of <b>amphetamine</b> and <strong>CPZ</strong> involve not only hypothalamic structures but more anterior telencephalic sites as well.
+CPZ	addiction	reward	825884	These findings, using <b>ICSS</b> as a behavioral measure, suggest that the effects of amphetamine and <strong>CPZ</strong> involve not only hypothalamic structures but more anterior telencephalic sites as well.
+CPZ	drug	amphetamine	825884	The prolonged actions of <b>amphetamine</b> and <strong>CPZ</strong> on caudate ICSS suggest that drugs acting, in part, on dopamine containing neurons will interfere with certain caudate mediated behavior.
+CPZ	addiction	reward	825884	The prolonged actions of amphetamine and <strong>CPZ</strong> on caudate <b>ICSS</b> suggest that drugs acting, in part, on dopamine containing neurons will interfere with certain caudate mediated behavior.
+CPZ	drug	benzodiazepine	169190	The effect of chlorpromazine (<strong>CPZ</strong>), imipramine (IMP), <b>nitrazepam</b> (NZP) and amobarbital sodium (AMOB) on the REM period of sleep (REMP) was investigated on four subjects by means of all night sleep polygraphy with the schedule PPPDDDPP where P is placebo and D active drug.
+CPZ	addiction	withdrawal	169190	<strong>CPZ</strong> 25 mg resulted in a slight increase in %REMP, and no significant change in REM density (1 second fraction method) and total REM activity during the drug and <b>withdrawal</b> nights.
+CPZ	drug	psychedelics	13739950	A representative psychotogen, lysergic acid diethylamide (<b>LSD</b> 25), in doses small enough to be devoid of gross effects, increases response latency in rats to a tone indicating the availability of water reward; this effect is greatly reduced by prophylactic administration of a representative phenothiazine tranquilizer, chlorpromazine (<strong>CPZ</strong>), in doses that per se do not affect performance.
+CPZ	addiction	reward	13739950	A representative psychotogen, lysergic acid diethylamide (LSD 25), in doses small enough to be devoid of gross effects, increases response latency in rats to a tone indicating the availability of water <b>reward</b>; this effect is greatly reduced by prophylactic administration of a representative phenothiazine tranquilizer, chlorpromazine (<strong>CPZ</strong>), in doses that per se do not affect performance.
+CCR5	drug	cocaine	31843646	<strong>CCR5</strong> and responses to <b>cocaine</b>: Addiction is not just about the brain.
+CCR5	addiction	addiction	31843646	<strong>CCR5</strong> and responses to cocaine: <b>Addiction</b> is not just about the brain.
+CCR5	drug	cocaine	31557508	Chemokine <strong>CCR5</strong> and <b>cocaine</b> interactions in the brain: <b>Cocaine</b> enhances mesolimbic <strong>CCR5</strong> mRNA levels and produces place preference and locomotor activation that are reduced by a <strong>CCR5</strong> antagonist.
+CCR5	drug	cocaine	31557508	Evidence that <strong>CCR5</strong> knockout mice display fewer dopamine neurons, lower striatal dopamine levels, and reduced locomotor activation compared to wild types also suggest a link between <strong>CCR5</strong> receptors and <b>cocaine</b> dependence.
+CCR5	addiction	dependence	31557508	Evidence that <strong>CCR5</strong> knockout mice display fewer dopamine neurons, lower striatal dopamine levels, and reduced locomotor activation compared to wild types also suggest a link between <strong>CCR5</strong> receptors and cocaine <b>dependence</b>.
+CCR5	drug	cocaine	31557508	Here, we tested the hypothesis using male Sprague Dawley rats that <b>cocaine</b> induced locomotor activation and conditioned place preference (CPP) are inhibited by a FDA approved <strong>CCR5</strong> antagonist (maraviroc), and that <strong>CCR5</strong> gene expression in mesolimbic substrates is enhanced by repeated <b>cocaine</b> exposure.
+CCR5	addiction	reward	31557508	Here, we tested the hypothesis using male Sprague Dawley rats that cocaine induced locomotor activation and conditioned place preference (<b>CPP</b>) are inhibited by a FDA approved <strong>CCR5</strong> antagonist (maraviroc), and that <strong>CCR5</strong> gene expression in mesolimbic substrates is enhanced by repeated cocaine exposure.
+CCR5	drug	cocaine	31557508	In rats treated repeatedly with <b>cocaine</b> (10 mg/kg × 4 days, IP), <strong>CCR5</strong> gene expression was upregulated in the nucleus accumbens and ventral tegmental area but mRNA levels of <strong>CCR5</strong> ligands (i.e., CCL3, CCL4 and CCL5) were not affected.
+CCR5	drug	cocaine	31557508	Our results suggest that mesolimbic <strong>CCR5</strong> receptors are dysregulated by <b>cocaine</b> exposure and, similar to CXCR4 and CCR2 receptors, influence behavioral effects related to the abuse liability of <b>cocaine</b>.
+CCR5	addiction	intoxication	31265902	The <b>binge</b> group showed increased expression of <strong>CCR5</strong> and PD 1 in NKCs, respective to the LR group, and decreased expression of TLR4, along with fewer CCR4+ cells.
+CCR5	drug	opioid	30970233	MCC22 consists of mu <b>opioid</b> receptor (MOR) agonist and chemokine receptor 5 (<strong>CCR5</strong>) antagonist pharmacophores connected through a 22 atom spacer and was designed to target a putative MOR <strong>CCR5</strong> heteromer localized in pain processing areas.
+CCR5	drug	opioid	30249618	Dose response curves for <b>morphine</b>, maraviroc (a <strong>CCR5</strong> antagonist), and AMD3100 (a CXCR4 antagonist) alone were established.
+CCR5	drug	opioid	30053832	A bivalent compound targeting <strong>CCR5</strong> and the mu <b>opioid</b> receptor treats inflammatory arthritis pain in mice without inducing pharmacologic tolerance.
+CCR5	drug	opioid	30053832	MCC22 is a novel bivalent compound containing a <strong>CCR5</strong> antagonist and mu <b>opioid</b> receptor (MOR) agonist pharmacophores linked through a 22 atom spacer.
+CCR5	drug	opioid	29578946	MCC22 consists of a mu <b>opioid</b> receptor agonist and a chemokine receptor 5 (<strong>CCR5</strong>) antagonist that are linked through a 22 atom spacer.
+CCR5	drug	opioid	29146238	<strong>CCR5</strong> mediates HIV 1 Tat induced neuroinflammation and influences <b>morphine</b> tolerance, dependence, and reward.
+CCR5	addiction	dependence	29146238	<strong>CCR5</strong> mediates HIV 1 Tat induced neuroinflammation and influences morphine tolerance, <b>dependence</b>, and reward.
+CCR5	addiction	reward	29146238	<strong>CCR5</strong> mediates HIV 1 Tat induced neuroinflammation and influences morphine tolerance, dependence, and <b>reward</b>.
+CCR5	drug	opioid	29146238	These effects may involve the C C chemokine receptor type 5 (<strong>CCR5</strong>); however, the behavioral contribution of <strong>CCR5</strong> on Tat/<b>opioid</b> interactions is not known.
+CCR5	drug	opioid	29146238	To assess the influence of <strong>CCR5</strong> on these effects, mice were pretreated with oral vehicle or the <strong>CCR5</strong> antagonist, maraviroc, prior to <b>morphine</b> administration.
+CCR5	drug	opioid	29146238	Protein array analyses revealed only minor changes to cytokine profiles when <b>morphine</b> was administered acutely or repeatedly; however, 24 h post <b>morphine</b> administration, the expression of several cytokines was greatly increased, including endogenous <strong>CCR5</strong> chemokine ligands (CCL3, CCL4, and CCL5), as well as CCL2.
+CCR5	drug	opioid	29146238	These data demonstrate that <strong>CCR5</strong> mediates key aspects of HIV 1 Tat induced alterations in the antinociceptive potency and rewarding properties of <b>opioids</b>.
+CCR5	addiction	intoxication	28481655	Compared to the low risk group, the <b>binge</b> group showed higher <strong>CCR5</strong> expression on PMNs, decreases in the CD69 percentage and positive PMNs per microliter, and decreased CXCR4 expression on monocytes.
+CCR5	drug	opioid	23682308	A Bivalent Ligand Targeting the Putative Mu <b>Opioid</b> Receptor and Chemokine Receptor <strong>CCR5</strong> Heterodimers: Binding Affinity versus Functional Activities.
+CCR5	drug	opioid	23682308	The steric hindrance generated from the spacer affected the binding affinity and Ca2+ flux inhibition function activity of bivalent ligand 1 at the chemokine receptor <strong>CCR5</strong> more profoundly than it did at the mu <b>opioid</b> receptor (MOR).
+CCR5	drug	opioid	22354464	Design and synthesis of a bivalent ligand to explore the putative heterodimerization of the mu <b>opioid</b> receptor and the chemokine receptor <strong>CCR5</strong>.
+CCR5	drug	opioid	22354464	<b>Morphine</b>, a mu <b>opioid</b> receptor (MOR) agonist, can accelerate HIV infection through up regulating the expression of the chemokine receptor <strong>CCR5</strong>, a well known co receptor for HIV invasion to the host cells and this has been extensively studied.
+CCR5	drug	alcohol	16105698	To test the hypothesis that chemokines exhibit previously undiscovered pleiotropic effects important for the behavioral actions of <b>ethanol</b>, we studied mutant mice with deletion of the Ccr2, <strong>Ccr5</strong>, Ccl2 or Ccl3 genes.
+CCR5	drug	alcohol	16105698	Ccr2 and <strong>Ccr5</strong> null mutant mice did not differ from wild type mice in <b>ethanol</b> induced loss of righting reflex (LORR), but mice lacking Ccl2 or Ccl3 showed longer LORR than wild type mice.
+CCR5	drug	alcohol	14560041	We and others have recently demonstrated that opioid enhances HIV infection of human macrophages through modulation of beta chemokines and the <strong>CCR5</strong> receptor and that this effect is reversed by <b>naltrexone</b>, a tertiary opioid antagonist.
+CCR5	drug	opioid	14560041	We and others have recently demonstrated that <b>opioid</b> enhances HIV infection of human macrophages through modulation of beta chemokines and the <strong>CCR5</strong> receptor and that this effect is reversed by naltrexone, a tertiary <b>opioid</b> antagonist.
+CCR5	drug	opioid	14560041	Furthermore, MNTX abolished <b>morphine</b> mediated up regulation of <strong>CCR5</strong> receptor expression.
+CCR5	drug	opioid	14560041	The ability of MNTX to block <b>opioid</b> induced <strong>CCR5</strong> expression and HIV replication at clinically relevant doses may have additional benefit for <b>opioid</b> abusers with HIV infection, or patients with AIDS pain receiving <b>opioids</b>.
+CCND1	drug	alcohol	28784931	<b>Alcohol</b> disrupted lipopolysaccharide (LPS) TLR4 ERK1/2 <strong>cyclin D1</strong> signaling and inhibited upregulation of Sca 1 and C/EBPβ expression by lineage negative marrow cells in response to bacteremia.
+CCND1	drug	alcohol	26786850	In addition, the <b>ethanol</b> inhibited basal neuroblasts proliferation was connected to decrease in <strong>cyclin D1</strong> and Rb phosphorylation indicating cell cycle arrest.
+CCND1	drug	alcohol	26786850	Further, in utero <b>ethanol</b> exposure in pregnant rats during E15 E18 significantly decreased Tbr2 and <strong>cyclin D1</strong> positive cell number in cerebral cortex of embryos as assessed by cell sorting analysis by flow cytometry.
+CCND1	drug	alcohol	26159875	Basal differences were observed between hPXR males and females in which females expressed higher levels of two principal enzymes responsible for EtOH metabolism, <b>alcohol</b> dehydrogenase 1 and aldehyde dehydrogenase 2, and two key mediators of hepatocyte replication and repair, <strong>cyclin D1</strong> and proliferating cell nuclear antigen.
+CCND1	drug	nicotine	26118026	The authors investigated the association of <strong>Bcl1</strong> polymorphism with predisposition to bronchial asthma, chronic obstructive pulmonary disease, with the <b>nicotine</b> addiction degree and with progressing disorders of pulmonary function in cystic fibrosis.
+CCND1	addiction	addiction	26118026	The authors investigated the association of <strong>Bcl1</strong> polymorphism with predisposition to bronchial asthma, chronic obstructive pulmonary disease, with the nicotine <b>addiction</b> degree and with progressing disorders of pulmonary function in cystic fibrosis.
+CCND1	drug	opioid	24469921	Furthermore HIV Tat and <b>morphine</b> exposure increased activation of extracellular signal regulated kinase 1/2 (ERK1/2), enhanced levels of p53 and p21, and decreased <strong>cyclin D1</strong> and Akt levels in NPCs.
+CCND1	drug	alcohol	23400686	In 289 patients with T3 4 (77.8%), node negative (84.1%) tumors of the larynx, high EGFR and <strong>CCND1</strong> mRNA correlated with no or ex smoking, (p = 0.003 and p = 0.029, respectively), while low Akt3 mRNA correlated with <b>alcohol</b> abuse, N0 stage, total laryngectomy, and absence of neck dissection.
+CCND1	drug	nicotine	23400686	In 289 patients with T3 4 (77.8%), node negative (84.1%) tumors of the larynx, high EGFR and <strong>CCND1</strong> mRNA correlated with no or ex <b>smoking</b>, (p = 0.003 and p = 0.029, respectively), while low Akt3 mRNA correlated with alcohol abuse, N0 stage, total laryngectomy, and absence of neck dissection.
+CCND1	addiction	relapse	23400686	In multivariate analysis, node positive status, subglottic transglottic location, surgery other than total laryngectomy and mTOR/<strong>CCND1</strong> mRNA interaction with a hazard ratio of 2.16 (p value for interaction: 0.0010) were independent predictors of <b>relapse</b>, while node positive status and subglottic transglottic location were associated with higher risk for death.
+CCND1	drug	alcohol	22901182	<strong>Cyclin D1</strong> overexpression is associated with the advanced stage of the cancer (P=0.029), but not with gender, age, stage of cancer, histological differentiation, anatomical site, smoking history and <b>alcohol</b> consumption history.
+CCND1	drug	nicotine	22901182	<strong>Cyclin D1</strong> overexpression is associated with the advanced stage of the cancer (P=0.029), but not with gender, age, stage of cancer, histological differentiation, anatomical site, <b>smoking</b> history and alcohol consumption history.
+CCND1	addiction	relapse	22901182	Overexpression of <strong>cyclin D1</strong> was correlated to shorter <b>relapse</b> free survival period (P<0.001).
+CCND1	addiction	relapse	22901182	Overexpression of <strong>cyclin D1</strong> can be used as a marker to predict <b>relapse</b> in patients with LSCC after primary curative resection.
+CCND1	drug	nicotine	20106947	We provide evidence for the first time that <b>nicotine</b> strongly activated Stat3, leading to <strong>Cyclin D1</strong> overexpression, cell cycle perturbations, and chemoresistance.
+CCND1	drug	nicotine	19221502	DNA damage dependent <strong>cyclin D1</strong> proteolysis: GSK3beta holds the <b>smoking</b> gun.
+CCND1	addiction	sensitization	19221502	(18) This work revealed that loss of <strong>cyclin D1</strong> regulation compromises the intra S phase response to DNA damage, promoting genomic instability and <b>sensitization</b> of cells to S phase chemotherapy, highlighting a potential therapeutic strategy for cancers exhibiting <strong>cyclin D1</strong> accumulation.
+AADC	drug	opioid	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (TH), <strong>DOPA decarboxylase</strong> (DDC), solute carrier family 6 member 3 (SLC6A3) and DA beta hydroxylase (DBH), with six important phenotypes of <b>heroin</b> dependence.
+AADC	addiction	dependence	32736537	This study aimed to identify the association between genetic polymorphisms of DA synthesis and metabolism genes, including tyrosine hydroxylase (TH), <strong>DOPA decarboxylase</strong> (DDC), solute carrier family 6 member 3 (SLC6A3) and DA beta hydroxylase (DBH), with six important phenotypes of heroin <b>dependence</b>.
+AADC	drug	opioid	27038750	This group had higher POMC in the arcuate nucleus (ARC), higher tyrosine hydroxylase (TH) in the VTA, higher <strong>dopa decarboxylase</strong> (DDc), higher D2R and μu <b>opioid</b> receptor in the NAc.
+AADC	drug	alcohol	24040111	A previous study of the <strong>DOPA decarboxylase</strong> substrate 6 [(18)F]fluoro L DOPA (FDOPA) with positron emission tomography (PET) detected no difference of the net blood brain transfer rate (Kin(app)) between detoxified <b>alcoholic</b> patients and healthy controls.
+AADC	drug	nicotine	26451072	Gamma aminobutyric acid B receptor 2 (GABBR2), <strong>dopa decarboxylase</strong> (DDC), and cholinergic receptor nicotinic alpha 4 (CHRNA4) are three examples of genes that have previously shown strong associations with <b>nicotine</b> dependence.
+AADC	addiction	dependence	26451072	Gamma aminobutyric acid B receptor 2 (GABBR2), <strong>dopa decarboxylase</strong> (DDC), and cholinergic receptor nicotinic alpha 4 (CHRNA4) are three examples of genes that have previously shown strong associations with nicotine <b>dependence</b>.
+AADC	drug	nicotine	21806388	The purpose of the present work was to examine the association of SNPs in the <strong>DOPA decarboxylase</strong> (DDC), dopamine receptor D2 (DRD2) and dopamine transporter (SLC6A3) genes with <b>smoking</b> cessation in a large retrospective study featuring approximately 900 cessation events.
+AADC	drug	alcohol	21797889	The relationship between rs3779084 in the <strong>dopa decarboxylase</strong> (DDC) gene and <b>alcohol</b> consumption is mediated by drinking motives in regular smokers.
+AADC	drug	nicotine	21797889	The relationship between rs3779084 in the <strong>dopa decarboxylase</strong> (DDC) gene and alcohol consumption is mediated by drinking motives in regular <b>smokers</b>.
+AADC	drug	amphetamine	19378464	At 14 days after 6 OHDA when <b>AMPH</b> evoked ipsiversive rotation is mediated by the intact hemisphere, rotation was dose dependently reduced by tyrosine hydroxylase (TH) inhibition with alpha methyl p tyrosine (alpha MPT) or <strong>dopa decarboxylase</strong> (DDC) inhibition with 3 hydroxybenzyl hydrazine (NSD 1015), indicating dependence upon newly synthesized DA.
+AADC	addiction	dependence	19378464	At 14 days after 6 OHDA when AMPH evoked ipsiversive rotation is mediated by the intact hemisphere, rotation was dose dependently reduced by tyrosine hydroxylase (TH) inhibition with alpha methyl p tyrosine (alpha MPT) or <strong>dopa decarboxylase</strong> (DDC) inhibition with 3 hydroxybenzyl hydrazine (NSD 1015), indicating <b>dependence</b> upon newly synthesized DA.
+AADC	drug	nicotine	17184203	<strong>DOPA decarboxylase</strong> gene is associated with <b>nicotine</b> dependence.
+AADC	addiction	dependence	17184203	<strong>DOPA decarboxylase</strong> gene is associated with nicotine <b>dependence</b>.
+AADC	drug	nicotine	17184203	To demonstrate the more powerful method, we re analyzed an existing dataset, which confirmed the association of the <strong>DOPA decarboxylase</strong> (DDC) gene on chromosome 7p11 with measures of <b>nicotine</b> dependence.
+AADC	addiction	dependence	17184203	To demonstrate the more powerful method, we re analyzed an existing dataset, which confirmed the association of the <strong>DOPA decarboxylase</strong> (DDC) gene on chromosome 7p11 with measures of nicotine <b>dependence</b>.
+AADC	drug	nicotine	16740595	Intronic variants in the <strong>dopa decarboxylase</strong> (DDC) gene are associated with <b>smoking</b> behavior in European Americans and African Americans.
+AADC	drug	nicotine	16740595	We report here a study considering association of alleles and haplotypes at the <strong>DOPA decarboxylase</strong> (DDC) locus with the DSM IV diagnosis of <b>nicotine</b> dependence (ND) or a quantitative measure for ND using the Fagerstrom Test for <b>Nicotine</b> Dependence (FTND).
+AADC	addiction	dependence	16740595	We report here a study considering association of alleles and haplotypes at the <strong>DOPA decarboxylase</strong> (DDC) locus with the DSM IV diagnosis of nicotine <b>dependence</b> (ND) or a quantitative measure for ND using the Fagerstrom Test for Nicotine <b>Dependence</b> (FTND).
+AADC	drug	alcohol	16055774	Positron emission tomography (PET) was used to map the net blood brain clearance of the <strong>dopa decarboxylase</strong> substrate 6 [18F]fluoro l dopa, an index of dopamine synthesis capacity, in the striatum of 12 detoxified male <b>alcoholic</b> patients and 13 age matched healthy men.
+AADC	drug	nicotine	15879433	Haplotype analysis indicates an association between the <strong>DOPA decarboxylase</strong> (DDC) gene and <b>nicotine</b> dependence.
+AADC	addiction	dependence	15879433	Haplotype analysis indicates an association between the <strong>DOPA decarboxylase</strong> (DDC) gene and nicotine <b>dependence</b>.
+SLC1A1	drug	amphetamine	31912366	Since <b>AMPH</b> is a transported inhibitor of both DAT and the norepinephrine transporter (NET), and <strong>EAAT3</strong> is also expressed in norepinephrine (NE) neurons, we explored the possibility that this signaling cascade occurs in NE neurons.
+SLC1A1	drug	amphetamine	31912366	We found that <b>AMPH</b> can cause endocytosis of NET as well as <strong>EAAT3</strong> in NE neurons.
+SLC1A1	addiction	dependence	31912366	However, <strong>EAAT3</strong> endocytosis is similar in all regards except its <b>dependence</b> upon CaMKII activation.
+SLC1A1	drug	amphetamine	31912366	RhoA activation is dependent on calcium, but not CaMKII, explaining a divergence in <b>AMPH</b> mediated endocytosis of DAT and NET from that of <strong>EAAT3</strong>.
+SLC1A1	addiction	withdrawal	30267744	Likewise, mice receiving the MA <b>withdrawal</b> regimen had high expression in mGluR5 protein but unaltered <strong>EAAT3</strong>, Homer2 expression in hippocampal tissues.
+SLC1A1	drug	alcohol	29786653	Earlier, we reported that gestational <b>ethanol</b> (E) can dysregulate neuron glutathione (GSH) homeostasis partially via impairing the <strong>EAAC1</strong> mediated inward transport of Cysteine (Cys) and this can affect fetal brain development.
+SLC1A1	drug	alcohol	29206135	<b>Ethanol</b> (E) Impairs Fetal Brain GSH Homeostasis by Inhibiting Excitatory Amino Acid Carrier 1 (<strong>EAAC1</strong>) Mediated Cysteine Transport.
+SLC1A1	drug	amphetamine	28927446	To evaluate the impact of reduced <strong>EAAT3</strong> expression in vivo, we studied male <strong>EAAT3</strong> heterozygous and wild type littermate mice using a battery of behavioral paradigms relevant to anxiety (open field test, elevated plus maze) and compulsivity (marble burying), as well as locomotor activity induced by <b>amphetamine</b>.
+SLC1A1	addiction	addiction	28927446	Compared to wild type littermates, <strong>EAAT3</strong> heterozygous male mice have unaltered baseline anxiety like, <b>compulsive</b> like behavior and locomotor activity.
+SLC1A1	addiction	addiction	28927446	Our results indicate that reduced <strong>EAAT3</strong> expression does not impact neurotransmitter content in the corticostriatal circuit nor alter anxiety or <b>compulsive</b> like behaviors.
+SLC1A1	drug	amphetamine	28507136	Using <b>amphetamine</b> as a probe, we found that <strong>EAAT3</strong> loss prevents expected increases in (i) locomotor activity, (ii) stereotypy, and (iii) immediate early gene induction in the dorsal striatum following <b>amphetamine</b> administration.
+SLC1A1	drug	amphetamine	28507136	<strong>Slc1a1</strong> STOP mice also exhibit reduced extracellular dopamine concentrations in the dorsal striatum both at baseline and following <b>amphetamine</b> challenge.
+SLC1A1	drug	amphetamine	28507136	Viral mediated restoration of <strong>Slc1a1</strong>/EAAT3 expression in the midbrain but not in the striatum results in partial rescue of <b>amphetamine</b> induced locomotion and stereotypy in <strong>Slc1a1</strong> STOP mice, consistent with an impact of EAAT3 loss on presynaptic dopaminergic function.
+SLC1A1	drug	amphetamine	28507136	Viral mediated restoration of <strong>Slc1a1</strong>/<strong>EAAT3</strong> expression in the midbrain but not in the striatum results in partial rescue of <b>amphetamine</b> induced locomotion and stereotypy in <strong>Slc1a1</strong> STOP mice, consistent with an impact of <strong>EAAT3</strong> loss on presynaptic dopaminergic function.
+SLC1A1	drug	opioid	28049029	We determined whether EAAT type 3 (<strong>EAAT3</strong>) played a role in <b>morphine</b> addiction.
+SLC1A1	addiction	addiction	28049029	We determined whether EAAT type 3 (<strong>EAAT3</strong>) played a role in morphine <b>addiction</b>.
+SLC1A1	drug	opioid	28049029	Six  to eight week old <strong>EAAT3</strong> knockout (<strong>EAAT3</strong> / ) mice and their wild type littermates received 3 intraperitoneal injections of 10mg/kg <b>morphine</b>, each on an alternative day, to induce conditioned place preference (CPP).
+SLC1A1	addiction	reward	28049029	Six  to eight week old <strong>EAAT3</strong> knockout (<strong>EAAT3</strong> / ) mice and their wild type littermates received 3 intraperitoneal injections of 10mg/kg morphine, each on an alternative day, to induce conditioned place preference (<b>CPP</b>).
+SLC1A1	drug	opioid	28049029	<b>Morphine</b> induced CPP in wild type and <strong>EAAT3</strong> /  mice.
+SLC1A1	addiction	reward	28049029	Morphine induced <b>CPP</b> in wild type and <strong>EAAT3</strong> /  mice.
+SLC1A1	drug	opioid	28049029	This conditioned behavior extinguished after <b>morphine</b> administration was stopped for 8 9days in wild type mice, while this extinction occurred 6days after discontinuation of <b>morphine</b> injection in <strong>EAAT3</strong> /  mice.
+SLC1A1	drug	opioid	28049029	A small dose of <b>morphine</b> similarly reinstated the conditioned behavior in the wild type and <strong>EAAT3</strong> /  mice.
+SLC1A1	drug	opioid	28049029	<b>Morphine</b> increased <strong>EAAT3</strong> expression in the plasma membrane of medial prefrontal cortex, nucleus accumbens and ventral tegmental area but did not affect <strong>EAAT3</strong> expression in the hippocampus.
+SLC1A1	drug	opioid	28049029	These results suggest that <strong>EAAT3</strong> delays the extinction of <b>morphine</b> induced CPP.
+SLC1A1	addiction	reward	28049029	These results suggest that <strong>EAAT3</strong> delays the extinction of morphine induced <b>CPP</b>.
+SLC1A1	drug	alcohol	26569416	Expressions of glutamate transporters, namely the excitatory amino acid transporter 2 (EAAT2) and <strong>EAAT3</strong>, in white blood cells were measured with the real time polymerase chain reaction (RT PCR) method in early (first day) and late (28(th) day) withdrawal in <b>alcoholic</b> patients and once in the controls.
+SLC1A1	addiction	withdrawal	26569416	Expressions of glutamate transporters, namely the excitatory amino acid transporter 2 (EAAT2) and <strong>EAAT3</strong>, in white blood cells were measured with the real time polymerase chain reaction (RT PCR) method in early (first day) and late (28(th) day) <b>withdrawal</b> in alcoholic patients and once in the controls.
+SLC1A1	addiction	withdrawal	26569416	EAAT2 and <strong>EAAT3</strong> expressions in the patients during both early and late <b>withdrawal</b> were higher than those of the controls.
+SLC1A1	drug	alcohol	26569416	The study revealed an upregulation of glutamate transporters EAAT2 and <strong>EAAT3</strong> during early and late withdrawal in patients with <b>alcohol</b> withdrawal.
+SLC1A1	addiction	withdrawal	26569416	The study revealed an upregulation of glutamate transporters EAAT2 and <strong>EAAT3</strong> during early and late <b>withdrawal</b> in patients with alcohol <b>withdrawal</b>.
+SLC1A1	drug	opioid	25839761	Chronic exposure to <b>morphine</b> decreases the expression of <strong>EAAT3</strong> via <b>opioid</b> receptors in hippocampal neurons.
+SLC1A1	drug	opioid	25839761	In this study, we used primary cultures of hippocampal neurons from neonatal rats to study the effects of chronic exposure to <b>morphine</b> on excitatory amino acid transporter 3 (<strong>EAAT3</strong>) expression and the roles of µ <b>opioid</b> receptor (MOR), δ <b>opioid</b> receptor (DOR), and κ <b>opioid</b> receptor (KOR) in the <b>morphine</b> dependent alterations in <strong>EAAT3</strong> expression.
+SLC1A1	drug	opioid	25839761	The results showed that the <strong>EAAT3</strong> protein and mRNA expression levels decreased significantly after chronic exposure to <b>morphine</b> (10μmol/L) for 48h, whereas the concentration of extracellular glutamate increased.
+SLC1A1	drug	opioid	25839761	In addition, we found that both the MOR inhibitor CTOP and the DOR inhibitor naltrindole could reverse the decreased expression of <strong>EAAT3</strong> after exposure to <b>morphine</b>, whereas the MOR activator DAMGO and the DOR activator DPDPE significantly decreased <strong>EAAT3</strong> expression.
+SLC1A1	drug	opioid	25839761	These results suggest that the down regulation of <b>morphine</b> dependent <strong>EAAT3</strong> expression in primary rat hippocampal cultures may be mediated by MOR and DOR and that KOR may not contribute significantly to this effect.
+SLC1A1	drug	alcohol	25743187	In the medial prefrontal cortex, 2.5g/kg <b>ethanol</b> decreased mRNA expression of brain derived neurotrophic factor, NMDA NR2A subunit, mGluR8 receptor, Homer1, the glutamate transporters <strong>SLC1a1</strong> and SLC1a6 and Srr.
+SLC1A1	drug	opioid	24120272	Altered δ <b>opioid</b> receptor (DOR) activity can affect the activity and function of excitatory amino acid transporter 3 (<strong>EAAT3</strong>), but the effects of DOR on <strong>EAAT3</strong> expression in <b>morphine</b> relapse remain unknown.
+SLC1A1	addiction	relapse	24120272	Altered δ opioid receptor (DOR) activity can affect the activity and function of excitatory amino acid transporter 3 (<strong>EAAT3</strong>), but the effects of DOR on <strong>EAAT3</strong> expression in morphine <b>relapse</b> remain unknown.
+SLC1A1	drug	opioid	24120272	Here, we show that <strong>EAAT3</strong> protein levels in C6δ cells decreased significantly after chronic exposure to <b>morphine</b> (10 μM) for 48 h and returned to normal 12 h after drug withdrawal.
+SLC1A1	addiction	withdrawal	24120272	Here, we show that <strong>EAAT3</strong> protein levels in C6δ cells decreased significantly after chronic exposure to morphine (10 μM) for 48 h and returned to normal 12 h after drug <b>withdrawal</b>.
+SLC1A1	drug	opioid	24120272	When C6δ cells were re exposed to 5 μM <b>morphine</b> for 4 h, <strong>EAAT3</strong> protein levels again decreased significantly.
+SLC1A1	drug	opioid	24120272	The selective μ <b>opioid</b> receptor (MOR) specific agonist DAMGO had a similar effect as <b>morphine</b>, and CTOP, a specific MOR blocker, reversed the declined expression of <strong>EAAT3</strong> protein triggered by <b>morphine</b> exposure.
+SLC1A1	drug	opioid	24120272	The selective DOR agonist [d pen2, 5] enkephalin (DPDPE) significantly increased <strong>EAAT3</strong> expression in C6δ cells and even reversed the decreased <strong>EAAT3</strong> expression caused by chronic <b>morphine</b> exposure.
+SLC1A1	drug	opioid	24120272	The non specific antagonist <b>naloxone</b>, but not the DOR inhibitor Naltrindole (NTI), reversed the decreased <strong>EAAT3</strong> expression in C6δ cells caused by chronic <b>morphine</b> exposure.
+SLC1A1	drug	opioid	24120272	In vivo, <strong>EAAT3</strong> levels in the prefrontal cortex of rats with <b>morphine</b> induced CPP reinstatement significantly decreased.
+SLC1A1	addiction	relapse	24120272	In vivo, <strong>EAAT3</strong> levels in the prefrontal cortex of rats with morphine induced CPP <b>reinstatement</b> significantly decreased.
+SLC1A1	addiction	reward	24120272	In vivo, <strong>EAAT3</strong> levels in the prefrontal cortex of rats with morphine induced <b>CPP</b> reinstatement significantly decreased.
+SLC1A1	drug	opioid	24120272	<b>Naloxone</b> completely suppressed reinstatement and reversed the decrease in <strong>EAAT3</strong> expression induced by <b>morphine</b> re exposure.
+SLC1A1	addiction	relapse	24120272	Naloxone completely suppressed <b>reinstatement</b> and reversed the decrease in <strong>EAAT3</strong> expression induced by morphine re exposure.
+SLC1A1	addiction	relapse	24120272	In contrast, NTI only weakened CPP <b>reinstatement</b> and exerted no influence on <strong>EAAT3</strong> expression.
+SLC1A1	addiction	reward	24120272	In contrast, NTI only weakened <b>CPP</b> reinstatement and exerted no influence on <strong>EAAT3</strong> expression.
+SLC1A1	drug	opioid	24120272	However, the <b>morphine</b> induced down regulation of <strong>EAAT3</strong> in C6δ cells and in the prefrontal cortex of rats may not be mediated by DOR.
+SLC1A1	drug	amphetamine	22540959	Changes in the neuronal glutamate transporter <strong>EAAT3</strong> in rat brain after exposure to <b>methamphetamine</b>.
+SLC1A1	drug	amphetamine	22540959	Therefore, this study examined the effects of acute and sub acute <b>METH</b> administration on the expression of the <strong>EAAT3</strong> in the hippocampal formation, striatum and frontal cortex.
+SLC1A1	drug	amphetamine	22540959	A significant increase in <strong>EAAT3</strong> was found in the hippocampal formation after sub acute, but not acute, <b>METH</b> administration.
+SLC1A1	drug	amphetamine	22540959	Our results of decreased <strong>EAAT3</strong> in striatum and frontal cortex suggest deficits of cortico striatal glutamatergic synapses after <b>METH</b> exposure.
+SLC1A1	drug	amphetamine	22540959	Increased <strong>EAAT3</strong> expression in the hippocampus may be a compensatory response to possible deficits of glutamatergic neurotransmission induced by <b>METH</b>.
+SLC1A1	drug	cannabinoid	15509898	Prenatal <b>cannabinoid</b> exposure down  regulates glutamate transporter expressions (GLAST and <strong>EAAC1</strong>) in the rat cerebellum.
+SLC1A1	drug	cannabinoid	15509898	This study analyzed the expression of the glial (GLAST) and neuronal (<strong>EAAC1</strong>) subtypes of glutamate transporter in the cerebellum of male and female offspring exposed pre  and postnatally to Delta9 <b>tetrahydrocannabinol</b> (<b>THC</b>, the main component of <b>marijuana</b>).
+SLC1A1	drug	cannabinoid	15509898	The expression of the glutamate transporter GLAST in astroglial cells and <strong>EAAC1</strong> in Purkinje neurons decreased in <b>THC</b> exposed offspring compared to controls.
+SLC1A1	drug	opioid	12805317	Cell surface biotinylation and immunoblot analysis showed that <b>morphine</b> withdrawal produced an increase in GLT1 expression rather than <strong>EAAC1</strong> (excitatory amino acids carrier 1), a neuronal subtype, at the cultured neuronal cell surface, whereas no significant change was observed in that of cultured astrocytes.
+SLC1A1	addiction	withdrawal	12805317	Cell surface biotinylation and immunoblot analysis showed that morphine <b>withdrawal</b> produced an increase in GLT1 expression rather than <strong>EAAC1</strong> (excitatory amino acids carrier 1), a neuronal subtype, at the cultured neuronal cell surface, whereas no significant change was observed in that of cultured astrocytes.
+SLC1A1	drug	amphetamine	11406296	<b>Amphetamine</b> administration does not alter protein levels of the GLT 1 and <strong>EAAC1</strong> glutamate transporter subtypes in rat midbrain, nucleus accumbens, striatum, or prefrontal cortex.
+SLC1A1	drug	amphetamine	11406296	The goal of this study was to determine whether repeated <b>amphetamine</b> administration influences the expression of two glutamate transporter subtypes, GLT 1 and <strong>EAAC1</strong>.
+SLC1A1	drug	amphetamine	11406296	We found no significant change in levels of GLT 1 or <strong>EAAC1</strong> in response to either acute or chronic <b>amphetamine</b> treatment.
+S100B	drug	alcohol	31533168	<strong>S100B</strong> Serum Level is Independent of Moderate <b>Alcohol</b> Intoxication.
+S100B	addiction	intoxication	31533168	<strong>S100B</strong> Serum Level is Independent of Moderate Alcohol <b>Intoxication</b>.
+S100B	drug	alcohol	31533168	On the other hand, studies have hypothesized that <b>alcohol</b> intoxication may lead to elevated <strong>S100B</strong> serum levels.
+S100B	addiction	intoxication	31533168	On the other hand, studies have hypothesized that alcohol <b>intoxication</b> may lead to elevated <strong>S100B</strong> serum levels.
+S100B	drug	alcohol	31533168	Therefore, the present study aims to investigate the relationship between the blood ethyl <b>alcohol</b> concentration and the <strong>S100B</strong> serum concentration in an experimental setting in young human adult volunteers.
+S100B	drug	alcohol	31533168	In a cohort of 58 healthy volunteers, serum <strong>S100B</strong> concentration and blood ethyl <b>alcohol</b> concentration were measured before and after liberately drinking <b>alcohol</b>.
+S100B	drug	alcohol	31533168	The <strong>S100B</strong> value ranged from to 0,021 to 0,115 µg/l after <b>alcohol</b> consumption (<strong>S100B</strong> standard value < 0,11 µg/l).
+S100B	drug	alcohol	31533168	By calculating the Pearson correlation of empirical correlation after drinking <b>alcohol</b> with r = 0.01181, a correlation between serum <strong>S100B</strong> concentration and ethyl <b>alcohol</b> concentration is not probable.
+S100B	drug	alcohol	31533168	The <strong>S100B</strong> concentrations were independent on the <b>alcohol</b> intake in low to medium <b>alcohol</b> levels.
+S100B	drug	alcohol	31533168	A relevant <b>alcohol</b> blood concentration (~ 1 g/l), in otherwise healthy volunteers, does not affect the serum concentration of <strong>S100B</strong>.
+S100B	drug	benzodiazepine	31022077	Using an animal model, we investigated serum <strong>S100b</strong> as an acute biomarker of cerebral hypoperfusion and cerebral cell dysfunction during hypotension, hypocapnia, or combined hypotension/hypocapnia during GA. Fifty seven sevoflurane <b>midazolam</b> anesthetized piglets aged 4 to 6 weeks were randomly allocated to control (n=9), hypotension (n=18), hypocapnia (n=20), or combined hypotension and hypocapnia (n=10).
+S100B	drug	opioid	28750172	Transgenerational modification of hippocampus TNF α and <strong>S100B</strong> levels in the offspring of rats chronically exposed to <b>morphine</b> during adolescence.
+S100B	drug	opioid	28750172	We examined the consequences of chronic <b>morphine</b> consumption by parents before mating on hippocampus TNF α and <strong>S100B</strong> levels in the parents and their offspring.
+S100B	drug	opioid	28750172	Hippocampus levels of <strong>S100B</strong> were significantly decreased in male (P < 0.05) but not female <b>morphine</b> consumer parents relative to control parents.
+S100B	drug	opioid	28750172	Both male and female offspring of <b>morphine</b> exposed parents showed significant decreases in hippocampus <strong>S100B</strong> levels (P < 0.05) compared to those of control offspring.
+S100B	drug	alcohol	24786333	<strong>S100B</strong> protein was increased in the cerebrospinal fluid (CSF) in the group treated with <b>alcohol</b>, and alterations in GFAP expression were also shown.
+S100B	drug	alcohol	23830006	<strong>S100B</strong> levels are affected by older age but not by <b>alcohol</b> intoxication following mild traumatic brain injury.
+S100B	addiction	intoxication	23830006	<strong>S100B</strong> levels are affected by older age but not by alcohol <b>intoxication</b> following mild traumatic brain injury.
+S100B	drug	alcohol	23830006	<b>Alcohol</b> intoxication had no effect on <strong>S100B</strong> levels (p = 0.65) and the performance of <strong>S100B</strong> remained unchanged in these patients.
+S100B	addiction	intoxication	23830006	Alcohol <b>intoxication</b> had no effect on <strong>S100B</strong> levels (p = 0.65) and the performance of <strong>S100B</strong> remained unchanged in these patients.
+S100B	drug	alcohol	23830006	<strong>S100B</strong> can be used reliably in mild TBI patients with <b>alcohol</b> intoxication.
+S100B	addiction	intoxication	23830006	<strong>S100B</strong> can be used reliably in mild TBI patients with alcohol <b>intoxication</b>.
+S100B	drug	alcohol	22411109	Clinical utility of the protein <strong>S100B</strong> to evaluate traumatic brain injury in the presence of acute <b>alcohol</b> intoxication.
+S100B	addiction	intoxication	22411109	Clinical utility of the protein <strong>S100B</strong> to evaluate traumatic brain injury in the presence of acute alcohol <b>intoxication</b>.
+S100B	drug	alcohol	22411109	To examine the role of the protein <strong>S100B</strong> as a biomarker for traumatic brain injury (TBI) in the presence of acute <b>alcohol</b> intoxication.
+S100B	addiction	intoxication	22411109	To examine the role of the protein <strong>S100B</strong> as a biomarker for traumatic brain injury (TBI) in the presence of acute alcohol <b>intoxication</b>.
+S100B	drug	alcohol	22411109	<b>Alcohol</b> consumption at the time of injury did not generally affect <strong>S100B</strong> levels.
+S100B	drug	alcohol	21897336	The influence of experimental <b>alcohol</b> load and <b>alcohol</b> intoxication on <strong>S100B</strong> concentrations.
+S100B	addiction	intoxication	21897336	The influence of experimental alcohol load and alcohol <b>intoxication</b> on <strong>S100B</strong> concentrations.
+S100B	drug	alcohol	21897336	However, whether <strong>S100B</strong> levels are influenced by <b>alcohol</b> itself remains to be unclear.
+S100B	drug	alcohol	21897336	Therefore, we performed a case control study of nontraumatized, <b>alcohol</b> intoxicated patients to prove if serum <strong>S100B</strong> is altered by <b>alcohol</b> uptake.
+S100B	drug	alcohol	21897336	Furthermore, we investigated if <b>alcohol</b> infusions combined with an initial oral <b>alcohol</b> load up to a blood <b>alcohol</b> steady state of 100 mg/dL affected <strong>S100B</strong> levels in healthy volunteers (n = 12).
+S100B	drug	alcohol	21897336	In contrast, compared with the control group (n = 60 sober and healthy), the ethyl <b>alcohol</b> intoxicated patients (n = 61; mean ethyl <b>alcohol</b>, 251 [SD, 87] mg/dL) had higher <strong>S100B</strong> concentrations (0.193 [SD, 0.45] vs. 0.063 [SD, 0.059] μg/L; P < 0.001), and 39% of them had levels greater than the pathologic cutoff at greater than 0.104 μg/L.
+S100B	drug	alcohol	21897336	However, no significant correlation was found between ethyl <b>alcohol</b> concentrations and <strong>S100B</strong> within the respective group.
+S100B	drug	alcohol	21897336	Our clinical data suggest that blood <b>alcohol</b> concentrations far in excess of 100 mg/dL are associated with increased <strong>S100B</strong> levels in <b>alcohol</b> intoxicated patients.
+S100B	drug	alcohol	20593192	<strong>S100B</strong> and homocysteine in the acute <b>alcohol</b> withdrawal syndrome.
+S100B	addiction	withdrawal	20593192	<strong>S100B</strong> and homocysteine in the acute alcohol <b>withdrawal</b> syndrome.
+S100B	drug	alcohol	20593192	Serum <strong>S100B</strong> levels are altered in different neuropsychiatric disorders but not well investigated in <b>alcohol</b> withdrawal syndromes.
+S100B	addiction	withdrawal	20593192	Serum <strong>S100B</strong> levels are altered in different neuropsychiatric disorders but not well investigated in alcohol <b>withdrawal</b> syndromes.
+S100B	drug	alcohol	20593192	Because of the close connection of <strong>S100B</strong> to ACTH and glutamate secretion that both are involved in neurodegeneration and symptoms of <b>alcoholism</b> the relationship of <strong>S100B</strong> and homocysteine to acute withdrawal variables has been examined.
+S100B	addiction	withdrawal	20593192	Because of the close connection of <strong>S100B</strong> to ACTH and glutamate secretion that both are involved in neurodegeneration and symptoms of alcoholism the relationship of <strong>S100B</strong> and homocysteine to acute <b>withdrawal</b> variables has been examined.
+S100B	drug	alcohol	20593192	<strong>S100B</strong> and homocysteine levels in serum were collected, and severity of withdrawal symptoms (AWS scale), applied withdrawal medication, initial serum <b>ethanol</b> levels and duration of addiction were recorded.
+S100B	addiction	addiction	20593192	<strong>S100B</strong> and homocysteine levels in serum were collected, and severity of withdrawal symptoms (AWS scale), applied withdrawal medication, initial serum ethanol levels and duration of <b>addiction</b> were recorded.
+S100B	addiction	withdrawal	20593192	<strong>S100B</strong> and homocysteine levels in serum were collected, and severity of <b>withdrawal</b> symptoms (AWS scale), applied <b>withdrawal</b> medication, initial serum ethanol levels and duration of addiction were recorded.
+S100B	drug	alcohol	20593192	As it is known for homocysteine, <strong>S100B</strong> revealed to decline rapidly over withdrawal treatment in <b>alcoholism</b>.
+S100B	addiction	withdrawal	20593192	As it is known for homocysteine, <strong>S100B</strong> revealed to decline rapidly over <b>withdrawal</b> treatment in alcoholism.
+S100B	drug	alcohol	20593192	<strong>S100B</strong> could be of relevance in the neurobiology of <b>alcohol</b> withdrawal syndromes.
+S100B	addiction	withdrawal	20593192	<strong>S100B</strong> could be of relevance in the neurobiology of alcohol <b>withdrawal</b> syndromes.
+S100B	drug	alcohol	20016383	Differential effects of <b>alcohol</b> intoxication on <strong>S100B</strong> levels following traumatic brain injury.
+S100B	addiction	intoxication	20016383	Differential effects of alcohol <b>intoxication</b> on <strong>S100B</strong> levels following traumatic brain injury.
+S100B	drug	alcohol	20016383	Although there seems to be a strong association between <strong>S100B</strong> levels and TBI, further research is required to establish the clinical role of <strong>S100B</strong> in patients with suspected TBI, particularly in patients whose clinical presentation is complicated by <b>alcohol</b> intoxication.
+S100B	addiction	intoxication	20016383	Although there seems to be a strong association between <strong>S100B</strong> levels and TBI, further research is required to establish the clinical role of <strong>S100B</strong> in patients with suspected TBI, particularly in patients whose clinical presentation is complicated by alcohol <b>intoxication</b>.
+S100B	drug	amphetamine	19598248	In WT mice, mEH like immunoreactivity was expressed in astrocytes labeled by GFAP or <strong>S100B</strong> after <b>METH</b> treatment.
+S100B	drug	psychedelics	18812013	<strong>S100B</strong> overexpressing mutant mice exhibit prolonged behavioural and biochemical responses towards repeated intermittent binge treatments with <b>MDMA</b>.
+S100B	addiction	intoxication	18812013	<strong>S100B</strong> overexpressing mutant mice exhibit prolonged behavioural and biochemical responses towards repeated intermittent <b>binge</b> treatments with MDMA.
+S100B	drug	psychedelics	18812013	Repeated binge treatment with <b>MDMA</b> (5 mg/kg, 3 times daily, 3 h apart, once per week for 4 wk) was found to increase gene expression of <strong>S100B</strong>, a neurotrophic factor that modulates neuronal plasticity.
+S100B	addiction	intoxication	18812013	Repeated <b>binge</b> treatment with MDMA (5 mg/kg, 3 times daily, 3 h apart, once per week for 4 wk) was found to increase gene expression of <strong>S100B</strong>, a neurotrophic factor that modulates neuronal plasticity.
+S100B	drug	psychedelics	18812013	Mutant mice overexpressing <strong>S100B</strong> were investigated to better understand how increased <strong>S100B</strong> expression may influence <b>MDMA</b> induced biochemical and behavioural responses.
+S100B	drug	psychedelics	18812013	In open field behaviour, the later <b>MDMA</b> binges decreased rearing and thigmotaxis in <strong>S100B</strong> mutant mice compared to wild type mice.
+S100B	drug	psychedelics	18812013	In the elevated plus maze, <b>MDMA</b> increased open arm entries in both genotypes, but less tolerance to this effect was found in <strong>S100B</strong> mutant mice.
+S100B	drug	psychedelics	18812013	<b>MDMA</b> treatment increased SERT in wild type mice, but did not further increase it in <strong>S100B</strong> mutant mice.
+S100B	drug	psychedelics	18812013	5 HT1B receptor density and G protein coupling were higher in <b>MDMA</b> treated <strong>S100B</strong> mutant mice than in saline treated mutant mice and <b>MDMA</b> treated wild type mice in the medial globus pallidus.
+S100B	drug	psychedelics	18812013	In conclusion, repeated <b>MDMA</b> treatment increases <strong>S100B</strong> mRNA.
+S100B	drug	psychedelics	18812013	Certain explorative and anxiolytic like behaviours in response to <b>MDMA</b> are potentiated and exhibit less tolerance in mice overexpressing <strong>S100B</strong>.
+S100B	drug	psychedelics	18812013	Our data indicate that genetic differences in <strong>S100B</strong> gene expression may predispose individual differences in the responsivity to repeated intake of <b>MDMA</b>.
+S100B	drug	psychedelics	17880365	In the present study, we investigated the effect of anaesthetics (thiopental, <b>ketamine</b> and halothane) on CSF concentrations of <strong>S100B</strong>, as well as a possible sex dependence, because several studies have suggested astrocytes as putative targets for oestrogen.
+S100B	addiction	dependence	17880365	In the present study, we investigated the effect of anaesthetics (thiopental, ketamine and halothane) on CSF concentrations of <strong>S100B</strong>, as well as a possible sex <b>dependence</b>, because several studies have suggested astrocytes as putative targets for oestrogen.
+S100B	addiction	dependence	17880365	Assuming CSF <strong>S100B</strong> as a marker of development, glial activation or even brain damage, investigations regarding the sex <b>dependence</b> of its concentration may be useful in gaining an understanding of sex variations in the behaviour and the pathological course of, as well as susceptibility to, many brain disorders.
+S100B	addiction	dependence	17880365	The findings of the present study reinforce the sex effect on synaptic plasticity and suggest a sex <b>dependence</b> of neural communication mediated by extracellular <strong>S100B</strong> without restricting the influence of astrocytes on the developmental phase.
+S100B	drug	alcohol	17091777	Serum levels of <strong>S100B</strong> protein have been extensively studied in several conditions of neural tissue injury but not in <b>alcohol</b> abuse.
+S100B	drug	alcohol	17091777	The aim of this study was to evaluate the serum levels of <strong>S100B</strong> in <b>alcohol</b> dependent individuals and to further investigate the effect of <b>alcohol</b> detoxification on the levels of <strong>S100B</strong>.
+S100B	drug	alcohol	17091777	The <strong>S100 B</strong> levels decreased in 10 patients with a moderate <b>alcohol</b> consumption over the last year, but increased in 10 patients with high <b>alcohol</b> consumption over the last year.
+S100B	drug	alcohol	17091777	<strong>S100B</strong> protein levels are affected differently in <b>alcohol</b> dependent individuals with either mild or high <b>alcohol</b> consumption during the period of up to one year before assessment.
+S100B	drug	alcohol	17091777	Although this is a preliminary study, the present data suggest a possible use of <strong>S100B</strong> protein measurements in detecting <b>alcohol</b> dependent individuals with high <b>alcohol</b> consumption and in further monitoring the <b>alcohol</b> detoxification treatment.
+PTN	drug	alcohol	32154588	Pleiotrophin (<strong>PTN</strong>) and midkine (MK) are cytokines that are up regulated in the prefrontal cortex (PFC) after <b>alcohol</b> administration and have been shown to reduce <b>alcohol</b> intake and reward.
+PTN	addiction	reward	32154588	Pleiotrophin (<strong>PTN</strong>) and midkine (MK) are cytokines that are up regulated in the prefrontal cortex (PFC) after alcohol administration and have been shown to reduce alcohol intake and <b>reward</b>.
+PTN	drug	alcohol	32154588	<strong>Pleiotrophin</strong> (<strong>PTN</strong>) and midkine (MK) are cytokines that are up regulated in the prefrontal cortex (PFC) after <b>alcohol</b> administration and have been shown to reduce <b>alcohol</b> intake and reward.
+PTN	addiction	reward	32154588	<strong>Pleiotrophin</strong> (<strong>PTN</strong>) and midkine (MK) are cytokines that are up regulated in the prefrontal cortex (PFC) after alcohol administration and have been shown to reduce alcohol intake and <b>reward</b>.
+PTN	addiction	relapse	32078975	Low <strong>PTN</strong> appears to be stable among adults with SUDs in the United States, presenting a potentially enduring barrier to treatment <b>seeking</b>.
+PTN	drug	alcohol	31054277	Inhibition of RPTPβ/ζ blocks <b>ethanol</b> induced conditioned place preference in <strong>pleiotrophin</strong> knockout mice.
+PTN	drug	alcohol	31054277	Pleiotrophin (<strong>PTN</strong>) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after <b>alcohol</b> administration and have been shown to reduce <b>ethanol</b> drinking and reward.
+PTN	addiction	reward	31054277	Pleiotrophin (<strong>PTN</strong>) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after alcohol administration and have been shown to reduce ethanol drinking and <b>reward</b>.
+PTN	drug	alcohol	31054277	<strong>Pleiotrophin</strong> (<strong>PTN</strong>) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after <b>alcohol</b> administration and have been shown to reduce <b>ethanol</b> drinking and reward.
+PTN	addiction	reward	31054277	<strong>Pleiotrophin</strong> (<strong>PTN</strong>) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after alcohol administration and have been shown to reduce ethanol drinking and <b>reward</b>.
+PTN	drug	alcohol	31054277	Since <strong>PTN</strong> knockout (<strong>Ptn</strong> / ) mice are more sensitive to the conditioning effects of <b>alcohol</b>, we aimed to test the effects of MY10, a small molecule inhibitor of RPTPβ/ζ, on <b>ethanol</b> induced CPP in <strong>Ptn</strong> /  mice.
+PTN	addiction	reward	31054277	Since <strong>PTN</strong> knockout (<strong>Ptn</strong> / ) mice are more sensitive to the conditioning effects of alcohol, we aimed to test the effects of MY10, a small molecule inhibitor of RPTPβ/ζ, on ethanol induced <b>CPP</b> in <strong>Ptn</strong> /  mice.
+PTN	drug	alcohol	31054277	The data presented here demonstrate for the first time that a regular dose of MY10, known to block <b>ethanol</b> consumption and reward in wild type mice, also blocks the rewarding effects of <b>ethanol</b> in the more vulnerable individuals lacking <strong>PTN</strong>, the endogenous inhibitor of RPTPβ/ζ.
+PTN	addiction	reward	31054277	The data presented here demonstrate for the first time that a regular dose of MY10, known to block ethanol consumption and <b>reward</b> in wild type mice, also blocks the rewarding effects of ethanol in the more vulnerable individuals lacking <strong>PTN</strong>, the endogenous inhibitor of RPTPβ/ζ.
+PTN	drug	alcohol	31054277	Overall, the data indicate that MY10 rescues <strong>Ptn</strong> /  mice from their increased susceptibility to the conditioning effects of <b>ethanol</b> and may induce anxiolytic effects in individuals with reduced or absent <strong>PTN</strong> functions.
+PTN	drug	alcohol	29753117	Pleiotrophin (<strong>PTN</strong>) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after <b>alcohol</b> administration and have been shown to reduce <b>ethanol</b> drinking and reward.
+PTN	addiction	reward	29753117	Pleiotrophin (<strong>PTN</strong>) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after alcohol administration and have been shown to reduce ethanol drinking and <b>reward</b>.
+PTN	drug	alcohol	29753117	<strong>Pleiotrophin</strong> (<strong>PTN</strong>) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after <b>alcohol</b> administration and have been shown to reduce <b>ethanol</b> drinking and reward.
+PTN	addiction	reward	29753117	<strong>Pleiotrophin</strong> (<strong>PTN</strong>) and Midkine (MK) are neurotrophic factors that are upregulated in the prefrontal cortex after alcohol administration and have been shown to reduce ethanol drinking and <b>reward</b>.
+PTN	drug	alcohol	27748122	For <b>ethanol</b> oxidation at <strong>Ptn</strong>/ITO, activity varies with size nonmonotonically, by more than an order of magnitude.
+PTN	drug	amphetamine	27642078	<strong>Pleiotrophin</strong> overexpression regulates <b>amphetamine</b> induced reward and striatal dopaminergic denervation without changing the expression of dopamine D1 and D2 receptors: Implications for neuroinflammation.
+PTN	addiction	reward	27642078	<strong>Pleiotrophin</strong> overexpression regulates amphetamine induced <b>reward</b> and striatal dopaminergic denervation without changing the expression of dopamine D1 and D2 receptors: Implications for neuroinflammation.
+PTN	drug	amphetamine	27642078	It was previously shown that mice with genetic deletion of the neurotrophic factor pleiotrophin (<strong>PTN</strong> / ) show enhanced <b>amphetamine</b> neurotoxicity and impair extinction of <b>amphetamine</b> conditioned place preference (CPP), suggesting a modulatory role of <strong>PTN</strong> in <b>amphetamine</b> neurotoxicity and reward.
+PTN	addiction	reward	27642078	It was previously shown that mice with genetic deletion of the neurotrophic factor pleiotrophin (<strong>PTN</strong> / ) show enhanced amphetamine neurotoxicity and impair extinction of amphetamine conditioned place preference (<b>CPP</b>), suggesting a modulatory role of <strong>PTN</strong> in amphetamine neurotoxicity and <b>reward</b>.
+PTN	drug	amphetamine	27642078	It was previously shown that mice with genetic deletion of the neurotrophic factor <strong>pleiotrophin</strong> (<strong>PTN</strong> / ) show enhanced <b>amphetamine</b> neurotoxicity and impair extinction of <b>amphetamine</b> conditioned place preference (CPP), suggesting a modulatory role of <strong>PTN</strong> in <b>amphetamine</b> neurotoxicity and reward.
+PTN	addiction	reward	27642078	It was previously shown that mice with genetic deletion of the neurotrophic factor <strong>pleiotrophin</strong> (<strong>PTN</strong> / ) show enhanced amphetamine neurotoxicity and impair extinction of amphetamine conditioned place preference (<b>CPP</b>), suggesting a modulatory role of <strong>PTN</strong> in amphetamine neurotoxicity and <b>reward</b>.
+PTN	drug	amphetamine	27642078	We have now studied the effects of <b>amphetamine</b> (10mg/kg, 4 times, every 2h) in the striatum of mice with transgenic <strong>PTN</strong> overexpression (<strong>PTN</strong> Tg) in the brain and in wild type (WT) mice.
+PTN	drug	amphetamine	27642078	<b>Amphetamine</b> caused an enhanced loss of striatal dopaminergic terminals, together with a highly significant aggravation of <b>amphetamine</b> induced increase in the number of GFAP positive astrocytes, in the striatum of <strong>PTN</strong> Tg mice compared to WT mice.
+PTN	drug	amphetamine	27642078	Given the known contribution of D1 and D2 dopamine receptors to the neurotoxic effects of <b>amphetamine</b>, we also performed quantitative receptor autoradiography of both receptors in the brains of <strong>PTN</strong> Tg and WT mice.
+PTN	drug	amphetamine	27642078	Finally, we found that <b>amphetamine</b> CPP was significantly reduced in <strong>PTN</strong> Tg mice.
+PTN	addiction	reward	27642078	Finally, we found that amphetamine <b>CPP</b> was significantly reduced in <strong>PTN</strong> Tg mice.
+PTN	drug	amphetamine	27642078	The data demonstrate that <strong>PTN</strong> overexpression in the brain blocks the conditioning effects of <b>amphetamine</b> and enhances the characteristic striatal dopaminergic denervation caused by this drug.
+PTN	drug	amphetamine	27642078	The data also suggest that <strong>PTN</strong> induced neuroinflammation could be involved in the enhanced neurotoxic effects of <b>amphetamine</b> in the striatum of <strong>PTN</strong> Tg mice.
+PTN	drug	opioid	26742526	Acute <b>Morphine</b>, Chronic <b>Morphine</b>, and <b>Morphine</b> Withdrawal Differently Affect <strong>Pleiotrophin</strong>, Midkine, and Receptor Protein Tyrosine Phosphatase β/ζ Regulation in the Ventral Tegmental Area.
+PTN	addiction	withdrawal	26742526	Acute Morphine, Chronic Morphine, and Morphine <b>Withdrawal</b> Differently Affect <strong>Pleiotrophin</strong>, Midkine, and Receptor Protein Tyrosine Phosphatase β/ζ Regulation in the Ventral Tegmental Area.
+PTN	addiction	addiction	26742526	<strong>PTN</strong> or MK, signaling through receptor protein tyrosine phosphatase β/ζ (RPTPβ/ζ), lead to the activation of extracellular signal regulated kinases (ERKs) and thymoma viral proto oncogene (Akt), which induce morphological changes and modulate <b>addictive</b> behaviors.
+PTN	drug	opioid	26742526	In the present work, we studied the effect of acute <b>morphine</b>, chronic <b>morphine</b>, and <b>morphine</b> withdrawal on <strong>PTN</strong>, MK, and RPTPβ/ζ expression and on their signaling pathways in the ventral tegmental area (VTA).
+PTN	addiction	withdrawal	26742526	In the present work, we studied the effect of acute morphine, chronic morphine, and morphine <b>withdrawal</b> on <strong>PTN</strong>, MK, and RPTPβ/ζ expression and on their signaling pathways in the ventral tegmental area (VTA).
+PTN	drug	opioid	26742526	Present results indicated that <strong>PTN</strong>, MK, and RPTPβ/ζ levels increased after acute <b>morphine</b> injection, returned to basal levels during chronic <b>opioid</b> treatment, and were upregulated again during <b>morphine</b> withdrawal.
+PTN	addiction	withdrawal	26742526	Present results indicated that <strong>PTN</strong>, MK, and RPTPβ/ζ levels increased after acute morphine injection, returned to basal levels during chronic opioid treatment, and were upregulated again during morphine <b>withdrawal</b>.
+PTN	drug	opioid	26222257	<strong>Pleiotrophin</strong> modulates <b>morphine</b> withdrawal but has no effects on <b>morphine</b> conditioned place preference.
+PTN	addiction	withdrawal	26222257	<strong>Pleiotrophin</strong> modulates morphine <b>withdrawal</b> but has no effects on morphine conditioned place preference.
+PTN	addiction	addiction	26222257	Pleiotrophin (<strong>PTN</strong>) is a neurotrophic factor with important functions in <b>addiction</b> and neurodegenerative disorders.
+PTN	addiction	addiction	26222257	<strong>Pleiotrophin</strong> (<strong>PTN</strong>) is a neurotrophic factor with important functions in <b>addiction</b> and neurodegenerative disorders.
+PTN	drug	opioid	26222257	<b>Morphine</b> administration induces an increase in the expression of <strong>PTN</strong> and Midkine (MK), the only other member of this family of cytokines, in brain areas related with the addictive effects of drug of abuse, like the Ventral Tegmental Area or the hippocampus.
+PTN	addiction	addiction	26222257	Morphine administration induces an increase in the expression of <strong>PTN</strong> and Midkine (MK), the only other member of this family of cytokines, in brain areas related with the <b>addictive</b> effects of drug of abuse, like the Ventral Tegmental Area or the hippocampus.
+PTN	drug	alcohol	26222257	In spite of previous studies showing that <strong>PTN</strong> modulates amphetamine and <b>ethanol</b> rewarding effects, and that <strong>PTN</strong> is involved in morphine induced analgesia, it was still unknown if the rewarding effects of morphine may be regulated by endogenous <strong>PTN</strong>.
+PTN	drug	amphetamine	26222257	In spite of previous studies showing that <strong>PTN</strong> modulates <b>amphetamine</b> and ethanol rewarding effects, and that <strong>PTN</strong> is involved in morphine induced analgesia, it was still unknown if the rewarding effects of morphine may be regulated by endogenous <strong>PTN</strong>.
+PTN	drug	opioid	26222257	In spite of previous studies showing that <strong>PTN</strong> modulates amphetamine and ethanol rewarding effects, and that <strong>PTN</strong> is involved in <b>morphine</b> induced analgesia, it was still unknown if the rewarding effects of <b>morphine</b> may be regulated by endogenous <strong>PTN</strong>.
+PTN	drug	opioid	26222257	Thus, we aim to study the role of <strong>PTN</strong> in the reward and physical dependence induced by <b>morphine</b>.
+PTN	addiction	dependence	26222257	Thus, we aim to study the role of <strong>PTN</strong> in the reward and physical <b>dependence</b> induced by morphine.
+PTN	addiction	reward	26222257	Thus, we aim to study the role of <strong>PTN</strong> in the <b>reward</b> and physical dependence induced by morphine.
+PTN	drug	opioid	26222257	We used the Conditioned Place Preference (CPP) paradigm in <strong>PTN</strong> genetically deficient (<strong>PTN</strong> / ) and wild type (WT) mice to assess the rewarding effects of <b>morphine</b> in absence of endogenous <strong>PTN</strong>.
+PTN	addiction	reward	26222257	We used the Conditioned Place Preference (<b>CPP</b>) paradigm in <strong>PTN</strong> genetically deficient (<strong>PTN</strong> / ) and wild type (WT) mice to assess the rewarding effects of morphine in absence of endogenous <strong>PTN</strong>.
+PTN	drug	opioid	26222257	Second, to study if <strong>PTN</strong> may be involved in <b>morphine</b> physical dependence, <b>naloxone</b> precipitated withdrawal syndrome was induced in <strong>PTN</strong> /  and WT <b>morphine</b> dependent mice.
+PTN	addiction	dependence	26222257	Second, to study if <strong>PTN</strong> may be involved in morphine physical <b>dependence</b>, naloxone precipitated withdrawal syndrome was induced in <strong>PTN</strong> /  and WT morphine dependent mice.
+PTN	addiction	withdrawal	26222257	Second, to study if <strong>PTN</strong> may be involved in morphine physical dependence, naloxone precipitated <b>withdrawal</b> syndrome was induced in <strong>PTN</strong> /  and WT morphine dependent mice.
+PTN	drug	opioid	26222257	Although the increase in the time spent in the <b>morphine</b> paired compartment after conditioning tended to be more pronounced in <strong>PTN</strong> /  mice, statistical significance was not achieved.
+PTN	drug	opioid	26222257	The data suggest that <strong>PTN</strong> does not exert an important role in <b>morphine</b> reward.
+PTN	addiction	reward	26222257	The data suggest that <strong>PTN</strong> does not exert an important role in morphine <b>reward</b>.
+PTN	addiction	withdrawal	26222257	However, our results clearly indicate that <strong>PTN</strong> /  mice develop a more severe <b>withdrawal</b> syndrome than WT mice, characterized as a significant increase in the time standing and in the total incidences of forepaw licking, forepaw tremors, wet dog shake and writhing.
+PTN	drug	opioid	26222257	The data presented here suggest that <strong>PTN</strong> is a novel genetic factor that plays a role in <b>morphine</b> withdrawal syndrome.
+PTN	addiction	withdrawal	26222257	The data presented here suggest that <strong>PTN</strong> is a novel genetic factor that plays a role in morphine <b>withdrawal</b> syndrome.
+PTN	drug	opioid	26164717	In the present work we studied the effect of acute <b>morphine</b> administration, chronic <b>morphine</b> administration, and <b>morphine</b> withdrawal on <strong>PTN</strong>, MK, and RPTPβ/ζ expression and on their signaling pathways in the nucleus accumbens.
+PTN	addiction	withdrawal	26164717	In the present work we studied the effect of acute morphine administration, chronic morphine administration, and morphine <b>withdrawal</b> on <strong>PTN</strong>, MK, and RPTPβ/ζ expression and on their signaling pathways in the nucleus accumbens.
+PTN	drug	opioid	26164717	Present results indicated that <strong>PTN</strong>, MK, and RPTPβ/ζ levels increased after acute <b>morphine</b> injection, returned to basal levels during chronic <b>opioid</b> treatment, and were up regulated again during <b>morphine</b> withdrawal.
+PTN	addiction	withdrawal	26164717	Present results indicated that <strong>PTN</strong>, MK, and RPTPβ/ζ levels increased after acute morphine injection, returned to basal levels during chronic opioid treatment, and were up regulated again during morphine <b>withdrawal</b>.
+PTN	addiction	addiction	25808239	Midkine and <strong>Pleiotrophin</strong> in the Treatment of Neurodegenerative Diseases and Drug <b>Addiction</b>.
+PTN	addiction	addiction	25808239	Pleiotrophin (<strong>PTN</strong>) and Midkine (MK) are neurotrophines with documented protective actions in experimental models of neurodegenerative diseases and beneficial effects on toxicity and <b>addictive</b> behaviours related to drug abuse.
+PTN	addiction	addiction	25808239	<strong>Pleiotrophin</strong> (<strong>PTN</strong>) and Midkine (MK) are neurotrophines with documented protective actions in experimental models of neurodegenerative diseases and beneficial effects on toxicity and <b>addictive</b> behaviours related to drug abuse.
+PTN	drug	amphetamine	25808239	Concerning the latter, both <strong>PTN</strong> and MK prevent the neurotoxic effects of <b>amphetamine</b> on nigrostriatal pathways and endogenous <strong>PTN</strong> also limits <b>amphetamine</b> reward.
+PTN	addiction	reward	25808239	Concerning the latter, both <strong>PTN</strong> and MK prevent the neurotoxic effects of amphetamine on nigrostriatal pathways and endogenous <strong>PTN</strong> also limits amphetamine <b>reward</b>.
+PTN	drug	alcohol	25808239	Moreover, endogenous <strong>PTN</strong> overexpression in the prefontral cortex abolishes <b>alcohol</b>  induced conditioned place preference.
+PTN	drug	opioid	25108770	Glial activation and midkine and <strong>pleiotrophin</strong> transcription in the ventral tegmental area are modulated by <b>morphine</b> administration.
+PTN	drug	opioid	25108770	Although a possible role for midkine and <strong>pleiotrophin</strong> cytokines in the field of synaptic plasticity has been proposed, it has not been assessed whether <b>morphine</b> administration regulates astrogliosis and midkine and <strong>pleiotrophin</strong> transcription.
+PTN	drug	opioid	25108770	Interestingly, single <b>morphine</b> injection and chronic <b>morphine</b> increased VTA midkine and <strong>pleiotrophin</strong> mRNA expression.
+PTN	drug	alcohol	25073406	<strong>Pleiotrophin</strong> differentially regulates the rewarding and sedative effects of <b>ethanol</b>.
+PTN	drug	alcohol	25073406	administration causes a significant up regulation of <strong>PTN</strong> mRNA and protein levels in the mouse prefrontal cortex, suggesting that endogenous <strong>PTN</strong> could modulate behavioural responses to <b>ethanol</b>.
+PTN	drug	alcohol	25073406	To test this hypothesis, we studied the behavioural effects of <b>ethanol</b> in <strong>PTN</strong> knockout (<strong>PTN</strong>( / )) mice and in mice with cortex  and hippocampus specific transgenic <strong>PTN</strong> over expression (<strong>PTN</strong> Tg).
+PTN	drug	alcohol	25073406	<b>Ethanol</b> (1.0 and 2.0 g/kg) induced an enhanced conditioned place preference in <strong>PTN</strong>( / ) compared to wild type mice, suggesting that <strong>PTN</strong> prevents <b>ethanol</b> rewarding effects.
+PTN	drug	alcohol	25073406	Accordingly, the conditioning effects of <b>ethanol</b> were completely abolished in <strong>PTN</strong> Tg mice.
+PTN	drug	alcohol	25073406	However, the sedative effects of <b>ethanol</b> (3.6 g/kg) tested in a loss of righting reflex paradigm were significantly reduced in <strong>PTN</strong> Tg mice, suggesting that up regulation of <strong>PTN</strong> levels prevents the sedative effects of <b>ethanol</b>.
+PTN	drug	alcohol	25073406	These results indicate that <strong>PTN</strong> may be a novel genetic factor of importance in <b>alcohol</b> use disorders, and that potentiation of the <strong>PTN</strong> signalling pathway may be a promising therapeutic strategy in the treatment of these disorders.
+PTN	drug	cocaine	24096156	Phosphoproteomic analysis of the striatum from <strong>pleiotrophin</strong> knockout and midkine knockout mice treated with <b>cocaine</b> reveals regulation of oxidative stress related proteins potentially underlying <b>cocaine</b> induced neurotoxicity and neurodegeneration.
+PTN	addiction	addiction	24096156	The neurotrophic factors pleiotrophin (<strong>PTN</strong>) and midkine (MK) are highly upregulated in different brain areas relevant to drug <b>addiction</b> after administrations of different drugs of abuse, including psychostimulants.
+PTN	addiction	addiction	24096156	The neurotrophic factors <strong>pleiotrophin</strong> (<strong>PTN</strong>) and midkine (MK) are highly upregulated in different brain areas relevant to drug <b>addiction</b> after administrations of different drugs of abuse, including psychostimulants.
+PTN	drug	amphetamine	24096156	We have previously demonstrated that <strong>PTN</strong> and MK modulate <b>amphetamine</b> induced neurotoxicity and that <strong>PTN</strong> prevents cocaine induced cytotoxicity in NG108 15 and PC12 cells.
+PTN	drug	cocaine	24096156	We have previously demonstrated that <strong>PTN</strong> and MK modulate amphetamine induced neurotoxicity and that <strong>PTN</strong> prevents <b>cocaine</b> induced cytotoxicity in NG108 15 and PC12 cells.
+PTN	drug	cocaine	24096156	In an effort to dissect the different mechanisms of action triggered by <strong>PTN</strong> and MK to exert their protective roles against psychostimulant neurotoxicity, we have now used a proteomic approach to study protein phosphorylation, in which we combined phosphoprotein enrichment, by immobilized metal affinity chromatography (IMAC), with two dimensional gel electrophoresis and mass spectrometry, in order to identify the phosphoproteins regulated in the striatum of <strong>PTN</strong> knockout, MK knockout and wild type mice treated with a single dose of <b>cocaine</b> (15mg/kg, i.p.).
+PTN	drug	cocaine	24096156	Most of these proteins are related to neurodegeneration processes and oxidative stress and their variations specially affect the <strong>PTN</strong> knockout mice, suggesting a protective role of endogenous <strong>PTN</strong> against <b>cocaine</b> induced neural alterations.
+PTN	drug	cocaine	23891929	To test this hypothesis, <b>cocaine</b> (10 and 15mg/kg) induced conditioned place preference (CPP) was rendered in <strong>PTN</strong> knockout (<strong>PTN</strong> / ), MK knockout (MK / ) and wild type (WT+/+) mice, and then extinguished after repeated saline injections (distributed in 4 extinction sessions).
+PTN	addiction	reward	23891929	To test this hypothesis, cocaine (10 and 15mg/kg) induced conditioned place preference (<b>CPP</b>) was rendered in <strong>PTN</strong> knockout (<strong>PTN</strong> / ), MK knockout (MK / ) and wild type (WT+/+) mice, and then extinguished after repeated saline injections (distributed in 4 extinction sessions).
+PTN	drug	cocaine	23891929	Particularly, 40% of MK /  mice did not extinguish <b>cocaine</b> (15mg/kg) induced CPP compared to WT+/+ and <strong>PTN</strong> /  mice (∼0 6%).
+PTN	addiction	reward	23891929	Particularly, 40% of MK /  mice did not extinguish cocaine (15mg/kg) induced <b>CPP</b> compared to WT+/+ and <strong>PTN</strong> /  mice (∼0 6%).
+PTN	addiction	reward	23891929	In contrast, a lower magnitude of <b>CPP</b> extinction correlates with increased phosphorylation of aconitase 2 in the prefrontal cortex of <strong>PTN</strong> /  mice, suggesting that the correlation between the tyrosine phosphorylation levels of aconitase 2 and magnitude of <b>CPP</b> extinction depends on the genotype considered.
+PTN	addiction	addiction	23889475	Targeting midkine and <strong>pleiotrophin</strong> signalling pathways in <b>addiction</b> and neurodegenerative disorders: recent progress and perspectives.
+PTN	addiction	relapse	23889475	In this review, evidence demonstrating that MK and <strong>PTN</strong> limit the rewarding effects of drugs of abuse and, potentially, prevent drug <b>relapse</b> is compiled.
+PTN	addiction	addiction	23889475	Exogenous administration of MK and/or <strong>PTN</strong> into the CNS by means of non invasive methods is proposed as a novel therapeutic strategy for <b>addictive</b> and neurodegenerative diseases.
+PTN	addiction	addiction	23889475	Identification of new molecular targets downstream of the MK and <strong>PTN</strong> signalling pathways or pharmacological modulation of those already known may also provide a more traditional, but probably effective, therapeutic strategy for treating <b>addictive</b> and neurodegenerative disorders.
+PTN	drug	amphetamine	23178526	It was previously shown that mice with genetic deletion of pleiotrophin (<strong>PTN</strong>), a neurotrophic factor upregulated in different brain areas after administration of <b>amphetamine</b>, show a longer lasting <b>amphetamine</b> induced conditioned place preference (CPP) when compared to wild type mice.
+PTN	addiction	reward	23178526	It was previously shown that mice with genetic deletion of pleiotrophin (<strong>PTN</strong>), a neurotrophic factor upregulated in different brain areas after administration of amphetamine, show a longer lasting amphetamine induced conditioned place preference (<b>CPP</b>) when compared to wild type mice.
+PTN	drug	amphetamine	23178526	It was previously shown that mice with genetic deletion of <strong>pleiotrophin</strong> (<strong>PTN</strong>), a neurotrophic factor upregulated in different brain areas after administration of <b>amphetamine</b>, show a longer lasting <b>amphetamine</b> induced conditioned place preference (CPP) when compared to wild type mice.
+PTN	addiction	reward	23178526	It was previously shown that mice with genetic deletion of <strong>pleiotrophin</strong> (<strong>PTN</strong>), a neurotrophic factor upregulated in different brain areas after administration of amphetamine, show a longer lasting amphetamine induced conditioned place preference (<b>CPP</b>) when compared to wild type mice.
+PTN	drug	amphetamine	23178526	In this work, we aimed to pursue the possibility of a different astrocytic response induced by <b>amphetamine</b> in <strong>PTN</strong> /  and <strong>PTN</strong>+/+ mice, which could underlie the higher vulnerability of <strong>PTN</strong> /  mice to maintain <b>amphetamine</b> CPP.
+PTN	addiction	reward	23178526	In this work, we aimed to pursue the possibility of a different astrocytic response induced by amphetamine in <strong>PTN</strong> /  and <strong>PTN</strong>+/+ mice, which could underlie the higher vulnerability of <strong>PTN</strong> /  mice to maintain amphetamine <b>CPP</b>.
+PTN	drug	amphetamine	23178526	In confirmation of previous studies, we found that <strong>PTN</strong> /  mice significantly maintained <b>amphetamine</b> (3mg/kg) induced CPP 5 days after the last drug administration compared to <strong>PTN</strong>+/+ mice.
+PTN	addiction	reward	23178526	In confirmation of previous studies, we found that <strong>PTN</strong> /  mice significantly maintained amphetamine (3mg/kg) induced <b>CPP</b> 5 days after the last drug administration compared to <strong>PTN</strong>+/+ mice.
+PTN	drug	amphetamine	23178526	However, we found that <strong>PTN</strong> /  mice showed significantly decreased numbers of astrocytes in CG and CPu compared to <strong>PTN</strong>+/+ mice independently of whether they maintained <b>amphetamine</b> induced CPP 5 days after the last drug administration or not.
+PTN	addiction	reward	23178526	However, we found that <strong>PTN</strong> /  mice showed significantly decreased numbers of astrocytes in CG and CPu compared to <strong>PTN</strong>+/+ mice independently of whether they maintained amphetamine induced <b>CPP</b> 5 days after the last drug administration or not.
+PTN	drug	amphetamine	23178526	The data demonstrate that maintenance of <b>amphetamine</b> induced CPP depends on the endogenous expression of <strong>PTN</strong>.
+PTN	addiction	reward	23178526	The data demonstrate that maintenance of amphetamine induced <b>CPP</b> depends on the endogenous expression of <strong>PTN</strong>.
+PTN	drug	amphetamine	23178526	The data tend to discard a correlation between activated astrocytes and maintenance of <b>amphetamine</b> conditioning effects and suggest <strong>PTN</strong> as a potential modulator of activation of astrocytes after <b>amphetamine</b> treatment.
+PTN	drug	amphetamine	21704677	Midkine regulates <b>amphetamine</b> induced astrocytosis in striatum but has no effects on <b>amphetamine</b> induced striatal dopaminergic denervation and addictive effects: functional differences between <strong>pleiotrophin</strong> and midkine.
+PTN	addiction	addiction	21704677	Midkine regulates amphetamine induced astrocytosis in striatum but has no effects on amphetamine induced striatal dopaminergic denervation and <b>addictive</b> effects: functional differences between <strong>pleiotrophin</strong> and midkine.
+PTN	drug	amphetamine	21704677	The data clearly suggest that endogenous MK limits <b>amphetamine</b> induced astrocytosis through Fyn , TrkA  and ERK1/2 independent mechanisms and identify previously unexpected functional differences between MK and <strong>pleiotrophin</strong>, the only other member of the MK family of growth factors, in the modulation of effects of drugs of abuse.
+PTN	addiction	addiction	21375485	Recent evidences have shown <strong>pleiotrophin</strong>, a growth factor with important functions in remodeling and repair of injured neural tissue, as an important factor involved in the pathogenesis of both diseases by preventing neurodegeneration in Parkinson's disease, neurotoxicity induced by drug abuse and by its ability to modulate drugs <b>addictive</b> effects.
+PTN	addiction	addiction	21375485	This review discusses targeting growth factors such as glial derived neurotrophic factor (GDNF) and brain derived neurotrophic factor (BDNF) to treat Parkinson's disease and/or drug <b>addiction</b> and compiles recent evidences to propose the <strong>pleiotrophin</strong>/receptor protein tyrosine phosphatase β/ζ signaling pathway as a new therapeutic target to treat Parkinson's disease and to prevent drug of abuse induced neurotoxicity and <b>addictive</b> effects.
+PTN	drug	amphetamine	20192945	The neurotrophic factor <strong>pleiotrophin</strong> modulates <b>amphetamine</b> seeking behaviour and <b>amphetamine</b> induced neurotoxic effects: evidence from <strong>pleiotrophin</strong> knockout mice.
+PTN	addiction	relapse	20192945	The neurotrophic factor <strong>pleiotrophin</strong> modulates amphetamine <b>seeking</b> behaviour and amphetamine induced neurotoxic effects: evidence from <strong>pleiotrophin</strong> knockout mice.
+PTN	drug	amphetamine	20192945	Pleiotrophin (<strong>PTN</strong>), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is up regulated in the nucleus accumbens after <b>amphetamine</b> administration suggesting that <strong>PTN</strong> could modulate <b>amphetamine</b> induced pharmacological or neuroadaptative effects.
+PTN	drug	amphetamine	20192945	<strong>Pleiotrophin</strong> (<strong>PTN</strong>), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is up regulated in the nucleus accumbens after <b>amphetamine</b> administration suggesting that <strong>PTN</strong> could modulate <b>amphetamine</b> induced pharmacological or neuroadaptative effects.
+PTN	drug	amphetamine	20192945	To test this hypothesis, we have studied the effects of <b>amphetamine</b> administration in <strong>PTN</strong> genetically deficient (<strong>PTN</strong>  / ) and wild type (WT, +/+) mice.
+PTN	drug	amphetamine	20192945	In conditioning studies, we found that <b>amphetamine</b> induces conditioned place preference in both <strong>PTN</strong>  /  and WT (+/+) mice.
+PTN	drug	amphetamine	20192945	When these mice were re evaluated after a 5 day period without <b>amphetamine</b> administration, we found that WT (+/+) mice did not exhibit <b>amphetamine</b> seeking behaviour, whereas, <strong>PTN</strong>  /  mice still showed a robust drug seeking behaviour.
+PTN	addiction	relapse	20192945	When these mice were re evaluated after a 5 day period without amphetamine administration, we found that WT (+/+) mice did not exhibit amphetamine <b>seeking</b> behaviour, whereas, <strong>PTN</strong>  /  mice still showed a robust drug <b>seeking</b> behaviour.
+PTN	drug	amphetamine	20192945	In immunohystochemistry studies, we found that <b>amphetamine</b> (10 mg/kg, four times, every 2 hours) causes a significant increase of glial fibrillary acidic protein positive cells in the striatum of <b>amphetamine</b> treated <strong>PTN</strong>  /  mice compared with WT mice 4 days after last administration of the drug, suggesting an enhanced <b>amphetamine</b> induced astrocytosis in the absence of endogenous <strong>PTN</strong>.
+PTN	drug	amphetamine	20192945	Interestingly, we found in concomitant in vitro studies that <strong>PTN</strong> (3 µM) limits <b>amphetamine</b> (1 mM) induced loss of viability of PC12 cell cultures, effect that could be related to the ability of <strong>PTN</strong> to induce the phosphorylation of Akt and ERK1/2.
+PTN	drug	amphetamine	20192945	To test this possibility, we used specific Akt and ERK1/2 inhibitors uncovering for the first time that <strong>PTN</strong> induced protective effects against <b>amphetamine</b> induced toxicity in PC12 cells are mediated by the ERK1/2 signalling pathway.
+PTN	drug	amphetamine	20192945	The data suggest an important role of <strong>PTN</strong> to limit <b>amphetamine</b> induced neurotoxic and rewarding effects.
+INSR	drug	opioid	30887859	The expression of <strong>Insr</strong> in the amygdala of control animals decreased over time while the opposite effect was seen in the rats that self administered <b>morphine</b>.
+INSR	drug	cocaine	30471157	Finally, intra VTA or intranasal insulin decreased locomotor responses to <b>cocaine</b>, an effect blocked by an intra VTA administered <strong>insulin receptor</strong> antagonist.
+INSR	drug	amphetamine	29698491	We found that rats fed a HF diet for only two weeks have reductions in striatal Akt activity, a marker of decreased striatal <strong>insulin receptor</strong> signaling and blunted striatal responsiveness to <b>AMPH</b>.
+INSR	drug	amphetamine	29698491	Because <b>AMPH</b> induces DA efflux and brain activation, in large part via DAT, these findings suggest that blunted central nervous system <strong>insulin receptor</strong> signaling through a HF diet can impair DA homeostasis, thereby disrupting cognitive and reward circuitry involved in the regulation of hedonic feeding.
+INSR	addiction	reward	29698491	Because AMPH induces DA efflux and brain activation, in large part via DAT, these findings suggest that blunted central nervous system <strong>insulin receptor</strong> signaling through a HF diet can impair DA homeostasis, thereby disrupting cognitive and <b>reward</b> circuitry involved in the regulation of <b>hedonic</b> feeding.
+INSR	drug	alcohol	29242853	<b>Ethanol</b>, NNK, and <b>ethanol</b> + NNK exposures significantly inhibited <strong>insulin receptor</strong> tyrosine phosphorylation, and IRS 1 and myelin associated glycoprotein expression.
+INSR	drug	alcohol	26586826	Here, we show that p70 S6 kinase (S6k), acting downstream of the <strong>insulin receptor</strong> (InR) and the small GTPase Arf6, is a key mediator of <b>ethanol</b> induced sedation in Drosophila.
+INSR	drug	alcohol	26586826	Here, we show that signaling from the <strong>insulin receptor</strong> in Drosophila neurons determines flies' sensitivity to <b>ethanol</b> induced sedation.
+INSR	drug	alcohol	26373814	<b>Ethanol</b> ± NNK, caused brain atrophy, inhibited insulin signaling through the <strong>insulin receptor</strong> and Akt, activated GSK 3β, increased protein carbonyl and 3 nitrotyrosine, and reduced acetylcholinesterase.
+INSR	addiction	intoxication	23363978	Insulin signaling in the hypothalamus, as assessed by <strong>insulin receptor</strong> and AKT phosphorylation, decreased after <b>binge</b> drinking.
+INSR	drug	alcohol	23363976	Binge <b>alcohol</b> exposure impairs hepatic insulin action by blunting <strong>insulin receptor</strong> signaling in the brain and enables the identification of a therapeutic target that may help treat <b>alcohol</b> induced insulin resistance (Lindtner et al., this issue).
+INSR	addiction	intoxication	23363976	<b>Binge</b> alcohol exposure impairs hepatic insulin action by blunting <strong>insulin receptor</strong> signaling in the brain and enables the identification of a therapeutic target that may help treat alcohol induced insulin resistance (Lindtner et al., this issue).
+INSR	drug	alcohol	20585647	Interestingly, myocardium from <b>ethanol</b> treated FVB mice displayed enhanced expression of PP2Calpha and PGC 1alpha, decreased <strong>insulin receptor</strong> expression as well as unchanged expression of Glut4, the response of which was unaffected by ADH.
+INSR	drug	opioid	17143271	In this study, we used viral mediated gene transfer in rat to show that chronic <b>morphine</b> induced downregulation of the <strong>insulin receptor</strong> substrate 2 (IRS2) thymoma viral proto oncogene (Akt) signaling pathway in the VTA mediates the decrease in dopamine cell size seen after <b>morphine</b> exposure and that this downregulation diminishes <b>morphine</b> reward, as measured by conditioned place preference.
+INSR	addiction	reward	17143271	In this study, we used viral mediated gene transfer in rat to show that chronic morphine induced downregulation of the <strong>insulin receptor</strong> substrate 2 (IRS2) thymoma viral proto oncogene (Akt) signaling pathway in the VTA mediates the decrease in dopamine cell size seen after morphine exposure and that this downregulation diminishes morphine <b>reward</b>, as measured by conditioned place preference.
+INSR	drug	alcohol	15592467	Here we show that genetic manipulations in Drosophila melanogaster that impair the function of insulin producing cells or of the <strong>insulin receptor</strong> signaling pathway in the nervous system lead to increased sensitivity to the intoxicating effects of <b>ethanol</b>.
+INSR	drug	opioid	11428713	The changes in <strong>insulin receptor</strong> number could be responsible for the improved glucose tolerance observed during <b>morphine</b> addiction.
+INSR	addiction	addiction	11428713	The changes in <strong>insulin receptor</strong> number could be responsible for the improved glucose tolerance observed during morphine <b>addiction</b>.
+IFNA1	drug	alcohol	31708974	Within these pathways, we identified four differentially methylated genes, namely, MSTN, <strong>IFNA13</strong>, ATP8B3, and GABBR2, that are involved in the onset of insulin resistance and adiposity, innate immune response, phospholipid translocation across cell membranes, and mechanisms of addiction to high fat diet, <b>alcohol</b>, and sweet taste.
+IFNA1	addiction	addiction	31708974	Within these pathways, we identified four differentially methylated genes, namely, MSTN, <strong>IFNA13</strong>, ATP8B3, and GABBR2, that are involved in the onset of insulin resistance and adiposity, innate immune response, phospholipid translocation across cell membranes, and mechanisms of <b>addiction</b> to high fat diet, alcohol, and sweet taste.
+IFNA1	addiction	addiction	19630716	Depression, anxiety, fatigue and irritability as typical <strong>IFN alpha</strong> associated side effects occur in 30 80% during antiviral treatment of hepatitis C. Patients with drug <b>addiction</b> were shown to have an increased risk to discontinue HCV treatment early in the first three treatment months, where most neuropsychiatric side effects appear.
+IFNA1	drug	opioid	19344248	Optimization of psychotropic and <b>opioid</b> replacement therapy with integrated psychiatric/addiction treatment prior to and during <strong>IFN alpha</strong> initiation produces optimal results.
+IFNA1	addiction	addiction	19344248	Optimization of psychotropic and opioid replacement therapy with integrated psychiatric/<b>addiction</b> treatment prior to and during <strong>IFN alpha</strong> initiation produces optimal results.
+IFNA1	drug	opioid	19322075	Cytokine interferon alpha (<strong>IFN alpha</strong>) is an immunomodulator and neuromodulator, which modulates central nervous system function partially by activating <b>opioid</b> receptors.
+IFNA1	addiction	relapse	19322075	However, the role that <strong>IFN alpha</strong> plays in <b>relapse</b> to drug abuse is still largely unknown.
+IFNA1	drug	opioid	19322075	These results indicate that <strong>IFN alpha</strong> is a stimulus for reinstatement of <b>morphine</b> CPP by activation of <b>opioid</b> receptors, which extends our understanding on the high comorbidity of <b>heroin</b> relapse and viral infection.
+IFNA1	addiction	relapse	19322075	These results indicate that <strong>IFN alpha</strong> is a stimulus for <b>reinstatement</b> of morphine CPP by activation of opioid receptors, which extends our understanding on the high comorbidity of heroin <b>relapse</b> and viral infection.
+IFNA1	addiction	reward	19322075	These results indicate that <strong>IFN alpha</strong> is a stimulus for reinstatement of morphine <b>CPP</b> by activation of opioid receptors, which extends our understanding on the high comorbidity of heroin relapse and viral infection.
+IFNA1	drug	opioid	16406668	Previous studies have indicated that interferon alpha (<strong>IFN alpha</strong>) can bind to <b>opioid</b> receptors and exerts an antinociceptive effect in both peripheral and central nervous systems.
+IFNA1	drug	opioid	16406668	The current study investigated the antinociceptive effect of <strong>IFN alpha</strong> unilaterally microinjected into the thalamic nucleus submedius (Sm) of rats on noxious thermal stimulus, and the roles of different subtypes of <b>opioid</b> receptors in mediating the Sm <strong>IFN alpha</strong> evoked antinociception.
+IFNA1	drug	opioid	16406668	The results indicated that unilateral microinjection of <strong>IFN alpha</strong> (4, 8, 16 pmol) into the Sm dose dependently increased the hind paw withdrawal latency from the noxious heat stimulus, and this effect was reversed by pretreatment with non selective <b>opioid</b> receptor antagonist <b>naloxone</b> (200 pmol) and specific mu <b>opioid</b> receptor antagonist beta FNA (1 nmol) into the same sites, whereas delta <b>opioid</b> receptor antagonist ICI174,864 (1 nmol) and kappa <b>opioid</b> receptor antagonist nor BNI (1 nmol) failed to alter the effect of <strong>IFN alpha</strong>.
+IFNA1	addiction	withdrawal	16406668	The results indicated that unilateral microinjection of <strong>IFN alpha</strong> (4, 8, 16 pmol) into the Sm dose dependently increased the hind paw <b>withdrawal</b> latency from the noxious heat stimulus, and this effect was reversed by pretreatment with non selective opioid receptor antagonist naloxone (200 pmol) and specific mu opioid receptor antagonist beta FNA (1 nmol) into the same sites, whereas delta opioid receptor antagonist ICI174,864 (1 nmol) and kappa opioid receptor antagonist nor BNI (1 nmol) failed to alter the effect of <strong>IFN alpha</strong>.
+IFNA1	drug	opioid	16406668	These results suggest that Sm is involved in <strong>IFN alpha</strong> evoked antinociception and mu  but not delta  and kappa <b>opioid</b> receptor mediates the Sm <strong>IFN alpha</strong> evoked antinociception.
+IFNA1	drug	opioid	16251417	These in vitro observations support the concept that <b>opioid</b> abuse favors HCV persistence in hepatic cells by suppressing <strong>IFN alpha</strong> mediated intracellular innate immunity and contributes to the development of chronic HCV infection.
+IFNA1	drug	amphetamine	16142050	Concerning the other monoaminergic systems, <strong>IFNalpha</strong> seems to have an <b>amphetamine</b> like effect at its first administration, followed by a decrease in dopaminergic tone with chronic administration.
+IFNA1	drug	opioid	16142050	Neuroendocrinian hypothesis    when administered through central or peripheral way, <strong>IFNalpha</strong> simulates/inhibits the corticotrope axis and alters endorphin system as shown by the induction of analgesia, catatonia and behavioural slowdown that can be suppressed by <b>opioid</b> antagonists.
+IFNA1	drug	alcohol	16142050	<strong>IFNalpha</strong> neurotoxic effects are successfully treated by <b>naltrexone</b>.
+IFNA1	drug	opioid	15317637	Data about sustained response and adherence in HCV infected <b>methadone</b> substituted patients were either comparable to control groups or to representative clinically controlled trials using the same treatment regimen (<strong>IFN alpha</strong> monotherapy or combined with ribavirin).
+IFNA1	drug	opioid	15317637	There is no clinical evidence suggesting that HCV treatment with <strong>IFN alpha</strong> should be limited to IDUs or <b>methadone</b> substituted patients.
+IFNA1	addiction	addiction	12540795	Psychiatric disorders or drug <b>addiction</b> are often regarded as contraindications against the use of interferon alfa (<strong>IFN alpha</strong>) in patients with chronic hepatitis C. Our aim was to obtain prospective data on adherence to as well as efficacy and mental side effects of treatment with <strong>IFN alpha</strong> in different psychiatric risk groups compared with controls.
+IFNA1	drug	opioid	12540795	In a prospective trial, 81 patients with chronic hepatitis C (positive hepatitis C virus[HCV] RNA and elevated alanine aminotransferase[ALT] level) and psychiatric disorders (n = 16), <b>methadone</b> substitution (n = 21), former drug addiction (n = 21), or controls without a psychiatric history or drug addiction (n = 23) were treated with a combination of <strong>IFN alpha</strong> 2a 3 MU 3 times weekly and ribavirin (1,000 1,200 mg/d).
+IFNA1	addiction	addiction	12540795	In a prospective trial, 81 patients with chronic hepatitis C (positive hepatitis C virus[HCV] RNA and elevated alanine aminotransferase[ALT] level) and psychiatric disorders (n = 16), methadone substitution (n = 21), former drug <b>addiction</b> (n = 21), or controls without a psychiatric history or drug <b>addiction</b> (n = 23) were treated with a combination of <strong>IFN alpha</strong> 2a 3 MU 3 times weekly and ribavirin (1,000 1,200 mg/d).
+IFNA1	drug	opioid	12540795	Preexisting psychiatric disorders or present <b>methadone</b> substitution should no longer be regarded as contraindications to treatment of chronic hepatitis C with <strong>IFN alpha</strong> and ribavirin in an interdisciplinary setting.
+IFNA1	drug	opioid	10962774	Psychosis in a <b>methadone</b> substituted patient during interferon alpha treatment of hepatitis C. Interferon alpha (<strong>IFN alpha</strong>) is the only effective treatment for chronic hepatitis B and C. Over 2/3 of <b>methadone</b> substituted patients suffer from chronic hepatitis C but a history of psychiatric disorders or drug addiction is still seen as a contraindication for <strong>IFN alpha</strong> because of a possible increased risk of severe psychiatric side effects such as depression, suicide attempts or psychotic episodes.
+IFNA1	addiction	addiction	10962774	Psychosis in a methadone substituted patient during interferon alpha treatment of hepatitis C. Interferon alpha (<strong>IFN alpha</strong>) is the only effective treatment for chronic hepatitis B and C. Over 2/3 of methadone substituted patients suffer from chronic hepatitis C but a history of psychiatric disorders or drug <b>addiction</b> is still seen as a contraindication for <strong>IFN alpha</strong> because of a possible increased risk of severe psychiatric side effects such as depression, suicide attempts or psychotic episodes.
+IFNA1	drug	alcohol	9347083	Accordingly, an increased concentration of this cytokine was detected in the supernatants of cirrhotic patients and active EtOH intake, particularly after <strong>IFN alpha</strong> stimulation (p < 0.05); whereas, in patients with at least 1 year of <b>alcohol</b> withdrawal, TNF alpha levels remained within normal range.
+IFNA1	addiction	withdrawal	9347083	Accordingly, an increased concentration of this cytokine was detected in the supernatants of cirrhotic patients and active EtOH intake, particularly after <strong>IFN alpha</strong> stimulation (p < 0.05); whereas, in patients with at least 1 year of alcohol <b>withdrawal</b>, TNF alpha levels remained within normal range.
+IFNA1	drug	opioid	9067644	The present study was undertaken to examine the immunomodulatory role of <b>morphine</b> on HIV protein induced lymphocyte proliferative responses, Sendai and Newcastle disease virus induced alpha IFN (<strong>IFN alpha</strong>) and IFN beta production by lymphocytes and fibroblast cells, respectively, and induction of apoptosis of normal lymphocytes in vitro.
+IFNA1	drug	opioid	9067644	Furthermore, <b>morphine</b> significantly inhibited both <strong>IFN alpha</strong> and IFN beta production by normal lymphocytes and fibroblasts but induced apoptosis of normal lymphocytes.
+IFNA1	drug	opioid	9067644	Inhibition of <strong>IFN alpha</strong> production by <b>morphine</b> could be reversed by the opiate receptor antagonist <b>naloxone</b>.
+HDAC1	drug	amphetamine	30811820	For single dose, <b>METH</b> affected H4ac by increasing its acetylation at class I <strong>Hdac1</strong> and class IIb Hdac10, decreasing it at class IIa Hdac4 and Hdac5.
+HDAC1	drug	amphetamine	30811820	We found that <b>METH</b> increased H4ac in class IIa Hdac4 and Hdac5 and decreased H3/H4ac at class I <strong>Hdac1</strong>, Hdac2, and Hdac8.
+HDAC1	drug	cocaine	30126647	<b>Cocaine</b> also increased testicular and germ cell acetylated histone 3 and 4 and decreased expression of histone deacetylases <strong>HDAC1</strong>/2.
+HDAC1	drug	cocaine	30126647	Analysis of mRNA expression in isolated germ cells shows decreased levels of <strong>Hdac1</strong>/2/8, Dnmt3b and Tet1 and increased levels of Dnmt3a gene expression after <b>cocaine</b> treatment.
+HDAC1	drug	amphetamine	30056065	In this study, we measured the effects of single dose injections of modafinil and <b>METH</b> on the protein levels of acetylated histone H3 (H3ac) and H4ac, deacetylases <strong>HDAC1</strong> and HDAC2, and of the NMDA subunit GluN1 in the medial PFC (mPFC) of mice euthanized 1 h after drug administration.
+HDAC1	drug	amphetamine	30056065	Acute modafinil and <b>METH</b> injections caused similar effects on total histone acetylation, increasing H3ac and decreasing H4ac, and they also increased <strong>HDAC1</strong>, HDAC2 and GluN1 protein levels in the mouse mPFC.
+HDAC1	drug	amphetamine	29397902	In contrast, HDAC5 knockdown in the dorsal striatum decreased <b>meth</b> seeking on withdrawal day 30 but not on day 2; this manipulation also altered other HDACs (<strong>Hdac1</strong> and Hdac4) and potential HDAC5 targets (Gnb4 and Suv39h1).
+HDAC1	addiction	relapse	29397902	In contrast, HDAC5 knockdown in the dorsal striatum decreased meth <b>seeking</b> on withdrawal day 30 but not on day 2; this manipulation also altered other HDACs (<strong>Hdac1</strong> and Hdac4) and potential HDAC5 targets (Gnb4 and Suv39h1).
+HDAC1	addiction	withdrawal	29397902	In contrast, HDAC5 knockdown in the dorsal striatum decreased meth seeking on <b>withdrawal</b> day 30 but not on day 2; this manipulation also altered other HDACs (<strong>Hdac1</strong> and Hdac4) and potential HDAC5 targets (Gnb4 and Suv39h1).
+HDAC1	drug	alcohol	28798030	We found that class I histone deacetylases (HDACs) regulate <b>ethanol</b> induced changes in α1 gene and protein expression as pharmacologic inhibition or knockdown of <strong>HDAC1</strong> 3 prevents the effects of <b>ethanol</b> exposure.
+HDAC1	drug	alcohol	28682229	Recent work in rodents has shown that systemic administration of pan HDAC class I and II inhibitors, TSA and N hydroxy N phenyl octanediamide [SuberoylAnilide Hydroxamic Acid] (SAHA), and of the more selective inhibitor (mainly <strong>HDAC1</strong> and HDAC9) MS 275, decrease binge like <b>alcohol</b> drinking in mice.
+HDAC1	addiction	intoxication	28682229	Recent work in rodents has shown that systemic administration of pan HDAC class I and II inhibitors, TSA and N hydroxy N phenyl octanediamide [SuberoylAnilide Hydroxamic Acid] (SAHA), and of the more selective inhibitor (mainly <strong>HDAC1</strong> and HDAC9) MS 275, decrease <b>binge</b> like alcohol drinking in mice.
+HDAC1	addiction	intoxication	28250112	Editorial: <b>Binge</b> drinking: lessons from ATF3 and <strong>HDAC1</strong> collaboration.
+HDAC1	addiction	intoxication	27260954	In <b>binge</b> drinking mice challenged with LPS, an up regulation of ATF3 and <strong>HDAC1</strong> and a concomitant decrease in TNF α were observed.
+HDAC1	drug	alcohol	27260954	Given that <strong>HDAC1</strong> was concomitantly induced in acute <b>ethanol</b> exposed monocytes and macrophages, we used the HDACi TSA or silenced <strong>HDAC1</strong> to explore the role of <strong>HDAC1</strong> in acute <b>ethanol</b> treated macrophages.
+HDAC1	drug	alcohol	27260954	Our results revealed that TSA treatment and <strong>HDAC1</strong> knockdown prevented acute <b>ethanol</b> induced ATF3 expression and the inhibition of TNF α transcription.
+HDAC1	drug	alcohol	27260954	These data indicated a dual role for <strong>HDAC1</strong> in acute <b>ethanol</b> induced LPS tolerance.
+HDAC1	drug	alcohol	27238566	nalmefene; (ii) the effects of nalmefene with increasing concentrations of <b>alcohol</b>; (iii) the efficacy of nalmefene on cocaine potentiated <b>alcohol</b> responding; and (iv) the gene expression profiles of histone deacetylases (<strong>Hdac1</strong> 11) in peripheral blood in vivo and in the prefrontal cortex, heart, liver and kidney post mortem.
+HDAC1	drug	cocaine	27238566	nalmefene; (ii) the effects of nalmefene with increasing concentrations of alcohol; (iii) the efficacy of nalmefene on <b>cocaine</b> potentiated alcohol responding; and (iv) the gene expression profiles of histone deacetylases (<strong>Hdac1</strong> 11) in peripheral blood in vivo and in the prefrontal cortex, heart, liver and kidney post mortem.
+HDAC1	drug	alcohol	26365275	We primarily found that acute <b>alcohol</b> binging reduced gene expression (<strong>Hdac1</strong> 10) in the peripheral blood of <b>alcohol</b> naïve rats and that this effect was attenuated following repeated <b>alcohol</b> binges.
+HDAC1	drug	nicotine	24789730	<b>Nicotine</b> inhibits the proliferation by upregulation of nitric oxide and increased <strong>HDAC1</strong> in mouse neural stem cells.
+HDAC1	drug	nicotine	24789730	Taken together, these data demonstrate that prolonged exposure of <b>nicotine</b> decreased proliferation of mNSCs by increased NO and inflammatory cytokine through increased <strong>HDAC1</strong>.
+HDAC1	drug	alcohol	24551070	Similarly, <b>ethanol</b> treatment was found to induce the translocation of <strong>HDAC1</strong>/4 and HMGB1 proteins from nuclear to cytosolic fractions.
+HDAC1	drug	alcohol	24551070	Furthermore, <b>ethanol</b> treatment reduced <strong>HDAC1</strong>/4 mRNA and increased acetylated HMGB1 release into the media.
+HDAC1	drug	amphetamine	24239129	Moreover, <b>METH</b> caused interactions of REST corepressor 1 and methylated CpG binding protein 2 with histone deacetylase 2 and of REST with <strong>histone deacetylase 1</strong>.
+HDAC1	drug	cocaine	23475113	Here we demonstrate that specific and prolonged blockade of <strong>HDAC1</strong> in NAc of mice increased global levels of histone acetylation, but also induced repressive histone methylation and antagonized <b>cocaine</b> induced changes in behavior, an effect mediated in part through a chromatin mediated suppression of GABAA receptor subunit expression and inhibitory tone on NAc neurons.
+HDAC1	drug	amphetamine	22470541	Our study investigated the effects of a non toxic <b>METH</b> injection (20 mg/kg) on gene expression, histone acetylation, and the expression of the histone acetyltransferase (HAT), ATF2, and of the histone deacetylases (HDACs), <strong>HDAC1</strong> and HDAC2, in that structure.
+HDAC1	drug	amphetamine	18632938	Accordingly, local knock out of <strong>HDAC1</strong> in striatum abolishes <b>amphetamine</b> induced desensitization of the c fos gene.
+EIF2S1	addiction	addiction	29539420	Reduced eukaryotic Initiation Factor 2 (<strong>eIF2</strong>)α phosphorylation (p eIF2α) enhances protein synthesis, memory formation, and <b>addiction</b> like behaviors.
+EIF2S1	drug	opioid	28546432	Compared with the <b>Heroin</b> group, mRNA and protein expression of PERK, <strong>eIF2a</strong>, CHOP, IRE1 and JNK in the hippocampus and VTA were significantly downregulated in the <b>Heroin</b>+acupuncture group (p<0.05).
+EIF2S1	drug	cocaine	27899881	New functional pathways were also identified for <b>cocaine</b> modulation (e.g., Rho GTPase signaling) and environmental enrichment (e.g., signaling of <strong>EIF2</strong>, mTOR, ephrin).
+EIF2S1	drug	alcohol	27527870	<b>Ethanol</b> induced endoplasmic reticulum stress was demonstrated by a significant increase in ATF6, CHOP, and the phosphorylation of PERK and <strong>eiF 2alpha</strong>.
+EIF2S1	drug	nicotine	26928076	When we investigated the influence of allelic variability of the <strong>Eif2s1</strong> gene (encoding eIF2α) on reward related neuronal responses in human <b>smokers</b>, we found that a single nucleotide polymorphism in the <strong>Eif2s1</strong> gene modulates mesolimbic neuronal reward responses in human <b>smokers</b>.
+EIF2S1	addiction	reward	26928076	When we investigated the influence of allelic variability of the <strong>Eif2s1</strong> gene (encoding eIF2α) on <b>reward</b> related neuronal responses in human smokers, we found that a single nucleotide polymorphism in the <strong>Eif2s1</strong> gene modulates mesolimbic neuronal <b>reward</b> responses in human smokers.
+EIF2S1	drug	alcohol	18334613	To date, <b>alcohol</b> induced alterations in <strong>eIF2</strong> and eIF2B content and activity are best investigated.
+EIF2S1	addiction	intoxication	18334613	The reduced eIF2B activity most likely is a consequence of twofold increased phosphorylation of the alpha subunit of <strong>eIF2</strong> on Ser(51) following acute <b>intoxication</b>.
+EIF2S1	drug	alcohol	18334613	The increase in <strong>eIF2alpha</strong> phosphorylation after chronic <b>alcohol</b> consumption is the same as that induced by acute <b>ethanol</b> intoxication, and protein synthesis is not further reduced by long term <b>alcohol</b> ingestion despite additional reduced expression of initiation factors and elongation factors.
+EIF2S1	addiction	intoxication	18334613	The increase in <strong>eIF2alpha</strong> phosphorylation after chronic alcohol consumption is the same as that induced by acute ethanol <b>intoxication</b>, and protein synthesis is not further reduced by long term alcohol ingestion despite additional reduced expression of initiation factors and elongation factors.
+EIF2S1	drug	alcohol	18334613	Indeed, pretreatment with Salubrinal, an inhibitor of <strong>eIF2alpha</strong>(P) phosphatase, before <b>ethanol</b> treatment does not further inhibit protein synthesis or increase <strong>eIF2alpha</strong> phosphorylation, suggesting that acute <b>ethanol</b> intoxication causes maximal <strong>eIF2alpha</strong> phosphorylation elevation and hepatic protein synthesis inhibition.
+EIF2S1	addiction	intoxication	18334613	Indeed, pretreatment with Salubrinal, an inhibitor of <strong>eIF2alpha</strong>(P) phosphatase, before ethanol treatment does not further inhibit protein synthesis or increase <strong>eIF2alpha</strong> phosphorylation, suggesting that acute ethanol <b>intoxication</b> causes maximal <strong>eIF2alpha</strong> phosphorylation elevation and hepatic protein synthesis inhibition.
+EIF2S1	drug	alcohol	18334613	In conclusion, sustained <strong>eIF2alpha</strong> phosphorylation is a hallmark of excessive <b>alcohol</b> intake leading to inhibition of protein synthesis.
+EIF2S1	drug	alcohol	18334613	Enhanced phosphorylation of <strong>eIF2alpha</strong> represents a unique response of liver to <b>alcohol</b> intoxication, because the <b>ethanol</b> induced elevation of <strong>eIF2alpha</strong>(P) is not observed in skeletal muscle or heart.
+EIF2S1	addiction	intoxication	18334613	Enhanced phosphorylation of <strong>eIF2alpha</strong> represents a unique response of liver to alcohol <b>intoxication</b>, because the ethanol induced elevation of <strong>eIF2alpha</strong>(P) is not observed in skeletal muscle or heart.
+EIF2S1	drug	alcohol	11331201	In contrast, <b>alcohol</b> does not produce consistent alterations in the control of translation initiation by the <strong>eIF2</strong> system.
+EIF2S1	drug	alcohol	11052957	Acute <b>alcohol</b> intoxication did not significantly alter the myocardial content of <strong>eIF2</strong> alpha or eIF2B epsilon, the extent of <strong>eIF2</strong> alpha phosphorylation, or the activity of eIF2B.
+EIF2S1	addiction	intoxication	11052957	Acute alcohol <b>intoxication</b> did not significantly alter the myocardial content of <strong>eIF2</strong> alpha or eIF2B epsilon, the extent of <strong>eIF2</strong> alpha phosphorylation, or the activity of eIF2B.
+EIF2S1	drug	alcohol	11052957	These data suggest that the acute <b>alcohol</b> induced impairment in myocardial protein synthesis results, in part, from an inhibition in peptide chain initiation, which is associated with marked changes in eIF4E availability and p70S6 kinase phosphorylation but is independent of changes in the <strong>eIF2</strong>/2B system and IGFs.
+EIF2S1	drug	alcohol	10776669	Hepatic eIF2B activity was decreased 24% in <b>alcohol</b> treated rats, and this was associated with a 95% increase in <strong>eIF2alpha</strong> phosphorylation.
+EIF2S1	drug	alcohol	10776669	In contrast to liver, neither eIF2B activity nor the phosphorylation of <strong>eIF2alpha</strong> was affected in muscle of <b>alcohol</b> treated rats.
+EIF2S1	drug	alcohol	3377809	The addition of <b>ethanol</b> to reticulocyte lysates led to increased phosphorylation of <strong>eIF 2</strong> alpha and to a decrease in the rate of exchange of guanine nucleotides bound to <strong>eIF 2</strong>.
+EIF2S1	drug	alcohol	3377809	Using purified components it was found that <b>ethanol</b> inhibited the ability of GEF to stimulate <strong>eIF 2</strong> and that this inhibition showed a similar temperature dependence to the effect of <b>ethanol</b> on overall protein synthesis.
+EIF2S1	addiction	dependence	3377809	Using purified components it was found that ethanol inhibited the ability of GEF to stimulate <strong>eIF 2</strong> and that this inhibition showed a similar temperature <b>dependence</b> to the effect of ethanol on overall protein synthesis.
+EIF2S1	drug	alcohol	3377809	Taken together, these results suggest that <b>ethanol</b> leads to inhibition of peptide chain initiation both through increased phosphorylation of <strong>eIF 2</strong> alpha and by directly inhibiting the productive interaction of <strong>eIF 2</strong> and GEF.
+CXCR4	drug	alcohol	32150428	Attentional set shifting in HAP3, <strong>LAP3</strong>, and cHAP mice is unaffected by either genetic differences in <b>alcohol</b> preference or an <b>alcohol</b> drinking history.
+CXCR4	drug	cocaine	31557508	Our results suggest that mesolimbic CCR5 receptors are dysregulated by <b>cocaine</b> exposure and, similar to <strong>CXCR4</strong> and CCR2 receptors, influence behavioral effects related to the abuse liability of <b>cocaine</b>.
+CXCR4	drug	opioid	31465771	However, the molecular mechanisms that underlie <strong>CXCR4</strong>, as well as <b>opioid</b> mediated regulation of dendritic spines are not completely defined.
+CXCR4	drug	opioid	31465771	Here, we will consolidate studies that describe the region specific synaptodendritic damage in the cerebral cortex of patients and animal models of HAND, describe the pathways by which <b>opioids</b> may contribute to cortical synaptodendritic damage, and discuss the prospects of using the <strong>CXCR4</strong> signaling pathway to identify new approaches to reverse dendritic spine deficits.
+CXCR4	drug	opioid	31465771	Additionally, we will discuss novel research questions that have emerged from recent studies of <strong>CXCR4</strong> and µ <b>opioid</b> actions in the cortex.
+CXCR4	drug	alcohol	31009094	The MIF axis, for example, MIF and MIF receptors invariant polypeptide of major histocompatibility complex, class II antigen associated (CD74), CXCR2, <strong>CXCR4</strong>, and CXCR7, was enhanced in the livers of <b>alcoholic</b> hepatitis (AH) patients as compared to healthy controls.
+CXCR4	drug	opioid	30249618	Dose response curves for <b>morphine</b>, maraviroc (a CCR5 antagonist), and AMD3100 (a <strong>CXCR4</strong> antagonist) alone were established.
+CXCR4	addiction	reward	29550625	The chemokine CXCL12 and its principal receptor target, <strong>CXCR4</strong>, are of particular interest because <strong>CXCR4</strong> activation enhances mesolimbic dopamine output that facilitates psychostimulant <b>reward</b>, <b>reinforcement</b>, and locomotor activation.
+CXCR4	drug	cocaine	29550625	Repeated <b>cocaine</b> enhances CXCL12 gene expression in the midbrain and produces conditioned place preference (CPP) that is inhibited by a <strong>CXCR4</strong> antagonist.
+CXCR4	addiction	reward	29550625	Repeated cocaine enhances CXCL12 gene expression in the midbrain and produces conditioned place preference (<b>CPP</b>) that is inhibited by a <strong>CXCR4</strong> antagonist.
+CXCR4	addiction	reward	29550625	We tested the hypothesis that an FDA approved <strong>CXCR4</strong> antagonist (AMD3100) inhibits MDPV induced <b>reward</b>, locomotor activation and positive affective state in rats using a triad of behavioral assays (<b>CPP</b>, open field, and 50 kHz ultrasonic vocalizations [USVs]).
+CXCR4	drug	cocaine	29550625	Our results identify the existence of chemokine/cathinone interactions and suggest the rewarding and stimulant effects of MDPV, similar to <b>cocaine</b>, require an active CXCL12/<strong>CXCR4</strong> system.
+CXCR4	addiction	intoxication	28481655	Compared to the low risk group, the <b>binge</b> group showed higher CCR5 expression on PMNs, decreases in the CD69 percentage and positive PMNs per microliter, and decreased <strong>CXCR4</strong> expression on monocytes.
+CXCR4	drug	cocaine	27575003	Chemokines and <b>cocaine</b>: <strong>CXCR4</strong> receptor antagonist AMD3100 attenuates <b>cocaine</b> place preference and locomotor stimulation in rats.
+CXCR4	drug	cocaine	27575003	To assess a role for the CXCL12/<strong>CXCR4</strong> system in behavioral effects of <b>cocaine</b>, we tested the hypothesis that AMD 3100 (Plerixafor), a <strong>CXCR4</strong> antagonist, would inhibit conditioned place preference (CPP) and locomotor activation produced by <b>cocaine</b>.
+CXCR4	addiction	reward	27575003	To assess a role for the CXCL12/<strong>CXCR4</strong> system in behavioral effects of cocaine, we tested the hypothesis that AMD 3100 (Plerixafor), a <strong>CXCR4</strong> antagonist, would inhibit conditioned place preference (<b>CPP</b>) and locomotor activation produced by cocaine.
+CXCR4	drug	cocaine	27575003	Our results suggest that the CXCL12/<strong>CXCR4</strong> system in the brain reward circuit is impacted by <b>cocaine</b> exposure and influences behavioral effects related to the abuse liability of <b>cocaine</b>.
+CXCR4	addiction	reward	27575003	Our results suggest that the CXCL12/<strong>CXCR4</strong> system in the brain <b>reward</b> circuit is impacted by cocaine exposure and influences behavioral effects related to the abuse liability of cocaine.
+CXCR4	addiction	intoxication	26151816	The <b>Binge</b> drinking group showed increased γGT together with increased expression of CD69 and reduced expression of TLR4, PD1, CCR2 and <strong>CXCR4</strong> in peripheral CD8 cells.
+CXCR4	drug	alcohol	26151816	PCA established 3 factors associated with <b>alcohol</b> consumption: "Early Activation" represented by CD69 and TLR4 expression in the CD8 population; "Effector Activation" by CD69 expression in CD8 CD127(+)CD137(+) and CD8 CD25(+) CD137(+); and Trafficking by <strong>CXCR4</strong> expression on total CD8 and CD8 GB(+)<strong>CXCR4</strong>(+), and CCR2 expression on total CD8.
+CXCR4	drug	alcohol	26151816	<b>Alcohol</b> consumption affects the immune phenotype of CD8 cells since binge drinking pattern was found to be associated with high CD69 and low TLR4, <strong>CXCR4</strong> and CCR2 expression, which suggest recent activation, decreased sensitivity to LPS and lower migration capacity in response to chemokines SDF 1 and MCP 1.
+CXCR4	addiction	intoxication	26151816	Alcohol consumption affects the immune phenotype of CD8 cells since <b>binge</b> drinking pattern was found to be associated with high CD69 and low TLR4, <strong>CXCR4</strong> and CCR2 expression, which suggest recent activation, decreased sensitivity to LPS and lower migration capacity in response to chemokines SDF 1 and MCP 1.
+CXCR4	drug	opioid	24401274	Previous studies indicated that μ <b>opioid</b> agonists specifically elevate neuronal levels of the protein ferritin heavy chain (FHC), which negatively regulates <strong>CXCR4</strong> signaling and affects the neuroprotective function of the CXCL12/<strong>CXCR4</strong> axis.
+CXCR4	drug	opioid	21465240	Levels of FHC as well as its effects on <strong>CXCR4</strong> activation increase in cortical neurons exposed to mu <b>opioid</b> receptor agonists such as <b>morphine</b>, an effect likely specific to neurons.
+CXCR4	drug	opioid	20627326	Disruption of neuronal <strong>CXCR4</strong> function by <b>opioids</b>: preliminary evidence of ferritin heavy chain as a potential etiological agent in neuroAIDS.
+CXCR4	addiction	relapse	20147779	The chemokine receptor <strong>CXCR4</strong> is emerging as an important target in cancer growth, metastasis, <b>relapse</b> and resistance to therapy.
+BEAN1	drug	alcohol	31898207	He was subsequently found to have some peculiar eating habits, including a fondness for <strong>bean</strong> curd and peanuts, and an aversion to <b>alcohol</b> and sweets.
+BEAN1	addiction	aversion	31898207	He was subsequently found to have some peculiar eating habits, including a fondness for <strong>bean</strong> curd and peanuts, and an <b>aversion</b> to alcohol and sweets.
+BEAN1	addiction	relapse	29320336	Chi square and ANOVA were used to compare <strong>bean</strong> health benefit knowledge, demographics, health risk factors, nutrition information <b>seeking</b>, and self efficacy by acculturation categories.
+BEAN1	drug	nicotine	29320336	Hispanic dominant and bicultural women reported significantly better health, higher <strong>bean</strong> consumption, and less cigarette <b>smoking</b> than English dominant women.
+BEAN1	addiction	reward	28774586	Utilization of chemically treated municipal solid waste (spent coffee <strong>bean</strong> powder) as <b>reinforcement</b> in cellulose matrix for packaging applications.
+BEAN1	drug	alcohol	27543189	In contrast, the dietary pattern rich in vegetables, fruits, and soya <strong>bean</strong> products, but low in animal foods, candied fruits, cakes, ice cream, sugared beverages, and <b>alcoholic</b> drinks is negatively associated with the prevalence of high depressive symptoms.
+BEAN1	drug	nicotine	26003578	Chasing the <strong>bean</strong>: prescription drug <b>smoking</b> among socially active youth.
+BEAN1	addiction	reward	20204549	Using histochemistry in combination with fluorescence microscopy we show that <strong>bean</strong> leaves from copper exposed plants displayed biochemical and structural modifications <b>reinforcing</b> the cell walls of their xylem tissues.
+BEAN1	drug	alcohol	11686489	This study examined the effects of 4 weeks of binge <b>ethanol</b> administration (<strong>BEAn</strong>) on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury.
+BEAN1	addiction	intoxication	11686489	This study examined the effects of 4 weeks of <b>binge</b> ethanol administration (<strong>BEAn</strong>) on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury.
+BEAN1	drug	alcohol	10517527	Both products, as well as a commercial sample of locust <strong>bean</strong> gum (LBG), were purified by precipitation in isopropyl <b>alcohol</b>.
+BEAN1	drug	nicotine	8811857	To investigate this problem, the expression of wild type and mutant alleles of the <strong>bean</strong> phytohemagglutinin (PHA) gene has been examined in <b>tobacco</b> cells and transgenic plants.
+BEAN1	addiction	sensitization	8521183	Factors related to the development of <b>sensitization</b> to green coffee and castor <strong>bean</strong> allergens among coffee workers.
+BEAN1	addiction	sensitization	8521183	Occupational allergic respiratory symptoms in coffee workers have been frequently reported, but the ultimate cause of <b>sensitization</b> is still debated, castor <strong>bean</strong> being considered besides green coffee beans.
+BEAN1	addiction	sensitization	8521183	This study was carried out to assess the prevalence of allergic respiratory symptoms and of <b>sensitization</b> to both green coffee beans and castor <strong>bean</strong> in the whole workforce of a coffee manufacturing plant.
+BEAN1	addiction	sensitization	8521183	The overall prevalence of skin <b>sensitization</b> was: 15% for green coffee beans, 22% for castor <strong>bean</strong>, 22% for common allergens.
+BEAN1	drug	nicotine	8521183	Our findings indicate that castor <strong>bean</strong> is the major cause of occupational sensitization among coffee workers, whereas <b>smoking</b> and atopy act as enhancing factors.
+BEAN1	addiction	sensitization	8521183	Our findings indicate that castor <strong>bean</strong> is the major cause of occupational <b>sensitization</b> among coffee workers, whereas smoking and atopy act as enhancing factors.
+BEAN1	drug	nicotine	1740436	In basic chitinases from dicotyledonous plants such as Arabidopsis thaliana, Phaseolis vulgaris (<strong>bean</strong>), Nicotiana tabacum (<b>tobacco</b>), and Solanum tuberosum (potato), as well as in the chitinase isolated from the monocotyledonous plant Hordeum vulgare (barley), this position is invariably occupied by a tyrosine.